ADVANCED PATHOPHYSIOLOGY EXAM.WITH
VERIFIED QUESTIONS AND ANSWERS
.2024/2025.A+ GRADED.
Chapter 1: Introduction to Pathophysiology
Describe an Action Potential ------CORRECT ANSWER-----Rapid, self-propagating electrical
excitations of the membrane
Mediated by voltage-gated ion channels that open (sodium flows into the cell) and close in
response to voltage changes across the membrane
Triggered by membrane depolarization
Propagated by sequential opening of voltage-gated sodium channels in adjacent sections of
membrane.
The action potential is regenerated in adjacent sections of membrane as more sodium channels
open. The initial segment repolarizes as sodium channels close and potassium ions move out.
Cardiac muscles: repolarization is prolonged from calcium influx
*Na+* initiates the action potential
*Only cells with voltage-gated channels have action potentials (not nerve cells)*
Describe a Resting Action Potential ------CORRECT ANSWER-----Electrical charge when there is
no net ion movement across plasma membrane
Major determinant: Ratio of Internal-to-External [K+]
This is dominated by potassium (K+)
Take Home Message About Action Potentials ------CORRECT ANSWER-----Resting Membrane
Potential Dominated by K+
Upstroke of Action Potential --> Na+
Repolarization --> K+
In cardiac tissue, plateau --> Ca++
Depolarization ------CORRECT 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
,2|Pa ge
Repolarization ------CORRECT ANSWER-----Sodium inflow is stopped and potassium efflux
increases
In cardiac muscles repolarization is prolonged from calcium influx
Hyperkalemia on Resting Membrane Potential ------CORRECT ANSWER-----Depolarizes the cell
Makes the membrane more negative
Hypokalemia on Resting Membrane Potential ------CORRECT ANSWER-----Hyperpolarizes the cell
Makes the membrane less negative (more positive)
*Chapter 4: Cell Injury, Aging, and Death* ------CORRECT ANSWER-----
Hyperplasia ------CORRECT 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 ------CORRECT 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 ------CORRECT 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 ------CORRECT 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 ------CORRECT 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
, 3|Pa ge
-Inflammation (fever, increased WBC, malaise)
-Loss of function
Coagulation Necrosis ------CORRECT ANSWER-----Most common type of necrosis
Process that begins with ischemia
Ends with degradation of plasma membrane
Caused by ischemia/infarction
Atrophy ------CORRECT 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 ------CORRECT ANSWER-----A rapid and often excessive spread or increase
Cell Differentiation ------CORRECT 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 ------CORRECT 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
Exocytosis ------CORRECT ANSWER-----The process of vesicles fusing with the plasma membrane
and releasing their contents to the outside of the cell
Exocytosis occurs when a cell produces substances for export, such as a protein, or when the
cell is getting rid of a waste product or a toxin.
Newly made membrane proteins and membrane lipids are moved on top the plasma
membrane by exocytosis.
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