Capstone College of Nursing
NUR 529 Exam 3 Blueprint
Pages referred to below are from Porth’s Pathophysiology: Concepts of Altered States, 11th ed.,
and the current e-book on coursepoint. Older versions are not included, this course does not
utilize older textbook versions. Format for page numbers below is Porth 10th ed “hard copy”
book/ Course Point Porth E-Book. Example: p. 967/975. If the pages correlate between editions
then only one will be listed.
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Unit 11. Disorders of GI Function. Chapters 36-39. There are 10 questions from this unit.
1. Chapter 36. Intestinal flora, roles. Essential vitamins in clotting, what are they and
how are they made? Pg. 1067.
p.1095
The major metabolic function of colonic microflora is the fermentation of
undigestible dietary residue and endogenous mucus produced by the epithelial cells.
The genetic diversity of the microorganisms in the gut provides various enzymes and
biochemical pathways that are distinct from those of the host. Fermentation of
nondigestible carbohydrates, including resistant starches, cellulose, pectins, and
unabsorbed sugars, is a major source of energy in the colon.
Colonic microorganisms also play a role in vitamin synthesis and in absorption of
calcium, magnesium, and iron. The colonic flora, for example, synthesizes vitamin
K. The newborn infant does not synthesize an adequate amount of vitamin K for the
first week or so of life until the normal colonic bacterial flora becomes established.
2. Chapter 37. Disorders of Gastrointestinal Function. Alterations in intestinal
absorption. Celiac disease. What are the dietary recommendations for celiac disease?
Pg. 1107.
(note: I am not expecting you to learn Table 37.2 but I do recommend printing this
table and putting it in your notebook/clipboard for clinicals).
p.1139
Celiac disease, also known as Celiac sprue and Gluten-sensitive enteropathy, is an
immune-mediated condition characterized by small intestinal enteropathy, systemic
symptoms related to malabsorption and/or immune activation, and autoantibodies to
tissue transglutaminase (TTG). It is unique among the autoimmune diseases in that
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, the trigger, dietary gluten-containing grains (including wheat, barley, and rye), has
been identified, and its removal results in resolution of symptoms and enteropathy in
the majority of patients (Lebwohl & Rubio-Tapia, 2021; Posner & Haseeb, 2020).
The primary treatment of celiac disease consists of removal of gluten and related
proteins from the diet. Gluten is the primary protein in wheat, barley, and rye. Oat
products, which are nontoxic, may be contaminated with wheat during processing.
Many gluten-free types of bread, cereals, cookies, and other products are available
(Posner & Haseeb, 2020). Meats, vegetables, fruits, and dairy products are free of
gluten as long as they are not contaminated during processing. Complete exclusion of
dietary gluten generally results in rapid and complete healing of the intestinal
mucosa.
3. Chapter 37. Disorders of the Stomach. Gastric mucosal layers. Which medications
affect the mucosal layer? Which ones increase the risk for GI bleeding? Pg. 1083.
p.1112
Nonsteroidal antiinflammatory drugs (NSAIDs) (e.g., aspirin) are commonly used for
relieving inflammation and pain. However, frequent usage is associated with GI
lesions (e.g., peptic ulcers) because the drug is able to cross the lipid layer and cause
damage to the superficial cells, which can result in acute erosions (Vakil, 2022).
Gastric irritation and occult bleeding due to gastric irritation occur in a significant
number of people who take aspirin on a regular basis. Alcohol, which like aspirin is
lipid-soluble, also disrupts the mucosal barrier. When aspirin and alcohol are taken in
combination, the permeability of the gastric mucosal barrier is significantly increased
and cellular damage occurs. Bile acids also attack the lipid components of the
mucosal barrier and afford the potential for gastric irritation when there is reflux of
duodenal contents into the stomach.
4. Chapter 38. Disorders of Hepatobiliary and Exocrine Pancreas Function. Bilirubin
elimination and jaundice. How do we get rid of bilirubin? Pg. 1122.
p.1157
Bilirubin is the final product of the breakdown of heme contained in aged red blood
cells. Bilirubin is the substance that gives bile its color. In the process of degradation,
the hemoglobin from the red blood cell is broken down to form biliverdin, which is
rapidly converted to free bilirubin (Fig. 38.7). Free bilirubin, which is insoluble in
plasma, is transported in the blood attached to plasma albumin. Even when it is bound
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