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Respiratory Flashcards

1
Q

COPD

Pathophysiology

A
  • Non-reversible, long-term deterioration in air flow in the lungs
  • Damage to lung tissue → obstruction of air flow → more difficult to ventilation lungs → more prone to infections
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2
Q

COPD

Causes

A
  • Smoking!
  • Alpha-1-antitrypsin deficiency
  • Cadmium
  • Coal
  • Cotton
  • Cement
  • Grain
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3
Q

COPD

Features

A
  • Cough - often productive
  • Dyspnoea
  • Wheeze
  • Recurrent respiratory infections
  • Severe cases: RHF → peripheral oedema
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4
Q

COPD

how to quantify breathlessness?

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 house due to breathlessness
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5
Q

COPD

Investigations

A

Clinical presentation and spirometry!

Spirometry:
- FEV1/FVC ratio < 70%

CXR:
- Hyperinflation, bullae, flat hemidiaphragm

High res CT scan:
- Emphysema/chronic airway disease

Others:
- ECG, echo, sputum, alpha1AT, FBC, BMI, TLCO

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6
Q

COPD

Severity

A

All with post-bronch FEV1/FVC < 0.7

FEV1 (% predicted):

  • Stage 1 (Mild): > 80% (+ symptoms)
  • Stage 2 (Mod): 50-79%
  • Stage 3 (Severe): 30-49%
  • Stage 4 (Very severe): < 30%
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7
Q

COPD

General management

A
  • Smoking cessation - offer nicotine replacement therapy
  • Vaccines = one-off pneumococcal and annual flu vaccines
  • Pulmonary rehabilitation - start early, as soon as feeling breathless with regular activity
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8
Q

COPD

Medications

A
  • SABA or SAMA

If asthmatic features:

  • SABA/SAMA + LABA + ICS
  • Then triple therapy (remove SAMA if add LAMA)

If no asthmatic features:

  • SABA + LABA + LAMA
  • Then triple therapy (+ ICS)
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9
Q

COPD

What are the asthmatic features

A
  • Any previous, secure diagnosis of asthma or atopy
  • Higher blood eosinophil count
  • Substantial variation in FEV1 over time (≥ 400 ml)
  • Substantial diurnal variation in peak expiratory flow (≥ 20%)
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10
Q

COPD

Oxygen therapy

A
  • If retaining COaim for oxygen saturations of88-92%titrated byventuri mask - start with 28%
  • If not retaining COand their bicarbonate is normal (meaning they do not normally retain CO) then give oxygen to aim for oxygen saturations> 94%
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11
Q

COPD

Complications

A
  • Polycythaemia

- Cor Pulmonale

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12
Q

COPD

Factors that improve survival

A
  • Smoking cessation
  • LTOT
  • Lung volume reduction surgery in selected patients
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13
Q

COPD

Exacerbation
Features

A
  • Increase in dyspnoea, cough, wheeze
  • May be increased in sputum suggestive of infective cause
  • May be hypoxic and in some cases, have acute confusion
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14
Q

COPD

Exacerbation
Causative bacterial organisms

A
  • Haemophilus influenzae (most common)
  • Streptococcus pneumoniae
  • Moraxella catarrhalis
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15
Q

COPD

Exacerbation
most common viral cause

A
  • Human rhinovirus
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16
Q

COPD

Exacerbation
Management

A
  • Increase frequency of bronchodilator
  • 30 mg Prednisolone PO for 5 days
  • Nebulisers
  • Abx only if sputum is purulent or there are clinical signs of pneumonia
    • Amoxicillin, Clarithromycin or Doxycycline
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17
Q

Lung cancer

Types

A

NSCLC (80%)

  • Adenocarcinoma
  • Squamous cell carcinoma
  • Large-cell carcinoma

SCLC (20%)
- Contain neurosecretory granules that can release neuroendocrine hormones –> responsible for many paraneoplastic syndrome

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18
Q

Lung cancer

Features

A
  • Persistent cough
  • Haemoptysis
  • Dyspnoea
  • Chest pain
  • Weight loss/anaemia
  • Recurrent pneumonia
  • Hoarseness (pancoast tumour on recurrent laryngeal nerve)
  • Superior vena cava syndrome
  • Fixed, monophonic wheeze
  • Supraclavicular lymphadenopathy or persistent cervical lymphadenopathy
  • Clubbing
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19
Q

Lung cancer

Investigations

A
  • 1st line = CXR
  • Staging CT scan
  • Bronchoscopy with biopsy
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20
Q

Lung cancer

Referral

A

2-week wait referral

  • CXR findings that suggest lung cancer
  • > 40 yrs with unexplained haemoptysis

OFFER urgent CXR (within 2 weeks):

  • > 40 yrs with 2 or more of following unexplained symptoms, or ever smoked and 1 of the following unexplained symptoms:
    • Cough
    • Fatigue
    • SOB
    • Chest pain
    • Weight loss
    • Appetite loss

CONSIDER urgent CXR (within 2 weeks):

  • > 40 yrs with any of following:
    • Persistent or recurrent chest infection
    • Clubbing
    • Supraclavicular lymphadenopathy or persistent cervical lymphadenopathy
    • Chest signs consistent with lung cancer
    • Thrombocytosis
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21
Q

Lung cancer

Management
NSCLC

A
  • Surgery if possible (lobectomy)
  • Mediastinopathy prior to surgery to show lymph node involvement
  • Curative or palliative radiotherapy
  • Poor response to chemo
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22
Q

Lung cancer

Management
SCLC

A
  • Surgery if early disease (T1-2a, N0, M0)
  • Combination of chemo and radiotherapy
  • Poorer prognosis than NSCLC
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23
Q

Pneumonia

Features
3 features on auscultation?

A
  • Productive cough
  • Chest pain - may be pleuritic
  • Dyspnoea
  • Fever
  • Tachycardia
  • Reduced O2 saturations
  • Auscultation:
    • Reduced breath sounds
    • Bronchial breathing
    • Focal coarse crackles
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24
Q

Pneumonia

Causes

A
  • Streptococcus pneumoniae
  • Haemophilus influenzae
  • Staphylococcus aureus
  • Mycoplasma pneumoniae
  • Legionella pneumophilia
  • Klebsiella pneumoniae
  • Pneumocystis jiroveci
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25
Q

Pneumonia

HAP time frame?

