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Respiratory Flashcards

1
Q

How do you grade dyspnoea

A
  • MRC Dyspnoea Scale
    • Grade 1 – Breathless on strenuous exercise
    • Grade 2 – Breathless on walking up hill
    • Grade 3 – Breathless that slows walking on the flat
    • Grade 4 – Stop to catch their breath after walking 100 meters on the flat
    • Grade 5 – Unable to leave the house due to breathlessness
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2
Q

spirometry findings in COPD

A
  • FEV1 /FVC ratio is <0.7
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3
Q

how is severity of airflow obstruction graded

A
  • Stage 1: FEV1 >80% of predicted
  • Stage 2: FEV1 50-79% of predicted
  • Stage 3: FEV1 30-49% of predicted
  • Stage 4: <30% of predicted
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4
Q

COPD investigations

A
  • CXR
    • To exclude other pathology like lung cancer
  • FBC
    • For polycythaemia which is a response to chronic hypoxia
  • BMI
    • As a baseline to assess weight loss (cancer or severe COPD) or weight gain (due to steroid therapy)
  • Sputum culture
    • To assess for chronic infections like pseudomonas
  • Serum alpha-1 antitrypsin
    • Alpha-1 antitrypsin deficiency leads to early onset and more severe COPD
  • Transfer factor for carbon monoxide
    • TLCO is decreased in COPD and can give an indication of severity of disease
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5
Q

Long term COPD management

A
  • Smoking cessation
  • Annual pneumococcal and flu vaccines
  • Pulmonary rehab
  • Stage 1
    • SABA (e.g. salbutamol) or SAMA (e.g. ipratropium) to use as needed
  • Stage 2
    • LABA (e.g. formoterol, salmeterol) plus LAMA (e.g. tiotropium)
  • Stage 3
    • LABA plus LAMA plus ICS
    • If no improvement in 3 months then switch back to LABA plus LAMA
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6
Q

management of acute exacerbation of COPD

A
  • Nebulised bronchodilators (salbutamol and ipratropium)
  • Steroids (hydrocortisone or oral prednisolone)
  • Antibiotics if evidence of infection
  • Physiotherapy
  • If not responding to first line treatment
    • IV aminophylline
    • Non-invasive ventilation
    • Intubation and ventilation with admission to intensive care
    • Doxapram
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7
Q

investigation of asthma in the community

A

fractional exhaled nitric oxide

spirometry with bronchodilator reversibility

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8
Q

how would you define good asthma control

A

No daytime symptoms.

No night-time waking due to asthma.

No need for rescue medication.

No asthma attacks.

No limitations on activity including exercise.

Normal lung function (FEV1 and/or PEF > 80% predicted or best).

Minimal side-effects from medication.

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9
Q

additional management of asthma in the community

A

yearly asthma review

emergency plan

yearly flu jab

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10
Q

describe asthma treatment ladder in adults

A
  1. everyone gets a SABA
  2. SABA + low dose ICS (beclametasone)
  3. SABA + low dose ICS + LTRA (montelukast)
  4. SABA + low dose ICS + LABA (salmeterol) +/- LTRA (depending on response to LTRA)
  5. MART (maintenance and reliever therapy) +/- LTRA
    • MART includes fast acting LABA and low dose ICS
    • used as daily maintenance and as a reliever
  6. Switch to a MART with moderate dose ICS +/- LTRA
  7. consider additional drug such as theophylline or switching to high dose ICS
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11
Q

asthma treatment ladder in children

A
  1. SABA
  2. SABA + low dose ICS (beclametasone)
  3. SABA + low dose ICS + LTRA (montelukast)
  4. SABA + low dose ICS + LABA (salmetarol)
  5. SABA + MART (low dose ICS in the MART)
  6. SABA + moderate dose ICS + LABA (either as MART or fixed dose regimen)
  7. here you can either increase to high dose ICS or trial new drug such as theophylline
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12
Q

how can you establish whether someone’s asthma is well controlled

A
  • answering no to all three of the RCP Three Questions is consistent with well controlled asthma
  1. are you having trouble sleeping because of your asthma symptoms?
  2. have you recently had your asthma symptoms during the day?
  3. has your asthma interfered with your normal activities?
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13
Q

how do you grade asthma attacks

A
  • Mild: PEFR >75%
  • Moderate: PEFR <75%
  • Severe:
    • PEFR <50%
    • can’t complete sentences
    • RR >25
    • PR >110
  • Life threatening (33 92 CHEST)
    • 33: PEFR <33%
    • 92: Sats <92%
    • Cyanosis
    • Hypotension
    • Exhaustion
    • Silent chest
    • Tachycardia
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14
Q

management for moderate asthma attack

A

Nebulised beta-2 agonists (i.e. salbutamol 5mg repeated as often as required)

Nebulised ipratropium bromide

Steroids. Oral prednisolone or IV hydrocortisone. These are continued for 5 days

Antibiotics if there is convincing evidence of bacterial infection

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15
Q

management of severe asthma attack

A
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16
Q

management of life threatening asthma attack

A

IV magnesium sulphate infusion

admission to HDU/ICU

Intubation - however this should happen early as it’s very difficult to intubate in bronchospasm

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17
Q

ABGs in an asthma attack

A

Initially patients will have a respiratory alkalosis as tachypnoea causes a drop in CO2.

A normal pCO2 or hypoxia is a concerning sign as it means they are tiring and indicates life threatening asthma.

A respiratory acidosis due to high CO2 is a very bad sign in asthma.

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18
Q

what are the different types of lung cancer and how common are they

list sub-types in order of prevalence

A
  • Non small cell lung cancer (80%)
    • adenocarcenoma
    • squamous cell carcinoma
    • large cell carcinoma
    • other
  • small cell lung cancer (20%)
    *
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19
Q

signs and symptoms of lung cancer

A

finger clubbing

coughing

haemoptysis

lymphadenopathy

recurrent pneumonia

weightloss

cough

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20
Q

investigations of lung cancer

A
  • chest x ray
  • contrast enhanced CT
  • bronchoscopy
  • biopsy (by bronchoscopy or percutaneously) and histological diagnosis
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21
Q

is prognosis generally better for small cell lung cancer or non-small cell lung cancer

A

non-small cell lung cancer generally has a better prognosis

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22
Q

treatment options for lung cancer

A
  • surgery
    • lobectomy
    • segmentectomy
    • wedge resection
  • radiotherapy
  • chemotherapy
    • curative
    • palliative
  • treatment for small cell lung cancer
    • outcomes usually worse so normally just radiotherapy and chemo
    • palliative
  • endobronchial treatment with stents and debulking works for palliative treatment of obstruction caused by cancer
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23
Q

list 9 extra pulmonary manifestations of lung cancer

A
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24
Q

what is recurrent laryngeal nerve palsy

A

presents as hoarse voice and is caused by lung cancer pressing on the recurrent laryngeal nerve

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25
Q

what is phrenic nerve palsy

A

due to compression of the phrenic nerve and results in diaphragm weakness - presents as shortness of breath

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26
Q

what happens with superior vena cava obstruction

A
  • it is a complication of lung cancer and is caused by direct compression of the tumour on the superior vena cava
  • it presents with
    • facial swelling
    • difficulty breathing
    • distended veins in the neck and upper chest
  • pemberton’s sign is where raising the hands over the head causes facial congestion and cyanosis - this is a medical emergency
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27
Q

what is horner’s syndrome

A

triad of partial ptosis, anhidrosis and miosis

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28
Q

why might a lung cancer cause a horner’s syndrome

A

it is caused by a pancoast tumour (tumout of the pulmonary apex) pressing on the sympathetic ganglion

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29
Q

why might lung cancer cause SIADH and how does it present

A

ectopic ADH secretion by a small cell lung cancer and presents with hyponatraemia

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30
Q

why might lung cancer cause cushing’s syndrome

A

ectopic ACTH secretion by a small cell lung cancer

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31
Q

why might lung cancer cause hypercalcaemia

A

ectopic parathyroid hormone secretion from a squamous cell carcinoma

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32
Q

what is limbic encephalitis and how is it caused

A
  • small cell lung cancer causes immune system to make antibodies to tissue in the brain - specifically the limbic system
  • this causes
    • hallucinations
    • confusion
    • seizures
    • memory impairment
  • associated with anti-Hu antibodies
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33
Q

what is lambert-eaton myasthenic syndrome and why do you get the specific symptoms

A
  • immune system produces antibodies against the small cell lung cancer
  • these cross-react with voltage gated calcium channels sited on presynaptic terminals in motor neurons
  • it mainly affects
    • proximal muscles
    • intraocular muscles
      • diplopia
    • levator muscles
      • ptosis
    • pharyngeal muscles
      • slurred speach and dysphagia
  • also causes autonomic dysfunction
    • dry mouth
    • blurred vision
    • impotence
    • dizziness
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34
Q

cxr findings in lung cancer

A

hilar enlargement

consolidation

lung collapse

pleural effusion

bony secondaries

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35
Q

rare causes of PE (i.e. not clot in legs)

A
  • right ventricular thrombosis (post MI)
  • septic emboli (right sided endocarditis)
  • fat embolus
  • air embolus
  • amniotic fluid embolus
  • neoplastic cells
  • parasites
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36
Q

what is the risk score for PE

A

wells criteria for PE

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37
Q

what are the wells criteria for PE

A
  • clinical signs and symptoms of DVT
  • PE is #1 diagnosis or equally likely
  • heart rate >100
  • immobilisation in the last 3 dats or surgery in the previous 4 weeks
  • previous, objectively diagnosed PE or DVT
  • hemoptysis
  • malignancy with treatment in the last 6 months or palliative
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38
Q

risk factors for PE

A

immobility

recent surgery

long haul flights

pregnancy

hormone therapy with oestrogen

malignancy

polycythaemia

systemic lupus erythematosus

thrombophilia

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39
Q

signs of PE

A

pyrexia

cyanosis

tachypnoea

tachycardia

hypotension

raised JVP

pleural rub

pleural effusion

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40
Q

thromboprophylaxis of patients admitted to hospital

A

low molecular weight heparin such as enoxaparin

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41
Q

investigations of PE based on wells score

A

likely: perform a CTPA
unlikely: d-dimer and if positive perform a CTPA

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42
Q

diagnosis of PE

A
  • CTPA
    • this is first choice
    • IV contrast highlights pulmonaty arteries to demonstrate blood clots
  • VQ scan
    • used in patients with
      • renal impairment
      • contrast allergy
      • risk from radiation
    • area of embolism will be ventilated but not perfused
  • CXR may be normal
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43
Q

cxr findings in PE

A
  • may be normal
  • oligaemia of affected segment
  • dilated pulmonary artery
  • linear atelectasis
  • small pleural effusion
  • wedge-shaped opacities
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44
Q

ecg findings in PE

A
  • may be normal
  • tachycardia
  • RBBB
  • right ventricular strain
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45
Q

initial management of PE

A
  • apixaban or rivaroxaban started immediately before confirming diagnosis
  • where there is massive PE and they are haemodynamically unstable
    • thrombolysis
      • inject fibrinolytic medication such as
        • alteplase
        • streptokinase
        • tenecteplase
      • either IV or catheter directed thrombolysis directly into pulmonary arteries
      • this is risky
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46
Q

long term anticoagulation following PE

A
  • options are
    • warfarin
      • target INR 2-3
    • a noac
      • apixaban
      • rivaroxaban
      • dabigatran
    • LMWH
      • first line treatment in pregnancy or cancer
  • continue anticoagulation for
    • 3 months if obvious reversible cause
    • beyond 3 months if cause unclear, if recurrent VTE or an irreversible underlying cause such as thrombophilia
    • 6 months in active cancer
    • then review
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47
Q

describe the bacteria that causes TB

A

mycobacterium tuberculosis

acid fast bacilli

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48
Q

what staining technique is used for TB

A

zeihl neelsen stain

this turns TB bright red against a blue background

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49
Q

disease course of TB

A
  • active TB is where there is active infection in various areas within the body
  • small granulomas (tubercles) form around the infection when host macrophages engulf the organism
  • in 80% of cases these tubercles heal spontaneously
  • in 20% of cases you get latent TB
    • this is where the infection is encapsulated but not eliminated
    • individual is otherwise healthy
  • if latent TB reactivates it is known as secondary TB
    • this is usually precipitated by impaired immune function
  • miliary TB occurs when primary infection is not adequately contained and invades the bloodstream
    • results in severe disseminated disease
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50
Q

TB presentation

A
  • 70% is pulmonary TB
  • lethargy
  • fever
  • night sweats
  • cough with or without haemoptysis
  • lymphadenopathy
  • erythema nodosum
  • spinal pain in spinal TB
    • this is AKA pott’s disease of the spine
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51
Q

investigating TB

A
  • difficult because bacteria grow slowly
  • two tests for immune response to TB
    • mantoux
    • interferon-gamma release assay
  • if active disease is suspected
    • X ray
    • sputum cultures
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52
Q

CXR findings in TB

A
  • pulmonary TB is unlikely with a normal CXR
  • primary TB
    • central apical portion with lower lobe infiltrate or pleural effusion
    • cavitation
  • reactivated TB
    • no pleural effusion and lesions are apical in position
    • cavitation
  • severe disease with poor immune response can produce a picture like millet seeds over the CXR
    • uniform 1-10mm shadows
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53
Q

obtaining samples for suspected pulmonary TB

A
  • need at least three sputum samples for culture and microscopy
    • including one early morning sample
  • if spontaneous not possible consider bronchoscopy and lavage
    • or in children gastric washing
  • start treatment without culture results if clinical signs and symptoms of TB
    • complete treatment even if culture results are negative
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54
Q

obtaining samples for suspected non-respiratory TB

A
  • needle aspiration
  • lymph node biopsies
  • early morning urine
  • start treatment if histology and clinical picture are consistent with TB before culture results are available
  • continue treatment even if results are negative
  • CXR should be done for co-existing respiratory TB in all patients with non-resp TB
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55
Q

how are TB samples analysed

A

staining with Ziehl-Neelsen stain

rapid direct microscopy for acid fast bacilli

they appear red on a blue background

culture on a lowenstein-jensen slope which takes 4-8 weeks due to slow bacterial growth

sensitivity cultures then take a further 3-4 weeks

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56
Q

contact screening in TB

A

mantoux testing to diagnose LTBI in people who are household contacts or close contaccts of all patients with TB

mantoux may well be positive in those with the BCG so offer interferon gamma as first line in these people

if positive refer to TB specialist

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57
Q

public health stuff following diagnosis of TB

A
  • all cases must be notified under the public health regulations 1988
  • admit to negative pressure single side-room vented to the outside until they are proven to be non-infectious
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58
Q

drug treatment of active TB without CNS involvement

A
  • start all at the same time
    • isoniazid for 6 months
    • rifampicin for 6 months
    • pyrazinamide for two months
    • ethambutol for two months
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59
Q

drug treatment of active TB of the CNS

A
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60
Q

side effects of rifampicin

A
  • red orange discolouration of urine and tears
  • cytochrome P450 inducer –> OCP
  • during first two months of rifampicin transient derangement of LFTs is common and generally doesn’t require change of treatment
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61
Q

side effects of isoniazid

A

peripheral neuropathy

prescribe pyridoxine (B6)

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62
Q

side effects of pyrazinamide

A

hyperuricaemia which may result in gout

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63
Q

side effects of ethambutol

A

can reduce visual acuity and cause colour blindness

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64
Q

which people should be treated for latent TB (LTBI)

A
  • people mantoux positive without prior BCG
  • people mantoux positive and interferon-gamma positive is prior BCG
  • people with TB scars on CXR without history of prior treatment
  • people with HIV who are close contacts of those with sputum-smear-positive respiratory TB
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65
Q

drug treatment of LTBI

A
  • either if no HIV
    • 6 months of isoniazid or
    • 3 months of isoniazid and rifampicin
  • any LTBI with HIV
    • 6 months of isoniazid
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66
Q

what are bronchial breath sounds

A

harsh breath sounds equally loud on inspiration and expiration

caused by consolidation of the lung tissue around the airway

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67
Q

how do you assess severity of pneumonia

A
  • in hospital
    • CURB65
    • Confusion
    • Urea >7
    • Resp rate >30
    • Blood pressure <90 systolic or <60 diastolic
    • 65 Age >65
  • in comunty
    • CRB65
    • no urea testing
    • if CRB score of anything other than 0 consider referring to hospital
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68
Q

CAP treatment in adults

A
  • CRB65 of 0 (low severity)
    • amoxicillin 500mg 3 times per day for 5 days
    • if penicillin allergy then
      • doxycycline 200mg on first day then 100mg once a day for 4 days
  • CRB65 of 1/2 (moderate severity)
    • amoxicillin 500mg 3 times a day for 5 days AND
    • clarithromycin 500mg twice a day for 5 days
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69
Q

CURB 65 interpretation

A

score 0/1: consider treatment at home

score 2 or more: consider admission

score 3 or more: consider intensive care assessment

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70
Q

most common atypical pneumonias

A

M. pneumoniae

C. pneumoniae

Legionella pneumophila

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71
Q

what is the definition of hap

A

hospital acquired pneumonia

new infection of lung parenchyma appearing more than 48hrs after admission to hospital

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72
Q

HAP occuring less than 5 days after hospital admission is normally caused by

A

S.pneumoniae

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73
Q

HAPs occuring more than 5 days after hospital admission are normally caused by

A

H.influenzae

MRSA

pseudomonas aeruginosa

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74
Q

legionella pneumophila presentation

A

typically caused by infected water supplies or air conditioning units. It can cause hyponatraemia (low sodium) by causing an SIADH.

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75
Q

treatment for atypical pneumonias

A

Macrolides such as clarithromycin

Quinolones such as levofloxacin

Tetracyclines such as doxycycline

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76
Q

mycoplasma pneumoniae presentation

A

causes a milder pneumonia and can cause a rash called erythema multiforme characterised by varying sized “target lesions” formed by pink rings with pale centres. It can also cause neurological symptoms in young patient in the exams.

77
Q

coxiella burnetii presentation

A

aka Q fever

linked to exposure to animals and their bodily fluids. The MCQ patient is a farmer with a flu like illness.

78
Q

chlamydia psittaci presentation

A

typically contracted from contact with infected birds. The MCQ patient is a from parrot owner.

79
Q

Pneumocystis jiroveci (PCP) management

A

Treatment is with co-trimoxazole (trimethoprim/sulfamethoxazole) known by the brand name “Septrin”. Patients with low CD4 counts are prescribed prophylactic oral co-trimoxazole to protect against PCP.

80
Q

should you prescribe abx in tonsillitis

A
  • centor criteria
    • history of fever
    • tonsillar exudates
    • no cough
    • tender anterior cervical lymphadenopathy
  • abx should be limited to patients with three or four criteria
81
Q

bacterial tonsilitis is most commonly caused by

A

Group A Streptococcus (GAS) mainly streptococcus pyogenes

82
Q

when should you give abx for tonsillitis and what should you give

A

if centor criteria is 3 or more

Penicillin V aka phenoxymethylpenicillin for a 10 day course

NICE guidelines are supportive of considering a delayed prescription in the community where patients can collect antibiotics if the symptoms don’t improve or get worse after 3 days.

83
Q

criteria for tonsillectomy

A

Sore throats are due to acute tonsillitis.

The episodes of sore throat are disabling and prevent normal functioning.

Seven or more well-documented, clinically significant, adequately treated sore throats in the preceding year; or

Five or more such episodes in each of the preceding two years; or

Three or more such episodes in each of the preceding three years.

84
Q

presentation of otitis media

management

A

difficult to distinguish between bacterial and viral otitis media. It presents with ear pain. Examination will reveal a bulging red tympanic membrane. If the ear drum perforates there can be discharge from the ear.

