test #29 4.19 Flashcards

1
Q

what surface marker (cell type) is deficient in Bruton’s X-linked agammaglobulimemia?

A

CD19 (no mature B cells in circulation)

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2
Q

B cell markers

A

CD19, 20, 21

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3
Q

CD15

A

neutrophil marker. also present in reed sternberg cells

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4
Q

CD16

A

NK cells (and others)

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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%

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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

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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

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8
Q

differentiation obesity hypoventilation syndrome from sleep apnea?

A

sleep apnea: normal arterial blood gas in day time

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9
Q

central sleep apnea

A

patient’s central DRIVE to initiate breaths is absent.

neurological problem (not mechanical)

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10
Q

tumor w/ fat, smooth muscle, blood vessel

A

angiomyolipoma (benign tumor)

associated w/ tuberous sclerosis

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11
Q

tuberous sclerosis inheritance

A

autosomal DOMINANT

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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

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13
Q

NF2

A

autosomal DOMINANT. bilateral acoustic neuromas.

also have multiple meningiomas, gliomas, ependymomas of spinal cord.

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14
Q

cerebellar hemangiomas, retinal hemangiomas, liver cysts, bilateral renal cell carcinoma, pheochromocytoma

A

von-hippel-lindau

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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)

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16
Q

hereditary hemorrhagic telangiectasia

A

Osler-Rendu-Weber syndrome

multiple tenangiectasia of skin & mucosa.

presentation is recurrent epistaxis or GI bleed (melena)

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17
Q

how does B agonists (increased camp) increase contractility?

A

cAMP increases conductance of Ca2+ channels in SR.

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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

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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!

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20
Q

mutation in NF1

A

mutation in NF1, tumor suppressor that regulates Ras

autosomal dominant

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21
Q

how does alcohol lead to pancreatitis?

A

obstruction via ductal concreations & direct parenchymal injury

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22
Q

three types of damage in pancreatitis

A

(1) pancreatic autodigestion - proteases
(2) vascular damage & hemorrhage - elastase
(3) fat necrosis - lipase / phospholipase

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23
Q

amylase makes..

A

hydrolyze starch into maltose (a glucose-glucose dissacharide), trisaccharide maltotriose, limit dextins

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24
Q

17 alpha hydroxylase needed for (2)

