Diabetes Melitus Flashcards

1
Q

What is the definition of diabetes mellitus?

A
  • > Metabolic disorder of multiple aetiology
  • > Characterised by chronic hyperglycaemia
  • > Disturbance of carb/fat/protein metabolism
  • > Resulting from insulin secretion/action defects
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2
Q

How is DM diagnosed as per WHO’s definition?

A
  • > Random BGL of <11.0mmol/L
  • > Fasting BGL of >8.0mmol/L
  • > Non-DM’s - BGL 3.0-5.6mmol/L.
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3
Q

List the types of diabetes mellitus:

A

Primary ->
> Type 1
> Type 2

Secondary ->
> Gestational
> Drug induced
> Decreased insulin secretion (disease related)

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4
Q

Describe T1DM.

A
  • > Insulin dependent DM.
  • > Absolute deficiency of insulin.
  • > Destruction of B-Islet cells of the pancreas by autoantibodies.
  • > Usually sudden onset at young age, often presents as life-threatening (DKA).
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5
Q

Describe T2DM.

A
  • > Non-insulin dependent DM.
  • > Gradual onset.
  • > Detected during routine check up or as a result of complications.
  • > Predisposing factors - obesity, sedentary lifestyle, age, genetics.
  • > Insulin secretion above/below normal, cells unable to take up insulin from ECF, due to insufficient activation of glucose transport mechanisms or receptors have become resistant so dysfunctional.
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6
Q

Describe the secondary causes of DM:

A
  • > Gestational: usually in the third trimester, ^ risk of dev T2DM later.
  • > Drug induced: (? more common in genetically predisposed), corticosteroids (enhance gluconeogenesis), phenytoin (suppresses insulin secretion), thiazide/diuretics (suppress insulin and peripheral glucose uptake).
  • > Decreased insulin secretion associated w/ other disease: pancreatitis, pancreatic Ca.
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7
Q

T1DM Symptoms:

A
Hyperglycaemia. 
Glucosuria. 
Polyuria. 
Polydipsia. 
Polyphagia. 
Weakness/fatigue. 
Weight loss. 
Ketonuria.
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8
Q

T2DM Symptoms:

A
Recurrent infections. 
Prolonged wound healing. 
Genital pruritus. 
Vaginal thrush. 
Visual changes. 
Retinopathy. 
Fatigue. 
Paraesthesia.
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9
Q

Pathophysiology of symptoms:

A
  • > Hyperglycaemia: cells can’t absorb glucose, glycogenesis impaired, gluconeogenesis stimulated due to lack of IC glucose.
  • > Glucosuria and Polyuria: glucose conc in glomerular filtrate same as blood, not all reabsorbed by tubules, remaining glucose ^ osmotic P - red water reabsorption (polyuria), -> electrolyte imbalance/dehydration/extreme thirst (polydipsia),
  • > Weight loss: alternative E producing pathways, gluconeogenesis from AA/proteins -> weight loss, muscle wastage, tissue breakdown, further ^BGL. Catabolism of fat bodies -> E and ketone bodies.
  • > Ketosis/Ketoacidosis: liver metabolism of ketones limited, if ketones accumulate then ketosis occurs and pH falls as buffers fail, excretion by ketonuria/breath.
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10
Q

Describe your assessment and management of hypoglycaemia:

A

> S/S: fatigue, sweating, headache, trembling, N/V, slurred speech, irritability, confusion, agitation, coma.

> Assessment: full set of jobs, BGL, FAST/Neuro Ax.

> Management: (BGL EVERY 5-10MINS)

  • Oral fast acting carb.
  • Glucogel 40% - repeated as necessary, if no airway comp.
  • IM Glucagon - induces glycogenolysis, 1mg adult dose, no repeats, 10 mins no response -> IV glucose.
  • IV Glucose - direct glucose delivery, 10g in 100ml, 30g max dose, dose interval 5mins,
  • ASHICE - if 5mmol/L or less or red GCS after treatment.
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11
Q

Hyperglycaemia - describe hyperosmolar hyperglycaemic state (HHS)

A

> Complication of T2DM.
BGL 30mmol/L w/out ketones.
Resultant state of hyperosmolality.
Characteristics - T2DM, hypovolaemia, dehydration or severely unwell.
Management: ASHICE, 0.9% NaCl as per JRCALC.

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12
Q

Hyperglycaemia - describe diabetic ketoacidosis

A

> Severely deranged cell metabolism.
Caused by stressors - infection, pregnancy, acute illness, missed insulin.
T1DM new onset may present as DKA.
S/S - ^BGL, metabolic acidosis, ^RR, urine acidification, polyuria, dehydration, hypovolaemia, electrolyte imbalance, confusion -> coma -> death.
Management - ASHICE, 0.9% NaCl as per JRCALC.

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13
Q

Chronic Complications of DM:

A

> CVS: atheroma and calcification, IHD, stroke, peripheral vascular disease (diabetic foot -> gangrene), diabetic retinopathy, peripheral neuropathy.
Infection: DM predisposes to infection (red cellular glucose suppresses phagocytic action), pyelonephritis, diabetic foot.
Renal failure: CKD -> diabetic nephropathy.
Visual impairment: diabetic retinopathy.
Diabetic foot: CVS impairs peripheral circulation, red sensation, minor wound may go unnoticed, delayed healing, infection -> ulcer -> gangrene -> amputation.

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