test #11 3.28 Flashcards Preview

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Flashcards in test #11 3.28 Deck (140)
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1
Q

compare distal and proximal radial n. lesion (i.e. motor & sensory involvement)

A

proximal lesion (i.e. midshaft of humerus) will injure radian n. & posterior cutaneous branch (which comes off above spiral groove). distal lesion near radial head / lateral epicondyle will not impair arm sensation, ONLY wrist extension (deep branch). no sensory defects

2
Q

lateral and medial branches of median n innervates

A

sensory innervatino of palmar & dorsral surfaces of distal 3 1/2 digits

3
Q

when an adult attempts to pull a child upward by the arm…

A

radial head subluxation “nurse-maid elbow”, can damage the deep branch of the radial n (paralysis of forearm extensor w/o affecting any sensory)

4
Q

boundaries of guyon’s canal? what n. passes through here?

A

between hook of hamate and pisiform bone (fibroosseus tunnel)

5
Q

fracture of the surgical neck of the humerus damages.. what will be lost (3)

A

axillary n. paralyzed (1) deltoid (2) teres minor (2) sensation on lateral upper arm

6
Q

immune response to Tb..

A

macrophage phagocytosis & antigen presentation –> CD4+ T cell stimulate macrophages –> activated macrophages form Langerhans giant cells (multiple nuclei organized peripherally in the shape of a horseshoe)

7
Q

what cell type is primary responsible for Giant cell formation?

A

CD4+ Th1 cells –> IFN-gamma

8
Q

Th2 cells activate..

A

mast cells, basophils, eosinophils

9
Q

heavy smoker w/ exertional dyspnea and airspace enlargement on CT likely has…

A

centriacinar emphysema

10
Q

descirbe pathophhysiology of centriacinar emphysema

A

oxidative injury to respiratory bronchioles –> activation & recruitment of resident macrophages –> neutrophil release of elastase, proteinase 3, cathepsin G, matrix metalloproteases, proteases, oxygen free-radicals (inhibit a1-antityrpsin). net protease-antiprotease & oxidant-antioxidant imbalance destroy’s acinar walls.

11
Q

clara cells histologically are.. located.. secrete..

A

non-ciliated, secretory constituents of terminal respiratory epithelium. secrete clara cell secretory protein (CCSP), which inhibits neutrophil recruitment and activation, as well as neutrophil-dependent mucin production.

12
Q

what 3 things can reduce pulmonary compliance?

A

(1) pulmonary fibrosis (2) insufficient surfactant (3) pulmonary edema

13
Q

coenzymes needed for pyruvate dehydrogenase

A

thiamine pyrophosphate (TPP), lipoic acid, CoA, FAD, NAD (mnemonic: tender love and care for nancy)

14
Q

lipoic acid needed for.. (2)

A

needed for the (1) decarboxylation of alpha ketoacids and (2) transfer of alkyl groups

15
Q

PDH is needed to.. absence leads to..

A

converte pyruvate acid to acetyl-CoA in the TCA cycle. w/o PDH or its 5 coenzymes, pyruvate –> lactic acid (lactate dehydrogenase)

16
Q

lipoic acid is an important coenzyme for..

A

alpha ketoglutarate dehydrogenase and branched-chain ketoacid dehydrogenase

17
Q

citrullinemia

A

urea cycle disorder that results from deficiency of arginosuccinate synthetase. ATP is cofactor required.

18
Q

homocysteinuria

A

deficiency in cystathione synthase. characterized by premature atherosclerosis. disposed by 2 pathways: (1) conversion to cysteine by the combined actions of two vitamin B6-requiring enzymes, cystathione synthase and cystathionase and (2) conversion to methionine by a folate & vitamin B12-dependent process.

