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PCOL Cardio Questions > PCOL Ischemic Heart Disease > Flashcards

PCOL Ischemic Heart Disease Flashcards

1
Q

When myocardial oxygen demand is increased WITHOUT a subsequent increase in oxygen supply this is known as:

A. Hemorrhage

B. Ischemia

C. Perfusion

D. Reflux

A

B

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2
Q

When the body increases it’s oxygen demand the supply should also ______

A. Increase

B. Decrease

C. Remain unchanged

A

A

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3
Q

What factors affect your Oxygen Demand?

A. Heart Rate

B. Contractility

C. Ventricular Wall Tension (VWT)

D. All of the above

A

D

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4
Q

How is Ventricular Wall Tension (VWT) related to preload and afterload (Select All)

A. Increased afterload leads to an increased VWT

B. Increased afterload leads to a decreased VWT

C. Increased preload leads to a decreased VWT

D. Increased preload leads to an increased VWT.

A

A, D

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5
Q

Myocardial oxygen supply is dependent on blood flow. What condition decreases your blood flow?

A. Low levels of LDL

B. Chronic Vasodilation

C. Atherosclerosis

D. Normal Sinus Rhythms

A

C

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6
Q

What is Variant (Prinzmetal) Angina?

A

Unexpected vasospasms that cause angina.

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7
Q

What precipitating factors can increase chances of anginal attacks?

A. Sympathetic Input

B. Sex

C. Exercise

D. Emotional Stress

E. All of the above

A

E

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8
Q

What other factors possibly increase chances of developing angina?

A. Increased HR

B. Decreased HR

C. Increased Contractility (contraction force)

D. Decreased VWT

E. Increased Preload and Afterload

A

A,C,E

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9
Q

Which of the following medications will decrease the workload of the heart (decrease in oxygen demand) (Select All)

A. Beta-blockers

B. Verapamil

C. Amlodipine

D. Alpha-1-agonists

E. Low-dose NTG

A

A, B, C, E

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10
Q

What is the effect of Statins and Anti-thrombin medications on myocardial oxygen supply?

A. Increases Oxygen supply

B. Decreases Oxygen supply

C. No change in oxygen supply

D. Maintains oxygen supply

A

D

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11
Q

What is the MOA of Aspirin?

A. Forms an irreversible covalent bond with the serine on COX-1 in order to prevent the production of TxA2

B. Forms a reversible ionic bond with the serine on COX-1 in order to prevent the production of ADP

C. Forms a reversible covalent bond with the serine on COX-1 in order to prevent the production of TxA2

D. Forms an irreverislbe covalent bond with the serine on COX-1 in order to prevent the production of ADP

A

A

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12
Q

What is the MOA of Ranolazine?

A. Blocks L-type calcium channels, lowering the contraction strength of the heart

B. Blocks the late-phase sodium channel lNa , Lowering the Heart Rate

C. Blocks the late-phase sodium channel lNa , Lowering the contraction strength of the heart.

D. Blocks the late-phase calcium channels, lowering the heart rate.

A
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13
Q

What triggers the opening of late-phase sodium channels (lNa) in heart muscle?

A. Hypoxia, Cardiac markers

B. Oxygen surplus

C. Voltage-gated Na Channels

D. L-type calcium channels

A

A

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14
Q

When can late phase sodium channel cause?

A. Increase in intracellular calcium, causing calcium overload

B. Causes the Na/Ca2+ exchanger (NCX) to reverse and pump calcium into the cell rather than out.

C. Decreased LV relaxation and increased LV diastolic tension

D. All of the above

A

D

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15
Q

What are the 3 rays calcium is removed from the cardiac cells to stop muscular contraction?

A. SERCA transport protein on Sarcoplasmic Reticulum (brings calcium back into the SR)

B. Ca2+/ 2H+ exchanger

C. 3 Na+/Ca2+ exchanger (NCX)

D. All of the above

A

D

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16
Q

What is the MOA of NTG?

