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Cancer & Exercise Lecture 1 > Lecture 7 - Metabolic Syndrome & Dyslipidaemia > Flashcards

Lecture 7 - Metabolic Syndrome & Dyslipidaemia Flashcards

1
Q

Dyslipidaemia in Aus

A

Based on measured data from the 2011-12 AHS, almost 2 in 3 people aged 18 and over [63%] have dyslipidaemia. This is comprised of:

  • 57% with uncontrolled abnormal blood lipids
  • 7% taking some form of lipid modifying medication but with normal lipid levels

Dyslipidaemia is common among both men and women, with rates over 50% for all age groups except those aged 18-24

1 in 3 aus adults [33%] have high levels of LDL [bad] cholesterol, almost 1 in 4 [23%] have low levels of HDL [good] cholesterol and 1 in 7 [14%] have high levels of triglycerides.
1 in 3 [33%] have a total cholesterol level that’s considered high.

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2
Q

Describe dyslipidaemia:

A

Dyslipidaemia - abnormal blood lipids - can contribute to the development of atherosclerosis, a build up fatty deposits in the blood vessels which may lead to the development of CV diseases

Dyslipidaemia is a risk factor for chronic diseases such as coronary heart disease and stroke

Dyslipidaemia referees to abnormal levels of lipids in the blood, typically:

  • high levels of total cholesterol [TC]
  • high levels of low density lipoprotein chol [LDL-C]
  • high levels of tryiglycerides [TG]
  • &/or low levels of high density lipoprotein chol [HDL-C]

Dys can also be described as hyperlipoproteinemia
Hyperlipidaemia [referring to abnormally high levels of TC, LDL-C, or TG]
Hypercholesterolemia [referring to elevated TC and/or LDL-C]

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3
Q

Hyperlipidaemia and Dyslipidaemia

A

Hyperlipidaemia: is a general term used to refer to chronic elevations in fasting blood concentrations of triglyceride, cholesterol.

Dyslipidaemia: is a combination of genetic, environmental, and pathological factors that can work together to abnormally alter blood lipids and lipoprotein concentrations

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4
Q

A closer look at blood lipids:

A

Blood lipids: cholesterol, triglycerides, phospholipids, fatty acids.

Play a crucial physiological role: energy storage, provision of body insulation, maintenance of bile acids, steroid hormone production, structure of cell membranes, and metabolic regulation

Blood lipids are transported in blood bound to proteins because they are not soluble

Lipid combine with profit a called Apolipoproteins and for lipoproteins

Lipoproteins = lipds + protein

Lipoproteins 98% of lipid in the plasma

Various classes of lipoproteins, identified according to density - each has distinct role, and when present in inappropriate amounts

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5
Q

Apolipoproteins

A

Lipid binding proteins contained within lipoprotein

Apolipoprotein A:
- facilitates cholesterol uptake by the liver and other tissues, allowing HDL cholesterol to help transport other cholesterol out of the blood plasma

Apolipoprotein B:

  • found in LDL cholesterol
  • combines with receptors that bring LDL cholesterol into other cells of the body

Apolipoprotein E:

  • synthesised in liver as part of VLDL
  • functions in transport of triglycerides to liver tissue and in cholesterol distribution among cells
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6
Q

Lipoproteins

A

Lipids are not soluble in aqueous solution and must combine with various proteins [apolipoproteins] to form a lipoprotein

Lipoproteins are necessary to transport lipids through the blood stream

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7
Q

Lipoprotein Classes:

A 
Chylomicrons
VLDL: very low density lipoprotein
IDL: intermediate density lipoprotein
LDL: low density lipoprotein
HDL: high density lipoprotein

2 pathways:

  • LDL receptor pathways
  • Reverse cholesterol transport
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8
Q

Chylomicrons

A

Originate from intestinal absorption of dietary or exogenous triglyceride

These triglyceride - rich lipoproteins [TRL] are distinguished from the liver-derived TRLs because they contain a single copy of apolipoprotein B-48

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9
Q

VLDL and IDL

A

VLDL:

  • Is synthesised in the liver and is the primary transport mechanism for endogenous triglyceride to body tissue
  • Are TG-rich particles, made in the liver
  • Transport FAs from liver to heart, muscles, adipose tissue

