Respiratory Flashcards
Characteristics of ARDS
- arterial hypoxia
- reduced thoracic compliance
- normal pulmonary capillary wedge pressure
- diffuse infiltrates on CXR
Management of acute Anaphyllaxis
- adrenaline 0.5ml of 1:1000 (1mg/ml) solution, I.e. 500 micrograms IM.
- repeat after 5mins if no improvement
- early oxygen
- IV fluid challenge if hypotension
- hydrocortisone 200mg slowly IV/IM + chlorphenamine 10mg slowly IV/IM after adrenaline
Differentials in breathless patient with no clinical signs (must exclude these before diagnosing ‘psychogenic’)
- early pulmonary congestion of LVF
- silent multiple pulmonary emboli (?diagnostic lung scan)
- lymphangitis carcinomatosis
- interstitial fibrotic pulmonary infiltrations
- metabolic acidosis e.g. Uraemia, DKA
- respiratory muscle weakness
Conservative treatment of asthma
Check precipitating factors e.g. Cold, exercise
Train to use peak flow and record values for 2w
Remove known allergens
Stop smoking
Step 1 treating asthma (mild intermittant asthma)
ICS low dose regular
(+Inhaled short acting B2 agonist)
SE: tremor and tachycardia (rarely hypokalaemia and lactic acidosis)
Step 2 treat asthma
Add LABA (combo inhaler) OR Increase dose inhaled corticosteroid (ICS) 200-800mcg/day (start e.g. 400mcg) according to severity OR try monteleukast if young.
Step 3 treat asthma
Check response to LABA (long acting B2 agonist)
If good response- continue LABA + increased ICS dose OR Add theophylline.
If response but inadequate control- increase ICS to 800mcg/day
If no response- stop LABA and increase ICS to 800mcg/day.
Step 4 treating asthma (persistent poor control)
Consider trials of
- increased dose of ICS up to 2000mcg/day
- add 4th drug e.g. Leukotriene R-antag; SR theophylline; B2 agonist tablet.
NB. Little evidence of benefit of ICS >800 in asthma. High risk of pneumonia. Warn about adrenal suppression if stop ICS suddenly.
Step 5 treating asthma (with continuous or frequent use of oral steroids)
- Add daily steroid tablet in lowest dose providing adequate control.
- Maintain high dose of ICS 2000mcg/day.
- Consider other treatments to minimise use of oral steroids.
- Refer for specialist care
Management of COPD (conservative)
Stop smoking
Lung rehab/exercise
Prevention: influenza and pneumococcal vaccine
Nutrition/lose weight
COPD management pharmacological
Bronchodilators (symptom management):
- SAB2A e.g. Salbutamol/terbutaline
- Anticholinergic Ipratropium (atrovent)/tiotropium
-?theophylline
- one or combination of above aerosol/Nebs
Inhaled corticosteroids (if documented Spirometry response to ICS) NB. little benefit >800mg ICS.
If chronic severe COPD consider long-term home oxygen >15l/day
COPD management of exacerbation
SHONA
Steroids (oral) v. Baseline. ?bone protection
Heparin (preventing DVT while immobile)
Oxygen (titrate carefully e.g. 24-28% Venturi)
Nebulised bronchodilators (?theophylline)
Antibiotics (amoxicillin & macrolide)
If PaCO2 continues to rise consider NIPPV, think about it early, before the patient tires.
Management of acute severe asthma
Continuous high flow oxygen.
Bronchodilators: SABA (salbutamol/terbutaline) + Ipratropium via oxygen Nebs OR IV infusion if unreliable inhalation.
Corticosteroids: oral prednisolone OR IV hydrocortisone. Continue oral prednisolone 30-50 mg daily >4days or recovery.
IV fluids: for initial dehydration until oral fluids taken, monitor urine output.
?IV Mg 8mmol over 8mins.
