Cardio Meds Flashcards
1
Q
HF drugs
- Digoxin: MOA, indication, secondary action w/ nerves, side effects, EKG findings, increased risk for tox and tx, effect w/ antiarrythmics
- milerione: indication, MOA
- naturietide: indication, MOA
A
- Digoxin: from foglove plant, Na/K atpase inhibitor, increases intracellular Na -> activated Na/Ca transporter -> increase intracellular Ca -> increase heart contraction, used for chronic heart failure, increase paraymspathetic tone through vagus -> bradycardia (Sa node) and heart block (AV node), can cause arrythmias, causes ST scoop, contraindicated in patient on meds for heart block, causes nausea, vommiting, abdominal pain, causes yellow vision, toxicity more common in patients with hypokalemia and kidney damage, antiarrythmics will cause longer half life of digoxin, use Fab on digoxin toxicity
- milerione: used for acute heart failure, inhibtits phosphodiesterase and increases CAMP, increase contractility of heart and dilates arteries
- naturietide: used for acute heart failure, syntheitc BNP -> increase cGMP, arterio/vaso dilate, natureisis
2
Q
- Aldosterone: suffix, MOA, side effects, used to treat which conditions, contraindications
- ARB: suffix, MOA, side effect
- Aliskiren: MOA, side effect
A
- ACE: -pril suffix; inhibit conversion of angiotensin I to angiotensin II, decrease GFR, decrease Na reabsorption at PCT, prevent increase in aldosterone -> decrease Na reabsorption and K excretion at DCT; increase creatinine when first given, cause hypotension and syncope in heart failure pts, cause hyperkalemia, dry cough; used to tx hypertension, diabetes (protein spilling), MI, and chronic heart failure (reduces mortality by preventing heart remodeling); hereditary angioedema, pregnant pts (teratogenic), pts on NSAIDS (cause AKI), pts with bilateral renal stenosis (chronic increase in creatinine),
- ARB: -sartan suffix; angiotensin receptor blocker; hyperkalemia
- Aliskiren: direct renin inhibitor, hyperkalemia
3
Q
Ca channel blockers
- MOA, both are used for (3)
- Dihydropyridine: work on, suffix, nifedipine info, other syndrome used for, side effects
- Non Dihydropyridines: types; v- moa, alternative use, side effects; d: MOA; PS use with both, contraindications with both
A
- block voltage dependent L type Ca channels on smooth and cardiac muscle -> decrease muscle contraction -> vasodilation and decrease contractility of heart; used for HTN (dipines given IV for hypertensive emergency), stable and vasospastic angina,
- dihydropyridines: for smooth muscle mainly -> vasodilation (systemisc and coronary vessels); suffix -dipine, nifedipine: used in pregnant patients, prevents vasospasm after subarachnoid hemmorrhage, and has a lot of negative side effects; raynauds phenomenon; light headedness and headache, peripheral edema and reflex tachycardia
- nondihydropyridines: verapamil- work mostly on heart -> decrease contration -> decrease O2 demand, used in migraines, constipation, gingival hypertrophy, ; dletiazem- work on heart and vessels; increase PS on AV and SA nodes -> bradycardia and anti-arrythmic properties -> contraindicated in pts with heart block and not to be used with beta blocker, canoot be used in patients with heart failure
4
Q
Hypertension Meds
- first line: meds and why should be given
- hypertensive emergency: sxs, tactic
A
- thiazide diuretics: better in AA; ACE inhibitors/ARBS: patients with hx of DMII, HF, or recent MI; Ca channel blockers: better for AA, pts with stable angina
- neuro sxs, blurry vision, lung crackles, BP> 180/120; reduce BP 10-20% over 1st hr, then 5-10% over next 23 hours; IV B1 blockers, lebatalol, Ca channel clboker (nicardipine, clovidipine), hydralazine (w/ beta blocker)
5
Q
Class I anti- arrythmics
- MOA
- binds to
- ECG findings
- 1A: examples, MOA and effects, binding, when is it used, side effects of each example
- 1B: example, binding, repolarization, used for, side effects
- 1C:
A
- Na channel blocker -> slow upstroke of cardiac electric signal
- inactivated/ activated state, not resting, so the more it is used the more binding there is -> tachy cardia will cause longer QRS complexes
- widened QRS -> can lead to prolonged QT -> torsades
- quinidine, procainimide, dysopiramide: blocks Na and K channels -> slower upstroke and longer depolarization/ repolarization; intermediate binding ability; used for supra and non supre ventricular tachycardia and Wolff parkinsons white; Q- headache, tinnitus, dizziness, thrombocytopenia, P- lupus like syndrome, D- exacerbate HF
