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Block 1 > Diabetes > Flashcards

Diabetes Flashcards

1
Q

What % of DM diagnoses are type 2?

A

85%

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2
Q

Name 3 places the body can get glucose from

A

Diet

Breakdown of glycogen stores (glycogenolysis)

Formation of glucose (gluconeogenesis)

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3
Q

Is glucose hydrophilic or hydrophobic?

What does this mean about transport into cells?

A

Hydrophilic

Diffuses slowly across lipid cell membrane
Requires specific transport proteins to move into cells

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4
Q

List some differences between GLUT and SGLT transporters

A

GLUT -
Facilitated diffusion
Not energy dependent

SGLT -
Use sodium to move glucose against concentration gradient

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5
Q

Where are the two types of SGLT transporters found?

A

SGLT-1
Intestines

SGLT-2
Kidneys

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6
Q

Which GLUT transporter is insulin dependent?

Where is it mainly found?

A

GLUT-4

Fat and muscle

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7
Q

Describe gluconeogenesis

A

Production of glucose from molecules that aren’t carbohydrates.

Substrates:

Lactate (non-oxidative metabolism, Kreb’s cycle)

Glycerol (fats)

Glutamine and alanine (protein)

Occurs in liver and kidneys

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8
Q

Describe glycogen and glycogenolysis

A

Multi branched polysaccharide of glucose, storage molecule of glucose

Stored in liver and muscle cells

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9
Q

Describe insulin

A

51 amino acids peptide hormone

2 protein chains (alpha and beta) linked by disulphide bonds

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10
Q

Where is insulin produced?

A

B-cells of Islets of Langerhans in the pancreas

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11
Q

Where is glucagon produced?

A

a-cells of Islets of Langerhans in the pancreas

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12
Q

Where is somatostatin produced?

What is its role?

A

gamma-cells

Strong inhibitor of insulin and glucagon

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13
Q

Describe biphasic insulin secretion

A

First phase - rapid onset, lasts 10 minutes

Second phase - prolonged plateau lasting as long as hyperglycaemia persists

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14
Q

Why is it presumed insulin levels are regulated by release rather than synthesis?

A

Only a portion of stored insulin is released even under maximal stimulation

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15
Q

Name 6 major actions of insulin

A

Release of GLUT-4 from storage vesicles to cell walls

Inhibit gluconeogenesis

Glycogen synthesis

Promotes protein synthesis

Promotes lipogenesis

Suppress ketogenesis

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16
Q

What can increase the levels of glucagon?

A

Fasting

Exercise

Stresses e.g. trauma, infection

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17
Q

List 5 major actions of glucagon

A

Stimulates gluconeogenesis

Stimulates glycogenolysis

Promotes proteolysis

Stimulates lipolysis

Promotes ketogenesis

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18
Q

What do L-cells of the small intestine produce?

A

Glucagon-like peptides (GLP)

Gastric inhibitory peptide (GIP)

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19
Q

Where is GLP and GIP made?

A

L cells of the small intestine

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20
Q

What stimulates the release of GLP and GIP?

A

Oral glucose loading

IV glucose has less of a response

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21
Q

How does adrenaline affect insulin and glucagon release?

A

Adrenaline inhibits insulin and promotes glucagon secretion

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22
Q

How does the autonomic nervous system affect insulin and glucagon release?

A

Sympathetic neurons - release noradrenaline - stimulates glucagon + inhibits insulin

Parasympathetic neurons - stimulate insulin, inhibit glucagon

23
Q

How is cortisol related to insulin?

A

Cortisol directly inhibits insulin secretion

24
Q

Cortisol and growth hormone promote _____ and inhibit ______

A

Promote gluconeogenesis

Inhibit glucose transport

25
Q

Define diabetes mellitus

A

A heterogeneous complex metabolic disorder characterised by elevated blood glucose concentration secondary to either resistance to the action of insulin, insufficient insulin secretion, or both

26
Q

What are the four classifications on the WHO spectrum of disorders of glucose metabolism

A

Normal

Impaired fasting glycaemia

Impaired glucose tolerance

Diabetes

27
Q

How is type 1 diabetes classified?`

A

Autoimmune disease with selective destruction of β-cells resulting in complete insulin deficiency

Can only be treated with insulin

28
Q

Who normally suffers from type 1 diabetes?