Otitis media usually resolves within 3-7 days without antibiotics. If systemically unwell consider admission.

amoxicillin if necessary in community

85
Q

subtypes of otitis media

A

acute otitis media

otitis media with effusion

chronic supperative otitis media

mastoiditis

cholesteatoma

86
Q

what is acute otitis media

A

acute inflammation of the middle ear

caused by bacteria or viruses

87
Q

what is otitis media with effusion

A

chronic otitis media without acute inflammation

often follows slowly resolving acute otitis media

effusion of glue like liquid behind the intact tympanic membrane

no signs of acute inflammation

88
Q

what is mastoiditis

A

acute inflammation of the mastoid periosteum and air cells occuring when acute otitis media spreads from middle ear

89
Q

what are the most common causative bacteria in otitis media

A

haemophilus influenzae

streptococcus pneumoniae

moraxella catarrhalis

streptococcus pyogenes

90
Q

what are the most common viral pathogens causing otitis media

A

RSV

rhinovirus

91
Q

abx in otitis media

A

usually resolves in 3-7 days

give amoxicillin on delayed prescription if it doesn’t resolve in 4 days

92
Q

different types of sinusitis

A

Acute: an infection lasting 7-30 days.

Subacute: the inflammation lasts 4-12 weeks.

Recurring: there are >3 significant acute episodes in a year lasting ≥10 days with no intervening symptoms.

Chronic: symptoms persist for >90 days (these may be caused by irreversible changes in the mucosal lining of the sinuses), with or without acute exacerbations

93
Q

risk factors for sinusitis

A

Upper respiratory tract infection.

Allergy.

Asthma.

Smoking.

Hormonal status (eg, pregnancy).

Nasal dryness.

Diabetes mellitus.

Presence of a foreign body.

Inhalation of irritants (eg, cocaine).

Iatrogenic (eg, nasogastric tubes, mechanical ventilation).

Dental problems (eg, trauma, infection).

Some sporting activities (eg, swimming, diving, high-altitude climbing).

Mechanical obstruction (eg, normal anatomical variations, nasal polyps).

Previous history of trauma (nose, cheeks).

Immunocompromise.

94
Q

diagnosis of acute sinusitis

A

acute sinusitis is diagnosed if there is:

  • Facial discomfort (often worse when bending forwards) or pain.
  • Nasal obstruction or (purulent) nasal discharge or postnasal drip.
  • Decreased or absent sense of smell.
95
Q

management of sinusitis

A

Symptoms for less than 10 days: No antibiotics.

No improvement after 10 days: 2 weeks of high-dose steroid nasal spray

No improvement after 10 days and likely bacterial cause: consider delayed or immediate prescription of antibiotics

96
Q

what is the most common interstitial lung disease

A

IPF

97
Q

most common causative organisms in infective exacerbation of COPD

A

streptococcus pneumoniae

moraxella catarrhalis

haemophilus influenzae

98
Q

antibiotic for infective exacerbation of COPD

A

co-amoxiclav

99
Q

medical management of COPD

A
100
Q

mnemonic for respiratory causes of clubbing

A

Asbestosis

Bronchiectasis

Cancer (lung)

Do not say COPD

Empyema

(There are some more respiratory causes such as interstitial lung disease)

101
Q

what is granulomatosis with polyangiitis

A

GPA is a systemic vasculitis that involves small and medium-sized vessels. It classically presents with upper and lower respiratory tract involvement and pauci-immune glomerulonephritis

102
Q

serology in GPA

A

granulomatosis with polyangiitis is usually cANCA-associated (c. 80%) but 10-15% is pANCA-associated.

103
Q

what is the best abx for penicillin allergic severe pneumonia

A

levofloxacin

104
Q

what is IPF

A

Idiopathic pulmonary fibrosis (IPF, also called cryptogenic fibrosing alveolitis) is specific form of

chronic,

progressive,

fibrosing

interstitial pneumonia of unknown cause,

occurring in adults and limited to the lungs.

It is associated with the histopathologic and/or radiologic pattern of usual interstitial pneumonia (UIP).

105
Q

what drugs are sometimes used to treat IPF

A

Idiopathic pulmonary fibrosis

Pirfenidone

106
Q

how is interstitial lung disease diagnosed

A

ground glass appearance on high resolution ct

107
Q

management of interstitial lung disease

A

Remove or treat the underlying cause

Home oxygen where they are hypoxic at rest

Stop smoking

Physiotherapy and pulmonary rehabilitation

Pneumococcal and flu vaccine

Advanced care planning and palliative care where appropriate

Lung transplant is an option but the risks and benefits need careful consideration

pirfenidone if recommended by nice

108
Q

life expectancy of idiopathic pulmonary fibrosis

A

median survival is 2.5 years from the time of diagnosis

109
Q

three types of fibrosis seen in the lungs and their causes

A
  • replacement fibrosis secondary to damage: e.g. infarction, tuberculosis and pneumonia
  • focal fibrosis in response to irritants: e.g. coal dust and silica
  • diffuse parenchymal lung disease: IPF and hypersensitivity pneumonitis
110
Q

median age of presentation of IPF

A

70

111
Q

presentation of IPF

A
  • age over 45
  • persistent breathlessness on exertion
  • persistent dry cough
  • bilareral inspiratory crackles on auscultation of chest
  • clubbing of fingers
  • spirometry may be normal, restrictive or obstructive
112
Q

diseases associated with IPF

A

thyroid disease

systemic sclerosis

rheumatoid arthritis

autoimmune liver disease

SLE

113
Q

who is pirfenidone suitable for

A

pirfenidone is recommended for the treatment of IPF if:

  • FVC is between 50% and 80% of expected
  • there is evidence of disease progression if the treatment is stopped
114
Q

who is nintedanib suitable for

A
  • nintedanib is recommended for the treatment of IPF if:
    • FVC is between 50% and 80% predicted
    • there is evidence of disease progression if the treatment is stopped
115
Q

which drugs can cause pulmonary fibrosis

A

amiodarone

cyclophosphamide

methotrexate

nitrofurantoin

116
Q

what is pirfenadone

A

antifibrotic and anti-inflammatory drug used to treat IPF

117
Q

what is nintendanib

A

monoclonal antibody that targets tyrosine kinase

118
Q

what diseases can pulmonary fibrosis be secondary to

A

Alpha-1 antitripsin deficiency

Rheumatoid arthritis

Systemic lupus erythematosus (SLE)

Systemic sclerosis

119
Q

what type of hypersensitivity reaction is hypersensitivity pneumonitis

A

type III

120
Q

hypersensitivity reactions associated with hobbies and their causes

A
  • farmer’s lung: mouldy hay
  • bird fanciers lung: avian proteins
  • cheese workers lung: cheese mould penicillium casei
  • malt worker’s lung: mouldy malt
  • hot tub lung: mycobacterium avium in poorly maintained hot tubs
  • chemical worker’s lung: manufacture of dyes, plastics, polyurethane foam and rubber
  • mushroom worker’s lung
121
Q

three forms of hypersensitivity pneumonitis

A

acute

subacute or intermittent

chronic

122
Q

difference between different forms of hypersensitivity pneumonitis

A
  • acute
    • 4-8hrs after exposure
    • flu like with fever, chest tightness and dry cough
    • symptoms directly related to level of exposure
  • subacute or intermittent
    • may be history of acute attacks
    • less severe symptoms with more gradual onset
    • after exposure removed it can take weeks or months for symptoms to resolve
  • chronic
    • often no systemic symptoms except weight loss
    • gradual loss of exercise tolerance
    • clubbing may develop
    • after antigen removed there may only be partial improvement
123
Q

management of hypersensitivity pneumonitis

A

remove exposure to antigen

corticosteroids but these don’t alter long term outcomes

azathioprine and mycophenolate can be used as steroid sparing agents

lung transplantation in specific cases

124
Q

complications of hypersensitivity pneumonitis

A

pneumothorax

pulmonary fibrosis

emphysema

respiratory insufficiency or failure

cor pulmonale

125
Q

what is sarcoidosis

A

a granulomatous inflammatory condition. Granulomas are nodules of inflammation full of macrophages. The cause of these granulomas developing is unknown.

126
Q

what is the typical exam patient with sarcoidosis

A

a 20-40 year old black woman presenting with a dry cough and shortness of breath, erythema nodosum and lymphadenopathy

127
Q

which organs does sarcoidosis affect

A

mainly lungs (90%)

but can affect almost any organ in the body

128
Q

effects of sarcoidosis by system

A
  • systemic
    • fever
    • weightloss
    • fatigue
  • liver
    • nodules
    • cirrhosis
    • cholestasis
  • lungs
    • mediastinal lymphadenopathy
    • pulmonary fibrosis
    • pulmonary nodules
  • eyes
    • uveitis
    • conjunctivitis
    • optic neuritis
  • skin
    • erythema nodosum
    • lupus pernio
    • granulomas in scar tissue
  • heart
    • arrhythmias
129
Q

what is lofgren’s syndrome

A
  • specific presentation of sarcoidosis characterised by the following triad
    • erythema nodosum
    • bilateral hilar lymphadenopathy
    • polyarthralgia
130
Q

investigations of sarcoidosis

A
  • bloods
    • raised serum ACE
    • hypercalcaemia
    • raised serum soluble IL-2 receptor
    • raised CRP
    • raised Ig
  • imaging
    • CXR - hilar lymphadenopathy
    • high res CT - hilar lymphadenopathy and pulmonary nodules
    • MRI may show cns involvement
    • PET can show active areas of inflammation
  • Biopsy and histology
    • this is gold standard
    • shows non-caseating granulomas with epithelioid cells
131
Q

treatment for sarcoid

A
  • mild or no symptoms
    • no treatment as 60% will resolve spontaneously within 6 months
  • first line
    • oral steroids with bisphosphinates to protect against osteoporosis from steroids
  • second line
    • azathioprine and methotrexate
  • lung transplant
    • rare
132
Q

what is the inheritance pattern of CF

A

autosomal recessive

133
Q

what is the mutation in CF

A

cystic fibrosis transmembrane conductance regulatory gene on chromosome 7.

