MRCP revision battle 18.1: Warfarin

Today is another 'octopus' day with 8 battles to embrace (three of which are mercifully brief)

So the topics are:

MRCP revision battle 18.1: Warfarin
MRCP revision battle 18.2: Psoriasis
MRCP revision battle 18.3: Beau's lines
MRCP revision battle 18.4: Elliptocytosis
MRCP revision battle 18.5: Aortic stenosis
MRCP revision battle 18.6: Polymyalgia rheumatica
MRCP revision battle 18.7: Threadworm
MRCP revision battle 18.8: Pseudohypoparathyroidism






MRCP revision battle 18.1: Warfarin


Ah, warfarin... everyone's favourite out-of-hours bleep as a houseofficer.  Originally made as a rat poison, it quickly became a favourite in the UK for the treatment of DVTs, PEs and prevention of clots associated with mechanical heart valves.


Warfarin works by inhibiting vitamin K epoxide reductase, which prevents vitamin K being recycled.  Since vitamin K is a cofactor for factors II, VII, IX and X it decreases coagulation.


Note however that vitamin K is also a cofactor for protein C and protein S, which help inhibit the clotting cascade.  As protein C is initially affected more than the clotting factors by lack of vitamin K warfarin is initially a procoagulant and when started therefore increases the risk of thrombosis.


Warfarin is monitored by INR.  The targets are:

• PE/DVT: INR 2-3
• metallic valve: INR 3-4

The duration of anticoagulation depends on the cause of the clot:

• below knee DVT after surgery: 6 weeks
• above knee DVT/PE after surgery: 3 months
• DVT/PE without precipitating factor identified: 6 months

1-2% of patients on warfarin have a haemorrhage per year.

Other complications of warfarin treatment include:

• increased risk of osteoporosis
• purple toe syndrome - toes turn purple ?secondary to cholesterol deposits 3 to 8 weeks after starting warfarin

Warfarin levels are notoriously difficult to regulate.

Things which increase the effect of warfarin include:

• erythromycine/clarithromycin
• metronidazole
• hyperthyroidism
• cranberry juice
• alcohol
• amiodarone
• propranolol
• fluconazole
• isoniazod
• cimetidine
• omeprazole

Things which decrease the effect of warfarin include:

• rifampacin
• carbamazepine
• chlordiazepoxide
• avocado in excess!

Management of INR outside the desired range depends both on the level and if there is bleeding:

• major bleed
• stop warfarin
• give vit K 5-10mg IV
• give prothrombin complex (II, VII, IX, X) or FFP if this is not available
• INR>8 but no/minimal bleeding
• stop warfarin
• give vit K 2.5-5mg PO/0.5-1mg IV
• restart warfarin when INR<5
• INR 5-8, no bleeding
• stop warfarin
• restart when INR<5
• INR 5-8 minor bleeding
• stop warfarin
• give 1-2.5mg vitamin K PO
• restart when INR<5

As an aside, with an eye on the future, a new drug called dabigatran is looking to usurp warfarin as king of the anticoagulants.  Trials such as RELY and RECOVER have shown dabigatran to be non-inferior to warfarin in preventing thrombosis, to cause fewer bleeding adverse effects and even better not require regular blood tests to check levels.  Of course its expensive and so not yet approved...



On to the second battle of the day, psoriasis...

MRCP revision battle 18.2: Psoriasis

Psoriasis is an autoimmune disease that classically causes a silver-scale topped rash on the skin.

It affects 1-2% of the population.

The cause is believed to be abnormal activity of the type 1 T helper cells.
It is associated wtih HLA CW6, B13, B17 and B27.


Females tend to be affected at a younger age than males.


The main 'types' of psoriasis are:

1. chronic plaque
2. generalised pustular
3. palmo-plantar pustulosis
• strong association with smoking
• tends to affect middle-aged females
4. guttate
• usually young adults/teenagers
• is often preceded by a strep infection 2-4 weeks before
• resolves spontaneously in 2-3 weeks
5. nail
6. flexural

Athropathy is a feature in 8% and may be in the form of :

• symmetric arthritis - appears rheumatoid-like; 50%
• asymmetric arthrtitis - 35% - dactylitis
• arthritis mutilans - <5%
• spondylitis
• distal interphalangeal predominant

Psoriasis can be worsened by multiple factors, including:

• trauma
• infection
• post-partum
• beta blockers
• lithium
• stress
• alcohol
• NSAIDs

Management for skin psoriasis is by a host of lotions and potions - coal tar, dithranol, topical vitamin D.... if these haven't already been drummed into you a brief visit to the BAD website (british association of dermatologists, trying to sound cool) to recap might be a good idea.



