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Pharmacology Lecture 4

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Anti-Hypertensive
Sites of Action
- nervous system

-renal system
Sympatholytics
suppress sympathetic action

1. beta-adrenergic blockers

2. alpha1 –adrenergic receptor blockers

3. alpha2 - agonists
Calcium channel blockers
(nervous system)

affect vascular smooth muscle, heart.
Direct-acting Vasodilators
(nervous system)

relax vascular smooth muscle
Angiotensin Converting Enzyme
Inhibitors (ACE Inhibitors)
(renal system)

prevent conversion of angiotensin I into angiotensin II.
Angiotensin II Receptors (ARB)
(renal system)

block angiotensin II receptors so prevents action of angiotensin II.
Diuretics
(renal system)

acts on renal tubules to promote Na and water excretion
Anti-Hypertensive Meds
-Beta-Adrenergic Blockers

-Alpha 1 -Adrenergic Receptor Blockers

-Alpha2-agonists

-Calcium Channel Blockers (CCB)
dihydropyridines
class of CCB

end in “dipine”

– potent vasodilators ONLY, no effects in heart.
amiodipine/norvasc
felodipine/plendil
nifedipine/adalat
isradipine/dynacirc
other – nondihydropyridines
class of CCB

vasodilators and affects the heart
diltiazem/cardizem (used a lot)
verapamil/isoptin, calan
Beta-Adrenergic Blockers

MOA
block Beta1 receptors in heart, blocks site and decreases sympathetic effects on heart.

Blocks Beta1 receptors in the kidney causing decrease in renin.

1. decrease heart rate

2. decrease force of contraction

3. reduced velocity of impulse conduction
Beta-Adrenergic Blockers

IN
HTN, angina, CHF, MI, dysrythmias
Beta-Adrenergic Blockers

AE
bronchoconstriction

bradycardia

reduced CO

AV heart block b/c impulses of node slowed down
Beta-Adrenergic Blockers

TYPES
end in “LOL”

atenolol/tenormin
bisoprolol/zabeta
carvediolol/coreg
labetalol/normodyne
metoprolol/lopressor
nadolol/corgard
propanolol/inderal
Alpha 1 -Adrenergic
Receptor Blockers

MOA
block the effects of alpha 1 receptors.

Results in:

1. dilated blood vessels: decrease BP

2. cardiac output decrease

Blocks sympathetic system effects
Alpha 1 -Adrenergic
Receptor Blockers

IND
HTN
Alpha 1 -Adrenergic
Receptor Blockers

AE
orthostatic hypotension

reflux tachycardia

Na retention and increased blood volume (b/c of decreased CO)
Calcium Channel Blockers
(CCB)

MOA
Blocks entry of Ca into cells – blood vessels and heart.
Calcium Channel Blockers
(CCB)

IND
HTN, angina, migraines, dysrythmias
Calcium Channel Blockers
(CCB)

DI
others:

digoxin- problems with liver: should avoid Beta-blockers
Calcium Channel Blockers
(CCB)

AE
both types: flushing, peripheral edema, gingival hyperplasia, HA

dihydropyridines:
reflex tachycardia

others: bradycardia, AV block
Vasodilators

MOA
relax smooth muscle in blood vessels

•Arterio-dilators: cause decrease in peripheral vascular resistance, decrease afterload -> decrease work of the heart, increase CO, increase tissue perfusion

•Venous–dilators: reduce force with which blood is returned to heart so decrease ventricular filling, decrease preload -> decrease force of contraction

•Result: decrease CO
Vasodilators

IND
HTN, angina, heart failure, MI, peripheral vascular disease.

Types:
hydralazine/apresoline: arterio–dilator minoxidil/loniten:

arterio–dilator, more potent, more severe SE reactions

sodium nitroprusside
/Nitropress-

arterio and venous; works rapidly, IV infusion, cardiac
emergencies, potent
Vasodilators

AE
postural hypotension

reflex tachycardia

expansion of blood/increased blood volume
Vasodilators

DI
other antihypertensive meds
Angiotensin Converting
Enzyme Inhibitors
(ACE Inhibitors)

MOA
Blocks the enzyme (angiotensin converting enzyme, kinase II) that converts angiotensin I to angiotensin II -> therefore decrease vasoconstriction and aldosterone
production.

