Medicine

Topics In This Section

Cardiology

Acute Coronary Syndrome
Atrial Fibrillation
Bradyarrhythmia
Dyslipidemia
Essentials Hypertension
Heart Failure
Pericarditis
Rheumatic Fever
Stable Angina
Supraventricular Tachycardia

Dermatology

Acne vulgaris
Ezcema
Psoriasis
Seborrhoeic Dermatitis

Endocrinology/Metabolic

Adrenal Insufficiency
Diabetes Insipidus
Diabetes Mellitus
Diabetic Ketoacidosis
Hypercalcaemia
Hyperkalaemia
Hyperthyroidism
Hypocalcaemia
Hypokalaemia
Paget's Disease of the Bone
Secondary Hyperparathyroidism

Gastroenterology

Autoimmune Hepatitis
Coeliac Disease
Haemochromatosis
Lactose intolerance
Non-Alcoholic Fatty Liver Disease
Primary Biliary Cirrhosis
Primary Sclerosing Cholangitis
Wilsons's Disease

Haematology and Oncology

Acute Lymphocytic Leukaemia
Chronic Myeloid Leukaemia
Haemophilia A
Hodgkin's Lymphoma
Multiple Myeloma
Thrombotic Thrombocytopaenic Purpura

Infectious Disease

HSV Encephalitis
Hepatitis A
Hepatitis B
Hepatitis C
HIV
Infective Endocarditis
Malaria
Meningitis
Osteomyelitis
Pneumocystitis Jiroveci Pneumonia
Pseudomembranous Colitis
Tuberculosis

Nephrology

Chronic Kidney Disease
Lower Urinary Tract Infection
Non-Proliferative Glomerulonephritis
Polycystitis Kidney Disease
Pyelonephritis

Neurology

Cluster Headache
Guillain-Barre Syndrome
Intracerebral Haemorrhage
Migraine
Myasthenia Gravis
Multiple Sclerosis
Parkinsons's Disease
Restless Legs Syndrome
Seizures
Stroke
Subarachnoid Haemorrhage
TIA

Respiratory

Asthma
Bronchiectasis
COPD
Cystic Fibrosis
Interstitial Lung Disease
Lung Cancer
Obstructive Sleep APnoea
Pneumothorax
Pneumonia
Pulmonary Embolism


Cardiology

Acute coronary syndrome

Clinical features:

  • Chest pain - dull, central crushing.
  • Shortness of Breath.
  • Nausea and Vomiting
  • Sweating.

Investigation:

  •  Initial & diagnostic: ECG and cardiac biomarkers (troponin T and CK-MB)

 Treatment:

  • Initial: Aspirin, GTN, Morphine & Oxygen (only if O2 <93%)
  • Best:
    • STEMI
      • If: Patient presenting <12 hours of symptom onset. Then: reperfusion therapy
        • If: PCI possible in <90 minutes from arrival at hospital. Then: PCI
        •  If: PCI NOT possible in <90 minutes from arrival at hospital. Then: Fibrinolysis.
      • If: Initially treated with fibrinolysis (e.g. in rural setting) → must arrange immediate transfer (< 24hrs) to PCI able hospital for possible angiography
    • NSTEACS
      • For all patients: Risk assessment
        • If: very high risk (i.e. on-going ischaemia, hemodynamically unstable). Then: Revascularization (PCI or CABG) recommended <2 hours of admission.
        • If: high risk. Then: Early revascularization strategy is recommended within 24 hours of admission.
        • If: Intermediate risk. Then: Invasive strategy recommended within 72 hours of admission followed by monitoring with non-invasive objective testing.
        • If: Low risk. Then: Aspirin and exercise stress test.
    • Discharge considerations should include: aspirin, dual antiplatelet therapy for 12 months, initiate highest dose of statin, beta-blocker in patients with normal LVEF/ACE


Atrial fibrillation

Clinical features:

  • Palpitations.
  • Syncope.
  • Features of precipitating cause: such as hyperthyroidism.
  • Complications: May precipitate heart failure and stroke.

Investigation:

  • Diagnostic: ECG
  • Underlying causes: TFT, CBE, echocardiogram

Treatment:

  • Best:
    • If: haemodynamically unstable OR AF started <48 hours ago and symptomatic. Then: Consider cardioversion. Either electrically or chemically (e.g. with amiodarone).
      • Patients should be anticoagulated for up to 12 months   following cardioversion.
    • If: otherwise. Then: Rate control:
      • 1st line: cardioselective beta-blocker (e.g. metoprolol)
      • 2nd line: Non-dihydropyridine calcium channel blocker (e.g. diltiazem or verapamil)
      • If: Heart failure. Then: Digoxin (in place of 1st or 2nd line)
      • When rate controlled, anticoagulation should be considered as per CHADSVASC score:
        • If: ≥2. Then: anticoagulate (with warfarin or NOAC)
        • If: 1. Then: anticoagulate or aspirin
        • If: 0. Then: aspirin or nothing

 

Bradyarrhythmia (including 2nd and 3rd degree heart block)

Clinical features:

  • Palpitations.
  • Syncope.
  • Stokes-Adams attacks.

Investigation:

  • Diagnostic: ECG

Treatment:

  • Initial:
    • If: Haemodynamically unstable.
      • ABCDE. Continuous cardiac monitoring. Avoid vagal manoeuvres.
      • 1st line: Atropine (while awaiting transcutaneous pacing)
      • 2nd line: If: atropine ineffective. Then: Transcutaneous pacing.
    • If: stable. Then:
      • If: 2nd or 3rd degree heart block, then: consider pacemaker insertion


Dyslipidemia

Clinical features:

  • Typically asymptomatic.
  • Severe cases (such as familial hypercholesterolaemias) may have xanthamata/xanthelasma, corneal arcus, and pancreatitis.

Investigation:

  • Diagnostic: Lipid studies

Treatment:

  • Best:
    • 1st line: Non-pharmacological. Diet (eat less saturated and trans fats, increase fibre intake) and exercise (>30 minutes moderate intensity exercise ≥5 times per week)
    • 2nd line: Pharmacological
      • If: predominantly elevated LDLs. Then: Statin.
        • 2nd line: ezetimibe
      • If: predominantly elevated triglycerides. Then: fenofibrate

 

 

Essential hypertension

Clinical features:

  • Asymptomatic typically

Investigation:

  • Diagnostic:
    • At least 2 blood pressure measurements > 1 week apart (or sooner if very high BP)
    • If: possibility of white coat hypertension is suspected. Then: 24 hours ambulatory BP monitoring

Treatment:

  • Best:
    • Target BP <140/90 with uncomplicated hypertension
    • Target BP <120 systolic if high CVS risk
      • 1st line: Non-pharmacological. Exercise, weight loss, assess/treat obstructive sleep apnoea, decrease salt intake, eat healthy, decrease alcohol (stopping smoking decreases CVS risk but not BP)
      • 2nd line: Pharmacological: ACE/ARB, CCB and thiazide are first line medications with similar monotherapy efficacy.
        • If: target not reached in 3 months. Then: add second drug.
        • If: target still not reached. Then: increase dose of one drug.
        • If: target still not reached. Then: add third drug
  • Drug combinations         
    • ACE/ARB plus CCB - useful in diabetes or lipid abnormalities
    • ACE/ARB plus thiazide - useful in CHF or post stroke
    • ACE/ARB plus beta blocker - recommended post MI or CHF

 

Heart failure (systolic failure)

Clinical features:

  • Right sided: peripheral oedema, hepatomegaly. Elevated JVP.
  • Left sided: Bibasal fine inspiratory crackles, SOB, PND.
  • Either: fatigue, nocturia, and 3rd heart sound.

