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ESR > Diabetes > Flashcards

Diabetes Flashcards

1
Q

How can mitochondrial disease lead to diabetes?

A
  • when mutant mitochondria predominate then oxidative capacity is reduced
  • means beta cells have reduced capacity to secrete insulin in response to glucose as insulin secretion is linked to glycolysis

Symptoms: muscle weakness, deafness, neurological problems and lactic acidosis
- maternally inherited diabetes and deafness (MIDD)

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2
Q

What is the sorbitol pathway?

A

1) Sorbitol is a sugar formed from glucose through aldose reductase which adds a hydrogen ion to the glucose
2) sorbitol is converted to fructose by sorbitol dehydrogenase which removes a hydrogen ion from sorbitol

The accumulation of sorbitol and fructose (as they diffuse slowly and are not absorbed) leads osmotic effects which damage cells such as lens cells and nerve cells

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3
Q

What happens to the kidneys in nephropathy?

A

1) microvascular injury
2) external surface is granular due to extensive sclerosis of cortical glomeruli
3) destruction of renal papillae and scarring consistent with previous attacks of pyelonephritis
4) can lead to kidney failure
5) accumulation of mesangial matrix
6) diffuse or focal/nodular (Kimmelstiel-Wilson nodules) glomerulosclerosis

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4
Q

What are some possible treatments for T1D?

A
  1. Islet transplantation
  2. Artificial islets
  3. Immunosuppressive therapy for those at risk - in trial
  4. Prophylactic injections of insulin - don’t prevent but delay
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5
Q

What can high levels of insulin stimulate?

A
  1. Some cells in the sympathetic nervous system can lead to hypertension
  2. It can also increase androgen production by ovaries which contributes to the hormonal disturbance seen in PCOS which may include masculinisation
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6
Q

What happens when you have too much adipose tissue?

A

1) sends signals of stress
2) activate endocrine tissue
3) produces leptin and cytokines
4) signals from cytokines pull in inflammatory cells e.g. T cells and macrophages
5) chronic inflammation in body
6) starts to store fat in liver, heart, muscle and pancreas
7) if in pancreas then defects in insulin secretion especially if beta cell compensation does not work

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8
Q

What can you see in diabetic retinopathy?

A

1) exudates
2) retinal infarcts
3) haemorrhage due to damage to BM of capillaries
5) cataracts
6) where you get bleeding blood vessels close off and you get retinal ischemia and new fragile blood vessels are made which leak blood into eye and blocks it
7) cataracts due to lens epithelium damage

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9
Q

What is macrovascular disease?

A

1) Disease is any large blood vessels in the body e.g. coronary arteries

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10
Q

What Abs have been identified and what is the significance?

A

1) islet cells
2) insulin
3) glutamic acid decarboxylase
4) protein tyrosine phosphatase

No. of Abs predictive of progression to overt divers rather than the type

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11
Q

What does acarbose do?

What does rosiglatazone do?

A
  • block carbohydrate metabolism
  • sensitive beta cells (thiazolidinediones)
    —> risk of fluid overload and heart failure
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12
Q

What increased glucose and lipids lead to?

A

1) oxidative stress
2) RAS activation
3) AGE effects

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13
Q

What is Fanconi-Bickel syndrome?

A

Mutation in GLUT2

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14
Q

What are the boundaries for impaired fasting glucose?

A

110-125mg/dL

5.6-6.9 mmol/L

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16
Q

How do anti-idiopathic antibodies work?

A
  1. Neutralising autoantibodies
  2. Inhibiting the secretion of autoantibodies
  3. B lymphocytes that produce autoantibodies function as auto-antigen presenting cells - can inhibit their binding to auto-antigen which would stop their production?
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17
Q

What is PC1 involved in?

A

Processing POMC

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18
Q

Where does insulin resistance first arise?

A
  • muscle and fat

- later stages liver

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20
Q

What are some of the genes that can cause type 2 diabetes?

A
  1. IRS1

2. IRS2

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21
Q

How does neuropathy occur?

A

1) glycation of BM

2) blood supply to nerves blocked

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22
Q

How does retinopathy occur?

A

1) glycation of BM
2) exudation
3) bleeding

22
Q

What causes retinopathy?

A

1) Glycation of BM

2) Leakage of protein

22
Q

What happens to the BM in the kidneys?

A

It thickens

25
Q

What other endocrine conditions can cause insulin resistance?

A
  1. Hyperthyroidism - reason unclear
  2. Acromegaly and GH
    - counter regulatory to insulin
    - GH deficient children are HYPOGLYCAEMIC
  3. Glucocorticoids
    - excess
    - endogenous tumour or exogenous
    - increase insulin resistance and frank type 2 diabetes
    - beta cells completely normal :. reducing response within pancreas
    - reversible with steroid level fall
    Mechanism: Decrease IRS1’s phosphorylation within the cell :. Decrease intracellular signalling
  4. Adrenaline
    - insulin resistance and blocks secretions
    - phaeochromocytoma or exogenous epinephrine
    - increases in glycogenolysis and excess glucose clearance
    - decreased tyrosine phosphorylation of IRS1 downstream effects
26
Q

How is a glucose tolerance test undertaken?

A
  • overnight fasting
  • rests during test
  • no smoking
  • fasting glucose taken
  • glucose solution of 75mg in 300ml of water
  • blood and urine samples taken after 2 hours
27
Q

What else can precipitate insulin resistance?

A
  1. Inflammatory mediators
  2. High levels of other hormones that antagonise insulin (glucagon, adrenaline, glucocorticoids)
  3. High levels of insulin

These can arise in obesity, metabolic syndrome and endocrine disorders such as a Cushing’s syndrome

28
Q

What other conditions can diabetes cause?

A

1) peripheral vascular disease
2) osteoarthritis
3) cataracts
4) glaucoma

28
Q

What is SOD? What happens when you glycate it?

A

1) detoxifies free radicals which are generated
2) takes free radicals and generates hydrogen peroxide
3) hydrogen peroxide is disposed of by catalase or detoxify using GSH peroxidase to produce water

—> When glycate it causes the accumulation of free radicals leading to oxidative stress

29
Q

How do you get skin infection?

A

1) Poor blood supply leads to poor healing

2) High glucose levels encourage pathogenic growth

30
Q

What is the most common cause of MODY?

A
  1. HNF1alpha - causes MODY type 3
31
Q

How does diabetes cause atherosclerosis?

A

1) Impaired endothelial function and NO production goes down
2) LDL particles are oxidised and glycated
3) Macrophages have receptors for AGE
4) profileraion

32
Q

What does AGE and oxidative stress lead to?

A

1) Inflammation leading to neuropathy

2) Inflammation can then combine with the RAS system to cause fibrosis and lead to retinopathy

32
Q

What can mitochondrial free radicals lead to?

A

1) Direct macromolecule damage

2) indirect oxidative stress which leads to insulin resistance and beta cell dysfunction

33
Q

How does Cataracts occur?

A

Accumulation of polyols in lens so light cannot pass through

34
Q

What do thiazolidinediones do?

A
  • binds to PPAR-gamma transcription factor which acts in fat cells
35
Q

What can shortage of exercise and hyperlipemia lead to?

A

Low blood flow in skeletal muscle

Dysfunction in the liver

37
Q

What is genetic risk of T1D attributed to?

A
  1. HLA region - 50% of genetic risk
    E.g. HLA-DR3/4 DQ8 (beta cell autoimmunity)
  2. Higher in individuals with DQA301 or DRB1*401
    (Diabetics either have both or one copy) - more than 50% of non diabetics don’t have these alleles
  3. MHC class-2 proteins make individuals susceptible to pancreatic autoimmune destruction
39
Q

Why does ulceration happen?

A

1) Skin breaks down areas of pressure

2) Toes can fall off when blood vessels are blocked

40
Q

What does the MC4 receptor do?

A

Controls appetite by controlling response of appetite in POMC in brain

40
Q

What kind of drugs can cause diabetes?

A

Steroids

41
Q

How are AGE proteins made?

A

1) CHO of glucose and NH2 of amino acid react together
2) if rapid then get reversible Shiff base
3) if slow then irreversible ketoamine which leads to advanced glycosylation end products (AGEs)

42
Q

How do elevated FFAs cause insulin resistance?

A
  1. Down-regulate sensitive to beta cells
    We can get FFAs when there is too much fat in our bodies and not enough insulin so hormone sensitive lipase is activated and TAG is broken down.

The FFAs are reconverted into TAGs by the liver and recirculated as VLDLA in high concentrations causing dyslipidaedimia

43
Q

Why do you get foot infections?

A

1) High levels of glucose means organisms can breed
2) contributed to by damage to small blood vessels
3) sensory neuropathy leads to foot numbness and damage e.g ill fitting shoes

43
Q

Are males or females more susceptible to type 1 diabetes?

A

Females

44
Q

How do B cell mass and B cell proliferative capacity differ?

A

1) B cell mass can increase up to a certain point depending on genetics and environment
2) B cell proliferative capacity decreases from the age of 10

44
Q

What is glucotoxicity?

A
  • hyperglycaemia can be toxic to beta cells
45
Q

What can cause a reduction in the expression of GLUT2?

A
  1. High fat diet

2. Mutation in galectin 9 which anchors GLUT2 to the plasma membrane

ESR (7 decks)

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