+Drugs-Cv

Front 1

what drugs are used to tx essential HTN?

Back 1

- diuretics (thiazides, retain Ca)
- ACE-I's
- ARB's
- Ca2+ chan blockers

Front 2

what anti-HTN drugs are used w/CHF?

Back 2

- diuretics (loop)
- K+ sparing diuretics (spironolactone)
- ACE-I's/ARB's
- b-blockers (in compensated CHF--don't give to a failing heart)

Front 3

what anti-HTN drugs are used w/DM?

Back 3

- ACE-I's/ARB's
- Ca2+ chan blockers
- diuretics
- b-blockers (but can mask signs of hypoglycemia)
- a-blockers

Front 4

what's the MOA of hydralazine?

Back 4

↑cGMP = SM relax = ↓ afterload
(vasodils arterioles > veins)

Front 5

when do you use hydralazine?

Back 5

- HTN crisis
- CHF
- 1st line for HTN in pregnancy w/methyldopa
- coadmin b-blocker to prevent reflex tachycardia

Front 6

what happens w/hydralazine toxicity?

Back 6

- compensatory tachycardia (contraind in angina/CAD)
- fluid retention
- nausea
- headache
- angina
- lupus like synd (remember, SHIP)

Front 7

what's the MOA of minoxidil?

Back 7

K+ chan opener
(hyperpols & relaxes vasc SM)

Front 8

what is minoxidil used for?

Back 8

severe HTN

Front 9

minoxidil toxicity

Back 9

- hypertrichosis (↑ hair)
- pericardial effusion
- reflex tachycardia (use b-block to prevent)
- angina
- salt retention

Front 10

calcium channel blockers

Back 10

- nifedipine
- verapamil, diltiazem

Front 11

calcium chan blockers MOA

Back 11

block volt-dept L-type Ca2+ chans of cardiac & smooth musc = ↓dp/dt
(vasc SM = nifedipine > diltiazem > verapamil)
(heart = verapamil > diltiazem > nifedipine)

Front 12

calcium chan blockers clinical use

Back 12

- HTN
- angina
- arrhythmias (not nifedipine)
- Prinzmetal's angina
- Raynaud's

Front 13

calcium chan blockers toxicity

Back 13

- cardiac depression
- AV block
- periph edema
- flushing, dizziness & constipation (SM in gut)

Front 14

nitroglycerin & isosorbide dinitrate MOA

Back 14

vasodil by releasing NO in SM = ↑cGMP & sm musc relaxation
(dils veins >>arteries)
(↓ preload)

Front 15

nitroglycerin & isosorbide dinitrate clinical use

Back 15

- angina
- pulm edema (get fluid out of lungs!)
- aphrodisiac & erection enhancer

Front 16

nitroglycerin & isosorbide dinitrate toxicity

Back 16

- reflex tachy
- hTN
- flushing
- HA
- "monday dz" in industry exposure
(probs of vasodil...)

Front 17

nitroprusside MOA

Back 17

↑cGMP via direct release of NO
(dil's arts/veins = ↓preload & afterload)
(short acting)

Front 18

nitroprusside toxicity

Back 18

can cause CN tox

Front 19

antianginal therapy

Back 19

- nitrates (affect preload)
- b-blockers (affect afterload)
- nitrates + b-blockers = ↓↓↓BP, no effect on dp/dt, ↓HR, ↓↓myocardial O2 consumption (additive)

Front 20

what b-blockers are contraindicated in angina?

Back 20

pindolol & acebutolol b/c they are partial b-agonists

Front 21

5 classes of drugs used to ↓ lipids

Back 21

1) HMG-CoA reductase inhibitors
2) Niacin
3) Bile acid resins
4) Cholesterol absorption blockers (eztimibe)
5) "Fibrates"

Front 22

HMG-CoA reductase inhibitors

Back 22

"statins"

- lovastatin
- pravastatin
- simvastatin
- atorvastatin
- rosuvastatin

Front 23

bile acid resins

Back 23

- cholestyrammine
- colestipol
- colesevelam

Front 24

what lipid lowering agent also bind to C. diff toxin in C. diff colitis?

