Topic 8: Metabolic Syndrome Flashcards
Indicate the extent to which prevalence of obesity has increased in western countries over the past 30 years
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
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
- 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:
- waist circumference,
- blood pressure and
- fasting trigylceride
Identify the major medical conditions that individuals with metabolic syndrome are at greater risk of developing
Heart Disease
Stroke
Type 2 Diabetes
Of the 5 risk factors for metabolic syndrome which is most commonly (a) measured (b) not measured
a) waist circumference, blood pressure and fasting triglyceride
b) HDL cholesterol, blood sugar
State the values for blood pressure (systolic & diastolic) and waist circumference (M and F Caucasian) above
which these become risk factors for metabolic syndrome
Blood pressure
SBP >130
DBP >85
Waist circumference
Males >102
Females >88
In addition to over-eating and physical inactivity, summarise other factors that can lead to obesity
- genetics - leptin deficiency
- childhood weight
- medications - antidepressants
- hormones - OCP
Explain the difference between visceral and subcutaneous fat and the relevance of waist/hip ratio
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
• State what best explains the current “obesity epidemic“ with terms of social trends in the last 30 years
Fueled by
economic growth
industrialisation - mechanised transport
sedentary lifestyle (office jobs)
processed & fast foods
high calorie foods
• Contrast healthy/unhealthy expansion of adipocytes in terms of (a) size (b) adiponectin levels (c) insulin
resistance
Healthy
- Size: small
- Adiponectin levels: high balanced hyperplasia/hypertrophy
- Insulin resistance: sensitive
Unhealthy
- Size: hypertrophic adipocytes - large
- Adiponectin levels: low
- Insulin resistance: insulin resistant
• State what is meant by lipotoxicity identifying the primary underlying cause of this state
Accumulation of excess fatty acids/tryglycerides in non-adipose tissue
Caused when nonadipose cells are exposed to chronic elevation of FFAs - diabetes
Identify the impact of lipotoxicity on the function of: heart, vasculature, liver, pancreas, skeletal muscle & kidney
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
State the impact of diabetes mellitus (DM) on glucose transport into cells and its impact on cellular and blood levels
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
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
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.
Compare and contrast the main pathophysiological basis of Type 1 and Type 2 Diabetes Mellitus (T1DM & T2DM)
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
Describe the genetic and immunological basis of T1DM referring to the role of “T cells” and “self tolerance”.
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
Describe how initially T2DM can result in hyperinsulinemia and how subsequent responses make this unsustainable
Hyperinsulinemia is caused by insulin resistance, where the body doesnt respond well and then makes more insulin leading to T2DM
Indicate the prevalence of DM worldwide stating the relative proportions of Type 1 & Type 2
Type 1 - 1 in 500
Type 2 - 1 in 3
Comment on the effect of age on blood glucose levels and the association between blood glucose levels and lifespan
> age causes elevated glucose and insulin levels.
lower blood glucose levels associated with low mortality. higher - prediabetes and mortality
Compare & contrast the 2 major acute complications of Diabetes: Diabetic Ketoacidosis (DKA) & Hyperosmolar Hyperglycemic State(HSS)
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
Explain the meaning and causes of the following common signs/symptoms in diabetics: glycosuria, polyuria, polydipsia, polyphagia
GLYCOSURIA: presence of reducing sugars in the urine
POLYURIA: excessive production of urine
POLYDIPSIA: feeling of extremem thirstiness
POLYPHAGIA: excessive/extreme hunger
Indicate how a diabetic state can impact on the function of the following systems: hepatic, renal, cardiovascular, respiratory
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
Describe how DM can be monitored and diagnosed (nb 1 mg/dL = 0.06 mmolL glucose – remember only HbA1c value)
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)
Explain how DM damages blood vessels & how this, coupled with nerve tissue damage, can lead to Retinopathy, Nephropathy, Neuropathy
& Ulcers
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
Summarise the general approach to the treatment and management of DM
Insulin
Diet - reduced CHO, fats, salts, alcohol + regular meals
Exercise
Summarise the mode of action of the following diabetic medications: Biguanides, Sulphonylureas, Thiazolidinediones, SGLT2 inhibitors
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
