Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Cardiovascular > Pharmacology Lipid Disorders > Flashcards

Pharmacology Lipid Disorders Flashcards

1
Q

Niacin mechanism

A

in adipose, inhibits FFA mobilization (GPR109A)

in liver, decreases VLDL-TG synth

inhibits uptake of HDL-apoA1

(main effect is to decrease TG)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
1
Q

adverse effects gemfibrozil, fenofibrate

A

increased creatine kinase is coadmin with statin > renal failure

gemfibrozil may block statin transport in liver (icnreased concentrations)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
1
Q

greatest LDL impact

A

HMG Coa reductase inhibitors

Atorvastatin

Lovastatin

Simvastatin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
1
Q

mechanism omega3 FA

A

unique TG lowering properties

results in very low density VLDL TG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
1
Q

pharmacokinetics MTP inhibitors

A

extensive CYP#A4 to inactive metabolites M1 and M3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

contraindications to statins

A

pregnant, lactating, could become pregnant

hypersensitivty

active liver disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

pharmocokinetics cholestyramien

A

not absorbed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

mechanism ezetimibe

A

acts at NPC1L1 to decrease absorption of cholesteryl ester incorporation into chylomicrons (reduced cholesterol flux from intestine to liver)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Dominant mechanism for controlling LDL plasma concentrations

A

Regulation of hepaatic LDL receptor pathway

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

associated polymorphism with statin myopathy

A

SLCO1B1

(lead to reduced hepatic uptake and increased plasma concentration)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

___ and ___ are admined as inactive lactones, which are transformed to active forms in liver

A

Simvastatin and lovastatin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

niacin mechanism - decrease synthesis of VLDL-TG

A

inhibit DGAT2 that catlayzes final TG synthesis

increases ApoB degradation (major protein of VLDL/LDL)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

pharmacokinetics niacin

A

oral admin, multiple formulations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Greatest HDL impact

A

Niacin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Ezetimibe lipoprotein pofile

A

TG decrease by 5%

LDL decrease by 15-20%

HDL increase by 1-2%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

only mechanism of cholesterol excretion

A

conversion to bile salts via 7a Hydroxylase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Statin lipid profile

A

TG decrease by 20-55%

LDL decrease by 5-10%

HDL increase by 5-10%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

adverse effecs cholestyramiune

A

constipation, bloating

interferes with other drug absorption

modest increase in TG (but normalizes)

gritty consistency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

lipoprotein profile gemfibrozil, fenofibrate

A

TG decrease 30-50%

LDL - decrease 15-20%

HDL - increase 5-15%

13
Q

Niacin mechanism - inhibit FFA mobilization from adipose

A

Niacin receptor 1 > decrease in cAMP

> PKA doesn’t phos perilipin and HSL

>TG not broken down into FFA and glycerol

14
Q

mechanism of action, statins

A

competitive inhibition of active site on HMG CoA reductase > rate limiting step of cholesterol biosynth

reduction leads to increased numbers of LFL-receptors and thus more uptake

16
Q

pharmokinetics of statins

(uptake via)

A

extensive first pass

uptake via OAT1B1

extensive plasma protein binding

18
Q

other beneficial effects of omega 3

A

reduced risk for fatal arrhythmias

enhanced plaque stability

reduced HR

improved endothelial function

19
Q

metabolism of statins primarily via

A

P450 CYP3A4

20
Q

specific HTP inhibitor indication

A

homozygous FH

22
Q

meechanism PCSK9 inhibitors

A

blocks PCSK9 targeting of LDR to lysosome for recyling > increase LDLR

23
Q

primary impact of Fibrates

A

lover levels of TG rich lipoproteins

24
Q

mechanism of statin induced myopathy

A

blockade of HMG CoA reductase also supprsses formation of isoprenoids required for normal muscle function

25
Q

pharmacokinetics fenofibrate, gemfibrozil

A

oral

plasma protein binding

fenofibraate metabolized to active

gemfibrozil metabolized to inactive

26
Q

pharmacokinetics ezetimibe

A

oral admin

metabolized to active form

half life 22

27
Q

niacin lipid profile

A

TG decrease 35-50%

LDL decrease by 25%

HDL - increase by 15-30%

Lpa reduced by 40%

28
Q

mechanism gemfibrozil, fenofibrate

A

bind as heterodimers to PPAR-a receptor in liver, adipose > regulates gene transcription, chief among those increase LPL that breaks down TG

lowers levels of TG rich lipoproteins

29
Q

first choice hyperchholesterolemia drugs

A

HMG Coa reductase inhibitors

30
Q

apoB 100 inhibitors adverse effects

A

injxn site

flu-like

elevation of liver enzyems (rsk hepatotoxicity)

31
Q

mechanism Cholestyramine

A

highly postive binds highly negative bile acids > large resins not absorbed and thus excreted

(excretion depletes bile acids, which are synthesized from cholesterol)

(reduced chol > activates SREBP > increase LDL receptor gene transcription

33
Q

drug of choice for hypertriglyceridemia

A

Gemfibrozil/fenofibrate

(then niacin, then Omega3)

34
Q

greatest TG impact

A

Fenofibrate, Gemfibrozil

36
Q

Class Atrovastatin

Lovastatin

Simvastatin

A

HMG CoA reductase inhibitors

37
Q

MTP inhibitors adverse effects

A

significant GI

hepatotoxicity

38
Q

ApoN-100 inhibtion mechanism

A

antisense oglionucleotide inhibit synthesis of apoB-100 in liver

(apo B binds LDL to receptor, crucial for transport)

40
Q

adverse effects niacin

A

intense cutaneous flsuh/pruritis (via PGD2 from macrophages)

.GI effects

hyperuricemia (gout concern)

Increase fasting glucose, insulin resistance

41
Q

cholestyramine liporotein profile

A

TG - transient increase (larger if higher baseline)

LDL - decrease by 12-25%

HDL - increase by 4-5%

42
Q

rarer, serious side effects statins

A

myositis or liver enzyme elevations

myopathy

rhabdomyolysis

43
Q

MTP inhibitors mechanism

A

prevent assembly of apo-B containing lipoproteins in entoerocytes and hepatocytes > reduced chylomicrons and VLDL > reduced plasma LAL-C concetration

44
Q

(statin use) when cholesterol decreases, ___ and ____ no longer bind, so SREBP-SCAP is transpoted to golgi and cleaved at ___ and ___

this leads to transcriptionally active SREBP > activates target genes

A

(statin use) when cholesterol decreases, **SCAP **and INSIG no longer bind, so SREBP-SCAP is transpoted to golgi and cleaved at S1P and S2P

this leads to transcriptionally active SREBP > activates target genes

Cardiovascular (39 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions