Block I: Dyslipidemia Flashcards
(149 cards)
1
Q
list lipids in order of their density
A
LEAST DENSE 1. chylomicron 2. VLDL 3. LDL 4. HDL MOST DENSE
2
Q
[] is in the intestine and transports dietary TG
A
chylomicron
3
Q
[] is in the liver and transports endogenous TG
A
VLDL
4
Q
[] is formed in circulation and delivers cholesterol to periphery
A
LDL
5
Q
[] takes systemic cholesterol to the liver for breakdown and excretion
A
HDL
6
Q
what is the role of plasma lipids
A
- cell membrane
- hormone synthesis
- source of free fatty acids
7
Q
what is the role of lipoprotines
A
- chylomicron and VLDL delivery tg to cells in body
- LDL delivers cholesterol to cells in body
- HDL involved in reverse cholesterol transport
8
Q
when should individuals have their lipids measured?
A
- 20 + every 4-6 years
2. adults with ASCVD every 3-12 months
9
Q
which lipoptorein is calculated, how?
A
LDL, friedewald formula
10
Q
that is the goal of total cholesterol
A
= 150
11
Q
what is the LDL goal
A
= 100
12
Q
what is the goal triglycerides
A
= 150
13
Q
what is the goal HDL
A
> /= 60
14
Q
what is the most arthrogenetic cholesterol
A
NON HDL (VLDL + LDL) Apo B
15
Q
what are arthrogenic cholesterols
A
- LDL
2. VLDL
16
Q
what is uncertain if it is arthrogenic
A
chylomicrons
17
Q
what is not arthrogenis
A
HDH
18
Q
a 1% redux in LDL with reduce ASVD risk by []
A
1%
19
Q
a 1% increase in HDL will reduce ASCVD risk by []%
A
2-3%
20
Q
how does LDL lead to ASCVD
A
LDL accumulated in endothelial layer of BV, engulged by macrophage, foam cell made, arthersclerosis forms, cad
21
Q
[] have an moa of: HMG-CoA reductase inhibitor. reduce cholesterol synthesis in liver by inhibiting enzyme that converts HMG-CoA to mevolonate.
rate-limiting step in cholesterol synthesis.`
A
Statins
22
Q
what is the MOA of statin
A
HMG-CoA reductase inhibitor. inhibts rate limiting step in cholesterol synthesis.
23
Q
what are some pleiotropic effects of statins?
A
- improve endothelial function
- inhibit platelet aggregation
- decrease LDL oxidation
- reduce vascular inflammation
- stabilize atherosclerotic plaque
24
Q
what is the clinical use of statins
A
first line therapy for dislipiemia in primary and secondary prevention CAD
25
what is the first line therapy for dyslipidemia in primary and secondary prevention of CAD
statins
26
Statins lower LDL by []%
21-63
27
statins lower TG by []%
8-37%
28
statins [] HDL
raise
29
what are two high intensity statins
1. rosuvastatin 20-40
| 2. atorvastatin 40--80
30
how much do high intensity statins affect LDL
50%
31
how much do moderate intensity statins affect LDL
30-49%
32
how much do low intensity statins affect LDL
< 30%
33
what intensity is atorvastatin 20
mod.
34
what intensity is rosuvastatin 10
mod
35
what intensity is simvastatin 20-40
mod
36
what intensity if prevastatin 40
mod
37
what intensity is lovastatin 40
mod
38
what intensity is fluvastatin
mod
39
what intensity is atorvastatin 40-80
high
40
what intensity is rosuvastatin 20-40
high
41
what intensity is simvastatin 10
low
42
what intensity is pravastatin 20
low
43
what intensity is lovastatin 20
low
44
how would you monitor a patient on statins
1. fasting lipids 4-12 weeks after initiation and every 3 months
- 12 months once stable
2. LFTS
only if symptoms occur (fatigure, loss apetite, abdominal pain, jaundice)
3. CPK
baseline if pt. at risk for myopathy & in symptomatic pts.
45
contraindications statins
1. liver disease
| 2. pregnancy
46
ADR statins
1. myalgias
2. rhabdo
3. GI
4. flu-like sx
5. increase LFT
6. increase rx DM in high dose
7. confusion, cognitive impairment
47
what drug does this SE profile belong to?
