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Quiz

PHA3112 Quiz: Cardiovascular Disease Notes
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9 Pages
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Winter 2017

Department
Pharmacology
Course Code
PHA 3112
Professor
Frank Feiner
Study Guide
Quiz

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Cardiovascular Disease Notes (Lecture 6)
RAAS System:
RAAS System
o Renin release from JG cells of kidney
o Triggered by decrease in BP, blood volume, plasma (Na+), and renal perfusion
o Negative feedback
o Renin angiotensinogen angiotensin I
o Angiotensin converting enzyme (ACE) = angiotensin I angiotensin II
o Angiotensin II stimulates aldosterone release from adrenals AND
vasoconstriction
Increases NE release from SNS nerves therefore increasing epinephrine
release from adrenal medulla and increases sympathetic outflow in CNS
o Aldosterone makes kidney retain water and sodium and lose K+
RAAS regulates BP, volume, fluid/e- balance
Woks 2 as…
o Water and Na+ reabsorption to increase volume; occurs slowly (days to months)
after RAAS activated
o Vasoconstriction increases BP by increasing resistance; occurs quickly (minutes
to hours) after RAAS activated
RAAS mediates pathological changes (MI, HTN, heart failure)
Dugs that suppess RAAS…the ok!
o Promote Na+ and water excretion
o Treatment for HTN, heart failure, MI, kidney disease, retinal disease in diabetes
o ACE inhibitors (enalapril)
Side effects of cough, 1st dose hypotension, hyperkalemia, angioedema
(rash but can be a fatal condition because of tissue swelling in the upper
head and neck), pregnancy category X!
o ARBS (losartan)
Angioedema, pregnancy category X!
o Direct renin inhibitors (aliskiren)
Same side effects as ACE inhibitors
o Aldosterone antagonists (eplerenone)
Hyperkalemia and gynecomastic (SPIROLACTONE)
Calcium Channel Blockers:
Prevent Ca2+ from entering cells especially in blood vessels and heart
Blood vessels
o Ca2+ into smooth muscle cells = contractions
o When BLOCKED = vasodilation
o CCBs are selective on peripheral arterioles and arteries of heart
o NO effect on veins
Heart
o Myocardium calcium entry and inotropic effect increases force of contraction
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Blocking DECREASES force
o SA node calcium regulates the pacemaker and opens channels for increased
discharge
Blocking DECREASES heart rate
o AV node blocking also decreases conduction speed through the AV node
Coupled @ beta 1 receptors
o Receptors activated or blocked depending on Ca2+ influx
3 chemical families
1. verapamil
2. diltizem
3. nifedipine (several more)
therapeutic uses
o verapamil and diltiazem block in arteries and heart
for hypertension, angina, dysrhythmias
block at peripheral arterioles dilation decrease BP
block at arteries of heart increased perfusion to heart muscule
suppresses AV node to help with dysrhythmia
no NET EFFECT on cardiac performance b/c direct effects are
counterbalanced by indirect effects from baroreceptor reflex
adverse constipation, dizziness, facial flushing, headache, gingival
hyperplasia, ankle edema
WORSENS dysrhythmias!
o nifedipine block only in arteries
for hypertension and angina NOT dysrhythmias
investigating suppression use in preterm labor
adverse sae as aoe…ot as uh ostipatio, efle tahadia
(Rx this with beta blockers)
safer with dysrhythmias
NOTE: immediate release nifedipine increases mortality in pts with MI
and unstable angina
o ***toxic doses suppress the heart
Vasodilators:
selective dilation of arteries CCBs, hydralazine, minoxidil
selective dilation of veins organic nitrates
dilate arteries and veins ACE inhibitors, ARBs, direct renin inhibitors, alpha adrenergic
blockers, nitroprusside
drugs that dilate arterioles decrease cardiac afterload and force to decrease cardiac
work and increase CO and tissue perfusion
drugs that dilate veins decrease blood to heart decreases ventricular fill and cardiac
preload therefore decreases force of contraction and work/CO/tissue perfusion
