test #14 4.2 Flashcards Preview

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Flashcards in test #14 4.2 Deck (159)
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1
Q

which n. can be affected by an acoustic schwanomma?

A

CN VII and CV by proximity

2
Q

parinaud syndrome (dorsal midbrain syndrome)

A

paralysis of vertical gaze & pupil issues

3
Q

germ cell tumors in the brain arise…

A

in pineal and suprasellar regions

4
Q

meningiomas are commonly found…

A

over the lateral hemispheric fissure & parasaggital aspect of the brain convexity

5
Q

prokaryotic ribosome is composed of…

A

3 types of rRNA and 50+ proteins

6
Q

30s ribosomal subunit in prokaryote contains..

A

16s subunit. essential for INITIATION of protein synthesis.

7
Q

16S rRNA expresses sequence

A

complementary to Shrine-Dalgarno sequence in all prokaryotic mRNA. [10bp upstream from AUG]

8
Q

shrine dalgarno sequence

A

sequence 10bp upstream AUG on mRNA. binds to 16s rRNA in 30s subunit of prokaryotic ribosome. allows mRNA & 30s ribosomal subunit to bind for protein translation.

9
Q

when does 50s ribosomal subunit associate?

A
  1. mRNA and 30s (w/ 16s rRNA and shrine dalgarno seq). (2) initiator tRNA binds to AUG (3) 50s subunit associates
10
Q

peptidyl transferase activity of 50s subunit conferred by..

A

23s rRNA on 50s subunit. facilitates peptide bond formation

11
Q

energy for translation translocation [where ribosome advances to next mRNA codon to be translated] in prokaryotes

A

facilitated by elongation factor G, energy by GTP

12
Q

tissues w/ surface ectoderm origins

A

rathke’s pouch (anterior pituitary), LENS & CORNEA, INNER EAR SENSORY ORGANS, olfactory epithelium, epidermis, salivary, sweat, & mammary glands

13
Q

tissues w/ neural crest (ectoderm) origins

A

autonomic, sensory & celiac ganglia. schwann cell, PIA & ARACHNOID MATER, aorticopulmonary septum & endocardial cushions, BRANCHIAL ARCHES (bones & cartilage), skull bones, melanocytes, adrenal mudella

14
Q

mesoderm

A

muscle (skeletal, cardiac, smooth), connective tissue, bone & cartilage, serosa linings (peritoneum), cardiovascular system, blood, lymphatic system, SPLEEN, internal genitalia, kidney & ureters, adrenal cortex

15
Q

endoderm

A

GI tract, liver, pancreas, lungs, thymus, parathyroids, thyroid follicular cells, middle ear, bladder & urethra

16
Q

gastrulation (formation of 3 germ layers) occurs.. initiated by..

A

3rd wk of embryogenesis. initiated by formation of PRIMITIVE STREAK: thickening of epiblast cell layer that appears caudally and extends cranially. epiblast cells undergo epithelial-to-mesenchymal transition, causing loss of cell-cell adhesion properties– allows migration downward through primitive streak to form mesoderm and endoderm layers. remainder of epiblast = surface ectoderm.

17
Q

notochord formation

A

2 days into gastrulation, some epiblasts migrate cranially through the primitive node (cephalic end of primitive streak) to form midline structure –> notochord. which induces overlying ectoderm to differentiate into neuroectoderm & form neural plate –> neural tube & neural crest cells (remainder of ectoderm –> surface ectoderm)

18
Q

notochord becomes…

A

nucleus pulposus of intervertebrae disk in adults

19
Q

clinical manifestation of Edwards syndrome (trisomy 18)

A
  1. FACE: microstomia, micropthalmia, cataracts, coloboma (hole in eye), low set & malformed ears, prominent occiput.
  2. CNS: microcephaly, neural tube defects, holoprosencephaly.
  3. MUSCULOSKELETAL: CLENCHED HANDS w/ overlapping fingers, rocker-bottom feet, short sternum, hypertonia.
  4. CARDIAC: VSD, patent duct arteriosus
  5. GI: Meckel’s diverticulum, malrotation
20
Q

ultrasound findings suggesting edwards syndrome

A

intrauterine growth restriction, polyhydramnios, fetus w/ abnormal hand arrangement

21
Q

direct thrombin inhibitors examples (2)? rx?

