Friday, 10 September 2010

MRCP revision battle 7.1: cardiac action potentials

I've got that Friday feeling so I've decided to indulge in a cardiology fest.  Today's revision battles will therefore be:

MRCP revision battle 7.1: cardiac action potentials
MRCP revision battle 7.2: the Vaugham-Williams classification system
MRCP revision battle 7.3: long QT
MRCP revision battle 7.4: adenosine
MRCP revision battle 7.5: cause of the broad complex tachycardia

Now I know that may look like a lot but quite a few of the battles are short and almost sweet, so lets get stuck in!




MRCP revision battle 7.1: cardiac action potentials


Understanding the basics of the cardiac action potential is essential to grasp how antiarrhythmic drugs work.  The basic cardiac action potential looks like this:

                                                                                                            thanks to http://commons.wikimedia.org for the image

In stage 0, there is a rapid influx of sodium
Stage 1 is then an efflux of potassium, followed by
Stage 2, which is an influx of calcium.  Finally in
Stage 3 the efflux of pottasium continues, terminating the action potential.


Try and keep this image in mind as we move on to the fabulous world of Vaughan-Williams classification...

MRCP revision battle 7.2: The Vaughan Williams Classification

The Vaughan-Williams classification is a way of dividing anti-arrhythmic drugs into groups based on their mechanism of action.  It was devised in the 1970s, and like some other inventions of that era (such as flares) it has a few flaws.  The main flaw is that many anti-arrhythmics actually work in several different ways, so although they can be put into a class based on their main mechanism of action this grouping only tells you part of how they work.

However, understanding it a) makes you seem clever (most consultants would have forgotten it within hours of passing MRCP) and b) helps you answer MRCP questions correctly.  So lets ignore its faults and embrace it whole-heartedly...



The original classification had groups I, II, III and IV.  A 'catch all' group of V has now been added for awkward drugs who just didn't fit in anywhere originally.  Lets look at each class in turn:


Class Ia:
  • works by blocking sodium channels - called a 'membrane stabiliser'
  • distinguishes itself from the other class Is by having intermediate association/dissociation with the sodium channels --> end result longer action potential
  • members include disopyramide, quinidine and procainamide

Class Ib:
  • works by blocking sodium channels - called a 'membrane stabiliser'
  • distinguishes itself from the other class Is by having fast association/dissociation with the sodium channels --> end result shorter action potential
  • members include lidocaine and phenytoin

Class Ic:
  • works by blocking sodium channels - called a 'membrane stabiliser'
  • distinguises itself from the other class Is by having slow association/dissociation with the sodium channels --> end result same action potential
  • members include flecanide and propafenone

Class II:
  • are beta blockers 
  • I'm sure you don't really need examples but think atenolol, bisoprolol, misoprolol...

Class III:
  • works by blocking potassium channels
  • this results in prolonged repolarisation
  • members include amiodarone and sotolol

Class IV:
  • works by blocking calcium channels
  • members include verapamil and diltiazem

(Class V: = last minute 'catch all', includes digoxin and adenosine)



Thats rather a lot to try and remember; understanding and linking it to the cardiac action potential makes it a bit easier to understand, then a bit of word-play might clarify things further:


To remember the broad classes of drugs, try recalling 'Sodium Blocks Potassium Channels' (just substitute calcium for channels and you have the 4 mechanisms of action)

To remember the members of each class, think "Double quarter pounder, lemonade please, fries please... and salt uh oh vomiting and diarrhoea..."



Got it?  Good, cos you'll need in for battle 7.3, long QT.

MRCP revision battle 7.3: long QT

The QT interval is that sneaky part of the ECG measured from the start of the QRS complex to the end of the T way.  I call it sneaky as as clinicians we rarely pay it much attention, then it just happens to get a bit on the long side and oh whoopsie we have a ventricular arrhythmia on our hands.


The first thing to learn about the QT interval is that it decreases as heart rate increases.  It is therefore necessary to correct it, which is achieved by using either Bazetts or Fridericas formula.

Bazetts = corrected QT = QT/square root of heart rate
Fridericas = corrected QT = QT/cube root of heart rate

Upper limit of normal is generally taken to be 450ms in a man and 470ms in a woman (for some bizarre reason I remember 450 by singing the song 'brimful of asha on the 45' then just remember that females are 20 more)


There are multiple causes of long QT:

  1. familial
    • Romano-Ward Syndrome (to be covered tomorrow)
    • Jervell-Lange-Nielson Syndrome (also to be covered tomorrow)
  2. metabolic
    • low Mg/Ca/K
    • low temp
    • low thyroid (also known as hypothyroidism.. :) )
  3. drugs
    • class I and III antiarrhythmics (which after the last revision battle you should be able to name)
    • erythromycin
    • TCA/haloperidol/risperidone/SSRIs
    • cocaine
    • organophosphates
    • antihistamines
  4. other
    • MI
    • myocarditis
    • SAH

Treatment is possibly beta blockers, possibly ICD.


Now on to revision battle 7.4, to meet a drug that fell into class V...

MRCP revision battle 7.4: Adenosine

Adenosine is a purine nucleoside which clinically is used to try and terminate SVTs/expose the underlying rhythm.  While doing so it has the potential to cause cardiac standstill, so it can have a unique dual action of increasing the adminstering doctor's heart rate in proportion to how much it decreases the receiving patients heart rate.

It's half life is 8 to 15 seconds, and it works by activating potassium channels which decreases AVN conduction.


The effect of adenosine is increased by dipridamol and carbamezepine.
The effect of adenosine is decreased by aminophylline.


A positive of adenosine is that it has no significant negatively inotropic effects.


Risks associated with its use include:
  • enhancing conduction through the accessory pathway in Wolff-Parkinson-White
  • causing a dangerously fast ventricular response in pre-excited AF/flutter

The side effects include:
  • anxiety
  • chest tightness
  • bronchospasm (avoid in asthma)
  • facial flushing
  • nausea

The usual dosing regime is 6mg, then if unsuccessful 12mg 2 mins later and if still unsuccessful another 12mg 2 mins after that.  Ensure cardiac monitoring is in place when it is given (it can cause cardiac standstill) and remember that given its short halflife it must be given as a rapid bolus, flushed instantly with saline.



So to the final revision battle of the day, with that most feared ECG pattern: the broad complex tachycardia.

MRCP revision battle 7.5: broad complex tachycardia

At some point an ECG will be shoved under your nose which shows an unnerving broad complex pattern going at a fast rate.  If in doubt, these must always be regarded as VT.  However, there are a few less scary possibilities, such as:
  • AF with LBBB
  • orthodromic tachycardic WPW
  • ventricular paced rhythm


Essentially the main call is whether the broad complex tachycardia is superventricular or ventricular in origin, and the features the MRCP exam expects you to pick up on to differentiate these two are:

  • AV dissociation - suggests VT
  • fusion/capture beats - suggest VT
  • positive QRS concordance in chest leads - suggests VT
  • marked left axis deviation - suggests VT
  • history of IHD - more likely VT
  • QRS>140ms - suggests VT
  • no response to adenosine/massage - suggests VT


Well thats if for today.  A quick test of yesterdays topics is available here if you still have the energy.

MRCP questions: War 6

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 6.1 to 6.5.

Jot your answers down on a piece of paper then compare them to the answers here

Question 1:
Which HLA is ankylosing spondylitis associated with?

Question 2:
List 5 symptoms/signs associated with acute iritis

Question 3:
What is the correct term for sterile pus in the anterior chamber of the eye?

Question 4:
List 7 infections associated with reactive arthritis


Question 5:
Name and describe a dermatological condition associated with reactive arthritis

Question 6:
What is reiters syndrome?

Question 7:
Define Light's criteria
    Question 8:
    List 5 possible causes of transudates and 5 possible causes of exudates

    Question 9:
    Which 5 causes of pleural effusion would cause a low pH (<7.3)?

    Question 10:
    List 3 associations of yellow nail syndrome




    answers here

    Thursday, 9 September 2010

    MRCP revision battle 6.1: ankylosing spondylitis

    Today's revision threw up a mixed bag of topics... a splash of rheumatology with a dash of respiratory and a hint of ophthalmology.

    So...

    Battle 6.1: ankylosing spondylitis
    Battle 6.2: acute iritis
    Battle 6.3: Reiters syndrome
    Battle 6.4: pleural effusion
    Battle 6.5 yellow nail syndrome

    Lets get started!


    6.1: Ankylosing spondylitis


    Ankylosing spondylitis (AS) is a chronic inflammatory disease of the spine and sacroiliac joints.


    It affects males more than females, intially around 6:1 but altering to around 2:1 by the age of 30.

     95% of patients are + for HLA B27


    Patients often present with low back pain which is worse at night and improves on moving.

    Clinically, the things to observe on regarding a patient with AS are:
    • a loss of lumbar lordosis
    • a fixed kyphosis which is compensated by extension of the cervical spine leading to the classical 
    • 'question mark' posture
    • if the patient turns their head to the side, the whole body may turn
    • there may be decreased chest expansion forcing increased diaphragmatic excursion and hence a
    • prominent abdomen
    A possible test to undertake is Schobers test - find L5 (roughly level with the sacral dimples) then mark a level 5cm below and 10cm above.  Get the patient to bend over; this 15cm distance should increase to at least 20cm, if it doesn't is suggests AS.

      Associations of AS include:
      • iritis
      • aortic regurgitation
      • fibrosis (rare)
      • cardiac conduction abnormalities (around 10%, mostly long PR)
      • secondary amyloidosis

      Management is keeping mobile, NSAIDs and in severe cases tumour necrosis factor alpha blockers such as infliximab.

      As an aside, if considering a TNF alpha blocker its a good idea to check TB status as it is likely to reactivate latent TB.


      Onwards.... 6.2!

      MRCP revision battle 6.2: acute iritis

      If you're anything like me eyes are a bit a vague part of the body... as an A&E SHO I hated dealing with 'the red eye'.  The good news is that MRCP doesn't have too many ophthalmology questions so there aren't too many topics you have to be familiar with.  One not to miss however is acute iritis.

      As an aside, acute irits and anterior uveitis are often used by doctors almost interchangeably, but technically anterior uveitis encompasses both iritis (inflammation of the iris) and iridocyclitis (inflammation of the iris and ciliary body).  Fortunately management is pretty much the same.


      Acute iritis presents as:
      • red eye ('circumcorneal redness'
      • pain
      • photophobia
      • blurred vision
      • lacrimation
      • small pupil (in reccurent cases the pupil may be irregular due to adhesions)

      You may be able to illicit a positive Talbot's test, which is an increase in the patient's pain when you get their eyes to converge (due to the pupils constricting)


      On slit lamp examination you may spot:
      • cells in the anterior chamber
      • white precipitates on back of cornea
      • sometimes a hypopyon (= sterile anterior chamber pus)

      It is associated with ankylosing spondylitis and also Bechets disease.
      It may relapse.


      Treatment requires ophthalmic input due to the need for steroids - and if steroids are given inappropriately to an infected eye the patient may become blind....



      On that happy note, lets move on to Reiters Syndrome

      MRCP revision battle 6.3: Reiters syndrome/Reactive Arthritis

      Reactive arthritis is one of the spondyloarthropathies (alongside ankylosing spondylitis, psoriatic arthritis and enteropathic arthritis).  It is characterised by a sterile arthritis which usually affects the lower limb days to weeks following an infection.  It is associated with being HLA B27 positive.


      Infections commonly associated with reactive arthritis fall into 2 groups:
      • GI infections 
        • campylobacter
        • salmonella
        • yersinia
        • shigella
      • GU infections
        • chlamydia
        • gonnorhora
        • ureaplasma

      The classical triad associated with reactive arthritis is Reiters Syndrome of uveitis/conjunctivitis, urethritis and arthritis ("can't see, can't pee, can't climb a tree")  Apparently in some parts this is becoming a politically incorrect term as Dr Reiter was a member of the Nazi party with a less than perfect record by the 1940s...

      Reactive arthritis can also be associated with keratoderma blenorrhagica, which is brown raised plaques on the hands and feet.  Rarely it can cause aortic incompetance.

      Treatment is generally resting/splinting the affected joint and NSAIDS.


      Now time for some diversification to the liquid world of the pleural effusion....

      MRCP revision battle 6.4: Pleural effusions

      Pleural effusions for me are one of the most interesting clinical signs.  A dull day can be made just that tad more interesting by the characteristic stoney dull percussion note, reminding you there is a reason you percuss everyone's chest.  A chest xray can then almost instantly confirm your clinical judgment (unlike with a murmur, which you may never know if you were just imagining or not) but then theres the 'oh bugger' moment as you realise you need to work out why this patient has an effusion... and most of the options aren't entirely positive....


      The main thing to establish with an effusion is if it is an exudate or a transudate.

