3. June 26, 2012 Total slide. 126 3
Clinical Biochemistry Gastrointestinal Disease
Gastrointestinal disease
Peptic ulcer disease
Chronic duodenal ulcer
Chronic benign gastric ulcer
Zollinger-Ellison syndrome
Gastritis
Gastric cancer
Post gastrectomy syndrome
Acute pancreatitis
Chronic pancreatitis
Insulinoma
Glucagonoma
Somatostatinoma
4. June 26, 2012 Total slide. 126 4
Clinical Biochemistry Gastrointestinal Disease
5. June 26, 2012 Total slide. 126 5
Clinical Biochemistry Gastrointestinal Disease
Peptic Ulcer Disease (PUD)
What is it?
Group of chronic disorders characterized by ulcerating
mucosal lesions in upper GI tract
chronic inflammatory condition
common forms are duodenal and gastric ulceration
Where does it occur?
Stomach, duodenum
What causes PUD?
H. pylori or drug induced (most commonly by chronic NSAID
use)
6. June 26, 2012 Total slide. 126 6
Clinical Biochemistry Gastrointestinal Disease
Drugs that can cause PUD
methotrexate
cyclophosphamide
azathioprine
erythromycin
iron
corticosteriods
potassium chloride
NSAIDS
7. June 26, 2012 Total slide. 126 7
Clinical Biochemistry Gastrointestinal Disease
Signs and Symptoms of PUD
Can be symptomatic
anorexia, nausea, vomiting, belching, bloating, heartburn,
epigastric pain (pain in the upper abdomen)
awakened at night (usu. around 3am,)
duodenal ulcers
epigastric pain, tenderness, burning, aching between xiphoid
process and belly button
relieved with food intake or antacids
gastric ulcer
diffuse pain over midepigastrium (midstomach)
worsened by food
8. June 26, 2012 Total slide. 126 8
Clinical Biochemistry Gastrointestinal Disease
Characteristics and Comparisons
Between Gastric and Duodenal Ulcers
Gastric ulcer formation involves inflammatory
involvement of acid-producing cells but usually occurs
with low acid secretion.
Duodenal ulcers are associated with high acid and low
bicarbonate secretion.
Increased mortality and hemorrhage are associated with
gastric ulcers.
10. June 26, 2012 Total slide. 126 10
Clinical Biochemistry Gastrointestinal Disease
Normal Stomach
11. June 26, 2012 Total slide. 126 11
Clinical Biochemistry Gastrointestinal Disease
Esophagus & Stomach Normal
12. June 26, 2012 Total slide. 126 12
Clinical Biochemistry Gastrointestinal Disease
Definition:
Ulceration (breach in mucosa) due to acid & pepsin
attack – peptic ulcer.
Deeper than just mucosa
Single, punched out, clean base
14. June 26, 2012 Total slide. 126 14
Clinical Biochemistry Gastrointestinal Disease
H. Pylori organisms- silver st.
15. June 26, 2012 Total slide. 126 15
Clinical Biochemistry Gastrointestinal Disease
Pathogenesis:
Helicobacter pylori infection
Colonization of gastric mucous
Urease ammonia neutralization of acid Rebound
acid production.
Protease – Mucous break down.
Weak mucosal resistance
Acid & Pepsin digestion of mucosa
Chronic Ulceration
16. June 26, 2012 Total slide. 126 16
Clinical Biochemistry Gastrointestinal Disease
Normal
Increased Attack
Hyperacidity
Weak defense
Helicobacter pylori
Stress, drugs, smoking
Etiology of PUD
17. June 26, 2012 Total slide. 126 17
Clinical Biochemistry Gastrointestinal Disease
Helicobacter pylori:
Most common infection in the world (20%)
10% of men, 4% women develop PUD
Positive in 70-100% of PUD patients.
H.pylori related disorders:
Chronic gastritis – 90%
Peptic ulcer disease – 95-100%
Gastric carcinoma – 70%
Gastric lymphoma
Reflux Oesophagitis.
Non ulcer dyspepsia
18. June 26, 2012 Total slide. 126 18
Clinical Biochemistry Gastrointestinal Disease
Peptic Ulcer Morphology:
90% ulcers in first portion of duodenum or
lesser curvature of stomach
80 to 90% cases single ulcer. Round Small
ulcers with sharply punched out edges
Small <2cm, clean base.
Microscopy: 4 zones.
Superficial necrotic layer.
Inflammatory cells zone.
Granulation tissue zone
Collagenous scar layer.
19. June 26, 2012 Total slide. 126 19
Clinical Biochemistry Gastrointestinal Disease
20. June 26, 2012 Total slide. 126 20
Clinical Biochemistry Gastrointestinal Disease
21. June 26, 2012 Total slide. 126 21
Clinical Biochemistry Gastrointestinal Disease
Gastric peptic ulcer
22. June 26, 2012 Total slide. 126 22
Clinical Biochemistry Gastrointestinal Disease
Gastric peptic ulcer:
23. June 26, 2012 Total slide. 126 23
Clinical Biochemistry Gastrointestinal Disease
Gastric Ulcer
Gastric ulcer:
24. June 26, 2012 Total slide. 126 24
Clinical Biochemistry Gastrointestinal Disease
Duodenal Peptic Ulcer
25. June 26, 2012 Total slide. 126 25
Clinical Biochemistry Gastrointestinal Disease
Peptic ulcer - Endoscopy
26. June 26, 2012 Total slide. 126 26
Clinical Biochemistry Gastrointestinal Disease
Gastric Ulcer
27. June 26, 2012 Total slide. 126 27
Clinical Biochemistry Gastrointestinal Disease
Gastric Ulcer
28. June 26, 2012 Total slide. 126 28
Clinical Biochemistry Gastrointestinal Disease
Gastric Ulcer
Punched out ulcer
Clean base
Small single
Radiating mucosal folds.
Benign ulcer.
No tumor.
29. June 26, 2012 Total slide. 126 29
Clinical Biochemistry Gastrointestinal Disease
Peptic Ulcer
30. June 26, 2012 Total slide. 126 30
Clinical Biochemistry Gastrointestinal Disease
Peptic Ulcer Microscopy:
32. June 26, 2012 Total slide. 126 32
Clinical Biochemistry Gastrointestinal Disease
CDU Camplications
Hemorrhage
Due to the ulcer’s eroding a blood vessel
Perforation
Through the anterior wall of the duodenal cap
Causing peritonitis
Penetration of the ulcer into the adjacent structures
Such as pancrease , biliary tract , liver, colon, abdominal wall, or
even long
Luminal abstruction
Caused by the gradual contraction of the ulser scar
33. June 26, 2012 Total slide. 126 33
Clinical Biochemistry Gastrointestinal Disease
Gastric Ulcer
34. June 26, 2012 Total slide. 126 34
Clinical Biochemistry Gastrointestinal Disease
Points to Remember:
A peptic ulcer is a sore in the lining of the
stomach or duodenum due to attack by acid &
Pepsin.
The major cause - H. pylori bacterium. Others
are NSAIDs. spicy food, stress are risk factors.
H. pylori can be transmitted from person to
person through close contact
A combination of antibiotics and H pump
inhibitors is the most effective treatment.
35. June 26, 2012 Total slide. 126 35
Clinical Biochemistry Gastrointestinal Disease
Helecobacter pylori
36. June 26, 2012 Total slide. 126 36
Clinical Biochemistry Gastrointestinal Disease
Toludine Blue stain – H pylori
37. June 26, 2012 Total slide. 126 37
Clinical Biochemistry Gastrointestinal Disease
Urease production test
40. June 26, 2012 Total slide. 126 40
Clinical Biochemistry Gastrointestinal Disease
41. June 26, 2012 Total slide. 126 41
Clinical Biochemistry Gastrointestinal Disease
Zollinger-Ellison syndrome
Increased numbers of
Increased numbers of
parietal cells with no
parietal cells with no
change in surface and
change in surface and
foveolar mucous cells.
foveolar mucous cells.
