Section 1
Preview this deck
General pathology
Front
| 5 | 0 | ||
| 4 | 0 | ||
| 3 | 0 | ||
| 2 | 0 | ||
| 1 | 0 |
Active users
1
All-time users
1
Favorites
0
Last updated
1 year ago
Date created
Mar 14, 2020
Cards (61)
Section 1
(50 cards)
General pathology
is concerned with the common reactions of cells and tissues to injurious stimuli
Where is fatty change principally encountered?
In organs that are involved in lipid metabolism
liquefactive necrosis
Occurs in the brain because of its lack of any substantial supporting stroma; thus necrotic neural tissue may totally liquefy There will be a glial reaction around the periphery, and the site of necrosis will be marked by an eventual cyst. This pattern of necrosis is seen in infections
Type of necrosis that is characterized by digestion of the dead cells resulting in transformation of the tissue into a liquid vicious mass.
Liquefactive necrosis
What is the hallmark of reversible cell injury in microscopy?
Cellular swelling and fatty change
What type of cell death is seen with tuberculosis?
Caseous necrosis
Physiological Apoptosis
Programmed destruction of cells during embryogenesis. Involution of hormone dependent tissues upon hormone withdrawal. Ex: Endometrial cell breakdown during menstrual cycle and ovarian follicular atresia in menopause. Cell loss in proliferating cell populations to maintain homeostasis. Ex: Immature lymphocytes in the bone marrow and thymus that fail to express useful antigen receptors. Elimination of potentially harmful self-reactive lymphocytes
Metaplasia
Mature cell type is replaced by a different mature cell type
Hypertrophy
increase in cell size Physiologic: Is caused by increased functional demand or by stimulation by hormones and growth factors. Example: Increased workload Pathologic: Develop response to stress signals. Example: Chronic Hemodynamic Overload
Hyperplasia
increase in number of cells Physiologic Hyperplasia Due to the action of hormones o growth factors when there is a need to increase functional capacity of hormone sensitive organs or when there is a need for compensatory increase after damage or resection Hormonal Hyperplasia Compensatory Hyperplasia Pathologic Hyperplasia Most forms of pathologic hyperplasia are cause by excessive hormonal or growth factor stimulation Example: Endometrial Hyperplasia
atrophy
reduction in the size of an organ or tissue due to a decrease in cell size and number.
Mechanism of atrophy
Nutrient deficiency and disuse → Activation of the ubiquitin proteasome pathway (Cellular proteins are target for degradation by proteosomes)
What is necrosis?
Damage to cell membranes and loss of ion homeostasis
Pro-apoptotic
Bax and Bak
caseous necrosis
degeneration and death of tissue with a cheese-like appearance A pattern of necrosis in which the dead tissue is structureless
Mechanism of metaplasia
Result of reprogramming of stem cells that are known to exist in normal tissues, or undifferentiated mesenchymal cell present in connective tissue.
Gangrenous Necrosis
death of tissue from severe hypoxic injury
When does fatty change occur?
in hypoxic injury and various forms of toxic or metabolic injury
Fibrinoid Necrosis
usually blood vessels death of a cell is replaced by fiber
causes of cell injury
Hypoxia, physical agents, toxins, immunological reaction, nutritional imbalances, protein energy malnutrition, obesity, aging, etc.
anti-apoptotic
Bcl-2 and Bcl-XL
systemic pathology
examines the alterations and underlying mechanisms in organ specific diseases such as ischemic heart disease.
Apoptosis vs. Necrosis
Necrosis causes cells to swell and burst, whereas apoptotic cells shrink and condense
Apoptosis in Pathological Conditions
1. Apoptosis eliminates cells that are injured beyond repair without eliciting a host reaction 2. DNA damage 3. Accumulation of misfiled proteins 4. Infections
Nucleare changes during necrosis
Assume one of the three patterns, all resulting from a breakdown or DNA and chromatin Pyknosis Kayorrhexis Karyolysis
Cell death: necrosis
The morphological appearance of necrosis is the result of denaturation of intracellular proteins and enzymatic digestion of the lethally injured cell. Necrotic cells are unable to maintain membrane integrity Their contents often leak out, a process that may elicit inflammation in the surrounding tissue.
