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PHAR152 > Dyslipidemia > Flashcards

Dyslipidemia Flashcards

1
Q

What is the definition of atherosclerosis?

A

a condition that afflicts the large and medium-sized arteries of almost every human, at least in societies in which cholesterol-rich foodstuffs are abundant and cheap
begins in childhood and in the absence of accelerating factors, develops slowly until it is widespread in old age

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2
Q

How is atherosclerosis accelerated?

A

genetic and environmental factors

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3
Q

What is the pathogenesis of atherosclerosis?

A

infiltration of LDL into the subendothelial region
the endothelium is subject to shear stress
most marked at points where the arteries branch, and this is where lipids accumulate to the greatest degree

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4
Q

Describe each layer of an artery.

A

inner layer (intima):
-endothelium that lines the lumen of all vessels
middle layer (media):
-smooth muscle cells and elastic fibers
outer layer (adventitia):
-collagen fibers

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5
Q

Describe the initiation of atherosclerosis.

A

transport of plasma LDL-cholesterol through the endothelial cell layer into the extracellular matrix of the subendothelial space
at low levels, this may not be problematic (LDL is naturally occurring)

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6
Q

How does an atherosclerotic plaque cause a heart attack?

A

plaque ruptures
the exposed core of an atherosclerotic plaque is highly stimulating to circulating platelets
platelets are fooled
blood flow is blocked

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7
Q

What are the most common plasma lipids in humans?

A

cholesterol
triglycerides

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8
Q

Describe cholesterol.

A

a “sterol” or modified steroid molecule
a type of lipid molecule synthesized by all animal cells
essential structural component of all animal cell membranes
allows cells to function without a cell wall

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9
Q

What is cholesterol a precursor for?

A

bile acids
vitamin D
steroid hormones
-includes glucocorticoids, mineralocorticoids, androgens,
estrogens, and progestogens

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10
Q

Describe triglycerides.

A

3 fatty acids connected by a glycerol backbone
fatty acids can be oxidized for energy by many tissues
-except brain
glycerol backbone can be used for gluconeogenesis

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11
Q

How are cholesterol and triglycerides transported?

A

not water soluble so must have specialized vehicles to circulate in the blood
these vehicles are made from apolipoproteins
apolipoprotein’s are proteins that bind lipids (to form lipoproteins)

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12
Q

How is the density of lipoproteins determined?

A

relative amount of protein vs lipid

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13
Q

What is the role of the protein component of lipoproteins?

A

provide structural stability and also may function as ligands in receptor interactions or as cofactors in enzymatic processes that regulate lipoprotein metabolism
the type of protein defines the use of the particle

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14
Q

What is contained within the lipid component of lipoproteins?

A

free cholesterol
esterified cholesterol (>1 cholesterol molecule linked together to improve storage efficiency)
triglycerides
phospholipids

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15
Q

What are the major lipoproteins?

A

chylomicrons
VLDL
LDL
HDL

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16
Q

What are chylomicrons?

A

large lipoproteins contains lots of TGs (80-95%)
major vehicle to carry dietary fat (and cholesterol) immediately after absorption from gut
present in plasma for 3-6h after a fat-containing meal has been ingested

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17
Q

What is the role of chylomicrons?

A

source of TG for adipose tissue and muscle (skeletal and cardiac)
-capillaries in these tissues contain LPL that liberates free fatty
acids for a cellular energy source
source of TG and cholesterol for liver to produce VLDL

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18
Q

What happens when chylomicron remnants are taken up by the liver?

A

chylomicron remnants contain cholesterol
when taken up by liver cells, increases intra-cellular cholesterol levels
liver responds by downregulation of LDL-receptors (to prevent further uptake of LDL from blood)
LDL accumulates in blood

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19
Q

What is VLDL?

A

very similar to chylomicron molecule
synthesized in liver
main source of FFA in the fasting (chylos are low)
provides FFA to tissues similar to chylomicrons (LPL in capillary bed steal the TG from VLDL)

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20
Q

True or false: blood tests measure VLDL and chylomicrons separately

A

false
blood tests measures all TG levels in the blood

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21
Q

What is the fate of VLDL?

A

eventually VLDLs are stripped of most of TG in the tissues and transform into IDLs

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22
Q

What would a blood test show for an individual with high VLDL and chylomicrons?

A

high TGs

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23
Q

What is the fate of IDL and where does this occur?

A

additional loss of TG by LPL will change IDL to LDL
occurs in the liver or peripheral tissues that use TG

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24
Q

Describe LDL.

A

main carrier of cholesterol in blood (60-70%)
most LDL is derived from VLDL metabolism
however, many tissues can synthesize their own cholesterol
contains apo B (affinity for LDL receptor)

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25
Q

What can a cell do if intracellular cholesterol is needed?

A

upregulate an LDL receptor
the LDL is internalized and degraded

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26
Q

Which cells express the LDL receptor constantly? Why?

A

liver cells
to eliminate excess LDL from the circulation
liver disposes of 3/4 of circulating LDL

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27
Q

What is familial hypercholesterolemia?

A

genetic trait that is associated with no LDL receptors
LDL is not cleared from the circulation and intracellular production is increased
people with FH has high LDL from young age and experience ACVD at very young ages

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28
Q

What will high levels of intracellular cholesterol result in?

A

inhibits intracellular production
decreases synthesis of LDL receptors
increased cholesterol storage within cells

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29
Q

How is LDL eliminated?

A

bile

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30
Q

What makes up the measurement of “non-HDL lipoproteins”?

A

chylomicrons
VLDL
IDL
LDL

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31
Q

When is non-HDL a useful measure?

A

when TG levels are high
can also be used as a target of cholesterol therapy

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32
Q

Where is HDL derived?

A

periphery (mainly gut) and in the liver
can be formed by remodeling of chylomicrons or by VLDL catabolism

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33
Q

Describe the role of HDL.

A

reverse cholesterol transport
excess cholesterol is acquired from cells and transferred to the liver for excretion
“full” HDL can donate cholesterol to LDL and VLDL
allowing tissues (such as coronary arteries) to eliminate excessive cholesterol may be a reason why HDL is considered protective

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34
Q

What has been associated with lower risks for ACVD events?

A

Apo A-I (major HDL apolipoprotein) and HDL levels

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35
Q

True or false: there are good drugs on the market that increase HDL levels

A

false
pharmaceutical companies have failed to produce HDL increasing drugs that protect against events

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36
Q

True or false: atherosclerosis is though to arise from transport of LDL through the endothelial layer into the subendothelial space

A

true

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37
Q

What is a chemical modification to LDL that makes it problematic?

A

oxidation

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38
Q

True or false: studies of atherosclerotic lesions show that LDL within plaques are rarely ever modified by oxidation

A

false
LDL within plaques are almost always modified by oxidation

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39
Q

What will oxidized LDL elicit?

A

oxidized LDL in the subendothelial space triggers signals to recruit monocytes into the artery wall
monocytes are attracted and are activated into macrophages

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40
Q

Describe the entire process of what occurs when LDL is oxidized.

A
  1. oxidized LDL stimulates endothelial cells to recruit monocytes and oxidized LDL also appears to stimulate T cells to secrete cytokines
  2. monocytes cross the subendothelial space and become macrophages (triggered by cytokines)
  3. macrophages take up oxidized LDL and become foam cells, the cytokines cause smooth muscle to proliferate
  4. under the influence of growth factors the smooth muscle moves to the subendothelial space and produce collagen to take up LDL, adding to the foam cells
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41
Q

What event appears to be a key trigger of the atherosclerotic process?

A

oxidization of LDL

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42
Q

True or false: HDL may serve to reduce the oxidation of LDL

A

true

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43
Q

What is the conclusion regarding the use of antioxidants to prevent the oxidation of LDL?