Back 24

cholestyramine

Front 25

"Fibrates"

Back 25

- gemfibrozil
- clofibrate
- bezafibrate
- fenofibrate

Front 26

main action of HMG-CoA reductase inhibitors

Back 26

↓ LDL

Front 27

S/E's of HMG-CoA reductase inhibitors

Back 27

- hepatotoxicity (↑ LFT's)
- rhabdomyolysis
- myocitis (inflam in musc)
- myalgia (musc pain)

Front 28

main action of Niacin

Back 28

↑ HDL

Front 29

S/E's of Niacin

Back 29

- red, flushed face (↓ w/aspirin & time)
- hyperglycemia (acanthosis nigricans)
- hyperuricemia (exacerbates gout--don't use)

Front 30

MOA of bile acid resins

Back 30

prevents intestinal reabs of bile acids

Front 31

bile acid resin S/E's

Back 31

- pt's hate it
- tastes bad
- GI discomfort
- cholest gallstones

Front 32

main action of cholest absorption blockers (eztimibe)

Back 32

↓ LDL

Front 33

S/E of cholest absorp blockers (eztimibe)

Back 33

- RARELY ↑'s LFT's
- ↑'s plaque thickness...

Front 34

main action of the "fibrates"

Back 34

↓ TG's
(imp to ↓ d/t risk of pancreatitis)

Front 35

S/E's of "fibrates"

Back 35

- same as for statins (never give w/a statin)
- myositis, hepatotox
- cholest gall stones

Front 36

cardiac glycosides

Back 36

digoxin, digitalis

Front 37

digoxin clinical use(s)

Back 37

- CHF (↑dp/dt)
- A fib (↓ conduction @AV node & depr SA node--rate control of resting HR, not during exercise)

Front 38

digoxin toxicity

Back 38

- cholinergic: n/v, diarrhea, blurry yellow vision (think Van Gogh)

- bradycardia (MC, tx w/atropine) OR tachycardia

- renally excr drug--> worsened by renal failure (↓excr), hypoK, quinidine (↓dig clearance; displaces from tissue binding sites)

Front 39

antidote for digoxin toxicity

Back 39

- slowly normalize K+
- atropine (for bradycardia, MC)
- lidocaine (for tachy-arrythmia)
- cardiac pacer (if atropine isn't effective)
- anti-dig Fab fragments
- Mg2+

Front 40

antiarrhythmic class IA drugs

Back 40

Na+ chan blockers
- Procainamide
- Disopyramide
- Quinidine
("Police Department Questioned")

Front 41

antiarrhythmic class IB drugs

Back 41

Na+ chan blockers
- Tocainide
- Lidocaine
- Mexiletine
("The Little Man")

Front 42

antiarrhythmic class IC drugs

Back 42

Na+ chan blockers
- Flecainide
- Propafenone
- Encainide
("For Pushing Ecstasy")

Front 43

quinidine toxicity

Back 43

- cinchonism: HA, tinnitus
- thrombocytopenia
- torsades de pointes d/t ↑QT int

Front 44

procainamide toxicity

Back 44

reversible SLE-like synd
(rememb, SHIP)

Front 45

class IB antiarrhythmics toxicity

Back 45

- local anesthetic
- CNS stim/depression
- CV depression

Front 46

class IC antiarrhythmics toxicity

Back 46

- proarrhythmic, esp post-MI (contraind)
- significantly prolongs refractory period in AV node

Front 47

____ causes ↑ toxicity for all class I antiarrhythmics.

Back 47

Hyperkalemia

Front 48

class II antiarrhythmics

Back 48

b-blockers:
- propranolol
- esmolol (short acting)
- metoprolol
- atenolol
- timolol

Front 49

class II (b-blockers) antiarrhythmics MOA

Back 49

- ↓cAMP, ↓Ca2+ currents
- suppress abnl pacemakers by ↓ slope of phase 4 (slows HR)

Front 50

class I antiarrhythmics (Na chan blockers) MOA

Back 50

- local anesthetics
- slow/block (↓) conduction
- ↓ slope of phase 4 depol
- ↑ threshold for firing in abnl pacemaker cells
- are state dependent (selectively depress tissue that's freq depol, e.g. fast tachy)

Front 51

class II antiarrhythmics (b-blockers) clinical use

Back 51

- V-tach
- SVT
- slow ventric rate during a-fib & a-flutter

Front 52

class II antiarrhythmics (b-blockers) toxicity

Back 52

- impotence
- exacerbation of asthma
- CV effects (bradycardia, AV block, CHF)
- CNS effects (sedation, sleep alterations)
- can mask signs of hypoglycemia in diabetics
- metoprolol can cause dyslipidemia
- tx overdose w/glucagon

Front 53

treat b-blocker overdose w/...?

Back 53

glucagon

Front 54

class III antiarrhythmics (K chan blockers)

Back 54

- sotalol
- amiodarone

Front 55

class III antiarrhythmics (K chan blockers) MOA

Back 55

(sotalol, amiodarone)
- ↑AP duration
- ↑ERP
- used when other antiarrhyths fail
- ↑QT int
- (rhythm control for Afib)

Front 56

sotalol toxicity
(class III antiarrhythmic / K chan blocker)

Back 56

- torsades de pointes
- excessive beta block

Front 57

amiodarone toxicity
(class III antiarrhythmic / K chan blocker)

Back 57

(Remember to check PFT's, LFT's, & TFT's when using amiodarone...)
- **pulmonary fibrosis
- **hepatotoxicity
- **hypo-/hyper-thyroidism (it's 40% iodine)
- corneal & skin deposits (blue/gray)
- photodermatitis (SAT for a photo)
- neuro effects
- constipation
- CV effects (bradycardia, heart block, CHF)

Front 58

what class effects does amiodarone have

Back 58

I, II, III, & IV...because it alters the lipid membrane. but it's primarily class III & works @myocyte phase 3.

Front 59

class IV antiarrhythmics (Ca chan blockers)

Back 59

verapamil, diltiazem

Front 60

class IV antiarrhythmics (Ca chan blockers) MOA

Back 60

(verapamil, diltiazem)
- primarily affect AV nodal cells
- ↓ conduction velocity
- ↑ERP
- ↑ PR int

Front 61

class IV antiarrhythmics (Ca chan blockers) clinical use

Back 61

(verapamil, diltiazem)
used to prevent nodal arrhythmias (e.g. SVT)

Front 62

class IV antiarrhythmics (Ca chan blockers) toxicity

Back 62

(verapamil, diltiazem)
- constipation
- flushing
- edema
- CV effects (CHF, AV block, sinus node depr)

Front 63

3 "other" antiarrhythmics that do not fall into class I-IV

Back 63

- adenosine
- K+
- Mg2+

Front 64

adenosine (antiarryth) MOA

Back 64

↑K+ leaving cells → hyperpols the cell & ↓I-Ca (can't depol...stops heart!)

Front 65

adenosine (antiarryth) clinical use

Back 65

- DOC in dx/tx supraventricular tachycardia
- slows heart down to see what the prob is
- very short acting (~15 sec)

Front 66

adenosine (antiarryth) toxicity

Back 66

- flushing
- hypotension
- chest pain

Front 67

what drug blocks the effects of adenosine?

Back 67

theophylline

Front 68

tx for chronic heart failure

Back 68

1) digoxin (↑dp/dt)
2) ACE-I/ARB's (↓BP by ↓'ing renin)
3) loop diuretics (to ↓ renin)
4) b-blockers (↑ symp)

Front 69

tx for acute heart failure

Back 69

"LMNOP"
1) loop diuretics/lasixs (furosemide)
2) morphine (for "air hunger")
3) nitrates (dil periph vasc to take blood from pulm)
4) O2
5) Positioning (sit on edge of bed to pool fluid to legs)
6) Pressors (dobutamine to ↑dp/dt)
(take off b-blockers!)

Front 70

DOC for empiric endocarditis

Back 70

vancomycin
(except, of course, for VRE endocarditis)