Altered Cell - CH. 4 Flashcards
Cellular Adaptation
Reversible
Atrophy
Decrease in cell size
Hypertrophy
Increase in cell size
Metaplasia
Reversible replacement of one mature cell type by another, less mature cell type or a change in cell phenotype.
Dysplasia
Deranged cellular growth, not considered a true cellular adaptation but rather atypical hyperplasia.
Physiologic Atrophy
Occurs with early development and is a normal event.
ex. thymus in childhood
Pathologic Atrophy
Result of decrease in workload, pressure, use, blood supply, nutrition, hormonal stimulation, or neural stimulation.
Disuse Atrophy
Occurs with prolonged bedrest or immobilization.
Also known as pathologic atrophy
Ex. arm in a cast
Atrophic cells contain less
ER, mitochondria, and myofilaments.
Mechanisms of atrophy
Decrease in protein synthesis, increase in protein degradation, or both.
Autophagic Vacuoles
Contain cellular debris and hydrolytic enzymes that degrade substances into simple units.
Vacuoles help ensure no uncontrolled destruction.
Lipofuscin
Yellow-brown pigmented granules; lipid-containing residue that persists after lysosomal destruction.
Become age spots in older adults
How does hypertrophy present clinically?
Muscle enlargement
Physiologic Hypertrophy
Result of increased demand, stimulation by hormones, and growth factors.
Pathologic Hypertrophy
Result of chronic hemodynamic overload (ex. hypertension or heart valve dysfunction)
What is pathologic hypertrophy associated with?
Increased interstitial fibrosis, cell death, and abnormal cardiac function.
Compensatory hyperplasia
Enables organs to regenerate
Callus
Thickening of the skin, considered compensatory hyperplasia
Hormonal Hyperplasia
Occurs in organs that respond to endocrine hormonal stimulation
Pathologic Hormonal Hyperplasia
Abnormal proliferation of normal cells, usually in response to excessive hormonal stimulation or to the action of growth factors on target cells.
Dysplasia is described as “low grade” or “ high grade” based on
The degree of variation from normal.
Why is metaplasia thought to develop?
The new cell type might be better suited to withstand an adverse environment. However, the change is usually not beneficial.
Metaplasia results from
A reprogramming of stem cells present in most epithelia or of undifferentiated mesenchymal (tissue from embryonic mesoderm) cells
Irreversible cell injury
Severe vacuolization of the mitochondria and Ca++ moves into the cell.
Hypoxia
Lack of sufficient oxygen within cells
Most common cause of cell injury
Ischemia
Reduced supply of blood and therefore oxygen
What does hypoxia negatively impact?
Differentiation, angiogenesis, proliferation, erythropoiesis, and overall cell viability.
Reactive Oxygen Species (ROS)
Reactive molecules from molecular oxygen formed as a natural oxidant species in cells during mitochondrial respiration and energy generation.
Anoxia
Total lack of oxygen
What happens when the Na+/K+ pump fails due to ischemia?
Ca++ and Na+ accumulate in the cell. K+ diffuses out of the cell. Na+ and H2O can freely enter the cell causing swelling of the cell. The cell is lysed.
Vacuolation
Formation of vacuoles
Occurs when Na+/K+ pump is broken and oxygen is not restored.
Ischemia-Reperfusion (reoxygenation) injury
Restoration of blood flow and oxygen to ischemic tissues that can help cells injured reversibly recover but also cause cell death. Can create free oxygen radicals that cause destruction.
Potential mechanisms for reperfusion injury
Oxidative stress, increased intracellular calcium concentration, inflammation, and complement activation
Oxidative Stress
Injury caused by ROS
Free radical
Electrically uncharged atom, or group of atoms, which has an unpaired electron that makes the molecule unstable.
Mechanisms for generation of free radicals
Reduction-oxidation reactions, absorption of extreme energy sources, enzymatic metabolism of exogenous chemicals or drugs, transition metals, or NO acting as an intermediate in reactions.
Potential damaging effects of free radicals
Lipid peroxidation, protein alteration, DNA damage, and mitochondrial effects.
Xenobiotics
Compounds and chemicals that have toxic, mutagenic, or carcinogenic properties.
Biotransformation
Enzymatic reactions convert one chemical into a less toxic or nontoxic compound
Antioxidants
Molecules that inhibit the oxidation of other molecules, thereby preventing the formation of free radicals.
Often terminate a chain reaction that would’ve resulted in free radical formation.
Ambient particulate matter
Particulate matter less than or equal to 2.5 micrometers in aerodynamic matter
Ozone
Special form of oxygen in a deep layer in the stratosphere.
Asphyxial Injuries
Failure of cells to receive or use oxygen
Suffocation
Process of dying as a result of lack of oxygen
Strangulation
Compression of the blood vessels and air passages resulting from external pressure on the neck.
Ligature strangulation
Does not require suspension
Manual strangulation
Assailant’s hands compress the neck of the victim to the point where death by asphyxiation occurs
Dry-lung drowning
Vagal-mediated laryngospasms closing off the airway
Cellular accumulations
Also known as infiltration
Can occur with both sustained cell injury and with normal but inefficient cell function.
Two categories of substances that can produce infiltrations
Normal cellular substances - excess water, protein, lipids, carbohydrates
Abnormal cellular substances - endogenous and exogeneous substances
Four mechanisms for accumulations
- Insufficient removal of the normal substance because of altered configuration or transport
- Accumulation of abnormal substance because of defects in protein folding, transport, or abnormal degradation.
- Inadequate metabolism of an endogenous substance, usually because of a lack of a lysosomal enzyme.
- Harmful exogenous materials
Cellular Swelling
Most common degenerative change
Result from a shift of extracellular water into the cells
Oncosis/vacuoler degeneration
Cytoplasmic swelling
Steatosis
Fatty changes of the liver, accumulation of intracellular lipids
Mechanisms for lipid accumulation in the liver
- Increased movement of free fatty acids into the liver
- Failure to convert fatty acids to phospholipids results in conversion into triglycerides
- Increased synthesis of triglycerides from fatty acids
- Decreased synthesis of apoproteins
- Failure of lipids to bind with apoproteins to form lipoproteins
- Failure of mechanisms that transport lipoproteins out of the cell.
- Direct damage to the ER by free radicals released by alcohol’s toxic effects
Hemoproteins
Endogenous pigments including cytochromes (hemoglobin and oxidative enzymes)
Hemosiderin
Intracellular, yellow-brown pigment
Hemosiderosis
Transient, localized deposition of iron that usually does not result in tissue damage
Dystrophic Calcification
Calcification occurring in dying or necrotic tissues
Commonly noted in chronic pulmonary tuberculosis
Psammoma bodies
Laminated, calcified structures. Concentric and commonly found within tumors
Metastatic calcification
Mineral deposits that occur in undamaged, normal tissues secondary to hypercalcemia
Urate
Major end product of purine catabolism
Necrosis
Form of cell destruction characterized by rapid loss of plasma membrane structure, swelling of organelles, mitochondrial dysfunction, and the lack of typical features of apoptosis.
Autolysis
A process of cellular self-digestion
Karyolysis
Enzymatic hydrolysis of nuclear chromatin
Pyknosis
Nucleus shrinks into a small, dense mass of genetic material
Karyorrhexis
Fragmentation of the nucleus into small particles or “nuclear dust”
Coagulative necrosis
Result of protein denaturation, where albumin is transformed into a firm opaque substance called an infarct
Infarct
Firm opaque substance (formerly albumin)
Liquefactive necrosis
Commonly results from ischemic injury to neurons and glial cells. Cysts form and are often triggered by infection
