GASTROINTESTINAL DISORDERS

Esophagus
- Passageway of food
Stomach
- Digestion of food
- 90 mins.
Sphincter
- Between esophagus and stomach
- For the food not to backflow
- Lower Esophageal Sphincter (LES)/Gastroesophageal Sphincter (GES)/
Or Cardiac Sphincter (CS)
o Cardiac: located near the heart
Antrum
- Inferior part of stomach
- Site of gastric ulcer
Pyloric Stenosis
- Between stomach and small intestine
- Should be closed after passing the food for it not to back flow
- Blockage (muscle): Olive shape mass
o Projectile vomiting (Increase pressure on the stomach)
 Vomit food with acid because it came from the stomach
 Non-bilious

*Intussusception - bilious vomiting

Small Intestine
- For absorption of nutrients
o Duodenum
o Jejunum
o Ileum

Accessory organ:
Liver - produce bile
Gallbladder - connected toward duodenum
-bile go towards duodenum
Large Intestine
- For absorption of water
Secum → ascending colon → transverse colon → descending colon → sigmoid
colon → rectum → anus → fecal matter

Etor, Evamie L.
Ileostomy
- Attached to ileum
- Food will not go to large intestine anymore
- Watery stools
- Prone to dehydration: Fluid Volume Deficit
Colostomy
- Attached to sigmoid or descending colon
- Dry waste: The food passed from colon

GASTROESOPHAGEAL REFLUX DISEASE (GERD)

- Backflow of gastric contents into esophagus
- Can cause cancer
o Barret Esophagus: Damage of lining of esophagus
 Esophageal Adenocarcinoma

Problem: weak sphincter

Cause: weak LES

Assessment:
- Common sign: Heartburn (Pyrosis)
- Pain: same with MI
o Substernal pain: Chest pain because of acid
 GERD pain location: Substernal chest pain feels like a “heart attack”
 Regurgitation: Sour-taste because of acid
 Dysphagia (difficulty swallowing) /Odynophagia (Painful swallowing): Stricture
 Aspiration: Trigger cough
o Asthma in adult: caused by GERD
 Asthma (Adult onset)
 Cough
 Damage of tooth enamel: because of constant exposure to acid

Diagnostic Test:
1. Esophagogastroduodenoscopy
- Can have sore throat after the procedure
- Patient will be sedated: Drowsiness
- Pre: 8hrs. NPO
- Post: After 4hrs, sips of water
 WOF:
>Aspiration: Because patient is sedated
>Signs of Peritonitis: Because of possible puncture

*All procedure from mouth: Should be NPO

*All procedure from anus: Enema

2. Upper GI Contrast
- From mouth to duodenum
- Givig dye
- Ingestion of contrast/barium then do Xray after
o Barium can cause constipation
- Pre: 8hrs. NPO
- Post: no drowsiness (not sedated), increase Oral Fluid Intake

*Stomach has parietal cell

Entrance:
1. G receptor: Gastrin
2. H2 receptor: Histamine
3. M receptor: Muscarinic Acetylcholine receptor
- or parasympathetic where acetylcholine bind
*Sympathetic: nore/epi
Exit:
Proton Pump or H/K ATPhase
o Stimulus: food

Etor, Evamie L.
Interventions:
Goal
- for food to go down
- no food that can low motility (fat)
- ↑ fiber for fast/increase motility

1. ↓ fat, ↑ fiber diet

- Fat slows gastric motility
2. Elevate HOB (6-8 blocks)
3. Drugs:
Goal: ↓HCl in the stomach
a. PPI
o Drug of choice
o Block the exit
o No exit of acid
o ↓acid/few: cannot digest the food
o Block HK ATPhase
o “prazole” meds

Ex: Omeprazole, Pantoprazole

- Give 30 min-1hr before breakfast
- S/E: Malabsorption: ↓ B12, Ca
 B12 is a component to make Hemoglobin
- WOF: Anemia & Fracture

*Vagus nerve – releases acetylcholine

*Vagotomy – block vagus nerve

b. H2 Receptor Blocker
o Block the H2 receptor
o Can still produce acid
o “tidine” meds

Ex. >Cimetidine: can cause gynecomastia/Endocrine S/E

>Famotidine
>Ranitidine
- Give before meals
- Acid can still exist
c. Antacids
o Neutralizes gastric acid
o Contains alkaline ions

Ex. >Aluminum Hydroxide (Amphojel)

