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Pharmacology 2 > Dyslipidaemia > Flashcards

Dyslipidaemia Flashcards

1
Q

Pathophysiology
Dyslipidaemia

A

Imbalance of lipids such as cholesterol, low-density lipoprotein cholesterol, (LDL-C), triglycerides, and high-density lipoprotein (HDL). This condition can result from diet, tobacco exposure, or genetic and can lead to cardiovascular disease with severe complications.

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2
Q

HDL VS LDL

A

HDL is high density lipoprotein = Hero found in health arteries

LDL is low density lipoprotein = Loser causes plaque buildup

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3
Q

What are triglycerides?

A

Type of fat in the body, in combination with high LDL leads to clogged arteries

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4
Q

Signs and symptoms
Dyslipidaemia

A
  • Chest pains or tightness
  • Dizziness
  • Heart palpitations
  • Exhaustion
  • Trouble breathing
  • Cold sweats
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5
Q

Drug rationale
Dyslipidaemia

A

Reduce progression of atherosclerosis, reduce risk of MI and stroke in patients with established CV disease, and improve survival.

Reduce premature CV morbidity and mortality in people at high risk of CV events.

Prevent pancreatitis due to hypertriglyceridaemia.

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6
Q

Drug treatment
Dyslipidaemia

A
  1. Statin
  2. If statin not tolerated ezetimibe, PCSK9 inhibitors
  3. Pt with High Cardiovascular risk = Statin + (2) OR Fibrate
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7
Q

Indication
Ezetimibe

A
  • Treat high blood cholesterol
  • Dyslipidaemia
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8
Q

MOA
Ezetimibe

A

Selectively inhibiting the absorption of cholesterol and phytosterol by the small intestine without altering the absorption of fat-soluble vitamins and nutrients.

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9
Q

Contraindications
Ezetimibe

A
  • Liver problems
  • Acute inflammation of the pancreas
  • Severe renal impairment
  • Abnormal liver function tests
  • Rhabdomyolysis
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10
Q

Adverse effects
Ezetimibe

A
  • Headache
  • Diarrhoea
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11
Q

HMG-CoA reductase inhibitors also known as…

A

Statins

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12
Q

MOA: HMG-CoA reductase inhibitors / Statin

A

Drugs for Dyslipidaemia
* Inhibit HMG-CoA reductase
* increase hepatic cholesterol uptake
* reduce cholesterol, LDL
* small increase in HDL

Competitively inhibit 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase (a rate-limiting enzyme in cholesterol synthesis). Increase hepatic cholesterol uptake from blood, reduce concentrations of total cholesterol, LDL and triglyceride (modest), and produce a small increase in HDL concentrations.

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13
Q

Indication: Statin / HMG-CoA reductase inhibitor

A
  • Hypercholesterolaemia
  • High risk of coronary heart disease, with or without hypercholesterolaemia

Used in low doses for primary CVD prevention (high risk CVD patients with no pt Hx of CVD yet)
Used in high doses for secondary prevention of CVD (pt with recent CVD Hx)

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14
Q

Adverse reactions
Statins / HMG-CoA reductase inhibitor

A
  • mild GI symptoms
  • headache
  • sleep disturbance
  • dizziness

Muscle symptoms (myalgia, myopathy, rhabdomyolysis)
Risk of myopathy (with or without CK elevation) and rhabdomyolysis is dose-related. Risk is also increased by age, illness (see Precautions) and certain drug interactions (see Statins).

Muscle symptoms are more likely in the first 4–6 weeks after starting or increasing the dose of a statin. Statin-associated muscle symptoms are often difficult to differentiate from other causes; for further information see www.nps.org.au/​sams.

There have been very rare reports of an autoimmune necrotising myopathy, generally with CK concentration >10 times ULN and anti-HMG-CoA reductase autoantibodies, which does not resolve solely on stopping the statin.

An effect on ocular muscles may cause visual disturbances (eg diplopia or blurred vision).

Aminotransferase concentrations
Elevated aminotransferases occur in 0.5–2% of patients treated with statins; it is dose-dependent, generally responds to a reduction in dosage.

Diabetes
Statins are associated with a slightly increased risk for new-onset diabetes which appears highest in those who are already more likely to develop diabetes.

A meta-analysis reported that, on average, treating 255 patients with statins for 4 years resulted in 1 additional case of diabetes (while possibly preventing >5 major coronary events).

