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HLTH 2511 > Module C: 14-17 > Flashcards

Module C: 14-17 Flashcards

1
Q

Describe the phases of the action potential of the autorhythmic cells of the heart, including the involvement of ion channels:

A

Phase 4: Pacemaker potential arises from “funny current” as sodium enters cell slowly through HCN channels. Membrane slowly depolarizes from -60 to -40mV

Phase 0: Membrane reaches threshold potenential and L-type Ca2+ channels open. Rapid depolarization from calcium influx.

Phase 3: L-type Ca2+ channels close at ~10mV while IKr potassium rectifier channels open, returning the cell to resting potential

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2
Q

What are three factors that determine the rate of spontaneous depolarization of the autorhythmic cells?

A
  1. Slope of the phase 4 pacemaker potential
  2. Value of the threshold potential
  3. Value of the maximum diastolic negative potential
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3
Q

Describe Phase 4 of the cardiomyocyte action potential, including the involvement of ion channels/pumps. Explain the significance of potassium in this phase

A
  • The resting membrane potential is held at a fairly constant -90mV by the action of the 3Na+/2K+ pump and the 3Na+/Ca2+ exchanger
  • Ion concentrations are restored to normal, post-depolarization by the action of these pumps
  • The membrane is most permeable to K+, so extracellular potassium has the greatest effect on cardiomyocyte RMP of any ion
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4
Q

Describe Phase 0 of the cardiomyocyte action potential, including the involvement of ion channels/pumps.

A
  • Influx of positive ions from a neighbouring cardiomyocyte or pacemaker cell causes membrane depolarization.
  • If threshold is reached (~70mV) voltage-gated sodium channels and L-type calcium channels open, causing a very rapid inward flux of positive charge
  • Membrane rapidly depolarizes to ~+50mV at which point sodium channels close, calcium channels remain open
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5
Q

Describe Phase 1 of the cardiomyocyte action potential, including the involvement of ion channels/pumps.

A
  • At ~+30mV votlage-gated sodium channels close and Ito1 potassium channels open
  • Membrane potential rapidly drops from +30mV
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6
Q

Describe Phase 2 of the cardiomyocyte action potential, including the involvement of ion channels/pumps.

A
  • “Plateau phase”, corresponds to ST-segment and ventricular systole!
  • Efflux of potassium through Ito2, IKR, and IKS potassium rectifier channels is matched by influx of calcium through L-type calcium channels such that there is no net change in membrane potential
  • Influx of calcium triggers myofibril contraction
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7
Q

Describe Phase 3 of the cardiomyocyte action potential, including the involvement of ion channels/pumps.

A
  • “Rapid Repolaization” phase
  • L-type calcium channels close while potassium channels remain open
  • Additional potassium rectifier channels (Ikr and Iks) and the IK1 channel open as well, allowing increased efflux of potassium
  • Membrane rapidly repolarizes to ~-90mV at which point the potassium rectifiers close
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8
Q

The absolute/effective refractory period (ERP) spans which phases of the cardiac action potential? What does this correspond to on the ECG?

A

Beginning of phase 0 to middle of phase 3, corresponding to the beginning of the Q-wave to the middle of the T-wave

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9
Q

The relative refractory period (RRP) spans which phases of the cardiac action potential? What does this correspond to on the ECG?

A

Spans from the middle of phase 3 to the early part of phase 4, corresponding to the downwards slope of the T-wave.

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10
Q

What is the cause of afterdepolarization?

A

abnormal influx of Ca2+ during the RRP, eg: with digitalis toxicity

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11
Q

The three main types of arrhythmia are:

A

tachycardias, bradycardias, irregular rhythms

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12
Q

The 4 Vaughan-Williams classes of antiarrhythmics are:

A
  1. Sodium-channel blockers
  2. Beta-adrenergic blockers
  3. Potassium-channel blockers
  4. Calcium-channel blockers

think NaB KC

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13
Q

Class 1 antiarrhythmics preferentially bind to sodium channels in the ________ (resting / open / inactivated) state.

