Download Common Gastrointestinal Problems

1|P age
MENNONITE COLLEGE OF NURSING
AT
ILLINOIS STATE UNIVERSITY
Family Nurse Practitioner III 475
Common Gastrointestinal Problems
Acute Abdominal Pain
What is it?
...A common problem that may pose diagnostic challenges for the FNP!
Is it a “quick” visit?
…Not usually! Need a longer appointment, if possible.
An understanding of the physiology of pain and basic anatomy is essential in the
evaluation of abdominal pain, but determination of an etiology can be difficult owing to
overlapping symptoms in pathologic processes and to the variable response of individuals
to pain.
The most powerful diagnostic tools are the history and physical examination.
Chronicity is a key determinant of the pace of assessment.
Prompt evaluation and appropriate treatment of acute abdominal pain are crucial.
Chronic abdominal pain usually may be evaluated in a more unhurried manner.
Differential Diagnosis
Intra-abdominal disorders
 Inflammatory (e.g., appendicitis, pyelonephritis, abscesses, salpingitis, PID)
 Mechanical (e.g., visceral obstructions, aneurysm, trauma, ectopic pregnancy,
ruptured ovarian cyst)
Extra-abdominal (e.g., pneumonia, myocardial infarction, shingles, sickle cell anemia,
diabetic ketoacidosis, depression, anxiety)
History
1.
Onset (chronic or acute)
2.
Progression (improving, worsening, or stable)
 Progression of pain from a dull, poorly localized pain to a sharp, well-defined
pain signals evolution of the disease process and the need for surgical
consultation
3.
Migration (has it moved?)
 Note: The more severe the visceral pain, the more likely it is to be referred to
the back.
4.
Localization (generalized, periumbilical, pelvic, or quadrantal)
2|P age
Some Causes of Perceived Pain in Anatomic Regions
Right Upper Quadrant
Cholecystitis
Hepatitis
Hepatomegaly
Fitz-Hugh-Curtis
Colitis
Diverticulitis
Pneumonia
Pulmonary embolus
Nephrolithiasis
Pyelonephritis
Right Lower Quadrant
Appendicitis*
Colitis
Diverticulitis
Inflammatory bowel disease
IBS
Ectopic pregnancy
Fibroids
Ovarian mass/torsion
PID
Nephrolithiasis
Pyelonephritis
Strangulated hernia
Epigastric
Cholecystitis
Myocardial infarction
Pericarditis
Esophagitis
Gastritis
Peptic ulcer
Pancreatitis
Aortic dissection
Mesenteric ischemia
Periumbilical
Intestinal obstruction
Acute pancreatitis
Early appendicitis*
Gastritis
Peptic ulcer
Mesenteric thrombosis
Abdominal aortic aneurysm
Aortic dissection
Mesenteric ischemia
Suprapubic
Appendicitis*
Colitis
Diverticulitis
Inflammatory bowel disease
IBS
Ectopic pregnancy
Fibroids
Ovarian mass/torsion
PID
Cystitis
Nephrolithiasis
Pyelonephritis
Left Upper Quadrant
Angina
Myocardial infarction
Pericarditis
Aortic aneurysm
Aortic dissection
Pneumonia
Esophagitis
Gastritis
Gastric ulcer
Pancreatitis
Ruptured spleen
Mesenteric ischemia
Perforated colon
Nephrolithiasis
Pyelonephritis
Left Lower Quadrant
Colitis
Diverticulitis
Inflammatory bowel disease
IBS
Ectopic pregnancy
Fibroids
Ovarian mass/torsion
PID
Nephrolithiasis
Pyelonephritis
Strangulated hernia
Any location
Abdominal wall: herpes zoster, muscle strain, hernia
Other: bowel obstruction, mesenteric ischemia, peritonitis, narcotic withdrawal, sickle cell crisis,
porphyria, inflammatory bowel disease, heavy metal poisoning
* Depending on location of appendix, may have LLQ discomfort at first.
Source: Cartwrigtht, SL & Knudson, MP (April 1, 2008). Evaluation of acute abdominal pain in adults. American Family Physician,
77(7), 971-978.
3|P age
5.
Character (e.g., colicky or continuous, cramping, or stabbing)
Quality and Onset of Abdominal Pain
Characteristic
Burning
Cramping
Colic
Aching
Knife-like
Gradual onset
Sudden onset
6.
Possible related condition
Peptic ulcer
Biliary colic, gastroenteritis
Appendicitis with impacted feces
Appendiceal irritation
Pancreatitis
Infection
Duodenal ulcer, acute pancreatitis, obstruction, perforation
Associated symptoms (e.g., nausea, vomiting, anorexia, change in bowel habits)
Also: “the order”.......If pain, then vomiting, think surgical
If vomiting, then pain, think medical
7.
Medical history and review of systems

