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UWorld mixed > #6 3/14 > Flashcards

#6 3/14 Flashcards

1
Q

fever (in Celsius)? hyperpyrexia temp and cause? temp that causes neurological sequelae? what temp is incompatible w/ life?

A

fever = >38.3 C. hyperpyrexia = >40; severe infection, malignant hyperthermia, neuroleptic malignant syndrome, heat stroke. neurological seq = > 42 (mental status change, convulsions, delirium, coma). incompatible w/ life = >43

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2
Q

pathogenesis of fever

A

exogenous pyrogens (i.e. LPS) stimulate synthesis of endogenous pyrogens (IL-1, IL-6, TNF). enter brain and stimulate release of arachodonic acid (phospholipase A2) and synthesis of PGE2 –> increases hypothalamic set-point

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3
Q

age at which aspirin can be used w/o fear of reyes?

A

> 12 y/o

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4
Q

acetaminophen mechanism?

A

anti-pyretic of choice in kids, inhibit cyclooxygenase in CNS, reduce PGE2 synthesis. oral or rectally = equally effective

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5
Q

symptoms of hypoglycemia (2; early and late).

A
  1. EARLY: adrenergic symptoms (sweating, tremor, palpitations, hunger, nervousness) from epinephrine and norepinephrine release.
  2. LATE & LOWER LEVELS: behavioral changes, confusion, visual disturbances, stupor. seizures
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6
Q

why is there a sympathetic surge when hypoglycemic (3)?

A
  1. stimulate lipolysis in peripheral tissue 2. stimulate gluconeogenesis in live 3. decrease peripheral glucose consumption
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7
Q

what drugs can make symptoms of hypoglycemia? (and therefore, be avoided in diabetics)

A

non-selective B-blockers (propanolol, timolol, nadolol). inhibit epinephrine and norepinephrine-mediated compensation to hypoglycemia.

specifically, B2 blockade inhibits hepatic gluconeogenesis and peripheral glycogenolysis and lipolysis

(use B1 blocker if needed)

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8
Q

golden yellow / brownish cytoplasmic granules (2)? distinguish using?

A

either lipfuscin or hemosiderin; prussian blue stain (detects intracellular iron) differentiates.
black = hemosiderin

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9
Q

prussian blue histochemical rxn

A

colourless potassium ferrocyanide converted by iron into blue-black ferric ferrocyanide

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10
Q

hemosiderin-containing alveolar marcophages indicate?

A

“siderophages” or “heart-failure cells”, indicate episodes of pulmonary congestion and edema (increased pulmonary capillary hydrostatic pressure) associated w/ chronic left-sided heart failure occurred previously.

increased intravascular pressure –> extravasation of iron-containing proteins & erythrocytes, eaten by macrophages –> converted to hemosiderin

note: pressure must be elevated at capillary beds for this to happen, not proximal to capillaries

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11
Q

what can cause granulomas in the lung (7)

A

TB, fungal infxn, inhalation of foreign particles, beryllium lung disease, granulomatosis w/ polyangiitis (wegners), sarcoidosis, histiocytosis X

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12
Q

describe HIV pathophysiology once intracellular. describe how raltegravir is an effective antiretroviral.

A

2 RNA strands. reverse transcriptase synthesizes complementary DNA strand –> makes DS DNA, integrates into host chromosome. uses HOST RNA pol II to make mRNA and ultimately proteins.

w/o integration, can’t use host RNA pol II to make mRNA

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13
Q

(2) HIV fusion inhibitors

A
  1. enfuvirtide (fusion inhibitor, binds to gp41) 2. maraviroc ( CCR5 inhibitor)
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14
Q

HIV polypeptide cleavage inhibitors

A

protease inhibitors -navirs

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15
Q

cleaved portion of proinsulin polypeptide in golgi is…

A

packaged along w/ insulin in secretory granules & secreted in equimolar concentrations

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16
Q

first line treatment for enterobiasis (infxn w/ enterobius vermicularis)? rx: in pregnant women?

