Tuesday, 7 September 2010

MRCP questions: War 3

As with previous 'wars' after 'battles' these are just a few quick questions to see if your brain cells have retained the information provided in battles 3.1 and 3.2.

Jot down your answers then look at my answers here

Question 1: 
Can you now state 10 causes of bilateral hilar lymphadenopathy?

Question 2: 
What are the two main causes of hypercalcaemia?

Question 3:
Name the 2 drugs mentioned that can cause hypercalcaemia

Question 4:
Toxicity of which 2 vitamins can cause hypercalcaemia?

Question 5:
Which 5 cancers are most commonly associated with boney mets?

Question 6:
What effect does vit D have on calcium and phosphate?

Question 7:
What will bloods show in secondary hyperparathyroidism?

Question 8: 
What is the commonest cause of primary hyperparathyroidism?

Question 9:
What is vitamin D made from?

Question 10:
What is the effect of PTH on calcium and phosphate levels?

answers here

MRCP revision battle 4.5: Clubbing

This clinical sign should be on one of those 'you know you're a medic when...' lists, as in "you know you're a medic when clubbing relates to fingers rather than a night out..."

As an undergraduate you probably spent cumulative hours staring purposefully at fingers to convince the examiner you were looking for clubbing, and now at MRCP you need to think about it again..

Firstly, for a definition: clubbing is defined as loss of the obtuse angle between the nail and the dorsum, with thickening of the nail bed and increased curvature of the nail bed in both directions.  There may also be increased fluctuation of the nail bed and the finger can sometimes have a 'drumstick like' appearence.

A picture can be found here

And now, for some causes, and a cry of 'ACE MILC (milk) MCFAB'!

Cardiac causes:
  • atrial myxoma
  • cyanotic congenital heart disease
  • endocarditis
GI causes:
  • malabsorption
  • inflammatory bowel disease
  • lymphoma
  • cirrhosis
Lung causes:
  • mesothioloma
  • CF and cancer
  • fibrosis
  • abscess
  • bronchiectasis

Thats all for today, but if you participated in battle 3 yesterday and fancy testing yourself go on for a brief test here...

MRCP revision battle 4.4: Lung fibrosis

You may need to be able to come up with a list of differentials for lung fibrosis... my way of remembering it is C BAR TAPS (mainly because at some point in the revision process I always get an urge to visit a drinking establishment and 'see' the bar taps, and possibly even purchase something from them...)

  • Cryptogenic fibrosing alveolitis
  • Bleomycin
  • Amiodarone
  • Radiation/rheumatological disease (=RA and SLE)
  • TB
  • Asbestosis
  • Paraquat/pigeon breeders lung
  • Sarcoid/siliosis

And finally for today, battle 4.5...

MRCP revision battle 4.3: Aspergillus

Aspergillus is a group of molds/fungi.  Allegedly they got their name from looking like water does when it falls from an aspergillum, which is an instrument for sprinkling holy water (that fact is unlikely to be necessary in MRCP but its nice for the brain to read bits its not obligated to remember every now and then)

Aspergillus can affect the lungs in 6 main different ways:
  1. It can cause asthma
    • a type 1 hypersensitivity reaction
    • prick test +, precipitans/culture +
  2.   It can cause an aspergilloma
    • = a fungal ball inside a pre-existing cavity
    • usually asymptomatic but may cause haemoptysis, lethargy or weight loss
    • treated by ?surgery ?amphotericin paste under bronchoscopy
    • prick test -, precipitans/culture ++
  3.  It can cause allergic bronchopulmonary aspergillosis
    • type 1 and type 3 hypersensitivity
    • CXR may show bronchietasis, lobar collapse or upper lobe fibrosis, or patchy lesions
    • prick test +, precipitans/culture +
    • also IgE levels are raised
  4. It can cause invasive aspergillosis
    • only occurs in immunocompromised individuals
    • prick test +/-, precipitans/culture +/-
  5. It can cause EAA
    • + serum precipitans to aspergillus clavatus
  6. It can simply colonise.

After that slightly heavy-going section, lets go on to think about BAR TAPS...

MRCP revision battle 4.2: Extrinsic Allergic Alveolitis

This is inflammation of lung tissue due to hypersensitivity to an allergen.  To get more scientific, it is a Gell and Coombs type 3 reaction acutely and a type 4 reaction chronically.

Clinically, an acute reaction occurs 4-6 hours post exposure and manifests as fever, rigors, dry cough, dyspnoea and myalgia.  Auscultation of the lungs might reveal crackles but no wheeze.

Chronically EAA causes dyspnoea, weight loss and can eventually lead to type 1 respiratory failure and cor pulmonale.

There are several different 'flavours' of EAA, each precipitated by something different.  These include:
  • Farmers lung: micropolyspora faeni or thermoactinomyces vulgaris or Saccharopolyspora rectivirgula
  • malt workers lung: aspergillos clavatus
  • mushroom workers lung: thermophilic actinomycetes
or, more modernly:
  • hot tub lung: mycobacterium avium in poorly maintaned hottubs!

A CXR acutely might show mid-zone mottling; chronically upper zone fibrosis might be seen.  It can also be a cause of bilateral hilar lymphadenopathy (remember battle 3.1?)

Spirometry gives a restrictive picture and lavage will show lymphocytes.

Treatment is oxygen, possibly steroids.

Allons-y to battle 4.3!

MRCP revision battle 4.1: lung function tests

After working an excessive number of hours and recovering thanks to chocolate cake (do click here to visit the ultimate chocolate cake recipe, which really is just amazing) I've managed a bit of a revision spurt, mainly through the world of lungs.

So today we have:
battle 4.1: pulmonary function tests
battle 4.2: extrinsic allergic alveolitis
battle 4.3: aspergillosis
battle 4.4: fibrosis
then bringing up the rear battle 4.5, that classic clinical sign clubbing.

Battle 4.1: Pulmonary function tests

Using a spirometer, ask your patient to blow as hard, as fast and as long as possible.  The spirometer will then give you their FEV1 (=forced expiratory volume in 1 second) and FVC (= forced vital capacity.)  These can be plotted, giving graphs that look like this.

In the exam you are far more likely to just get figures and need to be able to recognise them as representing either an obstructive or a restrictive picture.

Obstructive pattern

Obstructive lung function usually gives a very reduced FEV1 and a less severely reduced FVC.  This means that overall the FEV1/FVC ratio is <75%.

Classical causes of an obstructive pattern are COPD and asthma

Restrictive pattern

Restrictive lung function causes a reduced FVC, and FEV1/FVC remains either the same or may increase.

Causes include LONE K: lung fibrosis, obesity, neuromuscular problems, effusion, kyphoscoliosis.

That was short and sweet... onwards to battle 4.2...