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pharm > exam 2: lecture 3 > Flashcards

exam 2: lecture 3 Flashcards

1
Q

explain the exogenous pathway breifly.

A

in the gut, we have FA and cholestrol –> turned into MICELLES via bile salt, which are made in the liver

the micelles goes to the lumen of the enterocytes in the gut

micelels are packaged into triglyerides

cholestrol is taken up by the NEIMANN PICK C1L1, NPC1L1 and FAT takken up too

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2
Q

what are chylomicrons?

A

FA/triglerrides and cholestrol packaged tg are called chylomicrons

then the chylomircrons goes straight into the lymphatics to give tissue its energy before going to the liver to die

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3
Q

what does lipoprotein lipase do and what happens to the chylomirons remnant?

A

lipoprotien lipase breaks up the triglyerides and FA.

FA is absorbed by the fat tissues and skeletal muscules for energy

the remnants are PROATHEROGENIC!! (similiar to LDL) theyre taken up by liver via LDL receptors

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4
Q

what are the low intensity statin drugs? which is the FIRST DRUG to come out ? how much LDL do they decrease?

A

low intensitiy drugs decreases drugs by <30%

(LPSF)
lovastatin 20mg- 1ST DRUG TO COME OUT
pravastatin 10-20mg
simvistatin 10mg
fluvastatin20-40mg

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5
Q

in general, how do statin work?

A

statin are HMG-CoA reductase inhibitors.

HMG is needed to convert to mevalonate which is needed to make cholestrol synthesis

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6
Q

what are the moderate intensity statins? what % do they decrease LDL?

A

LDL by 30-50%
LPSF-P
lovastatin 40-80mg
pravastin 40-80mg
simvistatin 20-40mg
fluvastatin 80mg

pitavastatin 1-4mg

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7
Q

what are the high intentsisity statin drugs?

A

decrease LDL by 50-63%
(AR)
atorvsatain 40-80mg
rosuvastatn 20-40mg

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8
Q

between the statin drugs, which has a a modest inhibition of apoB production by the liver and modest decrease of VLDL?

A

ATORVASTATIN - uses to lower triglyceride mostly

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9
Q

what is the MOA of statins?

A

the statins are HMG co-A inhibitors!!
they STOP the production of cholestrol

to make up for this, the liver will INCREASE expression of LDL receptors and will pull LDL from the blood

statin will contribute to modest inhibtion of apoB proudction and modest decrease of VLDL –> usefull if soemone’s triglyeride is well elevated like above 200

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10
Q

what are two 2nd effects to statin drugs? good effects :)

A
  1. if you put someone on statin with normal HDL, statin will raise the HDL by 5-10%
    BUT, if you put someone on statin with RAISE than normal HDL, nothing will happen
  2. statin drugs inhibits ROS which will decrease inflammmation of atherosclerotic lesions –> which will STOP THE GROWTH OF LESIONS WOW!!!
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11
Q

what is the pharmokinetics of statins? think about if given PO, IV, etc and what two enzymes metabolzies the drugs

A

given PO at night!!! best time

These two metabolzies the drugs?
CYP2C9 - FPR - fluvastatin, pravastatin, rosuvastain
CYP3A4 - LAS - lorvastatin, atorvastatin, simvastatin

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12
Q

what are the indications for statin meds?

A
  • hypercholeserolemia obviouslly!!!
  • DM2 (to lower cholesterol levels
  • for acute coronary events ( it can LOWER coronary events

study has shown that a combo drug is really good than alone drug

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13
Q

what are some untoward effects for satin?

A
  1. Myalgia!!! (statin can inhbit coQ10 which is needed for ETC which can cause myalgia)
    - this is why you put people on satin + coQ10 supplement
    - always check CK levels since it can increase in blood with muscuels pain

severe cases: rhabdo

  1. DRUG TO DRUG! NEVER GIVE STATIN W NIACIN OR FIBRATE BC IT CAN CASUE SEVERE MYOPATHEIS
  2. NEVER GIVE STATIN W PREG PPL - it can go through the placenta to baby and cause teratogenic!
  3. ALWAYS CHECK liver enzymes. more than 3 is BAD
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14
Q

explain the MOA of ezetimibe? what year did it come out ?

A

it came out in 2002

it gets conjugated by the liver with glucoranic acid then it binds to the enterocyte on the lumen. this binding prevents cholestrol from binding and from being taken up via NC1L1 receptor

bc of this, the liver compenstates by taking up LDL from the blood and and increasing LDL receptors = THIS DECREASES LDL = GOOD THING

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15
Q

expplain the pharmokinetics of ezetimbie ?

A

taking PO
its a prodrug so its absorbed in the gut

gets conjugated with glucoronic acid in the liver so that it easily can bind to the NC1L1 receptor

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16
Q

what are the indication and untoward effect of ezetibmide?

A
  1. Hypercholesterolemia!!!
    - ezetimbine is better in combo therapy so with a statin or fibrate = decreases extra 10% of LDL

S/E:
HOWEVER, make sure you check hepatic function it can lead to liver diesease, cholesterokl gallstones,

bad for pregnancy people

17
Q

how do bile acid sequestrant work?

A

so normally, bile acid is made in the liver and stored in the gallblader. when we eat food, bile acid leaves the gallbadder and helps us reabsorbed the food in the gut, then it gets recylced back into the liver = enterohepatic recycling

normally BAS like cholestyramine is a catonic+ so CL- will bind to it but

when we take a bile acid sequestrant, the drug BINDS TO the bile acid and it prevent entoroheptatic

so this FORCES THE LIVER to make more bile acid so its not going back there anymore so LIVER INCREASES LDL RECEPTOR AND TAKES OUT LDL FROM THE BLOOD

18
Q

when is enterohepatic recycling ?

