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BIOC192 > Lecture 38: DIABETES > Flashcards

Lecture 38: DIABETES Flashcards

1
Q

What are the symptoms of diabetes?

A

fatigue, weight loss, intense thirst, frequent urination, hyperglycaemia, glycosuria and ketones

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2
Q

What are the other names for insulin dependent diabetes?

A

Juvenile onset and type 1 diabetes

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3
Q

What is the defect in insulin dependent diabetes?

A

autoimmune destruction of beta cells

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4
Q

What is the age of onset of insulin dependent diabetes?

A

1-25 years

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5
Q

What is the bodily physique in insulin dependent diabetes?

A

lean (weight diagnosis)

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6
Q

What is the prevalence of insulin dependent diabetes?

A

0.5%

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7
Q

What is the cause of insulin dependent diabetes?

A

genetic and environmental factors (viruses or toxins implicated)

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8
Q

What is the treatment of insulin dependent diabetes?

A

Insulin injections

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9
Q

What is the other names for non insulin dependent diabetes?

A

Maturity onset or type 2 diabetes

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10
Q

What is the defect in non insulin dependent diabetes?

A

Resistance to action of insulin

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11
Q

What is the age of onset of non insulin dependent diabetes?

A

> 40 years

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12
Q

What is the bodily physique of non insulin dependent diabetes?

A

obese

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13
Q

What is the prevalence of non insulin dependent diabetes?

A

2%

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14
Q

What is the cause of non insulin dependent diabetes?

A

Genetic and environmental factors (obesity, sedentary lifestyle implicated)

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15
Q

What is the treatment of non insulin dependent diabetes?

A

Diet, exercise, drugs

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16
Q

What may happen if blood glucose goes low?

A

Signal to eat; may get the shakes

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17
Q

What happens if blood glucose is very low <1 mmol L?

A

sweating, heartbeat increases, sympathetic nervous system may induce vomiting and cognitive impairment

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18
Q

Why may cognitive impairment occur if blood glucose goes low?

A

Because there is no glucose to provide energy for the brain; can cause aggressive moods, convulsions and coma

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19
Q

What happens if blood glucose goes too high?

A

Non-enzymatic glycation of protein; especially at Lys residues, can target crucial structural proteins and also constriction of blood vessels leads to gangrene and limb amputations

20
Q

What are examples of crucial proteins targeted when glucose is high?

A

collagen in basement membrane of capillaries and crystalline protein of the eye, making the eyes go opaque and impairing vision

21
Q

What are some long term implications of high glucose?

A

Retiopathy, nephropathy, neuropathy, cardiovascular disease and peripheral vascular disease

22
Q

What type of hormone is insulin?

A

Peptide

23
Q

Where is insulin synthesised?

A

In the pancreas by beta cells

24
Q

What is insulin secreted in response to?

A

High glucose (after a meal)

25
Q

What does insulin act on?

A

Liver, muscle and adipose tissue

26
Q

What does insulin inhibit (anti-catabolic)?

A

gluconeogenesis, ketogenesis, lipolysis, proteolysis and glycogenolysis

27
Q

What does insulin activate (uptake and storage of fuels - anabolic)?

A

glucose uptake in muscle and adipose tissue, protein synthesis, glycogen synthesis, TAG uptake and fatty acid synthesis

28
Q

What does a glucose tolerance test do?

A

Tests how well insulin is working

29
Q

What is involved in a glucose tolerance test?

A

fast overnight, consume 75g of glucose and measure the time to clear from blood (~1-1.5h)

30
Q

What are the metabolic consequences of lack of insulin?

A

Impaired glucose uptake and storage by muscle, increased mobilisation of glycogen, increased glucose synthesis, increased lipolysis, increased ketone body synthesis, reduced removal of triacylglycerols from blood and increased breakdown of tissue protein

31
Q

What does build up of TAG do?

A

Increases risk of atherosclerosis

32
Q

What signal doesn’t occur when insulin is absent?

A

The fed signal

33
Q

What are the impacts of insulin deficiency?

A

decreased glucose uptake, increased glucose production, increased lipolysis and increased proteolysis

34
Q

What do decreased glucose uptake and increased glucose production lead to?

A

Hyperglycaemia, glycosuria, osmotic diuresis, dehydration, thirst and diabetic coma

35
Q

What does increased lipolysis lead to?

A

fatty acids, ketone bodies, acidosis, vomiting, dehydration and diabetic coma

36
Q

What does increased proteolysis lead to?

A

Muscle breakdown, weight loss, wasting and weakness

37
Q

What is the equilibrium and formation of ketone bodies?

A

beta hydroxybutyrate <> acetoacetate > acetone

38
Q

When does ketoacidosis occur?

A

> 20 mmol L , ketouria

39
Q

Why is there dehydration?

A

Because of loss of osmotic imbalance and needing to accomodate by moving more fluid into the urine

40
Q

What happens when the kidney has >10 mmol L of glucose?

A

Osmotic pull of water from tissue and electrolyte loss leads to coma

41
Q

What is the treatment for type 1 diabetes?

A

Injections of human insulin (recombinant human insulin)

42
Q

What do insulin injections aim to do?

A

Mimic the normal rise in insulin caused by meals

43
Q

What is hypoglycaemia caused by?

A

Too much insulin

44
Q

When does a coma occur?

A

When glucose <1 mmol L

45
Q

What is the aim of type 2 diabetes treatment?

A

Tissues are resistant to insulin therefore aim to increase sensitivity of tissues to insulin

46
Q

What are some treatments for type 2 diabetes?

A

weight loss, increased exercise and hypoglycaemic drugs

47
Q

What are hypoglycaemic drugs?

A

sulphonylureas, glitazones, insulin injection if necessary

BIOC192 (38 decks)

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