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PHCY 310 > L 37 > Flashcards

L 37 Flashcards

1
Q

Complications of IHD: x3

A

Heart ischaemia, heart arrhythmia, heart failure

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2
Q

Principles of angina treatment x2 and how these occur

A

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

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3
Q

Principle of ACS treatment

A

Re-vascularisation/re-perfusion.

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4
Q

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

A

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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5
Q

What is angioplasty?

A

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

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6
Q

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

A

Nitrates, CCBs, ACEIs, ARBs, B blockers

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7
Q

Examples of drug classes that stabilise atherosclerotic plaques (x2)

A

Statins and other lipid lowering drugs

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8
Q

Examples of a drug class that prevents platelet aggregation

A

Anti-platelets

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9
Q

Examples of a drug class that prevents propagation of a thrombus

A

Anticoagulants

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10
Q

Examples of a drug class that breaks down a thrombus

A

Fibrinolytics

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11
Q

What are nitrates? MoA?

A

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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12
Q

Examples of nitrate drugs

Nitroglycerin (e.g glyceryl trinitrate - GTN)

A

Isosorbide mononitrate (ISMN)

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13
Q

What is the indication and dosing regimen of nitrates?

Are higher/more frequent doses better?

A

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

Higher/more frequent dosing is associated with tolerance.

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14
Q

Common side effects of nitrates? x4

Why?

A

Hypotension, facial flushing, headache, dizziness

These are typical effects from dilating blood vessels.

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15
Q

Side effects of CCBs

A

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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16
Q

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

A

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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17
Q

Side effects of ACEI and ARBs

A

Dizziness/postural hypotension

Hyperkalaemia

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18
Q

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

A

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

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19
Q

If we give a B1 blocker, we can anticipate…

A

If we give a B1 blocker, we can anticipate:

Decrease in heart rate —> less excertion and O2 demand

20
Q

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

A
  1. Increased heart rate
  2. Increased contractility
  3. 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
21
Q

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

A

ALWAYS LONG ACTING.

Short acting can worsen IHD

22
Q

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

A

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

23
Q

Quick MoA of statins

A

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

24
Q

Side effects of statins x3

A

Elevated liver enzymes, myopathy, rhabdomyolysis

25
Q

What are 3 examples of anti-platelet classes

A

Aspirin, thienopyridines, GPIIb/IIIa inhibitors

26
Q

How does aspirin work as an anti-platelet agent?

A

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

27
Q

How do thienopyridines work?

A

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.

28
Q 
How do GPIIb/IIIa inhibitors work? What class are they?
2x examples?
A

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

29
Q

Side effect of antiplatelet drugs

A

Bleeding.

30
Q

What is the general MoA for anti-coagulants?

A

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

31
Q

What does UFH and LMWHs stand for?

A

UFH: unfractionated heparin
LMWH: low molecular weight heparins

32
Q

What anti-coagulant is mainly used in ACS?

A

Heparins (e.g UFH and LMWHs)

33
Q

MoA of UFH?

A

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

34
Q

MoA of LMWHs

A

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

35
Q

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

A

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.

36
Q

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

A

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

37
Q

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

A

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)

38
Q

Side effects of anticoagulants

A

Bleeding, heparin-induced thrombocytopenia.

39
Q

MoA of fibrinolytic

A

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

40
Q

In what cases are fibrinolytic mainly used?

A

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

41
Q

Examples of a fibrinolytic class + 2x examples

A

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

42
Q

What is it mainly reserved for?

A

Bleeding

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

43
Q

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

A

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

44
Q

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

A

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

45
Q 
The focuses of IHD therapy are: (x5)
\+ which drug class targets each of these focuses?
A
  • 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)
46
Q

Giving a CCB will cause …

A

Vasodilation and decreased contractile strength (therefore decreased blood pressure)

PHCY 310 (65 decks)

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