The University of Alabama
Capstone College of Nursing
NUR 529 Exam 1 Blueprint
Pages below are from Porth’s Pathophysiology: Concepts of Altered States, 11th ed., and the
current e-book on Coursepoint. Older versions are not included, this course does not utilize older
textbook versions. Format for page numbers below is Porth 10th ed. “hard copy” book/ Course
Point Porth E-Book. Example: p. 967/975. If the pages correlate between editions then only one
will be listed.
Unit 1. Chapter 1. There are 2 questions from this unit. Starts on p. 2
1. Concepts of Health and Disease. Vocabulary:
Pathogenesis: explains how the disease process evolves
Morphology: refers to the fundamental structure or form of cells or tissues.
Histology: deals with the study of the cells and extracellular matrix of body tissues.
Clinical manifestations: Diseases can manifest in a number of ways. Sometimes, the condition
produces manifestations
Diagnosis: designation as to the nature or cause of a health problem
Clinical course: describes the evolution of a disease
2. Concepts of Health and Disease: Disease. The second question comes from the same
content section.
Unit 2. Chapters 2- 6. There are 16 questions from this unit. Starts on p. 49
2. Chapter 3.
Cellular Adaptation: Cells adapt to changes in the internal environment, just as the total
organism adapts to changes in the external environment. Cells may adapt by undergoing
changes in size, number, and type
3. Hyperplasia-physiologic: Hyperplasia refers to an increase in the number of cells in an organ
or tissue. There are two common types of physiologic hyperplasia: hormonal and
compensatory. Breast and uterine enlargements during pregnancy are examples of a
physiologic hyperplasia that results from estrogen stimulation. The regeneration of the liver
that occurs after partial hepatectomy (i.e., partial removal of the liver) is an example of
compensatory hyperplasia.
pathologic, examples.
Most forms of nonphysiologic hyperplasia are due to excessive hormonal stimulation or the
effects of growth factors on target tissues. Endometrial hyperplasia, or “thickened
endometrium,” is considered a high risk for developing endometrial cancer and is a
condition that is monitored carefully. Benign prostatic hyperplasia (BPH), which is a common
, disorder of people assigned male at birth older than 50 years of age, is related to the action
of androgens. BPH is a nonmalignant condition that causes lower urinary tract symptoms.
Although both BPH and prostate cancer share some common transcription factors and
signaling pathways.
4. Chapter 3. Cellular Adaptation:
Metaplasia, examples: Metaplasia represents a reversible change in which one adult cell
type (epithelial or mesenchymal) is replaced by another adult cell type. Usually occurs in
response to chronic irritation and inflammation. Chronic inflammation during
gastroesophageal acid reflux disease (GERD) is a primary risk factor of Barrett esophagus
(BE) and esophageal carcinogenesis. example of metaplasia is the adaptive substitution of
stratified squamous epithelial cells for the ciliated columnar epithelial cells in the trachea
and large airways of a habitual cigarette smoker.
5. Chapter 3. Cellular Adaptation:
Dysplasia, examples. Read about Pap smear: Dysplasia is characterized by deranged cell
growth of a specific tissue that results in cells that vary in size, shape, and organization. most
frequently encountered in areas of metaplastic squamous epithelium of the respiratory tract
and uterine cervix. In cancers of the respiratory tract and the uterine cervix, dysplastic
changes have been found adjacent to the foci of cancerous transformation. Through the use
of the Papanicolaou smear, it has been documented that cancer of the uterine cervix
develops in a series of incremental epithelial changes ranging from severe dysplasia to
invasive cancer. However, dysplasia is an adaptive process and as such does not necessarily
lead to cancer.
Preterm babies who are ventilated for long periods of time because of their prematurity and
lack of surfactant, and term infants who require intubation and ventilated oxygen in the first
month of life, often develop bronchopulmonary dysplasia (BPD). Research shows that
children with BPD are significantly more likely to have persistent respiratory symptoms at
school age such as airway obstruction and hyperinflation, and use asthma medications at
school age. The literature defines BPD as the need for oxygen supplementation at 28 days
postnatal or 36 weeks postmenstrual age.
6. & 7. Chapter 3. Cell Injury and Death: The mechanisms by which injurious agents cause cell
injury and death are complex. Some agents, such as heat, produce direct cell injury. Other factors, such
as genetic derangements, produce their effects indirectly through metabolic disturbances and altered
immune responses (Zemaitis et al., 2023). There seem to be at least three major mechanisms whereby
most injurious agents exert their effects:Free radical formation Hypoxia and ATP depletion Disruption of
intracellular calcium homeostasis (Fig. 3.6)
Mechanisms of Cell Injury: Types of necrosis
Necrosis refers to cell death in an organ or tissue that is still part of a living organism
Liquefaction necrosis occurs when some of the cells die but their catalytic enzymes are not destroyed
Example of liquefaction necrosis is the softening of the center of an abscess with discharge of its
contents
, During coagulation necrosis, acidosis develops and denatures the enzymatic and structural proteins of
the cell. Eg dry gangrene
and Ischemia vs Infarction (2 questions from this content).
Infarction (i.e., tissue death) occurs when an artery supplying an organ or part of the body becomes
occluded and no other source of blood supply exists.
8. Chapter 3. Cell Injury and Death-Intracellular Accumulations: Fatty necrosis
The accumulation of normal cellular constituents occurs when a substance is produced at a rate that
exceeds its metabolism or removal. An example of this type of process is fatty changes in the liver due to
intracellular accumulation of triglycerides. Liver cells normally contain some fat, which is either oxidized
and used for energy or converted to triglycerides. This fat is derived from free fatty acids released from
adipose tissue. Abnormal accumulation occurs when the delivery of free fatty acids to the liver is
increased, as in starvation and diabetes mellitus, or when the intrahepatic metabolism of lipids is
disturbed, as in alcoholism.
9. Chapter 3. Cell Injury and Death- Intracellular waste buildup.
Represent the buildup of substances that cells cannot immediately use or eliminate. The substances may
accumulate in the cytoplasm (frequently in the lysosomes) or in the nucleus. In some cases, the
accumulation may be an abnormal substance that the cell has produced, and in other cases, the cell may
be storing exogenous materials or products of pathologic processes occurring elsewhere in the body. An
example would be the accumulation of beta-amyloid fragments, which progresses to a skeletal muscle
disorder called myositis
10. Chapter 3. Cell Injury and Death-Pathologic Calcifications-dystrophic.
Pathologic calcification involves the abnormal tissue deposition of calcium salts, together with smaller
amounts of iron, magnesium, and other minerals.
Dystrophic calcification when it occurs in dead or dying tissues.
Dystrophic calcification represents the macroscopic deposition of calcium salts in injured tissues. It is
often visible to the naked eye as deposits that range from gritty, sandlike grains to firm, hard rock
material. The pathogenesis of dystrophic calcification involves the intracellular or extracellular formation
of crystalline calcium phosphate.
Dystrophic calcification is commonly seen in atheromatous lesions of advanced atherosclerosis and
areas of injury in the aorta and large blood vessels, and is the most prevalent mechanism of calcific
aortic valve disease. Dystrophic calcifications are seen in human tissues in the absence of known calcium
or phosphate imbalances—for example, in necrotic tissues or atherosclerotic plaques—and, when
found, are used for long-term management of chronic venous insufficiency
11. Chapter 3. Cell Injury and Death-Pathologic Calcifications-metastatic.
Metastatic calcification occurs in normal tissues.
result of increased serum calcium levels (hypercalcemia ). Almost any condition that increases the serum
calcium level can lead to calcification in inappropriate sites such as the lung, renal tubules, and blood
Capstone College of Nursing
NUR 529 Exam 1 Blueprint
Pages below are from Porth’s Pathophysiology: Concepts of Altered States, 11th ed., and the
current e-book on Coursepoint. Older versions are not included, this course does not utilize older
textbook versions. Format for page numbers below is Porth 10th ed. “hard copy” book/ Course
Point Porth E-Book. Example: p. 967/975. If the pages correlate between editions then only one
will be listed.
Unit 1. Chapter 1. There are 2 questions from this unit. Starts on p. 2
1. Concepts of Health and Disease. Vocabulary:
Pathogenesis: explains how the disease process evolves
Morphology: refers to the fundamental structure or form of cells or tissues.
Histology: deals with the study of the cells and extracellular matrix of body tissues.
Clinical manifestations: Diseases can manifest in a number of ways. Sometimes, the condition
produces manifestations
Diagnosis: designation as to the nature or cause of a health problem
Clinical course: describes the evolution of a disease
2. Concepts of Health and Disease: Disease. The second question comes from the same
content section.
Unit 2. Chapters 2- 6. There are 16 questions from this unit. Starts on p. 49
2. Chapter 3.
Cellular Adaptation: Cells adapt to changes in the internal environment, just as the total
organism adapts to changes in the external environment. Cells may adapt by undergoing
changes in size, number, and type
3. Hyperplasia-physiologic: Hyperplasia refers to an increase in the number of cells in an organ
or tissue. There are two common types of physiologic hyperplasia: hormonal and
compensatory. Breast and uterine enlargements during pregnancy are examples of a
physiologic hyperplasia that results from estrogen stimulation. The regeneration of the liver
that occurs after partial hepatectomy (i.e., partial removal of the liver) is an example of
compensatory hyperplasia.
pathologic, examples.
Most forms of nonphysiologic hyperplasia are due to excessive hormonal stimulation or the
effects of growth factors on target tissues. Endometrial hyperplasia, or “thickened
endometrium,” is considered a high risk for developing endometrial cancer and is a
condition that is monitored carefully. Benign prostatic hyperplasia (BPH), which is a common
, disorder of people assigned male at birth older than 50 years of age, is related to the action
of androgens. BPH is a nonmalignant condition that causes lower urinary tract symptoms.
Although both BPH and prostate cancer share some common transcription factors and
signaling pathways.
4. Chapter 3. Cellular Adaptation:
Metaplasia, examples: Metaplasia represents a reversible change in which one adult cell
type (epithelial or mesenchymal) is replaced by another adult cell type. Usually occurs in
response to chronic irritation and inflammation. Chronic inflammation during
gastroesophageal acid reflux disease (GERD) is a primary risk factor of Barrett esophagus
(BE) and esophageal carcinogenesis. example of metaplasia is the adaptive substitution of
stratified squamous epithelial cells for the ciliated columnar epithelial cells in the trachea
and large airways of a habitual cigarette smoker.
5. Chapter 3. Cellular Adaptation:
Dysplasia, examples. Read about Pap smear: Dysplasia is characterized by deranged cell
growth of a specific tissue that results in cells that vary in size, shape, and organization. most
frequently encountered in areas of metaplastic squamous epithelium of the respiratory tract
and uterine cervix. In cancers of the respiratory tract and the uterine cervix, dysplastic
changes have been found adjacent to the foci of cancerous transformation. Through the use
of the Papanicolaou smear, it has been documented that cancer of the uterine cervix
develops in a series of incremental epithelial changes ranging from severe dysplasia to
invasive cancer. However, dysplasia is an adaptive process and as such does not necessarily
lead to cancer.
Preterm babies who are ventilated for long periods of time because of their prematurity and
lack of surfactant, and term infants who require intubation and ventilated oxygen in the first
month of life, often develop bronchopulmonary dysplasia (BPD). Research shows that
children with BPD are significantly more likely to have persistent respiratory symptoms at
school age such as airway obstruction and hyperinflation, and use asthma medications at
school age. The literature defines BPD as the need for oxygen supplementation at 28 days
postnatal or 36 weeks postmenstrual age.
6. & 7. Chapter 3. Cell Injury and Death: The mechanisms by which injurious agents cause cell
injury and death are complex. Some agents, such as heat, produce direct cell injury. Other factors, such
as genetic derangements, produce their effects indirectly through metabolic disturbances and altered
immune responses (Zemaitis et al., 2023). There seem to be at least three major mechanisms whereby
most injurious agents exert their effects:Free radical formation Hypoxia and ATP depletion Disruption of
intracellular calcium homeostasis (Fig. 3.6)
Mechanisms of Cell Injury: Types of necrosis
Necrosis refers to cell death in an organ or tissue that is still part of a living organism
Liquefaction necrosis occurs when some of the cells die but their catalytic enzymes are not destroyed
Example of liquefaction necrosis is the softening of the center of an abscess with discharge of its
contents
, During coagulation necrosis, acidosis develops and denatures the enzymatic and structural proteins of
the cell. Eg dry gangrene
and Ischemia vs Infarction (2 questions from this content).
Infarction (i.e., tissue death) occurs when an artery supplying an organ or part of the body becomes
occluded and no other source of blood supply exists.
8. Chapter 3. Cell Injury and Death-Intracellular Accumulations: Fatty necrosis
The accumulation of normal cellular constituents occurs when a substance is produced at a rate that
exceeds its metabolism or removal. An example of this type of process is fatty changes in the liver due to
intracellular accumulation of triglycerides. Liver cells normally contain some fat, which is either oxidized
and used for energy or converted to triglycerides. This fat is derived from free fatty acids released from
adipose tissue. Abnormal accumulation occurs when the delivery of free fatty acids to the liver is
increased, as in starvation and diabetes mellitus, or when the intrahepatic metabolism of lipids is
disturbed, as in alcoholism.
9. Chapter 3. Cell Injury and Death- Intracellular waste buildup.
Represent the buildup of substances that cells cannot immediately use or eliminate. The substances may
accumulate in the cytoplasm (frequently in the lysosomes) or in the nucleus. In some cases, the
accumulation may be an abnormal substance that the cell has produced, and in other cases, the cell may
be storing exogenous materials or products of pathologic processes occurring elsewhere in the body. An
example would be the accumulation of beta-amyloid fragments, which progresses to a skeletal muscle
disorder called myositis
10. Chapter 3. Cell Injury and Death-Pathologic Calcifications-dystrophic.
Pathologic calcification involves the abnormal tissue deposition of calcium salts, together with smaller
amounts of iron, magnesium, and other minerals.
Dystrophic calcification when it occurs in dead or dying tissues.
Dystrophic calcification represents the macroscopic deposition of calcium salts in injured tissues. It is
often visible to the naked eye as deposits that range from gritty, sandlike grains to firm, hard rock
material. The pathogenesis of dystrophic calcification involves the intracellular or extracellular formation
of crystalline calcium phosphate.
Dystrophic calcification is commonly seen in atheromatous lesions of advanced atherosclerosis and
areas of injury in the aorta and large blood vessels, and is the most prevalent mechanism of calcific
aortic valve disease. Dystrophic calcifications are seen in human tissues in the absence of known calcium
or phosphate imbalances—for example, in necrotic tissues or atherosclerotic plaques—and, when
found, are used for long-term management of chronic venous insufficiency
11. Chapter 3. Cell Injury and Death-Pathologic Calcifications-metastatic.
Metastatic calcification occurs in normal tissues.
result of increased serum calcium levels (hypercalcemia ). Almost any condition that increases the serum
calcium level can lead to calcification in inappropriate sites such as the lung, renal tubules, and blood
