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NURS 5315 / NURS5315 Advanced Pathophysiology GASTROINTESTINAL (GRADED A+)
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NURS 5315 / NURS5315 Advanced Pathophysiology GASTROINTESTINAL (GRADED A+)
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N5315 Advanced PathophysiologyGastrointestinal
Core Knowledge Objectives with Advanced Organizers
Gastrointestinal Bleeds
1. Analyze the etiology, clinical manifestations, and pathophysiology of the upper and lower GI
bleed and describe the implications this has for your clinical practice as a nurse practitioner.
Disease Etiology Clinical Pathophysiology Implications for
Manifestations Practice
Upper Bleeding varices Frank, bright red or Any source of If left untreated or
GI (varicose veins) in “coffee ground” bleeding which if severe, can
Bleed the esophagus or (affected by occurs in the result in shock.
stomach, peptic stomach) emesis esophagus,
ulcers, gastritis, or Hematemesis = stomach, or
a Mallory-Weiss bright red, bloody duodenum.
tear (tearing of emesis= requires
esophagus from emergent
stomach) intervention.
Melena = black
tarry.
Shock symptoms if
untreated:
decreased CO,
hypotension, ARF,
tachycardia, and
anemia.
Lower Inflammatory Hematochezia: Any source of Occult GI bleed is
GI bowel disease, bright red blood in bleeding in the one that is not
Bleed cancer, stools and the jejunum, ileum, visible and results
diverticula, or presence suggest colon, or rectum. in iron deficiency.
hemorrhoids bleed in lower track Type of bleed
usually rectum, associated with
sigmoid colon, or colon cancer. =
descending colon. testing stools for
occult blood
Peptic Ulcer Disease
2. Analyze the etiology, clinical manifestations, and pathophysiology of gastric and duodenal
ulcers and describe the implications for clinical practice.
Disease Etiology Clinical Pathophysiology Clinical Implications
Manifestations
Gastric Ages 55-65, Epigastric pain Decreased Complications include
Ulcer typically which worsens mucosal protection bleeding or
s caused by when eating, or increased acid perforation. If a
, NSAIDs. melena, production. perforation occurs,
Chronic use of hematemesis or Infection with H. luminal contents can
NSAIDs coffee ground pylori. escape into the
suppresses emesis. peritoneum and cause
mucosal peritonitis.
prostaglandin Treatment is similar to
synthesis, duodenal ulcer
resulting in treatment. See p. 1437
decreased
bicarbonate
secretion and
mucin
production
Duodenal Younger Epigastric pain Acid and pepsin Endoscopic
Ulcers patients relieved by food. concentration in evaluation.
More common Pain will recur the duodenum Radioimmunoassay of
than any other when stomach is penetrating the gastrin levels to
type of ulcers empty, which may mucosal barrier identify ulcers
be 30min-2 hr and lead to associated with
after eating. Pain ulceration carcinomas. Urea
is relieved by breath test.
eating food or Management is aimed
antacids.Melena at relieving the causes
or hematemesis is and effects of acidity
also present and preventing
complications.
Antacids, PPI, H2
blockers, eradication
of H. pylori , ulcer
coating agents such as
sucralfate, surgical
resection for
perforation, obstruction
or peritonitis.
Risk of duodenal
ulcers may be reduced
with diet high in vit A
and fiber.
Disorders of the Intestines
3. Differentiate between the etiology, clinical manifestations, and pathophysiology of disorders
of the small and large intestines.
a. Analyze the etiology, clinical manifestations, and pathophysiology of ulcerative colitis and
crohn’s disease and describe the implications on nutritional status.
Disease Etiology Clinical Pathophysiology Nutrition
Manifestations Implications
, Ulcerative Unknown origin, Chronic, Inflammatory Complications
Colitis associated with recurrent, bloody disease of large include toxic
genetic factors, diarrhea. Febrile, intestine. Like megacolon, colon
alterations in polyarthritis, Crohn’s it has perforation, and
epithelial cell uveitis, sclerosing periods of remission colorectal
barrier functions, cholangitis, and exacerbations. adenocarcinoma.
immunopathology erythema Severe Increase risk for
related to nodosum, and inflammation and colon cancer.
abnormal T cell pyoderma ulcerations of large Nicotine has a
reactions to gangrenosum. intestine which protective effect.
commensal begins in rectum In extreme cases
microflora and and involves entire IV fluids and IV
other luminal large intestine. It nutrition
antigens only affects colon
(not small intestine)
and does not have
skipped lesions no
transmural
inflammations and
ulcerations = it
remains superficial.
Crohn’s Affects persons in Abdominal pain, Inflammatory Increased risk of
Disease their 20s-30s and diarrhea, disorder of GI tract colon cancer.
of Jewish descent. dehydration, with exacerbations If ileum is
Causes include bloody stools, and remissions. involved, one can
infectious agents malabsorption, May affect any have vit B12
(viruses or malnutrition, portion of the GI deficiency
bacteria), weight loss (most tract (mouth to anemia, folic acid
autoimmune, nutrients anus) but most and vit d and
psychosomatic, absorbed in small often in the ileum calcium. Loss of
and impaired T-cell intestine), or proximal colon. protein leading to
immunity. intestinal Pathophys includes hypoalbuminemia
obstruction from transmural
chronic involvement of the
inflammation, affected area (entire
fistulas (abnormal wall of the intestine
tracts/channels is affected) and
that develop in presence of skip
the presence of lesions. This means
inflammation), that there are
and perforation of healthy, unaffected
the intestine. tissue surrounded
They can develop by diseased tissue
strictures which which are randomly
cause obstruction present in the GI
or fistulas tract.
between
intestines,
bladder, and
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