respiratory

Question 1

what is the main abnormality seen in the CXR?

Answer 1

Left hilar mass

Question 2

DRUG HISTORY

i) name two resp symptoms that beta blockers may cause
ii) name two drugs that may cause interstitial lung disease (antiarrhythmic and abx)

Answer 2

i) b blockers can cause SOB and wheeze
ii) ILD - amiodarone & nitrofurantoin

Question 3

PNEUMONIA

i) what is community acquired? what is hospital acquired? what is healthcare associated? name three other causes
ii) name four symptoms? what imaging should be done? name five bloods to be done? what is urine dipped for?
iii) what is in the CURB65 score?
iv) what is the treatment for CURB 65 0-1? 2? >3?

Answer 3

i) CAP - pulm parenchyma infection w acute infection symptoms
* HAP - presents >48hrs post admin
* HCAP (healthcare assoc) - nursing homes
* also caused by aspiration (inhalation of contents in pts with altered mental state/stroke) > lung injury & infection, Ventilator assisted, PCP - opportunistic infection in HIV pts

ii) Fever, Cough - purulent sputum which may be blood stained, SOB, Malaise, loss of appetite, myalgia
Bloods - FBC, U&E, LFT, CRP, cultures
- Sputum for microscopy & culture
- Urine for legionella

iii) C onfusion
U rea >7
Resp rate > 30
Blood pressure <90/60

iv) * CURB65 0-1 = outpatient tx - amox 500mg TDS /clarith 500mg BD for 5 days
* CURB 2 - = inpatient tx (amox + clarith/doxycyc) oral/IV 500mg bd for 7 days
* CURB65 >3 = consider ITU admission (co-amox TDS + clarith/doxycyc IV) BD for 7 days

Question 4

TB

i) what is it? how is it transmitted?
ii) what process leads to latent TB? which acid is involved in establishing latent TB? which zone of the lung does it usually affect?
iii) name four general symptoms?
iv) name three extra pulm symptoms? name three RFs?

Answer 4

i) Granulomatous disease caused by mycobacteria
* Infection occ via droplet transmission

ii) latent TB > Mycobac are engulfed and replicate inside alveolar MPs
* Mycolic acid prev degred of mycobac > caseating granuloma (latent TB)
* Typically affects apical/upper zones of lung

iii) General - cough, fever, haemoptysis, malaise, weight loss

iv) Extra pulm - arthritis, meningitis, finger clubbing
* RF - endemic area, alcoholic, homless, immuno comp

Question 5

TB INVESTIGATION AND TX

i) what should be done first? what imaging is done? how many sputum samples should be taken?
ii) what blood is especially important to guide treatment? what two assays can detect latent TB?
iii) what may imaging show? what stain can be used and what is looked for on sputum culture?
iv) should you wait for culture results before starting treatment if clin suspic?
v) what treatment is given for 6 months? what is given for the next four months?

Answer 5

i) First isolate patient
- Imaging - CXR
- take aat least 3 sputum samples

ii) Bloods - FBC, UE, LFT (TB meds can be hepatotox so need baseline)
- if latent - mantoux skin test or IFNy rel assay
- seek HIV status

iii) CXR - apical changes or pl eff
- sputum - ziehl neeslen stain to look for acid fast bacilli / nuc amplific testing on at least one sample to isolate organism

iv) treatment should be started without waiting for culture results if clinical suspic of TB

v) 6 months total medical therapy - 2 months isoniazid, rifampicin, pyrazinamide and ethambuton
* then 4 months of just isonisazid and rifampicin - direct observed tx

Question 6

COPD

i) what is it? what happens to the airways because of it? what two things does it comprise of? explain each one?
ii) what is the most common cause? name two other causes? what should be suspected in a young person with symptoms? name four symptoms
iii) what is the best initial test? what is used to grade breathlessness? what imaging needs to be done to exclude other pathology? what is used to grade airway obstruction?
iv) what is the single most effective intervention? which two drugs are first line? what is used to guide treatment? what four drugs in combination can be given?
v) what should be given if PaO2 is <7.3? which two vaccines should be considered? what other therapy can be effective?

Answer 6

i) Airflow limitation second to abnormal inflammation
- airway remod 2 to chronic inflam of lung strucs, parenc & vasculature as a response to inhaled stim (smoke)
*emphysema + chronic bronchitis
* emphysema = alv wall destruction due to inflam change
* chronic bronchitis - goblet cell hyperplasia > inc mucus > chronic cough

ii) tobacco smoking is most common cause but air pollution and expos to toxic subs is also implicated
* a1 anti-trypsin defic should be suspected in a young person with emphysema
- symptoms exertional breathlessness, wheeze, regular sputum prod and bronchitis in the winter, haemoptysis, weight loss

iii) Spirometry - best initial test
* Grade breathlessness with MRC dyspnoea scale
* CXR to exclude any other pathology
* sputum culture to identify organisms

iv) smoking cessation - single most effective intervention`
- SABA or SAMA are first line
- use FEV1 to guide further tx - if FEV1 >50% then give LABA or LAMA & stop SAMA,
If FEV1 <50% give LABA + ICS or LAMA
- consider theophylline/mucolytics

v) LTOT if Pa02 < 7.3 - improves mort and should be on for at least 15 hrs/day (greater benefit at 20hrs/day)
* flu vacc and pneumococcal vacc
*physio/pulm rehab

Question 7

BRONCHIECTASIS

i) what is it? why do patients get recurrent episodes?
ii) name three things it can be characterised by? what is it secondary to
iii) name four causes?
iv) name three symptoms? what can be heard on auscultation? what may be seen in the hands?

Answer 7

i) irreversible airway dilat as a result of chronic inflam caused by imm response to infection
- dilated airways are more suscep to repeat colonisation > recurrent episodes

ii) charac by recurrent infection, chronic cough w purulent sputum & bacterial infec
- secondary to dilatation of the airways

iii) can be caused by immunodefic (HGG), rheumatoid, katagener syndrome, young synd, CF, post infectious

iv) wheeze, SOB, cough - espec with lots of purulent sputum
- coarse inspiratory crepitations on ausculatation
- hands - finger clubbing

Question 8

BRONCHIECTASIS INVESTIGATION AND TX

i) what is the gold standard imaging? what sign may be seen?
ii) what may be seen on CXR? name three blood tests to order
iii) what is the most important thing to target with therapy? what other health professional may be helpful? what should be done if patient has difficulty with ADLs?
iv) which two drugs should response be assessed against?
v) what should be started while awaiting sputum micro? what can be done if there is a poor response?

Answer 8

iii) High Resol CT is gold standard
- see signet ring sign (bronchus and artery should be same size but bronch is v dilated) and tree bud appearance

ii) CXR - tram tracks / fluid level
- bloods - order aspergillus, FBC, UE, serum Ig

iii) airway clearance is most important - chest physio and mucolytic therapy
- physio if - chronic cough and evidence of mucus plug on HRCT
- pulm rehab if pt has difficulty with ADLs

iv) assess response to b2 agonist/anticholinergic bronchidilator therapy

v) start abx - inhaled while awaiting sputum micro - init on amox/clarith
* poor response > lung sx

Question 9

CYSTIC FIBROSIS

i) what inheritance pattern does it have? which gene on which chromo is implicated? how does this lead to CF?
ii) which three organs are principally affected? and what happens in each
iii) name four resp symptoms seen? how may children present? (4)
iv) name three reproductive symptoms?
v) name three GI/endo symptoms?

Answer 9

i) Auto reccessive - defect in CFTR gene on chromosome 7
- leads to CF as CFTR mut affects cl transport - thick secretions - get bup of secretions

ii) secretions in in pancreas > blocks ducts / damage panc cells
- intestinal transport > block bile ducts
- secretions in lungs > predis to chronic infection/ colonisation

iii) Resp - wheeze, breathless, cough, purulent sputum, finger clubbing
- paeds - neonates have jaundice, fail to thrive, intest obstruc 2 to meconium ileus

iv) reprod - male infertility w absence of duct def, female subfert
v) GI/endo - DM, panc insuff, steatorrhea, liver disease, gallstones, osteoporosis

Question 10

CF TREATMENT

i) what test is diagnostic? how is it done?
ii) name two imaging test to be done? how can resp function be tested?
iii) where can a patient be referred for chest symptoms? name three drugs they may be put on? what is given if P aeruginosa is the causative organism
iv) when is a corticosteroid used?
v) name three treatments for GI symptoms?

Answer 10

i) dx with sweat test
- pilocarpine applied to stim sweating and collect sample > Cl conc of >60mmol/L on two diff occ is diagnostic

ii) imaging - CXR, HRCT
- spirometry to assess resp func

iii) chest symptoms = Chest physio and
- may be put on SABA PRN, mucolytics (dornase alfa) or neb tobramycin if P.aeruginosa, oral/IV abx

iv) CS use for acute exacerbation or in aspergillus infec
v) tx for GI/endo symp = panc enz and fat sol vit supp w high calorie meals, ursodeoxycholic acid in hepbil disease, stool softner, laxatives

Question 11

IDIOPATHIC PULMONARY FIBROSIS

i) what is it the most common presentation of? what does it involve? after what age do 2/3 patients present? what is the fibrosis/inflam secondary to? what causes the decreased lung function?
ii) name three symptoms? what may be seen in the hands? what may be heard on auscultation? what pattern is seen on pulm function tests?
iii) what should be done to exclude other dx? what is the gold standard imaging? what will spirometry show? what may be seen on imaging?
iv) what are the two mainstay of treatment? is medical tx beneficial? what may some patients be offered?
v) what is the prognosis?

Answer 11

i) Most common presentation of interstitial lung disease
* Progressive scarring and fibrosis of lung interstitium
* 2/3 of people presenting >60yrs
* fibrosis and inflam 2 to cytokine activation and medication > normal tissue repair is adversley affected
* fibroblastic foci formed in the interstit > disrup normal lung tiss > decrease in function
* tobacco smoking implicated

ii) Patients present at older age
* persistent and progressive dyspnoea, worse on exertion
* cough
* finger clubbing
* bilat inspiratory crackles on ausc
* restrictive pattern on pulm func tests

iii) Bloods to exclude other dx
* HRCT of thorax - gold standard > ground glass appearance
- spirometry > restrictive pattern (FEV1 normal/dec and FEV1:FVC inc)
* CXR - bilateral lower zone reticulonodular shadows

iv) Pulm rehab and supportive care are mainstay
* medical tx has little benefit
* some patients may be offered a lung transplant

v) Poor prognosis - avg life expectancy 3-5yrs after diagnosis

Question 12

SARCOIDOSIS

i) what is it? what is it characterised by? which ethnicities is there higher incidence in? how does it generally present?
ii) name two pulm features seen? name two cutaneous changes? what disease may it be associated with? how may eyes be affected?
iii) which imaging may be done? what may be seen? name three bloods that may be elevated? what will tuberculin skin test result be?
iv) how is asymp/bilateral hilar lymphado treated? how is symptomatic with infiltrates/fibrosis treated?
v) what type of drugs are given if severe or unresponsive? what can be given for cutaneous/ocular manifestations?

Answer 12

i) Chronic granulomatous disorder of unknown cause > aff multiple organ systems
* charac by non caseating granulomas
* higher incidence in afrocarrib/scand
generally presents w flu like illness - pyrexia

ii) pulm features are most common - dry cough and dyspnoea
* cutaneous change eg maculopap rash and erythema nodosum on legs
* assoc w lyme disease
* dry eyes/ant uveitis
* bell palsy, polyarthritis & hypercalc due to vit D change (2 to granulomatous change)

iii) CXR - use for staging - hilar lymphadenopathy, infiltrates or fibrosis
* Bloods - ca, esr, ace may be elevated, LFTs may be deranged
* tuberculin test will be negative

iv) If asymp and bilat hilar lymphado - observe
* if symp with HLNs, infiltrates or fibrosis give ICS

v) tx with cytotoxics (methotrexate/HCC) if severe or unresponsive
* topical corticosteroids for cutaneous and ocular manifestiations

Question 13

PLEURAL EFFUSION

i) what is it? what is transudate? what is exudate? name three causes of each?
ii) what criteria is used to differentiate between trans and exudate?
iii) how may a patient present? (2) what is seen if effusion is large? how may percussion sound? name two other features on exam?
iv) what three things may signal it is transudate? what should not be done in this case?
v) what should be done for exudate?

Answer 13

i) Greater than normal amount of fluid collects in the pleural space
- transudate (inc cap hydrostat pressure) - due to HF, liver fail, hypoalbuminm, meig syndrome (Peff+ascites+benign ovarian tumour), PE
- exudate (inc cap permeability - usually high protein) - due to inflam, neoplasia, infec eg pneum, TB, lung cancer

ii) differentiate with Light criteria - exudates usually have protein >35ng & transudates prot content <25 (if between 25 and 35 then criteria using LDH and prot ratios to classify)

iii) asymp or present with SOB and pleuritic chest pain
- tracheal deviation if large
- stony dull percussion
- reduced air entry and chest expansion

iv) transudate - look at clinical picture eg if LVF, dialysis, hypoalbumin (if transudate and bilateral do not perform asipiration)
v) exudate > pleural aspiration

Question 14

PLEURAL EFFUSION IX AND TX

i) name three things pleural fluid should be sent for? what should be suspic if pH is <7.2?
ii) what should be treated? how may symptoms be relieved? (2)
iii) what should be inserted into the safe triangle? what is the safe triangle?
iv) what is pleurodesis? when should this be done?
v) what should be done if empyema or para pneumonic? (2)

Answer 14

i) fluid testing - send for protein, LDH, gram stain, cytology, micro
- if pH <7.2 = suspcious of empyema or para pneumonic effusion (non infective P eff on bfround of pneumonia)

ii) treat underlying cause
- tap or chest drain to relieve symptoms

iii) chest drain in safe triangle (mid ax line, horiz line from the nipple and lat border of pec major) - drain in 4/5/6th IC space
iv) pleurodesis if req (adhere parietal and visc pleura with subs such as talc) if malignant or reccurent
v) if empyema or para pneyumonic then need antibiotics and chest drain

Question 15

ASTHMA

i) what three things is it characterised by? what causes airway inflamation? how is histamine implicated? name three things it can be associated with?
ii) what type of respiratory disease is it? what is the FEV1:FVC ratio? name four symptoms that point towards asthma? what may pt have a PMH of?
iii) what is the preferred first line test? what question should be asked? what peak flow result is expected between attacks? name two things that can be given in challenge testing?
iv) what test is a indirect marker of airway inflam? how may atopy be investigated for?
v) what is first line medication? what can be added to this? what can be added further? if there is poor control > what can be given?
vi) what immunotherapy can be used against IgE that prevents mast cell degranulation?

Answer 15

i) recurrent episodes of breathlessness, wheeze and bronchoconstriction secondary to reversible airway obstruc and hyper reactive airways
- airway inflam due to interac of inflam mediators and cytokines
- mast cell degran > histamine release after allergen exposure > mucus plug and airway bronchoconstric
* adult onset Is more severe
* interplat between genetics (atopy) and enviro facotrs > often hypersens to allergens eg house dust mite, fungi, pollen
* can be assoic with cold weather, exercise, GORD, emotions

ii) Obstructive resp disease > FEV1:FVC <0.7 (obstruc)
* mostly a clinical dx
Determine probability that symptoms are related to asthma
* episodic symptoms of wheeze, chest tight and cough exacerbated by allergens, cold or medication (NSAID/BB)
* evidence of diurnal variation - worse at night/early morning
* wheeze
* PMH of atopy eg eczema, allergic rhinitis

iii) Spirometry > pref first line test - looks for obstructive picture > is it reversible with bronchodilators?
* peak flow - usually normal between attacks (reduced during symptomatic episodes suggests obstructive)
* challenge testing > histamine or methacholine in a safe enviro

iv) fractional exhaled nitric oxide - indirect marker of airway inflam
* skin prick and serum IgE for investigation of atopy (normal level less likely to be asthma)

v) inhaled short acting B2 agonist eg salbut
*add inhaled corticosteroid (flutocasone, beclometasone) 400mcg starting
* add long acting beta agonist (salmeterol, formeterol) and assess response (also consider leukotriene r antag eg montelukast) if no repsonse to LABA/ICS
* if LABA is not enough, increase ICS dose, if no repsonse to LABA then stop > increase ICS , still no repsonse add LRA
* if still poor control > add daily steroid tablet alongside ICS

iv) consider immunotherapy eg omalizumab (monoclonal against IgE that prev mast cell degran)

Question 16

ACUTE ASTHMA

i) how is it characterised - PEFR? RR? HR? how is life threatening asthma charac? (4)
ii) what should be given first? how much/often should salbutamol nebs be given? what can be added to this? what can be added if still poor response?
iii) what is a bad prognostic sign on ABG? what can be given to reduce mortality? which drugs?
iv) what may be given as one off IV to help relax smooth muscle if poor responsive to therapy?

Answer 16

i) acute > PERF 33-50% of best, RR>25, HR >100bpm, cant complete sentence in one breath
- Life threat asthma > PEFR <33% of best, SPO2 <92%, normal PaCO2, cyanosis, hypotension, poor resp effeort, arrhythmia, silent chest

ii) Intervention > give oxgen, salbutamol nebs (5mg) every 15-30 mins, - add ipatropium bromide negs (0.6mg4-6hrly) to salbumatol for adults with acute/life threat ashtjma
- if poor initial repsonse to beta 2 agonist nebs

iii) ABG - normal or elevated PaCo2 is bad prognostic factor
* give steroids to reduce mortality > IV hydrocortisone 200mg or oral prednisolone 40mg

iv) may give single does IV magnesium sulphate if poor response ot therapy

Question 17

PNEUMOTHORAX

i) what is it? why does it happen? which group is it more likely to occur in? what is an open pthx? what is closed? what is tension? which one is a medical emergency?
ii) what is non tension primary? secondary? name an iatrogenic cause
iii) name two symptoms? what three things may be seen on exam? which type doesnt need a chest x ray? what influences management?
iv) what is done to manage tension? what is done for primary <2cm? primary >2cm? secondary <1cm? 1-2cm? >2cm?
v) what is done if bilateral of haemodynamically unstable?

Answer 17

i) abnormal amount of air accumulates within pleural space due to press gradient between alveoli (lower press in alv than pl space)
* more likely to occur in smokers (direct related to amount), men, chest trauma
* can be open (communicating with ext) or closed (chest wall in tact with accum of air in pleural space) or tension (air enters pl cavity via one way valve and compresses surr structures - med emergency)

ii) non tension spontaneous can be primary or secondary
* primary > occ in healthy indiv with no underlying lung disease, young tall, thin men who smoke
* secondary spont > underlying lung disease eg COPD, infection, TB
* iatrogenic eg insertion of central line

iii) sudden onset dyspnoea or pleuritic chest pain
* OE - decreased expansion, reduced breath sounds, hyper resonant percussion
if tension > clinical dx and don’t do CXR
* other types > do PA CXR
* look at degree of breathless > influences mx
* distinguish between primary and secondary spont (do they have underlying lung disease)

iv) Tension > insert large bore cannula intos econd IC space at mid clavic line > drain
* all other types either discharge and clinic review, high flow o2, aspirate with cannula or chest drain
- Primary > <2cm - discharnge and review in 2-4 weeks
- Primary >2cm or breathless > aspirate with wide bore cannula > success > discharge and clinic review (if unsuccess > chest drain)
- Secondary (lung disease, smoker, >50) - <1cm - high flow O2 and 24hr obs
- 1-2cm > aspirate with 16-18G cannula
>2cm/breathless > chest drain

v) If bilat or HD unstable > chest drain straight away

Question 18

PE

i) where does it come from? name two other causes? what is virchows triad? name three risk factors?
ii) name four symptoms? what are the two most commonly seen symptoms? what changes may be seen on ECG?
iii) what imaging should be done to exclude another pathology? what is done if a PE is likely? what is done if this cant be done immediately? what scan is done if the patient has a contrast allergy or renal failure?
iv) what are the seven components of a wells score? what may be seen on ABG? (2)
v) what treatment is given as soon as diagnosed? for how many days? what is given if patient has malignancy? what can be given if patient is in renal fail/high bleeding risk?
vi) what can be given to patients with recurrent emboli depsite anti coag?

Answer 18

i) consequence of thrombus from deep veins
* medical emergency with higher mort in men
* can also occ as a fat embolus from long bone fracture or air embolus second to trauma
* predis > cvirchows triad = hypercoag, venous stasis and endothelial damage
* RF = SPAM HD - surgery, pregnancy, age, malignancy, hormones (COCP, HRT), DVT

ii) chest pain (pleuritic), dyspnoea, haemoptysis, syncope
* most common sign is tachypnoea and tachycardia (may have low o2 sats)
S1Q3T3 - large S wave in lead I, a Q wave in lead III and an inverted T wave in lead III

iii) CXR to exclude other pathology
* wells score > if >4 - likely
* if PE likely > do CTPA (if cant be done immed then anti coagulate - alteplase 50mg IV bolus)
* if pt has contrast allergy, renal fail or cant have radiation > do VQ spect scan
* if PE unlikely > D dimer if negative consider different dx

iv) wells score - sign symp of PE, alt dx less likely, tachycardia, immobile, prev DVT/PE., haemoptysis, malignancy
- ABG - may see resp alkalosis and hypxaemia

v) put patient on O2 and ensure sitting up
* thombolysis in massive PE with circ fail
Pharma
* LMWH as soon as dx >c ontinue for 5 days until INR is >2 for >24hrs
* if pt has cancer > LMWH for 6 months
* use UFH if renal failure or high bleeding risk
* warfarin if known cause for three months

vi) vena cava filter in pts with recurrent emboli despite anticoag
* consider rivaroxaban

Question 19

NON INVASIVE VENTILATION

i) name five situations when it should be considered? how does it lessen respiratory effort and reduce work of breathing?
ii) what is FRC? how does NIV increase it?
iii) what is NIV positive pressure? what is the most basic level of support? how does it work? what condition is it often used fir?
iv) what is BIPAP? what is it most commonly used for? (3)
v) describe T1RF and T2RF

Answer 19

i) respiratory failure in chronic obstructive pulmonary disease, cardiogenic pulmonary oedema and other respiratory conditions without complications such as respiratory muscle weakness, upper airway trauma, ventilator-associated pneumonia, and sinusitis
- NIV > creating a positive airway pressure - the pressure outside the lungs being greater than the pressure inside of the lungs. This causes air to be forced into the lungs (down the pressure gradient), lessening the respiratory effort and reducing the work of breathing

ii) It also helps to keep the chest and lungs expanded by increasing the functional residual capacity (the amount of air remaining in the lungs after expiration) after a normal (tidal) expiration

iii) CPAP is the most basic level of support and provides constant fixed positive pressure throughout inspiration and expiration, causing the airways to remain open and reduce the work of breathing
- higher degree of inspired oxygen than other oxygen masks
- commonly used for patients requiring nocturnal CPAP for sleep apnoe at home
- High flow systems used in a hospital environment are designed to ensure that airflow rates delivered are greater than those generated by the distressed patient

iv) BIPAP provides differing airway pressure depending on inspiration and expiration. The inspiratory positive airways pressure (iPAP) is higher than the expiratory positive airways pressure (ePAP)[12]
- ventilation is provided mainly by iPAP, whereas ePAP recruits underventilated or collapsed alveoli for gas exchange and allows for the removal of the exhaled gas.
- In the acute setting, NIV is used in type 2 respiratory failure (for example in a COPD exacerbation), with respiratory acidosis (pH < 7.35
- Given in T2RF, acidotic exacerbation of COPD, weaning from trach intubation

v) Type I RF - PaO2 <8kPa with normal or low PaCo2
Type II RF - hypoxaemia with high PaCO2 >6kPa