Resp Flashcards

1
Q

Define vital capacity

A

Volume of air expired from the lungs from a maximal inspiration using a slow/relaxed manoeuvre

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2
Q

Define forced vital capacity

A

Volume of air that can be forcible expelled from the lungs from a position of maximal inspiration

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3
Q

Define forced expiratory volume

A

volume of air forcibly expelled from the lungs in the first second - following maximal inspiration

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4
Q

Pathophysiology of anaphylaxis

A

Sensitised individual exposed to specific antigen
Immunological response:
– IgE → antigen → mast cell & basophils ‡ → histamine ↑ → body response

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5
Q

Features of anaphylaxis

A

Uritus, urticaria & angioedema, hoarseness, progressing to stridor & bronchial obstruction, wheeze & chest tightness from bronchospasm

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6
Q

Management of anaphylaxis

A

DO NOT DELAY! GET HELP
• Remove trigger, maintain airway, 100% O2
• IM adrenaline 0.5 mg
(Repeat every 5 mins as needed to support CVS)
• IV hydrocortisone 200mg
• IV chlorpheniramine 10 mg
• If hypotensive: lie flat and fluid resuscitate
• Treat bronchospasm: NEB salbutamol
• Laryngeal oedema: NEB adrenaline

monitor for secondary deterioration; advice about epipens and wearing medic alert braclet
arrange f/u in clinic

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7
Q

Severity of asthma exacerbations

A

Mild:
• No features of severe asthma
• PEFR >75%
Moderate:
• No features of severe asthma
• PEFR 50-75%
Severe (if any one of the following):
• PEFR 33 – 50% of best or predicted
• Cannot complete sentences in 1 breath (or unable to feed/talk in children)
• Respiratory Rate > 25/min (2y/o - >40; >5; >30)
• Heart Rate >110/min (2y/o - >140; >5; >125)
Life threatening (if any one of the following):
• PEFR < 33% of best or predicted
• Sats <92% or ABG pO2 < 8kPa
• Cyanosis, poor respiratory effort, near or fully silent
chest
• Exhaustion, confusion, hypotension or arrhythmias
• Normal pCO2
Near Fatal:
• Raised pCO2

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8
Q

Acute asthma attack management

A

ABCDE
Oxygen - aim 94-98%
Salbutamol 5mg NEB (repeat after 15 min) - 2.5-5 if <11y/o
Hydrocortisone 100mg IV (or prednisolone 40mg PO)
(>2 = 20mg)
Ipratropium bromide 500mcg (250mcg in children) NEB
Theophyilline (IV amionophylline)
Magnesium sulphate
Escalate care - ITU

Consider IV salbutamol
Life threatening - portable CXR

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9
Q

Features of an infective COPD exacerbation

A

Change in sputum volume / colour
Fever
Raised WCC +/- CRP

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10
Q

Management of COPD exacerbation

A
Oxygen - 24-28% fixed performance face mask. AIm sats 88-92%
Antibiotics (if infective)
Salbutamol NEB
Ipratropium NEB
Steroids - prednisolone 30mg STAT and 7d

Consider IV aminophyline
Consider NIV if pH <7.35
ITU if pH <7.25

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11
Q

CURB -65

A

C Confusion, MMT 2 or more points worse
U Urea > 7.0
R >30/min
B < 90 mm Hg systolic or < 60 mm Hg diastolic 65 Age above 65 years

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12
Q

Treatment of pneumonia

A

ABCDE
If any features of sepsis – immediately treat using sepsis pathway – NO DELAY in initiating IV antibiotics and fluids
-ABx as per CURB-65 score, local pneumonia guidelines and awareness of any patient drug allergies
- analgiea; PT

CURB SCORE - amoxicillin <1 - home rx; 2 - hospital
- Co-Amoxiclav IV 1.2g tds and Doxycycline PO –> rx; 3 - itu or HAP

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13
Q

Features of pneumonia

A

Consolidation on CXR with fever +/- purulent sputum +/ raised WCC and / or CRP

  • May have malaise; dyspnoea; cough; pleuritic pain

Signs - tachypnoea; tachycardia; cyanosis; confusion; consolidation( reduced expansion; dull percussion; bronchial breathing; reduced air entry; crackles; pleural rub)

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14
Q

Classification of massive haemoptysis

A

> 240mls in 24 hours OR >100mls / day over consecutive days

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15
Q

Management of massive haemoptysis

A

• ABCDE
• Lie patient on side of suspected lesion (if known) • Oral Tranexamic Acid for 5 days or IV
• Stop NSAID’s / aspirin / anticoagulants
• Antibiotics if any evidence of respiratory tract
infection
• Consider Vitamin K
• CT aortogram – interventional radiologist may be able to undertake bronchial artery embolisation

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16
Q

Features of pneumothorax +/- tension

A
  • sudden onset dyspnoea, pleuritic chest pain which reduced chest expansion and breath sounds and resonant percussion
    TENSION
    o hypotension
    o tachycardia
    o deviation of the trachea away from the side of
    the pneumothorax
    o Mediastinal shift away from pneumothorax
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17
Q

Management of tension pneumothorax

A
  • ABCDE (no CXR)
  • Large bore intravenous cannula into 2nd ICS MCL
  • Chest drain into the affected side (0.9% saline-water seal)
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18
Q

