-
Clinical manifestations of GI dysfunction
- Anorexia
- Vomiting
- nausea
- constipation
- diarrhea
- abdominal pain
-
Bleeding that occurs in esophagus, stomach or duodenum
upper GI bleeding
-
Bleeding that occurs in jejunum, ileum, colon, or rectum
Lower GI bleeding
-
-
Causes of Lower GI bleeding
- Polyps
- iflammatory disease
- hemorrhoids
- cancer
-
Bloody vomitus
hematemesis
may be bright red or coffee groun appearance
-
Bright red blood from rectum
Hematochezia
-
Black sticky foul smelling stools
Melena
-
Trace blood detected
occult bleeding
Hemoccult test detects
-
Best indicators of gi bleed
-
Difficulty swallowing d/t mechanical obstruction or impaired esophageal motility
Dysphagia
-
painful swallowing
odynophagia
-
Lower esophageal sphincter fails to relax
achalasia
-
clinical manifestations of dysphagia
- discomfort w/swallowing
- regurgitation
- unpleasant taste
- vomiting
- weight loss
- aspiration
- nutritional deficiencies
-
dysphagia may be d/t
- tumors
- strictures
- diverticula
- CVA
- parkinsons
-
________________ is weak or incompetent. Increases in abdominal pressure contribute to reflux eophagitis. as a result, inflammatory responses are initaited. Edema, fibrosis and hyperplasia may occur. Metaplastic changes (barrett's esophagus) may occur.
Lower Esophageal sphincter in Gastroesophageal reflux
-
Clinical manifestations of GER
- heartburn
- regurgitation of acidic chyme w/in 1hr of eating
- symptoms worsen w/lying down or increased intraabdominal pressure
- respiratory-chronic cough, wheezing, hoarseness, asthma
-
Protursion of upper portion of stomach thru diaphragm into thorax
hiatal hernia
-
2 types of hiatal hernias
sliding-stomach slides or moves into thoracic cavity through esophageal hiatus
Paraesophageal-greater curvature of stomach herniates thru secondary opening in diaphragm and lies alongside the esophagus
-
clinical manifestations of hiatal hernia
- reflux
- dysphagia
- heartburn
- epigastric pain
- substernal discomfort
-
Accounts for 1% of all new cancers
Cancer of esophagus
-
Who is at greater risk for cancer of esophagus?
Males
-
Squamous cell types in cancer of esophagus d/t:
-
Adenocarcinomas in cancer of esophagus d/t
Barrett's esophagus-assoc w/GER
-
Pathogenesis of cancer of esophagus
esophageal dysfunction-food/drink prolonged contact
ulceration and metaplasia from reflux
chronic exposure to alcohol and tobacco
obesity
-
clinical manifestations of esophageal cancer
- dysphagia
- chest pain
- heartburn-#1
dysphagia may be late sign:1st w/bulky, then soft, then liquid
-
Can be caused by any condition that prevents normal flow of chyme thru intestinal lumen
intestinal obstruction
-
Mechanical blockage of lumen by lesion
adhesions
hernias
are all examples of:
Simple intestinal obstruction
-
Failure of motility
paralytic ileus
are examples of:
Functional Intestinal obstruction
-
Intestinal obstructions occur where?
Can occur in either small or large intestines
Simple obstructions of small is most common
-
obstruction in ___________ causes more pronounced distention
lower
-
obstruciton that can cause diarrhea or constipation
Partial
-
Causes of intestinal obstruction
- hernia
- intussusception
- volvulus
- diverticulosis
- tumor
- ileus
- adhesions
-
patho effects of intestinal obstruction
- F&E loss
- Acid base imbalance
- Distention d/t gas and fluid accumulation
- can lead to strangulation, gangrene, perforation, bacterial growth
-
clinical manifestations of intestinal obstruction
- colicky pain followed by vomiting (cardinal)
- sweating
- nausea
- hyptension
- distention
- atelectasis and pneumonia
-
rumbling heard w/mechanical obstruction trying to propel thru obstruction
borboygmus
-
inflammatory disorder of gastric mucosa
gastritis
-
Erodes surface epithelium and causes superficial erosions of gastric mucosa
acute gastritis
-
causes of acute gastritis
- NSAIDs
- chemicals
- alcohol
- histamine
- digitalis
- uremia-toxic waste in blood-kidney failure
-
clinial manifestations of acute gastritis
- abdominal discomfort
- epigastric tenderness
- bleeding
-
chronic inflammation changes lead to eventual atrophy of glandular epithelium of stomach. may progress to dysplasia
chronic gastritis
-
who's at risk for chronic gastritis?
