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brs round 2 - help me > respiratory > Flashcards

respiratory Flashcards

1
Q

cardinal features of asthma

A

wheeze +/- cough +/- dyspnoea

wheeze = expiratory

persistent symptoms + acute attacks (due to exertion/cold/allergen)

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2
Q

3 key features of asthma

A

atopy/allergen sensitisation

reversible airflow obstruction

airway inflammation
(eosinophilia + type 2 lymphocytes)

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3
Q

general pathophysiology of asthma

A

when well = airway narrowing due to thickened walls from eosinophilia + inflammation

acute attack = everything is exaggerated

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4
Q

why wheezing

A

normal airway = laminar flow

narrow airway = turbulent flow = wheeze

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5
Q

how does asthma show on a flow volume loop

A

Below x-axis: inspiratory = normal

Above x-axis: expiratory = reduced

improved after bronchodilators given

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6
Q

FEV1/FVC ratio in asthma

A

< 0.7 in adults
< 0.8 in children

(but must also look at pattern + if improved with bronchodilators)

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7
Q

what does a fixed (non-reversible) obstruction suggest

A

lung tumor

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8
Q

allergic asthma pathophysiology

A

healthy airway wall exposed to precipitant e.g. allergen

allergen binds dendritic cell in airway (APC)

DC presents allergen to CD4 t-cell via MHC2

CD4 differentiates to type 2 T-helper cell which releases IL4, IL5 and IL13

inflammation

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9
Q

what do IL4, 5 and 13 do

A

IL4: cause B-cells to produce IgE

IL13: stimulate mucous production from mucous cells

IL5: stimulate eosinophils (histamine release, GFs, chemokines, cytokines)

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10
Q

how do genetics play in asthma

A

multi-gene

genetic susceptibility + environment

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11
Q

tests for allergen sensitisation

A

skin prick test to common allergens
specific IgE antibodies to allergens in blood

eosinophils - bronchoscopy + sample taken (broncho-alveolar lavage) + microscopy

induced sputum eosinophil count

blood eosinophilia

exhaled nitric oxide

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12
Q

what is fraction of exhaled nitric oxide

A

non-invasive biomarker of airway inflammation

indirectly shows type-2 eosinophilic airway inflammation

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13
Q

what 3 things does FENO help with

A

diagnosis
predict steroid responsiveness
assess adherence to inhaled corticosteroids

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14
Q

how to test for the cardinal features of asthma

A

airway obstruction = spirometry = low FEV1/FVC ratio

reversible obstruction = spirometry + bronchodilator reversibility

exhaled NO

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15
Q

basic management of asthma

A

reduce long-term airway inflammation = ICS or leukocyte receptor agonists

acute symptomatic relief = smooth muscle relaxation via B-2 agonists + anticholinergic therapies

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16
Q

how do corticosteroids reduce inflammation

A

reduce numbers of eosinophils, mast cells and dendritic cells

reduce cytokine production from macrophages + t-cells

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17
Q

other functions of ICS

A

epithelial cells - reduce cytokine + mediator production

endothelium - reduce leakage

airway smooth muscle - increase b2 receptors + reduce cytokines

mucous glands - reduce secretion

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18
Q

why reduced antiviral response in asthma

A

low interferon-alpha, beta and gamma
increased viral replication = prolonged illness

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18
Q

how to make patients adhere to ICS better

A

SMART inhalers - Single inhaler Maintenance And Reliever Therapy (bronchodilator AND ICS)

use optimal device with a clear plain

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19
Q

how to treat severe asthma

A

biologics targeting IgE
biologics targeting airway eosinophils (IL5, 4,13)

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20
Q

anti IgE antibody therapy

A

humanised IgE monoclonal antibody
OMALIZUMAB
binds + captures circulating IgE = less around to cause inflammation

(unknown if preventative + £££)

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21
Q

anti-IL5 antibody therapy

A

MEPOLIZUMAB

(IL5 promotes eosinophil recruitment + increases survival)

treat severe eosinophilic asthma

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22
Q

anti-IL4/13 therapy

A

DUPILUMAB

anti-IL4-R-alpha

receptor that binds both IL 4 and 13

attacks rec + increases lung function

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23
Q

what is restrictive lung disease

A

low lung volume where expansion is restricted by intrinsic or extrinsic lung disease

