Respiratory 2 Flashcards
what is Wegener’s granulomatosis also known as?
granulomatosis with polyangitis (GPA)
what is the characteristic feature of Wegener’s granulomatosis?
necrotising granulomatous inflammation and vasculitis of small/medium vessels
name 3 respiratory features of Wegener’s granulomatosis
cough, haemoptysis, pleuritis, sinusitis, saddle-nose deformity, epistaxis, nasal obstruction
name 3 renal features of Wegener’s granulomatosis
proteinuria, haematuria, progressive glomerulonephritis
name 3 features, other than respiratory/renal features, of Wegener’s granulomatosis
skin purpura, peripheral neuropathy, mononeuritis multiplex. eye involvement - keratitis, conjunctivitis, scleritis, episcleritis, uveitis.
what would be the significant finding in the blood of Wegener’s granulomatosis patients?
ANCA +ve
how would you treat Wegener’s granuomatosis?
corticosteroids + cyclophosphamide for remission induction. Azathioprine + methotrexate for maintenance.
what prophylactic treatment would be given to Wegener’s granulomatosis patients? what does it protect against?
Co-trimoxazole. Pneumocystis jivorecii and staphylococcal colonisation.
list the possible sources of an embolus
FATBAT Fat Air Thrombus Bacteria Amniotic fluid Tumours
what is a likely cause of a PE?
DVT in pelvis/legs (iliofemoral veins)
give 4 risk factors for a PE
recent surgery (esp abdo/pelvis or hip/knee replacement). thrombophilia. immobility. malignancy. pregnancy/pill/HRT. previous PE. DVT.
list 3 steps taken to prevent PE in surgical patients
LMWH (e.g. dalteparin) given to all immobile patients. compression stockings. early mobilisation. stop HRT/Pill pre-op.
give 3 symptoms of PE
sudden onset dyspnoea, pleuritic chest pain, haemoptysis, dizziness, syncope
give 3 signs of PE
tachypnoea, pyrexia, cyanosis, tachycardia, hypotension, raised JVP, pleural rub
what 2 investigations are carried out to confirm a diagnosis of PE?
D dimer - neg result excludes, +ve doesn’t mean it is PE. CTPA (CT pulmonary angiography)
how would you manage a patient with a PE?
high flow oxygen, LMWH until INR 2-3, then start warfarin/stop heparin. massive PE - thrombolysis (alteplase)
what is the usual cause of the common cold? how is this spread?
rhinovirus infection. spread by droplets and close personal contact.
what 2 organisms usually cause sinusitis?
Strep pneumonia or H influenzae
how would you treat sinusitis?
broad spectrum abx (e.g. co-amoxiclav). topical corticosteroids, steam inhalation.
what is the surface of the influenza viruses coated with? what are these needed for?
haemaglutinin (H) and neuraminidase - needed for attachment to host respiratory epithelium.
give 3 clinical features of influenza
abrupt onset fever, generalised aching of limbs, severe headache, sore throat and dry cough
how would influenza be managed? what complication is the patient at risk of?
symptomatic - paracetamol, fluids, rest. pneumonia.
name 3 organisms that can cause community acquired pneumonia
common - *strep pneumoniae, H influenzae, Mycoplasma pneumoniae. also - staph aureus, Legionella spp, Moraxella catarrhalis and Chlamydia.
define nosocomial pneumonia
aka hospital-acquired. pneumonia acquired >48h after admission to hospital
name some common causative organisms of hospital acquired pneumonia
Gram -ve enterobacteria or *Staph aureus. also - Pseudomonas, Klebsiella, Bacterioides, Clostridia.
name 3 organisms that may cause pneumonia in immunocompromised patients
Strep pneumoniae, H influenzae, Staph aureus, M catarrhalis, M pneumonia, Gram -ve bacilli, Pneumocystic jivorecii.
give 3 symptoms of pneumonia
fever, rigors, malaise, anorexia, dyspnoea, cough, purulent sputum, haemoptysis, pleuritic pain
give 3 signs of pneumonia
pyrexia, cyanosis, confusion, tachypnoea, tachycardia, hypotension, signs of consolidation
name 3 signs of lung consolidation you might find on examination
diminished expansion, dull percussion note, increased tactile vocal resonance, bronchial breathing + pleural rub
list 3 differential diagnoses of pneumonia
PE, pulmonary oedema, pulmonary haemorrhage, bronchial carcinoma, hypersensitivity pneumonitis
if a pneumonia patient was found to have a pleural effusion, what type would it be?
exudate - high protein
what investigations might you perform in a case on pneumonia?
CXR - lobar infiltrates, cavitation or pleural effusion. blood tests and cultures. sputum MC&S. pleural fluid aspiration - MC&S.
what are the components of the CURB-65 score?
Confusion Urea >7mmol/L Resp rate >30/min BP >65yo 0-1 home treatment 2 hospital treatment 3+ - severe mortality risk, consider ITU
how would you treat a case of mild community acquired pneumonia? (CURB 1)
oral amoxicillin or erythromycin/clarithromycin if allergic.
how would you treat a case of severe community-acquired pneumonia? (CURB >2)
IV cefuroxime / co-amoxiclav
give 3 potential complications of pneumonia?
pleural effusion, empyema, lung abscess, respiratory failure, septicaemia, brain abscess, pericarditis, myocarditis, cholestatic jaundice
which at risk groups are given the pneumococcal vaccine to protect against pneumonia? (apart from childhood imms)
>65yo. chronic heart/liver/renal/lung conditions. DM. immunosuppression. AIDS. those on chemo/prednisolone.
name the causative organism of TB and how it can be transmitted
Mycobacterium tuberculosis/bovis. airborne - poor sanitation, overcrowding, coinfection with HIV
how would you stain for the causative organisms on TB? what would they look like? what culture medium would be used?
