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Pharmacology Lesson 2
Terms in this set (68)
1. List the long-term physical complications (cardiovascular risk) associated with poorly treated HTN.
a. Demenitai, retinopathy, kidney disease, death
b. Double every 20/10 increase
Discuss the general epidemiology of HTN
1/3 have HTN, Aferican americans, 70% aware, 60% treated, 35% under control
Discuss the general Pathophysiology of HTN
mean arterial pressure = cardiac output x total peripheral resistance; genetic influences account for 30-50%
Discuss issues of compliance in HTN management; why non-compliance is high; and why HTN is often called the "silent killer."
a. Issues: ¼ persons prescribed antihypertensive stops taking it within 6 months
b. Noncompliance: makes them feel run down
c. Silent killer: usually asymptomatic
What is normal blood pressure?
less than 120/80
What is high blood pressure?
What is Stage 1 HTN
What is stage 2 HTN
Discuss the general BP treatment goals
i. With CVD = <130/80
ii. High risk CVD = <130/80
iii. Low risk CVD = <140/90
iv. Frail older adults = <150/90
What is isolated systolic hypertension?
systolic number is high
What is ISH pathophysiology
arterial stiffness; little vessel accomodation during systole
What are common problems/difficult when treating ISH
Lowering systolic pressure without lowering diastolic
Recognize signs/symptoms of patients not tolerating a low diastolic number or a powerful vasodilator.
risk of syncope, dizziness, tachycardia, sweating, falls
What drugs cause or worsen HTN?
Corticosteriods, contraceptives, NSAIDs/COX 2 inhibitors, oral decongestants, nicotine &withdrawal
1. Discuss recommended lifestyle modification strategies.
a. Weight reduction - 10 kg drops 5-20 pts
b. Physical activity - 30min/day aerobic exercise
c. Heart healthy diet - fruits, veggies,
d. Dietary sodium reduction
e. Reduce alcohol consumption.
What are the acute effects of exercise on BP
prolonged reduction in resting BP, possible hypotensive rebound effect, may be intolerable
what are chronic effects of exercise on BP
lower resting HR, decrease circulating adrenaline, reduce inflammation, decreases triglycerides, increase HDL
What are safety tips when working with HTN patients
1. take vitals before/during/after exercise
2. encourage adequate hydration before/during/after
3. allow adequate warmup/cool down
4. normal breathing: valsalva effect
Alpha 2 agonists MOA/TU
MOA: stimulate alpha 2 receptors, reduced adrenaline
TU: chronic HTN, ADHD, withdrawal, Methyldopa = pregnancy
Alpha 1 blocker MOA/TU
MOA: block alpha 1 receptor
TU: lowers BP through vasodilation; relax smooth muscle of bladder neck
Beta Blockers Cardio-selective MOA/TU
MOA: block beta 1 receptors, reduce HR, reduce workload/O2 demand
TU: chronic HTN, CHF, angina, AFib, tachycardia
Beta Blockers non-selective MOA/TU
MOA: block beta 1 and beta 2 receptors
TU: better for hyperthyroidism, essential tremor, PTSD, migrane prophylaxis
alpha-1, beta-1, and beta-2 antagonist
TU: HTN, heart failure, post MI
ACE inhibitors MOA/TU
MOA: inhibit conversion of Ang1 to Ang2
TU: chronic HTN (improves morbidity/mortality), slows progression of kidney damage in diabetics
MOA - inhibit binding of angiotensin II to angiotensin type I receptor which causes vasodilation
TU: chronic HTN (improves morbidity/mortality),
CCBs (calcium channel blockers) MOA/TU
MOA: inhibit Ca entrance to smooth muscles surroind blood vessels; all vasodilators
TU: Chronic HTN, ISH, and angina
which CCBs are an exception?
