Topics that will be covered in the GI section:
GI tract organs and functions
Stomatitis
GERD
Gastritis
PUD
Peritonitis
Appendicitis
Ulcerative colitis
Crohn’s disease
Bowel diseases
Diverticular disease
Gastroenteritis
Herniation
Ostomies
Obstructions
IBS
Hemorrhoids
Liver function
Hepatitis
Cirrhosis
Cholecystitis
Pancreatitis
Chapters: 48-54
Clark College Department of Nursing
Nursing assessment and care of patients with upper gastrointestinal disorders
Nursing Student Learning Outcomes: Upon completion of this module, the student will:
1. Describe the structures and functions of the organs of the gastrointestinal tract.
a. Capriotti:
b. Upper GI: esophagus, stomach, small intestine - major digestion + absorption
c. Intestinal tract: propel digested food, absorb nutrient and water, excrete waste
and indigestible contents
d. Liver: multifunctional organ that synthesizes albumin, coagulation factors,
detoxifies blood, enables fat digestion, stores glucose, vitamins and minerals. It
makes bilirubin water-soluble and excretable.
e. Gallbladder - stores bile (bile digests fats)
f. pancreas - produces digestive enzymes and secretes them into the duodenum.
It digests fats, proteins, and carbohydrates. (lipase, amylase, trypsin,
chymotrypsin, bicarbonate)
g. Iggy: Secretion, digestion, absorption, motility, elimination
h. GI Tract:
i. Mouth - chewing, softening food
ii. Esophagus - muscular tube, weak lower sphincter (aka LES/caridac) is
often cause of GERD, upper sphincter prevents aspiration.
iii. Stomach - pyloric sphincter btwn stomach and duodenum. It digestive
by churning and by acid, pepsin (protein), and intrinsic factor (vitamin
B12). It makes chyme.
iv. Small intestine - duodenum, jejunum, ileum (ileostomy, ileocecal valve).
Movement, mixing (with digestive enzymes), digestion, and absorption.
Huge surface area for absorbing.
v. Large intestine - mainly absorbs water and electrolytes (think about
colostomies)
vi. Rectum - stores feces until defecation
i. Glands:
i. salivary gland - makes salivary amylase, begins carb breakdown, softens
food
ii. pancreas - secretes enzymes that digest carbs, fats, and proteins.
(amylase, lipase, protease) into the duodenum.
iii. liver - makes bile, receives a lot of blood. 400 functions! Storage: stores
iron, magnesium, vit DEAK, vit B12, glycogen. Protection: detoxifies
drugs, chemicals, alcohol, eats bacteria and defective RBCs. Metabolism:
gets ammonia out of the body (via urea), makes albumin, prothrombin,
fibrinogen (clotting factors). fatty acids and triglycerides - makes and
breaks them.
iv. gallbladder - stores bile from liver and secretes it into duodenum. biles
goes through a DUCT (this can cause problems if the duct is blocked)
2. Recognize when assessment findings vary from normal.
a. changes with aging:
i. less stomach acid - less digestion of iron, B12, higher chance of bacteria
overgrowth causing gastritis
ii. less peristalsis - risk of constipation and fecal impaction
iii. pancreas duct changes - less fat absorption, fatty stool
iv. decreased liver function - more risk of drug toxicity
v. gut flora changes increase obesity, inflammation, reduce immunity
b. assessment:
c.
i. Patient history
1. age (young- more likely to have IBS, old more likely to have
cancer), gender, culture, socioeconomic status. appetite? Weight
changes? stool quality and quantity? pain? Travel history camping? swimming?
2. Nutrition history - allergies? what types of food do you eat, what
time of day do you eat. Anorexia, nausea, vomiting? fasting?
lactose intolerant? alcohol and caffeine (risk for PUD). Heartburn
feeling? swallowing difficulties?
3. family history - some disorders have genetic risks.
4. current problem
a. find out about the timings of symptoms, medications,
treatments
b. find out about bowel habits, ask about distention and gas
c. weight and appetite
d. Pain - PQRST
i. P - provoke/palliative - what makes it better or
worse? what caused it?
ii. Q - quality - describe the pain - ache, burn,
stinging?
iii. R - region/radiating - where does the pain start and
go?
iv. S - severity/scale - rate it on a scale of 0-10
v. T - timing - when did it start?
e. Skin changes (usually due to liver/gallbladder) - rashes,
bleeding, bruising, jaundice, itchy skin, dry skin
ii. .Physical assessment
1. Inspection - symmetry, distention, scars, discoloration, umbilicus
position, (you should report if you see peristalsis right away, this
could mean there is an obstruction). Don’t touch a bulging mass it could be an aneurysm.
2. Auscultation - listen from RL, RU, LU, LL pattern (Iggy says to go
RU LU LL RL???). if you hear a swishing sound this may be bruits
and could mean an aneurysm. report that and don’t touch it
3. Percussion - nurses don’t really do this. could be used to find an
enlarged liver or spleen.
4. Palpation - same pattern as auscultation. light palpitations only
(0.5 inch to 1 inch). Looking for rigidity, masses, tenderness,
guarding.
iii. Psychosocial assessment - stressful life events, problems interfering with
work or life, embarrassment?
3. Describe the purposes and subsequent nursing responsibilities regarding diagnostic
studies of the gastrointestinal system.
a. CBC - anemia due to GI bleeds. Very common. ( Normal hemoglobin more than
12. normal hematocrit 35-50% ish). Also infection if WBC over 11. Possibly
immunosuppressed if WBC lower than 4.
b. INR/PT - know how good clotting is. (normal INR is close to 1, 0.7-1.8). Normal PT
is about 10 seconds. liver problems affect clotting
c. CMP - shows electrolytes (especially because nausea and vomiting can deplete
sodium (135-145) and potassium (3.5-5.2) and kidney labs. I think low potassium
can cause paralytic ileus.
d. AST/ALT - liver enzymes. Elevated in liver damage/disorders. Really high in
cirrhosis. ALT = 4-36, AST = 0-35.
e. Serum amylase/lipase - elevated during acute pancreatitis 24 hrs after onset,
lasts 5 days. Does not elevate during necrosis (since the tissue stops making the
enzymes). Amylase = 30-220, lipase = 0-160
f. Bilirubin - converted by the liver, can help to evaluate jaundice and liver
function. Bilirubin is a pigment in bile. Unconjugated (raw, indirect) bilirubin 0.2-0.8 - it can increase during liver damage or RBC breakdown, hemolysis.
