Resp Flashcards
1
Q
types of pneumothorax
A
primary spontaneous
- tall, thin males
- no history of lung disease
- family history, marfans, smoking
secondary spontaneous
- due to underlying lung disease
- most commonly COPD
- also
- > TB
- > pneumocystis jerovecii
- > cystic fibrosis
traumatic
- penetrating or blunt chest trauma
- iatrogenic
tension
-complication of any of above
2
Q
tension pneumothorax
A
- occurs when pleural pressure exceeds atmospheric during inspiration and expiration
- forms one way valve
- > air can enter pleural space with inspiration
- > less can exit with expiration
- increasing pressure compresses veins
- > reduced venous return
- > decreased CO and hypotension
- compression of lung tissue
- > resp failure
3
Q
hx and exam pneumothorax
A
hx
- dyspnoea
- pleuritic chest pain
- > usually ipsilateral
- spontaneous often occurs at rest
- > can recount it occuring
- risk factors
- tension
- > distressed
- > severe dyspnoea
exam
- typical
- > increased work of breathing
- > decreased chest expansion
- > ipsilateral hyperinflation with intercostal widening
- > tracheal deviation to contralateral
- > hyper-resonate to percussion
- > decreased breath sounds ipsilateral
- > subcut emphysema
- tension
- > cyanosis
- > decreased GSC
- > diaphoresis
- > hypotension
- > tachycardia
4
Q
ddx pneumothorax
A
EMPTIED
- embolus
- musculoskeletal
- pericarditis
- tamponade (haemopericardium)
- infarct
- effusion (eg haemothorax)
- dissection
5
Q
investigations pneumothorax
A
ABG
-resp alkalosis
ECG
FBC
trops
d-dimer
CXR
- visceral pleural line
- simple
- > no mediastinum shift
- tension
- > mediastinum and tracheal shift to contra
- > flaying of ribs
- > flattening diaphragm
consider
- ultrasound
- > in trauma
- > absence of lung sliding
- CT
- > in occult
- > more sensitive than CXR
6
Q
PE investigations
A
ECG -non specific changes (RV strain) ABG -hypoxia -alkalosis, hypocapnea
D-dimer Troponin -can be elevated (RV strain) FBC -leukocytosis EUC -contrast ESR LFTs Coags -INR and aPTT (anti-coagulation) bHCG -pregnant female (thrombolysis)
CXR -hamptoms hump -westermarks sign CTPA V/Q scan Compression U/S leg (proximal/whole)
7
Q
PE investigation pathway
A
Pretest probability
- Well’s PE
- Geneva
Score interpretation
- low=<2
- intermediate=2-6
- high=>6
PERC rule
-8 criteria to identify patients with low probability of PE where risk of testing outweighs risk of PE
Low
- fulfil 8 PERC criteria = no testing needed
- doesn’t fulfil all 8 = D-Dimer
- D-Dimer >500ng/mL = CTPA
- D-Dimer <500ng/mL = no further testing needed
Intermediate
- D-Dimer <500ng/mL = no testing (unless frail)
- D-Dimer >500ng/mL = CTPA
High
- negative D-dimer cannot rule out (5% risk)
- CTPA
8
Q
indications for intubation
A
Airway patency?
