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Phase 4 - GR > Resp > Flashcards

Resp Flashcards

1
Q

Name 2 features of asthma pres

A

wheezing, breathlessness, chest tightness, coughing

Worse at night and early morning
Wheeze (polyphonic and expiratory)
Episodic SOB 
Chest tightness
Cough - *worse at night
FHx atopy/nasal polyposis
Diurnal variation - *worse in morning
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2
Q

Name 2 triggers of allergic and 2 non allergic asthma

A

Allergic: house dust mite, pet fur, grass pollen -> IgE

Non: exercise, cold air, stress, strong emotion, viral infx, smoking

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3
Q

2 drugs you need to be careful prescribing asthmatic

A

Beta blockers - B2 cause airway constriction

NSAIDS or aspirin block COX-1 -> decrease prostaglandins + overproduction of pro-inflammatory leukotrienes

Carboprost

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4
Q

What happens in acute airway inflammation?

A

Constriction, oedema, mucus hypersecretion

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5
Q

2 Features of chronic airway inflammation

A

Airway remodelling, airway hyperresponsiveness

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6
Q

Basic pathology of early phase asthma. + Name 2 inflammatory mediators

A

Allergen ->
Mast cells release IgE

histamine, leukotrienes and TNFa

  • > Increase in Vascular permeability and hyper-secretion of mucus
  • > airway oedema

+ Increased smooth muscle and airway tone

-> Narrowed airways

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7
Q

Key cell in later phase asthma (6 hrs)? What happens/

A

eosinophil mediated (recruited by IL4 and IL5)

Increase goblet cells -> hyper-responsive airway

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8
Q

Effect of acute vs chronic inflammation?

Airway remodelling ->?

A

Acute inflammation = bronchoconstriction,

chronic = airway hyperresponsiveness,
airway remodelling = persistent obstruction

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9
Q

Name 3 questions to assess asthma control?

A

Inpast 4 weeks:\

How often felt SOB?
How often woken from sleep?
How often used reliever?
How often interfered with normal activities e.g. school/work?
How rate asthma control?
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10
Q

What should you always check in asthma (especially if poorly controlled)?

A

Inhaler technique

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11
Q

Name 3 Ix in asthma

A

PEFR (peak flow rate) - diurnal variation >20%, according height/weight

Reversibility testing FEV1 improves by 15% with SABA (or PEF - 20%)

Spirometry
FEV1 < 80% + *FEV1/FVC < 70% = obstructive

CXR: normal or hyperinflation

FBC -> ?eosinophilia

Skin prick test

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12
Q

Asthma pharma Mx stages

A

SABA

SABA + low ICS (<400 mcg budesonide) *step 1 if >3/week

SABA + low ICS + LTRA (montelukast)

SABA (±LTRA) + low ICS + LABA (depending on response LTRA

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13
Q

3 Key Ix in acute exacerbation asthma

A

PEF + SpO2 + ABG

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14
Q

Mx of acute asthma exacerbation ? If exhausted?

A

OSHITMS

O2 aim (94-98)
Salbutamol (neb)
Hydrocortisone /pred within 1 hour IV (4mg/kg hydrocortisone)
Ipratropium (neb)
Theophylline (IV)
Mag Sulf (IV)
Salbutamol (IV)

Intubate + ventilate if exhaustion

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15
Q

What is COPD

A

Chronic obstruction with irreversible airflow obstruction -> air trapping and hyperinflation

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16
Q

COPD genetic cause

A

A1ATD

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17
Q

Basic pathology of COPD

A

Chronic inflammation -> increased goblet cells, narrowing of airways, and vascular changes -> pulmonary HTN

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18
Q

Name 2 findings OE of COPD

A 
Barrel chest, 
CO2 flap, 
hyperresonant percussion, 
distant breath sounds (over bullae, 
hyperinflation and trapping), 
coarse crackles (exacerbation), wheeze (exacerbation)
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19
Q

Name 3 comps of COPD

A 
Cor pulminale 
Pneumonia - pneumococcal vaccine and yearly influenza vaccine
Depression* 
Polycythaemia
Respiratory failure
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20
Q

2 signs of cor pumonale

A

raised JVP, distended neck veins, hepatomegaly

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21
Q

Mx cor pulminale

A

Long term O2 therapy + loop diuretic

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22
Q

Difference between t1/2 resp failure pathology ? Description of people in these types

A

T1: Ventilation/perfusion mismatch
Pink puffer: emphysema –> old and thin, use of accessory muscles

COPD

T2: Alveolar hypoventilation
Blue bloater: peripheral oedema and overweight from RHF

