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Resp Flashcards

1
Q

presentation of asthma

A 
intermittemt dyspnoea
SOB
chets tightness
wheeze
cough (nocturnal)
Diurnal variation
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2
Q

signs o/e of asthma

A
  • hyperinflation (reduced chest exp and reduced crico sternal distance)
  • Hyperresonane on percussion
  • decrease in tactile vocal frem
  • polyphonic wheeze
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3
Q

other conditions that are associated with asthma

A

allergic rhinitis and eczema
GORD
Churg-straus- (eosinophillic granulomatosis with polyangiitis)

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4
Q

ix for ?asthma

A

spirometry- obstructive FEV1/FVC ratio <0.7 (FEV1 reduced more than FVC)

  • bronchodilator reversal - improvement in FEV1 by 12% or more
  • peak flow- varies >20%
  • fractional exhaled nitric oxide (FeNO)- eosinophils emit NP (>40ppb)
  • CXR- hyperinflation
  • challenge with histamine or methacholine- FEV falls by 20%
  • sputum culture
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5
Q

what tests do you do for screening once asthma has been diagnosed

A
  • skin prick
  • serum total and specific IgE
  • eosinophil count
  • exercise challenge- severity
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6
Q

Management of asthma

A
  • avoid precipitants
  • education
  • reduce NSAID dose

pharmac

  1. SABA (salbutamol)
  2. SABA + ICS (beclo, pred)
    - SABA + ICS +LTRA (montekukast)
  3. SABA +ICS+ LABA (salmeterol/formeterol) +- LTRA

then ask for specialist help

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7
Q

What specialist meds arethere for asthma

A
  • oral pred
  • LAMA- tiotropium/ipratropium
  • Theophylline/aminophylline- phosphodiesterase inhibs
  • omalizumab (anti- igE monocloncal Ab)
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8
Q

tx of subacute worsening of asthma- what could u do med wise?

A

double/triple/x4 ICS dose for 1 week

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9
Q

Types of asthma

A

Atopic
- type 1/igE mediated
- dust, pollens, food, animals
fhx and atopy triad present

Intrinsic/non-atopic/non-allergic

  • stress, cold air, anxiety, smoke, infections, aspirin
  • mechanism unknown

Eosinophillic

  • assoc with allergy
  • Th2 cells
  • overproduction of mucus- lumen plugging
  • ix autoimmune causesand vasculitis
  • responds well to steroids

Neutrophillic
- not well understood

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10
Q

things to cover in an asthmatic hx

A
  • diurnal/seasonal variation
  • cough at night
  • atopy
  • fam hx
    occupation and relation to work
  • severity- how many events/admissions in last year/how many times do they use SABA
  • inhaler technique
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11
Q

Management of acute asthma exacerbation

A 
ABCDE
Airways
Breathing
- RR, Sp02
- auscultate- polyphonic wheeze, air entry
- percuss- hyperres

OSHITME
O- 15L non rebreathe mask
S- Salbutamol- 2.5mg-5mg, neb in O2, repeat every 15min
H- hydrocortisone 100mg IV/pred 40mg PO
I- Ipratropium ** 0.5mg 4-6 hourly, neb in O2
T- Theophylline/aminophylline **1g in 1L saline at 0.5ml/kg/h
M- Mgsulphate 2g IV over **40min
E- escalate- anaesthetist, ICU, crash call

Circulation

  • IV access 2x wide bore
  • basic bloods, ABG
  • fluid bolus 250-500ml nomrla saline over 15min

Disability
Exposure
- rashes
- temp

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12
Q

ix for acute exacerbation of asthma

A

ABG-
T1/T2 resp failure
Pco2 may be decreased if hyperventilating

**Sputum and blood culture
CXR- infection, PTX
**ECG
SPO2
PEFR if stable
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13
Q

Grading severity of asthma

A

mod

  • increase in asthma sx
  • PEFR 50-70%

Severe

  • PEFR 35-50%
  • RR >25
  • HR >110
  • inability to complete sentences

Life- threatening

  • PEFR <33%
  • resp- <92%, silent chest, cyanosis, poor resp effort, bradycardia
  • confusion, exhaustion, coma

near fatal
- hypercapnia, requires mechanical ventilation

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14
Q

Types of lung cancers

A

Small cell

non small cell (sq, adeno, large cell)

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15
Q

presentation of lung cancer

A
  • cough, dyspnoea, wheeze, haemoptysis
  • hoarseness
  • pleurisy
  • head/neck/arm pain (SVCO)
  • horner’s syndrome (symp chain)
  • brachial plexus- shoulder/arm pain
  • Dysphagia
  • effusions
  • wt loss, fatigue, appetite
  • *- clubbing
  • *- lymphadenopthy
  • paraneoplastic sx- excessive **PTH, ADH, ACTH
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16
Q

where can lung cancers met to

A
  • brain
  • bone
  • liver
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17
Q

what is the 2ww criteria for ?lung cancer

A
  • CXR suggestive of lung cancer
  • > 40yo with unexplained haemoptysis

urgent 2-w CXR if

  • > 40 and 2 of the following (or 1 in they’ve ever smoked)
  • cough, wt loss, appeitie loss, dyspnoea, chest pain, fatigue
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18
Q

ix for ?lung cancer

A
  • CXR
  • CT to confirm
  • Bronchoscopu and biopsy
  • bloods - LFT (bone,- ALP, liver), UE (SIADH- low Na), Ca
  • Mets- CT head/abdo-pelvis
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19
Q

staging of lung Ca

A

I- <4cm
II- >4cm, +- lymph nodes
III- contralteral lymph nodes/eroded local strcutures
IV- extra-thoracic mets

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20
Q

management of lung Ca

A
  • stop smoking
  • lobectomy/pneumoectomy
  • RT
  • CT
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21
Q

complications of lung Ca

A
  • SVCO
  • Horners
  • Paraneoplastic syndromes (small cell)-
    • ADH- SIADH
    • PTH- hyperPT
    • ACTH- cushings
  • cauda equina
  • alopecia, neutropenia, bone marrow insuff due to CT
  • mucositis, pneumonitis, oesophagitis from RT
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22
Q

