Brainscape's Knowledge GenomeTM

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


See full index

CPT + Prescribing > Hyperlipidaemia > Flashcards

Hyperlipidaemia Flashcards

You may prefer our related Brainscape-certified flashcards:
NASM ® CPT flashcards
1
Q

Where is cholestrol synthesised?

A

Synthesised in body, with contribution from diet

  • Liver
  • Adrenal glands
  • Sex organs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

List some functions of cholestrol

Which type of cholestrol is most susceptible to oxidation via ROS?

A
  • Membrane integrity
  • Steroid hormone precursor
  • Bile acids
  • Vitamin D

LDL cholestrol (70% of cholestrol)

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

Why is the HDL carrier considered ‘good cholestrol’?

A

Carries cholestrol away from the circulation to liver for recycling

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

Briefly describe the pathophysiology of atherosclerosis

A
  • Oxidation of LDL at damaged endothelium by necrotic tissue + ROS
  • Adheres to proteoglycans
  • Lipid laiden core with fibrous external cap
  • Fibrous cap rupture
  • Platelet aggregation
  • Thrombus formation, MI, stroke
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Are high triglycerides treated as a modifiable risk factor?

A

No

High triglycerides not good, but limited data to suggest that it should be targeted as a modifiable risk factor

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

Why do we treat high cholestrol?

A

To reduce CVD risk

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

What type of cholestrol is targeted for CVD prevention?

A

LDL cholestrol lowering is target for CVD prevention

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

What sort of factors does the aggressiveness of treatment depend on?

A
  • Total CVD risk
  • Age
  • Familial hypercholestrolaemia (genetic); disorder of LDL receptor
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Briefly describe the processes leading to atheroma formation and atherosclerosis

A
  • Accumulation of LDL
  • Oxidation by local endothelial cells - oxidised LDL
  • Formation of foam cells in intima/endothelial space
  • Smooth muscle cell proliferation
  • Development of fatty streaks
  • Chronic inflammation + accumulation of disrupted endothelium/vascular smooth muscle

Development of fatty streaks due to oxidation of LDL cholestrol

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

What is a common site for the development of fatty streaks?

A

Descending aorta

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

Describe the mechanism of action of statins

A
  • Competitive inhibition of HMG-CoA reductase (rate limiting enzyme in mevalonate pathway)
  • Upregulation of hepatic LDL receptors
  • Increased clearance of circulating LDL
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Give some examples of statins

A
  • Atrovastatin; 1st line
  • Simvastatin
  • Fluvastatin
  • Pravastatin
  • Rosuvastatin
  • Lovastatin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Give some additional benefits of statin therapy which reduce CVD risk

A
  • Improved vascular endothelial function; increased NO and decreased endothelin signalling
  • Stabilisation of atherosclerotic plaque; reduced smooth muscle cell proliferation, increased collagen
  • Improved haemostasis; reduced fibrinogen, reduced platelet aggregation, increased fibrinolysis
  • Anti-inflammatory; reduced proliferation of inflammatory cells into plaque, reduced adhesion molecules + cytokines
  • Anti-oxidant; reduced superoxide production (ROS)

Thus, reduced risk of atheroma + atherosclerosis

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

What type of drugs are simvastatin and atorvastatin?

A

Pro-drugs; activated by 1st pass metabolism (into active derivatives)

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

Which has a longer half life; simvastatin or atorvastatin?

A

Atorvastatin (>30 hrs)

*Dose equity considerations

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

Give some warnings/contraindications for statins

A
  • GI disruption, nausea
  • Headache
  • Myalgia (diffuse muscle pain); raised CPK >10x normal limit)
  • Rhabdomyolysis (due to organic anion transporter/genetic differences?)
  • Muscle breakdown, pain, renal failure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Give some important interactions/considerations for statins

A
  • Renal impairment
  • Pregnancy, breast feeding
  • CYP 3A4; amiodarone, diltiazem, macrolides
  • Amlodipine; increase dose of statin
  • Withhold statin short term (eg if taking antibiotics)
  • Grapefruit juice (CYP 3A4)

Concurrent use of amlodipine and simvastatin causes a significant increase in blood levels of simvastatin such that, in practice, the effect is double that compared to uninhibited simvastatin. Therefore, in patients on amlodipine 10mg plus simvastatin 20mg, the effect is similar to receiving simvastatin 40mg alone.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Why is atrovastatin the most used/preferred statin?

A

Greatest dose dependent reduction in LDL cholestrol

ie at its highest dose (80mg), atorvastatin gives the greatest % reduction in LDL levels (compared to simvastatin, fluvastatin, pravastatin, rosuvastatin)

19
Q

When should statins be prescribed to employ primary prevention of CVD risk?

A

When 10 year CVD risk > 10% using QRISK

Patient considerations, risk/benefit

20
Q

What dose and type of statin is recommended for primary prevention?

A

20 mg atorvastatin once daily

21
Q

What dose and type of statin is recommended for secondary prevention (ie following a cardiovascular event eg MI/stroke)?

