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UWorld mixed > test #12 3.31 > Flashcards

test #12 3.31 Flashcards

1
Q

epithelium of ovary

A

simple cuboidal. also known as germinal epithelium. transitions to peritoneum at broad ligament of uterus

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2
Q

epithelium of fallopian tube

A

simple columnar: ciliated cells, help transport egg/embryo. peg cells: secrete nutrients

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3
Q

epithelium of uterus

A

simple (psuedostratified) columnar. contains tubular glands. divided into fxnal and basal layers

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4
Q

epithlium of cervix

A

endo: simple columnar. ecto: stratified squamous. contains cervical glands.

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5
Q

epithelium of vagina

A

stratified squamous. non keratinized. contains glycogen

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6
Q

acute hemolytic transfusion reaction

A

chills, shortness of breath, fever, hypotension, DIC, renal failure, hemoglobinuria. think: blood transfusion after MVA: ABO incompatibility: type II hypersensitivity Ab mediated –> activate COMPLEMENT

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7
Q

TNF-alpha released in response to..

A

bacterial endotoxin– SHOCK

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8
Q

kartagener inheritence and presentation

A

autosomal recessive: immotile cilia (microtubular defect): male infertility, recurrent sinusitis, bronchiectasis. situs inversus.

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9
Q

activation of trypsinogen to trypsin

A

trypsinogen secreted by pancreas –> enterokinase in duodenal lumen –> trypsin

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10
Q

2 protective mechanisms to limit amount of trypsinogen that becomes prematurely activated in pancreas

A

(1) SPINK1: serine peptidase inhibitor Kazal type I: secreted by pancreatic acinar cells: fxns as trypsin inhibitor. (2) trypsin cleaves other trypsin molecules (its own inhibitor)

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11
Q

hereditary pancreatitis

A

rare disorder: mutations in trypsinogen or SPINK1 genes. most common mutation: trypsinogen that is not susceptible to inactivating cleavage by trypsin.

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12
Q

helicobacter pylori is commonly associated w/

A

(1) peptic ulcer disease (2) gastric adenocarcinoma

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13
Q

treatment of choice for gestational diabetes?

A

INSULIN. diet and activity modifications alone are efficacious too.

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14
Q

why are oral hypoglycemic mediations avoided in gestational diabetes?

A

risk of fetal insulinemia and hypoglycemia

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15
Q

most effective motion sickness prevention meds work on…

A

(1) antimuscarinics or (2) antihistamines w/ antimuscarinic action

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16
Q

pathophysiology of motion sickness? rx?

A

muscarinic M1 and histaminic H1 pathways stimulated –> nausea and vomiting. first-generation antihistaminic drugs (meclizine and dimenhydrinate) scopolamine –> only anti muscarinic, also effective

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17
Q

H1 receptor blockers fxn by?

A

increasing proportion of inactive H1 receptors: REVERSE BLOCKADE utimate decreases the activity of H1 receptor

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18
Q

patients w/ amino acids in urine may have…

A

disorders of amino acid resoprtion: fanconi or hartnup

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19
Q

adult vs. infant botulism

A

ADULT botulism: consumed preformed TOXIN.

INFANT: consume c. botulinum SPORE

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20
Q

which cells directly mediate the vascular response to endothelial and intimal injury (leading to intimal hyperplasia // fibrosis)

A

reactive smooth muscle cells! injured endothelial cells secrete factors, (PDGF, FGF, endothelin-1) –> promote SMC migration, proliferation from media to intima & produce new connective tissue. macrophages help.

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21
Q

von Hippel-Lindau

A

rare, autosomal dominant condition characterized by (1) presence of capillary hemangioblastomas in retina/cerebellum, (2) congenital cysts/neoplasms in kidney, liver, pancreas. increased risk for (3) renal cell carcinoma (can be bilateral)

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22
Q

von Reckinghausen’s disease

A

NF1 (chromosome 12, 12 letters) inherited PERIPHERAL nervous system tumor. neurofibromas, optic nerve gliomas, lisch nodules (pigmented nodules of iris), cafe-au-lait (hyperpigmented cutaneous macules)

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23
Q

NF2

A

autosomal dominant nervous system tumor. bilateral cranial n VIII schwannomas & mult meningiomas

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24
Q

Sturge Weber (encephalotrigeminal angiomatosis)

A

rare congenital neurocutaneous disorder: cutaneous facial angiomas (port-wine stain) and leptomeningieal angiomas. skin: usu V1 or V2. mental retardation, seizures, hemiplegia, skull radiopacities: tram-track calcifications

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25
Q

tuberous sclerosis

A

cortical and subependymal HAMARTOMAS. cutaneous angiofibromas (adenoma sebaceum), visceral cysts (i.e. kidney, liver, pancreatic), renal angiomyolipoma and cardiac rhabdomyoma. SZ. other hamartomas too.