Note: A history of abdominal surgery, chronic disease, or prior pelvic
inflammatory disease should raise the index of suspicion for associated
sequelae (e.g., small bowel obstruction due to postoperative intra-abdominal
adhesions).
 Example: PID and development of Fitz-Hugh-Curtis

Study published in 2004 describes symptom pattern suggestive of ovarian
cancer: pelvic pain, abdominal pain, difficulty eating, bloating, increased
abdominal size, and urinary urgency. These symptoms were more frequent
(almost daily) compared to women without ovarian cancer, such as those with
symptoms associated with menses.
************** Case Study #1 **************
Clinical Findings
1.
Vital signs and general appearance (e.g., fever, shock, body position, jaundice)
Note:
 Clients with peritoneal pain lie still with legs drawn up to chest and resist
movement.
 Clients with colicky pain such as pain with renal stones are restless, frequently
shifting positions, and lacking peritoneal signs.
2.
Inspection (e.g., contour, scars, pulsations, skin or vascular lesions, visible
masses, or peristalsis)
4|P age
3.
Auscultation (e.g., murmurs or bruits, peristaltic sounds, succussion splash)
(“succussion” is the shaking of a person to detect the presence of fluid in the body
cavity by listening for a splashing sound, especially in the thorax)
4.
Palpation and percussion (e.g., light and deep, guarding and tenderness,
organomegaly, masses, hernias, ascites)
 Murphy’s sign: inspiratory arrest in response to RUQ palpation seen in acute
cholecystitis
 CVA tenderness
 Obturator sign: positive if abdominal pain occurs/increases in response to
passive internal rotation of the right hip from the 90-degree hip/knee flexion
position; suggests appendicitis.
 Psoas sign: positive if increased RLQ pain when patient lifts right thigh
against resistance; indicates irritation of the psoas by an inflamed appendix
 Rovsing’s sign: positive if RLQ pain increases with palpation in the LLQ
(early sign of peritoneal irritation, possible appendicitis)
5.
Rectal and/or pelvic examination (e.g., urethral or cervical discharge or bleeding,
prostate or adnexal tenderness or masses, stool impaction, rectal bleeding)

Note: The elderly person with an acute intraabdominal process may at first
show few signs of serious illness. Peritoneal signs may be absent or minimal.
The only early clues may be unexplained mild fever, tachycardia, and vague
abdominal discomfort. A high index of suspicion is needed.