- decreased level of conscious –> loss of protective resp reflexes
- PEF
Oxygenation/ventilation (respiratory failure)
- worsening hypoxia/hypercapnea
- RR>40
Clinical
- work of breathing
- exhaustion
- cyanosis
Expectation of need for intubation
- senior clinician expects deterioration
- need for transport out of ED
Non responsive to NIPPV
9
Q
investigations acute asthma
A
Pulse oximetry ABG PEF -normal = >80% -severe = <60% ECG
FBC EUC LFTs Trops NT- BNP/BNP D-Dimer
CXR
Consider
- CT chest (foreign body if non-opaque)
- tryptase (anaphylasis)
- spirometry (once stable)
- > safety to discharge (%FEV1)
- > useful in follow up
10
Q
ddx asthma
A
Immediately Page FACEM
- infection (pneumonia)
- pneumothorax
- foreign body
- Anaphylaxis
- COPD exacerbation
- Embolism
- MI (APO)
11
Q
asthma pathophys
A
Most commonly IgE mediated hypersensitivity
Airway inflammation
- mast cell activation central
- > sensitisation to allergen
- > degranulation of pulmonary mast cells with further exposure
- early phase
- > release of preformed mediators (eg. histamine)
- > production of eicosanoids (eg. PGD2, cysteinyl LTs)
- > direct stimulation of airway smooth muscle
- > mucous production
- > stimulation of neural reflex pathways (release of ACh)
- late phase
- > influx of inflammatory cells (basophils, eosinophils neutrophils, T helper cells)
- > release of cytokines activates smooth muscle
- > bronchoconstriction
Airway obstruction
- can be regional or global
- large and small airways involved
- initially obstruction -> air trapping and hyperinflation
- > predominately due to bronchoconstriction
- > oedema and thickening of airway wall
- > airway plugging with mucous and cellular debris
Airway remodelling
- irreversible structural change superimposed on effects of inflammation and bronchoconstriction
- histopath
- > loss of normal pseudostratified epithelium
- > increase in goblet cells
- > fibrosis and thickening of reticular layer of basement membrane
- > increased myofibroblasts
- > increased vascularity
- > increased smooth muscle mass and ECM
Bronchial hyper-responsiveness
- decrease in FEV1 20% with challenge (eg. histamine)
- alteration in smooth muscle function/mass
- enhanced sensitivity of neural pathways
- remodelling and structural abnormalities (eg. loss of airway parenchymal interdependence)
- > tethering forces maintaining patency
Additional histo
- Curschmann spirals
- > spiral of mucous plugs from subepithelial glands
- Charcot leyden crystals
- > eosinophilic binding protein in sputum
12
Q
Pathophys pneumonia
A
Gain access to lower respiratory tract
- aspiration from oropharynx most common
- > microaspiration normal, particularly in elderly
- > increased risk with decreased LOC
- > intubation
- > dysphagia/motility disorders
- haematogenous spread
- > eg. tricuspid IE
- local spread
- > pleural or mediastinum
Overcome mechanical factors
- gag and cough reflex
- > bypassed with intubation
- > decreased LOC
- > neuromusculuar dysfunction (eg. stroke)
- hairs and turbinates of nares
- > sufficiently small particles
- mucociliary elevator
- > impaired in chronic lung disease (eg. COPD/CF)
- > mucous thinned by influenza
- > chlamydia pneumoniae produce ciliostatic factor
- > mycoplasma pneumoniae shears off cilia
- normal flora crowds out potential pathogens
- > overwhelming inoculum
- > overgrowth of commensals
Evade innate immune system
-alveolar macrophage phagocytosis, destruction, mucociliary elevator or lympthatics
->overwhelming inoculum
->virulence factors (eg. mycobacterium resistant to phagocytes)
-IgA opsonisation
->Strep pneumoniae produce protease that splits IgA
Neutrophil response
-immunocompromise
->diabetes, HIV
-drugs
->anti TNF alpha
13
Q
path pneumonia
A
Pathology
Increased alveolar capillary permeability
-initially oedema (proteinaceous exudate)