A

open and inactivated

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14
Q

Xylocaine (Lidocaine)

A
  • Class 1B antiarrhythmic
  • Preferentially binds to sodium channels in the inactivated state
  • Has fast, rate-dependant kinetics. Slows conduction in rapidly depolarizing tissue and limits reentry
  • Used in the management of refractory Ventricular arrhythmias, esp. VTach and VFib
  • Second-line choice if amiodarone is unsuccessful
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15
Q

Class 1 antiarrhythmics delay conduction and extend refractory time, so they are known as ___________

A

membrane stabilizers

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16
Q

Class 1 antiarrhythmics only have a significant effect on ________ (atrial / autorhythmic / ventricular) tissue

A

ventricular

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17
Q

Iist 4 cardiac effects of the class 2 antiarrhythmics

A
  1. Decreased automaticity (negative chronotropes)
  2. Decreased AV nodal conduction (prolonged P-R interval)
  3. Increased AV node refractory time
  4. Decreased force of contraction (negative inotropes)
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18
Q

Class 2 antiarrhthmics are useful in __________ (life-threatening / non-life-threatening) arrhythmia

A

non-life-threatening

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19
Q

Give examples of all three subtypes of class 2 antiarrhythmics

A

Selective β1 - blockers: Atenolol, metoprolol, esmolol

Non-selective β - blockers: Propranolol

α and β blockers: Carvedilol

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20
Q

Class 2 antiarrhthmics are useful in __________ (supraventricular / ventricular) arrhythmia

A

supraventricular

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21
Q

the class 2 antiarrhythmic best suited to management of acute SVT is _______

A

Parenteral Esmolol

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22
Q

The most commonly utilized class 3 antiarrhythmic is __________

A

amiodarone

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23
Q

Amiodarone blocks potassium channels, as well as: (list 3)

A

sodium channels, calcium channels, beta-adrenoceptors

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24
Q

Class 3 antiarrhythmics exert their effect primarily by:

A

increasing refractory time

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25
Q

Amiodarone is generally given orally for __________ and IV for __________

A

Orally: supression of atrial and supraventricular dysrhythmias, VT, and VF

IV: termination of VT and VF

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26
Q

Cordarone (Amiodarone)

A
  • Class 3 antiarrhythmic, potassium channel blocker, thyroxine analog
  • also blocks sodium and potassium channels and beta-adrenoceptors
  • Decreases SA automaticity, prolongs AV nodal and ventricular refractory periods. Increases PR and QT intervals and may widen QRS.
  • Orally given to suppress both supraventricular and ventricular dysrhytmias
  • Given IV to terminate VT and VF
  • Many adverse effects; bradycardia, torsades de pointes, thyrotoxicity, photosensitivity, pulmonary fibrosis
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27
Q

Class 4 antiarrhythmics are primarily used for _________ (supraventricular / ventricular) arrhythmias

A

supraventricular

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28
Q

The calcium channel blockers which function as class 4 antiarrhythmics are:

A

Diltiazem and verapamil

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29
Q

Describe the mechanism of action of diltiazem as an antiarrhythmic

A

Blocks calcium influx, especially in SA and AV nodes. Prolongs phase 4 and phase 0, leading to a prolonged PR interval and decreased HR

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30
Q

Why might calcium channel blockers be particularly useful for patients with angina and AFib?

A

they act as a class 4 antiarrhythmic and an antianginal (negative inotrope, vasodilator)

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31
Q

Diltiazem and verapamil may be used to reduce ventricular rates in patients with _______ (list 2). How do they achieve this?

A

Atrial Fibrillation and Atrial Flutter. They inhibit AV Nodal conduction

the autorhythmic cell action potential is largely driven by calcium influx through L-type calcium channels which are inhibited by CCBs

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32
Q

Adenosine (A1) receptors are found in which three locations in the heart?