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23
Q

What spirometry finding in COPD

A

Obstructive pattern: FEV1/FVC < 0.7

Non-reversible and no diurnal variation

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24
Q

Name 3 Ix in COPD

A 
Spirometry 
ABG: may see hypoxia +- hypercapnia
CXR
FBC 
Sputum culture
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25
Q

Name 2 signs on XR of COPD

A

Flattened diaphragm
Increased intercostal spaces
Hyperlucent lungs
Increased AP diameter

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26
Q

What might you see on FBC of COPD

A

polycythaemia +Hb rise. Polycythaemia develops in response to hypoaemia which triggers erythropoietin release by the kidneys

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27
Q

Severity of COPD

A

Mild: FEV1 > 80%
Mod: FEV1 50-80%
Severe: FEV1 30-50%
V.Severe FEV1 < 30%

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28
Q

4 Non pharma Mx of COPD

A

Patient education
+ vaccination
+ depression screen
+ COPD nurse

Smoking cessation, exercise, obesity mgmt (pulmonary rehabilitation)

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29
Q

Pharma Mx of non controlled COPD

A

SABA/SAMA

If FEV1>50%

  • LABA
  • LABA+ICS

If FEV1<50%
-LABA + ICS

(Or LAMA for either)

Then
LABA+LAMA+ICS

LTOT
pka <7.3
pka >7.3 + one of pulmonary hypertension, polycythaemia

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30
Q

Name 2 bugs commonly causing COPD exacerbation

A

H. influenza, s. Pneumonia, m. catarrhalis

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31
Q

3 parts of Mx COPD ACUTE exacerbation? If resp insufficiency ?

A

SABA + SAMA neb (salbuamol + ipratropium)

+ O2 (24% venturi aim for 88-92%)

Oral corticosteroid (prednisolone) - prevents recurrence

Airway clearance - mucolytics + physio

BIPAP if respiratory insufficiency

Abx ….

Infective exacerbation management:

S - steroids
H - heparin
O - oxygen (88-92)
N - nebuliser bronchodilators
A - antibiotics
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32
Q

Abx in COPD exacerbation - community vs hospital

A

Community
amox / doxy

hospital
vanc / tazocin

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33
Q

2 places you might get cultures from in COPD

A

Blood culture and sputum culture

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34
Q

When would pneumonia be classified as hospital aquired

A

If LRTI @2 days post admission

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35
Q

Score for pneumonia risk

A 
CURB 65 
Confusion
Urea > 7
RR > 30
BP < 90 or < 60 diastolic
65

Score
0-1 - low risk, recommend outpatient care
2 - moderate risk - to hospital
3-5 - high risk = to ITU (30 day mortality = 15-40%)

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36
Q

CAP in younger adults - cause? how does it present slightly different?

A

Mycoplasma pneumoniae

Dry cough + atypical CXR + AI haemolytic anaemia + erythema multiforme

Tx = macrolide (C or E)

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37
Q

HAP in immunocompromised may be caused by fungal pneumocystis jirovecii - Mx?

A

Co-trimoxazole

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38
Q

3 parts of normal pneumonia pres

A

Cough with increasing sputum + expectoration
Fever (high in pneumococcal)
Dyspnoea
Pleuritic pain (assoc with bacteraemia)

[Arthralgia + myalgia + confusion]

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39
Q

3 findings OE pneumonia

A

Increased HR, RR, low BP ?sepsis, temperature

Dullness to percuss

On auscultation
-Crackles or bubbling 
-Reduced air entry (unilateral)
-Pleural friction rub
-Aegophony (E will sound like A)
Vocal fremitus
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40
Q

Name 4 Ix for pneumonia.

When might you check urinary antigen?

A

FBC, CRP (raised WCC, raised CRP)

ABG: may be low oxygenation

Sputum culture and sensitivity - for causative

CXR - lobar

Blood culture - for causative organism

*Urinary antigen: for legionella and pneumococcus

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41
Q

Name 2 findings on XR of pneumonia

A

Air bronchograms

Consolidation: homogenous opacification in lobe

Atelectasis if small airway obstruction

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42
Q

What is this describing

diffuse reticular or reticulonodular opacities (affects interstitium)

A

atypical pneumonia CXR

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43
Q

CURB scores decide the Mx of pneumonia in CAP
0-1
2
2+

A 
Low risk (0-1) CAP:
Oral 5 day amoxicillin or clarithro,

Mod (2) CAP:
7-10 days amoxicillin + clarithromycin

Mod and high risk (2+) CAP:
7-10 day
Co-amoxiclav + clarithromycin (IV)

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44
Q

In high risk pneumonia and penicillin allergic what can you use

A

cefotaxime

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45
Q

Mx of HAP

A

TAZ

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46
Q

Mx of legionella

A

Clarithromycin

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47
Q

Mx of chlamydia pneumonia

A

Doxy

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48
Q

Name 3 comps of pneumonia

A

Septic shock

ARDS - non-cardiogenic pulmonary oedema

Pleural effusion (50%) + empyema

*Hepatisation (histologically lungs start to look like liver)

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49
Q

Name 3 Rfs for Tb

A 
Birth endemic (asia etc), immunocompromised (e.g. HIV), exposure (v.infective)
Poor nutrition, overcrowding, IVDU, homeless, prisons
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50
Q

Screen for TB immunity? the issue with this? If +ve?

