lecture for pathophysiology

1. THE
GASTROINTESTI
NAL AND
HEPATOBILIARY
SYSTEMS
Barry University NUR 313

2. 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

3. 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

4. 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

5. 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

6. 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. 7

8. Structure and Function: Middle
and Lower GI Tract
8

9. 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

10. 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

11. 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

12. 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

13.  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

14. GERD
14

15. Risk Factors
Factors which reduce LES tone
Aging
Obesity
Pregnancy
High fat meals
15

16. 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

17. Diagnosis
 History and physical alone if symptoms
are typical
 Endoscopy and biopsy if symptoms are
atypical
 Complications
Barrett’s esophagus
Strictures
17

18. 18
Barrett’s Esophagus/Strictures

19. 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

20. 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

21. Gastric Ulcer
21

22. Duodenal Ulcer
22

23. Risk Factors
 Helicobacter pylori (H-Pylori) infection
90-95% of patients with duodenal
ulcers
60-70% of patients with gastric
ulcers
 NSAIDs
aspirin
23

24. 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
24

25. Complications
 Bleeding
 Hematemesis
 Coffee ground emesis
 Hematochezia
 Melena
 Occult bleeding
 Gastric Outlet Obstruction
 Caused by edema, spasm, scar tissue
 Perforation
 Peritonitis
25

26. 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

27. 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
27

28. Infectious Agents
 Rotavirus
 Clostridium difficile (C-diff)
pseudomembraneous colitis→ toxic
megacolon!
 Staphylococcus aureus
 Escherichia coli (E-coli)
 Shigella
 Salmonella
 Campylobacter
 Giardia lamblia
28

29. 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.
29

30. 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)
30

31. 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
31

32. 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
32

33. 33

34. Crohn’s Disease
34

35. 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

36. TREATMENT
 Gastroenterologist referral
 Corticosteroids
 Immunosuppressants
 Antibiotics- Metronidazole (Flagyl)
 Nutritious diet; residue free/bulk free to allow
bowel rest
36

37. Ulcerative Colitis
37

38. 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

39. Ulcerative Colitis
 Diagnosis
 H&P
 Colonoscopy
 Treatment
 Diet modifications
 Fiber reduces diarrhea
 Avoid caffeine, lactose, spicy, and gas-producing
foods
 Corticosteroids
 Immunosuppressants
 Surgery
39

40. 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

41. Diverticular Disease
41

42. 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

43. ACUTE DIVERTICULITIS
 LLQ ABDOMINAL PAIN (93-100%)
 Tender palpable mass in LLQ
 Fever
 Mild to moderate leukocytosis
 Nausea, vomiting, and anorexia
 Constipation/Diarrhea
43

44. 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

45. TREATMENT
 Increase dietary fiber
 Bowel retraining/ regular defacation
 Complications – Hospitalization
 NPO
 Nasogastric tube
 TPN
 Broad spectrum antibiotics
 Surgery
45

46. APPENDICITIS
46

47. 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
47

48. 48

49. DIAGNOSIS/TREATMENT
 Emergency Department
 History & Physical
 CT scan** (or U/S)
 Appendectomy (surgical)
 IV Antibiotics
 Complications
 Peritonitis
 Abscess formation
 Septicemia
49

50. 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

51. Intestinal Obstruction
51

52. Diagnosis
 Abdominal X-ray
 CT
 U/S
52

53. Treatment
 Nasogastric tube → Sxn for bowel
decompression
 Correct F&E imbalances
 Surgery if complete bowel obstruction or
strangulation
53

54. 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
54

55. COLORECTAL CANCER
55

56. Peritonitis
 Inflammatory response of the peritoneal
membrane
 Causes:
 Bacterial or chemical irritation
 Perforated ulcers, diverticulum, appendix
 Gangrenous bowel or gallbladder
56

57. Signs & Symptoms
 Pain & tenderness
 Rigid/board-like, distended, guarded abdomen
 Shallow respirations
 N/V
 Fluid losses; Dehydration
 Fever
 ↑WBC count
 Tachycardia
 Hypotension
57

58. 58

59. Peritonitis
 http://youtu.be/RxMIq4PfML4
59

60. Complications
 Paralytic ileus
 Hypovolemia
 Sepsis
 Shock
60

61. Treatment
 Correction of underlying cause
 Correction of F&E imbalances
 Surgery if indicated
 NPO
 NGT for decompression
 Antibiotics
 Analgesics
61

62. 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
62

63. 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

64. 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

65. 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

66. 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

67. TREATMENT
 Vaccination
 Administer HBIG
 Avoid medications metabolized by the liver
 Abstinence from alcohol
 Bleeding precautions
 Treat partners
 Treated by Gastroenterologist/ Hepatologist
67

68. 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

69. 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

70. 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

71. The Fate of Bilirubin…
Why would a man with liver failure
develop jaundice?
71

72. 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

73. 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

74. 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

75. Portal Hypertension
75

76. Biliary Tract
Hepatic
duct
Pancreatic
duct
Gall bladder
Cystic duct
Common bile
duct
Ampulla of Vater
Sphincter of Oddi
76

77. 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

78. Cholestasis and Intrahepatic
Biliary Disorders
78

79. Gall Stones
79

80. 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

81. 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

82. 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

83. The
Pancreas
Pancreas
Exocrine
pancreas
releases digestive
juices through a
duct
to the
duodenum
Endocrine
pancreas
releases hormones
into the blood
83

84. Exocrine Pancreas
 Acini produce:
 Inactive digestive
enzymes
 Trypsin inactivator
 These are sent to the
duodenum
 In the duodenum, the
digestive enzymes are
activated
84

85. 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
85
3. Blockage forms
in ampulla of Vater:
bile cannot enter
duodenum

86. Pancreatitis
86

87. 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

88. 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

89. 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

90. 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

91. 91