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DT3- EXAM 1 > Dislipidemia Drugs- Melissa (3)* > Flashcards

Dislipidemia Drugs- Melissa (3)* Flashcards

1
Q

4 disease states that raise cholesterol levels:

A
  1. Biliary Disease
  2. Renal Disease
  3. Hypothyroidism
  4. Diabetes Mellitus respond well to STATINS
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2
Q

Three disease states that raise TG levels:

A
  1. Alcoholism
  2. Renal Disaese
  3. Diabetes Mellitus
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3
Q

Ideal levels:

  1. cholesterol
  2. LDL-C
  3. TG
A

Cholesterol: UNDER 200
LDL-C: UNDER 100 (acceptable = 100-129)
TG: UNDER 150

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4
Q

Primary causes of hyperlipidemia (2)

A

diet

genetics

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5
Q

3 secondary causes of hyperlipidemia:

A

Drugs (Propranolol, HTZ), Disease (DM), ETOH abuse

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6
Q

What is the first line therapy in hyperlipidemia?

A

DIET MODIFICAITON:

  • Decrease fat (TGs, etc.), carbs, ETOH
  • Increase exercise–> ^HDL prodxn
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7
Q

Cholestyramine, Colesnvelam, Colestipol

Drug Class, ROA, MOA?

A

Resins: Aways start with chol/col

ROA:
PO w/ lots of fluid; NOT ABSORBED GI–> NO bioavailability!

MOA:
Bind bile acids in sm. intestine–>
^ Fecal bile acid excretion–>
DECREASE neg. feedback on 7a-HYDROXYLASE–>
^ Liver conversion cholesterol–> bile acid –>
DECREASE circulating cholesterol

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8
Q

How is Colesevelam administered? Why is this important?

A

Administered as a capsule w/ liquid; becomes gel in GI tract
Less GI sx; better patient compliance

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9
Q

Therapeutic use for Resin drugs?
How long do they take for max effect?
What is max effect?

A
  • Tx ^ cholesterol (~combo treatment for ^ TG/^C pts)

- 4 weeks to max effect= 20% reduction plasma LDL-C

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10
Q

Which patient populations can take resins safely (2)?

Why is this relevant?

A

preggos/ nursing; kiddos +6yrs

*Good alternative to statins which cannot be used in pregnancy or in children under 8yoa

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11
Q

Resins ADRs; when are they worse?

A

GI sx: bloating, constipation, abdominal pain

*Worse if patients don’t take enough fluid!

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12
Q

DD interactions with resins–what is the cause?

How do we avoid this?

A

Resins compromise absorption of fat sol vitamins and drugs

*Take drug 1 hr before or 4 hrs after resin

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13
Q

MOA for all statin drugs?

Recall the two ultimate effects:

A

Competitive inhib. HMG-CoA Reductase (RLS cholesterol synth.)–> DECREASE INDOGENOUS CHOLESTEROL SYNTH. –> ^ LDL-Rs in LIVER + ^ HDL levels

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14
Q

Therapeutic use for ALL statin drugs (2)?

Time to max effect?

A

Hypercholesterolemia; combo tx. in patients with ^ TGs

**2 weeks to max effect

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15
Q

Which two drugs are the most effective statins and can be used to treat ^ TGs?
Why are they so effective (2)?

A

Atorvastatin, Rosuvastatin

  • Longer t 1/2
  • ^ LDR # the most–> LDLR binds APOE–> ^ IDL clearance (w/TGs)
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16
Q

Which statin drug can treat kids 8+ yoa?
Why?
What is the age cut off for all other statin drugs?

A

Pravastatin 8+ yoa (less side effects)
Other Statins 10+ yoa

Pr= Prim, little sister (maybe 8 years old in the first hunger games movie?)

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17
Q

At what time of day does cholesterol synth. peak?

Which statin drugs are taken at night (3)?

A

Cholesterol synth. peaks b/w 12-2AM
Lova-, Fluva-, Simvastatin

Leah is Fast aSLeep at night. (LFS = night time drugs)
This was a good one, thank you! :)

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18
Q

Which statin drug should be taken at dinner (w. food)?

A

Lovastatin

Leah Loves Food!
Take the “L” drug with food!
Also excellent, thank you!!

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19
Q

Which two statin drugs can not be taken with food (dec. absorption)?

A

Prava-, Pitavastatin

Both start with “P”. Don’t take the “p” drugs when you eat your “peas”.
PRAy for PITA but don’t eat it!

