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Flashcards in test #29 4.19 Deck (184)
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1
Q
what surface marker (cell type) is deficient in Bruton's X-linked agammaglobulimemia?
A
CD19 (no mature B cells in circulation)
2
Q
B cell markers
A
CD19, 20, 21
3
Q
CD15
A
neutrophil marker. also present in reed sternberg cells
4
Q
CD16
A
NK cells (and others)
5
Q
two types of abnormal ventilation during sleep
A
(1) apnea (cessation of breathing for >10 seconds)
(2) hypopnea (reduced airflow causing SaO2 to decrease >4%)
6
Q
obstructive sleep apnea
A
noturnal hypoventilation w/ a transient upper airway obstruction due to poor pharyngeal muscle tone

most common cause of excessive daytime sleepiness

exam: erythrocytosis, obesity, increased soft tissue in oropharynx

arterial blood gas in day: normal
7
Q
obesity hypoventilation syndrome (aka Pickwickian syndrome)
A
obesity impedes expansion of chest and abdominal wall during breathing.

increased respiratory work & decreased respiratory drive.

underventilation during all hours (chronically elevated PaCO2 and reduced PaO2)

arterial blood gas = abnormal
8
Q
differentiation obesity hypoventilation syndrome from sleep apnea?
A
sleep apnea: normal arterial blood gas in day time
9
Q
central sleep apnea
A
patient's central DRIVE to initiate breaths is absent.

neurological problem (not mechanical)
10
Q
tumor w/ fat, smooth muscle, blood vessel
A
angiomyolipoma (benign tumor)

associated w/ tuberous sclerosis
11
Q
tuberous sclerosis inheritance
A
autosomal DOMINANT
12
Q
tuberous sclerosis symptoms
A
HAMARTOMAS

- hamartomas in CNS and skin
- angiofibromas (face, adenoma sebaceum)
- mitral regurgitation
- angiomyolipoma (renal)
- tuberous sclerosis
- autosomal dOminant
- mental retardation
- ash-leaf patch (hypopigmented)
- shagreen patch (thick leathery, dimpled, organge

also: subependymal astrocytoma and ungual fibromas
13
Q
NF2
A
autosomal DOMINANT. bilateral acoustic neuromas.

also have multiple meningiomas, gliomas, ependymomas of spinal cord.
14
Q
cerebellar hemangiomas, retinal hemangiomas, liver cysts, bilateral renal cell carcinoma, pheochromocytoma
A
von-hippel-lindau
15
Q
sturge-weber syndrome
A
STURGE:

Somatic
Tram track Ca2+ opposite gyrus
Unilateral leptomeningeal angioma& port-wine stain
Retardation
GNAQ (activating mutation)
& Glaucoma (episcleral hemangioma)
Epilepsy

port-wine stain -- nonblanching in V1/V2 distribution

developmental anomaly of neural crest derivatives (mesoderm/ectoderm)
16
Q
hereditary hemorrhagic telangiectasia
A
Osler-Rendu-Weber syndrome

multiple tenangiectasia of skin & mucosa.

presentation is recurrent epistaxis or GI bleed (melena)
17
Q
how does B agonists (increased camp) increase contractility?
A
cAMP increases conductance of Ca2+ channels in SR.
18
Q
when patient takes exogenous glucocorticoids, worry about..

how is this prevented?
A
acute adrenal insufficiency (when used for 3+ wks)

prevent by tapering off treatment
19
Q
where does suppression occur when extended exogenous glucocortoids are taken?
A
the WHOLE axis: hypothalamic, pituitary, and adrenal!

low CRH, low ACTH, low cortisol!
20
Q
mutation in NF1
A
mutation in NF1, tumor suppressor that regulates Ras

autosomal dominant
21
Q
how does alcohol lead to pancreatitis?
A
obstruction via ductal concreations & direct parenchymal injury
22
Q
three types of damage in pancreatitis
A
(1) pancreatic autodigestion - proteases
(2) vascular damage & hemorrhage - elastase
(3) fat necrosis - lipase / phospholipase
23
Q
amylase makes..
A
hydrolyze starch into maltose (a glucose-glucose dissacharide), trisaccharide maltotriose, limit dextins
24
Q
17 alpha hydroxylase needed for (2)
A
(1) pregnenolone -> 17 hydroxypregnenolone
(2) progesterone -> 17 hydroxyprogesterone
25
Q
17 alpha hydroxlase deficiency on secondary sex characterestics
A
prevents in both males & females.

no menarche in females
26
Q
5-alpha reductase deficiency on secondary sex characteristics?
A
abnormal external genitalia development, but will have normal secondary sex (increased muscle mass and phallus enlargement) bc of testosterone

prostate and hair = DHT
27
Q
urine from umbilicus
A
persistant allantois remnant
28
Q
allantois becomes..
A
URACHUS
29
Q
urachus
A
duct between bladder (urogenital sinus) and yolk sac
30
Q
failure of urachus to obliterate results in..
A
1. patent urachus: umbilicus to bladder: pee from belly button
31
Q
vesicourachal diverticulum
A
failure to close part of urachus adjacent to bladder.

outpouching of apex of bladder. commonly asymptomatic.
32
Q
urachal sinus
A
failure to close distal part of urachus (adjacent to umbilicus)

periumbicilical tenderness & purulent discharge from umilicus due to persistent and recurrent infection.
33
Q
vitelline duct
A
omphalo-mesenteric duct connect yolksac to midgut lumen.

connect small intestine w/ skin at umbilicus
34
Q
failure of vitelline duct to obliterate
A
(1) vitelline fistula
(2) meckel diverticulum
35
Q
vitelline fistula
A
failure of vitillene duct to obliterate

meconium from umbillicus
36
Q
meckel's diverticlum
A
partial closure of vitilline duct. patent portion attached to ileum (true diverticulum)

ectopic gastric mucosa / pancreatic tissue --> melena, periumbilical pain, ulcers

rule of 2!
2 inches, 2 feet from ileocecal valve, 2% of population, 2 epithelial
37
Q
omphalocele
A
incomplete closure of anterior abdominal wall.

-- failure of abdominal contents to return to body cavity

presents as ventral opening at the umbilicus, protruding viscera covered by peritoneum

SEALED in peritoneum
38
Q
gastroschisis
A
inadequate enlargement of peritoneal cavity during fetal life.

viscera PROTRUDE through defect in anterior abdominal wall adjacent to umbilicus

NOT covered by peritoneum.
39
Q
closure of abdominal wall (rostral, lateral, caudal)
A
rostral fold: sternal defects
lateral: omphalocele, gastroschisis
caudal fold: bladder extrophy
40
Q
duodenal atresia results from..
A
failure to recanalize
41
Q
jejunal, ileal, colonic atresia results from...
A
vascular accident -- apple peel atresia
42
Q
midgut development
A
6th wk: midgut herniates through belly button

10th: return to abdominal cavity, rotates around SMA, 90 degree counter clockwise
43
Q
granules in whipple's disease
A
diastase-resistant granules in macrophages (lysosomes w/ partially digested bacteria)
44
Q
what medication can decrease formation of adenomatous polyp formation?
A
aspirin! cox-2 overexpression in colon mucosa help lead to adenocarcinoma in adenoma-to-carcinoma sequence
45
Q
adenoma to carcinoma sequence
A
AK53 & DCC
1. APC (b-catenin) --> AT RISK
(cox-2 overexpression & methylation increase too)
2. K-ras -->ADENOMA
3. p53 & DCC --> CARCINOMA
46
Q
how does APC mutation lead to at risk colon?
A
APC keeps beta-catenin low --> maintains intercellular adhesion
47
Q
FAP --> carcinoma always involves..
A
RECTUM (left, despite being an "exophytic mass'
48
Q
HNPCC --> carcinoma always involves
A
PROXIMAL COLON (right, despite not being exophytic)
49
Q
febuxostat
A
like allopurinol, inhibits xanthine oxidase
50
Q
probenicid
A
blocks reabsorption of uric acid.

