GI and Hepatobiliary lecture

THE

GASTROINTESTI

NAL AND

HEPATOBILIARY

SYSTEMS

Barry University NUR 313

Objectives

At the completion of this lecture, the students will

be able to:

Describe the structure and function of the

gastrointestinal system

Verbalize the difference between the upper,

middle and lower GI tract.

Understand various disorders of the GI system

such as GERD, peptic ulcer disease, hepatitis,

pancreatitis, and gastroenteritis.

Describe diagnostic tests and treatments related

to various disorders of the GI system.

2

Structure and Function

Major Physiological Functions of the GI

system

Digestion of food

Absorption of nutrients into the blood stream

Motility, Secretion, Digestion, absorption

3

Structure and Function

GI tract is divided into 3 parts:

Upper: mouth, esophagus and stomach

Intake source

Middle: duodenum, jejunum and ileum

Digestion and absorption

Lower: cecum, colon, rectum

Storage and elimination

4

Structure and Function

Esophagus: straight, tube about 10 inches in

length

Smooth muscle layers with peristaltic movements

to move food

Connects oropharynx to stomach

Upper Pharyngoesophageal sphincter keeps air

from entering esophagus and stomach during

breathing

Lower Gastroesophageal Sphincter prevents

reflux of gastric contents

5

Stucture and Function

Stomach

Pouch-like structure on left side of

abdomen serves as food storage

Pyloric sphincter controls rate of

stomach emptying and prevents

regurgitation of intestinal contents back

into stomach

6

7

Structure and Function: Middle

and Lower GI Tract8

Structure and Function: Motility

Rhythmic intermittent contractions – mixing

and moving food

Esophagus, upper stomach, small intestines

Tonic movements is a constant contractions

Lower esophagus, ileocecal valve, anal sphincter

Autonomic nervous system

SNS

PNS

9

Structure and Function

Hormones:

Gastrin: stimulates gastric acid, blood flow

Cholecystokinin (CCK): Contraction of gallbladder

and secretion of pancreatic enzymes

Secretin: inhibits gastric acid secretion; stimulates

secretion of water from the pancreas

Ghrelin: peptide hormone stimulates food intake

and digestive function (appetite)

10

Digestion and Absorption

Digestion: The process of dismantling

food into parts

Requires hydrolysis, enzyme

cleavage, fat emulsification

Absorption: moving nutrients from

external intestinal lumen to internal

environment.

11

Disorders of the GI and Hepatobiliary

systems

Gastroesophageal

Reflux Disease

(GERD)

Peptic Ulcer

Disease

Gastroenteritis

IBD – Crohn’s &

Ulcerative Colitis

Diverticular Disease

Appendicitis

Intestinal

Colorectal CA

Peritonitis

Hepatitis

Cirrhosis

Liver Failure

Cholecystitis

Pancreatitis

12

Gastroesophageal Reflux Disease

Reflux of gastric contents into esophagus

as a result of

Reduction in lower esophageal sphincter

tone

Delayed gastric emptying

Increase gastric acid secretion

Irritation of esophageal mucosa

13

GERD

GERD14

Risk Factors

Factors which reduce LES tone

Aging

Obesity

Pregnancy

High fat meals

15

Signs and Symptoms

Pyrosis (heartburn) cardinal symptom

Belching

Atypical Symptoms

Esophageal pain referred to the neck,

mid-back, upper abdomen

Chest pain

Chronic cough, wheezing, Hoarseness

Chronic sore throat, dysphagia

16

Diagnosis

History and physical alone if symptoms

are typical

Endoscopy and biopsy if symptoms are

atypical

Complications

Barrett’s esophagus

Strictures

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Barrett’s Esophagus/Strictures