A

Develops > 48 hrs after admission and within 2 weeks of discharge

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26
Q

Pneumonia

Investigations

A
  • Sputum culture
  • Bloods - raised inflammatory markers, U&Es for urea for CURB65
  • ABG if low sats/COPD
  • CXR - consolidation
  • Atypicals antigen testing
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27
Q

Pneumonia

CURB-65 and scores

A 
Confusion (< 8/10)
Urea > 7mmol/L
R: RR > 30
B: BP < 90mmHg systolic or 60 mmHg diastolic
65: > 65 yrs

0-1: Home treatment
1-2: Hospital treatment
3+: Consider intensive care

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28
Q

Pneumonia

Management

A

Mild:
- 5 day course of PO Amoxicillin (or macrolide)

Mod-Sev:

  • 7-10 day course of dual Abx therapy
  • Amoxicillin and a macrolide

Repeat CXR at 6 weeks

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29
Q

Pneumonia

Complications

A
  • Sepsis
  • Pleural effusion
  • Empyema
  • Lung abscess
  • Death
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30
Q

Pneumonia

S. pneumoniae

A
  • 80% of pneumonia cases
  • High fever, rapid onset
  • Herpes labialis (cold sores!)
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31
Q

Pneumonia

H. influenza

A
  • Particularly common in COPD patients
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32
Q

Pneumonia

S. aureus

A
  • Often in patients with influenza infection or CF
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33
Q

Pneumonia

Mycoplasma pneumoniae

A
  • Atypical
  • Dry cough, atypical chest signs/XR findings
  • Autoimmune haemolytic anaemia
  • Erythema multiforme
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34
Q

Pneumonia

Legionella pneumophilia

A
  • Atypical pneumonia
  • Hyponatraemia
  • Lymphopenia
  • Air conditioning units (recent cheap holiday)
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35
Q

Pneumonia

Klebsiella pneumonia

A
  • Classically in alcoholics
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36
Q

Pneumonia

Pneumocystis jiroveci

A
  • FUNGAL
  • HIV
  • Dry cough
  • Exercise-induced desaturations
  • Absence of chest signs
  • Treat with co-trimoxazole (Trimethoprim and sulfamethoxazole)
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37
Q

PE

Features

A
  • Tachypnoea
  • Chest pain - typically pleuritic
  • Dyspnoea
  • Haemoptysis
  • Tachycardia
  • May have fever

Resp exam:
- Clear chest or crackles

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38
Q

PE

Risk factors

A
  • Immbolity
  • Long haul flihgts
  • Recent surgery
  • Pregnancy
  • Hormone therapy with oestrogen
  • Malignancy
  • Polycythaemia
  • SLE
  • Thrombophilia
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39
Q

PE

PERC criteria

A

All must be negative to rule out PE

  • Age > 50
  • HR > 100
  • O2 sats < 94%
  • Previous DVT or PE
  • Recent surgery or trauma in past 4 weeks
  • Haemoptysis
  • Unilateral leg swelling
  • Oestrogen use (e.g. HRT, contraceptives)
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40
Q

PE

Wells Score

A
  • Clinical signs and symptoms of DVT (3)
  • Alternative diagnosis is less likely (3)
  • HR > 100 bpm (1.5)
  • Immobilisation for > 3 days or surgery in past 4 weeks (1.5)
  • Previous DVT/PE (1.5)
  • Haemoptysis (1)
  • Malignancy (on treatment, treated in last 6 months, or palliative) (1)
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41
Q

PE

Investigations following Wells Score

A

If PE likely (> 4 Wells):

  • CTPA
  • Anticoagulation in the meantime (DOAC)
  • if negative –> proximal leg vein USS if DVT suspected

If PE unlikely (< 4 Wells):

  • D-Dimer
  • If positive –> CTPA
  • If negative –> PE unlikely, stop any anticoagulation

Renal impairment –> use V/Q scan instead of CTPA

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42
Q

PE

Other investigations

A
  • ECG: S1Q3T3
  • CXR: typically normal, use to rule out other pathology
  • ABG: sometimes respiratory alkalosis with low pO2
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43
Q

PE

Management

A
  • Anticoagulation with DOAC (unless renal impairment or antiphospholipid syndrome –> LMWH)
  • Provoked vs unprovoked: 3 months for provoked, 6 months for unprovoked, 6 months for active cancer
  • If haemodynamically unstable–> Thrombolysis (e.g. alteplase)
  • If repeat PEs despite adequate anticoagulation –> consider IVC filter
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44
Q

TB

Pathophysiology

A
  • Mycobacterium tuberculosis: rod-shaped, acid-fast bacilli
  • Macrophages engulf the TB bacteria but TB bacteria secretes enzymes to inhibit its own breakdown -> encapsulated within macrophage -> proliferates -> caseous necrosis -> Gohn Focus
  • Gohn Focus + hilar lymph nodes = Gohn Complex

Can stay like this as latent TB, then may reactivate if immunocompromised or in older age

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45
Q

TB

Types

A
  • Primary: Gohn complex etc
  • Secondary: reactivation, mostly in apex, cavitating lesions
  • Systemic miliary TB - spread via vascular system to other areas of the body
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46
Q

TB

Extra-pulmonary infection

A
  • CNS (Tb meningitis)
  • Vertebral bodies (Pott’s disease)
  • Cervical lymph nodes (scrofuloderma)
  • Cold abscesses - usually on the neck
  • Renal (sterile pyuria, WBCs in urine)
  • Adrenal glands (Addisons)
  • Liver (hepatitis)
  • Cutaneous TB
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47
Q

TB

Features

A
  • Fever
  • Night sweats
  • Weight loss
  • Haemoptysis
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48
Q

TB

Investigations

A

CXR

  • Primary TB: patchy consolidation, pleural effusions, bilateral hilar lymphadenopathy
  • Reactivated TB: patchy or nodular consolidation with upper lobe cavitation
  • Disseminated miliary TB: millet seeds appearance

Sputum smear

  • 3 specimen
  • Use hypertonic saline or bronchoscopy with lavage if not producing sputum
  • Ziehl Neelson stain -> red on blue background
  • Done on Lowenstein-Jensen growth medium

Sputum culture

  • Gold-standard
  • Can assess drug sensitivities
  • Can take 1-3 weeks
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49
Q

TB

bCG vaccine

A
  • Intradermal infection of live attenuated TB
  • Do Mantoux test prior to the vaccine - only give if negative
  • Assess for immunosuppression/HIV
  • Offer to high risk:
    • Neonates born in areas with high rates, with relatives from countries with high rates, Fx
    • Unvaccinated children/young adults (<35yrs) with close contact
    • Unvaccinated children/young adults who have recently arrived from high risk country
    • Healthcare workers
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50
Q

TB

Management of active TB

A

Initial 2 months:

  • Rifampicin
  • Isoniazid
  • Pyrazinamide
  • Ethambutol

Further 4 months:

  • Rifampicin
  • Isoniazid

PLUS Pyridoxine (Vit B6) for full 6 months

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51
Q

TB

RIfampicin SEs

A
  • Red and orange urine
  • Hepatitis
  • Liver enzyme inducer
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52
Q

TB

Isoniazid SEs

A
  • Peripheral neuropathy (Vit B6 helps)
  • Hepatitis
  • Liver enzyme inhibitor
  • Agranulocytosis
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53
Q

TB

Pyrazinamide SEs

A
  • Hyperuricaemia -> gout
  • Arthralgia and myalgia
  • Hepatitis
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54
Q

TB

Ethambutol SEs

A
  • Difficulty recognizing colours

- Check visual acuity before and during treatment

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55
Q

TB

Management of meningeal TB

A
  • Prolonged period of 12 months of treatment

- PLUS steroids

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56
Q

TB

DOTS

A
  • Directly observed therapy
  • 3 times a week
  • For those in certain groups, e.g. homeless people with active TB, likely to have poor concordance, all prisoners with active or latent TB
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57
Q

TB

Risk factors for reactivation of TB

A
  • Silicosis
  • Chronic renal failure
  • HIV
  • Solid organ transplantation with immuosuppression
  • IVDU
  • Anti-TNF treatment
  • Previous gastrectomy
  • Older age
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58
Q

TB

Screening for latent TB

A

Mantoux test

  • Purified protein derivative (PPD) - tuberculin
  • Injected intradermally
  • Result read 3 days later
  • Positive = had TB infection at some point
  • False negative may be seen in miliary TB, sarcoidosis, HIV, lymphoma, very young age (< 6 months)

Interferon-gamma blood test

  • Looks for evidence of previous TB infection
  • Used in mantoux positive or equivocal, people where tuberculin test may be falsely negative
  • If has BCG, does not show positive (a bonus)

If either are positive -> CXR to look for active infection

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59
Q

TB

Treatment of latent TB

A
  • 3 months or ‘RI’ (+ pyridoxine)
    OR
  • 6 months of Isoniazid (+pyridoxine)
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60
Q

Spirometry

Restrictive pattern

A
  • Reduced FEV1 < 80%
  • Reduced FVC <80%
  • Normal FEV1/FVC ratio >0.7/75%
  • Reduced TLCO
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61
Q

Spirometry

Obstructive pattern

A
  • Reduced FEV1 < 80%
  • Reduced FVC (but to a lesser extent than FEV1)
  • Reduced FEV1/FVC ratio <0.7/75%
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62
Q

Spirometry definitions

A
  • FEV1: forced expiratory volume - volume that has been exhaled at the end of the first second of forced expiration
  • FVC: forced vital capacity - volume that has been exhaled after a maximal expiration following a full inspiration
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63
Q

Spirometry graphs

A
  • Obstructive: more gradual upwards trajectory, less flat

- Restrictive: same shape of trajectory but lower on the graph

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64
Q

Interstitial lung disease

Definition

A

Umbrella term to describe conditions affecting the lung parenchyma

Fibrosis –> replacement of normal elastic and functional lung tissue with scar tissue that is stiff and does not function as effectively

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65
Q

Interstitial lung disease

Upper lobe diseases

A

CHARTS

Coal workers pneumonia
Histiocytosis/Hypersensitivity pneumonitis
Ankylosing spondylitis
Radiation
Tuberculosis
Silicosis/sarcoidosis
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66
Q

Interstitial lung disease

Lower lobe diseases

A

ICDA

Idiopathic pulmonary fibrosis
Connective tissue disorders, e.g. SLE
Drug-induced: amiodarone, bleomycin, methotrexate
Asbestosis

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67
Q

Interstitial lung disease

Diagnosis

A
  • CXR: ground glass changes

- Lung biopsy

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68
Q

Interstitial lung disease

Management

A
  • Remove/treat the underlying cause
  • Home oxygen is hypoxic at rest
  • Stop smoking
  • Physio and pulmonary rehabilitation
  • Flu and pneumococcal vaccines
  • Advanced care planning
  • Lung transplant - weigh up risks vs benefits
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69
Q

Idiopathic pulmonary fibrosis

Epidemiology

A
  • 50 - 70 yrs

- Twice as common in men

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70
Q

Idiopathic pulmonary fibrosis

Features

A
  • Insidious onset of SOB, dry cough > 3 months

- Bibasal fine inspiratory crackles and clubbing

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71
Q

Idiopathic pulmonary fibrosis

Investigations

A
  • Spirometry: restrictive picture
  • Reduced TLCO
  • High resolution CT = needed for diagnosis
  • CXR

Ground glass changes and honeycombing

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72
Q

Idiopathic pulmonary fibrosis

Management

A
  • Pulmonary rehabilitation
  • Supplementary O2
  • May need lung transplant eventually
  • Pirfenidone or Nintedanib may be used
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73
Q

Idiopathic pulmonary fibrosis

Prognosis

A

2-5 years

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74
Q

Drug causes of pulmonary fibrosis

A
  • Amiodarone
  • Cyclophosphamide
  • Methotrexate
  • Nitrofurantoin
  • Bleomycin
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75
Q

What is the TLCO

A

Total gas transfer!

The transfer factor describes the rate at which a gas will diffuse from alveoli into blood. Carbon monoxide is used to test the rate of diffusion.

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76
Q

What is KCO

A

TLCO that is corrected for lung volume

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77
Q

What might cause a high KCO and normal/reduced TLCO?

A
  • Pneumonectomy/lobectomy
  • Scoliosis/kyphosis
  • Neuromuscular weakness
  • Ankylosis of costovertebral joints, e.g. ankylosing spondylitis
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78
Q

Causes of raised TLCO

A
  • Asthma
  • Pulmonary haemorrhage (Wegener’s, Goodpasture’s)
  • L->R cardiac shunts
  • Polycythaemia
  • Hyperkinetic states
  • Male gender
  • Exercise
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79
Q

Causes of reduced TLCO

A
  • Pulmonary fibrosis
  • Pneumonia
  • Pulmonary emboli
  • Pulmonary oedema
  • Emphysema
  • Anaemia
  • Low cardiac output
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80
Q

Secondary pulmonary fibrosis

Causes

A
  • Alpha-1 antitripsin deficiency
  • Rheumatoid arthritis
  • Systemic lupus erythematosus (SLE)
  • Systemic sclerosis
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81
Q

Extrinsic allergic alveolitis / Hypersensitivity pneumonitis

Pathophysiology

A
  • Hypersensitivity induced lung damage due to inhaled organic particles
  • Largely caused by immune-complex mediate tissue damage (type III hypersensitivity)
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82
Q

Extrinsic allergic alveolitis / Hypersensitivity pneumonitis

Examples

A
  • Birds fancier lungs (avian proteins from bird droppings, chlamydia psittaci)
  • Farmers lung (spores of saccharopolyspora rectivirgula from wet hay)
  • Malt workers lung (aspergillus clavatus)
  • Mushroom workers’ lung (thermophilic actinomycetes)
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83
Q

Cryptogenic Organising Pneumonia

What
Dx
Tx

A

What?
- Focal area of inflammation of the lung tissue

Dx:

  • Present similarly to pneumonia
  • Lung biopsy is definitive Ix

Tx
- Systemic corticosteroids

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84
Q

Asbestosis

Pathophysiology

A
  • Inhalation of asbestos
  • Fibrogenic to lungs
  • Oncogenic too
  • Effects usually take decades to develop
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85
Q

Asbestosis

Features

A
  • Pleural plaques (benign, do not undergo malignant change, do not require follow up, occur after latent phase 20-40yrs)
  • Pleural thickening
  • Lung fibrosis
  • Asbestosis (severity is linked to length of exposure, latent period 15-30 yrs, lower lobe, SOB and reduced exercise tolerance)
  • Adenocarcinoma
  • Mesothelioma (malignant disease)
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86
Q

Mesothelioma

Which asbestos is most dangerous?

