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RESP (Physiology (Lung function test (Obstructive all forced volume…

- - - - dynamic compression of airway
        
        can occur in normal people in expiration
        
        is exaggerated in reduced lung compliance (e.g. emphysema)
        
        caused by increased intrapleural pressure, causing collapse of the small airways, leading to air trapping and so incrased airway resistance
        
        on the graph, is shown by the area in the positive pressure
  - - - D = A x (pressure dif)/T
        
        thickened barrier
        decreased SA
        exercise
      - can be unmasked by exercise due to reduced transit time
      - need significant impairment of O2 (less than 25%) for problem to occur, due to long transit time RBC spend around 0.75s in capillary but only takes around 0.25 for equlibration
        good response with O2
    - - responds to oxygen if it is ventilation problem
      - mismatch between ventilation and perfusion
    - - doesn't respond to oxygen
      - e.g. due to pneumonia = exudate in alveoli, diffusion can't occur
- - - - type 1 hypersensitivity allergy
      - first exposure = allergen taken by macrophages, presented to TH2 cells, causes IgE class switching of B cells
        B cells produce IgE, which binds to high affinity receptors for it in mast cells
        upon re-exposure, allergen binds to IgE on mast cells and degranulate it, releasing histamine (increases vascular permeability) and cytokines that recruit eosinophils, eosinophils then degranulate and release further cytokines causing inflammatory response and damages the respiratory epithelium, increases mucous production, causes bronchospasm
      - allergens have to be small soluble proteins, often are proteases
      - Hygiene hypothesis = early exposure to bacteria and virus may decrease risk of developing allergy later in life
      - changes seen in histology :star:
        
        airway inflammation - thickened basement membrane
        
        infiltration of eosinophils
        
        epithelium is damaged
        
        increased mucous production = hyperplasia of mucous glands and hyertrophy of goblet cells
        
        smooth muscle hypertrophy = bronchospasm
        - subepithelail fibrosis
      - treatment = allergen specific immunotherapy (graded exposure to allergen through alternative route = subcutaneous), pushes responses towards TH1, produce IgG mainly
        inhaler = salmeterol + fluticasone (LABA+glucocorticoid)
        salbutamol for acute attack
    - - Emphysema
        
        most common cause = smoking
        
        inhalation of toxins (e.g. smoking) which are free radicals (ROS) will cause inflammatory response
        epithelial cells, macrophages, and migrated leukocytes will all secrete inflammatory cytokines, particularly proteases which will break down elastin in the lung wall, causing lung to lose its elastic recoil = destruction of alveolar wall and elastic fibres
        can lead to air trapping => hyperinflated lungs, barreled chest
        
        features seen histologically :star:
        
        bullae (large alveolar space) due to destruction of alveolar wall
        
        goblet cel hyperplasia
        
        infiltration of neutrophils, macrophages
        
        thickening of bronchiole wall due to fibrosis and smooth muscle hypertrophy
      - Chronic bronchitis
        
        clinical diagnosis: cough productive of sputum for most days lasting 3 months for at least 2 consecutive years
        
        due to persistent exposure to: smoking, industrial chemicals
        exposure of the irritant/chemical causes inflammation => mucociliary dysfunction, hyperplasia of mucous glands and loss of serous glands, hypertrophy of SMC with constant coughing, thickened basement membrane due to fibrosis, goblet cell metaplasia (from psuedostratified ciliated columnar, can also be to squamous),
    - - Beta agonist
        
        binds and activates B1 receptors on airway bronchial smooth muscle, which activates AC, increases cAMP, activates PKA
        PKA increases conductance of Ca sensitive K channels, greater hyperpolarization - more relaxation
        effect on epithelial cAMP = increases mucociliary biliary frequency, creases mucous clearance
        symptom reliever
        SABA = salbutamol - symptom relief in acute asthma
        
        use as required
        
        prolonged use shows no effects and can build up tolerance
        LABA = salmeterol - symptom control
        
