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Respiratory Flashcards

1
Q

Asthma definition and presentation

A

Chronic inflammatory airway disease. Intermittent obstruction due to hypersensitivity

Recurrent episodes: wheeze, Breathlessness, Chest tightness, Coughing

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2
Q

Types of Asthma

A

Allergic (linked to atopy - Inc IgE production)

Non-allergic

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3
Q

Triggers

A

Allergic (IgE -> Mast cell): dust mites, pet fur, grass pollen

Non-allergic: Exercise, cold air, stress, strong emotion, viral infection, smoking

Drug causes: NAIDs/Aspirin block COX1 = dec prostaglandins and inc pro-inflam leukotrienes, Beta blockers (B2)

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4
Q

Acute and chronic changes to airway in asthma

A

Acute: airway bronchoconstriction, oedema, mucus hyper secretion

Chronic: airway remodelling, hyper responsiveness
- Gives more persistent obstruction

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5
Q

Hygiene hypothesis

A

Growing up in clean env suppresses the natural development of immune system

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6
Q

Asthma Pathopys: Early phase (constriction phase)

A

Exposure to allergen in presensitised individual

cross link IgE on mast cells

Release histamine, leukotrienes, TNFa

Migration of inflammatory cells

Inc vascular permeability (airway oedema) + mucus hyper secretion, inc airway tone through smooth muscle

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7
Q 
Asthma Pathopys:
Late phase (inflammation phase)
A

Eosinophil mediated (IL4/5 recruits) at 6 hours

Inc goblet cells
Epithelial denudation (leads to hyper responsiveness)

Deposition of matrix proteins and swelling (remodelling and SMC hyperplasia)

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8
Q

Asthma Presentation (when taking a Hx)

A

Worse at night and early morning

Wheeze
Episodic SOB
Chest tightness
Cough 
FH atopy
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9
Q

How to assess general asthma severity/control

A

In the past 4 weeks

  • How often SOB
  • How often woken from sleep
  • How often used reliever
  • How often interfered with ADL (e.g. school/work)
  • How do they rate asthma control
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10
Q

What is important to assess in asthmatic control

A

Inhaler technique

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11
Q

Asthma Investigations

A

Peak Expiratory Flow Rate (PEFR)

  • Diurnal variation over 20%
  • Reversibility testing: FEV1 improves 15% with SABA/ PEFR 20% improv

Spirometry: FEV1/FVC less than 70% + FEV1 less than 80% predicted.

FBC: Eosinophilia

Skin prick testing for allergen triggers

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12
Q

What is the aim of asthma management (2)

A

Good control on minimal meds

FEV1 and PEFR over 80% predicted

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13
Q

Asthma management

1 ->5

A

1) SABA
2) Add low ICS (400mcg budesonide)
3) Add LTRA (Montelukast)
4) Add LABA (LRTA can be kept or removed depending on response)
5) SABA + MART (Steroid+laba = can be used as maintenance AND releiver)

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14
Q

What are Theophylines and where do they come in on Asthma ladder?

A

Methylxanthine - phosphodiesterase inhibitor. inhibits leukotriene synthesis and TNFa

One of the final steps in management.

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15
Q

Acute asthma exacerbation management

A

OSHITMS

Oxygen (aim 94-98%)
Salbutamol (neb)
Hydrocortisone IV/Pred oral within one hour
Ipratropium (neb)
Theophylline (IV)
Mag Sulf (IV)
Salbutamol (IV)
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16
Q

Acute asthma exacerbation Investigations

A

Peak expiratory flow
SpO2
ABG

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17
Q

Moderate asthma exacerbation

A

PEF 50-75%

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18
Q

Severe asthma exacerbation

A

One of the following:

  • PEF 33-50%
  • RR over 25
  • HR over 110
  • Cant complete sentences
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19
Q

Life threatening asthma exacerbation

A 
One of the following:
- PEF less than 33%
- SpO2 less than 92%
- PaO2 less than 8kPa
- Silent chest
Exhaustion

May need these patients to be intubated

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20
Q

COPD

  • Definition
  • Types
A

Chronic & irreversible airflow obstruction giving air trapping and hyperinflation

Chronic bronchitis
Emphysema

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21
Q

What is Chronic Bronchitis

A

Narrowing of airways due to oedema of mucosa, mucous hyper secretion,

Cough due to excessive mucous and poor ciliary clearance
- Over 3M of the year for 2 yr

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22
Q

What is emphysema

A

Due to elastin breakdown causing permanent destruction and reduced SA in alveoli

Less elastin recoil/inc compliance = hyperinflation

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23
Q

COPD Aetiology & Pathophysiology

A

Cigarette smoking, A1AT

Emphysema: inc inflammation = inc neutrophils = inc oxidative stress + elastase to break down elastin in emphysema

Chronic bronchitis: Poor ciliary clearance and goblet cell hyperplasia (inc mucous)

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24
Q

COPD Pulmonary Pathology description

A

Chronic inflammation of central and peripheral airways/lung parenchyma/alveoli/vasculature

Increased goblet cells

Narrowing of airways

Vascular change = Pulm HTN

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25
Q

COPD Presentation

A

SOB - initially with exercise but this progresses

Cough

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26
Q

COPD examinatory findings

A

Barrel chest, CO2 flap, hyperresonant percussion, distant breath sounds (over bullae, hyperinflation and trapping), coarse crackles (exacerbation), wheeze (exacerbation)

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27
Q

COPD complications

A

Cor pulmonale: RHF secondary to long standing COPD (raised JVP, distended neck veins, hepatomegaly - Rx: long-term O2 therapy + loop diuretic)
Pneumonia - pneumococcal vaccine and yearly influenza vaccine
Depression
Polycythaemia
Respiratory failure (T1, T2)

