practice test Qs Flashcards
1
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2
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3
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4
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5
Q
what type of antiarrythmic is ibutilide
A
class III- work on K channels

6
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7
Q
the following tumor markers are associated with what type of tumors
- pancytokeratin
- calretinin
- chromogranin A
- synaptophysin
*
A
- pancytokeratin
- mesothelioma
- calretinin
- mesothelioma (highly sensitivie)
- chromogranin A
- neuroendocrine marker for small cell lung cancer
- synaptophysin
- neuroendocrine marker for small cell lung cancer
8
Q
+ describe the pathophysiology of the diagnosis

A

9
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10
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fast to slowest
purkinje –> atrial mycoytes –> ventricular myocytes –> AV node
**park at venture avenue**

11
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desmosomes= made of cadherins = cell-cell junctions
hemidesmosomes = cell-BM junctions

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14
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15
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16
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17
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18
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19
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20
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21
Q
why are there no cutaneous findings

A
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

22
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24
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most likely dx

A

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27
what are the AE of all the other drugs listed as well


28

histamine's role is probably via H4 receptors

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31

two hit hypothesis = loss of heterozygosity

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40
patient presents with N. gonnorrhea
what is this, who is this seen in

howell jolly bodies
asplenia
41

E

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45

presence of babinski sign indicates myelination problem ~~ B12 needed to myelinate neurons

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48
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

49
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
*
50
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
51
the loss of which tumor suppressor gene --\>
* x ubiquitin ligase component
* xurogenitcal differentiation
* x Wnt signalling
and which CAs/syndromes are they associated with

52


53


54


55
which mutations and CAs are associated with...
* Lynch Syndrome
* FAP
* VHL
* Li-Fraumenni
* MEN1
* MEN2

56
differentiate between the components that make up an MHCI vs MHCII molecule

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60
61


62
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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64

FSGS = most common cause of nephrotic syndrome

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66
lymphatic drainage of the abdomen goes through which LN

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70

transketolase = xthiamine --\> wernicke korsakoff + beri beri

71

POMC = a precursor for endogenous opioids, ACTH, and MSH
72
label the :
musculocutaneous N
axillary N
radial N
median N
ulnar N
subscapular Ns
suprascapular Ns


73

the plummer's van parked in the driveway

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75
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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79
aortic dissections usually occur where

80

endocardial cushion defect --\> VSD or aatrial defects --\> eisenmenger syndrome (presents later in life after the shunt reversal)

81

tightly bind your "CAB" -use dependence = 1C\>1A\>1C binding to Na channels

82
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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84

Strep viridans is bile INsoluble and so doesNOT grow in NaCl or bile

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91
what is seen when the probe is turned to look posteriorly?


92
pathogenesis of atherosclerosis
-what is the initial cell to be start the abnormal process, how does it progress

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94
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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101
effect of NE, epinephrine, phenylephrine, isoproteronol, and dobutamine on
heart contractility and SVR

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107
what is the diagnosis and pathophysiology


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120

B

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125

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.

126
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
127

normal heart changes = inc septal thickness and dec cavity volume

128
dx and pathophysiology of the given lesions


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131
pathophysiology of conduction abnormality seen in
* a flutter
* a fib
* wolf parkinson white
* AV node re-entrant tachy

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133

MC cause of sterile endocarditis = malignancy \>\> SLE

134
when would you see each answer choice


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139
differentiate between the murmur heard in aortic stenosis vs hypertrophic cardiomyopathy
