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PATHOLOGY > PATHOPHYSIOLOGY OF HYPERLIPIDAEMIA > Flashcards

PATHOPHYSIOLOGY OF HYPERLIPIDAEMIA Flashcards

1
Q

STATE THE CLINICAL MANIFESTATIONS OF FAMILIAL HYPERTRIGLYCERIDAEMIA.

A
  • ERUPTIVE XANTHOMA
  • LIPAEMIA RETINALIS
  • HEPATOSPLENOMEGALY
  • SERUM APPEARS TURBID AT THE BOTTOM AND CREAMY AT THE TOP LAYER
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2
Q

STATE THE INVESTIGATION FINDINGS IN FAMILIAL HYPERTRIGLYCERIDAEMIA.

A
  • 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.
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3
Q

STATE THE COMPLICATIONS OF FAMILIAL HYPERTG.

A
  • ACUTE PANCREARITIS
  • INCREASED RISK OF CVS DISEASE
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4
Q

STATE THE SERUM FINDING OF FAMILIAL HYPERCM.

A

CREAMY AT THE TOP LAYER

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5
Q

FAMILIAL HYPERCM OCCUR D/T

A

DEFICIENCY OF THE ENZYME LPL
DEFICIENCY OF APO Cii

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6
Q

FAMILIAL HYPERCM IS (DOMINANT/RECESSIVE) DISORDER

A

RECESSIVE

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7
Q

STATE THE CLINICAL MANIFESTATION OF FAMILIAL HYPERCM.

A
  • ERUPTIVE XANTHOMATA
  • RECURRENT ABDOMINAL PAIN CAUSED BY PANCREARITIS
  • LIPAEMIA RETINALIS
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8
Q

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

A. FALSE (DOMINANT)
B. TRUE
C. TRUE
D. FALSE (NO PRESENT OF TENDON XANTHOMATAIN THE FAMILIAL COMBINED HYPERLIPIDAEMIA)
E. TRUE

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9
Q

FAMILIAL HYPERALPHALIPOPROTEINEMIA IS DUE TO THE INCREASE IN ___.

A

HDL FRACTION

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10
Q

SECONDARY HYPERLIPIDAEMIA IS ___(MORE/LESS) COMMON THAN PRIMARY HYPERLIPIDAEMIA.

A

MORE

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11
Q

SECONDARY HYPERLIPIDAEMIA IS ___(MORE/LESS) COMMON THAN PRIMARY HYPERLIPIDAEMIA.

A

MORE

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12
Q

HOW IS THE OBESITY LEAD TO SECONDARY HYPERLIPIDAEMIA?

A
  • 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.
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13
Q

STATE THE PATHOGENESIS OF DM THAT RELATE WITH THE SECONDARY HYPERLIPIDAEMIA.

A
  • 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
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14
Q

HYPOALBUMINEMIA WILL CAUSE (INCREASED/DECREASE) IN HEPATIC PROTEIN SYNTHESIS.

A

INCREASE

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15
Q

HYPOALBUMINEMIA IN NEPHORTIC SYNDROME WILL CAUSE:

A
  1. INCREASED HEPATIC PRODUCTION
  2. DECREASED CLEARANCE OF VLDLS
  3. INCREASED LDL PRODUCTION
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16
Q

CHRONIC KIDNEY DISEASE WILL HAVE ACCUMULATION OF

A
  • VLDL
  • REMNANT OF LIPOPROTEIN IN THE CIRCULATION
17
Q

HOW THYROID DISORDERS LEAD TO SECONDARY HYPERLIPIDAEMIA?

A
  • 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.
18
Q

WHAT IS CHOLELITHIASIS?

A

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

19
Q

FH IS CHARACTERISED BY

A

ELEVATED LDL-C IN THE ABSENCE OF HYPERTG

20
Q

FH IS AUTOSOMAL

A

DOMINANT

21
Q

FH IS PRESENT FROM

A

EARLY CHILHOOD

22
Q

STATE THE CAUSES OF FH

A

MUTATION OF THE LDL-R
MUTATION OF THE APO-B
PCSK9 MUTATION

23
Q

STATE THE CHARACTERISTICS OF HOMOZYGOUS FH

A
  • 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
24
Q

STATE THE CHARACTERISTICS OF HETEROZYGOUS FH.

A
  • 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
25
Q

CLINICAL MANIFESTATION OF FH

A
  • TENDON XANTHOMATA
  • XANTHELASMA
  • CORNEAL ARCUS
  • SERUM: CLEAR
  • ATHEROSCLEROSIS
26
Q

MANAGEMENT OF FH

A

STATINS TO REDUCE RISK OF CHD
SCREEN OTHER FAMILY MEMBERS FOR EARLY DETECTION

27
Q

FAMILIAL HYPERTG AUTOSOMAL

A

DOMINANT

28
Q

FAMILIAL HYPERTG IS CHARACTERISED BY

A
  • HIGH TG W/O CLEAR CAUSE
  • AVERAGE BELOW LDL-C
  • LOW HDL-C
  • FAMILY H(X) OF HYPERTG
29
Q

FAMILIAL HYPERTG HAS
- ___ HEPATIC SYNTHESIS OF ____
- EXCESS ____ IN THE PLASMA
- NOT MANIFEST UNTIL ADULTHOOD

A

FAMILIAL HYPERTG HAS
- HIGH HEPATIC SYNTHESIS OF VLDL
- EXCESS VLDL IN THE PLASMA
- NOT MANIFEST UNTIL ADULTHOOD

30
Q

THE SERUM APPEARANCE FOR HYPERTG

A

TURBID AT THE BOTTOM
CREAMY AT THE TOP LAYER

31
Q

FAMILIAL COMBINED HYPERLIPIDAEMIA IS AUTOSOMAL

A

DOMINANT

32
Q

CAUSES OF FAMILIAL COMBINED HYPERLIPIDAEMIA

A
  • HEPATIC OVERPRODUCTION OF APOB
    1. INCREASED VLDL SECRETION
    2. INCREASED PRODUCTION OF LDL FROM VLDL

PATHOLOGY (13 decks)

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