A

SA node, Atria, AV Node

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33
Q

Adenosine causes _______ (depolarization / hyperpolarization) of AV nodal tissue

A

hyperpolarization

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34
Q

The main indication for adenosine is:

A

termination of PSVT

35
Q

Describe effects of adenosine that are not related to AV nodal blockade

A
  • Decreased HR
  • Decreased sensitivity to epinephrine
  • Decreased stroke volume
  • Increased coronary vasodilation
36
Q

Adenocard (Adenosine)

A
  • Antiarrhythmic, endogenous nucleoside, non-Vaughan-Williams class
  • Binds to A1 receptors to cause AV Nodal Blockade (may cause complete heart block and brief asystole). Causes increased potassium efflux and membrane hyperpolarization.
  • Used to terminate PSVT, including in WPW
  • Extremely short T1/2 (~10s)
  • May cause bronchoconstriction and reduces epinephrine sensitivity
37
Q

Digoxin is indicated as an antiarrhythmic for treatment of __________. Its mechanism of action is ___________. It ____ (is / is not) the preferred drug for this purpose.

A

Digoxin is indicated as an antiarrhythmic for treatment of atrial fibrillation. Its mechanism of action is increases vagal tone, decreases AV conduction. It is not the preferred drug for this purpose.

Digoxin has been shown to increase all-cause mortality in AFib patients and has largely been replaced by CCBs and Beta-blockers in this function

38
Q

List three cardiac indications for magnesium sulphate

A
  1. termination of Torsades de Pointes
  2. treat digitalis-induced ventricular dysrhythmias
  3. treat supraventricular dysrythmias associated with magnesium deficiency
39
Q

The two goals of rhythm control in active AFib/AFlutter are:

A
  1. control the ventricular rate (Beta-blockers or CCBs)
  2. convert to sinus rhythm (ibutilide or DC cardioversion)
40
Q

The most common cause of PSVT is:

A

a reentrant circuit in the AV Node

41
Q

Describe first-line and second-line pharmacotherapy for acute PSVT (as in WPW)

A

First line: Rapid IV push of adenosine

Second line: AV nodal blockade with esmolol or verapamil

42
Q

Long-term treatment of PSVT usually involves

A

surgical ablation of dysrythmogenic tissue

43
Q

The most common cause of sudden cardiac death is:

A

ventricular fibrillation

44
Q

Pharmacologic therapy for VF and VT includes:

A
  • IV infusion of amiodarone
  • IV Epinephrine in pulseless VF
  • IV Lidocaine in refractory VF/VT
45
Q

Use the provided chart to summarize treatments for different arrhythmias

A
46
Q

Define TLC in the management of hyperlipidemia and decribe 4 types

A

TLC = Therapeutic Lifestyle Changes

  1. Diet
  2. Exercise
  3. Weight Loss
  4. Other Changes (smoking cessation, stress reduction)
47
Q

High LDL to HDL ratio is associated with mortality due to __________

A

atherosclerotic disease

48
Q

Compare and contrast the biological functions of LDL and HDL and their role in atherosclerosis

A

Both are lipoprotein complexes that allow lipids to be transported in the blood

LDL is used to transport cholesterol from the liver to target tissues, but may also be taken up by macrophages at nascent atheromas to produce foam cells and plaques

HDL is a reverse transporter that is involved in the transport of lipids back to the liver for excretion and is associated with the dissolution of atheromas

49
Q

Describe the mechanism of action of statin medications for hyperlipidemia

A

statins competitively inhibit HMG-CoA reductase, which catalyzes the rate-determining step in hepatic cholesterol production

50
Q

Adverse effects of statins include:

A
  • muscle pain and potentially life-threatening muscle damage (rhabdo!)
  • GI Issues
  • Liver damage
  • Memory impairment
  • NIDDM
51
Q

Lipitor (Atorvastatin)