      Traditionally a transudate was defined as containing <3g/dl of protein.  However, some doctors prefer to use Light's criteria for determining which label to apply (a criteria which will misclassify 25% of transudates as exudates...)

      Lights criteria is that for a fluid to be an exudate it must either have:
      • pleural:serum protein > 0.5 or
      • pleural:serum LDH > 0.6 or
      • pleural LDH >2/3 upper limit of serum LDH

      So, obviously to make your diagnosis you need a pleural fluid sample and a blood sample.  You should send your pleural sample off for:
      • cell count
      • cytology
      • glucose
      • protein
      • LDH
      • amylase
      • pH
      • Ziel-nielson staining
      and remember to send bloods for glucose, LDH and amylase at the same time (plus any other bloods, like FBC, you might need)


      Armed with the knowledge of transudate or exudate, you can spin forth a list of diffentials:

      Causes of transudates:
      • heart failure
      • renal failure
      • liver failure
      • peritoneal dialysis
      • hypothyroidism
      • Meigs
      • constrictive pericarditis

      Causes of exudates:
      • infection: TB, pneumonia, subphrenic abscess
      • inflammation: Dresslers, pancreatitis, SLE, RA
      • malignancy: mesothelioma, local cancer, lymphoma
      • other: PE, uraemia, yellow nail syndrome


      As the list of differentials is still quite big, apart from your clinical acumen some of the other pleural fluid results can help narrow it out:


      Glucose <3.3 or pH <7.2 or raised LDH suggests:
      • TB
      • malignancy
      • empyema
      • SLE
      • RA
       Its worth noting that *really* low glucoses are usually due to RA or empyema


      Raised amylase suggests:
      • pancreatitis
      • carcinoma
      • bacterial pneumonia
      • oesophageal rupture

      Cytology results can give more clues:
      • neutrophils: pneumonia, TB
      • lymphocytes: malignancy, TB, RA, SLE, sarcoid
      • mesothial cells ++ : pulmonary infarction
      • multinucleated giant cells: RA
      • lupus cells: SLE

      Hopefully these lists should equip you well for any MRCP pleural effusion questions (or even, shock horror, real life on the wards!)


      On to the final battle of today, yellow nail syndrome

      MRCP revision battle 6.5: yellow nail syndrome

      Yellow Nail Syndrome falls into that subsection of clinical conditions that is rarely relevant in real life but disproportionately prevalent in MRCP questions.  Thankfully its fairly straightforward.

      Clinically:
      • thick nails which are
      • excessively curved from side to side and
      • pale yellow. They are
      • slow growing (showing uncovered bulbous fingertips) and have
      • absent lunulae (the little 'moon-shaped' white bits at the base of your nails)
      • onycholysis may be present

      The importance from an MRCP point of view is that they are associated with:

      Thats all for today.  If you fancy a quick little test on yesterday's topics, click here

      MRCP questions: War 5

      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 5.1 to 4.5.

      Jot down your answers on a piece of paper then compare to mine here



      Question 1:
      State the cardinal triad of nephrotic syndrome.

      Question 2:
      Try and list 10 potential complications of nephrotic syndrome

      Question 3:
      In a patient with nephrotic syndrome, what complication might be implied if the question states they develop 'loin pain'?

      Question 4: 
      What is the commonest glomerulonephritis in adults?

      Question 5:
      Does frank haematuria imply a good or bad prognosis in Bergers disease?

      Question 6:
      What HLA types is Bergers disease associated with?

      Question 7:
      What is the treatment for acute epiglottitis?

      Question 8:
      What is the commonest cause of nephrotic syndrome?

      Question 9:
      What tends to be raised in Bergers disease - C3 or C4?

      Question 10:
      Which gender is more affected by Bergers disease?



      Answers here

      Wednesday, 8 September 2010

      MRCP revision battle 5.1: Nephrotic Syndrome

      After yesterdays big push today's revision was less epic, mainly because I started reading "The Lovely Bones" by Alice Sebold and I just got too involved.  My motivation to revise also wasn't helped by the first onexamination question I did being 'renal based', with renal medicine being my personal black hole of knowledge... it doesn't matter how many facts I try to throw into it, it still remains just as black.

      So, today's battles are:
      5.1 nephrotic syndrome
      5.2 renal vein thrombosis
      5.3 IgA glomerulonephritis
      5.4 acute epiglottis



      Battle 5.1: Nephrotic syndrome


      Nephrotic syndrome is a classic triad of:
      • >3g proteinuria
      • hypoalbuminaemia <25 and
      • oedema
      It is also strongly associated with hypercholesterolaemia


      80% of the time it is associated with glomerulonephritis, a fiendishly complex set of conditions.


      The rest of the time its possible causes are many and varied:
      • diabetes mellitus
      • leprosy/malaria/HBV
      • myeloma/lymphoma
      • amyloidosis
      • SLE
      • gold/penicillamine/NSAIDS/captopril/interferon alpha/heroin
      • pre-eclampsia
      • accelerated hypertension
      • sickle cell disease
      • Alports
      • rarely visico-ureteric reflux
      I'm afraid I don't have a clever way/inclination to remember that list, I just hope that by reading it a few times in the exam a faint light of recognition may go on at the appropriate time.


      Happily I do have a way of remembering the potential complications of nephrotic syndrome, which is good since sneaky MRCP examiners may be trying to get you to guess nephrotic syndrome from a description of the complications alongside part of the classic triad.

      My mnemoric is BOB, I HIT HIM:
      • B12 deficiency
      • Osteomalacia
      • Budd-Chiari
      • Infections
      • Hyperlipidaemia
      • Immunosupression
      • Thrombosis (including renal vein thrombosis)
      • Hyponatraemia
      • Iron deficiency
      • Malnutrition

      Treatment for nephrotic syndrome is to restrict salt, treat the cause, prophylactic heparin, treat any hypertension and potentially give furosemide or ACE-i.


      On to 5.2... renal vein thrombosis

      MRCP revision battle 5.2: Renal vein thrombosis

      Renal vein thrombosis can occur due to:
      • nephrotic syndrome inducing a hypercoagulable state
      • invasion of the renal vein by renal cell carcinoma
      • thombophillia

      It is often asymptomatic, but equally may present with haematuria, loin pain, palpable mass or a sudden worsening of renal function.


      Treatment is with warfarin, anticoagulated to INR 2-3 for 3-6 months.

       Follow me to battle 5.3....

      MRCP revision battle 5.3: IgA Glomerulonephritis

      As if the glomerulonephropathies aren't tricky enough (hence why series 5 of the battles only discusses one of them) they can also have a series of pseudonyms/ 'nicknames.'  For example, IgA nephropathy also goes by the labels 'Bergers disease' and 'mesangioproliferative glomerulonephritis'.  For simplicity, I'll just refer to it as IgA nephropathy.


      IgA nephropathy is the commonest GN in adults, and it classically affects young males after an URTI.  So, in the exam look out for the 25 yr old man who has haematuria following a sore throat.

      Symptoms may just be micro/macro haematuria, or match the nephrotic syndrome triad.

      Incidence is increased in those from the far east, and those with HLA DQw7 or HLA B35.

      Associations include cirrhosis, dermatitis herpetiformis, ank spon, Wiskott-Aldrich syndrome and chronic liver or lung disease.


      IgA is positive in 50% of cases and C3 tends to be raised.


      25% of cases progress to end stage renal disease.

      Frank haematuria is associated with a good prognosis.
      Being male, having proteinuria, hypertension, smoking or high lipids are all associated with a poor prognosis.


      Phew, thats one of the GN covered... a few more to face at a later date... now lets diversify for the last battle of the day to acute epiglottis.

      MRCP revision battle 5.4: Acute Epiglottitis

      Since the introduction of the Hib vaccine the potentially life-threatening condition of acute epiglottitis has happily become rare.  Except, of course, in the MRCP exam.

      The commonest cause of acute epiglottis was always h.influenzae, but many other pathogens can also cause it.

      Presentation tends to be a 'toxic' looking patient with fever and stridor, often with a preceding sore throat.


      Treatment is with a 3rd generation cephalosporin.



      That's it for today, but if you fancy testing yourself on yesterday's battles click here to go to war 4...

      MRCP questions: War 4

      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 4.1 to 4.5.

      Jot down your answers on a piece of paper then compare them to my answers here


      Question 1: 
      What pattern would COPD produce on spirometry?

      Question 2:
      With what condition is thermoactinomyces vulgaris associated?

      Question 3:
      In which zone of the lungs would fibrosis secondary to EAA classically occur?


      Question 4:
      Can you name 11 causes of lung fibrosis?

      Question 5:
      Can you name at least 10 causes of clubbing?


      answers here

      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...)

      So, C BAR TAPS =
      • 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...