A. Cause vasoconstriction of smooth muscle

B. Decrease production of cGMP in order to stimulate vasodilation

C. Increase production of cGMP in order to stimulate vasodilation

D. Increase production of cGMP in order to stimulate vasoconstriction

A

C

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17
Q

Low-dose NTG has a higher affinity for the_____ side of the vasculature.

A. Venous

B. Arterial

A

A

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18
Q

With low-dose NTG you can expect to see: (select all)

A. A decrease in preload

B. A decrease in afterload

C. An increase in Oxygen supply

D. A decrease in oxygen demand

A

A, C, D

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19
Q

Based on this graph you can conclude: (Select All)

A. High doses of NTG produce a response from the venous side only

B. Low doses of NTG produce a response from the arterial side first

C. High doses of NTG produce a response from the arterial side

D. Low doses of NTG produce a response from the venous side first.

A

C,D

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20
Q

Why can it be a bad thing to use high doses of NTG in order to attempt decreaseing VWT and decrease myocardial oxygen demand?

A. Dropping the blood pressure too quickly on the venous and arterial sides may cause a reflex sympathetic output (tachycardia)

B. High dose NTG is not a problem for oxygen demand

C. High dose NTG can cause large amounts of vasoconstriction and lead to increased blood pressure

A

A

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21
Q

Why should PDE5 inhibitors NOT be given with NTG?

A. PDE5 inhibitors act against NTG and will decrease the vasodilatory effects of the NTG therapy

B. PDE5 inhibitors increase cGMP levels in the body and NTG will also cause a further increase in cGMP levels. Leading to large drops in blood pressure.

C. PDE5 inhibitors decrease cGMP levels in the body and NTG will also cause a further decrease in cGMP levels. Leading to large drops in blood pressure

A

B

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22
Q

What are the most common side effects of NTG?

A. Headache and flushing

B. Hypotension (syncope)

C. Reflex tachycardia at high doses

D. Evokes reflex stimulation of SNS

E. All of the above

A

E

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23
Q

What effects do beta-blockers have on the body?

A. Decrease in HR

B. Increase in HR

C. Decrease contractility (Contraction force)

D. Decrease VWT

E. Increase subendocardium prefusion by increasing diastolic perfusion time

A

A, C, D, E

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24
Q

What channel is blocked by calcium channel blockers?

A. T-Type calcium channels

B. I-Type calcium channels

C. L-Type calcium channels

D. Voltage-gated sodium channels

A

C

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25
Q

Verapamil is a ______ CCB that lowers myocardial oxygen ______

A. Dihydropyradine, Supply

B. Non-dihydropyradine, Demand

C. Non-dihydropyradine, Supply

D. Dihydropyradine, Demand

A

B

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26
Q

Dihydropyradines such as Amlodipine will lower myocardial oxygen_____ and increase myocardial oxygen _____

A. Supply, Demand

B Demand, Supply

A

B

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27
Q

Blocking coagulation factors such as VII, X, Xa etc. will lead to: (select all)

A. Increased bleeding

B. Decreased bleeding

C. Increased clotting

D. Decreased clotting

E. Increased PT time

A

A, D, E

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28
Q

T/F Fluidity is determined by the balance of coagulation and fibrinolysis

A

T

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29
Q

A clot that forms naturally in the body is known as a ______. When it is dislodged and begins flowing through the vasculature it is knonwn as a ______. When it lodges itself in a vessel and blocks blood supply it is known as an________

A. Embolism, Thrombus, Embolus

B. Thrombus, Embolism, Embolus

C. Thrombus, Embolus, Embolism

D. Embolism, Embolus, Thrombus

A

C

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30
Q

Heart attacks are usually caused by an embolus coming from the ______

A. Arterial side

B. Venous side

A

B

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31
Q

Strokes are usually caused by an embolus coming from the ________

A. Arterial side

B. Venous side.

A

A

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32
Q

In what ways can we manipulate the coagulation and fibrinolytic systems of our body?

