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Mechanisms of Hypokalaemia is usually, although not always, due to potassium action depletion. This may be because of, for example, diarrhoea, vomiting, or secondary hyperaldosteronism. By contrast, if losses are due to loopor thiazide-diuretic therapy, supplementation is largely ineffective. This is because although the serum potassium concentration is low, intake and output are in balance. Potassium supplementation results simply in increased potassium excretion and only minimal effect on serum concentration. Treatment with a potassium-sparing diuretic (or aldosterone antagonist) is therefore preferred. In redistributive hypokalaemia the total body potassium content is normal, but the serum concentration is low because of redistribution into cells. Important Oral potassium preparations are not very well tolerated, mainly because adverse effects they are unpalatable and cause gastrointestinal disturbance, including nausea, vomiting, pain, diarrhoea and fatulence. Modifedrelease preparations may be better tolerated, but these can cause gastrointestinal obstruction, ulceration and bleeding. Warnings Potassium supplements must be used with caution (lower dose and more intensive monitoring) in patients with renal impairment, due to the greatly increased risk of hyperkalaemia. Oral replacement is most commonly given as potassium chloride with potassium bicarbonate. Communication Advise patients that they have a low level of potassium in their blood, and without treatment this could upset their heart rhythm. Explain the common side effects and advise that these may be reduced by combining the doses with a meal or snack. These have high potassium content and, because the amount consumed inevitably varies, can make it diffcult to get the potassium dose right. Monitoring At baseline, an electrocardiogram should be recorded to confrm the absence of hypokalaemic changes. The frequency of monitoring is determined on a case-by-case basis, according to the severity and cause of the hypokalaemia. Clinical tip—Always beware of the risk of rebound hyperkalaemia when you are treating hypokalaemia. This is especially important if the patient has renal impairment or if there is a redistributive component to the hypokalaemia. Monitor the serum potassium concentration closely and stop potassium replacement as soon as possible. Prostaglandin analogues are generally preferred over topical β-blockers (the main alternative class) as they cause fewer systemic side effects. Mechanisms of Elevated intraocular pressure (ocular hypertension) is a risk factor for action open-angle glaucoma. Glaucoma is characterised by progressive optic nerve damage associated with visual feld loss and eventually blindness. It is usually, although not always, associated with elevated intraocular pressure. Analogues of prostaglandin F2α reduce intraocular pressure by increasing outfow of aqueous humour via the uveoscleral pathway. Locally adverse effects in the eye they may cause blurred vision, conjunctival reddening (hyperaemia), and ocular irritation and pain. They may also cause a permanent change in eye colour by increasing the amount of melanin in stromal melanocytes of the iris. This affects about one in three patients and is most noticeable when treatment is restricted to one eye. Warnings Caution is needed when contemplating prostaglandin analogue treatment in eyes in which the lens is absent (aphakia) or artifcial (pseudophakia); and in patients with or at risk of iritis, uveitis or macular oedema. In patients with severe asthma there is a theoretical risk of provoking bronchoconstriction, but in practice this does not seem to be a problem. All patients with confrmed open-angle glaucoma should be offered pharmacological treatment, again by a specialist. Communication Explain that the aim of treatment is to reduce the risk of sight loss. This advice may be tailored according to the patients’ eye colour, since it is most likely in those with mixed-colour irides. Explain that it is usually only slight and is not harmful, but if it occurs it is likely to be permanent. Monitoring Patients should be reviewed regularly by a suitably trained and experienced healthcare professional. The monitoring interval is determined according to intraocular pressure and risk of conversion to glaucoma. Cost Prostaglandin eye drops are relatively expensive, but with competition from non-proprietary products the cost is falling. At the time of writing, the leading latanoprost brand (Xalatan ) was about fve times the price of non-proprietary latanoprost. Clinical tip—Advice that may be given for all eye drops is that the patient should gently compress the medial canthus (the nasal ‘corner’) of the eye for about 1 minute, immediately after instilling the drop. Eradication of Helicobacter pylori infection, in which they are used in combination with antibiotic therapy. This is the ‘proton pump’ responsible for secreting H+ and generating gastric acid. An advantage of targeting the fnal stage of gastric acid production is that they are able to suppress gastric acid production almost completely. Patients at risk of osteoporosis should therefore be identifed and treated as appropriate. Understanding continues to evolve on this issue, but current evidence suggests that lansoprazole and pantoprazole have a lower propensity to interact with clopidogrel. Generally the lowest effective dose should be used for the shortest period possible. Ensure that both you and the patient are clear on the intended duration of therapy. Monitoring Response to treatment should be monitored in terms of symptomatic response and, in some cases. In prolonged use (>1 year) you should check serum magnesium levels due to the risk of hypomagnesaemia. Cost Relatively inexpensive non-proprietary formulations are available and should be preferred in most cases. Mechanisms of Leg cramps are caused by sudden, painful involuntary contraction of action skeletal muscle. Quinine is thought to act by reducing the excitability of the motor end plate in response to acetylcholine stimulation. In malaria, the mechanism of action of quinine is not well understood, but its overall effect leads to rapid killing of P. Important Although quinine is usually safe at recommended doses, it is potentially adverse effects very toxic and can be fatal in overdose. It can cause tinnitus, deafness and blindness (which may be permanent), gastrointestinal upset, and hypersensitivity reactions. Hypoglycaemia can occur and can be particularly problematic in patients with malaria, which also predisposes to hypoglycaemia. Warnings Quinine should be prescribed with caution in people with existing hearing or visual loss. It is teratogenic, so should not be prescribed in the frst trimester of pregnancy, although in the case of malaria its beneft may outweigh this risk. Communication For nocturnal leg cramps, explain that you are recommending a 4-week trial of quinine in the hope of reducing the frequency of cramps. Explain that if there is no improvement after 4 weeks they are unlikely to experience any beneft and should stop taking it. Ask your patient to report any adverse effects, such as hearing loss, visual disturbance and palpitations immediately, as quinine is potentially harmful to the ears, eyes and heart. Monitoring Review your patient’s symptoms after 4 weeks and advise them to stop taking quinine if there has not been a signifcant improvement.

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Within the first week, patients treated with tegaserod Metoclopramide Hydrochloride had significant improvements in abdominal pain and discomfort, constipation, and overall well-being. Tegaserod also demonstrated significant improvements Centrally, it is a dopamine antagonist, an action that is in the three bowel-related assessments (stool frequency, important both for its often desirable antiemetic effect stool consistency, and straining) within the first week, and other less desirable effects. Peripherally, it stimuand these improvements were sustained throughout the lates the release of intrinsic postganglionic stores of treatment period. The most common adverse events reacetylcholine and sensitizes the gastric smooth muscle ported thus far are headache and diarrhea. Peak label indication) to accelerate gastric emptying in diaplasma concentration is achieved within 40 to 120 minbetic gastroparesis and postoperative gastroparesis. With normal renal function, plasma half-life is Tachyphylaxis will occur, so it cannot be used uninterabout 4 hours. Since metoclopramide also can Diarrhea is the frequent passage of watery, unformed decrease the acid reflux into the esophagus that results stools. Extrapyramidal side effects Opioids seen following administration of the phenothiazines, thioxanthenes, and butyrophenones may be accentuated Most of the opioids have a constipating action; morby metoclopramide. Unfortunately, many of the the more widely used paregoric (camphorated opium opium preparations, while relieving diarrhea and tincture) is equally effective and is frequently used in dysentery, also produce such objectionable side effects combination with other antidiarrheal agents. Codeine as respiratory depression and habituation (see Chapter also has been used for short-term symptomatic treat26). These compounds usually produce an increase in segmentation and a deAlosetron crease in the rate of propulsive movement. Adsorbents and Bulking Agents Diphenoxylate (marketed in combination with atropine as Lomotil in the United States) is chemically reKaolin powder and other hydrated aluminum silicate lated to both analgesic and anticholinergic compounds. Kaolin is a naturally occurring hyhas a low incidence of central opioid actions. Diphendrated aluminum silicate that is prepared for medicinal oxylate is rapidly metabolized by ester hydrolysis to the use as a very finely divided powder. Lomotil hind its use in acute nonspecific diarrhea stems from its is recommended as adjunctive therapy in the manageability to adsorb some of the bacterial toxins that often ment of diarrhea. It is almost harmless and is effec2 years old and in patients with obstructive jaundice. In equal Bismuth subsalicylate (Pepto-Bismol) also binds indoses, loperamide protects against diarrhea longer than testinal toxins and may coat irritated mucosal surfaces. It reduces the daily fecal volume this compound is a salicylate and may therefore proand decreases intestinal fluid and electrolyte loss. Bismuth is the peristaltic reflex through depression of longitudinal radiopaque and may interfere with radiological examiand circular muscle activity. Its use may cause temporary gray-black discoltisecretory activity, presumably through an effect on inoration of the stool and brown pigmentation of the testinal opioid receptors. High dose Pepto-Bismol (8 tablets/day) has against a wide range of secretory stimuli and can be been efficacious in some patients with diarrhea secondused in the control and symptomatic relief of acute diary to collagenous or lymphocytic colitis. Hydrophilic substances such as calcium polycarbophil Adverse effects associated with its use include abdomi(FiberCon, Equalactin), methylcellulose (Citrucel), and nal pain and distention, constipation, dry mouth, hypervarious psyllium seed derivatives (Metamucil) are natural sensitivity, and nausea and vomiting. Its continual use, person to person; a