Diabetes Mellitus Flashcards

(29 cards)

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
What is proliferative retinopathy?
Retinal hypoxia and ischemia stimulate angiogenesis
26
What is nephropathy?
Progressive disease caused by damage to renal microvasculature due to poor glycaemic control
27
What are pathological changes in nephropathy?
Glomerular basement membrane thickening mesangial cell expansion ECM accumulation/fibrosis Decline in GFR
28
What is neuropathy?
Abnormalities of microvasculature that supply peripheral nerves -> basement membrane thickening, endothelial hyperplasia
29
What are pathological changes in neuropathy?
Increased vasoconstriction and oxidative stress Hypoxia and ischaemia non-traumatic lower extremity amputations