posteroinferior wall of left ventricle supplied by.. infarct on ECG?
posterior descending branch of RCA.
ST elevations in leads II, III, aVF
transmural ischemia of interventricular septum on EKG?
ST elevation in leads V1 V2
transmural ischemia of anterior left ventricular wall on EKG?
ST elevation in V3 V4
occlusion of proximal LAD infarcts.. causes on EKG?
infarts anteroseptal transmural ischemia. ST elevations in V1-V4
anterolateral infarct of left ventricle on EKG?
LCX or LAD – V4-V6
lateral wall of left ventricle infarct on EKG?
I, aVL & V5-V6
which segment of intestine is always involve w/ hirschsprung? why?
rectum, bc ganglion cells of submucosa & myenteric plexi travels caudally.
aganglionic segment -> constricted bc cannot relax
form of ventricular tachycardia.
polymorphic QRS complexes of varying amplitudes and cycle length.
give appearance that the tip of QRS is twisting around ECG baseline.
always associated w/ underlying prolonged QT
prolonged QT caused by..
class IA and III antiarrhythmics
lidocaine fxn by..
blocking Na+ channels
penicillins are structurally stimilar to
terminal d-ala-d-ala of peptidoglycan molecule
N-acetylmuramic acid and N-acetylglucosamine are
peptidoglycan precursor molesules of cell wall in bacteria
sulfonamide antibiotic mechanism? trimethoprim
sulfonamides: compete w/ PABA (paraaminobenzoic acid) for incorporation into folic acid..
trimethoprim: block dihydrofolate reductase
staph epidermidis infxn?
major cause of infection in pts w/ indwelling catheters or implanted foreign bodies.
produces biofilm (polysaccharide slime) allows adhesion.
diagnosis: recover from mult cultures (can be contaminant)
rx: initial aggressive. vancomycin w/ rifampin or gentamycin or both.
can be resistant to methicillin
rx for staph epidermidis bactermia. if not..?
aggressive! vancomycin + rifampin + gentamycin
w/o rx: indolent endocarditis after valve replacement. intracardiac abscess formation, dehiscence of prosthetic valve, septic embolization
AML blasts will stain positive for
peroxidase (since Aur rods have MPO)
TdT in lymphocytes
terminal deoxynucleotidyl tranferase
add nucleotides to V D J regions of Ab gene for diversity.
mature of immature B and T cells
hairy cell leukemia stains. what type of cells are they?
TRAP (tartare resistant acid phosphatase)
splenomegaly, fatigue, pancytopenia
glomus body & glomus tumor
small, encapsulated neurovascular organ. temp regulation
in dermis of nail bed, pads of fingers & toes, ears
afferent arteriole –> richly innervated, muscular arteriovenous anastomosis –> efferent vein.
COLD: shunt blood AWAY from skin surface: prevent heat loss
HEAT: direct blood TO skin, facilitate dissipation of heat.
form PAINFUL tumors under fingernail. arises from modified smooth muscle cells.
skin presentation of histiocytosis
erythematous papules, nodules, and/or scaling plaques
electrolyte presentation of primary adrenal insufficiency (Na, K, Cl, HCO3)
primary adrenal insufficiency vs. secondary / tertiary (i.e. pituitary / hypothal)
primary – loose aldosterone, cortisol, and androgens
secondary – loose cortisol only. aldosterone triggered by renin / angiotensin system!
Na+ in hyperaldosterone?
initial increase, but aldosterone loss –> intravascular hypervolemia –> ANP –> diuresis & compensatory Na+ loss
why is supraspinatus injury most common of rotator cuff?
repeated impingement trauma between humeral head & acromion
subacromial bursa location
under both acromion/clavicle & tendon of deltoid muscle.
sits on top of supraspinatus
why no hep C vaccine // why prone to chronic infection
variety in antigenic structure of HCV envelope proteins
- multiple genotypes & subgenotypes
- hypervariable region of envelope glycoprotein – prone to frequent mutation
- no proofreading 3-5’ exonuclease
constantly emerging mutant strains &much variety in a single person at one time
positive trendelenburg sign
hip dips to unaffected side when standing on affected sign (failure of gluteus medius/minimus to pull pelvis down and abduct thigh) –> superior gluteal n.
sciatic n. innervates all knee flexors except..
