NURS 337 Pathophysiology Gastrointestinal Disorders

Clinical Manifestations of Gastrointestinal Dysfunction

-Anorexia

-Nausea

-Vomiting

Anorexia

A lack of desire to eat

-Pathological

-Psychological

Vomiting

The forceful emptying of the stomach and intestinal contents through the mouth

-Can occur through Retching or Projectile Vomiting

Retching

Nonproductive Vomiting

Hematemesis

Vomiting Blood

Constipation

● Less frequent bowel movements

● Straining with defecation

● Small, lumpy hard stools

● Sensation of incomplete emptying

● Usually < 3/ week

Primary Constipation

-Normal transit of stool (functional)

-Slow Transit

-Pelvic floor or outlet dysfunction

Secondary Constipation

Due to diet, medications (opiates, irons), hypothyroidism, and aging

Transit Time

Time it takes for food to pass through the Digestive System

Constipation treatments

Manage underlying disease

○ Increase fluids and fibers

○ Enemas (inserting liquid into the rectum)

○ Stool softeners and laxatives

Diarrhea

● Increased frequency of bowel movements

○ 3-4/ day

● Loose, watery stools

● Types

○ Acute/ persistent – think infectious

○ Chronic – think inflammation

Mechanisms of Diarrhea

-Osmotic Diarrhea

-Secretory Diarrhea

-Motility Diarrhea

Osmotic Diarrhea

(Lactose Intolerance - Pulls water from the blood vessels)

Secretory Diarrhea

infectious

ex. (Gastroenteritis, Malabsorption - Bacterial Overgrowth)

Motility Diarrhea

(Drugs, Hyperthyroidism)

Signs and Symptoms of Diarrhea

-Dehydration

-Electrolyte Imbalance

-Rapid weight Loss

Treatment of Diarrhea

Fluid Intake, Antimotility, Casual Factors

BE CAUTIOUS when using antidiarrheal if C. DIFFICILE COLITIS, SALMONELLA infection, or SHIGELLOSIS are present

Abdominal Pain

Can be Visceral, Parietal, or Referred

Visceral Pain

Stretching of the organ -> Leading to poorly localized, characterized pain

-Dull, colicky, cramping, aching, burning sensation

Parietal Pain

Irritation of nerve fibers innervating the parietal peritoneum

-Localized to the size of the painful stimulus

-Sharp pain

Referred Pain

Pain or discomfort is identified as coming from one region like the shoulder when it's coming from a different region like the diaphragm

Gastrointestinal Bleeding

Can occur as Upper GI Bleeding (Mouth -> Duodenum) or Lower GI Bleeding (Jejunum-> Anus)

-Occurs as acute blood loss or occult blood loss (Occult blood loss determined by positive fecal occult blood test and/or iron deficiency anemia)

-Physiological response depends on the rate and amount of blood loss

Hematochezia

Blood in the stool (Bright red blood per rectum)

Melena

Dark/Black Tarry Stool

Gastroesophageal Reflux Disease (GERD)

Periodic, symptomatic reflux (backflow) of gastric (stomach) contents into the

esophagus causing erosion and inflammation

Pathogenesis of GERD

Resting tone of the lower esophageal sphincter (LES) tends to be lower than normal (Incompetent LES)

Bottom line: the LES opens more frequently and longer resulting in reflux

Symptoms of GERD

● Heartburn

● Indigestion

● Chest pain

● Hoarseness/laryngitis

● Chronic cough

● Asthma attacks (micro -aspirations)

● Globus

● Dysphagia

Heartburn

burning feeling in the lower chest, along with a sour or bitter taste (acid reflux) in the throat and mouth

Indigestion

is discomfort (pain) in your upper abdomen or a feeling of fullness soon after eating