- elderly
- alcohol
- smokers
- chronic nsaid users
-
major causative factor of chronic gastritis?
Other cause?
h. pylori
Autoimmune
-
Vit B12 deficiency -lacking intrinsic factor leading to B12 malasorption
Pernicious enemia
-
clinical manifestation of chronic gastritis
- anorexia
- fullness
- nausea
- vomiting
- epigastric pain
- gastric bleeding
-
break or ulceration in protective mucosal lining of lower esophagus, stomach, or duodenum that are exposed to acid-pepsin secretions.
peptic ulcers
acute,chronic, superficial or deep
-
risk factrs of peptic ulcers
- smoking
- advanced age
- habitual use of nsaids
- alcohol
- chronic disease-emphysema, ra, cirrohosis, diabetes
- infection of gastric and duodenal mucosa w/h pylori
-
most common type of ulcer
duodenal ulcers
-
Risk factors of duodenal ulcers
- younger persons
- type o blood-more conducive, lacking a and b antigens and less mucousal protection
-
major causes of duodenal ulcers
-
Patho of peptic ulcers
- increased parietal cells
- increased gastric acid levels
- rapid gastric emptying
- h pylori destruction of mucousal epith cells and release of toxins
- use of nsaids and inhibit prostoglandins
- acid producation r/t smoking
-
clinical manifestations of ulcers
- pain 2-3 hrs after eating when empty
- pain at night
- pain food relief pattern
- chronic intermittent epigastric discomfort
- constant unremitting pain-obstruction or perforation
-
1/4 as common as duodenal ulcers
gastric ulcers
- occur equally in males and females
- 55-65 yrs old
major cause-nsaids and h pylori
-
clinical manifestations of gastric ulcers
- pain food relief pattern
- may occur immediately after eating
- cause more anorexia, vomiting and weight loss
-
result of burn injury
curling ulcer
-
result of head injury, brain surgery
cushing ulcer
-
major factors of stress ulcer formation
- decreased mucousal blood flow
- ischemia
may develop hours after stressful event such as hemorrhage, trauma, burn, sepsis, and heart failure
-
clinical manifestations of stress ulcers
primary-bleeding
assess: color, vs changes, lab values
-
risk factors of cancer of stomach
- h pylori
- heavily salted and preserved foods
- low intake of fruits and veggies
- use of tobacco and alcohol
- males>females
- family hx
- blood type A
- pernicious anemia
May be asymptomatic until late
-
chronic inflammatory disease that causes ulceration of colonic mucosa
ulcerative colitis
-
most common sites for ulcerative colitis
colonic mucosa, left colon, usually rectum and sigmoid
-
risk factors of ulcerative colitis
- 20-40 yrs of age
- family hx
- jewish
- whites
- autoimmune
-
patho:inflammation at base of crypt of lieberkuhn, primarily in left colon
ulcerative colitis
inflammatory products cause tissue damage and small erosions and ulcers can form. abcesses, necrosis and edema may occur.