19
Q

orotic aciduria

A

results from a defective pyrimidine synthesis resulting from a deficiency of the enzyme orotate phosphoribosyl transferase (requires glutathione as a coenzyme)

20
Q

lipoic acid is a cofactor for which mitochondrial enzymes

A

(1) PDH (deficiency –> lactic acidosis) (2) alpha-ketoglutarate DH (3) branched-chain ketoacid DH (deficiency results in maple syrup urine disease)

21
Q

karyotype difference between complete vs. partial moles

A

complete mole: 46XX or XY (of paternal origin).

partial mole: 69XXX or XXY.

22
Q

evacuated uterine contents of complete vs. partial mole

A

complete: trophoblasts only, “bunch of grapes”.
partial: fetus, cord, amniotic membrane, some grossly enlarged villi

23
Q

microscopic appearance of complete vs. partial mole

A

complete: enlarged edematous villi and trophoblastic proliferation. no fetal tissue.
partial: some enlarged villi w/ trophoblastic proliferation. normal villi and fetal tissue also present.

24
Q

risk of complications w/ complete vs. partial mole

A

complete: 15-20% risk of malignant trophoblastic disease.
partial: low risk of malignancy (>5%)

25
Q

clinical presentation of complete mole

A

vaginal bleeding, uterus enlarged out of proportion to gestational age, pre-eclampsia, hyperthyroidism, theca-lutein cysts (hCG driven)

26
Q

clinical presentation of choriocarcinoma

A

after molar pregnancy, abortion, or normal pregnancy. presents w/ vaginal bleeding & symptoms of metastatic disease (eg cough w/ lung metastases). inappropriately elevated hCG levels

27
Q

missed abortion is…

A

embryonic death in utero. signs: vaginal bleeding w/ closed cervical os, small uterus, absence of fetal heart tones, & low hCG levels

28
Q

presentation of abruptio placentae

A

premature placental separation. can occur in 3rd trimester of pregnancy. manifests w/ vaginal bleeding, hypertonic uterus, intense painful contractions

29
Q

ruptured tubal pregnancy presents w/? curretage will reveal?

A

vaginal bleeding, abdominal pain, signs of hemorrhagic shock. curretage reveals endometrial lining w/ gestational changes. fetus and trophoblast are absent.

30
Q

phencyclidine (1) mode of action (2) symptoms (3) examination findings

A

(1) hallucinogen (2) agitation, dissociation, hallucinations, VIOLENT BEHAVIOR, memory loss (3) NYSTAGMUS, ataxia

31
Q

cocaine (1) mode of action (2) symptoms (3) examination findings

A

(1) stimulant (2) euphoria, increased arousal, agitation, CHEST PAIN, headaches, SEIZURES (3) tachycardia, hypertension, MYDRIASIS

32
Q

methamphetamine (1) mode of action (2) symptoms (3) examination findings

A

(1) stimulant (2) agitation, PSYCHOSIS, diaphoresis, violent behavior (3) tooth decay, HTN, tachycardia, choreiform movt

33
Q

LSD (1) mode of action (2) symptoms (3) examination findings

A

(1) hallucinogen (2) VISUAL HALLUCINATIONS, depersonalization, euphoria, occasional dysphoria, panic (3) mild tachycardia, mild HTN, ALERT & ORIENTED

34
Q

marijuana (1) mode of action (2) symptoms (3) examination findings

A

(1) psychoactive drug (2) increased appetite, euphoria, slowed reflexes, impaired time perception (3) dry mouth, CONJUNCTIVAL INJECTION, mild tachycardia

35
Q

heroin (1) mode of action (2) symptoms (3) examination findings

A

(1) opioid analgesic (2) mild euphoria or lethargy to coma (3) MIOSIS, DECREASED respiratory rate, DECREASED bowel sounds

36
Q

PCP mechanism

A

NMDA receptor antagonist. moderate – dissociative symptoms (detachment & withdrawal). higher – agitation, hallucinations, violent behavior. ataxia, nystagmus (both horizontal and vertical) and memory loss

37
Q

cocaine mechanism

A

blocks reuptake of dopamine, NE, and 5-HT at CNS synapses. tachycardia, HTN, blurry vision, euphoria, and agitation. ischemic side effects: i.e. MI and stroke can occur due to severe vasoconstriction. acute intoxication lasts for less than an hour.

