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Anatomy Step1 Buzzwords > First aid > Flashcards

First aid Flashcards

1
Q

Williams syndrome cardiac assoc

A

Supravalvualr aortic stenosis

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2
Q

Alcohol exposure in utero cardiac defect

A

VSD, PDA, ASD, TOF

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3
Q

Free wall rupture occurance in MI (timing, apperance at this time)

A

days 3-14. Macrophages are here, LV pseudoanerysm

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4
Q

aVL lead in MI- what artery

A

Lateral, LCS

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5
Q

avF lead in MI, what artery

A

Inferior (RCA)

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6
Q

V7-V9 in MI; what artery

A

Posteiror, PDA

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7
Q

Causes restrictive cardiomyopathy

A 
Puppy Leash
P: Postradiation fibrosis
uppy
L : loeffler syndrome (eosinophils will be present)
E: endocardiacal fibroelastosis
A: amyloidosis
S; sarcoidosis
H: hemochormatosis (dilated more common)
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8
Q

mortality reducing in HF

A

ace, angiotenesion II, B block, spironolactone (some people hydralazine with nitrates)

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9
Q

Tuberous sclerosis cardiac defect

A

Rhabdomyomas

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10
Q

Myxoma histological apperance

A

gelatinous, myxoma cells immersied in glycosaminoglycans (left atrial heart tumor)

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11
Q

What is the most common heart tumor

A

metastasis

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12
Q

Artery affect in Takaysu artertis, main symp

A

Pulseless disease; aortic arch (sweak upper extremity pulses)

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13
Q

Whati s spared in PAN; tell tale kidney sign

A

pulmonary arteries; renal microaneruysms

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14
Q

main artery involved in kawasakis

A

COronary artery

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15
Q

Granulomatosis iwth polyangitis triad, assoc labs

A

Focal necroizing vasculitis, granulmoas in lung and upper airway 9necrotizing), necrotizing glomerulonephritis
PR3-aanca, c-anca, antiproteinase 3

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16
Q

Difference between granulomatosis with polyangitis and microscopic polyangitis

A

no nasopharyngeal involvement in microscopic, also no granulomas

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17
Q

lab findings in microscopic polyangitis

A

MPO-Anca p-anca 9Anti myeloperoxidase)

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18
Q

What are unique findings in churg strauss/eosinophilic granulomatosis with poolyangitis

A

EOSINOPHILIA, Cardiac involvemnet (also gi and kidneys)

MPO-Anca, p-anca, increased IGE

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19
Q

What is Osler-Weber-Rendu syndrome

A

Inherited disorder of blood vessels
blancinhg skin lesions (telangiectasis), epistaxis, skin discolorations, AV malformations, GI bleeding, hematuria (also called hereditary hemorrhagic teleangatasia)

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20
Q

Main drug to prevent diabetic nephropathy in HF

A

ACEI/ ARBS (so give to DI people)

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21
Q

HTN in pregnancy tx

A

hydralazine, labetalol, methldopa, nifedipine

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22
Q

Clacium channel blockers MOA

A

Block voltage L-type calcium channels of cardiac and smooth muscle (decreases muscle contractility)

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23
Q

CCB drug names (both non-dihydro, dihydro)

A

dihydro: -dipines (vasc smooth muscle only)

nn-dihydro: dilatazem, verapamil ( act on heart)

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24
Q

unique side effects of dihydro CCBs

A

peripheral edema, gingiva hyperplasia

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25
Q

unique side ffects of nondihydro

A

hyper prolactinema

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26
Q

Hydralazine MOA

A

increases cGMP, smooth muscle relax. ARTEIROLES MORE THAN VEINS (decrease afterload)

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27
Q

Tx in hypertensive emregency

A

Clevidipine, fenolodopam, labetalol, nicarddipine, nitroprusside

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28
Q

MOA of nitrates

A

Vasodilate by increase NO in smooth muscle (Vascular)-> increase in cGMP and smooth muscle relax. DILATE VEINS MORE THAN ARTERIES. Decrease preload more.

