test #27 4.16 Flashcards Preview

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1
Q

why does C. perfringens make gas necrosis?

A

rapid metabolism of muscle tissue carbohydrate –> gas

2
Q

osmium tetroxide

A

fat = black

3
Q

fat embolism syndrome

A

(1) respiratory distress
(2) nonfocal neurological disturbance
(3) chest lesions consistent w/ thrombocytopenia

4
Q

describe path of fat emboli

A

dislodge from bone marrow, enter marrow vascular sinusoids,

  • occlude pulmonary microvessels –> impair gas exchange
  • occlude vasculature in CNS
5
Q

describe promotion of parenchymal destruction w/ fat emboli (2)

A
  1. platelet & mediators coat & adhere to emboli –> thrombocytopenia
  2. systemic activation of LPL (lipoprotein lipase) releases oleic acid systemically –> toxic levels
6
Q

wright stain

A

often hemotological stain. purple platelets

7
Q

iron stain // hemosiderin

A

brown on H&E

dark blue on prussian blue

8
Q

second trimester quad screen for down’s syndrome:

A

increased: b-HCG, inhibin A.
decreased: AFP, estriol

9
Q

first trimester findings in down’s syndrome:

A

ultrasound:
increased nuchal translucency &
hypoplastic nasal bone.

serum:
increased b-HCG
decreased PAPP-A

10
Q

edward’s syndrome (trisomy 18) screening findings

A

everything is down.

1st trimester:
DOWN: PAPP-A and b-HCG

quad screen:
DOWN: AFP, b-HCG, estriol, inhibin-A (could be normal)

11
Q

elevated b-HCG and inhibin in 2nd semester?

[low estriol and AFP]

A

down’s syndrome

12
Q

low bHCG, inhibin, estriol, and ADP

A

edward’s syndrome

13
Q

patau syndrome screening findings

A

first trimester:

DOWN: bHCG, PAPP-A

increased nuchal translucency

14
Q

low b-HCG and PAPP-A w/ nuchal translucency? without nuchal translucency

A

nuchal translucency: patau

w/o nuchal translucency: edwards

15
Q

vast majority of trisomy 21 occur due to..

A

nondisjunction in meiosis I

failure of homologous chromosomes to separate

16
Q

nondisjunction in meiosis I due to? nondisjunction in meiosis II due to?

A

meiosis I: failure of homologous chromosomes to separate

meiosis II: failure of sister chromatids to separate

17
Q

lagging strand is CONSTRUCTED in which direction? SYNTHESIZED in which direction?

A

constructed in 3’->5’ direction.

synthesized in 5’->3’ direction

18
Q

elder abuse

A

FIRST: try to speak to patient alone – to avoid intimidation.

ask:
1. do you feel safe at home
2. who prepares your meals
3. who handles your checkbook

REPORT only after information is collected

19
Q

anovulatory cycles

A

common in early menarche years.

immature HPA-axis

longer menstrual cycles and irregular bleeding patterns due to presence of anovulatory cycles

no ovulation -> no corpus luteum -> no progesterone -> continuous estrogen

results in continued proliferation.

becomes disorganized, fragile, w/ unstable venous capillaries –> irregular periods of stromal breakdown w/ variable (spotting) & heavy bleeding.

20
Q

three major causes of valvular aortic stenosis. most common world-wide? in USA?

A

(1) congenitally abnormal valve w/ calcification (i.e. biscuspid)
(2) calcified normal valve
(3) rheumatic heart disease

world-wide: rheumatic heart disease.
US: calcific aortic valve (either bicuspid/tricuspid)

21
Q

right horn of sinus venosus

A

originally receives blood from IVC. l

becomes smooth part of right atrium.

(smooth part of left from primitive pulmonary vein)

22
Q

bulbos cordis

A

forms beginning of ventricular outflow tract in embryonic heart. later –> smooth portion of left and right ventricles (adjacent to aorta and pulmonary artery, respectively)

23
Q

primitive atrium

A

receives blood from sinus venosus in embryonic heart, transmits to primitive ventricle.

primitive atrium –> rough portions of left and right atria

24
Q

close PDA? keep it open?

