CV Flashcards
big 4 that contribute to atherosclerosis
HTN (primary) hyperlipidemia (primary) DM (T2) smoking (obesity as well)
CV #1 killer in US primarily due to
ischemic heart disease and stroke
“athero” “sclerosis”
porridge - hardening
location of atherosclerosis
arterial intima, beneath inner endo. cell lining of large and medium-sized arteries–>narrowing of art. lumen
conditions that result from atherosclerosis
angina pectoris and MI
TIA and ischemic forms of stroke
cardiac arrhythmias and CHF
antiHTN drugs: diuretics
*hydrochlorothiazide (microzide) chlorthalidone (thalitone) indapamide *furosemide (lasix) triamterene (dyrenium) *spironolactone (aldactone) eplerenone (inspra)
primary vs secondary HTN
prim: don’t know cause, genetic, salt sensitivity
sec: i.e. pheochromocytoma triggers HTN
in HTN
elevation in vascular resistance +/- preceded by ^CO
we refer to SYSTEMIC pulmonary HTN rarely
non-drug tx
dietary (lower Na)
exercise
antiHTN drugs: adrenergic neuron blockers
- reserpine
- methyldopa
- clonidine (catapres)
antiHTN drugs: adrenergic receptor blockers
- Prazosin (Minipress)
- Doxazosin (Cardura)
- Terazosin (Hytrin)
loop diuretics
inhib. reabsorption of Na and Cl (water follows out in urine)
* more powerful than thiazides*
thiazide diuretics
inhib. reab of NaCl at distal tubule
antiK+ sparing diuretics
inhib. reab. of Na at collecting duct, K+ spared
antiHTN drugs: B-adrenergic rec blockers
Propranolol (Inderal‐LA)
- Nadolol (Corgard)
- Timolol
- Pindolol
- Atenolol (Tenormin)
- Metoprolol (Toprol‐XL)
- Acebutolol (Sectral
antiHTN drugs: a1/B Blocker and NO‐releasing β1 Blocker
- Labetalol (Trandate) (not NO-releasing)
* Nebivolol (Bystolic) (NO releasing)
antiHTN drugs: Direct Arteriolar Dilators
Hydralazine
Minoxidil
antiHTN drugs: Calcium Channel Blockers (CCB) (in cell mem.,–>less Ca2+ influx)
*Verapamil (Calan) Diltiazem (Cardizem) (dec cardiac contractions)
*Nifedipine (Procardia ‐ XL) (dec. sm. musc. contr in arterioles)
Felodipine
Amlodipine (Norvasc)
antiHTN drugs: Angiotensin Converting Enzyme (ACE) Inhibitors
*Captopril (Capoten) Enalapril (Vasotec) Lisinopril (Prinivil, Zestril) Quinapril (Accupril) Ramipril (Altace) **all "PRILS"**
antiHTN drugs: Angiotensin II Receptor Blockers (ARBs)
*Losartan (Cozaar)
Valsartan (Diovan)
Candesartan (Atacand)
“SARTANS”
antiHTN drugs: Renin Inhibitors
Aliskiren (Tekturna)
-inhibits AFTER released, dec. renin activity
ACE inhibitors
inhib. conversion of AngI to ACTIVE AngII
AngII causes: vasoconstriction and aldosterone secretion
if inhib: dec. resistance, dec.
AngII causes
vasoconstriction and aldosterone secretion
if inhib: dec. resistance, dec. MORE
Ezetimibe (Zetia)
cholesterol absorption inhibitor
Cholestyramine (Questran)
Colestipol (Colestid)
Colesevlam (WelChol)
bile acid binding resins
STATINS***
HMG-CoA Reductase Inhibitors *Lovastatin (Mevacor) Pravastatin (Pravachol) Simvastatin (Zocor) Atorvastatin (Lipitor) Rosuvastatin (Crestor)
importance of statins
HMG-CoA reductase** is rate limiting enzyme of cholesterol production in LIVER
triggers endogenic prod. pathway: VLDL–>IDL–>LDL–>tissue
antidiabetic agents
insulin preps
insulin secretory drugs (need more-directly stimulate)
insulin sensitizing drugs (help insulin along- Metformin)
a-glucosidase inhibitors (dec. gluc absorp)
incretin mimetics (stim. insulin release)
dipeptidyl peptidase IV inhibs (inhib. incretin brkdwn)
amylin analogs
insulin main action
stim. glucose uptake to tissue
inhib. glucose rel. from liver
* all to lower blood glucose* (hyperglycemia)
consequences of atherosclerosis
angina
antianginal agents: nitrates
*Nitroglycerin (Minitran, Nitrostat)
Isosorbide Dinitrate (Isordil)
Isosorbide Mononitrate (Ismo)
Amyl Nitrite
antianginal agents: Ca-channel blockers
*Nifedipine (Procardia XL) (vasculature) (misnomer!)
Amlodipine (Norvasc)
*Verapamil (Isoptin SR, Calan) (heart)
Diltiazem (Cardizem)
“DIPINES” dihydropyridines Ca2+ channel blockers in vasculature
antianginal agents: B-adrenergic blockers
[B1 and B2] *Propranolol (Inderal‐LA) *Nadolol (Corgard) *Timolol [B1 only] *Atenolol (Tenormin) *Metoprolol (Toprol‐XL)
3 types of angina: 1. atherosclerotic obstruction
plaque in large coronary arteries–>classic angina pectoris (effort or stable angina) most common!
triggered by exercise, not enough O2 reaching heart, switch over to other pathway creating toxic metabolites
-does not dilate very well, vasodilators will NOT help, make worse
3 types of angina: 2. vasospastic angina
reversible vasospastic reduction of flow in large coronary arteries (variant angina, Prinzmetal’s angina)
3 types of angina: 3. unstable or crescendo angina
combo of 1st 2:
or sudden marked platelet aggreg. with clot form. at site of ruptured plaque (rest or exertion)
may be immediate precursor to MI!!
other ways to help atherosclerotic obstruction
reduce O2 DEMAND in tissue blocked by obstructed vessel
preload dep. on
venous smooth muscle tone, venous fluid volume
how to dec. preload to to red. O2 demand
- dec. VENOUS smooth muscle tone–>nitrates: becomes NO (rarely: dec. arteriole tone)
dec. venous fluid volume (takes long time for diuretic to do that)
to dec. contractility/rate to red. O2 demand
B-blockers
Ca2+ chan. blockers (verapamil)
dec. afterload to red. O2
nifenampine, etc??
CHF drugs: digitalis glycosides and rel. agents
*Digoxin (Lanoxin)
Digitoxin
Digoxin Immune Fab (DigiFab)
CHF drugs: non-glycoside inotropic agents (+/- inotropic agents)
*Dobutamine *Dopamine
Inamrinone Milrinone
CHF drugs: ACE inhib.
*Captopril (Capoten)
Enalapril (Vasotec)
Fosinopril (Monopril)
Quinapril (Accupril)
CHF drugs: AngII rec-I blocker
*Losartan (Cozaar)
Valsartan (Diovan)
Candesartan (Atacand)
CHF drugs: diuretics
*Hydrochlorothiazide (Microzide)
*Furosemide (Lasix)
*Spironolactone (Aldactone)
Epleronone (Inspra)
CHF drugs: direct vasodilators
*Nitroglycerin (Minitran)
Hydralazine
Nitroprusside (Nitropress)
Isosorbide Dinitrate (Isosordil) Nesiritide (Natrecor)
CHF
chronic
impaired ability of ventricles to adequately fill AND/OR eject blood volume (diastolic or systolic failure)–>low ventr. output
causes of CHF
acute MI, pulmonary hypertension
CHF s/s
fesp, renal, musc, cardiac
preload is high/low in CHF?
it is HIGH, consequence of CHF
B receptors
stimulate Ca2+, inc. contractions in systole and diastole?
independent CHF mechanisms
- impaired contractile proteins
- inadequate reuptake and release of Ca2+ by SR
- dec. B-rec cAMP function (downreg.)
inc. PRELOAD
inc. Stroke Volume
in CHF, inc. PRELOAD
does not appropriately inc. Stroke Volume
have high venous pressure
inc. PRELOAD
dec. Stroke Volume
even more so in CHF
vasodilators will help this (nitro, need high does to dilate arteries)
inc. HR
inc. CO until LIMIT–>then dec. (fluttering, inadequate filling time)
tx with B blockers** (counter intuitive, but this is why it works!)
body attempts to compensate for CHF
hypertrophy–>exacerbates!
SNS and RAAS go into high gear–>also exacerbate
(SNS: tachycardiac, inc. HR, inc. afterload (constr) inc. preload)
why B rec. downreg.
chronic elevated SNS activity
B blockers prevent down regulation @ B rec!
the RAAS system may be detrimental to
structural changes of myocardium
digitalis glycoside mech
inhib of Na/K exchange–>increase Na–>dec. Na/Ca exchange (disrupted gradient due to inc. IC [Ca2+]–>inc. Ca2+–>inc. contraction
dec. automaticity in potential cardiac pacemaker cells
prevent ???
anti-CHF drugs: B-blockers
*Metoprolol (Toprol‐XL)
Bisoprolol (Zebeta)
Carvedilol (Coreg)
Class I antiarrhythmias
Class 1A Quinidine Procainamide Class 1B *Lidocaine (Xylocaine) Class 1C Flecainide (Tambocor)
Class II antiarrhythmias
*Propranolol (Inderal‐LA) *Acebutolol (Sectral) *Esmolol (Brevibloc)
Class III antiarrhythmias
*Amiodarone
Cordarone
Class IV antiarrhythmias
*Verapamil (Calan)
if slope not flat during phase 4
automaticity (slope suppressed with Ca rec. blocking drugs)
