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Pharm II > Lecture 1 (Cardio)-Exam 1 > Flashcards

Lecture 1 (Cardio)-Exam 1 Flashcards

1
Q

Overview

Explain the RAAS pathway including what organs are involved and what are the effects?

A
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2
Q

RAAS
* What are the events the lead up to activating the kidney? What does the kidney release?

A
  • Dehydration, low sodium, or hemorrhage causes a decrease in blood volume
  • Decrease in blood volume-> decreased blood pressure
  • Decreased blood pressure-> stimulates JG cells of kidney to release renin
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3
Q

RAAS
* What does Renin cleave? What does that new molcule do?

A
  • Renin cleaves angiotensinogen (from the liver) to angiotensin I
  • Angiotensin converting enzyme (from the lungs) converts angiotensin I into angiotensin II
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4
Q

What are 3 things that Angiotension II binds/stimulates?

A
  • Stimulates cells in the zona glomerulosa of the adrenal gland-> increases aldosterone
  • Binds AT II receptors in blood vessels
  • Stimulates posterior pituitary to release anti-diuretic hormone in the renal collecting ducts (CD)
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5
Q

Angiotensin II
* Stimulates cells in the zona glomerulosa of the adrenal glandð increases aldosterone. What does aldosterone do?

A
  • Aldosterone increases sodium and water reabsorption in the kidneys
  • Increases blood volume-> increases blood pressure
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6
Q

What happens when AT II binds to AT II receptors in the blood vessels?

A

Stimulates vasoconstriction-> increases blood pressure

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7
Q

Angiotensin II
* Stimulates posterior pituitary to release anti-diuretic hormone (ADH) in the renal collecting ducts (CD). What does ADH cause?

A
  • Increase CD aquaporins->increase water reabsorption
  • Increases blood volume->increases blood pressure
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8
Q

What are the three ways to block activity of AT II?

A

(1)Block the conversion of angiotensin I to angiotensin II
* Angiotensin converting enzyme inhibitors (ACEI)

(2)Block angiotensin II from binding its receptors in blood vessels
* Angiotensin II receptor blockers

(3)Inhibit renin release

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9
Q

How does ACEIs work?

A

Block the conversion of angiotensin I to angiotensin II

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10
Q

What do ARBs (antiotension II receptor blockers work)?

A

Block angiotensin II from binding its receptors in blood vessels

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11
Q

What are the examples of ACEIs?

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12
Q

What are the SE of ACEI?

A
  • Increase potassium
  • Hypotension
  • Cough (dry, hacking)
  • Angiodema (if you get this, the other ACEIs and ARBs are off the table)
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13
Q
  • What are the CI in ACEI? (4)
  • What do you monitor? (3)
A

CI
* PREGNANCY!
* Angioedema
* Bilateral renal artery stenosis
* Severe chronic kidney disease

Monitoring: electrolytes, SBP > 100 mmHg, renal function

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14
Q

SIDE EFFECTS OF ACEI

Normally, ACE breaks down what? What happens when you use ACEIs?

A
  • Normally, ACE breaks down bradykinin into inactive metabolites
  • ACE inhibitors prevent the breakdown of bradykinin Increased levels of bradykinin
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15
Q

What does increase levels of bradykinin cause?

A
  • Accumulation of protussive mediators in the respiratory tract – dry cough
  • Increased capillary permeation and vasodilation – edema and swelling
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16
Q

What drug will usually not have a cough since they do not increase bradykinin levels??

A

Angiotensin receptor blockers generally do not have these effects

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17
Q

What are the examples of ARBs?

A
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18
Q

ARB SE and CI?

A

SE:
* Increased potassium
* Hypotension
* Cough – less than ACEI
* Angioedema – less than ACEI

CI
* PREGNANCY!
* Bilateral renal artery stenosis
* Severe chronic kidney disease

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19
Q

What is an example of direct renin inhibitor? What does it do?

A

Aliskiren
* Blocks the conversion of angiotensinogen to angiotensin I

Not first line for cardio or renal unless they do not respond to ACEI and ARBs

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20
Q

DIRECT RENIN INHIBITOR (aliskiren)
* What are the Adverse effects and CI?

A

Adverse effects
* Diarrhea – MC
* Increased potassium
* Hypotension
* Cough
* Angioedema

CI
* PREGNANCY!
* Angioedema
* Bilateral renal artery stenosis
* Severe chronic kidney disease

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21
Q

Direct Renin inhibitor (Aliskiren)
* What are the disadvantages?
* No outcome data for patients with what? (3)
* Limited data on comparing aliskiren vs what?

A
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22
Q

What is the breakdown of the nervous system?

A
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23
Q

Adrenergic Nervous system:
* What are the receptor? where are they found?
* What is the normal physiology?

A

Beta Receptors
* Found on multiple different target organs and beta receptors
* Beta-1 and beta-2 receptors

  • Normal physiology: norepinephrine and epinephrine stimulate beta receptors during a flight or fight situation
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24
Q

Beta blockers
* What are they?
* What do they counter the effects of?
* What do they decrease?

A
  • Competitive inhibitors of beta-adrenergic receptors
  • Counter the effects of catecholamines (epinephrine / norepinephrine) on the sympathetic nervous system
  • Decreased sympathetic effects on the cardiovascular system
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Beta receptors-Heart * What receptor is there? * What happens when it reponds to stimulation?
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Beta receptors-Heart * What happens when the receptor is blocked?
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Beta receptors-Kidney * What receptor is it? * What happens when they are stimulated? * What happens when they blockage?
* Beta-1 * Stimulates JG cells to release renin * Decreased renin, decreased BP
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What is first generation beta-blockers?
Non-selective (Beta 1 and 2) * Nadolol * Pindolol * Propranolol * Sotalol * Timolol | N-Z = beta-1 and beta-
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What is a second gen beta blocker?
Selective (Beta 1) * Acebutolol * Atenolol * Bisoprolol * Esmolol * Metoprolol | A-M = beta-1 selective
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What are the 3rd generation beta blocker? What are the effects?
Beta 1, 2 + alpha blockade (more vasodilation) Examples: * Carvedilol * Decreases reactive oxygen species * Decreases atherosclerosis * Labetalol ## Footnote Different ending than “olol” * Alpha and beta blocker * Labetalol * carvedilol
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Beta blockers: * More beta 2 stimulations= * What are the SE?
* More beta 2 stimulation=more side effects * Bronchoconstriction, hypoglycemia unawareness
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Cavrvedilol * Increases and reduces what?
* Increases survival and reduces hospitalization risk in patients with mild to severe heart failure * Reduce cardiovascular mortality post MI with LVEF ≤40%.
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What is unique about Pindolol and acebutolol?
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# LY What are the BB indications?
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What are the SE of BB?
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* What Beta Blockers can pass the BBB to cause depression? * What type of patient do you need to be?
* Propranolol: Might want to get more hx on their depression if on this medication and on an antidepressent. * Hypoglycemia unwareness in diabetes pt-> The NE released is now blocked so you will not see the typical hypoglycemia sx (ex. sweating)
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What are the CI and warnings on BB?
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* What do you need to for a BB overdose? * What do you monitored when your patient is on a BB?
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CALCIUM CHANNEL BLOCKERS (CCB) - MOA * Calcium is needed for what? What does it normally bind to? * What happens when they are calcium is block?
Calcium needed for muscle contraction and cardiac conduction * Binds to and blocks voltage- gated L type calcium channels Calcium channel blockers * Calcium does not enter cell * No cell depolarization
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CALCIUM CHANNEL BLOCKERS- non-dihydrohyridines * What are the examples? (2) * Primarily works on what? * Both classifed as what? * What happens with the pacemaker and contractile cells?
