Lipid Lowering Medications Flashcards

1
Q

What is the desired outcome of lipid lowering agents?

A
  1. lower serum cholesterol
  2. lower serum LDLs
  3. prevention of CAD
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2
Q

How do lipid lowering agents help prevent CAD?

A
  • protect endothelial tissue
  • prevents plaque from rupturing
  • slow down the progression of atherosclerosis
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3
Q

What is cholesterol?

A

a lipid that is an essential part of bile acid & cell membranes

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4
Q

What lipid is insoluble in blood?

A

cholesterol

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5
Q

What lipid is a precursor of the steroid hormone?

A

cholesterol

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6
Q

What is a triglyceride?

A

a lipid made from fatty acid & glycerol

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7
Q

how are triglycerides aquired?

A

through the diet

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8
Q

Where are triglycerides stored?

A

adipose tissue

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9
Q

__________ levels correlate with LDL and are inverse to HDL

A

triglyceride

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10
Q

what are lipoproteins?

A

are carrier proteins that aid in transportation of cholesterol & triglycerides in the blood

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11
Q

Where are lipoproteins produced?

A

by the liver

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12
Q

What do LDLs enter circulation as?

A

tightly packed cholesterol, triglycerides, & lipids fom the liver to the peripheral tissue

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13
Q

____ are carried by proteins; broken down for energy or stored for future use as energy

A

LDLs

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14
Q

What are know as the “bad” cholesterol?

A

LDLs

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15
Q

What are the primary transport molecules for cholesterol?

A

LDLs

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16
Q

How do HDLs enter circulation?

A

as loosely packed lipids

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17
Q

________ are used for energy; pick up remnantsof fat & cholesterol from the peripheral tissues back to the liver where it is excreted in the bile

A

HDLs

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18
Q

What is considered to be the “good” cholesterol?

A

HDLs

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19
Q

What is the desired level for total cholesterol?

A

less than 200

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20
Q

What is the desired level for LDL?

A

less than 130

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21
Q

What is the desired level for HDL?

A

50 or higher

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22
Q

What are the desired levels from triglycerides?

A

less than 200

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23
Q

What do we want LDLs to be in diabetics & those at risk?

A

less than 70

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24
Q

What are non-modifiable CV risk factors?

A

genetic predisposition**
age
gender
- males greater than females
- equal after menopause