IDL:

  • What remains after TGS removed from VLDLs
  • Are the procures for LDL
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10
Q

LDL

A

End product of VLDL metabolism

Consists largely of cholesterol

Carries about 70% of all cholesterol in the plasma

Is taken up by liver & other tissues by LDL receptors

Causes of increased LDL:
-obesity, sat fats, trans fat

Causes of decreased LDL:
-monounsat fats, some polyunsaturated fats [linoleic]

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11
Q

HDL

A

Are known to be anti-atherogenic because they possess antioxidant effects and serve to transport cholesterol from the body’s tissue to the liver in a process known as reverse cholesterol transport

Key role in the reverse transport of cholesterol

Removes cholesterol from tissues and transfers it to the liver or other lipoproteins

Causes of decreased HDL:

  • obesity
  • trans fat
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12
Q

Classification of Dyslipidaemia

A

Hyper - cholestrerolemia

          - triglyceridemia
          - lipoproteinemia
          - lipoproteinemia
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13
Q

Genetic hyperlipidaemias:

A

Several forms of hyperlipidaemia have strong genetic components

  • familial hypercholesterolemia
  • polygenic familial hypercholesterolemia
  • familial combined hyperlipidaemia
  • familial dysberalipoproteinemia
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14
Q

Hypercholesterolemia:

A

Elevated fasting cholesterol Total-C >240mg/dl [6.2 mmol/L]

[genetic] familial hypercholesterolemia
-caused by defects in LDL receptor gene [defective LDL receptors or lack of LDL receptors]
- major RF for CHD
- Reduced LDL clearance rates - leads to:
=Xanthomas a disposition of yellowish cholesterol-rich material in tendons or in subcutaneous tissue in which lipids accumulate
= atheromas - lipid filled large foam cells in arteries

  • elevated Total-C, LDL>260mg/dl [6.7mmol/L]
  • premature atherosclerosis
  • 1 in 500 individuals
  • early detection critical
  • less than 10% are diagnosed
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15
Q

Hypercholesterolemia: [genetic] familial polygenic Hypercholesterolemia

A

High Total-C, LDL>220mg/dl [5.6mmol/L]
Result of multiple gene defects
Usually lower LDL-C than patients with nonpolygenic form
Remain at high risk for premature disease [atherosclerosis]
1 in 20 to 1 in 100 individuals

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16
Q

[Genetic] Familial combined Hypercholesterolemia:

A

Elevated Total-C and triglycerides levels
Multiple individuals in same family
Increased risk of premature atherosclerosis
1% of population

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17
Q

Hypertriglyceridemia:

Elevated Fasting Triglyceride Levels >15omg/dl [1.7mmol/L]

A

Results from following:

  1. Apolopprotein E2 genotype :
    = three apo E isoforms [E2,E3,E4]
    =Apo E2 unable to hydrolyse triglycerides in the liver due to ineffective binding to receptors = increased chylomicron and VLDL levels
  2. Familial lipoprotein lipase [LPL] defienciency:
    = Either defiency in apo C-II, which is responsible for LPL activation, or an insufficient production of LPL = limits clearance of chylomicron and VLDL
    = Elevate triglyceride, low HDL and LDL
  3. Familial hypertriglyceridemia:
    = Genetic condition abnormally high levels of endogenously produced triglycerides
    = Elevated TG’s, normal to mildly increase chol, reduced HDL
18
Q

Hyperlipoproteinemia:

Elevated Lipoprotein Levels

A

Familial trait, secondary to other disease [thyroid disease, diabetes], resutls of excess body weight, inactivity, poor nutrition

Hyper- B- lipoproteinemia
- produce too much Apo B- excess LDL

Hyper-A- lipoproteinemia

  • increased Apo A synthesis, and reduction in HDL clearance
  • =increased concentration of HDL
19
Q

HYPOlipoproteinemia:

Low lipoprotein levels

A

Familial trait, secondary to other diseases, result of excess body weight, inactivity, poor nutrition

A-B-lipoproteinemia

  • absence of B-band lipoprotein in plasma
  • no chylomicrons or VLDL is formed

Familial hypo-B-lipoproteinemia
-lower than normal LDL levels [-10 - 50%]

