GOGETA
Trying to get in PGY1
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for 1 is E
for 2 is C
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| Miradautas Vras
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looks like
for 1 it's C both of them do it.
for 2 it's D . Serum acids are not increased in hyperosmolar coma so A and B are gone.C doesn't look that specific to me.
E Supply is replenished by normal or half normal saline, not free water. And Heavy doses of insulin look out of place [ it's 5-10 u bolus followed by infusion] plus it can ppt hypoglycemia when given without iv glucose which is not mentioned.
D It's hyperosmolar coma so sodium is certainly elevated.]
correct me if i am wrong
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| hanialkhadher
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1-D
2-C
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| numita
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whats the answer prespara
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| peraspera
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#1. The answer is A.
Androgens increase libido, but their exact role in erectile dysfunction remains unclear. Individuals with castrate levels of testosterone can still achieve erections from visual or sexual stimuli.
 (I did not know it, but now WE KNOW!!)
Increased prolactin levels decrease libido by suppressing gonadotropins-releasing hormone (GnRH), which indirectly leads to a decreased serum testosterone level. Patients with diabetes mellitus have reduced amounts of nitric oxide synthase in both endothelial and neural tissues. Psychogenic erectile dysfunction is caused by a psychogenic stimulus to the sacral cord which inhibits reflexogenic responses. In addition, excess sympathetic stimulation may cause increased penile smooth muscle tone. Among the antihypertensive agents, the thiazide diuretics and beta blockers have been implicated most frequently.Calcium channel blockers and angiotensin-converting enzymes are less frequently sited.Alpha blockers are less likely to be associated with erectile dysfunction.
#2 the answer is C.
Diabetic, hyperosmolar, nonketotic coma is a medical emergency that usually occurs as a complication of maturity-onset diabetes. Typically,
affected persons are elderly (often living alone or in a nursing home), have a history ofrecent stroke or infection, and are unable to drink sufficient water to balance urinary fluid losses. These factors combine to cause sustained hyperglycemic diuresis with profound volume depletion and decreased urine output. Presenting features often include signs of circulatory compromise as well as central nervous system manifestations rangi ng from confusion or seizures to coma. Ketoacidosis is absent, perhaps because the concentration of portal-vein insulin is high enough to prevent full activation of hepatic ketogenesis.
Serum levels of free fatty acids are generally lower than in diabetic ketoacidosis, and although hypertonicity is marked, measured serum sodium concentration is kept from being significantly elevated by the profound hyperglycemia.
Infections are common, and disseminated intravascular coagulation can occur as a result of elevated plasma viscosity (both bleeding and in situ thrombosis have been reported). Although the administration of
free water eventually becomes necessary, the treatment of salt deficits has the highest initial therapeutic priority. Several liters of isotonic saline should be given over the first 2 h, followed by half-normal saline and then a 5% glucose solution when blood glucose levels
approach normal. Hypotonic fluids should not be used initially because most of the water enters the intracellular compartment, possibly leading to cerebral edema, rather than remaining in the plasma and interstitial spaces, where it is needed to support the circulation.
Insulin also is required, but usually in lower doses than in patients with diabetic ketoacidosis.
Edited by peraspera on 10/10/07 - 07:45 AM
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| aaroho
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1-E
2-E
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