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25
What are the modifiable risk factors?
metabolic syndrome cigarette smoking sedentary lifestyle high-stress levels HTN obesity diabetes untreated bacterial infection
26
What are modifiable CV risk factors related to?
inflammation
27
What medications are HMG CoA reductase inhibitors?
lovastatin pravastatin simvastatin atorvastatin rosuvastatin
28
What medications are fibrates?
gemfibrozil (lopid) fenofibrate (tricor) fenofibric acid (tripipix)
29
what medication is a cholesterol absorption inhibitor
ezetimibe
30
what medications are PCSK9 inhibitors?
evolocumab (repatha) alirocumab (praulent)
31
What medications are bile acid sequestrants?
colesevelam (welchol) cholestyramine (prevalite) colestipol (colestid
32
What medication is a lipid lowering medication that is not used much anymore?
niacin
33
What is the suffix of that HMG-CoA reductase inhibitors have?
"statin"
34
What is the most effective & most prescribed lipid lowering drug?
HMG-CoA reductase inhibitors
35
How do HMG-CoA reductase inhibitors work?
block synthesis of cholesterol in the liver by competitively inhibiting HMG-CoA reductase activity
36
What do HMG-CoA reductase inhibitors affect LDLs, triglycerides & HDLs?
- decreases LDL levels by 25-65% - modest decrease in triglycerides by 10-40% - modest increase in HDL by 5-17%
37
Can you take HMG-CoA reductase inhibitors during pregnancy?
no; pregnancy category x
38
What do statins do in the vascular system?
- reduce smooth muscle cell changes - reduce inflammatory c3ells inside plaque - stabilize the endothelium - reduce friction in the bloodflow - reduce proteins associated with inflammation
39
Who should be on a statin?
- adults with a hx of CV disease - those with LDL level greater than 190 - adults 40-75 with diabetes - adults 40-75 with LDL of 70-189 & a 5-19.9% 10-year risk of developing CV disease -adults 40-75 years with LDL lvel of 70-189 & a 20% or greater 10-year risk of developing CV disease
40
at what kind of dose should you start a HMG-CoA reductase inhibitor?
start with a lower dose & increase as needed
41
When should HMG-Coa reductase inhibitors be given?
should be given in the evening/bedtime
42
What HMG-CoA reductase inhibitors can be given in the morning
rosuvastatin atorvastatin
43
When should you checkk lipid panel when starting HMG-CoA reductase inhibitors?
4-6 weeks after starting
44
What is the most potent of the HMG-CoA reductase inhibitors?
rosuvastatin
45
What are the most common side effects of HMG-CoA reductase inhibitors?
CNS effects - headahces - dizziness - insomnia - fatigue GI effects - flatus - abd pain - N/V - constipation
46
What should you avoid eating when taking a HMG-CoA reductase inhibitor?
grapefruit
47
What drug class can cause myopathy?
HMG-CoA reductase inhibitors
48
What drug class may cause rhabdomyolysis?
HMG-CoA reductase inhibitors
49
how can the risk of myopathy with HMG-CoA reductase inhibitors be reduced?
- reduced by using the lowest effective dose - cautiously combine statins with fibrates
50
What can HMG-CoA increase?
liver enzymes
51
How do you manage the increase in liver enzymes with HMG-CoA reductase inhibitors?
- is dose-dependent - serious liver problems are rare - manage by reducing the dose or stopping until levels return to normal
52
What is a contraindication for HMG-CoA reductase inhibitors?
active liver disease
53
What drug class can cause coenzyme Q10 deficiency?
HMG-CoA reductase inhibitors
54
What causes oxidative stress & shredding of the blood vessels?
diabetes smoking HTN dyslipidemia obesity aging
55
What does oxidative stress lead to?
endothelial dysfunction & reduced nitric oxide bioavailabilty
56
What does endothelial dysfunction & reduced nitric oxide bioavailability cause?
- leukocyte adhesion & inflammation - lipid deposition - vascular smooth muscle cell proliferation - vasoconstriction - platelet aggregation & thrombosis
57
What is the result of endothelial dysfunction & reduced nitric oxide availability?
progression of atherosclerosis & CV disease
58
How do cholesterol absorption inhibitors work?
work in the small intestine to inhibit the absorption of cholesterol
59
What are indications for cholesterol absorption inhibitors?
- lower serum cholesterol levels - those who can not tolerate statins
60
Can cholesterol absorption inhibitors be given in combination with statins?
yes
61
What are the adverse effects of cholesterol absorption inhibitors?
- abd pain & diarrhea (most common) - upper airway infections - arthralgias
62
What are contraindications for cholesterol absorption inhibitors?
- allergy pregnancy & lactation
63
What are PCSK9s?
proteins produced by the liver; play a role in regulating LDL
64
Who are PCSK9 ibhibitors often reserved for?
people who have very high LDL levels or those who cannot tolerate statins
65
What are PCSK9 inhibitors often used in conjunction with?
statins
66
How do PCSK9 inhibitors affect LDL, cholesterol & triglycerides?
they decrease LDL, cholesterol & triglycerides
67
What medications are monoclonal antibodies?
PCSK9 inhibitors
68
How are PCSK9 inhibitors administered?
administration by SQ injection, either weekly or monthly
69
What are the side effects of PCSK9 inhibitors?
itching, swelling, pain or bruising at the injection site
70
how do bile acid sequestrants work?
- bind with cholesterol in the intestine; the complex can not be absorbed; and is excreted in the stool - by promoting an increase in bile acid excretion, they enhance the conversion of cholesterol to bile acids by the liver
71
Can bile acid sequestrants be used in those with active liver disease?
yes
72
What do bile acid sequestrants due to LDL, triglycerides & HDL?
- decrease LDL - may increase triglycerides - lightly increase HDL
73
What medication class has a strong record of efficacy & safety?
bile acid sequestrants
74
Are bile acid dequestrants used routinely?
no
75
can bile acid sequestrants be used in pregnancy?
yes
76
What can bile acid sequestrants be used with?
fibrates
77
What are the side effects of bile acid sequestrants?
constipation abd pain bloating diarrhea heartburn gallstones
78
What can bile acid sequestrants inhbit that absorption of?
fat soluble vitamins (A,D,E, & K)
79
What is niacin also known as?
nicotinic acid or vitamin B3
80
How does niacin work?
- inhbits the release of free fatty acid from adipose tissue - increases rate of triglyceride removal from plasma
81
How does niacin affect total cholesterol, triglycerides, LDL & HDL?
- lowers total cholesterol, triglycerides & LDL levels - elevates HDL
82
When should niacin be given?
bedtime
83
What are the adverse effects of niacin?
- flushing - nausea - abd pain - increase uric acid levels - liver toxicity
84
What are drug interactions with niacin?
- alcohol -statins - fibrates
85
What is often taken with niacin to help prevent flushing?
aspirin
86
How do fibrates work?
- inhibition of cholesterol & synthesis - decreases triglyceride synthesis - inhibition of lipolysis in adipose tissue
87
how do fibrates affect total cholesterol, triglycerides, LDL & HDL?
- lower total cholesterol, triglycerides, & LDL levels - elevate HDL
88
How often are lipid levels monitored when taking fibrates?
in 4 to 6 weeks, then every 3 to 4 months
89
What are adverse effects of fibrates?
- flushing of face & neck - increased uric acid levels - increased risk of rhabdomyolysis(rare) - GI tract - headaches
90
What are drug interactions with fibrates?
warfarin statins
91
What are omega 3 fatty acids derived from?
fish oil
92
How do omega 3 fatty acids affect triglycerides?
decreases triglyceride levels
93
What are side effects of omega 3 fatty acids?
- burping - fishy taste - diarrhea - change in taste
94
What do omega 3 fatty acids decrease the risk of?
pancreatitis
95
high doses of what may interfere with blood clotting?
omega 3 fatty acids
96
What are the drugs that are omega 3 fatty acids?
lovera vascepa epanova omtryg