Pathology Dr. Banan B. M Lecturer in pathology department
PathologyPathology literally translates to the study of suffering (Greek pathos = suffering, logos = study), the pathology is a branch of medical science that studies the causes , nature and effects of diseases. Traditionally the study of pathology is divided into general pathology and systemic pathology Disease: is the any abnormality in the structure and /or function of an organ or tissue.
Pathology has many branches: Cellular pathology: including -histopathology (the study of tissues) -cytopathology (the branch in which diagnosis of diseases are made from the study of separated cells). Forensic pathology: is the related branch concerned with medicolegal postmortem examinations. These are carried out under the aegis of a legal officer. Hematology : study the abnormalities of blood cells & clotting mechanism . Microbiology: the study of infectious diseases and their causes.
Genetics: the study of inheritance of characteristics and of diseases, or predisposition to diseases.Immunology : study the abnormalities in the immune mechanism which is responsible for defense mechanism .Chemical pathology or clinical biochemistry: is the study of body chemistry, usually by assaying the levels of substances – electrolytes, enzymes, lipids in blood or urine.
Biopsy: examination of tissue taken from living body (gross µscopical examination). Autopsy: Also known as a post-mortem examination . Is a procedure that consists of a thorough examination of the tissue taken from a human body after death to determine the cause and manner of death.
Types of biopsy: Incisional biopsy: a portion of tissue from a large lesion is taken -only diagnostic Excisional biopsy: the entire lesion is removed with a margin of adjacent normal tissue-diagnostic & therapeutic. Punch biopsy: by biopsy forceps in the uterus, cervix & oral cavity. 4) Core needle biopsy: by wide bore needle used percutaneously for sampling of internal organs. 5) Curettage biopsy: for diagnosis of internal diseases e.g. curettage of endometrium.
Cellular Responses to Stress and Toxic Insults:
- Cellular adaptations Atrophy, hypertrophy, hyperplasia, metaplasia -Cell injury *Reversible injury *Cell death (irreversible injury) 1-Necrosis 2-Apoptosis Intracellular accumulations Pathologic calcificationStages of the cellular response to stress and injurious stimuli
According to capacity of cell to division it divided into
High capacity (labile cell) Nil capacity (permanent cell) Epidermis Neurons Gastrointestinal epithelium Cardiac muscle Respiratory epithelium Bone marrow Low capacity (stable cell) Hepatocytes Pancreas Kidney Smooth muscle Bone cartilageCauses of cell injury:1-HypoxiaIschemiaCardiac & respiratory diseasesLow O2 carrying capacity ( anemia)2-Physical injury (temp, radiation, electrical shock, trauma, change in atmospheric pressure)3-Chemical agents & drugs4-Microbial agents (virus, bacterial, …..etc)5-Immunologic reactions (hypersensitivity reaction , anaphylactic shock & autoimmune diseases) 6-Genetic derangement (Down’s syndrome & sickle cell anemia)7-Nutritional imbalance (vitamin deficiency, protein deficiency, increase fat, alcoholism)8-Aging
General Principles related to cell injury: Cellular response to injurious stimuli depend on type of injury , its duration & its severity . Consequences of an injurious depend on type , status & genetic make up of the cell. Four intracellular systems are vulnerable to injury include : ATP , protein synthesis , integrity of genetic apparatus & cell membrane.
Free radical causes cell injury by: DNA fragmentation which lead to cell death & neoplasia Membrane damage through the process of lipid peroxidationCross link of proteins which enhance loss of enzyme activity or cause fragmentation of protein.Normally, there are several enzymatic and nonenzymatic systems to inactivate free radicals:glutathione peroxidase and superoxide dismutaseEndogenous or exogenous antioxidants (e.g. vitamin E, A & C & β carotene)
Cellular adaptations:1-hyperplasia:- increase in size of organ due to increase in no. of cell usually associated with hypertrophy. occurs in tissues whose cells are able to divide (labile cells), could be:Physiological: hormonal: proliferation of the breast glandular epithelium of female at puberty, or during pregnancy. compensatory: hyperplasia of the cell when part of the tissue is removed e.g. when part of the liver is resected. Pathological: Extensive hormonal stimulation e.g. endometrial hyperplasia.
Endometrial hyperplasia is an example of hormone-induced hyperplasia due to hyperestrogenism.
This is endometrial hyperplasia in which the amount of endometrium is abnormally increased.
left ventricular hypertrophy.
Hypertrophic cardiomyopathy is an example of pathological hypertrophy due to increase demand, this ultimately results in increase in the size of the organ3-Atrophy:- is the decrease in the size of the organ as a result of decrease in size of cells with loss of cell substances. causes: 1-Decrease in the workload 2-Denervation: e.g. paralysis of limb due to nerve injury or poliomyelitis. 3-Under nutrition as in starvation 4-Loss of endocrine stimulation e.g. atrophy of the gonads in hypopituitarism. 5-Aging 6-Diminish blood supply
On the left is a normal testis. On the right is a testis that has undergone atrophy
4-metaplasia: this refer to replacement of one mature cell type by an other mature cell type. It is a reversible process It may represents an adaptation of cells more sensitive to stress by other that are more resistant to the adverse environment, e.g: Squamous metaplasia of the laryngeal and bronchial respiratory epithelium due to habitual smoking. Columnar metaplasia of esophageal sq. epithelium. as a result of prolonged reflux esophagitis.Metaplasia of normal columnar (left) to squamous epithelium (right) in a bronchus
Barrett esophagus: Metaplastic transformation (arrow) of the normal esophageal stratified squamous epithelium (Lt) to mature columnar epitheliumSquamous metaplasia of bronchial epithelium
If the adaptation capacity is exceeded or if the cell cannot undergo adaptation the cell injury will occur &up to certain limit these changes are reversible and then cell can return to normal if the causative agent is remove however if the stress is severe or persistent this lead to irreversible cell injury.Cell Injury
Reversible cell injury :
It is a common type of cell injury usually due to ischemia (hypoxia) in this type of injury the cellular changes will regress and disappear when the injurious agent is removed; the cell will return to normal both morphologically and functionally Morphology of reversible cell injury: It is of two types :
2-Fatty changes(steatosis): Is abnormal accumulation of fat of triglyceride type within parenchymal cells rather than adipocytes. It is an example of reversible cell injury, seen often in the liver in which fat centrally metabolized & to less extend in heart & kidney
Causes of fatty change Toxins including alcohol Starvation & protein malnutrition Diabetes mellitus Oxygen lack (anemia & ischemia) Drugs & chemicals e.g., CCL4 Obesity Complicated pregnancy Reye syndrome
Morphology of Fatty liver Gross features : In the liver mild fatty changes shows no changes, but with further accumulation the organ enlarges & become increasingly yellow, soft & greasy to touch. Microscopically : In the early stages there are small fat vacuoles around the nucleus (microvesicular steatosis). With progression the vacuoles fuse together creating large clear space that displaces the nucleus to the periphery (macrovesicular steatosis) by H&E stain fat vacuole appear as empty space , however fat can be demonstrated by special stain ( oil red ).