respiratory Flashcards
chronic obstructive pulmonary disease
progressive airway obstruction with little or no reversibility
FEV1 <80%
FEV1/FVC <70%
COPD: chronic bronchitis
epithelial cell layer may ulcerate
when these heal, squamous epithelium may replace columnar
results in chronic cough and phlegm production
‘blue bloaters’
COPD: airway narrowing causes (in chronic bronchitis)
bronchial wall inflammation due to irritants- causes scarring
hypertrophy and hyperplasia of mucus secreting glands of bronchial tree- luminal occlusion
mucosal oedema
COPD: chronic bronchitis characteristics
submucosal bronchial gland enlargement
goblet cell metaplasia and mucus hypersecretion
airway oedema
inflamed bronchial tree
smooth muscle and connective tissue hypertrophy
airway epithelial squamous metaplasia
ciliary dysfunction
COPD: emphysema
dilation and destruction of lung tissue distal to terminal bronchioles
loss of elastic recoil- leads to airflow limitation and air trapping
‘pink puffers’
COPD: emphysema classification
centri-acinar emphysema
pan-acinar emphysema
irregular emphysema
COPD: centri-acinar emphysema
most common
upper lobe
more concentrated around resp bronchioles, more distal alveolar ducts and alveoli tend to be preserved
COPD: pan-acinar emphysema
lower lobe
emphysema affects whole acinus
associated with alpha-1-antitrypsin
COPD: small airway involvement
<2mm
involved early in COPD- obstructive bronchiolitis
major site of airway obstruction
COPD: pulmonary vascular changes
intimal thickening and endothelial destruction
collagen deposition and breakdown of collagen bed architecture
causes pulmonary hypertension and hypoxia
COPD: pink puffers
high alveolar ventilation (compensatory)
near normal PaO2 and normal or low PaCO2
breathless but not cyanosed
can progress to type 1 resp failure
COPD: blue bloaters
low alveolar ventilation, low PaO2 and high PaCO2
cyanosed but not breathless
can develop cor pulmonale
COPD: epidemiology
10-20% >40 y/o
COPD: causes
cigarette smoke alpha-1-antitrypsin cystic fibrosis industrial irritants resp infections- cause exacerbations
COPD: smoking
> 90%
cause mucus gland hypertrophy and inflammation
inactivates major protease inhibitor alpha-1-antitrypsin
COPD: alpha 1 antitrypsin deficiency
cause of early-onset emphysema
tend to have liver disease
low acinar of lungs affected
COPD: risk factors
smoking pollution occupational exposures family history increasing age poor lung development during gestation severe childhood resp infection
COPD: symptoms
cough sputum dyspnoea wheeze lethargy
COPD: signs
tachypnoea use of accessory muscles of respiration hyperinflation- barrel shaped chest wheeze cyanosis ankle swelling- if causes heart failure
COPD: complications
acute exacerbations polycythaemia resp failure cor pulmonale- oedema, raised JVP pneumothorax lung carcinoma
COPD investigations: spirometry
gold standard
obstruction and air trapping
FEV1 <80%
FEV1/FVC <70%
COPD investigations: CXR
hyperinflation
flat hemidiaphragms
large central pulmonary arteries
COPD investigations: FBC
increased PCV/haematocrit
COPD investigations: CT
bronchial wall thickening
scarring
air space enlargement
COPD investigations: ECG
right atrial and ventricular enlargement
COPD investigations: ABG
PaO2 high and normal PaCO2 in pink puffer
PaCO2 high and PaO2 low in blue bloater
COPD: lifestyle management
information and support smoking cessation exercise diet advice flu vaccination
COPD: stage 1 treatment
shot acting bronchodilator when needed (SABA= salbutamol) (SAMA= ipratropium bromide)
COPD: stage 2 treatment
regular LABA (salmeterol) or LAMA (tiotropium)
or LABA +LAMA
add pulmonary rehabilitation
COPD: stage 3 treatment
LABA+LAMA+ICS (budesonid or beclometasone)
COPD: stage 4 treatment
LABA+LAMA+ICS
add long term oxygen if in resp failure
consider surgery
COPD: treatment pathway
nebulised bronchodilators such as salbutamol
oxygen therapy if sats <88%- aim for 88-92
steroids- IV hydrocortisone or oral prednisolone
antibiotics if sign of infection
COPD: treatment for acute exacerbations
mild- short acting bronchodilators
moderate- SABA and antibiotics, maybe oral steroids
severe- hospitalisation
COPD: signs of life threatening resp failure
resp rate >30/min use accessory muscles acute changes in mental status persisting hypoxaemia hypercapnia acidosis
COPD: differentials
congestive heart failure bronchiectasis allergic fibrosing alveolitis pneumoconiosis asbestosis asthma
asthma
reversible chronic obstructive airway disease
hypersensitivity type 1 reaction
characteristics of asthma
airflow limitation
airway hyper-responsiveness
bronchial inflammation
non allergic asthma
intrinsic
exercise, cold air and stress
obesity associated
allergic asthma
atopic/eosinophilic
extrinsic
allergens
asthma: three characteristics that contribute to airway narrowing
bronchial muscle contraction
mucosal swelling/inflammation- mast cell and basophil degranulation
increased mucus production
asthma: immediate pathogenesis, IgE mediated type 1 hypersensitivity
- APC phagocytoses allergen and presents on surface as antigen
- T-helper binds to antigen and releases cytokines which cause B cells to become plasma cells
- Plasma cells release IgE which binds to mast cells
- next time allergen enters body it binds to IgE on mast cell which causes it to degranulate
asthma: immediate pathogenesis, mast cell degranulation
histamine
tryptase
prostaglandin 2
cytokines- TNF-alpha, IL-2/4/5_
asthma: immediate pathogenesis, histamine and cytokines release
cause:
bronchoconstriction
mucus production
inflammation
asthma: long term pathogenesis
airway remodelling:
- repeated airway constriction causes smooth muscle hyperplasia and hypertrophy
- increased goblet cells caused by mucus gland hyperplasia
- thickening of basement membrane
- reduced retractile forces
asthma: epidemiology
5-8% of population
1/11 children
common start is 3-5 y/o
asthma: allergic, genetic causes
atopy triad- asthma, hayfever, eczema
atopy= predisposition toward developing certain allergic hypersensitivity reactions
asthma: allergic, environmental stimuli
hygiene hypotheses= growing up in clean environment may predispose towards IgE response
maternal smoking
childhood exposure to allergens
asthma: non-allergic causes
stress
cold air
infection
asthma: precipitating factors
inflammatory factors irritants smoking/passive smoking drugs- NSAIDs, beta-blockers, ACE-i pollution obesity
asthma: inflammatory factors
infection
allergens- house dust mite, pollen, fur
asthma: irritants
cold air
exercise
emotion
stress
asthma: symptoms
intermittent dyspnoea wheeze cough sputum chest tightness
asthma: signs
tachypnoea audible wheeze hyperinflated chest hyper-resonant percussion decreased air entry
asthma: severe attack
inability to complete sentences
pulse >110bpm
resp rate >25/min
PEF 33-50% predicted
asthma: life-threatening attack
silent chest confusion exhaustion cyanosis bradycardia PEF <33% predicted
asthma: presentation pattern
diurnal variation
worse in morning
night time cough
asthma treatment: lifestyle
stop smoking
avoid allergens
education on good inhaler technique and PEF monitoring
asthma treatment: step 1
occasional SABA for symptom relief e.g salbutamol
if used more than one daily then step 2
asthma treatment: step 2
SABA and inhaled corticosteroids e.g beclometasone
asthma treatment: step 3
SABA +ICS + LABA e.g. salmeterol
if still uncontrolled increase ICS dose
asthma treatment: step 4
high corticosteroids
consider leukotriene receptor agonist/ modified release theophylline/LAMA
asthma treatment: step 5
step 4 + daily oral corticosteroid e.g. prednisolone
refer to asthma clinic
asthma treatment: beta- 2-agonists
selective to lungs
relax bronchial smooth muscle by increase cAMP- causes bronchodilation
asthma treatment: short acting beta agonist
4 hours
salbuatomol
can cause tachyarrhythmias
asthma treatment: long acting beta agonist
12 hours
salmeterol
lipophilic so remain in tissue longer
same S/E as SABA
asthma treatment: corticosteroids
decreased mucosal inflammation
rinse mouth after inhaled to prevent oral candidiasis
asthma treatment: theophylline
