Type 1 DM

Question 1

What is T1DM?

Answer 1

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.

Question 2

Why does T1DM develop?

Answer 2

Destruction of pancreatic beta cells in genetically susceptible individuals; probably triggered by environmental agents.
Insulin resistance has no role in the pathophysiology of T1DM.

Question 3

How will patients with T1DM present?

Answer 3

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)

Question 4

When does T1DM usually present?

Answer 4

Childhood or adolescence; typically 5-15 years.

Question 5

What investigations do you perform for T1DM?

Answer 5

1. Random plasma glucose - 11mmol/L or higher (in presence of symptoms of polyuria, polydipsia and weight loss)
2. Fasting plasma glucose - 6.9mmol/L or higher
3. 2-hour plasma glucose - 11 mmol/L or higher after 75mg oral glucose load
4. 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.

Question 6

What is diagnosis for T1DM based on?

Answer 6

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.

Question 7

The hallmarks of T1DM:

Answer 7

Weight loss
Ketoacidosis
AutoAbs - GAD, islet cell 
Presence of other autoimmune disease
Thirst and polyuria
Elevated plasma or urine ketones 
Low C-peptide

Question 8

Which genes are associated with T1DM?

Answer 8

Polymorphisms in the gene encoding preproinsulin and HLA-DQB, HLA-DR , PTPN22 and CTLA-4.

Question 9

What is mononeuritis multiplex?

Answer 9

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.

Question 10

Diagnosing diabetes in pregnant women:

Answer 10

Use OGTT.

Question 11

Monitoring diabetes in pregnant women/sickle cell patients/patients with increased red cell turnover:

Answer 11

Use fructosamine.

Question 12

How does DKA present?

Answer 12

Abdominal pain
Nausea
Vomiting
Coma
Tiredness
Kussmaul breathing
Ketotic breath
Signs of dehydration

Question 13

What are the microvascular complications of DM?

Answer 13

1. Neuropathy
2. Nephropathy
3. Retinopathy

Question 14

Neuropathy in DM:

Answer 14

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.

Question 15

Nephropathy in DM:

Answer 15

Microalbuminuria 
Proteinuria
Eventually renal failure
Chronic UTIs 
Renal papillary necrosis

Question 16

Retinopathy in DM:

Answer 16

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.

Question 17

Microvascular complications in DM:

Answer 17

Ischaemic heart disease, stroke/TIA, peripheral vascular disease.
Most patients with MI will have poorly controlled blood glucose.

Question 18

What are the complications of DM?

Answer 18

Microvascular (retinopathy, neuropathy, nephropathy), microvascular (ischaemic heart disease, stroke, TIA).
Susceptibility to infections (especially on feet/UTIs).
Complications of insulin treatment.

Question 19

What are the complications of insulin treatment?

Answer 19

Weight gain
Fat hypertrophy at injection sites
Hypoglycaemia - missing a meal or insulin overdose

Question 20

How does a hypoglycaemic episode present?

Answer 20

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.

Question 21

What is DKA?

Answer 21

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.

Question 22

What investigations do you perform for T1DM?

Answer 22

Blood glucose.
FBC, U&Es, lipid profile, urine albumin:creatinine ratio, urine dip, urine MC&S.
CXR - exclude infection.
ECG - ischaemic changes.

Question 23

What would bloods show in T1DM?

Answer 23

MCV, reticulocytes due to increased RBC turnover (may cause misleading HbA1c levels).

Question 24

Why U&Es in T1DM?

Answer 24

Monitor nephropathy and hyperkalaemia caused by ACE-Is.

Question 25

Why perform urine creatinine:albumin ratio?

Answer 25

To look for microalbuminuria - moderately increased levels of albumin due to nephropathy.

Question 26

What does urine show in T1DM?

Answer 26

Glycosuria, ketones.

May be evidence of UTI.

Question 27

Why do you get hyperkalaemia in DKA?

Answer 27

Insulin drives K+ into the cell; in ketoacidosis cells exchange H+ from acidosis for K+, which is then driven into the ECF and exacerbates hyperkalaemia.
This will rapidly fall on treatment.

Question 28

Treatment for normal blood pressure and microalbuminuria:

Answer 28

ACE-inhibitor.

Aim for 130/<80.

Question 29

What is the target BP in DM?

Answer 29

<130/<80