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PHYL2067 > L4 Diabetes and Obesity > Flashcards

L4 Diabetes and Obesity Flashcards

1
Q

what are the two metabolic states? explain them.

A

Absorptive State:
• After a meal: absorption of nutrient from diet (into the blood stream)
• Excess nutrients are stored in the body (used or stored)
Post-absorptive State:
• Between meals
• Stored energy is mobilised for use (energy supplied back into blood stream)
Note: blood concentration of nutrients (e.g. glucose) remain fairly stable during these states

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2
Q

define glucose

A

a monosaccharide (simple sugar) = only made up of one sugar

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3
Q

why is glucose control important

A

• Blood glucose levels are maintained between 70-110mg/100ml of plasma
• Most tissues can also generate ATP (cellular energy) from fats (adipose tissue)
• During starvation, we can break down proteins (muscle) to make ATP
BUT the brain can only get ATP from glucose SO blood glucose levels must be maintained

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4
Q

define glycogenesis & will it increase or decrease the blood glucose levels

A

glycogenesis: Building glycogen from glucose (glucose -> glycogen)

decrease blood glucose

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5
Q

define glycogenolysis & will it increase or decrease the blood glucose levels

A

glycogenolysis: Breaking down glycogen to release glucose (glycogen -> glucose)

increase blood glucose

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6
Q

define gluconeogenesis & will it increase or decrease the blood glucose levels

A

gluconeogenesis: Making new glucose molecules (amino acids -> glucose)

increase blood glucose

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7
Q

The breakdown of glycogen into glucose is called _______ whereas the production of glycogen from glucose is called _______. _______ is the creation of new glucose from non-carbohydrates.

A

The breakdown of glycogen into glucose is called GLYCOGENOLYSIS whereas the production of glycogen from glucose is called GLYCOGENESIS. GLUCONEOGENESIS is the creation of new glucose from non-carbohydrates.

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8
Q

_____ produces hormones to control blood glucose

A

PANCREAS produces hormones to control blood glucose

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9
Q

what are the effects of insulin on glucose

A

• Insulin favours glucose uptake and storage
o Facilitates glucose transport from blood into body cells (especially skeletal muscle and adipose tissue)
o Stimulates glycogenesis in liver and skeletal muscle
o Inhibits glycogenolysis and gluconeogenesis
• Promotes storage of fats (triglycerides) in adipose tissue
• Stimulate protein synthesis

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10
Q

what are the effects of glucagon on glucose

A

• Glucagon factors the release of glucose into the blood= stimulates glycogenesis, stimulates gluconeogenesis, inhibits glycogenesis
• Breakdown of stored fats
• Breakdown of proteins in live
• Insulin and glucagon have opposite effects on blood glucose
o Insulin: released during absorptive state when blood glucose is increased
o Glucagon: released during post absorptive state when blood glucose is decrease

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11
Q

what is hyperglycaemia

A

high blood glucose

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12
Q

what is hypoglycaemia

A

low blood glucose

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13
Q

describe glucose homeostasis

A

Increased blood glucose -> pancreas produces insulin -> stimulate glucose uptake by cell and stimulate glycogen formation by liver (increase glycogenesis) -> blood falls to normal range

Decreased blood glucose -> pancreas produces glucagon -> stimulates glycogen breakdown (increase glycogenolysis) -> blood glucose rises to normal range

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14
Q

what is diabetes mellitus

A

Impaired ability to utilise blood glucose = characterised by hyperglycaemia (high blood glucose)

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15
Q

regarding type 1 diabetes, describe the following:

  • old classification
  • % of cases
  • peak age of onset
  • pathophysiology
  • level of insulin
  • treatment
A
  • old classification: insulin-dependent diabetes mellitus (IDDM); juvenile onset
  • % of cases: 10-15% of diabetes cases (least common)
  • peak age of onset: < 20 years (children and adolescents)
  • pathophysiology: autoimmune destruction of B cells (produce antibodies that attack and destroy B cells) = inability to produce insulin
  • level of insulin: none or almost none
  • treatment: insulin injections, dietary management, exercise
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16
Q

regarding type 2 diabetes, describe the following:

  • old classification
  • % of cases
  • peak age of onset
  • pathophysiology
  • causes
  • level of insulin
  • treatment
A
  • old classification: non-insulin-dependent diabetes mellitus (NIDDM); adult onset
  • % of cases: 85-90% (most common)
  • peak age of onset: over 35-40
  • pathophysiology
    3 metabolic abnormalities
    1. Insulin Resistance: insulin is produced but insulin receptors are unresponsive or insufficient in number; pancreas compensates by increasing insulin production
    2. Decreased production of insulin: beta cells become fatigued; hyperglycaemia
    3. Inappropriate glucose production: liver releases glucose when not needed
  • causes: genetics; environmental factors (obesity, poor diet, lack of exercise); often associated with hypertension and hyperlipidaemia
  • level of insulin: may be normal or exceed normal
  • treatment: dietary control and weight reduction, exercise, oral hypoglycaemic drugs
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17
Q

what are the three methods for diagnosis

A
  • Fasting plasma glucose (glucose levels after fasting): ≥ 7mmol/L
  • Random plasma glucose: ≥ 11.1 mmol/L (also manifestations – symptoms – of diabetes: polyuria, polydipsia, weight loss)
  • Two-hour oral glucose tolerance test (OGTT): plasma glucose ≥ 11.1 mmol/L (glucose load after fasting
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18
Q

describe the oral glucose tolerance test

A
  • Patients consume 150g of carbohydrates/day for 3 days prior
  • Fast over night
  • On following morning: measure fasting plasma glucose
  • Ingest 75g glucose drink
  • Measure plasma glucose after 2 hours
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19
Q

T/F: Type 1 diabetes experience insulin resistance

A

F (type 2)

20
Q

T/F: Type 1 diabetes is due to autoimmune destruction of pancreatic alpha cells

A

F (B cells)

21
Q

what is prediabetes

A

intermediate stage of disordered carbohydrate metabolism

22
Q

what are the acute consequences of diabetes

A

glycosuria (glucose in the urine), polyuria (excessive urination), polydipsia (excessive thirst), polyphagia (excessive hunger), weight loss, fatigue, diabetic acidosis (if untreated: coma and death)
(for type I and II but type II is a slower progression and type I is quicker)

23
Q

describe what hyperglycaemia does to damage the blood vessels

A
  • Hyperglycaemia causes endothelial cells of blood vessels take in glucose and form glycoproteins by glycosylation (advanced glycation end products- AGEs) (protein + sugar = glycated protein)
  • These damages the basement membrane leading to microvascular and macrovascular disease
24
Q

describe what retinopathy is

A
  1. Retinal capillaries become leaky and develop microaneurysms
  2. Microaneurysms can haemorrhage causing bleeding in the retina
  3. Lack of oxygen to retina is compensated by growth of new blood vessels (neovascularisation)
    (microvascular disease)
25
Q

describe what nephropathy is

A

• Most common cause of end-stage kidney disease
• Damage to small blood vessels supplying the kidneys = leaky capillaries
• Associated with increase blood pressure and fluid retention
(microvascular disease)

26
Q

describe what a macrovascular disease is

A
  • Most common cause of death in type 2 diabetes
  • Coronary artery disease – atherosclerosis in coronary arteries – heart attack
  • Stroke – blockage of blood vessels in brain
  • Peripheral vascular resistance – reduction of blood flow to extremities (legs and feet)
27
Q

describe what neuropathy is and what are the chronic complications are

A

neuropathy:
- Neurons are insulin independent and can take up lots of glucose during hyperglycaemia. Glucose is converted into sorbitol inside the neurons which has an asmotic effect -> cell swelling and death
- Blood supply to nerves is impaired -> lack of oxygen and nutrients
chronic complications:
- nerve degeneration and delayed conduction

28
Q

what are the 5 reasons for increased infections

A

5 reasons for increased infections:

  1. Senses: numbness = decreased warning signs of damage
  2. Hypoxia: lack of oxygen = increased infection susceptibility
  3. Pathogens: like high glucose
  4. Blood supply: decreased blood supply = decreased supply of white blood cells (WBC)
  5. WBCs: impaired function in diabetics
29
Q

Before diagnosis, untreated diabetics often experience acute symptoms, such as increased urination (______), increased thirst (______), and glucose in the urine (______). Long term, poor blood glucose control can result in damage to nerves (______), the kidneys (______) and eye (______).

