Thorax Flashcards

1
Q

Types of bronchiolitis

A

Cellular
Constrictive fibrotic

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2
Q

Findings in constrictive fibrotic bronchiiolitis

Causes?

DD?

A

Air trapping
Mosaic attenuation.

Cause:
-post transplant
-connective tissue disease
-infection
-inhalation
-DIPNECH

DD: other fibrosing constrictive bronchiolitis
-Asthma
-Panlobular emphysema

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3
Q

Causes for bronchiectasis?

A

-Idiopathic

-Post infectious, most common, chronic or recurrent. Typical or atypical mycobacteria, staphylo, pertusis, pseudomonna, viral, fungal.

-Congenital: CF, primary cilliary dyskinesia, alfa 1 antitrypsin deficiency, williams-campbell syndrome, Mounier Kuhn syndrome.

-Immune mediated: ABPA, toxic inhalation, collagen, AIDS, ARDS.

-Obstructive: COPD, asthma, proximal obstruction .

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4
Q

Types of bronchiectasis (morphology)

A
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5
Q

Dx findings

A

Dx:
-Xray:** tram-track **opacities (Linear opacities that correspond to dilated airways and thickened airway walls)
-Rounded or branching tubular lucencies and cystic spaces that represent dilated airways;± air-fluid levels

-HRCT/thin CT: Best tool
Direct sign:
-↑ bronchoarterial ratio (B/A); signet ring sign (B/A > 1.5)
- Lack of bronchial tapering: Earliest and most sensitive sign
- Bronchiolectasis: Visualization of airway within 1 cm of costal pleura or abutting mediastinal pleura

Other associations:
-Bronchial wall thickening± mucoid impaction, fluid-filled bronchi
-Centrilobular nodules (tree-in-bud opacities)
-Mosaic attenuation (inspiratory) and air-trapping (expiratory) due to constrictive bronchiolitis

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6
Q

Diffuse Bronchiectasis, location and entities?

A

-Central
Allergic bronchopulmonary aspergillosis (ABPA),Mounier-Kuhn,Williams-Campbell

-Peripheral: Upper lobe predominant
Cystic fibrosis (CF), mycobacterial infection, non-TB, sarcoidosis, HP, AS.

-Peripheral: Lower lobe predominant
Pulmonary fibrosis (UIP, NSIP), chronic aspiration, immunodeficiency, autoimmune/collagen vascular disease,α-1 antitrypsin deficiency

-Peripheral: Middle lobe/lingular predominant
Atypical mycobacterial infection,primary ciliary dyskinesia (PCD),acute respiratory distress syndrome (ARDS)

-Peripheral: Diffuse involvement
Bronchiolitis obliterans syndrome (post-transplant)

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7
Q

Most common ILD pattern in RA
Findings in RA-ILD

A

UIP/ NSIP/ OP
Necrotic nodules
Airways: OB, bronchiectasis bronchiolectasis
pleural effusion, thickening.

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8
Q

Characteristic UIP pattern in CTD?

A

Straight line sign
Anterior uppler lobe fibrosis
Lower lobe exuberant honeycomb

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9
Q

CTD-ILD: which disease one is most likelty to express as NSIP

A

Scleroderma.

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10
Q

CTD-ILD in myositis, ILD expression?

A

OP+ NSIP

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11
Q

lung expression in LES

A

Serositis&raquo_space;» ILD (less likely)

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12
Q

Crazy Paving causes:

A

C: COP, Cancer
R: respiratory distress acute
A: Alveolar proteinosis
Z: zipper/fat= lipoid neumonia
Y: pulmonary haemorrage
P: PCP

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13
Q

Hemorrhagic metastasis to lung

A

RCC
Melanoma
Angiosarcoma
Choriocarcinoma

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14
Q

Cavitating mets

A

SCC
AdenoCA
Sarcoma

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15
Q

Name histological stages of lobar pneumonia

A

-Congestion: 2-6hs, vascular engorgement, intraalveolar edema fluid + bacterial proliferation + some N.
Macro: Red bogy heavy lung.

