-
What are common pathologies in these areas
-Airways
-Parenchyma
-Pleura
For each (inflammation, neoplasm,, infection, allergy, trauma)
- Airways
- Inflamm → tracheitis, bronchitis, asthma, bronchiectusis, COPD
- Neoplasm → Bronchial Ca-Infection
- Allergy → Asthma
- Trauma → post intubation
- Parenchyma
- Inflamm → pneumonitis,pulmonary fibrosis, asbestosis
- Neoplasm → Alveolar cell/Mets
- Infection → pneumonia
- Allergy → extrinsic allergic alveolitis
- Pleura
- Inflamm → pleuritis [fibrotic]
- Neoplasm → mesothelioma/mets
- Infection → empyema
- Allergy
-
For Asthma give the;
-Definition
-CF
-Patho
-Dx
- Definition
- reversible airway narrowing
- CF
- Dyspnoea
- Cough
- Wheeze
- often nothing
- Patho
- SM constriction & hypertrophy +Oedema → airway wall thickening
- Mucus & exudate in lumen
- remodelling→ ^vascular perm, goblet cell & SM hypertrophy
- Dx
- PEFR → airflow variability
- Histamine nebuliser → >20% drop in FEV
- Reversible → >15% ^FEV after salbutamol
-
Outline the pathophysiology of an Asthma Attack?
- Similar to T1 hypersensitvity
- APC presents allergen to T cell
- T cell activates B to prod IgE against allergen
- Mast cells primed with allergen
- 2nd contact → mast cell degranulation
- Preformed granules cause inflamm, bronchoconstriction & hypersecretion
- Later → influx of eosinophils → toxic to epithelium → remodelling
-
For Extrinsic Allergic Alveolitis give;
-Presentation
-Patho
-Mx
- Presentation
- Chills, cough, fever, Malaise, SoB
- Dry cough, loss of apetite, weight loss
- Patho
- breathe in allergen → acute inflammation
- C3b → tissue damage → pericapillary thrombosis & alveolar cell damage
- repeated exposure → chronic inflamm
- macrophages → foam cells → GF, IL-6
- collagen in interstitial spaces → impaired O2 t-port
- loss of surface tension → crackles
- Mx
- Avoid allergen
- ~prednisalone
-
Draw flow volume loops for;
-Obstructive lung disease
-Restrictive lung disease
-
For Pneumonia give
-Risk Factors
-Types [including pathology]
-Causative Orgs
Pneumonia
Risk factors → obstruction, aspiration, smoking, immunosuppression
- lobar
- spread → inflammatory oedema
- Red Hepatisation → RBC & fibrin in alveoli; fibrin organises, attracts polymorphs
- Grey Hepatisation → Fibrin & WBCs
- Resolution
- Broncho
- Lower lobes
- centred on bronchioles → spread to adjacent alveoli
- patchy
- abscess formation
- spread to pleura
- complications → resp failure, pleural effusion (leading to empyema), death, bronchiectusis
- Causative orgsS. Pneumoniae
- H. Influenzae
- C. Psitacci
-
For Pulmonary TB give
-Primary
-Secondary
-Treatment
- Primary
- sub pleural caseous granulomatous focal lesion → Gohn focus
- Infection → Hilar nodes → gohn complex
- clinically silent
- Secondary
- causes hypersensitivity → necrosis & cavitation [Granuloma]
- upper lobe
- heal by fibrosis & calcification
- other outcomes;→ miliary TB, systemic infection, blood spread→ MTB bronchopneumonia
- Tx [RIPE]
- Rifampicin
- Isoniazid
- Pyrazinamide
- Ethambutol
-
For COPD give
-Definition
-Risk Factors
- Definition
- Airflow obstruction, not fully revesible
- Chronic
- Exacerbations → ^SOB, ^^vol & purulence of sputum, URTI symptoms
- Risk factors
- Smoking → 10-20pack years
- air pollution
- occupation
- Nutritional → low fruit; low FEV, weight loss assoc w mortality
- Low socioeconomic status
- Bacterial colonisations → declining FEV, ^exacerbations
- Genetic → Alpha1-antitrypsin, early COPD
-
Outline the pathology of COPD
Oxidative stress > defences → patho changes in COPD
- Effects
- ^proteolysis → ^antigenicity → inflammmation
- Impaired membrance function → ^vascular perm, dec membrane receptors, dec memb enzyme function
- Impaired protective mechs → ^mucus, dec surfactant & cilia
-
What are the multisystem effects of COPD?
- CVS → ^IHD, ^systemic inflamm, Tx statins & ACEi
- Musculoskeletal → loss muscle, osteoporosis
- Anxiety & Depression
-
What is the Tx of COPD
- controlled O2 therapy → hypoxic, target 88-92%, ABGs check if CO2 sensitive
- Prednisalone → 30mg, 7-14d
- ^Bronchodilators → nebulisers
- Antibiotics → only if infected, amox/clarith, sputum for C+S
- Theophylline → bronchodilator & ^resp drive, monitor levels (esp w macrolides)
-
What is the definition of emphysema?
Different types?