38
Q

differentiate methampetamine and PCP intoxication.

A

BOTH can have violent behavior, but PCP will produce nystagmus and ataxia. methamphetamine intox typically lasts for up to 20 hours (much longer than PCP)

39
Q

narcolepsy clinical presentation (3).

A

excessive daytime sleepiness, episodic loss of motor tone triggered by emotion (cataplexy) and inability to move on awakening (sleep paralysis).

40
Q

narcolepsy is commonly caused by lack of which neuropeptides? where are these produced?

A

LACK of hypocretin-1 (orexin-A) and hypocretin-2 (orexin-B). promote wakefulness & inhibit REM sleep-related phenomena. produced only in neurons located in the lateral hypothalamus

41
Q

clinical diagnosis for narcolepsy (definition and inclusion)

A

recurrent lapsing into sleep or napping mult times within same day, occurring at least 3x/wk for 3 months. w/ at least one of the following: (1) cataplexy: conscious, brief episodes of sudden, bilateral muscle tone loss precipitated by emotions such as laughing or joking. or spontaneous abnormal facial movements w/o emotional triggers (2) hypocretin-1 deficiency by CSF analysis (3) rapid eye movement sleep latency <15min

42
Q

low CSF HIAA associated w/ what behaviour?

A

impulsive, destructive behaviors, particularly – aggression, suicide, and violence

43
Q

elevated amounts of 14-3-3 protein in CSF helps w/ diagnosis of..

A

Creutzfeldt-Jakob disease

44
Q

decreases of melatonin in CSF associated w/

A

progression to alzheimer’s disease

45
Q

two most frequent causes of eugonadotropic amenorrhea?

A

(1) incomplete canalization of the vaginal plate (agenesis or imperforate hymen) or (2) mullerian duct anomalies

46
Q

primary amenorrhea in a pt w/ fully developed secondary sexual characterestics?

A

anatomic defect in genital tract. most commonly imperforate hymen or mullerian duct anomaly. former presents w/ cyclic abdominal/pelvic pain w/ hematocolpos

47
Q

hematocolpos:

A

accumulation of blood in vaginal canal – distend vaginal, vaginal bulge or mass palpated anterior to rectum

48
Q

filtration fraction formula?

A

GFR/RPF

49
Q

mucosal neuromas

A

unencapsulated, thickened proliferations of neural tissue

50
Q

NF1 vs NF2

A

NF2 – the more ‘central’ form w/ bilateral acoustic neuromas, brain meningiomas, schwanommas of dorsal roots in spinal cord. NF1 – cafe au lait spots, cutaneous neurofibromas, axillary or inguinal freckling, optic glioma, iris hamartomas, ossessous lesions

51
Q

role of dynein

A

(1) retrograde transport in cells (2) cillary & flagellar movement

52
Q

ethambutol side effect

A

optic neuritis (decreased visual acuity, central scotoma, or colour-blindness). may be reversible w/ discontinuiation

53
Q

mesoderm derived organ that originates from the dorsal mesentary but receives blood supply by an artery of foregut

A

spleen (from splenic artery, branch of celiac artery). spleen = NOT a foregut derivative

54
Q

foregut includes?

A

esophagus through the 2nd part of duodenum (includes liver, gallbladder, and portion of pancreas)

55
Q

embryology of liver

A

endoderm-derivived foregut structure, forms from diverticulum of primitive gut tube within ventral mesentary

56
Q

loss to follow-up (disproportionately in exposed / unexposed groups) results in

A

attrition bias – type of SELECTION BIAS. results in over/underestimation of association between exposure and outcome

57
Q

sampling bias results from..

