Lipid Disorder
Structureof Lipoprotein
Apoprotein sa
Cholesterol Ester
Triacylglycerol
Phospholipid
Free Cholesterol
sghak kstts
Lipoproteinscompositions
Classification of Lipoproteins
"Bad" "Good"
(Non-HDL)
Chylomicron VLDL IDL LDL HDL
and Very Low Intermediate Low High
Chylomicron Density Density Density Density
remnant Lipoprotein Lipoprotein Lipoprotein Lipoprotein
Non-HIDL-C
Atherogenic lipoprotein
Chylomicron Chylomicron
VLDL
remnant
IDL
LDL
Lumen HDL
Intima
Endothelial cels Triglyceride Cholesterol
LDL Lp(a)
apo(B) apo(B)
S apo(a)
Post-prandial Biliary BAand
Gexcretion
Endogenous TG supply Dietary TG,
CandCE
Endogenous cholesteroi supply BA
Reverse cholesterol transport reabsorption
Billary excretionenterohepatic
circulation
LDLR iHDL Small
Lyrnph TG intestine
PCSK9
Chylomicron TG TG
CE Liver
TG
-LDLA
TG TG Chylomicron
CE
degraded in
lysosome
Peripheral Chylomicron Synthesis
tissues rermnant
LPL (
FFA Oxidation
Oxidation
iHDL
IHDL TG
FFA VLDL
TG
LPL
TG TG Apo B100
CE
IDL
Bile acids (BA)
LDLR
degraded
in ysoSome LDLR
IHDL Cholesterol
degraded in
Iysosme
HMGCOAR
Cholesterol LOL HL
IHDL
looipid-poor Apo A1 CE Synthesis
ABCA1
ABCG1
Lipid rafts
SRB1
HDL
Lipid measurement
Abnormalities of lipid metabolism
most commonly come to light
following routine blood testing
Is the measurement done in fasting (8-12hr) or
in Non fasting state?
And Why?
What is the age for measurement?
Classification of hyperlipidemia
Primary Hyperlipidemia
Secondary Hyperlipidemia
Predominant hypercholesterolaemia Predominant hypertriglyceridaemia
Xanthelasma" A Lipaernia rotinalis
Acute pancraatitis
Corneal arcus
Aortic stenosis
Lipaermic blood and
plasTia
Hepatosplenomegaly
Extensordigitorurn
xanthornas
Pre-patoilar xanthomas
Achilles tendon. Eruptive xanthoTias
Kanttormas
lipemia retinalis
Management of dyslipidaemia
Lipid-lowering therapies have a key role in
the secondary and primary prevention of
cardiovascular diseases.
Assessment of absolute risk, treatment of
all modifiable risk factors and optimization
of lifestyle, especially diet and exercise, are
central to management in all cases.
Non-pharmacological management
• Reduce intake of saturated and trans-unsaturated fat to less than 7–10% of total
energy
• Reduce intake of cholesterol to < 250 mg/day
• Replace sources of saturated fat and cholesterol with alternative foods, such as
lean meat, low-fat dairy products, polyunsaturated spreads and low glycaemic index
carbohydrates
• Reduce energy-dense foods such as fats and soft drinks, whilst increasing activity
and exercise to maintain or lose weight
• Increase consumption of cardio protective and nutrient-dense foods, such as
vegetables, unrefined carbohydrates, fish, pulses, nuts, legumes, fruit, etc.
• Adjust alcohol consumption, reducing intake if excessive or if associated with
hypertension, hypertriglyceridaemia or central obesity .
• Achieve additional benefits with supplementary intake of foods containing lipid-
lowering nutrients such as n-3 fatty acids, dietary fiber and plant sterols.
The response to diet is usually apparent within 3–4 weeks but dietary adjustment
may need to be introduced gradually.
Pharmacological management
+PSCK9 Inh.
To Convert LDL-C in mmol/L to mg/dL, multiply by 38.
To Convert TG in mmol/L to mg/dL, multiply by 88.
Monitoring of therapy
The effect of drug therapy should be
assessed after 6 weeks (12 weeks for
fibrates). .
At this point, it is prudent to review
side-effects, lipid response , CK and
liver function tests.
Monitoring of therapy
If myalgia or weakness occurs in association with
CK elevation over 5–10 times the upper limit of
normal, or if sustained alanine aminotransferase
(ALT) elevation more than 2–3 times the upper
limit of normal occurs that is not accounted for by
fatty liver , treatment should be discontinued and
alternative therapy sought.
European Treatment goals for LDL-C across categories of total
cardiovascular disease risk*
LDL-C goal +>50%
reduction from baseline
116 mg/dL Low -SCORE <1%
(3.0mmo/L)
-SCORE 1-5%
100 mg/dL
ModerateYoung patients (T1DM <35 years;T2DM<50years without other RF
(2.6 mmo/L)
-SCORE >5% and <10%
-Markedly elevated RF (TC310(8 mmo/) or LDL-C >190 (mmol/L)
-BP > 180/110
70mg/dL. -FH without other major risk factors
High
(1.8 mmol/L) -Moderate CKD (eGFR 30-59 ml/min)
-DM >10years or additional RF, w/o target organ danage
-SCORE >10%
-ASCVD (clinical/imaging)
55 mg/dl
Very High -FH with ASCVD or with another major RF
(1.4 mmol/L) -Severe CKD (eGFR <30ml/min)
-DM & target organ damage
40 mg/dl.
Very High** **2nd Event within 2 years
(1.0 mmol/L)
Low Moderate High Very High High with DM CV RISK
*Adapted from slideset available on www.escardio.org/guidelines which is from 2019 ESC/EAS Guidelines for the management of dvslipidaemias: lipid modification to reduce cardiovascular risk
Dyslipidemia In Pregnancy
Lipid Lowering agent Pregnancy Class
Statins X
Fibrates C
Ezetimabe C
Cholestyramine /Colesevelam B
Mipomersin ?
Lomitapide ?
PSCK-9Inhibitors ?
Evinacumab(ANGPTL3-inh.) ?
A: Safe
B :Animal studies safe but no adequate well controlled studies in humans
C: Animal studies have adverse effects on fetus but no adequate controlled studies
in humans
D: Positive evidence of human fetal risk but benefit may warrant use despite risk
19,25 Familial hypercholesterolaemia in adolescence
• Statin treatment: may be required from the age of about 10. It does not
Compromise normal growth and maturation.
• Smoking: patients should be strongly advised not to smoke.
• Adherence to medication: critically important to the success of treatment.
Simple regimens should be used and education and support provided.
