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Pathology > Respiratory II > Flashcards

Respiratory II Flashcards

1
Q

Chronic Obstructive pulmonary disease is charcterized by?

A

1) Decreased (↓) FEV [Forced Expiratory Volume]
2) ** Decreased FVC** [Forced Vital Capacity]
3) Decreased FEV : FVC ratio

*The “opposite” of Restrictive Pulmonary Disease

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2
Q

Group of diseases causing chronic Obstructive Pulmonary disease (COPD)

A

1) Emphysema
2) Chronic Bronchitis
3) Bronchial Asthma

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3
Q

Types of Asthma

A

1) Extrinsic (immune):
–> Mediated by type I hypersensitivity response
(IgE binding to mast cells)
–> Begin in childhood
–> Patients with a family history of allergy
2) Intrinsic (non-immune):
–> Association with chronic bronchitis, and exerciseor cold-induced asthma
–> Begin in adult life
–> NO history of allergy

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4
Q

Histopathologic findings:
 Smooth muscle hypertrophy of the bronchi
 Hyperplasia of bronchial submucosal glands and
goblet cells
 Thickening and hyalinisation of basement membranes
 Proliferation of eosinophils
 Airways plugged by viscid mucous containing
Curschmann spirals (whorl-like accumulations of epithelial cells) and Charcot-Leyden crystals
(crystaloids of eosinophil-derived proteins)

Are the features of what condition?

A

Bronchial Asthma

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5
Q

Clinical features of Asthma

A

1) Dyspnoea
2) Wheezing aspirtation (due to stenosis of the airways)

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6
Q

Complications of Bronchial Asthma

A

1) Superimposed infection
2) Chronic Bronchitis
3) Pulmonary Emphysema
4) Status asthmaticus:
* Prolonged bouts of asthma
* Lasts days
* Unresponsive to therapy
* Death

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7
Q

———————- :Persistent productive cough that
occurs during at least three consecutive months over
at least two consecutive years

A

Chronic Bronchitis

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8
Q

causes of Chronic Bronchitis

A

1) Cigarette smoking
2) Air-pollution
3) Infection
4) Genetic factors

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9
Q

Pathogenisis of Chronic Bronchitis

A

1) Causative agents (environmental irritants) : - Hypertrophy of mucous glands (trachea and main bronchi) +
-Increase in mucin-secreting goblet cells
–> Inflammation with infiltration of CD8+ lymphocytes, macrophages and neutrophils
2) airflow obstruction –> Small airway disease (goblet cell metaplasia, mucous plugging of the bronchiolar lumen,inflammation, bronchiolar wall fibrosis), Coexistent emphysema

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10
Q

Clinical features of Chronic Bronchitis

A

1) Prominent productive cough
2) Production of sputum
3) Development of COPD with outflow obstruction:
- Hypercapnia
- Hypoxaemia
- Cyanosis (“Blue bloaters”)

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11
Q

Complications of Chronic Bronchitis

A

1) Pulmonary Hypertension –> Cor pulmonale –>
Cardiac failure
2) Recurrent infections and Respiratory failure

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12
Q

Chronic Bronchitis is Charecterised by?

A

Cyanosis “BLUE BLOATERS”

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13
Q

Macroscopic features:
- Hyperaemic and swollen (by edema fluid) mucosal
lining of the larger airways
- Covering of the mucosa by a layer of mucinous or
muco-purulent secretions

are the features of what Condition?

A

Chronic Bronchitis

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14
Q

Microscopic findings:
* Hypertrophy of the mucous-secreting glands (Reid index: Ratio thickness of submucosal gland layer to thickness of the bronchial wall >0.4)
*** Mainly, mononuclear inflammatory cells, but
admixed with variable numbers of neutrophils **
Airway obstruction caused by:
- Goblet cell metaplasia
- Mucous plugging
- Inflammation
- Fibrosis

Are the features of what condition?

A

Chronic Bronchitis

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15
Q

cause of Emphysema

A

cigarette smoking

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16
Q

Types of Emphysema

A
  1. Centri-acinar (95% of cases)
  2. Pan-acinar
  3. Para-septal
  4. Irregular
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17
Q

Clinical features of Emphysema

A

1) “Pink puffer” vs. “Blue bloater” (Chronic Bronchitis)
2) ↑ Antero-posterior chest-diameter (“Barrel” chest)
3) ↑ Total vital capacity
4) Hypoxia
5) Cyanosis
6) Respiratory acidosis

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18
Q

cause of Emphysema

A
  • Action of proteolytic enzymes (e.g. elastase) on the
    alveolar wall
    1) Elastase:
    –> Induces destruction of elastin
    –> Neutralised by the opposing action of alpha1-
    antitrypsin
    2) Cigarette smoking:
    –> Attracts neutrophils and macrophages (sources of
    elastase)
    –> Inactivates alpha1-antitrypsin
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19
Q

pathogenisis of Emphysema

A

↑ in Neutrophil Elastase –> Tissue damage
*caused by tobacco

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20
Q

Complications of Emphysema

A

1) Chronic Bronchitis
2) Interstitial Emphysema: Tear in the airways
“Leakage” of air into the interstitial tissue of the chest
3) Rupture of a surface bleb (apical bulla) –> Pneumothorax

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21
Q

causes/patho of Interstital Emphysema

A

cause/Pathology: Coughing + bronchiolar obstruction
–> Sharply increased pressures within the alveolar sacs –> Alveolar tears –> Entrance of air into the lung’s stroma
Other Causes:
1) Wound of the chest –> Entrance of air within the lung substance
2) Fractured rib –> Puncture of the lung parenchyma 
Entrance of air within the lung substance

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22
Q

Patho of Bronchiectasis

A

Destruction of the muscle and elastic tissue, resulting from or associated with chronic necrotising infections

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23
Q

pre-disposing factors of Bronchiectasis

A

[1) Post-infectious conditions (necrotising pneumonia: caused by bacteria, viruses and fungi)
2) Bronchial obstruction (e.g. tumour)
3) Cystic fibrosis
**4) Kartagener Syndrome **
5) Rheumatoid Arthritis
6) Systemic Lupus Erythematosus
7) inflammatory Bowel Disease

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24
Q

Macroscopic features:
* Dilated airways (4x normal size)
* Lumen of bronchi and bronchioles can be followed
up to the pleural surfaces
*Cut surface of the lung: Appearance of dilated
bronchi as cysts filled with muco-purulent secretions

Are the features of what condition?

A

Bronchiectasis

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25
Q

Localisation of Bronchiectasis

A

lower lobes, bilaterally (of the lungs); Most severe in the more distal bronchi and bronchioles

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26
Q

Microscopic findings:
* Intense acute and chronic inflammatory exudation,
within the walls of the bronchi and bronchioles
* Desquamation of the lining epithelium
* Extensive areas of necrotising ulceration
* Possible, pseudo-stratification of the columnar cells
or squamous metaplasia of the preserved epithelium
* Complete necrosis of the bronchial or bronchiolar
walls –> Lung abscess
* Fibrosis both of the bronchial and bronchiolar walls
and peri-bronchiolar –> Subtotal or total obliteration
of bronchiolar lumens

Are the features of what condition?

A

Bronchiectasis

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27
Q

Clinical features of Bronchiectasis

A

1) Severe, persistent cough
2) foul-smelling, sometimes bloody sputum
3) Haemoptysis (life-threatening)
4) Dyspnoea and orthopnoea (severe cases)
5) Obstructive respiratory insufficiency –> Marked
dyspnoea and cyanosis
6) Recurrent pulmonary infection –> Lung abscess
7) Less frequent complications: Cor pulmonale, brain
abscesses, amyloidosis

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28
Q

Clinical features of restrictive pulmonary disesae

A

1) Dyspnoea
2) Tachypnoea
3) End-inspiratory crackles
4) Eventually: Cyanosis, secondary lung hypertension,
right-sided heart failure with Cor pulmonale

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29
Q

Chest radiograph of restrictive pulmonary disease

A

Bilateral infiltrative lesions, in form of
- Small nodules
- Irregular lines
- Ground-glass shadows