A

first-line: albendazole / mebendazole = first-line. pyrantel pamoate = preferred in pregnancy

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17
Q

diethylcarbamazine used for (2)

A
  1. Loa loa (loiasis) 2. wuchereria bancrofti (lymphatic filariasis)
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18
Q

ivermectin used for (2)

A
  1. strongyloides stercoralis 2. onchocerca volvulus
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19
Q

nifurtamox used for (1)

A

trypanosoma cruzi

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20
Q

praziquantel (3)

A
  1. schistosoma, 2. clonorchis sinensis, 3. paragonimus westermania
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21
Q

likelihood of plaque rupture depends on either (1) plaque stability or (2) plaque size?

A

(1) stability: mechanical strength of the overlying fibrous cap. balance of collagen synthesis and degradation. degradation –> chronic inflammation: macrophage secretion of metalloproteinases.

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22
Q

enzyme deficiency in Ehlers-Danlos syndrome? characterized by?

A

procollagen peptidase, cleaves terminal regions of procollagen molecule exocytosed by fibroblasts or SMC, transforming procollagen into insoluble tropocollagen. aggregate to form collagen fibrils

Ehlers-Danlos: disorganized collagen bundles, stretchable skin, hypermobile joints, short-stature

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23
Q

rule of thumb: if calcium levels are high, phosphate levels are…

A

low! and vice versa

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24
Q

PTHrP on phosphorous levels

A

low! PTHrP inhibits phosphorous reabsorption from proximal renal tubule

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25
Q

why does pregnancy increase the risk of DVT (5)?

A

increased clotting factors, decreased fibrinolysis, reduced levels of protein S, decreased venous tone, pressure of gravid uterus on IVC (predispose to venous stasis)

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26
Q

classic presentation of DVT (4)

A

unilateral leg pain, swelling, warmth. characteristic: tenderness of calf muscle on dorsiflexion of foot (Homan’ sign)

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27
Q

mainstay rx: for DVT in pregnancy?

A

heparin –> increased ATIII activity (coumadin is teratogenic!)

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28
Q

Conn’s syndrome. name 2 common causes. clinical presentation

A

primary hyperaldosteronism, 65% are aldosterone secreting adrenal adenomas. 30-40% idiopathic hyperaldosteronism, inclu primary adrenal hyperplasia.

hyperaldosteronism – HTN & hypokalemia & metabolic alkalosis

hypokalemia: muscle paresis
hypokalemic alkalosis: paresthesia

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29
Q

weight gain & easy bruising are symptoms of…

A

glucocorticoid excess (Cushing syndrome)

bruising: inhibited collagen and matrix glyocsaminoglycan synthesis (thin, weak skin)

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30
Q

excess hair growth & virilization can result from excess of..

A

androgens (adrenal cortex)

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31
Q

diarrhea and flushing can be seen w/

A

carcinoid syndrome, 5-HT secreting tumor derived from neuroendocrine cells of GI tract

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32
Q

relationship between gibbs free energy (deltaG0) and Keq

A

if deltaG0 is -, Keq is >1, conc of products will exceed substrates. if delta G0 is +, Keq is <1, formation of substrates is favored.

deltaG0 = -RTLnKeq

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33
Q

celiac disease

A

increased sensitivity to a group of dietary proteins in wheat, barely, and rye (collectively known as “gluten) .

celiac disease –> small intestine mucosa becomes inflamed and atrophic in response to gluten –> defective mucosal absorption of vitamins and nutrients.

poor fat absorption –> poor vitamin D absorption (rickets in kids, osteomalacia in adults)

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34
Q

vitamin D deficiency. effect on PTH. effect on Ca++ and PO4-

A

both calcium & phosphorous absorption impaired. low vit D & low Ca++ –> increase PTH, liberate Ca++ and PO4- from bone, but PTH also increases excretion of PO4-.

low Ca++, low PO4-

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35
Q

what can cause hypoparathyroidism? describe electrolyte abnormalities

A

severe hypomagnesium (i.e. diarrhea) –> hypoaparathyroidism. will see low Ca++, high PO4- [low Mg+]

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36
Q

chronic renal failure on Ca++ and PO4- levels

A

can’t make 1,25 dihydrox vit D. can’t absorb Ca++ and PO4- in GI tract, will stimulate PTH, which increases liberation from bones, but can’t trash phosphate (hyperphosphatemia) and normal-to-low Ca++

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37
Q

what is reactive arthritis? common findings?