42. June 26, 2012 Total slide. 126 42
Clinical Biochemistry Gastrointestinal Disease
Zollinger Ellison Syndrome
Tumour Location
Symptoms
Pancreas 50-60%
Duodenum 40-50%
20-25% Related to MEN-1
50-70% Malignant (lymphnode
metastases)
Gastrinoma Triangle 80%
Gastritis
Recurrent ulcers
Diarrhea (malabsorption)
43. June 26, 2012 Total slide. 126 43
Clinical Biochemistry Gastrointestinal Disease
Zollinger-Ellison syndrome
0.1 to 1 percent of patients with peptic ulcer disease .
Underestimation!
symptoms similar to typical peptic ulcer .
symptoms may be controlled by standard doses of an
antisecretory drug
patients may not be tested for hypergastrinemia
Gastrinomas can be either sporadic (80 percent) or
associated with multiple endocrine neoplasia type 1
44. June 26, 2012 Total slide. 126 44
Clinical Biochemistry Gastrointestinal Disease
Signs of ZES
Multiple ulcers
Diarrhea
ulcer in atypical site
resistant ulcer
enlarged folds
severe esophagirtis
45. June 26, 2012 Total slide. 126 45
Clinical Biochemistry Gastrointestinal Disease
Diarrhea in ZES
The high rate of acid volume load that cannot be
absorbed by the intestine
The excess acid exceeds the neutralizing capacity of
pancreatic bicarbonate . The exceptionally low pH of the
intestinal contents inactivates pancreatic digestive
enzymes, interferes with the emulsification of fat by bile
acids, and damages intestinal epithelial cells and villi.
The extremely high serum gastrin concentrations may
inhibit absorption of sodium and water by the small
intestine,
46. June 26, 2012 Total slide. 126 46
Clinical Biochemistry Gastrointestinal Disease
ZES diagnosis
Exclude hyperacidity!
>100mM/L in 12 hour overnight
secretion of HCl
Check gastrin,
if >1000=ZES.
<1000 but abnormal secretin
test to be performed
+200 pg/ml is ZES
Secretin chalenge test
47. June 26, 2012 Total slide. 126 47
Clinical Biochemistry Gastrointestinal Disease
ZES treatment
any patient with a sporadic gastrinoma and
without evidence of metastatic spread of disease
should be offered exploratory laparotomy with
curative intent
laparotomy is not routinely recommended for
patients with ZES as part of MEN 1 since the
multifocal nature of the tumors in this disorder
almost uniformly precludes cure of gastrin
hypersecretion
48. June 26, 2012 Total slide. 126 48
Clinical Biochemistry Gastrointestinal Disease
49. June 26, 2012 Total slide. 126 49
Clinical Biochemistry Gastrointestinal Disease
Definition
The term gastritis is used to denote
inflammation associated with mucosal injury
Gastritis is mostly a histological term that needs
biopsy to be confirmed
Gastritis is usually due to infectious agents
(such as Helicobacter pylori) and autoimmune
and hypersensitivity reactions.
50. June 26, 2012 Total slide. 126 50
Clinical Biochemistry Gastrointestinal Disease
Definition
Epithelial cell damage and regeneration without
associated inflammation is properly referred to
as “gastropathy”.
Gastropathy may be referred without histological
evidence and just according to gross
appearance in endoscopy or radiology
Gastropathy is usually caused by irritants such
as drugs (eg, nonsteroidal antiinflammatory
agents and alcohol), bile reflux, hypovolemia,
and chronic congestion.
51. June 26, 2012 Total slide. 126 51
Clinical Biochemistry Gastrointestinal Disease
Acute Esophagitis & Gastritis
52. June 26, 2012 Total slide. 126 52
Clinical Biochemistry Gastrointestinal Disease
Gross–histologic correlation?