-Red hepatisation: 12hs, massive exudation (RBCs, neutrophils & fibrin) filling alveolar spaces = red, firm, airless lung (liver-like consistency = hepatisation)

-Grey hepatisation: 1-10d. Fibrinopurulent exudate. Disintegration of red cells.
Greyish-brown, dry surface to lung

-Resolution: Exudate broken down (progressive enzymatic digestion) , produces granular, semifluid debris , ingested by macrophages, expectorated or organised (by fibroblasts)
Extension to pleura (pleuritis) often present- long-term fibrous thickening and/or permanent adhesions (organisation)

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16
Q

Name at least 5 most common bacterial causes for community acquired pneumonia?

Which one is the single most common?

A
  • *Streptococcus pneumoniae *– most common
  • Mycoplasma
  • Haemophilus influenzae (type B most virulent, hence vaccine),
  • Moraxella catarrhalis (esp. elderly & COPD),
  • Staphylococcus aureus (post-viral or IVDU; assoc. w/ lung abscess & empyema),
  • Pseudomonas aeruginosa (usually HAP hospital acquired pneumonia but occurs in CF & immuncompromised),
  • Klebsiella pneumoniae (chronic alcoholics)
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17
Q

Mention at least 5 clinical settings where pneumonia can arise

A

At least 7 specific clinical settings:
-Community acquired acute pneumonia
-Hospital acquired pneumonia
-Health care associated pneumonia
-Aspiration pneumonia
-Chronic pneumonia
-Necrotizing pneumonia
-Pneumonia in immunocompromised host.

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18
Q

Mechanism when local pulmonary defence is compromised?

A

-Loss or supression of cough reflex
-Dysfunction of mucociliary apparatus
-Accumulation of secretions
-Interference w/phagocytosis
-Pulmonary congestion and oedema
-Cell mediated deficiency
-Congenital innate immunity.

19
Q

Which are the patterns of distribution in bacterial pneumonia?

A

-Lobar pneumonia

-Bronchopneumonia

20
Q

Lobar pneumonia:
Population affected , most common cause, path.

A

Lobar pneumonia:
-Typically in healthy subjects.
-S. Pneumoniae most common. Klebsiela, legionella, H.I, Mycoplasmas, TB.
-Path: affects alveolar space (exudate/transudate/blood cells) leads to consolidation + air bronchogram.

21
Q

Bronchopneumonia:
Population affected , most common cause, path.

A

-At risk patients: young/elderly, OH, post op, supressed cough, immunosupressed, viral.
-Cause: S. Aureus, HI, viral
-Path: affects respiratory epithelium: foci of suppurative peribronchiolar inflammation in terminal bronchiles. Neutrophil-rich exudate filling bronchi/bronchioles and alveolar spaces.
Macro: granular grey-red-yellow foci.

22
Q

Complications of bacterial pneumonia?

A
  • Tissue destruction/necrosis = abscess formation (pneumococcus & klebsiella),
  • Spread of infection to pleural cavity and fibrinosuppurative reaction = empyema,
  • Bacteraemia systemic dissemination (heart valves, pericardium, brain, kidneys, spleen, joints causing abscesses, endocarditis, meningitis, suppurative arthritis)
23
Q

What organism is typically associated if patient has CF?

And what organism classically associate w/malnourised OH? Second most common in this population?

A

Pseudomona Aeruginosa.

Klebsiella pneumonia - thick sputum.
Moraxella catarrhalis 2nd most common in this population.

24
Q

Most common cuase of Gram Neg pneumonia?

A

Klebsiella

25
Q

Cause of bulging interlobular fissue, w/lobar expansion?

A

Klebsiella.

26
Q

Cause of pneumonia in IVDU?

A

S. Aureus

27
Q

3 causes of exacerbation of COPD?

A

H Influenzae most common
Moraxella 2nd most common
Legionella

28
Q

Etiologies of Atypical pneumonia?

A

Mycoplasma pneumoniae
Chlamydia pneumoniae
Legionella
Viruses
Zoonosis

29
Q

Pulmonary abscess:
-Common organisms?

A

Organisms: S. Aureus., S. pyogenes, Klebsiella, Anaerobes .

30
Q

How are causatve organisms introduced in lung abscess?

A

-Aspiration of infective material
-Antecedent primary lung infection
-Septic emboli
-Neoplasia (obstruction)
-Other (trauma, direct extension)
-Primary chryptogenic lung abscess.

31
Q

Cardinal histologic change in all abscess?

A

Suppurative destruction of the lung parenchyma within the central area of cavitation.

32
Q

Complications of lung abscess?

A

-Superimposed saprophytic infections
-Gangrene of lung
-Extension to pelural cavity
-Septic emboli: Brain abscess/menigitis
-Amyloidosis type AA (rarelly )

33
Q

Location and number of abscess in aspiration? If pneumonia/bronchopneumonia?

A

Aspiration: Lower segments. Right side. Tend to be single.

Pneumonia/bronchoneumonia: basal, scattered, multple.

34
Q

If ther is an abscess, what needs to be excluded?

A

Underlying malignancy (10-15%)

35
Q

What organisms are typically involved in pneumonia in immunocompromised? bacterial, viral and fungal

A

Bacterial: P aeruginosa, mycobacterium, legionella, listeria.

Viral: CMV, herpes

Fungal: PJP, candida, aspergillus, cryptococcus.

36
Q

CD4 counts and infections?

A

<200: CPC in 70%, atypical mycobacteria, primary TB
<100: CMV, disseminated cryptococcosis, mycobacterial infection.
<50: Mycobacterium avium complex, kansasi.

37
Q

Viral pneumonia: mechanism?

A

Starts as upper respiratory infection.
Progress to lower track in patients w/risk factors.
Virus attach to respiratory cells, replication, cell death, impariment of defence.
Predispose for superimposed bacterial infecition.

38
Q

Viral pneumonia: histological findings?

A

Interstitial inflammatory reaction to respiratory epithelium; less alveolar involvement.
Mononuclear infiltrate mainly (lymphocytes, macrophages)
Alveoli may be free of exudate, but in many patients there is intra alveolar proteinaceous material and cellular exudate.
Patchy lung involvement.

39
Q

Aspergillosis: name clinical presentations

A

-Allergic bronchopulmonary aspergillosis
-Aspergilloma
-Semi invasive aspergillosis
-Invasive aspergillosis (angio invasive, airway invasive)

40
Q

ABPA, who suffers from it? what type of immune reaction is it? Dx

A

Affects mainly CF 10% and asthmatics 1-2%.
Generally younger than 40yo.
Considered to be a type 1 IgE mediated hyerpsensitivity
Dx: peripheral eosinophilia, positive skin test, increased aspergillus specificl IgE, inreased precipitating IgG for aspergillous.

41
Q

Aspergilloma, who is affected? Physiopath? which location?

A

Needs a pre-existing strucutral lung cavity (TB, emphysema, CF, sarcoidosis, abscess, neoplasm)

Physiopath: colonized lung cavity.
Locaition: upper obe.

42
Q

Semi invasive aspergillosis: who? physiopath?

A

Similar to invasive but chronic course over months/year.
Mildly immunosupressed (OH, DM, COPD, Lung disease), malignancy.
Micro: aspergillus invades lung tissue leads to focal consolidation, over months becomes cavity w/thick walls, then thin walled and aspergilus ball.

43
Q

Invasive aspergillosis: who, classification

A

Affects severely immunocompromised patients w/neutropenia

Classification:
-Angio invasive aspergillosis: invasive necrotising pneumonia
-Airways invasive: bronchiolitis, bronchopneumonia.