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PATH30001 Mechanisms of Human Disease > L6 14 Mar 2019 > Flashcards

L6 14 Mar 2019 Flashcards

1
Q

normal lung structure

A
  • Trachea (lined with mucous gland with mucosa - surrounded by cartilage and smooth muscle)
  • Bronchus
  • Bronchiole
  • Alveoli
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2
Q

normal alvelolar structure

A
  • Type 1 pneumocytes: v. thin, 95% of alveolar surface, for gas exchange
  • Type 2 pneumocytes: synth surfactants - involved in repair of alveolar epithelium via ability to give rise to type 1 pneumocytes
  • Resident macrophages
  • Capillaries
  • Macrophages and other WBCs
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3
Q

pneumonia

A

respiratory disorder w/ acute inflammation of lung structure, mainly alveoli and bronchioles

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4
Q

classification of pneumonia by causative agent

A
  • infectious: bacterial, viral, fungal
  • non-infectious (usually ALI): chemical, inhalation
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5
Q

pneumonia syndromes

A
  • community acquired: usually streptococcus pneumoniae and atypical bacteria (mycoplasma, chlamydia and legionella) or viral
  • hospital acquired: much larger spectrum of pathogens, esp, bacterial ➡️ more difficult to treat
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6
Q

Causes of adult community acquired pneumonia

A
  • Streptococcus pneumoniae 48%
  • influenza 13%
  • Chlamydia pneumoniae13%
  • Unknown 20%
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7
Q

Streptococcus pneumoniae

A
  • part of normal flora
  • most dangerous lung infection and 2nd most common bacterial cause of death
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8
Q

Streptococcus pneumoniae infections

A
  • Nasopharyngeal commensal: 10% adults and 50% infants
  • Can cause: otitis media (mortality 0%), meningitis (mortality 20%)
  • Aspiration➡️pneumonia <75 per 100 000 colonisation
  • Septicaemia➡️ (after pneumonia) 1 in 25 (mortality 20%)
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9
Q

infectious pneumonia- AT RISK INDIVIDUALS

A
  • people with impaired host defences (immunocompromised individuals)
  • People with: AIDS, alcoholics, transplant immunosupression, pregnancy, cystic fibrosis, autoimmune, burns, cancer (chemo), v. old/young, chronic steroid, long-term diabetes
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10
Q

lung defences

A
  • mucociliary clearance: ciliated transport
  • goblet cell w/ mucus production
  • lamina propria: below epithelial cells and contains resident immune cells
  • Surfactant proteins: protect airways from infection and maintains alveolar integrity - reduce surface tension in air, liquid interface ➡️ air
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11
Q

lung defences: immune response to S. pneumoniae

A
  1. colonisation: physical defences, mucosal proteins, IgA (opsonisation to complement mediation) and IgG, phagocytes
  2. early lung infection: physical defences, mucosal proteins, alveolar macrophages activated (releases cytokines)
  3. established pneumonia: inflammatory exudate (drowns alveoli), phagocytes - neutrophils, CD4 and CD8 lymphocytes
  4. septicaemia: complement, circulating phagocytes: macrophages
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12
Q

alveolar macrophages (AMs)

A
  • first-line primary phagocytes in innate immune system
  • large range of receptros for: direct interaction w/ bacteria and indirect modulation of innate and adaptive immune systems
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13
Q

low dose vs. high dose of infectious bacteria on first line macrophage-mediated phagocytosis

A
  • low dose: <104 –> macrophage kills all bacteria within the hour
  • high dose: macrophage is overwhelmed, bacteria continues to spread
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14
Q

factors that affect bacterial clearance

A
  • bacterial factors: low inoculum (# of pathogen), low virulence strain (how dangerous/how well they can hide)
  • host factors: epithelium integrity, efficient alveolar macrophages, IgA and IgG concentration
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15
Q

impaired lung defences

A
  • loss/suppresion of cough reflex
  • injury to muco-ciliary apparatus
  • interference with phagocytic/anti-bacterial action of alveolar macrophages
  • accumulation of secretions
  • pulmonary congestion or oedema
  • low IgG and/or IgA
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16
Q

how does premature birth affect lung defence?

A

not all surfactant proteins are produced until late stage embryology

17
Q

inflammation in upper respiratory tract

A
  • bronchiole surrounded by WBCs
  • thickening of bronchiole –> problem in air flow and also tension stress –> smooth muscle cells proliferate to stretch out bronchiole
18
Q

bronchopneumonia

A
  • acute suppurative inflammation
  • often multilobular, freq. bilateral and basal - secretions tend to gravitate towards the lower lobes
  • neutrophil rich exudate in bronchi, bronchioles and adjacent alveolar spaces
  • patchy anatomy in the lung
19
Q

lobar pneumonia

A

affects the whole lobe

  1. congestion: vascular engorgement, intra-alveolar fluid, numerous bacteria
  2. red hepatisation: neutrophils, red cells and fibrin fill alveolar spaces
  3. grey hepatisation: disintegration of red cells, fibrosuppurative exudate persists
  4. resolution: exudate broken down –> produces granular, semifluid debris –> undergoes organisation = fibrinous thickening or permanent adhesions
20
Q