A

Crocidolite (blue)

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87
Q

Mesothelioma

Features

A
  • Progressive SOB
  • Chest wall pain
  • Pleural effusion (generally painless)
  • Clubbing
  • Weight loss
  • Hx of asbestos exposure in 85-90% (latent period of 30-40 years)
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88
Q

Mesothelioma

Tx

A
  • Palliative chemo
  • Limited role for surgery/radiotherapy
  • Industrial compensation
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89
Q

Mesothelioma

Prognosis

A

Poor

8-14 months = median survival

90
Q

Pleural effusion

Transudate causes

A

< 30 g/L

  • Heart failure (most common transudate cause)
  • Hypoalbuminaemia (liver disease, nephrotic syndrome, malabsorption)
  • Hypothyroidism
  • Meig’s syndrome
  • Kidney failure/nephrotic syndrome
91
Q

Pleural effusion

Exudate causes

A

> 30 g/L

  • Infection: Pneumonia (most common exudate cause), TB, subphrenic abscess
  • Connective tissue disease (RA, SLE)
  • Neoplasia (lung cancer, mesothelioma, metastases)
  • Pancreatitis
  • Pulmonary embolism
  • Dressler’s syndrome
  • Yellow nail syndrome
92
Q

Pleural effusion

Light’s criteria

A

If the protein level is between 25-35 g/L, Light’s criteria

An exudate is likely if at least one of the following criteria are met:

- Pleural fluid protein divided by serum protein >0.5
- Pleural fluid LDH divided by serum LDH >0.6
- Pleural fluid LDH more than two-thirds the upper limits of normal serum LDH
93
Q

Pleural effusion

Other characteristic pleural fluid findings

A
  • Low glucose: rheumatoid arthritis, tuberculosis
  • Raised amylase: pancreatitis,oesophageal perforation
  • Heavy blood staining: mesothelioma, pulmonary embolism, tuberculosis
94
Q

Pleural effusion

Features

A
  • Dyspnoea
  • Non-productive cough
  • Chest pain
  • Dullness to percussion
  • Reduced breath sounds
  • Reduced chest expansion
95
Q

Pleural effusion

Imaging

A
  • PA chest X-Ray
  • USS
  • Contrast CT
  • Aspiration
96
Q

Pleural effusion

Aspiration

A
  • As above, ultrasound is recommended to reduce the complication rate
  • A 21G needle and 50ml syringe should be used
  • Fluid should be sent for pH, protein, lactate dehydrogenase (LDH), cytology and microbiology
97
Q

Pleural effusion

Management

A
  • Depends on the cause, e.g. HF -> diuretics, Infection -> Abx
  • Recurrent aspiration
  • Pleurodesis
  • Indwelling pleural catheter
  • Drug management to alleviate symptoms, e.g. opioids to relieve dyspnoea
98
Q

Pleural effusion

CXR findings

A
  • Blunting of the costophrenic angle
  • Fluid in the lung fissures
  • Larger effusions will have a meniscus. This is a curving upwards where it meets the chest wall and mediastinum.
  • Tracheal and mediastinal deviation if it is a massive effusion
99
Q

Empyema

Define

A

Empyema is where there is an infected pleural effusion.

100
Q

Empyema

When to suspect?

A

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

101
Q

Empyema

Investigations

A

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

102
Q

Empyema

Management

A

Empyema is treated by chest drain to remove the pus and antibiotics

103
Q

Bronchiectasis

Causes

A
  • Post-infective: TB, measles, pertussis, pneumonia
  • Cystic fibrosis
  • Bronchial obstruction: lung cancer/foreign body
  • Immune deficiency: selective IgA, hypogammaglobulinemia
  • Allergic bronchopulmonary aspergillosis (ABPA)
  • Ciliary dyskinetic syndromes: Kartagener’s syndrome, Young’s syndrome
  • Yellow nail syndrome
104
Q

Bronchiectasis

Organisms

A
  • Haemophilus influenzae (most common)
  • Pseudomonas aeruginosa
  • Klebsiella spp.
  • Streptococcus pneumoniae
105
Q

Bronchiectasis

Features

A
  • Persistent cough
  • Copious purulent sputum
  • Intermittent haemoptysis
  • SOB
  • Recurrent chest infections
  • Clubbing
  • Coarse inspiratory crepitations
106
Q

Bronchiectasis

Investigations

A
  • Sputum culture
  • CXR: dilated bronchi, ring/cystic shadows, tram-tracks
  • High resolution CT: tram-tracks, wide bronchi, signet ring signs
107
Q

Bronchiectasis

Management

A
  • Physical training
  • Postural drainage
  • Abx for exacerbations and long-term rotating Abx in severe cases
  • bronchodilators
  • Immunisations
  • Surgery in selected cases (e.g. localised disease)
108
Q

Bronchiectasis

Pathophysiology

A

Permanent dilatation of the airways secondary to chronic infection or inflammation

109
Q

LTOT in COPD

A

LTOT should be offered to patients with a pO2 of < 7.3 kPa or to those with a pO2 of 7.3 - 8 kPa and one of the following:

  • Secondary polycythaemia
  • Nocturnal hypoxaemia
  • Peripheral oedema
  • Pulmonary hypertension
110
Q

Azithromycin in COPD

Criteria

A
  • Not smoker
  • Optimised standard treatment
  • Continue to have exacerbations
111
Q

Azithromycin in COPD

Prior to starting tx

A
  • CT thorax (exclude bronchiectasis)
  • Sputum culture (exclude atypical infections and TB)
  • LFTs
  • ECG to exclude QT prolongation
112
Q

Acute respiratory distress syndrome

Causes

A
  • Infection
  • Massive blood transfusion
  • Trauma
  • Smoke inhalation
  • Acute pancreatitis
  • Cardio-pulmonary bypass
113
Q

Acute respiratory distress syndrome

Features

A
  • Acute onset (within 1 week of known RF)
  • Dyspnoea
  • Elevated RR
  • Bilateral lung crackles
  • Low O2 sats
114
Q