A

lepirudin & agratroban. rx: heparin-induced thrombocytopenia

22
Q

ticlopidine and clopidergel use (3)

A

percutaneous coronary interventions (PCI), unstable angina, nonQwave MI

23
Q

folate deficiency inhibits formation of what substrate?

A

dTMP (deoxythymidine monophosphate). can reduce erythroid precursor cell apoptosis if supplement thymidine

24
Q

thymidylate synthase catalyzes what rxn?

A

methylation of dUMP (deoxyuridine monophosphate) to dTMP (deoxythymidine monophosphate) WHILE converting folate derivative 5-10 methylenetetreahydrofolate (methylene -THF) to dihydrofolate (DHF). de NOVO dTMP production. methylene-THF donates 1 carbon group to dUMP –> dTMP

25
Q

thymidylate synthase is essential in the supply of which nucleotide precursors?

A

all 4 precursors of DNA replication (directly – thymidine) indirectly (w/ DHF) – purines

26
Q

diminished dTMP synthesis w/ folate deficiency can be partially compensated w/

A

thymidine salvage pathway using thymidine kinase (normally accounts for 5-10% of dTMP synthesis). can use this w/ thymidine supplemenentation

27
Q

major source of nitrogen in synthesis of nucleotides?

A

glutamine. i.e. contributes nitrogen atom to biosynthesis of dUMP.

28
Q

withdrawal symptoms for alcohol & benzodiazepines? exam findings?

A

symptoms: tremors, agitation, anxiety, delirium, psychosis. benzo, also: perceptual disturbances (depersonalization), insomnia. exam: seziure, TACHYCARDIA, palpitations

29
Q

heroin withdrawal symptoms? exam findings?

A

symptoms: nausea, vomiting, abdominal cramping, muscle aches.

exam findings: DILATED PUPILS, YAWNING, piloerection, LACRIMATION, hyperactive bowel sounds

30
Q

stimulants (eg. cocaine & amphetamine) withdrawal symptoms? examination findings?

A

symptoms: increased appetite, hypersomnia, INTENSE PSYCHOMOTOR RETARDATION, SEVERE DEPRESSION (“crash”). no significant findings on exam.

31
Q

nicotine withdrawal? examination findings?

A

dysphoria, irritability, anxiety, INCREASED APPETITITE

32
Q

when does opiod withdrawal occur

A

as soon as 6-12 hrs after use, peaks 24-48 hrs. vitals usu normal.

33
Q

drug withdrawal w/ potentially fatal symptoms

A

ALCOHOL withdrawal. 12-24 hrs after, autonomic hyperactivity (tachycardia, HTN), also seizures

34
Q

layers of bone from middle to end

A

diaphysis, metaphysis, epiphyseal cartilage (growth plate), and epiphysis

35
Q

two effect of estrogen on bone growth

A

(1) stimulates rapid linear growth (stimulates osteoblasts, inhibit osteoclast), but also (2) encourage closure of epiphyseal plates (fusion of epiphysis and metaphysis).

36
Q

somatomedin C

A

also known as insulin-like growth-factor 1 (IGF-1)

37
Q

IGF-1 / somatomedin C on bone growth

A

differentiation and proliferation of chondrocytes in epiphyseal growth plate (increase in linear growth). unlike estrogen, does not accelerate epiphyseal closure.

38
Q

why does precocious puberty –> short stature but excess GH pre-puberty –> gigantism?

A

(1) excess sex steroids –> premature closure of epiphyseal growth plate –> short. (2) excess GH –> IGF-1 –> chondrocyte differentiate & proliferate in epiphyseal plate, no closure

39
Q

smoking can induce what change in hemoglobin

A

formation of carboxyhemoglobin – via inhalation of CO

40
Q

which cells in kidney increase EPO production in response to hypoxia?

A

cortical cells in kidney

41
Q

HELLP syndrome

A

hemolytic anemia, elevated liver enzymes, low platelets (thrombocytopenia)

42
Q

triad of pre-eclampsia

A

(1) hypertension, (2) proteinuria, (3) edema in pregnancy (diagnosis can be made w/o edema). occurs in <10% of pregnancies. typical onset after 20th wk of gestation.

43
Q

gestational diabetes associated w/ increased rates of

A

(1) still birth and (2) macrosomia (large baby)

44
Q

eclampsia vs. pre-eclampsia?

A

PRE-eclampsia: HTN, proteinuria, edema. ECLAMPSIA: w/ seizures.

45
Q

pre-eclampsia can progress to..

A

HELLP syndrome. hemolytic anemia, elevated liver enzymes, and low platelets.

46
Q

(1) older patient w/ (2) bone pain and (3) increase alkaline phosphatase level

A

Paget’s disease of the bone

47
Q

microscopic analysis of bone in Paget’s disease of the bone

A

increased osteoclastic activity —> increased osteoblastic activity. net result: mosaic pattern of lamellar bone w/ irregular sections linked by cement lines (representing previous areas of bone resorption)

48
Q

describe areas of bone affected by Paget’s disease

A

increased fibrous tissue deposition & vascularity (induced by proliferation of fibroblasts & endothelial cells)

49
Q

increased vascularity in Paget’s bone disease can result in..

A

arteriovenous shunting that can result in high-output heart failure.

50
Q

oil/water parition

A

used to describe pharmacokinetic properties of general anesthetics (relative solubility in oil vs. water)

51
Q

rx for narcolepsy? 2

A

1st line: modafinil – non-ampetamine stimulate. unclear mech, increase dopamine signaling.

2nd line: amphetamines

52
Q

carbamazepine rx (2)

A

trigeminal neuralgia and seizures

53
Q

zolpidem

A

non-benzodiazepine hypnotic used for insomnia

54
Q

melatonin rx (2)

A

jet-lag and age-related insomnia

55
Q

CEA (carcinoembryonic antigen)

A

inreased in 60-90% of patients w/ colorectal cancer. glycoprotein involved w/ cell adhesion. produced in embryonic pancreas, liver, and intestine. can be detected in healthy people.

56
Q

why can’t CEA be used to diagnose colon cancer? what can it be used for?

A

increased in pancreatic, gastric, and breast malignancies. also, benign diseases like inflammatory bowel disease, cirrhosis, and pancreatitis. smokers. sensitive indicator of colorectal cancer recurrence (measure pre-op and during surgery).

57
Q

tumor grade looks at

A

degree of tumor differentiation

58
Q

tumor stage reflects..

A

extent of spread

59
Q

most important factor determining survival of patients w/ colon cancer?

A

STAGE: lymph node involvement & distant mets.

60
Q

metabolic acidosis in diabetes caused by which 2 substrates?

A

ketones: (1) beta-hydroxybutyrate and (2) acetoacetate

61
Q

where can meningococci be isolated from in asymptomatic carriers?

A

oropharynx and nasopharynx (transmission w/ respiratory droplets)

62
Q

how does meningococci enter blood from pharynx?

A

pilus-mediated adherence and penetration of mucosal epithelium (to gain access to circulation). recall n. meningitidis makes IgA protease.

63
Q

recurrent lobar hemorrhages in elderly patient most likely results from..

A

cerebral amyloid angiopathy. (beta-amyloid deposited into arterial wall, weakining it, predispose to rupture). related to advanced age (not systemic amyloidosis)

64
Q

most common presentation of cerebral amyloid angiopathy?

A

recurrent HEMORRHAGIC strokes.

65
Q

HTN hemorrhagic strokes vs. amyloid-associated strokes

A

HTN: LARGE and involve basal ganglia. AMYLOID: cerebral hemisphere, involving smaller areas– lower mortality rate, more benign course

66
Q

carotid artery atherosclerosis & cardiac embolism are common causes of..

A

ISCHEMIC strokes

67
Q

great lakes, mississippi, ohio river valley

A

blastomycosis

68
Q

lung granulomatous inflammation w/ fungal infxn?

A

think blastomycoses. can cause illness in immunocompetent too.

69
Q

histology of blastomycoses

A

round yeast w/ thick, doubly refractive walls. each yeast –> single broad based bug.

70
Q

rx for blastomycoses?