A

close: indomethacin.

keep open: PGE2

25
Q

primitive pulmonary vein forms..

A

smooth part of left atrium

26
Q

left horn of sinus venosus

A

coronary sinus

right horn –> smooth part of right atrium

27
Q

right common cardinal vein & right anterior cardinal vein

A

SVC

28
Q

what is the first functional organ in human embryo? when does it function?

A

fetal heart. begins to pump 4 wks in.

29
Q

first heart loop establishes

A

left-to-right polarity.

30
Q

patent foramen ovalue

A

failure of septum primum and septum secundum to fuse. usu left untreated.

31
Q

embryological origin of AV values (tricuspid and mitral)

A

from fused endocardial cushions of AV canal

32
Q

embryological origin outflow valves (aortic/pulmonary)

A

endocardial cushion of outflow tract

33
Q

PTH and Ca2+ abnormalities in osteoperosis? osteopetrosis?

A

NONE

osteopetrosis might have low Ca2+

34
Q

PTH and Ca2+ in osteoperosis?

A

NORMAL

35
Q

high PTH, low Ca2+

A

renal failure, vitamin D deficiency

36
Q

causes of PTH-independent hypercalcemia?

A

humoral hypercalcemia of malignancy, vitamin D toxicity, excessive ingestion of Ca2+, thyrotoxicosis, immobilization

37
Q

age of calcification w/ bicuspid aortic valve? tricuspid

A

bicuspid: premature: 60-70
tricuspid: senile: 80-90

38
Q

damage to common peroneal n. sustained w/? physical finding?

A

lateral aspect of leg, fibular neck fracture.

foot dropPED & can’t feel foot dorsum
peroneal everts and dorsiflexes

39
Q

damage to tibial n. sustained w/? physical finding

A

knee trauma, proximal: baker’s cyst. distal: tarsal tunnel.

can’t TIP toe & sense sole of foot
tibial inverts and plantar flexes

40
Q

sensation to sole of foot? dorsum?

A

dorsum: superficial peroneal n.

41
Q

sensation to medial leg? lateral leg?

A

medial: saphenous n. branch of femoral n.
lateral: superficial peroneal

42
Q

superficial branch of common peroneal?

A

mostly lateral compartment: foot eversion & sensation of lateral leg & foot dorsum

43
Q

deep branch of common peroneal?

A

anterior compartment: dorsiflexors of foot and toes. inversion of foot.

sensation to only region between 1st and 2nd digits.

44
Q

where does the coronary sinus reside?

A

atrioventricular groove on posterior surface.

45
Q

describe placement of biventricular pacemaker

A

2 leads -> right heart
via left subclavian -> SVC -> right atrium & ventricle

1 lead -> left ventricle
via right atrium -> coronary sinus (atrioventricular groove of posterior heart) -> lateral venous tribituaries

46
Q

swan ganz catheter

A

insert catheter into pulmonary artery, diagnostic, test for heart failure

47
Q

cataracts, frontal balding, gonadal atrophy, and muscle atrophy / myotonia

A

myotonic muscular dystrophy type 1. (autosomal dominant)

2nd most common muscular dystrophy (after duchenne’s)

48
Q

typical symptom of myotonic muscular dystrophy type 1

A

difficulty loosening one’s grip after handshake. or inability to release doorknob.

49
Q

pathogenesis of myotonic muscular dystrophy

A

autosomal DOMINANT

CTG repeat expansion in gene for myotonia-protein kinase (DMPK gene)

has anticipation

50
Q

4 diseases w/ trinucleotide expansion

A

fragile X: CGG
friederich ataxia: GAA
huntington: CAG
myotonic dystrophy: CTG

51
Q

muscle histology in myotonic dystrophy

A

atrophy of type 1 muscle fibers (esp).

no necrosis or fibrofatty replacement (unlike duchenne’s)

52
Q

2 inflammatory myopathy

A

dermatomyositis and polymyositis

53
Q

ion channel myopathy

A

myotonia and episodes of hypotonic paralysis. often associated w/ exercise. no atrophy on light microscope.

