PATHOPHYSIOLOGY STUDY GUIDE ASSURED SUCCEED
Chapter 1
• ATP function in cell metabolism
• ATP = ENERGY currency for the cell
• Aerobic and Anaerobic metabolism
• Aerobic = requires oxygen to form CO2 and H2O as energy- Krebs cycle
• Anaerobic = no oxygen required; occurs in glycolysis = glucose pyruvic acid
• Lactic acid: what pyruvate turns during glycolysis when oxygen is not present
• Cell signaling and communication mechanisms
• Cell surface receptors:
• G protein-linked receptors: Function as an on/ off switch to
convert external signals (first messengers- proteins, small
peptides, amino acids, fatty acids) into internal signals (second
messengers- by the response of secretion, muscle contraction or
relaxation, or change in metabolism).
• Enzyme-linked receptors: Widely used in hormone control of cell function
• Ion channel linked receptors: Involved in rapid synaptic signaling between
electrically excitable
cells in nerve and muscle cells.
• Membrane potentials and their functions
• Movement of ions in water.
• Changes in membrane
potentials are necessary for the generation and conduction of nerve
impulses and muscle contraction.
Chapter 2
• Normal adaptive process (cell structure and function)
o Allows stressed tissue to survive or maintain function.
• Atrophy: Decrease in cell size
• Hypertrophy: Increase in cell size
• Hyperplasia: Increase in the number of cells
• Metaplasia: When one adult cell type is replaced by another adult cell type.
• Dysplasia: Deranged cell growth of a specific tissue.
• Two patterns of reversible cell injury
• cellular swelling: occurs with the
impairment of energy-dependent sodium
potassium pump, as a result of a hypoxic
cell injury.
• fatty changes: due to intracellular
accumulation of fat, indicates cell injury.
• Cell injury
• Hypoxic cell injury: Hypoxia deprives
the cell of oxygen and interrupts
oxidative metabolism and the generation
of ATP. The cell swells with water
• Nutritional imbalances contribute to cell injury
, • Apoptosis: Programmed cell death/ suicide.
Removes worn-out cells and unwanted tissue.
• Necrosis: unregulated cell death caused by injuries
to cells. Cell death and degradation of cells that are
part of living tissue. Cells swell and rupture which
results in inflammation. They are then destroyed by
WBCs.
• Dry gangrene: lack of arterial blood supply but
venous flow can carry fluid out of tissue, tissue
tends to coagulate.
• Wet gangrene: Lack of venous flow lets fluid accumulate in tissue, tissue tends to liquefy, and
infection is likely.
• Gas gangrene: Clostridium infection produces toxins and gas bubbles
Chapter 3
• Process of inflammation
• Acute Inflammation -Local Response
• Vascular stage:
• A brief phase of vasoconstriction, is followed by vasodilation.
• increases blood flow (vasodilation)and, structural changes (vascular permeability).
• Mediators include histamine and nitric oxide
• Redness and warmth result
• Capillaries become more permeable (vascular permeability)
• Allows exudate to escape into the tissues
• Mediators include histamine, bradykinin, and leukotrienes.
• Swelling, pain, and impaired function result.
• Cellular stage: immigration of leukocytes (neutrophils), at the site of injury.
• white blood cells enter the injured tissue
• destroys infective organisms
• removed damaged cells
• releases inflammatory mediators to control further inflammation and
healing.
• Stages:
• Margination and adhesion
• Transmigration
• Chemotaxis- leukocytes are brought to the site of infection
• Activation and phagocytosis
• Systemic response: Occurs in sepsis, when large quantities of microorganisms in the blood
result in an
uncontrolled inflammatory response, produce and release lots of inflammatory cytokines.
• Acute Phase Response:
• Leukocytes release interleukins (glycoproteins produced by
leukocytes regulating immune response) and tumor necrosis
factor.
• Affect thermoregulatory center fever
, • Affect the central nervous system lethargy
• Skeletal muscle breakdown
• White blood cell response:
• Inflammatory mediators cause WBC production.
• WBC count rises leukocytosis.
• Five cardinal signs of acute inflammation
• Rubor (redness), tumor (swelling), calor (heat), dolor (pain), and function less (loss of
function)
• Chronic inflammation:
• Involves infiltration with Macrophages, Lymphocytes, and Fibroblasts
• Leading to persistent inflammation, fibroblast proliferation, and scar formation
• Causes
• Foreign bodies (i.e. splinters, sutures, silica, and asbestos), viruses, bacteria,
fungi
• Autoimmune diseases
• Obesity (adipose tissue: a source of proinflammatory mediators)
• Plasma-derived mediators:
• Kinins: pain
• Coagulation and fibrinolysis proteins: contribute to the vascular phase of
inflammation through fibrin products formed during the final steps in the
coagulation process.
• Complement system: causes vasodilation and increased vascular
permeability, promotes leukocyte activation, adhesion, and
chemotaxis, augments phagocytosis
• Cell-derived mediators:
• Vasoactive amines: histamine, serotonin
• Eicosanoid family: prostaglandins, leukotrienes
• Omega 3 polyunsaturated fatty acids
• Platelet-activating factor
• Cytokines and chemokines
• Nitric oxide
• Reactive oxygen species
• Local from systemic
manifestations of
inflammation
• Systemic manifestation (fever)-
whole body
• Chemical mediators (cytokines)
• Five types of inflammatory exudates
• Serous: Watery fluid, low in protein
• Hemorrhagic: leakage of RBCs from capillaries
• Fibrinous: Large amounts of fibrinogen, thick meshy
• Membranous: develops in mucous membrane surfaces, composed of necrotic dead
cells.
, • Purulent: pus, degraded WBCs, proteins, and tissue debris.
Chapter 4
• Cell proliferation: a process of increasing cell numbers by mitotic division
• Cell differentiation: a process whereby a cell becomes more specialized in terms of structure
and function.
• Phases of tissue repair
• Hemostasis (the stopping of blood flow), angiogenesis (the development
of new blood vessels), and ingrowth of granulation tissue- vasodilation in
response to nitric oxide, increased permeability of preexisting vessels,
migration or endothelial cells
• Emigration of fibroblasts and deposition of the extracellular matrix-
growth factor, recruitment, and proliferation of fibroblasts
• Maturation and reorganization of the fibrous tissue (remodeling)- the transition of
granulation to scar tissue
• Usually begins within 24 hours of injury
• Granulation tissue = glistening red, moist conn. tiss.
• replacement: If the tissue is damaged by infection or inflammation, regeneration is
incomplete and accomplished by replacement with scar tissue
• Tissue regeneration: refers to the restoration of injured tissue to its normal structure and
function by the proliferation
of adjacent surviving cells
• scar formation: When
regeneration cannot occur, healing by replacement with a connective (fibrous)
tissue occurs
• Fibrosis: The formation of fibrous
connective tissue, as in the repair or
replacement of parenchymatous elements
• Organization: Fibrous tissue
grows into the area of damage,
converting it to a mass of fibrous
tissue.
• Adhesions: strands of collagen
• Describe healing by primary and secondary intention
• Infection: Impairs all dimensions of wound healing
• Wound separation (Dehisce): Mechanical factors that cause pressure
can cause wounds to pull apart
• Foreign bodies: Invite bacteria contamination and delay healing
• Phases of healing
• Inflammatory phase- hemostasis, vascular and cellular phases of inflammation
• Proliferative phase- key cell is fibroblasts
• Maturational or remodeling- begins 3 weeks after injury and can last for 6 months
• Factors of Influence
• Nutrition
• Infection
• Blood flow
Chapter 1
• ATP function in cell metabolism
• ATP = ENERGY currency for the cell
• Aerobic and Anaerobic metabolism
• Aerobic = requires oxygen to form CO2 and H2O as energy- Krebs cycle
• Anaerobic = no oxygen required; occurs in glycolysis = glucose pyruvic acid
• Lactic acid: what pyruvate turns during glycolysis when oxygen is not present
• Cell signaling and communication mechanisms
• Cell surface receptors:
• G protein-linked receptors: Function as an on/ off switch to
convert external signals (first messengers- proteins, small
peptides, amino acids, fatty acids) into internal signals (second
messengers- by the response of secretion, muscle contraction or
relaxation, or change in metabolism).
• Enzyme-linked receptors: Widely used in hormone control of cell function
• Ion channel linked receptors: Involved in rapid synaptic signaling between
electrically excitable
cells in nerve and muscle cells.
• Membrane potentials and their functions
• Movement of ions in water.
• Changes in membrane
potentials are necessary for the generation and conduction of nerve
impulses and muscle contraction.
Chapter 2
• Normal adaptive process (cell structure and function)
o Allows stressed tissue to survive or maintain function.
• Atrophy: Decrease in cell size
• Hypertrophy: Increase in cell size
• Hyperplasia: Increase in the number of cells
• Metaplasia: When one adult cell type is replaced by another adult cell type.
• Dysplasia: Deranged cell growth of a specific tissue.
• Two patterns of reversible cell injury
• cellular swelling: occurs with the
impairment of energy-dependent sodium
potassium pump, as a result of a hypoxic
cell injury.
• fatty changes: due to intracellular
accumulation of fat, indicates cell injury.
• Cell injury
• Hypoxic cell injury: Hypoxia deprives
the cell of oxygen and interrupts
oxidative metabolism and the generation
of ATP. The cell swells with water
• Nutritional imbalances contribute to cell injury
, • Apoptosis: Programmed cell death/ suicide.
Removes worn-out cells and unwanted tissue.
• Necrosis: unregulated cell death caused by injuries
to cells. Cell death and degradation of cells that are
part of living tissue. Cells swell and rupture which
results in inflammation. They are then destroyed by
WBCs.
• Dry gangrene: lack of arterial blood supply but
venous flow can carry fluid out of tissue, tissue
tends to coagulate.
• Wet gangrene: Lack of venous flow lets fluid accumulate in tissue, tissue tends to liquefy, and
infection is likely.
• Gas gangrene: Clostridium infection produces toxins and gas bubbles
Chapter 3
• Process of inflammation
• Acute Inflammation -Local Response
• Vascular stage:
• A brief phase of vasoconstriction, is followed by vasodilation.
• increases blood flow (vasodilation)and, structural changes (vascular permeability).
• Mediators include histamine and nitric oxide
• Redness and warmth result
• Capillaries become more permeable (vascular permeability)
• Allows exudate to escape into the tissues
• Mediators include histamine, bradykinin, and leukotrienes.
• Swelling, pain, and impaired function result.
• Cellular stage: immigration of leukocytes (neutrophils), at the site of injury.
• white blood cells enter the injured tissue
• destroys infective organisms
• removed damaged cells
• releases inflammatory mediators to control further inflammation and
healing.
• Stages:
• Margination and adhesion
• Transmigration
• Chemotaxis- leukocytes are brought to the site of infection
• Activation and phagocytosis
• Systemic response: Occurs in sepsis, when large quantities of microorganisms in the blood
result in an
uncontrolled inflammatory response, produce and release lots of inflammatory cytokines.
• Acute Phase Response:
• Leukocytes release interleukins (glycoproteins produced by
leukocytes regulating immune response) and tumor necrosis
factor.
• Affect thermoregulatory center fever
, • Affect the central nervous system lethargy
• Skeletal muscle breakdown
• White blood cell response:
• Inflammatory mediators cause WBC production.
• WBC count rises leukocytosis.
• Five cardinal signs of acute inflammation
• Rubor (redness), tumor (swelling), calor (heat), dolor (pain), and function less (loss of
function)
• Chronic inflammation:
• Involves infiltration with Macrophages, Lymphocytes, and Fibroblasts
• Leading to persistent inflammation, fibroblast proliferation, and scar formation
• Causes
• Foreign bodies (i.e. splinters, sutures, silica, and asbestos), viruses, bacteria,
fungi
• Autoimmune diseases
• Obesity (adipose tissue: a source of proinflammatory mediators)
• Plasma-derived mediators:
• Kinins: pain
• Coagulation and fibrinolysis proteins: contribute to the vascular phase of
inflammation through fibrin products formed during the final steps in the
coagulation process.
• Complement system: causes vasodilation and increased vascular
permeability, promotes leukocyte activation, adhesion, and
chemotaxis, augments phagocytosis
• Cell-derived mediators:
• Vasoactive amines: histamine, serotonin
• Eicosanoid family: prostaglandins, leukotrienes
• Omega 3 polyunsaturated fatty acids
• Platelet-activating factor
• Cytokines and chemokines
• Nitric oxide
• Reactive oxygen species
• Local from systemic
manifestations of
inflammation
• Systemic manifestation (fever)-
whole body
• Chemical mediators (cytokines)
• Five types of inflammatory exudates
• Serous: Watery fluid, low in protein
• Hemorrhagic: leakage of RBCs from capillaries
• Fibrinous: Large amounts of fibrinogen, thick meshy
• Membranous: develops in mucous membrane surfaces, composed of necrotic dead
cells.
, • Purulent: pus, degraded WBCs, proteins, and tissue debris.
Chapter 4
• Cell proliferation: a process of increasing cell numbers by mitotic division
• Cell differentiation: a process whereby a cell becomes more specialized in terms of structure
and function.
• Phases of tissue repair
• Hemostasis (the stopping of blood flow), angiogenesis (the development
of new blood vessels), and ingrowth of granulation tissue- vasodilation in
response to nitric oxide, increased permeability of preexisting vessels,
migration or endothelial cells
• Emigration of fibroblasts and deposition of the extracellular matrix-
growth factor, recruitment, and proliferation of fibroblasts
• Maturation and reorganization of the fibrous tissue (remodeling)- the transition of
granulation to scar tissue
• Usually begins within 24 hours of injury
• Granulation tissue = glistening red, moist conn. tiss.
• replacement: If the tissue is damaged by infection or inflammation, regeneration is
incomplete and accomplished by replacement with scar tissue
• Tissue regeneration: refers to the restoration of injured tissue to its normal structure and
function by the proliferation
of adjacent surviving cells
• scar formation: When
regeneration cannot occur, healing by replacement with a connective (fibrous)
tissue occurs
• Fibrosis: The formation of fibrous
connective tissue, as in the repair or
replacement of parenchymatous elements
• Organization: Fibrous tissue
grows into the area of damage,
converting it to a mass of fibrous
tissue.
• Adhesions: strands of collagen
• Describe healing by primary and secondary intention
• Infection: Impairs all dimensions of wound healing
• Wound separation (Dehisce): Mechanical factors that cause pressure
can cause wounds to pull apart
• Foreign bodies: Invite bacteria contamination and delay healing
• Phases of healing
• Inflammatory phase- hemostasis, vascular and cellular phases of inflammation
• Proliferative phase- key cell is fibroblasts
• Maturational or remodeling- begins 3 weeks after injury and can last for 6 months
• Factors of Influence
• Nutrition
• Infection
• Blood flow