A

seronegative spondyloarthropathyin 20-40 y/o patients following a primary infxn of urethritis or enteritis.

findings: synovitis (mainly of knees, ankles, feet), enthesitis (inflamm where tendon/ligament attaches to bone), conjunctivitis, mouth ulcerations, balantis circinata, keratoderma blennorrhagicum.

axial involvement in 20% of cases

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38
Q

reactive arthritis initiated by which pathogens (5)

A

urethritis: chlamydia trachomatic. enteritis: salmonella, shigella flexneri, campylobacter jejuni, yersinia.

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39
Q

triad of reactive arthritis? HLA-subtype association?

A
  1. non-gonnococcal urethritis 2. conjunctivitis (possibly w/ anterior uveitis 3. arthritis. associated w/ HLAB27.
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40
Q

what is keratoderma blennorrhagicum?

A

begins w/ vesicles on an erythematous base which become sterile pustules, followed by development of ketatotic scale.

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41
Q

esophageal dysmotility is a classic finding in…

A

scleroderma

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42
Q

ischemic events in the pons are associated w/ (6)

A

coma, bilateral paralysis, decerebrate rigidity, pinpoint pupils, often death

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43
Q

lesion of internal capsule causes…

A

motor defecit

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44
Q

pure sensory stroke on entire contralateral body

A

VPL and VPM of thalamus

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45
Q

chronic uncontrolled HTN or DM causes what brain lesion? what would autopsy findings be?

A

occlusion of small penetrating arteries feeding basal ganglia, posterior limb of internal capsule, pons, and cerebellum. leaves small 5mm cavities.

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46
Q

what are the primary causes of lacunar infarcts?

A

lipohyalinosis and microatheromas.

lipohyalinosis –> destructive vessel lesion characterized by loss of normal arterial architecture, mural foam cells, and in acute cases, fibrinoid vessel wall necrosis.

microatheromas – accumulation of lipid-laden macrophages within intimal layer.

chronic HTN and DM

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47
Q

what do the superficial inguinal lymph nodes drain? where are these nodes?

A

all cutaneous lymph from umbilicus to feet, including external genitalia and anus (up to the beginning of the rectum, the dentate line). lies in a region bounded by inguinal ligament, sartorius muscle, and adductor longus. overlie femoral nerve, artery, and vein.

EXCLUDES posterior calf – drains to popliteal lymph nodes.

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48
Q

prokaryotic DNA replication: what does DNA pol III do? DNA pol I? on lagging strand

A

DNA pol III, makes initial DNA segments on lagging strain. DNA pol I, removes RNA primers and replaces w/ DNA.

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49
Q

non-painful ulcerative sexually transmitted diseases (3)

A

(1) granuloma inguinale [donovanosis; klebsiella inguinale]. (2) syphillis [treponema pallidium] (3) lymphogranuloma venereum [chlamydia trachomatis]

50
Q

painful ulcerative sexually transmitted diseases (2)

A

(1) chancroid [haemophilius ducreyi] (2) genital herpes [herpes simplex virus 1 & 2]

51
Q

describe lesion w/ haemophilus ducreyi. painful? exudate? number?

A

STD. chancroid: PAINFUL (do cry!) lesion. multiple, deep. base = gray to yellow exudate. organisms clump in long parallel “school of fish” strands

52
Q

describe lesion w/ HSV1 and 2. painful? histology?

A

STD. genital herpes. painful. multiple, small ulcers. shallow w/ erythematous base. multinucleated giant cells w/ intranuclear cowdry type A inclusions.