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CALCIUM CHANNEL BLOCKERS- dihydrohyridines * What are the examples? * What does it primarily work on? * What does it cause?
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Indications for Non-dihydropyridines?
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Indications for dihydropyridines?
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CCB ADVERSE EFFECTS for Non- Dihydropyridines
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CCB ADVERSE EFFECTS for Dihydropyridines
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Diuretics: * increase production of what? Decrease What? * What are the five clases?
Increase production of urine; decrease water from the body * Loop diuretics * Thiazide diuretics * Potassium-sparing diuretics * Osmotic diuretics * Carbonic anhydrase inhibitors
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Diuretics: * **What are the examples of loop diuretics?** * **What are the examples of thiazide diuretics?**
* Loop diuretics – furosemide, bumetanide, torsemide, ethacrynic acid * Thiazide diuretics – chlorothiazide, chlorthalidone, hydrochlorothiazide, metolazone
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Diuretics: * What are the examples of potassium sparing diuretics? * Osmotic diurtics example? * Carbonic anhydrase inhibitors?
* Potassium-sparing diuretics – spironolactone, eplerenone, triamterene, amiloride * Osmotic diuretics - mannitol * Carbonic anhydrase inhibitors - acetazolamide
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Thiazide - Distal convluted tubule Carbonic- proximal convluted tubule Loop- ascending loop of henle Potassium -Sparing - collecting tubule and duct
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* Why are loop diuretics the most effective? * What are the examples? (Sulfonamides vs non-sulfonamides)
* Most effective"work at site with most Na reabsorption * Sulfonamides: Furosemide, torsemide, bumetanide (need to be carful about cross-senitivity * Non-Suldonamide: Ethacrynic acid (effective but IV and 2nd line)
52
Loop diuretic: * What is the site of action? * What is the MOA?
* Site: Thick ascending loop of henle * MOA: Inhibit Na,K, Cl cotransporter so it increases excretions of Na, H2O, Cl, K, Ca, MG
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Loop diuretic: * What are the indications? * What are the SE? * What are the CI?
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Thiazide diuretics: * What are the examples?
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Thiazide diuretics: * What is the site of action? * What is the MOA?
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Thiazide diuretics: * What are the indications? * What are the SE? * what are the CI?
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POTASSIUM SPARING DIURETICS * Works where?
Work in the DCT and CD
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POTASSIUM SPARING DIURETICS * What happens in the prinicipal cells?
Two pumps on apical side: * ATP-dependent K+ pump->pushes K+ into the tubule * Epithelial Na+ channel (ENac)->pushes Na+ into cell One pump on basal lateral surface * Na+-K+ ATPase pump->moves two K+ into cell for every three Na+ out
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POTASSIUM SPARING DIURETICS * What happens in intercalated cells?
Primarily remove H+ from blood Two pumps on apical side: * H+ ATPase->H+ into the tubule * H+-K+ ATPase->H+ into tubule in exchange for K+ into cell One pump on basal lateral surface * Na+-K+ ATPase pump->moves two K+ into cell for every three Na+ out
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POTASSIUM SPARING DIURETICS * Movement of all these electrolytes are controlled by what?
aldosterone
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POTASSIUM SPARING DIURETICS * Explain how Principal cells and intercalated cells are affected by aldosterone?
Principal cells: * Aldosterone enters cells->binds to steroid receptor->upregulates the synthesis of Na+-K+ ATPase pumps->net effect is more K+ secreted into urine and more Na+ secreted into blood Intercalated cells: * Aldosterone enters cell->binds to a steroid receptor->upregulates the synthesis Aldosterone increases the synthesis of H+ -K+ ATPase->increases hydrogen secretion
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POTASSIUM SPARING DIURETICS * How does it work? (2) * What is the net effect? (3)