->red hepatization (extravasation of RBCs and neutrophils)
->grey hepatization (neutrophils and fibrin deposition with bacterial clearance)
-resolution
->clearance of cell debris and fibrin by macrophage
14
Q
ddx pneumonia
A
BE ACCTIVE
- Bronchiectasis exacerbation
- Exacerbation COPD/Asthma
- Aspiration/foreign body
- Cancer/mets
- CCF
- TB
- ILD
- Viral (bronchitis/influenza)
- Empyaema (eg. IE)
15
Q
CXR pneumonia types
A
Lobar
- > most common strep pneumoniae
- > consolidation of alveolar spaces
- > homogenous opacification of lobe
- > sparing of bronchi -> air bronchogram
Bronchopneumonia (lobular)
- > associated with staph aureus
- > direct inhalation and colonisation of bronchi
- > patchy nodular or reticularnodular
- > asymetrical and bilateral
- > often lung bases
- > does not cross fissures
Atypical
- atypical bacteria, viruses and fungi
- inflammation confined to interstitium and interlobular septa
- patchy reticular pattern
- often involves hilum
- lack of consolidation
Round
- seen only in paediatric
- > lack of pores of Kohn
- rounded opacities
Cavitating
- complication of pneumonia
- radiolucency superimposed on consolidation
Hemorrhagic
16
Q
ddx PE
A
EMPPATHIIC
- exacerbation of COPD/asthma
- musculoskeletal
- pneumothorax
- pericarditis
- aortic dissection
- tamponade
- HTN (pulmonary - chronic emboli)
- infarct (MI)
- infection (pneumonia/bronchitis)
- CCF
DDx for DVT (BITCH Leg)
- bakers cyst (ruptured)
- injury (eg. tear)
- tumour (leading to venous congestion)
- cellulitis
- haematoma
- lymphagitis
17
Q
investigations pneumonia
A
ABG
FBC EUC -risk score LFT -liver failure = poor prognosis ESR -monitor treatment -non specific but high levels supports infection Procalcitonin -non specific -higher levels correlate with bacterial infection
Microbiology: -treatment is usually successful with empiric -diagnosis of causative agent rare -indicated here due to severity/treatment resistance Blood cultures -positive for causative oragnism Sputum culture and gram stain -prior to antibiotics PCR ->faster than bacterial culture ->improves sensitivity/specificity ->can provide information on resistance ->predominately for rapid identification of viral infection
CXR
-PA and lateral
Consider
-bronchoscopy
->bronchoalverolar lavage = 10^4 CFU/mL
->protected specimen brushing = 10^3CFU/mL
-urinary antigen
->once diagnosis has been made, if it can change therapy
->legionella
->strep pneumoniae
Serology for atypicals
->IgM for mycoplasma
->acute and convalescent phase (change in IgG status) for mycoplasma, chlamydophila, coxiella
18
Q
severity score pneumonia
A
Severity
- most sensitive is SMARTCOP
- > indicates mortality risk
- > predicts need for intensive respiratory support and pressor support
- > requires invasive testing and many investigations (eg. CXR)
- CORB
- > predicts need for intensive respiratory support and pressor support
- > Confusion (acute onset)
- > O2 <90%
- > RR >30
- > Blood pressure (SBP <90, DBP <60)
- > score of 2 or more = high risk and need for ICU
19
Q
Admission score pnuemonia
A
CURB 65
- > recommended by british thoracic society and eTG
- > Confusion (acute onset)
- > Uraemia
- > RR >30
- > BP (SBP <90, DBP <60)
- > Age >65
- scores
- > 0-1 = 30 day mortality <3% (outpatient)
- > 2 = 30 day mortality 9% (inpatient)
- 3-5 = 30 day mortality 15-40% (consider ICU)
Also CRB65
PSI no longer used
20
Q
pneumonia complications
A
SARACEN
- Sepsis/septic shock
- ARDS
- Rash (haemophilus: maculopapular, SJS)
- Abscess/empyema
- Cardiac (CCF, MI, arrhythmias)
- Effusion
- Necrotising
21
Q
pathogenesis COPD
A
Oxidative stress
- in a genetically susceptible individual
- chronic smoke exposure
- > great than 10-15 pack year
Protease/antiprotease
- oxidants activate macrophages and epithelial cells
