Chapter 36 - Alteration In Digestive Function Flashcards
Four layers of the digestive tract
- Mucosa
- Submucosa
- Muscularis externa
- Serosa
Small intestine (A) epithelial mucosa protection
Single layer
Large intestine (B) epithelial mucosa protection
Inner and outer layers
Structural and neural abnormalities can
Obstruct, slow, accelerate intestinal contents
Inflammatory and ulcerative conditions disrupt
Secretion, motility and absorption
Effects of accessory organs (liver pancreas and gallbladder) can alter
Metabolism
Emesis is Greek for
Vomiting
Vomiting
-forceful emptying stomach/intestinal contents through the mouth
Where is the vomiting center
Medulla oblong at a
Retching
Muscular event of vomiting without vomitus expulsion
Projectile vomiting
Spontaneous vomiting that does not follow nausea or retching
projectile vomiting is caused by
Direct stimulation of vomit center
Invitation of vomiting
Deep inhalation and glottis closes
Abdominal muscles create
Pressure from stomach to throat
Duodenum and stomach antrum
Spasm forcing chyme into esophagus
Upper esophageal sphincter stays closed =
Contents can’t enter mouth
Abdominal muscles relax =
Contents return to stomach
What replaces both esophageal sphincters
Parasympathetic
Abdominal muscles contract =
Force diaphragm high into thoracic cavity causing stomach chyme forced out of mouth
Constipation must be
Individually determined
Wide normal defecation range :
1-3 day to 1 week
Primary constipation
Impaired, infrequent and straining colonic movement
Secondary constipation
Neural pathways are altered, colon transit time delayed
Opiates (codeine)
Inhibit bowel movement
Notable change in constipation can be indicative of
Colorectal cancer
Manifestations of constipation
Straining to evacuate stool may cause hemorrhoids
Diagnosis of constipation
Assess sphincter tone and detect anal lesions
-colonoscopy to help direct lumen view
Treatment for constipation
-restoraLAX
-enemas to establish bowel routine
-collectomy
Colectomy
Remove part of the colon
Acute diarrhea
24 hours or less
Persistent diarrhea
14-28
Chronic diarrhea
Longer than 4 weeks
Osmotic diarrhea
Non absorbable substance in intestine draws excess water to intestine
Secretory diarrhea
Excessive mucosal secretion of fluid and electrolytes
-virus, bacterial toxins, rotavirus
Children and diarrhea, have high rates of
Morbidity and mortality
-younger than 5 years
Motility diarrhea
Excessive motility, causing decreased transit time, and decreased fluid reabsorption
Motility diarrhea is caused by
Surgical bypass of area of intestine
Treatment for diarrhea
-restoration of fluid and electrolyte balance
-anti motility or water absorbent medication
Rotavirus
RNA virus
-causing enteristis
Enteritis
Inflammation of intestinal system
Abdominal pain is caused by
Mechanical, inflammatory or ischemic
-abdominal organs stretching/distension = activation of pain receptors
Parietal pain
From parietal peritoneum
-localized and intense
Visceral pain
Distension, inflammation, ischemic of abdominal organs
-poorly localized with radiating pattern
Upper gastrointestinal intestinal bleeding is found in
Esophagus, stomach and duodenum
Upper gastrointestinal bleeding
Mostly Bright red or dark bleeding
-affected by stomach acids
Upper gastrointestinal bleeding is caused by
Peptic ulcers, tearing of esophageal gastric junction (due to severe retching)
Lower gastrointestinal bleeding is found in
Jejunum, ileum, colon, rectum
Lower gastrointestinal bleeding is caused by
Polyps, inflammatory disease, hemorrhoids
Occult bleeding is caused by
Slow chronic blood loss, not very obvious
Occult bleeding results in
Iron deficiency
-anemia
Presentation of gastrointestinal bleeding
-trace amount of blood in diarrhea or stools
-bp reduction
-compensating tachycardia
-vision loss
Dysphagia
Difficulty swallowing
Mechanical obstruction
Obstruction in esophageal wall
-tumours or herniating
Functional dysphagia
Neural and muscular disorders that interfere with swallowing
Achalasia
Rare form of dysphagia
-smooth muscle neurons of middle/lower esophagus are attacked by immune response
Result of achalasia
Altered esophageal peristalsis
-failure of LES to relax which causes obstruction
What can occur in achalasia
Cough and aspiration can occur
-since there is increased pressure of food being forced past LES
GERD
Gastroesophageal reflux disease
GERD is the reflux of
Acid/pepsin or bile salts into esophagus causing esophagitis
GERD is caused by
Abnormalities in LES function
-resting tone is lower than normal
+delayed gastric emptying of chyme
Severity of esophageal damage depends on
Composition and duration of reflux
Increased acidic chyme exposure =
Mucosal injury and inflammation
(GERD) Persistent =
Fibrosis thickening and precancerous lesions
Diagnosis of GERD
Esophageal endoscopy, tissue biopsy
TX GERD
Laparoscopic fundoplication to tighten junction between esophagus and stomach to prevent acid reflux
Hiatal hernia
Protrusion of superior aspect of stomach through diaphragm hiatal into thorax
Sliding hiatal hernia
So teach moves into thorax through esophageal hiatus
-via opening in diaphragm
Paraesophageal hiatal hernia
Stomach moves into thorax alongside esophageal
Paraesophageal hiatal hernia leads to
Gastritis and ulcer formation
Which type of hernia is GERD associated with
Sliding hiatal hernia
risk of hiatal hernia
Strangulation of hernia causing a medical emergency
Diagnosis of hiatal hernia
Radiology with barium swallow
TX for hiatal hernia
Sleeping with your head up, laparoscopic fundoplication
Intestinal obstruction
Any condition that prevents normal flow of chyme through the intestinal lumen
Paralytic ileus
Causes failure of intestinal motility due to dysfunctional neural activity after surgery
Paralytic ileus is a ____ obstruction
Functional
Large bowel obstruction
Less common
-related to cancer
S/s of large bowel obstruction
Abdominal distension and vomiting
Cause of small bowel obstruction
Postoperative adhesions
-herniation which lead to distension (enlargement)
Small bowel obstruction results in
Distension, causing impaired absorption and increased secretion —> accumulation of fluid, gas, solutes in lumen
Systemic ECF fluid osmotically moves into lumen causing
Decreased ECF —> tachycardia, dehydration and possible shock
Intestinal lumen becomes acidic and leaks..
Pathogens, into systemic circulation —> sepsis
-immune response with possibility of remote organ failure
Adhesions
Organs attacking to each other
Gastritis
Inflammatory disorder of gastric mucosa
acute gastritis
Erosion of protective stomach mucosal barrier by H. Pylori and NSAIDs
NSAIDs inhibit
Prostaglandin synthesis —> which normal stimulates global cell secretion of mucus
H.pylori
Burrows into mucus layers and disrupts function of mucosal layer—> triggers immune response which further destroys mucosal layer
Symptoms/ healing of gastritis
Pain, vomiting
-healing occurs within a few days
Chronic gastritis
Occurs in older adults
-chronic inflammation and mucosal atrophy
Chronic non immune antral gastritis is caused by
-involves only antrum and is caused by H.pylori
Chronic non immune antral gastritis
High levels of hydrochloric acid secretion = inc risk of duodenal ulcers
Sections of the stomach diagram
chronic immune fundal gastritis
-body and fungus
Associated with loss of T cell tolerance resulting in gastric mucosa being extensively degenerated in stomach fungus and body
Peptic ulcer is caused by
H.pylori and NSAIDs
peptic ulcer
Break or ulceration in protective mucosal lining
Duodenal ulcers
More frequent
-caused by H.pylori and NSAIDs
Causative factors of duodenal ulcers
Singly or in combination cause acid pepsin concentrations to penetrate mucosal barrier and cause ulceration
Host response (duodenal ulcers)
T and B cells, neutrophils to combat H. Pylori = damage to gastric epithelium by released cytokines
H. Pylori in duodenal ulcers
Releases toxin resulting in apoptosis of epithelial cells
Gastric ulcers
1/4 as common and caused by H. Pylori and NSAIDS
Gastric ulcers develop in
Gastric antrum
-next to acid producing gastric body
Defect of gastric ulcers
Increase in mucosal barriers permeability to hydrogen ions
H+ ions disrupts
Mucosal permeability and structure
Resulting cycle of gastric ulcers
Damaged mucosa liberates histamine causing inc HCL and pepsin production leading to mucosal destruction
Stress related mucosal disease
Acute from of peptic ulcer
-tends to accompany physiological stress, illness or major trauma
Where are Stress related mucosal disease found
Multiple sites of ulcers in stomach or duodenum
(Stress related mucosal disease) ischemic ulcers
Develop within hours of events
-hemorrhage, heart failure, sepsis
(Stress related mucosal disease) curling ulcers
Develop because of burn injury
(Stress related mucosal disease) Cushing ulcers
Develop because of brain trauma/surgery
Inflammatory bowel disease
Environmental factors or infections alter mucosal epithelium barrier
Result of Inflammatory bowel disease
-loss of body’s ability to discriminate harmful pathogens from commensal microorganism
Commensal
Association between two organisms in which one benefits and other derives neither benefit nor harm
Loss of ability to discriminate causes (three things)
- Activation of immune system
- Production of pro inflammatory cytokines
- Intestinal epithelium damage
Ulcerative colitis
Chronic inflammatory disease causing ulcers in colonic mucosa
Ulcerative colitis: disease begins in
Rectum and may extend to entire colon
Ulcerative colitis: small erosions coalesce into ulcers causing
Necrosis
Ulcerative colitis: necrosis results in
Thickening of muscularis mucosa, which narrows lumen and reduces transit time in colon
Ulcerative colitis: mucosal destruction and inflammation causes
Bleeding and urge to defecate
Ulcerative colitis causes
Frequent watery diarrhea with small amounts of blood and mucus
Ulcerative colitis has an intermittent period of
Remission and exacerbation
Symptoms of Ulcerative colitis
Diarrhea roughly 10-20 times a day
diagnosis of Ulcerative colitis
Endoscopy and biopsies
TX for Ulcerative colitis
Steroids, medication and surgery
Chrons disease
idiopathic inflammatory disorder
Chrons disease affects what area of the digestive tract
Any part, from mouth to anus
Chrons disease: inflammation begins in
Intestinal submucosa and spreads with discontinuous and transmural
Discontinuous
Skip lesions
Transmural
Across entire wall of organ
Most common sites of Chrons disease
Ascending and transverse colon
-but both large and small intestines are common
Chrons disease vs ulcerative colitis
C: discontinuous patchy inflammation + mucosal and submucosal layers
U: continous inflammation + transmural
Chrons disease ulcerations can produce
Fissures that extend inflammation into lymphoid tissue
Risks of Chrons disease
Smoking increases risk of developing serve disease and may cause a poorer response to treatment
Chrons disease TX and diagnosis `
D: endoscopy and biopsies
TX: steroids, medication or surgery
Fistulae
Abnormal opening or passage between two organs
Where are fistulae found
May form in peri anal area, or extend into bladder, rectum or vagina
IBS
-abdominal pain with altered bowel habits
-idiopathic with no specific bio markers for disease
IBS is more common in
Women, especially during youth and middle age
Manifestation of IBS
Lower abdominal pain or discomfort and bloating
Symptoms
Usually relieved with defecation and does not interfere with sleep
Appendicitis
Inflammation of appendix
Appendix hypothesis
That it contains lymphoid tissue which may provide a safe house for commensal bacterium for repopulation of intestinal system
What is the most common surgical emergency of abdomen
Appendicitis
Most common age appendicitis occurs
10 to 19 years
Manifestation of appendicitis
Mild pain, inc to intense pain in 3 to 4 hours
-nausea, vomiting
TX for appendicitis
Laparoscopic surgery
-allowing access to viscera without creating a large incision
Appendicitis: obstruction of appendix lumen causing
Block in the drainage of appendix
Appendicitis: as mucosal secretions continue
Intraluminal pressure inc
Appendicitis: inc pressure reduces blood flow
Appendix is hypoxia and ulcerative
Appendicitis: ulceration promotes bacterial invasion
Immune response and inflammation
-gangrene
Hepatic encephalopathy
A complex neurological syndrome characterized by impaired behavioural cognitive and motor function
Encephalopathy
Brain disease that alters brain function or structure
Hepatic encephalopathy: combination of biochemical alterations that affect
Neurotransmission and brain function
Liver dysfunction causes (Hepatic encephalopathy)
Development of collateral vessels that shunt blood around liver to systemic circulation
Hepatic encephalopathy: shunt permits
Toxins absorbed from GI tract to circulate to brain
-the toxins are usually removed by liver
Hepatic encephalopathy: toxins will alter
Cerebral energy metabolism, interfere with neurotransmisison and cause edema
Hepatic encephalopathy: most hazardous is
Ammonia causing astrocyte swelling
-alter BBB and promote cerebral edema
Jaundice
Yellowing pigmentation of skin
Jaundice is caused by
Hyperbilirubienmia which inc plasma
Bilirubin is normally
Removed from blood by liver
Inc plasma indicates
Liver damage
Obstructive jaundice
Occlusion of common bile duct by gall stones, tumour etc
-bilirubin cannot flow to duodenum and accumulates in liver
Obstructive jaundice results in
Enters blood stream causing jaundice
Hemolytic jaundice
Excessive production of bilirubin from excessive hemolysis of RBC
Hemolytic jaundice results in
Plasma exceeding liver ability to process = inc plasma bilirubin = jaundice
