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.Pharmacology > Part 21: Lipid Lowering Agents > Flashcards

Part 21: Lipid Lowering Agents Flashcards

1
Q

why can lipids and cholesterol lead to heart issues?

A

too much cholesterol and lipids can deposit into the walls of the arteries

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2
Q

the deposits of lipids and cholesterol are called_____

A

atherosclerotic plaques

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3
Q

atherosclerosis is also called the ____ and ____ of BV

A

hardening and stiffness

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4
Q

t/f saying atherosclerosis is the hardening of the arteries is misleading bc it doesnt actually make the BV hard like wood , but stiff bc they cant constrict / dilate

A

t

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5
Q

what is the issue with BV narrowing due to plaque build up?

A

restrict O2 delivery to the heart muscle , which results in angina and shortness of breath

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6
Q

what happens if coronary arteries get completely blocked?

A

the regions of the heart that would be supplied by that coronary artery begin to die, resulting in reduced heart function and possible heart failure

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7
Q

what can happen if plaque ruptures?

A

platelets are rapidly activated and can cause a blood clot, which can get lodged in a vessel, blocking O2 and causes a heart attack

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8
Q

plaque accumulation in peripheral vessels can cause ___

A

circulatory problems and pain bc the muscles are not adequately supplied with blood

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9
Q

blockages of the carotid and cerebral arteries can cause ___

A

stroke or transient ischemic attack (TIA)

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10
Q

narrowing of the carotid arteries obstructs blood flow from the heart to the ____

A

brain

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11
Q

blockages in the _____ vessels can cause ischemia in regions of the brain, often called mini strokes, of TIAs

A

intracranial

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12
Q

what is the difference between a stroke and a TIA?

A

in a stroke, a blood clot fully obstructs a vessel in the brain, a TIA occurs when blood flow is reduced for a short time, but is then restored and symptoms go away

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13
Q

t/f TIAs are typically very brief and some patients have several without knowing it before a real stroke happens

A

t

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14
Q

what is an embolism?

A

when a small piece of a blood clot travels through the blood stream and gets lodged in another vessel, which can cause a larger clot and vessel occlusion

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15
Q

_____ is a common complication of deep vein thrombosis, where blood clots form in the leg veins and travel back to the lungs where they plug pulmonary vessesl

A

pulmonary embolisms

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16
Q

cholesterol and triglycerides can come from which two places?

A
  1. dietary sources

2. made by the liver

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17
Q

in order to supply the body with sources of lipids, the liver packages them into _____ that circulate in the blood

A

lipoproteins

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18
Q

what liporpotein does the liver make when it wants to distribute triglycerides and cholesterol?

A

VLDL

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19
Q

triglycerides are delivered to target tissues which leaves the lipoprotein with less ____ and more ____, increasing the density of the particle into ____ lipoproteins

A

lipid; protein; IDL (intermediate density lipoproteins)

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20
Q

low density lipoproteins (LDL) is rich in ____

A

cholesterol

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21
Q

when LDL is taken up by cells, it is broken down into ____, or the LDL particle can be ___

A

cholesterol; returned to the liver for recycling

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22
Q

an excess of LDL particles can lead to ___

A

deposition in BV, making atherosclerotic plaques

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23
Q

what is the role of HDL?

A

picks up extra cholesterol and returns it to the liver

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24
Q

lipid lowering agents aim to lower which lipoprotein?

A

LDL

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25
Q

what are 2 main ways to target LDL pharmacologically?

A
  1. reduce amount of cholesterol and lipids coming into the system via the GI tract
  2. reduce production of new cholesterol in the liver
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26
Q

by limiting the amount of cholesterol available to hepatocytes, it forces the liver to increase _____

A

LDL recycling, thus removing LDL from the blood

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27
Q

what are two classes of drugs that act in the GI tract to 1. reduce the recycling of bile acids and 2. the absorption of lipids from food sources respectively?

A
  1. bile acid binding resins

2. cholesterol absorption inhibitors

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28
Q

do bile acid binding resins and cholesterol absorption inhibitors have a significant effect on lowering LDL?

A

only a modest effect bc hepatocytes are still able to make cholesterol from scratch

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29
Q

what are 2 classes of drugs that can reduce the making of new cholesterol?

A
  1. PCSK9 inhibitors

2. statins

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30
Q

statins are also known as ___

A

HMG-CoA reductase inhibitors

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31
Q

how does inhibiting the HMG-CoA reductase enzymes help reduce LDL cholesterol?

A

increases the expression of LDL receptors on hepatocytes, which causes more cholesterol to be taken up into cells out of the blood

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32
Q

cholestyramine belongs to which class of drug?

A

bile acid binding resins

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33
Q

bile acids are rich in ____ and play a major role in facilitating the absorption of lipids from the GI tract by acting as ____

A

cholesterol; detergents

34
Q

bile acids are typically recycled repeatedly, with ____ (much, little) being excreted in the feces

A

little

35
Q

if the reuptake of bile acids from the GI tract is impaired, the excretion of these cholesterol containing detergents will be ____ (increased/decreased) and stored bile acids are _____(depleted/built-up)

A

increased; depleted

36
Q

when bile acids are excreted and become depleted, what will hepatocytes do?

A

they will make new bile acids, using cholesterol in the process (liver will make cholesterol, or it will be pulled out of the blood)

37
Q

how do bile acid binding resins like cholestyramine work?

A

prevent the recycling of the bile acids, which lowers LDL bc the liver will constantly need to make more bile acid which requires pulling cholesterol out of the blood

38
Q

bile acid binding resins can be used with which other class of drugs to have a therapeutic benefit?

