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ENDO (Endocrinology) > Diabetes Mellitus - Type I Diabetes Mellitus > Flashcards

Diabetes Mellitus - Type I Diabetes Mellitus Flashcards

1
Q

What is Type I Diabetes Mellitus?

A

A disease where the pancreas stops being able to produce insulin.

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2
Q

Epidemiology of Type I Diabetes Mellitus.

A

Childhood/Early Adult Life.

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3
Q

Aetiology of Type I Diabetes Mellitus.

A
  1. Unclear Aetiology.
  2. Genetic Component.
  3. Triggers : Coxsackie B Virus and Enterovirus.
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4
Q

Pathophysiology of Type I Diabetes Mellitus.

A

Autoimmune disorder where the B-cells are destroyed by the immune system, resulting in an absolute deficiency of insulin.

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5
Q

Hormones Involved in Blood-Glucose Homeostasis (2).

A
  1. Insulin - B cells in Islets of Langerhans of Pancreas - anabolic hormone - reduces blood sugar.
  2. Glucagon - a cells in Islets of Langerhans of Pancreas - catabolic hormone - increases blood sugar.
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6
Q

Processes of Hormones in Blood-Glucose Homeostasis (3).

A
  1. Insulin - Glycogenesis (Uptake into Liver and Muscle Cells).
  2. Glucagon - Glycogenolysis (Liver Breakdown of Glycogen into Glucose).
  3. Glucagon - Gluconeogenesis ((Liver Conversion of Proteins and Fats into Glucose).
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7
Q

Ideal Blood Glucose Concentration.

A

Between 4.4 and 6.1 mmol/L.

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8
Q

What is Ketogenesis?

A

Hepatic conversion of fatty acids into ketones - water-soluble fatty acids when insufficient glucose supply and glycogen stores are exhausted.

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9
Q

Physiological Ketogenesis (2).

A
  1. Normal e.g. prolonged fasting or very low carbohydrate-high fat diets when buffered (using Bicarbonate) to prevent acidosis.
  2. Extreme Hyperglycaemic Ketosis - Metabolic Acidosis (Diabetic Ketoacidosis).
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10
Q

Important Aspects of Diabetic Ketoacidosis (3).

A

KDP :

  1. Ketoacidosis.
  2. Dehydration.
  3. Potassium Imbalance.
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11
Q

How is Dehydration caused by Diabetic Ketoacidosis? (5)

A
  1. Hyperglycaemia overwhelms kidneys.
  2. Glucose is filtered into the urine.
  3. Osmotic Diuresis.
  4. Polyuria - Severe Dehydration.
  5. Stimulation of Thirst Centre - Polydipsia.
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12
Q

How is Potassium Imbalance caused by Diabetic Ketoacidosis? (5)

A
  1. Insulin normally drives Potassium into cells.
  2. In DKA, serum Potassium is high/normal but total body Potassium is low.
  3. Treatment with Insulin means Potassium rapidly enters cells.
  4. Severe Hypokalaemia.
  5. Arrhythmias.
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13
Q

Clinical Features of Diabetic Ketoacidosis.

A
  1. Polyuria & Polydipsia.
  2. Nausea and Vomiting.
  3. Acetone ‘Pear-Drops’ Smell Breath.
  4. Dehydration & Hypotension.
  5. Altered Consciousness.
  6. Symptoms of Underlying Trigger e.g. Sepsis.
  7. Abdominal Pain.
  8. Kussmaul Respiration (Deep Hyperventilation).
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14
Q

Clinical Features of Type I Diabetes Mellitus (5).

A
  1. Weight Loss.
  2. Polydipsia.
  3. Polyuria.
  4. Secondary Enuresis (Bedwetting in a Previously Dry Child).
  5. Recurrent Infections.
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15
Q

Monitoring Blood Glucose (3).

A
  1. HbA1C - Glycated Haemoglobin (over last 3 months) : measure every 3-6 months in red-top EDTA bottle (target : 48 / 6.5%).
  2. Capillary Blood Glucose (target : 5-7 on waking and 4-7 before meals).
  3. Flash-Glucose Monitoring.
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16
Q

Diagnosis of Diabetic Ketoacidosis (3).

A
  1. Hyperglycaemia (Blood Glucose > 11).
  2. Ketosis (Blood Ketones > 3).
  3. Acidosis (pH < 7.35).
17
Q

Management of Diabetic Ketoacidosis (7).

A

FIG-PICK :

  1. F - IV Fluid Resuscitation with Normal Saline e.g. 1L STAT then 4L with added Potassium over next 12 Hours.
  2. I - Insulin Infusion e.g. Actrapid at 0.1 unit/kg/hour.
  3. G - Glucose (Monitor and Dextrose Infusion if below 14).
  4. P - Potassium (Monitor and Correct).
  5. I - Infection (Treat Underlying Triggers).
  6. C - Chart (Fluid Balance).
  7. K - Ketones (Monitor Directly or Use Bicarbonate Monitoring).
    * correct dehydration over 48 hours to reduce risk of cerebral oedema
18
Q

Important Consideration Before Stopping FIG-PICK.

A

Establish the patient on their normal SC Insulin regime prior to stopping the insulin and fluid infusion. Continue Long-Acting Insulin and Stop Short-Acting Insulin.

19
Q

Investigations in Type I Diabetes Mellitus (5).

A
  1. Urine Dipstick for Glucose and Ketones.
  2. Fasting and Random Glucose Levels.
  3. HbA1C NOT Accurate.
  4. C-Peptide : Low.
  5. Diabetes-Specific Antibodies.
20
Q

Give 4 Diabetes-Specific Antobodies.

A
  1. Antibodies to Glutamic Acid Decarboxylase (Anti-GAD).
  2. Islet Cell Antibodies (ICA) against Cytoplasmic Proteins in B-Cells.
  3. Insulin Autoantibodies (IAA).
  4. Insulinoma-Associated-2-Autoantibodies (IA-2A).
21
Q

Diagnostic Criteria for Type I Diabetes (2).

A
  1. Hyperglycaemia + 1 of : Ketosis, Rapid Weight Loss, Age < 50, BMI < 25 Personal/Family History of Autoimmune Disease.
  2. Consider C-Peptide and Diabetes-Specific Autoantibody Titres if Unsure Between Types.
22
Q

Management of Type I Diabetes Mellitus (5).

A
  1. Patient Education.
  2. SC Insulin Regimes (Combination of Background Long-Acting Insulin OD AND Short-Acting Insulin 30 minutes at meals).
  3. Monitor Dietary Carbohydrate Intake.
  4. Monitor Blood-Glucose on Waking, at each Meal and Before Bed.
  5. Monitor for and Manage Complications.
23
Q

Why should patients cycle their injection sites? (3)

A
  1. Injecting into the same spot can cause Lipodystrophy.
  2. Subcutaneous fat hardens.
  3. Patient does not absorb insulin properly from further injections into this spot.
24
Q

When is Metformin indicated in Type I Diabetes Mellitus?

A

If BMI is above 25.

25
Q

Sick-Day Rules of Diabetes Patients (4).

A
  1. Increase Frequency of Blood-Glucose Monitoring.
  2. Encourage Fluid Intake (3L in 24 hours).
  3. Sugary Drinks if struggling to eat.
  4. Continue Insulin (risk of DKA if stopping).
26
Q

Short-Term Complications of Type I Diabetes Mellitus (2).

A
  1. Hypoglycaemia.

2. Hyperglycaemia and DKA.

27
Q

Management of Hypoglycaemia (2).

A
  1. Combination of rapid-acting glucose (e.g. Lucozade) and slower-acting carbohydrates (e.g. biscuits and toast).
  2. Severe : IV Dextrose and IM Glucagon.
28
Q

Management of Hyperglycaemia (2).

A
  1. No DKA : Increase Insulin Dose.

2. DKA : Admission.

29
Q

Long-Term MACROVASCULAR Complications of Type I Diabetes Mellitus (4).

A
  1. Coronary Artery Disease.
  2. Peripheral Ischaemia - Poor Healing, Ulcers, Diabetic Foot.
  3. Stroke.
  4. Hypertension.
    * chronic exposure to hyperglycaemia causes damage to endothelial cells of blood vessels.
30
Q

Long-Term MICROVASCULAR Complications of Type I Diabetes Mellitus (3).

A
  1. Peripheral Neuropathy.
  2. Retinopathy.
  3. Nephropathy - especially Glomerulosclerosis.
    * leaky malfunctioning vessels that are unable to regenerate.
31
Q

Long-Term INFECTIOUS Complications of Type I Diabetes Mellitus (4).

A
  1. Urinary Tract Infections.
  2. Pneumonia.
  3. Skin/Soft Tissue Infections (e.g. Feet).
  4. Fungal Infections (e.g. Oral/Vaginal Candidiasis).
    * suppression of immune system
32
Q

Pathophysiology of Cerebral Oedema (4).

A
  1. Dehydration and Hyperglycaemia cause water to move from the intracellular space in the brain into the extracellular space.
  2. Shrinkage and Dehydration of Brain Cells.
  3. Rapid Correction of Dehydration and Hyperglycaemia causes a rapid shift into cells.
  4. Cerebral Oedema - Brain Cell Destruction and Death.
33
Q

Management of Cerebral Oedema (4).

A
  1. Monitor neurology e.g. GCS every hour and check for headaches, altered behaviour, bradycardia or changes to consciousness.
  2. Slow IV Fluids.
  3. IV Mannitol.
  4. IV Hypertonic Saline.
34
Q

Insulin Regimes in Type I Diabetes Mellitus.

A

BASAL - BOLUS REGIME :

  1. Basal - Injection of Long-Acting Insulin = Lantus in the evening.
  2. Bolus - Injection of Short-Acting Insulin = Actrapid TDS before meals.
35
Q

Complications of DKA (6).

A
  • Ketonaemia and Acidosis should resolve within 24 hours.
    1. Gastric Stasis.
    2. Thromboembolism.
    3. Arrhythmias.
    4. Cerebral Oedema, Hypokalaemia, Hypoglycaemia.
    5. ARDS.
    6. AKI.

ENDO (Endocrinology) (29 decks)

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