A

Younger, leaner patients

5-10% of all diabetes cases

Can be associated with other immune diseases e.g. thyroid disorders, coeliac disease

29
Q

Name four symptoms of type 1 diabetes

A

Polyuria

Polydipsia

Weight loss

Hyperglycaemia

30
Q

Why do diabetics have polyuria?

A

Hyperglycaemia results in glycosuria - exceeds renal capacity to reabsorb

Glucose in urine inhibits concentrating ability of kidney

Water is moved down a concentration gradient with glucose resulting in polyuria

31
Q

Why do diabetics have polydipsia

A

Polyuria due to hyperglycaemia, water needs replacing to maintain fluid balance

Hyperglycaemia also directly stimulates thirst response

32
Q

Why do diabetics experience weight loss?

A

Unopposed lipolysis and proteolysis (no insulin to appose these systems)

The results of these form gluconeogenesis precursors

33
Q

What is diabetic ketoacidosis?

A

When high levels of ketones are produced as an alternative energy source due to lack of glucose absorption into cells due to lack/insensitivity to insulin

34
Q

Give 3 symptoms of DKA

A

Shock (dehydration)

High respiratory rate

Abdominal pain

35
Q

Define type 2 diabetes mellitus

A

Heterogeneous condition

Characterised by insulin resistance and hyperinsulinemia

Loss of first phase of insulin response

B-cell exhaustion can occur

36
Q

What other symptoms are usually present with T2DM?

A

Central/visceral obesity
Dyslipidaemia
Cardiac factors (HTN)

37
Q

How does Metformin work?

A

Decreases hepatic gluconeogenesis

38
Q

What is first line treatment for T2DM?

A

Diet, exercise and lifestyle measures

39
Q

List the three broad categories of complications from diabetes

A

Hypoglycaemia

Microvascular

Macrovascular

40
Q

Name 3 microvascular complications of diabetes

A

Nephropathy

Retinopathy

Neuropathy

41
Q

Name 3 macrovascular complications of diabetes

A

IHD

Cerebrovascular disease (CVD)

Peripheral vascular disease

42
Q

Which type of glucose transporter is found on B-islet cells?

A

GLUT 2

43
Q

Where are SGLT1 and SGLT2 transporters found?

A

SGLT1 - intestines (absorption from food)

SGLT2 - kidneys (reabsorption)

1 intestine, 2 kidneys

44
Q

What is lipolysis?

A

The breakdown of fats and other lipids by hydrolysis to release fatty acids

45
Q

What affect does insulin have on glucose production, glucose utilisation, and lipolysis?

A

Glucose production - DECREASES

Glucose utilisation - INCREASES

Lipolysis - DECREASES

46
Q

What affect does glucagon have on glucose production, glucose utilisation, and lipolysis?

A

Glucose production - INCREASES

Glucose utilisation - DECREASES

Lipolysis - INCREASES

47
Q

List/draw the 6 steps to insulin secretion in response to glucose in B-cells in the pancreas

A

Glucose moves into B-cell via GLUT-2

Glucose is metabolised which increases ATP

ATP-dependent K+ channels close

This leads to membrane depolarisation

This leads to opening of voltage gated Ca2+ channels and influx

this leads to exocytosis of stored insulin vesicles

48
Q

Why does insulin have different affects on different target cells?

A

Insulin activates an insulin receptor but then different secondary pathways can be activated

49
Q

Describe the relationship between insulin and GLUT 4

A

GLUT 4 is stored in intracellular vesicles

Insulin promotes fusion of vesicles and transporter insertion into cell walls

This facilitates glucose transport into cells

50
Q

Which enzyme does insulin promote activation of?

A

Glycogen synthase

- makes glycogen from glucose

51
Q

What is glucagon secretion regulated by?

A

Blood glucose levels

Hypoglycaemia increases glucagon secretion

Hyperglycaemia inhibits glucagon secretion

52
Q

Is the post-absorptive state of glucose catabolic or anabolic?

A

Post-absorptive state is catabolic

53
Q

Is the post-prandial (fed) state of glucose catabolic or anabolic?

A

Post-prandial is anabolic

Block 1 (13 decks)

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