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
PUD: complications
HOP
hemorrhage - if BV involved
obstruction - scar tissue and strictures
perforation and peritonitis
appendicitis
inflam of appendix
etiology: obstructed, leads to inflam
complications cause biggest issues - gangrene, abscess, peritonitis
classic RLQ pain in periumbilical area - begins dull and steady and progress rapidly over 4-6 hrs; rebound pain, sudden relief - rupture = peritonitis
cm: low grade fever, n, anorexia, elevated wbc
peritonitis
serious membrane that covers abd cavity and visceral organs
inflam, fluid shifts and 3rd spacing (hypovolemic shock, sepsis), decreased peristalsis, paralytic ileus and intestinal obstruction -> bc gut shuts down and doesnt digest food
treat cause and anti inflam
appendicitis: dx
s/s, elevated wbc, abd sonogram (US), exploratory lap
peritonitis: causes
perforated ulcer, ruptured gallbladder, pancreatitis, ruptured spleen, ruptured bladder, ruptured appendix
peritonitis: cm
sudden/severe - cant move/talk/hard to breathe, abd pain!, tender, rigid abd, n/v, fever, elevated wbc, increase HR and decreased BP d/t SNS and fluid shift
irritable bowel s
chronic condition, alteration in bowel pattern d/t change in intestinal motility
constipation or diarrhea -> chronic and freq
almost never the result of psych distress -> can exacerbate, cyclic
cause is unknown but triggered by stress, food, hormone changes, GI infections, menses
IBS: cm
vary by individual
abd distention, fullness, flatus, bloat
intermittent abd pain exacerbated by stress and relieved by defecation
bowel urgency
intol to certain foods (sorbitol, lactose, gluten)
non bloody stool with excessive mucus
inflammatory bowel disease
chron’s and ulcerative colitis
characterized by chronic inflam of intestines, exacerbations and remission (periods)
group of lifechanging chronic illness
rf: white, F, jewish, smoke
autoimmune activated by infection
chron’s
lymph structures of GI tract blocked, tissue becomes engorged and inflammed, deep linear fissues and ulcers develop in patchy patterns in bowel wall (skip lesions - specific to chron’s, cobblestone appearance)
chron’s: complications
malN -> anemia
scar tissue and obstructions
fistulas - 2 structures connected innappropriately
cancer
chron’s: cm
crampy RLQ, watery d
systemic = weight loss, fatigue, no appetite, fever, malabs of nutrients
palpable abd mass, mouth ulcers, s/s fistulas -> depend on location
granulomas
increased r/o VTE
ulcerative colitis
inflam of mucosa of rectum and colon
3rd decade
rf: white (european descent), jewish, occassionally AA, asian rare
ulcerative colitis: patho
inflam begins in rectum and extends in continuous segment that may involve entire colon, large ulcerations, necrosis of epithelial tissue result in crypt abscesses
colon and rectum try to repair damage with new granulation tissue (fragile, bleed easily)
ulcerative colitis: cm
abd pain, bloody d - v common
systemic: weight loss, fatigue, no appetite, fever
complications: hemorrhage, perforation, cancer, increased r/o VTE, malN, anemia, strictures, fissures abscesses, colorectal carcinoma, toxic mega colon -> rapid dilation of LI, can be life threatening; liver disease - from inflam and scarring of bile ducts, F+E and pH imbalances
diverticular disease - diverticulosis: patho
development of diverticula -> small pouches in lining of colon that bulge outward through weak spots
congenital or acquired
though to be caused by low fiber diet with resulting chronic c
usually descending colon
inflammation of 1+ pouches (diverticula) -> retained fecal material
diverticular disease - diverticulitis: cm
LLQ pain, fever, elevated wbc, c/d (abn bowel pattern), acute (pass large quantity of frank blood), may resolve spont
usually asymp
discovered accidentally or with presentation of acute diverticulitis
complications: perforation, peritonitis, obstruction; depends on how inflammed, if they rupture, how many are there
GI system: structure
GI tract and related solid organs of digestion
7m
4th wk GA
GI system: function
provide nutrients for body with propulsive and mixing movements
secretion of digestive juices
abs of nutrients
esophageal sphincters
food is prevented from movement backwards by 2 sphincters (bundles of muscle)
normally closed at rest
UES prevents food and fluid from being aspirated into lungs
LES: cardiac sphincter, separates esophagus from stomach, prevents acidic contents of stomach from entering back into esophagus
stomach
elastic reservoir for food, mixing and initial digestion of proteins
capacity: 1000 - 1500 mL
lined with columnar epithelium containing millions of gastric glands
these glands contain special cells that secrete HCl, IF, and gastrin
stomach layers
mucosa layer: inner layer made up of special cells - G cells, parietal, chief, epithelial; also contain BV
2 muscle layers help propel food to SI
serosa: outer, act as covering
gastric cells in mucosa
G cells
parietal cells
chief cells
epithelial cells
G cells
produce gastrin - hormone that facilitates production of HCl
parietal cells
produce HCl to breakdown food
produce IF to protect mucosa
chief cells
secrete peptin
epithelial cells
secrete bicarbonate rich solution to coat and protect mucosa
SI: length
approximately 5-6m
duodenum: 22cm
jejunum: 2m
ileum: remainder
SI
entire inner wall has circular folds of a mucous membrane called plicae circulares
these are permanent ridges that contain millions of fingerlike projections - intestinal villi
each vilus has its own microscopic projections called microvilli
combined effect of circular folds, villi, and microvilli increase SA for digestion x600
special cells of SI
crypts of liberkuhn: intestinal glands that secrete about 2L of fluid per day into lumen of intestine, flui quickly reabs by villi
goblet cells and brunner glands: secrete large amounts of mucus to protect SI from damage of acidic gastric juices
SI cells have rapid turnover (58-72 hrs), one of fastest turnover rates in body
SI sphincter
ileocecal - area where food passes from SI to LI
distention of terminal ileum causes relaxation to allow contents to enter LI
distention of cecum prevents reflux back into ileum
LI: length
1.5m long, muscular tube that forms a frame around SI
6.5 cm in diameter, > than diameter of SI
includes appendix, ascending colon, transverse colon, descending colon, sigmoid colon, rectum
cells of LI
mucosa does not have villi and does not produce digestive enzymes
absoprtive cells absorb H2O and electrolytes
goblet cells produce mucous
endocrine cells are present and produce hormones but their function is not really understool
turnover is 3-8 days
GI tract motility
due to contractions of 2 layers of SM (longitudinal and circular)
2 types: propulsive (peristalsis) and mixing (segmental)
regulated by enteric NS, autonomic NS, and hormones
esophagus - function
transport food
stomach - function
stores and chums food
pepsin digests protein
HCl activates enzymes, breaks up food, kills germs
mucus protects stomach wall
limited abs
SI - function
completes digestion, mucus protects gut wall
abs nutrients, most water
peptidase digests P
sucrases digest sugars
amylase digests polysaccharides
LI - function
reabs some water and ions
forms and stores feces
rectum - function
store and expel feces