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30
Q

Restrictive pulmonary disease is charcterised by>

A
  • Reduced expansion of lung parenchyma and
  • Reduction in total lung capacity
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31
Q

Types of A.fibrosing Restrictive pulmonary disease

A

a. Usual Interstitial Pneumonia (UIP)
b. Non-Specific Interstitial Pneumonia (NSIP)
c. Cryptogenic Organising Pneumonia
d. Pneumoconioses:
- Anthracosis
- Coal worker’s Pneumoconiosis
- Silicosis
- Asbestosis
e. Associated with Connective Tissue Diseases:
- Rheumatoid Arthritis
- Scleroderma
- Systemic Lupus Erythematosus

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32
Q

Epi of Usual interstital Pneumonia (UIP)

A

Most common and with worst prognosis
interstitial pneumonia

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33
Q

Pathogenisis of Usual interstitial Pneumonia (UIP)

A

Unknown agent triggers repeated cycles of epithelial activation/injury –> Release of cytokines –> Abnormal epithelial repair –> Exuberant myo-/fibroblastic proliferation –> “Fibroblastic foci” –> Proximal dilatation of the small airways

TGF-β1
–> Driver of the process
–> Fibrogenic properties
–> Released by type I alveolar epithelial cells
–> Transformation of fibroblasts into myofibroblasts
–> Deposition of collagen and other ECM molecules

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34
Q

Macroscopic features:
* Pleural surfaces of the lungs: Cobblestone
appearance, due to retraction of scars along the
interlobular septa
* Cut surface: Fibrosis (firm, rubbery white areas) of the lung parenchyma; Lower-lobe predominance
and a distinctive distribution in the sub-pleural
regions and along the interlobular septa

Are the features of what Condition?

A

Usual Interstitial Pneumonia (UIP) (of Restrictive pulmonary disease)

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35
Q

Microscopic findings:
* Patchy interstitial fibrosis, variable in intensity and age of the lesion
* Coexistence of early (exuberant fibroblastic proliferation) and late lesions (more collagenous and less cellular foci)
* Dense fibrosis –> Destruction of alveolar architecture and formation of cystic spaces, lined by hyperplastic type II pneumocytes or bronchiolar epithelium (honeycomb fibrosis)
*Mild to moderate mixed inflammatory infiltrates
* Intimal fibrosis + Medial thickening (lung hypertension)

Are the features of what condition?

A

Usual Interstitial Pneumonia (UIP)

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36
Q

Causes of Non-Specific Interstitial Pneumonia (NSIP):

A

Secondary to a variety of aetiologic factors
(e.g. infection, collagen vascular disease,
hypersensitivity pneumonitis, drug reaction)

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37
Q

Pathological findings:
* Distinction in two patterns:
1) Cellular: Mild to moderate chronic interstitial
inflammation (mainly lymphocytes, few plasma cells) in a uniform or patchy distribution
2) Fibrosing: Diffuse or patchy interstitial fibrosis

Are the pahtological features of what type of restrictive pulmonary disease?

A

Non-Specific Interstitial Pneumonia (NSIP)

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38
Q

Clinical features of Non-Specific Interstitial Pneumonia (NSIP)

A

1) Dyspnoea
2) Cough

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39
Q

Prognosis of Non-Specific Interstitial Pneumonia (NSIP)

A
  • Better than for UIP (5 year survival > 80%)
  • Patients with cellular pattern (younger) better outcome than those with the fibrosing pattern (older)
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40
Q

Cryptogenic Organising Pneumonia (COP) is aka?

A

Bronchiolitis Obliterans Organising
Pneumonia (BOOP)

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41
Q

Microscopic findings:
- Polypoid plugs of loose organising connective tissue(“Masson bodies”) within alveolar ducts, alveoli and bronchioles
- The connective tissue is all of the same age
- Normal underlying lung architecture
- NO interstitial fibrosis or honey-comb lung

Are the features of what disease?

A

Bronchiolitis Obliterans Organising
Pneumonia (BOOP) [aka Cryptogenic Organising Pneumonia (COP)]

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42
Q

Clinical features of Cryptogenic Organising Pneumonia (COP)

A

1) Cough
2) Dyspnoea

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43
Q

Chest X-ray findings of Cryptogenic Organising Pneumonia

A

Sub-pleural or peri-bronchial patchy
areas of airspace consolidation

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44
Q

Treatment of Cryptogenic Organising Pneumonia

A

Oral administration of steroids for ≥6 months

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45
Q

The 4 Types of Pneumoconiosis

A

1) Anthracosis
2) Coal worker’s Pneumoconiosis
3) Silicosis
4) Asbestosis

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46
Q

Inhalation of inorganic dust particles (coal dust, silica, asbestos and beryllium) –> Interstitial fibrosis
Causes of what type of condition?

A

Pneumoconioses

note:
* Coal dust –> Least fibrogenic
* Silica, asbestos and beryllium –> Very fibrogenic

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47
Q

Pathogenisis of Pneumoconioses

A

Development of pneumoconiosis depends on following factors:
1) The amount of dust retained in the lung and airways
2) The ** size and shape, thus the resilience (elastic capacity) of the particles
3) Theparticle’s solubility**and physicochemical reactivity
4) The possible additional effects of other irritants
(e.g. concomitant tobacco smoking)

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48
Q

Etiology of Anthracosis

A

 Inhalation of carbon dust
 Usually asymptomatic

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49
Q

Macroscopic-/Microscopic findings:
- Irregular black patches, within lung tissue
- Carbon carrying macrophages (“dust cells”)

Are the features of what condition

A

Anthracosis (Type of Pneumoconioses)

50
Q

Epi of Coal worker’s Pnumocpniosis

A

Inhalation of coal dust (contains both carbon and silica)

51
Q

Simple va Complicated caol Workers’ Pneumoconiosis

A

1) Simple Coal Workers’ Pneumoconiosis:
Coal macules (<1cm; result of ingestion of coal dust
by macrophages) around the bronchioles of upper
lobes and upper portions of lower lobes

2) Complicated Coal Workers’ Pneumoconiosis (progressive massive fibrosis)
- Fibrotic nodules filled with necrotic black fluid
- Results in: Bronchiectasis, pulmonary hypertension,
Cor pulmonale, Caplan Syndrome (Rheumatoid
arthritis + Pneumoconiosis), death from respiratory
or right-sided heart failure

52
Q

Causes of Silicosis Pneumoconioses

A

Exposure to free silica dust

53
Q

patho of Silicosis Pneumoconioses

A

Ingestion of silica dust by alveolar macrophages –> Damage of macrophages –> Release of lysosomal enzymes and chemical mediators (e.g.
cytokines) –> Stimulation of fibrogenesis

54
Q

Macro-/ Microscopic findings:
Silicotic nodules: Concentric layers of collagen with or without central cavitation

A

Silicosis

55
Q

Cause of Asbestosis Pneumoconioses

A

Inhalation of asbestos fibers

56
Q

Patho of Asbestosis Pneumoconiosis

A

Uptake of asbestos fibers by macrophages –> Release of fibroblast-stimulating growth factors –> Diffuse interstitial fibrosis (lower lobes)

57
Q

Histopathologic findings:
- Ferruginous bodies: Fibers coated by iron and
protein; Yellow-brown, rod-shaped bodies,
with clubbed ends (Prussian blue [+])
- Hyalinised fibro-calcific plaques of the parietal
pleura

Are the features of what condition?

A

Abestosis Pneumoconioses

58
Q

Connective tissue diseases associated with Fibrosing Restrictive pulmonary disesae

A

1) Rheumatoid Arthritis
2) Scleroderma
3) Systemic Lupus Erythematosus

59
Q

Pathogenesis of Sarcoidosis

A

CD4Th cells interact with unknown airborne Ags (e.g. mold or mildew, pesticides) –> Release
of cytokines –> Formation of non-caseating granulomas

60
Q

Immunologic phenomena of Sarcoidosis

A
  • Reduced sensitivity and often anergy to skin test Ags
    (Tuberculin test [-])
  • Polyclonal hyperglobulinaemia
61
Q