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24
Q

intrinsic vs extrinsic lung disease

A

intrinsic = altered lung parenchyma e.g. interstitial (ILD)

extrinsic = compression of lungs + limited expansion

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25
Q

important cellular regions of lung parenchyma

A

alveolar type 1: gas exchange surface

alveolar type 2: stem cell + produce surfactant to decrease surface tension

fibroblasts: produce ECM e.g. type 1 collagen

macrophage: phagocytose foreign material + make surfactant

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26
Q

what is the interstitial space

A

space between alveoli + capillary endothelium

contains lymphatic vessels, fibroblasts + ECM

very thin to accommodate gas exchange

structural support of lung

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27
Q

5 causes of interstitial lung disease

A

idiopathic - e.g. idiopathic pulmonary fibrosis
autoimmune related - e.g. CTD - SSC/RA
exposure related - e.g. hypersensitivity pneumonitis
cysts and airspace filling
sarcoidosis

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28
Q

history of ILD

A

progressive breathlessness
non-productive dry cough
limited exercise tolerance

CTD symptoms
occupational/exposure history
medications
FHx (20% idiopathic)

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29
Q

clinical examination of ILD

A

low O2 sats (lower on exertion)
fine, bilateral inspiratory crackles at bases
may have digital clubbing

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30
Q

investigations for ILD

A

blood test - AI
pulmonary function test
6 minute walk test (O2 drop on exertion)
HRCT

invasive - bronchoalveolar lavage or surgical lung biopsy

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31
Q

lung pathophysiology in ILD

A

scarring = stiff lungs = less compliant
decreased lung volume
decreased FVC (BUT NORMAL FEV1/FVC RATIO)
reduced diffusing capacity of lung
reduced arterial PO2 especially with exercise

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32
Q

3 patterns seen on lung CT in ILD

A

UIP - usual interstitial pneumonia
NSIP - non-specific interstitial pneumonia
organising pneumonia

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33
Q

UIP view

A

seen in IPF (idiopathic pulmonary fibrosis)

honeycomb appearance
mainly at sides + bases = progresses towards middle

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34
Q

NSIP + OP view

A

ground glass change = immune cells fill airways
subpleural sparing - (in centre more than sides)

OP has consolidation

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35
Q

how to manage early ILD

A

pharmacological therapy - immunosuppressive drugs + anti-fibrotics
clinical trials
patient education
vaccinations
smoking cessation
treat co-morbidities
pulmonary rehab

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36
Q

co-morbidities with ILD

A

sleep apnoea
acid reflux
pulmonary hypertension

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37
Q

managing late ILD

A

supplement O2
lung transplant
palliative care

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38
Q

what is idiopathic pulmonary fibrosis

A

progressively scarring lung disease
in old, caucasian, male

patients decline at different rates
some patients have acute exacerbations - deadly

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39
Q

predisposing factors to IPF

A

genetic susceptibility (MUC5B, DSP)

environmental triggers (smoke, virus, pollutant)

cellular ageing (telomere attrition = shorter telomeres = cells age quicker)

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40
Q

mechanism of IPF

A

injury
alveolar/epithelial dysfunction
macrophage involvement - profibrotic
aberrant fibroblast activity = increased ECM
alveolar remodelling - less good at exchange

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41
Q

histopathology of IPF

A

normal: low ECM + high cells

progress to UIP (honeycomb cysts)

fibroblastic foci - proliferative fibroblasts or myofibroblasts = indicative of active disease

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42
Q

what is hypersensitivity pneumonitis

A

immune mediated response to people who are sucseptible + sensitised to an inhaled environmental trigger

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43
Q

2 key features of HP

A

involves both genetic and host factors (only some people exposed get HP)

involves small airways and parenchyma

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44
Q

classification of HP

A

acute = intermittent + high level exposure
(abrupt symptom onset, flu-like syndrome, short time after exposure)

chronic = long term + low level exposure
(non-fibrotic progressing to fibrotic)

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45
Q

epidemiology of HP

A

m=f
less frequent in smokers
affected by env you live in

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46
Q

pathophysiology of HP

A

antigen exposure + processing by innate IS
inflammatory response by cells = IgE antibodies
accumulation of lymphocytes + granuloma formation

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47
Q

triggers of HP

A

birds - esp African grey parrot droppings
bacteria
fungi
animal/plant protein

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48
Q

HP diagnosis

A

exposure history

inspiratory squeaks on auscultation (co-exisiting bronchiolitis)

specific IgG antibodies to potential antigens

HRCT changes

high lymphocyte count in bronchoalveolar lavage

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49
Q

HRCT changes in hypersensitivity pneumonitis

A

ground glass change
mosaic attenuation pattern
3 density pattern
air-trapping (narrowing of small airways)

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50
Q

HP treatment

A

complete antigen removal or avoidance

corticosteroids - not rec

immunosuppressants - no evidence
(MMF/azathioprine)

progressive + fibrotic = antifibrotics e.g. nintedanib

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51
Q

what is systemic sclerosis

A

ai diseases that involve the hardening and tightening of the skin

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52
Q

what auto-abs to test for in SSC

A

anti-centromeres
anti-SCL70

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53
Q

clinical features of systemic sclerosis

A

sclerodactyly
telengiectasis
abnormal nailfold capillaroscopy
raynauds
digital ulcers

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54
Q

2 types of SSC

A

limited cutaneous - pulmonary hypertension = more common

diffuse cutaneous - ILD more common

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55
Q

pathogenesis of SSC-ILD

A

tissue injury
vascular injury
inflammation
autoimmunity

(ALL DRIVE FIBROSIS)

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56
Q

what connective tissue disorders can lead to ILD

A

SSC
RA

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57
Q

HRCT for SSC vs RA

A

SSC: NSIP w/ ground glass change + subpleural sparing

RA: UIP

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57
Q

management of ssc-ild

A

determined by extent seen on HRCT + lung function trajectory

corticosteroids (pose renal crisis risk)
immunosuppressives

progressive fibrosis = anti-fibrotics e.g. nintedanib

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57
Q

examples of immunosuppressives used in SSC-ILD

A

cyclophosphamide
mycophenolate mofetil (MMF)

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58
Q

causes of lung cancer

A

smoking
asbestos exposure
radon exposure
indoor cooking fumes
chronic respiratory diseases (COPD/fibrosis)
air pollution
familial/genetic

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59
Q

pathogenesis of LC

A

interaction between inhaled carcinogens + upper/lower airway epithelium

formation of DNA adducts (pieces of DNA bound to cancer causing chemical)

persistent adducts = mutation + genomic alterations

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60
Q

2 main types of lung cancer

A

non-small cell lung cancer
(SCC, ADC, LCLC)

small cell lung cancer

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61
Q

squamous cell carcinoma

A

centrally located
bronchal epithelium

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62
Q

adenocarcinoma

A

peripherally located
mucous producing glandular tissue

cause: low tar cigarettes = more + deeper breaths

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63
Q

large cell lung cancer

A

heterogenous + poorly differentiated = poor prognosis

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64
Q

small cell lung cancer

A

pulmonary neuroendocrine cells
highly malignant

v-bad prognosis but if caught early, chemo can help

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65
Q

what are the important oncogenes that treatments target

A

EGFR (epidermal growth factor receptor) tyrosine kinase
ALK (anaplastic lymphoma kinase) tyrosine kinase
cROS-1 (cROS oncogene 1) receptor kinase
BRAF (cell signalling mediator)

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66
Q

EGFR

A

epidermal growth factor receptor tyrosine kinase

target in adenocarcinoma
mainly in women, asian + non-smokers

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67
Q

ALK

A

anaplastic lymphoma kinase tyrosine kinase

non-small cell lung cancer
mainly in young + non-smokers

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68
Q

cROS-1

A

cROS oncogene 1 receptor kinase

non small cell lung cancer
mainly in young + non-smokers

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69
Q

BRAF

A

BRAF cell signalling mediator

non small cell lung cancer
mainly in smokers

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70
Q

symptoms of lung cancer

A

Persistant cough
Weight loss
Breathlessness
Fatigue
Chest pain: can be shoulder/arm/back
Haemoptysis

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71
Q

why is lung cancer detected so late

A

lungs are big = less volume of pain receptors so often asymptomatic

when presents late - presents with metastasis e.g. seizures, spinal cord compression, bone pain, paraneoplastic syndrome

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72
Q

symptoms of paraneoplastic syndrome

A

clubbing
hypercalaemia
hyponatraemia
cushings

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73
Q

signs of late stage lung cancer

A

clubbing
cachexia

pembertons sign: arms raised = red face - due to superior vena cava obstruction

horners syndrome: contracted pupil + droopy eyelid

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74
Q

what is the general diagnostic strategy for lung cancer

A

1 - establish most likely diagnosis
2 - establish fitness for investigation or treatment
3 - confirm diagnosis + histology (genomic testing if considering systemic treatment)
4 - confirm staging

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75
Q

methods of investigation of lung cancer

A

CXR (mass + pleural effusion)

CT (high res - small tumours + mets to liver/LNs)

PET-CT (useful to exclude occult mets)

biopsy (bronchoscopy, EBUS-TBNA, CT guided lung biopsy)

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76
Q

bronchoscopy

A

for tumours of central + segmental airways
useful for pre-surgery to see where the tumour is

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77
Q

EBUS-TBNA

A

endo-bronchial ultrasound + transbronchial-needle aspiration of mediastinal lymph nodes

if LN involvement
stage mediastinum +/- achieve tissue diagnosis

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78
Q

CT-guided lung biopsy

A

CT scan to mark where tumour is

anaesthetic - use needle to biopsy at spot of tumour to assess peripheral lung tumours

