NEET MDS Lessons
General Pathology
Bacillus anthrax
- large Gram (+) rods that produce heat resistant spores; Clostridia and Bacillus species are the two bacterial spore formers; they do not form spores in tissue; produces a powerful exotoxin.
- contracted by direct contact with animal skins or products
- four forms of anthrax are recognized → cutaneous (MC), pulmonary, oraloropharyngeal, and gastrointestinal.
- cutaneous anthrax (90 to 95% of cases) occurs through direct contact with infected or contaminated animal products.
- lesions resemble insect bites but eventually swell to form a black scab, or eschar, with a central area of necrosis ("malignant pustule").
Lymphangitis
is the acute inflammation due to bacterial infections spread into the lymphatics most common are group A β-hemolytic streptococci.
lymphatics are dilated and filled with an exudate of neutrophils and monocytes.
red, painful subcutaneous streaks (the inflamed lymphatics), with painful enlargement of the draining lymph nodes (acute lymphadenitis).
subsequent passage into the venous circulation can result in bacteremia or sepsis.
INFLAMMATION
Response of living tissue to injury, involving neural, vascular and cellular response.
ACUTE INFLAMMATION
It involves the formation of a protein .rich and cellullar exudate and the cardinal signs are calor, dolor, tumour, rubor and function loss
The basic components of the response are
Haemodynamic changes.
Permeability changes
Leucocyte events.
1. Haemodynamic Changes :
- Transient vasoconstriction followed by dilatation.
- Increased blood flow in arterioles.
- More open capillary bed.
- Venous engorgement and congestion.
- Packing of microvasculature by RBC (due to fluid out-pouring)
- Vascular stasis.
- Change in axial flow (resulting in margination of leucocytes)
.2. Permeability Changes:
Causes.
- Increased intravascular hydrostatic pressure.
- Breakdown of tissue proteins into small molecules resulting in
- increased tissue osmotic pressure.
- Increased permeability due to chemical mediators, causing an
- immediate transient response. .
- Sustained response due to direct damage to microcirculation.
3. White Cell Events:
.Margination - due to vascular stasis and change in axial flow.
Pavementing - due to endothelial cells swollen and more sticky.
Leucocytes more adhesive.
Binding by a plasma component
Emigration - of leucocytes by amoeboid movement between endhothe1ial cells and beyond the basement membrane. The passive movement of RBCs through the gaps created during emigration is called diapedesis
Chemotaxis - This is a directional movement, especially of polymorphs and monocytes towards a concentration gradient resulting in aggregation of these cells at the site of inflammation. .Chemotactic agents may be:
- Complement components. (C3and C5 fragments and C567)
- Bacterial products.
- Immune complexes, especially for monocyte.
- Lymphocytic factor, especially for monocyte.
Phagocytosis - This includes recognition, engulfment and intracellular degradation. It is aided by .Opsonins., Specific antibodies., Surface provided by fibrin meshwork.
Functions of the fluid and cellular exudate
1. Dilution of toxic agent.
2. Delivers serum factors like antibodies and complement components to site of inflammation.
3. Fibrin formed aids In :
- Limiting inflammation
- Surface phagocytosis
- Framework for repair.
4. Cells of the exudate:
Phagocytose and destroy the foreign agent.
Release lytic enzymes when destroyed, resulting in extracellular killing of organisms- and digestion of debris to enable healing to occur
Plasma Cell Pathology
A. Multiple myeloma
1. Plasma cell neoplasm that results in the proliferation of monoclonal plasma cells. These tumor cells produce nonfunctional immunoglobulins.
2. Laboratory findings include:
a. Monoclonal IgG spike.
b. Bence-Jones proteins found in urine.
3. Radiographic findings: characteristic “punched-out” radiolucencies in bones.
Pathology gives explanations of a disease by studying the following four aspects of the disease.
1. Etiology,
2. Pathogenesis,
3. Morphologic changes and
4. Functional derangements and clinical significance.
1. Etiology Etiology of a disease means the cause of the disease. If the cause of a disease is known it is called primary etiology. If the cause of the disease is unknown it is called idiopathic. Knowledge or discovery of the primary cause remains the backbone on which a diagnosis can be made, a disease understood, & a treatment developed. There are two major classes of etiologic factors: genetic and acquired (infectious, nutritional, chemical, physical, etc).
2. Pathogenesis Pathogenesis means the mechanism through which the cause operates to produce the pathological and clinical manifestations. The pathogenetic mechanisms could take place in the latent or incubation period. Pathogenesis leads to morphologic changes.
3. Morphologic changes The morphologic changes refer to the structural alterations in cells or tissues that occur following the pathogenetic mechanisms. The structural changes in the organ can be seen with the naked eye or they may only be seen under the microscope. Those changes that can be seen with the naked eye are called gross morphologic changes & those that are seen under the microscope are called microscopic changes. the morphologic changes will lead to functional alteration & to the clinical signs & symptoms of the disease.
4. Functional derangements and clinical significance The morphologic changes in the organ influence the normal function of the organ. By doing so, they determine the clinical features (symptoms and signs), course, and prognosis of the disease.
Thalassaemia. Genetic based defect in synthesis of one of the normal chains.
Beta thalassaemia ---> reduced Hb A and increased HbF (α2, Y2) HBA2(α2)
Alpha thalassaemia ---> reduced Hb-A, Hb-A2 and Hb-F-with formation of Hb-H(β4) and Hb Barts (Y4).
Thalassaemia may manifest as trait or disease or with intermediate manifestation.
Features:
• Microcytic hypochromic RBC is in iron deficjency.
• Marked anisopoikilocytsis with prominent target cells.
• Reticulocytosis and nucleated RBC seen.
• Mongoloid facies and X-ray findings characteristic of marrow hyperplasia
• Decreased osmotic. fragility.
• Increased marrow iron (important difference from iron deficiency anaemia).
• Haemosiderosis, especially with repeated transfusions.
Diagnosis is by Hb electrophoresis and by Alkali denaturation test (for HbF).
DEGENERATION
Definition: Reversible cell injury.
(1) Water accumulation in the form of
(i) Cloudy swelling.
(ii) Vacuolar degeneration.
.(ill) Hydropic degeneration.
This change is commonly seen in parenchymal cells e.g. kidneys.
Gross appearance: The organ is swollen, soft and pale.
Microscopic appearance: Cells show varying degrees of swelling. Cytoplasm may be granular, vacuolated, homogenously pale and ballooned out.
(2) Fatty change An excessive, demonstrable accumulation of fat is common in parenchymal cells of liver and heart
In the liver, it can be due to: .
(i) Excess fat entry into the liver as occurs in starvation and in steroid excess due to mobilization from stores.
(ii) Excess triglyceride formation
(iii) Reduced phosphorlyation of fat.
(iv) Decreased release as lipoprotein due to protein deficiency.
Causes
(i) Hypoxia as in severe anaemia and venous stasis
(ii) Protein malnutrition.
(iii) Hepatotoxins like CCl4.
(iv) Alcoholism
(v) Metabolic defects like Diabetes mellitus
(vi) Infections.
Gross appearance: The organ is enlarged, soft and greasy, with a pale yellowish colour. It may involve the organ uniformly or patchily ( thrush breast or tabby cat heart)
Microscopic appearance: The cells contain clear vacuoles (stainable by fat-sudan stains on frozen sections). These may be small and dispersed or large, displacing the nucleus peripherally. Several such cells may fuse to form fat cysts.
(3) Hyaline degeneration
In alcoholic liver damage, the cytoplasmic organelles are damaged and give the cytoplasm a deep eosinophilic staining-Mallory hyaline.