What is NITROglycerin's mechanism of action for variant angina?
Acts by relaxing or preventing coronary artery spasms
NTG increases oxygen supply
Tell me about the absorption and metabolism of Nitroglycerin
HIGHLY lipid soluble so you can give it multiple ways (SL, Transdermal, PO, IV)
Does have big 1st pass effect (most of PO dose is destroyed)
Rapidly metabolized by liver-short 1/2 life of 5-7 minutes
TRUE or FALSE
NITROglycerin patches should be on intermittently (taken off at night for 8hrs)
TRUE but can use nitro if attack occurs
Can you use Nitroglycerin as an ointment?
Yes, onset is 20-60min and lasts 12hrs so it provides sustained protection.
NOT for use during attack (doesn't work quickly enough!)
TRUE or FALSE
You must taper Nitroglycerin slowly when discontinuing to prevent risk of vasospasm
TRUE
TRUE or FALSE
It's okay to chew and swallow the sub lingual Nitroglycerin.
FALSE. SL dose is meant to have no 1st bypass effect so it contains a much lower dose than the PO form.
DO NOT CHEW or SWALLOW SL dose!
Name 3 side effects of NITROglycerin
HA, Orthostatic HYPOtension, Tachycardia
but generally well tolerated
TRUE or FALSE
Nitroglycerin (SL) bottle is good for 12months
FALSE! It's good for 24months. Teach patient to discard after it's expired...otherwise dose may be ineffective in an emergency (and that would suck!)
Bob is on a Phosphodiesterase Type 5 inhibitor (Viagra, Cialis, or Levitra) and and wants to take Nitroglycerin. Can he?
NO! Vasodilation is greatly increased when taking these medications together
PS. this was the only medication questions I had on my NCLEX :)
What happens if Bob takes a betablocker (or Ca Channel blocker like Verapamil or Diltazem) with his Nitroglycerin?
It could suppress the NTG induced tachycardia.
What is the goal HR of Betablockers?
50-60bpm
Name some uses of Betablockers (There are a ton!)
STABLE ANGINA (not vasospasms!)
Makes heart more efficient
Dec. cardiac O2 demand
Dec. afterload
Dec. HR (allows longer filling time)
Dec. contracility (caution w/CHF patients!)
Dec. intensity and frequency of angina
INCREASEs exercise tolerance (eventually)
TRUE or FALSE
You should never stop a Beta blocker abruptly
TRUE! IT could cause a very intense angina attack and lead to an MI
Name some side effects of a betablocker
Bradycardia
Decreased AV node conduction
Decreased contractility (caution in HF)
Can block Beta 2 as well (caution w/asthma and COPD)
Insomnia, bizarre dreams
Sexual dysfunction (educate pt!)
If your patient has asthma and needs to be on a betablocker, which one is best?
Metoprolol (more Beta 1 selective) but still be cautious!
Calcium channel blockers are used to treat what two types of angina?
Stable and Variant
Name the three drug categories used in prevention of an MI for the patient w/chronic stable angina.
Anti-platelet (ASA or plavix)
Cholesterol lowering drug (for all pt w/stable angina)
ACE (for most pt's w/CAD and strongly recommended for those w/DM bc it's renal protective)
Explain the strategy for angina treatment (start with one drug class, if not effective then....etc.)
SL Nitroglycerin, if not effective...
Add a beta blocker, (gold standard for previous MI) if not effective....
Add a Ca channel blocker, if not effective....
Add a long-acting nitrate.....if not effective
Get a referral!
What is the first line of treatment for management of HF and what does it do?
Diuretics are the 1st line of therapy.
Decreases preload/afterload and pulmonary/peripheral edema (decreases fluid to LV...so it doesn't have so much to pump out!)
Vasodilators are used to treat CHF. Name three types and how they work.
ACE, ARB, and Nitrates
Reduces workload of the heart, increases O2 demand, and decreases afterload
Inotropic agents can be used to treat HF (sometimes). How do they work?
Increases the strength of the contraction (increased contractility of a weak ventricle)
TRUE or FALSE
Betablockers can be used for treatment of HF and are indicated if history of MI
TRUE!
Thiazide diuretics (like Hydrocholorthiazide) are used for early stage HF (1st line therapy). Can you use it in a patient w/low GFR?
NO it will be ineffective, use a loop diuretic (Lasix, Bumex, or Demadex)
What is an adverse effect of both Thiazide and Loop diuretics?
Hypokalemia (caution w/ Digoxin because it can cause toxicity!)
TRUE or FALSE
High ceiling loop diuretics are drug of choice for MODERATE to SEVERE CHF
TRUE! They are good because they can mobilize a lot of water and are NOT DEPENDENT on GFR and cardiac output.