Investigation:

  • Initial: CXR, BNP, ECG (cause of CHF)
  • Diagnostic: Echocardiogram (left ventricular EF <40%)

Treatment:

  • Emergency department (for APO):
    • Sit patient up
    • O2 via mask
    • Frusemide IV
    • Treat precipitating factor
    • GTN (provided systolic BP > 100mmHg)
    • If: Not responding to above measures. Then: CPAP
    • If: Anxious/distressed. Then: Morphine
  • Best (for long term):
    • Non-pharmacological: salt restricted diet (<6 grams/day), fluid restriction <1.5L/day, daily weighs, weight loss, exercise
    • Pharmacological (mortality benefits):
      • All: ACE inhibitor/ARB
      • All: Beta blocker (extended-release metoprolol, bisoprolol, carvedilol)
      • If: Symptoms not controlled by optimum dose of ACE inhibitor + beta-blocker + frusemide. Then: Aldosterone antagonist (spironolactone).
      • If: unable to tolerate ACE inhibitor /ARB. Then: Hydralazine + isosorbide dinitrate
    • Pharmacological (2nd line treatments):
      • Almost all: Loop diuretics (symptomatic relief)
      • If: sinus rhythm but symptoms not controlled by ACE inhibitor + beta-blocker + diuretic + aldosterone antagonist. Then: Digoxin
      • If: rapid Atrial Fibrillation. Then: Digoxin

 

Heart failure (with preserved systolic function)

Clinical features:

  • Similar to systolic heart failure
  • Symptoms/signs of underlying cause may differ

Investigation:

  • Initial: CXR
  • Diagnostic: Echocardiogram (≥45% left ventricular EF)

Treatment:

  • Best, treat underlying cause:
    • If: Hypertensive. Then: ACE inhibitor/ARB,
    • If: Diabetic. Then: Strict glycaemic and BP control (ACE inhibitor/ARB)

 

Pericarditis

Clinical features:

  • Sharp chest pain.
  • Postural change (worse lying down, better sitting up).
  • Associated SOB.

Investigation:

  • Initial/diagnostic: ECG (diffuse up-scooping ST elevation)
    • Then: Echo (to assess size of pericardial effusion).
  • Look for underlying cause

Treatment:

  • Initial: If: tamponade present. Then: Pericardiocentesis 
  • Best: 
    • Treat underlying cause
    • If viral pericarditis:
      • 1st line: NSAIDs
      • 2nd line: paracetamol
    • If: Recurrent. Then: Colchicine
    • If: uraemic pericarditis. Then: haemodialysis

 

Rheumatic fever

Clinical features:

  • See Jones criteria below
  • Investigation:
    • Diagnostic: Jones Criteria (2 major or 1 major + 2 minor)
      • Major:
        • Migratory polyarthritis
        • Sydenham chorea
        • Carditis (+/- subclinical echo findings dependent on at-risk population)
        • Erythema marginatum
        • Subcutaneous nodules
      • Minor:
        • Raised inflammatory markers (ESR/CRP)
        • Fever >38C
        • Polyarthralgia or aseptic monoarthritis
        • Elongated PR interval
      • Evidence of Group A Streptococcus (GAS):
        • Positive culture for GAS
        • Anti-streptolysin O antibodies
        • Anti-DNase B antibodies

Treatment:

  • Best:
    • If: persistent URTI present. Then: benzathine penicillin/oral penicillin
    • If: arthritis present. Then: aspirin or naproxen
    • If: chorea present. Then: anticonvulsant
    • If: carditis present. Then: treat as per heart failure

 

Stable angina

Clinical features:

  • Dull central chest pain on exertion.
  • SOB.
  • Symptoms resolve with rest.
  • Not crescendo pattern

Investigation:

  • Diagnostic: exercise stress test

Treatment:

  • Initial:
    • See acute coronary syndromes
  • Best:
    • Non-pharmacological: smoking cessation, healthy diet and exercise
    • Prevention of further disease: aspirin, statin, ACEI, metoprolol
    • Symptomatic: GTN

 

Supraventricular tachycardia (i.e. AV nodal re-entry tachycardia)

Clinical features:

  • Palpitations. Syncope/presyncope.

Investigation:

  • Diagnostic: ECG (narrow QRS < 0.12, tachycardia, p waves often not visible – buried)

Treatment:

  • Initial/best:
    • If: haemodynamically unstable. Then: DC cardioversion.
    • If: haemodynamically stable. Then: Vagal manoeuvres and/or IV Adenosine
      • 2nd line: IV non-dihydropyridine calcium channel blocker or IV beta blocker
    • Consider beta-blocker as prophylaxis for recurrent SVT.

 

Dermatology

Acne vulgaris

Clinical features:

  • Comedones, papules, pustules, nodules and pseudocysts occurring in on pilosebaceous units
  • Often affects face, neck, chest and back

Investigation:

  • Diagnostic: Clinical diagnosis
  • Grading of mild/moderate/severe based on number of comedones, inflammatory lesions and presence of pseudocysts

Treatment:

  • Best:
    • If: mild. Then: Topical benzoyl peroxide cream and topical retinoid.
    • If: moderate. Then: consider COCP and doxycycline (or erythromycin).
    • If: Severe/not responding to treatment. Then: referral to dermatologist for consideration of oral isotretinoin (Roaccutane)
      • Side effects of Isotretinoin – dry skin/mucosal membrane, lipid dysfunction, arthralgia
      • Teratogen. If female of child-bearing age, then consider two simultaneous types of contraception

 

Eczema (atopic dermatitis)

Clinical features:

  • Erythematous weepy patches with poorly demarcated edges
  • Pruritic with excoriations.
  • Dry and lichenified skin
  • Infants – commonly affects cheeks with sparing of nappy area
  • Toddlers – localised to extensor surfaces
  • Older children/adults – typical flexural pattern of involvement

Investigation:

  • Diagnostic: Clinical diagnosis
  • Consider patch testing to exclude allergic dermatitis

Treatment:

  • Avoid triggers
  • First line: Emollients and intermittent topical corticosteroids for acute flares
  • Second line: consider topical calcineurin inhibitors, antibiotics, antihistamines, oral corticosteroid and phototherapy.
  • Immunosuppressive agents (such as ciclosporin, azathioprine or methotrexate) can be used for severe and chronic eczema.

 

Plaque Psoriasis

Clinical features:

  • Well demarcated plaques with silvery scale
  • Commonly over extensor surfaces and scalp.
  • Auspitz’s sign

Investigation:

  • Diagnostic: Usually clinical diagnosis.
  • If: uncertain. Then: Skin biopsy (hyperkeratosis, parakeratosis, Munro’s microabscesses, elongated rete ridges)

Treatment:

  • General Measures – dermatology referral, sunlight, baths, emollients, wet wraps, removal of stress
  • If: Localised or mild psoriasis. Then: consider topical emollients, coal tar, dithranol, topical steroids and calcipotriol.
  • If: widespread psoriasis. Then: consider use systemic treatment, such as methotrexate, cyclosporin, acitretin or phototherapy
  • If: extensive disease not responding to systemic treatment. Then: Consider application for biologics (e.g. infliximab or adalimumab)

 

Seborrhoeic dermatitis

Clinical features:

  • Not particularly itchy compared to atopic dermatitis
  • Often present as defined scaly patches or diffuse scale
  • Commonly affecting scalp and face
  • Also known as “cradle cap” in infants

Investigation:

  • Diagnostic: Clinical diagnosis

Treatment:

  • Best:
    • If: scalp involvement present. Then: medicated shampoos (containing ketoconazole, ciclopirox, salicylic acid or coal tar) in combination with topical steroids to reduce itch.
    • If: non-scalp involvement. Then: Consider ketoconazole or ciclopirox cream + hydrocortisone cream/calcineurin inhibitors.
    • If: resistant to above treatment. Then: oral itraconazole, tetracycline antibiotics or phototherapy.

 

Endocrinology

Adrenal insufficiency (incl. Addison’s disease)

Clinical features:

  • Nausea and vomiting.
  • Hypotension.
  • Hypoglycaemia - weakness, sweating and shaking.