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26
Q

osler-weber-rendu

A

hereditary hemorrhagic telangiectasia. autosomal DOMINANT. rupture –> epistaxis, GI bleed, hematuria. cysts not common

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27
Q

two common scenarios where antibiotics are prescribed but not needed

A

(1) VIRAL URI (2) acute otitis media (which resolves spontaneously often)

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28
Q

cutaneous lateral aspect of leg? medial aspect of leg

A

lateral: common peroneal (L4-S2). medial: femoral (L2-L4)

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29
Q

formula for number needed to treat

A

1/ARR. ARR (event rate in placebo - event rate in treatment)

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30
Q

rare disease assumption

A

approximate odds ratio and relative risk when studying rare diseases

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31
Q

how does mannitol reduce cerebral edema but increase pulmonary edema?

A

retain plasma // tubular fluid osmolality – extract water from interstitial space into vascular space // tubular lumen. brain: redistribute of water from tissue into plasma. but this causes increase hydrostatic pressure in vasculature –> can cause pulmonary edema

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32
Q

mechanism of morphine

A

mu opiod g-protein coupled receptor –> one pathway: (1) increased K+ conductance (efflux) –> hyperpolarize and decrease pain transmission. ALSO, inhibit adenylyl cyclase, (2) inhibit Ca2++ conductance (less NTX release

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33
Q

silent GERD presentation

A

no heartburn; dysphagia, nocturnal cough, sore throat

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34
Q

histological findings in GERD (3)

A

basal zone hyperplasia, elongation of laina propria papillae, inflammatory cells (eosinophils, neutrophils, lymphocytes)

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35
Q

pill-induced esophagitis seen w/ (3)

A

(1) tetracyclines (2) KCl (3) bisphosphonates

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36
Q

most common cause of infectious esophagitis

A

candida albicans. herpes simplex is other.

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37
Q

achalasia

A

(1) impaired relaxation of LES (2) impaired peristalasis of esophagus

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38
Q

absent esophageal peristaltic movt in (2)

A

achalasia and scleroderma

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39
Q

posterior & anterior urethra

A

posterior: prostatic segment & membranous segment (above bulb of penis.
anterior: bulbous segment & penile segment (within bulb and remainder of corpus spongiosum)

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40
Q

which part of urethra is most susceptible to damage from trauma?

A

membranous segment of posterior urethra. unsupported & weak.

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41
Q

falling on crossbar of bicycle or top of a fence, ‘straddle injury’ in male?

A

crushing injury to bulbous urethral segment

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42
Q

cuneate vs. lingual gyrus of striate cortex

A

cuneate – superior lobe, inferior visual field. lingual – inferior lobe, superior visual field.

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43
Q

Wallenberg syndrome

A

contralateral loss of pain and temp. ipsilateral loss of CN V, VIII, IX, X, XI, and horner’s syndrome

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44
Q

rightward shift of venous return curve

A

increased MAP

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45
Q

acute and chronic arteriovenous fistula

A

acute: decreased TPR (increased cardiac output, increased venous return). overtime: sympathetics and kidney compensates for fistula by increased CO, vascular tone, and circulating blood volume. this results in increased cardiac function curve, and increased mean systemic pressure (rightward shift of venous return curve)

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46
Q

acute GI bleed (on venous return curve)

A

decreased MAP: leftward shift

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47
Q

phenylephrine on cardiac output / venous return curve

A

increased sympathetic tone (vasoconstriction) decrease both CO and venous return

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48
Q

MI on cardiac output / venous return curve

A

isolated decrease in CO, no change in blood volume / venous return

49
Q

anaphylaxis on cardiac output / venous return curve

A

widespread venous / arteriolar dilation. increased capillary permeability – 3rd spacing on fliud. DROP in venous return

50
Q

GH stimulates linear growth of long bones via..