Conjugated (direct, liver changed it) - 0.1-0.3 - could rise if there is a biliary
blockage.
g. Ammonia - liver helps to get rid of ammonia, so high ammonia shows low liver
function. Normal - 10-80.
h. Urine - amylase can show acute pancreas, urobilinogen in urine can occur before
jaundice.
i. Stool - apparently stool tests can be used for colorectal cancer screening. Other
reasons: parasites, eggs, blood, fat, and c.diff. Dark blood = GI bleed. Fresh red
blood = typically from constipation/hemorrhoids.
j. X-ray - very easy, not too invasive - can show mass, tumor, stricture, and
obstruction (can see gas). Can also show hernia.
i. Nurse: pt. in hospital gown with no metal
k. CT/MRI - Nurse: if contrast medium is used: assess kidneys, metformin, allergies,
NPO. MRI: metal stuff in body - joints, implants, etc.
l. Endoscopy/EGD - looks at upper GI - takes a look, can take samples. Can look for
bleeding, inflammation, ulcers, tumors. EGD: Looks around esophagus, stomach,
duodenum. It can fix GI bleeds, dilate esophageal strictures, look at lesions, and
confirm celiac.
i. Nursing considerations: ask pt. to not use NSAIDs, anticoagulants, aspirin.
NPO for a few hours. Take out dentures. Moderate sedation (assess
respirations). No gag reflex. Be careful of swallowing. After: PREVENT
ASPIRATION, NPO until gag reflex, check vitals after sedation, look for
pain, bleeding, infection. They can’t drive home because of the sedation.
ii. “After esophagogastroduodenoscopy (EGD), monitor vital signs, heart
rhythm, and oxygen saturation frequently per agency protocol until they
return to baseline. In addition, frequently assess the patient’s ability to
swallow saliva. The patient’s gag reflex may initially be absent after EGD
because of anesthetizing (numbing) of the throat with a spray before the
procedure. After the procedure, do not allow the patient to have food or
liquids until the gag reflex has returned!”
m. Colonoscopy - indications: cancer screening, polyps, GI bleed source, find the
cause of diarrhea. It looks at the large intestine.
i. Prep: Similar to endoscopy, NPO, no NSAIDs, anticoagulants, aspirin.
Bowel prep: clear liquid diet, liquid stools, gatorade. IV access for
moderate sedation
ii. After: frequent vitals, NPO. look for signs of perforation: severe pain and
guarding. Hemorrhage: rapid drop in BP. After flatus is passed and
peristalsis returns, fluids are allowed. There may be a little bleeding if a
biopsy was performed.
4.
a. MRCP: MRI of liver, gallbladder, bile duct, and pancreas. No metal.
b. ERCP: Looks at liver, gallbladder, bile duct, pancreas for obstructions. Usually to
treat, not to diagnose. A papillotomy may be performed (gallstone removal).
Stricture treatment like stent. Biopsy
i. Nurse: prep is similar to EGD. This involves x-rays and dye. Remove metal,
deactivate defibrillators,
ii. Severe pain and fever a few days afterwards is BAD. Usually it means
gallbladder or pancreas inflammation, perforation, sepsis.
5. Explain the pathogenesis, clinical manifestations, complications, nursing,
pharmacological and surgical management of disorders of the mouth and esophagus.
a. Stomatitis
i. Inflammation, ulcers (canker sore) in the mouth
ii. Pathogenesis: primary - noninfectious, herpes, or trauma as cause
(allergies too). Secondary - infection by bacterial, fungi, virus - common
is candida. Risk: medicines that dry mouth, inhaled steroids, poor oral
hygiene.
iii. S/S: pain, lesions in mouth
iv. Labs
v. Treatment: warm saline or bicarb rinse, anti-fungi, viral, bacterial
medications, frequent oral care (no alcohol mouthwash), oral hygiene,
eating soft foods. Pain: lidocaine, Aluminum hydroxide, magnesium
hydroxide, and simethicone suspension
vi. Complications: bleeding, infection, dysphagia, anorexia.
b. GERD
i. Acidic stomach content flows into the esophagus and causes damage
ii. Risk: increased pressure in abdomen (obesity, pregnancy, ascites,
bending, sleep apnea, tight clothes), h. pylori causing gastritis, NG tubes,
diet: coffee, mint, tomatoes, caffeine, alcohol, chocolate, nitrates.
Smoking.
iii. S/S: Heartburn, indigestion, feeling full, gas, bloating,
epigastric/abdominal pain
iv. Labs: normally none, if things are really weird do an endoscopy,
esophageal pH testing.
v. Treatment: Lifestyle: small, frequent meals, no fatty, spicy, caffeine or
fried foods. Sitting up after eating. Don’t eat too close to bedtime. Avoid
heavy lifting and bending. CPAP helps in OSA pts.
vi. Surgery: Stretta (non-invasive), fundoplication. LINX - a device that
augments the LES with a ring composed of rare earth magnets. NO LINX
WITH MRI!!!
vii. Meds: eliminate harmful meds: birth control, NSAIDs, anticholinergics.
Antacids, histamine blockers, and proton pump inhibitors (PPIs). They
block gastric acid secretion, promote gastric emptying, protect gastric
lining.
1. Famotidine: histamine antagonist
2. Sucralfate - GI protectant
3. Omeprazole - proton-pump inhibitor - caution: risk of fracture
4. Pantoprazole - proton-pump inhibitor - caution: risk of fracture
5. Calcium Carbonate - antacid
6. Aluminum hydroxide with magnesium hydroxide ::antacid
7. Aluminum hydroxide with simethicone: antacid
viii. Complications: Barret esophagus (tissue changes), stricture (narrow
esophagus), cancer, asthma, hemorrhage, aspiration pneumonia,
dental issues, respiratory issues.
6. Differentiate between acute and chronic disorders of the stomach, including the
etiologies, pathophysiology and care management.
a. Gastritis
i. Inflammation of stomach lining
ii. Risk: Damage to the protective lining of the stomach, the acid makes
everything worse. Long-term NSAID use. Alcohol, coffee, caffeine,
smoking, toxic chemicals. Drugs: SSRIs, spironolactone, steroids.
Chronic: h. pylori, stomach surgery, radiation, smoking.
iii.
iv. Healthy diet - avoid chocolate, peppers, mustard, caffeine
v. S/S: epigastric pain, heartburn, bright red -coffee ground vomit, dark
tarry stool, severe nausea and vomiting. Chronic: nause, vomiting,
anorexia, usually few symptoms unless there are ulcers. periodic
epigastric pain.
vi. Labs: EGD w/biopsy- gold standard. Can test for H. pylori. Better results
if no PPI/antacid has been taken for a week prior. From ppt: CBC for
H+H, CMP if N/V
vii. Treatment: Acute - often supportive treatment, remove the cause,
sometimes need blood transfusions and fluid support for massive bleeds.
Electrolyte replacement for major vomiting. Diet - bland, no irritating
foods. Stress reducing techniques.
1. Chronic - Get rid of the cause, treat any h. pylori, B12
supplements
viii. Surgery: Acute - gastrectomy sometimes to remove areas of significant
ulcer/bleeding. It could also reduce acid secretion
ix. Meds:
1. Famotidine: histamine antagonist
2. Sucralfate - GI protectant
3. Omeprazole - proton-pump inhibitor - caution: risk of fracture
4. Pantoprazole - proton-pump inhibitor - caution: risk of fracture
5. Calcium Carbonate - antacid - (risk of rebound acid secretion)
6. Aluminum hydroxide with magnesium hydroxide ::antacid
7. Aluminum hydroxide with simethicone: antacid
x. Complications: Pernicious anemia, permanent stomach damage ( no
longer secretes acid), cancer, hemorrhage
b. PUD
i. The protective lining of the stomach is broken through, exposing the
tissue to harsh acid, causing ulcer.
ii. Risk: H. pylori (mouth to mouth, fecal to oral). Family history. Same risk
factors as gastritis. Duodenal: high-protein, high calcium food, vagus
nerve stimulation increases gastric acid. Gastric: bile back-flowing
through pyloric sphincter. Stress ulcer: medical crisis situation, critically
ill people, sepsis pts.
iii. S/S: Midline epigastric pain, Peritonitis - rigid, boardlike belly. Initial
hyperactive tones, later less tones. Dyspepsia (heartburn). orthostatic
hypotension, dehydration from GI bleed. N/V.
iv. Labs: H. Pylori tests (stool, breath, or blood). Occult blood. H+H. EGD is
the main diagnostic tool. lets look at the ulcer
v. Treatment/med:
1. Pain relief - NO NSAIDS!!!!!
2. Treat h. pylori infection: 2 types of antibiotics, bismuth (Don’t
take aspirin)
3. Heal ulcer: PPI (1st choice, possible osteoporosis risk, don’t
suddenly stop taking), H2 antagonist
4. Prevent more ulcer
5. Diet: try to avoid caffeine, eat healthy, possibly eat bland to
reduce symptoms, try not to eat near bedtime, avoid alcohol and
smoking
6. Stress reduction - yoga?
vi. Surgery: lap ulcer removal, gastrectomy
vii. Complications: Hemorrhage - this is an RRT call
viii. Critical Rescue - “Recognize that your priority for care of the patient with
upper GI bleeding is to maintain airway, breathing, and circulation
(ABCs). Respond to these needs by providing oxygen and other
ventilatory support as needed, starting two large-bore IV lines for
replacing fluids and blood, and monitoring vital signs, hematocrit, and
oxygen saturation.” the nurse might also do an ng tube in order to:
“determine the presence or absence of blood in the stomach, assess the
rate of bleeding, prevent gastric dilation, and administer gastric lavage”
ix. It may be treated with an EGD
x.
xi. Perforation - hole in GI tract, things leak out. S/S: sharp pain,
apprehension, rigid and boardlike abdomen (Peritonitis). Pt. takes a fetal
position. Life threatening emergency!!
xii. Blockages, permanent (intractable) ulcers
Nursing care of patients with lower gastrointestinal, hepatic and pancreatic disorders
Nursing Student Learning Outcomes: Upon completion of this module, the student will:
1. Explain the pathogenesis and the medical and nursing management of peritonitis.
a. Peritonitis
b. The sterile fluid in the peritoneum get a pathogen. Inflammation and infection.
Blood gets shunted to the peritoneum, fluid gets shifted to the cavity (3rd
spacing), causing hypovolemic shock. Decreased perfusion to the kidney. Risk of
sepsis and death. Peristalsis may stop and bad things accumulate in the GI tract.
Respiratory effects due to the pressure. High mortality rate - 20%
c. Risk: Perforation (PUD, diverticulitis, appendicitis). Wounds, surgeries. Leakage
of bile or pancreatic enzymes.
d. S/S: Pain, fever. Fetal position. The cardinal signs of peritonitis are abdominal
pain, tenderness, and distention
e.
f. Labs: WBC (often elevated to 20,000), neutrophils high. Blood culture. CBC
(H+H), CMP (electrolytes and kidney function), oxygen saturation. X-ray or CT
scan.
g. Treatment: Patient will likely be in critical care. Monitor vitals frequently for
shock signs, monitor mental status. Asepsis and strict handwashing around this
patient. Sterile when doing urinary catheter stuff. Monitor wounds for drainage.
Oxygen as needed. Fluids: Give Hypertonic IV fluid, NG tube to decompress
stomach, monitor weight
h. Surgery: To find and repair the cause. It usually removes the inflamed organ,
controlling infection from spreading, draining fluid. Cleaning the cavity.
i.
Action Alert
j. Monitor the patient’s level of consciousness, vital signs, respiratory status
(respiratory rate and breath sounds), and intake and output at least hourly
immediately after abdominal surgery. Maintain the patient in a semi-Fowler
position to promote drainage of peritoneal contents into the lower region of the
abdominal cavity. This position also helps increase lung expansion.
k. Meds: Broad spectrum antibiotics.
l.
Complications: Sepsis, hypovolemic shock, respiratory issues, death
2. Compare and contrast inflammatory vs non-inflammatory bowel diseases.
3.
a. Ulcerative colitis
i. chronic inflammation of rectum/sigmoid colon. (could go to the entire
colon if disease is extensive). Lining can bleed and ulcers can occur.
abscess and necrosis can occur.
ii. Risk: Not fully known. Genetic, immunologic, environmental.
Exacerbation causes: infection
iii. S/S: Bloody and mucus stools. Tenesmus - unpleasant and urgent sense
to defecate. Pain. Malaise, anorexia, anemia, dehydration, fever, weight
loss.
iv. Labs: H+H may be low, High WBC, C-reactive protein, sed rate. Diarrhea
- low sodium, potassium, chloride. Low albumin - not being absorbed.
MRE (MRI). CT scan to confirm diagnosis sometimes. Endoscopy or
colonoscopy, especially after 10 years.
v. Treatment: Risk of dehydration, hypokalemia. Psychosocial. Rest.
Notebook for stool and diet. Peri-care. Nutrition therapy and rest: severe
- NPO, bowel rest, TPN. Some people need to cut out caffeine, alcohol,
high-fiber foods, lactorse, carbonated beverages, pepper, nuts, corn,
dried fruits, smoking bad. But each person is different. Pt. needs to rest.
vi. Always monitor for lower GI bleeds. Critical Rescue
1. Recognize that it is important to monitor stools for blood loss for the patient with
2.
ulcerative colitis. The blood may be bright red (frank bleeding) or black and tarry
(melena). Monitor hematocrit, hemoglobin, and electrolyte values and assess vital
signs. Prolonged slow bleeding can lead to anemia. Observe for fever,
tachycardia, and signs of fluid volume depletion. Changes in mental status may
occur, especially among older adults, and may be the first indication of
dehydration or anemia.
