First Aid, UWorld sets > practice test Qs > Flashcards

practice test Qs Flashcards

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5
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what type of antiarrythmic is ibutilide

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class III- work on K channels

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7
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the following tumor markers are associated with what type of tumors

  • pancytokeratin
  • calretinin
  • chromogranin A
  • synaptophysin
    *
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  • pancytokeratin
    • mesothelioma
  • calretinin
    • mesothelioma (highly sensitivie)
  • chromogranin A
    • neuroendocrine marker for small cell lung cancer
  • synaptophysin
    • neuroendocrine marker for small cell lung cancer
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8
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+ describe the pathophysiology of the diagnosis

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10
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fast to slowest

purkinje –> atrial mycoytes –> ventricular myocytes –> AV node

**park at venture avenue**

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11
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desmosomes= made of cadherins = cell-cell junctions

hemidesmosomes = cell-BM junctions

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21
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why are there no cutaneous findings

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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

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24
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most likely dx

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what are the AE of all the other drugs listed as well
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histamine's role is probably via H4 receptors
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two hit hypothesis = loss of heterozygosity
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patient presents with N. gonnorrhea what is this, who is this seen in
howell jolly bodies asplenia
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E
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presence of babinski sign indicates myelination problem ~~ B12 needed to myelinate neurons
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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
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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 *
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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
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the loss of which tumor suppressor gene --\> * x ubiquitin ligase component * xurogenitcal differentiation * x Wnt signalling and which CAs/syndromes are they associated with
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which mutations and CAs are associated with... * Lynch Syndrome * FAP * VHL * Li-Fraumenni * MEN1 * MEN2
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differentiate between the components that make up an MHCI vs MHCII molecule
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which autonomic receptors set off which G-couple receptors
a1 = q a2= i B(1,2,&3) = s "queens inspire songs"
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FSGS = most common cause of nephrotic syndrome
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lymphatic drainage of the abdomen goes through which LN
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transketolase = xthiamine --\> wernicke korsakoff + beri beri
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POMC = a precursor for endogenous opioids, ACTH, and MSH
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label the : musculocutaneous N axillary N radial N median N ulnar N subscapular Ns suprascapular Ns
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the plummer's van parked in the driveway
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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
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aortic dissections usually occur where
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endocardial cushion defect --\> VSD or aatrial defects --\> eisenmenger syndrome (presents later in life after the shunt reversal)
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tightly bind your "CAB" -use dependence = 1C\>1A\>1C binding to Na channels
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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
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Strep viridans is bile INsoluble and so doesNOT grow in NaCl or bile
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what is seen when the probe is turned to look posteriorly?
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pathogenesis of atherosclerosis -what is the initial cell to be start the abnormal process, how does it progress
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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
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effect of NE, epinephrine, phenylephrine, isoproteronol, and dobutamine on heart contractility and SVR
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what is the diagnosis and pathophysiology
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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.
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which leads correspond to STEMI of... * LAD * left circumflex * Right coronary A
* LAD * V1-V4 (distal LAD is only 3-4, proximal only 1-2) * left circumflex * I, avL, V5-V6 * Right coronary A * II, III, avF
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normal heart changes = inc septal thickness and dec cavity volume
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dx and pathophysiology of the given lesions
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pathophysiology of conduction abnormality seen in * a flutter * a fib * wolf parkinson white * AV node re-entrant tachy
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MC cause of sterile endocarditis = malignancy \>\> SLE
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when would you see each answer choice
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differentiate between the murmur heard in aortic stenosis vs hypertrophic cardiomyopathy
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