A

type of SELECTION BIAS; results from nonrandom sampling of target population. characteristics of study population differ from target population: results are not generalizable.

58
Q

nondisjunction in meiosis I or II can cause…

A

monosomy or trisomy

59
Q

differentiating bet meiosis I or II nondisjunction events

A

nondisjunction in meiosis I: 2 diff alleles inherited from one parent (homologous chromosomes – child has 3 diff bands). nondisjunction in meiosis II: 2 same alleles inherited from one parent (sister chromatid) – child: 2 0bands, 2x normal amt of one

60
Q

majority of nondisjunction trisomy 21 occurs during

A

meiosis I (inherit mom’s homologous chromosomes)

61
Q

classic triad of congenital rubella

A

(1) sensorineural hearing loss (2) cataracts (3) PDA

62
Q

IFN-alpha approved for rx of..

A

hepatitis B and C, hairy cell leukemia, condyloma acuminatum, kaposi sarcoma

63
Q

naturally competent bacteria that can undergo transformation (3)

A

(1) streptococcus pneumoniae (2) haemophilus influenza (3) neisseria gonorrhoeae & meningitidis

64
Q

generalized transduction vs. specialized transduction

A

Generalized: during lytic infxn, RANDOM bacterial genes accidentally packaged into viral capsid. Specialized: lysogenic ifxn, SELECT bacterial genes near viral insertion site are excised & packaged into viron

65
Q

normal relationship between LAEDP (left atrium end diastolic pressure) and LVEDP (left ventricle end diastolic pressure)

A

equivalent! mitral senosis elevates LAEDP and PCWP relative to LVEDP

66
Q

kartagener’s is related to..

A

microtubular dynein arm defect (also have sinusitis, bronchiectasis, and situs inversus)

67
Q

tuberous sclerosis

A

AD, angiofibromas (adenoma sebaceum) seizures, and mental retardation

68
Q

main cardiovascular pathology / developmental defect in down’s?

A

endocardial cushion defect (ostium primum ASD, regurgitant AV valves)

69
Q

main cardiovascular pathology / developmental defect in di george?

A
  1. Conotruncal - truncus arteriosus
  2. tetrology of fallot
  3. interrupted aortic arch (atretic or segment is absent)
70
Q

main cardiovascular pathology / defect in friedrich’s ataxia?

A

hypertrophic cardiomyopathy

71
Q

main cardiovascular pathology / defect in Marfan’s?

A

cystic medial necrosis of aorta –>

  1. dissection
  2. Thoracic aneursym
  3. aortic valve incompetence
72
Q

main cardiovascular pathology / defect in tuberous scerlosis?

A

valvular obstruction due to cardiac rhabdomyomas

73
Q

GI loss of K+ leading to hypokalemia results from..

A

prolonged diarrhea

74
Q

early serum marker of thiamine deficiency

A

erythrocyte transketolase activity (solely uses thiamine as cofactor).

75
Q

transketolase fxns to..

A

in hexose monophosphate pathway (HMP).
w/ phosphopentose isomerase

converts ribulose 5-p (derivived from glucose) to

Ribose 5-phosphate
glyceraldehyde 3P (intermediary of glycolysis)
fructose-6 phosphate

76
Q

if give glucose to alcoholic / malnourished patient, must also..

A

give thiamine! needed for glucose utilization. w/o thiamine, may cause acute cerebral damage

77
Q

glucose-6-6 phosphate dehydrogenase is important for..? low levels suggest..?

A

rate limiting step in pentose phosphate pathway, needed for (1) NADPH production (2) fxn of the erythrocyte antioxidant system. decrease G6PD suggests hemolytic anemia

78
Q

methylmalonyl CoA mutase

A

uses B12 as cofactor. converts methylmalonic acid –> succinyl coA. methylmalonic acid is a product of fatty acid oxidation

79
Q

why is hypernatremia rarely observed w/ mineralcorticoid excess?

