MRCP revision battle 37.1: TB

Today has a respiratory feel....


MRCP revision battle 37.1: TB
MRCP revision battle 37.2: DVT/PE in pregnancy
MRCP revision battle 37.3: Asthma
MRCP revision battle 37.4: Cor pulmonale
MRCP revision battle 37.5: alpha-1 antitrypsin deficiency
MRCP revision battle 37.6: Cystic fibrosis
MRCP revision battle 37.7: HPOA





MRCP revision battle 37.1: TB


TB is an infection caused by mycobacterium tuberculosis.  Primary infection is usually in the lungs (ghon focus, usually in the mid or lower zones).  Second favourite site for primary infection = GI, ileocaecal area.


Incidence =7000/yr in UK


Spread is by droplet infection. Household contacts have 1 in 4 chance of infection therefore contact tracing is very important and TB is a notifiable disease.


Primary TB is often symptomless. Although it may cause fever, sweats, anorexia, cough or erthyema nodosum.  If the immune system ‘wins’, the TB is walled off by calcification; however, the TB remains active in ~ 20% calcified areas and may be reactivated when immune system is weakened, eg steroids, diabetes, HIV.


Post-primary TB makes you ill – fever, malaise, weight loss, anorexia, tiredness, cough, haemoptysis, rarely night sweats.



 It can spread to:

• brain = meningeal TB
• spine = Potts fracture
• blood = miliary
• skin = lupus vulgaris

Diagnosis:
•    CXR
•    Sputum cultured/stained with Zielh-Nielsen – looking for acid-fast bacilli
•    Mantoux test of little help in the UK due to BCG

BCG = bacilli calmette-guerin – decreases risk of TB by 50%


Treatment: DOTS
•    2 months rifampicin, isoniazid, pyrazinamide and ethambutol (=RIPE)
•    then 4 months rifamicin and isoniazid
•    Pyridoxine throughout to protect against neuropathic effects of isoniazid



MRCP (and real life) side effects of TB meds to be aware of:

Rifampicin turns bodily excreations orange
Isoniazid and rifampicin cause cirrhosis – check LFTs
Pyrazinamide decreases urea excreation = risk of gout and CI in gout sufferers
Ethambutol can affect the optic nerve - check colour vision



On to DVT and PE in pregnancy...

MRCP revision battle 37.2: DVT/PE in pregnancy

It is one of those unfortunate situations: pregnancy makes DVT/PE more likely (increases risk around 6x), but the presence of a fetus also makes your preferred investigative tests more risky.


Risk is more increased if:

• >35 yrs
• higher parity
• raised BMI
• smoker
• sickle cell
• anaemic
• dehydration
• not blood group O

The consensus on management of ?PE in pregnancy seems to be:

• CXR in all cases
• compression doppler in all cases - if this shows DVT you can just treat without needing to investigate further

In terms of the next investigation if you clinically suspect PE but the doppler is normal there is a lack of consensus:

• CTPA delivers 10-30% less radiation to the fetus but
• V/Q scan causes less radiation to the maternal breast tissue

In general CTPA seems to 'win'



Note that d-dimer is usually 'normal' in the first trimester of pregnancy, rises in the second to third and then returns to baseline at 4-6 weeks post-partum.  However, it is generally not recommended as an investigation in pregnant women.



Treatment for DVT/PE in pregnancy is LMWH, continued for 6 months (with at least 6 weeks of anticoagulation post-partum)

For the really keen:

Patient plus article on DVT/PE in pregnancy

Next... MRCP revision battle 37.3...

MRCP revision battle 37.3: Asthma

Asthma is a condition characterised by periods of dyspnoea, cough and wheeze caused by reversible airways obstruction.


Asthma diagnosis

The table below (from the 2009 BTS/SIGN guidelines) lists the factors that increase or decrease the probability of the presentation being asthma:

If from history/examination you believe there is a:

• high probability the patient has asthma --> being a trial of treatment
• intermediate probability of asthma --> perform spirometry:
• FEV1/FVC <0.7 - trial asthma treatment
• FEV1/FVC >0.7 - refer to specialist

After a trial of treatment >400mls improvement in FEV1 or PEFR >15% is significant


In a peakflow diary, look for diurnal variation >25%


Treatment of asthma

Treatment of asthma follows a stepwise approach (BTS/SIGN guidelines):

1. Mild intermittent asthma
•  SABA (short-acting inhaled beta 2 agonist) PRN 
• salamol, salbutamol
2. Regular preventor therapy
• corticosteroid 200-800mcg per day
• beclometasone, fluticasone, budesonide
3. Initial add-on therapy
• LABA (long-acting inhaled beta 2 agonist (eg salmeterol))
• if this doesn't work, stop and trial an oral therapy such as leukotriene receptor antagonist or theophylline
4. Persistant poor control
• increase steroid inhaler up to 2000mcg per day
• add leukotriene receptor antagonist or theophylline
5. Continuous or frequent oral steroids

If stable for 3 months, consider stepping down a step.




Severity of asthma

In acute asthma attacks, severity may be graded as follows:

Severe:

• unable to complete sentences
• RR>25
• PEFR<50% predicted or best
• pulse >110

Life-threatening:

• silent chest
• PEFR <33% predicted or best
• bradycardia
• hypotension
• normal or raised CO2
• exhaustion

Management of acute severe asthma

Think 'O! sip Ma':

• high flow oxygen
• 5mg salbutamol neb
• 500mcg ipratropium neb
• 30mg prednisolone (or 100mg hydrocortisone IV)
• magnesium 1.2g and aminophylline if still not improving

And make sure ITU know if things aren't going well....


Now for a battle with cor pulmonale...

MRCP revision battle 37.4: Cor pulmonale

Cor pulmonale is right heart failure caused by chronic pulmonary hypertension

Normal pulmonary artery pressure = 15mmHg.

Pulmonary hypertension = pulmonary artery pressure >25mmHg at rest or >30mmHg on exercise

Causes of cor pulmonale include:

• lung disease - of which COPD is by far the commonest
• pulmonary vascular disease - PE
•  rib cage deformity

Presentation is:

• dyspnoea
• fatigue
• syncope

Signs:

• raised JVP, a and v waves
• RV heave
• loud P2
• pansystolic murmur - tricuspid regurgitation
• peripheral oedema
• hepatomegaly
• Graham Steell murmur = high-pitched early diastolic murmur, best heard 2nd left intercostal space with pt in full inspiration = pulmonary regurgitation

Investigations:

• CXR
• FBC - look for secondary polycythaemia
• ECG - R axis deviation, right ventricular hypertrophy

Management:

• treat cause
• treat symptoms
• ?heart-lung transplant

Next up: alpha-1 antitrypsin deficiency

MRCP revision battle 37.5: alpha-1 antitrypsin deficiency

alpha-1 antitrypsin is a serine protease inhibitor produced in the liver.


In the lung it prevents neutrophil elastase from breaking down the alveolar wall.
It is inactivated by cigarette smoke.


Genetic varients of alpha-1 antitrypsin exist and are labelled based on their electrophoresis mobility, with M (medium), S (slow) and Z (very slow).  MM is 'normal' while 'ZZ' has the worst prognosis with panlobular emphysema.


Patients with an alpha-1 antitrypsin defiency are likely to develop COPD early (even without smoking) and liver cirrhosis is common.



Now for a very straightforward battle - cystic fibrosis

MRCP revision battle 37.6: Cystic fibrosis

CF is an autosomal recessive genetic disorder which results in a mutation of CFTR, leading to Cl not leaving cells and so more Na and water entering, resulting in thick, sticky secreations.



The mutation is on chromosome 7.  70% are ΔF5O8


Incidence = 1/2000.  Carriers = 1/25


Presentation in neonates is failure to thrive, meconim ileus or rectal prolapse.
Later presentation tends to be recurrent respiratory infections, cough, wheeze, bronchiectasis.  85% have steatorrhoea.


Signs include:
-    cyanosis
-    clubbing
-    bilateral course crackles


Diagnosis is by pilocarpine sweat test.  Na/Cl>60mmol/l, usually Cl>Na.  CXR may show bronchietasis.  PCR can pick up 90% of mutations.  Faecal elastase is a good screening tool for exocrine pancreatic dysfunction.  Spirometry shows obstruction.


Treatment is MDT, physio, enzyme replacement, heart/lung transplant.


Complications include  

• diabetes (1/3) 
• gallstones
• cirrhosis
• OP
• male infertility (no vas deferens or epididimus)
• vasculitis
• nasal polyps (1/3) 
• HPOA (if you don't know what this is you will by the end of the next battle)
• infections
• s.aureus
• h.influenzae
• pseudomonas
• s.pneumoniae
• burkholderia cepacia (gram negative)
• aspergillos

It tends to be the upper lobes of the lungs that are damaged.




Mean age of death ~30.



So to the final battle of the day, HPOA...

MRCP revision battle 37.7: HPOA

HPOA = hypertrophic pulmonary osteoarthropathy is a paraneoplastic syndrome consisting of periostitis, arthritis and clubbing.



It is seen in around 50% of patients with mesothelioma.

Of the 'usual' lung cancers it is most commonly associated with adenocarcinomas and least commonly associated with small cell lung cancer.



Thats it for today