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USMLE® Step 1 flashcards
1
Q

hyponatremia, abd pain with fasting, worsens with barbitruates

A

Acute Intermittent Porphyria

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2
Q

blisters on skin, tea colored urine that turns pink under woods lamp

A

porphyria cutanea tarda

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3
Q

Snail

A

schistoma

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4
Q

tsetse fly

A

trapanosoma brucei; african sleeping disease

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5
Q

Treatment for bacillus ceres

A

supportive

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6
Q

Infective steatorrhea

A

Giardia

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7
Q

Naegleria fowleri sx

A

abd pain, N/V, CNS changes–>rapid coma

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8
Q

Counsilman bodies

A

eosinophilic round granules in hepatocytes…yellow fever

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9
Q

HNPCC–>name 2 cancers

A

colon and endometrial

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10
Q

Ileal resection –>at risk for what?

A

Gall stones; B12 deficiency

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11
Q

Gastroparesis treatment?

A

metoclopromide, erythromycin

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12
Q

What is a drug contraindication when using Allopurinol?

A

azathioprine–>will accumulate due to allopurinol inhibition of XO; will cause hemolytic anemia

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13
Q

Drugs for Gaves?

A

PTU methimazole–>inhibition of thyroid peroxidase

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14
Q

hyperglycemia, weightloss, diarrhea–>doesn’t respond to metformin
necrolytic migratory erythemia
dx?

A

glucagonoma

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15
Q

acromegaly treatment

A

Octreotide

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16
Q

short 4th and 5th metacarpals

A

psuedohypoparathyroidism–>high PTH low calcium because organs cannot sense PTH

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17
Q

Pt has hashimoto’s what else in predisposition

A

DM1; and celiac’s

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18
Q

thyroid hormone is what kind of hormone?

A

steroid

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19
Q

PTU side effect?

A

agranulocytosis

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20
Q

air above liver upon xray

A

GI perforation

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21
Q

still born baby with edematous hands and feet

A

Turner syndrome

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22
Q

lung mass, hypercalcemia on labs. what is dx? why is calcium high?

A

spquamous cell carcinoma; due to PTHrP

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23
Q

pt admitted for angina or MI. develops DVT a couple days later. What do you suspect? how do you treat?

A

HIT. treat with direct thrombin inhibitors (bivalirudin, dabigatran, argatroban)

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24
Q

abciximab, eptifibatide mech?

A

IIb/IIIa inhibitor. thus platelet aggregation inhibitor

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25
Q

how does estrogen affect thyroid hormone?

A

decreases TBG catabolism. thus increasing bound Thyroid hormone… thus increasing over all pool of thyroid hormone. NO difference in free/active thyroid hormone.

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26
Q

what is chromatolysis?

A

neuronal changes post axonal damage. neuron revs up protein synthesis and nissl body expands

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27
Q

Dystrophic versus metastatic calcification. location/diseases/serum calcium status?

A

dystrophic is due to damage/necrosis (aging heart valve, TB, monkeberg, psammoma body). pt is normocalcemic

metastatic caclification is due to overall hypercalcemia –>such as in sarcoidosis, vitaminosis D…etc. you see calcifications everywhere

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28
Q

prepatellar bursa is where?

pes anserina is where?

A

-pretellar bursa is in the lower pole of patella

pes anserina is on the medial leg

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29
Q

first line tx for RA? others? which is the fastst thing for sx relief?

A

methotrextate= firstline tx; corticosteroids=fastest relief. leflunomide, TNFalpha inhibitors, and steroids

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30
Q

is stool usually lower or higher in osmolarity than blood? in what case will this gap increase?

A

it’s usually lower. the gap will increase with indigestible things which will osmotically hold on to the water making it even more hypoosmotic (ex: lactose intolerance)

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31
Q

centrilobular necrosis of the liver

A

acetaminophen toxicity–>liver damage/failure

or ischemic damage

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32
Q

which lung cancer is nonsurgical

A

small cell carcinoma

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33
Q

alpha amatoxin causes what symptoms?

A

because it halts RNA pol II–>stops protein synthesis thus cells with rapid turnover are affected.

N,V,D/ liver failure/renal failure (PT especially)

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34
Q

NK cells express what CDs?

A

16, 56

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35
Q

what activates NK cells

A

cytokines: IFNY, IL12

lack of MHCI on cell

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36
Q

which drugs are used to treat mild rheumatoid arthritis?

A

sulfasalazine, hydroxychloroquine, minocycline

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37
Q

heterophile antibody negative mono?

A

CMV. READ YOUR QUESTIONS CAREFULLY

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38
Q

patient on opioid has severe abdominal pain. Why?

A

mu agonists will cause smooth muscle contraction (hence constipation? hence miosis?)

therefore contraction of sphincter of oddi may lead to colicky obstructive pain

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39
Q

opioid pain treatment of choice for biliary/pancreatic pain source?

A

meperidine. mu agonist but has less effect on Oddi constriction compared to other mu agonists

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40
Q

what is the mechanism of organophosphates?

A

they’re irreversible cholinesterase inhibitors

treat: atropine, prailadoxime

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41
Q

how do you treat serotonin syndrome/SSRI overdose?

A

cyproheptadine (first generation histamine inhibitor with 5HT blocking properties)

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42
Q

Ecthyma gangrenosum

causal organism? factors?

A

pseudomonas. pyocyanin (ROS), exotoxin A, phospholipase C, elastase

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43
Q

name 2 H1 inhibitors

A

chlorpheniramine, diphenhydramine

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44
Q

what are sedatives that should not be used together?

A

alcohol, benzodiazepine, barbiturates, antihistamines, antipsychotics

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45
Q

brain tumor with hemorrhage and necrosis. what type of cell is the tumor made of?

A

this is glioblastoma multiforme. therefore, astrocytes

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46
Q

brain tumor with calcifications? what kind of tumors could this be?

A

oligodendoglioma (or it could also be meningioma with psammoma bodies)
cranial pharyngioma

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47
Q

brain tumor with calcifications? what kind of tumors could this be?

A

oligodendoglioma (or it could also be meningioma with psammoma bodies)

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48
Q

name the enteroviruses? are they acid labile or stable?

A

echovirus, poliovirus, and coxackie virus

these are all acid STABLE thus enterovirus!
Rhinovirus is the only acid labile picornavirus…thus it’s in the nasal passage

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49
Q

what are hnRNA?

A

heterogenous nuclear RNA. these are the newly transcribed RNA that have not gone through RNA processing. they’re in the nucleus, duh!

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50
Q

what is the RNA processing/storage center in the cytoplasm called?

A

P bodies

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51
Q

you hear holosystolic murmur…what could it be?

A

mitral valve regurg, tricuspid regurg, VSD

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52
Q

holosystolic murmur that increases with inspiration

A

tricuspid valve regurgitation

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53
Q

mucosal bleeding, petechiae are seen in what kind of bleeding disorders?

A

platelet aggregation disorders—>vWBD

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54
Q

hemearthrosis, intramuscular bleeds, prolonged bleeding with dental work? bleeding disorder?

A

hemophilia

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55
Q

G6PD is deficient in what?

A

NADPH; thus can’t reduce glutathione

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56
Q

what is Osler-Weber-Rendu

A

hereditary hemorrhagic telangiectasia; autosomal dominant

arteriovenous malformations, telangiectasia/skin discoloration, epistaxis, hematuria, GI bleeds

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57
Q

syncope, angina, and dyspnea. with heart murmur

A

aortic stenosis

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58
Q

sudden cardiac death in a young person. What do you have to think about?

A

HCM, WPW, cor pulmonale

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59
Q

etiology of WPW?

what do you see on EKG

A

reentrant circulation through bundle of KENT by passing slow AV node.
EKG: delta wave, and shortened PR interval, resulting in SVT

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60
Q

what mutation will predispose someone to disseminated mycobacteria infections?

A

IFNY R

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61
Q

What receptor does IFNY act through?

