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Pharmacotherapeutics Theory 1 > CHD CUE CARDS > Flashcards

CHD CUE CARDS Flashcards

1
Q

What is cadiac ischaemia?

A

Refers to the lack of blood flow and oxygen to heart muscle

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2
Q

What are the causes of cardiac ischaemia?

A

> Atherosclerosis and thrombosis (stable angina, ACS)

> Vasospasm (variant angina [prinzmetals])

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3
Q

What is angina?

A

> Angina is the crushing/squeezing/burning chest pain or diffuse discomfort that can radiate to shoulders, down arms, to throat, jaw or back

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4
Q

What is the difference between stable angina and variant angina?

A

> Stable angina is inadequate blood supply for myocardial demand due to atherosclerotic narrowing of coronary artery
Variant angina is caused by the constriction of blood flow due to intense coronary artery spasm (not associated with atherosclerosis)

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5
Q

What are the symptoms of Coronary Ischaemia?

A

> Pain (squeezing, tightness): radiating from chest, brought on by exertion, may be relieved by rest
Other ‘anginal equivalent’ symptoms: SOB, weakness, nausea, sweating
‘Silent Ischaemia’: no symptoms present (e.g. poorly controlled diabetes - problems with nerve function - don’t feel events)

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6
Q

When is stable angina diagnosed?

A

For at least the past month, angina has been precipitated by the same amount of exertion

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7
Q

How is stable angina diagnosed?

A

> Clinical Hx: symptoms, medical, family, lifestyle hx

> Investigations: BP, ECG, stress test, coronary angiogram, blood tests, chest xray

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8
Q

How is stable angina managed? What are the aims of this management?

A

> Management by pharmacotherapy or surgical revascularisation procedures

> Aims are to: Relieve acute attacks, prevent acute attacks (by improving exercise tolerance, symptoms rapid in onset but predictable) and improving prognosis (slowing progression of atherosclerosis and preventing progression to ACS)

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9
Q

What are the treatment principles of stable angina? (in terms of supply vs. demand)

A

> Treat or prevent symptoms
Slow progression of CHD
Supply: reduce atherosclerosis and increase vessel diameter
Demand: reduce HR, reduce myocardial contractility

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10
Q

Discuss TE prevention in terms of stable angina to improve the prognosis

A

> Patients are at high CV (stable angina) and more likely to go on to have MI
Beyond 12 month period: aspirin (or clopidogrel if intolerant)
To prevent further CV events: antiplatelet drug used because events are in coronary arteries (high shear) - rupture of plaque - initial factor that triggers these events is platelet activation

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11
Q

In terms of TE prevention, although antiplatelets are used, justify the use of potentially anticoagulants

A

> Coagulation pathways all feedback together eventually and clotting factors become involved as the clot forms and enlarges - so can justify potential benefit of anticoagulants such as rivaroxaban (much lower dose) because balancing benefit of preventing an atherosclerotic event/CV event with risk of bleeding

> Targeting at high risk group where you’re more likely to see benefit

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12
Q

Discuss secondary prevention in stable angina (LLT)

A

> Drug therapy is important for lowering lipid levels
Need to aim for targets as increased CV risk already
Initiate and continue indefinitely, the highest tolerated dose of statin (maximise dose as they tolerate - if not reaching target + ezetimibe)

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13
Q

Discuss secondary prevention in stable angina (BP targets)

A

> Not preventing this group from having first event, these people have symptomatic CVD
More intense treatment - aiming to a target of <120mmHg
Higher doses of antihypertensives and more combinations - Increase risk of S/Es but can justify this risk to prevent them from getting heart attack

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14
Q

What are the types of planned revascularisation?

What are they used for?

A

> Percutaneous Coronary Intervention (PCI) (stent insertion)
Coronary Artery Bypass Graft

> They are used to open narrow or blocked coronary arteries

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15
Q

What is CABG?