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28
Q

Resp failure

  • Types
  • Reasons
  • Description
A

Type 1 & 2

  • T1 = VQ mismatch. PaO2 less than 8kPa (can get rid of CO2 but O2 not going to right place for oxygenation)
  • T2 = Alveolar hypoventilation. PaO2 less than 8kPa, PaCO2 over 6kPa (large collapse, secretions blocking etc)

Pink puffer - emphysema
Blue bloater - Bronchitis

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29
Q

Pink puffer (emphysema)

A 
CO2 responsive
Pink skin
Purse lip breathing and accessory muscle use
Inc Res rate
Old and cachectic
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30
Q

Blue bloater (Bronchitis)

A 
CO2 retention (T2) means insensitive to it
Obese
Peripheral oedema (RHF)
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31
Q

COPD Investigations

A

Spirometry

  • Obstructive pattern (FEV1/FVC less than 0.7)
  • Non-reversible

Decreased pulse oximetry

ABG: hypoxia + hypercapnia may be seen

CXR: flattened diaphragm, increased intercostal spaces, hyper lucent lungs

FBC: may have polycythemia (HCT over 0.55 - venesection, too viscus)

Sputum culture - infectious exacerbation

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32
Q

COPD severity score

A

Mild FEV1 less than 80%

Moderate FEV1 50-80%

Severe FEV1 30-50%

V Sev less than 30%

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33
Q

COPD management

A

Patient education + Lifestyle (smoking, exercise, obesity management)

Vaccination (Pneumococcal, Flu)

Depression screen

Inhaled therapy

Long term O2 therapy (if PaO2 less than 7.3, sats less than 88% or congestive HF

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34
Q

COPD inhaled therapy

A

1) SABA or SAMA

2) If still uncontrolled
- FEV1 over 50% add LABA/LAMA
- FEV1 under 50% add LABA+ICS

3) LABA + LAMA + ICS

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35
Q

COPD exacerbation Tx

A

Similar to OSHITMS

SABA + SAMA neb (salbutamol+ipratropium)
O2 (24% venturi - aim 88-92%)
Oral Prednisolone

Airway clearance - mucolytic + physio
If respiratory insufficiency - BIPAP

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36
Q

Why can BIPAP be used in T2 RF

A

Because it doesnt have to be 100% O2.

It works more by keeping airways open rather than high O2 which can take away rest drive in T2RF patients

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37
Q

COPD exacerbation organisms + Investigation

A

H. influenza
Strep Pneumonie
Moraxella catarrhalis

Blood + Sputum culture and gram stain

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38
Q

Abx for COPD exacerbation

Extra therapies.

A

Community acquired (less severe) - amoxicillin or Doxycycline + PREDNISALONE

Hospital acquired - Vancomycin or Tazocin (piperacillin/tazobactam)

Oral Theophyline
Mucolytics (acetylcysteine)
O2 therapy
Furosemide in HF

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39
Q

Difference Between Asthma Vs COPD

A

Reversible/Irreversible

Airway hyperactivity only in asthma

Mast cells/ Eosinophils (A) Vs Neutrophils and macrophages (C)

Peak flow diurnal variation (A), minimal variation (C)

Spirometry may be ok (A) but always bad (C)

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40
Q

Total Lung Capacity

Tidal Volume

Expiratory reserve volume

Residual volume

A

6L

  1. 5L
  2. 25L
  3. 25L
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41
Q

Obstructive and restrictive effects on spirometry

A

Obstructive gives decrease in inspiratory reserve as tidal volume occurs at higher total volume (more air conserved)

Restrictive gives less total lung volume but also less expiratory volume moving the tidal volume at lower lung volume

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42
Q

Types of pneumonia

A

Community acquired

Hospital acquired

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43
Q

Pneumonia score

A

CRB65 (add U if in secondary care setting - can get urea)

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44
Q

CURB65 and how to use

A

Confusion
Urea (over 7)
Resp (over 30)
BP (less than 90 systolic, 60 dias)

65yrs+

0-1 low risk - outpatient
2 mod risk - hospital
3-5 high risk - ITU (15-40% 30 day mortality)

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45
Q

Community acquired pneumonia

  • RF
  • Causes
  • Atypical caused
A

over 65, Care home, COPD (h.influena), smoking, alcohol (Klebsiella),

S.pneumonia (rusty sputum in 30%) most commonly

Mycoplasma pneumonia (different symptoms)
chlamydia psitacci (Bird fanciers)
Legionella pneumophilia (aircon, asco with hyponatraemia)
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46
Q

Hosp acquired pneumonia

A

Gram negative bacilli

E.coli, Klebsiealla (upper lobes), Pseudomonas aeruginosa, MRSA

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47
Q

Mycoplasma pneumonia (atypical - diff pres, diff, Tx)

A

Dry cough
Haemolytic anaemia
Erythema multiforme

Interstitial opacities (nodular) on CXR

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48
Q

Pneumonia

  • Presentation
  • Examinatory findings
A

Cough + Sputum
Fever (high in pneumococcal)
Bacteraemia
Arthralgia, myalgia, confusion

Inc HR, RR, temp
Dullness to percuss, crackles/reduced air entry/vocal fremitus on auscultation

If septic - low BP

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49
Q

Pneumonia investigations

A

FBC (Raised WCC)

CRP - raised

ABG - low O2x

Sputum culture and sensitivity for ABx

CXR - For lobar pneumonia to looks for consolidation. Atelectasis - small airway obstruction

Blood cultures for causative organism

Urinary antigen - legionalla, pneumococcus

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50
Q

Pneumonia Management

A

O2 if needed IV fluids if needed

Low risk: (0-1)
- Amoxicillin or macrolide (ACE: azithro, clarithro, erythro)

Mod risk: (2)
- Amoxicillin + Clarithromycin (Doxy if allergic)