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20
Q

Two prominent ADRs of statin drugs:

A
  • Hepatic dysfunciton (^ALT, AST)

- Myalgia (^CPK) STOP DRUG

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21
Q

Factors that increase hepatic ADRs of statin drugs (3)

A
  • ^dose statin
  • gemfibrosil or nicotinic acid
  • CYP3A4 inhibitors (ketoconazole, erythromycin)
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22
Q

Which two statins cause the LEAST ADRs?

A

Fluvastatin, Pravastain (KIDDOS 8+ yoa!)

–> Consequently, these are also the least potent/ cause the smallest cholesterol reduction.

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23
Q

3 contraindications for statins:

A
  • PREGGOS X!!!/ nursing
  • Liver disease
  • Kiddos under 8/10
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24
Q

Which two statins are prodrugs?

Two potential factors compromising their safety of use?

A

Lova-, Simvastatin
CYP3A4 inhibitors, Grapefruit juice
*Atorvastatin not prodrug, but met. by CYP3A4

“LOve SIMone; she’s a pro.”
or “Leah’s SIMply a PRO at school :)”

25
Q

Which 2 statins are metabolized by CYP2C9?

A

Rosuva-, Fluvastatin

It would be *Freaking *Ridiculous 2 C 9 monkeys at the BCC!

26
Q

Which statin is metabolized by CYP2D6?

2 clinical implications?

A

Simvastatin

  1. CYP2D6*4 allele–> slow metabolizers–> longer t 1/2
  2. SCLO1B1 SNP–> poor hepatic uptake–> ^ plasma levels
    - -> more ADRs (MSK pain!)
27
Q

SCLO1B1 SNP: clinical significance?

A

Simvistatin; low hepatic absorption and more MSK pain!

Give these patients lower Simvastatin doses.

28
Q

Ezetimibe:
MOA?
Describe administration regimen?

A

Targets DIETARY cholesterol
Once daily dosing

MOA:
INHIBIT NPC1L1 transporter–> DECREASE cholesterol absorption at brush boarder enterocytes (sm. intestine)

29
Q

Therapeutic uses for Ezetimibe (2) :

A

Hypercholesterolemia (decrease LDL-C 20%) independently or combo tx

DOUBLE Statin effectiveness

30
Q

2 ADRs of Ezetimibe:

A

Diarrhea with fatty meals; Hepatic dysfxn.

Your poops come out too EZ :)💩

31
Q

Contraindications to Ezetimibe use (2):

A
  • Hepatic disease (enterohepatic recirculation)

- Resins decrease absorption

32
Q

Alirocumab, Evolocumab:
Drug class + MOA?
ROA + Dosing regimine?

A

Remember. –mab = monoclonal antibody

PCSK9 Inhibitors
Inhibit PCSK9 binding LDL-Rs–>
STOP targeting endocytosed receptors for destruction–>
^ LDL-R recycling–> ^ # LDL-Rs

*IV infusion every 2-4 weeks

33
Q

ADRs of PCSK9 Inhibitors:

A

Hypersensitivity

-others really unknown because these are so new

34
Q

Gemfibrozil, Clofibrate, Fenofibrate, Benzafibrate

Drug Class?
MOA ( + 3 effects)?

A

Fibrates (have fibr in name)

MOA: 
Bind + stimulate PPAR-a --> 
1. ^ FA oxidation/LPL--> DECREASE FFA
2. ^ APO AI/AII--> ^ HDL (15%)
3. DECREASE APO CIII--> ^LPL--> DECREASE VLDL
35
Q

2 ADRs of Fibrate drugs–which drugs/ circumstances are worst?

A

-Gallstones (worst = Clofibrate)
-Myopathy (statin combo»>)
(worst = Gemfibrosil, Clofibrate)

36
Q

Which fibrate drug causes the LEAST myopathy?

A

Fenofibrate

FEeel NO pain with FENOfibrate

37
Q

Describe why fibrate drugs cause worsened myopathy when combined with statins:

Which statins are affected the worst (3)?

A

Block OATP2 transporter–> can’t clear statins from liver–> ^ conc. in circ–> ^ MSK sx.

*statins affected = prava-, atorva-, rosuvastatin

When the fibrates ruin the OATs, the PARty is ruined! We can’t have no bake cookies without OATmeal. No cookies = sucky PARty.
PAR = prava, atorva, rosuvastatin

38
Q

3 contraindications for fibrate drugs

A

gallbladder/ liver/ renal disease

39
Q

Nicotinic Acid:

MOA (2)

A
  1. INHIBIT hormone sensitive lipase (adipose cells) –> Decrease lipolysis of fats –> DECREASE FFA return to liver
  2. ^LPL –> ^ VLDL clearance

(Thank you! :) )

40
Q

Which two classes of drugs are used to treat elevated blood triglycerides?
How do they work?

