Assessment Flashcards
Asthma Pathophysiology
Increased airway episodic hyper reactivity to unknown triggers causes inflammation, narrowing and hypersecretion
During episode, bracho-constriction, smooth muscle hypertrophy, hyperplasia of mucus glands, mucosal oedema, infiltrated inflammatory cells such as eosinophils and neutrophils.
Long term this leads to airway remodelling. Collagen deposition, denuding of epithelium, thickening of smooth muscle, oedema.
Airway narrowing causes air-trapping and increased expiratory resistance puts stress on expiratory muscles.
Asthma Aetiology/Epidemiology
Extrinsic (allergic) TH2 humoral immunity, triad (asthma, rhinitis, eczema) 60%
Late on-set environmental or occupational
Low birth weight, wheezy infant, maternal smoking, anxiety, obesity, hyper hygiene
Most common chronic childhood disease. 5.4 million UK recieving treatment
90% deaths avoidable
Western disease
More males in childhood, females persist
Asthma assessment
Diagnosis: Spirometry,
Reversibility, Airways inflammation, PEFR
ABGs, Chest X-Ray, Pulse oximetry, breathing pattern, auscultation, Mod ified Borg scale of Dyspnoea, NEWS
Aspiration pneumonia Pathophysiology
Inhalation of secretions (stomach contents)
Acute inflammation of alveoli and adjacent airways. Restrictive.
Chemical (stomach acid, respiratory compromise after an hour)/Baterial (from upper airways, most common)/Mechanical (non-toxic fluids). Not exclusive.
Congestion (24hrs cellular exudates replace alveolar air, pleura inflammation)/ Red hepatisation (RBC into alveolar air, solidification, neutrophils and fibrin+) 2-4 days/ Grey hepatisation (RBC disintigrate)/ Resolution (cleared by enzymes and macrophages or cough) 3 weeks
Aspiration pneumonia Aetiology/ Epidemiology
Most common cause of death in dysphagic patients due to neuro conditions. Represent 10% of hospitalised pneumonias.
Silent aspiration, poor swallow (e.g. motor neurone), long term -aspiration
Due to compromised response: CVA, alcoholic, seizure, general anaesthetic
Aspiration pneumonia assessment
Diagnosis: Blood count, blood culture, sputum culture, chest x-ray (right middle and lower)
Auscultation, Breathing Pattern, BORG scale of dyspnoea, MRC, Chest expansion, Peak expiratory flow rate (PEFR)
Cystic Fibrosis Pathophysiology
Chronic, progressive multisystem disorder affecting exocrine glands, mostly lungs.
Characterised by abnormal transport of sodium and chloride across epithelial membranes leading to thick sticky secretions that cause blockages, inflammation and infection.
Thickened sol layer makes cilia unable to stand upright. CFTR protein.
Dilated bronchi and enlarged cyst formation.
Affects pancreas, islets of langerhans (diabetes). Begin with type 1 respiratory failure, becomes type 2 over time.
Cystic Fibrosis Aetiology/Epidemiology
1/2,500 in Caucasian, 1/17,000 African, 1/30,000 Asian
Aprox 9,000 in UK
Median survival 47, but newborns 50+
Faulty gene on Chromosome 7, 2000 variations, most common delta F508 (70%), recessive
Cystic Fibrosis Assessment
Spirometry BORG, MRC Auscultation Breathing Pattern, Chest Expansion, peak expiratory flow rate PEFR
Anaesthetic Pathophysiology
Hemicolectomy (colon)
Thoracotomy (lung)
Median Sternotomy (heart)
Airway obstruction (no cough reflex and tongue laxity Reduced ventilation (- tidal volume and resp rate) Atelectasis (20-69% post op) compression and absorbtion Changes in Functional Residual Capacity (FRC) -20%, VQ and airway function (reduced ciliary tract activity and mucus plugging
Anaesthetic Aetiology/Epidemiology
Thoractomy results in greater atelectasis on that side, close to diaphragm basally
Risk increased if: over 65, >180 mins surgery, visceral handling, smoking, BMI, pre-existing conditions
Anaesthetic Assessment
Auscultation, VAS, Goniometry for shoulder RoM, ABGs, Breathing pattern, resp. rate, MRC, BORG
COPD Pathophysiology
Common preventable, progressive lung disease characterised by irreversible or partially reversible airflow obstruction and enhanced chronic inflammatory response to noxious particles or gases. Leads to fibrosis, alveolar wall destruction and mucus hypersecretion. Elastic recoil loss of alveoli is irrevesible.
Chronic bronchitis (cough and excessive mucus 3 months+), emphysema (abnormal destruction and enlargement of terminal airways and alvolar sacks) and asthma
Emphysema can be centrilobular (upper) or panacinar (lower).
COPD Aetiology/Epidemiology
900,000 in England and Wales, half as many undiagnosed
Insidious beginning
35+, more in industrial, 5th most common cause of death
Smoking - 80% of cases
air pollution/ fumes
2% genetic
