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NURS 5315 Module 1 Study Guide- University of Texas Arlington

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NURS 5315 Module 1 Study Guide- University of Texas Arlington/NURS 5315 Module 1 Study Guide- University of Texas Arlington/NURS 5315 Module 1 Study Guide- University of Texas Arlington/NURS 5315 Module 1 Study Guide- University of Texas Arlington/NURS 5315 Module 1 Study Guide- University of Texas Arlington

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N5315 Advanced Pathophysiology
Altered Cellular Function and Cancer

Module Core Concepts and Objectives with Advanced Organizers

Cellular Physiology
1. Analyze the steps of the action potential.
● Sodium permeability increases, sodium ions move into the cell increasing positivity,
depolarization is occurring, action potential threshold is reached as cell becomes more
positive, potassium permeability increases, potassium ions leave the cell, repolarization is
occurring, resting membrane potential is reestablished.

· The action potential carries signals along the nerve or muscle cell and conveys
information from one cell to another.
· When a resting cell is stimulated with voltage the membrane becomes permeable to
sodium.
· Movement of sodium into the cell, the membrane potential decreases, moves to a
negative or zero is known as depolarization. Depolarized cells are positively charged.
· To generate an action potential and the resulting depolarization is known as threshold
potential. It happens when the cell has depolarized by 15-20 millivolts. When the threshold is
met the cell continues to depolarize with no further stimulation. This makes the sodium rush
out of cell causing the membrane potential to reduce to zero and become positively
(depolarization). This rapid reversal in polarity results in action potential.
· Repolarization is negative polarity of the resting membrane potential. Membrane
permeability to sodium decreases, and potassium increases with outward movement of
potassium. This makes the membrane potential more negative.
· During most of the action potential the plasma membrane cannot respond to any
additional stimulus is known as absolute refractory period. Its related to changes in sodium.
· If potassium increases, a stronger stimulus can evoke an action potential is relative
refractory period.
· A membrane potential more negative than normal, requires a larger stimulus to reach the
threshold potential is hyperpolarized (less excitable). occurs when the membrane is
repolarizing.
· A membrane that is more positive than normal, needs smaller stimuli to reach threshold
potential is hypopolarized (more excitable than normal).
2. Discuss how the action potential is altered by calcium and sodium imbalances and the
clinical significance
· Na has a greater concentration in the ECF. When a neuron is excited by a stimulus, the
stimulus-gated Na+ channels open allowing Na+ to move intracellularly. This moves the
resting membrane potential of -70mV more towards 0. Once the threshold potential is
reached (-59mV) the voltage gated Na+ channels open allowing for more Na+ to move into
the cell and complete the depolarization to a maximum of +30mV. If the depolarization does
not reach a minimum of -59mV (threshold potential) the voltage gated Na+ channels will not
open and the cell will simply repolarize to -70mV without generating an action potential.

, 2


· Hyponatremia: Cellular swelling and deficits of intracellular Na alter the ability of cells
to depolarize and repolarize normally. Causes neurological changes headaches, lethargy, and
seizures.
· Hypernatremia: Na is largely in the ECF, increase concentration of Na causes
intracellular dehydration and hypervolemia. Causes hypotension, tachycardia, thirst.
· Hypercalcemia decreases cell permeability to sodium. This causes the threshold potential
to become more positive and is further away from the membrane potential. It takes more of a
stimulus to initiate an action potential. The cells are far less excitable and do not initiate
action potentials. This leads to weakness, hyporeflexia, fatigue, lethargy, confusion,
encephalopathy, a shortened QT segment and depressed widened T waves on EKG.
· Hypocalcemia- calcium deficits causes partial depolarization of the nerves and muscle as
the threshold potential becomes more negative and approaches resting membrane potential
(hypopolarization). A smaller stimulus is needed to start the action potential. This means the
cells are more excitable. This results in tetany, hyperreflexia, paresthesias, prolonged QT
interval, seizures, muscle spasms, laryngospasm.

Topic Describe the How is the action potential How is the action
Action Potential altered by a potassium potential altered by a
imbalance? calcium imbalance?
Action Potential The action Low K: ECF potassium is Low Ca: the cell has
Physiology potential carries depleted, ICF potassium increased permeability
signals along leaves cell easily, cell to Na which can cause
nerves or muscles becomes more negative a progressive
to convey info (HYPERPOLARIZED) and is depolarization, the
from one cell to less likely to transmit cells become more
the other. When impulses. This results in excitable resulting
resting cells
neuromuscular excitability, frequently occurring
become stimulated
weakness, smooth muscle action potential
the membrane
become more atony, paresthesia and causing tetany,
permeable to NA, cardiac dysrhythmias. hyperreflexia,
causing it to move circumoral
into the cell. This High K: ECF potassium paresthesia, seizures
results in increases, cell becomes and dysrhythmias.
depolarization. more positive
This allows Na and (HYPOPOLORIZED), cells High Ca: cell has
K to move into and are more excitable decreased
out of the cell. This (elevated T waves present), permeability to Na
is how the Na K depolarization is not causing it to become
pump works possible. Cardiac stand still more negative and
is possible and paralysis less excitable resulting
and paresthesia will occur. in more stimuli to
create action potential
causing weakness,
hyporeflexia, fatigue,
lethargy, confusion,

, 3


encephalopathy,
shortened QT segment
and depressed
widened T waves on
EKG.


Cellular Adaptation Patterns
1. Analyze the differences between cellular adaptation patterns.
a. Differentiate between the etiology and the pathophysiology of atrophy,
hypertrophy, hyperplasia, dysplasia, and metaplasia and identify an example of
each.
Disease Etiology Pathophysiology Example
Atrophy The shrinkage of There is an imbalance Physiologic atrophy
cell size between protein synthesis occurs with early
and degradation (an development; for
increase in the catabolism example, the thymus
of the intracellular gland involutes and
organelles). There is a atrophies .
reduction of the cell Pathologic atrophy
structure (less occurs as a result of
mitochondria, decreases in
myofilaments and ER). workload, use,
This causes a reduction in pressure, blood
cell size with diminished supply, nutrition,
function. hormonal
stimulation, and
Mechanisms of action nervous stimulation.
include decreased protein Disuse Atrophy is
synthesis, increased skeletal muscle
catabolism or both atrophy that occurs
from a person being
Up-regulation of immobilized for a
proteasome (protein prolonged period of
degrading complex) is a time. This is what
characteristic of atrophic happens in persons
changes. who are paralyzed.
Hypertrophy Increase in cell Hormonal stimulation or Skeletal muscle
size d/t hormonal increased functional hypertrophy is a
stimulation or demand causes an physiologic
increased increase in the cellular adaptation pattern in
functional demand protein in plasma those persons who
membrane, ER, do heavy work or
myofilaments and weight lifting
mitochondria which exercises. When a

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