normal stool frequency may vary therefore, is contraindicated, although its occasional adfrom three stools per week up to three stools per day. It Constipation is defined as the infrequent passage of is employed primarily in patients who must avoid stool. It may be secondary to sluggish colonic motility, in straining at stool, including persons with hemorrhoids which soft stool is seen throughout the colon, or to difand other painful anal lesions. Leakage of mineral oil ficulties with evacuation in which firm stool is seen pripast the anal sphincter may lead to soiling of clothing. Docusate dioctyl sodium sulfosuccinate (Colace), the dangers of excessive purging are salt and fluid dioctyl calcium sulfosuccinate (Surfak), and dioctyl loss and gradually increasing desensitization of the potassium sulfosuccinate (Diocto-K) are surface-active bowel to normal stimuli; the latter effect forces the agents that produce fecal softening in 1 or 2 days. Orally ingested dolaxatives and pure osmolar laxatives do not predispose cusate may also act as a stool softener by stimulating patients to formation of a cathartic-type colon and the secretion of water and electrolytes into the intesshould be the initial agents used for chronic constipatinal lumen. Docusate has been used both alone and in tion after a structural obstructing lesion has been excombination with other laxatives. Laxatives are also used before radiological, enappears to be relatively nontoxic, it may, when taken in doscopic, and abdominal surgical procedures; such combination with other laxatives, increase their absorppreparations quickly empty the colon of fecal material. Caution is necessary when Nonabsorbable hyperosmolar solutions or saline laxadocusate is prescribed together with mineral oil, since tives are used for this purpose. Bulk Forming Laxatives Stool Softeners the bulk-forming laxative group includes the hyFecal softeners are substances that are not absorbed drophilic substances described previously: calcium from the alimentary canal and act by increasing the polycarbophil (FiberCon, Equalactin), methylcellulose bulk of the feces and softening the stool so that it is eas(Citrucel), and various psyllium seed derivatives ier to pass. All act by increasing the bulk of the feces, either as the oil or as a white emulsion; it is a mixture of part of this action being due to their capacity to attract liquid hydrocarbons. Their action may not be evident for 2 to 3 and appears in the mesenteric lymph nodes, and if it is days after starting treatment. These salts should always be given with substantial the use of high-fiber diets has recently received a amounts of water; otherwise the patient may be purged great deal of publicity, and many claims have been at the expense of body water, resulting in dehydration. Fiber in the diet is deSodium-containing laxatives should not be used in parived entirely from plant material, either from fruit and tients with congestive heart failure, since the patient vegetables or from cereals, the latter being known as may absorb excessive sodium. The fiber content in each case is a complex carbofailure, magnesium or phosphate-containing products hydrate in the form of cellulose, pectin, and lignin. A high-fiber diet is effective in the prevention of Enemas may contain water, salts, soap, mineral deconstipation and diverticulitis. Claims also have been tergent (docusate potassium), or hypertonic (sorbitol, made that such diets prevent cancer of the colon. Many of Since clear advantages accrue from a high-bran diet these solutions irritate the mucosa and may produce ex(a reduction in both constipation and diverticulitis) and cessive mucus in the stool. Excessive use of these enema since there is no associated toxicity, a bulk-forming laxproducts may result in water intoxication and hyponaative is the laxative of choice for constipated patients. A new formulation of a saline laxative, Visicol, that Osmotic Laxatives is useful to prepare patients for procedures, was approved for use in 2001. Visicol tablets, taken in two creases, and fluid movement occurs secondary to osdoses of 30 g approximately 12 hours apart, induce dimotic pressure. Each administration has a purgative effect for mammalian enzyme is capable of hydrolyzing it to its approximately 1 to 3 hours. It therefore reaches the colon unchanged and is metabolized by colonic bacteria to lactic acid and to small quantities of formic and acetic Stimulant Cathartics acids. Since lactulose does contain galactose, it is conthe stimulant cathartics contain a variety of drugs traindicated in patients who require a galactose-free whose exact mode of action is not known, although it is diet. Metabolism of lactulose by intestinal bacteria may thought that they act on the mucosa of the intestine to result in increased formation of intraluminal gas and stimulate peristalsis either by irritation or by exciting abdominal distention. Polyethylene glycol (Miralax) is another osmotic They produce irritation of the mucosa if given in large laxative that is colorless and tasteless once it is mixed. However, a direct local irritation may not be essential to Saline Laxatives their action. It has been suggested that these drugs may Saline laxatives are soluble inorganic salts that contain act by stimulating afferent nerves to initiate a reflex inmultivalent cations or anions (milk of magnesia, magcrease in gut motility. These charged particles do not readily cross the senna, and rhubarb) are among the oldest laxatives intestinal mucosa and therefore tend to remain in the known. Cascara sagrada is one of the mildest of the the colon and producing a physiological stimulus for anthraquinone-containing laxatives. This Phenolphthalein is partially absorbed (about 15% explanation of the mechanism by which the saline laxaof a given dose) and excreted into the bile; hence, if it tives exert their effects, however, may be too simplistic, is taken constantly, it will accumulate and exert too since active secretion of fluid into the gut lumen has drastic an action. The ricinoleic acid acts larly dopamine) stimulation, is connected to the emetic on the ileum and colon to induce an increased fluid secenter through the fasciculus solitarius. The dose is 4 L ingested over 2 to 4 hours either orally or through a nasogastric tube. There is minimal Emetics net absorption or excretion of fluid or electrolytes, and the most commonly used emetics are ipecac and apothus these are safe to use in patients with renal insuffimorphine. The patient has repeated liquid stools until the emptying the stomach in awake patients who have inadministered solution has been expelled. If gastric empgested a toxic substance or have recently taken a drug tying is slow, patients may have abdominal distention overdose.

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The cytoplasmic membrane component harnesses intracellular energy to capture, in cooperation with the periplasmic component, drug molecules from the periplasm, which are then channeled out of the cell across the outer membrane component. Periplasmic substrate capture by the multicomponent system protects against antibiotics acting in the periplasm. In addition, it amplifies the resistance afforded by efflux pumps that extrude drugs from the cytosol into the periplasm in a multiplicative manner [239, 240]. The cell wall in mycobacteria has two membranes, and therefore the same considerations just outlined for the Gram-negative cell wall should apply here as well. Drug efflux across the mycobacterial outer membrane has not been experimentally characterized, however [241]. Bacterial metabolism and chemotherapy Apart from the cell wall, there are other metabolic distinctions between bacterial and mammalian cells that can provide targets for chemotherapy. For example, Escherichia coli can thrive on a minimal growth medium that contains no organic compound other than glucose, indicating that the bacterium can synthesize all those molecu1 In rapidly proliferating bacterial cultures, we must also consider dilution, since the increase in cellular volume due to cell division counteracts the penetration of polar drug molecules. Biosynthetic enzymes exclusive to bacteria are potential drug targets, provided that the bacterial cell lacks the ability to acquire the product from the environment instead. An example is dihydropteroate synthase, which functions in the bacterial synthesis of folic acid; this enzyme is inhibited by sulfonamides (see Section 1. Another interesting and practically important class of drugs that exploit metabolic diversity are nitroimidazole derivatives such as metronidazole (see Figure 11. These are selectively toxic for bacteria and also some eukaryotic parasites that are anaerobic, meaning that they thrive only in the absence of oxygen. Aerobic human or bacterial cells are not affected because they don’t contain sufficiently strong reducing agents. Inside the mycobacterial cell, it is first activated to a reactive radical by a bifunctional catalase/peroxidase enzyme, KatG. The latter participates in the synthesis of mycolic acids, the long chain fatty acids that occur in the mycobacterial cell wall (Figure 11. Its toxicity for humans is tolerable and caused by metabolism in the liver (see Section 4. Many plasmids encode an elaborate apparatus of multiple proteins that enables their own transfer from one bacterial cell to another, often crossing species boundaries in the process. Through successive transposition events, resistance genes from multiple sources can be collected on a single plasmid molecule. Such plasmids, sometimes referred to as R factors, will greatly aid the survival of bacterial hosts exposed to multiple antibiotics and therefore be effectively selected for in a hospital environment. This became manifest only a few years after the introduction of antibiotic therapy, when bacterial species that had originally been susceptible began to acquire resistance to multiple antibiotics, often including ones that had not even been used on the individual patients from whom the resistant bacteria were isolated. While Mycobacterium tuberculosis actually propagates rather slowly, it is killed by antibiotics even more slowly, meaning that multiple successive generations of bacteria are exposed to them and have a chance to develop resistance. When a manifest case of tuberculosis is treated with a single antibiotic only, the emergence of resistant mutants is almost certain. Assuming that each of these drugs by itself is lethal, a bacterial cell would have to develop resistance to all of them at the same time to actually survive. With mutation rates on the order of 10-6 per drug and bacterial generation, 1 Plasmids may also encode enzymes that mediate resistance to heavy metal ions; mercury, for example, is disposed of by reduction to its volatile elemental form. Apart from conferring resistance, plasmids may provide other benefits to the bacterial host, such as increased pathogenicity. When cured of this plasmid, the dreaded Bacillus anthracis turns into a rather agreeable fellow. In contrast, chloramphenicol and sulfonamides merely cause biosynthesis and proliferation to stall, but the bacteria will survive and resume growth after dilution or removal of the antibiotic. Very broadly speaking, a bacterial infection will overwhelm the host only if the bacteria multiply faster than they can be killed by the host’s immune system. In most