Grand Canyon University NUR 631 Midterm Study Guide.

NUR 631 Topic 8 Midterm Study Guide 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)
oEx: liver, hepatocyte growth
oAdaptive mechanism that enables certain organs to regenerate
oEven with removal of 70% of the liver, it will regenerate within about 2 weeks
oCompensatory 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)
oBenign 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.
oSome 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
1 BENIGN TUMORS MALIGNANT TUMORS
Grow slowly
Have a well-defined capsule
Are not invasive
Are well differentiated; look like
the tissue from which they arose
Have a low miotic index; dividing cells are rare
Do not metastasizeGrow rapidly
Are not encapsulated
Invade local structures and tissues
Are poorly differentiated; may not be able to determine the tissue of orgin
High miotic index; many dividing cells
Can spread distantly; often through blood vessels and lymphatics
Genetics
Recurrence of autosomal diseases (152-154, 155-156)
oAutosomal 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. oAutosomal 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)
oCauses
Chromosomal disorder XXY – genotype
Genetically male – due to Y
Male XY, female XX
Random, not inherited – nondisjunction in the X chromosomes in the mother
oSigns 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 2 oTesting
Clinical Exam
Chromosomal testing
Hormones Immunology
Rickets disease (1599-1600)
oDisorder in which growing bones fails to become mineralized, resulting in “soft” bones and skeletal deformity. oResults 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
oMost common form is x-linked hypophosphatemic rickets in industrialized nations
oIn US it happens in children due to lack of dietary vitamin D – can lead to early fracture or slow bone healing after fracture
oCan 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
oNormalization of calcium, phosphorus, and vitamin D levels before surgical intervention, deformity often improves when bone metabolism improves
oHypocalcemia
Epstein-Barr Virus (318t, 1078-1079, 1011)
oAdenovirus, herpesviruses – transmitted via saliva, disease: mono, burkitt lymphoma
oStrongly associated with non-hodgkin lymphoma in children
oEBV and African Burkitt Lymphoma
oEtiologic agent for mono: EBV – ubiquitous, lymphotrophic, gamma-group herpesvirus accounting for approximately 85% of mono cases
oEarly EBV infections are usually asymptomatic and provide immunity to EBV later in life
Human Herpes Virus (HHV) 8 (382, 383, 1645)
oKaposi’s Sarcoma
Commonly occurs in older men but now occurs in a markedly more virulent form in immunocompromised individuals (AIDS)
oLinked to several rare lymphomas
oAssociated with cancer in humans
oMember of Herpesviridae family
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