High risk:

  • Co-amox/3rd gen ceph + macrolide
  • Co-amoxlclav + Clarithromycin

Hosp acquired:
- IV cefotaxime + Gentamicin

Legionalla:
- Clarithromycin + fluoroquinolone

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51
Q

Pneumonia complications

A

Sepsis

ARDS: non-cariogenic pulmonary oedema

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52
Q

TB

  • Types
  • RF
  • Cause
  • Type of infection
A

Pulmonary (latent, active - primary or reactivation of latent), Extra-pulmonary (military)

immunocompromised (e.g. HIV), exposure, poor nutrition, overcrowding, IVDU, homeless, prisons

M.tuberculosis, M.bovis

Granulomatous

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53
Q

What is a granuloma

A

A collection of epithelioid histiocytes (macrophages). These might also fuse to form multinucleate langerhans giant cells

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54
Q

TB prevention

A

BCG vaccine

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55
Q

TB screen

A

Tuberculin skin test (cant distinguish between active and latent disease

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56
Q

Latent TB

A

Infections with M.tuberculosis but no clinical, bacteriological or radiographic evidence of active TB

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57
Q

Gohn Complex

A

Gohn focus (Calcified focus from TB, often in mid to lower lung zones)

PLUS an affected lymph node

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58
Q

TB pathophysiology

A

Macrophage in mid zone of lung engulfs bacteria

Results in Granuloma formation, MP presentation to T-cell –> Caseation

Caseation heals and calcifies

Mediastinal LN involvement

Secondary lesions in lung apices (after 1-2 year)

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59
Q

TB Presentation

A

Cough (haemoptysis) + fever + weight loss + night sweats + RF

Pleuritic chest pain, erythema nodosum

Examination: crackles, bronchial breathing

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60
Q

TB investigations

A

CXR:

  • Primary: consolidation, hilar enlargement
  • healed primary: Gohn focus

Sputum acid fast (Ziehl-Neelsen) bacilli smear X3

Sputum culture shows no growths

FBC - leukocytosis and anemia

Nucleic acid amplification test +ve for TB

HIV concurrent infection possible

CT, urinalysis, Ascitic fluid analysis for extra-pulmonary TB

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61
Q

TB Tx

A

RIPE DOTS

Rifampicin - 6m (hepatotoxic, p450 inducer)

Isoniazid - 6m (hepatotoxic, peripheral neuropathy)

Pyrazinamide - 2m (liver toxic, hepatitis)

Ethambutol - 2m (optic neuritis: loss of acuity)

Directly Observed Therapy for 3 weeks

Isolate patient, contact tracing + Tx. infectivity decreased after 2w tx

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62
Q

Extra pulmonary TB

A 
Pleura: effusion
GU: hameaturia/dysuria
Bone: osteomyelitis, Pott's - vertebral fracture assoc with TB
Brain: meningitis
Abdo: ascites

Miliary = haematogenous seeding. liver spleen, lung. Can be seen on CT

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63
Q

DVT RF

A 
Cancer
Trauma
Major surgery
Hopitalisation
Immobilisation (including limb immobilisation and long haul travel)
OCP
Obesity
Pregnancy (high oestrogen)

Genetics: Factor V leiden, Protein C deficiency
Protein S deficiency, antithrombin deficiency, antiphospholipid syndrome

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64
Q

Virchows triad

A

Three broad categories contributing to thrombosis:

1) Venous stasis
2) Vessel injury
3) Activation of clotting system/hypercoagulable state

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65
Q

Where do DVT form

A

Deep venous system of leg, often behind a valve

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66
Q

DVT marker

A

Active thrombus breakdown by fibrinolytic system releases cross linked fibrin breakdown products esp. D-dimer (also acute phase protein - poor specificity, more helpful if -ve)

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67
Q

DVT pres

A

Unilateral calf swelling and pain along venous system

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68
Q

DVT score

A

Wells

  • Active Ca in last 6 months
  • Paralysis, paresis or recent plaster immobilisation
  • Recently bed ridden for 3+ days
  • Localised tenderness alone deep venous system
  • Entire leg swollen
  • Calf swelling more than 3cm more than other
  • pitting oedema
  • Previous DVT
  • contralateral superficial non-varicose veins
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69
Q

Using Wells score

A

0-1: D-dimer and if positive then proximal venous USS (if negative then repeat at 6 days

2+ Proximal venous USS, +ve = tx, -ve = repeat in 6-8 days

If USS not available within 4 hours then anticoagulant and do within 24 hours

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70
Q

PE

  • Definition
  • Complications
  • Causes
A

Life threatening condition resulting from dislodged thrombi occluding pulmonary vasculature

If not Tx –> RHF and cardiac arrest

Distal vein thrombosis (50% will embolise), Amniotic fluid embolus, Fat/Air embolus, tumour embolus

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71
Q

PE RF (try to get 5)

A 
Cancer
Trauma
Major surgery
Hopitalisation
Immobilisation (including limb immobilisation and long haul travel)
OCP
Obesity
Pregnancy (high oestrogen)

Genetics: Factor V leiden, Protein C deficiency
Protein S deficiency, antithrombin deficiency, antiphospholipid syndrome

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72
Q

PE presentation

A

Chest pain (pleuritic), dyspnoea, tachypnoea, cough, fever

Large PE: shock, collapse, acute RHF, sudden death

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73
Q

PE signs

A 
Tachycardia
Tachypnoea
Elevated JVP
Hypoxia
Shock (low BP)
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74
Q

Classical CXR PE

A

Wedge-shaped lesion against the pleura

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75
Q

PE Ddx

A

ACS
Aortic dissection (tearing pain - anticoagulant here fatal)
Pneumothorax

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76
Q

PE investigation

A 
2 level wells
DVT
PE most likely cause
Tachy Card
Immobilisation (Surg, bed for 3 day+)
Hx DVT/PE
Haemoptysis
Malig last 6 month

