Mf1 Drugs

Front 1

quinidine

Back 1

depresses normal increase in Na+ permeability of cardiac muscle membrane during generation of AP

can be used to block rhythmic discharge of focal point causing a paroxysmal tachycardia attack

Front 2

lidocaine

Back 2

depresses normal increase in Na+ permeability of cardiac muscle membrane during generation of AP

can be used to block rhythmic discharge of focal point causing a paroxysmal tachycardia attack

Front 3

To reduce tachycardia

Back 3

Digitalis glycosides act primarily by increasing vagal tone at the AV node.

Beta blockers decrease sympathetic tone.

Calcium channel blockers directly interfere with conduction by impairing the cellular entry of calciumions, which play a major role in electrical impulse transmission in the AV node.

Front 4

mechanism of action inotropic effect of digitalis

Back 4

1) inhibition sarcolemmal Na+K+ ATPase = ^ intracellular Na+
2) reduced transmembrane gradient Na+ = reduced action of Na+ Ca++ exchanger driving Ca++ out of cell
3) extra Ca++ taken up into sarcoplasmic reticulum
4) stronger contractile force due to ^ Ca++ released at AP

Front 5

mechanism of action of chronotropic effects of digitalis

Back 5

modification of ANS output
= ^ vagal tone
= reduction sympathetic activity

= decrease frequency of transmission through AV node

** beneficial in reducing ventricular rate in supraventricular arrhythmias

** many toxic effects!

Front 6

treatment of digitalis induced tachyarrhythmias

Back 6

potassium if hypokalemia

IV lidocaine

may require temporary pacemaker therapy if high-grade AV block

*digoxin-specific antibodies

Front 7

ramipril

Back 7

ACE inhibitor

dose 2.5 - 20mg
tablets in 1.25, 2.5, 5, 10mg

use in HTN, CHF, post-MI

major elimination pathway = renal

Front 8

ACE inhibitors

Back 8

Mixed vasodilator
block formation of AII
= decrease systemic arterial pressure
= facilitate natriuresis
= reduce adverse ventricular remodeling

inhibit normal ACE degredation of bradykinin (natural vasodilator)
= stim endothelial release NO

Front 9

Omeprazole

Back 9

PPI

decreases gastric acid secretion by inhibiting the parietal cell H+/K+ ATP pump

It might decrease the incidence of NSAID-induced peptic ulcers and can be used to help prevent peptic ulcers in long-term NSAID users at high risk.It might decrease the incidence of NSAID-induced peptic ulcers and can be used to help prevent peptic ulcers in long-term NSAID users at high risk

Front 10

lansoprazole

Back 10

PPI

decreases gastric acid secretion by inhibiting the parietal cell H+/K+ ATP pump

It might decrease the incidence of NSAID-induced peptic ulcers and can be used to help prevent peptic ulcers in long-term NSAID users at high risk.

Front 11

Rabeprazole

Back 11

PPI

decreases gastric acid secretion by inhibiting the parietal cell H+/K+ ATP pump

used for short-term (4-8 wk) treatment and relief of symptomatic erosive or ulcerative gastroesophageal reflux disease GERD

Front 12

Esomeprazole

Back 12

PPI

S-isomer of omeprazole

inhibits gastric acid secretion by inhibiting the H+/K+-ATPase enzyme system at the secretory surface of gastric parietal cells

used in severe cases and in patients who have not responded to H2 antagonist therapy

treat and relieve symptoms of active duodenal ulcers,

treat all grades of erosive esophagitis.

Front 13

Pantoprazole

Back 13

PPi

suppresses gastric acid secretion by specifically inhibiting the H+/K+-ATPase enzyme system at the secretory surface of gastric parietal cells

intravenous preparation has only been studied for short-term use (ie, 7-10 d)

Front 14

cimetidine

Back 14

H2 R Blocker

can be used as primary therapy to heal ulcers not associated with H pylori infection. The duration of treatment is 6-8 weeks. A longer treatment course might be required for gastric ulcers.

Front 15

famotidine

Back 15

H2 R blocker

competitively inhibits histamine at H2 receptor of gastric parietal cells, resulting in reduced gastric acid secretion, gastric volume, and hydrogen ion concentrations.

Front 16

nizatidine

Back 16

H2 R Blocker

competitively inhibits histamine at H2 receptor of gastric parietal cells, resulting in reduced gastric acid secretion, gastric volume, and hydrogen ion concentrations.

Front 17

ranitidine

Back 17

H2 R Blocker

inhibits histamine stimulation of the H2 receptor in gastric parietal cells, which, in turn, reduces gastric acid secretion, gastric volume, and hydrogen ion concentrations.

Front 18

H2 Receptor Blockers

Back 18

antihistamine agents are used in the short-term treatment of an active duodenal ulcer and as prophylaxis in the long term

act at parietal cells
result in reduced gastric acid secretion etc

Front 19

Cytoprotective Agents

Back 19

stimulate mucus production and enhance blood flow throughout the lining of the gastrointestinal tract.