Investigation:

  • Initial: EUC (showing hyponatraemia and hyperkalaemia), BGL
  • Diagnostic: Low plasma morning cortisol + plasma ACTH + Short synacthen test (failure of cortisol rise following ACTH administration) and elevated plasma renin levels

Treatment:

  • Initial treatment for Addisonian crisis: Intravenous fluids and commencement of IV steroids (hydrocortisone or dexamethasone). Hyperkalaemia should resolve with steroids.
  • Best:
    • Primary adrenal insufficiency: Glucocorticoid (hydrocortisone) and mineralocorticoid (fludrocortisone) replacement
    • Secondary adrenal insufficiency: Glucocorticoid (hydrocortisone) replacement only (RAAS intact)

Note: Increase dose of replacement (Stress dose) if patient sick or going to have surgery

 

Diabetes insipidus

Clinical features:

  • Polyuria.
  • Polydipsia
  • Precipitating cause: head trauma or brain surgery (central), lithium (nephrogenic)

Investigation:

  • Diagnostic: Water deprivation test (high serum osmolarity and low urine osmolarity) to distinguish from primary polydipsia
    • Then: Desmopressin test.
      • If: urine osmolarity increases. Then: central.
      • If: urine osmolarity stays low. Then: Nephrogenic.

Treatment:

  • Initial: Rehydration
  • Best:
    • If: Central. Then: Desmopressin replacement
    • If: Nephrogenic. Then: salt restriction and thiazide diuretic

 

Diabetes mellitus type 2

Clinical features:

  • Polyuria.
  • Polydipsia.
  • Fatigue.
  • Frequent infections.
  • Acanthosis nigricans.

Investigation:

  • Initial: Urine dipstick (or BSL or HbA1c)
  • Diagnostic: HbA1c >6.5% or fasting BSL >7 mmol/L or random BSL >11 mmol/L or OGTT >11 mmol/L
  • Follow-up for complications: Podiatry, urinary albumin: creatinine ratio and fundoscopy.

Treatment:

  • Initial: (for hyperglycaemic hyperosmolar state): IVT, IV insulin +/- potassium
  • Best:
    • Target: Aim for HbA1c <7% (although targets should be individualised). Check HbA1c every 3-6 months.
    • Keep stepping up treatment regime if HbA1c control is inadequate. Frequent podiatry review is recommended.
      • 1st line: Non-pharmacological. Healthy diet and exercise
      • 2nd line: Add Metformin
      • 3rd line: Add sulfonylurea (Gliclazide)
      • 4th line: Add DPP-4 inhibitor (sitagliptin) or acarbose or thiazolidinedione (pioglitazone) or direct to insulin

 

Diabetic ketoacidosis

Clinical features:

  • Sharp and non-specific abdominal pain
  • Nausea and vomiting.
  • Thirst and polyuria.
  • Confusion.
  • Recent trigger (e.g. recent illness or insulin non-compliance).

Investigation:

  • Initial/diagnostic: Urine dipstick (ketones), BSL
  • EUC (for potassium)

Treatment:

  • Initial: Intravenous fluids. Insulin infusion + glucose +/- potassium.
  • Best: Treat underlying cause

 

Hypercalcaemia

Clinical features:

  • Decreased neuronal/muscular excitability manifesting as fatigue, depressed mood, weakness and constipation.
  • Polyuria/polydipsia.
  • Abdominal pain and kidney stones.

Investigation:

  • Diagnostic: Serum calcium levels (also correct for albumin levels)
  • PTH levels: if high/inappropriately normal, then likely primary hyperparathyroidism (or familial hypocalciuric hypercalcaemia). If low, then concern regarding malignancy
  • ECG (wide QRS, short QT, bradyarrhythmias)

Treatment:

  • Initial:
    • If: severe hypercalcaemia (total calcium >3.5 or ionised calcium >2.5). Then: give IVT, frusemide (only to treat fluid overload) and IV bisphosphonates.
  • Best:
    • Treat underlying cause

 

Hyperkalaemia

Clinical features:

  • Weakness.
  • Fatigue.
  • Nausea and vomiting.
  • Palpitations.

Investigation:

  • Diagnostic: EUC
  • Priority: ECG (for peaked T waves, prolonged PR, QRS prolongation)
  • Further workup to investigate underlying causes:
    • GFR, adrenal insufficiency, drugs, haemolysis

Treatment:

  • Initial:
    • Membrane stabilizer to prevent arrhythmias: Calcium gluconate
    • Insulin and dextrose infusion (+/- Salbutamol nebuliser)
    • Resonium (resin administered PO or PR to remove potassium)
    • If: Above measures are unsuccessful. Then: Dialysis
  • Best:
    • Treat underlying cause

 

Hyperthyroidism

Clinical features:

  • Increased metabolic rate (weight loss despite decreased appetite, heat intolerance)
  • Increased sympathetic stimulation (fine bilateral postural tremor, sweating, anxious, palpitations).
  • Proptosis and lid retraction
  • Goitre
  • Hyperreflexia.

Investigation:

  • Initial: Thyroid Function Tests
  • Diagnostic:
    • If: Graves. Then: TSI +ve (anti-TPO also often +ve). Radioiodine uptake scan diffusely increased.
    • If: toxic multinodular goiter. Then: anti-TPO -ve. Radioiodine uptake scan multifocally elevated.
    • If: Toxic adenoma. Then: anti-TPO -ve. Radioiodine uptake scan focally elevated.
    • If: Subacute thyroiditis. Then: anti-TPO -ve or low titre. High ESR. Radioiodine uptake scan diffusely decreased.
    • If: Hashimoto’s thyroiditis (painless sporadic thyroiditis). Then: Clinically painless. Anti-TPO high titre. Normal ESR. Radioiodine uptake scan diffusely decreased.

Treatment:

  • Initial: Beta blockers to control hyperthyroid symptoms
  • Best:
    • If: Graves. Then: antithyroid medication (such as carbimazole), radioiodine ablation or thyroidectomy (see “Graves disease” in Surgery section for details)
    • If: Toxic adenoma. Then: Radioiodine ablation or ipsilateral lobectomy
    • If: Toxic multinodular goiter. Then: Radioiodine ablation or total thyroidectomy
    • If: Subacute thyroiditis or Hashimoto’s. Then: Beta-blockers for symptom control +/- NSAID for pain (subacute thyroiditis likely painful). Patient will likely require thyroxine for hypothyroid phase.

Note: Patient must be euthyroid before radioiodine ablation or thyroidectomy. Consider Lugol’s iodine prior to thyroidectomy.

 

Hypocalcaemia

Clinical features:

  • Perioral and peripheral paraesthesia.
  • Muscle cramps. Seizures.
  • Chvostek’s and Trousseau’s signs.

Investigation:

  • Diagnostic: Serum Calcium levels (correct for albumin)
  • PTH levels
  • ECG (QT prolongation, tachyarrhythmias – torsades de pointes)

Treatment:

  • Initial: If: symptomatic. Then: IV calcium gluconate. Consider HDU/ICU admission and continuous infusion for 1-2 days.
  • Best:
    • 1st line: Calcitriol and calcium carbonate

 

Hypokalaemia

Clinical features:

  • Weakness and Fatigue
  • Palpitations
  • Constipation

Investigation:

  • Diagnostic: EUC
  • ECG (T wave flattening, U waves)
  • Look for underlying causes (in particular diuretics)

Treatment:

  • Initial: Oral potassium supplements.
  • Best:
    • Treat underlying cause

 

Paget’s disease of the bone

Clinical features:

  • Incidental finding, often asymptomatic
  • Dull and aching bone pain, commonly affecting the hip
  • Pathological fractures
  • Headache from overgrowth of skull

Investigation:

  • Diagnostic: XR (increased density, cortical thickening) and raised ALP.