A
  • Statin, antihyperlipidemic
  • HMG-CoA inhibitor, reduces LDL by 20-50%
  • Shown to reduce mortality due to atherosclerosis
  • adverse effects include muscle damage, GI issues, memory impairment, and NIDDM
  • Lipitor has a long half life and can be taken at any time of day
52
Q

Pravachol (Pravastatin)

A
  • Statin, antihyperlipidemic
  • HMG-CoA inhibitor, reduces LDL by 20-50%
  • Shown to reduce mortality due to atherosclerosis
  • adverse effects include muscle damage, GI issues, memory impairment, and NIDDM
  • Pravachol has the lowest rate of adverse effects and drug interactions of any statin
53
Q

Tissue factor (TF) is required to activate the ________ (extrinsic / intrinsic) pathway, the function of which is measured using ________

A

Extrinsic pathway, PT or INR

54
Q

The first clotting factor in the common pathway is factor _____, which cleaves ______ into ________

A

The first clotting factor in the common pathway is factor X, which cleaves prothrombin into thrombin

55
Q

Vitamin K is required for the production of clotting factors ___, ___, ___, and ___. The first clotting factor to be cleared from the blood (due to short T1/2) is factor ___, which is involved in the ________ (intrinsic / extrinsic) pathway

A

Vitamin K is required for the production of clotting factors II, VII, IX, and X. The first clotting factor to be cleared from the blood (due to short T1/2) is factor VII, which is involved in the Extrinsic pathway

56
Q

Because warfarin has a delayed onset of action, it is usually co-administered with _______ during initial administration

A

a low molecular weight heparin

57
Q

Coumadin (Warfarin)

A
  • anticoagulant
  • Inhibits production of clotting factors II, VII, IX, and X, thereby inhibiting both intrinsic and extrinsic pathways, but especially extrinsic
  • Delayed onset of action (3-5 days), initially given with LMWH
  • effectiveness is assessed by INR (should be 2-3 for warfarin. 1.1 or less is normal)
  • Used in long term PO prophylactic treatment for DVT, with artificial heart valves, and AFib
58
Q

The effectiveness of Warfarin is measured using ____

A

INR

59
Q

While unfractionated and fractionated heparin (LMWH) both promote inactivation of _____, only unfractionated heparin promotes inactivation of _______

A

While unfractionated heparin, fractionated heparin (LMWH), and direct thrombin inhibitors all promote inactivation of Factor XA, only unfractionated heparin promotes inactivation of Thrombin

60
Q

Heparin and related drugs act primarily by:

A

increasing the activity of antithrombin III (ATIII), to inactivate factor Xa, and thrombin (only unfractionated heparin)

61
Q

Unfractionated heparin activity is measured using _____

A

aPTT

62
Q

LMWH drugs _____ (do / do not) require aPTT monitoring

A

do not!

low molecular weight heparins have highly predictable anticoagulation

63
Q

Heparin (unfractionated)

A
  • Anticoagulant
  • promotes antithrombin III (ATIII) activity, inactivating factor Xa and thrombin.
  • Only given parenterally (IV, SC)
  • Requires ongoing aPTT monitoring
  • Used acutely (PE, DVT, DIC) and prophylactically in surgery or in patients at high risk for clotting disorders
  • Antidote is Protamine if excessive bleeding is present
64
Q

Lovenox (Enoxaparin)

A
  • Anticoagulant, fractionated heparin / LMWH
  • promotes antithrombin III (ATIII) activity, inactivating factor Xa
  • Only given parenterally (IV, SC)
  • Does not require ongoing aPTT monitoring
  • Used acutely (PE, DVT, DIC) and mainly prophylactically in surgery or in patients at high risk for clotting disorders
  • Antidote is Protamine if excessive bleeding is present
65
Q

A major hematologic complication of heparin and related drugs is:

A

Heparin induced thrombocytopenia (HIT)

66
Q

Protamine (Protamine sulphate)

A
  • heparin antidote
  • used to treat uncontrollable bleeding in the context of heparin administration
67
Q

Pradaxa (dabigatran)

A
  • Anticoagulant, direct thrombin inhibitor
  • Competitively inhibits thrombin protease site, which inhibits fibrin formation
  • no INR monitoring is required
  • is increasingly replacing warfarin for chronic management of DVT, AFib due to lower risk of adverse events, no need for monitoring, and fewer food interactions
  • not for patients with valve replacement!
68
Q

Why is aspirin given in a lower dose for antiplatelet function than for pain management?