inhibits phosphodiesterase, decreasing bronchoconstriction by increasing cAMP levels
asthma treatment: anticholinergics
decrease muscle spasm
e.g. ipratropium (short term) or tiotropium (long term)
asthma treatment: leukotriene receptor antagonist
block effects of cysteinyl leukotrienes in airways
e.g. montelukast
asthma: treatment summary
SABA
SABA+ICS
SABA+ICS+LABA
SABA+LABA+high dose ICS+biological therapy
SABA+LABA+ HD ICS+ BT+ oral corticosteroid
asthma: ABCDE O SHIT ME- acute management
ABCDE checks Oxygen- maintain sats 94-98% Salbutamol nebulised Hydrocortisone IV Ipratropium bromide- 4 to 6 hourly Theophylline- usually in ICU Magnesium sulphate- one off dose if life threatening, before doing theophylline Escalate care- intubation and ventilation
asthma: associated diseases
acid reflux 40-60%
polyarthritis nodosa
churg-strauss syndrome
allergic bronchopulmonary aspergillosis
asthma: differentials
pulmonary oedema COPD large airway obstruction pneumothorax PE bronchiectasis
asthma: distinguishing from COPD
COPD later disease- mainly in smokers
less day to day variation
winter symptoms and sputum production on COPD
overlap can occur
asthma investigations: RCP3 questions
daytime symptoms
effect on daily life
difficulty sleeping from cough
asthma investigations: initial diagnosis
spirometry, FEV1/FVC <70%
reversibility to distinguish from COPD
peak flow diary
asthma investigations: acute attack
PEF sputum culture FBC, U&E, CRP, cultures ABG CXR
chronic asthma investigations
PEF monitoring spirometry CXR skin prick tests to identify allergens histamine challenge aspergillus serology
bronchial carcinoma: small cell
20%, worse prognosis
arise from endocrine cells in central bronchus
often secrete polypeptide hormones in paraneoplastic syndrome
70% are disseminated at presentation
bronchial carcinoma: non small cell
80% squamous cell carcinoma 35% adenocarcinoma 27% large cell carcinoma 10% adenocarcinoma in situ- rare, <1%
bronchial carcinoma: non small cell- squamous cell
most strongly associated lung cancer with smoking
arise from epithelial cells
bronchial carcinoma: non small cell- adenocarcinoma
most common type
most common for non-smokers
arise from mucus-secreting glandular cells
bronchial carcinoma: sites of metastatic spread
liver bone adrenal glands brain pleura and ribs
bronchial carcinoma: epidemiology
second most common cancer in UK
third most common cause of death in UK
more common in men
bronchial carcinoma: cigarette smoke
causes 90% of lung carcinomas
passive smoking also causes carcinomas
bronchial carcinoma: occupational risk factors
asbestos chromium arsenic iron oxides coal, nickel, petroleum
bronchial carcinoma: environmental risk factors
ionising radiation
radon gas
bronchial carcinoma: host risk factors
cystic fibrosis
HIV infection
bronchial carcinoma: symptoms
haemoptysis- red flag cough dyspnoea chest pain weight loss lethargy
bronchial carcinoma: signs
cachexia- weakness/wasting of the body
anaemia
clubbing
supraclavicular or axillary lymph nodes
bronchial carcinoma: chest signs
may be none
consolidation
collapse
pleural effusion
bronchial carcinoma: metastatic signs
bone tenderness
hepatomegaly
bronchial carcinoma: non metastatic skeletal manifestations
clubbing
hypertrophic osteoarthropathy
bronchial carcinoma: non metastatic cutaneous manifestations
dermatomyositis
herpes zoster
acanthosis nigricans
bronchial carcinoma: non metastatic vascular manifestations
thrombophlebitis migrans
anaemia
disseminated intravascular coagulation
bronchial carcinoma: non metastatic neurological manifestations
cerebellar degeneration
myopathy
polyneuropathy
bronchial carcinoma: non metastatic endocrine manifestations
ectopic secretion:
ACTH-cushing’s
ADH- dilutional hyponatraemia
TH- hypercalcaemia
bronchial carcinoma: local complications
recurrent laryngeal nerve palsy phrenic nerve palsy SVC obstruction Rib erosion pericarditis AF
bronchial carcinoma: metastatic complications
brain
bone- anaemia, hypercalcaemia
liver
adrenals- addison’s
bronchial carcinoma: non-metastatic neurological complications
confusion fits cerebellar syndrom proximal myopathy polymyositis
bronchial carcinoma: chest x ray
peripheral nodule hilar enlargement consolidation lung collapse pleural effusion bony secondaries
bronchial carcinoma: cytology
sputum and pleural fluid
bronchial carcinoma: CT scan
for Staging
bronchial carcinoma: bronchoscopy
give histology
assess operability
bronchial carcinoma: lung function test
assess suitability for lobectomy
bronchial carcinoma: bone scan
if suspected mets
bronchial carcinoma: PET scan
helps with staging
bronchial carcinoma: non-small cell treatment
surgical excision- lobectomy
radiotherapy for stages I-III
chemo and radio for more advanced
bronchial carcinoma: small cell, treatment
surgery
chemo and radio if well enough
pharmacological, palliative and treat complications
bronchial carcinoma: small cell, palliative care
radiotherapy- for bronchial obstruction, SVC obstruction, haemoptysis, bone pain and cerebral mets
bronchial carcinoma: small cell, treat complications
SVC obstruction- stent, RT and dexamethasone
endobronchial therapy- tracheal stenting, cryotherapy, laser brachytherapy
pleural effusion- drainage
bronchial carcinoma: small cell, pharmacological treatment
analgesia steroids anti0emetics cough linctus bronchodilators antidepressants
bronchial carcinoma: prevention
stop smoking
prevent occupational exposure
bronchial adenoma: pathology
rare
slow growing
90% carcinoid
10% cylindromas
bronchial adenoma: treatment
surgery
hamartoma: pathology
rare
benign
irregular proliferations of benign tissues that are not normally found in that pattern within lung tissue
hamartoma: investigation
CT- lobulated mass, potential flecks of calcification
hamartoma: treatment
excision to exclude malignancy
malignant mesothelioma: pathology
malignant tumour of mesothelial cells that usually occurs in the pleura
malignant mesothelioma: epidemiology
more common in men
presents 40-70 y/o
malignant mesothelioma: aetiology
asbestos is main cause- 90%
latent period can be up to 45 years
malignant mesothelioma: symptoms
chest pain dyspnoea weight loss fatigue recurrent pleural effusions
malignant mesothelioma: signs
finger clubbing
signs of metastasis- lymphadenopathy, hepatomegaly, bone pain/tenderness
abdo pain
malignant mesothelioma: investigation
CXR/CT- pleural thickening/effusion
aspiration- bloody pleural fluid
thorascopy w/ biopsy= diagnostic
malignant mesothelioma: treatment
poor prognosis- presents late and progresses quickly, average survival is 8 months
chemo can improve survival
cancers that spread to the lung
breast
bowel
kidney
bladder
causes of nodule in the lung
malignancy, primary or secondary abscess granuloma cyst foreign body skin tumour
complications of resp viruses
pharyngitis sinusitis otitis media bronchitis pneumonia
viral illnesses of resp tract
influenza
coronavirus
adenovirus
respiratory syncytial virus
emergency respiratory infections
severe acute respiratory syndrome
avian influenza
tonsillitis: pathology
pharyngitis and tonsillitis are infections in the throat that cause inflammation
either affecting pharynx or tonsils
tonsillitis: viral causes
adenovirus= most common cause
rhinovirus
epstein barr virus
acute HIV infection
tonsillitis: bacterial causes
lancefield group A beta-haemolytic streptococci
strep pyogenes
tonsillitis: symptoms
sore throat
fever
tonsillitis: signs
oropharynx and soft palate are red
tonsil inflammation and swelling
lymph nodes enlarge
tonsillitis: viral presentation
red swollen tonsils
throat redness
tonsillitis: bacterial presentation
white pus filled spots
grey furry tongue
swollen uvula
red swollen tonsils and throat
tonsillitis: investigations
clinical diagnosis
self limiting tonsillitis: treatment
symptomatic treatment- pain relief
no antibiotics required
persistent tonsillitis: treatment
phenoxymethylpenicillin
cefaclor
sinusitis: pathology
infection of paranasal sinuses
mostly bacterial but can be fungal
sinusitis: causes
streptococci pneumoniae= 40%
haemophilus influenzae= 30-35%
sinusitis: symptoms
purulent rhinorrhoea
facial pain, unilateral with tenderness
fever
frontal headache
sinusitis: signs
past medical history of upper resp tract infection- cold
sinusitis: complications
brain abscesses
sinus vein thrombosis
orbital cellulitis
sinusitis: investigations
clinical diagnosis
sinusitis: treatment
nasal decongestants- xylometazoline
broad spectrum antibiotics- co-amoxiclav
acute epiglottitis: pathology
inflammation of epiglottis
acute epiglottitis: causes
haemophilus influenzae= most severe
causes of pharyngitis
acute epiglottitis: symptoms
high fever
severe airway obstruction
odynophagia- pain when swallowing
acute epiglottitis: signs
inspiratory stridor- high pitch wheezing when breathing in
acute epiglottitis: complications
meningitis
septic arthritis
osteomyelitis
acute epiglottitis: investigations
clinical diagnosis
acute epiglottitis: treatment
IV antibiotics- ceftazidime
may require emergency endotracheal intubation
whooping cough: pathology
caused by bordatella pertussis- gram -ve coccobacillus
highly contagious
spread via droplets
whooping cough: epidemiology
mainly occurs in childhood
90% <5 y/o
whooping cough: catarrhal phase presentation
highly infectious, 1-2 weeks malaise anorexia rhinorrhoea conjunctivitis
whooping cough: paroxysmal phase presentation
chronic cough >14 days
coughing spasms which may end in vomiting
classic whoop= breath through partially closed vocal cords
whooping cough: complications
pneumonia
encephalopathy
sub-conjunctival haemorrhage
whooping cough: investigations
PCR- nasal/throat swab
culture sensitivity
whooping cough: treatment
macrolides- clarithromycin
vaccination in pregnancy
croup: pathology
aka acute laryngotracheobronchitis
complication of URTI- particularly from parainfluenza virus and measles
croup: pathogenesis
inflammatory oedema extends to vocal cords and epiglottis
causes narrowing of airway
associated tracheobronchitis
progressive airway obstruction
croup: symptoms
barking cough- croup
croup: signs
hoarse voice
audible stridor- high pitch wheeze breathing in
tachypnoea
cyanosis
croup: investigation
clinical diagnosis
croup: treatment
nebulised adrenaline
oral corticosteroids- dexamethasone
oxygen
IV fluids
pneumonia
acute lower resp tract infection associated with fever, symptoms and signs in the chest and abnormalities on CXR
pneumonia: methods of spread
inhalation of airborne particles
aspiration of gastric contents or nasopharyngeal flora
haematogenous spread- septic arthritis
pneumonia: pathogenesis
bacteria translocate in normally sterile distal airway
multiply in lung- overwhelm host defence
alveolar macrophages release chemicals resulting in inflammation and entry of neutrophils
community acquired pneumonia
pneumonia occurs in person with no underlying immunosuppression or malignancy
community acquired pneumonia: epidemiology
occurs in all ages but commoner in extremes of age
community acquired pneumonia causes: typical
streptococcus pneumonia= most common
haemophilus influenzae
community acquired pneumonia causes: atypical
water cooler/air conditioner mycoplasma pneumonia staph. aureus legionella chlamydia
community acquired pneumonia causes: viral
account for 15%
CMV
VZV
SARS
hospital acquired pneumonia
defined as >48 hours after hospital admission
hospital acquired pneumonia: epidemiology
mostly in elderly, ventilated and post-op
2nd most common Hospital acquired infection
hospital acquired pneumonia causes: common
gram -ve enterobacteria
(E.coli, pseudomonas aeruginosa)
Staph. aureus
hospital acquired pneumonia causes: less common
bacteriodes
clostridia
pneumonia causes: aspiration
acute aspiration of gastric contents into lungs
stroke, myasthenia, bulbar palsies, loss of consciousness, poor dental hygiene
pneumonia causes: immunocompromised patients
pneumocystis jiroveci- HIV strep. pneumonia haemophilus influenzae staph. aureus gram -ve bacilli fungi
pneumonia: risk factors
infants and elderly COPD cystic fibrosis immunocompromised smoking excess alcohol diabetes impaired swallowing CVD
pneumonia: symptoms
fever dyspnoea productive cough purulent sputum pleuritic chest pain haemoptysis
pneumonia: signs
confusion tachypnoea tachycardia hypotension pyrexia cyanosis
pneumonia: signs of consolidation
reduced expansion
dull percussion
increased tactile vocal resonance
bronchial breathing
pneumonia investigations: examination
dull percussion
reduced breath sounds
pneumonia investigations: chest x ray
gold standard
lobar or multilobar infiltrates
pleural effusion
pneumonia investigations: microbiology
sputum sample
serology
pleural fluid aspiration
pneumonia investigations: CURB 65
Confusion Urea >7mmol/L Resp rate >30/min Bp<90 systolic 65y/o or higher
pneumonia investigations: CURB 65 implications
0-1=mild, oral antibiotic, home treatment
2= moderate- admit to hospital
3-5= severe=admit and closely monitor
4-5= consider admission to CCU
pneumonia treatment: mild community acquired
oral amoxicillin or clarithromycin
pneumonia treatment: moderate community acquired
oral amoxicillin or clarithromycin
pneumonia treatment: severe community acquired
oral co-amoxiclav or clarithromycin
pneumonia treatment: atypical community acquired
legionella- fluoroquinolone and clarithromycin
chlamydia- tetracycline
pneumonia treatment: hospital acquired patients
IV aminoglycoside and IV antipseudomonal penicillin
pneumonia treatment: aspiration patients
IV cephalosporin and IV metronidazole
pneumonia treatment: neutropenic patients
IV aminoglycoside and IV antipseudomonal penicillin
pneumonia treatment: supportive therapy
oxygen- keep sats >94% (if COPD, 88-92%)
IV fluids- for anorexia, dehydration and shock
pneumonia treatment: analgesia
paracetamol for pleuritic chest pain
pneumonia: prevention
smoking cessation
influenza vaccine
pneumococcal vaccine for at risk groups
pneumonia: complications
pleural effusion empyema resp failure hypotension AF lung abscess jaundice septicaemia pericarditis brain abscess
pneumonia complications: pleural effusion
inflammation of pleura by adjacent pneumonia
may cause fluid exudation into pleural space
if small then no consequences
if large or infected then drainage required
pneumonia complications: empyema
pus in pleural space
should be suspected if a pt. with resolving pneumonia develops a recurrent fever
should be drained
pneumonia complications: resp failure
type 1 is relatively common
treat with high flow oxygen, aim for normal sats
pneumonia complications: hypotension
may be due to combination of dehydration and vasodilation from sepsis
treat with IV fluids
pneumonia complications: atrial fibrilation
common in elderly
usually resolves with treatment of pneumonia
beta-blocker or digoxin can be used short term
pneumonia complications: septicaemia
may occur as result of bacteria spread from lung into blood stream
treat with IV antibiotics according to sensitivities
pneumonia complications: Jaundice
usually cholestatic and may be due to sepsis or secondary to antibiotic therapy- especially flucloxacillin and co-amoxiclav
pneumonia complications: lung abscess
cavitating area of localised, suppurative infection within the lung
pneumonia complications: lung abscess causes
inadequate treat pneumonia
aspiration
bronchial obstruction
septic emboli
pneumonia complications: lung abscess presentation
swinging fever cough purulent, foul selling sputum malaise finger clubbing anaemia weight loss
pneumonia complications: lung abscess CXR
walled cavity
often with a fluid level
pneumonia complications: lung abscess CT scan
exclude construction
pneumonia complications: lung abscess bronchoscopy
obtain diagnostic samples
pneumonia complications: lung abscess treatment
antibiotics
postural drainage
repeated aspiration
pneumonia differential diagnosis
TB
lung cancer
pneumococcal pneumonia
most common cause of bacterial pneumonia
affects all ages but common in elderly, alcoholics, immunocompromised and chronic heart failure
pneumococcal pneumonia: treatment
amoxicillin
staphylococcal pneumonia
may complicate influenza infection
occurs in young, elderly or those with underlying disease
causes bilateral cavitating bronchopneumonia
staphylococcal pneumonia: treatment
flucloxacillin
if MRSA- vancomycin
