CV1-Pharm Flashcards
what is the pathophysiology of ischemic heart disease?
imbalance between cardiac oxygen needs and supply
what are the two branches of ischemic heart disease?
- chronic stable angina
- acute coronary syndrome
what are the three types of acute coronary syndrome?
- unstable angina
- non ST segment elevation MI
- ST segment elevation MI
what are are the reasons someone can have angina which is a type of ischemic heart disease?
- athrosclerosis
- atheroscleorosis and vasospasm
- vasospasm alone
what are the characteristics of stable angina? what is an example of this?
CHRONIC
stable pattern with known inducers
Ex: stable athrosclerosis >70% narrowing
what are the characteristics of unstable angina which is a type of ischemic heart disease? what is the example?
increase in frequency, severity, duration
Ex: plaque rupture with platelet and fibrin thrombus
what is acute coronary syndrome caused by? and what type of ischemic heart disease is this?
what are four things that can increase the chances of this?
UNSTABLE ANGINA, STEMI, NSTEMI
- athroschlerosis plaque rupture with subsequent thrombrus +/- increased oxygen demand
- tobaccing smoking, coccaine, hyperventilation, cold temps
what is the acute drug class that can be used to treat chronic stable angina?
what drug falls under this?
nitrates
- isosorbide dinitrate
- nitroglycerin
what are the long term therapy drug classes that are used to treat chronic stable angina? (5)
- nitroglyerin: isosorbide dinitrate
- beta blockers
- calcium channel blockers
- sodium channel inhibitor
- ASA/clopidigrel
what are the two adjunct therapies that are used to treat chronic stable angina? (2)
ACE inhibitors/ARBs
HMG-CoA reductase inhibitors (statins)
what are the two drug classes that are included as vasodilators?
- nitrates
2. calcium channel blockers
what are the two drugs under nitrates drug class?
- isosorbide dinitrate
2. nitroglycerin
what are the two subcategories and four total drugs that are under the calcium channel blocker drug class?
Dihyrdropyridine (DCCBs)
- amlodipine - nefedipine
Nondihydropyridine (NDCCBs)
- diltiazem - verapamil
what is the drug class that is a sympatholytic?
beta blockers
what are the two non selective beta blocker drugs?
- propanolol (B1 +B2)
2. carvedilol (B1 + B2 + a1)
what are the two selective beta blocker drugs?
- metoprolol
2. atenolol
what is a miscellaneous drug that is used for chronic angina?
ranolazine
what is heart failure?
a clinical syndrome arising from numerous etiologies (HTN, CAD, Cardiomyopathy)
inability of the heart to pump enough blood to meet the metabolic demands of the body
what are the four goals of the therapy for heart failure treatment?
- improve cardiac function
- reduce the clinical symptoms
- reduce hospitalizations
- reduce the risk of death
what are 7 symptoms of clinical heart failure?
- fatigue/weakness/exercise intolerance
- polyuria
- nocturia
- JVD
- dyspnea, orthopnea, PND
what are the three loop direutics?
- furosemide
- torsemide
- ethycrinic acid
what are the two anti-aldosterone agents?
- spironolactone
2. eplenerone
what are the 3 ACE-I drugs?
captopril
lisinopril
fosinopril
what are the three vasodilating classes?
nitrates
calcium channel blockers
hydralazine (direct acting vasodilator)
what is the inotropic cardiac glycoside agent?
digoxin
what is a miscellaneous recombinant BNP drug?
nisiritide
what is the direct renin inhibitor drug?
aliskiren
what is a miscellaneous drug that is totally random that you wanna know?
invabradine
what is your fast friend for heart failure?
diuretics
what do diuretics do?
improve fluid overload rapidly
what must you watch for when giving a patient diuretics?
electrolyte imbalance
general dehydration
for congestive heart failure, it is good to start direutics while other therapies are being started?