A

Jak 1 and 2, upregulating phagocytosis, MHC, and antimicrobial elements

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62
Q

recurrent lower respiratory tract infections and recurrent Giardia infections? what is the immune def

A

X linked Agammaglobulinemia=Bruton’s

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63
Q

C3 deficiency leads to recurrent what infections?

A

encapsulated

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64
Q

delayed detachment of umbilical cord, poor wound healing with no pus production. what is the dx and what receptor is missing?

A

defect in leukocyte adhesion. lack of CD18 is a common defect of integrins

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65
Q

RBC lifespan

A

120 days

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66
Q

what bacterium has protein A as its virulence factor? what does it do?

A

Staph aureus–> binds Fc of IgG

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67
Q

bacterium with cytoplasmic polyphosphate granules upon methylene blue

A

diphtheria

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68
Q

diphtheria toxin ribosylates elatongation factor 2. what does elongation factor 2 do?

A

protein synthesis elongation

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69
Q

Which class of antiarrhythmics has use dependent sodium channel blocking ability? list the subclasses

A 
class 1-->the sodium channel blockers. 
subclasses listed by duration of binding 1C>1A>1B
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70
Q

What is the action of class 1c antiarrhythmics and why is it rarely used?

A

prolonging K channels and inhibiting Na/Ca channels can both elongate QT interval and thus may allow reentrance and arrythmias

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71
Q

How long must a couple wait after vastectomy to not use contraception? why

A

viable sperm remain in the proximal vas–>thus must wat 3 months or 20 ejaculations

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72
Q

why is there still a significant amount of ejaculate post vasectomy?

A

ligation is done at vas that is near the testes…thus not affecting the seminal vesicle, prostate, and bulbourethral glands

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73
Q

ambiguous genitalia at birth; normal male sex characteristics develop at puberty. what is missing?

A

5 alpha reductase

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74
Q

17 alpha hydroxylase deficiency
what is low and what is high?
what are the sx/characteristics of these patients?

A

High: mineralcorticoids
low: glucocorticoids and sex hormones (both estrogen and androgens)

genetic males will have female external genitalia and male internal genitalia.
all pts will fail to develop secondary sexual characteristics due to general lack of sex hormones
Hypertension, hypokalemia, and low renin will be seen.

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75
Q

which structure of the celiac trunk is not endodermal derived? what is its origin?

A

liver and pancreas ARE endoderm outpouching derived.

Spleen is NOT–> it’s mesodermal from dorsal mesentery

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76
Q

Gottron’s nodules

A

Dermatomyositis

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77
Q

which spinal levels are in the femoral nerve?

A

L2-L4

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78
Q

Which spinal levels are in the sciatic nerve?

A

L4-S3

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79
Q

can’t plantar flex is injury of what nerve?

can’t dorsi flex is injury of what nerve?

A

plantar flexion is accomplished by S1

dorsiflexion is accomplished by L5

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80
Q

what is diastolic depolarization. How is it affected by calcium channel blockers?

A

diastolic depolarization occurs in SA and AV node where sodium current drift into cells in phase 4 (repolarization). at the end of phase 4 calcium flows in until action potential is triggered in phase 0.

thus calcium channels block the end of phase 4 and phase 0 therefore slowing the pacing of the heart.

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81
Q

resistance is the greatest where in the lung? it’s the least where in the lung?

A

greatest at 2-5th generation of lung due to turbulent flow.

least in the small branches/alveoli due to large cross area

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82
Q

what is natural competency? what bacteria are naturally competent?

A

abilityto uptake naked DNA strands drom environment (transformation)

Strep pneumo
haemophilus
neisseria gon and mening

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83
Q

alkaptonuria is a result of defect in which pathway (which amino acid is converting to what?)

A

Tyrosine to fumarate; homogenisate oxidase is defective

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84
Q

what is leucine metabolized to?

A

acetoacetate and acetyl coa

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85
Q

what are isoleucine and valine metabolized to?

A

succinyl coa

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86
Q

name the vessels most affected by atherosclerosis?

A

abd aorta, coronary artery, popliteal artery, internal carotid artery, circle of willis

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87
Q

anticholinergic meds, severe head ach and eye pain

A

close angle/narrow angle glaucoma

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88
Q

what are 4 classes of drugs used for glaucoma? what are the mechanisms?

A

beta blockers and acetazolaminde–> decrease aqueous humor production from ciliary epithelium

prostaglandin F2a ( latanoprost, unoprostone, travoprost) and cholinomimetics (pilocarpine, carbachol) increase outflow

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89
Q

what produces aqeous humor?

A

ciliary epithelium in the ciliary body…which is in the posterior chamber

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90
Q

hemoptysis, nasal mucus ulceration, chronic sinusitis, renal disease. dx

A

wegener C anca

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91
Q

what kind of skin changes can you see in chronic venous insufficiency

A

venous insufficiency=varicose veins…

you can see dermatitis, dermal fibrosis, and hyperpigmentation

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92
Q

which enzyme involved in some glycolytic pathways may be affected in gestational diabetes?

A

glucokinase. It’s pancreas’s way of sensing and trapping glucose. Therefore this may be overwhelmed in pregnancy. The direct glycolytic enzymes do NOT cause gestational DM

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93
Q

what’s similar and what’s different about Rubella and Rubeola?

A

both start on head and spread downward (rash)

Rubella travels faster and is not as dark/convelscent, postauricular lymphadenopathy
Rubeola is dark and convelscent but spreads slower

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94
Q

what is german measels, what is measels?

A

measles is rubeola;

german measels is rubella

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95
Q

Rubeola is what kind of virus?

A

paramyxovirus

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96
Q

German measles is what kind of virus?

A

togavirus

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97
Q

postauricular lymphadenopathy is associated with rubeola or rubella?

A

Rubella

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98
Q

What is winter’s formula. What do you use it for?

A

to determine if low pCO2 in metabolic acidosis is due to compensation or due to a mixed disease.

paCO2=1.5(HCO3)+8 +/-2

if it’s not predicted then this is likely a MIXED disorder. meaning metabolic acidosis + respiratory alkalosis/acidosis

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99
Q

what kind of metabolic abnormalities do you see in salicylate poisoning?

A

first you get respiratory alkalosis
few hours in you will get worsening metabolic acidosis because salicylate UNCOUPLES ELECTRON CHAIN TRANSP, inhibits TCA cycle, and increases lipolysis–>build up of pyruvate, ketoacids, lactate

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100
Q

what is the mechanism of reflex tachycardia

A

dilation of arterial vessels–>drop in pressure–>decreased baroreceptor firing–>triggers SNS–>tachycardia/contraction/REnin/angiotensin system activation

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101
Q

What may be the benefit of giving hydralazing and a beta blocker togeter?

A

hydralazine will dilate the vessels, and beta blocker will prevent SNS activation of reflex tachycardia AND renal sodium retention

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102
Q

congenital bilateral absence of vas deferens

A

CF! (or unilat renal agenesis)

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103
Q

what is azoospermia

A

no sperm in semen

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104
Q

what does xeroderma pigmentosa literally mean

A

pigmented dry skin

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105
Q

statin indication? side effects?

A

high LDL; SE: hepatic injury, increased LDL

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106
Q

niacin indication? side effects?

A

indicated for low HDL;

Flushing, hyperglycemia, hyperurecemia, hepatic injury

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107
Q

cholestyramine indication? side effect?

A

indication: high LDL
SE: GI sx, malabsorption, gall stones

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108
Q

Fibrates indication? side effects?

A

indication: high Triglycerides
SE: gallstones, myopathy with statins

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109
Q

phenylephrine stimualtes which receptor(s)?

A

alpha 1

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110
Q

Dopamine stimulates waht receptors?

