NR 507 PATHO MIDTERM STUDY GUIDE / NR507 PATHO MIDTERM STUDY GUIDE:NEWEST-2022,CHAMBERLAIN
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Course
NR 507 (NR507)
Institution
Chamberlain College Of Nursing
NR 507 PATHO MIDTERM STUDY GUIDE / NR507 PATHO MIDTERM STUDY GUIDE:NEWEST-2022,CHAMBERLAINNR 507 PATHO MIDTERM STUDY GUIDE / NR507 PATHO MIDTERM STUDY GUIDE:NEWEST-2022,CHAMBERLAINNR 507 PATHO MIDTERM STUDY GUIDE / NR507 PATHO MIDTERM STUDY GUIDE:NEWEST-2022,CHAMBERLAIN
NR 507 PATHO MIDTERM STUDY GUIDDE
Pathophysiology classmates, lets all contribute to filling out the midterm study
guide as a team! This not only helps us to fill out the whole study guide
quickly but it also is a great way to see important information that maybe you
didn’t understand or missed in your own reading!! Also please put page
numbers if the information is from the textbook =)
Chapters
Chapter 1: Cellular Biology
Chapter 2: Altered Cellular and Tissue Biology
Chapter 6: Epigenetics and Disease
Chapter 7: Innate Immunity: Inflammation
Chapter 8: Adaptive Immunity
Chapter 9: Alterations in Immunity and Inflammation
Chapter 10: Infection
Chapter 12: Cancer Biology
Chapter 13: Cancer Epidemiology
Chapter 14: Cancer in Children
Chapter 30: Alterations in Hematologic Function in Children
Chapter 34: Structure and Function of the Pulmonary System
Chapter 35: Alterations in Pulmonary Functions
Chapter 36: Alterations in Pulmonary Function in Children
Chapter 37: Structure and Function of the Renal and Urologic Systems
Chapter 38: Alterations of Renal and Urinary Tract Function
,Chapter 39: Alterations of Renal and Urinary Tract Function in Children
Epigenetics (Note, Chapter 6 should be reviewed)
Epigenetics and its role on human development
Compare and contrast Prader-Willi syndrome and Angelman syndrome
Cellular Proliferation
the role of inactive MLH1 in the development of some forms of inherited colon
cancer (p. 1468-1470) p.186
MLH1 is a deoxyribonucleic acid (DNA) mismatch repair gene, essentially a
tumor suppressor gene in this case. If MLH1 is inactive, repair is unable to
be made to the DNA mismatches and the hereditary factor of colon cancer
(see below) is able to proliferate.
Progression from polyps to colon cancer (1) activation of proto-oncogenes
(promote cell growth) (2) loss of tumor-suppressor gene activity (inhibit cell
growth]); and (3) abnormalities in DNA mismatch repair (MMR) genes (fix
errors in DNA replication and recombination
Microsatellite instability = genetic hypermutability (predisposition to
mutation) that results from DNA MMR. Usually right sided colon proximal
to splenic flexure, associated with autosomal dominant hereditary polyposis
colorectal cancer.
Inflammation as an etiology for cancer-note conditions in which this may occur (p.
403)
Chronic inflammation caused by infiltrating immune cells help to create a
permissive tumor progressing environment. Also thought to precede and
initiate malignant change in many cancers (colon, liver, lung)
Numerous environmentally-linked reasons for inflammation (tobacco
smoke, exhaust, asbestos, fine particles in air) and can be linked to many
cancers (lung)
Chronic inflammation and cancer development = continuous presence of
cytokines (soluble factor that affects neighboring cell, can be pro- or anti-
inflammatory, interleukins or interferons)(p203-205), chemokines (low-
molecular weight peptide that induce leukocyte chemotaxis or directional
movement of cells on a chemical gradient)(p203-205), reactive oxygen
species (free radical that damages cell membrane)(p59-60), oncogenes
, (mutant genes that in their normal nonmutant state direct synthesis of protein
that positively regulate or accelerate proliferation), amongst others
Cancer
In terms of epigenetic modifications, the role of environmental stressors associated
with development of cancer
Defects in Mechanism of Defense
Hemolytic defects in the newborn
Understand the meaning of infectivity: Ability of the pathogen to establish an
infection.
Most effective treatment for HIV - Page 327 - Antiretroviral therapy (ART) in
different combinations. In general, at least three drugs used as a cocktail (2 NRTIs
and one from another class (NNRTI, PI, INSTI or CCR% antagonist). Death
reduced significantly with compliance. Without meds, death in 9 to 10 months.
No cure, just good response with decades of life. Even with success avoiding
oportunistic infections, HIV patients at higher risk for comorbidities
(cardiovascular disease, renal disease, diabetes, liver disease). Development of
effective vaccine greatest hope in fight against AIDS. Providers recommend to
screen adults 15 – 65 for the disease. Those younger and older with increased risk
should be tested. 😀
Defected cells of HIV
Signs of T-Lymphocyte deficiency
Pulmonary Alterations
Pulmonary function tests (see pages 1243-1243)
Spirometry: measures volume and flow rate during forced expiration
Alveolar-arterial oxygen gradient: evaluates cause of hypoxia
Diffusing Capacity: a measure of the gas diffusion rate at the
alveolocapillary membrane
Arterial blood gas: used to determine pH, oxygen, and CO2 concentrations
Radiographic chest exams: evaluates air trapping, consolidation, cavity
formation, or presence of tumors
, ABG used to determine pH and o2 and CO2 concentrations (most accurate).
Diffusing capacity measure of the gas diffusion rate at alveolocapillary
membrane Ex. residual volume, total lung capacity, functional reserve
capacity. Determine cause of hypoxiua use alveolar-arterial oxygen
gradient.
Chest xray views air trapping, consolidation, tumors, and cavity formation
Relationship of lung compliance and residual volume
Chest wall compliance decreases with age losing some of its ability to
expand, respiratory muscle strength and endurance decreases. These mechanical
changes in the lung and chest wall reduces ventilatory capacity in older adults. As
vital capacity decreases, residual volume increases, but total lung capacity remains
the same. (see pages 1244-1245)
Relationship of lung compliance and residual volume: decreased lung
compliance=vital capacity decrease=residual volume increases Ex. as seen in
normal aging
Shifts in the oxyhemoglobin dissociation-pg. 1241-1242 (Pam Grant)
Shifts in the oxyhemoglobin dissociation: (process in which oxygen is released
from hemoglobin occurring the body tissues at the cellular level), oxyhemoglobin
is when hemoglobin molecules wind with oxygen this occurs in the lungs and is
called oxyhemoglobin association or hemoglobin saturation.
The shift occurs right or left on the curve. Right shift oxygen moved into the
cells such as by acidosis and hypercapnia. A left shift means association in
the lungs and dissociation in the tissues by alkalosis and hypocapnia..
When hemoglobin saturation and desaturation are plotted on a graph, the result is a
distinctive S-shaped curve known as oxyhemoglobin dissociation curve. Several
factors can change the relationship between Pao2 and Sao2, causing the
oxyhemoglobin dissociation curve to shift to the right or left.
A shift to the right depicts hemoglobin's decreased affinity for oxygen or an
increase in the ease with which oxyhemoglobin dissociates and oxygen
moves into the cells. The curve is shifted right by acidosis (low pH) and
hypercapnia (increased Paco2).
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