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Chapter 38

Alterations of Digestive
Function

Clinical Manifestations of
Gastrointestinal Dysfunction
UPPERGASTRO.
•Esophagealvarices
INTESTINALBLEEDING Mallory-Weisstear

• Gastrointestinal bleeding Gastriculcer

Hemorrhagic
gastritis
Upper gastrointestinal bleeding
DINKenalTicer

• Esophagus, stomach, or duodenum

• Lower gastrointestinal bleeding SMALLINTESTINALBLEEDING

• Jejunum, ileum, colon, or rectum Ischemicboweldisease.

Intussusception
• Occult bleeding Meckeldiverticulum

• Physiologic response depends on rate and


LOWERINTESTINALBLEEDING
amount of blood loss
Angiodysplasia

• Hematochezia: bright red stools


Melena: black or tarry stools
Coloniccarcinoma

Rectosigmoidcarcinoma Inflammatory
boweldisease
Hemorrhoids
Diverticulosus
Pathophysiology of Gastrointestinal Bleeding

Disorders of Motility
• Dysphagia
• Difficulty swallowing
• Mechanical obstruction: Tumors, Strictures, Diverticula
• Functional disorders
• Caused by neural/muscular disorders that interfere with voluntary swallowing.

• Stroke, Parkinson’s Disease, Multiple Sclerosis, Muscular Dystrophy

• Manifestations
• Pain at the level of obstruction
• Regurgitation of undigested food, vomiting, and/or aspiration
• Weight loss

• Symptoms managed by eating small meals slowly, taking fluid with meals,
and sleeping with the head elevated to prevent regurgitation and
aspiration
Disorders of Motility
• Gastroesophageal reflux disease (GERD)
• Backflow of gastric and duodenal contents into the esophagus
• Loss of tone in the lower esophageal sphincter
• Reflux of acid and pepsin from the stomach to the esophagus
esophagitis

• Conditions that increase abdominal pressure or delay gastric


emptying can contribute to the development of reflux esophagitis
– Hiatal hernia, pyloric stenosis, impaired gastric emptying,
obesity
• Manifestations
• Heartburn (pyrosis)

• Acid regurgitation
• Dysphagia
• Chronic cough
• Asthma attacks
• Laryngitis, hoarseness

Disorders of Motility
• Intestinal obstruction
• An intestinal obstruction is any condition that
prevents the flow of digestive contents
(chyme) through the intestinal lumen
• Simple obstruction
• Mechanical blockage of the lumen
• Hernia

• Neoplasm

• Stool impaction

• Foreign object

• Functional obstruction (paralytic ileus)


• Failure of intestinal motility
• Often occurs after intestinal or abdominal
surgery, pancreatitis, or hypokalemia
Disorders of Motility

• Intestinal obstruction
• Signs of small intestinal obstruction
• Colicky pains
• Nausea and vomiting

• Signs of large intestine obstruction


• Hypogastric pain and abdominal distention

Gastritis
• Inflammatory disorder of the gastric mucosa
• Common causes: overuse of NSAIDs, H. pylori infection, &
physiologic stress-related mucosal changes
• NSAIDs inhibit prostaglandin synthesis, which normally
stimulates the secretion of mucus

• Acute gastritis
• Caused by injury of the protective mucosal barrier
• Symptoms are vague
• Anorexia, fullness, nausea, vomiting, epigastric pain
Peptic Ulcer Disease
• A break or ulceration in the protective mucosal lining
• Usually in stomach or proximal duodenum
• Sometimes in esophagus
• Acute and chronic ulcers
• Superficial
• Erosions
• Deep

Causes of Peptic Ulcer Disease (PUD)


• Helicobacter Pylori
• Bacterium that has learned to live in the thick
mucous lining of the stomach. Its presence can
lead to ulcers.
• Autoimmune Gastritis
• Stomach lining is attacked by the immune
system leading to loss of certain stomach cells.
The result is acute and chronic inflammation
which can results in pernicious anemia.
• Aspirin & NSAID Use/Overuse
• Non-steroidal anti-inflammatory drugs (NSAIDs)
reduce a protective substance in the stomach
called prostaglandin that can lead to
gastritis/ulcer formation
• Alcohol Overuse
• Causes inflammation and injury to the stomach.
Duodenal Ulcers
• Most common of the peptic ulcers
• Causative factors:
• Helicobacter pylori infection
• NSAIDs – INHIBITS PROSTOGLANDIN SYNTHESIS
• Characterized by burning pain in
midepigastric area 2 to 3 hours after a meal.
• Relieved rapidly by ingestion of food or antacids

• Management aimed at eliminating causes


and mitigate effects of hyperacidity and
erosion
• Antibiotics (for H. pylori)
• PPI
• H2 blockers