cases, therefore, application of bacteriostatic antibiotics will suffice to decisively tip the balance in favor of the host. However, this may not be the case in patients with severely compromised immune function. For example, patients recovering from bone marrow transplants go through a precarious period of several weeks during which they have essentially no immune system, and therefore should be treated with bactericidal antibiotics if at all possible. The bactericidal action of some antibiotics, particularly β-lactams, applies only to actively growing bacteria. Since growth stalls under the influence of bacteriostatic agents, these will negate the effect of β-lactams. Its biosynthesis starts in the cytosol, where monomeric peptidoglycan precursors are assembled on a membrane-associated lipid carrier. Fosfomycin is an antimetabolite of phosphoenolpyruvate in the enzymatic synthesis of muramic acid (reaction 1 in Figure 11. It contains an epoxy group, which covalently reacts with a cysteine residue in the enzyme’s active site. Fosfomycin is taken up into the cell by active transport, piggybacking on the glycerolphosphate transporter, and cells can become resistant by inactivation of this nonessential transport protein. Cycloserine is an antimetabolite of d-alanine and inhibits both alanine racemase and d-alanine ligase (steps 2 and 3 in Figure 11. The lipopeptide antibiotic amphomycin inhibits transfer of the precursor to the undecaprenol phosphate carrier lipid (step 4). It inhibits similar transfer reactions in mammalian metabolism and therefore is not suitable for therapy; however, the 1 In a typical combination of tuberculostatic drugs, some are cheap, whereas others are expensive. When uninsured patients skip the expensive ones, this subverts the principle of combination therapy and gives Mycobacterium tuberculosis the opportunity to acquire resistance in a piecemeal fashion. The consequences for society are certainly more costly than subsidized therapy could ever have been. The free end of this peptide contains two d-alanine residues that are supplied by alanine racemase (2) and d-alanine ligase (3). This nascent building block is transferred to the lipid carrier undecaprenol phosphate (4) and subsequently extended by another molecule of N-acetylglucosamine and five glycine residues. The glycopeptide moiety is transferred to a growing murein strand in the transglycosylase reaction (6). The final transpeptidase (7) reaction crosslinks the new subunit to an adjacent murein strand, releasing the terminal d-alanine residue. The final polymerization stage of murein synthesis is particularly interesting for chemotherapy, because it occurs outside the cytoplasmic membrane. It involves two separate reactions, both of which are catalyzed by the bifunctional enzymes known as penicillin-binding proteins. The transpeptidation reaction (7) is inhibited by β-lactams and by glycopeptides such as vancomycin. B: d-cycloserine is an antimetabolite of d-alanine in the alanine racemase and d-alanine ligase reactions. Considering its widespread and frequent use, development of resistance has been remarkably slow. However, resistant bacterial strains have begun to emerge, and other antibiotics have begun to take its place. The name of the class derives from the four-membered β-lactam ring that occurs in each of these molecules. The amide bond in this ring resembles the peptide bond between the two d-alanine residues in the substrate, and it undergoes a similar reaction with the enzyme. The active site of muramyl-transpeptidase contains a serine residue, which transiently forms an amide bond with the penultimate d-alanine residue of the substrate, thereby releasing the terminal d-alanine. In the second step, the amino group of the second substrate’s terminal glycine substitutes and releases the catalytic serine. The β-lactam bond in the antibiotic resembles the peptide bond between the two dalanine residues (Figure 11. The four-membered ring is spring-loaded because of the strained bond angles within, which facilitates the covalent reaction of the drug with the catalytic serine. The covalent adduct typically undergoes hydrolysis with a half-life of several hours, but usually the bacterium will be dead long before this occurs. The ring tension of the β-lactam ring that promotes its reaction with penicillin-binding proteins also makes it prone to side reactions. One side reaction is hydrolysis; aqueous solutions of β-lactams therefore are not very stable.

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If the airman is on a Special Issuance for drug or alcohol condition(s) and they have a new event, they should not fly under 61. The airman must take a separate action to report a conviction or administrative action to security. Upon receipt and review of all of the above information, additional information or action may be requested. Submit a complete copy of your driving records from each of these for the past 10 years. Any evidence or concern the airman has not been compliant with the recovery program? Were the records clear and in sufficient detail to permit a a certified satisfactory evaluation of the nature and extent of any previous mental disorders. Occupational problems such as absenteeism or tardiness at work; reduced productivity, demotions or frequent job changes or loss of job. Economic problems such as frequent financial crises or bankruptcy or loss of home or lack of credit f. Include if you agree or disagree with previous diagnosis or findings from the records you reviewed and why. Specifically mention if any of the following regulatory components are present or not: a. Any evidence of any other personality disorder, neurosis, or mental refer to their letter health condition to determine what f. Discuss any weaknesses or concerning deficiencies that may potentially affect safe performance of pilot or aviation-related duties (if any). Recommendations: additional testing, follow-up testing, referral for medical evaluation. Submit your report along with the CogScreen computerized summary report (approximately 13 pages) and summary score sheet for all additional testing performed. Additional reports If the airman has other conditions that require a special issuance, those reports should also be submitted according to the Authorization Letter. Drug and/or alcohol testing results summarized, how often tested, how many tests performed to date. Substance use disorders, including abuse and dependence, not in satisfactory recovery make an airman unsafe to perform pilot duties. These evaluations are required to assess the disorder, quality of recovery, and potential other psychiatric conditions or neurocognitive deficits. Due to the differences in training and areas of expertise, separate evaluations and reports are required from both a qualified psychiatrist and a qualified clinical psychologist for determining an airman’s medical qualifications. Recommendations should be strictly limited to the psychiatrist’s area of expertise. The neuropsychologist’s report as specified in the portal, plus:  Copies of all computer score reports; and 415 Guide for Aviation Medical Examiners  An appended score summary sheet that includes all scores for all tests administered. Recommendations should be strictly limited to the psychologist’s area of expertise. In that event, authorization for release of the data by the airman to the expert reviewer will need to be provided. Interval evaluations (every 3 months or as required by Authorization Letter) were unfavorable? Not Yes No Due  Report(s) is/are favorable (no anticipated or interim treatment changes). I have no other concerns about this airman and recommend re-certification for Special Issuance. State if the airman meets all the requirements of the Authorization Letter or describe why they do not. Interval treatment records if any, such as clinic or hospital notes, should also be submitted. The exam should be timed so that the medical certificate is valid at the time of solo flight. The previous requirement to transmit student exams within 7 days no longer applies. Administrative Changed coversheet to 2020 and added monthly update schedule for the calendar year. Includes Initial Certificate Consideration Requirements and Renewal Certificate Requirements. Removed block for Metabolic Syndrome, Glucose Intolerance, Impaired Glucose Tolerance, Impaired Fasting Glucose, Insulin Resistance, and Pre-Diabetes. Medical Policy In Disease Protocols, updated and reorganized Protocol for Cardiac Valve Replacement. Medical Policy In Pharmaceuticals, updated chart of Acceptable Combinations of Diabetes Medications. Medical Policy In Protocol for Binocular Multifocal and Accommodating 434 Guide for Aviation Medical Examiners Devices, added a new Visual Acuity Standards table. Administrative Changed coversheet to 2019 and added monthly schedule of when updates will take place. General Systemic, Blood and Blood-Forming Tissue Disease, revised the disposition table to provide guidance for Chronic Lymphocytic Leukemia. Medical Policy In Specifications for Psychiatric and Psychological Evaluations, updated testing information. Medical Policy In Disease Protocols Attention Deficit/Hyperactivity Disorder, revised section to include links to new information pages. Administrative In Security Notification/ Reporting Events, reworded link information. Heart revised guidance for Other Cardiac Conditions, including that anticoagulants may be allowed, if the condition is allowed. Medical Policy Substances of Dependence/Abuse (Drugs and Alcohol) main page was revised to add index of new documents. Medical Policy In Substances of Dependence/Abuse (Drugs and Alcohol), added new Drug Use – Past or Present Disposition Table. Medical Policy In Substances of Dependence/Abuse (Drugs and Alcohol), added Security Notification/Reporting Events information. Psychiatric, revised language in disposition table notes which referenced substances of abuse. Medical Policy Moved language from Substances of Dependence/Abuse into the Pharmaceuticals section to clarify reasons as to why there is no list of acceptable medications. Medical Policy In Pharmaceuticals, Erectile Dysfunction and Benign Prostatic Hyperplasia Medications, added daily Cialis (Tadalafil) use as allowed with limitations. Validity of Medical Certificates, removed redundant note regarding typing or hand-writing medical certificates. Near and Immediate Vision, revised to remove requirement to test both corrected and uncorrected visual acuity. Added Note: If correction is required to meet standards, only the corrected visual acuity needs to be tested and recorded. Medical Policy In Pharmaceuticals, updated the Do Not Issue – Do Not Fly list to provide examples within classes of medications. Medical Policy Revised language In Pharmaceuticals – Glaucoma Medications, Item 31. Applicants using miotic or mydriatic eye drops or taking an oral medication for glaucoma may be considered for Special Issuance certification following their demonstration of adequate control. Abdomen and Viscera, updated Malignancies Disposition Table with information on colon cancer. Medical Policy In General Information, Who May Be Certified, and in Student Pilot Rule Change, revise information on language requirements. Chart has new 449 Guide for Aviation Medical Examiners title and content. Hearing, and Disease Protocol for Musculoskeletal, revise language to clarify process.