Globus

sensation of something in the back of the throat

Dysphagia

difficulty or pain on swallowing

Barret esophagus

• METAPLASTIC COLUMNAR EPITHELIUM REPLACES THE STRATIFIED SQUAMOUS EPITHELIUM THAT NORMALLY LINES THE DISTAL ESOPHAGUS

• INCREASED RISK OF ESOPHAGEAL ADENOCARCINOMA

• DUE TO CHRONIC GERD

• MANAGED WITH ENDOSCOPIC SURVEILLANCE

• LES DYSFUNCTION

Risk Factors for GERD

-Increased abdominal pressure

• Obesity

• Pregnancy

• Hiatal Hernia

-Delay Gastric Emptying (Gastroparesis)

-Medications: Calcium Channel Blockers

-HELICOBACTER PYLORI

History of GERD

-OCCURS 30-90 MINUTES AFTER A MEAL

- Sleeps with 2-3 pillows (30 – 40 degree incline)

-Worsens with reclining

-Improves with antacids, sitting, or standing

Diagnosis for GERD

Clinical Diagnosis/History Alone

Diagnostics:

-Upper Endoscopy + Biopsy (Always try to do this first)

-Esophageal Manometry

-24-hour pH Testing

-Barium Esophagram

Treatment of GERD

-Weight Loss

-Head Elevation

-Avoidance of meals 2-3 hours before bedtime

-Trigger foods elimination

-Medications

• Proton Pump Inhibitors (Prilosec) (Take at night before bed)

• H-2 Antagonists (Cimetidine)

• Antacids

• Surgery: laparoscopic fundoplication

Peptic Ulcer Disease

Damage to or Break in the mucosal barrier of the stomach and duodenum

Pathogenesis of Peptic Ulcer Disease

-Inadequate Blood Supply

• caused by vasoconstriction (e.g. by stress, smoking, shock, circulatory impairment, scar tissue, and anemia)

• interferes with rapid regeneration of the epithelium

-Excessive glucocorticoid secretion or medication

-Ulcerogenic substances break down mucous layer

• (Aspirin, NSAIDs, and alcohol)

-Atrophy of Gastric Mucosa

• (Chronic Gastritis)

Causes of Peptic Ulcer Disease

-Non-Steroidal Anti-Inflammatory Drugs

-Helicobacter Pylori

Pathogenesis of Peptic Ulcer Disease Through NSAIDs

-Systemic anti-prostaglandin Effect

• Loss of cytoprotection - decrease prostaglandin

  • Minimize mucosal secretion

  • stops bicarbonate (HCO3-)

• Less blood flow

-Topic Caustic Effects

• NSAIDs - Weak acid ionize in the stomach

• Acid enters cell -> trapped

• Uncouple oxidative-phosphorylation-increase cell permeability

Pathogenesis of Peptic Ulcer Disease Through Helicobacter Pylori

-Gram Negative Rod

-Found only in gastric epithelium

-Produces NH3 ammonia (a urease) to decrease acid production

-Produces protease - allow bacteria to burrow or move into the mucosa

-Produce auto-antibodies

Complications of Peptic Ulcers

-Hemorrhage - Caused by erosion of blood vessels and may be the first sign of a peptic ulcer

