(E2) Gastrointestinal System

GI LECTURE OBJECTIVES AFTER REVIEWING THESE CHAPTERS, THE LEARNER SHOULD BE ABLE TO: • DESCRIBE THE PATHOPHYSIOLOGIC ALTERATIONS THAT LEAD TO DIARRHEA AND CONSTIPATION. • LIST AND BRIEFLY EXPLAIN THE VARIOUS DISORDERS OF MOTILITY OF THE GASTROINTESTINAL TRACT. • IDENTIFY THE PATHOPHYSIOLOGY AND MANIFESTATIONS OF VARIOUS OBSTRUCTIONS OF THE GASTROINTESTINAL TRACT. • DESCRIBE THE CAUSES AND MANIFESTATIONS OF GASTRITIS. • COMPARE THE PATHOPHYSIOLOGY, CAUSATIVE AGENTS, AND MANIFESTATIONS OF PEPTIC ULCERS DISEASE. • DISCUSS THE PATHOPHYSIOLOGY AND CLINICAL MANIFESTATIONS OF IRRITABLE BOWEL SYNDROME. • DISCUSS THE RISK FACTORS, CELL TYPE, INCIDENCE, MANIFESTATIONS, MORBIDITY, AND MORTALITY OF THE VARIOUS DISCUSSED CANCERS (GASTRIC, COLON, AND RECTUM) OF THE DIGESTIVE SYSTEM.

Upper Esophageal Sphincter (UES)

Lower Esophageal Sphincter (LES)

Pyloric Sphincter

Ileocecal Sphincter

Important things to know about the Mucosa Layer of GI tract

= innermost layer

-has villi a “brush border” that increase the surface area for absorption

-secretion of protective factors: bicarbonate, mucus, prostaglandin

-cells: parietal, goblet, chief, gastric mucosal cells

Layers of the GI tract (outer to inner)

1) Muscularis

2) Serosa

3) Submucosa

4) Mucosa

Muscularis Layer

-circular muscle layer

-longitudinal muscle layer

Serosa Layer

-connective tissue layer

-peritoneum

Submucosa Layer

-Gland in submucosa

-Duct from gland

Mucosa Layer

-Mucous epithelium

-Lamina propria

-Muscularis mucosae

*Note: remember the other important things abt this layer too… secretion of stuff, villi, etc….

3 Phases of Digestive Process

1) Cephalic Phase

2) Gastric Phase

3) Intestinal Phase

1) Cephalic Phase

-Secretion of Acetylcholine (PSNS), Gastrin, Histamine

*acetylcholine = NT that stimulates rest & digest

2) Gastric Phase

*Know what each cell type does

-parietal cells

-goblet cells

-chief cells

-gastric mucosal cells

-G cells

3) Intestinal Phase

Begins with chyme entering the small intestine

-Moves into Small Intestine first, then the Large Intestine

Fundus of Stomach

Upper part of stomach

Body of Stomach

Main central region of the stomach

Antrum of Stomach

Lower portion of the stomach that leads to the pylorus.

Intestinal Villi

“brush border”

-increases surface area for absorption

-secretion of mucus, bicarbonate, PEG2 = “protective / defensive factors”

3 Pieces of the Small Intestine

1) Duodenum

2) Jejunum

3) Ileum

Duodenum of S.I.

-digestion continues and nutrients begin to be absorbed

-It receives chyme from the stomach and bile from the liver

Pyloric Sphincter

-found between stomach and duodenum of S.I.

Senses pH of chyme going into S.I.

*if pH <3.5 (very acidic), it will slow dumping of chyme and generate more protective factors (bases) to increase pH

Jejunum of S.I.

-Absorbs fat soluble vitamins: A, D, E, K

Ileum of S.I.

Last, Longest part of S.I.

-Absorbs Vitamin B12

-Bile acids are reabsorbed into liver

Typical Questions of G.I. Assessment

Swallowing → Odynophagia? Dysphagea?

Indigestion → Eructation? Burning?

Weight Loss?

Appetite?

N/V? → timing in relation to meals? character of emesis?

Pain → type? timing in relation to meals/sleep? what makes it worse/better?

Elimination → bowel movement frequency, quantity, appearance

Family Hx

Odynophagia

painful swallowing

Dysphagia

difficulty swallowing

Substances affecting Upper GI

Alcohol, Smoking, NSAIDS

What is the largest organ of the GI system?

Small Intestine (20ft long!!)

function: absorption + digestion

Pertinent Dx Tests

Upper + Lower GI Endoscopy

Videocapsule Endoscopy

Laparoscopy + Laparotomy (open)

Upper GI Series (barium study)

Role of Upper + Lower GI Endoscopy

-biopsies

-remove polpys (clumps of cells that can be cancerous)

Role of Videocapsule Endoscopy

Swallowing camera to view S.I.

Role of Laparoscopy + Laparotomy (open)

-Diagnostic

-Surgery

Role of Upper GI Series (barium study)

A series of X-rays taken after the patient drinks a barium solution, used to visualize the esophagus, stomach, and duodenum.

