Flashcards in Dislipidemia Drugs- Melissa (3)* Deck (59)
4 disease states that raise cholesterol levels:
1. Biliary Disease
2. Renal Disease
4. Diabetes Mellitus *respond well to STATINS*
Three disease states that raise TG levels:
2. Renal Disaese
3. Diabetes Mellitus
Cholesterol: UNDER 200
LDL-C: UNDER 100 (acceptable = 100-129)
TG: UNDER 150
Primary causes of hyperlipidemia (2)
3 secondary causes of hyperlipidemia:
Drugs (Propranolol, HTZ), Disease (DM), ETOH abuse
What is the first line therapy in hyperlipidemia?
- Decrease fat (TGs, etc.), carbs, ETOH
- Increase exercise--> ^HDL prodxn
Cholestyramine, Colesnvelam, Colestipol
Drug Class, ROA, MOA?
Resins: Aways start with chol/col
PO w/ lots of fluid; NOT ABSORBED GI--> NO bioavailability!
Bind bile acids in sm. intestine-->
^ Fecal bile acid excretion-->
DECREASE neg. feedback on *7a-HYDROXYLASE*-->
^ Liver conversion cholesterol--> bile acid -->
DECREASE circulating cholesterol
How is Colesevelam administered? Why is this important?
Administered as a capsule w/ liquid; becomes gel in GI tract
*Less GI sx*; better patient compliance
Therapeutic use for Resin drugs?
How long do they take for max effect?
What is max effect?
- Tx ^ cholesterol (~combo treatment for ^ TG/^C pts)
- 4 weeks to max effect= 20% reduction plasma LDL-C
Which patient populations can take resins safely (2)?
Why is this relevant?
preggos/ nursing; kiddos +6yrs
*Good alternative to statins which cannot be used in pregnancy or in children under 8yoa
Resins ADRs; when are they worse?
GI sx: bloating, constipation, abdominal pain
*Worse if patients don't take enough fluid!
DD interactions with resins--what is the cause?
How do we avoid this?
Resins compromise absorption of fat sol vitamins and drugs
*Take drug 1 hr before or 4 hrs after resin
MOA for all statin drugs?
Recall the two ultimate effects:
Competitive inhib. HMG-CoA Reductase (RLS cholesterol synth.)--> DECREASE *INDOGENOUS* CHOLESTEROL SYNTH. --> **^ LDL-Rs in LIVER** + **^ HDL levels**
Therapeutic use for ALL statin drugs (2)?
Time to max effect?
Hypercholesterolemia; combo tx. in patients with ^ TGs
**2 weeks to max effect
Which two drugs are the most effective statins and can be used to treat ^ TGs?
Why are they so effective (2)?
- Longer t 1/2
- ^ LDR # the most--> LDLR binds APOE--> ^ IDL clearance (w/TGs)
Which statin drug can treat kids 8+ yoa?
What is the age cut off for all other statin drugs?
Pravastatin 8+ yoa (less side effects)
Other Statins 10+ yoa
Pr= Prim, little sister (maybe 8 years old in the first hunger games movie?)
At what time of day does cholesterol synth. peak?
Which statin drugs are taken at night (3)?
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! :)**
Which statin drug should be taken at dinner (w. food)?
Leah Loves Food!
Take the "L" drug with food!
**Also excellent, thank you!!**
Which two statin drugs can not be taken with food (dec. absorption)?
Both start with "P". Don't take the "p" drugs when you eat your "peas".
**PRAy for PITA but don't eat it!**
Two prominent ADRs of statin drugs:
-Hepatic dysfunciton (^ALT, AST)
-Myalgia (^CPK) ***STOP DRUG***
Factors that increase hepatic ADRs of statin drugs (3)
-gemfibrosil or nicotinic acid
-CYP3A4 inhibitors (ketoconazole, erythromycin)
Which two statins cause the LEAST ADRs?
Fluvastatin, Pravastain (KIDDOS 8+ yoa!)
--> Consequently, these are also the least potent/ cause the smallest cholesterol reduction.
3 contraindications for statins:
-PREGGOS X!!!/ nursing
-Kiddos under 8/10
Which two statins are prodrugs?
Two potential factors compromising their safety of use?
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 :)"
Which 2 statins are metabolized by CYP2C9?
It would be *Freaking *Ridiculous 2 C 9 monkeys at the BCC!
Which statin is metabolized by CYP2D6?
2 clinical implications?
1. CYP2D6*4 allele--> slow metabolizers--> longer t 1/2
2. SCLO1B1 SNP--> poor hepatic uptake--> ^ plasma levels
--> more ADRs (MSK pain!)
SCLO1B1 SNP: clinical significance?
Simvistatin; low hepatic absorption and more MSK pain!
Give these patients lower Simvastatin doses.
Describe administration regimen?
Targets *DIETARY cholesterol*
Once daily dosing
INHIBIT NPC1L1 transporter--> DECREASE cholesterol absorption at brush boarder enterocytes (sm. intestine)
Therapeutic uses for Ezetimibe (2) :
Hypercholesterolemia (decrease LDL-C 20%) independently or combo tx
*DOUBLE Statin effectiveness*