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Cardio Renal II Midterm > Pharmacology - Dyslipidemia Part 2 > Flashcards

Pharmacology - Dyslipidemia Part 2 Flashcards

(96 cards)

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1
Q

2 lipid lowering agents (not statins) that interact with statins to increase the risk of myopathy

A

gemfibrozil
niacin

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2
Q

atorvastatin + digoxin interaction

A

digoxin toxicity - levels increased by 20%

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3
Q

statin + grapefruit juice

A

grapefruit inhibits CYP3A4 - increased statin levels and potential myopathy

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4
Q

dr prescribes atorvastatin + cyclosporine

what is recommendation

what if it’s another drug that reacts

A

do not go over 10mg of atorvastatin QD

use caution when going over 20mg of atorvastatin – lowest dose should be used

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5
Q

statin + resin counseling points

A

statin should be given at least 1 hour before the resin

if pt already took the resin, have to wait AL LEAST 4 HOURS before taking the statin

this is bc the absorption of the statin will decrease

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6
Q

true or false

pravastatin is not a prodrug

A

true

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7
Q

pravastatin is CI with what gout agent

A

colchicine

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8
Q

when giving rosuvastatin with ___ or ___, low doses of rosuvastatin should be used due to risk of myopathy

A

gemfibrozil and cyclosporine

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9
Q

in general, if fibrates are given with a statin, which fibrate is preferred bc it has less risk of causing myopathy?

A

fenofibrate over gemfibrozil

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10
Q

for which statin are polymorphisms in CYP2C19 a concern

A

rosuvastatin

if pts have low activity of the enzyme, they have higher risk of myopathy and liver damage

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11
Q

a patient with _____ may be predisposed to rhabdomyolysis from statins

A

renal failure

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12
Q

what do statins do to INR

A

increase INR – bleeding risk for warfarin. time to clot is increased

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13
Q

statins increase or decrease transaminases?

A

increase

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14
Q

true or false

chronic alcohol drinkers can take statins

A

not really – too much hepatotoxicity

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15
Q

which group of people are predisposed to myopathy from rosuvastatin and why

A

japanese and chinese bc of CYP2C19 polymorphisms

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16
Q

proteinuria when taking statins can be a sign of….

A

muscle damage, kidney damage
(rhabdomyolysis damages the kidney)

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17
Q

pitavastatin is contraindicated with ___ and ____

A

fibrates and cyclosporine

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18
Q

advantage of pitavastatin over other statins

A

does not affect warfarin! no increased bleeding risk

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19
Q

name 3 bile acid-binding resins

A

colestipol
cholestyramine
colesevelam

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20
Q

bile acid-binding resins are a _____-exchange copolymer

A

ANION EXCHANGE

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21
Q

Do bile acid-binding resin drugs get absorbed?

A

NO - they are too large

they dont need to be absorbed to do their mechanism. they work in the GI tract and then get excreted through the feces, bound to the bile acid

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22
Q

in what organ is bile acid made?

in what organ is bile acid stored?

A

made in the liver, stored in the gallbladder

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23
Q

what is the major, endogenous role of bile acids?

A

they emulsify the fat that we eat and convert it to chylomicrons

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24
Q

explain the MOA of bile acid-binding resins

A

they go into the GI tract where they bind bile acids. (bc the resins are highly positively charged and the bile acids themselves are highly NEGATIVELY charged)

these bile acids can no longer be reabsorbed into the body through enterohepatic circulation

instead, the bile acid resin + the bile acid go through the hepatic portal vein, get converted to bile, and eventually excreted through the feces

the liver responds to less bile acids in the body by making more bile acids with lipids. to do this, more LDL receptors are produced and LDL is taken from the blood – and therefore LDL goes down!

