• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/82

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

82 Cards in this Set

  • Front
  • Back
4 therapies for essential HTN
Diuretics
ACE inhibitors
AII receptor blockers
Ca-channel blockers
4 treatments for CHF-induced HTN
Diurectics
ACEI/ARBs
B-blockers (compensated CHF)
K-sparing diuretics
In a patient with CHF, when are b-blockers

a. indicated
b. contraindicated
a. compensated CHF

b. decompensated CHF
5 treatments for Diabetes Mellitus-induced HTN
ACEI/ARBs
Ca-channel blockers
Diuretics
B-blockers
a-blockers
What type of drugs are protective against diabetic nephropathy, used as an antihypertensive in DM
ACE inhibitors
Drug to use for
-severe HTN
-CHF
-First line drug for hypertension in pregnancy (given with methyldopa)

what is the drug and what is it often co-administered with?
hydralazine, often coadministered with a b-blocker to prevent reflex tachycardia
Hydralazine

MOA
increases cGMP --> smooth muscle relaxation

vasodilates arterioles > veins --> lowers afterload
Adverse effects of what antihypertensive drug

Compensatory tachycardia
Fluid retention
Nausea
Headache
Angina
Lupus-like syndrome
Hydralazine
what are 2 contraindications of hydralazine?

why?
angina, coronary artery disease

the drug vasodilates --> can cause compensatory tachycardia
Nifedipine, verapamil, diltiazem

class
MOA

How does the effectiveness of each drug differ in vascular vs. cardiac muscle
Ca-channel blockers

block voltage-gated L-type Ca channels of cardiac and smooth muscle --> reduce contractility

Vascular: nifedipine > diltiazem > verapamil

Heart: verapamil > diltiazem > nifedipine
5 clinical uses of Ca channel blockers


which one do you NOT use nifedipine for
HTN, angina, arrhythmias, Prinzmetal's, Raynaud's

no nifedipine for arrhythmias
Cardiac depression
AV block
peripheral edema
flushing
dizziness
constipation

adverse effects of which drugs
Ca channel blockers = nifedipine, diltiazem, verapamil
2 drgus that are used in angina, pulmonary edema, and as an erection enhancer/aphrodesiac

MOA?
Nitroglycerin, isosorbide dinitrate

Releases NO in smooth muscle --> increase in cGMP --> smooth muscle relax; dilates veins a lot, reduces preload
Reflex tachycardia, hypotension
flushing
headache

-workers who work with these substances develop tolerance during the week, lose it over the weekend, and come back to work on monday with tachycardia, dizziness, and headache
Nitroglycerin, isosorbide dinitrate
A short-acting treatment for malignant HTN that can cause CN toxicity

MOA?
Nitroprusside

Increases cGMP by directly releasing NO
a treatment for malignant HTN that works as a D1 (dopamine) receptor agonist

where does it act?
Fenoldopam

Relaxes renal vascular smooth muscle
Treatment for Malignant HTN that acts by opening K channels, leading to hyperpolarization and relaxation of vascular smooth muscle

what is the side effect
diazoxide

hyperglycemia (reducees insulin release)
What is the fundamental goal of anti-anginal therapy

what are 5 possible targets
decrease myocardial oxygen consumption

need to reduce
1. end diastolic volume
2. BP
3. HR
4. Contractility
5. Ejection time
Nitrates vs. B-blockers

which affects preload?
afterload?
Nitrates = preload (dilates veins)

B-blockers = afterload (dilates arteries)
Effect of nitrates on
a. end diastolic volume
b. BP
c. Contractility
d. HR
e. ejection time
f. Myocardial O2 consumption
a. down
b. down
c. up (reflex)
d. up (reflex)
e. down
f. down
What are the effects of b-blockers on
a. end diastolic volume
b. bp
c. contractility
d. hr
e. ejection time
f. myocardial O2 consumption
a. up
b. down
c. down
d. down
e. up
f. down
What are the effects of using b-blockers AND nitrates on
a. end diastolic volume
b. bp
c. contractility
d. hr
e. ejection time
f. myocardial O2 consumption
a. no effect or down
b. down
c. no effect
d. down
e. no effect
f. way down!
Ca channel blockers

a. which one acts more similarly to nitrates

b. which one acts more similarly to b-blockers
a. Nifedipine more like Nitrates

b. verapamil more like b-blockers
2 beta blockers contraindicated in angina and why?
pindolol and acebutolol

partial b-agonists
Lovastatin, pravastatin, simvastatin, atorvastatin, rosuvastatin

class?
MOA?
inhibits what compound?
side effects?
HMG-CoA reductase inhibitors, inhibit cholesterol precursor, mevalonate

Hepatotoxicity (inc. LFTs), rhabdomyolysis
Lovastatin, pravastatin, simvastatin, atorvastatin, rosuvastatin

Effect on
a. LDL
b. HDL
c. TGs
a. way down
b. up
c. down
Niacin

MOA?

