Test 1 Flashcards
What ace inhibitors have long 1/2 life, which is not a pro drug like all others
Fosinopril and ramipril have long 1/2 lives
Captopril is not a pro rug
ARB receptor blockers dosing
1 day orally.
Renin inhib. What other drug reduces it’s efficiency?
NSAIDs
Therapeutic uses for BB
HTN patients with arrhythmia, prev heart attack, agnina, chronic heart failure, migraine, anxiety, glaucoma.
Longest half life of calcium channel blockers
Amlodipine
Adverse effects/contra for calcium channel blockers
Most AE due to hypotension- dizzy, peripheral edema, reflex tachycardia, headache, fatigue.
Contra in HF patient
Hydrazaline usually take what with it
Vasodilator. Usually take BB to help with reflex tachycardia (prevent adverse effects of arrhythmia and angina) and a diuretic to help with reflex water retention.
Monotherapy in pregnancy ok
How does minoxidil work
Hyperpolarizes K+ channels. Oral admin for severe, non responsive HTN.
How to treat diabetes insidious symptoms of polyuria and polydipsia?
Thiazide
Most common diuretic
Most efficacious
Common- Thiazide
Loop works best- use in HF
CAI location of action and what are they used for
Avoid in pts with
PCT.
used to tx glaucoma, mountain sickness and pseudotumor cerebri.
Acetazolamide- 2 250 tablets for glaucoma.
Avoid in pts with liver problems.
What drug may reduce effects of loop diuretics
NSAIDS
Loop diuretic DOC
Adverse effects
Used to reduce acute pulmonary edema due to HF.
Also treats hyperglycemia and hyperkalemia.
Adverse effects: ototoxicity and hyperuricemia, hypovolemia (shock)
Thiazide diuretics are derived from
Sulfa.
How long does it take thiazide diuretics to work? Adverse effects
1-3 weeks.
Hyperuricemia= gout
Aldosterone antag Potassium Sparing diuretics adverse effects
Gi upset, peptic ulcer, chemical resembles sex hormones.
Resistance is influenced by what 2 things
Diameter (Direct)
____
Blood vol (indirect)
most common cardiovascular disease
HTN
How do baroreceptors control CO and peripheral resistance
Fall in BP causes baroreceptors to send fewer impulses to cardiovascular centers in the spinal cord. Reflex response of increase sympathetic and decrease parasympathetic. Vasoconstriction and inc erase CO
2 systems that control CO and peripheral resistance
Baroreceptors (quick)
RAAS (Slow)
Conversion of angiotensinogen to angiogtension II
Angiotensinogen converted by renin to angiotensin 1. Then converted by ace to angiotensin II
Role of angiotensin II
Vasoconstrictor
Increases levels of aldosterone, which causes reabsorption of sodium and water= increasing blood volume.
Induces cardiac hypertrophy. Causes myocardial stiffness and fibrosis and apoptosis
How do baroreceptors increase sympathetic activity
When they sense a decrease in blood pressure, they stimulate B1 to increase heart rate and force of contraction.
They also stimulate alpha 1 to cause vasoconstriction.
4 tips to manage HF
Decrease activity
Decrease Na intake
Treat co-morbid conditions
Avoid NSAIDS, alcohol, calcium channel blockers
Pharmacokinetics of digoxin
Little metab- leads body the same
Long 1/2 life bc accumulates in muscle. High Vd.
Digoxin adverse effects
Toxicity- arrhythmia, Gi probs, HA, confusion, fatigue
**blurred vision, halos, color distortion. Flashes, yellow vision.
Drug/drug interactions with other drugs that also decrease K+ levels in blood: erythromycin, tetracycline, verapamil, quinidine
Milrinone MOA and admin
PDE 5 inhibitor- cannot break down cAMP, which results in an increased level of calcium inside cell.
IV
Aldosterone antagonists. Why are these good to use in HF and which one has less side effects
Good to use in HF because HF patients have increased levels of aldosterone.
Sprironolactone has more side effects due to sex hormones.
Epelerone has less.
Vasodilators
Hydrazaline
Minoxidil
Isosorbide dinitrate and isosorbide mononitrate release NO (also organic nitrates)
2 BB approved for chronic HF
carvedilol and metoprolol. Only use in chronic
What drugs to use for high risk/no symptoms to lots of symptoms of HF patients
High risk/no symptoms
Risk factor reduction and inform patient
ACE or ARB
ACE + BB
Digoxin + diuretic + diet restriction
Lots of symptoms
Quinidine adverse effects
Na channel blocker Type IA
Increase concentration of digoxin
GI
blurred vision due to anticholinergic activity
Procainide adverse effects
Lupus, CNS side effects Metabolites show class III activity
Disopyramide adverse effects
Dry mouth, urine retention, blurred vision, constipation. Similar to anticholinergic.
Flecainide and propafenone (1C) adverse effects
Metallic taste, constipation, induce arrhythmia
How does each class affect the heart contraction? Class I thru 4
1: Na blocker. Slows phase 0, also affects phase 3
2: BB. Slows AV node. Slows phase 4.
3: K+. Prolongs phase 3 and QT interval (4)
4. Refractory period prolonged (phase 4) AV and SA node prolonged. Slows depol (phase 0)
0 and 3
4
3 and 4
0 and 4
Potassium channel blocker drugs
Amiodarone long half life, lots of side effects, Whorl keratopathy, NAION.
Dronedarone- short half life, less side effects
Ibutalide-
Dofetilide
Sotalol- BB but high Class III activity
Amiodarone
Complex- has class 1-4 actions DOC for atrial fib and anti anginas
Long half life and lots of side effects -pulmonary fibrosis -GI -CNS: dizzy, tremor -Blue skin NAION Whorl keratopathy
4 other anti-arrhythmic drugs
Adenosine- caffeine decreases effectivity
Digoxin- Positive inotropic? ocular toxicity!
Magnesium- unknown MOA
Potassium- balance
Arrhythmias have disfunction of
- Impulse generation
- Impulse conduction
Both cause CO to decrease
Worsened by ischemia, acidosis, electrolyte imbalances
tricky to treat!
phases of heart contraction
phase 0: depol. Na+ flows into cell.
Phase 1: K+ channels open, then quickly close. Na+ channels inactivated.
Phase 2: Ca++ channels open and Ca++ enters cell, K+ leaks out. Plateau
Phase 3: Ca++ channels cost. K+ opens and K+ exits cell causing repol.
Phase 4: gradual increase in Na+ permeability. Na+ can start entering cell, causing depol.
Force of contraction is directly related to unbound intracellular calcium levels. Sources of intracellular calcium.
- Voltage sensitive channels that cause calcium to move into cell
- Exchange with sodium
- Release from SR and mitochondria
Abnormal automaticity causing arrhythmia
When sites other than SA show enhanced automaticity. Ex: Damaged myocardial cells may remain partially depolarized, allowing them to reach threshold sooner.
Tx with drugs that decrease calcium or sodium
Abnormal impulse conduciton
Blocked nerve impulse may cause short circuit= premature contraction and re-entry defect.
Tx: Slow conduction or increase refractory period. Converts unidirectional block that may cause flutter into bidirectional block.
How to treat angina
Decrease myocardial O2 requirements by decreasing cardiac work or increase 02 delivery with vasodilators.
Determinants of cardiac O2 demand
Wall stress
HR
Contractility
Any increase = increase 02 demand. Often during physical activity
Determinants of coronary blood flow
Perfusion pressure (diastolic)
Duration of diastole
Coronary vascular resistance
Determinants of vascular tone
Arteriole tone (controls peripheral vascular resistance, systolic wall stress)
Venous tone (controls amount of blood returning to heart. Diastolic wall stress)
3 types of angina
- Stable/classic/typical. usually due to blockage of coronary artery. Short lasting, happens during activity. Treat with rest or nitroglycerin.
- Variant/vasospastic. Occurs at rest. Unrelated to activity or HR. Respond well to vasodilators and calcium channel blockers.
- Unstable. (maybe due to plaque rupture) Classic angina getting worse- attacks with less exertion. Rest and nitroglycerin do not work.
Organic nitrates
- 3 types
- Admin
Nitroglycerin
Isosorbide di- and mono nitrate
Admin sublingual or patch (first pass inactivates)
Tolerance develops quickly- do 12 hours on/12 off.
DOC for acute angina
nitroglycerin.
Nitroglycerine adverse effects
HA, tachycardia due to vasodilation, orthostatic hypotension, 12 hours on/12 off to avoid tolerance. Do to combine with PDE type 5 inhibitor.
Preferred BB for angina
Atenolol, metoprolol
What type of angina is BB not helpful for
Vasospastic angina because BB is not a vasodilator.
DOC for chronic angina
BB or Ranolzaine (Sodium channel blocker)
MOA of ranolzaine
Sodium channel blocker. Tx chronic angina. Inhibits late phase of Na+ current during depol.
Improves diastolic function and increases O2 supply
3 type 5 PDE inhibitors
Sildenafil
Tadalafil - more selective to PDE 5, not 6.
Vardenafil
MOA and side effects of PDE 5 inhibitors
MOA: Prevents inactivation of cGMP. No increases cGMP inside the cell, which leads to vasodilation.
Type 5 usually breaks it down.
Ocular side effects bc similar to PDE 6 inside the eye, a phototransductor. Causes mild impairment of color vision- blue/yellow/pink tinge. Last mins to hours.
Also causes blurred vision.
Do not take with organic nitrates= severe vasodilation.
ADP receptor blockers have what side effects
Severe bruising, life threatening TTP
PP bound, 450 met
What anti-thrombin med is excreted by the liver
Argatroban.
DOC for dabigitran
prevent stroke because atrial fib
administration for Xa inhibiting drugs
Apixiban and rivaroxaban are oral
Fondaparinux is Sub Q
What thrombolytic drug is only approved for pulmonary emboli and is produced naturally by the liver
Urokinase.
What thrombolytic agent is fibrin selective and a DNA recombinate
Alteplase
What additional meds should you take with thrombolytic agents?
Aspirin. As it breaks down clot, may induce more clotting.
