GASTROINTESTINAL DISORDERS

• Sigmoid
DIGESTIVE TRACT • Rectum (vascular)
→ AKA alimentary canal o If high risk for bleeding → invasive
→ Starts in the mouth procedures are contraindicated
• Mechanical digestion (mastication/chewing) • Anus (opening)
• Chemical digestion (salivary amylase to break
down starch into sugar) Quadrants
o Mechanical and Chemical Digestion is → Pancreatitis - LUQ
inversely proportional → Liver and gallbladder - RUQ
▪ ↓chew = ↑HCL → Appen - RLQ
▪ ↑chew = ↓HCl → Rectum - LLQ
→ Upon swallowing, food reaches the esophagus → Sigmoid - LLQ
• Dysphagia
→ Lower Esophageal Sphincter/Cardiac Sphincter Assessment:
• Ensures downward and prevents reflux, → IAPePa
regurgitation → To get an accurate assessment on bowel sounds
• GERD auscultation is done first → any pressure to the
→ LES closes once food reaches the stomach abdomen will cause changes/alter to the peristalsis or
• Stomach can be divided into two: bowel sounds
o Fundus - upper portion
o Antrum - lower portion GASTROESOPHAGEAL REFLUX DISEASE (GERD)
▪ Antrectomy - removal of the distal portion → Weak LES
of the stomach • Anything that may decrease LES pressure, inc
• Stomach has parietal cells which produces HCl to HCl
dilute food and intrinsic factor which absorbs vit b • Substances to Avoid: (5CAFPS)
12 o Coffee
o Pernicious anemia if intrinsic factor became o Citrus Fruits
dysfunctional o Cigarette Smoking
o HCl is acidic (ph 1.5 - 3.5) o Carbonated Drinks/Cola
→ Pyloric Sphincter opens around 2-3 hours (gastric o Chocolate
emptying) o Alcohol
• But depends on the content of food: o Fatty foods
o Fastest to digest: carbohydrates o Peppermint
o Fats and proteins stays longer in the stomach o Spicy
→ Small Intestine → Backflow, regurgitation, and reflux of gastric contents
• Duodenum connected to the hepatobiliary tract into the esophagus
o Pancreas → pancreatic enzymes → Signs and Symptoms:
▪ Amylase → breaks down carbohydrates • Pyrosis (heartburn) burning sensation after eating
▪ Lipase → breaks down fats • Nausea and Vomiting + Hypersalivation
▪ Trypsin → breaks down protein • Dyspepsia or Indigestion
o Liver → produces bile (stomach contents that • Dysphagia (difficulty swallowing)
would enter the small intestine should be • Injury because esophagus has no mucosal layer
water soluble → fats are needed to be → Odynophagia
emulsified (to go along with the water) → bile → Management:
would be the emulsifier) • “Food should go down”
o Gallbladder → storage of bile • High carbs, low fat, low protein diet
• Jejunum absorbs nutrients • High fiber diet → increase feeling of fullness
• Ileum absorbs bile salt and vitamin b12 (satiety) → prevents overeating
o ↓absorption of bile salt → steatorrhea (foul • Small frequent feeding
smelling) → stool will be more dense • Position: Upright → elevate HOB and turned to left
(lumulutang) → esophagus will be above → food will not
o Resection of the ileum → dec vit b12 regurgitate
absorption → pernicious anemia • Avoid anything that may increase pressure in the
→ Large Intestine absorbs water and formation of stool or abdomen
feces o Do not bend after eating
• Peristalsis (movement of the colon) o Do not wear tight clothing
o Is directly proportional with bowel sounds o Avoid heavy lifting
▪ ↑peristalsis → ↑bowel sound → irritation o (X) Obesity
of the intestine → diarrhea → Medication:
▪ ↓peristalsis → ↓bowel sound → • Avoid medications that increases HCl
constipation o E.g. NSAIDS, Aspirin
▪ (+) pain → decreased peristalsis • Antacids
o Is indirectly proportional with absorption of • Proton Pump Inhibitor
water • Histamine 2 blocker
▪ ↑peristalsis → ↓absorption of water → • Prokinetics (meds to increase motility) for food to
stool will be wet (diarrhea) descend
▪ ↓peristalsis → ↑ absorption of water → o Metoclopramide
stool will be dry (constipation) • Antiemetics
o Immobility will cause decrease peristalsis → Fundoplication
resulting to constipation • Fundus is wrapped around the LES
▪ Advice the patient to exercise to increase → Diagnostics
peristalsis → Endoscopy
• Ascending Colon → Checking of gastric pH
• Transverse Colon
• Descending
PEPTIC ULCER DISEASE
→ Related to low food → Career stage
Causes: intake
1. Helicobacter pylori → from raw meat → burrows in the
GIT → causes ulceration Malnourished (weight loss) Well nourished
• DOC: Metronidazole
o Should not be mixed with alcohol → disulfiram → Pain - ½ - 1 hour after → Pain - 2-3 hours after
like effect/reaction meal (with food) meal (empty)
2. ↑HCl and ↑Pepsin → Pain is triggered by food → Pain is relieved by food
3. ↓mucus → ↓protection intake intake
→ Pain relieved by → Pain is common at night
• Burn injury → fluid shifting → edema → dec blood
vomiting (pressure is (empty)
volume → dec blood flow to the stomach → less relieved)
production of mucus → curling’s ulcer
Nausea, vomiting and Melena
Pathophysiology: hematemesis

