Anti-Hypertensive Agents Flashcards
What is the pre-hypertensive state?
Systolic < 120 AND Diastolic < 80
What is considered pre hypertension?
Systolic 120-129 AND Diastolic < 80
What is Stage I HTN?
Systolic of 130-139 or Diastolic of 80-89
What is Stage II HTN?
Systolic ≥ 140 OR Diastolic ≥ 90
What Blood Pressure is considered a Hypertensive Crisis
Systolic > 180 AND/OR Diastolic > 120
What are the 4 sites of action for HTN drugs?
- Arterial resistance
- Venule capacitance
- Kidney volume
- Cardiac output
What drugs alter arteriole resistance?
Diuretics Calcium Channel Blockers (CCBs) Alpha Adrenergic Blockers Beta Adrenergic Blockers (BBs) Vasodilators Angiotensin Receptor Blockers (ARBs)
What drugs alter venous capacitance?
Vasodilators
What drugs alter cardiac output?
Beta-blockers
What drugs alter the volume excreted by the kidneys?
Diuretics
ACE Inhibitors
Beta-blockers (inhibit renin)
What are the drugs of choice for uncomplicated HTN?
Diuretics
Thiazide MOA
Inhibits Na+/Cl co-transporter
Thiazide SE
Hyponatremia
Hyperglycemia
Increased LDL/HDL
Hypokalemia
How do thiazides stimulate hypokalemia?
Low Na stimulate aldosterone which causes increased delivery of Na+ to collecting duct cells increases Na+ diffusion.
K+ loss from principal cells and H+ loss from intercalated cells due to resulting neg. charge on lumen side following Na reuptake.
What are the 4 first line drugs for HTN?
- Diuretics
- Calcium Channel Blockers (CCBs)
- Angiotensin Converting Enzyme inhibitors (ACEIs) *Angiotensin Receptor Blockers (ARBs)
What are the interactions of thiazides with NSAIDs and beta blockers?
NSAIDs – inhibits prostaglandin production, reduces efficacy
ß-blockers – enhances hyperlipidemia and hyperglycemia
Thiazide Contraindications
Hypokalemia
Pregnancy (starting after pregnant)
Loop Diuretic MOA
Blocks Na+/K+/Cl co-transporter, causes venous dilation via prostaglandins
Loop Diuretic SE
Dehydration/hyponatremia Hypokalemia Increased LDL/HDL Impaired diabetes control Ototoxicity
What are the drug interactions of the loop diuretics?
NSAIDS - inhibit prostaglandins which are required for efficacy
Aminoglycosides – enhance ototoxicity and nephrotoxicity
K+ Sparing Diuretics MOA
Aldosterone receptor blocker – combine with diuretics, not used for monotherapy of HT
K+ Sparing Diuretics SE
Hyperkalemia
Gynecomastia (spironolactone)
K+ Sparing Diuretics Contraindications
Renin System Inhibitors (they will inhibit aldosterone which will further contribute to hyperkalemia)
Ca Channel Blockers MOA
All reduce vascular resistance by reducing calcium influx in VSM Non-dihydropyridines also reduce pacemaker potentials, AV node conduction, and contractility
CCB - Nifedipine Action and SE
Nifedipine – dihydropyridine, limited effect on pacemaker or conduction
SE: acute tachycardia, peripheral edema (arteriolar dilation > venodilation)
CCB - Diltiazem Action and SE
Diltiazem – non-dihydropyridine, reduces pacemaker and conduction currents
SE: bradycardia
CCB - Verapamil Action and SE
Verapamil – non-dihydropyridine, more pronounced reduction of currents
SE: constipation, bradycardia
CCB - non-dihydropyridine Contraindications
Non-dihydropyridines are contraindicated in pts with conduction disturbances.
- Use with care in patients on beta blockers
Clonidine MOA
Alpha-2 agonist that causes peripheral vasoconstriction but decreases sympathetic outflow from CNS resulting in vasodilation
Clonidine SE
Sedation
Dry Mouth
Dermatitis
Rebound HTN with withdrawal of the drug
What is the analog of clonidine that has less chance of rebound?
Guanfacine
Methyldopa MOA
It is converted to methylnorepinephrine and is a α2-adrenergic receptor agonist