gi Flashcards
upper GI anatomy
esophagus, stomach, beginning of SI
esophageal issues = GERD, hiatal hernia
inflam of stomach = gastritis, acute gastroenteritis, PUD
lower GI anatomy
SI, colon (LI), rectum/anus
dysphagia
difficulty swallowing: solids -> liquids (progress)
causes: mechanical and NM dysF, trach, intubated
mechanical: stenosis/stricture, diverticula (in esophagus), tumors (block)
NM dysF: CVA, achalasia, (LES doesn’t open properly, LES connects esophagus to stomach)
GERD
upper GI, esophagus
LES doesnt close properly, backflow of stomach contents into esophagus (highly acidic) pass through and cause s/s of heart burn
gerd: etiology
sphincter strength altered or abd P increases
ex: fatty foods, spicy, tomato based, citrus, caffeine, large amount of OH, cig smoking, sleep position, obesity, preg, pharm agents
GERD: cm
heart burn (pyrosis), dyspepsia, regurgitation, chest pain, dysphagia, pulm S, hot burps
tooth decay, gingivitis, bad breath
chronic cough, worsening asthma, recurrent pna
abd bloating, belching
earache
hoarseness, chronic sore throat, throat clearing, laryngitis, lump in throat, post nasal drip
gerd: complications
ulcerations, scaring, strictures
barret’s esophagus (dev of abn metaplastic tissue premalignant) -> 3x increase risk of adenocarcinoma of esophagus
not really treatment - just control gerd
GERD: tm
not really pharm for complications, prevention, treat gerd and avoid triggers
hiatal hernia
diaphragm defect that allows part of stomach to pass into throax
types: sliding, paraesophageal (rolling), mixed (more severe, type 3 + 4)
hitatal hernia: sliding
type 1
small, no treatment, peritoneum intact and restrains size of hernia
hiatal hernia: paraesophageal
type 2
part of stomach pushes through diaphragm and stays there
peritoneum membrane is thinner so sac sits above diaphragm and expand into thoracic
peritoneum becomes thin, enters into intrathoracic P = becomes larger
hiatal hernia: patho
exact cause unknown, age related, injury or other damage to weaken diaphragm muscle, repeated P around stomach (severe cough, v, c and straining for BM, smoking, obesity
rf = age, smoke, obesity
hitatal hernia: cm
asymp, belching, dysphagia, chest or epigastric pain
GERD coexist -> bc LES is weak
hitatal hernia: tm
conservative
small and freq meals, dont lay down after eating
no tight clothes and or abd support
weight control (for obese)
antacid for gerd S
sx of other tm dont work (usually due to noncompliance)
gastritis
stomach inflam
gastritis: acute
temp, not intestines - just stomach
2-10 days
irritating substances (OH), drugs - ex:
NSAIDs - inhibit prostaglandins and therefore diminish protective coating
infectious agents - H. pylori + others
gastritis: chronic
progressive, wks - yrs
immune (attack on parietal cells) or non immune (H. pylori)
complications: PUD, bleeding ulcers, anemia, gastric cancers
gastritis: H. pylori
gram -
thrives in acid, destructive when overgrown, persistent inflam which leads to chronic gastritis, PUD, stomach cancer
transmitted via saliva, fecal matter, v, contaminated food or water
gastritis: cm
same for acute or chronic
asymp or anorexia, n/v, postprandial discomfort, intestinal gas, hematemesis, tarry stools, anemia
acute gastroenteritis
stomach and SI
1-3 days, up to 10
viral infections = norovirus, rotovirus
bacterial = E. coli, salmonella, campylobacter
parasitic
mostly let it play out, prevent dehyd, abx, see provider if last >48-72 hr
acute gastroenteritis: cm
diff btw gastritis (not just upper GI issues)
watery d (bloody if bacteria), abd pain, n/v, fever, malaise
complication = FVD!
PUD
ulcerative disorder of upper GI
esophageal, stomach -> stomach ulcers, duodenum -> peptic ulcer in 1st part of SI
when GI tract exposed to too much acid and H. pylori
natural body defenses: mucus, bicarb, BF, prostaglandins
PUD: etiology
H. pylori, injury causing substances (NSAIDs - decrease prostaglandins, ASA, OH), excessive acid, smoking, fam hx, stress -> increase gastric acid secretion (not cause but can worsen)
rf: age, high NSAID dose, hx of PUD, corticosteroids and anticoags, serious systemic disorders, H. pylori infection
PUD: patho
mucosa damage, histamine secreted (increase acid and pepsin secretion - more damage, vasodilate - edema), blood vessels destroyed = bleeding!
PUD: classify
duodenal ulcer: most common, any age (early adulthood)
gastric/peptic ulcer: 50-70 yo -> high NSAIDs, corticosteroids, anticoags, more likely to have serious systemic illness
PUD: cm
none
n/v, anorexia, weight loss, bleed (if BV involved), mid abd burning (worse when stomach empty)
gastric = burning, cramp, gas; epigastrium, back; 1-2 hrs after eating
duodenal = same except 2-4 hrs after eating