GASTROINTESTINAL DISORDERS
DIGESTIVE TRACT
→ AKA alimentary canal
→ Starts in the mouth
• Mechanical digestion (mastication/chewing)
• Chemical digestion (salivary amylase to break
down starch into sugar)
o Mechanical and Chemical Digestion is
inversely proportional
▪ ↓chew = ↑HCL
▪ ↑chew = ↓HCl
→ Upon swallowing, food reaches the esophagus
• Dysphagia
→ Lower Esophageal Sphincter/Cardiac Sphincter
• Ensures downward and prevents reflux,
regurgitation
• GERD
→ LES closes once food reaches the stomach
• Stomach can be divided into two:
o Fundus - upper portion
o Antrum - lower portion
▪ Antrectomy - removal of the distal portion
of the stomach
• Stomach has parietal cells which produces HCl to
dilute food and intrinsic factor which absorbs vit b
12
o Pernicious anemia if intrinsic factor became
dysfunctional
o HCl is acidic (ph 1.5 - 3.5)
→ Pyloric Sphincter opens around 2-3 hours (gastric
emptying)
• But depends on the content of food:
o Fastest to digest: carbohydrates
o Fats and proteins stays longer in the stomach
→ Small Intestine
• Duodenum connected to the hepatobiliary tract
o Pancreas → pancreatic enzymes
▪ Amylase → breaks down carbohydrates
▪ Lipase → breaks down fats
▪ Trypsin → breaks down protein
o Liver → produces bile (stomach contents that
would enter the small intestine should be
water soluble → fats are needed to be
emulsified (to go along with the water) → bile
would be the emulsifier)
o Gallbladder → storage of bile
• Jejunum absorbs nutrients
• Ileum absorbs bile salt and vitamin b12
o ↓absorption of bile salt → steatorrhea (foul
smelling) → stool will be more dense
(lumulutang)
o Resection of the ileum → dec vit b12
absorption → pernicious anemia
→ Large Intestine absorbs water and formation of stool or
feces
• Peristalsis (movement of the colon)
o Is directly proportional with bowel sounds
▪ ↑peristalsis → ↑bowel sound → irritation
of the intestine → diarrhea
▪ ↓peristalsis → ↓bowel sound →
constipation
▪ (+) pain → decreased peristalsis
o Is indirectly proportional with absorption of
water
▪ ↑peristalsis → ↓absorption of water →
stool will be wet (diarrhea)
▪ ↓peristalsis → ↑ absorption of water →
stool will be dry (constipation)
o Immobility will cause decrease peristalsis
resulting to constipation
▪ Advice the patient to exercise to increase
peristalsis
• Ascending Colon
• Transverse Colon
• Descending
•
•
•
Sigmoid
Rectum (vascular)
o If high risk for bleeding → invasive
procedures are contraindicated
Anus (opening)
Quadrants
→ Pancreatitis - LUQ
→ Liver and gallbladder - RUQ
→ Appen - RLQ
→ Rectum - LLQ
→ Sigmoid - LLQ
Assessment:
→ IAPePa
→ To get an accurate assessment on bowel sounds
auscultation is done first → any pressure to the
abdomen will cause changes/alter to the peristalsis or
bowel sounds
GASTROESOPHAGEAL REFLUX DISEASE (GERD)
→ Weak LES
• Anything that may decrease LES pressure, inc
HCl
• Substances to Avoid: (5CAFPS)
o Coffee
o Citrus Fruits
o Cigarette Smoking
o Carbonated Drinks/Cola
o Chocolate
o Alcohol
o Fatty foods
o Peppermint
o Spicy
→ Backflow, regurgitation, and reflux of gastric contents
into the esophagus
→ Signs and Symptoms:
• Pyrosis (heartburn) burning sensation after eating
• Nausea and Vomiting + Hypersalivation
• Dyspepsia or Indigestion
• Dysphagia (difficulty swallowing)
