GIT NOTES

 Mouth
o Mastication/Chewing
o Salivary Amylase/Ptyalin
 Chewing and Hydrochloric Acid are inversely proportional (Decreased Chewing = Increased HCl)
 Esophagus
o Lower Esophageal Sphincter – Prevents backflow
 Stomach – Digestion/Dilution of food
o Parietal Cell – HCl – Activates – Pepsin
o Gastric pH – 1.5 – 3.5
o Mucus Barrier – Protection
o Fundus – Upper Portion
o Antrum – Lower Portion
o Pylorus
 Pyloric Sphincter – Opens 2 – 3 hours after meal (Max. 5 hours)
 Gastric Emptying
o Carbs – Fastest
o Fats and Protein – Slow
o Fiber – Delays Emptying – Increase Satiety
 Small Intestine
o Duodenum – 1st portion
 Connected to Hepatobiliary
 Liver – Bile
 Gall Bladder – Storage of Bile
 Pancreas – Enzymes
nd
o Jejunum – 2 portion
 Absorption of nutrients
o Ileum – Absorption of Bile Salts and Vitamin B12
 Large Intestine – Absorption of Water
o Rectum – Very Vascular
 High Fiber – High Risk for Bleeding
Gastroesophageal Reflux Disease
 Cause:
o Weak LES
o Pyloric Stenosis Backflow – Gastric Contents
o Decreased Motility
 Clinical Manifestations: “Indigestion Burns your throat, larynx and esophagus”
o Dyspepsia: Nausea and Vomiting (Increased Saliva)
o Pyrosis – Heart Burn
o Globus – Feeling of fullness in the throat
o Laryngitis – Dry Cough and Hoarseness
o Dysphagia – Difficulty Swallowing
o Odynophagia – Painful Swallowing
 Intervention: “Food Should go Down”
o Avoid “5CAFPS” – Decreases Pressure of LES and GIT Irritants.
 Caffeine
 Citrus
 Cigarettes
  Carbonated
 Chocolate
 Alcohol
 Fatty/Fried
 Peppermint
 Spicy
o Diet:
 Carbs – High
 Fiber – High – Prevent Over Eating
 Meal – Small Frequent Feeding – 6 to 10 meals/day
o Position
 Head of the Bed – Elevated (30 – 45 degrees/Semi-Fowler)
 Turned to Left
o Avoid
 High Intra-Abdominal Pressure
 Low Motility
 Aspirin
 NSAIDS
 Anticholinergic/Antispasmodic – Atropine and Propantheline
 Calcium Channel Blocker
o Medications:
 Antacids
 Histamine 2 Blocker
 Proton Pump Inhibitor
 Prokinetics – Increase Motility
o Surgery: Severe
 Nissen Fundoplication – Narrow or Tighten LES
Peptic Ulcer Disease: Causative Agent: H. Pylori (Raw Meat)
 Drug of Choice: Metronidazole – Avoid – Alcohol it will cause Disulfiram-like Reaction
 Increased HCI and Pepsin
 Decreased Mucus Production = Decreased Protection
o Ex: Burn – Fluid Shifting (Edema) – Decreased Blood Volume – Decreased Blood Flow – Stomach
(Hypoactive) – Decreased Mucus = Curling’s Ulcer
 Factors:
o Stress – Chronic (Increased Acetylcholine/Increased PNS) – Vagus Nerve – Gastrin – Histamine 2 –
Parietal Cell – HCI
o Cigarette Smoking
o Alcohol Gastric Irritants
o Caffeine
o Aspirin and NSAID
o Zollinger-Ellison Syndrome – Pancreatic Tumor – Increase Gastrin – Increase HCI
o Irregular & Hurried Meals – Less Chewing = Increased HCI
o Type A Personality – Workaholic – Prone to Stress
o Type O Blood – Increased Pepsin
o Genetics – Increased Parietal Cell – High HCI
 Management:
o Monitor for signs of bleeding “Hematemesis and Melena” – NPO
o Diet:
 Milk – Avoid Large Quantity – Increase HCI
  Feeding – SFF – Less Food – Less HCI
 Chew – Slow and Thoroughly – Decreases HCI
 Foods – As tolerated; Acute/Painful = Bland
 Avoid Factors
 Stress Reduction – Rest and Relaxation
 Medications:
o Antacids (Starts with “Elements”) – Neutralize Acid – Decreases Acidity – Increases Gastric pH: 5
 Take – 1 – 2 hours after meal/chewable
 Aluminum Hydroxide – SE: “Ala tae” – Constipation
 Magnesium Hydroxide – SE: “Mag tae” – Diarrhea (Taken with Aluminum Hydroxide)
 Calcium Carbonate
 Sodium Bicarbonate – SE: Metabolic Alkalosis
o Histamine 2 Receptor Blocker “Tidine”
 Ranitidine – Decrease HCI
 Take – Bed Time
o Proton Pump Inhibitors “Prazole”
 Omeprazole – Decrease HCI
 Take – Before meal
o Hormone – Increase Somatostatin – Decrease Gastrin – Decrease HCI
 Octreotide
 Take – Before meal
 Used for ZES – Pancreatic Tumor – Increases Gastrin – Increase HCI
o Cytoprotective Drugs “Protect Fate”
 Sucralfate – Barrier/Coating
 Take – Before meal
o Prostaglandins – Decreases HCI and Increases Mucus (Other Use: Stimulates Inflammation and Uterine
Contraction)
 Misoprostol (Cytotec)
 Take – With meal
 Used if PUD is caused by NSAID
 Surgery
o Vagotomy – Decrease production of HCI – Decrease Acidity – Increase Gastric pH
o Gastrectomy – Decrease Parietal Cells – Decrease HCI/To Prevent Perforation
 Total – Esophagus is reconnected – small intestine
 Subtotal/Antrectomy – Removal of Lower Half (2/3)
o Anastomosis – “Reconnection”
 Billroth 1 – Gastroduodenostomy
 Billroth 2 – Gastrojejunostomy
Gastric Ulcer Duodenal Ulcer
Poor Man’s or Laborer’s Ulcer – Less Food Intake Executive Ulcer – Stress
20% Incidence 80% Incidence Most Common
Common in people 50 years old and above – Less Food Common in people 25 – 50 years old – Career Stage
Intake
Malnourish (Weight Loss) Well Nourished
Pain – ½ - 1 hour after meal (with food) Pain – 2 – 3 hours after meal (Empty)
Pain is triggered by food intake Pain is relieved by food intake
Pain relieved by vomiting Pain is common at night (Empty)
Nausea, Vomiting & Hematesis Melena
Dumping Syndrome: Rapid Gastric Emptying – Highly Concentrated food will be dumped (Hyperglycemia – Increase
Insulin – Post Prandial Hypoglycemia 1 – 2 hours after meal) – Small Intestine (Increase Concentration and Increases
Fluids) = Blood – Decrease Concentration – Decrease Blood Volume – Shock Like (30 mins. after meal)
 Small Intestine – Increase Fluid – Diarrhea – Increase Peristalsis – Increase Bowel Sound (borborygmi) = Crampy
Abdominal Pain
o Bloated/Distended; N and V
 Shock – Pallor
o Low BP – High HR – High RR (Hypo-Tachy-Tachy)
 Post Prandial Hypoglycemia – Diaphoresis
o Lightheadedness
 Management: “Food Should Stay”
o Diet:
 Protein – High
 Fiber – High
 Carbohydrate – Low (Simple)
 Meals – SFF
 Fluids – Avoid During Meals; “Drink in Between Meals”
 Salt, Sugar, Milk and Caffeine – Avoid
o Position: Lie Down 20 – 30 minutes after meal; Turn to left
o Medication – Anticholinergic/Antispasmodic
Diverticulosis: Outpouching of intestinal mucosa “Diverticula”
 Common Site: Sigmoid
 Cause: Decrease Fiber Diet – Constipation
Diverticulitis: Inflammation of 1 or more diverticula.
