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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?

A
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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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25
Q

Beta receptors-Heart
* What receptor is there?
* What happens when it reponds to stimulation?

A
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26
Q

Beta receptors-Heart
* What happens when the receptor is blocked?

A
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27
Q

Beta receptors-Kidney
* What receptor is it?
* What happens when they are stimulated?
* What happens when they blockage?

A
  • Beta-1
  • Stimulates JG cells to release renin
  • Decreased renin, decreased BP
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28
Q

What is first generation beta-blockers?

A

Non-selective (Beta 1 and 2)
* Nadolol
* Pindolol
* Propranolol
* Sotalol
* Timolol

N-Z = beta-1 and beta-

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29
Q

What is a second gen beta blocker?

A

Selective (Beta 1)
* Acebutolol
* Atenolol
* Bisoprolol
* Esmolol
* Metoprolol

A-M = beta-1 selective

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30
Q

What are the 3rd generation beta blocker? What are the effects?

A

Beta 1, 2 + alpha blockade (more vasodilation)

Examples:
* Carvedilol
* Decreases reactive oxygen species
* Decreases atherosclerosis
* Labetalol

Different ending than “olol”
* Alpha and beta blocker
* Labetalol
* carvedilol

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31
Q

Beta blockers:
* More beta 2 stimulations=
* What are the SE?

A
  • More beta 2 stimulation=more side effects
  • Bronchoconstriction, hypoglycemia unawareness
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32
Q

Cavrvedilol
* Increases and reduces what?

A
  • 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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33
Q

What is unique about Pindolol and acebutolol?

A
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34
Q

LY

What are the BB indications?

A
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35
Q

What are the SE of BB?

A
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36
Q
  • What Beta Blockers can pass the BBB to cause depression?
  • What type of patient do you need to be?
A
  • 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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37
Q

What are the CI and warnings on BB?

A
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38
Q
  • What do you need to for a BB overdose?
  • What do you monitored when your patient is on a BB?
A
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39
Q

CALCIUM CHANNEL BLOCKERS (CCB) - MOA
* Calcium is needed for what? What does it normally bind to?
* What happens when they are calcium is block?

A

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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40
Q

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?

A
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41
Q

CALCIUM CHANNEL BLOCKERS- dihydrohyridines
* What are the examples?
* What does it primarily work on?
* What does it cause?

A
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42
Q

Indications for Non-dihydropyridines?

A
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43
Q

Indications for dihydropyridines?

A
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44
Q

CCB ADVERSE EFFECTS for Non- Dihydropyridines

A
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45
Q

CCB ADVERSE EFFECTS for Dihydropyridines

A
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46
Q

Diuretics:
* increase production of what? Decrease What?
* What are the five clases?

A

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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47
Q

Diuretics:
* What are the examples of loop diuretics?
* What are the examples of thiazide diuretics?

A
  • Loop diuretics – furosemide, bumetanide, torsemide, ethacrynic acid
  • Thiazide diuretics – chlorothiazide, chlorthalidone, hydrochlorothiazide, metolazone
48
Q

Diuretics:
* What are the examples of potassium sparing diuretics?
* Osmotic diurtics example?
* Carbonic anhydrase inhibitors?

A
  • Potassium-sparing diuretics – spironolactone, eplerenone, triamterene, amiloride
  • Osmotic diuretics - mannitol
  • Carbonic anhydrase inhibitors - acetazolamide
49
Q
A

Thiazide - Distal convluted tubule
Carbonic- proximal convluted tubule
Loop- ascending loop of henle
Potassium -Sparing - collecting tubule and duct

50
Q
A
51
Q
  • Why are loop diuretics the most effective?
  • What are the examples? (Sulfonamides vs non-sulfonamides)
A
  • 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
Q

Loop diuretic:
* What is the site of action?
* What is the MOA?