A

IGF-1 secreted from LIVER

51
Q

Laron dwarfism

A

decreased linear growth due to defective growth hormone receptors –> serum levels of growth hormone high w/ low levels of circulating IGF-1

52
Q

mechanism underlying hypoxic pulmonary vasoconstrictoin

A

direct hypoxemia-induced increase in smooth muscle cytosolic Ca2++, w/ Ca2++ sensitization factor

53
Q

when does hypoxemia cause arteriolar dilation in cerebral circulation

A

PaO2 < 50mmHg

54
Q

length constant // space constant

A

how far along an axon an electrical impulse can propagate. specifically: distance at which originating potential decreases to 37% of its original amplitude. decreased w/ demyelination.

55
Q

time constant

A

time it takes for a change in membrane potential to achieve 63% of the new value. related to membrane capacitance. myelination DECREASES membrane capacitance (decreases time constant). low time constant, quicker change in membrane potential, increase axonal conduction speed.

56
Q

PRPP synthetase

A

enzyme responsible for synthesis of activated ribose, which is needed for de novo purine/pyrimidine synthesis. increased purine production –> hyperuricemia –>

57
Q

glucose-6-phosphatase deficiency

A

von Gierke disease

58
Q

acid maltase deficiency

A

Pompe disease

59
Q

negatively birefringent crystal under polarized light

A

monosodium urate crystals: gout

60
Q

cell responsible for intense inflammatory response in acute gout?

A

neutropils – phagocytose monosodium urate crystals.

61
Q

colchicine

A

acute management of gouty arthritis: reduce inflammatory response by interfering w/ adhesion molecules and microtubules (neutrophil chemotaxis) and decreasing tyrosine phosphorylation in response to monosodium urate crystals (decreased neutrophil activation)

62
Q

starvation for 16-24 hours causes..

A

peripheral tissue shift to rely on lipid-derived fuels (free fatty acis & ketones) instead of glucose for energy.

63
Q

beta oxidation

A

within mitochondria of the liver. yields significantly more energy per carbon atom than carbohydrate.

64
Q

each round of fatty acid beta-oxidation produces

A

1 NADH, 1 FADH2, 1 acetyl-CoA. acetyl-CoA –> TCA cycle: 3 NADH, 1 FADH, 1 GTP. rapid beta-oxidation overwhelms TCA, shunt to ketone production.

65
Q

failure to produce ketone bodies when fasting suggests

A

impaired beta oxidation. most commonly due to defects in first enzyme in pathway: acyl-CoA dehydrogenase

66
Q

acetyl-CoA carboxylase

A

first step in fatty acid synthesis.

67
Q

glycogen phosphorylase

A

mediates glycogenolysis. removes single glucose residues form alpha-1,4-linkages within glycogen molecules.

68
Q

deficiency in muscle glycogen phosphorylase

A

muscle cramping and fatigue w/ exercise, McArdle’s glycogen storage disease type V

69
Q

intracellular breakdown of glycogen

A

most: by cytosolic phosphorylase. some by lysosomal enzyme alpha-1,4-glucosidase (acid maltase).

70
Q

pompe disease (glycogen storage disease II

A

deficiency of alpha-1,4-glucosidase (lyososmal enzyme) glycogen accumulation in lyososmes. cardiomegaly, hypotonia, occasional hypoglycemia, early demise

71
Q

most common predisposing factor to native valve bacterial endocarditis

A

mitral valve prolapse: platelet and fibrin deposition spontaneously occur, causing nonbacterial thrombotic endocarditis. then, colonized by microorganisms. rheumatic valvular disease is a potential, but less common cause of NVBE

72
Q

degenerative mitral annual calcification

A

can result in mitral regurg due to loss of sphincteric action of annulus. can predispose to bacterial endocarditis. most common in females over 60 with prior history of myxomatous degeneration of valve and in pts w/ chronically elevated left ventricular pressure

73
Q

when in gestation does differentiation and development of external genitalia occur

A

8-15 wks.

74
Q

fate of urogenital folds in female vs. male

A

female: urogenital folds do NOT fuse; labia minora. male: urogenital folds fuse to form ventral aspect of penis and penile raphe.

75
Q

genital tubercle goes on to become what in female vs. male?

A

clitoris or penis

76
Q

bifid scrotum occurs when..

A

malunion of labioscrotal folds.

77
Q

de Quervain’s thyroiditis also known as..

A

subacute granulomatous thyroiditis. mixed cellular infiltrate w/ occasional multinucleate giant cells.

78
Q

thyrotoxicosis in subacute granulomatous thyroiditis caused by..