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79
Q

TNM staging

A

tumour (1-4)
nodes (0-3)
metastasis (0-1c)

N = stage 2, M = stage 4

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80
Q

what determines treatment

A

patient fitness
cancer histology
staging
patient preference
health service factors

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81
Q

what determines patient fitness

A

WHO performance status
0 = asymptomatic (live as normal)
1 = symptomatic - can still do light work
2 = symptomatic - active up to 50% of day
3 = symptomatic + sometimes confined to chair
4 = completely disabled - no self care
5 = dead

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82
Q

what levels of WHO performance status do you treat

A

radical therapy restricted to PS 0-2

(co-morbidities + lung function also important)

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83
Q

LC treatment: surgery

A

surgical resection in early stages

involves both lobectomy + lymphadenectomy
(stage 1 = sublobar resection)

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84
Q

types of LC surgery

A

wedge resection
segmental resection
lobectomy
pneumonectomy (whole lung)

(smallest to largest)

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85
Q

why is a wedge resection often bad

A

not useful as you cant guarantee you’ve cleared microscopic resection margins

86
Q

how to treat a lung cancer patient unfit for surgery

A

radical radiotherapy

STEREOTACTIC ABLATIVE BODY THERAPY (SABR)

high precision targeting using multiple convergent beams

87
Q

why higher recurrence in SABR than surgery

A

SBAR doesn’t target lymph nodes = possible mets

88
Q

stage 4 LC treatments + what they’re used for

A

oncogene directed - metastatic NSCLC WITH mutation

immunotherapy - metastatic NSCLC with NO mutation + PDL>50%

cytotoxic chemotherapy - metastatic NSCLC with NO mutation + PDL <50%

89
Q

oncogene directed therapy for LC
(target, type of cancer, toleration/SE)

A

targets EGFR, ALK, ROS-1
to treat metastatic NSCLC with mutation - first line for driver mutations

well tolerated tablets but can have rash, diarrhoea + sometimes pneumonitis

90
Q

immunotherapy for LC
(target, type of cancer, toleration/SE)

A

blocks PD-L1/PD-1 binding

(PDL-1 on tumour cell + PD-1 on T-cell bind to stop killing of tumour cell - blocks = kills tumour cell)

for metastatic NSCLC without mutation + high PDL

well tolerated but can cause immune related disease (e.g. thyroid, skin, bowels etc)

91
Q

cytotoxic chemotherapy for LC
(target, type of cancer, toleration/SE)

A

targets rapidly dividing cells
not helpful alone - requires immunotherapy e.g. pembrolizumab

metastatic NSCLC with no mutation + low PDL

fatigue, nausea, BM suppression, nephrotoxicity

92
Q

what does palliative care for LC consist of

A

symptom control
psychological support
education
practical support
financial support
plans for EOL care

93
Q

factors affecting exercise capacity

A

neurological - motor control/coordination
respiratory - ability to ventilate, pulmonary perfusion, gas exchange
cardiovascular - heart’s ability to receive + pump blood
muscular - local perfusion + muscle cell enzymes

94
Q

what does the cardiopulmonary test entail

A

uses cycle ergometer/treadmill
intensity = incremental
close clinical supervision + controlled environment

95
Q

cardiopulmonary test outputs

A

nine-panel chart - relationship between key measured + derived variables

Main: peak VO2 (O2 consumption)
ECG
Ventilation
O2, CO2

96
Q

advantages of cardiopulmonary test

A

quantifies performance in relation to metabolism
precise and reproducible
continuous monitoring for safety

97
Q

disadvantages of cardiopulmonary test

A

skilled technical support e.g. calibration
expensive - initial + ongoing costs
needs dedicated space

98
Q

what does the 6 minute walk test entail

A

20-30m flat course e.g. corridor
objective - cover biggest distance in 6 minutes

externally timed by assessor
sub-maximal test

99
Q

whats a sub-maximal test

A

evaluates adaptation of oxygen transport to exercise below the max intensity, so main energy system being used and therefore monitored is aerobic

100
Q

outputs for 6 minute walk test

A

main: total distance walked in 6 minutes
‘perceived exertion’ scales
heart rate
pulse oximetry

101
Q

advantages of 6 minute walk test

A

patient-driven pace - speeding up, slowing down and resting is allowed
cheap to deploy
validated in many clinical populations

102
Q

disadvantages of 6 minute walk test

A

needs significant unobstructed course - often undertaken in a public hospital corridor

pace not re-regulated

103
Q

what does an incremental shuttle walk test entail

A

10m circuit
externally paced by an audio recording e.g. bleep test

each minute has one extra length than the previous minute

104
Q

incremental shuttle walk output

A

main: total distance walked before volitional end
‘Perceived exertion’ scales
Heart rate
Pulse oximetry