- > release of cytokines and influx of inflamm cells (neutrophils)
- > imbalance of protease/antiprotease
- > elastase from neutrophils, MMP from macrophages
- > degradation products of both activate each other
- > destruction of elastic fibres and ECM
Oxidant/antioxidant
- deactivation of histone deacytelases
- > transcription of proinflammatory genes
- recruitment and activation of CD8 T cells and neutrophils
- > imbalance in oxidant/antioxidant pathways
- > drives inflammation and immune cell activation
Apoptosis and ineffective repair
- chronic inflammation continues long after smoking cessation
- drives apoptosis
- impaired phagocytosis of cellular debris
- > inadequate release of growth factors
- septation and alveologenesis does not appear possible in adult lung
22
Q
pathology COPD
A
Large airways
- chronic inflammation
- > predominantly lymphocytes, macrophages, neutrophils
- > hyeraemia and oedema of mucosa
- hyperplasia and hypertophy of mucous glands
- > trachea, bronchi and bronchioles
- > hypersecretion and mucopurelent sputum
- squamous cell metaplasia
- > carinogenesis
- > impaired mucociliary apparatus
- smooth muscle hypertrophy
Small airways
- Replacement of Clara cells by goblet cells
- > increase mucous secretion and plugging
- > increased surface tension and narrowing
- further obstruction
- > oedema
- > inflammatory infiltrate
- > fibrosis
- airflow obstruction
- > progresses to hyperinflation
Parenchyma (Emphysema)
- perforation and obliteration of gas exchanging spaces
- > coalesce into enlarged airspaces distal to terminal bronchioles
- > respiratory bronchioles, alveolar ducts, alveoli
- different types
- > centrilobular most common, seen in smokers = resp bronchiole
- > panlobular, alpha 1 antitrypsin = everything distal to resp bronchiole
- > distal-lobular = pneumothorax
Vasculature
- chronic hypoxia
- > intimal hyperplasia
- > smooth muscle hypertrophy/plasia
- emphysema
- > loss of capillary bed
- all leads to HTN
23
Q
ddx COPD
A
BATCHED
- Bronchiectasis
- Asthma
- TB
- Constrictive bronchiolitis
- Heart failure
- Esophageal reflux
- Drugs (eg. ACEI)
24
Q
investigations COPD
A
ABG -respiratory failure ->type 1 = PaO2 <60 ->type 2 = hypoxia with PaCO2 >50 -resp acidosis -HCO3 compensation to chronic resp acidosis ->increase 4 mmol/L for every 10mmHg increase in CO2 ECG
FBC -anaemia -WCC EUC -electrolytes -acidosis BNP TSH Glucose -lethargy
CXR
- ddxs
- hyperinflation
- > 6 anterior ribs mid clavicular line
- flattened diaphragm
- increased retrosternal airspace
- attentuation of vascular markings
- bullae
- pulmonary HTN
- > pulmonary artery prominent
- > hilar vascular shadows
- > cardiothoracic ration >0.5
Spirometry
- pre and post bronchodilator
- > obstruction (GOLD criteria) = FEV1/FVC <0.7 post
- no reducibility in COPD
Consider:
- sputum culture/stain
- flow/volume loops
- DLCO
- > emphysema
- body plesthismography
- > hyperinflation vs restriction
- alpha 1 anti trypsin
- > if family hx
25
Q
lights criteria
A
if anyone one of following is present = exudate
- pleural/serum protein >0.5
- pleural/serum LDH >0.6
- pleural LDH >2/3 upper limit normal
26
Q
pleural effusion ddx
A
exudative (PAINTERS)
- pneumonia
- abscess
- infarct
- neoplasia
- TB
- empyema
- rheumatoid pleurisy
- SLE/sarcoid/scleroderma
transudative (CHARM
- CCF/cirrhosis
- hypothyroidism
- albumin
- renal failure
- mets to draining nodes
27
Q
pleural effusion investigations
A
Urinalysis
Glucose
ECG
ABG
FBC EUCs -kidney failure LFTs -cirrhosis CMP Albumin Serum protein CRP LDH BNP/NT BNP
CXR
->ultrasound if positive to localise fluid
Thoracocentesis
-pleural fluid analysis
Consider
- chest CT
- > malignancy and TB
- culture/gram stain (if signs of infection)
- > blood
- > sputum
- > pleural fluid
28
Q
hx and exam PE
A
DVT
-wells criteria
PE Hx
- dyspnoea (and orthopoea)
- pleuritic chest pain
