12. Type 1 Diabetes Flashcards
Define type 1 diabetes.
What are the 2 types?
2
Insulin deficiency leading to metabolic disorder characterized by hyperglycaemia due to autoimmune destruction of beta cells by T lymphocytes
Autoimmune - Type 1a
- Islet cell antibodies
- GAD antibodies
- Insulin autoantibodies
- A/w other autoimmune disorders
- Increased risk of coeliac disease
Non-Autoimmune - Type 1b
- Antibody negative
- More common in ethnic population
Describe the epidemiology of type 1 diabetes.
What are the clinical presentations?
(6)
How do you diagnosis T1D?
(4)
Begins in childhood (young age)
Short history of osmotic symptoms
No complications at time of dx
Require life-long therapy
CP
- Weight loss
- Polyphagia: excessive eating
- Polyuria
- Polydypsia
- Glycosuria
- Glucose not resorted in renal tubules, so filtered out in urine - High serum glucose (lack of insulin = decrease of glucose uptake into adipose tissue and skeletal muscle = increase in glucose in blood)
DX
- Random glucose ≥ 11.1mmol/l with osmotic symptoms or
- Fasting glucose ≥ 7.0 mmol/l on 2 occasions or
- 2 hour glucose value post 75gm oral glucose tolerance test of ≥ 11.1mmol/l or
- HbA1c ≥ 6.5% (48mmol/mol)
What are the treatment options for type 1 diabetes?
(2)
What are examples of basal and bolus injections?
(5)
What are the aims of the treatment?
(6)
TX
- Insulin (basal – bolus regime)
- 4-5 injections/day
- SE’s: hypoglycaemia and weight gain - Mixture Insulin
- (Novo Mix 30 —> 3/10 of novrapid, 7/10 insulatard // Humalog Mix 25 —> 1/4 Humalog, 3/4 Insulatard)
- Twice a day, inflexible regime
- High risk of hypoglycaemia
BASAL
- NPH or Insulatard
- Glargine or Lantus
- Levemir or Detemir
- Degludec
- Insulin Tuojeo (glargine U300)
- Levemir and Glargine cause less hypoglycaemia particularly at night when compared to NPH insulin
- Usually given at bedtime
- Levemir is given usually twice a day
- Degludec and Tuojeo are long acting basal insulins
BOLUS
- Actrapid (Regular)
- NovoRapid (Aspart)
- Humalog (Lispro)
- Glulisine (Apidra)
- FiAsp (fast acting novorapid
AIMS
- Glycated Hemoglobin (HBA1c) £ 7.0% or £ 53mmol/mol
- Pre-prandial blood glucoses 5 to 7mmol/l
- Post-prandial blood glucose <10mmol/l
- No severe hypoglycaemic episodes
- Avoid complications of diabetes
- Maintain quality of life
What is glycated hemoglobin?
- Glucose binds to the valine portion of the hemoglobin side chain
- Reflects glucose control over a 2 to 3 month period
- Aim in type 1 diabetes is a HBA1c of <7.0%
- Hemoglobinopathies, hemolytic or iron deficiency anaemias interfere with interpretation of test
What are the microvascular complications of diabetes?
(3)
What are the macrovascular complications of diabetes?
(3)
MICROVASCULAR
- Retinopathy
- Nephropathy
- Neuropathy
MACROVASCULAR
- Coronary artery disease
- Cerebrovascular disease
- Peripheral arterial disease
Describe retinopathy.