Treatment

Medication

Avoid recumbence after eating

Elevate head of bed when sleeping

Reduce size of meals

Reduce fat, acid, spices, caffeine, sweets,

peppermints, chocolate, and alcohol

Avoid constrictive garments

19

Peptic Ulcer Disease

A group of ulcerative disorders that occur in

areas of the upper gastrointestinal tract that

are exposed to acid-pepsin secretions

Erosion of the gastric membrane

Gastric ulcers

Duodenal ulcers

Stress ulcers- Curling’s ulcer

20

Gastric Ulcer21

Duodenal Ulcer22

Risk Factors

Helicobacter pylori (H-Pylori) infection

90-95% of patients with duodenal

ulcers

60-70% of patients with gastric

ulcers

NSAIDs

aspirin

23

Signs and Symptoms

Pain

Burning, gnawing, cramp-like

Frequently when stomach empty

Midline epigastric, near xiphoid…may

radiate to back or right shoulder

Relieved by foods or antacids

Periodicity: daily for weeks, then remits

until next occurrence

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Complications

Bleeding

Hematemesis

Coffee ground emesis

Hematochezia

Melena

Occult bleeding

Gastric Outlet Obstruction

Caused by edema, spasm, scar tissue

Perforation

Peritonitis

25

TREATMENT

Antibiotics for H-Pylori

Proton pump inhibitors (protonix), H2 Blockers

(pepcid)

Bismuth (Maalox, pepto bismol)

Avoid symptom triggers

Alcohol

High fat

Tobacco

Spicy food

26

Infectious Enterocolitis

Acute infection causing inflammation of the

intestinal linings resulting in vomiting, diarrhea,

and fever.

Etiology

Infection is by fecal-oral route.

Risk Factors

Improper hand washing and food preparation

Day care center attendance (children)

Recent use of antibiotics

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Infectious Agents

Rotavirus

Clostridium difficile (C-diff)

pseudomembraneous colitis→ toxic

megacolon!

Staphylococcus aureus

Escherichia coli (E-coli)

Shigella

Salmonella

Campylobacter

Giardia lamblia

28

Symptoms

Diarrhea and abdominal pain

Treatment

Supportive for 48 hours

Avoid anti-diarrheal agent

Rehydrate! – especially in pediatric and geriatric population

Stool for WBC, stool cultures, stool for ova, cysts, and parasites

Monitor hydration with BUN, urine specific gravity, electrolytes.

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INFLAMMATORY BOWEL

DISEASE (IBD)

Idiopathic chronic disorders of the GI

tract distinguished by the recurrent

inflammatory involvement of intestinal

segments.

Two main types

Crohn’s disease

Ulcerative colitis (UC)

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Incidence

Peak age of onset 20-30’s (Crohn’s), and

30’s(UC)

Family history

Genetic predisposition – triggered by dietary

antigen or microbial agent

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Crohn’s Disease

Definition Granulomatous inflammatory lesions of the GI tract.

Location Mouth to anus. Mostly small intestine & proximal colon.

Pattern “cobblestone” inflammatory appearance of submucosal

layer Skip lesions if multiple

Manifestations Intermittent diarrhea, steatorrhea, colicky pain, weight loss,

F/E imbalances, nutritional deficiencies, malaise, low-grade fever.

Complications: anal & perianal fistulas, abscesses, intestinal obstruction

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Crohn’s Disease34

Diagnosis

H&P

Sigmoidoscopy & Colonoscopy with biopsy:

inflammation; biopsy often reveals

granulomatous inflammation

X-rays

CT scan

Sedimentation rate: elevated

CBC: possible anemia

Electrolytes: imbalances

35

TREATMENT

Gastroenterologist referral

Corticosteroids

Immunosuppressants

Antibiotics- Metronidazole (Flagyl)

Nutritious diet; residue free/bulk free to allow

bowel rest

36

Ulcerative Colitis37

Ulcerative Colitis

Definition Inflammatory condition confined to the mucosal layer of the

rectum and colon

Location Starts in rectum and spreads proximally through colon

Pattern Confluent inflammatory pattern (no “skip” lesions)

Lead to pinpoint mucosal hemorrhages; may develop into crypt abscesses; may become necrotic & ulcerate

