T1DM Flashcards

1
Q

Definition?

A

Metabolic disorder characterised by persistent hyperglycaemia, with disturbances of carbohydrate, protein and fat metabolism, due to deficits in insulin secretion and/or insulin action.
10% of diabetes cases are T1

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2
Q

Risk factors?

A
  • Genetic factors-polygenic
  • Low vit D
  • Diet
  • Obesity
  • Enteroviruses as a child
  • SE class
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3
Q

Differentials?

A
  • Monogenic diabetes-non-obese, young-family history
  • Neonatal-AD, under 6 months
  • Latent autoimmune diabetes in adults-over 30’s, responsive to treatment, non-obese
  • T2DM
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4
Q

Epidemiology?

A

Age: Youths-under 20’s
Sex:1:1
Ethnicity: More in Europeans and less in Asians
Prevalence: 1 million worldwide

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5
Q

Aetiology?

A
  • HLA-DR and HLA-DQ increase susceptibility
  • Environment/genetic triggering auto-immune destruction of beta pancreatic cells
  • Low vit D
  • Enteroviruses
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6
Q

Clinical Presentation?

A
  • Hyperglycaemia
  • Ketosis
  • Rapid weight loss
  • Age<50
  • BMI<25
  • Polydipsia
  • Polyuria
  • Weight loss
  • Lethargy
  • Blurred vision
  • Diabetic ketoacidosis
  • N and V
  • Abdominal pain
  • Tachypnoea
  • Tachycardia
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7
Q

Pathophysiology?

A
  • Type 4 hypersensitivity response
  • Cell mediated immune response
  • Self-tolerance-genetic abnormality-loss of this so T-cell targets islets of Langerhans
  • Less insulin
  • Glucose collects in blood as it is not taken up- cells starved of glucose, osmolality increases, cannot be reabsorbed in PCT, RAAS system regulation depletes so ADH increases thirst
  • HLA-genes on c6 code for MHC-imp for recognising foreign molecules-needed for self-tolerance/presentation
  • 90% of cells destroyed before symptoms show
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8
Q

Investigations-first line and findings?

A
  • Exam/history-vascular, foot, eye
  • Random plasma glucose -≥11 mmol/L (≥200 mg/dL)
  • Fasting plasma glucose-≥6.9 mmol/L (≥126 mg/dL)
  • 2-hr plasma glucose after 75g oral glucose load-≥11 mmol/L (≥200 mg/dL)
  • Plasma or urine ketones-med/high
  • HbA1c-≥48 mmol/mol (≥6.5%)
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9
Q

Investigations-second line and findings?

A
  • Fasting C-peptide-low
  • Autoimmune markers-glutamic acid decarboxylase, insulin, islet cells, islet antigens (IA2 and IA2-beta), and the zinc transporter ZnT8-positive
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10
Q

Management-first line non-pharm?

A
  • Individual care plan-
    • Medical assessment of diagnosis, acute care, compounding risk factors
    • Environment-social lifestyle, diet and PA
  • Education programme
    • Self-monitoring
  • Lifestyle management
    • Carbohydrate counting
    • Low fat, sugar and salt and 5 a day
    • Eating disorders/healthy weight, HT or CKD management
    • Avoid alcohol on empty stomach
    • Each week, accumulate at least 150 minutes of moderate intensity activity (such as brisk walking or cycling), or 75 minutes of vigorous intensity activity (such as running), or shorter durations of very vigorous intensity activity (such as sprinting or stair climbing), or a combination of moderate, vigorous, and very vigorous intensity activity.
    • Smoking cessation
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11
Q

Management-first line pharm?

A
  • Basal-bolus insulin/pump-
    • Basal-long lasting-once a day
    • Bolus-30 mins before meals
    • Adults-0.2 to 0.4 units/kg/day
    • In children an initial daily dose will be 0.5 to 1.0 units/kg/day
    • 1 unit for 15g of carbs a day
  • Pre-meal correction dose-
    • 1800/Total Daily Dose = the predicted point drop in blood glucose per unit of rapid acting insulin.
  • Amylin analogue-
    • co-secreted usually with insulin and increases emptying time/delays glucose absorption-used in post-prandial hyperglycaemia
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12
Q

Management-second line pharm?

A

• Fixed dose insulin-managed well, cannot manage 3-4 injections a day or have trouble mixing it

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13
Q

Management pregnancy?

A

Consider low-dose aspirin to minimise risk of pre-eclampsia

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14
Q

monitoring?

A
  • Screen for complications every 6 months

* Provide CVD/complication lowering medications

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15
Q

Prognosis?

A
  • If poorly controlled, can lead to severe morbidity and mortality
  • CVD major cause of death
  • Can have successful pregnancies if managed well
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16
Q

Complications?

A
DKA
• Hypoglycaemia
• Retinopathy
• Diabetic kidney disease
• Peripheral or autonomic neuropathy
• CVD
• Stroke 
• HT
• UTI
• Pneumonia
• Fungal infections
• Skin infections
17
Q

DKA?

A

• In events of stress
• Lipolysis converts into ketone acids -acetoacetic acid and b-hydroxybutyrate-energy and increased acidosis of blood
• Kussmaul resp-deep/laboured breathing
• Increased K/H transport and lack of Na and K transporter-hyperkalaemia but low K in cells, high anion gap
• Acetone-fruity breath
• N and V
Mental status changes/cerebral oedema
• I-VBG, ketones and U and E
• Treatment depends on BP and serum potassium levels
• If<90-IV,potassium replacement, insulin, monitor for complications/markers-sodium bicarb and thromboprophylaxis
• If >90-do as above but refer to critical care