3- pathology of respiratory tract Flashcards

1
Q

what is pneumonia?

A
  • infection of long parenchyma (functional tissue of an organ)
  • infection involving distal airspaces, usually with inflammatory exudation (localised oedema)
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2
Q

what are the classifications of pneumonia by morphology?

A
  • lobar pneumonia (whole lobes)
  • bronchopneumonia (bits of lobes)
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3
Q

what are the classifications of pneumonia by clinical setting?

A
  • community
  • hospital

= either where infection acquired or how/why patient acquired it - again, doesn’t necessarily tell you what but helps narrow done list

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4
Q

what are the classification of pneumonia by organisms?

A

stupid question soz - just saying that definitive classification is by what organism caused it = specific treatment can be made

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5
Q

what is lobar pneumonia?

A

= confluent consolidation involving most/all of lung lobe

  • Consolidation is when lung tissue solidified because of accumulation of inflammatory cells, fluid, and debris in alveoli
  • areas of consolidation within a lobe merge together to form larger, continuous patches of affected lung tissue
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6
Q

what organisms is most common cause of lobar pneumonia?

A

strep pneumoniae

(usually community acquired in healthy, younger adult)

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7
Q

what are some less common organisms that can also cause lobar pneumonia?

A
  • Klebsiella pneumoniae - commonly in debilitated or malnourished adults – DM, alcoholics
  • Legionella pneumophila – individuals with co-morbidities – heart, renal, haematological disease, immunosuppressed, transplant patients
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8
Q

what is bronchopneumonia?

A
  • infection starts in terminal airways and spreads adjacent to alveolar lung
    • widespread, patchy
    • often bilateral, basal
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9
Q

what organisms cause bronchopneumonia?

A

wide variety = strep pneumoniae, haemophilus influenza, staphylococcus, anaerobes, coliforms

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10
Q

what may help narrow down wide variety of organisms that can cause bronchopneumonia?

A

clinical context may help e.g. staph/anaerobes/coliforms seen in aspiration

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11
Q

when is bronchopneumonia mostly seen in?

A

most seen in context of pre-existing disease:
- COPD
- Cardiac failure (elderly)
- Complication of viral infection (influenza)
- Aspiration of gastric contents

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12
Q

what is differences in appearance of microscopy in pneumonia stages?

A
  • normally, the alveoli look like big white spaces with thin walls
  • during acute period, alveoli filled with neutrophils
  • as infection progresses exudate(mostly made of neutrophils but also macrophages, fibrin) within alveoli begins to organise
  • exudate becomes formed masses of macrophage & fibroblasts.

= this can either be broken down by enzymes or reabsorbed by phagocytes by macrophages (resolution) or undergo fibrosis (scarring)

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13
Q

what are complications of pneumonia?

A
  • fibrous scarring
  • abscess
  • empyema
  • bronchiectasis
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14
Q

what is a lung abscess?

A

Localised collection of pus → leads to necrosis of involved lung parenchyma

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15
Q

when do lung abscess mostly occur?

A
  • Most result as a complication of aspiration = foreign material, such as food, liquids, or vomit, is inhaled into the lungs instead of being swallowed into the digestive system →in that case mixed infections so Mixed organisms causing abscess
  • Can occur after any bacterial pneumonia
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16
Q

what is empeyema?

A
  • collection of pus in pleural cavity
  • can organise leading to fibrous adhesions within pleural cavity
17
Q

what is bronchiectasis?

A
  • abnormal fixed dilation of bronchi & bronchioles usually due to fibrous scarring following infection (pneumonia, TB, cystic fibrosis) or with tumour
  • the dilated airways accumulate purulent secretion and that makes sort of cycle of infection
18
Q

what is tuberculosis?

A

chronic pulmonary & systemic disease
- primary infection occurs in lung then chronic infection in many sites (lung, gut, kidneys, lymph nodes, skin)

19
Q

what is cause of tuberculosis?

