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function of GI tract
starts in the mouth
motility - movement of food
peristalsis
secretion - secretion of acids, mucus, hydroclous pumps breaking down the food
digestion - breaking down of the actual food
absorption - absorption in the small intestines
parasympathetic nervous system (PNS)
primarily is the vagus nerve
when stimulated it triggers an increase in peristalsis
things that stimulate it
food stretching stomach (NOT OVERSTRETCHING)
increase in Ph
pleasent smells and hunger
PNS: rest and digest
sympathetic nervous system (SNS)
conversely inhibits gastrointestinal activity (ex: overstretching of the stomach)
cause vasoconstriction
reduces secretions
reduces regeneration of epithelial cells
cells that sit in the GI tract and as food moves through it takes some of these cells with it
these cells are important cause without them you will get irritation and breakdown of the stomach
SNS: fight or flight
nausea and vomiting
initiated when vagus nerve is triggered and sent to the medulla and the medulla tells us to throw up
nausea and vomiting are initiated by the medulla
distention or irritation of the digestive tract
smells or sights
pain or stress (anxiety)
inner ear imbalance
medications
some meds on an empty stomach can cause you to throw it back up
chemotherapy
noxious (poision) substances or stimuli
IICP
increased inercranial pressure
ex: brain bleed
hematemesis
“coffee grounds” partially digested food mixed with old blood
significance in vomitus
hematemesis: “coffee grounds” partially digested food mixed with old blood
deeper brown color may be content from lower instestine (stool) - obstruction
recurrent projectile vomiting may be pyloric stenosis - usually seen in children
pyloric sphincter: the gate from the stomach to the small intestine
with pyloric stenosis that gate becomes inflammed and is now narrow and tight so whenever they eat anything, all of it puts pressure on that sphincter and will shoot back out
dehydration - can lead to metabolic acidosis
first with throwing up it will lead to alkalosis because they are throwing up the acid but after severe long vomiting, the body will become dehydrated making the body hypovolemic. due to the small amounts of blood, there is not enough blood with nutrients getting to the tissues with oxygen so the body has to revert to anerobic metabolism to make energy which builds up lactic acid therefore making us acidodic in the end
vomitus
the actual throw up
emesis
the action of throwing up vomitus
diarrhea
excessive frequenncy of loose stools
to be considered for having diarrhea you have to have 3-4 loose stools within 24hrs
diarrhea - large volume (osmotic)
short transit time, excess fluid volume flooding intestine, lactose intolerance, leads to hypovolemia and metabolic acidosis
ex: eating something that has bacteria in it or cdiff causes inflammation to bowels causing their to be excess flow to the intestine and for poop to flow out in large amounts with out being filtered
diarrhea - small volume
bowel disease, may contain blood, pus or mucous
ex: ulcerative colitus
diarrhea- steatorrhea
“fatty diarrhea” greasy, loose and foul odor
malabsorption syndromes
occurs if fats arent getting absorbed in the small intestine bc the food is moving so fast through the gi tract
diarrhea - blood diarrhea
occult: small hidden amounts of blood
fecal occult system
melena: dark colored (tarry stools)
old blood in stool
tells us there is high bleeding up in the GI tract so its further from the rectum making it take a minute to get to the end making it rust making it look darker
hematochezia: passing fresh (frank) red blood
this tells us there is bleeding lower in the GI tract because it is more red
ex: hemmorides - these are closer to the rectum so when they break open it looks more red
constipation
can lead to an impaction
can be acute or chronic
acute: holding you poop in during the day and ignoring signals that you need to go because your in public or like constipation for a couple days
causes
increased age
inadequate fiber
inadequate fluid intake
ignore urge
muscle weakness and inactivity
neuro disorders (MS, spinal cord injuries, etc)
drugs (opiates, drugs that block PNS, etc)
obstruction
upper GI disorders - Mouth
cleft lip and/or palate - neural tube disorder
aphthous ulcers - canker sores or stomatitis
candidiasis - thrush
herpes - HSV-1 - transmitted through kissing or close contact - reactivates with stress
dental issues
ex : having dentures and you forgot to bring them so now you can eat
leukoplakia - precancerous lesions
upper GI disorders - dysphagia
difficulty in swallowing
causes
neurological deficit (MS, stroke, infection in brain, brain damage)
achalasia - failure in esophageal sphincter to relax
congenital atresia - blind pouch
fibrosis - stenosis or stricture
compression
diverticulum

upper GI disorders - hiatal hernia
a part of the stomach protrudes through the opening (hiatus) in the diaphragm
sliding - slides up and back down with positiion changes (esp. laying down)
paresophageal - part of the fundus of stomach moves above diaphragm (leads to mechanical constriction of blood vessels in stomach)
medical emergency
loosing blood flow and its going to become necrotic

Upper GI disorders - Gastroesophageal reflux disease (GERD)
this is chronic heart burn/chronic reflux of food
stomach contents chronically regurgitate into esophagus
causes
weak esophageal sphincter
obesity
hiatal hernia
pressure causes gerd - aka pregnancy
Upper GI disorders - esophageal cancer
usually squamous cell carcinoma
mostly found in distal esophagus
causes
chronic irritation
reflux (gerd)
esophagitis
achlasia
hiatal hernia
alcohol abuse
smoking
poor prognosis
Upper GI disorders - acute gastritis
gastric mucosa inflamed, red, edematous and ulcerated. could bleed in the mucosal barrier is damages
causes:
infection
allergies to food or drugs
ingesting irritants frequently (ex:spicy foods)
excessive alc intake
ingestion of aspirin or other ulcerogenic drugs esp. on an empty stomach
radiation and chemotherapy
usually self limiting
Upper GI disorders - chronic gastritis
atrophy of mucosa of stomach and loss of secretory glands
causes
same causes as with acute, but continued insult
infection - helicobacter pylori (bacteria that may times lead to ulcers)
Upper GI disorders - peptic ulcers
gastric and duodenal ulcers
patho
most commonly found in the proximal duodenum (duodenal ulcers)
also found in antrum of the stomach or lower esophagus (gastic ulcers)
usually small cavity develops in mucousa that continues to erode into further layers below mucosa
eventually invades blood vessels (which causes bleeding)
may perforate stomach or intestinal wall and spill gastric contents into peritoneal cavity
peptic ulcers causes
helicobacter pylori bacteria (most common)
inadequate blood supply (vasoconstriction caused by stress, smoking, shock, elederly, severe anemia)
ulcerogenic substances
atrophy of gastric mucosa (chronic gastritis)
increased number of acid-pepsin secretory cells in the stomach (a genetic anomaly)
increased stimulation of acid-pepin secretion (alcohol, caffine, or certian foods)
this ultimately can lead to gastric cancer
peptic ulcer symptoms
epigastric aching, burning pain 2-3 hours after meals or at night relieved by ingestion of food or antiacids
heartburn
nausea
intake of spicy food exacterbates symptoms
stress ulcers
result from severe trauma
burns: curlings ulcers
head injury: cushings ulcers
can quickly progess to hemorrhage
sepsis
medications usually given to prevent
upper GI disorders - dumpting syndrome
control of gastric emptying is lost (many times seen after gastric resection or partial gastrectomy)
appropriate dilution of chyme is lost
hyperosmolar chyme leaves the stomach and draws too much water into the intestine
distention hyper-activates PNS increasing peristalsis and gastric dumpting
dizziness and weakness
rapid pulse and sweating
hypoglycemia
Upper GI disorders - pyloric stenosis
narrowing and obstruction of the pyloric sphincter
can be seen in infants and adults
infant form (congenital)
sphincter hypertrophied
projectile vomiting
adult form (acquired)
acquired due to surgical adhesions/scars
decreased gastric emptying
persistent feeling of fullness
eventually vomiting as sphincter becomes more constricted
disorders of liver and pancreas - gall bladder disorders
cholelithiasis
cholecystitis
cholangititis
choledocholithiasis
cholelithiasis
formation of gallstones (calculi) that form in bile in the gallbladder
cholecystitis
stones obstruct duct and leads to inflammation of gallbladder and bile duct
cholangitis
inflammation and infection of bile ducts
choledocholithiasis
obstruction by gallstones of the biliary tract
gallbladder disorder symptoms
severe upper right quadrant discomfort (biliary colic) that leads to waves of deferred pain
epigastric pain
nausea and vomiting
later stages
jaundice
fever
leukocytosis
hepatitis
inflammation of the liver
causes
idiopathic (fatty liver)
viral hepatitis
infectious mononucleosis
chemical or drug toxicity
chronic inflammation that begins to cause irreparable liver cell damage
viral hepatitis
virus that specifically attacks the liver
acute forms
hep a and e
transmitted by oral/fecal route
self limiting
chronic forms
hep b, c, and d
transmitted by blood and body fluids
life-long liver damage
produces a chronic or carrier state
hepatitis - preicteric (or prodromal) stage
insidious onset
fatigue, anorexia and muscle aching
fever, headache, and distaste for cigarettes
mild upper right quadrant discomfort
AST and ALT begin to become elevated
hepatitis - icteric stage
onset of jaundice and increase in serum bilirubin levels
stools become light colored and urine dark
pruitis
liver tender and hepatomegaly
clotting ability decreases
stage lasts longest with hep b
hepatitis - posticteric or recovery stage
reduction in symptoms
extends over weeks
acute (esp. hep a) 8-10 weeks
prolonged (esp.hep b) over 16 weeks
cirrhosis
progressive destruction of liver tissue leading to liver failure
categories
alcoholic liver disease (largest group)
biliary cirrhosis (stones or cystic fibrosis)
postnecrotic cirrhosis (chronic hepatitis or long term exposure to toxic materials)
metabolic (storage disorders such as hemochromatosis)
cirrhosis complications - functional losses
decreased removal and conjugation of bilirubin
Decreased production of bile
Impaired digestion and absorption of nutrients
Decreased production of blood clotting factors and plasma proteins
Impaired glucose/glycogen metabolism
Inadequate storage of iron and vit B12
Decreased inactivation of hormones (aldosterone and estrogen)
Decreased removal of toxic substances, such as ammonia and drugs
cirrhosis complications - R/T obstruction of bile ducts and blood flow by fibrosus tissue
Reduction of the amt. of bile entering the intestine
Back-up of bile in liver – obstructive jaundice
Blockage of blood flow through liver – leads to increased pressure in portal veins – portal hypertension
Congestion in the spleen -Splenomegaly – due to increasing hemolysis
Congestion in intestinal walls and stomach, impairing digestion and absorption
Development of esophageal varices
Development of ascites in the peritoneal cavity
cirrhosis symptoms
Fatigue
Anorexia
Weight loss
Anemia
Diarrhea
Dull aching pain in URQ
Ascites
Esophageal varices
Encephalopathy
Edema
Increased bruising
Jaundice
acute pancreatitis
Inflammation of the pancreas resulting from autodigestion of the tissues.
Premature activation of proenzymes in pancreas
Activation of proenzyme trypsinogen into trypsin
Trypsin converts other proenzymes and chemicals into active forms of amylase and lipase
These enzymes digest pancreatic tissue
Leads to massive inflammation, bleeding and necrosis
acute pancreatitis - etiology and symptoms
Gallstones and excessive alcohol intake
Symptoms:
Severe epigastric or abdominal pain
Signs of shock – low B/P, pallor, sweating
Low-grade fever
Abdominal distention and decreased bowel sounds
Leukocytosis
upper GI disorders - celiac disease
malabsorption syndrome that prevents the breakdown of gluten - leads to malnutrition and intestinal inflammation
Genetic link – defect in intestinal enzyme
Steatorrhea
Muscle wasting
Failure to thrive
Must be on a gluten free diet
Higher risk for intestinal cancers
upper GI disorders - chrons disease
chronic inflammatory bowel disease – most frequently in small intestine
Occurs in the mucosal layer
Develops shallow ulcerations
Leads to thickened walls that can lead to obstruction
Destructive masses form (Granulomas) in the intestine walls and regional lymph nodes
Decreased ability of small intestine to metabolize and absorb nutrients
Increased intestinal motility
crohns symptoms
Diarrhea
Cramping
Melena
Pain and tenderness RLQ
Anorexia
Weight loss
Fatigue
ulcerative colitis
Inflammation begins in the rectum and then progresses through the colon
Mucosa and submucosa inflamed
Tissue becomes edematous and fragile and ulcerations develop
Granulation tissue forms but is fragile, vascular and bleeds easily
Tissue destruction interferes with absorption of fluid and electrolytes
Inflammation impairs peristalsis, leading to swelling and possible obstruction
High risk for colon cancer
ulcerative colitis symptoms
Severe abdominal cramping
Tenesmus (rectal spasms)
Bleeding with diarrhea
Could lead to medical emergency
Relentless extension of the disease can lead to intestinal paralysis and necrosis of entire colon (toxic megacolon)
During severe episodes of diarrhea electrolyte disturbances may take place
Diverticulum
herniation or outpouching of the mucosa through the muscle layer of the colon wall, frequently the sigmoid colon
Diverticulosis
asymptomatic diverticular disease – ususally multiple diverticula are present
Diverticulitis
refers to inflammation of the diverticula
diverticular disease - causes and comps
Causes:
Low-residue diets
Irregular bowel habits
Aging
Complications
Intestinal obstruction
Perforation with peritonitis
Abscess formation
diverticular disease - symptoms
Mild lower abdomen pain
Diarrhea or constipation
Flatulence
When there is stasis of feces in pouches forming diverticula there is:
LLQ pain and tenderness
Nausea & vomiting
Fever
Leukocytosis
intestinal obstruction - Functional obstruction
Abdominal surgery - effects of anesthetic combined with inflammation
Spinal cord injuries
Inflammation with severe ischemia
Infection in the abdominal cavity
intestinal obstruction - mechanical obstruction
Adhesions
Hernias
Strictures
Masses
Intussusception
Volvulus
Hirschsprung’s disease
Gradual obstruction from chronic inflammation
colicky abdomen
pain develops as peristalsis increases
borborygmi
extreme rumbling bowl sounds caused by building and movement of gas
intestinal rushes
heard before the obstruction in an attempt to propel intestinal contents forward
intestinal obstruction - symptoms
Colicky abdomen – pain develops as peristalsis increases
Borborygmi (extreme rumbling bowel sounds caused by building and movement of gas)
Intestinal rushes heard before the obstruction in an attempt to propel intestinal contents forward.