?aminophylline (BW dependent)
Consider bacterial infection trigger (?antibiotics) usually strep pneumoniae or H. Influenzae
Consider mechanical ventilation if persisting/increasing high PaCO2 OR worse hypoxia esp if + exhaustion.
Discharge when PEFR >75% of best with
Steriods prescribe for asthma/COPD
Asthma: 30-40 mg prednisolone for 5d.
COPD: 30mg OD 7-14d
NB. If prx high dose steroids for >3weeks you need to implement a weaning period to prevent addisonian crisis (2a addison’s)
SABA example
Salbutamol
-10-30% absorbed, distrib 5-15mins, peak 30min-2h
SE: tremor (skeletal muscle B2) tachycardia (atrial B1) dose dependent.
NB. rarely causes: hypokalaemia (Na-K pump by B2 activation); interaction with steroids (decrease K); lactic acidosis.
LABA
Salmeterol
12h action, enables steroid reduction.
Add LAMA/LABA if stable COPD with SOB or have exacerbations >2y. If FEV1>50%
If FEV1
Qvar?
Beclometasone inhaled
Ipratropium
Muscarinic antagonist (also tiotropium)
Short acting
SE: dry mouth, slow GI, bitter, glaucoma (para block)
Theophylline
Methylxanthine
- competitive non-selective PDE inhibitor, raises ICF cAMP, activate PKA, inhibits TNF-a/LK synthesis/reduce inflam and innate immunity.
- non-selective adenosine R antagonist (A1,A2,A3) tachycardia, arrhythmia (careful in AF)
ADR: insomnia, palpitations, headache, nausea/vomit HYPOKALAEMIA, diarrhoea.
NB. Narrow therapeutic window! Toxicity: seizures, tachyarrhythmia, CNS stimulation (esp. Resp centre)
Aminophylline
2Theophylline + 1ethylenediamine
Improves solubility.
Less potent, shorter action (vs theophylline)
Clenil inhaler?
Beclometasone
Flixotide
Fluticisone inhaler
Causes of haemoptysis
Common: 1. Bronchitis 2. Bronchial Ca 3. Bronchiectasis 4. Pneumonia
Uncommon: Pulmonary infarction; CF; Abscess; TB; Foreign body; Goodpasture’s; after vigorous coughing.
CV: severe mitral stenosis; acute LVF.
Bleeding diatheses.
Causes of stridor
Congenital- Laryngomalacia (congenital flaccid larynx)
Foreign body
Laryngeal oedema: anaphylaxis, inhalation injury
Infection: epiglottitis, retropharyngeal abscess.
Iatrogenic: post-tracheostomy/intubation stenosis, post-thyroid surgery.
Rheumatoid Arthritis: cricoarytenoid RA
Goitre
Malignancy: intraluminal- larynx, trachea, bronchus; external compression- malignant nodes; bilateral vocal cord palsy- brainstem stroke, thyroid Ca, oesophageal Ca.
Pulmonary fibrosis differentials
BREAST CARDS- Upper lobe: BREAST; Lower lobe: CARDS Berylliosis Radiation Extrinsic allergic alveolitis Ankylosing spondylitis/ ABPA Sarcoidosis/Silicosis Cryptogenic fibrosing alveolitis (IPF) Asbestosis Radiation Drugs Systemic sclerosis and other CTDs
Minimum presentation of normal respiratory examination
On examination of X’s respiratory system I found him to be comfortable at rest with a respiratory rate of 12/minute and pulse of 72 beats per minute. There are no peripheral stigmata of respiratory disease. The trachea is central. Chest shape is normal. Chest movement is equal bilaterally with 6cm expansion. Percussion note is resonant in all areas. Breath sounds are vesicular throughout with no added sounds. In conclusion this patient presents with a normal respiratory examination.
Pleural fluid aspirate findings ‘normal’
Normal
Cytology: macrophages, mesothelial cells, lymphocytes and some erythrocytes
Pleural fluid cytology findings and differentials
- NEUTROPHILIC: acute inflammatory response. Empyema/Pneumonia. NB. May also see reactive mesothelial cells. These may mimic/hide malignancy.
- Eosinophilic (>10%): usually reaction to haemo/pneumothorax.
- Lymphocytic majority
- Malignant cells.
Causes of eosinohphilic pleural aspirate
- Reaction to air/blood in pleural cavity
- Drug reactions
- Parasitic infections
- Churg-Strauss Syndrome (E-GPA, eosinophilic granulomatosis with polyangiitis)
Differentials for a lymphocytic effusion on pleural aspirate
- Inflammatory disease e.g. Rheumatoid
- Infection, including mycobacteria
- Malignancy, solid or lymphoma
- Post CABG and others
Pleuritic chest pain indicates inflammation/irritation of parietal or visceral pleura
Parietal, has sensory innervation for pain. The visceral pleura has no sensory innervation.
Where is pleural fluid secreted and absorbed? Normal volume?
Parietal pleura secretes fluid, it is absorbed by the visceral pleura, draining into the lymphatics and returns to the blood. Normally there is 10-20ml.
Radiological findings of Pleural effusion
- Homogenous density
- density in dependent portion ‘meniscus sign’ (concave upper border)
- ?fissures visible
- loss of normal silhouette e.g. Obscures hemidiaphragm, loss of costophrenic angle
+/- mediastinal shift (contralateral in massive effusions)
Normally confirmed by PA and lateral CXR (more sensitive than PA)
At what size is a pleural effusion visible on CXR
> 200ml on average needed.
Lateral CXR >50ml obliterates ant/post costophrenic angle (CP)
PA CXR >200ml obliterates lateral CP angle
PA CXR >500ml obliterates/elevates ipsilateral hemidiaphragm.
Confirm with lateral decubitus film OR USS (effusions from 5ml)
Signs of pleural effusion on Supine/AP CXR?
- hazy diffuse opacity (but can see normal lung marking through it)
- Ill-defined hemidiaphragm
- capping of apex with pleural shadow >500ml
- apparent elevation of diaphragm.
Variations on pleural effusion presentation on CXR
- Encysted pleural fluid (commonly CCF): obliterates oblique CP angles, ‘vanishing tumour’
- Loculated effusion: fluid doesn’t shift to dependent portion, ?adhesion between pleura. Lenitform opacity against chest wall (convex to lung) mimics chest wall mass. Haemothorax/empyema.
Findings in USS for pleural effusion
Anechoic (Black, echo free) = transudate (sometimes exudate)
Complex non-septated (echogenic/bright material in anechoic fluid) = Exudate
Complex septated (fibrin strand/septa floating in anechoic fluid) = Exudate
Echogenic (homogenous echogenic- bright fluid) = exudate/haemorrhage/empyema/chylothorax.
Pros and cons of using CT for pleural effusions
Pros: differentiates pleural/parenchymal lesions, free/Loculated fluid, pleural fluid/pleural thickening, acute bleed/saline (high density in acute bleed), free flowing/trapped (dependent portions?). Precise location.
Cons: can’t reliably differentiate exudate/transudate, can’t separate normal pleura from adjacent structures (
Distinguishing features of CXR in pleural effusions of different aetiology?
- Heart failure: most common cause of transudative effusion
Bilateral > unilateral (R>L); Kerley B-lines; enlarged heart; enlarged central pulmonary arteries; fissural fluid; improve rapidly on diuretics. - Malignant effusion ~25% of all effusions in older pts. 1a or 2a (but 2a = 90%); ill-defined density; nodular/irregular pleural thickening; unilateral mostly; rib destruction. Pleural thickening nodular/mediastinal/parietal/circumferential. Common causes of pleural 2a: lung>breast>leukaemia/lymphoma. Most common 1a = malignant mesothelioma (>80% asn with asbestos exposure); if suspicious need biopsy + image guidance; focal pleural plaques seen in 50%; 60% have a large unilateral pleural effusion at diagnosis; ‘frozen mediastinum’.