105
Q

advantages of incremental shuttle walk test

A

cheap to deploy
validated in many clinical populations

external pacing helps to achieve maximum levels

106
Q

disadvantages of incremental shuttle walk test

A

requires unobstructed course
incremental nature is difficult

ceiling affect of 1020m (measurement limitation that occurs when the highest possible score is reached)

patient penalised for poor pace management

107
Q

signs of upper respiratory tract infection

A

cough
sneezing
runny/stuffy nose
sore throat
headache

108
Q

signs of lower resp tract infection

A

productive cough (phlegm)
muscle aches
wheezing
breathlessness
fever
fatigue

109
Q

signs of pneumonia

A

chest pain
blue tinting of the lips
severe fatigue
high fever

110
Q

bacterial causes of RTI

A

streptococcus pneumoniae
myxoplasma pneumonia
haemophilus influenzae
myobacterium tuberculosis

111
Q

viral causes of RTI

A

influenza A/
respiratory synctial virus
human metapneuovirusm
human rhinovirus
coronaviruses

112
Q

risk factors for bacterial RTI (pneumonia)

A

demographic + lifestyle factors

specific factors for certain pathogens e.g. geography

certain meds

social contact

medical history

113
Q

what medications are a risk factor for developing bacterial RTI

A

inhaled corticosteroids
immunosuppressants e.g. steroids
proton pump inhibitors

114
Q

streptococcus pneuomoniae properties

A

gram +ve, extracellular, opportunitistic pathogen

115
Q

methods of categorising bacterial pneumonias

A

community/hospital acquired/ventilator associated

typical/atypical

116
Q

typical vs atypical pneumonia

A

typical - most common + by common bacteria
(presenting with rapid progression, fever, breathlessness, confusion, decreased movements)

atypical - less frequent + by distinct bacterial species
(slower onset + milder symptoms)

117
Q

examples of bacteria causing typical pneumonia

A

Streptococcus pneumoniae
Haemophilus influenzae
Moraxella catarrhalis

118
Q

examples of bacteria causing atypical pneumonia

A

Mycoplasma pneumoniae
Chlamydia pneumoniae
Legionella pneumophilia

119
Q

treatments for typical vs atypical pneumonia

A

typical = penicillin
atypical = additional macrolides

120
Q

examples of community acquired pneumonia bacteria

A

Streptococcus pneumoniae
Mycoplasma pneumoniae
Staphylococcus aureus
Chlamydia pneumoniae
Haemophilus Influenzae

121
Q

examples of hospital acquired pneumonia bacteria

A

Staphylococcus aureus
Psuedomonas aeruginosa
Klebsiella species
E. coli
Acinetobacter spp.
Enterobacter spp.

122
Q

examples of ventilator associated pneumonia bacteria

A

Psuedomonas aeruginosa
Staphylococcus aureus
Enterobacter

123
Q

how does acute bacterial pneumonia actually cause damage

A

lung injury = arterial hypoxemia = ARDS

bacteraemia = organ infection = organ injury/dysfunction = sepsis

systemic inflammation = organ injury/dysfunction = sepsis

124
Q

bronchitis vs bronchiolitis vs pneumonia

A

bronchitis = inflammation + swelling of bronchi

bronchiolitis = inflammation + swelling of bronchioles

pneumonia = inflammation + swelling of alveoli

125
Q

how to grade bacterial pneumonia

A

CURB-65 - each = 1 point

confusion
urea = (if in hospital) >7mmol/L
resp rate = >30 bpm
BP = < 90 systolic or < 60 diastolic
65 years/+

(0 = home treatment, 1-2 = hospital referral, 3-4 = urgent admission + empirical abs)

126
Q

treatments for bacterial pneumonia

A

supportive therapy = oxygen, fluids, analgesia

other = nebulised saline + chest physiotherapy

antibiotics = penicillins, macrolides

127
Q

what is the key to increasing success of antibiotics

A

time of administration (need to be fast - every hour = less survival)

use an effective antibiotic

combination is better

128
Q

how does penecilin work

A

beta lactams that bind proteins in the bacterial cell wall to prevent transpeptidation

129
Q

how do macrolides work

A

bind to the bacterial ribosome to prevent protein synthesis

130
Q

how do you get bacterial pneumonia

A

many bacteria exist in the oropharynx - inc. strep pneumoniae

commensal = become pathogenic due to change in env e.g. virus or smokw

131
Q

Opportunistic Pathogen

A

microbe that takes advantage of a change in conditions (often immuno-suppression)

132
Q

Pathobiont

A

microbe that is normally commensal, but if found in the wrong environment (e.g. anatomical site) can cause pathology.

