Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Year 5 Path Charis > Histopathology - Lung > Flashcards

Histopathology - Lung Flashcards

1
Q

What are

o Curschmann’s spiral
o Charcot Leyden crystals

and where are they seen?

A

o Curschmann’s spiral – spiral-shaped mucous plugs/ whorls of shed epithelium
o Charcot Leyden crystals – found in oesinophils/basophil granules

seen in asthma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Define chronic bronchitis (COPD)

A

o Chronic cough productive of sputum, most days for >=3 months over >=2 consecutive years

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Histology of COPD

A

Goblet cell hyperplasia
Hypertrophy of mucous glands
Dilation of airways

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Histology of asthma

A 
Hyperaemia 
Mucous plugging and inflammation 
Eosinophilic inflammation
Goblet cell hyperplasia
Hypertrophied constricted muscle

Curschmann spirals
Charcot Leyden crystals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Complications of chronic bronchitis (COPD)

A

Repeated infections - most common cause of hospital admission + death

Chronic hypoxia:

  • reduced exercise tolerance
  • pulmonary HTN
  • cor pulmonale
  • RHF

Lung cancer (independent of smoking)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Bronchiectasis complications

A

Recurrent infections
Pulmonary HTN + RHF

Haemoptysis
Amyloidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Which gene is responsible for CF?

A

CFTR (CF transmembrane conductance regulator) gene on Chr 7

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Histology of emphysema

A

Loss of alveolar parenchyma distal to the terminal bronchiole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Where are iron-laden macrophages found?

A

Pulmonary oedema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How does diffuse alveolar damage present in adults vs neonates?

A

Adults - ARDS

Neonated - RDS (=hyaline membrane disease of the newborn)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Diffuse alveolar damage changes

A

Capillary congestion –> Exudative phase –> Hyaline membranes –> organising phase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Histology of bronchopneumonia

A

Patchy bronchial and peribronchial distribution

Inflammation surrounding bronchioles themselves + is within the alveoli

Lower lobes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Causes of bronchopneumonia vs lobar pneumonia

A

Bronchopneumonia –> Low virulence organisms

Staph
Strep
Haemophilus
Pneumococcus

Lobar pneumonia –> high virulence organisms
Pneumococcus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Histology of lobar pneumonia

A

Widespread fibrinosuppurative consolidation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Stages of lobar pneumonia

A

Congestion of the lungs - hyperaemia, intra-alveolar fluid

Red hepatisation - intra-alveolar neutrophils, hyperaemia (neutrophilia)

Grey hepatisation - intra-alveolar connective tissue (fibrosis)

Resolution
Complications - abscess, pleuritis, pleural effusion, empyema, fibrosis, sepsis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is atypical pneumonitis?

A

Interstitial inflammation without the accumulation of intra-alveolar inflammatory cells

17
Q

How does cigarette smoke cause emphysema

A

Activates neutrophils + macrophages

These in turn activate proteases (Elastase) which leads to tissue damage

alpha 1 antitrypsin normally inhibits these proteases but in A1AT deficiency these proteases cannot be inhibited

18
Q

Emphysema damage

Smoking vs A1AT deficiency

A

Smoking - loss centered around bronchiole = centrilobular

A1AT deficiency - diffuse loss of aleveolae = panacinar

19
Q

Causes of lung granulomas

A

TB - caseating
Sarcoid - non caseating
Occupational lung disease (extrinsic allergic alveolitis)

20
Q

Extrinsic allergic alveolitis histology

A

Polypoid plugs of loose connective tissue within alveoli/bronchioles
Granuloma formation
Organising pneumonia

21
Q

Extrinsic allergic alveolitis acute vs chronic presentation

A

• Acute presentation
o Inhalation of antigenic dust in sensitised individual – systemic symptoms (fever, chills, chest pain, SOB) within hours of exposure
o Usually settle by the following day

• Chronic presentation
o Progressive persistent productive cough + SOB
o Finger clubbing
o Severe weight loss

22
Q

What is interstitial lung disease?