Symptoms and signs of PE

A
Sx
– Chest pain (pleuritic)
– SOB
– Syncope
– Haemoptysis
– Massive --> RHF - hypotension, raised JVP, loud P2, +/- cardiac arrest 

Signs
- fever, cyanosis, tachycardia, tachypnoea, evidence of DVT

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19
Q

Risk factors for PE

A
Thrombopillia/ antiphospholipid syndrome
Hx PE/VTE
Recent travel
Obstetric - pregnancy/ OCP
Malignancy
Break lower limb/ varicose veins
Old age
Surgery / smoking
Immobility
Sex (F)
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20
Q

Management of PE

A

A - sit up and 100% oxygen
B - CXR (exclude pleural effusion/ consolidation)
C - ECG, bloods (Trop, FBC, U+E, Clotting, D-Dimer), ABG
D -
E -

• Fluid resuscitation (if hypotensive), analgesia +/- anti-emetic
• Thrombolysis should be considered if a massive PE
is confirmed on Echo or CT scan ( IV Alteplase) –> senior!
• LMWH and Ted Stockings

Wells score
<4 –> if D-dimer -ve - exclude; if +ve –> CTPA
>4 –> CTPA
Ongoing - Graduated compression stockings for 2 years if sign of DVT; Start warfarin -3m if known cause; 6m if unknown

ECG –> T wave inversion, AF, RBBB, RAD –> ?S1Q3T3

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21
Q

Absolute thrombolysis contraindications

A
Haemorrhagic stroke or Ischaemic stroke < 6 months 
CNS neoplasia
Recent trauma or surgery
GI bleed < 1 month
Bleeding disorder
Aortic Dissection
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22
Q

Relative thrombolysis contraindications

A

Warfarin
Pregnancy
Advanced Liver Disease
Infective Endocarditis

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23
Q

Complications of thrombolysis

A
  • Bleeding
  • Hypotension
  • Intracranial haemorrhage / stroke
  • Reperfusion arrhythmias
  • Systemic embolisation of thrombus
  • Allergic reaction
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24
Q

Pathophysiology of asthma

A

Airway epithelial damage – shedding and subepithelial fibrosis, basement membrane thickening
• An inflammatory reaction characterised by eosinophils, T-lymphocytes (Th2) and mast cells. Inflammatory mediators released include histamine, leukotrienes, and prostaglandins
• Cytokines amplify inflammatory response
• Increased numbers of mucus secreting goblet cells
and smooth muscle hyperplasia and hypertrophy
• Mucus plugging in fatal and severe asthma

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25
Q

define asthma and features

A
  • Asthma is a chronic inflammatory disease of the airways
  • Airway obstruction that is reversible (but not completely so in some subjects), either spontaneously or with treatment
  • Increased airway responsiveness (bronchoconstriction) to a variety of stimuli

Features
sx- cough, wheeze (high pitched polyphonic), dyspnoea, diurnal variation, chest tightener
signs - increased RR and HR, widespread polyphonic wheeze, hyperinflated chetst, ? reduced air entery, tracheal tug/recession, nasal flaring/ accessory muscle use

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26
Q

Differentials of a wheeze

A
> Acute Asthma Exacerbation
• Bronchitis – viral or bacterial
Other causes of wheeze less likely:
• Pulmonary oedema
• PE
• Vocal cord dysfunction
• Gastro-oesophageal reflux
• Foreign body
• Allergy
• Hyperventilation / psychosocial
• Cardiac disease
• Vasculitides – Churg-Strauss syndrome, polyarteritis nodosa, Granulomatosis with Polyangiitis (Wegener’s granulomatosis)
• Carcinoid syndrome with hepatic metastases – release of HIAA
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27
Q

Criteria for safe asthma discharge after exacerbation

A

• PEFR >75%
• Stop regular nebulisers for 24 hours prior to discharge
• Inpatient asthma nurse review to reassess inhaler
technique and adherence
• Provide PEFR meter and written asthma action plan
• At least 5 days oral prednisolone
• GP follow up within 2 working days
• Respiratory Clinic follow up within 4 weeks
• For severe or worse, consider psychosocial factors

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28
Q

Differentials of eosinophilia

A
  • Airways inflammation (asthma or COPD)
  • Hayfever / allergies
  • Allergic Bronchopulmonary Aspergillosis
  • Drugs
  • Churg-Strauss / vasculitis
  • Eosinophilic Pneumonia
  • Parasites
  • Lymphoma
  • SLE
  • Hypereosinophilic syndrome
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29
Q

Asthma trigger factors

A

• Smoking
• Upper respiratory tract infections – mainly viral
• Allergens – pollen, house dust mite, pets
• Exercise – also cold air
• Occupational irritants
• Pollution
• Drugs – aspirin, beta blockers (including eye drops)
• Food and drink – dairy produce, alcohol, orange
juice
• Stress
• Severe asthma – consider inhaled heroin, pre-menstrual, psychosocial aspects

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30
Q

NICE definition of COPD

A

COPD is characterised by airflow obstruction. The airflow obstruction is usually progressive, not fully reversible and does not change markedly over several months. The disease is predominantly caused by smoking.