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In addition, patients may become psychically Effects on Gastric Mucosa dependent on steroids as a result of their euphoric efSteroid administration was once thought to lead to the fect, and withdrawal of the treatment may precipitate formation of peptic ulcers, with hemorrhage or perforaan emotional crisis, with suicide or psychosis as a consetion or reactivation of a healed ulcer. Patients with Cushing’s syndrome may also exthat this effect is principally observed in patients who hibit mood changes, which are reversed by effective have received concomitant nonsteroidal antiinflammatreatment of the hypercortisolism. Since there is a minimal increase in the the hippocampus is a principal neural target for gluincidence of ulcers in patients receiving glucocorticoid cocorticoids. It contains high concentrations of glucotreatment alone, prophylactic antiulcer regimens are corticoid and mineralocorticoid receptors and has usually not necessary. Hyperglycemic Action Fluid and Electrolyte Disturbances In about one-fourth to one-third of the patients receivthe normal subject may retain sodium and water during ing prolonged steroid therapy, the hyperglycemic effects steroid therapy, although the synthetic steroid ana60 Adrenocortical Hormones and Drugs Affecting the Adrenal Cortex 695 logues represent a lesser risk in this regard. The functional state of the hyponisolone produces some edema in doses greater than 30 thalamic–pituitary axis can be evaluated by tests involvmg; triamcinolone and dexamethasone are much less liing basal plasma cortisol determinations, low and high able to elicit this effect. Glucocorticoids may also prodoses of cosyntropin (peptide fragment of cortiduce an increase in potassium excretion. Muscle weakcotrophin), insulin hypoglycemia, metyrapone, and ness and wasting of skeletal muscle mass frequently corticotrophin-releasing hormone. The expanGlucocorticoids are not withdrawn abruptly but sion of the extracellular fluid volume produced by are tapered. The doses are altered so that the condition steroids is secondary to sodium and water retention. Tapering vascular smooth muscle suggests that glucocorticoids the dose may reduce the potential for the development are also more directly involved in the regulation of of Addison-like symptoms associated with steroid withblood pressure. Alternate-day therapy will relieve the clinical coids on the cardiovascular system include dyslipidemia manifestations of the inflammatory diseases while allowand hypertension, which may predispose patients to ing a day for reactivation of endogenous corticosteroid coronary artery disease. A separate entity, steroid myoutput, thereby causing less severe and less sustained opathy, is also improved by decreasing steroid dosage. This is feasible with doses of shorter-acting corticosteroids, such as prednisolone. The usual daily dose is doubled and is given in Pseudorheumatism the early morning to simulate the natural circadian variIn certain patients, whose large dosages of corticoation that occurs in endogenous corticosteroid secretion. It Although not always predictable, the degree to which is tempting to increase the dosage of steroid in this sita given corticosteroid will suppress pituitary activity is reuation, but continued maintenance at the lower dosage lated to the route of administration, the size of the dose, with a subsequent gradual decrease in the dose usually and the length of treatment. Hypothalamic–pituitary suppression also may result if large doses of a steroid aeroAdditional Effects sol spray are used to treat bronchial asthma. Patients Other side effects include acne, striae, truncal obesity, given high concentrations of steroids for long periods deposition of fat in the cheeks (moon face) and upper and subsequently exposed to undue stress. Acute adrenal insufficiency will, of course, occur from an abrupt cessation of steroid therapy. The causation of fever, myalgia, arthralgia, and malaise may be Iatrogenic Adrenal Insufficiency difficult to distinguish from reactivation of rheumatic In addition to the dangers associated with long-term use disease. Steroid treatment should be reduced gradually of corticosteroids in supraphysiological concentrations, over several months to avoid this potentially serious withdrawal of steroid therapy presents problems. Also, continued suppression may be avoided suppression of the hypothalamic–pituitary axis obby administering daily physiological replacement doses served with modest doses and short courses of gluco(5 mg prednisone) until adrenal function is restored. However, Although tapering of dose may not facilitate recovery steroid therapy with modest to high doses for 2 weeks of the hypothalamic–pituitary–adrenal axis, it may reor longer will depress hypothalamic and pituitary activduce the possibility of adrenal insufficiency. This is imity and result in a decrease in endogenous adrenal portant, since severe hypotension caused by adrenal insteroid secretion and eventual adrenal atrophy. Adrenal patients have a limited ability to respond to stress and insufficiency should always be considered in patients an enhanced probability that shock will develop. Longwho are being withdrawn from prolonged glucocortiacting steroids, such as dexamethasone and betamethacoid therapy unless metyrapone or insulin hyposone, suppress the hypothalamic–pituitary axis more glycemia tests are performed to exclude this possibility. Thus, osteoporosis can be a sequela of rheumavirtually every phase and component of the inflammatoid arthritis, and the physician is left to determine tory and immune responses, they have assumed a major whether the untoward effect is iatrogenic or is merely a role in the treatment of a wide spectrum of diseases sign of the disease being treated. Thus, the problems astions have proven to be efficacious, particularly in chilsociated with withdrawal from long-term steroid therdren. However, the detrimental effects of glucocortiapy in rheumatoid arthritis are additional reasons coids on growth are significant for children with active steroid treatment should be initiated only after rest, arthritis. Although steroids offer symptomatic relief physiotherapy, and nonsteroidal antiinflammatory from this disorder by abolishing the swelling, redness, drugs or after methotrexate, gold, and D-penicillamine pain, and effusions, they do not cure. Inhaled preparations are particularly Replacement Therapy effective when used to prevent recurrent attacks. Adrenal insufficiency may result from hypofunction of this therapy is often combined with an inhaled bronthe adrenal cortex (primary adrenal insufficiency, chodilator such as a -adrenergic agonist. The use of Addison’s disease) or from a malfunctioning of the adrenergic agonists or theophylline enables use of a hypothalamic–pituitary system (secondary adrenal inlower dose of glucocorticoid, especially in patients relasufficiency). In treating primary adrenal insufficiency, tively resistant to therapy (see Chapter 39). A doubling of the may also be used at lower doses in combination with cortisol dose may be required during minor stresses or other drugs for the treatment of vasculitis, lupus infections. Steroids are valuable in the mentation, prednisone can be substituted for cortisol to prevention and treatment of organ transplant rejecavoid fluid retention. In Guillainconsidered, since patients with deficient corticotrophin Barré syndrome glucocorticoids reduce the inflammasecretion generally do not have abnormal function of tory attack and improve final outcome, while in chronic the zona glomerulosa. Since cortisol replacement therinflammatory demyelinating polyneuropathy glucocorapy is required for life, adequate assessment of patients ticoids suppress the immune reaction but may not reis critical to avoid the serious long-term consequences tard the progression of the disease. In many cases, the exert a facilitatory action on neuromuscular transmisdoses of glucocorticoid used in replacement therapy are sion that may contribute to their efficacy in certain neuprobably too high. To limit the risk of tor antibodies are responsible for the neuromuscular osteoporosis, replacement therapy should be carefully transmission defect in myasthenia gravis has provided a assessed on an individual basis and overtreatment rationale for exploiting the immunosuppressive effects avoided. Overproduction of androgens causes virilization, particularly frequent and possibly severe in patients accelerated growth, and early epiphysial fusion. Treattreated with steroids, they have been used as short-term ment of this condition requires administration of glucoadjunctive therapy to reduce the severe symptoms assocorticoid in amounts adequate to suppress adrenal anciated with such bacterial infections as acute H. These patients may decystis carinii pneumonia, demyelinating peripheral neuvelop potentially fatal salt-wasting if not treated. Steroids transported by transcortin enter the target cell by diffuLeukemia sion and then form a complex with its cytosolic receptor Steroids are important components in the treatment of protein. Their efficacy in chronic coid receptors containing two subunits of the heat lymphocytic leukemia and multiple myeloma stems shock protein that belong to the 90-kDa family. The from their lympholytic effects to reduce cell proliferaheat shock protein dissociates, allowing rapid nuclear tion, promote cell cycle arrest, and induce cell death by translocation of the receptor–steroid complex. However, the developcalled glucocorticoid response elements in the proment of resistance may limit the effectiveness of steroid moter–enhancer regions of responsive genes (Fig. Because their side effects are thought to be a Prompt intensive treatment with corticosteroids may be consequence of gene induction, glucocorticoids that can lifesaving when an excessive inflammatory reaction has repress inflammatory genes without inducing gene tranresulted in septic shock. This protective role of steroids may cellular responsiveness are directly proportional to the be due to a direct effect on vascular smooth muscle. A decrease in glucocombination of glucocorticoids and dopamine therapy corticoid receptor number (down-regulation) produced preserves renal blood flow during shock. Downregulation of glucocorticoid receptors also is a potential Congenital Adrenal Hyperplasia mechanism for terminating glucocorticoid-dependent Congenital enzymatic defects in the adrenal biosynresponses and for curtailing excessive cell stimulation thetic pathways lead to diminished cortisol and aldowhen circulating levels of steroids are high. In these conditions, tiveness of glucocorticoids will also be compromised by corticotrophin secretion is increased, and adrenal hythe concomitant administration of other drugs that enperplasia occurs, accompanied by enhanced secretion of hance the clearance of glucocorticoids (ephedrine, steroid intermediates, especially adrenal androgens. However, in other tissues glucoMembrane phospholipids corticoids may exert their actions through mineralocorticoid receptors. Several actions of glucocorticoids that are too rapid to be explained by actions on transcription are mediated by effects on membrane receptors. Because glucocorticoids regulate gene expression and Glucocorticoids (induce lipocortin) protein synthesis, there is generally a lag of several hours before their effects are manifest. This may account for the fact that side effects elicited by Arachidonic acid steroids can be minimized by alternate-day therapy. Steroids may exert a primary effect at the inflammatory site by inducing the synthesis of a Glucocorticoids group of proteins called lipocortins. Although may also contribute to the antiinflammatory effects of the short cosyntropin test is recognized as a valid glucocorticoids.

