Trachte Rx Flashcards

Question

Propanolol

Answer 1

nonspecific b blocker block b1: decrease HR and contractility block b2: decrease bronchodilation (not as important) decrease BP

Answer 2

b1 antagonist b1 blocker block b1: decrease HR and contractility decrease BP *specific to b1 = specific to heart

Answer 3

b1 antagonist b1 blocker block b1: decrease HR and contractility decrease BP *specific to b1 = specific to heart

Answer 4

vascular SM contractility | VASOCONSTRICTION

Answer 5

1 heart = b1 increase HR and contractility

Answer 6

don't need to care about it inhibit neural NE release

Answer 7

2 lungs = b2 vascular SM relaxation VASODILATION BRONCHODILATION decreased uterine tone

Answer 8

3rd gen cephalosporin CELL WALL INHIBITOR blocks transpeptidation fo peptidoglycan in bacterial cell walls Tx: MSSA, strep, some gram (-)

Answer 9

CELL WALL INHIBITOR binds D-ala-D-alanine to prevent transglycosylation Tx: MRSA, broad gram (+)

Answer 10

ceftriaxone and vancomycin

Answer 11

CELL WALL INHIBITOR beta-lactam binds pbp and blocks transpeptidation of peptidoglycan in bacterial cell walls Tx: some gram (+), basically strep

Answer 12

penicillin G strep viridans = gram (+)

Answer 13

CELL WALL INHIBITOR AMINO-beta-lactam binds pbp and blocks transpeptidation of peptidoglycan in bacterial cell walls Tx: some gram (+) = mainly strep, some gram (-) can still be inactivated by beta-lactamases, so give with clavulanate

Answer 14

beta-lactamase resistant

Answer 15

t-PA tissue plasminogen activator: converts plasminogen to plasmin --> break down fibrin clots Tx: non-hemorrhagic stroke or clot (emboli or thrombi) CONTRAINDICATED IN ENDOCARDIDITS

Answer 16

OPIOD PAIN RELEIVER/ANALGESIC acts on mu receptors in three locations: - presynatpic nociception pathway (blocks calcium pump --> blocks vesicle release) - postsynatpic nociception pathway (increases K permeability --> blocks depolarization) - presynatpic descending inhibitory pathway (blocks GABA release --> allos inhibior neuron firing and blocking nociception pathway)

Answer 17

VENOdilator forms free radical NO -> activates guanylyl cyclase --> incrase cGMP --> increase MLC phosphatase --> increase MLC dephosphorylation --> SM relaxation --> VEINS vasodilate --> decreased blood returning to heart --> decrease preload Tx: decrease myocardial activity and oxygen demand --> decrease ischemic damage

Answer 18

ANTI-COAGULANT INHIBITS PLATELET ACTIVATION blocks ADP receptors on platelets --> inhibits platelet activation Tx: post MI anticoagulation therapy

Answer 19

ANTI-COAGULANT INHIBITS FIBRIN FORMATION increases activity of antithrombin III --> Inhibits thrombin --> blocks conversion of fibrinogen to fibrin = NO CLOT Tx: post MI anticoagulation therapy

Answer 20

ANTI-COAGULANT INHIBITS PLATELET AGGREGATION binds GPIIb/IIIa receptor on activated platelets --> inhibits binding of fibrinogen --> block initiatino of coagulation cascade post-platelet plug Tx: post MI anticoagulation therapy

Answer 21

ANTI-COAGULANT INHIBITS PLATELET AGGREGATION irreversibly inhibits COX1/2 --> blocks production of TXA2 --> inhibits platelet aggregation Tx: used IMMEDIATELY upon suspected MI UNLESS patient recently took aspirin

Answer 22

INHIBIT CHOLESTEROL SYNTHESIS inhibit HMG-CoA reductase reduces plaque formation in vessels Tx: dyslipidemia --> decrase atherosclerosis and risk of CAD

Answer 23

angiotensin converting enzyme inhibitor SUPPRESSES RAAS system suppresses RAAS system by inhibitng conversion of angiotensin I to angiotensin II --> decreased aldosterone release --> decreased Na reabsorption in kidney --> DECREASED BLOOD VOLUME AND PRELOAD DECREASED VASOCNX --> DECREASED AFTERLOAD Tx: post MI management, chronic CHF management

Answer 24

ACE inhibitor suppresses RAAS system --> dec aldosterone --> DECREASE BLOOD VOLUME AND PRELOAD DECREASED VASOCNX --> DECREASED AFTERLOAD Tx: post MI, chronic CHF

Answer 25

ACE inhibitor suppresses RAAS system --> dec aldosterone --> decreased Na reabsorption in kidney --> DECREASED BLOOD VOLUME --> DECREASED PRELOAD DECREASED VASOCNX --> DECREASED AFTERLOAD Tx: post MI, chronic CHF

Answer 26

block b1 receptors: MAIN ACTIVITY ON HEART: DECREASE HR AND CONTRACTILITY decrease myocaridal oxygen demand decrease BP Tx: MI to reduce ischemia, post MI, chronic CHF *contraindicated in acute CHF (need to preserve heart function and complete diuresis first)

Answer 27

specific b1 blocker: block b1 receptors: MAIN ACTIVITY ON HEART: DECREASE HR AND CONTRACTILITY decrease myocaridal oxygen demand decrease BP Tx: MI to reduce ischemia, post MI, chronic CHF

Answer 28

nonspecific beta blocker (blocks b1 and b2) block b1 receptors: MAIN ACTIVITY ON HEART: DECREASE HR AND CONTRACTILITY decrease myocaridal oxygen demand decrease BP Tx: MI to reduce ischemia, post MI, chronic CHF

Answer 29

same mech as NO NO --> binds SM --> G-protein coupled receptor --> activates guanyly cyclase --> increase cGMP --> decrease intracellular Ca --> relaxes SM --> VENOdilator --> decrases preload *longer half-life than NO (60-90 min)

Answer 30

increases NO synthesis in endothelium --> NO --> binds SM --> g-protein coupled receptor --> incrase cGMP --> dec intracell Ca --> relaxes SM --> VENOdilator --> decreases preload *HIGHER SELECTIVITY FOR ARTERIOLES = decrease afterload

Answer 31

ARBs Block aldosterone action --> decrease Na reabsorption in kidney --> DECREASES BLOOD VOLUME --> DECREASES PRELOAD *causes an increase in aldosterone and renin plasma concentration = INHIBITION OF NEGATIVE FEEDBACK

Answer 32

ARB | block aldosterone --> decrease BV --> decreases preload

Answer 33

ARB | blocks aldosterone --> decrease BV --> decreases preload

Answer 34

Inhibits Na/K/ATPase POSITIVE INOTROPE: increases CONTRACTILITY NEGATIVE CHRONOTROPE: decreases HR

Trachte Rx Flashcards

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