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Clinical Biochemistry Gastrointestinal Disease
In the name of God
Clinical Biochemistry Gastrointestinal Disease
By: Amir Nader Emami Razavi
April 11, 2023 Total slide. 126 3
Clinical Biochemistry Gastrointestinal Disease
Gastrointestinal disease
Peptic ulcer diseaseChronic duodenal ulcerChronic benign gastric ulcerZollinger-Ellison syndromeGastritisGastric cancerPost gastrectomy syndromeAcute pancreatitisChronic pancreatitisInsulinomaGlucagonomaSomatostatinoma
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Clinical Biochemistry Gastrointestinal Disease
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Clinical Biochemistry Gastrointestinal Disease
Peptic Ulcer Disease (PUD)
What is it?Group of chronic disorders characterized by ulcerating mucosal lesions in upper GI tractchronic inflammatory conditioncommon 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)
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Clinical Biochemistry Gastrointestinal Disease
Drugs that can cause PUD
methotrexate
cyclophosphamide
azathioprine
erythromycin
iron
corticosteriods
potassium chloride
NSAIDS
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Clinical Biochemistry Gastrointestinal Disease
Signs and Symptoms of PUD
Can be symptomaticanorexia, nausea, vomiting, belching, bloating, heartburn, epigastric pain (pain in the upper abdomen)awakened at night (usu. around 3am,)
duodenal ulcersepigastric pain, tenderness, burning, aching between xiphoid process and belly buttonrelieved with food intake or antacids
gastric ulcerdiffuse pain over midepigastrium (midstomach)worsened by food
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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.
Clinical Biochemistry Gastrointestinal Disease
Pathology of Peptic Ulcer
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Clinical Biochemistry Gastrointestinal Disease
Normal Stomach
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Clinical Biochemistry Gastrointestinal Disease
Esophagus & Stomach Normal
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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
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Clinical Biochemistry Gastrointestinal Disease
Etiology:
Helicobacter pylori infection.
Hyperacidity - eg. zollinger ellison.
Drugs - anti-inflammatory (NSAIDs) & Corticostroids.
Cigarette smoking, Alcohol,
Rapid gastric emptying
Personality and stress
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Clinical Biochemistry Gastrointestinal Disease
H. Pylori organisms- silver st.
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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
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Clinical Biochemistry Gastrointestinal Disease
Normal
Increased Attack Hyperacidity
Weak defense Helicobacter pylori Stress, drugs, smoking
Etiology of PUD
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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
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Clinical Biochemistry Gastrointestinal Disease
Peptic Ulcer Morphology:
90% ulcers in first portion of duodenum or lesser curvature of stomach80 to 90% cases single ulcer. Round Small ulcers with sharply punched out edgesSmall <2cm, clean base.Microscopy: 4 zones.
Superficial necrotic layer.Inflammatory cells zone.Granulation tissue zone Collagenous scar layer.
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Clinical Biochemistry Gastrointestinal Disease
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Clinical Biochemistry Gastrointestinal Disease
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Clinical Biochemistry Gastrointestinal Disease
Gastric peptic ulcer
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Clinical Biochemistry Gastrointestinal Disease
Gastric peptic ulcer:
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Clinical Biochemistry Gastrointestinal Disease
Gastric UlcerGastric ulcer:
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Clinical Biochemistry Gastrointestinal Disease
Duodenal Peptic Ulcer
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Clinical Biochemistry Gastrointestinal Disease
Peptic ulcer - Endoscopy
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Clinical Biochemistry Gastrointestinal Disease
Gastric Ulcer
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Clinical Biochemistry Gastrointestinal Disease
Gastric Ulcer
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Clinical Biochemistry Gastrointestinal Disease
Gastric Ulcer
Punched out ulcer
Clean base
Small single
Radiating mucosal folds.
Benign ulcer.
No tumor.