A

mycobacterial infection, commonly:
- Mycobacterium tuberculosis (most common)
- Mycobacterium bovis – infection seen in places with infected dairy cows and no routine pasteurisation of milk (not really seen in scotland)

  • Other mycobacteria cause atypical infection especially in immunocompromised host
20
Q

what helps the pathogenicity of mycobacterium?

A
  • ability to avoid phagocytosis
  • ability to stimulate host T cell response
21
Q

what characterises the pathology of tuberculosis?

A
  • delayed (type IV) hypersensitivity reaction
  • granulomatous inflammation which necrosis

= T cell response to organism enhances macrophage ability to kill mycobacteria & T cell response causes granulomatous inflammation, tissue necrosis & scarring

22
Q

what is primary TB?

A

what happens in first exposure and up to 5 years afterward

  • Inhaled organism phagocytosed and carried to hilar lymph nodes
  • Immune activation (few weeks) leads to a granulomatous response in nodes (and in lung) usually leading to killing of organism

*can lead to progressive disease but not very common (5%)

23
Q

what is secondary TB?

A
  • Reinfection or reactivation of disease in a person with some immunity
  • Disease tends initially to remain localised, often in apices of lung
  • Can progress to spread by airways and/or bloodstream
24
Q

why does TB re-activate/re-occur?

A

you get re-infected as host defences lowered like decreased T cell function (age, coincident disease causing immunocompromised (e.g. HIV), immunosuppressive therapy (steroids, cancer chemotherapy))

25
Q

usually, where is primary TB?

A

near pleura, lower part of upper lobe or upper part of lower lobe

26
Q

what is ghon focus and ghon complex?

A
  • both aspects of primary TB

ghon focus = focused areas of consolidation in lung
ghon complex = ghon focus + enlarged hilar nodes (granulomatous inflammation

27
Q

what happens to tissues in secondary TB?

A

fibrosing (scarring + fibrosis) and cavitating apical lesion (lesion that has hollow space in it due to necrosis)

28
Q

what is the final stage/most severe form of tuberculosis?

A

= haematogenous (bacteria travels through blood stream to infect different sites of body)
- disseminated TB = miliary TB due to looking like millet seeds - seed like lesions scattered (tiny granulomas)

29
Q

what is key characteristic of tuberculosis under microscope?

A

granulomas with caseous necrosis centre

granuloma = aggregate of epithelioid macrophages

*caseous necrosis = think TB

30
Q

what stain can be used for testing TB?

A

Ziehl Neelsen (ZN) stain = highlights mycobacteria (small rod shaped organisms staining purple)

stain because alcohol acid fast bacilli = something in cell wall that highlights (called alcohol fast because unlike lots of other organisms retain dye even after alcohol & acid)

31
Q

what is difference in microscopy for people who are immunocompromised in TB?

A

can see way more of the purple rods than in normal people with ZN stain

(alveolar spaces also filled with amorphous debris in TB)

32
Q

what are common pathogens that affect immunocompromised people
a) virus
b) bacteria
c) funghi
d) protozoa

A
  • virus (cytomegalovirus, herpesvirus)
  • bacteria (Mycobacterium avium intracellulare)
  • fungi (aspergillus, candida, pneumocystis, cryptococcus)
  • protozoa (cryptosporidia, toxoplasma)
33
Q

what is different about symptoms in immunocompromised people?

A

muted signs or symptoms or completely different ones = High index of suspicion required for diagnosis

34
Q

what is involved in diagnosis of TB in immunocompromised?

A
  • High index of suspicion
  • Multidisciplinary (physician, radiologist, microbiologist, pathologist)
  • Broncho-alveolar lavage (BAL) = flushing out airways to try and collect cells & mucus etc
  • Cytology/biopsy (with lots of special stains)
35
Q

what is special stain for pneumocystitis jiroveci?

A

grocott = stains black when positive