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The disorder is associated with alcoholism cheap 30 mg nimotop with visa muscle relaxer kick in, electrolyte disturbances cheap 30 mg nimotop visa spasms 14 year old beagle, malignant disease, and malnutrition, and it relates particularly to the rapid correction of hyponatremia. A 78-year-old woman is transported to the emergency department after being “found down” by a fami- ly member. Upon arrival at the emergency department, the patient is pulseless and apneic. A “code 10” is called, and advanced cardiac life support is initiated. Chest compressions are performed, and the patient is intubated and oxygenated with 100% fraction of inspired oxygen (FIO2). Pharmacologic therapy with epinephrine and atropine is administered. After the second round of epinephrine and atropine, the patient regains a pulse. She is transferred to the medical inten- sive care unit for further care. You are concerned about the possibility of anoxic-ischemic encephalopa- thy secondary to circulatory arrest. Which of the following statements regarding anoxic-ischemic encephalopathy is accurate? In the mature nervous system, white matter is generally more vulnera- ble to ischemia than gray matter 20 BOARD REVIEW B. In the mature nervous system, the brain stem is more vulnerable to ischemia than the cerebral cortex C. The persistent vegetative state is characterized by the return of the sleep-wake cycle, but wakefulness is without awareness D. Brain death is defined as the loss of all cerebral activity for at least 48 hours Key Concept/Objective: To understand the characteristics of the persistent vegetative state and the definition of brain death The persistent vegetative state is characterized by the return of sleep-wake cycles and of various reflex activities, but wakefulness is without awareness. Recent studies have indi- cated that the minimally conscious state, which is characterized by inconsistent but clear- ly discernible behavior of consciousness, can be distinguished from coma and a vegetative state by the presence of behavioral conditions not found in either of those two conditions; this distinction is important because outcome appears to be different in minimally con- scious patients. Brain death is defined as the loss of all cerebral activity, including activity of the cerebral cortex and brain stem, for at least 6 hours if confirmed by electroen- cephalographic evidence of electrocerebral inactivity or for 24 hours without a confirma- tory electroencephalogram. A 68-year-old woman with a history of alcohol abuse and dependence presents to the primary care clin- ic for evaluation of confusion. The patient is accompanied by her daughter, who is concerned about her mother’s forgetfulness and who feels that her mother has been “making things up. On the basis of the physical exami- nation and a history of confabulation, you make the diagnosis of Wernicke encephalopathy. A deficiency of which of the following is responsible for this condition? Thiamine (vitamin B1) Key Concept/Objective: To understand that thiamine (vitamin B1) deficiency is responsible for Wernicke encephalopathy Thiamine (vitamin B1) deficiency is responsible for the hallmark features of Wernicke encephalopathy. These features include ophthalmoplegia, gait ataxia, and fluctuating con- fusional states. Pathologic changes occur in characteristic regions of the brain stem, espe- cially in the mamillary bodies and thalamus. Diffusion-weighted magnetic resonance imaging may show signal changes in these characteristic midline locations. As with Wernicke encephalopathy, Korsakoff encephalopathy is attributed to thiamine deficiency, though the precise pathophysiology is unknown. Selective disturbance of memory is the predominant clinical abnormality in Korsakoff encephalopathy. Thiamine replacement therapy rarely leads to improvement. There is marked impairment of recent memory and difficulty in incorporating new memories, though immediate recall is intact. Patients are unaware of any deficit and often confabulate. The disorder is common in chronic alcoholics, often occurring in association with Wernicke encephalopathy. The pathologic changes are similar in distribution to those in Wernicke encephalopathy.

