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PAT Patho Pharma Flashcards

1
Q

complication of acute tonsilitis

A
  1. Spread of infection:
    a. Direct: Peritonsillar abscess (Quinzy) - otitis media – pharyngitis- laryngitis.
    b. Lymphatic spread: Cervical lymph nodes (lymphadenitis).
    c. Blood spread: Bacteremia- septicemia- toxemia- pyemia.
  2. Hypersensitivity :
    to streptococcal sore throat or URT infections may result in
    © Rheumatic Fever Or
    © Post Streptococcal Glomerulonephritis.
  3. Chronicity: Chronic tonsillitis.
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2
Q

complications of otitis media

A
  • include mastoiditis, meningitis, and brain abscess.
  • Inflammation may persist and become chronic with hear loss.
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3
Q

Definition of Diphtheria

A

Diphtheria is a life-threatening disease characterized by a pseudo-membranous inflammation of throat and tonsils of young children.

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4
Q

Gross of pseudomembranous inflammation

A

Multiple small yellowish foci of necrosis gradually enlarge, fuse together and form a continuous membrane.
The membrane:
is slightly raised and adherent, but if removed by force it leaves bleeding ulcerating surface and reforms again

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5
Q

causes of pyemic abscess of lung

A

septic empoli from septic thrombophlebitis of systemic veins
infective endocarditis of the right side of the heart

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6
Q

Gross of the pyemic abscess

A

multiple , very small and always next to a blood vessel, yellow spots surrounded by a zone of congestion

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7
Q

It is the type of emphysema that occurs with alpha 1 antitrypsin deficiency

A

Panacinar
(panlobular)

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8
Q

Distention of all air spaces distal to the terminal bronchiole i,e. the whole lobular unit

A

Panacinar
(panlobular)

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9
Q

emphysema occurs more commonly in the lower lung zones

A

Panacinar
(panlobular)

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10
Q

what is Centriacinar
(bronchiolar
emphysema)

A

§ Distention of the central part of the acinus formed by the respiratory bronchioles while distal alveoli are spared.
§ The lesions are more common and severe in the upper lobes, particularly the upper segments.
§ This type is common in cigarette smokers & coal workers’
Pneumoconiosis

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11
Q

Definition of Emphysema

A

Permanent over distention of air spaces distal to the terminal
bronchioles, with destruction of their walls

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12
Q

location of centriacinar emphysema

A

distention of respiratory bronchioles more common in the upper lobes, particularly the upper segments

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13
Q

cause of the panacina emphysema

A

alpha 1 antitrypsin defeciency

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14
Q

what is panacinar emphysema

A

Distention of all air spaces distal to the terminal bronchiole i,e. the whole lobular unit

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15
Q

other names of the centri, pan, disatalacinar emphysema

A

bronchiolar
panlobular
paraseptal

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16
Q

location of the panacinar emphysema

A

lower lung zones

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17
Q

emphysema occurs adjacent to areas of pulmonary scarring, or atelectasis

A

Distal acinar (paraseptal)

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18
Q

location of the paraseptal emphysema

A

usually in the upper half of the lung

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19
Q

Pathogenesis of the emphysema

A
  • Alveolar wall destruction in emphysema likely results from imbalances between pulmonary proteases and their inhibitors
  • Tobacco smoke and air pollutants:
    ü recruit neutrophils and macrophages.
    ü Smoking enhance elastase release from macrophages and neutrophils
    ü at the same time inhibit alpha 1 antitrypsisn.
    increase the elastases over the antitrypsin degrades the extracellular matric and the elastic tissue of the alveoli thus preventing the alveoli from returning to normal size after their inflation with air during inspiration
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20
Q

the microscopic picture of the emphysema

A

enlargment and dilation of the air spaces of thinning and destruction of the alveolar wall
and number of alveolar capillaries are diminshed

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21
Q

the gross of emphysema

A

panacinar: pale, dry, and voluminous lungs that obscure the heart
centriacinar: less pale and less voluminous and upper two thirds of the lung are more severely affected

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22
Q

Clinical picture of emphysema

A

1) Dyspnea
2) Iassociated with chronic bronchitis there is coughing and wheezing.
3) Barrel chest (increased antero-posterior diameter) due to lung
overinflation.
4) Finger clubbing due to hypoxia.