53. June 26, 2012 Total slide. 126 53
Clinical Biochemistry Gastrointestinal Disease
CLASSIFICATION
GASTRITIS
ACUTE COMMON CHRONIC
EMAG
AMAG
BILE HP
STRESS
NSAID
54. June 26, 2012 Total slide. 126 54
Clinical Biochemistry Gastrointestinal Disease
CLASSIFICATION
Acute vs. chronic
Acute refers to short term inflammation
Acute refering to neurophilic infiltrate
Chronic referring to long standing forms
Chronic referring to mononuclear cell infiltrate
especially lymphocyte and maccrophages
56. June 26, 2012 Total slide. 126 56
Clinical Biochemistry Gastrointestinal Disease
Acute hemorrhagic erosive
hemorrhagic and erosive lesions shortly after
exposure of the gastric mucosa to various
injurious substances or a substantial reduction in
mucosal blood flow
57. June 26, 2012 Total slide. 126 57
Clinical Biochemistry Gastrointestinal Disease
Acute hemorrhagic erosive
nonsteroidal antiinflammatory drugs [NSAIDs],
alcohol, or bile acids) or to mucosal hypoxia
(such as in trauma, burns [Curling's ulcers] or
sepsis) or to a combination of factors such as
with antineoplastic chemotherapy
58. June 26, 2012 Total slide. 126 58
Clinical Biochemistry Gastrointestinal Disease
Acute hemorrhagic erosive
Gastric and duodenal ulceroinflammatory ulcers
occurring during severe damage to the central
nervous system (Cushing's ulcers) are often
considered in this group
59. June 26, 2012 Total slide. 126 59
Clinical Biochemistry Gastrointestinal Disease
Acute hemorrhagic erosive
specific pathogenetic factor in NSAID-induced
acute hemorrhagic and erosive gastropathy is
the inhibition of prostaglandin production.
Prostaglandins, especially those of the E class,
protect against acute mucosal injury due to
NSAIDs and other injurious substances by
several mechanisms, including the stimulation of
mucus and bicarbonate secretion, and
maintenance of mucosal blood flow
60. June 26, 2012 Total slide. 126 60
Clinical Biochemistry Gastrointestinal Disease
Acute hemorrhagic erosive
Hemorrhagic or erosive gastropathy may be
associated with the development of gastric or
duodenal ulcers. Acute ulceration is most likely
to occur in relation to shock-induced
hemodynamic instability (ie, the stress ulcer
syndrome).
61. June 26, 2012 Total slide. 126 61
Clinical Biochemistry Gastrointestinal Disease
Risk factors
Prior history of an adverse GI event (ulcer,
hemorrhage) increases risk four to fivefold
Age >60 increases risk five to sixfold
High (more than twice normal) dosage of a
NSAID increases risk 10-fold
Concurrent use of glucocorticoids increases risk
four to fivefold
Concurrent use of anticoagulants increases risk
10- to 15-fold
62. June 26, 2012 Total slide. 126 62
Clinical Biochemistry Gastrointestinal Disease
HP and NSAID
Patients with a history of uncomplicated or
complicated peptic ulcers (gastric, duodenal)
should be tested for H. pylori prior to beginning a
NSAID or low dose aspirin. If present, H. pylori
should be treated with appropriate therapy, even
if it is believed that the prior ulcer was due to
NSAIDs
63. June 26, 2012 Total slide. 126 63
Clinical Biochemistry Gastrointestinal Disease
Helicobacter pylori
Helicobacter pylori is a
spiral shaped, gram
negative bacterium
measuring
approximately 3.5
microns in length and
0.5 microns in width
64. June 26, 2012 Total slide. 126 64
Clinical Biochemistry Gastrointestinal Disease
Helicobacter pylori
Urease appears to be
vital for its survival
and colonization; it is
produced in
abundance, making
up more than 5
percent of the
organism's total
protein weight.