A

clinical studies of antioxidant supplementation have been disappointing
the risk ratio was basically 1 in every trial=they arent good
evidence suggests antioxidant supplements do now lower risk for ACVD events

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44
Q

What does oxidized LDL trigger the LDL receptor to change to?

A

scavenger receptor in macrophages and migrated muscle cells

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45
Q

What do scavenger receptors result in?

A

scavenger receptors are not governed by lvl of intracellular LDL
as a result, macrophages and migrated muscle cells consume enormous volumes of oxidized LDL and become foam cells

46
Q

What happens to an atherosclerotic plaque as time progresses?

A

vascular smooth muscle cells proliferate and lay down collagen and other matrix molecules, and contribute to the bulk of the lesion
repeated injury and repair eventually leads to a fibrous cap protecting the plaque
endothelial dysfunction appears to occur frequently

47
Q

How do low levels of atheroscleroris appear?

A

low levels of atherosclerosis appear as fatty streaks in blood vessels that can be seen in the first 10 years of life

48
Q

What are the factors affecting the progression of fatty streaks into atherosclerosis?

A

extent of oxidation of LDL and extent of inflammatory response
level of plasma lipids (diet, genetics, demand for cholesterol)
metabolic factors/classic risk factors/endothelial damage
-hypertension, sugar, smoking, etc

49
Q

What are the outcomes of atherosclerosis?

A

cerebral circulation
-ischemic stroke, vascular dementia
abdominal aorta
-aneurysmal dilation and rupture of the vessel
renal vessels
-renovascular hypertension
legs (PAD)
-vascular insufficiency, intermittent claudication), gangrene
coronaries
-CHD, CAD, ACVD

50
Q

What are the three groups of people listed under primary prevention for cholesterol management?

A

low risk:
-FRS < 10%
intermediate risk:
-FRS 10-19.9%
-AND LDL >3.5mmol or non-HDL >4.2mmol or ApoB >1.05g/L
or men >50 years and women > 60 years with one additional
risk factor: low HDL, IFG, high waist circumference, smoker,
HTN or other risk modifiers (high Lp(a), CRP, CAC)
high risk:
-FRS > 20%

51
Q

Describe the recommendations for a low risk patient under primary prevention for cholesterol management.

A

statin therapy not recommended unless:
-LDL > 5.0 mmol or ApoB > 1.45g/L or non-HDL > 5.8mmol
-FRS is 5-9.9% with LDL > 3.5mmol or ApoB > 1.05g/L or non-
HDL > 4.2 mmol (particularly with other CV modifiers)
health behaviour modifications:
-smoking cessation
-diet
-exercise

52
Q

Describe the recommendations for an intermediate risk patient under primary prevention for cholesterol management.

A

discuss health behaviour modifications
initiate statin treatment
-if LDL >2.0mmol or ApoB >0.8g/L or non-HDl>2.6mmol on
maximally tolerated dose then discuss add-on therapy
(ezetimibe as first line)

53
Q

Describe the recommendations for a high risk patient under primary prevention for cholesterol management.

A

discuss health behaviour modifications
initiate statin treatment
-if LDL >2.0mmol or ApoB >0.8g/L or non-HDl>2.6mmol on
maximally tolerated dose then discuss add-on therapy
(ezetimibe as first line)

54
Q

What are the goals we want to obtain for LDL, non-HDl, and ApoB for an intermediate or high risk patient who is primary prevention?

A

LDL < 2.0 mmol
non-HDL < 2.6 mmol
ApoB < 0.8g/L

55
Q

What is the definition of “family history” for ACVD?

A

first degree relative with established ACVD at young age (<55 males or <65 females)

56
Q

What is Lp(a)?

A

an LDL molecule covalently bonded to an Apo A
highly genetic predisposition that is associated with higher risk

57
Q

What is CAC?

