The University of Alabama
Capstone College of Nursing
NUR 529 Exam 1 Blueprint
Pages below are from Porth’s Pathophysiology: Concepts of Altered States, 10th 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, morphology and histology,
clinical manifestations, diagnosis, and clinical course.
Pathogenesis: explains how the disease process evolves. Sequence of cellular and tissue events
that take place from the time of initial contact with an etiologic agent until the ultimate expression of a
disease.
Morphology: Refers to the fundamental structure or form of cells or tissues. Morphologic
changes are concerned with both the gross anatomic and microscopic changes that are characteristic of
a disease.
Histology: Deals with the study of the cells and extracellular matrix of body tissues. Histologic
sections play an important role in the diagnosis of many types of cancers.
Clinical Manifestations: Sometimes, the condition produces manifestations, such as fever, that
make it evident that the person is sick.
Diagnosis: Designation as to the nature or cause of a health problem. The diagnostic process
requires a careful history, physical examination, and diagnostic tests.
Clinical Course: Describes the evolution of a disease. A disease can have an acute, subacute, or
chronic course. Acute disorder is one that is relatively severe, but self-limiting. Chronic disease implies a
continuous, long-term process. Subacute disease is an intermediate or between acute and chronic; not
as severe as an acute disease and not as prolonged as a chronic disease.
2. Concepts of Health and Disease: Disease. The second question comes from the same
content section.
A disease is considered an acute or chronic illness that one aquires or is born with that causes
physiologic dysfunction in one or more body systems. Each disease generally has specific signs and
symptoms that characterize its pathology and identifiable etiology.
Unit 2. Chapters 2- 6. There are 16 questions from this unit. Starts on p. 49
, 3. Chapter 3. Cellular Adaptation: Hyperplasia-physiologic vs pathologic, examples.
Hyperplasia refers to an increase in the number of cells in an organ or tissue. It occurs in tissues
with cells that are capable of mitotic division, such as the epidermis, intestinal epithelium, and glandular
tissue.
There are two common types of physiologic hyperplasia: hormonal and compensatory.
Hormonal examples include: breast and uterine enlargement during pregnancy. Compensatory
examples include: regeneration of liver after partial hepatectomy.
Most forms of nonphysiologic hyperplasia are due to excessive hormonal stimulation or the
effects of growth factors on target tissues. Example: excessive estrogen production can cause
endometrial hyperplasia and abnormal menstrual bleeding; benign prostatic hyperplasia is related to the
action of androgens.
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. Metaplasia is thought to involve the
reprogramming of undifferentiated stem cells that are present in the tissue undergoing the metaplastic
changes. Usually occurs in response to chronic irritation and inflammation and allows for substitution of
cells that are better able to survive under circumstances in which a more fragile cell type might
succumb. Examples: 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. Minor degrees of dysplasia are associated with chronic irritation or
inflammation. Dysplasia is strongly implicated as a precursor of cancer. Examples: In cancers of the
respiratory tract and uterine cervix, dysplastic changes have been found adjacent to the foci of
cancerous transformation.
Pap 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.
6. & 7. Chapter 3. Cell Injury and Death: 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: softening of the center of an abscess with discharge of its contents.
Coagulation necrosis: acidosis develops and denatures the enzymatic and structural proteins of
the cell. Characteristic of hypoxic injury and is seen in infarcted areas. Infarction occurs when an artery
supplying an organ or part of the body becomes occluded and no other source of blood supply exists.
Caseous necrosis: form of coagulation necrosis in which the dead cells persist indefinitely. Most
commonly found in the center of TB granulomas.
and Ischemia vs Infarction (2 questions from this content).
, Ischemia: Characterized by impaired oxygen delivery and impaired removal of metabolic end
products such as lactic acid. In contrast to pure hypoxia, which depends on the oxygen content of the
blood and affects all cells in the body, ischemia commonly affects blood flow through limited numbers of
blood vessels and produces local tissue injury.
Infarction: occurs when an artery supplying an organ or part of the body becomes occluded an
no other source of blood supply exists. As a rule, the shape of the infarction is conical and corresponds
to the distribution of the artery and its branches. An artery may be occluded by an embolus, thrombus,
disease of arterial wall, or pressure from outside the vessel.
8. Chapter 3. Cell Injury and Death-Intracellular Accumulations: Fatty necrosis
9. Chapter 3. Cell Injury and Death- Intracellular waste buildup.
Intracellular accumulations represent the buildup of substances that cells cannot immediately
use or eliminate. The substances may accumulate in the cytoplasm or in the nucleus. The accumulation
may be 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. Example:
accumulation of beta-amyloid fragments, which progress to a skeletal muscle disorder called myositis.
10. Chapter 3. Cell Injury and Death-Pathologic Calcifications-dystrophic.
Dystrophic calcifications represent the macroscopic deposition of calcium salts in injured tissue.
Often visible to the naked eye as deposits that range from gritty, sand-like grains to firm, hard rock
material. Pathogenesis involves the intracellular or extracellular formation of crystalline calcium
phosphate. Components of the calcium deposits are derived from the bodies of dead or dying cells as
well as from the circulation and interstitial fluid. Commonly seen in atheromatous lesions of advanced
atherosclerosis, areas of injury in the aorta and large blood vessels, and damaged heart valves.
11. Chapter 3. Cell Injury and Death-Pathologic Calcifications-metastatic.
Metastatic calcification occurs in normal tissues as a result of increased serum calcium levels.
Almost any condition that increases the serum calcium level can lead to calcification in inappropriate
sites such as lung, renal tubules, and blood vessels.
Major causes are hyperparathyroidism, increased metabolism of calcium from bone, cancer with
bone lesions, or immobilization
12. Chapter 3. Cell Injury and Death-Injury from physical agents: lead poisoning, clinical
manifestations, vulnerable population.
Lead poisoning: particularly toxic metal. Flaking paint, lead-contaminated dust and soil, lead
contaminated root vegetables, lead water pipes or soldered joints, pottery glazes, newsprint, and toys
made in foreign countries. Lead is absorbed through the gastrointestinal tracts or the lungs into the
blood. A deficiency of calcium, iron, or zinc increases lead absorption.
Clinical manifestations: toxicity of lead is related to its multiple biochemical effects. Has the
ability to inactivate enzymes, compete with calcium for incorporation into bone, and interfere with
Capstone College of Nursing
NUR 529 Exam 1 Blueprint
Pages below are from Porth’s Pathophysiology: Concepts of Altered States, 10th 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, morphology and histology,
clinical manifestations, diagnosis, and clinical course.
Pathogenesis: explains how the disease process evolves. Sequence of cellular and tissue events
that take place from the time of initial contact with an etiologic agent until the ultimate expression of a
disease.
Morphology: Refers to the fundamental structure or form of cells or tissues. Morphologic
changes are concerned with both the gross anatomic and microscopic changes that are characteristic of
a disease.
Histology: Deals with the study of the cells and extracellular matrix of body tissues. Histologic
sections play an important role in the diagnosis of many types of cancers.
Clinical Manifestations: Sometimes, the condition produces manifestations, such as fever, that
make it evident that the person is sick.
Diagnosis: Designation as to the nature or cause of a health problem. The diagnostic process
requires a careful history, physical examination, and diagnostic tests.
Clinical Course: Describes the evolution of a disease. A disease can have an acute, subacute, or
chronic course. Acute disorder is one that is relatively severe, but self-limiting. Chronic disease implies a
continuous, long-term process. Subacute disease is an intermediate or between acute and chronic; not
as severe as an acute disease and not as prolonged as a chronic disease.
2. Concepts of Health and Disease: Disease. The second question comes from the same
content section.
A disease is considered an acute or chronic illness that one aquires or is born with that causes
physiologic dysfunction in one or more body systems. Each disease generally has specific signs and
symptoms that characterize its pathology and identifiable etiology.
Unit 2. Chapters 2- 6. There are 16 questions from this unit. Starts on p. 49
, 3. Chapter 3. Cellular Adaptation: Hyperplasia-physiologic vs pathologic, examples.
Hyperplasia refers to an increase in the number of cells in an organ or tissue. It occurs in tissues
with cells that are capable of mitotic division, such as the epidermis, intestinal epithelium, and glandular
tissue.
There are two common types of physiologic hyperplasia: hormonal and compensatory.
Hormonal examples include: breast and uterine enlargement during pregnancy. Compensatory
examples include: regeneration of liver after partial hepatectomy.
Most forms of nonphysiologic hyperplasia are due to excessive hormonal stimulation or the
effects of growth factors on target tissues. Example: excessive estrogen production can cause
endometrial hyperplasia and abnormal menstrual bleeding; benign prostatic hyperplasia is related to the
action of androgens.
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. Metaplasia is thought to involve the
reprogramming of undifferentiated stem cells that are present in the tissue undergoing the metaplastic
changes. Usually occurs in response to chronic irritation and inflammation and allows for substitution of
cells that are better able to survive under circumstances in which a more fragile cell type might
succumb. Examples: 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. Minor degrees of dysplasia are associated with chronic irritation or
inflammation. Dysplasia is strongly implicated as a precursor of cancer. Examples: In cancers of the
respiratory tract and uterine cervix, dysplastic changes have been found adjacent to the foci of
cancerous transformation.
Pap 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.
6. & 7. Chapter 3. Cell Injury and Death: 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: softening of the center of an abscess with discharge of its contents.
Coagulation necrosis: acidosis develops and denatures the enzymatic and structural proteins of
the cell. Characteristic of hypoxic injury and is seen in infarcted areas. Infarction occurs when an artery
supplying an organ or part of the body becomes occluded and no other source of blood supply exists.
Caseous necrosis: form of coagulation necrosis in which the dead cells persist indefinitely. Most
commonly found in the center of TB granulomas.
and Ischemia vs Infarction (2 questions from this content).
, Ischemia: Characterized by impaired oxygen delivery and impaired removal of metabolic end
products such as lactic acid. In contrast to pure hypoxia, which depends on the oxygen content of the
blood and affects all cells in the body, ischemia commonly affects blood flow through limited numbers of
blood vessels and produces local tissue injury.
Infarction: occurs when an artery supplying an organ or part of the body becomes occluded an
no other source of blood supply exists. As a rule, the shape of the infarction is conical and corresponds
to the distribution of the artery and its branches. An artery may be occluded by an embolus, thrombus,
disease of arterial wall, or pressure from outside the vessel.
8. Chapter 3. Cell Injury and Death-Intracellular Accumulations: Fatty necrosis
9. Chapter 3. Cell Injury and Death- Intracellular waste buildup.
Intracellular accumulations represent the buildup of substances that cells cannot immediately
use or eliminate. The substances may accumulate in the cytoplasm or in the nucleus. The accumulation
may be 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. Example:
accumulation of beta-amyloid fragments, which progress to a skeletal muscle disorder called myositis.
10. Chapter 3. Cell Injury and Death-Pathologic Calcifications-dystrophic.
Dystrophic calcifications represent the macroscopic deposition of calcium salts in injured tissue.
Often visible to the naked eye as deposits that range from gritty, sand-like grains to firm, hard rock
material. Pathogenesis involves the intracellular or extracellular formation of crystalline calcium
phosphate. Components of the calcium deposits are derived from the bodies of dead or dying cells as
well as from the circulation and interstitial fluid. Commonly seen in atheromatous lesions of advanced
atherosclerosis, areas of injury in the aorta and large blood vessels, and damaged heart valves.
11. Chapter 3. Cell Injury and Death-Pathologic Calcifications-metastatic.
Metastatic calcification occurs in normal tissues as a result of increased serum calcium levels.
Almost any condition that increases the serum calcium level can lead to calcification in inappropriate
sites such as lung, renal tubules, and blood vessels.
Major causes are hyperparathyroidism, increased metabolism of calcium from bone, cancer with
bone lesions, or immobilization
12. Chapter 3. Cell Injury and Death-Injury from physical agents: lead poisoning, clinical
manifestations, vulnerable population.
Lead poisoning: particularly toxic metal. Flaking paint, lead-contaminated dust and soil, lead
contaminated root vegetables, lead water pipes or soldered joints, pottery glazes, newsprint, and toys
made in foreign countries. Lead is absorbed through the gastrointestinal tracts or the lungs into the
blood. A deficiency of calcium, iron, or zinc increases lead absorption.
Clinical manifestations: toxicity of lead is related to its multiple biochemical effects. Has the
ability to inactivate enzymes, compete with calcium for incorporation into bone, and interfere with
