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• No gender predilection: ~2/3 of malignant pleural effusions occur in women.Platelet-rich plasma efficacy versus corticosteroid injection treatment for chronic severe plantar fasciitis. Foot Ankle Int. 2014;35(4):313–318. • Peterlein CD, Funk JF, Hölscher A, et al. Is botulinum toxin A effective for the treatment of plantar fasciitis? Clin J Pain. 2012;28(6):527–533. SEE ALSO Algorithm: Heel Pain CODES ICD10 M72.2 Plantar fascial fibromatosis CLINICAL PEARLS • Plantar fasciitis occurs due to degeneration of plantar fascia at origin (medial calcaneal tuberosity) with characteristic pattern of pain. • Pain with weight bearing (especially first few steps in the morning or after prolonged rest) is hallmark presentation. • Conservative treatment is preferred. Supportive footwear helps avoid excess pronation and provides adequate cushion. Modify activity, stretch plantar fascia, ice (water bottle roll), massage (golf ball roll), and provide arch support. • Weight loss helps control symptoms, particularly for BMI ≥25. PLEURAL EFFUSION Felix B. Chang, MD, DABMA, FAAMA BASICS Abnormal accumulation of fluid in the pleural space DESCRIPTION Types: transudate, exudate • Congestive heart failure: 40%: transudate • Pneumonia 25%, malignancy 15%, and pulmonary embolism (PE) 10% account for exudative effusions • Malignant: lung cancer and metastases of breast, ovary, and lymphoma EPIDEMIOLOGY Incidence Estimated 1.5 million cases/year in the United States; CHF: 500,000; pneumonia: 300,000; malignancy: 150,000; PE: 150,000; cirrhosis: 150,000; TB: 2,500; pancreatitis: 20,000; collagen vascular disease: 6,000 Prevalence • Estimated 320 cases/100,000 people in industrialized countries; in hospitalized patients with AIDS, prevalence is 7–27%. • No gender predilection: ~2/3 of malignant pleural effusions occur in women.• Transudates result from imbalances in hydrostatic and oncotic forces.– Increase in hydrostatic and/or low oncotic pressures; increase in pleural capillary permeability; lymphatic obstruction or impaired drainage; movement of fluid from the peritoneal or retroperitoneal space • Transudates – CHF: 40% of transudative effusions; 80% bilateral.

Analogous to their favorable and detrimental roles in inflammation, increasing evidence suggests that TLRs act as a double-edged sword in cancer cells too, pointing to a dual function of TLRs as anti- and pro-tumor modulators (Basith _et al._ , 2012).The nature of RIG-I and MDA5 interactions with adaptor proteins on the peroxisome is not yet fully understood and is therefore depicted with a '?'. IRF3 and IRF7 translocate to the nucleus and initiate transcription of type 1 IFN (4). The TF NF-κB is also activated by RIG-I-MAVS interaction, ultimately leading to transcription of a number of pro-inflammatory cytokines. Combinatorial sensing of diverse ligands can result in simultaneous or sequential activation of multiple pathways, which may be important for generating a tailored, specific response to a potential pathogen. Activation of TLRs on antigen-presenting cells such as macrophages, DCs and B cells, strongly influences the development of adaptive immune responses by controlling several essential processes such as the upregulation of co-stimulatory or accessory molecules like CD80 and CD86, enhancement of antigen presentation, B-cell proliferation and maturation, activation of T cells, and suppression of regulatory T cell activity (Iwasaki and Medzhitov, 2010), thereby mediating effective host defense to a wide range of pathogens. However, an unchecked TLR-induced inflammatory response can be deleterious to the host resulting in a variety of immune disorders. TLRs are implicated in the pathogenesis of autoimmune diseases, such as SLE, rheumatoid arthritis, atherosclerosis, hepatitis, diabetes, kidney disease, and certain other disorders (Li _et al._ , 2009). Recent studies have shown that functional TLRs are expressed not only on immune cells, but also on cancer cells, implicating a role of TLRs in tumor biology. Analogous to their favorable and detrimental roles in inflammation, increasing evidence suggests that TLRs act as a double-edged sword in cancer cells too, pointing to a dual function of TLRs as anti- and pro-tumor modulators (Basith _et al._ , 2012).Thus, apart from their protective role against various pathogens, the involvement of TLRs in autoimmune diseases and tumorigenesis indicates the need for further studies to delve into the potential of targeting TLR signaling for therapeutic benefit under these conditions.

This produces multiple QRS morphologies.Used with permission._ Multiform ventricular couplet comes from two or more ventricular ectopic foci._Rhythm strip provided by Riley Hospital for Children.Used with permission._ AJR occurs when the AV junctional pacemaker rate exceeds the rate of the sinus node. AJR heart rates range between 60 and 100 bpm. Sinus bradycardia follows this AJR. Rhythm | Regular (AJR) | Regular (bradycardia) ---|---|--- Rate | 94 | 56 bpm P waves | Not visible | Wide and upright LAE PRI | Unable to determine | 220 ms first-degree AV block QRS | 144 ms | QT/QTc | 458/425 ms | 66Junctional Tachycardia (JT) Rhythm Strip 6.16 Junctional tachycardia (1-week-old). _Rhythm strip provided by Riley Hospital for Children. Used with permission._ Junctional tachycardia has a heart rate of over 100 bpm. This tracing has no P waves seen, has a narrow QRS, and is over 100 bpm. Rhythm | Regular ---|--- Rate | 150 bpm P waves | Not visible PRI | Unable to determine QRS | 64 ms QT/QTc | 254/401 ms 67Premature Ventricular Complexes/Contractions (PVC) Rhythm Strip 6.17 Premature ventricular contractions. _Rhythm strip provided by Riley Hospital for Children. Used with permission._ Premature ventricular contractions (PVCs) are characterized by a premature, wide QRS complex followed frequently (but not always) by a T wave that points in the opposite direction of the normal beat for the patient. These PVCs are in bigeminal and trigeminal patterns. Rhythm | Irregular (for frequency of PVC events, see Chapter 4) ---|--- Rate | 110 bpm P waves | Normal and upright PRI | 136 ms QRS | 66 ms QT/QTc | 336/454 ms 68Multiform Ventricular Couplet Rhythm Strip 6.18 Multiform ventricular couplet. _Rhythm strip provided by Riley Hospital for Children. Used with permission._ Multiform ventricular couplet comes from two or more ventricular ectopic foci. This produces multiple QRS morphologies._Rhythm strip provided by Riley Hospital for Children.Used with permission._ Ventricular tachycardia (VT) originates in the ventricles and produces a regular rhythm of at least three PVCs or more.VT has a rate of >100 bpm.This VT has a regular rhythm of 10 uniform PVCs.The other PVCs are called isolated uniform PVCs.They are located singularly and have the same morphology.

A tourniquet is placed around the upper thigh of the affected side.77.5).The patient is placed in a supine position with a folded sheet under the ipsilateral buttock which causes a slight elevation and endorotation (Fig.Arthroscopic treatment of ankle instability cannot be performed with joint distraction, since distraction prevents adequate visualization of the fibula tip and ATFL. Distraction counteracts tightening of the ATFL. When the ankle joint is distracted, the anterior neurovascular structures are more at risk for iatrogenic damage with introduction of instruments [12, 13]. Fig. 77.1 Placement of noninvasive ankle distraction device. The device is attached to a belt around the surgeon's waist Fig. 77.2 By leaning against the foot sole of the involved foot, the ankle is brought into dorsiflexion, thereby creating an anterior working space (see also Fig. 77.3c) Fig. 77.3 Ankle joint with distraction (a), in neutral position (b) and in dorsiflexion (c) The increased working area in dorsiflexion allows the surgeon to use a larger-diameter arthroscope which gives the advantage of an increased inflow of saline, thus allowing the use of a large-diameter shaver (Figs. 77.3c and 77.4). Fig. 77.4 (a) Anterior view in a right ankle without distraction. Inspection of the complete anterior joint compartment is thus possible. (b) Distraction creates intra-articular workspace. Distraction is only needed in case of treatment of symptomatic osteochondral lesions ## 77.3 Dorsiflexion Method: General Setup Anterior ankle arthroscopy is performed as outpatient surgery under general anesthesia or spinal anesthesia. The patient is placed in a supine position with a folded sheet under the ipsilateral buttock which causes a slight elevation and endorotation (Fig. 77.5). A tourniquet is placed around the upper thigh of the affected side.Fig.77.5 Routine supine position for anterior ankle arthroscopy ## 77.4 Instruments For anterior ankle arthroscopy, a 4.0 mm ankle arthroscope can be used.An alternative is a 12 cm long 2.7 mm scoop with a 4.6 mm high volume sheath.A large-diameter arthroscope sheath can irrigate a larger amount of fluid per time which is beneficial when large-sized motorized instruments are used.

When asked to oppose the index finger to the thumb in a tapping motion, patients often start with reasonably fast, large-amplitude movements, but the speed and amplitude then rapidly decrease and the movement fades away.There is a particular difficulty with sequential and concurrent self-paced movements."26 Voluntary movements tend to be of low amplitude and to show increased fatigability.PD also involves the ascending serotonergic, noradrenergic, and cholinergic projections to the cortex and basal ganglia.22 Clinicopathologic studies have demonstrated that coexisting neuropathology within the striatum and in other areas of the brain is extremely common in older subjects with histologically confirmed PD.23 Braak and colleagues have proposed that the primary degenerative process in PD, based on the assumption that the presence of Lewy bodies indicates neuronal loss, begins not in the substantia nigra but in the olfactory tracts, lower brainstem, and enteric nervous tissue.24 This model fits well with the increasing recognition that rapid eye movement (REM) sleep disorders, hyposmia, and constipation may precede the motor symptoms of PD by several years. The proposed pattern of disease progression also indicates the potential for interaction with environmental agents via the olfactory system and gut. #### Motor Features Akinesia is the central motor abnormality in PD that refers to a lack of spontaneous voluntary movement, slowness of movement (bradykinesia), and faulty execution of movement.25 Marsden brilliantly described akinesia as the "failure to execute automatic learned motor plans. "26 Voluntary movements tend to be of low amplitude and to show increased fatigability. There is a particular difficulty with sequential and concurrent self-paced movements. When asked to oppose the index finger to the thumb in a tapping motion, patients often start with reasonably fast, large-amplitude movements, but the speed and amplitude then rapidly decrease and the movement fades away.Older patients often find bedside tests for akinesia difficult to execute and may perform poorly because of cognitive impairment, painful arthritis, restricted joint range, and muscle weakness.Action tremor from any cause can interfere with the quality of normal hand and finger movements, and this can make the assessment of akinesia difficult in the presence of essential or dystonic tremor.

## Psychiatric Work-Related Disability Evaluation This is a formal report format for the evaluation of an individual who is believed to be unable to work due to psychiatric disability.Recommendations.14.Summary.13.Significant Test Results.12.Referral Source: Should include who will have access to the report and if the evaluator is to review the report with the patient once completed or is the patient directed to another clinical source for a review of the report upon completion. 7. Reason for Referral: To gain a deeper more complete understanding of a presenting problem(s). It may not be an overly complex clinical issue, just a desire for additional information to aid in refining the best fit of intervention for evidence-based practice. 8. Identifying Information: Age, marital status, children, occupation, etc. 9. Relevant Background Information (historical and of current problem): A. Psychological/psychiatric history (personal/family) medical history, i.e., significant illnesses, injuries, hospitalizations and dates (personal/family). B. Personal history: family history, brief description of childhood, adolescence, early adulthood. C. Legal history: history of arrests and convictions, if any, including current status. D. Military history: age at the onset of military career, dates, duration, and geographic locations of all deployments as well as occupation and rank during each circumstance of discharge and date. E. Lifetime history of stressful events (if applicable). A brief documentation of stressful events reported by the patient. Indicate date, geographic location, the circumstances surrounding each, and the emotional response reported by the patient. 10. Behavioral Observations and Mental Status. 11. Assessment Validity: Provide a description of the validity of the assessment results (i.e., coherence, internal validity, symptom validity, symptom exaggeration/minimization, etc.). 12. Significant Test Results. 13. Summary. 14. Recommendations. ## Psychiatric Work-Related Disability Evaluation This is a formal report format for the evaluation of an individual who is believed to be unable to work due to psychiatric disability.According to Taiwo, Cantley, and Schroeder (2008), approximately 10.9 million people are not able to work and approximately 8.1 million people require some form of accommodation in the amount or type of work they can perform as a result of a chronic health condition.

The response to naloxone and the presence of reflex eye movements (see later) assist in distinguishing these.Even smaller reactive pupils (<1 mm) characterize narcotic or barbiturate overdoses but also occur with extensive pontine hemorrhage.Reactive and round pupils of midsize (2.5–5 mm) essentially exclude midbrain damage, either primary or secondary to compression. A response to light may be difficult to appreciate in pupils <2 mm in diameter, and bright room lighting mutes pupillary reactivity. One enlarged and poorly reactive pupil (>6 mm) signifies compression or stretching of the third nerve from the effects of a cerebral mass above. Enlargement of the pupil contralateral to a hemispheral mass may occur but is infrequent. An oval and slightly eccentric pupil is a transitional sign that accompanies early midbrain–third nerve compression. The most extreme pupillary sign, bilaterally dilated and unreactive pupils, indicates severe midbrain damage, usually from compression by a supratentorial mass. Ingestion of drugs with anticholinergic activity, the use of mydriatic eye drops, and direct ocular trauma are among the causes of misleading pupillary enlargement. Unilateral miosis in coma has been attributed to dysfunction of sympathetic efferents originating in the posterior hypothalamus and descending in the tegmentum of the brainstem to the cervical cord. It is therefore of limited localizing value but is an occasional finding in patients with a large cerebral hemorrhage that affects the thalamus. Reactive and bilaterally small (1–2.5 mm) but not pinpoint pupils are seen in metabolic encephalopathies or in deep bilateral hemispheral lesions such as hydrocephalus or thalamic hemorrhage. Even smaller reactive pupils (<1 mm) characterize narcotic or barbiturate overdoses but also occur with extensive pontine hemorrhage. The response to naloxone and the presence of reflex eye movements (see later) assist in distinguishing these.Lid tone, tested by lifting the eyelids and noting their resistance to opening and the speed of closure, is progressively reduced as unresponsiveness progresses.Horizontal divergence of the eyes at rest is normal in drowsiness.As coma deepens, the ocular axes may become parallel again.Spontaneous eye movements in coma often take the form of conjugate horizontal roving.

A final note about this popular drug concerns its frequent dance partner: alcohol.When the drug is withdrawn these adaptive changes are no longer needed and lead to physical and emotional symptoms of withdrawal within a few hours.Some of these effects have led to the idea that a nicotine patch might be used to treat cognitive decline in the elderly—the drug can improve some aspects of attention and memory—but the unlikelihood of being able to take anything long term without incurring compensatory adaptations, or substantial side effects, has so far kept these out of the clinic. It is notoriously hard to quit smoking, a combination of habits being hard to change and nicotine's particular form of withdrawal. After chronic exposure, withdrawal produces a profound syndrome of craving characterized by irritability, anxiety, attention deficits, trouble sleeping, and increased appetite. The reason for this, of course, is the _b process,_ which in smokers is largely accounted for by an upregulation of nAChRs. Usually we think that a drug that acts as an agonist by stimulating receptors as nicotine does would produce a downregulation. Why should activating a receptor cause it to become more sensitive and more numerous? Though at first it may seem contrary, recall that nicotine's long-lasting presence results mostly in nAChR desensitization, and the homeostatic response to desensitized receptors is upregulation. So what is the effect of all those extra-sensitive nicotinic receptors? Because nAChRs affect the release of virtually every major transmitter, neuro-adaptations from chronic exposure lead to widespread and general alterations in neurotransmission throughout the brain. Many neurotransmitters that are regulated by acetylcholine transmission such as glutamate, GABA, dopamine, and opioids have their activity altered by the changes in acetylcholine signaling, and all of this adjustment combines to produce the experience of dependence. When the drug is withdrawn these adaptive changes are no longer needed and lead to physical and emotional symptoms of withdrawal within a few hours. A final note about this popular drug concerns its frequent dance partner: alcohol.There are several hypotheses, each of which may explain part of the relationship.For one, any drug that stimulates dopamine greases the rails for another.Because they are both addictive, they can also serve as reminders of addiction, and especially when smoking was okay in bars, the contextual cues were largely overlapping.

Administration of aminophylline (A.d) or 5-HT (A.e) following 4 h IMZ also induced profound membrane damage and edema.Perivascular edema (arrowheads), membrane damage (arrows) and vacuolation (*) are quite common in these drug treated rats.; A.c) did not prevent IMZ induced cell changes.However, treatment with 5,7-DHT (i.c.v., A.b) or 6-OHDA (i.c.v.These observations are the first to suggest that early neutralization of TNF-α is injurious to the brain [111, 179]. This indicates that the TNF-α has a dual role in inducing BBB disruption and brain pathology (results not shown). Taken together it appears that a reduction in the BBB or BSCB disruptions induced by antibodies appears to be largely responsible for neuroprotection following stress induced brain damage. ### 9.11.2 Neurochemical Synthesis Inhibitors Reduce BBB Permeability and Brain Pathology The neurochemical mediators such as serotonin or prostaglandins are known to induce BBB disruption and brain damage [10, 12, 13, 23, 25, 26, 73, 74, 151, 180–182]. Thus, it is likely that inhibition of prostaglandin or serotonin synthesis prior to CNS insults in stress is neuroprotective (Fig. 9.15). Weused p-chlorophenylalanine (p-CPA) and indomethacin to inhibit serotonin and prostaglandin synthesis, respectively in separate groups of rats [2–14, 22–28, 150, 151, 181–190] and then subjected them to different stressful situations (see Table 9.6). In these animals, the BBB permeability in relation to neural injuries was determined [12, 13, 25, 26, 185]. Fig. 9.15 Ultrastructural changes in the brain at the time of the BBB permeability in stress and neuroprotection by various agents. Ultratstructural changes in stress and their modification with drugs. (A) Pretreatment with p-CPA markedly attenuated cell damage following 8 h immobilization (IMZ) stress (A.a). However, treatment with 5,7-DHT (i.c.v., A.b) or 6-OHDA (i.c.v. ; A.c) did not prevent IMZ induced cell changes. Perivascular edema (arrowheads), membrane damage (arrows) and vacuolation (*) are quite common in these drug treated rats. Administration of aminophylline (A.d) or 5-HT (A.e) following 4 h IMZ also induced profound membrane damage and edema.Pretreatment with 6-OHDA (i.c.v., B.b) did not reduce cell damage following HS.On the other hand, heat adapted (HA) rats either reared at high environmental temperature (B. g, h) or chronically exposed to heat stress for 7 days (B. i, j) when subjected to HS did not show any cell damage.

This is especially true if the antibiotic is given for the wrong reason or for too long a period of time.If antibiotics are given to babies or young children this can also set the scene for adverse reactions to foods.It is unlikely that one single course of antibiotics will cause too much trouble, but repeated courses almost certainly will cause some digestive imbalance or other.**Relevant Tests: Stool Analysis (Comprehensive Parasitology)** The best method of testing for parasites is with a stool sample, or two, which are analysed by powerful microscopy. This should be accompanied by appropriate antibody testing, which means the lab also looks for whether your body is making antibodies to the bugs. This increases the tests' accuracy by about 40 per cent. The test that IWDL offer is one of the best and most accurate in the world (see Resources). ### A Note about Unwelcome Bacteria **Since the signs and symptoms of unwelcome bacteria such as _Proteus_ species, _Klebsiella pneumoniae, Citrobacter freundii_ and _Pseudomonas aeruginosa_ are identical to those of parasites or yeast overgrowth, there is no specific questionnaire to help identify the presence of these. Your answers to the yeast and parasite questionnaires should give you the course of action that will help you address these. ** # [8 Prescription and Over-the-Counter Drugs](003-toc.html#ch08) #### Antibiotics Since antibiotics alter the bowel bacteria and inhibit probiotics, they can affect functions within the intestinal lining, lowering intestinal immunity and paving the way for the growth of unwanted bacteria. These can further deplete intestinal immunity and increase the risk of leaky gut syndrome. It is unlikely that one single course of antibiotics will cause too much trouble, but repeated courses almost certainly will cause some digestive imbalance or other. If antibiotics are given to babies or young children this can also set the scene for adverse reactions to foods. This is especially true if the antibiotic is given for the wrong reason or for too long a period of time.This diminishes the friendly bacteria and further increases the likelihood that the young child will develop other intolerances.Antibiotics are also well known for permitting the growth of yeast in the colon.This is because antibiotics inhibit the growth of bacteria but do not have any impact on yeast, which is a different kind of microbe.

Commonly used devices are the following: 1.The disk space is usually filled with allograft bone blocks or fusion cages [1].A posterior approach is often preferred in the lumbar spine because the pedicle screws and rods or plates can be placed before dural retraction and dissection of the intervertebral disk, restoring normal disk height and decompressing the neural foramina.Imaging plays a crucial role in the assessment of the postoperative spine, and adequate evaluation of spinal hardware necessitates a detailed understanding of the initial spinal pathologic condition, the surgical procedure performed, the clinical presentation of the patient, and the time interval from the surgery to the imaging study. Imaging is essential in identifying the location and integrity of surgical implants, in evaluating the success of decompression procedures, in delineating fusion status, and in identifying postoperative complications. Keywords Postoperative spineArthrodesisSurgical complicationsComputed tomographyMagnetic resonance imaging ## Background Spinal fusion surgeries are performed for a wide spectrum of indications (i.e., deformities, trauma, infections, and tumors) to restore anatomic alignment and functional biomechanics [1]. In spinal fusion surgeries, surgical implants are used to stabilize the spine, replace resected components, and maintain anatomic alignment during the period osseous fusion occurs [2, 3]. Metallic hardware always serves a temporary purpose, allowing bone fusion to occur. The surgical approach to spinal fusion can be anterior, posterior, or lateral [3]. The anterior approach is preferred in the cervical spine because of the risk of cord injury. A posterior approach is often preferred in the lumbar spine because the pedicle screws and rods or plates can be placed before dural retraction and dissection of the intervertebral disk, restoring normal disk height and decompressing the neural foramina. The disk space is usually filled with allograft bone blocks or fusion cages [1]. Commonly used devices are the following: 1.Rods and transpedicular screws are usually attached to the vertebral bodies in the thoracic and lumbar spine.Lateral mass screws and other screws tend to be used in the cervical spine [2, 4].2.Translaminar or facet screws: These devices can be used when posterior elements are intact to attach the laminae of two adjacent vertebrae [2].3.

Despite three decades of physicians using beta-blockers for hypertension, the authors of the state-of-the-art paper noted that no study has shown that beta-blocker therapy reduces death in hypertensive patients, even when compared with placebos.The latest review of the evidence was presented in a 2007 issue of the _Journal of the American College of Cardiology_.The hormone angiotensin can affect cell survival and angiogenesis (formation of new blood vessels), two important factors in tumor growth. The issue here is the concern that these medications may promote the growth of blood vessels that could enable the growth of tumors and cancers. To determine whether taking ARBs affects cancer risk, scientists performed a meta-analysis of several studies. They determined that ARBs carry a significantly increased risk of a new diagnosis of any cancer (8 percent) and a seriously higher risk of lung cancer (25 percent). The study also revealed increased rates of sudden cardiac death, death from heart attack, and death from stroke in the subjects taking an ARB compared to those taking placebos in two studies; this data is still being reviewed by the FDA. Consider another blood pressure drug class: beta-blockers. In the large POISE (Perioperative Ischemic Evaluation) trial, conducted in twenty-three countries, all 8,351 enrolled patients were randomized to either metoprolol (a common beta-blocker) or a placebo. After thirty days, overall mortality (death) was higher in the group treated with the beta-blocker—3.1 percent vs. 2.3 percent—and the drug-treated group had almost double the incidence of stroke. Additional analyses did not identify any subgroup that benefited from metoprolol. The artificially lowered blood pressure had clear risks; the drugs caused more harm than good. In fact, there is no data to suggest that these drugs prevent heart attacks in healthy people with only mildly elevated blood pressure. The latest review of the evidence was presented in a 2007 issue of the _Journal of the American College of Cardiology_. Despite three decades of physicians using beta-blockers for hypertension, the authors of the state-of-the-art paper noted that no study has shown that beta-blocker therapy reduces death in hypertensive patients, even when compared with placebos.The liberal use of medications in an attempt to reduce the effects of our toxic diet-style has its own set of unique risks, as these research findings suggest.Medications to lower blood pressure also cause fatigue, lightheadedness, and loss of balance.