Pseudopolyps of mucosal layer

Manifestations Bloody diarrhea, nocturnal diarrhea, mild abdominal

cramping

Complications: Colon cancer risk; toxic megacolon in severe fulminant type

38

Ulcerative Colitis

Diagnosis

H&P

Colonoscopy

Treatment

Diet modifications Fiber reduces diarrhea

Avoid caffeine, lactose, spicy, and gas-producing foods

Corticosteroids

Immunosuppressants

Surgery

39

DIVERTICULAR DISEASE

Diverticulum – saclike protrusions of the

mucous membrane that herniates outward

through muscular layer. (outpouches or

outpocketings)

Diverticula – plural for diverticulum

Diverticulosis – the presence of diverticula

Diverticulitis – diverticula become inflamed

and may perforate (undigested food, fecal

matter, and bacteria become trapped forming

fecalith)

40

Diverticular Disease41

DIVERTICULAR DISEASE

Increases dramatically with age

More common in North America, Australia, and

Europe

Affects men and women equally

Risk Factors

Low fiber diet

↓strength of colon musculature

↓physical activity

Poor bowel habits

42

ACUTE DIVERTICULITIS

LLQ ABDOMINAL PAIN (93-100%)

Tender palpable mass in LLQ

Fever

Mild to moderate leukocytosis

Nausea, vomiting, and anorexia

Constipation/Diarrhea

43

DIAGNOSIS

Diverticulosis

Usually no symptoms – picked up on routine

colonoscopy or plain X-ray

Vague abd discomfort, change in bowel habits,

bloating, flatulence

Flat and Upright abdominal films

CT scan**

Colonoscopy

Barium enema—not for acute diverticulitis!

44

TREATMENT

Increase dietary fiber

Bowel retraining/ regular defacation

Complications – Hospitalization

NPO

Nasogastric tube

TPN

Broad spectrum antibiotics

Surgery

45

APPENDICITIS46

APPENDICITIS

Inflammation of the vermiform appendix

Can lead to gangrene and perforation

Cause: Intraluminal obstruction w/ fecalith

Signs and Symptoms

Initially: vague epigastric or periumbilical pain

Nausea, vomiting, anorexia

Follow onset of pain

RLQ McBurney’s point rebound tenderness

75% have leukocytosis 10-18,000/mm3

Fever

Psoas sign/ Obturator test

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DIAGNOSIS/TREATMENT

Emergency Department

History & Physical

CT scan** (or U/S)

Appendectomy (surgical)

IV Antibiotics

Complications

Peritonitis

Abscess formation

Septicemia

49

Intestinal Obstruction

Mechanical vs. Paralytic Mechanical:

Hernias, adhesions, strictures, tumors, foreign bodies, intussusception, volvulus

Severe colicky pain Borborygmy

Paralytic: “adynamic” Neurogenic or muscular impairment of peristalsis Paralytic ileus Absent bowel signs

S/S: Abdominal distention, pain, constipation, vomiting, F&E

disturbances.

50

Intestinal Obstruction51

Diagnosis

Abdominal X-ray

CT

U/S

52

Treatment

Nasogastric tube → Sxn for bowel

decompression

Correct F&E imbalances

Surgery if complete bowel obstruction or

strangulation

53

COLORECTAL CANCER

Uncontrolled growth of malignant cells in the

large intestine

Risk Factors - >40, polyps, family history, DM,

Tobacco, diets rich in fats and red meats,

ethnicity

S/S – Change in bowel habits, occult blood,

bloating, anorexia, weight loss

Pain is a LATE sign!

Diagnosis – Colonoscopy, CEA

Treatment – Surgery, chemo, radiation

Screening recommendations

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COLORECTAL CANCER55

Peritonitis

Inflammatory response of the peritoneal

membrane

Causes:

Bacterial or chemical irritation

Perforated ulcers, diverticulum, appendix

Gangrenous bowel or gallbladder

56

Signs & Symptoms

Pain & tenderness

Rigid/board-like, distended, guarded abdomen

Shallow respirations

N/V

Fluid losses; Dehydration

Fever

↑WBC count

Tachycardia

Hypotension

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Peritonitis

http://youtu.be/RxMIq4PfML4

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Complications

Paralytic ileus

Hypovolemia

Sepsis

Shock

60

Treatment

Correction of underlying cause

Correction of F&E imbalances

Surgery if indicated

NPO

NGT for decompression

Antibiotics

Analgesics

61

VIRAL HEPATITIS

Viral infection affecting the liver

Five viral causative agents: A,B,C,D,E

Hepatitis B,C, and D can cause chronic infections

Risk Factors:

HAV & HEV

Transmitted via fecal-oral route

Travel to endemic areas

Ingestion of contaminated food, water, milk, or shellfish

IgM anti-HAV, IgG anti-HAV

Hep A vaccine available

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RISK FACTORS B&C

HBV, HCV –blood/body fluids

Shared needles

Multiple sexual partners

Tattoo recipients; body piercings

Health care workers

Can cause chronic hepatitis & cirrhosis

All adolescents are considered high-risk for HBV

Risk for hepatocellular CA w/ HCV

HBV vaccine available

63

SIGNS AND SYMPTOMS

Many are asymptomatic

Nausea, vomiting, anorexia, RUQ abdominal

pain, liver enlargement

Malaise, fever

Sclera become yellow (icteric)

Jaundice, dark urine, clay-colored stools

Elevated ALT, AST, bilirubin levels

64

DIAGNOSIS

Liver function tests

ALT, AST – hepatic injury

ALT – Think Hepatitis B

AST – Alcohol, Statins, Tylenol

PT/albumin – measure synthetic activity of

liver

Bilirubin – measure of excretory function of

liver

65

HEPATITIS B Serologies

HBsAg- detected in acute or chronic HepB-

infectious

Anti-HBs or HBsAb- indicates recovery,

immunity

HBeAg

Anti-HBe

HBcAg

Anti-HBc – previous or ongoing infection

IgM Anti-HBc – acute infection

IgG Anti-HBc

66

TREATMENT

Vaccination

Administer HBIG

Avoid medications metabolized by the liver

Abstinence from alcohol

Bleeding precautions

Treat partners

Treated by Gastroenterologist/ Hepatologist

67

CIRRHOSIS

End stage chronic liver disease

Irreversible inflammatory disease

Disrupts liver structure and function

Inflammation causes structural fibrotic

changes

Disruption of blood flow…portal HTN

Obstruction of biliary system…jaundice

68

Signs & Symptoms

Most common

Weight loss (masked by ascites)

Weakness

Anorexia

Ascites

Diarrhea

Jaundice

Abdominal pain (epigastric or RUQ)

If portal HTN & liver failure: esophageal varices, bleeding, encephalopathy, splenomegaly.

69

The Fate of

Bilirubin Hemoglobin from old red blood

cells becomes bilirubin

The liver converts bilirubin into conjugated bilirubin

Bilirubin passes on to the

intestine

Bacteria convert it to

urobilinogen

º Some is lost in feces

º Most is reabsorbed into

the blood via portal

circulation

Returned to the liver to be

reused

unconjugated

bilirubin in

blood

bilirubinemia

jaundice

liver links it

to

gluconuride

conjugated

bilirubin

bile

70

The Fate of Bilirubin…

Why would a man with liver failure

develop jaundice?

71

Liver Failure Leads To …

Hematologic disorders

Anemia, thrombocytopenia (low platelet),

coagulation defects, leukopenia (WBC)

Metabolic disorders

Fluid retention, hypokalemia, disordered

sexual functions

Which hormones would cause these

endocrine disorders?

72

Liver Failure Leads To …(cont.)

