This document discusses lipoproteins and drugs that lower lipid levels. It begins by defining lipoproteins and how they transport lipids in blood, classifying them into six groups. It then discusses the functions of different lipoproteins and causes of hyperlipoproteinemias. The document focuses on statins, how they work by inhibiting HMG-CoA reductase, and their effects on cholesterol, LDL, HDL, and triglyceride levels. It covers the pharmacokinetics of statins, their adverse effects and uses. Other drug classes discussed include bile acid sequestrants, fibrates, nicotinic acid and their mechanisms and uses for treating different lipid abnormalities.

2.  Drugs which lower the level of lipids
and lipoproteins in blood.
 Lipids are transported in plasma as
lipoproteins.
 Lipoproteins are classified into six
classes based on their particle size and
density

3. LIPOPROTEIN FUNCTION
1. Chylomicrons Dietary TG transport
2. Chylomicrons.rem Dietary cholesterol
transport
3. VLDL Endogenous TG
transport
4. IDL Transport
cholesterylesters and
TG to liver
5. LDL Transport cholesterol
to tissues and liver
6. HDL Removal of cholesterol
from tissues
FUNCTIONS OF LIPOPROTEIN

4. HYPERLIPOPROTEINAEMIAS
DUE
TO
•Single gene defect
{or}
•Multiple
genetic,dietary &
physically related
activities
DUE TO
• Myxoedema
• Nephrotic
syndrome
• Chronic alcholism
• Diabetes

5. SOURCES OF CHOLESTEROL

8. HMG CoA
HMG CoA reductase
Mevalonic acid
 Decreases CH synthesis by inhibition of rate limiting HMG
CoA reductase
LDL 20-55%
HDL 5-15%
TG 10-35%

9. 


 First clinically used statin
 Absorption is incomplete
 1st pass metabolism extensive
 Excreted in bile
 T1/2 is short {1-4}hrs

10. Head ache ,nausea,bowel
upsets,rashes
Sleep disturbances
Increased serum
transaminase
Muscle tenderness & rise in
CPK levels occur
infrequently
Myopathy is more common.
Adverse effects

11. 1st choice of drugs for Primary hyper lipidaemia
with raised LDL & total CH levels.
Secondary hypercholesterolaemia.
Used in patients with MI,angina,stroke to lower
cholesterol levels.

12. BILE ACID SEQUESTRANTS:

13. • These are basic ion exchange resins supplied in
chloride form
• They are neither digested nor absorbed in gut
• They bind to bile acids in the intestine
• They increase faecal excretion of bile salts and CH
• resins can retard atherosclerosis
• Not popular clinically because they are
unpalatable,have to be taken in large doses,causes
flatulence and interfere with absorption of many
other drugs
• Have poor patient acceptability

14. GEMFIBROZIL,BEZAFIBRATE,FENOFIBRATE
Activity of lipoprotein lipase

15. • Effectively lowers Plasma TG level by enhancing breakdown &
suppressing hepatic synthesis of TG‘s
ADDITIONAL ACTION: decreases level of clotting factor VII phospholipid
complex & promotion of fibrinolysis
PHARMACOKINETICS: completely absorbed orally ,Metabolized by
glucuronidation & excreated in urine
ADVERSE EFFECT:
 Epigastric distress
 Skin rashes
 impotence
USES:
 Drug of choice in patient with increased TG levels

16.  It lowers TG & LDL-CH
 It raises HDL-CH
 It is used in combination with
statins

17. Nicotinic acid

18.  To lower ldl-ch are statins.
 Statin therapy should be commenced at low dose.
 In adequate response,dose should be doubled at
6 wks interval.
Treatment based on LDL-CH level

19. Treatment of low HDL-CH level
 The primary approaches of therapy is to reduce LDL–CH
level
 Nicotinic acid has highest efficacy to rise HDL-CH level
followed by fibrates

20.  Primary tg lowering drugs are fibrates and
nicotinic acid
 Treatment depend on cause and severity
Treatment of raised TG level