MCCANCE PATHOPHYSIOLOGY THE
BIOLOGIC BASIS FOR DISEASE IN ADULTS AND
CHILDREN 8TH EDITION 2026 KEY DISEASE
MECHANISMS AND SYSTEM REVIEW A+
◉ Take Home Message About Action Potentials. Answer: Resting
Membrane Potential Dominated by K+
Upstroke of Action Potential --> Na+
Repolarization --> K+
In cardiac tissue, plateau --> Ca++
◉ Depolarization. Answer: As the sodium rushes back into the cell
the positive sodium ions raise the charge inside the cell from
negative to positive. Once the interior of the cell becomes positively
charged, depolarization of the cell is complete.
This triggers the action potential
◉ Repolarization. Answer: Sodium inflow is stopped and potassium
efflux increases
In cardiac muscles repolarization is prolonged from calcium influx
,◉ Hyperkalemia on Resting Membrane Potential. Answer:
Depolarizes the cell
Makes the membrane more negative
◉ Hypokalemia on Resting Membrane Potential. Answer:
Hyperpolarizes the cell
Makes the membrane less negative (more positive)
◉ *Chapter 4: Cell Injury, Aging, and Death*. Answer:
◉ Hyperplasia. Answer: Increase in functional capacity related to an
increase in cell number due to mitotic division
-Usually in response to increased physiologic demands or hormonal
stimulation
-Other causes: persistent cell injury, chronic irritation of epithelial
cells
-Usually result from increased functional demand
◉ Hypertrophy. Answer: Increase in cell mass accompanied by an
augmented functional capacity in response to physiologic and
pathophysiologic demands
-General cause:increased cellular protein content
-Usually result from increased functional demand
,◉ Dysplasia. Answer: Disorganized appearance of cells because of
abnormal variations in size, shape, and arrangement
-Represents an adaptive effort gone astray
-Significant potential to transform into cancerous cells
(preneoplastic lesions)
-Result from a persistant injury
◉ Metaplasia. Answer: Replacement of one differentiated cell type
with another
-Common cause: adaptation to persistent injury, with replacement of
a cell type that is better suited to tolerate injurious stimulation
-Fully reversible when injurious stimulation is removed
-Result from persistent injury
◉ Necrosis. Answer: Usually occurs as a consequence of ischemia or
toxic injury
Necrosis occurs when the injury is too severe or prolonged to allow
adaptation
-Usually from a disruption in blood supply
Local and systemic indicators of cell death
, -Pain
-Elevated serum enzyme levels
-Inflammation (fever, increased WBC, malaise)
-Loss of function
◉ Coagulation Necrosis. Answer: Most common type of necrosis
Process that begins with ischemia
Ends with degradation of plasma membrane
Caused by ischemia/infarction
◉ Atrophy. Answer: Cells shrink and reduce their differentiated
functions in response to normal and injurious factors
-General causes: disuse, denervation, ischemia, interruption of
endocrine signals, persistent cell injury
-Results from decreased functional demand or chronic ischemia
Results from decreased functional demand or chronic ischemia
◉ Proliferation. Answer: A rapid and often excessive spread or
increase
◉ Cell Differentiation. Answer: How generic embryonic cells become
specialized cells. This occurs through a process called gene
BIOLOGIC BASIS FOR DISEASE IN ADULTS AND
CHILDREN 8TH EDITION 2026 KEY DISEASE
MECHANISMS AND SYSTEM REVIEW A+
◉ Take Home Message About Action Potentials. Answer: Resting
Membrane Potential Dominated by K+
Upstroke of Action Potential --> Na+
Repolarization --> K+
In cardiac tissue, plateau --> Ca++
◉ Depolarization. Answer: As the sodium rushes back into the cell
the positive sodium ions raise the charge inside the cell from
negative to positive. Once the interior of the cell becomes positively
charged, depolarization of the cell is complete.
This triggers the action potential
◉ Repolarization. Answer: Sodium inflow is stopped and potassium
efflux increases
In cardiac muscles repolarization is prolonged from calcium influx
,◉ Hyperkalemia on Resting Membrane Potential. Answer:
Depolarizes the cell
Makes the membrane more negative
◉ Hypokalemia on Resting Membrane Potential. Answer:
Hyperpolarizes the cell
Makes the membrane less negative (more positive)
◉ *Chapter 4: Cell Injury, Aging, and Death*. Answer:
◉ Hyperplasia. Answer: Increase in functional capacity related to an
increase in cell number due to mitotic division
-Usually in response to increased physiologic demands or hormonal
stimulation
-Other causes: persistent cell injury, chronic irritation of epithelial
cells
-Usually result from increased functional demand
◉ Hypertrophy. Answer: Increase in cell mass accompanied by an
augmented functional capacity in response to physiologic and
pathophysiologic demands
-General cause:increased cellular protein content
-Usually result from increased functional demand
,◉ Dysplasia. Answer: Disorganized appearance of cells because of
abnormal variations in size, shape, and arrangement
-Represents an adaptive effort gone astray
-Significant potential to transform into cancerous cells
(preneoplastic lesions)
-Result from a persistant injury
◉ Metaplasia. Answer: Replacement of one differentiated cell type
with another
-Common cause: adaptation to persistent injury, with replacement of
a cell type that is better suited to tolerate injurious stimulation
-Fully reversible when injurious stimulation is removed
-Result from persistent injury
◉ Necrosis. Answer: Usually occurs as a consequence of ischemia or
toxic injury
Necrosis occurs when the injury is too severe or prolonged to allow
adaptation
-Usually from a disruption in blood supply
Local and systemic indicators of cell death
, -Pain
-Elevated serum enzyme levels
-Inflammation (fever, increased WBC, malaise)
-Loss of function
◉ Coagulation Necrosis. Answer: Most common type of necrosis
Process that begins with ischemia
Ends with degradation of plasma membrane
Caused by ischemia/infarction
◉ Atrophy. Answer: Cells shrink and reduce their differentiated
functions in response to normal and injurious factors
-General causes: disuse, denervation, ischemia, interruption of
endocrine signals, persistent cell injury
-Results from decreased functional demand or chronic ischemia
Results from decreased functional demand or chronic ischemia
◉ Proliferation. Answer: A rapid and often excessive spread or
increase
◉ Cell Differentiation. Answer: How generic embryonic cells become
specialized cells. This occurs through a process called gene