mucousal destruction occurs
-
clinical manifestations of ulcerative colitis
- remissions and exacerbations
- diarrhea (10-20)
- stool w/blood and mucous
- cramping
- anorexia
- weakness and fatigue
-
recurrent, granulomatous type of inflammatory response that can affect both large and small intestines
crohns disease
aka-regional enteritis
-
risk factors of crohns
- family hx
- similiar to ulcerative colitis
- altered immune response
-
Most common site of crohns
ascending and transverse
-
multiple lesions interspersed b/t normal bowel layers
skip lesions
crohns
-
clinical manifestations of crohns
- diarrhea
- lower abdominal pain
- weight loss
- f/e disorders
- less bloody than ulcerative colitis
-
herniation or saclike outpouching of mucosa thru muscle layers
diverticula
-
asymptomatic diverticular disease
diverticulosis
-
inflammation of pouchings
diverticulitis
-
most frequent site for diverticulitis
sigmoid colon
-
patho for diverticula
form at weak points in colon wall, usually where arteries penetrate tunica mucularis to nourish mucosal layer. colonic mucosa herniates through smooth muscle layers. muscle hypertrophy and contraction occurs
-
risk factors of diverticula
-
clinical manifestations of diverticula
- may be vague or absent
- cramping
- diarrhea, constipation, distention, flatulence
- inflammation and abcesses may occur
- fever, leukocytosis tenderness, LLQ
-
inflammation of vermiform appendix. obstruction of lumen w/stool, tumors, foreigh occurs w/bacterial infection, inflammation. obstruction results in decreased mucosal blood flow, hypoxia, inflammation and edema. gangrene and perforation can occur
appendicitis
-
most common surgical procedure of abdomen
appendicitis
20-30 yrs of age most common
-
clinical manifestations of appendicitis
- epigastric or periumbilical pain
- vague at first w/increased intensity
- may shift to RLQ-rebound tenderness
- mcburney's point
- n/v/d
- anorexia
- increased wbc w/increased neutorphils
-
variable combination of chronic and recurrent intestinal symptoms not explained
irritable bowel syndrome
-
IBS more common in:
women
-
clinical manifestations of IBS
- abd pain
- n/v
- flatus
- bloated
- change in stools
-
mass that protrudes into lumen of gut. benign neosplasm
adenomatous polyp
-
raised mucosal nodules of adenomatous polyp
sessile
-
attached by stalk of adenomatous polyp
pedunculated
-
most common site of adenomatous polyp
rectosigmoid colon
-
3rd most common cause of cancer and cancer death in us for men and women
most begin with adenomatous polyp
> 50 years of age
colorectal cancer
-
risk factors of colorectal cancer
- family hx
- ulcerative colitis
- high fat, lowfiber diet
- alcohol
- sedentary lifestyle
- smoking
-
clinical manifestations of colorectal cancer
- depends on site
- bleeding
- change in bowel habits
- pain is late sign
-
abnormally high accumulation of bilirubin
billi > 2.5-3.0
jaundice (icterus)
may see 1st in sclera
-
abnormally high pressure in portal venous system > 10 mm Hg
portal hypertension
normal is 3 mm Hg
d/t obstruction, thrombosis, inflammation, cirrhosis
-
patho of viral hepatitis
hepatic cell necrosi, scarring, hyperplasia, cellular injury, inflammatory response can damage bile canaliculi
-
begins _____ wks after exposure and ends with appearance of jaundice
highly infectious
fatigue, anorexia, n/v, ruq pain, weight loss, malaise, ha, hyperalgia, cough, low grade fever
2 wks
Prodromal (preicterus) phase- 1st phase
-
begins about ________ wks after prodromal phase and lasts 2-6 wks.
juandice, dark urine, clay colored stools, liver enlarged and tender. actual phase of illness.
icteric phase
-
begins with resolution of jaundice after approx 6-8 wks. liver function tests return to normal w/in 2-12 wks after onset of jaundice.
symptoms diminish. liver remains large and tender
convalescent (recovery) phase
- chronic hepatitis may persist. abn liver fx tests for > 6 mo
- B,C,D infections
-
functional liver tissue replaced by fibrous tissue. fibrous replaces normally functioning liver tissue and forms constrictive bands that disrupt flow in vascular channels and iliary duct systems of liver
cirrhosis
-
cirrhosis usually assoc with _____________ but can develop from other disorders
alcoholism
- manifestions:
- weakness
- fatigue
- anorexia
- hepatomegaly
- jaundice
-
one of main effects of alcohol is accumulation of fat in hepatocytes (steatosis) liver becomes yellow and enlarges owing to excessive fat accumulation
fatty liver
-
inflammation and necrosis of liver cels. intermediate stage b/t fatty changes and cirrhosis
alcoholic hepatitis
-
liver changes occur d/t toxic effects of chronic, excessive alcohol intake, acetyladehye formed by alcohol metabolism damages hepatocytes. cellular damage initiates an inflammatory response that results in necrosis and excessive collagen formation. bands of fibrosis and scarring disrupt stucture of liver
- alcoholic cirrhosis
- laennec cirrhosis
liver becomes fatty d/t deposits of triglycerides w/in liver
-
damage and inflammation leading to cirrhosis begin in bile canaliculi and bile ducts, rather than in hepatocytes
biliary cirrhosis
-
d/t autoimmune disease that destroys small intrahepatic ducts
primary biliary cirrhosis
-
d/t prolonged partial or complete obstruction of common bile duct or its branches
secondary biliary cirrhosis
-
etiologic agents:
chronic viral hepatitis
cirrhosis
chemical agents
cancer of liver
-
clinical manifestations of cancer of liver
- insidious onset
- weakness
- fatigue
- abdominal fullness
- ascites
- jaundice
- hepatomegaly
- elevated alpha fetoprotein
-
risk factors of cholelithiasis include:
- obesity
- middle age
- female
- native american
- gallbladder disease
- pancreas and leal disease
- rapid weight loss
- genetics
-
factors contributing to gallstones
1.abnormalities in composition of bile
2. stasis of bile
3. inflammation of gallbladder
-
form in bile that is supersaturated with cholesterol produced by liver. supersaturation promotes crystalization into stones. may lay in gallbladder or become lodged in cystic or bile duct
cholesterol gallstones
-
form from increased levels of unconjugated bilirubin which binds with calcium
pigmented stones
-
cardinal signs of cholelithiasis
other signs
abd pain and jaundice
epigastric, ruq pain, intolerant of fatty foods, heartburn, flatus
-
biliary colic d/t:_________________________
gallstones in cystic or common duct
may c/o ruq pain that radiates to back ,right shoulder, right scapula, midscapular region
-
what does jaundice indicate in cholelithiasis
stone blocking CBD(common bile duct)- post hepatice jaundice
-
acute or chronic cholecystitis d/t:
lodging of gallstone in cystic duct
gallbladder becomes distended and inflamed with potential for ischemia, necrosis, and perforation. Fever, leukocytosis, rebound tenderness, and guarding may be present.
bilirubin and alkaline phosphatse levels may elevate
-
most common causes of acute pancreatitis
alcoholism and stones
-
develops as result of injury or disruption of pancreatic ducts or acini, permitting leakage of enzymes into tissue. leaked enzymes activated, initiating autodigestion
acute pancreatitis
amylase and lipase are enzymes that break down
-
most common initial symptom of acute pancreatitis
sever epigastric and abdominal pain that radiates into back
-
clinical manifestations of pancreatitis
- fever
- leukocytosis
- n/v
- abdominal distention
- cullen's
- turners
- elevated amylase and lipase
-
why is person at risk for hyptension
plasma volume is lost d/t release of enzymes and kinins that increase vascular permeability and dilate vessels
-
complications of acute pancreatitis
- acute resp distress syndrome (ards)
- acute tubular necrosis-kidneys
- hypocalcemia
- increased wbcs and glucose
-
client may complain of continuous or intermittent abdominal pain, which intensifies after meals. enzyme deficiency may cause steatorrhea (fatty stools) or a malabsorption
chronic pancreatitis
-
chronic alcohol abuse is most common cause of:
chronic pancreatitis
complications include fibrosis, strictures, inflammation, cysts
risk for pancreatic cancer
-
smoking is a major risk factor of
cancer of pancreas
- other risks include:
- diet
- obesity
- diabetes
- chronic pancreatitis
-
clinical manifestations of cancer of pancreas
- asymptomatic at first
- vague back pain
- jaundice
- weight loss
- malabsorption
- most panc cancers metastasized by time of diagnosis
- 5 year survival < 5%
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