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​Pathology - Cystic Fibrosis
Cystic fibrosis is an autosomal recessive illness resulting from a mutation, most commonly the delta 508 mutation, on chromosome 7. This mutation leads to a malfunctioning membrane CI channel (CFTR), resulting in impaired chloride and water transportation in epithelial cells.

Pathophysiology: A mutation in the CI channel results in the production of viscous mucus that accumulates in the lungs, liver, and pancreas.
Lung: Mucus plugs blocking bronchioles due to an increase in the number and size of goblet cells.
Liver: Biliary cirrhosis caused by the obstruction of bile canaliculi by mucus plugs.
The pancreatic ducts are blocked by mucus plugs, leading to fibrosis of the exocrine gland.

This condition is characterized by a persistent lung illness that leads to a productive cough, pulmonary infections, bronchiectasis, cyanosis, and a barrel-shaped chest. Additionally, it causes pancreatic insufficiency resulting in steatorrhea, diabetes, and malabsorption. Newborns with this condition may experience meconium ileus, which is a blockage in the small bowel. Lastly, men with this condition may also experience infertility.
Laboratory results include elevated amounts of chloride ions in the sweat test, hypoxia, and an increased ratio of residual volume to total lung capacity (TLC).

Treatment options for respiratory conditions include antibiotics, inhaled bronchodilators, airway secretion clearance procedures, and lung transplantation.
The median age of survival is 31 years. Pulmonary problems lead to death.
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​Pathology - Acute and Neonatal Respiratory Distress Syndrome
Acute respiratory distress syndrome (ARDS) can be caused by various factors such as lung infections, toxin inhalation, sepsis, trauma, pancreatitis, and shock. DIC stands for Disseminated Intravascular Coagulation.
Neonatal respiratory distress syndrome (NRDS) is a medical condition characterized by breathing difficulties in newborns. Prone to being affected by preterm and maternal diabetes. Caesarean section delivery is caused by a deficiency of pulmonary surfactant.
ARDS, or Acute Respiratory Distress Syndrome, occurs when cytokines and endotoxin cause damage to the walls of the alveolar capillaries and alveoli. This damage results in increased permeability of blood vessels and a decrease in surfactant production. As a consequence, pulmonary edema and collapse of the alveoli occur. 

Study of the nature and causes of diseases. 
Unpleasant: Dense and crimson pulmonary organ. Under microscopic examination, there is evidence of intra-alveolar edema and inflammation accompanied by the presence of hyaline membranes. If the condition is not fatal, it can lead to the formation of long-lasting scars.
Surfactant insufficiency leads to elevated surface tension within the lung, which in turn causes the collapse of the alveoli. 
Gross: The lung is enlarged and its blood vessels are filled with blood, giving it a purple color. Minuscule.
Alveoli containing eosinophilic hyaline membranes.

Symptoms and signs 
ARDS is characterized by symptoms such as difficulty breathing (dyspnea), rapid breathing (tachypnea), and bluish discoloration of the skin (cyanosis). Imaging reveals the presence of diffuse infiltrates in both lungs on the chest X-ray. Additionally, there is a discrepancy observed on the ventilation-perfusion scan. Laboratory results: Hypoxia is defined as a condition when the ratio of arterial oxygen pressure (Pao) to the fraction of inspired oxygen (Fio) is less than 200.
NRDS: The newborn experiences difficulty breathing, rapid breathing, and bluish discoloration of the skin shortly after birth. If not fatal, potential consequences include abnormal development of the bronchopulmonary system. Personal Digital Assistant. Intraventricular brain hemorrhage. and the condition known as necrotizing enterocolitis

Therapeutic interventions 
ARDS should be managed by addressing the root cause and implementing mechanical ventilation with low-tidal volumes, supplementary oxygen, and positive end-expiratory pressure.
NRDS: Administer exogenous surfactant to infants born before 28 weeks of gestation; administer corticosteroids to the mother before to birth; take caution with oxygen therapy due to the potential danger of oxygen toxicity and damage caused by oxygen-free radicals.
The mortality rate of ARDS ranges from 30% to 60%.
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​Pathology - Pneumoconiosis ( Silicosis, Coal Worker, Anthracosis) 
Pneumoconiosis refers to a group of lung diseases, including silicosis, coal worker pneumoconiosis, and anthracosis.

The act of breathing in inorganic particles, such as carbon dust (anthracosis), coal dust (coal worker's pneumoconiosis), and silica dust (silicosis).
Coal worker pneumoconiosis: Straightforward: Coal macules are present surrounding the bronchioles in the higher lobes.
Complex: Progressive large fibrosis is characterized by the presence of blackened fibrotic nodules with a necrotic center in the lung.
Silicosis is a condition characterized by the presence of silicotic nodules in the lungs, which can block airways or blood vessels. These nodules can eventually turn into collagenous scars, leading to a condition known as honeycomb lung.

Anthracosis is characterized by the presence of irregular black patches, which are caused by macrophages that consume carbon, along the lung lymphatics.

Signs and symptoms 
Coal miner pneumoconiosis is a condition that can be either simple or complicated. In its simple form, it does not cause any symptoms. However, in its complicated form, it can lead to the development of bronchiectasis. Pulmonary hypertension. Or pulmonary heart disease. 
Imaging reveals the presence of small opacities located beneath the lung, as observed on the chest X-ray.
Silicosis is a respiratory condition characterized by difficulty breathing (dyspnea) and an elevated risk of developing tuberculosis (TB). Imaging reveals the presence of nodules in the upper lung and calcification resembling an eggshell in the hilar lymph nodes, as observed on a chest X-ray.

Treatment for anthracosis is mostly focused on alleviating symptoms.
Laboratory results: Reduced total lung capacity (TLC) seen across all variations.
Treatment involves providing supportive care by the administration of oxygen and discontinuing the use of the causative substance.
Asbestosis is classified as a kind of pneumoconiosis, as seen in the Asbestosis card.
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​Pathology - Asbestosis

The inhalation of asbestos fibers is exacerbated by the act of smoking cigarettes.
Pathophysiology refers to the study of the functional changes that occur in the body as a result of a disease or injury. Alveolar macrophages phagocytose asbestos fibers, leading to a fibroblastic reaction.

Lung: Widespread scarring of the lung tissue; presence of asbestos bodies (yellow-brown ferruginous structures in the lungs that indicate the presence of asbestos fibers coated with hemosiderin); formation of collagenous plaques on the pleura and diaphragm.
Patients exhibit symptoms of difficulty breathing and coughing up phlegm 20-40 years after being exposed to asbestos.
The physical examination shows the presence of clubbing and dry inspiratory crackles.
Imaging: CT scan reveals the presence of interstitial fibrosis and pleural plaques, primarily affecting the lower lobes.
Pulmonary function test results: Reduced total lung capacity (TLC); reduced diffusion capacity of the lungs for carbon monoxide (DICO).

Administration of oxygen as a form of supportive treatment is recommended, as there is currently no known remedy for the condition.
Individuals diagnosed with asbestosis have a higher likelihood of getting bronchogenic carcinoma and malignant mesothelioma of the pleura. Malignant mesothelioma is characterized by a dense sheet of white tumor that has both fibrous and glandular epithelial components. This tumor surrounds and envelops the lung.
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​Pathology - Hypersensitivity pneumonitis
The condition is a result of sensitivity to certain antigens, such as actinomycetes commonly present in hay, animal proteins, wood bark, and some chemicals.
Pathophysiology: IgG antibodies bind to the antigen, forming an antibody-antigen complex. This complex triggers an inflammatory response in the alveoli, leading to the release of cytokines and prostaglandins. These substances then attract lymphocytes and macrophages to the lung tissue.

Lung: The acute form is characterized by the presence of mononuclear cells infiltrating the tissue, along with large cells and poorly developed granulomas that do not contain caseous material. These granulomas are mainly found around the bronchial tubes. The chronic type exhibits peripheral irregular fibrosis, especially in the peribronchial area, accompanied with remaining granulomas.

The acute manifestation emerges within a timeframe of 4-12 hours following exposure and encompasses symptoms such as fever, cough, malaise, and dyspnea.
The chronic manifestation is characterized by a gradual onset of difficulty in breathing, gradual loss of weight, and persistent coughing.
Imaging reveals the presence of interstitial fibrosis and ground-glass opacities on CT scans, primarily affecting the upper lobes.
Pulmonary function test results indicate reduced total lung capacity (TLC) and forced capacity (FC), as well as decreased diffusing capacity of the lungs for carbon monoxide (DLCO).

Treatment involves eliminating the causative factor and administering corticosteroids for chronic cases.
Farmer's lung and Bird Fancier's lung are both types of hypersensitivity pneumonitis that result from being exposed to actinomyces (which is present in rotting hay) and avian antigen, respectively.
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Pathology - Goodpasture Syndrome
Resulting from the presence of antibodies targeting the glomerular basement membrane (a type II hypersensitivity reaction)
Prevalent among males in the age range of 20 to 30 years.

Pulmonary organ: Intra-alveolar hemorrhages refer to bleeding within the small air sacs of the lungs. Fibrosis thickening of the septa indicates the thickening of the walls that separate these air sacs. Hemosiderin-laden macrophages are cells within the air sacs that contain iron pigment due to the presence of blood.
Kidney: This condition, known as rapidly progressive crescentic glomerulonephritis, occurs when macrophages, proliferating parietal cells, and fibrin come together to create crescents in Bowman space. These crescents eventually lead to the destruction of Bowman space and the compression of the glomerular capillaries.

Immunofluorescence investigations: Immunoglobulins are deposited in a linear pattern along the glomerular basement membranes (GBMs) of the alveoli.
The patient is experiencing hemoptysis, as well as symptoms of nephritic syndrome including edema, hypertension, and hematuria.
Laboratory results indicate the presence of Anti-GBM antibodies and iron deficient anemia.
Plasmapheresis is a medical procedure used to remove harmful substances from the blood. Corticosteroids and cyclophosphamide are medications that may be used to treat the condition. Hemodialysis may be necessary if the patient experiences renal failure.

Anti GBM glomerulonephritis is defined by the presence of nephritic syndrome, which is caused by the deposition of anti GBM antibodies in the kidney. It is important to note that this condition does not affect the lungs. 
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​Pathology - Sarcoidosis
The cause is unclear. While the possibility of immunological malfunction has been suggested.
The highest occurrence is observed in African American women between the ages of 20 and 41.
The tissues most frequently affected are the lung, lymph nodes, spleen, liver, bone marrow, skin, eyes, and salivary glands.

The specimen exhibits a microscopic finding of a noncaseating granuloma with a fibrotic center. The granuloma is surrounded by epithelioid cells and Langhans giant cells. Additionally, there are asteroid bodies (inclusions inside giant cells) and Schaumann bodies (calcium concretions) present. However, they may also be found in other granulomatous conditions.

The individual presents with a range of symptoms including malaise, fever, enlargement of the liver and spleen, difficulty breathing, inflammation of the lung tissue, skin rash characterized by painful nodules, inflammation of many joints, inflammation of the uvea (middle layer of the eye), damage to the central nervous system and peripheral nerves, and a condition where the heart muscle becomes stiff and less able to pump blood efficiently.
Imaging: The chest X-ray reveals the presence of enlarged lymph nodes on both sides of the chest and abnormal lung tissue infiltration. The laboratory results are also available. Reduced total lung capacity. Reduced diffusion capacity of the lungs for carbon monoxide (DLCO). elevated erythrocyte sedimentation rate (ESR). Elevated ACE enzyme activity, excessive levels of calcium in the blood and urine, elevated levels of gamma globulins, decreased responsiveness to skin test antigens


Corticosteroids are prescribed for people who are experiencing symptoms or have complications affecting their organs.
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​Pathology - Idiopathic Pulmonary Fibrosis 
Idiopathic Pulmonary Fibrosis is a condition characterized by fibrosis of the lungs, and its cause is still unknown. A proposed process involves the initial insult to the alveolar epithelium, which subsequently triggers abnormal activation of fibroblasts, resulting in damage to the lung tissue.

The microscopic examination reveals a significant increase in fibrous tissue and the growth of fibroblast cells, leading to the distortion of the walls separating the air sacs in the lungs. This results in a honeycomb-like structure, with enlarged bronchioles that are lined by scarred and fibrotic lung tissue.

Patients have a gradual onset of difficulty breathing and a non-productive cough.
The physical examination reveals the presence of hypoxemia, inspiratory crackles throughout the lungs, and clubbing.
Imaging: CT scan reveals a subpleural honeycombing pattern and patchy bibasilar reticular opacities.
Pulmonary function test results: Reduced total lung capacity (TLC) and reduced diffusing capacity of the lungs for carbon monoxide (DLCO).

Treatment options include providing additional oxygen and considering the possibility of a lung transplant.
The prognosis is unfavorable, with an average survival rate of 2-5 years following diagnosis.
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​Pathology - Pulmonary embolism
Emboli may consist of air, amniotic fluid, fat, foreign substances, or malignant cells. Thromboemboli, which typically arise from deep vein thrombosis (DVT) in the leg, account for the majority (93%) of emboli.

Gross: Hemorrhage or infarction of the lung typically occurs in the lower lobes. Infarction only happens in individuals with insufficient blood flow due to lung or heart disease. In such cases, it is possible to observe a venous thrombus, which appears dark red with pale-gray fibrin strands and has a hard consistency, stuck in a pulmonary conduit.

The individual may experience tachycardia, dyspnea, pain upon inspiration, and potential symptoms of deep vein thrombosis such as a sore and swollen calf. Additionally, there is a possibility of syncope and tachyarrhythmias. or hypotension in the case of a major pulmonary embolism (PE)
Imaging: An inconsistency was observed on the ventilation-perfusion scan, and a region with incomplete filling was observed on the high-resolution CT scan of the chest.
Laboratory results: The presence of hypoxia and increased levels of D-dimer are observed in cases of thromboembolism.
Anticoagulation should be administered. If the patient is not eligible for anticoagulation, an IVC filter should be considered. Thrombolysis may be appropriate if the patient is experiencing hypotension or showing signs of right ventricular strain. In cases of extensive PE, surgical thrombectomy should be contemplated.

Hospitalized patients rank PE as the third most common cause of mortality.
The presence of Virchow triad, which consists of venous stasis, hypercoagulable condition, and vascular wall damage, increases the likelihood of developing deep vein thrombosis (DVT) and consequently pulmonary embolism (PE).
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​Pathology - Idiopathic Pulmonary Arterial Hypertension
The cause is unclear.
Primarily impacts females in the age range of 20 to 40.
Lung: Medial hypertrophy and intimal fibrosis of the pulmonary arterioles.
Cardiac findings: Right ventricular hypertrophy and dilatation, observed in cases of acute cor pulmonale.

Patients exhibit symptoms of dyspnea, tiredness, chest discomfort, and exertional syncope.
The physical examination reveals a prominent P wave, an S3 sound on the right side, a noticeable enlargement of the right ventricle, and indications of right-sided heart failure such as swelling in the lower extremities, distended jugular veins, and fluid accumulation in the abdomen (ascites).

Complications including cyanosis, thrombosis, enlargement of the right ventricle, and cor pulmonale (heart failure on the right side due to pulmonary hypertension).

Treatment options for this condition include administering oxygen, using diuretics to address right heart failure, prescribing anticoagulant medications, utilizing phosphodiesterase 5 inhibitors, employing prostacyclin analogues, administering endothelin receptor blockers, and considering calcium channel blockers for individuals who have a good response to vasodilator challenge during right heart catheterization.

The prognosis is uncertain, with an estimated 3-year survival rate of approximately 60%.
Increased pressures in the pulmonary vasculature can also be linked to connective tissue disorders such as systemic lupus erythematosus (SLE) and CREST syndrome, congenital heart disease with left-to-right shunts, left heart failure, interstitial lung diseases such as chronic obstructive pulmonary disease (COPD), sarcoidosis, and chronic thromboembolic disease, obstructive sleep apnea (OSA), cirrhosis, or HIV infection.
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