4 points = PE likely

Other: FBC, US, clotting, Trops (MI rule out), ECG, CXR (late sign = wedge), ABG (reduced PaO2, high lactate)

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77
Q

PE management algorithm

A

Well under 4 D-dimer, if +ve CTPA

If Wells over 4 CTPA immediately (if renal impair V/Q scan - contrast) if positive Tx, if negative but suspect Proximal vein USS

If CTPA not available immediately then anticoagulant until available

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78
Q

VTE Tx

A

PE: O2, IV access for fluids, Morphine

Haemodynamically stable - LMWH (dalteparin) or Fondaparinux (10a inhibitor)

Active Ca - LMWH 6m
Other people get Warfarin for 3 months then reassess (6m if unprovoked DVT)

Mechanical prevention = graduated compression stocking

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79
Q

Investigating cause of DVT

A 
Cancer screen:
- Physical examination, CXR, Bloods (FBC, Ca2+),
Ca markers BhCG - Testis
CA125 - Ovary
CA19-9 - Pancreas
PSA - Prostate

Thrombophila testing:
Antiphospholipid Ab
Protein C/S (deficiency)

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80
Q

VTE prevention

A

Early mobilisation and hydration post surgery

Avoid OCP

Graduated pressure stockings (TED)

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81
Q

Pulmonary fibrosis

  • Pathophys
  • Spirometry
  • Presentation
A

Interstitial lung damage and fibrosis leading to decreased compliance

Restrictive - FVC low, FEV1/FVC high

4Ds: Dry cough, Dyspnoea, Digital clubbing, Diffuse inspiratory crackles

82
Q

Where is pulmonary interstitium

A

Areas in-between alveoli and capillary basement membrane

83
Q

Types of pulmonary fibrosis

A

Replacement fibrosis:
- Secondary to lung damage e.g. infarction, TB, pneumonia

Focal fibrosis:

  • due to irritants
  • coal, dust, silica

Diffuse parenchymal lung disease:

  • Idiopathic pulmonary fibrosis
  • EAA
84
Q

Causes of PF

A

CTDs: RA, SLEm SSc, Sjogren’s

Occupational: asbestos, coal dust, silica

Medications: amiodarone, bleomycin, MTX

Inhaled irritants: hypersensitivity pneumonitis, birds, mould

Radiation

85
Q

Upper lobe fibrosis causes

A

Granulomatous diseases - SCHART

silicosis, sarcoidosis

coal workers pneumoconiosis

histiocytosis

ank spond

radiotherapy

TB

86
Q

Lower lobe fibrosis

A

Systemic diseases RASCO

RA
Asbestosis
Scleroderma/SLE
Cryptogenic fibrosing alveoli's (IPF)
Other (e.g. drugs)
87
Q

Idiopathic PF Cause, RF and Pathophys

A

No known aetiology

Smoking, infection, dust exposure, aspiration (GORD)

Insult giving pro-inflammatory, for-fibrotic response

Influx of macrophages, increased fibroblast and myofibroblast activity = fibroblastic foci + collagen/EC matriculates deposition

88
Q

IPF presentation

A

dry cough, dyspnoea, diffuse inspiratory crackles, digital clubbing, weight loss (increased work)

89
Q

IPF complications

A

Pulmonary HTN (Cor Pulmonale)

90
Q

Important thing to ask about in IPF

A

OCCUPATION!

91
Q

Investigations and findings in Pulmonary fibrosis

A

CXR

  • net-like shadowing of lung peripheries/bases
  • shaggy heart border

High resolution CT

  • honeycombing, reticular pattern
  • Ground glass opacification marital air space filling by exudate OR interstitial thickening

Lung function tests

  • restrictive pattern
  • impaired gas exchange: decreased DLCO, increased PaCO2, decreased PaO2

ANA: SLE
RF: RA

Lung biopsy: fibroblastic foci, interstitial fibrosis

92
Q

IPF management and prognosis

A

6 monthly assessment for pulmonary rehab

O2 therapy

Physiotherapy

Weight loss

Vaccination (pneumococcal)

Smoking cessation

PPI for GORD + opiated for cough

acute exacerbation: admit + high dose oral prednisolone, sputum culture and ABx

Extreme cases - lung transplant

Median survival 2-5 years

93
Q

Scleroderma PF

A

Chest wall fibrosis
Leading cause of death
Pneumonia from aspiration from stiff oesophagus
ANA in 95%

94
Q

RA PF

A

Interstitial lung disease

Rheumatoid nodules

MTX also give pneumonitis - stipend use Steroids instead

Caplan’s: PF in coal workers with RA
CXR well defined nodules, may capitate at lung peripheries

95
Q

Tx of systemic causes of PF (scleroderma, RA etc)

A

Immunosuppression with steroids

96
Q

SLE pneumonitis

A

Interstitial inflammation leading to interstitial fibrosis

97
Q

What is a lagerhans giant cell

A

This is formed by the fusion several histiocyte (Macrophages)

98
Q

Granulomatous lung diseases

A

TB
Sarcoidosis (non-caveating)
EAA

Tx: Oral Prednisalone

99
Q

Extrinsic allergic alveolitis (Hypersensitivity pneumonitis)

  • RF
  • Pathophys
  • Types of granuloma
A

RF: hx of exposure to organic dust (birds, agricultural, mould)

Non-IgE inflammation of alveoli and distal bronchioles
Sensitised individuals inhale allergens giving hypersensitivity reaction (Type 3 or 4)

Widespread inflammation of small airways, cellular infiltrate (neutrophils, macrophage), non-caveating granulomas (reticulo-nodular)