65. June 26, 2012 Total slide. 126 65
Clinical Biochemistry Gastrointestinal Disease
Helicobacter pylori
urease forms
ammonia and
bicarbonate that
neutralize gastric acid
and form a protective
cloud around the
organism
66. June 26, 2012 Total slide. 126 66
Clinical Biochemistry Gastrointestinal Disease
Helicobacter pylori
spiral shape, flagella
facilitate its passage
through the mucus
layer
67. June 26, 2012 Total slide. 126 67
Clinical Biochemistry Gastrointestinal Disease
Helicobacter pylori
H. pylori then
attaches to gastric
epithelial cells by
means of specific
receptor-mediated
adhesion
68. June 26, 2012 Total slide. 126 68
Clinical Biochemistry Gastrointestinal Disease
Chemical gastritis (acute ・ chronic)
Alcoholic gastritis
Drug induced gastritis (e.g., NSAID)
Reflux ( due to duodenal juice or bile) gastritis
Other chemical gastritis
Radiation gastritis
Allergic gastritis
Autoimmune gastritis
Special forms of gastritis
Non HP gastritis
69. June 26, 2012 Total slide. 126 69
Clinical Biochemistry Gastrointestinal Disease
Stress ulcer pathophysiology
Hypersecretion of acid –head trauma.
Defects in gastric glycoprotein mucus –In
critically ill patients, increased concentrations of
refluxed bile salts or the presence of uremic
toxins can denude the glycoprotein mucous
barrier
Ischemia – Shock, sepsis, and trauma can lead
to impaired perfusion of the gut.
70. June 26, 2012 Total slide. 126 70
Clinical Biochemistry Gastrointestinal Disease
Stress ulcer risk factors
Shock
Sepsis
Hepatic failure
Renal failure
Multiple trauma
Burns over 35 percent of total body surface area
Organ transplant recipients
Head or spinal trauma
Prior history of peptic ulcer disease or upper GI
bleeding
71. June 26, 2012 Total slide. 126 71
Clinical Biochemistry Gastrointestinal Disease
73. June 26, 2012 Total slide. 126 73
Clinical Biochemistry Gastrointestinal Disease
WHO Classification
5 main categories
Adenocarcinoma, Adenosquamous cell carcinoma,
squamous cell carcinoma, undifferentiated carcinoma
and unclassified carcinoma
Adenocarcinoma – subdivided
Papillary, tubular, mucinous, signet ring
Further subdivided based on differentiation
74. June 26, 2012 Total slide. 126 74
Clinical Biochemistry Gastrointestinal Disease
Cancer of Stomach
1. Incidence
a. Worldwide common cancer, but less common in US
b. Incidence highest among Hispanics, African Americans,
Asian Americans, males twice as often as females
c. Older adults of lower socioeconomic groups higher risk
2. Pathophysiology
a. Adenocarcinoma most common form involving mucus-
producing cells of stomach in distal portion
b. Begins as localized lesion (in situ) progresses to
mucosa; spreads to lymph nodes and metastasizes early in
disease to liver, lungs, ovaries, peritoneum
75. June 26, 2012 Total slide. 126 75
Clinical Biochemistry Gastrointestinal Disease
Cancer of Stomach
3. Risk Factors
a. H. pylori infection
b. Genetic predisposition
c. Chronic gastritis, pernicious anemia, gastric polyps
d. Achlorhydria (lack of hydrochloric acid)
e. Diet high in smoked foods and nitrates
4. Manifestations
a. Disease often advanced with metastasis when diagnosed
b. Early symptoms are vague: early satiety, anorexia,
indigestion, vomiting, pain after meals not responding to
antacids
c. Later symptoms weight loss, cachexia (wasted away
appearance), abdominal mass, stool positive for occult blood
76. June 26, 2012 Total slide. 126 76
Clinical Biochemistry Gastrointestinal Disease
Cancer of Stomach
5. Collaborative Care
a. Support client through testing
b. Assist client to maintain adequate nutrition
6. Diagnostic Tests
a.CBC indicates anemia