- lidocain, phenytoin, mexilitene; poor binding -> little effect on cardiac upstroke, speed up repolarization; used for ischemia induced ventricular arrythmias; paresthesias, tremor, neuro def
- flecanide, proprfinone; binds the best to Na channel -> slows the upstroke the most -> increases QRS even more and does not block K channels so normal repolarization; treat supraventricular and ventricular arrythias (afib); hx of structural or ischemic heart disease
6
Q
Class II anti arrythmics
- MOA
- alternate MOA
- kinds of arrythmias
- side effects
A
- Beta blockers -> block sympathetic input to SA and AV nodes -> decrease cAMP -> close Ca channels
- supraventricular, afib/flutter (prevent rapid ventricular response)
- heart block (prolonged PR interval)
7
Q
Class III antiarrythmics
- MOA
- amneodarone: MOA, toxic
- common class III suffix
- sotalol
- kind of arrythmias
A
- K channel blocker -> prolong phase 3 -> porlonged refractory period
- acts like 1-4 anti-arrythmics, neuro tox, gray corneal spots, iodine -> TSH changes, palm tox w/ restrictive lung dx, heart block, heart dx, lung tox, blue/gray rash, phototox, CYP450 inhibitor -> build up of various drugs
- tilide (dofetilide and ibutelide)-> causes Q-T elongation (torsades)
- beta blocker and k channel blocker
- supra and ventricular tachy, a-fib (rhythm control)
8
Q
Type IV antiarrythmics
- MOA
- effects
- used for which type of arrythmias
- side effects
A
- Ca channel blocker -> nondihyrdopyridines -> verapamil and deltiazem
- effects SA and AV nodes -> phase 4 prolongation -> pr prolongation
- only supraventricular tachy -> especiall afib (rate control)
- heart block
9
Q
No Class anti-arrythmics
- Digoxin: MOA; which arrythmia
- Mg
- Adenosine: structure; MOA; side effects; which arrythmias; blocks effects
A
- works on vagus nerve to increase PS innervation, afib,
- used for tosades
- purine nucleotide, binds to A1 receptors on AV nodes and stops Ca current and increase potassium out -> prolongs depolarization and hyperpolarizes, also vasodilates by binding to A2; heart block, flushing, SOB, chest pain, headache, hypotension; supraventricular; energy drinks block A1
10
Q
Beta blockers
- suffix
- MOA
- work on
- side effect
- used for
- difference between alpha and beta
- carvedilol
- lebtalaol
- IV
- thyroid
- tox
A
- lol
- decrease cardiac contractility and inhibit renin production by antagonizing beta 1 receptors
- SA and AV node
- heart block, reduce cardiac remodeling, exacerbate asthma, impotence
- stable angina
- reduce mortality in pts with MI and heart failure
- beta 2s are cardio selective; used after MI and heart failure - non selective beta blocker and alpha 1 blocker
- nonselective beta blocker and alpha 1 blocker -> used for HTN (especially in pregnancy) and hypertensive emergencies
- used for hypertensive emergencies and aortic dissection
- symptomatic treatment of thyroid storm
- glucagon
11
Q
Ca channel blockers
- dihydropyridines: examples, suffix, indications; side effects
- non dihydropyridines: examples; indications
- nimodipine
- nicardipine/ clevidipine
A
- amlodipine=nifedipine, - pines; HTN, angina, raynauds; peripheral edema, flushing, dizziness
- verapamil and diltiazem; HTN, angina, afib; heart block, constipation
- subarachnoid hemmorrhage
- hypertensive emergency
12
Q
Hydralazine
- MOA
- location of effects
- indications
- pregnancy
- given with and why
- side effects
A
- increase cGMP -> smooth muscle relax
- arteries> vein -> afterload reduction
- severe HTN, HF
- safe
- Beta blocker, to prevent reflex tachy
- SLE like syndrome, fluid retention, headache
13
Q
Other HTN emergency drugs
- nitroprusside
- fenoldopam
A
- increase cGMP via direct release of NO; cyanide tox;
- Dopamine D1 receptor agonist causing coronary, peripheral, renal and splanchnic vasodilation; increase BP and decrease naturesis; hypotension and tachycardia
14
Q
Nitrates
- MOA
- location of effect and effect
- indication
- side effect
A
- vasodilate by increasing NO in vasc smooth muscle
- dilates veins >> arteries; decrease preload
- angina, acute coronary syndrome, pulm edema
- reflex tachy, hypotension
15
Q
Ranolazine
- MOA
- indication
- side effects
A
- inhibits late phase of Na current reducin diastolic wall tension and oxy consumption
- refractory angina
- constipation, dizziness, headache
