First aid Flashcards

(93 cards)

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
unique side ffects of nondihydro
hyper prolactinema
26
Hydralazine MOA
increases cGMP, smooth muscle relax. ARTEIROLES MORE THAN VEINS (decrease afterload)
27
Tx in hypertensive emregency
Clevidipine, fenolodopam, labetalol, nicarddipine, nitroprusside
28
MOA of nitrates
Vasodilate by increase NO in smooth muscle (Vascular)-> increase in cGMP and smooth muscle relax. DILATE VEINS MORE THAN ARTERIES. Decrease preload more.
29
"Monday disease"
industrial exposure of nitrateS: get tolerance during week, lose tolerance over weekend, get back and get tachy, dizzy, headache
30
Milrinone
PDE inhibitor; used in acute decompansated HF (Goal is to inhibig MLCK, vasodilate, lower afterload)
31
Statins side effects
hepatotaxicity, myopathy (increased with fibrates or niacin). somewhat tetragoenic
32
bile acid resins, names, main side effects
Cholestyramine, colestipol, colsevalam. INCREASES TRIGLYCERIDES SLIGHTLY. GI upset, decreased absorption fat soluble stuff and drugs (it does focus on terminal ileum), increase cholesteral gallstones
33
Ezetimide MOA, main side effects
Prevent chlesterol absorption at small intestine brush border. Diarrhea
34
Fibrates MOA, what they do best
Upreguilate LPP, ativate PPAR-alpha. REALLY good at lower triglyceride. MYopathy risk (with statin sesp), cohlesteral gallstones
35
Niacin MOA, main side effects, what it does best
Increases HDL the most; reduces hepatic VLDL syntheiss, inhibit lyoplysis, hyperglyceima, hyperuricemia
36
PCSK9 inhibitor names; main side effects, moa
Alirocumab, evolocumab, inactive LDL receptor degradation (so more LDL receptor clearing). Myalgia, delirium, dementia, other neurocog effects
37
tx digoxin toxicity, main signs
Cholingeric toxicity; bluury yellow vision, arrhythmia, AV block, hyperkalemia. Tx with antidigoin FAB fragments, Mg2+, fix potassium
38
Class 1A antiarrhythmic names, MOA
Qunidine, procaminide, disopyramide (prom queen disappears). increase AP duratino, lengethne QT (some potassium block). Mostly slow phase 0 upstroke (na+)
39
Class 1b antiarrhythmic name, moa, best use
Lidocaine, mexiletine BEST POST MI lowerse AP duration, again slow upstroke phase 0
40
class 1c antiarrhythmic name, moa
Flecaine, Propafenocane, slow upstroke phase 0, prolong ERP in AV node and accessory tracts
41
Quinidine unique side effect
cinchonism (headache, tinitus)
42
Procanimide nuique side effect
drug induced lupus
43
Class 1a main concerning side effect
torsades due to long QT
44
Class II antiarrhythmic side effects, MOA
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
Propanolol unique side effect
vaso spasm exacerbatin in prinsmetal angina
46
tx for beta blocker overdose
glucagon, atropine, saline
47
Class III antiarrhythmic names, MOA
AIDS: Amidodarone, Ibutilide, Dofetiline, sodalol (also a eta blocker). K+ blok Longer AP, prolong ERP and QT, basically prolong repolarization
48
Amidarone concerning side effects
Pulm fibrosis, both hyper/hypothyroid, corneal deposits (acting like haptin), blue grey skin deposits
49
Class IV antiarrhythmic names, MOA
Verapamil, dilatazem (Ca2+) block. Slow rise of aP at av node, prolong repol
50
Adenosine moa
increaess K+ out of cells, decrease AV Node conduction, very slow acting
51
unique side effects adenosine, what can blunt effect
effect blunted: caffine, theophylline | sense of impending doom, bronchospasm, flsuhing
52
origin of thyroid tissue and parafollicular cells (calcitonin)
Endoderm
53
Adrenal cortex orgiin, medulla orgin
Mesoderm, neural crest (Respectively)
54
Adrenal cortex layers, products
``` 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
Anterior pituitary origin
oral ectodemr; rathke pouch
56
Posterior pituitary origin
neuroectoderm
57
Where are ADH and oxytocin made
supraoptic, paraventiruclar nuclei
58
where is glucagon made
alpha pancreas
59
sites insulin dependent glucose uptake
adipose tissue, striated muscle (GLUT4, exercise increase expression too)
60
sites insulin independent glucose uptake
BRICK L (Brain, RBCs, intestine, cornea, kidney, liver)
61
Desmopressin drug uses
Central DI, nocturnal enuresis, vWF disease, hemophilia A
62
apperance of 17 alpha hydroxylase def
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
21 hydroxylase apperance
``` No Aldosterone (so high K+), high renin, high sex hormones virilization, procisous puberty ```
64
11b hydroxylase apperance
Increased BP, low renin, low K+, low aldost, high sex hormones
65
What is inactive form of vitamin D made when calcium is sufficient
24,25 OH
66
what cna alter pH secretion
Calcium (free), and pH
67
What is the wolff-chaikoff effect
excess iodine temporarily inhibts thyroid peroxidase
68
What makes thyroid hormone
follicles of thyroid
69
what makes calcitonin, effect?