- Retinopathy
- Background diabetic retinopathy
o Microaneurysms
o Exudates
o Haemorrhages (dot and blot)
—> Visual acuity is normal, but problems can arise
- Nonproliferative diabetic retinopathy
o Dot aneurysms: hypercellular, saccular outpouchings of the capillary wall)
o Blot hemorrhages resulting from vascular occlusion
o Cotton-wool spots: retinal nerve fiber infarcts due to ischemia)
o Hard exudates: lipid and protein exudates due to excessive vascular permeability),
o Venous beading: abnormal appearance of retinal veins with localized swellings and constrictions resembling sausage links - Pre-proliferative
- Proliferative
o New Vessels at Disc (NVD)
o New Vessels Elsewhere (NVE)
o Vitreal haemorrhage
—> Neovascularisation of iris: budding of the capillaries on the venous side of the circulation and is in 2 sites, either on the optic disc or at the junction of normal and ischaemic retina
—> Growth of vessels onto posterior surface of vitreous gel occurs and as vitreous degenerates vessels are stretched = vitreous haemorrhage
—> Can cause intraocular pressure (becomes neovascular glaucoma) - Advanced Diabetic Retinopathy
o Vitreous haemorrhage
o Tractional retinal detachment
o Rubeosis iridis: causes neovascular glaucoma (painful blind eye)
—> No perception light vision within 5 years due to vitreous haemorrhage and tractional detachment of the retina
Describe nephropathy.
- Ward dipstick (not used as a screening test)
- Early morning urine corrected for creatinine – albumin creatinine ratio (UACR)
- UACR screens for microalbuminuria
—> ≥ 2.5mg/mmol in males
—> ≥ 3.5mg/mmol in females
Describe neuropathy (peripherally polyneuropathy).
Peripheral polyneuropathy: clinical neuropathic syndromes described in patients with diabetes mellitus include dysfunction of almost every somatic peripheral and autonomic nervous systems
o Can cause:
—> Small nerve fibre dysfunction: hyperalgesisa, reduced light tough and sensation
• Example: contractures —> hammer toe —> improper weight-bearing —> ulcer —> infection —> osteomyelitis —> amputation
—> Large nerve fibre dysnfunction: reduced vibration, weakness, muscle wasking, depressed tendon reflexes
- Motor neuropathy
- Sensory neuropathy
- Mixed sensori-motor neuropathy
- Compression neuropathies
- Cranial nerve palsies
- Mononeuritis multiplex
- Autonomic neuropathy
- Focal neuropathies: mononeuritis and entrapment syndromes
—> Mononeuropathies due to vasculitis and subsequent ischemia or infarction of nerves
- Carpal tunnel syndrome occurs in 2x as much in diabetic people
What is diabetic ketoacidosis (DKA)?
What criteria is used to make a diagnosis?
(3)
What are risk factors?
(7)
What is the clinical presentation?
(3)
What are the symptoms?
(9)
What are the signs?
(4)
How do you manage DKA?
(5)
- Characterized by excess serum ketones
- Life threatening hyperglycaemic complication of diabetes
—> In younger patients may be first presentation of DM - Arises w/ stress = epinephrine stimulates glucagon = increase in glucogneogensis, glycolysis, and lipolysis = increase in FFAs = ketone bodies (synthesized in liver)
CRITERIA
- Ketonaemia: >3.0mmol/L or significant ketonuria (more than 2+ on standard urine sticks)
- Blood glucose: >11.0mmol/L or known diabetes mellitus
- Bicarbonate (HCO3-): <15.0mmol/L and/or venous pH <7.3
RISK FACTORS
- Diagnosis of T1DM
- Poor nutrition
- Missed/inadequate insulin doses
- Sepsis
- Trauma
- Surgery
- Corticosteroid use or substance abuse
CP
- Hyperglycaemia > 300 mg/dL
- Anion gap metabolic acidosis
- Hyperkalemia
SYMPTOMS
- Polyuria
- Polydipsia
- Weight loss
- Lethargy
- N+V
- Abdominal pain
- Muscle cramps
- Kussmal breathing
- Fruity breath (b/c ketones)
SIGNS
- Tachypnoea: ketotic breath & Kussmaul’s breathing
- Neurological signs: reduced GCS, confusion/coma, seizures
- Volume depletion: decreased skin turgor, dry mucous membranes, tachycardia, low JVP, hypotension, oliguria
- Absent bowel sounds
MANAGEMENT
- Correction of volume deficits
- Insulin therapy
- Potassium monitoring/replacement
- Acidosis correction
- IV antibiotics
How would you educate a patient on diabetes?
5
- Teach how to inject
- Teach how to test their blood glucose
- Teach how to treat hypoglycaemia
- Advise re dose adjustment for alcohol, exercise, sickness etc.
- Quality of life