It can also interconvert weak and potent estrogens such as estrone and estradiol generic nimotop 30 mg overnight delivery muscle relaxant robaxin. Testosterone in turn can be produced from androstene- dione generic 30 mg nimotop amex muscle relaxant tablets. To date, seven types of human 17ß-HSDs have been cloned, sequenced, and characterized, designated active within the sebaceous gland and in keratinocytes types 1–7 in the chronological order of their isolation [20– derived from the infrainfundibular region of piloseba- 23]. Recently, the type 8 17ß-HSD also known as Ke6 ceous follicle (from the base of the epidermis to the point gene was shown to efficiently transform estradiol to estro- of insertion of the sebaceous duct) [3, 29]. The type 2 iso- gen in transfected HEK-293 cells. The type 2 isozyme zyme is most active in the prostate gland where it can be of 17ß-HSD appears to be the most active within the seba- inhibited by drugs such as finasteride. While the type 1 ceous gland where it prefers to oxidize testosterone back 5·-reductase has a broad alkaline pH optima of 6. In this regard, the 17ß-HSD and demonstrates relatively moderate affinity for steroid enzyme may play a protective role in the skin by metabo- substrates (Km = 1–5 ÌM), the type 2 5·-reductase has a lizing testosterone back to the less potent precursor, narrow acidic pH optimum of 5. It may also represent a regulatory point high affinity for substrates (Km = 4–50 nM) [30, 31] in androgen and estrogen metabolism within the skin. Activity of 5·-reductase and 17ß-HSD exhibits region- Dihydrotestosterone is produced from testosterone al differences depending upon the source of the sebaceous within peripheral tissues such as the skin by the action of glands [25, 29] (fig. In skin that is prone to acne, such the 5·-reductase enzyme. Recently, two isozymes of 5·- as facial skin, activity of the type 1 5·-reductase in seba- reductase have been identified. The type 1 isozyme is ceous glands is greater than in sebaceous glands obtained Update and Future of Hormonal Therapy Dermatology 2003;206:57–67 59 in Acne from nonacne-prone skin. Enzymes involved in lipogenesis in human sebaceous being produced in sebaceous glands from facial skin com- glands pared to other areas of the body that are not prone to Enzymes involved in Enzymes involved in develop acne. In contrast, the oxidative activity of the cholesterol synthesis fatty acid synthesis type 2 17ß-HSD enzyme is greater in sebaceous glands from nonacne-prone areas compared to sebaceous glands Acetoacetyl CoA thiolase Acetyl CoA carboxylase obtained from facial skin. Since the predominant activity HMG CoA synthetase Fatty acid synthetase HMG CoA reductase of this isozyme is to transform testosterone back to its less Mevalonic acid kinase active precursor, it may be inferred that facial skin is less Mevalonate decarboxylase able to metabolize testosterone to its less potent precur- Isopentenyl pyrophosphate isomerase sor. The net effect of the activity of these two enzymes is Geranyl transferase the greater production of potent androgens such as T and Squalene synthetase Squalene oxidocyclase DHT within sebaceous glands of facial areas that may in part account for the development of acne in these areas. Site of Androgen Action in Acne The sebaceous gland is known to be a site of androgen regulating the production of growth factors by dermal action within the pilosebaceous unit. The stromal/epithelial interaction of sex ste- hypothesized that androgens may play a role in follicular roid hormones and growth factors is an important phe- hyperkeratinization in acne in addition to their effects on nomenon in the local regulation of other endocrine- stimulating sebum secretion [1, 2]. Indirect evidence in responsive tissues such as the prostate, breast, endometri- support of this hypothesis includes the finding of andro- um and ovary. Evidence exists for the importance of these gen receptors in the outer root sheath of sebaceous folli- autocrine and paracrine effects of androgens and growth cles, the clinical observation that antiandrogens may factors in the regulation of sebaceous glands. In addition reduce follicular casts and the finding of activity of andro- to androgen receptors, sebocytes also possess receptors for gen-metabolizing enzymes such as 3ß-HSD, 17ß-HSD growth factors such as epidermal growth factor (EGF) and and 5·-reductase in follicles. Furthermore, the activity of insulin-like growth factor I (IGF-I). Evidence exists 17ß-HSD and 5·-reductase is significantly greater in for the role of EGF, IGF-I and keratinocyte growth factor infrainfundibular keratinocytes compared to keratino- (KGF) in modulating sebaceous gland growth. For exam- cytes obtained from the interfollicular epidermis, suggest- ple, growth of sebocytes is enhanced by supplementation ing that follicular keratinocytes have a greater propensity of cell culture medium with EGF and insulin. Direct evidence in sup- of experimental animals with KGF stimulates growth of port of the effects of androgens on follicular keratiniza- hair and sebaceous glands [34, 35]. Mechanism of Androgen Action in Acne Several important enzymes involved in lipid metabo- Androgens are thought to stimulate the growth and dif- lism have been identified in sebaceous glands. These ferentiation (sebum production) of sebaceous glands. The include 3-hydroxy-3-methylglutaryl-coenzyme A (HMG- exact mechanism by which this is accomplished has not CoA) reductase which is the rate-limiting enzyme in the been defined. Androgens such as testosterone and DHT synthesis of cholesterol and acetyl CoA carboxylase which form complexes with nuclear androgen receptors.