A

itraconozole

71
Q

typical ECG of atrial fibrillation

A

absent P waves, chaotic fibrillatory (f) waves, irregularly irregular R-R intervals, narrow QRS complexes (narrow –> tachycardia)

72
Q

pathophysiology of atrial fibrillation

A

normally. SA node –> right atrium –> interatrial pathway –> left atrium.

AFIB: atrial excitability is heightened, mult impulses generated in areas other than SA node. some regions = shortened refractory period. other = decreased conductivity. all in all, multiple re-entrant impulses travel.

some abnormal atrial impulses reach AV nodes –> ventricles. majority do not go through bc AV node refractory period.

refractory period in AV node prevents then average atrial rate of 300-500 in afib from transmitting to ventricles

73
Q

note: SA node and AV node abnormal in atrial fibrillation?

A

NO! the atria are hyperexcitable and have multiple impulses generated in regions other than SA node. but SA node is fine, so will NOT have new site of impulse generation

74
Q

effect of competitive & noncompetitive antagonists on ED50 and Emax

A

competitive = change ED 50 = shift right. noncompetitive = change Emax = shift down (on a effect v. dose curve)

75
Q

granulosa-theca tumors commonly present in

A

postmenopausal women

76
Q

describe histology of granulosa cell tumor

A

small, cuboidal cells that grows in cords/sheets. can see gland-like structures w/ acidophillic materia: call-exner bodies –> immature follicles

77
Q

what 2 tissues normally produce AFP?

A

fetal liver and yolk-sac

78
Q

AFP is a tumor marker for..

A

hepatocellular carinoma, nonseminomatous testicular carcinoma, ovarian carcinoma

79
Q

CA-125 is found in elevated amounts on the surface of which 3 tumors

A

malignanct ovarian epithelial cells in (1) serous (2) endometroid (3) clear cell carcinomas

80
Q

Bohr effect (hemoglobin)? how does this happen? Haldane effect?

A

BOHR: peripheral tissue, release of O2 from hemoglobin facilitated by increase PCO2 and resultant decreased pH (H2CO3 = HCO3- and H+). due to histidine side chains on alpha and beta hemoglobin side chains. HALDANE: in lungs, rise in pO2 increases binding of oxygen to hemoglobin and release of H+ and CO2 from hemoglobin (H + HCO3- back into RBC, to be converted to CO2)

81
Q

where is the chloride concentration of RBCs highest?

A

in venous blood (exchanged bicarb into plasma or Cl-)

82
Q

combined cardiac and vascular fxn curves

A

cardiac: as cardiac muscle is stretched, cardiac output increases [frank-staring effect]. venous return curve: describes how venous return changes w/ variations in right atrial pressure

83
Q

when venous return curve intersects w/ x-axis..

A

means no more venous return. venous pressure = right atrial pressure. the mean systemic filling pressure (measure of the degree of FILLING of the circulatory system relative to the circulatory CAPACITY.

84
Q

on cardiac - vascular fxn curves, what shifts venous return x-intercept to right? left?

A

right: increased blood volume i.e. excessive hydration. left: acute hemorrhage

85
Q

how does increased TPR affect cardiac/vascular fxn curve? decrease?

A

increased TPR –> decrease slope of both curve, bc higher vascular resistance restricts venous return, and increases afterload.

86
Q

CREST syndrome symptoms

A

Calcinosis, Raynaud syndrome, Esophageal dysmotility, Sclerodactyly, Telangiectasia

87
Q

crest syndrome is.. pathogenesis?

A

a systemic sclerosis variant that mostly involves SKIN of the FACE & fingers. pathogenesis unclear: unknown antigen stimulates accumulation of CD4+ lymphocytes in skin and other tissues. CD4+ cells stimulate fibroblasts to product collagen

88
Q

hallmark of systemic sclerosis

A

excessive tissue fibrosis

89
Q

GI issues in CREST syndrome

A

esophageal dysmotility, result of atrophy & fibrous replacement of esophageal muscles (muscularis). esophageal body and LES become atonic & dilated – REFLUX: heartburn, regurgitation, dysphagia. dilated esophagus w/ absent peristalisis.

90
Q

what disorder results in an increase resting lower esophageal sphincter tone & diminished LES relaxation during meals?

