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Year 3 - CR > Respiratory infections - Pathology 2 > Flashcards

Respiratory infections - Pathology 2 Flashcards

1
Q

What is an infection of the lung called

A

pneumonia or pneumonitis

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2
Q

Describe how the size of the air micron affects where it is deposited in the airway

A
  • particles that are more than 10 micron in size are held in the upper airways
  • 3-10 microns are trapped in the tracheobronchial mucus
  • 1-5 microns(bacteria) are deposited in terminal airways and alveoli
  • less than 1 micron is suspended in alveolar air
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3
Q

What are the defence mechanisms of the lung

A
  • Nasal clearance
  • Tracheobronchial clearance: mucociliary action
  • Alveolar clearance: Alveolar macrophages
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4
Q

How can lung mechanisms be disturbed

A
  • Suppression of cough reflex = due to coma, anaesthesia, drugs, chest pain, neuromuscular disease
  • Injury to mucociliary apparatus = due to smoking, inhalation of hot/corrosive gases, congenital
  • disturbance of macrophage function = due to smoking, alcohol, anoxia, oxygen toxicity
  • pulmonary congestion and oedema
  • accumulation of secretions
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5
Q

What is pneumonia

A
  • Alveolar inflammation
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6
Q

What are the types of pneumonia

A
  • lobar pneumonia
  • bronchopneumonia
  • atypical pneumonia
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7
Q

what is lobar pneumonia also known as

A
  • community acquired pneumonia
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8
Q

what part of the lobe does lobar pneumonia affect

A
  • affects large part or the entire lobe
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9
Q

what causes lobar pneumonia

A
  • 90% caused by streptococcus pneumonia
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10
Q

What are the clinical features of lobar pneumonia

A
  • high grade fevers with riggers
  • productive cough
  • rusty sputum
  • pleuritic chest pain
  • signs of consolidation - when you look at the chest X ray, when you tap there chest, when you listen to the chest (bronchial breath sounds)
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11
Q

describe what the pathology of lobar pneumonia looks like

A
  • the lobe that is affected looks more consolidated

- has 4 different stages

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12
Q

Describe the pathogenesis of lobar pneumonia

A
  1. Congestion (24 Hours)
    - vessel engorged
    - oedema in alveoli
    - heavy, red lung
  2. Red hepatisation (2-4 days)
    - outpouring of neutrophils and RBC’s into alveoli, red, solid, airless, liver-like lung (resembles the liver)

3l. Grey hepatisation(4-8 days)
- fibrin and macrophage replace neutrophils and RBC’s, grey, solid, airless lung

  1. Resolution (8-10 days)
    - gradual return to normal
  • these stages are not seen with prompt treatment
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13
Q

What are the complications of lobar pneumonia

A
  • rarely you can have suppurative complications such as lung abscess or emyema especially with Klebsiella or staphylococcus infections
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14
Q

What is the commonest type of pneumonia

A
  • Bronchopneumonia
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15
Q

Where do you see bronchopneumonia

A
  • chronic debilitating illness
  • secondary to viral infections
  • infancy
  • old age
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16
Q

How does bronchopneumonia begin

A
  • begins as bronchitis and bronchiolitis and then spreads to alveoli
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17
Q

What causes bronchopneumonia

A
  • Low virulence bacteria such as staph, street viridian’s, H influenzas, pseudomonas, coliform
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18
Q

describe the pathology of bronchopneumonia

A
  • bilateral - affects both lung
  • worse in the basal as there is more statsis and the air supply is worse
  • patchy
  • grey or grey-red spots of consolidation
  • microscopically acute inflammatory infiltrate in bronchioles and alveoli
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19
Q

What are the complications of bronchopneumonia

A
  • death - because usually complicating/terminal event in other debilitating illness or extremes of age
  • resolution
  • scarring
  • abscess/empyema - rare
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20
Q

what are the x ray differences between lobar pneumonia and bronchopneumonia

A

Lobar
- X ray and clinical signs: complete lobar opacity

bronchopneumonia
- Focal opacities, clinical sign less pronounced

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21
Q

What is more important that the difference between the lobar and bronchopneumonia

A
  • Correct identification of causative agent

- determination of extent of disease

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22
Q

What is interstitial (atypical) pneumonia

A
  • caused by different organisms
  • inflammation is restricted to alveolar septa and interstitial tissues: interstitial pneumonitis
  • no or minimal alveolar exudate
  • can be patchy or extensive
  • congested subcrepitant lungs
  • rarely intra-alveolar proteinancous material forming hyaline membrane
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23
Q

what can you get in interstitial (atypical) alveoli

A

rarely intra-alveolar proteinancous material forming hyaline membrane

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24
Q

Why is interstitial pneumonia atypical

A
  • they don’t have the normal symptoms of pneumonia

- don’t have a normal X ray that you would see in pneumonia

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25
Q

What can cause interstitial pneumonia atypical

A
  • mycoplasma pneumonia
  • Viruses: influenza A and B, RSV, acino, rhino, rubeola, varicella
  • chlamydia
  • coxiella
  • often undetermined
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26
Q

What are the predisposing conditions to interstitial atypical pneumonia

A
  • malnutrition
  • alcoholism
  • debilitating illnesses
27
Q

What is the clinical course of interstitial pneumonia

A
  • variable
  • clinically general rather than localised symptoms, out of proportion to signs
  • usually sporadic form usually mild and self limiting
  • epidemic forms associated with higher mortality
  • secondary bacterial infections common
28
Q

What is pulmonary tuberculosis

A
  • infection of the lungs by mycobacterium tuberculosis or M Bovis
29
Q

how does infection occur in endemic areas of pulmonary tuberculosis

A
  • infection occurs early in childhood
30
Q

How does spread of pulmonary tuberculosis occur

A
  • infection is airborne from open cases (not under control)
31
Q

describe the pathogenesis of pulmonary tuberculosis

A
  • pathogenicity is due to the ability to resist macrophage killing and induction of cell-mediated or delayed type IV hypersensitivity
  • cell mediated hypersensitivity is central to the development of characteristic tissue destruction through caseous necrosis and cavitation
  • macrophages phagocytes bacilli but cannot kill; multiply, lyse and infect other cells

T cell mediated immunity (2-3 weeks after infection)

  • CD4 mediated interferon gamma secretion; intracellular killing and granuloma formation
  • CD8 mediated lysis of macrophages and killing
  • CD4/CD8 mediated lysis of macrophages and caseation necrosis; bacilli are killed in anoxic acid environment
32
Q

what is a first tb infection called

A

primary TB

33
Q

describe what forms in primary TB

A
  • Ghon complex; typically 1cm focus in mid zone with draining lymph node
  • heals with fibrosis and calcification
34
Q

Is primary TB symptomatic

A
  • usually asymptomatic
35
Q

where is the Ghon complex in primary tb in the lung

A
  • mid zone of the lung
36
Q

describe what causes secondary TB

A
  • due to a heavy reinfection or reactivation

- sometimes it can be caused by progressive primary TB

37
Q

where do the bacteria relocate in secondary TB

A
  • bacterial relocate to areas that have high oxygen in the lungs therefore they go to the upper portion of the lung
38
Q

Describe where secondary TB is in the lung

A
  • usually apical about 3cm at clinical presentation
39
Q

what type of hypersensitivity is TB

A
  • type IV hypersensitivity
40
Q

describe the microscopic pathology of TB

A
  • granulomas with caseous necrosis, langhan’s giant cells and epithelioid macrophages (macrophages that resemble epithelial cells)
41
Q

What is a granuloma

A
  • collection of activated macrophages
42
Q

what stain is used to find the microscopic pathology bacteria of TB

A
  • ziehl-Neelson stain - this reveals the characteristic of the bacteria which have cell walls that are acid-fast bacilli - when you stain the tissue red everything will go red but when you decolourise with acid the red fades except in the bacteria which stay red due to the cell wall
43
Q

What is used for the definitive and most accurate diagnosis of TB

A
  • sputum culture (can take up to 6-7 weeks)
44
Q

What are the complications of pulmonary TB

A
  • progressive firbocavitary TB

- Miliary TB

45
Q

What is progressive fibrocavitary TB

A
  • progressive firbocavitary TB = gradually destroys lung through necrosis cavitation and fibrosis
46
Q

What happens in miliary TB

A
  • bloodborne dissemination within the lung or throughout the body
  • seed-like foci consisting of granulomas in meninges, bone marrow, liver or any organ
47
Q

Name some examples of fungal infections that can effect the lung

A
  • HIV: Pneumocystis carinii (PCP) - harmless to a healthy person but with immune compromise it can cause a life threatening infection (AIDs defining infection)
  • histoplasma
  • coccidiosis
  • candida
  • aspergillus
  • mucor
  • cryptococcus
48
Q

Who do fungal infections tend to affect

A

seen with immune compromise

49
Q

Name another example of a route of lung infection

A
  • route of lung infection may also be aspiration or blood borne (aspiration pneumonia)
50
Q

Name the symptoms of tuberculosis if it is in the lung

A
  • night sweats
  • weight loss
  • cough
  • fever
51
Q

Name the signs of tuberculosis in the lung

A
  • pleural effusion
  • clubbing
  • ## erythema nodosum
52
Q

What are differential diagnosis of Haemoptysis

A
  • Haemothorax
  • Pulmonary embolism
  • lung cancer
  • bronchiectasis
53
Q

How does TB present in the lymph nodes

A
  • painless enlargement of cervical or supraclavicualr lymph nodes
54
Q

How does TB present in the GI tract

A
  • disease is ileocaecal
  • causes colicky abdominal pain and vomiting
  • bowel obstruction can occur due to bowel wall thickening, stricture formation or inflammatory adhesions
55
Q

How does TB present in the spinal cord (Potts disease)

A
  • local pain and bony tenderness for weeks-months

- can cause bone destruction, vertebral collapse and soft tissue abscess

56
Q

Name the two diagnostic tests used for latent TB

A
  • tuberculin skin testing = Mantoux test
  • Interferon gamma release assays

these tests cannot diagnose or exclude active disease

57
Q

Name 4 tests used to diagnose active pulmonary TB

A
  • CXR
  • Sputum spear
  • sputum culture
  • nucleic acid amplification test
58
Q

Describe what a chest x ray would show in active pulmonary TB

A
  • fibronodular/linear opacities in upper lobe (typical) or middle or lower lobes (atypical)
  • Cavitation
  • calcification
  • military disease
  • effusion
  • lymphadenopathy
59
Q

What is the difference between a sputum smear or sputum culture

A

Sputum culture is more sensitive than smear testing and can assess drug sensitivity

60
Q

How long does a sputum culture take

A

Culture takes 1–3 weeks (liquid media) or 4–8 weeks (solid media)

61
Q

How does a nucleic acid amplification test work

A
  • direct detection of M.tuberculosis in sputum by DNA or RNA amplification
  • rapid diagnosis is in less than 8 hours
  • can also detect drug resistance
62
Q

What is DOTs strategy

A
  • aim to achieve completion treatment rates
  • treatment directly supervised by a healthcare professional or family member where the person is observed swallowing there medication
63
Q

Describe how the BCG vaccine works

A
  • BCG is a live attenuated vaccine that is derived from M.Bovis that has lost its virulence
  • it reduces the risk of disseminated and CNS TB

Year 3 - CR (44 decks)

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