There are many variants of this mutation, the most common is the delta-F508

134
Q

how common is it to be a carrier of CF mutation

A

1 in 25 are carriers of the mutation

135
Q

how common is CF

A

1 in 2500 children have CF

136
Q

what are 3 key consequences of CF mutation

A
  • thick pancreatic and biliary secretions
    • block the ducts resulting in lack of digestive enzymes such as pancreatic lipase
  • low volume thick airway secretions
    • reduced clearance
    • susceptibility to infections
    • bacterial colonisation
  • congenital bilateral absence of the vas deferens
137
Q

what is commonly the first sign of CF

A

meconium ileus almost always means CF

happens in about 20% of babies with CF

it means not passing meconium within 24hrs of birth

138
Q

presentation of CF

A
  • screened for with newborn blood spot test
  • meconium ileus
  • if not picked up ad birth may present later in childhood
    • recurrent lower resp tract infections
    • failure to thrive
    • pancreatitis
139
Q

symptoms of CF

A
  • chronic cough
  • thick sputum
  • steatorrhoea
  • recurrent resp tract infections
  • abdo pain and bloating
  • failure to thrive
140
Q

signs of CF

A

lower weight or height on growth charts

nasal polyps

finger clibbing

crackles and wheezes on auscultation

abdo distention

141
Q

causes of clubbing in children

A

Hereditary clubbing

Cyanotic heart disease

Infective endocarditis

Cystic fibrosis

Tuberculosis

Inflammatory bowel disease

Liver cirrhosis

142
Q

diagnosis of CF

A
  • Newborn blood spot testing is performed on all children shortly after birth and picks up most cases
  • The sweat test is the gold standard
  • Genetic testing for CFTR gene by amniocentesis or chorionic villous sampling
143
Q

what happens during sweat test for CF

A

pilocarpine applied to skin patch

electrodes placed either side of patch with small current running through

this causes skin to sweat

sweat absorbed by gauze

chloride concentration >60mmol/L is diagnostic

144
Q

what are the two key colonisers to remember with CF

A

staph aureus: patients with CF take long term prophylactic flucloxacilling to prevent staph aureus infection

pseudomonas aeruginosa: remember because it’s particularly hard to treat and worsens prognosis

145
Q

How is pseudomonas aeruginosa infection managed in patients with CF

A

dangerous ass leads to increased mortality and morbidity and v difficult to eliminate

CF patients with pseudomonas treated in seperate clinic rooms

long term nebulised abx such as tobramycin and ciprofloxacin for infected pts

146
Q

what vaccines should CF pts get

A

influenza

pneumococcal

varicella

147
Q

8 aspects of CF management

A
  • chest physio
  • high calorie diet
  • CREON to replase missing lipase in pancreatic insufficiency
  • prophylactic flucloxacillin to reduce risk of bacterial infections such as staph aureus
  • bronchodilators such as salbutamol
  • nebulised DNAse (dornase alpha) breaks down DNA material making secretions less viscous and easier to clear
  • nebulised hypertonic saline
  • vaccination for pneumococcus, varicella and influenza
148
Q

difference between exudate and transudate

A

exudate is >3g/dL

transudate is <3g/dL

149
Q

exudative causes of pleural effusion

A

lung cancer

pneumonia

rheumatoid arthritis

tuberculosis

150
Q

Transudative causes of pleural effusion

A

congestive cardiac failure

hypoalbuminaemia

hypothyroidism

meig’s syndrome

151
Q

what is meig’s syndrome

A

triad of benign ovarian tumor with ascites and pleural effusion

152
Q

how does pleural effusion appear on x ray

A

blunting of costophrenic angle

fluid in lung fissures

larger effusions will have a meniscus

tracheal and mediastinal deviation if it is a massive effusion

153
Q

Investigations of pleural effusion

A
  • CXR
  • sample of pleural fluid by aspiration or chest drain to analyse for:
    • protein count
    • pH
    • glucose
    • LDH
    • microbiology
154
Q

what is an empyema

A

this is an infected pleural effusion

155
Q

how do you know if someone’s pleural effusion is empyema

A

Suspect an empyema in a patient who has an improving pneumonia but new or ongoing fever.

Pleural aspiration shows pus, acidic pH (pH < 7.2), low glucose and high LDH.

156
Q

how is empyema treated

A

antibiotics

chest drain to remove the pus

157
Q

what is the treatment for pleural effusion

A

conservative if small as they will resolve on their own

pleural aspiration although you may need to do this more than once

chest drain to drain effusion and it also prevents it recurring

158
Q

how do you measure a pneumothorax

A

measure horizontally from the lung edge to the inside of the chest wall at the level of the hilum on x ray

