PATHOPHYSIOLOGY OF HYPERLIPIDAEMIA Flashcards
STATE THE CLINICAL MANIFESTATIONS OF FAMILIAL HYPERTRIGLYCERIDAEMIA.
- ERUPTIVE XANTHOMA
- LIPAEMIA RETINALIS
- HEPATOSPLENOMEGALY
- SERUM APPEARS TURBID AT THE BOTTOM AND CREAMY AT THE TOP LAYER
STATE THE INVESTIGATION FINDINGS IN FAMILIAL HYPERTRIGLYCERIDAEMIA.
- HIGH LEVEL OF TG
- LOW LEVEL OF HDL
- AVERAGE OR LOW LEVEL OF LDL
- IF THE TG IS MORE THAN 4.5, THEN THE LDL CANNOT BE CALCULATED.
STATE THE COMPLICATIONS OF FAMILIAL HYPERTG.
- ACUTE PANCREARITIS
- INCREASED RISK OF CVS DISEASE
STATE THE SERUM FINDING OF FAMILIAL HYPERCM.
CREAMY AT THE TOP LAYER
FAMILIAL HYPERCM OCCUR D/T
DEFICIENCY OF THE ENZYME LPL
DEFICIENCY OF APO Cii
FAMILIAL HYPERCM IS (DOMINANT/RECESSIVE) DISORDER
RECESSIVE
STATE THE CLINICAL MANIFESTATION OF FAMILIAL HYPERCM.
- ERUPTIVE XANTHOMATA
- RECURRENT ABDOMINAL PAIN CAUSED BY PANCREARITIS
- LIPAEMIA RETINALIS
TRUE/FALSE:
REGARDING FAMILIAL COMBINED HYPERLIPIDAEMIA:
A. IT IS AN AUTOSOMAL RECESSIVE DISORDER.
B. IT IS DUE TO THE HEPATIC OVERPRODUCTION OF APO B
C. PLASMA CHOLESTEROL OR TG OR BOTH MAY BE ELEVATED.
D. PRESENCE OF TENDON XANTHOMATA AS CLINICAL MANIFESTATION
E. A SECONDARY CAUSE OF HYPERLIPIDAEMIA.
A. FALSE (DOMINANT)
B. TRUE
C. TRUE
D. FALSE (NO PRESENT OF TENDON XANTHOMATAIN THE FAMILIAL COMBINED HYPERLIPIDAEMIA)
E. TRUE
FAMILIAL HYPERALPHALIPOPROTEINEMIA IS DUE TO THE INCREASE IN ___.
HDL FRACTION
SECONDARY HYPERLIPIDAEMIA IS ___(MORE/LESS) COMMON THAN PRIMARY HYPERLIPIDAEMIA.
MORE
SECONDARY HYPERLIPIDAEMIA IS ___(MORE/LESS) COMMON THAN PRIMARY HYPERLIPIDAEMIA.
MORE
HOW IS THE OBESITY LEAD TO SECONDARY HYPERLIPIDAEMIA?
- OBESITY HAS INCREASE IN ADIPOCYTE MASS AND DECREASED IN THE INSULIN SENSITIVITY WHICH CAN AFFECT THE LIPID METABOLISM.
- MORE FREE FA FROM THE ADIPOSE TISSUE WILL BE DELIVERED TO THE LIVER.
- THIS FA WILL BE REESTERIFIED IN HEPATOCYTES TO FORM TG WHICH ARE PACKAGED INTO VLDL FOR SECRETION INTO THE CIRCULATION
- THEREBY, THIS WILL LEAD TO EXCESSIVE HEPATIC VLDL PRODUCTION.
- HENCE, HIGH TG, LOW HDL AND VARIABLE/NORMAL LDL CAUSING THE SECONDARY HYPERLIPIDAEMIA.
STATE THE PATHOGENESIS OF DM THAT RELATE WITH THE SECONDARY HYPERLIPIDAEMIA.
- INSULIN RESISTANCE A/W TYPE II DM.
- IT WILL CAUSE THE LPL ACTIVITY TO BE REDUCED.
- LPL IS USED TO DEGRADE THE TG INTO FREE FA AND GLYCEROLS
- SINCE THERE IS REDUCTION IN THE LPL ACTIVITY, THE CATABOLISM ACTIVITY OF THE CM AND VLDL WOULD BE REDUCED AS WELL.
- AS A RESULT, THERE WILL BE AN INCREASE IN THE RELEASE OF FREE FA FROM THE ADIPOSE TISSUE, FA SYNTHESIS IN THE LIVER AS WELL AS HEPATIC VLDL PRODUCTION.
- THEREBY, THERE WILLL BE AN ELEVATED LEVEL OF TG
HYPOALBUMINEMIA WILL CAUSE (INCREASED/DECREASE) IN HEPATIC PROTEIN SYNTHESIS.
INCREASE
HYPOALBUMINEMIA IN NEPHORTIC SYNDROME WILL CAUSE:
- INCREASED HEPATIC PRODUCTION
- DECREASED CLEARANCE OF VLDLS
- INCREASED LDL PRODUCTION
CHRONIC KIDNEY DISEASE WILL HAVE ACCUMULATION OF
- VLDL
- REMNANT OF LIPOPROTEIN IN THE CIRCULATION
HOW THYROID DISORDERS LEAD TO SECONDARY HYPERLIPIDAEMIA?
- THYROID HORMONE INCREASE THE HEPATIC EXPRESSION OF THE LDL R.
- HYPOTHYROIDISM IS A/W HIGH LEVEL OF LDL
- IN A THYROID DISORDER, THERE WILL BE LACK OF LDL R.
- THERE WILL BE A REDUCTION IN HEPATIC LDL R FUNCTION IN A THYROID DISORDER PT.
- HENCE, THERE WILL BE A DELAT IN THE CLEARANCE OF LDL.
- THEREFORE, THE LDL LEVEL IN THE HYPOTHYROID PT IS ELEVATED, BUT IT IS LOW IN HYPERTHYROID PT.
WHAT IS CHOLELITHIASIS?
CHOLILETHIASIS:
- A MAJOR PATHWAY BY WHICH CHOLESTEROL IS EXCRETED FROM THE BODY IS VIA SECRETION INTO THE BILE
- CHOLESTHASIS WILL BLOCKS THIS CRITICAL EXCRETORY PATHWAY RESULTING IN HIGH LDL LEVEL
FH IS CHARACTERISED BY
ELEVATED LDL-C IN THE ABSENCE OF HYPERTG
FH IS AUTOSOMAL
DOMINANT
FH IS PRESENT FROM
EARLY CHILHOOD
STATE THE CAUSES OF FH
MUTATION OF THE LDL-R
MUTATION OF THE APO-B
PCSK9 MUTATION
STATE THE CHARACTERISTICS OF HOMOZYGOUS FH
- NO FUNCTIONAL RECEPTORS ARE PRESENT
- CAUSED BY MUTATION IN BOTH ALLELES
- PLASMA CHOLESTEROL CONC. USUALLY MORE THAN 15MMOL/L
- DEVELOPS CAD IN CHILDHOOD
- IF LEFT UNTREATED, RARELY SURVIVE TO ADULTHOOD
STATE THE CHARACTERISTICS OF HETEROZYGOUS FH.
- TOTAL CHOLESTEROL: 7.5- 12 MMOL/L
- INHERITANCE OF ONE MUTANT LDL- R ALLELE
- HYPERCHOLESTEROLEMIA SINCE BIRTH
- DISEASE RECOGNITION: DURING ROUTINE SCREENING
- DEVELOP CAD 20 YRS EARLIER THAN GENERAL POPULATIONS
- MORE THAN HALF OF THOSE UNTREATED DIE BEFORE THE AGE OF 60 YRS
CLINICAL MANIFESTATION OF FH
- TENDON XANTHOMATA
- XANTHELASMA
- CORNEAL ARCUS
- SERUM: CLEAR
- ATHEROSCLEROSIS
MANAGEMENT OF FH
STATINS TO REDUCE RISK OF CHD
SCREEN OTHER FAMILY MEMBERS FOR EARLY DETECTION
FAMILIAL HYPERTG AUTOSOMAL
DOMINANT
FAMILIAL HYPERTG IS CHARACTERISED BY
- HIGH TG W/O CLEAR CAUSE
- AVERAGE BELOW LDL-C
- LOW HDL-C
- FAMILY H(X) OF HYPERTG
FAMILIAL HYPERTG HAS
- ___ HEPATIC SYNTHESIS OF ____
- EXCESS ____ IN THE PLASMA
- NOT MANIFEST UNTIL ADULTHOOD
FAMILIAL HYPERTG HAS
- HIGH HEPATIC SYNTHESIS OF VLDL
- EXCESS VLDL IN THE PLASMA
- NOT MANIFEST UNTIL ADULTHOOD
THE SERUM APPEARANCE FOR HYPERTG
TURBID AT THE BOTTOM
CREAMY AT THE TOP LAYER
FAMILIAL COMBINED HYPERLIPIDAEMIA IS AUTOSOMAL
DOMINANT
CAUSES OF FAMILIAL COMBINED HYPERLIPIDAEMIA
- HEPATIC OVERPRODUCTION OF APOB
1. INCREASED VLDL SECRETION
2. INCREASED PRODUCTION OF LDL FROM VLDL
