Anti-hypertensive Therapy Flashcards
What are the BP classifications for Normal, Pre-HTN, HTN Stage 1, HTN Stage 2?
Normal: less than 120/80 Pre-HTN: 120/180-139/89 HTN Stage 1: 140/90-159/99 HTN Stage 2: 160/100 & above **NOTE: if the systolic or diastolic requirement is met-->belong to that stage
What are the therapeutic goals for patients with HTN that are less than 60 yo?
less than 140/90
What are the therapeutic goals for patients with HTN that are over 60 yo?
less than 150/90
guidelines loosened for this pop b/c of the side effects elderly people were experiencing.
What are the therapeutic goals for patients with HTN also have kidney disease or diabetes?
less than 140/90
WHat is essential HTN? What % of HTN patients belong in this category?
cause isn’t known
85-90%
What are some causes of secondary HTN?
Sleep apnea Drug-induced or related causes Chronic kidney disease Primary aldosteronism Renovascular disease Chronic steroid therapy and Cushing’s syndrome Pheochromocytoma Coarctation of the aorta Thyroid or parathyroid disease
What are some contributing factors to essential HTN?
Obesity Stress Lack of exercise Diet (excess dietary salt) Alcohol intake Smoking
What is the prevalence of HTN? Gender difference? Age difference?
30% of adults
men & women equal
more common in elderly
Which ethnicity has the highest rates of HTN?
African AMericans–42%
Are people aware of their HTN? Which ethnicity & age group is least aware?
83% of people with HTN were aware, 76% of them are on meds
Asians & young people are least aware
What are some complications of HTN?
risk of cardiovascular disease, renal damage, retinal damage increases with HTN
risk double for heart disease w/ each increase of 20/10 mmHg
What is the treatment strategy for HTN?
Lifestyle modification
Antihypertensive drugs
Follow-up and monitoring
What are some lifestyle modifications used in the treatment of HTN?
Reduce weight to normal BMI, <25 DASH eating plan (8-14 mmHg) Reduce your salt intake! (2-8 mmHg) Increase your activity! (4-9 mmHg) Stop smoking & reduce your drinking.
For each 10 kg loss in weight…how much reduction do you get in your systolic BP?
5-20 mmHg
What is the DASH diet?
similar to Mediterranean
fruits, veggies, low fat dairy, low salt
whole grains, poultry, fish, nuts
LESS red meat, sugar, saturated fat
What is the formula for mean arterial pressure?
MAP=CO X PVR
CO=HR X SV
What are some factors that affect cardiac output?
Heart rate & contractility
- Autonomic Nervous system
- Blood Volume
- Venous Tone
What are some factors that can affect peripheral vascular resistance?
determined by the radius of resistance of arteries & arterioles
circulating factors: NE, ANG II, Sympathetic Nervous System, Local Reactions
T/F Blocking the NE receptor will increase BP.
False. Will decrease by decreasing PVR.
GIve the different types of antihypertensive medications.
- Diuretics
- Agents affecting adrenergic function
- vasodilators
- RAAS target
What are the 3 types of diuretics?
Thiazides
Loop Diuretics
Potassium sparing diuretics
Which of the diuretics are most commonly used? What are 2 examples?
thiazides
ex: chlorothiazide, hydrochlorothiazide
Give 3 examples of loop diuretics? When are they usu used?
Ex: Furosemide, bumetanide, ethacrynic acid
used for severe HTN & heart failure
Give 3 examples of potassium sparing diuretics. What is the usual indication for this?
spironolactone, triamterene, amiloride
Reduction in heart failure mortality
What is the initial effect of diuretics? Effect after 6-8 weeks?
Initially: increase excretion of sodium & water
decrease blood volume–decrease CO–>decrease MAP
After some time: CO returns to normal, but PVR decreases (vasodilation)
How much do diuretics usu lower BP?
usu lower by 10-15 mmHg
What are some possible toxic effects of diuretics?