## Bemigride A central nervous system stimulant; may be used to counter barbiturate poisoning.Some ewes require CAESAREAN SECTION.The rams weigh about 90 kg (198 lb) and the ewes 70 kg (154 lb).They are polled and have no wool on the head or feet.The breed entered Britain in 1989.Megestrol (Ovarid) may be useful where the behavioural problem is hormonally triggered (spraying, aggression); or tranquillising drugs may be prescribed. ## Belgian Blue Cattle A beef breed noted for exceptional double hindquarter muscling. The British name is a misnomer, and it is now called BRITISH BLUE. DYSTOKIA may be a problem, in pure breeds and ones with Blue blood in them, partly due to a relatively narrow pelvis. Problems are much less in dairy type cattle, e.g. Holsteins. Maiden heifers should not become pregnant to a Belgian Blue bull or cows that have previously had dystokia after mating with Blue bulls. ## Belgian Shepherd Dog It is a breed in which cataract can be inherited as a dominant trait. Hip dysplasia is multifactorial while in the Tervueren form of the breed, epilepsy may be inherited by an unknown mechanism. ## Belladonna Belladonna is another name for the deadly night-shade flower (Atropa belladonna). (See ATROPINE.) ## Belted Galloway Cattle A beef breed, often called 'Belties', it is a variety of Galloway with a distinctive wide white strip around the abdomen in both black and dun animals. They are often slightly smaller and more dairy-like than the main beef breed type. (See GALLOWAY CATTLE.) ## Beltex Sheep A portmanteau name of Belgium and Texel; it is an offshoot of the Texel, with double muscling, used as a terminal sire for meat production. The breed entered Britain in 1989. They are polled and have no wool on the head or feet. The rams weigh about 90 kg (198 lb) and the ewes 70 kg (154 lb). Some ewes require CAESAREAN SECTION. ## Bemigride A central nervous system stimulant; may be used to counter barbiturate poisoning.(See ANTIHISTAMINES.## Benazepril A medicine for congestive heart failure in dogs and chronic renal insufficiency in cats.It is rapidly absorbed from the intestinal tract and forms benazeprilat which is a potent inhibitor of angio-tensin converting enzyme reducing the conversion of angiotensin I to angiotensin II.

_Diagrams the chain of events that are initiated by the arterial baroreceptor reflex to compensate for a change in arterial pressure_._Describes how the sympathetic and parasympathetic outputs from the medullary cardiovascular centers change in response to changes in arterial pressure_.an increased mean circulatory filling pressure_ _c. an increased central venous pressure_ _d. distended jugular veins_ _e. decreased cardiac output_ _8–7. If you gave a blood transfusion to a patient who had recently experienced a severe hemorrhage, you would expect_ _a. to expand arterial volume_ _b. to expand venous volume_ _c. to decrease central venous pressure_ _d. to decrease the mean circulatory filling pressure_ _e. to reduce cardiac output_ _8–8. Which of the following would directly (by themselves in the absence of any compensatory responses) tend to_ decrease _central venous (cardiac filling) pressure?_ _a. increased sympathetic nerve activity to only the heart_ _b. increased parasympathetic nerve activity to only the heart_ _c. increased blood volume_ _d. decreased total peripheral resistance_ _e. immersion in water up to the waist_ ## **9 Regulation of Arterial Pressure** * * * ### **OBJECTIVES** _The student understands the mechanisms involved in the short-term regulation of arterial pressure:_ _Identifies the sensory receptors, afferent pathways, central integrating centers, efferent pathways, and effector organs that participate in the arterial baroreceptor reflex_. _States the location of the arterial baroreceptors and describes their operation_. _Describes how changes in the afferent input from arterial baroreceptors influence the activity of the sympathetic and parasympathetic preganglionic fibers_. _Describes how the sympathetic and parasympathetic outputs from the medullary cardiovascular centers change in response to changes in arterial pressure_. _Diagrams the chain of events that are initiated by the arterial baroreceptor reflex to compensate for a change in arterial pressure_._Describes and indicates the mechanisms involved in the Bezold–Jarisch reflex, the cerebral ischemic response, the Cushing reflex, the alerting reaction, blushing, vasovagal syncope, the dive reflex, and the cardiovascular responses to emotion and pain_.

The number of mitotic figures is variable, but atypical mitoses may be found (Figure 4.16D).The nuclei are large and chromatic, with prominent nucleoli, and display moderate pleomorphism.The neoplastic cells have intracytoplasmic lipid vacuoles, but the degree of lipidization varies from cell to cell.##### Growth and metastasis Local infiltration is most often found with sebaceous epitheliomas so recurrence occurs with incompletely excised neoplasms but metastases are rarely found. In cases that metastasize, the primary neoplasms are most often on the head and metastasis is via lymphatics to mandibular lymph nodes. #### Sebaceous carcinoma This is a malignant neoplasm with cells showing sebaceous differentiation. ##### Incidence, age, breed, and sex Sebaceous carcinomas are uncommon in dogs and cats and rare in other species. In dogs the peak incidence is between 10 and 13 years of age. Breeds at increased risk are cavalier King Charles spaniel (6.6), cocker spaniel (4.8), Siberian husky (4.4), Samoyed (3.2), and West Highland white terrier (2.4). No sex predilection has been noted. In cats the peak incidence is between 8 and 15 years of age. No breed or sex predilection has been noted. ##### Sites and gross morphology Sebaceous carcinomas arise primarily on the head (39%) and neck (11%) in dogs and on the head, thorax, and perineum in cats. The neoplasms are similar on gross examination and cut section to sebaceous adenoma and epithelioma. A multilobulated intradermal mass is the most common finding. ##### Histological features The neoplasm is subdivided by fibrovascular connective tissue trabeculae into lobules of varying size. The neoplastic cells have intracytoplasmic lipid vacuoles, but the degree of lipidization varies from cell to cell. The nuclei are large and chromatic, with prominent nucleoli, and display moderate pleomorphism. The number of mitotic figures is variable, but atypical mitoses may be found (Figure 4.16D).The multilobulated appearance of the neoplasm allows it to be differentiated from a liposarcoma.Differentiation from a sebaceous adenoma is based on cells with greater cellular and nuclear pleomorphism, mitoses in sebocytes and on rare occasions infiltration of peripheral lymphatics.##### Growth and metastasis Local infiltration is most often found with sebaceous carcinomas.

Whether this is the result of blood group incompatibility between the mother and fetus is still open to debate1.**Blood Group Links** There is an association with blood group O women and the risk of toxemia of pregnancy and subsequent loss of the fetus.Toxemia of pregnancy is also known as pre-eclampsia or eclampsia, depending on its severity.Clinical and subclinical thyroid disorders associated with pernicious anemia. Observations on abnormal thyroid-stimulating hormone levels and on a possible association of blood group O with hyperthyroidism. _Arch Intern Med._ 1982;142:1465-1469. **TOOTH DECAY** – _SeeDental caries_ **TOXEMIA, PREGNANCY** – _Dangerous hypertension during the final weeks of pregnancy._ **Symptoms** ■ Elevated blood pressure on two blood pressure readings, 6 hours apart ■ Edema ■ Rapid excessive weight gain ■ Gastric pain ■ Headache ■ Visual disturbance ■ Apprehension **About Toxemia of Pregnancy** Toxemia is a disorder of pregnant women that is characterized by elevated blood pressure, swelling of the feet and hands, and loss of protein in the urine. It occurs in the third trimester, usually after the 20th week of gestation. The cause of toxemia is not known. It is more common in women who are carrying twins, who have high blood pressure before pregnancy, and who are pregnant for the first time. Toxemia is also more common in women 35 years of age and older. If severe, toxemia of pregnancy may progress to serious problems for both mother and child—including MISCARRIAGE. Toxemia of pregnancy is also known as pre-eclampsia or eclampsia, depending on its severity. **Blood Group Links** There is an association with blood group O women and the risk of toxemia of pregnancy and subsequent loss of the fetus. Whether this is the result of blood group incompatibility between the mother and fetus is still open to debate1.Liver Support Protocol 2.Detoxification Protocol **BLOOD GROUP B:** 1.Liver Support Protocol 2.Detoxification Protocol **BLOOD GROUP AB:** 1.Liver Support Protocol 2.Detoxification Protocol **BLOOD GROUP O:** 1.Liver Support Protocol 2.Detoxification Protocol **Related Topics** Cardiovascular disease Infertility Insulin resistance Obesity REFERENCES 1.

• Procedures requiring prophylaxis – Oral/upper respiratory tract: any manipulation of gingival tissue or periapical region of teeth or perforation of the oral mucosa (1)[B]; invasive respiratory procedures involving incision; or biopsy of the respiratory mucosa merit prophylaxis. Amoxicillin 2 g PO (if penicillin allergic, clindamycin 600 mg PO) 30 to 60 minutes before procedure or ampicillin 2 g IV/IM are first-line prophylactic choices. For penicillin-allergic patients, use clindamycin 600 mg IV, or cephalexin 2 g PO, or azithromycin/clarithromycin 500 mg PO, or cefazolin/ceftriaxone 1 g IV/IM 30 minutes before procedure. Pediatric doses are amoxicillin 50 mg/kg PO (max 2 g), cephalexin 50 mg/kg PO (max 2 g), clindamycin 20 mg/kg PO (max 600 mg), and ampicillin or ceftriaxone 50 mg/kg (maximum 1 g) IM/IV. – GI/GU: Only consider coverage for Enterococcus (with penicillin, ampicillin, piperacillin, or vancomycin) for patients with an established infection undergoing procedures (1)[B]. – Cardiac valvular surgery or placement of prosthetic intracardiac/intravascular materials: perioperative cefazolin 1 to 2 g IV 30 minutes preop or vancomycin 15 mg/kg (maximum 1 g) (penicillin-allergic patients) 60 minutes preop (1)[B] – Skin: incision and drainage of infected tissue; use agents active against skin pathogens (e.g., cefazolin 1 to 2 g IV q8h or vancomycin 15 mg/kg q12h; max 1 g) if penicillin allergic or if methicillin-resistant Staphylococcus aureus (MRSA) suspected.Signs of heart failure (rales, edema) if valve function is compromised.

After three to five days, the titrating formula for increasing the evening injection if the fasting/waking glucose is still not ideal is as follows: • If glucose is higher than 180 mg/dL, increase by 4–8 units.Ideally it's lower than 90 mg/dL, but starting out at lower than 110 mg/dL is acceptable to prevent lows in a patient just getting used to using insulin.• Complications are developing or they are at risk of developing due to elevated glucose and A1C. • They have acute onset of severe T2DM with high glucose numbers and high A1C. It is always best to start at a lower starting dose of basal insulin and then titrate up. Avoiding a hypoglycemic reaction is best to earn a patient's trust and faith. The typical way of starting basal insulin in patients with T2DM is to start with one shot of basal at bedtime, using either a syringe and vial or a pen. There are two dosing methodologies: • Start with 10 units—a typical starting dose. • Body weight starting dose—0.15–0.2 units per kilogram of body weight. For example, if you weigh 200 pounds (approximately 91 kg): 91 × 0.15 = 13.65. So, 13 units would be your starting dose. Unless your patient weighs less than 150 pounds, injecting 10 units will always be less than when calculating based on body weight. If your patient weighs 150 pounds and has T2DM, then use the body weight formula. However, since most T2DM patients (who are not mistakenly LADA) are overweight, starting with 10 units is a typical methodology. Once the starting dose is decided, and the patient knows the proper way to inject, she must wait three to five days to see how low her fasting glucose levels go before raising her evening basal insulin dose. I usually wait four days. It takes basal insulin a few days to get settled in the body and start having a consistent effect on fasting glucose; patients can notice day by day that their fasting glucose is lowering. The target fasting glucose is lower than 100 mg/dL. Ideally it's lower than 90 mg/dL, but starting out at lower than 110 mg/dL is acceptable to prevent lows in a patient just getting used to using insulin. After three to five days, the titrating formula for increasing the evening injection if the fasting/waking glucose is still not ideal is as follows: • If glucose is higher than 180 mg/dL, increase by 4–8 units.• If glucose is 120–140 mg/dL, increase by 2–4 units.• If glucose is 110–120 mg/dL, increase by 1–2 units.I usually increase by the lowest amount, to be safe, so if it says 2–6 units, I'll usually recommend my patient go up just 2 units.It is better to be cautious and not cause a low glucose event than be aggressive and have the patient develop hypoglycemia.

This defect can occur between the left subclavian artery and descending thoracic aorta (type A), the left subclavian and carotid arteries (type B), or the left carotid and brachiocephalic arteries (type C).Rarely in adults, the arch or the descending aorta is completely interrupted.These injuries are often result of transection of the descending thoracic aorta at the level of the ligamentum arteriosum, a point of fixation of the mobile aortic arch, but can also occur in the distal thoracic or abdominal aorta (Fig. 5.6). The mechanism of injury involves a combination of increased shear stress due to rapid deceleration and acute increases in intraluminal pressure. Little is known about the management and long-term outcomes of chronic traumatic thoracic aortic aneurysms [6, 7]. Fig. 5.4 Classification of traumatic aortic blunt injury . By permission of Mayo Foundation for Medical Education and Research. All rights reserved Fig. 5.5 Imaging findings of traumatic aortic blunt injury . Reprinted from Journal of Vascular Surgery, 55(1), Starnes BW, Lundgren RS, Gunn M, Quade S, Hatsukami TS, Tran NT, et al., A new classification scheme for treating blunt aortic injury, 47–54, Copyright 2012, with permission from Elsevier Fig. 5.6 Traumatic blunt aortic injury associated with fracture-dislocation of lower thoracic spine (a) was treated by endovascular repair and reduction of dislocation (b). By permission of Mayo Foundation for Medical Education and Research. All rights reserved ## Classification of Aortic Coarctation Aortic coarctation is a congenital arch disease that is anatomically described in relationship to the ductus arteriosus (ligamentum arteriosum). The narrowing can be preductal, ductal, or postductal. Most commonly, in adults an aortic coarctation is immediately distal to the atrophied ductus (postductal), but such cases are often associated with a hypoplastic, more proximal aortic arch. Rarely in adults, the arch or the descending aorta is completely interrupted. This defect can occur between the left subclavian artery and descending thoracic aorta (type A), the left subclavian and carotid arteries (type B), or the left carotid and brachiocephalic arteries (type C).Arch aneurysms can be isolated or representing proximal extension of a thoracic aortic aneurysm or distal extension of ascending aortic aneurysm (Fig.5.7).Fig.5.7 A schematic illustration comparing the normal ascending aorta to three common patterns of ascending aortic aneurysmal disease : supracoronary, annuloaortic ectasia (also known as Marfanoid-type aneurysm), and tubular.

We are getting these superior products because Apple wants to make money.Owing to Apple's existence, PCs are better than they otherwise would be.I use their products because I think they are superior (so much so that I even pay more for them).I'm glad the Apple computer company wants to make money.It's how our economy works.Money I don't think there's anything wrong with making money."But," he said, "there isn't a person on the planet who doesn't believe that this drug substantially reduces the risk of hip fracture." I begged to differ. I told him he was sitting next to one. This got a good laugh. And his demeanor changed markedly. It turned out he was a pretty nice guy. He was interested to learn that there was a medical school filled with other doctors who might ask him similar questions. And then he let his guard down. "You know, if we really wanted to prevent hip fractures we'd take a different approach. Patients get hip fractures because they fall. Preventing falls in the elderly would go a longer way towards reducing hip fractures than all the medications in the world." I told you these guys were smart. But the bottom line is that drug reps are salespeople—men and women whose job is to help pharmaceutical companies make money, and pharmaceutical companies have a strong financial interest in pushing early treatment for all kinds of diseases. Incidentally, the Forteo study was stopped early. It was supposed to be a three-year study, but it was stopped short of two years because rats in a long-term study of it developed bone cancer. While the FDA approved the drug, it required the company to conduct a ten-year trial looking for increased osteosarcoma in users of the drug (in the meantime, the FDA forbade the company to distribute free samples to physicians or to conduct direct-to-consumer advertising). Unfortunately, no results of the postmarketing surveillance were available nearly ten years later. As of this writing, Forteo is still on the market. Money I don't think there's anything wrong with making money. It's how our economy works. I'm glad the Apple computer company wants to make money. I use their products because I think they are superior (so much so that I even pay more for them). Owing to Apple's existence, PCs are better than they otherwise would be. We are getting these superior products because Apple wants to make money.I use their product because it helps me save money on car rentals (and because I'm glad to see William Shatner on TV again).Rental-car companies use Priceline for the simple reason that it helps them rent more cars.We are getting this more efficient market because Priceline wants to make money.Unlike most of my medical-school classmates, I was not a biology or biochemistry major in college.

Fig.* Stage IV tumor extends into the cranial cavity.* Stage III tumor extends into one or more of the following: antrum, ethmoid sinus, pterygomaxillary and infratemporal fossae, orbit, and/or cheek.* Stage II tumor extends into the nasal cavity and/or sphenoid sinus.[8]: * Stage I tumor remains confined to the nasopharynx.Email: elaws@partners.org Keywords JuvenileNasopharyngealAngiofibromaEpistaxisNasal obstructionSinonasalVascular ## 49.1 Epidemiology and Clinical Presentation * Juvenile nasopharyngeal angiofibroma (JNA) is a rare, histologically benign skull base tumor that develops in adolescents and young adults, almost exclusively in males [1, 2]. * JNAs represent less than 1 % of head and neck tumors. * The median age at diagnosis is 15 years [3]. * The incidence rate of JNA is 0.4 per million persons per year and as high as 3.7 per million males per year [3]. * Patients typically present with epistaxis and nasal obstruction [2]. * JNA may be related to familial adenomatous polyposis (FAP) [4]. ## 49.2 Imaging Features * JNAs typically arise in the region of the pterygopalatine fossa, and erosion of the bone posterior to the sphenopalatine foramen is a common sign on CT scans (Fig. 49.1) [5]. * The cancellous bone of the sphenoid is commonly involved (68 % of patients), and the degree of involvement of the sphenoid bone correlates with outcome [5, 6]. * On MRI, intratumoral flow voids and strong contrast enhancement are hallmarks of the vascularity typically seen with JNAs [5]. * On angiographic studies, unilateral blood supply is seen in up to 85 % of JNAs and is typically from the internal maxillary artery (Fig. 49.1f) [7]. * The most common staging system for JNA is the system proposed by Chandler et al. [8]: * Stage I tumor remains confined to the nasopharynx. * Stage II tumor extends into the nasal cavity and/or sphenoid sinus. * Stage III tumor extends into one or more of the following: antrum, ethmoid sinus, pterygomaxillary and infratemporal fossae, orbit, and/or cheek. * Stage IV tumor extends into the cranial cavity. Fig.(a) Sagittal contrast-enhanced CT image.(b) Axial contrast-enhanced CT image.(c) Coronal contrast-enhanced CT image.(d) Sagittal precontrast T1-weighted MR image.(e) Axial T1-weighted post-gadolinium, fat-saturated MR image.

The German Commission E approved the use of camomile for the treatment of skin and mouth irritation, bacterial skin diseases, and irritation of the respiratory tract, as well as the internal treatment of gastrointestinal spasm.EXPOSURE Sources Flos chamomillae consists of the dried flowering heads of Chamomilla recutita L. The yield of essential oil is typically at least 0.4% wet weight ranging up to about 1.5% wet weight. Powdered flos chamomillae is greenish yellow to yellowish brown. Medicinal Uses Traditional The water and ethanol extracts of pulverized flower heads from German and Roman chamomile are popular, old remedies used for spasmolytic, wound-healing, antibacterial, anti-inflammatory, and sedative effects.1,2 Traditional indications for chamomile tea include insomnia, indigestion, anxiety, fever, upper respiratory tract infections, headaches, skin and eye irritation, and burns. Chamomile is used both as an herbal tea and as an essential oil in cosmetics. Current Chamomile teas and extracts are traditional treatment for a variety of illnesses related to inflammation of the skin, upper respiratory tract, lungs, and gastrointestinal tract. The essential oil of chamomile is popular in aromatherapy. Previously, chamomile was evaluated as a mouthwash for the treatment of 5-fluorouracil-induced stomatitis with equivocal results.3 There is an absence of clinical data evaluating the sedative properties of chamomile. An uncontrolled clinical series of 10 cardiac patients associated a "deep sleep" for 90 minutes with the administration of chamomile tea.4 Regulatory Status Chamomile is regulated as a dietary supplement in the United States. The German Commission E approved the use of camomile for the treatment of skin and mouth irritation, bacterial skin diseases, and irritation of the respiratory tract, as well as the internal treatment of gastrointestinal spasm.

A gentle form of non-digestible carbohydrate, it makes its way through the gut, flushing out toxic wastes as it transits through the digestive system.It neutralizes acidity, coating the mucous membrane lining of the gastrointestinal tract.Its moisturizing action eases an upset digestion, protects the stomach and eases diarrhea and intestinal cramps.Gingerols and zingerones are the active anti-inflammatory constituents of this pungent spice. It is a natural remedy for heartburn, as well as nausea caused by motion sickness, so it is helpful for travelers. As a digestive tonic, ginger helps normalize the digestive process. Before eating anything, the wise sage Confucius would ginger up his food by sprinkling a little of this yang spice onto his meal. He knew that some ginger would promote appetite, prevent nausea, and help expel gases from the stomach and intestinal tract. Ginger root can be bought in any supermarket. The root can be grated and made into a warming ginger tea that is helpful for soothing nausea. ### Slippery Elm Bark (Ulmus fulva)—Gut Soother Native Americans used the powdered inner bark of the elm tree to make poultices to soothe damaged skin and to draw out poisons from boils and abscesses. European settlers used it to calm the terrible digestive problems of typhoid sufferers. Today this herb is a popular remedy for digestive discomfort, such as acid dyspepsia, irritable bowel syndrome, or for the type of problems associated with eating a food that disagrees with you. Soothing, nutritive, and demulcent in action, slippery elm bark has calming properties. Its moisturizing action eases an upset digestion, protects the stomach and eases diarrhea and intestinal cramps. It neutralizes acidity, coating the mucous membrane lining of the gastrointestinal tract. A gentle form of non-digestible carbohydrate, it makes its way through the gut, flushing out toxic wastes as it transits through the digestive system.Slippery elm bark comes in powder form and it can be used to make a soothing tea for irritation of the digestive tract.The powder can be sprinkled on muesli or oatmeal, helpful in healing the lining of the gut in leaky gut syndrome.

It is important to visualize one-sided defects, such as those resulting from a structural asymmetry as seen in hemifacial microsomia, hypoplasia or palatal palsy.On rare occasions, tonsils can be seen within the velopharynx at the level of (attempted) closure but usually they are below this plane.Ideally the moveable tip of the endoscope should be angled and rotated so that the velopharynx is in full view at rest. In the cleft palate population, structural abnormalities may restrict such optimum positioning. Velopharyngeal structure and function are assessed at rest, during speech and non-speech tasks, using the speech sample previously described for videofluoroscopy and, in a similar way, tailored to the patient based on the perceptual speech assessment. It may be important to try and stress the mechanism by encouraging speaking at speed and/or counting from 60 to 70. It is essential that the procedure is recorded (e.g. DVD) and the data archived for subsequent viewing. By moving the scope up and down through the mechanism, the anatomical structures in the naso- and oropharynx can be observed, and the three-dimensional nature of activity is appreciated. Sell et al. (2008) outlined the possible features that should be evaluated, although the focus of the evaluation will depend on the surgical philosophy of the team. Anatomical features include observation of the nasal surface of the soft palate. A v-shaped notch is suggestive of the incorrect insertion of the levator palatini muscles into the back of the hard palate, commonly associated with the spectrum of submucous cleft palate (SMCP) or a poorly repaired cleft palate. A flat nasal surface might suggest an absence or hypoplasia of musculus uvulae, also associated with SMCP. Visualization of adenoids is useful, and in particular their presentation, be they projecting, irregular or indented (Sell et al., 2008), together with some impression of size. On rare occasions, tonsils can be seen within the velopharynx at the level of (attempted) closure but usually they are below this plane. It is important to visualize one-sided defects, such as those resulting from a structural asymmetry as seen in hemifacial microsomia, hypoplasia or palatal palsy.Following pharyngeal flap surgery, its position and width, and some impression of its level and any residual gaps either side of the flap during speech can be seen and documented.

JA stimulates the transcription of genes encoding proteinase inhibitor ( _PIN2_ ) and other wound response proteins locally and in remote tissue to which JA is transported.Prosystemin is proteolytically processed to the peptide hormone systemin, which activates synthesis of JA from linolenic acid (C18:3).PIs are small defense proteins that interfere with the invertebrate digestive system by inhibiting serine, cysteine and aspartyl proteinases and thereby reduce the uptake of essential amino acids and retard the herbivore's growth and development. Many of the immediate biochemical changes in injured cells are shared with those of other abiotic and biotic stresses (see Figures 15.30 and 15.41): production of ROS, induction of secondary metabolism and accumulation of phenolics, tannins and phytoalexins, and increased synthesis of ethylene, jasmonates and salicylic acid. As a consequence of the export of signal molecules from a wound site via the vascular system, wounding often stimulates systemic responses in the whole plant. Wounding promotes proteolytic processing of the 200-amino acid precursor **prosystemin** to form the 18-amino acid peptide hormone **systemin**. Systemin engages with a receptor in the plasma membrane and activates the oxylipin pathway of jasmonic acid (JA) synthesis (see Chapter 10), as well as the transcription of genes encoding a PI ( _PIN2_ ). JA is believed to move through the phloem to remote undamaged tissues where it induces synthesis of PIN2 and other systemic wound response proteins (Figure 15.43). Figure 15.43 Local and systemic responses to wounding mediated by systemin and jasmonic acid (JA). Prosystemin is proteolytically processed to the peptide hormone systemin, which activates synthesis of JA from linolenic acid (C18:3). JA stimulates the transcription of genes encoding proteinase inhibitor ( _PIN2_ ) and other wound response proteins locally and in remote tissue to which JA is transported.Among the volatiles emitted by plants are methanol, acetone, formaldehyde and other short-chain carbonyl compounds, plus a host of terpenoids (including isoprene—see Section 15.5.2), phenylpropanoids and fatty acid derivatives.Plant-to-plant signaling by volatiles is a relatively new field of research and details of mechanisms and ecological significance remain to be discovered.