ABSOLUTELY
get some of that fluid off!!
when is furosemide most commonly used? (this is lasix)
both inpatient and out patient settings
are the oral and IV dosing of torsemide equivalent?
yes they are!! they are the same
what is the chemistry of ethacrynic acid?
non-sulfa chemistry
what is the MOA of diuretics?
block the reabsorption of Na, K, and Cl ions glomular filtrate
why are diuretics effective in heart failure?
decrease preload, increase renal blood flow, and promote sodium excretion
what are 3 potential side effects of loop diuretics?
- electrolyte imbalance
- orthostatic hypertension
- dehydration
which diuretic carries the highest risk of kypokalemia and dehydration?
furosemide!!!!
what are most diuretics made of?
what do you need to watch patients closely for?
most are sulfa based so patients might be hesitant if they have a sulfa allergy, there is NO evidence of this however
YOU DO NEED TO WATCH CLOSELY FOR DECREASED PROFUSION…since you are decreasing the volume of fluid
what do you need to watch closely when a patient is taking diuretics because of the decreased volume of fluid?
watch for decreased profusion
what are 3 things you want to monitor when a patient is taking a diuretic?
- electrolyte levels
- BUN/creatine
- MONITOR DAILY BODY WEIGHT AS MEASURE OF EFFECTIVENESS OF TX
when do MOST reactive electrolyte imbalance and renal functions changes changes STABALIZE in a pt taking a diuretic?
MOST within 2-3 weeks….but you gotta keep monitoring them at follow up visists
what are the three classes of beta blockers?
- nonselective B1 and B2 beta blockers
- selective B1 blocker
- nonselective B1, B2, alpha1 blocker
what is the nonselective B1 and B2 beta blocker?
propranolol
what are the 3 SELECTIVE B1 beta blockers?
- metropolol tartrate
- metroprolol succinate (XL)
- atenolol
what is the non selective B1, B2, Alpha1 blocker?
carvedilol
what are the three things that antagonists of B-adrenergic receptors do? AKA beta blockers
- decrease HR
- decrease stroke volume
- decrease TPR via decreasing renin and angiotension II
how do beta blockers decrease TPR?
by decreasing renin and angiotensin II
what is the current thought of why beta blockers are used in heart failure?
poorly understood mechanism but WELL DOCUMENTED IT DOES HAVE AN EFFECT!!
possible from blockade of excessive sympathetic influences (aka it stops the heart from becoming overly stimulated)
what do you want to monitor on the patient when taking a beta blocker?
THEIR HR!!!
what are the 4 contraindications to beta blockers in HF?
- bradycardia
- heart block
- uncompensated HF
- severe depression
what additional substance does carvedilol have that increases the changes that hypotension could occur?
it blocks NOREPINEPHRINE so has additive effect in lowering BP
theoretically this decreases the negative side effects seen with the beta blocker class
carvedilol reduces….
do you start at a high or low dose? what do you need to monitor for?
BP and periphrieal vascular resistance
start at very low does 3.125 mg BID initital….monitor for weight gain!!
what might a patient note about their symptoms when taking carvedilol?
symptoms may increase for 4-10 days before any improvement is noted
what are four side effects of carvedilol?
dizziness, drowsiness, diarrhea, fatigue
What population of people should ALWAYS be put on a ACE inhibitor?? why??
ALL PATIENTS WITH LEFT VENTRICULAR DYSFUNCTION
it improves symptoms and survival in patients with HF
what is the site of action for ACE inhibitors?
kidneys in the renin-angiotension system
what is the MOA of ACE inhibitors?
what are 3 things that it lowers?
inhibits the conversion of antiotensin I to angiotensin II
lowers:
- arteriolar resistance
- increases venous capacity
- cardiac output and volume
Explain the 5 functions of a ACE inhibitor in HF?
- reduced the afterload
- reduces preload
- decreases sympathetic activation
- improves O2 supply
- prevents angiotensin from triggering cardiac remodeling
how do you reduce afterload?
enhance stroke volume and EF
how often should you increase the dose of ACE inhibitors?
every two weeks?
what are the target dosing for the two ACE inhibitor?
captopril
linsinopril
captopril- 50 mg TID
linsinopril-40 mg daily
start these drugs low and gradually increase them every two weeks to the target levels
what do you want to monitor for TWO labs in patients taking ACE inhibitors?
potassium and creatinine, within 1-2 weeks after starting treatment and continue to monitor but less frequently
weekly-> monthly->yearly
what are three things that make using ACE inhibitors contraindicated?