Skin disorders

Jaundice, red palms, spider nevi

Hepatorenal syndrome

Azotemia, increased plasma creatinine,

oliguria

Hepatic encephalopathy

Asterixis, confusion, coma, convulsions

Ammonia not converted to urea

73

Veins Draining into the Hepatic

Portal System

Portal hypertension causes pressure in these veins to increase

Varicosities and shunts develop

Organs engorge with blood

74

Portal Hypertension75

Biliary Tract

Hepatic

duct

Pancreatic

duct

Gall bladder

Cystic duct

Common bile

duct

Ampulla of Vater

Sphincter of Oddi

76

Disorders of the Gallbladder

Cholelithiasis (gallstones) Cholesterol, calcium salts, or mixed

Acute and chronic cholecystitis Inflammation caused by chemical

irritation due to concentrated bile. Can result in ischemia from mucosal swelling

Choledocholithiasis Stones in the common bile duct

Cholangitis Inflammation of the common bile duct

77

Cholestasis and Intrahepatic

Biliary Disorders78

Gall Stones79

Cholecystitis

Gall bladder disease

Acute – Complete or partial obstruction of the

cystic or common bile ducts.

Inflammation caused by chemical irritation

from the concentrated bile, mucosal swelling

and ischemia.

Bacterial infection

Mucosal necrosis gangrene perforation

Risk Factors

The Five F’s

80

SIGNS AND SYMPTOMS

RUQ pain that radiates to the tip of the right

scapula

Murphy’s sign

Excessive belching

Flatus

Nausea and vomiting

Low-grade fever

Elevated WBC count

Worsening symptoms after ingesting fried

foods.

81

DIAGNOSIS/ TREATMENT

Ultrasound

Gallbladder scan

Treatment

Bowel rest, intravenous hydration, analgesia, and

intravenous antibiotics. For mild cases of acute

cholecystitis, antibiotic therapy with a single

broad-spectrum antibiotic is adequate

Laparoscopic cholecystectomy (“Lap Chole”)

82

The

Pancreas

Pancreas

Exocrine

pancreas

releases digestive

juices through a

duct

to the

duodenum

Endocrine

pancreas

releases hormones

into the blood

83

Exocrine Pancreas

Acini produce: Inactive digestive

enzymes

Trypsin inactivator

These are sent to the duodenum

In the duodenum, the digestive enzymes are activated

84

Biliary Reflux

5. Bile in

pancreas

disrupts

tissues;

digestive

enzymes

activated

4. Bile

goes up

pancreatic

duct

1. Gallbladder

contracts

2. Bile is sent

down common

bile duct

3. Blockage forms

in ampulla of Vater:

bile cannot enter

duodenum

85

Pancreatitis86

ACUTE PANCREATITIS

Rapidly developing, potentially fatal,

inflammatory disease of the pancreas

Escape of pancreatic enzymes cause

autodigestion of the pancreas and fat necrosis

Causes:

Gall stones/Alcohol/GI surgery

87

Autodigestion of the Pancreas

Activated enzymes begin to digest the

pancreas cells

Severe pain results

Inflammation produces large volumes of serous

exudate hypovolemia

Elevated enzymes (amylase, lipase) appear in

the blood

Areas of dead cells undergo fat necrosis

Calcium from the blood deposits in them

º Hypocalcemia

88

Acute Pancreatitis

Signs & Symptoms

Severe abrupt abdominal pain that may radiate to the back.

Pain worse in supine position

N/V

Hyperglycemia

Hypotension & tachycardia

Fever

Elevated pancreatic enzymes – Amylase, Lipase,

Tx – aggressive hydration, antibiotics, NPO, NGT, pain management, surgery

89

Chronic Pancreatitis and Pancreatic

Cancer

Have signs and symptoms similar to acute

pancreatitis

MOST common cause: ETOH

Permanent destruction of exocrine function and

later stages also endocrine fxn destruction

Often have:

Digestive problems because of inability to deliver

enzymes to the duodenum

Glucose control problems because of damage to islets

of Langerhans

Signs of biliary obstruction because of underlying bile

tract disorders or duct compression by tumors

90

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