respiratory Flashcards
3 factors characterizing asthma
reversible airway inflammation
airway hyper responsiveness
inflammation of bronchi
causes of asthma
atrophy hygiene hypothesis aspirin induced occupational exercise induced
describe atrophy and related conditions
genetic predisposition to IgE mediated allergen sensitivity
allergic asthma, atopic dermatitis, allergic rhinitis
what are the 3 phases of asthma
early phase
late phase
chronicity
describe early phase of asthma
type 1 hypersensitivity->IgE release activating mast cells
mast cells degranulate w/ histamine
what role does histamine play in early phase of asthma
smooth muscle contraction + bronchoconstriction
describe late phase of asthma
recurrence of inflammatory cells such as polymorphonuclear/ T cells
beta agonist cannot accomplish complete reversal
describe chronic phase of asthma
airway remodelling (non reversible) persistent inflammation w/ airways filled with fibrous tissue
diagnostic of asthma
spirometry: obstructive pattern
FeNO: eospinopilic airway inflammation is raised
peak flow tests daily recorded
obstructive vs restrictive pattern spirometry
obstructive:
FVC: normal/ reduced, FEV1: reduced
FEV1/FVC: <70%
restrictive:
both decreased, ratio is normal %
treatment of asthma
SABA
SABA+ low dose ICS
low dose ICS+ LABA
higher ICS+ LABA
(move to second stage when there is uncontrolled symptoms)
acute attacks of asthma
salbutamol (SABA)
oxygen (94-98%)
steroids (prednisolone/ IV hydrocortisone)
ipratropium bromide
mode of action: ipratropium bromide
SAMA: muscarinic antagonist
mode of action: adrenaline
alpha agonist
define COPD
non reversible long term blockage in air flow to lung tissue damage: smoking, alpha 1 antitrypsin deficiency
COPD vs ASTHMA
COPD not reversible w/ bronchodilators, symptoms will exacerbate during lung infections
describe COPD: chronic bronchitis
- chronic inflammation of bronchi with neutrophilic, CD8+ t lymphocytes and macorphages infiltration
- chronic productive cough for 3 months over 2 consecutive years
pathological changes in chronic bronchitis
goblet cell hyperplasia
mucus hypersecretion
narrowing of small airways
describe COPD: emphysema
abnormal air sac enlargement distal to terminal bronchioles causing reduced area for gas exchange->chronic hypoxia
what causes alveoli destruction in emphysema
^proteases due to neutrophils and macrophages-> protease elastase cause decrease elastin-> collapse/ dilation and bullae formation
COPD symptoms
productive cough, SOB, wheeze, recurrent respiratory infections
diagnosis of COPD
spirometry
CXR, FBC, BMI
COPD: long term management
smoking cessation+ flu vaccines
- SABA/ SAMA
- LABA/LAMA
- LABA + ICS
when is long term oxygen therapy used in COPD
PaO2< 7.3 kPa
or
PaO2< 8 kPa with:
pulmonary hypertension, peripheral oedema
symptoms of COPD exacerbation
pyrexia, SOB, sputum
CO2 retention-> flapping tremor/ confusion
cracked wheeze on auscultation
define type 1 respiratory failure
normal pCO2 and low pO2
define type 2 respiratory failure
raised pCO2 and low pO2
ie, COPD
effect of CO2 and HCO in lungs
^CO2= acidic (low pH)
^ HCO= basic (high pH)
2 rules for oxygen saturations in COPD
- if retaining CO2: aim for O2 at 88-92% with Venturi mask
2. not retaining CO2 + bicarbonate is normal: aim for oxygen sat 94% +
at home COPD exacerbation treatment
prednisolone
inhalers or nebulizers
antibiotics for infections
in hospital non severe COPD exacerbation treatment
nebulised bronchodilators
steroids
antibiotics for infection
physiotherapy for sputum
in hospital severe COPD exacerbation cases treatment
IV aminophylline
non-invasive ventilation, intubation
Doxapram
define pneumonia
inflammation of the lung parenchyma where normal air-filled lungs is filled with infective liquid known as consolidation
what are the three route for bacteria to reach the lungs
inhalation
aspiration
hematogenous
name the organisms involved in CAP: typical pneumonia
streptococcus pneumonia
haemophilus influenza
name the organisms involved in CAP: atypical pneumonia
mycoplasma pneumoniae coxiella burnetti (Q fever)
presentation of streptococcus pneumoniae
cough, pleuritic pain, pyrexia
leukocytosis and raised CRP
describe mycoplasma pneumoniae (type, patient type, symptoms, diagnostic)
rod shaped bacterium, no cell wall
young ppl
arthralgia, haemolytic anaemia
serology
define hospital acquired pneumonia
pneumonia contracted> 48 hours after hospital admission
organisms in hospital acquired pneumonia
gram negative bacteria:
