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DIABETES MELLITUS > PATHOPHYSIOLOGY > Flashcards

PATHOPHYSIOLOGY Flashcards

1
Q

What is the origin of type 1 diabetes

A

Environmental trigger on a genetically susceptible individual

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2
Q

What is LADA

A

Type 1 diabetes presenting in adults

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3
Q

Genes linked to type 1 diabetes

A

HLA antigens in chromosome 6
Insulin gene polymorphisms on chromosome 11
PTPN22
IL2RA
CTLA-4

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4
Q

Environmental triggers for Type 1 diabetes

A

Early exposure to cow’s milk
Lack of breastfeeding
Gut bacteria
Certain viruses

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5
Q

Viruses that can trigger pathogenesis of type 1 diabetes in a agenetically susceptible individual

A

Rotavirus
Enterovirus

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6
Q

Which vitamin deficiency is more prevalent in type 1 DM

A

Vitamin D deficiency

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7
Q

Most common autoantibodies in type 1 DM

A

ICA - Islet Cell Autoantibodies

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8
Q

Other antibodies found in Type 1 DM apart from ICA

A

Antibodies formed to
Insulin
Glutamic acid decarboxylase 65 (GAD65)
Insulinoma-associated antigen 9 (IA-2)
Zinc transporter 8 (ZnT8)

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9
Q

Autoimmune disorders common in type 1 DM

A

Hashimoto’s thyroiditis
Graves’ disease
Addison’s disease
Vitiligo
Celiac sprue

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10
Q

Apart from insulin, which other hormone is deficient in type 1 DM

A

Amylin

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11
Q

What causes type 2 DM

A

Beta cell dysfunction coupled with insulin resistance

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12
Q

Why is type 2 diabetes polygenetic

A

many geenetic defects contribute to its pathogenesis

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13
Q

Defects in type 2 DM that impair glucose regulation (7)

A
  1. Deficiency and resistance to insulin
  2. Deficiency and resistance to incretins
  3. Excess glucagon secretion
  4. Increased hepatic glucose production
  5. Upregulation of SGLT2
  6. Systemic inflammation
  7. Diminished satiety
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14
Q

People with type 2 DM lose approximately ……….. of
β-cell function per year.

A

5% to 7%

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15
Q

Glucotoxicity occurs when glucose levels chronically exceed……………..

A

140
mg/dL (7.8 mmol/L)

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16
Q

What is glucotoxicity

A

When β-cell is unable to maintain sufficient
insulin secretion and, paradoxically, releases less insulin as glucose
levels increase

17
Q

Causes of progressive beta cell loss in type 2 DM

A

(1) glucotoxicity
(2) lipotoxicity
(3) insulin resistance
(4) age
(5) genetics
(6) incretin deficiency.

18
Q

What causes impaired glucose tolerance in the early stages of beta cell dysfunction

A

Deficient first-phase insulin release

19
Q

Cause of decreased posprandial insulin secretion in type 2 DM

A

Impaired beta cell function
Diminished stimulus from gut hormones (mostly incretins)

20
Q

How is abdominal fat different from subcutaneous fat

A

Presence of o excess lipids in non-adipose tissue
Abdominal fat is resistant to antilipolytic effects of insulin

21
Q

Causes insulin resistance in type 2 DM

A

1.Release of excess free fatty acids by abdominal fat
2. Excess fat inhibits secretion of adiponectin
3. Oversecretion of inflammatory adipokines
4. Excess stored fatsalso causes adipocytes to become too large and inhibit further fat storage

22
Q

how adoes abdominal fat causes insulin resistance

A
23
Q

Which tissues or organs does insulin resistance affect

A

Muscle
Adipose tissue
Liver

24
Q

Function of adinopectin

A

Suppresses the attachment of monocytes to endothelial cells,
thereby protecting against vascular damage.

25
Q

Adipokines released in type 2 DM by Visceral adipose tissue

A

Plasminogen activator inhibitor-1
TNF-alpha
Interleukin-6
Resistin
Angiotensinogen

26
Q

Role of resistin in type 2 DM

A

Causes insulin resistance

27
Q

Surrogate market for visceral adipose tissue

A

Central obesity

28
Q

Renal threshold for glucose in normal people and diabetics

A

Normal - 10 mmol/l
Diabetes- 12.2-13.3 mmol/l

29
Q

What accounts for increased reabsorption of glucose in the proximal renal tubules in diabetes

A

Upregulation of the SGLT-2 receptors

30
Q

What is type A insulin resistance

A

Clinical syndrome characterized by acanthosis nigricans,
virilization in women, polycystic ovaries, and hyperinsulinemia.

31
Q

What is type B insulin resistance

A

When anti-insulin receptor antibodies block the binding of insulin

32
Q

Clinical presentation of type 1 DM

A

Polyuria
Polydipsia
Polyphagia
Fatigue
Lethargy
Blurred vision

33
Q

Components metabolic syndrome

A

Abdominal Obesity
Triglycerides
High LDL or Low HDL cholesterol
High blood pressure
Hyperglycaemia

34
Q

Components metabolic syndrome

A

Abdominal Obesity
Triglycerides
High LDL or Low HDL cholesterol
High blood pressure
Hyperglycaemia

35
Q

Components metabolic syndrome

A

Abdominal Obesity
Triglycerides
High LDL or Low HDL cholesterol
High blood pressure
Hyperglycaemia

36
Q

Acute complications of diabetes or diabetic emergencies

A

Diabetic ketoacidosis in type 1
Hyperosmolar hyperglycaemic state for type 2
Hypoglycaemia

37
Q

Microvascular complications of diabetes

A

Nephropathy
Neuropathy
Retinopathy

38
Q

Macrovascular complications of diabetes

A

Cardiovascular disease
Cerebrovascular disease
Peripheral vascular disease

39
Q

Combined macrovascular and microvascular complication

A

Diabetic foot problems

DIABETES MELLITUS (12 decks)

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