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Pathology - Hypersensitivity pneumonitis
Definition: An interstitial lung disease resulting from an immunological response to inhaled antigens. Synonyms include extrinsic allergic alveolitis. Various versions of the disease are referred to by numerous alternative names, such as farmer’s lung, humidifier lung, maple bark stripper’s lung, mushroom worker’s lung, pigeon breeder’s lung, and bird fancier’s lung, among others.
Epidemiology: Rare occurrence.
Aetiology: • Thermophilic bacteria (found in moldy hay, compost, and air conditioning ducts), • Fungi (present in moldy maple bark, barley, or wood dust). • Avian proteins (excrement and plumage of birds).
Pathogenesis: Inhaled antigens provoke an aberrant immune response in the pulmonary system. • Comprises a synthesis of antibody-mediated (type 2), immune complex-mediated (type 3), and cell-mediated (type 4) hypersensitivity reactions
. Presentation • Acute illness occurs upon exposure to substantial quantities of antigen, resulting in severe dyspnea, cough, and fever 4–6 hours post-exposure. Resolution transpires within 12 to 18 hours following the cessation of exposure. Chronic illness arises from extended exposure to little quantities of antigen, leading to a gradual onset of dyspnea, nonproductive cough, and exhaustion.
Radiology • High-resolution computed tomography (CT) reveals linear interstitial opacities and tiny nodules predominantly in the middle to upper lobes. • Frequently accompanied by traction bronchiectasis and honeycomb formations. Histopathology: Cellular chronic interstitial pneumonia with peribronchiolar accentuation. • Foci of organized pneumonia and ill-defined granulomas may also be observed.
Prognosis: Generally favorable if the culprit antigen is identified and exposure is prevented. Prolonged exposure may result in permanent pulmonary fibrosis and respiratory failure.
Definition: An interstitial lung disease resulting from an immunological response to inhaled antigens. Synonyms include extrinsic allergic alveolitis. Various versions of the disease are referred to by numerous alternative names, such as farmer’s lung, humidifier lung, maple bark stripper’s lung, mushroom worker’s lung, pigeon breeder’s lung, and bird fancier’s lung, among others.
Epidemiology: Rare occurrence.
Aetiology: • Thermophilic bacteria (found in moldy hay, compost, and air conditioning ducts), • Fungi (present in moldy maple bark, barley, or wood dust). • Avian proteins (excrement and plumage of birds).
Pathogenesis: Inhaled antigens provoke an aberrant immune response in the pulmonary system. • Comprises a synthesis of antibody-mediated (type 2), immune complex-mediated (type 3), and cell-mediated (type 4) hypersensitivity reactions
. Presentation • Acute illness occurs upon exposure to substantial quantities of antigen, resulting in severe dyspnea, cough, and fever 4–6 hours post-exposure. Resolution transpires within 12 to 18 hours following the cessation of exposure. Chronic illness arises from extended exposure to little quantities of antigen, leading to a gradual onset of dyspnea, nonproductive cough, and exhaustion.
Radiology • High-resolution computed tomography (CT) reveals linear interstitial opacities and tiny nodules predominantly in the middle to upper lobes. • Frequently accompanied by traction bronchiectasis and honeycomb formations. Histopathology: Cellular chronic interstitial pneumonia with peribronchiolar accentuation. • Foci of organized pneumonia and ill-defined granulomas may also be observed.
Prognosis: Generally favorable if the culprit antigen is identified and exposure is prevented. Prolonged exposure may result in permanent pulmonary fibrosis and respiratory failure.
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Pathology - Lung carcinoma
Definition • A malignant epithelial neoplasm originating in the lung.
Epidemiology • The most prevalent and lethal cancer, resulting in over 1 million fatalities per year.
Aetiology • As much as 90% of instances can be directly linked to smoking. Carcinogenesis • TP53 mutations are prevalent across all varieties of lung cancer. • Overexpression of HER2 and KRAS in adenocarcinomas. • Overexpression of EGFR and deletion of 3p in squamous cell carcinomas. • The inactivation of RB is nearly ubiquitous in small cell carcinomas.
Presentation• Symptoms associated with localized tumor growth encompass increasing dyspnea, cough, thoracic discomfort, dysphonia or voice loss, hemoptysis, weight reduction, and recurrent pneumonia. Metastases may result in abdominal pain, bone pain, and neurological problems. A minority of small cell carcinomas manifest with paraneoplastic syndromes or superior vena cava syndrome.
Macroscopy • A solid white/grey neoplastic tumor located within the lung. Yellow consolidation may be observed in the lung parenchyma distal to substantial proximal tumors as a result of obstructive pneumonia. Pleural puckering may be observed over peripheral tumors that have infiltrated the pleura. • Metastatic tumor deposits may be observed in hilar lymph nodes.
Histopathology
Adenocarcinoma is a malignant epithelial tumor characterized by glandular development and/or mucus secretion. Squamous cell carcinoma is a malignant epithelial tumor characterized by keratinization and/or intercellular bridges. Small cell carcinoma is a malignant epithelial neoplasm characterized by diminutive cells with minimal cytoplasm, poorly defined cell boundaries, finely granular chromatin, and the absence of nucleoli. The mitotic count is elevated, and necrosis is frequently widespread. Large cell carcinoma is an undifferentiated (non-small) cell carcinoma that exhibits no signs of squamous or glandular differentiation.
Prognosis: • Dismal, with 5-year survival rates ranging from 7% to 10% in the majority of countries.
TNM 7 pathological staging of lung carcinomas
Primary tumour (T)
T1a: tumour d 2cm in size, confi ned to the lung.
T1b: tumour > 2–3cm in size, confi ned to the lung.
T2: tumour 3–7cm in size; tumour of any size that involves the main
bronchus 2cm or more distal to the carina, invades visceral pleura,
causes partial atelectasis.
T3: tumour > 7cm in size; tumour of any size that invades the chest wall,
diaphragm, pericardium, mediastinal pleura, main bronchus <2cm distal< />pan>
to the carina, causes total atelectasis; multiple tumour nodules in same
lobe.
T4: tumour of any size that invades the mediastinum, heart, great vessels,
carina, trachea, oesophagus, vertebra; multiple tumour nodules in same
lung, but different lobes.
Regional lymph nodes (N)
N0: no regional lymph node metastasis.
N1: metastasis in ipsilateral peribronchial or hilar lymph nodes.
N2: metastasis in ipsilateral mediastinal or subcarinal lymph nodes.
N3: metastasis in contralateral mediastinal or hilar lymph nodes or any
scalene or supraclavicular lymph nodes
Definition • A malignant epithelial neoplasm originating in the lung.
Epidemiology • The most prevalent and lethal cancer, resulting in over 1 million fatalities per year.
Aetiology • As much as 90% of instances can be directly linked to smoking. Carcinogenesis • TP53 mutations are prevalent across all varieties of lung cancer. • Overexpression of HER2 and KRAS in adenocarcinomas. • Overexpression of EGFR and deletion of 3p in squamous cell carcinomas. • The inactivation of RB is nearly ubiquitous in small cell carcinomas.
Presentation• Symptoms associated with localized tumor growth encompass increasing dyspnea, cough, thoracic discomfort, dysphonia or voice loss, hemoptysis, weight reduction, and recurrent pneumonia. Metastases may result in abdominal pain, bone pain, and neurological problems. A minority of small cell carcinomas manifest with paraneoplastic syndromes or superior vena cava syndrome.
Macroscopy • A solid white/grey neoplastic tumor located within the lung. Yellow consolidation may be observed in the lung parenchyma distal to substantial proximal tumors as a result of obstructive pneumonia. Pleural puckering may be observed over peripheral tumors that have infiltrated the pleura. • Metastatic tumor deposits may be observed in hilar lymph nodes.
Histopathology
Adenocarcinoma is a malignant epithelial tumor characterized by glandular development and/or mucus secretion. Squamous cell carcinoma is a malignant epithelial tumor characterized by keratinization and/or intercellular bridges. Small cell carcinoma is a malignant epithelial neoplasm characterized by diminutive cells with minimal cytoplasm, poorly defined cell boundaries, finely granular chromatin, and the absence of nucleoli. The mitotic count is elevated, and necrosis is frequently widespread. Large cell carcinoma is an undifferentiated (non-small) cell carcinoma that exhibits no signs of squamous or glandular differentiation.
Prognosis: • Dismal, with 5-year survival rates ranging from 7% to 10% in the majority of countries.
TNM 7 pathological staging of lung carcinomas
Primary tumour (T)
T1a: tumour d 2cm in size, confi ned to the lung.
T1b: tumour > 2–3cm in size, confi ned to the lung.
T2: tumour 3–7cm in size; tumour of any size that involves the main
bronchus 2cm or more distal to the carina, invades visceral pleura,
causes partial atelectasis.
T3: tumour > 7cm in size; tumour of any size that invades the chest wall,
diaphragm, pericardium, mediastinal pleura, main bronchus <2cm distal< />pan>
to the carina, causes total atelectasis; multiple tumour nodules in same
lobe.
T4: tumour of any size that invades the mediastinum, heart, great vessels,
carina, trachea, oesophagus, vertebra; multiple tumour nodules in same
lung, but different lobes.
Regional lymph nodes (N)
N0: no regional lymph node metastasis.
N1: metastasis in ipsilateral peribronchial or hilar lymph nodes.
N2: metastasis in ipsilateral mediastinal or subcarinal lymph nodes.
N3: metastasis in contralateral mediastinal or hilar lymph nodes or any
scalene or supraclavicular lymph nodes
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Pathology – Pneumothorax
Definition • The accumulation of air in the pleural cavity.
Epidemiology: Prevalent. • Males are impacted more significantly than females.
Aetiology
Spontaneous pneumothorax generally manifests in slender, tall young males. The phenomenon is believed to originate from the rupture of small, fragile apical blebs in lung tissue caused by lung expansion. • Preexisting pulmonary conditions, such as COPD, asthma, pneumonia, tuberculosis, cystic fibrosis, sarcoidosis, lung cancer, and idiopathic pulmonary fibrosis (IPF). Uncommon disorders frequently linked to pneumothorax encompass pulmonary Langerhans cell histiocytosis, pulmonary lymphangioleiomyomatosis, and thoracic endometriosis. • Trauma, such as penetrating thoracic injury and rib fractures. • Iatrogenic, for instance, subclavian vein cannulation and lung biopsy.
Pathogenesis
Air escapes from the compromised lung into the pleural cavity until the pressures equilibrate. The lung collapses to a varying extent, contingent upon the magnitude of the pneumothorax. • Infrequently, the tissues next to the pulmonary lesion function as a unidirectional valve, obstructing pressure equalization. The persistent accumulation of pressure and volume in the pleural cavity displaces mediastinal structures, resulting in cardiorespiratory arrest (tension pneumothorax).
Presentation:
• Abrupt onset of unilateral pleuritic thoracic discomfort. • Breathlessness may occur, contingent upon the magnitude of the pneumothorax. Individuals with preexisting pulmonary conditions typically observe an exacerbation of their symptoms.
Radiology
• Air is present in the pleural space alongside various degrees of lung collapse. Histopathology: Apical lung tissue removed from patients with spontaneous pneumothoraces has one or more bullae linked to subpleural alveolar collapse and fibrosis. The superficial visceral pleura exhibits reactive mesothelial hyperplasia and inflammation, frequently characterized by an abundance of eosinophils.
Prognosis: Approximately one-third of patients with spontaneous pneumothorax experience recurring episodes, typically on the same side.
Definition • The accumulation of air in the pleural cavity.
Epidemiology: Prevalent. • Males are impacted more significantly than females.
Aetiology
Spontaneous pneumothorax generally manifests in slender, tall young males. The phenomenon is believed to originate from the rupture of small, fragile apical blebs in lung tissue caused by lung expansion. • Preexisting pulmonary conditions, such as COPD, asthma, pneumonia, tuberculosis, cystic fibrosis, sarcoidosis, lung cancer, and idiopathic pulmonary fibrosis (IPF). Uncommon disorders frequently linked to pneumothorax encompass pulmonary Langerhans cell histiocytosis, pulmonary lymphangioleiomyomatosis, and thoracic endometriosis. • Trauma, such as penetrating thoracic injury and rib fractures. • Iatrogenic, for instance, subclavian vein cannulation and lung biopsy.
Pathogenesis
Air escapes from the compromised lung into the pleural cavity until the pressures equilibrate. The lung collapses to a varying extent, contingent upon the magnitude of the pneumothorax. • Infrequently, the tissues next to the pulmonary lesion function as a unidirectional valve, obstructing pressure equalization. The persistent accumulation of pressure and volume in the pleural cavity displaces mediastinal structures, resulting in cardiorespiratory arrest (tension pneumothorax).
Presentation:
• Abrupt onset of unilateral pleuritic thoracic discomfort. • Breathlessness may occur, contingent upon the magnitude of the pneumothorax. Individuals with preexisting pulmonary conditions typically observe an exacerbation of their symptoms.
Radiology
• Air is present in the pleural space alongside various degrees of lung collapse. Histopathology: Apical lung tissue removed from patients with spontaneous pneumothoraces has one or more bullae linked to subpleural alveolar collapse and fibrosis. The superficial visceral pleura exhibits reactive mesothelial hyperplasia and inflammation, frequently characterized by an abundance of eosinophils.
Prognosis: Approximately one-third of patients with spontaneous pneumothorax experience recurring episodes, typically on the same side.
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Pathology - Malignant mesothelioma
It is a malignant tumor originating in the pleura from mesothelial cells, characterized by a diffuse growth pattern throughout the pleural surfaces.
Epidemiology • The majority of occurrences occur in males over 60 years of age. • The incidence continues to increase owing to the prolonged incubation period between asbestos exposure and tumor formation.
• The incidence is anticipated to reach its zenith between 2015 and 2020.
Aetiology Over 90% of instances can be directly linked to asbestos exposure. Amphibole asbestos is the most potent kind, succeeded by chrysotile, and subsequently amosite. • Additional potential causes encompass non-asbestos mineral fibers and therapeutic radiation.
Pathogenesis • Inhaled asbestos fibers stay permanently lodged in the lung. • The majority do not elicit a tissue response, and they are likely the fibers responsible for carcinogenic effects. A minority become enveloped in iron, resulting in the formation of asbestos bodies.
Presentation • Dyspnea, frequently resulting from a significant unilateral pleural effusion, accompanied by thoracic pain. • Marked weight loss and malaise are commonly observed.
Macroscopy • Initially, several tiny nodules are observed on the parietal pleura. • As the tumor progresses, the nodules coalesce to create a tumor mass that envelops the entire lung and adheres to the chest wall.
Cytopathology • Epithelioid mesotheliomas are more prone to disseminate into pleural fluid, where malignant cells are observed organizing into sheets, clusters, and papillae.
Histopathology • Epithelioid mesothelioma consists of spherical cells that create tubules and papillae. Sarcomatoid mesothelioma consists of elongated spindle-shaped cancerous cells. Biphasic mesothelioma comprises a combination of epithelioid and sarcomatoid variants. Desmoplastic mesothelioma is a variation characterized by a limited number of malignant cells embedded in highly dense collagenous tissue.
Prognosis: Extremely unfavorable
It is a malignant tumor originating in the pleura from mesothelial cells, characterized by a diffuse growth pattern throughout the pleural surfaces.
Epidemiology • The majority of occurrences occur in males over 60 years of age. • The incidence continues to increase owing to the prolonged incubation period between asbestos exposure and tumor formation.
• The incidence is anticipated to reach its zenith between 2015 and 2020.
Aetiology Over 90% of instances can be directly linked to asbestos exposure. Amphibole asbestos is the most potent kind, succeeded by chrysotile, and subsequently amosite. • Additional potential causes encompass non-asbestos mineral fibers and therapeutic radiation.
Pathogenesis • Inhaled asbestos fibers stay permanently lodged in the lung. • The majority do not elicit a tissue response, and they are likely the fibers responsible for carcinogenic effects. A minority become enveloped in iron, resulting in the formation of asbestos bodies.
Presentation • Dyspnea, frequently resulting from a significant unilateral pleural effusion, accompanied by thoracic pain. • Marked weight loss and malaise are commonly observed.
Macroscopy • Initially, several tiny nodules are observed on the parietal pleura. • As the tumor progresses, the nodules coalesce to create a tumor mass that envelops the entire lung and adheres to the chest wall.
Cytopathology • Epithelioid mesotheliomas are more prone to disseminate into pleural fluid, where malignant cells are observed organizing into sheets, clusters, and papillae.
Histopathology • Epithelioid mesothelioma consists of spherical cells that create tubules and papillae. Sarcomatoid mesothelioma consists of elongated spindle-shaped cancerous cells. Biphasic mesothelioma comprises a combination of epithelioid and sarcomatoid variants. Desmoplastic mesothelioma is a variation characterized by a limited number of malignant cells embedded in highly dense collagenous tissue.
Prognosis: Extremely unfavorable
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Pathology - Gastrointestinal anomalies
Oesophageal atresia occurs in 1 in 3,500 live births. • Outcomes from improper segmentation of the foregut into the tracheal and esophageal pathways during the initial month of embryonic development. • In most instances, there exists a link between the distal esophagus and the trachea referred to as a tracheoesophageal fistula. • Neonates exhibit coughing and choking during feeding. Approximately fifty percent of impacted infants exhibit other congenital anomalies, with heart problems constituting the predominant cause of mortality in infants diagnosed with oesophageal atresia.
Duodenal atresia is less prevalent than esophageal atresia. • Correlated with Down's syndrome in 30% of instances. • Resulting from the failure of epithelial apoptosis and inadequate canalization of the intestinal lumen by eight weeks of gestation. • The obstruction typically occurs distal to the ampulla of Vater. • Prenatal ultrasonography reveals dilatation of the proximal duodenum and stomach accompanied by polyhydramnios.
Exomphalos • A defect in the anterior abdominal wall at the umbilicus, resulting in the protrusion of abdominal contents through the umbilicus. • The protrusion is encased in a fragile, transparent sac formed by amniotic membrane and peritoneum. • Occurs due to the failure of the midgut to retract into the abdomen from the umbilical coelom during embryonic development.
Gastroschisis • A defect in the front abdominal wall located adjacent to the umbilicus, through which intestinal loops extrude. • In contrast to exomphalos, there is an absence of a protective covering sac.
Malrotation • Abnormal placement of the intestine and mesentery resulting from inadequate rotation of the growing gut as it retracts from the umbilical coelom to the abdomen during development. A malrotated bowel typically exhibits a constricted mesenteric base, increasing the risk of volvulus around the superior mesenteric artery. • Impaired arterial blood flow results in ischemic necrosis of the complete midgut, from the duodenum to the transverse colon. • Necrosis induces hemorrhage within the intestine and significantly increases the risk of perforation. • In the absence of immediate surgical intervention, the situation may be lethal.
Meckel's diverticulum • A remnant of the vitellointestinal duct, which connects the primitive gut to the yolk sac. • Estimated prevalence in the normal population • The mucosa of the diverticulum may exhibit regions of gastric or pancreatic tissue (heterotopia). • The majority of children with Meckel’s diverticulum are asymptomatic. • The predominant symptom is painless rectal hemorrhage resulting from ulceration in a diverticulum harboring acid-secreting gastric mucosa. • Small bowel obstruction may furthermore arise, associated with intussusception or incarceration.
Imperforate anus • Comprehensive designation for any atretic ailment affecting the rectum or anus. • Lesions vary in severity from a stenosed anal canal to anorectal agenesis. • Surgically, they are classified as either high or low anomalies, based on the termination level of the bowel relative to the pelvic floor. • Low defects are simpler to rectify, and post-operative function is favorable. Higher abnormalities are more challenging to rectify, as they are more prone to being linked with fistulae between the rectum and the genitourinary tract, in addition to a compromised pelvic floor.
Hirschsprung disease • Not precisely a deformity, but a congenital gastrointestinal disorder characterized by the absence of ganglion cells from a variable length of the intestinal wall. • Outcomes resulting from the inability of neuroblasts to move from the esophagus to the anal canal during gestational weeks 5 to 12. • The lack of ganglion cells results in spasms within the aganglionic segment. • It manifests as intestinal obstruction and an inability to pass meconium within 24 hours post-birth. The rectal suction biopsy is the definitive method for diagnosing Hirschsprung's disease. The primary characteristic is the lack of ganglion cells in the submucosa and the presence of unusually thick nerve fibers in the mucosal layer.
Oesophageal atresia occurs in 1 in 3,500 live births. • Outcomes from improper segmentation of the foregut into the tracheal and esophageal pathways during the initial month of embryonic development. • In most instances, there exists a link between the distal esophagus and the trachea referred to as a tracheoesophageal fistula. • Neonates exhibit coughing and choking during feeding. Approximately fifty percent of impacted infants exhibit other congenital anomalies, with heart problems constituting the predominant cause of mortality in infants diagnosed with oesophageal atresia.
Duodenal atresia is less prevalent than esophageal atresia. • Correlated with Down's syndrome in 30% of instances. • Resulting from the failure of epithelial apoptosis and inadequate canalization of the intestinal lumen by eight weeks of gestation. • The obstruction typically occurs distal to the ampulla of Vater. • Prenatal ultrasonography reveals dilatation of the proximal duodenum and stomach accompanied by polyhydramnios.
Exomphalos • A defect in the anterior abdominal wall at the umbilicus, resulting in the protrusion of abdominal contents through the umbilicus. • The protrusion is encased in a fragile, transparent sac formed by amniotic membrane and peritoneum. • Occurs due to the failure of the midgut to retract into the abdomen from the umbilical coelom during embryonic development.
Gastroschisis • A defect in the front abdominal wall located adjacent to the umbilicus, through which intestinal loops extrude. • In contrast to exomphalos, there is an absence of a protective covering sac.
Malrotation • Abnormal placement of the intestine and mesentery resulting from inadequate rotation of the growing gut as it retracts from the umbilical coelom to the abdomen during development. A malrotated bowel typically exhibits a constricted mesenteric base, increasing the risk of volvulus around the superior mesenteric artery. • Impaired arterial blood flow results in ischemic necrosis of the complete midgut, from the duodenum to the transverse colon. • Necrosis induces hemorrhage within the intestine and significantly increases the risk of perforation. • In the absence of immediate surgical intervention, the situation may be lethal.
Meckel's diverticulum • A remnant of the vitellointestinal duct, which connects the primitive gut to the yolk sac. • Estimated prevalence in the normal population • The mucosa of the diverticulum may exhibit regions of gastric or pancreatic tissue (heterotopia). • The majority of children with Meckel’s diverticulum are asymptomatic. • The predominant symptom is painless rectal hemorrhage resulting from ulceration in a diverticulum harboring acid-secreting gastric mucosa. • Small bowel obstruction may furthermore arise, associated with intussusception or incarceration.
Imperforate anus • Comprehensive designation for any atretic ailment affecting the rectum or anus. • Lesions vary in severity from a stenosed anal canal to anorectal agenesis. • Surgically, they are classified as either high or low anomalies, based on the termination level of the bowel relative to the pelvic floor. • Low defects are simpler to rectify, and post-operative function is favorable. Higher abnormalities are more challenging to rectify, as they are more prone to being linked with fistulae between the rectum and the genitourinary tract, in addition to a compromised pelvic floor.
Hirschsprung disease • Not precisely a deformity, but a congenital gastrointestinal disorder characterized by the absence of ganglion cells from a variable length of the intestinal wall. • Outcomes resulting from the inability of neuroblasts to move from the esophagus to the anal canal during gestational weeks 5 to 12. • The lack of ganglion cells results in spasms within the aganglionic segment. • It manifests as intestinal obstruction and an inability to pass meconium within 24 hours post-birth. The rectal suction biopsy is the definitive method for diagnosing Hirschsprung's disease. The primary characteristic is the lack of ganglion cells in the submucosa and the presence of unusually thick nerve fibers in the mucosal layer.
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Pathology - Diseases of the oral cavity
Candidiasis • A fungal illness prevalent among immunosuppressed individuals. • Clinically characterized by erythema and pseudomembrane development.
Actinomycosis • Gram-positive anaerobic bacteria that constitute a component of the normal oral flora, colonizing tonsillar crypts, dental plaque, and gingival tissues. • Pathological infection may arise if these organisms penetrate deeper tissues via trauma (e.g., tooth extraction).
Lichen planus • Frequently affects the oral cavity.Pemphigus vulgaris typically affects the oral cavity.
Mucous membrane pemphigoid, also referred to as cicatricial pemphigoid. Autoimmune blistering disease mostly impacting mucosal regions. • Manifestations occur between the ages of 50 and 70 years, characterized by mouth blistering. • Involvement of the conjunctiva, upper respiratory tract, and skin is also common. Histological examination reveals detachment of the squamous epithelium from the subjacent connective tissue accompanied by a heterogeneous inflammatory infiltrate. Direct immunofluorescence reveals linear deposition of IgG and C3 along the basement membrane zone.
Squamous papilloma • Benign exophytic growth of squamous epithelium. • Predominantly observed in people aged 30 to 50 years. • Preference for hard and soft palates, as well as the uvula. • Histological examination reveals papillary fronds covered by mature squamous epithelium.
Fibroma • Nonmalignant expansion of fibrous tissue due to inflammation. • The majority manifest as a painless oral mass in adults aged 30 to 50 years. Histological examination reveals a subepithelial mass composed of thick collagenous tissue.
Pyogenic granuloma • A benign vascular lesion more accurately referred to as 'lobular capillary hemangioma'. • Exhibits a dark red polypoid mass that frequently undergoes ulceration. • Histological examination reveals a lobulated proliferation of tiny blood vessels.
Squamous cell carcinoma • The most prevalent cancer of the oral cavity. • Significant correlation with alcohol consumption and tobacco use. • 30% present with regional lymph node metastases. • Cumulative 5-year survival around 50%
Candidiasis • A fungal illness prevalent among immunosuppressed individuals. • Clinically characterized by erythema and pseudomembrane development.
Actinomycosis • Gram-positive anaerobic bacteria that constitute a component of the normal oral flora, colonizing tonsillar crypts, dental plaque, and gingival tissues. • Pathological infection may arise if these organisms penetrate deeper tissues via trauma (e.g., tooth extraction).
Lichen planus • Frequently affects the oral cavity.Pemphigus vulgaris typically affects the oral cavity.
Mucous membrane pemphigoid, also referred to as cicatricial pemphigoid. Autoimmune blistering disease mostly impacting mucosal regions. • Manifestations occur between the ages of 50 and 70 years, characterized by mouth blistering. • Involvement of the conjunctiva, upper respiratory tract, and skin is also common. Histological examination reveals detachment of the squamous epithelium from the subjacent connective tissue accompanied by a heterogeneous inflammatory infiltrate. Direct immunofluorescence reveals linear deposition of IgG and C3 along the basement membrane zone.
Squamous papilloma • Benign exophytic growth of squamous epithelium. • Predominantly observed in people aged 30 to 50 years. • Preference for hard and soft palates, as well as the uvula. • Histological examination reveals papillary fronds covered by mature squamous epithelium.
Fibroma • Nonmalignant expansion of fibrous tissue due to inflammation. • The majority manifest as a painless oral mass in adults aged 30 to 50 years. Histological examination reveals a subepithelial mass composed of thick collagenous tissue.
Pyogenic granuloma • A benign vascular lesion more accurately referred to as 'lobular capillary hemangioma'. • Exhibits a dark red polypoid mass that frequently undergoes ulceration. • Histological examination reveals a lobulated proliferation of tiny blood vessels.
Squamous cell carcinoma • The most prevalent cancer of the oral cavity. • Significant correlation with alcohol consumption and tobacco use. • 30% present with regional lymph node metastases. • Cumulative 5-year survival around 50%
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Pathology - Pulmonary hypertension
Definition: A mean pulmonary artery pressure above 25 mmHg at rest or 30 mmHg during exertion.
Categories Secondary pulmonary hypertension is a consequence of chronic pulmonary or cardiac conditions. Primary pulmonary hypertension manifests in the absence of chronic pulmonary or cardiac conditions.
Epidemiology
• Secondary pulmonary hypertension is prevalent. Primary pulmonary hypertension is uncommon.
Aetiology
Common etiologies of secondary hypertension encompass COPD, interstitial lung disease, left ventricular failure, and chronic pulmonary thromboemboli. Primary pulmonary hypertension may be idiopathic or linked to specific medications, HIV infection, collagen vascular disorders, and congenital systemic-to-pulmonary shunts.
Pathogenesis: Chronic hypoxia and obliterative pulmonary fibrosis contribute to elevated pressure in the pulmonary arterial circulation.
Presentation • Secondary pulmonary hypertension exacerbates the symptoms of the pre-existing illness, resulting in increased breathlessness. • Primary pulmonary hypertension manifests as exertional dyspnoea and exhaustion. Dizziness and syncope are prevalent as well.
Macroscopy • The identification of atherosclerosis in major pulmonary arteries indicates potential underlying pulmonary hypertension. • Right ventricular hypertrophy may also be observed.
Histopathology: All cases have muscular hypertrophy and intimal proliferation of tiny pulmonary arteries, together with muscularization of pulmonary arterioles. • Severe instances have plexiform lesions, marked by the proliferation of slit-like vascular gaps originating from the arterial wall. • Extremely severe cases may present with fibrinoid necrosis of the arterial wall.
Prognosis • Secondary pulmonary hypertension typically indicates substantial cardiac or pulmonary pathology with a bad prognosis. The prognosis for primary pulmonary hypertension is bleak, with 5-year survival rates ranging from 25% to 50%.
Definition: A mean pulmonary artery pressure above 25 mmHg at rest or 30 mmHg during exertion.
Categories Secondary pulmonary hypertension is a consequence of chronic pulmonary or cardiac conditions. Primary pulmonary hypertension manifests in the absence of chronic pulmonary or cardiac conditions.
Epidemiology
• Secondary pulmonary hypertension is prevalent. Primary pulmonary hypertension is uncommon.
Aetiology
Common etiologies of secondary hypertension encompass COPD, interstitial lung disease, left ventricular failure, and chronic pulmonary thromboemboli. Primary pulmonary hypertension may be idiopathic or linked to specific medications, HIV infection, collagen vascular disorders, and congenital systemic-to-pulmonary shunts.
Pathogenesis: Chronic hypoxia and obliterative pulmonary fibrosis contribute to elevated pressure in the pulmonary arterial circulation.
Presentation • Secondary pulmonary hypertension exacerbates the symptoms of the pre-existing illness, resulting in increased breathlessness. • Primary pulmonary hypertension manifests as exertional dyspnoea and exhaustion. Dizziness and syncope are prevalent as well.
Macroscopy • The identification of atherosclerosis in major pulmonary arteries indicates potential underlying pulmonary hypertension. • Right ventricular hypertrophy may also be observed.
Histopathology: All cases have muscular hypertrophy and intimal proliferation of tiny pulmonary arteries, together with muscularization of pulmonary arterioles. • Severe instances have plexiform lesions, marked by the proliferation of slit-like vascular gaps originating from the arterial wall. • Extremely severe cases may present with fibrinoid necrosis of the arterial wall.
Prognosis • Secondary pulmonary hypertension typically indicates substantial cardiac or pulmonary pathology with a bad prognosis. The prognosis for primary pulmonary hypertension is bleak, with 5-year survival rates ranging from 25% to 50%.
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Pathology – Asthma
Definition
• A chronic inflammatory condition of the major airways marked by recurring episodes of reversible airway constriction.
Epidemiology: Highly prevalent, impacting over 10% of children and 5% of adults.
Aetiology • The majority of cases are linked to atopy, a hereditary predisposition of the immune system to generate IgE in reaction to prevalent environmental allergens. • The aetiology of non-atopic asthma remains ambiguous; nevertheless, some propose a connection with gastro-oesophageal reflux syndrome.
Pathogenesis: Atopic individuals react to prevalent environmental allergens by generating substantial quantities of allergen-specific IgE, which attaches to the surface of mast cells. • Subsequent exposure to the allergen results in the cross-linking of allergen-specific IgE antibodies and the degranulation of mast cells. Degranulated mast cells provoke airway inflammation and bronchospasm. Chronic inflammation leads to hypersensitive airways that respond to many stimuli, such as physical exertion, cold air, and tobacco smoke. Presentation: Intermittent episodes of dyspnea, wheezing, and chest constriction. Coughing, especially during nocturnal hours, is prevalent.
Macroscopy • The lungs of the majority of asthmatics may appear macroscopically normal. • In severe illness, thick mucus plugs may be observed in the airways.
Histopathology • The airways exhibit signs of inflammatory activity characterized by the presence of eosinophils, which are typically absent in normal airways. • Additionally, there may be thickening of the basement membrane, hyperplasia of goblet cells, and pronounced smooth muscle.
Prognosis: Generally favorable with suitable treatment. • A minor fatality rate is linked to severe acute asthma.
Definition
• A chronic inflammatory condition of the major airways marked by recurring episodes of reversible airway constriction.
Epidemiology: Highly prevalent, impacting over 10% of children and 5% of adults.
Aetiology • The majority of cases are linked to atopy, a hereditary predisposition of the immune system to generate IgE in reaction to prevalent environmental allergens. • The aetiology of non-atopic asthma remains ambiguous; nevertheless, some propose a connection with gastro-oesophageal reflux syndrome.
Pathogenesis: Atopic individuals react to prevalent environmental allergens by generating substantial quantities of allergen-specific IgE, which attaches to the surface of mast cells. • Subsequent exposure to the allergen results in the cross-linking of allergen-specific IgE antibodies and the degranulation of mast cells. Degranulated mast cells provoke airway inflammation and bronchospasm. Chronic inflammation leads to hypersensitive airways that respond to many stimuli, such as physical exertion, cold air, and tobacco smoke. Presentation: Intermittent episodes of dyspnea, wheezing, and chest constriction. Coughing, especially during nocturnal hours, is prevalent.
Macroscopy • The lungs of the majority of asthmatics may appear macroscopically normal. • In severe illness, thick mucus plugs may be observed in the airways.
Histopathology • The airways exhibit signs of inflammatory activity characterized by the presence of eosinophils, which are typically absent in normal airways. • Additionally, there may be thickening of the basement membrane, hyperplasia of goblet cells, and pronounced smooth muscle.
Prognosis: Generally favorable with suitable treatment. • A minor fatality rate is linked to severe acute asthma.
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Pathology - Pulmonary thromboembolism
Definition: Occlusion of a pulmonary artery by an embolic thrombus.
Epidemiology: Highly prevalent and frequently underdiagnosed.
Aetiology • Pulmonary emboli arise from deep vein thromboses, thus sharing identical risk factors, including immobility, acute medical conditions, recent surgical procedures, malignancy, pregnancy, and both inherited and acquired thrombotic diseases.
Pathogenesis: A piece of a detached thrombus from deep vein thrombosis embolizes via the right side of the heart into the pulmonary arterial circulation and becomes lodged in a pulmonary artery.
The clinical presentation is contingent upon the size of the pulmonary artery obstructed by the embolus. • Blockage of a large pulmonary artery usually leads to rapid death due to a sudden massive rise in pulmonary arterial pressure, acute right ventricular failure, and cardiac arrest. • Occlusion of medium-sized arteries results in a region of ventilation-perfusion imbalance in the lungs, leading to dyspnea. • Minor pulmonary emboli may produce mild manifestations of dyspnea, thoracic discomfort, and vertigo; these symptoms can often remain undetected.
Macroscopy
• Emboli appear as thrombi pieces within pulmonary arteries. • Thrombi are solid and brown, with the sliced surface potentially displaying discernible bands (lines of Zahn). Histopathology: Fresh thromboemboli consist of a composite of fibrin and interwoven blood cells, frequently organized in alternating linear bands that align with the macroscopic lines of Zahn. • Thromboemboli undergo organization after 2–3 days, characterized by the proliferation of granulation tissue consisting of fibroblasts and capillaries derived from the vessel wall. • Aged thromboemboli may manifest as fibrous nodules protruding from the vessel wall or as fibrous bands traversing the lumen of a pulmonary artery.
Prognosis
• Approximately 30% of all patients succumb to pulmonary embolism. • The mortalityz risk significantly increases if the diagnosis is not promptly established.
Definition: Occlusion of a pulmonary artery by an embolic thrombus.
Epidemiology: Highly prevalent and frequently underdiagnosed.
Aetiology • Pulmonary emboli arise from deep vein thromboses, thus sharing identical risk factors, including immobility, acute medical conditions, recent surgical procedures, malignancy, pregnancy, and both inherited and acquired thrombotic diseases.
Pathogenesis: A piece of a detached thrombus from deep vein thrombosis embolizes via the right side of the heart into the pulmonary arterial circulation and becomes lodged in a pulmonary artery.
The clinical presentation is contingent upon the size of the pulmonary artery obstructed by the embolus. • Blockage of a large pulmonary artery usually leads to rapid death due to a sudden massive rise in pulmonary arterial pressure, acute right ventricular failure, and cardiac arrest. • Occlusion of medium-sized arteries results in a region of ventilation-perfusion imbalance in the lungs, leading to dyspnea. • Minor pulmonary emboli may produce mild manifestations of dyspnea, thoracic discomfort, and vertigo; these symptoms can often remain undetected.
Macroscopy
• Emboli appear as thrombi pieces within pulmonary arteries. • Thrombi are solid and brown, with the sliced surface potentially displaying discernible bands (lines of Zahn). Histopathology: Fresh thromboemboli consist of a composite of fibrin and interwoven blood cells, frequently organized in alternating linear bands that align with the macroscopic lines of Zahn. • Thromboemboli undergo organization after 2–3 days, characterized by the proliferation of granulation tissue consisting of fibroblasts and capillaries derived from the vessel wall. • Aged thromboemboli may manifest as fibrous nodules protruding from the vessel wall or as fibrous bands traversing the lumen of a pulmonary artery.
Prognosis
• Approximately 30% of all patients succumb to pulmonary embolism. • The mortalityz risk significantly increases if the diagnosis is not promptly established.
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Pathology - Chronic obstructive pulmonary disease (COPD)
Definition: A chronic pulmonary ailment marked by dyspnea resulting from poorly reversible and increasing airflow restriction.
Epidemiology • Extremely prevalent. Primarily a condition affecting middle-aged to older adult smokers.
Aetiology • The majority of instances are attributable to smoking. • Instances in younger individuals may result from A-1-antitrypsin deficiency. Pathogenesis Inflammation and scarring of tiny bronchioles are considered the primary cause of airflow obstruction. • An imbalance between proteases and antiproteases leads to the degradation of lung parenchyma, resulting in the dilatation of terminal airspaces (emphysema) and air trapping. • Hyperplasia of mucous glands and the irritative effects of smoking contribute to a productive cough (chronic bronchitis).
Presentation • Abrupt emergence of dyspnea during exertion, occurring against a history of chronic cough and sputum expectoration. • Spirometric analysis generally reveals a diminished FEV1 and a reduced FEV1/FVC ratio (Fig. 5.1). Macroscopy • The lungs exhibit hyperinflation, characterized by thick mucus in the airways and dilated terminal airspaces. • Bullae may be observed.
Histopathology • Persistent inflammation and fibrosis of tiny bronchioles (chronic obstructive bronchiolitis). • Highly pigmented macrophages in respiratory bronchioles (respiratory bronchiolitis). • Enlarged terminal airspaces (emphysema). Larger airways may exhibit mucus gland hyperplasia
.
Prognosis • Progressive deterioration of lung function accompanied by bouts of acute exacerbation resulting from infection, pneumothorax, or pulmonary embolism. • Subsequently, pulmonary hypertension and right ventricular failure manifest. Left ventricular failure frequently coexists with ischemic heart disease. • Mortality frequently associated with a conjunction of respiratory and heart failure
Definition: A chronic pulmonary ailment marked by dyspnea resulting from poorly reversible and increasing airflow restriction.
Epidemiology • Extremely prevalent. Primarily a condition affecting middle-aged to older adult smokers.
Aetiology • The majority of instances are attributable to smoking. • Instances in younger individuals may result from A-1-antitrypsin deficiency. Pathogenesis Inflammation and scarring of tiny bronchioles are considered the primary cause of airflow obstruction. • An imbalance between proteases and antiproteases leads to the degradation of lung parenchyma, resulting in the dilatation of terminal airspaces (emphysema) and air trapping. • Hyperplasia of mucous glands and the irritative effects of smoking contribute to a productive cough (chronic bronchitis).
Presentation • Abrupt emergence of dyspnea during exertion, occurring against a history of chronic cough and sputum expectoration. • Spirometric analysis generally reveals a diminished FEV1 and a reduced FEV1/FVC ratio (Fig. 5.1). Macroscopy • The lungs exhibit hyperinflation, characterized by thick mucus in the airways and dilated terminal airspaces. • Bullae may be observed.
Histopathology • Persistent inflammation and fibrosis of tiny bronchioles (chronic obstructive bronchiolitis). • Highly pigmented macrophages in respiratory bronchioles (respiratory bronchiolitis). • Enlarged terminal airspaces (emphysema). Larger airways may exhibit mucus gland hyperplasia
.
Prognosis • Progressive deterioration of lung function accompanied by bouts of acute exacerbation resulting from infection, pneumothorax, or pulmonary embolism. • Subsequently, pulmonary hypertension and right ventricular failure manifest. Left ventricular failure frequently coexists with ischemic heart disease. • Mortality frequently associated with a conjunction of respiratory and heart failure