A

coronary artery calcium
an imaging test that can reveal how much disease activity is/was present in the coronary arteries
high CAC indicates higher risk

58
Q

What are the groups of people under secondary prevention/statin indicated conditions for cholesterol management?

A

LDL > 5.0 mmol:
-or ApoB > 1.45g/L or non-HDL > 5.8 mmol
-likely FH or genetic dyslipidemia
most patients with diabetes:
-age>40
-age>30 and DM >15yr duration
-microvascular disease
chronic kidney disease:
-age>50 and eGFR<60ml/min or ACR>3mg/mmol
atherosclerotic cardiovascular disease
-MI, ACS
-stable angina, documented CAD using angiography
-stroke, TIA, documented carotid disease
-PAD, claudication, and/or ABI<0.9
-abdominal aorta aneurysm

59
Q

Describe the recommendations for a patient with FH under secondary prevention/statin indicated conditions.

A

initiate statin treatment
-if LDL > 2.5mmol (or <50% reduction) or ApoB >0.85g/L or
non-HDl > 3.2 mmol then discuss add on therapy (ezetimibie
or PCSK9 inhibitor)

60
Q

Describe the recommendations for a patient with diabetes or CKD under secondary prevention/statin indicated conditions.

A

initiate statin treatment
-if LDL >2.0 mmol or ApoB >0.8g/L or non-HDl>2.6mmol on
maximally tolerated statin dose then discuss add on therapy
(ezetimibe)

61
Q

Describe the recommendations for a patient with ACVD under secondary prevention/statin indicated conditions.

A

initiate statin treatment
-if LDL > 1.8mmol or ApoB > 0.7g/L or non-HDL >2.4mmol on
maximally tolerated statin dose then discuss intensification of
therapy

62
Q

What are the lipoprotein goals for the following patients:
FH
diabetes/CKD
ACVD

A

FH:
-LDL<2.5
-non-HDL<3.2
-ApoB<0.85
diabetes/CKD:
-LDL<2.0
-non-HDL<2.6
-ApoB<0.8
ACVD:
-LDL<1.8
-non-HDL<2.4
-ApoB<0.7

63
Q

What is the official name of statins?

A

HMG CoA reductase inhibitors

64
Q

True or false: statins main effect is on HDL levels in the blood

A

false
main effect is on LDL levels in the blood

65
Q

What are some statins listed in the Sask formulary?

A

atorvastatin
fluvastatin
lovastatin
pravastatin
rosuvastatin
simvastatin

66
Q

What are the most commonly used statins?

A

atorvastatin and rosuvastatin

67
Q

What is the MOA of statins?

A

inhibits an enzyme (HMG CoA reductase) in the pathway for intracellular synthesis of cholesterol
cellular levels of cholesterol become depleted
cell upregulates LDL receptor
LDL levels in the blood decrease

68
Q

Where is the primary site of action of statins?

A

hepatic cells

69
Q

Which statins and their associated doses are correlated with the highest decrease in LDL?

A

rosuvastatin:
-20mg: 55%
-40mg: 63%
atorvastatin:
-80mg: 55%

70
Q

True or false: lipid reduction is not a cure for ACVD

A

true

71
Q

Which patients get the greatest absolute benefit from statins?

A

patients with a statin-indicated condition

72
Q

True or false: dose doesn’t matter for statins

A

false
dose-related benefits of statins have been confirmed in specific trials

73
Q

A large number of trials showed a ___% additional reduction in events with ___ dose statins vs ___ dose statins.

A

15%
high
low

74
Q

What is the strength of statin recommended for MOST patients?

A

high or moderate
pending tolerability

75
Q

How much LDL reduction do we typically get when we double the dose of a statin?

A

6-7% further reduction

76
Q

What are the high intensity statins?

A

atorvastatin 40-80mg
rosuvastatin 20-40mg
LDL lowering >50%

77
Q

What are the moderate intensity statins?