A

80 mg atorvastatin once daily

(CKD- 20 mg, amended based on adverse reactions, drug interactions)

22
Q

What blood tests need to be carried out before prescription of a statin?

A

Full lipid profile, HDL, non-HDL, triglycerides (TG’s), LFT’s, LDL cholestrol

23
Q

What effect is aimed for with statins?

A

>40% reduction in non-HDL cholestrol at 3 months

*Grapefruit juice/whole grapefruit- avoid*

24
Q

Why is it recommended to take statins at night?

A
  • Due to circadian rhythm of LDL receptor synthesis/activity
  • Short half life of simvastatin, thus more effective if taken at night (atrovastatin = longer half life)
25
Q

Describe the mechanism of action of fibric acid derivatives (fibrates)

A
  • Activates nuclear transcription factor PPAR-alpha (peroxisome proliferation-activated receptor)
  • PPAR-alpha regulates expression of genes that control lipoprotein metabolism
  • Thus, increased production of lipoprotein lipase
  • Increased triglyceride internalisation + breakdown
  • Increased triglycerides from lipoprotein in plasma; thus increased TG breakdown
  • Increased fatty acid uptake by liver
  • Increased levels of HDL
  • Increased LDL affinity for receptor
26
Q

Give an example of a fibric acid derivative (fibrate)

A

Fenofibrate

27
Q

Are fibrates used alone or alongside statins?

A

Rarely used alone, often co-prescribed with statins (eg if high dose statin not tolerated)

28
Q

Give some warnings/contraindications of fibrates

A
  • Cholelithiasis (gall stones)
  • Myositis
29
Q

Give an interaction/consideration of fibrates

A

Warfarin potentiation; increased bleeding risk

30
Q

Describe the mechanism of action of cholestrol absorption inhibitors

A
  • Inhibit NPC1L1 transporter
  • Reduces absorption of cholestrol by the gut
  • Hepatic LDL receptor expression increases
  • Reduced total cholestrol
31
Q

Give an example of a cholestrol absorption inhibitor

A

Ezetimibe

Standard single dose of 10 mg (no dose escalation)

Not 1st line treatment for hypercholestrolaemia; co-prescribed with statins

Adjunct to statin, familial hypercholestrolaemia

32
Q

List some features of cholestrol absorption inhibitors

A
  • Pro-drug
  • Hepatic metabolism
  • Remain in enterohepatic circulation; thus limits systemic exposure
  • Secreted by bile
33
Q

Give some warnings/contraindications of cholestrol absorption inhibitors

A

GI upset, abdominal pain

34
Q

Give some interactions/considerations of cholestrol absorption inhibitors

A

Hepatic failure; as they require hepatic metabolism

(within enterohepatic circulation)

35
Q

What is the standard dose of ezetimibe?

What is the advantage of prescribing exetimide with a statin?

A

10 mg SID (no dose escalation)

Benefits in CKD and secondary CVD prevention

Useful in those that can only tolerate low dose statin; additive + synergistic effect

36
Q

What are the target concentrations of LDL cholestrol and total cholestrol for those being treated for secondary prevention?

A

LDL cholestrol: 2.0 mmol/L

Total cholestrol: 4.0 mmol/L

37
Q

What is the benefit of prescribing 10 mg ezetimibe with simvastatin?

A

Additive + synergistic effect

Simvastatin-ezetimibe combination reduces event rate more than simvastatin alone

38
Q

Describe the mechanism of action on monoclonal antibodies eg PCSK9 inhibitors in lowering cholestrol

A
  • Normally, LDL attaches to LDL receptor, receptor is internalised, LDL is catabolised and the receptor is degraded/recycled within the cell
  • PCSK9 = protein that binds to the internalised LDL-receptor and directs it for degradation
  • PCSK9 inhibitors reduce degradation of the internalised LDL receptor, so that more receptors are expressed on cell surfaces to take up more LDL
  • Thus, PCSK9 inhibitors reduce LDL cholestrol
39
Q

Give 2 examples of PCSK9 inhibitors

A

Alirocumab

Evolocumab

40
Q

What are PCSK9 inhibitors used for currently?

A

Lifetime injections

For primary and secondary prevention in resistant familial hypercholestrolaemia (resistant to statins)

And some high risk secondary prevention patients

41
Q

List some non-pharmacological management options for hypercholestrolaemia

A
  • Plant sterols; LDL cholestrol lowering effects
  • Naturally occuring in grains, legumes; structurally similar to cholestrol thus compete for absorption

Work with statins, not with ezetimibe

  • Fish oils/oily fish
  • Fibre, whole grains
  • Vit C/E
42
Q

Describe the effect of alcohol on lipid profiles

A

Increased HDL cholestrol

BUT

Increased triglycerides

43
Q

Which method is used to assess a patient’s CVD risk?

A

QRISK (2)

Based on age, smoking, cholestrol, hypertension, statins, DM etc

CPT + Prescribing (7 decks)

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