Cellular Adaptation Flashcards
Cellular Adaptation
Change in cell structure and/or function in response to changes inside the body
Atrophy
A decrease or shrinksge in cellular size
Ex; muscle tissue/ muscle shrinking after a cast
Atrophy Causes and exmaples
- Disuse
- decreased nervous/ hormonal stimulation
- ischemia leading to cell hypoxia
- cell isnt getting enough oxygen ( neurons in the brain shrink)
Atrophy patho
- Decreased number of organelles ( lower mitochondria & atp)
- decreased actin/myosin
Hypertrophy
An increase in the size of cells & thicker (compensates to increase work load)
Hypertrophy causes and exmaples
-Increased Workload
ex. working out; building skeletal muscle (not making more muscle just getting bigger)
-Increased hormonal stimulation
Hypertrophy of cells in uterus during hormonal increase in pregnancy
Hypertrophy Patho
- NOT swelling of the cell
- Increase in actin/myosin
- Increase in organelles (more mito, atp and myosin)
Hyperplasia
An increase in the NUMBER of cells, through cell division and mytosis
Hyperplasia causes and examples
-Compensatory hyperplasia;
allows certsin organs/tissues to regenerate
ex: scrape skin; cell division occurs and grows back
- Hormonal hyperplasia
Occurs chiefly in estrogen-dependent organs
ex; uterine cells growing
-Pathologic hyperplasia
Abnormal proliferation or normal cells usually as the result of excessive hormone situation
ex; benign prostatic hyperplasia (enlarged prostate) from an increase in testosterone
Hyperplasia Patho
Metaplasia
Abnormal change in the tissue, reversible replacment of on mature cell type by another - usually insult or injury
Metaplasia Cause and Examples
-Prolonged Insult
Columnar cells change shape. become less specified multiple layer of skin cells formed
Metaplasia patho
ADAPTATION of injury to protect
Dysplasia (atypical hyperplasia)
Abnormal changes in the size, shape and organization
of mature cells- Cells less normal, one step closer to cancer
Dysplasia Cause and example
-DNA mutations - inherited, random or due to cell injury (e.g. free radical injury)
ex; Cervical dysplasia seen on a pap smear (from hpv) ..dysplasia is a pre-cancerous condition
Hypoxic Injury
Lack of oxygen in the tissues leading to altered cell metabolism and function
Hypoxic Injury causes
-Decreased oxygen CONTENT blood (hypoxemia)
respiratory oxygen such as asthma/ high altitude
-Decreased Oxygen CARRYING CAPACITY of blood (anemia)
low hemoglobin count
-Decreased blood FLOW to the tissue (ischemia)
ex; blocked arterial, not allowing blood flow (blokced blood flow)
Reperfusion injury
Reperfused: Restoring flow of blood to organ or tissue
If Hypoxic tissue is reperfused, cell injury because introducing oxygen to tissue has been hypoxic causes formation of reactive oxygen species (ROS) (i.e. free radicals)
hypoxic cells produce xanthine oxydase >
> when O2 is reintroduced >
> reascts w/ O2 to create oxygen free radicals
Free Radical Injruy
Free radicals are molecules that have an unpaired electron (unstable molecule)
Free Radical causes and formation
- Absorption of extreme energy sources
absorp. of ionizing radiation breaks apart molecules and liberates free radicals
-Endogenous, usually oxidative, rxns from nomal metabolic processes
ex; ATP production in ETC
- Inflammation
ex. phagocytosis..kills things in free radicals, the rest not killed is dumped into the body
-Enzymatic metabolism or exogenous chemicals/drugs
ex; chemotherapy agents
-other sources- cigarette smoke, alcohol,transfate, etc.
Free Radical Effects
In high levels, FR cause “oxidative stress” cell injury
-DNA damage
FR can fragment strands of DNA causing mutations/ireeversible injury to cells
-Fragmented Proteins
enzymes and structural proteins
-Lipid Peroxidation
attracted to carbon double bonds in lipid moelcules. & breaks apart this bond {lipid very stable,FR love them}
Free Radical Clinical Example
-FR injury and aging
-FR injury causes disease
>CANCER
fr> damage dna > mutate DNA > form cancer tumors
> Cardiovascular disease
damage to endothelial lining by FR circulating in the blood
Molecules that inactive Free Radicals
ANTIOXIDANTS
- Vitamin A & E
- Betacarotene
- lypocene
- flavonoids
- omega 3 & 6 fatty acids
Necrosis (Cell death)
Loss of plasma membrane structure, swelling of organelles, mitochondrial dysfunction leading to death of cell {primarily autodigestion}
Coagulative Necrosis
-Caused by protein denaturing & coagulation
typically has a lot of protein initially
-Occurs with hypoxic injury to kidneys, heart and adrenal glands
Liquefactive Necrosis
-Tissue becomes soft and liquefies
Little tissue present
-Occurs with hypoxic injury to brain tissue and bacterial infections
Caseous Necrosis
- Combination of coag & liqeufactive necrosis cause by tuberculosis
- primarily in the lungs
Fat necrosis
-Caused by release of lipase
ex; lipase auto digests, fat takes over space where tissue was
-most commonly occurs in breast,liver, pancreas
Gangrenous necrosis
-Death of a series of tissues from severe hypoxic injury
ex; leg or toe (lack of blood supply to limb)
-GAS GANGRENE
occurs with anaerobic bacterial infections.. gas build up in dead/dying tissue
Gas gangrene
occurs with anaerobic bacterial infections
-gas build up in dead/dying tissue
Apoptosis
Programmed Cell death
-Cell turns on internal mechanisms to initiate self-destruction
Signals that induce Apoptosis
- Extracellular signals (death ligands, withdrawl of hormones, toxic agents, etc)
- intracellular signals
Mechanisms of Apoptosis
- Nucleus condenses and cell shrinks
- > activation of intracellular enzymes that breakdown structural proteins and DNA
- > Apoptic bodies are ingested by neighboring cells and local phagocytes (WBC) or just degenerate
**NOTE; inflammatory response NOT stimulated
Clinical examples of apoptosis
-Apoptosis during embryonic development
ex; embryo to child .. fingers unwebbed
-Apop. in cancer cells
50% of cancer has mutation in apop gene