_Prescription No 1_.Slippery Elm.Garlic.Lobelia.Iceland Moss._Tablets/capsules_.Add honey and eat with a spoon, as desired.Cannot be strained.It gels into a viscous mass._Irish Moss (Carragheen)_ – 1 teaspoon to cup water gently simmered 20 minutes.A pinch of Cayenne assists action.1 cup 2-3 times daily.1 heaped teaspoon to cup water simmered 5 minutes in closed vessel.Mix.The sucking of a clove (or single drop of oil of Cloves in honey) has given temporary relief. _Aromatherapy_. Inhalants or chest-rub – Eucalyptus, Cajeput, Hyssop, Rosemary, Sandalwood. **Diet**. Wholefoods. Low fat, low salt, high fibre. Avoid all dairy foods. _Supplementation_. Vitamin B-complex. Vitamin E for increased oxygenation. Vitamins A, C, D, F. _Outlook_. Relief possible from regular herbal regime as dispensed by qualified practitioner. Requirements of each individual case may differ. **BRONCHITIS, ACUTE**. Inflammatory condition of the bronchial tubes caused by cold and damp or by a sudden change from a heated to a cold atmosphere. Other causes: viral or bacterial infection, irritating dust and fumes, colds which 'go down to the chest'. **Symptoms** : short dry cough, catarrh, wheezing, sensation of soreness in chest; temperature may be raised. Most cases run to a favourable conclusion but care is necessary with young children and the elderly. Repeated attacks may lead to a chronic condition. **Alternatives**. _Teas_ – Angelica, Holy Thistle, Elecampane leaves, Fenugreek seeds (decoction), Hyssop, Iceland Moss, Mouse Ear, Mullein, Nasturtium, Plantain, Wild Violet, Thyme, White Horehound, Wild Cherry bark (decoction), Lobelia, Liquorice, Boneset. With fever, add Elderflowers. _Tea. Formula_. Equal parts: Wild Cherry bark, Mullein, Thyme. Mix. 1 heaped teaspoon to cup water simmered 5 minutes in closed vessel. 1 cup 2-3 times daily. A pinch of Cayenne assists action. _Irish Moss (Carragheen)_ – 1 teaspoon to cup water gently simmered 20 minutes. It gels into a viscous mass. Cannot be strained. Add honey and eat with a spoon, as desired. _Tablets/capsules_. Iceland Moss. Lobelia. Garlic. Slippery Elm. _Prescription No 1_.Thyme 2; Lungwort 2; Lobelia 1.OR _Prescription No 2_.Morning and evening and when necessary.Iceland Moss 2; Wild Cherry bark 1; Thyme 2._Doses_ :– Powders: one-third teaspoon (500mg) or two 00 capsules.Liquid Extracts: 30-60 drops.Tinctures: 1-2 teaspoons._Practitioner_.Alternatives:– (1) Tincture Ipecacuanha BP (1973).Dose, 0.25-1ml.(2) Tincture Grindelia BPC (1949).Dose, 0.6-1.2ml.

This is most commonly required for potential femoral neck fractures.** --- * * * • CT can be used for any bone or joint where there is ongoing clinical suspicion of a fracture despite normal X-rays.Therefore, a normal CT does not exclude significant injury and an MRI may be required.There is significant posterior displacement of the superior fracture fragment and resultant spinal canal narrowing._ _**Image B:** Axial image showing the significant encroachment of the fracture fragment into the spinal canal. Note how the spinal canal and other soft tissue structures (intervertebral discs and ligaments) cannot be clearly seen._ ### CT IN ORTHOPAEDICS CT can be used to investigate potential fractures at sites other than the cervical spine: • CT is extremely useful for assessing and characterising fractures of the thoracic and/or lumbar spine. Accurate assessment is needed to determine whether a spinal fracture is potentially stable or unstable. • CT is very helpful in the assessment of facial fractures, which can be complex and are often difficult to identify fully on facial X-rays. CT also has the advantage in this setting of identifying any associated intracranial abnormality, such as intracranial haemorrhage. • Other examples where CT is commonly used include the further evaluation of tibial plateau fractures of the knee and Lisfranc fractures of the foot. Both of these types of injury require accurate assessment prior to surgical fixation; however, this is usually not possible using X-rays alone. * * * **KEY POINT** **CT provides very limited assessment of the intervertebral discs, ligaments and spinal cord. Therefore, a normal CT does not exclude significant injury and an MRI may be required. ** --- * * * • CT can be used for any bone or joint where there is ongoing clinical suspicion of a fracture despite normal X-rays. This is most commonly required for potential femoral neck fractures.MRI is preferred to CT in cases of suspected scaphoid fractures with normal X-rays.### CT CHEST • Chest CT is performed with the patient holding their breath in full inspiration (to prevent respiratory motion artefact degrading the images of the lungs and other tissues).• It can be performed as a non-contrast scan or with IV contrast depending on the indication.

**Homeopathic—** _Nux vomica_ (poison nut) 6C: Use Schedule 6(a).Schedule 2.**Homeopathic—** _Belladonna_ (deadly nightshade) 30C: This is most useful for the stage of fever, restless agitation, hot head, and dilated pupils, and is often the first remedy to use.One of the following remedies can also be helpful.(¼ teaspoon is about 1,000 milligrams.)Therefore, as you can imagine, inflammation of the liver (hepatitis) and other disturbances of this vital organ are very serious conditions. Symptoms of liver trouble include nausea, vomiting, loss of appetite, jaundice (yellowing of the tissues, best observed in the whites of the eyes or inside the ears in animals), perhaps the passing of light-colored or "fatty"-looking bowel movements (from insufficient bile and poor digestion), and the swelling of the abdomen from fluid accumulation. Liver malfunction is caused by many conditions. Viral infections or the swallowing of poisonous substances are factors, but in most cases, it's hard to tell just what initiated the problem. ### **T REATMENT** Because the liver is so central to the whole process of breaking down and using food, treatment includes minimizing the work it must do by fasting or feeding small, frequent, easily digested meals. In the early, acute stage of liver inflammation, fasting is best, especially if a fever is present. Follow the directions for fasting given in chapter 15. Keep your dog or cat on a liquid diet for a few days until his or her temperature returns to normal or there is some improvement. During this period, give the following treatments. Vitamin C: 500 to 2,000 milligrams four times a day, depending on size. This is most easily given as sodium ascorbate powder dissolved in a small amount of water. (¼ teaspoon is about 1,000 milligrams.) One of the following remedies can also be helpful. **Homeopathic—** _Belladonna_ (deadly nightshade) 30C: This is most useful for the stage of fever, restless agitation, hot head, and dilated pupils, and is often the first remedy to use. Schedule 2. **Homeopathic—** _Nux vomica_ (poison nut) 6C: Use Schedule 6(a).These animals are usually thirsty, vomit easily, have diarrhea, or very narrow, hard stools.As the animal improves and the symptoms subside, ease it onto a diet similar to that for kidney failure.You should, however, reduce the fat content by using lean meat and eliminating the added oil.Eggs are usually well-tolerated by the liver patient, as are grains.

Further physical investigations can be necessary in order not to lose the patient.Therefore, they should not be interpreted by the therapist at the beginning of treatment Begin with the body by allowing as much physical and medical therapy as is necessary to win the patient's co-operation (establishing therapy alliance)._Case report_ A twenty-six-year-old male patient comes to the psychosomatic clinic after finishing his examination in administration science abroad. One month earlier, he had broken off his outpatient treatment in a special headache clinic. A neurological examination with CCT had been carried out. His complaints were diagnosed as tension headaches. The symptom has been occurring daily for the past three years. He finished his exams with a high grade and had good prospects for his job, but he felt handicapped because of the impression that he could not rely on himself and face his daily work without breaks. During his studies, he always used to take breaks when the headache set in. _Table 9.12_. Guidelines for treatment of patients with chronic pain disorders. View the physical symptoms as material for interpretation, not defence No immediate search for the primary cause in the background of the physical symptoms Use the thoughts of the patient concerning his body as a key to his connection to his own self (body as an object) The obvious connection between symptoms and psychosocial problems (as seen by the physician) cannot be recognised by the patient. Therefore, they should not be interpreted by the therapist at the beginning of treatment Begin with the body by allowing as much physical and medical therapy as is necessary to win the patient's co-operation (establishing therapy alliance). Further physical investigations can be necessary in order not to lose the patient.Not to have a "real" (physical) pain often means for him that he suffers from an imaginary illness --- The headache is accompanied by a strong feeling of pressure on both sides of the head.It occurs in rest periods after high levels of intellectual stress.During the night he is free from pain, but in the morning he anxiously waits for the headache to start again.

In addition, alveolar rhabdomyosarcomas are translocation tumors, and most display a translocation involving PAX3-FKHR/FOXO1 or PAX7-FKHR/FOXO1 partners [t(2;13) and t(1;13), respectively].##### Immunohistochemical Work-Up Rhabdomyosarcomas display skeletal muscle differentiation and thus are variably immunoreactive for: myogenin and desmin.As in all cases, a clinical history is essential.(a–c) The core needle biopsy of the breast mass reveals loosely cohesive nests of small round blue cells separated by delicate fibrous septae. The cells display high nuclear-to-cytoplasmic ratio, nuclear hyperchromasia, and focally eosinophilic cytoplasm ##### Differential Diagnosis The differential diagnosis of rhabdomyosarcoma includes other small round blue cell tumors including lymphoma, Ewing's sarcoma/peripheral neurectodermal tumor (PNET), desmoplastic round cell tumor, Wilm's tumor, neuroblastoma and small cell osteosarcomas and chondrosarcomas. Other tumors in the differential which are more common in adult patients would include primary invasive lobular carcinoma, metastatic small cell carcinoma and Merkel cell carcinoma. The differential diagnosis of a neoplasm exhibiting skeletal muscle differentiation also includes primary spindle cell metaplastic carcinoma, malignant peripheral nerve sheath tumor with skeletal muscle differentiation (Triton tumor) and a malignant phyllodes tumor with heterologous elements. As in all cases, a clinical history is essential. ##### Immunohistochemical Work-Up Rhabdomyosarcomas display skeletal muscle differentiation and thus are variably immunoreactive for: myogenin and desmin. In addition, alveolar rhabdomyosarcomas are translocation tumors, and most display a translocation involving PAX3-FKHR/FOXO1 or PAX7-FKHR/FOXO1 partners [t(2;13) and t(1;13), respectively].#### Other Rare Sarcomas ##### Microscopic Features, Differential Diagnosis, and Immunohistochemical Work-Up In addition to leiomyosarcoma and rhabdomyosarcomas, other sarcomas have been reported to metastasize to the breast.

The following qualifiers describe fracture types and affect treatment: • Simple: the overlying skin is intact.Fractures are some of the most common pathologic conditions affecting bone.### Fractures A fracture is defined as loss of bone integrity due to mechanical injury and/or diminished bone strength.Key Concepts Acquired Disorders of Bone and Cartilage ▪ Osteopenia and osteoporosis represent histologically normal bone that is decreased in quantity, but osteoporosis is sufficiently severe to significantly increase risk of fracture. The disease is very common with marked morbidity and mortality from fractures. Multiple factors including peak bone mass, age, activity, genetics, nutrition and hormonal influences contribute to its pathogenesis. ▪ Paget disease is a disorder of locally increased but disordered bone. Typically asymptomatic, it is usually discovered incidentally. A mosaic pattern of mineralization is the histologic hallmark at the late stage of the disease. Genetic and possibly viral infectious etiologies have been proposed. ▪ Osteomalacia is characterized by bone that is insufficiently mineralized. In the developing skeleton, the manifestations are characterized by a condition known as rickets. ▪ Hyperparathyroidism arises from either autonomous or compensatory hypersecretion of PTH and can lead to osteoporosis, brown tumors, and osteitis fibrosa cystica. However, in developed countries, where early diagnosis is the norm, these manifestations are rarely seen. ▪ Renal osteodystrophy represents the constellation of bone abnormalities (osteopenia, osteomalacia, hyperparathyroidism, and growth retardation) from chronic renal failure. The mechanisms are complex but stem from decreased tubular, glomerular, and hormonal functions of the kidney. ### Fractures A fracture is defined as loss of bone integrity due to mechanical injury and/or diminished bone strength. Fractures are some of the most common pathologic conditions affecting bone. The following qualifiers describe fracture types and affect treatment: • Simple: the overlying skin is intact.• Comminuted: the bone is fragmented.• Displaced: the ends of the bone at the fracture site are not aligned.

He had recently been diagnosed with autism.#### Joey's Story _Joey was just shy of three years old when I met him.Behavioral and educational interventions are great therapies, and your child will need them, but they can't treat underlying medical conditions in the gut.If you're skeptical, let me assure you— _so was I._ But what do you have to lose at this point?That is why you must focus on breaking the constipation before going on to other gastrointestinal interventions such as probiotics and antimicrobials. But I don't mean you should just rely on laxatives. Once your child is free of chronic constipation and the resulting symptoms, he will probably calm down a _lot_. In addition, his improved behavior will mean the doctor will be far less likely to suggest psychiatric medications such as risperidone. #### This Is Your Child's Brain on Drugs What kinds of problems do these opiate-like neuropeptides contribute to? Take a look, and see if you recognize any of your child's problems in this list: _Sound familiar?_ Social withdrawal Limited use of language, even if he can speak Addictive eating patterns Constipation, or diarrhea _and_ constipation Reflux Fuzzy thinking, being "zoned out" Poor concentration Poor eye contact Disrupted sleep patterns Irritability and aggression Anger-related issues (easily angered) Lack of impulse control Self-injuring behaviors High pain tolerance Obviously, these opioid peptides cause lots of symptoms that can make children seem autistic, or more autistic than they really are. Our son Evan had many of the problems on this list; they began to clear up dramatically when we removed the opioid peptides from his diet (which was our best course of action, because we didn't have the enzymes back then). If he accidently ate wheat or cheese, the bizarre behaviors and anger returned. If you're skeptical, let me assure you— _so was I._ But what do you have to lose at this point? Behavioral and educational interventions are great therapies, and your child will need them, but they can't treat underlying medical conditions in the gut. #### Joey's Story _Joey was just shy of three years old when I met him. He had recently been diagnosed with autism.Her health was good and she did not smoke, use drugs, or drink.Little Joey had never been bothered by colic or thrush, had rarely been sick, and had "slept like a dream from day one."He did not have allergies, asthma, or sinus infections; he had not had diaper rashes or the telltale red ring around the anus; and he had normal bowel movements once or twice a day, with normal odor and texture.

## The six tastes ( _rasas_ ) As with the Chinese view, the effects of foods and the pharmacology of medicines were classified in terms of their immediate impact on the body.This is a _kapha_ -like influence, being generally cold, slimy, heavy and dense, with phlegm and mucus, loss of taste and appetite, indigestion, depression and irritability as common symptoms, and may arise from emotional difficulties as well as physical reasons. It lies at the root of much chronic disease and immune disturbance. Where there is evidence of _ama_ , improving eliminations is the first priority of treatment, a universal theme in herbal therapeutics. The prime herbal influences in the elimination of _ama_ are the bitter and pungent herbs, often in that sequential order, perhaps after a fast. (This is exactly the strategy for the Galenic elimination of 'damp'.) Sweet, salty and sour herbs can increase _ama_. The treatment of _ama_ is, however, complicated by its combinations with the _doshas_ (in which case it has the suffix _sama_ ). Combined with _kapha_ ( _kapha sama_ ), it is marked by severe mucus conditions and is a clear indication for pungent with bitter herbs. _Pitta sama_ is the classic Galenic damp-heat condition, with yellow tongue coating, urine and faeces, congestive anorexia, loss of thirst and biliousness. Bitter herbs lead the treatment, with modest amounts of pungent, as appropriate. _Vata sama_ is associated with constipation, painful abdominal congestion and flatulence, anorexia and bad breath, and is treated with pungent herbs, warming aromatic digestives and carminatives combined with laxatives as required. ## The six tastes ( _rasas_ ) As with the Chinese view, the effects of foods and the pharmacology of medicines were classified in terms of their immediate impact on the body.The choice of both medicines and foods is thus often determined by such assessments, the distinction between them again being a function of their effects on the body: foods nourish, medicines balance and poisons disturb.The effects of _rasas_ on the body are complex and rarely isolated.

Another limitation of the DSM-IV is that the criteria are, to a certain extent, arbitrary.Thus, in the future, defining disorders by their **neurobiology** , or biological cause, may lead to more specifically targeted, and therefore more effective, treatment approaches.Further, one process may respond to a particular treatment while another does not.I'm not recommending that you purchase the DSM; my point is to make you aware that it is readily available. The American Psychiatric Association, the national organization for physicians specializing in psychiatry, publishes the DSM-IV. It outlines the diagnostic criteria for all psychiatric disorders. Additionally, it provides supplementary information about disorders, such as familial pattern or inheritability, other disorders that may be similar, and the prevalence and course of illness. The DSM is written by prominent psychiatrists and other mental health professionals based on the evidence suggesting how psychiatric disorders should be defined. It is updated periodically as new information becomes available. The DSM is the gold standard for defining mood disorders. However, it is important for you to know about its limitations. The main problem with the DSM is that it is not based on the biological causes of disorders. In medicine, almost all disorders are defined, at least in part, by the underlying pathology. As discussed above, we do not yet understand the causes of psychiatric conditions well enough to use pathology as a part of the definition. As science advances, this will likely be possible in the future. For now, we are limited to definitions based on the existence of symptoms. The problem is that more than one pathological process may lead to the same set of symptoms. Further, one process may respond to a particular treatment while another does not. Thus, in the future, defining disorders by their **neurobiology** , or biological cause, may lead to more specifically targeted, and therefore more effective, treatment approaches. Another limitation of the DSM-IV is that the criteria are, to a certain extent, arbitrary.But what if someone has had many episodes of serious depression but the longest lasted twelve days?It would be illogical to say that person doesn't suffer from major depressive disorder, but technically she or he would not meet the DSM-IV criteria.

Brittle hair, fine hair, hypertrichosis of the eyebrows, and increased hair and nail growth have also been observed occasionally in patients with AIDS.The mechanism of action is unknown but it has been compared to a vitiligo-like process.#### **M ANAGEMENT** There is no specific treatment other than controlling HIV infection and supporting the patients' nutritional status. Trimming of the eyelashes may be required as needed for comfort. The presence of trichomegaly with systemic symptoms in a patient without a known immune deficiency disorder should prompt an evaluation for such, as these may be physical signs of HIV infection. ### **OTHER HAIR ABNORMALITIES** Hair straightening is a characteristic sign of HIV infection, especially in black patients.,– The hair is described as lighter, thinner, and softer, and the alteration occurs predominantly in advanced HIV disease. Unfortunately, improvement of immune function with antiretroviral therapy has not been shown to reverse the changes. Various explanations have been suggested for this phenomenon including HIV-induced regression of hair to its fetal stage, deficiencies in zinc, selenium, and copper, and endocrine changes. Smith _et al_. suggest that hormonal changes occurring in HIV infection such as decreased androgen levels and increased levels of estradiol, cortisol, and thyroid hormone may play a role. Premature graying of the hair (canities) has also been described in HIV-infected patients., It is noted to occur with other signs of aging such as premature skin aging and diffuse hair loss. The mechanism of action is unknown but it has been compared to a vitiligo-like process. Brittle hair, fine hair, hypertrichosis of the eyebrows, and increased hair and nail growth have also been observed occasionally in patients with AIDS.### **ONYCHOMYCOSIS** #### **D EFINITION/OVERVIEW** Onychomycosis is often a sign of HIV disease progression in an otherwise asymptomatic individual.Onychomycosis refers to an infection of the nail that is caused by dermatophyte fungi, nonderma-tophyte fungi, or yeast.Tinea unguium is onychomycosis that is limited to the nail plate.

Researchers argue that this is a probable reason why statins have been associated with greater mortality in recent trials.As patients take the statins for many years, starting earlier in the disease process, more dangers accrue as the years go by.This may be an important reason why statins fail in primary prevention.After all-cause mortality, "hard" cardiovascular endpoints—cardiovascular death, myocardial infarction, and stroke—are the most reliable because they minimize subjective input and are least vulnerable to bias in adjudication._ _With no reduction in all-cause mortality and no evidence of reduction in total serious adverse events for patients with five-year cardiovascular risk of ˂10%, the net benefit-harm equation has zero overall benefit and ignores the clear evidence of harm that has been demonstrated in clinical trials and observational studies. A retrospective cohort study found that 18% of statin-treated patients had discontinued therapy (at least temporarily) because of statin-related adverse events. Forty percent of the adverse events were related to musculoskeletal symptoms. At the same time, 18% or more of this group experienced side effects, including muscle pain or weakness, decreased cognitive function, increased risk of diabetes, cataracts or sexual dysfunction._ And wait—it gets worse. Research scientists are finding eventual damage to the heart from statin use, possibly even increasing the risk of heart failure with long-term use. Supporting these findings is that these drugs interfere with muscle function, even in people without muscle complaints or lab findings of muscle breakdown. Remember, the heart is a muscle, and over years, it may be subtly damaged, just like skeletal muscles. This may be an important reason why statins fail in primary prevention. As patients take the statins for many years, starting earlier in the disease process, more dangers accrue as the years go by. Researchers argue that this is a probable reason why statins have been associated with greater mortality in recent trials.• Statins are mitochondrial toxic, depleting coenzyme Q10, heme A, and adenosine triphosphate production, leading to muscle degeneration.This can have long-term negative effects on the heart muscle, even without muscular complaints.• Statins inhibit selenium-containing protein synthesis, creating cardiac muscle stress, which leads to cardiomyopathy and heart muscle disease.

I believe that over time, she had obtained prescription opiates while she was out on passes.• • • When I was working at a state rehab as an RN, a patient who had been on an outing returned to the center.If this bill had been in effect in the state where I practiced nursing, it could have potentially helped me to save a life.Naloxone, which we talked about in chapter 9 as an ingredient in Suboxone, blocks the effect of the opiate by binding to the same receptor in the brain as the opiate and knocking it off. It reverses the overdose, and if the victim has stopped breathing, allows him or her to begin breathing again. When naloxone is given as an injection or nasal spray, the overdose may be reversed immediately; with the nasal spray, the victim can wake up in as little as two to five minutes. Here is part of the bill as it was originally written: _This bill would . . . authorize a licensed health care provider who is permitted by law to prescribe an opioid antagonist [naloxone] and is acting with reasonable care to prescribe and subsequently dispense or distribute an opioid antagonist for the treatment of an opioid overdose to a person at risk of an opioid-related overdose or a family member, friend, or other person in a position to assist a person at risk of an opioid-related overdose._ I can almost hear some people yelling at me right now, calling this "The Enabler Bill." But it is not about enabling—it is about saving the life of someone who is going to use opiates no matter the circumstances. Some people will ask why a health care professional would prescribe opiates to someone suspected of abusing the medication. Well, sometimes doctors cannot tell if they are prescribing for true pain or addiction. Also, some extreme chronic pain patients are legitimately on high doses of opiates that are potentially dangerous. If this bill had been in effect in the state where I practiced nursing, it could have potentially helped me to save a life. • • • When I was working at a state rehab as an RN, a patient who had been on an outing returned to the center. I believe that over time, she had obtained prescription opiates while she was out on passes.I was in the kitchen eating an oatmeal cookie and was in my seventh month of pregnancy with my son, Max, when I heard the other female patients hysterically yelling for my help.I screamed to the cook who was in the kitchen with me to get more staff up to the second floor.I bounded up the stairs, ripping the CPR mask off the wall as I rounded a corner, instinctively knowing it would be needed.

Presence of haemorrhage indicates an acute injury.## 73.3 Tips and Pearls The identification of acute and chronic injures is difficult.The preliminary results of these techniques are interesting, but a longer follow-up is needed to demonstrate the real validity of the techniques.We can observe the suture performed after arthroscopic capsuloligamentodesis [24] Another arthroscopic technique, which aims to repair the volar part of the scapholunate joint, has been proposed by Del Pinal. This technique needs a volar portal, and an arthroscopic retensioning of volar ligaments is performed in order to close the volar SL space [18]. Other techniques of arthroscopic reconstruction have been recently proposed which necessitate the creation of two bone tunnels, one in the scaphoid and another in the lunate bone with the passage of a tendon which has the function to approximate the two bones and reconstruct the SL ligament. According to Ho, the two tunnels are performed in the sagittal plane in the proximal pole of scaphoid and in the lunate which allows the passage of a tendon graft, which is tightened with a knot [25]. Corella proposed to use a part of FRC to be passed in scaphoid tunnel from anterior to posterior and then in a lunate tunnel from posterior to anterior [26]. In the technique by Della Rosa, the tunnels are performed in the frontal plane and the tendon graft is a bone-tendon-bone graft which is fixed with interference screws [27]. These techniques are technically demanding and should be performed by experienced hand surgeons. The major complications are scaphoid proximal pole necrosis or fracture of scaphoid and lunate bone, so they are not still widely used. The preliminary results of these techniques are interesting, but a longer follow-up is needed to demonstrate the real validity of the techniques. ## 73.3 Tips and Pearls The identification of acute and chronic injures is difficult. Presence of haemorrhage indicates an acute injury.## 73.4 Complications Complications of wrist arthroscopy are rare.Nevertheless, they can be related to traction (paraesthesia, skin injuries at traction site) or due to arthroscopy itself (cartilage damage, rupture of instruments in the joint, swelling, compartment syndrome for fluid extravasation).Infection is extremely rare.