A

released of STORED thyroid hormones secondary to inflammation. NOT excess production (iodine uptake is decreased). followed by hypothyroid state for few months

79
Q

recent viral illness, increased ESR, markedly reduced radioactive iodine intake, thyrotoxicosis, tender thyroid

A

de Quervain (subacute granulomatous thyroiditis)

80
Q

ground-glass nucleus w/ intranuclear grooving (orphan annie eyes)

A

papillary thyroid cancer

81
Q

chronic lymphocytic thyroiditis

A

hashimoto’s thyroiditis: formation of germinal centers – diffuse mononuclear infiltration. normal ESR, nontender thyroid, high antithyroid peroxidase (anti-TPO antibody)

82
Q

anti-TPO

A

hashimoto’s thyroiditis

83
Q

phenytoin, carbamazepine, and valproic acid…

A

inhibit neuronal high-frequency firing by reducing ability of voltage-gated Na+ channels from recovering from inactivation.

84
Q

differential media vs. selective media

A

differential: differeniate organsims based on metabolic / biochemical properties. selective: kills all else

85
Q

thayer-martin VCN

A

Neisseria specific. vancomycin kills gram positives. colistin kills gram negs other than neisseria. nystatin kills fungi.

86
Q

side effect of opiods

A

BILIARY COLIC. contraction of smooth muscles in sphincter of Oddi –> increased pressure in bile duct & gallbladder.

87
Q

intestinal malrotation

A

cecum found in right upper quadrant, fixed w/ fibrous bands (Ladd’s bands) to second aspect of duodenum. entire midgut fixed to SMA. INTESTINAL obstruction –> due to adhesive bands compressing duodenum –> bilious vomiting. can have midgut volvulus – twisting of gut around SMA, decreasing perfusion –> intestinal gangrene and performation

88
Q

normal rotation in GI development

A

6th wk: midgut herniates through umbilical ring. returns at 10th wk, completing 270 degree counterclockwise rotation around SMA. allows for proper placement and fixation of intestine in abdominal cavity.

89
Q

pancreatic divisum

A

failure of ventral and dorsal pancreatic buds to fuse during 8th wk of embryonic life. incidental.

90
Q

omphalomesenteric duct. failure to obliterate?

A

connects lumen of midgut to yolk sac. failure to obliterate –> vitelline fistula (connection between ileum and outside body at umbilicus. partial failure –> Meckel diverticulum

91
Q

hindgut descent

A

along IMA after midgut returns to abdominal cavity.

92
Q

two main manifestations of intestinal malrotation

A

(1) intestinal obstruction – compression via adhesive bands (2) midgut volvulus – intestinal ischemia due to twisting around blood vessels

93
Q

pili

A

hair-like protein polymers projecting from surface of cell. involved in attachment of organism to mucosal surfaces. HIGH antigenic variation (developing vaccine against gonococcal pilus –> challenging)

94
Q

calcineurin

A

protein phosphatase –> dephosphorylates NFAT (nuclear factor of activated T cells), allows it to enter nucleus and bind to IL-2 promoter (stimulate growth & differentiation of T cells)

95
Q

inhibition of calceneurin (2)

A

cyclosporin and tacrolimus

96
Q

low back pain & morning stiffness in young man suggest…

A

ankylosing spondylitis (chronic inflammatory condition). most commonly affects: sacroiliac and apophyseal joints of spine. progressive exacerbation / remission. mild-moderate disease w/o permanent disability.

97
Q

HLA-B27

A

seronegative spondyloarthropathies PAIR: psoriasis, ankylosing spondylitis, inflammatory bowel disease, reiter syndrome. NO rheumatoid factor

98
Q

ankylosing spondylitis involves which 4 systems. in what way?

A

(1) musculoskeletal: peripheral enthesitis: calcaneus, tibial tuberosity, patella, trochanters, distal ulna most common. (2) pulmonary involvement due to enthesopathy of costovertebral & costosternal junctions –> hypoventilation. TEST CHEST EXPANSION. (3) cardiovascular: ascending aortitis –> dilatation of aortic ring and aortic insufficiency. (4) eye: anterior uveitis – blurred vision, photophobia, conjunctival erythema

99
Q

most common benign vascular tumor

A

cherry hemangioma / angioma. small, bright-red, papular lesion. appear in 3rd-4th decade of life. do not regress spontaneously & number increases w/ age –> ‘senile hemangiomas’. always cutaneous, not on mucosa / deep tissue. histologically: sharply circumscribed areas of congested capillaries and post-capillary venules in papillary dermis.

