MRCP revision battle 8.1: Cluster headache

Its Saturday and sunny so I'm not particularly feeling the MRCP revision love.  But the battle must continue, and today's topics are:

Revision battle 8.1: Cluster headache
Revision battle 8.2: Arsenic poisoning
Revision battle 8.3: Mee's lines
Revision battle 8.4: Reversible causes of cardiac arrest
Revision battle 8.5 Pituitary tumours
Revision battle 8.6: Romano-Ward and Jervell-Lange-Nielson



Revision battle 8.1: Cluster headache


Cluster headaches appear in the MRCP exam (and occasionally real life) as:

• severe unilateral pain focused around one eye with
• redness of the eye and possibly
• lid swelling with
• lacrimation and
• nasal congestion

It is worth noting that up to 20% will also get ptosis, which in a minority of cases can be permanent.


Cluster headaches are more common in males (5:1).
Risk of suffering from cluster headache is increased if you are a smoker.


Classically patients will suffer from severe 15 minute to 2 hour bouts of pain once or twice a day over a period of 4 to 12 weeks.


Treatment acutely is 100% oxygen.  S/C sumitriptan and nasal lidocaine are also proposed as treatments.

Prophylactic options include verapamil, prednisolone or lithium.


So onwards to a slightly curveball topic - arsenic poisoning...

MRCP revision battle 8.2: Arsenic poisoning

Arsenic poisoning used to be both a favourite method of murder (allegedly involved in the demise of Napoleon) and a substance commonly found in paint and water pipes.  It is now thankfully carefully controlled so it tends to be found mainly in MRCP exam questions...


Arsenic is still used in the glass, smelter and microelectronic industries, and is found in wood preservatives.


Acute poisoning tends to cause features in 30 mins to 2 hours.

Features of acute arsenic poisoning include:

• severe gastroenteritis
• garlic ordour
• hypersalivation

Treatment for acute poisoning is DMPS.


Symptoms of chronic arsenic poisoning present at different times post-exposure; for example, skin symptoms tend to show clinically around 10 years afterwards.  There are multiple, multiple possible complications of chronic arsenic poisoning but a few which may pop up are:

• keratoses
• Mees lines (if you don't know what these are you'll find out in the next battle!)
• hyperpigmentation
• neuropathy
• muscle fasciculation and wasting

So on to explore Mees lines...

MRCP revision battle 8.3: Mees lines

Mees lines are white transverse lines that go all the way across the nail.

An image of Mees lines can be found here


Mees lines are found in:

• arsenic poisoning
• thalium poisoning
• heavy metal poisoning
• renal failure

 Next up: battle 8.4!

MRCP revision battle 8.4: Reversible causes of cardiac arrest

A little bit of a random one to throw into MRCP revision but a quick recap of the reversible causes of cardiac arrest, famously recalled as the 4 Hs and 4 Ts, can never go amiss...


4 H's:

• hypoxia
• hypovolaemia
• hypothermia
• hypoglycaemia/hyper/hypokalaemia/ other electrolyte imbalance

4 T's:

• Tension pneumothorax
• cardiac Tamponade
• Thombus
• Toxins

I remember the 4 H's in the format of a little picture of a man standing on top of a snow-covered mountain.  He is struggling to breath as there's not much oxygen up there (hypoxia) and  is shivering as its so cold (hypothermia).  He is looking sad and in one hand is an empty water bottle (hypovolaemia) and in the other an empty lunchbox (hypoglycaemia... then remember the hypo/hyper kalaemia from that).

For the 4 T's I think of the less happy phrase of 'Thomas has Ten Toxic Tampons' (= Thombus, tension pneumothorax, toxins, tamponade)



So after a couple of nice straightforward battles let face a juicier one: pituitary tumours...

MRCP revision battle 8.5: Pituitary tumours

Most pituitary tumours are benign adenomas.


Symptoms from pituitary tumours are either due to:

• local pressure
• hormone secretion
• hypopituitism

Local pressure symptoms include:

• bitemporal hemianopia (pressure on CN III)
• palsies of CN III/IV/VI (remember the cavernous sinus anatomy at the end of battle 1.1?)

The commonest hormone secreted by pituitary tumours is prolactin (35%) followed by GH (20%).

30% of pituitary tumours secrete no obvious hormone


Potentially a pituitary tumour can disturb hypothalamic control of temperature, sleep or appetite.

If the tumour erodes the floor of the sella the patient may get CSF rhinorrhoea


Histologically, pituitary tumours fall into the following catagories:

• 70% - chromophobes
• 30% cause a pressure effect
• can produce prolactin, ACTH, GH
• 15% - acidophils
• 10% cause a pressure effect
• can produce GH, prolactin
• 15%  - basophils
• rarely cause a pressure effect
• can produce ACTH

The investigation of choice for suspected pituitary tumours  is MRI.


Finally, in this section we need to cover Nelsons Syndrome.  Nelsons syndrome is a condition that occurs after adrenalectomy for pituitary-dependent cushings.  The adrenalectomy removes the negative feedback on the pituitary which causes ACTH levels to rise massively, leading to hyperpigmentation +/- an invasive pituitary tumour.


Tomorrow we will look at craniopharyngioma, but to finish today on a lighter note onwards to Romano Ward and Jervell-Lange-Nielson Syndromes.

MRCP questions: War 7

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 7.1 to 7.5.

Grab a piece of paper, jot down your answers then compare them to my answers here

Question 1:
An efflux of which ion terminates the cardiac action potential?

Question 2:
What is the mechanism of action of class III antiarrhythmics?


Question 3: 
Name 2 class IV antiarrhythmic drugs

Question 4:
What is the relationship between heart rate and QT?

Question 5:
How do you calculate QT using the Bazzett formula?

Question 6:
State the upper limit of a normal QT

Question 7: 
Name 5 drugs that prolong QT

Question 8:
State 5 metabolic conditions that can prolong QT

Question 9:
Name 2 drugs that increase the effect of adenosine and one that decreases it.

Question 10:
Does positive concordance in the chest leads make a broad complex tachycardia more or less likely to be VT?


answers here

MRCP revision battle 8.6: Romano Ward and Jervell-Lange-Nielson Syndomes

Both Romano-Ward and Jervell-Lange-Nielson Syndrome are congenitial causes of a long QT.

Both are believed to be caused by mutations in the potassium subunit.

The differences are:

1. Romano-Ward is autosomal dominant while Jervell-Lange-Nielson is autosomal recessive
2. Jervell-Lange-Nielson is associated with bilateral deafness; Romano Ward is not.

Thats all for today; if you want to test your recall of topics covered yesterday click here