        ADRs = tremor, reflex tachycardia, hyperkalemia
        do NOT use with beta blockers as they target same receptor and have opposite effects
      - glucocorticoid
        
        prednisone (oral)
        
        tluticasone (inhaled)
        
        steroid, binds to intracellular receptor, which then translocate to nucleus and binds to HRE, causes transcriptional effect
        
        upregulation of lipocortin, phospholipase A2 inhibitor
        
        upregulate anti-inflammatory, inlterleukin receptor antoagnost
        
        downregualte pro = iNOS, COX, phospholipase A2
        overall, ger reduced inflammatory cell recruitment and number, so less cytokines released = less inflammatory effect
        
        also decreases vascular permeability, by decreasing histamine release by mast cells
        
        decreases macrophage function, so less immune response
        no effect on bronchodilation
        doesn't reverse airways remodelling in poorly controlled asthma
        not used in COPD
        
        ADRs
        
        osteoporosis
        
        fat distribution, towards belly and face (moon face)
        
        hyperglacemia
        
        immunosuppressed - increased risk of oropharyngeal candidiasis
        
        suppressed HPA axis, due to reduced production of cortisol (can't directly withdraw)
        
        muscle wasting
        
        poor wound healing
      - muscarinic receptor antagonist = ipratropium
        
        blocks M2 receptors (Ach) = blocks parasympathetic effect = block bronchoconstriction
        
        used in COPD, with SABA for synergistic effect for reversible bronchospasm
  - - - continuous cycle of infection, inflammation and healing by fibrosis
        
        in CF, reduced mucous clearance, so bacteria can be in mucous and cause disease
        
        inflammatory response follows infection, with production of cytokines and inflammatory mediators
        
        inflammation causes increased mucous secretion, and with chronicity causes hyperplasia of mucous glands
        
        healing occurs with fibrosis, causing loss of elastic fibres in bronchiole wall, leading to dilated lumen
        
        constant coughing in attempt to get rid of mucous leads to SMC hypertrophy
  - - - CFTR genes:
        I = no production at all = G542x = nonsense mutation
        II = blocked in processing = p508del
        III = blocked in regulation (gets to membrane) = G551D
    - - biofilm infection
        biofilm = a group of bacteria that adheres together and works together (commensal relationship) to survive in a harsh environment, embedded in a self-produced matrix = extracellular polymer substance
        biofilm are more resistant to antibiotics because they have a EBS barrier and efflux pumps
        quorum sensing of amount of autoinducers corresponds to conc. of bacteria
      - treatment = nebulised aminoglycoside and oral ciprofloxacin
  - - - acid fast stain
      - sputum culture
      - PCR (nucleic acid amplification)
      - Tuberculin test = test for cell mediated type 4 hypersensitivity response, inject tuberculin, measure induration
      - IGRA = test for cell mediated type 1 response, test for IFN-gamma produced by CD4 T cells, no false positives from vaccinations and non-mycobacetrium TB
  - - - from neuroendocrine progenitor cells
    - - keratin pearls
        intracellular bridges
    - - glandular appearanc
    - - multi-nucleated giant cell
        lots of mitoses
        no differentiation
- - - - upper 1/3 = olfactory
        lower 2/3 = respiratory
      - conchae = finger-like projections from the lateral of nasal cavity
        allow swirling of air to improve filtration and moisten
        superior, middle, inferior nasal conchae
        inferior nasal conchae is separate bone, the rest is part of ethmoid bone
      - meatus = pathway of air
        sphenoethmoidal meatus
        superior meatus (above middle)
        middle meatus (above inferior)
        inferior meatus (below inferior)
    - - nasopharynx
        
        tubal tonsils
        
        pharyngeal tonsils
        
        auditory tube
        
        posterior nares (chonae)
      - oropharynx
        
        oropharyngeal isthmus
        
        to epiglottis
        
        palatine tonsils
        
        lingual tonsils
        
        palatoglossal and palatopharngeal arches
      - laryngopharynx
        
        laryngeal inlet
    - - cartilages:
        
        cricoid (C6 level), thyroid, epiglottis
        
        arytenoid, cuneiform, corniculate
      - laryngeal vestibule
        laryngea ventricle = pouch
        infraglottic space
      - vocal fold and vesticular fold
        fold = + mucosa
  - - - extrapulmonary = right main bronchus, left main bronchus, right superior lobar bronchus
        intrapulmonary = rest
      - right main bronchus is more vertical, larger diameter and shorter c.f. left main bronchus