Flashcards in test #45 5.4 Deck (197):
when to involve ethics committee or risk management?
basically never on USMLE. handle it on your own.
sudden onset headache and nuchal rigidity
meningeal irritation from blood
can also see papilledema and pupillary dilation, but no other focal neurological signs
blood in CSF
diff between intracerebral hemorrhage & subarachnoid hemorrhage
intracerebral: focal neurological impairment
subarachnoid: no focal issues
carrier frequency for mom 1/30
carrier frequency for dad: 1/100
chance child will have disease?
(1/30 x 1/2) x (1/100 x 1/2)
what % of observations fall in 1 standard deviation of mean
what % of observations fall in 2 standard deviations of mean
what % of observations fall in 3% of standard deviation of mean
normal pulmonary arterial pressure
definition of pulmonary artery hypertension
major causes of pulmonary artery HTN
-hereditary (AD: BMPR2 mutation)
-left heart failure
-chronic hypoxia: obstructive sleep apnea, COPD
idiopathic pulmonary artery HTN inheritence
autosomal dominant w/ variable penetrance
1. mutation in BMPR2. normally suppresses smooth muscle proliferation
2. activates disease process (i.e. infxn, drug)
cardiac sounds that can arise w/ pulmonary HTN (2)
1. accentuated S2
2. holosystoic tricuspid regurg (diastolic) due to increased 'afterload'
etiology of pulmonary HTN in COPD, obstructive sleep apnea, interstitial lung disease
compensation for chronic respiratory acidosis
(at least 24hr)
kidney excrete acid & retain HCO3-
shallow breathing seen in diabetic ketoacidosis, attempt to blow off CO2 to compensate for metabolic acidosis (low bicarb, low CO2, low pH)
adverse effects of succinylcholine (3)
1. malignant hyperthermia in genetically susceptible people
2. hyperkalemia in pts w/ burns, myopathy, crush injury, denervation -> quadriplegia, guillan-barre
(due to upregulation of muscle nAChR & rhabdomyolysis --> increase K+ efflux)
3. bradycardia, from parasympathetic stimulation or tachycardia, from sympathetic ganglion effects
side effects of atracurium
1. release histamine ->
bp drop, flushing, bronchoconstriction
2. spontaneous degradation to laudanosine --> seziure
but, good for renal/hepatic insufficiency
GABAb at level of spinal cord
phase I of succinylcholine
strong agonist of nAChR
binds & depolarizies
insensitive to AChE, so prolonged depolarization --> twitching
potentiate: AchE inhibitors, bc Ach will help further depolarize & inactivate muscle.
eventually degraded by plasma cholinesterases
phase II of succinylcholine
w/ continuous infusion or SLOW metabolizers
eventually nAChR insensitive to succinylcholine, which can bind & block site, but can no longer depolarize
--> becomes nondepolarizing blocker
antidote: AChE inhibitors (increase Ach concentration)
infective dose of shigella, salmonella, and vibrio cholera, ETEC
least --> most
shigella -- 10 - 10^2
salmonella -- 10^ 7
vibrio cholera: 10^5- 10^7
ETEC: 10^ 8-10^ 10
why is shigella so infective? when does infxn start
- survive stomach acid & bile
- uniquely bind to mucosal M cells in peyer's patches
24-72 hrs incubation
painful spasm of rectum associated w/ urge to defecate, yet little passage of stool occurs
infective dose of c. perfinges
organisms that can cause diarrhea w/ small innoculum
- camplyobacter jejuni - 500
- entamoeba histolytica - as few as 1
- giardia lamblia - as few as 1
TB virulence factor: cord factor
- inhibit macrophage & neutrophil maturation
- induce release of TNF-alpha
- damages mitochondria
mycoside (2 mycolic acid molecules bound to disaccharide trehalose)
correlates w/ virulence.
no cord factor -> no disease.
TB virulence factor: sulfatides (surface glycolipids)
- inhibit phagolysosomal fusion
thick, ropelike cords of mycobacterial organisms in twisted "serpentine" pattern
TB, consistent w/ presence of cord factor
eyes, lies, and capsize
-opthalmoplegia / nystagmus:
anterograde amnesia: mamillary body
ataxia : cerebellum
what nutrient is often deficient in alcoholics
give IV dextrose & thiamine
wernicke encephalopathy is exacerbated when..
IV dextrose WITHOUT THIAMINE
thiamine needed for pyruvate dehydrogenase (pyruvate --> acetyl CoA for glycolysis -> TCA)
acute thiamine def:
ataxia, nystagmus, opthalmoplegia, anterograde amnesia
chronic thiamine def:
- anterograde & retrograde amnesia, apathy, lack of insight, confabulation
what brain structure is most affected by thiamine deficiency
mammillary body, undergoes necrosis.
papez circuit, neural pathway of limbic system involved in cortical control of emotion & memory.
originate from hippocampal subiculum, projects to mamillary body
alexia w/o agraphia
suggests corpus callosum lesion
before giving dextrose to alcoholic / malnourished, must give..
THIAMINE! to avoid ppt of wernicke encephalopathy.
virus w/ nuclear membrane envelope
herpes, CMV, EBV, etc
how do antithyroid drugs work (3)
1. oxidation of iodine
2. iodination of tyrosine residues
3. coupling of iodotyosine molecules
different between PTU and methimazole (3)
1. propylthiouracil also blocks peripheral conversion of T4 -> T3
2. PTU shorter half life
3. PTU for pregnancy!
methimazole = teratogen
both PTU and methimazole as associated with..
preferred rx for hyperthyroidism in US
definition of agranulocytosis
absolute neutrophil count of less than 500/mL
presentation of agranulocytosis
fever & sore-throat
often induced by medication
drugs that cause agranulocytosis
drugs cccrush myeloblasts & promyeloblasts
how to check for agranulocytosis?
WBC & differential
patient w/ hyperthyroidism w/ fever & throat pain?
worry about methimazole / PTU induced agranulocytosis
PO2 in venous blood
PCO2 in venous blood
PCO2: 47 mmHg
PO2 in arterial blood
PCO2 in arterial blood
describe bronchial arterial supply
left & right arise from descending thoracic aorta
oxygenated to bronchi & bronchioles
w/ pulmonary artery, form dual blood supply to lungs
describe bronchial drainage
-part to right heart via azygous, accessory hemiazygous, intercostal veins
- MOST drain to left heart via pulmonary veins
DEOXYGENATED blood into LEFT ventricle
explain why pO2 (100) in left ventricle is lower than pO2 (104) in pulmonary capillaries
bc admixture w/ venous blood from bronchial VEINS
most drain into right heart via pulmonary vein
what normally limits blood gas exchange in alveoli
CO2 & O2: usu perfusion limited
CO2 equilibrates really fast
O2 also does
what shifts hemoglobin curve to the right
high temp, pCO2, 2,3DPG
more codons (61) than there are amino acids (20)
each tRNA molecule = specific for an AA
multiple tRNA can code for same aa
explain basis of wobble in tRNA
5' tRNA has different spatial orientation than other 2 bases
may be inosine, which can hydrogen bond w/ uracil, adenine, and cytosine
allows for different codons to = same amino acid
3 categories of vitamin A toxicity
think: intracranial HTN, skin changes, hepatosplenomegaly
-n/v, vertigo, blurred vision
-alopecia, dry skin, hyperlipidemia, hepatoxicity, hepatosplenomegaly, visual difficulty, papilledema (pseudotumor cerebri)
1st trimester: microcephally, cardiac anomalies, fetal death
thiamine deficiency associated w/
beri beri wet & dry
large doses of vitamin C associated w/
diarrhea, abdominal bloating
false negative stool guaiac results
large doses of vitamin E
-hemorrhagic stroke in adult
-necrotizing enterocolitis in infants
major use of ELISA
to measure AMOUNT of protein in body fluid
indirect vs. direct ELISA
indirect: test antigen to see if patient has antibody
indirectly assume if you Ab, you must have antigen
direct: test antibody to see if patient has antigen
[directly see if you have antigen]
look for patient antibody
name loop diuretics (4) & major use
furosemide, toresemide, bumetanide, ethacrynic acid
use for volume overloaded state: CHF
name thiazide diuretic (4) & major use (2)
hydrochlorothiazide, chlorthalidone, indapamide, metolazone
use: HTN, calcium nephrolithiasis prophylaxis
ENaC blockers (2)
mineralcorticoid receptor antagonist (2)
which diuretic is most likely to produce hyponatremia
have normal corticomedullary concentration, better able to retain free water in response to ADH
(loop diuretics loose some corticomedullar gradient in TAL, less able to absorb free water in loop of henle & CD)
diuretic causing hypocalcemia?
loop (furosemide etc)
BAD for renal nephrolithiasis
hepatitis w/ isoniazid presentation
fever, anorexia, nausea
how can isoniazid peripheral neuropathy be averted?
administer vitamin B6
fever, urticaria, arthalgia, proteinuria, lymphadenopathy 5-10 days after drug exposure
type III HSR
fatigue & new onset cardiac murmur in young adult
nephritic issues with bacterial endocarditis?
can have circulating immune complexes --> diffuse proliferative glomerulonephritis
inheritance of hemophilia A? hemophilia B?
A: factor 8; X-linked recessive
B: factor 9; X-linked recessve -> christmas disease
difference between hemophilia A & B
common cause of PT prolongation
common causes of increased bleeding time
von willebrand disease
general side effect of sulfonylurea?
1st generation risk?
2nd generation risk?
general: hypoglycemia w/ renal failure
1st gen: disulfram-like rxn
2nd gen: hypoglycemia
risk of rapid acting insulin
hypoglycemia, rare HSR
side effect of metformin
CONTRAINDICATED in renal failure
diabetes drug contraindicated w/ renal failure
can cause lactic acidosis
side effect of thiazolidinediones (4)
1. weight gain (fluid)
4. heart failure (bc of fluid retention)
which diabetes drug can cause weight gain, edema, hepatoxicity, and heart failure
which diabetes drugs can cause hypoglyemia
insulin & sulfonylureas
not TZD or metformin
drugs associated w/ pulmonary fibrosis
amiodarone, bleomycin, mitomycin C, busulfan, methysergide
how to identify lunate on X-ray
most medial articulation w/ radius!
be careful when counting!
how to identify scaphoid on X-ray
lateral articulation w/ radius
be careful when counting
what carpal bone articulates w/ thumb?
thumb swings on trapezium
stomach wall grossly thickened & leathy, diffuse stomach adenocarcinoma
progression of gastric adenocarcinoma
early aggrssive local spread & node/liver mets
1. virchow node
2. krukenberg tumor
3. sister mary joseph node
signet cells in stomach
diffuse adenocarcinoma, associated w/ linitis plastica
nodular, polypoid-well demarcated masses in stomach.
microscopy: well-formed glands w/ columnar/cuboidal cells
resembles colon cancer
prognostic factors of gastric adenocarcinoma
depth of invasion through gastric wall & regional lymph involvement
what type of gastric carcinoma can ulcerate
intestinal type, can present as upper GI bleed
rugal thickening w/ acid hypersecretion in stomach
think zollinger-ellison; bc gastrin increases acid secretion & parietal cell growth factor
hypertrophy of brunner's gland
suggests peptic ulcer disease
brunner gland in duodenum --> secrete mucous via crypts of lieberkuhn
bicarbonate in small intestine comes from.. (2)
1. pancreatic duct secretions
2. brunner's gland (only in duodenum)
brunner gland. where am i?
crypt of lieberkuhn. where am i?
anywhere from small intestine to colon.
