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Comprehensive practice flashcards covering cardiovascular and renal pharmacology, anticoagulation, and hematopoietic agents based on the module transcript.
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ACEIs Suffix
The common pharmacological suffix "prils" refers to this drug class.
ACEIs MOA (Angiotensin)
Inhibit ACE which inhibits conversion of angiotensin I to angiotensin II.
ACEIs MOA (Aldosterone)
Decreases the production of aldosterone, leading to decreased sodium and water retention.
ACEIs MOA (Bradykinin)
Prevent breakdown of bradykinin, which increases vasodilation but may cause bronchial irritation.
ARBs Suffix
The common pharmacological suffix "sartans" refers to this drug class.
ARBs MOA
Block the angiotensin II receptor, affecting vasoconstriction and aldosterone secretion without affecting bradykinin.
DRIs Example
aliskiren [Tekturna] is the prototype for this drug class.
DRIs MOA
Inhibit the conversion of angiotensinogen to angiotensin I, reducing the formation of both angiotensin I and II.
RAAS (Abbreviation)
Stands for the Renin-Angiotensin-Aldosterone System.
Renin Site of Origin
According to the RAAS diagram, the kidney is the source of this enzyme.
Angiotensin II Effects
Causes vasoconstriction and triggers aldosterone secretion from the adrenal gland.
ACEIs, ARBs, & DRIs Combination Rule
None of these drugs should be combined; use one or the other.
Bilateral renal artery stenosis
A major contraindication for ACEIs, ARBs, and DRIs.
Angioedema
A life-threatening adverse effect associated specifically with ACEIs and DRIs.
Pregnancy
A contraindication for RAAS inhibitors due to risk of fetal harm.
ACEI-induced Cough
Bronchial irritation caused by increased bradykinin levels.
Hyperkalemia
A common electrolyte adverse effect for ACEIs, ARBs, and DRIs.
Renoprotection
The clinical effect of ACEIs and ARBs for patients who have proteinuria.
First-line HTN for Diabetes Mellitus
ACEIs and ARBs are the first-line therapy for this population.
Black Patient HTN therapy
ACEIs and ARBs are characterized as not as effective in this population, with an increased risk of angioedema.
ACEI Post-MI benefit
Early initiation helps decrease mortality in patients who have suffered a myocardial infarction.
ACEI HF benefit
Decreases remodeling, hospitalization, and mortality in heart failure patients.
ACEI/ARB Monitoring (Renal)
Evaluate serum creatinine prior to prescribing and during therapy.
Calcium Channel Blockers MOA
Block the influx of calcium to inhibit cardiac and vascular smooth muscle contraction.
Dihydropyridines (Type 2) Suffix
The common pharmacological suffix "dipines" refers to this CCB sub-class.
Dihydropyridines Effect Profile
Focus on vasodilation with less cardiac effect; they do not affect conduction through the AV node.
Non-dihydropyridines (Type 1) Examples
Referred to as "mil & dil" (verapamil and diltiazem).
Non-dihydropyridines Effect Profile
Focus on cardiac effects over vasodilation; they affect conduction through the AV node to decrease heart rate.
Non-dihydropyridines Contraindication
Should be avoided in heart failure (HF) and bradycardia.
Dihydropyridines Contraindication
Should be avoided in significant peripheral edema and unstable angina.
Verapamil specific adverse effect
Constipation is a common side effect, which is noted to be worse with this specific drug.
Reflex Tachycardia
An adverse effect specifically associated with Dihydropyridine CCBs.
Peripheral Edema
A common adverse effect for Dihydropyridines.
CYP3A4
The enzyme system responsible for metabolizing CCBs; inhibitors like grapefruit juice increase drug levels.
Grapefruit Juice Interaction
Inhibits the CYP3A4 system, which can increase free drug levels of Calcium Channel Blockers.
Prinzmetal’s Angina
A clinical use for Calcium Channel Blockers.
HTN therapy for Black Patients
Calcium Channel Blockers are considered better for this population than ACEIs/ARBs.
SVT/a-fib CCB choice
Non-dihydropyridines are used for rate control in these conditions.
Raynaud’s Syndrome
A clinical use for Calcium Channel Blockers involving peripheral vasoconstriction.
CCB Monitoring
Check liver function before initiating, heart rate, and monitoring for edema or HF symptoms.
Loop Diuretics MOA
Inhibit sodium reabsorption in the ascending loop of Henle.
furosemide [Lasix]
The prototype drug for Loop Diuretics.
Thiazide-type Diuretics MOA
Inhibit sodium reabsorption in the distal renal tubule.
chlorthalidone [Thalitone]
An example of a Thiazide-type diuretic.
hydrochlorothiazide [HCTZ]
A common Thiazide-type diuretic used for HTN.
Potassium-sparing Diuretics MOA
Inhibit sodium reabsorption and potassium excretion in the distal renal tubule.
spironolactone [Aldactone]
The prototype drug for Potassium-sparing diuretics.
Diuretic Threshold for Renal Impairment
Precautions are needed if CrCl is <30mL/min.