53
Q

describe lesion w/ klebsiella inguinale. painful? histology?

A

STD. granuloma inguinale (donovanosis). NOT PAINFUL. extensive and progressive, base = granulation tissue. deeply staining gram neg intracytoplasmic cysts (donovan bodies) = DIAGNOSTIC. untreated = can result in lymphedema = elephantiasis.

vs. chlamydia lymphogranuloma venerum; inguinale less commonly has lymphadenopathy.

54
Q

describe lesion w/ treponema pallidum.

A

STD. syphilis, single, indurated, well-circumscribed ulcer. clean base. thin, delicate, corkscrew shaped organisms on darkfield microscopy. NOT PAINFUL

55
Q

describe lesion w/ chlamydia trachomatis

A

STD. lymphogranuloma venerum. NOT PAINFUL. small, shallow ulcer. intracytoplasmic hlamydial inclusion bodies present in epithelial cells & leukocytes. heals rapidly.

56
Q

chlaymdia serotypes.

A 
A-C = ocular infxn, trachoma, in children.
D-K = urogenital (sexually-transmitted) and inclusion conjunctivitis
L1-L3 = lymphogranuloma venereum.
57
Q

describe lymphogranuloma venereum. rx? what happens if untreated?

A

painless ulcer –> painful lymphadenopathy

painless ulcer on genital w/ chlamydia infected cells. weeks later –> swollen, painful inguinal nodes that coalesce, ulcerate, and rupture (buboes). develop into stellate abscesses.

doxycycline. untreated – fibrosis, lymphatic obstruction, anogenital stricture/fistula.

58
Q

how does UV light damage DNA? how do prokaryotes fix this? eukaryotes?

A

pyrimidine-pyrimidine dimers. thymine dimers –> covalent bond. inhibits proper transcription and replication. eukaryotes: UV-specific endonucleases detect abnormalities, nicks damaged site. DNA pol excises (5’-3’ exonuclease) and synthesizes new DNA.

59
Q

xeroderma pigmentosum enzyme deficiency?

A

lack of UV-specific endonuclease to repair thymidine dimers.

60
Q

how does ionizing radiation (X-ray and gamma-ray) damage DNA? how is it repaired?

A

double-stranded breaks. joined together by nonhomolgous or homologous re-ligation.

61
Q

deamination of bases. what do they become. how it is repaired?

A
  • cytosine –> uracil (spontaneous).
  • adenine and guanine –>hypoxanthine and xanthine, respectively. base excision repair. removed by specific glycosylases w/o disruption of phosphodiester backbone. apurinic/apyridimidinic sites cleaved by nucleases. gap filled w/ DNA pol & ligases.
62
Q

mismatch repair in DNA replication

A

adenine methylation in template strand, absence of methylation in newly synthesized strand.

63
Q

when do protons dissociate from amino acids

A

when pH exceeds pKa. (when pH below pKa, will be protenated)

64
Q

embryonic kidney development: fate of pronephros, mesonephros, and metanephros

A

derived from nephrogenic cord (develops from urogenital ridge formed by intermediate mesoderm).

  • pronephros: regresses
  • mesonephros: persist in male as wolffian duct (ductus deferens and epididymis). females –> regress and becomes vestigal gartner’s ducts.
  • metanephros –> true kidney
65
Q

describe development of true kidney from metanephros (ureteric bud/metanephric diverticulum and metanephric mesoderm/blastema)

A

formation of metanephric diverticulum (ureteric bud), which penetrates sacral intermediate mesoderm to induce formation of metanephric mesoderm (metanephric blastema).

  • ureteric bud –> collecting system of kidney (collecting tubule, ducts, major/minor calyces, renal pelvis, ureters.
  • metanephric blastema -> glomeruli, bowman’s space, proximal tubules, loop of Henle, DCT.
66
Q

enzyme specific to mast cell (marker of mast cell activation & anaphylactic reaction)

A

tryptase (i.e. anaphylaxis to cephalosporin)

67
Q

screen for carcinoid tumors

A

5-hydroxyindoleacetic acid, breakdown product of serotonin.