A

low dose–>D1–>increased GFR and mesenteric blood flow (BOTH BY VASODILATION)
med dose–>D1 and beta 1–>cardiac output/renal increase GFR (BETA WILL CAUSE VASOCONSTRICTION)
high dose D1, beta1, alpha 1–>increase BP

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111
Q

why might implementation of ACE inhibitors lead to rise in creatinine? especially in patients with renal artery stenosis

A

ACE keeps GFR up in renal stenosis by vasoconstriction. ACE I will targetedly dilate efferent arteriole, so if there’s underlying GFR compromise, the compensatory mechanism is taken away

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112
Q

pleuritic pain is transmitted to where? along what nerve?

A

to the shoulder/neck area via phrenic nerve C3-5

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113
Q

4 features of neurleptic malignant syndrome? what drugs cause this?

A

sx: hyperthermia, muscle rigidity, unstable ANS, and altered mental status

Drugs: antipsychotics especially ones that have D2 inhibition

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114
Q

mitral valve thickening small vegetations on both sides

A

SLE LIBMAN SACKS

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115
Q

preeclampsia sx

A

edema, hypertension, proteinuria

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116
Q

crohn’s disease is associated with what type of kidney stones? how does this occur?

A

oxalate stones;
poor reabsorption of fats in the GI tract lead to fat binding Calcium and are excreted. This results in increased oxalate (unable to bind calcium) absorption and thus accumulates

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117
Q

How long after MI will red wavy fibers, edema, and punctate hemorrhage show up?

A

4-12 hrs

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118
Q

tetanus toxin is transported retrograde in neurons and inhibit what neurotransmitters?

A

GABA glyciine

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119
Q

what are the risk genes for EARLY onset alzheimer’s

A

APP on Chr 21, Presenillin 1 (chr 14) and Presenillin 2 (chr1)

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120
Q

What genes are indicated as risk factors in LATE onset alzheimers? what’s protective?

A

ApoE4 is risk factor. ApoE2 is protective

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121
Q

common mutation in HCM?

A

beta myosin chain

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122
Q

Von Hippel Lindau gene does what? why does this make sense given clinical presentatioN?

A

VHL gene induces Hypoxia Inducible Factor–> endothelia and blood vessel proliferation. THIS IS why you get the hemagiomas, RCC, and pheochromocytoma…

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123
Q

what chromosome is Von hippel Lindau on?

A

chr 3

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124
Q

3 classic histology signs of B6, B12 deficiency

A

megaloblastic anemia, hypersegmented neutrophils (6+ lobes), and crazy platelets

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125
Q

what is side chain cleavage enzyme? what if it’s deficient?

A

It catalyzes conversion of cholesterol to pregnenolone. without it cholesterol will accumulate in adrenals and lead to damage of adrenal gland. There also will not be ANY steroid hormones

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126
Q

what is the amino acid mutation of Sickle Cell?

A

Glu to Val

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127
Q

what is the amino acid mutation of HbC?

A

Glu to Lys

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128
Q

HbA, HbS, and HbC. what are the expected charges?

A

HbA is negative charged
HbS–>Glu to Val–> Neg charged to neutral charged. Still negative but less so than HbA
HbC–>Glu to Lys–>more positive than BOTH HbA and HbS

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129
Q

false neutrophil elevation. What’s probably the cause?

A

corticosteroids–> demargination of neutrophils; while decreasing all the other leukocytes

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130
Q

dry mouth, tachycardic, hyperphagia, inappropriate laughter, conjunctival injection. What drug is this?

A

Marijuana

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131
Q

what are Ruffini receptors?

A

slow adapting mechano receptors in skin

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132
Q

What do Golgi Organs prevent? how do they do it?

A

too much muscle contraction. travel through Ib–to InhiBit alpha motor neurons

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133
Q

What do intrafusal fibers prevent? how do they doit?

A

too much muscle lengthening–travel through Ia and II neurons to trigger alpha motor neuron (contraction)

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134
Q

thalamic strokes knocks out what?

internal capsule strokes knock out what?

A

thalamic is sensory body/face

internal capsule is mortor body/face

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135
Q

pink patches in white matter tracts; oligodendrocyte apoptosis. dx?

A

MS

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136
Q

yello renal tumor; microscopically polygonal cells filled with glycogen and lipid with eccentric nucleus. Where in the kidney/nephron did this tumor originate?

A

Proximal tubule, clear cll carcinoma

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137
Q

renal pelvis tumor. What is it called? and what’s the histology?

A

transitional cell carcinoma; it often is papillary

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138
Q

Renal Oncocytoma. Where is it usually found? what is a characteristic histo feature?

A

collecting duct; it has abundant mitochondria

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139
Q

why might you hear a murmur with ASD?

A

L to R shunting will cause volume increase in R heart… increased flow across Pulmonic valve is the reason for the murmur.

In ASD you usually don’t hear a murmur

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140
Q

why does hyperventilation cause you to pass out?

A

hypocapnea causes vasoconstriction–>decreased perfusion to brain.

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141
Q 
Antivirals...what are the
vudines?
cyclovirs?
fovirs?
navirs?
Raltegravir?
A 
vudines=reverse transcriptase inhibitors
cyclovirs=nucleoside analogs that need viral T kinase
fovirs=nucleotide analogs
navirs=protease inhibitors
raltegravir=integrase inhibitor
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142
Q

ambiguous genitalia in baby girl; maternal hirsutism in pregnancy. what’s missing? what will happen at puberty?

A

aromatase is missing; at puberty the female will NOT get period, be tall in stature, and have early osteoporosis (all due to lack of estorgens)

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143
Q

what type of patient is most at risk for mucormycosis?

What type of patient is most at risk for aspergillosis?

A

mucor=DM pt

aspergillus=neutropenia

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144
Q

black eschar in nasal mucosa; diabetic ketoacidosis. What is it? how do you find out?

A

Mucormycosis/Rhizopus, do biopsy

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145
Q

what type of patient is most at risk for mucormycosis?

What type of patient is most at risk for aspergillosis?

A

mucor=DM pt, neutropenia

aspergillus=neutropenia

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146
Q

middle meningeal artery/vein pass through what hole in the skull?

A

foramen spinosum

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147
Q

vancomycin generally is used to treat what class of bacteria?

A

G+

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148
Q

Polymyxin=Colistin is used for waht class of bacteria? what does it NOT work against?

A

G- bacteria EXCEPT for Neisseria

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149
Q

heated blood agar with vancomycin, colistin, nystatin, and trimetheprim…what is this agar?

A

theyar martin

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150
Q

which antibiotic has a disulfram-like side effect?

A

metronidazole

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151
Q

Sabouraud agar grows what?

A

Coccidioides immitis

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152
Q

LOC due to severe hypoglycemia is treated how in in hospital? NOT in hospital?

A

If there’s IV access–> push dextrose/glucose slowly

If no IV access–> IM glucagon (IM glucose is NOT useful)

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153
Q

What are TWO effects of digoxin

A

increase contractility via potentiation of intracellular calcium. decrease
AV node conduction via increasing PNS stimulation

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154
Q

mullerian inhibition factor is secreted by what cells?

A

sertoli

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155
Q

why do you get alcoholic hepatic steatosis?

A

because alcohol DH and acetaldehyde DH are taking up all the NAD and reduced it to NADH. This stops TCA cycle and beta oxidation, and gluconeogenesis. thus accumulates fats (especially as triglyceride synthesis is also increasing)

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156
Q

glucocorticoids increase protein synthesis in waht organ?

A

liver (gluconeogenesis and glycogenesis proteins)

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157
Q

CF. what is the amino acid mutation?

A

deleted phenylalanine

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158
Q

What organism produces acid in glucose fermentation?

A

shigella

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159
Q

what organism produces H2S?

A

Salmonella

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160
Q

what happens in the first few weeks of TB primary infection

A

the respiratory drops carry TB in to lungs, and they replicate until Mphage burst…they continue to replicate and infect macrophages to prevent T cell signalling…thus T cell response will occur about 3 weeks post exposure.

Then the Th1 and macrophages will attack TB and wall it off in granulomas

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161
Q

aconitase contains what elements

A

iron, sulfur

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162
Q

which steps in Gluconeogenesis are in the mitochondria? what is the enzyme that leaves the mitochondria?

