DMP 715 Path Exam 1 Objectives Overview
Terms
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- Disease defn:
- Disease defn: absence of health; dyshomeostasis
- Factors affecting Disease (2)
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Host
Environmental - Host Factors affecting Disease (6)?
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Host Factors affecting Disease (6)
heredity, age, sex, species, immune status, mental status - External Factors affecting Disease (5)
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External Factors affecting Disease (5)
poor management, climate, microorganisms, chemicals, physical factors -
Pathology defn:
must understand what to understand pathology?
Pathology is: -
Pathology defn: study of disease
must understand what to understand pathology? normal
Pathology is: a process - Nomal cell is focal point for:
- Nomal cell focal point for: studying pathology
- cell components (7):
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cell components (7):
plasma membrane
cytosol
mitochondria
endoplasmic reticulum and golgi
lysosomes and peroxisomes
cytoskeleton
nucleus - Cell cycle phases:
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Cell cycle phases:
G0, G1, S, G2, M - Cell Cycle Regulation:
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Cell Cycle Regulation:
complex and critical - Different _____ _____ go through the ____ _____ at different ________. ________ _______ are important.
- Different cell types go through the cell cycle at different rates. Local Conditions are important.
- Labile cells:
- Labile cells always in cell cycle, need to constantly replace like intestinal epithelium
- Stable cells:
- Stable cells are resinging in G0, rarely need additional cells, injury or other reason can go to G1 to grow
- Permanent cells:
- k. Permanent cells are cells that are highly differentiated and do not divide, do not enter cell cycle, include neurons and cardiac myocytes
- G1
- G1 – (growing) cell increases its biosynthetic activities to the level of a majure cell during G1 phase
- S
- S phase (b4 mitosis) initiated when DNA synthesis begins and ends when DNA content is doubled
- G2
- G2 – gap between DNA synthesis and cell division
- M
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M phase – cell division occurs
Mitosis = nuclear divison
Cytokinesis – process of cytoplasmic division
Result = two genetically identical cells - G0
- G0 phase: (resting)cell has exited the cell cycle and is not directing its metabolism towards replication
- Cell Functions (5)
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Cell Functions (5)
Exocytosis
Endocytosis
Communication
Cell Aging
Apoptosis - Exocytosis
- Exocytosis: process by which large molecules can leave the cell and be released into the extracellular space
- Endocytosis (2 types)
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Endocytosis: process by which extracellular molecules are taken into a cell
Pinocytosis: uptake of fluid or small molecules
Phagocytosis: uptake of large particles - Communication (3 types and definitions)
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Communication (3 types and definitions)
1)Autocrine signals involve a single cell – self stimulation
-Cell produces factor or cytokine that stimulates its own membrane receptors
2) Paracrine – affect cells in close proximity
-One cell may release a mediator that stimulates receptors on nearby cells, e.g. inflammatory
3) Endocrine – systemic and can affect cells anywhere in the body (e.g. hormones in endocrine tissues and organs) - Cell Aging (3 mechanisms)
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Cell Aging (3 mechanisms)
a. alterations in gene expression
i. inhibit cell cycle, express certain genes to enhance aging, cumulative damage to DNA
b. telomere shortening
i. telomerase maintains telomere length and is not present in somatic cells – if present predispose to neoplasia
c. cell damage resulting from normal metabolism
i. collective damage over life of cell - Apoptosis defn:
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Apoptosis defn:
programmed cell death - cell junction
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cell junction
18. understand the role of the basement membrane and its importance in pathology
a. basement membranes form the border between the ECM and plasma membrane of cells that are fixed within the ECM
b. specialized component of ECM
c. functions include selective permeability and scaffolding - Extracellular matrix (3 components)
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Extracellular matrix (3 components)
1) Structural component: collagen and elastin
2) Absorptive component: glycosaminoglycans and proteoglycans
3) Adhesive component: Fibronectin, laminin - Adaptation defn:
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Adaptation:
Change in the demands on the cell, nutrients, cell microenvironment - 3 outcomes to Altered/injured cell:
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3 outcomes to Altered/injured cell:
Adaptation
Sublethal damage (injury)
Cell Death - Cell Adaptation (4 ways)
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Cell Adaptation (4 ways)
Hyperplasia
Hypertrophy
Atrophy
Metaplasia - Hyperplasia defn:
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Hyperplasia defn:
increased cell number
physiologic or pathologic - Hypertrophy defn:
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Hypertrophy defn:
increase cell size
predominately in myofibers
physiologic or pathologic
most hyperplasitc cells show some hypertrophy - Atrophy defn:
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Atrophy defn:
Decrease in cell size and also number
Physiologic or pathologic
Affected organs are small - Metaplasia defn:
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Metaplasia defn:
Replacement of one cell type with another
protective response
rarely beneficial - cell injury mechanisms (3)
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cell injury mechanisms (3)
loss of membrane integrity
loss of ability to produce energy
genetic damage - Loss of membrane integrity (3 methods)
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Loss of membrane integrity (3 methods)
free radical - induced injury (many protective (antioxidant) substances)
Phospholipase-induced injury - activated by increased cytoplasmic calcium and others
direct injury -
Loss of ability to produce energy
How is energy formed?
What results (4)? -
Loss of ability to produce energy
How is energy formed? ATP is produced by oxidative phosphorylation or glycolysis
What results?
