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Pharm > Ch 39 > Flashcards

Ch 39 Flashcards

1
Q

HTN

A

Increase in blood pressure (BP) → systolic blood pressure (SBP) > 90 mm Hg and diastolic blood pressure (DBP) > 90 mm Hg

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2
Q

essential HTN (what is it, origin, contributing factors)

A

Most common: affecting 90% of persons with high blood pressure.

ii. Exact origin is unknown
iii. Contributing factors include
1. Stress
2. Aging
3. Diabetes
4. Obesity
5. Smoking
6. Family history
7. Hyperlipidemia
8. Excessive alcohol
9. African-American background

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3
Q

secondary HTN

A

10% of hypertension cases are related to renal and endocrine disorders and classified as secondary hypertension

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4
Q

BP regulators

A

KIDNEYS (work with blood vessels to regulate/maintain normal BP.)
-Regulate by control of fluid and volume, and RAAS system
-control sodium and water elimination/retention > affecting cardiac output, and arterial blood pressure
BARORECEPTORS: In aorta, carotid sinus, and vasomotor center in the medulla aid in regulation of blood pressure. Catecholamine (norepinephrine and epinephrine) increase blood pressure through vasoconstriction activity.
HORMONES
1. ADH- antidiuretic hormone
2. ANP- atrial natriuretic peptide
3. BNP- brain natriuretic peptide

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5
Q

physiologic risk factors for HTN

A

i. Obesity → affects cardiovascular and sympathetic systems
ii. Alcohol consumption increases renin secretion
iii. Diet high in saturated fat and simple carbohydrates

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6
Q

cultural responses to antihypertensive agents

A
  1. African Americans are more likely to develop hypertension at an earlier age. Also have higher mortality rate from hypertension. Susceptible to low-renin hypertension, therefore use of beta blockers and ACE-I are less effective in controlling blood pressure, unless combined with a diuretic. Better response to alpha 1 blockers, calcium channel blockers, diuretics
  2. Asian Americans are 2x more sensitive to antihypertensive medication than Caucasians
  3. Native Americans have a reduced or lower response to beta blockers compared to Caucasians
  4. Caucasians usually have high-renin hypertension and respond well to all antihypertensive agents.
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7
Q

HTN with adults

A

i. 70 million American adults (1 in 3) have hypertension

ii. 65% of individuals > 60 yo have developed hypertension

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8
Q

HTN with older adults

A

iii. Oder adults affected by orthostatic (postural) hypotension with use of antihypertensive medications
1. Sudden drop in BP when going from lying or sitting to upright position, causing dizziness d/t blood pooling in lower extremities

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9
Q

nonpharma control of HTN

A

a. Nonpharmacologic measures should be instituted first, to attempt to decrease blood pressure. These include stress-reduction techniques, exercise, salt restriction, ↓ alcohol intake, smoking cessation
b. Antihypertensive medications are usually initiated with consistent systolic readings of >140

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10
Q

JNC BP guidelines

A

purpose: reduce risk of CVD.
pre: SBP 120-139, DBP 80-89
stage 1: 140/90-159/99
stage 2: 160/100 or up

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11
Q

is SBP or DBP more important for CVD risk in HTN?

A

sbp

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12
Q

pharma control of HTN

A
  1. diuretics
  2. sympatholytics
  3. direct acting arteriolar vasodilators
  4. ACE-I (pril)
  5. ARBs
  6. calcium channel blockers (calcium blockers)
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13
Q

how do diuretics control bP

A

Promote sodium depletion > decreases extracellular fluid volume. Effective for first line drugs for mild hypertension

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14
Q

sympatholytics for BP?

