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Medicine Notes Endocrinology Notes

Diabetes Notes

Updated Diabetes Notes

Endocrinology Notes

Endocrinology

Approximately 28 pages

Complete set of notes on endocrinology. Covering the most common endocrine problems, with the basic science and anatomy along with investigations and management of both chronic disease and acute presentation and crises. Colour-coded per topic and using flow diagrams and images for visual learners. Ideal for clinical finals...

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The following is a more accessible plain text extract of the PDF sample above, taken from our Endocrinology Notes. Due to the challenges of extracting text from PDFs, it will have odd formatting:

Diabetes

Type 1 Diabetes

Epidemiology

  • Can occur at any age, usually juvenile onset (13 years)

Aetiology

  • Genetic predisposition (HLA DR3 + HLA DR4) + environmental trigger (? Viral)

Pathophysiology

  • Autoimmune destruction of Beta cells of Islet of Langerhan (pancreas)

  • Complete insulin deficiency

Clinical features

  • Classic triad

    • Polydypsia

    • Polyuria

    • Weight loss

May present in DKA

Fatigue

Investigations

  • Hx + postitive test or 2 positive tests on separate occasions

    • Fasting plasma glucose 7.0mmol/L

    • Random blood glucose 11.0 mmol/L

    • Oral glucose tolerance test 11.0 mmol/L (75g in 300ml water)

  • Urine dip for glycosuria

  • HbA1c < 7.5% normally, <6.5% if increased CV risks (previous stroke/MI)

Management

  • MDT (nurse specialist, dietician, GP/consultant, podiatrist)

  • Education

    • BMs, exercise, diet (reduce sat fats, sugar and increase starch carbs, moderate protein), smoking cessation, foot care

    • Inform DVLA (patient)

  • Insulins

    • Dose adjustable regime to suit lifestyle

      • BD regime = twice daily premixed insulin by pen injector e.g novomix 30

      • QDS regime = before meals

      • Once daily regime before bedtime – intermediate or long-acting insulin

    • DAFNE course (dose adjustment for normal eating)

      • If ill, insulin requirements increase even if food intake decreases

      • Increase BMs

      • Increase insulin if glucose is higher

      • Admit if patient is vomiting, dehydrated or ketotic

Diabetic Ketoacidosis (DKA)

Lipolysis Free fatty acids ketone bodies Ketoacidosis (low pH)

Symptoms

  • Sluggish, extreme tiredness, extreme thirst, constant urination, fruity smell to breath (ketotic breath), hyperventilation, nausea, vomiting, abdominal pain, coma

Precipitants

  • Infection

  • Surgery

  • MI

  • Non-compliance

  • Wrong insulin dose

For diagnosis need ketosis + acidosis

Investigations

  • Bloods

    • Glucose

    • U+E (risk of hypokalaemia with treatment of DKA, hyperkalaemia without)

    • Amylase (pancreatitis often present)

    • FBC (infection screen, WCC, platelets)

    • ABG (acidosis)

    • Cultures (infection screen)

  • Imaging

    • CXR (Infection)

  • Urinalysis (ketones)

  • ECG (hyperkalaemia)

Management

  • Iv access

  • Fluids (resuscitation with saline – boluses)

  • Check plasma glucose

  • NG tube if vomiting or unconscious

  • Start insulin sliding scale

  • Treat underlying cause

  • K+ replacement +/- phosphate replacement

Complications

  • Cerebral oedema

  • Aspiration

  • Hypokalaemia

  • Thromboembolism

Type 2 Diabetes

Aetiology

  • Genetic predisposition

  • Overweight

  • Metabolic syndrome

  • Asians

Pathophysiology

  • Slow progressive loss of B cells with disorders of insulin secretion and tissue resistance to insulin

  • Relative insulin deficiency

Clinical features

  • Often asymptomatic

  • Fatigue, persistent infections, slow healing, minor skin damage or visual problems

  • May progress from glucose intolerance

    • Fasting < 7mmol/L, OCTT >7.8 but <11.1 mmol/L

Management

MDT (podiatrist, dietician, nurse specialist)

Education

1st line – diet and exercise

2nd Line – oral hypoglycaemics, followed by insulin when necessary

  • Sulphoylureas (e.g gliclazide 12hours, BD)

    • Closes K+ channels on B cells = depolarized = increased insulin secretion

    • ADRs = Hypos, weight gain

    • Requires Beta cells so useful in early diabetes

  • Biguanides (e.g metformin)

    • Mechanism not fully understood but increases glucose uptake + utilization, decreases hepatic gluconeogenesis, reduces VLDLs, LDLs

    • ADRs = GI disturbance, lactic acidosis (don’t give in renal/liver disease, hypoxic pulmonary disease, HF or shock)

    • Doesn’t cause hypos or weight gain

  • PPAR gamma agonists e.g glitazones

    • Improve insulin sensitivity + B cell function

      • Increase transcription of GLUT 1 + 4 by activating PPAR gamma receptors

    • Weight gain

    • Add-on therapy

    • ADR = hepatotoxicity, hypos, fluid retention

  • Alpha glucosidase inhibitors (acarbase)

    • Block conversion of carbohydrates to monosaccharides, therefore delay absorption = less increase in glucose levels after a meal

    • Gives B cells time to augment response

    • ADR = flatulence, loose stools, abdominal pain, bloating

Diabetic complications

  • Microvascular

    • Retinopathy – leaky vessels

    • Nephropathy – hyper-filtration – thickening of GBM - microalbumaenia

    • Neuropathy

      • Damage to vessels nourishing peripheral nerves (glove and stocking neuropathy)

      • Cranial nerves VI + VII...

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