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Pharmacology > Statins (drugs to treat hyperlipidemia) > Flashcards

Statins (drugs to treat hyperlipidemia) Flashcards

1
Q

What is the most associated species with hyperlipidemia?

A

LDL (not triglycerides)

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2
Q

What are lipoprotein particles composed of?

A

1) lipid membranes
2) hydrophobic core
3) apolipoproteins

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3
Q

How do LDL differ from HDL?

A

LDL is 60% cholesterol while HDL is 20% cholesterol

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4
Q

What enzyme makes cholesterol?

A

HMG-CoA reductase

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5
Q

In normal cholesterol states, where does LDL go?

A

binds to LDL receptor and is degraded in the lysosome into cholesterol which goes to membranes, steroid hormones, bile acids, lipoproteins

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6
Q

When does LDL become a problem?

A

When there is too much of it and it isn’t taken up into the cell - stays in blood

  • endothelial injury allows entry of LDL
  • macrophages take up LDL becoming FOAM cells
  • necrosing FOAM cells release cholesterol into matrix making fatty streak
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7
Q

How might HDL prevent atherosclerosis?

A

HDL promote the REVERSE cholesterol transport (from periphery back to liver where it can be secreted as bile)

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8
Q

What is target LDL?

A
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9
Q

What is target HDL?

A

> 50mg/dL

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10
Q

What is target triglyceride?

A
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11
Q

What 4 drug classes inhibit LDL?

A

1) statins
2) bile acid-resins
3) chol. absorption inhibs
4) PCSK9 inhibitors

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12
Q

What is the NUMBER ONE causative role of atherosclerosis?

A

high levels of LDL

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13
Q

What 2 drug classes inhibit triglycerides?

A

1) niacin

2) fibrates

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14
Q

What is the treatment for moderate hypercholesterolemia with LOW cv risk?

A

lifestyle change

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15
Q

What is the LDL level that indicates statins?

A

> 190mg/dL

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16
Q

What are the 6 statins?

A 
atorvastatin
fluvastatin
lovastatin
simvastatin
pravastatin
rosuvastatin
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17
Q

What are the 3 bile acid binding resins?

A

cholestryamin
colestipol
colesevelam

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18
Q

What is the primary clinical effect of statins?

A

REDUCE LDL

moderate reduction in triglycerides and increase in HDL

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19
Q

What is the MOA of statin?

A

as an analog of the HMG CoA substrate, they inhibit HMG CoA reductase

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20
Q

What is the role of HMG CoA reductase?

A

to make cholesterol

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21
Q

What is the SREBP transcription factor?

A

a protein that is activated in the face of reduced cholesterol synthesis and works to INCREASE expression of LDL receptor which increases clearance of serum LDL

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22
Q

What turns SREBP on?

A

decreased cholesterol levles

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23
Q

What 2 ways do statins decrease cholesterol?

A

1) reduced cholesterol formation

2) increase LDL receptor expression to sop up serum LDL

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24
Q

True or false: statins are effective at reducing CHD risk irrespective of initial baseline LDL

A

TRUE (can prevent primary and secondary CHD)

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25
Q

If you double the dose of statins, do you double the effects?

A

NO (only increases like 5-6% but significantly increasing it can cause adverse effects)

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26
Q

What is the main side effect of statins/

A

Rhabdomyolysis (also causes myalgia)

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27
Q

Which statin is the best choice for minimizing drug interactions?

A

Pravastatin

28
Q

Where are statins absorbed?

A

intestine (metabolized by CYP3A4)

29
Q

How are statins taken up into the liver?

A

OATP2

30
Q

How are statins excreted?

A

bile and feces

31
Q

What is the only statin that is eliminated via the liver and the kidney?

A

pravastatin

32
Q

How do CYP3A4 inhibitors affect the potency of statins?

A

increases it - statins can no longer be metabolized

increases risk of rhabdo

33
Q

What 2 statins are metabolized via CYP2C9?

A

fluvastatin and rosuvastatin

34
Q

What are 5 known inhibitors of CYP3A4?

A 
cyclosporin
ritonavir
itraconazole
erythromycin
grapefruit juice
35
Q

What are inducers of CYP3A4?

A

phenytoin
barbiturates
rifampin
thiazolidnediones

36
Q

What is Gemfibrozil?

A

a fibrate drug that is strongly associated with INCREASED risk of STATIN induced myopathy

37
Q

What does Gemfibrozil do?

A

inhibits OAT2P transporter - statins not taken up (increased serum statins)

38
Q

True or false: gemfibrozil does NOT affect pravastatin

A

FALSE - causes an increase in systemic levels of all statins

39
Q

In what 2 ways does gemfribrozil increase serum statins?

A

1) inhibits OAT2P

2) inhibits glucoronyl transferases

40
Q

What are 2 big contraindications of statins?

A

1) pregnancy

2) liver disease

41
Q

True or false: statins should be prescribed earlier in life

A

TRUE - usually the arteriolar damage has already been done by the time they are prescribed in the patient’s 40s-50s

42
Q

What is the clinical effect of bile acid binding resins?

A

modest reduction in LDL

can increase serum triglycerides

43
Q

What is the MOA of bile acid binding resins?

A

resins (cationic) bind to negatively charged bile acids and prevent their absorption in the small intestine

44
Q

What is the therapeutic benefit of making bile not absorbable in the small intestine

A

makes liver make more bile therefore resulting in a decrease in hepatic cholesterol clearance (causing upregulation of LDLR)

45
Q

Why do bile acid binding resins increase serum triglycerides?

A

because bile acids usually serve to suppress endogenous triglyceride synth

46
Q

Can bile acid resins be used in combo with a statin?

A

YES - to aggressively reduce LDL

47
Q

When are bile acid resins really important?

A

for pregnant/nursing women

48
Q

True or false: bile acid resins have serious adverse effects

A

FALSE very safe/few side effects but GI disturbances and occasionally impair absorption of ADEK vitamins (fat soluble)

49
Q

What are the contraindications for bile acid resins?

A

elevated triglycerides

50
Q

What does ezetimibe do?

A

inhibit cholesterol absorption (both dietary and biliary cholesterol in small intestine) - results in decreased delivery of cholesterol to the liver reducing VLDL

51
Q

What receptor does ezetimibe block?

A

NPC1L1

52
Q

When might ezetimibe be beneficial?

A

in patients who do not have an intact LDLR (so like familial hypercholesterolemia)

53
Q

What are the new anti-hypercholesterolemia drugs?

A

inhibitors of PCSK9 (a protein that is mutated in patients with FH) which prevents LDLR recycling and instead degrades it

54
Q

True or false: PCSK9 mutations can be both LOF and GOF

A

TRUE

55
Q

What 2 drugs inhibit PCSK9?

A

alirocumab
evolocumab

(antibodies specific for PCSK9)

56
Q

Why is there a need for anti-hypercholesterolemia drugs other than statins?

A

because statins target the LDLR mostly; patients with FH don’t have a functional LDLR

57
Q

What 2 drugs can treat homozygous FH?

A

lomitapide

mipomersen

58
Q

How does mipomersen work?

A

reduces expression of apoB100 resulting in reduced production of chylomicrons and VLDLs

59
Q

How does lomitapide work?

A

inhibits microsomal triglyceride transfer protein (MTP) which is needed for the assembly of chylomicrons and VLDLs

60
Q

What is the official lab cut off for hypertriglyceridemia?

A

> 500mg/dL

61
Q

What pathology is particularly concerning with hypertriglyceridemia?

A

pancreatitis

62
Q

True or false: elevated serum triglycerides are associated with a decreased serum conc of HDLs

A

TRUE (so drugs will have the corollary effect of increasing HDL)

63
Q

What 2 drugs are used for the treatment of hypertriglyceridemia?

A

niacin

fibrates

64
Q

What is the most effective drug at raising HDLs?

A

Niacin (often combined with statins to lower LDL and also increase HDL)

65
Q

What is Lp(a) lipoprotein and what does it do?

A

a modified LDL that can block the conversion of plasminogen to plasmin

Niacin BLOCKS this (promoting thrombolysis)

66
Q

What is the main adverse effect of niacin?

A

skin flushing (due to prostaglandins - take an NSAID)

also uric acid build up (gout) and peptic ulcer disease

Pharmacology (21 decks)

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