A

five groups of medications: (1) Beta-adrenergic blockers (2) alpha2 agonists (3) alpha adrenergic blockers (4) adrenergic neuron blockers (5) alpha 1 and beta1 adrenergic blockers. (lecture focus on 1, 2 and 3)

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15
Q

beta adrenergic blockers

A

sympatholytics.
(beta blockers).
Used as antihypertensive drugs, or in combination with diuretics. Can also be used as antianginals and antidysrhythmics. Reduce cardiac output by diminishing sympathetic nervous system response to decreased basal sympathetic tone. Reduce heart rate, contractility, and release of renin. Nonselective and selective
i. Nonselective - affect beta 1(heart) & beta 2 (bronchial) receptors: Heart rate slows, BP ↓, bronchoconstriction occurs
ii. Selective – preferred because they affect mainly beta1 heart receptors, so bronchoconstriction is less likely to occur

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16
Q

metoprolol (lopressor) PD/PT/CI/PREC

A

pd: blocks beta1 receptors (cardioselective).
PT: HTN, HF, acute MI, angina.
CI: heart block, cardiogenic shock, hypotn, acute HF, sinus brady.
prec: hep/renal, thyroid dysfx, asthma, PVD, DM, depression

17
Q

metoprolol adv/se/dfl/ni/pt ed

A

adv: Bradycardia, thrombocytopenia, stroke, diabetes mellitus
-Life threat: AV heart block, bronchospasm, agranulocytosis, HF
SE: Fatigue, weakness, dizziness, dry mouth, n/v/d, short-term memory loss, drowsiness, headache, blurred vision, photosensitivity, nasal congestion, peripheral edema, tinnitus, erectile dysfunction, depression
Drug: Increased bradycardia with digitalis, clonidine, SSRIs, MAOIs, cimetidine. Increased hypotensive effect with other antihypertensives, alcohol, anesthetics.
NSAIDs decrease effect of beta blockers
Lab:Increased hepatic enzymes
NI: Obtain medication/herbal hx for possible interactions, base VS. Baseline liver and renal labs and cardiac enzymes. Monitor vital signs, especially BP and pulse, Monitor lab values: BUN, CRT, AST, LDH
PT ED: Check blood pressure and pulse (heart rate) before taking. Report any adverse effects to your healthcare provider immediately. If diabetic educate potential for hypoglycemia. Rise slowly from sitting to standing due to risk of orthostatic hypotension. Wear a medic-alert bracelet. Avoid taking herbs and OTC medications without first discussing with healthcare provider. Teach nonpharmacologic methods to decrease BP

18
Q

centrally acting alpha 2 agents

A

Decrease sympathetic response from the brainstem into peripheral vessels

b. Stimulate Alpha2 receptors > decreases sympathetic activity > increased vagus activity > decreases cardiac output > all result in reduce peripheral vascular resistance, and increased vasodilation
c. Minimal effect on cardiac output, and blood flow to the kidneys

19
Q

clonidine (catapres)

A

centrally acting alpha 2 agonist.

i. Can cause sodium and water retention in high doses > peripheral edema
ii. Frequently administered with diuretics
iii. Available as a transdermal patch worn for 7 days at a time
iv. Cannot abruptly discontinue > risk for rebound hypertension

20
Q

alpha adrenergic blockers

A

a. Block alpha-adrenergic receptors> vasodilation, and decreased blood pressure
b. Help maintain renal blood flow rate
c. Useful in treating hypertension in patients with lipid abnormalities  can decrease VLDL, and LDL responsible for buildup of fatty plaques in the arteries, and increase HDL
d. Safe for patients with diabetes; they do not affect glucose metabolism
e. Do not affect respiratory funcion
f. Given to patients with BPH (benign prostatic hypertrophy)

21
Q

prazosin (minipress) PD, PT, CI, PREC

A

PD: Dilates peripheral blood vessels by blocking alpha-adrenergic receptors
PT: HTN, refractory HF, bPH
CI: Renal disease
PREC: Angina, orthostatic HT, syncope, pregnancy, breastfeeding