Wright-Giemsa stain on epithelial cells scraped from ulcer base.
see multinucleated giant cells w/ some intranuclear inclusions – HSV & VZV
primary vs. reactivation HSV-1 infxn
- usu one side
- much less extensive area involved (limited)
- favor skin around mucosal orifice (lips & nose)
- larger area
- gingivostomatitis: gums & oral mucosa
primary vs. reactivation of VZV infxn
reactivation won’t cross midline either
full viral genome persists in host cells, but infectious virons cannot be recovered from those cells that harbour the virus.
slow virus infection
prolonged incubation period, months to years. virus persistently infects host & multiplies before gradually causes clinically apparent disease.
predominantly progressive, degenerative disorder of CNS – SSPE, PML
early in diastole. sudden deceleration of entering blood column as ventricle reaches its elastic limit
reverberation of blood between ventricle walls. low frequency
- forceful, rapid filling of a ventricle w/ normal or elevated compliance
- normal, or even decreased filling rates when compliance is low
- blood flowing into an overfilled ventricle w/ high end-systolic volume
murmur associated w/ HCM
dynamic LVOT – mitral regurgitation – systolic. or ‘aortic stenosis’ like??
pattern of drug administration for nitrates?
nitrate free interval every day. rapid tolerance
due to decreased vascular sensitivity & increased sensitivity to vasoconstriction
MAO inhibitors (phenelzine) fxn by..
IRREVERSIBLY bind. takes 2 wks post discontinuation to regenerate enzyme
wait before giving SSRI
SSRI + MAOi =
serotonin syndrome. wait 2 wks after discontinuing MAOi before giving SSRI
drug of choice for paroxysmal supraventricular tachycardia?
adenosine – open K+ channels, hyperpolarize AV node.
acts in manner similar to muscarinic cholinergics
side effects of adenosine for PSVT?
flushing, chest burning (bronchospasm), hypotension, high grade AV block
side effects of amiodarone
blue-grey skin discoloration, photodermatitis, pulmonary fibrosis, hypo/hyperthyroidism
lidocaine side effects/toxicity
neurologic symptoms usu
usu drug-induced lupus syndrome
verapamil side effects
gingival hyperplasia and constipation
digoxin/digitalis side effects / toxicity
fatigue, blurry vision, changes in colour perception, nausea & vomiting, diarrhea, abdominal pain, confusion, delirium
drug used for chemical stress test?
adenosine! causes bronchospasm, flushing, high grade block!
proprionylCoA –> methymalonylCoA
(propionylCoA carboxylase + biotin)
methylmalonylCoA –> succinylCoA
malonyl CoA comes from..
acetylCoA + acetylCoA carboxylase
methylmalonyl CoA comes from..
propionylCoA + propionylCoA carboxylase
hydrolysis in urea cycle
arginine to ornithine via arginase
converts alpha-ketoacids to amino acids (via transfer of amino group from one amino acid to alpha-keto acid)
usu requires B6
defet in isomerization rxn. transforms methylmalonyl CoA to succinyl COA – TCA
parvovirus infxn in adult:
arthritis involving proximal interphalangeal, metacarpal knee, and ankle
usu symmetric (like RA) but spontaneously resolves (unlike RA)
hyaline membranes in ARDS
alveolocapillary membrane leakage. fibrin exudate and plasma protein-rich edema fluid mixed w/ cytoplasmic and lipid remnants of necrotic epithelial cells.
exudate-like. not transudate.
smell is from..
dermis / subcutaneous fat of breast areolae, axillae, genital.
membrane bound vesicles “sweat” into hair follicles. rather than directly to skin.
innervated by adrenergic fibers of sympathetic nervous system. not fxn until puberty.
women – cyclical changes secondary to hormonal influence w/ menstrual cycle.
usu odorless when secreted. malodorous secondary to activity of commensal bacteria in skin.
associated w/ SEBACEOUS glands. discharge of entire cell undergo breakdown to release secretory product & meibomian glands in eye
skin throughout body. except lips and glans penis.
merocrine glands secret watery fluid rich in Na and Cl “sweat” directly to skin
mammary glands (lactation)
modified sweat glands. apocrine secretion.
aldosterone functions by..
