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PATHPROS > LUNG PATHOLOGY-1 > Flashcards

LUNG PATHOLOGY-1 Flashcards

Non Neoplastic lung conditions

1
Q

3 asbestos exposure related conditions

Deborah Dalmeida MD

A
  1. Pleural plaques
  2. Adenocarcinoma
  3. Mesothelioma

Deborah Dalmeida MD

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2
Q

Ghon focus/ Ghon Complex?

Deborah Dalmeida MD

A

Ghon Complex

The image shows a combination of parenchymal lung lesion and regional nodal involvement

Refer Slide 98 of the Lung ppt

Deborah Dalmeida MD

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3
Q

1. Diagnosis?

Gross- Cobblestoned lung surface

C/F: Fine bibasilar crackles

2. What is the cause for the finding seen on radiology?

Deborah Dalmeida MD

A
  1. Idiopathic pulmonary fibrosis
  2. Retraction of interlobular septa due to scarring is responsible for the honeycomb fibrosis seen on radiology

Deborah Dalmeida MD

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4
Q

Identify the pneumoconioses based on description provided for each:

1. • increased susceptibility to tuberculosis, egg shell calcification on Xray, birefringent particles on polarizing microscopy

  1. multiple, intensely blackened scars larger than 2 cm, necrotic center, coal miner
  2. See the image. What stain has been used to identify this characteristic finding ? Which condition is this?

Deborah Dalmeida MD

A
  1. Silicosis (see slide 57 for microscopic image of silicotic nodule)
  2. Complicated coal worker’s pneumoconioses (CWP)

(See slide 56 for gross lung image)

  1. Perl’s Prussian Blue; asbestos body.

An asbestos body- golden brown, fusiform or beaded rods with a translucent center and consist of asbestos fibers coated with an iron-containing proteinaceous material

Deborah Dalmeida MD

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5
Q
  1. Miliary pulmonary disease- does spread occur thorugh venous /arterial blood?
  2. Systemic miliary tuberculosis - does spread occur through venous/ arterial blood?

Deborah Dalmeida MD

A
  1. occurs when organisms draining through lymphatics enter the venous blood and circulate back to the lung.
  2. Systemic miliary tuberculosis : occurs when bacteria disseminate through the systemic arterial system

Deborah Dalmeida MD

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6
Q

Primary/ reactivation Tuberculosis?

Deborah Dalmeida MD

A

Reactivation Tuberculosis

The key here is to observe the cavitation, typically assoc with reactivation

Deborah Dalmeida MD

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7
Q

List some fibrogenic cytokines produced by the activated alveolar epithelial cells in IPF?

Deborah Dalmeida MD

A

TNF-alpha, TGF-beta, PDGF

Deborah Dalmeida MD

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8
Q

What is the major source of the event represented in the image?

Deborah Dalmeida MD

A

The event shown is a saddle embolus; cause in 95% is DVT.

Deborah Dalmeida MD

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9
Q

Identify this condition using the clues and Xray given:

Local suppurative process

secondary to Aspiration of infective material

or an

Antecedent primary lung infection

Deborah Dalmeida MD

A

Lung abscess

Deborah Dalmeida MD

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10
Q

What is the echocardiogram finding associated with this condition?

See attached image

Deborah Dalmeida MD

A

Coronary sinus dilatation

Deborah Dalmeida MD

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11
Q

Diagnosis?

abrupt onset of high fever, chills, purulent sputum, chest pain that increases on inspiration

Deborah Dalmeida MD

A

Bronchopneumonia

Deborah Dalmeida MD

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12
Q

1. What type of atelectasis is this?

Resorption of oxygen trapped in dependent alveoli due to complete obstruction of the bronchial airway

Mediastinum shifts toward affected side

2. Name the other 2 types of atelectasis

Deborah Dalmeida MD

A
  1. Resorption atelectasis
    2a. . Compression
    2b. Contraction

(If you cannot remember these, study slide 11 of the Lung ppt)