Treatment:

  • Best: Bisphosphonates

 

Secondary hyperparathyroidism

Clinical Features:

  • Features of chronic kidney disease
  • Nonspecific

Investigation:

  • Initial: EUC (CKD)
  • Diagnostic: PTH, Calcium, Vitamin D levels

Treatment:

  • Best:
    • 1st line: Calcium supplements. Restrict phosphate, phosphate binders (calcium carbonate).

 

Gastroenterology

Autoimmune hepatitis

Clinical features:

  • RUQ pain.
  • Jaundice.
  • Nausea and vomiting

Investigation:

  • Initial: LFTs
  • Diagnostic: ANA, anti-smooth muscle antibody (type 1 autoimmune hepatitis), LKM-1 (type 2 autoimmune hepatitis), raised IgG, typical histology on liver biopsy (absence of viral hepatitis).

Treatment:

  • Initial: Corticosteroids
  • Best:
    • 1st line: Corticosteroids and azathioprine

 

Coeliac disease

Clinical features:

  • Diarrhoea. Steatorrhoea
  • Weight loss.
  • Fatigue.

Investigation:

  • Initial: Anti-tissue transglutaminase antibodies (sensitive and specific) OR anti-endomysial antibodies OR anti-gliadin antibodies
  • Diagnostic: Endoscopy and duodenal biopsy (villous atrophy)
  • Further workup: Test for deficiency of nutrients including iron, folate, vitamin D

Treatment:

  • Best:
    • 1st line: Gluten free diet (avoid food containing wheat, rye, barley and oats)

 

Hemochromatosis

Clinical features:

  • Cirrhosis.
  • Joint pain.
  • Bronze skin.
  • Erectile dysfunction.
  • Diabetes mellitus type 2.

Investigation:

  • Initial: Iron studies showing elevated ferritin
  • Diagnostic: HFE mutation analysis
  • If: mutation positive. Then: family screen recommended.

Treatment:

  • Best:
    • 1st line: Venesection

 

Lactose intolerance

Clinical features:

  • Diarrhoea.
  • Bloating abdominal pain.
  • Symptoms present after meals containing lactose (e.g. dairy)

Investigation:

  • Diagnostic: Hydrogen breath test

Treatment:

  • Avoid lactose in diet

 

Non-alcoholic fatty liver disease

Clinical features:

  • Usually asymptomatic.

Investigation:

  • Initial: LFTs (hepatocellular picture)
  • Diagnostic: Liver biopsy. (A presumptive diagnosis is usually made by ruling out other causes)

Treatment:

  • Best:
    • 1st line: Improve diet and exercise. Vitamin E supplements. Optimise control of diabetes, dyslipidaemia and hypertension

 

Primary biliary cirrhosis

Clinical features:

  • Jaundice/pruritus (generally asymptomatic until cirrhosis is present)

Investigation:

  • Initial: LFTs (cholestatic picture)
  • Diagnostic: antimitochondrial antibodies, high IgM, liver biopsy (also absence of duct narrowing on MRCP)

Treatment:

  • Best: Ursodeoxycholic acid

 

Primary sclerosing cholangitis

Clinical features:

  • RUQ pain.
  • Jaundice/pruritus.
  • Associated with ulcerative colitis.

Investigation:

  • Initial: LFTs (cholestatic picture)
  • Diagnostic: ERCP/MRCP showing multiple biliary strictures (causes ‘bead-like’ appearance). Liver biopsy shows ‘onion-skin’ appearance.

Treatment:

  • Best:
    • Early/mild disease: urosdeoxycholic acid. No proven benefit for survival.

 

Wilson’s disease

Clinical features:

  • Early onset Parkinsonism.
  • Psychiatric disturbances.
  • Cirrhosis.
  • Kayser-Fleischer rings.

Investigation:

  • Initial: Decreased ceruloplasmin, increased 24 hour urinary copper excretion
  • Diagnostic: Liver biopsy (genetic analysis imperfect as many possible mutations)
  • If: positive liver biopsy. Then: Screen relatives

Treatment:

  • Best: Penicillamine


Haematology and Oncology

Acute lymphocytic leukaemia

Clinical Features:

  • Pallor/fatigue.
  • Easy bruising/bleeding.
  • Frequent Infections.
  • Bone pain.
  • Weight loss.
  • Splenomegaly.

Investigation:

  • Initial: CBE with blood film (blast cells, no aeur rods)
  • Diagnostic: Bone marrow biopsy

Treatment:

  • Best:
    • 1st line: Chemotherapy: Induction, consolidation and maintenance chemotherapy and CNS prophylaxis (intrathecal methotrexate). 
    • Tyrosine kinase inhibitor (if BCR-ABL positive). Fluid therapy and allopurinol (preventing tumour lysis syndrome). Prophylactic anti-microbials or broad-spectrum antibiotics if febrile. RBC and platelet transfusion.

 

Chronic myeloid leukaemia

Clinical features:

  • Fatigue/pallor.
  • Splenomegaly.
  • Features of thrombocytopenia and immunosuppression (late stage)

Investigation:

  • Initial: CBE
  • Diagnostic: bone marrow biopsy, genetic test for BCR-abl translocation on cancer cells (Philadelphia chromosome)

Treatment:

  • Best: 
    • 1st line: Tyrosine-kinase inhibitor (imatinib)

 

Haemophilia A

Clinical features:

  • Bleeding diathesis.
  • History of other affected males on maternal side

Investigation:

  • Initial: Prolonged aPTT, normal INR
  • Diagnostic: Decreased factor VIII

Treatment:

  • Best:
    • If: Mild. Then: desmopressin
    • Otherwise: Recombinant factor VIII concentrate

 

Hodgkin’s lymphoma

Clinical features:

  • Lymphadenopathy.
  • Night sweats.
  • Weight loss.
  • Generalised pruritus.
  • Tender lymph nodes with consumption of alcohol.

Investigation:

  • Initial: CBE, CXR (mediastinal mass).
  • Diagnostic: Lymph node biopsy (Reed-Sternberg cells)

Treatment:

  • Best:
    • 1st line: Radiotherapy and chemotherapy

 

Multiple myeloma

Clinical features:

  • CRAB syndrome – hypercalcaemia, renal impairment, anaemia and bone pain.

Investigation:

  • Initial: EUC demonstrating hypercalcaemia and decreased renal function, CBE showing anaemia, and plain XR showing lytic lesions (vs smouldering multiple myeloma – no CRAB features)
  • Diagnostic: Serum protein electrophoresis (increased monoclonal proteins). Urine protein electrophoresis (Bence-Jones proteins). Bone marrow biopsy (>10% plasma cells) (vs MGUS – fewer plasma cells on biopsy)

Treatment:

  • Best:
    • 1st line: Chemotherapy. Radiotherapy for bone pain.

 

Infectious diseases

HSV Encephalitis

Clinical features:

  • Confusion/personality change.
  • Memory deficit.
  • Seizures.
  • Headache

Investigation:

  • Initial: brain MRI
  • Diagnostic: LP (CSF PCR)

Treatment:

  • Initial: start IV acyclovir empirically and continue until HSV ruled out

 

Hepatitis A

Clinical features:

  • Self-limiting infection
  • Can be associated with nausea and vomiting, diarrhoea and RUQ pain.
  • May rarely take fulminant course.

Investigation:

  • Initial: LFTs
  • Diagnostic: Hepatitis A serology

Treatment:

  • Initial: Hydration, anti-emetics. Avoid alcohol and paracetamol.
  • Prevention: Vaccine

 

Hepatitis B

Clinical features:

  • Can be asymptomatic until cirrhosis is well established.
  • Associated with RUQ pain, jaundice, fever, nausea and vomiting

Investigation:

  • Initial: LFTs
  • Diagnostic: Hepatitis B serology +/- liver biopsy
  • Screen for HIV and hepatitis C

Treatment:

  • Prevent: vaccine
  • Initial: Supportive care
  • Best:
    • 1st line: Pegylated interferon
  • Also: avoid alcohol

 

Hepatitis C

Clinical features:

  • Primary infection usually asymptomatic.
  • May have RUQ pain, fever and jaundice.
  • Usually first symptoms are of cirrhosis.

