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Z-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? Whats a side effect?

A

Dilates arterioles by inducing NO production in the endothelium
Cause a rash that looks like SLE

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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
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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
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25
What is classic angina or angina of effort?
* Chest pain induced by increased O2 demands (exercise) * Coronary artery flow not being increased proportionately leads to ischemia * Relieved after rest
26
What is vasospastic angina?
* O2 delivery is decreased due to coronary vasospasm
27
What is unstable angina?
* Angina at rest due to small clots in the vicinity of atherosclerotic plaque
28
What is the treatments for classic and variant angina?
* Classic - reduces cardiac demand * Variant - Potent vasodilators, nitrates, CCB
29
What are the determinants of cardiac oxygen consumption?
* Heart rate * Wall tension * Contractile state
30
How is coronary blood flow related to duration of diastole?
Coronary vessels only get flow during diastole, the longer diastole is, the more flow the arteries get
31
Draw the molecular pathway of vascular tone and drug targets.
## Footnote NO increases cGMP
32
What is the MOA and pharmokinetics of nitroglycerin?
* 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
Describe Amyl Nitrite?
* Older use, inhaled NO and very volatile
34
What are concerns with overexposure to nitrates and nitrites?
You can build a tolerance
35
Why are beta blockers useful for angina?
They decrease myocardial oxygen demand by reducing HR, BP, and contractility
36
What are the receptor differences in the epicardial and micro-arteries of the heart? Why is this important for durg treatment in angina?
* 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
What are the targets of pFOX inhibitors? What is an example?
* They decrease fatty acid oxidation and increase glucose utilization which is more efficent, leading to decreased O2 demand during cardiac metabolism * Ranolazine
38
Why is combination of nitrates with a BB of CCB better than with nitrates alone?
BB and CCB when given in combination with nitrates prevent the adverse effects associated with either drug given alone.
39
What are the non-pharmalogical treatments for angina?
* CABG * Stenting -These usually require interventions after fixation and are not always permanent solutions
40
What is heart failure and how does it develop?
* When the heart fails to meet the metabolic demands of the tissues * Typically caused by CAD * Can be systolic or diastolic dysfunction
41
What are the 4 factors of cardiac performance? How are they altered in heart failure?
* 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
Describe the Frank-Starling law?
The strength of contraction increases with increased stretch of fibers (increased preload) Rubber band analogy
43
What contributes to EDV?
* Passive filling * Atrial contraction * ESV synonomous with preload; the volume available for a contraction
44
Draw and describe the molecular mechanisms controlling normal cardiac contractility?
45
What is the MOA of digitalis and its major effects?
* 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
What other drugs besides digitalis are positive ionotropes?
* Milrinone * Dopamine * Dobutamine
47
How do diuretics, ACE inhibitors/ARBs, and vasodilators effect the heart in HF?
* Diuretics - reduce salt and water retention - reduces preload * ACE inhibitors/ARB- Reduce compensatory mechanisms to failure - lowers afterload * Vasodilators-reduces preload and afterload
48
Why are BB used for treatment in HF?
They can reduce the stress on the heart and reduce mortality
49
What are some non-pharmaceutical interventions for HF?
* Cardioverter/defibrillator * Heart transplant * Cellular cardiomyoplasty
50
List the different types of arrhythmias
* Bradycardia * Block * Tachycardia -SVT, ST, Vtach * Fibrillation
51
What is the intrinsic conduction system? How does this relate on an EKG?
* SA node * AV node * Bundle of His * Purkinjie fibers
52
Describe the sodium channel positions during an action potential?
* Closed - M gate closed, H gate open * 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
Describe calciums role in the cardiac action potential?
* Calcium influx occurs through L-type voltage gated Ca++ channels * Happens more slowly (causes plateau of AP) * Occurs at more positive potentials
54
Describe the phases of the cardiac action potential and what is occuring at each phase?
## Footnote Repolarization occurs via the NaKATPase to put ions "back where they came"
55
Describe the differences between disturbances in impulse conduction and impulse formation?
* Disturbances in impulse formation -SA/AV node abnormalities -Ion changes -SNS stimulation * Disturbances in impulse conduction -Block -Reentry
56
What are early and delayed afterdepolarizations?
* **Early**- Phase 2 or 3 by sodium or calcium channels * **Delayed** - Occur before a normal action potential via elevated ICF Ca++
57
Describe the different EKG in hear blocks?
58
What are the 4 classes of antiarrhythmic drugs and their discreption?
* Class I: Sodium channel blockade * Class II: Sympatholytic * Class III: prolong action potential duration (other mechanisms beside sodium channels * Class IV: block cardiac calcium channel currents
59
List and describe the drugs in class I and its subgroups?
* **Class IA**: *Quinidine and procainimide* - prolongs APD (lengthens QT), increases the ERP * **Class IB**: Lidocaine - Shortens APD, decreases ERP * **Class IC**: Flecanide - minimall effects on APD, slow dissociation, no effect on ERP (Na+ channels still blocked).
60
What are some class II drugs and their effects?
* Propanolol * Esmolol Supress ventricular ectopic depolarization, antiarrhythmic
61
What are some class III drugs and their effects?
* Amiodarone - blocks K+ channels, actually has all 4 class effects -Drug of choice for VT, lengthens AP
62
What is the side effects in amiodarone?
* Bradycardia or HB * Drug precipitates in tissues * Very long 1/2 life
63
List a drug in class IV and its effects?
* Verapamil - blocks activated and inactivated Ca++ channels * Can reduce ventricular rate
64
What are the effects of adenosine in SVT?
* Increases K+ conductance * Inhibits cAMP induced Ca+ influx * 10 second half life * Converts to sinus rhythm
65
What are the non-pharmalogical therapies for arrhythmias?
* Vagal maneuvers * Pacemakers * Cardioversion * Ablation * Surgery
66
Organize the treatments for arrythmics for acute and chronic care?
67
What is the hydraulic equation?
BP= CO x PVR
68
What'sthe major side effect of ACE inhibitors? Why?
Cough Increases bradykinin and prostaglandins
69
What is the shape of the heart in systolic and diastolic HF?
* Systolic - heart walls are thinned * Diastolic - heart walls are thickened with less room to fill

Z-Advanced Pharmacology (17 decks)

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