Type 1 DM Flashcards
What is T1DM?
A metabolic disorder characterised by hyperglycaemia due to an absolute insulin deficiency.
Destruction of pancreatic beta cells (mostly by autoimmune, T cell mediated mechanisms).
Can be idiopathic.
Why does T1DM develop?
Destruction of pancreatic beta cells in genetically susceptible individuals; probably triggered by environmental agents.
Insulin resistance has no role in the pathophysiology of T1DM.
How will patients with T1DM present?
Hyperglycaemia
Anion gap metabolic acidosis
Polyuria, polydipsia (needing to get up at night is typical)
Blurred vision - higher or fluctuating levels of glucose
Weight loss
Lassitude, generalised weakness
Infections - particularly of the skin, UTIs
Some patients will present with symptoms of DKA (abdominal pain, nausea, tachypnoea, tachycardia, lethargy and coma)
When does T1DM usually present?
Childhood or adolescence; typically 5-15 years.
What investigations do you perform for T1DM?
- Random plasma glucose - 11mmol/L or higher (in presence of symptoms of polyuria, polydipsia and weight loss)
- Fasting plasma glucose - 6.9mmol/L or higher
- 2-hour plasma glucose - 11 mmol/L or higher after 75mg oral glucose load
- HbA1c - 48 mmol/mol or higher (reflects past 3 months)
CONSIDER - fasting C-peptide (low or undetectable); indicates the absence of insulin secretion from pancreatic beta cells.
What is diagnosis for T1DM based on?
Random plasma glucose >11 mmol/L in a symptomatic patient.
Fasting plasma glucose >6.9 mmol/L
Plasma glucose >11 mmol/L 2 hours after a 75g oral glucose load
HbA1c > 48 mmol/L. 2 readings, 4 weeks apart.
Repeat tests in asymptomatic patients
Elevated plasma or urine ketones in the presence of hyperglycaemia is suggestive of T1DM over T2DM.
Low C-peptide/autoimmune markers are consistent with T1DM.
Random blood glucose is better as it may be sudden onset.
The hallmarks of T1DM:
Weight loss Ketoacidosis AutoAbs - GAD, islet cell Presence of other autoimmune disease Thirst and polyuria Elevated plasma or urine ketones Low C-peptide
Which genes are associated with T1DM?
Polymorphisms in the gene encoding preproinsulin and HLA-DQB, HLA-DR , PTPN22 and CTLA-4.
What is mononeuritis multiplex?
Cranial mononeuropathy III - diabetic type.
Painless III nerve palsy; most common cranial nerve disorder in people with diabetes. Causes double vision and eyelid drooping (ptosis), and sometimes pain in the head or behind the eye.
May occur along with diabetic peripheral neuropathy.
Due to damage to the small blood vessels that feed the III nerve.
Preservation of pupillary response.
Also cranial nerve VI.
Diagnosing diabetes in pregnant women:
Use OGTT.
Monitoring diabetes in pregnant women/sickle cell patients/patients with increased red cell turnover:
Use fructosamine.
How does DKA present?
Abdominal pain Nausea Vomiting Coma Tiredness Kussmaul breathing Ketotic breath Signs of dehydration
What are the microvascular complications of DM?
- Neuropathy
- Nephropathy
- Retinopathy
Neuropathy in DM:
Distal symmetrical sensory neuropathy, painful neuropathy, carpal tunnel syndrome, diabetic amyotrophy (wasting of asymmetrical proximal muscle), mononeuritis, autonomic neuropathy (e.g. postural hypotension), gastroparesis (pain, n/v), impotence, urinary retention.
Nephropathy in DM:
Microalbuminuria Proteinuria Eventually renal failure Chronic UTIs Renal papillary necrosis
Retinopathy in DM:
Dot and blot haemorrhages, hard exudates Cotton wool spots, venous beading New vessels on the disc and elsewhere Macular oedema, exudates within 1 disc diameter of the centre of the fovea; haemorrhage within 1 disc diameter of the centre of the fovea and a decrease in acuity. Patients are also prone to glaucoma.
Microvascular complications in DM:
Ischaemic heart disease, stroke/TIA, peripheral vascular disease.
Most patients with MI will have poorly controlled blood glucose.
What are the complications of DM?
Microvascular (retinopathy, neuropathy, nephropathy), microvascular (ischaemic heart disease, stroke, TIA).
Susceptibility to infections (especially on feet/UTIs).
Complications of insulin treatment.
What are the complications of insulin treatment?
Weight gain
Fat hypertrophy at injection sites
Hypoglycaemia - missing a meal or insulin overdose
How does a hypoglycaemic episode present?
Neuroglycopenic and adrenergic symptoms: Personality change Coma Fits Confusion Pallor Sweating Tremor Tachycardia Palpitations Dizziness Hunger Focal neurological symptoms
Symptoms may be masked by autonomic neuropathy, B-blockers or adaptation after recurrent episodes.
What is DKA?
Low insulin and an increase in counter-regulatory hormones increases hepatic gluconeogenesis and decreases peripheral glucose utilisation.
The renal resorptive capacity of glucose is exceeded; causes glycosuria, osmotic diuresis and dehydration.
Increased lipolysis leads to ketogenesis and metabolic acidosis (high anion gap).
DKA may be precipitated by infection, errors in management, newly diagnosed diabetes, other disease.
What investigations do you perform for T1DM?
Blood glucose.
FBC, U&Es, lipid profile, urine albumin:creatinine ratio, urine dip, urine MC&S.
CXR - exclude infection.
ECG - ischaemic changes.
What would bloods show in T1DM?
MCV, reticulocytes due to increased RBC turnover (may cause misleading HbA1c levels).
Why U&Es in T1DM?
Monitor nephropathy and hyperkalaemia caused by ACE-Is.