Diltiazem and Verapamil - similar to beta 1 blocker; not cardio protective
Thiazide diuretics MOA/TU
MOA: block reabsorption of Na; vasodilator
TU: chronic HTN and ISH; mild to moderate edema
Loop Diuretics MOA/TU
MOA: block Na reabsorption in loop of Henle
TU: moderate to severe edema, CHF, respiratory failure, HTN in patients w/fluid overload
Potassium sparing diuretics MOA/TU
MOA: block aldosterone, cause Na wasting and Potassium retention
TU: CHF, portal vein HTN in liver failure, prevent hypokalemia, resistant HTN
Alpha 2 Agonists ADRs
orthostatic hypertension, dizziness
s/s: anticholinergic, rebound fluid retention
Alpha 1 Blocker ADRs
orthostatic hypotension, reflex tachycardia, fluid retnetion
s/s: dizziness, lack of energy, drowsiness, nasal congestion, headache
Beta Blockers cardio ADRs
hypotension, bradycardia and AV block, active HF, sexual dysfunction
Beta blockers non-selective ADRs
peripheral vasoconstriction, bronchoconstriction, reduce ability to rebound from low BG
fatigue, sexual impairment, low blood sugar mask, orthostatic hypotension, does NOT include tachycardia
ACE inhibitors ADRs
hypotension, bradykinin related ADRs, hyperkalemia, acute renal failure
s/s: dry hacky cough, nonallergic rash, angioedema
Drug Interactions: NSAIDs can increase BP
hypotension, hyperkalemia, acute renal failure
Drug interactions: NSAIDs can increase BP/renal failure
constipation, dizziness, hypotension, flushing, peripheral edema, headache, gingival enlargement
Thiazide diuretics ADRs
orthostatic hypotension, dehydration, electrolyte imbalance, gout attacks, hypokalemia
Loop Diuretics ADRs
orthostatic hypotension, dizziness, dehydration, electrolyte imbalance, hypokalemia, gout attacks
Potassium sparing diuretics ADRs
gynecomastia (male breast enlargement)
Generic name of alpha 1 blocker
Generic name of beta blocker
Generic name of ACE inhibitor
Generic name of ARBs
Generic name of CCBs
which antihypertensives reduce long-term morbidity/mortality associated with HTN
Thiazides, ACE, ARB, CCB
Beta blockers if there is a cardiac side kick
which antihypertensives just reduce BP
a. alpha 2 agonist, alpha 1 blocker,
Describe the physiological differences between the cardio-selective and non-selective b-blockers
a. Cardio-selective: have higher affinity for beta 1 receptors; more selective
b. Non-selective: block beta 1 and beta 2 receptors
Discuss why b-blockers must not be stopped suddenly.
Need to be tapered, because of withdrawal symptoms: tachycardia, heart attack, increase in contraction force
Discuss how β-blockers with intrinsic sympathomimetic activity are different than regular β-blockers.
Partial agonist activity, little effect on resting HR (less bradycardia), do NOT reduce CV risk
Discuss how β-blockers mask the signs/symptoms of hypoglycemia in diabetic patients
Beta blocker mask early warning signs like rush of adrenaline, hungry feeling, thus the patient doesn't know they are low until it is too low.
Similarities between ACEs and ARBs
therapeutic use, adverse effects, drug interactions
Differences between ACEs and ARBs
ARBs dont cuase bradykinin related ADRs
What is the most powerful diuretic?
Loop diuretics because it works in the ascending loop of Henle, blocking the most sodium thus keeping water out as well
What is the least powerful diuretic?
Aldosterone Channels because it blocks aldosterone activity too far down the line
What is considered a mild diuretic?
Thiazide diuretic; it blocks salt but is in the distal convoluted tubule
why thiazide diuretics are usually better to treat hypertension than loop diuretics?
Thiazide diuretics are vasodilators
Name two classes of antihypertensive that may precipitate gout attacks?
Thiazide and Loop Diuretics
How to avoid excessive nocturnal diuresis in patients taking loop diuretics?
Take doses in the AM and avoid doses after 6PM
What are clinical symptoms of hyper/hypokalemia?
Muscle weakness, cramps, patesthesias, hypotension, ECG changes, bradycardia
Why is it important to report symptoms of hyper/hypokalemia?
Because if potassium levels are too high or too low the heart can stop
What drugs can increase serum potassium levels?
ACEs, ARBs, potassium sparing diuretics
What drugs can decrease serum potassium levels?
thiazide and loop diuretics
Provide patient instructions regarding fall avoidance in persons with orthostatic hypotension
make sure to stand up slowly, exercise calf muscles before standing, avoid bending at the waist, instead, squat. Dont get dehydrated, sit/lie down immediately if lightheaded
What are two oral medications sometimes used to treat orthostatic hypotension?
Midodrine and fludrocortisone
List of Antihypertensives that cause orthostatic hypotension
all antihypertensives can cause orthostatic hypertension
What is the role of beta blockers and verapamil and diltiazem in Afib
they inhibit entrance of Ca into smooth muscles of coronary and arterial vessels. It causes negative inotropes and negative chronotropes
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