A

Tuberculin skin test: > 5mm
- no distinction between active and latent TB

If +ve - interferon gamma release assay

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51
Q

What type of infection is active TB

A

Granulomatous

[multinucleate/Langhans giant cell, MP, LC]

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52
Q

3 ix in TB

A

CXR

3 x sputum acid fast bacilli smear

Sputum culture - Dont get much growth

FBC - leukocytosis and anaemia

NAAT - +ve for m.tuberculosis

?HIV test - for concurrent infection

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53
Q

Stain for TB

A

Ziehl-Neelsen stain - pink

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54
Q

Seen on CXR of TB
Primary?
Healed primary?
Most important = post primary?

Need to know post primary - focus on that

A

Primary: consolidation + ipsilateral hilar enlargement (lymphadenopathy)

Healed primary: Ghon focus: large round calcified lesion near hilum

Post primary: fibronodular upper zone opacities with cavitation + calcification + consolidation to hilum

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55
Q

TB mx - What needa to be checked before Mx and monitored?

A

RIPE DOTS (check LFTs before and monitor, check vision with Snellen)

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56
Q

TB drug Mx and 1 SE of each

A

6M Rifampicin: liver tox, orange secretions, induces hepatic enzymes (accelerate oestrogens, steroids, anticoagulants, phenytoin)

6M Isoniazid: liver tox, peripheral neuropathy (give w/ pyridoxine B6)

2M Pyrazinamide: liver tox, hepatitis

2M Ethambutol: *visual disturbance: optic neuritis, loss of acuity
[E - for EYES]

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57
Q

What is meant by DOTS in TB Mx

A

DOTS: directly observed therapy 3x/week

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58
Q

Who gets screened with Dx of TB

A

Screen household and close contacts

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59
Q

When is infectivity decreased in TB

A

2 weeks of treatment + 3 consecutive -ve AFB smears

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60
Q

Name 3 systems and pres of extra pulmonary TB

A

Pleura - pleural TB leads to pleural effusion

LN - scrofula - swelling and discharge

GU - frequency/dysuria/haematuria

Bone - osteomyelitis starting in growth plates of bone Pott’s disease - vertebral fracture associated with TB

Brain - TB meningitis - Rich foci

Abdomen - ascites (peritoneal) and abdominal LN

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61
Q

Whats seen on CT of disseminated TB

A

millet seed appearance

Liver/spleen/lung

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62
Q

Name 2 thromboembolic and 2 genetic RFs for DVT

A

Thromboembolic risk factors:
Cancer, trauma, major surgery, hospitalisation, immobilisation, oral contraception, obesity/preg (high oestrogen), recent flight (immobilisation)

Genetic risk factors: (Family history)
Factor V leiden, protein C deficiency, protein S deficiency, antithrombin deficiency, antiphospholipid

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63
Q

What is virchows triad in DVT

A

venous stasis,
vessel injury,
activation of clotting system

(hypercoaguable state)

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64
Q

DVT score

A

Wells (>2)

Alternative diagnosis more likely
Symptoms: DVT, haemoptysis, tachy
PMH: previous VTE, immobilisation 4 days, active malignancy

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65
Q

Ix in wells 0-1?

2?

A

D dimer

if +ve / wells 2
PVUSS - venous duplex USS

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66
Q

2 Main comps of PE

A

-> RHF and cardiac arrest

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67
Q

Name 3 types of embolus for PE

A 
thrombus 
Amniotic fluid embolus
Fat embolus (at long bone fracture)
Air embolus
Tumour embolus
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68
Q

Name 3 signs of PE OE

A

Pleural rub, tachy, tachyp, elevated JVP, hypoxia, shock

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69
Q

Name 2 DDx of PE

A

ACS, aortic dissection (anticoag fatal), pneumothorax

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70
Q

IX in PE

A 
Wells 
CXR 
ECG: sinus tachycardia
ABG: reduced PaO2, high lactate
D-dimer
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71
Q

Late sign of PE on CXR

A

wedge shape infarction

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72
Q

Key Ix in PE if wells >4 or D-dimer +ve

A

CTPA

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73
Q

What OE finding would indicate massive PE

A

Systolic <90

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74
Q

Initial resus for PE? Mx of haeomdynamically stable / unstable?