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31
Q

Pathophysiology of COPD

A

COPD is an umbrella term which encompasses emphysema and chronic bronchitis:
• Mucous gland hyperplasia
• Loss of cilial function
• Emphysema – alveolar wall destruction causing
irreversible enlargement of air spaces distal to the
terminal bronchiole
• Chronic inflammation (macrophages and
neutrophils) and fibrosis of small airways

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32
Q

Causes of COPD

A

> Smoking
• Inherited α-1-antitrypsin deficiency
• Industrial exposure, e.g. soot

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33
Q

Members involved in MDT management of COPD

A
  • Physicians
  • G.P.’s
  • Specialist nurses
  • Physiotherapists
  • Pharmacists
  • Occupational therapists
  • Dieticians
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34
Q

Outpatient COPD management

A
  • ‘COPD Care Bundle’
  • SMOKING CESSATION
  • Pulmonary Rehabilitation
  • Bronchodilators
  • Antimuscarinics
  • Steroids
  • Mucolytics
  • Diet
  • LTOT if appropriate
  • LUNG VOLUME REDUCTION if appropriate
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35
Q

Criteria for long term oxygen therapy in COPD

A

> pO2 consistently below 7.3 kPa, or below 8 kPa with cor pulmonale
• Patients must be non-smokers and not retain high levels of CO2

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36
Q

Reason for pulmonary rehabilitation in COPD

A

Many COPD patients with COPD avoid exercise and physical activity because of breathlessness
• This may lead to a vicious cycle of increasing social isolation and inactivity leading to worsening of symptoms
• Pulmonary Rehabilitation aims to break this cycle – an MDT 6-12 week programme of supervised exercise, unsupervised home exercise, nutritional advice, and disease education

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37
Q

CXR consolidation differentials

A
Pneumonia
TB (usually upper lobe)
Lung cancer
Lobar collapse (blockage of bronchi) 
Haemorrhage
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38
Q

Investigations for pneumonia

A
CXR
FBC, UE, CRP
Sputum culture - MC+S
Blood culture (if febrile)
Serology and urine legionella test (if high CURB65)
ABG
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39
Q

Pneumonia follow up

A
• HIV test 
• Immunoglobulins
• Pneumococcal IgG serotypes
• Haemophilus influenzae b IgG
F/u in clinic in 6 weeks with a repeat CXR to
ensure resolution
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40
Q

Causes of non-resolving pneumonia and other complications

A

CHAOS
• Complication – empyema, lung abscess
• Host – immunocompromised
• Antibiotic – inadequate dose, poor oral absorption
• Organism – resistant or unexpected organism not
covered by empirical antibiotics
• Second diagnosis – PE, cancer, organising
pneumonia

Complications - respiratory failure; hypotension; AF; pleural effusion (exudate); sepsis; pericarditis; jaundice (sepsis/drugs)

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41
Q

Clinical features of TB

A
  • fever
  • nocturnal sweats
  • Weight loss (weeks – months)
  • Malaise
  • Respiratory TB: cough ± purulent sputum/ haemoptysis, (+/-pleural effusion)
    Non-Respiratory TB: Skin (erythema nodosum); Lymphadenopathy; Bone/joint; Abdominal; CNS (meningitis); Genitourinary; Miliary (disseminated); Cardiac (pericardial effusion)
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42
Q

Differentials of Haemoptysis

A
Infection:
• Pneumonia
• Tuberculosis
• Bronchiectasis / CF
• Cavitating lung lesion (often fungal) 
Malignancy:
• Lung cancer
• Metastases 
Haemorrhage:
• Bronchial artery erosion
• Vasculitis
• Coagulopathy 
Others:
• PE
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43
Q

Risk factors for TB

A

Past history of TB
Known history of TB contact
Born in a country with high TB incidence
Foreign travel to country with high incidence of TB
Evidence of immunosuppression–e.g. IVDU, HIV, solid organ transplant recipients, renal failure/ dialysis, malnutrition/ low BMI, DM, alcoholism

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44
Q

Management for respiratory TB

A

ABCDE
CXR
Admit to side room and start infection control
3 x early morning sputum samples (AAFB and TB culture)
FBC,LFT, UE, vit D levles
HIV test
CT chest if CXR not clear
MRI/Spine if milary
Abx for pneumonia if diagnosis not clear
If highly likley TB - start anti-TB therapy (after cultures)
Notify TB nurse specialist (initiate contact tracing - Mantoux test to those at risk; IFN gamma if had bcg); notify public health etc)
TB culture can take 6-8 weeks

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45
Q

Anti-TB therapy

A

4 antibiotics for 2 months
(Rifampicin, Isoniazid, Pyrazinamide, Ethambutol) followed by 4 months on two antibiotics (Rifampicin, Isoniazid)
+ Pyridoxine as prophylaxis against peripheral neuropathy

  • Dose is weight dependent
  • check baseline LFT’s and monitor closely
  • Check visual acuity

Compliance is crucial and Directly Observed Therapy (DOT) sometimes used for patients
Provide leaflets on treatment & ensure patient is aware of common and serious SE
Corticosteroids sometimes used, mainly seen in those with TB meningitis

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46
Q

Side effects of TB treatment

A

Rifampicin – Hepatitis, rashes, febrile reaction, orange/red secretions (N.B. contact lenses), many drug interactions including warfarin and OCP