A
  • Site: Thick ascending loop of henle
  • MOA: Inhibit Na,K, Cl cotransporter so it increases excretions of Na, H2O, Cl, K, Ca, MG
53
Q

Loop diuretic:
* What are the indications?
* What are the SE?
* What are the CI?

A
54
Q

Thiazide diuretics:
* What are the examples?

A
55
Q

Thiazide diuretics:
* What is the site of action?
* What is the MOA?

A
56
Q

Thiazide diuretics:
* What are the indications?
* What are the SE?
* what are the CI?

A
57
Q

POTASSIUM SPARING DIURETICS
* Works where?

A

Work in the DCT and CD

58
Q

POTASSIUM SPARING DIURETICS
* What happens in the prinicipal cells?

A

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

59
Q

POTASSIUM SPARING DIURETICS
* What happens in intercalated cells?

A

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

60
Q

POTASSIUM SPARING DIURETICS
* Movement of all these electrolytes are controlled by what?

A

aldosterone

61
Q

POTASSIUM SPARING DIURETICS
* Explain how Principal cells and intercalated cells are affected by aldosterone?

A

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

62
Q

POTASSIUM SPARING
DIURETICS
* How does it work? (2)
* What is the net effect? (3)

A

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+

can give if use furomide to help preserve K+ or you can just give k+

63
Q

POTASSIUM SPARING
DIURETICS
* What are the examples?

A
64
Q

POTASSIUM SPARING
DIURETICS
* What is the site of action?
* What is the MOA and the sites?

A
65
Q

POTASSIUM SPARING DIURETICS
* What is the indicatinos?
* What are the SE?
* What is the CI?

A
66
Q

ALDOSTERONE RECEPTOR ANTAGONISTS

A
67
Q

ALPHA STIMULATION AND BLOCKADE
* What are the different type of receptors?
* Where are they located?

A
68
Q

Where is alpha one located? What is response to stimulation? What is the response to blockage?

A
  • Located: Blood vessels
  • Receptor: Alpha-1
  • Response: Vasoconstriction
  • Block: Vasodilation; decreased SVR, afterload, BP
69
Q
A
70
Q

SELECTIVE ALPHA BLOCKERS
* What does this block?
* Where will we see this? What does it cause?

A
71
Q

SELECTIVE ALPHA BLOCKERS
* What happens when you block alpha-1 receptors on vascular smooth muscle (α1b)?

A

Vasodilation->decrease SVR = decrease afterload = decrease blood pressure

72
Q

Alpha1 Blockers:
* What are the examples (3)?
* Is it first line?

A
  • Terazosin, dozazosin, prazosin
  • Not first line in cardio isssues: no benfits on mortality, increase SE and used in BPH
73
Q

Alpha1 blockers
* What are the incidications and SE?
* What are the CI?

A

IFIS: if patient to have cataract surgery, it makes surgery very difficult on these drugs (hold durg for surgery)

74
Q

VASODILATORS-cGMP mediated vasodilators
* What is the pathophysio of normal vasodilation?

A
  • 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
Q

VASODILATORS - NITRATES (antianginal agents)
* What type of drugs are they? What does it stimulate?
* What predominates? What does that cause?

A

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

76
Q

VASODILATORS - NITRATES (Antianginal agents):
* Besides venodilation, what else happens?
* Whar does it decrease?
* What does it increase?

A
77
Q
A
78
Q

VASODILATORS - NITRATES
* What are the CI?

A

CI: Right-sided infarct – hypotension; concomitant use with drugs for erectile dysfunction

Not enough venous return so bottom out

79
Q
A
80
Q

VASODILATORS - ANTIHYPERTENSIVES
* Hydralazine: What is the MOA and incations?

A
81
Q

VASODILATORS - ANTIHYPERTENSIVES
* Hydralazine:What are the SE?

A
82
Q

VASODILATORS - ANTIHYPERTENSIVES
* Nitroprusside: what is the MOA and Indications?