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It is possible that in patients predisposed to Parkinson’s disease there is some breakdown of the patients’ protective mechanisms in those neurons. In experimenting with amphetamine, he was finding with individual neuron investigation that amphetamine, in both low and high doses, was inhibitory in some neurons. In other neurons it was inhibitory in low doses, and in high doses it became excitatory. But in this investigation he claimed that he was finding some substance in the brain that was counteracting the effect of the amphetamine and, by analysis, he said it was determined to be ascorbic acid. Now the use of molecular psychiatry of ascorbic acid in schizophrenia by Linus Pauling and others, where there seems to be some relationship to dopamine neurons, and fmding that dopamine-dopaminergic neurons or receptors are present in twice the normal amount, makes this an intriguing area of investigation. Rebec also said that the brains on post mortem studies of schizophrenics tended to be mushy and to have very low levels of ascorbic acid in their constituent tissue. We deprived them of their scorbic acid contents, then exposed them to amphetamine. In those studies we found that the ascorbutic animals were protected from some of the neurotoxicities of the amphetamines. It is not just a matter of adding vitamin C or ascorbic acid and getting protection; it can work as a double-edged sword. So I feel very sure that in the chronic state there will come a time when this is not reversible. Do you have any explanation for why depression is not seen in humans if serotonin neurons have been damaged by these drugs? We have talked about this a lot with fenfluramine, and we have done studies with parachloroamphetamine in which we have given it orally to rats at relatively low doses, but still anorectic doses, over 90 days. But I don’t feel comfortable about relying on the lack of reporting of depression as real evidence that there is no neurotoxicity. In the primate, to get the kind of Parkinsonism that people talk about in animal models, that animal model actually turns out to be very difficult to produce in chronic Parkinsonism. The problem is developing an animal that has 90 to 95 percent depletion of dopamine on a chronic basis. As you know, it is a very narrow window, and it is very difficult to produce that kind of animal preparation. So I think you have to consider the possibility that lack of symptoms after serotonergic lesions could, perhaps, be related to the fact that we are dealing with preparations where there is a 50, 60, 70 percent depletion where we don’t have enough of a lesion to produce an overt behavioral disturbance. There may be systems in which you must have a lot of depletion to see a functional change, and there may be others where it doesn’t take very much. I think that if you did a proper neuropsychological exam that you would pick up even smaller depletion effects. I think if you are looking for an overt complete terminal Parkinson situation, yes, you need a 99 percent depletion. But part of the problem is that the Parkinson situation involves not only the nigrostriatal system but also the mesolimbic dopamine system. There are plenty of studies in rats, and it is very easy to produce a Parkinsonian rat with a very discrete 352 injection of 6-hydroxydopamine in the right place. I can take 2 micrograms of 6-hydroxydopamine and put it in exactly the right location in the ventral tegmental area, and I can produce a Parkinsonian rat that will die, So I think you can debate that issue about 99 or 95 percent depletion. I think that if you probe those animals with the proper pharmacological agents and proper environmental situation, you will pick up deficits. I think the lack of knowledge about what the serotonin systems do is the basis of the problem here. If we have proper probes for exaggerating serotonergic function or proper probes for exaggerating deficits associated with serotonergic function we would easily pick up things. Whether that is important or not, you know it might be good to trim our serotonin neurons slightly. But I think we have the tools in behavioral pharmacology to conduct tests in rats that will be sensitive to serotonin depletion. One of the striking aspects of this toxicity of compounds is selective destruction terminals and the cell bodies that are left intact. De Souza has recently reported some biochemical evidence for recovery of serotonin. We have now found anatomic evidence for reinnervation of depleted areas by serotonin neurons. But it is going to be a while before we figure out whether their reinnervation is appropriate or perhaps aberrant. Do they end up with complete recovery, do they end up with a better system than they started with or one that malfunctions? Inhibition of 5-hydroxytryptamine accumulation and deamination by substituted phenylalkylamines in hypothalamic synaptosomes from normal and reserpine-pretreated rats. A functional response to D1 dopamine receptor stimulation in the central nervous system: Inhibition 3 of the release of [H]-serotonin from the rat substantia nigra. Ultrastructural relationships between serotonin and dopamine neurons in the rat arcuate nucleus and medial zona incerta: A combined radioautographic and immunocytochemical study. Endogenously produced 5,6-dihydroxytryptamine may mediate the neurotoxic effects of para-chloroamphetamine. Long-term changes in dopaminergic innervation of caudate nucleus after continuous amphetamine administration. Further studies on the long-term depletion of striatal dopamine in iprindole-treated rats by amphetamine. Comparison of the oxime and the hydroxylamine derivatives of 4-chloroamphetamine as depletors of brain 5hydroxyindoles. Long-term effects of 4-chloroamphetamine on brain 5-hydroxyindole metabolism in rats. Catecholamine toxicity: A proposal for the molecular pathogenesis of manganese neurotoxicity and Parkinson’s disease. Autooxidation versus covalent binding of quinones as the mechanism of toxicity of dopamine, 6-hydroxydopamine and related compounds toward Cl300 neuroblastoma cells in vitro. Fenfluramine: Evidence for a neurotoxic action on midbrain and a long-term depletion of serotonin. Serotonin axon terminals in the ventral tegmental area of the rat: Fine structure and synaptic input to dopaminergic neurons. Long-term effects of multiple doses of methamphetamine on tryptophan hydroxylase and tyrosine hydroxylase activity in rat brain. Parkinsonism-inducing neurotoxin, N-methyl-4-phenyl-1,2,3,6tetrahydropyridine: Uptake of the metabolite N-methyl-4-phenylpyridine by dopamine neurons explains selective toxicity. Evaluation of the neurotoxic effects of p-chloroamphetamine: A histological and biochemical study. Alphamethyldopamine, a key intermediate in the metabolic disposition of 3,4-methylenedioxyamphetamine in vivo in dog and monkey. Metabolic activation of the serotonergic neurotoxin para-chloroamphetamine to chemically reactive intermediates by hepatic and brain microsomal preparations. Decrease of cerebral 5-hydroxytryptamine and 5-hydroxyindoleacetic acid by an arylalkylamine. Nerve terminal & generation after a single injection of d-amphetamine in iprindole-treated rats: Relation to selective long-lasting dopamine depletion. Long-term effects of p-chloroamphetamine on tryptophan hydroxylase activity and on the levels of 5-hydroxytryptamine and 5-hydroxyindoleacetic acid in brain. In vitro demonstration of dopamine uptake by neostriatal serotonergic neurons of the rat. Formation of 6-hydroxydopamine in caudate nucleus of the rat brain after a single large dose of methylamphetamine. Correlation between brain levels and biochemical effects of the optical isomers of p-chloroamphetamine. Plasma prolactin changes following fenfluramine in depressed patients compared to controls: An evaluation of central serotonergic responsivity in depression. Lack of morphological changes in the neurons of the B-9 group in rats treated with fenfluramine. A comparative study of the therapeutic effects of some 4-chlorinated amphetamine derivatives in depressive patients. Amphetamine induces depletion of dopamine and loss of dopamine uptake sites in caudate. The effects of a single dose of amphetamine and iprindole on the serotonergic system of the rat brain. Kinetics of serotonin accumulation into synaptosomes of rat brain-effects of amphetamine and chloroamphetamines.

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Tolerance develops within a few days if potent opioids are given at frequent intervals, such as every 4 Extent and Pattern of Abuse to 6 hours. Development of tolerance requires several Sympathomimetic stimulant drugs have very high abuse weeks if the opioid is given only twice a day. They are typically used repeatedly for a short the continued use of opioids results in the developperiod during which time the user escalates the dose to ment of physical dependence, as demonstrated by the greater and greater levels to attain the desired degree of appearance of a characteristic abstinence syndrome euphoria. Extended uninterrupted use of stimulants for upon interruption or cessation of use. The symptoms of 24 to 72 hours is often referred to as a run and usually withdrawal include hyperactivity, anxiety, restlessness, ends in a crash (24–36 hours of sleep) once the individyawning, diarrhea, vomiting, chills, fever, lacrimation, ual is exhausted physically. Piloerection (gooseflesh or cold stimulants, approximately 5 billion doses of these drugs turkey), mydriasis, increased blood pressure and heart are prescribed per year, and there appears to be a sigrate, and hyperpyrexia may be observed. Drug craving is an important feature of opioid withmethylphenidate, are taken orally, others are either drawal. In contrast to some other drugs of abuse, volatilized for inhalation or snorted as the solid (nasal withdrawal is not life threatening. It is necessary to convert cocaine and methamphetamine to their free base so that they can be Treatment of Opioid Dependence volatilized. Although the ultimate goal of treatment programs is to achieve drug-free status as quickly as possible, it is Pharmacological Aspects rarely achieved without pharmacotherapy. The most commonly used strategy is to switch the patient from a Most of the sympathomimetic stimulants exhibit similar short-acting opioid, such as heroin, to a long-acting agpharmacological properties, differing primarily in the 35 Contemporary Drug Abuse 411 magnitude of their effects. Intravenous injections of cocaine and amphetamine can Pharmacological Actions produce a very intense rush of sensations that resemble sexual orgasm. At small doses cognition increases and the behavioral effects of nicotine have been defined as mood is elevated. As the dose of drug escalates during a both stimulant and depressant, effects that are influrun, the overall activity of the individual changes from enced by the present mental status and expectations of task performance to one generally characterized by the smoker. The person starts performing Nicotine produces myriad effects on the central nervous certain behaviors repeatedly. Many continuously touch or pick at their face or ated through nicotinic receptors. Acute toxic prominent effects is stimulated release of dopamine, paranoid psychosis can develop, but it usually requires particularly in the nucleus accumbens, which is a major a longer period of abuse than a single acute session. Autonomic hyperactivity is also expressed as hyperthermia Tolerance and Dependence and mydriasis. More serious effects include the possibility of myocardial infarction, cerebrovascular hemorTolerance to nicotine’s effects develops rapidly and rhage, seizure, and death. It has been proMechanism of Action posed that rapid tolerance or desensitization occurs to the sympathomimetic drugs are discussed in Chapter the behavioral or reinforcing effects of nicotine. In brief, the most commonly abused of these drugs, effects are of such a short duration that a smoker consuch as cocaine, work primarily as indirect agonists of tinually cycles between a sensitized and desensitized the catecholamine neurotransmitter systems via instate. This notion is consistent with the fact that drugs hibitory actions upon the transmitter reuptake system. There is also Regardless of the mechanism of tolerance, nicotine evidence that blockade of serotonin uptake may conis a highly addicting drug. Although most smokTolerance and Dependence ers wish to quit, only about one-third attempt to do so Tolerance to stimulants develops fairly rapidly, even in each year. It is the rapid development of tolerance that leads to the escalation of dose during drug abuse runs. As the medical Chronic stimulant abuse alters the personality of the use of barbiturates decreased, primarily because of abuser. These