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NSG 530 Exam 2 Study Guide (2025) | Advanced Pathophysiology – Wilkes | Key Concepts & Clinical Prep – PDF

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**INSTANT DOWNLOAD PDF** – This NSG 530 Exam 2 Study Guide is tailored for the 2025 Wilkes University Advanced Pathophysiology course. It summarizes high-yield disease processes, clinical markers, and organ-specific pathologies. Perfect for NP and graduate nursing students preparing for Exam 2, this guide is organized by system and focused on what you really need to know for success. What’s Included: ️ Exam 2 Core Topics ️ Simplified Disease Pathways ️ System-Based Layout ️ Clinical Clarity for NP Students --- study guide, exam prep, nursing exam, pathophysiology notes, np student, wilkes university, clinical content, key concepts, advanced nursing, test review, pdf download, nurse practitioner, 2025 nursing

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NSG 530 / NSG 530
EXAM 2 STUDY GUIDE

Advanced Pathophysiology – Wilkes




THIS GUIDE CONTAINS:
 tailored to advanced practice nursing students

at Wilkes University.

 Focusing on key concepts

 is organized for clarity and comprehensive review.

 Expert-Verified

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Autoimmunity

Disturbance in the immunologic tolerance of self-antigens. Tolerance state
of immunologic control so that the individual doesn’t make a detrimental
immune response towards own cells and tissues. Autoimmunity results
from breakdown in tolerance. Occurs mainly in women.



Common autoimmune disorders

Systemic Lupus Erythematous (SLE)- most common, complex, and serious.
Production of a large variety of antibodies against self-antigens including
nucleic acids, erythrocytes, coagulation proteins, phospholipids,
lymphocytes, platelets, and many other self- components. SLE can produce
type II hypersensitivity destruction of RBS, lymphocytes, and platelets. Can
also produce type III hypersensitivity which forms circulating immune
complexes which attacks systems like the brain, heart, spleen, lung, GI,
peritoneum, and skin.



Common clinical findings associated with SLE

Individual may go through periods of remission and be disease free until
the onset of a flare. S/S arthralgias or arthritis (90%), vasculitis and rash
(70-80%), renal disease (40- 50%), hematologic abnormalities (50%-
anemia most common), cardiovascular disease (30-50%). Because it
affects almost every body system, it is difficult to diagnosis.

LIST Common Clinical Finding: Rash, photosensitivity, arthritis, serositis,
renal dysfunction, neurologic disorders, and hematologic manifestations—
when they occur together are highly suggestive of SLE. Presence of
antinuclear antibodies further supports diagnosis.



Vaccines-general principles and virulence

Vaccines are biologic preparations of antigens that stimulate production of
protective antibodies or cellular immunity against a specific pathogen
without causing potentially life-threatening disease. PURPOSE induce a
long-lasting protective immune responses under safe conditions.

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AIDS syndrome- Patho/expected lab findings

Secondary immune deficiency. Develops in response to viral infection HIV
infects and destroys the CD4+ Th cells, which are necessary for the
development of B cells (humoral immunity) and cytotoxic T cells (cellular
immunity). Advanced stage of HIV infection.

Pathogenesis- retrovirus. Virus attaches to dendritic cells, which carries
the virus to the lymph nodes, where it infects its primary target cell Th
lymphocyte. Viral attachment begins with the binding of gp120 and CD4
molecules.
-HIV reverse transcriptase- enzyme that converts RNA into dsDNA.

-HIV integrase- viral enzyme used to insert DNA is inserted into the
infected new cell’s genetic material.
-HIV protease- viral enzyme that processes production of long strand viral
components.
-Antivirals are developed to prevent the action of all 3 of these enzymes.

Lab Findings- HIV diagnosed by measuring HIV antibodies and HIV p24
antigen in blood.- Positive tests are confirmed by HIV DNA (nucleic acid
tests [NATs])

Diagnosis of AIDS is made when the HIV infection becomes associated with
various clinical conditions. Decreased CD4+ and T cell numbers. Diagnosis
can be made if CD4+ T cell numbers decrease to <200/mm3



Cancer terminology and characteristics: neoplasm, benign, malignant and in
situ
Neoplasm a new and abnormal growth of tissue.

Benign- encapsulated with connective tissue and contain well-differentiated
cells and well-organized stroma (tumor microenvironment). Recognizable
normal tissue structure and do not invade beyond their capsule, nor do
they spread to regional lymph nodes or distant locations. Mitotic cells are
rarely present. They are named according to the tissues with the suffix “-
oma”.

Malignant- some benign tumor can progress to cancer. Distinguished by

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more rapid growth rates and specific microscopic alterations. Loss of
differentiation and absence of normal tissue organization. Microscopic
HALLMARK anaplasia, loss of cellular differentiation. They are also
pleomorphic, marked variability of size and shape. Often have a large
darkly stained nuclei, and mitotic cells are common. Substantial stroma,
but is disorganized, with loss of tissue structure. Lack a capsule and grow
to invade nearby blood vessels, lymphatics, and surrounding structures.
Ability to spread far beyond tissue of origin- metastasis. Named according
to the cell type.

Carcinoma In Situ (CIS) preinvasive epithelial tumors of gradular or
squamous cell origin. early stage cancers are localized to the epithelium and
have not penetrated the local basement membrane or invaded the
surrounding stroma.



Cancer staging (I-IV)

TNM System: TUMOR size and extent of primary tumor, NODES presence
and extent of regional lymph node involvement, MESTASTASIS presence of
absence of distant metastasis.

STAGE 0: sometimes referred to as carcinoma in situ (CIS). Very early stage
where the cancer cells are confined to the layer of cells where they were
first developed and have not yet invaded nearby tissues.
STAGE I: Cancer confined to the organ of origin.
STAGE II: Cancer that is invasive locally.
STAGE III: Cancer that has spread to regional structures such as lymph nodes.

STAGE IV: Cancer that has spread to distant sites



Routes of metastases

Metastasis requires cells to have abilities to invade, survive, and proliferate
in a new environment. Carcinomas undergo a process called EMT
epithelial-mesenchymal transition, where epithelial-like characteristics are
lost, resulting in increased migratory capacity, increased resistance to
apoptosis, and a dedifferentiated stem cell-like state that favors growth in
the foreign microenvironments and establishment of metastatic disease.

Invasion consists of loss of cell-to-cell contact, degradation of extracellular
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