Deborah Dalmeida MD

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13
Q

Identify the lesion represented in the image provided

  • extends to the periphery of the lung substance as a wedge with the apex pointing toward the hilus of the lung
  • hemorrhagic

Deborah Dalmeida MD

A

Pulmonary infarction

Deborah Dalmeida MD

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14
Q

1. Identify this condition

  • greater prevalence in African-Americans
  • noncaseating granulomas, Schaumann bodies & asteroid bodies
  • hypercalcemia, elevated ACE, hypercalcemia

2. Describe the radiologic finding

Deborah Dalmeida MD

A
  1. Sarcoidosis
  2. Bilateral hilar lymphadenopathy

Deborah Dalmeida MD

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15
Q

PaO2 / FiO2 in ARDS

Deborah Dalmeida MD

A

Less than 200

Deborah Dalmeida MD

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16
Q

Identify this lesion that primarily involves the alveoli , immunologically mediated & is predominantly interstitial

  1. harvested humid, warm hay -
  2. proteins from serum, excreta, or feathers of birds
  3. thermophilic bacteria in heated water reservoirs

Deborah Dalmeida MD

A

Hypersensitivity pneumonitis

  1. Farmer’s lung
  2. Pigeon breeder’s lung
  3. Humidifier/air conditioner lung

Deborah Dalmeida MD

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17
Q
  1. What is the Reid Index?
  2. Which condition is this condition increased?
  3. In terms of the alphabets represented in the image, what represents the ratio?

Deborah Dalmeida MD

A
  1. ratio of the thickness of the mucous gland layer to the thickness of the wall between the epithelium and the cartilage .(normally 0.4)
  2. Chronic bronchitis
  3. bc/ad

Deborah Dalmeida MD

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18
Q

Pulmonary function test findings in restrictive airway diseases

Deborah Dalmeida MD

A

Decreased FVC and TLC

Increased FEV1/FVC ratio

Decreased lung volumes

Reductions in carbon monoxide diffusing capacity

Deborah Dalmeida MD

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19
Q

List 2 drugs causing pulmonary fibrosis

Deborah Dalmeida MD

A

Bleomycin

Busulfan

Amiodarone

Deborah Dalmeida MD

20
Q

What is the cause for appearance of honeycomb fibrosis in IPF?

Deborah Dalmeida MD

A

Fibrosis destroys alveolar architecture and forms cystic spaces lined by hyperplastic type 2 pneumocytes / bronchiolar epithelium and fibrotic wall

Deborah Dalmeida MD

21
Q

Identify the conditions from the microscopic descriptions below:

  1. loss of alveolar walls, Dilated airspaces, abnormally large alveoli separated by thin septa
  2. enlargement of the mucus-secreting glands of the trachea and bronchi, numbers of goblet cells increase slightly, mucous gland hyperplasia

Deborah Dalmeida MD

A
  1. Emphysema
  2. Chronic Bronchitis

Deborah Dalmeida MD

22
Q

Identify industries/occupations associated with the following pneumoconioses

  1. Coal mining industry
  2. Foundry work, sandblasting, hard rock mining
  3. Shipbuilding yard, roofing, insulation

Deborah Dalmeida MD

A
  1. Coal worker’s pneumoconioses
  2. Silicosis
  3. Asbestosis

Deborah Dalmeida MD

23
Q

Causes for pulmonary eosinophilia

Deborah Dalmeida MD

A
  • D - Drugs
  • N - Neoplasm
  • A - Allergy, asthma
  • A - Addison’s
  • A - Acute interstitial nephritis
  • C - Collagen vascular disease
  • P - Parasites

Deborah Dalmeida MD

24
Q

Which condition do you see this?

hyperinflation(> 6 ribs anterior above diaphragm, mid-clavicular line)