klebsiella pneumonia
rare
occurs in elderly, diabetic and alcoholics
klebsiella pneumonia: treatment
cefotaxime
pseudomonas treatment
antipseudomonal penicillin and aminoglycoside
mycoplasma pneumonia treatment
clarithromycin or doxycycline
legionella pneumophilia
colonises water tanks kept at 65 degrees
treat with clarithromycin or fluoroquinolone
chlamydia pneumonia treatment
clarithromycin or doxycycline
viral pneumonia causes
influenza= most common swine flu measles CMV varicella zoster
pneumocystis pneumonia treatment
high dose co-trimoxazole
TB: causes
mycobacterium tuberculosis
mycobacterium bovis
mycobacterium africanum
mycobacterium microti
TB: bacteria features
M. tuberculosis:
- intracellular bacteria
- aerobic, non-motile, non-spore forming, slightly curved
- slow growing
- cell wall contains mycolic acid (phagocytosis resistant)
- acid fast bacteria (ziehl-neelsen stain)
TB: active infection
occurs when containment by immune system (t cells/macrophages) is inadequate
it can arise from primary infection or re-activation of previously latent disease
-transmission is via inhalation of aerosol droplets
TB: latent pathophysiology
- infection without disease
- granuloma forms, preventing bacteria growth and spread
- lifetime risk of reactivation is 5-10%
- asymptomatic, non-infectious
- normal sputum/CXR
- positive skin test
TB: risk factors for reactivation
new infection, <2yrs HIV organ transplant immunosuppression silicosis illicit drug use malnutrition haemodialysis
TB: risk factors
immunocompromised HIV diabetes mellitus IV drug use homeless alcoholic viral hepatitis
TB presentation: systemic features
low grade fever anorexia weight loss malaise night sweats erythema nodosum
pulmonary TB presentation:
productive cough
haemoptysis
pleurisy
pleural effusion
extra-pulmonary TB presentation: lymph
tuberculous lymphadenitis
painless enlargement of cervical or supraclavicular lymph nodes
extra-pulmonary TB presentation: GI
most disease is ileocaecal colicky abdo pain vomiting bowel obstruction from wall thickening ascites
extra-pulmonary TB presentation: spinal/bone
local bone pain and tenderness
bone destruction
vertebral collapse
extra-pulmonary TB presentation: milliary
haematogenous dissemination
discrete foci throughout lung (millet appearance)
extra-pulmonary TB presentation: CNS
haematogenous spread
meningism
raised ICP
extra-pulmonary TB presentation: GU
dysuria
frequency
loin pain
granulomas can cause infertility, ulceration and strictures
extra-pulmonary TB presentation: cardiac
pericardial involvement- pericarditis, pericardial effusion, constrictive pericarditis
extra-pulmonary TB presentation: skin
lupus vulgaris- persistent, progressive, cutaneous TB (red brown nodules)
latent TB investigations: tuberculin skin testing
intradermal injection of purified protein derivative tuberculin
size of skin induration is used to determine positivity
latent TB investigations: interferon-gamma release assays
diagnose exposure to TB by measuring the release of interferon-gamma from T-cells reacting to TB antigen
active TB investigations: CXR
fibronodular, linear opacities in upper lobe cavitation calcification miliary disease effusion
active TB investigations: sputum smear
Ziehl-neelsen for acid fast bacilli
three specimens are needed
active TB investigations: sputum culture
cultured with lowenstein-jensen medium
ziehl-neelsen stain
active TB investigations: NAAT
direct detection of M. tuberculosis
active TB investigations: histology
caesating granuloma
extra-pulmonary TB investigations: aspiration or biopsy
lymph node, pleura, bone, synovium, GI/GU
AFB staining
histology
culture
extra-pulmonary TB investigations: NAAT
any sterile fluids- CSF, pericardial
lumbar puncture
TB treatment: 1st line treatment RIPE
Rifampicin
Isoniazid
Pyrazinamide
Ethambutol
TB treatment: rifampicin
6 months
bactericidal
blocks protein synthesis
TB treatment: isoniazid
6 months
bactericidal for rapidly growing bacilli
block cell wall synthesis
inhibits formation of active vitamin B6 which causes peripheral neuropathy
TB treatment: pyrazinamide
2 months
bactericidal
TB treatment: ethambutol
2 months
bactericidal
TB treatment: rifampicin side effects
Red/orange bodily fluids- urine, sweat, tears
renal failure
rash
hepatitis
TB treatment: isoniazid side effects
peripheral neuropathy
tingling, numb feet/hands
TB treatment: pyrazinamide side effects
hepatitis
hyperuricaemia/gout
TB treatment: ethambutol side effects
Eye problems
optic neuritis
TB treatment: side effect management
prophylactic vitamin B6
eye and liver screening
TB: 2nd line treatment
fluoroquinolones- ciprofloxacin
augmentin
clarithromycin
TB: prevention
active case finding
vaccination- BCG
respiratory failure
occurs when gas exchange is inadequate, resulting in hypoxia
PaO2 <8kPa
type 1 respiratory failure
hypoxia with normal or low PaCO2
ventilation/perfusion mismatch
type 1 respiratory failure causes
V/Q mismatch= pneumonia, pulmonary oedema, pulmonary embolism, asthma, emphysema
Hypoventilation
Abnormal diffusion
type 2 respiratory failure
hypoxia with hypercapnia
caused by hypoventilation w/ or w/o V/Q mismatch
type 2 respiratory failure causes: pulmonary disease
asthma
COPD
pneumonia
end stage pulmonary fibrosis
type 2 respiratory failure causes: reduced respiratory drive
sedative drugs
CNS tumour
trauma
type 2 respiratory failure causes: neuromuscular disease
cervical cord lesion
diaphragmatic paralysis
myasthenia gravis
guillain-barre syndrome
type 2 respiratory failure causes: thoracic wall disease
flail chest
kyphoscoliosis
causes of respiratory failure: perfusion
PE
cardiac failure
shunt
pulmonary hypertension
causes of respiratory failure: diffusion
IPF
emphysema
causes of respiratory failure: hypoventilation
COPD
neuromuscular weakness
obesity
chest wall deformity
causes of respiratory failure: obstructive
asthma
COPD
OSA
pneumonia
hypoxia: symptoms
dyspnoea restlessness agitation confusion central cyanosis
hypoxia: signs
polycythaemia
pulmonary hypertension
cor pulmonale
hypercapnia: symptoms
headache peripheral vasodilation tremor confusion drowsiness
hypercapnia: signs
bounding pulse
tachycardia
papilloedema
respiratory failure investigations
aimed at finding cause ABG CXR sputum culture spirometry
type 1 resp failure treatment
treat underlying cause
oxygen by facemask
assisted ventilation if sats remain low
type 2 resp failure treatment
resp centre may be insensitive to CO2 and resp drive is usually because of hypoxia
treat cause
controlled oxygen therapy- aim for 88-92% sats
recheck ABG after 20 mins
ABG result of metabolic alkalosis:
pH= high PaCO2= normal, high when compensated HCO3-= high
ABG result of metabolic acidosis:
pH= low
PaCO2=normal, low when compensated
HCO3-=low
ABG result of resp alkalosis:
pH= high
PaCO2= low
HCO3-=normal, low when compensated
ABG result of resp acidosis:
pH= low PaCO2= high HCO3-= normal/high when compensated
interstitial lung disease pathology
generic term to describe conditions affecting mainly ling parenchyma in a diffuse manner
chronic inflammation and/or progressive interstitial fibrosis
interstitial lung disease clinical features
dyspnoea on excretion
non-productive cough
abnormal breathing sounds
abnormal chest x ray or CT
interstitial lung disease pathological features
fibrosis and remodelling of interstitium
chronic inflammation
hyperplasia of type II pneumocytes
interstitial lung disease with known cause
occupational/environmental- asbestos, cotton worker lung etc. drugs hypersensitivity reactions infections- TB gastro-oesophageal reflux
interstitial lung disease associated with systemic disorders
sarcoidosis
RA
SLE
idiopathic interstitial lung disease
idiopathic pulmonary fibrosis
non-specific interstitial pneumonitis
causes of fibrotic shadowing on CXR: upper zone
TB
hypersensitivity pneumonitis
ankylosing spondylitis
Radiotherapy
causes of fibrotic shadowing on CXR: mid zone
sarcoidosis
histoplasmosis
causes of fibrotic shadowing on CXR: lower zone
idiopathic pulmonary fibrosis
asbestosis
hypersensitivity pneumonitis
hypersensitivity reaction to inhaled allergens- affecting small airways and alveoli.
