Module 4 Forum Questions Flashcards
What is bradykinin and what role does it play in the cough some patients develop while taking angiotensin-converting enzyme inhibitors (ACEIs)?
Bradykinin is a peptide that causes contraction of smooth muscle and dilation of blood vessels.
ACEIs prevent the breakdown of bradykinin which can lead to swelling (i.e. angioedema) and cough (due to build up in lungs).
Is the cough caused by an ACEI specific to a single drug or is it related to the class of ACEIs? Would it be prudent to switch to a different ACEI if a patient develops a cough? Explain why or why not. Would the same effect be expected in angiotensin II receptor blockers (ARBs)? What type of patient is highest risk?
If a patient experiences an ACEI cough-the should no longer take any ACEI as it is class related. They can be switched to an ARB because they do not affect bradykinin.
Pts at higher risk: Women-twice as likely
What is angioedema? Which of the drugs discussed in this module list angioedema as a potential adverse reaction? What are the risk factors for this adverse reaction? Are any populations more at risk than others?
Angioedema=swelling under the skin that can become life-threatening.
Medications that cause it: ACEI, ARBs, Direct renin inhibitors
Higher risks: Black pts, older, smoking
A patient presents to your clinic concerned about shoulder pain believed to be directly related to taking a statin. How may a statin be associated with the patients’ pain? What would you do?
Statins have a high risk of rhabdomylosis/muscle pain. The medication should be stopped immediately and labs checked (creatine kinase, thyroid and myoglobinuria). If symptoms resolve, restart the statin to determine causal relationship
Highest risk statin: Simvastatin
Other possible concerning cause of shoulder pain: MI
Are ACEIs, ARBs, and/or ANRIs routinely combined? Why or why not? Are these classes of medications safe in pregnancy?
ACEI and ARBs should not be combined because it leads to more adverse effects.
They should not be used in pregnancy because they work on the RAAS. Can cause injury and death to the developing fetus.
What are the acceptable antihypertensive medications during pregnancy?
ACOG: Labetalol (beta-blocker), nifedipine (CCB), methyldopa, and hydrochlorothiazide (HCTZ)
HCTZ: lexicomp suggests third trimester risk as it crosses the placenta. Neonatal bleeding seen.
Methyldopa: improves fetal outcomes per lexicomp
Are there any potential problems with prescribing beta-adrenergic blockers to patients with diabetes? Please Explain. Are beta-blockers contraindicated in patients with diabetes? Please explain.
1st gen (propranolol) can cause hypoglycemia, 2nd gen do not. Both can mask hypoglycemia symptoms (HR not allows to increase and blocks tremors)
What are some important patient teaching points when starting warfarin (Coumadin)? What medical conditions OR medications might require a different starting dose?
Vitamin K can reduce effectiveness of coumadin. High risk of hemorrhage and requires lab monitoring
Lower dosing: elderly, malnourished, HF, liver disease, genetic differences
LOTS of D2D interaction
What education would you provide for someone prescribed Warfarin (Coumadin)?
Monitor for any unusual bleeding. Report accidents/falls/injuries to care provider.
Avoid foods high in vitamin K, but consistency in diet is the most important vs limiting.
Always notify providers that you are on warfarin.
Do not take ASA or NSAIDs.
What education would you give to a patient taking spironolactone? What education would you provide about salt substitutes (like No-Salt or Morton Lite Salt)? Explain your answer.
Do not take any other medications that act on the RAAS (ACE, ARBS) or KCl supplements due to risks of hyperkalemia. They also work on the endocrine system, so Gynocomastia, erectile dysfunction, deep voice, and irregular menstruation are possible side effects.
black box warning that it has caused tumors in rats
The medication has been shown to decrease mortality and hospital stays.
Avoid salt substitutes, many of which contain potassium. The aldosterone receptor antagonists cause the patient to excrete Na and Cl but hold on to potassium. Hyperkalemia is already a risk on these medications. Taking a salt substitute with high K exacerbates that risk.
Explain in one sentence the definition of anticoagulants. Differentiate the mechanism of action (MOA) of warfarin (Coumadin) compared to other anticoagulants. Briefly discuss the MOA of antiplatelets.
Anticoagulants (Heparin, Warfarin) disrupt the clotting cascade and thereby suppress the production of fibrin, while Anti-platelets (ASA, Clopidogrel) inhibit platelet aggregation, and thrombolytics (Alteplase) promote the lysis of fibrin, causing the dissolution of the thrombi.