A

100%O2
IV access: fluids
Morphine

stable:
LMWH (dalteparin) or fondaparinux (10a inhibitors)

Haemodynamically unstable (?renal fail): 
Unfractionated heparin ± thrombolysis (alteplase)
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75
Q

how long do you give Mx in PE?
If active Ca?

What other Mx do you give [always continue on this]?

A

5 days OR till INR > 2 for 24 hours (longer)
LMWH for 6 months

VKA (warfarin) for 3 months then reassess

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76
Q

mx recurrent DVT + anticoagulation is CI

A

inferior vena caval filters

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77
Q

Mx symptomatic DVT

A

Catheter directed thrombolytic - Eg dalteparin

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78
Q

2 methods of prevention VTE

A

Early mobilisation and hydration post surgery

Avoid the pill

Graduated pressure stockings

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79
Q

Seen on spirometry of pulm fibrosis

A

restictive

FVC low, FEV1/FVC normal/high

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80
Q

3 things on pres / OE of PF

A

4Ds: dry cough, dyspnoea, digital clubbing, diffuse inspiratory crackles

81
Q

Name 3 causes of PF

A

Connective tissue disease: RA, SLE, SS, Sjogren’s

Occupational exposure: asbestos, coal dust, silica

Medication: amiodarone, bleomycin, methotrexate

Inhalation of irritants: hypersensitivity pneumonitis, birds, mould

Radiation

82
Q

Name 3 RFs for IPF

A

Smoking, infectious agent, dust exposure, chronic aspiration (GORD)

83
Q

Most important q in IPF

A

Occupation

84
Q

Main comp of IPF

A

Pulmonary hypertension -> cor. Pulmonale

85
Q

Name 3 Ix in IPF

A

CXR

CT

LuFT - restictive

ANA (SLE…_, RF

lUNG BIOPSY

86
Q

Name 1 XR findings IPF

A 
reticular shadowing (net-like) of lung peripheries + bases, 
shaggy heart border
87
Q

Name 2 findings on High resolution CT of IPF

A

Ground glass
honeycombing
reticular pattern

88
Q

General supportive Mx for IPF - 3 things

A 
O2 therapy
Physiotherapy
Exercise and weight loss
Vaccination 
Smoking cessation
89
Q

What pharma Mx can be used in IPF

A

Antifibrotic: pirfenidone (inhibits TGFB collagen synth)

90
Q

Give 2 differentials for Upper vs Lower lung fibrosis

A 
Upper - ESCHART (granulomatous diseases)
Extrinsic allergic alveolitis
Sarcoidosis/silicosis
Coal worker’s pneumoconiosis
Histiocytosis X
Ankylosing spondylitis
Radiotherapy
TB
Lower - RASCO (systemic diseases)
RA
Asbestosis
Systemic sclerosis/SLE
Cryptogenic fibrosing alveolitis
Other (drugs)
91
Q

3 main systemic causes of PF

Mx

A

SLE, RA, systemic sclerosis

Generally immunosuppression with steroids

92
Q

2 ways RA could lead to PF

A

Rheumatoid nodules may lead to small effusion

Methotrexate associated pneumonitis -> stop and Rx with steroids

93
Q

What is caplans syndrome

A

pulmonary fibrosis in coal workers with RA

94
Q

EAA - RFs, basic pathology

A

History of exposure to organic dust
Birds, agricultural, mould

Non-IgE mediated inflammation of alveoli and distal bronchioles

95
Q

3 Ix in EAA

A

Raised inflamm markers (WCC, CRP)

CXR: diffuse micronodular interstitial shadowing - upper zone

CT: reticulo-nodular shadowing, ground glass, micronodules

LuFT: restrictive, decreased DLco (diffusing lung capacity of carbon monoxide), decreased SpO2
Inhalation challenge: provocation testing - NP and LC levels, LuFT

BAL (bronchoalveolar lavage): predominant CD8 cells

96
Q

Mx of EAA ? Acute/chronic?

A

Allergen avoidance + facemask
Acute or subacute: O2 + prednisolone (oral) taper
Chronic: low dose corticosteroids

97
Q

What is histiocytosis X also called?
What happens?
Where is affected?

A

Langerhan’s cell histiocytosis

Usually in kids

clonal proliferation of Langerhan’s cells (Dendritic cell in skin) and CK overproduction

Bone, skin, lung

98
Q

2 Ix of histocytosis X? Mx?

A

Bone XR - punched out lytic lesions

Chest XR - reticulo-micronodular infiltration

Tissue biopsy - Langerhan’s cells

Chemotherapy

99
Q

What are Pneumoconioses? How long for Sx?

What is important to remember?

A

Group of chronic lung diseases by exposure to mineral dust or metal:
Includes coal workers, silicosis, asbestosis

10 years coal
15-60 years asbestos

Notifiable industrial disease - may be eligible for compensation

100
Q

Coal worker who has RA will probs have what in exam?

A

Caplans syndrom

101
Q

3 Ix in coal workers

A

Occupational history

LuFT: restrictive

CXR: large nodular fibrotic mass in upper lobes

Sputum microscopy: black

102
Q

Mx of coal workers lung

A

Avoid exposure
CXR, CT, LuFT for monitoring - incurable

Financial implications

Smoking cessation

103
Q

What 2 conditions might give black sputum

A

coal workers

silicosis

104
Q

Ix in asbestosis

A

Occupational history

LuFT: restrictive

CXR: ground glass opacification, small nodular opacities (asbestos bodies - in alveoli at lung bases), shaggy cardiac sillhouette

Sputum microscopy: asbestos bodies

105
Q

Mx asbestosis

A

Avoid exposure
CXR, CT, LuFT for monitoring - incurable

Financial implications

Smoking cessation

106
Q

Usual cause of pleural mesothelioma

A

asbestosis

107
Q

3 sx of pleural mesothelioma.

Make sure you know the key recurrent one

A

Dry cough, dyspnoea, dig club + pleuritic chest pain (*recurrent pleural effusion)

Symp of pleural effusion: diminished breath sounds, dull to percuss

Constitutional symptoms: weight loss, fatigue, fever, night sweats

108
Q

3 Ix in pleural mesothelioma

A

CXR

CT

Thoracentesis

pleural biopsy - (*epithelioid mesothelioma)

109
Q

Seen on thoracentesis of pleural mesothelioma

A

Exudate with malignant cells

110
Q

2 things seen on CXR of pleural mesothelioma

A

Irregular pleural thickening, reduced lung vol, ev asbestosis, unilateral pleural effusion

111
Q

Mx of pleural mesothelioma

A

operable at stage 1 + chemo

Chemoradio for others

ENTITLED TO COMPENSATION

112
Q

What is a pleural effusion

A

fluid in the potential space between visceral and parietal pleura

113
Q

What are the 2 main types of effusion and difference? If its hard to tell what can be used?

A

Transudate (low protein <30g/L)

exudate (high protein >30g/L)
[exercise likes lots of protein]

Light criteria if protein 25-35

114
Q

Pathology of transudate pleural effusion

A

disruption of hydrostatic and oncotic forces across pleural membranes (increase venous P or hypoproteinemia)

115
Q

pathology of exudative pleural effusion

A

increased permeability of pleura from inflammatio

116
Q

2 Causes of transudative plerual effusion

A

Increase hydrostatic or low oncotic:

Heart failure, cirrhosis, hypoalbuminaemia, nephrotic syndrome

117
Q

What syndrome has pleural transudative effusion and 2 other things?

A

Meig’s =
right pleural effusion
+ ovarian fibroma
+ ascites

118
Q

2 Causes of exudative plerual effusion

A

Pneumonia, malignancy, TB, AI disease (RA) comp of MI (Dressler’s)

119
Q

3 findings OE pleural effusion

A

Unilateral reduced chest expansion,
stony dullness on percussion,
decreased breath sounds,
if large -> tracheal deviation away

120
Q

What CXR finding in small pleural effusion

A

Blunted costophrenic angle

121
Q

Unilateral pleural effusion .
Transudative clinical picture mx?
If no transudative picture?

A

Yes -> treat cause (LVF, hypoalbuminaemia)

No -> USS guided pleural aspiration/thoracentesis

122
Q

pleural effusion on thoracentesis - if it is
Clear/straw?
turbid / yellow?
red?

A

Clear/straw = trans or ex

Turbid/yellow = empyema, parapneumonic

Haemorrhagic = haemothorax - malignancy, PE, trauma

123
Q 
Cytology of pleural effusion aspirarion .
Neutrophils?
Multinucleated giant cells?
Abnormal mesothelium? 
Lymphocytes?
A

Neutrophils = parapneumonic effusion,

multinucleated giant cells = RA,

abnormal mesothelium = mesothelioma,

Leukocytes = TB, malignancy

124
Q

Is a bilateral effusion likely to be trans or ex?

A

transudate

125
Q

Mx difference between trans and ex effusion

A

Trans - Do not tap!

Ex - Symptomatic: pleural tap
Max 1.5l - otherwise will result in fluid shift and pulmonary oedema

126
Q

Mx of malignant cause effusion

A

pleurodesis (with talc)

Likely to recur

127
Q

Causes of bilateral hilar lymphadenopathy

A

TIMES

TB
Inorganic dust - silicosis, berylliosis
Malignancy: lymphoma, carcinoma, mediastinal
EAA: e.g. bird fanciers lung
Sarcoidosis
128
Q

What is a pneumothorax?