68
Q

cystic fibrosis; inheritance, mutation gene and chromosome.

A

autosomal recessive. mutations in cystic fibrosis transmembrane conductance regulator (CFTR) gene, chr 7. deltaF508 mutation (deletion of three nucleotides coding for phenylalanine at position 508 of CFTR protein is most commonly implicated.

69
Q

describe fxn of CFTR. fxn in airway, bowel, exocrine pancreas, sweat.

A

ATP-binding cassette transmembrane ion transporter, pumps Cl- out of epithelial cells against concentration gradient. water follows. hydrates mucosal surfaces (airway and bowel). also hydrates and promotes secrertion from ducts of exocrine pancreas. also, formation of hypotonic sweat (eccrine gland, initially isotonic w/ plasma. salt removed by CFTR.

70
Q

what organs are affected in cystic fibrosis patients?

A

airways, bowel, exocrine pancreas, eccrine sweat glands.

71
Q

osteitis fibrosa cystica

A

increased bone turnover and resorptive bone lesions in hyperparathyroidism

72
Q

renal osteodystrophy pathogenesis (ESRD)

A

low vitamin D (1-25 dihydroxycholecalciferol vit D, calcitriol). low intestinal absorption of Ca++.

ESRD also associated w/ PO4-retention, binds Ca++, exacerbates hypocalcemia.

both hypocalcemia + hyperphosphatemia –> increase PTH, increased bone resorption –> osteitis fibrosa cystica

73
Q

ESRD uremia on thyroid fxn?

A

decreased peripheral conversion of T4 to T3 (functional hypothyroidism)

74
Q

drug-induced lupus

A

classically test: hydralazine, isoniazid, procanimide, phenotyoin.

QCHIMPP-
quinidine, chlorpromazine, hydralazine, isoniazide, methyldopa, phenytoin, procainamide

75
Q

hydralazine and procainimide metabolism. effect on drug-induced lupus

A

phase II N-acetylation in liver. acetylator phenotype determined via genetic predisposition. most patients will develop anti-histone antibodies; not all symptomatic. only discontinue is symptomatic.

76
Q

name a drug excreted w/o metabolism

A

very few: the diuretic chlorothiazide

77
Q

drugs metabolized via liver sulfate conjugation (2)

A

phenol and chloramphenicol

78
Q

drug metabolized via liver hydroxylation (2)

A

pentobarbitol and phenobarbitol

79
Q

drug metabolized by liver hydrolysis (3)

A

usu preceeds phase II metabolism, involves esterase or amidase. procaine, lidocaine, and aspirin

80
Q

drug metabolized by plasma hydrolysis (3)

A

plasma esterase cleave ester linkages to biotransform or inactivate rapidly. short-acting profile of many agents. many are anesthesia: succinylcoline, tetracaine, remifentanil.

81
Q

which drugs inhibit dihydrofolate reductase (reduction of folic acid to tetrahydrofolate) [3]

A

trimethoprim, methotrexate, pyrimethamine.

pyrimethamine – antimalarial & toxoplasmosis (parasitic dihydrofolate)

82
Q

how does sulfamethoxazole work?

A

structural analogue of PABA (para-aminobenzoic acid). competes with PABA to inhibit dihydrofolic acid synthesis (intermediate step in formation of THF)

83
Q

metronidazole mechanism

A

binds to DNA, unravel and breaths.

84
Q

why imipenem + cilastatin

A

cilastatin prevents renal metabolism of imipenem by inhibiting dehydropeptidase on renal tubule brush border.

85
Q

describe extrathyroidal manifestations of grave’s disease (2)

A
  • infiltrative opthalmopathy: edema and infiltration of lymphocytes into extraocular muscles and CT. stimulates retro-orbital fibroblasts, which are then stimulated by Th1 cells –> produce excessive glycosaminoglycans.
    clinically: eyes pop out, red and tender. diplopia.
  • pretibial myxedema

rx: glucocorticoids. (antithyroid drugs do not have a direct effect on this)

86
Q

describe iodide organification

A

inorganic iodide oxidized into iodine via thyroid peroxidase. iodine + tyrosine residue on thyroglobulin.

87
Q

rx for symptoms of hyperthyroidism prior to definitive therapy

A

beta blockers: i.e. propanol

88
Q

which GLUT transporter is responsive to insulin? which tissue is it expressed in?

A

only GLUT-4; predominately expressed in muscle cells and adipocytes

89
Q

GLUT-1 (cellular distribution & distinctive feature)

A

RBCs and CNS; basal glucose transport

90
Q

GLUT-2 (cellular distribution & distinctive feature)

A

hepatocytes, pancreatic beta-cells; regulation of insulin release

91
Q

GLUT-3 (cellular distribution & distinctive feature)

A

placenta, brain, kidney

92
Q

GLUT-4 (cellular distribution & distinctive feature)

A

muscle cells & adipocytes; INSULIN MEDIATED

93
Q

GLUT-5 (cellular distribution & distinctive feature)

A

spermatocytes & GI tract (fructose transport)

94
Q

warfarin metabolism. 4 major drugs that can decrease warfarin’s activity.

A

elimination -> almost entirely by hepatic metabolism by cytochrome P-450. inducers (i.e. rifampin, phenobarb, phenytoin) and cholestyramine (which binds warfarin).

95
Q

4 impt drug interaction w/ warfarin. why?

A
  • amiodarone-> inhibits warfarin metabolism, both given for atrial fibrilation
  • cimitidine, metronidazole and bactrim (TMP-SMX)-> also inhibit warfarin metabolism
96
Q

majority of Down syndrome cases caused by…

A

meiotic non-disjunction prior to conception (failure of chromosomes to separate during first meiotic division of ovum. chances increase w/ maternal age.

96
Q

majority of Down syndrome cases caused by…

A

meiotic non-disjunction prior to conception (failure of chromosomes to separate during first meiotic division of ovum. chances increase w/ maternal age.

97
Q

process whereby same genetic abnormality causes different disorders when inherited from the mother of the father? 2 classic examples?

A

imprinting –> selective inactivation of maternal or paternal alleles. prader-willi and angelman syndromes

97
Q

inherited down’s syndrome caused by..?

A

robertsonian translocation. break near the centromeres of two chromosomes, w/ transfer of genetic material between the chromosomes. 3-4% of cases. usu inherited from mother. common translocations t(14,41) and t(21,22)

97
Q

process whereby same genetic abnormality causes different disorders when inherited from the mother of the father? 2 classic examples?

A

imprinting –> selective inactivation of maternal or paternal alleles. prader-willi and angelman syndromes

98
Q

inherited down’s syndrome caused by..?

A

robertsonian translocation. break near the centromeres of two chromosomes, w/ transfer of genetic material between the chromosomes. 3-4% of cases. usu inherited from mother. common translocations t(14,21) and t(21,22)

99
Q

inherited diseases caused by loss of part of chromosome (Deletion) [3]

A
  • cri-du-chat syndrome (5p deletion)
  • diGeorge syndrome (22q11 microdeletion)
  • prader-willi (15q deletion)
99
Q

inherited diseases caused by loss of part of chromosome (Deletion) [3]

A
  • cri-du-chat syndrome (5p deletion)
  • diGeorge syndrome (22q11 microdeletion)
  • prader-willi (15q deletion)
100
Q

pulmonary infarcts are almost always..

A

hemorrhagic (dual blood supply from pulmonary and bronchial arteries)

100
Q

pulmonary infarcts are almost always..

A

hemorrhagic (dual blood supply from pulmonary and bronchial arteries)

101
Q

most common cause of tricuspid endocarditis in IV drug users? 2nd most?

A

1st: s. aureus
2nd: p. aeruginosa
can have multiple emboli w/ fever

101
Q

most common cause of tricuspid endocarditis in IV drug users? 2nd most?