A

(1) pregnenolone -> 17 hydroxypregnenolone

(2) progesterone -> 17 hydroxyprogesterone

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25
17 alpha hydroxlase deficiency on secondary sex characterestics
prevents in both males & females. no menarche in females
26
5-alpha reductase deficiency on secondary sex characteristics?
abnormal external genitalia development, but will have normal secondary sex (increased muscle mass and phallus enlargement) bc of testosterone prostate and hair = DHT
27
urine from umbilicus
persistant allantois remnant
28
allantois becomes..
URACHUS
29
urachus
duct between bladder (urogenital sinus) and yolk sac
30
failure of urachus to obliterate results in..
1. patent urachus: umbilicus to bladder: pee from belly button
31
vesicourachal diverticulum
failure to close part of urachus adjacent to bladder. outpouching of apex of bladder. commonly asymptomatic.
32
urachal sinus
failure to close distal part of urachus (adjacent to umbilicus) periumbicilical tenderness & purulent discharge from umilicus due to persistent and recurrent infection.
33
vitelline duct
omphalo-mesenteric duct connect yolksac to midgut lumen. connect small intestine w/ skin at umbilicus
34
failure of vitelline duct to obliterate
(1) vitelline fistula | (2) meckel diverticulum
35
vitelline fistula
failure of vitillene duct to obliterate meconium from umbillicus
36
meckel's diverticlum
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
omphalocele
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
gastroschisis
inadequate enlargement of peritoneal cavity during fetal life. viscera PROTRUDE through defect in anterior abdominal wall adjacent to umbilicus NOT covered by peritoneum.
39
closure of abdominal wall (rostral, lateral, caudal)
rostral fold: sternal defects lateral: omphalocele, gastroschisis caudal fold: bladder extrophy
40
duodenal atresia results from..
failure to recanalize
41
jejunal, ileal, colonic atresia results from...
vascular accident -- apple peel atresia
42
midgut development
6th wk: midgut herniates through belly button 10th: return to abdominal cavity, rotates around SMA, 90 degree counter clockwise
43
granules in whipple's disease
diastase-resistant granules in macrophages (lysosomes w/ partially digested bacteria)
44
what medication can decrease formation of adenomatous polyp formation?
aspirin! cox-2 overexpression in colon mucosa help lead to adenocarcinoma in adenoma-to-carcinoma sequence
45
adenoma to carcinoma sequence
``` AK53 & DCC 1. APC (b-catenin) --> AT RISK (cox-2 overexpression & methylation increase too) 2. K-ras -->ADENOMA 3. p53 & DCC --> CARCINOMA ```
46
how does APC mutation lead to at risk colon?
APC keeps beta-catenin low --> maintains intercellular adhesion
47
FAP --> carcinoma always involves..
RECTUM (left, despite being an "exophytic mass'
48
HNPCC --> carcinoma always involves
PROXIMAL COLON (right, despite not being exophytic)
49
febuxostat
like allopurinol, inhibits xanthine oxidase
50
probenicid
blocks reabsorption of uric acid. so does HIGH dose of salicylates
51
caspase
cysteine protease
52
what two enzymes can act on fructose intracellularly
fructokinase (fructose 1-phosphate) and hexokinase (fructose 6-phosphate)
53
where is fructose absorbed
proximal intestine, facilitative hexose transporter GLUT 5
54
how is fructose metabolised in essential fructosuria?
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
aldolase B converts..
fructose 6-phosphate --> DHAP (dihydroxyacetone P) and glyceraldehyde glyceraldehyde --> glyceraldehyde 3-phoshpate via triose kinase
56
galactose metabolism
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
aldose reductase
[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
which tissues (4) lack sorbitol dehydrogenase? what is the manifestations of this?
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
acute interstitial pancreatitis vs. acute necrotic pancreatitis
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
mesenteric ischemia on gross
bowel is dusky red and congested. see subserosal ecchymoses, edema, defined necrosis (probably related to arcades, mult sources of blood to bowel)
61
calcification on bowel mesentary, omentum, etc
pancreatitis. lipase release free fatty acids, which bind Ca2+ and ppt calcium salts
62
gastroesophageal mural injury: mallory-weiss vs. boerhaave syndrome?
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
ethanol metabolism
in cytosol: ethanol --> acetaldehyde (alcohol dehydrogenase, makes NADH) in mitochondria: acetaldehyde --> acetate (acetaldehyde dehydroganse, makes NADH) overall increase in NADH/NAD+
64
why does alcohol cause lactic acidosis?
high NADH/NAD+ need NAD+ for glycolysis, will regenerate AND+ via lactic acid production pyruvate -> lactate consume NADH --> NAD+
65
why does alcohol cause steatosis in liver (2)?
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
what 4 metabolic pathways are affected by alcohol?
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
supine hypotension syndrome
aortocaval compression syndrome hypotension, pallor, sweating, nausea, dizziness when preggers lady > 20wks lay on back
68
inheritance of hemochromatosis
autosomal recessive fairly common among northern europeans intestinal absorption of iron usu C282Y mutation on chr 6 in HFE gene
69
symptoms of hemochromatosis (5)
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
most common source of e. coli bacteremia
URINARY TRACT! urosepsis risk: BPH, fecal incontinence, neurogenic bladder secondary to diabetes, frequent indwelling catheterization.
71
why does mucor, rhizopus, absidia <3 diabetic ketoacidosis
have ketone reductase. proliferate in vasculature, causes downstream tissue necrosis --> black eschar
72
differentiate paranasal infxn w. aspergillus and mucor?
histology. aspergillus: acute angle septate mucor: broad angle, nonseptate
73
diagnosis of allergic bronchopulmonary aspergillosis
SEROLOGICAL TESTING. increased IgE and Ab to aspergillus fumigatus = diagnostic
74
quadratus lumborum
muscle of posterior abdominal wall
75
erector spinae
large group of back muscle. longitudinally along spinous processes. contraction = spine extension
76
transversus abdominis (transversalis)
most internal component of anterior abdominal wall musculature. below inferior oblique
77
ligamentum flava
paired elastic ligaments, connect vertebral laminae. form posterior wall of spinal canal. help hold body erect.
78
psoas major
anterior surface of transverse processes & lateral surface of vertebral bodies of T12-L5
79
long delay between diet change and vitamin deficiency (~4yr) suggests..
cobalamin B12 | hepatic reserves last for up to several years
80
which vitamins present w/ deficiency rapidly
WATER SOLUBLE, quickly wash out of body (except B12 and folate -- have stores in liver)
81
time frame of B12 and folate deficiency
B12: hepatic reserves last for years folate: about 1/2 stored in liver, lasts 3-4 months. folate deficiency faster
82
storage of vitamin D (25-vitD)
in adipose tissue. deficiency takes a few months
83
vitamin A storage
90% stored in liver, perisinusoisal stellate (Ito cells) last 6 months
84
vitamin K storage
small amount in liver, lasts 1-3 weeks only. heavily dependent on that made from large intestinal microbes
85
diagnosis of hashimoto
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
characterestics of papillary thyroid cancer (3) tall variant?
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
in thyroid; follicular hyperplasia lined by tall epithelial cells in older individual?
tall variant of papillary thyroid carcinoma. worse prognosis.
88
mixed cellular infiltration w/ occasional multinuclear giant cells in thyroid
subacute thyroiditis or, de Quervain thyroiditis or, granulomatous thyroiditis
89
presentation of subacute thyroiditis, de Quervain, granulomatous thyroiditis
painful tender thyroid. first thyroxoticosis, then hypothyroid usu post-viral illness
90
origin of Riedel's thyroiditis
IgG4-related systemic illness
91
Riedel's thyroiditis vs. anaplastic carcinoma
both are firm, fixed, painless masses, but.. Riedel -- young female. anaplastic -- old people.
92
rapid relief for rheumatoid arthritis
glucocorticoids NSAIDs woud help too
93
sulfasalazine, hydroxychloroquine, minocycline in rheumatoid arthritis
used to treat mild, early, seronegative rheumatoid arthritis. do NOT have anti-inflammatory. effects work as immune modulators (disease modifying)
94
colchicine
NOT used in rheumatoid arthritis. binds to tubulin and inhibts MT polymerization of neutrophils. reduce inflammatory response to uric acid crystals
95
rx for acute gout:
NSAID, glucocorticoids (short-term only), colchine
96
rx for chronic gout:
allopurinol, febuxostat, probenicid, also colchine
97
mechanism of pain in migraines
(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
sumatriptan for cluster headache and migraines
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
buprprion activity
NDRI and nicotine agonist
100
which drugs block presynaptic reuptake of 5-HT and NE?
(1) TCA (2) SNRI (venlafaxine and duloxetine) note: TCA also have.. (1) anti-alpha adrenergic (2) anti-muscarinic (3) anti-H1 histamine
101
SNRI used for? specific extra use of each>
rx: depression. venlafaxine also: generalized anxiety disorder & panic duloxetine: also peripheral diabetic neuropathy
102
drugs used for migraine prophylaxis
b-blockers antidepressants (TCA and SNRI) anticonvulsants (valproate and topiramate)b
103
didanosine
nucleoside reverse transcription inhibitor. side effect: pancreatitis
104
ganciclovir toxicity
interfere w/ human host cell DNA synthesis
105
zidovudine toxicity
inhibit mammalian cellular and mitochondria DNA polymerases bone marrow suppression (anemia, granulocytopenia)
106
common side effect in non-nucleotide reverse transcriptase inhibitors (nnRTIs: efavirenz, nevirapine, delaviridine) specific ones?
rash and hepatotoxicity efavirenz: vivid dreams and CNS delaviridine and efavirenz contraindicated in pregnancy
107
rx for reducing risk of fetal transmission of HIV?
zidovudine
108
common side effect of nucleotide reverse transcriptase inhibits (nRTIs)
bone marrow suppression (reverse with G-CSF and EPO) peripheral neuropathy, lactic acidosis (nucleosides) anemia: zidovidine didanosine: pancreatitis
109
what is more toxic: acyclovir or gancyclovir?
gancyclovir
110
toxicity with gancyclovir
bone marrow suppression & renal toxicity
111
toxicity with acyclovir
obstructive crystalline nephropathy & acute renal failure
112
foscarnet toxicity
nephropathy, results in electrolyte abnormalities: hypocalcemia, hypokalemia, hypomagnesemia, hypophosphatemia
113
cidofovir toxicity
nephrotoxic! give w/ probenecid and IV saline to reduce toxicity
114
nonselective beta and alpha blockers
carvedilol and labetalol (modified endings)
115
nebivolol
combines cardioselective B1 blockage w/ stimulation of B3 (activates NO synthase in vasculature)
116
short acting benzo (<10hr)
MOAT midazolan, oxazepam, alprazolam, triazolam
117
medium acting benzo (10-20)
LET lorazepam, estazolam, temazepam
118
long acting benzo (days)
chlordiazepoxide, clorazepate, diazepam, flurazepam
119
choosing duration of a benzo?
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
association between risk of dependence and rate of clearance.
directly proportional. rate of clearance high, more dependence
121
association between duration of action and withdrawal symptoms
shorter duration of action, more likely withdrawal symptoms will occur
122
short acting benzo vs. zolpidem
short acting benzo = addictive. zolpidem = rapid onset of action & short half-life, but LOW POTENTIAL for tolerance and dependence
123
normal P50 (partial pressure of oxygen at which hemoglobin is 50% saturated)
26mmHg. shifted to lower numbers in lungs (LEFT = lungs) shifted to higher numbers in tissue (RIGHT = tissue)
124
oxygen dissociation curve for sickle cell
shifted to RIGHT (easier to release oxygen)
125
subperiosteal thinning w/ cystic degeneration filled with brown fibrous tissue?
hyperparathyroidism! usu cortical bones
126
excessive osteoid matrix accumulation around trabeculae. and widening between osteoid seems (as measured by bone histomorphometry and double tetracycline labeling)
vitamin D deficiency
127
trabecular thinning w/ few interconnections
osteoperosis
128
lamellar bone structure resembling mosaic?
paget's disease of bone
129
spongiosa filling medullar canal with no mature trabeculae
osteopetrosis
130
after vitamin D is absorbed from GI tract or skin..
must be activated by LIVER and KIDNEY
131
genu varus, rachitic rosary, harrison's sulci, craniotabes, growth retardation
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
strong neutrophil chemotactic agents
leukotriene B4, C5a, 5-HETE
133
3 fates of arachodonic acid
(1) cox 1-2: prostacyclin, prostaglandin, thromboxane (2) 5-lipooxygenase: leukotrienes (3) 12-lipooxygenase: lipoxin
134
fxn of lipoxins
made from arachadonic acid via 12-lipooxygenase lipoxin A4 and B4 1. vasodilate 2. inhibit neutrophil chemotaxis 3. stimulate monocyte adhesion
135
LTC4, LTD4, LTE4
made from arachadonic acid via 5-lipooxygenase 1. increased bronchial tone 2. vasoconstriction 3. increased permeability think: constrict everything
136
LTB4 & 5-HETE
neutrophil chemotaxis
137
prostacyclin (PGI2)
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
prostaglandins (PGD2, PGE2, PGF2a)
made from arachadonic acid via cyclooxygenase 1. vasodilate 2. increase permeability 3. increase uterine tone 4. reduce bronchial tone
139
main difference between prostacyclin and prostaglandins?
prostaglandin (PGD2, PGE2, PGF2) INCREASE uterine tone prostacyclin reduces uterine tone and reduces platelet aggregation
140
misoprostol
PGE1 analogue. used to increase production of gastric mucosa & decrease acid production. also an abortifactant, increases uterine tone
141
thromboxane
made from arachodonic acid via cyclooxygenase counteracts prostacyclin (PGI2) (1) increases platelet aggregating (2) vasoconstriction (3) increases bronchial tone 'increases everything'
142
important neutrophil chemoattractants (6)
``` 5-HETE LTB4 C5a IL-8 PAF kallikrein ```
143
bradykinin on vasculature
- vasodilation - increases vascular permeability - stimulates muscular contraction - mediates pain
144
initial concern w/ given ACE inhibitors?
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
don't combined ACE with.. (2)
1. beta blockers, won't help much | 2. thiazides, will give too much hypotension
146
three exposures related to liver angiosarcoma
- arsenic (pesticides) - thorotrast (radioactive contrast) - polyvinyl chloride
147
angiosarcoma on stain
CD31+, PECAM, impt for leukocyte extravasation
148
QT interval encompasses
start of QRS and end of T wave
149
inherited long QT? predisposed to
- K+ channel - predisposed to torsades de pointes (1) romano-warD autosomal Dominant no deafness (2) lange-jervell-nielsen autosomal recessive sensorineural deafness
150
mutations in cardiac cell cytoskeleton & mitochondrial enzymes of oxidative phosphorylation related to..
inherited dilated cardiomyopathy
151
progressive fibrofatty replacement of right ventricular myocardium
arrhythmogenic right ventricular cardiomyopathy -- mutation in calcium-binding sarcoplasmic reticulum protein
152
follicular carcinoma on histology
sheets of follicular cells or large cells w/ eosinophilic cytoplasm (hurthle) adenoma: no capsular / vascular invasion carcinoma: capsular / vascular invasion
153
urease test
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
distinguish ARDS from cardiogenic pulmonary edema?
pulmonary capillary wedge
155
histology: extreme myofiber disarray w/ interstitial fibrosis
hypertrophic cardiomyopathy
156
immunity to hepB indicated by
Anti-Hbs (HbsAb)
157
HbsAg
- detectable during acute infection | - persistence after 6 months -- chronic infection
158
anti-HBc IgM vs IgG
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
window period in hep B
no HbsAg or HbsAb. | can have HbcAb IgM
160
HBeAg
another component of core - appears AFTER HBsAg - marker for viral replication activity - detetable in chronic infectoin
161
HBeAb
present after recovery from acute infection - HBeAg/anti-HBe seroconversion indicates transition of chronic infection from high to low viral replication & infectivity
162
hepatitis B infection presentation
- long asymptomatic incubation period (6-8 wks) | - acute disease, lasting several week to months
163
when does HBsAg appear in blood? when does it peak?
appear in blood: before symptom onset peak: when patient is most ill undetectable in 3-6 months
164
markers for active viral replication (hep B)? what else rises in this time
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
exacerbation of chronic hepatitis B?
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
acute hepatitis that has progressed to chronic hepatitis w/ low infectivity
HbsAg (>6 months), HbeAb, HbcAb no HbeAg, no HbsAb
167
acute hepatitis that has progressed to chronic hepatitis w/ high infectivity
HbsAg (>6 months), HbeAb, HBV DNA no HbeAb, no HBsAb
168
vaccinated against Hep B? resolved HepB?
vaccine: HbsAb, no anything else resolved hepB: HbsAb, HbcAb
169
inguinal hernia vs. direct hernia
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
hernia in scrotum? hernia above inguinal ligament? hernia below inguinal ligament?
in scrotum: indirect inguinal above inguinal ligament: direct below inguinal ligament: femoral
171
hernias relative to inferior epigastrics
indirect: lateral. direct: medial
172
deep inguinal nodes receives drainage from?
reside under fascia lata, medial side of femoral vein. glans penis // clitoris & superficial nodes
173
superficial inguinal nodes receives drainage from?
scrotum & all cutaneous structures inferior to umbillicus. including genitalia and anus up to pectinate line
174
testes drain to? scrotum? glans penis?
testes: para-aortic nodes. scrotum: superficial inguinal nodes --> deep glans penis --> deep inguinal nodes
175
specific iron deficiency signs (anemia)
dysphagia, spoon nails or koilonychia (disfigured finger nails)
176
filgastrim
G-CSF
177
what help w/ iron absorption
vitamin C, reduces it to Fe2+ state
178
factor V leiden
resistant to cleavage by protein C -- thrombophilia
179
antiphospholipid presents with (3) abnormal lab finding?
1. venous thromboembolism 2. arterial thromboembolism 3. frequent fetal loss LONG aPTT
180
most common cause of long PTT?
lupus anticoagulant
181
why is folic acid deficiency --> prothrombotic?
hyperhomocysteinemia
182
lipofuscin is composed of..
product of lipid peroxidation. lipid polymers and protein-complexed phospholipids. 'wear & tear' seen in heart & liver of aging or cachectic, malnourished patients.
183
mediators of cachexia?
TNF-alpha!!!! also: IFN-gamma, IL-6
184
chromogranin + lung cancer?
small cell carcinoma! also: neuron specific enolase, synaptophysin. secretory granules on EM