Side effects? (3)
Inhibits lipolysis of adipose tissue, reduces hepatic VLDL secretion into circulation

1. Red, flushed face (dec. by aspirin)
2. hyperglycemia (acanthosis nigricans)
3. hyperuricemia (exacerbates gout)
Niacin

Effect on
a. LDL
b. HDL
c. TGs
a. down
b. up
c. down
Cholestyramine, colestipol, colesevalam

class?

MOA?

adverse? (4)
bile acid resin

prevents intestinal reabsorption of bile acids, so liver must use more cholesterol

1. tastes bad
2. GI discomfort
3. decreases absorption of fat-solube vitamins
4. cholesterol gallstones
Cholestyramine, colestipol, colesevelam

Effect on
a. LDL
b. HDL
c. TGs
a. down
b. slightly up
c. slightly up
Ezetimibe

class

MOA

Side effects
Cholestrol absorption blockers

Prevents cholesterol reabsorption at small intestine brush border

rare increase in LFTs
gemifibrozil, clofibranate, fenofibrate

class
MOA
side effects (3)
"fibrates"

upregulate LPL --> increases TG clearance

Myositis, hepatotoxicity (high LFTs), cholesterol gallstones
Ezetimibe

Effect on
a. LDL
b. HDL
c. TGs
a. down
b. none
c. none
gemifibrozil, clofibranate, fenofibrate
Effect on
a. LDL
b. HDL
c. TGs
a. down
b. up
c. way down
6 structures of cardiac excitation contraction coupling (start with Na/K ATPase)
1. Na/K ATPase sends Na out, K in
2. Na/Ca exchanger sends Ca out, Na in
3. L-type Ca channel (voltage gated) brings Ca in
4. Ca pump in wall of SR (closely coupoled to L-type Ca channel)
5. Ryanodine receptors and Ca-release channels in wall of SR
6. Ca interaction in troponin-tropomyosin system
Where does digoxin work
Na/K ATPase channel in cardiac cell membrane
Where do Ca channel blockers and b-blockers work

effect
L-type Ca channels in cell membrane

Decrease cardiac contraction
Where does ryanodine work

effect?
Inhibits ryanodine receptor in SR
Where do "Ca sensitizers" work in the cardiac excitation-contraction coupling
increases Ca binding to troponin/tropomysoin
How do B1 receptors increase contractility
B1 receptor --> Gs --> ^cAMP --> PKA --> phosphorylates L-type Ca channel and phospholamban (SR Ca-Channel inhibitor) --> increases intracellular Ca during contraction
Digoxin

a. bioavailability
b. % protein bound
c. t (1/2) =
d. Mechanism of excretion
a. 75%
b. 20-40%
c. 40hrs
d. urinary excretion
Drug used to treat CHF (increases contractility), atrial fibrillation (decreases conduction at AV node, depresses SA node)
Digoxin
-cardiac glycoside
Drug that is used to increase contractility, treat atrial fibrillation

Adverse:
-anti-cholinergic
-ECG - high PR, low QT, Twave inversion, arrhythmia, hyperkalemia
Digoxin
Digoxin

MOA (2)
1) inhibits Na/K ATPase (Na builds up inside) --> directly inhibits Na/Ca exchanger (Na can't enter cell so Ca can't leave) --> increases Ca --> positive intropy

2) also stimulates vagus
3 contraindications of digoxin
-renal failure (dec. excretion)
-hypokalemia
-quinidine (decreases digoxin clearance, displaces digoxin from tissue-binding sites
antidote to digox poinsong
-slowly normalize K
-lidocaine
-cardiac pacer
-anti-dig Fab fragments
-Mg
What is the MOA of drugs that serve as local anesthetics
Na channel blockers (class I antiarrhythmics)
class I antiarrythmics

3 effects
Na channel blockers

1. slows/blocks conduction i(n depolarized cells especially)

2. decreases slope of phase 0 depol. (slows HR)

3. increases threshold for firing abnormal pacemaker cells
What does it mean that Na-channel blockers (class I antiarrhythmics) are state dependent
selectivly depress tissue that is frquently depolarized (ex. fast tachycardia)
Quinidine
Procainamide
DisoPYRAMIDe

class?
3 effects?
Class IA antiarrhythmic (Na channel blocker)

"the Queen Proclaims Disco's Pyramid" (Quinidine, procainamide, disopyramide)