A

achalasia. barium swallow –> distended esophageal body w/ narrow LES “bird beak”

91
Q

abnormal location of gastroesophageal junction

A

sliding hiatal hernia. prone to GERD

92
Q

periodic non-peristaltic esophageal muscle contractions are seen in..

A

diffuse esophageal spasm. clinical manifestation = dysphagia and chest pain. barium esophagus = “corkscrew esophagus”

93
Q

bird-beak esophagus –> stomach in barium swallow

A

achalasia

94
Q

corkscrew esophagus on barium swallow

A

diffuse esophageal spasm

95
Q

earliest visceral manifestation of systemic sclerosis

A

esophageal hypomotility & incompetence of LES (due to atrophy and fibrous replacement of esophageal muscles). esophageal dilation –> reflux.

96
Q

caspofungin is most active against which 2 fungi? not active/limited against which 2?

A

most active against: candida and aspergillus. not active: cryptococcus neoformas. limited: mucor / rhizopus

97
Q

normal QRS duration

A

0.08-0.12 seconds ( 2-3 little boxes)

98
Q

how does QRS change w/ exercise

A

normally, QRS interval shortens during exercise (normal = 80-120msec)

99
Q

antiarrhythmic that exhibits strong use dependence?

A

normal QRS interval at baseline, prolonged when exercise i.e. FLECAINIDE (class IC antiarhythmic)

100
Q

explain use dependence of Class IC antiarrhythmics

A

IC bind to fast Na+ channels; responsible for phase 0 depolarization (block inward Na+ current, prolong QRS). IC are SLOWEST to dissociate from Na+ channel –> so Na+ blocking effects INTENSIFY as HR increases (bc less time between AP for mediation to dissociate from receptor)

101
Q

which antiarrhythmic drugs do NOT affect QRS interval:

A

selective B1 blockers (lower HR), digoxin (lower HR), dofetilide, verapamil (slow SA and AV node conduction)

102
Q

which drug can cause false ST segment depression during exercise?

A

digoxin

103
Q

which antiarrythmic drug displays reverse use-dependence?

A

class III (i.e. dofetilide), block outward K+ currents during repolarization. prolongs QTc interval. the slower the heart rate, the more QT interval is prolonged.

104
Q

2 toxins w/ clostridium difficile

A

enterotoxin A: watery diarrhea. cytotoxin B: colonic epithelial cell necrosis & fibrin deposition

105
Q

clinical presentation of c. diff

A

(1) range from watery diarrhea to fulminant colitis (toxic megacolon (2) sigmoidoscopy shows characterestic white/yellow pseudomembranes

106
Q

best method of diagnosis C. diff colitis?

A

PCR detection of toxin A and B genes in stool

107
Q

ingestion of undercooked shellfish is associated w/ (3)

A

(1) vibrio cholerae (2) norwalk virus (3) hepatitis A infxn

108
Q

vaccine preventable causes of diarrhea (2)

A

(1) hepatitis A (2) typhoid fever

109
Q

white/yellow membrane-like plaques on colonoscopy are virtually pathognomonic for…

A

clostridium difficile colitis

110
Q

histopatholgoy of acute rejection (usu 1-4 wks following transplant)

A

dense infiltrate of mononuclear cells usu composed primarily of T-lymphocytes.

111
Q

histopathological presentation of hypersensitivity myocarditis

A

perivascular infiltrate w/ abundant eosinophils. often due to initiation of new drug therapy, against which body mounts an atopic response

112
Q

presentation of chronic rejection

A

scant inflammatory cells w/ interstitial fibrosis

113
Q

ulcer found in distal duodenum suggests..

A

Zollinger-Ellison

114
Q

suggests of Zollinger-Ellison induced duodenal ulcers?

A

(1) distal duodenum (2) multiple (3) refractory to therapy (4) recurrence of ulcer after acid-reducing surgery

115
Q

where are Zollinger-Ellison tumors located. malignant?

A

majority in pancreas, but some in duodenum, stomach, etc. 2/3 of tumors are malignant.

116
Q

clinical presentation of zollinger-ellison?