PAS+ intracytoplasmic inclusions

54
Q

side effect of corticosteroid treatment for atoptic dermatitis?

A

good: reduces inflammatory response
bad: decreases fibroblast production of ECM collagen and glycosaminoglycans

  • -> atrophy of dermis w/ loss of collagen, drying, cracking, tightening in skin.
  • -> also teleangiectasia, ecchymoses from mild trauma, atrophic striae
55
Q

rx for conn syndrome

A

primary hyperaldosteronism

spironolactone / epeleperone

56
Q

most common CNS tumor in immunosuppresed?

A

CNS lymphoma

57
Q

describe CNS lymphoma

A

micropscopically: dense cellular aggregates of uniform, atypical lymphoid cells. majority: B cells.

diffuse large B cell = most common type. (CD20, CD79a+)

associated w/ EBV

nonspecific clinical presentation

usu high grade, poor response to chemo

solitary mass in brain.

58
Q

presentation of sporothrix schenckii. biopsy of innoculation site?

A

infects immunocompetent!

dimorphic fungi. via thorn pick. spread along lymphatics forming subcutaneous nodules & ulcers

biopsy of innoculation site: granuloma w/ histiocytes, multinucleated giant cells, neutrophils, surrounded by plasma cells.

59
Q

fungus from animal contact?

A

dermatophytoses – microsporum species. i.e.

microsporum canis –> tinea capitis

60
Q

woolsorter’s disease

A

pulmonary anthrax!

exposure to animal products (hair, infected hides, hide-based clothing pdt, wool).

GOAT HAIR: most common implicated exposure

61
Q

antiphagocytic D-glutamate capsule?

A

bacillus anthracis. required for pathogenicity.

62
Q

describe pathogenesis of pulmonary anthrax:

A

ingested by pulmonary macrophages –> move to mediastinal lymph nodes –> cause hemorrhagic mediastinitis

when spores germinate into vegetative cells, begin to produce 3-part anthrax toxin. symptoms follow.

63
Q

progression of symptoms of pulmonary anthrax

A

myalgia, fever, malaise.

rapidly progress to hemorrhagic mediastinitis (widened mediastinum on chest x-ray), bloody pleural effusions, septic shock, death

64
Q

hemorrhagic mediastinitis?

A

pulmonary anthrax

65
Q

long chain “serpentine” or “medusa head” colonies. nonhemolyzing, standard culture medium?

A

b. anthracis

66
Q

protein A (bind Fc portion of IgG)

A

staph aureus

67
Q

peritrichous flagella

A

proteus mirabilis.

flagella distributed uniformly over entire surface of bacterial cell.

characteristic of highly motile organisms.

68
Q

anterior hypothalamic nuclei? destruction?

A

cooling via parasympathetics. destruction = hyperthermia

69
Q

posterior hypothalamic nuclei? destruction?

A

heating via sympathetics. destruction = hypothermia

70
Q

ventromedial hypothalamic nuclei? destruction?

A

satiety.
stimulated by leptin.

destruction = chubs.

71
Q

lateral hypothalamic nuclei? destruction?

A

hunger.
inhibited by leptin.

destruction = skinny.

72
Q

arcuate nucleus of hypothalamus

A

secretes:

  1. dopamine (inhibit prolactin)
  2. GHRH
  3. GnRH
73
Q

paraventricular nucleus of hypothalamums

A

secrete oxytocin, ADH, TRH, CRH

74
Q

supraoptic nucleus of hypothalamus

A

ADH and oxytoxin

75
Q

suprachiasmatic nucleus

A

input from retinohypothalamic tract (specialized photosensitive ganglion cells in retina)

secrete NE –> pineal gland –> melatonin

also regulates body temperature and production of cortisol.

regulate circadian rhythm.