Radiological and Labratory findings of Sarcoidosis

A

1) Radiologic findings:
- Bilateral hilar lymphadenopathy
- Interstitial lung disease (diffuse reticular densities)

2) Laboratory findings:
- Hypercalcaemia and hypercalciuria
- Hypergammaglobulinaemia
- Increased activity of serum Angiotensin-Converting
Enzyme

62
Q

Clinical features of Sarcoidosis

A

1) Interstitial lung disease
2) Enlarged hilar lymph nodes
3) Anterior uveitis
4) Erythema nodosum of the skin
5) Polyarthritis

63
Q

Macro-/Microscopic findings:
- Granulomas located in the interstitium, and
mediastinal and hilar nodes
- Granulomas containing multinucleated giant cells
- Schaumann bodies and “asteroid” bodies

Are the features of what condition?

A

Sarcoidosis

64
Q

Histopathologic picture:
- Patchy mononuclear cell infiltrates in the
pulmonary interstitium (typical peri-bronchiolar accentuation)
- Mainly lymphocytes, but also plasma cells and
epithelioid cells; In acute forms: Also neutrophils
- Interstitial non-caseating granulomas, in peribronchiolar location
- Chronic cases: Diffuse interstitial fibrosis

Are the histopathological feature of what condition?

A

Hypersensitivity Pneumonitis

65
Q

Characteristic condition of Hypersensitivity Pneumonitis

A

Farmer’s lung –> casued by moldy hay

66
Q

Describe the features of the First exposure , Second exposure and chronic phase of farmer’s lung caused by hypersensitivity Pneumonitis

A
  • First exposure: Development of IgG Abs
  • Second exposure: Binding of Abs to inhaled
    allergens –> Formation of immune complexes
    (Type III hypersensitivity reaction)
    *Chronic: Granulomatous inflammation (Type IV
    hypersensitivity reaction)
67
Q

Immunological findings of Hypersensitive Pneumonitis

A

1) Bronchio-alveolar lavage specimens: ↑ numbers of T lymphocytes, of both CD4+ and CD8+ phenotype
2) Presence of specific precipitating Abs in patients’ serum, and Complement and Igs within the vessel walls (Type III hypersensitivity reaction).
3) Presence of non-caseating granulomas –> Type IV reaction

68
Q

Categories of Pulmonary Eosinophilia

A
  1. Acute Eosinophilic Pneumonia with respiratory failure
  2. Simple Pulmonary Eosinophilia (Loeffler Syndrome)
  3. Tropical Eosinophilia
  4. Secondary Eosinophilia
  5. Idiopathic Chronic Eosinophilic Pneumonia
69
Q

CM of Acute Eosinophilic Pneumonia with respiratory failure

A

Rapid onset of fever, dyspnoea, hypoxia

70
Q

chest X-ray/ Labratory test of Acute Eosinophilic Pneumonia with respiratory failure

A

X-RAY: diffuse pulmonary infiltrates
Labratory test: Broncho-alveolar lavage: >25% eosinophils

71
Q

Causes of Loeffler Syndrom (simple Pulmonary eosinophilia)

A
  • Unidentifiable aetiologic agent in up to 1/3 of patients
  • Parasitic infections (especially Ascaris lumbricoides)
  • Drugs (aspirin, penicillin)
    –> Self-limiting condition; Resolution of the lung opacities
    within a month
72
Q

Causes of Tropical Eoisnophilia

A

infection with
microfilariae and helminthic parasites

73
Q

Secondary Eosinophilia is associated with?

A

1) Asthma
2) Drug allergies
3) Certain forms of vasculitis

74
Q

Clinical features of Idiopathic Chronic Eosinophilic Pneumonia

A

High fever, night sweats and dyspnoea

75
Q

Eosinophilic Granuloms is aka?

A

Unisystem Langerhans Cell Histiocytosis

76
Q

Clinical features of Eosinophilic Granuloma

A

i. Bone pain,
ii. Pathologic fractures

77
Q

Radiological findings of Eosinophilic Granuloma

A

Unifocal lytic lesions in skull, ribs
and femur

78
Q

Histopathology:
- Localised proliferation of histiocytic cells (similar to
Langerhans cells of the skin)
- Characteristic cytoplasmic inclusions (“Birbeck
granules”; tennis racket appearance)
- Presence of monocytes-macrophages, lymphocytes
and eosinophils

Are the features of what condition?

A

Eosinophilic Granuloma

79
Q

Smoking related Restrictive Pulmonary lung disease

A

Desquamative Interstitial Pneumonia (DIP)

80
Q

Epi of Desquamative Interstitial Pneumonia (DIP)

A
  • Smokers in their 30s or 40s
  • Association with respiratory bronchiolitis-interstitial
    lung disease
81
Q

Histopathologic picture:
- Alveolar spaces, filled with macrophages
- Preservation of alveolar architecture
- Minimal fibrosis

Are the features of what condition?

A

Desquamative Interstitial Pneumonia (DIP)

82
Q

Clinical features of Pneumonia

A

1) Chills and fever
2) Productive cough
3) Blood-tinged or rusty sputum
4) Pleuritic pain
5) Hypoxia with shortness of breath
6) Cyanosis (sometimes)
7) Neutrophilic leukocytosis (if bacterial cause)

82
Q

cause of Lober Pneumonia

A

Streptococcus pneumoniae

83
Q

Macro-/Microscopic picture:
-Intra-alveolar exudate (involving an entire lobe
of lung) –> Consolidation

Macroscopic featurs of what type of Pneumonia?

A

Lobar Pneumonia

84
Q

stages of Lobar Pneumonia

A

1) Congestion
2) Red Hepatisation
3) Gray Hepatisation
4) Yellow Hepatisation
5) Resolution

85
Q

cause of Broncho-Pneumonia

A

1) Staphylococcus aureus,
2) Haemophilus influenzae,
3) Klebsiella pneumoniae,
4) Streptococcus pyogenes

86
Q

Macro-/Microscopic picture:
- Extension of acute inflammatory exudate
from the bronchioles into the adjacent alveoli
- Patchy distribution, involving one or more
lobes

Are the features of what type of Pneumonia

A

Broncho-Pneumonia

87
Q

Causes of interstital Pneumonia

A

Viruses, Mycoplasma pneumoniae

88
Q

Macro-/Microscopic picture:
- Involvement of more than one lobes
- Diffuse, patchy inflammation localised to
interstitial areas of the alveolar walls

Are the features of what type of Pneumonia?

A

Interstitial Pneumonia

89
Q

Epi of Mycoplasma Pneumoniae Pneumonia

A

Most common interstitial pneumonia
* Children and young adults
* Possible occurrence in epidemics

90
Q

Clinical features of Mycoplasma pneumoniae Pneumonia

A

1) Insidious onset
2) Mild, self-limited course

91
Q

Macro-/Microscopic findings:
- Inflammatory reaction limited to the interstitium
- NO exudate in the alveolar spaces
- Intra-alveolar hyaline membranes
Are the features of what type of Pneumonia?

A

Mycoplasma

92
Q

Epi of Viral Pneumonia

A

Most common types of pneumonia in childhood

93
Q

Causes of Viral Pneumonia

A

1) Influenza viruses,
2) Adenoviruses,
3) Rhinovirus,
4) Expiratory Syncytial Virus,
5) Varicella Zoster Virus (Chickenpox and Shingles) or,
6) Rubeola (Measles)
*Rubeola virus –> Giant cell pneumonia (numerous
giant cells), complicated by tracheo-bronchitis

94
Q

causative agent of Candidiasis

A

Candida albicans

95
Q

Candida albicans is the most frequent casue of Human fungal infections.
These infections can manifest as:

A

1) Superficial lesions in healthy persons
2) Disseminated infections in immuno-compromised
patients
3) Pulmonary, renal and hepatic abscesses and vegetative endocarditis
4) Invasive form (Invasive Candidiasis) –> Blood-borne
dissemination

96
Q

causative agent of Nocardiosis

A

Nocardia

97
Q

Causative agent of Actinomycosis

A

Actinomyces israelii

98
Q

Macro-/Microscopic features:
- Formation of abscess and sinus tract
- Exudate, with sulfur granules (yellow clusters of
the organism)

Are the features of what pulmonary infection?

A

Actinomycosis

99
Q

Causative agent of Coccidioidomycosis

A

Coccidioides immitis

100
Q

Causative agent of Cryptococcosis

A

Cryptococcus neoformans

101
Q

Histopathology:
- Encapsulated organism
- India ink: Visualisation of the capsule in cerebral spinal fluid (zone of clearance or “halo” around the cells)
- Mucicarmine stain: Staining of polysaccharide cell wall in tissue

Are the features of what pulmonary infection?

A

Cryptococcosis

102
Q

Causative agent of Histoplasmosis

A

Histoplasma capsulatum

103
Q

Clinical feature of Rickettsial Pneumonias

A

Q- Fever

104
Q

causative agent of Aspergillosis

A

Aspergillus fumigatus

105
Q

patho of Aspergillosis

A

1) Aspergillus spores (2-3 μm) reach alveoli –>
Engulfment and killing of Aspergillus conidia by
alveolar macrophages –> Secretion of cytokines and chemokines (by macrophages), thus stimulating adaptive immune responses –> T lymphocytes confer protective immunity

106
Q

Cause of Q-fever

A

inhalation of Coxiella burnetti

107
Q

Ornithosis (Psittacosis) is caused by?

A

Chlamydia species

108
Q

Pathogens causing Lung Abscess

A

I. Staphylococcus
II. Pseudomonas
III. Klebsiella
IV. Proteus, combined with anaerobes

109
Q

Patho of Lung abscess

A
  • Bronchial obstruction
  • Aspiration of gastric contents (due to loss of
    consciousness; from alcohol or drug overdose,
    neurologic disorders, general anesthesia)
  • Complication of bacterial pneumonia
110
Q

Clinical features of lung abcess

A

1) Fever
2) Foul smelling purulent sputum
3) Fluid-filled cavity (X-ray)

111
Q

causative agent of Tbc

A

Mycobacterium tuberculosis

112
Q

cause of Pulmonary and non-pulmoary Tbc

A
  • Pulmonary form: Inhalation of droplets with the organism
  • Non-pulmonary form: Ingestion of infected milk
113
Q

patho of Tbc

A
  • Ingestion of organism by macrophages–>
    Presentation of Ags to CD4 Th cells –> Proliferation of CD4 Th cells and secretion of cytokines
  • Attraction of lymphocytes and macrophages
  • Macrophages either ingest and kill some of the
    organisms or undergo alteration and form epithelioid
    cells and Langhans multinucleated giant cells
114
Q

Clinical picture of Primary Tbc

A

Asymptomatic; No clinically evident
disease

115
Q

Primary Tbc is characterised by?

A

Initial infection, characterised by primary or Ghon complex (Peripheral sub-pleural parenchymal
lesion + Hilar lymph nodes)

116
Q

Histopathology:
- Central caseous necrosis
- Langhans giant cells

Are the features of what lung infection ?

A

primary Tbc

117
Q

Secondary Tbc is charcaterised by?

A

Activation of a prior Ghon complex, with spread to a
new pulmonary or extra-pulmonary site

118
Q

Clinical featurs of secondary Tbc ?

A

1) Progressive disability
2) Fever
3) Haemoptysis
4) Bloody pleural effusion
5) Generalised wasting

119
Q

Macroscopic picture:
 Localised lesions: Apical or posterior segments of
the upper lobes
Involvement of hilar lymph nodes

Are teh features of what lung infection?

A

Secondary Tbc

120
Q

Microscopic picture:
 Liquefaction and expulsion of the caseous contents
 Formation of cavitary lesions
Cavitation
Caseation
 Scarring and calcification

Are the features of what lung infection

A

Secondary Tbc

note:
- Cavitation: Only in secondary Tbc
- Caseation: Both primary and secondary Tbc

121
Q

what are the 3 types of Tuberculosis?

A

1) Primary
2) Secondary
3) Miliary

Pathology (11 decks)

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