A

> A healthy artery or vein from the body is connected or grafted to the blocked coronary artery
This creates a new path for oxygen-rich blood to flow to the heart muscle

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16
Q

What is PCI

A

> A catheter is inserted into the blood vessels either in the groin or arm
Catheter placed where coronary artery is narrowed
When tip in place, balloon tip covered with stent inflated
Balloon tip compresses the plaque and expands the stent
Once stent in place, balloon is deflated and withdrawn
Stent stays in the artery, holding it open

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17
Q

What are the risks associated with PCI?

A

> Stent Insertion: re-stenosis (endothelium inside the vessel grows over the top of stent and narrows back down again, limiting blood supply - angina), thrombosis (metal looks a bit like a break in the vessel - platelets may stick and triggers the formation of a clot - blockage of vessel - MI)
Contrast induced nephropathy: damage kidneys
Catheter insertion and balloon inflation: movement of plaque, vessel occlusion

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18
Q

How are the risks of PCI managed?

A

> Stent Insertion: re-stenosis (drug-eluting stents - reduce overgrowth of endothelial cells), thrombosis (antiplatelet drug to reduce risk of blood clots)
Contrast induced nephropathy: avoid other nephrotoxins, ensure hydration, sodium bicarbonate to adjust urinary pH

19
Q

What are the steps taken to reduce the risk of thrombosis when PCI?

A

> Antiplatelet drugs (2 - prior to stent insertion) because it’s a high risk environment for clot to form. Clot formation will initially be triggered by platelet activation
Use aspirin + clopidogrel OR ticagrelor OR prasugrel (loading doses to ensure platelets are knocked out at the time the stent is being inserted)
Possibly Gp IIb/IIIa inhibitor

20
Q

How is thrombosis risk managed post-PCI?

A

Post-procedure antiplatelet therapy

dual - aspirin continued for life + another

21
Q

Compare how antiplatelet drugs clopidogrel, prasugrel and ticagrelor bind to their drug targets and how this effects the way they are dosed?

A

> Clopidogrel: binding to drug target is irreversible - once bound to platelet, target is inactivated permanently (doesn’t matter what t1/2 is, irreversible inhibition - give 1d).
However, clopidogrel is a prodrug (get converted to active metabolite) - conversion provides opportunity for variability between people (some people don’t respond optimally)

> Prasugrel: prodrug, acts irreversibly, not as subject to variation

> Ticagrelor: doesn’t need to be converted to active metabolite. Binds to drug target reversibly - entirely dependent on maintaining drug concentration in plasma to exert its effect. Short t1/2 = bd administration (compliance)

22
Q

Discuss the choice between P2Y12 inhibitors

A

> Clopidogrel: recommended for patients who can’t receive ticagrelor or prasugrel

> Ticagrelor: shortness of breath in some people (A/E) can lead to people wanting to stop medication

> Prasugrel: tends towards bleeding more and shouldn’t be used for patients >75yrs, of low body weight (<60kg) or with hx of TIAs or stroke

23
Q

Discuss the risks associated with ticagrelor and statins

A

> Ticagrelor is CYP3A4 substrate
Usually taken in groups with atherosclerosis (taking statin)
Statin also CYP3A4 substrate (atorv and simv) but difference in interaction profiles
CYP3A4 has broad open active site, multiple drugs can fit in slightly different ways
Risk of muscle toxicities = make patients aware

24
Q

What are the Types of ACS?

A

> Non-ST elevations (NSTEACS): unstable angina, myocardial infarction)

> ST Elevation Myocardial Infarction (STEMI)

25
Q

What are the Characteristics of STEMI?

A

> Significant changes to ECG (ST segment elevated)
Transmural myocardial damage
Indicates complete occlusion and full-thickness heart muscle injury

26
Q

What are the characteristics of NSTEMI?

A

> Minor changes to ECG (Non-ST Segment elevation MI)
Subendocardial damage
Involves partial occlusion and partial thickness damage to heart muscle (less severe MI)

27
Q

What are the symptoms of a Heart Attack?

A

> Chest discomfort (at rest or lasting longer than 10 mins, not relieved by sublingual nitrates or recurs, associated with syncope or acute heart failure)
Classically crushing central chest pain
Other presentations include: back, neck, arm or epigastric pain, chest tightness, dyspnoea, nausea, vomiting, diaphoresis

28
Q

What investigations are conducted for ACS diagnosis?