so does HIGH dose of salicylates
51
Q
caspase
A
cysteine protease
52
Q
what two enzymes can act on fructose intracellularly
A
fructokinase (fructose 1-phosphate) and hexokinase (fructose 6-phosphate)
53
Q
where is fructose absorbed
A
proximal intestine, facilitative hexose transporter GLUT 5
54
Q
how is fructose metabolised in essential fructosuria?
A
absent fructokinase, cannot make fructose-1-phosphate. mostly loose in urine.

BUT small amount converted by hexokinase in liver into fructose-6-phosphate --> phosphoglucomutase turns it into --> glucose 6 phosphate.

can be used for glycogenesis, glycolysis, HMP, etc.
55
Q
aldolase B converts..
A
fructose 6-phosphate --> DHAP (dihydroxyacetone P) and glyceraldehyde

glyceraldehyde --> glyceraldehyde 3-phoshpate via triose kinase
56
Q
galactose metabolism
A
galactose --> galactose-1-phosphate
(via galactokinase)

galactose 1-phosphate --> glucose 1-phosohate
(via galacose-1-uridyltransferase, which also converts UDP-glucose --> UDP-galactose

UDP glucose is regenerated from UDP galactose with UDP-galactose-4-epimerase
57
Q
aldose reductase
A
[low affinity for glucose, only relevant when glucose is high]

converts glucose --> sorbitol.
also galactose --> galactitol

will accumulate if there is no sorbitol dehydrogenase to convert sorbitol ---> fructose
58
Q
which tissues (4) lack sorbitol dehydrogenase? what is the manifestations of this?
A
lens, schwann cells, retina, kidney.

glucose --> sorbitol via aldose reductase. sorbitol accumulates (can't convert to fructose).

has osmotic pull. results in..

cataracts, peripheral neuropathy, retinopathy, nephropathy (as seen in diabetes)
59
Q
acute interstitial pancreatitis vs. acute necrotic pancreatitis
A
acute interstitial: GROSS EDEMA: microscopic: calcifications. l

ipase digests adipose cells, form fatty acids that bind Ca2+ & ppt calcium salts.

if inflammation continues, trypsin activated, autodigestion of pancreas --

acute necrotic pancreatitis: GROSS CHALKY. destroy vessels --> white chalky fat necrosis. spread onto mesentery, omentum, other parts of abdominal cavity.
60
Q
mesenteric ischemia on gross
A
bowel is dusky red and congested. see subserosal ecchymoses, edema, defined necrosis

(probably related to arcades, mult sources of blood to bowel)
61
Q
calcification on bowel mesentary, omentum, etc
A
pancreatitis. lipase release free fatty acids, which bind Ca2+ and ppt calcium salts
62
Q
gastroesophageal mural injury: mallory-weiss vs. boerhaave syndrome?
A
both caused by forceful vomiting

mallory-weiss: MUCOSAL tear. submucosal arterial or venous plexus bleeding

boerhaave: esophageal TRANSMURAL tear. esophageal air/fluid leakage into mediastinum & pleura
63
Q
ethanol metabolism
A
in cytosol:
ethanol --> acetaldehyde
(alcohol dehydrogenase, makes NADH)

in mitochondria:
acetaldehyde --> acetate
(acetaldehyde dehydroganse, makes NADH)

overall increase in NADH/NAD+
64
Q
why does alcohol cause lactic acidosis?
A
high NADH/NAD+
need NAD+ for glycolysis, will regenerate AND+ via lactic acid production

pyruvate -> lactate
consume NADH --> NAD+
65
Q
why does alcohol cause steatosis in liver (2)?
A
high NADH/NAD+

