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MET 2 > Diabetes mellitus > Flashcards

Diabetes mellitus Flashcards

1
Q

Define diabetts

A

Chronic, non-communicable disease characterised by hyperglycaemia

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2
Q

What is type 1 diabetes

A

Chronic autoimmune disease characterised by immune mediated disruption of pancreatic beta cells within islets of Langerhans

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3
Q

What must always be injected in type 1 diabetes

A

Insulin deficiency

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4
Q

Name 3 pieces of evidence that suggest T1D is an immune-mediated disease

A
  • Infiltration of pancreas islets by mononuclear cells
  • Almost 90% of patients possess autoantibodies against islets
  • Immunosupression after diagnosis delays beta cell disruption
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5
Q

What % of people with diabetes have T2D

A

85-90%

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6
Q

What characterises type 2 diabetes

A

Abnormal insulin action adn secretion

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7
Q

What genes are suspected to be responsible for T2D

A

GKRP, PPARG

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8
Q

Name some risk factors for T2D

A 
Obesity
Family history
Age
Ethnicity
Environemental factors (urbanisation)
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9
Q

Briefly describe how obesity is suspected to cause T2D

A
  • Accumulation of lipids and their metabolites/ increased concentration of circulating free fatty acids
  • Adipose tissue releases factors called adipokines which affect insulin resistance
  • Chronic inflammation
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10
Q

Why does hyperinsulinaemia occur in T2D? What is the effect of this

A

Pancreas produces more insulin in response to the body not responding to insulin anymore
Increases lipid synthesis which worsens situation

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11
Q

How do levels of circulating adipokines contribute to insulin resistance

A
  • Act as level or IRS so phosphorylate IRS in another residue
  • Because its phosphorulated can’t be phosphorylated on tyrosine anymore
  • Pathway is blocked at this stage
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12
Q

Which 2 physiological conditions is insulin resistance associated with in healthy people

A

Pregnancy

Body weight gain

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13
Q

How is physiological insulin resistance different to pathological insulin resistance

A

In physiological insulin resistance new beta cells can be generated so beta cells can compensate

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14
Q

How do islets change during insulin resistance

A

Increase in size (beta cells increase in size and number)

Increased beta function

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15
Q

How do islets change during T2D

A

Number of islets decrease

Signification decrease in number of beta cells per islet

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16
Q

What types of genes are the susceptability genes associated with T2D

A

Regulators of cell turover or regeneration

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17
Q

What happens to glucagon in diabetics

A

Excessive circulating levels of glucagon because theres no regulation
HYPERGLUCAGONAEMIA

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18
Q

Why does hyperglucagonaemia occur in T1D

A

No insulin in the body to regulate glucagon

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19
Q

Why does hyperglycagonaemia occur in T2D

A

Reduction of beta cells, alpha cells could also be resistant to insulin and hyperglycaemia

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20
Q

What is MODY

A

Maturity onset diabetes of the young- autosomal dominantly inherited form
Pancreatic beta cell dysfunction

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21
Q

What is LADA

A

Latent autoimmune diabetes of the adult

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22
Q

2 situations in which diabetes can be diagnosed

A
  • One abnormal plasma glucose in presence of symptoms

- Two fasting venous plasma in abnormal range

23
Q

What should plasma glucose be in oral glucose tolerance test in healthy person

A 
Fasting= <6.1
2h= <7.8
24
Q

What should plasma glucose be in oral glucose tolerance test in person with diabetes

A

Fasting>7

2h> 11.1

25
Q

What are the advantages of measuring HbA1c

A

Reliable
Stable
Patient convenience

26
Q

What is the recommended cut off point of HbA1c for diagnosing patients

A

48mmol/mol (6.5%)

27
Q

Aims of diabetes treatment

A

Reduce insulin resistance or reduce hyperglycaemia

28
Q

What drug is the first line treatment for treating diabetes

A

Metformin

29
Q

Functions of metformin

A

Improve function of insulin receptor

Improve transport of glucose from blood into muscle

30
Q

What does tzd do

A

Tackles insulin resistance

Resistant muscles pushed to uptake glucose as well as preventing the liver from producing glucose

31
Q

Why does the liver produce glucose in diabetes

A

Essentially in starvation condition

32
Q

Where can drug targets be to prevent excessive insulin secretion

A

Potassium channels

Calcium channels

33
Q

Name 2 drugs that work at the level of potassium channels

A

Sylfonylureas and meglifinides

34
Q

What is the role of GLP-1

A

Inhibits secretion of glucagon

35
Q

Effect of metformin on GLP-1

A

Increases GLP-1 secretion

36
Q

What drug inhibits DDP-4

A

Sitagliptin

37
Q

What is the threshold for hypoglycaemia

A

<70mg/dL

<3.9mmol/L

38
Q

Name 5 causes of hypoglycaemia

A 
Alcohol excess
Insulinoma
Excessive exercise
Reactive hypoglycaemia
Type 1 diabetes
39
Q

How does alcohol excess lead to hypoglycaemia

A

Gluconeogenesis inhibited at the level of lactate dehydrogenase

40
Q

Symptoms of hypoglycaemia

A
  • Trembling
  • Palpitation
  • Sweating
  • Anxiety
  • Hunger
  • Tingling
41
Q

What hormones are secreted in hypoglycaemia

A

Growth hormone

Cortisol

42
Q

What are the consequences of prolonged hypoglycaemia

A
  • Neuroglycopaenia
  • Permenant brain damage
  • Loss of cognitive function
43
Q

Name 3 microvascular complications of diabetes

A
  • Nephopathy
  • Neuropathy
  • Retinopathy
44
Q

What pathway does glucose activate that isn’t normally activated

A

protein kinase C pathways

45
Q

How does hypoeractivation of PKCs can damage blood vessels

A
  • Increased permeability
  • Increased occlusion
  • Increased reactive oxygen species
  • Increased inflammation
  • Mitochondrial dysfunction
46
Q

How do glycation end products mediate cellular damage

A

Lipids modified when they attach molecule of glucose

Products from glucose attach to the proteins leading to changes in activity

47
Q

What is non proliferative diabetic retinopathy

A

Dilation of retina veins and microaneurysms can cause internal haemorrhaging and oedema in the retina.
Oedema in central retina is main cause of vision loss

48
Q

What is proliferative diabetic retinopathy

A

Fragile, new blood vessels form near the optic disc and grow on vitreous chamber
Bleed, reducing vision and leads to separation and detachment of areas of retina

49
Q

What characterises diabetic nephopathy

A

Proteinuria
Glomerular hypertrophy
Decreased GFR
Renal fibrosis

50
Q

What is peripheral diabetic neuropathy

A

Pain or loss in feelings in hands/ arms/ feet/ legs

51
Q

What is autonomic diabetic neuropathy

A

Changes in digestion, bowel and bladder control problems, erectile dysfunction

52
Q

What is proximal diabetic neuropathy

A

Pain in thighs and hips

Weakness in legs

53
Q

What can promote macrovascular disease

A

Advanced glycation end production formation

54
Q

How does AGE formation promote macrovascular disease

A

AGE modification of oxidised LDLR leads to enhanced LDL uptake
Induces pro-inflammatory cytokine production

MET 2 (32 decks)

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