hyperlipidemia 33333& Anemia111111113.ppt

hyperlipidemia & Anemia

1. Sunday, June 2, 2024 1
Classes of Plasma lipoproteins
1. Chylomicrons:
-Formed in GIT & after meal.
-It transports dietary C & TGs from GIT to muscles & fat.
2. VLDL:-Synthesized by the liver & rich in TGs.
–Carry endogenous TGs from liver to muscles & fatty tissues.
3. LDL: -Atherogeniclipoprotein (bad cholesterol) & rich in cholesterol.
-Carries cholesterol from the liver into the blood.
4. HDL: -Antiatherogeniclipoprotein (good cholesterol).
–Carries cholesterol from blood and tissues into the liver to be cleared from
the body.

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When Hyperlipoproteinemiashould be treated?
•If total C 200 mg/dl
LDL C 130 mg/dl.
•If total C 200-239 mg/dl
LDL C 130-159 mg/dl.
–If no risk factorsdiet therapy may be sufficient.
–Any risk factors both drug and diet therapies are needed.
•If total C 240 mg/dl
LDL C 160 mg/dl
–Require urgent drug and diet therapies (even no risk factor).
Normal & no risk
high ‘border line’
high C levels

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Approaches used in the treatment of hyperlipoproteinemia
1. Non-drug therapy of hyperlipidemia
a)Diet therapy:
–saturated fat(animal fat)
–unsaturated fat(vegetable fat e.g., olive oil).
first line management in high border line & hyper-lipidemia
b) Cigarette smoking:should be stopped at once.
c) Obesity:Must be reduced by:
-physical activity +
-dietary regimen.
d) Stop alcohol drinking.

4. Antihyperlipidemic drugs
1. HMG-CoA reductase inhibitors
Atrovastatin Fluvastatin
Lovastatin Simvastatin
2. Fibrates
Fenofibrate Gemfibrozil
3. Niacin
4. Bile acid sequesterants
Colestipol Cholestyramine
5. Cholesterol absorption inhibitors
Ezetimibe

5. Acetyl-CoA
cholesterol
HMG-CoA
reductase
statins
LDL
R
LDL
MECHANISM
LDL
R
LDL
R
LDL
R
LDL
R
LDLLDL
LDL
LDL
LDL
LDL
LDL
LDL
LDL
LDL
HMG-CoA Rate limiting
step in
cholesterol
synthesis

6. Mechanism of action
They lower plasma cholesterol by ↓cholesterol
biosynthesis + ↑catabolism of LDL
Inhibition of HMG CoA reductase: deplete intracellular
cholesterol
Effective in lowering plasma cholesterol levels in all
typesof hyperlipidemia
Therapeutic uses

7. Adverse effects
1. Liver:
Evaluate liver function periodically.
They return to normal when the drug
is stopped
2. Muscle:
Myopathy and rhabdomyolysis
(rare), most cases have renal
insufficiency
Contraindicated in pregnancy,
lactation and children

8. 2. Niacin (nicotinic acid)
The most effective agent for increasing
HDL
Can reduce LDL
Uses: -Lowers bothcholesterol and TG
-Forraising HDL

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Fibricacid (fibrate) derivatives
Members:
–Clofibrate(Atromid-S)
–Gemfibrozil(Lopid)
Mode of action:
VLDL breakdown(lipoprotein lipase activity)
Activation of LDL receptors: shift LDL formed from VLDL from
the blood into the liver LDL.
Net effect: TGs by 40 %
Use: Treatment of hypertriacylglycerolemiasand some types of
familial hyperlipidemia

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2. Bile-Acid Binding Resins
Members:
Cholestyramine(Questran) & colistipole(Colestid)
Mode of action:
•Resins are not absorbed from GIT and given orally.
•They bind with bile acids in the GIT absorption
of bile acids bile acids levels in the bloods :
–The net effect: LDL levels in the blood.

11. Antianemic Drugs

12. Def:Below-normal plasma hemoglobin concentration resulting from a
decreased number of circulating RBCs.
Anemiais usually caused by either:
a)Reduction in blood hemoglobin(Hb) level.
b)Reduction in number of RBC’s.
Anemia

13. Both required for normal DNA
synthesis.
Deficiency causes megaloblastic
Anemia.
Role of Vit B
12and Folic acid
Nutritional Causes of Anemia:
Deficiency
Iron
Vitamin B
12
Folic acid

14. Oral iron and Parenteral iron are available
Treatment aimed to raise 1% haemoglobin a day
Oral Iron :
Avoid to be taken with: antacids , with tea (
absorption).
Preferred to be taken with vitamin C-Why?: because
VitC reduces ferric iron to ferrous →absorption.
I-Iron

15. Adverse effects & poisoning of iron salts:
Oral iron:GIT side effects: nausea, vomiting & constipation due to
irritation.
Parenteral iron:Risk of severe and even fatal hypersensitivity reactions.
Acute iron poisoning:Causes liver & brain damages, nausea and vomiting
as well as ulceration in GIT.
Treated by deferoxamine: Deferoxamine acts by binding free iron in the
bloodstream and enhancing its elimination in the urine.
Parenteral treatment considerations:

16. Source:Diet (all foods from animal origin).
Administered parentally to both patients with pernicious
anemiaand megaloblastic anemia.
III-Folic acid (Pteroylglutamicacid)
In most fruits and vegetables; over cooking destroys
more than 90% of it.
II-Vit. B
12(Cyanocobalamin)