1) failure of membrane pumps
2) decrease cell pH and protein synthesis
3) membrane and cytoskeleton degradation
4) organelle dysfunction and leakage -
Genetic Damage
Definition & results (3): -
Genetic Damage
Definition & results (3):
Genetic damage is a mutation
1) Most damage is repaired
2) unrepaired damage leads to apoptosis
3) Mutated cells that replicate can lead to:
- disease or increased incidence of disease
- neoplastic transformation
+ interference with cell cycle, repair or apoptosis pathways
+ anaplasia and pleomorphism - Morphology of injured cells (3 changes due to):
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Morphology of injured cells (3 changes and description):
1) Cell Swelling (oncosis)
-membrane injury or lack of energy for pumps
2) fatty change (lipidosis)
-may reflect cell overload or true injury
3) intracellular accumulations
-metabolic products
-pigments
-exogenous substances - Apoptosis (5 points)
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Apoptosis:
1) programmed/Physiologic death
2) Requires energy
3) Multiple pathways ending with caspase activation
4) A balance between pro- and anti- apoptotic influences
5) Morphology: Shrunken and no-tissue damage - Necrosis (4 points)
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Necrosis
1) a manifestation of cell injury and damage
2) does not require energy
3) can be activated by similar stimuli that activate apoptosis
4) morphology: cell swelling and disintegration with tissue damage -
Tissue Injury
Combination of:
Primary injury usually to:
Some times primary injury to: -
Tissue Injury
Combination of: cells & ECM
Primary injury usually to: cells
Some times primary injury to: ECM - Primary Cell Injury (5 types)
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Primary Cell Injury (5 types)
1) coagulative necrosis (hypoxia)
2) liquefactive necrosis (lymphocytes --> pus & abscesses)
3) caseous necrosis (chronic inflammation, type of coagulative)
4) gangrenous necrosis (coagulative w/bacteria undergo putrefaction)
5) fat necrosis (action of lipases on adipose tissue) - Primary ECM damage (4 types)
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Primary ECM damage (4 types)
1) Increased destruction (inflammation)
2) Decreased production
3) Excessive production (fibrosis)
4) Abnormal deposits
-calcification (dystrophic and metastatic)
-amyloidosis (primary AL and secondary AA abnormal deposits) - amyloid defn:
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amyloid defn:
acellular, amorphous material
95% fibril proteins, 5% P component protein and other glycoproteins - amyloidosis defn:
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amyloidosis defn:
b. Amyloidosis – due to deposition of a chemically diverse protein that has a beta pleated sheet structure, can be systemic or local - Primary amyloidosis:
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Primary amyloidosis:
i. Primary: not common, associated with immunologic dyshomeostasis with type AL protein usu animal with plasma cell neoplasms (multiple myeloma) - secondary amyloidosis:
- secondary amyloidosis: associated with chronic inflammation and deposition of type AA protein, stimulated by cytokines, occurs with inflammation due to Abnormal breakdown of SAA (serum amyloid associated protein) or structural abnormalities in SAA
- dystrophic calcification:
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dystrophic calcification:deposition of calcium in necrotic tissue
i. Initiated extracellularly by phospholipids which are derived from degenerating or aging cells
ii. Calcium bound to phospholipids or membrane components binds phosphate to form a calcium phosphate microcrystal
iii. Occurs in necrotic tissue -
Developmental disease defn:
causes and examples(2) -
Developmental disease defn: abnormal embryogenesis or postnatal development
causes and examples(2):
1) genetic - chromosomal defects, single gene anomalies, multifactor abnormalities
2) environmental - infectious agents, chemicals, nutritional - Mechanisms of abnormal development (6)
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Mechanisms of Abnormal Development (6)
1) Arrest or inhibition of development
2) persistence of fetal structures
3) Failure of groove/fissure closure
4) aberrant growth
5) duplicaitons
6) lack of coordination - Developmental Disease types and examples (5)
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Developmental disease types and exapmles (5)
1) Musculoskeletal - arthrogryposis, Chondrodysplasia, Osteopetrosis
2) Nervous System - Holoprosencephaly, hydrocephalus/hydranencephaly
3) Cardiovascular system - Patent ductus arteriosus, septal defects, Tetralogy
4) Reproductive system - Hermaphrodites and pseudohermaphrodites
5) Integumentary system - ichthyosis, hypotrichosis, epitheliogenesis imperfecta - Metabolic Disease cause/due to:
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Metabolic Disease cause/due to:
Dyshomeostasis - Causes of Metabolic Disease: (3 and examples)
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Causes of Metabolic Disease: (3 and examples)
1) Genetic - inherited storage disease
2) Nutritional - inadequate ration, uptake or absorptoin
3) Hormonal - disregulation of metabolic processes - Central metabolic organs/tissues (5)
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Central metabolic organs/tissues (5):
1) liver
2) kidney
3) endocrine system
4) gastrointestinal system
5) bone - Two types of metabolic disease:
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two types of metabolic disease:
reversible vs. irreversible - Pathogenesis of disease (involves what? (2 aspects))
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Pathogenesis of disease (involves what? (2 aspects))
central metabolic organs
primary disease vs. secondary disease
e.g. chronic renal failure in dogs -
Morphology of disease
specific?
type?
eg? -
Morphology of disease
specific? - non-specific
type? primary vs. secondary disease
eg? hepatic inflammation / neoplasia vs. lipidosis