Ziehl-Neelsen stain. Acid-fast bacilli (bright red). Lowenstein-Johnston medium.
describe the typical granulomatous lesions of TB
central areas of CASEATION surrounded by epithelioid cells and Langhan’s giant cells
give 3 features of pulmonary TB
cough, sputum, malaise, weight loss, night sweats, pleurisy, haemoptysis, pleural effusion
what is miliary TB?
occurs following haematogenous dissemination of primary TB
describe the features of miliary TB
nonspecific, overwhelming signs. nodular opacities on CXR. retinal disease. biopsies of lung/liver/lymph nodes or marrow show AFB or granuloma.
give 3 GU features of TB
dysuria, frequency, loin pain, haematuria, sterile pyuria
give 1 bone feature of TB
vertebral collapse. Pott’s vertebra.
give 2 abdominal features of TB
peritonitis, GI upset.
give 3 signs of TB seen on CXR
consolidation, cavitation, fibrosis, calcification
describe 3 different methods of testing for TB
Mantoux test - tuberculin sensitivity skin test - identifies latent TB, active TB and BCG exposure. Quantiferon TB gold (IFN gamma test). MC&S for AFB of 3+ sputum samples (also pleural fluid, urine, pus ascites etc). PCR - for identifying drug resistance.
how would you treat TB?
isoniazid, rifampicin, pyrazinamide and ethambutol for 2mths. then isoniazid and rifampicin for 4 further months. DOTS - directly observed therapy to ensure compliance + avoid resistance.
give 1 main side effect of each of the drugs used to treat TB
rifampicin - orange urine/tears, inactivation of Pill, flu symptoms. isoniazid - neuropathy, low WCC. ethambutol - optic neuritis. pyrazinamide - hepatitis, arthralgia.
how do steroids work to help in an asthma attack?
corticosteroids inhibit phospholipase A2 - this inhibits the inflammatory cascade, so dampening down the inflammatory reaction that occurs in an asthma attack
anti-muscarinics are used in severe asthma, what is their mechanism of action? what cardiac drug also works in a similar way?
blocks the muscarinic ACh receptors (competitive inhibition of ACh) - causes smooth muscle relaxation. atropine also acts on these receptors.
why are beta-blockers CI in asthmatics?
beta-blockers can act on the beta2 receptors within the bronchi - blocking them induces bronchospasm, causing an asthma attack/worsening.
why in type 2 respiratory failure do you not start the patient immediately on high flow O2? what respiratory disease is this common in?
common in COPD. px with type 2 resp failure is hypoxic but hypercapnic due to alveolar hypoventilation. due to chronic high CO2, body becomes desensitised to CO2 and so relies on hypoxic drive to breathe - if you raise their oxygen levels too quickly, they will lose this drive to breathe.
how do antihistamines work?
block the H1 receptor, blocking the effects of excess histamine, which is usually released from mast cells in response to an antigen to induce features of immediate type 1 hypersensitivity.
give 2 examples of antihistamines
cetirizine, loratadine, fexofenadine, chlorphenamine.
give 2 examples of antimuscarinics used as bronchodilators
ipratropium, tiotropium, glycopyrronium
give an example of a short-acting beta2 agonist and a long-acting beta2 agonist
SABA - salbutamol LABA - salmeterol, formoterol
how do beta2 agonists work to improve asthma symptoms?
stimulate G protein coupled beta 2 receptors found in smooth muscle of bronchi and blood vessels - activates a signalling cascade leading to smooth muscle relaxation. airflow in constricted airways is improved.
give some possible side effects of beta2 agonists
tachycardia, palpitations, tremor - activation of ‘fight or flight’ receptors
give some examples of inhaled corticosteroids
beclometasone, budesonide, fluticasone
how do inhaled corticosteroids work in COPD/asthma?
corticosteroids pass through the plasma membrane and interact with receptors in the cytoplasm. activated receptor passes into nucleus to modify transcription of lots of genes. downregulates pro inflammatory interleukins, cytokines and chemokines, upregulates anti inflammatory proteins. reduces mucosal inflammation, widens the airways, reduces mucus secretion.
what class of drug is theophylline?
xanthine = non-selective phosphodiesterase inhibitors
how does theophylline work?
a competitive non-selective phosphodiesterase inhibitor - inhibits leukotriene synthesis (major cause of bronchiole inflammation) - reduces inflammation and immunity
give an example of a leukotriene receptor antagonist
montelukast, zafirlukast
how do leukotriene receptor antagonists work to improve asthma symptoms?
block action of leukotrienes on the CsyLT1 receptor on bronchial smooth muscle cells and mast cells - blocks the effects of leukotrienes such as inflammation, mucous secretion, bronchoconstriction
give some examples of indications for mucolytic inhalers/nebulisers
treatment of abnormal, sticky or thick mucous secretions - chronic emphysema, bronchitis, pneumonia, CF, COPD
how do mucolytics work? name an example.
acetylcysteine. dissolve thick mucus by splitting disulphide chemical bonds between mucoproteins in secretions, and lowers viscosity by altering the mucin containing components.
give 2 examples of obstructive lung diseases
COPD asthma
give 2 examples of restrictive lung diseases
interstitial fibrosis sarcoidosis pneumoconiosis interstitial pneumonias connective tissue diseases pleural effusion obesity kyphoscoliosis neuromuscular problems
how would you treat a case of hospital-acquired pneumonia?
gentamicin IV + antipseudomonal penicillin (e.g. piperacillin) IV or cefotaxime (3rd gen cephalosporins)
