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zfoundations of pathophysiology > Topic 9- Insulin and Diabetes > Flashcards

Topic 9- Insulin and Diabetes Flashcards

1
Q

Define diabetes mellitus

A

metabolic disorder characterised by abnormal chemical reactions that alter normal metabolic processes

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2
Q

Define diabetes

A

a disease that causes polyuria, glucosuria, polyphagia, polydipsia

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3
Q

What is diabetes insipidus?

A

characterised by abnormal secretions of ADH

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4
Q

What is insulin?

A

secreted from B cells of the Islets of Langerhans in the pancreas, in response to increased blood glucose level

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5
Q

What are the two main glucose transporters and what do they do?

A

GLUT 2: bidirectional flow in the liver, pancreas and renal tubules (all these organs need bidirectional flow of glucose)
GLUT 4: one-directional, skeletal muscles and adipose tissue

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6
Q

Glycogenesis

A

glucose –> glycogen

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7
Q

Lipogenesis

A

glucose –> triglycerides

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8
Q

Glycogenolysis

A

glycogen –> glucose

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9
Q

Gluconeogenesis

A

glucose from non-carb sources

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10
Q

Lipolysis

A

triglyceride breakdown

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11
Q

What is glucagon/

A

secreted from alpha cells in the Islets of Langerhans in the pancreas in response to low blood glucose levels

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12
Q

What are ketone bodies?

A

resulting from no glucose breakdown during ATP production - fatty acids cannot enter the kreb’s cycle without glucose so instead they are sent to the liver where ketones are produced as energy

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13
Q

Why are ketones harmful in high levels?

A

makes blood acidic

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14
Q

What occurs in a fed state?

A

increased insulin, decreased glucagon

increased: lipogenesis, glycogenesis, protein synthesis
decreased: glycogenolysis, gluconeogenesis, lipolysis, ketogenesis

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15
Q

What occurs in a fasted or starved state?

A

increased glucagon, decreased insulin

decreased: lipogenesis, glycogenesis, protein synthesis
increased: glycogenolysis, gluconeogenesis, lipolysis, ketogenesis

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16
Q

What kind of inflammation is diabetes?

A

stress response or para-inflammation

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17
Q

What is type 1 diabetes?

A

catabolic disorder characterised by:

  • lack of insulin
  • B cell destruction
  • elevated BGL (hyperglycaemia)
  • increased fat/protein breakdown
  • at the level of the pancreas
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18
Q

What is the difference between type 1A and 1B?

A

1A: immune-mediated destructionof beta cells by T cells
1B: idiopathic, no immune component

19
Q

What is type 2 diabetes?

A

insulin resistance caused by:

  • genetic predisposition
  • obesity
  • certain ethnicities
20
Q

What occurs to cells over time due to hyperglycaemia?

A

hypotrophy, hypoplasia, apoptosis, glucose toxicity, lipotoxicity

21
Q

How are diabetes and obesity related?

A

obesity puts the body in a pro-inflammatory state

insulin usually suppresses inflammatory mediators, but insulin resistance = increased inflammation

22
Q

polyphagia

A

excessive hunger

23
Q

polyuria

A

excessive urination

24
Q

polydipsia

A

excessive thirst

25
Q

glucosuria

A

glucose in urine

26
Q

Treatment for type 1?

A

lifelong insulin injection

27
Q

Treatment for type 2?

A

diet and exercise modifications

28
Q

How is diabetes detected?

A

fasting blood glucose levels, oral blood glucose, glycated haemoglobin test

29
Q

Fasting blood glucose levels

A

normal: less than 5.5mmol/
DM: more than 7.7mmol/L

30
Q

OGTT (oral blood glucose test) levels

A

normal: less than 7.8mmol/L
DM: 11.1 mmol/l

31
Q

Glycated haemoglobin levels

A

normal: less than 6.5%
DM: greater than 6.5%

32
Q

Casual BGT levels

A

normal: less than 11.1mmol/L
DM: greater than 11.1mmol/l

33
Q

What is pre-diabetes?

A

can be reversed
elevated BGL but not in range of DMT2
early detection and changes can prevent onset of DMT2

34
Q

Acute complications of hypoglycaemia?

A
  • failure to eat
  • incorrect insulin doage
  • increased exercise
  • excessive alcohol
  • altered cerebal functions: headache, disturbed behaviour
  • ANS changes: anxiety, sweating, cool clammy skin
35
Q

Chronic complications of diabetes?

A

macrovascular, microvascular, neurophaties,

36
Q

Macrovascular

A

cerebral vascular, coronoary artery, peripheral vascular, atherosclerosis, stroke, HBP

37
Q

Microvascular

A

nephropathies, retinopathies

38
Q

Neuropathies

A

somatic, autonomic

39
Q

What are some other complications of diabetes?

A
  • thickening of basement membrane - hypoxia
  • glycostation - protein and glucose accumulating in vessels
  • damaged cells - glucose –> sorbitol = increased pressure/water influx
  • damaged myelin - impaired nerve transmission
40
Q

What occurs in retinopathies?

A

damage to blood vessels, cataracts

41
Q

What occurs in nephropathies?

A

-basement membrane thickening –> efferent and afferent arterioles, glomeruli, Bowman’s capsule, nodular lesions, glomerulosclerosis

42
Q

What occurs in neuropathies?

A
  • ischaemia to nerves
  • damage to myelin = slow impulses
  • decreased ability to empty bladder, cardiac response, vasomotor function
43
Q

Foot uclers

A
  • decreased blood supply and nerve damage
  • decreased pain = decreased sensory information –> unnoticed ulcers
  • poor circulation and immune function –> poor healing: infections, gangrene, amputations

zfoundations of pathophysiology (10 decks)

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