Management:
→ Monitor for signs of bleeding
→ Anything that can cause perforation or rupture →
peritonitis (compilation)
→ Signs and symptoms:
• Board like and rigid abdomen
→ Diet:
• Avoid milk → causes hyperacidity
o Milk can also increase ph → alkaline →
stomach will try to return acidity of the
stomach by ↑HCl
• Small frequent feeding
• Chew food properly
• Foods as tolerated; not bland
→ Avoid risk factors
→ Stress reduction
• Any form of rest/relaxation

Medications:
→ Antacids
• Neutralizes acid
• Taken 1-2 hrs after meal
→ Vagotomy: (X) vagus nerve → low production of HCl • If empty stomach → longer duration
(decrease stimulus for the production of HCL) • Aluminum Hydroxide (phosphate binder for
→ Histamine 2 blocker → (x) proton pump → ↓hcl hyperphosphatemia)
production o To be taken with meals
→ Proton pump inhibitor → ↓HCL production o WOF: constipation
→ Octeroride → mimics the action of somatostatin → • Magnesium Hydroxide
↓gastrin → ↓histamine → ↓HCl o WOF: Diarrhea
• Aluminum Magnesium hydroxide
Factors: • Calcium Carbonate
→ Stress • Sodium Bicarbonate
• ↑acetylcholine → ↑HCl o Can cause metabolic alkalosis
→ Cigarette Smoking o Can enter bloodstream
→ Alcohol → Histamine 2 receptor blockers
→ Caffeine • Ranitidine
→ Aspirin and NSAID • Taken at bedtime
• ↑HCL → Proton Pump Inhibitors
→ Zollinger - Ellison Syndrome • Omeprazole
• Pancreatic tumor → ↑gastrin → ↑HCl • Taken before meals
→ Irregular and Hurried Meals → Cytoprotective Drugs
• Dec chewing → ↑HCl • Sucralfate
→ Type A personality • Coats the stomach; acts a protective barrier
• Workaholic → prone to stress → Prostaglandins
→ Type O blood • Misoprostol
• ↑pepsin level • Dec HCl, ↑mucus, for inflammation, induces
→ Genetics uterine contraction
• ↑parietal cells → ↑HCl non • Contraindicated to pregnant → abortifacient
→ Hormone
• Octreotide
GASTRIC ULCER DUODENAL CANCER • Increases somatostatin
Poor Man’s or Laborer’s Executive Ulcer
Ulcer → Related to stress The cause of peptic ulcer is NSAIDS, which medications
→ Related to low food will you give?
intake A. Histamine 2 receptor blocker
B. Proton Pump Inhibitor
20% incidence 80% incidence C. Cytoprotective Drugs
D. Prostaglandin
Common in people 50 yrs Common in people 25-50 ● NSAID is an anti-inflammatory → antiprostaglandin
old and above yrs old ● WOF: pregnant, do not give Misoprostol
Surgery: • Chronic constipation with episodes of diarrhea
1. Vagotomy
• To dec stimuli for the production of HCl Management: (Diverticulosis)
2. Gastrectomy 1. High fiber Diet
• Before imperforation happens / removal of parietal 2. Increase fluid intake to counter constipation
cells 3. Medication: Laxative to move bowel
• Total - usually done on gastric cancer
• Subtotal/Antrectomy - removal of the lower half of Acute Phase: “painful episodes” (priority is to rest the
the stomach bowel) → dec peristalsis (Diverticulitis)
3. Anastomosis: → Low fiber diet
• Billroth I - gastroduodenostomy → Oral Intake
o Reconnect the stomach to the duodenum • Patient will be placed on NPO status
• Billroth II - gastrojejunostomy → Activity
o Done If the damage in the duodenum is • Bed rest
extensive → Medication
o Rapid gastric emptying → dumping syndrome • Antispasmodic/Anticholinergic
• Propantheline
DUMPING SYNDROME → Monitor for perforation
• Complication: Peritonitis

APPENDICITIS
→ Appendix is found on the cecum
→ Where fecalith could be dislodged d/t irregular bowel
pattern → obstruction → injury → necrosis →
infection → inflammation sets in → inc peristalsis →
rupture (sudden disappearance of pain) → peritonitis
(diffused pain)
→ Management: (To dec peristalsis)
• NPO status
• IV fluids
• Bed rest
• Avoid enema, hot application, laxatives
• Position: dorsal recumbent, knees flexed
• Appendectomy:
o If the patient will cough, instruct them to splint
to prevent dehiscence or evisceration
▪ Cover with gauze soaked with NSS
→ Clinical Manifestations
• McBurney’s Point – RLQ
Management:
→ Food should stay in the stomach
1. Diet
o High fat, high protein, low carb
o Small frequent feedings
o Avoid fluids during meals
▪ Should be in between meals
• Rovsing’s Sign
o Avoid salt, sugar and milk
o Pain elicited in the right lower quadrant when
2. Position:
pressure is applied on the left lower quadrant
o Supine
• Dunphy’s Sign
o Left Side Lying → food will be pulled in the
o Pain is triggered when coughing d/t inc
stomach → will not descend immediately
intraabdominal pressure
• Blumberg’s Sign
DIVERTICULOSIS
o Rebound tenderness → pain is felt upon
→ Asymptomatic
release
→ Outpouching of intestinal mucosa
• Inc WBC
→ Common site: Sigmoid Colon
• Bowel Sound
→ Cause: low fiber diet → constipation
o Decreased or absent
• Reversible through dietary modifications
• Psoas’ Sign
→ ↑pressure in the intraluminal/wall of the colon →
o Left-side lying while the right leg is flexed
weakening of the wall of the colon → outpouching →
backward → triggers pain because iliopsoas
trapping of stool → obstruction → injury → infection
stretches and hits the appendix
→ inflammation
• Obturator Sign
o Supine position while knees are flexed at 90
DIVERTICULITIS
degrees → obturator muscle will hit the
→ Inflammation/infection of 1 or more diverticula
appendix → triggering pain
→ Cause: Accumulation of fecal material

Manifestations:
1. Inflammation
• Abdominal pain in the LLQ (anatomical position of
the sigmoid)
• Crampy pain
2. Infection → Fever
3. Injury → blood in stool
4. Obstruction (d/t accumulation of gas in the colon)
• Bloating and flatulence
LIVER CIRRHOSIS ▪ ↑vasodilation
→ d/t repeated injury to the hepatocytes (basic ❖ Palmar erythema
functioning unit of the liver) → fibrosis (scar tissues) → ❖ Spider angioma/telangiectasia
loss of function o Therapeutic communication d/t altered body
• Loss of liver function d/t scarring image
→ Heart gives blood supply to the kidneys through renal
Types: arteries → heart gives blood to the GIT → portal vein
→ Laennec’s Cirrhosis → liver → filters blood → blood goes back to the heart
• Alcoholic cirrhosis (d/t alcohol) through IVC
→ Post necrotic
• Caused by hepavirus or hepatotoxins (found in
analgesics)
→ Biliary Cirrhosis
• d/t obstruction/blockage of
gallstones/cholelithiasis
→ Cardiac Cirrhosis
• Right sided heart failure