A

Accumulation of air in the pleural space

129
Q

3 RFs for pneumothorax

A

Primary spontaneous: tall thin males, smoking, Marfan’s, family history

Secondary spontaneous: pre-existing lung disease: COPD (bullae), CF, TB, PCP

Trauma

130
Q

What happens in a tension pneumothorax

A
  • occurs when intrapleural pressure > atmospheric -> results from ball valve mechanism letting air in but not out

Lung deflates and mediastinum shifts contralaterally compressing great veins and causing decreased venous return to heart

131
Q

Pres of pneumothorax

A

pain *on same side as pneumothorax on breathing in + dyspnoea

132
Q

2 findings OE of pneumothorax

A

Hyper-resonant
Reduced expansion
Decreased breath sounds

133
Q

Pres / OE of tension pneumothorax

A

Respiratory distress with rapid shallow breathing

Distended neck veins

Tracheal deviation away

Hyperexpanded ipsilateral hemithorax

TachyC/TachyP

134
Q

2 findings XR of pneumothorax ? extra if tension?

A

Visceral pleural line
no lung markings

Tension
+ increased intercostal space + contralateral mediastinal shift + depression of hemidiaphragm

135
Q

Mx pneumothorax? If this doesnt work?

A

High flow o2

Aspirate 16-18G cannula, 2nd IC space, mid clavicular line

Chest drain and admit

136
Q

Where does a chest drain go?

A

Mid axillary IC 4-6

137
Q

Where do you put needles with regard to ribs for needle thoracostomy

A

2nd IC mid clavicular

Aim for just above a rib (rather than just below) to avoid neurovascular bundle

138
Q

Give 3 DDx of pleuritic chest pain

A 
ACS
Aortic dissection
Pneumothorax
PE
Pneumonia
Malignancy
139
Q

What is bronchiectasis and characteristic features

A

Permanent dilatation and thickening of the airways due to recurrent infection and inflammation

Recurrent (chronic daily) cough, excessive sputum
-Prone to infections

140
Q

Give 3 causes of bronchiectasis

A

Post infectious: measles/flu/pertussis, aspergillus fumigatus (ABPA), pneumonia

Immunodeficiency: HIV, Ig deficiency

Genetic: CF, ciliary dyskinesia, A1ATD

Connective tissue disease: RA, Sjogren’s

IBD: CD, UC

141
Q

Name 2 bugs often in bronchiectasis

A

aspergillus fumigatus

S.aureus, h.inf, s.pneum, pseudomonas aeruginosa

142
Q

Pres of infective bronchiectasis

A

Cough and daily sputum (bloody at 50%)
Mild - yellow/green sputum
More severe - khaki sputum
Intermittent haemoptysis

Obstructive symptoms: dyspnoea + wheeze

Weight loss and fatigue

143
Q

2 findings OE of bronchiectasis

A

Inspiratory coarse crackles (shift on cough),
high pitched inspiratory squeaks and pops,
low pitched brhonci (snoring sounds),
clubbing

144
Q

Cause of early vs late inspiratory crackles

A

Early inspiratory: airway disease e.g. bronchiectasis

Late inspiratory: interstitial disease: e.g. IPF

145
Q

3 Ix in bronchiectasis and whats seen

A

CXR
Normal/dilated bronchi with thickened walls + cysts (cystic shadows)
Tubular or ovoid opacities
TRAM-TRACK SIGN

*CT - imaging of choice
Thickened, dilated airways with or without air fluid levels, cysts

FBC - high eosinophils in ABPA, neutrophilia -> bacterial infection

Sputum culture and sensitivity

[For cause 
Serum A1AT phenotype, 
serum immunoglobulins (low), 
sweat test, serum HIV,
 aspergillus fumigatus skin prick test]
146
Q

Bronchiectasis bugs if gram +ve vs -ve? Which in CF

A

G- = pseudomonas aeruginosa (high risk if CF)

G+ = s.aureus, s.pneumonia

147
Q

Mx bronchiectasis

A

Exercise + improved nutrition
+ airway clearance physio (postural drainage, percussion)
+ mucolytics

Inhaled bronchodilator
+ inhaled hypertonic saline

Vaccinations and prophylactic antibiotics

148
Q

Mx recurrent pseudomonas

A

nebulised gentamicin

149
Q

Mx severe exacerbation of bronciectasis? Mild?

A

Iv ciprofloxacin

Oral amoxicillin§

150
Q

Who gets allergic bronchopulmonary aspergillosis?

what is it?

A

Asthma / CF

hypersensitivity to aspergilllus fumigatus

-> fibrosis / bronchiectasis

151
Q

3 Ix allergic bronchopulmonary aspergillosis

A

Skin test for aspergillus fumigatus sensitivity - positive

Serum IgE elevated

FBC with eosinophil count elevated

CXR *upper or middle lobe infiltrates

152
Q

Mx allergic bronchopulmonary aspergillosis

A

Avoid mold

Optomise CF/asthma mx

oral corticosteroid

oral antifungal - Eg co-trimoxazole

153
Q

Gene in CF ?

A

CFTR - cl channel

154
Q

3 organs affected in CF

A

Lungs, bowel, pancreatic duct, sweat glands, reproductive organs

-> thick sticky secretions

155
Q

When is screening for CF

A

Serum immunoreactive trypsinogen on 5d heel prick (Guthrie)

156
Q

Give 3 parts of Pres of CF

A

Neonates + infants: failure to pass meconium, failure to thrive, large appetite (pancreatic insufficiency), chronic wet cough

Resp:
Recurrent infection, chronic cough, wheeze, thick mucus, nasal polyps

GI
Gallstones, decreased motility

Panc
Insufficiency -> bulky, greasy, foul smelling stool
May develop DM from autodigestion

Reproductive system
Absent VAS - infertility

Digital clubbing

157
Q

3 Ix for CF

A

Serum immunoreactive trypsinogen

Sweat test - high Na/Cl

Genetic testing

pancreatic assessment: feacal elastase

158
Q

Usual bug in CF - key Ix for this

A

Pseudomonas aeruginosa (70%) - *highly transmissible

Sputum C+S

159
Q

2 comps of CF

A

Bone disease from malnutrition,
depression,
short stature,
cor pulmonale -> RVH

160
Q

3 parts of the mx for cf

A

Stop smoking

Chest physio

Inhaled bronchodilator

Inhaled mucolytic: dornase alfa + hypertonic saline

Segregate in hospital

Vaccination: influenza and pneumococcal

Prophylactic ABX: fluclox or amoxi

Pancreatic enzyme replacement, fat soluble vitamins DEAK

161
Q

Mx of advanced lung disease in CF

A

Bilateral transplant

162
Q

What is cor pulmunale

A

RVH/RHF due to disease of the lungs or the pulmonary blood vessels.(HTN)

163
Q

pressure for pulm HTN

A

Mean pulmonary artery pressure >25mmHg at rest

164
Q

2 egs of vasoconstrictors in pulm vasculature

A

endothelin-1, thromboxane A2 (+ platelets), low NO

165
Q

OE pulm HTN

A

Accentuated P2 (pulmonary component of second heart sound)

Tricuspid regurgitation murmur (high pitched holosystolic)

Pulmonary regurgitation murmur (Graham Steell) - high pitched early diastolic at pulm area (normally if pul HTN secondary to mitral stenosis)

RHF: oedema, exertional syncope, visible RV heave, pulsatile hepatomegaly, ascites, raised pulsatile JVP

166
Q

3 ix and findings in pulm HTN

A

CXR: pruning - attenuated peripheral arteries, enlarged pulmonary artery shadow

ECG: RVH (tall R wave and small S in V1), RAD, right atrial enlargement (p-wave > 2.5mm in II, III, aVF)

Transthoracic echo: Tricuspid regurge

Right heart catheterisation (Swan-Ganz) - >25mmHg pul art pressure with pulmonary capillary wedge pressure < 15mmHg

167
Q

3 parts of Mx pulm HTN

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

168
Q

2 main types and breakdown of lung Ca

A

Small cell (least common) 15%

Non-small cell (most common) 85%

  • Adenocarcinoma
  • Squamous cell carcinoma
  • Large cell carcinoma
169
Q

What would get you a 2 week wait for lung Ca

A

> 40 + 2 of following

Cough, fatigue, SOB, chest pain, weight loss, appetite loss, smoking

170
Q

Name 2 Paraneoplastic features of small cell lung Ca

A

ADH, ACTH, Lambert-Eaton syndrome (muscle weakness - NMJ)

SIADH - hyponatraemia

ACTH - HTN, hyperglycaemia, hypokalaemia, alkalosis, muscle weakness

LES - weakness that improves with muscle contraction

171
Q

Name a paraneoplastic feature os squamous cell Ca

A

PTH-rp, clubbing, TSH

PTH - bone pain and hypercalcaemia

TSH -> Hyperthyroidism

172
Q

Name a paraneoplastic feature of adenocarcinoma

A

gynaecomastia

173
Q

What tumour is from neuroendocrine cells-? presentation

A

carcinoid

serotonin secretion -> flushing and diarrhoea

174
Q

Where are adenocarcinomas usually found

A

peripheral lung

175
Q

Where does squamous cell carcinoma usually found? what does this mean for pres?

A

central airway

-> present as obstructive lesion

176
Q

Mets in Adeno/squamous/large cell?

A

Adeno
brain, adrenal, bone

squamou (well differentiated cells)
mets late

Large
mets early
undifferentiated

177
Q

Where might a pancoast tumour invade? features?

A

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

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

Recurrent laryngeal nerve -> hoarseness

178
Q

Where is a pancoast tumour found?

A

superior sulcus

179
Q

Signs of Lung Ca

A

Fixed monophonic wheeze

Pleural effusion -> stony dullness on percussion

Signs of SVC compression - facial congestion, distension of neck veins

Signs of hypertrophic arthropathy - finger clubbing (more common @NSCLC)

180
Q

Name 2 ways you might get a sample of Lung Ca

A

Cytology sputum and pleural fluid

Bronchoscopy - for histological diagnosis, endobronchial lesions may be biopsied

Surgical biopsy - transthoracic needle aspiration, peripheral lesions and LNs

181
Q

Ix for lung Ca

A

CXR

CT/MRI brain

LuFT

FBC - anaemia

LFT - mets

Bone scan - skeletal mets

U+E: Na, Ca - hyponatraemia = small cell, hyperCa = squamous

Sampling

182
Q

Common mets of lung Ca

A

Liver, bones, brain, adrenals

Hilar, mediastinal, supraclavicular LNs

183
Q

Give 2 times when surgery for NSCLC is CI

A

Stage 3b or 4 - mets present
*FEV1 < 1.5
Malignant pleural effusion
Vocal cord paralysis/ superior vena cava syndrome

184
Q

Mx SCLC

A

Not surgery

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

185
Q

Palliative support in Lung Ca .
Breathlessness

Obstruction

Pleural effusion

Cough

Hoarseness

SVCO

Bone pain

Spinal cord compression

A

Breathlessness
Opiate

Obstruction
External beam radiotherapy

Pleural effusion
Aspiration/drainage

Cough
Opiate

Hoarseness
ENT

SVCO
Chemo + radio

Bone pain
Radio

Spinal cord compression
Dex

186
Q

What is good pastures? presentation? precede?

A

Anti-glomerular basement membrane disease

Kidney symptoms: oedema, *reduced urine output

Lung symptoms: cough + haemoptysis + SOB + fever

*likely to have had recent URTI

187
Q

3 Ix goodpastures

A

Kidney tests:

  • Urinalysis - proteinuria + haematuria
  • Renal function - raised Ur and Cr (azotaemia - raised nitrogen compounds)
  • Renal biopsy - crescentic glomerulonephritis and linear IgG staining on immunofluorescense

Lung tests
-CXR: lower zone pulmonary infiltrates (blood)

Anti GBM titre raised - by immunofluorescence

[ANCA (type 2 cytotoxic reaction therefore may be ANCA +ve)
ANA normal to rule out lupus nephritis
Complement levels - normal to rule out lupus, infection and other nephritis
Anti-streptolysin O to rule out post strep glomerulonephritis]

188
Q

Mx goodpastures with pulm involvement

A

Oral corticosteroid
+ plasmapheresis
+ cyclophosphamide (remove and suppress Aab)

O2 +- blood products for severe pulmonary haemorrhage

189
Q

CO2 levels in 2 types of resp failure? how do they present?

A

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

Type 2 hypoxia + hypercapnia

T1: COPD (pink puffer), pneumonia, pulmonary oedema, fibrosis, asthma, PE, ARDS

T2: COPD (blue bloater), asthma, myasthenia gravis, polyneuropathy

190
Q

Ix resp failure

A

ABG, CXR, FRB, ECG

191
Q

mx respt failure ? what do you have to be cautious of

A

Admission and resuscitation

Treat hypoxaemia - aim SATS > 90%
ALWAYS start on high flow

Beware prolonged high conc O2 if lost hypercapnic drive -> elevating PaO2 may reduce RR

192
Q

Resp failure ventilation options

A

conscious
O2
BiPAP

Unconcious
O2
Intubate / ventilate

193
Q

What is ARDS

A

Non-cardiogenic pulmonary oedema and diffuse lung inflammation

dyspnoea, decreased sats despite ventilation

194
Q

2 most common causes of ARDS

A

sepsis

pancreatitis

195
Q

Who gets ARDS

A

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

196
Q

Ix ARDS

A

Low tidal volume ventilation

CXR (bilateral infiltrates), ABG, blood culture, sputum culture, urine culture

Criteria

  • acute
  • non-cardiogenic
  • CXR pulmonary oedema
  • Po2 <40
197
Q

Mx ARDS

A

Supportive care - resus and then slightly negative fluid balance

ABX + treat cause

198
Q

What is seen on an atypical pneumonia CXR

A

diffuse reticular or reticulonodular opacities (affects interstitium)

Phase 4 - GR (22 decks)

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