NU 545
Unit 4 Study Guide
Advanced Pathophysiology
University of South Alabama.
This document provides a focused
study guide
It summarizes key concepts, lecture highlights, and
exam-relevant material to support efficient last-minute
review. The guide is structured to help students
reinforce understanding, identify weak areas, and prepare
confidently for the assessment.
, Unit 4 Study Guide
Below is a list of the specific topics that you should know for exam 4.
1. Know Infectious mononucleosis: patho, clinical manifestations, diagnostics,
treatment & complications. (p 945)
• Benign, acute, self limiting, lymphoproliferative clinical syndrome characterized by acute viral
infection of B lymphocytes (B cells)
• Assoc. with human tumors, such as B- cell and T- cell lymphoma, Hodgkin lymphoma, and
nasopharyngeal carcinoma,
• Linked to posttransplant lymphoproliferative diseases and gastric carcinoma
• Most common cause: EBV; HSV
SYMPTOMS
• Pharyngitis, lymphadenopathy, fever
• Individuals with immunodeficiency the proliferation of infected B Cells may be uncontrolled and can
lead to B Cell lymphomas/those with malaria/HIV increased risk of EBV ass lymphomas, include.
Burkitt lymphoma.
• EBV not documented from environmental sources, HUMANS are major reservoir
• More than 90% of individuals have antibodies to EBV
• 50-85% of children are infected by age 4, usually asymptomatic and provide immunity
• Symptomatic IM usually affects young adults btwn 15-24 yrs old ,males have a later peak 18-24.
• Overall incidence 6-8 cases/1000 persons/yr
• IM uncommon in >40, if does occur, commonly from CMV
TRANSMISSION
• Person to person (virus is shed in salivary secretions at high levels for a prolonged time) viral oral
shedding persists for about 6 months, once infected, virus may be intermittingly shed in oropharynx for
decades
• Breastfeeding
• Sexual transmission
• Virus initially infects the oropharynx, nasopharynx, and salivary epithelial cells with later spread into
lymphoid tissue inro and B cells. Once the virus enters the blood stream, the infection spreads
systemically.
PATHOPHYSIOLOGY
1 1
, • Immunocompetent- unaffected B cells produces antibodies (IgG,IgA,IgM) against the virus. At the
same time, massive activation and proliferation of cytotoxic T cells (CD8) directed against EBV
infected cells. Immune response against EBV infected cells is largely responsible for cellular
proliferation in the lymphoid tissue (lymph nodes, spleen, tonsils, and occasionally liver) Sore throat
and fever are caused by inflammation at the site of initial viral entry and initial infection (mouth and
throat )
CLINICAL MANIFESTATIONS:
• Incubation period for IM 30-50 days
• Early flu like symptoms-h/a, malaise, joint pain, fatigue, may appear during first 3-5 days although
some people are without symptoms
• At the time of diagnosis, commonly present with class group of symptoms:
Fever, sore throat, cervical lymph node enlargement, and fatigue
• Pharyngitis is diffuse with whitish/grayish green thick exudate, can be painful
• Progression: generalized lymphadenopathy, enlarged spleen, atypical activated T lymphocytes
(mononucleosis cells) in the blood
• Self-limiting, recovery occurs in a few weeks; fatigue 1-2 months after resolution
• Splenomegaly clinically evident 50% of the time, rare, but most common cause of death
Complications:
• liver or spleen enlargement, hepatic failure, meningitis, encephalitis, Guillain-Barre syndrome, Bell
palsy, pleural effusion. Eye manifestations, eyelid and periorbital edema, dry eyes, keratitis,
conjunctivitis. Reyes syndrome in children with ebv infection. Pulm and resp failure have been
documented but in immunocompromised.
Diagnostics & treatment:
• based on Hoagland's criteria of at least 50% lymphocytes and at least 10% atypical lymphocytes in the
blood in the presence of fever, pharyngitis, and adenopathy confirmed by a positive serologic test.
Serologic tests are used to determine a heterophile antibody response.
