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CPT > L7 - Hyperlipidaemia > Flashcards

L7 - Hyperlipidaemia Flashcards

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1
Q

Where is cholesterol synthesised

A

Liver
Sex organs
Adrenal glands
Dietary intake

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2
Q

What is cholesterol used for

A

Phospholipid membrane integrity
Precursor of steroid hormones
Vitamin D
Bile acids

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3
Q

Effects of high cholesterol

A

LDLs are susceptible to oxidation at damaged endothelium by ROS
Macrophages can engulf LDLs to form foam cells
Adhere to proteoglycans causing atherosclerosis
Increased risk of MI or stroke if the fibrous cap ruptures

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4
Q

Reduction in cholesterol

A

10% reduction - 15% reduced risk of CHD mortality and 11% reduced risk of total mortality

For every 1 mmol reduction , there is a 20% reduction reduced risk of CVD

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5
Q

Process of atherosclerosis

A
  1. Increased oxidative stress due to toxins, infection or fat
  2. Increased ROS damages the endothelium
  3. Platelets aggregate to site
  4. Macrophages uptake oxidised LDLs forming foam cells
  5. Foam cell aggregation causing fatty streaks to develop
  6. Proliferation of smooth muscle to form the fibrous cap which concludes the vessel and may rupture
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6
Q

Statin mechanism of action

A
  • Competitive inhibition of HMG- CoA reductase therefore inhibiting the rate controlling enzyme in cholesterol production
  • Upregulation of hepatic LDL receptors
  • Increased clearance of circulating LDLs
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7
Q

Examples of statins

A 
Atorvastatin - 1st line 
Simvastatin 
Fluvastatin 
Pravastatin 
Rosuvastatin 
Lovastatin
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8
Q

Additional benefits of statins

A

Antioxidant - decreases superoxide formation

Improves vascular endothelial function by:

  • increasing nitric oxide
  • increasing vascular endothelial growth factor
  • decreasing endothelin ( vasoconstriction)

Stabilises atheromatous plaques by:

  • decreasing the proliferation of smooth muscle
  • increasing collagen

Decreased haemostasis by

  • decreasing plasma fibrinogen
  • decreasing platelet aggregation
  • increasing fibrinolysis

Anti inflammatory by decreasing proliferation of inflammatory cells into plaque I.e.

  • CRP
  • cytokines
  • adhesion molecules
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9
Q

Simvastatin

A

Prodrug activated in the liver by CYP 450

Short half life

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10
Q

Atorvastatin

A

Prodrug activated in the liver by CYP 450
Longer half life
Best efficacy
Lowest number needed to treat

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11
Q

Contraindications and interactions of statins

A

Contraindications:

  • GI disruption
  • Nausea
  • Headache
  • Myalgia - increased creatine phosphokinase
  • Rhabdomyolysis

Interactions:

  • renal impairment
  • pregnancy
  • breastfeeding
  • CYP 3A4 - do not drink grapefruit juice
  • amiodarone - anti-arrythmetic medication
  • diltiazem - CCB
  • macrolides - stop statin short term whilst on antibiotics
  • amlodipine - give higher dose statin
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12
Q

Grapefruit juice effect on CYP 3A4

A

Inhibits CYP 3A4 which normally metabolises lovastatin

Therefore higher statin dose in plasma

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13
Q

Rosuvastatin

A

Greatest efficacy

But interacts with diabetes and can cause many side effects

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14
Q

Cerivastatin

A

Withdrawn as interacting with fibrates and can cause:

  • death
  • rhabdomyolysis
  • renal failure
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15
Q

NICE guidelines with statin use

A

Primary prevention:

  • 10+% QRISK
  • low dose atorvastatin once daily

Secondary prevention:

  • already had a CVD event e.g. MI
  • high dose atorvastatin once daily
  • CKD patients - lower dose

Check lipid profile and triglycerides before prescribing
Check LFTs for liver function before prescribing

  • aim for more than 40% reduction in non HDLs at three months
  • avoid grapefruits
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16
Q

When should atorvastatin and simvastatin be taken

A

Most cholesterol and LDL receptor synthesis occurs at night via circadian rhythm

  • simvastatin has a short half life so should be taken at night
  • atorvastatin has a longer half life so can be taken in the morning
17
Q

Fibric acid derivatives aka fibrates mechanism of action

A

Activation of nuclear transcription factor - PPAR - alpha within the nucleus

  • lowers triglycerides from lipoprotein in plasma
  • decreases fatty acid uptake by the liver
  • increased HDLs
  • increases LDL affinity for the receptor
18
Q

PPAR alpha

A

Peroxisome proliferation activated receptor
Regulates gene expression that controls lipoprotein metabolism
Increased lipoprotein lipase production

19
Q

Fibrate use

A

Normally co-prescribed with statins when high dose statins are not tolerated
Rarely prescribed by itself

20
Q

Contraindications and interactions with fibrates

A

Contraindications:

  • choleliathiasis - gall stones
  • myositis - inflammation of muscles

Interactions:
- warfarin - increased risk of bleeding

21
Q

Example of fibrate

A

Fenofibrate

22
Q

Cholesterol absorption inhibitors mechanism of action

A

Prodrug - activated by first pass metabolism by CYP 450 on the liver
Enters the enterohepatic circulation via bile

Inhibit NPC1L1 transporter on brush border of the intestines
Reduces cholesterol absorption from the gut
Increases hepatic LDL receptor expression
- decreases cholesterol by 15% and LDLs by 20%

23
Q

Significance of enterohepatic circulation of cholesterol absorption inhibitors

A

Less systemic exposure
Less side effects and good tolerability
Replaced resins and sequestrants

24
Q

When are cholesterol absorption inhibitors used

A

Adjunct with statin in familial hypercholesterolemia
No dose escalation with ezetimibe
Secondary prevention
Patients that cannot tolerate high dose statin

  • benefits in CKD and secondary CVD prevention
25
Q

Contraindic and interaction of cholesterol absorption inhibitors

A

Contraindications:

  • abdominal pain
  • GI upset

Interactions:
- hepatic failure

26
Q

Name of cholesterol absorption inhibitor

A

Ezetimibe

27
Q

Alirocumab

A

Monoclonal antibodies for PCSK9
Less internalisation of LDL receptors
Therefore increases LDL reuptake into the liver

28
Q

Why is alirocumab or evolocumab not used

A

Require lifetime injections
More expensive

Only used when resistant to statins in familiar hypercholesterolemia

29
Q

Plant sterols

A

Structurally similar to cholesterol therefore competitive antagonist
Lower LDL cholesterol a bit (0.8mmol)
Works with statins but not ezetimibe

Can get from:

  • grains
  • legumes
  • modified butter
  • omega 3 in fish oil
  • vitamin C/E
30
Q

Alcohol

A

Increases HDL cholesterol

Increases triglycerides therefore not effective

CPT (23 decks)

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