A

Pyruvate is converted to Oxaloacetate in the mitochondria by pyruvate carboxylase to malate, which leaves

malate is converted back to oxaloacetate in the cytoplasm

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163
Q

cataplexy is often triggered by what? what’s the other presentation?

A

emotions–> loss of muscle tone pt is conscious;

OR abnormal facial movements without emotional trigger

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164
Q

14-3-3 protein in CSF?

A

creuzfeld jakob

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165
Q

homovanilic acid is a metabolite of what?

A

dopamine (thus Epi/NE too)

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166
Q

increased AFP in gestation can indicate what 3 things?

A

multiple gestation
open neurotube
open anterior abd wall

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167
Q

low AFP, low conjugated estriol, high hCG, high inhibin A.

what is this?

A

This is the QUAD screen of second trimester

screening for down syndrome

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168
Q

Which two parental things can lead to higher risk of downsyndrome?

A

maternal age >35; and robertsonian translocation of 21 and 14

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169
Q

what is in the gonadal “round ligament”?

A

artery of sampson. rarely a source of bleeding

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170
Q

how can you tell the difference between absolute erythrocytosis versus relative erythrocytosis?

A

(relative erythrocytosis=volume contraction…NOT bleeding)

LOOK AT RBC MASS!!!

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171
Q

erythropoitin production site in adults? fetuses?

A

kidney in adults; liver in fetuses

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172
Q

when in the respiratory cycle is the perfusion the best?

A

its the best at the end of tidal volume since the stretch from inspiration is the least yet the pressure is not dominated by postitive inward pressure

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173
Q

what are the correlated events in venous pulse wave?

a, c, x, v, y

A 
a=atrial contraction
c=trCuspid bulge
x=atrial relaXation
v=ventricular contraction
y=passive flow in to atrium
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174
Q

what could steep y decend wave indicate?

A

restrictive pericarditis

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175
Q

What causes carboxyhemoglobinemia

what causes methemoglobinemia?

A

carboxy=CO–>CARBON MONOXIDE!

met=Fe3+ –>Nitro drugs/sulf drugs

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176
Q

how does carboxyhemoglobinemia affect oxygen curve? PaO2?

A

it will L shift the curve and bring it down…it decreases amount of Hb available to bind O2 and decreases Hb ability off load O2.

HOWEVER. PaO2=/=HbSaturation=/=O2 content. PaO2 is dependent on atm PaO2 and diffusion/perfusion.

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177
Q

TNFalpha, catecholamines, glucocorticoids, and glucagon induce insulin resistance. How is this accomplished?

A

Serine/thr kinase phosphorylates IRS complex, so that the receptor cannot send the signals in.

178
Q

ACL inserts on the anterior or posterior aspect of Tibia?

A

anterior

179
Q

Isoniazid resistance by TB is accomplished how?

A

decrease in activating enzyme catalase peroxide

mutation in binding protein

180
Q

what is acrolein?

A

toxic metabolite of cyclophosphamide when metabolized by kidneys. Mesna can bind acrolein to reduce risk of hemorrhagic cystitis

181
Q

sterile small non destructive fibrinous vegetations lining the closure cusps of heart valves. what is this?

A

non-bacterial thrombotic endocarditis. MARANTIC. due to procoagulant state

182
Q

marantic valvular vegetations/nonbacterial thrombotic endocarditis is associated with with what diseases?

A

CANCERS…pancreatic adenocarcinoma or lung adenocarcinoma

183
Q

what is the function of lysysl oxidase in collagen?

A

disulfide crosslinking between collagen

184
Q

rabies virus binds to what receptor?

A

nicotinic ach receptor–>then retrograde travel

185
Q

Rhinovirus binds to what receptor?

A

ICAM1 (CD54)

186
Q

cytomegalovirus binds to what receptor?

A

Integrins

187
Q

EBV binds to what receptor?

A

CD21 (CR2)

188
Q

which pneumoconeosis resembles sarcoidosis?

A

Berrylliosis—> LOOK FOR EXPOSURE TO MINES

189
Q

How does N acetylcystein help acetaminophen toxicity?

How does N acetyl cystein help CF patients?

A

Acetaminophen tox–> it regenerates glutathione

CF–>cleaves disulfide bonds in mucin glycoproteins–>looser mucus

190
Q

thiopental is a barbiturate anesthetic. What is the mechanism responsible for patients waking up quickly from it?

A

It is NOT metabolized rapidly. Rather it is distributed to skeletal muscles and fat

191
Q

fever, maculovesicular rash, renal failure with RBCs, eosinophils and neutrophils in urine.

What is this called? what is it caused by?

A

Acute Interstitial Nephritis.

-Sulfonamides, Rifampin, NSAID, diuretics
maybe you should listen to goljian tell you about this

192
Q

Acute Interstitial Nephritis you see peripheral eosinophilia with waht stains?

A

Hansel stain

wright stain

193
Q

papillae necrosis of kidneys; 3 ddx?

A

SICKLE CELL, pyelonephritis, DM

194
Q

why is busprione only used for GAD?

what are some advantages of buspirone over benzos?

A

GAD because it takes weeks to become effective..thus not for acute relief

advantages is there’s no dependency, no sedation, no muscle relaxant, no seizure prophylactic effect. JUST aniety

195
Q

What are two advantages of Celecoxib?

A

No interaction with thromboxane (therefore nl platelet fxn),
No corrosive actions in GI

196
Q

Hypertensive emergency and patient has renal concomitant renal insufficiency. WHAT DO you use?
WHY?

A

Fenoldapam–> SELECTIVE D1 agonist. with NO effect on alpha and beta receptors.
It vasodilates as well as maintain renal perfusion and promotes diuresis

197
Q

Wilm’s tumor mutation?

A

WT1

198
Q

spontaneous bursts of random eye movements and myoclonus+hypotonia in child. Abdominal mass. what is this disease? what’s the mutation?

A

This is neuroblastoma of the adrenal medulla due to N-myc amplification.
this results in increased metanephric precursors

199
Q

what is the disease if a child presents with pheochromocytoma like sx?

A

neuroblastoma

200
Q

spontaneous bursts of random eye movements and myoclonus+hypotonia in child. Abdominal mass. what is this disease? what’s the mutation?

A

Opsoclonus-myoclonus
This is neuroblastoma of the adrenal medulla due to N-myc amplification.
this results in increased metanephric precursors

201
Q

isolated systolic hypertension. calcification of abdominal aorta see on xray

A

monkenberg sclerosis

202
Q

acute intermittent porphyria… what’s the def?

A

porphobilinogen deaminase

203
Q

Urine that darkens… ddx?

A

alkaptonuria

acute intermittent porphyria

204
Q

how do you make acute intermittent porphyria better?

A

you try to stop ALAsynthase so that less products are sent down the heme synthesis pathway.

Use HEME and GLUCOSE to stop ALAs via neg feedback

205
Q

what makes intermitten porphyria worse?

A

CYPP450 inducers

206
Q

what makes intermitten porphyria worse?

A

CYPP450 inducer durgs, alcohol, smoking

207
Q

two types of bone ossification

A

endochondral–long;

intramembranous

208
Q

two types of bone ossification

A

endochondral–long;

intramembranous-flat bones

209
Q

three main compensatory components of reduced cardiac output?

A

increase SNS stimulation,
Renin-ang-aldo pathway increase
Increased ADH release

210
Q

three main compensatory components of reduced cardiac output?

how can this be bad?

A

increase SNS stimulation,
Renin-ang-aldo pathway increase
Increased ADH release

fluid/sodium retention will worsen afterload thus put more pressure on the heart. Aldosterone also lead to cardiac remodeling and fibrosis

211
Q

what cells participate in late phase anaphylaxis?

A

mainly eosinophils, but also neutrophils and basophils

212
Q

What is the main component of eosinophil granules?

A

major basic protein

213
Q

what is the main component of basophil granules

A

histamin, heparin, and SRSA

214
Q

What is the main component of eosinophil granules?

A

major basic protein–>destroys outer membrane of helminths

215
Q

what is the role of mTOR?

A

activation leads to cell proliferation.

216
Q

What activates mTOR? what inhibits it?

A

PI3K–>AKT–>mTOR pathway is activating

PTEN inhibits mTOR

217
Q

why are Turner syndrome patients usually short?

A

they’re ususally missing a SHOX gene from the missing X which influences long bone growth

218
Q

Which X is usually missing in Turner syndrome?

A

paternal

219
Q

dihydrorhodamine test. what is it used to test?

A

presence of superoxides and thus Neutrophilic NADPH oxidase activity..if deficient–>chronic granulomatous disease

220
Q

Nitroblue tetrazolium. what is it used for?

A

testing for ROS in neutrophil in chronic granulomatous disease… if ROS is present the yellow liquid will turn blue

221
Q

what are two tests used for chronic granulomatous disease?

A

nitroblue tetrazolium, dihydrorhodamine

222
Q

loss of hearing and finding of a brain tumor +/- facial/trigemnal nerve palsy. what is this likely? where is the tumor?

A

Neurofibromatosis 2–>schwannoma

location=cerebellar pontine angle

223
Q

where is the pineal gland located?

A

dorsal midbrain

224
Q

falcine superficial brain tumor. what is it?

A

meningioma

225
Q

what is the difference between Pica and normal pregnancy cravings?

A

pica is often due to iron deficiency anemia.
However the difference is pica is eating nonfoods/nonstaple foods
versus cravings are of normal foods

226
Q

what drugs cause Serotonin syndrome?

A

You were dancing when you tripped over a line and caused trauma…and now you’re depressed.

Ondansetron, Tryptans, Linezolid, Tramadol, antidepressants (SSRI, SNRI, MAO, Tricyclics)

227
Q

Doxycycline sideeffects

A

this is just all the tetracycline SE: photophobia, pill esophagitis, teeth stains

228
Q

what is a common gene mutated in dilated cardiomyopathy?

A

dystrophin

229
Q

what are SE of first gen antihistamines that second generation does not have?

A

antimuscarinic, antiserotonergic, anti alpha adrenergic, and more CNS sedation

230
Q

name 4 first generation antihistamines

A

diphenhydramine, chlorpheniramine, hydroxyzine, promethazine

231
Q

warfarin is metabolized how?

A

CYP2C9

232
Q

what is neurophysin

A

chaperone protein for ADH and Oxytocin.

233
Q

Autosomal dominant inherited Diabetes Insipidus is caused by what?

A

point mutation in neurophysin…which causes misfolding and removal of the hormones from ER. Thus pt will lack ADH and oxytocin

234
Q

first, second, and third line of gout tx?

A

NSAID (don’t use with renal failure, hepatic failure, GI bleed), colchicine (GI SE), and corticosteroids

235
Q

endothelin action

A

vasoCONSTRICTION

236
Q

pt >50 years old with systolic hypertension but nl diastolic. what is the mechanism causing this?

A

aortic stiffening (possibly monkenberg?)

237
Q

normal MABP?

A

90-100

238
Q

how to calculate MAP using DBP and SBP?

A

DBP+ 1/3(SBP-DBP)=MAP

239
Q

renal failure’s effect on calcium, PTH, calcitriol, and phosphate?

A

high phosphate, low calcitriol–>low calcium–>high PTH

240
Q

common pathogens for reactive arthritis?

A

Campylobacter, chlamydia, shigella, salmonella, Yersinia, and Bartonella

241
Q

C1 inhibitor deficiency is linked to what?

A

hereditary angioedema (due to lack of C1 inhibition thus overactive complement system)

242
Q

What is the process by which bruises become green and then brown?

A

Heme is oxidized by heme oxidase into biliverdin (green) then spontaneously oxidizes further to bilirubin.

243
Q

what are c diff’s toxin’s and what do they do? what’s the mechanisms?

A

C diff has toxin A (enterotoxic) and toxin B (cyto toxic)

but their mechanism of action are the same. disruption of Rho protein thus destabilizing actin, also disrupting tight junctions leading to diarrhea

244
Q

clostridium perfringens… what’s the toxin?

A

Lecithinase

245
Q

lens dislocation. ddx? wht are they at risk for?

A

marfans –> dissection; and homocysteinuria –>thromboses

246
Q

homocysteinuria…what enzyme is missing?

A

cystathione synthetase

247
Q

what dietary thing can worsen homocysteinuria?

A

excess methionine in diet..increases homocystein even more

248
Q

what dietary thing can worsen homocysteinuria?

what dietary supp can make it better?

A

excess methionine in diet..increases homocystein even more

B6

249
Q

AIDS patient with ring enhancing brain lesions. How do you treat?

A

pyrimethamine and sulfadiazine

250
Q

two top diagnoses for ring enhancing brain lesions in AIDs pt?

A

toxo and primary CNS lymphoma

251
Q

what is the microbe responsible for CNS lymphoma?

A

EBV

252
Q

drug of choic for myotonic seizures?

A

Valproate

253
Q

what kinds of seizures can valproate be used for?

A

myoclonic, tonic clonic, and absence

254
Q

hemachromatosis. what is the mutation on what gene? what chromosome?

A

Cysteine to Tyrosine at amino acid 282 on HFE gene on chromosome 6

255
Q

MTMP is oxidized to MPP and can damage dopaminergic neurons. What enzyme catalyzes this?

A

MAO B

256
Q

Why is it useful to use MAO I in parkinson’s?

A

it’s helpful because dopamine breakdown leads to ROS that damages substantia nigra. thus. MAO Inhibition will lower monoamine breakdown

257
Q

inhaled glucocorticoids…what’s the most common SE? what are some others? how do you prevent?

A

oral candidiasis is most common. You can also get cataracts and osteoporosis. Prevent by oral rinsing

258
Q

which layer of the stomach is are parietal cells located?

A

the upper glandular layer that is right underneath the epithelial layer

259
Q

pure red cell aplasia is associated with what two causes?

A

thymoma and parvoB19 infection

260
Q

how are eosinophils able to kill helminths?

A

helminths are coated with IgG which then bind to eosinophils causing degranulation

THIS IS ANTIBODY DEPENDENT CYTOTOXICITY

261
Q

how are eosinophils able to kill helminths?

A

helminths are coated with IgG which then bind to eosinophils causing degranulation

THIS IS ANTIBODY DEPENDENT CELL MEDIATED CYTOTOXICITY

262
Q

rotavirus infection. what comes before the diarrhea?

A

upper respiratory infection

263
Q

white OR blue spots with underlying erythema on buccal mucosa

A

koplik spots. measles=rubeola

264
Q

name the top few risk factors for cervical carcinoma

A

HPV, HIV, low socioeconomic status, multiple sex partners, and smoking

265
Q

dual blood supply of lung?

A

pulmonary arteries and bronchial arteries

266
Q

ppost op hydration helps with what

A

renal function

267
Q

post op breathing exercise prevent what?

A

atalectasis

268
Q

how to prevent post op PE?

A

heparin

269
Q

how are particles 10micron+, 2-10 microns, and

A

10+ will be coughing/sneezing
2-10 microns will be mucociliary transport
and

270
Q

what decreases risk of ovarian cancer?

A

OCP, multiparity, breast feedng

271
Q

able to follow command and answers questions appropriately. However has trouble writing and has slowed speech. What region of brain is affected?

A

Broca’s area

272
Q

Wiskott Aldrich syndrome. when does it onset?

A

about 6 months after maternal passive immunity has worn off.

273
Q

fevers chills, back pain, hemoglobinuria hours after blood transfusion. What is this called? what type of hypersensitivity?

A

acute hemolytic transfusion reaction.

This is type II hypersensitivity mediated by Ab and Complements

274
Q

Crohn’s and UC. which one is more likely to have bloody diarrhea, which one is more likely to have abdominal pain?

A

UC-bloody diarrhea,

Crohn’s abd pain

275
Q

process of liquifactive necrosis?