pseudomonas aeruginosa
staphylococcus aureus
legionella pneumophila
describe pseudomonas aeruginosa (type, risk factor, sputum)
gram negative bacillus
immunosuppressed patients (ie, bronchiectasis due to cystic fibrosis)
green sputum
pseudomonas aeruginosa treatment
cephalosporin, amino glycoside
define aspiration pneumonia
inhalation of oropharyngeal or gastric contents
what type of patient may get aspiration pneumonia
neuro/muscular problems
oesophageal conditions
mechanical interventions like endotracheal tubes
complications of pneumonia
pulmonary effusion, pneumothorax
sepsis, AF
what does CURB-65 measure for
mortality risk of pneumonia
what does CURB-65 stand for
C: confusion U: urea>7 R: respiratory rate> 30 B: blood pressure < 90/60 65 years of age or older
what does CURB-65 score mean
0-1=low risk/ mild
2= intermediate risk / moderate
3-5= high risk / severe
CAP treatment
mild: amoxicillin (use clarithromycin/ doxycycline instead for allergy)
moderate: amoxicillin + clarithromycin
severe: IV co-amoxiclav and clarithromycin
2 types of lung cancer
small cell
non small cell (adenocarcinoma, squamous cell, large cell)
(also mesothelioma: asbestos)
adenocarcinoma vs squamous cell
Adeno: non-smoker, lung peripheries
squamous: smoker, PTHcentral part of lungs (bronchus)
unique features of small cell lung cancer
poor prognosis, fast doubling time
cancer of APUD (neuroendocrine) cell find in lungs
smokers
symptoms that may present with small cell carcinoma
ectopic ADH/ACTH production (Cushing’s syndrome=^ cortisole)
weight gain, easy bruising and hyperpigmentation
lung cancer: signs of pleural effusion
exudative
dull/ stony percussion
reduced vocal resoncance/ breath sound
when should CXR be ordered for lung cancer
patient over 40 + concerning symptoms:
weightloss, hemoptysis
diagnosis of lung cancer
CXR: focal lesion, pleural effusion , widen mediastinum
CT for suggestive CXR, include neck and upper abdomen for staging
T in TNM staging
T0 - tumour not visible but found in sputum culture / bronchial fluids
T1 - 3cm or less
T2 - 3 < x
N in TNM staging
N0 - no lymph node metastases
N1 - ipsilateral hilar lymph node
N2 - ipsilateral mediastinal or subcarinal lymph nodes
N3 - contralateral mediastinal or hilar lymph nodes
M in TNM staging
M0 - no distant metastases
M1 - distant metastases
cause and spread of TB
caused by mycobacterium spread via aerosolized droplets
characteristics of mycobacterium
aerobes
facultative intracellular
acid fast bacilli
primary vs progressive primary vs latent TB
prim: initial infection, suppressed in majority of individuals
1a. latent: non infectious state after primary infection
1b. progress: primary infection not suppressed, prolonged infection
what is the ghon complex
lesion seen in children w/ TB
ghon focus+ ipsilateral mediastinal lymph node
symptoms of TB
fever, weightless, malaise
diagnosis of TB
Active: CXR, Ziehl-Neelson stain(AFB, langhans type giant cells)
Latent: Tuberculin skin test
CXR findings in TB
Ghon focus
Bilateral hilar lymphadenopathy
Miliary shadowing
active TB treatment
- Rifampicin, Isoniazid, Pyrazinamide and Ethambutol for 4 months
- Rifampicin and Isoniazid for a further 2 month
latent TB treatment
Rifampicin and Isoniazid for 3 months
OR
Isoniazid for 6 months
side effects of TB drugs
Rifampicin: hepatitis, orange urine/sweat
Isoniazid: peripheral neuropathy
Pyrazinamide: ^ uric acid, gout
Ethambutol: optic neuritis
define pneumothorax
air in intrapleural cavity (between visceral pleura and parietal pleura)
what are the 2 types of pneumothorax
spontaneous (no trauma)
traumatic (yes trauma)
2 types of spontaneous pneumothorax and their risk groups
primary: no pathophysiological lungs (tall/thin male)
secondary: pathological lungs (50+ and COPD/ asthmatic patients)
symptoms of spontaneous pneumothorax
sudden onset dyspnoea and chest pain
hyper resonance on percussions
decrease air entry
what is tension pneumothorax
spontaneous pneumothorax patients who are hemodynamically (abnormal bp, arrhythmias) unstable
tension pneumothorax treatment
urgent needle decompression inserted through 2nd intercostal space midclavicular line
procedure for haem stable patients w/ spontaneous pneumothorax
send for CXR
treatment for primary pneumothorax patients
large (>2cm) or breathless: needle aspiration (14-16G)
small (<2cm) and asymptomatic: outpatient followup
treatment for secondary pneumothorax
(>2cm) or breathless: chest drain
(1-2) : needle aspiration (14-16G)