What cell type is small cell lung ca

A

neuroendocrine

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23
Q

whihc type of cancer has the worse prognosis

A

small cell

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24
Q

which type of cancer is most common

A

non-small cell- adeno

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25
Q

sx of SIADH

A 
vomiting
**headache
lethargy
**cramps
confusion
**seizures

hyponatraemia due to water retention

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26
Q

sx of cushings

A
  • central obesity
    moon face
    thinning skin
    striae
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27
Q

cell type of non small cell lung cancer

A

Adenocarcinoma- most common overall, and also most common in people who have never smoked
Sq- more linked with smoking than adenocarcinoma
Large cell

NSCLCs are all linked with hx of smoking, however, SCLCs are way more strongly linked with smoking, with the vast majority of the cases being in smokers

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28
Q

mutations NSCLC assoc with

A

Epidermal growth factor receptor
Anaplastic lymphoma kinase
Programmed ligand death 1

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29
Q

what type of lung Cancer is a pancoast cell usually

A

NSCLC- sq

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30
Q

presentaiton of pancoast tumour

A

Most Pancoast tumours are NSCLC- adeno, sq, large cell

  • *- Horner’s syndrome- miosis, anhidrosis, ptosis- ipsilaterally
  • *- brachial plexus compression- pain in shoulder radiating to scapula, pain/weakness in arm, thoracic outlet syndrome (vasculature)
  • recurrent laryngeal- hoarseness, bovine cough (non-explosive)
  • SVCO- facial swelling, cyanosis, neck veins
  • rib erosion (chest pain)
  • *- 1/4 of cases have spinal involvement/compression at presentation- screen for weakness, neuropathic pain
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31
Q

histology of mesothelioma

A

epithelioid, on pleura

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32
Q

causes of mesothelioma

A

asbestos

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33
Q

progression of mesothelioma

A
  1. pleural plaques
  2. asbestos effusion and pleural thickening
  3. asbesotsis (fibrosis)
  4. Mesothelioma
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34
Q

presentation of mesothelioma

A
  • recurrent pleural effusion
  • dyspnoea, cough
  • pleuritic pain
  • B sx
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35
Q

ix for ?mesothelioma

A

Biopsy- GOLD STANDARD
CXR- white spots, plerual mass, rib destruction, pleural thickening, effusion
CT
Pleural aspiraton- straw coloured

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36
Q

management of mesothelioma

A
  • palliative- CT, RT, debulking surgery
  • indwelling intrapleural drain
  • chemical, mechnical pleurodesis (fusion)
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37
Q

What is a pneumothorax

A

air in the pleural space

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38
Q

Causes of pneumothorax

A

spontaneous/idiopathic

Secondary- due to underlying disease

  • emphysema
  • COPD
  • fibrosis etc

Trauma- broken rib, stab wound

Iatrogenic- pleural biopsy, hgih pressure vent

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39
Q

Why does PTX have effect on lung ventilation

A

loss of pressure gradient (pressure in lung is increased so less air is sucked in)

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40
Q

who do you usually see spontenous PTX in

A

young, slim male

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41
Q

RF for PTX

A 
reps cond- asthma, COPD, LRTI
connective tissue disorder
**A1- antitrypsin deficiency
**CF
SMoking, smoking cannabis
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42
Q

presentaion of PTX

A
  • acute onset dyspnoea
  • pleuritis chest pain
  • Sensation of not being able to take full breath
  • beware of the pt who rapidly declines (BP, sats, tachycardia) after intubation- the ventilation is making the tension PTX worse
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43
Q

signs of PTX o/e

A
  • diminished breath sounds/silent chest
  • hyperresonance on percussion
  • reduced tactile vocal fremitus (which is only raised in colsol, reduced in effusion)
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44
Q

Ix of PTX

A
  • monitor obs
  • ABG
  • CXR on insp
  • bloods- A1AT
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45
Q

Clasificaiton of PTX (size)

A
  • small- <2cm between chest wall and lung border

- Large- 2cm

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46
Q

Management of PTX

A
  • high flow O2 15L non rebreath
  • if small and not in resp distress- can discharge
  • chest drain- 14-16G, no lower than 5th ICS mid-axillary line/2nd ICS mid-clavicular

always admit if secondary cause for observation (more serious presentations and outcomes)

pt education

  • stop smoking
  • advice on recurrence
  • avoid flying until resolution
  • avoid diving permanently
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47
Q

tx of recurrent PTX

A

pleurodesis

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48
Q

why is tension PTX an emergency

A

pleural cavity expands, compressing lung and other thoracic structures

  • Resp distress
  • Impaired venous return leading to less contractility
  • Reduced CO
  • -> lead to hypoxaemia and haemodynamic comprimise
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49
Q

causes of tension ptx

A

ventilated pts
trauma, CPR
acute presentations of asthma/COPD
blocked/displaced chest drains

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50
Q

presentation of tension PTX

A

SOB
Chest pain, pleurisy
profuse diaphoresis

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51
Q

signs of tension pTX

A 
tachypnoea
tachycardia
cyanosis
mass effect
- tracheal deviation away from PTX
- displaced apex beat
- raised JVP
  • beware of the pt who rapidly declines (BP, sats, tachycardia) after intubation- the ventilation is making the tension PTX worse
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52
Q

Causes of PE

A
  • embolisation from DVT
  • septic vegetation (endocard)
  • parasitic
  • fat
  • air
  • amniotic fluid
  • neoplastic cells
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53
Q

presentation of PE

A

acute SOB
pleuritic chest pain
haempotysis
syncope

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54
Q

signs o/e of PE

A 
cyanosis
tahcypnoea
tachycardia
hypotension
***raised JVP
**pleural rub (sounds like squeaky leather on ausc)
pleural effusion- stony dull percussion
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55
Q

What criteria is used for ?PE

A

Wells

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56
Q

What is the cut off thresholds for PE on the Well’s score and tx

A

> 4– likely
- CTPA or V/Q scan

<=4- unlikely

  • D- dimer
  • if raised, do CTPA or V/Q sc
  • if normal- observe, consider other dx

if pt is haemodyn unstable- do CTPA straight away, give anticoags w/o delay

tx-

  • alteplase if haemodyn unstable
  • DOAC (or LMWH followed by dabigatran; heparin if renally impaired)
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57
Q

ix for PE

A
  • assess legs for signs of DVT (>2cm increase in diameter, redness)
  • FBC, UE, clotting, D-dimer
  • CTPA
  • V/Q
  • ECG- RBBB. right axis deviation, inverted T waves, sinus tachy
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58
Q

Management of PE

A

ABCDE

  • O2 15L non rebreathe
  • Consider Alteplase IV if haemodyn unstable

anticoag

  • DOAC- apixiban/rivaroxiban- 15mg BD for 21 days, then 20mg OD
  • can offer LMWH (dalteparin)
  • continue DOAC for at least 3m
  • vena cava filter if anticoag CIed
  • surgical thrombectomy/embolecomty if massive
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59
Q

what are the contraindications for a CTPA

A

renal impairement
contrast allergy
pregnant

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60
Q

thrombolysis contraindications

A
  • *- recent surgery (3m)
  • *- active malignancy
  • active bleeding
  • hx haemorrhagic stroke
  • *- BP uncontrolled/>180 systolic
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61
Q

how are PEs prevented in anyone at at risk of them eg after surgery

A
  • thromboprophylaxis- daily dalteparin SC
  • compression stockings
  • avoid dehydration
  • stop meds like COCP
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62
Q

what is the prophylactic dose of dalteparin

A

2500U once every 24hours

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63
Q

what is tx dose dalteparin

A

7,500, 10,000, 12,500, 15,000, 18,000u depending on weight

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64
Q

Causes of interstitial lung disease

A

primary/idiopathic

secondary

  • toxins- asbestosis, bird dander, silica, hot tubs
  • medications- methotrexate, amiodarone, abx- nitrofurantoin, rituximab, *radiation
    • conditions- sjogrens, SLE, RA, Sarcoidosis, connective tissue disorders
    • infective- mycoplasma pneumonia, penumonocystis pneumonia (jiroveci)
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65
Q

what is intersitial lung disease

A
  • inflammation and fibrosis of the lung intersitium
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66
Q

presentation of interstitial lung disease

A
  • slowly progressive exertional dyspnoea
  • dry cough
  • malaise, fatigue
  • sx of underlying condition
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67
Q

signs of intersitial lung disease

A
  • fine end-respiratory crackles
  • dullness to percussion
  • finger clubbing
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68
Q

ix ffor ?intersitial lung disease

A
  • sats
  • spirometry (restrictive- FEV1/FVC >0.7 reduced FVC, normal FEV1)
  • bloods- anaemia of chronic disease
  • urine dip- haema/proeinturia= vasculitis
  • antibodies- anti-ccp+ RF (RA, sjorgens), ANA (lupus, sjogren’s), ANCA (vasculitis), dsDNA (biliary cirrhosis, mononucl., hepatitis, lupus) antiRo (lupus, sjogrens), anti-La (sjogrens, lupus)
  • RAST- igE in blood
  • CXR- fine opacities
  • CT lung- honeycombing, reticular opacities, traction bronchiectasis
  • bronchoscopy, bronchial lavage, biopsy
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69
Q

management of interstitial lung disease

A
  • avoid cause- meds, toxins, smoking
  • pulm rehab
  • annual flu vacc
  • tx cause- often w steroids
  • IPF: pirfenidone (antifibrotics)
  • LTOT (spO2 <88%, paO2 <7.3)
  • lung transplant
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70
Q

complications of instersitial lung disease

A
  • pulm HTN–> right HF, cor pulmonale
  • resp failure
  • anxiety, depression
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71
Q

what is idiopathic pulmonary fibrosis

A
  • chronic, progressive intersitial lung disease

- unknown origin

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72
Q

presentation of IPF (immune pulm fibrosis)

A
  • SOB
  • persistent cough (dry usually, hacking)
  • fatigue
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73
Q

signs of ITP

A

BL fine insp crackles

clubbing

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74
Q

ix for ?IPF

A
  • lung function/spirometry (restrictive >0.7)
  • CXR
  • CT thorax
  • bronchoalveolar lavage/biopsy if no dx can be made from above
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75
Q

managament of Idiopathic pulmonary fibrosis disease

A
  • review 6m after diagnosis to assess deterioration
  • smoking cessation
  • pulm rehab
  • LTOT
  • ***- opioids/thalidomide for cough
  • **- pirfenidone (antifibrotic)
  • palliative care referral

median survival is 4 years

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76
Q

RF Idiopathic pulmonary fibrosis

A
  • smoker
  • GORD
  • *- >70y/o
  • fam hx
  • *- viral infections
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77
Q

what is hypersensivity pneuomnitis

A
  • extrinsic allergic alveolitis

- allergic sensitisation, leading to inflammation and then fibrosis

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78
Q

causes of hypersensitivity pneuomonitis

A

**bacterial, fungal
animals
pollen
**insecticides, plastics

Occupational:
bird fanciers
farmers lung (mould spores in hay- micopolyspora)
**malt workers lung (aspergillus)
**bagassosis/sugar workers lung
**Coal workers pnemoconiosis
**silicosis
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79
Q

presentation of hypersensitivity pneumonitis

A
  • progressive SOB
  • worse after contact with allergen
  • wheeze
  • fevers, rigors, myalgia, headache, wt loss
    can be acute (4-6hours after exposure, flu-like) or chronic (insidious dyspnoea)
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5
Perfectly
80
Q

signs of hypersensitivity pneumonitis

A

fine basal crackles

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81
Q

ix ?hypersensitivity pneumonitis

A
  • CRP, ESR
  • serum igG antibodies
  • spirometry (restrictive)
  • CXR- upper zone consoliation/fibrosis/honeycombing
  • CT thorax
  • Bronchoalveolar lavage/biopsy- lymphocytes, mast cells
82
Q

tx of hypersensitivity pneumonitis

A 
avoid allergen-preventative
chest physio, bronchodilators, cough suppressors
O2 
pred LT
lung transplant
83
Q

sx of asbestosis

A
  • SOB
  • persistent cough
  • wheeze
  • shoulder/chest pain
  • extreme fatigue
  • finger clubbing
84
Q

high risk jobs for asbestos exposure

A
  • heating, ventilation engineers
  • demolition workers
  • plumbers
  • construction workers
  • electricians
85
Q

