Brainscape's Knowledge GenomeTM

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


See full index

CVS: Pharmacology > Atherosclerosis + lipid-lowering drugs > Flashcards

Atherosclerosis + lipid-lowering drugs Flashcards

1
Q

What is hypercholesterolaemia?

What does it lead to?

A

Elevated plasma cholesterol

Leads to atherosclerosis

Atherosclerosis is when plaques on the inner surface of an artery

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

What does atherosclerosis cause/lead to?

A

Ischaemic heart disease

Peripheral vascular disease

Cerebrovascular disease

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

State the risk factors for atherogenesis (formation of plaque in arteries) + CVD in general

A

Genetic

Hypercholesterolaemia (raised LDL or lowered HDL)

Hypertension

Smoking

Obesity

Hyperglycaemia

Reduced physical activity

Infection

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

What drugs can induce dyslipidaemia?

Abnormal amount of lipids (e.g. triglycerides, cholesterol and/or fat phospholipids) in the blood

A

Beta-blockers

Thiazides

Corticosteroids

Retinoids - monitor

Oral Contraceptives

Anti-HIV - monitor lipid levels

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

What are lipoproteins?

What are the 4 major types?

A

Central core of hydrophobic lipid, encased in phospholipid, cholesterol and apolipoproteins

The 4 major types types:

  1. HDL
  2. LDL
  3. VLDL
  4. Chylomicrons
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Function of chylomicrons

A

Transport triglycerides and cholesterol from GI tract to liver.

Free FA released and cholesterol is stored, oxidised to bile salts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Function of VLDL

A

Transports cholesterol + triglycerides to the tissues

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

Function of LDL

A

Large component of cholesterol

Delivers cholesterol to liver and tissues, via endocytosis via an LDL receptor.

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

Function of HDL

A

Absorbs cholesterol from cell breakdown and transfers it to VLDL & LDL

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

What should the ideal cholesterol levels be?

A

<5.0mmol/l

25 - 30% middle aged population have hypercholesterolaemia (.6.5mmol/l)

Important to know if it is high LDL or low HDL

Hypercholesterolaemia can cause Xanthomata - deposition of yellowish cholesterol-rich material that can appear anywhere in the body

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

Describe the process of atherogenesis + how this is affected by lifestyle

A

Summary

  • damage to the blood vessel
  • inflammatory response
  • cholesterol-rich deposits form
  • inflammatory mediators may lead to growth of VSM/connective tissue
  • plaques form
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How do you manage atherogenesis?

A

Modify risk factors

  • Stop smoking
  • Exercise
  • Treat HT/DM
  • Drug-induced

Low cholesterol diet

  • only 25-30% cholesterol comes from diet (rest from liver)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Describe the mode of action of statins

A

HMG-CoA reductase inhibitors

Competitively inhibit the activity of HMG-CoA reductase, the rate-limiting enzyme in cholesterol synthesis

Inhibition of this enzyme results in a decrease in cellular cholesterol concentration

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

Example of statins

A

Simvastatin

Pravastatin

Atorvastatin

Fluvastatin

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

Describe the clinical pharmacology of statins

A

Reduce plasma cholesterol

Reduction in hepatic cholesterol synthesis leads to an upregulation of hepatic LDL receptors, promoting LDL uptake

Less effective in homozygous familial hypercholesterolaemia

  • They cannot make LDL receptor
  • Atorvastatin may be effective
  • Statins effective in heterozygous disease

Statins are hepatoselective

  • liver is the main site of cholesterol synthesis, extrahepatic sites synthesise essential cholesterol
  • 1st pass metabolism: 5% reaches systemic circulation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

When should statins be taken?

A

At night

Offsets a nocturnal increase in cholesterol synthesis

Except atrovastatin

17
Q

What are the drug interactions + contraindications of simvastatin?

A

Contraindicated with macrolides

Interaction with amlodipine, verapamil, diltiazem

If amlodipine needs to be taken with a statin:

  • pravastatin should be used instead (does not interact)
  • 20mg simvastatin as maximum dose
18
Q

Name the uses and limitations of statins as OTC medicines.

A

10mg simvastatin without cholesterol test

For patients at high risk:

  • All males > 55
  • Males 45-55 + females > 55 with…
    • family history of IHD
    • smokers
    • overweight
    • S Asians Indian sub-continent ethnicity

Refer angina to GP

Monitoring - signs of hepatoxicity (jaundice, dark urine, itching)

Counsel re muscle pains

Interactions - HIV protease inhibitors, ciclosporin, azoles, fibrates, anticoagulants, macrolides

Treatment might not be documented with GP

Patients may buy a packet for christmas

19
Q

Briefly describe the mode of action of fibrates

A

Activate PPAR-alpha = alters lipoprotein metabolism

Promote breakdown in VLDL (w/ small reduction in LDL + increase in HDL)

Reduce triglycerides - used w/ statins when TGs (+cholesterol) raised

Decrease glucose, use in DM

Reduce IHD but not mortality

Adverse effects = rhabdomyolysis

20
Q

Example of a cholesterol absorption inhibitor

A

Ezetimibe

Prevents cholesterol absorption

Use on top of a statin

21
Q

Fill in the gaps

A

CVS: Pharmacology (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions