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Pud Gastritis Lecture[1]
 

Pud Gastritis Lecture[1]

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    Pud Gastritis Lecture[1] Pud Gastritis Lecture[1] Presentation Transcript

    • 55 yo male c/ epigastric pain on/off x 1 mo
    • History
      • Awoke him from sleep
      • Relieved by food, but pain worsened 1-3 hrs later
      • Fatigue
      • Dyspepsia/ bloating/ belching/ burning
      • Wt loss
      • No SOB/ pain radiation/N/V/D/F
      • Wife states that his diet is “poor”
    • History
      • PMH
        • No DM
        • No CAD
        • Etc.
      • Family History
        • Mother died 75 MI
        • Father died 70 stroke
      • Surgical Hx
        • None
      • Social History
        • + Smoker 1ppd
      • Medications
        • “ some arthritis med”
        • “ some HTN med”
      • NKDA
    • Physical Exam
      • + Epigastric tenderness
      • Guiaic +
    • Differential Diagnosis?
      • Cardiac
        • MI
      • Aortic Dissection
      • Pulmonary
      • GI
        • PUD
        • Pancreatitis
        • Gallstones
        • Inflammatory bowel ds. (crohn’s/UC)
        • Colon Ca
    • Dx tests
      • CBC (blood loss)
      • Chem c/ BUN/creat
      • Type & cross
      • H. pylori
      • EKG
      • CXR (free air)
      • Barium study
    • Procedures
      • NG tube (if upper GI bleed)
      • IVF
      • Endoscopy
      • ? Sig vs. colonoscopy?
    • Tx
      • Antacids
      • GI cocktail
      • H2 blockers
      • PPI’s
      • Abx
    • Reflux Esophagitis Peptic Ulcer Disease, Gastritis, & GI Bleeding Pascale Gèhy-Andrè, PA-C
    • Anatomy & Physiology of the stomach
      • The blood supply is from the Celiac artery
      • The vagus nerve stimulates the stomach
      • The epithelium is columnar cells pieced by numerous glands
      • The cardia and antrum have mostly mucous cells
    • Normal Gastric Function
      • 1. Primary function of the stomach
        • A. secretion of substances important to digestion & absorption
        • B. movement of gastric contents downstream to small bowel
      • 2. Classes of secretory cells
        • A. Mucous secreting cells of the cardia :
          • 1. Protect underlying cells from mechanical forces of digestion
          • 2. Lubrication of mucosa to move food over surface
          • 3. Retain water within the mucous gel providing aqueous environment for underlying cells.
          • 4. Forming an unstirred layer above the mucosa impending but not blocking diffusion of hydrogen ions from the lumen to the superficial epithelial cells.
    • Normal Gastric Function
      • 2. Classes of secretory cells (cont.):
        • B. HCL -Secreting parietal cells of the body which also secrete intrinsic factor.
        • C. Pepsinogen -Secreting chief cells of the body.
        • D. Gastrin -Secreting G cells of the Antrum (body has 2 sources of Gastrin stomach and pancreas).
    • Gastric Function (cont.)
      • 3. Neural & Hormonal influence on gastric function:
        • A. Cephalic phase : (smell/thinking) initiates cholinergic impulse via the vagus nerve stimulating parietal secretion of acid & G cell secretion of Gastrin which also stimulates acid.
        • B. Gastric phase : causes distention of the stomach by food which causes further secretion of acid and gastrin. Protein will also stimulate G cells to produce Gastrin and acid.
        • C. Intestinal phase : will cause gastric acids to stimulate secretion of secretin & cholecystokinin which will also inhibit the action of gastrin on the parietal cells.
    • Reflux Esophagitis
      • Definition: Recurrent reflux of gastric contents in the distal esophagus
      • Commonly called heartburn
      • 20% of normal population at least one week
      • May cause erosions that leads to Barrett’s esophagitis which can predispose to malignancy
    • Reflux Esophagitis
      • Contributing Factors:
        • Hiatal hernia
        • Delayed gastric emptying (gastroparesis/obstruction)
        • Incompetent Lower esophageal sphincter
        • Irritant effects of gastric juices (refluxate)
      • Clinical features:
        • Heartburn most common presenting feature
        • Hoarseness, cough, hiccup, atypical chest pain, sore throat
    • Reflux Esophagitis
      • Laboratory studies
        • Barium swallow may indicate a large hiatal hernia
        • ENDOSCOPY with BIOPSY standard procedure describes the presence and extent of mucosal damage
        • Endoscopy when symptoms do not respond to medical therapy
        • pH monitoring can be done
    • Reflux Esophagitis
      • Treatment: Life style modification ( DC smoking)
        • Pharmacotherapy
          • Antacids or alginic acid(gaviscon)
          • Histamine (H2 blockers)
          • Prokinetic drugs ( e.g. metoclopramide, cisapride, bethanechol) increase gastric emptying and can be combined with H2 blockers
          • Acid-suppressant proton-pump inhibitor (e.g. omeprazole, lansoprazole) may be tried as last resort
          • Anticholinergic, B - adrenergic, and calcium channel-blocking agents decrease lower esophageal sphincter pressure and should be avoided
      • Complication: Barrett’s Esophagagus
    • Gastritis
      • Acute Gastritis is an inflammation of the gastric mucosa.
      • Gastropathy : epithelial or endothelial damage without inflammation
      • Gastritis has 3 basic types:
        • Acute (erosive/ hemorrhagic)
        • Non-erosive, Non-specific/Chronic
        • Special Forms
    • Acute Gastritis (Erosive/Hemorrhagic)
      • Most common causes:
        • NSAIDS gastric injury by diminishing prostaglandin production in stomach and duodenum
        • Alcohol use is the leading cause of gastritis
        • Stress from CNS injury burns, sepsis, surgery
        • Portal hypertension (portal gastropathy)
      • Other causes:
        • Caustic ingestion
        • radiation
    • Chronic Gastritis Nonerosive/nonspecific
      • Infectious gastritis Type B: H Pylory
        • Involves antrum and body of stomach
      • majority of patients asymptomatic
        • Strong association with PUD
        • 2 to 6 fold risks of gastric adenocarcinoma and also gastric lymphoma
      • Autoimmune gastritis Type A: Pernicious anemia
        • Body and fundus, It usually spares the antrum & affects the parietal cells.
        • Pernicious anemia caused by impaired absorption of vitamin B-12 occurs due to lack of intrinsic factor from parietal cells and decrease in acid production
        • Increased risk of adenocarcinoma
    • Special forms of Gastritis
      • Infectious (Phlegmonous or necrotizing gastritis)
        • Emergency gastric resection, and Abx therapy
        • CMV, candidal (fungal) in immunocompromised pt’s
        • Larvae ingestion requires endoscopic removal
      • Eosinophilic Gastritis
      • Giant Cell (Menetrier’s disease) (Hypertrophic Gastropathy)
        • only found on biopsy
      • Lymphocytic Gastritis
      • Granulomatous Gastritis
        • Tuberculosis
        • Syphilis
        • Fungal
        • Sarcoid
        • Crohn’s
    • Gastritis Symptoms
      • Clinical features of gastritis generally reflects the underlying syndrome rather than the gastric injury itself
      • Acute:
        • Dyspepsia and abdominal pain are common indicators of gastritis
        • Mild epigastric discomfort
        • Occasional N/V
        • Headache, excessive salivation, flatus
      • Chronic:
        • Non specific symptoms c/ chronic abdominal discomfort
      • Key signs: (usually none)
        • Hematemesis, bloody nasogastric aspirate
        • Abdominal tenderness
        • Bloating
        • Emesis
    • Gastritis
      • Lab:
        • Endoscopy c/ biopsy is the gold standard
        • A urea breath test can be used to detect HP
        • Specific test for underlying conditions (e.g) B12 and CBC for pernicious anemia
      • Differential Diagnosis:
        • 1. Peptic ulcer 2. Gastroparesis
        • 3. Gastric carcinoma 4. GERD
        • 5. Pancreatitis 6. Lymphoma
      • Treatment: (same as duodenal ulcers)
        • Remove irritant
        • Treat for H pylori
        • Antacids & H2 blockers
        • Avoid smoking & alcohol
    • Peptic Ulcer Disease
      • Definition : PUD is describes any ulcer of the upper digestive tract. (duodenal # 1) and stomach (gastric #2)
      • Break in the duodenal or gastric mucosa extending through the musularis mucosae, and are usually 5mm-1cm.
    • Zollinger-Ellison Syndrome
      • Ulcers-associated with the Zollinger-Ellison (ZE) Syndrome (#3 ) are caused by gastrin-releasing islet cell tumors (gastrinomas), & are also considered a form of peptic ulcer.
    • Zollinger-Ellison Syndrome
      • A tumor of the pancreas that secretes gastrin ( Gastrinoma)
      • Usually found in head of pancreas but can also be found in duodenum, liver & lung
      • 75-80% of ulcers produced develop in the duodenal bulb
      • Suspect in any patient with:
        • Multiple or recurring duodenal ulcers
        • Post bulbar or jejunal ulcers
        • Ulcers associated with diarrhea
        • Elevated serum gastrin levels
          • Usually only tested when suspect ZE syndrome
    • Peptic Ulcer Disease (PUD)
        • Men 1.3 : 1 Women
        • Most commonly occur in :
        • #1 Duodenum (Duodenal)
        • #2 Stomach (Gastric)
        • Esophagus
        • Gastroenteric anastomoses
        • Meckel’s Diverticulum
    • PUD
      • The spectrum of the disease is broad from mild mucosal injury to frank ulcerations.
      • Symptoms vary and are not related to the severity of tissue damage.
      • 1-2% of population have an ulcer at the present time
      • 10% of population will have ulcer in their lifetime
      • Gastric and Duodenal ulcers tend to recur in the same location.
      • Recurrent hemorrhage occurs in 50% of patients who have had a prior bleed.
    • Duodenal Ulcer vs. Gastric Ulcer
      • Duodenal
        • Increased acid production
        • H. pylori
        • relieved by food & typically awakens patient around 1:00am
      • Gastric
        • Normal or decreased acid production
        • Decreased mucosal resistance
        • H. pylori
        • NSAIDS
        • worsened by food
    • Duodenal Vs. Gastric (cont)
      • Duodenal
        • Onset more common age 25 to 55
        • never malignant
        • mostly located in the duodenal bulb or immediately post bulbar.
        • Ulcers distal to the duodenal bulb should raise suspicion for Zollinger-Ellison Syndrome (also c/ multiple frequently occurring duodenal ulcers.)
        • Men 2:1 Women
        • Duodenal 5 times more common than gastric
        • 60-80% have recurrence within one year.
      • Gastric
        • Onset more common age 40 to 70
        • Benign more likely @ lesser curvature/ antrum
        • Gastric ulcers are more common @ lesser curvature
        • Malignancies more likely @ greater curvature
        • 1-3% occur in carcinomas
    • PUD Etiologies
      • 1. Helicobacter pylori (H. pylori) infection: (#1 cause)
        • A. Associated c/ 70-95% of Peptic ulcers.
        • B. Treatment of H. pylori improves healing rate & markedly decreases the recurrence rate.
      • 2. NSAIDS: (#2 cause) (inhibit prostaglandins which normally stimulate production of mucous secretions & bicarb.)
        • A. may cause gastric or duodenal ulcers (steroids also)
        • B. accounts for the majority of non H. pylori ulcers
    • PUD Etiologies (cont)
      • 3. Hypersecretion states: (#3 although uncommon)
        • Gastrinomas (Zollinger-Ellison Syndrome)
        • Multiple endocrine neoplasia (MEN-1)
        • Systemic mastocytosis (mast cells infiltrate intestinal wall, release histamine- stimulates acid. Symptoms are diarrhea, flushing, urticaria. Histamine in blood. Confirmed by biopsy.)
      • 4. Stress: physiologic stress (eg. Burns, surgery, & severe medical conditions)
      • 5. Rare causes: viral, radiation, vascular insuff.
      • Diseases assoc. c/ peptic ulcers:
        • Cirrhosis, renal failure, pulmonary ds.
          • Any pt. c/ systemic ds. (COPD, renal failure, cirrhosis of liver) are prone to ulcers so should be started on H2 blockers.
    • The pathogenesis of PUD is related to the imbalance between normal protective factors and injurious factors
      • No Ulcer
        • Normal
      • Ulcer
      • Aggressive forces
        • Gastric acid
        • Digestive enzymes
      • Vs.
      • Defensive forces
        • Mucus
        • Bicarb
        • Prostaglandins
        • Epithelial regeneration
    • Ulcers result from:
      • 1. Increased aggression
        • H. pylori infection
        • NSAIDS
        • Cigarettes
        • ETOH
      • Or
      • 2. Impaired Defense
        • Ischemia
        • Prostaglandin Inhibition (NSAIDS)
        • Delayed gastric emptying
    • PUD
      • ADVERSE EFFECTS OF SMOKING
        • 1. Interferes c/ action of H2 antagonists
        • 2. Increases rate of gastric emptying
        • 3. Increases duodenogastric reflux
        • 4. Decreases pancreatic bicarb secretion
        • 5. Decreases mucosal blood flow
        • 6. Depresses gastric mucosal prostaglandin synthesis
    •  
    • Peptic Ulcer Disease Facts
      • Most ulcers are caused by H. pylori infection, not spicy food, acid or stress.
      • You can test for H. pylori infection.
      • H. pylori / ulcers can be tx’d c/ antibiotics.
      • Complications:
        • A Major complication is bleeding & perforation
        • Erosion of a small vessel at the base of the ulcer is the cause of the bleeding
        • Perforation is usually catastrophic causing peritonitis
    • What is H. pylori
      • Helicobacter pylori ( H. pylori ) is a gram negative spiral-shaped bacillus found in the gastric mucous layer or adherent to the epithelial lining of the stomach.
      • H. pylori causes more than 90% of duodenal ulcers and up to 80% of gastric ulcers.
    • How do people get infected with H. pylori ?
      • It is not known how H. pylori is transmitted or why some patients become symptomatic while others do not.
      • The bacteria are most likely spread from person to person through fecal-oral or oral-oral routes.
      • Possible environmental reservoirs include:
        • contaminated water sources
        • Iatrogenic spread through contaminated endoscopes has been documented but can be prevented
    • What can people do to prevent H. pylori infection?
      • Since the source of H. pylori is not yet known, recommendations for avoiding infection have not been made.
      • In general, it is always wise for persons to wash hands thoroughly, to eat food that has been properly prepared, and to drink water from a safe, clean source.
    • H. pylori infection
      • Before this bacterium was discovered, spicy food, acid, stress, and lifestyle were considered the major causes of ulcers.
      • The majority of patients were given long-term medications, such as H2 blockers, and more recently, proton pump inhibitors, without a chance for permanent cure.
      • These medications relieve ulcer-related symptoms, heal gastric mucosal inflammation, and may heal the ulcer, but they do NOT treat the infection.
    • H. Pylori infection
      • When acid suppression is removed, the majority of ulcers, particularly those caused by H. pylori , recur.
      • Since we now know that most ulcers are caused by H. pylori , appropriate antibiotic regimens can successfully eradicate the infection in most patients, with complete resolution of mucosal inflammation and a minimal chance for recurrence of ulcers.
    • What illnesses does H. pylori cause?
      • Most persons who are infected with H. pylori never suffer any symptoms related to the infection; however, H. pylori causes chronic active, chronic persistent, and atrophic gastritis in adults and children.
      • Infection with H. pylori also causes duodenal and gastric ulcers. Infected persons have a 2- to 6-fold increased risk of developing gastric cancer and mucosal-associated-lymphoid-type (MALT) lymphoma compared with their uninfected counterparts.
      • The role of H. pylori in non-ulcer dyspepsia remains unclear.
    • Peptic Ulcer Disease Symptoms
      • #1. Epigastric Pain
        • Burning
        • Occurs 1-3 hrs p/ meals
        • Relieved by food
        • May occur @ night
        • May radiate to back or shoulders if perforated
      • Nausea
      • Vomiting
        • May be related to partial or complete gastric outlet obstruction
      • Dyspepsia
        • Belching/ Bloating
      • Heartburn
      • Chest Discomfort
      • Anorexia
      • Weight loss
        • In gastric ulcers (also in pancreatic ds.)
      • Weight gain
        • In duodenal ulcers
      • Hematemesis or melena
        • Due to GI bleeding
        • If severe = hematochezia
    • Chinese Proverbs
      • Man with one chopstick go hungry.
      • Man who scratch ass should not bite fingernails.
      •   Man who eat many prunes get good run for money.
      • Baseball is wrong: man with four balls cannot walk.
      • Panties not best thing on earth! But next to best thing on earth.
      • Man who fight with wife all day get no piece at night.
      • It take many nails to build crib, but one screw to fill it.
      • Man who drive like hell, bound to get there.
    • Who should be tested and treated for H. pylori ?
      • Persons with active gastric or duodenal ulcers or documented history of ulcers should be tested for H. pylori , and if found to be infected, they should be treated.
      • To date, there has been no conclusive evidence that treatment of H. pylori infection in patients with non-ulcer dyspepsia is warranted.
    • PUD Tests
      • Laboratory Test:
        • Routine tests are of little importance. Having a CBC is helpful.
      • Upper GI endoscopy c/ biopsy*
      • Upper GI series (barium) (limited today)
      • Serum Test
        • Amylase
        • Electrolytes
        • Serum Gastrin level if ZE syndrome is suspected
          • Frequently occurring duodenal ulcers or multiple Duodenal Ulcers*
    • How is H. pylori infection diagnosed?
      • Several methods may be used to diagnose H. pylori infection.
      • Serological tests that measure specific H. pylori IgG antibodies can determine if a person has been infected.
        • The sensitivity and specificity of these assays around 80%
      • Fecal Antigen Assay
      • Urea Breath test
        • In this test, the patient is given either 13C- or 14C-labeled urea to drink.
        • H. pylori metabolizes the urea rapidly, and the labeled carbon is absorbed.
        • This labeled carbon can then be measured as CO2 in the patient's expired breath to determine whether H. pylori is present.
        • The sensitivity and specificity of the breath test ranges from 94% to 98%.
        • PPI’s can give false negative results
    • How is H. pylori infection in PUD diagnosed?
      • Upper endoscopy (esophagogastroduodenal) is considered the reference method of diagnosis.
    • Dx of H. pylori by Endoscopy
      • During endoscopy, biopsy specimens of the stomach and duodenum are obtained and the diagnosis of H. pylori can be made by several methods:
        • The biopsy urease test - a colorimetric test based on the ability of H. pylori to produce urease; it provides rapid testing at the time of biopsy.
        • Histologic identification of organisms - considered the gold standard of diagnostic tests.
        • Culture of biopsy specimens for H. pylori, which requires an experienced laboratory and is necessary when antimicrobial susceptibility testing is desired
    • Peptic Ulcer Disease Therapy
      • Non-Pharmacological
        • Diet change is of no value
        • Smoking Cessation
          • Smoking delays healing
        • DC medications that enhance the progression
          • NSAIDS
      • Pharmacological Therapy
        • Inhibit secretion of acid
        • Neutralizing gastric acids
        • Augmentation of protection of mucosa
        • Antibiotics prn
      • Maintenance Therapy
        • Prevention c/ colloid bismuth
        • Bedtime dosage of H2 blockers
    • Peptic Ulcer Disease Therapy
      • Pharmacological Therapy
        • Inhibition of acid
          • H2 blockers
          • Antacids
          • Proton pump inhibitors
          • Anticholinergics
          • Prostaglandins
          • Augmentation protection
    • Peptic Ulcer Disease Therapy
      • Antacids (magnesium, aluminum, & calcium based)
        • cause diarrhea
      • Moderate to high doses of H2 blockers result in improved healing rates
        • Used 1 hr PC & HS for 6-8 wks
        • Side effects:
          • Hypermagnesemia (careful in renal patients)
          • Aluminum causes phosphate depletion & osteoporosis
          • Sodium overload in CHF
          • Hypercalcium causing Milk alkali syndrome
          • Inhibits absorption of antibiotics, digoxin, warfarin
    • PUD Therapy (cont)
      • Proton Pump Inhibitors:
        • Inhibit the H,K-ATPase pump
        • Healing rate 80-100%
        • Prilosec (Omeprazole)
      • Anticholinergics: reduce acid by 50% and cause blurred vision
        • pupil dilation, consider pt’s occupation or driving restriction
    • PUD Therapies (cont)
      • Prostaglandins (Do not use in pregnancy)
        • Inhibit the parietal cell cyclic AMP function in response to histamine
        • Healing rate are equal to H2 blockers
        • Primary role is to be used as a prophylactic agent to prevent NSAID induced ulcers. Not used as a primary therapy
        • Mosoprostol (Cytotec)
      • Sucralfate (Carafate) its action is unknown
        • It forms a viscous shield over the mucosa
        • Absorbs bile & pepsin
    • Screw the environment carpooling is bad
    • What are the treatment regimens used for H. pylori eradication?
      • Current therapy for H. pylori infection consists of 10 days to 2 weeks of one or two effective antibiotics,
        • amoxicillin,
        • tetracycline
          • not to be used for children <12 yrs
        • metronidazole, or
        • clarithromycin,
      • Plus either
        • ranitidine bismuth citrate (H2 blocker),
        • bismuth subsalicylate (pepto-bismol),
        • or proton pump inhibitor.
    • PUD Therapies (cont)
      • Acid suppression by the H2 blocker or proton pump inhibitor in conjunction with the antibiotics helps
        • alleviate ulcer-related symptoms (i.e., abdominal pain, nausea),
        • helps heal gastric mucosal inflammation,
        • and may enhance efficacy of the antibiotics against H. pylori at the gastric mucosal surface.
    • H. Pylori Tx
      • Currently, eight H. pylori treatment regimens are approved by the Food and Drug Administration (FDA); however, several other combinations have been used successfully.
      • Antibiotic resistance and patient noncompliance are the two major reasons for treatment failure.
      • Overall, triple therapy regimens have shown better eradication rates than dual therapy. Longer length of treatment (14 days versus 10 days) results in better eradication rates.
    • FDA-approved treatment options
      • 1. Omeprazole 40 mg QD + clarithromycin 500 mg TID x 2 wks, then omeprazole 20 mg QD x 2 wks
      • -OR-
      • 2. (Zantac) Ranitidine bismuth citrate (RBC) 400 mg BID + clarithromycin 500 mg TID x 2 wks, then RBC 400 mg BID x 2 wks
      • -OR-
      • 3. Bismuth subsalicylate (Pepto Bismol®) 525 mg QID + metronidazole 250 mg QID + tetracycline 500 mg QID* x 2 wks + H2 receptor antagonist therapy as directed x 4 wks
      • -OR-
      • 4. Lansoprazole 30 mg BID + amoxicillin 1 g BID + clarithromycin 500 mg TID x 10 days
    • FDA-approved treatment options (cont.)
      • 5. -OR- Lansoprazole 30 mg TID + amoxicillin 1 g TID x 2 wks**
      • 6. -OR- Rantidine bismuth citrate 400 mg BID + clarithromycin 500 mg BID x 2 wks, then RBC 400 mg BID x 2 wks
      • 7. -OR- Omeprazole 20 mg BID + clarithromycin 500 mg BID + amoxicillin 1 g BID x 10 days
      • 8. -OR- Lansoprazole 30 mg BID + clarithromycin 500 mg BID + amoxicillin 1 g BID x 10 days
    • Long-term consequences of H. pylori infection?
      • Recent studies have shown an association between long-term infection with H. pylori and the development of gastric cancer .
      • Gastric cancer is the second most common cancer worldwide ; it is most common in countries such as Colombia and China, where H. pylori infects over half the population in early childhood.
      • In the United States, where H. pylori is less common in young people, gastric cancer rates have decreased.
    •  
    • GI Bleeding
    • Gastrointestinal Bleeding
      • May present as:
        • Occult blood (not visualized)
        • Melena (black stool)
        • Hematemesis (vomiting blood)
        • Hematochezia (passage of BRBPR in stool)
    • Kinds of GI Bleeding
      • Hematemesis
        • Rapid bleed: vomiting bright red blood
        • Slow bleed: “coffee-grounds”
      • Melena
        • Black tarry stool
        • Source:
          • Upper GI
          • Or lower GI to right colon
      • Hematochezia
        • Bright red blood in stool
        • Source:
          • Lower GI
          • Or Upper GI if massive
    • Occult blood
      • Hemacult/Guiaic is the most commonly used test
      • False positives <2%
      • Obtain 2 different samples from 2 stools over a 3 day period
      • Laxatives alter results causing both false-positive and false-negative results
      • False positive results from food rich in peroxidase
        • Bloody meats
        • Broccoli
        • Turnips
        • Cauliflower
      • False negatives from taking Vit. C or food containing vitamin C
      • Neoplasms is #1 cause of occult blood loss
    • Guiaic/ Hemoccult
    • Causes of GI bleeding by location
      • Upper GI
        • #1 PUD
          • Duodenal
          • Gastric
        • Esophageal varices
          • (Secondary to portal HTN)
        • Mallory-Weiss tear
          • (Mucosal laceration @ EG junction)
        • Gastritis
      • Lower GI
        • #1 Hemorrhoids
        • #2 Anal Fissure
        • Diverticulosis
        • IBD
        • Intussusception
      • Upper & Lower GI
        • Neoplasms
        • Angiodysplasias
          • (Osler’s disease)
    •  
    • GI Bleed
      • GI bleeding is a powerful laxative
      • GI bleeding may be life threatening
      • GI bleeding may be acute or chronic
      • Adult anemia is secondary to GI bleeding until proven otherwise
      • GI bleeding is secondary to cancer until proven otherwise
    • GI Bleed
      • Nature & duration helps with evaluation
      • Presence of pain is important
      • Watch for associated symptoms: fever, weight loss
      • Medication and past surgery history
      • The initial step is assessment of hemodynamic status. A systolic BP <100mm Hg is high risk c/ acute bleeding.
      • CAN BE MASSIVE AND DEADLY
      • MUST BE TREATED RAPIDILY AND AGGRESSIVELY
      • ALWAYS R/O CANCER
    • Upper GI bleed
      • 4x more common than lower GI bleed
      • R/O upper GI source by NG tube aspirate
    • Upper GI Differential Dx aids
      • Signs of chronic liver disease implicates bleeding due to portal HTN.
      • A hx of dyspepsia, NSAID use, or PUD, suggests Peptic Ulcer.
      • Acute bleeding after heavy alcohol ingestion or retching suggests a Mallory-Weiss tear.