K+ Depletion (except K+-sparing diuretics)
Can be minimized by limiting Na+ intake
Mg2+ depletion, impaired glucose tolerance, and increase serum lipid concentration
Gout (increased uric acid)
What are the targets of drugs affecting the adrenergic system?
sympathetic nerves release NE that act on beta 1 receptors in the heart & alpha 1 receptors in blood vessels.
beta 1: causes increase in contractility, HR, & conduction velocity. Increase in CO, MAP.
alpha 1: increase in smooth muscle contraction in bv–>increase in PVR–>increase in MAP.
WHat is a good target to reduce NE release from sympathetic stimulation?
alpha 2
Give 4 categories of drugs that decrease adrenergic function.
- Agents that prevent adrenergic transmission.
- selective alpha 1 blockers
- beta adrenergic blockers
- agents directly affecting the CNS
What is an example of an agent preventing adrenergic transmission? What is its MOA?
depletes neurotransmitters (e.g. NE) in the nerve endings in the brain and periphery.
Main effects: depress SNS function centrally and peripherally decreased HR, contractility and PVR
Ex: reserpine
used infrequently b/c of the side effects
What are the negative side effects of reserpine? What are its pharmacokinetics?
Adverse effects: depression, insomnia, nightmares, ulcers, diarrhea, abdominal cramping, nasal stuffiness, orthostatic hypotension, dry mouth, impotence
Pharmacokinetics: onset is slow and full effect is seen in weeks
What are some examples of alpha 1 blockers? What is its mechanism? WHen is this commonly used?
(prazosin, terazosin, doxazosin)
Mechanism: block 1 receptors in vasculature
Main effects: decreased PVR decrease BP
stage 1 & 2 HTN used in conjunction w/ diuretics & beta blockers
What are the adverse effects of alpha 1 blockers?
Adverse effects: 1st dose phenomenon, fluid retention, dizziness, headache
1st dose: when you first take it can have a dramatic reduction in BP…need to take before bed or something not while driving in your car.
What are the 2 types of beta blockers?
nonselective, blocks beta 1 & beta2
cardioselective for beta 1
What is the MOA for beta blockers?
Block cardiac beta1 receptors –> lower CO
Block renal beta 1 receptors –> lower renin, lower PVR
Describe the characteristics of propranolol.
nonselective beta blocker
decrease HR
use in stage 1 & 2 HTN
What are possible adverse effects of propranolol? Bad drug interactions?
bradycardia, depression, aggravates asthma (beta2 blockade in airways)
Drug Interactions: verapamil, diltiazem, digitalis (possible AV Block)
What are the more commonly used beta blockers?
Metoprolol & Atenolol
Cardioselective
Most widely used β-blockers for hypertension
More selective for β1 vs. β2 (less bronco constriction)
What is a good med to use for hypertensive emergencies?
Labetalol
Combined nonselective beta and alpha-1 blocker. Beta blocking action is more prominent
What are some agents that act directly on the CNS? What is its mechanism?
alpha-methyldopa
clonidine
become alpha 2 agonists. Suppresses sympathetic output.
Effect: decreases PVR & HR
What is the clinical indication for methyldopa? for clonidine? Adverse effects?
Methyldopa: HTN during pregnancy
Clonidine: Stage 1 & 2 HTN
Adverse effects: sedation, drowsiness, dry mouth, impotence, bradycardia, withdrawal syndrome (rebound HTN)
What are 3 types of vasodilator drugs?
- calcium channel blockers
- direct acting vasodilators
- potassium channel openers
What are 3 types of calcium channel blockers & examples of each? MOA?
mechanism: inhibit Ca2+ entry through L-type voltage gated Ca2+ channels
Phenylalkylamines: verapamil
Benzothiazepines: diltiazem
Dihydropyridines: amlodipine
What is the category of meds that amlodipine belongs to? What is its MOA ?
calcium channel blocker, dihydropyridine
blocks vascular calcium channels
vasodilation–>lower PVR–>lower BP
Used for HTN & angina, effective in AA pop.
What are the adverse effects of amlodipine?
headache, flushing, nausea, dizziness, ankle edema, reflex tachycardia
What category do verapamil & diltiazem belong to?
calcium channel blockers verapamil-phelyalkylamine diltiazem-benzothiazepine MOA: block calcium in vasculature, heart muscle, AV node Vasodilation-->lower PVR-->lower mAP
What are the adverse effects &contraindications for verapamil & diltiazem?
headache, flushing, nausea, dizziness, ankle edema
contraindications: Caution for AV block when used with beta blockers, and digitalis (amlodipine does not have this effect)
Does amlodipine carry increased risk for AV block, like verapamil & diltiazem?