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25
bile acid resins vs bile acids which have a positive charge and which have a negative charge?
bile acids have a negative charge and resins have a positive charge
26
true or false bile acid resins can be used as monotherapy
true - or with statins
27
true or false bile acid-binding resins increase triglyceride synthesis by the liver
true therefore, contraindicated in severe hypertriglyceriedemia!!! can cause pancreatitis
28
what is an advantage of using bile acid-binding resins with statins
the dose of each can be reduced - less prone ot statin side effects
29
when are bile acid resins taken
at breakfast or dinner remember - if pt taking statin - need to take at least an hour before resin, or at least 4 hours after
30
which 2 bile acid resins come as a powder in which the patient has to make a slurry and have it as a juice? which comes as a tablet?
powder - cholestyramine, colestipol tab - colesevelam
31
true or false bile acid resins are generally well tolerated
true due to chloride salts, there are rare cases of hyperchloremic acidosis
32
bile acid resins are contraindicated if patients have high levels of ___
triglcyerides!! bc the resins increase synthesis of TG CI bc too much TG can cause pancreatitis
33
bile acid resins can cause malabsorption of ____
vitamin K bc it will be removed with the bile acid. it's a fat soluble vitamin
34
name some potential side effects of bile acid resins
heartburn (bc acidic) malabsorption of vitamin k bloating dyspepsia constipation
35
true or false bile acid resins are contraindicated in diverticulitis
true
36
these 2 bile acid resins bind and interfere with the absorption of many drugs name some of them
cholestyramine and colestipol thiazides, furosemide, propranolol, levothyroxine, digoxin, warfarin, some statins (BC ACIDIC!!!!)
37
TRUE OR FALSE acidic drugs are contraindicated with bile acid resins
FALSE not contraindicated, just not given at the same time because the drug will bind the resin and not be absorbed
38
of the 2 fibrates, which is a prodrug
fenfibrate
39
which fibrate is mostly excreted unchanged? explain the metabolism of the other fibrate
unchanged - gemfibrozil glucuronidation - fenofibrate
40
which fibrate is highly protein bound, undergoes enterhepatic circulation, and readily passes the placenta
gemfibrozil
41
what happens when PPAR-a is activated? WHEN is it activated? explain WHAT DRUGS ARE PPAR-A AGONISTS??
fatty acid oxidation is induced activated in times of fasting the fatty acids are broken down and used for energy - maintain blood sugar the fibrates
42
explain how fibrates affect these activities in the liver: -Apoprotein synthesis -Triglyceride secretion and synthesis -fatty acids
increase "good" apoprotein synthesis (I and II) decreased bad apoprotein synthesis (III) decreased synthesis and secretion of TG increased fatty acid oxidation
43
what class of receptor is PPAR-a
nuclear receptor
44
true or false fibrates decrease fatty acid oxidation
FALSE - increase
45
true or false fibrates increase the synthesis of lipoprotein lipase
true
46
which fibrate is more effective at increasing HDL levels?
fenofibrate
47
is apoprotein CIII good or bad and why
bad - inhibits lipolysis
48
how do fibrates affect thrombosis?
they have antithrombotic effects -- inhibit clotting, and enhance the fibrinolysis of clots
49
***true or false fibrates have very little effect on LDL cholesterol
TRUE really only decrease triglycerides
50
fibrates are useful drugs in hypertriglyceridemias in which ____ predominates
VLDL (has very high triglyceride content. only chylomicrons have higher)
51
5 potential AE of fibrates
liver toxicity, rashes, myopathy cholesterol gallstones, pancreatitis
52
the risk of myopathy from fibrates ALONE is pretty rare. however, this risk increases when...
combined with a reductase inhibitor (statin)
53
DDI concern with fibrates
potentiation of warfarin - bleeding risk
54
true or false fibrates react with alcohol
true - increased risk of necrotizing myopathy
55
**general mechanism of ezetimibe
inhibits intestinal absorption of sterols (ie - cholesterol) does this by inhibiting NPC1L1, a transport protein that uptakes cholesterol into the intestines
56
explain the synergy effect of zetia + statin
bc zetia reduces cholesterol absorption by 50%, there is a compensatory increase in cholesterol synthesis in the liver. HOWEVER, statins inhibit this cholesterol synthesis!!! the 2 different MOA's work together to significantly decrease LDL
57
true or false because the mechanism of zetia is to decrease the absorption of dietary cholesterol, it is NOT effective against cholesterol that is endogenously produced