Work by either: * Blocking the steroid receptor-> aldosterone cannot bind * Blocking ENaC channels on the cell membrane Net effect: * Increased excretion of Na+ (water follows) * Increased water loss through urine * Decreased excretion of H+ and K+ ## Footnote can give if use furomide to help preserve K+ or you can just give k+
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POTASSIUM SPARING DIURETICS * What are the examples?
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POTASSIUM SPARING DIURETICS * What is the site of action? * What is the MOA and the sites?
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POTASSIUM SPARING DIURETICS * What is the indicatinos? * What are the SE? * What is the CI?
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ALDOSTERONE RECEPTOR ANTAGONISTS
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ALPHA STIMULATION AND BLOCKADE * What are the different type of receptors? * Where are they located?
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Where is alpha one located? What is response to stimulation? What is the response to blockage?
* Located: Blood vessels * Receptor: Alpha-1 * Response: Vasoconstriction * Block: Vasodilation; decreased SVR, afterload, BP
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SELECTIVE ALPHA BLOCKERS * What does this block? * Where will we see this? What does it cause?
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SELECTIVE ALPHA BLOCKERS * What happens when you block alpha-1 receptors on vascular smooth muscle (α1b)?
Vasodilation->decrease SVR = decrease afterload = decrease blood pressure
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Alpha1 Blockers: * What are the examples (3)? * Is it first line?
* Terazosin, dozazosin, prazosin * Not first line in cardio isssues: no benfits on mortality, increase SE and used in BPH
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Alpha1 blockers * What are the incidications and SE? * What are the CI?
## Footnote IFIS: if patient to have cataract surgery, it makes surgery very difficult on these drugs (hold durg for surgery)
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VASODILATORS-cGMP mediated vasodilators * What is the pathophysio of normal vasodilation?
* Tunica intima – endothelial cells that produce nitric oxide (NO) * NO produced in tunica intima moves to tunica media and activates guanylyl cyclase that converts GTP to cGMP * cGMP induces vascular smooth muscle relaxation
75
VASODILATORS - NITRATES (antianginal agents) * What type of drugs are they? What does it stimulate? * What **predominates**? What does that cause?
Prodrugs converted to nitric oxide – stimulates vasodilation of veins and arteries * Venodilation predominates – decreased venous return to heart – decreased preload * Preload – volume of blood the heart must pump with each contraction
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VASODILATORS - NITRATES (Antianginal agents): * Besides venodilation, what else happens? * Whar does it decrease? * What does it increase?
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VASODILATORS - NITRATES * What are the CI?
CI: Right-sided infarct – hypotension; concomitant use with drugs for erectile dysfunction | Not enough venous return so bottom out
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VASODILATORS - ANTIHYPERTENSIVES * Hydralazine: What is the MOA and incations?
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VASODILATORS - ANTIHYPERTENSIVES * Hydralazine:What are the SE?
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VASODILATORS - ANTIHYPERTENSIVES * Nitroprusside: what is the MOA and Indications?
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VASODILATORS - ANTIHYPERTENSIVES * Nitroprusside: What are the adverse effects?
84
Explain what comes and out during a cardiac action potential?
85
What are the medications that suppress the rate through AV node (rate control)?
* Beta blockers * Calcium channel blockers * Adenosine * Digoxin ## Footnote ABCDs
86
Explain how Medications that shut down re-entrant circuits (rhythm control) work?
87
CLASS 1 - SODIUM CHANNEL BLOCKERS * list the examples and the trick to help you remember them
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CLASS 1 - SODIUM CHANNEL BLOCKERS * How do they work? * Why are there 3 classes? Rank them * What should you do with patients?
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Type 1c: * Strongest what? * Decreases what? * No chage in what? * What are the examples?
* Strongest Na channel blockage * Decreases slope of phase 0 * No change in action potential (AP) duration * Ex: Flecainide, propafenone
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Type 1a: * Moderate what? Less what? * Some what blockage? * Prolonged what? * Longer what? * What are the examples?
* Moderate Na blockage-> Less decrease in phase 0 slope compared to type 1c * Some K channel blockade * Prolonged refractory period * Longer action potential duration * Examples: Disopyramide, Quinidine, Procainamide
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Type 1B * Weakest what? What happens? * Blocks and inactive what? What happens? * What examples?
Weakest Na channel blockage * Smallest decrease in phase 0 slope Blocks inactive and active Na channels configurations * Alters the plateau and repolarization phases * Shorter AP duration - decreased Example: Lidocaine
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Class 2-Beta blockers * Prevent what? * What is the MOA? * What does it rate control?
Prevent influx of L-type calcium Decrease the conduction of action potentials through the AV node * Primarily decreases the slope of phase 4 * May also decrease the slope of phase 0 * No change in phase 3 Rate control * A. fib * A. flutter * SVT
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Fill in for Class 2 BB?
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What is class 3- potassium channel blockers
* A – amiodarone * I – ibutilide * D – dofetilide * S – sotalol
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CLASS 3 – POTASSIUM CHANNEL BLOCKERS * What is the MOA? (4) * Cardiovert patients out of what?
* Block voltage-gated potassium channels I * Decreases rate at which potassium leaves the cell at phases 1, 2, and 3 * Increases AP duration and refractory period * Can increase QTc interval * Decreases myocyte ability to be stimulated * Cardiovert patients out of AF, A flutter, V. tachycardias (rhythm control)
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Amiodarone: * MC used what? * Actions of what? * Used for most types of arrythmias?
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Aminodarone: * What are the SE?
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Amiodarone:
100
Amiodarone:
101
Sotalol (class 3) * What is the MOA? * How does affect HR and contracility? * What are the inications (3)
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Sotalol (class 3) * What are the SE?
103
Class IV-Calcium channel blockers * What is the MOA? * What rates does it control?
Prevents influx calcium at L-type calcium channels * Decreases the conduction of action potentials through the AV node * Primarily decreases the slope of phase 4 * May also decrease the slope of phase 0 * No change in phase 3 Rate control * A. fib * A. flutter * SVT
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Class IV-Calcium channel blockers * Similar effects as what? * Which class has cardiac activity?
* Similar effects as beta-blockers * Only non-dihydropyridines have cardiac activity
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Class IV-Calcium channel blockers * Diltiazem: Less what? What does it txt? * Verapamil: More specific for what? What does it treat?
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Class 5-digoxin * What are the two primary cardiac effects?
* Slows cardiac conduction – pacemaker cells * Increases cardiac contractility – cardiac myocytes
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Class 5- digoxin * How does it slows cardiac conduction – pacemaker cells?
* Stimulates increased acetylcholine release from the Vagus nerve * Slow conduction throught the AV node
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Class 5-Digoxin * How does it increases cardiac contractility – cardiac myocytes?
Increases cardiac contractility – cardiac myocytes * Inhibits sodium/potassium ATPase pumps * Increases intracellular Na * Na leaves cell via Na / Ca exchanger * Ca accumulates inside the cell * Increases myocardial contractility
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Dignoxin * What are the SE?
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Dignoxin * What are the levels? * What are the risk factors for toxicity?
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DIGOXIN TOXICITY TREATMENT * How do you tx digoxin toxicity?
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Adenosine: * What is the MOA?
Binds to adenosine1 receptors on pacemaker cells * Blocks L-type calcium channels * Decreases Ca entering cells * Opens potassium channels - Hyperpolarizes cell Slows conduction through the AV node
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Adenosine: * What are the indications? * What are the pharmacokinetics?
116
Adenosine: * What are the adverse effects?
* Feeling of impending doom * Hypotension * Dyspnea afd * Chest pain * Bronchoconstriction * Flushing
117
What drug was given with this EKG?

Pharm II (14 decks)

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