22
Q

prazosin (minipress) ADV, SE, DFL, NI, PT ED

A

ADV: Orthostatic hypotension, palpitations, tachycardia, pancreatitis, elevated liver enzymes
SE: Dizziness, drowsiness, nervousness, blurred vision, tinnitus, fatigue, headache, depression, nasal congestion, dry mouth, n/v/d/c, abdominal pain, impotence, urinary incontinence, peripheral edema, erectile dysfunction
DRUG: Increased hypotensive effect with other antihypertensives, nitrates, alcohol. Decreased effects with NSAIDs
LAB: Increased hepatic enzymes
NI: Baseline VS, Medication history. Report probable drug/herbal interactions. Check urinary o/p →drug contraindicated if renal dx present. report sudden decrease in BP and tachycardia. Check for peripheral edema and ↑weight. Prazosin may cause sodium and water retention
PT ED: Check blood pressure and pulse (heart rate) before taking. in high doses > impotence can occur in males > contact healthcare provider. Report any adverse effects to your healthcare provider immediately. Rise slowly from sitting to standing due to risk of orthostatic hypotension. Must take exactly as prescribed > do not abruptly stop > risk of rebound hypertension. Avoid taking OTC medications without first discussing with healthcare provider. Wear a medic-alert bracelet. May cause peripheral edema > monitor weight due to risk of fluid retention

23
Q

direct acting arteriolar vasodilators

A

i. Act by relaxing smooth muscles of the blood vessels, mainly arteries
ii. Promote increased blood flow to brain and kidneys
iii. Vasodilation> decrease in blood pressure, however, sodium and water are retained > peripheral edema > may need to give with diuretic

24
Q

hydralazine (apresoline) PD, PT, CI, PREC

A

direct acting arteriolar vasodilator.
PD: Relaxes smooth muscles > vasodilation
PT: Hypertension, hypertensive emergency, preeclampsia, eclampsia. May be used in conjunction with diuretic or beta blocker
CI: Pregnancy category C
PREC: tachycardia

25
Q

hydralazine (apresoline) ADV, SE, NI, PT ED

A

ADV/SE: Dizziness, tremors, headache, reflex tachycardia, palpitations, edema, nasal congestion, GI bleeding, numbness and tingling
NI: Assess baseline vital signs, before administering, Monitor HR and BP regularly throughout treatment.
PT ED: Check blood pressure before taking. Notify healthcare provider if palpitations develop or become short of breath

26
Q

ACE inhibitors

A

end in pril.

i. Names of some ACE inhibitors are benazepril, captopril, enalapril maleate, fosinopril, lisinopril
ii. Inhibits formation of angiotensin II (potent vasoconstrictor) blocking the release of aldosterone
1. When aldosterone is blocked, sodium is excreted along with water, potassium is retained, and BP is lowered
iii. Primarily used to treat hypertension, and some agents are effective in treatment of heart failure
iv. Cannot be given during pregnancy due to decrease in placental blood flow
v. Need to reduce dose, if renal insufficiency is present
vi. Can cause a chronic, dry hacking cough if present, need to change medications
vii. Should not be taken with potassium-sparing diuretics like spironolactone due to risk of hyperkalemia

27
Q

benazepril (lotensin) PD/PT/CI/PREC

A

ace II drug.
PD: Inhibit ACE> inhibiting formation of angiotensin II, and blocks release of aldosterone
PT: Hypertension
CI: Pregnancy category D. Do not take with potassium-sparing diuretics
PREC: Hypotension

28
Q

benazepril ADV/SE/NI/PT ED

A

ADV: i. Hyperkalemia
ii. First-dose hypotension
iii. Angioedema: swelling of face, larynx, mucous membranes, extremities
SE: Hyperkalemia, headache, dizziness, nausea, diarrhea, constipation, hypotension, and !!!dry irritating cough!!!!
NI: obtain drug/herbal hx for interactions, assess baselin VS BEFORE admin, assess bUN/Cr, K, protein. report sudden drop in bP. monitor labs for renal fx and blood glucose (hypoglycemic rxn in pt with dm).
pt ed: dry irritating cough, call doc. check/record BP before med. report adv eff immediately. dont abruptly stop: rebound htn. dont take salt substitutes (contain K) or additional potassium sparing meds. if become pregnant or planning, let doc know(may harm fetus)

