GI pathology

esophagus

connects mouth to stomach

peristalsis

waves of muscular contractions to propel food downwards towards stomach

top 1/3 of esophagus has

voluntary control

bottom 2/3 esophagus has

involuntary control

lower esophageal sphincter

band of muscle around esophagus preventing stomach contents from refluxing upward into esophagus (involuntary control)

stomach

site of food digestion into chime, has a low pH to kill off bacteria

small intestine

site of food/chime absorption, mucosa in villi and microvilli increase SA for absorption of nutrients

pyloric sphincter

where stomach meets SI, bands of muscle pinching off stomach and duodenum to control passage

large intestine

cecum, colon and rectum, pulls out water and solidifies stool for elimation

signs and symptoms of GI disease

nausea, vomiting, diarrhea, anorexia, constipation, dysphagia, GI bleeding, heartburn, abdominal pain, fecal incontinence

constipation

infrequent, incomplete or difficult passage of stools, <3 BMs/week

causes of constipation

failure to response to defecation urge, inadequate dietary fiber/fluids, weak abdominal muscles, inactivity, pregnancy

transit time

time from eating to elimination in stool

slow transit time can be a result of

decreased neuromuscular function of colon

PT implication of constipation

low back pain via muscle guarding or compressed sacral nerves, pelvic floor or anal sphincter dysfunction

upper GI bleeding would result in

blood in vomit or stool

esophageal bleed result

vomit bright red

stomach bleed result

"coffee ground" appearance, blood interacted with digestive enzymes

duodenum bleed result

dark black stool, interacted with all digestive enzymes

a bleed below the duodenum is a

lower GI bleed

lower GI bleed appearance

only in stool, no enzyme interaction so bright red blood (jejunum, ileum, colon, rectum)

dysphagia is associated with

neurological disorders, local trauma, muscle damage, mechanical obstruction or musculoskeletal cause

musculoskeletal causes of dysphagia

forward head posture and anterior cervical vertebral osteophytes

heart burn

gastric contents leaking - symptoms worse in supine

age related changes to oral cavity

reduced saliva and taste bud atrophy (decreased taste sensation and altered appetite)

age related changes to esophagus

degenerative changes to smooth muscle lining esophagus, slower/weaker peristalsis, reduced resting pressure of LES (likely heartburn), increased likelihood of stomach content reflux

gastritis and gastropathy

disruption of protective mechanisms for mucosa and formation of peptic ulcers

protective mechanisms of mucosa

mucin secretion forms thin layer of mucus, mucus has neutral pH, rich blood supply helps buffer with washout of acidity

peptic ulcers

painful sores in stomach lining - can cause cell death

gastritis will have

inflammatory cells, from infection

gastropathy will have

no inflammatory cells, usually from decreased BF

chronic gastropathy

infection with the bacillus Hpylori causes increased acid production, repeated peptic ulcers (could also be caused by autoimmune disease or chronic NSAID use)

symptoms of gastritis and gastropathy

(may be asymptomatic) variable degrees of epigastric pain, nausea, vomiting, mucosal erosion/hemorrhage

treatments for gastritis and gastropathy

antibiotic and proton pump inhibitors

proton pump inhibitors

treat production of acid to decrease stress on cell layer

gastroesophageal reflux disease

chronic backflow or stomach and duodenal contents into the esophagus resulting in inflammation and scarring

GERD is not the same as

heartburn, but heartburn is a symptom of GERD