Type 3 hypersensitivity reaction due to immune complex deposition
hypersensitivity pneumonitis: pathogenesis
in sensitised individuals, repetitive inhalation of allergens provokes a hypersensitivity reaction. This varies in intensity and clinical course depending on the allergen
hypersensitivity pneumonitis: acute phase
alveoli are infiltrated with acute inflammatory cells
results in pneumonitis
hypersensitivity pneumonitis: chronic phase
granuloma formas and obliterative bronchiolitis
results in fibrosis, emphysema, and permanent lung damage
hypersensitivity pneumonitis causes: farmer’s/ mushroom worker’s lung
due to exposure of mouldy hay
bacteria= micropolyspora faeni, thermoactinomyces vulgaris
hypersensitivity pneumonitis causes: pigeon-fancier’s lung
due to exposure of avian proteins in bird droppings
hypersensitivity pneumonitis causes: malt worker’s lung
due to exposure of aspergillus clavatus
hypersensitivity pneumonitis causes: bagassosis or sugar worker’s lung
due to exposure of thermoactinomyces sacchari
hypersensitivity pneumonitis causes: cheese worker’s lung
due to exposure of mouldy cheese- penicillium casei
hypersensitivity pneumonitis: risk factors
pre-existing lung disease
specific occupations
bird keeping
regular hot tub use
acute hypersensitivity pneumonitis: presentation
4-6 hr post exposure fever rigors myalgia dry cough dyspnoea fine bilateral crackles
chronic hypersensitivity pneumonitis: symptoms
increasing dyspnoea
weight loss
exertional dyspnoea
chronic hypersensitivity pneumonitis: signs
finger clubbing
type 1 resp failure
cor pulmonale
acute hypersensitivity pneumonitis investigations: bloods
serum antibodies- may indicated exposure and previous sensitisation rather than disease
acute hypersensitivity pneumonitis investigations: CXR
upper zone mottling/consolidation
acute hypersensitivity pneumonitis investigations: lung function tests
reversible restrictive defect
reduced gas transfer during attack
chronic hypersensitivity pneumonitis investigations: bloods
serum antibodies
chronic hypersensitivity pneumonitis investigations: CXR
upper zone fibrosis
honey comb lung
chronic hypersensitivity pneumonitis investigations: CT chest
nodules
ground glass appearance
fibrosis
chronic hypersensitivity pneumonitis investigations: lung function test
restrictive defect
chronic hypersensitivity pneumonitis investigations: bronchoalveolar lavage
fluid shows an increase in lymphocytes and plasma cells
acute hypersensitivity pneumonitis: treatment
remove allergen
give oxygen
oral prednisolone
chronic hypersensitivity pneumonitis: treatment
allergen avoidance
long term steroids
hypersensitivity pneumonitis: differentials
infection
connective tissue disorder
pulmonary fibrosis
asthma
occupational lung disorders
response to inhalation of fumes, dust, gas or vapour at work
occupational lung disorders: acute bronchitis
from irritants such as sulphur dioxide, chlorine, ammonia, oxides of nitrogen
occupational lung disorders: pulmonary fibrosis
from inhalation of inorganic dust- coal, silica, asbestos, iron, tin
occupational lung disorders: occupational asthma
most common industrial lung disease in developed world
occupational lung disorders: bronchial carcinoma
due to asbestos, polycyclic hydrocarbons, radon mines
coal workers pneumoconiosis
pneumoconiosis is accumulation of dust in the lungs and reaction of the tissue
coal workers pneumoconiosis: pathology
most common dust disease in countries with coal mines
results in inhalation of coal dust over 15-20 years
these are ingested by macrophages which die, releasing enzymes that cause fibrosis
coal workers pneumoconiosis: presentation
asymptomatic
co-existing bronchitis is common
coal workers pneumoconiosis: investigations
chest x ray- round opacities, especially upper lobe
coal workers pneumoconiosis: treatment
avoid coal dust exposure
treat chronic bronchitis
progressive massive fibrosis
due to progression of coal workers pneumoconiosis
progressive massive fibrosis: presentation
progressive dyspnoea
fibrosis
cor pulmonale
progressive massive fibrosis: investigations
CXR- bilateral, upper-mid zone fibrotic masses
develop from periphery to hilum
progressive massive fibrosis: treatment
avoid coal dust exposure
silicosis
caused by inhalation of silica particles which are very fibrogenic
jobs include- metal mining, stone quarrying, sand blasting, pottery
silicosis: presentation
progressive dyspnoea
high incidence of TB
silicosis: investigations
CXR- diffuse miliary/nodular pattern in upper-mid zones, egg shell calcification of hilar nodules
Spirometry- restrictive ventilatory defect
silicosis: treatment
avoid silica exposure
asbestosis
inhalation of asbestos fibres
the degree of roofing exposure related to degree of fibrosis
high risk of bronchial adenocarcinoma and mesothelioma
asbestosis: presentation
similar to other fibrotic lung diseases progressive dyspnoea clubbing fine end-inspiratory crackles pleural plaques
asbestosis: treatment
symptomatic treatment- corticosteroids
berylliosis
caused by inhalation of beryllium
copper alloy used in aerospace industry, atomic reactors and electrical devices
byssinosis
caused by prolonged inhalation of textile fibre dust- cotton
chest tightness, cough, dyspnoea
idiopathic pulmonary fibrosis
progressive chronic pulmonary fibrosis of unknown aetiology
most common cause of interstitial lung disease
idiopathic pulmonary fibrosis: pathogenesis
thought to develop from repetitive injury to alveolar epithelium
wound healing mechanisms become uncontrolled leading to overproduction of fibroblasts
patchy fibrosis occurs in interstitium
structural integrity of parenchyma is lost as well as elasticity
idiopathic pulmonary fibrosis: risk factors
factors that trigger aberrant wound healing:
cigarette smoke, infectious agents (hep C), occupational dust exposure, drugs (methotrexate) GORD
idiopathic pulmonary fibrosis: symptoms
dry cough
exertional dyspnoea
malaise
weight loss
idiopathic pulmonary fibrosis: signs
cyanosis