2. Know the leukemias: patho, clinical manifestations, diagnostics, treatment &
complications p. 947
• Clonal malignant disorder of the bone marrow and usually but not always of the blood
2 2
, • Common pathological feature of all forms is uncontrolled proliferation of malignant leukocytes,
causing overcrowding bone marrow and decreased production of and function of normal hematopoietic
cells
• Chromosomal abnormalities and translocations common
• When genes become mutated, they create genomic aberrations that block cell maturation and activate
pro-growth signaling pathways that prevent apoptic cell death
• World Health Organization (WHO) groups lymphoid neoplasms into 5 broad categories, defined by
cell of orgin:
1. Precursor B-cell neoplasms (immature B cells)
2. Peripheral B-cell neoplasms (mature B cells)
3. Precursor T-cell neoplasms (immature T cells)
4. Peripheral T-cell and NK (natural killer)-cell neoplasms(mature T cells and NK Cells)
5. Hodgkin Lymphoma (Reed Sternberg [RS] cell and variants)
• Acute Leukemia characterized by undifferentiated or immature cells, usually a blast cell. Onset
ABRUPT and RAPID. Without tx, short survival time.
• Chronic Leukemia, predominant cell is more differentiated but does not function normally, with
SLOW progression
• Four General Types of Leukemia:
-Acute Lymphocytic (ALL)
-Acute Myelogenous (AML)
-Chronic Lymphocytic (CLL)
-Chronic Myelogenous (CML)
• Leukemia is more common in adults/higher incidence in males
• Rates of induced remission and survival in most types has increased
PATHOPHYSIOLOGY
• Most lymphoid neoplasms arise from B-cell and T-cell differentiation pathways
• Hypothesis of origin for leukemias is “clonal disorders driven by genetically abnormal progenitor cells
or stem like cancer cells (SLCCs) 85-90% of lymphoid neoplasm are of B-cell origin, followed by T-
cell tumors, and rarely NK cell tumors.
• Abnormal immature white blood cells, called leukemic blasts, fill bone marrow and spill into the
blood. They “crowd out” the bone marrow, compete for growth factors and cause cellular proliferation
of the other cell lines to decrease or cease.
3 3
Unit 4 Study Guide
Advanced Pathophysiology
University of South Alabama.
This document provides a focused
study guide
It summarizes key concepts, lecture highlights, and
exam-relevant material to support efficient last-minute
review. The guide is structured to help students
reinforce understanding, identify weak areas, and prepare
confidently for the assessment.
, Unit 4 Study Guide
Below is a list of the specific topics that you should know for exam 4.
1. Know Infectious mononucleosis: patho, clinical manifestations, diagnostics,
treatment & complications. (p 945)
• Benign, acute, self limiting, lymphoproliferative clinical syndrome characterized by acute viral
infection of B lymphocytes (B cells)
• Assoc. with human tumors, such as B- cell and T- cell lymphoma, Hodgkin lymphoma, and
nasopharyngeal carcinoma,
• Linked to posttransplant lymphoproliferative diseases and gastric carcinoma
• Most common cause: EBV; HSV
SYMPTOMS
• Pharyngitis, lymphadenopathy, fever
• Individuals with immunodeficiency the proliferation of infected B Cells may be uncontrolled and can
lead to B Cell lymphomas/those with malaria/HIV increased risk of EBV ass lymphomas, include.
Burkitt lymphoma.
• EBV not documented from environmental sources, HUMANS are major reservoir
• More than 90% of individuals have antibodies to EBV
• 50-85% of children are infected by age 4, usually asymptomatic and provide immunity
• Symptomatic IM usually affects young adults btwn 15-24 yrs old ,males have a later peak 18-24.
• Overall incidence 6-8 cases/1000 persons/yr
• IM uncommon in >40, if does occur, commonly from CMV
TRANSMISSION
• Person to person (virus is shed in salivary secretions at high levels for a prolonged time) viral oral
shedding persists for about 6 months, once infected, virus may be intermittingly shed in oropharynx for
decades
• Breastfeeding
• Sexual transmission
• Virus initially infects the oropharynx, nasopharynx, and salivary epithelial cells with later spread into
lymphoid tissue inro and B cells. Once the virus enters the blood stream, the infection spreads
systemically.
