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8 Cards in this Set
- Front
- Back
- 3rd side (hint)
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49♀, SOB, cough, chest pain, hilar lymphadenopathy,
1 DIAGNOSIS
1 BIOPSY?
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SARCOIDOSIS epithelioid histiocytes
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Pathologic findings associated with sarcoidosis:
Noncaseating granulomas with epithelioid histiocytes
Multinucleated giant cells of Langhans
Asteroid bodies
Schaumann bodies
The predominant cell type is the epithelioid macrophage (also known as histiocyte).
They are transformed macrophages and can, but not invariably, fuse to form a multinucleated giant cell.
pale pink cytoplasm and indistinct cell boundaries.
Schaumann bodies, or multinucleated giant cell features may be present, but are not required for the diagnosis of sarcoidosis granulomas.
This image shows a non-necrotizing granuloma consisting of epithelioid histiocytes admixed with lymphocytes. A prominent multinucleated giant cell is in the center. CD4 T-helper cells are in the center of the granuloma, which is surrounded by CD8 T-suppressor lymphocytes and B cells.
Aschoff bodies→acute rheumatic myocarditis
Calcifications in lymph node → silicosis, tuberculosis
Caseous necrosis → active TB
Fibroblast proliferation → Over time, fibroblasts proliferate (choice E) within the core of old, inactive granulomas, eradicating the histiocytes and stereotypical appearance and producing a dense collagenous scar. This feature is not required for the diagnosis of granulomas.
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25♂, chlronic relapsing hemolytic anemia, multiple treatments, SOB, wesk, smear → microcytic hypochromic cells electrophoresis → near complete absence of β globin chains, pitting edema in LE, rales, 1 DISEASE 2 ACUMULATION OF WHAT CAUSES Sx |
1 β thalassemia major 2 IRON → CHF |
heart is also damaged by the chronic high output state needed to compensate for the anemia. Patients with beta thalassemia major require repeated blood transfusions, which can cause hemosiderosis or acquired iron overload. Iron deposition in cardiac tissue can cause restrictive cardiomyopathy and result in congestive heart failure. severe hemolytic anemia characterized by failure to produce the beta chains of hemoglobin, resulting in unpaired alpha chains. near absence of beta chains on hemoglobin electrophoresis, as opposed to thalassemia minor, in which case electrophoresis would show some beta chains. The excess alpha chains are insoluble, leading to intra- and extravascular hemolysis. Eventually, further cardiac accumulation of iron and cellular damage can lead to dilated cardiomyopathy in these patients. heart is also damaged by the chronic high output state needed to compensate for the anemia. Calcium deposiotion in hyperparahyyroidism |
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27♂, warm, pleasant, happy, works, lives with parents, didnt complete high school, speaks in 3 word sentences ASSOCIATED A. Defect in chromosome 15 B. Deficits in early parental attachment C. Difficulty sleeping D. Maternal alcohol use E. Treatment with methylphenidate |
D. Maternal alcohol use |
Fetal alcohol syndrome is the most common known cause of intellectual disability (intellectual developmental disorder) formerly known as mental retardation. incorporates a range of physical, mental, behavioral, and cognitive effects developmental delays, global cognitive or intellectual defects and other CNS-related features. Chromosome 15 → autism (also ch. 11), Angelman intellectual disability is not linked to poor parenting or poor parental attachment Difficulty sleeping (choice C) is a common complaint for about 50% of all psychiatric disorders, ADHD is often managed with methylphenidate (choice E) as well as dextroamphetamine, pemoline, or atomoxetine. |
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43♀, 3m ↑weight, irregular menses, weakness, tingling sensation in hands feet, ↑↑↑urinary frequency, depressed, 170/100, n TSH, n free T, ↑cortisol secretion 1 DISEASE 2 K 3 Na |
u 2 ↓ 3 ↑ |
Primary adrenal hyperfunction causes increased secretion of cortisol, aldosterone, and adrenal androgens. Increased aldosterone can cause hypervolemia, hypokalemia, and hypernatremia. Increased cortisol can cause hypercalcemia, hypercalciuria, and hyperglycemia. W tej chorobie ±catecholamines After a few days (usually when patients gain ~3 kg in weight), the hypernatremia and hypervolemia are largely corrected during a phenomenon known as “aldosterone escape”. Aldosterone escape is believed to be mediated in part by hypervolemia-induced release of atrial natriuretic peptide (ANP) from the cardiac atria and decreased Na reabsorption by the proximal tubule. For reasons that are not completely understood, hypertension persists, along with mild hypervolemia. Typical symptoms of hypokalemic alkalosis include episodic weakness, paresthesias, transient paralysis, and tetany. Cushing → irregular menstrual preiods |
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4♂, ingests a toy, block will be forced through the GI tract during one of periodic sequential contractions that begin in the stomach and gradually migrate to ileum during fasting WHAT INTESTINAL HORMONE? |
