NU606 STUDY GUIDE 2026
COMPREHENSIVE ANSWER DIGEST
◉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
expression. Gene expression is the specific combination of genes
that are turned on or off (expressed or repressed), and this is what
dictates how a cell functions.
◉Endocytosis. Answer: The process of capturing a substance or
particle from outside the cell by engulfing it with the cell membrane.
The membrane folds over the substance and it becomes completely
enclosed by the membrane.
At this point a membrane-bound sac, or vesicle, pinches off and
moves the substance into the cytosol.
There are two main kinds of endocytosis:
(1) Phagocytosis, or cellular eating, occurs when the dissolved
materials enter the cell. The plasma membrane engulfs the solid
material, forming a phagocytic vesicle.
(2) Pinocytosis, or cellular drinking, occurs when the plasma
membrane folds inward to form a channel allowing dissolved
substances to enter the cell
COMPREHENSIVE ANSWER DIGEST
◉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
expression. Gene expression is the specific combination of genes
that are turned on or off (expressed or repressed), and this is what
dictates how a cell functions.
◉Endocytosis. Answer: The process of capturing a substance or
particle from outside the cell by engulfing it with the cell membrane.
The membrane folds over the substance and it becomes completely
enclosed by the membrane.
At this point a membrane-bound sac, or vesicle, pinches off and
moves the substance into the cytosol.
There are two main kinds of endocytosis:
(1) Phagocytosis, or cellular eating, occurs when the dissolved
materials enter the cell. The plasma membrane engulfs the solid
material, forming a phagocytic vesicle.
(2) Pinocytosis, or cellular drinking, occurs when the plasma
membrane folds inward to form a channel allowing dissolved
substances to enter the cell
