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Flashcards related to Pathology for Radiology Technologist I lecture notes.
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Pathology
The science that deals with the study of diseases.
Gross Features (Macroscopic)
Change in size, color, and consistency of the diseased organ.
Microscopic Features
Cellular and extracellular changes, such as the detection of malignant cells.
Biopsy
Examination of a tissue specimen.
Autopsy
Examination of tissue obtained from dead bodies.
Frozen Section Examination
Used for rapid diagnosis during surgery.
Cytology
Examination of body fluids or smears to detect any abnormal cells, such as malignant and inflammatory cells.
Purpose of Fixation
To prevent autolysis, bacterial decomposition, and putrefaction.
Lesions
The changes in tissues and cells produced by diseases.
Etiology
Factors and causes of disease.
Pathogenesis
Mechanism of disease.
Complication
Secondary effect of disease.
Prognosis
The course and fate of disease.
Cell Injury
Adaptive capability of cells to stimulus are exceeded or no adaptive response is possible.
Ischemia
Obstruction of arterial blood flow
Infectious agents
Viruses, bacteria, fungi, protozoa and metazoa all cause diseases.
Physical agents
Extremes of temperature, radiation, and electric shock.
Immunologic reactions
Autoimmune reactions against one's own tissues.
Reversible injury (Degeneration)
caused by mild injury, resulting in intracellular accumulation of water, fat, Protein, cholesterol, glycogen, iron, calcium or pigments.
Necrosis
Irreversible injury, resulting in death of groups of cells in living tissue. It is accompanied by acute inflammatory reaction
Apoptosis
death of individual cells surrounded by viable cells
Cellular Swelling
Is the first manifestation of almost all forms of injury to cells, it occurs due to incapability of cells to maintain ionic & fluid homeostasis.
Steatosis (fatty change)
intracellular accumulation of triglycerides within parenchymal cells
Point of no return
Irreversible mitochondrial damage and disturbances in cell membrane function
Necrosis
Irreversible injury, resulting in death of groups of cells
Apoptosis
Death of individual cells surrounded by viable cells with activation of an internally suicide program
Hyaline Degeneration
Alteration within cells or in the extracellular space that gives a homogeneous glassy pink appearance in routine histologic sections stained with hematoxylin and eosin
Russel bodies
This is hyaline change in plasma cells in chronic inflammation due to distension with immunoglobulins
Neurofibrillary tangle
Aggregation of proteins that are present in the brain of Alzheimer disease
Mucoid Degeneration
Accumulation of excessive amount of mucin in unusual location
Xanthomas and xanthelasma
Clusters of foam cells in tumor-like masses
Intracellular Accumulation
Metabolic derangements in cells can lead to the intracellular accumulation of abnormal amounts of various substances that remains either transiently or permanently
Amyloidosis
Extracellular accumulation of abnormal folded protein →→cell death
Lipofuscin pigment
An insoluble pigment, also known as lipochrome or wear-and tear pigment (aging pigment).
Melanin
Most common ; brown black pigment normally present in hair , skin, choroid of eye, meninges and adrenal medulla.
Leukoderma
Patchy skin hypopigmentation. May be congenital or acquired as in leprosy.
Hemosiderin (iron)
Systemic overload of iron.
Hemosiderosis
When accumulation of hemosiderin is primarily within tissue macrophages & is not associated with tissue damage
Hemochromatosis
When there is more extensive accumulation of hemosiderin, often within parenchymal cells, which leads to tissue damage, scarring & organ dysfunction
Bilirubin
A yellowish pigment, mainly produced during the degradation of hemoglobin. Excess accumulation of bilirubin causes yellowish discoloration of the sclerae, mucosae, & internal organs
Anthracosis
inhalation of carbon particles engulfed by macrophages. This pigment blacken the tissues of the lungs e.g. cigarette smoking, , air pollutant of urban life. coal dust in coal workers
Pathological Calcification
Abnormal intracellular or extracellular depositions of calcium salts.
Dystrophic Calcification
Occurs locally in dying tissue.
Metastatic Calcification
Calcification of normal tissues due to hypercalcemia
Inflammation
A local protective response of living vascularized tissues to kill and remove injurious agents& prepare for repair.
Add the suffix ―itis‖ to organ name
Examples:- - Tonslitis, Rhinitis,
Transient Vasoconstriction
A neural mechanism that lasts for few seconds or minutes followed by vasodilatation
Permanent Vasodilatation
result of redness and hotness in inflamed area
Increase hydrostatic pressure
lead to transudation of fluid into extracellular space
exudate
The protein-rich fluid which is now found in the extravascular space
margination
When blood slowing occurs, some leukocytes (mainly neutrophils and monocytes) fall out of the central column and begin to line the endothelium
pavementing
Adhesion of the marginating leukocytes to the endothelial surface occurs, aided by complementary receptors on the surfaces of leukocytes and endothelial cells
Emigration of leucocytes
Insertion of leukocyte pseudopodia into the junction between the endothelial cells → escape of leukocytes into the extravascular space
Chemotaxis
It is the directed movement of emigrating leukocytes to the site of injury.