A

Before diagnosis, untreated diabetics often experience acute symptoms, such as increased urination (POLYURIA), increased thirst (POLYDIPSIA), and glucose in the urine (GLYCOSURIA). Long term, poor blood glucose control can result in damage to nerves (NEUROPATHY), the kidneys (NEPHROPATHY) and eye (RETINOPATHY).

30
Q

what are the causes of obesity?

A

Obesity occurs from positive energy balance: energy from food intake is greater than energy expenditure

Energy input (food) = energy output (external and internal work) +/- stored energy

However, the reasons for this imbalance are complex – regulation of body weight involved complicated feedback systems that results in changes in appetite, energy intake and energy expenditure

31
Q

describe the change of size in the adipose cells when weight changes

A
  • Increase weight: cell size increase (hypertrophy) (to hold more triglycerides)
  • Increase weight substantially: cell size increases, cell number increase (hyperplasia)
  • Lose weight: cell size decreases, cell number remains
32
Q

adipose cells produce a collection of hormones (______) that are involved in appetite and blood glucose regulation

A

adipose cells produce a collection of hormones (ADIPOKINES) that are involved in appetite and blood glucose regulation

33
Q

leptin function

A

Supresses appetite, dominant long-term regulator of energy balance and body weight

34
Q

adiponection function

A

Increases sensitivity to insulin, decreases body weight by increasing energy expenditure, suppressed in obesity

35
Q

resistin function

A

Leads to insulin resistance. Released in obesity

36
Q

describe the short term and long term control of food intake done by the hypothalamus

A
  • Short-term control = controls meal size and frequency
  • Long term control = controls satiety and hunger in the long term (not a moment-to-moment response to mealtimes- that’s short term- but it’s the bodies way of thinking more long term about your energy intake)
37
Q

describe long term energy control

A

• Insulin and leptin act on the hypothalamus to suppress long-term food intake
o Inhibits the appetite stimulant neuropeptide Y (NPY)
o Stimulates the appetite suppressants melanocortins

38
Q

describe short term energy control

A
  • Ghrelin stimulates appetite before a meal (makes you hungry)
  • PYY, CCK and stomach distention after a meal stimulate
39
Q

T/F: Ghrelin controls appetite in the short-term, whereas leptin controls appetite in the long term

A

T

40
Q

T/F: When adipose cells increase in size it is called hyperplasia

A

F

41
Q

what are the ways of diagnosing obesity

A

BMI, waist circumference, body shape

42
Q

what is BMI

A
  • Index of weight-for-height measurements
  • Classify healthy, overweight and obesity
  • An estimate of body fat
  • BMI = weight (kg) / height squared (m squared) e.g. 75/1.75squared =24.5
43
Q

what are the BMI limitations

A
  • Does not distinguish between lean mass and fat mass
  • Overestimates body fat if: body builders, broad frame, pregnant
  • Underestimates body fat if: elderly, muscle wasting
44
Q

what is waist circumference.

A
  • Indication of location of body fat
  • May be better indicator of health risk than BMI
  • Abdominal fat is higher risk than fat around hips and buttocks- best determinant of truncal obesity and hence metabolic risk
45
Q

are all categories of obesity the same?

A

• There is a clear link between ‘visceral’ obesity and cardiometabolic risk
• The location of excess fat is just as important as the amount of excess fat
• Visceral obesity is associated with an increased risk of:
o Insulin resistance and type 2 diabetes
o Dyslipidemia (increase triglycerides, decrease HDL cholesterol)
o Cardiovascular disease

46
Q

describe the difference between subcutaneous fat and visceral fat

A

subcutaneous fat:

  • underneath the skin
  • pear shape, hold fat around the hips and buttocks
  • gynoid obesity
  • lower risk of obesity-relatef complication

visceral fat:

  • deeper inside the body; visceral fat is located inside the abdominal wall- around organs
  • apple shape, hold fat around the stomach
  • android obesity
  • higher risk of obesity-related complications
47
Q

prevention for obesity?

A

increase energy expenditure (exercise), decrease energy intake

PHYL2067 (9 decks)

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