In my clinical experience, athletes and people with magnesium deficiency conditions may require 10–15 mg/kg per day.For a 150-pound woman that would be 400–680 mg per day.For a 220-pound man that would be 600–1,000 mg per day.Early in the second half, eleven players became disoriented and had difficulty walking. Their speech was slurred, they complained of muscle spasms, and they were breathing very deeply. Within an hour, eight of the boys collapsed into full-blown seizures; two had repeated seizures. Those having the worst symptoms had been playing the hardest. Thirteen more players reported headaches, blurred vision, muscle twitching, nausea, and weakness. Eventually all the boys recovered, but what happened to create such a frightening scene in this group of healthy young men? With the increased magnesium loss from excessive sweating plus the calcium supplement, their magnesium stores had been driven dangerously low. Magnesium deficiency may also play a role in sudden cardiac death syndrome, which can affect athletes. Another study concluded that the sudden death of athletes and other individuals during extreme exertion is triggered by the detrimental effects of persistent magnesium deficiency on the cardiovascular system. In a study of young, healthy, well-conditioned men, strenuous exercise was reported to give rise to persistent magnesium deficiency and a related long-term increase in cholesterol, triglycerides, and blood sugar. ## **MAGNESIUM SUPPLEMENTS FOR EXERCISERS AND ATHLETES** Dr. Seelig, an internationally recognized magnesium expert, recommends that athletes in training obtain at least 6–10 mg/kg/day (or 2.7–4.5 mg/lb/day) of magnesium to help replace the losses from exertion, sweating, and stress. For a 220-pound man that would be 600–1,000 mg per day. For a 150-pound woman that would be 400–680 mg per day. In my clinical experience, athletes and people with magnesium deficiency conditions may require 10–15 mg/kg per day.However, as I've indicated previously, you must go by your clinical symptoms and your magnesium RBC blood test to define your magnesium requirements—and be aware they can shift according to the many variables I outline throughout the book.# 5 # **The CNS, Stroke, Head Injury, Brain Surgery** **THREE THINGS YOU NEED TO KNOW ABOUT MAGNESIUM AND THE BRAIN** 1.

PIC was found to be a very efficient inducer of apoptosis in this ex vivo assay as well [12].The antileukemic properties of PIC were also assessed using primary, leukemic lymphoblasts from 21 patients suffering from childhood lymphoblastic leukemia.### 9.2.2 Induction of Apoptosis #### 9.2.2.1 Hematologic Tumor Cells ##### Multiple Myeloma (MM) and Lymphoma MM is a clonal B cell cancer characterized by proliferation of malignant plasma cells in the bone marrow. Although the introduction of immunomodulatory drugs like bortezomib or lenalidomide has improved patient survival, MM is still incurable, and new treatment options are needed. Treatment of MM cell lines (AMO-1, U266, and RPMI8226) as well as primary MM cells with PIC reduced proliferation and stromal cell-derived factor-1 alpha induced migration [9]. PIC induced apoptosis of MM cells, as revealed by reduced expression of procaspase 3, increased cleavage of poly(ADP-ribose) polymerase(PARP)-1 and enhanced release of cytochrome c (cyt c). The anti-proliferative and proapoptotic activities of PIC in MM cells appear to be mediated through suppression of Syk [9]. Aberrant activation of Wnt/β-catenin signaling promotes development and progression of various malignant neoplasms. The Wnt signaling pathway is constitutively activated in MM, which exaggerates cell proliferation. PIC inhibited Wnt/β-catenin signaling in murine plasmocytoma MPC11 cells as well as human MM (OPM-2, RPMI-8226, and U-266) cells. PIC induced apoptosis and suppressed the proliferation of these cells [10]. The combination of PIC with ethacrynic acid or ciclopirox olamine had a significant additive effect on the vitality of MM cells compared to single-agent application, while healthy cells remained unaffected [11]. PIC induced apoptosis in BJAB Burkitt-like lymphoma cells as evidenced by activation of caspase-3 and perturbation of mitochondrial permeability transition [12]. The antileukemic properties of PIC were also assessed using primary, leukemic lymphoblasts from 21 patients suffering from childhood lymphoblastic leukemia. PIC was found to be a very efficient inducer of apoptosis in this ex vivo assay as well [12].Among the seven cell lines, HL-60 and HSC-2 cells were the most sensitive to the cytotoxic action of these compounds.PIC induced internucleosomal DNA fragmentation and activation of caspases-3, -8, and -9 in HL-60 cells.[13].PIC treatment to the human leukemia cell line U937 induced the formation of apoptotic bodies, DNA fragmentation, and the accumulation of the sub-G1 phase [14].

Information about infectious diseases (e.g., childhood diseases, otitis media), immunizations, allergies (including adverse reaction to drugs), and sleeping disturbances should be obtained.It should review hospitalizations, illnesses, traumatic injuries, and previous and current medical treatment.Such factors as the parents' occupations, the number of children in the family, and the child's attendance at day‐care institutions and schools, are important in selecting a realistic plan for preventive and restorative dental care. The family history should also include the occurrence of inherited diseases, oral or general. It should be emphasized that the information required for an adequate family history is considered confidential by many parents. Thus, the dentist`s questions should be restricted to issues and diseases of relevance in the clinical situation. Some parts of such information may be considered confidential, and national guidelines on informed consent for transferal of information between health professionals should be observed. ### General medical history The general medical history should place the oral problems into a broader perspective of total patient care. Congenital or acquired diseases or functional disturbances may, directly or indirectly, cause or predispose to oral problems (e.g., craniofacial syndromes, juvenile rheumatoid arthritis, diabetes, hematologic diseases; see Chapters 23, and ) or they may have effects on the delivery of care and treatment of oral disease in the individual child. The general medical history includes information about pregnancy, delivery, the neonatal period, and early childhood. It should review hospitalizations, illnesses, traumatic injuries, and previous and current medical treatment. Information about infectious diseases (e.g., childhood diseases, otitis media), immunizations, allergies (including adverse reaction to drugs), and sleeping disturbances should be obtained.neuropsychiatric disorders, information on these child characteristics are important (see Chapters 6 and ).Finally, current and past problems as well as any current signs and symptoms of disease in the head, respiratory, cardiovascular, gastrointestinal, neuromuscular, and skeletal systems should be included in the general medical history.

S.'s room was in the center of the corridor across from the main desk, and when the pack rounded on it, the visiting surgeon hung back and leaned on the desk.And that was that—the scrum was on to the next room, the next presentation.The visiting surgeon nodded seriously, even solicitously, I thought.(In a subsequent telephone call, this cardiologist confirmed S.'s course, denied absolutely that the staff had ever stopped rounding on her, expressed regret over the surgeon's suggestion about her being overweight, and said, summarizing the situation, "It was felt that a second attempt [at surgical repair] would be too difficult, and we wanted the best possible person for this patient. . . . Other centers might try and try again, and they'd wind up with a dead patient on their hands and nobody'd know about it. We did the right thing.") What made this situation unique was that the surgeon who'd done the unfortunate job was planning to visit the clinic the following week. He would arrive, by coincidence, while S. was still in the PICU. The surgeon had traveled here to observe Dr. Mee and his staff. He'd brought his perfusionist along and was especially interested in watching the team's perfusion technique, he told me. His patients—his center performed about a hundred congenital cases a year—tended to be more edematous, or bloated, than normal, pointing to a perfusion problem. On the first day of the surgeon's visit, I did my best during rounds to stick close to Mee. Fairly early on, while the scrum was between rooms in the PICU corridor, the visitor asked about S. Mee told him she was here and doing all right. The surgeon then asked what had been wrong with his repair. Mee responded quietly but peevishly, explaining it to him exactly as he had explained it to me: "Patches don't turn corners," he said. He then went into some detail, using the curve between his thumb and index finger to represent the branching pulmonary artery, and also mentioned the loose patch. The visiting surgeon nodded seriously, even solicitously, I thought. And that was that—the scrum was on to the next room, the next presentation. S.'s room was in the center of the corridor across from the main desk, and when the pack rounded on it, the visiting surgeon hung back and leaned on the desk.I was wearing a badge that said I was an ambassador (the honorific given to hospital volunteers), and the surgeon noticed it and asked why I was here.For a book on congenital heart surgery, I said.He asked if it was a medical text, and I replied no; then he asked if I'd written other books.

Vitamin B6 Vitamin B6 (pyridoxine) is important for nerve function, energy metabolism, amino acid metabolism, and synthesis of neurotransmitters, including norepinephrine and serotonin, which strongly influence pain perception.** Good food sources include lean pork, kidney, liver, beef, eggs, fish, beans, nuts, and some whole grain cereals, if the hull and germ are present.It is currently known that vitamin C daily doses above 400 milligrams (mg) are not used by the body, and that taking 1,000 mg daily increases the risk of kidney stones in people with kidney problems, so megadosing with vitamin C is not necessary (Simons, Travell, and Simons 1999, 207). Women taking estrogen or oral contraceptives may need 500 mg per day. Do not take vitamin C together with antacids. Since vitamin C is ascorbic acid and the purpose of an antacid is to neutralize acid, antacids will neutralize vitamin C and make it ineffective. Vitamin B1 Vitamin B1 (thiamin) is essential for normal nerve function and the production of energy within muscle cells. Diminished sensitivity to pain and temperature and an inability to detect vibrations are indicators of vitamin B1 deficiency. You may also experience cramping of your calves at night, slight swelling, constipation, and fatigue. B1 is needed for the body to produce adequate amounts of thyroid hormones (for more on this topic, see "Organ Dysfunction and Disease" in chapter 6). Abuse of alcohol reduces absorption of vitamin B1, and liver disease will further reduce absorption. Antacids, the tannins in black tea, or a magnesium deficiency can also prevent the absorption. Because vitamin B1 is water soluble, it will be excreted too rapidly if you're taking diuretics or drinking an excessive amount of water. Vitamin B1 can be destroyed by processing foods, and by heating them to temperatures above 212°F (100°C). **Self-help technique: Get enough vitamin B 1. ** Good food sources include lean pork, kidney, liver, beef, eggs, fish, beans, nuts, and some whole grain cereals, if the hull and germ are present. Vitamin B6 Vitamin B6 (pyridoxine) is important for nerve function, energy metabolism, amino acid metabolism, and synthesis of neurotransmitters, including norepinephrine and serotonin, which strongly influence pain perception.It can also lead to a hormonal imbalance.Deficiency of B6 will manifest as symptoms of deficiency of one of the other B vitamins, since B6 is needed for all of the others to perform their functions.The need for B6 increases with age and with eating a high proportion of protein.Tropical sprue (a malabsorption disease) and alcohol use interfere with the body's uptake of B6.

Figure 104: Two identical abdominal radiographs showing a 'bamboo spine' in a patient with ankylosing spondylitis.9.The right radiograph shows the position of the missing pedicle shown with a white circle.The normal dense oval shape of the left pedicle of L3 is no longer visualised.Figure 98: Two pairs of identical radiographs showing multiple sclerotic bone lesions. There are multiple areas of increased density throughout the pelvis. In this elderly male patient the most likely cause is prostate metastasis. The right radiograph shows the sclerotic lesions marked in red. 4. Figure 99: Two pairs of identical radiographs showing a lucent bone lesion. If you compare the left and right sides, you can see an ill-defined area of lucency in the right pubic bone, with loss of the normal dense bone appearance. In this case the lucent lesion was a metastasis. The right radiograph shows the lucent lesion marked in red. 5. Figure 100: (1a) AP and (1b) lateral radiographs of the lumbar spine in the same patient showing an example of a wedge compression fracture of the L2 vertebral body. Note how there is loss of height of the L2 vertebral body (white arrow) when compared to the vertebrae above and below. (2a) AP and (2b) lateral radiographs of the lumbar spine in the same patient showing an example of a compression fracture of the L3 vertebral body. Note how there is loss of height of the L3 vertebral body (white arrow) when compared to the vertebrae above and below. There is also spinal metal work in situ providing mechanical support to the lumbar spine either side of the fracture. 6. Figure 101: A radiograph of a patient with thoraco-lumbar scoliosis. The thoraco-lumbar spine is curved with concavity to the right. 7. Figure 102: Diagram of a vertebra as seen from above with both left and right pedicles marked in yellow. 8. Figure 103: Two identical abdominal radiographs showing absence of the left L3 pedicle due to destruction by a spinal metastasis. The normal dense oval shape of the left pedicle of L3 is no longer visualised. The right radiograph shows the position of the missing pedicle shown with a white circle. 9. Figure 104: Two identical abdominal radiographs showing a 'bamboo spine' in a patient with ankylosing spondylitis.There is fusion (ankylosis) of the vertebrae by marginal syndesmophytes (white arrows).This gives the overall appearance of a spine that looks a bit like a bamboo stick.The right radiograph shows the 'Bamboo spine' marked in yellow.10.Figure 105: Two identical abdominal radiographs showing a Riedel's lobe (normal variant).The right lobe of the liver is enlarged and extends inferiorly.

It may be constant or sporadic, and although often temporary, it affects some people for many years.The pain varies in severity from mild to excruciating, and tends to be localized to a specific area.Vitamin B6 (see here) A randomized, double-blind, placebo-controlled study on pregnant mothers in Obstetrics and Gynecology looked at the effectiveness of 25 mg of vitamin B6 given every eight hours to control vomiting. After three days, only 26 percent of patients in the vitamin B6 group vomited, compared to 54 percent of the placebo group. Cold therapy (see here) A cold compress placed on the forehead will soothe feelings of nausea, especially if the symptoms are associated with a migraine. Quick fix Pressure on the sixth point on the Pericardium pathway in Chinese medicine, the exact point targeted by a motion sickness bracelet, quickly calms an upset stomach. (See Acupuncture and acupressure, here.) Gently press your middle and index finger on the point about 2 inches (5 cm) above your wrist crease on the palm side, right in between the two tendons. * * * See your doctor Go directly to the emergency room if you think the vomiting is related to poisoning or you notice blood or coffee-colored material in your vomit. Call your doctor if: • you vomit more than three times in a day or if the vomiting lasts for longer than 24 hours • you are unable to keep any fluids down for 12 hours • you have a stiff neck or severe belly pain. * * * See also Gastroenteritis ## NEURALGIA NEURALGIA IS THE MEDICAL TERM FOR nerve pain, which is often described as sharp, burning, cold or like an electric shock, and is sometimes accompanied by numbness, itching or tingling. The pain varies in severity from mild to excruciating, and tends to be localized to a specific area. It may be constant or sporadic, and although often temporary, it affects some people for many years.Treatment varies according to its cause and severity, and may involve making changes to your lifestyle to relieve pressure on affected nerves, as well as taking medication to relieve pain.Different natural therapies may also bring some relief.

Previously, anterior surgery was frequently performed, but of late, many surgeons prefer the all-posterior approach, in which the anterior debridement and reconstruction and posterior stabilization are performed through a single-stage posterior approach.The introduction of antitubercular chemotherapy in the 1960s achieved spectacular success in the control of disease. Although a significant number of patients could be treated with chemotherapy, those who presented late had significant morbidity due to kyphosis and neurologic deficit. Over half a century ago, Hodgson and Stock34 attempted surgical excision of an infected lesion along with chemotherapy, and achieved good results. Hodgson popularized the concept of anterior surgery for spinal tuberculosis with radical debridement and placement of rib strut grafts (known as the Hong Kong surgery). The approach enabled complete clearance of the abscess and cord decompression, acquired tissue for diagnosis, and enabled reconstitution of the anterior column. Soon it was realized that such a radical surgery is unnecessary in spinal tuberculosis, and most patients can be treated with an ambulant short course of chemotherapy with surgery being performed in select cases (known as the middle-path regimen).35 Currently, surgery in spinal tuberculosis is performed to achieve debridement and drainage of large cold abscesses, decompression of spinal cord and neural structures, spinal deformity correction, and stabilization and reconstruction of the anterior column. These goals can be achieved through different surgical approaches selected on an individual basis. The different surgical techniques include a direct anterior approach, a combined anterior and posterior approach, and an all-posterior approach. The addition of instrumentation in spinal tuberculosis is well accepted and advised, especially where instability is present or expected after decompression. Previously, anterior surgery was frequently performed, but of late, many surgeons prefer the all-posterior approach, in which the anterior debridement and reconstruction and posterior stabilization are performed through a single-stage posterior approach.10.18).** The availability of the pedicle screw system, which provides excellent reconstruction possibilities, along with the development of surgical techniques that enable anterior reconstruction through a posterior approach, have recently tilted the balance in favor of all-posterior surgeries in spinal tuberculosis.**Fig.

I was staring into the crib, and _I didn't know who my baby was_.He got me to stand up and walk into the boys' room.I didn't know who he was."When I finally came to, I couldn't remember anything.I was having a severe seizure—I was convulsing, my eyes rolled back, I was drooling, and I bit my tongue almost all the way through."My husband thought I was going to die.The label said such side effects were experienced by "less than one percent" of the patients taking Floxin. Two women who worked less than a mile from each other being stricken by the same lightning didn't sound like a "less than one percent" risk to him. He promised to put me in touch with her. Speaking to litigator Stacy Phillips* was an immense relief. Now I knew that Diane wasn't the only person in America who considered herself Floxed. But the experience was also pretty chilling, because Stacy still wasn't feeling great, nearly a _year_ after taking Floxin. In her case, it was two pills. Stacy was thirty and had two kids. Not long after the birth of her second son, on Christmas Eve 1991, she began having pain that she suspected was a recurrence of a pelvic infection. She wanted to catch it right away this time, so she went to her doctor and asked for a prescription for Keflex (cephalosporin), the antibiotic she had used to treat it before. "He said, 'Well, Keflex can clear it up, but I have something that's supposed to be as good or better,' " she recalled. "He prescribed Floxin and some Motrin [ibuprofen] for the pain, and I went to the pharmacy and got them." She took one Floxin that morning, and another before going to sleep. She woke up hours later with her husband screaming at her. "This was the single most terrifying experience of my life," she said. "My husband thought I was going to die. I was having a severe seizure—I was convulsing, my eyes rolled back, I was drooling, and I bit my tongue almost all the way through. "When I finally came to, I couldn't remember anything. I didn't know who he was. He got me to stand up and walk into the boys' room. I was staring into the crib, and _I didn't know who my baby was_.I called the doctor the next morning, and he had me go in for an MRI and EEG.The EEG was abnormal—it showed a seizure disorder, and the doctor said I probably had some preexisting seizure disorder."Stacy's descriptions of how she had felt since her drug reaction were eerily similar to things Diane was telling me as her weeks in treatment began turning into months.

* All patients require antiseptic mouth wash and body bathing.).Bolus enteral feeding is preferred over continuous tube feeds (see Chap.While a general polymeric formula is acceptable, we prefer a semi-elemental diet high in omega-3 FFA.If the patient cannot take orally enteral nutrition should be started within 12 h of ICU admission.* Normal * Increased * Decreased * Does this patient have evidence of impaired tissue/organ perfusion * Decreased urine output * Cold/clammy skin * Mottled peripheries * Hypotension * The patients code status, preferences for life supportive therapy and goals/expectations of treatment MUST be determined when the patient s admitted to the ICU * Determine the adequacy of venous access * Communicate with the patients' nurse and respiratory therapist * Keep the family informed * Measure the patients height and weight on admission ## Initial "Generic" Treatment Orders * Fluids * Sate the type of fluid and the infusion rate * Oxygenation or * Nasal canula or face mask or BiPAP * Initial ventilator settings * AC rate 6–8 mL/kg IBW# * Flow rate 60 L/min * FiO2 100 % * PEEP 5–10 cm H2O * ICU patients are at a high risk for deep venous thrombosis (DVT) and therefore ALL ICU patients require DVT prophylaxis. This should be individualized based on the patients risk of DVT, risk of bleeding, risk of HIT and renal function (see Chap. ) * subcutaneous heparin (5,000 U BID, TID) * subcutaneous low-molecular weight heparin (Enoxaparin 40 mg daily or equivalent) * subcutaneous fondaparinux (2.5 mg daily) * sequential compression devices * combination of SCD and anticoagulant * Routine stress ulcer prophylaxis is not required * Nutrition (see Chap. ) * Unless specifically contraindicated or the patients length of stay in the ICU is expected to be less than 24 h all patients should be fed enterally once they have been resuscitated. If the patient cannot take orally enteral nutrition should be started within 12 h of ICU admission. While a general polymeric formula is acceptable, we prefer a semi-elemental diet high in omega-3 FFA. Bolus enteral feeding is preferred over continuous tube feeds (see Chap. ). * All patients require antiseptic mouth wash and body bathing.Reference 1.Rissmiller R. Patients are not airplanes and doctors are not pilots[Letter].Crit Care Med.2006; 34(11):2869.Footnotes 1 Estimated GFR (Cockcroft-Gault equation): (140 – age) × (Weight in kg) × (0.85 if female) / (Creatinine × 72).© Springer International Publishing Switzerland 2015 Paul Ellis MarikEvidence-Based Critical Care10.1007/978-3-319-11020-2_5 # 5.

The patient is usually aware of the deficit and appropriately concerned about it.Repetition is impaired, but comprehension of spoken language is normal.The patient has difficulty naming even simple objects.##### **A. Broca's Aphasia** Broca's aphasia is common, and is usually caused by a lesion in the inferior frontal gyrus in the dominant hemisphere (Broca's area; Fig 21–1).In testing for aphasia, the clinician first listens to the patient's spontaneous speech output and then explores the patient's speech during conversation. Speech may be categorized as _fluent_ (more than 50 words per minute, effortless, absence of dysarthria, normal phrase length, and normal intonation). In contrast, _nonfluent_ aphasia is effortful, with decreased verbal output (less than 50 words per minute), poor articulation, degradation of inflection and melodic aspects of speech, and agrammatism (ie, the tendency to omit small, grammatical words, verb tenses, and plurals and to use only nouns and verbs). Naming (which is usually examined by asking patients to name objects presented to them), repetition of phrases such as "dog," "automobile," "President Kennedy," "no ifs, ands, or buts," and comprehension of spoken language are also tested. Comprehsion can be assessed in patients with impaired speech output by observing the response to yes-no questions of graded difficulty ("is your name John?" "Are we in a hospital room?" "Are we in a church?" "Do helicopters eat their young?") **TABLE 21–1 The Aphasias**. #### **Aphasia With Impaired Repetition** In most common forms of aphasia, the ability to repeat spoken language is impaired. Broca's, Wernicke's, and global aphasia are frequently seen in clinical practice. ##### **A. Broca's Aphasia** Broca's aphasia is common, and is usually caused by a lesion in the inferior frontal gyrus in the dominant hemisphere (Broca's area; Fig 21–1). The patient has difficulty naming even simple objects. Repetition is impaired, but comprehension of spoken language is normal. The patient is usually aware of the deficit and appropriately concerned about it.Patients are often hemiplegic, with the arm more affected than the leg.Broca's aphasia often occurs as a result of strokes, most commonly affecting the middle cerebral artery territory.##### **B. Wernicke's Aphasia** This common form of aphasia is caused by a lesion in or near the superior temporal gyrus, in Wernicke's area (see Figs 21–1 and 21–2).

Studies that combined industry funding with nonprofit support fell between the two on the spectrum, with 57 percent offering favorable results.Trials funded by nonprofits, however, were about as likely to support the drugs or devices as to oppose them: only 49 percent of these articles were positive.NitroMed also loaded the statistical dice by claiming special efficacy in blacks, then testing the medication only in blacks. But the most enduring type of clinical-trial manipulation is purchased bias. Although many assume that peer-reviewed studies, which are published only after they have been critiqued and evaluated by experts, are objective, several recent empirical studies suggest otherwise, at least when drug companies are involved. This extensive conflict of interest is important not only for medical publications but for vetting medications: groups such as the National Institutes of Health, the Institute of Medicine, and health-care insurers, including Medicaid and Medicare, examine the peer-reviewed medical literature to determine which drugs should be made available to patients and entered into formularies. But clinical-trial results favor the products of those who fund them. We've suspected this since at least 1994, when Paula Rochon and her team analyzed all the trials bankrolled by the makers of nonsteroidal anti-inflammatory drugs (NSAIDs), painkillers for arthritis. Every one of the fifty-six trials found the funder's drug study superior to the medication to which it was compared. Not one study published results unfavorable to the drug maker. Drs. Paul M. Ridker and Jose Torres at Harvard Medical School found that two-thirds of the results of industry-sponsored trials published between 2000 and 2005 in the three most influential medical publications—the _Journal of the American Medical Association_ , the _New England Journal of Medicine_ , and the UK's _Lancet_ —favored experimental heart drugs or medical devices. Trials funded by nonprofits, however, were about as likely to support the drugs or devices as to oppose them: only 49 percent of these articles were positive. Studies that combined industry funding with nonprofit support fell between the two on the spectrum, with 57 percent offering favorable results.Similarly, Lisa Bero, professor of clinical pharmacy at the University of California, San Francisco, looked at two hundred trials comparing similar medications in 2007 in medical journals that were chosen because of their reputation for publishing high-quality, peer-reviewed studies.

The medication bupropion (which is popularly known as Wellbutrin or Zyban) modulates dopamine pathways in the reward system.Gamblers taking opiate blockers are not compelled to seek reward-system stimulation through further gambling, possibly because they feel reduced pleasure from the financial ups and downs.Some experts speculate that people with a competitive nature, such as athletes, are susceptible to developing gambling problems. They want to win against the gods, even though the gods of the odds play by different (mathematical) rules. # **REDUCING GAMBLING** Medications, psychotherapy, and educational interventions have all been studied as treatments for pathological gambling. Medication treatments use one of three neural strategies: (1) improving impulse control in the prefrontal cortex, (2) increasing fear of loss in the amygdala, or (3) decreasing gambling cravings by bolstering the reward system. Psychological treatments, such as psychotherapy, target cognitive distortions that minimize losses and the social costs of gambling. Education about mathematical probabilities did not change gambling behavior in one study, indicating that the decision to gamble tends to be an emotional, not an intellectual, process. Warnings that describe irrational gambling beliefs do decrease gambling behavior, which implies that irrational beliefs and expectations can be changed when they are directly contradicted (as can happen in psychotherapy). The most widely used medication treatment for pathological gambling is naltrexone. Both naltrexone and nalmefene are medicines that block mu opiate receptors, and they have both been found useful in reducing gambling among gambling addicts. In the reward system, mu opiate receptors stimulate dopamine release. Blocking opiate receptors with naltrexone decreases dopamine release in the nucleus accumbens, which results in decreased subjective feelings of pleasure. Gamblers taking opiate blockers are not compelled to seek reward-system stimulation through further gambling, possibly because they feel reduced pleasure from the financial ups and downs. The medication bupropion (which is popularly known as Wellbutrin or Zyban) modulates dopamine pathways in the reward system.# **SUMMARY** Pathological gambling is not a lifelong illness.It often waxes and wanes over one's lifetime.It can arise unexpectedly in previously disciplined investors, or it can suddenly disappear after years of struggle.Many celebrities have experienced problem gambling.