1. increases AP duration
2. increases effective refractory period
3. increases QT interval
Drugs to use for
-reentrant and ectopic supraventricular and ventricular tachycardia
class IA antiarrhythmics (Na channel blockers)

quinidine, procainamide
disopyramide
Quinidine toxicity
cinchonism = headache, tinnitus
prcainamide toxicity
reversible SLE-like syndrome
class IA antiarrhythmic toxicity
(2)
-thrombocytopenia
-torsades de pointes (due to long QT)
Lidocaine
Mexiletine
Tocainide

class of drugs?
effect?
class IB (Na Channel blockers) antiarrhytmics

I'd Buy LIDy's MEXIcan Tacos"

(can also include phenytoin)

decreases AP duration
Drug to use in acute ventricular arrhythmias (esp. post MI) and digitalis-induced arrhythmias

what tissue do these drugs target
Lidocaine, Mexiletine, Tocainide (class IB)

targets ischemic or depolarized Purkinje and ventricular tissue
3 consequences of class IB antiarrythmic toxicity
1. local anesthetic
2. CNS depressant/stimulant
3. CV depression
Flecainide, Encainide, Propafenone

class of drug?

effect on action potential?
Class IC antiarrhythmic (Na channel blocker)

no effect on AP duration

Chiptle's Food has Excellent Produce)
drug useful in
-V-tachs that progress to Vfib
-intractable SVT
-last resort for refractory tachyarrhytmias
Flecainide, Encainide, Propafenone (class IC)
What are 2 contraindications for class IC antiarrhythmics
1. structural abnormalities
2. post MI
1. proarrhythmic post-MI
2. prolongs refractory period in AV node

toxicities of which drug
class IC antiarrhythmics
Class I antiarrhytmic

a. best after MI
b. contraindicated post-MI
a. IB = best after MI
b. IC = contra after MI
effect of hyperkalemia on class I antiarrhythmics
increases toxicity for all class I
Propanolol, esmolol, metoprolol, atenolol, timolol

class?
beta blockers (class II antiarrhythmics)
b-blockers

MOA

effect on abnormal pacemakers?

effect on AV node?

2 manifestations of this
decrease cAMP, decrease Ca currents

suppresses abnormal pacemakers and AV node -->
decreased slope of phase 4, inc. PR interval
Drug to use for
-Vtach
-SVT
-slow ventricular rate during atrial fibrillation and atrial flutter
beta blockers (class II antiarrhytmics)
Very short acting beta blocker
esmolol
-Impotence
-exacerbation of asthma
-bradycardia, AV block, CHF
-sedation, sleep alteration
-mask hypoglycemia

adverse effects of what drugs
beta blockers
adverse effect of metoprolol

how do you treat overdose
dyslipidemia

glucagon
Sotalol, ibutilide, bretylium, dofetilide, amiodarone

class of drug
class III antiarrhythmic (K channel blocker)
Drug to use when other antiarrhytmics fail -->
-increased AP
-increased refractory time
-increased QT interval
class III antiarrhythmic (K channel blocker)

Sotalol, ibutilide, bretylium, dofetilide, amiodarone
class III antiarrhytmic (k channel) that has toxicity -->
-torsades de pointes
-excessive beta block
sotalol
class III antiarrhytmic (k channel) that has toxicity -->
-new arrhytmias
-hypotension
bretylium
class III antiarrhytmic (k channel) that has toxicity -->
-pulmonary fibrosis
-hepatotoxicity
-hypothyroidism / hyperthyroidism
-corneal deposits
-skin deposits (blue/gray) --> photodermatitis
-neuro effects
-constipation
-bradycardia, CHF, heart block
amiodarone

check PFTs, LFTs, and TFTs with amiodarone
what are the effects of amiodarone
alters lipid membrane --> has class I, II, III, and IV effects
Verapamil, Diltiazem

class of drug?
class IV antiarrhythmic (ca channel block)
Drug used to prevent nodal arrhythmias, causes
-decreased conduction velocity
-increased refractory
-increased PR interval
class IV (Ca channel blockers)
class of antiarrhytmics that causes
-consipation
-flushing
-edema
-CHF, AV block, sinus node depression
Ca channel blockers (IV)
Other antiarrhytmics

-very short acting drug that is the drug of choice in abolishing supraventrcular tachycardias

MOA
adenosine

increases K out of cells --> hyperpolarization, decreased Ca current
Other antiarrhytmics

3 negative effects of adenosine

how can you block these
flushing, hypotension, chest pain

blocked by theophylline
Other antiarrhytmics

Used to depress ectopic pacemakers in hypokalemia (ex. digoxin toxicity)
Potassium
Other antiarrhytmics

Used to treat torsades de pointes and digoxin toxicity
Mg