L 37 Flashcards by Md Ashiqur Rahman

Complications of IHD: x3

Heart ischaemia, heart arrhythmia, heart failure

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Principles of angina treatment x2 and how these occur

Increase myocardial O2 supply (by dilating cardiac vasculature)
Decrease O2 demand (by decreasing heart rate, myocardial contractility and afterload)

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Principle of ACS treatment

Re-vascularisation/re-perfusion.

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How is re-vascularisation/re-perfusion for ACS treatment achieved?

Mechanically/surgically:
- Percutaneous coronary intervention (PCI) (e.g angiography, angioplasty)
- Coronary artery bypass graft (CABG)
Chemically:
- Antiplatelets, anticoagulants, clot blusters (fibrinolytics)

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What is angioplasty?

Using a balloon or a stent to open up an artery.

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Examples of drug classes that dilate blood vessels and reduce cardiac load (x5)

Nitrates, CCBs, ACEIs, ARBs, B blockers

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Examples of drug classes that stabilise atherosclerotic plaques (x2)

Statins and other lipid lowering drugs

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Examples of a drug class that prevents platelet aggregation

Anti-platelets

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Examples of a drug class that prevents propagation of a thrombus

Anticoagulants

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Examples of a drug class that breaks down a thrombus

Fibrinolytics

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What are nitrates? MoA?

They are prodrugs that donate nitric oxide.

MoA: this donated NO increases intracellular cGMP –> relaxation of smooth muscle cells and vasodilation

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Examples of nitrate drugs

Nitroglycerin (e.g glyceryl trinitrate - GTN)

Isosorbide mononitrate (ISMN)

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What is the indication and dosing regimen of nitrates?

Are higher/more frequent doses better?

Given prn or regularly to relieve angina-related chest pain.

Higher/more frequent dosing is associated with tolerance.

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Common side effects of nitrates? x4

Why?

Hypotension, facial flushing, headache, dizziness

These are typical effects from dilating blood vessels.

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Side effects of CCBs

Headache, flushing, dizziness/postural hypotension, peripheral oedema, constipation
Non DHP CCB side effects
Be careful if…
Bradycardia
Be careful if patient is also on a B blocker.

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If we give an ACEI or ARB, we can anticipate….How is this used in ACS?

Vasodilation.
Used mainly in ACS to reduce the risk of ventricular hypertrophy and HF (reduce afterload = reduce the need for dead myocytes to undergo hypertrophy and expand ventricle size)

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Side effects of ACEI and ARBs

Dizziness/postural hypotension

Hyperkalaemia

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ACEI can cause a cough? Why do ACEI cause a cough?

ACEI can cause a cough due to an increased build-up of bradykinin (which is usually broken down by ACEI)

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If we give a B1 blocker, we can anticipate…

If we give a B1 blocker, we can anticipate:

Decrease in heart rate —> less excertion and O2 demand

What are some examples of what stimulation of the B1 receptor would cause? x3

Increased heart rate
Increased contractility
Increased conduction velocity
…. are used to prevent angina attacks and improve survival following ACS
B blockers are used to prevent angina attacks and improve survival following ACS

Are long or immediate release B blockers used in angina attacks?

ALWAYS LONG ACTING.

Short acting can worsen IHD

If we give a patient a B blocker, then we anticipate ….. (more related to B2 than B1)

If we give a patient a B blocker, then we anticipate bronchial constriction (more related to B2 than B1)

Quick MoA of statins

Statins inhibit the conversion of HMG-CoA to L-mevalonic acid and subsequently cholesterol, therefore decreasing cholesterol and stabilising atherosclerosis.

Side effects of statins x3

Elevated liver enzymes, myopathy, rhabdomyolysis

What are 3 examples of anti-platelet classes

Aspirin, thienopyridines, GPIIb/IIIa inhibitors

How does aspirin work as an anti-platelet agent?

Aspirin inhibits COX-1 which would NORMALLY increase TxA2 and increase platelet activation and aggregation. (Therefore they decrease platelet aggregation and activation)

How do thienopyridines work?

What class are they? 2x examples? Antiplatelet drugs. e.g clopidogrel and ticagrelor They inhibit the ADP receptor P2Y12 on the platelets to reduce their aggregation and secretion.

``` How do GPIIb/IIIa inhibitors work? What class are they? 2x examples? ```

Antiplatelet drugs e/g abciximab, tirofiban They inhibit GP IIb and IIIa receptors to decrease platelet activation and adherence to the subendothelium.

Side effect of antiplatelet drugs

Bleeding.

What is the general MoA for anti-coagulants?

They inhibit the formation and propagation of thrombi in arteries and veins.

What does UFH and LMWHs stand for?

UFH: unfractionated heparin LMWH: low molecular weight heparins

What anti-coagulant is mainly used in ACS?

Heparins (e.g UFH and LMWHs)

MoA of UFH?

UFH increases the inhibitory action of anti-thrombin (AT) on factors 10a and 2a (Xa and IIa) NOTE: also increases the inhibitory action of anti-thrombin on 12a, 11a and 9a

MoA of LMWHs

LMWHs increase the inhibitory action of anti-thrombin on 10a and 2a.

What are the differences between LMWH and UFH? + example of LMWH

LMWH example: enoxaparin LMWH's have a smaller molecular weight than UFH, and a longer half life. LMWHs can also be self-administered subcutaneously = easier dosing for patient.

... is a natural way to deactivate clotting factors. ... enhance the effect of ... on these factors.

Anti-thrombin is a natural way to deactivate clotting factors. Heparins enhance the effect of anti-thrombins on these factors.

What do Xa and IIa mean compared to factors X and II?

The 'a' means that the factor has been activated in the clotting cascade. (e.g factor X gets activated into Xa which in turn activates factor II into IIa)

Side effects of anticoagulants

Bleeding, heparin-induced thrombocytopenia.

MoA of fibrinolytic

Fibrinolytics break down fibrin stabilized clots (amplifying the body's natural clot-breakdown mechanism)

In what cases are fibrinolytic mainly used?

Mainly for severe IHD (e.g stroke and sometimes pulmonary embolism)

Examples of a fibrinolytic class + 2x examples

Class: synthetic tissue plasminogen activators (tPA) and examples: alteplase, reteplase Side effects of fibrinolytic

What is it mainly reserved for?

Bleeding | Reserved for very serious clots as it has the highest risk of bleeding compared to other cardiac medicines.

Variability in beneficial effects tends to be related to the ... and ... of the drugs used.

Variability in beneficial effects tends to be related to the PK and PD of the drugs used.

Variability in side effects is also related to the ... and ... of the drugs, as well as the .... and ....

Variability in side effects is also related to the PK and PD of the drugs, as well as the drug combination and drug interactions

``` The focuses of IHD therapy are: (x5) + which drug class targets each of these focuses? ```

- Reducing oxygen demand of heart (nitrates, CCBs, ACEI/ARBs, B blockers) - Improving oxygen supply (nitrates, CCBs, ACEI/ARBs, B blockers) - Stabilising atherosclerosis (statins) - Revascularisation (nitrates, CCBs, ACEI/ARBs, B blockers) - Preventing platelet adhesion, activation, and aggregation (anticoagulants, antiplatelets, fibrinolytic)

Giving a CCB will cause ...

Vasodilation and decreased contractile strength (therefore decreased blood pressure)