-S/E: Constipation
>Magnesium Hydroxide (Milk of magnesia)
-S/E: Diarrhea
>Aluminum-Magnesium Hydroxide (Maalox) (Simethicone)
-can avoid the S/E of the 2 meds above
-give after meals

Etor, Evamie L.
Surgery:
- Cut the fundus & connect to Lower Sphincter, so the sphincter is no longer
weak.
- Nissen Fundoplication
o Wrapping the fundus around the lower esophagus
- Position: Right side-lying when sleeping

Avoid:
o Fatty foods: can slow down motility
o Alcohol
o Chocolate\coffee
o Smoking
o Peppermints
o Food/drinks 2hr before HS: can cause regurgitation
o Tight clothes: can compress stomach
o NSAIDS: can increase gastric acid
- Blocks chemicals (prostaglandin) that stimulate pain in the body

Prostaglandin
-an advantage in stomach
-gastric protectant
-rule: ↑HCO3 in the stomach (Alkaline)

*Wine – gastric irritant

*Coffee – okay for pregnant: 200mg/2cups

Etor, Evamie L.
 PEPTIC ULCER DISEASE

Gastric Peptic (↑acid)

o weakened stomach muscle o Wound in the duodenum
because of the wound. o Too much/high acid w/out wound in
o Pain when eating the stomach
o When vomits, pain fades away o Pain fades away when eating
o Pain in daytime because the acid is used for
digestion
o Pain in night
o Pain on empty stomach
Location
o Lesser Curvature of Antrum o Anterior duodenum
Patho
o Weak gastric mucosa o ↑HCl
o ↓HCO3
Cause
H. Pylori, NSAIDS
Zollinger-Ellison Syndrome, Smoking, Stress
Malignancy
o Common cancer because of o Rare
weakened muscle
Pain
o 30 – 60 mins. after meals o Empty stomach
o Daytime o 90 mins. – 3hrs. after meal
o Night time
Relief
o After vomiting o After eating
Site of Pain
o Left of the mid-epigastric area o Right of the mid-epigastric area
Complication
o Gastric Cancer o Acute Pancreatitis

Diagnostic Test:
1. Esophagogastroduodenoscopy
- best test for UGI Bleeding
2. Upper GI Contrast
3. Urea Breath Test
- Urea: Produce by H. Pylori
- Test to see the bacteria (H. Pylori)
4. Stool Culture
- To detect H. Pylori antigen

Complications:
1. Bleeding (most common)
- UGB: Dark red
- Most common complication
- Melena
- Hematemesis
2. Perforation
- There’s a hole already
- Constant pain, radiate to back
3. Peritonitis
- Inflamed
- Rigid, board-like abdomen
- Fever, leukocytosis (↑WBC)

Etor, Evamie L.
 *bleeding → bleeding → perforation → peritonitis

Intervention:
Drugs:
1. PPI
2. H2 Receptors
3. Antacids
4. Mucosal Protectant: Because of the wound
a. Sucralfate
-protecting coating on the ulcer
-give before meal
-take 1hr before meal
b. Bismuth Salicylate
-protective coating
-before meals: but can eat right after
-S/E: Darkening of tongue
c. Misoprostol
-activates prostaglandin: reason why there’s pain
-bicarbonate and mucus production
-S/E:
o Uterine Contraction
o Miscarriage
o Diarrhea

*Methotrexate – meds for ectopic pregnancy

Triple Therapy 14 days:

PCA
- Any PPI
- Clarithromycin 500 mg BID
o All meds end “thromycin” can cause diarrhea
- Amoxicillin 100 mg BID

*1st gen: Ceph

*2nd gen: Cef + vowel
3rd gen: Cef + consonant

Surgery:
1. Total Gastrectomy (anastomosed to remaining portion)
- Removal of entire stomach
2. Vagotomy
- Dissection of vagus nerve

Billroth I:
- Upper portion + duodenum is connected
- Gastroduodenostomy:
-Distal portion of stomach is removed
-Anastomosed to duodenum
Billroth II:
- Aka Gastrojejunostomy
- Removal of distal portion of stomach
-anastomosed to jejunum

Post-op:
1. Diet: NPO:
- clear liquid: Cathedral (Jello) → full liquid
2. Monitor for complications:
o Bleeding
o Vit. B12 Deficiency
o Hypoglycemia

