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Pathophysiology 1 > Jan 12 - Coronary Heart Disease Part 2 > Flashcards

Jan 12 - Coronary Heart Disease Part 2 Flashcards

1
Q

Name the 8 steps of progression to acute coronary syndromes (ACS)

A
  1. Destabilization of atherosclerotic plaque (fibrous cap ruptured) due to shearing forces of blood flow
  2. Endothelial lining is disrupted - collagen is exposed triggering platelets to repair the injured vessel
  3. Platelets adhere to the exposed collagen, and change their shape or activate in response to binding GPIb to von Willebrand factor
  4. After activating, the platelets release thromboxane A2, adenosine diphosphate and other prothrombotic substances
  5. The ADP released binds to P2Y12 receptors on the platelets which activates another receptor (GP IIb/IIIa) on the platelet
  6. With the activation of the GP IIb/IIIa receptor, neighbouring platelets can crosslink fibrinogen as part of the clotting cascade
  7. More platelets aggregate due to more TxA2, serotonin, thrombin and epinephrine released from activated platelets
  8. Fibrinogen converted to fibrin using thrombin (clotting cascade)
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2
Q

Name 5 different groups of drugs used in ACS

A 
Aspirin
Eptifibatide, abciximab, tirofiban
Alteplase or tenectiplase
Clopidogrel, ticagrelor
Heparin or low molecular weight heparins (enoxaparin)
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3
Q

What is the mechanism of action of aspirin?

A

It is a thromboxane A2 inhibitor (prevents sticky platelets; blood thinner)

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4
Q

What is the mechanism of action of eptifibatide, abciximab and tirofiban?

A

GP IIb/IIIa inhibitor (occupies receptor so fibrin crosslink cannot occur)

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5
Q

What is the mechanism of action of alteplase or tenectiplase?

A

Fibrinolytic (breaks fibrin clots)

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6
Q

What is the mechanism of action clopidogrel and ticagrelor?

A

Blocks the P2Y12 receptor (therefore GP IIb/IIIa is not activated)

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7
Q

What is the mechanism of action of heparin and low molecular weight heparin (enoxaparin)?

A

Disrupts clotting cascade (heparin factors IX, X, XI, XII, inactivates thrombin) and LMWH (anti-Xa activity)

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8
Q

What are the two types of clots?

A

White clots and red clots

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9
Q

Describe white clots

A

There are more platelets than fibrin
There is an incomplete artery occlusion
It’s more common in NSTEMI

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10
Q

Describe red clots

A

There are more fibrin than platelets
There is usually a complete artery occlusion
It’s more common in STEMI

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11
Q

How can you differentiate stable angina from acute coronary syndrome?

A

Stable angina resolves with rest and lasts a short duration

Acute coronary syndromes do not resolve with rest, the pain is severe and they last a long duration.

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12
Q

How can you differentiate STEMI from NSTEMI/Unstable angina?

A

Via a 12-lead ECG. ST-segment elevation indicates STEMI. ST-segement depression and/or T-wave inversion indicates NSTEMI/Unstable angina

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13
Q

How can you differentiate between NSTEMI and unstable angina?

A

Do a blood test for troponin T and creatine kinase. Elevated levels of troponin T indicate necrosis (NSTEMI). Normal levels of troponin T indicate unstable angina

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14
Q

How many leads are their in a 12-lead ECG?

A

4 limb-leads and 6-precordial leads

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15
Q

Why is a 12-lead ECG named so?

A

10 leads + heart (technically a lead) = 12 pieces of information

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16
Q

What do the 12 leads do?

A

They give you information to tell you what areas of the heart may be affected; each one takes a different picture of the heart

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17
Q

What does lead II do?

A

It looks from the right leg to the right arm. It looks at the bottom of the heart (the apex). It’s also known as the sinus rhythm. It follows the correct direction that electricity travels

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18
Q

What does lead I do?

A

It looks from the left arm to the right arm. It looks across the heart at the left side

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19
Q

What does lead III do?

A

It looks from the left leg to the left arm

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20
Q

What does the aVL do?

A

It looks diagonally into the left side of the heart

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21
Q

What does the aVR do?

A

It looks at the right side of the heart

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22
Q

What does the aVF do?

A

It looks from the feet up at the bottom side of the heart

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23
Q

What do V1 and V2 do?

A

They look at the septum of the heart (the centre of the heart)

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24
Q

What do V3 and V4 do?

A

They look at the anterior part of the left ventricle

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25
Q

What do V5 and V6 do?

A

They look at the lateral side of the heart

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26
Q

What side of the heart is hard to “see” with a 12-lead ECG?

A

The posterior of the heart

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27
Q

Which leads look at the lateral side of the heart?

A

Lead I, aVL, V5 and V6

28
Q

Which leads look at the inferior wall?

A

Lead II, lead III and aVF

29
Q

Which lead looks at the right atria?

A

aVR

30
Q

Which leads look at the septum of the heart (septal leads)?

A

V1 and V2

31
Q

Which leads look at the anterior left ventricle?

A

V3 and V4 (and V2 a little bit)

32
Q

Why is the 12-lead ECG so important?

A

If you see these changes in a certain lead (ST elevation, T-wave inversion, ST depression), you can determine the area of the heart that is ischemic/dying

33
Q

What is troponin? How many types are there? Which type(s) come from the heart?

A

Troponin is a protein. There are three types of troponin: troponin C, I and T. Troponin I and T come from the heart.

34
Q

What is the importance of troponin?

A

Elevated levels of troponin T implies that there is tissue damage in the heart (NSTEMI)

35
Q

What is creatine kinase?

A

It is a protein that is important for transferring high energy phosphates to the muscles so they are able to work harder

36
Q

What is the importance of creatine kinase with regards to cardiology?