A

(1) duodenal / gastric ulcers (2) diarrhea (bc pancreatic / intestinal enzymes inactivated by gastric acid, cannot digest nutrients

117
Q

stress-related mucosal erosions (acute erosive gastritis)

A

after surgery, head trauma, burns, or heavy NSAID use. multiple shallow mucosal defects seen in the stomach. EROSIONS, by definition, DO NOT PENETRATE MUSCULARIS MUCOSA

118
Q

chronic gastritis w/ antral sparing…

A

autoimmune gastritis

119
Q

chronic antral-predominant gastritis

A

h. pylori infxn

120
Q

gastric ulcers are commonly found..

A

on lesser curvature.

121
Q

peptic ulcer disease duodenal ulcer…

A

usu located 3cm from pylorus

122
Q

ipratropium / tiotropium

A

blocks action of acetylcholine at muscarinic receptors in lungs (less effective at bronchodilation compared to B2-agonist)

123
Q

methylxanthines, like theophylline and aminophylline…

A

bronchial dilitation by (1) decreasing phosphodiesterase activity (increase cAMP) and (2) block adenosine receptors

124
Q

zileuton

A

inhibits 5-lipoxygenase. prevents leukotriene formation. prophylatic. use in (1) allergic rhinitis (2) bronchial asthma

125
Q

flunisolide

A

inhaled glucorticoid, prophylactic rx

126
Q

most preferred prophylatic rx: of bronchial asthma?

A

inhaled glucocorticoids like flunisolide

127
Q

1st line treatment for most patients w/ acute gouty arthritis? 1st line in elderly? overall 2nd line?

A

1st line most: NSAID (cox inhibitors). avoid in elderly, pts w/ hepatic and renal fxn [GI bleed risks, fluid retention, aggravation of hypertension, precipitation of CHF). 1st line elderly: systemic or intra-articular glucocorticoids. overall 2nd line: colchicine (bc side effects of nausea and diarrhea)

128
Q

when are uricosuric agents contrainidicated?

A

during acute gouty attacks

129
Q

most important factor in diagnosis tetanus?

A

strong clinical suspicion! history & physical exam: HISTORY: (1) immunization status (2) length of time since las tetanus vaccine / booster (3) history of penetrating trauma (piercing wound, burn, illicit drug use, contaminated soil, MVA) PHYSICAL EXAM: (1) trismus (2) risus sardonicus (3) opisthotonos – extension of truncal muscles.

note: NO SERUM TOXIN ASSAY AVAILABLE for TETANOSPASM. blood cultures are of little use – local infxn. also, takes long to identify even when it does grow. no Ab test

130
Q

3 unidirectional enzymes in glycolysis

A

(1) hexokinase (2) phosphofructokinase (3) pyruvate kinase

131
Q

4 enzymes needed to ‘reverse’ glycolysis (gluconeogenesis)

A

(1) pyruvate carboxylase (2) PEP carboxykinase (3) fructose 1,6 bisphophosphatase (4) glucose-6-phosphatase

132
Q

role of fructose 2,6-bisphosphate

A

control balance between gluconeogenesis and glycolysis. allosterically inhibits fructose-1,6-bisphosphatase. allosterically activates PFK-1.

133
Q

conversion of glucose to alanine begins w..

A

transamination of alanine to pyruvate

134
Q

how does glucagon & insulin affect gluconeogenesis vs. glycolysis

A

via interconversion of fructose-6-phosphate and fructose-2,6-bisphosphate. BIFUNCTIONAL enzyme. GLUCAGON PHOSPHORYLATES it: activating the fructose-2,6-bisphosphatase.

INSULIN DEPHOSPHORYLATES, activating phosphofructokinase-2

135
Q

fatty acid synthesis is upregulated by increased… (2)

A

(1) insulin (2) citrate – which is increased when acetyl-CoA is abdundant, as w/ active glycolysis.

136
Q

foramen ovale is patent in..

A

20-30% of normal adults. usu remains fxnally closed due to pressure. consider when pt w/ DVT has STROKE

137
Q

in patients w/ persistent truncus arteriosus, always see associated…

A

ventricular septal defect

138
Q

persistent ductus arteriosus usu closes..

A

by 3rd month of life, due to high O2 from left to right.

139
Q

attributable risk percent

A

ARP = (relative risk - 1)/RR or..

