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ELM3 - metabolism > lecture 3 - diabetes mellitus > Flashcards

lecture 3 - diabetes mellitus Flashcards

1
Q

What is the threshold of blood glucose concentration for hypoglycaemia?

A

<4.0mmol/L

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2
Q

What is the threshold of blood glucose concentration for hyperglycaemia?

A

> 15mmol/L

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3
Q

What are the symptoms of hypoglycaemia?

A

tachycardia, sweating, weakness, intense, confusion

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4
Q

What is neuroglycopenia?

A

Low glucose delivery to the brain

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5
Q

How does alcohol cause hypoglycaemia?

A

It inhibits endogenous glucose production

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6
Q

What are the treatments for severe hypoglycaemia?

A

Intramuscular/subcutaenous glucagon, IV glucose

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7
Q

What are the symptoms of acute hyperglycaemia?

A

glycosuria, osmotic diuresis, dehydration

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8
Q

What are the symptoms of Diabetic Ketoacidosis (DKA)?

A

hyperventilation, abdominal pain, nausea/vomiting, dehydration, fruity breath, psychosis

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9
Q

What are the blood glucose levels required for a diagnosis of diabetes?

A

Fasting glucose >7.0mmol/L or
Random glucose >11.1mmol/L

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10
Q

What is the ‘Type 1 Triad’?

A

The 3 most common symptoms at diagnosis with T1D: polydipsia, polyuria, polyphagia

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11
Q

What is the pathophysiology of T1D?

A

Autoimmune destruction of the beta-cells in the islets of the pancreas means the pancreas cannot release insulin in response to glucose.

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12
Q

What is the treatment for T1D?

A

Carbohydrate counting, insulin replacement

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13
Q

What are the 2 types of insulin used in T1D treatment?

A

Short-acting - given as a bolus after meals
Long-acting - given to maintain basal insulin levels over the day

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14
Q

What are the 3 key modifiable risk factors for developing T2D?

A

Weight loss, Exercise, Glycaemic control

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15
Q

What is MODY?

A

Maturity Onset Diabetes of the Young
a rare cause of type 2 diabetes in younger patients, causes by mutations to genes involved in glucose metabolism or insulin production

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16
Q

What are the symptoms of T2D?

A

Obesity, polyphagia, polyuria, polydipsia, signs of peripheral disease (blurred vision, neuropathy, itchiness, fatigue, ulcers)

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17
Q

What is the basic pathophysiology of T2D?

A

Obesity and genetic factors lead to insulin resistance which causes chronic hyperglycaemia. B-cells increase their activity to compensate, but eventually fail and die, perpetuating the hyperglycaemia.

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18
Q

What is the biggest risk factor for insulin resistance?

A

Obesity - visceral fat and central obesity

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19
Q

What are the 3 key ways that obesity causes insulin resistance?

A
  1. obesity causes a state of chronic inflammation because adipocytes release inflammatory cytokines. Cytokines impede insulin signalling.
  2. Excess intracellular FFAs overwhelm oxidative pathways and generate toxic intermediates that interfere with insulin signalling.
  3. Adipocytes fail to release sufficiency adiponectin, which is needed to increase insulin sensitivity.
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20
Q

What are the mechanisms through which Beta-cells are damaged with insulin resistance?

A

excess circulating glucose and FFAs is damaging to beta cells, reduced incretin production by the gut reduces insulin secretion, excess GLUT-2 receptor activation can cause down-regulation to avoid gluco-toxicity but this reduces insulin secretion

21
Q

What changes occur to fat metabolism in T2D?

A

Increased lipolysis, less activity of LPL, increased lipogenesis.

22
Q

Why does T2D cause increased lipogenesis and fatty liver disease?

A

Lipogenesis is a process usually stimulated by insulin. The liver is less resistant to insulin than other tissues, so in T2D hyperinsulinaemia stimulates liver lipogenesis resulting in a fatty liver

23
Q

Why is there decreased VLDL storage in T2D?

A

Lipoprotein Lipase, which is needed for VLDL processing, is insulin-dependent, so diabetes means that VLDL cannot be broken down into TAGs and fatty acids for storage in adipose tissue

24
Q

What are the non-pharmacological treatments for T2D?