Liver Functions
→ Metabolism of nutrients (breakdown/processing of
proteins, fats, etc.,)
→ Kupffer cell → swallow/engulf/trap microorganisms
(phagocytosis; part of immunity)
→ Excretion of hormones:
• Glucocorticoids (cortisol; sugar)
• Mineralocorticoids (aldosterone; potassium,
sodium and water)
• Androgen (testosterone and estrogen)
o Estrogen is a vasodilator
→ Breakdown of hemoglobin
• Heme - iron; globin - protein
• Iron → bilirubin → enter the liver → mixed with
bile (for emulsification of fats) → fats are for → Liver produces albumin (most abundant protein) →
absorption of vit ADEK → vitamin K (clotting maintains oncotic/osmotic pressure → attracts water
factor) going into the intravascular space while hydrostatic
o Bile pressure draws fluid out → if liver is damaged →
▪ GIT → urobilin → urine ↓albumin → ↓oncotic pressure → fluids will go out →
▪ stercobilin → color of the stool edema → ↓fluids in the intravascular space → RAAS
→ If the liver is not functioning: activate → ↑aldosterone and ADH → worsen edema
• Bilirubin will be retained in the blood → → Excrete waste product of protein
accumulation in the skin → jaundice/icterus → • Ammonia → goes to liver to be converted into
pruritus urea → once combined with blood it will be
o Warm bath converted into BUN (blood urea nitrogen) →
o Cool environment excreted by the kidneys
o Oatmeal bath • If the liver is damaged → ammonia will
• Kidneys → dark urine accumulate and is neurotoxic → resulting in
• (X) bile → fats will enter the stools → steatorrhea hepatic encephalopathy (fatal; brain damage)
• (X) clotting → high risk for bleeding → Hepatic encephalopathy
o Bleeding precautions: • Asterixis (flapping hand tremor)
▪ Use of electric razor • Changes in LOC
▪ Soft bristled toothbrush • Constructional apraxia (hindi magaya yung
▪ Avoid dental floss drawing/sinulat)
▪ Avoid anticoagulants • Fetor hepaticus
• (x) urobilin or stercobilin → clay/pale colored stool
Laboratory Tests:
Clinical Manifestations → Albumin (3.5-5 g/dL) - low
→ ↓metabolism → anorexia & decreased body weight → Partial Thromboplastin time or prothrombin time/INR
• High caloric intake (↑carbs & ↑protein) (25-35 sec. / 11-14sec./.8-1.2)
• Bed rest • Prolonged if there is bleeding
→ (X) Kupffer cell → low immunity → high risk for → Serum Bilirubin (.03-1.9 mg/dL) - increased
infection → Aspartate Aminotransferase (AST/SGOT) (10-40 U/L)
• Aseptic technique - increased
• Handwashing → Alanine Aminotransferase (ALT/SGPT) (7-56 U/L) -
→ (X) excretion of hormones → retention of hormones increased
resulting to ↑GMA → BUN - low d/t high levels of ammonia
• ↑cortisol → ↑sugar
o Monitor blood glucose level Management:
o (X) gluconeogenesis → dec blood glucose → High calorie intake
level → Low protein to prevent hepatic encephalopathy
• Retention of sodium and water → edema • High protein if there is no hepatic encephalopathy
o Sodium and water restriction → Low fat
• Low potassium → Low sodium
o Spironolactone (potassium sparing diuretics) → Low fluid intake
• ↑androgens: → Hepatic Encephalopathy
o Female: hirsutism, amenorrhea • Asterixis
o Male: gynecomastia, atrophy of the genitals • Constructional Apraxia
 •LOC • Murphy’s sign
o Check if oriented o Client is in supine; nurse placed the hands on
o Avoid sedatives the hepatic margin → tell the client to inhale
• Fetor hepaticus → upon inhalation diaphragm will contract →
o Assess breath inflamed gallbladder will be palpated → pain
→ Esophageal varices • Abdominal pain in the RUQ
• Prevent rupture • Rebound tenderness
o Avoid anything that might increase pressure • Radiating
o Beta blockers are used to decrease pressure o To the right shoulder
(prevent bleeding) • Usually after a heavy or fatty meal
• (+) rupture → balloon tamponade through the use o Contraction of the gallbladder to release bile
of sengstaken blakemore tube → pain
o Patient should be closely monitored: near the → Indigestion of fats → this would accumulate in the
nurse’s station colon → gas formation
o Esophageal balloon for pressure • N&V
o Gastric balloon for anchoring • Belching
▪ Can be deflated → displaced/dislodged • Flatulence
→ airway obstruction (DOB/dyspnea) → → Obstruction
scissors at bedside to cut the 2-balloon • Skin → yellow (jaundice)
lumen (esophageal and gastric to deflate) • Stool → steatorrhea or pale/clay colored
• Urine → dark
• Vitamin Deficiency of vitamin ADEK
→ Infection
• Fever → increase insensible fluid loss
• Dehydration