100
Q

strawberry (infantile/capillary) hemangioma

A

appear during first weeks of life. intially grow rapidly, then frequently regress by 5-8 years. bright red when near epidermis, violaceous when deeper.

101
Q

spider angiomas

A

bright red central papule surrounded by several outwardly radiating vesselse that blanch w/ pressure & refill centrifugally on release. dilitation of central arteriole & superficial capillary network. ESTROGEN dependent

102
Q

cavernous hemangiomas

A

dilated vascular spaces w/ thin-walled endothelial cells. present as soft BLUE, compressible mass (few cm in size). appear on skin, mucosa, deep tissue, viscera. when on skin – usu based in dermis. less likely to regress spontaneously. when in brain & viscera, associated w/ VHL

103
Q

cystic hygroma

A

lymphatic cysts, lined by thin endothelium. present at birth, most commonly on neck / lateral chest wall. neonates w/ turner / down syndrome

104
Q

differential cyanosis (cyanosis in lower extremity, not in upper)

A

reduced arterial oxygen in aorta distal to left subclavian. patent PDA which transforms into right-to-left shunt due to pulmonary HTN. note: eisenmenger & tetrology of fallot would cause cyanosis in upper & lower equally

105
Q

fantasy vs. denial defense mechanism

A

fantasy: substituting imaginary scenarios. denial: behaving as if an aspect of reality doesn’t exist (refusing to acknowledge)

106
Q

defense mechanism

A

means of protecting oneself from painful awareness of feelings

107
Q

what antiseizure med causes generalized lymphadenopathy?

A

phenytoin. also causes undesirable cosmetic effects (hirsutism, coarsening of facial features, acneiform skin rash, gingival hypertrophy)

108
Q

most feared complication of carbamazepine

A

agranulocytosis

109
Q

complication from valproic acid

A

severe hepatoxicity

110
Q

features of type II pompe’s disease

A

deficiency of lysosomal alpha-glucosidase: NORMAL blood sugar level, severe cardiomegaly, GLYCOGEN ACCUM in LYSOSOMES, normal glycogen structure, hepatomegaly, macroglossia, hypotonia. mental retardation

111
Q

feature of type V mcArdle’s disease

A

deficiency of glycogen phosphorylase deficiency: weakness and fatigue w/ exercise, little/no rise in blood lactate w/ exercise, high levels of glycogen in muscles

112
Q

features of type I von Gierke’s disease

A

deficiency on glucose-6-phosphatase in liver: hepatomegaly, fasting hypoglycemia, lactic acidosis, hyperuricemia and hyperlipidemia, increased glycogen storage but normal strxr

113
Q

releasing glucose from glycogen

A

cytosolic glycogen phosphorylase shorts glycogen chains by cleaving alpha 1,4 glycosidic linkages. until 4 residues left before branching point. branching enzyme (1) transferase cleaves outer three residues and transfers to non-releasing end of other strand. (2) alpha 1,6 glucosidase releases free glucose. glycogen phosphorylase makes glucose-1-phosphate. converted to glucose-6-phosphate by phosphoglucomutase. in liver, glucose-6-phosphotase converts to glucose. small amounts of glycogen broken down by lysosomal enzyme alpha-1,4-glucosidase (acid maltase). deficiency –> pompe disease.

114
Q

debranching enzyme deficiency

A

Cori or Forbes disease. childhood hepatomegaly, growth retardation, hypoglycemia, hyperlipidemia. muscle weakness.

115
Q

galactokinase deficiency

A

normally: catalyzes phosphorylation of galactose in presence of ATP. cataracts is predominant manifestation of deficiency.

116
Q

pyruvate kinase deficiency

A

chronic hemolytic anemia, splenomegaly, poor exercise inolerance

117
Q

clinical manifestation of left vs. right side colorectal carcinoma

A

left: infiltrate intestinal wall, encircle lumen: symptoms of partial intestinal obstruction –> change in stool caliber, constipation, cramping abdominal pain, abdominal distension, nausea. vomiting.
right: exophytic mass. usu not obstructive bc larger caliber lumen, usu iron deficiency anemia (fatigue, pallor) due to ongoing blood loss. nonspecifc symptoms of anorexia, malaise, weight loss.

118
Q

tenesmus & thin stool suggest

A

space occupying lesion of rectum, i.e. rectal adenocarcinoma.

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