stomach: has gastric glands
CCK and secretin on pancreatic secretions
CCK stimulates mostly acinar cells (enzymes)
secretin stimulates mostly ductal cells (bicarb)
CCK and secretin on gallbladder
CCK stimulates gallbladder contraction & sphincter of Odi opening
secretin stimulates bile secretion
chronic gastritis w/ h. pylori leads to..
diffuse gland atrophy & intestinal emtaplasia
increase risk of gastric carcinoma
resistance to rifampin
mutation in DNA-dep RNA pol
best indicator of MR severity?
presence of S3 gallop
reflects increase rate of left ventricular filling due to large volume of regurgitant flow re-entering ventricle during mid diastole
functional diastolic rumbling?
suggests mitral regurg leading to high rate of regurgitant flow across MV in diastole
is intensity of murmur a good indicator of mital regurg?
no, bc low intensity means larger regurg orifice --> worse!
what causes mid systolic click in MVP?
tensing of chordae tendineae as they are being pulled taut by valve leaflets into atrium.
connect papillary muscles to AV valves leaflets (mitral & tricuspid)
collagen & elastin
most common cause of aortic stenosis?
degenerative senile calcification of valves
result of prolonged hemodynamic stress on valves
common >65 y/o
physical exam of aortic stenosis (3)
1. pulsus parvus et tardus:
-small & slow rise in carotid pulse
2. diminished aortic component to S2
3. harsh systolic crescendo-decrescendo murmur right upper border
valve issues w/ rheumatic fever (3)
1. mitral stenosis (late)
2. mitral & aortic regurg
what type of valvular issue is caused by infectious endocarditis
insufficiency of any valve
cystic medial necrosis can lead to what valve issue
(dilation of ascending aorta)
non-musculoskeletal issues associated w/ ankylosing spondylitis
apical pulmonary fibrosis
medical to prevent calcium stone formation
DON'T GET CONFUSED
reduce calcium in tubules
diuretic that worsens calcium stones
looses Ca2+ means more in the tubules
how to thiazides reduce hypercalciuria (2)
1. block Na/Cl -->
-less Na+ in tubular cell, activates basolateral Na/Ca2+ antiporter, which pumps Na into cell in exchange for Ca2+
-this increases uptake of Ca2+ across apical membrane
2. hypovolemia --?
increases Na and H20 absorption in PCT, leading to passive Ca2+ too
acetazolamide on calcium levels
induces metabolic acidosis -> increase bone release of Ca2+ PO4-
hypercalciuria, worsens calcium stones
DCIS w. solid sheets of pleomorphic, high grade cells w/ central necrosis
chroni inflammation & periductal concentrib fibrosis
calcify necrosis --> mammographic detection
paget's disease of nipple
malignant cells spread from DCIS into nipple w/o having crossed basement membrane
erythema and scale crust
medullary breast carcinoma
invasive, lymphocytic infiltrate
solid sheets of vesicular, pleomorphic, mitotically active cells w/ lymphoplasmacytic infiltrate around & within tumor & pushing noninfiltrating border
central acinar compression & distortion by surrounding fibrotic tissue w/ peripheral ductal dilation
slight association w/ carcinoma risk
breast ductal dilation, inspissated breast secretion, chronic granulomatous inflammation in periductal & interstitial area
mammary duct ectasia
like fibroadenoma but increased cytological atypia & stromal cellularity & overgrowth
how long will myocardium look normal on histology post MI
up until 4 hours post MI.
then waviness in myofibrils (due to relaxation) will start, w/ edema, hemorrhage, early coagulative necrosis
earliest sign of coagulative necrosos of cardiac myocytes
also: punctate hemorrhage & edema
when do neutrophils come into myocardium post MI
when do macrophages come into myocardium post MI
when does granulation tissue form post MI
10-14 days post MI
when does collagen start to lay down post MI
2 weeks post MI -> 2 months
causes of acute pancreatitis (common & uncommon)
usu gallstones & alcoholism
1. drugs: azathioprine, sulfasalazine, furosemide, valproic acid
2. infxn: mumps, coxsackie virus, mycoplasma pneumoniae
4. structure abnormalities of pancreatic duct (stricture, cancer, divisum) or ampulla (choledochal / bile duct cyst, stenosis of sphincter of odi)
6. surgery of stomach / bilary tree
7. recent endoscopic retrograde cholangiopancreatography
repeated acute pancreatitis that resolves on fasting w/ no risk factors in young patient?