Gastric Ulcer
H.pylori,bilesalts,NSAIDs,alcohol,ischemia

Damagedmucosalbarrier

~Functionofmucosalcells
• Gastric ulcers tend to develop in the antral §Qualityofmucus
Lossoftightjunctionsbetweencells
region of the stomach, adjacent to the acid-
secreting mucosa of the body Back-diffusionofacidintogastricmucosa

• Causes: Use of aspirin and NSAIDs ,


Helicobacter pylori infection, chronic Conversionofpepsinogen Formationandliberation

gastritis, smoking, advanced age topepsin ofhistamine

• Pathophysiology
†Acidsecretion

• The primary defect is an increased mucosal Localvasodilation

permeability to hydrogen ions disrupt


Furthermucosalerosion
permeability and cellular structure H.pylori Destructionofbloodvessels
Increasedcapillarypermeability
Lossofplasmaproteins
Bleeding Mucosaledema
Lossofplasmaintogastriclumen
• Damaged mucosa releases histamine
stimulate increased production of acid and
Stimulationofcholinergic
pepsinogen Mucosal
injury
Ulceration intramuralplexus,causing
musclespasm

• Manifestations and treatment similar to Copyright©2020,ElsevierInc.Allrightsreserved.

duodenal ulcers except food causes pain


• Gnawing, sharp pain in or to the left of the
midepigastric region occurs 1-2 hours after a
Symptoms

• Abdominal pain after eating


• Nausea
• Abdominal indigestion
• Nausea
• Vomiting, particularly coffee-ground/bloody emesis
• Black tarry stools

Inflammatory Bowel Disease

• Ulcerative colitis and Crohn disease


• Chronic, relapsing inflammatory bowel disorders
• Genetics
• Environmental factors or infections
• Alterations of epithelial barrier functions
• Altered immune reactions to intestinal flora
Ulcerative Colitis
• Chronic inflammatory disease that causes ulceration of the colonic
mucosa
• Sigmoid colon and rectum
• Begins in the rectum and may extend proximally to the entire colon
• Damages bowel in a continuous fashion
• Intermittent periods of remission and exacerbation
• Symptoms
• Diarrhea (10 to 20/day)
• Urgency
• Bloody stools
• Cramping
• Treatment is individualized and depends on severity of symptoms
and extent of mucosal involvement

Crohn Disease
• Idiopathic inflammatory disorder; affects any part of the
digestive tract, from mouth to anus
• Most commonly the distal small intestine and proximal large colon
• Causes “skip lesions”
• Discontinuous pattern of bowel damage
• Ulcerations can produce fissures that extend into the
lymphatics
• Symptoms similar to ulcerative colitis: diarrhea, weight loss,
abdominal pain
• Rectal bleeding or bloody stools if the colon is involved
• Anemia may result from malabsorption of vitamin B12 and folic
acid
• Treatment similar to ulcerative colitis
Irritable Bowel Syndrome
• Disorder of brain-gut interaction characterized by recurrent abdominal pain
with altered bowel habits
• More common in women
• Associated with anxiety, depression, and reduced quality of life
• Manifestations
• Lower abdominal pain or discomfort and bloating
• Can be grouped
• Diarrhea-predominant
• Constipation-predominant

• Alternating diarrhea/constipation

• Symptoms including gas, bloating, and nausea are usually relieved with
defecation and do not interfere with sleep
• Diagnostic procedures to rule out other causes
• No cure, and treatment is individualized
• Laxatives and fiber, antidiarrheals, antispasmodics, prosecretory drugs, dietary
interventions

Diverticular Disease of the Colon

• Diverticula
• Herniations or saclike outpouchings of
mucosa through the muscle layers of
the colon wall, especially the sigmoid
colon
• Diverticulosis
• Asymptomatic diverticular disease
• Diverticulitis
• Inflammation of one or more
diverticula
Diverticular Disease of the Colon

• Diverticula can occur anywhere in the gastrointestinal tract, particularly at


weak points in the colon wall
• Complicated diverticulitis includes abscess, fistula, obstruction, bleeding,
or perforation
• Symptoms of uncomplicated diverticular disease may be vague or absent
• Cramping pain, diarrhea, constipation, distention, or flatulence
• If diverticula become inflamed or abscesses form fever, leukocytosis, abdominal
tenderness
• Evaluation: Diagnostic imaging and/or procedures
• Treatment is individualized: increased fiber; bowel rest with liquid diet;
antibiotics; laparoscopic surgical resection

Appendicitis

• Inflammation of the appendix


• Possible causes:
• Obstruction of the lumen with stool, tumors or foreign bodies infection
• Patho: obstructed lumen does not allow drainage of the appendix increased
intraluminal pressure decreased mucosal blood flow appendix becomes
hypoxic, inflamed and edematous
• Periumbilical pain that descends to the RLQ with increasing intensity
• Rebound tenderness and abdominal rigidity
• Nausea, vomiting, anorexia, and low-grade fever
• Elevated WBCs
• Perforation, peritonitis, and abscess formation are the most serious
complications
• Treatment is antibiotics and appendectomy
Functions of the Liver