Isoniazid – Hepatitis, rashes, peripheral neuropathy, psychosis

Pyrazinamide – Hepatitis, rashes, vomiting, arthralgia

Ethambutol – Retrobulbar neuritis

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47
Q

Definition of bronchiectasis

A

Chronic dilatation of one or more bronchi. The bronchi exhibit poor mucus clearance and there is predisposition to recurrent or chronic bacterial infection

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48
Q

Ix for bronchiectasis

A
  • High Resolution CT (diagnositic) - dilated and thickened airways
  • sputum culture; bloods; CXR? (tramlines and rings); spirometry (obstructive); ?bronchoscopy; ?CF sweat teast
49
Q

Causes of bronchiectasis

A

• Post infective – whooping cough, TB, measles, bronchiolitis
• Immune deficiency – Hypogammaglobulinaemia
• Genetic / Mucociliary clearance defects – Cystic
fibrosis, primary ciliary dyskinesia, Young’s syndrome (triad of bronchiectasis, sinusitis, and reduced fertility), Kartagener syndrome (triad of bronchiectasis, sinusitits, and situs inversus)
• Obstruction – foreign body, tumour, extrinsic LN, Ca
• Toxic insult – gastric aspiration (particularly post lung transplant), inhalation of toxic chemicals/gases
• Allergic bronchopulmonary aspergillosis
• Secondary immune deficiency – HIV, malignancy
• Rheumatoid arthritis
• Associations – inflammatory bowel disease; yellow
nail syndrome

50
Q

Common organisms that cause bronchiectasis

A
• Haemophilus influenzae
• Pseudomonas aeruginosa
• Moraxella catarrhalis
• Stenotrophomonas maltophilia
• Fungi – aspergillus, candida
• Non-tuberculous mycobacteria
• Less common - Staphylococcus aureus (think about
CF)
51
Q

Management of bronchiectasis

A

• Treat underlying cause (CF - DNAase; ABPA - steroids; immune def - IVIg)
• PT – mucus clearance/ expectoration; drainage
• Abx according to sputum cultures /
sensitivities for acute exacerbations and often
chronic suppressive therapy
• Supportive – flu vaccine, bronchodilators if required
• Pulmonary Rehab – MRC Dyspnoea Score >3

52
Q

Definition of CF

A

CF is an autosomal recessive disease leading to mutations in the Cystic Fibrosis Transmembrane Conductance Regulator (CFTR). This can lead to a multisystem disease (most commonly affecting the respiratory and GI systems) characterised by thickened secretions - impairs mucociliary clearance.

53
Q

Diagnostic criteria for CF

A

One or more of the characteristic phenotypic features -
• Or a history of CF in a sibling
• Or a positive newborn screening test result (increased immunoreactive trypsinogen)
And
• An increased sweat chloride concentration
(> 60 mmol/l) – SWEAT TEST
• Or identification of two CF mutations – genotyping
• Or demonstration of abnormal nasal epithelial ion
transport (nasal potential difference)

54
Q

Presenting features of CF

A

Neonates
- failure to thrive; meconium ilies; rectal prolapse

Children/ young adults

  • chronic sinusitis
  • nasal polyps (infancy/childhood)
  • repeated LRTI (throughout life)
  • bronchiectasis
  • Liver disease; portal hypertension; gallstones
  • DIOS
  • Steatorrhoea
  • Abnormal sweat secretions
  • Pancreatic insufficiency (malabsorption/ steatorrhoea and DM)
  • Finger clubbing
  • Osteoporosis
  • Male infertility (as teenager)
  • Arthritis

Signs - clubbing; arthritis; cyanosis; bilateral creps

Meconium ileus - bowel is blocked by sticky secretions, Signs of intestinal obstruction soon after birth with bilious vomiting, abdominal distension and delay in passing meconium. (+/- jaundice)

55
Q

Common complications of CF

A

1.Respiratory Infections
- Needs aggressive therapy with PT and
Abx +/- prophylactic Abx
common organisms - p. aeruginosa (s.aurues in early life)
2.Low Body Weight
- needs careful monitoring
? pancreatic insufficiency–> Creon (pancreatic enzyme replacement therapy)
- high calorie intake and often extra supplements
- may need NG or PEGf eeding
- may need insulin
3.Distal Intestinal Obstruction Syndrome (DIOS)
- DIOS vs.constipation faecal obstruction in ileocaecum versus whole bowel
- Due to intestinal contents in the distal ileum and proximal colon (thick, dehydrated faeces)
-Often insufficient prescription of pancreatic
enzymes or non-compliance, also salt deficiency / hot weather
- Often presents with palpable RIF mass (faecal)
-Diagnosis: Symptoms; palpable RightIliacFossaMass,
AXR demonstrating faecal loading at junction of small
and large bowel
4. CF Related Diabetes

56
Q

CF lifestyle advice advice

A

• No smoking
• Avoid other CF patients
• Avoid friends / relatives with colds / infections
• Avoid jacuzzis (pseudomonas)
• Clean and dry nebulisers thoroughly
• Avoid stables, compost or rotting vegetation – risk of
aspergillus fumigatus inhalation
• Annual influenza immunisation
• Sodium chloride tablets in hot weather / vigorous
exercise

57
Q

Types of pneumothorax

A
  1. Spontaneous
    i. Primary (no lung disease) ii.Secondary (lung disease) 2.Traumatic (penetrating)
  2. TENSION: emergency
  3. Iatrogenic (e.g. post central line or pacemaker insertion)
58
Q

Risk factors for pneumothorax

A
  • Pre-existing lung disease -COPD; pulmonary fibrosis
  • Height
  • Smoking/ Cannabis
  • Diving
  • Trauma/ Chest procedure
  • Association with other conditions e.g. Marfan’s
    syndrome/ Ehler’s danlos
59
Q

Ix and Management for pneumothorax

A

Ix - ABG and bloods; CXR (translucent, collapse, mediastinal shift +/- depressed hemidiaphragm; surgical emphysema)

Mx
Primary – If symptomatic and rim of air >2cm on
CXR give O2 and aspirate. If unsuccessful consider re-aspiration or intercostal drain. Remove drain after full re-expansion / cessation of air leak.

Secondary – if 1-2cm; >50 and SOB –> insert ICD; otherwise as above - admit for 24 hours

If persistent air leak >5 days (bronchopleural
fistula) refer to thoracic surgeons - chemical pleurosis/pleurectomy etc

Traumatic - ABCDE, analgesia, 3 sided wet dressing and ICD

Discharge advice – No flying or diving until
resolved

60
Q

Investigations for pleural effusion

A

USS guided pleural aspiration

  • biochemistry (protein, pH, LDH)
  • Cytology
  • Microbiology
  • CXR
  • ECG
  • Bloods: FBC, U+E’s, LFT’s, CRP, Bone profile, LDH, clotting
  • ECHO (if suspect heart failure)
  • Staging CT (with contrast) if suspect exudative cause
61
Q

Indications for urgent chest drain for new pleural effusion

A

underlying empyema (pH of pleural fluid <7.2 or visible pus on aspirate).

62
Q

Causes of transudate effusion

- pleural protein <30g/L

A

Common:
“ Heart failure
“ Cirrhosis
“ Hypoalbuminaemia (nephrotic syndrome or
peritoneal dialysis) Less common:
“ Hypothyroidism, mitral stenosis, pulmonary embolism
Rare:
“ Constrictive pericarditis, superior vena cava
obstruction, Meig’s syndrome

63
Q

Causes of Exudate effusions

- pleural protein >30 g/L

A

Common:
“ Malignancy
“ Infections – parapneumonic, TB, HIV (kaposi’s) Less common:
“ Inflammatory (rheumatoid arthritis, pancreatitis, benign asbestos effusion, Dressler’s, pulmonary infarction/pulmonary embolus), Lymphatic disorders, Connective tissue disease
Rare:
“ Yellow nail syndrome, fungal infections, drugs

64
Q

Lights criteria - and when is it used

A

If pleural fluid protein level between 25 and 35 g/L (i.e. borderline) use Light’s criteria
– exudate if one or more of the following:
– Pleural fluid/Serum protein >0.5
– Pleural fluid/Serum LDH >0.6
– Pleural fluid LDH > 2/3 of the upper limit of normal

65
Q

Management of pleural effusion

A
Transudate
Often no diagnostic tap is required
• Treat the underlying cause
• If effusion resolves, stop or reduce treatment
• If effusion persists, then therapeutic
aspiration/drainage is required

Exudate

  • treat underlying cause
  • if established diagnosis - drain/ ICD
66
Q

Causes of interstitial lung disease and commonest type of pulmonary fibrosis

A
  • asbestos, silicon, drugs (bleomycin, amiodarone, sulfasalasime, methotrexate), EAA, TB
  • Assoc systemic disease - sacoid, RA, SLE, systemic sclerosis, UC, A.S.
  • Usual Interstitial Pneumonia
67
Q

Classical findings in UIP and other sx

A

Classical Findings:
• clubbing, reduced chest expansion
• Auscultation – fine inspiratory crepitations (like pulling Velcro slowly) – usually best heard basal / axillary areas
• Cardiovascular – may be features of pulmonary hypertension

Other sx -Dry cough, dyspnoea, malaise, wt loss, arthralgia, OSA, cyanosis

68
Q

Cause and clinical presentation of extrinsic allergic alveolitis

A

Inhalation of organic Ag to which the individual has been sensitised

–ACUTE – short period from exposure, 4-8 hrs. Usually reversible: spontaneously settle 1-3 days. Can recur.
- Fevers, rigors, malaise, dry cough, dyspnoea, crackles

–CHRONIC – chronic exposure (months – years). Less reversible
- Increasing dyspnoea, weight loss, t1 resp failure, cor pulmonale

69
Q

Define and presentation sarcoidosis

A

Multisystem inflammatory condition of unknown cause
• Non-caseating granulomas

Presentation - GRANULOMAS

  • General - fever, reduced wt, fatigue, lyphadenopathy and HSM
  • Resp - otitis/sinusitis; dry cough, SOB, Chest pain
  • Arthraligia
  • Neuro - peripheral and cranial polyneuropathy, headache
  • Urine - hypercalciuria (stones, DI)
  • Low hormones (amenorrhoea)
  • Opthamology - uveitis, keratoconjunciticis, sjogrens
  • Myocaridal - restrictive cardiomyopathy, effusion
  • abdo - HSM
  • Skin - erythema nodosum, lupus pernio
70
Q

Investigations and management of sarcoidosis

A

Ix
• PFTs: (obstructive until) fibrosis
• CXR: 4 stages (BHL –> mid zone fibrosis)
• Bloods: renal function, ACE (increased) , Calcium
• Urinary Calcium
• Cardiac involvement: ECG, 24 tape, ECHO, cardiac MRI • CT/MRI head: headaches – Neuro sarcoid