Etor, Evamie L.
 o Dumping Syndrome

DUMPING SYNDROME
-rapid emptying of gastric contents

Goal:
-slow down of food/motility
-↓fiber, ↑fat

Cause: Gastric resection

Assessment:
 Symptoms occur 15-30 mins. after meal
 N/V
 Abdominal pain
 Diarrhea
 Tachycardia
 Perspiration

Interventions:
1. No sugar, dairy & salt
a. -sugar: can ↑motility
b. -dairy: protein
2. Eat high in fat, low carb
3. Lie down after meals: Diversion of gravity to slow down motility
4. Avoid fluids during meals
5. Teach to eat small frequent feeding

HIATAL HERNIA
-like GERD
-part of the stomach herniates through diaphragm

Risk Factors:
o ↑ Abdominal pressure: The stomach herniates when the pressure is high
o Straining
o Heavy lifting
o Obesity
o Pregnancy
o Aging: The weaker of diaphragm

Assessment:
-same with GERD

Surgery:
o Hiatal Hernia Repair
+
o Nissen Fundoplication

VITAMIN B12 DEFICIENCY

-lack of Intrinsic factor
o Aka Pernicious Anemia
o Most common cause
-Lack of B12 Intake
o Absorb in the last part of the intestine (ileum)

Parietal cell
-secrete intrinsic factor
-go with the B12 in ileum
- B12 is need to make myelin sheath in neurons
Etor, Evamie L.
 -No stomach → no parietal cell → no intrinsic factor → no B12 absorption
-B9 & B12
- need to make hemoglobin
- Both: Anemia → macrocytic anemia: The RBC has no hemoglobin

B9 B12
o No neurologic signs o Has neurologic signs
o Folic acid o Cobalamin
o Green leafy vegetables
Absorbed
Jejunum Ileum
Deficiency
o Macrocytic
o Megaloblastic anemia
o Spinal cord degeneration
o (+) neurologic signs because of
myelin sheaths

*B12 food: animal products

Assessment:
 Pallor
 Numbness: B12 deficiency
 Paresthesia: B12 deficiency
 Difficulty walking
 Beefy red tongue

Diagnostic Test:
o Schilling’s Test
- To determine the cause

Interventions:
1. If lack of intake, give:
 Liver
 Organ meats
 Poultry, eggs, milk products
 Citrus fruits
 Grenn leafy vegetables
2. If no intrinsic factor, give:
 Lifelong monthly Vit. B12 injection (IM route): 90⁰ angle

APPENDICITIS
-inflammation of the appendix
o r/t obstruction of appendiceal lumen
-part of the lymphoid organ
-producing lymphatic fluid: for fighting infection
o should be drain upward

Cause:
 anything that can obstruct
 fecalith (most common): obstruct appendix
 hypertrophy of the lymphoid tissue
 seeds
 intestinal worms

Etor, Evamie L.
 Continuing Secretion of Appendiceal fluid
Pathophysiology:

Lumen Obstruction

Bacterial Multiplication

Inflammation of the

Acute Appendicitis

Progressive distention r/t infarction & periappendiceal abcess

Perforation

Assessment:
 Periumbilical pain
 McBurney’s Point
o -pain from umbilicus to RLQ
 Anorexia
 Murphy’s triad
o -abdominal pain
o -vomiting
o -fever
 Rovsing sign
o -pain of RLQ when LLQ is palpated

Report
 Rigid board-like
 Distended abdomen
 Increase pain
 High fever
 Diminished bowel sound

Avoid
 Hating pads or hot compress
 Enema
 Laxatives
 Pain reliever: it can mask any pain

Diagnostic Test:
1. CT scan (best test)
2. CBC (Leukocytosis)
3. Ultrasound
- wall thickening with periappendiceal fluid
- most sensitive

Interventions:
1. Non-surgical method
 Antibiotics: to relieve infection
 Fluids
 Bowel rest
 Percutaneous drainage
2. Surgical
 Open Appendectomy: RLQ incision
 Laparoscopic Appendectomy: fewer surgical site infections (SSI)

LIVER CIRRHOSIS
Etor, Evamie L.
 - “Bantok”
- Degeneration & destruction of hepatocytes
- Formation of scar
- All blood from the GI tract ends at the liver by the use of portal vein
- All food nutrients & even chemical ends at the liver
- Blood cannot enter the liver; it stays in portal vein
↓
↑ pressure
↓
portal hypertension
↓
backflow of blood to esophagus (esophageal varices): risk for rupture
↓
Some blood goes to abdomen: Ascites – visible veins

