Dyslipidemia Flashcards

1
Q

Hyperlipemia

A

Excess tag

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2
Q

Hyperlipidemia

A

Hyperlipoproteinemia

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3
Q

Cholesterol

A

Hydrophilic

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4
Q

Cholesteryl ester

A

Hydrophilic

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5
Q

Chylomicrons carrying dietary TAGs to the liver

A

Can’t be decreased or increased with any intervention

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6
Q

Hyper TAG

A

DM
Myxedema
Alcohol
Estrogen
Uremia
Corticos
GSD
Hypopituutarism and acromegaly

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7
Q

Hyperchol.

A

Hypothyroidism
Early nephrosis
Resolving lipemia
Anorexia nervosa
Cholestasis
Hypopituitarism
Corticos

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8
Q

Hypolipidemic drugs

A

Statins
Niacin
Fabric Acid Derivatives (Fibrates)
Bike acid - binding resins
Inhibitors of Intestinal Sterol Absorption

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9
Q

Statins - HMG-CoA reductase inhibitors
(3 - hydroxy, 3-methyl glutaryl CoA recuctase)

A

Lovostatin
Simvastatin
Pravastatin
Atrovastatin
Fluvaastatin
Ruaovastatin
Pitavastatin

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10
Q

Statins

A

Decreases chol.
And LDL receptors
Decreasing LDL in plasma
Increasing HDL
Decreases TAG

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11
Q

Pleutropic effect of statins

A

Improved endothelial function
Reduced inflammation reduced platelet aggregation
Neivascularisation jnductuon in ischaemic tissues
Antithrombotic
Enhanced fibrinolysis and immune suppression

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12
Q

Statins taken orally excreted jn bile, urine and feces

A

Taken at bed time because long half life (1-3hrs except:
Atrova (14hrs), rosuva (12hrs) and pitava statin (19hrs)

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13
Q

Statins used in

A

All types of hyperlipidemia
-alone or with others like resins, niacin or ezetimibe
Use immediately after ACE

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14
Q
A
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15
Q

Adverse effects

A

High ALT and AST (×3)

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16
Q

Myopathy and rhabdomolysis

A

Break down of muscles
In blood stream
Pain
Dark cola red

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17
Q

Potentiate oral anticoagulants and antidiabetic ad they displace them from plasma proteins

A

Statins

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18
Q

Not used in pregnancy and lactation

A

No chol. for hormones and milk

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19
Q

Niacin - nicotinic acid

A

Decreases bothe VLDL and LDL and increases HDL so they can be combined with statins for synergism

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20
Q

Mechanism of Niacin (absorbed orally)

A

Adipose tissue
Liver
Plasma

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21
Q

In adipose

A

Niacin binds to it’s receptors decreasing mobilisation of FA so no TAG and no VLDL

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22
Q

In the liver (no synthesis and esteeification of fat)

A

Inhibits DAG acetyl transferase so no TAG synthesis and no VLDL

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23
Q

In plasma

A

Increases LipoProtein Lipase activity that clears VLDL and chylomicron

24
Q

Niacin used for

A

Mixed hyperlipidemia
Taken with oher drugs

25
Q

Niacin causes puritis and flushing

A

Because Prostaglandin that can be treated with aspirin

26
Q

Nausea, pain and gastric distress

A

Because niacin induces histamine release

27
Q

Nicotinic acid also dependent on OASS

A

So causes hyperurecemia

28
Q

Also elevates Hepatic enzymes (×2) without liver toxicity as well

29
Q

Take Niacin and potentiate

A

Anti hypertensive (this can be accompanied by atherosclerosis so it treats that)

30
Q

Fibric acid (fibrates) - Decrease VLDL and some LDL

A

Gemfibrozil and fenofibrate

31
Q

Fibrates, agonist of peroxisome proliferator activated receptor alpha

A

Decreases TAG
Increases LPL which hydrolyzes TAG and Decreases VLDL

32
Q

Directly increases lipolysis decreasing TAG and VLDL

A

Fibrates (also increases HDL by inhibiting it’s catabolism

33
Q

Take fibrates with

34
Q

Also used in mixed hyperlipidemia

35
Q

Most common adverse dibrates effecf

36
Q

Arrhythmias in

37
Q

You have gall stones in excess chol. with fjbrates

A

As doesn’t get directed towards TAG synthesis

38
Q

Also causes myopathies and myositis

A

When fibrates taken with statins

39
Q

Potentiate oral anticoagulants and antidiabetics

40
Q

Firates can cause

A

Hepatotoxicity

41
Q

No fibrates in

A

Pregnancy and lactation
Gall bladder release
Hepatic and renal dysfunction

42
Q

Bike acid binding resins

A

Colestipol
Cholestyramine
Colesevelam

43
Q

Resins used in

A

Isolated increase in LDL

44
Q

No absorption of resins orally

A

So goes to be excreted and affects natural enetrogepatic circulation of bile

45
Q

Uregulates LDLreceptoprs and scavangas

46
Q

Resins for

A

Treattment of peeps with hyperchol.

47
Q

Adverse resins

A

Constipation
Decreases absorption fat soluble vitamins

48
Q

Interactions with resins

A

Digoxin
Thiazide
Wayfaring
Aspirin
Phenylbutazone
Pamrava and flucastatin
Tetracycline
Thyroxine
Iron salts
Folic acid
Ascorbic acid

49
Q

Take drugs 1 - 2 hrs before

A

Resin (unless niacin)

50
Q

Coleselvam

A

No digoxin
Wayfaring
Reductase inhibitors

51
Q

Ezetimibe

A

Inhibitors of intestinal steroid absorption

52
Q

Inhibits chol. Absorption, both dietary adln

54
Q

Less than 10yrs no statins

A

Unless Pravastatin

55
Q

No lipophilic statin with CYP inhibitors

A

Increases myopathy and rhabdomyolysis