Why diuretic can cause otoxicity?
LASIX (FUROSEMIDE)=High ceiling loop diuretic
Why bother giving Aldactone to a patient w/CHF if it only promotes a scant diuresis?
It is used to counteract K+ loss by thiazides and loop diuretics.
When prescribing Aldactone, what three drugs do you need to use caution with?
ARBs, ACE inhibitors, and Digoxin
d/t risk for hyperkalemia!!
TRUE or FALSE
Aldactone is the only K+ sparing diuretic proven to prolong survival in HF patients
TRUE
How does Aldactone work?
It blocks aldosterone receptors
TRUE or FALSE
ACE inhibitors (think -pril) are the drug of choice for HF patients and should be prescribed to ALL HF patients unless contraindicated
TRUE! They increase functional status and prolong life. They also decrease morbidity and mortality.
How do ACE inhibitors (-pril) work?
They block Angiotensin II production which in turn decreases the release of aldosterone from adrenal cortex. This also suppresses the degradation of kinins.
They dilate arterioles and veins (decreased afterload and workload, increased CO and SV, increased renal bld flow)
ACE inhibitors decrease edema, pre load and ventricular dilation. HOW?
By decreasing aldosterone, kidneys will secrete fluid and retain K+ (watch for hyperkalemia)
Also increase renal blood flow so the kidneys can excrete more water and Na+
What are two major side effects of ACE inhibitors that can be attributed to the accumulation of bradykinin?
Intractable cough, may improve after 3M
Angioedema
TRUE or FALSE
ACE inhibitors are safe to use when pregnant
FALSE! Fetal lung injury in 2nd and 3rd trimester!
What is a major contraindication to using an ACE inhibitor (-pril)?
Bilateral renal artery stenosis!
Kidney's release Renin to increase angiontensin II to preserve GFR. If this is inhibited, then decreased GFR and decreased UO
ARBs are similar to ACE inhibitors, so why switch from an ACE inhibitor to an ARB?
ARBs don't increase the level of kinins like ACE inhibitors....so you won't get the cough!
What is the only ARB (-sartan)currently used for tx of HF?
Valsartan.
Although you can use the others (Candesartan or Losartan)..just use caution and monitor symptoms
TRUE or FALSE
After 2 weeks, the full benefits of a betablocker should be reached
FALSE. Full benefits are not seen for 1-3 months. START LOW and GO SLOW. A gradual increase will minimize effects of decreased contractility.
How do Betablockers (-lol) work to protect the heart?
They protect the heart from excessive sympathetic stimulation and protect against dysrhythmias.
Help exercise tolerance, improve LV function, slow progression of HF, and reduce hospitalization and mortality.
Why do you need to use caution in placing a patient w/CHF on a beta blocker?
A side effect of Betablockers is fluid retention and worsened HF from the decreased contractility.
Also can have SOB, night cough, weight gain, and extremity swelling (from same problem)
TRUE or FALSE
Digoxin (inotropic agent) is a second line agent in treatment of HF and does not prolong life, it's actually less effective in women.
TRUE! And it has a narrow therapeutic window so it's a very risky drug!
How does digoxin work?
It increases contractile force
Decreases sympathetic tone
Increases urine production
Decreases renin release
It takes ___ days for Digoxin levels to plateau.
SIX. Check levels at routine intervals until at goal and then recheck is S/S of digoxin toxicity.
What kind of labwork do you need to monitor w/Digoxin?
Renal function (BUN/Cr)
BMP (K+, Na, Mg, Ca)
ABG for hypoxemia or acidosis.
How do antacids and kaopectate interact with digoxin?
They decrease absorption and you will have subtherapeutic Dig levels
How do chloestyramine and metoclopropamide effect Digoxin levels?
They impair absorption (so space the dosing!)
TRUE or FALSE
Ca Channel blockers can increase digoxin levels.
TRUE=toxicity risk!
How is digoxin metabolized?
In the liver and gut by bacteria. So if you give abx, then you may increase digoxin levels d/t interference w/bacterial flora!
*20-30% of Digoxin is protein bound....
Todd is a bit earthy crunchy and is taking siberian ginseng and licorice that his herbal store recommended. Can you prescribe Digoxin to him?
NO! It will enhance Digoxin toxicity. NEED to ask patients about any OTC and herbal supplements!
TRUE or FALSE
Decreased renal function can increase half life of Digoxin from 30-40hours to FOUR days.
TRUE
Why should you always get an EKG prior to beginning Digoxin.
Toxicity can cause non-specific ST depression or T wave flattening
PS. I hate getting EKGs
Visual disturbances of Digoxin toxicity are....
yellow and green halos!
HYPOkalemia or HYPERkalemia can cause Digoxin toxicity?