acute inflammation time course

A
  1. 1 - 2 days: lung heavy, full of blood - oedema
  2. 2 - 4 days: lung red, heavy, full of liquid and some fibrin - stasis and congestion
  3. 4 - 8 days: lung solid, heavy, grey-white alveoli full of fibrin and neutrophils, red cells disintegrate
  4. > 8 days: RESOLUTION - exudate break down and removal in a healthy person –> where phlegm comes from
21
Q

acute inflammation in lung: histology

A
  • normal lung: very thin blood vessels + no cells in alveoli
  • vascular congestion and stasis: large blockage of red –> congested blood vessels
  • leukocyte infiltrate: large numbers of infiltrating neutrophils in alveoli
  • neutrophil exudate: congested capillaries and exudate in alveoli - no gas exchange - red hepatisation
  • pores of Kohn: little connections between alveoli, as one alveolus becomes swollen, some of the exudate will infect close healthy alveolus via pores of Kohn
  • organisating pneumonia: transformation of exudate to fibrous masses - infiltrated by macrophages and fibroblasts
22
Q

complications with lobar pneumonia/acute inflammation in lung

A
  • tissue destruction and necrosis
  • spread of infection and inflammation to pleural cavity: pleurisy
  • bacteraemic dissemination: endocarditis, pericarditis, meningitis, nephritis
23
Q

symptoms of complications with lobar pneumonia/acute inflammation in lung

A
  • acute onset, malaise, fever, chills, productive cough
  • chest pain secondary to pleurisy
  • ARDS –> if symptoms aren’t relieved
24
Q

how can symptoms of complications with lobar pneumonia/acute inflammation in lung be aleviated?

A
  • corticosteroids - if severe
  • antibiotics - need to rapidly ID what bacteria it is to be able to administer appropriate antibiotic
25
Q

ARDS

A

acute respiratory distress syndrome: rapid onset of loss of lung function - can’t breathe properly/can’t exchange gas efficiently

26
Q

histopathology of chronic inflammation in lung

A
  • collection of chronic inflammatory cells - clustered around fibrous tissue
  • no type I pneumocytes –> cuboidal epithelium - oxygen exchange problems
  • collagen: rigid lung, can’t stretch to take in normal amount of oxygen
27
Q

acute lung injury

A
  • AKA: ARDS, shock lung, traumatic wet lungs
  • diffuse alveolar damage: high mortality (40-60%)
  • due to damage of: alveolar capillaries, epithelium and surfactant layer
  • can be due to many reasons, usually direct injury to lung (direct chemical exposure and trauma), but also severe infectious end-stage pneumonia
28
Q

common causes of ARDS

A
  • gastric aspiration
  • pulmonary contusion, penetrating lung injury
  • ionising radiation
  • near drowning
  • inhalation injury e.g. NO2, SO2, Cl2, smoke
  • reperfusion pulmonary oedema after lung collapse/transplant
29
Q

What are the key factors in diagnosing for ARDS?

A
  • timing: always acute onset of respiratory failure
  • location: (almost) always seen as bilateral infiltrate on CXR
30
Q

damages to alveolus during acute phase of ALI/ARDS

A
  • rapid death of bronchila epithelium
  • inactivated surfactants fall away
  • type I pneumocytes die –> necrosis e.g. from toxic gases
    • cause cellular debris
  • some fibrosis begins
  • innate immune response storm: causes more problems
31
Q

ARDS progression and morphology

phase 1: exudative (acute)

A
  • day 1: interstitial/alveolar oedema, lots of cell death of parenchymal cells; lymphocytes, plasma cells and macrophages enter
  • day 2: sloughing of type 1 cells: basement membrane is exposed, hyaline membrane starts to form
  • day 4-5: peak of hyaline membrane formation
  • day 7: peak of interstitial inflammatory infiltrate; type 2 pneumocytes proliferate and spread along basement membrane, thrombi in aleveolar capillaries and pulmonary arterioles
32
Q

hyaline membrane

A

lining of “inappropriate” material: dead cells + proteins = hyaline membrane = very poor gas exchange

33
Q

ARDS progression and morphology

phase 2: organising phase (slower)

A
  • macrophages breakdown hyaline membrane and debris
  • > day 14: interstitial fibroblasts proliferate and produce collagen
34
Q

if one survives ARDS, then what are the two possible outcomes?

A
  1. resolution OR
  2. end-stage fibrosis (more often)
35
Q

resolution of ARDS

A

= complete recovery and restoration of normal lung function

  • alveolar exudate and hyaline membrane is resorbed
  • normal alveolar epithelium restored
  • fibroblast proliferation ceases
  • extra collagen metabolised
  • requires:
    • Na+/K+-ATPase = sodium pump
    • ENaC = epithelial sodium channel
    • Aquaporins: water transport channels
36
Q

end-stage fibrosis in ARDS

A
  • large amount of scar tissue produced
  • lung architecture remodelled (loss of branching): cyst like spaces = “honeycomb lung”
  • spaces separated from each other by fibrous tissue, lined with type II pneumocytes, bronchiolar epitheliuim or squamous cells
37
Q

treatment of ARDS

A
  • mechanical ventilation
  • inhalation of vasodilator, e.g. NO
  • high O2 concentrations - but not too high (toxic)
  • surfactant therapy
  • anti-inflammatory drugs - glucocorticoids
  • w/ treatment: mortality is still high (40-60%)
  • stem cell treatment?

PATH30001 Mechanisms of Human Disease (14 decks)

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