and related changes are the result of neutheir high addiction liability and the danger of acute rotoxicity and are not characterized as either acute drug lethality, the use of the benzodiazepine anxiolytics ineffects or withdrawal signs. The most commonly abused barbiturates are of being pursued or persecuted and therefore become secobarbital, pentobarbital, and amobarbital. They become self-occupied barbital is not generally abused, because of its slow onand hostile toward others. The most commonly abused anxiolytics duce toxic psychosis that closely resembles schizophreinclude diazepam, chlordiazepoxide, midazolam, lonia and must be treated with neuroleptic drugs razepam, and flurazepam. These drugs to alcohol and the barbiturate sedatives, withdrawal are abused for their euphoric effects and as a means to from benzodiazepines is not life threatening. The difference between the classes of drugs is primarily Ethanol is the most widely abused drug in the world. Intoxication progresses from mild There are more than 10 million alcoholics in the United to severe over a relatively narrow dose range in the case States alone. The benzodiazepine dose–response ages has been linked to as many as half of all traffic accurve is such that great increases in dose are necessary cidents, two-thirds of homicides, and three-fourths of to make such a transition. Thus, the benzodiazepines are suicides, and it is a significant factor in other crimes, in a safer class of depressant drugs. The annual cost to the American economy has ria, anxiety reduction, anticonvulsant activity, sedation, been estimated to exceed $100 billion in lost productivataxia, motor incoordination, impaired judgment, anesity, medical care, and property damage. The physiological effects of high-dose by the procurement and consumption of alcoholic bevdepressants include miosis, shallow respiration, and reerages and when this behavior interferes with personal, duction in reflex responses. A light drinker generally is defined as one who consumes an average of one drink or less per day, usually Tolerance and Dependence with the evening meal; a moderate drinker is one who has approximately three drinks per day; and a heavy Tolerance to many of the effects of the depressants dedrinker is one who has five or more drinks per day (or velops. Unlike opioids, barbiturate and benzodiazepine in the case of binge drinkers, at least once per week with tolerance develops slowly. The lethal dose in a tolChemistry erant individual is not much different from that of the Ethanol (ethyl alcohol, alcohol) is a simple organic molgeneral population. Cross-tolerance develops to some ecule composed of a single hydroxyl group and a short degree between the depressant classes of drugs. The hydroxyl 3 2 Dependence on benzodiazepines, as evidenced by a and ethyl moieties confer both hydrophilic and withdrawal syndrome, can develop to large doses of lipophilic properties on the molecule. Once the Absorption, Distribution, Metabolism, and withdrawal syndrome has dissipated, the abusers of Excretion benzodiazepines are not as likely to resume drug consumption as are alcoholics. Withdrawal signs appear to After oral administration, ethanol is almost completely be more likely following chronic exposure to shortabsorbed throughout the gastrointestinal tract. The rate acting benzodiazepines, such as alprazolam (half-life of of absorption is largely determined by the quantity conless than 15 hours) or lorazepam than long-acting drugs. Eating food before or during drinking retards abing, clouded sensorium, heightened sensory perception, sorption, especially if the food has a high lipid content. Withdrawal signs brain, liver, lungs, and kidney, equilibrium occurs rappeak the second day after abrupt withdrawal and last idly. Conversely, in organs with low blood flow, such as 35 Contemporary Drug Abuse 413 muscle, equilibrium occurs more slowly. Ethanol readily In adults, ethanol is metabolized at about 10 to passes through the blood–placenta barrier into the fetal 15 mL/hour. Although the concentration of ethanol in tion must be controlled to prevent accumulation and inthe blood can be quite predictable, measurements of toxication. There is little evidence that chronic ingestion blood ethanol, especially when the concentrations are of ethanol leads to a significant induction of alcohol derising, may lead to erroneous conclusions, since the valhydrogenase, even in heavy drinkers. The sympceedings in drunk-driving cases where blood ethanol toms include facial flushing, vasodilation, and tachycarconcentrations are considered an accurate and legally dia. These individuals apparently have a genetic defiacceptable determinant of the amount of ethanol conciency of the enzyme aldehyde dehydrogenase, which sumed. The best-studied and most drugs such as metronidazole, griseofulvin, quinacrine, important enzyme is zinc dependent: alcohol dehydrothe hypoglycemic sulfonylureas, phenothiazines, and genase. Salient features of the reaction can be seen in phenylbutazone are coadministered with ethanol, a simFig. The rate of metabolism catalyzed by alcohol ilar accumulation of acetaldehyde may occur. These actions result in powerful suppression of nerve cell activity, which is consistent with 60 the depressant actions of alcohol in the brain. This Blood alcohol concentration (mg/dL) after the consumption stimulation is expressed as decreased social and psychoof various amounts of alcohol (for an adult of about 150 lb). The behavioral and physiological eftance in the metabolism of ethanol in humans, it may be fects are associated with different blood ethanol conceninvolved in some of the reported interactions between trations. As the blood ethanol concentration begins to inethanol and other drugs that are also metabolized by crease, behavioral activation, characterized by euphoria, this system. Microsomal mixed-function oxidases may talkativeness, aggressiveness, and loss of behavioral conbe induced by chronic ethanol ingestion.

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When precocious puberty is documented on physical examination, endocrine lab studies are not necessary prior to advanced imaging F. Panhypopituitarism, hyperprolactinemia, symptoms or signs of tumor mass effect. Children with no evidence of malignancy, Crohn’s disease, renal disease, hypothyroidism or Turner syndrome and one of the following i. For isolated growth hormone deficiency two measurements of growth hormone with stimulation are performed iv. After 3 years, then every other year for the next 6 years, then every 5 years unless new signs and symptomsif stable. Common syndrome inherited in an autosomal dominant manner (50% risk to offspring) affecting 1 in 2500 people. Cranial nerve palsy (See Suspected tumor of or affective one or more cranial nerves above) 2. Cranial nerve palsy (See Suspected tumor of or affecting one or more cranial nerves above) 6. Vision loss Page 143 of 885 10. Short stature with height 2 standard deviations below the mean 71 for age and gender [One of the following] A. Growth hormone levels below normal (≤ 10 ng/mL [micrograms/L]) for isolated growth hormone deficiency, two measurements of growth hormone with stimulation are performed. Proptosis including thyroid eye disease and exophthalmus [One of the following] A. Examples include drop attacks, seizures, coincident headache, ataxia, aura or focal neurological findings 4. Equivocal or unusual nystagmus findings, including direction changing or persistent downbeat nystagmus 5. Confusion including memory loss and disorientation Page 145 of 885 E. New onset of severe headache Page 146 of 885 15. Horner’s syndrome, miosis and ptosis (contraction of the iris, drooping eyelid) E. Recurrent Laryngeal Palsy – the following can be considered with unilateral vocal cord/fold palsy identified by 84 laryngoscopy: A. Atypical Parkinsonism because ofunusual clinical features (for example, persistent unilateral signs and symptoms, young onset under age of 50, rapid progression), incomplete or uncertain medication responsiveness, or clinical diagnostic uncertainty. Evaluation for surgical treatment or Essential Tremor or Parkinson’s disease, including Deep Brain Stimulator placement. This clinical evaluation should also include family history and (whenever possible) the accounts of eyewitnesses to the event(s). First-time seizure in child ≥ 12 months of age that has no known cause and is not associated with fever b. First-time seizure in child < 12 months of age that has no known cause and is not associated with fever if the infant has an open fontanelle. Due to the length of time for image acquisition and the need for stillness, anesthesia is required for almost all infants and young children (age < 7 years), as well as older children with delays in development or maturity. If requesting clinicians indicate that a non-contrast study is being requested with specific concern for gadolinium retention, the exam can be approved. Suspected normal pressure hydrocephalus with gait disturbance and either dementia or urinary incontinence f. Recognition and treatment of a comorbid sleep disorders is paramount, and a complete neurologic history and examination should precede any request for advanced imaging. Orbital and/or Intracranial complications with ocular and/or neurological deficit 1. A new obstructing sinus mass, including retention cysts and nasal polyps, that obscures the physician’s view on endoscopy 1. Any head and neck cancer with neurological findings or suspicion of skull base invasion 1. Pediatric-specific imaging considerations include suspected congenital brain infection and neonatal meningitis. The common causes of prenatal infections of the central nervous system are cytomegalovirus, Toxoplasma gondii, herpes simplex type 2 virus and most recently zika virus. The findings suggesting prenatal brain infection include microcephaly, microphthalmia, chorioretinitis, cataracts, hypotonia, and seizures. The following imaging is considered for newborn infants with suspected prenatal brain infection regardless of inciting organism. Neonatal meningitis is most often caused by bacterial pathogens and usually occurs as a complication of sepsis in the first week of life. In older infants and children, meningeal inoculation occurs secondary to hematogenous spread or penetrating trauma. The following imaging is considered for newborns or older infants with and open fontanelle and suspected meningitis. Congenital lesions (cephalocele-discussed above, dermoid cysts, epidermoid cyst), 2. Extracranial hemorrhage related to birth trauma (caput succedaneum, cephalohematoma, subgaleal hematoma). After the first year of life, malignant tumors, such as Langerhans cell histiocytosis metastases from neuroblastoma and rhabdomyosarcoma are an additional cause of a scalp mass. The following imaging is considered for newborns with palpable scalp and skull lesions. Page 153 of 885 1. Diagnostic criteria for idiopathic intracranial hypertension, Neurology, 2002; 59:1492-1495. Practice parameter: neuroimaging in the emergency patient presenting with seizure (summary statement). American College of Emergency Physicians, American Academy of Neurology, American Association of Neurological Surgeons, American Society of Neuroradiology. American College of Radiology Appropriateness Criteria – Orbits, Vision and Visual Loss. American College of Radiology Appropriateness Criteria – Hearing Loss and/or Vertigo. Page 154 of 885 16. Clinical practice guideline: sudden hearing loss, Otolaryngol Head Neck Surg, 2012;146:S1-S35. Recommendations for the Management of Intracranial Arteriovenous Malformations: A Statement for Healthcare Professionals from a Special Writing Group of the Stroke Council, American Stroke Association, Stroke, 2001; 32:1458-1571. Clinical Practice Advisory Group of the British Association of Otorhinolaryngologists Head and Neck Surgeons. Clinical Effectiveness Guidelines: Acoustic Neuroma (Vestibular Schwannoma), 2002. Diagnosis of cerebral venous thrombosis with echo-planar T2*weighted magnetic resonance imaging. Diagnosis and management of cerebral venous thrombosis: A statement for Healthcare Professionals from the American Heart Association/American Stroke Association, Stroke, 2011; 42:1158-1192. Page 155 of 885 40. American Association of Clinical Endocrinologists medical guidelines for clinical practice for growth hormone use in growth hormone-deficient adults and transition patients – 2009 update, Endocr Pract, 2009; 15 Suppl 2:1-29. Testosterone therapy in adult men with androgen deficiency syndromes: An Endocrine Society Clinical Practice Guideline, J of Cl Endocrinol Metab, 2010; 95:2536-2559. Diagnosis and treatment of hyperprolactinemia: An Endocrine Society Clinical Practice Guideline, J of Clinical Endocrinology and Metabolism, 2011; 96:273-288.