133
Q

why viral infections cause diease when theyre not pathobionts

A

cell inflammation
mediator release
local immune memory

damage to epithelium:
(loss of chemoreceptors, poor barrier to antigen, bacterial growth, loss of cillia)

134
Q

what causes severe disease in viruses

A

RNA sequences, viral load, DNA and environment

all lead to:
cell stress, mediator release, epithelial damage, viral spread

135
Q

where do different viruses target (influenza + avian flu)

A

H1N1 influenza A: haemogglutinin binds alpha-2,6 sialic acids in pharynx

H5N1 avian flu:
haemogglutinin binds alpha-2,3 sialic acids in lower tract

(avian flu doesn’t affect humans as doesn’t target pharynx)

136
Q

smokers and SARS-COV2

A

sars-cov 2 has spike protein that targets ACE-2 in nasal epithelium + type 2 pneumocytes

high ACE-2 in smokers

137
Q

how epithelial cells provide first line of defence against respiratory tract infections

A

TIGHT junctions = stop systemic infection

MUCOUS lining and CILIAL clearance

ANTIMICROBIALS - kill microbes

PRR - pathogen recognition receptors

INTERFERON pathways - upreg of antiviral proteins + apoptosis

137
Q

Serotypes

A

pathogens which cannot be recognised by serum (antibodies) that recognise another pathogen

137
Q

viral immunity in the body

A

humoral immunity
(adaptive + dependant on prior exposure)

b-cells activated to differentiate into antibody secreting plasma cells

138
Q

2 types of ab involved in viral immunity

A

IgA: nasal cavity
(epithelial cells = poly IgA receptor - allows export of IgA to mucosal surface)

IgG: in lung
(thin walled alveolar space = easy transfer from circulation)

139
Q

properties of influenza immunity

A

no re-infection by same strain

imperfect vaccines - immunity rapidly wanes, mainly homotypic

140
Q

properties if RSV immunity

A

recurrent re-infection with similar strains

no vaccine as of yet

141
Q

SARS-COV-2 immunity

A

no prior immunity

potential for reinfection - only help dampen symptoms, waning immunity

142
Q

RSV bronchiolitis in children occurence

A

half of the population get it before the age of 1

whole population gets it before the age of 3

143
Q

risk factors for developing severe RSV in an infant

A

premature birth
congenital heart and lung disease

144
Q

symptoms of RSV bronchiolitis in infants

A

nasal flaring

hypoxaemia + cyanosis

croupy cough

expiratory wheezing, prolonged expiration, rales + rhonchi

tachypnea + apneic episodes

chest wall retractions

145
Q

treatment for viral resp tract infections

A

supportive - O2/fluids/analgesia (+ nebulised saline, chest physio)

preventative/prophylactic (vaccines)

therapeutic (anti-inflammatory)

anti-virals

146
Q

types of vaccine targets

A

major surface antigen e.g. spike protein in COVID

viral vetor e.g. adenovirus vaccine

mRNA vaccine

147
Q

anti-inflamm drugs to help treat respiratory viruses

A

Dexamethasone (steroids)

Tocilizumab (anti-IL-6R) or Sarilumab (anti-IL-6)

148
Q

antiviral examples

A

Remdesivir
Paxlovid
Casirivimab and imdevimab

149
Q

Remdesivir

A

broad spectrum antiviral – blocks RNA-dependent RNA polymerase activity

150
Q

Paxlovid

A

antiviral protease inhibitor

151
Q

Casirivimab and imdevimab

A

monoclonal neutralising antibodies for SARS-CoV-2

152
Q

relationship between viral and bacterial respiratory tract infections

A

viral infection = damage to cellular environment = commensal bacteria more likely to become pathogenic

153
Q

examples of how chronic lung diseases can interplay with respiratory tract infections

A

viral bronchitis = associated with asthma

rhinovirus = cause asthma + COPD exacerbations

154
Q

respiratory failure

A

inadequate gas exchange due to dysfunction of one or more components of the respiratory system

155
Q

what components play a role in respiratory failure

A

nervous system (CNS/BS/PNS/NMJ)

respiratory muscles
(diaphragm, thoracic muscles. extra-thoracic muscles)

pulmonary (airways, alveoli, circulation etc)

156
Q

male + female risk factors for respiratory failure - most common

A

male = smoking

female = household air pollution from solid fuels

157
Q

ventilation at top of lung

A

Ppl (pressure in pleural space) = more negative

greater transmural pressure gradient

alveoli larger + less compliant

LESS VENTILATION

158
Q

ventilation at bottom of lung

A

Ppl (pressure in pleural space) = less negative

smaller transmural pressure gradient

alveoli smaller + more compliant

MORE VENTILATION

159
Q

perfusion at top of lung

A

lower intravascular pressure (gravity)

less recruitment

greater resistance

lower flow rate

LOW PERFUSION

160
Q

perfusion at bottom of lung

A

high intravascular pressure

more recruitment

less resistance

higher flow rate

HIGHER PERFUSION

161
Q

3 types of respiratory failure

A

acute
chronic
acute on chronic

162
Q

pulmonary causes of acute respiratory failure

A

infection
aspiration
primary graft dysfunction (following lung transplant)