A

lysosomal degradation
phagocytic removal of material
astrocyte proliferation and gliosis

276
Q

necrosis with preserved architecture?

A

coagulative

277
Q

necrosis with giant cells and granulomas

A

caseous

278
Q

most prominent atrophy in brain regions of alzheimer’s?

A

temporoparietal and hippocampus

279
Q

achondroplasia. what gene is mutated? pattern of inheritance?

A

FGFR3; autosomal dominant. homozygous is lethal

280
Q

medusa head/serpentine on microscopy. micro

A

Bacillus anthracis

281
Q

wool sorter

A

bacillus anthracis

282
Q

bacillus anthracis disease progression

A

inhaled and generates toxin in mediastiunal lymphnodes… fever, malaise, then hemorrhagic mediastinitis/pleural effusion

283
Q

name the three dihydrofolate inhibitor drugs

A

methotrexate, pyrimethamine, nd trimethoprim

284
Q

antismith ab…is against what exactly?

A

snRNP

285
Q

Pt with musculoskeletal pain, fatigue, and depression. dx?

A

Fibromyalgia

286
Q

Young female pt with musculoskeletal pain, fatigue, and depression. dx?

A

Fibromyalgia

287
Q

Young female pt with musculoskeletal pain, fatigue, and depression. dx? tx?

A

Fibromyalgia. exercise, SSRI, and anticonvulsant

288
Q

Primase; what kind of polymerase is it?

A

DNA dependent RNA pol

289
Q

where are ribosomal proteins synthesized? where are they assembled? and where do they function?

A

after transcription in the nucleolus, the proteins are synthesized in the cytoplasm. They target back to nucleolus and are assembled as rRNA/60S/40S structures. then it’s sent out to cytoplasm for tranlsation functions

290
Q

what is lactose also known as?

A

galactose beta 1,4 glucose

291
Q

techoic acid of strep A is a part of what structure?

A

peptidoglycan

292
Q

What does protein M do?

A

antiphagocytic and cytotoxic to neutrophils, inhibit complement activation, and facilitates attachment

293
Q

why is liver resistant to infarct?

A

dual blood supply of hepatic artery and portal vein. Also arteries from phrenic branches, adrenal branches will supply it.

294
Q

apical subpleural blebs are associated with what?

A

tall thin males in their 20s, and smoking

295
Q

what kind/shape of nucleic acid do herpes viruses have? what kind of core?

A

linear dsDNA, icosahedron

296
Q

Dane particle. what is it? what kind of nucleic acid? waht kind of core?

A

partially double stranded circular DNA. hexagonal core. This is HepB!

297
Q

“worst headache of my life”…name 3 types of people at risk for this the most

A

this is subarachnoid hemorrhage

Ehler Danlos, Polycystic kidney disease (AD), atrioventricular malformation

298
Q

aortic regurgitation is best heard how?

A

patient leaning forward during expiration.

299
Q

high pitched blowing diastolic decrescendo murmur. +/- presence of A2

A

aortic regurgitation

300
Q

What is A2 heart sound?

A

S2=A2 and P2; A2 is first and loud. P2 is usually very quite and only heard in the P area

301
Q

high pitched blowing early diastolic decrescendo murmur. +/- presence of A2

A

aortic regurgitation

302
Q

what are two diuretics that work in the PT? what are their sideeffects?

A

inhibitors of carbonic anhydrase (Acetazolamide); SE=metabolic acidosis

osmotic diuretics Mannitol; SE pulmonary edema, increased intracranial pressure

303
Q

pseudotumor cerebri tx?

A

Acetazolamide

304
Q

sweating is controlled by what ANS branch and how

A

SNS via cholinergic stimulation

305
Q

succinylcholine mechanism of action?

A

it mimics acetylcholine and depolarizes NMJ resultingin paralysis

306
Q

How does neostigmine affect succinylcholine action in phase I and phase II?

A

Phase I neostigmine potentiates succinylcholine and results in prolonged paralysis
Phase II neostigmine inhibits succinylcholine and stops paralysis

307
Q

What is syrup of Ipecac

A

emetic to induce vomiting immediately post ingestion of poison…but this is only effective if given immediately prior to metabolic derangements

308
Q

what is in cryoprecipitate?

A

VWBF, fibrinogen, factors XIII and factorVIII

309
Q

What do you give in rat poisoning?

A

this leads to depletion of vitamin K and all the factors

Thus give vitamin K and fresh frozen plasma

310
Q

molecular effect of NO?

A

increase in cGMP –>decreased calcium–>myosin light chain kinase dephosphorylation–>relaxation

311
Q

acne in adult athelete…what do you think of?

A

taking androgens

312
Q

4 key components of acne

A
  1. excessive epidermal follicular proliferation
  2. excessive sebum production
  3. inflammation
  4. p. acnes
313
Q

cushingoid habitus. glucocorticoid excess causes this, but what OTHER pharm therapy causes this?

A

HAART therapy for HIV. mostly protease inhibitors inhibit chylomicron uptake and triglyceride clearance

314
Q

babies can be falsely positive for HIV in the first few months why?

A

anti-gp120 crosses placenta…thus it will be positive on ELISA and western

315
Q

do you treat osteoarthritis with steroids?

A

injections yes, systemic NO

316
Q

H. pylori destroys what cells?

A

D cells (somatostatin decrease thus elevated acid)

317
Q

what cancers are associated with H pylori?

A

gastric adenocarcinoma, gastric lymphoma, MALToma

318
Q

what cancers are associated with H pylori?

A

gastric adenocarcinoma, gastric lymphoma

319
Q

pulsus paradoxus definition? what is associated with it?

A

drop in systolic BP of more than 10 mmHg with inspiration

cor pulmonale and constrictive pericarditis

320
Q

sharp mid sternal pain that gets better with sitting up and worse with breathing

A

pericarditis

321
Q

common causes of pericarditis. name 3

A

MI, rheumatic fever, uremia

322
Q

cherry hemagioma

A

benign in elderly due to venous congestion. nevus looking but redder

323
Q

strawberry hemagioma

A

AKA superficial hemagiomas

in infants either bright if superficial or purple if deeper. often spontaneously disappears in late infancy

324
Q

spider angiomas

A

increased estrogen due to pregnancy, OCP, or cirrhosis (decreased metabolism of estrogen)

325
Q

HIV uses what receptor to bind CD4 and CCR5?

A

gp120

326
Q

which part of the aorta is most suseptible to tearing during blunt trauma like a car accident? which part is the next susceptible part?

A

very first part of descending arota at the site of ligamentum arteriosum
distal ascending aorta

327
Q

which part of the aorta is most suseptible to tearing during blunt trauma like a car accident? which part is the next susceptible part?

A

very first part of descending arota at the site of ligamentum arteriosum
distal ascending aorta is the next most susceptible

328
Q

what reaction is most important in containing TB and subsequently causes damage?

A

delayed hypersensitivity

329
Q

precision is the same as what

A

reliability

330
Q

accuracy is the same as what

A

validity

331
Q

Inhibition of mast cell degranulation is what drug?

A

Cromolyn (and Nedocromil)

332
Q

intravenous/centra catheters are associated with increased incidence of what?

A

bacteremia. esp things that are naturally apart of skin flora… Staph epi, staph aureus, candida, enterococcus

333
Q

What is “preexcitation syndrome”? what’s the classic EKG findings (3 things)

A

It’s wolff parkinson white… where the ventricle is “preexcited” by the bundle of kent.
Result: short PR interval, delta wave, and long QRS

334
Q

what are the branches of celiac trunk?

A

common hepatic, L gastric, and splenic artery

335
Q

What branches off the splenic artery?

A

Left gastroepiploic, short gastric

336
Q

what branches off L gastric artery?

A

esophageal artery, and L gastric

337
Q

What are the two large branches off common hepatic, and waht are their tributaries?

A
  1. gastroduodenal–> supraduodenal, R epiploic, and superior pancreaticoduodenal
  2. proper hepatic–>L/R hepatic, and cystic artery, R gastric artery
338
Q

How can you tell acute respiratory acidosis from chronic respiratory acidosis?