1. myalgias
2. rhabdo
3. GI
4. flu-like sx
5. increase LFT
6. increase rx DM in high dose
7. confusion, cognitive impairment
Statins
48
increased risk myopathy if statins are taken with []
other CYP3A4 drugs (except pravastatin, rosuvastatin)
49
what re some common drug interactiosn with statins
1. CCB
2. amiodarone
3. ketoconazole
4. fibric acid derivative
5. rifampin
inhib. statin metabolism
50
what should you counsel your stain pateitns on about diet and statin
a ton of grapefruit juice will impair absorbtion
51
what are some statin cautions
1. age > 75
| 2. decrease if LDL < 40 on 2 occaisons
52
MOA exetimibe
cholesterol absorbtion inhibitor, inhibits absorbtion in small intestine
53
[] is a cholesterol absorbtion inhibitor, inhibits absorbtion in small intestine
ezetimibe
54
ezetimibde can decrease LDL levels by []%
17
55
[] can be used second like if stain is not tolerated well, or LDL not controled on statin alone
ezetimibe, either second line or in combo with statin
56
what is the clinical use ezetimibde
2nd line if statin contI, not tolerated, or not meeting goal
can be added to statins well
57
[] can be useful in diabetic patients who cannot tolerate high dose statin therapy
ezetimibe
58
ezetimibe has a formulation mized with []
atorvastatin or simvastatin
59
what are contraindications ezetimibe
1. acute liver disease
| 2. pregnancy (adverse effects in animals)
60
what are SE ezetimibe
1. HA
2. rash
* usually well tolerated
61
how would you monitor an ezetimibe patient
1. fasting lipid panel and LFT at baseline
| - +6-8 week after initiation and dose titration
62
when should ezetimibe be d/c
if ALT > 3x
63
[] bind bile acid and cholesterol, intestines, and decrease biliary cholesterol absorption
bile acid sequestrants
64
what is the MOA BAS
bind bile acid and cholesterol in intestines, decrease biliary cholesterol absorption
65
BAS decrease LDL by []%
15-30
66
BAD increase HDL by []%
3-5%
67
what is the clinical use for BAS
LDL lowering after statin and niacin maxed or not tolerated
68
[] is used when statin and niacin are maxed and pt. still not at goal
BAS
69
cholestyramine is a []
BAS
70
Colestipol is a []
BAS
71
Colesevelam is a []
BAS
72
what is the ROA BAS
1. tablet
2. powder
3. oral suspension
73
contraindications BAS
1. complete biliary obstruction
2. TG > 300
3. hyperlipoproteinemia
74
what drug has these AE
1. GI distress
2. constipation
3. hypernatremia
4. hyperchloremia
5. impaired fat soluble vitamin absorbtion
BAS
75
what are some AE BAS
1. GI distress
2. constipation
3. hypernatremia
4. hyperchloremia
5. impaired fat soluble vitamin absorbtion
76
what caution is assoc. with BAS
other meds that can cause constipation
| -TAC, fiber sup, narcotics
77
what drug interactions with BAS
can bind other drugs and excrete them,
should take other meds 2-4 hours apart
78
how should you monitor a patient on BAS
1. fasting lipid panel baseline and 6-8 weeks after initiation
- every 6-12 months therefter
2. d/c if TG exceeds 400 mg/dL while on thereapy
79
what is the MOA of PCSK9 inhib
binds PCSK9 to prevent degradation of LDL-c receptors,
- maintain functionality of LDL-c receptors that take in LDL from bloodstream into cell
- decrease LDL from circulation
80
what is the clinical use of PCSK 9 inhib
1. heterozygous familial hypercholesteroleemia
| 2. clnical ASCVD
81
PCSK9 inhib decrease LDL by [] %
50%
82
PCSK9 inhib decrease TC by []%
30
83
PCSK9 inhib decrease lipoprotein []%
26
84
PCSK9 inhib increase HDL by []%
6
85
how should you monitor a patient on PCSK9 inhib
1. fasting lipid panel
- reassess 4-8 weeks after initiation/titration
2. assess for hypersensitivity reactions
86
alirocumad belongs to what class
PCSK9 inhibitor
87
Evolocumab belongs to what class
PCSK9 inhibitor
88
contraindication PCSK9 inhib
hypersensitivity
89
1. nasopharyngitis
2. flu sx
3. increased LFT
4. injection site reaction
5. myalgia
6. cough
side effect profile fo []
PCSK9 inhib.
90
what is the MOA of bempepoidic acid
ATP citrate lyase inhibitor (ACL)
| halts LDL synthesis by inhibiting ACL (higher up on cholesterol synthesis than statin)
91
what are some indications for bempedoidic acid/ACL inhib.
ASVCD, HeFH
usually in combo with max tolerated statin
92
bempedoidic acid decreases LDL by [] %
16.5
93
[] is a prodrug
bempedoidic acid/ACL inhib
94
drug interactions with bempedoici acid
1. antivrials
2. max dose simvastatin 20, pravastatin 40
- due to inhibitor OATP...