PATHOPHYSIOLOGY
1 1
, • Immunocompetent- unaffected B cells produces antibodies (IgG,IgA,IgM) against the virus. At the
same time, massive activation and proliferation of cytotoxic T cells (CD8) directed against EBV
infected cells. Immune response against EBV infected cells is largely responsible for cellular
proliferation in the lymphoid tissue (lymph nodes, spleen, tonsils, and occasionally liver) Sore throat
and fever are caused by inflammation at the site of initial viral entry and initial infection (mouth and
throat )
CLINICAL MANIFESTATIONS:
• Incubation period for IM 30-50 days
• Early flu like symptoms-h/a, malaise, joint pain, fatigue, may appear during first 3-5 days although
some people are without symptoms
• At the time of diagnosis, commonly present with class group of symptoms:
Fever, sore throat, cervical lymph node enlargement, and fatigue
• Pharyngitis is diffuse with whitish/grayish green thick exudate, can be painful
• Progression: generalized lymphadenopathy, enlarged spleen, atypical activated T lymphocytes
(mononucleosis cells) in the blood
• Self-limiting, recovery occurs in a few weeks; fatigue 1-2 months after resolution
• Splenomegaly clinically evident 50% of the time, rare, but most common cause of death
Complications:
• liver or spleen enlargement, hepatic failure, meningitis, encephalitis, Guillain-Barre syndrome, Bell
palsy, pleural effusion. Eye manifestations, eyelid and periorbital edema, dry eyes, keratitis,
conjunctivitis. Reyes syndrome in children with ebv infection. Pulm and resp failure have been
documented but in immunocompromised.
Diagnostics & treatment:
• based on Hoagland's criteria of at least 50% lymphocytes and at least 10% atypical lymphocytes in the
blood in the presence of fever, pharyngitis, and adenopathy confirmed by a positive serologic test.
Serologic tests are used to determine a heterophile antibody response.
2. Know the leukemias: patho, clinical manifestations, diagnostics, treatment &
complications p. 947
• Clonal malignant disorder of the bone marrow and usually but not always of the blood
2 2
, • Common pathological feature of all forms is uncontrolled proliferation of malignant leukocytes,
causing overcrowding bone marrow and decreased production of and function of normal hematopoietic
cells
• Chromosomal abnormalities and translocations common
• When genes become mutated, they create genomic aberrations that block cell maturation and activate
pro-growth signaling pathways that prevent apoptic cell death
• World Health Organization (WHO) groups lymphoid neoplasms into 5 broad categories, defined by
cell of orgin:
1. Precursor B-cell neoplasms (immature B cells)
2. Peripheral B-cell neoplasms (mature B cells)
3. Precursor T-cell neoplasms (immature T cells)
4. Peripheral T-cell and NK (natural killer)-cell neoplasms(mature T cells and NK Cells)
5. Hodgkin Lymphoma (Reed Sternberg [RS] cell and variants)
• Acute Leukemia characterized by undifferentiated or immature cells, usually a blast cell. Onset
ABRUPT and RAPID. Without tx, short survival time.
• Chronic Leukemia, predominant cell is more differentiated but does not function normally, with
SLOW progression
• Four General Types of Leukemia:
-Acute Lymphocytic (ALL)
-Acute Myelogenous (AML)
-Chronic Lymphocytic (CLL)
-Chronic Myelogenous (CML)
• Leukemia is more common in adults/higher incidence in males
• Rates of induced remission and survival in most types has increased
PATHOPHYSIOLOGY
• Most lymphoid neoplasms arise from B-cell and T-cell differentiation pathways
• Hypothesis of origin for leukemias is “clonal disorders driven by genetically abnormal progenitor cells
or stem like cancer cells (SLCCs) 85-90% of lymphoid neoplasm are of B-cell origin, followed by T-
cell tumors, and rarely NK cell tumors.
• Abnormal immature white blood cells, called leukemic blasts, fill bone marrow and spill into the
blood. They “crowd out” the bone marrow, compete for growth factors and cause cellular proliferation
of the other cell lines to decrease or cease.
3 3