76
Q

jetlag

A

dysynchrony between body’s circadian rhythm (sleep/wake cycle) and local environmental rhythm

77
Q

diurnal variation: melatonin levels? cortisol levels

A

melatonin: high at night, low in day. secreted by pineal gland.
cortisol: high in day, low at night.

78
Q

superficial candidiasis (thrush, esophagitis, cutaneous, vulvovaginitis) directly related to?

hematogenous candidiasis related to?

A

superficial: low T-LYMPHOCYTE
hematogenous: NEUTROPENIA

79
Q

what type of candida infection are HIV pts susceptible?

what about neutropenic?

A

HIV: low T count: superficial (oral, cutaneous, etc)

neutropenic: disseminated (right sided endocarditis, liver & kidney abscesses, candidemia)

(note if HIV + neutropenic: susceptible to both)

80
Q

C1 esterase deficifiency

A

hereditary angioedema

ACE inhibitors contraindicated

81
Q

C3 deficiency

A

(1) recurrent pyogenic sinus, respiratory tract infection.

(2) susceptible to type III HSR

82
Q

C5-9 deficiency

A

both Neisseria (gonorrhea & meningitidis)

83
Q

nitroglycerin

A

venodilator (large veins) reduce preload (decreased myocardial oxygen demand and treats angina pectoris)

note: reflex tachycardia and contractility, but overall low O2 demand in heart

84
Q

large veins

A

modulated by nitroglycerin (venodilate)

85
Q

small arteries & arterioles

A

primary site of hormonal regulation of systemic blood pressure & site of action of vasoactive antihypertensive drugs (nifedipine and prazosin)

large doses; nitrates affect arteries – flushing, headache

86
Q

large arteries

A

primary conduits for blood delivery to tissues. contain large amount of smooth muscle to regulate blood pressure and withstand high pressures

87
Q

precapillary sphincters

A

bands of smooth muscles at junction of capillary and arteriole. limit flow of blood. respond to NE & E (contract or relax)

also directly responsive to local environment (histamine, low O2, high CO2, decreased pH)

88
Q

equinovarus posture

A

plantarflexed and inverted
damage to common peroneal n.

paralysis of peroneus longus and peroneus brevis muscle (eversion), tibialis anterior (dorsiflexion), and extrinsic extensors of toe.

89
Q

what three rxns is pyrodoxine B6 important for

A

(1) transamination and (2) decarboxylation of amino acids. (3) gluconeogenesis.

90
Q

transamination

A

between amino acid and alpha-keto acid

91
Q

transamination w/ oxaloacetate (alpha-keto-acid) & glutamate (amino acid)

A

aspartate (amino acid) & alpha-ketoglutarate (keto-acid)

92
Q

transaminases require what cofactor

A

pyridoxine B6

93
Q

hypertensive crisis defined as..

A

persistent diastolic pressure exceeding 130mmHg.

associated w/ acute vascular damage

94
Q

hyperplastic arteriolosclerosis histology:

A

malignant hypertension

onion-like concentric thickening of walls:

due to (1) laminated smooth muscle cells & (2) reduplicated basement membranes

95
Q

major toxicity of statins

A

hepatoxicity and myopathy (elevated creatinine kinase)

96
Q

statins post MI?

A

decrease both incidence of 2nd MI and mortality. lower cholesterol & directly stabilize atheromatous plaques

97
Q

statin myopathy amplified w/

A

concomittant use of fibrates & niacin

98
Q

myopathy-inducing drugs

A

statins, fibrates, nitrates, hydroxychloroquine, glucocorticoids, colchicine, interferon alpha, penicillinaime.

99
Q

reliability?

A

reproductability (test, retest).
measured in terms of coefficient of variation (CV) = standard deviation of the set of repeated measurments divided by mean

100
Q

validity (accuracy)?