A

aldosterone escape – increase in Na+, increased volume, increase RBF and GFR –> increase Na+ excretion. also increased volume –> increased ANP –> naturesis

80
Q

snRNPs are needed for

A

small nuclear ribonucleoproteins –> splicesosome

81
Q

transcription factor II D

A

transcription factor that binds to TATA promoter region.

82
Q

elongation factors

A

facilitate tRNA binding and translocation step of protein synthesis

83
Q

releasing factors

A

recognize stop codon (UGA, UAA, UAG) to terminate protein synthesis.

84
Q

severe intellectual disability, history of seizures, and abnormal pallor of catecholaminergic brain nuclei, hair, eye, skin. also classic musty / mousy body odor

A

phenylketonuria – inability to convert phenylalanine to tyrosine (phenylalanine hydroxylase, requires BH4 (tetrahydrobiopterin; tetrahydropteridine reductase)

85
Q

hypopigmentation of skin, hair, eyes, catecholaminergic brain nuclei in PKU results from..

A

inhibitory effect of excess phenylalanine on melanin synthesis.

86
Q

absence of dopamine hydroxylase

A

results in rare form of dysautonomia, characterized by ptosis, orthostatic hypotension, hypoglycemia, and hypothermia. can’t convert dopamine to NE

87
Q

alkaptonuria

A

autosomal recessive disorder of tyrosine degradation – deficiency of homogentisic acid oxidase. accumulation of homogentisic – hyperpigmentation and degenerative joint disease

88
Q

albinism

A

autosomal recessive, defects in biosynth/distribution of melanin. most commonly due to depressed/absent TYROSINASE activity. [melanin synth = tyrosine –> DOPA –> dopaquinone by tyrosinase in melanocytes]

89
Q

deficiency in which two proteins can lead to phenylketonuria?

A

phenylalanine hydroxylase or cofactor tetrahydrobiopterin (or enzyme dihydropteridine reductase)

90
Q

first line treatment for isolated systolic hypertension (common in elderly)

A

thiazide diuretics and dihydropyridine calcium antagonists, like amlodipine and nifedipine (in non-diabetics. diabetics: ACE-I or ARB)

91
Q

side effect profile of nifedipine

A

bilateral ankle swelling and flushing

92
Q

gynecomastic caused by which 2 diuretic?

A

spironolactone (9%), epeleperone (1%)

93
Q

adverse effects from verapamil

A

constipation and gingival hyperplasia

94
Q

mechanism of thiazolidinediones

A

decrease insulin resistance. bind to PPAR-gamma (perioxisome proliferator activated receptor gammA) transcriptional regulator of genes involved in glucose and lipid metabolism. CRUCIAL GENE regulated by PPAR-gamma: adiponectin (cytokine released by fat tissue). adiponectin low in type II diabetics. thiazolidinediones increase adiponectin

95
Q

genes altered by PPAR-gamma (upregulated by thiazolidinediones)

A

(1) crucial: adiponectin (2) fatty acid transport protein (3) insulin receptor substrate (4) glucose transporter-4 (glut-4)

96
Q

main side effects of thiazolidinediones?

A

fluid retention, weight gain, precipitation of CHF

97
Q

blood/gas partition coefficient

A

anesthetics w/ higher blood solubility have larger blood/gas partition coefficients. high solubility –> dissolve easily in blood –> larger amounts must be absorbed before blood is saturated –> delayed rise in partial pressure

98
Q

if partial pressure rises rapidly in blood..

A

gas is not very soluble in blood –> rapid onset in brain

99
Q

speed of anesthetic induction determined by…

A

rate of uptake in brain –> dependent on solubility of anesthetic in blood. very soluble (high blood/gas partition) –> slower onset

100
Q

example of poorly soluble gas? highly soluble has?