finger clubbing
fine end-inspiratory crepitation
idiopathic pulmonary fibrosis: complications
resp failure
increased risk of lung cancer
idiopathic pulmonary fibrosis: bloods
high CRP
high immunoglobulins
ABG- low PaO2
idiopathic pulmonary fibrosis: CXR
bilateral lower zone reticulo-nodular shadows
honeycomb lung
idiopathic pulmonary fibrosis: Chest CT
similar to XR but more sensitive and essential for diagnosis
idiopathic pulmonary fibrosis: spirometry
restrictive
idiopathic pulmonary fibrosis: bronchoalveolar lavage
high lymphocytes- good prognosis
high neutrophils and eosinophils- poor prognosis
idiopathic pulmonary fibrosis: lung biopsy
may be needed for diagnosis
idiopathic pulmonary fibrosis: supportive care
oxygen
pulmonary rehab
opiates
palliative care
idiopathic pulmonary fibrosis: treatment
lung transplant
DO NOT give high dose steroids
idiopathic pulmonary fibrosis: differentials
COPD asthma congestive heart failure pneumonia lung cancer asbestosis hypersensitivity pneumonitis
sarcoidosis
multisystem granulomatous disorder of unknown cause
sarcoidosis: pathogenesis
typical sarcoid granulomas consist of focal accumulations of epitheloid cells, macrophages and lymphocytes
affects any organ system
sarcoidosis: histology
non-caseating granuloma (aggregation of epitheloid histiocytes)
sarcoidosis: epidemiology
affects adults, 20-40 y/o
more common in women
afro-caribbeans are more affected
acute sarcoidosis: presentation
usually resolves spontaneously fever erythema nodosum polyarthralgia bilateral hilar lymphadenopathy
sarcoidosis: pulmonary symptoms
dry cough progressive dyspnoea decreased exercise intolerance chest pain abnormal CXR
sarcoidosis: non-pulmonary signs
lymphadenopathy hepatomegaly splenomegaly uveitis conjunctivitis neuropathy space occupying lesions arrhythmia renal stones
sarcoidosis presentation: SARCOID
Skin- erythema nodosum
Arthritis- hands and feet
Respiratory- BHL
Cardiac- heart block, heart failure
Ocular- anterior uveitis
Intracranial- chronic meningitis, seizures
Derangement of liver and renal function- hypercalcaemia
sarcoidosis investigations: bloods
high ESR lymphopenia high LFT high serum ACE high calcium
stage 0 sarcoidosis investigations: CXR
normal
stage 1 sarcoidosis investigations: CXR
BHL
stage 2 sarcoidosis investigations: CXR
BHL and peripheral pulmonary infiltrates
stage 3 sarcoidosis investigations: CXR
peripheral pulmonary infiltrates
stage 4 sarcoidosis investigations: CXR
progressive pulmonary fibrosis
bulla formation
pleural involvement
sarcoidosis investigations: ECG
arrhythmias
BBB
sarcoidosis investigations: lung function tests
may be normal
potential reduced lung volumes
impaired gas transfer and a restrictive ventilatory impairment
sarcoidosis investigations: bronchoalveolar lavage
shows increase in lymphocytes in active disease
increase in neutrophils in pulmonary fibrosis
sarcoidosis investigations: ultrasound
may show nephrocalcinosis or hepatosplenomegaly
sarcoidosis investigations: bone X ray
punched out lesions in terminal phalanges
sarcoidosis investigations: CT/MRI
may be useful in assessing severity of pulmonary disease or diagnosing neuro-sarcoidosis
acute sarcoidosis: treatment
bed rest
NSAIDS
stages I-III sarcoidosis: treatment
remission likely
stage IV sarcoidosis: treatment
corticosteroids- prednisolone
if parenchymal lung disease/uveitis/hypercalcaemia/neuro or cardio involvement
severe sarcoidosis: treatment
IV methylprednisolone
immunosuppressants- methotrexate
anti-TNF-alpha
lung transplant
differentials for sarcoidosis
RA lymphoma metastatic malignancy TB lung cancer SLE idiopathic pulmonary fibrosis multiple myeloma
differentials for granulomatous disease: infections
bacterial- TB, leprosy, syphilis
fungi- cryptococcus neoformans
protozoa
differentials for granulomatous disease: autoimmune
primary biliary cholangitis
granulomatous orchitis
differentials for granulomatous disease: vasculitis
giant cell arteritis
polyarteritis nodosa
differentials for granulomatous disease: idiopathic
crohn’s disease
sarcoidosis
causes of bilateral hilar lymphadenopathy
sarcoidosis infection- TB malignancy- lymphoma organic dust disease- silicosis hypersensitivity pneumonitis
bronchiectasis
chronic inflammation of the bronchi and bronchioles, leading to permanent dilation and thinning of these airways
bronchiectasis: characteristics
irreversible dilation of the bronchioles- due to recurrent damage and inflammation
build-up of mucus increasing risk of infection
ciliary dysfunction
bronchiectasis: pathogenesis
damage to bronchi and bronchioles widening due to scarring and inflammation increased mucus production stagnant bacteria cause infection damage to the tract widening cycle continues
bronchiectasis: main organisms
H. influenzae
pseudomonas aeruginosa
strep. pneumoniae
staph. aureus
bronchiectasis: epidemiology
more common in women
bronchiectasis: post-infection causes
most common previous pneumonia TB measles whooping cough bronchiolitis HIV
bronchiectasis: congenital causes
CF
young’s syndrome
bronchiectasis: other causes
bronchial obstruction- tumour, foreign body allergic bronchopulmonary aspergillosis RA Ulcerative colitis idiopathic
bronchiectasis: symptoms
persistent cough
copious purulent sputum
intermittent haemoptysis
dyspnoea
bronchiectasis: signs
finger clubbing
coarse inspiratory crepitations
wheeze
bronchiectasis: complications
pneumonia
pleural effusion
pneumothorax
amyloidosis
bronchiectasis: high resolution CT
gold standard
asses extent and distribution of disease
thickened, dilated bronchi (larger than associated blood vessels) and cysts at end of bronchioles
bronchiectasis: sputum culture
look for infectious agents
bronchiectasis: CXR
cystic shadows
thickened bronchial walls
bronchiectasis: spirometry
often shows an obstructive pattern
reversibility should be assessed
bronchiectasis: bronchoscopy
locate site of haemoptysis
exclude obstruction and obtain samples for culture
bronchiectasis: non-pharmacological treatment
can’t be cured.