CT features of empyema
Lenticular shape Uniform enhancing wall Compression of adjacent lung Obtuse angle with chest wall 'Split-pleura' separation of pleural layers May have air fluid level Tends to loculate.
Histological findings for malignant mesothelioma
Asbestos fibres near peripheries of lung. - Crocidolite (blue) = most dangerous - Amosite (brown) = also dangerous - Crysotile (white) = least dangerous (serpentine type) Histological types of mesothelioma: - epithelioid - sarcomatoid - biphasic - Desmoplastic
Histological findings in different mesotheliomas.
- Epithelioid: glandular tissue with tubular and microcystic spaces lined by cuboidal epithelia with papillary buds projecting into them. Most commonly confused with adenocarcinoma
- Sarcomatoid: elongated, spindled, fibroblastic looking cells in non-distinctive sheets, with much fibrous tissue.
- Biphasic: majority of cases. both Histological types present, but with one type predominating.
- Desmoplastic: worst prognosis, difficult to diagnose, extensive scar tissue seen, ?originating in scarred lung.
What is an epithelioid mesothelioma? Importance?
Histological diagnosis of mesothelioma type; most common at 60%
- commonly confused with pulmonary adenocarcinoma.
Findings: tubular and microcystic spaces lined with cuboidal epithelia, disorganised; small papillary buds projecting into spaces.
Sarcomatoid mesothelioma histology, prevalence?
20% (joint 2nd most common subtype)
- due to mesenchymal origin of pleural cells
- spindled, fibroblastic-appearing in non-distinctive sheets
- looks like a fibrosarcoma.
Other mesothelioma types (after 1+2)
Biphasic: both Histological types present with one or other type prevailing 20%
Desmoplastic: originating from scar tissue, difficult to diagnose, worst prognosis
Prognosis for mesothelioma
94% die within 2y. Median survival 10months. Eligible for industrial benefits; treated by chemo; min role for surgery. Pleural plaques are NOT precursor lesions.
Benign pleural tumours
- Hamartoma (mesenchymoma AKA coin lesion): benign, disorganised normal tissue, no malignant potential but DO note in records to prevent further investigations. Typically: cartilage, epithelia, connective tissue. ‘A tumour formed of mature but disorganised elements normally found at that site’
- Lymphoma
- Bronchial adenoma: usually benign but can invade locally, often a pedunculated intrabronchial made causing cough/haemotptysis. 90% phenotypically ‘carcinoid’ but few are symptomatic.
‘Tell me about ‘lung cancer’…? Who gets it?
Mainly disease of old; M=F; rising incidence in developing world; main UK cause of cancer deaths (21% of female Ca deaths, more than breast cancer!)
Causes of lung cancer?
Smoking (prop to no of cigarettes); urban living (diesel, coal fires); asbestos (multiplicative with smoking); radon gas; Radiation/radiotherapy; Others rare (Arsenic, Chromium, nickel, polycyclic aromatic compounds)
Types of lung cancer?
Non-small cell lung cancer (NSCLC)
- Squamous cell carcinoma 40-50% (falling incidence)
- Adenocarcinoma 30% (rising incidence)
- Large cell carcinoma 10-20% (lots of subtypes but poor prognosis)
Endocrine Lung cancers:
- Small AKA Oat cell lung cancer 10% (high grade malignancy)
- Carcinoid lung cancer
Squamous cell carcinomas prognosis, presentation?
Presentation: smokers; M>F; centrally located; bronchial obstruction symptoms; non-mets symptoms Hypercalcaemia and HPOA. Exposure to irritants in main bronchi = metaplastic squamous epithelia.
Prognosis: slow growing; metastasise late; may be resectable; recognised precursor lesion.
Adenocarcinoma presentation, prognosis, cause, subtypes?
Presentation: M=F; rising incidence; non-smoker’s lung cancer (?asn with passive smoking); typically peripheral in areas of pre-existing scarring; may present as pneumonia-like consolidation. HPOA (non-mets symptoms) in 2-3%
Mets symptoms- pathological fracture; CNS symptoms; hepatomegaly/jaundice
Prognosis: slow growing, smaller than SCC; Metastasise early.
Subtypes: 1. Acinar; 2. papillary; 3. solid carcinoma with mucin production; 4. Bronchoalveolar carcinoma (Clara cells/TII pneumocystis)- A. multifocal diffuse infiltrative (consolidation) B. Single grey tumour mass D
Adenocarcinoma precursor lesions
Atypical adenomatous hyperplasia
In situ ‘lepidic’ Adenocarcinoma (mucinous or non-mucinous)
Bronchoalveolar pattern of spread in pre-invasive stage.
Small cell carcinoma presentation, prognosis, histology.
Presentation: M>F, 10-20%, associated with smoking, central, paraneoplastic syndromes (SIADH; ectopic ACTH; Lambert-Eaton Myaesthenia syndrome; Metastases present at diagnosis in most (mets symptoms); mediastinal lymph nodes may be bigger than primary.
Prognosis: neuroendocrine cancer; All are high grade malignancy; untreated survival ~3months, 1-2y with chemo; rarely operable; rapid rate of growth.
Histology: from bronchial endocrine/APUD cells; round-oval cells with little cytoplasm; appear dark with mitotic figures, poorly defined borders; grow in clusters, salt and pepper pattern (granular nuclear chromatin); background necrosis; few dense secretory granules
Large cell carcinoma: presentation, prognosis, histology
Presentation: 10-20%; M>F; smokers; central; often widely disseminated at diagnosis; fast rate of growth
Prognosis: poor, aggressive carcinoma; mets common; subtypes
Histology: no glandular/squamous/small cell differentiation (so bad you can’t even tell where they’re from micro- ultrastructure may retain features on EM); ?squamous/adenocarcinoma origin; large cells with pleimorphic nuclei and giant cell forms; necrosis (outgrow blood supply quickly
- commonest subtype: Large cell Neuroendocrine (LCNET) histology features of small cell/immunohistochemistry; organoid nesting/trabecular/rossette-like/palisading patterns.
Treatment for active TB
PE and IR (P)
PE for 2 months: pyrazinamide and ethambutol
IR (P) for 6 months: isoniazid (+ pyridoxine) and rifampicin
Side effect of each drug used for TB
Pyrazinamide: hepatotoxicity
Ethambutol: optic neuritis and RG colour vision/acuity reduced
Rifampicin: deranged LFTs, red urine
Isoniazid: peripheral neuropathy (give with pyridoxine), encephalopathy
Immune tests for TB
Tuberculin skin test: detects delayed type hypersensitivity to PPD (purified protein derivative, mix of TB antigens) e.g. Mantoux test: Subcut inoculation and 48-72h measurement of skin response
Interferon-gamma assay: test blood of pt + TB specific antigens NOT present in BCG. (inc ESAT-6 and CFP10- early secretory antigen target 6,culture filtrate protein 10). T cells produce IFN-g if latent/active infection.
Mutation and patholophysiology of Cystic Fibrosis
Mutation: CF transmembrane conductance regulator on Ch7. cAMP regulated Cl channel on apical surface.
Autosomal recessive 1 in 3000 live births
Production of abnormally thick secretions from glandular tissue affecting lung and pancreas = lung damage 2a recurrent infections and pancreatic insufficiency.
Lung signs: Bronchiectasis, lung abscesses, recurrent small haemoptysis, clubbing, pneumothorax, persistent productive cough.
Pathogens: S. Aureus and H. Influenzae and gram-neg bacteria -> pseudomonas (poor prognosis)
GI: meconium ileus in neonate, diabetes mellitus, biliary obstruction, azoospermia (>90% males). (Male sterility and female subfertile).