Mx

  • acute - bed rest and NSAIDS
  • chronic - steroids +/- methotrexate/ ciclosporin
  • stop smoking
  • remove occupational exposure
71
Q

Treatment for Interstitial lung disease

A
• Occupational exposure – remove
• Drug associated – avoid
• Stop smoking
• ? N-Acetylcysteine ? Immunosuppressant ? Pirfenidone 
• Transplantation
• Treatment of infections (atypical)
• Oxygen
• MDT
• Palliative care
? pul rehab
72
Q

Clinical features of lung cancer

A

Asymptomatic, incidental finding
• Any respiratory symptom/systemic deterioration
- Chronic cough +/- haemoptysis (or chnage in smokers cough); chest pain; recurrent chest infection; hoarse voice; stridor; malaise; weight loss; SOB
• SVCO
• Horner’s syndrome
• Metastatic disease – liver, adrenals (Addison’s),
bone, pleural, CNS
• Paraneoplastic – clubbing, hypercalcaemia,
anaemia, SIADH, Cushing’s syndrome, Lambert- Eaton myasthenic syndrome, thrombo-embolic disease

73
Q

Risk factors for lung cancer

A
  • Large number of smoking pack years
  • Airflow obstruction
  • Increasing age
  • Family history of lung cancer
  • Exposure to other carcinogens, e.g. asbestos
74
Q

WHO performance status

A

0 Normal - Fully active without restriction

1 Restricted in physically strenuous activity but
ambulatory and able to carry out light work e.g.,
light house work, office work

2 Ambulatory and capable of all self-care but
unable to carry out any work activities. Up and
about more than 50% of waking hours

3 Capable of only limited self-care, confined to
bed or chair more than 50% of waking hours

4 Completely disabled. Cannot self-care. Totally
confined to bed or chair

5 Dead

75
Q

Investigations of lung cancer

A

Bloods – FBC, U+E, Calcium, LFT’s, INR
•CXR (? hilar enlargement; consolidation; collapse; effusion; bony secondaries)
• Staging CT – Spiral CT Thorax and Upper Abdo –
helps to stratify TNM stage
•PET (detect small mets)

Histology
• US guided neck node FNA for cytology if
lymphadenopathy
• Bronchoscopy – endobronchial, transbronchial,
endobronchial USS (if mediastinal
lymphadenopathy) + biopsy
• CT Biopsy
• Thoracoscopy if pleural effusion present

Lung function test and WHO performance status

76
Q

Treatment for NCSLC

A
  • Curative surgery for stages I+II – assuming fit for surgery
  • Surgery + adjuvant chemotherapy clinical trial for stage IIIa – assuming fit for surgery + chemo
  • Chemotherapy – consider in patients with stage III/IV disease and PS 0-2
  • Radiotherapy – curative (CHART = continuous hyperfractionated accelerated radiotherapy) for people not fit for surgery OR palliative
  • Palliative Care (SVCO stent; analgesia; pleural drainage etc)
  • Do nothing / watch & wait
77
Q

Prognosis for SCLC

A

Rapid growth rate and almost always too extensive for surgery at time of diagnosis
• Mainstay of treatment is chemotherapy
• Also palliative radiotherapy (for bronchial obstruction, haemoptysis, bone or CNS mets)
• Untreated – median survival is 4-12 weeks
• Combination chemotherapy – median survival 6- 15 months

78
Q

Define Obstructive Sleep Apnoea

A

upper airway narrowing,
provoked by sleep, causing sufficient sleep fragmentation to result in significant daytime symptoms, usually excessive sleepiness

79
Q

Pathophysiology of OSA

A
  • Upper airway patency depends on dilator muscle activity. All muscles relax during sleep (including pharyngeal dilators).
  • Some narrowing of the upper airway is normal
  • Excessive narrowing can be due to either an
    already small pharyngeal size during awake state which undergoes a normal degree of muscle relaxation during sleep causing critical narrowing OR excessive narrowing occurring with relaxation during sleep
80
Q

Risk factors for OSA

A
  • Fatty infiltration of pharyngeal tissues and external pressure from increased neck fat and/or muscle bulk
  • Large tonsils
  • Craniofacial abnormalities
  • Extra submucosal tissue, e.g. myxoedema
  • NMD - greater loss of dilator muscle tone, e.g. stroke, MND, myotonic dystrophy
  • Muscle relaxants – sedatives, alcohol
  • Increasing age
81
Q

Clinical effects for OSA

A
  • repetitive upper airway collapse, with arousal required to re-activate the pharyngeal dilators.
  • associated hypoxia and hypercapnia –>corrected during the inter-apnoeic hyperventilatory period.
  • Recurrent arousals lead to highly fragmented and unrefreshing sleep – snoring and apnoea attacks often witnessed by partner
  • Excessive daytime sleepiness results (Epworth Sleepiness Scale score >9)
  • With every arousal there is a rise in BP, often over 50 mmHg. It is not clear if this damages the CVS. There is also a rise in daytime BP.
  • Nocturia
  • Less common - Nocturnal sweating, reduced
    libido, oesophageal reflux
82
Q

