Cellular Pathology Flashcards
Robbins List Causes of Cell Injury
Oxygen Deprevation (Vascular)
Chemical Agents (Intoxication)
Infectious Agents (Infectious)
Immunologic Reactions (Inflammatory)
Genetic Factors (Congenital)
Nutritional Imbalances (Environmental, Metabolic)
Physical Agents (Trauma)
4 types of adaptions
Hypertrophy
Hyperplasia
Atrophy
Metaplasia
Hypertrophy
Increase in cell size
Hyperplasia
Proliferation
Atrophy
Decrease in cell size
Metaplasia
change of one type of differentiated cell into another type of differentiated cell
Hx GERD. What cellular change might you see at the gastroesophageal junction
Protective metaplasic changes result in intestinal epithelium at lowe GE junction
45 year old M with barretts esophagus. What might you see?
A small region of red, velvet-like mucosa in the lower esophagus
27 year old M with N x 1 week, scleral icterus, and elevated AST and ALT
Defect in cell membrane
19 year old previously healthy collapeses playing bball. Died.
Age related atheromatous plaque buildup
MI due to CAD
Septal hypertrophy (congenital)
Congenital narrowing of the aorta with poor blood flow to the legs
Cardiac myxoma (pedunculated tumor within the L atrium)
Septal Hypertrophy
6 types of necrosis
Coagulative
Liquefactive
Gangrenous
Caseous
Fat necrosis: Saponification
Fibroid necrosis
Coagulative Necrosis
Seen in ischemia/ infarcts in most tissues (except brain)
Due to ischemia or infarction: proteins denature, then enzyme degredation
Liquefactive necrosis
Seen in bacterial abcesses, brain infarcts (due to increased fat content)
Due to neutrophil release lysosomal enzynes that digest tissue. Enzymatic degredation first, then proteins denature
Gengrenous Necrosis
Seen in distal extremity after chronic ischemia
Due to:
Dry: ischemia
Wet: superinfection
Caseous Necrosis
Seen in TB, systematic fungi
Due to macrophages wall off the infecting microorganisms lead to granular debris
Fat necrosis
Seen in enzymatic acute pancreatitis (saponification of pancreatic fat) and nonenzymatic traumatic (eg breaest injury)
Damaged cells release lipase which breaks down triglycerides in fat cells
Chalkiness
Fibrinoid necrosis
Immune reaction in vessels
Immune complexes combine with fibrin leading to vessel wall damage
Diseases due to misfolded proteins (think neurodegenerative)
Huntingtons
Parkinsons
Alzheimers
Failure to degrade a metabolite due to inherited enzyme deficiencies
storage diease
Cellular accumulation of normal substance
most neurodegenerative dz, fatty liver: acquired by inadequate removal of a normal substance
Cellular accumulation of abnormal endogenous substance
cystic fibrosis, alpha1antitrypsin, other. Accumulation of an abnormal endogenous substance as a result of genetic or acquired defect
Failure to degrade a metabolite
inborn errors of metabolism/ storage dz. Failure to degrade a metabolite due to inherited enzyme deficiencies
accumulation of abnormal exogenous substance
pneumoconioses, scoliosis, asbestosis, berylliosis. deposition and accumulation of an abnormal exogenous substance
Dystrophic calcification
dystrophic calcification is encountered in areas of necrosis of any type. It is virtually inevitable in the atheromas of advanced atherosclerosis, associated with intimal injury in the aorta and large arteried and is characterized by the accumulation of lipids