If a Peptic Ulcer Disease (PUD) is suspected, what Dx test is done?

Presence of H. Pylori Antibody in blood test

If a GI bleed is suspected, what Dx test is done?

Fecal occult blood test (FOBT)

or “Hemoccult”

Most common dysfunction of GI system

Constipation

Constipation definition

Infrequent or difficult defecation

Causes of constipation

-Neurogenic Disorders

-Functional/Mechanical Conditions

-Low Residue Diet (low fiber)

-Sedentary Lifestyle

-Changes in Bowel Habits

-Medications

What do we monitor for in severe constipation?

Bowel Obstruction

Meds linked to constipation

-Benzodiazepines

-Diuretics

-Opiates (pain killers)

-Antidepressants

With more mobility, comes more ????

motility = more pooping

Diarrhea

Increased frequency of bowel movements

-increased vol, fluid, and weight of feces

3 Major Mechanisms of Diarrhea

1) Osmotic Diarrhea (mild)

2) Secretory Diarrhea (severe)

3) Motility Diarrhea

Osmotic Diarrhea (mild)

-Malabsorption syndromes (lactose intolerance), laxatives

Secretory Diarrhea (severe)

Infections (toxins), medications (chemo)

Motility Diarrhea

Irritable bowel

GERD: Gastroesophageal Reflux Disease

A chronic condition where stomach acid flows back into the esophagus, causing heartburn and possible damage to the esophageal lining.

-common in infants and people over 40

Issues that occur with GERD

-Relaxation of the LES (inadequate closure)

-Gastroparesis - delayed emptying from stomach to duodenum

During GERD, Gastroparesis occurs. What damage does this cause?

-Damages the esophageal epithelium

-Can lead to metaplasia at gastroesophageal junction → Barrett’s Esophagus → esophageal CA

Manifestations of GERD

-Dyspepsia

-Regurgitation of chyme

-Mid-epigastric pain within 1HR of eating

-Dry cough

-Laryngitis

GERD can lead to….

GI bleed

Aspiration Pneumonia

Contributing Factors to GERD

-Laying flat / bending over

-Alcohol, Chocolate, Coffee

-Fatty meals (slows digestion)

-Medications (see other slide)

*NICOTINE

*HIATAL HERNIA

Hiatal Hernia

Part of the stomach pushes up through the opening in diaphragm and protrudes into the thoracic cavity

-Allows stomach acid to reflux back into esophagus

-Many are undiagnosed, asymptomatic, and discovered incidentally

S/S of Hiatal Hernia

-Esophagitis

-Dysphagia

-Sub-sternal burning

-Belching

-Epigastric discomfort

CXR with a hiatal hernia

Displacement of the stomach into thoracic cavity

Lifestyle changes to decrease GERD and Hiatal Hernia risk

-Weight loss

-Small meals

-Coffee limitation

-Smoking cessation

-Refrain from lying down after eating → eat an early dinner

-Elevate head of bed or use 2 pillows to sleep (decreases gastric reflux)

-Avoid certain foods

Disorders of GI Motility

-Bowel Obstruction

-Paralytic Ileus

Bowel Obstruction

any condition that prevents the flow of chyme through the intestinal lumen

-can be partial or complete (emergency)

-can be SBO p.747 or LBO p.768-769

Paralytic Ileus

failure of normal intestinal motility (in the absence of an obstructing lesion)

Clinical Manifestations of GI motility disorders

-Crampy, colicky (intermittent) pains

-N/V → results in electrolyte depletion

-abdominal distension

-sweating, restlessness

-diarrhea w/ partial blockage

Common bowel surgeries

Ileostomy

Colostomy

Expandable Stents

Ileostomy

surgery where the ileum of the small intestine is surgically brought out to the exterior abdominal wall through an incision in the anterior abdominal wall

Colostomy

surgery where colon is brought out to the anterior abdomen through an opening known as a stoma

-can be reversible or irreversible

Expandable stents

a surgery where they are used endoscopically to relieve large bowel obstructions

Hernia

protrusion of intestine through weakness in abdominal muscles

Intussusception

telescoping of one part of intestine into another

Torsion (volvulus)

twisting of intestine on its mesenteric pedicle, with occlusion of blood supply

-associated w/ fibrous adhesions

-occurs mostly in middle-aged and elderly men

Tumor

abnormal growth into intestinal lumen

-adenocarcinoma of colon and rectum is the most common tumoral obstruction

-common in individuals 60+ years old

Paralytic (adynamic) ileus

Loss of peristaltic motor activity in intestine

-associated w/ abdominal surgery, peritonitis, hypokalemia, ishchemic bowel, spinal trauma, pneumonia

Fibrous Adhesions

peritoneal irritation from surgery, trauma, or chron’s disease

-leads to formation of fibrin and adhesions that attach to intestine, omentum, or peritoneum and can cause obstruction

-most common in S.I.