• Synthesis of absorbed nutrients


• Serum glucose regulation
• Lipid (fat) metabolism
• Protein metabolism
• Ammonia is a byproduct of protein metabolism

• Synthesis of prothrombin for normal clotting mechanisms


• Vitamin and mineral storage
• Produces and stores vitamins A & D
• Vitamin B12 and iron are stored in the liver
• Drug metabolism
• Production of bile and bile salts

Disruption of Liver Function

• Hepatocyte injury disrupts the liver’s functions


• Decreased clotting synthesis
• Decreased albumin
• Decreased detoxification activity
• Excess accumulatio of drugs, hormones, and metabolites
• Decreased storage of nutrients
• Decreased conjugation of bilirubin
Disorders of the Liver

• Cirrhosis
• Chronic, progressive disease of the liver
characterized by diffuse degeneration and
destruction of hepatocytes.
• Repeated destruction of hepatic cells scar tissue
• Biliary channels become obstructed and cause
portal hypertension
• Severity and rate of progression depend on the
cause
• Long-term alcohol abuse

• Hepatitis B and C
• Non-alcoholic fatty liver disease

• Nonalcoholic steatohepatitis

• Early signs are vague and nonspecific: fatigue,


significant weight changes, GI symptoms, anorexia,
vomiting, abdominal pain, and liver tenderness

Alcoholic Liver Disease


• Related to toxic effects of alcohol and coexisting liver disease
• Alcoholic fatty liver
• Can be caused by relatively small amounts of alcohol; reversible with
cessation of alcohol

• Alcoholic steatohepatitis
• Increased hepatic fat storage, inflammation, and degeneration and
necrosis of hepatocytes stimulates irreversible fibrosis

• Alcoholic cirrhosis
• Caused by the toxic effects of alcohol metabolism in the liver,
immunologic alterations, inflammatory cytokines and malnutrition.

• Anorexia, nausea, jaundice, and edema develop with advanced


fatty infiltration or the onset of alcoholic steatohepatitis
Disorders of the Liver
• Primary biliary cholangitis
• Chronic, slowly progressive, autoimmune, cholestatic liver
disease
• Begins in bile canaliculi and bile ducts

• Often accompanies other autoimmune diseases


• Manifestations
• Pruritus, hyperbilirubinemia, jaundice, light/clay colored stools
• Progresses to cirrhosis, portal hypertension, encephalopathy

Disorders of the Liver


• Hepatitis
• Widespread inflammation of the liver
• Caused by virus, drugs, or toxic substances
• Inflammatory process causes hepatic cell degeneration and
necrosis.
• 5 Types (A, B, C, D, and E)
• B and C are most common causes: bloodborne
• Hep A and E are transmitted via fecal-oral route
• Vaccinations available for Hep A and B only
Disorders of the Liver
• Hepatitis
• Can cause acute, icteric illness (jaundice)
• Prodromal, icteric, and recovery phases
• Possible clinical manifestations: jaundice, fatigue, anorexia, malaise,
nausea, vomiting, headache, dark urine, clay-colored stools, pruritus,
liver enlargement (hepatomegaly) and tenderness.
• Diagnostics:
• Antigen and antibody markers
• Increased alanine aminotransferase (ALT), aspartate
aminotransferase (AST), and serum bilirubin levels
• Treatment and prevention

Complications of Liver Disorders


• Portal hypertension
• Abnormally high blood pressure in the portal venous
system caused by resistance to portal blood flow, most
commonly as a result of liver cirrhosis
• Vomiting of blood from bleeding esophageal varices is
the most common clinical manifestation and increases
mortality in those with cirrhosis.
• Varices
• Distended, tortuous collateral veins – particularly in
the lower esophagus and stomach
• Rupture of varices life-threatening hemorrhage
• Splenomegaly
• Enlargement of the spleen caused by increased
pressure in the splenic vein (branches from portal
vein)
Complications of Liver Disorders
• Hepatic encephalopathy
• A neurologic syndrome of impaired behavioral, cognitive, and motor
function caused by failure of the diseased liver to detoxify neurotoxic
agents such as ammonia.
• Early symptoms
• Subtle changes in personality, memory loss, irritability, disinhibition, lethargy, and
sleep disturbances

• Later symptoms
• Confusion, disorientation to time and space, flapping tremor of the hands
(asterixis), slow speech, bradykinesia, stupor, convulsions, and coma