A

Lifestyle changes: diet, exercise, weight loss,
Bariatric surgery

25
Q

What classes of medications are used to treat T2D?

A

Biguanides (e.g. metformin), Sulphonylureas (e.g. gliclazide), synthetic insulin

26
Q

What is the first line medication for T2D?

A

Metformin

27
Q

What is the mechanism of action of metformin?

A

decreases hepatic glucose production, decreases intestinal absorption of glucose, and improves insulin sensitivity by increasing peripheral glucose uptake and utilization.

28
Q

What are the acute complications of hyperglycaemia?

A

Glycosuria increases UTI risk, Osmotic diuresis can cause dehydration, erectile dysfunction, ketoacidosis

29
Q

What are the chronic complications of hyperglycaemia?

A

Retionopathy, cataracts, nephropathy, neuropathy, cardiomyopathy, cardiovascular disease (atherosclerosis)

30
Q

Why does diabetes cause nephropathy?

A

A combination of ischaemia and AGE reactions leads to long term changes to the blood vessels in the kidneys.

31
Q

What is the first clinical sign of nephropathy in patients with diabetes?

A

Microalbuminuria - sclerosis causes leaky glomerular basement membranes

32
Q

What are glomerular changes seen in diabetic nephropathy?

A

basement membrane thickening, diffuse mesangial sclerosis, nodular glomerulosis

33
Q

What are the initial signs of diabetic peripheral neuropathy?

A

Decreased sensation with a ‘glove and stocking’ distribution (hands and feet). Vibration sense is the first type of sensation to be lost

34
Q

Why does diabetes cause neuropathy?

A

It causes narrowing of the small blood vessels that supply the nerves

35
Q

What are AGEs?

A

Advanced Glycation End-products - products produced by non-enzymatic glycation of side-chains of proteins. These become oxidised to aldehydes and form cross links with collagen and elastin.

36
Q

What is the consequence of AGE cross-linking?

A

AGEs form cross links with collagen and elastin which causes basement membrane thickening and endothelial injury. This causes damage by thickening arteries, promoting atherosclerosis, and thickening renal basement membranes.

37
Q

What are RAGEs?

A

Receptors for Advance Glycation End-products:
Receptors on inflammatory, endothelial and vascular smooth muscle cells that bind to AGE and trigger inflammation.

38
Q

What are the consequences of AGE-RAGE binding?

A

Triggers inflammation leading to decreased neutrophil function, release of inflammatory cytokines, reactiive oxygen species, procoagulant activity and atherosclerotic plaque deposition.

39
Q

What causes the development of AGEs?

A

An increase in blood glucose

40
Q

What is the early stage of diabetic retinal damage?

A

Non-proliferative retinopathy

41
Q

What causes early diabetic non-proliferative retinopathy?

A

AGE/RAGE causes damage to the endothelium and basement membrane of small vessels in the retina. These become weak and cause micro-aneurysms and oedema.

42
Q

What causes the progression from non-proliferative to proliferative retinopathy in diabetes?

A

Over time, the early onset vasculopathy causes ischaemia to the retina, which responds by neovascularising/proliferating to improve supply to the ischaemic areas. These vessels are prone to bleeding and bursting, causing damage to the retina.

43
Q

What is the polyol pathway in diabetes?

A

The excess sugars due to hyperglycaemia are converted to sorbitol, which accumulates in the nerves and eyes, causing cataracts and nerve conduction defects

44
Q

What are the direct effects of diabetes on immune function?

A

Hyperglycaemia provides optimal condition for bacterial growth by providing glucose for energy.
Immune cells are dysfunctional due to AGE/RAGE

45
Q

What are the indirect effects of diabetes on immune function?

A

Atherosclerosis and vessel narrowing decreases blood supply to areas of infection leading to poor wound healing

46
Q

How does exercise reduce insulin resistance?

A

Activates AMPK and adiponectin

47
Q

Why is insulin sensitivity greater in athletes, especially sprinters?

A

There is increased expression of GLUT4 transporters in muscle and adipose, allowing for greater glucose uptake during rapid bursts of exercise.

48
Q

How does adiponectin protect against insulin resistance and T2D?

A

Increases muscular glucose uptake and expenditure, decreases glucose and production in the liver, and reduces overall inflammation protecting against CVD

ELM3 - metabolism (15 decks)

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