What is sarcoidosis

A
  • autoimmune
  • inflammation, granulomas
  • affects lungs mainly, but also lymph nodes, skin and other organs
86
Q

presentation of sarcoidosis

A
  • wheeze
  • SOB
  • persistent dry cough
  • arthralgia
  • red spots on skin

sign- hepatosplenomegaly

87
Q

ix for sarcoidosis

A
  • Kveim test- SC injection of sarcoid tissue- induced granulomas
  • lung function tests
  • **- serum ACE increase due to granulomas
  • CXR/CT
  • bronchoscopy, biopsy
88
Q

management of sarcoidosis

A
  • watch and wait
  • corticosteroids (pred)plus bisphosphonates
  • infliximab
  • paracetemol/NSAIDs
89
Q

What is Caplan’s syndrome

A

RA patients with diffuse lung fibrosis (pneumoconiosis) with nodules on CXR

90
Q

Tx of radiation pneumonitis

A
  • long course corticosteroids
  • NSAIDs
  • O2
  • *- bronchodilators
91
Q

What type of vasculitis can affect the lungs

A

Small vessels:
Goodpastures
Granulomatosis with polyangiitis (wegners)

92
Q

sx of good pastures with lung involvement

A

haematuria, proteinuriea, kidney failure
General discomfort, pain
anaemia
chets pain, SOB, cough, haempotysis

93
Q

ix for ?goodpastures/anti glomerular basement membrane

A
  • kidney biopsy- ***cresentic glomeruloneohritis
  • CXR- infiltrates, lower zones
  • anti glomerular membrane antibodies
  • **- ANCA
  • **- alpha 3 subunit of type 4 collegen (goodpastures antigen)
94
Q

tx of goodpastures

A

corticosteroids, cyclophosphamides

plasmapheresis/dialysis

95
Q

what is granulomatosis with polyangiitis

A

(Wegners)
small vessels
ear, nose, sinuses, kidneys, lungs

96
Q

sx of granulomatosis with polyangiitis

A

fatigue, pyrexia, wt loss
sinusitis, inflam of nose, epistaxis
scleritis, episcerlitis
renal disease, glomerulonephritis- haematuria
cough, haemoptysis, pleuritis
purpura, peripheral neuropathy, arthritis

97
Q

Ix of ?granulomatosis with polyangiitis

A 
cANCA
urinanalysis - proteinuria, haematuria
CXR- haemorrhage, nodules, infiltrates
CT
renal biopsy
98
Q

tx granulomatosis with polyangiitis

A
  • steroids
  • with cyclophosphamide, rituximab
  • LT may be given- rituximab, methotrexate, azathioprine, mycophenolate.
  • plasmaphoresis, haemodyalysis
99
Q

What mutation causes CF

A

autosomal recessive
cystic fibrosis transmembrane conductance regulator gene (CFTR)
on chromosome 7

100
Q

What is the pathophysiological process that occurs in CF

A
  • defective CFTR channel which transports CL- into/out of cells channel
  • Less Cl- absorbed into cell
  • therefore less Na+ absorbed, as Na+ follows Cl-
  • More water moves into cell due to osmotic gradient
  • mucus is dehydrated (more viscous)
  • salty sweat
  • Pancreatic ducts blocked (malabs)
  • Lumen of bile duct plugged, local damage, bile deficiency
  • Meconium ileus
  • resp mucous plugging, infection, intersitial damage
  • Male infertility- vas deferens absence
  • female infertility- plugging of fallopian tubes, cervical mucous thickening
101
Q

How common is CFTR mutation

A

1/25

102
Q

Presentation of CF

A 
productive cough
Wheeze
*finger clubbing
BL coarse crackles
Recurrent resp infections, *bronchiectasis
*PTX

weak infant with meconium ileus/rectal prolapse

Steatorrhea
*intestinal obstruction
*gallstones
*liver cirrhosis (jaundice)
*haemorrhage (vit K malabs)
Malnutrition/FTT
infertility 
*OP, arthritis
103
Q

Ix for ?CF

A
  • newborn screening- heel prick test for immunoreactive trypsinogen
  • genetic screening
  • sweat test (Na+ and Cl- >60mmol/L. Cl- higher then Na+)
  • **- FAECAL ELASTASE= decreased– panc insuff
  • bloods- deranged LFTs, deranged clotting (vit K malabs)
  • sputum culture
  • CXR- hyerpinfl, bronchiectasis
  • spirometry- obstructive
  • semen analysis- aspermia
104
Q

Management of CF

A

resp

  • Resp physio
  • muclytics (boranse alfa, hypertnoic saline)
  • infection prophylaxis
  • regular sputum MC&S
  • lung, liver transplant

GI/malabs

  • Pancreatin (creon), insulin replacement
  • vit supplements, Ca/vit D
  • ursodeoxycholic acid to improve bile flow
  • regular DEXA for OP, bisphosphonates
  • high calorie intake (130%)
  • psych support
  • biannual f/u
105
Q

What organism is common in CF penumonia

A

pseudomonas aeruginosa

106
Q

What is primary ciliary dyskinesia

A
  • autosomal recessive

- cilia- ineffective movement of mucous

107
Q

What is Kartagener’s syndrome

A
  • causes primary ciliary dyskinesia and situs inversus totalis (everything in body is other side)
108
Q

presentation of primary ciliary dyskinesia

A
  • CF but less severe
  • chronic/recurrent resp infection
  • infertility
  • *- hearing loss, otitis media
109
Q

ix for ?primary ciliary dyskinesia

A

Spirometry

biopsy of bonchial airway cilia

110
Q

Management of primary ciliary dyskinesia

A
  • same as CF
  • mucolytics
  • mucous clearance physio
  • infection prophylaxis
111
Q

What is acute resp distress syndrome

A
  • fluid build up in the lungs

- causes reduced O2 exchange

112
Q

Causes of acute resp distress syndrome

A
  • pleural trauma
  • inhalation of dense smoke or chemical fumes,
  • pneumonia (esp aspiration)
  • cerebral trauma
  • hypovolaemic shock

Systemic inflammatory resposne-

  • sepsis
  • acute pancreatitis
  • burns
  • massive trauma (esp if shcok /mult transfusions neede)
  • near drowning
113
Q

sx of ARDS

A
  • SEVERE SOB!
  • cough
  • chest pain- esp with deep breathing
  • confusion
  • exhaustion
  • dizziness
114
Q

sings o/e of ARDS

A
  • hypotension
  • tachypnoea
  • tachycardia
  • fever
  • cyanosis
  • oedema (fluid is leaving blood into tissues)
  • peripheral vasodilation
  • BL fine end resp crackles
115
Q

ix for ?ARDS

A
  • FBC, UE, LFT
  • amylase, CRP
  • blood cultures
  • ABG
  • clotting
  • CXR- BL alveolar shadowing
  • CT (Trauma)
  • echo if ?cardiac /HF cause instead
116
Q

What criteria is used for ARDS

A

Berlin
- onset within 1 week of known clinical insult
or
- a pt recognising a worsening of resp sx

  • presence of BL opacities on CXR/CT, not fully explained by effusion/lobar or lung collapse/nodules
  • diagnosis of resp failure is not fully explained by cardiac failure or fluid overload
  • presence of hypoxaemia
117
Q

tx of ARDS

A
  • ICU
  • CPAP- 40-60% O2, intubation, ventilate prone
  • arterial line- haemodynamic monitoring
  • inotropes- dobutamine
  • vasodilators
  • antiplatelets- clopi
  • fluids= with careful fluid balance, on some cases, negative fluid balance
  • haemofiltration/blood transfusion
  • enteral feeding
118
Q

What is type 1 resp failure

A

Hypoxia, normo/hypocapnia
<8kPa (<60mmHg) O2
<=6KPa (<50mmHg) CO2

  • assoc with damage to the lung tissue, preventign oxygenation but CO2 is still able to be excreted
119
Q

causes of T1 resp failure

A 
Lung tissue damage:
pulm oedema, HTN, ARDS
chronic pulm fibrosis
pneumonia, COVID 19
asthma
PTX, PE
120
Q

What is type 2 resp failure

A

hypoxaemia with hypercapnia
<8kPa (<60mmHg)
>6kPa (>50mmhg)

  • alveolar ventilation is insufficient to excrete CO2
121
Q

causes of T2 resp failure

A 
Ventilation issues:
COPD
Severe asthma
chest wall deformities
resp muscle weakness
CNS depression (reduced resp drive)- sedatives, strong opioids, MG
Hypothyroidism
122
Q

sx of resp failure

A
  • confusion, anxiety, restlessness, seizures, coma

- reduced consciousness

123
Q

signs of resp failure

A

tachycardia +- arrhythmias
cyanosis
polycythemia if chronic cause
cor pulmonale- pulmonary HTN induces RSHF– hepatomegaly and peripheral oedema

124
Q

ix ?resp failure

A
  • ABG
  • CXR
  • FBC- anaemias, polycythemia
  • UE LFT- Mg, K, PO4- may aggravate resp failure
  • serum CK, trop- exclude recent MI/myositis
  • TFT
  • Spirometry
  • Echo- cardiac causes suspected
  • ECG- cardiac causes suspected
  • sputum/blood culture
125
Q

Management of resp failure

A
  • immediate resus
  • O2
    • –>CPAP- expiratory positive pressure, keeps alveoli open during exp– T1RF
  • –> BiPAP- insp and exp pressure– T2RF, as pressure on insp improves ventilation and solves CO2 issues
  • Tx the cause
126
Q

complications resp failure

A

PE
MI, Arrhythmias, pericarditis
polycythemia if chronic
AKI, abnormalities in electrolytes, Acid-base balance issues

gastric ileus, pneumoperitoneum, duodenal ulceration

127
Q

What is the pathophysiology of bronchiectasis

A

Not fully understood

  • initial insult (infection)
  • leads to excessive mucus
  • persistent colonisation in mucus
  • chronic inflam leads to permanent damage of bronchial airways and dilation
  • thickened walls
  • vicious cycle of infeciton, inflamm, damage/dilation
128
Q

causes of bronchiectasis

A
  • post infectious
  • pulm disease
  • congenital
  • connective tissue disease
  • idiopathic (most cases)
129
Q

what are some post infective causes of bronchiectasis

A
  • recurrent childhood LTRI
  • pulm TB
  • allergic bronchopulmonary aspergillosis
130
Q

What are some pulm diseases that causes bronchiectasis

A

asthma

COPD

131
Q

what are some congenital causes of bronchiectasis

A

CF
Primary ciliary dyskinesia
alhpha1 antitrypsin deficiency

132
Q

what are some autoimmune conditions that may lead to bronchiectasis

A

RA
SLE
sarcoidosis

133
Q

Presentation of bronchiectasis

A

daily cough

  • productive (copious amounts, mucopurulent)
  • haemoptysis in 50%
  • extertional dyspnoea, may progress to at rest
  • fatigue
  • rhinosinusitis- nasal discharge, nasal obstruction, facial pressure
  • onset over months/years
134
Q

things to cover in hx of ?bronchiectasis

A
  • no of exacerbations/hospitalisations
  • exercise tolerance- recent change?- hx to
  • sputum quantity and colour- recent change? blood?
  • hx of childhood LRTI
  • hx of asthma, COPD, TB. aspergillosis
  • fam hx of RA, CF
  • smoking hx, oets, mould in house

ddx exclusion

  • COPD- smoking, o/e absence of high pitched sounds, CT normal
  • Asthma- diurnal variation? hx of atopy, bronchodilator reversibility
  • Pneumonia- acute presentation
  • Chronic sinusitis- lack of productive cough
  • lung cancer- wt loss, fatgue, haemoptysis
135
Q

Sings o/e in bronchiectasis

A
  • finger clubbing
  • coarse creps- exp and insp
  • rhonchi– low pitched noises like snoring
  • high pitched inspiratory squeaks and pops
136
Q

Ix ?bronchiectasis

A
  • CT- GOLD STANDARD
  • sats
  • sputum culture
  • lung function tests- obstructive/normal
  • echo- pulm HTN, vent function
  • CXR- exclude other pathologies, tramline/ring shadows seen in severe disease
  • FBC- neutrophilia, CRP
  • autoimmune- Anti-ccp, ANA, ANCA, antiro/la, dsDNA
  • CF/primary ciliary genetic testing
137
Q

conservative tx bronchiectasis

A
  • pulm rehab- physio
  • smoking cessation
  • annual flu and one off pneumococcal vacc
138
Q

medical tx of bronchiectasis

A
  • mucoactive- neb saline and carbocisteine
  • prophylactic abx- azithromycin 3x a week >=3 exacerbations year
  • bronchodilators- LABA (formoterol/salmeterol)
  • LTOT

Acute exacerbation

  • amoxicillin, clarithro, doxy oral
  • coamx IV
139
Q

surgical tx of bronchiectasis

A
  • lung resection if localised

- lung transplant if <65, with rapid deterioration despite above tx

140
Q

The two ‘presentations’ of COPD

A

Blue bloater- Bronchitis

Pink puffer- emphysema

141
Q

What is th epathophysiology of bronchitis

A
  • cough and sputum on most days for 3m in 2 consecutive years
    hypersecretion of mucus
  • hypertrophy of glands
  • goblet cells hyperplasia
  • epithelial cells become ulcerate, collumnar replace sq ep
142
Q

Pathophysiology of emphysema

A
  • large airspaces distal to terminal bronchioles due to destruciton of alveolar walls
  • inflam and scarring decreased lumen size
143
Q

sx of COPD

A 
chronic cough- productive
dyspnoea- exertional SOB
- wheeze
- chest pain
- haemoptysis
144
Q

signs of COPD

A

tachypnoea
cyanosis
hyerinflation (reduced cricosternal dist., chets expansion)
use of accessory muscles
coarse crackles, wheeze, quiet breath sounds
hyperesonant percussion
corpulmonale

145
Q

Presentation of pink puffer

A
  • SOB main sx
  • anxious, jerky, short sentences
  • prolonged exp time, breath with pursed lips to increased pressure in lungs for gas exchange
  • cachectic
  • decresase breath sounds
  • orthopnoeic
  • barrel chest
  • RSHF
  • hypoxic, normocapnic
146
Q

presentation of blue bloater

A

chronic bronchitis

  • Productive cough main sx
  • cyanotic
  • oedema
  • exertional dyspnoea
  • hypoxic and hypercapnic (t2RF)
  • acidotic
147
Q

How do you grade COPD

A

Medical research council breathlessness score

1- none, except on strenuous exercise
2- SOB when hurrying, walking up slight hill
3- walks slower than contempories on level ground due to breathlessness, or has to stop when walking at own pace
4- stops fro breath after walking ~100m/few mins level ground
5- cannot leave house due to SOB, SOB when dressing

148
Q

COPD diagnosis, ix

A

none

> 35
presence of RF (smoker, occupation exposure, air pollutions, A1AT deficiency)
typical sx
obstructive <0.7 on spirometry

ABG- hypoxia +- hypercapnia
sats
FBC- secondary polycythemia
- ECG, serum antriuretic peptide, echo (if cor pulmonale and pulm htn sx- oedema, cyanosis)
- sputum culture
- CXR- hyperinfl
- high rec CT
- PHQ-9, GAD-7
- serum A1AT- if early onset, no smoking, fam hx
149
Q

tx of acute exacerbation of COPD

A
  • cnsider admission
  • increase dose/freq of SABA/SAMA-
  • nebs SABA
  • px oral corticosteroids (pred OD 1-2w)
  • abx if purulent sputum/signs of pneumonia- amox, doxy, clarithro (oral or IV)
  • f/u- review management, technique
  • LTOT

NB- no acute IV steroids or inhaled steroids advised by NICE

150
Q

Management of stable COPD

A
  • smoking cessation, exercise, wt loss
  • influenza, pneumococcal vacc
  • cardiopulm rehab
  • antimucolytics- carbocysteine
  1. SABA (salbut)/SAMA (IpratropiuM- I(pratropium) need it now!)
  2. no asthma features/steroid responsiveness– +LABA+LAMA (tiotropium)
    asthma/steroid- +LABA (salmet)+ICS

3.LABA+LAMA+SABA+ICS

SABA continue throughout the steps

Specialist add-ons

  • roflumilast
  • theophylline
  • prophylactic azithromycin

asthma features= high eosinophil, atopy hx, variation in FEV1, diurnal variation)

151
Q

What baseline tests must you do before starting someone on prophylactic azithromycin, then how often do u monitor?

A
  • CT thorax
  • baseline ECG (can cause QT prolongation)
  • LFTs
  • review after 1st 3m
  • then 6 monthly
152
Q

Mciroorganisms that commonly cause pharyngitis

A 
rhinovirus
influenza
adenovirus
coronavirus
parainfluenza
153
Q

sx of pharyngitis

A 
sore throat 
hoarseness
mild cough
fever, headache, nausea, tiredness
dysphagia
154
Q

signs of pharyngitis

A

lymphadenopathy in neck

may see pus on tonsil

155
Q

tx of pharyngitis

A
  • usually goes within 1 week
  • can last longer (10%)
  • keep fluid intake up
  • NSAIDs, paracetemol
  • lozenges
  • gargling warm salt water
  • humidifier
  • feverPAIN- pheoxymethylpenicillin (erythro/clarithro if allergic)
156
Q

