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Flashcards in Diabetes Deck (23)
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1
Q

What are the clinical features of diabetes mellitus?

A

Acute presentation- young people, 2-6 week history of thirst, polyuria and weight loss. Ketoacidosis if symptoms aren’t recognised
Subacute presentation- older patients, less marked symptoms and extending over months. Lack of energy, visual problems and pruritus vulvae or balanitis due to candida
Retinopathy
Asymptomatic

2
Q

What are the investigations for diabetes?

A

Fasting (no calorie intake for at least 8 hours) plasma glucose >7
Random plasma glucose >11
1 value in symptomatic patients, 2 values in asymptomatic
HbA1c of 48

3
Q

What is the management plan for diabetes?

A

Achieving goof glycemic control
Advice regarding exercise, weight loss and improvement in glycemic control in type 2
Aggressive treatment of hypertension and hyperlipidaemia
Regular checks of metabolic control and physical examination of diabetic complications

4
Q

What is checked at least once a year in diabetics?

A

Biochemical assessment of metabolic control (e.g. glycosylated haemoglobin test)
Measure body weight
Measure blood pressure
Measure plasma lipids (except in extreme old age) Measure visual acuity
Examine state of retina (ophthalmoscope or retinal photo) Test urine for proteinuria/microalbuminuria
Test blood for renal function (creatinine)
Check condition of feet, pulses and neurology Review cardiovascular risk factors
Review self-monitoring and injection techniques Review eating habits
Review and reinforce structured education

5
Q

What is metformin?

A

Biguanide
Reduces glucose production by the liver and sensitises target tissues to insulin
First line treatment after diet control
Reduces cardiovascular risk
Doesn’t cause weight gain like sulphonyureas
Side effects- anorexia and diarrhoea

6
Q

What are short acting (soluble) insulins?

A

Start working within 30–60 minutes and last
for 4–6 hours. They are given 15–30 minutes before meals in patients on multiple-dose regimens and by continuous intravenous infusion in labour, during medical emergencies, at the time of surgery and in patients using insulin pumps.

7
Q

What are short-acting insulin analogues?

A

The human insulin analogues (insulin aspart, insulin lispro, insulin glulisine) have a faster onset and shorter duration of action than soluble insulin. They have a reduced carry-over effect compared to soluble insulin and are routinely used in type 1 diabetes.

8
Q

What are longer-acting insulins?

A

Longer-acting insulins. Insulins premixed with retarding agents (either protamine or zinc) are intermediate (12–24 hours) or long acting (more than 24 hours). The protamine insulins are also known as isophane or Neutral Protamine Hagedorn (NPH) insulins
Used in type 2, intensified therapy, troublesome hypoglycaemia

9
Q

What are the classic insulin regimens?

A

Basal bolus regimen, with one or two subcutaneous injections of an intermediate or long- acting insulin a day (the basal component) and a bolus of rapid-acting insulin with meals and substantial snacks
Twice-daily regimen of premixed rapid and intermediate or long-acting insulin is suitable (type 2)

10
Q

What are the complications of insulin therapy?

A

Hypoglycaemia
Lipohypertrophy at injection site, allergic reactions, injection site abscesses
Insulin resistance
Weight gain

11
Q

What are the symptoms of hypoglycaemia?

A

When levels fall below 3
Hunger, sweating, pallor, tachycardia
Untreated- confusion, personality change, fits, hemiparesis, coma

12
Q

How is hypoglycaemia treated?

A

Rapidly absorbed carbohydrate or glycogen given orally
Unconcious- IV dextrose (50ml of 20%)
Intramuscular glucagon (1mg)

13
Q

What is diabetic ketoacidosis?

A

Results from insulin deficiency
Results from: previously undiagnosed diabetes, interruption of insulin therapy, stress on intercurrent illness
Common error- insulin stopped when patient is not eating or vomiting in type 1

14
Q

What are the clinical features of ketoacidosis?

A
Profound dehydration and vomiting 
Eyes are sunken, tissue turgor reduced, tongue is dry, hypotension 
Kussamul's respiration (deep rapid)
Breath smells of ketones 
Disturbance of consciousness
15
Q

What are the investigations for ketoacidosis?

A
Hyperglycaemia >11
Ketoanaemia >3 (finger prick)
Acidosis pH <7 and/or bicarb <15
Urine dipstick- glycosuria and ketonuria
Urea and creatinine raised (dehydration)
Elevated white cell count
16
Q

What is the hyperosmolar hperglycaemic state?

A

This is a life-threatening emergency characterized by marked hyperglycaemia, hyperosmolality and mild or no ketosis
Uncontrolled type 2 diabetes
Precipitated by infection (pneumonia)

17
Q

What are the clinical features of the hyperosolar hyperglycaemic state?

A

Insulin levels are reduced, but sufficient to prevent ketogenesis
Glucose production is unrestrained
Profound dehydration
Reduced level of unconsciousness
Urea, glucose and serum osmolality are higher than in ketoacidosis

18
Q

What is diabetic eye disease?

A

Diabetic retinopathy with lesions developing in the retina and the iris
Cataracts develop earlier in diabetics than in the general population. Temporary blurred vision also occurs caused by reversible osmotic changes in the lens in patients with acute hyperglycaemia.
External ocular palsies – the sixth and third nerve are most commonly affected.

19
Q

What is the classification of diabetic retinopathy?

A

Non-proliferative- tiny red dots (capillary microanerysms), larger red spots (intraretinal blot haemorrhages), hard exudates (capillary leaks of plasma rich in lipids and protein)
Pre-proliferative- venous bleeding/loops, growth of intraretinal new vessels, multiple cotton wool spots (oedema from retinal infarcts)
Proliferative- preretinal blood vessel formation, preretinal or subhyaloid haemorrhage, vitreous haemorrhage
Advanced retinopathy- retinal fibrosis, traction retinal detachment
Maculopathy- macula oedema, perimacular hard exudates

20
Q

What is diabetic nephtopathy?

A

On microscopy there is thick- ening of the glomerular basement membrane and later glomerulosclerosis, which may be a diffuse or nodular form (Kimmelstiel–Wilson lesion)
Intermittent albuminuria followed by persistent proteinuria
UTIs are common
Ischaemic lesions

21
Q

When should a second drug be added in type 2 diabetes?

A

If HbA1c >58 mol/mol

22
Q

What are the type 2 diabetes blood pressure targets?

A

No organ damage <140/80

End-organ damage <130/80

23
Q

What are patients with a DKA at high risk if getting?

A

Thromboembolism