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Exam 1 Year 3 > Coronary Heart Disease > Flashcards

Coronary Heart Disease Flashcards

1
Q

What thromboembolic diseases are arterial?

A

Acute Myocardial Infarction (AMI)
Transient Ischaemic attacks (TIA’s)
Cerebral Vascular infarcts / accidents (CVA’s)

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2
Q

What thromboembolic diseases are venous?

A

DVT
PE

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3
Q

What causes arterial thrombosis?

A

Ruptured atherosclerotic plaques

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4
Q

What causes venous thrombosis?

A

Often occurs in normal vessels, majority deep vein of the leg

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5
Q

What type of thrombi causes arterial thrombosis?

A

White

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6
Q

What type of thrombi causes venous thrombosis?

A

Red - fibrin rich!

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7
Q

What is CHD?

A

CHD is a condition in which the vascular supply to the heart is impeded by atheroma thrombosis or spasm

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8
Q

What is atheroma?

A

Fatty plaques on blood vessel

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9
Q

What can an inadequate blood supply to the heart cause?

A

Ischaemic chest pain
-Stable angina
-Acute Coronary Syndrome (ACS)
-Sudden death

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10
Q

Who is more susceptible to CHD?

A

Males - until women reach the menopause! Risk increases with age

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11
Q

Atherosclerosis is caused by?

A

*Complex inflammatory process initiated due to injury or dysfunction of the endothelium
*Increases permeability to oxidised lipoproteins, macrophages and then lipid-laden foam cells cause fatty-streaks
*Smooth muscle cells secrete collagen proteoglycans, elastin and glycoproteins
*Fibrous cap forms plaque
*Narrowing of blood vessels and decreases blood flow
*Plaque ruptures and a clot is formed

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12
Q

Where can the fatty streaks be seen?

A

Endothelium - microscopic

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13
Q

What are the risk factors of CHD?

A

Age, Gender, Family history, Smoking, Diet, Obesity, HTN, Hyperlipidaemia, DM, Sedentary lifestyle, Ethnicity, Alcohol, Stress

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14
Q

What group of people have a 45% increased chance of having CHD?

A

S.Asians

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15
Q

What group of people have a 50% less chance of death from CHD?

A

Black African Caribbean

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16
Q

If a patient has a QRISK of >10% what should they be initiated on for primary prevention?

A

Statins!

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17
Q

What is the pathophysiology of CHD in regards to O2 demand?

A

-HR, contractility, & systolic wall tension

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18
Q

What is the pathophysiology of CHD in regards to O2 demand?

A

-Coronary blood flow and O2 carrying capacity of blood

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19
Q

What induces stable angina?

A

Exercise

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20
Q

When the coronary arteries narrow due to atheromatous plaques, this reduces blood supply, therefore when there is an excess oxygen demand for the heart increases, what happens?

A

*Chest pain caused by exercise, stress, heavy meals or extremes of temperature

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21
Q

What can be given to relieve stable angina?

A

Rest or S/L GTN

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22
Q

‘Demand ischaemia’ is a name for?

A

Stable Angina

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23
Q

Narrowed coronary arteries unable to meet the increased oxygen demand during exercise and stress is known as?

A

Stable Angina

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24
Q

If a patient has central crushing chest pain which can radiate to the jaw, neck or arms, this could be?

A

Stable angina

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25
Q

If a patient describes the chest pain as constricting, choking, heavy weight, stabbing, burning, like a knife or elephant on the chest, what could this be?

A

Stable angina

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26
Q

With what type of angina is there a lack of ECG/cardiac enzyme changes, such as troponin?

A

Stable angina

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27
Q

What is first line for Stable Angina?

A

B-blockers or CCB

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28
Q

What is ‘add on’ therapy for Stable Angina?

A

Long acting nitrate (isosorbide), Ivabradine, Ranolazine, or Nicorandil

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29
Q

What is secondary prevention for a patient with stable angina?

A

*Lifestyle changes
*Antiplatelet (aspirin 75mg OD)
*Atorvastatin 20mg

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30
Q

What is given for symptom control for Stable Angina?

A

S/L GTN

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31
Q

What is ACS?

A

Acute Coronary Syndrome

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32
Q

What medical issues class as having ACS?