- Loss of elastin → airway compression-obstruction-hyperinflation
- maldistribution of ventilation
- Centri-lobar → alveoli around resp bronchioles, ^[upper lobes]
- Pan-lobar → uniform dam of airspaces, ^[Lower lobes]
-
What is the Tx for Emphysema?
- LTOT → long term O2, 17hr/day, ^QoL
- Surgery → if single large bullae, FEV <50%, lung TPx/reduction coil
-
For NIV give;
description [+ indication]
CPAP
BiPAP
- Description
- +ve pressure w/o endotracheal tube
- used after 1hr maximal medical Mx + controlled O2
- T2RF
- CPAP
- constant positive airway pressure
- recruit collapsed
- T1RF
- BiPAP
- alternate betw → ^insp P & low exp P
- reduces work
- recruit collapsed
- more efficient gas exchange
-
For NIV give
-Criteria [4]
-Rationale
- Criteria
- Primary Dx of COPD exacerbation
- Pt able to protect airway
- Pt conscious & co-operative
- Potential for recovery suitable to Pt
- Rationale
- reduce need for intubation
- reduced mortality
- Reduced in-Pt stay
- not ITU specific
-
Outline the monitoring of a Pt on NIV, including
-O/E
-Bloods
- O/E
- chest wall movement
- ?accessory muscles [dificulty breathing]
- Pt co-ordination w machine → HR, RR & GCS
- Pulse Ox → continuous measurement
- ABGs → 0, 1 & 4-6hrs, then variable
-
For Lung cancer give
-CF [signs & symptoms]
-Pathogenesis
- CF
- Cough, haemoptysis, chest pain, effects of Mets
- Peripheral Ca → few symptoms
- Central Ca → retention pneumonia
- Pathogenesis
- Chronic irritation/stim of cells by carcinogens
- ^cell turnover
- Accumulation of DNA abnormalities (cell cycle & angiogenesis)
-
What are the 4 classses of Lung Ca?
- Adenocarcinoma
- most common
- peripheral & incidentaloma
- Appearance → glandular/solid/papillary/lepidic (scaly), ~mucin
- Squamous cell
- localised central mass, arise from squamous metaplasia
- form cavitating lesions → retention pneumonia & lung collapse
- Appearance → ~ keratinisation, intercellular bridges (desmosomes)
- RF; Smoker
- Small cell
- Most aggresive
- early mets, various locations
- Appreance → oval/spindle shaped cells, inconspicuous nucleoli, scant cytoplasm, nuclear moulding
- Tx → good resp to Ct (many relapse)
- RF; Smoking
- Large Cell
- Dx of exclusion
- Central tumour
- Appearance → poorly differentiated malignant epithel tumour, lacks signs of other cancers
-
What are other tumours affecting the lung?
-Neuroendocrine
-Pleural
-Lymphatic
-Benign
- Neuroendocrine [Carcinoid]
- Endobrachial/peripheral
- Appearance → yellow colour, resemble carcinoid in appendix
- Typical = low met risk
- Atypical = >50% met
- Pleural [Mesothelioma]
- primary pleural tumour (also in serosal membranes)due to asbestos, >40y lag
- Appearance → epithelial/sarcomatoid/mixture (biphasic)
- Malignant → encase lung & spread thru fissures, secondary pneumonias
- Pt entitled to compensation
- Lymphatic
- Lungs can get lymphoma → see haemotology
- Benign
- Chondroid Hamartoma
Most common cancer in lungs is metastatic
-
What are the non-metastatic effects of Lung Ca?
- Endocrine
- Secretion of ACTH → ^cortisol, Cushing's syndrome
- ADH analogue → water retention → dilutional hyponatraemia
- PTH-related peptide → ^osteoclastic activity, hypercalcaemia
- Others
- Encephalopathy
- Cerebellar Degeneration
- Neuropathy
- Myopathy
- Eaton Lambert → Muscle weakness (a.k.a Lambert-Eaton Myasthenic syndrome [LEMs])
- Retinopathy
-
What are the Metastatic Effects of Lung Ca?
[Local & Distal]
- Local
- Pleura → haemorrhagic pleural effusion
- Hilar lymph nodes
- Adjacent lung tissue → large BV [haemoptysis]
- Pericardium → Pericardial Effusion
- Mediastinum → SVC obstruction, recurrant laryngeal n (coarseness) Phrenic n (diaphragmatic paralysis)
- Pancoasts Tumour
- → apex, non-small cell, local spread (brachial plexus, sympathetic ganglion), Horner Syndrome (Ptosis, Miosis & anhydrosis)
- Distal
- Haematogenous → liver, bone, brain, adrenal
- Lymphatic → cervical lymph node chain
-
What are the typical ABGs & definitions of the following
-T1RF
-T2RF
- T1RF
- Ventilation/perfusion inequality
- Low PaO2 [<8kpa]
- normal/low PaCO2 (^pCO2 drives resp)
- Tx → ^FiO2 (40-60%) target sats 94-98%
- T2RF
- Ventilatory Failure
- Low PaO2 [<8kpa] (low pO2 = respiratory drive)
- ^PaCO2 [>6kpa]
- Tx → 'controlled' oxygen, target 88-92%
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