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Y3 Diseases > Diabetes > Flashcards

Diabetes Flashcards

1
Q

How is diabetes characterised?

A

High levels of insulin, low concentration of receptors with high affinity

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2
Q

How was insulin first isolated?

A

Banting and Best tied off dog pancreas and accumulated extract

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3
Q

What is insulin?

A

A hormone that promotes glucose uptake for cells
Synthesised in pancreatic β-cells as preproinsulin
Hexamer
Part of the negative feedback chain with glucagon apposing it

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4
Q

What are the features of type I diabetes?

A

Typically adolescent onset
Genetic origin
Auto immune- pancreatic β-cells broken down
Loss of mass
Monozygotic concordance 30%
Associated with HLA
Familial
No obesity

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5
Q

What are the features of type II diabetes?

A

Maturely onset
May not require insulin
Can be modified by diet an insulin
Monozygotic 40-100%
No HLA association
Associated with obesity

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6
Q

What is glucagon?

A

Hormone synthesised in pancreatic α-cells
Increases gluconeogenesis, glycogenolysis and decreases lipogenesis
Controlled by ATP levels and glucose metabolism in mitochondria

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7
Q

How is glycolysis inhibited?

A

PKA synthesising phosphofructokinase-2

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8
Q

What components of β-cells are involved in glucose uptake?

A

Kir6.2 is a K+ channel and moves K+ out the cell.
Ca2+ channel
Glut-2 imports glucose

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9
Q

What effects does glucogon have in the brain?

A

Lower appetite
Higher satiety

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10
Q

What effects does glucogon have in the pancrease?

A

Higher insulin secretion

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11
Q

What effects does glucogon have in the liver?

A

Gluconeogenesis
Lipid breakdown
Less lipogenesis

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12
Q

What effects does glucogon have in the heart?

A

Higher heart rate

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13
Q

What effects does insulin have in the skeletal muscle?

A

increased glucose uptake
Glycogenesis

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14
Q

What effects does insulin have in the fat cells?

A

Glucose uptake
Lipogenesis
Less lipolysis

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15
Q

What effects does insulin have in the liver?

A

Glycogenesis
Lipogenesis
Less glycogenolysis
Less gluconeogenesis

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16
Q

What effects does insulin have in the pancreas?

A

β-cell growth
Less glucagon

17
Q

Explain insulin signalling

A

Insulin binds to receptor, this dimerises, allowing it to self-phosphorylate
IRS-1 binds to the phosphorylated receptor
IRS-P -> PI3K-P -> PDK1-P -> AKT-P -> cytoskeletal arrangements allowing Glut4 to insert into cell membrane

18
Q

How can hyperglycaemia occur from diabetes?

A

As insulin levels fall, so does β-cell mass and productivity

19
Q

How can insulin promote candida?

A

Glucose in urine can damage tubules and the glucose-rich bladder promotes candida to grow

20
Q

Explain the pathogenesis of insulin

A

Initial loss of response to insulin signalling
Glucose remains high, driving increased insulin production by β-cells.
β-cell mass and productivity fall
After insulin has fallen, blood glucose rises

21
Q

How do glucose meters work?

A

Engineered glucose oxidase coupled to a test strip

22
Q

What does glucagon do in the liver?

A

Coverts fatty acids to triglycerides
LDL and HDL increases in the blood
Circulating lipids are associated with increased atherosclerosis risk

23
Q

What types of amylod form in type 2 diabetes?

A

Islet amyloid polypeptide (IAPP) produced by β-cells

23
Q

What happens under insulin resistance?

A

Weight loss can reverse this in early stages
Akt signalling becomes refractory
Low level inflammation produced by visceral fat

24
Q

What is insulinitis?

A

β-cells being silently destroyed and insulin production fades

24
Q

What biomarkers can forecast type 1 diabetes in adolescence?

A

Autoantibodies against β-cell proteins:
Glutamic acid decarboxylase (GAD)
Insulin
Zinc transporter 8
Insulin-associated antigen-2

25
Q

How can polyuria and polydipsia result from diabetes

A

Blood ciruclates through glomerulus of nephron and filtrate diffuses through capillary lining
Scarring makes the nephrons more fibrous, meaning glucose isn’t reabsorbed

26
Q

What microvascular complications can occur from diabetes?

A

High glucose concentration toxic to endothelial cells lining capillaries
Fibronetic growth factors PDGF and TGF-β increase deposition of matrix
Vessel walls thicken, loss of elasticity
Loss of cirulation in ischaemia

27
Q

What macrovascular complications can occur from diabetes?

A

Scarring response, leading to deposition of lipids in supportive layers of the vessel

28
Q

What neuropathy complications can occur from diabetes?

A

Progressive less of nerve function associated with poor control of glucose levels
High glucose is toxic to nerve cells, leading to cell death, causing
tingling, pain, erectly dysfunction, loss of sensation and infection and microvascular problems

29
Q

What genes are associated with diabetes?

A

Calpain 10- polymorphisms disrupt insulin release
Glucokinase- Hexokinase IV with defective glucose sensing
GLUT2- transports glucose to the cell. Gene variants may disrupt glucose regulation

30
Q

Explain the Pima Indian study

A

Migration and change of lifestyle increased instance of type 2 DM
Usually had a calorie deficient lifestyle

31
Q

What inflammatory mediators are associated with diabetes

A

IL-2- regulatory cytokine for T-cells
Idd5-CTLA4 - key regulator of T-cell antigen response

32
Q

Does islet transplantation work?

A

For type I, no as patient is still autoimmune
β-cells destroyed over time

33
Q

Explain how the adaptive immune repertoire is reset?

A

Entire immune cells in bone marrow are killed
These are given back
Do not have autoreactive T and B cells

34
Q

Why is diabetes a major risk factor for atherosclerosis?

A

Hyperglycaemia modifies macromolecules, forming advanced glycation end (AGE) products
When AGEs bind to their receptor RAGE, proinflammatory cytokines in vascular endothelial cells are produced.
Diabetic state also promotes oxidative stress by ROS

Y3 Diseases (5 decks)

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