A

1st: s. aureus
2nd: p. aeruginosa
can have multiple emboli w/ fever

102
Q

gestational choriocarcinoma is often preceeded by [4]

A
  • most common: evacuated hydatidiform mole
  • abortion
  • normal pregnancy
  • ectopic pregnancy
102
Q

gestational choriocarcinoma is often preceeded by [4]

A
  • most common: evacuated hydatidiform mole
  • abortion
  • normal pregnancy
  • ectopic pregnancy
103
Q

histology of gestational choriocarcinoma vs. hydatidiform mole

A

choriocarcinoma: proliferation of cytotrophoblast and syncitiotrophoblast. no villi.
vs. hydatidiform mole: cystic swelling of chorionic VILLI and proliferation of chorionic epithelium (only trophoblast)

103
Q

histology of gestational choriocarcinoma vs. hydatidiform mole

A

choriocarcinoma: proliferation of cytotrophoblast and syncitiotrophoblast. no villi.
vs. hydatidiform mole: cystic swelling of chorionic VILLI and proliferation of chorionic epithelium (only trophoblast)

104
Q

manifestations of measles

A

4 C’s
-cough, coryza (runny nose), conjunctivitis, and Koplik spots.

maculopapular rash.

rare complication: subacute scerlosing encephalitis. strain that lacks M protein antigen. neurological deficits. fatal. high titer of Ab in serum and CSF. oligoclonal bands. NO ANTIBODIES TO M-COMPONENT.

105
Q

vitamin C deficiency

A

scurvy: impaired CT strength. often manifests as fragile capillary walls –> easy bruising and propensity to bleed. gum disease. children: bony deformities and subperiosteal hemorrhages = characterestic.

106
Q

thiamine B1

A

coenzyme in decarboxylation rxn. necessary for conversion of pyruvate to acetyl-CoA and of alpha-ketoglutarate to succinyl coA in citric acid cycle. deficiency = dry beri beri: peripheral neuropathy. wet: high output cardiac failure

107
Q

vit B6 (pyridoxine)

A

cofactor in many rxn that involve amino acids (transamination, decarboxylation, deamination). deficiency: seborrheic dermatitis, glossitis, peripheral neuropathy.

108
Q

vitamin B12

A

synthesis of methionine and synthesis of succinyl coA from methylmanonyl coA. deficiency: megaloblastic anemia and subacute combined degeneration of spinal cord.

109
Q

2 possibilities w/ lymphadenopathy

A

reactive hyperplasia (inflammatory changes within lymph node) or malignant transformation.

110
Q

types of reactive hyperplasia of lymph nodes? how does malignant transformation look?

A

refers to all benign, reversible, enlargement of the lymphoid tissue secondary to an antigenic stimulus. multiple genetically distinct cells undergo limited monoclonal expansion–> POLYCLONAL (prolif of many diff cell types). pleomorphism, increased mitoses, and nuclear changes are commonly seen.

follicular hyperplasia, sinus hyperplasia (fill w/ histiocytes), or diffuse hyperplasia.

malignant transformation: effacement/distortion of normal architecture. MONOCLONAL. (unchecked prolif of single genetically unique cell)

111
Q

when lymphoma is suspected…

A

evaluate for monoclonality of lymphocyte population. PCR for rearrangement of T-cell receptor genes. if a single allele for V predominates –> monoclonal prolif suspected. same for B cell. NOTE: admixture of several lymphoid types may be seen in Hodgkin (reed-sternberg cells attract non-malignant cells to lymph nodes)

112
Q

differentiate ARDS from pulmonary edema

A

ARDS – normal pulmonary capillary pressure

113
Q

2 signs of increased PTH activity

A
  1. increased urinary cAMP (indicate PTH fxn in PCT)

2. increased hydroxyproline (indicate PTH fxn on bone)

122
Q

psuedohyperparathyroidism

A

autosomal dominant end-organ resistance to PTH. mental retardation, short 4th and 5th metacarpals. knuckle-knuckle-dimple-dimple

UWorld mixed (60 decks)

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