- CHON: ↑ammonia (fat soluble)

o Convert by the liver into urea
o Ammonia travel to brain (because the liver is damage): Hepatic
Encephalopathy

Cause:
- Chronic Injury of the liver
- Schistosomiasis /Hepatitis

Bile Duct System

 Liver
o Produce bile
 Bile
o For fat emulsification (“dugmokon”)
-including the fat-soluble vitamins: ADEK
 When there’s obstruction in the hepatic duct, bile go back to liver & circulate into
blood & into skin
o Jaundice: pruritis
 When fat is in duodenum, the duodenum releases cholecystokinin to signal the
gallbladder to release the bile by contracting.
 Bile in the duodenum can go to kidney & will give color to the urine as yellowish
o Dark orange urine: Gallstone
o Clay-colored stool: no bile in the duodenum that give its color because of
gallstone
 When gallstone is in the Sphincter of Oddi, there’s no enzymes will be release from
pancreas because of obstruction. The enzymes in the pancreas will auto digest
(“malata”)
Pancreas
Etor, Evamie L.
  Exocrine: secrete enzymes
1. Lipase: fats
2. Amylase: carbs (CHO)
3. Trypsin: Proteins
 Endocrine
1. Alpha cell: glucagon
2. Beta cell: Insulin

Bile Duct Physiology

- Bile originates from RBC
- RBC: 1-3 days lifespan

RBC destruction

Hemoglobin

Heme Globin

Unconjugated Bilirubin “Hilaw”

Indirect bilirubin
Go to liver (conjugation) “lutuon”

Conjugated bilirubin Direct bilirubin

Delivered in gallbladder

Bile (called when it’s in gall bladder

Liver Cirrhosis: ↑ indirect bilirubin/unconjugated

Gallbladder problem/Gallstone: ↑ direct bilirubin/conjugated

Main function of the liver:

 Production of bile
 Protein Synthesis
o No protein can cause edema (↓ protein)
o Protein: Pull force of water from interstitial to intravascular (oncotic pressure)
o No protein: water is in interstitial
 Give albumin then 1hr after, administer furosemide
 Clotting factors
o ↓Vit. K
o Prone to bleeding
 Detoxification
 Stores sugar
 Metabolizes estrogen

Etor, Evamie L.
 Assessment:
1. Portal Vein Hypertension
o ↑ pressure of portal vein
o Due to ↑ intrahepatic resistance
S/Sx:
 Ascites
 Splenomegaly
 Portosystemic Shunts
- Esophageal varices: risk for bleeding
- Caput medusae
- Hemorrhoids
o Hepatorenal Syndrome
2. Esophageal Varices
o Distended esophageal vein that may rupture
- Give vasopressin (Very potent vasoconstrictor)
-to prevent further bleeding
3. Coagulation defects
o Decrease absorption of fat-soluble Vitamins (ADEK)
o Decrease production of clotting factors
4. Jaundice
o r/t inability to conjugate bilirubin
5. Hepatic Encephalopathy
o r/t inability of liver to detoxify toxins such as ammonia
S/Sx:
 Asterixis: hand flapping tremors
 Decrease LOC
 Coma
6. Hepatorenal Syndrome
o Everytime there’s portal hypertension, rena artery will constrict
o Renal Hypertension
↓
Renal Vasoconstriction
↓
Decrease blood flow to kidney
↓
Hepatorenal Syndrome
7. Hyperestrinism
o Elevated estrogen
S/Sx:
 Gynecomastia
 Spider angioma
 Palmar erythema

Diagnostic Test:
1. Liver Biopsy: Confirmatory test
2. SGPT (ALT) - ↑
3. SGOT (AST) - ↑
4. Indirect Bilirubin - ↑
5. PTT/PT - ↑
o Warfarin: PT
o Heparin: PTT
6. Pancytopenia
o ↓ WBC, ↓ RBC, ↓ Platelet
7. Abdominal Ultrasounds

Etor, Evamie L.
Interventions:
1. Nutrition
o Give high biologic protein
o No to protein restriction
2. Lactulose
o To defecate
o DOC for H.E (best drug)
o Goal: 2-3 soft stools/day
3. Antibiotics
o Neomycin 250 mg BID
o Metronidazole 500 mg BID