-Perforation - Ulcer erodes through the wall resulting in chemical peritonitis

-Obstruction - May result later because of the formation of scar tissue

Signs and Symptoms of Peptic Ulcers

Epigastric burning or localized pain, usually following stomach emptying

Diagnostic Tests for Peptic Ulcers

-Fiberoptic Endoscopy with Biopsy

-Barium X-Ray

Treatment of Peptic Ulcers

Determine cause

-Antimicrobial and proton pump inhibitor to eliminate H. pylori infection

-Reduction of exacerbating factors

Duodenal Ulcers

Most common of the peptic ulcers

-Pathogenesis includes the use of NSAIDs and Helicobacter pylori infection

-Intermittent pain in the epigastric area

• RELIEVED RAPIDLY BY INGESTION OF FOOD OR ANTACIDS

• PAIN 2-3 HOURS AFTER MEAL

• PAIN AT NIGHT

Management of Duodenal and Gastric Ulcers

-Relieving the causes and effects of hyperacidity

-Preventing complications

Gastric Ulcer

Location: antrum of the stomach

-Pathogenesis

• increased mucosal permeability to hydrogen ions

• Gastric secretion usually normal

Treatment is similar to duodenal ulcers

Inflammatory Bowel Disease

Chronic, idiopathic, relapsing inflammatory bowel disorders

Types: Ulcerative Colitis and Crohn's Disease

Pathogenesis of Inflammatory Bowel Disease

-Alterations of epithelial barrier functions

-Altered immune reactions to intestinal flora

-Genetics

-Environmental Factors

Ulcerative Colitis

Chronic inflammatory disease that causes ulceration of the colonic mucosa

-involves sigmoid colon and rectum

-Begins in the rectum and may extend proximally to the entire colon

-Intermittent periods of remission and exacerbation

- Lesion: continuous, limited to the mucosa

Symptoms of Ulcerative Colitis

-Diarrhea (Small volume type and 10 to 20/day)

-Urgency

-Bloody Stools

-Cramping

Crohn's Disease

Idiopathic, Granulomatous, inflammatory disorders, affect any part of the digestive tract from the mouth to the anus

-Other terms: regional enteritis or granulomatous colitis

-"Skip lesions"

-One side of the intestinal wall may be affected and not the other

-Complications: adhesions, fissures, or fistulas

-Interference with digestion and absorption

- Prolonged diarrhea with abdominal pain, fatigue, and weight loss

• Hypoproteinemia, malnutrition, possibly steatorrhea (fatty stool)

• Anemia - Malabsorption of vitamin B12 and Folic Acid

Characteristics of Crohn's Disease

Region Affected: any part of the digestive tract, usually the Terminal ileum, and sometimes colon

Distribution of Lesions: Transmural, all layers, Skip lesions

Characteristic Stool: Loose, semi-formed

Granuloma: Common

Fistula, Fissure, Abscess: Common

Stricture, Obstruction: Common

Malabsorption, Malnutrition: Yes

Characteristics of Ulcerative Colitis

Region Affected: Colon, rectum

Distribution of Lesions: Mucosa only, Continuous, diffuse

Characteristic Stool: Frequent, watery, with blood and mucus

Granuloma: No

Fistula, Fissure, Abscess: No

Stricture, Obstruction: Rare

Malabsorption, Malnutrition: Not Common

Treatment for Inflammatory Bowel Disease

-Goals/Team Approach

• Achievement of Remission (Induction): disappearance or decrease in signs and symptoms

• Prevention of Disease Flares (Maintenance)

-Anti-inflammatory Medications

• Sulfasalazine (aspirin)

• Glucocorticoids

-Immunotherapeutic Agents (Immunomodulators)

-Antimotility Agents

-Antimicrobials

-Diet, lifestyle, and nutritional supplements

-Surgical resection (LAST RESORT)

• Usually an ileostomy or colostomy

Clostridioides difficile (formerly Clostridium difficile)

-Contains endospores that can survive the acidity of the stomach and reach the large intestine

-The normal gut flora is altered by broad-spectrum antibiotics, most notably clindamycin, cephalosporins, ampicillin, amoxicillin, and fluoroquinolones

-flourishes within the colon

-Toxins A & B cause mucosal damage

-The most common cause of nosocomial (hospital-acquired) diarrhea

-pseudomembranes colitis; yellowish plaques form over damage epithelium

C. difficile symtoms

fever, crampy abdominal pain, diarrhea

Colorectal cancer

-3rd most common cancer diagnosis

-3rd leading cause of cancer death

-22 million people are not up-to-date with screening recommendations

-risk increases with age

-Screenings reduce mortality by 53%

Risk Factors for Colorectal Cancer

• older age

• personal or family history of colorectal cancer or polyps

• inflammatory bowel disease

• hereditary syndromes (such as lynch syndrome)

• Type 2 diabetes

Screening Guidelines for Colorectal Cancer with No past Medical or Family history

Starting at age 50-75:

