Type 1 Diabetes Mellitus Flashcards

1
Q

Pathophysiology

A

T cell-mediated autoimmune destruction of beta cells in the islets of Langerhans in the pancreas, perhaps triggered by environmental factors (eg viruses) in people with genetic predisposition
Insulin deficiency => decreased glucose utilisation + increased gluconeogenesis => hyperglycaemia => osmotic diuresis => polydipsia, polyuria, weight loss => loss of H2O, Na+, K+
Insulin deficiency => increased lipolysis => increased katoacids => ketonuria => ketoacidosis => dehydration metabolic acidosis
The above two pathways => Dehydration metabolic acidosis

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2
Q

Clinical features

A
Peak age 7-15 years
Polyuria
Polydipsia
Weight loss
DKA (abdo pain, vomiting, severe dehydration, acidosis. younger children develop more severe consequences)
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3
Q

Diagnosis

A

Symptoms + random >1
Fasting >7
Raised Hba1c
2 hour after ingesting 75g >11.1

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4
Q

Management basics

A
Insulin replacement
Diet
Exercise
Monitorung
Education and psychological support
Management of complications
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5
Q

Insulin replacement

A

Average 0.5 - 1.0 unit/kg/day (can have honeymoon period)
1) one, two or three injections of comnination of rapid acting and intermediate acting
2) basal bolus - rapid acting before meals plus one or more injections of long acting
3) continuous insulin infusion using a pump
During puberty, insulin requirements increase
Multiple injections may result in better glycaemic control

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6
Q

Diet and exercise

A

High fibre, complex carbs (sustained release) to avoid rapid swings
Three main meals + snacks
Food intake increased before or after heavy exercise
Work with dietician for carb counting

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7
Q

Monitoring of BM

A

Finger prick
Readings recorded in diary to enable changes to regimens
HbA1c reflects glycaemic control over past 6-8 weeks - recommended <7.5% (but beware hypos)

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8
Q

DKA

A

Hyperglycaemia, acidosis, ketonaemia
Precipitation conditions: infection, inadequate insulin/non-compliance, other medical illnesses, cardiovascular stuff, alcohol

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9
Q

DKA clinical features

A
More common in young people and in women
Insidious onset polydipsia
Worsening polyuria
Weight loss (esp if first presentation)
Nausea and vomiting
Abdominal pain
Lassitude, weakness, fatiguability
SoB (hyperventilating to blow off CO2)
Confusion, disorientation => coma
Dehydration (dry membranes, decreased skin turgor, sunken eyes, slow cap refill, tachycardia with weak pulse, hypotension)
(Pear drops)
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10
Q

DKA management

A

Resusitation - ABC
Rehydration - SLOOOWLY (over 48 hours) - risk of cerebral haemorrhage
Insulin (plus K+ plus dextrose once BM drops to teens)
Monitor potassium
Frequent neuro obs
Treat precipitating illness
Patient education

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