29
Q

ARBs

A

angiotensin II receptor blockers.

i. Losartan, valsartan, irbesartan, candesartan, eprosartan are examples of some ARBs
ii. ARBs are similar to ACE-I because they both prevent the release of aldosterone
iii. Acts on RAAS system
iv. Main difference between ACE-I and ARB’s is:
1. ARB’s block Angiotensin II from the Angiotensin I receptors found in tissues
2. ACE inhibitors inhibit angiotensin-converting enzyme from forming angiotensin II
3. ARBs do not cause the constant, irritated cough like ACE inhibitors
v. Cause vasodilation, and decreased peripheral vascular resistance
vi. Should not be taken during pregnancy

30
Q

valsartan (diovan) PT/PT/CI/PREC

A

ARB.
PD: Potent vasodilator, inhibits binding of angiotensin II
PT: Hypertension and heart failure
CI: Hypersensitivity
PREC: Pregnancy, breastfeeding, Renal and hepatic impairment, hypotension, heart failure hypovolemia, hyperkalemia
ADV: Orthostatic hypotension, hyperkalemia, elevated hepatic enzymes, rhabdomyolysis
-Life threatening: Renal dysfunction, neutropenia
SE: Dizziness, drowsiness, cough (rare), palpitations, blurred vision, headache, diarrhea, arthralgia, fatigue, erectile dysfunction
DRUG: Antihypertensives, diuretics, MAOI’s, and alcohol may increase hypotensive effects
-ACEI and ASA may increase hyperkalemia and renal dysfunction
LAB: May increase AST, ALT, ALP, bilirubin, BUN, creatinine, Hct, Hgb
NI: Obtain drug and herbal hx for possible interactions
ii. Assess baseline vital signs
iii. Assess baseline labs including: BUN, creatine, potassium, WBCs. Assess if patient is pregnant > cannot be taken during pregnancy. Monitor BP and report a sudden drop. Monitor labs including: renal function, blood glucose and potassium
PT ED: Check and record blood pressure before taking
b. Inform patients not to take OTC medication w/o consulting provider
c. Report any adverse effects to your healthcare provider immediately
d. Do not take salt substitutes as they contain potassium, or additional potassium sparing medications
e. If you become pregnant, or are planning on becoming pregnant notify your healthcare provider immediately

31
Q

Calcium channel blockers

A

(aka calcium blockers)
i. Names of some calcium blockers: Verapamil, diltiazem, amlodipine, nifedipine
ii. Block calcium channels in the vascular smooth muscle (VSM) > vasodilation
Calcium channels are found in the myocardium (heart muscle) and VSM cells
—- Large central arteries are not as sensitive to calcium blockers as coronary and cerebral arteries, and peripheral vessels

32
Q

amlodipine (Norvasc) PD/PT/CI/PREC

A

PD: Blocks calcium channels in vascular smooth muscle> vasodilation
PT: (KNOW WHY YOUR PATIENT IS TAKING THE MEDICATION)
a. Angina
b. Hypertension
c. Dysrhythmia
3. Contraindications
a. Pregnancy category C
b. Bradycardia, AV block
c. Beta blocker usage due to decreased myocardial contractility
ADV/SE: Flushing, headache, dizziness, ankle edema, bradycardia, AV block
NI: Assess baseline vital signs, before administering
PT ED: Check blood pressure before taking
b. Report any adverse effects to your healthcare provider immediately
c. When would you need to recheck the blood pressure? (see onset, peak and duration)

Pharm (20 decks)

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