 Cause: Accumulation of fecal material
 Symptoms:
o Inflammation
 Abdominal Pain – Crampy, LLQ worsens when straining (Increase IAP)
o Infection
 Fever – High WBC
o Injury
 Blood in stool (Hematochezia)
o Obstruction – Increase GAS
 Bloating & Flatulence
o Chronic Constipation with episodes of diarrhea.
 Management:
o Diverculosis – Constipation
 High Fiber Diet
 High Fluid Intake
 Medication – Laxative
o Diverticulitis
 Acute Phase: Painful Episode – Goal is to decrease peristalsis.
 Fiber – Low
 Oral Intake – NPO
 Activity – Bed Rest
 Medication – Anticholinergic/Antispasmodic
 Monitor for perforation – Peritonitis – board-like rigid abdomen; Paralytic Ileus – Absent Bowel
Sounds
Appendicitis
 Cause: Fecalith – Obstruction of blood flow leading to injury – infection and inflammation
o Increase Peristalsis – Rupture (Sudden Relief of Pain) – Peritonitis (Diffused Pain)
o Client is positioned/turned to right side.
 Clinical Manifestation
o McBurney’s Point – 3 Point Pain (Umbilical Area, Ischial Spine, RLQ)
o Rovsing’s Sign – Palpate LLQ – Pain triggers in RLQ
o Dunphy’s Sign – Cough = Pain
o Blumberg’s Sign – Rebound Tenderness (Pain after release)
o WBC – High
o Bowel Sound – Decrease
o Psoas Sign – Left Lateral
 Right Leg Flexed Backward – Pain
o Obturator Sign – Supine
 Right Knee Flexed at 90 Degree – Pain
 Management: Goal – Decrease Peristalsis
o Oral Intake – NPO
o Fluids – IV
o Activity – Bed Rest
o Cold Compress
o Analgesics – Avoid
o Increase Peristalsis – Avoid
 Laxative
 Enema
 Heat Application
o Surgery: Appendectomy
 Deep Breathing and Coughing – Splint
 Dorsal Recumbent
 Drain – Turn to right – Increase Drainage
 Early Ambulation
 WOF: Evisceration
 Dehiscence
o Cover with moist sterile dressing – Report
Liver Cirrhosis: Repeated Injury – Hepatocytes – Fibrosis (Scarring) – Loss of Function
 Types:
o Laennec’s Cirrhosis – Caused by Alcohol (Most Common)
o Post Necrotic – Hepa B and C (Hepatotoxin)
o Biliary Cirrhosis – Obstruction – Gall Stone
o Cardiac Cirrhosis – Caused by Right Hearted Failure
 Clinical Manifestation:
o Metabolism of Nutrients:
 Weight – Malnourished/Weight Loss
 Appetite – Decreased/Anorexia
 Fatigue – Pain = RUQ
o Kupffer Cells: Malfunctioning Phagocytosis – Decreased Immunity – Infection
o Gluconeogenesis – Production of Glucose = Low
o Storage of Vitamins – ADEK (Fat Soluble) and B12 (Water Soluble)
o Removal of Hormones = Decreased
 Testosterone – Female – Virilization – Hirsutism and Menstrual Changes
  Estrogen – Male – Gynecomastia and Genital Atrophy
 Excessive Vasodilation – Palmar Erythema – Spider Angioma
o Decreased Albumin (Most Abundant Protein in the Blood) – Exerts Oncotic Pressure – Pulling Force –
Attracts Water
 Hydrostatic Pressure