These agents also work by forming a coating that protects the ulcerated tissue.

Ex: misoprostol and sucralfate.

Front 20

Sucralfate

Back 20

cytoprotective agent

binds with positively charged proteins in exudates and forms a viscous adhesive substance that protects the GI lining against pepsin, peptic acid, and bile salts; adhesion to the ulcer base, adsorption of bile acids, inactivation of pepsin, and stimulation of bicarbonate and mucus secretion

- used for short-term management of ulcers, may be used as primary therapy for PUD (at a dose of 1g orally four times daily)
- also effective in preventing duodenal ulcer relapse (at a dose of 1g twice daily).

Front 21

Misoprostol

Back 21

cytoprotective agent

prostaglandin analog that can be used to decrease the incidence of peptic ulcers and complications in long-term NSAID users at high risk.

Front 22

cardiac inotropic drugs

Back 22

dobutamine (b1)
isoproternol (b1/b2)
dopamine (NE > E; b1/b2)
PDE inhibitors

if use these drugs long term, will lead to more harm than good (^ mortality)
vs digoxin - can use longer term bc not as good of an inotrope

Front 23

PDE inhibitors
phosphodiesterase

Back 23

get increased cAMP (blocks met)

amironone
milronone
dont use, chronically = kill pts

Front 24

digoxin

Back 24

only inotrope consider using chronically for CHF
IV
PO (85% absorption)

therapeutic window narrow (0.6-1.6)

Front 25

digoxin metabolism

Back 25

15% liver
85% renal

therefore kidney probs = build up (v narrow therapeutic window)

BUT short acting

Front 26

digoxin toxicities

Back 26

- nausea
- decreased appetite
- vision changes (colour)
- increase PR interval in EKG (bc chronotropic effects) -> first degree heart block as get higher levels dig
- ST changes (not pathological, also w ^ dose)

serious**
- PAT with block (paroxysmal atrial tachy) bc atrial stim combined w dec AV node conduction
- ventricular premature beats (VPB) -> can lead to death

Front 27

digoxin OD

Back 27

digibind - Immunologic mop up
(Ag-Ab)

$$$
when see OD or ventricular irritability (not with just block, or PAT with block; only ventricular irregs worrisome)

Front 28

digoxin w renal impairment

Back 28

can still use but at decreased dose and with very consistent monitoring (starting at 5th half-life - which is longer in renal impairment, up to 48 hours vs 12 hr norm)

also concerned about K+ and Mg++

Front 29

vasodilators

Back 29

arteriole dilators: reduce afterload
ACE inhibs (stops conversion angiotensin I-->II; blocks inactivation of bradykinin -> probably creates dry cough prob of ACE inhibs; use ARB if someone gets this)

ARBs (blocks effects of angio II at site of effect = arterioles/caps, no effect on bradykinin** one of fundamental diff) bit more $$

hydralazinne - dilates arteries directly (use in combo w NTG, alternative to using ACE inhib, although not as desirable)

venodilators: reduce preload
Nitroglycerine (high doses effects on arterioles as well)

nitropusside - IV only in H, only ICU, short term use; 1* used to lower bp in emergent situation

Front 30

Angiotensin II

Back 30

decreases resistance in capillary beds - more blood can leave heart

Front 31

ACE inhibitors

Back 31

ramipril - 1x day
captopril - 1st, but not used much anymoore bc need 3x day
enalapril
lisinopril
forinopril
quinapril

Front 32

ARBs

Back 32

losarten - 2xday
candesaten - 1xday
irbesarten
telmisarten
valarten

no evidence that one better than other, just some have been studied more than others

Front 33

adverse events ARBs and ACE inhibs

Back 33

decrease renal fn

can get ^ K+ (block of aldosterone; not a prob on its own necessarily, if combo with other drug that is affecting K+)

angioedema (swelling in neck, face;prob bradykinin effect, less than 1% pop will get; will still get some angioedema with ARBs oddly)

- dry cough in ACE inhibs

Front 34

main types diuretics

Back 34

- loop (at loop of henle in kidney, changes circ volume - mainstay of symptom management in HF with volume XS)

- thiazide: also get rid of salt, but at more distance site, but not as effective as loops

- K+ sparing (by giving with other diuretic, "adds life" w/o being particularly strong diuretic - prob just related to K+ and Mg++ loss)

Front 35

hydrochlorothiazide

Back 35

thiazides

Front 36

furosemide

Back 36

loop diuretic

Front 37

Spironolactone

Back 37

K+ sparing

ADEs: if use too much in presence of drugs that also increase K+ (ACE inhib) than can cause ^K+
- anti-androgenic effect (impotence, breast growth)

Front 38

K+ sparing drugs

Back 38

spironolactone
triamterene (not HF)
amiloride (not HF)

Front 39

beta blockers in HF

Back 39

use in HF prolongs life but start with low dose, titrate slow, only use in stable patients