Epworth sleepiness scale

A
Points for following:
0=would never doze, 
1=slight chance, 
2=moderate chance, 
3=high chance
  • Sitting and reading
  • Watching TV
  • Sitting in a public place, e.g. theatre
  • Passenger in a car for an hour
  • Lying down to rest in the afternoon
  • Sitting and talking
  • Sitting quietly after lunch without alcohol
  • In a car, while stopped in traffic
83
Q

Diagnosis of OSA

A
  • Overnight oximetry alone
  • Limited sleep study – oximetry, snoring, body
    movement, heart rate, oronasal flow, chest/abdominal movements, leg movements – usual study of choice
  • Full polysomnography – limited study plus EEG, EMG
84
Q

Management of OSA

A

Given based on symptoms/quality of life – NOT on severity seen on sleep study

  • Weight loss
  • sleep decubitus rather than supine
  • avoid/reduce evening alcohol intake

FOR SNORERS +MILD OSA:
- Mandibular advancement devices, consider
pharyngeal surgery as last resort
FOR SIGNIFICANT OSA:
- Nasal CPAP (upper airway splinted open with 10cm H20 This prevents airways collapse, sleep fragmentation, and ultimately daytime somnelence)
- consider gastroplasty/bypass, and rarely tracheostomy
FOR SEVERE OSA & CO2 RETENTION:
- May require a period of NIV prior to CPAP if
acidotic, but compensated CO2 may reverse with CPAP alone

85
Q

Driving advice for OSA

A
  • Tell all patients with OSA to NOT drive while sleepy; stop and have a nap. On diagnosis the patient should notify the DVLA
  • The doctor can advise drivers to stop altogether (e.g. HGV drivers)
86
Q

Action of salbutamol, salmeterol

A

ß2-selective adrenergic agonists

Increase cAMP in SMC’s resulting in relaxation and thus bronchodilation

87
Q

SE of salbutamol, salmeterol

A

Tremor, headache, GI upset, palpitations, tachycardia, hypokalaemia

88
Q

Action of Ipratropium/ Tiotropium

A

Muscarinic antagonist Decreases cGMP which affects intracellular calcium resulting in decreased SMC contractility

89
Q

SE Ipratropium/ Tiotropium

A

Dry mouth, constipation, cough, headache

90
Q

CI of Ipratropium/ Tiotropium

A

angle- closure glaucoma +Benign Prostatic Hypertrophy

91
Q

Action of aminophylline

A

Block phosphodiesterases resulting in decreased cAMP breakdown causing bronchodilation

Positive chronotropic and inotropic effects, diuretic action

92
Q

SE and toxic effects aminophylline

A

Headache, GI upset, reflux, palpitations, dizziness

TOXIC - serious arrhythmias, seizures, N+V, hypotension

93
Q

Action of inhaled steroids e.g. beclomethasone

A

Increase airway calibre by decreasing bronchial inflammation +/- modifying allergic reactions

94
Q

SE of inhaled steroids e.g. beclomethasone

A

Cough, oral thrush, unpleasant taste, hoarseness

95
Q

Advice after use inhaled steroids

A

good oral hygiene

96
Q

Examples of corticosteroids

A

Prednisolone (PO), Hydrocortisone (IV/IM), Dexamethasone (PO/IV), Triamcinolone (IM)

97
Q

Actions of corticosteoids

A

Supress inflammation, allergy + immune responses by altering gene transcription

98
Q

SE of corticosteroids

A

Adrenal suppression (especially courses > 3 weeks), hyperglycaemia, psychosis, insomnia, indigestion, mood swings

Other Side Effects

Diabetes, cataracts, glaucoma, peptic ulceration, susceptibility to infections, osteoporosis, muscle wasting, skin thinning, Cushingoid appearance

99
Q

Additional medication to prescribe with long-term steroids and patient information

A

May need PPI (reduce GORD), Bisphosphonates (bone protection) and steroid card.

100
Q

MRC Dyspnoea Score

A

1 Not troubled by breathlessness except on strenuous exercise
2 Short of breath when hurrying or walking up a slight hill
3 Walks slower than contemporaries on level ground because of breathlessness, or has to stop for breath when walking at own pace
4 Stops for breath after walking about 100m or after a few minutes on level ground
5 Too breathless to leave the house, or breathless when dressing or undressing

101
Q

Management of chronic asthma - BTS guidelines

A

Assess symptoms, measure lung function, check inhaler technique and adherence, adjust dose, update self-management plan. Use spacer in children.
STEPWISE
Short acting β2 agonists as required – consider moving up if using three doses a week or more

1) Low-dose ICS (V. low in kids) - <5y/o - LTRA
2) + inhaled LABA (<5 y/o - LTRA +v. low ICS)
3) - No response to LABA – stop LABA and consider
increased dose of ICS
- If benefit from LABA but control still inadequate- continue LABA and increase ICS to med dose (low in kids)
- If benefit from LABA but control still inadequate
- continue LABA and ICS and consider trial of other therapy - LTRA (adults - also SR theophylline, LAMA)
4) Increasing ICS up to high dose (med - kids)
- Addition of a fourth drug, eg SR theophylline (or LTRA, beta agonist tablet, LAMA in adults)
- Refer to specialist care
5) Use daily steroid tablet and Maintain high-dose ICS (med - kids)

