NEET MDS Lessons
General Pathology
Lymphomas
A. Hodgkin’s disease
1. Characterized by enlarged lymph nodes and the presence of Reed-Sternberg cells (multinucleated giant cells) in lymphoid tissues.
2. Disease spreads from lymph node to lymph node in a contiguous manner.
3. Enlarged cervical lymph nodes are most commonly the first lymphadenopathy observed.
4. The cause is unknown.
5. Occurs before age 30.
6. Prognosis of disease depends largely on the extent of lymph node spread and systemic involvement.
B. Non-Hodgkin’s lymphoma
1. Characterized by tumor formation in the lymph nodes.
2. Tumors do not spread in a contiguous manner.
3. Most often caused by the proliferation of abnormal B cells.
4. Occurs after age 40.
5. Example: Burkitt’s lymphoma
a. Commonly associated with an EpsteinBarr virus (EBV) infection and a genetic mutation resulting from the translocation of the C-myc gene from chromosome 8 to 14.
b. The African type occurs in African children and commonly affects the mandible or maxilla.
c. In the United States, it most commonly affects the abdomen.
d. Histologically, the tumor displays a characteristic “starry-sky” appearance.
Biochemical examination
This is a method by which the metabolic disturbances of disease are investigated by assay of various normal and abnormal compounds in the blood, urine, etc.
Parvoviruses
- smallest DNA virus
- erythema infectiosum (fifth disease) is characterized by a confluent rash usually beginning on the cheeks ("slapped face") which extends centripetally to involve the trunk; fever, malaise and respiratory problems; and arthralgias and joint swelling (50%).
other associations:
- aplastic anemia in patients with chronic hemolytic anemias (e.g., sickle cell disease, spherocytosis).
- repeated abortions associated with hydrops fetalis.
- pure RBC aplasia by involving the RBC precursors (no reticulocytes peripherally).
-chronic arthritis
HEALING
Definition. Replacement of damages tissue by healthy tissue. It is an attempt to restore the tissue to structural and functional normalcy.
Healing may be of 2 types
A. Regeneration.
B. Repair by granulation tissue.
A. Regeneration
Where the replacement is by proliferation of parenchymatous cells of type destroyed. This depends upon:
(1) Regenerative capacity of cells. Cells may be :
(a) Labile cells which are constantly proliferating to replace cells continuously shed off or destroyed
Epithelial cells of skin and lining surfaces.
Lymphoid and haemopoietic tissue.
(b) Stable cell. Cells mostly in resting-phase, but capable of dividing when necessary e.g.
- Liver and other parenchymatous and glandular cells.
- Connective tissue cells.
- Muscle cells have a limited capacity to divide.
(c) Permanent cell. These cells, once differentiated are not capable. of dividing e.g.-nerve
(2) The extent of tissue loss. If there is extensive destruction including disruption of the framework, complete.regeneration is not possible. even with labile an stable cell
B. Repair by granulation tissue
Granulation tissue is formed by proliferation of surrounding connective tissue elements. which migrate into the site to be repaired.
Granulation tissue formation seen in :
- Wound healing.
- Organisation of exudates.
- Thrombi.
- Infarcts.
- Haematomas.
The process of repair can be best studied in clean incised wounds, where there is .no or minimal tjssue loss or the_edges or the edges of the wound are approximated closely as in a surgical wound. This is called Primary union (healing by first intention).
1. The blood in the incised area clots and the fibrin binds the edges together.
2. During the first 24 hours, an acute inflammation sets in to .bring protein and phagocyte rich exudates to the site.
3. The superficial part of the clot get dry and dehydrated{scab). The surface epithelium proliferates just beyond the cut edges and the cells migrate-deep to dry scab. Epithelialisation is usually complete by 24- 48 hours.
4 Granulation tissue, with actively growing fibroblasts and capillary buds invades the clot (stage of vascularisation). These fibroblasts 'posses contractile myofibrils & hence are termed as myofibroblasts'.
5. Simultaneously, demolition of the debris and clot components takes place.
6 The granulation tissue initially lays down a mucopolysacharide rich ground substance
7.Reticulin and later collagen fibrils are formed by the fibroblasts (with 5 days)
8 with progressive maturation of collagen, some of the capiliary buds develop into arterioles and venules and majority of them are obliterated (stage of devascularisation).
9. With time (weeks to months) the tensile strength of the scar increases and it shrinks.
Secondary union (excised wound-healing by secondary intention).
1. Coagulum forms and fills the gap.
2. Inflammatory reaction is seen as in primary union but is more intense, as a lot more debris has to be removed. .
3. Epithelial proliferation starts covering the surface from the periphery by proliferation beyond the edges and migration under scab.
4.Debridement starts and simultaneously granulation tissue grows into the coagulum from the sides and base of the wound. This is much more exuberant than in primary union. The surface now looks red and granular.
5. Wound contraction. This is early contraction (starts after 3 days and is complete in 2 weeks) and must be differentiated from contraction after scar formation Wounds can contract by up to 80% of original size of that the gap to be filled is much reduced, resulting in faster healing with a smaller scar.
Wound contraction is probably caused by:
- Dehydration
- Collagen contraction.
- Granulation tissue contraction .(myofibroblasts).
The exact mechanism is not known.
6. Laying down of collagen.
7 Maturation to form a scar which later shrinks and devascularises.
Factors affecting wound healing
Wound healing is delayed by :
A. Local factors
1. Poor blood supply.
2. Adhesion to bony surfaces (e.g. over the tibia).
3. Persistent injurious agents (infective or particulate) results in chronicity of inflammation and ineffective healing. .
4. Constant movement (especially in fracture healing).
5. ionizing radiation (in contrast, ultraviolet rays hasten healing).
6. Neoplasia.
B. General factors
I. Nutritional deficiency, especially of.
(i) Protein
(ii) Ascorbic acid (Vitamin C).
(iii) Zinc
2. Corticoids adversely affect wound contraction and granulation tissue formation
(anabolic steroids have a favorable effect).
3. Low temperature.
4. Defects (qualitative or quantitative) in polymorphs and macrophages
.Complication of wound healing
1. Wound dehiscence
2. Infection
3. Epidermal inclusion (implantation) cysts.
4. Keloid formation
5. Cicatrisation resulting in contract Ires and obstruction(in hollow viscera).
6. Calcification and ossification.
7. Weak scar which could be a site for incisional hernia
8. Painful scar if it involves a nerve twig.
9. Rarely neoplasia (especially in burn scars).
Acute tubular necrosis
Characterized by impaired kidney functions due to the destruction of the renal tubule epithelium.
Caused by a variety of conditions that lead to ischemia of the renal tubules, usually resulting from renal tubular injury or problems with vascular flow. It can also be induced by ingesting toxins or drug-related toxicity (e.g., gentamicin).
The most common cause of acute renal failure.
Is a reversible condition, although it can be fatal.
Diagnostic techniques used in pathology
The pathologist uses the following techniques to the diagnose diseases:
a. Histopathology
b. Cytopathology
c. Hematopathology
d. Immunohistochemistry
e. Microbiological examination
f. Biochemical examination
g. Cytogenetics
h. Molecular techniques
i. Autopsy
Pemphigoid
1. Ulcerative lesions on the skin and oral mucosa.
2. An autoimmune disease in which patients have autoantibodies against basal cells (desmosome attachment to the basement membrane).
3. Histologically, the entire epithelium appears to separate from the connective tissue. There is no acantholysis.
4. A positive Nikolsky sign is observed.
5. Complications include blindness, due to ocular lesions present in some patients.
6. Treatment: corticosteroids.