Week 4 Cardiac Pharmacology Flashcards
what is first pass metabolism
goal medications have to go through the intestinal epithelium and the portal venous system and the liver before they can enter the circulation. So, the drugs will undergo metabolism in the intestines and then has to be excreted into the intestines from the liver. All of this will decrease is bioactivity, and reduces the amount of drug that actually makes it to the systemic circulation.
what is half life
the time required for 50% of the first order process to complete. so this means that 50% of the drug is eliminated after one half life.
what does half life determine?
the time for the drug to disappear, and the the time we need to be able to dose the drug, and know what the plasma steady state is. Need to know how long it will last.
what is steady state
the amount of the drug administered per unit of time. like with an IV, the drug is at a steady state. oral administration, and taking it at the same time, ensures equal amounts in the system.
TF: there is a natural fluctuation in the amount of drugs in the system
true
how do oral and IV doses differ
oral doses have to be much larger, because they are metabolized before they enter the circulation. IV drugs need a much smaller dose
can nitroglycerine be orally administered?
no, because it is completely extracted before it reaches the circulation. it undergoes pre systemic metabolism, so you need to administer it either IV or under the tongue.
what is always present before the plasma drug concentration exceeds the minimum effective concentration of the desired effect
a lag period
what are the temporal characteristics of drug effects
you have a lag time, and then you have the response to the drug that you wanted. the response will build until you start to sag off, and then it disappears.
what is the difference between a selective and a non-selective drug
selective means it can only bind to one receptor, ad then a nonselective drug can bind to many areas, like EPI… which can attach in the lungs and the heart.
what is an agonist
binds to a specific membrane and activates the cell and opens membranes
what is an antagonist
binds specially, but blocks the agonist. Does not influence the cell function, but can block people out
what does a non-competitive antagonist do
binds to the allosteric (non-agonist) site on the receptor to prevent the activation of the receptor. it doesn’t compete, it just prevents action. binds to a different part.
what does a competitive antagonist do
binds to the same site as the agonist, but doesn’t activate it. it blocks. Cock block.
what side effect does beta blockers have that can affect PT
beta blockers reduce the HR at rest, and suppresses chronotropic responses to exercise.
when dealing with HTN, what is always our first treatment option
lifestyle modifications
when treating HTN, what is our goal BP
less than 140/90mmHg, or less than 130/80mmHg in people with diabetes or kidney disease.
what is the initial mediation for most HTN patients
thiazide type diuretics
what is the usual 2 drug combo for HTN
ACE inhibitor and thiazide diuretic
what is the goal of diuretics
decrease blood pressure by reducing the blood volume, via the kidneys.
what are the 3 most common types of diuretics
Loop (lasix)
Thiazide (hydrochorothiazide)
aldosterone receptor antagonists.
what do loop diuretics do
they block the Na/K/Cl reabsorption in the loop of Henle, they knock off a lot of volume, but also you lose a lot of Na and K
what patients get loop diuretics as a drug of choice
HF, CAD and CKD
what does thiazide do
blocks Na reabsorption int he distal tubule of the nephron
what does aldosterone receptor antagonists do
blocks aldosterone and interferes with Na/K exchange at the distal table.
what are the types of sympatholytics
beta blockers, and alpha 1 backers and alpha 2 agonists.
what is a beta blockers “word”
“olol”
what do beta blockers do
they target beta 1 receptors, which are in the heart, and they reduce HR, BP, sympathetic tone, can decrease anxiety.
in which patients do we need to be cautious giving beta blockers
kidney or renal dysfunction, pulmonary dysfunction (especially if we use non-specific beta blockers that can bind to the lungs and cause bronchoconstriction. and diabetics because it will reduce the reduce the tachy and shaky stuff and we don’t get the normal hypoglycemic response.
what are alpha 1 blockers?
“zosin”
block alpha 1 receptors on smooth muscle, so the TPR and BP decreases. can treat prostate hypertrophy.
what are alpha 2 agonists
reduces vascular tone by centrally mediated methods, suppresses sympathetic outflow to vasomotor centers in the brainstem
what are ACE inhibitors
angiotensin converting enzyme inhibitors
what do ACEi end in
“pril”
what do ACEi do
block the conversion of Ang 1 to Ang 2, it lowers the BP.
what do ACEi do in patients with HF
it decreases afterload and improves survival in patients
what do ACEi do post MI
increases survival and prevents left ventricular dilation
what are ARBs
angiotensin 2 receptor blockers
what do ARBs end with
“sartan”
when are ARBs used
when patients don’t respond well to ACEi side effects coughing.
ARBs can also treat
obstructive sleep apnea.
what are calcium channel blockers
they selectively block Ca entry into the vascular smooth muscle, which manages HTN, angina, SVT,
what is the “ “ for calcium channel blockers
“dipine”
what is hydralazine
a smooth muscle relaxant used to treat HTN by acting as a vasodilator of arteries and arterioles. it reduces BP by reducing TPR
what is the side effect of hydralazine, and what is it usually given with
Na retention, and fluid retention, and often given with a diuretic
what three drugs may have a sudden excessive hypotension post exercise?
alpha blockers
calcium channel blockers
vasodilator drugs.
what two drugs may interfere with thermoregulation
beta blockers and diuretics.
what are drugs we can use to treat hyperlipidemia
HMG-CoA reductase inhibitors, or statins.
what do statins do
they block LDL synthesis and increase HDLs, and some can have anti-inflammatory things.
what are the 4 groups that may benefit from statin therapy
- patients with ASCVD
- patients with LDL over 190
- patients with DM, 40-70 with LDL between 70 and 189
- patients without DM, 40-75, 10 year ASCVD over 7.5%
what is rhabdo associated with? and what re the three conditions it presents with
statins, dark urine, muscle pain and weakness.
TF: rhabdo is more common in distal muscle groups,
false, it is more common in proximal muscles like thighs and shoulders.
what does unfractionated heparin do
blocks clotting factors in blood, given post op to prevent clots, DVT. takes 24 hours.
what does low molecular weight heparin do
faster then unfractionated heparin, takes 3-5 hours.
what does Coumadin do
warfarin, blocks effect of vitamin K epoxide reductase, used for long term anticoagulation. (a fib, aflutter)q
what does aspirin do
prevents platelet aggregation, used in chronic low doses, and given during MI
what does clopidogrel go
ADP inhibitor, that prevents platelet aggregation
what is a thrombolytics
tissue plasminogen activators (TPA) are clot busters. they facilitate the breakdown of clots that have already been formed by converting plasminogen to plasmin.
what “ “ does clot busters have
“kinase”
what are the 4 classes of anti arrhytmics
Class 1: Na channel blockers (VTACH and VFIB)
Class 2: beta blockers (AFIB and SVT)
Class 3: K blockers (SVT and VTACH and VFIB, slows the repolarization phase)
Class 4: Ca blockers. (SVT)
what do you give in acute coronary syndrome (4 of them)
anti anginals: like sublingual nitro, rapid vasodilator. reduces pre and after load, and reduces angina.
aspirin: prevent platelet aggregation
morphine: vasodilator
beta blockers: reduce VO2 and prevent arrhythmia.
what else can be given in acute coronary syndromes
O2,
anticoagulation drugs
ACEi
statins
what are the 3 goals of treatment for HF meds
decrease preload
decrease afterload
control sympathetic stimulation
TF: Ca blockers are given to those with HF
false, they have adverse effects.
what are some of the drugs given to people with HF (5 things)
ACEi or ARBs beta blockers diuretics aldosterone digoxin (inotrope)
what is given in decompensated HF
positive inotropes. and afterload reducers. we want to increase the hearts ability to pump, but decrease afterload.
what is a cardiac glycoside
digoxin, can have a positive inotrope without increasing VO2, and controls sympathetic tone, and can decrease arrhythmia’s. But these are being phased out because they can also cause arrhythmia, or prolonged QT intervals.