- renal artery stenosis
- hypersensitvitiy
- pregnancy!!
the angiotensin 2 receptor blocker LOSARTAN acts on what site?
smooth muscle cells of the blood vessels cause dilation
what is the MOA of LOSARTAN (angiotensin receptor blocker)?
Selectively and competitively blocks AT1 and AT2 receptors
who do you use angiotensin receptor blocker LOSARTAN in?
patients who can’t tolerate ACE inhibitors because they basically have the same efficacy!!!
BUT DON’T USE THEM TOGETHER!!! DUH.
what are the adverse effects of angiotensin 2 receptor blocker LOSARTAN ? (3)
muscle cramps
increased K+
impotence
what four populations of people do you not want to sue angiotensin 2 receptor blocker LOSARTAN in?
pregnant
severe renal disease
liver disease
pts with elevated k
of the calcium channel blockers, which ones do you WANT to use in CF patients? which ones do you NOT use?
USE: DIHYDROPYRIDINES (DCCBS) aka AMLODIPINE, these have little to no effect on cardiac contractability
DO NOT USE…..nondihydropyridines (NCCBS) because they have cardiac impact which is negative!!!
which calcium channel blockers do you want to use in a patient with CF?
DCCBS…..
they “D” stands for “duh”, use this ;)
what is the site of action for dihydropridines aka amlodipine?
vascular smooth muscle
what is the MOA of dihydropridines aka amlodipine?
blocks Ca channel and prevents contraction resulting in vascular relaxation and decreased TPR, vasodilation of coronary arteries
what are the severe portenital side effects seen with calcium channel blockers??
(includes diltiazem, verpampil, amlodipine)
- INCREASED MORTALITY IN POST MI PT
- INCREASED DOSES INCREASE RISK OF ACUTE MI
**these assume that the med is given in a high dose, but must be cautious of this and selective in regards to using this in HF patients
what population of people are hydralazine reccomended for who are not optimized using other therapy?
african american people
can use as adjunct therapy or replacement therapy nonblack populations if tolerant to ACE, ARB, and diuretic
what effect can hydralizine cause?
a reflex sympathetic (stimulating) of the heart….so actually can cause it to get worked up and work harder
what is a interesting autoimmune disorder that can be caused by using hydralazine?
SLE!!!!!
so you need to check the ANA of the patient before using it!!!
what is the DOC for treatment of hypertension in an EMERGENCY of a pregnant woman usually due to preeclampsia or preexisting HTN?
hydralazine!!!
what is the drug class for digoxin?
positive inotropic agents: cardiac glycosides
what signs would you see on a EKG with someone who is taking glycosides like digoxin? (5)
- prolonged P-R interval
- inverted T wave
- S-T segment depression
- shortened Q-T interval
- PVCs
what levels do you want to maintain Digoxin between?
.5 and .8 ng/mL
what should the initial dose of digoxin be?
.125-.25
what are four negative side effects of digoxin?
- visual disturbances
- AV block
- EKG changes
- toxic psychosis
what plants can you find glycosides in? (4)
milkweed
lilly of the valley
foxglove
oleander
natural plant analogs of glycosides have been used for over 300 years!
what is the drug class for dobutamine?
positive inotropic agents: B-agonists
what does dobutamine play a role in?
in HF patients who are awaiting a heart transplant because it can improve their quality of life
what is the drug class for milrinone?
phosphodiesterase inhibitor
what is the MOA of milirinone?
increase cAMP in heart and vascular muscle positive inotrope and vasodilator
what is the drug class for tekturna?
aliskiren
what is the MOA of tekturna?
inhibits reninin, therefor lowering BP
DONT USE IN PTS WITH RENAL DISEASE OR DIABETES!!!!
who is ivabradine indicated for?
HF patients with EF 70
what is the MOA of ivabradine?
selective and specific inhibition of If within SA node & prolonging diastolic depolarization and reducing HR