A

ability to measure that which it is supposed to measure

test can be highly reliable but invalid

101
Q

minute ventillation vs. alveolar ventilation

A

minute ventilation: total volume of air entering (or leaving) lungs per minute
Ve = Vt x RR

alveolar ventillation: air entering (or leaving) alveoli per minute
Va = (Vt - Vd) x RR

differ on dead space

102
Q

formula for physiological dead space

A

Vd: Vt x ((PaCO2 x PeCO2)/PaCO2)

Taco, Paco, Peco, Paco

103
Q

what part of bone is usu affected in hematogenous osteomyelitis in children? why?

A

metaphysis: has slow-flowing sinusoidal vasculature that is conducive to microbial passage.

104
Q

progression of osteomyelitis

A

seeding event –> acute cellulitis of bone marrow. inflammation in confined boney space leads to increased intramedullarly pressure –> compromises blood flow and forces infectious exudate through vascular chanels into cortex & periosteal region (further compromises blood flow –> ischemia –> necrosis)

can progress to suppurative osteomyelitis (condition where necrotic bone [sequestrum] serves as reservoir for infection and becomes covered by poorly constructed shell of new bone [involcrum]

1+ sinus tracts develop to drain purlent material to soft tissue / out of skin surface

105
Q

how does flat bone (skull, sternum, pelvis) osteomyelitis often occur?

A

contiguous spread of infection (mastoiditis or dental abscess)

106
Q

most common site for hematogenous osteomyelitis in adults? children?

A

adult: vertebral body (location of pott’s disease, TB)
children: metaphysis of long bone.

(adults less likely to have osteomyelitis bc of changes due to epiphyseal closure)

107
Q

which drugs are metabolized by liver (i.e. affected by inducers / inhibitors)

A

warfarin, cyclosporine, tacrolimus, phenytoin, isoniazid, rifampin, oral hypoglycemics

108
Q

how do beta-blockers (i.e. timolol) help open-angle glaucoma?

A

reduce production of aqueous humor by ciliary epithelium

109
Q

what does schlemm’s canal drain into

A

drains into episcleral and conjunctival veins

110
Q

what drugs precipitate narrow angle glaucoma crisis?

A

anticholinergics (exacerbate small angle in posterior chamber) during mydriasis

111
Q

what drugs reduce aqueous humor production in the eye?

A

(1) nonselective beta blockers (like timolol)

(2) acetazolamide

112
Q

what drugs increase outflow of aqueous humor

A

(1) prostaglandin F2a (latanoprost, unoprostone, travoprost)

2) cholinomimetics (pilocarpine, carbachol

113
Q

latanoprost, unoprostone, travoprost

A

prostaglandin F2a. increase drainage of aqueous humor: glaucoma

114
Q

epinephrine & brimonidine for glaucoma

A

alpha-2 agonists: decreases aqueous humor secretion BUT causes mydriasis.

can use for open angle, but NOT closed angle glaucoma

115
Q

exonuclease vs. endonuclease

A

exonuclease: remove nucleotide from the END of a DNA molecule
endonuclease: cut DNA at very specific DNA sequences within molecule (i.e. restriction endonucleases)

116
Q

secondary structure (alpha helices & beta sheets) of amino acids dictated by..

A

hydrogen bonding

  • alpha, between every 4th AA
  • beta, between all residues of antiparallel strands)
117
Q

tertiary structures form what bonds

A

many; ionic, hydrophobic, hydrogen, disulfide

118
Q

what is the first step in the pathogenesis of atherosclerosis?

A

endothelial injury!

from HTN, hyperlipidemia, smoking, diabetes, homocysteine, toxins (inclu alcohol), viruses, immune rxn

119
Q

gallstone ileus

A

rare type of mechanical bowel obstruction, when a large gallstone (> 2.5cm) erodes into the intestinal lumen (via cholecystoenteric fistula)

eventually gets stuck in ileum: smallest lumen in intestinal tract

imaging: pneumobilia (air in billiary tree)

120
Q

GI causes of left pleural effusion

A

pancreatitis, esophageal rupture

121
Q

progression of irreversible neuronal injury? 12-48 hrs

A

“red neurons” – eosinophilic cytoplasm, pynkinotic nuclei, loss of nissl substance