A. Promote Clotting

B. Prevent Clotting

C. Promote Clot breakdown

D. All of the above

A

D

However for the sake of preventing clotting we are mostly focused on B and C

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33
Q

An inactive factor such as VII is known as a ___ while the ACTIVE factor is known as a _____

A. Protease, Zymogen

B. Zymogen, Protease

A

B

34
Q

What protease is responsible for converting the zymogen X into Xa?

A. VII

B. II

C. IIa

D. VIIa

A

D

35
Q

Which zymogen connects the extrinsic and intrinsic pathways into the common pathway?

A. VII

B. X

C. XII

D. IX

A

B

36
Q

What drug is responsible for preventing a white clot from forming (stopping platelet aggregation)?

A. Clopidogrel

B. Dabigatran

C. Rivaroxaban

D. Warfarin

A

A

White clots are made by connecting platelets with fibrinogen . Therefore the other drugs that affect the factors such as Xa and IIa will only affect the red clot formation. Clopidogrel is the only one that actually stops the activation of the platelets, thus preventing the white clots from forming.

37
Q

What is the first step in beginning platelet aggregation?

A. Release of TxA2 and ADP from platelets.

B. Endothelial damage and release of TF which then binds to platelets

C. Binding of Fibrinogen to platelets

D. Intracellular calcium increase within platelets.

E. Platelet shape change

A

B.

Tissue Factors (TF) is required to bind to platelets in order to begin the process of increasing intracellular calcium levels. This leads to the release of ADP and TxA2 along with a change in platelet shape. In other words these processes must come after TF has been released from endothelial cell damage.

38
Q

What active protease is responsible from converting prothrombin (II) to the active protease thrombin (IIa)?

A. X

B. Xa

C. VII

D. Plasminogen

A

B

39
Q

What is the function of the active protease thrombin (IIa)? (select all)

A. Conversion of fibrinogen to fibrin

B. Forming the white clot

C. Forming the red clot

D. Activating the cofactors VIII and V to VIIIa and Va

E. Breakdown of the red clot

A

A, C, D

40
Q

The intrinsic pathway includes all of the following factors: (Select All)

A. VII

B. IX

C. X

D. XII

E. VIIa

F XI

A

B, C, D, F

41
Q

What active protease from the intrinsic pathway causes the conversion of X to Xa?

A. IXa

B. IX

C. XIa

D. XII

E. XIIa

A

A

42
Q

What is the functions of proteins C and S? (select all)

A. Inhibit active protease VIIIa

B. Inhibit active protease VIIa

C. Inhibit active protease Va

D. Inhibit inactive zymogen VIII

E. Inhibit Inactive zymogen V

A

A, C

43
Q

What is the MOA of Heparin?

A. Increase rate of thrombin-antithrombin reactions (binding) in order to inactivate thrombin and Xa.

B. Directly binds to Xa and IIa and inhibits their actions

C. None of the above

A

A

heparin will bind to thrombin and cause a conformational change that binds to antithrombin more easily. Thus increasing the rate of thrombin-antithrombin reactions.

44
Q

What is Pro-thrombin (PT) time? And what pathway does it measure?

A. Intrinsic pathway

B. Extrinsic pathway

A

Its the amount of time it takes the blood to clot. Larger PT times means it takes the blood a longer period of time to clot. It measures the

B.

45
Q

What is PTT? What pathway does it measure?

A. Intrinsic Pathway

B. Extrinsic Pathway

A

PTT stands for Partial Thromboplastin Time. It is similar to PT time in the sense that it also measures the time it takes for the blood to clot. The difference is that it is a measure of the INTRINSIC pathway while PT time is a measure of the EXTRINSIC pathway.

A. Intrinsic Pathway

46
Q

Anticoagulant medications such as Warfarin will increase: (select all)

A. PT time

B. Clot formation

C. Bleeding Time

D. Bleed risk

A

A, C, D

47
Q

Anticoagulant medications such as Heparin will cause an increase in:

A. PTT

B. The amount of time it takes to form clots

C. Clot formation

D. Bleeding time

E. Bleed Risk

A

A, C, D, E

48
Q

What does warfarin block?

A. VII

B. VIIa

C. X

D. IX

E, II

F. Proteins C and S

A

A, C, D, E, F

49
Q

Heparin acts on _____factors circulating in the blood while Warfarin acts on _____ factors circulating in the blood.

A. Inactive, Active

B. Inactive, Inactive

C, Active, Active

D. Active, Inactive

A

D

50
Q

What is Heparin Associated Thrombocytopenia (HAT)?

A

It is a condition that has three main characteristics:

  1. Fall in platelet count less than 150,000
  2. NOT IMMUNE MEDIATED
  3. Drop in platelet count can cause bleeding and hemorrhage. (Opposite effect of HIT)
51
Q

What is Heparin-Induced Thrombocytopenia (HIT)?

A

It is a condition that is defined by three main characteristics:

  1. Leads to Platelet Aggregation
  2. THIS IS ANTIBODY MEDIATED (IgG)
  3. Produces exact OPPOSITE effect of HAT
52
Q

What is the antidote for Heparin overdoses?

A. NAC

B. Protamine Sulfate

C. Vitamin K

D. Vitamin B

A

B

53
Q

What is the advantage of Low molecular weight heparin such as Enoxaparin in comparison to Heparin?

A. Lower incidence of HIT and HAT

B. More selective to Xa so it has less side-effects

C. Lower incidence of bleeding

D. All of the above

A

D

54
Q

What is the difference between Fondaparinux and Enoxaparin?

A. Fondaparinux only has affinity for IIa receptors

B. Enoxaparin has a higher affinity for Xa than Fondaparinux

C. Fondaparinux only has affinity for Xa receptors

D. Enoxaparin has equal affinity for the IIa and Xa receptors while Fondaparinux only has affinity for Xa receptors

A

C

55
Q

What are the advantages dabigatran has over warfarin and other anticoagulants?

A. Does not need an INR

B. No injections

C. No drug-food DDI

D. All of the above

A

D

56
Q

What is the difference between Dabigatran and the other thrombin inhibitors? (select all)

A. Dabigatran is an oral medication

B. Dabigatran can also bind to Xa

C. Dabigatran requires INR

D. Other direct thrombin inhibitors (Lepirudin, Bivalirudin, Argatroban) are given parenterally

A

A, D

57
Q

What makes Lepirudin different than Bivalirudin and Argatroban?

A. Lepirudin binds irreversibly

B.

A
58
Q

With initial doses of warfarin what will you see?

A. Rapid decrease in coagulation

B. Initial increase in coagulation due to blocking Proteins C and S

C. Increases vitamin K epoxide synthesis

D. None of the above

A

B

59
Q

What form of vitamin K is required to activate factors VII, IX, X and II?

A. Vitamin K (epoxide)

B. Vitamin K (oxidized)

C. Vitamin K (reduced)

D. VItamin K

A

C

60
Q

What are the two primary reasons warfarin is given with heparin when first beginning warfarin treatment (known as bridging)?

A. Warfarin takes a long period of time to start working

B. Heparin can override the initial clotting effect of warfarin (since warfarin blocks proteins C and S)

C. Both and A and B

A

C

61
Q

What is the antidote given for warfarin overdoses?

A. Protamine sulfate

B. Vitamin K

C. NAC

D. Rifampin

A

B

62
Q

Warfarin acts_____ because it affects the ______ of factors wheras Heparin acts _____ because it inactivates active protease factors already in circulation.

A. Quickly, synthesis, slowly

B. Slowly, synthesis, rapidly

C. Slowly, synthesis, slowly

D. Rapidly, synthesis, Rapidly

A

B

63
Q

What effects do the drugs Clopidogrel and Aspirin have in common?

A. Both are antiplatelet medications

B. Both interfere with platelet aggregation

C. Both increase decrease calcium levels

D. A and B only

E. A and C only

A

D

64
Q

Under normal conditions ADP binds to which receptors? (Select All)

A. GPIIb/IIIa receptors

B. P2Y12 receptors

C. TxA2 receptors

D. P2Y1 receptors

A

B, D

65
Q

What signals are needed to activate platelets?