o LOW risk of orthostatic hypotension
Therapeurtic uses HTN, HTN crisis, angina, heart failure, MI, pheochromocytosis,
peripheral vascular disease, pulmonary arterial hypertension, production of controlled
hypotension in surgery
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Adverse effects
o Postural or orthostatic hypotension
Relaxation of venous smooth muscle makes the blood pool in the veins
and decreases blood return to the heart
Decreased CO and BP leads to lightheadedness and fainting
o Reflex tachycardia from baroreceptor reflex
Drop in BP signals baroreceptors in aortic arch and carotid sinus relay to
vasomotor center in medulla
Increases HR in attempt to restoe to oal BUT….
Causes undue stress on heart
Negates vasodilator action to reduce BP
Prevent this by administering with beta blocker
o Epasio of lood olue fo pologed loeed BP though…
Aldosterone renal retention of Na+ and water
Decreased renal blood flow, decreased GFR, increased reabsorption of
Na+ and water
This NEGATES vasodilation
Prevent this by administering with diuretics
Hydralazine
o For HTN, HTN crisis, heart failure
o Adverse reflex tachycardia, systemic lupus erythematosus (like rheumatoid
syndrome of muscle and joint pain, fever, nephritis, pericarditis, antibodies)
Minoxidil
o For severe HTN (BECAUSE VERY DANGEROUS) and as topical agent to promote
hair growth in bald
o Adverse reflex tachycardia, Na+ and water retention, hypertrichosis (excess
hair growth), pericardial effusion
Sodium Nitroprusside
o For HTN emergency, HF, MI
o Adverse hypotension, cyanide poisoning
Drugs for HTN:
Lifelong treatment required but without treatment causes heart disease, kidney disease,
and stroke
Usually you cannot cure, drug only reduce Sx
Most people ae’t diagosed ith HTN
Types
o Primary essential HTN (92%)
Non-identifiable cause
A rule-out diagnosis
Gradual rise in BP seen in 30% adults
Risks = age, menopause, race (African and Hispanic)
Dugs a loe BP ut do’t eliiate ause
o Secondary HTN (8%)
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Description
Cardiovascular Disease Notes (Lecture 6) RAAS System: RAAS System o Renin release from JG cells of kidney o Triggered by decrease in BP, blood volume, plasma (Na+), and renal perfusion o Negative feedback o Renin angiotensinogen angiotensin I o Angiotensin converting enzyme (ACE) = angiotensin I angiotensin II o Angiotensin II stimulates aldosterone release from adrenals AND vasoconstriction Increases NE release from SNS nerves therefore increasing epinephrine release from adrenal medulla and increases sympathetic outflow in CNS o Aldosterone makes kidney retain water and sodium and lose K+ RAAS regulates BP, volume, fluide balance Works 2 ways o Water and Na+ reabsorption to increase volume; occurs slowly (days to months) after RAAS activated o Vasoconstriction increases BP by increasing resistance; occurs quickly (minutes to hours) after RAAS activated RAAS mediates pathological changes (MI, HTN, heart failure) Drugs that suppress RAASthey work! o Promote Na+ and water excretion o Treatment for HTN, heart failure, MI, kidney disease, retinal disease in diabetes o ACE inhibitors (enalapril) st Side effects of cough, 1 dose hypotension, hyperkalemia, angioedema (rash but can be a fatal condition because of tissue swelling in the upper head and neck), pregnancy category X! o ARBS (losartan) Angioedema, pregnancy category X! o Direct renin inhibitors (aliskiren) Same side effects as ACE inhibitors o Aldosterone antagonists (eplerenone) Hyperkalemia and gynecomastic (SPIROLACTONE) Calcium Channel Blockers: Prevent Ca2+ from entering cells especially in blood vessels and heart Blood vessels o Ca2+ into smooth muscle cells = contractions o When BLOCKED = vasodilation o CCBs are selective on peripheral arterioles and arteries of heart o NO effect on veins Heart o Myocardium calcium entry and inotropic effect increases force of contraction
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