Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pharmacology Yr2 > Angina and myocardial infarction > Flashcards

Angina and myocardial infarction Flashcards

1
Q

What do we do to manage an angina attack?

A

Reassure patient
Call 999
If sublingual GTN doesn’t help a MI maybe in progress.
Chewable aspirin + MUST tell ambulance it has been given.
High flow O2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the three usual causes of angina perctoris?

A

Restriction (usually incomplete) in blood supply to working heart muscle.

Partial occlusion of blood vessels
> atheroma
> thrombus

Vasospasm in coronary arteries
> overly reactive vessels
> drugs e.g. cocaine, smoking

Severe anaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How does an atheroma form?

A

Endothelium damaged

Cholesterol accumulation
- oxidation

Monocyte invasion
- convert to macrophages, phagocytose cholesterol to become foam cells

Foam cell degeneration
- Deposition of atherosclerotic plaque, increases stiffness at margin and narrows artery.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How is HDL associated with coronary heart disease and heart attacks?

A

HDL is strongly associated with a -ve risk of heart attack incidence to due increasing HDL/LDL ratio.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How do platelets have a central role in the formation of an atheroma?

A

When platelets are activated when they come in contact with the tunica intima, they shed microparticles which attract monocytes.

Monocytes then proliferate and differentiate into phagocytes

Phagocytes consume cholesterol/lipoprotein and become foam cells.

Foam cells die and deposit atheroscleoritc plaque in artery.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Name two HMG CoA reductase inhibitors

A

Lovastatin and atorvastatin

  • decrease liver cholesterol synthesis
  • increase VLDL and LDL receptor expression to decrease blood LDL levels
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are some of the side effects of HMG CoA reductase inhibitors?

A

Muscle cramps

Gi tract disturbances

Malabsorption of lipid soluble vitamins (ADEK) and lipid soluble drugs.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

In which patients are HMG CoA reductase inhibitors seen to have the best efficacy?

A

In patients with known cardiovascular disease.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the mechanism of action of ezetimibe?

A

inhibits absorption of cholesterol at the brush border of the small intestines

This means more is uptaken from the circulation into the liver cells.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

When is eztimibe most commonly used?

A

In statin intolerant patients or as an adjunct to statin treatment.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Name two fibrates?

A

Bezafibrate Ciprofibrate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the mechanism of action of fibrates?

A

Agonists of PPAR alpha receptor.

This leads to increased lipoprotein lipase activity which decreases VLDL.

Increases HDL via apolipoprotein A

Decreased hepatic triglyceride secretion.

Increased B oxidation in the liver.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the main use for fibrates?

A

Mainly used for hypercholesterolaemia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are some side effects of fibrates?

A

Mild stomach upset

Gallstones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Name two Bile acid binding agents

A

Cholestipol & cholestyramine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the mechaism of action of Cholestipol & cholestryamine?

A

Bind to bile acid in the gut leading to increased cholesterol loss due to

Decreased enterohepatic recirculation of bile.

Increased synthesis of bile salts by liver

Decreased liver cholesterol

Increased LDL receptor expression leading to greater LDL uptake

17
Q

What is the main uses for Bile acid binding agents such as Cholestipol?

A

Hyperlipidaemias.

18
Q

What are some side effects of bile acid binding agents such as cholestipol?

A

GI tract disturbances

Increase in VLDL and triacylglyceride synthesis

Malabsorption of lipid soluble vitamins

Malabsorption of lipid soluble drugs.

19
Q

What is the mechanism of action of Nitrate in the treatment of angina?

A

Increase the production of NO.

NO is an endothelium derived relaxing factor.

NO stimulates guanylate cyclase to produce cGMP.

cGMP leads to increased myosin light chain phosphatase activity

Myosin light chains in the smooth muscle in the tunica media are dephosphorylated, relaxing the smooth muscle.

20
Q

Why cant we orally administer NO?

A

Has a half life of a minute and undergoes nearly 100% first pass metabolism in the liver.