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Code for Term House fire X00 Locate the E-code for House fire: House fire (uncontrolled) X00. General Instructions the main axis of classification for land transports (V01-V89) is the victim’s mode of transportation. The vehicle of which the injured person is an occupant is identified in the first two characters since it is seen as the most important for prevention purposes. Refer to these definitions when any means of transportation (aircraft and spacecraft, watercraft, motor vehicle, railway, other road vehicle) is involved in causing death. Motor vehicle accidents where the type of vehicle is unspecified are classified to V87-V89. Vehicle accidents where the type of vehicle is unspecified are classified to V87-V89. Heavy transport vehicle includes armored car, dump truck, fire truck, panel truck, semi, tow truck, tractor-trailer, 18-wheeler d. This table is referenced with any land transport accident if the mode of transportation is known. For V01-V09, the fourth character indicates whether a pedestrian was injured in a nontraffic accident, traffic accident, or unspecified whether traffic or nontraffic accident. Each means of transportation is preceded by its set of fourth characters in Volume 1. From Volume 1, determine the fourth character is 9, unspecified car occupant injured in traffic accident. Classifying accidents as traffic or nontraffic If an event is unspecified as to whether it is a traffic or nontraffic accident, it is assumed to be: a. A traffic accident when the event is classifiable to categories V02-V04, V10-V82, and V87. Consider category V05 to be unspecified whether traffic or nontraffic if no place is indicated or if the place is railroad (tracks). Consider accidents involving occupants of motor vehicles as traffic when the place is railroad (tracks). When a motor vehicle strikes another vehicle or object, assume the collision occurred on the highway unless otherwise stated. Refer to these instructions for clarification of the status of the victim when not clearly stated. Codes for Record I (a) Multiple internal injuries T065 (b) Crushed by car on highway T147 V031 Code to pedestrian injured in collision with car, pickup truck or van, traffic (V031). In classifying motor vehicle traffic accidents, a victim of less than 14 years of age is assumed to be a passenger provided there is evidence the decedent was an occupant of the motor vehicle. A statement such as thrown from car, fall from struck head on dashboard, drowning, or carbon monoxide poisoning is sufficient. Female, 4 years old Codes for Record I (a) Fractured skull S029 (b) Struck head on windshield when V476 (c) car struck tree that had fallen across road Code to car occupant injured in collision with fixed or stationary object, passenger (V476). When the transport accident descriptions do not specify the victim as being a vehicle occupant and the victim is described as: pedestrian versus (vs) any vehicle (car, truck, etc. If drowning results from a specified type of motor vehicle accident, code the appropriate E-code for the specified type of motor vehicle accident. When falls from transport vehicles occur, apply the following instructions: (1) Consider a transport vehicle to be in motion unless there is clear indication the vehicle was not in transit. Refer to Table of land transport accidents, specified type of vehicle reported, noncollision. Refer to Volume 1 for fourth character and select 3, unspecified occupant of pick-up truck, nontraffic accident. Refer to Volume 1 for fourth character and select 4, person injured while boarding or alighting. Select occupant of motor vehicle (traffic), noncollision transport accident (V892). Codes for Record I (a) Third degree burns T303 (b) Auto accident car overturned V489 (c) Code to car occupant injured in noncollision transport accident, unspecified (V489). Occupant of special all-terrain or other motor vehicle designed primarily for off-road use, injured in transport accident (V86) this category includes accidents involving an occupant of any off-road vehicle. The fourth character indicates whether the decedent was injured in a nontraffic or traffic accident. Codes for Record I (a) Multiple injuries T07 (b) Driver of snowmobile which V860 (c) collided with auto Code to driver of all-terrain or other off-road motor vehicle injured in traffic accident since the collision occurred with an automobile (V860). Codes for Record I (a) Head injuries S099 (b) Overturning snowmobile V869 Code to unspecified occupant of all-terrain or other off-road motor vehicle injured in nontraffic accident (V869). Traffic accident of specified type but victim’s mode of transport unknown (V87) Non-traffic accident of specified type but victim’s mode of transport unknown (V88) a. If more than one vehicle is mentioned, do not make any assumptions as to which vehicle was occupied by the victim unless the vehicles are the same. If reported types of vehicles are not indexed under Accident, transport, person, collision, code V877 for traffic and V887 for nontraffic. Codes for Record I (a) Head injuries S099 (b) Bus and pick-up truck collision, driver V877 (c) Do not make any assumption as to which vehicle the victim was driving. Collision between bus and pick-up is not indexed under Accident, transport, person, collision. Water transport accidents (V90-V94) the fourth character subdivision indicates the type of watercraft. Air and space transport accidents (V95-V97) For air and space transport accidents, the victim is only classified as an occupant. Military aircraft is coded to V958, Other aircraft accidents injuring occupant, since a military aircraft is not considered to be either a private aircraft or a commercial aircraft. Where death of military personnel is reported with no specification as to whether the airplane was a commercial or private craft, code V958. When multiple deaths occur from the same transportation accident, all the certifications should be examined, and when appropriate, the information obtained from one may be applied to all. When classifying accidents which involve more than one kind of transport, use the following order of precedence: aircraft and spacecraft (V95-V97) watercraft (V90-V94) other modes of transport (V01-V89, V98-V99) Codes for Record I (a) Multiple fractures T029 (b) Driver of car killed when V973 (c) a private plane collided with (d) car on highway after forced landing Code to person on ground injured in air transport accident following order of precedence. When no external cause information is reported and the place of occurrence of the injuries was highway, street, road(way), or alley, assign the external cause code to person injured in unspecified motor vehicle accident, traffic. Falls with other external events When fall is reported more information must be obtained in order to assign the most appropriate code. Codes for Record I (a) Drowned T751 X37 (b) Car which decedent was driving was washed (c) away with bridge during hurricane Code to victim of cataclysmic storm (X37). Codes for Record I (a) Suffocation T71 X36 (b) Covered by landslide Code to victim of avalanche, landslide and other earth movements (X36). Codes for Record I (a) Suffocated by smoke T598 X00 (b) Home burned after being (c) struck by lightning Code to exposure to uncontrolled fire in building or structure (X00). Category X33 includes only those injuries resulting from direct contact with lightning. Codes for Record I (a) Ruptured diaphragm S278 (b) Driver of auto which struck V475 (c) landslide covering road Code to car occupant injured in collision with fixed or stationary object, driver (V475). When the following statements are reported, see Table of drugs and chemicals for the external cause code and code as accidental poisoning unless otherwise indicated. Codes for Record I (a) Poisoning by barbiturates T423 X41 Code to X41, accidental poisoning by and exposure to anti-epileptic, sedative-hypnotic, anti-parkinsonism and psychotropic drugs, not elsewhere classified. Interpret intoxication by drug to mean poisoning by drug unless indicated or stated to be due to drug therapy or as a result of treatment for a condition. Codes for Record I (a) Respiratory failure J969 (b) Digitalis intoxication T460 X44 Code to X44, digitalis intoxication as poisoning when there is no indication the drug was given for therapy. Use the following codes for the different manners of death: Suicide X64, Homicide X85 and Undetermined Y14. Codes for Record I (a) Drug intoxication T509, X44 (b) Digitalis & cocaine intoxication T460 T405 Code to X44, accidental poisoning by and exposure to other and unspecified drugs, medicaments, and biological substances. Codes for Record I (a) Acute respiratory failure J960 (b) due to synergistic action T519 X45 T404 X42 (c) of alcohol and darvon Code to X42, accidental poisoning by and exposure to narcotics and psychodysleptics (hallucinogens), not elsewhere classified. Synergistic action of alcohol and a medicinal agent is classified to poisoning by the medicinal agent. Codes for Record I (a) Alcohol and barbiturate intoxication T519 X45 T423 X41 Code to X41, accidental poisoning by and exposure to antiepileptic, sedative-hypnotic, antiparkinsonism and psychotropic drugs, not elsewhere classified. Alcoholic intoxication or poisoning reported in combination with medicinal agents is classified to poisoning by the medicinal agents. Carbon monoxide poisoning Code carbon monoxide poisoning from motor vehicle exhaust gas to noncollision motor vehicle accident (traffic) according to type of motor vehicle involved unless there is indication the motor vehicle was not in transit.

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Such ‘limbless perception’ is thought to reflect the mental representation of body parts generated within the brain (body schema), such that perception is carried out without somatic peripheral input. Reorganization of cortical connections following amputation may explain phantom phenomena such as representation of a hand on the chest or face, for which there is also evidence from functional brain imaging. Phantom Vision this name has been given to visual hallucinations following eye enucleation, by analogy with somaesthetic sensation experienced in a phantom limb after amputation. Similar phenomena may occur after acute visual loss and may overlap with phantom chromatopsia. Unformed or simple hallucinations are more common than formed or complex hallucinations. Phonagnosia is the equivalent in the auditory domain of prosopagnosia in the visual domain. Cross References Agnosia; Auditory agnosia; Prosopagnosia; Pure word deafness Phonemic Disintegration Phonemic disintegration refers to an impaired ability to organize phonemes, the smallest units in which spoken language may be sequentially described, resulting -277 P Phonetic Disintegration in substitutions, deletions, and misorderings of phonemes. Phonemic disintegration is relatively common in aphasic disorders, including Broca’s aphasia, conduction aphasia, and transcortical motor aphasia. The neural substrate may be primary motor cortex of the left inferior precentral gyrus and subjacent white matter, with sparing of Broca’s area. Clinical–anatomical correlation in a selective phonemic speech production impairment. Cross Reference Hyperacusis Phosphene Phosphenes are percepts in one modality induced by an inappropriate stimulus. The perception of flashes of light when the eyes are moved has been reported in optic neuritis, presumably reflecting the increased mechanosensitivity of the demyelinated optic nerve fibres; this is suggested to be the visual equivalent of Lhermitte’s sign. Eye gouging to produce phosphenes by mechanical stimulation of the retina is reported in Leber’s congenital amaurosis. Noise-induced visual phosphenes have also been reported and may be equivalent to auditory-visual synaesthesia. Cross References Auditory-visual synaesthesia; Gaze-evoked phenomena; Lhermitte’s sign; Photism; Synaesthesia Photism Photisms are transient positive visual phenomenon, such as geometrical shapes or brightly coloured spectral phenomena, occurring in the context of epilepsy, migraine, or in blind visual fields (hence overlapping with photopsia). It is associated with a wide range of causes and may result from both peripheral and central mechanisms:. Intracranial disease: migraine, meningitis, and other causes of meningeal irritation, central photophobia (? Cross References Dazzle; Meningism; Retinitis pigmentosa Photopsia Photopsias are simple visual hallucinations consisting of flashes of light which often occur with a visual field defect. They suggest dysfunction in the inferomedial occipital lobe, such as migraine or an epileptogenic lesion. Cross References Aura; Hallucination; Photism Physical Duality A rare somaesthetic metamorphopsia occurring as a migraine aura in which individuals feel as though they have two bodies. Cross Reference Geophagia, Geophagy Picture Sign the ‘picture sign’ is present when a patient believes that individuals seen on the television screen are actually present in the home; indeed they may be reported -279 P ‘Picture Within a Picture’ Sign to emerge from the television set into the room. This may occur as part of the cognitive disturbance of Alzheimer’s disease or dementia with Lewy bodies, or as part of a psychotic disorder. Like the ‘mirror sign’, the ‘picture sign’ may be classified as a misidentification phenomenon. Cross References ‘Mirror sign’; Misidentification syndromes ‘Picture Within a Picture’ Sign Following a right parieto-occipital infarction, a patient complained of seeing people moving about in the left lower quadrant of the visual field whilst vision was normal in the remainder of the visual field, a phenomenon labelled the ‘picture within a picture’ sign. Cross References Froment’s sign; ‘Straight thumb sign’ Pinhole Test Impairments in visual acuity due to refraction defects (changes in shape of the globe or defects in the transparent media of the eye) may be improved or corrected by looking through a pinhole which restricts vision to the central beam of light. The first response of the hallux is the critical observation, which may be facilitated by having ones line of vision directly above the axis of the toe. An extensor response of the big toe in an adult (Babinski’s sign), with or without fanning (abduction) of the other toes (fan sign, signe de l’éventail), is a reliable sign of upper motor neurone pathology. Use of the term ‘negative Babinski’s sign’ or ‘negative Babinski response’ to mean ‘flexor plantar response’ is incorrect and should not be used. This normal plantar response is a superficial cutaneous reflex, analogous to abdominal and cremasteric reflexes, whereas the pathological response is often accompanied by activity in other flexor muscles. In some individuals the toes do not move at all, in which case the response is labelled as ‘mute’ or absent. Assessment of the response may be confounded by withdrawal of the foot in ticklish individuals. Differentiation from the striatal toe seen in parkinsonian syndromes is also important. The plantar response may be elicited in a variety of other ways which are not in routine clinical use. Of these, perhaps the most frequently used are Chaddock’s sign (application of a stimulus in a circular direction around the external malleolus or the lateral aspect of the foot from heel to little toe) and Oppenheim’s sign (application of heavy pressure to the anterior surface of the tibia from patella to ankle). These may be helpful in ticklish patients who object to having their feet stroked. If the plantar response thus elicited is upgoing, this suggests a spread of the ‘receptive field’ of the reflex. Babinski’s sign is the earliest to occur in the presence of upper motor neurone pathology. It is often difficult to form a definite judgment on the plantar response and reproducibility is also questionable. A study of 24 experienced clinicians invited to examine plantar responses ‘blind’ found that the interobserver percentage agreement beyond chance was on average only 16. There remains a persistent belief, particularly amongst trainees, that an experienced neurologist can make the plantar response go which ever way s/he chooses. Cross Reference Dystonia Plexopathy Lesions confined to the brachial, lumbar, or sacral plexi may produce a constellation of motor and sensory signs (weakness, reflex diminution or loss, sensory loss) which cannot be ascribed to single or multiple roots (radiculopathy) or peripheral nerves (neuropathy). This may be likened to ‘echoes’ of the image, and eye movement may produce a trailing effect. Polyopia may occur as part of the visual aura of migraine and has also been associated with occipital and occipito-parietal lesions, bilateral or confined to the non-dominant hemisphere, and with drug abuse. It has also been described in disease of the retina and optic nerve and occasionally in normal individuals. The pathophysiology is unknown; suggestions include a defect of visual fixation or of visual integration; the latter may reflect pure occipital cortical dysfunction. Cross Reference Winging of the scapula Poriomania A name sometimes given to prolonged wandering as an epileptic automatism, or a fugue state of non-convulsive status epilepticus. Cross References Automatism; Seizures Porropsia Porropsia, or teliopsia, is a form of metamorphopsia characterized by the misperception of objects as farther away from the observer than they really are (cf. Postural and righting reflexes depend not only on the integration of labyrinthine, proprioceptive, exteroceptive, and visual stimuli, mostly in the brainstem but also involve the cerebral cortex. However, abnormalities in these reflexes are of relatively little diagnostic value except in infants. One exception is extrapyramidal disease (parkinsonism, Huntington’s disease, but not idiopathic dystonia) in which impairment or loss of postural reflexes may be observed. In the ‘pull test’ the examiner stands behind the patient, who 284 Presbyastasis P is standing comfortably, and pulls briskly on the shoulders; if balance is normal, the patient takes a step back; with impaired postural reflexes, this may provoke repetitive steps backwards (retropulsion, festination) or even en bloc falling, due to the failure of reflex muscle contraction necessary to maintain equilibrium. Pushing the patient forward may likewise provoke propulsion or festination, but this manoeuvre is less safe since the examiner will not be placed to catch the patient should they begin to topple over. Cross References Dystonia; Festinant gait, Festination; Parkinsonism; Proprioception; ‘Rocket sign’ Pourfour du Petit Syndrome Pourfour du Petit syndrome is characterized by mydriasis, widening of the palpebral fissure, exophthalmos, hyperhidrosis. Cross Reference Horner’s syndrome Pouting, Pout Reflex the pout reflex consists of a pouting movement of the lips elicited by lightly tapping orbicularis oris with a finger or tendon hammer, or by tapping a spatula placed over the lips. This myotactic stretch reflex is indicative of a bilateral upper motor neurone lesion, which may be due to cerebrovascular small vessel disease, motor neurone disease or multiple sclerosis. It differs from the snout reflex, which refers to the reflex elicited by constant pressure on the philtrum. Cross References Frontal release signs; Primitive reflexes Prayer Sign An inability to fully oppose the palmar surfaces of the digits with the hands held in the praying position, recognized causes of which include ulnar neuropathy (main en griffe), Dupuytren’s contracture, diabetic cheiroarthropathy, and camptodactyly. Vestibular rehabilitation therapy and avoidance of vestibular suppressant medications may be helpful. Presbycusis Presbycusis is a progressive sensorineural hearing loss, especially for high frequencies, developing with increasing age, which may reduce speech discrimination. It is thought to be due to age-related attrition of hair cells in the organ of Corti and/or spiral ganglion neurones. Cross Reference Age-related signs Presbyopia Presbyopia is progressive far-sightedness which is increasingly common with increasing age, thought to be due to an age-related impairment of accommodation.

References:

  • https://chemistry.osu.edu/sites/chemistry.osu.edu/files/CDC%27s%20Biosafety%20in%20Biomedical%20Labs%20Guidelines.pdf
  • https://accesstomedicinefoundation.org/media/uploads/downloads/5d25b3dd5f128_5cb9b00e8190a_Access-to-Medicine-Index-2018.pdf
  • http://phrma-docs.phrma.org/sites/default/files/pdf/biologics2013.pdf
  • https://dphhs.mt.gov/Portals/85/dsd/documents/DDP/MedicalDirector/UrinaryTractInfections.pdf
  • https://anatomy.med.utah.edu/diganat/SOM/unit_2/lec/Unit%2002%20Practice%20Lecture%20Exam.doc.pdf

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