Exam (elaborations)
Patho Exam 2 UNMC
- Module
- GOVT 350 Exam 1
- Institution
- GOVT 350 Exam 1
Exam of 20 pages for the course GOVT 350 Exam 1 at GOVT 350 Exam 1 (Patho Exam 2 UNMC)
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Patho Exam 2 UNMCTrachea-esophageal fistula - ANS--Cells of the embryonic foregut fail to differentiate
during the developmental period.
-Foregut fails to separate into a totally separate esophagus and trachea, resulting in a
patent fistula between the two structures.
Esophageal atresia - ANS--Cells of the embryonic foregut fail to develop.
-Incorrect development leads to a pouch at the end of the esophagus and no connection
to the stomach.
Clinical Manifestations of Trachea-esophageal fistula and Esophageal atresia -
ANS-Manifestations are similar. Manifestations relate to the fact that there is no normal
pathway from the esophagus down to the stomach, and that there is an opening
between the trachea and either the esophagus or the stomach.
Manifestations of Trachea-esophageal fistula and esophageal atresia cont. -
ANS--Infants are unable to handle oral secretions and usually have what appears to be
increased oral secretions.
Coughing/choking/spitting up of feedings
-Aspiration into the lungs is a potential complication
-Abdominal distention with the type in example C (they swallow air)
Pyloric Stenosis - ANS-Genetically influenced abnormal narrowing of the pyloric
sphincter connecting the stomach and small intestine.
Patho of Pyloric Stenosis - ANS-Sphincter muscle hypertrophies during development.
This hypertrophy narrows the opening of the sphincter. This causes a delayed stomach
emptying into the small intestine.
Clinical Manifestations of Pyloric Stenosis - ANS-Vomiting is the primary manifestation.
There is increased pressure and fullness due to the stomach not emptying correctly.
This vomiting usually occurs during or after feedings.
,Constipation. The delayed stomach emptying also can slow things down in the GI tract
causing some constipation.
General Causes of Malabsorption - ANS-Incomplete digestion of nutrients. For example,
having deficient enzymes of digestions such as lactase so lactose cannot be broken
down.
Abnormalities of the absorptive surface. Biochemical or genetic. Inflammatory or
infectious disorders causing abnormalities with the absorptive surface.
Lack of absorptive surface area.
Patho of Ulcerative Colitis - ANS-Begins in the rectum and extends into the sigmoid
colon. Inflammatory process usually begins at the bases of the crypts of Lieberkuhn.
Inflammation causes the mucosa to become swollen and engorged with blood, and dark
red. Erosions of the mucosa form and lead to mucosal hemorrhages. This leads to
further ulcerations, and mucosal destruction. Bowel lumen often is narrowed, and there
is sloughing off of the mucosa and the bowel fills with a bloody, mucousy secretion.
Main problem is the loss of absorptive surface in the sigmoid area. Ulcerative colitis is
characterized by periods of exacerbations and remissions.
Clinical Manifestations of Ulcerative Colitis - ANS-• Cramping abdominal pain
• Bloody, mucousy diarrhea
• Fluid and electrolyte imbalances
• Weight loss
• Anemia
Patho of Crohns Disease - ANS-An inflammatory process starts in the submucosa. The
process spreads inward and outward leading to transmural lesions (lesions that affect
the entire width of the intestinal wall). These lesions can affect certain segments but not
others, therefore are also called skip lesions.
Clinical Manifestations of Crohns Disease - ANS-• Individuals may have nonspecific
diarrhea for several years.
• Non-bloody diarrhea
• Abdominal pain (usually right lower quadrant)
• Fluid and electrolyte imbalance
• Vitamin deficiencies and hypoproteinemia
• Weight loss
, • A complication that can occur related to the strictures is intestinal obstruction.
• A complication that can occur related to formation of fissures is fistulas, and possible
peritonitis.
Patho of Stress Ulcers - ANS-Related to ischemia. The major insult to the body leads to
shunting of blood away from the gut. This leads to decreased metabolism of mucosal
cells, and then degeneration of the mucosal lining. The mucosa is then unable to protect
itself from the acid in the GI tract.
Usually occur after a major insult to the body (shock, burns, drug ingestion, severe
infections).
Patho of Gastric Ulcers - ANS-The mucosal barrier has an increased permeability to H+.
This leads to a "Back-Diffusion of acid" back into the mucosa and stomach lining. This
leads to ulceration.
Clinical Manifestations of Gastric Ulcers - ANS-• Pain, usually upper abdominal pain, is
normally intermittent, but has no particular pattern.
•Hemorrhage/perforation
• Tend to be more chronic
Patho of Duodenal Ulcers - ANS-increased acid concentrations --> penetrate the
mucosal barrier --> ulceration
Clinical Manifestations of Duodenal Ulcers - ANS-• Chronic intermittent epigastric pain
that usually follows a particular pattern of "pain --food--relief".
• Pain occurs, and is usually relieved after eating.
• Pain may recur 2 to 3 hours after eating.
•Hemorrhage/perforation
Patho of Musculoskeletal Traumatic Injuries - ANS--Inflammatory exudate develops
between torn ends.
-Repair process - granulation (healthy, new) tissue.
-Collagen formation (connective tissue).
-Vascular fibrous tissue fuses tissues into single mass.
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