Sweat with Na >70mmol/l is characteristic.
Clinical presentation and causes of Bronchiectasis.
Clinical presentation: - chronic cough (?postural) - copious sputum (+acute infections) - halitosis - febrile episodes - haemoptysis (alone in 'dry Bronchiectasis') ?severe - dyspnoea - coarse basal crepitations + wheeze - cyanosis and clubbing - wt loss or cor pulmonale (advanced disease) Causes: - post acute childhood resp infection esp. Measles, whooping cough, pneumonia - cystic fibrosis - predisposition by bronchial obstruction - TB (less common) - congenital causes.
Define Bronchiectasis and Congential causes
Bronchiectasis: dilatation of airways. Clinically significant only if infection/haemoptysis.
Congenital causes:
- Primary ciliary dyskinesia
- Kartenger syndrome: Bronchiectasis, sinusitis, situs inversus.
Causes of recurrent bacterial pneumonia
- chronic bronchitis
- aspiration
- bronchial carcinoma (preventing drainage)
- Bronchiectasis
- cystic fibrosis
- Achalasia of cardia (25% present as chest disease, pharyngeal pouch, Neuromuscular disease of oesophagus e.g. bulbar palsy) = apsiration!
- hypogammaglobulinaemia and myeloma
- opportunistic infections of immunosuppressed e.g. AIDS or treated myeloproliferative disorders.
58yo man presents with SOB, fever, dry cough, malaise. Not responded to amoxicillin. Recent caving holiday. What are your DD and what signs would you look for?
DD: Psitticosis pneumonia (Chlamydia psittaci- bacterial) OR histoplasmosis (Histoplasma caspulatum- fungus)
Psitticosis: headache, rash, splenomegaly (+hepatitis, encephalitis, renal failure, haemolysis). Treat: tetracycline OR erythromycin.
Histoplasmosis: 2-3weeks post exposure, erythema nodosum and arthritis (soil of Australasia, SE Asia, Southern USA- bird/bat guano). Florid CXR changes (diffuse patchy shadowing, bilateral Hilar lymphadenopathy). Treat: supportive (or antifungals)
Antifungals used in respiratory fungal infection and side effects
Amphotericin: Nephrotoxic, hepatotoxic, cardiotoxic
Fluconazole: diarrhoea, Stevens Johnson syndrome
Nystatin: rashes, diarrhoea
Itraconazole: peripheral neuropathy, cholestatic jaundice
Griseofulvin: peripheral neuropathy, photosensitivity, enzyme inducer
Ketoconazole: hepatitis, gynacomastia
65yo lady with 20y pack history presents with rust coloured sputum, fever and bad CXR. Most likely organism? Treatment?
Streptococcus pneumoniae. Treat with Penicillin (or erythromycin if penicillin allergic)
65yo man presents with 2 week history of flu-like symptoms, now worsened SOB, fatigue and polyarthritis, Non-productive cough. What is the likely organism? How is best diagnosed? How to treat?
Mycoplasma pneumoniae. (1/3 do not have a cough/sputum)
Diagnosis: mycoplasma IgM
Treat: erythromycin OR tetracycline.
(CXR typically shows patchy consolidations and small effusions)
Organisms causing atypical pneumonia?
Legionella spps.
Staphylococcus pneumoniae
Chlamydia psittaci.
65y Man presents with acute delerium, D+V, SOB and dry cough. CXR shows lung base consolidation. Likely organism? Management?
Legionella spps. (Also asn with flu-like prodrome or renal failure)
Treat: erythromycin OR ciprofloxacin.
50y woman presents with headache, fever, dry cough, and splenomegaly (flu like prodrome). Likely organism? Management?
Chlamydia psittaci (5-14d incubation)
Management: Erythromycin, or tetracycline.
Other signs: border spots (macular rashes inc. face), haemolysis, hepatitis, encephalitis.
