Diabetes Mellitus Flashcards

1
Q

Why is diabetes mellitus characterized by?

A

High blood sugar levels and an insufficiency of insulin

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2
Q

What is the difference between type 1 and 2 diabates?

A

Type 1 - insulin deficiency caused by pancreatic beta cell destruction (autoimmune)
Type 2 - insulin insufficiency caused by insulin resistance in normal target tissue and beta cell exhaustion

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3
Q

What is diabetes mellitus’ metabolism disorders?

A

Hyperglycaemia
Ketonemia/ketonuria
Glucosuria
Ketoacidiosis or HONK/HHS

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4
Q

What is diabetes mellitus’ symptoms?

A

Polydipsia
Polyuria
Blurred vision
Hyperglycemia
Glucosuria
Long term micro and macrovascular complication

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5
Q

How can you diagnose diabetes mellitus?

A

Elevated 2h post glucose load
Fasting hyperglycemia

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6
Q

How is glycosylated Hb formed?

A

Spontaneous reaction between glucose and Hb
Non-enzymatic
over 8.0 is bad

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7
Q

What are characteristics of type 1 diabetes?

A

Early onset
autoimmune destruction of beta cells - loss of insulin production
complex metabolic derangements
hyperglycemia
protein breakdown
ketoacidosis

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8
Q

What is the treatment for type 1 diabetes?

A

Lifelong insulin replacement therapy

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9
Q

What is the genetic susceptibility for type 1?

A

Linkage to HLA locus (chromosome 6)
DR3 allele increases risk X5
DR4 allele increases risk X8

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10
Q

What are environmental triggers in type 1?

A

Childhood viral infections eg coxsackie, mumps and rubella

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11
Q

What does reduced glucose entry lead to?

A

Hyperglycemia

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12
Q

What does insulin deficiency lead to?

A

Hepatic gluconeogensis -> increasing plasma glucose
cells are ‘starved’ of glucose (energy)

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13
Q

What does switching to FA metabolism as an energy source lead to?

A

Excessive FA oxidation leads to increased production of ketone bodies

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14
Q

What happens in diabetic ketoacidosis?

A

Increased protein breakdown, lipolysis, beta oxidation (acetyl CoA) and ketone bodies
leads to drop in pH and acidosis

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15
Q

What causes diabetic ketoacidosis?

A

Insufficient insulinisation

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16
Q

How does respiratory compensation reverse metabolic acidosis?

A

Lowering CO2 by hyperventilation will drive bicarbonate buffering system away from H+ correcting acidosis

17
Q

What two factors lead to diabetes type 2?

A

Genetic predisposition and obesity

18
Q

How is insulin resistance overcome?

A

Continued secretion of insulin -> after a while beta cells become exhausted

19
Q

What are the 2 types of fat distribution?

A

Android (visceral)
Gynoid (subcutaneous)

20
Q

Which fat is more metabolically active?

A

Visceral - constant flux of TG and FA between liver and visceral adipose tissue

21
Q

How does expanded and inflamed adipose tissue affect the liver?

A

Increases FFA, inflammatory cytokines, insulin resistance
Lowers adiponectin

22
Q

What are the 7 oral hypoglycemic agents?

A

Biguanides and Thiazolidinediones - improve insulin sensitivity
Sulfonylureas GLP-1 receptor agonists - increase insulin secretion
alpha glucosidase inhibitors - reduce glucose GIT absorption
SGLT2 inhibitors - reduce renal glucose reabsorption

23
Q

What is retinopathy?

A

Changes in retinal microvasculature due to poor glycemic control

24
Q

What is non-proliferative retinopathy?

A

Increased vascular permeability/macular oedema

25
Q

What is proliferative retinopathy?

A

Retinal hypoxia and ischemia stimulate angiogenesis

26
Q

What is nephropathy?

A

Progressive disease caused by damage to renal microvasculature due to poor glycaemic control

27
Q

What are pathological changes in nephropathy?

A

Glomerular basement membrane thickening
mesangial cell expansion
ECM accumulation/fibrosis
Decline in GFR

28
Q

What is neuropathy?

A

Abnormalities of microvasculature that supply peripheral nerves -> basement membrane thickening, endothelial hyperplasia

29
Q

What are pathological changes in neuropathy?

A

Increased vasoconstriction and oxidative stress
Hypoxia and ischaemia
non-traumatic lower extremity amputations