- cough
- wheezing
- haemoptysis
- calf pain
- palpitations
- syncope
PE exam
- tachypnea
- tachycardia
- obstructive shock
- rales
- wheeze
- soft breath sounds
- prominent P2
- elevated JVP
- tender, erythematous, swollen calf
29
Q
post acute care asthma
A
Don’t discharge until
- Spiro FEV1 >60% predicted
- SABA <4 hrly
Hx:
- consider patient context (eg. help at home/time of day)
- psych factors
- risk factors for life threatening (eg. previous ICU)
If discharged:
- > continue oral prednisone 5-10 days
- > start/continue ICS
- > review inhaler technique
- > assess adherence to drug regime
- > identify triggers, discuss avoidance
- > formulate and discuss asthma action plan
- > GP within 2 days
- > consider specialist review
30
Q
spiro asthma
A
FEV1/FVC normal range
- 0.85 for teenager
- minus 0.05 every decade after
FEV1 improvement
- after 4 puffs salbutamol
- after 15 mins
- increase 12% or 200mL
31
Q
asthma control and risk assessment
A
Risk
- asthma flare ups within 12 months
- no action plan
- ED/ICU visits
Good Control:
- daytime symptoms <2 per week
- use SABA <2 per week
- no limitation on ADLs
- no night symptoms
Poor Control:
-absence of above criteria
32
Q
asthma triggers
A
PADDIES
- Pollen
- Animal dander
- Drugs (aspirin, beta blockers)
- Dust/dust mites
- Infection (viral URTI)
- Exercise
- Smoking/smoke/air pollution
33
Q
monitoring asthma
A
Timing
- following flare ups and hospital admissions
- 6 monthly
- opportunistically for non-asthma appointment
Assess
- symptom control
- > Primary care Asthma Control Screening tool
- > frequency reliever medication
- > spirometry annually
- treatment issues
- > inhaler technique (6 monthly)
- > adherence
- > understanding/review of asthma action plan (annually)
- > comorbidities
34
Q
ddx caveatting lesion on CXR
A
CASINO
- Cyst/bullae
- Autoimmune/vasculitis (granulomatosis with polyangitis)
- Septic emboli
- Infarct
- Neoplasia
- Organising pneumonia
35
Q
hx and exam COPD
A
HPC -chronic cough -sputum production ->usually mucoid, purulent during exacerbation ->less than bronchiectasis -dyspnoea ->initially exertional then at rest -wheezing -chest tightness -weight gain or loss -lethargy -ddx ->fever, night sweats, infective symptoms ->coryzal symptoms = post nasal drips ->atopy = asthma PMH -exacerbations -asthma -GORD -comorbid ->lung cancer ->bronchiectasis ->CCF ->anxiety and depression FHx -COPD -alpha 1 anti trypsin -lung cancer Meds -ACEI Social .-impact on ADLs -pack year history -occupational exposure ->dust, smoke etc -travel ->TB
Exam
- appearance
- > can be cyanotic
- > cachexic
- increased work of breathing
- > accessory muscles
- > tripod
- > pursed lips
- barrel chest
- diaphragm
- > harrisons sulcus
- > hoovers sign
- hands
- > nicotine staining
- > asterixis
- auscultation
- > wheeze
- > crepitations
- > reduced air entry
- percussion = hyper-resonate
- heart
- > elevated JVP
- > distant heart sounds
- > hepatomegaly
- > kussmauls sign
36
Q
spiro measures
A
FEV1:
- most important for monitoring progress/severity
- normal
- > 4L man
- > 3L women
- abnormal
- > best if lower 5th percentile
- > below 80% predicted
- COPD
- > normal less than 1-1.5L
FEV1/FVC
- most important for identifying obstruction
- abnormal
- > best is lower 5th percentile
- > less than 0.7
37
Q
flow loops
A
Graph
- flow on Y axis, volume on X
- FEF50/FIF50
- > flow at mid vital capacity for insp/exp
- > normal = <1
- variable intrathoracic obstruction
- > FEF/FIF reduced
- > normal inspiratory curve
- > flattened exp
- variable extrathoracic
- > FEF/FIF increased
- > normal expiratory curve
- > flattened inspiratory
- lower airway obstruction (COPD)
- > scooped out expiratory curve
- > loss of elastic recoil/compliance during effort-independent phase
- restrictive (ILD)
- > sharp rise and fall in expiratory (increased elasticity)