Watch closely for cough, bronchospasm, and tachypnea.• Monitor respiratory status carefully.Stay alert for fever, flulike symptoms, and EENT infections.• Assess body temperature.Watch closely for blood pressure changes and tachycardia.• Monitor vital signs and ECG.#### **Administration** • Dilute with dextrose 5% in water, dextrose 5% in normal saline solution, dextrose 5% in 0.2% sodium chloride solution, dextrose 5% in 0.33% sodium chloride solution, dextrose 5% in 0.45% sodium chloride solution, normal saline solution, or lactated Ringer's solution for injection. • Give I.V. bolus over at least 1 minute with ifosfamide dose and at prescribed intervals after ifosfamide doses. Don't use multidose vial (contains benzyl alcohol) in neonates or infants. In older children, use with caution. • If patient vomits within 2 hours of oral mesna dose, repeat oral dose or switch to I.V. route. #### **Adverse reactions** **CNS:** fatigue, malaise, irritability, headache, dizziness, drowsiness, hyperesthesia, rigors **CV:** hypertension, hypotension, ST-segment elevation, tachycardia **EENT:** conjunctivitis, pharyngitis, rhinitis **GI:** nausea, vomiting, diarrhea, constipation, anorexia, flatulence **Hematologic:** hematuria **Musculoskeletal:** back pain, joint pain, myalgia **Respiratory:** coughing, tachypnea, **bronchospasm** **Skin:** flushing, rash **Other:** arm or leg pain, injection site reactions, fever, flulike symptoms, allergic reactions #### **Interactions** **Drug-diagnostic tests. ** _Hepatic enzymes:_ increased levels _Urinary erythrocytes:_ false-positive or false-negative results _Urine tests using Ames Multistix:_ false-positive for ketonuria #### **Patient monitoring** • Monitor nutritional and hydration status. • Monitor vital signs and ECG. Watch closely for blood pressure changes and tachycardia. • Assess body temperature. Stay alert for fever, flulike symptoms, and EENT infections. • Monitor respiratory status carefully. Watch closely for cough, bronchospasm, and tachypnea.Reassure him that he will be monitored closely.• Encourage patient to request analgesics or other pain-relief measures for headache, back or joint pain, hyperesthesia, or muscle ache.Advise patient to immediately report breathing difficulties and allergic symptoms.• Inform patient about drug's adverse CNS effects.Explain safety measures used to prevent injury.

There again is no good data suggesting that this treatment works in autism.Potential side effects of the treatment include stomach upset and, rarely, allergic reactions.Also, they are not bothered by the fact that many women who have mild yeast infections have children who are perfectly fine.(This can be tested for in both mothers and their children.)The medicines, like all medicines, can have serious side effects. Sometimes they "activate" the child—that is, they make her seem more "hyper" or energetic. This may give the impression that the child has suddenly made developmental gains—but these gains are lost over time as the child's system becomes used to the medication. Parents who have themselves been on steroids may know exactly what we are talking about here! At present, there are not good data to support the use of anticonvulsants or steroids for an abnormal EEG in the absence of a clear seizure disorder. You can talk with your child's neurologist about this in more detail. ## **Drug Treatments for Infections** One group of alternative therapies holds that autism results from infections (either from bacteria, viruses, or yeast) and that treatment of the underlying infection should lead to improvement in the child's symptoms. Yeast infections probably have gotten the most notice. Many women have chronic but very, very mild yeast infections, and someone suggested that maybe mothers of children with autism were more likely to have such infections that had never been recognized. This led a number of doctors to try medicines, such as nystatin, to treat yeast infections in children with autism. Somewhat surprisingly, many of the advocates of this treatment are not particularly concerned about whether or not the mother can be shown to have a yeast infection. (This can be tested for in both mothers and their children.) Also, they are not bothered by the fact that many women who have mild yeast infections have children who are perfectly fine. Potential side effects of the treatment include stomach upset and, rarely, allergic reactions. There again is no good data suggesting that this treatment works in autism.There are no good data at present to support this idea.As with other medicines, antibiotics can have serious side effects.## **Intravenous Immunoglobulin Infusion** Some people have thought that perhaps autism might represent an immune problem, particularly an autoimmune problem (where the body develops some adverse reaction to something within itself).

You can add parsley (fresh or dried) to essentially any savory dish, including soups, stews, salads (particularly quinoa and bean salads), sandwiches, pasta, marinades, dressings, dips, and even smoothies.Dried parsley offers a concentrated source of apigenin—it's a nice shortcut when I don't have fresh around!You can store parsley for up to 1 week in the fridge.Cooking paprika also releases its full flavor profile and may help your body absorb many of the antioxidants. STUDIES SHOW THAT PAPRIKA MAY: Protect skin cells from UV damage and the effects of aging Stunt the growth and spread of cancer cells, including leukemia and pancreatic, prostate, and colon cancers Protect the eyes from macular degeneration (the leading cause of vision loss) Boost HDL cholesterol and lower LDL cholesterol Lower the risk of Alzheimer's and Parkinson's diseases Parsley Something that drives me crazy is seeing parsley used only as a decoration—especially when it's the healthiest item on a plate! I understand that it's a bitter herb, so I don't expect anyone to go to town on a parsley salad. But parsley is a true power herb: Its primary phytonutrient (apigenin) may kill cancer cells, prevent tumor cell invasion and metastasis, and inhibit a cancer cell's ability to take in glucose as fuel, thus stunting its growth. Parsley is also packed with vitamins C, A, and K as well as folate, iron, calcium, magnesium, potassium, and manganese. But it's not just a multivitamin. You'll find two types of fresh parsley in grocery stores: curly leaf and flat leaf (also called Italian). Flat-leaf parsley has a stronger flavor, but both convey similar health benefits. You can store parsley for up to 1 week in the fridge. Dried parsley offers a concentrated source of apigenin—it's a nice shortcut when I don't have fresh around! You can add parsley (fresh or dried) to essentially any savory dish, including soups, stews, salads (particularly quinoa and bean salads), sandwiches, pasta, marinades, dressings, dips, and even smoothies.Rosemary This herb, often a staple in Italian cooking, boasts a powerful fragrance that enhances the flavor of your dishes and improves your health.Rosemary leaves contain an essential oil rich in organic acids (carnosic, rosmarinic, and ursolic acids) that work together synergistically on a cellular level to magnify their antioxidant and anti-inflammatory effects.

Management of these reactions is essentially the same as for anaphylaxis.Anaphylactoid reactions may occur after first exposure to a drug.Reactions may include any combination of the following: pruritus, urticaria, angioedema, bronchospasm, hypotension, syncope, nausea, emesis, and flushing.Patients may have a genetic defect or defects in metabolic pathways that lead to the accumulation of toxic metabolites. These metabolites may have direct toxic effects or act through a hapten-mediated mechanism to activate cytotoxic T lymphocytes, with the subsequent release of inflammatory cytokines. Complications include stomatitis and mucositis, which hinder oral intake. Buccal, nasopharyngeal, pulmonary tract, esophageal, and perineal desquamation and erosion may also occur. About 50% of cases of Stevens-Johnson syndrome and 80% of cases of toxic epidermal necrolysis are drug induced. More than 100 drugs have been associated with these two conditions. The medications with the highest relative risk are sulfonamides, β-lactam antibiotics, imidazole agents, and NSAIDs. Drugs in the moderate-risk category include quinolones, aromatic anticonvulsants, and allopurinol. ### 9.3.10 9.3.10 Anaphylactoid Drug Reactions Anaphylactoid drug reactions are caused by the direct release of mediators from mast cells and basophils without IgE cross-linking. Clinically, the signs and symptoms resemble those of anaphylaxis, but IgE is not involved. These reactions can occur with a large number of medications and excipients, most commonly with opiates, aspirin, and radiocontrast material. Reactions may include any combination of the following: pruritus, urticaria, angioedema, bronchospasm, hypotension, syncope, nausea, emesis, and flushing. Anaphylactoid reactions may occur after first exposure to a drug. Management of these reactions is essentially the same as for anaphylaxis.The more frequent and potentially serious organ involvement includes lymphadenopathy, hepatitis, nephritis, pneumonitis, and hematologic conditions.The prodrome of this syndrome includes fever, malaise, and pharyngitis, followed by skin lesions.Skin lesions range from an exanthematous eruption to erythroderma and a toxic epidermal necrolysis-like pattern.

Proof that OT is involved in mediating these very specialized behavioral patterns came from experiments that demonstrated that OT centrally injected to female prairie voles facilitated the development of partner bonding in the absence of mating and that the mating-induced partner bond formation was blocked by central administration of an OT antagonist before mating.Detailed microinjection studies with OT antagonists injected into discrete brain areas implicate the medial preoptic area and the ventromedial nucleus of the hypothalamus in OT-mediated lordosis, whereas the ventral tegmental area appears to regulate OT-mediated social behaviors. For studies of OT effects on social attachment and affiliation, two types of voles, the prairie and the montane vole, have provided a valuable model system. Despite their close relation, these two species differ markedly with respect to their social behaviors. The prairie vole manifests the classic features of monogamy. A breeding pair shares the same nest and stays together until "death do them part," and even then a new mate is accepted by the surviving mate only one-fifth of the time. In contrast, montane voles live in isolated burrows, have little social contact, and clearly are not monogamous. Despite an overall similar distribution of neuropeptide receptors, these two species differ very radically in the neural distribution of OT as well as AVP receptors, and both are expressed within very different pathways. Whereas prairie vole OT receptors are found in brain regions associated with reward, such as the nucleus accumbens and the prelimbic cortex, montane vole OT receptors are found in the lateral septum, where they may be responsible for the effect of OT in this species on self-grooming. Proof that OT is involved in mediating these very specialized behavioral patterns came from experiments that demonstrated that OT centrally injected to female prairie voles facilitated the development of partner bonding in the absence of mating and that the mating-induced partner bond formation was blocked by central administration of an OT antagonist before mating.Maternal behavior is another complex behavior that can be induced in virgin, steroid-primed female rats, and the natural occurrence of the behavior following parturition can be blocked by central OT antagonist application.Typical OT-induced maternal behavior includes nest building and recognition and acceptance of the pups, as well as retrieval of the pups into the nest.

Fig.6.15 Temporal dispersion of the compound muscle action potential (CMAP) from first dorsal interosseous at the elbow.Fig.6.14 Slowing of the evoked motor response from adductor digiti minimi, maximal across the elbow.Fig.6.14–6.16).If routine motor studies recording from adductor digiti minimi are inconclusive, conduction studies should then be made using the first dorsal interosseus muscle, or vice versa, as nerve fibre bundles to individual muscles may be differentially affected in compressive lesions of the ulnar nerve at the elbow. Peripheral nerves have a complex internal arrangement, comprising fascicles in which nerve fibres bound for a particular target are organised together. In a partial nerve lesion, fascicular involvement will be determined by proximity of a specific fascicle to the injurious lesion. Short segment conduction studies ("inching") significantly increase detection of ulnar nerve lesions at the elbow (Gooch et al. 2003), and may also provide precise localisation, such as to the cubital tunnel region where the nerve is vulnerable to compression by the fascia connecting the two heads of the flexor carpi ulnaris muscle. The technique of inching involves movement of the stimulating electrode over small distances, looking for abrupt change in CMAP amplitude, morphology or latency (Campbell and Geiringer 1998); it can be utilised for the localisation of many focal neuropathies in upper and lower limbs. Whilst the typical electrophysiological findings in ulnar neuropathy at the elbow are attenuation or loss of the ulnar digital sensory response, and conduction slowing around the elbow, other features of demyelination, such as temporal dispersion and conduction block may also be present (Figs. 6.14–6.16). Fig. 6.14 Slowing of the evoked motor response from adductor digiti minimi, maximal across the elbow. Fig. 6.15 Temporal dispersion of the compound muscle action potential (CMAP) from first dorsal interosseous at the elbow. Fig.Intra-operative electroneurography at the time of ulnar nerve exploration can assist precise localisation of the site of ulnar nerve compression – Campbell and colleagues have employed peri-operative stimulation for this purpose, and to identify residual compression in patients undergoing re-exploration (Campbell et al.1988).

If such damage cannot be avoided, taking means of preemptive analgesia should be considered (i.e., continuous epidural analgesia during the perioperative period in the case of lime amputation).As such, clinicians are encouraged to minimize, as much as possible, nerve damage during surgical or other medical procedures.#### 22.2.5.4 Surgery Surgical procedures, such as neurolysis, nerve, and neuroma transection with or without intraosseous transposition, venous rapping, and nerve-to-nerve anastomosis, all used in the treatment of neuropathic pain associated with nerve injury with various degrees of success. However, the detailed description of these procedures is beyond the scope of this chapter. Yet, surgical procedures can be considered in patients with chronic intractable pain that fail to respond to alternative treatments, even though complete pain relief can be rarely achieved [68]. #### 22.2.5.5 Prevention Cohort studies and clinical practice repeatedly show that neuropathic pain is often persistent and resistant to multiple analgesic interventions. The need to prevent the development of this type of pain is therefore obvious. Evidence show that the administration of local anesthetics, anti-inflammatory drugs, opioids, NMDA receptor antagonists, and other agents can prevent the development of long-term hyperalgesia and pain-like behavior in animals. In contrast, a relatively small number of studies aimed to prevent chronic neuropathic pain after injuries in humans have been conducted thus far, and yielded much less consistent results. Nonetheless, it is generally accepted that an effective pain treatment at the time or early after nerve injury has the potential to reduce the incidence of chronic neuropathic pain. As such, clinicians are encouraged to minimize, as much as possible, nerve damage during surgical or other medical procedures. If such damage cannot be avoided, taking means of preemptive analgesia should be considered (i.e., continuous epidural analgesia during the perioperative period in the case of lime amputation).## 22.3 Complex Regional Pain Syndrome (CRPS) Complex regional pain syndrome (CRPS) is a painful disorder of unclear etiology, typically involving the distal part of one limb, represented by spontaneous and evoked pain as well as autonomic, motor, and trophic abnormalities.CRPS typically appears subsequent to a traumatic event [55].

Nerve Posterior interosseous nerve C6–C8.Action Abducts and extends the thumb at the carpometacarpal joint.Insertion Base of the first metacarpal.Origin Posterior surfaces of the ulna and the radius, and interosseous membrane.ABDUCTOR POLLICIS LONGUS **Latin** , _abducere_ , to lead away from; _pollicis_ , of the thumb; _longus_ , long.Adductor pollicis, supine with the forearm supported.Origin Flexor retinaculum, and tubercles of the scaphoid and trapezium. Insertion Lateral side of the base of the proximal phalanx of the thumb. Action Abducts the thumb and helps oppose it. Nerve Deep ulnar nerve C8, T1. ADDUCTOR POLLICIS KINETIC CHAIN COMMENT This muscle decelerates abduction of the thumb. MYOFASCIAL TRIGGER POINT COMMENT Aching pain is felt on the outside of the thumb and on the hand at the base of the thumb, which has a tendency to lock. Patients find it difficult to control movement of the thumb and have difficulty holding a pen. Difficulty fastening buttons or performing actions that require fine muscle control becomes evident. Myofascial trigger point pain can be felt in the thumb web space and the thenar eminence. It is worth pointing out at this stage to remember which other muscles refer pain into these areas—the scalenes, brachialis, supinator, extensor carpi radialis longus, and brachioradialis. Remember to check these muscles first (in the order of most medial and superior). PRACTITIONER GUIDELINES ### Patient positioning Patient is supine, with the forearm supported. ### Needle type Use 0.14 to 0.16mm × 15mm needle. ### Needling directions The muscle is needled through the posterior skin surface between the thumb and the first finger. ### Precautions Fine, short needles are recommended. Adductor pollicis, supine with the forearm supported. ABDUCTOR POLLICIS LONGUS **Latin** , _abducere_ , to lead away from; _pollicis_ , of the thumb; _longus_ , long. Origin Posterior surfaces of the ulna and the radius, and interosseous membrane. Insertion Base of the first metacarpal. Action Abducts and extends the thumb at the carpometacarpal joint. Nerve Posterior interosseous nerve C6–C8.MYOFASCIAL TRIGGER POINT COMMENT The abductor pollicis longus is one of a number of muscles that can generate stiffness in the hand and fingers, often mistaken for arthritis.Patients have reported waking from their sleep because of cramping.As a result of inhibitory influences, the fingers and forearm lose local endurance, and fatigue sets in early on.Skilled control of the thumb reduces.

There can be primary disorders of structures in the bronchi (cartilage defects), diseases of mucus clearance (CF), infectious aetiologies (severe childhood bronchial infections) and inflammatory diseases (ulcerative colitis).87 Bronchiectasis can present with generalised effects on the lungs as seen with CF or the pattern may be more localised in a segment of the lung.The family and the person with CF have a great financial and emotional burden. The cost of medication, special equipment and healthcare is often a financial hardship. Because most CF patients live to childbearing age, family planning and genetic counselling are important. The burden of living with a chronic disease at a young age can be emotionally overwhelming. Community resources are often available to help the family. In addition, associations such as Cystic Fibrosis Australia and the Cystic Fibrosis Association of New Zealand can be of assistance (see Resources on pp 727–728). As the person continues towards and into adulthood, nurses and other skilled health professionals should be available to help the patient and family cope with complications resulting from the disease. # Bronchiectasis ## AETIOLOGY AND PATHOPHYSIOLOGY **Bronchiectasis** is characterised by permanent, abnormal dilation of one or more large bronchi in either a localised or diffuse pattern. The pathophysiological change that results in dilation is destruction of the elastic and muscular structures supporting the bronchial wall. The disease process results in a reduced ability to clear mucus from the lungs and decreased expiratory airflow. Thus bronchiectasis is classified as an obstructive lung disease. A variety of pathophysiological processes can result in bronchiectasis. There can be primary disorders of structures in the bronchi (cartilage defects), diseases of mucus clearance (CF), infectious aetiologies (severe childhood bronchial infections) and inflammatory diseases (ulcerative colitis).87 Bronchiectasis can present with generalised effects on the lungs as seen with CF or the pattern may be more localised in a segment of the lung.Bronchiectasis can follow a severe pneumonia with a wide variety of infectious agents initiating bronchiectasis, including adenovirus, influenza virus, _S.aureus_ , _Klebsiella_ and anaerobes.Infections cause the bronchial walls to weaken and pockets of infection begin to form (see Fig 28-20).

**22 Genital infestations** 14.**21 Anogenital warts and human papilloma virus infection** 13.**20 Molluscum contagiosum and normal genital lumps** 12.**19 Epididymo-orchitis and sexually-acquired reactive arthritis** 11.**18 Genital ulcers: tropical infections** 10.**17 Genital herpes** 9.**16 Syphilis** 8.**15 Trichomonas vaginalis** 7.**14 Vulvovaginal candidiasis** 6.* Oral contraception: EE and progestogens are absorbed from the small bowel and therefore small bowel disease and malabsorption may reduce efficacy. Large bowel disease is unlikely to affect efficacy of oral methods * Progestogen-only injectables and implant, non-oral CHC methods, and intrauterine devices are good alternatives if malabsorption is a concern * Barrier methods are not reliable enough in women taking teratogenic (or potentially teratogenic) medications. Rectally administered therapies for IBD can in theory spread onto the genital skin and damage barrier methods * DMPA has possible detrimental effects on BMD and as osteopenia and osteoporosis are more common in women with IBD, consideration should be given to the risks and benefits before using this in those who have the condition * Laproscopic sterilization in women who have had previous abdominal or pelvic surgery carries twice the complication rate of those with no previous surgery. Hysteroscopic sterilization would be a safe alternative or sterilization at the time of other abdominal surgery * CHC methods should be stopped at least 4 weeks before major elective surgery to reduce the risks of VTE # Part 3 Sexual Health **Chapters** 1. **10 Chlamydia trachomatis** 2. **11 Gonorrhoea and non-gonococcal urethritis** 3. **12 Vaginal discharge** 4. **13 Bacterial vaginosis** 5. **14 Vulvovaginal candidiasis** 6. **15 Trichomonas vaginalis** 7. **16 Syphilis** 8. **17 Genital herpes** 9. **18 Genital ulcers: tropical infections** 10. **19 Epididymo-orchitis and sexually-acquired reactive arthritis** 11. **20 Molluscum contagiosum and normal genital lumps** 12. **21 Anogenital warts and human papilloma virus infection** 13. **22 Genital infestations** 14.**24 Viral hepatitis A, B and C** 16.**25 HIV** 17.**26 Sexual assault** Don't forget to visit the companion website at www.ataglanceseries.com/sexualhealth where you can test yourself on these topics.# Chapter 10 Chlamydia trachomatis ### Background In 2008 the World Health Organization (WHO) estimated there were 105 million new cases of chlamydia worldwide.

Exercise gave me an unanticipated, wonderful benefit in addition to the ones you'd expect.Originally, I swam; now I do power walking."My eating was always healthy, so my diet didn't have to change much, but I began a committed exercise program that has become an important part of my life.In the few months after diagnosis, Jan made a number of changes in her life."Myeloid metaplasia" means that marrowlike tissue is growing in a different place from where it should be—in this case, in the spleen. "Agnogenic" is a choice word meaning "of unknown cause" (or, perhaps better, "We haven't a clue as to why you have this condition or what we can do to fix it"). The root problem is replacement of functioning marrow by fibroblasts, the cells that make connective tissue. In response to this life-threatening process, the spleen takes over the job of manufacturing blood cells; its enlargement is a compensatory—or healing—response to the disease, which is why splenectomy would be disastrous. The prognosis in primary myelofibrosis is uncertain. Most people who acquire it are older than Jan, often in their sixties or seventies, and they may die of other causes. In some people, the marrow disorder turns into leukemia. "They told me it was rare in my age group and that the average life expectancy was ten years," Jan recalls. "But they gave me some other statistics that were more hopeful, like twenty-five percent of people had no further problems. I thought, 'That's not so bad. I can be in that twenty-five percent.' " No treatment was offered or recommended. "I'm actually grateful for that," Jan says. "Since there were no drugs or surgery to help me, it left me to do all the work on my own." She was told to have regular blood counts to determine whether the condition was progressing. In the few months after diagnosis, Jan made a number of changes in her life. "My eating was always healthy, so my diet didn't have to change much, but I began a committed exercise program that has become an important part of my life. Originally, I swam; now I do power walking. Exercise gave me an unanticipated, wonderful benefit in addition to the ones you'd expect.Jan says the most significant changes were psychological."First of all, I gave myself permission to take care of myself.I resolved never to apologize for nurturing myself.I dropped out of an overtaxing school program in nursing and went instead for a master's degree in experiential education.(My experience was living with this diagnosis and coming to a holistic philosophy of health.)

A research study showed that normal dogs fed b/d were able to learn new tasks more quickly than dogs fed a regular diet.Hill's Prescription Diet Canine b/d contains antioxidants, brain-specific fatty acids, and other nutrients to help slow the breakdown of brain cells.There's also a prescription dog food designed to fight aging changes in the brain."** Some dogs do develop a sort of Alzheimer's disease as they get older. The veterinary term for it is canine cognitive dysfunction (CCD). The symptoms can include failure to recognize familiar locations or people, wandering or pacing, restlessness at night, and loss of housebreaking. Because there aren't any practical ways to test a dog's thinking ability, CCD is diagnosed by ruling out physical explanations for the symptoms, such as failing eyesight or blindness, a urinary tract infection, or pain that causes the dog to feel irritable and distracted. The drug Anipryl (selegiline/deprenyl) reduces the symptoms of CCD in some dogs. Other dogs are either not helped by Anipryl or show an increase in symptoms such as restlessness and trembling. Anipryl should not be given to a dog who is taking either phenylpropanolamine (for urinary incontinence) or an anti-depressant, because the combination of drugs can produce extreme restlessness and agitation. A dog taking Anipryl should not use a Preventic collar or other products that contain amitraz. Melatonin is a natural supplement that's often recommended for dogs who display sleeplessness, restlessness, or agitation at night, but it shouldn't be used in diabetic dogs. See page 196 for other alternative-medicine options for treating canine cognitive dysfunction. There's also a prescription dog food designed to fight aging changes in the brain. Hill's Prescription Diet Canine b/d contains antioxidants, brain-specific fatty acids, and other nutrients to help slow the breakdown of brain cells. A research study showed that normal dogs fed b/d were able to learn new tasks more quickly than dogs fed a regular diet.#### UNDERSTANDING AGGRESSION **"When I took my Chihuahua to the vet for a nail trim, the assistant asked me whether he was aggressive.I said of course not, she tried to pick him up, and he growled and snapped at her.The girl jerked her hand back and said to me, 'Not aggressive, huh?'in a nasty tone, and I got mad and left.What was her problem?

