Week 08 - Respiratory updated

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mewinstanley@googlemail.com
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128951
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Week 08 - Respiratory updated
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2012-02-02 09:42:14
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Respiratory week - updated
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  1. 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
  2. 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
  3. 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
  4. 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
  5. Draw flow volume loops for;
    -Obstructive lung disease
    -Restrictive lung disease
  6. 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 orgs
    • S. Pneumoniae
    • H. Influenzae
    • C. Psitacci
  7. 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

    • R & I = 6m
    • P & E = 2m
  8. 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
  9. 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
  10. What are the multisystem effects of COPD?
    • CVS → ^IHD, ^systemic inflamm, Tx statins & ACEi
    • Musculoskeletal → loss muscle, osteoporosis
    • Anxiety & Depression
  11. 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)
  12. 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]
  13. What is the Tx for Emphysema?
    • LTOT → long term O2, 17hr/day, ^QoL
    • Surgery → if single large bullae, FEV <50%, lung TPx/reduction coil
  14. 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
  15. 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
  16. 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
  17. 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)
  18. 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
  19. 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
  20. 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
  21. 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
  22. 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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