b.Upper GI series, ultrasound identifies a mass
c.Upper endoscopy: visualization and tissue
biopsy of lesion
77. June 26, 2012 Total slide. 126 77
Clinical Biochemistry Gastrointestinal Disease
Cancer of Stomach
7. Treatment
a. Surgery, if diagnosis made prior to metastasis
1.Partial gastrectomy with anastomosis to
duodenum: Bilroth I or gastroduodenostomy
2.Partial gastrectomy with anastomosis to
jejunum: Bilroth II or gastrojejunostomy
3.Total gastrectomy (if cancer diffuse but limited
to stomach) with esophagojejunostomy
78. June 26, 2012 Total slide. 126 78
Clinical Biochemistry Gastrointestinal Disease
Fungating Carconoma
80. June 26, 2012 Total slide. 126 80
Clinical Biochemistry Gastrointestinal Disease
81. June 26, 2012 Total slide. 126 81
Clinical Biochemistry Gastrointestinal Disease
Post gastrectomy syndrome
b. Complications associated with gastric surgery
1. Dumping Syndrome
a.Occurs with partial gastrectomy; hypertonic, undigested
chyme bolus rapidly enters small intestine and pulls fluid into
intestine causing decrease in circulating blood volume and
increased intestinal peristalsis and motility
b.Manifestations 5 – 30 minutes after meal: nausea with
possible vomiting, epigastric pain and cramping, and diarrhea;
client becomes tachycardic, hypotensive, dizzy, flushed,
diaphoretic
c.Manifestations 2 – 3 hours after meal: symptoms of
hypoglycemia in response to excessive release of insulin that
occurred from rise in blood glucose when chyme entered
intestine
82. June 26, 2012 Total slide. 126 82
Clinical Biochemistry Gastrointestinal Disease
Post gastrectomy syndrome
Treatment: dietary pattern to delay gastric emptying
and allow smaller amounts of chyme to enter
intestine
Liquids and solids taken separately
Increased amounts of fat and protein
Carbohydrates, especially simple sugars, reduced
Client to rest recumbent or semi-recumbent 30 – 60
minutes after eating
Anticholinergics, sedatives, antispasmodic
medications may be added
Limit amount of food taken at one time
83. June 26, 2012 Total slide. 126 83
Clinical Biochemistry Gastrointestinal Disease
Post gastrectomy syndrome
Common post-op complications
Pneumonia
Anastomotic leak
Hemorrhage
Relux aspiration
Sepsis
Reflux gastritis
Paralytic ileus
Bowel obstruction
Wound infection
Dumping syndrome
84. June 26, 2012 Total slide. 126 84
Clinical Biochemistry Gastrointestinal Disease
Post gastrectomy syndrome
Nutritional problems related to rapid entry of food into the
bowel and the shortage of intrinsic factor
Anemia: iron deficiency and/or pernicious
Folic acid deficiency
Poor absorption of calcium, vitamin D
Radiation and/or chemotherapy to control metastasic spread
Palliative treatment including surgery, chemotherapy; client
may have gastrostomy or jejunostomy tube inserted
85. June 26, 2012 Total slide. 126 85
Clinical Biochemistry Gastrointestinal Disease
86. June 26, 2012 Total slide. 126 86
Clinical Biochemistry Gastrointestinal Disease
Pancreas
87. June 26, 2012 Total slide. 126 87
Clinical Biochemistry Gastrointestinal Disease
Function
Exocrine
precursor digestive enzymes
lipases
Endocrine
metabolic hormones
Insulin from β cells
Glucagon from α cells
88. June 26, 2012 Total slide. 126 88
Clinical Biochemistry Gastrointestinal Disease
Exocrine Pancreas
The final product of the exocrine pancreas is a
clear isotonic solution with a pH in the range of
8. The 2 distinct components of exocrine
secretion are enzyme secretion and
water+electrolyte secretion.
Cholecystokinin is the most potent endogenous
hormone known to stimulate enzyme secretion.
Secretin is the most potent endogenous
stimulant of pancreatic electrolyte secretion.
