GI - Patho E3 Flashcards
IBS key points
-IBS D&C
-distention, fullness, bloating, flatus
-intermittent
-exacerbated by stress, relieved by defecation
-intolerance to certain foods (sorbitol, lactose, gluten)
-non bloody stools
what can trigger IBS
stress, food, hormone changes, GI infections, menses
IBD is most common in
women
Caucasians
jewish descent
smokers
etiology of IBD
genetically autoimmune activated by an infection
Crohn’s patho
lymph structures get blocked -> tissues become engorged & inflamed -> fissures & ulcers develop in patchy patterns skip lesions w/ cobblestone apperance
complications of Crohn’s disease
-malnutrition (anemia)
-scare tissue & obstructions
-fistulas
-cancer
Crohn’s disease clinical manifestations
-cramping in RLQ
-watery diarrhea
-systemic wt loss, fatigue, no appetite, fever, malabsorption
-palpable abdominal mass (RLQ)
-mouth ulcers
-s/s of fistulas
Crohn’s disease affects what part of the GI tract
mostly the upper portion and small intestines with a little bit of the rectum
UC affects what what part of the GI tract
the rectum & colon
UC pathogenesis
inflammation begins in the rectum & extends in a continuous segment that may involve the entire colon -> inflam leads to large ulcerations & necrosis which can cause crypt abscesses -> body tries to repair w/ new granulation tissue but tissue is fragile & and bleeds easily
UC clinical manifestations
-abdominal pain
-bloody diarrhea
-systemic: wt loss, fatigue, no appetite, fever
complications of UC
hemorrhage, perforation, cancer, malnut, anemia, liver disease, fluid/lyte/pH imbalances
toxic megacolon: rapid dilation of the large intestine that be life threatening
both UC & Crohn’s disease put a patient at risk for
DVTs & PEs
what causes diverticulosis
low fiber diet resulting w/ chronic constipation
clinical manifestations of diverticulitis
abdominal pain (LLQ)
fever
inc WBCs
constipation or diarrhea
acute passage of frank stool
complications of diverticulitis
peritonitis
obstruction
perforation
the upper GI includes
esophagus
stomach
beginning of the small intestine (duodenum)
the lower GI includes
small intestine
colon
rectum
anus
what do we want to prevent in people w/ gerd
barrett esophagus (development of abnormal metaplastic tissue that - premalignant)
3 fold increase of developing esophageal cancer
hiatal hernia
a defect in the diaphragm that allows part of the stomach to pass into the thorax
sliding hiatal hernia
usually small & often does not need treatment
paraesophageal hiatal hernia
part of the stomach pushes through the diaphragm & stays there
hiatal hernia clinical manifestations
-belching
-dysphagia
-chest or epigastric pain
-too much pressure on the muscles around stomach leading to severe coughing, vomiting, & constipation
hiatal hernia treatment / education
-SFM
-don’t lay after meals
-avoid tight clothing
-wt control
-antacids
acute gastritis
temporary inflammation of only the stomach lining (no intestines included) that lasts 2-10 days
acute gastritis etiology
irritating substances (alc)
drugs (NSAIDs)
infectious agents (H.pylori)
chronic gastritis
progressive disorder with chronic inflammation in the stomach
complications of chronic gastritis
PUD
bleeding ulcers
anemia
gastric cancers
chronic gastritis etiologies
1) autoimmune -> attacks the parietal cells
2) H.pylori infection
what can H.pylori cause
chronic gastritis
PUD
stomach cancer
how is H.pylori transmitted
-person to person via salvia, fecal matter or vomit
-contaminated food or water
acute or chronic gastritis sx
anorexia
N/v
postprandial discomfort
intestinal gas
hematemesis
tarry stools
anemia
acute gastroenteritis
inflammation of the stomach & small intestine
acute gastroenteritis etiologies
1) viral infections- norovirus & rotavirus
2) bacterial infections- E.col, salmonella, campylobacter
3) parasitic infections
acute gastroenteritis clinical manifestations
-watery diarrhea (possibly w/ blood if bacteria)
-abdominal pain
-N/v
-fever, malaise
acute gastroenteritis complication
fluid volume deficit because of mass amount of diarrhea
acute gastroenteritis treatment
let the patient right it out but may need to give fluids
when does PUD develop
when the GI tract is exposed to acid and h. pylori
(+NSAIDs, ASA, Alc)
+smoking
+stress bc inc gastric acid is a stress response
why can NSAIDs induce PUD
they inhibit prostaglandins synthesis so the upper GI loses the mucus coating
PUD clinical manifestations
-N/v
-anorexia
-wt loss
-bleeding
-burning pain (middle abdomen)
gastric ulcer
CM: burning, cramping, gas like
location: epigastrium, back
timing: 1-2 hr after eating
duodenal ulcer
CM: burning, cramping, gas like
location: epigastrium, back
timing: 2-4 hrs after eating
complications of PUD
hemorrhage
obstruction
perforation / peritonitis
complications of appendicitis
gangrene
abscess formation
peritonitis
key points of appendicitis
-RLQ pain
-rebound pain
-sudden relief of pain if it ruptures
peritonitis
inflammation of the peritoneum that causes 3rd spacing which can lead to hypovolemic shock, sepsis, & decreased peristalsis -> paralytic ileus
peritonitis clinical manifestations
-sudden & severe pain
-abdominal pain
-tenderness
-rigid, board like abdomen
-N/v
vitals/labs seen during peritonitis
fever
elevated WBCs
increased HR
decreased BP