A

Fibrates and Nicotinic Acid

  1. Fibrates: through PPARa
  2. Nicotinic acid through hormone sensitive lipase
41
Q

Two caveats to administration of nicotinic acid:

A
  1. CAN’T INTERCHANGE immediate and XR versions
    (will ^ ADRs)
  2. MUST TITRATE DOSE over 4 weeks to the therapeutic dose of 2-6 g/d (will ^ ADRs otherwise…. Like flushing and itching)
42
Q

6 Most common ADRs asstd. with nicotinic acid:

A
  • Itching/ Flushing** (admin ASA **to prevent flushing)
  • PEPTIC ULCERS***
  • HYPERURICEMIA (Gout)***
  • GLUCOSE INTOLERANCE (DM)***
  • Liver disease
  • Myopathy w/ Statins
43
Q

3 Contraindications for nicotinic acid use:

A

Bleeding disorders, peptic ulcers, Liver disease

probably gout and DM too if conditions are severe…

44
Q 
Familial Hyperchylomicronemia (type 1): 
Describe disease + Treatment
A

Defective LPL or APOCII–> ^ TG/chylomicrons w. 12 hr fast

TX:

  • Diet (limit carbs + fats)
  • Fibrates + Nicotinic acid- because this is a TG problem! Not cholesterol.
45
Q 
Familial Hypercholesterolemia (IIa):
Describe disease + Drug Treatment
A

Impaired LDL-C clearance HIGHEST RISK CVD

TX:
#1 Statins
-possible combo w/ Ezetimibe or Resin
B/c this is a CHOLESTEROL problem!

46
Q

Familial Combined Hyperlipoproteinemia (IIb):

Describe disease + Drug Treatment

A

^ TG, ^ Cholesterol

TX:
#1 Statins (Atorvastatin or Rosuvastatin are best- because this is a TG AND CHOLESTEROL problem)
Possible combo w/ nicotinic acid

47
Q 
Familial Dysbetalipoproteinemia (III):
Describe disease + Drug Treatment
A

Abnormal APOE2–> Can’t clear VLDL properly–>
^ TG/cholest., ^IDL + chylomicrons
…Basically, all of the levels are messed up.

TX: #1 Fibrates (DECREASE TG 50%)
*I don’t know a logical reason for not treating the cholesterol issue. *Me either, this perplexed me.

48
Q 
Familial hypertriglyceridemia (IV)
Describe disease + Drug Treatment

Which drug makes it worse?

A

^ TG/ VLDL w/ asstd. hyperuricemia + glucose intolerance

TX: #1 Fibrates

NICOTINIC ACID will WORSEN uricemia/ glucose intol.!

49
Q

Thiazide diuretics effect on lipid profile:

A

^ cholesterol + ^ TG 10-15%

50
Q

Non-specific B-Blockers (propranolol) effect on lipid profile:

A

^ TG

DECREASE HDL

51
Q

OCPs effect on lipid profile:

A

^TG

52
Q

Of all drugs to treat Dislipidemia, which are not labeled to cause hepatic dysfunction/ aren’t specifically contraindicated in hepatic failure?

A

Resins (Because they have no bioavailability)

PCSK9i’s (maybe because not enough research yet)

53
Q

NPC1L1 transporter is inhibited by which drug?

A

Ezetimibe

54
Q

Worst three statins to combine with fibrate drugs:

A

prava-, atorva-, rosuvastatin

55
Q

What do you give patients to prevent itching/ flushing induced by nicotinic acid?

A

ASA prophylaxis

56
Q

Which familial lipid disorder has the highest associated risk for CVD?

A

Familial Hypercholesterolemia (IIa)

57
Q

Three well known CYP3A4 inhibitors

A
  • -Azoles (antifungals)
  • -grapefruit juice
  • -erythromycin
58
Q

What are types:

I, IIA, IIB, III, and IV dislipidemia?

A 
I. Hyperchylomicronemia 
IIA. Hypercholesterolemia 
IIB. Combined Hyperlipidemia 
III. Dysbetalipoproteinemia 
IV. Hypertriglyceridemia (the one with glucose/utricle acid issues)
59
Q

Which drugs have the following effects?
^TG/cholesterol
^ TG
^TG/ decreased HDL

A

^TG/cholesterol- Thiazides
^ TG- OCPs
^TG/ decreased HDL- BBers

DT3- EXAM 1 (26 decks)

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