Acute respiratory distress syndrome

Investigations

A
  • ABG
  • CXR: bilateral infiltrates (pulmonary oedema)
  • Non-cardiogenic (pulmonary artery wedge pressure needed if doubt)
  • pO2/FiO2 < 40 kPa (200 mmHg)
115
Q

Acute respiratory distress syndrome

Management

A
  • ITU
  • Oxygenation/ventilation to treat hypoxaemia
  • General organ support (e.g. vasopressors)
  • Tx of underlying cause
  • Prone positioning and muscle relaxation
116
Q

Asthma

Stepdown therapy

A

In the step-down treatment of asthma, aim for a reduction of 25-50% in the dose of inhaled corticosteroids

117
Q

Extrinsic allergic alveolitis

Features

A

Acute (4-8 hrs after exposure):

  • Dyspnoea
  • Dry cough
  • Fever

Chronic (weeks-months):

  • Weight loss
  • Productive cough
  • Dyspnoea
  • Lethargy
118
Q

Extrinsic allergic alveolitis

Investigations

A
  • Imaging: upper/mid-zone fibrosis
  • Bronchoalveolar lavage: lymphocytosis
  • Serologic assays for specific IgGs
  • Blood: NO eosinophilia
119
Q

Extrinsic allergic alveolitis

Management

A
  • Avoid triggers

- Oral glucocorticoids for severe cases or failure to avoid triggers

120
Q

Kartagener’s syndrome

Features

A
  • Dextrocardia or complete situs inversus
  • Bronchiectasis
  • Recurrent sinusitis
  • Subfertility (secondary to diminished sperm motility and defective ciliary action in the fallopian tubes)
121
Q

Kartagener’s syndrome

Pathophysiology

A
  • Primary ciliary dyskinesia
  • Dextrocardia = quiet heart sounds, small volume complexes in lateral leads
  • Dynein arm defect results in immotile cilia
122
Q

Lung cancer

Small cell
Paraneoplastic features

A

SIADH
- Hyponatraemia

ACTH (not typical)

  • Hypertension
  • Hyperglycaemia
  • Hypokalaemia
  • Alkalosis
  • Muscle weakness
  • CUSHINGS

Lambert-Eaton Syndrome

123
Q

Lung cancer

Squamous cell
Paraneoplastic features

A
  • Hypercalcaemia
  • Clubbing
  • Hypertrophic pulmonary osteoarthropathy (HPOA)
  • Hyperthyroidism due to ectopic TSH
124
Q

Lung cancer

Adenocarcinoma
Paraneoplastic features

A
  • Gynaecomastia

- Hypertrophic pulmonary osteoarthropathy (HPOA)

125
Q

Pneumothorax

Features

A

RAPID onset

  • Dyspnoea
  • Chest pain - pleuritic
  • Sweating
  • Tachypnoea
  • Tachycardia
126
Q

Pneumothorax

Risk factors

A
  • Pre-existing lung disease (COPD/asthma/CF/lung cancer/pneumocystis pneumonia)
  • Connective tissue disease (Marfans/RA)
  • Ventilation!
  • Catamenial pneumothorax (related to menstruation)
127
Q

Pneumothorax

Types

A
  • Primary: no underlying lung disease

- Secondary: underlying lung disease present

128
Q

Pneumothorax

Tx of primary pneumothorax

A
  • If rim of air < 2cm and no SOB -> consider discharge
  • Otherwise ASPIRATION
  • If this fails (> 2cm still or SOB) then chest drain
129
Q

Pneumothorax

Tx of secondary pneumothorax

A
  • If > 50 yrs and rim of air > 2cm +/- SOB then CHEST DRAIN
  • Otherwise ASPIRATION
  • If < 1cm then O2 and admit for 24 hrs
130
Q

Pneumothorax

Iatrogenic Tx

A
  • Less likely to recurs than spontaenous
  • Majority resolve with observation
  • Aspiration if Tx required
  • If COPD/ventilation, may consider a chest drain
131
Q

Pneumothorax

Discharge advise

A
  • NEVER scuba dive
  • No travel by air for 1 week post check XR
  • Avoid smoking to reduce risk of further episodes
132
Q

Obstructive sleep apnoea

Predisposing factors

A
  • Obesity
  • Macroglossia: acromegaly, hypothyroidism, amyloidosis
  • Large tonsils
  • Marfan’s syndrome
133
Q

Obstructive sleep apnoea

Consequences

A
  • Snoring
  • Period of apnoea
  • Daytime somnolence
  • Compensated respiratory acidosis
  • HYPERTENSION
134
Q

Obstructive sleep apnoea

Assessment of sleepiness

A
  • Epworth sleepiness scale

- Multiple Sleep Latency Test (MSLT) - measures time to fall asleep in a dark room

135
Q

Obstructive sleep apnoea

Diagnostic tests

A

Sleep studies (polysomnography)

  • Ranging from monitoring of pulse oximetry at night to full polysomnography
  • Full includes: EEG, respiratory airflow, thoraco-abdominal movement, snoring and pulse oximetry
136
Q

Obstructive sleep apnoea

Management

A
  • Weight loss
  • CPAP = 1st line for moderate-severe
  • Intra-oral devices (e.g. mandibular advancement) if CPAP not tolerated or mild OSAHS with no daytime sleepiness
  • DVLA should be informed if excessive daytime sleepiness
137
Q

Causes of haemoptysis

A
  • Lung cancer
  • Pulmonary oedema
  • TB
  • PE
  • LRTI
  • Bronchiectasis
  • Mitral stenosis
  • Aspergilloma
  • Granulomatosis with polyangiitis
  • Goodpasture’s syndrome
138
Q

Aspergilloma

Pathophysiology

A
  • Mass-like fungus ball (mycetoma)

- Colonises an existing lung cavity (e.g. secondary to malignancy, TB, CF)

139
Q

Aspergilloma

Features

A
  • Usually asymptomatic
  • Cough
  • Haemoptysis
140
Q

Aspergilloma

Investigations

A
  • CXR: round opacity

- High titres Aspergillus precipitins

141
Q

Acute bronchitis

Pathophysiology

A
  • Self-limiting chest infection
  • Result of inflammation of trachea and major bronchi
  • Oedematous large airways and production of sputum
142
Q

Acute bronchitis

Features

A
  • Cough
  • Sore throat
  • Rhinorrhoea
  • Wheeze
  • Sometimes low-grade fever
143
Q

Acute bronchitis

Differentiating from pneumonia

A
  • Hx: sputum, wheeze, breathlessness may be absent in acute bronchitis
  • Examination: only wheeze in acute bronchitis. In pneumonia would see dullness to percussion, creps, bronchial breathing
144
Q

