Conditions - Diabetes Flashcards

1
Q

What is the defining feature of diabetes?

A

Hyperglycaemia

Random blood sugar > 11.1
Fasting blood sugar > 7
HbA1c > 6.5%

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2
Q

What are the two types of diabetes?

A

Primary (absolute)

  • most common form
  • Type 1 (absolute deficiency of insulin)
  • Type 2 (relative deficiency of insulin)

Secondary:
- secondary to another pathology (ie: cystic fibrosis, corticosteroid abuse)

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3
Q

What are some of the conditions that can cause secondary diabetes?

A

Pancreatic disease (cystic fibrosis)

Iatrogenic (corticosteroids)

Conditions with excessive insulin antagonists

  • growth hormone
  • cortisol
  • thyroid hormone
  • pregnancy (human placental lactogen)
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4
Q

Which hormones are excessive insulin antagonists and can be implicated in secondary diabetes?

A

Growth hormone
Cortisol
Thyroid hormone
Human placental lactogen (pregnancy)

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5
Q

What are the incidence rates for diabetes in Australia?

A

5% diabetes (88% Type 2)

17% pre-diabetes (impaired glucose tolerance or impaired fasting glucose)

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6
Q

Which factors are involved in the aetiology of Type 1 Diabetes?

A

Genetics + environmental factors

Viral infections that damage beta cells

  • rubella (in utero)
  • mumps
  • cytomegalovirus
  • epstein barr virus

Autoimmunity:
- circulating antibodies attack and destroy islet cells
(85% of Type 1 Diabetes)

Combined hypothesis:
- a virus triggers the autoimmune response in a genetically vulnerable patient

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7
Q

Which cells produce insulin in the pancreas?

A

Beta cells in pancreatic islets

- hyperglycaemia occurs after 90% of islet cells are destroyed in Type 1 Diabetes

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8
Q

What are the aetiological factors involved in Type 2 Diabetes?

A
  1. Genetics
  2. Obesity
    - diabetogenic in those genetically predisposed to T2DM
    - inflammatory mechanisms involved
  3. Metabolic Syndrome
  4. Tobacco (30-40% higher risk)
  5. Age (70% > 50)
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9
Q

What is the connection between obesity and Type 2 Diabetes?

A
  1. oxidative stress
    - excessive nutrients cause oxidative stress (stress insulin sensitive tissues - adipose tissue, liver, muscle)
  2. adipose tissues release pro-inflammatory cytokines (TNFa, interleukin 1B)
  3. cytokines interact with insulin receptors and impair intracellular signalling
  4. cells become less responsive to insulin
  5. obesity also associated with decreased insulin receptor density and damaged beta cells
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10
Q

What is insulin resistance?

A

In Type 2 Diabetes: enough insulin is produced, but cells have become resistant to the effects of insulin

  1. initial stages: compensatory hyperinsulinaemia (prevents appearance of diabetes for years) - initial stage T2DM has high levels of insulin
  2. late stage: beta cell exhaustion / dysfunction - causes insulinpaenia
    - late stage T2DM has low levels of insulin
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11
Q

What mechanism does insulin use to interact with target cells?

A

GLUT-4 mechanism

  • insulin binds to insulin receptors on cell wall
  • GLUT-4 transport channels on cell wall activated so glucose can enter cell
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12
Q

What are the clinical features of T1DM?

A

Onset: several weeks

“starvation in the midst of plenty”

Osmotic diuresis:
– polyuria

Dehydration:

  • polydipsia
  • tachycardia
  • hypotension

Malnutrition:

  • weight loss
  • fatigue

Increased gluconeogenesis:

  • mm wasting
  • weakness

Glycosuria

  • vulvitis
  • balanitis
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13
Q

What are the clinical features of T2DM?

A

Onset - insidious (months to years)

Hyperglycaemia and glycosuria increase infection risk:

  • skin infections
  • recurrent UTIs
  • vulvitis and balanitis

Diabetic Vascular Disease

Diabetic Neuropathy

Diabetic Foot

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14
Q

What are the complications associated with T1DM and T2DM?

A

T1:

  • hypoglycaemia
  • diabetic ketoacidosis

T2:

  • diabetic vascular disease
  • diabetic neuropathy
  • diabetic foot
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15
Q

Describe the complication of hypoglycaemia

A

Complication of T1DM

  • without sufficient glucose to fuel brain, neuro SSX occur (when B.G. < 2.5)

CNS features:

  • drowsiness
  • confusion
  • speech difficulties
  • lack of concentration
  • headache
  • fatigue

ANS features:

  • sweating
  • trembling
  • pounding heart
  • hunger
  • anxiety
  • nausea

Severe hypoglycaemic attack:

  • coma
  • convulsions
  • brain damage
  • stroke
  • fatal

Causes:

  • misuse of insulin or hypoglycaemic medication
  • missed meals
  • unusual / excessive exercise
  • alcohol intake
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16
Q

Describe the complication of diabetic ketoacidosis

A

Complication of T1DM

Pathology:

  • fatty acids become main energy source when glucose levels low
  • excessive catabolism of fatty acids causes ketone formation
  • accumulation of ketones lowers pH of body (ketoacidosis)

Clinical features:

  • thirst, frequent urination
  • nausea, vomiting
  • acetone breath
  • respiratory compensation (increased respiratory rate, deep laboured breathing)
  • mental disturbance (inattention to coma)
  • peripheral vasodilation (hypotension, hypothermia)

Medical emergency - can be fatal

17
Q

Describe the complication of diabetic vascular disease

A

Complication usually seen in T2DM

Umbrella term:
- range of blood vessel pathologies (atherosclerosis and arteriosclerosis)

Atherosclerosis (diabetic macroangiopathy)
- risk for AMI, PVD, stroke

Arteriosclerosis (diabetic microangiopathy)
- risk for retinopathy, nephropathy, neuropathy

Diabetic retinopathy

  • common cause of blindness
  • late stage of disease
18
Q

What is diabetic neuropathy?

A
  • affects PNS

Changes:

  1. thickened basement membrane of intra-neural capillaries
  2. axonal degeneration
  3. patchy demyelination

Sensory polyneuropathy:

  • decreased reflexes
  • impaired vibration sense
  • ‘glove and stocking’ sensory impairment
  • paraesthesia
  • pain
  • ataxia

Motor neuropathy:
- generalized mm wasting and weakness

Mononeuropathy:
- involvement of single peripheral nerve affecting eye

Autonomic neuropathy:

  • postural hypotension
  • tachycardia
  • dysphage, nausea, vomiting
  • diarrheoa, constipation
  • impotence
  • sweating
19
Q

Describe the condition of diabetic foot

A

Foot trauma and ulceration caused by:

  • peripheral neuropathy
  • peripheral vascular disease
  • hyperglycaemia and ketosis (impairs immune function)
  • untreated infection can result in gangrenous necrosis requiring amputation
  • regular podiatry necessary for monitoring and treating minor wounds (impaired healing and sensation)
20
Q

What is the pharmacology used in the treatment of diabetes?

A
  1. exogenous insulin
  2. oral hypoglycaemic agents (T2DM)
    - biguanides (1st line - increase glucose uptake, decrease gluconeogenesis and glucose absorption)
    - sulphonylureas (increase insulin secretion)
    - thiazolidineodiones (increase insulin sensitivity by increasing uptake of fatty acids by adipocytes)
    - alpha glucosidase inhibitors (decrease digestion of starch and reduce post-meal BG levels)
  3. other:
    - exenatide (increased insulin secretion and decreased glucagon secretion)