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Daily Flashcard Quizzes > 7/12 > Flashcards

7/12 Flashcards

1
Q

what is Kinesin

A

a microtubule motor protein that provides anterograde (away from nucleus to the axon) transport of NT-vesicles towards synaptic terminals

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2
Q

what is the most common hepatic malignancy

A

metastatic from another primary site

HCC can present multi focally, univocally, or as diffusely infiltratively. It’s more common in a pt w/ h/o cirrhosis or Hep B/C

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3
Q

what is cryptogenic stroke frequently associated with

A

Patent foramen ovale and atrial septal defect

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4
Q

how does a PFO close

A

after delivery, umbilical cord is clamped and there’s decreased pulmonary vascular resistance, which lowers RA pressure and raises LA pressure.

This pushes the septum premium against the septum secundum, closing the foramen ovale

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5
Q

differentiate between ASD and PFO

A

ASD:
results from APLASIA of septum primum or septum secundum during development;
may lead to embolism, but much less common than PFO
FIXED SPLITTING OF S2

PFO:
more common
incomplete FUSION of atrial septum premium and secundum

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6
Q

what will exztraperitoneal structures have layered on top of them

A

skin, fascia, abdominal muscle layers, anterior abdominal aponeurosis

(no peritoneum)

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7
Q

what are 2 antiretroviral therapy drugs that do not require kinase activation

A

Cidofovir and Foscarnet

Both are viral DNA polymerase inhibitors

both particularly useful in CMV and acyclovir-resistant HSV

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8
Q

what is unique about tRNA

A

noncoding RNA that contains many chemically modified bases (ex dihydrouridine, ribothymidine)

contains a “CCA” sequence at its 3’ end used as a recognition sequence by proteins

the 3’ terminal -OH on the CCA tail serves as the amino acid binding site, ensuring correct tRNA recognition by the proper aminoacyl tRNA synthetase

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9
Q

what are the tRNA secondary structure regions

A

acceptor stem:
base-pairing of the 3’ CCA + OH tail and 5’ nucleotides

D loop:
dihydrouridine residues that also help facilitate correct tRNA recognition by aminoacyl tRNA synthetase

Anticodon loop:
contains sequences complementary to the mRNA codon.
Ribosome complexes select the proper tRNA based solely on anticodon sequence.

T loop:
contains “TgreekYC” sequence necessary for binding of tRNA to ribosomes

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10
Q

what is Riboflavin a precursor for, and what enzyme is inhibited in defiancy

A

Vit B2 is a precursor for coenzymes FMN and FAD.

FAD participates in the TCA cycle with succinate dehydrogenase,
which converts succinate to fumarate

FAD and FAM are derived from riboFlavin
(B2 = 2 ATP)

deficiency = the 2 C’s of B2:
Cheilosis
Corneal vascularization

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11
Q

what does an elevated serum ACE level suggest

A

sarcoidosis

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12
Q

what is hyper acute rejection

A

type 2 hypersensitivity

Pre-existing antibodies react to donor antigen and activate complement.
Examples incl anti-ABO and anti-HLA antibodies

causes immediate (min-hrs) thrombosis, ischemia, and necrosis

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13
Q

what is acute organ rejection

A

cell mediated
usually weeks-months

exposure to donor antigens induces humoral and cellular activation of NAIVE immune cells

has a cellular and a humoral component

causes vasculitis with dense interstitial lymphocytic infiltrate.
prevent/reverse with immunosuppressants.

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14
Q

what is the cellular component of acute organ rejection

A

Cellular:
lymphocytic interstitial infiltrate and endotheliitis. These are CD8+ T cells activated against donor MHCs, which is Type 4 hypersensitivity rxn.

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15
Q

what is the humoral component of acute organ rejection

A

Humoral:
similar to hyper acute (recipient antibodies react to donor antigens), except the antibodies develop after the transplant.
There’s C4d deposition, neutrophilic infiltrate, and necrotizing vasculitis

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16
Q

what is the difference between a manic and a hypomanic episode

A 
manic:
severe symptoms
>1 week unless hospitalized
marked impairment in functioning!
may have psychotic features, which would make it automatically manic
hypomanic:
less severe
>4 consecutive days
change from baseline, but not severe enough to cause marked impairment or necessitate hospitalization 
NO psychotic features
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17
Q

what is viral reassortment

A

when viruses with segmented genomes (BOAR) exchange genetic material.

For example, novel H1N1 pandemic emerged via reassortment of human, swine, and avian virus genes.

Has potential to cause antigenic shift, and highly mutagenic viruses (influenza, ex)

reaSSortment = Segmented = Species = Shift

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18
Q

what is viral recombination

A

exchange of 2 genes between2 chromosomes by CROSSING OVER within region of significant homology. The progeny have gene traits from both parents.

reCombination = Crossing over

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19
Q

what is phenotypic mixing

A

when a host cell is simultaneously infected with 2 viruses.

Virus A’s genome can be covered by Virus B’s surface proteins.
This means Virus B’s coat determines the tropism (infectivity) of the hybrid virus.

However, the progeny of this infection will have Virus A’s coat, since Virus A is the one donating the genetic material.

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20
Q

what is transformation

A

the uptake of (viral) DNA and incorporation into host cell chromosomes (lysogeny)

this alters the genetic composition of host cell but typically causes no genomic changes in progeny virions

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21
Q

what is pancreas divisum

A

ventral and dorsal parts fail to fuse at 8 weeks

the pancreatic ductal systems remain separate, with the accessory duct draining the majority of the pancreas

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22
Q

what is annular pancreas

A

ventral pancreatic bud abnormally encircles 2nd part of duodenum, forms a ring, and may cause duodenal narrowing and bilious vomiting

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23
Q

where does the spleen arise

A

mesentery of stomach. it’s mesodermal

it has foregut blood supply

24
Q

what forms the majority of pancreatic tissue

A

dorsal pancreatic bud

it forms body, tail, and most of head

25
Q

what does the ventral pancreatic bud form

A

ventral pancreatic bud is the precursor of the uncinate process, inferior/posterior portion of the head, and major pancreatic duct

26
Q

when is K+ permeability highest in an action potential

A

during repolarization phase

not hyper polarization

27
Q

what is adenosine’s MOA

A

reduces rate of spontaneous depolarization in cardiac pacemaker cells.

interacts with A1 receptors to activate K channels and inhibit L-type Ca channels. this prolongs phase 4 and slows the sinus rate and AV nodal conduction delay

28
Q

what are rheumatoid arthritis antibodies

A

Rheumatoid factor,
which is and IgM auto-antibody against Fc component of IgG

also anti-citrullinated protein antibodies
(anti-CCP)

29
Q

which joints are spared in rheumatoid arthritis

A

DIP joints are spared

small joints (PIP, MCP, MTP) are affected

30
Q

what antibodies are in CREST syndrome

A

anti-centromere antibodies

31
Q

what antibodies are seen in PBC

A

anti-mitochondrial antibodies

32
Q

what patients would you see with antiphospholipid antibodies

A

patients with SLE and antiphospholipid antibody syndrome

33
Q

what does antiphospholipid antibodies cause

A

Antiphospholipid antibodies cause a hyper coagulable state with a paradoxical PTT prolongation

34
Q

what does aromatase do

A

converts androgens into estrogens

35
Q

what is aromatase deficiency

A

inability to convert androgens to estrogens

manifests with high androgen and low estrogen in female fetuses.

maternal virilization commonly occurs during pregnancy 2/2 transfer of baby’s androgens to maternal circulation.

