Summary NUR-631-Midterm Exam Study Guide

Study Guide for Midterm – Spring 2018
This study guide provides a content outline that can be used to prepare for the topic quiz. This
outline may not be inclusive of all quiz content.
Cellular biology and Alterations
 Compensatory hyperplasia after partial resections (mod 1) (51-53)

o Ex: liver, hepatocyte growth
o Adaptive mechanism that enables certain organs to regenerate
o Even with removal of 70% of the liver, it will regenerate within about 2 weeks
o Compensatory hyperplasia occurs in epidermal, intestinal epithelia, hepatocytes,
bone marrow and fibroblasts. Some type off hyperplasia is noted in bone,
cartilage and smooth muscles – Example- callus, wound healing as part of
inflammation process


 Tumor progress from benign to malignant (364-366)

o Benign tumors are usually encapsulated and well differentiated. They retain some
normal tissue structure and do not invade the capsules surrounding them or spread
to regional lymph nodes or distant locations.
 Generally named according to the tissues from which they arise, and
include the suffix –oma.
o Some benign tumors can progress to cancer and are then referred to as malignant.
They have more rapid growth rates and specific microscopic alterations, including
loss of differentiation and absence of normal tissue organization.
 One hallmark is anaplasia – loss of cellular differentiation, irregularities of
the size and shape of the nucleus, and the loss of normal tissue structure.
 May present with different degrees of encapsulation; some lack a capsule,
and even if one is apparent, it’s integrity has been compromised so that
tumor cells can grow to invade nearby blood vessels, lymph and
surrounding structures.
 Most deadly characteristic is their ability to spread far beyond the tissue of
origin – metastasis




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, BENIGN TUMORS MALIGNANT TUMORS
 Grow slowly  Grow rapidly
 Have a well-defined capsule  Are not encapsulated
 Are not invasive  Invade local structures and tissues
 Are well differentiated; look like the tissue  Are poorly differentiated; may not be
from which they arose determine the tissue of orgin
 Have a low miotic index; dividing cells are  High miotic index; many dividing ce
rare  Can spread distantly; often through b
 Do not metastasize vessels and lymphatics

Genetics
 Recurrence of autosomal diseases (152-154, 155-156)

o Autosomal dominant - Affected offspring are produced by the union of a normal
parent with an effected heterozygous parent
 Affected parent can pass either a disease gene or a normal gene to his or
her children
 Each event has a probability of 0.5, so on average half the children will be
normal and half will express the disease.
o Autosomal recessive – individual must be homozygous for a recessive allele to
express the disease – can survive the population one generation to the next
 Characterized by delay of onset, incomplete penetrance, and variable
expressivity – most common is cystic fibrosis
 Recurrence risk for the offspring of carrier parents is 25%

 Klinefelter’s syndrome (mod 1) (148, 156, 914)

o Causes
 Chromosomal disorder XXY – genotype
 Genetically male – due to Y
 Male XY, female XX
 Random, not inherited – nondisjunction in the X chromosomes in the
mother
o Signs and Symptoms
 Both male and female sexual characteristics
 Decreased T  more female hormones causing
 Less body and facial hair
 Gynecomastia (risk breast CA)
 Weak muscles and bones (osteoporosis), shy (tall, lanky, shy)
 Can result in decreased IQ
 Higher risk of AI disorders
 Majority - Infertility



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, o Testing
 Clinical Exam
 Chromosomal testing
 Hormones


Immunology
 Rickets disease (1599-1600)

o Disorder in which growing bones fails to become mineralized, resulting in “soft”
bones and skeletal deformity.
o Results from insufficient vitamin D, insensitivity to vitamin D, wasting of
Vitamin D by the kidney, or inability to absorb Vitamin D and calcium in the gut
o Most common form is x-linked hypophosphatemic rickets in industrialized
nations
o In US it happens in children due to lack of dietary vitamin D – can lead to early
fracture or slow bone healing after fracture
o Can lead to short stature, bowing of the limbs with broad, irregular growth plates,
often listless and irritable with hypotonia and muscle weakness may be unable to
walk without support; abnormal parietal flattening and frontal bossing occur in
the skull
o Normalization of calcium, phosphorus, and vitamin D levels before surgical
intervention, deformity often improves when bone metabolism improves
o Hypocalcemia

 Epstein-Barr Virus (318t, 1078-1079, 1011)

o Adenovirus, herpesviruses – transmitted via saliva, disease: mono, burkitt
lymphoma
o Strongly associated with non-hodgkin lymphoma in children
o EBV and African Burkitt Lymphoma
o Etiologic agent for mono: EBV – ubiquitous, lymphotrophic, gamma-group
herpesvirus accounting for approximately 85% of mono cases
o Early EBV infections are usually asymptomatic and provide immunity to EBV
later in life

 Human Herpes Virus (HHV) 8 (382, 383, 1645)

o Kaposi’s Sarcoma
 Commonly occurs in older men but now occurs in a markedly more
virulent form in immunocompromised individuals (AIDS)
o Linked to several rare lymphomas
o Associated with cancer in humans
o Member of Herpesviridae family


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