resp conditions Flashcards
what would a CXR of someone with asbestosis look like?
pulmonary fibrosis
dense calcified pleural plaques
pleural thickening
(restrictive defects)
asthma drug therapy
1 - SABA (salbutamol) as required + low dose ICS (beclomethasone)
2 - + LABA (salmeterol)
3 - 4th drug - leuketriene (montelukast), methylxanthines (theophylline), LAMA (tiotropium), sodium cromoglicate in kids
4 - increase ICS dose or oral steriod (prednisolone) - used in primary exacerbation
5 - consider trials of anti-IgE (omalizumab)
how do you diagnose bronchiectasis?
HRCT showing -
dilation of airways - larger than accompanying pulmonary artery
thickening of bronchial walls
lack of tapering airways
who does bronchiolitis usually affected and what are the common causes?
viral respiratory condition that affects those ages 0-2 + causes inflammation of the bronchioles obstructing them
80% = respiratory syncytial virus (RSV)
metapneumovirus
drug therapy in COPD exacerbation
oxygen 24-28% - keep SaO2 between 88-92%
nebulised high dose salbutamol (SABA) + ipratropium (SAMA)
antibiotics if infection
when is triple therapy recommended for COPD patients?
LABA/LAMA/ICS
if frequent exacerbator or high eosinophilic count (>300)
what is Cor pulmonale?
right heart failure secondary to lung disease caused by chronic pulmonary hypertension
most common cause = COPD
clinical presentation of cor pulmonale
SOB peripheral oedema syncope hypoxia, cyanosis raised JVP 3rd heart sound
name 2 anti-fibrotic drugs
pirfenidone - also anti-inflammatory
nintedanib - monoclonal antibody targeting tyrosine kinase
signs + symptoms of pulmonary fibrosis
progressive breathlessness exertional dyspnoea dry cough cyanosis, clubbing fine-end inspiratory crackles reduced lung volume (restrictive) honeycomb lung on CT - advanced
whats the difference between transudates + exudates?
transudates = <30 g/L
–> fluid moving across into pleural space (congestive HF, hypoalbuminaemia, hypothyroidism)
exudates = >30g/L
–> increase leakiness of tissues into pleural space (malignancy, infection, inflammation)
signs + symptoms of pleural effusion
pleuritic chest pain
stoney dull to percuss
diminished breath sounds on affected side
blunting of costophrenic angles
management of pneumothorax
no SOB + <2cm = no treatment - follow up in 2-4weeks
SOB and/or >2cm = aspiration
if aspiration fails twice - chest drain
where do you insert a chest drain?
triangle of safety
- 5th ICS
- mid axillary line
- anterior axillary line
management of tension pneumothorax
insert large bore cannula to 2nd ICS in midclavicular line
once pressure relieved, insert chest drain
will the aspiration of empyema be acidic or alkalotic?
acidic
what is first line treatment for patients with non small cell lung cancer?
surgery - if isolated to a single area
lobectomy, segmentectomy
name some extrapulmonary manifestations associated with lung cancer
recurrent laryngeal nerve palsy - hoarse voice, cancer pressing on recurrent laryngeal nerve
phrenic nerve palsy - weak diaphragm, SOB, ^ same cause
SVC obstruction - facial swelling, bulging neck + chest veins
–> pembertons sign
what is pembertons sign?
raising hands over head causes facial congestion + cyanosis
due to SVC obstruction - potential extra-pulmonary manifestation of lung cancer
name some paraneoplastic syndromes associated with small cell lung cancer
syndrome of inappropriate ADH (SIAD)
cushing’s syndrome - excessive cortisol
limbic encephalitis
lambert-eaton syndrome - autoimmune @ neuromuscular junctions
what is horner’s syndrome and what causes it?
triad of -
partial ptosis (drooping eyelid)
anhidrosis (difficulty sweating)
miosis (excessive constriction of pupil)
caused by pancoast tumour = tumour in pulmonary apex
–> presses on sympathetic ganglion
what causes SIADH?
SIADH = syndrome of inappropriate ADH (anti-diuretic hormone)
caused by ectopic ADH secretion by small cell lung cancer
–> presents with hyponatraemia
what is cushings syndrome? how does it present?
high levels of cortisol
ectopic ACTH (stimulation of cortisol) secretion by a small cell cancer
weight gain, easy brusing, stretch marks, depression
name some paraneoplastic syndromes associated with non-small cell lung cancer
horner’s syndrome - pancoast tumour
hypercalcaemia - caused by ectopic parathyroid hormone
–> from squamous cell carcinome
what is lambert-eaton syndrome?
paraneoplastic syndrome from SMALL cell lung cancer
a result of antibodies produced by immune system against cancer but also target + damage voltage-gated calcium channel @ presynaptic terminals in motor neurones
symptoms - muscle weakness, ptosis, slurred speech, blurred vision
what are 3 auscultatory features you’d see in someone with pneumonia?
bronchial breath sounds - harsh breath sounds, equally loud on inspiration + expiration –> due to consolidation of tissue around airway
focal coarse crackles - air passing through sputum
dullness to percussion - lung tissue collapse and/or consolidation
what does CURB 65 predict?
predicts mortality
1 = <5%
3 = 15%
4/5 = > 25%
treatment based on score
0/1 - home
>=2 - hospital
>= 3 - ICU assessment
what parameters does CURB65 involve?