This patient is likely to have a large deficit in total body potassium purchase 30mg nimotop muscle relaxant vecuronium, and with hydration and insulin treatment order 30 mg nimotop muscle relaxant vitamin, his serum potassium level will decrease. Failure to adequately replace potassium can have severe consequences in patients with DKA, and potassium should be started immediately unless urine output is compromised or hyperkalemia exists. Administration of bicarbonate is not generally required in most cases of DKA and is generally reserved for treatment of severe acidosis (pH < 7. Studies have indicated that the use of bicarbonate does not affect the course of most cases of DKA, and there is some theoretical rationale for not using bicar- bonate unless clearly necessary. A 49-year-old man was referred from a walk-in clinic when he was discovered to have a blood glucose level of 246 mg/dl during evaluation of an acute GI syndrome. Subsequently, a diagnosis of diabetes was confirmed by a finding of fasting blood glucose values of 190 mg/dl and 176 mg/dl, measured when the patient was not ill. He has not received medical treatment or been evaluated for many years but reports being in generally good health. Perform 24-hour urine collection, obtain an estimate of his creati- nine clearance, and measure total protein excretion B. Measure the albumin-creatinine ratio on a spot urine sample C. Defer specific assessment because he has just been diagnosed, and diabetic nephropathy is unlikely to have developed D. Measure serum BUN and creatinine concentrations E. Perform renal ultrasound Key Concept/Objective: To know that urinary albumin excretion is the most sensitive means of detecting early diabetic nephropathy An abnormally high rate of albumin excretion is the earliest manifestation of diabetic nephropathy, and microalbuminuria can be detected well before changes in creatinine clearance and pathologic proteinuria occur. Microalbuminuria is predictive of the pro- gression of renal disease in most cases, and its occurrence marks the point in the course of nephropathy at which treatment is most efficacious. Therefore, all patients who are diagnosed with diabetes should undergo screening for renal albumin excretion. For patients with type 1 diabetes, formal evaluation can be deferred for several years because the time of disease onset is generally clear, and abnormalities in renal function do not occur during the first 5 years after onset. Patients with type 2 diabetes should be screened at the time of diagnosis because the time of onset of type 2 diabetes is often hard to discern, and asymptomatic hyperglycemia may have been present for several years. Screening for microalbuminuria can be done with a 24-hour urine collection, an overnight collection, a 4-hour timed collection, or a spot collection with determination of albumin-creatinine ratio. All these measures require a specific assay for albumin because standard clinical laboratory measurements of urinary protein are not sensitive enough to detect microalbuminuria. Diabetic nephropathy is usually quite advanced before changes in the BUN and serum creatinine levels occur. Although one of the ear- liest renal manifestations of diabetes is transient kidney enlargement, renal ultrasound is not useful for screening for diabetic nephropathy. A 52-year-old woman presents to the emergency department after experiencing 4 days of worsening men- tal status. Physical examination shows a somnolent, obese woman with dry mucous membranes. Results of laboratory studies are as follows: sodium concentration, 128 mEq/L; potassium concentration, 4. Which of the following would be the most appropriate intervention in the care of this patient? Demeclocycline Key Concept/Objective: To be able to recognize hyperglycemic hyponatremia Hyperglycemia lowers the plasma sodium concentration; in the absence of insulin, glu- cose is an effective osmole that attracts water from cells and thereby dilutes extracellu- lar sodium. Therefore, the blood glucose level should always be examined when a low plasma sodium concentration is being evaluated. The plasma sodium concentration falls by approximately 3 mEq for every 200 mg/dl (10 mmol) increase in blood glucose and will increase by this amount when hyperglycemia is corrected with insulin. To eval- uate hyponatremia in the presence of hyperglycemia, the serum sodium concentration must be "corrected" for the osmotic effect of glucose. In this patient, the corrected sodi- um concentration is within normal limits, and the sodium value will normalize once the high glucose level is treated.