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Clinical Biochemistry Gastrointestinal Disease
Peptic Ulcer
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Clinical Biochemistry Gastrointestinal Disease
Peptic Ulcer Microscopy:
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Clinical Biochemistry Gastrointestinal Disease
PUD - Diagnosis
Endoscopy
Barium meal – contrast x-ray
Biopsy – bacteria & malignancy
H.Pylori:Endoscopy cytology
Biopsy – Special stains
Culture
Urease Breath test.
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Clinical Biochemistry Gastrointestinal Disease
CDU Camplications
HemorrhageDue to the ulcer’s eroding a blood vessel
PerforationThrough the anterior wall of the duodenal cap
Causing peritonitis
Penetration of the ulcer into the adjacent structuresSuch as pancrease , biliary tract , liver, colon, abdominal wall, or even long
Luminal abstructionCaused by the gradual contraction of the ulser scar
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Clinical Biochemistry Gastrointestinal Disease
Gastric Ulcer
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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.
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Clinical Biochemistry Gastrointestinal Disease
Helecobacter pylori
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Clinical Biochemistry Gastrointestinal Disease
Toludine Blue stain – H pylori
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Clinical Biochemistry Gastrointestinal Disease
Urease production test
Clinical Biochemistry Gastrointestinal Disease
“You get ulcer, not from what you eat, but from what’s eating
you..!”
Clinical Biochemistry Gastrointestinal Disease
Hmmmm……… H.pylori
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Clinical Biochemistry Gastrointestinal Disease
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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.
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Clinical Biochemistry Gastrointestinal Disease
Zollinger Ellison Syndrome
Tumour Location
Symptoms
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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
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Clinical Biochemistry Gastrointestinal Disease
Signs of ZES
Multiple ulcers Diarrhea ulcer in atypical site resistant ulcer enlarged folds severe esophagirtis
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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,
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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
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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
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Clinical Biochemistry Gastrointestinal Disease
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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.
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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 radiologyGastropathy is usually caused by irritants such as drugs (eg, nonsteroidal antiinflammatory agents and alcohol), bile reflux, hypovolemia, and chronic congestion.
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Clinical Biochemistry Gastrointestinal Disease
Acute Esophagitis & Gastritis
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Clinical Biochemistry Gastrointestinal Disease
Gross–histologic correlation?
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Clinical Biochemistry Gastrointestinal Disease
CLASSIFICATION
GASTRITIS
ACUTE COMMON CHRONIC
EMAG
AMAG
BILE HPSTRESS
NSAID
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Clinical Biochemistry Gastrointestinal Disease
CLASSIFICATION
Acute vs. chronicAcute 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
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Clinical Biochemistry Gastrointestinal Disease
Mucosal congestion, edema, inflammation & ulceration
ACUTE GASTRITIS MORPHOLOGY
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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
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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
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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
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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
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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).
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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
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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
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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
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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.
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Clinical Biochemistry Gastrointestinal Disease
Helicobacter pylori
urease forms ammonia and bicarbonate that neutralize gastric acid and form a protective cloud around the organism
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Clinical Biochemistry Gastrointestinal Disease
Helicobacter pylori
spiral shape, flagella
facilitate its passage through the mucus layer
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Clinical Biochemistry Gastrointestinal Disease
Helicobacter pylori
H. pylori then attaches to gastric epithelial cells by means of specific receptor-mediated adhesion
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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
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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.