A

*Myocardial Infarction (MI)
*ST Elevated MI (STEMI)
*Non-ST elevated MI (NSTEMI)
*Unstable Angina (Troponin Positive ACS

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33
Q

What signs/symptoms could indicate a differential diagnosis?

A

-History of ischaemic chest pain (type of pain/is it indigestion)
-ECG Changes
-Cardiac Enzymes increasing

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34
Q

Where is an ECG elevated in someone with a STEMI?

A

ST Elevation

35
Q

What conditions is ST elevation NOT seen in?

A

NSTEMI and Unstable Angina

36
Q

If an ECG has T wave inversion/ST segment depression or changes in the Q wave, what could this represent?

A

NSTEMI

37
Q

If a patient has Left Bundle Branch Block (LBBB), what condition is this associated with?

A

STEMI

38
Q

What are the Cardiac Enzymes?

A

Troponin T and Troponin I (Trop I)

39
Q

When is Troponin released?

A

2-4 hours after, peaks at 12 hours and can persist up to 7 days (can aid in a late diagnosis)

40
Q

When do you get your Standard Troponin repeat measured?

A

Repeat after 10-12 hours

41
Q

Why do you get high sensitivity troponin assay repeated every 3 hours?

A

To rule out NSTEMI, if not raised NSTEMI can be ruled out

42
Q

When there is some change in Troponin levels but not enough for the patient to be having an MI what is this classed as?

A

MI

43
Q

Pt X Troponin levels comes back as less than <0.4ng/ml, what does this rule out?

A

ACS is unlikely

44
Q

What are other causes of increased Troponin levels?

A

PE, HF, Myocarditis, CKD, Sepsis

45
Q

What are the three enzymes which rise during a STEMI / NSTEMI but aren’t specific enough to be used alone to diagnose?

A

Creatine Kinase (CK) Aspartate Transaminase (AST)
Lactate dehydrogenase (LDH)

46
Q

When would you expect Creatine Kinase (CK) to rise during a STEMI / NSTEMI?

A

*Peaks within 24 hours
-Will be normal within 48 hours

47
Q

When would you expect Aspartate Transaminase (AST) and Lactate Dehydrogenase (LDH) to peak during a NSTEMI or STEMI?

A

LDH peaks 3-4 days and remains increased for up to 10 days, - can be useful in late presentations

48
Q

What happens during a Myocardial Infarction?

A

1) Thrombosis forms at site of rupture of atheromatous plaque = blood clot formation
2) Severe and prolonged ischaemia
3) Death of cardiac muscle cells -> release of enzymes (Troponin) from cells

49
Q

How much of the heart muscle does a STEMI damage?

A

Full thickness of all cardiac muscle

50
Q

How much of the heart muscle does a NSTEMI damage?

A

Damage to partial thickness of cardiac muscle
-Partial

51
Q

What is the pathophysiology and a Myocardial Infarction and Unstable Angina?

A

*Supply ischaemia vs demand ischaemia of stable angina
*Decrease coronary blood flow and a decrease in oxygen supply due to thrombus formation
*Partial blockage in UA
*Complete blockage in STEMI/NSTEMI
*Thrombus forms as a result of plaque rupture and activation ad aggregation of platelets

52
Q

Pt D has severe chest pain with a sudden onset, often at rest and constant constricting pain which has not been relieved by rest or GTN spray, Pt also appears to be sweaty, breathless, feels sick, restless and is pale, with a grey tinge, what would you diagnose this patient with?

A

STEMI/NSTEMI

53
Q

What type of people are more at risk of a silent MI?

A

Elderly and DM

54
Q

What percent of Acute Myocardial Infarctions have no symptoms?

A

20%

55
Q

Pt A has had a sudden deterioration in angina symptoms, this is happening at risk and is not relived by s/l GTN, there is no ECG change, but a small increase in Troponin, what is this patients diagnosis?

A

Unstable Angina

56
Q

Pt Q has ST elevation what is this?

A

ST elevation MI
STEMI

57
Q

How do you manage a STEMI acutely?

A

-Pain relief
-Thrombolysis/reperfusion
-Minimisation of infarct size

58
Q

How do you manage a STEMI/NSTEMI/Unstable Angina immediately?

