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Urinary Symptoms and thirst > Complications of diabetes mellitus > Flashcards

Complications of diabetes mellitus Flashcards

1
Q

What are the types of diabetes?

A

Type 1: autoimmune destruction of insulin-producing beta-cells (8%)
• Type 2: combination of insulin resistance and relative insulin
deficiency (90%)
• Gestational diabetes
• Other:
✓ Type 3c – damage to the pancreas (pancreatitis, pancreatic cancer,
hemochromatosis, cystic fibrosis)
✓ Steroid induced diabetes
✓ Maturity onset diabetes of the young (MODY)
✓ Neonatal diabetes

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2
Q

What are type 1 diabetes?

A

autoimmune destruction of insulin-producing beta-cells

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3
Q

What cells produce insulin

A

islet cells

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4
Q

How do you get type diabetes from being fat

A
  • Fatty liver (resistant to insulin)
  • Impaired insulin-mediated suppression of gluconeogenesis
  • Liver paradoxically produces excess of glucose
  • Fatty pancreas
  • Destruction and/or Impaired function of beta-cells
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5
Q

What does insulin do?

A

Icreases glucose uptake
increases glycogen synthesis
Deccreases lipolysis

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6
Q

What does glucagon do?

A

Increase Glycogenolysis
Increase Gluconeogenesis
Increase Lipolysis

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7
Q

What is used as an emergency treatment for type 1 diabetes?

A

Glucagon

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8
Q

What happens if insulin is inhibited in hyperglycemia?

A

High glucose in blood
Protein breakdowwn - muscle wasting
Lipolysis
Formation of ketone bodies

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9
Q

What is an acute complication of Type 1 diabetes ?

A

Diabetes ketoacidosis

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10
Q

What is an acute complication of Type 2 diabetes ?

A

Hyperglycaemic hyperosmolar state HHS

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11
Q

What does an increase in ketone bodies do?

A

Metabolic acidosis
Increase in osmotic diuresis hypovolaemia and less glomerular filtration which leads to hyperosmolality leasds to dehydration

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12
Q

What does increase in hyperglycemia do?

A

Increase in osmotic diuresis hypovolaemia and less glomerular filtration which leads to hyperosmolality leads to dehydration

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13
Q

What are the differences in DKA and HHS?

A

Glucose- Mainly more hyperglycemia in HHS
Osmolality- Serum hyper osmolality in HHS, variable in DKA
Ketonemia- Absence in HHS, + in DKA
Acidosis - Absence in HH, pH< 7.3 / bicarbonate <15mmol/l
Hypovolaemia- Severe in HHS, Less Severe in DKA

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14
Q

What are chronic complications of diabetes?

Microvascular

A

Retinopathy-disease of the small retinal blood vessels(endothelial cells in the retina)
Nephropathy- deterioration of kidney function (attack on cells in renal glomerulus)
Neuropathy- type of nerve damage (neurons and schwaan cells)

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15
Q

What are chronic complications of diabetes?

Macrovascular

A

Coronary artery disease
Cerebrovascular disease
Peripheral vascular disease

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16
Q

What is the polyol pathway?

A

Glucose shunted through aldose reductase into sorbitol -> fructose
all these things are going through reactive oxygen species,cause damage to blood vessels and to endothelium

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17
Q

What do AGE do?

A

Advanced glycation end products cause connective tissue to become stiff therefore:
contractures in collagenous tissue in their hands
lose heparin sulphate proteoglycans important for normal basement membrane drummer of functioning

18
Q

What is the protein kinase C pathway?

A

Increase in vascular endothelial growth factor causes new vessel formation in the back of the eye not useful causes proliferative retinopathy

19
Q

What can treat diabetic retinal disease?

A

anti-VEGF treatment

20
Q

What is the Hexosamine pathway

A

Increase in oxygen reactive series = toxic

21
Q

What treatment is given for someone with protein in urine?

A

ACE inhibitors

22
Q

What do ACE inhibitors do?

A

preferential efferent arteriole vasodilatation

23
Q

What does metformin do?

A

Suppression of hepatic gluconeogenesis

24
Q

What does Sulfonylurea do?

A

Increase in insulin secretion from beta-cells

25
Q

What does Meglitinides do?

A

Increase in insulin secretion from beta-cells

26
Q

What does DPP-4 inhibitors do?

A

Inhibit GLP-1 degradation – promotes glucose

dependent insulin secretion

27
Q

What does GLP-1 agonists do?

A

Promotes glucose dependent insulin secretion

28
Q

What does SGLT-2 inhibitors

do?

A

Increased glucosuria through inhibition of SGLT-2 in the kidney

29
Q

What does Alpha-glucosidase inhibitors do?

A

Reduce intestinal glucose absorption

30
Q

What does Thiazolidinediones do?

A

Reduce insulin resistance

31
Q

What does Amylin analogs do?

A

Reduce glucagon release, reduce gastric emptying

32
Q

Which drugs suppress hepatic gluconeogenesis

A

metformin

33
Q

Which drugs increase insulin secretion from beta-cells

A

Sulfonylurea

Meglitinides

34
Q

Which drugs promotes glucose

dependent insulin secretion by inhibiting GLP-1 degradation

A

DPP-4 inhibitors

35
Q

Which drugs promotes glucose

dependent insulin secretion

A

DPP-4 inhibitors

GLP-1 agonists

36
Q

Which drugs increase glucosuria through inhibition of SGLT-2 in the kidney

A

SGLT-2 inhibitors

37
Q

Which drugs reduce intestinal glucose absorption

A

Alpha-glucosidase inhibitors

38
Q

Which drugs reduce insulin resistance

A

Thiazolidinediones

39
Q

Which drugs reduce glucagon release and reduce gastric emptying

A

Amylin analogs

40
Q

What is the Incretin effect?

A

oral glucose elicits higher insulin secretory responses than does intravenous glucose for healthy patients

41
Q

What happens to the incretin effect for people with Type 2 diabetes?

A

Reduced effect

Urinary Symptoms and thirst (4 decks)

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