Results in:

1. vasodilation

2. decrease blood volume/BP

3. prevent or reverse pathological changes in heart, vessels
Angiotensin Converting
Enzyme Inhibitors
(ACE Inhibitors)

IND
HTN, CHF, MI, left ventricular dysfunction, nephropathy

TYPES:

end in “PRIL”
benazepril/lotensin
captopril/capoten
enalapril/vasotec
lisinopril/zestril
ramipril/altace
fosinopril/monopril
Angiotensin Converting
Enzyme Inhibitors
(ACE Inhibitors)

AE
cough

first dose syncope- b/c BP drops rapidly

hyperkalemia- don’t give with potassium

renal failure

angioedema
Angiotensin Converting
Enzyme Inhibitors
(ACE Inhibitors)

DI
other anti HTN

potassium sparing diuretics or drugs that raise K

diuretics
Angiotensin II Receptor
Blockers (ARBs)

MOA
Angiotensin II receptor blocker competes with angiotensin II at tissue binding sites: blocks effects of angiotensin II.

Effects similar to ACE inhibitors:

1. vasodilation

2. reduces blood volume/BP

3. reverses pathological changes in the heart
Alpha2-agonists

MOA
Centrally acting

– reduces firing of sympathetic neurons

– suppresses sympathetic
activity to heart and blood vessels.

Decreases vasoconstriction

– decrease BP
Alpha2-agonists

IND
HTN, severe pain


Ex: clonidine/catapres
Alpha2-agonists

AE
rebound hypertension

drowsiness

xerostomia (dry mouth)
Angiotensin II Receptor Blockers

(ARBs)

MOA
Angiotensin II receptor blocker competes with angiotensin II at tissue binding sites: blocks effects of angiotensin II.

Effects similar to ACE inhibitors:

1. vasodilation

2. reduces blood volume/BP

3. reverses pathological changes in the heart
Angiotensin II Receptor Blockers

(ARBs)

TYPES
Types: end in ‘sartan”
losartan/cozaar
valsartan/diovan
irbesartan/avapro
candesartan/atacand
Angiotensin II Receptor Blockers

(ARBs)

AE
renal failure

hyperkalemia (but less than ACEI)
Diuretics


definition
Drugs that increase renal excretion of water, Na, and other e-lytes

– results in an increase in urine output.
Diuretics

Indications
HTN

remove edematous fluid

prevent renal failure- to stimulate renal output
Diuretics

Classifications
1. High – ceiling: Loop

2. Thiazides

3. Potassium – Sparing diuretics

4. Osmotic diuretics
High – ceiling: Loop

MOA
inhibits Na and Cl reabsorption in ascending loop of Henle, getting more fluid out
High – ceiling: Loop

IN
multiple uses – HTN, heart failure, pulmonary edema, renal disease

Ex: Furosemide/Lasix
High – ceiling: Loop

AE

DI
dehydration,

electrolyte imbalances esp K (hypokalemia) and Na,

hypotension,
ototoxicity (ear toxicity, temporary and can be reversed)

DI: digoxin
Thiazides

MOA
decrease reabsorption of Na, H2O, Cl, bicarbonate in distal convoluted tubule.

⬢Most common diuretic and HTN medication given
Thiazides

IND
HTN, edematous states, diabetes insipidus

Ex: HCTZ – hydrochlorothiazide
Thiazides

AE

DI
AE: similar to loop diuretic, risk for hypokalemia, no ototoxicity

DI: similar to loop diuretics
Potassium – Sparing diuretics

MOA
blocks aldosterone in distal nephron – decrease Na reabsorption and K excretion
Potassium – Sparing diuretics

IND
HTN, edema, severe heart failure, cirrhosis

Ex: spironolactone/aldactone
Potassium – Sparing diuretics

AE

DI
AE: hyperkalemia

DI: do not take with other agents that increase K levels, or with other potassium sparing
diuretics; foods high in K; watch IV fluids
Osmotic diuretics

MOA
creates osmotic forces in lumen of nephron – draws water into renal tubule.

Not
metabolized; rapid acting, very strong, used in emergencies
Osmotic diuretics

IND

DI
prophylaxis of renal failure, reduction of intracranial pressure with cerebral edema, reduction of intraocular pressure

Ex: mannitol/osmitrol


DI: edema
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