A

Inflammation + fibrosis of the pulmonary connective tissue

Can be
- Fibrosing
Idiopathic pulmonary fibrosis (cryptogenic fibrosing alveolitis)
Pneumoconiosis (industrial lung disease)

  • Granulomatous
    Sarcoid
    Extrinsic Allergic alveolitis
23
Q

Pneumoconiosis vs extrinsic allergic aleveolitis

A

Pneumoconiosis - occupational lung disease caused by inhalation of mineral dusts or inorganic particles (fibrosing interstitial lung disease)

Extrinsic allergic alveolitis - intense/prolonged exposure to organic antigens (granulomatous interstitial lung disease)

24
Q

Idiopathic pulmonary fibrosis/ cryptogenic fibrosing alveolitis histopathology

A 
Interstitial pneumonia (required for dx)
Interstitial fibrosis 
Honeycomb fibrosis
Loss of normal lung architecture 
Usually sub-pleural

Hypertrophy of type II pneumocytes –> cyst formation

diagnosis by HRCT +/- biopsy

25
Q

Define pulmonary HTN

A

Mean pulmonary arterial pressure >25mmHg at rest

26
Q

Causes + classes of pulmonary HTN

A

Pre-capillary

  • Vasoconstriction due to chronic hypoxia
  • Thromboembolism (class 4)
Capillary
- Widespread pulmonary fibrosis (class 3)

Post-capillary

  • LHF (class 2)
  • Veno-occlusve disease
class 1 - primary PAH, idiopathic, hereditary, drugs/toxins
Class 5 - pulmonary HTN with unclear multifactorial mechanisms
27
Q

Where is nutmeg liver found?

A

RHF

can be caused by a large pulmonary embolus (saddle embolus)

28
Q

Complications of small emboli

A

Localised haemorrhagic infarct

Repeated small emboli –> increasing occlusion of the pulmonary vascular bed –> pulmonary HTN

29
Q

Commonest type of cell from which lung cancers arise

A

Endothelial

30
Q

Types of malignant tumours

A

 Non-small cell carcinoma - less chemosensitive

  • SCC (30%) – smokers, central (airways), spread locally, late metastasis, PTHrP, cavitation
  • Adenocarcinoma (30%) – non-smokers, females, peripheral (peripheral alveolar spaces), early metastasis, extra thoracic metastases common and early
  • Large cell carcinoma (20%)

 Small cell carcinoma- chemoradiotherapy
• SCLC (20%) – smokers, central, SIADH, ACTH, Lamber-Eaton Myasthenic syndrome (LEMS)
• poor prognosis

31
Q

Adenocarcinoma precursor lesion

A

AAH

Atypical adenomatous hyperplasia

32
Q

Adenocarcinoma progression

A

Atypical adenomatous hyperplasia –> non-mucinous adenocarcinoma in situ –> mixed pattern invasive adenocarcinoma

histology –> glandular differentiation

33
Q

Large cell carcinoma histology

A

No histological evidence of glandular/ squamous differentiation

BUT on electron microscopy many show some evidence of glandular, squamous or neuroendocrine differentiation
– i.e are probably very poorly differentiated adeno/squamous cell carcinomas

34
Q

Small cell lung cancer - which cells do they arise from?

A

Neuroendocrine cells

35
Q

Small cell lung cancer histology

A

– Small poorly differentiated cells

– p53 and RB1 mutations common

36
Q

Biopsy of central vs peripheral tumours

A

Central
- Biopsy at bronchoscopy

Peripheral
- Percutaneous CT guided biopsy

37
Q

Molecular treatments in lung cancer

A

EGFR mutation - TKI inhibitor - cetuximab

ALK translocation - crizotinib

Ros1 translocation - crizotinib

PDL1 expression inhibition (high levels of PD1 or PDL1 protein expression may inhibit immune response- inhibit cytotoxic T cells)

Year 5 Path Charis (44 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions