Topic 8: Metabolic Syndrome Flashcards

1
Q

Indicate the extent to which prevalence of obesity has increased in western countries over the past 30 years

A

Since 1975 it has trippled
2016 39% of adults aged 18 and over were overweight and 13% were obese
Most of the population of world lives in countries where overweight and obesity kills more than underweight

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2
Q

Identify the 5 factors that are considered in evaluating if a person has metabolic syndrome and state how many
of these need to be met to diagnose this syndrome

A
  • Waist circumference: >102 males, >88 females
  • triglycerides: >1.7 mmol/L
  • blood pressure: >130 SBP or >85 DBP
  • HDL cholesterol: <1.0 mmol/L male, <1.3 mmol/L female
  • blood sugar: fasting glucose > 5.6 mmol/L

Need to be met:

  1. waist circumference,
  2. blood pressure and
  3. fasting trigylceride
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3
Q

Identify the major medical conditions that individuals with metabolic syndrome are at greater risk of developing

A

Heart Disease
Stroke
Type 2 Diabetes

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4
Q

Of the 5 risk factors for metabolic syndrome which is most commonly (a) measured (b) not measured

A

a) waist circumference, blood pressure and fasting triglyceride
b) HDL cholesterol, blood sugar

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5
Q

State the values for blood pressure (systolic & diastolic) and waist circumference (M and F Caucasian) above
which these become risk factors for metabolic syndrome

A

Blood pressure
SBP >130
DBP >85

Waist circumference
Males >102
Females >88

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6
Q

In addition to over-eating and physical inactivity, summarise other factors that can lead to obesity

A
  • genetics - leptin deficiency
  • childhood weight
  • medications - antidepressants
  • hormones - OCP
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7
Q

Explain the difference between visceral and subcutaneous fat and the relevance of waist/hip ratio

A

Visceral fat: lies between abdominal organs and in tissue called the omentum

Subcutaneous fat: is between the skin and the out abdominal wall

Relevance to waist/hip:
- quicky measurement adn indicator of visceral fat which is linekd to chronic diseases such as CHD, hypertension and diabetes

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8
Q

• State what best explains the current “obesity epidemic“ with terms of social trends in the last 30 years

A

Fueled by
economic growth

industrialisation - mechanised transport

sedentary lifestyle (office jobs)

processed & fast foods

high calorie foods

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9
Q

• Contrast healthy/unhealthy expansion of adipocytes in terms of (a) size (b) adiponectin levels (c) insulin
resistance

A

Healthy

  • Size: small
  • Adiponectin levels: high balanced hyperplasia/hypertrophy
  • Insulin resistance: sensitive

Unhealthy

  • Size: hypertrophic adipocytes - large
  • Adiponectin levels: low
  • Insulin resistance: insulin resistant
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10
Q

• State what is meant by lipotoxicity identifying the primary underlying cause of this state

A

Accumulation of excess fatty acids/tryglycerides in non-adipose tissue

Caused when nonadipose cells are exposed to chronic elevation of FFAs - diabetes

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11
Q

Identify the impact of lipotoxicity on the function of: heart, vasculature, liver, pancreas, skeletal muscle & kidney

A

HEART: coronoary atherosclerosis & CVD = decreased diastolic filling and increased epicardial fat

VASCULATURE: atherscolerosis and CVDs, icnreased SNS activty and BP

LIVER: steatosis, inflammation = Increased oxidaitve stress and VLDL production

PANCREAS: beta cell dysfunction and increased insulin resistance

SKELETAL MUSCLE: insulin resistance and decreased ATP synthesis

KIDNEY: inflammation and TNF a, I-6,, apoptosis and Fibrosis

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12
Q

State the impact of diabetes mellitus (DM) on glucose transport into cells and its impact on cellular and blood levels

A

Impaired glucose transport in diabetes is secondary to intracellular transporter depletion and to the presence of inhibitory factors interfering with the full expression fo glucose transporters at the plasma membrane contributing to postreceptor insulin resistance

Blood glucose levels is impacted by carbohydrate ingestion and regulated by insulin

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13
Q

Identify the 2 hormones that regulate blood glucose levels, indicating their sites of production (incl. cell types) and their principal impacts on
glucose metabolism

Summarise how these 2 hormones regulate blood glucose levels identifying their principal target tissues/organs

A

The pancrease produces Insulin and glucagon to stabilise blood sugar levels

Insuin helps the cells absorb glucose, reducing blood sugar and providing cells with glucose for energy.