85yo man has deteriorated over the past 2d, after improving respiratory symptoms for ?influenza. He is febrile, vomited, and CXR shows changes bilateral infiltrates. Likely organism? Management?
Staphylococcal pneumonia (secondary to influenza)
Management: flucloxacillin
Is he MRSA+? -> if so ?vancomycin for MRSA pneumonia.
Features to look for in ?chalmydia psittaci pneumonia?
Splenomegaly Horder spots (macular rash) Hepatitis Encephalitis (photophobia, headache) Haemolytic anaemia
What is Ritter disease?
Scalded skin syndrome: rare toxin-mediated disorder with superficial fragile blisters that burst and leave a tender base. Often accompanying fever, and mucopurulent eye discharge.
Empirical treatment for aspiration pneumonia
Penicillin/amoxicillin + metronidazole
What is Mendelson syndrome?
Severe chemical pneumonitis + pulmonary oedema + bronchospasm. Due to significant aspiration of gastric contents. -> ARDS
Key features of interstitial lung disease?
Alveolar structure affected
Decreased elasticity -> restrictive deficit
Decreased gas exchange (increased capillary-alveolar distance for diffusion exchange)
Granulomatous interstitial lung diseases?
Sarcoidosis
Hypersensitivity pneumonitis
Signs of life threatening asthma:
33-92-CHEST PEFR <33% of predicted/best SpO2 ≤92% Cyanosis Hypotension Exhaustion Silent chest Tachycardia/bradycardia
4 signs of severe asthma?
Unable to complete sentences in one breath RR>25 HR>110 PEFR <50% predicted/best Need any of these.
Blood gas markers of severity of asthma
SpO2≤92%
Severe hypoxia pO2<8
pCO2 normal or high (would expect low pCO2 as it’s easier to blow off)
Management of severe asthma?
OSHITMe Oxygen: 15l non rebreathe + resevoir (Hudson mask) Salbutamol nebs back to back (every 15mins) Hydrocortisone IV Ipratropium Theophylline MgSO4 And get the anaesthetist!
Organisms causing CAP in order of prevalence?
CAP SHMELS Strep pneumoniae Haemophilus Morexella catarrhalis/Mycoplasma Enterobacter Legionella Staph (or pSeudomonas in CF)
Causes of Hopsital acquired pneumonia in prevalence?
Pseudomonas/Proteus E. Coli Serration Klebsiella MRSA-> but why? (Y) PESKY
Causes of Atypical pneumonias?
MIRACKL Mycoplasma Influenza (or parainfluenza) RSV Adenovirus Chlamydophila (psittaci or pneumoniae) Klebsiella Legionella
CURB-65 scale?
Confusion AMTS <8 Urea > 19mg/dl or 7mmol RR >30 BP <90 systolic or <60 diastolic Age >65y. If >3: severe, use HDU; 2: mx in hospital; 2 or 1: amoxicillin/co-amoxiclav? <1 community care.
Treatment of Staphylococcal infection?
Flucloxicillin
Diagnostic test for mycoplasma?
Cold agglutinin test
50y pt with dry cough, erythema mutliformae, hyponatraemic, anaemic. Likely organism
Mycoplasma
Features of mycoplasma infection
Young pts, Skin: erythema multiformae/nodosum Diarrhoea Cold haemolytic anaemia Bullous miringitis, otitis media -> meningitis Hyponatraemia (SIADH) Immune complex glomerulonephritis Transaminitis (raised LFTs)
Risk factors for staph pneumonia
Ventilation, secondary to viral infection, aspiration pneumonia, alcoholics
72y man comes in with fever, productive cough of brown rusty sputum and basal consolidation. Likely organism?
Strep. Pneumoniae
65y homeless man comes in with slow onset basal consolidation and red current jelly sputum and fever. Alcoholic. Likely organism?
Klebsiella
Organism most likely to cause IECOPD?
Haemophilus
Organisms causing interstitial pneumonia
PCP, viral, mycoplasma,