21
Q

What are the actions of NO?

A

Venous vasodilation

  • reduction in preload which reduces the stress put on the heart so the cardiac muscles need less energy.

Arterial dilation

  • reduced arterial resistance so heart has to beat less hard.

Coronary artery dilation

  • increased blood flow to the cardiac myocytes which in turn means more O2.

Some antiplatelet/antithrombotic effects - can break down atheroma / thrombus which could be causing blockage.

22
Q

What are some ways in which nitrates are administered?

A

Via buccal mucosa

Transdermal patches (long acting)

Alkyl nitrates (abused as poppers).

23
Q

What are some side effects of nitrates?

A

Headache, flushing (vasodilation), palpitations

24
Q

What drugs may Nitrates have an adverse effect with when combined?

A

Drugs for impotence (such as viagra) has potential to cause hypotensive crisis.

25
Q

Why are B blockers useful for treatment of angina?

A

B blockers reduce myocardial oxygen demand.

26
Q

What is the first line therapy in the treatment of chronic stable angina?

A

B blockers

27
Q

What is atenolol?

A

B1 selective beta blocker

28
Q

What is Carvedilol?

A

A receptor antagonists, caused peripheral vasodilation which can lead to greater coronary perfusion.

29
Q

What are some side effects of B blockers

A

Hypotension

Consitpation

Indigestion

Insomnia.

30
Q

How are Ca2+ channel blockers used in the treatment of angina?

A

Ca2+ in cardiac myocytes is what causes the muscle contraction.

Ca2+ enters the cardiac myocytes from votage gated ion channels (L-type VDCC) from the outside, therefore if we block the channels no Ca2+ can enter the cells and no smooth muscle contraction can occur.

31
Q

What are the 3 main classes of L type calcium channel blocker and give an example of a drug from each class.

A

Dihydropyridines - Nifedipine

Phenylalkyamines - Verapamil

Benzothiazepine - Diltiazem

32
Q

What are some side effects of Voltage gated calcium channel blockers?

A

Peripheral vasodilation

Consitpation

Gingival overgrowth

33
Q

What is an important factor to consider when choosing which class of Ca2+ channel blocker to use?

A

We need to consider their selectivity - wether they mainly target the myocardium or have more widespread peripheral effects. If the drug chosen also has widespread peripheral effects, such as dihydropiridines (nifedipine) it may cause a drop in blood pressure and incite a baroreceptor reflex which will in turn increase myocardial O2 demand which could worsen the angina.

Therefore it is good to use Phenylalyklamine calcium channel blockers such as Verapamil which are more selective for the myocardium.

34
Q

Give an example of an antiplatelet drug?

A

Clopidogrel, aspirin

35
Q

What is the mechanism of action of clopidogrel?

A

Blocks platelet ADP receptors

Blocks the formation of cross links between platelets by fibrin.

Side effects: hemorrhage

Neutropenia

36
Q

What is the mechanism of action of aspirin?

A

Metabolised to salicylic acid

Inhibits thromboxane production via Cox-1 inhibition.

Low dose aspirin is used long term to prevent heart attacks, strokes and blood clots.

  • Low dose to inactivate Cox in platelets but not endothelial cells that produce PGI2.
  • Doses may be given straight after heart attack to reduce risk.
37
Q

What are the side effects of aspirin?

A

GI ulcers, bleeding as inhibits Cox-1 which is involved in the maintenance of mucosal health.

38
Q

What are some treatments after the first MI?

A

Ranolazine - Blocks late Na+ entry and appears to reduce cardiac dysfunction in angina

  • decreases angina episodes.

Aspirin - reduced clot formation by targeting platelets and inhibiting the production of thromboxane A2.

Bypass surgery, stents, angioplasty.

39
Q

What are some side effects of Ranolazine?

A

Increases QT interval which could lead to risk of sudden cardiac death.

Pharmacology Yr2 (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions