Exam I Review Guide
Cell Death: Necrosis vs. Apoptosis (slide 3)
Necrosis Apoptosis
Irreversible Regulated or programmed cell process
“Dropping off” of cellular fragments
Rapid loss of the plasma membrane
structure, organelle swelling,
mitochondrial dysfunction
Passive or accidental, occurs after severe Active process of cellular self-destruction
and sudden injury
Enlarged cell size (swelling) Reduced cell size (shrinkage)
Pathologic (accumulation of irreversible Physiologic (means of eliminating unwanted cells; may be
cell injury) pathologic after some forms of cell injury, especially DNA
damage)
Hypoxia #1 cellular injury (MI) Elimination of harmful lymphocytes that may be self-
Ischemia, toxin exposure, infection, reactive and cause deaths of cells after they perform useful
trauma functions
Cellular Adaptation (slide 4): when cells adapt to the environment to escape & protect themselves from injury
An adapted cell is neither normal nor injured
Adaptations are reversible changes in cell size, number, phenotype, metabolic activity or functions of cells
Atrophy: Decrease or shrinkage in cellular size, can affect any organ, most common in skeletal muscle (heart), secondary
sex organs, and the brain
Physiologic-early development (thymus gland undergoes physiologic atrophy during childhood)
Pathologic- result of decreases in workload, use, pressure, blood supply, nutrition, hormonal stimulation, and
nervous stimulation (immobilized person in bed for a prolonged time aka disuse atrophy)
Less ER and fewer mitochondria and myofilaments
Nerve loss, oxygen consumption, and amino acid uptake are rapidly reduced
Decreased protein synthesis or increased
protein degradation
Malnutrition
Hypertrophy: Increase in the size of cells and thus
consequently increases the size of the affected organ
Heart or Kidneys
Physiologic- Caused by increased demand
Stimulation by hormones (ANP) and growth
factors
Skeletal muscle by heavy work
Pregnancy
Pathologic- Chronic hemodynamic overload
Hypertension or heart valve dysfunction
Cardiac hypertrophy by mechanical signals (stretch) and trophic signals (growth factors and vasoactive agents)
, Hyperplasia: Increase in the number of cells in an organ or tissue resulting from an increased rate of cellular division
Response to injury
Main mechanism is the production of growth factors, which stimulate the remaining cells to synthesize new cell
components and ultimately to divide
Increased output of new cells from tissue stem cells
Compensatory hyperplasia: adaptive mechanism that enables certain organs to regenerate (Liver)
Pathologic hyperplasia: abnormal proliferation of normal cells and can occur as a response to excessive hormonal
stimulation or the effects of growth factors on target cells (Endometriosis; imbalance of estrogen and progesterone)
Metaplasia: Reversible replacement of one mature cell type by another
Found in association with tissue damage, repair, and regeneration
Usually change is not beneficial
Normal columnar ciliated epithelial cells of the bronchial lining have been replaced by stratified squamous
epithelial cells
Can be reversed if irritant stopped (smoking)
Cellular Metabolism (slide 5): All chemical tasks of maintaining essential cellular function, provides the cell with the
energy it needs to synthesize (produce) cellular structures
Energy-using process: Anabolism
Energy-releasing: Catabolism
Adenosine Triphosphate (ATP)
“Fuel” inside living cells, needed for biological reactions for cells to function & energy stored in ATP can be used
in energy-requiring reactions (anabolism)
The function of ATP is not only to store energy but also to transfer it from one molecule to another
Energy is stored by molecules of carbohydrate, lipid and protein which when catabolized, transfer energy to ATP
Used by cells for muscle contraction and active transport of molecules across cellular membranes
ATP = energy BUT needs Oxygen (Aerobic)
Food & Production of Cellular Energy: Catabolism (energy-releasing) of proteins, lipids, and polysaccharides found in
food can be divided into 3 phases
Phase 1: Digestion
Large molecules broken down into smaller subunits-protein into amino acids, polysaccharides into simple sugars
and fats into fatty acids and glycerol
Processes occur outside the cell by the action of enzymes
Phase 2: Glycolysis and Oxidation
Small molecules enter the cells and are further broken down in the cytoplasm
Sugars into pyruvate acid
Pyruvate enters mitochondria and converted into acetyl groups of acetyl coenzyme A
Acetyl CoA (like ATP) releases energy when it is hydrolyzed
Glycolysis (lysis) splitting of glucose-produces 2 net molecules of ATP per glucose molecule through oxidation
(removal and transfer of a pair of electrons)
Occurs when O2 reserves are depleted
Phase 3: Citric Acid Cycle (Krebs cycle)
Most ATP generated in this phase