Hypokalemia
An adverse effect associated with loop and thiazide-type diuretics.
Hyperuricemia
An adverse effect of diuretics that can trigger gout.
Gynecomastia
A specific adverse effect associated with spironolactone.
NSAIDs and Diuretics
These drugs decrease the effectiveness of all diuretic classes.
First-line HTN Monotherapy
Thiazide-type diuretics are recommended as first-line for this purpose.
Diuretic for Low CrCl
Loop diuretics are the most effective and can be used when CrCl is <30mL/min.
Potassium Supplementation Threshold
Required if potassium levels are <3.5mEq/L during diuretic therapy.
Diuretic Education (Timing)
Instruct the patient not to take the medication after 4p (4 PM).
HTN Lifestyle Modifications
Should be the first step for all patients diagnosed with hypertension.
Stage 1 HTN First-line Classes
ACEIs, ARBs, CCBs, and thiazide diuretics.
Alternative for ACEI Intolerance
An ARB is usually chosen if the patient is unable to take an ACEI.
Labetalol [Trandate]
Recommended for the management of HTN in pregnant patients.
Methyldopa [Aldomet]
Recommended for the management of HTN in pregnant patients.
HFrEF Compelling Indication
Requires ACEI or ARB, beta blocker, diuretic, and aldosterone antagonist.
Post-MI Compelling Indication
Requires ACEI or ARB, beta blocker, and aldosterone antagonist.
Proteinuric CKD Indication
An ACE inhibitor or ARB is the specific antihypertensive drug class indicated.
Benign Prostatic Hyperplasia Comorbidity
Alpha blockers are likely to have a favorable effect on symptoms.
Essential Tremor Comorbidity
Noncardioselective beta blockers are likely to have a favorable effect.
Osteoporosis Comorbidity
Thiazide diuretics are likely to have a favorable effect.
Bronchospastic Disease Contraindication
Do not use a non-selective beta blocker.
Gout Contraindication
Generally avoid loop or thiazide diuretics in this condition.
Hyponatremia Precaution
Generally avoid thiazide diuretics in this condition.
Cardiac Glycosides MOA
Inhibit the Na+/K+ ATPase pump to increase intracellular sodium and calcium.
Inotropic Effect of Digoxin
It is positive, meaning it increases contractility.
Chronotropic Effect of Digoxin
It is negative, meaning it slows conduction through the AV node to decrease heart rate.
digoxin [Lanoxin]
The primary drug listed under Cardiac Glycosides.
Digoxin Toxicity Threshold
Occurs with serum drug levels >2ng/mL.
Digoxin Visual Disturbances
Signs of toxicity include blurred vision and green/yellow halos around lights.
Digoxin Immune Fab [Digibind]
The antidote for severe or life-threatening digoxin toxicity.
Hypokalemia and Digoxin
This electrolyte abnormality increases the risk of digoxin toxicity.
Antiarrhythmics Class Ia
Sodium channel blockers that prolong the action potential; e.g., quinidine.
Antiarrhythmics Class Ib
Sodium channel blockers that shorten the action potential; e.g., lidocaine.
Antiarrhythmics Class Ic
Sodium channel blockers with no effect on the action potential; e.g., flecainide [Tambocor].
Antiarrhythmics Class II
Standard drug class consists of beta blockers.
Antiarrhythmics Class III
Potassium channel blockers; e.g., amiodarone [Cordarone] and sotalol [Betapace].
Antiarrhythmics Class IV
Calcium channel blockers, specifically "mil & dil" (verapamil and diltiazem).
Amiodarone Thyroid Effects
Can cause both thyrotoxicosis and hypothyroidism.
Amiodarone Skin Side Effect
Can cause a distinct blue-gray skin tone.
Amiodarone Organ Toxicities
Includes pulmonary fibrosis, hepatitis, and corneal deposits.
Amiodarone Monitoring
Requires CXR/PFTs, thyroid function tests, and eye exams.
Nitrates MOA
Vasodilators that relax smooth muscle to decrease afterload and preload, reducing myocardial oxygen demand.
Nitrate Examples
isosorbide mononitrate/dinitrate [Imdur/Isordil] and NTG.
PDE-5 Inhibitors Nitrate Interaction
Concurrent use of drugs like sildenafil [Viagra] is a major contraindication.
Nitrate Tolerance
To prevent this, patients need a nitrate-free period of 10−12 hours each day.
Nitrate Headache
A common adverse effect due to vasodilation.
Exertional Angina Education
Take NTG 5−10 minutes before activity.
Acute Angina Protocol
Take 1 NTG every 5 minutes up to 3 doses; call 911 if no relief after the 2nd tablet.
Nitrate Storage
Keep in a glass bottle, protect from heat/light, and replace every 6 months.
Peripheral Vasodilators Examples
hydralazine [Apresoline] and minoxidil [Loniten].
Peripheral Vasodilators Adverse Effect
Commonly associated with reflex tachycardia.
Peripheral Vasodilators Clinical Use
Indicated for resistant HTN, but not as first-line therapy.
Bile-acid Sequestrants Examples
colestipol [Colestid] and cholestyramine [Questran].