Acute Gastritis

aka. “Erosive Gastritis,” an inflammatory disorder of the gastric mucosa

Causes of acute gastritis

Medications: aspirin, NSAIDS, corticosteroids (blocks prostaglandin)

Factors: infection, allergy, acute stress, bile reflux, alcohol abuse, radiation, and direct trauma

Symptoms of acute gastritis

heartburn, nausea, epigastric pain

Dx of acute gastritis

take a thorough Hx & possibly EGD (upper endoscopy)

Confirmed with an endoscopy and biopsy of affected tissue

Tx of acute gastritis

based around the on antigen causing inflammation

-PPIs (proton pump inhibitors)

Chronic Gastritis

aka. “nonerosive gastritis”

-causes atrophy of the stomach lining

What is the most common cause of Chronic Gastritis?

Presence of the Helicobacter pylori (H. pylori) bacterium

S/S of Chronic Gastritis

-Gnawing, burning epigastric pain

-Nausea

-Weight loss

-Anorexia

-Hematemesis (vomiting blood or coffee ground material)

Tx for Chronic Gastritis

Antibiotics given for H. pylori

PPIs (proton pump inhibitors)

Peptic Ulcer Disease (PUD)

Inflammatory erosion in the Stomach or Duodenal lining (S.I.)

-ulceration occurs 4x more often in the duodenum

-use of endoscopy and tissue biospy

Contributing factors to Peptic Ulcer Disease (PUD)

*H pylori (bacterium)

*NSAIDs use

-Stress

-Alcohol abuse

-Excessive caffine

-Smoking

-Genetic susceptibility

Pathophysiology of Peptic Ulcer Disease (PUD) → what happens?

-Hypersecretion of HCl

-Ineffective GI mucus production

-Poor cellular repair

-Toxin secretion

Why does Hypersecretion of HCl occur with PUD?

The erosion permits the diffusion of Hydrochloric Acid (HCl) into the stomach wall and BV

Why does Ineffective Mucus Production occur with PUD?

-NSAIDs counteract Prostaglandin E secretion

-Protective mechanisms of the intestinal mucosal barrier are damage by H. pylori

Why does Poor Cellular Repair occur with PUD?

H. Pylori secretes toxins which perpetuate inflammation

S/S of Peptic Ulcer Disease (PUD)

-Epigastric pain = intensifies with eating

-Duodenal pain = improved after eating

Pain is INTENSE. — burning and gnawing sensation is present that can be slightly relieved by food and strong enough to wake up someone from sleep

-perforation of the stomach or intestinal wall → sudden, excruciating abdominal pain / ridigity, pale skin, hematemesis, and cold sweat

Irritable Bowel Syndrome (IBS)

-"irritable bowel” “colitis” “spastic colon”

Recurrent abdominal pain and discomfort associated with altered bowel habits

What causes Irritable Bowel Syndrome (IBS)?

No specific structural or biochemical alterations as a cause of disease

-no pathological changes

-however, IBS is associated w/ anxiety, depression, and chronic fatigue syndrome

IBS Risk Factors

Female

Under 40 y/o

Family Hx of IBS

Stress

Food Triggers → dairy, fructose, sorbitol, etc.

Manifestations of Irritable Bowel Syndrome (IBS)

-Abdominal pain and other symptoms >6 months

-Change in normal bowel habits

-Pain caused by eating, relieved with bowel movement

-Flatulence

-ABD distension/bloating

-Mucus in stool

True or False: IBS can be diarrhea-predominant or constipation-predominant.

True

Alternating diarrhea/constipation, gas, bloating, and nausea is a symptom of…

Irritable Bowel Syndrome (IBS)

2 types of CA in GI tract

Esophageal

& Colorectal

Risk Factors for Esophageal Cancer

Male

GERD & Barrett’s Esophagus

Chronic Alcohol Consumption, esp. whiskey

Tobacco use

Genetics

Pathophysiology of Esophageal Cancer

-Chronic irritation of the epithelial cells causes cell injury and leads to metaplastic changes

-Metaplasia becomes dysplasia

-Proliferation of cancer cells

S/S of esophageal CA

Dysphagia

Changes in eating patterns

Weight Loss

Dyspepsia

Sore throat or hoarseness

Cough

Dx of esophageal CA

EGD, biopsy, CT

Risk Factors for Colorectal CA

Genetics *highest risk

Polyps

Hx IBD (UC, Div, Chron’s)

High refined carbs, low fiber, high fat diets

Eating lots of red meat

Obesity, Sedentary Lifestyle

Clinical Manifestations of Colorectal CA

-Asymptomatic for years

-Fatigue, weakness

-Changes in bowel habits

-Slow GI bleed → anemia

-Bloody stool → anemia

-Pain

-Mass

-Obstruction

Parietal Cells

secrete HCl (acid), Acetylcholine, Histamine, and Gastrin Binds

-trigger proton pump (more H+ ions)