A

statins

39
Q

what are some of the ADRs of bile acid binding resins?

A

bloating, constipation, can reduce the absorption of drugs and essential nutrients

40
Q

cholestyramine is not soluble and some patients describe the administration to be comparable to ____

A

drinking sand

41
Q

the doses of cholestyramine are typically up to ____g/day

A

30

42
Q

what is the MOA of Ezetimibe?

A

inhibits absorption of cholesterol contained in dietary sources by binding to intestinal sterol transport protein (NPC1L1), preventing uptake of cholesterol in the GI tract

43
Q

does ezetimibe alter the absorption of other lipids, fat soluble vitamins, or steroid hormones?

A

no, just cholesterol

44
Q

reducing the amount of cholesterol absorbed from food sources will also promote hepatocyte ____ of LDL cholesterol

A

recycling

45
Q

ezetimibe can often be combined with ____ (drug class) to be more effective

A

statins

46
Q

LDL receptors are expressed on ____ and ____

A

cell membranes of target tissues and on the surface of hepatocytes

47
Q

what happens after the LDL binds to the LDL receptor?

A

endocytosis brings the LDL particle into the cell, in hepatocytes, the LDL is broken down so cholesterol can be recycled an dthe LDL receptor is brought back to the cell membrane so more LDL can be brought in

48
Q

what is PCSK9?

A

an endogenously produced protein whose function is to regulate whether the LDL receptor is recycled or downregulated after endocytosis with LDL particles

49
Q

what happens if PCSK9 is bound to the LDL receptor?

A

the whole complex is taken up by the hepatocyte by endocytosis and cholesterol is taken back for re-use and signals fo rthe cell to degrade the LDL receptor (not good, leads to too much cholesterol in the blood)

50
Q

what class of drug is Evolocumab?

A

PCSK9 inhibitor

51
Q

what is the MOA of PCSK9 inhibitors like Evolocumab?

A

inhibit PCSK9 to reduce LDL receptor downregulation in order to facilitate LDL cleasrance from the blood and into hepatocytes

52
Q

how often is Evolocumab dosed?

A

biweekly or monthly by SC injection

53
Q

what is Evolocumab?

A

a MAB that binds to circulating PCSK9 to prevent its interaction with the LDL receptor, so that when LDL receptor is endocytized, it will be returned to the cell surface to remove more cholesterol from the blood

54
Q

for who is Evolocumab indicated?

A

patients with genetic causes of hyperlipidemia, and heart disease when statin therapy wasnt enough

55
Q

t/f there have been some studies that have shown that adding a PCSK9 inhibitor to a statin is more effective than doubling the statin dose

A

t

56
Q

the LDL levels can be reduced up to ___% in some patients after Evolocumab

A

70%

57
Q

what are statins?

A

aka HMG-CoA reductase inhibitors, work by inhibiting the key enzyme involved in cholesterol making in hepatocytes

58
Q

which class of drug is the first line patients at risk of CAD or a CV event?

A

statins

59
Q

statins increase the expression of ____

A

LDL receptor

60
Q

what are some of the ADRs of statins?

A
  1. muscle soreness or weakness

2. liver toxicity at high doses

61
Q

muscle soreness / weakness from statin use may indicate ____, which can cause ___

A

elevated levels of creatine kinase (CK); kidney damage

62
Q

t/f blood tests are routine for statin use

A

t

63
Q

t/f statins can be used as preventative treatment for MI and stroke

A

t

64
Q

t/f statins can be beneficial for some patients even if they have so-called “normal” cholesterol and LDL

A

t

65
Q

what is the Framingham risk score (FRS)?

A

a tool used to estimate the risk of a patient having a CV event or developing CVD (especially coronary artery disease) in the next 10 years

66
Q

what is the first step of the FRS?

A
  1. using patient data to determine the # of risk points
67
Q

what is step 2 of the FRS?

A

the points are converted to % and patients are categorized to a yellow, blue, or red zone for risk

68
Q

what do the red, yellow, and blue zones of the FRS mean?

A

red: high risk
yellow: intermediate risk
blue: low risk

69
Q

if a patient is 30-59 and has a 1st degree relative who has had an early CVD disease (meaning <55 y/o males or <65 y/o females), what happens to the FRS score?

A

it gets doubled (risk is doubled)

70
Q

what is the 3rd step of the FRS?

A

what to do for the patient to manage their risk based on what has been found out

71
Q

lipid lowering agents are indicated for which patients?

A

diabetes, renal impairment, and the high risk category of FRS (>20%)

72
Q

what % risk is considered “high risk” by the FRS?

A

> 20%

73
Q

what % risk is “intermediate risk” based on the FRS?

A

10-19%

74
Q

what % risk is “low risk” based on the FRS?

A

<10%

75
Q

are people with an FRS <10% typically treated with statins?

A

no

76
Q

t/f patients with a high risk FRS score are typically recommended a statin regardless of their lipid panel results

A

t

77
Q

patients with intermediate FRS score are “treated to target”, what does this mean>

A

often treated with statins and or lifestyle modification until their LDL lipid levels reach less than 2 mmol/L

78
Q

when can the use of statins be thought of as more beneficial than the risk?

A

if the patient has high cholesterol, high LDL and other risk factors for CVD

79
Q

t/f patients with a low FRS are typically not treated with statins, even if their LDL levels are mildly elevated

A

t

80
Q

t/f the risk score on the FRS can change over time for a patient, so it should be done at multiple intervals in their life

A

true, one of the risk factors is age, so it will be constantly changing

.Pharmacology (55 decks)

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