A

> ECG

> Blood tests

29
Q

What indicates the magnitude of damage of ACS?

A

The magnitude in ECG change (ST elevation) and rises in cardiac enzymes (CK-MB and troponin) indicates magnitude

30
Q

How are STEMIs managed?

A

> Relieve pain
Reperfuse myocardium to limit infarct size (larger infarct results in mechanical complications)
Prevent formation of intramural thrombus

31
Q

How is pain relieved in STEMI?

A

Morphine

32
Q

How are arrhythmias prevented and managed in STEMI?

A

Antiarrhythmics

33
Q

How are intramural thrombus prevented in STEMI?

A

Anticoagulants

34
Q

Discuss how myocardium is reperfused in STEMI to limit infarct size?

What drugs are also used?

A

> Reperfusion (PCI, thrombolytics or CABG) therapy is determined by the balance of achieving rapid reperfusion with the risks of procedure
The time since onset of the ACE is a major determinant of the potential benefits of reperfusion (once damage is done - can’t reverse it)
Thrombolysis carries significant bleeding risk (haemmohragic stroke) therefore PCI is preferred reperfusion technique unless it will take too long for PCI to occur
Antiplatelet, anticoagulant, nitrates and beta blockers used

35
Q

How are reperfusion risks managed in PCI?

A

> Stent Insertion: re-stenosis (drug-eluting stents - reduce overgrowth of endothelial cells), thrombosis (antiplatelet drug to reduce risk of blood clots)
Contrast induced nephropathy: avoid other nephrotoxins, ensure hydration, sodium bicarbonate to adjust urinary pH

36
Q

How are reperfusion risks managed in Thrombolysis?

A

> Minimise by careful patient selection
Contraindicated - previous haemorrhagic stroke or internal bleeding
Caution - uncontrolled BP, anticoagulant therapy, recent trauma or major surgery or prolonged CPR

37
Q

Why is anticoagulation required in MI management?

A

> Prevent the coronary artery clot from getting bigger and prevent intramural thrombus formation
Full doses of enozaparin (LMWH) used

38
Q

What drugs are used in secondary prevention of MI?

A 
> Beta blockers
> ACE inhibitor/ATII antagonists
> Eplerenone
> Statin
> Aspirin
> Clopidogrel/Ticagrelor/Prasugrel
> Short acting nitrates
39
Q

Discuss the use of ACE inhibitors in ACS secondary prevention

A

> Significant long term morbidity and mortality benefits (particularly those with significant LV dysfunction)
Patient must be haemodynamically stable before initiation
Start at low dose and uptitrate
If not tolerated, consider ATII antagonist

40
Q

Discuss the use of eplerenone, statins and short acting nitrates in ACS secondary prevention

A

> Eplerenone: reduce mortality in those with LV dysfunction (start 3-14 days post MI in those patients with a LVEF of <40%)
Statin: if patient not already on a cholesterol lowering drug, then one should be commenced (start at moderate dose)
Nitrates: prn use if not already using

41
Q

Management of NSTEACS is guided by what?

A

> Guided by risk of MI
High risk being treated similar to STEMI patient (not thrombolytics) and low risk patients being treated with drugs for stable angina (if already managed - uptitrate)

42
Q

NSTEACs patients who haven’t received a coronary artery stent will be discharged on what?

A

NSTEAC patients who haven’t received coronary artery stent will still be discharged on dual anti platelet therapy (at least 1 month - up to 12 months) particularly those who have experienced NSTEMI

43
Q

What is Prinzmetal’s angina?

What does it occur?

What is the treatment?

A

> Spasm of vessels, not caused by atherosclerosis
Most occur spontaneously at night (at rest) [not associated with exertion or stress]
Treatment: DHP CCBs, Nitrates
Symptoms may pass (reduce treatment after 6-12 months)

Pharmacotherapeutics Theory 1 (17 decks)

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