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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
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Clinical Biochemistry Gastrointestinal Disease
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Clinical Biochemistry Gastrointestinal Disease
Gastric Neoplasia
BenignGastric polyps
Ectopic pancreas
MalignantGastric Adenocarcinoma
Gastric Lymphoma
Gastric Sarcoma
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Clinical Biochemistry Gastrointestinal Disease
WHO Classification
5 main categories Adenocarcinoma, Adenosquamous cell carcinoma, squamous cell carcinoma, undifferentiated carcinoma and unclassified carcinoma
Adenocarcinoma – subdividedPapillary, tubular, mucinous, signet ring
Further subdivided based on differentiation
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Clinical Biochemistry Gastrointestinal Disease
Cancer of Stomach
1. Incidencea. Worldwide common cancer, but less common in US b. Incidence highest among Hispanics, African Americans, Asian Americans, males twice as often as femalesc. Older adults of lower socioeconomic groups higher risk
2. Pathophysiologya. Adenocarcinoma most common form involving mucus-producing cells of stomach in distal portionb. Begins as localized lesion (in situ) progresses to mucosa; spreads to lymph nodes and metastasizes early in disease to liver, lungs, ovaries, peritoneum
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Clinical Biochemistry Gastrointestinal Disease
Cancer of Stomach
3. Risk Factorsa. H. pylori infectionb. Genetic predispositionc. Chronic gastritis, pernicious anemia, gastric polypsd. Achlorhydria (lack of hydrochloric acid)e. Diet high in smoked foods and nitrates
4. Manifestationsa. Disease often advanced with metastasis when diagnosedb. Early symptoms are vague: early satiety, anorexia, indigestion, vomiting, pain after meals not responding to antacidsc. Later symptoms weight loss, cachexia (wasted away appearance), abdominal mass, stool positive for occult blood
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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
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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
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Clinical Biochemistry Gastrointestinal Disease
Fungating Carconoma
Clinical Biochemistry Gastrointestinal Disease
Gastric Surgical Procedures
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Clinical Biochemistry Gastrointestinal Disease
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Clinical Biochemistry Gastrointestinal Disease
Post gastrectomy syndrome
b. Complications associated with gastric surgery1. 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
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Clinical Biochemistry Gastrointestinal Disease
Post gastrectomy syndrome
Treatment: dietary pattern to delay gastric emptying and allow smaller amounts of chyme to enter intestineLiquids and solids taken separatelyIncreased amounts of fat and proteinCarbohydrates, especially simple sugars, reducedClient to rest recumbent or semi-recumbent 30 – 60 minutes after eatingAnticholinergics, sedatives, antispasmodic medications may be addedLimit amount of food taken at one time
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Clinical Biochemistry Gastrointestinal Disease
Post gastrectomy syndrome
Common post-op complicationsPneumoniaAnastomotic leakHemorrhageRelux aspirationSepsisReflux gastritisParalytic ileusBowel obstructionWound infectionDumping syndrome
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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 spreadPalliative treatment including surgery, chemotherapy; client may have gastrostomy or jejunostomy tube inserted
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Clinical Biochemistry Gastrointestinal Disease
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Clinical Biochemistry Gastrointestinal Disease
Pancreas
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Clinical Biochemistry Gastrointestinal Disease
Function
Exocrineprecursor digestive enzymes
lipases
Endocrinemetabolic hormones
Insulin from β cells
Glucagon from α cells
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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.
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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
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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
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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
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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
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Clinical Biochemistry Gastrointestinal Disease
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Clinical Biochemistry Gastrointestinal Disease
Acute Pancreatitis
Nonbacterial inflammatory disease caused by activation, interstitial liberation, and autodigestion of the pancreas by its own enzymes.
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Clinical Biochemistry Gastrointestinal Disease
Acute Pancreatitis Aetiology
Gallstones and Alcohol account for 90%HyperlipidemiaHypercalcemiaFamilial Pancreatic duct obstruction
TumourPancreas divisum
Viral infectionScorpion venomDrugsIdiopathic
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Clinical Biochemistry Gastrointestinal Disease
Acute PancreatitisSymptoms 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)
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Clinical Biochemistry Gastrointestinal Disease
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Clinical Biochemistry Gastrointestinal Disease
Acute PancreatitisDiagnosis
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
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Clinical Biochemistry Gastrointestinal Disease
Acute PancreatitisDiagnosis
Elevated amylase levels may occur in other acute abdominal conditions, though levels rarely exceed 500 IU/dLUrinary 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 HaematocritHypocalcaemia (Calcium being complexed with fatty acids)
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Clinical Biochemistry Gastrointestinal Disease
Acute PancreatitisGlasgow prognostic system
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Clinical Biochemistry Gastrointestinal Disease
Acute PancreatitisTreatment
Goals of medical treatmentReduction of pancreatic secretory stimuli
Correction of fluid and electrolyte derangements
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Clinical Biochemistry Gastrointestinal Disease
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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.