Acute bronchitis

Investigations

A
  • Typically a clinical diagnosis

- CRP can guide the need for Abx

145
Q

Acute bronchitis

Management

A
  • Analgesia
  • Good fluid intake

Consider Abx therapy if:

  • Systemically very unwell
  • Pre-existing co-morbidities
  • CRP of 20-100 (delayed prescription) or > 100 (immediately)
  • Doxy would be 1st line if Abx needed. NOT in children/pregnancy -> Amoxicillin.
146
Q

Acute asthma

Moderate

A
  • PEFR 50-75% best or predicted
  • Normal speech
  • RR < 25
  • HR < 110
147
Q

Acute asthma

Severe

A
  • PEFR 33-50%
  • Can’t complete sentences
  • RR > 25
  • HR > 110
148
Q

Acute asthma

Life-threatening

A
  • PEFR < 33%
  • O2 sats < 92%
  • Silent chest
  • Cyanosis
  • Feeble resp effort
  • Bradycardia
  • Dysrhythmia
  • Hypotension
  • Exhaustion
  • Confusion
  • Coma
  • NORMAL CO2 = EXHAUSTION
149
Q

Sarcoidosis

Indications for steroids

A
  • CXR stage 2 or 3 disease AND symptomatic
  • Hypercalcaemia
  • Eye. heart and neuro involvement
150
Q

Sarcoidosis

Features

A

Acute:

  • Erythema nodosum
  • Bilateral hilar lymphadenopathy
  • Swinging fever
  • Polyarthralgia

Insidious:

  • Dyspnoea
  • Non-productive cough
  • Malaise
  • Weight loss

Skin:
- Lupus pernio

Hypercalcaemia:
- Macrophages inside the granulomas cause increased conversion of Vit D to 1, 25-dihydroxycholecalciferol

151
Q

Sarcoidosis

Pathophysiology

A
  • Mutilsystem disorder

- Non-caseating granulomas

152
Q

Sarcoidosis

Epidemiology

A

More common in

  • Young adults
  • African descent
153
Q

Asbestosis

Ethics

A
  • Suffers are eligible for compensation if they develop asbestos related health conditions (except isolated pleural plaques).
  • All patients that die with known exposure to asbestos need to be referred to the coroners.
154
Q

Mesothelioma

Pathophysiology

A
  • Malignancy of mesothelial cells of pleura
  • Metastases to contralateral lung and peritoneum
  • Right lung affected more often than left
155
Q

Mesothelioma

Investigations

A
  • CXR: pleural effusions or pleural thickening
    If pleural effusion -> send for MC&S, biochemistry and cytology
  • Pleural CT
  • Local anaesthetic thoracoscopy
  • Image-guided pleural biopsy if pleural nodularity seen on CT
156
Q

Pulmonary hypertension

Pathophysiology

A
  • Increased resistance and pressure of blood in pulmonary arteries
  • Causes strain on the right side of the heart
  • Back pressure of blood into systemic venous system
157
Q

Pulmonary hypertension

Causes

A

5 groups

  • Group 1: Primary pulmonary hypertension or connective tissue disease (e.g. SLE)
  • Group 2: LHF - usually due to MI/systemic HTN
  • Group 3: Chronic lung disease (e.g. COPD)
  • Group 4: Pulmonary vascular diseases (e.g. PE)
  • Group 5: Misc, e,g, sarcoidosis, glycogen storage disease, haematological disorders
158
Q

Pulmonary hypertension

Features

A
  • SOB
  • Syncope
  • Raised JVP
  • Hepatomegaly
  • Peripheral oedema
159
Q

Pulmonary hypertension

Investigations

A
  • ECG: RH strain - R ventricular hypertrophy, right axis deviation, RBBB
  • CXR: Dilated pulmonary arteries, right ventricular hypertrophy
  • Others: Raised NT-proBNP (RVF), Echo to estimate pulmonary artery pressure
160
Q

Pulmonary hypertension

Management

A

Primary:

  • IV prostanoids (e.g. epoprostenol)
  • Endothelin receptor antagonists (e.g. macitentan)
  • Phosphodiesterase-5-inhibitors (e.g. sildenafil)

Secondary:
- Treat underlying cause

Supportive treatment for resp failure, arrhythmias, HF

161
Q

Goodpasture’s Syndrome / Anti-glomerular basement membrane (GBM) disease

Epidemiology

A
  • More common in men
  • Bimodal age distribution (20-30 yrs and 60-70 yrs)
  • Associated with HLA DR2
162
Q

Goodpasture’s Syndrome / Anti-glomerular basement membrane (GBM) disease

Features

A
  • Pulmonary haemorrhage

- Rapidly progressive glomerulonephritis

163
Q

Goodpasture’s Syndrome / Anti-glomerular basement membrane (GBM) disease

Investigations

A
  • Renal biopsy: linear IgG deposits along basement membrane, crescentic glomerulonephritis
  • Raised transfer factor, secondary to pulmonary haemorrhages
  • Anti-GBM antibodies
164
Q

Goodpasture’s Syndrome / Anti-glomerular basement membrane (GBM) disease

Management

A
  • Plasma exchange (plasmapheresis)
  • Steroids
  • Cyclophophamide
165
Q

Factors that increase the likelihood of pulmonary haemorrhage

A
  • Smoking
  • Lower respiratory tract infection
  • Pulmonary oedema
  • Inhalation of hydrocarbons
  • Young males
166
Q

Granulomatosis with polyangiitis (Wegener’s)

Features

A
  • URT: epistaxis, sinusitis, nasal crusting
  • LRT: dyspnoea, haemoptysis
  • Rapidly progressive glomerulonephritis
  • Saddle-shaped nose
  • Vasculitis rash
  • Eye involvement
  • Cranial nerve lesions
167
Q

Granulomatosis with polyangiitis (Wegener’s)

Investigations

A
  • Renal biopsy: epithelial crescents in Bowman’s capsule
  • CXR: cavitating lesions
  • cANCA (90%)
  • pANCA (25%)
168
Q

Acute asthma

Features

A
  • Progressively worsening SOB
  • Use of accessory muscles
  • Tachypnoea
  • Symmetrical expiratory wheeze on auscultation
  • Tight chest, reduced air entry
169
Q

Acute asthma

Near fatal asthma

A
  • High CO2 (respiratory acidosis)

- Mechanical ventilation requirement

170
Q

Acute asthma

Management

A

O SHIT ME

O: Oxygen
S: Salbutamol nebs
H: Hydrocortisone/Pred for 5 days
I: Ipratropium bromide nebs
T: Theophylline/aminophylline (severe)
M: Magnesium sulphate (LT)
E: Escalate - HDU/ITU/intubation (LT)
171
Q