Parafollicular cells (C cells) of thyroid, decreased Ca2+ absorption
70
PTU moa, Methiamazole MOA, Glucorticoid MOA in thyroid
PTU: inhibit thyroid peroxidase and peripheral 5' deiodinase Methimazole: inhibit thyroid peroxidase only glucocort peripheral only
71
Receptor tyrsoine kinase endocrine hormones
``` GROWTH FACTORS (IGF-1, FGF, PDGF, EGF, Insulin) MAP Kinase mediated ```
72
cGMP endocrine hormones
BNP, ANP, EDRF (NO). BAD GRAMPA (vasodilators)
73
cAMP endocrine hormones
FLAT ChAMP (FSH, LH, ASTH, TSH, CRH, hCG, ADH, MSH, PTH, calcitonin, GHHR, glucagon, histamine)
74
NON RECEPTOR TYRSOINE KINASES
JAK/STAT Mediated (Acidophils, cyotkines) PIGGLET Prolacitn, immunomodulators (IL-2, i-6, IFN), GH, G-CSF, Erythproetin, Thrombopoetin
75
SHBG impact on free testosterone
lowers it (so can lead to like gynecomastia whne its up)
76
Neuroblastoma presentation
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
pheocromocytoma gene assocs
NF-1, HL, RET (MEN2A/B)
78
drugs to give before pheochormocytoma surgey
alhpa block (phenoxybenzamine0 then a beta block
79
hashimoto main moa, histology
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
Congenital hypothyroidism presentation
Pot pellied, pale, puffy faced child, protuding umbilicus, protuberant tongue, poor brain development, can be a bit floppy
81
Hard, painless goiter
Ribel thyroditis
82
Thyroid storm treamtent
Beta blockers (Propanolol), propythiouracil, corticosteroids, potassium iodine (The 4 Ps)
83
Graves disaese main MOA, Gene assoc
Thyroid stimmulating immunglobuilin (IgG, type II hypersens) stims TSH receptor on thyroid (and dermal fibroblasts hence edema). HLADR3-HLAB8. SCALLOPED colloid
84
Papillary carcinoma unique histology, gene assoc
Orphan annie eyes, psammoma bodies, nuclear grooves. RET, BRAF (Also childhood radiation)
85
Follicular carcinoma unique feature
tends to spread hematogenously
86
Medullary carcinoma features
from parafollic T cells; stains in congo red (amyloid presence). MEN21/2B/ret assoc
87
What is albright hereditary osteodystrophy
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
What is Nelson syndrome
ACTH secreting adenoma gets bigger after adrenals are removed (No negative feedback)
89
What is laron syndrome
defective growth hormone receptors, short, increased GF, no IGF1, short height, sadal nose
90
longa cting insulins
determine glargine
91
rapid acting insulins
lispro, aspart, glulisine
92
Glitazone/thiazolditene names, MOA
-glitazone | Increased insulin sensitivity in peripheral tisuse, PPARgamma nuclear transcription regulator (bind intracellularly)
93
sulfonyura names
-amide (chlorpropamide, tobutamide) | second generation are glimepiride, glipizine (short guy), glyburide (long acting guy)