Investigation:

  • Initial: LFTs
  • Diagnostic: serum Hep C PCR +/- liver biopsy
  • Screen for hepatitis B and HIV

Treatment:

  • Acute hepatitis C: Pegylated interferon alpha (increases chance of viral clearance)
  • Best:
    • Depends on genotype, however, as a general rule
    • If: Types 1-3. Then: 1st line Sofosbuvir
    • If: Types 4-6. Then: Pegylated interferon alpha + ribavirin
  • Also: avoid alcohol. Hepatitis A and B vaccination (if not previously exposed).

 

HIV

Clinical features:

  • Seroconversion approximately 6 weeks following primary infection
  • Associated with rash, diarrhoea, myalgia, headache and fever (flu-like illness).
  • Immunosuppression (e.g. opportunistic infections and associated malignancies) at later stages

Investigation:

  • Initial: anti-HIV antibody serology (ELISA).
  • Diagnostic: If: serology positive. Then: confirm with Western blot
  • Once confirmed: Measure CD4 count (AIDS if <200) and viral load.
  • Further workup: Hepatitis B and C serology. CMV, VZV. Tuberculin skin test

Treatment:

  • Initial: Mandatory notification and contact tracing
  • Best:
    • Counselling.
    • Immunisations (including influenza, pneumococcal, hepatitis A/B).
    • If: CD4 T cell count <500 OR opportunistic infection OR pregnant OR at risk of transmitting to sexual partners
    • Then: Highly active anti-retroviral therapy (HAART) and monitor response with CD4 count and viral load.
    • Therapy may include combination of NRTI, NNRTI, PI, integrase inhibitors and entry inhibitor.

 

Infective endocarditis

Clinical features:

  • See Diagnostic criteria

Investigation:

  • Diagnostic (Duke modified criteria: 2 major OR 1 major+3 minor OR 5 minor)
  • Major: positive blood cultures (at least 2 with organisms typical of infective endocarditis). Make sure to collect 3 cultures that are 1 hour apart.
  • Major: Echocardiogram showing oscillating intracardial mass, abscess or new valvular regurgitation
  • Minor: Predisposing condition, fever, vascular phenomena (Petechiae. Janeway lesions. Emboli), immunologic phenomena (Osler nodes. Splinter haemorrhages. Roth spots), positive blood cultures not meeting major criteria.

Treatment:

  • Initial: Empiric (benzylpenicillin, gentamicin, vancomycin)
  • Best:
    • 1st line: Targeted antibiotics
    • 2nd line: If: severe heart failure or antibiotics fail or prosthetic valve. Then: Surgery.

 

Malaria

Clinical features:

  • General features: fatigue and spiking fever, haemolysis, splenomegaly.
  • Plasmodium falciparum: Most severe
  • Plasmodium vivax/ovale: Some remain dormant in liver as hypnozoites. Fever may present every 48 hours
  • Plasmodium malariae: fever once every 72 hours.

Investigation:

  • Initial/diagnostic: Blood smear (with Giemsa or Wright stain) thick and thin films

Treatment:

  • Prophylaxis: Mefloquine. Must start 2-3 weeks before trip and continue prophylaxis for 4 weeks after returning. Or doxycycline.
  • Best:
    • Quinine + doxycycline (or + clindamycin)
    • If: vivax/ovale. Then: primaquine required to eradicate hypnozoites (must be aware of severe reaction between primaquine and G6PD)

 

Meningitis

Clinical features:

○    Headache.
○    Fever.
○    Meningisms (photophobia, neck stiffness/pain, Kernig’s and Brudzinski’s signs).
○    Seizures.
○    Confusion/impaired level of consciousness.

Investigation & treatment

  • Initial:
    • Take blood culture.
    • Then:
      • If: lumbar puncture (LP) not contraindicated and no features of raised ICP. Then: LP. Then: Dexamethasone + ceftriaxone.
      • If: LP not contraindicated and features of raised ICP. Then: Dexamethasone + ceftriaxone followed by head CT. +/- LP based on CT result.
  • Best:
    • If: bacterial, then: targeted antibiotics
    • If: viral, then: supportive
    • If: fungal, then: consider amphotericin B and consult local guideline.

 

Osteomyelitis

Clinical features:

  • Pain.
  • Fever.
  • Erythema/swelling.

Investigation:

  • Initial: Plain XR (may show soft tissue swelling, lytic bone destruction, formation of new bone) and blood culture.
  • Diagnostic: MRI is gold standard for diagnosis, followed by bone biopsy for culture and sensitivities. Nuclear imaging is an alternative if MRI is contraindicated.

Treatment:

  • Initial: Empiric antibiotics (e.g. Flucloxacillin). If: allergic. Then: vancomycin
  • Best:
    • 1st line: Targeted antibiotics. If: abscess present. Then: Incision and drainage.

 

Pneumocystis jiroveci pneumonia

Clinical features:

  • Dry cough.
  • Desaturation with exertion.
  • Immunosuppression (especially with HIV).

Investigation:

  • Initial: CXR (can show bilateral, diffuse opacities but may also be unremarkable)
  • Diagnostic: Sputum MC&S
  • If: Not already diagnosed with HIV. Then: HIV serology

Treatment:

  • Initial: ABCs to stabilise patient
  • Best:
    • 1st line: trimethoprim + sulfamethoxazole
    • 2nd line: Pentamidine

Note: Prophylaxis is required in patients with established AIDS

 

Pseudomembranous colitis

Clinical features:

  • Diarrhoea (may be bloody).
  • Abdominal pain.
  • Recent course of antibiotics (typically 5-10 days ago).

Investigation:

  • Diagnostic: Combination of Clostridium difficile toxin assay and culture from stool (culture alone limited value)

Treatment:

  • Initial: Barrier precautions. Note to autoclave bedpans as alcohol rubs are insufficient.
  • Best:
    • 1st line: Metronidazole
    • 2nd line: Vancomycin (oral)
    • If: severe recurrent disease. Then: consider faecal microbiota transplant

 

Tuberculosis (active)

Clinical features:

  • Cough.
  • Haemoptysis.
  • Weight loss, night sweats.
  • History of travel to endemic areas.

Investigation:

  • Initial: Chest X-ray
  • Diagnostic: Sputum MC&S (Zeihl-Neelsen stain). NAAT on sputum.

Treatment:

  • Initial: Respiratory precautions and negative air pressure room (isolation for at least 2 weeks while on treatment). Mandatory notification. Contact tracing and testing.
  • Best (May require directly observed therapy. Before treatment assess baseline LFTs, colour vision):
  • Short course: “Four for two, and two for four”.
  • 2 months on RIPE. Followed by 4 months on isoniazid and rifampicin. Give pyridoxine with isoniazid to decrease likelihood of peripheral neuropathy.

 

Tuberculosis (latent)

Clinical features:

  • Asymptomatic during latent period.

Investigation:

  • Initial: Chest X-ray (CXR)
  • Diagnostic: Positive mantoux test (intradermal infection) or interferon gamma release assay in conjunction with history, exam and radiological findings

Treatment:

  • Best: Isoniazid for 9 months. OR Rifampin for 4 months.

 

Nephrology

Chronic kidney disease

Clinical features:

  • Often asymptomatic until GFR greatly reduced.
  • Generalised pruritus.
  • Anorexia.
  • Nausea and vomiting.
  • Fatigue.
  • Anaemia.
  • Peripheral oedema.
  • Can have features of underlying cause: e.g. lupus, diabetes mellitus
  • Complication: Pericarditis.

