Altered Cellular and Tissue Biology Flashcards
What are the 4 most significant cellular adaptive changes
- atrophy
- hypertrophy
- hyperplasia
- metaplasia
Dysplasia
atypical hyperplasia (not an adaptive change) abnormal change in size, shape and organization of mature tissue cells.
NOT cancer and may not progress to cancer. Dysplastic tissues that do not involve the entire thickness of the epithelium may be completely reversible.
What are the causes of cellular injury (8)
- hypoxia
- free radicals
- chemicals
- Infection
- Inflammation
- Genetic factors
- Starvation
- Physical trauma
Pathologic Calcification
calcium accumulation within surrounding damaged tissue
Autophagy
occurs during times of cellular stress and is typically triggered by deficiency of nutrients or growth factors.
What 4 biochemical themes are important to cell inury
- Hypoxia
- Depletion of ATP
- Increased concentration of intracellular calcium and loss of calcium steady state
- Defects in membrane permeability
Effects Hypoxia on a cell
-Can induce inflammation and inflamed areas can become hypoxic
-Common in: bacterial infections, wounds, CV defects and cancer
Reperfusion Injury Cause and effect
Caused by the generation of highly reactive oxygen intermediates or radicals and
-promotes proinflammatory neutrophil adhesion to the endothelium
Oxidative Stress
-Can activate intracellular signaling pathways modulate enzymes, and transcription factors.
-Difficult to control and can initiate chain reactions
Effect of Free radicals
- Lipid peroxidation or the destruction of unsaturated fatty acids
- alterations of proteins, protein loss, and protein misfolding
- Mutations in DNA
Livor mortis
the purple discoloration caused by blood pooling in the most dependent, or lowest tissues.
Begins in 30 min to 1 hour after death and becomes fixed 6-8 hours after death
Coagulative necrosis
result of protein denaturization where albumin is transformed from gelatinous state to firm opaque substance (infarct)
Caseous necrosis
commonly results from pulmonary TB infection. curdled or cheese like gross appearance. combines elements of both coagulative and liquefactive necrosis.
Dead cells disintegrate but the debris is not completely hydrolyzed causing a granulomatous inflammatory response resulting in formation of soft granular tissues resembling clumped cheese.
Atrophy
decrease in cellular size
Hypertrophy
increase cellular size
Hyperplasia
increase in the number of cells
Metaplasia
reversible replacement of one mature cell type by another, sometimes less differentiated, cell type. Associated with tissue damage, repair, and regeneration.
what changes does a cell undergo due to ischemia
-Lack of oxygen leads to decreased ATP
-decreases the Na pump and increases anaerobic glycolysis
-Na & Ca increase in the cell, K increases OUTside the cell. At the same time lactic acid is increasing
-Intracellular water increases as swelling, pH is falling, protein synthesis falls.
IS REVERSIBLE IF O2 IS DELIVERED QUICKLY
Liquefactive necrosis
digestion of the dead cells transforming tissue into viscous liquid. Common in CNS hypoxic injury, also seen in bacterial and fungal infections. (creation of pus)
Gangrene
Tissue necrosis caused by hypoxia and subsequent bacterial infection
Suffocation vs strangulation
Suffocation: process of dying as a result of lack of oxygen. can be from an airway obstruction or environmental
Strangulation: compression of blood vessels and air passages externally on the neck.
Penetrating vs perforating bullet wounds
Penetrating: bullet remains in the body
Perforating: bullet exited the body
dystrophic calcification vs metastatic calcification
Dystrophic: accumulation of calcium salts. always a sign of pathologic change, as it only occurs in injured or dead cells. (ca in the cytosol can cause activation of protein kinases, activation of phospholipases and membrane damage)
Metastatic: can occur in uninjured cells in those with hypercalcemia.
Rigor mortis
muscle stiffening or rigidity that begins within a few hours of death.
Starts in smaller muscles and increases over time, maintains for about 12 hrs, then diminishes in the same order as it started over the next 12-14 hrs.
Apoptosis vs necrosis
Apoptosis: regulated or programmed cell process by the “dropping off” of cellular fragments called apoptotic bodies.
Necrosis: rapid loss of the plasma membrane structure, organelle swelling, mitochondrial dysfunction, and the lack of typical features of apoptosis
Effect of excess hormonal stimulation on cells
hypertrophy
Effect of reduced hormonal stimulation on cells
Atrophy
Heavy metal poisoning, what metals and what is the physiology
Metals: lead, mercury, arsenic, and cadmium
Physiology: alteration to:
1. DNA repair mechanisms
2. tumor suppressor functions
3. signal transduction pathways
Effect of deprivation of essential nutrients
cellular injury altering:
1. cellular structure
2. Function particularly of transport mechanisms
3. chromosomes, the nucleus and DNA
What is cellular swelling and what causes it
the accumulation of excessive water in the cell, caused by the failure of transport mechanisms.
Is a sign of many types of cellular injury
Mechanism of gout
disturbance of urate metabolism, resulting in hyperuricemia and deposition of sodium urate crystals in tissue
Autophagy
a recycling factory, a self destructive process and survival mechanism where it degrades cytoplasmic components and organelles in lysosomes and and salvages key metabolites to promote metabolic and nutrient homeostasis.
Important in development, cell proliferation, remodeling, aging, cancer, heart disease, neurodegenerative disease, inflammation, infection, metabolic diseases and cell death.
Fatty necrosis
cellular dissolution caused by lipases, that break down triglycerides, releasing free fatty acids that combine with calcium, magnesium and sodium ions creating soaps (saponification). Necrotic tissue appears opaque and chalky white.
Fibrinoid necrosis
Unique vascular damage typically seen immune reactions involving blood vessels. Occurs from injury, and complexes of antigens and antibodies are deposited in the walls of arteries.
Also called immunologically mediated vasculitis syndromes.
Senescence
Growing OLD
Results in loss of tissue repair capacity and produces proinflammatory and matrix degrading molecules known as the senescence associated secretory phenotype (SASP)
process of permanent proliferative arrest or nondividing state called replicative senescence.
Inflammaging
increased levels of circulating cytokines and proinflammatory markers associated with aging.
Somatic Death
Death of the organism. Does not involve the inflammatory response
What are the 7 stages of death and possible 8th
- pallor mortis
- algor mortis
- rigor mortis
- livor mortis
- putrefaction
- decomposition
- skeletonization
- fossilization
Chemical Asphixiants
Carbon monoxide
cyanide
hydrogen sulfide
methane
all displace or interfere with O2 delivery or use.
Pallor mortis
First change after death where the skin becomes pale and yellowish.
Algor mortis
Post mortem decrease in body temperature. Immediately after death the body temp gradually falls and then decreases more rapidly (1-1.5F/hr) until body temp is equal to environmental temp
Liopfuscion
Yellow brown age pigment
Karyolysis
Nuclear dissolution and lysis of chromatin
Sarcopenia
loss of skeletal muscle and strength
Pyknosis
shrunken nucleus, appearing as a small dense mass
Steatosis
fatty changes in the liver
Caspase
aspartic acid specific enzymes that trigger proteolytic activity in response to signals inducing apoptosis.