89. June 26, 2012 Total slide. 126 89
Clinical Biochemistry Gastrointestinal Disease
Endocrine Pancreas
The release of insulin into the portal blood is controlled
by the concentration of blood glucose, vagal
interactions, and local concentrations of somatostatin.
The major stimulus for glucagon release is a fall in
serum glucose.
Pancreatic polypeptide appears to function for
regulation of pancreatic exocrine secretion and biliary
tract motility.
Somatostatin has a broad inhibitory spectrum of
gastrointestinal activity
90. June 26, 2012 Total slide. 126 90
Clinical Biochemistry Gastrointestinal Disease
Factors Leading to Pancreatitis
Alcohol intake – usually 5
to 10 years
Prior biliary disease
Abdominal surgery or
diagnostics
Trauma
Recent viral infections
Medications
Mostly middle aged men
91. June 26, 2012 Total slide. 126 91
Clinical Biochemistry Gastrointestinal Disease
Pathophysiology
Inflammation from an insult or injury
Causes activation of pancreatic enzymes
Enzymes autodigest and cause fibrosis
Leads to thrombi and necrosis of tissue
Fat necrosis occurs
Fats bind to calcium
Results in hypocalcemia
92. June 26, 2012 Total slide. 126 92
Clinical Biochemistry Gastrointestinal Disease
More Patho
Necrosis of blood vessels
Fibers in blood vessels and ducts are dissolved
Vasodilation starts due to vessel damage
Results in bleeding and hemorrhage
May be acute or chronic
May be mild to necrotizing
93. June 26, 2012 Total slide. 126 93
Clinical Biochemistry Gastrointestinal Disease
94. June 26, 2012 Total slide. 126 94
Clinical Biochemistry Gastrointestinal Disease
Acute Pancreatitis
Nonbacterial inflammatory disease caused by
activation, interstitial liberation, and
autodigestion of the pancreas by its own
enzymes.
95. June 26, 2012 Total slide. 126 95
Clinical Biochemistry Gastrointestinal Disease
Acute Pancreatitis Aetiology
Gallstones and Alcohol account for 90%
Hyperlipidemia
Hypercalcemia
Familial
Pancreatic duct obstruction
Tumour
Pancreas divisum
Viral infection
Scorpion venom
Drugs
Idiopathic
96. June 26, 2012 Total slide. 126 96
Clinical Biochemistry Gastrointestinal Disease
Acute Pancreatitis
Symptoms and signs
Midepigastric abdominal pain, radiating to
the back
Nausea and vomiting
Fever and tachycardia
Epigastric tenderness
Abdominal distention
Bluish discoloration in the flank (Grey
Turner’s sign)
97. June 26, 2012 Total slide. 126 97
Clinical Biochemistry Gastrointestinal Disease
98. June 26, 2012 Total slide. 126 98
Clinical Biochemistry Gastrointestinal Disease
Acute Pancreatitis
Diagnosis
It is supported by appropriate laboratory
determinations and radiographic findings
Serum amylase is the most widely used lab
test
Hyperamylasemia is commonly observed
within 24 hrs. of the onset and gradually
returns to normal
99. June 26, 2012 Total slide. 126 99
Clinical Biochemistry Gastrointestinal Disease
Acute Pancreatitis
Diagnosis
Elevated amylase levels may occur in other acute
abdominal conditions, though levels rarely exceed
500 IU/dL
Urinary amylase excretion is increased and this
may be very helpful in cases where the serum
amylase level has returned to normal.