Flat hemidiaphragms

hyperlucency of the lungs

Deborah Dalmeida MD

A

Emphysema

Deborah Dalmeida MD

25
Q

Histologic pattern associated with idiopathic pulmonary fibrosis

Deborah Dalmeida MD

A

Usual interstitial pneumonia (UIP)

Major findings consistent with UIP pattern:

  1. Dense fibrosis
  2. Patchy and peripheral / perilobular involvement
  3. Fibroblastic foci
  4. Honeycomb (Cystic spaces lined by bronchiolar epithelium and fibrotic wall)

Deborah Dalmeida MD

26
Q

Identify the pattern of emphysema from the description

  1. Acini are uniformly enlarged from the level of the respiratory bronchiole to the terminal blind alveoli
  2. The central or proximal parts of the acini are affected,distal alveoli are spared
  3. proximal portion of the acinus is normal, and the distal part is predominantly involved, tendency for spontaneous pneumothorax due to rupture of bullae (MEMORIZE THIS IMAGE)

Deborah Dalmeida MD

A
  1. Panacinar
  2. Centriacinar
  3. Paraseptal

Deborah Dalmeida MD

27
Q

1. Identify the condition described

a. circulating neutralizing antibodies specific for GM-CSF
b. sputum that often contains chunks of gelatinous material.

2. What will you see on Light microscopy in this condition?

Deborah Dalmeida MD

A
  1. Pulmonary alveolar proteinosis
  2. Dense, homogeneous, granular precipitate containing surfactant proteins within the alveoli

Deborah Dalmeida MD

28
Q
  1. Microscopic features of advanced Pulmonary hypertension
  2. List one important Complication of pulmonary hypertension

Deborah Dalmeida MD

A

1. Plexiform pulmonary arteriopathy

Characterized by:

a. medial hypertrophy
b. tuft of capillary formations is present, producing a network, or web, that spans the lumens of dilated thin-walled, small arteries

2. Cor Pulmonale

Deborah Dalmeida MD

29
Q

Describe the microscopic findings in the 1st image and name the structures seen in the 2nd and 3rd

Deborah Dalmeida MD

A

1st image - bronchial cartilage at the right, bronchial lumen filled with mucus at the left , submucosa widened by smooth muscle hypertrophy, edema, and inflammation (mainly eosinophils).

  1. Curschmann’s Spirals
  2. Charcot-Leyden crystals

Deborah Dalmeida MD

30
Q

autosomal recessive condition

immotile cilia due to a defect of dynein arms (primary ciliary dyskinesia)

bronchiectasis, chronic sinusitis, and situs inversus

Deborah Dalmeida MD

A

Kartagener syndrome

Deborah Dalmeida MD

31
Q
  1. What is this condition?

abrupt onset of significant hypoxemia and diffuse pulmonary infiltrates in the absence of cardiac failure

  1. What is the most severe form of this condition called?

Deborah Dalmeida MD

A
  1. Acute Lung Injury.
  2. The most severe form is ARDS.

Deborah Dalmeida MD

32
Q

List some organisms that can cause necrotizing pneumonias and therefore lead to bronchiectasis

Deborah Dalmeida MD

A

Pseudomonas

Staphylococcus aureus

Hemophilus influenzae

Mycobacterium tuberculosis

Aspergillus

Deborah Dalmeida MD

33
Q

Bronchopneumonia or lobar pneumonia?

Deborah Dalmeida MD

A

Lobar pneumonia

Deborah Dalmeida MD

34
Q

Pulmonary function test findings in Obstructive airway diseases

Deborah Dalmeida MD

A

Increased FRC, Increased RV, Increased TLC.

Markedly decreased FEV1, Decreased FVC,

Decreased FEV1/FVC ratio

Increased lung volumes

Deborah Dalmeida MD

35
Q

1. Diagnosis?

anti–basement membrane antibodies directed against α3 chain of collagen IV

rapidly progressive glomerulonephritis and a necrotizing hemorrhagic interstitial pneumonitis

Light microscopy- focal necrosis of alveolar walls +intra-alveolar hemorrhages. +hemosiderin-laden macrophages

2. Immunofluoresence finding?

Deborah Dalmeida MD

A
  1. GOODPASTURE SYNDROME
  2. Immunofluorescence - linear deposits of immunoglobulins along the basement membranes

Deborah Dalmeida MD

36
Q
  1. Characteristic finding on bronchoalveolar lavage fluid in sarcoidosis
  2. Marker of disease activity of sarcoidosis

Deborah Dalmeida MD

A
  1. accumulation of CD4+ T cells (CD4:CD8 ratio 10:1)
  2. high TNF levels

Deborah Dalmeida MD

37
Q
  1. Identify the clinical condition described.

Sudden onset dyspnea, pleuritic chest pain, petechial rash, confusion, tachypnea, tachycardia, V/Q scan shows V/Q mismatch

Deborah Dalmeida MD

A

Pulmonary embolism

Deborah Dalmeida MD

38
Q

PaO2 / FiO2 in Acute lung injury

Deborah Dalmeida MD

A

Less than 300

Deborah Dalmeida MD

39
Q
  1. What is the composition of the structure indicated by the black arrows in the image ?
  2. What is the Xray finding of this condition?

Deborah Dalmeida MD

A
  1. fibrin-rich edema fluid mixed with the cytoplasmic and lipid remnants of necrotic epithelial cells (hyaline membranes)
  2. diffuse bilateral infiltrates (ground glass opacifications)

(See slide 17 of the ppt)

Deborah Dalmeida MD

40
Q

Red hepatization/ Gray hepatization?

  1. disintegration of red cells and the persistence of a fibrinosuppurative exudate ; grayish brown, dry surface
  2. massive confluent exudation with neutrophils, red cells, and fibrin filling the alveolar spaces ;affected lobe is distinctly red, firm, and airless, with a liver-like consistency

Deborah Dalmeida MD

A
  1. Gray hepatization
  2. Red hepatization

Deborah Dalmeida MD

41
Q

1. Identify the condition described

permanent dilation of bronchi and bronchioles caused by destruction of the muscle and elastic tissue, resulting from or associated with chronic necrotizing infections

2. Name one important complication of this condition

3. What are the classic clinical features?

Deborah Dalmeida MD

A
  1. Bronchiectasis
  2. Lung abscess
  3. Severe, persistent cough- particularly frequent when the patient rises in the morning; expectoration of foul-smelling, sometimes bloody sputum

Deborah Dalmeida MD

42
Q
  1. What is this lesion?
  2. Describe it ?
  3. Causative organism

Deborah Dalmeida MD

A
  1. Granuloma
  2. granulomatous inflammatory reaction with caseation necrosis,enclosed within a fibroblastic rim punctuated by lymphocytes, Multinucleate Langhans giant cells
  3. Mycobacterium Tuberculosis

Deborah Dalmeida MD

43
Q

1. What kind of pneumonia is this?

Scant amount of sputum, no consolidation, lack of alveolar exudate, confined to the alveolar septa and pulmonary interstitium

mononuclear inflammatory infiltrate

2. Name 2 causative organisms

Deborah Dalmeida MD

A
  1. Community acquired pneumonia (Atypical Pneumonia)
  2. Mycoplasma pneumoniae, influenza virus types A and B, Chlamydia pneumoniae

Deborah Dalmeida MD

44
Q

Gene defect observed in 50% familial and 25% idiopathic pulmonary hypertension

Deborah Dalmeida MD

A

BMPR2 gene

Deborah Dalmeida MD

45
Q

What are the components of airway remodeling in Asthma?

Deborah Dalmeida MD

A
  1. Overall thickening of airway wall
  2. Sub-basement membrane fibrosis
  3. An increase in size of the submucosal glands and mucous metaplasia of airway epithelial cells
  4. Hypertrophy and/or hyperplasia of the bronchial wall muscle

Deborah Dalmeida MD

PATHPROS (36 decks)

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