36
Q

what is serum sickness

A

type 3 hypersensitivity rxn to nonhuman proteins

characterized by vasculitis 2/2 tissue deposition of circulating immune complexes.

clinical findings include fever, pruritic skin rash, arthralgia, and LOW SERUM C3 AND C4 COMPLEMENT LEVELS

37
Q

which 2 types of hypersensitivity rxns activate complement

A

Type 2 (cytotoxic) and Type 3 (immune complex) activate complement

38
Q

what is Infliximab’s MOA

A

it targets soluble TNF-alpha to be used in autoimmune disease, including IBD, RA, ankylosing spondylitis, and psoriasis

39
Q

what other drugs have a similar MOA to Infliximab

A

Adalimumab and Certolizumab

these all target TNF-alpha

40
Q

what is Etanercept’s MOA

A

it is a TNF-alpha receptor decoy

it’s not a monoclonal antibody

41
Q

what paraneoplastic syndrome is seen in squamous cell carcinoma of the lung

A

severe hypercalcemia 2/2 PTHrP

this acts like PTH so you have increased bone respiration and decreased renal excretion of Ca

42
Q

what is rat poisoning made of, and how do you reverse it

A

“super warfarin”

you reverse it quickly with FFP, which contains all blood clotting factors and proteins.

43
Q

how do you reverse a Heparin overdose

A

Protamine sulfate

it binds to heparin, forming a complex that has no anticoagulant activity

44
Q

What is Conn Syndrome

A

primary hyperaldosteronism from an aldosterone-producing adenoma

this is a yellow-brown tumor

presents with:
excess Na retention
excess urinary K and H+ secretion
HTN, hypokalemia, metabolic alkalosis
paresthesias and muscle weakness
45
Q

what is aldosterone escape

A

the mechanism that limits fluid volume expansion when a pt has hyperaldosteronism

it limits edema
it limits hypernatremia

the HTN and high blood volume:
increases RBF
increases GFR
increases ANP
all 3 of these increase Na excretion
46
Q

what are the 2 pentose phosphate pathways

A

an oxidative (irreversible) branch

a non oxidative (reversible) branch

each function independently based on cellular requirements

47
Q

what is the enzyme in the non oxidative step of the HMP shunt

A

Transketolase

this is a reversible enzyme

48
Q

what does transketolase do

A

it interconverts ribose-5-phosphate and fructose-6-phosphate in the HMP shunt

49
Q

what is the significance of ribose-5-phosphate

A

ribose-5-phosphate is a nucleotide precursor that is made in the HMP shunt.

when ribose-5-phosphate is in excess, you produce glycolytic intermediates to get back to the glycolysis pathway for ATP generation (via reversible non-oxidative pathway).

when ribose-5-phosphate is in demand and exceeds the capabilities of the oxidative (irreversible) path, then the non oxidative reverses so that the transketolase reverts fructose-6-phosphate away from ATP-producing glycolysis pathway and toward the HMP shunt

50
Q

what is the significance of fructose-6-phosphate

A

fructose-6-phosphate is a glycolytic intermediate

it can be converted to ribose-5-phosphate via transketolase

51
Q

what is the rate-limiting enzyme in the oxidative path of the HMP shunt

A

the oxidative path of the HMP shunt is irreversible

the rate-limiting enzyme is glucose-6-phosphate dehydrogenase (G6PD)

52
Q

what is the significance of the oxidative path of the HMP shunt

A

the oxidative path uses G6PD to produce NADPH

NADPH is required for cholesterol and fatty acid synthesis, as well as a glutathione antioxidant mechanism

53
Q

what is penicillin’s MOA

A

they’re structural similar to D-alanine-D-alanine

they inhibit transpeptidase by binding covalently to its active site

transpeptidase normally catalyzes the final cross-linking of the peptidoglycan wall

this means failed synthesis of the bacterial peptidoglycan wall

54
Q

what is Vancomycin’s MOA

A

binds directly to D-ALA-D-ALA residues

the binding prevents incorporation into the cell wall.

55
Q

what is trimethoprim/sulfonamide’s MOA

A

Trimethoprim:
blocks a step in folic acid synthesis by inhibiting the dihydrofolate reductase enzyme

Sulfonamide:
competes with para-aminobenzoic acid for incorporation into folic acid

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