A

*Oxygen to relieve ischaemia
*Diamorphine - pain relief, opens blood vessels
*Aspirin 300mg STAT
*Antiplatelet - Clopidogrel 300mg STAT or 180mg Ticagrelor STAT or 60mg Prasugrel STAT

59
Q

What is the Golden First line treatment for a STEMI?

A

PPCI (surgery)
Primary Percutaneous Coronary Intervention

60
Q

If a patient can not have PPCI for a STEMI, what is offered next?

A

-Thrombolysis (break clot)
-Reperfusion - limit damage
-Steptokinase, Alteplase, Tenecteplase, Reteplase

61
Q

What is the ‘call to needle time’ with a STEMI?

A

1 hour

62
Q

What is the ‘door to needle time’ with a STEMI?

A

30 mins

63
Q

What is contraindicated to thrombolysis medications?

A

CVA, recent surgery, peptic ulcer, uncontrolled HTN, more than 6 hours since symptoms started!

64
Q

What are the side effects of Thrombolysis?

A

Haemorrhage, stroke, reperfusion arrythmias, allergy

65
Q

Why can you have an allergy to Streptokinase? (SK)

A

It is allergenic

66
Q

When is Heparin given during a STEMI?

A

For the first 48 hours after thrombolysis, to prevent a further clot!

67
Q

What side effects can thrombolysis for a STEMI cause?

A

Arrythmias
Heart failure

68
Q

What is the Gold Standard secondary prevention for a patient who has had a STEMI?

A

5 Drugs when they leave the hospital
-Antiplatelets
1) Aspirin
2) Clopidogrel, ticagrelor, prasugrel
3) Beta-blocker
4) ACEi ‘prils’
5) Atorvastatin 80mg OD

69
Q

What is given to a patient who is having a NSTEMI / Unstable Angina?

A

Fondaparinux - until stable

70
Q

What is Fondaparinux?

A

10a Inhibitor - injection

71
Q

What must NOT be given in a NSTEMI/Unstable angina?

A

No Thrombolysis or PPCI

72
Q

What happens after a patient has had the inital treatment?

A

1) Further investigations to predict 6 month risk of mortality / further cv event chance
2) Use GRACE scoring system

73
Q

If GRACE system identifies pt at Intermediate / higher risk >3% what is the next treatment?

A

Angio and PCI

74
Q

If the GRACE system identifies pt as low risk, <3% what is the next treatment?

A

Conservative management

75
Q

What is the Gold Standard secondary prevention for a patient who has had a NSTEMI / Unstable Angina?

A

-Antiplatelets
1) Aspirin
2) Clopidogrel, ticagrelor, prasugrel
3) Beta-blocker
4) ACEi ‘prils’
5) Atorvastatin 80mg OD

76
Q

What is the procedure called when a catheter is put into the coronary circuclation through wrist or groin, with Xray contrast, this is done to observe the severity of the narrowing due to the plaque?

A

Angiography

77
Q

What type of surgery is a CABG?

A

Coronary Artery By-pass Graft - open heart surgery

78
Q

When a balloon is mounted on the tip of a very thin catheter is then inserted through obstruction and inflated,, and often needs restenosis what is this procedure called?

A

Angioplasty

79
Q

When a wire mesh is inserted with a balloon to keep a stenosis open what is this called?

A

Stenosis

80
Q

Why is long term Aspirin and 12 months of clopidogrel / ticagrelor / Prasugel given to a patient with a stent?

A

Both angioplasty and stents can damage vessel wall and this increases the clotting (in-stent thrombosis)
-Therefore these agents are given to prevent in stent clotting - lower chance of getting a stent in the clot!

81
Q

What is the benefit of having a drug eluting balloon, which is covered in a proliferative drug?

A

The drug is lipophilic and absorbed into the vessel wall, this reduces the chance of restenosis and there is no issues with in stent thrombosis

82
Q

When is a primary PCI used?

A

Alternative treatment for STEMI instead of thrombolysis
Better outcomes and less people contraindicated compared to thrombolysis
-Clot is removed during procedure

83
Q

What is the call to balloon time for a primary PCI?

A

120 min

84
Q

What is the door to balloon time for a primary PCI?

A

30 mins

Exam 1 Year 3 (40 decks)

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