FALSE - it still is, bc it inhibits the reabsorption of cholesterol into the bile
58
*true or false ezetimibe is a non-competitive inhibitor. it does NOT compete with sterols
true binds an allosteric site - not the same site
59
true or false zetia can be given with bile acid resins
FALSE - CONTRAINDICATED the absorption of ezetimibe will be inhibited
60
metabolism of ezetimibe
water insoluble - so gets metabolized glcuronidation
61
how is zetia mainly excreted
in feces
62
zetia + fibrates
the concentration of ezetimibe in the plasma will be increased
63
ezetimibe is only used as monotherapy in what scenario
in patients intolerant to statins
64
zetia is particularly useful in which disease?
phytosterolemia ( too many plant sterols)
65
true or false zetia is generally well tolerated
true
66
name 2 PCSK9 antibodies used for dyslipidemia
evolocumab (repatha) alirocumab (praluent)
67
explain the MOA of PCSK9 antibodies to lower cholesterol
in the presence of PCSK9, the endosome with PCSK9 + receptor + LDL cholesterol, ALL BREAKS DOWN, so there is very little LDL receptor cycling back to the surface of the hepatocyte. this means that there is LESS LDL CHOLESTEROL BINDING TO LDL RECPETORS -- resulting in less elimination and ultimately higher levels in the blood HOWEVER, PCSK9 antibodies bind PCKS9 protease and PREVENT it from going into the endosome and degrading the receptor. instead, ONLY the LDL particle is destroyed, and the receptor is recycled back to the surface to take in and ELIMINATE MORE LDL cholesterol
68
explain the synergy of statins + PCSK9 inhibitors
statins upregulate the production of LDL receptors, while at the same time PCKS9 inhibitors prevent these new receptors' destruction
69
PCSK9 is a ____ that binds to ____ on the surface of ____ and enhances ____ what is the result
protease that binds LDL receptor on the surface of hepatocytes this enhances the lysosomal degradation of the LDL receptor which is BAD because less LDL will be eliminated so LDL plasma concentrations will be higher
70
true or false the PCSK9 inhibitors increase LDL receptor concentration
true!! these receptors enhance the elimination of LDL through the liver
71
route of administration of PCSK9 inhibitors
subq injection either q 2 weeks or monthly
72
true or false there are NO myopathy issues with PCSK9 inhibitors
true
73
Niacin is the component of...
vitamin B3
74
in general, niacin decreases what 3 things
triglycerides LDL production VLDL secretion (from the liver)
75
what does niacin increase
HDL
76
dose of niacin to have positive effects on LDL and HDL
need very high dose
77
true or false niacin is excreted unchanged
true or only the major metabolite - nicotinuric acid is found in urine
78
***2 places in the body where niacin acts
adipose (fat) tissue the liver
79
explain the MOA of niacin in adipose tissue
INHIBITS the lipolysis of triglycerides decreases number of free fatty acids sent to liver, thus decreasing triglyceride synthesis
80
explain the MOA of niacin in the liver
inhibits synthesis and esterification of fatty acids decreased VLDL production and TG synthesis decreased LDL
81
true or false niacin enhances LPL activity
true
82
true or false niacin decreases HDL levels
FALSE - raises
83
niacin is indicated for...
hypertriglyceridemia high LDL-c
84
true or false niacin can be used in combo with a statin or a resin
true
85
*true or false niacin only affects LDL levels
FALSE also decreases triglycerides
86
rare AE of niacin. if it occurs, must be discontinued
arrhythmias
87
3 AE niacin (besides arrhythmia)
flushing dyspepsia hepatoxicity
88
fish oil is only used for....
reducing VLDL triglycerices adjunct to diet in patients with severe hypertriglyceridemia
89
proposed MOA of fish oil
not really well known - but thought to act on PPAR-a (like fibrates)
90
when is prescription strength fish oil given
for pancreatitis -- triglycerides higher than 1000
91
bempedoic acid is a ___ inhibitor
ATP citrate lyase
92
what is the ATP citrate lyase enzyme
an enzyme that is upstream of HMG-CoA reductase in the cholesterol biosynthesis pathway
93
How does bempedoic acid decrease LDL
inhibits ATP citrate lyase - an enzyme in the cholesteorl synthesis pathway
94
AE of bempedoic acid
hyperuricemia (gout!) tendon rupture muscle pain counsel to watch for joint pain!
95
what is inclisiran and when is it used
a siRNA (small interfering RNA) that is directed at inhibiting PCSK9 mRNA as adjunct to diet and to high dose statin therapy
96

Cardio Renal II Midterm (14 decks)

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