    • Lower GI bleeds
      • Hematochezia
        • (however, 10% is from upper GI source)
      • Defined as below ligament of Treitz
        • (divides duodenum/ jejunum)
      • 95% from Colon
      • Less likely than Upper GI bleed to present in shock, or require transfusion
      • 85% spontaneous cessation
    • Complications of GI bleed
      • DIC from both massive blood loss & coagulation
      • Multi-organ failure
      • Hemodynamic collapse
      • Hyper-ammonia toxicity
      • Hepatorenal failure
      • Encephalopathy
    •  
    •  
    •  
    • MCC of GI Bleeding 2006 Current
      • Upper GI
        • PUD
        • Portal HTN
        • Mallory Weiss
        • Vascular abn
        • Gastric Neoplasms
        • Erosive gastritis
        • others
      • Lower GI
        • Under 50 y/o
          • Infectious colitis
          • Anorectal ds
          • Inflammatory bowel ds
        • Over 50 y/o c Major Bleed
          • Diverticulosis
          • Vascular ectasias
          • Malignancy
          • ischemia
    •  
      • LABS
      • CBC
      • PT/PTT/Thrombin time- DIC panel (FSP fibrin split products, fibrinogen, FDP fibrin degradation products, clotting time, D dimer assay)
      • Electrolytes/BUN/creatinine
      • Blood Type and Cross match
      • CXR/ AXR rarely helpful only if perforated
      GI BLEED
    • CXR Pneumoperitoneum
    • Anoscopy/ Sigmoidoscopy VS. Colonoscopy
      • Anoscopy/ Sigmoidoscopy
        • Acceptable in <45 yo otherwise healthy to evaluate for:
          • Anorectal ds.
          • Inflammatory bowel ds.
          • Infectious colitis
        • If lesion found, no further eval needed
      • Colonscopy
        • Used Diagnostically and Therapeutically
        • All >40-45 yo c/ + guiaic or Fe+ deficiency anemia
    • Flex Sig
    • Anoscopy/ Rigid Sigmoidoscopy
    • Super Duper Pooper Scooper
    • Colonoscopy
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    • Urgent management of Upper GI bleeds
      • 2 Large bore IV lines need started c/ colloid solution started until PRBC can be infused, if needed.
      • Octreotide - Decreases portal HTN (it is administered promptly to all patients with active upper GI bleeds, and liver ds, or known portal HTN, until source can be ID’d by endoscopy.
      • PPI’s reduce risk of rebleed in PUD
      • Endoscopy
        • To ID source
        • Determine risk of rebleed
        • Hemostasis
      • Other Tx modalities (used only if endoscopy fails)
        • Angiographic embolization
        • Transvenous shunts (for portal HTN, and variceal bleeds)
    • Chinese Proverbs
      • Man who stand on toilet is high on pot.
      • Man who live in glass house should change clothes in basement.
      • Man who fish in other man's well often catch crabs.
      • Man who fart in church sit in own pew.
      • Crowded elevator smell different to midget.
    • Review
      • Acute Erosive Gastritis
        • D/C NSAIDS or add misoprostol
        • If bleeding caused by ASA; consider platelet administration
        • Sucralfate/ H2 antagonists
      • Chronic Gastritis (Nonerosive)
        • Type A
          • Eradicate H. pylori: amox + tetracycline + PPI
        • Type B
          • Treat pernicious anemia: monthly lifelong IM B12
      • Specific Types of Gastritis
    • Review
      • Peptic Ulcer Disease
        • Almost all need Pepsin, Acid, & H. pylori to form ulcer
        • Eradicate H. pylori
        • Endoscopic bx to exclude adenocarcinoma recommended for all patients
        • If refractory: obtain fasting serum gastrin levels to exclude Zollinger-Ellison
        • Consider parietal cell vagotomy.
          • Partial gastrectomy c/ gastro-duodenostomy (Billroth I) or gastrojejunostomy (Billroth II) are rarely used now.
    • Review
      • Upper GI Bleed
        • Evaluate hemodynamic status, stabilize
        • Nasogastric tube
        • Octreotide
        • Endoscopy if bleeding is severe enough to require blood transfusions
        • Bleeding from esophageal varices: endoscopic sclerotherapy preferred
    • Review
      • Lower GI Bleed
        • The most common cause of significant bleeding is diverticular bleeding; that of intermittent minor hematochezia is hemorrhoidal bleeding
        • Evaluate hemodynamic status, stabilize
        • Colonoscopy if bleeding is severe or patient >50 yrs (neoplasms)
        • If bleeding continues consider nuclear bleeding scan or mesenteric angiography (often of limited use if bleeding is slow or intermittent), or Intra-arterial vasopressin or embolization.
        • Surgery as last resort
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