Causes of laryngitis

A

viral
- adenovirus, rsv , influenza, parainfluenza, herpes, HIV, coxsackievirus

bacterial

  • H. influenza type B
  • strep pneumonia
  • S aureus
  • group A beta haemolytic strep
  • moraxella catarrhalis
  • kelbsiealla
  • candidiasis

Trauma
- voice misuse

157
Q

Management of laryngitis

A
  • should be self limiting
  • vocal hygeine- resting, avoid smokig, humidifcation, hydration
  • crhonic- voice therapy, tx underlying cond eg GORD
158
Q

causes of pneumonia

A

cancer

viral

  • influenza
  • RSV
  • SARS-CoV-2

bacterial

  • strep pneumonia
  • H influenza
  • legionella, mycoplasma, chlamydia pneumoniae

Fungi
- histoplasmosis
cryptococcus
pneumocystis jiroveci (HIV)

Mycobacterial- tuberculosis

Aspiration

159
Q

what organisms tend to cause HAP vs CAP

A

CAP- strep pnuemoniae

HAP- occurs >=48hours after hosp admission

  • pseudomonas
  • S.arueus- methicillin resistant and susceptible
  • klebsiella
  • E.coli
160
Q

What features of a pneumonia suggest strep. pneumonia is the causative agent

A
  • lobar

- rust coloured sputum

161
Q

Sx of pneumonia

A 
Dyspnoea, SOB
Weakness, pale, fatigue
fever
productive cough- pus/blood/rust
chest pain
back pain
162
Q

signs of pneumonia o/e

A

dullness on percussion (consolidation)
increase tactile vocal fremitus
**bronchial breath sounds
late insp crackles– rales (crackles, larger airways, on insp, pneumonia/CHF), rhonchi (low pitched snore, larger airways, on exp, pnuemonia/COPD)

163
Q

How do you calculate mortality risk of someone with pneumonia

A

CURB65

  • Confusion
  • Urea (blood urea nitrogen >7mmol/L)
  • raised RR (>=30pm)
  • BP <90 S or 60 D (one of the two)
  • Age >=65

0- low risk
1-2= intermediate (1-10%)
3-4- high risk (>10%)

164
Q

ix of ?pneumonia)

A 
CXR
procalcitonin (high in bacterial)
sputum culture
bronchoalveolar lavage
blood culture
165
Q

tx of pneumonia

A

CAP
low/mod severity:
amoxicillin 500mg TDS 5 days
doxy, clarithro, erythro if allergic/pregnant /atypical pathogen suspected

High severity:- oral or IV
coamox with ***clarithro 7-10d
oral erythro if allergic

HAP
co-amox 500/125mg TDS 5 days
severe- IV- Tazocin
if MRSA- add vancomycin

pain meds
CPAP, non invasive vent

166
Q

what is a pleural effusion

A
  • collection of fluid in pleural space

reduces decrease lung expansion

167
Q

causes of pleural effusion

A

Transudative (fluid leaving capillaries due to increase hydrostatic pressure/decrease in oncotic pressure)

  • HF with pulmonary oedema
  • liver cirrhosis (less proteins made)
  • nephrotic syndrome (increase exc. of proteins causing hypoalbuminaemia)

Exudative- inflammation, caps leaky

  • *- trauma
  • malignancy
  • *- inflammatory conditions/autoimmune (lupus)
  • infection eg pneumonia
  • *- PE
  • **lymphatic/cyclothorax
  • thoracic duct occlusion
  • damage during surgery
    • mesothelioma (recurrent effusions)
168
Q

sx of pleural effusion

A
  • chest pain (pleurisy)
    SOB
    dyspnoea
    orthopnea
169
Q

signs of pleural effusion

A
  • decreased breath sounds
  • dull percussion
  • decreased tactile vocal fremitus- only increased in inflammed or denser lung TISSUE! (pneumonia)- decreased with air or fluid in lungs/pleura (eg asthma, COPD, effusions)
  • tracheal deviation away from effusion
  • blurring of costophrenic angle on CXR when standing
170
Q

Ix for ?pleural effusion

A

CXR
thoracenesis
- transudative- translucent (less protein)
- Exudative- Cloudy (immune cells, protein)
- lymphatic- milky (fats)

171
Q

What criteria do you use for analysing aspirated fluid following thoracentesis

A

Light criteria

NB-

  • EXudative means proteins EXit the capillaries into pleural space (leaky)– fluid/serum protein >=0.5= exudative (increased proteins in fluid)
  • TRANSudative is just increase pressure/decrease oncotic, so things that already wouldve gone across TRANSfer across– fluid/serum protein <0.5– transudative (less proteins in fluid)

Fluid Lact dehydrogenase/serum LD (protein)

  • > =0.6= exudative
  • <0.6- transudative

LDH

  • > 2/3 of upper limit of normal serum LDH- exudative
  • <2/3 of upper limit of normal serum LDH- transudative
172
Q

tx of pleural effusion

A

HF (transudative)- loop diuretics, Na restriction

Pneumonia/TB (exudative)- removal by surgery as fluid can thicken and form empyema

large effusion- thoracentesis drainage

173
Q

Causes of pulm HTN

A

Grade 1 -idiopathic

Grade 2- LH disease

  • valvular heart disease
  • restrictive cardiopmyopathy
  • HF

Grade 3- lung disease/environmental hypoxemia

  • COPD
  • interstitial
  • sarcoidosis
  • vasculitis
  • pulm venous occlusive disease

Grade 4- chronic thrombotic disease/embolic
- PE

Grade 5- metabolic disorders/systemic disorder/haem/other misc disorders

  • thyroid disease
  • chronic renal failure
  • hepatitis–> portal HTN
  • drugs, toxins
  • congenital
  • haem: HIV, myeloproliferative, splenectomy
  • tumour obstruction in venous/arterial system
174
Q

what is pulm hypertension

A
  • HTN in ateries in the lungs and right side of heart
175
Q

sx of pulm HTN

A
  • 0SOB- orthopnea, PND in venous HTN
  • oedema
  • cyanosis
  • *chest pain , palpitations, fainting, lightheadedness
  • poor appetite, fatigue
  • *- R abdo pain
  • haemoptysis
176
Q

signs of Pulm HTN

A

tachycardia
cyanosis
peripheral oedema
3rd heart sounds- inflow of large volume of blood into LV in early diastole, best heard at apex and when pt leans to L

parastenal heaves due to R atrial hypertrophy

RSHF

  • jugular venous distension
  • ascites
  • hepatojugular reflux

RS valve dysfunctions due to large volume of blood in pulmonary arteries:

tricuspid regurg (RA->RV)

  • high pitched
  • holosytolic (all of sytsole)
  • L lower sternal border (5th ICS)
  • intensity increases on inspiration

pulmonic regurg (RV-> pulm arts)

  • early diastolic murmur
  • high pitched
  • decrescendo
  • L upper sternal border
  • louder pt holds breath at end- exp and sits upright
177
Q

Ix for ?pulm HTN

A

Echo

  • pulm/tricuspid regurg
  • RA hypertorphy
  • RSHF
  • **CT
  • enlarged pulmonary trunk
  • calcification pulm arteries
  • CXR
  • ABG
  • pulm function
  • *- RH catheterisation
178
Q

tx of pulm HTN

A

tx underlying cause
- pulm endarterectomy- remove clots

  • replace, repair RSH valves
  • Anticoags- warfarin, NOACs, heparin, if caused by clot
  • O2 if due to hypoxia/lung disease
Meds
- diuretics
- digoxin for tachycardia, inotrop
Vasodilation:
- CCBs- eg amlodipine
- Prostaglandins (prostacyclin, iloprost nebs)- also prevent platelets aggregation
- Endothelin
- sildenafil
  • angioplasty
  • atrial septostomy- hole made to reduce pressure in RSH
  • lung/heart transplant
179
Q

what is pulm oedema

A

fluid build up in lung interstium

- decreased gaseous exchange–> hypoxia

180
Q

Causes of pulmonary oedema

A

Cardiogenic

  • LSHF
  • severe systemic HTN
Non-cardiogenic-
Reduced oncotic pressure (less proteins):
  - malnutrition
  - liver failure
  - nephrotic syndrome
ARDS: damage to pulmonary caps or alveoli- inflammation- cap permeability
   - pulm infection
   - inhalation of toxic substances
   - chest trauma
   - sepsis
181
Q

sx pulm oedema

A
  • Severe SOB

* ****- orthopnea due to LSHF (increased congestion when lying down)

182
Q

ix for ?pulm oedema

A

CXR

CT- fluid in interstitial space

183
Q

tx pulm oedema

A
  • O2
  • *- cardiogenic- antiHTN, betablockers, ivadradine, digoxin
  • *- antiinflams: diclofenac, high dose aspirin
  • loop diuretics if LVHF (furosemide)
  • tx liver failure, nephrotic syndrome, malnutrition
184
Q

What species of mycobacterium are there

A

Tuberculosis
africanum
bovis
microti

185
Q

where has high prevalence of TB

A

South asia- india, pakistan, indonesia, bangladesh

Sub saharan africa

Russia

China

South america

186
Q

stages of TB infection

A

primary

  • mild flu like sx/asymptomatic
  • granuloma and caseous necrosis- gohn focus
  • spread to hilar lymph nodes
  • bacteria may be eliminated

Secondary

  • fever, night sweats, malaise, wt loss, haempotysis, chest pain, SOB
  • gohn focus activated
  • upper lobe spread
  • cavities form
  • bronchopneumonia
  • solid necrosis
  • systemic TB
187
Q

Systemic TB locations

A
  • kidneys (sterile pyuria), loin pain, dysuria

Meninges

Lumbar vertebrae

Adrenals- Addisons (low cortisol, aldosterone- fatigue, wt loss, low mood, loss of appetite, increased thirst)

Liver- heaptitis, RUQ pain, jaundice

Cervical lymph nodes-neck

  • skin- erythema nodosum- red, lumpy rash
188
Q

Ix ?TB

A
  • Montoux./uberculin skin test
  • INterferon gama release assay (blood)
  • CXR
  • Sputum/bronchoalveolar lavage samples- Zhiel Neelson, PCR, culture
189
Q

tx TB

A

Latent

  • isoniazid 9m
  • rifampicin and isoniazid for 3m
Active
Rifamicin- 6m
Isonizaid- 6m
Pyrazinamide- 1st 2 months
Ethambutol- 1st 2m

will be infective 2-3w into course

CNS involved- Rid and ison for 10m instead of 6m
TB in brain/pericardium - give pred to reduce swelling

190
Q

SE of TB meds

A

Rifampicin- red/orange excretions

Isoniazid- Peripheral neuropathy

Pyrazinamide- hepatitis

Ethambutol- optic neuritis (diplopia, hemianopia)

191
Q

what drug do you give for prophylaxis for close contacts of TB

A

isoniazid

192
Q

causative organism in pt with bronchial breath sounds and productive cough who suffered from flu recently

A

S.aureus causes pneumonia following influenza

193
Q

most likley causative organism of pneumonia in COPD pt

A

HiB

194
Q

sx legionnaire’s disease

A

flu like
dry cought
confusion

195
Q

signs of legionnaires

A

lymphopenia
hyponatraemia
deranged LFTs
pleural effusion

196
Q

transmission of legionella

A

warm stagnant water- water tanks

197
Q

diagnosis of legionnaire’s disease

A

urinary antigen

198
Q

tx of legionnaire’s

A

erythro/clarithro

199
Q

sx and signs mycoplasma pneumonia

A

similar to legionnella:

  • flu like
  • dry cough
  • **- deranged LFTs
But also has:
peri/myocarditis- chets pain
**haemolysis- jaundice
**ITP- bruising/bleeding
**erythema multiforme- targetoid lesions/rash
200
Q

diagnosis of mycoplasma pneumonia

A 
serology/culture/PCR of:
polymerase chain reaction of 
- nasopharyngeal swab
- aspirate (lavage)
- sputum
201
Q

tx mycoplasma pneumonia

A

macrolide- erythro

202
Q

atypical pneumonia typically seen in alcoholics

A

klebsiella

Finals (15 decks)

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