Other lab. Findings
Moderate leukocytosis
Mild bilirubin elevation (<2mg/dL)
Raised Haematocrit
Hypocalcaemia (Calcium being complexed with fatty
acids)
100. June 26, 2012 Total slide. 126 100
Clinical Biochemistry Gastrointestinal Disease
Acute Pancreatitis
Glasgow prognostic system
101. June 26, 2012 Total slide. 126 101
Clinical Biochemistry Gastrointestinal Disease
Acute Pancreatitis
Treatment
Goals of medical treatment
Reduction of pancreatic secretory stimuli
Correction of fluid and electrolyte derangements
102. June 26, 2012 Total slide. 126 102
Clinical Biochemistry Gastrointestinal Disease
103. June 26, 2012 Total slide. 126 103
Clinical Biochemistry Gastrointestinal Disease
Chronic Pancreatitis
Is an entity encompassing recurrent or persistent
abdominal pain of pancreatic origin combined
with evidence of exocrine and endocrine
insufficiency and marked pathologically by
irreversible parenchymal destruction.
It is associated with alcohol abuse,
Hyperparathyroidism, congenital anomalies of
the pancreatic duct and pancreatic trauma. It
may also be idiopathic.
104. June 26, 2012 Total slide. 126 104
Clinical Biochemistry Gastrointestinal Disease
Chronic Pancreatitis
Patients typically present in the fourth or fifth
decade with a history of alcohol abuse and with
epigastric or back pain.
Anorexia and weight loss may be present.
1/3 of pts. Have insulin-dependent diabetes
1/4 of pts have steatorrhea.
Narcotic abuse is common
105. June 26, 2012 Total slide. 126 105
Clinical Biochemistry Gastrointestinal Disease
Chronic Pancreatitis
pancreatic calcifications in ~50%
pancreatic parenchymal nodularity,
calcifications and pancreatic ductal dilatation.
106. June 26, 2012 Total slide. 126 106
Clinical Biochemistry Gastrointestinal Disease
Signs and Symptoms of
Chronic Pancreatitis
Abdominal pain: intense, burning,
Abdominal tenderness
Ascites
Steatorrhea
Jaundice
107. June 26, 2012 Total slide. 126 107
Clinical Biochemistry Gastrointestinal Disease
More S & S of Chronic
Dark urine
Signs and symptoms of diabetes
Dyspnea
Orthopnea
Weight loss
108. June 26, 2012 Total slide. 126 108
Clinical Biochemistry Gastrointestinal Disease
Diagnostics
Elevated amylase, lipase, and urine amylase
Elevated glucose, bilirubin, alkaline phosphatase
Elevated WBCs
Hypocalcemia
Hypomagnesia
109. June 26, 2012 Total slide. 126 109
Clinical Biochemistry Gastrointestinal Disease
Chronic Pancreatitis
Medical Treatment
Control of abdominal pain
Treatment of endocrine and exocrine
insufficiency
110. June 26, 2012 Total slide. 126 110
Clinical Biochemistry Gastrointestinal Disease
111. Clinical Biochemistry Gastrointestinal Disease
Insulinoma
•Characteristic clinical manifestation is fasting
hypoglycemia with symptoms
• insulinomas arise from cells of ductular/acinar
system of the pancreas
112. June 26, 2012 Total slide. 126 112
Clinical Biochemistry Gastrointestinal Disease
Insulinoma
Incidence
0.4/100,000 person-yrs (4 cases/million/year)
So rare that few institutions have accrued
enough experience to provide data
113. June 26, 2012 Total slide. 126 113
Clinical Biochemistry Gastrointestinal Disease
Insulinoma
Symptoms
Confusion, visual changes, unusual behavior
Sympathoadrenal symptoms include
palpitations, diaphoresis, and tremulousness
Amnesia as well
114. June 26, 2012 Total slide. 126 114
Clinical Biochemistry Gastrointestinal Disease
Insulinoma
Information based on a collection of 224 patients
out of Olmsted County, Minnesota
Of those 224, 8% had MEN neoplasia
Tumor distribution:
87% had single benign lesions
7% benign tumors-multiple
6% had malignant insulinomas
115. June 26, 2012 Total slide. 126 115
Clinical Biochemistry Gastrointestinal Disease
Insulinoma
Established by demonstrating inappropriately
high serum [insulin] during a spontaneous or
induced episode of hypoglycemia
Virtually all insulinomas are islet cell tumors
After diagnosis, imaging used to localize tumor