1. glyceradehyde-3-phosphate --> glycerol-3-phosphate. combine w/ fatty acids --> triglycerides
2. high acetyl-CoA (due to inhibition of TCA) promotes lipogenesis

TCA inhibited bc oxaloacetate is converted to malate (to regenerate NAD+)
66
Q
what 4 metabolic pathways are affected by alcohol?
A
high NADH/NAD+

1. pyruvate -> lactate
(consumes NADH--> NAD+)
2. oxaloacetate -> malate
(consumes NADH --> NAD+)
3. glyceraldehyde-3-phosphate --> glycerol-3-phosphate
(combines w/ fatty acids to make triglyceride)

4. blocked TCA, build up acetyl-CoA, permits ketogenesis & lipogenesis
67
Q
supine hypotension syndrome
A
aortocaval compression syndrome

hypotension, pallor, sweating, nausea, dizziness

when preggers lady > 20wks lay on back
68
Q
inheritance of hemochromatosis
A
autosomal recessive
fairly common among northern europeans

intestinal absorption of iron
usu C282Y mutation on chr 6 in HFE gene
69
Q
symptoms of hemochromatosis (5)
A
1. micronodular cirrhosis
2. diabetes mellitus
3. skin pigmentation
4. testicular atrophy
6. CHF

increased risk of HCC

all related to DEPOSITS of Fe2+
70
Q
most common source of e. coli bacteremia
A
URINARY TRACT!

urosepsis risk: BPH, fecal incontinence, neurogenic bladder secondary to diabetes, frequent indwelling catheterization.
71
Q
why does mucor, rhizopus, absidia <3 diabetic ketoacidosis
A
have ketone reductase.

proliferate in vasculature, causes downstream tissue necrosis --> black eschar
72
Q
differentiate paranasal infxn w. aspergillus and mucor?
A
histology.
aspergillus: acute angle septate

mucor: broad angle, nonseptate
73
Q
diagnosis of allergic bronchopulmonary aspergillosis
A
SEROLOGICAL TESTING.

increased IgE and Ab to aspergillus fumigatus = diagnostic
74
Q
quadratus lumborum
A
muscle of posterior abdominal wall
75
Q
erector spinae
A
large group of back muscle. longitudinally along spinous processes. contraction = spine extension
76
Q
transversus abdominis (transversalis)
A
most internal component of anterior abdominal wall musculature. below inferior oblique
77
Q
ligamentum flava
A
paired elastic ligaments, connect vertebral laminae.

form posterior wall of spinal canal. help hold body erect.
78
Q
psoas major
A
anterior surface of transverse processes & lateral surface of vertebral bodies of T12-L5
79
Q
long delay between diet change and vitamin deficiency (~4yr) suggests..
A
cobalamin B12
(hepatic reserves last for up to several years)
80
Q
which vitamins present w/ deficiency rapidly
A
WATER SOLUBLE, quickly wash out of body (except B12 and folate -- have stores in liver)
81
Q
time frame of B12 and folate deficiency
A
B12: hepatic reserves last for years

folate: about 1/2 stored in liver, lasts 3-4 months.

folate deficiency faster
82
Q
storage of vitamin D (25-vitD)
A
in adipose tissue.

deficiency takes a few months
83
Q
vitamin A storage
A
90% stored in liver, perisinusoisal stellate (Ito cells)

last 6 months
84
Q
vitamin K storage
A
small amount in liver, lasts 1-3 weeks only.

heavily dependent on that made from large intestinal microbes
85
Q
diagnosis of hashimoto
A
usu (1)hypothyroidism, (2) high TSH, low T4/T3, and (3) anti-TPO antibody

can do biopsy: see intense mononuclear infiltration w/ lymphocytes and plasma cells. germinal centers.
86
Q
characterestics of papillary thyroid cancer (3)

tall variant?
A
MOST COMMON. GOOD PROGNOSIS.