- > decreased vital capacity
- abnormal inspiratory and expiratory
- > normal FEF/FIF
- > tracheal stenosis
- > severe COPD
38
Q
pleural effusion pathophys
A
INCREASED FLUID ENTRY
increased permeability (exudative)
- eg. tumour
- > local release of cytokines such VEGF
- > mast cell release of tryptase
- as protein content is not altered by fluid absorption
- > high protein content
increased pressure (transudative)
- increase sieving of proteins
- > low protein content in fluid
- usually due to elevation in venous pressure
- > systemic for parietal pleura
- > pulmonary for visceral pleura
- cardiogenic
- > increase pulmonary venous pressure
- > increase in bronchial capillary pressure
- > interstitial oedema (interlobular septae and peribronchovascular space)
- > filter across visceral pleura
decrease pleural pressure
- seen in atelectasis
- decreases extravascular hydrostatic force
decrease plasma oncotic pressure
-hypoalbuminaemia
DECREASED FLUID EXIT
lymph exit dependent on…
decreased lymph contractility
- hypothyroidism
- exotoxins
resp motions
-paraylsis
patency
-pleural fibrosis or malignancy
lymphatic or venous verus pleural pressure
- decrease in pleural pressure with atelectasis
- increase in systemic venous
- > eg superior vena cava syndrome
- increase in lymphatic
- > eg. malignancy of draining lymphatics
39
Q
pleural fluid analysis
A
gross observation
- pale straw coloured = transudate
- blood = malignancy or trauma
- milky = chylothorax
lights
- protein
- LDH
transudate
- BNP/NT BNP in pleural fluid
- LFTs
- EUCs/urinalysis
exudate
- cholesterol
- > high in exudative
- triglycerides
- > high in chylothorax
- glucose
- > low in infection/neoplasia/rheumatoid
- pH
- > low in infection
- cell count and differential
- > lymphocytes = ?TB
- > eosinophilia = low in malignancy
- adenosine deaminase
- > TB
40
Q
whooping cough pathophys
A
aetiology
- bordetella pertussis
- > also other bordetella species
pathophys
- spread by aerosol droplets
- > highly infectious
- > 80% of susceptible household contacts with develop clinical disease after sick contact
- adhesins
- > binding to resp epithelium of upper tract and nasopharynx
- tracheal cytotoxin
- > local tissue damage
- > micro aspiration and cough
- pertussis toxin
- > lymphocytosis
- eventually colonisation
- > alveolar macrophages
- > ciliated resp epithelium
- adenylate cyclase
- > evades phagocytosis and immune destruction
- > chronic cough
41
Q
whooping cough clinical stages
A
stage 1: catarrhal
- URTI symptoms
- 1-2 weeks
stage 2: paroxysmal
- usually last 6 weeks
- cough
- > becomes progressively worse then improves within this time
- typical symptoms
- > post tussive emesis
- > inspiratory whoop
stage 3: convalescent
- 2-3 weeks
- cough
- > declining in frequency
- exacerbations
- > common with URTI for many months after
42
Q
investigations whooping cough
A
SpO2/ABG
- > apnea
- > hypoxic encephalopathy
FBC
-lymphocytosis
EUC
-electrolytes with vom
nasopharyngeal
- swab
- > culture
- > fastideous
- > neg culture does not rule out diagnosis
- aspirate
- > PCR
- > high sensitivity and specificity
consider
- serology
- > IgA/IgG
- > only indicates previous infection or immunisation
- CXR
- > pneumonia is complication
- > atelectasis, perihilar infiltrates
43
Q
ddx whooping cough
A
Uncontrolled Apnea GASP
- URTI
- > viral
- Aspiration foreign body
- GORD
- Asthma
- Sinusitis
- > allergic
- > post nasal drip
- Pneumonia
- > CAP
44
Q
ddx haemoptysis
A
CHAIN
- cardiovascular
- > LV failure with mitral stenosis
- > AVM
- haematological
- > coagulopathy
- autoimmune
- > rheumatoid pleurisy
- > wegeners
- infectious
- > bronchitis (most common)
- > bronchiectasis
- > pneumonia
- > TB
- neoplasia
- > primary (mainly SCLC)
- > mets (skin, breast, colon, renal)
- > lymphoma
