practice test Qs Flashcards
what type of antiarrythmic is ibutilide
class III- work on K channels
the following tumor markers are associated with what type of tumors
- pancytokeratin
- calretinin
- chromogranin A
- synaptophysin
*
- pancytokeratin
- mesothelioma
- calretinin
- mesothelioma (highly sensitivie)
- chromogranin A
- neuroendocrine marker for small cell lung cancer
- synaptophysin
- neuroendocrine marker for small cell lung cancer
+ describe the pathophysiology of the diagnosis
fast to slowest
purkinje –> atrial mycoytes –> ventricular myocytes –> AV node
**park at venture avenue**
desmosomes= made of cadherins = cell-cell junctions
hemidesmosomes = cell-BM junctions
why are there no cutaneous findings
acute intermittant porphyria = no cutaneous sx
porphyria cutaenou tarda = painful, blistering skin lesions that develop on sun-exposed skin (photosensitivity). Affected skin is fragile and may peel or blister after minor trauma
most likely dx
what are the AE of all the other drugs listed as well
histamine’s role is probably via H4 receptors
two hit hypothesis = loss of heterozygosity
patient presents with N. gonnorrhea
what is this, who is this seen in
howell jolly bodies
asplenia
E
presence of babinski sign indicates myelination problem ~~ B12 needed to myelinate neurons
at the two day mark of little to no eating, what clinical finding can differentiate between a patient presenting with defect in gluconeogenesisi vs defect in beta oxidation
ketone levels in urine
hypoglycemic hypoketotic = beta oxidiation abnormality
- severe vomiting, seizures..
vs: gluconeogenesis mess up- @ 24 hrs, when the main switch is to gluconeogenesis, they are not able to last that long - vs beta oxidation can last a lil longer than 24 hours
- x gluconeo= more severe, full body - LOC
both present in youngish people, but xgluconeo probs younger children
which TUMOR SUPPRESSOR GENES are turned off –> can’t set off apoptosis –> CA
associated with what CA/syndrome
TP53 = in most CAs ,
- genomic stability
- Li Fraumenni Syndrome
RB = retinoblastoma, osteosarcoma
- G1/S transition inhibitor
*
which PROTO-ONCOGENES –> GOF in CAs
- result in inc growth signals
associated with which CAs
MYC
- TF –> Burkitt Lymphoma
RAS
- GTP-binding protein –> cholangiocarcioma, pancreatic adenocarcinoma
EGFR
- (aka ERBB1 ) RTK= lung adenocarcinoma
HER2
- RTK = breast CA
ABL
- CML (chronic myelogenous leukemia)
BRAF
- (Ras signalling) hairy cell leukemia, melanoma
the loss of which tumor suppressor gene –>
- x ubiquitin ligase component
- xurogenitcal differentiation
- x Wnt signalling
and which CAs/syndromes are they associated with
which mutations and CAs are associated with…
- Lynch Syndrome
- FAP
- VHL
- Li-Fraumenni
- MEN1
- MEN2
differentiate between the components that make up an MHCI vs MHCII molecule
which autonomic receptors set off which G-couple receptors
a1 = q
a2= i
B(1,2,&3) = s
“queens inspire songs”
FSGS = most common cause of nephrotic syndrome
lymphatic drainage of the abdomen goes through which LN
transketolase = xthiamine –> wernicke korsakoff + beri beri
POMC = a precursor for endogenous opioids, ACTH, and MSH
label the :
musculocutaneous N
axillary N
radial N
median N
ulnar N
subscapular Ns
suprascapular Ns
the plummer’s van parked in the driveway
differentiate the histo between
AML vs ALL
AML vs CML
CML = only lots of mature lymphotcytes (has granules) and <2% blast cells (the v dark nucleus takes up the entire cell, no granules)
CLL= no myeloblasts at all
AML = auer rod cells, ALL= none
aortic dissections usually occur where
endocardial cushion defect –> VSD or aatrial defects –> eisenmenger syndrome (presents later in life after the shunt reversal)
tightly bind your “CAB” -use dependence = 1C>1A>1C binding to Na channels
which of the following increase or decrease LV volume
- valsalva
- abdrupt standing
- nitroglycerin
- sustained hand grip
- squatting
- passive leg raise
DEC LV VOLUME
- valsalva —-> push out to bladder, legs,
- abdrupt standing
- nitroglycerin —> dec work of the heart
INC LV VOLUME
- sustained hand grip –> work out hand, thighs, leg
- squatting
- passive leg raise
Strep viridans is bile INsoluble and so doesNOT grow in NaCl or bile
what is seen when the probe is turned to look posteriorly?
pathogenesis of atherosclerosis
-what is the initial cell to be start the abnormal process, how does it progress
how will the administration of alpha 1 agonists change the heart rate
what is the effect of alpa 1, alpha 2, beta 1, beta 2, m2, and m3 receptors
effect of NE, epinephrine, phenylephrine, isoproteronol, and dobutamine on
heart contractility and SVR
what is the diagnosis and pathophysiology
B
Gamma-glutamyl carboxylase is an enzyme that catalyzes the posttranslational modification of vitamin K-dependent proteins. Many of these vitamin K-dependent proteins are involved in coagulation so the function of the encoded enzyme is essential for hemostasis.[5] Most gla domain-containing proteins depend on this carboxylation reaction for posttranslational modification.[6] In humans, the gamma-glutamyl carboxylase enzyme is most highly expressed in the liver.
normal heart changes = inc septal thickness and dec cavity volume
dx and pathophysiology of the given lesions
pathophysiology of conduction abnormality seen in
- a flutter
- a fib
- wolf parkinson white
- AV node re-entrant tachy
MC cause of sterile endocarditis = malignancy >> SLE
when would you see each answer choice
differentiate between the murmur heard in aortic stenosis vs hypertrophic cardiomyopathy