(1) branching papillary structure
(2) psamomma bodies
(3) ground glass nucleus w/ intranuclear grooving "orphan annie eyes'

tall variant: follicular hyperplasia, lined by tall epithelial cells. older individuals, worse prognosis compared to well-differentiated papillary thyroid cancer.
87
Q
in thyroid; follicular hyperplasia lined by tall epithelial cells in older individual?
A
tall variant of papillary thyroid carcinoma. worse prognosis.
88
Q
mixed cellular infiltration w/ occasional multinuclear giant cells in thyroid
A
subacute thyroiditis or,
de Quervain thyroiditis or,
granulomatous thyroiditis
89
Q
presentation of subacute thyroiditis, de Quervain, granulomatous thyroiditis
A
painful tender thyroid. first thyroxoticosis, then hypothyroid

usu post-viral illness
90
Q
origin of Riedel's thyroiditis
A
IgG4-related systemic illness
91
Q
Riedel's thyroiditis vs. anaplastic carcinoma
A
both are firm, fixed, painless masses, but..

Riedel -- young female. anaplastic -- old people.
92
Q
rapid relief for rheumatoid arthritis
A
glucocorticoids

NSAIDs woud help too
93
Q
sulfasalazine, hydroxychloroquine, minocycline in rheumatoid arthritis
A
used to treat mild, early, seronegative rheumatoid arthritis.

do NOT have anti-inflammatory.

effects work as immune modulators (disease modifying)
94
Q
colchicine
A
NOT used in rheumatoid arthritis.

binds to tubulin and inhibts MT polymerization of neutrophils. reduce inflammatory response to uric acid crystals
95
Q
rx for acute gout:
A
NSAID, glucocorticoids (short-term only), colchine
96
Q
rx for chronic gout:
A
allopurinol, febuxostat, probenicid, also colchine
97
Q
mechanism of pain in migraines
A
(1) trigeminal afferents to meninges activated
(2) release substance P and CGRP (calcitonin gene related peptide)
(3) causes neurogenic inflammation --> vasodilation and plasma protein extravasation
98
Q
sumatriptan for cluster headache and migraines
A
agonist of 5-HT 1B/1D on post-synaptic vasculature & presynaptic trigeminal neuron. inhibit release of vasoactive peptides. blocks vasodilation.

ABORTIVE.

contraindicated in prinzmetal angina and CAD bc can cause coronary vasospasm
99
Q
buprprion activity
A
NDRI and nicotine agonist
100
Q
which drugs block presynaptic reuptake of 5-HT and NE?
A
(1) TCA
(2) SNRI (venlafaxine and duloxetine)

note: TCA also have..
(1) anti-alpha adrenergic
(2) anti-muscarinic
(3) anti-H1 histamine
101
Q
SNRI used for? specific extra use of each>
A
rx: depression.
venlafaxine also: generalized anxiety disorder & panic
duloxetine: also peripheral diabetic neuropathy
102
Q
drugs used for migraine prophylaxis
A
b-blockers
antidepressants (TCA and SNRI)
anticonvulsants (valproate and topiramate)b
103
Q
didanosine
A
nucleoside reverse transcription inhibitor.

side effect: pancreatitis
104
Q
ganciclovir toxicity
A
interfere w/ human host cell DNA synthesis
105
Q
zidovudine toxicity
A
inhibit mammalian cellular and mitochondria DNA polymerases

bone marrow suppression (anemia, granulocytopenia)
106
Q
common side effect in non-nucleotide reverse transcriptase inhibitors (nnRTIs: efavirenz, nevirapine, delaviridine)

specific ones?
A
rash and hepatotoxicity

efavirenz: vivid dreams and CNS

delaviridine and efavirenz contraindicated in pregnancy
107
Q
rx for reducing risk of fetal transmission of HIV?
A
zidovudine
108
Q
common side effect of nucleotide reverse transcriptase inhibits (nRTIs)
A
bone marrow suppression (reverse with G-CSF and EPO)

peripheral neuropathy, lactic acidosis (nucleosides)