• RF is an IgM autoantibody that has specificity for the Fc portion of IgG.RA: activated CD4 + T cells release proinflammatory agents b. Inflamed synovial cells express an antigen that triggers B cells to produce rheumatoid factor (RF).One proposed mechanism is CD4 + helper T cells (cell-mediated type IV) are activated leading to release of proinflammatory agents (e.g., tumor necrosis factor).a.Use of a cane c. Analgesics (NSAIDs, acetaminophen; do not use at the same time refer to [Chapter 20]) d. Viscosupplementation (questionable usefulness) • Oral chondroitin sulfate, glucosamine e. Joint replacement E **Neuropathic arthropathy (Charcot joint)** 1. Definition—noninflammatory joint disease secondary to a neurologic disease • Loss of proprioception and deep pain sensation leading to recurrent trauma Neuropathic joint: loss of proprioception and deep pain sensation, leading to recurrent trauma 2. Causes a. Diabetes mellitus (15% of cases) • Primarily affects the tarsometatarsal joint b. Syringomyelia (20%–25% of cases) • Primarily affects the shoulder, elbow, wrist joints Common causes: DM, syringomyelia, tabes dorsalis c. Tabes dorsalis (10%–20% of cases) • Primarily affects the hip, knee, and ankle joints 3. Treatment a. Immobilization b. Pneumatic walking braces F **Rheumatoid arthritis (RA)** 1. Epidemiology a. Definition—systemic disorder associated with chronic joint inflammation that most commonly affects peripheral joints b. Occurs more often in women 30 to 50 years of age RA: women > men; HLA-DR4 c. HLA-DR4 association d. ? Initial inciting agents • Epstein-Barr virus, parvovirus, human herpesvirus 6, _Mycoplasma_ e. Risk factor for septic arthritis • Medications may suppress the immune system, making infections more likely to occur. 2. Pathogenesis of joint disease involves both type III and type IV reactions. a. One proposed mechanism is CD4 + helper T cells (cell-mediated type IV) are activated leading to release of proinflammatory agents (e.g., tumor necrosis factor). RA: activated CD4 + T cells release proinflammatory agents b. Inflamed synovial cells express an antigen that triggers B cells to produce rheumatoid factor (RF). • RF is an IgM autoantibody that has specificity for the Fc portion of IgG.RA: RF forms ICs with IgG → activate complement system d. ICs activate the complement system to produce C5a, a chemotactic agent for neutrophils and other leukocytes to enter the joint space.e. Chronic synovitis and pannus formation eventually occur (Fig.24-8A).24-8: **A,** Schematic of rheumatoid arthritis in a joint.

Senile Dementia, Senility Senility refers to mental deterioration and infirmity that is often associated with old age, as in severe memory problems.It can also reflect the person reacting to possible separation or tension between their parents, something happening with the father that results in a sense of separation from the mother.As always, see when the symptom began, and also when the symptom was diagnosed and what was happening in the person's life at that time. Scotopic Sensitivity Syndrome – See Meares–Irlen Syndrome Scurvy Scurvy is a disease that occurs when there is a severe lack of vitamin C (ascorbic acid) in the diet. It causes general weakness, anaemia, gum disease and a rash on the legs, reflecting root chakra tensions and insecurity about money, home, job and mother. Seasickness – See Motion Sickness Seasonal Affective Disorder (SAD) Seasonal affective disorder or SAD, also known as winter depression, winter blues, summer depression, summer blues or seasonal depression, is a disorder in which people who have normal mental health throughout most of the year experience depressive symptoms in the winter or summer. Depression is a sense of powerlessness to do something about an unhappy situation, and can then be related to the situation the person is unhappy about during the season in which they feel affected. Seizures Seizures happen because of sudden, abnormal electrical activity in the brain, which is associated with the crown chakra. Thus, there is tension about father/authority, or a sense of separation from someone. Often the symptom is triggered by fear, and the person goes out of their body, pointing to root chakra tensions about money, home, job or mother. It can also reflect the person reacting to possible separation or tension between their parents, something happening with the father that results in a sense of separation from the mother. Senile Dementia, Senility Senility refers to mental deterioration and infirmity that is often associated with old age, as in severe memory problems.There may also be crown chakra considerations; feeling isolated or separated from others due to society's attitudes toward aging.Sepsis/Septicaemia Septicaemia, formerly called blood poisoning, is an infection resulting from the presence of bacteria in the blood.It often begins with a high fever, chills, weakness and excessive sweating, followed by a decrease in blood pressure.

Observation of the catheter for misplacement or slippage is important.Catheter and insertion site assessment includes inspection of the site for redness, oedema, warmth, drainage and tenderness or pain.Although there may be specific institution policies and procedures regarding different types of CVADs, there are some general guidelines to be followed too.The port is accessed via the septum by means of a special Huber-point needle that has a deflected tip, which prevents damage to the septum that could make the port useless (see Fig 16-20, B).15 Huber-point needles are also available with the tip at a 90° angle for longer infusions. Implanted ports are good for long-term therapy and have a low risk of infection. Because the port is hidden it offers cosmetic advantages. Implanted ports have been developed that are safe for injections of radio-opaque contrast media at high pressures and controlled rates. For patients who already have poor peripheral venous access, the ability to use the port to inject contrast media decreases discomfort from venipuncture and helps lower the risk for extravasation of vesicant contrast media.17 Care requirements include regular flushing. Formation of 'sludge' (accumulation of clotted blood and drug precipitate) may also occur within the port septum. ## COMPLICATIONS The potential for complications associated with CVADs is always present. Astute monitoring and assessment may assist in early identification of potential complications. Table 16-20 lists common possible complications, potential causes, clinical manifestations and interventions. ## NURSING MANAGEMENT: CENTRAL VENOUS ACCESS DEVICES Nursing management of CVADs includes assessment, dressing change and cleansing, injection cap changes and flushing. Although there may be specific institution policies and procedures regarding different types of CVADs, there are some general guidelines to be followed too. Catheter and insertion site assessment includes inspection of the site for redness, oedema, warmth, drainage and tenderness or pain. Observation of the catheter for misplacement or slippage is important.Transparent semipermeable dressings or gauze and tape can be used.If the site is bleeding, a gauze dressing may be preferable; otherwise, transparent dressings have some advantages over gauze and tape.For example, they allow observation of the site without dressing removal and may be left in place for up to 1 week if clean, dry and intact.

Plasminogen is converted to plasmin by proteolytic cleavage.### Test Explanation Plasminogen is a protein involved in the fibrinolytic process of intravascular blood clot dissolution (see Figure 2-12 on p. ).Certain GPI-anchored proteins protect red blood cells from destruction; others are involved in blood clotting, whereas others are involved in fighting infection. Therefore the majority of the disease manifestations (i.e., hemolytic anemia, thrombosis, and infection) result from a deficiency of these GPI-anchored proteins. Individuals without PNH have normal expression of all PI-linked antigens—CD14 (monocytes), CD16 (neutrophils and NK cells), CD24 (neutrophils), and CD59 (RBCs). Other GPI-linked antigens noted to be absent in PNH include CD55, and CD59. In addition, FLAER, a fluorescently labeled inactive variant of aerolysin, binds directly to the GPI anchor and can be used to evaluate the expression of the GPI linkage. ### Procedure and Patient Care #### Before Explain the procedure to the patient. Tell the patient that no fasting is required. #### During • Collect a venous blood sample in a yellow (ACD)-top tube. #### After • Apply pressure or a pressure dressing to the venipuncture site. ### Test Results and Clinical Significance #### Decreased Levels PNH: _These GPI linked antigens are reduced or absent in patients with PNH. Determining which antigen is most significantly reduced will highlight the disease manifestations._ ## Plasminogen (Fibrinolysin) ### Normal Findings 2.4-4.4 Committee on Thrombolytic Agents (CTA) units/mL ### Indications This test is used to diagnose suspected plasminogen deficiency in patients who present with multiple thromboembolic episodes. ### Test Explanation Plasminogen is a protein involved in the fibrinolytic process of intravascular blood clot dissolution (see Figure 2-12 on p. ). Plasminogen is converted to plasmin by proteolytic cleavage.Plasmin can destroy fibrin and dissolve clots.This fibrinolytic system helps maintain a normal homeostatic balance between coagulation and anticoagulation.Plasminogen levels are occasionally measured during fibrinolytic therapy (for coronary and peripheral arterial occlusion) and are diminished.

Neither drug is appropriate for women with a Factor V Leiden mutation, those who have (or have had) blood clots, or those taking estrogen replacement or certain cholesterol-reducing drugs, including Locholest and Questran.These medications also increase the chance of stroke and blood clots, particularly in those who smoke or have clotting disorders.If you decide to take tamoxifen and you already take Paxil, Prozac, Wellbutrin, or another antidepressant, discuss it with your doctor, who may consider an alternative such as Celexa, Effexor, or Lexapro. Your doctor can also determine if any of your other medicines, vitamins, or supplements should be reconsidered. If you currently take tamoxifen, don't abruptly quit your antidepressant. Your doctor can help decide whether any change in medication is warranted and, if so, the best way to wean away from one drug or switch to a substitute. ##### **Side Effects of SERMs** Tamoxifen and raloxifene are reliable and effective multitasking medications. Aside from potentially preventing breast cancer, they improve bone density. Both, however, have side effects. Taking either medication may cause hot flashes, vaginal dryness, mood changes, and other menopause-like symptoms, which may be mild and well tolerated by some women; others need medication to address their symptoms. SERMs can also cause vaginal bleeding or discharge, headaches, nausea, leg cramps, rashes, and other serious side effects. Tamoxifen slightly increases a woman's risk for endometrial cancer—the risk is still relatively low, about two chances in 1,000 per year. Raloxifene has less risk of uterine cancer. Unlike tamoxifen, it doesn't have an estrogen-like effect on the uterus. These medications also increase the chance of stroke and blood clots, particularly in those who smoke or have clotting disorders. Neither drug is appropriate for women with a Factor V Leiden mutation, those who have (or have had) blood clots, or those taking estrogen replacement or certain cholesterol-reducing drugs, including Locholest and Questran.For survivors, AIs work more effectively than tamoxifen against advanced breast cancer; following five years of tamoxifen with five years of an AI continues to reduce your risk of recurrence.Health experts are hoping AIs prevent breast cancer in postmenopausal previvors as successfully as they treat breast cancers in women with sporadic, hormone-positive breast cancers.

• CML is characterized by the presence of Philadelphia-chromosome (reciprocal translocation between chromosomes 9 and 22 resulting in a BCR-ABL fusion gene).• This topic focuses on the classic MPNs.Therapy-related myelodysplastic syndrome: morphologic subclassification may not be clinically relevant. Am J Clin Pathol. 2007;127(2):197–205. CODES ICD10 • D46.9 Myelodysplastic syndrome, unspecified • D46.4 Refractory anemia, unspecified • D46.B Refract cytopenia w multilin dysplasia and ring sideroblasts CLINICAL PEARLS • MDS constitutes a heterogeneous group of acquired, hematopoietic stem cell disorders characterized by cytologic dysplasia in the bone marrow and blood and by various combinations of anemia, neutropenia, and thrombocytopenia. • The natural progression of this malignant disease evolves as cellular maturation becomes more arrested and blast cells accumulate. MYELOPROLIFERATIVE NEOPLASMS Tarsheen K. Sethi, MBBS • Sanjay Mohan, MD, MSCI BASICS DESCRIPTION • Myeloproliferative neoplasms (MPNs) are a group of clonal disorders that share a common cell of origin in the pluripotent hematopoietic stem cell. • MPNs are characterized by proliferation of cells of myeloid lineage—granulocytic, erythroid, megakaryocytic or mast cell. They share common clinical features including risk of thrombosis, spleen and/or liver enlargement and constitutional symptoms related to a hypermetabolic state. • The "classic" MPNs include chronic myelogenous leukemia (CML), polycythemia vera (PV), essential thrombocythemia (ET), and primary myelofibrosis (PMF). World Health Organization (WHO) MPN classification also includes chronic neutrophilic leukemia, chronic eosinophilic leukemia not otherwise specified (CEL-NOS), systemic mastocytosis, and MPN unclassifiable. • This topic focuses on the classic MPNs. • CML is characterized by the presence of Philadelphia-chromosome (reciprocal translocation between chromosomes 9 and 22 resulting in a BCR-ABL fusion gene).• The following three MPNs are characterized by varying degree of presence of JAK2 V617F mutation and are negative for BCR-ABL fusion gene.

This may have its basis in the lymphatic drainage, which helps detoxify tissue.There is a long tradition for the use of Cleavers in the treatment of ulcers and tumours.It is helpful in the treatment of cystitis and other urinary conditions where there is pain and may be combined with urinary demulcents for this.Externally it makes a good compress or poultice to speed up the healing of wounds and ulcers. Eczema and psoriasis may also be treated this way externally, but it must be remembered that such skin problems can only be healed from within and with the aid of internal remedies. _Combinations_ : For skin problems, combine with _Yellow Dock, Red Clover_ or _Cleavers_. _Preparation and dosage_ : Decoction: put 1 teaspoonful of the root into a cup of water, bring to the boil and simmer for 10–15 minutes. This should be drunk three times a day. For external use see further information in the section on the skin in Chapter 6. _Tincture_ : Take 2–4ml of the tincture three times a day. CLEAVERS | _Galium aparine_ ---|--- _Common names_ : Goosegrass, clivers. _Part used_ : Dried aerial parts and the fresh expressed juice. _Collection_ : The plant should be gathered before flowering and dried in the shade. _Constituents_ : Glycoside asperuloside, gallotannic acid, citric acid. _Actions_ : Diuretic, alterative, anti-inflammatory, tonic, astringent, anti-neoplastic. _Indications_ : This is a remedy with a long tradition of folk usage. Much of the 'old wives' wisdom has a good solid foundation in herbal therapy. It is a very valuable plant, being perhaps the best tonic to the lymphatic system available. As a lymphatic tonic with alterative and diuretic actions it may be used safely in a wide range of problems where the lymphatic system is involved. These include swollen glands (lymphadenitis) anywhere in the body and especially in tonsillitis and in adenoid trouble. It is helpful in a wide variety of skin conditions, especially in the dry kind such as psoriasis. It is helpful in the treatment of cystitis and other urinary conditions where there is pain and may be combined with urinary demulcents for this. There is a long tradition for the use of Cleavers in the treatment of ulcers and tumours. This may have its basis in the lymphatic drainage, which helps detoxify tissue._Combinations_ : for the lymphatic system it will work well with _Poke Root, Echinacea_ and _Marigold_.For skin conditions it is best combined with _Yellow Dock_ and _Burdock_._Preparation and dosage_ : Infusion: pour a cup of boiling water onto 2–3 teaspoonsful of the dried herb and leave to infuse for 10–15 minutes.This should be drunk three times a day.

In Otto CM, Bonow RO, editors.(From Otto CM: Echocardiographic evaluation of valvular heart disease.B, The short-axis view allows accurate planimetry of the mitral orifice area if care is taken to identify the smallest opening by scanning slowly from apex toward the base.Left atrial enlargement is present.(From Otto CM: Echocardiographic evaluation of valvular heart disease. In Otto CM, Bonow RO, editors. Valvular Heart Disease: A Companion to Braunwald's Heart Disease, 4th ed. Philadelphia, Saunders, 2014.) VIDEO 63-8B Bicuspid aortic valve. A, The parasternal long-axis view shows diastolic sagging and systolic doming of the leaflets. B, In the short-axis view, only two leaflets (arrows) are shown to open in systole with the commissures at 4- and 10-o'clock positions. (From Otto CM: Echocardiographic evaluation of valvular heart disease. In Otto CM, Bonow RO, editors. Valvular Heart Disease: A Companion to Braunwald's Heart Disease, 4th ed. Philadelphia, Saunders, 2014.) VIDEO 63-9A Mild rheumatic mitral stenosis. A, The parasternal long-axis view shows the typical doming of the anterior mitral leaflet as a result of commissural fusion. Left atrial enlargement is present. B, The short-axis view allows accurate planimetry of the mitral orifice area if care is taken to identify the smallest opening by scanning slowly from apex toward the base. (From Otto CM: Echocardiographic evaluation of valvular heart disease. In Otto CM, Bonow RO, editors. Valvular Heart Disease: A Companion to Braunwald's Heart Disease, 4th ed. Philadelphia, Saunders, 2014.) VIDEO 63-9B Mild rheumatic mitral stenosis. A, The parasternal long-axis view shows the typical doming of the anterior mitral leaflet as a result of commissural fusion. Left atrial enlargement is present. B, The short-axis view allows accurate planimetry of the mitral orifice area if care is taken to identify the smallest opening by scanning slowly from apex toward the base. (From Otto CM: Echocardiographic evaluation of valvular heart disease. In Otto CM, Bonow RO, editors.Philadelphia, Saunders, 2014.)VIDEO 63-10A Planimetry of mitral valve area.Long-axis (A) and short-axis (B) views show thickened and calcified leaflet tips.Note the diastolic doming and severe commissural fusion.Valve area as calculated by two-dimensional planimetry is 0.6 cm2.In addition, severe left atrial enlargement is present.

Blood too thick and too viscous will have a much slower passage through these capillaries, reducing the flow of oxygen, glucose and other nutrients to eyes and ears.If sluggish blood is a problem in large vessels, it is even more of a problem in the fine capillaries that feed the eyes and ears.#### **Causes of age-related hearing loss** Noise is known to be a major cause of hearing loss, whether it's a sudden loud whistle or explosion, or the continuous clamour of a noisy workplace. A serious concern is the amount of noise ears are exposed to at a young age through personal listening devices turned up way too high. These devices operate in proximity to the sensitive hair cells of the ear that are easily damaged. Rock musicians typically suffer premature hearing loss. Exposed to excessive noise, the small sensory hair cells in the inner ear may die. These cells convert sound energy into electrical signals that travel through the auditory nerve to the brain. Death of the hair cells (apoptosis) may be caused by circulatory problems and diseases such as diabetes. Once damaged, those cells are not easily replaced. Magnesium has been shown to protect ears from noise-induced hearing loss and in some cases even reverse it. In one interesting experiment, 300 U.S. military recruits were given a fairly small dose (173 mg a day) of magnesium, while another group of recruits was given a placebo. The objective was to see if magnesium would protect them from hearing loss brought on by repeated exposure to gunfire over a two-month training period. Recruits who had daily magnesium were less likely to experience hearing loss than those who were given a placebo, and if they did, it was less severe. #### **Other causes of gradual hearing loss** Hyperviscosity of the blood can affect hearing as well as vision. Blood may thicken as we age, causing it to travel more slowly through blood vessels, which puts us at increased risk of blood clots and stroke. If sluggish blood is a problem in large vessels, it is even more of a problem in the fine capillaries that feed the eyes and ears. Blood too thick and too viscous will have a much slower passage through these capillaries, reducing the flow of oxygen, glucose and other nutrients to eyes and ears.Diets high in saturated fats increase blood viscosity, while diets high in fruits, vegetables and omega-3 fats found in fish and fish oils will keep blood thin naturally.Eating two or more servings of fish a week has been shown to reduce the risk of age-related hearing loss by 42 percent compared to those eating less than one serving a week.

If pain persists, stop the irrigation.• If pain occurs, decrease the pressure.• Do not use blasts or bursts of sudden pressure.• Apply gentle but firm continuous pressure, allowing the water to flow against the top of the canal.When the occluding material is cerumen, management options include watchful waiting, manual removal, and the use of ceruminolytic agents followed by either manual irrigation or the use of a low-pressure, electronic, oral irrigation device (Holcomb, 2009). The canal can be irrigated with a mixture of water and hydrogen peroxide at body temperature (Fig. 51-2), following best practices for proper irrigation (Chart 51-2). Removal of a cerumen obstruction by irrigation is a slow process and may take more than one sitting. When it is the cause of hearing loss, cerumen removal may improve hearing. Between 50 and 70 ml of solution is the maximum amount that the patient with an impaction usually can tolerate at one sitting. FIG. 51-2 Irrigation of the external canal. Cerumen and debris can be removed from the ear by irrigation with warm water. The stream of water is aimed above or below the impaction to allow back-pressure to push it out rather than further down the canal. Chart 51-2 Best Practice For Patient Safety & Quality Care Ear Irrigation • Wash your hands. • Use an otoscope to check the location of the impacted cerumen; ascertain that the eardrum is intact and that the patient does not have otitis media. • Gather the proper equipment: basin, syringe (without needle), otoscope, towel. • Warm tap water (or other prescribed solution) to body temperature. • Fill a syringe with the warmed irrigating solution. • Place a towel around the patient's neck. • Place a basin under the ear to be irrigated. • Place the tip of the syringe at an angle so that the fluid pushes on one side of and not directly on the impaction (this helps loosen the impaction instead of forcing it further into the canal). • Apply gentle but firm continuous pressure, allowing the water to flow against the top of the canal. • Do not use blasts or bursts of sudden pressure. • If pain occurs, decrease the pressure. If pain persists, stop the irrigation.• Continue to irrigate the ear with about 70 mL of fluid.• If the cerumen does not drain out, wait 10 minutes and repeat the irrigation procedure.• Monitor the patient for signs of nausea.• If the patient becomes nauseated, stop the procedure.

These structures run down the back of the abdominal cavity and enter the bladder where it sits within the pelvis.The physiology of the ureters The ureters receive a steady flow of urine from the renal pelvis at a rate of 20–100 milliliters/hour.For this reason, kidney disease can be a cause of the disease of weakening of the bones known as osteomalacia.When blood oxygen levels drop, the secretion of EPO is stimulated, and this in turn increases the production of red blood cells from the bone marrow. These blood cells are then available to carry more oxygen, and thereby to increase the level of oxygen in the blood. The kidneys and the control of blood pressure Healthy kidneys are essential for the control of blood pressure, and disease of the kidneys is one of the causes of hypertension. In addition, the kidneys act in a situation of shock (low blood pressure) to conserve fluid, and so to prevent its loss into the urine. There are at least two important hormone systems that cause the kidney to excrete more fluid when the blood pressure is high and to conserve fluid when the blood pressure drops. The hormones involved in the kidneys' control of blood pressure include aldosterone, renin, angiotensin I and II, and atrial natriuretic factor (ANF). ACE (angiotensin-converting enzyme) inhibitors and angiotensin II receptor blockers are drugs used in the treatment of hypertension and heart failure. They act by blocking the formation of one of these hormones (angiotensin II). The kidneys and vitamin D metabolism Although vitamin D is mostly manufactured as a response to the action of sunlight on the skin, it requires conversion within the kidneys to become active in the body. For this reason, kidney disease can be a cause of the disease of weakening of the bones known as osteomalacia. The physiology of the ureters The ureters receive a steady flow of urine from the renal pelvis at a rate of 20–100 milliliters/hour. These structures run down the back of the abdominal cavity and enter the bladder where it sits within the pelvis.The urine that enters the bladder passes through a narrowing, akin to a valve, as it enters the bladder.This important structure prevents the return of urine back into the ureter (known as reflux) from the bladder.The urine enters the bladder in little spurts, which occur every 10 seconds or so.

Malignant tumours and their precursor conditions are of major pathological importance.As in other systems, a wide range of pathological conditions may occur in these organs.#### Cross-reference: Chapters 15 and 16 17 # Female reproductive system ## Introduction The female reproductive tract comprises the vulva, vagina, uterus, fallopian tubes and ovaries.This mixed inflammatory cell background with R-S cells is typical of several variants of classical Hodgkin lymphoma. #### Cross-reference: Chapter 16 ### Chapter 16 Answer 4 #### Correct answer with explanation: * D) Correct. There is a lymphoepithelial lesion, typical of gastric MALT-type lymphoma. The image shows a damaged gastric gland infiltrated by small lymphocytes, forming a lymphoepithelial lesion. * A, B) Incorrect. The background cells are mainly small lymphocytes, not neutrophils or macrophages. * C) Incorrect. There is no goblet cell metaplasia, although this can occur in association with chronic Helicobacter infection and is associated with a risk of dysplasia and carcinoma. * E) Incorrect. Helicobacter has a well-defined pathogenetic role in the development of gastric MALT-type lymphoma (extranodal marginal zone lymphoma) and, in some early cases, Helicobacter eradication therapy may result in regression of the lymphoma. #### Cross-reference: Chapters 13 and 16 ### Chapter 16 Answer 5 #### Correct answer with explanation: * E) All of the above. The bony trabeculae are surrounded by pale, malignant glands and cribriform patterns, typical of metastatic adenocarcinoma (A). Prostatic carcinoma is unusual in commonly producing sclerotic metastases (B), rather than more typical osteolytic metastases (C). This is due to factors produced by the tumour cells which activate osteoblasts. Serum PSA levels can be used in prostate cancer screening but are often of greater use in tracking the progression of disease and the effectiveness of treatment in patients with known disease (D). #### Cross-reference: Chapters 15 and 16 17 # Female reproductive system ## Introduction The female reproductive tract comprises the vulva, vagina, uterus, fallopian tubes and ovaries. As in other systems, a wide range of pathological conditions may occur in these organs. Malignant tumours and their precursor conditions are of major pathological importance.For example, serous adenocarcinoma is most commonly found in the ovary but can also present in the uterus and cervix.## Disorders of the vulva and vagina The vulva is subject to many of the conditions affecting skin elsewhere in the body, including inflammatory conditions such as dermatitis and lichen planus (see Ch.