 Increase Fluid in the Interstitial Space
o Edema
o Ascites
o Decreased Blood Volume – Triggers RAAS = Increases ADH – Fluid Retention
o Hemo (Iron) globin (Protein)
 Iron – Turns to Bilirubin – Processed in Liver = Bile (500 – 1000ml/day) Ingredients: Bilirubin and
Cholesterol – Gall Bladder – Contract – Duodenum (Bilirubin – Urobilin – Urine/Stercobilin –
Stool) – Emulsify Fats – Absorption of Vitamin ADEK – Clotting Factor
 Malfunctioned Liver – Increases Bilirubin – Skin = Jaundice accompanied by Pruritus –
Kidney – Dark Urine
 Emulsify – Fatty Stool – Steatorrhea – Absorption of Vit. ADEK – Clotting Factor = High
Risk for Bleeding
 Bilirubin – Urobilin and Stercobilin = Stool = Pale/Clay Colored
o Protein – Amino Acid – Increase Ammonia – Liver – Low Urea - Low BUN – Kidneys
 Increased Ammonia
 Neurotoxic
o Hepatic Encephalopathy – Asterixis (Flapping Tremor)
o Decreased LOC
o Constructional Apraxia (Inability to Draw 3D Shapes)
o Fetor Hepaticus
o Portal Circulation – Heart – GIT (Increase Fluid “Portal HPN” = Ascites – Caput Medusae – Hemorrhoids
– Esophageal Varices)– Liver (Portal Circulation) – Fibrosis – Obstruction – Increase Blood –
Hepatomegaly and Portal Hypertension = Low Blood Flow – Kidneys = Hepatorenal Syndrome
 Laboratory Test:
o Albumin (3.5 – 5g/dl)
 Low
o PTT or PT/INR (25 – 35 sec./11 – 14 sec/.8 – 1.2)
 Prolonged (High Risk for Bleeding)
o Serum Bilirubin (.03 – 1.9mg/dl)
 High (Jaundice)
o Aspartate Aminotransferase (AST/SGOT) (10 – 40u/l)
 High
o Alanine Aminotransferase (ALT/SGPT) (7 – 56u/l)
 High
o BUN (10 – 20mg/dl)
 Low
 Management:
o Decreased Body Weight
 Calories – High (Carbs)
 Procedure – TPN
o Low Bile
 Diet – Low Fat
o Decreased Vitamins
 Supplement – ADEK and B12
 o Low Immunity
 Avoid – Crowded and Visiting
o Fluid Status – Edema and Ascites
 Monitor – Daily Weight and Abdominal Girth
 Diet – Low Sodium
 Fluid Intake – Decreased
 Position – Semi Fowler’s
 DOC – Diuretics and IV Albumin
 Procedure – Paracentesis
 WOF: Shock
o Hepatic Encephalopathy (Increased Ammonia)
 Asterixis – Extend the Arm = Flapping Tremors
 Constructional Apraxia – Inability to draw 3D Shape.
 Decreased LOC – Monitor and Avoid Sedatives
 Fetor Hepaticus – Monitor Breath
 Diet – Limit Protein
 DOC
 Lactulose – Laxative – Increase Defecation – Decreases Ammonia
 Neomycin – Antibiotic – Decreases Bacteria (GIT) – Decrease Protein – Decrease
Ammonia
o Portal Hypertension
 DOC: Beta Blockers – Decreases Portal Pressure – Decreases Risk for Bleeding
 Procedure: “TIPS”
 Trans jugular Intrahepatic Portosystemic Shunt
o Esophageal Varices
 Avoid – Anything that increases pressure in the esophagus (Coughing, Spicy, Bending, Heavy
Lifting)
 Rupture – Balloon Tamponade – Application of Pressure to stop bleeding.
