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Semester 1 TxWes Updated Fall 2024 > Pharm Unit 3 > Flashcards

Pharm Unit 3 Flashcards

1
Q

Per pharm lecture, what is the intrinsic rate of the SA node and AV nodes?

A

75 and 40

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2
Q

What part of the cardiac conduction system travels down the septum?

A

Bundle of His

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3
Q

What part of the cardiac conduction system travels through the ventricular muscle?

A

Purkinje fibers

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4
Q

What are 4 possible causes of an arrhythima?

A

Site of origin - scar tissue on a node
Rate - tachy vs brady
Regularity - inconsistent, like A. Fib
Conduction - heart block

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5
Q

What are the primary ions driving cardiac AP?

A

K, Na and Ca

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6
Q

Describe what happens during each phase of cardiac contraction

A

Phase 0: Peak Na influx, sharp rise from phase IV
Phase 1: Na gates slam shut, K efflux begins, small amount of repolarization occurs
Phase 2: plateau phase, K and Ca are coming in/out and maintain a fairly stable membrane potential creating the plateaus
Phase 3: Ca gates shut. K efflux returns the cycle to Vrm
Phase 4: back to Vrm, slow increase in potential until threshold is reached and Phase 0 begins

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7
Q

How does a beta blocker slow down HR?

A

It lowers Vrm, making it take longer to reach threshold

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8
Q

What are the 4 basic classes of anti-arrhythmics? Name a drug for each

A

Class I: Na channel blockers (Quinidine, Lidocaine, Flecainide)
Class II: Sympatholytics (beta blockers, propranolol)
Class III: Prolong AP duration other than by blocking Na channels (usually done via K channel manipulation)(Amiodarone)
Class IV: Block calcium channels (CCBs, verapamil)

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9
Q

What are the 3 subclasses of class I arrhythmics? Name a drug for each

A

Class IA: Quinidine (prolong AP duration, don’t get to phase 4 as fast)
Class IB: Lidocaine (shorten AP duration, get to phase 4 faster)
Class IC: Flecainide (no effect on AP duration, slows dissociation of Na channels, making less available and reducing ectopic beats)

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10
Q

What is a concern with Quinidine?

A

Toxicity, torsades can occur in 2 - 8% even at sub-therapeutic doses

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11
Q

What are some of the “other” anti-arrhythmics?

A

Digoxin (positive inotrope, does have some anti-arrhythmic effects)
Adenosine
K and Mg (if the levels are low)

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12
Q

Describe Adenosine’s MOA

A

It enhances K conductance, helps “reset” HR to normal from a fast SVT. Extremely short half life

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13
Q

What is a non-pharmacologic method to treat SVT?

A

Vagal maneuver

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14
Q

Describe symptomatic vs chronic treatment for bradycardia

A

S = Atropine first, epi or dopamine second
C = pacemaker

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15
Q

Describe symptomatic vs chronic treatment for a heart block

A

S = atropine, transcutaneous pacing
C = pacemaker

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16
Q

Describe symptomatic vs chronic treatment for SVT

A

S = adenosine
C = CCBs, beta blockers

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17
Q

Describe symptomatic vs chronic treatment for ST

A

S = Adenosine, CCBs, Cardioversion
C = Ablation

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18
Q

Describe symptomatic vs chronic treatment for V-tach

A

S = Amiodarone
C = Amiodarone, Sotalol

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19
Q

Describe symptomatic vs chronic treatment for A. Fib

A

S = Diltiazem, Verapamil
C = Beta blockers, Amiodarone

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20
Q

Describe symptomatic vs chronic treatment for V. Fib

A

S = CPR, defibrillation
C = Amiodarone, Lidocaine

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21
Q

What is the mechanism of action for class IA anti-arrythmic?

A

Blocks Na channels, slows phase 0 depolarization

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22
Q

What is the mechanism of action for class IB anti-arrythmic?

A

Blocks Na channels, shortens phase 3 repolarization

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23
Q

What is the mechanism of action for class for class IC anti-arrythmic?

A

Blocks Na channels, markedly slows phase 0 depolarization

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24
Q

What is the mechanism of action for class II anti-arrythmic?

A

B-adrenoceptor blocker, or beta blocker. Inhibits phase IV depolarization in the SA and AV nodes

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25
Q

What is the mechanism of action for class for class III anti-arrythmic?

A

K channel blocker, prolongs phase 3 repolarization

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26
Q

What is occurring during diastolic HF?

A

The heart is “thicker” because the heart is pumping against a higher pressure, making the ventricles smaller. EF is the same, just less total volume

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27
Q

What is occurring during systolic HF?

A

The heart is thinner, EF is reduced, usually due to an MI.

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28
Q

Where is congestion with RV dysfunction? LV?

A

RV = peripheral congestion/edema
LV = pulmonary congestion/edema

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29
Q

What type of ventricular dysfunction does respond to inotropes?

A

Systolic

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30
Q

What is high output failure? How do you treat it?

A

Where the CO/heart function is normal, but it is not enough to cover the bodies metabolic demands, such as with hyperthyroidism or beriberi. Fix the underlying cause, the heart itself is fine

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31
Q

What is preload? How does it affect CO?

A

The amount of stretch placed on the heart, sensitive to fluid volume status. Direct relationship, more preload = more CO.

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32
Q

What is afterload?

A

The pressure the heart beats against

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33
Q

What factors make up CO?

A

HR x SV

34
Q

What parts of the heart are low pressure? Moderate? High?

A

Low = the atria and SVC
Mod = the RV and PA’s
High = LV
Mod/high = the Aorta

35
Q

Describe the Frank-Starling law

A

The strength of contraction increases when streched

36
Q

What factors make up end diastolic volume (EDV)?

A

Passive filling from the atrium + atrial contraction + ESV = EDV

37
Q

What makes up stroke volume?

A

EDV - ESV

38
Q

What is the pre-dominate factor contributing to preload?

A

EDV

39
Q

How do you treat increased preload?

A

Dilate with nitro, diuresis and restrict salt

40
Q

Why is chronic high afterload dangerous in an at risk heart?

A

The high afterload creates a drop in CO, which creates SNS outflow, which further increases afterload. In a weak or at risk heart, this vicious cycle can lead to heart remodeling and eventual failure.

41
Q

What is the relationship between preload and SV?

A

Direct, increased preload = increase SV

42
Q

What is the long term drugs of choice for CHF?

A

ACE, ARBs, vasodilators, diuretics

43
Q

Describe how trigger Ca causes muscle contraction, and how the Ca is put back into storage (likely essay question).

A

Trigger Ca comes in, binds to ryanodine receptors, which triggers calcium efflux from the SR into the cell. Contraction occurs. SERCA pumps the Ca back into the SR to reset. The trigger Ca is pumped out via an Na/Ca antiporter (1 Ca out, 3 Na in), then the Na/K (3 Na out, 2 K in) pump gets the Na out.

44
Q

What is the relationship of amount of trigger calcium to amount released from the SR?

A

Direct, if trigger Ca is increased, released Ca is increased

45
Q

How do beta agonists increase force of contraction?

A

By keeping the L-type Ca channels open longer

46
Q

What is digoxin’s main effect?

A

Blocking the Na/K pump. Na accumulates, reverses the Na/Ca transporter, now there is more trigger Ca, increasing strength of contraction. Does not affect the SA/AV nodes, so minimal effect on HR. Does have a narrow TI and arrhythmia concerns.

47
Q

What is the digitalis effect?

A

Increase in PR interval and decrease in QT, and creation of the “swoop” shape after the QRS complex

48
Q

What is a contraindication for digoxin?

A

Hyperkalemia, it decreases the effect of digoxin by compete with it for the Na/K pump. And Hypercalcemia, increases the risk of arrhythmias because digoxin increases Ca, so if there is already a lot of trigger calcium this can cause massive calcium efflux.

49
Q

What is the phosphodiesterase inhibitor? How does it work?

A

Milrinone, it inhibits PDE3, an enzyme which breaks down cAMP and cGMP. More cAMP = more contraction of the heart, more cGMP = vasodilation of the smooth muscle. So it reduces afterload and increases CO

50
Q

Why are arrhythmia concerns lesser with milrinone as opposed to digoxin?

A

Milrinone does not affect the Na/K pump

51
Q

What is the preferred beta adrenergic agonist? Why?

A

Dobutamine. Less arrhythmogenic than digoxin, more beta 1 selective than other agonists, and empirically works very well in CHF.

52
Q

What are meds to avoid in CHF?

A

Anything that raises BP. NSAIDS, diabetes meds like avandia and acto (they can cause fluid retention) and metformin (causes acidosis when you have CHF).

53
Q

What are the 4 stages of CHF? Treatment for each stage?

A

A = no s/sx, but at risk (you have HTN, prior MI, an arrythmia)

B = No s/sx, but evidence of heart remodeling (decrease salt intake, fix HTN & HLD, promote exercise, treat DM)

C = Structural disease and s/sx present (start BBs, digoxin)

D = Need special intervention (IV inotropes, transplant, VADs)

54
Q

What are the classes of diuretics?

A

Carbonic Anhydrase Inhibitors
Loop diuretics
Thiazides
Potassium Sparing
Agents that Alter Water Excretion
SGLT2 Inhibitors

55
Q

What are the 3 principal activities of the nephron?

A

Filtration, reabsorption, excretion

56
Q

What is the job of the glomerulus?

A

Filter out large particles, like drugs, RBCs

57
Q

What happens in the proximal tubule?

A

This is where 80% of filtrate re-absorption occurs

58
Q

What does Bowmans capsule do?

A

Catches all the small ions/molecules

59
Q

What is the vascular pole? What important structure also resides here?

A

Where afferent/efferent arterioles bring blood in/out. The JGA

60
Q

What are the 2 capillary systems allowing movement in the tubules? Which specific parts?

A

The peritubular capillaries surround the proximal tubules and the Vasa Recta surrounds the loop of Henle

61
Q

What direction is secretion going? Reabsorption (both from a renal standpoint)?

A

Secretion = going from blood to the nephron
Reabsorption = going from nephron to the blood

62
Q

How much of the filtrate is reabsorbed?

A

99%

63
Q

What makes up the JGA? What is each of their functions?

A

Macula Densa = monitors the osmolality and volume of fluid
Juxtaglomerular cells = synthesize renin
Extraglomerular Mesangial cells = make sure we aren’t filter out too much

64
Q

What happens if flow drops at the JGA?

A

Renin is released, and the JGA starts to release NO to increase flow to the kidneys

65
Q

How many JGA’s are there in the body?

A

~2 million, one for each nephron

66
Q

What is the cycle of getting rid of H+ ions with bicarb?

A

H binds with bicarb to make carbonic acid. This goes up to the lungs and is then broken down into CO2 and H2O.

67
Q

Why are Carbonic Anhydrase inhibitors not our first choice diuretic?

A

Because they waste bicarb, raising the risk of acidosis

68
Q

What non-medicine mentioned in lecture functions as a diuretic, what does it antagonize?

A

Caffeine, and it competes with adenosine to bind to adenosine receptors

69
Q

What kick starts the filtration process once the filtrate clears Bowmans capsule?

A

the NHE3 transporter

70
Q

How does the NHE3 transporter work?

A

The NHE3 transporter which pulls Na out of the urine and puts H into the urine, which then binds to bicarb and makes carbonic acid -> CO2 and H2O. CO2 diffuses away into the tubule, where via the Carbonic Anhydrase enzyme it is turned into Bicarb and is then sent into the blood

71
Q

What is the prototype CA inhibitor? How does it work?

A

Acetazolamide, stops the CA enzyme from working, which does not allow carbonic acid to be broken down, and is instead excreted. This also shuts down the Na/H anti-porter, and water follows Na, so we get more water into the urine and more Na.

72
Q

Where does mannitol work in the body? How does it work there?

A

In the proximal tubule, it raises the osmolality, so that less water leaves it, and more can be excreted

73
Q

Where are large substances excreted back into circulation?

A

The S2 segment of the proximal tubule

74
Q

How do you get the osmolality of the loop of Henle back to 300?

A

By getting rid of excess ions

75
Q

How does the loop of Henle move ions? Include ALL ion movement

A

Via the NKCC2 pump, which moves 1 Na, 1 K, and 2 Cl into the loop, from there, K leaks back into the urine, whose + charge forces Mg and Ca back into the blood. In the loop, a K/Cl symporter moves both into the blood, and an Na/K pump is getting Na into the blood and K into the loop.

76
Q

What is the general trend of movement through the tubules?

A

As its going “down” water leaves the tubules, as it goes up, solutes leave.

77
Q

How do loop diuretics work?

A

By blocking NKCC2, which keeps all affected ions (K, Na, Cl, Mg, Ca) in the urine, which then holds onto water.

78
Q

What are the concerns with lasix?

A

Hypokalemia, dehydration, allergic reaction (it is a sulfonamide), loss of other ions (Na, Cl, Mg, Ca) and alkalosis

79
Q

Where do thiazides work? How do they work?

A

In the distal convoluted tubule. The block the NCC pump (Na/Cl). Does inhibit some Ca reabsorption. Keeping them in the urine, and holding onto water. It is also a sulfonamide

80
Q
A

Semester 1 TxWes Updated Fall 2024 (7 decks)

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