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15
Q

Practice points
Statins / HMG-CoA reductase inhibitor

A
  • do not stop if symptoms of ACS
  • 1st choice for hypercholesterolaemia
  • TIMING : simvastatin better at night, must be taken consistently
  • Monitor Creatine (affects muscle issues)
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16
Q

Drug Class

Atorvastatin

A

Statin / HMG-CoA reductase inhibitor

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17
Q

Drug Class

Fluvastatin

A

Statin / HMG-CoA reductase inhibitor

18
Q

Drug Class

Pravastatin

A

Statin / HMG-CoA reductase inhibitor

19
Q

Drug Class

Rosuvastatin

A

Statin / HMG-CoA reductase inhibitor

20
Q

Drug Class

Simvastatin

A

Statin / HMG-CoA reductase inhibitor

21
Q

Generic names of Statins / HMG-CoA reductase inhibitors

A

Atorvastatin
Fluvastatin
Pravastatin
Rosuvastatin
Simvastatin

22
Q

Generic drug names
PCSK9 inhibitors

A

Alirocumab
Evolocumab

23
Q

Suffix
PCSK9 inhibitors

A

“cumab”

24
Q

“cumab” Suffix

A

PCSK9 inhibitors

25
Q

Indication
PCSK9 inhibitors

A

Dyslipidaemia

26
Q

MOA
PCSK9 inhibitors

A

Bind to proprotein convertase subtilisin/kexin type 9 (PCSK9) and inhibit its activity, increasing LDL clearance from the blood.

27
Q

HDL and LDL

A

Cholesterol travels through the blood on proteins called “lipoproteins.” Two types of lipoproteins carry cholesterol throughout the body:
LDL = loser = High LDL –> increased risk of heart disease and stroke

HDL = hero = absorbs cholesterol = high HDL –> lowered risk of heart disease and stroke

28
Q

Adverse effects
PCSK9 inhibitors

A

injection site reactions

29
Q

Drug class and indication

Alirocumab

A

PCSK9 inhibitor
Hypercholesterolaemia, add-on to optimised lipid-lowering treatment in patients with ischaemic cardiovascular disease

Primary hypercholesterolaemia after an inadequate response to, or intolerance of, statins

30
Q

Drug class and indication

Evolocumab

A

PCSK9 inhibitor
Hypercholesterolaemia, add-on
Primary hypercholesterolaemia after an inadequate response to, or intolerance of, statins

31
Q

Generic names of Fibrates contain …

A

“fib”

32
Q

Drug class containing ‘fib’

A

Fibrates

33
Q

Generic drug names
Fibrates

A

Fenofibrate
Gemfibrozil

34
Q

Indication
Fibrates

A

Dyslipidaemia

35
Q

MOA
Fibrates

A

Activate peroxisome proliferator-activated nuclear receptors and modulate lipoprotein synthesis and catabolism. They reduce plasma triglyceride, moderately increase HDL and have a variable effect on LDL concentrations.

36
Q

Precautions
Fibrates

A

Renal
Contraindicated in severe impairment.

Hepatic
Contraindicated when hepatic impairment, primary biliary cirrhosis, gallstones or gall bladder disease are present.

37
Q

Adverse effects
Fibrates

A

GI disturbances (eg dyspepsia, abdominal pain), increased creatinine concentration (reversible)

38
Q

Practice points
Fibrates

A

Affects creatine
Therefore … check baseline creatine

39
Q

Drug class and indication

Fenofibrate

A

Fibrates
Severe hypertriglyceridaemia
Dyslipidaemia associated with type 2 diabetes (second line)

Having a high level of triglycerides in your blood can increase your risk of heart disease.
triglycerides are fat (lipids)
Triglycerides and cholesterol are different types of lipids that circulate in your blood:
* Triglycerides store unused calories and provide your body with energy.
* Cholesterol is used to build cells and certain hormones.

40
Q

What are triglycerides

A

Having a high level of triglycerides in your blood can increase your risk of heart disease.
triglycerides are fat (lipids)

41
Q

Drug class and indication

Gemfibrozil

A

Fibrate
Drug for dyslipidaemia
Severe hypertriglyceridaemia with risk of pancreatitis
Mixed hyperlipidaemia and dyslipidaemia associated with diabetes (second line)

Pharmacology 2 (41 decks)

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