Flashcards in test #9 3.23 Deck (153)
which antidepressant is good for (1) depression w/ psychomotor retardation or hypersomnia (2) depression w/ smoking cessation desire (3) w/o sexual dysfxn
buproprion (NDRI and nAch-agonist). has stimulatory effects.
which antidepressant is good for patients w/ insomnia. side effect?
trazodone (highly sedating antidepressant, but can cause priapism & other sexual side effects. SARI -- 5-HT antagonist and reuptake inhibitor.
SSRI-induced sexual dysfxn in what %age? what 3 types?
50%. decreased libido, anorgasmia, and increased latency to ejaculation.
electrolyte abnormalities w/ hyperaldosteronism
hypokalemia, metabolic alkalosis. normal Na+ bc of aldosterone escape
describe aldosterone escape
hypernatremia is not seen w/ hyperaldosteronism. increased Na+ reabsorption --> intravascular hypervolemia --> promote ANP release --> diuresis --> compensatory Na+ loss.
presentation of primary mineralcorticoid excess
HTN, hypokalemia, suppressed renin, non-suppressible aldosterone
normal serum Na+, hypokalemia, metabolic acidosis suggests..
renal tubular acidosis
renal tubular acidosis types (1, 2, and 4)
1: distal: failure of H+ secretion by alpha-intercalated cells (hypokalemia) 2: proximal: failed HCO3- reabsorption in PCT 4: adrenal: aldosterone deficiency or resistance
renal tubular acidosis explanation
inability to acidify urine
how do CAG repeats in huntingtin gene lead to disease
code for abnormal huntingtin protein that decreases expression of OTHER genes by inhibiting transcription (hypermethylation of histone fragments). SILENCE of other neurotrophic genes
mutation of homeodomain gene would lead to..
alteration in body structure // spontaneous abortion
is macrocephaly a typical feature of common chromosomal syndromes
cleft palate, polydactylyl, rocker-bottom feet associated w/
trisomy 13 (patau syndrome)
down's syndrome have increased risk of..
AML-M7 and ALL in childhood. Alzheimer's in adulthood
common presentation of trisomy 21 (5)
mental retardation, facial dysmorphism, single palmar crease, endocardial cushion defects, duodenal atresia
select those w/ disease & w/o disease. then look back to look at exposure. calculate odds ratio
controls in a case-control experiment
individuals w/o disease (w/ and w/o exposure). goal: exposure frequency among non-disease general population
carcinoid heart disease (associated w/ carcinoid syndrome)
fibrous intimal thickening w/ endocardial plaques limited to the RIGHT heart (bc both 5-HT and bradykinin in blood are inactivated distally by pulmonary vascular endothelial monoamine oxidase). can result in pulmonic stenosis and restrictive cardiomyopathy.
carcinoid syndrome symptoms. results from?
skin flushing, abdominal cramping, nausea, vomiting, diarrhea. results from production of serotonin, kallikrein, bradykinin, histamine, prostaglandins and/or tachykinins produced by carcinoid tumor.
degree of endocardial fibrosis seen in carcinoid heart disease correlates w/..
plasma levels of serotonin and urinary excretion of 5-HIAA (5-hydroxyindoleacetic acid)
elevated plasma levels of homocysteine associated w/..
arterial and venous thrombosis. also atheroscerlosis
common way to injur PCL
lateral vs. medial meniscus
lateral -- rounder and covers a larger portion of the articular surface
lateral vs. medial articular surface of knee size
medial articular surface is larger, as it bears more body weight
characterized by neurological symptoms (nonepileptic seizures, blindness, loss of sensation, weakness, paralysis) that are anatomically or physiologically inconsistent w/ neurologic disease but are NOT FEIGNED.
2 most important mechanisms involved in the development of complications w/ diabetes
(1) advanced glycosylation end products (2) polyol pathway impairment
describe how advanced glycosylation end products --> diabetic complications (microangiopathy, neuropathy, atheroscerlosis)
attach glucose to amino acids (reversible --> irreversible), accumulate & cross-link w/ collagen in blood vessel walls & interstitial tissue (MICROANGIOPATHY and NEUROPATHY). cross-linking also facilitates inflammatory cell invasion & deposition of LDL in vascular walls --> ATHEROSCLEROSIS
describe how polyol pathway impairment --> diabetic complications (cataracts & peripheral neuropathy)
in tissues that do not depend on insulin for glucose transport (lens, peripheral nerves, blood vessels, kidney). glucose --> sorbitol (via aldose reductase). sorbitol --> fructose. both sorbitol & fructose increase osmotic pressure in tissue --> osmotic cellular injury. increased water in lens fiber cells --> rupture of cells --> opacification of lens and CATARACT formation. osmotic injury of Schwann cells --> PERIPHERAL NEUROPATHY
which main tissues do not rely on insulin for glucose transport
lens, peripheral nerves, blood vessels, and kidney