Now for a brief skirmish with Beau's lines

MRCP revision battle 18.3: Beau's lines

Beau's lines are transverse depressions in nails due to temporary arrest in their growth.

They are associated with:

• psoriasis
• diabetes
• metabolic disturbances

Now onwards to another very brief battle, elliptocytosis

MRCP revision battle 18.4: Elliptocytosis

Elliptocytosis is an autosomal dominant condition which results in cigar-shaped elliptocytes:

In severe cases they can cause haemolytic anaemia; happily the majority of people with elliptocytosis have no ill effects from it at all.


Now on to a more substantial battle again: aortic stenosis

MRCP revision battle 18.5: Aortic stenosis

Aortic stenosis may be detected incidentally (keen houseofficer noticing the classical ejection systolic murmur radiating to the carotids) or may present with its classical triad of symptoms that can be remembered as 'DAD':

• exertional dyspnoea
• etertional angina
• exertional dizziness

Signs of aortic stenosis include:

• ejection systolic murmur radiating to carotids
• slow rising pulse
• narrow pulse pressure
• heaving apex beat

Things which suggest severe aortic stenosis include:

• LVF
• soft S2
• paradoxically split A2
• S4

 The formal divisions of severity are as follows:

• mild: area >1.5cm, gradient <25
• moderate: area 1-1.5cm, gradient 25-50
• severe: area <1cm, gradient >50
• critical: area <0.7cm, gradient >80

The main causes of aortic stenosis are:

• calcification of the valve
• bicuspid aortic valve

ECG changes which may be associated with aortic stenosis include:

• p mitrale
• LVH
• LAD
• poor R wave progression
• complete heart block if calcification involves the conduction tissue.

Treatment is surgical.  The operative mortality is around 20-25% if there is LVF, 2-8% if not.



So from the very factual aortic stenosis on to the slightly touchy-feeling PMR...

MRCP revision battle 18.6: Polymyalgia rheumatica

Polymyalgia rheumatica (PMR) is a slightly nebulous condition which the Oxford handbook defines as 'symmetrical aching, tenderness and morning stiffness in shoulders and proximal limb muscles, +/- systemic features'.  These systemic features can include anything from fatigue to anorexia...


It generally affects over 70s and is rare in under 60s.


Bloods tend to show a raised ESR


Treatment is with prednisolone (15mg PO OD) which tends to produce a dramatic improvement in days.  This should be decreased by 1mg per month, and of course anti-OP treatment should be given concurrently.

If symptoms recur on decreasing the dose and you have a lovely little old lady stuck on >10mg OD for over a year, it is worth considering methotrexate or azothioprine to try and allow you to decrease the steroid.


As a random aside, 10% of patients with PMR will suffer from carpal tunnel syndrome.



Now get ready to itch as we move on to the penultimate battle of the day, threadworm....

MRCP revision battle 18.7: threadworm

Threadworm, AKA enterobius vernicularis, appears frequently in MRCP questions, usually in relation to patients in institutions.

They tend to present with perianal itching.

Treatment is mebendazole 100mg (or piperazine if the patient happens to be under 2 yrs of age)



On that pleasant note, on to the last battle of the day, pseudohypoparathyroidism

MRCP revision battle 18.8: Pseudohypoparathyroidism

Pseudohypoparathyroidism is an autosomal dominant condition that occurs when a person is insensitive to PTH.


Features include:

• short metacarpals (esp 4th and 5th)
• short stature
• round face
• obese
• low IQ
• dental hypoplasia

It can be diagnosed by a failure of cAMP to increase after injection of parathyroid hormone.  More traditionally, the clinical picture of low calcium, high PTH and normal/raised alk phos is enough.


Treatment is with alfacalcidol.

It is worth noting it is associated with slipped femoral epiphysis.



To end today's battles on an almost comic note (and the fact I find this comic is a reflection that I really should get out more) there also exists a pseudopseudohypoparathyroidism, which is essentially the morphological features of pseudohypoparathyroidism but with normal biochemistry.  Hopefully that'll make you smile if it comes up!


A few questions on yesterday's battles are now online here, otherwise see you tomorrow!

MRCP questions: War 17

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 11.1 to 11.4.

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


Question 1:
What haematological picture do you get in DIC?


Question 2:
What symptoms are associated with jugular foramen syndrome?


Question 3:
Name the commonest form of thyroid cancer.



Question 4:
List 3 causes of unilateral pleural calcification



Question 5:
What condition is associated with a 'plucked chicken skin' appearence?



Question 6:
Legionella is a gram positive bacteria.  True or false?




Question 7:
Which biochemical disturbance is classically associated with legionella?


The answers are here