100
Q

Types of EAA

A

Farmer’s lung (hay mould)
pigeon fanciers lung (dropping proteins)
Maltworkers lung
Cheese makers lung

Always ask about pets, Occupation etc

101
Q

EAA presentation

A

Acute (4-8hrs): flu like illness- fever, chest tightness, dry cough, dyspnoea, aches and pains

Sub-acute” less severe more gradual onset.. dyspnoea, fatigue, anorexia

Chronic: weight loss, cyanosis, RH

102
Q

Investigations EAA

A

Blood: Raised WCC and CRP

CXR: diffuse micro nodular interstitial shadowing

CT: reticula-nodular shadowing, ground glass, micro nodules

Lung function: restrictive spirometry, decreased diffusing lung capacity of carbon monoxide (DLCO), decreased SpO2

Bronchoalveolar lavage: CD8

103
Q

EAA Tx

A

Allergen avoidance/removal is best

Acute/subacute presentation: O2 +oral Prednisolone

Chronic: low dose ICS

104
Q

Pneumoconiosis

  • Definition
  • E.G
  • Latency according to cause
A

Group of chronic lung diseases due to exposure to mineral dust or metal.

Coal workers pneumoconiosis, silicosis, asbestosis

Coal - 10 years
Asbestos - 15-60 years

Notifiable industrial disease: may be eligible for compensation

105
Q

Coal workers pneumoconiosis

  • Pathology
  • what is caplans
  • Presentation
A

1) Coal particles retained in alveoli
2) Engulfed by macrophages
3) Immune response
4) Fibrosis (interstitial)

When assoc with RA (Rheumatoid nodules + fibrosis)

Dry cough, dyspnoea, Black sputum, SOBOE

106
Q

Coal workers pneumoconiosis

  • Investigations
  • Management
  • Prevention
A

Occupational Hx,
Lung function testing (restrictive),
CXR (upper lobes large nodular fibrotic mass)
Sputum microscopy (black)

Avoid exposure
incurable, CT/CXR/LuFT oto monitor
smoking cessation

In those working with coal: adequate ventilation, low dust, facemasks

107
Q

Abestosis

  • Latency
  • Presentation
  • Hx
A

5-10 years

Dry cough, dyspnoea, digital clubbing. Diffuse inspiratory crackles can be heard

Occupational hx:
Building trade. Asbestos used for fireproofing

108
Q

Asbestosis

  • Investigations
  • Management
A

Lung function (Spirometry = restrictive and reduced DLCO)

CXR: Ground glass opacification, small nodular opacities (asbestos bodies at lung bases) shaggy cardiac sillouette

Sputum microscopy: asbestos bodies

Prevent: adequate ventilation, low dust, facemasks

109
Q

Asbestosis complication

A

Mesothelioma

110
Q

Pleural Mesothelioma

  • Latent period
  • Definition
  • RF
A

50 years

Aggressive epithelial neoplasm from lining of the lungs

Asbestos (80% of cases) or asbestiform minerals

111
Q

Mesothelioma pathophys

A

Asbestos fibres recruit and activate alveolar macrophages and neutrophils

Generate ROS (oxidative stress), chronic inflammation, DNA damage and altered gene expression

112
Q

Mesothelioma presentation

A

Dry cough, dyspnoea, digital clubbing and pleuritic chest pain (recurrent pleural effusion)

113
Q

Mesothelioma staging

A

1a: ipsilateral parietal pleura
1b: ipsilateral visceral pleura
2: diaphragm or lung involvement
3: ipsilateral bronchopulmonary or hilar LN
4: contralateral or distant mets

114
Q

Mesothelioma investigations

A

CXR: irregular pleural thickening, reduced lung volume, unilateral pleural effusion

CT: pleural thickening, pleural plaques, hilare LN enlargement

Thoracocentesis: exudate contains malignant cells

Pleural biopsy: Epithelioid mesothelioma

115
Q

Mesothelioma treatment and prognosis

A

Surgery: only curable for stage 1 disease

Platinum based pre+post op chemo ± radio

Pleurectomy/Pleurodesis for recurrent pain/effusions

if inoperable: chen-radio

Survival = 1 year

116
Q

Pleural effusion

  • Definition
  • Types
A

Excessive fluid in potential space between visceral and parietal pleura

Transudate: low protein (less than 30g/L
- Disrupted hydrostatic and oncotic forces across pleura membranes (inc venous pressure or hypoproteinaemia)

Exudate (high protein (over 30g/L
- Increased permeability of pleura from inflammation/malig

Pulmonary, pleural or extra pulmonary

117
Q

Malignant causes of pleural effusion

A

40% lung mets
25% breast mets
10% malignant mesothelioma

118
Q

Pleural effusion: Mechanism & Causes of transudate

A

Increased hydrostatic, low oncotic

HF (LVF), cirrhosis, hypoalbuminaemia, nephrotic syndrome

119
Q

Pleural effusion: Mechanism & Causes of exudate

A

Increased vascular permeability due to inflammation

Pneumonia, malignancy, TB, AI disease (RA), Dressler’s (complication of MI causing pericardial + pleural inflammation

120
Q

Pleural effusion Presentation + examination findings

A

Pleuritic chest pain, SOBOE, cough

unilateral reduced chest expansion, stony dullness on percussion, decreased breath sounds
If large - tracheal deviation (away)

121
Q

Pleural effusion investigations

A

CXR: blunted costophrenic angle Effusion is visible on AP if over 200ml

USS guided pleural aspiration (if clinical picture suggests exudate rather than transudate)
- clear = trans or ex
- turbid/yellow = empyema, parapneumonic
- Haemorrhagic = haemothorax, malignancy, PE, trauma
Low pH/Glucose = RA, SLE, TB, Malig

Bilateral strongly suggests transudate

122
Q

Pleural effusion management

A

Underlying cause
DO NOT TAP
(will result in fluid shift and pulmonary oedema)

Chest drain - controlled removal

If malignant then recurrence likely - may attempt pleurodesis (with talc)

123
Q

Causes of Bilateral lymphadenopathy

A

TIMES

TB

Inorganic dust - silicosis

Malignant - lymphoma, Lung Ca

EAA e.g. bird fanciers

Sarcoidosis

124
Q

Pneumothorax

  • Definition
  • Important when…
  • Aetiology
A

Air in pleural space

Tension pneumothrax (like a one way valve which keeps filling)

Primary spontaneous: tall, thin males, SMOKING, Marfan’s, FH

Secondary: pre-exhisting lunge disease, COPD (bullae), CF, TB,

125
Q

Pneumothorax Pathophys

A

Normally pressure in alveoli high than in pleural space.

If communication between alveolus and pleural space then gases follow pressure to equalise gradient

Thoracic cavity enlarges and lungs shrink

126
Q

What is tension pneumothorax

A

MEDICAL EMERGENCY

intrapleural pressure is able reach exceed atmospheric due to ball valve mechanism letting air in but not out

Lung deflates, mediastinum shifts contra laterally, compression of great veins and decreased venous return to heart

127
Q

Pneumothorax presentation

A 
chest pain (on same side, pleuritic - on inhale)
Dyspnoea (size determines sev)
128
Q

Pneumothorax examinatory findings

A

Hyper-resonant
Reduced expansion
Dec breath sounds

129
Q

Tension Pneumothorax près

A

Resp distress with rapid shallow breathing
Distended neck veins (block great arteries)
Tracheal deviation
Tachycardia Tachypnoea

130
Q

Pneumothorax investigations

A

CXR: Visceral pleural line can be seen (dark area with no leg markings)

TP CXR: contralateral mediastinal shift, depression of hemidiaphragm

131
Q

Pneumothorax Tx

A

Primary:

  • if less than 2cm discharge
  • if more than 2cm, aspirate (2nd intercostal space mid clavic). If this not success chest drain and admit

Secondary:

  • if SOB or over 2cm then admit for chest drain
  • if less than 1cm admit for high flow O2, observe 24 hours
  • 1-2cm aspirate then chest drain if not success

Supplemental O2 for all

132
Q

Safe triangle for chest drain

A

Lateral border pec major
Anterior border lat dorsi
Horizontal line through nipples

Mid axillary line, IC space 4-6, pain relief

133
Q

Tension Pneumothorax Tx

A

Immediate needle thoracostomy 2nd IC mid clavicular line

134
Q

Recurrent pneumothorax

A

Hospitalisation and high flow O2

Pleurodesis may be considered

135
Q

Chest drains in relation to ribs

A

Aim just above rib to avoid Neuromuscular bundles

136
Q

Causes of pleuritic chest pain

A 
ACS
Aortic dissection
Pneumothorax
PE
Pneumonia
Malignancy
137
Q

Bronchiectasis

  • Def
  • Characteristics
  • Types
A

Permanent dilatation and thickening of airways from recurrent infection/inflammation

Recurrent (chronic daily) cough, excessive sputum, bacterial colonisation gives recurrent infection

Diffuse or Local

138
Q

Bronchiectasis

  • Pathophysiology
  • Aetiology
A

Failed mucociliary clearance, impaired immune function gives chronic inflammation = continued bronchial wall insult

Post infection: Measels, peruses, aspergillus, pneumonia

Immunodeficiency: HIV, Ig deficiency

Genetic: CF, ciliary dyskinesia, A1ATD

CTDs: RA, sjogren’s

IBD: UC, CD

139
Q

Cyst forming bacteria (RF bronchiectasis)

A 
Staph aureus
Bordatella pertussis (paeds)
Pseudomonas aeruginosa
H influenza
Strep pneumoniae
140
Q

Bronchiectasis Presentation

A

Cough and daily sputum (bloody in 50%)

  • mild = yellow/green
  • more severe = khaki

Intermittent haemoptysis

Obstructive symptoms: dyspnoea and wheeze

Weight loss

141
Q

Bronchiectasis examinatory findings

A

Inspiratory coarse crackles
and squeaks and pops

Low pitched rhonci (snoring sounds)

Clubbing

142
Q

Early inspiratory Vs Late inspiratory crackles

A

Early = airway disease e.g. bronchiectasis

Late = interstitial disease e.g. IPF

143
Q

Bronchiectasis Investigations

A

CT ( imaging modality of choice): thickened dilated airways ± air fluid levels, cysts

CXR: normal/dilted bronchi with thickened walls + cysts. Ovoid opacities

FBC: high eosinophils if aspergillosis, Neutrophilia = bacterial infection
Serum A1AT

Sputum culture:
G+ = s.aureus, s.pneumoniae
G- = pseudomonas

144
Q

Bronchiectasis Tx

A

Lifestyle: exercise and nutrition

Physio + mucolytics

Inhaled: Bronchodilator + hypertonic saline (thins mucous through drawing water)

Acute exacerbation:

  • Mild = oral amoxicillin
  • Severe = IV ABX with pseudomonas cover (ciprofloxacin)
145
Q

Cystic fibrosis

  • Detected
  • Def
A

Mostly at birth (newborn heel prick-Guthrie test)

Genetic disease with mutation in CFTR gene (Cl channel)

146
Q

Locations of CFTR

A

Lunges, bowel, pancreas, sweat glands, reproductive organs

147
Q

Epidemiology and Pathophysiology

A

1/2500 white people in UK
1 in 25 carriers

Failure of Cl channel in response to cAMP in epithelial cell. Decreased excretion of Cl to lumen, increased Na reabsorption decreased H2O excretion.

Results in thick sticky secretion

148
Q

Organ specific explain CF

A

Pancreas: block of exocrine ducts, early pancreases duct activation = autodigestion

Intestine: bulky stools, intestinal block, prolapse in paeds

Lung: mucous retention, chronic infection, inflammation

Skin: NaCl channels reabsorbing from gut doesn’t work leaving increase in sweat

149
Q

Screening CF

A

Guthrie test (5d) shows serum immunoreactive trypsinogen

150
Q

CF presentation

A

Neonates/infants: failure to pass meconium, fail to thrive, large appetite (pancreases insufficiency- foul smelling stools), chronic wet cough

VAS absent - infertility

Digital clubbing

Very salty sweat (rusts glasses)

151
Q

CF Investigations

A

Sweat test: +ve Na and Cl over 60mmol/L (CL more than Na)

Genetic testing

Pancreatic assessment: faecal elastase (low)

Chest infect: Sputum culture and sensitivity

  • Pseudomonas (70%): highly transmissible esp the contact other CF
  • Burkholderia cepacia
  • S.aureus and mycobacterium abscessus
152
Q

CF:

  • Tx referral
  • Prog
  • Burden & complications
A

Very complex, lots of drugs, physio and high cal diet.
Refer to specialist CF centre

Median survival 40

Huge burden of drugs (lots) and high cal.
Bone disease from malnutrition, depression, short, cor pulmonate (RHF), infertility/subfertility

153
Q

Tx CF

A

Abx

  • Prophylactic Oral Co-amoxiclav/Fluclox
  • If IV needed: Gentamycin + cover pseudomonas.staph - Tazocin)

Chest physio
Inhaled bronchodilator
Inhaled mucolytic (hypertonic saline, dornase alfa)

Segregate in hosp. (prev pseudomonas)

Vaccine: influenza, pneumococcal

Pancreatic enzyme replace, Fat soluble vitamins
PPI for GORD

Bilateral lung transplant

154
Q

Pulmonary HTN

  • Prognosis
  • Definition
A

Poor as most patients develop RHF - cor. Pulmonale

Disease with HTN in small pulmonary arteries characterised by vascular proliferation and remodelling

155
Q

Diagnostic criteria Pulm HTN

A

Mean pulmonary artery pressure >25mmHg at rest with pulmonary capillary wedge pressure <15mmHg
(pressure in LA)

156
Q

Causes of pulmonary HTN

A

CTDs: CREST syndrome

COPD, Interstitial Lung disease

Heart disease: structural, valvular failure

157
Q

Pulmonary HTN Pres + Examinatory findings

A 
Dyspnoea
Accentuated P2 (pulmonary component of second heart sound)

Tricuspid regurgitation murmur/other causative murmurs

RHF: oedema, exertional syncope, pulsatile JVP, hepatomegaly (pulsatile)

158
Q

Pulmonary HTN Investigation

A

CXR: enlarged pulmonary artery shadow

ECG: Tall R in V1 = RVH, Large in II, III, aVF = RA enlarge

Right heart catheter shows pressure over 25mmHg in pulmonary artery and less than 15mmHg cap wedge

159
Q

Pulmonary HTN Tx

A

CCB (nifedipine or amlodipine) or sildenafil (PDE5 inhibitor - augments pulmonary vascular response to nitric oxide)
Anticoagulant: warfarin target 1.5 to 2.5
Lifestyle: low level graded exercise
Oedema: furosemide and low salt diet
Supplemental O2 if needed

160
Q

Types of Lung Ca

& Epidemiology

A

Small cell (least common) 15%

Non-small cell (most common) 85%

Adenocarcinoma

Squamous cell carcinoma

Large cell carcinoma

Most common non-cutaneous cancer: M>F (x3)

161
Q

Lung Ca RF

A

Occupational, Smoking asbestos, radiation, COPD

162
Q

Two week referral in Lung Ca

A

> 40 + 2 of following:

Smoking. Cough, fatigue, SOB, chest pain, weight loss, appetite loss

Refer if:
Supraclavicular lymphadenopathy, finger clubbing

163
Q

Paraneoplastic features of:

SC

Squam

Adeno

A

SC
SIADH (hyponatraemia)

Sq
PTH (hyperCa, bone pain), hyperthyroid

Ad
Gynaecomastia

164
Q

NSCLC

  • Location
  • Mets
  • Other
A

Adeno (40%)

  • peripheral
  • brain, adrenal, bone
  • most common in smokers and non-smokers

Sq (20%)

  • central
  • mets late, local spread common

Large cell (10%)

  • central
  • mets early and large
165
Q

Lung Ca Pres

A

Cough + dyspnoea + haemoptysis (new or persistent)
Requires imaging

Fixed monophonic wheeze

Chest pain (lung has no pain fibres therefore this suggests invasion of pleura or chest wall)

Constitutional symptoms: Weight loss, fatigue

Other: SVC obstruct, bone pain, clubbing (Sq)

166
Q

Pancoast tumour Pres

A

invasion of brachial plexus -> weakness, parasthesia, pain in C8-T1, shoulder pain

Invasion of sympathetic chain -> Horner’s syndrome
Ptosis, miosis/constrict, ipsilateral anhydrosis

167
Q

Lung Ca prognosis

A

10 year survival = 5%

SCLC worse prognosis than NSCLC (70% have extensive)

168
Q

Lung Ca Mets

A

Liver, bones, brain, adrenals

LN
Hilar, mediastinal, supraclavicular

169
Q

Lung Ca Investigations

A

CXR: opacity (Periph = adeno), Hilar enlarge, boney secondaries

Contrast CT: chest, liver, adrenals

Bronchoscopy may allow for biopsy

Cytology from sputum/pleural effusion (if pres)

Surgical biopsy: Transthoracic needle aspiration

CT/MRI brain, FBC (anaemia), LFT (mets), Bone scan (mets), U+E (hyperCa - mets or Sq, hypoNa+ SC)

170
Q

Staging Lung Ca

A

T1: < 3cm
T2: 3-7cm, assoc atelectas

N1: ipsilateral bronchopulmonary or hilar
N2: ipsilateral mediastinal or subcarinal

Extensive =
Metastatic lesions in contralateral lung
Distant mets: brain, bone, liver, adrenal

171
Q

NSCLC Lung Ca Tx

A

Stage 1 or 2: surgical resection lobar resection (lobectomy) or pneumonectomy + hilar/mediastinal LN sampling + pre-op cisplatin chemotherapy

If not operable:
Radical radiotherapy +
chemotherapy - cisplatin based + bevacizumab (anti-angiogenic)
If EGFR mutation use EGFR-tyrosine kinase inhibitors
E.g. Afatinib

172
Q

SCLC management

A

chemo (cisplatin + etoposide) 4-6 cycles + radio + prophylactic cranial irradiation

173
Q

Lung Ca palliative Tx:

Breathless

Lung Obstruction

Effusions

Cough

SVCO

Bone pain

Spinal cord compression

A

Breathlessness
Opiate

Obstruction
External beam radiotherapy

Pleural effusion
Aspiration/drainage

Cough
Opiate

SVCO
Chemo + radio

Bone pain
Radio

Spinal cord compression
Dexamethasone

174
Q

Types of Respiratory fail

A

Type 1: hypoxia (<8kPa) without hypercapnia Type 2 hypoxia + hypercapnia (>6kPa)

175
Q

Causes of Resp failure and names given

A

T1: COPD (pink puffer), pneumonia, pulmonary oedema, fibrosis, asthma, PE, ARDS
T2: COPD (blue bloater), asthma, myasthenia gravis, polyneuropathy

176
Q

Resp failure pres

A

Confusion and reduced consciousness

177
Q

Resp failure investigations

A

ABG, CXR, Functional residual volume, ECG

178
Q

Resp failure management

A

Admit and resuscitate

Treat hypoxia aim for sats 90%

Always start on high flow

Beware of prolonged high conc O2 if lost hypercapnia drive (may reduce RR) - BIPAP may be better

179
Q

When to intubate Resp failure

A

If unstable

If unconscious

180
Q

What is ARDS and what can cause

A

Non-cariogenic pulmonary oedema + diffuse lung inflammation
Dyspnoea and hypoxaemia which may progress to resp failure

SEPSIS and Pancreatitis most common

181
Q

ARDS Presentation

A

Low SATS, RFs (sepsis, aspiration, pneumonia, blood trans, panc), respiratory failure

182
Q

ARDS investigations

A

CXR (bilateral infiltrates), ABG, blood culture, sputum culture, urine culture
(due to common in SEPSIS)

183
Q

ARDS Tx

A

Low tidal volume ventilation (6cc/kg)

Supportive care - resus and then slightly negative fluid balance

ABX + treat cause

184
Q

ABCD for Hypersensitivity types

A

I = Allergic Anaphylaxis and Atopy

II = antBody

III = immune Complex

IV = Delayed

185
Q

T1RF causes and Tx

A

Inadequate oxygenation (alveolar collapse: pneumonia, Fluid in alveoli: LHF)

VQ mismatch

CPAP: alveoli forced open, fluid removed

186
Q

T2RF causes and Tx

A

Limited Alveolar expansion: COPD, Muscular dystrophy

BiPAP: expands and holds open collapsing airways allow oxygenation and CO2 release

187
Q

Cough + Wheeze + Nasal polyps

- Suspected disease + test

A

Churg strauss

pANCA

188
Q

Productive cough plus glomerulonephritis and Saddle shaped nose

A

GPA

Wegners, Granulomatosis with Polyangitis.

189
Q

Relevance of Kartagener syndrome in resp

A

Dysfunction of cilia reversal of organs + recurrent chest infections.

190
Q

COPD exacerbation, no consolidation. Cause and Tx?

A

H.Influenzae (S.pneumoniae usually more common, Hi more in COPD)
Amoxicillin + Prednisalone

191
Q

COPD features on CXR

A

Hyperinflation
Hyperlucent (v black) lung fields
Flattened diaphragm

192
Q

Preferd Tx to stop smoking in preg

A

Nicotine patches are the only pharmacological intervention for smoking cessation in preg

193
Q

Lambert Eaton syndrome

A

Myasthenic like disease seen with small cell LC

Lower limbs more than upper
May have oesophageal motility (dysphagia)

Weakness improves with use

194
Q

What is diagnostic of COPD

A

FEV1/FVC ratio less than 70% PLUS symptoms suggestive of COPD

195
Q

Sarcoidosis Tx

A

None initially for early stage (some take ibuprofen)

parenchymal lung disease, uveitis, hypercalcaemia and neurological or cardiac involvement

196
Q

Oxygen targets

  • Acutely ill
  • COPD
A

94-98%

88-92%

197
Q

Hx of TB, Round lesion with air around rim, haemoptysis and fever

A

Aspergilloma

198
Q

A1AT Vs COPD

  • Imaging
  • Age
A

A1AT more basal changes Vs Apical in COPD

A1AT in younger patients

199
Q

Testing adult for suspected Asthma

A

FeNO (nitrous oxide exhaled) and bronchodilator reversibility testing

200
Q

Raised ACE level, lung and joint involvement diagnosis

A

Sarcoidosis

201
Q

Who offered Long term O2 Therapy

A

PaO2 under 7.3kPa on two occasion

OR pO2 of 7.3 - 8 kPa PLUS: Polycythemia, peripheral oedema, pulmonary HTN

202
Q

Resp complication of Pancreatitis

What else can cause this

A

ARDS

COPD, Trauma, Shock

Final (26 decks)

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