Manifested by the appearance of triglycerides containing lipid vacuoles in the cytoplasm
Fatty change
Pathology
study of the structural, biochemical, and functional changes in cells, tissues, and organs that underlie disease
What type of necrosis occurs in the brain?
Liquefactive necrosis
Ultrastructural Changes of Reversible Cell Injury
Plasma membrane alterations, such as blebbing, blunting, and loss of microvilli. Mitochondrial changes, including swelling and the appearance of small amorphous densities Dilation of the ER, with detachment of polysomes Nuclear alterations with disaggregation of granular and fibrillar elements
Fat necrosis
Fatty tissue is broken down into fatty acids
Autophagy
"self-eating it occurs in an attempt to reduce nutrient demands → formation of autophagy vacuoles.
Necrosis changes to the cell
Lysosomal enzymes enter the cytoplasm and digest the cell Cellular contents also leak through plasma membrane (inflammation) Results from ischemia, toxins, infections, trauma
Intrinsic pathway of apoptosis
mitochondrial leakage of cytochrome c into the cytosol with eventual activation of caspases 1. BCL family 2. Anti-apoptotic 3. Pro- Apoptotic
Pathologic atrophy
occurs as a result of decreases in workload, pressure, use, blood supply, nutrition, hormonal stimulation, and nervous stimulation
Histological changes in apoptosis
Cell shrinkage Chromatin condensation Formation of cytoplasmic blebs and apoptotic bodies Phagocytosis of apoptotic cells or cell bodies, usually by macrophages
Reversible Injury
Swelling of the cell and its organelles. Blobbing of the plasma membrane Detachment of ribosomes from the ER, and clumping of nuclear chromatin Decreased generation of ATP Loss of cell membrane integrity. Defects in protein synthesis, cytoskeletal damage, and DNA damage Persistent or excessive injury →I Irreversible injury and cell death
What is hypoxia?
deficiency in the amount of oxygen reaching the tissues
What are some causes of hypoxia?
Reduced blood flow (ischemia- in addition result sin a deficiency of essential nutrients and a build up of toxic metabolites) Cardiorespiratory failure Decreased oxygen-carrying capacity of the blood (anemia or carbon monoxide poisoning)
Mechanisms of apoptosis
1. Apoptosis results from the activation of enzymes called caspases 2. Caspases exist as inactive proenzymes, or zymogens 3. Initiation Phase: During which some caspases become catalytically active 4. Execution Phase: During which other caspases trigger the degradation of critical cellular components
necrosis morphology
1. increase eosinophilia (H&E) 2. appear with a glassy homogenous appearance (as a result of glycogen particles 3. The cytoplasm becomes vacuolated and appears moth-eaten 4. Dead cells may be replaced by large, whorled phospholipid masses called myelin figure that are derived from damaged cell membranes 5. Those phospholipid are degraded into fatty acids; calcification of such fatty acid residues results in the generation of calcium soaps.
Necrosis
death of tissue
Apoptosis
programmed cell death Pathway of cell death in which cells activate enzymes that degrade the cells own nuclear DNA and nuclear cytoplasmic proteins
What is the most common form of necrosis?
Coagulative necrosis
Cell injury
results when cells are stressed so severely that they no longer are able to adapt or when cells are exposed to inherently damaging agents or suffer from intrinsic
What is cellular swelling?
Appears whenever cells are incapable of maintaining ionic and fluid homeostasis and is the result of failure of energy-dependent ion pumps I'm the plasma membrane
BCL family
Family of proteins that regulate mitochondrial permeability
Type of necrosis that occurs from acute inflammation affecting tissues with numerous adipocytes such as the pancreas and breast tissue?
Fat necrosis
Coagulative necrosis
Most common form of necrosis and can occur in most organs Following devitalization, the cells, retain their outline as their protein coagulate and metabolic activity ceases Default patter of necrosis associated with ischemia or hypoxia in every organ in the body except the brain
Fatty change
Manifested by the appearance of lipid vacuoles in the cytoplasm Seen mainly in cells involved in an d dependent on fat metabolism, such as hepatocytes Principally involved in organs that are involved in lipid metabolism The cytoplasm or injured cells also may become redder (eosinophilic)- Becomes much more pronounced with progression of necrosis
Section 2
(11 cards)