LMWH is more effective than standard low-dose heparin in general surgical patients 30 mg nimotop fast delivery spasms coughing, patients undergoing elective hip surgery buy discount nimotop 30 mg on line spasms after hysterectomy, and patients with stroke or spinal injury. For those undergoing genitourinary, neurologic, or ocular surgery, intermittent pneumatic compression, with or without graduated compression stockings, is effective prophylaxis against venous thrombosis and does not increase the risk of bleed- ing. An 80-year-old patient of yours is scheduled to undergo total knee replacement. He is in excellent health, and except for osteoarthritis, his medical history is not significant. The orthopedic surgeon asks you for advice regarding VTE prophylaxis. LMWH is contraindicated because of the risk of bleeding; intermittent pneumatic compression devices would be preferable ❏ B. Intermittent pneumatic compression devices are contraindicated because of the location of the surgery; LMWH is preferable ❏ C. LMWH and intermittent pneumatic compression devices are equally effective in preventing VTE after knee surgery ❏ E. The risk of VTE after knee replacement is so low as to make prophylax- is unnecessary Key Concept/Objective: To know the prophylaxis for DVT after knee-replacement surgery LMWH and intermittent pneumatic compression devices have been shown to be equally effective in preventing DVT after knee-replacement surgery. Aspirin has been shown to decrease the risk of DVT after hip fracture, but its efficacy relative to LMWH or intermit- tent pneumatic compression devices has never been studied, and the standard of care for postoperative DVT prophylaxis in North America does not call for its use. After knee- replacement surgery, the risk of postoperative DVT is 10% to 20%, and the rate of fatal pul- monary embolism is 1% to 5%, so prophylaxis is indicated. A 28-year-old woman who is 18 weeks pregnant and is G1P0 is referred to you by her obstetrician for advice regarding management of a possible VTE diathesis. Although she has no personal history of VTE, she reports that her mother and a cousin both had blood clots during pregnancy; she does not know whether they were tested for clotting disorders. She is feeling well, and her physical examination is remarkable only for her pregnancy. Which of the following actions would you take for this patient? Educate her about the symptoms of VTE and advise her to seek care immediately if she notes one of them; otherwise, no further testing or treatment is necessary ❏ B. Start warfarin therapy with a target INR of 2 to 3 ❏ C. Test for antithrombin-III deficiency; if she has the deficiency, start LMWH therapy Key Concept/Objective: To understand the management of inherited thrombophilias in pregnancy It is possible that this woman has an inherited thrombophilia. Pregnant women with antithrombin-III deficiency have an especially high rate of VTE. If this patient tests posi- tive, she should receive prophylactic anticoagulation therapy throughout the rest of her pregnancy. The benefits of prophylactic anticoagulation in pregnant women with protein C or protein S deficiency outweigh the risks only if they have a history of VTE. Because this patient has never had VTE, the results of testing her for these disorders would not lead to a change in management. In pregnant women with factor V Leiden mutation or G20210A prothrombin mutation, no anticoagulation therapy is recommended unless they develop a clot during the current pregnancy. In any case, LMWH is preferable to warfarin therapy because of the teratogenic effects of warfarin. Aspirin does not provide effective anticoagulation therapy for VTE. Although this woman should be educated about the signs and symptoms of VTE, this alone is not sufficient. A 56-year-old white man presents to you in clinic complaining of increasing shortness of breath. His symptom began several months ago and has gotten progressively worse over time. On further review of systems, he reports chronic sinusitis, some fatigue, and a new nonpainful, nonpruritic rash on his lower extremities. His medical history is significant only for hypertension. On physical examination, you note nasal ulcerations and a mildly erythematous, papular rash with occa- sional nodules on his lower extremities. His pulmonary examination is notable for fine, bilateral crack- les.