95
what drug has the following SE profile
1. gout
2. tendon rupture
3. a fib
4. GI distress
5. anemia
6. leukopenia
9. increased BUN/Scr
bempedoidic acid/ACL inh
96
what drug may cause gout
ACL in /bempedoic acid
97
what drug may cause tendon rupture
ACL/bempedoic acid
98
what drug may increase BUN/Scr
ACL in /bempedoic acid
99
how would you monitor a patient on ACL inhib
1. lipid levels 8-12 wk
2. uric acid levels
3. s/sx tendon rupture
100
if a pt TG are 174-499 how would you treat?
lifestyle mod
101
if pt TG are > 500 what do you rec
statin init.
102
if pt TG > 1,000 what do you rec
very low fat diet
avoid ref carb
avoid alcohol
initiate fibrates/omega-3
103
[] has an MOA of activating PAR-alpha, the gene that regulates/controls lipid metabolism, reduces hepatic production VLDL and increases lipoprotein lipate-mediated clearance
fibrates
104
clinical use fibrates
reserved for pt with TG > 500
105
fibrates decrease tg []%
20-50
106
fibrates increase HDL [] %
10-20
107
gemfibrozil is a [] drug
fibrate
108
fenofibrate is a [] drug
fibrate
109
fenofibritic acid is a [] drug
fibrate
110
what is the MOA gemfibrozil
activate PPAR-alpha to reduce TG
111
contraindications fibrates
1. hepatic disease
| 2. statins, may increase rhabdo
112
what drug should NOT be mixed with a statin
gemfibrozil
113
what drug has this side effect profile
1. GI upset
2. dyspepsia
3. rash
4. gallstones
5. myopathy
6. LFT and Scr elevatoin
fibrates
114
what drug may cause gall stones
fibrates
115
how would you monitor fibrates
1. fastin lipid
2. ALT
3. CPK if muscle pain
116
MOA omega 3
inhibit hepatic secretion of TG and promote metabolism TG
117
omega 3 decreases Tg by [] %
20-30
118
what is the clinical use of omega 3
1. dietary aduvant for very high TG levels
119
what is a safe dose omega 3
< 3 G
| 2-4 may be needed
120
AE omega 3
1. GI disturbance
2. fishy aftertate
3. increased bleeding risk
4. worsening glycemic control
5. increased LDL
6. abnormal LFT
121
1. increased bleeding risk
2. worsening glycemic control
3. increased LDL
4. increased LFT
SE profile of what
omega 3
122
what drug comes with an increased risk bleeding
omega 3
123
DI omega 3
1. antiplatelets and anticoagulants
| * bleeding risk
124
how to monitor omega 3
1. TG baseline
2. ALT
3. eval GI dis. skin change, bleeding
125
lovaza belongs to what class
omega 3
126
omtyg belongs to what glass
omega 3
127
epanova belongs to what class
omega 3
128
vascepa belongs to what class
omega 3
129
MOA inhibit mobilization free fatty acids from peripheral adipose tissue to liver and reduce VLDL synthesis
niacin
130
what is MOA niacin
inhibit mobilization free fatty acids from peripheral adipose tissue to liver and reduce VLDL synth
131
niacin decreased tg by [] %
20-50
132
niacin decreased LDL by [] %
5-25%
133
niacin increased HDL by [] %
15-35%
134
what is the clnical use of niacin
if TG > 500
135
can is niacin sometimes combined with?
1. lovostatin
| 2. simvastatin
136
how are you monitoring your niacin pt
1. CPK if statin
2. fasting lipid
3. blodo glucose
4. uric acid
5. lft
137
niacin with [] increasing myopathy risk
statin or gemfibrozil
138
interactions with niacin
1. statin/gemfibrozil (increased myopathy risk)
2. alcohol
3. antidiabetic
139
CI niacin
liver disease
sever gout
peptic ulcer disease
AST/ALT > 2-3x
140
[] can cause persistent hyperlgycemia, cutaneous symptoms, acute gout
niacin
141
what drug causes facial flushing
niacin
142
ADR niacin
1. flushing
2. hyerglycemia
3. hyperuricemia
4. upper gi distress
4. hepatotox
6. myopathy
143
[] is contraindicated in pregnancy (category x)
statin
144
[] is category C, no harm in animal studies
niacin
d/c if hyperlipidemia
d/c if hypertriglyceridemia
145
B/C not systemically absorbed, may interfere with vitamin absorbtion
BAS
146
[] C harm shown in animal studies, other agents pref.
cholesterol absorbtion inhbit
147
[] C adverse events observed in animal studies, maternal toxicity rare
fibrates
148
in a ASCVD pt. less than 75 yoa what is the treatment and what is the goal
high intesnity stain
LDL 50% lowering
149
clinical ASVCD on max tolerated dose statin, next step
ezetimibde
| or PCKS9 if severe risk