What would you say to a patient about crushing or dissolving nitrates in liquid? Discuss Nitrate Tolerance
Nitrates should never be crushed or altered. Nitrate tolerance develops with chronic use, and is when the drug no longer is effective, so it is recommended to take an 8-hour nitrate-free break.
What is the difference between short-acting and long-acting nitrates? What patient teaching is indicated when prescribing nitrates? Include safety concerns.
Short-acting = acute episode relief
Long-acting = prevention of angina
Keep short-acting on them at all times in a tightly sealed container. Replace every six months. Take 0.3-0.4mg q 5 minutes up to three doses. If symptoms worsen after the first dose or do not improve after 3, call 911.
Provide patient education when prescribing bile acid sequestrants.
As bile acid resins block cholesterol reabsorption from food, they must be taken during meals. Please avoid taking them with other medications (e.g., thyroid, antibiotics), as this can block their absorption. Take these meds 1 hour before or four after other any other medications. Bile acid sequestrants may decrease the absorption of fat-soluble vitamins. Take vitamins four or more hours before bile acid resins. Bloating and constipation are a concern
Which labs would you monitor for a patient taking warfarin (Coumadin)?
PT/INR
Which drug listed as a class III antidysrhythmic agent poses a risk for a patient taking warfarin (Coumadin) and what is the risk?
Amiodarone=increased risk of bleeding
Should we have patients double up on missed doses of coumadin?
No. Do not double up.
How does the mechanism of action (MOA) of a loop diuretic differ from the MOA of an aldosterone antagonist?
Loops decrease NaCl reabsorption in the loop of Henle, and aldosterone antagonists block receptors in the distal nephron, causing excretion of NaCL and holding on to K. The effects of aldosterone are not as drastic or as fast as Loop diuretics.
Discuss the reversing the effects of Warfarin (Coumadin) & Direct Oral Anticoagulants?
Reversal agent for Warfarin is Vitamin K
Reversal agent for direct Oral Anticoagulants like Dabigatran (Pradaxa) is Idarucizumab (Praxbind)
discuss the mechanism of action of bile acid sequestrants and pharmacokinetics?
MOA: it prevents absorption of bile acids. As a response, more LDL receptor sites are presented, decreasing the amount of LDLs in the circulatory system. To aid in the potential side effects of bloating and constipation, drink plenty of water and increase fiber intake.
Should potassium levels be monitored for patients taking diuretics? Which diuretics require monitoring of potassium levels and are there diuretics that do not require monitoring of potassium levels?
Thiazide and Loop diuretics have a risk of hypokalemia. Potassium-sparing diuretics have a risk of hyperkalemia. All should be monitored
Provide a brief discussion of one or two classifications of antidysrhythmic drugs? Discuss the Black Box warning for Amiodarone.
Pacerone, cardarone, nexterone –> anti-arrhythmic drugs, indicated use for ventricular arrhythmias and atrial fibrillation.
MOA: potassium channel blocker that delays repolarization, but are contraindicated in AV block, 2nd-3rd degree block, long QT syndrome, electrolyte imbalance. QT prolongation drug.
BBW: can cause thyroid disorders, pulmonary toxicity, hepatotoxicity, life threatening arrhythmias.
What role does the renin-angiotensin-aldosterone system have in heart failure?
When the body senses low blood pressure, the RAAS system, through various mechanisms of sodium and water retention as well as vasoconstriction, will cause the body to increase blood pressure. This can lead to an increase in the heart’s workload to pump out more blood, which is dangerous in heart failure where the heart is already struggling with contractility, decreased ejection fractions, and low volume output.
Identify a cardiac glycoside. Discuss patient education when prescribing a cardiac glycoside. Are there safety concerns? Please explain
Digoxin. Narrow therapuetic index, hypokalemic dysrythmias, and lots of D2D interactions.
What are the first line antihypertensives?
Thiazides, CCBs, ACIs, ARBs
In black patients with HTN and without HF. CKD or DM, what antihypertensives should be included
Thiazide or CCB
How many antihypertensive medications are recommended for BP target of 130/80 in those with HTN (esp black adults)?
Two or more
What are the recommended antihypertensives for pregnancy?
Methyldopa, nifedipine and labetalol
What antihypertensives should not be given in pregnancy?
ACEI, ARBs, or direct renin inhibitors
What is the main concerning side effect with Loop diuretics (Lasix)? What D2D interaction should be considered?
Hypokalemia-ototoxicity
D2D: digoxin
