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Advanced Pharmacology > Exam 2 - Hypertension, heart failure, arrhythmias > Flashcards

Exam 2 - Hypertension, heart failure, arrhythmias Flashcards

1
Q

Desribe the categories of blood pressure?

A
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2
Q

What are the 4 factors that effect blood pressure?

A
  • Peripheral reistance
  • Vessel elasticity
  • Blood volume
  • CO (SVxHR)
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3
Q

Where are the 4 anatomic sites of blood pressure control?

A
  1. Resistance - arterioles
  2. Capacitance - venules
  3. Pump output - heart
  4. Volume - kidneys
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4
Q

What are the 4 major groups of antihypertensives?

A
  1. Diuretics - deplete sodium
  2. Sympathoplegics - deacrease PVR, reduce CO (alpha and beta blockers)
  3. Direct vasodilators - relax vascular smooth muscle
  4. Anti-angiotensins - block activity or production
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5
Q

What is the only available drug that acts on renin to decrease blood pressure?

A

Aliskiren

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6
Q

What are the targets for centrally acting sympathoplegics? What 2 drugs are in this category?

A
  • Methyldopa - alpha 2 agonist in brainstem
  • Clonidine - alpha 2 agonist in brainstem and alpha 1 agonist in arterioles
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7
Q

What is the primary indication for methyldopa?

A

Pregnancy induced hypertension, does not cross the placenta

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8
Q

What are the uses of clonidine? Side effects?

A
  • Back up hypertensive
  • ADHD, Tourettes, anxiety, PTSD
  • Causes sedation
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9
Q

What is the side effects of alpha 1 blockers? What is the treatment?

A
  • Retention of salt and water (less flow to renal tubules)
  • More effective when used with beta blocker or diuretic
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10
Q

How do vasodilators work in general?

A

They cause relaxation of smooth muscle of arterioles and veins causing reduction in PVR and MAP.

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11
Q

Describe how vasodilators elicit compensatory responses and require combination therapy?

A
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12
Q

Describe the MOA of hydralazine?

A

Dilates arterioles by inducing NO production in the endothelium

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13
Q

Describe the MOA of minoxidil?

A

Opens K+ channels in smooth muscles (hyperpolarizes, less likely to contract) leading to dilation of arteries and arterioles

Well absorbed orally and topically (Rogaine)

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14
Q

What is the MOA of sodium nitroprusside? What is a treatment concern?

A
  • Dilates arterial and venous vessels by NO release and increasing cGMP (relaxes smooth muscle)
  • In high doses can cause CN toxicity, worse in pt’s with renal insufficency
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15
Q

What are the 4 classes of vasodilators and some examples?

A
  • Oral - hydralazine and minoxidil
  • Parenteral - nitroprusside and fenoldopam
  • Combination - CC blockers
  • Nitrates
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16
Q

What is the MOA of fenoldopam?

A

Peripheral arteriolar dilator, agonizes D1 receptors in renal arterial bed.
Acts as a diuretic by increaseing BF to kidneys

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17
Q

What are the 3 classes of CCB and their targets?

A
  • Verapamil - Heart arterioles
  • Diltiazem - peripheral and heart arerioles
  • Dihydropyridines - peripheral arterioles (-pine)
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18
Q

Draw the RAAS pathway and the targets of treatment.

A
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19
Q

What are the differences between the two types of angiotensin antagonists?

A
  • ACE inhibitors (-pril) - prevent the conversion of angiotensin I to angiotensin II, prevents metabolisim of bradykinin
  • Angtiotensin Receptor Blockers (ARB, -sartan) - prevents binding of angtiotensin II, preventing vasoconstriction and aldosterone secretion.
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20
Q

What are the drugs used to treat pulmonary hypertension and their MOA?

A
  • Prostaglandins (Epoprostanol) - continuous IV infusion that prevents formation of ET-1 which is responsible for vasoconstriction proliferation
  • Endothelin receptor antagonists (-sentan) - block binding of ET- 1 to receptors
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21
Q

What is the suggested treatment for mild hypertension?

A
  • Weight loss and reduction in sodium intake
  • First line drugs: diuretic, BB, CCB
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22
Q

What are hypertensive urgency and hypertensive crisis?

A
  • Urgency is BP >180/110 without acute end organ damage
  • Emergency - BP >180/110 with acute end organ damage
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23
Q

What are the treamtents for hypertensive emergencies?

A
  • Parenteral drugs to reduce BP quickly: sodium nitroprusside and fenoldopam
24
Q

What are the differences between arteriolar, capillary, and venous tone?

A
  • Arteriolar - have ability to squeeze tightly due to increased amount of smooth muscle
  • Capillaries - no real tone
  • Veins - some tone, much less than arteries
25
Q

What is classic angina or angina of effort?

A
  • Chest pain induced by increased O2 demands (exercise)
  • Coronary artery flow not being increased proportionately leads to ischemia
  • Relieved after rest
26
Q

What is vasospastic angina?

A
  • O2 delivery is decreased due to coronary vasospasm
27
Q

What is unstable angina?

A
  • Angina at rest due to small clots in the vicinity of atherosclerotic plaque
28
Q

What is the treatments for classic and variant angina?