If symptoms of GI bleeding begin, respond by notifying the Rapid Response Team
or primary health care provider immediately. Blood products are often prescribed
for patients with severe anemia. Prepare for the blood transfusion by inserting a
large-bore IV catheter if it is not already in place. Chapter 37 outlines nursing
actions during blood transfusion.
vii. Surgery: Ileostomy (give prophylactic antibiotics). Protocoletomy with
ileo pouch-anala anastomosis - gold standard.
1. Critical Rescue
2. The ileostomy stoma (Fig. 52.3B) is usually placed in the right lower quadrant of
the abdomen below the belt line. It should not be prolapsed or retract into the
abdominal wall. Assess the stoma frequently after stoma placement. Recognize
that it should be pinkish to cherry red to ensure an adequate blood supply. If the
stoma looks pale, bluish, or dark, respond by reporting these findings to the
surgeon immediately ( Stelton, 2019 )!
3. Initial: loose, dark green liquid w/some blood. High output at first.
Then, the small intestine will start to do some colon things and
absorb water. Stool becomes paste-like and yellow-green,
yellow-brown, with less output.
4. giver 500 mL extra water to reduce dehydration.
viii. Meds: aminosalicylates, glucocorticoids (long-term use effects:
osteoporosis, infection, hyperglycemia, don’t suddenly stop using) ,
antidiarrheal (risk for toxic megacolon), immunomodulator.
ix. Complications: Colon cancer
b. Crohn’s disease
i. chronic inflammatory disease, anywhere in the GI tract from mouth to
anus. Common: terminal ileum.
ii. Risk: unknown. Family history, genetics, environment. Tobacco use,
living in urban areas. Exacerbated by infection.
iii. S/S: Cobblestone appearance. Severe diarrhea, malabsorption of vital
nutrients (especially small intestine), anemia from malabsorption. Bowel
tones: decreased/absent due to inflammation, high-pitched or rushing
sounds over narrow bowel loops. Common: diarrhea, ab pain, low-grade
fever. RLQ.
iv. Labs: ESR, C-reactive protein. X-rays show stricutres, fistulas, narrowing,
ulceration. MRE.
v. Treatment: Similar to UC. Possible TPN and bowel rest. Nutritional
supplements including vitamin B12. Avoid GI stimulant foods.
vi. Fistula care: Action Alert
vii. Adequate nutrition and fluid and electrolyte balance are priorities in the care of the patient
with a fistula. GI secretions are high in volume and rich in electrolytes and enzymes. The
patient is at high risk for malnutrition, dehydration, and hypokalemia (decreased serum
potassium). Assess for these complications and collaborate with the health care team to
manage them. Carefully monitor urinary output and daily weights. A decrease in either
measurement indicates possible dehydration, which should be treated immediately by
providing additional fluids.
viii. Action Alert
ix. For patients with fistulas, preserving and protecting the skin are the nursing priorities. Be
sure that wound drainage is not in direct contact with skin because intestinal fluid enzymes
are caustic! Clean the skin promptly to prevent skin breakdown or fungal infection, which
can cause major discomfort for the patient.
x.
xi. 3,000 calories a day to heal a fistula. Prevent skin breakdown, use drains.
xii. Surgery: Resections (unfortunately, surgery is not as effective in CD as it
is in UC). Stricturoplasty to increase bowel diameter.
xiii. Meds: SImilar to UC. But be careful with glucocorticoids (they mask
infection signs that might come from fistula or abscess.
xiv. Complications: fistula development. Hemorrhage (more common in UC
than CD). Obstruction. Peritonitis, nutritional and fluid imbalances.
Bowel cancer
c. appendicitis
i. A blockage in the appendix causes inflammation, infection, swelling,
possibly bursting.
ii. Risk: Young adults.
iii. S/S: Initial pain could be anywhere, then moves to McBurney point. RLQ
pain. Later: pain at McBurney’s point. (Pain 1st, then N/V note:
gastroenteritis - N/V first, then pain). Rebound tenderness. Peritonitis pain relieved by fetal position.
iv. Labs: WBC 10-18. Ultrasound to show appendix. CT scan shows the
fecaloma.
v. Treatment: NPO in case of surgery, some pain relief
vi. Action Alert
vii. For the patient with suspected appendicitis, administer IV fluids as prescribed to maintain
fluid and electrolyte balance and replace fluid volume. If tolerated, advise the patient to
maintain a semi-Fowler position so that abdominal drainage can be contained in the lower
abdomen. Once the diagnosis of appendicitis is confirmed and surgery is scheduled,
administer opioid analgesics and antibiotics as prescribed. The patient with suspected or
confirmed appendicitis should not receive laxatives or enemas, which can cause
perforation of the appendix. Do not apply heat to the abdomen because this may increase
circulation to the appendix and result in increased inflammation and perforation!
viii. Surgery: typically an appendectomy
ix. Meds: ABX, pain relief, fluids
x. Complications: perforation, Peritonitis, gangrene, sepsis, abscess
d. gastroenteritis
i. inflammation of the stomach and intestinal tract (often viral)
ii. Risk: foodborne illness, fecal-oral route, living in crowded areas, travel
iii. S/S: Diarrhea/vomiting. N/V first, then cramping and diarrhea. possibly,
weakness and dysrhythmias due to low potassium from diarrhea.
Dehydration - dry membranes, oliguria, even could cause mental status
changes
iv. Labs: CMP (potassium, kidney?)
v. Treatment: typically self-limiting and lasts 3 days. Worries about
dehydration. Fluid replacement. Peri-care - avoid TP or harsh soaps. USe
gentle warm water with a nice gel or cream. Sitz baths. Good peri-care.
vi. Surgery: none?
vii. Meds: Sometimes antidiarrheal such as loperamide (but diarrhea can be
good to help eliminate the bacteria/virus). Antibiotics (bacterial
infection).
viii. Complications: hypovolemia, hypokalemia
e. diverticular disease
i. Pouches in the intestine that get inflamed (diverticulitis).
ii. Risk: typically sigmoid colon. Age, lack of fiber in diet. Food or bacteria
get trapped in a diverticulum, reducing blood supply. Constipation, less
bulky stool have been implicated.
iii. S/S: LLQ pain. low-grade fever, nausea, abdominal pain. Constipation.
iv. Labs: High WBC< low H + H. occult blood. x-ray to show free air and fluid.
CT scan. Diverticuli (not inflamed) are often found with routine
colonoscopy.
v. Treatment: Rest. Refrain from lifting or straining - risk of perforation.
Diet - low fiber or clear liquid - initially. Possibly NPO. After: teaching
what foods to avoid - nuts, corn popcorn, cucumbers (small seeds are
bad), tomatoes (small seeds), figs. Strawberry.
Diverticulitis - older adult considerations
• Provide antibiotics and analgesics as prescribed. Observe older patients carefully for side effects of these
drugs, especially confusion (or increased confusion), and orthostatic hypotension.
• Do not give laxatives or enemas. Teach the patient and family about the importance of avoiding these
measures.
• Encourage the patient to rest and to avoid activities that may increase intra-abdominal pressure, such as
straining and bending.
• While diverticulitis is active, provide a low-fiber diet. When the inflammation resolves, provide a highfiber diet. Teach the patient and family about these diets and when they are appropriate.
• Because older patients do not always experience the typical pain or fever expected, observe carefully for
other signs of active disease, such as a sudden change in mental status.
• Perform frequent abdominal assessments to determine distention and tenderness on palpation.
• Check stools for occult or frank bleeding.
vi.
vii. Surgery: colon resection. Emergency surgery to deal with complications.
viii. Meds: Broad spectrum antimicrobial. Mild anagelgis. IV fluid for
dehydration. NO laxatives or enemas (increased intestinal motility)
ix. Complications: perforation, peritonitis, lower GI bleeds
Non-inflammatory
f. IBS
i. chronic diarrhea, constipation, bloating, abdominal pain.
ii. Risk: most common digestive disorder. unknown cause. sometimes
foods like dairy, caffeine, carbonated beverages. Stress, anxiety,
depression.
iii. S/S: chronic diarrhea, constipation, bloating, abdominal pain.
iv. Labs: Routine laboratory values (including a complete blood count [CBC], serum
albumin, erythrocyte sedimentation rate [ESR], and stools for occult blood) remain
normal in IBS. Possible hydrogen breath test (NPO)
v. Treatment: Often get rid of dairy, raw fruit, grains. Dietary fiber and
bulk. 30-40 g of fiber. lots of water, chew slow, regular meals. probiotics.
peppermint oil. stress management.
vi. Surgery:
vii. Meds: Bulk-forming laxatives, bulk-forming psyllium, antidiarrheals.
Amitriptyline for pain.
viii. Complications: mental health
g. Hemorrhoids
i. swollen, distended veins in the anorectal region.
ii. Risk: Increased intra-abdominal pressure. Pregnancy, constipation,
obesity, heart failure, sitting or standing too long, weight lifting.
iii. S/S: bleeding, swelling, bulging, bright red blood on toilet paper. Pain.
iv. Labs: Inspection and digital exam.
v. Treatment: constipation - more fiber in diet, more whole grains, veggies,
fruit, lots of water. avoid straining. healthy weight. Cold packs. Sitz
baths. lidocaine for severe pain. steroid for itching or inflammation.
Moist tissue wipes rather than paper.
vi. Surgery: remove hemorrhoids. Action Alert
vii. Tell the patient who has had surgical intervention for hemorrhoids that the first
postoperative bowel movement may be very painful. Be sure that someone is with or near
the patient when this happens. Some patients become light-headed and diaphoretic and may
have syncope (temporary loss of consciousness) related to a vasovagal response.
viii.
ix. Meds:
x. Complications: pain, bleeding
h. herniations
i. segment of bowel goes through a weakness in a abdominal muscle wall.
1. Reducible - can be placed back with gentle pressure
2. incarcerated/irreducible - can not go back in - immediate surgical
eval needed.
3. strangulated - blood supply is cut off, risk for ischemia and
obstruction. s/s: ab distension, n/v, pain, fever, tachycardia.
Absent bowl sounds.
ii. Risk: muscle weakness, intra-abdominal pressure (obesity, pregnancy,
heavy lifting)
iii. S/S: lump or protrusion.
iv. Labs:
v. Treatment: Hernies are never forcibly reduced. A truss to wear.
vi. Surgery: same-day surgeries. Hernia repair surgery. NPO before
procedure, need someone to drive you home. THEY SHOULD AVOID
COUGHING (deep breath and ambulate instead). Avoid strain and lift for
several weeks. Showers OK in a few days. Don’t lift more than 10 lbs. Eat
high-fiber foods to avoid constipation. Go back to work about 1-2 weeks.
vii. Meds:
viii. Complications: strangulation of the intestine (risk of necrosis, sepsis and
perforation), a leak that could eventually cause peritonitis
4. Compare and contrast the anatomic and physiologic differences among the various
ostomies.
a. ostomies - for ileostomy - see ulcerative colitis
i. basically just think about infection, skin breakdown, bleeding. Wellfitting pouch. Psychosocial.
ii. Ileostomy - foods to reduce gas, drink extra water to stay hydrated.
Typically has a lot of drainage at first, then less later.
iii. no extended-release medications
iv. Colostomy - reddish pink, dark red to pink and protruding is good. After
creation - small bleeding and slight swelling is normal. Assess skin. Start
working 2-3 days after surgery. empty ⅓-½ full. liquid at first but
becomes more solid. Nutrition - control gas. (veggies). psychosocial.
Financial concerns.
v.
5. Describe the etiologies, clinical manifestations and management of intestinal
obstructions.
a. Obstructions
i. Physically blocked or functionally blocked bowel.
ii. Risk: adhesions, tumors, hernias, fecal impactions, strictures, Non
Mechanimal: post op. Surgery, tumors, older age.
iii. S/S: distention. mid-ab pain or cramping. Could be sporadic. Vomiting.
Full - obstipation, no flatus, partial - diarrhea, ribbon stool. visible
peristalsis waves. Borborygmi (high-pitched sounds), could become
absent later.
iv. Labs: CT snac, MRI. ultrasound, endoscopy. Normal WBC. H+H, BUN
high - dehydration. Electrolytes.
v. Treatment: NPO w/ NG tube. IV fluid replacement and maintenance. NG
tube - assess for placement, patency, output, skin, peristalsis. Fecal
impaction - disimpaction, enema. pain meds often held so we know if
there is perforation or peritonitis. . Semi-fowler
vi.
vii. Surgery: laparotomy to explore cause. get an NG until peristalsis returns
and fluids are tolerated.
viii. Meds: alvimopan - increase motility (for post-op ileus), metoclopramide
(increase gastric motility). ABX for complications.
ix. Complications: hypovolemic shock (fluid changes, plasma leak in
peritoneal cavity). Fluid and electrolyte balance, acid-base
balance.Peritonitis, perforation. Strangulated obstruction, closed-loop
obstruction, gangrene, ischemia. .
6. Describe the liver’s metabolic functions.
a. Liver: multifunctional organ that synthesizes albumin, coagulation factors,
detoxifies blood, enables fat digestion, stores glucose, vitamins and minerals. It
makes bilirubin water-soluble and excretable. Excretes ammonia from protein.
7. Differentiate between the types of viral hepatitis including the etiology, clinical
manifestations, complications and their management.
a. hepatitis
i. widespread inflammation and infection of liver.
ii. Risk: viral is most common. uncommon: chemicals, drugs, herbs. Living
in close contact with other people (dorms, prisons).
1. Hep A - mild, flu like. fecal-oral wrote, consuming contaminated
food or water. Shellfish. Not usually life threatening. Usually like
a normal GI illness with uneventful recovery.
2. Hep B - blood transmitted. Needles, sexual intercourse, sharing
toothbrush, razers, transfusions, hemodialysis, birth, contact
with blood. Many ppl have no symptoms.
3. Hep C - leading cause of end-stage liver disease. Blood to blood.
Not by casual contact, but be careful with razors or toothbrushes
because it may have some blood on it. Usually becomes a chronic
infection. Causing chronic inflammation and scarring. Leads to
cirrhosis.
iii. S/S: Abdominal pain, yellow sclera, joint or muscle pain, N/V, diarrhea,
constipation, anorexia, light-clay colored stools, dark yellow/brown
urine, JAUNDICE, fever, fatigue, malaise, dry skin, itching.
iv. Labs: acute elevations of ALT and AST (into the 1,000s!!) Increased
bilirubin. Antibody screen. Liver biopsy to find cause. Ultrasound
v. Treatment: Prevent - hep b and A vaccines. Proper handwashing.
Prevent needlesticks. Treatment: prevent dehydration. Encourage meals
with high calories and find appealing foods to counteract anorexia. Rest.
vi. Surgery:
vii. Meds: Antivirals, immunomodulating drugs. Make sure to avoid crowds.
Teaching: avoid alcohol, prevent fatigue by resting and planning, small
meals with high carbs.
viii. Complications: cirrhosis, liver cancer. Necrosis, fulminant hepatitis (fatal,
acute type of hepatitis).
8. Explain the pathogenesis, clinical manifestations, complications and management of
cirrhosis.
a. cirrhosis
i. extensive, irreversible scarring of the liver.
ii. Risk: chronic reaction to inflammation and necrosis. Postnecrotic - viral
hepatitis, some drugs, toxins. Alcoholic - chronic alcoholism. Biliary chronic biliary obstruction. Nonalcoholic fatty liver disease can cause
chirrosis (NAFLD is assoicated with aging, obesity, t2dm, metabolic
syndrome).
iii. S/S: Early - fatigue, weight changes, GI - anorexia, vomiting, pain in the
abdomen and liver tenderness. Often early is compensated and pt. will
not notice symptoms. Hepatomegaly. splenomegaly. Late: Gi bleed,
jaundice, ascites (measure girth), bruising.
iv. Other: occur blood, vomit blood - from bleeding or varices. Fetor
hepaticus - fruity or musty breath odor of chronic liver disease and
hepatic encephalopathy. No period, testicular atrophy, gynecomastia,
impotence. Mental status changes!!!! asterixis - tremor of the hands.
Alcohold withdrawal symptoms.
v.
vi. Labs: High AST, ALT. Bilirubin - high, indirect bilirubin - high. Urine
urobilinogen - high. Fecal urobilinogen - low (for obstructive liver
disease)). Low albumin. High PT/INR. Low RBC and WBC (low platelets).
High ammonia. X-ray to show enlargement or ascites. CT or MRI too.
Ultrasound. Biopsy - bleeding risk. EGD for varices, ulcers, irritation.
ERCP.
vii.
viii. Treatment: Fluid volume management - Low sodium diet, late stage - IV
vitamin supplements - thiamine, folate, multivitamins (liver can’t story
vitamins).
1. Be careful of giving drugs that are eliminated by the liver.
2. for itching - avoid being too warm, do moisturize, avoid irritants,
some creams such as corticosteroid, cool compresses.
3. No alcohol, tylenol, smoking, or illicit drugs.
ix. Surgery: Paracentesis - remove abdominal fluid. TIPS (not really a
surgery) - diverting blood vessels. Risks: elevated pulmonary artery
pressure and strain on the right heart. More toxins in the body - give
lactulose.
1.
x. Meds:
1. Diuretics to reduce fluid accumulation (possibly with potassium
supplement).
2. Propranolol - decrease HR and hepatic venous pressure gradient,
lowers the chance of varices bleeding.
3. Octretide - leads to decreased GI blood flow and helps reduce
pressure in the varices (helps with variceal bleeding and the
decrease portal hypertension, also has an antidiarrheal effect).
4. Lactulose - get rid of ammonia via the stool (also has a laxative
effect) Thiamine and benzo for alcohol withdrawel.
xi. Complications: end-stage liver disease.
1. Portal hypertension
2. Ascites - risk for spontaneous bacterial peritonitis from stagnant
fluid - if this happens, abx are needed. First for hepatopulmonary
syndrome - respiratory problems due to increased pressure. Risk
for f/e imbalance and hypovolemia. TIPS: shunt that controls
long-term ascites and reduces variceal bleeding.
3. Esophageal varices - risk of hemorrhage. treatment - preventive
therapy - propranolol. If you already had a bleed antibiotics to
prevent infection. Bleeds are emergencies!! - octreotide can be
given. Ligate the bleeding. sclerotherapy may be used to stop
bleeding. Rescue procedures - balloon tamponade, stents,
shunting. Pt. typically gets a NG tube to detect new bleeding, get
RBC, plasma, destran, albumin, platelets.
4. Biliary obstruction
5. Hepatic encephalopathy - due to ammonia build-up. Should only
eat moderate protein (not high protein). Lactulose to get rid of
ammonia buildup. Monitor mental status frequently. check for
asterixis and fector hepaticus.
6. hepatorenal syndrome - oliguria, increased osmolarity.
9. Explain the pathogenesis, clinical manifestations, complications and management of
gallbladder disorders.
a. Cholecystitis
i. gallbladder inflammation
ii. Risk: adults in affluent countries. Obesity, sedentary lifestyle, genetics,
high cholesterol intake. Pregnancy, hormones. Women. Rapid weight
loss or prolonged fasting.
1. Typically, diets high in fat, high in calories, low in fiber, and high in refined
white carbohydrates place patients at high risk for developing gallstones.
Consuming low-fat diets can contribute to chronic cholecystitis in young thin
women.
2. Acute: Calculos - the cause is gallstone (cholelithiasis) the stone
causes bile to be reabsorbed and it irritates the gallbladder wall.
Acalculous - often due to sepsis, severe trauma, burns, TPN,
MODS, major abdominal surgery, hypovolemia.
3. Chronic: young thin women, athletic, veterinary diet low in fat.
iii. S/S: Abdominal pain. could be in the RUQ and radiate to the right
shoulder. Pain AKA “gallbladder attacks”. Temp up, tachycardia,
dehydration. Chronic - Jaundice and icterus - more common in chronic.
Itching, burning. clay-colored stool, dark urine full of bilirubin,
steatorrhea.
1. Critical Rescue
2. The severe pain of biliary colic is produced by obstruction of the cystic duct of
the gallbladder or movement of one or more gallstones. When a stone is moving
through or is lodged within the duct, tissue spasm occurs in an effort to get the
stone through the small duct. Biliary colic may be so severe that it occurs with
tachycardia, pallor, diaphoresis, and prostration (extreme exhaustion). Assess the
patient for possible shock caused by biliary colic. Notify the health care provider
or Rapid Response Team if these symptoms occur. Stay with the patient and keep
the head of the bed flat if shock occurs.
3. Older adults may have atypical symptoms such as only delirium
or localized tenderness.
4.
iv. Labs: rule out similar things such as PUD, hepatitis, pancreatitis.
Increased WBC, possible elevation of AST, LDH, AST, Bilirubin if liver is
involved. Possibly also amylase and lipase if pancreas is involved. X-ray
clearly shows calcified gallstones. Ultrasonography. ERCP, MRCP.
v. Treatment: Treating pain is a high priority. Dehydration is important in
older adults- iv fluids. Diet: avoid fatty foods, high -fiber, no food and
fluid if n/v occur.
vi. Surgery: Lap chole (gold standard), lithotripsy (waves to break up
gallstones, not surgery)), & cholecystectomy (removal of gallbladder).
Biliary drains.
1. Action Alert
2. After a laparoscopic cholecystectomy, assess the patient’s oxygen saturation level
using pulse oximetry frequently until the effects of the anesthesia have passed.
Remind the patient to perform deep-breathing exercises every hour.
3. Some people will need to carefully avoid high-fat foods after the
lap chloe.
4. Postcholecystectomy syndrome - pain, n/v following procedure.
vii. Meds: Analgesics, opioids - but they can cause sphincter of Oddi spasm.
Ketorolac - potent NSAID - risk of GI bleeding. Antiemetics. ABX.
viii. Complications: reduced nutrition status. Infection. Risk of ischemia,
infection, necrosis and gangrene, rupture, abscess, peritonitis.
10. Describe the pathogenesis, pathophysiology, clinical manifestations, complications and
management of pancreatic disorders.
a. Pancreatitis (acute)
i. serious (possibly life-threatening) inflammation of the pancreas.
Enzymes activate early in the pancreas.
ii. Risk: Half the cases are caused by gallstones. Biliary tract disease.
Surgery, trauma. Alcohol consumption. Childbirth.
iii. S/S: “severe boring abdominal pain “ severe, constant abdominal pain.
Mid-epigastric area or LUQ. often radiates to back, left flank, left
shoulder. WORSE WHEN LYING FLAT. Gray-blue discoloration
(Turner/Cullen’s sign). Ask about alcohol intake. paralytic ileus.
Cullen’s sign - blue gray discoloration around the umbilicus.
Turner’s sign - ecchymosis on flanks (side).
iv. Critical Rescue
v. For the patient with acute pancreatitis, monitor for significant changes in vital signs that
may indicate the life-threatening complication of shock. Hypotension and tachycardia may
result from pancreatic hemorrhage, excessive fluid volume shifting, or the toxic effects of
abdominal sepsis from enzyme damage. Observe changes in behavior and level of
consciousness (LOC) that may be related to alcohol withdrawal, hypoxia, or impending
sepsis with shock.
vi.
vii. Labs: HIgh amylate, lipase (useful). It is accompanied by biliary
dysfunction - high bilirubin, ALT. WBC, ESR, and glucose are often high.
Low calcium and magnesium. High BUN, triglycerides.
Hemoconcentration due to 3rd spacing. Low platelets. C-reactive
protein.
1. Ab ultrasound to find gallstones. CT w/ contrast is most reliable.
X-ray to show stones, and pleural effusion. ERCP for stones.
viii. Treatment: Manage pain. Support breathing - monitor often. Decrease
GI activity - NPO, possible NG suction - keep nutrition in mind. Position side-lying fetal position. Once food is tolerated - small, frequent meals,
high protein, low-fat, bland with little spice, avoid caffeine, alcohol.
1. IV fluids - calcium and magnesium, pain control 0 PCA, opioids .
ix. Surgery: ERCP with sphincterotomy (not a surgery). Other surgeries
usually not indicated. Possible lap chloe to remove stones. abscess/cyst
drainage
x. Meds: Famotidone, PPIs (prazoles). ABX if indicated.
xi. Complications: Necrotizing hemorrhagic pancreatitis (could lead to
MODS). Jaundice (due to a bile duct obstruction). Diabetes. Pleural
effusion, atelectasis, pneumonia. ARDS. (pulmonary failure is
responsible for half of deaths). Hypercoagulation and DIC. Shock.
b. Pancreatitis (chronic)
i. Progressive, destructive disease, has flare ups and calm periods.
ii. Risk: Alcoholism, biliary tract disease (cholecystitis/cholelithiasis),
autoimmune
iii. S/S: Steatorrhea (clay colored, frothy stool), jaundice, intense
abdominal pain (continuous, burning, gnawing), abd. tenderness,
ascites, weight loss, dark urine, possible LQ mass, resp. compromise,
polyuria, polydipsia, polyphagia (DM)
iv. Labs: ERCP, CT, MRI, EUS. (Check amylase & lipase levels, bilirubin &
alkaline ph levels)
Increase- amylase, lipase, WBCs, bilirubin, glucose,
Decrease- calcium, magnesium, platelets
Stool specimen - steatorrhea
v. Treatment: Manage pain, maintain adequate nutrition (similar to acute,
low fat, high calories, no alcohol), & prevent ds. recurrence. Opioids,
analgesics, abx, pancreatic enzymes (give wit meal/snacks).
Prevention of Exacerbations of Chronic Pancreatitis
• Avoid things that make your symptoms worse, such as drinking caffeinated beverages.
• Avoid alcohol ingestion; refer to self-help groups for assistance.
• Avoid nicotine.
• Eat bland, low-fat, high-protein, and moderate-carbohydrate meals; avoid gastric stimulants such as
spices.
• Eat small meals and snacks high in calories.
• Take the pancreatic enzymes that have been prescribed for you with meals.
• Rest frequently; restrict your activity to one floor until you regain your strength.
vi. Surgery: not a primary intervention. Lap - abscess drain,
sphincterotomy. Pancreas resection.
vii. Meds: opioid or nonopioid analgesics. PO pancreatic enzymes. Possibly diabetes meds. H2 blocker and PPIs to protect the pancreatic enzymes.
viii. Complications: Fibrosis leading to insufficiency and pancreas
dysfunction. Weight loss and muscle wasting due to fat malabsorption.
DM. Pulmonary complications (effusions, infiltrates, even ARDS.)
Chapters to read: 48-54
Students! FYI, notes are NOT complete, please remember to complete your own notes as
you study.
Random med notes:
-PO vs IV vs IM, which one works faster? Lasts longer?
-Delayed release vs immediate release capsules. Why wouldn’t you crush you delayed
release medication? Why is this important to consider in a patient with an ostomy?
-Side effects: expected, unexpected, black box warnings
-Do they interact with another drug? Food?
-Ask your patient about OTC medications/herbs/vitamins they are taking to assess for
drug
Interactions
Medications to study:
Anti-pain
Acetaminophen - T: antipyretic, nonopioid analgesic
Ketorolac: T: NSAID, nonopioid analgesic. Reduces inflammation, super strong. can help with
inflamed gall bladder.
Ibuprofen - T: antipyretic, NSAID, nonopioid analgesic P: nonopioid analgesic
Antibiotics
Trimethoprim/sulfamethoxazole (bactrim) - T: anti-infective, antiprotozoal
Ciprofloxacin - antibiotic - cipro can be used to treat infections in UC and CD.
Amoxicillin - T: anti-infective, antiulcer agent. P: aminopenicillin - can help treat h. pylori
Cefotaxime - T: anti-infectives P: second-gen cephalosporin
Narcotics (listed) - probably for sedation for procedures
-
Naloxone - T:opioid antidote P: opioid antagonist
Propofol - T: general anesthetics
Midazolam - T: sedative/hypnotic P:benzodiazepine. Sugergies, alcohol withdrawel
Antiulcers/less stomach acid
Famotidine: T: antiulcer agent P: histamine antagonist
Sucralfate - T: antiulcer agent P: GI protectant
Omeprazole - T: antiulcer agent P: proton-pump inhibitor. Fracture risk (decreased calcium
and protein absorption). Messes with Plavix. Use for PUD, gastritis, GERD, pancreatitis
Pantoprazole - T: antiulcer agent P: proton-pump inhibitor. Fracture risk. (decreased calcium
and protein absorption)
Calcium Carbonate - T: mineral and electrolyte replacement/supplement P: antacid (risk of
rebound acid secretion)
Aluminum hydroxide with magnesium hydroxide : T: antiulcer agent P:antacid (mag by itself if
a laxative, aluminum by itself has a side effect of constipation, they kind of cancel each other
out)
Aluminum hydroxide with simethicone: T: antiulcer agent p: antacid
Steroid
Solumedrol (methylprednisolone): T: corticosteroids,systemic, antiasthmatic (according to
saunders, this is used as an anti-emetic???? it can help in UC)
Vitamin
Thiamine T: vitamin B1, P: water soluble vitamin
Diuretic
Furosemide: T: diuretic P: loop diuretic
Spironolactone: T: diuretic P: potassium-sparing diuretic
Beta-blocker
Propranolol - T: antianginal, antiarrhythmic, antihypertensive, vascular headache suppressant
- helpful in cirrhosis
Anti-diarrhea
Octreotide -T:antidiarrheal, hormone - helpful in cirrhosis
Laxative/Encephalopathy treatment
Lactulose - T: laxative P: osmotics - treats constipation and encephalopathy
Atropine: T: antiarrhythmic P:anticholinergic, antimuscarinic (diphenoxylate with atropine
sulfate can be an antidiarrheal)
Acetaminophen
-Analgesic/antipyretic
- Used for minor aches, pains, reducing fevers, combined in other medications
Shouldn’t use more than 4g in 24 hr period. Can damage the liver (since it is primarily
metabolized here)
-Side effects:
NSAID’s
Ketorolac- shouldn’t be used for more than 5 days due to increased risk of bleeding
-Can cause AKI
Ibuprofen
-Used for aches/pain, antipyretic, inflammation
-Can cause bleeding
-Take with food
-Side effects:
Antibiotics
Trimethoprim/sulfamethoxazole (combo)
-Antibiotic
-Used to treat infections
-Metabolized in the liver
-Side effects:
Ciprofloxacin
-Fluoroquinolone (used to treat bacterial infections)
-Can cause problems with bones, joints, and surrounding joint tissue, nerve
damage
Amoxicillin
-Antibiotic- Penicillin class- stops bacterial growth
-Can make birth control less effective
Narcotics: Typically used to treat moderate-severe pain, acute and chronic.
Oxycodone, Hydrocodone (cough suppressant), Morphine, Hydromorphone
(dilaudid), Fentanyl (More potent than morphine).
-Primarily metabolize in the liver
-Nurse assessment:
-ask about other medications
-Be aware of age and ETOH consumption
-bowel regiment
-Might need to pre-medicate for nausea
S/S of an overdose: Unconsciousness, small pupils, decreased respiratory effort,
vomiting, purple lips, limp body
Naloxone (Narcan)- opioid antagonist used to reverse the effects of opioids very quickly
It has a short half-life and may need to be used more than once
Monitor for withdrawal symptoms: changes in vs, mood changes, sweat,
nausea/vomiting, tremors.
Propofol
General anesthetic- IV
Used for sedation.
Monitoring is required: Telemetry, oxygen, blood pressure
No driving after receiving
Metabolized in the liver
Midazolam
Benzodiazepine
Used for sedation, anxiety
Grapefruit can increase effects
Reversal drug: Flumazenil (reverses effects of benzodiazepines)
Atropine
Antimuscarinic and increases cardiac output
Used: treats bradycardia, decrease secretions
Adverse effecs: blurred vision, tachycardia,
Famotidine- decreased the amount of acid the stomach produces
Antihistamine (used in combination with other drugs for anaphylaxis) and antacid
Used: GERD, ulcers, heartburn
Sucralfate- antacid
Helps treat and prevent ulcers by forming a barrier over the ulcer, protecting it so it can
heal
Proton-pump inhibitors (PPI): Block gastric acid secretion
Helps treat symptoms and damage caused by back flow of acid from the stomach
Omeprazole, Pantoprazole (protonix)
Antacids: help neutralize stomach acid
Used to treat heartburn, indigestion and upset stomach.
Aluminum hydroxide with magnesium hydroxide, Aluminum hydroxide with
simethicone, calcium carbonate
Take with caution: Acid rebound, microcytic anemia, osteopenia, hypercalcemia.
Amitriptyline- antidepressant and nerve pain medication