• The condition develops rapidly during acute hepatitis or slowly during


course of liver disease
• Cells in the nervous system are vulnerable to neurotoxins absorbed from
the GI tract that, because of liver dysfunction, circulate to the brain

Complications of Liver Disorders

• Jaundice (icterus)
• Caused by hyperbilirubinemia
• Obstructive jaundice
• Extrahepatic obstruction
• Intrahepatic obstruction
• Hemolytic jaundice
• Prehepatic jaundice
• Excessive hemolysis of red blood cells
• Characterized by dark urine, yellow discoloration of sclera and skin, and
light-colored stools
Complications of Liver Disorders

• Ascites
• Accumulation of fluid in the peritoneal cavity
• Most common cause is cirrhosis
• Development associated with
• Portal hypertension
• Decreased synthesis of albumin by the liver
• Splanchnic arterial vasodilation
• Renal sodium and water retention
• 25% mortality in 1 year if associated with
cirrhosis
• Causes abdominal distention and increased
abdominal girth and weight gain
• Paracentesis

Disorders of the Gallbladder

• Gallstones
• Formation called cholelithiasis
• Risk Factors:
• Obesity, middle age, female, oral contraceptive use, rapid weight loss, Native American
ancestry, genetic predisposition, and gallbladder, pancreas, or ileal disease

• Clinical manifestations
• Often asymptomatic or vague (heartburn & flatulence)
• Epigastric and right hypochondrium pain
• Intolerance to fatty foods
Disorders of the Gallbladder

• Cholecystitis
• Inflammation of gallbladder or cystic duct
• Almost always caused by a gallstone lodged in
the cystic duct
• Result in gallbladder becoming distended and inflamed

• Pain localized in RUQ and triggered by a high-fat or


high-volume meal
• Fever, leukocytosis, rebound tenderness, and
abdominal muscle guarding are common findings
• Serum bilirubin and alkaline phosphatase levels may be
elevated

• + Murphy’s sign – cannot take a deep breath when the


examiner palpates below the hepatic margin due to
pain

• Acute attacks usually require laparoscopic


cholecystectomy

Disorders of the Pancreas


• Pancreatitis
• Inflammation of the pancreas
• Most common causes include obstructive biliary
tract disease (cholelithiasis), chronic alcohol
abuse, hyperlipidemia, peptic ulcer disease
• Develops because of obstruction to the outflow of
pancreatic digestive enzymes caused by bile and
pancreatic duct obstruction
• Results in a backup of pancreatic secretions and
activation and release of enzymes within the
pancreatic acinar cells.
• Activated enzymes cause autodigestions of
pancreatic cells and tissues inflammation,
vascular damage, necrosis, and formation of
pseudocysts (walled-off collections of pancreatic
secretions).
Disorders of the Pancreas

Acute Pancreatitis Chronic pancreatitis


• Occurs suddenly as one attack or • Continual inflammation of and
can be recurrent, with resolutions destruction of the pancreas, with
scar tissue replacing pancreatic
• Usually mild and resolves
tissue
spontaneously, but about 20% with
the disease have a severe case • Process of progressive fibrotic
requiring hospitalization. destruction of the pancreas

• May result from direct cellular • Related to chronic alcohol abuse


injury from alcohol, drugs, or viral (cause in > 50% cases)
infection • Continuous or intermittent
• Cardinal manifestation is abdominal pain and weight loss
midepigastric or LUQ pain with are common
radiation to the back • Manifestations of pancreatic
• N/V, abdominal distension & enzyme deficiency (steatorrhea
or malabsorption syndrome)

Cancer of the Gastrointestinal Tract

• Esophagus
• Squamous cell carcinoma
• Associated with smoking tobacco and chronic alcohol consumption

• Adenocarcinoma
• Associated with obesity, GERD, and smoking tobacco

• Frequent symptoms are chest pain and dysphagia


Cancer of the Gastrointestinal Tract

• Stomach
• Associated with chronic gastritis and Helicobacter pylori
• Sporadic and associated with consumption of heavily salted, processed, and
preserved foods (especially those containing nitrates)
• Poor intake of fruits and vegetables
• Tobacco and alcohol abuse
• Early symptoms are vague
• loss of appetite, malaise, and indigestion

• Later symptoms
• Unexplained weight loss, upper abdominal pain, vomiting, change in bowel habits, and
anemia

Cancer of the Gastrointestinal Tract

• Colon and rectum


• Colorectal polyps are closely associated with development of
cancer.
• Most are sporadic or associated with a family history of colorectal
cancer
• Caused by multiple gene alterations and environmental
interactions
• Familial adenomatous polyposis

• Hereditary nonpolyposis, or Lynch syndrome

• Low fiber diets at risk


• Most common location: rectum
• Colorectal cancers carry the highest incidence and number of
deaths of all GI cancers
Signs & Symptoms of Colorectal Cancer by Location

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