Hypo-a-lipoproteinemia

  • low levels of HDL [ <40mg/dl]
  • results from lack of Apo A or insufficient LPL activity, excess body weight, smoking
20
Q

Genetic Hyperlipidaemias

A

Familial combined hyperlipidaemia [FCHL]

  • 2+ family members have serum LDL/TG >90% percentile
  • several lipoprotein patterns may be seen
  • can have:
    1. elevated LDL with normal TG
    2. Elevated LDL with elevated TG
    3. Elevated VLDL
  • 15% of patients who have an MI before 60 have FCHL

Familial dysbetalipoproteinemia:

  • relatively uncommon [1 in 10 000]
  • Apo E gene defect
21
Q

What are some Diagnostic and Lab evualtuions used:

A
  1. Complete blood lipid profile = forearm venepuncture, 12 hours postprandial [fasted]
  2. General analyses = Total C, LDL, HDL, TRIG
  3. Lipid specialist analyses= lipoprotein subtractions [IDL] and apolipoprotein
22
Q

What are the RACGP clinical guidelines?

A

Adults should do fasting blood lipids starting at age 45, every 5 years

Lipids Levels should be interpreted in context of absolute CV risk assessment after 45yr

Aboriginal and Torrest strait islanders should have FLT performed every 5 years after age 35

23
Q

Blood lipid profile targets:

A

NORMAL:
Tot Chol <5.5 mmol/L
HDL Chol >1.0 mmol/L
LDL Chol <3.0 mmol/L

IF AT HIGH RISK:
Tot Chol <4.0 mmol/L
HDL Chol >1.0 mmol/L
LDL Chol  <2.5 mmol/L
TG < 2.0 mmol/L
24
Q

Converting Chol and blood glucose level measurements

A

World standard: mmol/L

US measurement: mg/dl

25
Q

Converting mmol/L = mg/dl

DIVIDE BY CONVERSION FACTOR!

A

Trig [0.01129]
= 1.7mmol/L / 0.01129
=150mg/dl

HDL,LDL, TC [0.02586]
=1.3mmol/L / 0.02586
=50mg/dl

BGLs [0.05551]
= 5.6mmol/L / 0.05551
=100mg/dl

26
Q

Converting mg/dl - mmol/L

MULTIPLE BY CONVERSION FACTOR!

A

Trig [ 0.01129]
=150mg/dl x 0.01129
=1.7mmol/L

HDL,LDL, TC [0.02586]
=40mg/dl x 0.02586
=1.03mmol/L

BGLs [ 0.05551]
=100mg/dl x 0.05551
=56mmol/L

27
Q

What is Metabolic syndrome?

A

Used to be called “syndrome X”

Not a chronic disease per se, but a collection of risk factors

Closely related to obesity

28
Q

What are the characteristics of MetaSynd:

A
  1. Abdominal obesity = excessive fat tissue in and around the abdomen
  2. Atherogenic dyslipidemia = high TRIG, low HDL and high LDL
  3. hypertension = elevated BP
  4. Insulin resistance or glucose intolerance = the body cant properly use insulin or manage BGL

Also:
5. Pro-inflammatory state - elevated C-reactive protein [CRP] in the blood

  1. Pro-thrombotic state - high fibrinogen or plasminogen activator inhibitor-1 in blood
29
Q

Criteria for MetabSynd:

A

According to IDF, for a person to be defined as have MS they must have:
- central obesity

-plus any 2 of the following 4 factors:
=Raised TRIG [ >150mg/dl ; 1.7mmol/L
=Reduced HDL [<40mg/dl ;1.03mmol/L in males, <50mg/dl; 1.29mmol/L in females]
=Raised BP [systolic > 130, or diastolic > 85mmhg]
=Raised fasting plasma glucose [ FPG >100mg/dl; 5.6mmol/L]

30
Q

What is the distribution of Body Fat:

A

Located in 2 general areas:

  • subcutaneous fat
  • visceral fat

Genes play a role in determining body shape and whether the individual loses or gains fat easily

31
Q

Patterns of body fat distribution:

A

Abdominal adipose tissue accumulation - Android

Lower body/ gluteofemoral adipose tissue accumulation - Gynoid

32
Q

What is Visceral Fat:

A

Android obesity: more V adipose tissue

Visceral adipose tissue [VAT] is associated with the individual components of the MS in contrast to subcutaneous adipose tissue

VAT volume is an independent prediction of elevated blood pressure, myocardial infarction, and insulin resistance

Association of VAT, with obesity related complications recognised in 1950’s

Insulin resistance, diabetes, hypertension dyslipidaemia and CV morbidity and mortality all shown to be relate to the extent of visceral adipose tissue

METABOLIC OBESITY = visceral fat accumulation in either lean or obese people

33
Q

How it affects organ function?

A

The lipid content of every organ increases in overweight and obesity

However, the liver, heart and muscle cells may be the most altered by excess fat

Nonalcoholic fatty liver disease [NAFLD] is the most common cause of liver abnormalities and clinical follow up

34
Q

Describe NAFLD

A

Occurs in up to 1/3 of adults and is present in most obese people

Unaddressed will progress to end-stage liver disease or liver cancer

Leads to CVD, T2D, and is closely linked with metabolic syndrome

35
Q

How does it affect heart function?

A

Epicardium VAT under normal conditions is used for energy, is anti-inflammatory, and provides mechanical protection

In excess, its inflammatory, correlates with CAD and AFib, may interfere with cardiac nervous system

36
Q

Cardiometabolic risks;

Greatly increased by:

A 
Associated with metabolic consequences:
T2D
Gall bladder disease
Hypertension
Dyslipidaemia 
Insulin resistance
Atherosclerosis
Associated with weight :
Sleep apnoea 
SOB
Asthma
Social
Isolation/depression
Daytime sleepiness/fatigue
37
Q

Cardiometabolic risks;

Moderately increased by:

A

Metabolic Consequences:
CHD
Stroke
Gout/hyperuricaemia

Weight:
Musculoskeletal problems
OA
Respiratory disease
Hernia
Psychological problems
38
Q

Is CVD mortality increased in metabolic syndrome:

A

YES

39
Q

Pathophysiology

A

The excess adipose tissue releases large quantities of free fatty acids

The FFA cause an increase hepatic potuput of glucose and TRIG in the form of VLDL Chol.
Associated with the increase in VLDL is an increase in LDL and a decrease in HDL.

In the muscle, the FFA inhibit insulin action for glucose uptake. The excess glucose produced by the liver cant be utilities by the muscle when the insulin is disabled.

The excess glucose also signals the pancreas to increase insulin production and secretion.

The result of the insulin resistance in the muscle is hyperglycemia.
Because there is less glucose for the muscle to use as fuel, the muscle with deplete its glycogen stores

And the muscle then uses more FFA for fuel. The FFA also accumulates in the muscle cell as TRIG.

The excess insulin secreted from the pancreas in response to the excess hepatic glucose production creates a hyperinsulinemia.
This may increase sodium reabsorption in the kidneys and increase sympathetic output from the CNS.

Both of these activities increase BP and contribute to hypertension assoc with MetabSynd.

Thus, the connection among excess fat, insulin resistance, hyperlipidaemia and hypertension.

But the adipocytes is not just passive. It has an endocrine function.

The release of angiotensinogen is increased in excess body fat.
Angiotensinogen, through a series of reactions, is a potent vasoconstrictors increasing hypertension .

Cytokines are released from the fat cell in excess in conditions of high body fat
TNF- alpha promotes insulin resistance and Interleukin 6 [IL6] increases the liver’s production of glucose.

IL-6 also increases hepatic VLDL production, contributing to the dyslipidaemia of decreased HDL and increased LDL.

Plasminogen activator inhibitor [PAI-1] release is decreased from the adipocytes

Together with increased fibrinogen from the liver [due to increased cytokines] the vascularise become prothrombotic.

40
Q

In summary:

A 
Many factors can contribute:
1. Insulin resistance
2. FFA - obesity - main culprit 
=release many adipocytes derived hormones and cytokines [TNF-a, IL6, PAI-1, Leptin]
3. Hypertension

Cancer & Exercise Lecture 1 (8 decks)

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