A

acute will not have renal HCO3 compensation (30)

339
Q

What is contraction alkalosis?

A

loss of volume–>aldosterone increase–>increased Na reabsorption and loss of H and K thus resulting in metabolic alkalosis

340
Q

which cells are affected by sorbitol in DM and why?

A

lens, pheripheral nerve (schwann cells), blood vessels, kidney

because they don’t depend on insulin to uptake glucose

341
Q

which cells are affected by sorbitol in DM and why?

A

lens, pheripheral nerve (schwann cells), blood vessels, kidney

because they don’t depend on insulin to uptake glucose. conversion to sorbitol increases osmotic pressure

342
Q

what does stimulation of mu receptor do down stream?

A

mu receptor is a G protein…downstream it will inhibit adenylyl cyclase and cause decreased calcium. It will also increase Potassium efflux

343
Q

constrictive lung diseases versus obstructive lung diseases…which one would benefit from lower frequency breathing which one would benefit from higher frequency breathing.

A

constrictive lung diseases=faster
obstructive= slower

both are trying to optimize workload. Elastic forces are greater at higher tidal volumes (AKA slower rate), and obstructive forces are greater at low volumes (AKA high er rate)

344
Q

during ischemia… at what time point does myocyte stop contracting?

A

within a minute due to ATP depletion.

345
Q

during ischemia…at what time point does myocyte dysfunction become permanent?

A

30 minutes

346
Q

If ischemic myocyte is perfused after less than 30 min of injury… the myocyte will return to normal slowly over days. what is this called?

A

this is myocyte stunning

347
Q

In global cerebral ischemia…what cells are most susceptible to injury?

A

hippocampal pyramidal cells and purkinje cells of the cerebellum

348
Q

which vitamin deficiency develops after YEARS of dietary insufficiency?

A

cobalamin, B12

349
Q

NADPH synthesized via HMP shunt is used to do what?

A

synthesize fatty acids, cholesterol, and steroids

350
Q

Ribulose 5-phosphate is produced where and what are its fates?

A

HMP shunt.

it can be catabolized in glycolysis OR used anabolically to build nucleotides and aromatic aminoacids

351
Q

what is the committed step in purine syntehsis?

A

PRPP conversion to IMP via PRPP amidotransferase

352
Q

PRPP is used in what pathways?

A

both de novo (PRPP amidotransferase) and salvage (HGPRT) pathways.

353
Q

what is the committed step in purine syntehsis?

A

PRPP conversion to 5 phosphoribosylamine via PRPP amidotransferase

354
Q

PRPP is used in what pathways?

A

both de novo (PRPP amidotransferase) and salvage (HGPRT) pathways.

355
Q

Lesh Nyhan…what is decreased enzyme what is the increased enzyme?

A

decreased is HGPRT. increased PRPP leads to an increased activity of PRPP amidotransferase

356
Q

what is Shiga toxin also called?

A

Verotoxin

357
Q

what virulence factor does E. coli use to cause meningitis?

A

K1 antigen =CAPSULE. Most meningeal species have capsule

358
Q

What does E. Coli use as virulence factor to cause spetic shock?

A

Lipid A –>recruitment of Macrophages –>IL6, IL1, TNFa

359
Q

Ethambutol mechanism. SE?

A

mech: inhibits arabinosyl transferase–>inhibition of TB cell wall cross linking
SE: visual changes, and hepatic toxicity

360
Q

Rifampin mechanism?SE??

A

RNA pol inhibitor. SE: orange secretions, hepatotoxicity

361
Q

Isoniazid mechanism?SE?

A

inhibits mycolic acid synthesis. hepatotoxicity and peripheral neuropathy

362
Q

Which elements are in the bronchi that are not in the bronchioles? what is the cell feature that disappears last in bronchioles

A

cartillage, serous, mucus glands stop at the smallest bronchi
Cilia continues in bronchioles to sweep up the fallen mucus.

363
Q

how does cavedilol decrease overall mortality in CHF

A

it decreases cardiac work and decreases afterload

364
Q

Milrinone mechanism? functional use?

A

it is a phosphodiesterase inhibitor. It increases cardiac contractiility and decrease BOTH preload and afterload (smooth muscle vasodilatioN)

365
Q

tricyclic antidepressants can be effective for insomnia in what kind of pt

A

depressed pts

366
Q

Buproprion. mechanism of action? use?

A

blocks Dopamine (mostly) and norepinephrin reuptake. Used for major depression (atypical antidepressant), smoking sessation.

Does NOT have sexual dysfunction SE thus great!

367
Q

Buproprion contraindication

A

seizure pts, pts with hx of anorexia and bulimia

368
Q

Potential seizure causing drugs? name 5

A

Buproprion, Isoniazid, clozapine, ciprofloxacin, Imipenem

369
Q

Clozapine serious SE

A

agranulocytosis

370
Q

persisting vitellin duct is related to what

A

meckles diverticulum

371
Q

delayed puberty; cannot smell

A

Kallman syndrome. hypogonadotrophic hypogonadism

372
Q

delayed puberty; cannot smell

A

Kallman syndrome. hypogonadotrophic hypogonadism due to hypothalamic dysfunction

373
Q

Cryptococcus neoforman. Three types of stains for it?

A

India ink, mucicarmine (bright red), methenamine silver

374
Q

which type of erythroblastosis fetalis can occur in the very first pregnancy, and which type occurs in the second pregnancy.

A

A/B antibody type in O mothers occur in the first pregnancy because A/B antigen exposure is likely through food throughout life.

Rh antibodies occur after exposure in the first pregnancy and affect the second baby.

375
Q

Which antibody/antibodies cross placenta

A

only IgG

376
Q

metformin SE?

A

GI and lactic acidosis.

377
Q

metformin contraindications?

A

liver dysfunction, renal dysfunction, CHF, alcoholics, and sepsis

378
Q

metformin general biochem action?

A

increase glycolysis, decrease GI glucose absorption, and decrease gluconeogenesis

379
Q

multiple lesions in liver what is it? why is this common?

A

mets,

liver is large, highly perfused via dual blood supply, and Kupffer cell filter all the bad things and keep it.

380
Q

hepatic adenoma in a female? in a male? risk?

A

OCP=female; steroids=male; risk of rupture

381
Q

hepatoblastoma is associated with what two conditions?

A

children with FAP, Beckwith-Weidemann

382
Q

When is oral glucose tolerance test preferred over the fasting glucose measurement?

A

gestational diabetes

383
Q

Type 1 diabetes could onset following what?

A

viral infection; especially in young white person

384
Q

transmural segmental necrotizing inflammation of small and medium arteries. what is this? what organs are MOST affected?

A

this is polyarteritis nodosa. most affected are Kidney, GI, heart, and liver

385
Q

esophageal varices without liver abnormalities?

A

portal vein thrombosis

386
Q

what’s the difference between budd chiari syndrome and portal vein thrombosis

A

budd chiari is in the hepatic vein…thus you will see hepatic congestion
portal vein thrombosis is in the portal vein prior to the liver. thus will NOT have any liver abnormlaities

387
Q

mutation of neurofibromin in NF1 results the unchecked upregulation of what?

A

Ras

388
Q

Tuberous sclerosis. Pts get rhabdomyomas and what other cardiac abnormality?

A

mitral valve regurgitation

389
Q

what types of tissues may be in meckle’s diverticulum? how is this detected?

A

gastric and pancreatic.

99mmTc Pertechnetate detects ectopic gastric mucosa (acid causes bleeding)

390
Q

what types of tissues may be in meckle’s diverticulum? how is this detected?

A

gastric and pancreatic.

99mmTc Pertechnetate detects ectopic gastric mucosa

391
Q

Why can meckle’s diverticulum lead to bleeding?

A

ectopic gastic mucosa… leading to acid excretion in to small bowel

392
Q

what types of tissues may be in meckle’s diverticulum? how is this detected?

A

gastric and pancreatic.

99mmTc Pertechnetate detects ectopic gastric mucosa in RLQ

393
Q

how is copper excreted from the body? 2 routes…which one is the main one?

A

Mainone is bile excretion of copper and ceruloplasmin bound copper.

about 10% is excreted via renal tubular secretion.

394
Q

what are the 2 defense mechanisms of fungal infections?

A

T cells and neutrophils

395
Q

what kind of patient is at high risk for disseminated candidaiasis?

A

neutropenic. (NOT low T cell. low T cell=mucocutaneous candidiasis)

396
Q

spaghetti meat ball with cigar shapped ends. what organism? treatment?

A

tinea versicolor; Selsun blue is treatment (selenium shampoo)

397
Q

Tamoxifen raises risk of what? why?

A

it’s a partial agonist of estrogen receptors in bones, endometrium, and heart.

Thus it raises risk of endometrial cancer and thrombosis

398
Q

anastazole/letrazole (aromatase inhibitors) are best for what two kinds of breast cancers?

A

post menopausal and metastatic

399
Q

Gliosis scarring is what material?

A

astrocyte processes

400
Q

eosinophilic foamy alveolar material in lung biopsy of pneumonia.

Silver stain/Giemsa stain with cup in saucer appearance

A

Pneumocystic jiroveci

401
Q

what shifts potassium out of cells?

A 
Digitalis
Osmolarity
Lysis
Acidosis
beta blockers
402
Q

causes of increased anion gap metabolic acidosis?

A 
Methanol
Uremia
Dka
Propylene glycol
Iron or Isoniazide
Lactic acidosis
Ethylene glycol
Salicylate
403
Q

Normal anion gap metabolic acidosis causes?

A 
Hyperalimentation
Addison's
Renal tubular acidosis
Diarrhea
Acetazolamide
Spironolactone
Saline
404
Q

Ketamine mechanism of action?

A

blocks NMDA

405
Q

opioid receptor cause what? how is tolerance achieved?

A

opioid is a Gi protein–>decrease in cAMP–>increase K efflux and decrease Ca depolarization.

tolerance is likely protein kinase phosphorylation leading to increased cAMP in cells

406
Q

what can prevent opioid tolerance

A

NMDA blockers thus preventing protein kinase signalling to phosphorylate opioid receptors.

407
Q

eye pain, history of arm pain, fatigue after hot shower. dx?

A

MS

408
Q

eye pain, history of arm pain, fatigue after hot shower. dx?

A

MS

decreased axonal transmission following heated environments.

409
Q

lead inhibits which 2 enzymes of heme synthesis?

A

ALAdehydratatse

Ferrochetalase

410
Q

child with neurological sx, anemia, and lives in an Old house…what do you think of?

A

lead poisoning

411
Q

how to diagnose princemetal angina?

A

ergonovine test–> causes vasospasm via stimulation of alpha1 and serotonin receptors.

412
Q

describe calcium flow in skeletal muscle contraction?

A

excitation leads to L type calcium channel openning and immediate opening of Ryanidine receptors. They are coupled. and almost all calcium comes from the SR–>binding to troponin C

413
Q

describe calcium flow in cardiac muscle contraction?

A

excitation leads to opening of L type receptors…the influx of calcium opens ryanidine receptors (Calcium induced calcium release)…thus most of calcium is from extracellular compartment. This then binds troponinC

414
Q

Describe calcium flow in smooth muscle contraction?

A

calcium enters via L type channel upon deoplarization… induces ryanidine channel release of calcium…which binds myosin light chain kinase.

415
Q

decreased B6 causes what kind of anemia?

A

sideroblastic

416
Q

spoon nails (koilonychia) and dysphagia with anemia…what kind of anemia?

A

iron deficiency

417
Q

dementia, ataxia, incontinence. dx?

A

normopressure hydrocephalus

418
Q

what are the three control centers of micturition?

A 
Sacral micturition center (PNS dominant induces bladder contraction)
Pontine micturition center (coordinates sphincter relaxation and bladder contraction in urination)
Cerebral cortex (inhibits sacral micturition center)
419
Q

what is 16S rRNA? what does it do?

A

the Shine Dalgarno sequence 10 bp upstream of AUG codon. 30S ribosome is recuited here to start protein synthesis… 50S will join at AUG

420
Q

what is 16S rRNA? what does it do?

A

the Shine Dalgarno sequence 10 bp upstream of AUG codon. 30S ribosome is recuited here to start protein synthesis… 50S will join at AUG (prokaryotes)

421
Q

what class of drug is Oxybutinin? what is used for?

A

Oxybutinin is a antimuscarinic. It’s used for urge incontinence/bladder spasm…

422
Q

Organophosphate poisoning. If you give Atropine. what is the patient still at risk of?

A

Organophosphates irreversibly take out cholinesterases…so you have a ton of cholines floating around

Atropine is antiMuscarinic…thus acetylcholine excess at nicotinic receptor is still are exposed. Thus pt can have depolarization of NMJ and paralysis.

Pralidoxime regenerase cholinesterases…so it’s the ultimate solution

423
Q

what are some environemental ways of lead exposure?

A 
old home, 
old pottery/glaze
moonshine
batteries
ammunition
alloys
occupational-Inhaled
consumer-ingested
424
Q

How to reduce flushing in Niacin use?

A

Asprin prophylaxis

425
Q

Nniacin reduces synthesis of what?

A

VLDL. and thus also LDL because VLDL is converted to LDL when broken down

426
Q

hypertriglyceridemia is associated with which lipid lowering drug?

A

cholestyramine

427
Q

Two mechanisms of DM peripheral neuropathy?

A
  1. small vessel hyalinization leading to nerve necrosis

2. sorbitol accumulation in schwann cells leading to apoptosis

428
Q

Lipid within muscle finbers?

A

carnitine palmitoyltransferase deficency

429
Q

pt with small cell lung cancer develops ataxia. what is this?

A

neuronal paraneoplastic syndrome. anticancer antibodies are formed to crosslink with purkinje cells of cerebellum…
Anti Yo, Anti Hu, AntiP/Q

430
Q

Anti Yo, Anti Hu, anti P/Q are seen in what? specific types?

A

paraneoplastic syndromes of small cell lung cancer, breast, ovarian, uterine cancer

431
Q

pt with small cell lung cancer develops ataxia. what is this?

A

neuronal paraneoplastic syndrome. anticancer antibodies are formed to crosslink with purkinje cells of cerebellum leading to degeneration…
Anti Yo, Anti Hu, AntiP/Q

432
Q

Anti Yo, Anti Hu, anti P/Q are seen in what? specific types?

A

paraneoplastic cerebellar degeneration syndromes of small cell lung cancer, breast, ovarian, uterine cancer

433
Q

What are somethings that will predispose someone to SMA syndrome?

A

mesentaric fat loss, lordosis, scoliosis correction

434
Q

bowel ischemia due to blood loss is going to affect what portion of bowel? how might these patients present?

A

systemic hypotension affects splenic flexture.

These patients will present will abd pain and bloody diarrhea due to ischemic shedding.

435
Q

what kind of amyloidosis can occur with dialysis?

A

beta microglobulinemia

436
Q

Name 5 unusual conditions associated with carpal tunnel sydrome?

A 
Pregnancy, 
hypothyroidism
DM
rheumatoid arthritis
DIALYSIS! (amyloidosis)
437
Q

IgG oligoclonal band on electrophoresis from pt with neuro symptoms

A

MS

438
Q

Oligodendrocyte depletion is seen in what two diseases?

A

MS and PML (JC virus)

439
Q

pathogenesis of centriacinar emphysema related to smoking?

A

Smoke and damage activates alveolar MACROPHAGES AND NEUTROPHILS–>release of proteases, which leads to breakdown of the tissue

440
Q

What are club cells/Cara cells

A

non ciliated cells in terminal respiratory epithelium. it detoxifies inhaled smoke and it produces surfactant (in addition to type II pneumocytes)

USMLE (9 decks)

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