HYPOkalemia!
(Increased K can cause Subtherapeutic levels)
Digoxin is like Goldilocks-K needs to be JUST RIGHT!
What three agents do you need to avoid in HF?
Antidysrthymic agents (Amio and Defetilide) will make HF worse
Ca Channel blockers (make HF worse)
NSAIDS: increase fluid retention and peripheral vasoconstriction
First line of therapy for HF includes three drugs.....name them!
Diuretics
ACE or ARB
Beta blocker
*only add Digoxin if symptoms can't be managed w/these three*
Which category of Dislipidemic agents are most effective at lowering LDL-C?
HMG-COA REDUCTASE INHIBITORS (STATINS)
Statins have very few SE but what is the common one?
Leg cramps..
Myopathy/rhabdomyolysis (renal caution!)
Also can cause hepatoxicity
STATINS (HMG-COA Reductase Inhibitors) should be given AT NIGHT, why?
Endogenous cholesterol increases during the night (increased synthesis)
most effective before bed (don't need to worry about taking w/ or w/out meals)
What's so great about STATINS (HMG-COA Reductase inhibitors)
Decrease LDL-C (25-63%)
Increase HDL-C (5-17%)
Name some non-lipid benefits of Statins...there are quite a few!
Promote plaque stability
Reduces inflammation
Slows progression of CAD
Improves endothelial dysfunction
Enhances vasodilation
Reduces risk of A-fib
Reduces risk of thrombosis
What is the MOA for STATINS (HMG-COA Reductase inhibitors)?
Competitive inhibitor of HMG-COA Reductase that is responsible for conversion of HMG-CoA to mevalonate which is a precursor of cholesterol.
Stimulates synthesis of LDL receptors leading to an increase in uptake of LDL particles
How often should you monitor LFTs when when your patient is on STATINS?
Check LFTs Q3M, then Q6M, then QYR
TRUE or FALSE
Pregnant patients can take STATINs
FALSE!
Name 5 drugs that interact with STATINs
Cimetidine
Aldactone (increases risk of endocrine dysfunction)
Digoxin (can elevate levels)
Erythromycin/Genfibrozil (increased risk of rhabdomyolysis)
Warfarin (increased anticoagulant effect)
How do NICOTINIC acids work?
They inhibit lipolysis in adipose tissue which decreases hepatic esterification of triglycerides
Increase lipoprotein lipase activity
Reduces serum cholesterol & TG levels
Nicotonic Acids (Niacin) is good for triclycerides. It's also good for ___.
Good for HDL but not as good for LDL
What are some indications to give Niacin?
Adjunct tx of hyperlipidemia & hypercholesteremia
Pellagara (vitamin B deficiency)
Peripheral Vascular disease
Patients often complain of _____ so they should take Niacin at night and not have hot food or drink with it.
Flushing (d/t excessive peripheral vasodilation)
Regular schedule and starting low and going slow will decrease SE.
Niacin can also cause ___ and ____ so use caution in patients with DM or gout.
Hyperglycemia and Hyperuricemia
Niacin is contraindicated with these four things...
Hepatic dysfunction
Active Peptic Ulcer Disease
Severe hypotension
Arterial hemorrhage
(seriously, is someone is hemorrhaging don't give Niacin, should probably fix the hemorrhage first....)
Niacin is used with caution in the following situations (tricky Nancy might ask...hateful!)
Liver disease (contraindicated w/dysfunction)
PUD (contraindicated if ACTIVE)
Gout
DM
Gallbladder disease
What happens if you give ASA with Niacin (nicotinic acid)?
Decreased metabolic clearance of nicotinic acid
what happens if you give a sympathetic blocker with Niacin?
Causes vasodilation and hypotension
How does Gemfibrozil (fibrate) work?
It decreases TG levels and VLDL while increasing HDL
Inhibits lipolysis of adipose tissue
Reduces hepatic TG synthesis
*Good for high TG and Low HDL*
TRUE or FALSE
Giving a Fibrate (Gemfibrozil) and a statin together will increase occurance of myopathy.
TRUE
Why should you advise the patient to call you if they experience diarrhea, nausea, epigastric pain, chills, fever, or sore throat when they are taking a fibrate (Gemfibrozil)?
Could indicate leukopenia!
Your patient is on a fibrate (Gemfibrozil) and when you check their serum lipoprotein concentration, there was NOT a significant change What do you do now?
DC the drug.
What labwork should you obtain for your patient on a fibrate (Gemfibrozil)?
Serum lipoprotein concentration
LFTs/BUN/Cr (ensure appropriate metabolism and excretion)
CBC & Electrolytes
If on anticoagulant then PT/INR (Fibrates can increase effects of oral anticoagulants)