ARP = risk in exposed - risk in unexposed / risk in exposed

140
Q

which branch of MCA supplies Broca (inferior frontal)? Wernicke (posterior superior temporal)>

A

broca –> superior division. wernicke –> inferior division

141
Q

power (1-B)? depends on.. (2)?

A

probability of rejecting null when its truly false. depends on sample size & diffference in outcome between two groups

142
Q

sheehan’s syndrome

A

high estrogen in pregnancy –> growth of pituitary –> larger & more vascular. hypotension w/ postpartum hemorrhage –> ISCHEMIC NECROSIS of pituitary –> hypopituitary. present w/ inability to lactate, also hypothyroid, hypocortisol

143
Q

autoimmune hypophysitis: when does it occur? presentation?

A

sometimes seen late preg / early postpartum – anterior & posterior inflammation. presentation: (1) ACUTE headaches, (2) visual defects, (3) cortisol deficiency (unknown why, but cortisol deficiency before others)

144
Q

pituitary apoplexy? presentation?

A

HEMORRHAGE into a preexisting pituitary adenoma. MEDICAL EMERGENCY. present: acute, severe headache, opthalmoplegia, altered sensorium. give steroids.

145
Q

how would infiltration (i.e. sarcoid, histiocytosis X, mets) into the pituitary present?

A

compress stalk, decrease hypothalamic dopamine –> loss of inhibition of lactotrophs –> elevated prolactin

146
Q

most common location for intussusception? presentation

A

ileocolic junction (small ileum into larger cecum). in pts < 2 = no structural cause, viral infxn. in pts >2 = look for cause i.e. meckle diverticulum, foreign body, tumor. presentation = colicky, intermittent abdominal pain, nausea, vomiting, “currant jelly” stools – blood & mucous

147
Q

inspiration on cardiac parameter. increase murmur? decrease?

A

increase R venous return. decrease L venous return. increase right sided murmurs, decrease left sided.

148
Q

valsalva strain / rapidly standing on cardiac parameter? increase murmur? decrease?

A

decrease preload and afterload(?). INCREASE HCM and MVP murmurs (due to decrease LV volume) *. decrease most others (i.e. flow through stenotic valve or regurg)

149
Q

squatting on cardiac parameter? increase murmur? decrease?

A

increase preload & afterload. increase most murmurs (stenosis / regurg). decrease MVP and HCM.

150
Q

passive leg raise on cardiac parameter? increase murmur? decrease?

A

increase preload. like squating, increases most murmurs (regurg/stenosis). decrease HCM and MVP.

151
Q

handgrip on cardiac parameter? increase murmur? decrease?

A

increase afterload. increase AR, MR, VSD. decrease HCM and AS

152
Q

what is valsalva

A

forced exhalation against a closed glottis, increase intrathoracic pressure

153
Q

why does MVP murmur decrease w/ increase preload / afterload?

A

increased LV volume brings valve leaflets into more normal anatomic arrangement (facilitating proper closure)

154
Q

defect in MVP

A

mitral incompetency resulting from elongation & redundancy of valve leaflets and chordae tendineae. click –> chordae tendinae as they are pulled taut by ballooning leaflets. murmur – impaired coaptation of valve margins during systole

155
Q

most common cause of MVP in developed countries? what else can?

A

most common: sporadic myxomatous degeneration of mitral valve. could also be Marfan or Ehler-Danlos

156
Q

histology of sporadic myxomatous degeneration of mitral valve?

A

attenuation of fibrosa (collagen) layer of valve. thickening of spongiosa layer (deposition of mucoid/myxomatous material). also, thinning of collagenous core of chordae tendinae

157
Q

AIDs patients have risk of which malignant proliferation

A

EBV associated –> non-Hodgkin’s lymphoma (including aggressive diffuse large B-cell lymphomas and Burkitt’s)

158
Q

what 2 diseases does BK virus cause?

A

(1) nephropathy (typically post-transplant when latent virus is reactivated (2) hemorrhagic cystitis

159
Q

potential causes of dilated cardiomyopathy (4)

A

viral myocarditis, alcohol toxicity, diptheritic myocarditis, chemo (doxorubicin / daunorubicin)