A

The creatine kinase specific to the heart is the myocardial band. It can also be used as a marker for a heart attack (not as much anymore; it’s not as sensitive as troponin T)

37
Q

Why do patients have to get blood work done every six hours?

A

It can take 1-2 days for troponin T levels to be at its peak; blood levels might be normal at earlier stages

38
Q

What are the steps for treating acute coronary syndromes?

A
  1. Percutaneous coronary intervention - go in and yank the clot out
  2. Fibrinolytics - break up the clot (especially if it’s a red clot)
  3. Medical management - if there is a partial occlusion, the clot can be left alone, use drug intervention and hope it goes away on its own
  4. Coronary artery bypass graph - worst case scenario
39
Q

What should be done if a patient is experiencing symptoms of ACS?

A

MONA

Morphine, oxygen, nitrates, aspirin

40
Q

What is the importance of morphine (MONA)?

A

It is given for pain and it diverts the blood away from the middle of the body (which takes the burden of the heart)

41
Q

What is the importance of oxygen (MONA)?

A

Oxygen is for shortness of breath (SOB) and to get oxygen to the tissues (which helps with chest pain)

42
Q

What is the importance of nitrates (MONA)?

A

Nitrates are for vasodilation and preload

43
Q

What is the importance of aspirin (MONA)?

A

It makes the platelets less sticky

44
Q

What follows MONA?

A

A 12-lead ECG to determine if there is ST-elevation, ST-depression or T-wave inversion

45
Q

After determining that the patient is experiencing a STEMI, what’s the next step?

A

Is there access to the cath lab? If yes, do an angiogram followed by PCI, stent, CABG. If not, give fibrinolytics (alteplase, tenecteplase) and do an angiogram once access to the cath lab is gained followed by PCI, stent, CABG

46
Q

After determining that the patient is experiencing an NSTEMI/UA, what is the next step?

A

Check troponin T and CK levels to decipher between NSTEMI and UA

47
Q

What follows measuring troponin T and CK levels in the case of NSTEMI/UA?

A

Determine the risk of death or ischemic events using the TIMI risk score. A risk score of 2 or below indicates conservative therapeutic options (drug intervention - heparin/LMWH, clopidogrel, GP IIa/IIIb aka eptifibatide). A risk score of 3 or above requires invasive therapy (angiogram followed by PCI, stent, CABG)

48
Q

How is the TIMI risk score determined?

A

One point is awarded for each of the following:
Age 65 or older
3 or more of the following heart disease risk factors: smoking, hypercholesterolemia, hypertension, diabetes, family history of premature CV events/death
Known coronary artery disease (50% or over stenosis)
ASA use in past 7 days
2 or more episodes of chest discomfort in the past 24 hours
ST-segment depression of 0.5 mm or more (on ECG)
Positive biochemical marker for infarction

49
Q

What is considered low risk by TIMI?

A

0-2 points; 0 to 8.3% risk of death/MI or severe ischemia

50
Q

What is considered moderate risk by TIMI?

A

3 to 4 points; 13.2 to 19.9% risk of death/MI or severe ischemia

51
Q

What is considered high risk by TIMI?

A

5 to 7 points; 26.2 to 40.9% risk of death/MI or severe ischemia

52
Q

How is an angiography performed?

A

A catheter is inserted through an artery in the forearm, thigh, upper groin or neck and threaded to the coronary artery in question. A dye is released, allowing for X-rays to illuminate the arteries and show areas of poor blood flow

53
Q

What is the most common place to insert a catheter during an angiogram?

A

Femoral artery

54
Q

What is PCI?

A

Percutanous coronary intervention aka angioplasty/stenting

55
Q

Explain how PCI works

A

A tiny catheter runs from the femoral artery (or jugular vein depending on the side of the heart) to the affected area. A balloon at the tip squashes the athersclerotic plaque and holds the artery open. A bare-metal or drug eluting stent (looks like chicken wire) is placed, like a little cage to keep the artery open

56
Q

Why is PCI dangerous?

A

The ballon could cause the clot or parts of the clot to break off

57
Q

Describe the steps of coronary revascularization (bypass)

A

Harvest a blood vessel (great saphenous vein, left internal mammary artery (LIMA))
Sew one end of the vessel above the blocked coronary artery and one end below “by-passing” the blockage to restore blood flow.
The number of blockages determine how many bypasses need to be done (i.e. triple, quadruple, quintuple)

58
Q

What is the mechanism and the goal of morphine?

A

It takes the blood away to provide pain relief

59
Q

What is the mechanism and the goal of nitrates?

A

Venous vasodilation to provide ischemic relief

60
Q

What is the mechanism and goal do the aspirin?

A

It makes platelets not sticky (thromboxane A2 inhibitor) to prevent clotting

61
Q

What is the mechanism and goal of beta-blockers?

A

They block beta-1 receptors in the heart to provide ischemic relief

62
Q

What is the mechanism and goal of thienopyridines?

A

They block P2Y12 receptors to prevent clotting

63
Q

What is the goal of GP IIb/IIIa inhibitors?

A

Prevent clotting

64
Q

What is the mechanism and goal of heparin?

A

Inhibits factors IX, X, XI and XII to prevent clotting

65
Q

What is the mechanism and the goal of fibrinolytics?

A

Breaks up fibrin to break up clots

66
Q

What is the mechanism and the goal of statins?

A

They stop cholesterol synthesis pathway to lower cholesterol. They are only administered once the patient is stable

67
Q

What is the mechanism and the goal of ACEIs?

A

They are angiotensin converting enzyme inhibitors; they stop the conversion of angiotensin 1 into angiotensin 2 so the blood pressure can’t increase. This controls blood pressure and prevents future events. These drugs are only administered once the patient is stable

Pathophysiology 1 (11 decks)

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