A

ASA is a selective thromboxane A2 inhibitor at low doses, but inhibits prostacyclin at higher doses, which reduces its antiplatelet effect

69
Q

Aspirin (Acetylsalicylic acid)

A
  • NSAID, antiplatelet
  • non-competitive cyclooxygenase inhibitor. At low doses selectively inhibits thromboxane A2 production without affecting prostacyclins
  • prevents platelet aggregation
  • given prophylactically or acutely for MI and stroke
70
Q

Persantine (Dipyridamole)

A
  • antiplatelet
  • relatively weak antiplatelet effect, but also acts as a coronary vasodilator by causing adenosine release
  • Often combined with aspirin for post-CVA therapy
71
Q

Describe the general mechanism of action of thrombolytic drugs

A

they activate plasminogen to plasmin, which degrades fibrin, leading to thrombus dissolution

72
Q

The major indications for fibrinolytic/thrombolytic drugs are:

A
  1. Stroke
  2. MI
  3. Pulmonary embolism: relative indication, often first line treatment is with LMWH
73
Q

The major adverse effect of thrombolytics is:

A

adverse bleeding

74
Q

TNKase (Tenecteplase)

A
  • fibrinolytic, thrombolytic, recombinant tPA
  • causes plasmin activation from plasminogen, with high specificity for fibrin-bound plasminogen
  • longer duration of action than alteplase
  • used in resolution of STEMI
75
Q

Activase (Alteplase-Recombinant)

A
  • fibrinolytic, thrombolytic, recombinant tPA
  • causes plasmin activation from plasminogen, with moderate-to-high specificity for fibrin-bound plasminogen
  • only thrombolytic recommended for acute PE
  • also used in stroke and MI management (tenecteplase preferred for STEMI)
76
Q

TXA (Tranexamic Acid)

A
  • procoagulant, antiplasmin
  • inhibits activation of plasmin from plasminogen
  • used in management of heavy menstrual bleeding, hemophilia, and traumatic hemorrhage
77
Q

Iron deficiency causes a ________ (hyperchromic / hypochromic) _________ (macrocytic / mycrocytic) anemia

A

hypochromic, microcytic anemia

78
Q

iron is transported in blood bound to ________ and is stored in cells bound to ________

A

trasnferrin, ferritin

79
Q

The major adverse effects of iron supplementation are:

A
  • GI distress
  • N/V
  • Black stools
80
Q

Deficiency in folic acid may lead to: (list 2)

A
  • congenital abnormalities (spinda bifida)
  • Megaloblastic anemia
81
Q

vitamin B12 causes a _________ anemia

A

megaloblastic

82
Q

Care most be taken when giving folate supplementation because it can mask a _________ deficiency

A

vitamin B12

83
Q

The most powerful class of V-W antiarrhythmic in extending ERP is:

A

Class III - Potassium-channel blockers

84
Q

What are the three categories of antithrombotics? Give an example of each.

A
  1. Anticoagulants (inhibit fibrin formation)
    • Warfarin, Heparin, Deltaparin, Tinzaparin, Dabigitran
  2. Antiplatelets (inhibit platelet aggregation)
    • Aspirin, clopidogrel, persantine
  3. Thrombolytics/fibrinolytics (promote clot breakdown by plasmin)
    • Tenecteplase, Alteplase

HLTH 2511 (11 decks)

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