anemia: zidovidine

didanosine: pancreatitis
109
Q
what is more toxic: acyclovir or gancyclovir?
A
gancyclovir
110
Q
toxicity with gancyclovir
A
bone marrow suppression & renal toxicity
111
Q
toxicity with acyclovir
A
obstructive crystalline nephropathy & acute renal failure
112
Q
foscarnet toxicity
A
nephropathy, results in electrolyte abnormalities: hypocalcemia, hypokalemia, hypomagnesemia, hypophosphatemia
113
Q
cidofovir toxicity
A
nephrotoxic! give w/ probenecid and IV saline to reduce toxicity
114
Q
nonselective beta and alpha blockers
A
carvedilol and labetalol (modified endings)
115
Q
nebivolol
A
combines cardioselective B1 blockage w/ stimulation of B3 (activates NO synthase in vasculature)
116
Q
short acting benzo (<10hr)
A
MOAT

midazolan, oxazepam, alprazolam, triazolam
117
Q
medium acting benzo (10-20)
A
LET

lorazepam, estazolam, temazepam
118
Q
long acting benzo (days)
A
chlordiazepoxide, clorazepate, diazepam, flurazepam
119
Q
choosing duration of a benzo?
A
long-acting: more severe drowsiness, but less addicting/dependent

older people: short acting or they will fall
drug addict: long acting, or they will get addicted!
120
Q
association between risk of dependence and rate of clearance.
A
directly proportional.

rate of clearance high, more dependence
121
Q
association between duration of action and withdrawal symptoms
A
shorter duration of action, more likely withdrawal symptoms will occur
122
Q
short acting benzo vs. zolpidem
A
short acting benzo = addictive.

zolpidem = rapid onset of action & short half-life, but LOW POTENTIAL for tolerance and dependence
123
Q
normal P50 (partial pressure of oxygen at which hemoglobin is 50% saturated)
A
26mmHg.

shifted to lower numbers in lungs (LEFT = lungs)

shifted to higher numbers in tissue (RIGHT = tissue)
124
Q
oxygen dissociation curve for sickle cell
A
shifted to RIGHT (easier to release oxygen)
125
Q
subperiosteal thinning w/ cystic degeneration filled with brown fibrous tissue?
A
hyperparathyroidism! usu cortical bones
126
Q
excessive osteoid matrix accumulation around trabeculae. and widening between osteoid seems

(as measured by bone histomorphometry and double tetracycline labeling)
A
vitamin D deficiency
127
Q
trabecular thinning w/ few interconnections
A
osteoperosis
128
Q
lamellar bone structure resembling mosaic?
A
paget's disease of bone
129
Q
spongiosa filling medullar canal with no mature trabeculae
A
osteopetrosis
130
Q
after vitamin D is absorbed from GI tract or skin..
A
must be activated by LIVER and KIDNEY
131
Q
genu varus, rachitic rosary, harrison's sulci, craniotabes, growth retardation
A
vitamin D deficiency

-genu varus: bowed legs
-rachitic rosary: bony prominence at costochondral junction
-Harrison's sulci: indentations in lower ribs
-craniotabes: softening of skull
132
Q
strong neutrophil chemotactic agents
A
leukotriene B4, C5a, 5-HETE
133
Q
3 fates of arachodonic acid
A
(1) cox 1-2: prostacyclin, prostaglandin, thromboxane

(2) 5-lipooxygenase: leukotrienes

(3) 12-lipooxygenase:
lipoxin
134
Q
fxn of lipoxins
A
made from arachadonic acid via 12-lipooxygenase

lipoxin A4 and B4
1. vasodilate
2. inhibit neutrophil chemotaxis
3. stimulate monocyte adhesion
135
Q
LTC4, LTD4, LTE4
A
made from arachadonic acid via 5-lipooxygenase

1. increased bronchial tone
2. vasoconstriction
3. increased permeability

think: constrict everything
136
Q
LTB4 & 5-HETE
A
neutrophil chemotaxis
137
Q
prostacyclin (PGI2)
A
made from arachadonic acid via cyclooxygenase (PGH2 intermediate)