binding to intracellular receptor and altering gene expression
(1) more Na/K pumps
(2) ENaC on principal cells
(3) increase K+ secretion from principal cells
(4) increase H+ secretion from intercalated cells
which chemical increases urea transport in collecting ducts
inheritance of phenylketonuria?
autosomal recessive. mental retardation, eczema, mousy musty body odor
ritodrine and terbutaline
b2 agonist. tocolysis. relaxes uterus. defer premature labor
inheritance of glucose 6 phosphate dehydrogenase
MOST structural abnormalities are inherited as..
autosomal dominant (i.e. hereditary spherocytosis)
MOST enzyme deficiencies inherited as..
X-linked dominant? example
100% risk to female offspring of an affected male.
when does mismatch repair (i.e. that mutated in lynch: MSH2 and MLH1) function
shortly after daughter strands synthesized.
DNA deaminating agents. repair?
base pair excision repair: glycosylase detect, create an empty sugar-phosphate residue (apurinic site)
how does alcohol cause pancreatitis
induces pancreatic secretions w/ high protein concentration and low fluid content – prone to ppt.
also causes spasm of sphincter of Oddi – direct toxic effect on acinar cells
main causes of acute pancreatitis (2)
2. alcohol abuse!
alcohol abuse leads to what hematological abnormality
macrocytosis (MCV) secondary to…
(1) poor nutrition: folate / b12
(2) direct toxicity of alcohol on bone marrow
3 indicators of chronic alcohol abuse
(1) macrocytosis (RBC)
(2) AST:ALT ratio > 2
(3) elevated gamma-glutamyltransferase (GGT)
macrocytosis can occur independently of folate or cobalamin deficiency
defect in LYST – lysosomal regulator gene. MT dysfunction in phagolysome-lysosome function.
- bleeding and bruising (platelet deficiency)
- albinism (partial oculocutaneous albinism)
- infxn w/ staph strep peripheral
B and T cel disorder
mutation in WAS
T cells unable to reorganize actin.
B cells can’t anchor membrane bound receptors well
low to normal IgG and IgM
high IgE and IgA
fewer and smaller platelets
increased risk of non-hodgkin’s lymphoma
immunodeficiency with partial oculocutaneous albinism and neurological defects (i.e. nystagmus)
chediak-higashi (defective neutrophil phagolysosome function)
side effects of lithium
lithium movement (tremor) nephrogenic diabetes insipidus hypOthyroidism pregnancy -- ebstein's anomaly
monitor BUN/creatinine and TSH
clozapine atypical antipsychotic can cause
agranulocytosis & seizures
risperidone can cause..
galactorrhea and amenorrhea
trazodone side effects
painful erection (priapism), orthostatic hypotension, sedaition
olanzipine/clozapine side effect
ziprasidone side effect
atypical antipsychotic with least side effect
presentation of polycythemia vera
plethoric face, splenomegaly.
increase incidence of..
- peptic ulcerative (altered blood viscosity)
- itching (histamine release from basophils)
- gouty arthritis (increased cell turnover)
examples of JAK STAT signalling
describe JAK STAT signalling
nonreceptor tyrosine kinase.
ligand binds –> JAK comes and phosphorylates. attracts STAT, which is phosphorylated –> then goes to nucleus for effect
examples of RTK activity
insulin, IGF-1, EGF
li-fraumeni syndrome associated w/ which cancers
- sarcomas and tumor of breast
- adrenal cortex
photosensitivty in porphyria due to
formation of porphyrin-mediated superoxide free radicals from oxygen upon sunlight exposure
where does H. pylori like living in the stomach?
antrum: in prepyloric area, where there are few acid-secretory parietal cells.
will cause gastric metaplasia of duodenum (due to increased acid secretion), and will THEN colonize duodenum
where can H. pylori live?
ONLY in areas of gastric metaplasia!
can’t live in normal duodenum
myocardial biopsy with interstitial collection of mononuclear inflammatory cells * scattered multinucleated giant cells, surrounded by fibrosis?
interstitial myocardial granulomas: aschoff bodies)
acute rheumatic carditis.
plump macrophages w/ abundant cytoplasm & central, round-to-ovoid nuclei w/ central, slender, chromatin ribbons – Anitschkow cells “caterpillar”.
Aschoff giant cells: when larger macrophages become multinucleated.
can be found in any 3 layers of heart. later replaced by fibrous scar tissue.
preceeded by episode of group A strep 10 days to 6 wks earlier
predominantly lymphocytic interstitial inflammatory infiltrate w/ focal necrosis of myocytes adjacent to inflammatory cells
interstitial inflammatory infiltrate of mononuclear inflammatory cells & eosinophils in heart
circualting toxin produced by primary focus of infxn in upper aerodigestive tract (tonsilopharyngitis)
pleomorphic interstitial infiltrate of macrophages w/o distinct Ascoff-body type granulomas
distension of individual myofibers w/ intracellular trypanosomes in heart?
chagas disease, trypanosoma cruzi
most common cause of end state renal failure in US
kidney disease w/ hyperuricemia?
monosodium urate crystal ppt in medullary interstitium –> fibrosis and foreign-body granulomas (gouty nephropathy).
can result in chronic renal failure.
microscopically – negatively birefringent under polarized light
psychogenic erectile dysfunction
usually sudden & have spontaneous morning erections (integrity of neurologic / vascular disease)
what sexual features decrease w/ age
longer refractory period, take longer to achieve erection
sexual desire does not fall
most common mediations causing impotence
SSRI and sympathetic blockers (clonidine, methyldopa, beta blockers)
signs of irreversible injury in heart
appearance of vaculoes and phospholipid-containing amorphous densities WITHIN mitochondria
implies permanent inability to generate ATP via oxidative phosphorylation.
[simple mito swelling = reversible]
myofibril relaxation results from..
within 30min of injury.
corresponds w/ intracellular ATP depletion & lactate accumulation due to anaerobic glycolysis
disaggregation of polysomes is a sign of
dissociation of rRNA from mRNA.
disaggregation of granular and fibrillar elements of nucleus is a sign of..
clumping of nuclear chromatic is a sign of..
both: reversible cell injury.
perhaps due to change in pH
glycogen loss in myocardium is a sign of…
reversible cell injury.
less mito ATP – use glycogen
glycogen stores can be depleted within 30 min of severe ischemia
triglyceride droplet accumulation in cells is a sign of..
reversible injury, esp in hepatocytes. also in striated muscle injury and renal cells.
results from decreased synthesis of intracellular proteins within cell injury.
hepatocytes: decrease production of lipid acceptor proteins –> prevents incorporation of lipid into lipoproteins –> accumulate in cell
vascular dementia vs. alzheimer’s
multiple lacunar infarcts: STEP-WISE decline in cognition
alzheimer’s: gradual decline
which cells in testes are temperature sensitive
sertoli cells must more temperature sensitive (seminiferous tubules in general)
which hormone is decreased in cryptoorchidism?
sertoli cells are very temperature sensitive and prone to heat-induced damage.
seminferous tubules become atrophic and hyalinized –> low sperm count.
leydig cells are NOT very temperature sensitive –> secondary sexual characteristics develop just fine.
broadly speaking, tests that evaluate hepatobilary disease assess what 3 things
(1) liver functionality: PTT, bilirubin, albumin, cholesterol
(2) structural integrity & cellular intactness of liver (transaminase)
(3) bililary tract (ALP, gamma-glutamyl transferase)
group of enzymes associated w/ metabolic activity in a number of tissues (liver, bone, intestine, kidney, placenta, leukocytes, some neoplasms)
primary source: BONE & LIVER
3x elevation = nonspecific finding for many liver disease.
GGT (gamma glutamyl transpeptidase)
enzyme primarily in hepatocytes and biliary epithelia.
can be found in various extrahepatic tissues (kidney, spleen, pancreas, heart, lung, and brain)
NOT present much in bone.
therefore, useful to determine whether ALP is of hepatic or bony origin
determine if ALP is of bony / hepatic origin
look at GGT
lactate dehydrogenase measures
nonspecific test, evaluation of tissue injury or death
CML vs. leukomoid reaction
CML: low leukocyte alkaline phosphatase score
macrophage and monocyte.
receptor for LPS (activates macrophage)
atypical reactive T cells in EBV are..
CD8+ T cells – ready to attack EBV infected B cells
how does EBV get into B cells