 Sengstaken Blakemore Tube
o Dislodged – Airway Obstruction – Scissor – Cut Two Balloon Lumen – To Deflate
 Liver, Gallbladder, Pancreas, and Bile Passage
o Gallbladder – Fats – GIT – Secretin – Gall Bladder – Contract – Bile
o Pancreas – Food – HCI – Activate – Pancreatic Enzyme (Digestion) Eg; Amylase (Carbs), Lipase (Fats),
Protease (Protein)
Cholecystitis – Inflammation of the Gall Bladder
 Type:
o Calculous – Gall Stone (Most Common)
o Acalculous – Caused by Injury, Surgery, Infection
 Cholelithiasis – Super Saturation – Bile – Cholesterol (Most Common) and Bilirubin/Pigment (Hemolysis)
o Factors: “5Fs”
 Fair – Caucasian
 Fat – Obese
 Female
 Fertile – Multi-gravid
 Forty Years Old
 Obstruction (Trapped Bile- Indigestion of Fats) will cause – Distention – Will Cause
Inflammation
 Clinical Manifestations
o Inflammation
 Biliary Colic – Severe Pain
 Murphy’s Sign – Supine – Nurse’s Hand – Hepatic Margin – Inhale – Pain
 Abdominal Pain – RUQ and Guarding
 Rebound Tenderness
 Radiating – Right Shoulder
 Usually after a fatty or heavy meal
o Indigestion – Fats – Increase GAS
 Nausea and Vomiting
 Belching
 Flatulence
o Obstruction
 Skin – Jaundice and Pruritus
 Stool – Pale/Clay and Steatorrhea
 Urine – Dark
 Vitamin Deficiency – Decrease Vit. K – High Risk Bleeding
o Infection
 Fever – Increase insensible fluid loss.
 Dehydration
 Management:
o Acute Phase – Goal – Decrease GIT
 Oral Intake – NPO
 Fluids – IV
 N&V – NGT – Decompression
 Medication – Anticholinergic/Antispasmodic
o Diet
 Fat – Low
 Meal – SFF
 Gas Forming Foods – Avoid
o Medication – Mild Cases – To Dissolve the Stone
 Ursodeoxycholic Acid (UDCA)
 Chenodeoxycholic Acid (chenodiol or CDCA)
 Surgery:
o Cholecystectomy
o Choledocholithotomy – Removal of Stone (Common Bile Duct)
o T-Tube
 Position – Semi-Fowler’s
 Drainage
 Below
 Color – 1st 24 hours = Red; after 24 hours – Brown or Green
o WOF: Abnormal – Report
 Amount – 500 – 1000ml/day – Abnormal – Report
 Irrigation, Aspiration and Clamping – As prescribed
 Before Meal – Clamp
 WOF: N&V/Abdominal Cramps – Unclamp – Report
Acute Pancreatitis:
 Cause: Alcohol and Gall Stone – Obstruction – Trapped P.Enzyme – Autodigestion – Bleeding – Inflammation
o Inflammation
 Pain – LUQ, Guarding and Radiating at the Back
 Aggravated By:
 Diet – Fat
 Beverage – Alcohol
 Position – Recumbent (Flat)
 Bowel Sound – Decreased
 N&V – Indigestion
o Bleeding
 Dehydration
 Weight Loss
 Cullen’s and Grey Turner’s Sign
 Laboratory Findings:
o WBC – High
o Glucose – High
o Bilirubin – High
o Alkaline Phosphate – High
o Serum and Urinary Amylase – High (Parameters for Recovery)
o Serum Lipase – High (Parameters for Recovery)
 Management: Food – HCI – P.Enzyme – Injury
o Acute Phase – Goal – Decrease GIT
 Oral Intake – NPO
 Fluids – IV
 Nutrition – TPN
 N&V – NGT – Decompression
 Medication – Anticholinergic/Antispasmodic
o Medication
 H2 Receptor Blocker
 Proton Pump Inhibitor
 Both are 1st line – to decrease HCI – Decrease P.Enzyme – Decrease Injury
 Morphine – Analgesic
 Avoid – Demerol – Cause – Seizure
Chronic Pancreatitis: Repeated Injury – Healing – Fibrosis – Loss of Function – Decrease P.Enzyme and Insulin
 Inflammation
o Abdominal Pain - LUQ
 Fibrosis
o Mass – LUQ
o Calcium – Low (Hypocalcemia)
 Loss of Function
o Weight – Loss
o Bilirubin – High
o Stool – Steatorrhea
o Glucose – High
 Management:
o Diet
 Food – Bland and Avoid Gastric Stimulant
 Meals – SFF
  Fat – Low
 Protein – Low
 Calorie – High (Carbs)
o Medication: “Same with acute”
 Pancreatin
 Pancrelipase – Less grease on stool – Negative Steatorrhea
 Insulin and OHA – For Hypoglycemia and DM