122
Q

progression of irreversible neuronal injury? 24-72 hrs

A

necrosis & neutrophil invasion

123
Q

progression of irreversible neuronal injury? 3-5 days

A

macrophage infiltration and phagoytosis

124
Q

progression of irreversible neuronal injury? 1-2wks

A

reactive gliosis & vascular proliferation around necrotic area

macroscopic: see liquefactive necrosis: well demarcated soft area (1wk-1month)

125
Q

progression of irreversible neuronal injury > 2 wks

A

glial scar

macroscopic: cystic area surrounded by gliosis (>1 month)

126
Q

severe skin & subcutaneous fat necrosis soon after initiating warfarin?

A

related to early prothrombotic effects, as warfarin inhibits protein C early (shortest half-life), intitially pro-thrombotic

pronounced w/ high doses of warfarin & patients w/ preexisting protein C deficiency

127
Q

definition of polycythemia in men? women

A

hematocrit > 52% in men

>48% in women.

128
Q

differentiate between relative vs. absolute polycythemia?

A

measure RBC mass

129
Q

secondary erythrocytosis can be driven by what level of hypoxia?

A

SaO2 < 92% (PaO2 < 65 mmHg)

130
Q

‘classic’ phases of acid secretion within stomach

A

cephalic: ACh and vagal influence (thought sight, smell)
gastric: mediated by gastrin (which stimulates histamine, and therefore, acid secretion)
intestinal: when protein-containing food enters duodenum. THIS ACTUALLY DOWNREGULATES gastric acid secretion

131
Q

role of the intestinal phase in gastric acid secretion

A

presence of protein in duodenum actually downregulates acid secretion.

ileum and colon release peptide YY, bind to receptors on ECL cells, inhibits gastrin-stimulated histamine release.

132
Q

receptive relaxation

A

reflex that allows gastric fundus to dilate in anticipation of food passing through pharynx and esophagus.

133
Q

prostprandial alkaline tide

A

increase in plasma HCO3- and decrease in plasma Cl- secondary to surge of acid within gastric lumen.

does not play a role in downregulating post-prandial gastric secretion

134
Q

delusional disorder

A

presence of a NON-BIZARRE delusion for at least one month.

unlikely, but possible, like being followed, cheated, or poisoned (as opposed to covert alien activity)

usu single overriding delusion w/ preserved occupational and social functioning. does not meet diagnostic criteria for SZ

135
Q

paranoid personality vs. delusional disorder

A

paranoid personality disorder: pervasive pattern of suspiciousness vs. one fixed delusion (delusional disorder)

136
Q

coagulative necrosis

A

after ischemic injury in most tissue (except brain)

  • architecture PRESERVED after death (due to denaturation of lytic enzymes & disrupted proteolysis)
  • cell = ANUCLEATED w/ eosinophilic cytoplasm
  • leukocytes eventually infiltrate & digest
137
Q

liquefactive necrosis

A
  • seen w/ focal BACTERIAL infection that stimulate MASSIVE leukocyte recruitment
  • occurs in CNS infarcts due to LACK of substantive supporting STOMA.
  • necrotic cells completely digested by hydrolytic enzymes, forming VISCOUS LIQUID MASS
  • often creamy yellow due to dead leukocytes (PUS)
  • associated w/ ABSCESS formation in peripheral tissue. brain = CSF-FILLED SPACES
138
Q

fat necrosis

A

-acute pancreatitis

  • release of active pancreatic enzymes, included LIPASES, digest adipose cells & release free fatty acids
  • SAPONIFICATION (CHALKY-WHITE DEPOSITS) form when fatty acids combine w/ calcium.
139
Q

Caseous necrosis

A
  • most commonly withTB INFECTION
  • also w/ FUNGAL (histo, cryptococcus, coccidioides)
  • necrotic tissue = CHEESY TAN-WHITE gross appearance & consists of fragmented cells & acellular proteinaceous material.
  • surrounded by macrophages & other inflammatory cells, forming GRANULOMA
140
Q

TB in brain parenchyma

A

could cause CASEOUS NECROSIS (even though brain is often liquefactive necrosis)

141
Q

fibrinoid necrosis

A

histologic pattern of injury seen in walls of blood vessels affected by vasculitis syndromes (i.e. polyarteritis nodosa), malignant HTN, and diabetes mellitus

142
Q

nonenzymatic fat necrosis

A

following trauma, female breast = common example. often mistaken for breast tumor.