A

atorvastatin 10-20mg
rosuvastatin 5-10mg
simvastatin 20-40mg
pravastatin 40-80mg
lovastatin 40-80mg
LDL lowering 30-49%

78
Q

What are the low intensity statins?

A

simvastatin 10mg
pravastatin 10-20mg
lovastatin 20mg
fluvastatin 20-40mg
LDL reducing <30%

79
Q

What are the effects of statins on other plasma lipids?

A

HDL may increase 5-10% (up to 15% or not at all)
TG may decrease up to 30% (higher baseline TG=greater effect)
benefit of these is unclear

80
Q

What is the NNT that is generally accepted as reasonable for statins in regards to low risk patients?

A

NNT of <50 over 5 years
some believe NNT should be <30 to consider treatment worth the money and risk

81
Q

What is the conclusion on diet/lifestyle and LDL?

A

limited benefits for LDL specifically
although diet/lifestyle is critical for global CV risk reduction
perhaps these interventions are undertaken too late

82
Q

True or false: you should pay attention to the reference ranges on lab tests for cholesterol rather than the recommendations from guidelines

A

false
we care about recommendations from guidelines

83
Q

True or false: more intensive LDL reduction is clearly associated with greater protection against ACVD events

A

false

84
Q

What are the exceptions to high dose statins?

A

intolerance
drug interactions
patient preference

85
Q

How long should we wait to ensure statins are inducing their full effect?

A

6-12 weeks

86
Q

What are recommendations for patients with ACVD who are not meeting their goals on a maximally tolerated statin dose?

A

if LDL >1.8mmol or ApoB >0.7g/L or non-HDL is >2.4mmol:
-LDL 1.8-2.2 or ApoB 0.7-.8 or non-HDL 2.4-2.9: ezetimibe +/-
PCSK9 inhibitor
-if LDL >2.2 or ApoB >0.8 or non-HDL >2.9 or high PCSK9 inhibitor benefit patient: PCSK9 inhibitor +/- ezetimibe
if TG >1.5-5.6 mmol:
-consider Icosapent ethyl 2000mg BID

87
Q

What does PCSK9 inhibitor stand for?

A

proprotein convertase subtilisin kexin 9 inhibitor
potash corporation of Saskatchewan

88
Q

What are the two PCSK9 inhibitors?

A

evolocumab
alirocumab

89
Q

What dosage form do the PCSK9 inhibitors come in?

A

SQ injections

90
Q

What does the enzyme PCSK9 do?

A

an enzyme that promotes degradation of the LDL receptors on hepatocytes

91
Q

What is the MOA of PCSK9 inhibitors?

A

monoclonal antibodies to PCSK9
result is increased expression of LDL receptors on hepatocytes and increased clearance of LDL from blood

92
Q

True or false: PCSK 9 inhibitors are not safe to use with statins

A

false
safe because the mechanism is totally different

93
Q

How often is evolucumab injected?

A

q2wks or qmonth

94
Q

What is the major barrier of the PCSK9 inhibitors?

A

cost

95
Q

True or false: PCSK9 inhibitors are associated with lots of side effects

A

false
they seem to be very safe

96
Q

Describe ezetimibe.

A

inhibits luminal cholesterol absorption in small intestine
decreased cholesterol absorption=decreased chylomicron formation
decreased chylomicron remnants to the liver=decreased hepatocyte cholesterol
increased LDL expression in liver=greater clearance of LDL

97
Q

How much LDL reduction is seen with ezetimibe as monotherapy?

A

15-20%

98
Q

What is the role of ezetimibe?

A

limited (no) role as monotherapy due to small LDL effect
combine with statins when:
-statin escalation impossible-tolerability
-statin dose maxed out-LDL still not at goal

99
Q

What are some other lipid drugs in the pipeline?