1. inhibit platelet aggregation
2. vasodilate
3. reduce bronchial tone
4. reduce uterine tone
5. increases permeability

relaxes everything
138
Q
prostaglandins (PGD2, PGE2, PGF2a)
A
made from arachadonic acid via cyclooxygenase

1. vasodilate
2. increase permeability
3. increase uterine tone
4. reduce bronchial tone
139
Q
main difference between prostacyclin and prostaglandins?
A
prostaglandin (PGD2, PGE2, PGF2) INCREASE uterine tone

prostacyclin reduces uterine tone and reduces platelet aggregation
140
Q
misoprostol
A
PGE1 analogue. used to increase production of gastric mucosa & decrease acid production.

also an abortifactant, increases uterine tone
141
Q
thromboxane
A
made from arachodonic acid via cyclooxygenase

counteracts prostacyclin (PGI2)

(1) increases platelet aggregating
(2) vasoconstriction
(3) increases bronchial tone

'increases everything'
142
Q
important neutrophil chemoattractants (6)
A
5-HETE
LTB4
C5a
IL-8
PAF
kallikrein
143
Q
bradykinin on vasculature
A
- vasodilation
- increases vascular permeability
- stimulates muscular contraction
- mediates pain
144
Q
initial concern w/ given ACE inhibitors?
A
hypotension, esp if using a diuretic, hyponatremic, renal impairment

esp worry if taking a thiazide!

reduce venous return, secondary to decrease in angiotensin II levels

can activate Bezold-Jarisch reflec: vagally mediated hypotension and bradycardia
145
Q
don't combined ACE with.. (2)
A
1. beta blockers, won't help much

2. thiazides, will give too much hypotension
146
Q
three exposures related to liver angiosarcoma
A
- arsenic (pesticides)
- thorotrast (radioactive contrast)
- polyvinyl chloride
147
Q
angiosarcoma on stain
A
CD31+, PECAM, impt for leukocyte extravasation
148
Q
QT interval encompasses
A
start of QRS and end of T wave
149
Q
inherited long QT? predisposed to
A
- K+ channel
- predisposed to torsades de pointes

(1) romano-warD
autosomal Dominant
no deafness

(2) lange-jervell-nielsen
autosomal recessive
sensorineural deafness
150
Q
mutations in cardiac cell cytoskeleton & mitochondrial enzymes of oxidative phosphorylation related to..
A
inherited dilated cardiomyopathy
151
Q
progressive fibrofatty replacement of right ventricular myocardium
A
arrhythmogenic right ventricular cardiomyopathy -- mutation in calcium-binding sarcoplasmic reticulum protein
152
Q
follicular carcinoma on histology
A
sheets of follicular cells or large cells w/ eosinophilic cytoplasm (hurthle)

adenoma: no capsular / vascular invasion
carcinoma: capsular / vascular invasion
153
Q
urease test
A
H. pylori

give isotopic urea.

H. pylori converts urea into CO2 and ammonia. isotpically labelled CO2 absorbed in blood and exhaled. measured 30min later.
154
Q
distinguish ARDS from cardiogenic pulmonary edema?
A
pulmonary capillary wedge
155
Q
histology: extreme myofiber disarray w/ interstitial fibrosis
A
hypertrophic cardiomyopathy
156
Q
immunity to hepB indicated by
A
Anti-Hbs (HbsAb)
157
Q
HbsAg
A
- detectable during acute infection
- persistence after 6 months -- chronic infection
158
Q
anti-HBc IgM vs IgG
A
IgM:
- present acute infection & window phase when HbsAg and HbsAb absent

