NEET MDS Synopsis
Psoriasis
General Pathology
Psoriasis
1. Characterized by skin lesions that appear as scaly, white plaques.
2. Caused by rapid proliferation of the epidermis.
3. Autoimmune pathogenesis; exact mechanism is unclear.
FUNGAL INFECTION- Aspergillosis
General Pathology
FUNGAL INFECTION
Aspergillosis
Opportunistic infections caused by Aspergillus sp and inhaled as mold conidia, leading to hyphal growth and invasion of blood vessels, hemorrhagic necrosis, infarction, and potential dissemination to other sites in susceptible patients.
Symptoms and Signs: Noninvasive or, rarely, minimally locally invasive colonization of preexisting cavitary pulmonary lesions also may occur in the form of fungus ball (aspergilloma) formation or chronic progressive aspergillosis.
Primary superficial invasive aspergillosis is uncommon but may occur in burns, beneath occlusive dressings, after corneal trauma (keratitis), or in the sinuses, nose, or ear canal.
Invasive pulmonary aspergillosis usually extends rapidly, causing progressive, ultimately fatal respiratory failure unless treated promptly and aggressively. A. fumigatus is the most common causative species.
Extrapulmonary disseminated aspergillosis may involve the liver, kidneys, brain, or other tissues and is usually fatal. Primary invasive aspergillosis may also begin as an invasive sinusitis, usually caused by A. flavus, presenting as fever with rhinitis and headache
Agranulocytosis
General Pathology
Agranulocytosis. Severe neutropenia with symptoms of infective lesions.
Drugs. are an important cause and the effect may be due to .
-Direct toxic effect.
-Hypersensitivity.
Some of the 'high risk drugs are.
-Amidopyrine.
-Antithyroid drugs.
-Chlorpromazine, mapazine.
-Antimetabolites and other drugs causing pancytopenia.
Bloodpicture: Neutropenia with toxic granules in neutrophils. Marrow shows decrease in granulocyte precursors with toxic granules in them.
NEOPLASIA
General Pathology
NEOPLASIA
An abnormal. growth, in excess of and uncoordinated with normal tissues Which persists in the same excessive manner after cessation of the stimuli which evoked the change.
Tumours are broadly divided by their behaviors into 2 main groups, benign and malignant.
Features
Benign
Malignant
General
Rate of growth
Mode of growth
Slow
Expansile
Rapid
Infiltrative
Gross
Margins
Haemoeehage
Circumscribed often Encapsulated
Rare
III defined
Common
Microscopic
Arrangement
Cells
Nucleus
Mitosis
Resemble Parent Tissues
Regular and uniform in shape and size
Resembles parent Cells
Absent or scanty
Varying degrees of structural differentiation
Cellular pleomorphism
Hyper chromatic large and varying in shape and size
Numerous and abnormal
Through most tumours can be classified in the benign or malignant category . Some exhibits an intermediate behaviours.
CLASSIFICATION
Origin
Benign
Malignant
Epithelial
Surface epithelium
Glandular epithelium
Melanocytes
Papilloma
Adenoma
Naevus
Carcinoma
Adenoca cinoma
Melanocarcinoma(Melanoma)
Mesenchymal
Adipose tissue
Fibrous tissue
Smooth tissue
Striated muscle
Cartilage
Bone
Blood vessels
Lymphoid tissue
Lipoma
Fibroma
Leiomyoma
Rhabdomyoma
Chondroma
Osteoma
Angioma
Liposarcoma
Fibrosarcoma
Leimyosarcoma
Chondrosarcoma
Osteosarcoma
Angiosarcoma
Lymphoma
Some tumours can not be clearly categorized in the above table e.g.
Mixed tumours like fibroadenoma of the breast which is a neoplastic proliferation of both epithelial and mesenchmal tissues.
Teratomas which are tumours from germ cells (in the glands) and totipotent cells
(in extra gonodal sites like mediastinun, retroperitoneum and presacral region). These are composed of multiple tissues indicative of differentiation into the derivatives of the three germinal layers.
Hamartomas which are malformations consisting of a haphazard mass of tissue normally present at that site.
Mental Age Assessment
PedodonticsMental Age Assessment
Mental age can be assessed using the following formula:
Mental Age = (Chronological Age × 100) / 10
Mental Age Descriptions
Below 69: Mentally retarded (intellectual disability).
Below 90: Low average intelligence.
90-110: Average intelligence. Most children fall within
this range.
Above 110: High average or superior intelligence.
Acid-Peptic disorders
Pharmacology
Acid-Peptic disorders
This group of diseases include peptic ulcer, gastroesophageal reflux and Zollinger-Ellison syndrome.
Pathophysiology of acid-peptic disorders
Peptic ulcer disease is thought to result from an imbalance between cell– destructive effects of hydrochloric acid and pepsin on the one side, and cell-protective effects of mucus and bicarbonate on the other side. Pepsin is a proteolytic enzyme activated in gastric acid (above pH of 4, pepsin is inactive); also it can digest the stomach wall. A bacterium, Helicobacter pylori, is now accepted to be involved in the pathogenesis of peptic ulcer.
In gastroesophageal reflux the acidic contents of the stomach enter into the oesophagus causing a burning sensation in the region of the heart; hence the common name heartburn or other names such as indigestion and dyspepsia.
However, Zollinger-Ellison syndrome is caused by a tumor of gastrin secreting cells of the pancreas characterized by excessive secretion of gastrin that stimulates gastric acid secretion.
These disorders can be treated by the following classes of drugs:
A. Gastric acid neutralizers (antacids)
B. Gastric acid secretion inhibitors (antisecretory drugs)
C. Mucosal protective agents
D. Drugs that exert antimicrobial action against H.pylori
Neutropenia
General Pathology
Neutropenia: Neutropenia is an abnormally low number of neutrophils
Causes
-Typhoid, paratyphoid. .
-Viral and ricketseal infections.
-Malaria, Kala azar.
-Hypersplenism.
-Aplastic and megaloblastic anaemia.
-Marrow infiltration by malignancies, lymphomas etc.
-SLE.
PNEUMONIAS
General Pathology
PNEUMONIAS
Pneumonia is defined as acute inflammation of the lung parenchyma distal to the terminal bronchioles which consist of the respiratory bronchiole, alveolar ducts, alveolar sacs and alveoli. The terms 'pneumonia' and 'pneumonitis' are often used synonymously for inflammation of the lungs, while 'consolidation' (meaning solidification) is the term used for macroscopic and radiologic appearance of the lungs in pneumonia.
PATHOGENESIS.
The microorganisms gain entry into the lungs by one of the following four routes:
1. Inhalation of the microbes.
2. Aspiration of organisms.
3. Haematogenous spread from a distant focus.
4. Direct spread from an adjoining site of infection.
Failure of defense mechanisms and presence of certain predisposing factors result in pneumonias.
These conditions are as under:
1. Altered consciousness.
2. Depressed cough and glottic reflexes.
3. Impaired mucociliary transport.
4. Impaired alveolar macrophage function.
5. Endobronchial obstruction.
6. Leucocyte dysfunctions.
CLASSIFICATION. On the basis of the anatomic part of the lung parenchyma involved, pneumonias are traditionally classified into 3 main types:
1. Lobar pneumonia.
2. Bronchopneumonia (or Lobular pneumonia).
3. Interstitial pneumonia.
BACTERIAL PNEUMONIA
Bacterial infection of the lung parenchyma is the most common cause of pneumonia or consolidation of one or both the lungs. Two types of acute bacterial pneumonias are distinguished—lobar pneumonia and broncho-lobular pneumonia, each with distinct etiologic agent and morphologic changes.
1. Lobar Pneumonia
Lobar pneumonia is an acute bacterial infection of a part of a lobe, the entire lobe, or even two lobes of one or both the lungs.
ETIOLOGY.
Following types are described:
1. Pneumococcal pneumonia. More than 90% of all lobar pneumonias are caused by Streptococcus pneumoniae, a lancet-shaped diplococcus. Out of various types, type 3-S. pneumoniae causes particularly virulent form of lobar pneumonia.
2. Staphylococcal pneumonia. Staphylococcus aureus causes pneumonia by haematogenous spread of infection.
3. Streptococcal pneumonia, β-haemolytic streptococci may rarely cause pneumonia such as in children after measles or influenza.
4. Pneumonia by gram-negative aerobic bacteria. Less common causes of lobar pneumonia are gram-negative bacteria like Haemophilus influenzae, Klebsiella pneumoniae (Friedlander's bacillus), Pseudomonas, Proteus and Escherichia coli.
MORPHOLOGY. Laennec's original description divides lobar pneumonia into 4 sequential pathologic phases:
1. STAGE OF CONGESTION: INITIAL PHASE
The initial phase represents the early acute inflammatory response to bacterial infection and lasts for 1 to 2 days.
The affected lobe is enlarged, heavy, dark red and congested. Cut surface exudes blood-stained frothy fluid.
Microscopic Examination
i) Dilatation and congestion of the capillaries in the alveolar walls.
ii) Pale eosinophilic oedema fluid in the air spaces.
iii) A few red cells and neutrophils in the intra-alveolar fluid.
iv) Numerous bacteria demonstrated in the alveolar fluid by Gram's staining.
2. RED HEPATISATION: EARLY CONSOLIDATION
This phase lasts for2 to 4 days. The term hepatisation in pneumonia refers to liver-like consistency of the affected lobe on cut section.
The affected lobe is red, firm and consolidated. The cut surface of the involved lobe is airless, red-pink, dry, granular and has liver-like consistency.
Microscopic Examination
i) The oedema fluid of the preceding stage is replaced by strands of fibrin.
ii) There is marked cellular exudate of neutrophils and extravasation of red cells.
iii) Many neutrophils show ingested bacteria.
iv) The alveolar septa are less prominent than in the first stage due to cellular exudation.
3. GREY HEPATISATION: LATE CONSOLIDATION This phase lasts for4 to 8 days.
The affected lobe Is firm and heavy. The cut surface is dry, granular and grey in appearance with liver-like consistency. The change in colour from red to grey begins at the hilum and spreads towards the periphery. Fibrinous pleurisy is prominent.
Microscopic Examination
i) The fibrin strands are dense and more numerous.
ii) The cellular exudate of neutrophils is reduced due to disintegration of many inflammatory cells. The red cells are also fewer. The macrophages begin to appear in the exudate.
iii) The cellular exudate is often separated from the septal walls by a thin clear space.
iv) The organisms are less numerous and appear as degenerated forms.
COMPLICATIONS. Since the advent of antibiotics, serious complications of lobar pneumonia are uncommon. However, they may develop in neglected cases and in patients with impaired immunologic defenses.
These are as under:
1. Organisation. In about 3% of cases, resolution of the exudate does not occur but instead it is organised. There is ingrowth of fibroblasts from the alveolar septa resulting in fibrosed, tough, airless leathery lung tissue.
2. Pleural effusion. About 5% of treated cases of lobar pneumonia develop inflammation of the pleura with effusion.
3. Empyema. Less than 1% of treated cases of lobar pneumonia develop encysted pus in the pleural cavity termed empyema.
4. Lung abscess. A rare complication of lobar pneumonia is formation of lung abscess.
5. Metastatic infection. Occasionally, infection in the lungs and pleural cavity in lobar pneumonia may extend into the pericardium and the heart causing purulent pericarditis, bacterial endocarditis and myocarditis.
CLINICAL FEATURES. The major symptoms are: shaking chills, fever, malaise with pleuritic chest pain, dyspnoea and cough with expectoration which may be mucoid, purulent or even bloody. The common physical findings are fever, tachycardia, and tachypnoea, and sometimes cyanosis if the patient is severely hypoxaemic. There is generally a marked neutrophilic leucocytosis. Blood cultures are positive in about 30% of cases. Chest radiograph may reveal consolidation.
II. Bronchopneumonia (Lobular Pneumonia)
Bronchopneumonia or lobular pneumonia is infection of the terminal bronchioles that extends into the surrounding alveoli resulting in patchy consolidation of the lung. The condition is particularly frequent at extremes of life (i.e. in infancy and old age), as a terminal event in chronic debilitating diseases and as a secondary infection following viral respiratory infections such as influenza, measles etc,
ETIOLOGY.
The common organisms responsible for bronchopneumonia are staphylococci, streptococci, pneumococci, Klebsiella pneumoniae, Haemophilus influenzae, and gram-negative bacilli like Pseudomonas and coliform bacteria.
Bronchopneumonia is identified by patchy areas of red or grey consolidation affecting one or more lobes, frequently found bilaterally and more often involving the lower zones of the lungs due to gravitation of the secretions. On cut surface, these patchy consolidated lesions are dry, granular, firm, red or grey in colour, 3 to 4 cm in diameter, slightly elevated over the surface and are often centred around a bronchiole. These patchy areas are best picked up by passing the fingertips on the cut surface.
Microscopic Examination
i) Acute bronchiolitis, ii) Suppurative exudate, consisting chiefly of neutrophils, in the peribronchiolar alveoli, iii) Thickening of the alveolar septa by congested capillaries and leucocytic infiltration, iv) Less involved alveoli contain oedema fluid.
COMPLICATIONS.
The complications of lobar pneumonia may occur in bronchopneumonia as well. However, complete resolution of bronchopneumonia is uncommon. There is generally some degree of destruction of the bronchioles resulting in foci of bronchiolar fibrosis that may eventually cause bronchiectasis.
CLINICAL FEATURES. The patients of bronchopneumonia are generally infants or elderly individuals. There may be history of preceding bed-ridden illness, chronic debility, aspiration of gastric contents or upper respiratory infection.
VIRAL AND MYCOPLASMAL PNEUMONIA (PRIMARY ATYPICAL PNEUMONIA)
Viral and mycoplasmal pneumonia is characterised by patchy inflammatory changes, largely confined to interstitial tissue of the lungs, without any alveolar exudate. Other terms used for these respiratory tract infections are interstitial pneumonitis, reflecting the interstitial location of the inflammation, andprimary atypical pneumonia, atypicality being the absence of alveolar exudate commonly present in other pneumonias. Interstitial pneumonitis may occur in all ages.
ETIOLOGY. Interstitial pneumonitis is caused by a wide variety of agents, the most common being respiratory syncytial virus (RSV). Others are Mycoplasma pneumoniae and many viruses such as influenza and parainfluenza viruses, adenoviruses, rhinoviruses, coxsackieviruses and cytomegaloviruses (CMV).
Depending upon the severity of infection, the involvement may be patchy to massive and widespread consolidation of one or both the lungs. The lungs are heavy, congested and subcrepitant. Sectioned surface of the lung exudes small amount of frothy or bloody fluid.
Microscopic Examination
I) Interstitial Inflammation: There is thickening of alveolar walls due to congestion, oedema and mononuclear inflammatory infiltrate comprised by lymphocytes, macrophages and some plasma cells. illness, chronic debility, aspiration of gastric contents or upper respiratory infection.
ii) Necrotising bronchiolitis: This is characterised by foci of necrosis of the bronchiolar epithelium, inspissated secretions in the lumina and mononuclear infiltrate in the walls and lumina.
iii) Reactive changes: The lining epithelial cells of the bronchioles and alveoli proliferate in the presence of virus and may form multinucleate giant cells and syncytia in the bronchiolar and alveolar walls.
iv) Alveolar changes: In severe cases, the alveolar lumina may contain oedema fluid, fibrin, scanty inflammatory exudate and coating of alveolar walls by pink, hyaline membrane similar to the one seen in respiratory distress syndrome.
COMPLICATIONS.
The major complication of interstitial pneumonitis is superimposed bacterial infection and its complications. Most cases of interstitial pneumonitis recover completely.
CLINICAL FEATURES.
Majority of cases of interstitial pneumonitis initially have upper respiratory symptoms with fever, headache and muscle-aches. A few days later appears dry, hacking, non-productive cough with retrosternal burning due to tracheitis and bronchitis. Chest radiograph may show patchy or diffuse consolidation.
C. OTHERTYPES OF PNEUMONIAS
I. Pneumocystis carinii Pneumonia
Pneumocystis carinii, a protozoon widespread in the environment, causes pneumonia by inhalation of the organisms as an opportunistic infection in neonates and immunosuppressed people. Almost 100% cases of AIDS develop opportunistic infection, most commonly Pneumocystis carinii pneumonia.
II. Legionella Pneumonia
Legionella pneumonia or legionnaire's disease is an epidemic illness caused by gramnegative bacilli, Legionella pneumophila that thrives in aquatic environment. It was first recognised following investigation into high mortality among those attending American Legion Convention in Philadelphia in July 1976. The epidemic occurs in summer months by spread of organisms through contaminated drinking water or in air-conditioning cooling towers. Impaired host defenses in the form of immunodeficiency, corticosteroid therapy, old age and cigarette smoking play important roles.
III. Aspiration (Inhalation) Pneumonia
Aspiration or inhalation pneumonia results from inhaling different agents into the lungs. These substances include food, gastric contents, foreign body and infected material from oral cavity. A number of factors predispose to inhalation pneumonia which include: unconsciousness, drunkenness, neurological disorders affecting swallowing, drowning, necrotic oropharyngeal tumours, in premature infants and congenital tracheo-oesophageal fistula.
1. Aspiration of small amount of sterile foreign matter such as acidic gastric contents produce chemical pneumonitis. It is characterised by haemorrhagic pulmonary oedema with presence of particles in the bronchioles.
2. Non-sterile aspirate causes widespread bronchopneumonia with multiple areas of necrosis and suppuration.
IV. Hypostatic Pneumonia
Hypostatic pneumonia is the term used for collection of oedema fluid and secretions in the dependent parts of the lungs in severely debilitated, bedridden patients. The accumulated fluid in the basal zone and posterior part of lungs gets infected by bacteria from the upper respiratory tract and sets in bacterial pneumonia.
V. Lipid Pneumonia Another variety of noninfective pneumonia is lipid pneumonia. It is of 2 types:
1. Exogenous lipid pneumonia. This is caused by aspiration of a variety of oily materials. These are: inhalation of oily nasal drops, regurgitation of oily medicines from stomach (e.g. liquid paraffin), administration of oily vitamin preparation to reluctant children or to debilitated old patients.
2. Endogenous lipid pneumonia. Endogenous origin of lipids causing pneumonic consolidation is more common. The sources of origin are tissue breakdown following obstruction to airways e.g. obstruction by bronchogenic cancer, tuberculosis and bronchiectasis.