A
83
Q

VASODILATORS - ANTIHYPERTENSIVES
* Nitroprusside: What are the adverse effects?

A
84
Q

Explain what comes and out during a cardiac action potential?

A
85
Q

What are the medications that suppress the rate through AV node (rate control)?

A
  • Beta blockers
  • Calcium channel blockers
  • Adenosine
  • Digoxin

ABCDs

86
Q

Explain how Medications that shut down re-entrant circuits (rhythm control) work?

A
87
Q

CLASS 1 - SODIUM CHANNEL BLOCKERS
* list the examples and the trick to help you remember them

A
88
Q

CLASS 1 - SODIUM CHANNEL BLOCKERS
* How do they work?
* Why are there 3 classes? Rank them
* What should you do with patients?

A
89
Q

Type 1c:
* Strongest what?
* Decreases what?
* No chage in what?
* What are the examples?

A
  • Strongest Na channel blockage
  • Decreases slope of phase 0
  • No change in action potential (AP) duration
  • Ex: Flecainide, propafenone
90
Q

Type 1a:
* Moderate what? Less what?
* Some what blockage?
* Prolonged what?
* Longer what?
* What are the examples?

A
  • 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
91
Q

Type 1B
* Weakest what? What happens?
* Blocks and inactive what? What happens?
* What examples?

A

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

92
Q
A
93
Q

Class 2-Beta blockers
* Prevent what?
* What is the MOA?
* What does it rate control?

A

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

94
Q

Fill in for Class 2 BB?

A
95
Q

What is class 3- potassium channel blockers

A
  • A – amiodarone
  • I – ibutilide
  • D – dofetilide
  • S – sotalol
96
Q

CLASS 3 – POTASSIUM CHANNEL BLOCKERS
* What is the MOA? (4)
* Cardiovert patients out of what?

A
  • 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)
97
Q

Amiodarone:
* MC used what?
* Actions of what?
* Used for most types of arrythmias?

A
98
Q

Aminodarone:
* What are the SE?

A
99
Q

Amiodarone:

A
100
Q

Amiodarone:

A
101
Q

Sotalol (class 3)
* What is the MOA?
* How does affect HR and contracility?
* What are the inications (3)

A
102
Q

Sotalol (class 3)
* What are the SE?

A
103
Q

Class IV-Calcium channel blockers
* What is the MOA?
* What rates does it control?

A

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

104
Q

Class IV-Calcium channel blockers
* Similar effects as what?
* Which class has cardiac activity?

A
  • Similar effects as beta-blockers
  • Only non-dihydropyridines have cardiac activity
105
Q

Class IV-Calcium channel blockers
* Diltiazem: Less what? What does it txt?
* Verapamil: More specific for what? What does it treat?

A
106
Q
A
107
Q

Class 5-digoxin
* What are the two primary cardiac effects?

A
  • Slows cardiac conduction – pacemaker cells
  • Increases cardiac contractility – cardiac myocytes
108
Q

Class 5- digoxin
* How does it slows cardiac conduction – pacemaker cells?

A
  • Stimulates increased acetylcholine release from the Vagus nerve
  • Slow conduction throught the AV node
109
Q

Class 5-Digoxin
* How does it increases cardiac contractility – cardiac myocytes?

A

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

110
Q

Dignoxin
* What are the SE?

A
111
Q

Dignoxin
* What are the levels?
* What are the risk factors for toxicity?

A
112
Q

DIGOXIN TOXICITY TREATMENT
* How do you tx digoxin toxicity?

A
113
Q
A
114
Q

Adenosine:
* What is the MOA?

A

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

115
Q

Adenosine:
* What are the indications?
* What are the pharmacokinetics?

A
116
Q

Adenosine:
* What are the adverse effects?

A
  • Feeling of impending doom
  • Hypotension
  • Dyspnea afd
  • Chest pain
  • Bronchoconstriction
  • Flushing
117
Q

What drug was given with this EKG?

A

Pharm II (14 decks)

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