IgG:
- detectable w/ HbsAb & HbeAb after recovery
- present w/o HbsAb in chronic infxn
-not present after vaccination
159
Q
window period in hep B
A
no HbsAg or HbsAb.
can have HbcAb IgM
160
Q
HBeAg
A
another component of core
- appears AFTER HBsAg
- marker for viral replication activity
- detetable in chronic infectoin
161
Q
HBeAb
A
present after recovery from acute infection
- HBeAg/anti-HBe seroconversion indicates transition of chronic infection from high to low viral replication & infectivity
162
Q
hepatitis B infection presentation
A
- long asymptomatic incubation period (6-8 wks)
- acute disease, lasting several week to months
163
Q
when does HBsAg appear in blood? when does it peak?
A
appear in blood: before symptom onset

peak: when patient is most ill

undetectable in 3-6 months
164
Q
markers for active viral replication (hep B)? what else rises in this time
A
HBeAg and HBV DNA in serum. rises shortly after HBsAg comes in.

also increase in anti-HBc IgM and serum transaminases [shortly after symptoms arise]
165
Q
exacerbation of chronic hepatitis B?
A
abrupt increase in liver enzyme, increased levels of HBV DNA.

exacerbation frequently occurs w/ HbeAg seroconversion & accompanying transition from high infectivity to low infectivity.
166
Q
acute hepatitis that has progressed to chronic hepatitis w/ low infectivity
A
HbsAg (>6 months), HbeAb, HbcAb

no HbeAg, no HbsAb
167
Q
acute hepatitis that has progressed to chronic hepatitis w/ high infectivity
A
HbsAg (>6 months), HbeAb, HBV DNA

no HbeAb, no HBsAb
168
Q
vaccinated against Hep B? resolved HepB?
A
vaccine: HbsAb, no anything else

resolved hepB: HbsAb, HbcAb
169
Q
inguinal hernia vs. direct hernia
A
inguinal hernia: failure of processus vaginalis to oliterate, travels through indirect inguinal. out of external inguinal canal, scrotum

external hernia: weakness in abdominal wall (hesselbach's triangle, between rectus abominus, inferior epigastric, inguinal ligament). come out near external inguinal ring. NOT in scrotum bc has no passage (no processus vaginalis)
170
Q
hernia in scrotum? hernia above inguinal ligament? hernia below inguinal ligament?
A
in scrotum: indirect inguinal

above inguinal ligament: direct

below inguinal ligament: femoral
171
Q
hernias relative to inferior epigastrics
A
indirect: lateral.
direct: medial
172
Q
deep inguinal nodes receives drainage from?
A
reside under fascia lata, medial side of femoral vein.

glans penis // clitoris & superficial nodes
173
Q
superficial inguinal nodes receives drainage from?
A
scrotum & all cutaneous structures inferior to umbillicus. including genitalia and anus up to pectinate line
174
Q
testes drain to? scrotum? glans penis?
A
testes: para-aortic nodes.
scrotum: superficial inguinal nodes --> deep
glans penis --> deep inguinal nodes
175
Q
specific iron deficiency signs (anemia)
A
dysphagia, spoon nails or koilonychia (disfigured finger nails)
176
Q
filgastrim
A
G-CSF
177
Q
what help w/ iron absorption
A
vitamin C, reduces it to Fe2+ state
178
Q
factor V leiden
A
resistant to cleavage by protein C -- thrombophilia
179
Q
antiphospholipid presents with (3) abnormal lab finding?
A
1. venous thromboembolism
2. arterial thromboembolism
3. frequent fetal loss

LONG aPTT
180
Q
most common cause of long PTT?
A
lupus anticoagulant
181
Q
why is folic acid deficiency --> prothrombotic?
A
hyperhomocysteinemia
182
Q
lipofuscin is composed of..
A
product of lipid peroxidation.

lipid polymers and protein-complexed phospholipids.

'wear & tear'

seen in heart & liver of aging or cachectic, malnourished patients.
183
Q
mediators of cachexia?
A
TNF-alpha!!!!

also: IFN-gamma, IL-6
184
Q
chromogranin + lung cancer?
A
small cell carcinoma!

also: neuron specific enolase, synaptophysin. secretory granules on EM