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23
Q

Complications of emphysema

A

1) pulmonary hypertension and right sided heart failure (cor pulmonale)
2) Respiratory failure from defective ventilation, perfusion & diffusion ofgases with increased C02 in blood, respiratory acidosis & death.
3) Rupture bullae containing air into pleura producing pneumothorax (air in pleural cavity)

heart and respiratory failure and pneumothorax

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24
Q

what is compensatory emphysema

A

compensatory dilatation of alveoli in response to loss of the lung substance due to fibrosis or atelectasis

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25
Q

Definition of the chronic bronchitis

A

Chronic bronchitis is defined clinically as persistent productive cough for at least 3 consecutive months, for 2 consecutive years.

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26
Q

what is bullous emphysema?

A

It is a localized accentuation of any form of emphysema which there are large cystic spaces (bullae) greater than 1 cm

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27
Q

What is Interstitial
emphysema?

A

§ air collects out of the air spaces in the connective tissue
septa of the lung and track into the connective tissue of the
mediastinum and the neck.
§ It may occur spontaneously with sudden increase in intraalveolar pressure (as violent coughing in children with
whooping cough), or from perforating injuries of the lung.
§ There is marked swelling of the neck with crepitus under the
skin.
§ Air is absorbed spontaneously

air from connective tissue of lung to C.T of the mediastinum and neck

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28
Q

What is senile or atrophic emphysema

A

Occurs as a result of senile loss of elasticity of tissues
accompanying the atrophic changes of aging.

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29
Q

Etiology of the chronic bronchitis

A

The most important causative factor is cigarette smoking

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30
Q

pathology of chronic bronchitis

A

hypersecretion of mucus in trachea and large bronchi
due to
hypertrophy of submucosal mucous glands

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31
Q

Definition of Chronic Interstitial Lung Diseases

A

Chronic interstitial lung diseases are a heterogeneous group of
disorders characterized by bilateral, patchy, chronic Involvement of the interstitium of the lung.

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32
Q

the main clinical manifestation of Chronic Interstitial Lung Diseases

A

Chronic interstitial lung diseases are a heterogeneous group of
disorders characterized by bilateral, patchy, chronic Involvement of the interstitium of the lung

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33
Q

Pathogenesis of Chronic Interstitial Lung Diseases

A

reduced compliance
More pressure is required to expand the lungs because they are stiff
dypnea
affection of ventilation and perfusion causes hypoxia
ground glass shadows
honey-comb lung appearance
respiratory failure often with pulmonary
hypertension and cor pulmonale

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34
Q

Types of Chronic Interstitial Lung Diseases

A

1) Idiopathic pulmonary fibrosis.
2) Non- specific chronic interstitial pneumonia
3) Cryptogenic organizing pneumonia
4) Pulmonary involvement in collagen
diseases as rheumatoid arthritis and
systemic lupus erythematosus).
5) Sarcoidosis.
6) Pneumoconiosis

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35
Q

Definition of Pneumoconiosis

A

Lung disease caused by inhaled dust. Dust may be inorganic (mineral) or organic.

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36
Q

stages of Coal worker’s pneumoconiosis

A

Simple anthracosis: presence of coal dust pigments which are taken by alveolar macrophages.
Macules and nodules
1) of dust-laden macrophages with delicate collagen fibers.
2) Can lead to centilobular emphysema.
Complicated stage Progressive massive fibrosis with black pigment.

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37
Q

the most prevalent occupational disease

A

Silicosis

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38
Q

increase the susceptibility to tuberculous infection

A

silicosis

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39
Q

increase risk of mesothelioma

A

asbestosis

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40
Q

definition of atelectasis and collapse

A

Atelectasis is failure of expansion of the lung or collapse of previously
inflated lung, affecting part or all of one lung

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41
Q

types of atelectasis

A
  • Resorption atelectasis
  • Compression atelectasis
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42
Q

the 5 % non carcinoma tumors of the lung

A

carcinoid tumor,
fibrosarcoma,
leiomyosarcoma
lymphoma

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43
Q

the most common benign tumor of the lung is

A

hamartoma

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44
Q

what is hamartoma?

A

benign tumor of the lung which spherical coin like-shadow on X ray
It consists mainly of mature cartilage admixed with fat, fibrous tissue and blood vessels

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45
Q

Gross of the squamous cell carcinoma

A

Centrally located mass:
85% of tumors arise in major bronchi and present as;
* An endobronchial growth
* An infiltrative tumor that invade the bronchial wall and surrounding lung tissue.

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46
Q

Microscopic picture of squamous cell carcinoma

A

Squamous cell carcinoma with various grades of differentiation and Keratin pearl formation.

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47
Q

Most common type of lung cancer in women

A

Adenocarcinoma

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48
Q

Gross of Adenocarcinoma

A
  • Most are peripherally located, and may be multiple.
  • Can occur centrally in men.
  • Seeding of the pleura occur early.
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49
Q

what is Large cell carcinoma

A

Large cell undifferentiated carcinoma that have no glandular or keratin formation

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50
Q

Keratin pearl formation related to

A

squamous cell carcinoma

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51
Q

Gross of the small cell carcinoma

A

a central mass which is rapidly growing and early metastasizing

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52
Q

Microscopic picture of small cell carcinoma

A
  • Cells are twice the size of small lymphocytes with scant cytoplasm.
  • Necrosis is always present and may be extensive.
  • These tumors often secrete a variety of polypeptide hormones that may result in paraneoplastic syndromes
  • The tumor cells can be stained by anti chromogranin which is a marker of neuroendocrine cells.
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53
Q

inflammatory ulcers of the tongue and oral cavity

A

Dental ulcer
Apthous ulcer
Herpitic ulcer
Tuberculous ulcer
Syphilitic ulcer (primary, secondary, Teritiary)

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54
Q

sharp teeth producing a single superficial ulcer (simple ulcer)
on the edges of the tongue.

A

Dental ulcer

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55
Q

idiopathic, possibly autoimmune. Occur as multiple, small,
shallow, recurrent painful ulcers

A

Apthous ulcer

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56
Q

herpes simplex vesicles which ulcerate

A

Herpitic ulcer

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57
Q

what is dental ulcer

A

inflammatory ulcer of the tongue which is sharp teeth producing
single superficial ulcer
on the edges of the tongue

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58
Q

location of tuberculous ulcer

A

tip of tongue

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59
Q

what is tuberculous ulcer of the tongue

A

o Ulcer occurs at tip of tongue from coughed sputum.
o The ulcer have undermined edge and caseous floor

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60
Q

what is syphilitic ulcer of the tongue

A

Primary syphilis ulcerated chancre (describe from general).
Secondary syphilis ulcerated mucous patches.
Tertiary syphilis ulcerated gumma (precancerous)

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61
Q

the neoplastic ulcer of the tongue

A

squamous cell carcinoma malignant ulcer on the anterior 2/3 of the tongue

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62
Q

what is leukoplakia

A

whitish mucosal patch which is squamous hyperplasia with hyperkeratosis

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63
Q

complication of leukoplakia

A

squamous cell carcinoma

64
Q

Predisposing factors of squamous cell carcinoma of the tongue

A

1) leukoplakia
2) tobacco chewing
3) HPV 16&18
4) tertiary syphilitic (gumma ulcer)

65
Q

Gross of squamous cell carcinoma of the tongue

A

anterior 2/3 of the tongue as a polypoid fungating mass or a malignant ulcer
Edge: raised everted
floor: necrotic
base: fibrotic

66
Q

Microscopic picture of the squamous cell carcinoma of the tongue

A

cell nest of malignant cell
outer columnar
middle polyhydral cells
inner flat cells and keratin in center

67
Q

complication of the squamous cell carcinoma of the tongue

A

Direct spread:
producing fixation of tongue, restriction of its mobility & improper speech.
Lymphatic: Cervical lymph nodes
Blood spread: to systemic circulation (early)

68
Q

what is sialadenitis

A

Inflammation of the salivary glands (minor or major)

69
Q

causes of sialadenitis

A

Viral: mumps and cytomegalovirus
Bacterial: Acute abscess and chronic sialadenitis

70
Q

is the most common tumor of salivary glands tumor

A

pleomorphic adenoma

71
Q

80% of salivary glands tumors occur in the

A

parotids

72
Q

other name of the pleomorphic adenoma

A

Benign Mixed Salivary Gland Tumor

73
Q

Gross Picture of Pleomorphic adenoma

A

Capsule: benign tumor with an incomplete capsule
outer surface: Lobulated outer surface
color: bluish white in color
consistency: Soft, Gelatinous Consistency
Cut section: Bulging With Rounded Borders & Cystic Areas.

74
Q

Microscopic Picture of pleomorphic adenoma

A

mixed epithelial & mesenchymal differentiation
* Epithelial gland
* myoepithelial cells in solid groups
* Myxoid, hyaline, chondroid (pseudo-cartilage)

75
Q

complication of pleomorphic adenoma

A

May undergo malignant transformation producing malignant mixed salivary gland tumor

76
Q

It is a benign tumor formed of cystic spaces lined by eosinophilic cells and surrounded by dense lymphoid stroma

A

Warthin tumor

77
Q

named adenolymphoma

A

Warthin tumor

78
Q

is the most common primary malignant salivary gland tumor

A

Mucoepidermoid Carcinoma

79
Q

A malignant tumor, more common in minor salivary glands

A

Adenoid cystic carcinoma

80
Q

tumor of salivary gland has a tendency for perineural spread

A

Adenoid cystic carcinoma

81
Q

microscopic picture of mucoepidermoid carcinoma

A

It consists of mucus-secreting cells, squamous cells and intermediate cells

82
Q

microscopic picture of Adenoid cystic carcinoma

A

It is formed of small cells arranged in islands with microcystic changes

83
Q

is a failure of embryological canalisation of the esophagus, & it is usually associated with an abnormal connection (fistula) between the patent proximal part of the esophagus and the trachea

A

Atresia

84
Q

effect of atresia

A

The affected child cannot swallow and develops aspiration bronchopneumonia.

85
Q

what is atresia

A

is a failure of emryological canalisation of the esophagus & it is usually associated with abnormal connection (fistula) between patent proximal ppart of the esophagus and the trachea

86
Q

what is diverticulum

A

An outpouching of the wall of a hollow structure in the body, which can be saccular dilation of the full thickness or formed of herniation of mucosa and submucosa through defect in the muscle wall

87
Q

types of diverticulum

A

traction (external forces pulling on the wall) or pulsion (forcible distension)

88
Q

effect of diverticulum

A

difficulties in swallowing (dysphagia)

89
Q

definition of the hiatus hernia

A

It is defined as the protrusion of the upper part of the stomach
into the thorax via the diaphragmatic orifice

90
Q

Etiology of the hiatus hernia

A

increased intra-abdominal pressure and loss of diaphragmatic muscular tone with aging
predisposing factors: obesity, tear clothes, bending, lifting heavy weights, frequent coughing fits

91
Q

Etiology of achalasia

A

o Patients usually present with
1) recurrent progressive dysphagia (difficulty in swallowing) and
2) vomiting of undigested food.
o Achalasia may be primary due to
1) neural degeneration
2) neurotropic infection with
- Trypanosoma cruzi (Chagas’ disease),
- varicella-zoster virus,
- measles and HSV1 .
o Achalasia also occurs in patients with autoimmune disease such as
- multiple sclerosis,
- Sjogren’s syndrome,
- patients with antibodies against myenteric neurons or
- other diseases impairing nerve function such as diabetes and alcoholism.

92
Q

C/P of Achalasia

A

Achalasia results in slowing or retention of the food bolus with increasing obstruction and dilatation of the esophagus.

93
Q

Treatment

A
94
Q

Treatment of Achalasia

A

pneumatic dilatation or surgical myotomy of the lower sphincter

95
Q

defintion of Esophageal varices

A

Dilated congested tortuous submucosal veins, in the lower end of the
esophagus, due to portal hypertension

96
Q

etiology of esophageal varices

A

liver fibrosis or cirrhosis : the blood flow through the liver is
impaired leading to portal hypertension & opening of porto-systemic
anastomosis.

97
Q

complications of Esophageal varices

A

Ulceration and Hematemesis

98
Q

etiology of acute esophagitis

A
  1. Infections :
    - Herpes simplex type 1 virus, cytomegalovirus or Candida albicans
  2. Ingestion of corrosive substances
99
Q

pathogenesis of REFLUX ESOPHAGITIS, GASTRO-ESOPHAGEAL REFLUX DISEASE (GERD)

A
  • Reflux of gastric juices is the major source of mucosal injury.
  • Conditions which contribute to GERD are
    1) smoking,
    2) alcohol,
    3) increased abdominal pressure,
    4) pregnancy,
    5) hiatal hernia
    6) obesity.
100
Q

gross of GERD

A

Hyperemia

101
Q

microscopic picture of GERD

A
  • Basal zone hyperplasia (exceeding 20% of the epithelium) & thinning of superficial epithelial layers.
  • Neutrophil &/or eosinophil infiltration
102
Q

symptoms of GERD

A

Dysphagia, heartburn, & regurgitation of gastric contents into the mouth

103
Q

Complication of GERD

A

Ulceration, hematemesis, melena, stricture, or Barrett esophagus

104
Q

what is Barrett esophagus

A

a complication of long standing GERD characterized by foci of
intestinal metaplasia (columnar epithelium with goblet cells) in the esophageal squamous mucosa

105
Q

complication of barrett esophagus

A

develop esophageal adenocarcinoma

106
Q

endoscopy of Barrett esophagus

A

appears as salmon-colored tongues replacing the pearly white
squamous epithelium of the esophagus

107
Q

most frequently encountered benign esophageal tumors

A

smooth muscle
tumors (leiomyoma)

108
Q

The only benign epithelial tumor of esophagus

A

squamous cell papilloma which may be linked to human papillomavirus (HPV) infection

109
Q

risk factors of squamous cell carcinoma of esophagus

A
  1. Tobacco
  2. Alcohol
  3. Nitrosamine in pickled food, or fungus contaminated food.
  4. Vitamin deficiencies.
  5. Repeated thermal injury due to hot beverages.
  6. Human papillomavirus infection.
  7. Squamous cancers develop from squamous epithelium and may be preceded by
    dysplastic changes.
110
Q
A
111
Q

Gross of squamous cell carcinoma of esophagus

A
  • Half of the tumors are in the middle third of esophagus.
  • It starts as insitu carcinoma on top of dysplasia
    and appears as grey white thickening.
  • With invasion they present as
    ( polypoid mass - malignant ulcer or diffuse annular stricture )
112
Q

spread of squamous cell carcinoma of esophagus

A
  1. Local spread
    - Spread to trachea and bronchi causing pneumonia.
    - Spread to the mediastinum and pericardium.
    - Spread to aorta causing severe hemorrhage.
  2. Lymphatic spread:
    - Tumors in upper third spread to cervical lymph nodes
    - Tumors in middle third fspread to mediastinal, pretracheal and
    tracheobronchial lymph nodes.
    - Tumors in lower third spread to gastric and celiac lymph nodes.
113
Q

complications of squamous cell carcinoma of esophagus

A
  1. Dysphagia
  2. Hematemesis
  3. Tracheo-esophageal fistula
114
Q

Risk factors of adenocarcinoma of esophagus

A

Gastro-esophageal reflux disease and Barrett’s esophagus

115
Q

Gross Picture of the adenocarcinoma

A
  • Adenocarcinoma occurs in the distal third of esophagus.
  • They present as exophytic mass, ulcer or diffuse annular stricture
116
Q

Microscopic of adenocarcinoma of esophagus

A
  • Tumors typically produce mucin & form glands.
  • Barrett esophagus frequently is seen adjacent to the tumor
117
Q

lining of the cardia

A

mucin secreting columnar cells

118
Q

li

lining of the antral

A

mucin secreting cells and G cells that secrete gastrin

119
Q

lining of the fundus and body

A

parietal cells that secrete acids

120
Q

lining of the fundus

A

parietal cells and chief cells that secrete pepsin

121
Q

An abnormal hypertrophy of the circular muscle coat at the pylorus

A

Congenital Stenosis PYLORIC STENOSIS

122
Q

clinical picture of the pyloric stenosis

A

projectile vomiting

123
Q

pathogenesis of the acute gastritis

A

chemical agents 1) damage the epithelial cells
2) diminish secretion of mucus which protects against acid
3) inhibit prostaglandins synthesis by mucosal cells

124
Q

causes the acute gastritis

A

1- Alcohol
2- Aspirin & non-steroidal anti-inflammatory agents (NSAIDs),
3- Cortisone & cytotoxic drugs.
4- stress
5- shock
6- sepsis

125
Q

Gross Picture of the acute gastritis

A
  • Edema & hyperemia.
  • If injury is severe, erosions and hemorrhage occur (acute erosive hemorrhagic gastritis).
126
Q

microscopic picture of acute gastritis

A
  • Neutrophils invade the epithelium, with superficial epithelial erosion.
  • Fibrinous luminal exudate.
127
Q

Clinical picture of acute gastritis

A
  • Dyspepsia (epigastric discomfort).
  • Epigastric pain.
  • Hematemesis or melena.
  • Nausea & vomiting.
128
Q

fate of acute gastritis

A

Healing by regeneration

129
Q

what is type A gastritis

A

Autoimmune associated gastritis

130
Q

Pathogenesis of autoimmune associated gastritis

A
  • Destruction of parietal cells is the major pathogenic mechanism by cell mediated autoimmunity.
  • Autoantibodies to parietal cells & intrinsic factor are also present in the serum.
  • Parietal cell destruction leads to defective gastric acid secretion (achlorhydria),
  • Reduced intrinsic factor production impedes B12 absorption & causes pernicious anemia.
131
Q
A
132
Q

which type of gastrits causes prenicious anemia?

A

Autoimmune associated gastritis

133
Q

which type of gastrits causes achlorhydria

A

Autoimmune associated gastritis

134
Q

Gross Picture of autoimmune associated gasrtritis

A
  • Fundus & body are affected (typically spares the antrum).
  • Mucosa appears thin paper like with loss of rugae & pallor.
135
Q

Tumors Of The Nasopharynx

A

Juvenile Angiofibroma
Nasopharyngeal Carcinoma

136
Q

Micro of nasopharyngeal carcinoma

A

[It may take one of three histological variants]:
* Keratinizing squamous cell carcinoma.
* Non-keratinizing squamous cell carcinoma.
* Undifferentiated carcinoma with excess lymphocytes in the stroma
lymphoepitheliomal

137
Q

Complications of diphteria

A

1) Asphyxia
2) 2) Acute toxaemi may cause toxic myocarditis and necrosis of supra renal cortex and temporary paralysis

138
Q

Nasal Polyp gross and micro

A

¶ Gross:
Multiple, soft, pink polyps projecting from mucosa of nose & sinuses
¶ Microscopic: 2 C [ cover + core ]
Ø Cover:
* Pseudostratified columnar ciliated (respiratory) epithelial cover,
but with chronic irritation it may changes to squamous (metaplasia)
* Thickened, pink basement membrane
Ø Core:
* Thick, very wide edematous core with many eosinophils,
* lymphocytes and plasma cells.
* Increased number of mucous glands (hyperplasia).

139
Q

complication of nasal polyps

A

Nasal obstruction leading to 2ry infection & spread of the infection, & epistaxis

139
Q

def of adenoids

A

Adenoids denote hyperplastic lymphoid tissue at the posterior wall of the nasopharynx, due to chronic infection in infants and children

140
Q

characteristic adenoid face

A

Opened mouth, short upper lip, protruding upper incisors,
narrow nasal openings, absent nasolabial folds

141
Q

Rhinoscleroma micro and gross

A

Morphology:
Ä Gross:
* The lesions appear as small hard nodular mass or masses filling the nasal cavity.
Ä Microscopic:
* There is a chronic inflammatory infiltrate involving the submucosa ,
* The inflammatory cells comprise:
Þ Mickulicz cells:
o these are the predominant cells.
o They are macrophages with foamy cytoplasm.
o They are large with a small pyknotic nucleus.
Þ Plasma cells and Russell bodies:
( Plasma cells with hyaline change due to accumulated immunoglobulin)
* Later there is fibrosis

142
Q

related to mickulicz cells

A

Rhinoscleroma

143
Q

causative agent of Nasopharyngeal Carcinoma

A

EBV

144
Q

Squamous Cell Papilloma Of Larynx caused by

A

HPV 6 & 11

145
Q

Squamous Cell Papilloma Of Larynx G&M

A

¶ Gross: Fine finger-like surface protrusions.
¶ Microscopic: 2 C [cover + core ]
Ø Cover:
covered by hyperplastic stratified
squamous epithelium, showing hyperkerotosis,
parakeratosis and acanthosis.
Ø Core: Papillary thin fibrovascular core

146
Q

Squamous Cell Carcinoma- Larynx G&M

A

Morphology:
Ø Gross: Ulcerating or fungating tumors.
Ø Microscopic: Squamous cell carcinoma. Glottic tumors are usually keratinizing and better differentiated than others.

146
Q

Squamous Cell Carcinoma- Larynx complications

A

Ø Spread:
- Direct to nearby structures (esophagus, trachea & pharynx)
- Lymphatic to cervical lymph nodes, especially supraglottic tumors because this area is rich in lymphatics.

146
Q

Malignant Mesothelioma GM

A

Gross:
§ Mesothelioma is usually unilateral, starting as small nodules on the visceral pleura and extends to cover the whole lung and obliterate the pleural cavity.
§ The tumor is yellowish white.
Microscopic:
Epithelioid type Cuboidal cells forming papillae and acini (looks like adenocarcinoma)
Sarcomatoid type sheets of spindle malignant cells (looks like sarcoma)
Mixed type (biphasic): Epithelial + sarcomatous

146
Q

Causes of hemoptysis

A

Causes:
1. Bronchitis, bronchiectasis, pneumonia, lung abscess
2. Chronic fibrocaseous tuberculosis
3. Carcinoid tumor, carcinoma of the lung and secondaries of the lung.
4. Chronic venous congestion of the lung
5. General causes as leukemia, hemophilia , purpura, vitamin C and K
deficiency.

146
Q

Bronchopneumonia G&M

A

Gross: Usually bilateral lower lobe affection
* Bronchioles: contain pus
* Patchy areas of yellow consolidation (purulent exudate in alveoli), some areas may become confluent.
* Pleurisy.
* Enlarged hilar lymph nodes (lymphadenitis).
Microscopic:
- Suppurative (neutrophilic) exudation filling bronchi, bronchioles, and alveoli.
- Alveoli: The alveoli are full of pus (patchy areas of consolidation)

147
Q

adult respiratory distress syndrome ARDS related to

A

Atypical pneumonia

147
Q

causative agent of atypical pneumonia

A

Mycoplasma pneumoniae

147
Q

bronchoectasis GM

A

Gross:
§ Site: is mostly bilateral, Most severe changes occur in peripheral lower lobes.
Medium sized bronchi & bronchioles:
ü Airways can be dilated up to four times the normal size.
ü The bronchi appear thickened, with suppuration of their lining.
ü The dilated bronchi could be seen from hilum till the pleura

Microscopic:
Bronchi
§ Lumen: filled with pus & blood.
§ Lining respiratory epithelium shows areas of ulceration.
§ Wall shows intense acute and chronic inflammatory cells and fibrosis.
Alveoli
§ Adjacent alveoli undergo fibrosis.
§ Patches of compensatory emphysema (to compensate for
nonfunctioning alveoli).
Pleura § Fibrosis and adhesions.

147
Q

Bronchoecatasis complications

A

a. Hemoptysis with abundant foul smelling, yellowish red sputum (pus + blood).
b. Lung abscess- gangrene.
c. Spread of infection (see septic bronchopneumonia).
d. Bilateral lung fibrosis , pulmonary hypertension & right sided heart failure
(cor pulmonale).
e. Secondary amyloidosis (chronic destructive condition).
f. Squamous metaplasia

147
Q

Pulmonary Hypertension causes

A

a. Chronic obstructive or interstitial lung disease.
b. Recurrent pulmonary emboli.
c. Mitral stenosis.
d. Congenital left to right shunt due to increased pulmonary blood flow
e. Idiopathic or primary pulmonary hypertension

147
Q

lung cancer complication

A

Direct:
§ to the pericardium, medi
astinum and esophagus.
§ Pleural seeding especially in adenocarcinoma
Lymphatic:
§ To the hilar and mediastinal lymph node.
§ The supraclavicular node affection (Virchow’s node) may be the first
presentation.
Ä Blood spread: To the brain, bones, liver, adrenals or other lung.
B) Hemoptysis.
C) Obstruction leading to collapse, secondary infection, bronchiectasis or lung
abscess.
D) Paraneoplastic syndrome:
§ 3-10% of patients with lung cancer develop clinical paraneoplastic syndrome
due to secretion of polypeptide hormones.
§ It presents in one or more of the following forms:
ü Hypercalcemia.
ü Cushing syndrome.
ü Myasthenia gravis.
ü Excess ADH.

PAT (5 decks)

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