A

poor solubility –> nitrous oxide N20 (small amt needed to saturate blood, rapid rise in blood partial pressure, rapid equilibration in brain, rapid onset of action.

high solubility –> halothane. large amount needed to saturate blood, slow rise in PP in blood, slow equilibration in brain, slow onset of action.

101
Q

potency of gas determined by…

A

minimal alveolar concentration. potent –> lower partial pressure needed to be effective.

102
Q

nitrates cause reflex..

A

tachycardia. block w/ beta-blockers

103
Q

hydralazine

A

direct-acting arteriolar dilator

104
Q

phenylephrine

A

alpha-agonist – vasopressor

105
Q

2 uses of N-acetylcysteine

A

(1) antidote in acetaminophen/tylenol overdose (2) renal protective agent prior to IV iodine contrast for radiologicalstudies

106
Q

in parkinson’s, prescribe L-dopa with…

A

(1) carbidopa – peripheral dopa decarboxylase inhibitors (2) entacapone – COMT inhibitor. COMT – catechol-O-methyl-transferase impt in methylation of levodopa. entacapone inhibits peripheral COMT. tolcapone inhibits central and peripheral COMT, but is hepatotoxic.

107
Q

how does amantadine enhance the effect of endogenous dopamine

A

increase synthesis, release, and reuptake of dopamine

108
Q

name some dopamine agonists (4)

A

bromocriptine, pergolide, pramipexole, ropinerole

109
Q

selegiline

A

inhibitor of MAO-B. decreases central dopamine degradation.

110
Q

anticholinergics used for parkinsons (2)

A

trihexyphenidyl and benztropine

111
Q

2 causes of peptic ulcer disease

A

(1) helicobacter pylori infxn (80-90%) (2) NSAID use.

112
Q

rx for h. pylori

A

2 antibiotics (metronidazole, tetracycline, amoxicillin, clarithromycin) and PPI and/or bismuth for 14 days

113
Q

PPI vs. H2 blockers for peptic ulcer disease?

A

PPI superior

114
Q

sucralfate

A

binds to base of mucosal ulcers, protecting against gastric acid. can help duodenal ulcers heal.

115
Q

metoclopramide? rx?

A

dopamine antagonist w/ central & peripheral effects. prokinetic & antiemetic. rx: GI motility disorders, gastroparesis. prevent nausea and vomiting.

116
Q

misoprostol GI rx?

A

prostaglandin E1 analog. prevent NSAID induced peptic ulcer disease

117
Q

three main causes of acute urethritis in healthy young?

A

N. gonorrhea, C. trachomatis, HSV. if engage in anal sex: e. coli

118
Q

rx for gonococcal urethritis?

A

ceftriaxone or fluoroquinolone.

119
Q

rx for chlamydia urethritis?

A

single dose of azithromycin or multi-day doxycycline.

120
Q

pentamidine (3 rx)

A

prophylaxis and treatment of (1) PCP pneumonia. rx: (2) leishmaniasis and (3) African sleeping sickness.

121
Q

nifurtimox rx:

A

trypanosoma cruzi Chagas’ disease

122
Q

mebenzaole rx (4)

A

ascariasis, truchuriasis, hookworm, pinworm

123
Q

nitroprusside use? toxicity? sign? antidote?

A

use: emergent setting where quick onset of action needed to control BP and prevent target organ damage; mixed arterial and venous vasodilation. could cause cyanide toxicity. metabolized into cyanide and nitric oxide –>

cyanide metabolized in liver (by liver rhodanase to thiocynate (excreted in urine).

sign: altered mental status and lactic acidosis. rx: Na2S2O4 (sodium thiosulfate) –> donates sulfur to lier rhodanase –> enhance metabolism and detox of cyanide to thiocyanide.

oxygen also given to prevent cyanide inhibition of cytochrome oxidase (needed for respiration)

124
Q

bicornuate uterus

A

partially septate uterus attached to a single cervix and vagina. results from failure of paramesonephric ducts to fuse. total nonfusion: uterus didelphys – two sep vaginas, cervices, and uterine horns

125
Q

mesonephric ducts in female and male

A

female: from Gartner duct. male: epididymis, ductus deferens, seminal vesicles, and ejaculatory duct

126
Q

paramesonephric ducts in female and male

A

female: uterine tubes, uterus, cervix, and superior 1/3 of vagina.
male: involute, leaving only vestige appendices of the testes

127
Q

concentric vs. eccentric left ventricular hypertrophy

A

concentric: pressure overload: aortic stenosis, chronic HTN. thickens wall uniformly, outer dimension of ventricle remaining unchanged (narrowed cavity).
eccentric: volume overload: aortic or mitral regurgitation, myocardial infarction, dilated cardiomyopathy.

128
Q

structural heart changes w/ aging (after 65)

A

decreased LV size, predominately through shortening of the apex-to-base dimension, accompanied by leftward bowing or lower interventricular (sigmoid) septum.

129
Q

ventricular remodeling post-MI

A

often results in volume overload, poor contractile fxn – eccentric cardiac hypertrophy

130
Q

lynch syndrome (HNPCC)

A

autosomal dominant. microsatellite instability –> DNA mismatch repair defect. inherit one allele, acquire one later.

131
Q

HNPCC-associated colon adenocarcinoma vs. sporadic

A

HNPCC: younger than 50, usu right sided, mult cancers are common: synchronous (same time w/ primary) and metachronous (occur after resection). arises from macroscopically-normal areas of dysplastic mucosa. mutation: DNA mismatch repair: MLH-1, MSH-2, MSH-6, PMS-2)

sporadic: older than 50, predominantly left, uncommon to have mult cancer, adenomatous polyp is source. “adenoma-to-carcinoma” sequence (mutation in APC, k-ras, p53 and DCC)

132
Q

Lynch I and II

A

Lynch I: familial predisposition to colon adenocarcinoma.

Lynch II: predisposition to colon cancer AND increased incidence of extraintestinal cancers (i.e. endometrial, ovarian, stomach, pancreas, urothelial tract

133
Q

APC gene

A

intracellular attachment. mutation: formation of adenomatoius polyp from normal mucosa. mutation detected in MOST sporadic colon cancers and ALL familial polyposis

134
Q

MEN 2b

A

medullary carinoma of thyroid (calcitonin), pheochromocytoma, mucosal neuromas & marfinoid habitus

135
Q

pancreatic tumor in Men 1

A

often gastrinoma –> zollinger-ellison. rarely: insulinoma –> hypoglycemia. vasoactive intestinal polypeptide: massive diarrhea

136
Q

pathogenesis of typhoid fever

A

fecal-oral. penetrate gut mucosa via transporters on enterocytes & phagocytosis by M cells in peyer’s patches. phagocytosed by macrophages (specially designed to live there. macrophages carry to liver, spleen, bone marrow , gallbladder –> hepatosplenomegaly.

in gut lumen –> inflammation of peyer’s patches, intestinal hemmorhage, gut performation – polymicrobial peritonitis & sepsis –> death.

can be carrier in gallbladder: typhoid mary (bile –> stool).

presentation: rose spots on abdomen.

137
Q

hodgkin’s disease age presentation?

A

usu bimodal, peak in 20-30s and 50’s. B symptoms, reed-sternberg cell surrounded by normal lymphocytes in node.

138
Q

histology of follicular lymphoma. 2 major cell types.

A

aggregates of closely packed lymph follicles. 2 major cell types (1) centrocytes: small cleaved cells. centroblasts: large noncleaved cells.

139
Q

histology of large B-cell lymphoma

A

diffuse sheets of large lymphocytes w/ nuclei at least 5x size of small lymphocytes.

140
Q

describe Reed-Sternberg cells

A

abdundant cytoplasm, bilobed/double nuclei, inclusion-like eosinophilic nucleoli.