A. Decrease in intracellular cAMP levels

B. Increase in intracellular Ca2+ levels

C. Increase in intracellular cAMP levels

D. Decrease in intracellular Ca2+ levels

E. Formation of TxA2

F. Tissue Factor (TF)

A

A, B, E, F

66
Q

Which receptor is responsible for decreasing intracellular cAMP levels in platelets?

A. P2Y1 coupled to Gq

B. P2Y12 coupled to Gi

C. GPIIb/IIIa

D. TxA2 Receptor

A

A

67
Q

Which recetpros are responsible for increasing intracellular calcium levels in platelets? (select all)

A. TxA2 coupled to Gq

B. TxA2 coupled to Gi

C. P2Y12 coupled to Gi

D. P2Y1 coupled to Gq

E. P2Y1 coupled to Gi

A

A,D

68
Q

What are the contraindications with giving aspirin?

A. Bleeding Disorders

B. Hypersensitivity reactions to aspirin

C. Reye’s syndrome

D. All of the above

A

D

69
Q

What are the effects of giving clopidogrel on platelet cells?

A. Prevention of platelet aggregation

B. Increase in cAMP

C. Decrease in cAMP

D. Platelet shape change and aggregation

E. A and B

F. C and D

A

E

70
Q

Which of the following P2Y12 inhibitors are irreversible?

A Ticagrelor

B. Clopidogrel

C. Ticlopidine

D. Cangrelor

E. Prasugrel

A

B, C, E

71
Q

What does Clopidogrel and Dipyridamole have in common?

A. Both increase levels of cAMP through different mechanisms.

B. Both decrease intracellular calcium

C. Both interfere with platelet aggregation

D. Both prevent formation of red clots

E. A and C

A

E

72
Q

What is the major metabolizing enzyme that activates the prodrug clopidogrel?

A. CYP2C19

B. CYP2C9

C. CYP3A4

D. CYP3A5

A

A

73
Q

Which of the following facts is true about clopidogrel?

A. Its activation is affected by CYP2C19 polymophisms

B. It is a prodrug

C. Has DDIs with PPIs

D. All of the above

A

D

74
Q

What is the MAJOR side effect of Ticlopidine?

A. Low GI motility

B. Constipation

C. Coagulation

D. Fatal Agranulocytosis

A

D

75
Q

Ticagrelor and Cangrelor are known as ____ P2Y12 antagonists

A. Reversible

B. Irreversible

A

A

76
Q

Why does the antiplatelet Dipyridamole have a chance at causing angina?

A. Causes vasoconstriction at the arterioles

B. Can possibly cause an increase in cAMP levels in cardiac cells, leading to an increase in contraction strength and heart rate.

C. Causes vasodilation in coronary arteries, leading to less blood supply to the heart

A

B

77
Q

Platelet Aggregation is mediated by _____ causing a crosslink with between many platelets

A. Fibrin

B. Fibrinogen

A

B

Fibrinogen is needed to start aggregation. Fibrin is only a stronger form that causes a red clot.

78
Q

Which of these drugs are GPIIb/IIIa antagonists?

A. Rivaroxaban

B. Eptifibatide

C. Tirofiban

D. Enoxaparin

E. Clopidogrel

F. Abciximab

A

B, C, F

79
Q

What natural factors in the body keep t-PA from converting plasminogen to plasmin?

A. Antiplasmin

B. Vitamin K reduced

C. PAI-1 and PAI-2

D. A and C

A

D

80
Q

What natural factor do the fibrinolytic drugs resemble?

A. Antiplasmin

B. PAI-1 and PAI-2

C. t-PA

D. Plasminogen

A

C

81
Q

T/F Urokinase and Streptokinase are knonwn to not be clot-specific while Alteplase abd Reteplase are clot-specific

A

T

82
Q

What is the antidote for Fibrinolytic drug overdoses?

A. Vitamin K

B. Protamine sulfate

C. Aminocaproic Acid

D. NAC

A

C

PCOL Cardio Questions (4 decks)

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