-Stool guaiac (FOBT) annually

-FIT annually

-Colonoscopy every 10 years

-Sigmoidoscopy every 5 years

-Multitargeted sDNA (Cologuard) every 3 years

-CTC every 5 years

Screening Guidelines for Colorectal Cancer with First-degree relative with colon cancer

-Colonoscopy every 5 years starting at age 40 or a Colonoscopy every 5 years starting 10 years prior to the age of the affected family member at the time of diagnosis (whichever comes first)

-i.e. If affected family member was 35 at the time of diagnosis, get a Colonoscopy every 5 years starting at age 25

Complications of Liver Disorders

- Portal hypertension

-Ascities

-Encephalopathy

-Hepatorenal

-Jaundice

Portal Hypertension

High blood pressure in the portal venous system is caused by resistance to portal blood flow (Intrahepatic, Post-hepatic)

-Varices

-Splenomegaly

-Vomiting of blood from bleeding esophageal varices is the most common clinical manifestation

Ascites

-Accumulation of fluid in the peritoneal cavity

-Most common cause is -> Cirrhosis

• 25% mortality if associated with cirrhosis

-Abdominal distention, increased abdominal girth, and weight gain

-Treatment: Paracentesis: needle is inserted into the peritoneum cavity and fluid is drained

Hepatic Encephalopathy (acute)

Spectrum of neuropsychiatric abnormalities in patients with liver dysfunction, after exclusion of brain disease

Signs and Symptoms of Hepatic Encephalopathy

-Personality changes and irritability

-Intellectual impairment and memory loss

-Depressed level of consciousness (stupor/coma)

-Flapping tremor of the hands (asterixis)

-Stupor, coma, death

Pathogenesis of Hepatic Encephalopathy

-Astrocyte dysfunction

-Excess plasma ammonia

Hepatorenal Syndrome

Functional renal failure that develops as a complication of advanced liver disease

-Manifestations include oliguria (abnormally small amounts of urine), hypotension, peripheral vasodilation associated with advanced liver disease —--May be acute or gradual onset

Jaundice (Icterus)

Caused by hyperbilirubinemia

-Types include

• Prehepatic

• Intrahepatic,

• Extrahepatic (post hepatic) obstruction

How is Jaundice characterized?

Dark urine, yellow discoloration of sclera and skin, and light-colored stools

Prehepatic Jaundice

Transfusion reactions, sickle cell anemia, thalassemia, autoimmune disease

Hepatic Jaundice (Intrahepatic)

Hepatitis, cancer, cirrhosis, congenital disorders, drugs, alcohol consumption

Posthepatic Jaundice

Gallstones, inflammation, scar tissue, or tumors block the flow of bile into the intestines, pancreatic cancer

Alcoholic Liver Cirrhosis

-Irreversible inflammatory, fibrotic liver disease

-Biliary channels become obstructed and cause portal hypertension

-Severity and rate of progression depend on the cause

Three Stages of Cirrhosis: Alcoholic Liver Disease

-Initial Stage (Fatty Liver)

-Second Stage (Alcoholic Hepatitis)

-Third Stage (End Stage Cirrhosis)

Initial Stage - Fatty Liver (steatosis)

-Enlargement of the liver

-Asymptomatic and reversible with reduced alcohol intake

Second Stage - Alcoholic Hepatitis

-Inflammation and cell necrosis

-Fibrous tissue formation-irreversible change

Third Stage - End-Stage Cirrhosis

-Fibrotic Tissue replaces normal tissue

-Little normal function remains

Manifestations of Alcoholic Liver Cirrhosis

Initial manifestations are often mild and vague

• Fatigue, anorexia, weight loss, anemia, diarrhea

• Dull aching pain may be present in the upper right abdominal quadrant

Advanced Cirrhosis

• Ascites and peripheral edema

• Increased bruising

• Esophageal varices (May rupture, leading to hemorrhage, circulatory shock)

• Jaundice

• Encephalopathy: neurological dysfunction

Treatment of Cirrhosis

-Avoidance of Alcohol

-Supportive or symptomatic treatment (Paracentesis)

-No dietary restrictions

-Antibiotics to reduce intestinal flora

-Lactulose/lactitol: draws ammonia and other fluid from the blood to the colon, where it is excreted

-Emergency treatment if esophageal varices rupture

-Liver transplantation

Cholelithiasis

Gallstones

Cholecystitis

Inflammation of the gallbladder from obstruction of the cystic duct

Choledocholithiasis

Gallstone obstructing the biliary tract, i.e., the common bile duct

Cholangitis

Bacterial infection superimposed on an obstruction of the biliary tree

Gallstones

Pathogenesis: impaired metabolism of cholesterol, bilirubin, and bile acids

• Supersaturation of bile with cholesterol

• Nucleation of crystals

• Hypomotility → allowing stone growth

-Type of Gallstone depends on the chemical composition

• Cholesterol - Bile that is supersaturated with cholesterol

• Pigmented or (calcium) bilirubinate

  • Brown - Infected Bile

  • Black - Stasis: Parenteral nutrition or chronic liver disease and hemolytic disease (excess unconjugated bilirubin)

Risks for Gallstones (4-Fs)

-Fat (Obesity)

-Forty (Middle age)

-Female

-Fertile (multiparity)

- Oral contraceptive use

-Rapid weight loss

-Native American ancestry

Acute Cholecystitis

Gallstone lodged in the cystic duct

-Pain in the upper right quadrant or epigastric region

• Rebound tenderness and abdominal muscle guarding

-Intolerance to fatty foods

Diagnosis of Acute Cholecystitis

CBC, SMA7, liver panel, amylase, lipase

-Ultrasound (Procedure of choice)

Treatment of Acute Cholecystitis

Surgery - most often elective

• Laparoscopic cholecystectomy - preferred

• transluminal endoscopic

• Endoscopic retrograde cholangiopancreatography (ERCP)

-Medical - dissolve stones (chenodeoxycholic or ursodeoxycholic acid)

Endoscopic retrograde cholangiopancreatography (ERCP)

-a medical procedure used to diagnose and treat problems in the bile ducts, pancreas, and gallbladder.

-it involves passing a flexible tube with a camera (an endoscope) down the throat into the stomach and duodenum, then injecting a dye to visualize the ducts on x-rays

Transluminal endoscopy

a minimally invasive surgical approach where procedures are performed through natural body openings (like the mouth or anus) instead of through abdominal incisions

Laparoscopic cholecystectomy

a minimally invasive procedure where the gallbladder is removed through several small incisions in the abdomen

Pancreatitis

Inflammation resulting in autodigestion of the tissue

-May be acute or chronic (acute form considered a medical emergency)

Pathogenesis of Acute Pancreatitis

-Obstruction to pancreatic outflow

-May progress to surrounding tissue/organ

-Substance released by necrotic tissue led to widespread inflammation (Hypovolemia and circulatory collapse may follow)

Causes of Acute Pancreatitis

#1 - Alcohol Abuse

#2 - Gallstones

Pathophysiology of Acute Pancreatitis

● Injury or damage to pancreatic cells and ducts → leakage of pancreatic

enzymes into the pancreatic tissue → cause autodigestion of pancreatic

tissue and leak into the bloodstream → leading to injury to blood vessels and other organs

Signs and symptoms of Acute Pancreatitis

● Fever

● Nausea & vomiting

● Severe epigastric or mid-abdominal pain

● Pain radiating to the back

● Signs of shock

● Low-grade fever until infection develops

● Abdominal distention and decreased bowel sounds

Diagnostic Tests for Acute Pancreatitis

-Serum AMYLASE-P levels - first rise, then fall after 48 hours

-Serum LIPASE levels are elevated

-Liver panel

-CBC, SMA7

Treatment for Acute Pancreatitis

-Intravenous Fluids

-Oral intake is stopped (NPO)

-Nasogastric tube insertion and suctioning

-Treatment of shock and electrolyte imbalances

-Analgesics for pain relief