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Benign paroxysmal positional vertigo

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Benign paroxysmal positional vertigo (BPPV) describes a condition in which there is:
  • Rotational Vertigo 
  • Provoked by turning head/change in position 
  • Lasts around 10-30 seconds 
  • Possibly with nausea 

Most patients are over 40 years of age 
Women > men (2:1)

Aetiology – believed to be due to free-floating endolymph particles in semi-circular canal. 
  • Most cases (60-70%) are idiopathic. 
  • Secondary BPPV may be due to 
    • Head trauma (7-17% of all cases of BPPV) 
    • Viral (up to 15% of all cases of BPPV)
    • Meniere’s disease (around 5% of cases of BPPV) 
    • Migraines (less than 5% of all cases of BPPV) 

Diagnosis:  Dix-Hallpike manoeuvre – look for nystagmus 

Treatment: Epley’s manoeuvre – series of head movements with the purpose of encouraging any foreign material out of the canal and into the utricle 



References

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Hypertrophic cardiomyopathy

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Hypertrophic cardiomyopathy is an autosomal dominant cardiac condition characterized by marked left ventricular hypertrophy with a non-dilated ventricular cavity, and in around 20% of patients left ventricular outflow obstruction. 

It is the commonest genetic cardiac disease (incidence 1 in 500) and the commonest cause of sudden cardiac death in the young. 

Presentation may be: 
  • Sudden death 
  • Syncope 
  • Shortness of breath 
  • Angina 
  • Palpitations 

Clinical findings may include: 
  • Ejection systolic murmur 
    • If obstruction is present this murmur may be increased by valsalva 
  • Prominent A wave in JVP
  • Bifid pulse (obstructive only) 
  • ? MR 
  • ? split S2 

Investigation 
  • Echocardiography 
    • Hypertrophied and non-dilated left ventricle 
  • ECG
    • ? LVH 
    • ? AF 
    • ? Q waves 
    • ? TWI 

Prognosis include:
  • Sudden death (classically stated at 6% per year but now believed to be lower – around 1%) 
  • Atrial fibrillation (20-25%) 
  • Heart failure symptoms 
  • No symptoms 

Risk factors for sudden death 
  • Family history of sudden death 
  • Unexplained syncope 
  • Massive LV hypertrophy (thickness >30mm)
  • Non-sustained VT on ambulatory ECG 
  • Hypotensive on exercise 

Management – depends on severity and symptoms 
  • Medical 
    • Beta blockers 
    • Verapamil 
  • Surgery 
  • Percutaneous alcohol septal ablation 
  • Dual chamber pacing
  • ICD 
  • Avoid nitrates/ACE-i/digoxin in outflow tract obstruction 


References 

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Metabolic acidosis

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Definition of metabolic acidosis: low pH and low PHCO3

Metabolic acidosis may be due to:
  • Accumulation of acids (= high anion gap) or
  • Loss of bicarbonate (= hyperchloraemic metabolic acidosis, normal anion gap) 

Anion gap =  (Na + K) - (Cl + HCO3)
The normal anion gap is 14-16 mmol/l


  • Causes of a high anion gap metabolic acidosis: MUDPILES
    • Methanol (formic acid)
    • Uraemia
    • Diabetic ketoacidosis
    • Paraldehyde (acetic and chloroacetic acid)
    • Isoniazid
    • Iron
    • Inborn errors of metabolism
      • Glucose 6 phosphate deficiency
    • Lactic acid
    • Ethylene glycol (oxalic acid)
    • Salicylates
      • Also:
      • Toluene OD (an aromatic hydrocarbon used as a solvent in paints, glues etc)
      • Paracetamol OD – either due to lactic acidosis or pyroglutamic acidosis

Pyroglutamic acid (=intermediate in the gamma glutamyl cycle). Excess associated with ingestion of several medications, including flucloxacilin, vigabatrin and paracetamol.

  • Causes of a hyperchloraemic (=normal anion gap) metabolic acidosis
    • Gastrointestinal bicarbonate loss:
      • Diarrhoea
      • Intestinal fistula
      • Urinary tract diversion to intestine
      • Ileal conduit
      • Ureterosigmoidoscopy
      • Medications
        • Magnesium sulphate
        • Laxative abuse
        • Cholestyramine
    • Renal causes
      • Renal tubular acidosis
      • Renal failure
      • Drug-induced hyperkalaemia with renal insufficiency
        • spironolactone
        • ACE-i
    • Administration of fluid containing chloride


Small print gem: a major decrease in extra cellular fluid volume will raise the HCO3, so the diagnosis of metabolic acidosis may be missed in the diabetic patient who has vomited lots and is severely dehydrated with concurrent DKA, or the cholera patient who has had massive diarrhoea 


References

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Glaucoma

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Glaucoma describes a range of disorders with a characteristic type of optic disc damage usually due to raised intraocular pressure.

Upper limit of normal intraocular pressure is 21mmHg. 

2 main divisions of glaucoma are: 
  • Open angle = chronic 
  • Closed angle = acute 


Open angle glaucoma 

Primary open angle glaucoma occurs in 1-2% of over 40s and over 4% of over 80s 

Patients are often asymptomatic – visual losses tend to occur late in the course of the disease and is often peripheral. 

Fundoscopy may reveal optic disc cupping

  • Major risk factors 
    • FH in a first degree relative 
    • Myopia 
    • Advanced age
    • Afro-caribean origin 
    • Raised intra-occular pressure 
  • Other risk factors 
    • Diabetes 
    • Hypertension 
    • Hypothyroidism 
    • Steroid use 
    • Migraine 
    • Sleep apnoea 

Patients of afro-caribbean origin are at higher risk of progression to blindness 

Management 
  • Medical 
    • Eye drops 
      • First line: prostaglandin analogues (increase aqueous outflow from eye through the uveoscleral pathway) or beta blockers (reduce secretion of aqueous) 
      • Second line: carbonic anhydrase inhibitors and alpha agonists 
    • Oral medication: carbonic anhydrase inhibitors (reduce secretion of aqueous) 
  • Surgical 
    • Argon laser trabeculoplasty 
    • Trabeculectomy 


Closed angle glaucoma 

Closed angle glaucoma is a sight-threatening ophthalmic emergency characterized by a rapid rise in intraocular pressure as a result of obstruction of aqueous humour drainage from the anterior chamber of the eye. 

Presentation 
  • Painful red eye 
  • Semi-dilated, non-reactive pupil 
  • Periocular headache 
  • Halos around light
  • Loss of vision 
  • Nausea and vomiting 
  • Systemically unwell 
  • Affected eye is tender and feels hard to the touch

Risk factors for closed angle glaucoma include: 
  • Advanced age 
  • Female gender 
  • Far eastern origin 
  • Hypermetropia 
  • Medications (due to their pupil-dilating effects) 
    • SSRIs 
    • TCA 
    • Anticholingergics 

Treatment 
  • Acetazolamide IV
  • Pilocarpine 4% eye drops 
  • Laser iridotomy or iridoplasty 
  • Iridectomy if laser treatment fails 

Small print gem: carbonic anhydrase drugs are strucurally similar to sulfonamides so should be avoided if patients have an allergy to these 



References 

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Gout

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Gout is an inflammatory arthritis caused by monosodium urate crystals in and around joints. 

The most commonly affected joint is the first metatarsophalangeal joint. When this is affected it is called a podagra. 

Tophi may develop in chronic disease.

The most important risk factor for developing gout is hyperuricaemia. 

Hyperuricaemia may be caused by: 
  • Urate overproduction: 
    • Psoriasis
    • Excessive dietary purine intake 
    • Cytotoxics 
    • B12 
    • Alcohol 
  • Urate underexecretion 
    • Renal impairment 
    • Diuretics 
    • Low-dose aspirin (but not this should still be given for cardioprotection if indicated) 
    • Hypothyroidism 
    • Lead poisoning 

Investigation
  • Microscopy of joint aspirate - monosodium urate crystals are fine, needlelike and negatively birefringent under polarized light. 
  • Serum urate level – usually raised but may be normal during an acute attack
  • XR 
    • Usually normal until chronic disease and then may show extra-articular erosions and widened joint space 

Management 
  • Acute gout 
    • Rest joint 
    • NSAIDs 
    • Colchicine if NSAIDs contraindicated 
    • Corticosteroids (orally or intraarticularly) if NSAIDs/colchicine not sufficient 
    • Do not start allopurinol during an acute attack 
  • Preventative options 
    • Diet inclusive of soy beans, cherries and skimmed milk
    • Avoidance of liver, kidneys, shellfish and yeast extracts/purine rich foods
    • Restrict alcohol intake 
    • Allopurinol 
      • Works by inhibiting xanthine oxidase 
      • Give if 
        • Second attack or 
        • Tophi or 
        • Renal insufficiency or 
        • Uric acid stones or 
        • On diuretics 
      • Start 1-2 weeks after inflammation has settled 


Small print gem: a side effect of colchicine is diarrhoea 


References 

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Polycystic ovarian syndrome

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The definition for polycystic ovarian syndrome varies, but the one adopted by the RCOG is 2 of 3 of: 
  • Polycystic ovaries (12 or more peripheral follicles or ovarian volume >10cm^3) 
  • Oligo or anovulation 
  • Clinical and/or biochemical signs of hyperandrogenism (hirsuitism, acne, alopecia) 

Features associated with polycystic ovarian syndrome include: 

Biochemically:
  • Raised LH (40% of women) 
  • Raised testosterone 
  • Low or normal FSH 

Management 
  • Lifestyle changes to encourage weight loss 
  • OCP to block androgen effects
  • Topical eflornithine hydrochloride (an inhibitor of the enzyme ornithine decarboxylase) for hirsuitism 
  • Metformin
  • Clomifene if fertility issues 
  • ?ovarian drilling 


References

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Secret collector of interesting anonymised ECGs. Fan of the Bath Photomarathon. Lover of cream teas. [Sarah Hudson] (Your Picture)