Cell Death: Necrosis vs. Apoptosis (slide 3)
Necrosis Apoptosis
Irreversible Regulated or programmed cell process
“Dropping off” of cellular fragments
Rapid loss of the plasma membrane
structure, organelle swelling,
mitochondrial dysfunction
Passive or accidental, occurs after severe Active process of cellular self-destruction
and sudden injury
Enlarged cell size (swelling) Reduced cell size (shrinkage)
Pathologic (accumulation of irreversible Physiologic (means of eliminating unwanted cells; may be
cell injury) pathologic after some forms of cell injury, especially DNA
damage)
Hypoxia #1 cellular injury (MI) Elimination of harmful lymphocytes that may be self-
Ischemia, toxin exposure, infection, reactive and cause deaths of cells after they perform useful
trauma functions
Cellular Adaptation (slide 4): when cells adapt to the environment to escape & protect themselves from injury
An adapted cell is neither normal nor injured
Adaptations are reversible changes in cell size, number, phenotype, metabolic activity or functions of cells
Atrophy: Decrease or shrinkage in cellular size, can affect any organ, most common in skeletal muscle (heart), secondary
sex organs, and the brain
Physiologic-early development (thymus gland undergoes physiologic atrophy during childhood)
Pathologic- result of decreases in workload, use, pressure, blood supply, nutrition, hormonal stimulation, and
nervous stimulation (immobilized person in bed for a prolonged time aka disuse atrophy)
Less ER and fewer mitochondria and myofilaments
Nerve loss, oxygen consumption, and amino acid uptake are rapidly reduced
Decreased protein synthesis or increased
protein degradation
Malnutrition
Hypertrophy: Increase in the size of cells and thus
consequently increases the size of the affected organ
Heart or Kidneys
Physiologic- Caused by increased demand
Stimulation by hormones (ANP) and growth
factors
Skeletal muscle by heavy work
Pregnancy
Pathologic- Chronic hemodynamic overload
Hypertension or heart valve dysfunction
Cardiac hypertrophy by mechanical signals (stretch) and trophic signals (growth factors and vasoactive agents)
, Hyperplasia: Increase in the number of cells in an organ or tissue resulting from an increased rate of cellular division
Response to injury
Main mechanism is the production of growth factors, which stimulate the remaining cells to synthesize new cell
components and ultimately to divide
Increased output of new cells from tissue stem cells
Compensatory hyperplasia: adaptive mechanism that enables certain organs to regenerate (Liver)
Pathologic hyperplasia: abnormal proliferation of normal cells and can occur as a response to excessive hormonal
stimulation or the effects of growth factors on target cells (Endometriosis; imbalance of estrogen and progesterone)
Metaplasia: Reversible replacement of one mature cell type by another
Found in association with tissue damage, repair, and regeneration
Usually change is not beneficial
Normal columnar ciliated epithelial cells of the bronchial lining have been replaced by stratified squamous
epithelial cells
Can be reversed if irritant stopped (smoking)
Cellular Metabolism (slide 5): All chemical tasks of maintaining essential cellular function, provides the cell with the
energy it needs to synthesize (produce) cellular structures
Energy-using process: Anabolism
Energy-releasing: Catabolism
Adenosine Triphosphate (ATP)
“Fuel” inside living cells, needed for biological reactions for cells to function & energy stored in ATP can be used
in energy-requiring reactions (anabolism)
The function of ATP is not only to store energy but also to transfer it from one molecule to another
Energy is stored by molecules of carbohydrate, lipid and protein which when catabolized, transfer energy to ATP
Used by cells for muscle contraction and active transport of molecules across cellular membranes
ATP = energy BUT needs Oxygen (Aerobic)
Food & Production of Cellular Energy: Catabolism (energy-releasing) of proteins, lipids, and polysaccharides found in
food can be divided into 3 phases
Phase 1: Digestion
Large molecules broken down into smaller subunits-protein into amino acids, polysaccharides into simple sugars
and fats into fatty acids and glycerol
Processes occur outside the cell by the action of enzymes
Phase 2: Glycolysis and Oxidation
Small molecules enter the cells and are further broken down in the cytoplasm
Sugars into pyruvate acid
Pyruvate enters mitochondria and converted into acetyl groups of acetyl coenzyme A
Acetyl CoA (like ATP) releases energy when it is hydrolyzed
Glycolysis (lysis) splitting of glucose-produces 2 net molecules of ATP per glucose molecule through oxidation
(removal and transfer of a pair of electrons)
Occurs when O2 reserves are depleted
Phase 3: Citric Acid Cycle (Krebs cycle)
Most ATP generated in this phase