Confusion
Urea > 7
Respiratory rate >=30
BP - <90 systolic / <= 60 diastolic
65 or older
2 most common causes of pneumonia
streptococcus pneumoniae
haemophilus influenzae
clinical features of mycoplasma pneumoniae
erythema multiforme - target lesions (pink rings with pale centres)
how do you diagnoses interstitial lung disease?
clinical features + HRCT (ground class appearance)
if unclear - biopsy
what is hypersensitivity pneumonitis (extrinsic allergic alveolitis)? causes?
type III hypersensitivity reaction to environmental allergen that causes parenchymal inflammation + destruction
causes - bird-fanciers lung - bird droppings farmers lung - mouldy hay spores mushroom workers lung malt workers lung - mould on barely
how is hypersensitivity pneumonitis diagnosed?
bronchoalveolar lavage
– involves collecting cells from airway during bronchoscopy by washing with fluid then collecting fluid for testing
–> shows raised lymphocytes + mast cells
why do patients with a PE commonly have a respiratory alkalosis when an ABG is performed?
high respiratory rate causes them to blow off extra CO2
low CO2 = alkalotic
PE pO2 = low
initial management of PE
first line = apixaban or rivaroxaban (factor Xa inhibitors)
LMWH (enoxaparin) where not suitable (antiphospholipid syndrome)
–> given before diagnosis if DVT / PE suspected
long term anticoagulation
warfarin - target INR = 2-3
NOACs/DOACs - apixaban, dabigatran, rivaroxaban
LMWH = first line in pregnancy + cancer
how long should you anticoagulate for post PE?
obvious reversible cause = 3 months
unclear cause, recurrent VTE, thrombophilia = >3 months
active cancer = 6 months then review
when would you use thrombolysis for a PE?
where there is a massive PE with haemodynamic compromise
thrombolytic agents = streptokinase, alteplase
what type of bacteria causes tuberculosis?
myobacterium tuberculosis
gram positive aerobic bacillus - acid-fast characteristics (resistant to staining)
transmission = respiratory droplets
investigations for TB
ziehl-neelson stain - TB bacteria goes red against blue background
CXR - linear opacities in upper lobe, lymphadenopathy, calcification, miliary disease, effusion, cavitation (reactivated)
skin test - for LATENT TB
what would a CXR of someone with silicosis look like?
egg-shell calcification of hilar lymph nodes
inhalation of silica particles
what type of hypersensitivity reaction is TB?
type IV (cell-mediated - delayed)
caseating granuloma
what is the treatment for active + latent TB?
rifampicin
isoniazid
pyrazinamide
ethambutol
active = RIPE for 2 months + RI for further 4 months
latent = RI for 3 months
what are the side effects of the medication given for TB?
rifampicin - orange urine + tears
isoniazid - neuropathy
pyrazinamide - hyperuricaemia (excess uric acid in blood), V+D
ethambutol - colour blindness
RIP - all associated with hepatotoxicity
a patient is started on 4 medications to treat their TB. They start experiencing symptoms of neuropathy, what medication should be prescribed?
pyridoxine (vitamin B6) - usually prescribed prophylactically
isoniazid causes neuropathy
how can latent TB become reactivated?
becoming immunocompromised
–> HIV
clinical features of sarcoidosis
non-caseating - type IV hypersensitivity
dry cough erythema nodosum uveitis bilateral hilar lymphadenopathy fever, malaise, weight loss
increase serum ACE + Ca2+
peripheral nodular infiltration
what is the gold standard for confirming diagnosis of sarcoidosis?
US guided biopsy of mediastinal lymph nodes
–> non-caseating granulomas with epithelioid cells
what causes alpha-1 antitrypsin deficiency? what can it cause?
common inherited conditon caused by lack of protease inhibitor produced by liver
role of A1AT is to protect cells from enzymes such as neutrophil elastase
–> causes emphysema (COPD) in young, non-smokers
how would you differentiate between acute tonsillitis and quinsy?
quinsy = a complication of tonsillitis
trismus (difficulty opening the mouth) = a feature of quinsy (peritonsillar abscess)
what would an ABG of someone with long standing COPD look like?
type 2 resp failure (low pO2 + high pCO2)
respiratory acidosis - over time becomes compensated by HCO₃
patients with longstanding COPD rely on hypoxic drive in order to drive respiration because the respiratory centre in their brain is insensitive to CO₂. Patients are therefore hypercapnic and exhibit type 2 respiratory failure. The longstanding hypercapnia eventually causes a respiratory acidosis which over time becomes compensated by HCO₃. These patients classically have a low % O2 and high CO2.
Which organism commonly causes pneumonia in immunocompromised patients?
Pneumocystis jiroveci
What is the pattern of inheritance shown by alpha-1 antitrypsin deficiency?
autosomal recessive
