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Pharmacy Y3- Cardiovascular diseases > Week 9- Dyslipidemia+lipid lowering drugs > Flashcards

Week 9- Dyslipidemia+lipid lowering drugs Flashcards

1
Q

what is dyslipidemia?

A

high fat levels in your blood stream

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2
Q

is dyslipidemia a risk factor for cardiovascular disease?

A

yeah

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3
Q

how can you reduce cardiovascular risk through lipids?

A
  • change diet to less fat

- and medication if they still have high cholesterol levels

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4
Q

when does LDL get deposited in the blood vessels? leads to what?

A

when it is oxidised leading to atherosclerosis

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5
Q

why is HDL considered as a antioxidant?

A

because it decreases the adverse effects of the LDL by transporting excess cholesterol from peripheral tissues to the liver

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6
Q

what are the NICE guidlines for TC, LDL, HDL,TG levels?

A

aim for a 40% decrease in NON-hdl CHOLESTROL TC= <5

LDL<3

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7
Q

what is the epidemiology for cholestrol levels?

A
  • increases as you get older
  • western diet leads to high TC/LDL
  • South asian populations- higher % of population with HDL <1.0mmol/l
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8
Q

what is the aetiology of high cholestrol?

A
  • Primary dyslipidemia 60% , combination of diet and genetics (5 inherited conditions), high saturated fat, physically inactive, overweight or obese, smoking, large waist circumference
  • secondary dyslipidemia 40%, underlying cause eg. disease or drugs, natural rise as age and after menopause
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9
Q

what is familial hypercholestrolaemia?

A

-inherited high levels from birth
mutation in LDLR or APOB or PCSK9
-Homzygous mutation- >20mmol/l
-hetrozygous mutation- >8mmol/l

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10
Q

what is familial combined hyperlipidemia?

A
  • high cholestrol and trigylceride by 20-30yrs
  • raised VLDL and more compact and dense LDL than normal
  • fasting TG>1.5MMOL/L
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11
Q

what is type 3 hyperlipidemia?

A
  • inherited
  • high cholsterol and trigylceride
  • mutation in ApoE
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12
Q

what is polygenic hypercholesterolemia?

A
  • More than 1 gene with changes

- >12 genes linked to high cholesterol

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13
Q

what is primary hypertriglyeridaemia?

A

 Lipoprotein lipase deficiency
 Affects 1 in a million
 Very high TG

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14
Q

what is lysosomal acid lipase deficeny?

A

 Breaks down fat in lysosomes normally but instead fat builds up
in cells
 Rare condition – affects <1/1 million in UK

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15
Q

what are some signs of hyperlipidemia?

A
  • corneal arcus (ring of white around eye)
  • tendon xanthomas (deposition at joins in skin)
  • xanthelesma (pockets aroudn the eye)
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16
Q

what are some underlying disorders that can cause secondary dyslipidemia?

A 
Diabetes mellitus 
Hypothyroidism 
Chronic renal failure 
Alcoholism 
Liver disease
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17
Q

what certain drugs that can cause dyslipidemia?

A 
Thiazide diuretics
Loop diuretics
 Beta blockers
Oral contraceptves
Ciclosporin
Glucocorticoids
Isotretinoin
Tamoxifen
Protease inhibitors for HIV
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18
Q

what is the risk associated with lipoprotein a?

A 
-Apo(a) receptor– structurally similar to
plasminogen
-Lp(a) inhibits binding of
plasminogen to receptors on
endothelial cells – leads to less
plasmin generation and promotion
of thrombosis
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19
Q

what is the role of plasminogen?

A

it breaks down clots

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20
Q

what are some non-pharmacological treatments

A

-dietary modification
 Low saturated fat, low trans fat, high mono or polyunsaturated fat – to decrease LDL and increase HDL
 Oily fish twice weekly
 Plant sterols and stanols to decrease cholesterol absorption from gut
 High fibre – soluble fibre (from fruit and veg) may decrease cholesterol absorption from gut
-weight loss BMI <25
-smoking
-physical activity 30mins 5xtimes per week
-reduce alcohol

21
Q

15:43 what are the main fats?

A

cholesterol and triglycerides which is taken in from diet

22
Q

what is the main drug for lipid lowering?

A

statin

23
Q

what are statins not great at lowering?

A

triglycerides

24
Q

what type of drug is a statin?

A

HMG-CoA reductase inhibitors

25
Q

how do statins work?

A
  • in the liver we have acetyl CoA through a series of enzymes forms cholesterol in the liver, one of these enzymes is HMG CoA reductase so statins inhibit this i.n the liver
  • they are competitve with HMG CoA reductase
  • decreased in cholesterol synthesis
  • this makes the liver think it needs to make more cholestrol so it upregulates LDL receptors on the surface of its cells
  • this allows LDL to be taken up from the blood
  • so serum LDL levels go down
26
Q

what percentage of cholesterol traveling in the body is made by the liver?

A

80-85% and 10-15% comes from diet

27
Q

what are the main statin drugs?

A

atorvastatin, rosuvastatin, simvastatin, fluvastatin, pravastatin

28
Q

what are the main 3 things that statins do?

A
  • reduce LDL levels
  • reducdes plasma TG slightly
  • increases HDL
29
Q

which statins are the fast acting ones?

A

simvastatin, lovastatin, pravastatin

30
Q

whcih statins are the long lasting statins?

A

atorvastatin and rosuvastatin

31
Q

why is simvastatin an interesting statin?

A

its a prodrug and is inactive until it reaces the liver where its metabolised and activated

32
Q

what are statins other protective effects?

A
  • plaque stability= decrease risk. oflast stages of atherosclerosis before plaque ruptures, increse collage so the plaque is more stable, neovascularisation of ischemic tissue that is dead
  • anti-thrombotic=can decrease clotting through platelet aggregation, can increase fibrinolytic activity whih is the break down of the clot
  • anti-oxidant= decrease oxidation of LDL which causes atherosclerosis
  • anti inflammatory=smooth muscle cell proliferation and affects adhesion molecules
33
Q

what are some genetic variations that influence reposnce to statin?

A

-CYP’s
-HMG CoA redcutase
-Lipoprotein lipsase affects the breakdown of TG
-Apoproteins on the surace of lipoproteins
-Cholesteryl ester transfer protein
-Lecithin cholesterol acyltransferase
-PPAR alpha
-SREBP1 and 2
-IL1β, IL6 polymorphisms influence response to
pravastatin

34
Q

what are some of the benefits and effectveness of these statins?

A
  • reduce LCL by 20-40%
  • reduce TG by 10-20%
  • 5-10% increase in HDL
  • used as primary and secondary preventations of cvd
35
Q

what is a negative for using the more lipophyllic statins?

A

can develop Type II diabetes

36
Q

what are fibrates?

A

-not used routinely
used for paitents that have hypertriglyceridemia serum TG>10MMOL/L and nothing else is helping or if statins alone dont work or they have adverse afects
-derivates of fibric acids and structurally related to thiazolidinediones

37
Q

how do fibrates work?

A
  • they switch on a transcription factor called PPAR alpha

- 2 of the important genes they switch on is lipoprotein lipase and ApoA1/5

38
Q

what is PPAR alpha?

A

its a nuclear receptor that binds directly to DNA and switches on certain genes that are involved in lipid metabolisim.

39
Q

what does lipoprotein lipase do?

A

results in breakdown of VLDL, removes TG from blood stream and to the liver

40
Q

what does ApoA1/5 do?

A

results in increase HDL production

41
Q

what are the results of fibrates?

A

-Increase hepatic LDL-C uptake – form LDL with higher affinity to the LDL
receptor
-Increase fatty acid uptake and conversion to acyl co-A by liver therefore not
available for TG synthesis
-Decrease secretion of VLDL from liver and hence TG levels reduced
-Anti-inflammatory effects
Decrease APP synthesis – CRP and fibrinogen
Inhibit VSMC inflammation via NF-κB

42
Q

What are some drugs that inhibit cholesterol absorption?

A

-ezetimibe– inhibits cholesterol absorption –
used where statin contraindicated or in addition
to statin
-Bile-acid binding resins – no longer
recommended except in special circumstances
as can aggravate hypertriglyceridemia
-Plant stanols and sterols – supplements and
functional foods

43
Q

what does ezetimibe do?

A

-its blocks proteins involved in the cholestrol transport in the epithelial cells.
-, incl
NCPC1L1, aminopeptidase N and caveolin1-Annexin A2 complex
-Conjugated in the intestine to ezetimibe glucuronide (also
pharmacologically active) and excreted in stools
-lowers diet LDL by 17%

44
Q

what does bile acid binidn resins do?

A

Sequester bile acids in intestine and prevent reabsorption
and enterohepatic circulation – promotes conversion of
cholesterol into bile acids, resulting in increased LDL-R in
liver and LDL clearance from plasma
Decrease plasma LDL, unchanged HDL and can
increase TG
13% fall in plasma cholesterol

45
Q

what does nicotinic acid derivaties do?

A

-Nicotinic acid - water-soluble B vitamin
-1.5-3g day – lowers both LDL-cholesterol and TG by inhibiting
synthesis
Increases HDL-cholesterol
Inhibits hepatic TG production and VLDL secretion

46
Q

why are nicotinic acid derivities not recommended by NICE anymore?

A

No longer recommended by NICE for primary/secondary
prevention of CAD, or CKD or diabetes because of
vasodilatory effects

47
Q

what are Alirocumab and Evolocumab and how do they work?

A

Monoclonal Abs that inhibit PCSK9, involved in regulation
of LDL receptors on liver cells and by binding of mAb,
results in increasing receptor number and LDL uptake
Treatment of primary hypercholesterolemia or mixed
dyslipidemia as adjunct to diet
Combination with statin or with other lipid-lowering drugs
if statin not tolerated
Approved by NICE in summer 2016

48
Q

what are fish oils and hwhy arent they recommended by NICE anymore?

A

No evidence that reduce hyperlipidemia
No longer recommended by NICE for primary/
secondary prevention of CAD, or CKD or diabetes
However, eating oily fish reduces risk of ischemic
heart disease

Pharmacy Y3- Cardiovascular diseases (8 decks)

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