Advice - avoid triggers and personal asthma action plan for emergencies

102
Q

Management of chronic COPD - stable management

A
General
- smoking cessation advice
- annual influenza vaccination
- one-off pneumococcal vaccination
FEV1 --> Mild = >80%; mod 50-79%; severe <50%

1) SABA or SAMA
2) FEV1 > 50% - LABA or LAMA e.g. tiotropium
- FEV1 < 50% - LABA + ICS or: LAMA
3) Then LABA +ICS
- + LAMA

  • Mucolytics = productive cough
103
Q

Management of pulmonary oedema

A

 Sit up and give high-flow O2
 Morphine 2.5mg IV (± metoclopramide 10mg IV)
 Frusemide 120-250mg IV over 1h
 GTN spray ± ISMN IVI (unless SBP <90)
 If no response consider:
 CPAP
 Haemofiltration / haemodialysis ± venesection

104
Q

Causes of clubbing

A
C - CHD
L - lung  - Abscess; Bronchiectasis; CF; Disease (IL) Empyema/ TB
U - UC/ CD
B - baby coming - pregnancy
B - Biliary cirrhosis 
I - IE; idiopathic; familial
N - Neoplasm - Bronchial/ mesothelioma
G - GI lymphoma/graves
105
Q

Stages of clubbing

A

1) fluctuant nail bed
2) loss of nail angle
3) curvature of nail
4) broadening of distal phalnx

106
Q

Organisms causing pneumonia

A

CAP
o Streptococcus pneumoniae
o Haemophilus influenza
o Moraxella cattarrhalis

HAP
o Gram –‘ve enteric bacteria - 10%
o Staphylococcus aureus

Immunocompromised

  • Above +
  • PCP; TB; fungi; CMV/HSV
107
Q

Causes, features, ix and mx of lung abscess

A

Causes

  • Aspiration
  • bronchial obstruction (ca/FB)
  • septic emboli
  • pulmonary infarction
  • hepatic disease

Features

  • swinging fever
  • cough, foul purulent sputum, haemoptysis
  • malaise, wt loss
  • pleuritic pain
  • clubbing
  • empyema

Ix - bloods; sputum; CXR; ?CT/bronchoscopy

Mx - Abx, aspiration/ surgical excision

108
Q

Features of Bronchiectasis

A
Symptoms 
- persistent cough and purulent sputum
- haemoptysis 
- fever, wt loss
Signs
- clubbing
- coarse inspiratory crackles
- wheeze
- ?situs inversus (kartageners)/ splenomegaly (immune def)
109
Q

Complications of bronchiectasis

A
  • pneumonia
  • pleural effusion
  • pneumothorax
  • pulmonary HTN
  • massive haemoptysis
  • Cerebral abscess
  • Amyloidosis
110
Q

Allergic Bronchopulmonary Aspergillosis

- features, ix and rx

A

hypersensitivity to aspergillus
sx - wheeze; productive cough; dyspnoea +/- recurrent pneumonia
Ix - CXR (bronchiectasis); aspergillus in sputum; high IgE/Eosinophils
Rx - steroids +/- bronchodilators

111
Q

Features of COPD

A

Sx - cough + sputum; SOB; wheeze; wt loss
signs - increased RR, prolonged expiratory phase, hyperinflation and hyperesonant (air trapping), wheeze, ?early inspir crackles, cyanosis, cor pulmonale, signs of steroid use, accessory muscles

112
Q

COPD complications

A
  • acute exacerbation
  • pneumothorax
  • cor pulmonale
  • polycythaemia
  • lung ca
113
Q

Ix for COPD

A
  • spirometry (obstructive pattern)

- CXR - hyperinflation, flat hemi-diaphragm, decreased lung markings, bulla, prominent hila

114
Q

Sx and signs of pleural effusion

A

Sx
- asymptomatic; dyspnoea; pleuritic chest pain

Signs

  • tracheal deviation away; reduced expansion; stony dull percussion; reduced air entry; bronchial breathing just above effusion
  • Of associated disease e.g. Ca, CLD, Cardiac failure
115
Q

Causes of cavity in lungs

A

C: cancer –> SCC/ mets
A: AI; granulomas - granulomatosis with polyangiitis, RA
V: vascular (both bland and septic pulmonary emboli)
I: infection (bacterial/fungal); abscess; TB
T: trauma - pneumatoceles
Y: youth –> CPAM (congenital pulmonary airway malformation); pulmonary sequestration; bronchogenic cyst

116
Q

Cause of ILD on location

A

Upper zone
- Aspergillus, coal, silica, EAA, TB, A.S, radiation

Lower zone
- Sarcoid(mid), toxins, asbestos, UIP, rheum

117
Q

Features and Ix for pulmonary fibrosis

A

Features
- SOB (progressive); dry cough; clubbing, sx of disease e.g. RA/SLE
Signs - dyspnoea, reduced expansion and fine end-inspiratory crepitations

Ix

  • CXR
  • High-resolution CT (honeycombing and ground glass changes)
  • Spirometry (restrictive +/- reduced transfer factor)
  • blood tests for cause
  • lung biopsy
  • ?BAL
118
Q

Ix and Mx of EAA

A

Ix

  • bloods (neutrophiia, raised inflam markers)
  • CXR - honeycomb lung
  • spirometry (restrictive)
  • BAL - increased lymphocytes and mast cells

Mx

  • steroids
  • avoid exposure