Investigations:

  • Initial: EUC, urinalysis, CBE, urine albumin:creatinine ratio, 
  • Diagnostic (definition of CKD): GFR <60 for >3 months OR evidence of renal damage (blood, protein in urine) for >3 months
  • Diagnostic of underlying cause: Renal biopsy (not always done)

Treatmentt

  • Best:
    • Treat underlying condition
      • Stage 1 (GFR >90) or 2 (GFR 60-89): Patient is normal (no CKD yet). 
        • If: Hypertension present. Then: BP control with ACEi/ARB. If: dyslipidemia present. Then: statin. BGL control
      • Stage 3 (GFR 30-59) or 4 (GFR 15-29):
        • Blood Pressure control with ACE inhibitor/ARB (target <130/80).
        • Salt and water restriction.
        • Treat anaemia with EPO stimulating agent and iron supplementation.
        • Manage secondary hyperparathyroidism (calcium supplements) and hyperphosphataemia (phosphate binders and dietary phosphate restriction)
        • Consider Oral sodium bicarbonate for metabolic acidosis
      • Stage 5 (GFR <15) or any stage with uraemia:
        • Dialysis. Kidney transplantation

Lower urinary tract infection

Clinical features:

  • Dysuria.
  • Increased urinary frequency.
  • Cloudy appearance to urine.
  • Foul smell of urine.

Investigation:

  • Initial: Urine dipstick (Nitrates, blood, leucocytes)
  • Diagnostic: Urine MC&S

Treatment:

  • Best:
    • 1st line: Trimethoprim (contraindicated in pregnancy)
    • 2nd line: Cephalexin

 

Non-proliferative glomerulonephritis (causes nephrotic syndrome)

Clinical features:

  • Frothy urine.
  • Peripheral and periorbital oedema.
  • Fatigue.
  • DVT/PE.
  • Frequent infections

Investigation:

  • Initial (to establish nephrotic syndrome): 24-hour urinary protein collection (>3.5 grams in 24 hours). Serum albumin. Hyperlipidaemia.
  • Diagnostic (for underlying process):  Renal biopsy
    • Minimal change disease: Light microscopy (LM) - normal. Immunofluorescence (IF) - negative. Electron Microscopy (EM) - podocyte effacement.
    • Membranous nephropathy: LM - thickening of capillary wall/basement membrane. No mesangium thickening. IF - Diffuse IgG and C3 deposits (granular). EM - Subepithelial deposits (beneath podocytes) causing spikes (“spike and dome”)
    • Focal Segmental Glomeruloscleorsis: LM- Focal and segmental sclerosis. IF= Focal IgM and C3. EM- Loss of foot processes (similar to minimal change disease)
    • Diabetic nephropathy:  Mesangial expansion. Glomerular sclerosis. Thickening of glomerular basement membrane. Hyaline arteriosclerosis
    • Lupus nephritis: Mesangial proliferation. Subendothelial immune complex deposition.
    • Membranoproliferative (often nephritic syndrome): “train-track” double-layered basement membrane

Treatment:

  • Best:
    • 1st line: Corticosteroids (or, if: Diabetes is present. Then: treat T2DM)
    • Symptom & Risk management: Frusemide for oedema. Aspirin to decrease risk of DVT. Statin to decrease risk of atherosclerosis. Restrict salt intake.

 

Polycystic kidney disease (autosomal dominant)

Clinical features:

  • Can be asymptomatic.
  • Ballotable kidneys.
  • Family History.
  • Back/flank pain.
  • Dull, aching or sharp pain (with cyst rupture).
  • Haematuria.

Investigation:

  • Diagnostic: Ultrasound or CT. Can also do genetic testing.

Treatment:

  • Best:
    • Early management of UTIs and adequate blood pressure control.
    • Eventually may require dialysis or renal transplant

Note: Autosomal recessive PKD presents in infancy and may be fatal in first few years of life.

 

Proliferative glomerulonephritis (causes nephritic syndrome)

Clinical features:

  • Haematuria.
  • Headaches.
  • Oliguria
  • Hypertension
  • Features of underlying cause (e.g. purpuric rash or haemoptysis).

Investigation:

  • Initial: Urinalysis (blood and protein), EUC.
  • Diagnostic (to determine underlying cause): c-ANCA (GPA), anti-GBM (Goodpasture’s)
  • ASO titre (post-streptococcal), serum complement (C3 low in post-streptococcal), Lupus autoantibodies (lupus nephritis – low C3 and low C4). Renal biopsy.

Treatment:

  • Best:
    • All: Salt and water restriction, diuretics. Can require dialysis.
    • If: GPA or Goodpasture’s. Then: Immunosuppression (prednisolone or cyclophosphamide)
    • If: IgA nephropathy. Then: Treat hypertension with ACEi (or immunosuppression)

 

Pyelonephritis

Clinical features:

  • Flank pain.
  • Haematuria.
  • Fever.
  • Features of lower UTI (dysuria, urinary frequency, cloudy urine
  • Nausea and vomiting.

Investigation:

  • Initial: Urine MC&S, Urinalysis, CBE
  • Diagnostic: Systemically unwell and positive urine MC&S

Treatment:

  • Initial: Empiric antibiotics: Amoxicillin + clavulanate and gentamicin. Tailor empiric antibiotics to severity of disease
  • Best:
    • Targeted antibiotics

 

Neurology

Cluster headache

Clinical features:

  • Headache – unilateral, retro-orbital severe sharp pain (like “red hot poker in the eye).
  • Last from 10 minutes up to several hours.
  • Accompanied by autonomic features (unilateral tearing and rhinorrhoea).
  • May have up to 5-10 episodes in one day, occurring for weeks to months at a time.
  • Patients may have months-years symptom free periods between clusters.

Investigation:

  • Diagnostic: Clinical diagnosis

Treatment:

  • During attacks:
    • 1st line: 100% oxygen
    • 2nd line: Sumatriptan
  • Preventative: Verapamil

 

Guillain-Barre syndrome

Clinical features:

  • Weakness (LMN signs) and paraesthesia.
  • Back pain.
  • Recent illness.

Investigation:

  • Initial: Spirometry. Lumber puncture (albuminocytological dissociation = high protein, normal WCC) supports diagnosis
  • Diagnostic: Nerve conduction studies.
  • Further workup: ECG (can get arrhythmias).

Treatment:

  • Initial: If respiratory compromise, then ICU admission +/- intubation and ventilation
  • Best:
    • 1st line: Plasmapheresis and IVIG

 

Migraine

Clinical features:

  • Headache: typically (but not always) unilateral, throbbing, temporal/frontal, worse with bright lights/loud sounds/physical activity.
  • Triggers may include stress, lack of sleep some foods (e.g. salty foods, wine and skipping meals) and certain smells.
  • May be preceded by aura (approximately 20 minutes before headache usually). Aura may take many forms, most classically a visible jagged white or colourful line that moves gradually across the field of vision. Aura may also involve tingling/weakness, which progress gradually up a limb (compared with TIA which has maximal weakness at onset). Migraine aura may occur without subsequent headache.
  • Nausea and vomiting.

Investigation:

  • Diagnostic: Clinical diagnosis (sometimes head CT/MRI is required to rule out other pathology, namely stroke)

Treatment:

  • During attack:
    • 1st line: simple analgesia. Ibuprofen (or other NSAID) or, if: contraindicated. Then: paracetamol
    • 2nd line: Triptan (e.g. sumatriptan)
    • If: persistent attack requiring hospitalisation/rehydration. Then: chlorpromazine
  • Preventing attacks
    • Non-pharmacological: Avoid triggers. CBT
    • 1st line: Propranolol or amitriptyline
    • 2nd line: verapamil

Note: If having migraine with aura the COCP is contraindicated.

 

Myasthenia gravis

Clinical features:

  • Fatiguable weakness (i.e. weakness worsens with repeated movements).
  • May affect extraocular muscles (causing diplopia and ptosis), oropharyngeal/respiratory muscles (dysphagia, dysarthria, difficulty breathing) and/or limbs (proximal muscle weakness).
  • Weakness typically worse at the end of the day.