Manifestations of jaundice
-darkened urine, several days before onset
-bacterial infections may occur
-yellow discolouration of sclera followed by inc yellowing of skin
Cirrhosis
Irreversible fibrotic scarring of liver in response to inflammation and tissue damage
Liver cirrhosis is
Final step of various chronic liver diseases
Pathophysiology cal hallmark of cirrhosis
Development of scar tissue due to fibrosis
Chaotic fibrosis
Obstructus blood flow and produces jaundice, inc portal hypertension and cellular dysfunction
Cirrhosis regeneration is disrupted by
Hypoxia = necrosis= atrophy= liver failure
Manifestation of cirrhosis
Liver acquires a cobble appearance and is hard upon palpitation
Alcoholic cirrhosis
Toxic effects of alcohol on liver, and immune alterations
Alcoholic cirrhosis: alcohol is transformed into
Acetaldehyde which activates hepatic Stellate cells
Alcoholic cirrhosis: hyperactivation of stellate cells results in
Collagen formation = fibrosis scarring
Alcoholic cirrhosis: damage results in
Translocation of gut microbiota
Non alcoholic fatty liver disease
Infiltration of hepatocutes with triglycerides
-obesity, high blood triglycerides and cholesterol
Biliary cirrhosis
Damage and inflammation leading to cirrhosis begins in bile ducts rather than hepatocytes
Primary biliary cirrhosis
Caused by chronic autoimmune liver disease
-damage bile ducts = fibrosis = bile duct obstruction
Secondary biliary cirrhosis is caused by
Caused by obstruction of common bile ducts by gallstones, tumours etc
Viral hepatitis
Common systemic disease that primarily affects the liver
-ABCDE
Viral hepatitis
-all cause jaundice
-infiltration of pathogens = hepatic cell necrosis/scarring
Further cellular injury is promoted by
Immune response
Most severe damage (hepatitis)
Hep B and C
Co infection fo hep and hiv occurs because
Virus share same route of transmission
-contact between infected body fluids
Diagnosis of viral HEP
Presence of viral antibodies
TX for viral HEP
Directed at viral replication suppression and HEP B vaccine
Common gallbladder disorders
Obstruction and inflammation
Gallstones
Block flow of bile in and out of gallbladder
-causes inflammation
Cholelithaiasis
Gallstone formation
Cholecystitis
Gallbladder inflammation
Obstructive pancreas disease
Causes backup of pancreatic secretion, release and activation of pancreatic enzymes within acinar cells
Enzymes causes (pancreas)
Autodigestion of pancreatic cells and tissues = inflammation
Autodigestion of pancreas causes
Vascular damage, necrosis and pseudocysts formation
Pseudocysts
Walled off collections of pancreatic secretions
Alcohol abuse is the
Main cause of further developments in pancreas
-acinar cell metabolizes ethanol = toxic metabolites that release acinar digestive enzymes
Chronic alcohol to pancreas =
Destruction of acinar cells = tissue destruction replaced with fibrosis = pancreatic cysts
treatment for pancreas
Alcohol cessation
Cancer of the esophagus
Carincoma and adenocarinomas of epithelium
Adenocarcinoma initiates in
Epithelial glandular cells
Carcinoma initaiates in
Epithelial squamous cells
Manifestations of esophageal cancer
Dysphagia and chest pain
Risk for cancer of esophagus
Alcohol combined with smoking or chewing tobacco
Gastric adenocarcinoma is associated with
H.pylori
Cancer of the stomach inc risk by
Heavily salted and preserved foods
-salt enhances conversions of nitrates to carcinogenic nitrosamines
Most common form of cancer
Carcinoma
-imitates in epithelial tissue of skin or internal organs
Adenocarcinoma
Is a subtype of carcinoma that initiates in glands
Pre existing polyps are highly associated
With colon adenocarcinoma
Manifestations of cancer in colon and rectum
Pain, bloody stools and change in bowel habits
Rectal carcinomas occur close to
Anus
-spread to vaginal and prostate
Leading cause of world wide cancer deaths
Cancer of the liver
Cancers of the over are associated with
Chronic liver diseases
-cirrhosis and HEP b
Hepatocellular carcinomas arise from
Hepatocytes
cholangiocellular carcinomas
Rare and develop in bile ducts
Liver cancers have high risk of
Metastasizing to other organs
Msot common cancer between 50 and 60 years of age
Cancer of gallbladder
Most common type within gallbladder cancer
Adenocarcinoma
Cancer of gallbladder metastases to
Lymph vessels and usually occurs before diagnosis
What is the fourth leading cause of cancer death in Canada
Cancer of pancreas
Adrencarinoma in pancreas cancer occurs in
Exocrine component of pancreas
Cancer of pancreas often metastasizes before
Diagnosis