upper and lower GI Flashcards
what organs are part of the upper GI?
esophagus
stomach
beginning of small intestines
what organs are part of the lower GI?
small intestines, colon, rectum, anus
esophageal disorders
GERD
Hiatal hernia
Inflammatory disorders of the stomach
gastritis
acute gastroenteritis
PUD
dysphagia
difficulty swallowing
begins with solids and processes to liquids
common causes of dysphagia
mechanical obstruction
neuromuscular dysfunction
what is a mechanical obstruction
stenosis or stricture
diverticula
tremors
what is a neuromuscular dysfunction
CVA ( intubation or trachs)
achalasia (lower esophageal sphincter cant open properly)
GERD
backflow of gastric acid from stomach to esophagus
occurs when LES doesn’t close properly
causes of GERD
anything that alters closure strength of LES or increases abdominal pressure
(fatty, spicy, acidic, tomato, citrus, caffeine, alcohol, smoking, sleep, obesity, pregnancy)
what symptoms can GERD cause in the mouth?
tooth decay
gingivitis
bad breath
what symptoms can GERD cause in the chest
chronic cough
worsening asthma
recurrent pneumonia
what symptoms can GERD cause in the abdomen
bloating
belching
what symptoms can GERD cause in the ears
earache
what symptoms can GERD cause in the throat
hoarseness chronic sore throat throat clearing laryngitis lump in throat post nasal drip
clinical manifestations of GERD
heartburn (pyrosis) dyspepsia regurgitation chest pain dysphagia pulmonary symptoms
complications of GERD
ulceration
scarring
strictures
barrettes esophagus
what are the risks with barrettes esophagus?
premalignant
three-fold increased risk of developing esophageal cancer
overall survival rate 17%
hiatal hernia
defect in diaphragm that allows part of stomach to pass into thorax
what are the 2 types of hiatal hernias?
sliding
paraoesophageal
sliding hernia
usually small
does not need tx
peritoneum stays intact
paraoesophageal hernia
part of stomach pushes through diaphragm and stays there, peritoneum thins and ruptures
risk factors for hiatal hernias
age
obesity
smoking
manifestations of hiatal hernia
asymptomatic belching dysphagia chest or epigastric pain common for GERD and hiatal hernia to coexist
tx for hiatal hernia
conservative small frequent meals, avoid lying after meals avoid tight clothes and abd supports weight control antacids
acute gastritis
temporary inflammation of stomach lining
lasts 2-10 days
aggregators of acute gastritis
alcohol
nsaids ( r/t decreased prostaglandins)
infectious agents (h. pylori)
chronic gastritis
progressive, chronic inflammation
lasts weeks to years
immune related/ non immune related
complications of chronic gastritis
PUD
bleeding ulcers
anemia
gastric cancers
2 main causes of chronic gastritis
autoimmune- attacks own cells
chronic h. pylori infections
h. pylori thrives in what kind of enviornment?
acidic
what is h. pylori
destructive pattern of persistent inflammation
can cause Chronic Gastritis, PUD, stomach cancer
how is H. Pylori transmitted?
person to person via saliva, fecal matter, or vomit
contaminated food or water
symptoms of gastritis (acute or chronic)
vomiting stomach burning upset stomach loss of appetite vomiting blood black stool postprandial discomfort
acute gastroenteritis
inflammation of stomach and small intestine
usually lasts 1-3 days
caused by viral, bacterial, parasitic infections
let infections play out.. usually no abx
manifestations of acute gastroenteritis
watery diarrhea (can be bloody is bacterial), abdominal pain, N/V, fever, malaise
what is a complication of gastreoenteritis
fluid volume deficit
What is PUD
ulcerative disorder of upper GI tract esophageal stomach - gastric ulcers duodenum- peptic ulcer develops when GI tract exposed to acid and h. pylori
aggressive factors of GI tract
h. pylori NSAIDS acid pepsin smoking
defensive factors or GI tract
mucus
bicarbonate
blood flow
prostaglandins
causes of PUD
H. pylori nsaids asa alcohol excessive secretion of acid smoking family fx stress
risk factors for NSAID induced PUD
age high doses of NSAIDS chronic corticosteroids chronic anticoagulants autoimmune disorders h. pylori infection
how does PUD develop?
mucosa damage
histamine secretion resulting in increased acid and pepsin production, vasodilation
if blood vessels are destroyed results in bleeding
duodenal ulcer
most common type
can occur at any age
gastric/peptic ulcer
peak at age 50-70
caused by increased of NSAIDs, corticosteroids, anticoagulants, more likely to have systemic illness
clinical manifestations of PUD
sometimes none unless bleeding n/v, anorexia wt loss bleeding burning pain in middle of abd, worse when stomach is empty
gastric ulcer
Characteristics
location
timing
burning, cramping, gas like
epigastrium, back
1-2 hours after eating
duodenal ulcer
characteristics
location
timing
burning, cramping, gas like
epigastrium, back
2-4 hours after eating
complications of PUD “HOP”
hemorrhage
obstruction
perforation and peritonitis
appendicitis
inflammation of appendix
caused is obstructed which leads to inflammation
complications of appedicitis
gangrene
abscess formation
peritonitis
key points of appendicits
RLQ pain, periumbilical area
rebound pain at McBurney’s point
sudden pain relief may indicate rupture/peritonitis
manifestations of appendicitis
age 10-12 starts as dull, steady pain in periumbilical area progresses over 4-6 hours RLQ low grade fever nausea elevated WBC
peritonitis
inflammation of peritoneum
fluids shift causing third spacing can lead to hypovolemic shock and sepsis
decreased peristalsis
can lead to paralytic ileus and intestinal obstruction
causes of peritonitis
think ruptured or perforated perforated ulcer ruptured gallbladder pancreatitis ruptured spleen ruptured bladder ruptured appendix
clinical manifestations of peritonitis
sudden and severe abdominal pain (worst pain of life) rigid board like abdomen INCREASED HR DECREASED BP
IBS
changes in intestinal motility
can be IBSC or IBSD
symptoms vary by individual
intermittent abdominal pain relieved by deification
bowel urgency
intolerance to certain foods (sorbitol, lactose, gluten)
non-bloody mucous stool
psychological stress and IBS
cause unknown, triggered by stress, food, hormone changes, GI infections, menses
IBD
life changing chronic illness
2 types: crohns and UC
causes chronic inflammation, exacerbations and remission in intestines
autoimmune activated by infection
IBD is more common in
women
Caucasians
Jewish descent
smokers
crohns
lymph structures of GI tract are blocked, tissues become engorged and inflamed
deep linear fissures and ulcers
skip lesions
cobblestone appearance
complications of crohns
malnutrition anemia scar tissue and obstructions fistulas cancer
GALS (crohns disease)
granulomas, all layers, skip lesions
clinical manifestations of crohns
crampy RLQ pain watery diarrhea weight loss fatigue no appetite malabsorption of nutrients PALPABLE RLQ mass mouth ulcers
UC
inflammation of mucosa of rectum and colon
usually develops in third decade of life
UC is more common in
white people of European descent, esp. Ashkenazi Jewish
occasionally in black/African
rare in Asians
pathogenesis of UC
inflammation begins in rectum extends in CONTINUOUS segment that involves entire colon
inflammation leads to large ulcerations
necrosis of epithelial tissues
CRYPT ABSCESSES
damage repaired with new granulation tissue
why is new granulation tissue a problem with IBD?
tissue is fragile and bleeds easily
clinical manifestations of UC
abdominal pain bloody diarrhea (not seen with crohns) wt loss fatigue no appetite fever
complications of UC
hemorrhage perforation cancer fissures Crypt abscesses toxic megacolon increased risk of colo/rectal cancer liver disease fluid, electrolyte, and PH balances increased risk of VTE and PE
diverticulosis
small pouches bulging outwards through weak spots can be congenital or acquired caused by low fiber diet usually in descending colon discovered accidentally
diverticulitis
inflammation retained fecal matter LLQ pain increased WBC acute passage of large frank blood
complications of diveritculitis
perforation
peritonitis
obstruction
g-cells
produce gastrin, facilitates production of HCl
parietal cells
produce HCl to break down food
produce intrinsic factor to protect mucosa
chief cells
secrete pepsin
epithelial cells
secrete bicarbonate-rich solution to coat and protect stomach
order of small intestine
duodenum
jejunum
illeum
crypts of lieberkuhn
intestinal glands
secretes 2l fluid daily into lumen of intestine
Crypt abscesses in UC
goblet and brunner cells
secrete mucus to protect small intestine from acidic gastric juices
ileocecal sphincter
area where food passes from small to large intestine
large intestine includes
appendix, ascending colon, transverse colon, descending colon, sigmoid colon and rectum