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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
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Clinical Biochemistry Gastrointestinal Disease
Chronic Pancreatitis
pancreatic calcifications in ~50%
pancreatic parenchymal nodularity, calcifications and pancreatic ductal dilatation.
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Clinical Biochemistry Gastrointestinal Disease
Signs and Symptoms of Chronic Pancreatitis
Abdominal pain: intense, burning,
Abdominal tenderness
Ascites
Steatorrhea
Jaundice
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Clinical Biochemistry Gastrointestinal Disease
More S & S of Chronic
Dark urine
Signs and symptoms of diabetes
Dyspnea
Orthopnea
Weight loss
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Clinical Biochemistry Gastrointestinal Disease
Diagnostics
Elevated amylase, lipase, and urine amylase
Elevated glucose, bilirubin, alkaline phosphatase
Elevated WBCs
Hypocalcemia
Hypomagnesia
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Clinical Biochemistry Gastrointestinal Disease
Chronic PancreatitisMedical Treatment
Control of abdominal pain
Treatment of endocrine and exocrine insufficiency
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Clinical Biochemistry Gastrointestinal Disease
Clinical Biochemistry Gastrointestinal Disease
Insulinoma
•Characteristic clinical manifestation is fasting hypoglycemia with symptoms• insulinomas arise from cells of ductular/acinar system of the pancreas
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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
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Clinical Biochemistry Gastrointestinal Disease
Insulinoma
Symptoms
Confusion, visual changes, unusual behavior
Sympathoadrenal symptoms include palpitations, diaphoresis, and tremulousness
Amnesia as well
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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
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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
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Clinical Biochemistry Gastrointestinal Disease
Insulinoma/diagnosis
Serum glucoseMale<55mg/dl
Female<35mg/dl
Plasma insulin level>15 mu/l
Plasma proinsulin level>40 pmol/l
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Clinical Biochemistry Gastrointestinal Disease
Insulinoma/treatment
Surgical removal
partial pancreatectomy
enucleation of insulinomasurgeon’s choice
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Clinical Biochemistry Gastrointestinal Disease
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Clinical Biochemistry Gastrointestinal Disease
Glucagonoma Syndrome
Tumour Location
Symptoms
Pancreas>90% malignant
Necrolytic migratory erythemaWeight lossAnemiaTrombosisImpaired glucose toleranceDiarrhoea
Glocagenoma Syndrome
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Clinical Biochemistry Gastrointestinal Disease
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Clinical Biochemistry Gastrointestinal Disease
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Clinical Biochemistry Gastrointestinal Disease
Histopathology
Tumour Markers
Radiology
Agyrophil staining, CgA, glucagon:500pg/ml glicentin
p-CgA, p-glucagon
Octreoscan, Endoscopic ultrasound,CT-angiography, MRI
GlocagenomaSyndrome/Diagnosis
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Clinical Biochemistry Gastrointestinal Disease
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Clinical Biochemistry Gastrointestinal Disease
Somatostatinoma Syndrome
Tumour Location
Symptoms
DuodenumPancreasColon/Rectum>80% mixed tumours
GallstonesSteatorrheaImpaired glucose toleranceOften “non-functioning” tumours!
Somatostatinoma Syndrome
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Clinical Biochemistry Gastrointestinal Disease
Somatostatinoma Syndrome/Diagnosis
Histopathology
Tumour Markers
Radiology
Argyrophil staining, CgASomatostatin
p-CgA, p-Somatostatin(s-Gastrin, p-Glucagonom, mixed tumour)
Endoscopic ultrasonographyCT-angiography, MRIColonoscopyUS (liver metastases)
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Clinical Biochemistry Gastrointestinal Disease