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29
Q

“Monday disease”

A

industrial exposure of nitrateS: get tolerance during week, lose tolerance over weekend, get back and get tachy, dizzy, headache

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30
Q

Milrinone

A

PDE inhibitor; used in acute decompansated HF (Goal is to inhibig MLCK, vasodilate, lower afterload)

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31
Q

Statins side effects

A

hepatotaxicity, myopathy (increased with fibrates or niacin). somewhat tetragoenic

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32
Q

bile acid resins, names, main side effects

A

Cholestyramine, colestipol, colsevalam. INCREASES TRIGLYCERIDES SLIGHTLY. GI upset, decreased absorption fat soluble stuff and drugs (it does focus on terminal ileum), increase cholesteral gallstones

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33
Q

Ezetimide MOA, main side effects

A

Prevent chlesterol absorption at small intestine brush border. Diarrhea

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34
Q

Fibrates MOA, what they do best

A

Upreguilate LPP, ativate PPAR-alpha. REALLY good at lower triglyceride. MYopathy risk (with statin sesp), cohlesteral gallstones

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35
Q

Niacin MOA, main side effects, what it does best

A

Increases HDL the most; reduces hepatic VLDL syntheiss, inhibit lyoplysis, hyperglyceima, hyperuricemia

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36
Q

PCSK9 inhibitor names; main side effects, moa

A

Alirocumab, evolocumab, inactive LDL receptor degradation (so more LDL receptor clearing). Myalgia, delirium, dementia, other neurocog effects

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37
Q

tx digoxin toxicity, main signs

A

Cholingeric toxicity; bluury yellow vision, arrhythmia, AV block, hyperkalemia.

Tx with antidigoin FAB fragments, Mg2+, fix potassium

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38
Q

Class 1A antiarrhythmic names, MOA

A

Qunidine, procaminide, disopyramide (prom queen disappears). increase AP duratino, lengethne QT (some potassium block). Mostly slow phase 0 upstroke (na+)

39
Q

Class 1b antiarrhythmic name, moa, best use

A

Lidocaine, mexiletine
BEST POST MI
lowerse AP duration, again slow upstroke phase 0

40
Q

class 1c antiarrhythmic name, moa

A

Flecaine, Propafenocane, slow upstroke phase 0, prolong ERP in AV node and accessory tracts

41
Q

Quinidine unique side effect

A

cinchonism (headache, tinitus)

42
Q

Procanimide nuique side effect

A

drug induced lupus

43
Q

Class 1a main concerning side effect

A

torsades due to long QT

44
Q

Class II antiarrhythmic side effects, MOA

A

Basically beta blockers. Slow phase 4 depolarization and prolong repol at AV node. Great in AFIB, A flutter. Main side effect is concern for exacerbating COPD, masking hyperglycemia

45
Q

Propanolol unique side effect

A

vaso spasm exacerbatin in prinsmetal angina

46
Q

tx for beta blocker overdose

A

glucagon, atropine, saline

47
Q

Class III antiarrhythmic names, MOA

A

AIDS: Amidodarone, Ibutilide, Dofetiline, sodalol (also a eta blocker). K+ blok

Longer AP, prolong ERP and QT, basically prolong repolarization

48
Q

Amidarone concerning side effects

A

Pulm fibrosis, both hyper/hypothyroid, corneal deposits (acting like haptin), blue grey skin deposits

49
Q

Class IV antiarrhythmic names, MOA

A

Verapamil, dilatazem (Ca2+) block. Slow rise of aP at av node, prolong repol

50
Q

Adenosine moa

A

increaess K+ out of cells, decrease AV Node conduction, very slow acting

51
Q

unique side effects adenosine, what can blunt effect

A

effect blunted: caffine, theophylline

sense of impending doom, bronchospasm, flsuhing

52
Q

origin of thyroid tissue and parafollicular cells (calcitonin)

53
Q

Adrenal cortex orgiin, medulla orgin

A

Mesoderm, neural crest (Respectively)

54
Q

Adrenal cortex layers, products

A 
Zona Glomerulosa (antiotension II- aldosteorne)
Zona Fasiculata (ACTH/CRH-> cortisol)
Zona Reticularis (ACTH/CRH)-> DHEA (androgens)
Medulla: Chormaffin cells pregang symp fibers (ACh)-> Epi, NE
55
Q

Anterior pituitary origin

A

oral ectodemr; rathke pouch

56
Q

Posterior pituitary origin

A

neuroectoderm

57
Q

Where are ADH and oxytocin made

A

supraoptic, paraventiruclar nuclei

58
Q

where is glucagon made

A

alpha pancreas

59
Q

sites insulin dependent glucose uptake

A

adipose tissue, striated muscle (GLUT4, exercise increase expression too)

60
Q

sites insulin independent glucose uptake

A

BRICK L (Brain, RBCs, intestine, cornea, kidney, liver)

61
Q

Desmopressin drug uses

A

Central DI, nocturnal enuresis, vWF disease, hemophilia A

62
Q

apperance of 17 alpha hydroxylase def

A

no androgen or glcocrticoids (so low sex hormones, low cortisol, low K+)–have aldosterone hence low K+, also increasedm ineral corticoids
more ambigious sexes, no 2nd sex dvelopment in girls

63
Q

21 hydroxylase apperance

A 
No Aldosterone (so high K+), high renin, high sex hormones
virilization, procisous puberty
64
Q

11b hydroxylase apperance

A

Increased BP, low renin, low K+, low aldost, high sex hormones

65
Q

What is inactive form of vitamin D made when calcium is sufficient

66
Q

what cna alter pH secretion

A

Calcium (free), and pH

67
Q

What is the wolff-chaikoff effect

A

excess iodine temporarily inhibts thyroid peroxidase

68
Q

What makes thyroid hormone

A

follicles of thyroid

69
Q

what makes calcitonin, effect?

