Diabetes mellitus Flashcards

1
Q

What is type 1 diabetes mellitus?

A

Metabolic hyperglycaemic condition caused by absolute insufficiency of pancreatic insulin production

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2
Q

What is the aetiology of type diabetes mellitus?

A
  • Caused by destruction of the pancreatic insulin producing B cells, resulting in absolute insulin deficiency. The B cell destruction is caused by an autoimmune process in 90% of patients - Likely to occur in genetically susceptible subjects and is probably triggered by environmental agents. Polymorphisms of a number of genes may influence the risk of type 1 diabetes. These include the gene encoding preproinsulin and a number of genes related to immune system function - Pancreatic B cell autoantigens may play a role in the initiation or progression of autoimmune islet injury. These include gluatmic acid decarboxylase (GAD) insulin, insulinoma associated protein 2 and cation efflux zinc transporter (ZnT8)
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3
Q

What is the epidemiology of type 1 diabetes mellitus?

A
  • On of the most common chronic diseases in childhood with a prevalence of 0.25% in UK - Considerable geographic variation in incidence
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4
Q

What are the presenting symptoms of type 1 diabetes mellitus?

A
  • Often of juvenile onset (under 30yrs). Polyuria/nocturia (osmotic diureses caused by glycosuria), polydipsia (thirst), tiredness, weight loss. Symptoms of complications. Diabetes ketoacidosis: Nausea, vomiting, abdominal pain, polyuria, polydipsia, drowsiness, confusion, coma, Kussmaul breathing (deep and rapid) ketotic breath, signs of dehydration (e.g. dry mucous membranes & reduced tissue turgor) - Signs of complications: examination of feed, test for neuropathy - Signs of associated autoimmune conditions e.g. vitiligo, Addison’s disease, autoimmune thyroid disease
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5
Q

What are the investigations for type 1 diabetes mellitus?

A

Blood glucose: Fasting blood glucose over 7mmol/L or random blood glucose over 11 mmol. 2 pos results needed before diagnosis HbA1C: Estimates overall blood glucose levels in past 2-3 months FBC: MCV, reticulolytes ( raised erythrocyte turnover causes misleading HbA1c levels) U&E: Monitor for nephropathy and hyperkalaemia caused by ACE inhibitors Lipid profile Urine albumin creatinine ratio CXR: exclude infection ECG: Look for ischaemic changes

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6
Q

How is type 1 diabetes mellitus managed?

A

Diabetes keoacidosis consider HDU/ICU input, central line, arterial line and urinary catheter if severe acidosis, hypotensive or oliguric - Insulin - Fluids - Potassium replacement - Monitor blood glucose - Broad spectrum antibiotics if infection suspected - NBM for at least 6h (gastroparesis is common) - NG tube: If GCS is reduced to prevent vomiting and aspiration - Refer to diabetes team for patients education

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7
Q

What does glycaemic control involve in type 1 diabetes mellitus?

A
  • Advice and patient education: Diabetes nurse specialist dietitians. SC insulin: Short acting insulin (e.g. Lispro, aspart, glusine) three times daily before each meal and one long-acting insulin. Injection sites should be rotated - Insulin pumps slightly better glycaemic control but are costly and cumbersome for some patients and ketoacidosis may occur if pump malfunction - Monitor: control of symptoms, regular finger prick tests by patient, monitoring HbA1c levels - Screening and management of complications Treatment of hypoglycaemia
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8
Q

What are the possible complications of type 1 diabetes mellitus?

A
  • Diabetic ketoacidosis: reduced insulin and increased counter-regulatory hormones result in raised hepatic gluconeogenesis and decreased peipheral glucose utilisation. - Microvascular: Retinopathy, nephropathy, neuropathy - Macrovascular: Peripheral vascular disease, ischaemic heart disease, stroke (TIA) - Complications of insulin treatment: Weight gain, fat hypertrophy at insulin injection sites - Hypoglycaemia caused by missed a meal r overdosage of insuline
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9
Q

What is the prognosis of type 1 diabetes mellitus?

A

Depends on early diagnosis, good glycaemic control and compliance with screening and treatment - Vascular disease and renal failure are major causes of increased morbidity and mortality

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10
Q

What is type 2 diabetes mellitus?

A

Characterised by increased peripheral resistance to insulin action, impaired insulin secretion and increased hepatic glucose output

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11
Q

What is the aetiology of type 2 diabetes mellitus?

A
  • Multi-factoiral ( fenetic and environmental - Obesity: raised plasma free fatty acid levels and adipokines secreted by adipocytes (e.g. leptin, adinonectin, TNF-a, resistin) contribute to peripheral insulin resistance. Chronic hyperglycaemia can have a toxic effect on B cells - Secondary diabetes: Pancreatic diseases (chronic pancreatitis, hereditary haemochromatosis, pancreatic cancer, surgical removal of pancreas), Endocrinopathies (Cushings), Drugs (eg. corticosteroids
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12
Q

What is the epidemiology of type 2 diabetes mellitus?

A

People of Asian, African and Hispanic descent are at greater risk. Incidence has increased over last 20 years, in parallel with increased obesity worldwise

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13
Q

What are the presenting symptoms of type 2 diabetes mellitus?

A
  • May be incidental finding - Polyuria, polydipsia, tiredness. Patients may present with hyperosmolar hyperglycaemic state (also known as hyperosmolar, non ketotic state). Infections - Assess for other cardiovascular risk factors: hypertension, hyperlipidaemia and smoking
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14
Q

What are the signs of type 2 diabetes mellitus on examination?

A
  • Measure weight and height, weight circumference, blood pressure - Look for signs of complications - Diabetic foot: both ischaemic and neuropathic signs. Dry skin, reduced subcutaneous tissue, corns and calluses, ulceration, gangrene - Charcot’s arthropathy and signs of peripheral neuropathy, foot pulses are decreased in ischaemic foot - Skin changes: aNecrobiosis lipoidica diabeticorum (well-dermacated plaques on the shins or arm with shiny atrophic surface and red-brown edges), granuloma annulare (flesh coloured paplules coalescing in rings on the back of hands and fingers), diabetic dermopathy (depressed pigmented scars on shins)
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15
Q

What are the investigations for type 2 diabetes mellitus?

A

Diagnosed if one or more of the following are present - Symptoms of diabetes and random plasma glucose over 11.1mmol/L - Fasting plasma glucose over 7mmol - Two hour plasma glucose over 11.mmol after a 75g oral glucose tolerance test Monitor: HbA1c, U&Es, lipid profile, estimated glomerular filtration rate using MDRD calculator - Spot urine albumin. Creatinine ratio (to detect microalbuminaria)

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16
Q

How is type 2 diabetes mellitus managed?

A
  • Glycaemic control - Sulphonylureas (gliclazide) block ATP-sensitive K channels in B cells, stimulating insulin release. Metformin inhibits hepatic gluconeogenesis. Plioglitazone activate PPAR gamma & reduced peipheral insulin resistance - Retinopathy: Regular digital retinal photography, ophthomology referral and laser photo-coagulation if necessary - Nephropathy: Monitor U&Es and estimated GFR using MDRD calculator, spot urine analysis - Neuropathy: Regular examination and inspection of the feet for ulcers, 10g monofilament testing, joint vibration, foot hygeine, amitriptuline - Vascular disease: Regular examination of foot pulses - Diabetic foot: Educate to examine foot regularly. Diabetic footwear. Podiatry assessment. For infections, clean and dress regularly, swan for culture and sensitivity - Screen for and test cardiovascular risks: Lose weight, exercise, stop smoking, BP control, all diabetics patients should be started on a statin. Aspirin in patients with diabetes and additional cardiovascular risk factor
17
Q

What does glycaemic control in type 2 diabetes mellitus involve?

A
  • At diagnosis: Lifestyle & metformin - If HbA1c more than 7% after 3 months: Lifestyle & metformin & sulphonurea - If HbA1c more than 7% after 3 months: Lifestyle & metformin % basal insulin - If HbA1c more than 7% and fasting blood glucose less than 7mmol/L: Add premeal rapid acting insulin - Sulphonurea may be given as monotherapy in patients who cannot tolerate metformin
18
Q

What advice and patient education should be given to type 2 diabetics?

A

INFORM PT - Information: Diabetic nurses, leaflets, websites etc, explaining diabetes control, complications - Nutrition: Optimizing meal plans, diet - Foot care: Regular inspection, appropriate footwear, role of chiropodist - Organisations: Local and national support groups - Recognition and treatment of hypoglycaemia - Monitoring capillary blood glucose and charting it. Monitoring for ketones during intercurrent illness - Pregnancy: Strict glycaemic control and planning of conception - Treatment: Action, duration and administration, technique for insulin, change the site of injection, explain the need to plan exercise

19
Q

What are the possible complications of type 2 diabetes mellitus?

A
  • Hyperosmolar hyperglycaemic state: Due to insulin deficiency as diabeteic ketoacidosis but patient is usually old and may be presenting for the first time, history is longer (e.g. 1 week). Distal symmetrical sensory neuropathy, painful neuropathy, carpal tunnel syndrome, diabetic amyotrophy, mononeuritis, autonomic neuropathy, gastroparesis, impotence, urinary retention. Nephropathy: Microambinuria, proteinuria and eventually renal failure. - Retinopathy: Backgroun: dot and blot haemorrhages, hard exudates. Pre-proliferative: Cotton wool spots, venous beading. Proliferative: New vessels on the disc and elsewhere. Maculopathy: Macular oedema, exudates within 1 disc diameter of the centre of the fovea, haemorrhage within 1 disc diameter of centre of the fovea associated with reduced visual acuity. Also prone to glaucoma, cataracts, transient visual loss - Macrovascular: ischaemic heart disease, stroke, pvd
20
Q

What is the prognosis of type 2 diabetes mellitus?

A
  • Intensive therapy to achieve lower levels of glycaemia, lowers the risk of development and progression of diabetic microvascular complications