This is especially true for people with prediabetes.Well, it turns out that making changes to the foods you eat or exercising more can reduce your risk for diabetes.Why does prediabetes matter?One out of three American adults has prediabetes, although many don't know they have it; nine out of ten Americans who have prediabetes are undiagnosed.Women with preexisting type 2 diabetes should try to have their blood glucose on target before they become pregnant. They also need to exercise, eat healthy foods, and often take medications to manage their blood glucose during pregnancy. All pregnant women should be tested for gestational diabetes during the 24th to 28th week using the oral glucose tolerance test (see Chapter 9 for more details on tests to diagnose gestational diabetes). Then women with gestational diabetes should get a test for type 2 diabetes 4–12 weeks after giving birth and every 3 years thereafter. ### Other types of diabetes Type 1, type 2, and gestational diabetes are the main types of diabetes. However, they're not the only ones. Other forms of diabetes occur because of mutations in single genes. You can inherit these gene mutations, or they can occur out of the blue. Maturity-onset diabetes of the young (MODY) and neonatal diabetes mellitus are two of the most common forms. Cystic fibrosis–related diabetes is another type of diabetes common in people with cystic fibrosis, which occurs because of scarring of the pancreas. This also destroys beta cells and stops insulin production. ### Prediabetes Prediabetes is another term you've probably heard alongside type 2 diabetes. And it's exactly what it sounds like. _Prediabetes_ is a higher than normal blood glucose level that isn't high enough to be diabetes. One out of three American adults has prediabetes, although many don't know they have it; nine out of ten Americans who have prediabetes are undiagnosed. Why does prediabetes matter? Well, it turns out that making changes to the foods you eat or exercising more can reduce your risk for diabetes. This is especially true for people with prediabetes.In one study called the Diabetes Prevention Program, people with prediabetes who lost 5–7 percent of their body weight through changes to diet and exercise reduced their risk of developing diabetes by 58 percent during the 3-year course of the study.This was a landmark study that showed that people at risk for type 2 diabetes can make changes to prevent or delay the disease.

Alimentary hypoglycemia occurs in response to rapid glucose absorption.The mechanism of the hypoglycemia is unclear but is thought not to be related to excessive insulin secretion.It occurs following meals and is associated with high-energy, type A personalities.Functional hypoglycemia is the most common type.Gestational diabetes portends an increased risk for diabetes later in life. It also predisposes newborns to macrosomia, hypoglycemia, and respiratory distress syndrome. ### Case 8-12 A 42-year-old registered nurse complains of episodes of tremor, diaphoresis, and palpitations several hours after eating. She also notes similar symptoms when first waking in the morning. Symptoms are alleviated by eating. Her plasma glucose is low during symptomatic episodes, ranging from 30 to 60 mg/dL (she has access to a glucometer because her husband is diabetic). Review of systems is significant only for a 15-lb weight gain in recent months. Physical examination is unrevealing. ## 1 What is the differential diagnosis for hypoglycemia in this woman? Hypoglycemia can be "reactive" or can be due to insulin excess. Reactive or postprandial hypoglycemia can occur in various situations (more on this later). Excess insulin can be due to either an endogenous source (insulinoma, nesidioblastosis) or an exogeneous source (factitious hypoglycemia). For boards, realize that a patient with a significant psychiatric history or with access to prescription drugs (e.g., nurses, doctors) is suspect for exogenous insulin administration (factitious hypoglycemia). ## 2 What is reactive (postprandial) hypoglycemia? Reactive hypoglycemia can be categorized as functional or alimentary or representing early (occult) diabetes. Functional hypoglycemia is the most common type. It occurs following meals and is associated with high-energy, type A personalities. The mechanism of the hypoglycemia is unclear but is thought not to be related to excessive insulin secretion. Alimentary hypoglycemia occurs in response to rapid glucose absorption.Symptoms will often respond to reduced carbohydrate intake as well as smaller, more frequent meals.Early or occult diabetes mellitus can also cause hypoglycemia.The mechanism is felt to be related to a delay in early insulin release from beta cells, resulting in hyperglycemia.An exaggerated late-phase insulin secretion then occurs in response to the hyperglycemia.

###### _Heart murmurs (seeFig.• Back of chest for collateral vessels in coarctation.• Over lungs for signs of congestion (crackles which do not clear with coughing) as opposed to infection (crackles which may clear after coughing), pericardial effusion (may have scratchy rubbing sound, like walking on dry snow) or pulmonary effusion (diminished breath sounds).Feel at carotid and/or brachial for character, e.g. collapsing (see Chapter 7.6, Aortic regurgitation), slow rising (see Chapter 7.7, Aortic stenosis). • Chest wall: for respiratory expansion (?symmetrical, if not unilateral lung disease likely), for apex beat and character (displaced in left ventricular hypertrophy (LVH), left ventricular (LV) enlargement, tapping in mitral stenosis; see Chapter 7.4, Mitral stenosis), for RV heave in right heart overload, e.g. right to left shunt, pulmonary hypertension. • Over heart: effectively indicate a high-intensity heart murmur. • Oedema detection: look for pitting oedema at ankles, or sacrum if bed bound. • Liver edge for hepatic congestion of right heart failure. • Spleen edge palpable if enlarged. • Feel for enlarged ballotable kidneys in polycystic disease. ##### _Percussion_ • To detect pulmonary effusion, cardiac enlargement or pneumothorax and differential diagnosis for chest pain and dyspnoea. ##### _Auscultation_ ###### _Where to listen_ • Listen over arteries for bruits and shunts. • Chest wall: listen in aortic, mitral pulmonary and tricuspid areas for best determination of murmurs. Use augmentation strategies, e.g. ask patient to breathe out and stop while leaning forward to accentuate aortic murmurs. • Over lungs for signs of congestion (crackles which do not clear with coughing) as opposed to infection (crackles which may clear after coughing), pericardial effusion (may have scratchy rubbing sound, like walking on dry snow) or pulmonary effusion (diminished breath sounds). • Back of chest for collateral vessels in coarctation. ###### _Heart murmurs (seeFig.crescendo, decrescendo, or crescendo-decrescendo, and radiation of the murmur, pitch (high pitch best heard by diaphragm, low by bell) and quality (such as blowing, harsh, rumbling or musical).**Fig.1.1.1** Murmurs.See also Plate 1.• Ejection systolic murmur: in aortic area, accentuated by leaning forward, late crescendo murmur, can have soft A2: aortic stenosis.

See **fibrocystic disease of the breast.** chronic cystic mastitis.See **Huntington's disease.chronic chorea.See **cholecystitis**.chronic cholecystitis.See **cervicitis**.chronic cervicitis.chronic carrier, an individual who acts as host to pathogenic organisms for an extended period without displaying any signs of disease.See **care of the chronically ill**.chronic care.Prolonged expiratory phase, prominent cough, cyanosis, and acute attacks of respiratory distress with rapid, labored respirations may result. Common laboratory findings include elevated hematocrit, with or without respiratory acidosis; abnormal liver function caused by right-sided heart failure and hepatic congestion; pathogenic bacteria in the sputum; abnormal pulmonary function test results; and often chest x-ray signs of increased bronchial markings. INTERVENTIONS: Patients with chronic bronchitis should be immunized against influenza and pneumococcal infections. Broad-spectrum antibiotics are usually prescribed during acute exacerbations of symptoms. Bronchodilators, such as albuterol, and sympathomimetic drugs, such as terbutaline and metaproterenol, are prescribed to prevent worsening of the condition. Adrenergics and anticholinergics, like albuterol and Atrovent, are used to maintain lung function. Heart failure is managed with appropriate medication. NURSING CONSIDERATIONS: The nurse encourages the patient to discontinue smoking and to avoid exposure to toxic inhalants, such as hair sprays, aerosol insecticides, and occupational irritants and poisons. The use of low-flow oxygen in the home requires patient/family education and monitoring. Exercise, especially walking, is often indicated. See also **asthma,** **chronic obstructive pulmonary disease,** **cor pulmonale,** **emphysema,** **respiratory failure**. chronic calcific pancreatitis, pancreatitis with calcification in the ducts, usually associated with exocrine insufficiency and diabetes mellitus. chronic care. See **care of the chronically ill**. chronic carrier, an individual who acts as host to pathogenic organisms for an extended period without displaying any signs of disease. chronic cervicitis. See **cervicitis**. chronic cholecystitis. See **cholecystitis**. chronic chorea. See **Huntington's disease. ** chronic cystic mastitis. See **fibrocystic disease of the breast.The condition is sometimes associated with exhaustion, malnutrition, and wasting.chronic dieting syndrome, the extreme practice of following fad diets, often leading to harmful physical and psychological effects.Also called **dieting syndrome**.chronic disease, a disease that persists over a long period.

Advice on the diet is usually also given, particularly with respect to the type of protein that is fed.• Other drugs that may be used include antibiotics, vitamins, drugs to promote blood flow to the kidneys, to control vomiting and several others.Drinking replaces the water which is being lost in the very dilute urine which affected cats must pass (their kidneys are unable to concentrate the urine as normal due to poor function). Appetite should be tempted as much as possible. It is likely that, during bad spells, affected cats feel nauseous and thus reluctant to eat. However this compounds the problem by leading to dehydration and a negative energy balance. Try tempting with small meals of white meat, fish, scrambled eggs, etc. Warming the food often helps and many cats like sardines in tomato sauce, which is also a good source of potassium. Although red meats are generally advised against in kidney disease, small amounts may help to get the appetite started again if the cat particularly likes this. Vitamin supplements may be prescribed by the veterinary surgeon and well as periodic use of other drugs, e.g. antibiotics. Good nursing and grooming, gentle cleaning of the nose and eyes, etc. and communication with the cat can do wonders to improve demeanour and make a significant contribution to overall wellbeing. Try to avoid stressful situations if possible. Entering catteries may be associated with a deterioration in condition – whenever possible, cats with chronic renal failure should be looked after at home when the owners are away. ### Veterinary treatment • Kidney disease is diagnosed after blood and urine tests and its progress is monitored by repeat tests to check how effectively the kidneys are removing body toxins from the bloodstream. • Initial treatment may involve intravenous fluids (a drip) to correct problems with body fluid balance, and this treatment may need to be repeated during bouts of illness to 'rescue' the failing kidneys. • Other drugs that may be used include antibiotics, vitamins, drugs to promote blood flow to the kidneys, to control vomiting and several others. Advice on the diet is usually also given, particularly with respect to the type of protein that is fed.• The long-term trend is always downwards with chronic renal failure, however many cats can maintain a good quality of life for some time with appropriate treatment.Euthanasia is required when quality of life is poor, since appetite then tends to disappear, the cat becomes very subdued and may have distressing symptoms such as severe vomiting or even fits.

**Benefits** Like other B group vitamins, pantothenic acid is vital for many energy-yielding metabolic reactions involving carbohydrates, fats and protein.Despite its wide distribution in foods, many people do not obtain optimum levels of pantothenic acid, as it is easily destroyed by food processing and by deep freezing.One of the richest supplementary sources is royal jelly.When used for medicinal purposes, higher doses of 50 mg niacin a day may be taken. Doses as high as 1500 mg nicotinamide may be prescribed daily for certain medical disorders. Therapeutic use of high-dose niacin usually needs regular blood liver function tests. **Side effects** High-dose niacin (especially in the form of nicotinic acid) can produce a red flush and warming of the skin similar to blushing. People who blush easily seem to be more sensitive to this effect. For those who are very sensitive, a low dose of aspirin (75–300 mg) taken half an hour before the dose of niacin can reduce this effect. **Excess** Symptoms of niacin toxicity can occur at very high doses, including thickening and darkening of patches of skin (acanthosis nigricans), palpitations, worsening of pre-existing conditions such as diabetes and peptic ulceration. Gout and liver inflammation (hepatitis) can also be triggered. **Contraindications** Niacin should not be taken by sufferers of diabetes, low blood pressure, gout, liver disease, glaucoma or peptic ulcers except under medical advice. Niacin has been shown to increase absorption of dietary zinc and iron from the gut. **B5** Vitamin B5, or pantothenic acid, is a water-soluble vitamin widely found in foods such as whole grains, beans, vegetables, nuts, eggs, meats and yeast extract. One of the richest supplementary sources is royal jelly. Despite its wide distribution in foods, many people do not obtain optimum levels of pantothenic acid, as it is easily destroyed by food processing and by deep freezing. **Benefits** Like other B group vitamins, pantothenic acid is vital for many energy-yielding metabolic reactions involving carbohydrates, fats and protein.It has also been suggested that supplements containing pantothenic acid may help during weight-loss diets by ensuring that fatty acids released from body fat stores are fully broken down.This will reduce the formation of ketones so that hunger pangs and weakness are reduced.

When detected early, growth modification treatment may be a possibility and an option.Excessive vertical growth may create an open bite, while deficient vertical growth may create a deep bite.It seems evident that problems arise from the postural position of the tongue at rest as opposed to during function (Figures 6.3, 6.4). When planning treatment for correction of malocclusions in these patients, a combined approach with a speech pathologist to help train a new tongue position after treatment is recommended. This training may prevent or minimize future relapse tendencies. Figure 6.3 Eight-year-old boy with a tongue thrusting habit. (a) Facial picture showing a mild anterior open bite and (b) intraoral view showing the dental occlusion with a mild anterior open bite due to the anterior tongue position, with constricted upper arch and maxilla. (c–e) After expansion treatment, combined with speech therapy to retrain tongue posture, the open bite closed. (f) The patient was followed up for a year, during which no relapse was observed. Figure 6.4 Four-year-old girl with enlarged tonsils and adenoids, chronic mouth breathing and lower tongue posture. (a) Facial picture showing an enlarged mandible with a deficient maxilla and (b) intraoral view showing the dental occlusion with an anterior crossbite and increased spacing in the lower anterior teeth. Growth-Related Problems It is commonly understood that problems with craniofacial growth can result in functional impairments of the masticatory system as well as esthetic concerns. The manifestations of growth-related problems will depend on the craniofacial region or jaw being affected, the direction of growth, and the cause of the problem. Deficiencies such as in cases of Class II malocclusions caused by lack of sufficient growth of the mandible, or too much growth in cases of Class III malocclusions, caused by excessive mandibular growth, are examples of such craniofacial problems. Excessive vertical growth may create an open bite, while deficient vertical growth may create a deep bite. When detected early, growth modification treatment may be a possibility and an option.Therefore, a functional shift resulting from a crossbite should be corrected early, so that unfavorable growth of the mandible can be reduced or even prevented (Figure 6.5).Patients with lateral shifts of the mandible due to bite problems may develop asymmetries in condylar height (Kilic et al., 2008) (Figure 6.6).

In previously sedentary adults, the addition of regular exercise increases the plasma HDL cholesterol by a modest ~2 mg/dL (~0.05 mM).Nonsteroidal antiinflammatory drugs (NSAIDs) may reduce the flushing.Nicotinic acid often has side effects, such as flushing, that prevent patients from taking this drug.The resulting HDL recirculate and can transport more cholesteryl esters. However, the smaller the HDL, the shorter their lifetime in the circulation. Catalyzed by the cholesteryl ester transfer protein (CETP), VLDL exchange lipids with HDL (Fig. 29.7). HDL thus gain triglycerides and lose cholesteryl esters. Subsequently, hepatic lipase removes triglycerides from the HDL. This leaves poorly lipidated HDL, which are then degraded. This series of reactions is clinically important and accounts for the observed low value for HDL cholesterol in patients who have hypertriglyceridemia. Fig. 29.7 Cholesteryl ester transfer protein (CETP)-mediated exchange of lipids between high-density lipoproteins (HDL) and chylomicrons or very-low-density lipoproteins (VLDL) leads to low HDL cholesterol. FA, fatty acids; LCAT, lecithin-cholesterol acyltransferase; TG, triglycerides. ### 3.3 Treatment of a Low Concentration of HDL Cholesterol Most patients who have HDL cholesterol levels below 20 mg/dL (0.5 mM) have severe hypertriglyceridemia. The low HDL is a consequence of CETP-catalyzed triglyceride versus cholesteryl ester exchange between VLDL and HDL (see Fig. 29.7). When the triglyceride-enriched, cholesteryl ester–depleted HDL lose their triglyceride, they are poorly lipidated and therefore degraded prematurely. The treatment of hypertriglyceridemia often involves a statin, a fibric acid drug, and supplementary ω-3 fatty acids (see Chapter 32). Nicotinic acid (niacin, vitamin B3) reduces VLDL production and increases HDL cholesterol in part through reduced CETP-mediated lipid exchange between HDL and VLDL, which allows HDL to remain in the circulation longer. Nicotinic acid often has side effects, such as flushing, that prevent patients from taking this drug. Nonsteroidal antiinflammatory drugs (NSAIDs) may reduce the flushing. In previously sedentary adults, the addition of regular exercise increases the plasma HDL cholesterol by a modest ~2 mg/dL (~0.05 mM).About 1 in 400 people are heterozygous for an ABCA1 deficiency.These individuals have only about two-thirds to one-half of the normal HDL cholesterol, yet they do not have a markedly increased risk of ischemic heart disease.

In the early twentieth century, European "neuromuscular technique" emerged, primarily through the work of Stanley Lief and Boris Chaitow.NMT emerged on two continents almost simultaneously, but the methods had little connection to each other until recent years.Although some skill is necessary to apply this technique effectively, it is simple to learn and easily applied. The practitioner uses light and deep pressure, depending on the target structures, to palpate motion restriction within the fascia and moves toward or away from the restriction. The position is held until a "release," or softening, is felt, the perception of which is the most difficult aspect of application. The tissues are then slowly returned to their original position. The release can be the relaxation of muscles, changes in the viscosity of the ground substance of the fascia, the slow breaking of fascial adhesions, or the realignment of the fascia to a more appropriate orientation. Figure 16-8 A crossed-arm myofascial release (MFR) can be applied broadly to the tissues to alter the ground substance of the fascia. (Modified from Salvo S: _Massage therapy: principles and practice_ , ed 3, St. Louis, 2007, Saunders.) ## Myofascial–Soft Tissue Technique The myofascial–soft tissue technique is a combination direct-indirect massage technique for reducing muscle spasm and fascial tension. It is similar to pétrissage, except that more parts of the hand are typically employed. This technique can be used as a prelude to the high-velocity low-amplitude technique. # NEUROMUSCULAR THERAPY (NEUROMUSCULAR TECHNIQUES) Neuromuscular therapy (NMT) is a precise and thorough examination and treatment of the soft tissues of a joint or region that is experiencing pain or dysfunction. As a medically oriented technique, it is primarily used for the treatment of chronic pain or as a treatment for recent (but not acute) trauma; however, it can also be applied to prevent injury or to enhance performance in sports. NMT emerged on two continents almost simultaneously, but the methods had little connection to each other until recent years. In the early twentieth century, European "neuromuscular technique" emerged, primarily through the work of Stanley Lief and Boris Chaitow.The protocols of North American "neuromuscular therapy" also derived from a variety of sources, including chiropractic (Raymond Nimmo), myofascial trigger point therapy (Janet Travell, David Simons), and massage therapy (Judith DeLany, Paul St. John).

The genes involved here are known as tumor suppressor genes, and normally code for inhibitors of growth.The next change is the insensitivity to growth inhibitors.Among its numerous functions is a stimulation of cell division, and it is often found as a gain-of-function mutation in human cancers.* * * The first type of defect needed to establish a cancer is independence from growth factors for continued division. The mutations bringing this about are those that generate oncogenes, which are genes that can cause changes in tissue culture cells that resemble cancerous behavior, such as loss of contact inhibition. Oncogene products are often elements of the signaling systems that control growth and other aspects of development, either the growth factors themselves, or growth factor receptors, or components of the signal transduction pathways, or transcription factors activated by these pathways. Gain-of-function mutations may create constitutively active forms of the proteins, for example human tumors often contain constitutive mutations of the GTP exchange protein Ras, a component of the ERK pathway activated by receptor tyrosine kinases such as EGFR and FGFR. Oncogenic mutations may also act by causing an inappropriate expression of otherwise normal gene products. For example many tumors secrete growth factors, and these may be factors normally supplied by neighboring tissues in order to create a stem cell niche. When the tumor itself makes the factors, or activates the pathway independent of the presence of the factors, then its growth will no longer be controlled by the neighboring tissue and will become autonomous. Another very important oncogene is Myc, a transcription factor which upregulates a great many genes by recruitment of histone acetyl transferases. Among its numerous functions is a stimulation of cell division, and it is often found as a gain-of-function mutation in human cancers. The next change is the insensitivity to growth inhibitors. The genes involved here are known as tumor suppressor genes, and normally code for inhibitors of growth.An example is the product of the Retinoblastoma (Rb) gene.This is an inhibitor of the cell cycle, normally upregulated by factors of the TGFβ family.If both copies of the Rb gene are lost from a retinal cell then it will develop into a retinoblastoma.

These results indicate a selectivity of LESP for prostate cells. Several studies have further investigated the in vitro activities of fatty acids found in LESP on 5-AR. Using the eukaryotic (baculovirus-directed insect cell) expression system, IC50 values were determined at 4 μg/mL for myristic acid and 19 μg/mL for lauric acid on the type II isozymes of 5-AR.28 Long unsaturated fatty acids (oleic and linolenic) were much less active. In contrast, IC50 values for 5-AR inhibition in rat liver microsomes were 54 and 66 μg/mL for oleic and lauric acids, respectively.29 Using the same model, the IC50 ranged from 42 to 68 μg/mL for linoleic, oleic, myristic and lauric acids, and was 101 μg/mL for LESP.30 In a reflection of earlier work that compared different extracts, the testing of a range of commercial LESPs (including different batches of the same extract) found a wide variation in the inhibition of 5-AR activity using prostatic co-cultured epithelial and fibroblast cells.31 While extracts tested were able to inhibit both isoforms of 5-AR, the relative potencies varied by a factor of 24 for type I and 237 for type II inhibition. The lowest observed IC50 for type II inhibition was around 4 μg/mL of extract. The authors suggested this variability indicates the potential for a wide diversity of clinical activity for these different extracts of saw palmetto. A novel LESP (extraction methodology not defined) demonstrated relatively good inhibition of 5-AR type II in transfected human embryonic kidney cells (IC50 2.9 μg/mL).32 However, while the authors state that this bioactivity 'corresponds favourably... to the established prescription drug... finasteride', in fact the IC50 in the same model for finasteride was found to be 3.2 nM (or about 0.0012 μg/mL), around 2000 times lower on a weight for weight basis.

Consideration must also be given to the course, orientation, and disease state of the cervical portion of the carotid and vertebral arteries.Increased tortuosity of the great vessels, which is common with increasing age, or aberrant branching patterns from the arch can make it difficult to pass a catheter or can decrease its stability during the treatment.Although there are different types and sizes of aneurysms, occurring at many locations within the cerebral vasculature and in patients of all ages, the general approach to the endovascular management of these lesions requires the same basic steps: (1) diagnosing the aneurysm and determining its suitability for endovascular treatment; (2) gaining endovascular access to the aneurysm; (3) excluding the aneurysm from the circulation; (4) avoiding complications during treatment; and (5) following up to monitor the durability of the treatment. This article explores these general technical considerations for the endovascular management of intracranial aneurysms. ## Relevant anatomy and pathophysiology ### Endovascular Access In contrast with open surgical treatment of aneurysms, in which the focus is on the regional intracranial vascular anatomy, during endovascular treatment of aneurysms consideration must also be given to peripheral vascular anatomy, aortic arch, and great vessel anatomy in addition to the intracranial vascular anatomy. Gaining endovascular access to the arteries of the brain requires first accessing the peripheral vascular system, usually by a transfemoral route (although transbrachial or transradial routes may be used),1 navigating the aortic arch, and selecting the desired carotid or vertebral artery. Increased tortuosity of the great vessels, which is common with increasing age, or aberrant branching patterns from the arch can make it difficult to pass a catheter or can decrease its stability during the treatment. Consideration must also be given to the course, orientation, and disease state of the cervical portion of the carotid and vertebral arteries.The final step of endovascular access is navigation of the intracranial vessels, and, again, review of preoperative imaging is important, because individual variability is high.The use of biplane angiography and biplane roadmapping is the standard of care in the endovascular treatment of cerebral aneurysms.

Ask yourself, "Which is the best indicator of hemorrhage?"Pain at the biopsy site is expected due to the procedure.No.Does this indicate the client is hemorrhaging?"Pain at the biopsy site."4.Shock is a result of hemorrhage.An increased pulse, a decreased blood pressure, and increased respirations indicate shock.Yes.Does this indicate that the client is hemorrhaging?The NCLEX-RN **®** exam asks few minimum-competency questions at the comprehension level. It assumes you know and understand the facts you learned in nursing school. Minimum-competency NCLEX-RN **®** exam questions are written at the application and/or analysis level. Remember, the NCLEX-RN **®** exam tests your ability to make safe judgments about client care. Your ability to solve problems is not tested with questions at the recall/recognition or comprehension level. Let's look at this same question written at the application level. 1. Which of the following symptoms observed by the nurse during the first 24 hours after a percutaneous liver biopsy would indicate a complication from the procedure? 1. Anorexia, nausea, and vomiting 2. Abdominal distention and discomfort 3. Pulse 112, blood pressure 100/60, respirations 20 4. Pain at the biopsy site Can you select an answer based on recall or recognition? No. Let's analyze the question and answer choices. The question is: What is a complication of a liver biopsy? In order to begin to analyze this question, you must _know_ that hemorrhage is the major complication. However, it's not listed as an answer. Can you find hemorrhage in one of the answer choices? **_ANSWERS:_** 1. "Anorexia, nausea, and vomiting." Does this indicate that the client is hemorrhaging? No, these are not symptoms of hemorrhage. 2. "Abdominal distention and discomfort." Does this indicate that the client is hemorrhaging? Perhaps. Abdominal distention could indicate internal bleeding. 3. "Pulse 112, blood pressure 100/60, respirations 20." Does this indicate that the client is hemorrhaging? Yes. An increased pulse, a decreased blood pressure, and increased respirations indicate shock. Shock is a result of hemorrhage. 4. "Pain at the biopsy site." Does this indicate the client is hemorrhaging? No. Pain at the biopsy site is expected due to the procedure. Ask yourself, "Which is the best indicator of hemorrhage?"Abdominal distention can be caused by liver disease.The correct answer is (3).This question tests you at the application level.You were not able to answer the question by recalling or recognizing the word _hemorrhage_.You had to take information you learned (hemorrhage is the major complication of a liver biopsy) and select the answer that best indicates hemorrhage.