how does hypertriglyceridemia lead to acute pancreatitis
DIRECT TISSUE TOXICITY
high TG -> increased production of free fatty acids within pancreatic capillaries via pancreatic lipase
normally is bound to albumin
when TG >1000mg/dl -> will exceed albumin's binding capacity & directly injure pancreatic acinar cells
increased cholesterol predisposes to.. (3)
1. coronary artery disease
2. peripheral vascular disease
hemachromatosis on pancreas
pancreatic fibrosis --> secondary diabetes
does NOT cause pancreatitis
things that can cause pancreatitis mnemonic
3. trauma (seat belt)
7. scorpion sting
8. hypercalcemia / hypertriglyceridemia
10. drugs (esp sulfa)
wilson disease signs
Copper is Hella BAD
unable to loose Cu2+ in bile
1. low ceruloplasmin, cirrhosis, corneal deposit (kaiser-fleisher ring), hepatocellular carcinoma
2. hemolytic anemia
3. basal ganglia degeneration (parkinsonian)
5. dementia, dyskinesia, dysarthria
suggests lots of chylomicrons in blood stream
(think: turbid blood 30min post hamburger!)
lipoprotein lipase deficiency
1 form of hyperchylomirconemia:
childhood: hyperlipidemia, abdominal pain (pancreatitis), lipema retinalis, xanthomas, hepatosplenomegaly
reduced LPL response to heparin
what converts nascent HDL to mature HDL
LCAT: which esterifies cholesterol
role of CETP
cholesterol ester transfer protein: transfers cholesterol liporotein particles from mature HDL to VLDL, IDL, LDL
hyperchylomicronemia can develop with what 2 deficiencies
1. deficiency of lipoprotein lipase
2. mutation in apo C-II
recall, apo C-II activates LPL
hypertriglyceridemia results from..
hepatic overproduction of VLDL
increased blood levels of VLDL and TG
presentation of hyperchylomicronemia
increased chylomicrons & TG
PANCREATITIS, hepatosplenomegaly, eruptive/pruritic xanthoma
no increase risk of atherosclerosis
heparin on lipase activity
heparin releases endothlium-bound lipases, encourage triglyceride clearance from circulation.
pain w/ hyperchylomicronemia / hypertriglyceridemia?
pain w/ hypercholesterolemia?
high chylomicron & TG --> abdominal pain --> PANCREATITIS
high LDL cholesterol --> chest pain --> MI
hallmark of familial hypercholesterolemia
tubular xanthomas (tendon)
also have: xathelasma & acrus cornea
what increases risk of pancreatic cancer?
what increases risk of gastric cancer?
-dietary nitrates (smoked food)
-alcohol & tobacco
what increases risk of liver cancer?
- hep B & C
- liver cirrhosis
- carbon tetrachloride
what increases risk of colorectal cancer?
-hereditary colorectal cancer
-inflammatory bowel disease
-charred / fried food
what increases risk of renal cancer?
what increases risk of bladder cancer
-occupational exposure to..
-aromatic amine-containing dyes (benzidine, 2-napthylamine,
what increases risk of breast cancer
what increases risk of prostate cancer
african american race
what increases risk of leukemia / lymphoma
what increases risk of angiosarcoma in liver
what increases risk of papillary thyroid cancer?