163
Q

extra-pulmonary causes of acute respiratory failure

A

trauma
pancreatitis
sepsis

164
Q

neuromuscular causes of acute respiratory failure

A

myasthenia gravis

165
Q

pulmonary/airway cause of chronic respiratory failure

A

COPD
lung fibrosis
CF
lobectomy

166
Q

musculoskeletal cause of chronic respiratory failure

A

muscular dystrophy

167
Q

causes of acute on chronic respiratory failure

A

infective exacerbation of COPD/CF
myasthenic crisis
post-op

168
Q

type 1 respiratory failure + PaO2

A

hypoxemic - failure to oxygen exchange

PaO2 > 60 at sea level

169
Q

properties of type 1 RF

A

increased shunt fraction

due to alveolar flooding

hypoxemia not improved by supplemental oxygen

NORMAL CO2

170
Q

causes of type 1 resp failure

A

collapse
aspiration
pulmonary oedema
fibrosis
pulmonary embolism
pulmonary hypertension

171
Q

what is type 2 respiratory failure + PaCO2

A

hypercapnic - failure to exhange/remove CO2

PaCO2 > 45

172
Q

properties of type 2 resp failure

A

decreased alveolar minute ventilation

dead space ventilation

173
Q

causes of type 2 respiratory failure

A

nervous system
neuromuscular
muscle failure
airway obstruction
chest wall deformity

174
Q

what is type 3 respiratory failure

A

peri-operative
during/after surgery

175
Q

what are the properties of type 3 respiratory failure

A

increased atelectasis (part of lungs collapse = less air in)

low FRC (air left in lungs after breathing out = lower than normal)

abnormal abdo wall (muscles not moving properly)

hypercapnia / hypoxemia

176
Q

how to prevent type 3 respiratory failure

A

better anaesthetic/operative techniques
posture
incentive spirometry (encourages deep breaths)
analgesia
attempts to lower intra-abdo pressure

177
Q

what is type 4 respiratory failure

A

occurs when body is in shock (septic, cardiogenic, neurogenic) and patient has been intubated as a result

positive pressure ventilation using a ventilator

178
Q

how shock can cause respiratory failure

A

peripheral pooling of blood → drop in pulmonary perfusion

poor perfusion of lung → gas doesn’t meet blood + cannot transfer across alveolar capillary membrane

179
Q

how to help in type 4 shock

A

optimise ventilation = improves gas exchange + unloads respiratory muscles

lowers O2 consumption

180
Q

how does positive ventilation affect the heart

A

LV: reduced afterload = reduced distress

RV: increased pre-load (as pressure in thorax is higher)

181
Q

causes of SOB leading to acute respiratory failure

A

lower respiratory tract infection (viral/bacterial)

aspiration

trauma - need for transfusion

pulmonary vascular disease (pulmonary embolus/haemoptysis)

extrapulmonary (pancreatitic/new meds)

182
Q

what is sequelae

A

pathological condition resulting from a prior disease, injury, or attack

183
Q

sequelae of acute respiratory distress syndrome

A

poor gas exchange = inadequate oxygenation, poor perfusion, hypercapnia

infection - sepsis

inflammation - inflammatory response

systemic effects
(ARDS patients mainly die from organ failure)

184
Q

process of acute lung injury

A

injury + inflamm = damage tissue between alveoli
macs = activated = sk release (IL-6, 8 + TNF-a)
TNFR-1 signalling pathway also = IL 8/TNF-a

fluid rich proteins collect in lung (oedema)
surfactant breakdown = hard to inflate

inflammation attracts wbcs from BVs to lung tissue = worsens swelling + damage tissue

respiratory failure

185
Q

cells in alveoli

A

alveolar macrophages and type II pneumocytes

type 2 can become type 1

186
Q

what is some evidence that proves the acute lung injury pathway

A

blocking TNFR1 pathway + blocking mac activation or nph migration = REDUCED LUNG INJURY

DAMP (damage associated molecular patterns) release observed e.g. HMGB-1, RAGE

CYTOKINE release observed - IL6, IL8, IL1B, IFN-y

CELL DEATH observed = lung necrosis + apoptotic mediators

187
Q

some ineffective pharmacological therapies for acute lung injury

A

steroids
salbutamol
surfactant
n-acetylcysteine
neutrophil esterase inhibitor
GM-CSF
statins

