Study your flashcards anywhere!

Download the official Cram app for free >

  • 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

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key

image

Play button

image

Play button

image

Progress

1/24

Click to flip

24 Cards in this Set

  • Front
  • Back
Hypertension treatment

What are the 5 general drug categories for treatment?
Diuretics, Sympathoplegics, Vasodilators, ACE inhibitors, A II receptor blockers
Diuretics for HTN

1)Name and Side effects
1)Hydrochlorothiazide- hypokalemia, hyperlipidemia, hyperuricemia, hypercalcemia,hyperglycemia

2)Loop Diuretics- K+ wasting, metabolic alkalosis (volume contraction), ototoxic
Clonidine
1) MOA
2) side effects
1)central agonist at alpha2 to prevent further release

2) dry mouth, sedation, rebound hypertension
Methyldopa
same as clonidine

Causes (+) Coomb's test
Hexamethonium
1)MOA
2)Side effects
1) Blocks Vasovagal response to increase HR and BP

2) Orthostatic Hypotension
Reserpine
1)MOA
2)Side Effects
1) Blocks Dopamine uptake into vessicles ---> decreases NE stores

2) Sedation, Depression
Prazosin
1)MOA
2)Side Effects
1) selective alpha 1 antagonist

2) 1st dose hypotension
Beta Blockers
1) MOA
2)Side Effects
1) Drugs that start with A-M selectively block increased HR to drop CO. The rest act on Beta2 as well to prevent bronchodilation

2)Impotence, Asthma exacerbation, Sedation, CHF, bradycardia
Hydralazine
1)MOA
2)Use
3)Toxicity
1)Vasodilator in arteries via cGMP

2)Severe HTN, CHF

3) SLE like syndrome, reflex tachy (use B blocker)
Nifedipine, Verapamil, Diltiazem
1)MOA
2)side-effects
3)uses
1) Block voltage gated L-type Ca+ channel to reduce contractility
Vascular muscle-nifedipine>diltiazem>nifedipine
Heart muscle- Verapamil>Diltiazem>Nifedipine

2)Dizziness, flushing, nausea, constipation (verapamil)
3)HTN,Angina, Arrythmias (not nifedipine)
Nitroprusside
1)MOA
2)Side Effects
1)increase NO release and vaso/veno dilates, but it is metabolized into cyanide.
2)Causes cyanide poisoning
Captopril
1)MOA
2)Side Effecs
1)ACE inhibitor to block Renin/Angiotensis system

2) CAPTOPRIL
Cough, Angioedema (decreases C1 Esterase), Proteinura, Taste Change, hypOtension, Pregnancy problems (renal damage to fetus), Rash (erythema multiforma, Stevens Johnson), Increase Renin, Low AT II
Nitroglyceride, isosorbide
1)MOA
2)Use
3)Side Effects
1) vasodilates veins via cGMP to decrease preload (decrease cardiac work)
2)Angina
3)Headache, Tachy (due to decrease CO), Hypotension
Tolerance develops
Monday Disease- if exposed to nitratse in industry, tolerance develops through work week, but showing up on Monday will cause Headache, Hypotension, and Tachy
Anginal Therapy
Goal is to decrease O2 consumption of myocardium via decreasing EDV, Afterload, Contractility, or HR

Nitrates- decrease Preload with reflex increase HR/

B-Blockers- decrease afterload by decreasing contraction and HR

Combo- drastically decrease O2 consumption via decreased HR and BP
Cardiac Glycosides - Digitalis, Digoxin

1)Facts
2)MOA
3)Use
1) 75% bioavailable, 20-40% protein bound, and t1/2 = 40 hours, urinary excretion

2)Inhibits Na/K pump which builds up Na inside cell --> lowers Na/Ca exchanger so that intracelluar Ca+ increases --> (+) inotropy
Also increases PR interval

3) used in CHF (inc inotropy), and Afib (dec conduction AV node)
Digoxin
4) Toxicity
5) Antidote
4) Nausea, Vomiting, Yellow Vision, Arrythmias

Risk increases with Renal Failure (less excretion), hyokalemia (synergistic effect), and Quinidine (displaces from Plamsa Protein to increase levels)

5) Stop Dig, give K+, use Lidocaine for arrhythmia, anti-Dig Fab fragments
Class I Antiarrhythmics

-What channels do they all block??
They are Na Channel blockers, specifically the fast Na+ channels involved in Phase 0 upstroke.
They can also slow Phase 4 upstroke Na+ funny channels in abnormal pacemaker cells.
Class Ia
1)Names
2)Effect
3)Uses
4)Toxicity
1) Quinidine, Procainamide, Amiodarone (also Class III), and Disopyramide

2) Moderate blockade of upstroke, and Prolongs the Repolarization --> net increase in Refractory Period to slow down abnormal re-entry circuits (long QT)

3) Afib, SVT, Vfib

4) Quinidine- cinchonism (headache, tinnitus, thrombocytopenia), and Torsades de Pointe
Procainamide- SLE like syndrome
Class Ib
1) Names
2) Effect
3) Use
4) Toxicity
1) Lidocaine, Tocainide

2) Weakest block of Na fast channels, and shortens repolarization to cause a decrease in Refractory Period. Only works on infarcted tissue

3)Post-MI arrythmias and digitalis induced

4) Local anesthesia, CNS depression,
Class Ic
1) Names
2) Effects
3) Uses
4) Toxicity
1) Flecainide, Ecainide, Propafenone

2) Strongest slow down of Na fast channels, but no effect on Repolarization (same Refractory Period)

3) Used in life threatening Vtachs, SVT (last resort)

4) Can induce arrythmias
Class II - Beta Blockers

1)MOA
2)Toxicity
1) Decrease cAMP which prevents phosphorylation of Rianodine receptors --> less Ca+ for contraction
Prolongs upstroke of Phase 4 in pacemaker cells (long PR interval)

2) Impotence, exacerbate asthma, bradycardia, sedation, may mask hypoglycemia (because it releases Glucagon)
Class III - K+ Blockers

1)Names
2)MOA
3)Uses
4)Toxicity
1) Sotalol, Amiodarone, Ibutilide

2) Prolongs the time for K+ to leave the cell -->increase Refractory Period (QT)

3)Used in SVT and Vtach when other drugs fail

4) Sotalol- torsades de pointe
Amiodarone- Pulmonary Fibrosis, Hepatotoxic, Hyper/hypothyroid (check PFTs, LFTs, and TFTs). Also visual changes, and skin deposits


4)
Class IV- Ca+ Blockers

1)Names
2)MOA
3)Uses
4)Toxicity
1) Verapamil, Diltiazem (Nifedipine not used)

2) They block Ca+ currents, which are the fast channels in Pacemaker cells.
Prolong ERP and conduction velocity of AV node

3) Prevention of nodal Arrhythmias (SVT)

4) Constipation, flushing, edema, CHF (decreases contraction force), AV block
Adenosine
Causes flat line for 15 seconds --> abolishes AV node arrhythmia (cardioversion)