Management:
→ NPO initially: (+) pain
→ Diet
• Low fat
• Small frequent meals
• Avoid gas forming foods
o Eggs
o Cabbage
o Broccoli
o Cauliflower
→ Medications
• Ursodeoxycholic acid (UDCA) - mild cases; to
Medications: dissolve the stone
→ Spironolactone (potassium sparing diuretic) → edema, • Chenodeoxycholic acid (chenodiol or CDCA) -
ascites, hypokalemia mild cases; to dissolve the stone
→ IV albumin to increase oncotic pressure • Antispasmodics/Anticholinergics (Propanthalin) -
→ Lactulose - laxative → increased defecation → for pain
decreased level of ammonia through bowel elimination → Surgery: cholecystectomy (laparoscopic)
→ Neomycin (antibiotic) to decrease the bacteria in the • Can survive without gallbladder because it is only
GIT → ↓protein → ↓ammonia for storage of bile. Production of bile occur in the
liver
CHOLECYSTITIS
→ Inflammation of the gallbladder ACUTE PANCREATITIS
→ Can lead to cholelithiasis → Obstruction leading to trapping of pancreatic enzymes
inside the pancreas → autodigestion → bleeding and
Types: inflammation
→ Calculous - gallstone • Pancreatic enzymes aid in digestion
→ Acalculous - trauma → Inflammation
• Pain in the LUQ radiating at the back because the
CHOLELITHIASIS pancreas is located at the back of the stomach
→ Formation of stone → d/t supersaturation (substance • Aggravated by:
separates from solution) o Diet: fatty
• Cholesterol → d/t high fat diet → stones o Beverage: alcohol
• Bilirubin (pigment stone) → from hemolysis o Position: flat on bed
→ Gallstone will cause obstruction → injury to gallbladder • Bowel sound: decreased d/t pain
→ infection → inflammation → bile will not be excreted • N&V
→ trapping in the gallbladder → indigestion of → Bleeding
nutrients (fats) • Dehydration
• Weight loss
Factors: “5 F's” • Cullen’s & Grey turner’s Sign
→ Fair o Cullen’s: bluish discoloration in the umbilical
→ Fat area
→ Female o Grey Turner’s: bluish discoloration in the flank
→ Fertile (multigravid) area
→ Forty ▪ “Turn your back”

Clinical Manifestations:
→ Inflammation
• Biliary colic (severe pain) - cholelithiasis
o Stones gets trapped in the biliary duct
Laboratory Findings:
→ ↑WBC
→ ↑Glucose
→ ↑Bilirubin
→ ↑Alkaline phosphate
→ ↑Serum and urinary amylase
→ ↑Serum lipase
→ Refer to serum amylase & serum lipase during
recovery (should return to normal)

Management:
→ Acute phase
• NPO
o Presence of food increases HCl → stimulates
release of pancreatic enzyme
• TPN
• NGT
o To suction hydrochloric acid
▪ (X) HCL → (X) stimulus for pancreatic
enzymes
• NPO and TPN until the patient is stable (normal
amylase and lipase)
→ Medications:
• H2 receptor blocker
• Proton pump inhibitor
• Morphine for pain
o Given with antispasmodic/anticholinergic
(atropine)
▪ Morphine can cause spasm of sphincter
of oddi
o (X) demerol as it can cause seizures

CHRONIC PANCREATITIS
→ Repeated injury → fibrosis (scarring) → loss of
function
• Exocrine → (X) pancreatic enzyme
• Endocrine → (X) insulin
→ Inflammation
• Abdominal pain in the LUQ
→ Fibrosis
• Palpable mass at LUQ
• Hypocalcemia → used in the healing process
→ Loss of function
• ↓body weight
• ↑Bilirubin
• Stool → steatorrhea d/t indigestion of fats
• ↑Glucose → DM

Management:
→ Diet
• Food
o Bland
o Avoid gastric stimulants → ↑HCl →
↑production of pancreatic enzyme → causing
damage
• Small frequent meals
• ↓Fat
• ↓Protein
→ Medications
• Synthetic pancreatic enzymes (oral)
o Pancreatin
o Pancrelipase → decreases fats in stool
• Insulin & OHA