Phagocytosis
the process by which the phagocytic cells recognize then engulf abnormal particles such as bacteria, dead cells, fibrin and articles to be phagocytized
opsonization
bacteria are coated by an opsonin which is an immunoglobulin or complement factor
Degranulation
performed granule-stored products are discharged or secreted into phagosomes
Chemical mediators of acute inflammation
Any substances that secreted and activated to help inflammatory process acts on blood vessels, inflammatory cells or other cells
Fate of acute inflammation - Spread
Spread (Septicemia , toxemia, lymphangitis, lymphadenitis Thrombophlebitis)
Fibrosis (Scarring): a.
a. After extensive tissue destruction. b. When the inflammatory injury involves tissues that are incapable of regeneration. c. When there is abundant fibrin exudation.
Fibrosis (Scarring): b.
a. After extensive tissue destruction. b. When the inflammatory injury involves tissues that are incapable of regeneration. c. When there is abundant fibrin exudation.
Fibrosis (Scarring): c.
a. After extensive tissue destruction. b. When the inflammatory injury involves tissues that are incapable of regeneration. c. When there is abundant fibrin exudation.
Another name for Abscess Formation Progression to Chronic Inflammation
thrombophlebitis
Suppurative/ Purulent acute inflammation Characteristic
pus is purulent thick, turbid yellowish inflammatory exudate
Serous inflammation:
Examples:- Skin blisters due to skin burns. Inflammation of serous membranes (pleura, pericardium and peritoneum)
Fibrinous inflammation
Characterized by: - an inflammatory exudate rich in fibrin, with poor fluid. Examples:- Lobar pneumonia or inflammation of serous membranes
Catarrhal inflammation
A mild form of acute inflammation of mucous membranes with excess mucus secretions
Pseudomembranous /Membranous inflammation
Occur in mucous membrane with dirty grayish false membrane forming on surface e.g. toxins of diphteria and irritant gases
Allergic inflammation
characterized by: - the presence of excessive serous fluid and many eosinophils in the inflammatory exudate. Examples:- Allergic rhinitis or Allergic conjunctivitis
Chronic Inflammation
Inflammation of prolonged duration weeks to years, in which inflammation, tissue destruction occur in same time
Granulomas/ granulomatous inflammation
A special form of chronic inflammation characterized by nodular collections of many macrophages with mixture of lymphocytes, plasma cells, giant cells.
Chronic Specific Inflammations
Show microscopic features of chronic inflammation with additional features specific to its type.
Granulomas/ granulomatous inflammation Characteristic
Macrophages have an important role
Healing by regeneration
Proliferation of cells to replace the damaged components by same type of cells and return to a normal state
Healing By Fibrosis
Replace the damaged components by scar formation due to deposition of connective (fibrous) tissue
Fibrogenesis
Migration and proliferation of fibroblasts to the site of damage by action of growth factors include PDGF, FGF, TGF – beta & Cytokins e.g. TNF, IL-1
Angiogenesis
Formation of new blood vessels by action of growth factors include VEGF, PDGF, FGF &TGF – beta
First intention healing (primary union)
Small wounds that easily close edges with epithelial regeneration predominating over fibrosis
Second intention healing (Second union)
Larger wounds that have large gap, large amount of granulation tissue & fibrosis
Bone Healing
The repair of a bone fracture
Routes of infection
Inhalation, ingestion or local contact with skin or mucous membranes, blood or blood product transfusion
Mycobacterium tuberculosis
Rod shaped Acid fast bacilli that cause tuberculosis
Primary tuberculosis
The first time TB bacilli enter the body
Organism reach organ again thru endogenous or exogenous routes
Patient has acquired secondary tuberculosis
Ghon`s focus in the Primary Pulmonary Tuberculosis
Small yellow subpleural granuloma in mid lung field
Caseating granuloma
Central caseous necrosis surrounded by epitheloid cells , Langhan‘s giant cells& lymphocytes in the granulomas of tuberculosis
Leprosy
Hansen disease, is a chronic, slowly progressive, destructive infective granulomatous disease involving peripheral nerves, skin, and mucous membranes, caused by Mycobacterium leprae
Leprosy
Chronic, slowly progressive, destructive infective granulomatous disease involving peripheral nerves, skin, and mucous membranes, caused by Mycobacterium leprae
Tuberculoid leprosy
In which lesion of tuberculosis lack caseous necrosis, occurs in patients with high resistance and is the mildest form of Leprosy
Lepromatous leprosy
Exhibits multiple tumor like lesions of the skin, eyes, testes, nerves, lymph nodes, and spleen caused by nodular infiltrates of foamy macrophages loaded with bacilli
Actinomycosis
Granulomatous disease caused by gram-positive anaerobic bacteria Actinomyces Israeli, normally present in the oral cavity and intestine as harmless commensals
Cervicofacial Actinomycosis
In which bacterial invasion of buccal mucosa may sometimes follow dental extraction and blood spread causes pulmonary
Gross pathology due to
C/b Multiple abscesses with indurated fibrotic walls in Pulmonary Actinomycosis
Tuberculosis
Chronic infectious granulomatus inflammation
Infection - causes
Bacterial, viral, protozoal, or fungal
2 Types of Exogenous
Bacterial as E.coli and Endotoxins
Define INFLAMMATION
Local protective response of living vascularized tissue to irritant
Microbial infections
Bacteria and their toxins, viruses, fungi, and parasites
Physical irritants
Burns, excess cold, ultraviolet light, irradiation
Mechanical irritants?
Trauma