A

Parafollicular cells (C cells) of thyroid, decreased Ca2+ absorption

70
Q

PTU moa, Methiamazole MOA, Glucorticoid MOA in thyroid

A

PTU: inhibit thyroid peroxidase and peripheral 5’ deiodinase
Methimazole: inhibit thyroid peroxidase only
glucocort peripheral only

71
Q

Receptor tyrsoine kinase endocrine hormones

A 
GROWTH FACTORS (IGF-1, FGF, PDGF, EGF, Insulin)
MAP Kinase mediated
72
Q

cGMP endocrine hormones

A

BNP, ANP, EDRF (NO). BAD GRAMPA (vasodilators)

73
Q

cAMP endocrine hormones

A

FLAT ChAMP (FSH, LH, ASTH, TSH, CRH, hCG, ADH, MSH, PTH, calcitonin, GHHR, glucagon, histamine)

74
Q

NON RECEPTOR TYRSOINE KINASES

A

JAK/STAT Mediated (Acidophils, cyotkines)
PIGGLET
Prolacitn, immunomodulators (IL-2, i-6, IFN), GH, G-CSF, Erythproetin, Thrombopoetin

75
Q

SHBG impact on free testosterone

A

lowers it (so can lead to like gynecomastia whne its up)

76
Q

Neuroblastoma presentation

A

MOST COMMON TUMOR OF ADRENAL MEDULLA in kids. CROSSES MIDLINE (unlike wimls tumor). Can get opsoclonus-myocolouns syndrome. HVA and VMA in urine; homer wright rosettes. N-myc oncogene. Bombesin, NSE +

77
Q

pheocromocytoma gene assocs

A

NF-1, HL, RET (MEN2A/B)

78
Q

drugs to give before pheochormocytoma surgey

A

alhpa block (phenoxybenzamine0 then a beta block

79
Q

hashimoto main moa, histology

A

autoimmune to antithyroid peroxidase, anti thyroglobulin antibodies. Increasedn on hodgkin lymphoma risk.

Histology: Hurtle cell (lymphoid aggregates with germinal center). kind of look like an egg

80
Q

Congenital hypothyroidism presentation

A

Pot pellied, pale, puffy faced child, protuding umbilicus, protuberant tongue, poor brain development, can be a bit floppy

81
Q

Hard, painless goiter

A

Ribel thyroditis

82
Q

Thyroid storm treamtent

A

Beta blockers (Propanolol), propythiouracil, corticosteroids, potassium iodine (The 4 Ps)

83
Q

Graves disaese main MOA, Gene assoc

A

Thyroid stimmulating immunglobuilin (IgG, type II hypersens) stims TSH receptor on thyroid (and dermal fibroblasts hence edema). HLADR3-HLAB8. SCALLOPED colloid

84
Q

Papillary carcinoma unique histology, gene assoc

A

Orphan annie eyes, psammoma bodies, nuclear grooves. RET, BRAF (Also childhood radiation)

85
Q

Follicular carcinoma unique feature

A

tends to spread hematogenously

86
Q

Medullary carcinoma features

A

from parafollic T cells; stains in congo red (amyloid presence). MEN21/2B/ret assoc

87
Q

What is albright hereditary osteodystrophy

A

pseudohypoparathyroidism1A; kdney just doens’t respond to PTH. Shortened 4th/5th digits, short stature, autosomal dominant. (without hte 1a is basically just the same with a gs mutation from dad instead)

88
Q

What is Nelson syndrome

A

ACTH secreting adenoma gets bigger after adrenals are removed (No negative feedback)

89
Q

What is laron syndrome

A

defective growth hormone receptors, short, increased GF, no IGF1, short height, sadal nose

90
Q

longa cting insulins

A

determine glargine

91
Q

rapid acting insulins

A

lispro, aspart, glulisine

92
Q

Glitazone/thiazolditene names, MOA

A

-glitazone

Increased insulin sensitivity in peripheral tisuse, PPARgamma nuclear transcription regulator (bind intracellularly)

93
Q

sulfonyura names

A

-amide (chlorpropamide, tobutamide)

second generation are glimepiride, glipizine (short guy), glyburide (long acting guy)

Anatomy Step1 Buzzwords (11 decks)

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