Investigation:

  • Initial: spirometry
  • Diagnostic: Tensilon test (not really done any more), ice test, anti-ACh antibodies (and anti-MuSK antibodies), Nerve conduction studies (NSC)/electromyography (EMG) with repetitive nerve stimulation (showing decrement), Single-fiber EMG (showing increased jitter).
  • Chest CT (to scan for thymoma) and anti-striated muscle antibodies

Treatment:

  • Initial: If: respiratory compromise. Then: intubation and ventilation
  • Best (unless as an emergency, wait until diagnosis confirmed before commencing therapy):
    • Short-term:
      • 1st line: pyridostigmine.
      • If: severe. Then: plasmapheresis or IVIG
    • Long-term:
      • Thymectomy beneficial whether thymoma present or not. However, in elderly who are poor surgical candidates, the risks outweigh and benefits.
      • Consider immunosuppression such as with corticosteroids or azathioprine.

 

Multiple sclerosis

Clinical features:

  • Variable as lesions may occur in multiple locations within the CNS.
  • Common features include: optic neuritis (pain on eye movement, red-green colour blindness, decreased visual acuity), transverse myelitis (weakness/paraesthesia with a spinal level, bladder/bowel dysfunction), and cerebellar abnormalities.

Investigation:

  • Diagnostic: MRI (can show 2 lesions disseminated in time/space – McDonald diagnostic criteria. Typically involve periventricular region, brainstem, cerebellum and corpus callosum. Can also show Dawson’s fingers). Lumbar puncture showing oligoclonal bands, raised WCC and protein.

Treatment:

  • Acute treatment: IV methylprednisolone. Alternative plasmapheresis or IVIG
  • Best (to prevent disease progression):
    • 1st line: Interferon beta
    • Other options include glatiramer, natalizumab (be wary of JC virus, causes progressive multifocal leukoencephalopathy), IVIG and plasmapheresis

 

Parkinson’s disease

Clinical features:

  • Motor features: Tremor (asymmetrical 4-6 hz resting tremor), bradykinesia and rigidity. Postural instability in late stage.
  • Non-motor features: REM sleep behaviour disorder. Autonomic dysfunction (constipation, gastroparesis and orthostatic hypotension). Dementia.

Investigation:

  • Diagnostic: Clinical diagnosis (MRI if doubt)

Treatment:

  • Currently no treatments shown to modify disease course.
  • Aim for symptomatic control with: dopamine replacement - levodopa. Given with peripheral dopadecarboxylase inhibitor (carbidopa) to improve availability and minimise side effects, dopamine agonists (pramipexole, apomorphine).
  • When motor fluctuations (wearing off/on-off fluctuations/freezing) develop, use: more frequent, smaller doses of levodopa. MAOI (rasagiline) and COMT inhibitors (entacapone) help to increase duration of levodopa effect. Further motor fluctuations may be managed with deep brain stimulation or duodopa administration in good candidates.

 

Restless legs syndrome

Clinical features:

  • Discomfort in legs alleviated by movement.
  • Diurnal variation (worse at night).

Investigations:

  • Initial: Iron studies (for iron deficiency), EUC (for CKD), consider drugs related cause (beta blockers, antidepressants), pregnancy test
  • Diagnostic: clinical diagnosis

Treatment:

  • Initial/best:
    • Treat underlying cause (e.g. iron supplementation, dialysis, cease medication or wait for delivery of baby)
  • Otherwise:
    • Sleep hygiene and smoking cessation
    • 1st line (Medical therapy): Ropinirole

 

Seizures

Clinical Features:

  • Depends on seizure type – focal (simple vs complex) vs. generalised

Investigation:

  • Diagnostic: Clinical diagnosis (or EEG)
  • Investigate cause

Treatment:

  • Initial:
    • If: status epilepticus (>30 mins). Then: IV midazolam followed immediately by phenytoin.
  • Best:
    • Treat underlying cause
    • Anticonvulsant choice depends on multiple patient factors however as a general rule:
    • If: generalised, then: first line sodium valproate
    • If: focal, then: first line carbamazepine
    • If: ineffective. Then: add second anticonvulsant

Note: driving restrictions will apply following seizure. Duration varies depending on cause and treatment. General rule: 6 months no driving

 

Stroke (ischaemic)

Clinical features:

  • Sudden onset focal neurological deficit conforming to a vascular territory.

Investigation:

  • Initial: Head CT (to rule out haemorrhage) then CTA.
  • If: no evidence of stroke but looks suspicious. Then: MRI with diffusion-weighted imaging
  • After acute management, look for underlying cause: ECG +/- echocardiogram, carotid Doppler.

Treatment:

  • Initial:
    • 1st line: If: <4.5 hours from symptom onset and significant deficit (NIHSS score cut-off in local guidelines). Then: consider thrombolysis (e.g. Alteplase).
    • If: thrombolysis fails and it is a proximal arterial occlusion, then: consider intra-arterial clot retrieval
    • All: Aspirin (hold for 24 hours if given alteplase).
    • If: malignant stroke that looks like cerebral oedema will cause herniation. Then: consider hemicraniectomy.
  • After acute management:
    • All: Swallowing assessment. Only lower BP in first 48 hours after stroke if given alteplase or malignant hypertension. DVT prophylaxis (early mobilisation, hydration, antiplatelet and enoxaparin).
    • All: statin, antihypertensive (e.g. ACE inhibitor) and continue antiplatelet.
    • Treat any underlying cause found (e.g. Atrial fibrilation or carotid stenosis)

 

Subarachnoid haemorrhage

Clinical features:

  • Thunderclap headache.
  • Worst headache of life.
  • Instantaneous onset.
  • May occur in setting of raised ICP (e.g. cough, straining).
  • History of sentinel bleed (similar symptoms).

Investigation:

  • Diagnostic: Head CT
  • If: CT negative but suspect SAH, Then: LP – may identify xanthochromia
  • To find aneurysm: CTA or MRA

Treatment:

  • Initial: Check coagulation. Admit to ICU (or NICU). Elevate head of bed 30˚.
  • Best:
    • Nifedipine (aim for BP <160mmHg and prevention of vasospasm). Seizure prophylaxis (levetiracetam)
    • Consider: aneurysm intervention (e.g. coiling, clipping)

 

TIA

Clinical features:

  • Transient focal neurological deficit that adheres to a vascular territory.

Investigation:

  • Initial: Head CT (to rule out cerebral haemorrhage). BSL to rule out hypoglycaemia
  • Diagnostic: Brain MRI with diffusion-weighted imaging (to rule out stroke)
  • Look for underlying cause: ECG +/- echocardiogram, carotid Doppler

Treatment:

  • Initial: Aspirin (after excluding haemorrhage)
  • Best:
    • If: carotid stenosis. Then: urgent carotid endarterectomy (within 2 weeks) depending on degree of stenosis
    • If: Atrial fibrillation. Then: oral anticoagulant immediately (with aspirin, or IV unfractionated heparin if high risk, bridging until INR therapeutic if using warfarin)

Note: TIA should be regarded as medical emergency. ABCD2 determines need for transfer/admission.

 

Respiratory

Asthma

Clinical features:

  • Episodic cough, wheeze and SOB.
  • Commonly part of atopic triad with atopic dermatitis (eczema) and allergic rhinitis.
  • Aggravated by triggers such as cold air, smoke and cleaning products.

Investigation:

  • Diagnostic: Spirometry
  • Trigger identification/identification of variable expiratory airflow limitation: Measure peak expiratory flow BD and keep a diary.

