Gen Path Exam 1 - Cell Injury/Death, Inflammation, Wound Healing, and Hemostasis Flashcards
Give examples of continuously dividing tissue
Skin, mouth, vagina, cervix, GI, exocrine ducts
Give examples of stable tissue that divide only in response to injury
Endothelial cells, fibroblasts, SM, solid organs (kidney, liver, pancreas)
Give examples of permanent tissue that never proliferate after birth
Neurons, heart muscle, skeletal muscle
Name endogenous causes of stress/injury
Hypoxia (most common)
Immunologic rxns
Genetic abnormalities
Aging
Name exogenous causes of stress/injury
Toxins (pollutants, asbestos, cig smoke)
Infectious pathogens
Nutritional imbalance
Physical agents (trauma)
Increase in size of cell and organ
Hypertrophy
Occurs in cells with limited capacity to divide (ex: skeletal muscle)
Hypertrophy
Give an example of physiologic hypertrophy
Uterus during pregnancy
Give an example of pathologic hypertrophy
Heart during hypertension
Increase in # of cells (controlled)
Hyperplasia
Occurs in tissue capable of division
Hyperplasia
Give an example of physiologic hyperplasia
Breast development (hormonal)
Liver regeneration (compensatory)
Give an example of pathologic hyperplasia (caused by excessive hormonal or growth factor stimulation)
Endometrial hyperplasia
Benign prostatic hyperplasia
Decrease in size of cells
Atrophy
Loss of cell substance by decreased protein synthesis or increased protein degradation
Atrophy
What are the causes of atrophy?
Decreased workload, blood supply, and endocrine stimulation
Inadequate nutrition
Aging
One cell type replaced by another cell type
Metaplasia
New type may better withstand stress, but can predispose to malignant transformation
Metaplasia
Give an example of metaplasia
Ciliated columnar cells become stratified squamous in bronchi of smokers
Disordered growth
Dysplasia
Division of precancerous cells, may be reversible, but may progress to cancer
Dysplasia
Failure of cell production in embryogenesis
Aplasia
Decrease in cell production in embyrogenesis
Hypoplasia
Describe the tolerance for ischemia without irreversible injury for:
Neurons
Heart cells
Skeletal muscle
Neurons = 3-5 mins
Heart cells = 1-2 hrs
Skeletal muscle = hrs
When stress exceeds cell’s adaptive ability
Cell injury
What are the 4 types of cell injury in this course?
Hypoxia
Oxidative stress
Reversible
Irreversible
Oxygen deficiency
Hypoxia
Examples of hypoxia
Lung disease
Anemia
Specific type of hypoxia
Ischemia
Reduced blood supply leads to oxygen deficiency (ex: blocked artery)
Ischemia
ATP needs _______ and cell metabolism needs ________
oxygen; ATP
Induced by reactive oxygen species
Oxidative stress
Oxygen derived free radicals
Reactive oxygen species
Chemically unstable, attack nucleic acids, proteins, and lipids
Free radicals
What do small amounts of reactive oxygen species normally result from?
Respiration and energy production
What do reactive oxygen species do normally? Where are they produced?
Destroy microbes
Produced in phagocytic leukocytes
Accumulation of reactive oxygen species is BAD. When does this happen?
Radiation
Exogenous chemicals
Inflammation
What mechanisms are there to minimize injury by reactive oxygen species?
Free radical scavengers
Anti-oxidants
Name the 3 free radical scavengers
Superoxide dismutase
Glutathionine peroxidases
Catalase
Block formation of free radicals and scavenge after they have been formed
Anti-oxidants
Can be exogenous or endogenous
Anti-oxidants
Name 4 anti-oxidants
Vitamins E, A, C
Beta carotene
What are the mechanisms of injury by reactive oxygen species?
Membrane damage
DNA damage
Protein cross-linking
Normal function/morphology returns when stimulus leaves
Reversible cell injury
What is the most common change in reversible cell injury?
Cellular swelling
Cells can’t recover and will die
Irreversible cell injury
What are the main causes of irreversible cell injury?
Loss of mitochondrial function
Loss of structure/function of membranes
Loss of DNA/chromatin structural integrity
What can happen to the nucleus during cell death?
Condensation (pyknosis)
Fragmentation (karyorrhexis)
Dissolution (karyolysis)
What are the 2 different mechanisms of cell death?
Necrosis
Apoptosis
Describe necrosis
Cell membranes fall apart
Enzymes leak out and digest cell
Inflammation
Messy
Damages surrounding cells
Describe apoptosis
Programmed cell death
Cell shrinks
Nucleus condenses and fragments
Apoptotic bodies fall from cell and removed by macrophages
NO inflammation
Which necrosis?
Caused by infarct in solid organs; does NOT occur in brain
Coagulative necrosis
Which necrosis?
Tissue looks firm
Coagulative necrosis
Which necrosis?
Cell outlines preserved, NO NUCLEUS, eosinophilic (pink)
Coagulative necrosis
Which necrosis?
Caused by bacterial/fungal infections and hypoxia in CNS
Liquefactive necrosis
Which necrosis?
Dissolution of tissue into viscous liquid
Liquefactive necrosis
Which necrosis?
Ischemia of limb
Gangrenous necrosis
Which necrosis?
Coagulative necrosis -> looks like mummified tissue
Can have superimposed liquefactive necrosis
Gangrenous necrosis
Which necrosis?
Caused by TB infections because body tries to wall off infection
Caseous necrosis
Which necrosis?
Cheese-like, friable yellow/white necrotic tissue
Caseous necrosis
Which necrosis?
Caseating granulomas
Caseous necrosis
Granuloma with central necrosis
Caseating granuloma
Group of macrophages that form in response to infection, inflammation, foreign material
Granuloma
Which necrosis?
Caused by lipase breaking down fat cells, Ca2+ accumulates, seen in pancreatitis
Fat necrosis
Which necrosis?
Chalky, white deposits in fat
Fat necrosis
Which necrosis?
Outlines of dead fat cells, NO NUCLEUS
Fat necrosis
Which necrosis?
Caused by immune-mediated conditions, hypertension, occurs in vessels
Fibrinoid necrosis
Which necrosis?
Eosinophilic (pink) deposits in walls of blood vessels
Fibrinoid necrosis
Normal response to injury, cells travel where they’re needed to kill infectious agents and clean damage
Inflammation
Name the cardinal signs
Heat (calor)
Redness (rubor)
Swelling (tumor)
Pain (dolor)
Loss of function (functio lasea)
Main cell type in acute inflammation
Neutrophils
How long does acute inflammation develop?
Mins/hrs
How long does acute inflammation last?
Hrs/days
Describe the tissue injury in acute inflammation
Mild and self-limited
Main cell types in chronic inflammation
Lymphocytes and macrophages
How long does chronic inflammation develop?
Days
Describe the tissue injury in chronic inflammation
Severe/progressive
What are the 4 causes of inflammation?
Infection (bacteria, fungus, parasite)
Necrosis
Foreign bodies (exogenous, endogenous)
Immune reactions (allergies, autoimmune diseases)
What are the 5 “Rs” of the inflammatory response?
Recognition of injurous agent
Recruitment of leukocytes
Removal of agent
Regulation of response
Resolution
What are the 3 key features of “Recognition of injurous agent”
Toll-like receptors
Inflammasomes
Circulating proteins
Receptors for microbes
Toll-like receptors
Where are Toll-like receptors found?
Plasma membranes for extracellular microbe detection
Endosomes for ingested microbe detection
What are Toll-like receptors expressed by?
Macrophages and dendritic cells