2nd leading cause of lung cancer?
aggressive & difficult to treat
gross appearance of transitional cell carcinoma of bladder?
gross cystoscopy: multifocal sessile or papillary tumors
histology: pleomorphic, hyperchromatic nuclei, increased NC ratio, disrupted oritentation & polarity
how does cyclophosphamide & ifosfamide cause hemorrhagic cystitis
acrolein -- irritates bladder mucosa
carcinoma, mesothelioma, thymoma, sarcoma, trophoblastic tumor, desmoplastic small round cell tumor all..
stain positive for ketatin!
desmin, caldesmon, actin +
muscle tissue stain
stain for endothlium
CD34+, von willebrand factor
presentation of dermatomyositis (3)
- red violaceous fat-topped papules w/ light scale. over bony prominences.
heloptrope rash: erythematous or violaceous edematous eruption on upper eye-lid & periorbital skin
proximal muscle weakness!
serum findings in dermatomyositis
elevated creatinine kinase
prognosis of dermatomyositis
if present after age 50 --> increased risk of underlying occult malignancy
dermatomyositis is associated w/ underlying
elevated white lesion near vagina
acute pyelonephritis pathogenesis
must have vesicoureteral reflux in some way
fat embolism syndrome triad
1. acute onset neuro issues
3. petechial rash
trauma of long bone/pelvis
pathogenesis of fat embolism syndrome
1. trauma dislodge fat in marrow
2. travels in bone marrow sinusoud
- pulmonary vasculature
- CNS (via AV shunt)
- thrombocytopenia & petechial rash due to platelet coating fat microglobules
why see petechial rash in fat embolism syndrome?
platelet coats fat globule in vasculature
presentation of epidural hematoma
talk and die
may loose consciousness after injury. then lucid interval -> loss of consciousness
epicranial aponeurosis & periosteum cover..
outer surface of skull
why is there a physiological drop in systolic pressure with inspiration
increased pulmonary vascular capacitance --> reduced left ventricle preload
what is there a exacerbated drop in systolic pressure w/ inspiration w/ pulsus paradoxus?
physiologic: increased pulmonary capacitance -> reduced preload
increased filling of right heart, normally bulges into pericardium, but when filled will blood -> push against interventricular septum, reducing LV stroke volume
low potency antipsychotics associated with
histamine block: sedation
alpha-1 block: orthostatic hypotension
name 2 low potency 1st generation antipsychotics
name 2 high potency 1st generation antipsychotics
migratory thrombophlebitis suggests
underlying visceral malignancy
explain trousseau's sign
bc common paraneoplastic syndrome: hypercoagulability, esp adenocarcinoma (of pancreas, lung, colon)
secrete thromboplastin-like substance -> cause chronic intravascular coagulation --> disseminated & tend to migrate
superficial venous thromboses that appear in one site, resolves & appears elsewhere
migratory thrombophlebitis --> underlying visceral malignancy
WBC casts ppt by what in renal tubular cells
Tamm-Horsfall protein, secreted by tubular epithelial cells
what will have highest rate of metabolism in glycolytic pathway: glucose 6-phosphate, mannose 6-phosphate, galactose 1-phosphate, fructose 1-phosphate, glucose 1-phosphate
fructose 1-phosphate, bypasses rate limiting step of PFK-1
all others enter before PFK-1
rate limiting enzyme in glycolysis
F 6-phosphate -> F 1,6 bisphosphate
formed from metabolism of several polysaccharides & glycoproteins
phosphorylated to mannose 6-P, converted to fructose 6-P (by mannose isomerase) then acted on by PFK-1
galactoskinase makes galatose 1-P
transfer of UDP to galactose 1-phosphate, then epimerization to UDP-glucose (by galactose 4-epimerase).
resultant glucose 1-P -> glucose 6-P via phosphoglucomutase
F 1P--> DHAP & glyceradehyde
via aldolase B
glyceraldehyde -> glyceraldehyde 3-P
becomes pyruvate eventually
hepatosplenomegaly, aseptic necrosis, gaucher cells
presentation of fabry's
1. peripheral neuropathy of hand and feet
3. cardiovascular / renal disease (COD)
DNR means (3)
1. no intubation or mechanical ventillation
2. no defibrillation or IV drugs to acutely treat terminal rhythm
3. no chest compressions
can otherwise specify additionally:
-no artificial feeding