A

so normally, bile acid is made in the liver and stored in the gallblader. when we eat food, bile acid leaves the gallbadder and helps us reabsorbed the food in the gut, then it gets recylced back into the liver = enterohepatic recycling

19
Q

what are the bile acid sequesrant drugs examples?

A

B-CCC
* Colestipol
* Cholestyramine
* Colesevelam

20
Q

which bile acid sqeusret is NOT SYSEMICALLY ABSORBED and what is the benefit?

A

cholestryamine is not systemically absrobed so its SAFE to give to preg pt or those trying to get preg

21
Q

what are the indication for bile acid sequesrants?

A
  1. hypercholesterolemia! decreases LDL
  2. PRUITITS + LIVER DISEASE!!!!
    - those with liver disease have bile salts getting to the blood and spilling onto the skill casuing nasty prurities. so a bile acid sequerants is perfect to help bring this down!
22
Q

what are the untoward effect to bile sequesrants?

A
  • GI : bloating and constipation
  • VIT K: so bile acids are needed to absorb VIT K for clotting factors
  • DRUG TO DRUG –> ezitimide, digoxin, duritiecs, levothyroxin, warfarin, BB

-metabolic acidosis: someone with COPD has a buildup CO2 and someone w diabeties can get ketoacidosis
–> so what happens is that the drug binds to bile salt so CL builds up in the blood and the body will try to compensate and remove another anion so it will remove bicarb and removing bicarb causing metabolic acidosis

23
Q

what are the two fibrates medication and their half life?

A

GF
Gemfibrozil - earlier generation, short half life
Fenofibrate - long half life of 18 hours

24
Q

what is the MOA for fibrates?

A

fibrates bind to PPAR-a which is a transcription factor for lipid homeostasis. it does the folowing:

casues expression of LPL

LPL is sig becasue it PULL MORE fat/lipids out of blood

it also upregulate apoA1 and 2 which is a component of HDL (remember apoB is a component of LDL)

and it inhibits apoC3 which inhibit lipoprotein lipase

25
Q

what is the net effect and indication of fibrate?

A
  • net effect is that fibrate works on VLDL and reduces VLDL
  • it also midly decreases LDL and increases HDL
  • its used for hypertriglyceridemia and genetic disorders such as those with type 3 hyperlipoproteinemia or those w high chylomicron levels
26
Q

what is the untwoard effect for fibrates?

A
  • GI issues
  • elevated liver enzymes
  • cholestrol gallstones - can increase cholestrol content of bile
  • mypathy - combo of fibrate and station is bad
  • rash
  • vertigo
  • preg NOT SAFE!!! (only Bile acid squeesrant is)
27
Q

which lipid lowering agent is safe in pregnacny?

A

BILE ACID SEQUESRANTS LIKE CHOLESTRYAMINE SINCE IT IS NOT SYSTEMICALLY ABSROBED

28
Q

whar are the diff names for naicin?

A

nicotnic acid
VIT B
niacor, niaspan

29
Q

how does naicin work in the liver and adipose tissue?

A

In the liver there is diacylgylcerol acyltransferase 2 which is needed to make trigyleride. NIACIN inhibits this and this decreases VLDL and LDL

naicin also inhbits the catabolism of apo1 which is esstensial for HDL

in the adipose tissue, naicin increases LPL which increases lipoprteoin lipase which breaks trigylerides and it inhibits HSL

30
Q

what is the net effect for naicin ?

A

decreases VLDL, LDL, increases HDL, decreases trigylerides

31
Q

what is the pharmcokinetics and indication for niacin? CT

A

naicin is taking PO and its indication are hypertrigyleridemia and hyperchoelsterolema

32
Q

what are the many untowards effect for niacin? ALOT

A
  1. niacin flush –> langerhands cell have niacin receptors so naicain binds to it that gives off inflamamtory repsonse and release cyclooxygenase enzymes which contributes to the inflammation and increases prostalgandins
  • recommended to give cox-i 2 hours before

comes w red flush and warth

can also casue vasodilation so its not good to take it w HTN med

  1. hyperuricemia –> blocks the OAT receptors on the kidney. so gout increeases
  2. GI issues duh
  3. myopathies – not good w statin
  4. liver damange in high dose duh
  5. stops coagulation factors so bad w those w GI bleeding or ulcers
  6. homocystenin levels increases in blood which is bad - increases CV events

NOT SAFE W PREGNANCTY

33
Q

what are the two PCSK9i and when did they come out? what is the PO and untoward effects ?

A

AE = both came out in 2015 VERY NEW

Alirocumab (praluent) AP
Evolocumab (repatha) ER

given SUBQ every 2-4 weeks really expensive

untoward effect: injection site irritation and flu like sx

34
Q

what is the MOA and what did the studies show for PSCK9i?

A

MOA:
normaly PCSK binds to LDL receptors and takes it to the lysosome to destroy it

PCSKi inhibiting the binding to LDL and LDL receptors are higher than normal, and more LDL are pulled out of the bloodstream which lowers cholesterol ode

studies show that combo drugs is BETTER so PCSKi + statin

35
Q

which drugs has an S/E of homocysteine and coagulation issues

A

naicin

bile acid = vit k absortion effected

36
Q

which drugs increases gout levels as one of the s/e?

A

naicin

37
Q

which drugs has a rash and vertigo s/e?

A

fibrates

38
Q

which drugs can casue metabolic acidosis?

A

BAS

pharm (13 decks)

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