📖 General Pathology
Malnutrition
Malnutrition
A. Marasmus - calorie malnutrition
A child with marasmus suffers growth retardation and loss of muscle. The loss of muscle mass results from catabolism and depletion of the somatic protein compartment.
With such losses of muscle and subcutaneous fat, the extremities are emaciated; by comparison, the head appears too large for the body. Anemia and manifestations of multivitamin deficiencies are present, and there is evidence of immune deficiency, particularly of T cell-mediated immunity.
B. Kwashiorkor - protein malnutrition - importance of protein quality as well as quantity
Marked protein deprivation is associated with severe loss of the visceral protein compartment, and the resultant hypoalbuminemia gives rise to generalized, or dependent, edema.
The weight of children with severe kwashiorkor is typically 60% to 80% of normal.
However, the true loss of weight is masked by the increased fluid retention (edema).
Children with kwashiorkor have characteristic skin lesions, with alternating zones of hyperpigmentation, areas of desquamation, and hypopigmentation, giving a "flaky paint" appearance.
Hair changes include overall loss of color or alternating bands of pale and darker hair, straightening, line texture, and loss of firm attachment to the scalp.
An enlarged, fatty liver (resulting from reduced synthesis of carrier proteins) and a tendency to develop early apathy, listlessness, and loss of appetite.
The bone marrow in both kwashiorkor and marasmus may be hypoplastic, mainly because of decreased numbers of red cell precursors. How much of this derangement is due to a deficiency of protein and folates or to reduced synthesis of transferrin and ceruloplasmin is uncertain. Thus, anemia is usually present, most often hypochromic microcytic anemia, but a concurrent deficiency of folates may lead to a mixed microcytic-macrocytic anemia.
C. Most cases of severe malnutrition are a combination of A and B usually characterized by:
• Failure of growth
• Behavioral changes
• Edema (kwashiorkor)
• Dermatosis
• Changes in hair
• Loss of appetite
• Liver enlargement
• Anemia
• Osteoporosis
Muscle pathology
General PathologyMuscle pathology
1. Myasthenia gravis
a. An autoimmune disease caused by autoantibodies to acetylcholine receptors at the neuromuscular junctions.
b. Characterized by muscle weakness or the inability to maintain long durations of muscle contractions; this worsens during exercise but recovers after rest.
c. Affects various muscle groups, including:
(1) Eyes—diplopia, ptosis.
(2) Neck—dysphagia, problems swallowing or speaking.
(3) Extremities—arms and legs.
d. Treatment: cholinesterase inhibitors(neostigmine), anti-immune therapy.
2. Muscle tumors
a. Rhabdomyoma—benign tumor of skeletal muscle.
b. Leiomyoma
(1) Benign tumor of smooth muscle.
(2) Most common tumor found in women.
(3) Usually affects the uterus, although it can occur anywhere.
c. Rhabdomyosarcoma
(1) Malignant tumor of skeletal muscle.
(2) Most common sarcoma found in children.
(3) Usually affects head and neck region—orbit, nasal cavity, and nasopharynx.
Immunodeficiency
General PathologyImmunodeficiency
This may be :-
- Congenital (Primary)
- Acquired (Secondary)
Features : Complete or near complete lack of T & B lymphoid tissue. Fatal early in life Even with marrow grafting, chances of graft versus host reaction is high.
B. T Cell Defects :
- Thymic dysplasia
- Digeorge’s syndrome
- Nazelof’s syndrome
- Ataxia teltngiectaisa
- Wiscott Aldrich’s syndrome
These lessons show predominantly defective cell mediated immunity. But they may also show partial immunoglobulin defects cell mediated immunity. But they may also show partial immunoglobulin defects due to absence og T-B co-operation.
C. Humoral immunity defects.
Bruron type- aggammaglobulinaemia.
- Dysgammaglobulinaemias-variable immunodeficiency’s of one or more classes.
Acquired deficiency
A. Immuno suppression by :
- Irradiation.
- Corticoids.
- Anti metabolites.
- Anti lymphocyte serum.
B. Neaplasia of lymphoid system :
- Hodgkin's and Non Hodgkin's lymphomas.
- Chronic lymphocytic leukaemia..
- Multime myeloma and other paraproteinaemias (normal immunoglobulins reduced in spite of hyperglobulinaemia).
c. excessive protein loss.
- Nephrotic Syndrome.
- Protein losing enteropathy.
DEGENERATION
General PathologyDEGENERATION
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.