gastrointestinal

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 GASTROINTESTINAL

gi system overview
MAIN FUNCTIONS TYPES of DIGESTION
① Digest and absorb ingested nutrients mechanical chemical
② Excrete waste products of digestion Physical breakdown of Chemical breakdown of food
food into smaller pieces by enzymes found in saliva &
aka chewing pancreas
UPPER gi TRACT FUNCTIONS
Mouth / Oral cavity
Ingests & breaks down food

pharynx & esophagus

Carries food from mouth to stomach

Stomach
→ Storage site until passed to small intestine
→ Food mixes with gastric acid to form chyme (paste)
→ Absorbs fat-soluble minerals

lower gi TRACT FUNCTIONS

small intestine
→ Digests contents from stomach
→ Absorption of water & electrolytes

large intestine
→ Absorption of water & electrolytes
→ Storage & elimination of waste

anus
Excretion of waste

accessory digestive organs

Liver pancreas gall bladder
Stores bile produced
by the liver
→ Metabolism of fats, proteins & carbs → Secretes glucagon and insulin
→ Detoxification → Secretes enzymes to break down foods Bile:
→ Regulates blood sugar levels lipase → digests fats → Digests fatty foods
amylase → digests carbs → Absorbs fat soluble vitamins
→ Regulates blood clotting
protease → digests protein → Carries waste out of the liver
© nurse well versed

digestion process
mechanical chemical
1 Ingestion 2 propulsion 3 digestion 4 digestion 5 absorption 6 defecation
Act of ingesting or Movement of food Physically breaking Food molecules Products of digestion Elimination of
consuming along the digestive down food broken down with are absorbed by the undigested material
something orally tract through substances into enzymes blood to be supplied from the body
peristalsis smaller particles to rest of body
aka eating
Involuntary contractions that
move food through digestive tract

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 Gastrointestinal System Overview
med-surg

gastro
nurse in the making

N IC AL DIGE
ST I C A L D I G ES T
HA EM I
ORAL CAVITY COMPONENTS

ON
C

CH
IO
ME

N amylase protease lipase

When food is broken When food is broken

down into smaller down by enzymes and pancreas
pieces digestive juices
amylase:
Examples: TIP Enzymes end in "-ase" breaks down carbs into glucose
• Chewing protease:
• Churning of the stomach Protease think Proteins breaks down proteins
Lipase think Lipids (fat) lipase:
breaks down fats
(lipids = fats)

ESOPHAGUS STOMACH
A hollow muscular tube A hollow muscular organ
that carries food & Functions:
liquid from the mouth • Stores food during eating
to the stomach using • Secretes digestive fluids
peristalsis • Moves partially digested
LIVER food (chyme) into the
small intestine
Functions:
• Filters the blood
• Metabolizes sugar, protein & fat
• Synthesizes lipoproteins (VLDL & HDL)
• Makes vitamin D PANCREAS LARGE INTESTINE
• Detoxifies/excretes bilirubin Helps make By the time food reaches the large intestines, most
and other toxins pancreatic juice of the absorption & digestion have been completed.
• Forms bile (enzymes), which breaks down In the large intestines, stool begins to form and is
• Metabolizes drugs sugar, fat & starch. The pancreas pushed toward the rectum.
• Helps in blood clotting has both exocrine & endocrine
Functions:
• Synthesizes proteins functions.
• ABSORPTION of water and electrolytes from food
such as albumin & that has not been digested yet
coagulation factors
• defecation rids the body of any waste left over from
food & removes it through the rectum & anus
SMALL INTESTINE
Transverse
The longest portion of the GI tract colon
(longer than the large intestine)
Functions:
• Digestion of food from the stomach Ascending
Descending
colon
• Absorption of nutrients, fats, carbohydrates, colon
vitamins, minerals & water
from food into the
bloodstream to be Proximal Duodenum Cecum
used by the body
Jejunum
Proximal Cecum
distal Ileum Ascending colon Sigmoid
Rectum
Transverse colon colon
Descending colon
Anus
Sigmoid colon
To remember the order of Proximal
Rectum
to Distal think DJ Ileum in the club! distal Anus

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 GASTROINTESTINAL

gi system assessment
typical
Assessment order: gi Assessment:
ï ïnspection ï ïnspection Order is changed to prepare for assessment ask
P Palpation A Auscultation to avoid altering
bowel sounds
patient to:
Percussion ★ Empty bladder
P Percussion P
★ Lie in supine position with pillow under the head
A Auscultation P Palpation

1 focused gi history 2 inspection

Ask the patient about any: Assess for:
→ Change in appetite → Nausea and vomiting → Bulges
→ Weight gain or loss → Change in bowel habits → Masses
→ Difficulty swallowing (dysphagia) → Abdominal pain
→ Hernias
→ Ascites
→ Intolerance to certain foods → Diarrhea or constipation
→ Enlarged veins
Could be early sign of malignancy or other GI disorder → Spider nevi

3 auscultation 4 percussion
© nurse well versed
sequence of quadrants Dullness
Start in RLQ & move clockwise
3
Hear elsewhere
2 3 → Soft, muffled, thud- like tone may indicate
RUQ LUQ → Heard over fluid & solid structures tumor or mass
Auscultate for 1 full minute to determine if: (full bladder or liver)
RLQ LLQ
normal 5-30 bowel sounds per minute
1 4
hypoactive <5 bowel sounds per minute tympany
→ High pitched, drum-like sound
hyperactive >30 bowel sounds per minute → Heard over air filled structures
absent No bowel sounds (large intestine)

Could mean: Could mean:

Must listen if ascites present:
▶ Ileus for at least ▶ Bowel obstruction Will have shifting dullness/ tympany with position change
▶ Peritonitis 5 minutes to ▶ Malabsorption
▶ Constipation confirm absent ▶ Infectious enteritis supine side lying
▶ Ischemic bowel disease bowel sounds ▶ GI bleeding

tympany tympany
dullness
5 palpation dullness

→ Use fingers of dominant hand DIAGNOSTICS

→ Use light, gentle, and dipping motions
→ Warm the palms before Contraindicated Guaiac test: stool sample to test for blood
→ Palpate clockwise if suspected:
→ Abdominal aortic aneurysm colonoscopy: Endoscope inserted through anus
light palpation (1-2 cm) → Appendicitis to visualize colon
→ Polycystic kidney disease
Should feel soft with no rigidity or pain → Kidney transplant Esophagogastroduodenoscopy (EGD):
→ Tumor Endoscope inserted through mouth to visualize esophagus,
deep palpation (4-5 cm) upper GI tract, and duodenum
Assess for tenderness, lumps, masses
Small bowel series: X-Rays taken after
ingestion of contrast agent/barium to obtain clear picture
No tenderness should be felt on light or deep palpation of small bowel

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 Lab Values Related to the Gastrointestinal System
med-surg

gastro
nurse in the making

Expected Range Interpretation Description

Lipase
AMYLASE
30 - 110 U/L is a better indicator
Pancreatic enzyme
of pancreatitis than
↑ levels amylase because
could indicate serum lipase lipase think
pancreatitis longer
remains elevated
LIPASE
< 200 U/L for a longer period
Pancreatic enzyme
of time.

Jaundice
normal
is a yellow discoloration
↑ levels
BILIRUBIN Total of the skin due to high
could indicate
Produced by the liver 0.2 – 1.2 mg/dL levels of bilirubin. It
liver dysfunction jaundice
is visible when serum
bilirubin is > 2 mg/dL.

↑ levels
Albumin helps keep
ALBUMIN 3.5 - 5.5 g/dL could indicate
fluid in the bloodstream.
dehydration

↓ levels
PREALBUMIN 15 - 36 mg/dL could indicate Prealbumin is great for assessing
malnutrition nutritional status.

AST
0 - 35 U/L
Part of the liver function

Liver enzyme
↑ levels AST must be taken with ALT.
test (LFT)

could indicate AST is a less specific marker of

liver dysfunction liver function than the enzyme ALT.
ALT
0 - 48 U/L
Liver enzyme

Ammonia (NH3) is produced

by cells throughout the body and is
used by the liver to make urea.
↑ levels
If the liver stops working,
AMMONIA 10 - 80 mcg/dL could indicate
ammonia increases
liver dysfunction
in the body.
Too much ammonia is very toxic,
especially to the brain.

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 GASTROINTESTINAL

CHOLECYSTITIS
all bla
hy g
WHAT IS IT? h ealt
dd
er
cho
lecystitis
Inflammation of the gall bladder
chole cyst Itis
Bile Membranous sac Inflammation
The gall bladder is connected Gall bladder becomes inflamed or blocked
and bile cannot exit properly
to the liver & stores bile

Bile helps: If inflammation becomes severe enough

★ Digests fatty foods can lead to hepatitis (liver inflammation) or
★ Absorb fat soluble vitamins perforation which can lead to sepsis
★ Carry waste (including bilirubin) out of liver

RISK FACTORS DIAGNOSTICS

remember the 5 F’s → HIDA Scan: assess for abnormal flow in gall
bladder
F Family History → Abdominal US: will show thickening in gall bladder
F Female wall
© nurse well versed

F Fat (obesity) → CT scan/ MRI

F Forty or older → ERCP (Endoscopic Retrograde Cholangiopancreatography):
Diagnostic/ treatment procedure to visualize gall bladder
F Fertile (pregnant) with endoscope & x-rays after admin of dye

SYMPTOMS Will get worse

TREATMENT
after a fatty meal
→ Severe RUQ/epigastric pain → Antibiotics for infection
→ Nausea/ vomiting → Antiemetics for nausea
→ Bloating → Cholycysectomy: removal of gall bladder
→ Fever
→ Steatorrhea (fatty stools) → ERCP: Diagnostic & remove gall stones
→ Tachycardia Breathing stops upon
→ T-tube: placed in common bile duct to drain bile
→ Positive Murphy's Sign RUQ palpation while → Lithotripsy: non-surgical procedure to break up
in supine position stones
signs of
biliary obstruction NURSING INTERVENTIONS
If bile duct gets blocked, bile cannot leave the gall
bladder, causing bile to back up into the liver → NPO preoperatively
Symptoms → NGT insertion (for gastric decompression)
▶ Jaundice
Most commonly → IV fluids for hydration
caused by → Monitor VS & electrolytes
▶ Clay-colored stool
Gall Stones gall → Monitor T-tube site & drainage
▶ Dark colored urine stone
▶ Pruritis → NO FATTY FOODS
▶ Elevated AST/ALT & billirubin common
bile duct

Gall stones are formed due to impaired metabolism of bile &

get stuck in bile duct causing inflammation

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 GASTROINTESTINAL

pancreatitis
WHAT IS IT? The pancreas has two main functions:
Inflammation of the pancreas
Endocrine Exocrine
Secretes digestive enzymes
Occurs due to autodigestion of pancreas Secretes insulin &
lipase → digests fats
glucagon to regulate
amylase → digests carbs
Pancreatic duct becomes blocked & digestive enzymes can't blood glucose levels
protease → digests protein
move out of pancreas causing them to activate early while still in
the pancreas, causing inflammation & damage

CAUSES & RISK FACTORS DIAGNOSTICS

→ labs
→ Alcohol abuse most common ▶ ↑ Lipase & Amylase ▶ ↓ Calcium
→ Gallstones causes ▶ ↑ Bilirubin ▶ ↑ Glucose
▶ ↑ WBC ▶ ↓ Platelets
→ Cholecystitis
→ Cystic Fibrosis © nurse well versed
→ ct Scan: may show enlarged pancreas
→ ERCP (can cause trauma to pancreatic duct)
→ ERCP (Endoscopic Retrograde Cholangiopancreatography):
→ Smoking Diagnostic/ treatment procedure to visualize gall bladder
→ Hyperlipidemia & pancreatic ducts

acute chronic
Abrupt onset & recovery Persistent for months &
within a few days may get worse overtime
Symptoms Symptoms Chronic inflammation leads
to fibrosis of pancreas
→ Epigastric LUQ pain that radiates to back → Chronic, persistent abdominal pain tissue leading to inability to
→ Fever (worse after consuming fatty meals) produce digestive enzymes
→ Tetany (from hypocalcemia) → Steatorrhea (fatty stool)
→
→
Nausea/ vomiting
Turner sign (bruising on flank) T C
→ Unintended weight loss
(no enzymes to digest food)
→ Cullen sign (bruising around navel) → Dark urine (from excessive bile)

COMPLICATIONS TREATMENT
→ Antibiotics for infection
ards
Inflammatory chemicals leak into blood stream causing
→ Antiemetics for nausea
widespread inflammation & alveoli to fill with fluid → Antacids: decrease acid production
▶ Shortness of breath signs of → ERCP: Diagnostic & remove gall stones
▶ Restlessness
hypoxia
▶ Tachycardia

peritonitis NURSING INTERVENTIONS

Bile or bacteria from the pancreas can leak into → NPO at least 24 hrs (eating stimulates enzymes!)
abdominal cavity causing inflammation of stomach lining → NGT insertion (for gastric decompression)
→ IV fluids for hydration
▶ Rigid board-like abdomen
▶ Rebound tenderness → Opioid analgesics for pain
▶ Fever → Monitor for hyperglycemia diet
→ Monitor VS & electrolytes ▶Low fat
▶Low sugar
Can lead to sepsis if not treated promptly! → Give pancreatic enzymes before meals ▶No alcohol

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 Acute vs. Chronic Pancreatitis
med-surg

gastro
nurse in the making

Pathology
Pancreatitis is
AUTODIGESTION of the ACUTE VS. CHRONIC
pancreas by its own Sudden inflammation that is
digestive enzymes that Chronic inflammation
reversible with prompt
are released improperly in that is irreversible
recognition and treatment
the pancreas. This causes
the pancreatic enzymes ∙ Gallstones ∙ Repeated episodes of acute pancreatitis
to destroy its own tissue, ∙ Block the bile duct
∙ Excessive & prolonged consumption of
CAUSES

leading to inflammation. ∙ Alcohol (ETOH) alcohol (ETOH)

∙ Damages the cells of the pancreas ∙ Recurrent damage to the cells
∙ Infection ∙ Medications of the pancreas
If the pancreas isn't
working, the enzymes ∙ Tumor ∙ Trauma ∙ Cystic fibrosis
aren't working properly
either. In Acute, there will still be working In chronic, you will see different S&S
functions of the pancreas due to the prolonged damage & loss of function
DIGESTIVE ENZYMES (exocrine)
Amylase: ∙ Sudden, severe PAIN
∙ Chronic epigastric pain or no pain
• Breaks down carbs to glucose ∙ Mid-epigastric pain LUQ
Protease: ∙ Pain increases after drinking alcohol
∙ Nausea & vomiting
• Breaks down proteins or eating a fatty meal
SIGNS & SYMPTOMS

∙ Fever
Lipase: ∙ Steatorrhea or "fatty stools"
• Breaks down fats ∙ ↑ HR & ↓ BP ∙ Oily/greasy, frothy stool
∙ ↑ Glucose ∙ Weight loss
Labs ∙ Mental confusion & agitation ∙ Can't digest food properly
normal
Amylase ∙ Abdominal guarding ∙ Jaundice
∙ Yellowish color of the
Lipase ∙ Rigid/board-like abdomen
skin from buildup of bile
WBCs ∙ Grey Turner's sign
∙ Diabetes mellitus jaundice
∙ Bluish discoloration at the flanks
Bilirubin ∙ Damage to the islet of Langerhans
Glucose ∙ Cullen's sign
∙ Dark urine
∙ Bluish discoloration of the umbilicus
Platelets ∙ From excess bile in the body
Ca+ & Mg Cullen's = Circle belly button

Cullen’s
Nursing Considerations Medications
∙ Rest the pancreas! ∙ Opioid analgesics
∙ NPO (we don't want stimulation of the enzymes) ∙ Antibiotics
Grey-Turner’s
∙ Administer IV fluids ∙ Pancreatic enzymes
∙ Manage pain ∙ Insulin
∙ Position the patient: ∙ Proton pump inhibitors (PPIs),
Side lying → Fetal position H2 antagonists, antacids
NOT supine
∙ Insert NG tube
∙ Remove stomach contents Patient Education
Diet Modifications
∙ Monitor:
∙ Avoid alcohol
• Glucose
• Blood pressure ∙ Protein
• Intake & output (I&O) ∙ Complex carbohydrates (fruits, vegetables, grains)
• Laboratory values ∙ Fat (no greasy, fatty foods)
• Stools ∙ Limit sugars
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 GASTROINTESTINAL

inflammatory bowel disease

Term that encompasses two conditions (crohn's & ulcerative colitis)
similarities causes
→ Have flare ups & remissions Causes not fully known
→ Increase risk of colon cancer ▶ Genetics ▶ Smoking
→ Cause inflammation & ulcers ▶ Illness ▶ Stress

crohn's ulcerative
colitis
PRIMARY DIFFERENCES
location Affects entire GI tract location Affects colon & rectum

thickness Affects full thickness of bowel wall thickness Affects mucosa layer of bowel wall

ulcerations Patchy & scattered (skip lesions) ulcerations Continuous throughout

symptoms symptoms
→ Diarrhea (not usually bloody) → Severe diarrhea with pus/blood (10-20 stools/ day)
→ Abscesses in bowel wall → Electrolyte imbalances
→ Mouth or GI ulcers → Weight loss
→ RLQ pain → Bowel urgency

complications complications
☛ Malnourishment: if affects small intestine ☛ toxic megacolon: dilation of colon due to
(site of nutrient absorption) severe inflammation
☛ Fistula: abnormal tunnel forms between two ☛ Peritonitis: severe inflammation can cause
body parts (worsening of abscess) bowel to rupture
☛ Obstruction: from severe swelling & ☛ dehydration: due to inability to absorb water
formation of scar tissue from inflammation

treatment treatment
NO CURE: goal is symptom management
① Protocolectomy (+ permanent illeostomy)
→ Bowel Resection: cut out diseased parts of bowel
only cure is: ② Ileoanal anastomosis (no ostomy)
→ Sulfasalazine: ↓ inflammation → Sulfasalazine: ↓ inflammation
→ Corticosteroids: ↓ inflammation & immune response → Corticosteroids: ↓ inflammation & immune response
→ Antibiotics: during flare ups to prevent infection → Antibiotics: during flare ups to prevent infection
→ Anti-diarrheals → Anti-diarrheals

EDUCATION
foods to avoid during flare ups
© nurse well versed

U High fiber foods ★ Low fiber

U Hard to digest foods (nuts, raw vegetables) ★ High protein
U Spicy foods ★ Adequate water intake
U Gas causing foods (beans, onions)
★ Low residue

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 nurse in the making

Ulcerative Colitis vs. Crohn’s Disease

med-surg

gastro

Types of Inflammatory Bowel Disease (IBD) This is not the same

thing as irritable bowel
syndrome (IBS)

MOST
N
ULCERATIVE Colitis Crohn’s disease
C MMO
O
description

Chronic ulceration Inflammation of the

& inflammation gastrointestinal tract wall
of the rectum at ANY point through
& colon ALL layers
location

Affects the large intestine Can affect anywhere in the GI tract

& rectum only (mouth to anus)
thickness

Inflammation affects the Inflammation is transmural

submucosa or mucosa (occurring across the entire wall)

Patches of inflammation
APPEARANCE

Inflamed areas are

are present throughout
continuous with no
ulcerative the bowel
patches showing the Crohn's think
colitis think This makes a
appearance of ulcers Cobblestone
bloody ulcers cobblestone appearance
no! but surgical intervention (colectomy)
complications cure

no cure, but surgery can help with symptoms

can help with symptoms

Toxic megacolon,
rupture of bowel, Increased risk for Abscess, fistulas Increased risk for
dehydration hemorrhage/shock infection (sepsis)

• Diarrhea ULCERATIVE COLITIS

symptoms

• Abdominal pain
classic

Can have mucus, pus, or blood in the stool

• Weight loss
• Nutritional deficiencies CROHN’S DISEASE
• Fatigue Steatorrhea (fat in the stool)
Diagnostic

Colonoscopy

Both: Diet modifications for both:

similarities

• Are a form of inflammatory bowel disease (IBD) fiber

• Have causes that are not completely known Small,
protein
frequent
• Increase the risk for colon cancer calories meals
• Cause inflammation & ulcers fluids

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 GASTROINTESTINAL

diverticular disease
risk factors
Two diseases that mainly affect the large intestine
▶ Diet ↓fiber & ↑red meat ▶ Obesity
▶ Age (over 40) ▶ Medications
diverticula form in weak spots of the colon ▶ Smoking & alcohol abuse (steroids, opioids, NSAIDs)
Small pouches that form on the intestinal walls ▶ Genetics ▶ Sedentary lifestyle

colon
diverticulosis diverticulitis
Formation of multiple hollow Complication of diverticulosis
diverticula pouches throughout the colon where pouches become inflamed
most common site: sigmoid colon Undigested food or stool gets trapped
in pouches inflamed
pouch
symptoms symptoms
Usually asymptomatic until complications develop → Severe LLQ pain
→ Change in bowel patterns → Bloating
(constipation or diarrhea) → Bloody stool
→ Bloating → Nausea/ vomiting
→ Mild cramping → Fever & chills

complications complications
bleeding ▶ Painless bleeding abscess ▶ Fever
Arterial walls of intestine become ▶ Bright red stools Pouches become infected & ▶ Elevated WBC
weak overtime & rupture ▶ Abdominal cramping filled with pus ▶ Abdominal tenderness

obstruction ▶ Constipation Peritonitis ▶ Rigid board-like abdomen

Narrowing of colon called ▶ Abdominal distention Diverticulum rupture and contents ▶ Rebound tenderness
strictures where stool can't pass ▶ Vomiting spill into peritoneal cavity ▶ Fever

diagnostics
colonoscopy: endoscope inserted through rectum to assess colon for diverticula
labs: WBC & inflammatory markers (CRP) will be elevated (Diverticulitis)
ct scan: assess for abnormalities in GI tract Patients often find out they have
diverticulosis through routine
colonoscopy

treatment treatment
Usually requires no treatment because asymptomatic
▶ Antibiotics for infection
▶ OTC analgesics for pain (Acetaminophen)
If recurrent symptoms:
▶ High fiber diet ▶ NPO (to rest bowel)
▶ Fiber supplements ▶ IV fluids
▶ Probiotics ▶ Bowel resection may be needed in severe cases

EDUCATION
during flare up recovery & maintenance
© nurse well versed

▶ NPO to rest bowel if severe ♥ Gradually introduce low fiber foods

▶ No high fiber foods ♥ Build up to high fiber foods
▶ No solid foods ♥ Psyllium supplements
▶ Clear liquids for 2-3 days ♥ Adequate hydration

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 GASTROINTESTINAL

gerd vs gastritis vs pud

Conditions that result from abnormal acid production

gerd gastritis pud

gastroesophageal peptic ulcer
reflux disease Inflammation of the disease
stomach lining Ulcer formation in
Acid backflow from
stomach into esophagus lining of GI tract

risk factors risk factors risk factors

→ Weak LES (lower esophageal sphincter) → H. pylori (bacteria) → H. pylori (bacteria)
→ Obesity → Long term NSAID use → Long term NSAID use
→ Pregnancy → Stress → Stress caused by
→ Hiatal hernia → Smoking → Smoking gastritis
→ Smoking → Alcohol abuse → Alcohol abuse

symptoms symptoms symptoms

→ Heartburn → Indigestion gastric ulcer
▶ Abdominal pain 30 m-1 hr after eating
→ Epigastric pain → Nausea/ vomiting ▶ Eating makes it worse
→ Regurgitation while supine → Bloating ▶ Bloody emesis
→ Bitter taste in mouth → Abdominal pain duodenal ulcer
→ Dry cough → Decreased appetite ▶ Abdominal pain 2-3 hrs after meals
▶ Eating makes it better
▶ Bloody stool

diagnostics diagnostics diagnostics

→ EGD: insert camera down → Urea breath test: assess for → EGD: assess for ulcers
esophagus to assess for erosion or presence of H. Pylori
changes → CBC: if actively bleeding
→ EGD & biopsy: sample is taken → Urea breath test: assess for
→ Manometry: assess ability of of GI lining to assess for bacteria
esophagus to squeeze food down H. Pylori

treatment treatment treatment

→ Elevate head of bed Medication
→ IV fluids
Medication → Antibiotics for H. Pylori
→ NPO if vomiting
→ H2 Antagonists
→ H2 Antagonists → Proton Pump Inhibitors
→ Proton Pump Inhibitors Medication → Antacids
→ Antacids → H2 Antagonists → Sucralfate: coats stomach lining
procedures → Proton Pump Inhibitors
→ Antacids
if actively bleeding ulcer
→ Nissen Fundoplication: wrapping → Antibiotics for H. Pylori ▶ Cauterization: stop bleeding
fundus around lower esophagus ▶ IV fluids: maintain fluid volume
→ Antiemetics for nausea
▶ Blood products

EDUCATION
Lifestyle Modifications avoid
© nurse well versed

U Alcohol U Citrus
▶ Smoking cessation ▶ Small, frequent meals
U Spicy & fried foods U Peppermint
▶ Weight management ▶ Adequate hydration U Red meat U Overeating
▶ Stress management ▶ Probiotics U Dairy U Carbonated beverages
U Coffee & tea U NSAIDs

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 GASTROINTESTINAL

gastrointestinal bleed
Bleeding that occurs in the GI tract due to an underlying cause
Can range from mild to life-threatening
UPPER gi bleed mallory-weiss esophogeal
Bleeding occurs in the lining of tear varices
esophagus, stomach or duodenum
gastric ulcer gastritis
CAUSES duodenal
→ Esophageal varices ulcer

→ Mallory-weiss tear (tear in lower esophagus)

→ Ulcers
→ Erosive gastritis

SYMPTOMS ischemic bowel

→ Dark, tarry stool

→ Hemoptysis (bright red, bloody emesis)
→ Tachycardia
→ Abdominal pain
→ Paleness
→ Dizziness inflammatory
bowel disease

lower gi bleed
Bleeding occurs in the large
intestine or rectum
CAUSES
→ Tumors
→ IBD (Crohn’s or Colitis) tumor
diverticulosis
→ Hemorrhoids
intussusception diverticulitis
→ Anal Fissures
→ Diverticulitis or Diverticulosis hemorrhoids
anal fissure
SYMPTOMS
→ Frank, bright red blood in stool complication: Hypovolemic Shock
© nurse well versed

→ Tachycardia
→ Abdominal pain Severe cases can lead to severe & acute blood loss
→ Paleness ▶ ↓ BP ↑ HR ↑ RR ▶ Confusion
→ Dizziness ▶ Pale, cool, clammy ▶ ↓ urine output
medical emergency

DIAGNOSTICS TREATMENT
→ Find & treat source of bleeding (cauterization)
→ CBC: will see drop in HGB
→ Blood products (if active bleeding & ↓ HGB)
→ Guaiac Test: to confirm bleeding → Protonix infusion: ↓ acid to prevent further ulceration
→ Endoscopy: assess & treat source of → Isotonic fluids (NS or LR)
bleeding → Vitamin K: promote clotting

NURSING INTERVENTIONS
Monitor
→ Vital signs → Keep patient NPO → Maintain 2 large bore IV's
→ EKG
→ Administer oxygen as needed → Make sure type & screen is current
→ I &O
→ Trends in hemoglobin → Stop NSAIDs, aspirin & blood → Fall precautions
→ Bowel movements (frequency & color) thinners (may have orthostatic hypotension from bleeding)

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 GASTROINTESTINAL

hepatitis
WHAT IS IT? memory trick
Inflammation of the liver acute types= Hep A & E
Both transmitted through fecal-oral route
hepat Itis all
chronic types= Hep b, c & d consanants
Liver Inflammation All transmitted through blood & body fluids

type transmission diagnostics treatment prevention

Anti-HAV
Hepatitis Fecal-oral Rest & supportive ▶ Hep A vaccine

a (Contaminated food & water) ▶ + IgM= active infection treatment ▶ Hand hygiene
▶ + IgG= past infection (resolves on own)
(recovered)
acute only

Hepatitis ACUTE ▶ Hep B vaccine

Blood & body fluids ▶ + HBsAg= active infection Supportive

b (Childbirth, sex, IV drug use) ▶ Hand hygiene

▶ + Anti-HBS= past infection chronic
(recovered) ▶ Sharp precautions
Anti-virals
acute & chronic

Hepatitis ACUTE ▶ Hand hygiene

Blood & body fluids + Anti-HCV Supportive

c
(Childbirth, sex, IV drug use) ▶ Sharp precautions
most common chronic no vaccine
among iv drug use Anti-virals
acute & chronic

Hepatitis ACUTE
Occurs in conjuction
▶ + Anti-HDV Supportive ▶ Hep B vaccine

d with Hepatitis B
remember b & d are
best buds
▶ + HDAg (Hep D antigen) chronic
Anti-virals
▶ Hand hygiene
no vaccine
acute & chronic

Hepatitis Fecal-oral
+ Anti-HEV Rest & supportive ▶ Fully cook food

e
(Contaminated food & water) treatment (resolves ▶ Hand hygiene
most common in 3rd on own)
no vaccine
world countries
acute only

SYMPTOMS education
→ Jaundice → Fatigue ★ Strict hand hygiene
© nurse well versed

→ Abdominal discomfort → Fever ★ Do not share personal hygiene products

→ Nausea/ vomiting → ↑ AST/ ALT ★ Eat small, frequent meals
→ Dark urine → ↑ Bilirubin ★ Adequate rest (to allow liver to heal)
→ Clay-colored stools → ↑ Ammonia ★ Avoid liver toxic meds (Acetaminophen + Aspirin)

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 Types of Hepatitis
med-surg

gastro
nurse in the making

HEPATITIS CAUSED BY:

MOST
• Virus (A, B, C, D, E) COMMON
• Excessive use of alcohol
liver inflammation • Hepatotoxic medications
"Inflammation of the liver"
TRANSMISSION SIGNS & SYMPTOMS DIAGNOSTIC TREATMENT VACCINE

A
Anti-HAV

H V Fecal & oral

Food & water
IgM =
Active infection
Supportive
therapy &
ACUTE ONLY Igg = REST
Recovered (it’s gone)

BV
GI symptoms

H
B think Body fluids (N&V, stomach pain, anorexia) HBsAg = ACUTE
(blood, semen, saliva)
Active infection Supportive
• Childbirth therapy & rest
• Blood Dark-colored urine
ACUTE & CHRONIC Anti-HBs =
• Sex CHRONIC
• IV drugs Immune/recovered Antivirals
Clay-colored stool

CV
Vomiting ACUTE

H
Anti-HCV Supportive
Body fluids therapy & rest
Most common: Flu-like symptoms
IV drug users
No post-exposure CHRONIC
ACUTE & CHRONIC immunoglobulin • Antivirals
Jaundice
• Interferon

DV
ACUTE
Depends on B
H
HDAg Supportive
B & D = BuDs therapy & rest
Hep D only occurs Anti-HDV CHRONIC
ACUTE & CHRONIC • Antivirals
with Hep B YELLOW DISCOLORATION
of the skin from the • Interferon

EV
buildup of bilirubin

H Fecal & oral

Food & water Anti-HEV
Supportive
therapy &
ACUTE ONLY
(uncooked meats,
REST
developing countries)
normal jaundice

Patient Education for all types of hepatitis Labs All will

∙ Rest elevate be
Diet modifications: Liver enzymes: dw
hepatit ith
∙ Practice proper hand hygiene ALT: 0–48 U/L is
Carbohydrates
∙ Do not share personal hygiene products AST: 0–35 U/L
Calories Small,
∙ Avoid sex until hepatitis antibodies are negative Bilirubin: 0.2–1.2 mg/dL
Protein & fat frequent
∙ Avoid hepatotoxic substances: meals Ammonia: 10–80 mcg/dL
∙ Alcohol, acetaminophen,
aspirin, sedatives

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 GASTROINTESTINAL

CIRRHOSIS
hy liver cirr
hosis
alt
WHAT IS IT? he
Healthy liver cells are replaced with
fibrotic (scar) tissue
Known as end stage liver disease
Build up of scar tissue prevents liver from
Once at this stage damage is irreversible!
functioning normally (becomes hard & stiff from scarring)
functions of the liver:
Also connects to the hepatic portal vein
★ Produces bile to digest fats ★ Makes albumin
Blood vessel that carries blood from GI tract,
★ Regulates clotting & glucose ★ Detoxifies the body
spleen, gall bladder & pancreas to the liver
★ Turns ammonia into urea ★ Metabolizes nutrients & drugs

CAUSES & RISK FACTORS DIAGNOSTICS

→ Chronic alcohol abuse → labs
→ Chronic hepatitis (B, C & D) → ↑ AST & ALT → ↓ Albumin & calcium (bind together)
→ ↑ Bilirubin → ↓ Platelets
→ Non-alcoholic fatty liver disease → ↑ Ammonia → ↑ PT/PTT & INR
▶ Obesity gold
▶ Diabetes → liver
standard biopsy: sample taken to assess extent of
▶ Hyperlipidemia damage to liver
→ Cystic fibrosis → ct scan/ mri: assess for fatty tissue & damage
→ Biliary cirrhosis (damage to biliary ducts)
→ Toxins & hepatotoxic drugs
→ abdominal us: assess for ascites

SYMPTOMS
early signs late signs
Liver is able to cope with damage & Liver is no longer able to maintain
maintain important functions functioning due to damage
→ Jaundice → Anemia
→ Fatigue
© nurse well versed

→ Ascites → Bleeding & easily bruised

→ Hepatomegaly
→ Edema → Portal hypertension
→ Nausea/ vomiting
→ Pruritis (itchy skin) ▶ Splenomegaly
→ Abdominal pain
→ Clay-colored stool ▶ Caput madusae
→ Decreased appetite (enlarged veins on abdomen)

COMPLICATIONS TREATMENT
Causes loss of ammonia through stool
hepatic encephalopathy Medications & deemed effective when patients

High ammonia level in body

→ Lactulose: ↓ ammonia mental status improves

causes toxic effects to brain → Albumin: ↓ ascites & edema

→ Diuretics: ↓ edema
▶ Severe AMS
▶ Asterixis procedures
(flapping hand when extended)
→ Paracentesis: drain fluid in peritoneum (ascites)
esophogeal varices → Liver transplant
Severe pressure from portal hypertension
causes enlarged esophogeal veins Diet bleeding precautions
high risk for hemorrhage ▶ No alcohol ▶ Soft toothbrush
▶ No NGT tubes ▶ ↓ protein ↓ sodium ▶ Electric razor
▶ No straining ▶ Limit fluid intake ▶ Monitor for bloody stools

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 Cirrhosis
med-surg

gastro
nurse in the making

• Liver cells are DESTROYED and replaced with fibrotic (scar) tissue
• Normal function of the liver is compromised

Stages of Liver Damage Functions of a healthy liver

healthy liver 1 DETOXES the body If the fu

2
nction
of the
Helps to CLOT the blood
liver is
disrupte
d, then
none o

3
functio f these
Helps to METABOLIZE
ns will
w
properl ork
y

fatty cirrhosis (break down) drugs

liver
liver
liver
liver cell
4 SYNTHESIZES (makes) albumin
enlargement destruction
due to fat
deposits
Causes MOST
∙ Alcoholic cirrhosis COMMO
N
∙ Caused by excessive
alcohol intake • Viral hepatitis B or C
fibrosis liver ∙ Nonalcoholic • Autoimmune disorders
healthy liver tissue • Hepatotoxic drugs
fatty liver disease
replaced with scar tissue • Toxins & parasites
(NAFLD)
• Fat collection in the liver
(obesity, diabetes, ↑ cholesterol)
When
Signs & Symptoms th
is unab e liver
Labs
toxins le to filter
like am
mo
∙ Hepatic encephalopathy/coma they bu
ild up in nia,
∙ Asterixis “liver flap”
blood
and e the Bilirubin & ammonia
reach t ventually BLEEDING PRECAUTIONS
∙ Jaundice
he brain Platelets
∙ Use electric razor
∙ Yellow discoloration ∙ Risk for bleeding
∙ Use soft-bristled
of the eyes & skin WBCs toothbrush
∙ Itchy skin ∙ Risk for infection ∙ Hold pressure on
∙ From buildup of toxins scrapes/cuts to
minimize bleeding
∙ Ascites
∙ Edema
∙ Abdominal pain
Medications
normal jaundice
∙ Heartburn Lactulose Lactulose think
• ↓ Serum ammonia Lactuloose because
through the stool it loosens the bowels
Treatment Acid reducers
Treat underlying cause of cirrhosis (antacids & Histamine (H2) Receptor Antagonists)

∙ Fibrosis (scarring) of liver cannot be reversed, Diuretics

but progression can be slowed Vitamins
∙ Possibly a paracentesis
for those with ascites Removal AVOID:
∙ In severe cases, of fluid from
the peritoneal Narcotics
a liver transplant cavity
may be needed Acetaminophen

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 GASTROINTESTINAL

acute liver failure

WHAT IS IT? for diagnosis must have: & onset
Sudden, rapid loss of liver function in ① Acute liver injury (↑ LFT) <26 weeks
patient without history of liver disease ② Coagulopathy (↑ INR) (unless reactivation of hepatitis
③ Encephalopathy (AMS) or Wilson's disease)
medical emergency

CAUSES DIAGNOSTICS
→ Acetaminophen overdose most common Labs
→ Toxins → ↑ AST & ALT → ↓ Platelets
▶ Amanita phalloides (poisonous wild mushroom) → ↑ Bilirubin → ↑ PT/PTT & INR
▶ Alcohol or cocaine → ↑ Ammonia → ↑ Lactate
→ Hepatitis A, B, D & E
→ blood cultures: assess for infection
→ Budd-Chiari syndrome (clot blocks hepatic veins)
→ Wilson’s disease (elevated copper levels) → Autoimmune markers: assess for hepatitis
→ Malignancy © nurse well versed

→ HELLP Syndrome (pregnancy) → ct scan/ mri/ ultrasound

→ Shock

SYMPTOMS GRADES of ENCEPHALOPATHY

→ Jaundice characteristics
severity
→ RUQ pain
▶ Behavioral changes
→ Nausea and vomiting grade I ▶ Altered sleep-wake cycle
→ Fatigue ▶ Mild confusion
→ Hepatic encephalopathy
→ Ascites ▶ Lethargy
grade II ▶ Moderate confusion
▶ + Asterixis
Complications
Cerebral edema: Due to elevated ammonia ▶ More severe confusion
grade III ▶ Stuporous (wakes with stimulation)
sepsis: Increased risk of infection due to liver injury ▶ Incoherant speech
bleeding/ clotting: liver regulates coagulation
hypoglycemia: Liver stores glycogen
▶ Coma
grade IV ▶ Unresponsive to stimuli
TREATMENT
find & treat underlying cause! NURSING INTERVENTIONS
Medications will need icu management
→ Acetylcysteine: antidote for acetaminophen → Prepare for possible intubation
→ Bleeding precautions
→ Osmotic diuretics: ↓ cerebral edema → Keep HOB elevated 30 degrees
→ FFP or Vitamin K for bleeding
→ Lactulose: ↓ ammonia close monitoring
→ Q1 neuro checks
→ Continuous VS & heart monitoring
procedures → Blood glucose checks
→ Emergent liver transplant (in severe cases) → ICP monitoring
→ I&O

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 GASTROINTESTINAL

bowel obstruction
WHAT IS IT? Can affect both the
Blockage in bowel prevents effective
absorption & elimination small & large intestine
Blockage can be partial or complete
large
GI tract is narrowed but some
partial: contents can still pass through
intestine
small
intestine
GI tract is completely blocked &
complete: nothing can pass through
medical emergency
↓ blood flow to bowel causes tissue death &
can lead to perforation & shock

SYMPTOMS
TYPES of BOWEL OBSTRUCTION
mechanical functional small bowel obstruction
→ Colicky abdominal pain
Physical blockage in bowel Muscles & nerves not working
preventing movement properly & disrupt peristalsis → Frequent nausea/ vomiting
→ Severe fluid & electrolyte imbalances
hernia aka paralytic ileus → Metabolic alkalosis
Portion of intestine protrudes
into other part of body
→ Abdominal surgery large bowel obstruction
volvulus → Gastroenteritis → Lower abdominal cramping
Intestine twists around itself → Hypothyroidism
→ Abdominal distention
→ Sepsis
Intussusception → Medications → Vomiting fecal matter (late sign)
Part of bowel telescopes into
adjacent segment ▶ Opioids → Constipation
▶ Anticholinergics
Adhesions → Neuromuscular disorders
Bands of scar tissue form ▶ Parkinson's
hyperactive bs above blockage
between bowel loops ▶ Spinal cord injury &
hypoactive bs below blockage
other causes:
© nurse well versed
Foreign body, tumor, fecal impaction

DIAGNOSTICS NURSING INTERVENTIONS

→ abdominal x-ray: assess for presence of gas or fluid → Keep patient NPO
→ ct scan w/ contrast: assess for cause of obstruction → Ostomy care + education
(also contact wound care RN)
→ Labs: CBC & BMP → Emotional support
→ Pain management

TREATMENT monitor
→ NGT output (amount & color)
partial obstructions may resolve without surgery → Electrolytes
→ IV fluids → Bowel sounds
→ Antibiotics: for infection → VS & heart monitoring
→ Antiemetics: for nausea → I&O
→ NGT placement: for gastric decompression education
→ Colon resection: removal of part of the colon ▶ Small, frequent meals ▶ Low fiber 6-8 weeks
▶ Eat slowly & chew thoroughly ▶ Avoid foods that cause gas
→ Colostomy: part of colon redirected through opening in ▶ Adequate hydration ▶ Add new foods back slowly
abdomen (stoma)

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