Treatment:

  • Initial (acute exacerbation):
    • If: O2 sats <95%. Then: Supplemental oxygen (aim for 92-96%)
    • Nebulised salbutamol (+/- ipratropium)
    • Steroids (oral prednisolone or, if: unable to be taken orally, then: IV hydrocortisone or methylprednisolone)
    • Consider HDU/ICU admission depending on severity
  • Best (long term):
    • Non-pharmacological: Avoid triggers, make an asthma action plan
    • Pharmacological: Stepwise progression (see steps below). If: Using SABA > 2 days per week. Then: Indicates inadequate control. Then: consider stepping up.
      • (1) SABA
      • (2) + ICS
      • (3) ICS/LABA combination (low dose)
      • If: still poorly controlled, then: increase dose or refer

Note: Always check inhaler technique

 

Bronchiectasis

Clinical features:

  • Chronic productive cough.
  • Copious amounts of sputum.
  • Haemoptysis.
  • SOB & Wheeze
  • Clubbing.
  • Inspiratory coarse crackles.

Investigation:

  • Diagnostic: Chest CT
  • After diagnosis: Conduct baseline spirometry (obstructive picture)

Treatment:

  • Best:
    • All: Chest physiotherapy. Mucolytic agents.
    • If: infective exacerbation being treated empirically. Then: amoxicillin
    • If: Pseudomonas aeruginosa cultured. Then: ciprofloxacin.

 

COPD

Clinical features:

  • Chronic productive cough.
  • SOB and Wheeze.
  • Smoking history.
  • Barrel chest.
  • Diminished breath sounds and vocal resonance.
  • Wheeze and inspiratory/expiratory coarse crackles.

Investigation:

  • Initial: CXR
  • Diagnostic: Spirometry (obstructive) shows FEV1:FVC <0.7 post-bronchodilator (and FEV1 <80% predicted)

Treatment:

  • Initial (for acute exacerbation):
    • Salbutamol (+/- ipratropium). Steroids (oral prednisolone or, if: can’t be given orally, then: IV hydrocortisone)
    • If: O2 saturation <88%. Then: Consider supplemental O2 but be wary of CO2 retainers
    • If: Clinical/investigation evidence of infection. Then: amoxicillin (or doxycycline)
  • Best (stable, long term):
    • Severity indicates prognosis:
    • FEV1 60-80% of predicted (mild COPD).
    • FEV1 40-59% of predicted (moderate COPD).
    • FEV1 <40% of predicted (severe COPD):
    • Treatment considerations:
      • Non-pharmacological: Smoking cessation, pneumococcal and annual influenza vaccination, exercise/pulmonary rehabilitation.
      • Pharmacological:
        • SABA (+/- ipratropium)
        • LABA and/or LAMA
        • If: frequent infective exacerbations. Then: LABA/ICS combination
        • If: severe, then: Consider domiciliary oxygen therapy (proven survival benefit) and Advanced care directive

Note: Always check inhaler technique.

 

Cystic fibrosis

Clinical features:

  • Meconium ileus.
  • Steatorrhoea
  • Failure to thrive.
  • Frequent respiratory infections.
  • Clubbing.
  • Crackles/wheezes.

Investigation: 

  • Initial: New-born screening for high serum trypsinogen levels (misses 5%) or sweat test (increased chloride in sweat)
  • Diagnostic: Genetic tests

Treatment:

  • Best:
    • Respiratory: Chest physiotherapy, mucolytics, infection control, bronchodilators, antibiotics (azithromycin)
    • GI: Pancreatic enzyme replacement and high calorie diet

 

Interstitial lung disease

Clinical features:

  • Varies depending on individual and aetiology
  • Common features include dry cough, weight loss, fatigue, SOB on exertion, clubbing and fine inspiratory crackles.

Investigation:

  • Initial: CXR, spirometry
  • Diagnostic: high resolution chest CT

Treatment:

  • Initial: treat exacerbations with prednisolone
  • Best:
    • All: pulmonary rehabilitation, oxygen. Can require lung transplant.
    • Most aetiologies (e.g. idiopathic, sarcodosis and hypersensitivity pneumonitis.) require prednisolone.

 

Lung cancer

Clinical features:

  • Cough
  • Haemoptysis
  • Weight loss, night sweats, fatigue.
  • Symptoms of paraneoplastic syndromes including Lambert-Eaton myasthenic syndrome, hypercalcaemia, Cushing’s syndrome and SIADH.

Investigation:

  • Initial: CXR, Chest CT, sputum cytology
  • Diagnostic: Biopsy
    • If: central. Then: via bronchoscopy
    • If: peripheral. Then: percutaneously under CT guidance
  • Staging: standard bloods (including LFTs), CT chest/abdomen, whole body bone scan, brain MRI

Treatment:

  • Best (General overview):
    • If: Small cell. Then: treat with radiotherapy and chemotherapy (no surgery)
    • If: non-small cell and localised. Then: surgical resection and chemotherapy
    • If: any lymph node involvement. Then: Non surgical and treat with chemo radiotherapy

 

Obstructive sleep apnoea

Clinical features:

  • Snoring.
  • Apnoeic episodes – Temporary cessation of breathing at night
  • Daytime somnolence.
  • Morning headache.
  • Difficulty concentrating.
  • Large neck circumference.

Investigation:

  • Diagnostic: Polysomnography (respiratory disturbance index >5)

Treatment:

  • Best:
    • Weight loss, sleep on side, smoking cessation
    • CPAP is gold standard.
  • Other: maxillary advancement splint. Surgery

 

Pneumothorax

Clinical features:

  • Sharp chest pain
  • SOB and cough.
  • Hyper-resonant percussion note
  • Decreased breath sounds over affected side.

Investigation:

  • Diagnostic: CXR
  • Proceed to treatment before investigation if suspecting tension pneumothorax

Treatment:

  • Best:
    • If: suspected tension pneumothorax. Then: large bore needle into 2nd intercostal space on affected side, mid-clavicular line
    • If: primary spontaneous pneumothorax >20% collapse.  Then: chest drain.
    • If: primary spontaneous pneumothorax <20% collapse
    • Then: aspirate if symptomatic and observe if asymptomatic
    • If: secondary and traumatic pneumothorax. Then: chest drain.

 

Pneumonia

Clinical features:

  • Sharp chest pain – often pleuritic and worse with inspiration and coughing
  • Productive cough (may have haemoptysis) and fever
  • Dullness to percussion over affected area and increased vocal resonance.
  • May have bronchial breath sounds and coarse crackles.

Investigation:

  • Initial: CXR, CBE
  • Diagnostic: Sputum MC&S

Treatment:

  • Initial: Empiric antibiotics
  • Community Acquired: If Moderate: Then treat with Benzylpenicillin + doxycycline. If severe: Then treat with ceftriaxone + azithromycin
  • Hospital-acquired: If Moderate: then treat with ceftriaxone (consider adding cover for aspiration pneumonia)
  • If Aspiration pneumonia: then treat with ceftriaxone + metronidazole
  • To cover broad spectrum (e.g. severe): Piperacillin + tazobactam
  • Best: Targeted antibiotics

 

Pulmonary embolism

Clinical features:

  • Sharp chest pain (pleuritic and worse with inspiration and coughing)
  • Cough (may have haemoptysis).
  • Shortness of Breath (SOB).
  • Features of DVT (leg pain, swelling and erythema).

Investigation:

  • If: Wells score ≤4 (low likelihood). Then: D dimer.
  • If D-Dimer: Positive. Then proceed to diagnostic investigation.
  • Diagnostic:
    • If: Wells score ≥5 and renal function good and no contrast allergy. Then: CTPA
    • If: Wells score ≥5 and bad renal function or contrast allergy. Then: V/Q scan

Treatment:

  • Initial: O2, analgesia
  • Best:
    • 1st line:
    • If: No haemodynamic compromise or right ventricular strain. Then: Therapeutic enoxaparin followed by warfarin (as in DVT, heparin to last until INR >2 for 2 consecutive days, minimum 5 days)
    • If: Haemodynamic compromise or right ventricular strain (on echocardiogram/troponin/severe hypoxia).
    • Then: treat as above, with addition of alteplase followed by heparin

 

Rheumatology

See separate rheumatology and orthopaedics page.