Upper GI disorders Flashcards
cholelithiasis
gallstones bile states -> formed stones 3 factors - supersaturatoin of Bile w/ cholesterol - nucleation of crystals - hypomotility
risk factors for cholelithiasis
high spinal injury TPN prolonged fasting rapid wt. loss pregnancy oral contraceptive obesity DM women IN CHILDREN - cystic fibrosis - sickle cell
chronic cholelithiasis
intermittent biliary colic, persistent epigastric or RUQ pain
chronic cholelithiasis s/s
pain radiates to back
N/V
sweating
gas
acute cholecystitis s/s
severe RUQ pain radiates to back tenderness fever cystic duct obstruction bacterial infection
acalculous cholecysitis
without preexisting gallstones
- major surgery
- critical illness
- trauma
- burns
- TPN
GERD
function and structure alteration of the gastroesophageal junction anything that dec. LES pressure or inc. intraabdominal pressure
GERD risk factors
fatty foods caffeine alcohol smoking sleep position obesity
GERD s/s
heartburn
regurgitation
chest pain
dysphagia
persistent GERD can lead to
esophageal strictures barrett esophagus pulmonary s/s - cough - laryngitis
N/V
disturbances in gastric motility
alteration in vestibular system/ taste/olfaction
gastric dysrhythmia
inc. release of nitric oxide
down-regulation of stimulatory G protein expression
up-regulation of inhibitory G protein expression
-> dec. gastric contractility and emptying
abdominal bloating and constipation
changes in H2O absorption mechanical factors dietary factors dec. physical activity hormonal effects
dysphagia d/t nervous system
postpolio syndrome
multiple sclerosis
muscular dystrophy
parkinsons
dysphagia d/t immune system
inflammation and weakness
- polymyositis
- dermatomyositis
dysphagia d/t scleroderma
tissues of the esophagus become hard and narrow
dysphagia d/t blockages
GERD
diverticula
tumors/growth
Achalasia
LES fails to relax Loss of intrinsic inhibitory innervation - aperistalsis - incomplete relaxation - inc. resting tone
achalasia ->
dysphagia
mucosal inflammation and ulceration
squamous cell carcinoma
Sliding Hiatal hernia
portion of stomach and gastroesophageal junction slide into thorax
visceral peritoneum remains intact and restrains the size of hernia
paraesophageal hiatal hernia
greater curvature of stomach rolls through the diaphragmatic defect
membrane becomes thinned out or defection -> true peritoneal sac to protrude into the posterior mediastinum where negative intrathroacic pressure causes it to enlarge.
hiatal hernia risk factors
inc. intraabdominal pressure
- ascites
- preg
- obesity
- chronic straining/coughing
hiatal hernia s/s
GERD
ulceration on the mucosal surface: cameron ulcers
anorexia nervosa
lack of desire to eat despite stimuli that normally produces hunger
- poor body image
- can lose 25-30% of ideal body weight d/t fat and muscle depletion/atropy
- can lead to starvation induced cardiac failure
- females -> absence of menstruation
Bulimia nervosa
body wt remains near normal but with aspirations for wt. loss
- recurrent binge eating
- self-induced vomiting -> pitted teeth, pharyngeal and esophageal inflammation, and tracheoesphageal fistulae
- fasting to oppose the effect of binge eating, or excessive exercise
- overuse of laxatives -> rectal bleeding and relying on laxatives
Long-term starvation
Kwashiorkor
Marasmus
- stunted physical and mental development
- presence of subQ fat, hepatomegaly
- fatty liver differentiates between the 2
Kwashiorkor
lack of proteins causes liver to swell due to the inability to produce lipoproteins for cholesterol synthesis
Marasmus
liver function continues, but overall caloric intake is too low to support cellular protein synthesis
- deficiency of all nutrients
retching
nonproductive vomiting
projectile vomiting
spontaneous vomiting that does not follow nausea or retching
Abdominal pain
may be first sign of GI disorder 3 types - visceral - somatic - referred
visceral abd. pain
stretching/distending abd. organ
inflammation
- diffuse, poorly localized
- gnawing, burning, cramping
somatic abd. pain
injury to abd. wall, parietal peritoneum, root of mesentery, or diaphragm
- sharper more intense, localized
referred pain
felt at distant location from source
- same dermatome/neurosegments
sharp, well localized, skin or deeper tissues
peptic ulcer disease
break or ulceration in the protective mucosal lining of the lower esophagus, stomach, or duodenum
- superficial: erosions
- deep: true ulcer
caused by hydrocholoric acid and pepsin
hydrochloric acid and injury to mucosa
potentiates pepsin and other injury substances with aspirin and NSAID use
duodenal ulcer
most common peptic ulcer development factors - H. pyloryi -> lower bicarb levels in duodenum - inc. stomach acid and pepsin - NSAIDS - inc. gastrin - acid production by smoking - stress: glucocorticoid release -> inc. acid production - heredity
H. pylori virulence
unique, lengthy DNA sequences
- pathogenicity islands
peptic ulcer s/s
epigastric burning, relieved with eating or antacids - worse with empty stomach (gastric) - worse 2-3 hr after meal (duodenal) nausea abd. pain/upset chest discomfort
gastric ulcer
tends to be in antral region of stomach, adjacent to the acid-secreting mucosa
- inc. mucosal permeability to H+
- gastric secretion is normal or less than nml
gastric ulcer patho
damaged mucosal barrier
- > dec. function of mucosal cells, loss to tight junctions
- > back diffusion of acid into gastric mucosa
- > pepsinogen converts to pepsin
- > further mucosal erosion, destruction of blood vessels, bleeding
- > ulceration
stress ulcer
peptic ulcer that is r/t severe illness, neural injury, or systemic trauma
- ischemic
- cushing: r/t burn injury
stress ulcer s/s
bleeding
gastritis
inflammation of stomach lining /mucosa Triggered by toxins - ETOH - aspirin - irritating substances (viral, bacterial, autoimmune) - tobacco
Acute gastritis
H. pylori
NSAIDs
Chronic gastritis
chronic fundal gastritis chronic antral gastritis - s/s often do not correlate with disease severity. Atrophy intestinal metaplasia lymphoid aggregates neutrophil infiltrates
gastritis s/s
anorexia
N/V
postprandial discomfort
Peptic ulcer bed 4 layers
necrotic debris (top most)
inflammatory layer
granulation tissue
fibrous scar (deepest)
damaging forces to gastric mucosa
gastic acidity
peptic enzymes
H. pylori
drugs
defensive forces of gastric mucosa
mucus secretion bicarbonate mucosal blood flow apical surface membrane transport epithelial regenerative capacity Elaboration of prostaglandins
Esophageal varices
impaired hepatic portal blood flow
- associated with alcoholic cirrhosis
~ 2/3 of cirrhosis pts
esophageal varices complication
rupture
-> hematemesis
20-30% die on each episode
70% recurrence rate
cholesterol gallstone 3 phases
- superstauration of bile with cholesterol -> precipitation
- nucleation of crystals
- hypomotility (stasis of bile) allow for stone growth