The establishment of this pH gradient is the chemiosmotic potential that is coupled with the production of ATP.Activated adenylate cyclase leads to increased production of cAMP and the concomitant activation of PKA with the result being phosphorylation and activation of hormone-sensitive lipase. The released free fatty acids bind to UCP1 triggering an uncoupling of the proton gradient and the release of the energy of the gradient as heat. **19. ** A 21-year-old man is brought to the ER after being found unconscious. He is gasping, and respirations are 24/min. There is evidence that he has vomited recently. Two capsules containing potassium cyanide are found in his shirt pocket. Blood lactate concentration is 3.3 mEq/L (normal = 0.8 ± 0.4 mEq/L). Which of the following processes is most likely inhibited in this patient? **A. ** conversion of pyruvate to alanine **B. ** glycolysis **C.** mitochondrial electron transport **D.** mobilization of fatty acids from adipose tissue **E.** release of insulin from pancreas **Answer C:** Cyanide is a poison that acts by inhibiting electron flow through complex IV of the oxidative phosphorylation machinery. This prevents further mitochondrial electron transport leading to rapid decline in ATP synthesis capacity and ultimately cellular death. **20. ** Addition of an uncoupling agent to respiring mitochondria carrying out oxidative phosphorylation has which of the following metabolic effects? **A. ** activity of the TCA cycle ceases **B. ** ATP formation ceases, but O2 consumption continues **C.** fatty acid oxidation ceases **D.** formation of ATP continues, but O2 consumption ceases **E.** NADH oxidation ceases **Answer B:** The normal flow of electrons, through the proteins of the oxidative phosphorylation machinery, is coupled with the establishment of a proton gradient across the inner mitochondrial membrane. The establishment of this pH gradient is the chemiosmotic potential that is coupled with the production of ATP.Since the PMF across the membrane is lost, there is no longer a gradient to restrict the rate of electron flow; as a result electron transport accelerates resulting in increased oxygen consumption.**21.

Fig.12.7).Move the second, upper ligature, 1-2 cm above the place of the planned aorta incision and cut the anterior side of the aorta 1-1.5 cm below the upper ligature (Fig.6.Use either the vascular clamp, your fingers or the second upper ligature to close the abdominal aorta below renal arteries.12.1 Thoracic surgeons during major thoracic vessel cannulation * Scrub nurses * Anaesthetist * Transplant coordinator(s) (Fig. 12.2) Fig. 12.2 Divide the tasks amongst the OR personnel ATTENTION! * Remember that you are not alone in the operating room; try to communicate adequately with everybody on a professional level. ## 12.2 12.2 Ligation and Cannulation of the Abdominal Aorta and IVC ### 12.2.1 12.2.1 Surgical Steps 1. Move the right colon together with the small bowel to the upper part of the abdomen and to the thorax and fix them with an abdominal retractor blade or ask the thoracic surgeon or your assistant to hold it (Fig. 12.3). Fig. 12.3 1 - IVC, 2 - left renal vein, 3 - abdominal aorta, 4 - ligature placed around the aorta, 5 - ligatures placed around the IVC, H - head, F - feet, R - right, L - left 2. Bowel fixating with the retractor blade gives your assistant the opportunity to use both hands and rally help (Fig. 12.4). Fig. 12.4 1 - IVC, 2 - abdominal aorta, 3 - left renal vein, 4 - IMV, H - head, F - feet, R - right, L - left 3. With the first, lowest ligature, ligate the aorta at the level of the bifurcation (Fig. 12.5). Fig. 12.5 1 - Abdominal aorta at the level of bifurcation, 2 - first lowest ligature placed around the aorta and ligated, 3 - abdominal aorta above ligation, 4 - IVC, 5 - sigmoid, 6 - right kidney, H - head, F - feet, R - right, L - left 4. Outside the abdominal cavity, fix the ligated ligature with a clamp (Fig. 12.6). Fig. 12.6 1 - Ligated abdominal aorta, 2 - ligatures are fixed with the clamps outside abdominal cavity, H - head, F - feet, R - right, L - left 5. Use either the vascular clamp, your fingers or the second upper ligature to close the abdominal aorta below renal arteries. 6. Move the second, upper ligature, 1-2 cm above the place of the planned aorta incision and cut the anterior side of the aorta 1-1.5 cm below the upper ligature (Fig. 12.7). Fig.Insert the aortic cannula into the abdominal aorta and secure it with the upper ligature (ligate the aorta on the cannula) and avoid leakage of blood (Fig.12.8).Fig.12.8 1 - Aortic cannula, 2 - Abdominal aorta, 3 - IVC, 4 - Ligatures placed around the IVC, H - head, F - feet, R - right, L - left 8.

Diagnosis of osteoarthritis Your GP will probably be able to diagnose OA if you present with these symptoms and signs.Increased pain might suggest that you have done too much and need to rest, or that you've been sitting in one position for too long and need to get up and move around.The pain of arthritis may indicate joint swelling, inflammation, or damage.Swelling Swelling of the joints might be due to the synovium swelling slightly and producing more synovial fluid, or it may be down to the presence of osteophytes. The knees are especially prone to swelling after exercise. Loss of balance Instability, or loss of balance, when moving about. Some OA sufferers say that their joints 'give way'. Reduced mobility and flexibility All of these symptoms, depending on their severity, can make you less mobile and less able to carry out everyday tasks. For example, if your hips and knees are affected, you may find walking difficult, and if your fingers and thumbs are affected, you may have problems turning a tap on and off, or opening a jar. Calcification This is a fairly common complication of OA. It occurs when calcium deposits form in the cartilage. If these deposits work their way into the synovium, they can cause irritation and hot, painful, swollen joints. Why do we feel pain? Pain is the body's way of telling you that something is wrong. Irritation or injury triggers the nerves nearby to release chemicals that in turn stimulate nerve fibres to send messages to the brain, which are interpreted as pain. Pain is often a warning that you need to take action - for example if you touch a hot iron you will automatically respond by removing your hand, to avoid further injury. The pain of arthritis may indicate joint swelling, inflammation, or damage. Increased pain might suggest that you have done too much and need to rest, or that you've been sitting in one position for too long and need to get up and move around. Diagnosis of osteoarthritis Your GP will probably be able to diagnose OA if you present with these symptoms and signs.Your GP may also ask if your joints 'creak' or 'crunch' when you move them and may suggest a blood test to rule out other inflammatory forms of arthritis, such as RA.An x-ray may be requested to confirm OA, because it shows changes to the bone caused by cartilage thinning, calcification and bony outgrowths on the joints.

By the time the United States entered World War II, Americans were consuming more than a billion barbiturates annually, and as production grew to meet demand, so did addiction and overdose.More recently, their co-prescription with opiates has been thought to contribute to a surge in lethal overdoses.Very early on it was recognized that these drugs could help epileptic patients, too. This was discovered accidentally by a doctor who was frustrated that his own sleep was interrupted by epileptic patients having seizures during the night, so he gave them phenobarbital. He was pleasantly surprised to find a dramatic dip in the frequency and intensity of his patients' seizures, many of whom were then able to leave institutions and live relatively normal lives. Phenobarbital is currently the most widely prescribed antiepileptic drug in the world, aptly dubbed "king of the barbiturates." Many analogs have been synthesized—some that have better efficacy (strength) and shorter action, obviating drowsiness the next day. Soon Amytal (amobarbital), Seconal (secobarbital), Nembutal (pentobarbital), and Pentothal (thiopental) arrived on the market. In short order, people other than psychiatric or epileptic patients began taking these pills to help them sleep or relax, and a large portion began exploiting some of the non-medicinal benefits—though admittedly it's sometimes hard to make the distinction—and becoming addicted. Despite regulation in 1938 by the U.S. Food and Drug Administration (FDA), these drugs only became more popular. Many also began combining barbiturates with alcohol to increase the effect or took them alternately with stimulants to mitigate drowsiness. More recently, their co-prescription with opiates has been thought to contribute to a surge in lethal overdoses. By the time the United States entered World War II, Americans were consuming more than a billion barbiturates annually, and as production grew to meet demand, so did addiction and overdose.According to her death certificate, Marilyn Monroe died of "acute poisoning by overdose of barbiturates" on August 5, 1962, after taking nearly fifty Nembutals.

However, two-thirds of them instead express a CD8 αα homodimer, which is almost exclusively found only on IELs.One-third of them possess the conventional form of CD8, which is a heterodimer composed of a CD8 α chain and a CD8 α chain.Of those bearing an γδ TCR, most are CD8+ positive and in mice can be divided into two populations.T- and B-cells also appear in the lymphoid tissue of the lung and in other mucosal sites guided by the interactions of specific homing receptors with appropriate HEV addressins as discussed earlier. It is noteworthy that intranasal immunization is particularly effective at generating antibody production in the genitourinary tract. **Intestinal lymphocytes** The LPAM-1 integrin ligand, MAdCAM-1, is present on the intestinal lamina propria postcapillary venules (Figure 7.13) and thus facilitates the arrival of the intestinal T-cells. These cells bear a phenotype roughly comparable to that of peripheral blood lymphocytes: namely >95% T-cell receptor (TCR) **αβ** and a CD4:CD8 ratio of 7 : 3, and seem to mainly be activated or memory cells. Unwarranted immune responses in the gut may be dampened down following the secretion of IL-10 and transforming growth factor-β (TGFβ) by inducible regulatory T-cells. Within the lamina propria there is also a generous sprinkling of activated B-cells and plasma cells secreting IgA for transport by the poly-Ig receptor to the intestinal lumen (cf. p. 68). Intestinal **intraepithelial lymphocytes** (IELs) are quite a different "kettle of fish." Both they, and intraepithelial dendritic cells, express high levels of the αEβ7 integrin, which binds E-cadherin on the intestinal epithelial cells thereby localizing the IELs between the epithelial cells (Figure 7.14). They are mostly T-cells, about 10% of which in humans bear a γδ TCR. In other species γδ T-cells may represent up to 40% of the IEL T-cells. Of those bearing an γδ TCR, most are CD8+ positive and in mice can be divided into two populations. One-third of them possess the conventional form of CD8, which is a heterodimer composed of a CD8 α chain and a CD8 α chain. However, two-thirds of them instead express a CD8 αα homodimer, which is almost exclusively found only on IELs.**Figure 7.13.** **Selective expression of the mucosal vascular addressin MAdCAM-1 on endothelium involved in lymphocyte homing to gastrointestinal sites.

(From Craig SA: Radiology.Figure 157-1 Radiopaque iron tablets _(arrow)_ seen on abdominal radiograph.157-1).11,12 Repeated radiographs can also demonstrate the efficacy of gastrointestinal decontamination efforts.The presence of tablets on a radiograph correlates with the severity of the ingestion (Fig.### Diagnostic Strategies The presence of gastrointestinal symptoms suggests a potentially serious ingestion, whereas their absence is reassuring.5 A serum iron level measured at its peak, 3 to 5 hours after ingestion, is the most useful laboratory test to evaluate the potential severity of an iron overdose. Sustained-release or enteric-coated preparations may have erratic absorption, so a second level 6 to 8 hours after ingestion should also be checked. Peak serum iron levels below 350 µg/dL are generally associated with minimal toxicity; 350 to 500 µg/dL, with moderate toxicity; and above 500 µg/dL, with potentially severe toxicity (Table 157-2).5 Because iron is rapidly cleared from the serum and deposited in the liver, the level of iron after a substantial ingestion may be deceptively low if it is measured after its peak. TIBC is a crude test and is not useful to gauge the severity of iron poisoning.9 Table 157-2 Toxicity of Iron by Amount Ingested and Peak Serum Levels ELEMENTAL IRON (mg/kg) | PEAK SERUM IRON LEVEL (µg/dL) | TOXICITY ---|---|--- <20 | 50-150 | None 20-40 | 150-300 | Mild 40-60 | 300-500 | Moderate >60 | >500 | Severe When serum iron levels are not immediately available, elevations of the serum glucose level above 150 mg/dL and leukocyte count above 15,000 are 100% specific for prediction of serum iron levels of more than 300 µg/mL. However, a sensitivity of only 50% limits their sole use as indicators of toxicity.10 Most tablets that contain a significant amount of elemental iron are radiopaque, although a false-negative radiograph may occur with chewable, liquid, and completely dissolved iron compounds. The presence of tablets on a radiograph correlates with the severity of the ingestion (Fig. 157-1).11,12 Repeated radiographs can also demonstrate the efficacy of gastrointestinal decontamination efforts. Figure 157-1 Radiopaque iron tablets _(arrow)_ seen on abdominal radiograph. (From Craig SA: Radiology.Philadelphia, WB Saunders, 2001, p 62.)### Management Gastric Emptying Decontamination may prevent absorption of additional iron from the gastrointestinal tract and can be performed concomitantly with interventions that address drug that has already been absorbed (see later section on deferoxamine).

Signs appear in all susceptible birds in a flock within three to seven days of infection having been spotted in individuals.## Quail Bronchitis A highly contagious infection caused by an adenovirus.Q fever from contaminated clothing This was the presumed cause of 16 out of 32 employees at a truck-repair plant becoming ill with the disease. Serological tests on a cat were positive for C. burnetii. The cat was fed at home by one of the workers at the plant. ## QMS (See QUALITY MEAT SCOTLAND.) ## Quadriceps Quadriceps means having four heads, and is the collective name applied to the powerful muscles situated above the stifle-joint. These are medial and lateral vasti, and the rectus femoris; the fourth muscle (vastus intermedius) in the horse combined with the medial vastus. It is a useful muscle for giving intramuscular injections in rabbits and large rodents. ## Quadriplegia (adjective, Quadriplegic) Paralysis of all four limbs. It is also called TETRAPLEGIA. It results from a spinal cord injury or lesion in the cervical region; it can be progressive or sudden in onset, depending on the nature of the lesion and cause. Most cases are due to trauma but some are inherited. In dog breeds it is common in IRISH SETTERS. (See PARALYSIS; TICK PARALYSIS; RACCOONS; CURARE.) ## Quail Small, rapidly-maturing game birds included as poultry in British legislation. Females start to lay eggs at five to six weeks of age; the first eggs laid are usually infertile, but thereafter high fertility can be obtained. Males are sexually active at five weeks. The nutritional requirements of quail are usually met by basic turkey starter diets. Among the diseases they may suffer are: BOTULISM, LYMPHOID LEUKOSIS, MAREK'S DISEASE, NEWCASTLE DISEASE, pasteurellosis, MYCOPLASMOSIS, SALMONELLOSIS, QUAIL DISEASE (ulcerative enteritis), quail bronchitis and COCCIDIOSIS. ## Quail Bronchitis A highly contagious infection caused by an adenovirus. Signs appear in all susceptible birds in a flock within three to seven days of infection having been spotted in individuals.## Quail Disease, Ulcerative enteritis of quail A severe bacterial infection caused by Corynebacterium perdicum.Birds may die suddenly without showing clinical signs; these birds are usually in good condition with feed in their crop.Birds less acutely affected are listless, huddling with eyes partly closed and with ruffled feathers.Emaciation develops within a week.Survivors become immune.

Intraventricular hemorrhage, one of the major types of bleeds, is graded by severity: infants with grades III and IV hemorrhages, which are the most severe, are the most likely to develop cerebral palsy.And finally, the brain is also vulnerable to bleeds and ischemia at such a young age.Anemia can also be caused by bleeding (e.g. menstruation or ulcers); it can be due to decreased red blood cell production; or it can be caused by an increased breakdown in red blood cells. In the case of folate and iron, deficiencies are most typically associated with reduced red blood cell production. The body simply cannot make enough red blood cells to carry oxygen where it needs to go. In the fetus this can be especially detrimental. Scientists have found that during early brain growth, iron deficiency dramatically alters neuron development and impairs learning and memory well after the deficiency has resolved (Tran et al., 2008). It may also exacerbate the effects of other risk factors, particularly inflammation. Using animal models, researchers have found that pregnant rats who are iron-deficient produce more inflammatory molecules when exposed to lipopolysaccharide (a bacterial mimic) than mothers who aren't deficient (Harvey & Boksa, 2014). Together, these data indicate that iron deficiency can have some extreme consequences and is a basic substrate to life. PREMATURITY Approximately 13 percent of all births are premature, defined as occurring at or before 36 weeks gestation (reviewed in Rais-Bahrami & Short, 2013). The greatest challenge for preterm infants is living in a world for which most of their organs are developmentally unprepared. For instance, because the preemie lungs don't produce enough surfactant, this can lead to significant respiratory distress. Their gastrointestinal tracts may also not receive enough blood supply, leading to a condition called "necrotizing enterocolitis," which is when gastrointestinal tissue start to necrotize or die off. And finally, the brain is also vulnerable to bleeds and ischemia at such a young age. Intraventricular hemorrhage, one of the major types of bleeds, is graded by severity: infants with grades III and IV hemorrhages, which are the most severe, are the most likely to develop cerebral palsy.Research has shown that about one quarter of ex-preterm infants who weighed 1500g or less at birth score positively on toddler autism screening tools like the Child Behavior Checklist and the Vineland Adaptive Behavior Scale (Limperopoulos et al., 2008).

Here you will find some facts about each disease, its connection with oxidation, and sources of super antioxidants to counteract it.| CHAPTER FOUR **Reactive Oxygen Species in Specific Diseases** This chapter will discuss several diseases that are generated by reactive oxygen species (ROS).In 1993, an outbreak of this single-cell parasite in Milwaukee caused an estimated 370,000 people to become ill and may have led to 142 deaths. Despite this astounding figure, less than 10 percent of the 4.6 million home water-purification systems sold in this country in 1994 protected against cryptosporidium. Next to oxygen, water is the most important element for sustaining life. We can live for a while without food, but only forty-eight hours without water. Water makes up 70 percent of our bodies' weight, with the average adult having about sixteen gallons of water in his or her system. Water is so important for the functioning of our bodies. Water lubricates all of our moving parts and regulates all body processes such as digestion, elimination, circulation, and absorption. Water also transports nutrients through the body, dilutes toxins, and flushes out waste and poisons. Water is essential in controlling body temperature as well. If we don't drink enough water daily, we'll become dehydrated. Signs of dehydration include: fatigue, frontal headaches, kidney disease, constipation, arthritis, circulatory diseases, and colds. Remember, not all water is created equal! Eliminate tap water from your diet if possible. Chlorine and fluoride are poisons. Drink at least eight 8-ounce glasses of good, pure water per day. Get a good in-home water filter or drink bottled water. I have long preferred steam-distilled water. Distilled water is healthier for you, tastes better, and will not leach minerals from your bones and organs. I have recently been introduced to Oxy-Water™, which contains 34 mg of pure O2 added to each liter of filtered and distilled water. | CHAPTER FOUR **Reactive Oxygen Species in Specific Diseases** This chapter will discuss several diseases that are generated by reactive oxygen species (ROS). Here you will find some facts about each disease, its connection with oxidation, and sources of super antioxidants to counteract it._Phyto_ is Greek for "plant," and familiarity with this term is important to your understanding of the foods I suggest that contain phytonutrients or chemicals!These are the plant elements that have antioxidant properties such as flavonoids, carotenoids, and enzymes.**Cancer** In the United States, a person dies from cancer every minute of every day.

* * * ###### ANTIDIURETIC HORMONE Also known as **vasopressin** , ADH plays a major role in determining whether the kidney produces and excretes concentrated or dilute urine (Figure 8-23).* * * **CLINICAL CORRELATION** Potassium-sparing diuretics such as spironolactone inhibit the actions of aldosterone in the distal nephron.* * * Angiotensin II only persists in the blood for 1–2 minutes before it is inactivated by angiotensinase. For this reason, the angiotensin II stimulation of aldosterone production is more influential in restoring arterial BP than its direct vasoconstrictive actions. * * * **KEY FACT** Overall, angiotensin II serves to ↑ intravascular volume and ↑ BP. * * * ###### ALDOSTERONE A mineralocorticoid synthesized in the zona glomerulosa of the adrenal cortex. Whereas adrenocorticotropic hormone (ACTH) is the primary regulator of the corticosteroid hormones, aldosterone's synthesis and secretion are mainly regulated by changes in ECF volume via the RAAS and changes in serum K+ levels. **Late distal tubule:** Aldosterone exerts its action via stimulation of the mineralocorticoid receptors (MRs) on **principal cells**. This action increases the permeability of their apical (luminal) membrane to Na+ and K+ by adding newly synthesized proteins (epithelial sodium channels [ENaC], ROMK channels) as well as basolateral Na+–K+-ATPases and enzymes of the citric acid cycle, which stimulate ATP hydrolysis, reabsorption of Na+ and water into the blood, and K+ secretion into the urine. **Collecting duct:** Aldosterone also stimulates H+ secretion by α **-intercalated cells** , thereby regulating plasma HCO3– levels and acid-base balance. * * * **CLINICAL CORRELATION** Potassium-sparing diuretics such as spironolactone inhibit the actions of aldosterone in the distal nephron. * * * ###### ANTIDIURETIC HORMONE Also known as **vasopressin** , ADH plays a major role in determining whether the kidney produces and excretes concentrated or dilute urine (Figure 8-23).It is also produced in response to angiotensin II as part of the RAAS, which acts to increase blood volume and BP.**FIGURE 8-23.Regulation of water balance**.The two major pathways for altering total body water: On the left, changes in antidiuretic hormone (ADH) release from the posterior pituitary are triggered by changes in blood volume.

Most notably, this has been used in the critically ill obese patient.HFNC has also been used for preoxygenation and to provide apneic oxygenation for patients undergoing rapid sequence intubation.As a result, the use of HFNC in patients with hypercapnic respiratory failure cannot be routinely recommended.Additional benefits of HFNC devices include the ability to decrease dead space in the upper airway through a washout of carbon dioxide and improved minute ventilation. Finally, the heated and humidified air improves patient tolerance of the device and may enhance mucociliary clearance. At present, the best evidence for the use of HFNC is in the patient with isolated hypoxemia due to pneumonia that does not require immediate airway management and mechanical ventilation. A prospective, multicenter, randomized, controlled trial in patients with hypoxemic respiratory failure and normal work of breathing demonstrated decreased mortality with the use of HFNC compared with NIV. Importantly, mortality was a secondary outcome, and the benefit was primarily seen in patients with pneumonia. Patients with chronic lung disease were excluded from this trial. HFNC may also be used in patients with hypoxemia due to other etiologies (i.e., congestive heart failure); however, the evidence that supports its use is less robust. The use of HFNC for patients with hypercapnic respiratory failure is limited to case reports. It is important to note that HFNC devices do not have a direct effect on tidal volume or respiratory rate, the two primary determinants of ventilation and carbon dioxide exchange. Risks of HFNC use in this specific patient population include the administration of high levels of oxygen that may mask worsened pulmonary function and delayed intubation. As a result, the use of HFNC in patients with hypercapnic respiratory failure cannot be routinely recommended. HFNC has also been used for preoxygenation and to provide apneic oxygenation for patients undergoing rapid sequence intubation. Most notably, this has been used in the critically ill obese patient.Given the size of the device and lack of robust clinical data, the use of HFNC in this setting should not be considered standard care.If HFNC is used to preoxygenate select patients prior to endotracheal intubation, consider using a jaw-thrust maneuver to maintain a patent airway and maximize its effect.

Bursitis in the heel can result from wearing shoes that are too tight or that don't fit properly, or from running long distances.Wear elbow and knee pads during athletic activities to cushion your elbows and knees from falls that could cause bursitis.To prevent bursitis in your elbow, avoid resting your elbows on the table or desk while working or studying.**Bursae in the knee** Bursae (fluid-filled sacs for cushioning joints) in the knee are located between the tendon and the bone. ### _**Treatment**_ Bursitis usually subsides on its own after a few days. Rest the affected area and use an ice pack to ease the pain and help absorb the excess fluid into your bloodstream. Take a nonsteroidal anti-inflammatory drug such as aspirin to help relieve pain and reduce inflammation. If your symptoms persist, your doctor may remove the excess fluid through a needle and apply a bandage tightly over the area to prevent fluid from reaccumulating in the area. If the fluid contains pus, the doctor will prescribe antibiotics to help fight a bacterial infection. He or she may also inject a local anesthetic to relieve pain and a corticosteroid drug to reduce inflammation. Surgery to remove a bursa, called a bursectomy, is performed only if bursitis recurs repeatedly or if the bursa is infected and the infection seems to be spreading. ### _**Preventing Bursitis**_ Bursitis tends to develop in joints that are repeatedly placed under a lot of pressure. You can prevent bursitis by taking steps to protect your joints from prolonged pressure. For example, if you spend much of your working day kneeling, as carpet layers or roofers do, wear knee pads to reduce pressure on the bursae of your kneecaps. To prevent bursitis in your elbow, avoid resting your elbows on the table or desk while working or studying. Wear elbow and knee pads during athletic activities to cushion your elbows and knees from falls that could cause bursitis. Bursitis in the heel can result from wearing shoes that are too tight or that don't fit properly, or from running long distances.## **Baker's Cysts** Baker's cysts are fluid-filled sacs that form behind the knee.The cyst usually develops from inflammation of the knee joint that causes the membrane around the joint to swell backward and, sometimes, down into the calf muscles.