Nope.
What is a direct acting vasodilator? What is its MOA?
sodium nitroprusside
NO donor-vasodilator
vasodilation–>lower PVR–> lower BP
What are possible adverse effects of sodium nitroprusside? PHarmacokinetics? What are its indications?
Adverse Effects: Reflex tachycardia, severe hypotension, possible cyanide poisoning
Pharmacokinetics: rapid acting, i.v. drip, short plasma half-life
Use: Hypertensive emergencies
What is an example of a potassium channel opener? How does it work?
minoxidil Opens K+ channels Smooth muscle hyperpolarization smooth muscle relaxation arterial dilation decreased PVR decreased BP **adverse effect: hair growth
What are 3 categories of drugs affecting the RAAS system?
- ACE inhibitors
- Angiotensin II Receptor Blockers
- Renin Inhibitors
What are some examples of ACE inhibitors? What is its MOA?
(captopril, enalapril, lisinopril, rampiril)
Mechanism: inhibit ACE –> lower circulating Ang II Levels –>decreased PVR –>decreased BP
Review the RAAS system.
Liver produces angiotensinogen.
Decreased renal perfusion (decreased BP) sensed by juxtaglomerular apparatus. Renin released.
Angiotensinogen + Renin–>Ang I.
Ang I + ACE–>Ang II
Ang II increases simp activity, tubular Na+ & H2O reabsorption, aldosterone secretion
vasoconstriction, ADH secretion
BP goes up mainly b/c of water & salt retention
Adverse effects of ACE inhibitors? Indication?
Adverse effects: skin rash, taste, cough, hyperkalemia (decreased K+ excretion from aldosterone)
Use: Stage 1 and 2 HT; also for congestive heart failure
What is the MOA of aldosterone & ADH?
Aldosterone: tubular Na+ & H2O retention. K+ excretion
ADH: increases collecting duct absorption
T/F ACE inhibitors have negative effects on plasma lipids, glucose.
False.
Which pop should ACE inhibitors be used in? Not be used in?
Should be used in: patients with diabetes
Not used in: pregnancy, less effective in AA
What are different types of ARBs? What is its MOA?
(losartan, valsartan, irbesartan)
Mechanism: selectively block Ang II AT-1 receptor –> decrease PVR –> decrease BP
Negative effects of ARBs?
skin rash, taste, hyperkalemia
fetal toxicity
What’s the deal with renin inhibitors? Contraindications?
new drug, prevents the formation of Ang I
Aliskiren
Equally effective (or better) at lowering BP as ACE Inhibitors and ARBs.
Reported side effects: Diarrhea, stomach pain, heartburn, cough, rash, dizziness, headache, back pain. Fetal Toxicity.
Contraindicated for use with ARBs or ACE inhibitors in patients with diabetes and/or CKD
What is resistant HTN?
BP > 140/90 mmHg (130/80 with diabetes and CKD) for patients prescribed 3 or more antihypertensive medications at optimal doses
or
BP controlled with 4 or more antihypertensive drugs
What % of HTN patients have resistant HTN?
up to 40%
What are the adherence rates for HTN treatment? How are adherence rates for lifestyle mod ?
Meds: 20-80% adherence
Lifestyle: 10-20% adherence
What appear to be the med combos/strategies that elicit the highest adherence rates?
Adherence is higher for single drug and/or lower number of doses per day
Adherence may be higher for RAS drugs and Ca2+ channel blockers vs. diuretics and β-blockers.
What is the BP goal for patients with CKD or diabetes?
less than 140/90
With patients who have CKD…what are the meds used?
ACEI or ARB alone or in combo w/ another class
With patients who have diabetes w/o CKD…what is the dosing strategy?
thiazide-type diuretic or ACEI or ARB or CCB
If African American: thiazide type diuretic or CCB
**same for all other HTN patients
What are 3 titration dosing strategies?
- Max dose of 1st med before adding a second
- Add second med before reaching max dose of 1st
- Start with 2 meds @ the beginning