A

eicosapent ethyl: purified ester of EPA
inclisiran: interferes with PCSK9 mRNA
bempedoic acid: inhibitor of ATP citrate lyase

100
Q

Is statin tolerability quite variable or do most people experience the same side effects?

A

extremely variable
-some people can take high dose statins without any problem
-other people cant take statins at all due to side effects

101
Q

What are the nuisance side effects of statins?

A

GI discomfort
fatigue

102
Q

What are the major concerns of statins that are often portrayed in the media?

A

muscle effects–>rhabdomyolysis
diabetes: like TZD diuretics, risk is small
cognitive impairments: considering benefits to vessels, statins should decrease the risk of vascular dementia

103
Q

What is the range of experiences that people get from the muscle effects of statins?

A

no noticeable muscle effects
muscle aches/myalgia
stiffness and cramps
weakness
severe pain
extensive muscle breakdown–>rhabdomyolysis

104
Q

How do we evaluate the severity of muscle symptoms associated with statins?

A

creatinine kinase

105
Q

What is the difference between myalgia, myositis, and rhabdomyolysis?

A

myalgia: CK<ULN
myositis: CK>ULN
rhabdomyolysis: CK>10x ULN

106
Q

How do we approach statin myopathy?

A

identify any DI that may increase statin levels
ask about muscle diseases, wasting/frailty–>may indicate higher risk for statin myopathy
if the risk for muscle effects is high, consider a baseline CK
CK levels only ordered if symptoms appear

107
Q

How can we confirm if muscle effects are actually from a statin?

A

symptoms resolve when statin dc
symptoms recur when statin restarted
symptoms recur when another statin tried

108
Q

What are our approaches to trying to improve muscle effects that an individual is experiencing from a statin?

A

dc statin for short period, re-challenge after res of sx
lower doses/every other day dosing
lower potency statins (ex: fluvastatin)
non-statin drugs

109
Q

Describe the ADME of statins.

A

all statins undergo extensive first pass effect
all are metabolized by the liver, more than 70% of metabolites are excreted by the liver
hepatic metabolism is the most likely origin of DI for statins
3A4/GJ interaction

110
Q

Which statins are more concerning for an interaction with grapefruit juice?

A

GJ may increase serum concentration of older statins
avoid high quantities of GJ with atorvastatin

111
Q

Describe rosuvastatin and atorvastatin based on the following: efficacy, safety, drug interactions, convenience, CI/precautions

A

efficacy:
-excellent effectiveness from RCTs in preventing events
-indicated in ALL ppl with clinical atherosclerosis regardless of
LDL levels
safety:
-muscle sx most common ADR (can be associated with
increased CK and rare rhabdo) DOSE RELATED
-may increase blood sugar slightly
-reduce dose if CrCl <30ml/min for ROSUV (atorv does not
require dosage adjustments in renal dysfx)
drug interactions:
-atorvastatin is a substrate of CYP3A4 and weak inhibitor
(macrolides, azoles, non-DHP CCB)=consider lower dose
-fibrates can increase risk of muscle ADRs
-rosuvastatin has fewer drug interactions
convenience:
-OD dosing, older statins require HS dosing for better LDL
effect (not necessary for rosuv and atorv cause better t1/2)
CI/precautions:
-people with muscle diseases
-gemfibrozil

112
Q

What are some lipid lowering drugs that are rarely used today?

A

niacin:
-B complex vitamin
-related to niacinamide, but only niacin lowers lipid lvls
-reduces TG synthesis and VLDL production
-increases HDL by decreased clearance of Apo A1
-higher doses required for LDL effect but cause flushing
fibric acid derivates (fibrates):
-gemfibrozil, fenofibrate, bezafibrate
-used for elevated TG (small LDL effect)
-bind to PPAR
-can elevate risk for myopathy when used with statins
omega-3 fatty acids:
-EPA and DHA esters reduce VLDL, TGs
-high doses required for effect (3-4g/d)

PHAR152 (21 decks)

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