stop smoking
vaccinations for infections
airway clearance techniques- physio, flutter valves
bronchiectasis: pharmacological treatment
bronchodilators- nebulised salbutamol
corticosteroids- prednisolone
antibiotics- according to sensitivities (amoxicillin for H. influenzae, flucloxacillin for s. aureus)
bronchiectasis: surgery
may be indicated in localised disease or to control severe haemoptysis
bronchiectasis: differentials
COPD asthma TB cough due to acid reflux pneumonia cancer inhalation of foreign body
cystic fibrosis (CF)
chronic disease resulting in thickened and sticky mucus
CF: genetics
autosomal recessive
mutation in CF transmembrane conductance regulator (CFTR) gene on chromosome 7
CF: pathogenesis
mutation in CFTR Cl- channel protein
Cl- cannot be transported into lumen
water does not move out by osmosis
CF: characteristics
thick and sticky mucus which blocks ducts
affects all ducts that produce mucus
predisposes lung to chronic infections
CF: epidemiology
one of the most common life-threatening autosomal recessive conditions
presents in childhood
CF: aetiology
mutation in CFTR gene on chromosome 7
F508 deletion is most common- 70%
CF: risk factors
family history
caucasian
CF: neonate presentation
failure to thrive
meconium ileus
rectal prolapse
CF: resp symptoms
cough wheeze recurrent infections bronchiectasis pneumothorax resp failure
CF: GI symptoms
pancreatic insufficiency- diabetes, steatorrhoea
distal intestinal obstruction syndrome
CF: other symptoms
male infertility osteoporosis arthritis vasculitis nasal polyps
CF: signs
cyanosis
finger clubbing
bilateral coarse crackles
CF complications
infertility
pancreatitis
resp infections
bronchiectasis
CF investigations: sweat test
diagnostic
sweat sodium and chloride >60mmol/L
abnormal NaCl collected as it can’t be pumped into lumen so removed via skin
CF investigations: genetic testing
diagnostic
screen for common CF mutations
CF investigations: faecal elastase
screening test in newborns
low or no levels of elastase- marker for exocrine pancreatic dysfunction
CF treatment
no cure
symptomatic management
life expectancy of about 50 years
CF non-pharmacological treatment
physiotherapy- postural drainage, airway clearance techniques
CF pharmacological treatment
antibiotics mucolytics bronchodilators pancreatic enzyme replacement fat soluble vitamin supplements- A,D,E,K ursodeoxycholic acid
CF pharmacological treatment: antibiotics
for acute infective exacerbations
prophylactically
flucloxacillin for s. aureus
amoxicillin for H. influenzae
CF pharmacological treatment: mucolytics
clear airways of mucus
DNase e.g. dornase alpha
CF pharmacological treatment: bronchodilators
salbutamol and beclometasone
symptom relief
CF pharmacological treatment: treat complications
CF related diabetes- insulin
osteoporosis- bisphosphonates
malabsorption, GORD, fertility
CF surgery
lung transplant
CF monitoring
annual chest x ray
screening for osteoporosis- DEXA scan
CF, advanced lung disease: treatment
oxygen
diuretic
non-invasive ventilation
lung and heart transplants
pleural effusion: haemothorax
blood in pleural space
pleural effusion: empyema
pus in pleural space
pleural effusion: chylothorax
chyle (lymph with fat) in pleural space
pleural effusion: haemopneumothorax
both blood and air in pleural space
pleural effusion: exudate
protein conc. >35g/L
pleural effusion: transudate
protein conc. <25g/L
pleural effusion: transudate pathogenesis
excessive production of pleural fluid or resorption of the fluid is reduced
mostly due to fluid being pushed out of the vessels and into the space
pleural effusion: exudate pathogenesis
results from damaged pleura
mostly due to increased leakiness of pleural capillaries secondary to infection, inflammation or malignancy
pleural effusion: increased venous pressure, transudate causes
heart failure
constrictive pericarditis
fluid overload
pleural effusion: hypoproteinaemia transudate causes
cirrhosis
nephrotic syndrome
malabsorption
pleural effusion: other transudate causes
hypothyroidism
meig’s syndrome- R pleural effusion and ovarian fibrom
pleural effusion: exudate causes
pneumonia TB PE lung cancer SLE RA
pleural effusion: risk factors
previous lung damage
asbestos exposure
pleural effusion: symptoms
can be asymptotic
dyspnoea
pleuritic chest pain
pleural effusion: signs
decreased expansion
stony dull percussion notes
diminished breath sounds
pleural effusion: signs of associated disease
malignancy- clubbing, lymphadenopathy stigmata of chronic liver disease cardiac failure hypothyroidism RA SLE- butterfly rash
pleural effusion investigation: CXR
white fluid
small effusions blunt the costophrenic angles
larger effusions are seen as water-dense shadows with concave upper borders
pleural effusion investigation: ultrasound
useful in identifying the presence of pleural fluid and guiding diagnostic or therapeutic aspiration
pleural effusion investigation: diagnostic aspiration
clinical chemistry (protein, glucose, pH), bacteriology (TB culture, MC&C), cytology, immunology
pleural effusion investigation: pleural biopsy
if pleural fluid analysis is inconclusive
pleural effusion treatment
treat cause drainage pleurodesis intra-pleural alteplase and dornase alpha surgery
pleural effusion treatment: drainage
small needle or tube inserted and draws out the fluid
pleural effusion treatment: pleurodesis
recurrent effusions for more severe cases
injection of ‘glue’, the two pleural surfaces stick together so no more fluid can come in between
pleural effusion treatment: intra-pleural alteplase and dornase alpha
IPA= thrombolytic, DA= mucolytic
may help empyema
pleural effusion treatment: surgery
persistent collections and increasing pleural thickness on USS requires surgery
pneumothorax
air in pleural space
causes lung on affected side to collapse and is unable to inflate
simple pneumothorax
no communication with atmosphere
no mediastinal shift
non-expanding
pleural cavity pressure less than atmosphere
tension pneumothorax
progressive build up of air in pleural space from each inspiration
mediastinum is pushed over into contralateral hemithorax
can lead to cardiorespiratory arrest
communicating pneumothorax
loss of integrity of a chest wall, secondary to penetrating chest trauma
causes collapse of affected lung on inspiration
pneumothorax: primary spontaneous causes
young thin men- connective tissue disorders, marfan’s, elhers-danlos
due to rupture of subpleural bulla- thing walled air containing spaces
usually apical- due to congenital defects
pneumothorax: secondary spontaneous causes
chronic lung disease- asthma, COPD, FC, sarcoidosis
infection- TB, pneumonia
carcinoma
pneumothorax: traumatic causes
traumatic- fractured rib, stab wound, gunshot
iatrogenic- CVP line insertion, pleural aspiration
pneumothorax: risk factors
male smoking tall underweight use of mechanical ventilation
pneumothorax: symptoms
can be asymptomatic sudden onset of dyspnoea pleuritic chest pain sudden deterioration hypoxic
pneumothorax: signs
reduced expansion
hyper-resonance to percussion
diminished breath sounds
tension pneumothorax: signs
respiratory distress tachycardia hypotension distended neck veins trachea deviation away from side of pneumothorax
pneumothorax: CXR
should not be performed if suspected tension as it delays treatment
look for an area devoid of lung markings, peripheral to edge of collapsed lung
pneumothorax: ABG
if dyspnoeic/chronic lung disease
hypoxia
small spontaneous pneumothorax: treatment
heal on their own
pneumothorax due to trauma or medical intervention: treatment
chest drain
tension pneumothorax: treatment
needle aspiration then chest drain
pneumothorax: surgery
if:
bilateral
lung fails to expand in 48 hours of drain insertion
persistent air leak
pneumothorax: differentials
pleural effusion
chest pain
pulmonary embolism
pulmonary embolism
blockage of pulmonary artery or one of its branches in the lung by a venous thromboembolism
pulmonary embolism: pathogenesis
PEs usually arise from a venous thrombosis in pelvis or legs
clots break off and pass through the veins and right side of heart before lodging in pulmonary circulation
pulmonary embolism: risk factors and causes
deep vein thrombosis septic emboli fat air recent surgery leg fracture malignancy old age obesity combined pill
pulmonary embolism: symptoms
acute dyspnoea
pleuritic chest pain
haemoptysis
syncope
pulmonary embolism: signs
cyanosis tachypnoea tachycardia hypotension pleural effusion
pulmonary embolism: bloods
FBC
U&E
baseline clotting
pulmonary embolism: D-dimer
non-specific fibrin degradation product
normal excludes diagnosis
positive does not confirm
pulmonary embolism: ABG
may show type 1 resp failure, low O2 and low Co2
pulmonary embolism: CXR
may be normal or show dilated pulmonary artery, or pleural effusion
pulmonary embolism: CT pulmonary angiography
sensitive and specific
test of choice in high risk or those with positive D-dimer
pulmonary embolism: ECG
may be normal or show tachycardia, RBBB, RV strain