When blood sugar levels are too low, glycagon instructs liver to released stored glucose causing rise in blood sugar.

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14
Q

Compare and contrast the main pathophysiological basis of Type 1 and Type 2 Diabetes Mellitus (T1DM & T2DM)

A

TYPE 1:
due to pancreatic islet B cell destruction by autoimmne process causing proneness to keto-acidosis

TYPE 2:
more prevelent form resulting from insulin resistance with a defect in compensatory insulin secretion

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15
Q

Describe the genetic and immunological basis of T1DM referring to the role of “T cells” and “self tolerance”.

A

Type 1 diabetes is a disease in which tolerance to self-antigens, e.g insulin, is borken leading to expansion of autoreactive T cells that attack pancreatic B cells causing loss of insulin production

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16
Q

Describe how initially T2DM can result in hyperinsulinemia and how subsequent responses make this unsustainable

A

Hyperinsulinemia is caused by insulin resistance, where the body doesnt respond well and then makes more insulin leading to T2DM

17
Q

Indicate the prevalence of DM worldwide stating the relative proportions of Type 1 & Type 2

A

Type 1 - 1 in 500

Type 2 - 1 in 3

18
Q

Comment on the effect of age on blood glucose levels and the association between blood glucose levels and lifespan

A

> age causes elevated glucose and insulin levels.

lower blood glucose levels associated with low mortality. higher - prediabetes and mortality

19
Q

Compare & contrast the 2 major acute complications of Diabetes: Diabetic Ketoacidosis (DKA) & Hyperosmolar Hyperglycemic State(HSS)

A

DKA =
- free fatty acids in adipose tissue; cause hyperketonemia; acidemia (increased ventillation) adn coma or death

HHS =
- amino acids from peripheral tissue cause liver to hyperglycemia; osmotic diuresis; profound dehydration; hypertension; circulatory failure and coma or death

20
Q

Explain the meaning and causes of the following common signs/symptoms in diabetics: glycosuria, polyuria, polydipsia, polyphagia

A

GLYCOSURIA: presence of reducing sugars in the urine

POLYURIA: excessive production of urine

POLYDIPSIA: feeling of extremem thirstiness

POLYPHAGIA: excessive/extreme hunger

21
Q

Indicate how a diabetic state can impact on the function of the following systems: hepatic, renal, cardiovascular, respiratory

A

HEPATIC: raises risk of nonalcoholic fatty liver disease

RENAL: damage to blood vessel clusters in the kidneys that filter waste from blood

CARDIOVASCULAR: overtime blood sugar can damage blood vessels and nerves that control your heart

RESPIRATORY: decreased lung capacity and function due to inflammation

22
Q

Describe how DM can be monitored and diagnosed (nb 1 mg/dL = 0.06 mmolL glucose – remember only HbA1c value)

A

Diagnosis = glycated hemoglobin assay (HbA1C) +ve if >6.5%
Amount of glucose attached to your hemoglobin

Monitored through: finger pricking: HbA1C is tested using venous blood, any time of day (no fasting)

23
Q

Explain how DM damages blood vessels & how this, coupled with nerve tissue damage, can lead to Retinopathy, Nephropathy, Neuropathy
& Ulcers

A

Excess glucose decreases the elasticity of blood vessels and causes them to narrow, impeding blood flow - reduced supply of blood and oxygen

Retinopathy = retina disease

Nephropathy = deterioration of kidney function

Neuropathy = damage to nerves causing tingling, muscle weakness, numbness

24
Q

Summarise the general approach to the treatment and management of DM

A

Insulin
Diet - reduced CHO, fats, salts, alcohol + regular meals
Exercise

25
Q

Summarise the mode of action of the following diabetic medications: Biguanides, Sulphonylureas, Thiazolidinediones, SGLT2 inhibitors

A

BIGUANIDES: prevent liver form converting fats and amino acids into glucose

SULPHONYLUREAS: stimulate release of insulin from pancreatic beta cells adn lower blood glucose concentrations

THIAZOLIDINEDIONES: activation of PPARY and involves redistribution of surplus fatty acids to peripheral fat

SGLT2 INHIBITORS: reducing renal tubular glucose reabsorption, producing blood glucose reduction without stimulating insulin release