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Block 1 > Pathophysiology of diabetes > Flashcards

Pathophysiology of diabetes Flashcards

1
Q

How do GLUT transporters work?

A

Facilitated diffusion, not energy dependent

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2
Q

Where are GLUT transporters found?

A

GLUT 1: Everywhere, provide basal glucose to all cells
GLUT 2: Beta-islet cells
GLUT 3: Mainly in neurons
GLUT 4: Adipose tissue and muscles

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3
Q

Which GLUT transporters work independently of insulin?

A

GLUT 1, 2 and 3

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4
Q

Which GLUT transporter is dependent on insulin?

A

GLUT 4, responsible for insulin dependent response in fat and muscles

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5
Q

How do the SLGT transporters work?

A

Sodium dependent glucose transporter, requires ATP.

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6
Q

Where are SLGT 1 transporters found? What is their role?

A

Intestines: responsible for uptake of dietary glucose

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7
Q

Where are SLGT 2 transporters found? What is their role?

A

Kidneys: responsible for glucose reabsorption

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8
Q

What substrates are used for gluconeogenesis?Where does it occur?

A

Production of glucose from molecules: lactate (non-oxidative metabolism), glycerol (from fats), glutamine and alanine (from protein)
Occurs in liver and kidneys

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9
Q

Where is glycogen stored?

A

Liver and muscles cells primarily

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10
Q

What are the functions of insulin?

A

Decrease glucose production and lipolysis, increase glucose utilisation

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11
Q

What are the functions of glucagon?

A

Increase glucose production and lipolysis, decrease glucose utilisation

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12
Q

What are the effects of adrenaline on glucose?

A

Increases glucose production and lipolysis, decreases glucose utilisation

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13
Q

What are the effects of cortisol on glucose?

A

Increases glucose production and lipolysis, decreases glucose utilisation

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14
Q

What are the effects of free fatty acids (FFAs) on glucose?

A

Increases glucose utilisation, decreases glucose production

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15
Q

What are the effects of growth hormone on glucose?

A

Increases glucose production and lipolysis, decreases utilisation

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16
Q

Where is insulin produced?

A

Beta cells of Islets of Langerhans within the pancreas

17
Q

What are the functions of the Islets of Langherhans?

A 
Provide pancreatic endocrine function
3 major cell types:
-Alpha- glucagon
-Beta- insulin
-Delta- somatostatin (inhibitor of insulin and glucagon)
18
Q

Describe the process of insulin secretion

A

Glucose enters the pancreatic Beta-cell via GLUT-2 and is metabolised to ATP increasing ATP:ADP ratio within the cell. This causes K+ channel to close leading to cell membrane depolarisation which activates calcium channels causing an influx of calcium into the cell which triggers release of insulin vesicles by exocytosis.

19
Q

Describe the phases of insulin release

A

First phase: rapid onset, lasts approx 10 mins.
Release of pre-docked, primed insulin vesicles.
Second phase: prolonged, lasts as long as hyperglycaemia persists. Transport, docking, priming, fusion.

20
Q

Describe the actions of insulin

A

Anabolic
Activates insulin receptor on target cell membrane- outcome depends on secondary pathway.
Facilitates glucose transport into cells by promoting the fusion of GLUT-4 intracellular vesicles into cell membranes.
Increases glycogen synthesis by promoting activation of glycogen synthase.
Promotes protein synthesis and inhibits breakdown
Promites lipogenesis and prevents lipolysis via hormone sensitive lipase.
Promotes mitogenesis- insulin like growth factor homology.

21
Q

What regulates the secretion of glucagon?

A

Hypoglycaemia increases and hyperglycaemia inhibits.
Levels rise with fasting, exercise and physiological stresses (trauma, infection)
Suppressed by insulin secretion.

22
Q

Describe the actions of glucagon

A

Stimulates gluconeogenesis and glycogenolysis
Increases fatty acid oxidation and ketone formation.
Stimulates lipolysis in adipose cells which increases circulation free fatty acids and reduces adipocyte glucose uptake.

23
Q

How are blood glucose levels maintained in the fasted state? (14-16 hours fasting)

A

Catabolic state
80% of glucose provided by liver:
-50% from glycogenolysis, 50% gluconeogenesis
As fasting progresses this shifts: 90% gluconeogenesis by 48 hours.

Kidneys contribute by gluconeogenesis, amount is comparable to liver.

24
Q

Describe the post-prandial state

A

Increased insulin and decreased glucagon.
Anabolic state
Acute exposure to FFAs increases basal and stimulated insulin production

25
Q

Describe the activation of the ANS effects on glucose homeostasis

A

Activation of the sympathetic nervous system: adrenaline inhibits insulin and promotes glucagon secretion.
ANS directly innervates the pancreatic islets: noradrenaline stimulates glucagon and inhibits insulin.

26
Q

What are the actions of cortisol and growth hormone on glucose homeostasis?

A

Promote gluconeogenesis and inhibit glucose transport.

Cortisol directly inhibits insulin secretion.

27
Q

What causes type 1 diabetes?

A

Autoimmune destruction of pancreatic beta cells causing insulin deficiency

28
Q

What causes hyperglycaemia in type 1 diabetes?

A

Loss of insulin secretion
Lack of ability to uptake glucose into cells
Inability to store glucose into glycogen
Unapposed glucagon action: gluconeogenesis and glycogenolysis.

29
Q

What causes polyuria in diabetes?

A

Hyperglycaemia causes glycosuria. Glucose in urine impedes the ability of the kidney to concentrate urine.

30
Q

What causes polydipsia in diabetes?

A

Physiological response to dehydration from polyuria.

High BG also stimulates thirst response directly.

31
Q

What causes DKA in type 1 diabetes?

A

The body cannot uptake glucose so produces ketones for fuel which leads to acidaemia.

32
Q

How does DKA present?

A

Shock from severe dehydration
Vomiting
High respiratory rate (respiratory compensation)
Abdominal pain

33
Q

Define T2DM

A

Insulin resistance and initially hyperinsulinaemia.

Loss of first phase insulin response with eventual beta cell exhaustion

34
Q

What are the modifiable risk factors for T2DM?

A

Obesity (esp central obesity)
Lack of physical exercise
Smoking
Poor diet (high fat low fibre)

35
Q

What are the non-modifiable risk factors for T2DM?

A 
Age (over 40)
Family history
Ethnicity (afrocaribbean, south asian)
Hx of gestational diabetes
HTN, cardiovascular disease
Low birth weight
Polycystic ovarian syndrome
36
Q

What are the complications of diabetes?

A 
Hypoglycaemia (from treatment)
Nephropathy
Retinopathy
Neuropathy
IHD
Cerebrovascular disease
PVD

Block 1 (31 decks)

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