pulmonary embolism: treatment
LMHW thrombolysis anticoagulants oxygen morphine IV fluids
pulmonary embolism: LMWH
short term anticoagulation
fondaparinux
pulmonary embolism: thrombolysis
if haemodynamically unstable
alteplase
pulmonary embolism: long term anticoagulants
DOAC- rivaroxaban- inhibit factor Xa
warfarin
pulmonary embolism: length of treatment
pregnancy- LMWH until delivery
malignancy- LMWH for 6 months or until cure of cancer
unprovoked- continue for > 3 months
provoked- 3 months then reassess risk
pulmonary embolism: prevention
LMWH to all immobilised patients
stop HRT and combined pill
hydration
early mobilisation
wegener’s granulomatosis
multisystem disorder of unknown cause characterised by necrotising granulomatous inflammation and vasculitis of small and medium vessels
wegener’s granulomatosis: pathogenesis
anti-neutrophil cytoplasmic antibody (ANCA) attaches to neutrophils and activated them before then enter the tissue
this results in recruitment of more neutrophils and so more activation
reactive oxygen species produced and neutrophil degranulation occurs
this generates microabscesses, recruits monocytes and produces granulomas by macrophages
wegener’s granulomatosis: upper airway disease presentation
nasal obstruction
ulcers
nose bleed
destruction of nasal septum
wegener’s granulomatosis: renal disease presentation
rapidly progressive glomerulonephritis
proteinuria
haematuria
wegener’s granulomatosis: pulmonary involvement presentation
cough
haemoptysis
pleuritic chest pain
wegener’s granulomatosis: general presentation
skin purpura
peripheral neuropathy
arthritis
wegener’s granulomatosis: bloods
cANCA positive
high ESR/CRP
wegener’s granulomatosis: urinalysis
look for proteinuria and haematuria
wegener’s granulomatosis: CXR
nodules present
possible fluffy infiltrate of pulmonary hemorrhage
wegener’s granulomatosis: CT
diffuse alveolar haemorrhage
wegener’s granulomatosis: treating severe disease
corticosteroids- prednisolone- induces remission
methotrexate for maintenance
wegener’s granulomatosis treatment: plasma exchange
severe renal disease or pulmonary haemorrhage
wegener’s granulomatosis treatment: co-trimoxazole
prophylaxis against pneumocystis jiroveci and staph colonisation
wegener’s granulomatosis: differentials
churg-strauss syndrome:
- affects small arteries
- males in 40s
- rhinitis, eosinophilia and vasculitis
- high eosinophil count
- ANCA +ve
goodpasture’s syndrome: epidemiology
more common in males
usually presents >16 yrs
goodpasture’s syndrome: lung disease presentation
pulmonary haemorrhage sneezing, nasal discharge, fever cough dyspnoea anaemia
goodpasture’s syndrome: acute glomerulonephritis presentation
nephritic glomerulonephritis
haematuria
proteinuria
hypertension
goodpasture’s syndrome: autoantibodies
diagnostic test
anti-GBM
goodpasture’s syndrome: CXR
infiltrates due to pulmonary haemorrhage- often in lower zones
goodpasture’s syndrome: kigney biopsy
crescent glomerulonephritis
goodpasture’s syndrome: treatment
vigorous immunosuppressants
treat shock
plasma exchange
goodpasture’s syndrome treatment: vigorous immunosuppressants
corticosteroids- prednisolone
cyclophosphamide
goodpasture’s syndrome: differentials
SLE
RA
idiopathic pulmonary haemosiderosis
goodpasture’s syndrome
acute glomerulonephritis and lung symptoms caused by antiglomerular basement membrane antibodies
type 2 hypersensitivity
autoimmune disease
acute respiratory distress syndrome
caused by direct lung injury or occur secondary to severe systemic illness
lung damage and release of inflammatory mediators cause increased capillary permeability and non-cariogenic pulmonary oedema
acute respiratory distress syndrome: pulmonary causes
pneumonia gastric aspiration inhalation injury vasculitis
acute respiratory distress syndrome: other causes
shock septicaemia haemorrhage multiple transfusions acute liver failure trauma burns
acute respiratory distress syndrome: risk factors
sepsis trauma pneumonia gastric aspirin pregnancy drugs burns smoke inhalation head injury raised ICP malaria
acute respiratory distress syndrome: symptoms
cyanosis
peripheral vasodilation
acute respiratory distress syndrome: signs
tachypnoea
tachycardia
bilateral fine inspiratory crackles
acute respiratory distress syndrome: investigations
blood test
ABG
CXR
pulmonary artery catheter
acute respiratory distress syndrome: CXR
bilateral pulmonary infiltrates
acute respiratory distress syndrome: pulmonary artery catheter
measure pulmonary capillary wedge pressure- normal
acute respiratory distress syndrome: diagnostic criteria
the following:
- acute onset
- CXR- bilateral infiltrates
- PCWP normal
- refractory hypoxaemia with PaO2:FiO2 <200
acute respiratory distress syndrome: treatment
admit to ITU supportive therapy treat cause nutritional support resp and circulatory support treat sepsis
acute respiratory distress syndrome treatment: respiratory support
1st line- continuous positive airway pressure with 40-60% O2
2nd line- mechanical ventilation
acute respiratory distress syndrome treatment: circulatory support
conservative fluid management
inotropes, vasodilators, blood transfusions
low dose NO to treat hypertension
acute respiratory distress syndrome treatment: sepsis
identify organism
give appropriate antibiotics
pulmonary hypertension
mean pulmonary artery pressure above 25mmHg
occurs due to increased pulmonary vascular resistance or increased pulmonary blood flow
pulmonary hypertension: pathogenesis
hypoxic vasoconstriction, inflammation or cell proliferation results in narrower vessels increasing right ventricular pressure causing hypertension.
leads to development of RV hypertrophy, dilation and eventually failure
pulmonary hypertension: pulmonary vascular disorders causes
pulmonary embolism
primary pulmonary hypertension
pulmonary hypertension: disease of lung parenchyma causes
COPD
chronic lung disorders
pulmonary hypertension: MSK disorders causes
poliomyelitis
myasthenia gravis
pulmonary hypertension: disturbance of resp drive causes
obstructive sleep apnoea
morbid obesity
cerebrovascular disease
pulmonary hypertension: cardiac causes
mitral stenosis
LV failure
congenital heart failure
pulmonary hypertension: symptoms
exertional dyspnoea lethargy fatigue ankle swelling chest pain
pulmonary hypertension: signs
loud pulmonary second sound
right parasternal heave
pulmonary hypertension investigations: CXR
enlarged proximal pulmonary arteries which taper distally
pulmonary hypertension investigations: ECG
RVH and P pulmonale
right axis deviation
pulmonary hypertension investigations: echo
RV dilation
pulmonary hypertension investigations
LFT detects portal hypertension autoimmune screen Echo ECG CXR
pulmonary hypertension: treatment
treat cause oxygen warfarin diuretics for oedema pulmonary vasodilators
pulmonary hypertension: differentials
cor pulmonale cardiomyopathies primary right ventricular heart failure congestive cardiac failure portal hypertension
cor pulmonale
right heart failure and abnormal enlargement
caused by chronic pulmonary arterial hypertension
cor pulmonale: caused by lung disease
COPD
bronchiectasis
pulmonary fibrosis
lung resection
cor pulmonale: caused by pulmonary vascular disease
pulmonary emboli
pulmonary vasculitis
ARDS
sickle cell
cor pulmonale: caused by thoracic cage abnormality
hyphosis
scoliosis
thoracoplasty
cor pulmonale: neuromsuclar disease
myasthenia gravis
poliomyelitis
motor neuron disease
cor pulmonale: hypoventilation
sleep apnoea
enlarged adenoids
cor pulmonale: symptoms
dyspnoea
fatigue
syncope
cor pulmonale: signs
cyanosis tachycardia raised JVP loud P2 pansystolic murmur
cor pulmonale: bloods
FBC- high haematocrit, secondary polycythaemia
cor pulmonale: ABG
hypoxia
hypercapnia
cor pulmonale: CXR
enlarged right atrium and ventricle, prominent pulmonary arteries
cor pulmonale: ECG
P pulmonale
right axis deviation
right ventricular hypertrophy
cor pulmonale: treat cause
COPD
pulmonary infections
cor pulmonale: treating resp failure
in acute situation
give 24% oxygen
cor pulmonale: treating cardiac failure
diuretics- furosemide
cor pulmonale: venesection treatment
if haematocrit >55%
cor pulmonale: surgery
if the patient is young
heart-lung transplant
beta 2 agonists: indications
COPD asthma
beta 2 agonists: examples
salbutamol- SABA
salmeterol- LABA
beta 2 agonists: route of administration
inhaler
nebuliser
beta 2 agonists: mechanism
bind to B2 receptor which causes smooth muscle relaxation and bronchodilation
B@R’s found in the smooth muscle of the bronchi, GI tract, uterus and blood vessels
beta 2 agonists: types
short acting
long acting- take longer to act but last longer
beta 2 agonists: adverse effects
hypokalaemia
tremor
palpitations
corticosteroids: examples
prednisolone
methylprednisolone
dexamethasone
corticosteroids: mechanisms
supress multiple inflammatory genes
leads to reduced inflammation
corticosteroids: adverse effects
osteoporosis
increased risk of infection
weight gain