• Injury because esophagus has no mucosal layer
→ Odynophagia
→ Management:
• “Food should go down”
• High carbs, low fat, low protein diet
• High fiber diet → increase feeling of fullness
(satiety) → prevents overeating
• Small frequent feeding
• Position: Upright → elevate HOB and turned to left
→ esophagus will be above → food will not
regurgitate
• Avoid anything that may increase pressure in the
abdomen
o Do not bend after eating
o Do not wear tight clothing
o Avoid heavy lifting
o (X) Obesity
→ Medication:
• Avoid medications that increases HCl
o E.g. NSAIDS, Aspirin
• Antacids
• Proton Pump Inhibitor
• Histamine 2 blocker
• Prokinetics (meds to increase motility) for food to
descend
o Metoclopramide
• Antiemetics
→ Fundoplication
• Fundus is wrapped around the LES
→ Diagnostics
→ Endoscopy
→ Checking of gastric pH
PEPTIC ULCER DISEASE
Causes:
1. Helicobacter pylori → from raw meat → burrows in the
GIT → causes ulceration
• DOC: Metronidazole
o Should not be mixed with alcohol → disulfiram
like effect/reaction
2. ↑HCl and ↑Pepsin
3. ↓mucus → ↓protection
• Burn injury → fluid shifting → edema → dec blood
volume → dec blood flow to the stomach → less
production of mucus → curling’s ulcer
→
Related to low food
intake
Career stage
Malnourished (weight loss)
Well nourished
→
→
→
→
Pain - ½ - 1 hour after
meal (with food)
Pain is triggered by food
intake
Pain relieved by
vomiting (pressure is
relieved)
Nausea, vomiting and
hematemesis
Pathophysiology:
→
→
→
Pain - 2-3 hours after
meal (empty)
Pain is relieved by food
intake
Pain is common at night
(empty)
Melena
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
→ Vagotomy: (X) vagus nerve → low production of HCl
(decrease stimulus for the production of HCL)
→ Histamine 2 blocker → (x) proton pump → ↓hcl
production
→ Proton pump inhibitor → ↓HCL production
→ Octeroride → mimics the action of somatostatin →
↓gastrin → ↓histamine → ↓HCl
Factors:
→ Stress
• ↑acetylcholine → ↑HCl
→ Cigarette Smoking
→ Alcohol
→ Caffeine
→ Aspirin and NSAID
• ↑HCL
→ Zollinger - Ellison Syndrome
• Pancreatic tumor → ↑gastrin → ↑HCl
→ Irregular and Hurried Meals
• Dec chewing → ↑HCl
→ Type A personality
• Workaholic → prone to stress
→ Type O blood
• ↑pepsin level
→ Genetics
• ↑parietal cells → ↑HCl non
GASTRIC ULCER
DUODENAL CANCER
Poor Man’s or Laborer’s
Ulcer
→ Related to low food
intake
Executive Ulcer
→ Related to stress
20% incidence
80% incidence
Common in people 50 yrs
old and above
Common in people 25-50
yrs old
Medications:
→ Antacids
• Neutralizes acid
• Taken 1-2 hrs after meal
• If empty stomach → longer duration
• Aluminum Hydroxide (phosphate binder for
hyperphosphatemia)
o To be taken with meals
o WOF: constipation
• Magnesium Hydroxide
o WOF: Diarrhea
• Aluminum Magnesium hydroxide
• Calcium Carbonate
• Sodium Bicarbonate
o Can cause metabolic alkalosis
o Can enter bloodstream
→ Histamine 2 receptor blockers
• Ranitidine
• Taken at bedtime
→ Proton Pump Inhibitors
• Omeprazole
• Taken before meals
→ Cytoprotective Drugs
• Sucralfate
• Coats the stomach; acts a protective barrier
→ Prostaglandins
• Misoprostol
• Dec HCl, ↑mucus, for inflammation, induces
uterine contraction
• Contraindicated to pregnant → abortifacient
→ Hormone
• Octreotide
• Increases somatostatin
The cause of peptic ulcer is NSAIDS, which medications
will you give?
A. Histamine 2 receptor blocker
B. Proton Pump Inhibitor
C. Cytoprotective Drugs
D. Prostaglandin
● NSAID is an anti-inflammatory → antiprostaglandin
● WOF: pregnant, do not give Misoprostol
Surgery:
1. Vagotomy
• To dec stimuli for the production of HCl
2. Gastrectomy
• Before imperforation happens / removal of parietal
cells
• Total - usually done on gastric cancer
• Subtotal/Antrectomy - removal of the lower half of
the stomach
3. Anastomosis:
• Billroth I - gastroduodenostomy
o Reconnect the stomach to the duodenum
• Billroth II - gastrojejunostomy
o Done If the damage in the duodenum is
extensive
o Rapid gastric emptying → dumping syndrome
DUMPING SYNDROME
•
Chronic constipation with episodes of diarrhea
Management: (Diverticulosis)
1. High fiber Diet
2. Increase fluid intake to counter constipation
3. Medication: Laxative to move bowel
Acute Phase: “painful episodes” (priority is to rest the
bowel) → dec peristalsis (Diverticulitis)
→ Low fiber diet
→ Oral Intake
• Patient will be placed on NPO status
→ Activity
• Bed rest
→ Medication
• Antispasmodic/Anticholinergic
• Propantheline
→ 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
o Avoid salt, sugar and milk
2. Position:
o Supine
o Left Side Lying → food will be pulled in the
stomach → will not descend immediately
DIVERTICULOSIS
→ Asymptomatic
→ Outpouching of intestinal mucosa
→ Common site: Sigmoid Colon
→ Cause: low fiber diet → constipation
• Reversible through dietary modifications
→ ↑pressure in the intraluminal/wall of the colon →
weakening of the wall of the colon → outpouching →
trapping of stool → obstruction → injury → infection
→ inflammation
DIVERTICULITIS
→ Inflammation/infection of 1 or more diverticula
→ 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
•
•
•
•
•
•
•
Rovsing’s Sign
o Pain elicited in the right lower quadrant when
pressure is applied on the left lower quadrant
Dunphy’s Sign
o Pain is triggered when coughing d/t inc
intraabdominal pressure
Blumberg’s Sign
o Rebound tenderness → pain is felt upon
release
Inc WBC
Bowel Sound
o Decreased or absent
Psoas’ Sign
o Left-side lying while the right leg is flexed
backward → triggers pain because iliopsoas
stretches and hits the appendix
Obturator Sign
o Supine position while knees are flexed at 90
degrees → obturator muscle will hit the
appendix → triggering pain
LIVER CIRRHOSIS
→ d/t repeated injury to the hepatocytes (basic
functioning unit of the liver) → fibrosis (scar tissues) →
loss of function
• Loss of liver function d/t scarring
Types:
→ Laennec’s Cirrhosis
• Alcoholic cirrhosis (d/t alcohol)
→ 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
absorption of vit ADEK → vitamin K (clotting
factor)
o Bile
▪ GIT → urobilin → urine
▪ stercobilin → color of the stool
→ If the liver is not functioning:
• Bilirubin will be retained in the blood →
accumulation in the skin → jaundice/icterus →
pruritus
o Warm bath
o Cool environment
o Oatmeal bath
• Kidneys → dark urine
• (X) bile → fats will enter the stools → steatorrhea
• (X) clotting → high risk for bleeding
o Bleeding precautions:
▪ Use of electric razor
▪ Soft bristled toothbrush
▪ Avoid dental floss
▪ Avoid anticoagulants
• (x) urobilin or stercobilin → clay/pale colored stool
Clinical Manifestations
→ ↓metabolism → anorexia & decreased body weight
• High caloric intake (↑carbs & ↑protein)
• Bed rest
→ (X) Kupffer cell → low immunity → high risk for
infection
• Aseptic technique
• Handwashing
→ (X) excretion of hormones → retention of hormones
resulting to ↑GMA
• ↑cortisol → ↑sugar
o Monitor blood glucose level
o (X) gluconeogenesis → dec blood glucose
level
• Retention of sodium and water → edema
o Sodium and water restriction
• Low potassium
o Spironolactone (potassium sparing diuretics)
• ↑androgens:
o Female: hirsutism, amenorrhea
o Male: gynecomastia, atrophy of the genitals
↑vasodilation
❖ Palmar erythema
❖ Spider angioma/telangiectasia
o Therapeutic communication d/t altered body
image
→ Heart gives blood supply to the kidneys through renal
arteries → heart gives blood to the GIT → portal vein
→ liver → filters blood → blood goes back to the heart
through IVC
▪
→ Liver produces albumin (most abundant protein) →
maintains oncotic/osmotic pressure → attracts water
going into the intravascular space while hydrostatic
pressure draws fluid out → if liver is damaged →