143
Q

gallbladder hypomotility? risk factors?

A

slow / incomplete gallbladder emptying in response to cholecystokinin stimulation

pregnancy, rapid weight loss, prolonged use of parenteral nutrition or ocreotide, high spinal cord injury.

144
Q

describe biliary sludge

A

consequence of gallbladder hypomotility. results from bile ppt.

contains cholesterol monohydrate crystals, calcium billirubinate, & mucus.

known precursor to stone

acute cholecystitis can occur in 20% of patients w/ biliary sludge.

145
Q

brown GB pigment stones

A

arise in cases of biliary tract infection

146
Q

black GB pigment stones

A

arise in causes of intravascular hemolysis

147
Q

cystinuria presents w/ defective transport of..

A

autosomal recessive
COLA

cysteine, ornithine, lysine, and arginine

148
Q

when does scarlet fever begin post group A strep infection? symptoms?

A

1-5 days

  • fever, malaise, abdominal pain, sore throat
  • “strawberry tongue” - inflammed red papillae
  • pharynx: erythematous, swollen, covered w/ gray-white exudate

after 1-2 days:

  • rash on neck, armpit, groin.
  • subsequently generalizes to rest of body

early:
- ‘boiled lobster’ appearance - scarlet spots / blotches
spread:
- “sandpaper-like” - sunburn w/ goose pimples

cheeks: flushed, giving area around mouth circumoral pallow.

end of 1st wk:
- desquamation in armpits, groin, tips of fingers, toes

predispose to glomerulonephritis / rheumatic fever

149
Q

differentiate kawasaki vs. scarlet fever

A

tonsilar exudate: scarlet fever

bilateral conjunctivitis: kawasaki

coronary aneursym: kawasaki

both have strawberry red tongue, desquamation

150
Q

3 different neuro manifestations of measles

A

acute: encephalitis
recovery: acute disseminated encephalomyelitis

years later: subacute sclerosing panencephalitis

151
Q

factor V leiden

A

DVT, cerebral vein thrombosis, recurrent pregnancy loss.

most common inherited thrombophilia.

hets have 5-10x risk of thrombosis
homoz have 50-100x risk

  • factor V has less susceptibility to protein C cleavage
  • factor V cannot support activated protein C activity

(increased coag, decreased anticoag)

152
Q

renal artery stenosis primary caused by (2)

A

atherosclerosis

fibromuscular disease

153
Q

where does malignant melanoma arise

A

typically skin.

can arise in: eye, esophagus, meninges, mucosal surfaces

risk factors: sun exposure, hereditary, history of pre-existent dysplastic nevus in same location.

154
Q

describe appearance of melanoma gross?

A

either asymptomatic or pruitic. -

  • usu > 1cm.
  • demonstrated change in color, size, shape.
  • variability in pigment: shades of black, brown, red, navy blue, gray
  • borders irregular/notched
155
Q

histology of melanoma?

A

congregate in poorly formed nests. large w/ irregular nuclei, clumped chromatin. prominent nucleoli.

156
Q

risk of melanoma metastasis

A

based on growth phase.

radial growth: remain superficial and extend horizontal within epidermis / superficial dermis. no risk of metastasis

vs.

melanoma w/ vertical growth – atypical immature cells travel down into deep dermal layeres – increase risk of mets.

157
Q

most important prognostic factor in malignant melanoma?

A

depth of invasion (breslow thickness)