NURS 5315 Advanced Patho Exam 1 STUDY
GUIDE 2026 COMPLETE QUESTIONS WITH CORRECT
DETAILED ANSWERS || 100% GUARANTEED PASS
<LATEST VERSION>
1. Atrophy - ANSWER ✔ E. Cells decrease in size
P. Still functional; imbalance between protein synthesis and degradation.
Essentially there is an increase in the catabolism of intracellular organelles,
reducing structural components of cell
Physiologic: thymus gland in early childhood
Pathological: disuse (muscle atrophy d/ decrease workload, pressure, use,
blood supply, nutrition, hormonal stimulation, or nervous stimulation)
2. Hyperplasia - ANSWER ✔ E: cells increase in number, mitosis (cell
division) must occur, size of cell does not change
Phys: increased rate of division, increase in tissue mass after damage or
partial resection; may be compensatory, hormonal, or pathologic
Patho: abnormal proliferation of normal cells usually caused by increased
hormonal stimulation (endometrial). increase of production of local growth
factors
Ex: removal of part of the liver lead to hyperplasia of hepatocytes. uterine or
mammary gland enlargement during pregnancy
3. Dysplasia - ANSWER ✔ E. Not true adaptation; Cells abnormal change in
size, shape, organization (classified as mild, moderate, severe)
P. caused by cell injury/irritation, characterized by disordered cell growth.
aka atypical hyperplasia or pre-cancer, a disorderly proliferation
Physiologic: N/A
Pathologic: squamous dysplasia of cervix from HPV shows up on pap
smear, breast cancer development; pap smears often show dysplastic cells of
the cervix that must undergo laser/surgical tx
,4. Metaplasia - ANSWER ✔ E: reversible change, one type of cell changes to
another type for survival
P: reversible; results from exposure of the cells to chronic stressors, injury,
or irritation; Cancer can arise from this area, stimulus induces a
reprogramming of stem cells under the influence of cytokines and growth
factors
Ex: Patho: Columnar cells change to squamous cells in lungs of smoker or
normal ciliated epithelial cells of the bronchial linings are replaced by
stratified squamous epithelial cells.; Phys: Barrett Esophagus- normal
squamous cells change to columnar epithelial cells in response to reflux, aka
intestinal metaplasia
5. Hypoxia injury - ANSWER ✔ E. inadequate oxygenation of tissues
P. decrease in mitochondrial function, decreased production of ATP
increases anaerobic metabolism. eventual cell death.
C.M. hypoxia, cyanosis, cognitive impairment, lethargy
6. Free radical and ROS - ANSWER ✔ E. normal byproduct of ATP
production, will overwhelm the mitochondria- exhaust intracellular
antioxidants
P. lipid peroxidation, damage proteins, fragment DNA
C.M. development in Alzheimer's, heart disease, Parkinson's disease,
Amyotrophic Lateral Sclerosis
7. Role of the hepatocytes - ANSWER ✔ Role: liver cell, ketogenesis occurs in
the mitochondria of the hepatocyte Clinical Implications: result of
unavailability of glucose
8. Role of the mitochondria - ANSWER ✔ Role: Ketogenesis is the formation
of ketone bodies and occurs mostly in the mitochondria of the hepatocytes
, (liver cells) Clinical Implications:- level of ketone bodies too high, pH drops
= ketoacidosis (commonly seen in uncontrolled DM1 and alcoholics
9. Triggers for ketogenesis - ANSWER ✔ Role:lack of glucose Clinical
Implications:occur from the depletion of carbohydrate stores or may occur
bc the cell is not able to use glucose but the individual is hyperglycemic
(type 2 DM)
10.Role of Acetyl-CoA - ANSWER ✔ Role:processed by hepatocytes and
undergoes transformation to 3 ketone bodies: Acetoacetate, Acetone and B-
hydroxybutyrate (basis of ketoacidosis) Clinical Implications:States of
starvation or uncontrolled DM, cells do not receive enough glucose to
produce energy, resulting in acceleration of the B-oxidation cycle and
increasing oxidation of fatty acids or energy. B-oxidation cycle results in
formation of acetyl-CoA
11.Effect on oxaloacetate - ANSWER ✔ Role:Oxaloacetate is also used in
gluconeogenesis, during starvation & uncontrolled DM oxaloacetate levels
are insufficient due to gluconeogenesis... this depletion furthers the amount
of acetyl-CoA which activates ketogenesis Clinical
Implications:Oxaloacetate (an intermediate) is involved in: Citric acid
cycle*gluconeogenesis*urea cycle*amino acid synthesis*fatty acid synthesis
12.action potential - ANSWER ✔ The process by which excitable cells transmit
information from one to another.
13.How is the action potential altered by a potassium imbalance?
(Hyperkalemia) - ANSWER ✔ The ECF has more K+ ions. The membrane
potential becomes more positive (hypopolarized).
Cells become MORE excitable.
T waves peak.
, QRS complexes widen.
Causes dysrhythmias, weakness, paresthesia.
{If membrane potential becomes equal to threshold potential cardiac
standstill occurs}
14.How is the action potential altered by a potassium imbalance?
(Hypokalemia) - ANSWER ✔ The ECF has less K+ ions. The membrane
potential becomes more negative or hyper-polarized.
The cell becomes less excitable, depolarization takes longer, and takes a
stronger stimulus.
Causes weakness, atony, cardiac dystrhythmias.
15.How is the action potential altered by a calcium imbalance? (hypercalemia) -
ANSWER ✔ Increase in ECF calcium to >10.5 mg/dL. It decreases the cell
permeability to calcium.
The cell becomes hyperpolarized (the distance between membrane potential
and threshold potential widens).
The cell is less excitable and take more stimulus to depolarize.
Causes: weakness, hyporeflexia, lethargy, confusion, shortened QT wave,
depressed T wave.
16.How is the action potential altered by a calcium imbalance? (hypocalemia) -
ANSWER ✔ Decreased ECF calcium <9.0 mg/dL. <5.5 ionized.
Increases the cell permeability to Na+. Resting membrane potential gets
hypo-polarized.
Cells become excitable and threshold and membrane potential get closer.
Causes: tetany, hyperreflexia, parathesias, seizures, dysrhythmias.
17.Atrophy - ANSWER ✔ Catabolism of intracellular organelles causing a
reduction in the intracellular contents.
The cell shrinks
-The thymus gland shrinks in childhood
-Disuse atrophy
GUIDE 2026 COMPLETE QUESTIONS WITH CORRECT
DETAILED ANSWERS || 100% GUARANTEED PASS
<LATEST VERSION>
1. Atrophy - ANSWER ✔ E. Cells decrease in size
P. Still functional; imbalance between protein synthesis and degradation.
Essentially there is an increase in the catabolism of intracellular organelles,
reducing structural components of cell
Physiologic: thymus gland in early childhood
Pathological: disuse (muscle atrophy d/ decrease workload, pressure, use,
blood supply, nutrition, hormonal stimulation, or nervous stimulation)
2. Hyperplasia - ANSWER ✔ E: cells increase in number, mitosis (cell
division) must occur, size of cell does not change
Phys: increased rate of division, increase in tissue mass after damage or
partial resection; may be compensatory, hormonal, or pathologic
Patho: abnormal proliferation of normal cells usually caused by increased
hormonal stimulation (endometrial). increase of production of local growth
factors
Ex: removal of part of the liver lead to hyperplasia of hepatocytes. uterine or
mammary gland enlargement during pregnancy
3. Dysplasia - ANSWER ✔ E. Not true adaptation; Cells abnormal change in
size, shape, organization (classified as mild, moderate, severe)
P. caused by cell injury/irritation, characterized by disordered cell growth.
aka atypical hyperplasia or pre-cancer, a disorderly proliferation
Physiologic: N/A
Pathologic: squamous dysplasia of cervix from HPV shows up on pap
smear, breast cancer development; pap smears often show dysplastic cells of
the cervix that must undergo laser/surgical tx
,4. Metaplasia - ANSWER ✔ E: reversible change, one type of cell changes to
another type for survival
P: reversible; results from exposure of the cells to chronic stressors, injury,
or irritation; Cancer can arise from this area, stimulus induces a
reprogramming of stem cells under the influence of cytokines and growth
factors
Ex: Patho: Columnar cells change to squamous cells in lungs of smoker or
normal ciliated epithelial cells of the bronchial linings are replaced by
stratified squamous epithelial cells.; Phys: Barrett Esophagus- normal
squamous cells change to columnar epithelial cells in response to reflux, aka
intestinal metaplasia
5. Hypoxia injury - ANSWER ✔ E. inadequate oxygenation of tissues
P. decrease in mitochondrial function, decreased production of ATP
increases anaerobic metabolism. eventual cell death.
C.M. hypoxia, cyanosis, cognitive impairment, lethargy
6. Free radical and ROS - ANSWER ✔ E. normal byproduct of ATP
production, will overwhelm the mitochondria- exhaust intracellular
antioxidants
P. lipid peroxidation, damage proteins, fragment DNA
C.M. development in Alzheimer's, heart disease, Parkinson's disease,
Amyotrophic Lateral Sclerosis
7. Role of the hepatocytes - ANSWER ✔ Role: liver cell, ketogenesis occurs in
the mitochondria of the hepatocyte Clinical Implications: result of
unavailability of glucose
8. Role of the mitochondria - ANSWER ✔ Role: Ketogenesis is the formation
of ketone bodies and occurs mostly in the mitochondria of the hepatocytes
, (liver cells) Clinical Implications:- level of ketone bodies too high, pH drops
= ketoacidosis (commonly seen in uncontrolled DM1 and alcoholics
9. Triggers for ketogenesis - ANSWER ✔ Role:lack of glucose Clinical
Implications:occur from the depletion of carbohydrate stores or may occur
bc the cell is not able to use glucose but the individual is hyperglycemic
(type 2 DM)
10.Role of Acetyl-CoA - ANSWER ✔ Role:processed by hepatocytes and
undergoes transformation to 3 ketone bodies: Acetoacetate, Acetone and B-
hydroxybutyrate (basis of ketoacidosis) Clinical Implications:States of
starvation or uncontrolled DM, cells do not receive enough glucose to
produce energy, resulting in acceleration of the B-oxidation cycle and
increasing oxidation of fatty acids or energy. B-oxidation cycle results in
formation of acetyl-CoA
11.Effect on oxaloacetate - ANSWER ✔ Role:Oxaloacetate is also used in
gluconeogenesis, during starvation & uncontrolled DM oxaloacetate levels
are insufficient due to gluconeogenesis... this depletion furthers the amount
of acetyl-CoA which activates ketogenesis Clinical
Implications:Oxaloacetate (an intermediate) is involved in: Citric acid
cycle*gluconeogenesis*urea cycle*amino acid synthesis*fatty acid synthesis
12.action potential - ANSWER ✔ The process by which excitable cells transmit
information from one to another.
13.How is the action potential altered by a potassium imbalance?
(Hyperkalemia) - ANSWER ✔ The ECF has more K+ ions. The membrane
potential becomes more positive (hypopolarized).
Cells become MORE excitable.
T waves peak.
, QRS complexes widen.
Causes dysrhythmias, weakness, paresthesia.
{If membrane potential becomes equal to threshold potential cardiac
standstill occurs}
14.How is the action potential altered by a potassium imbalance?
(Hypokalemia) - ANSWER ✔ The ECF has less K+ ions. The membrane
potential becomes more negative or hyper-polarized.
The cell becomes less excitable, depolarization takes longer, and takes a
stronger stimulus.
Causes weakness, atony, cardiac dystrhythmias.
15.How is the action potential altered by a calcium imbalance? (hypercalemia) -
ANSWER ✔ Increase in ECF calcium to >10.5 mg/dL. It decreases the cell
permeability to calcium.
The cell becomes hyperpolarized (the distance between membrane potential
and threshold potential widens).
The cell is less excitable and take more stimulus to depolarize.
Causes: weakness, hyporeflexia, lethargy, confusion, shortened QT wave,
depressed T wave.
16.How is the action potential altered by a calcium imbalance? (hypocalemia) -
ANSWER ✔ Decreased ECF calcium <9.0 mg/dL. <5.5 ionized.
Increases the cell permeability to Na+. Resting membrane potential gets
hypo-polarized.
Cells become excitable and threshold and membrane potential get closer.
Causes: tetany, hyperreflexia, parathesias, seizures, dysrhythmias.
17.Atrophy - ANSWER ✔ Catabolism of intracellular organelles causing a
reduction in the intracellular contents.
The cell shrinks
-The thymus gland shrinks in childhood
-Disuse atrophy