159
Q

managment of pneumothorax

A
  • if no SOB AND <2cm rim of air on CXR then no treatment
    • follow up in 2-4 weeks
  • if SOB or >2cm rim of air then aspiration
  • if aspiration fails twice then chest drain
  • chest drain straight away for
    • unstable patients
    • bilateral pneumothorax
    • secondary pneumothorax
160
Q

signs of a tension pneumothorax

A
  • tracheal deviation away from side of pneumothorax
  • reduced air entry to affected side
  • increased resonance to percussion on affected side
  • tachycardia
  • hypotension
161
Q

what is the management of a tension pneumothorax

A
  • “Insert a large bore cannula into the second intercostal space in the midclavicular line.”
  • do not wait for investigations
  • once pressure relieved with cannula then insert chest drain for definitive treatment
162
Q

where are chest drains inserted

A
  • into triangle of safety between:
    • 5th intercostal space
    • mix axillary line
    • anterior axillary line
  • insert needle just above the rib to avoid neurovascular bundle that runs below the rib
  • once inserted get a chest x ray to check positioning
163
Q

when is BiPAP used

A
  • for TYPE 2 respiratory failure
  • the criteria for initiating are:
    • pH <7.35
    • PaCO2 >6
    • despite adequate medical treatment
164
Q

what is NIV

A

non invasive ventilation can be either BiPAP or CPAP

165
Q

contraindictations for BiPAP

A
  • untreated pneumothorax
  • if it doesn’t delay they should have a CXR to exclude pneumothorax before the BiPAP is initiated
166
Q

IPAP and EPAP for BiPAP

A
  • IPAP (inspiratory positive airway pressure)
    • sensible starting point for average male pt: 16-20cmH2O
  • EPAP (expiratory positive airway pressure)
    • sensible starting point for average male pt: 4-6cmH2O
167
Q

monitoring BiPAP

A

repeat ABG 1hr after every change and every 4hrs after that until stable

IPAP is increased by 2-5cm increments until the acidosis resolves

168
Q

causes of pulmonary hypertension

A

can be split into 5 groups

  1. primary pulmonary hypertension or connective tissue disease like SLE
  2. left heart failure usually due to myocardial infarction or systemic hypertension
  3. chronic lung disease like COPD
  4. pulmonary vascular disease such as pulmonary embolism
  5. misc causes
    1. sarcoid
    2. glycogen storage disease
    3. haematological disorders
169
Q

signs and symptoms of pulmonary hypertension

A
  • SOB main symptom
  • others
    • syncope
    • tachycardia
    • raised JVP
    • hepatomegaly
    • peripheral oedema
170
Q

ECG changes in pulmonary hypertension

A
  • right sided heart strain produces:
    • right axis deviation
    • right bundle branch block
    • right ventricular hypertrophy
      • larger R waves on the right sided chest leads (V1-3)
      • S waves on the left sided chest leads (V4-6)
171
Q

how do you treat primary pulmonary hypertension

A
  • IV prostanoids (e.g. epoprostenol)
  • endothelin receptor agonists (e.g. macitentan)
  • phosphodiesterase-5 inhibitors (e.g. sildenafil)
172
Q

what is the way of assessing someone for sleep apnoea

A

epworth sleepiness scale

173
Q

what is GPA

A

granulomatosis with polyangiitis - rare form of vasculitis

174
Q

how is GPA classified

A

ELK classification:

  • E indicates ear nose and throat as it most commonly affects URT
  • L indicates lung involvement (most patients)
  • K indicates kidney involvement (>75% patients)

can also affect many other areas of the body - i.e. joints

175
Q

symptoms of GPA

A

can be literally anything :

Fatigue, malaise

Fever, night sweats

Weakness

Loss of appetite

Weight loss

Rhinorrhoea

Sinusitis

Facial pain

Hoarseness

Cough

Dyspnoea

Wheezing

Chest pain

Joint pains

Hearing loss

176
Q

distinctive signs in GPA

A

subglottic stenosis causing hoarseness, stridor, dyspnoea or cough

rashes - petychial or purpuric

177
Q

investigations for GPA

A

ESR

U&E for renal involvement

c-ANCA and p-ANCA detectible in nearly all patients with active severe GPA

biopsy of affected tissue looking for presence of vasculitis and granulomas

178
Q

treatment for GPA

A
  • asymptomatic patients with no organ damage
    • methotrexate to induce remission
  • patients with life-threatening organ damage
    • cyclophosphamide
    • with prednisolone
  • rituximab if they can’t have cyclophosphamide
    • with prednisolone
  • once in remission switch to methotrexate with prednisolone
    • titrate this down or up if relapses
  • if relapse they may need plasma exchange
179
Q

what is GPA AKA

A

wegeners granulomatosis

180
Q

what is goodpastures

A

co-existence of acute glomerulonephritis and pulmonary alveolar haemorrhage

it is a specific autoimmune disease caused by type II antigen-antibody reaction

181
Q

what antibodies circulate in goodpastures

A

anti-glomerular basement membrane antibodies

anti-GBM

this is diagnostic

182
Q

which HLA type is goodpastures linked to

A

HLA-DRB1

183
Q

typical presentation of goodpastures

A

Typically presents as acute kidney injury caused by a rapidly progressive glomerulonephritis, accompanied by pulmonary haemorrhage that may be life-threatening

184
Q

management principles of goodpastures

A
  1. remove circulating antibodies with plasmapheresis
  2. stop further production of antibodies with immunosuppression
    1. IV methylprednisolone with cyclophosphamide or azathioprine
  3. remove identifiable causes of antibody production
185
Q
A
186
Q
A
187
Q
A
188
Q
A
189
Q
A

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