A
  • Classic - reduces cardiac demand
  • Variant - Potent vasodilators, nitrates, CCB
29
Q

What are the determinants of cardiac oxygen consumption?

A
  • Heart rate
  • Wall tension
  • Contractile state
30
Q

How is coronary blood flow related to duration of diastole?

A

Coronary vessels only get flow during diastole, the longer diastole is, the more flow the arteries get

31
Q

Draw the molecular pathway of vascular tone and drug targets.

A

NO increases cGMP

32
Q

What is the MOA and pharmokinetics of nitroglycerin?

A
  • Causes NO release in vascular smooth muscle in veins and arteries
  • NO increases cGMP which increases dephosphorylation of MLC leading to relaxation
  • Low oral bioavailibilty
  • T 1/2 of 2-8 minutes
33
Q

Describe Amyl Nitrite?

A
  • Older use, inhaled NO and very volatile
34
Q

What are concerns with overexposure to nitrates and nitrites?

A

You can build a tolerance

35
Q

Why are beta blockers useful for angina?

A

They decrease myocardial oxygen demand by reducing HR, BP, and contractility

36
Q

What are the receptor differences in the epicardial and micro-arteries of the heart? Why is this important for durg treatment in angina?

A
  • The epicaridal arteries are beta 1 receptors
  • The microarteries are beta 2 recepors
  • If we can give a selective beta 1 antagonist, we can get dilation of the microarteries improving myocyte oxygen delivery
37
Q

What are the targets of pFOX inhibitors? What is an example?

A
  • They decrease fatty acid oxidation and increase glucose utilization which is more efficent, leading to decreased O2 demand during cardiac metabolism
  • Ranolazine
38
Q

Why is combination of nitrates with a BB of CCB better than with nitrates alone?

A

BB and CCB when given in combination with nitrates prevent the adverse effects associated with either drug given alone.

39
Q

What are the non-pharmalogical treatments for angina?

A
  • CABG
  • Stenting
    -These usually require interventions after fixation and are not always permanent solutions
40
Q

What is heart failure and how does it develop?

A
  • When the heart fails to meet the metabolic demands of the tissues
  • Typically caused by CAD
  • Can be systolic or diastolic dysfunction
41
Q

What are the 4 factors of cardiac performance? How are they altered in heart failure?

A
  • Preload: increased due to retention of blood bc of ineffective pumping
  • Afterload: Increases as cardiac output decreases (vicous cycle)
  • Contractility: Reduced
  • Heart rate: increases as compensatory mechanism
42
Q

Describe the Frank-Starling law?

A

The strength of contraction increases with increased stretch of fibers (increased preload)

Rubber band analogy

43
Q

What contributes to EDV?

A
  • Passive filling
  • Atrial contraction
  • ESV
    synonomous with preload; the volume available for a contraction
44
Q

Draw and describe the molecular mechanisms controlling normal cardiac contractility?

A
45
Q

What is the MOA of digitalis and its major effects?

A
  • Inhibits the Na+/K+ ATPase pump
    • increases ICF Na+ - prevents action of NCX - Increases ICF Ca+ = increased ionotropy
  • Increases PR and reduces QT (arrythmic)
46
Q

What other drugs besides digitalis are positive ionotropes?

A
  • Milrinone
  • Dopamine
  • Dobutamine
47
Q

How do diuretics, ACE inhibitors/ARBs, and vasodilators effect the heart in HF?

A
  • Diuretics - reduce salt and water retention - reduces preload
  • ACE inhibitors/ARB- Reduce compensatory mechanisms to failure - lowers afterload
  • Vasodilators-reduces preload and afterload
48
Q

Why are BB used for treatment in HF?

A

They can reduce the stress on the heart and reduce mortality

49
Q

What are some non-pharmaceutical interventions for HF?

A
  • Cardioverter/defibrillator
  • Heart transplant
  • Cellular cardiomyoplasty
50
Q

List the different types of arrhythmias

A
  • Bradycardia
  • Block
  • Tachycardia
    -SVT, ST, Vtach
  • Fibrillation
51
Q

What is the intrinsic conduction system? How does this relate on an EKG?

A
  • SA node
  • AV node
  • Bundle of His
  • Purkinjie fibers
52
Q

Describe the sodium channel positions during an action potential?

A
  • Closed - M gate closed, H gate ope
  • Activated - M and H gate open
  • Deactivated - M gate open, H gate closed
  • Inactivated - M gate and H gate closed - need repolarazation to return to resting
53
Q

Describe calciums role in the cardiac action potential?

A
  • Calcium influx occurs through L-type voltage gated Ca++ channels
  • Happens more slowly (causes plateau of AP)
  • Occurs at more positive potentials
54
Q

Describe the phases of the cardiac action potential and what is occuring at each phase?

A

Repolarization occurs via the NaKATPase to put ions “back where they came”

55
Q

Describe the differences between disturbances in impulse conduction and impulse formation?

A
  • Disturbances in impulse formation
    -SA/AV node abnormalities
    -Ion changes
    -SNS stimulation
  • Disturbances in impulse conduction
    -Block
    -Reentry

Advanced Pharmacology (3 decks)

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