motilin |
Motilin is released by the small intestine during the fasting state. Motilin causes migrating motor complexes (MMCs) to occur. MMCs begin in the stomach and will migrate to the ileum, where they stop. Cleansing function During passage of an MMC, the pyloric sphincter dilates and allows larger pieces of bone, plastic building blocks (for example), and other organic and inorganic detritus to be cleared from the stomach and eliminated in preparation for the next meal. Eating a meal interrupts MMC activity. CCK → I cells, intestinal phase of dig, It induces pancreatic enzyme secretion and bile release through contraction of the gallbladder and relaxation of the sphincter of Oddi. Gastrin → G cells, gastric phase, stimulates gastric acid production and tends to increase stomach motility, although the rate of emptying is decreased because gastrin also causes the pyloric sphincter to contract. increase in ileal and colonic motility as part of the gastroileal and gastrocolic reflexes, respectively. GRP gastrin releasing peptide → vagal nerve efferents that stimulates the G cells to secrete gastrin. Secretin → S cells, when duodenal pH↓4,5, Secretin stimulates bicarbonate production by the pancreas and tends to decrease the rate of stomach emptying. Somatostatin → D cells, inhibition of gastrin secretion that occurs when the pH of the gastric juice falls below 3. It also acts directly on the parietal cell to decrease acid secretion. |
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25♀, acetaminophen poisoning, ↑HR, RR 20, 1 WHAT DRUG 2 MECH OF ACTION OF THE DRUG |
1 N acetylcysteine NAC 2 replenished glutathione |
Acetylcysteine (N-acetylcysteine) is the antidote for acetaminophen overdose. Acetylcysteine is most effective if administered within 8 hours of acetaminophen ingestion. Acetylcysteine replenishes depleted hepatic stores of glutathione caused by acetaminophen metabolism. Management includes stabilization, decontamination (activated charcoal), and administration of N-acetylcysteine (NAC). Acetaminophen is extensively metabolized in the liver to form nontoxic sulfate and glucuronide conjugates (see figure below). A small proportion of the drug can be metabolized, however, by the cytochrome P450 mixed oxidase enzyme system to form a potentially toxic, intermediate metabolite (NAPQI), which, under normal circumstances, is conjugated with glutathione (a sulfydryl donor) to form nontoxic cysteine and mercapturic acid derivatives. In an overdose setting, the glucuronide and sulfate conjugation pathways often become saturated. A large proportion of the drug is then shunted into the P450 pathway, which results in the depletion of hepatic stores of glutathione and the subsequent binding of NAPQI to hepatic proteins, leading to centrilobular necrosis. Serious hepatotoxicity is uncommon if NAC is administered within 8 hours of overdose. Penicillamine → Wilson, poisoning with copper, lead, arsenic, and gold, and is used in the treatment of severe rheumatoid arthritis. Sodium thiosulfate → facilitates the rhodanese-catalyzed conversion of cyanide to less toxic thiocyanate (choice C). This agent is indicated for the treatment of cyanide overdose. Pralidoxime is an acetylcholinesterase reactivating agent (choice D) that is used in organophosphorus cholinesterase inhibitor poisoning. |
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hospital lenght of stay → mean= 7,6d, median=5 days, standard deviation=3.1d WHICH A. Binomial distribution B. Cannot tell from the information provided C. Negatively skewed distribution D. Normal distribution E. Positively skewed distribution F. t-statistic distribution |
E. POSITIVELY SKEWED DISTRIBUTION |
Positive skew: Mean > Median Negative skew: Median > Mean For skewed distributions, the median is better representation of central tendency than the mean there are two types of graphs the classical Gaussian or bell-shaped curve and skewed curves. The binomial distribution (choice A) yields a normal curve with the mean equal to the median. A t-statistic distribution (choice F) is derived from a statistical test and is not a descriptor of primary data, as in this case. Remember, a t-test compares the means of 2 groups from a single nominal variable, using means from an interval variable to see whether the groups are different. |
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Stent → has to return in 2 weeks for CDC cuz ↑ risk of neutropenia causwed by 1 DRUG 2 MECHANISM |
1 TICLOPIDINE Prevents adenosine diphosphate from binding to platelet receptors IRREVERSIBLY |
Ticlopidine is an oral platelet-aggregation inhibitor that is structurally related to clopidogrel It has a rare side effect of bone marrow toxicity (neutropenia/agranulocytosis) (2%) that limits its use. It works by inhibiting ADP from binding to platelet receptors. Subsequently, ADP-induced expression of glycoprotein receptors is reduced, resulting in less fibrinogen binding. Binds and potentiates antithrombin III → heparins inhibit the binding of fibrinogen (not fibrin) to glycoprotein IIb/IIIa receptors. → abciximab, eptifibatide, tirofiban Converts plasminogen to plasmin → alteplase Inhibits vitamin K-dependent carboxylation of clotting factors → vitamin K |