↓albumin → ↓oncotic pressure → fluids will go out →
edema → ↓fluids in the intravascular space → RAAS
activate → ↑aldosterone and ADH → worsen edema
→ Excrete waste product of protein
• Ammonia → goes to liver to be converted into
urea → once combined with blood it will be
converted into BUN (blood urea nitrogen) →
excreted by the kidneys
• If the liver is damaged → ammonia will
accumulate and is neurotoxic → resulting in
hepatic encephalopathy (fatal; brain damage)
→ Hepatic encephalopathy
• Asterixis (flapping hand tremor)
• Changes in LOC
• Constructional apraxia (hindi magaya yung
drawing/sinulat)
• Fetor hepaticus
Laboratory Tests:
→ Albumin (3.5-5 g/dL) - low
→ Partial Thromboplastin time or prothrombin time/INR
(25-35 sec. / 11-14sec./.8-1.2)
• Prolonged if there is bleeding
→ Serum Bilirubin (.03-1.9 mg/dL) - increased
→ Aspartate Aminotransferase (AST/SGOT) (10-40 U/L)
- increased
→ Alanine Aminotransferase (ALT/SGPT) (7-56 U/L) increased
→ BUN - low d/t high levels of ammonia
Management:
→ High calorie intake
→ Low protein to prevent hepatic encephalopathy
• High protein if there is no hepatic encephalopathy
→ Low fat
→ Low sodium
→ Low fluid intake
→ Hepatic Encephalopathy
• Asterixis
• Constructional Apraxia
•
LOC
o Check if oriented
o Avoid sedatives
• Fetor hepaticus
o Assess breath
→ Esophageal varices
• Prevent rupture
o Avoid anything that might increase pressure
o Beta blockers are used to decrease pressure
(prevent bleeding)
• (+) rupture → balloon tamponade through the use
of sengstaken blakemore tube
o Patient should be closely monitored: near the
nurse’s station
o Esophageal balloon for pressure
o Gastric balloon for anchoring
▪ Can be deflated → displaced/dislodged
→ airway obstruction (DOB/dyspnea) →
scissors at bedside to cut the 2-balloon
lumen (esophageal and gastric to deflate)
Medications:
→ Spironolactone (potassium sparing diuretic) → edema,
ascites, hypokalemia
→ IV albumin to increase oncotic pressure
→ Lactulose - laxative → increased defecation →
decreased level of ammonia through bowel elimination
→ Neomycin (antibiotic) to decrease the bacteria in the
GIT → ↓protein → ↓ammonia
CHOLECYSTITIS
→ Inflammation of the gallbladder
→ Can lead to cholelithiasis
Types:
→ Calculous - gallstone
→ Acalculous - trauma
CHOLELITHIASIS
→ Formation of stone → d/t supersaturation (substance
separates from solution)
• Cholesterol → d/t high fat diet → stones
• Bilirubin (pigment stone) → from hemolysis
→ Gallstone will cause obstruction → injury to gallbladder
→ infection → inflammation → bile will not be excreted
→ trapping in the gallbladder → indigestion of
nutrients (fats)
Factors: “5 F's”
→ Fair
→ Fat
→ Female
→ Fertile (multigravid)
→ Forty
Clinical Manifestations:
→ Inflammation
• Biliary colic (severe pain) - cholelithiasis
o Stones gets trapped in the biliary duct
•
Murphy’s sign
o Client is in supine; nurse placed the hands on
the hepatic margin → tell the client to inhale
→ upon inhalation diaphragm will contract →
inflamed gallbladder will be palpated → pain
• Abdominal pain in the RUQ
• Rebound tenderness
• Radiating
o To the right shoulder
• Usually after a heavy or fatty meal
o Contraction of the gallbladder to release bile
→ pain
→ Indigestion of fats → this would accumulate in the
colon → gas formation
• N&V
• Belching
• Flatulence
→ Obstruction
• Skin → yellow (jaundice)
• 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
dissolve the stone
• Chenodeoxycholic acid (chenodiol or CDCA) mild cases; to dissolve the stone
• Antispasmodics/Anticholinergics (Propanthalin) for pain
→ Surgery: cholecystectomy (laparoscopic)
• Can survive without gallbladder because it is only
for storage of bile. Production of bile occur in the
liver
ACUTE PANCREATITIS
→ Obstruction leading to trapping of pancreatic enzymes
inside the pancreas → autodigestion → bleeding and
inflammation
• Pancreatic enzymes aid in digestion
→ Inflammation
• Pain in the LUQ radiating at the back because the
pancreas is located at the back of the stomach
• Aggravated by:
o Diet: fatty
o Beverage: alcohol
o Position: flat on bed
• Bowel sound: decreased d/t pain
• N&V
→ Bleeding
• Dehydration
• Weight loss
• Cullen’s & Grey turner’s Sign
o Cullen’s: bluish discoloration in the umbilical
area
o Grey Turner’s: bluish discoloration in the flank
area
▪ “Turn your back”
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