188
Q

what does the ARDSNET study conclude about ARDS treatment

A

physically increases ventilation to improve exchange but extreme lung expansion causes further injury

189
Q

what does the PROSEVA study conclude about ARDS treatment

A

patients should be placed in prone position as early as possible to improve outcomes

190
Q

what does the FACCT study conclude about ARDS treatment

A

conservative fluid management

fluid restriction in patients may improve lung function but would jeopardise extra pulmonary organ perfusion

191
Q

what are some trial treatments for ARDS

A

mesenchymal stem cells
keratinocyte growth factor
microvesicles
high dose vitamin C, thiamine, steroids (for sepsis)

ECCO2R: extra-corporeal CO2 removal

192
Q

ARDS therapeutic interventions

A

treating underlying disease e.g. antibiotics/antivirals
respiratory support

multiple organ support incl: CVS support, renal assistance, immune support

193
Q

what CVS support can help in ARDS

A

ionotropes
fluid restriction
vasopressors
pulmonary vasodilators

194
Q

how do ionotropes help ARDS

A

e.g. adrenaline → increases forces of contractions

195
Q

how do pulmonary vasodilators help ARDS

A

e.g. NO

improved hypoxemia
lower pulmonary arterial pressure
improved RV function + cardiac output

196
Q

what renal things help in ARDS

A

haemofiltration
haemodialysis

197
Q

how to treat underlying disease in ARDS

A

inhaled therapies: bronchodilators + pulmonary vasodilators

steroids
antibiotics
anti-virals

drugs: pyridostigmine, plasma exchange, IViG, rituximab

198
Q

respiratory support in ARDS

A

physiotherapy
oxygen
nebulisers
high flow oxygen
non-invasive ventilation
mechanical ventilation
extra-corporeal support

199
Q

types of ventilation used for ARDS

A

volume controlled
pressure controlled
assisted breathing modes
advanced ventilatory modes

200
Q

what is compliance

A

amount of lung that opens for the pressure used

ARDS: using more pressure to get the same volume

201
Q

what is the LIP on a PV loop and how is it significant in ARDS

A

lower inflection point

minimum pressure needed for alveolar recruitment

dropping pressure too much below LIP = lot of the lung collapses

202
Q

what is the UIP on a PV loop and how is it significant in ARDS

A

upper inflection point

pressure above which additional alveolar recruitment requires disproportionate increases in applied airway pressure

Above = damages lungs = lung becomes more inflamed = more oedema

203
Q

what is PEEP

A

positive end expiratory pressure

the positive pressure that remains in the airways at the end of exhalation that is greater than the atmospheric pressure

204
Q

intrinsic vs extrinsic PEEP

A

intrinsic = due to incomplete exhalation
(expiratory time < time needed to fully deflate lungs so lung + chest wall cant reach elastic eqbm point)

extrinsic = pressure applied by ventilator

205
Q

why cant you efficiently ventilate a COPD patient

A

Patients with COPD/asthma/high thoracic volume/barrel chest
don’t exhale completely
trapping
increased pressure within lungs
cannot efficiently ventilate patient

low minute ventilation (volume of gas inhaled/exhaled per min) + V/Q mismatch (ventilation without exchange)

206
Q

how to prevent ventilator-induced lung injury in patients with high intrinsic PEEP

A

must set time of exhalation to be long enough to allow full exhalation

avoid very low pressures (lung would have to work much harder)

use driving pressure (difference between peak + plateau pressure)

207
Q

what is lung recruitment

A

temporary airway pressure is increased during mechanical ventilation → opens up the collapsed alveoli → improves oxygenation

208
Q

what is the murray score (factors + what numbers mean)

A

used to grade the severity of lung injury in acute respiratory distress syndrome (ARDS)

considers: PaO2, CXR, PEEP, compliance

0 = normal, 1-2.5 = mild, 2.5+ = severe, 3 = ECMO

209
Q

what is ECMO

A

extracorporeal membrane oxygenation

helps blood get oxygen + gets rid of carbon dioxide when lungs or heart can’t

210
Q

inclusion criteria for ECMO

A

severe respiratory failure with non-cardiac cause (murray lung injury > 3.0)

positive pressure ventilation is not appropriate

211
Q

exclusion criteria for ECMO

A

contraindication to active treatment
significant co-morbidity leading to dependancy
significant life-limiting co-morbidity

212
Q

advantages of ecmo

A

improved O2 delivery
improved CO2 removal
rest lung + prevent ventilator associated lung injury
resolve respiratory acidosis
reduce multiple organ dysfunction

213
Q

issues with ECMO

A

time
referral system logistics
costs
consideration of referral
technical difficulties

214
Q
A

brs round 2 - help me (4 decks)

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