Procedures:
 Esophagogastric Balloon Tamponade (Sengtaken Blakemore Tube)
o Balloon: compress and anchor
o To control esophageal & gastric varices
o Prepare a pair of scissors
o Respiratory distress: Cut all balloon lumen & remove the tube

ACURE PANCREATITIS
-sudden inflammation of pancreas
-most common cause is pancreas
-autodigestion
-priority is hydration

Cause:
 Gallstone (most common)
 Alcoholism
 Viral/Bacterial infection
o Mumps is most common
 Trauma
 Epigastric abdominal pain
o Radiates to the back
o After a fatty meal, enzymes cannot go out from pancreas because of
gallstone
o Tenderness & guarding\
 N/V
 Weight loss
 Elevated serum lipase (stay longer in blood) & amylase
o Normal serum lipase: 0-160 U/L
o Normal serum amylase: 30-100 U/L
 Cullen’s sign
o Bluish discoloration of the periumbilical area
 Turner’s sign
o Bluish discoloration of the flank

*Priority is fluid resuscitation

Complication:
1. Shock!!!
- Due to pancreatic hemorrhage (“nalata”)
2. Pseudocyst
- Presents as abdominal mass
- Prone to rupture
- Due to inflamed pancreas
3. DIC (Disseminated Intravascular Coagulation)
- All platelet and clotting factor are used up
4. Hypocalcemia
- Once there’s steatorrhea, calcium will also go out together
5. Diabetes Mellitus

Etor, Evamie L.
 6. ARDS (acute respiratory distress syndrome)
- Pancreatic enzymes damage the alveoli
Intervention:
1. Fluid Resuscitation
2. Address the pain
o Meperidine (Demerol)
- DOC for pancreatitis
- Opioid analgesic
- Disadvantage:
-if not eliminated (defecate/urinate), it can cause seizure to patient
with impaired kidney function.

*Morphine: can cause spasm of Oddi

3. Nutrition
o NPO during acute pain
o IV Hydration
o Parenteral nutrition
o NGT for gastric decompression
4. Infection
o Antibiotics
C – Ceftriaxone
I – Imipenem
A – Ampicillin

Procedure:
 ERCP (Endoscopic Retrograde Cholangiopancreatography)
- Uses endoscopy & Xray
- Injects dye in the bile duct &pancreatic duct
- Both diagnostic & therapeutic
- Note: NPO before the test
- Test

CHOLECYSTITIS
- inflammation of gallbladder
- r/t gallstone (cholelithiasis)

Cause: bacteria (acalculous cholecystitis)

Pain: after a fatty meal because the gallbladder contracts, there’s inflammation (painful)

Gallstone: made up of fat & cholesterol

Risk factors:
 ↑ Fat
o the more fat, the more estrogen
 Forty
o end point of fertility
o beyond is not risk
 Fertile
o The more fertile, the more estrogen
 Female
 Family history
 Pregnant

Diagnostic Test:
1. Abdominal ultrasound
- The best test for Gallstone
2. Oral Cholecystogram
- Dye + Xray to see the stone

Etor, Evamie L.
Assessment:
 RUQ Pain
o after a fatty meal
 Murphy’s sign
o breathing stops upon RUQ palpation
 Boa’s sign
o Pain radiates to the tip of right scapula
 Ortners sign
o Pain when palm taps the edge of Right Costal Arc (RCA)
 Guarding
 Fever
 N/V

Signs & symptoms:

 Jaundice
 Clay-colored urine
 Dark orange urine
 Pruritus
 Steatorrhea

Interventions:
Pre-op:
 Low fat diet
 If severe N/V & Pain
o NPO
o Nasogastric decompression: to remove the gastric content
Surgery:
1. Cholecystectomy
- Removal of gallbladder
2. Choledocholithotomy
- Incision of Common Bile Duct to remove the stone

T-tube
- to preserve the patency of the duct
- after cholecystectomy, there’s post-op blood that would possibly clot; t-tube is
attached to drain the blood
- to retain the patency
- Drainage: with blood is normal with some bile in 1st 24hrs

Care of T-tube:
1. Maintain semi-fowler position
2. Monitor output
1st 24hr
o ≤500ml (bloody)
o Beyond: report to physician
2 – 3rd day
nd

o ≤200ml/day (green brown)

o Beyond: report to physician
3. Assess for skin irritation
4. Avoid: Irritation, Clamping, Aspiration without doctor’s order
o The nurse will just empty the bag & record the drainage
5. Clamp 1-2hr before & after meal

Etor, Evamie L.