Acute asthma

Monitoring response

A
  • Respiratory rate
  • Respiratory effort
  • Peak flow
  • Oxygen saturations
  • Chest auscultation
  • Monitorserum potassium when on salbutamol
172
Q

Acute asthma

Admission criteria

A
  • Life-threatening acute attack
  • Severe and not responding to initial treatment
  • Previous near-fatal asthma attack
173
Q

Acute asthma

Criteria for discharge

A
  • Beenstable on their discharge medication (i.e. no nebulizers or oxygen) for 12–24 hours
  • Inhaler technique checked and recorded
  • Check compliance with meds
  • PEF >75% of best or predicted
  • Asthma action plan and possible rescue pack
  • Referral to a respiratory specialist if > 2 attacks in 12 months
174
Q

Chronic asthma

Pathophysiology

A
  • Causes episodic exacerbations of bronchoconstriction
  • A reversible airway obstruction
  • Responds to bronchodilators, e.g. Salbutamol
  • Caused by Type I hypersensitivity
175
Q

Chronic asthma

Common triggers (7)

A
  • Infection
  • Night time or early morning
  • Exercise
  • Animals
  • Cold/damp
  • Dust
  • Strong emotions
176
Q

Chronic asthma

Risk factors (9)

A
  • Personal/family Hx of atopy
  • Antenatal factors: maternal smoking, viral infection during pregnancy (especially RSV)
  • Low birth weight
  • Not being breastfed
  • Maternal smoking
  • Exposure to high concentrations of allergens (e.g. house dust mite)
  • Air pollution
  • Hygiene hypothesis
  • Occupation
177
Q

Chronic asthma

Presentation

A
  • Episodic symptoms
  • Diurnal variability, typically worse at night
  • Dry cough with wheeze and SOB
  • Hx of atopic conditions, such as eczema, hayfever and food allergies
  • Family Hx
  • Bilateral widespread expiratory polyphonic wheeze
  • A number of patients with asthma are sensitive toaspirin. Patients who are most sensitive to asthma often suffer from nasal polyps (Samter’s triad).
178
Q

Chronic asthma

Presentations that may indicate a diagnosis other than asthma

A
  • Wheeze related to coughs and colds more suggestive of viral induced wheeze
  • Isolated or productive cough
  • Normal investigations
  • No response to treatment
  • Unilateral wheeze → suggests focal lesion of infection
179
Q

Chronic asthma

Investigations

A
  • 1st line = spirometry with bronchodilator reversibility and FeNO

Spirometry:
- Reduced FEV1, normal FVC, FEV1/FVC < 70%
Reversibility:
- FEV1 improve by 12% or increase in volume by 200 ml
FeNO:
- > 40 parts per billion

Peak expiratory flow variability > 20%

180
Q

Chronic asthma

Drug management

A
  1. SABA
  2. ICS
  3. LABA or Montelukast
  4. The one that wasn’t added preivously
  5. Maintenance and reliever therapy (MART): ICS and LABA combined
181
Q

Chronic asthma

Stepping down treatment

A
  • Consider stepping down treatment every 3 months or so

- When reducing inhaled steroids, do this by 25-50% at a time

182
Q

Chronic asthma

Additional management

A
  • Individual asthma self-management programme
  • Yearly flu jab
  • Yearly asthma review
  • Advise exercise and avoid smoking
183
Q

Occupational asthma

Associations

A
  • Isocyanates (spray painting/foam moulding)
  • Platinum salts
  • Soldering flux resin
  • Glutaraldehyde
  • Flour
  • Epoxy resins
  • Proteolytic enzymes
184
Q

Occupational asthma

Diagnosis

A
  • Serial peak flows when at work and away from work
185
Q

Occupational asthma

Management

A

Referral to resp specialist

186
Q

Silicosis

Pathophysiology

A
  • Fibrosing lung disease caused by the inhalation of fine particles of crystalline silicon dioxide (silica)
  • It is a risk factor for developing TB (silica is toxic to macrophages)
187
Q

Silicosis

Occupations at risk

A
  • Mining
  • Slate works
  • Foundries
  • Potteries
188
Q

Silicosis

Features

A
  • Fibrosing lung disease

- ‘Egg-shell’ calcification of hilar lymph nodes

189
Q

Coal workers pneumoconiosis

Pathophysiology

A
  • Long term exposure to coal dust particles
  • Coal dust (2-5 nanometres) enters the lungs
  • Dust reaches terminal bronchioles and is engulfed by alveolar and interstitial macrophages
  • Moved by macrophages to mucociliary elevator and removed from body as mucus
  • In over exposure to coal dust -> system is overwhelmed -> macrophages accumulate in alveoli -> immune response -> damage to lung tissue
190
Q

Coal workers pneumoconiosis

Epidemiology

A
  • Higher in populations with higher levels fo exposure (many coal mines)
  • Severity linked to length of exposure
  • Male (likely due to prevalence in coal mines)
  • Makes up 7% of all pneumoconiosis
  • Diagnosis usually made 15-20 yrs after initial exposure
191
Q

Coal workers pneumoconiosis

Simple penumoconiosis

A
  • Most common type
  • Most are asymptomatic
  • Increases risk of lung disease, e.g. COPD
  • May lead to progressive massive fibrosis (PMF)
192
Q

Coal workers pneumoconiosis

Staging

A

Category 1: some opacities but normal lung markings visible
Category 2: large number of opacities but normal lung markings visible
Category 3: large number of opacities with normal lung not visible

193
Q

Coal workers pneumoconiosis

Investigations

A
  • CXR: Upper zone fibrosis
  • Spirometry: Restrictive pattern
    A normal or slightly reduced FEV1 and a reduced FVC
194
Q

Coal workers pneumoconiosis

Management

A
  • Avoid exposure to coal dust and other resp irritants, e.g. smoking
  • Manage symptoms of chronic bronchitis
  • Patients eligible for compensation via Industrial Injuries Act
195
Q

What is a pneumoconiosis

A

Pneumoconiosis = accumulation of dust in the lungs and the response of the bodily tissue to its presence, most commonly used in relation to coal workers’ pneumoconiosis.

196
Q

Progressive Massive Fibrosis

A
  • Dust exposure causes patients to develop round fibrotic masses which can be several centimeters in diameter
  • These are most commonly in the upper lobes.
  • The exact pathogenesis is not known.
  • Patients are often symptomatic and have both breathlessness on exertion and cough, some may have black sputum.
  • Lung function testing shows a mixed obstructive/restrictive picture.
197
Q

Signs of respiratory distress

A
  • Raised respiratory rate
  • Use of accessory muscles of breathing, such as the sternocleidomastoid, abdominal and intercostal muscles
  • Intercostal and subcostal recessions
  • Nasal flaring
  • Head bobbing
  • Tracheal tugging
  • Cyanosis (due to low oxygen saturation)
  • Abnormal airway noises
198
Q

Bronchiolitis

Epidemiology

A
  • < 1 year, peak 3-6 months

- Very common in winter

199
Q

Bronchiolitis

Who is it more severe in?