< 1cm: observe for at least 24h
symptoms of traumatic pneumothorax
hypotension + tachycardia
chest pain + hypoxaemia
treatment of traumatic pneumothorax
immediate needle decompression
define bronchiectasis
irreversible + abndomal dilatation of airways
commonly secondary to cystic fibrosis
what is the predominant inherited cause of bronchiectasis
primary ciliary dyskinesia
symptoms of bronchiectasis
persistent sputum production and cough over years
may have immune disorders/ COPD
diagnostic of bronchiectasis
high resolution CT scan
what is bronchiectasis exacerbation
infections cause worsening symptoms
H. influenzae, S. aureus, P. aeruginosa, and S. pneumoniae.
define cystic fibrosis
autosomal recessive mutations to the CFTR gene on the long-arm of chromosome 7
when and what test is used to screen CF
day 5 after birth
newborn heel prick test (measure Immuno-reactive trypsin)
what are some confirmatory testings for CF
Sweat test: sweat chloride > 60mmol/L = +++
Genetic testing: screen for common mutations or entire CFTR gene
define pleural effusion
abnormal collection of fluid in pleural cavity (between visceral pleura and parietal pleura)
what are the 3 serous membranes that line the lung
Visceral pleura: inner layer. Covers the lungs, blood vessels and bronchi
Pleural space: Contains ~10 mL of fluid
Parietal pleura: outer layer. Attaches to the chest wall
function of pleural cavity fluid
Lubricates: easier for the layers to slide over one another during respiration
Generates surface tension: pulls the two layers (parietal and visceral) adjacent to one another
where does the pleural cavity get the liquid from?
vessels at the parietal and visceral pleura
define hydrostatic pressure and the role it has on pleural cavity fluid
Hydrostatic: pressure exerted by a fluid against a membrane, Increases lead to fluid leaking from blood vessels
define oncotic pressure and the role it has on pleural cavity fluid
Oncotic pressure: osmotic pressure produced by large macromolecules (e.g. proteins). Exerts a ‘pulling power’ on fluid
define lymphatic drainage and the role it has on pleural cavity fluid
Lymphatic drainage: drains body fluid and returns it to the systemic circulation. Can alter the hydrostatic pressure
3 reasons that increase fluid entry to pleural cavity
Increased vasculature permeability
Increased microvascular pressure
Decreased plasma oncotic pressure
what causes Increased vasculature permeability
infection, malignancy: loss of fluid and macromolecules from ‘leaky’ vessels
what causes increase microvascular pressure
heart failure: increased venous pressure affects hydrostatic pressure forcing fluid out
what causes decreased plasma oncotic pressure
cirrhosis: leading fluid accumulation
transudative vs exudative pleural effusion
Transudate: no protein/ cellular content, due to change in hydrostatic and oncotic pressure (HF, cirrhosis)
Exudate: high protein/ cellular content, from inflammatory conditions that affect vessel permeability /lymphatic drainage. (infection/ malignancy)
symptoms of pleural effusion
reduced vocal resonance/ breath sounds
stony dull percussion
SOB + non productive cough
diagnostic of pleural effusion
CXR
symptoms of pulmonary embolism
SOB, pleuritic chest pain, pleural rub,
sinus tachycardia, DVT symptoms
diagnostic of PE
well’s score 4+: CTPA, not available-> anticoagulation if safe.
well’s score ≤ 4: d-dimer . positive= send for CTPA
what is d-dimer
fibrin-degradation product, produced when blood clots are broken down by fibrinolytic system
management for PE/ DVT initial and long term
initial: apixaban or rivaroxaban-> LMWH-> thrombolysis
long term: warfarin, a DOAC or LMWH
key features of sarcoidosis
mostly black
CXR: Bilateral hilar lymphadenopathy
red lesions/ erythema nodusum
key features of pulmonary fibrosis/ interstitial lung disease
chronic exertion dyspnea
honeycombing (clusters of cystic air spaces)
reticular opacities
TLC formula
VC+ RV
vital capacity + residual volume
describe type 1 pneumocytes
thin squamous cell covering 97% of alveolar surface
describe type 2 pneumocytes
cuboidal cells, secret surfactant
may not produce enough until 35 weeks causing premature babies being prone to respiratory distress
law of Laplace+ example
tension/ pressure exerted on spherical wall, is inversely proportional to sphere’s thickness (thin wall=more pressure/tension)
ie, alveoli are prone to collapse due to alveolar surface tension and surfactant increase alveolar thickness reducing surface tension
describe coup symptoms and treatment
inspiratory stridor, cough, and hoarseness
dexamethasone and supportive care
What does wells score PE look for
Clinical signs of DVT PE is likely Tachycardia > 100 Surgery in the past Monet Prior DVT/PE Haemoptysis Malignancy
Treatment for HAP
Amoxicillin and metronidazole
If sevré give in IV form
Acute exacerbation of asthma treatment
oxygen (94-98%) salbutamol (neb) Hydrocortisone (IV) OR oral prednisolone Ipratropium (neb) Theophylline (oral) Magnesium sulphate (IV) An anesthetist (to intubate)
Acute exacerbation of COPD treatment
Ipratropium Salbutamol oxygen (target 88-92%) Amoxicillin (/doxycycline) Prednisolone
Define tidal vs vital volume
Tidal: normal passive air intake and out
Vital: force inspiration and expiration
Sevré asthma symptoms
Life threatening asthma symptoms