A
  • Congenital heart problems
  • Downs syndrome
  • CF
  • Bronchopulmonary dysplasia (premature)
  • Dual infection with metapneumovirus
200
Q

Bronchiolitis

Causative organisms

A
  • RSV (75-80%)
  • Mycoplasma
  • Adenoviruses
201
Q

Bronchiolitis

Presentation

A
  • Coryzal symptom preceding
  • Dry cough
  • Wheeze
  • Respiratory distress signs
  • Fine end-inspiratory crackles
  • SOB
  • Feeding difficulties (children)
  • Mild fever
  • Apnoeas
  • Tachypnoea
202
Q

Bronchiolitis

When to admit?

A
  • If Downs/congenital heart disease/CF etc
  • < 3 months
  • RR > 70 bpm, head bobbing, grunting, recessions
  • Child looks seriously unwell to HCP
  • Apnoea
  • SpO2 < 92%
  • Central cyanosis
203
Q

Bronchiolitis

Investigations

A
  • Pulse oximetry
  • Viral throat swab
  • Nasopharyngeal secretion immunofluorescence may reveal RSV
  • If severe -> CXR, blood gas, FBC
204
Q

Bronchiolitis

Management

A
  • Most = self-limiting (peak 3-5 days)
  • Nasogastric feeding if cannot drink/eat
  • Suction if excessive secretions
  • Humidified O2 if sats < 92%
  • Maybe PEEP/CPAP
  • Intubation if required, monitor using cap blood gases
  • Poor ventilation = high CO2, falling pH
  • RIBAVIRIN → for immunocompromised and heart/lung conditions
205
Q

Bronchiolitis

Prophylaxis

A
  • Palivizumab = monoclonal antibody that targets RSV. Given as prophylactic monthly injection to high risk babies, such asex-premature and those withcongenital heart disease
  • Maternal IgG can protect newborns against RSV
206
Q

Cystic fibrosis

Pathophyisology

A
  • Autosomal recessive disorders
  • Causes increased viscosity of secretions (e.g. lungs and pancreas)
  • Due to defect in cystic fibrosis transmembrane conductance regulator gene (CFTR) which codes a cAMP-regulated chloride channel
  • In UK - 80% are due to delta F508 on long arm of chromosome 7
  • Affects 1 per 2500 births
  • Carrier rate is 1 in 25
  • Around 5% are diagnosed after 18yrs
207
Q

CF

Consequences of mutation

A
  • Thick pancreatic and biliary secretions→ blockage of theducts → lack of digestiveenzymessuch aspancreaticlipasein thedigestive tract
  • Low volume thick airway secretions→ reduce airway clearance →bacterial colonisationand susceptibility to airwayinfections
  • Congenital bilateral absence of thevas deferensin males. Patients generally have healthy sperm, but the sperm have no way of getting from the testes to the ejaculate, resulting in male infertility
  • Female subfertility
208
Q

CF

Organisms that may colonise

A
  • S. aureus (prophylactic fluclox)
  • Pseudomonas aeruginosa (neb tobramycin)
  • Burkholderia cepacia
  • Aspergillus
  • Escherichia coli
  • Klebsiella pneumoniae
  • Haemophilus influenza
209
Q

CF

Features

A
  • Neonatal period: meconium ileus (abdo distension and vomiting), prolonged jaundice
  • Recurrent chest infections (40%)
  • Malabsorption (30%): steatorrhorea, failure to thrive
  • Liver disease, pancreatitis
  • Chronic cough
  • Thick sputum production
  • Salty taste when kissing (concentrated salt in sweat)
  • Delayed puberty
  • Rectal prolapse (due to bulky stools)
  • Diabetes mellitus
  • Short stature
  • Nasal polyps
  • Clubbing
  • Crackles and wheeze on auscultation
  • Male infertility, female subfertility
210
Q

CF

Investigations

A
  • Newborn blood spot test
  • Genetic testing for CFTR gene (amniocentesis, chorionic villous sampling)
  • Sweat test (> 60 mEq/L of Cl-)
211
Q

CF

Causes of false-positive sweat test

A
  • Malnutrition
  • Adrenal insufficiency
  • Glycogen stroage disease
  • Nephrogenic diabetes inspidus
  • Hypothyroidism, hypoparathyroidism
  • G6PD
  • Ectodermal dysplasia
212
Q

CF

Cause of false-negative sweat test

A

Skin oedema, often due to hypoalbuminaemia / hypoproteinaemia secondary to pancreatic exocrine insufficiency

213
Q

CF

Management

A
  • Chest physiotherapy and postural drainage (>BD)
  • High calorie diet and high fat intake
  • Exercise
  • Minimise contact with each other to prevent cross infection with Burkholderia cepacia complex and Pseudomonas aeruginosa
  • Vitamin supplementation
  • Pancreatic enzyme supplements taken with meals (CREON tablets)
  • Bronchodilators (e.g. Salbutamol) can help treat bronchoconstriction
  • Nebulised DNase or hypertonic saline
  • Vaccinations: pneumococcal, influenza, varicella
  • Fertility treatment and genetic counselling

Lung transplantation

Lumacaftor/lvacaftor (Orkambi):
- Used in CF patients who are homozygous for delta F508 mutation

214
Q

CF

MoA of Ivacaftor

A

Potentiator of CFTR that is already at cell surface, increasing the probability that the defective channel with be open and allow chloride ions to pass through the channel pore

215
Q

Cf

MoA of Lumacaftor

A

Increases CFTR protein numbers that are transported to cell surface

216
Q

CF

Lung transplantation CI

A

Chronic infection with Burkholderia cepacia is an important CF-specific CI to lung transplantation

217
Q

CF

Monitoring

A
  • Followed up every 6 months
  • Regular monitoring of sputum for colonisation
  • Monitoring for DM, osteoporosis, Vit D deficiency, liver failure
218
Q

CF

Prognosis

A
  • 90% of patients with CF developpancreatic insufficiency
  • 50% of adults with CF developcystic fibrosis-related diabetesand require treatment withinsulin
  • 30% of adults with CF developliver disease
  • Most males are infertile due to absent vas deferens
219
Q

What are the boundaries of the ‘safe triangle’ for chest drain insertion?

A
  • Anterior edge latissimus dorsi
  • Lateral border of pectoralis major
  • Line superior to the horizontal level of the nipple (5th intercostal space)
  • Apex below the axilla
220
Q

Causes of an anterior mediastinal mass?

A

4 T’s

  • Teratoma
  • Terrible lymphadenopathy
  • Thymic mass
  • Thyroid mass

Finals (21 decks)

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