Note: Examining for nerve and muscle wall injury is often overlooked in the
urgency of searching for more worrisome pathology. Two important signs of
nerve involvement are pain in a dermatomal distribution and
hyperesthesia. Both occur with nerve injury due to herpes zoster or nerve
root impingement; however, hyperesthesia is also seen with focal peritoneal
irritation. Testing is performed by gentle stroking of the skin overlying the
area of pain.
Tests to Consider
1.
CBC with differential
2.
Urinalysis
3.
Serum electrolytes, BUN, creatinine, glucose if vomiting or other symptoms are
present
4.
Serum lipase and amylase if pancreatic process is suspected
5.
Serum bilirubin (conjugated and unconjugated), transaminase levels (AST, ALT),
and albumin if hepatic process is suspected. If jaundice is present, PT and PTT
may also be indicated.
6.
Urine pregnancy test
 Rule out ectopic pregnancy in all women of childbearing age who present
with acute abdominal pain
5|P age
7.
Diagnostic imaging (e.g., flat and upright abdominal films, CXR,
abdominal/pelvic U/S or abdominal/pelvic CT, upper and lower bowel contrast
studies)
Recommended Imaging Studies Based on Location of Abdominal Pain
Location of Pain
Imaging
Right upper quadrant
Ultrasonography
Left upper quadrant
CT
Right lower quadrant
CT with IV contrast media
Left lower quadrant
CT with oral and IV contrast media
Suprapubic
Ultrasonography
Source: Cartwrigtht, SL & Knudson, MP (April 1, 2008). Evaluation of acute abdominal pain in adults. American
Family Physician, 77(7), 971-978.
8.
9.
10.
Abdominal paracentesis
Direct visualization by endoscopy, laparoscopy, or surgery
With acute upper abdominal pain, CXR and EKG
NOTE: Look at the total picture, not just one test…don’t forget to look at the
patient!!!
Beware of common misconceptions:
 “The white blood cell count is normal; the patient can’t have a surgical abdomen.”
 Studies of patients with appendicitis demonstrate sensitivities ranging from
42-90%
 “The white blood cell count is elevated; the patient must have a surgical abdomen.”
 Almost 11% of normal individuals have elevated WBC counts and 13% have
left shifts. These left shifts are felt to be due to the stress response.
 “The patient has right lower quadrant pain, but the urinalysis shows evidence of a
UTI.”
 Up to 30% of appendicitis cases have white blood cells in the urine secondary
to periureteral inflammation.
 “Abdominal radiographs are often helpful in the work-up of nonspecific abdominal
pain.”
 Abdominal radiographs are rarely helpful unless bowel obstruction,
perforation, or foreign body is suspected. In healthy young individuals, these
diagnoses can usually be made clinically, thus prompting the ordering of plain
radiographs for confirmation.
 Note: They may, however, be helpful with the elderly patient.
Management
Although the management of abdominal pain is specific to the causative pathology, the
following general measures may be useful in the management of acute abdominal pain.
6|P age

Any evidence suggestive of peritoneal irritation, obstruction, or acute vascular
compromise is an indication for immediate hospitalization and surgical
consultation.

In general, patients with unexplained abdominal pain in conjunction with
recurrent nausea and vomiting, jaundice, fever, weight loss of > 10% of body
weight, or the presence of blood in the stool will require more invasive testing.

In patients who are older or frail:



If low risk (stable vital signs, limited comorbidities), consider UTI or
diverticulitis and conduct general work-up for abdominal pain
If high risk (unstable vital signs, significant comorbidities), consider
sepsis, perforated viscus, or ischemic bowel. Perform CT and consider
hospitalization.
Occult urinary tract infection, perforated viscus, and ischemic bowel
disease are potentially fatal conditions commonly missed or diagnosed late
in older patients.
Medication
Note: There is the idea that due to the fear of masking abdominal symptoms, analgesics
should not be given until a probable diagnosis is made and a course of treatment is
determined. Recent information suggests that some analgesics (especially parenteral
NSAIDS) may not significantly interfere with the evaluation of acute abdominal pain.
Meds to consider:
 Narcotic and non-narcotic parenteral analgesics
 Antiemetics and other symptomatic medications
 Specific pharmacotherapy as indicated (e.g., PPI in ulcer disease)
Diet
Nothing by mouth until a diagnosis is made; thereafter, the diet is determined by the
disease.
Activity
Usually bedrest (especially if there is risk of medication-related falls or aortic aneurysm)
Patient Education
 The patient should promptly report changes in symptoms.
 Medication information
Follow-up
 In acute abdominal pain, even if the cause is known, follow-up may be as frequent
as every few minutes.
7|P age

In chronic abdominal pain, re-evaluation may be as infrequent as every several
months depending on the patient, the suspected or confirmed cause, and the
FNP’s degree of comfort.
“Practice Pearls”
 Determine whether pain is acute or chronic. If acute, work-up should proceed
rapidly.
 History and physical examination should guide focused selection of diagnostic
studies.
 Keep patients with acute abdominal pain NPO initially.
 For chronic pain, recording of symptoms on a calendar along with menses, diet, and
other features may be helpful.
Three different categories of acute abdominal pain:
 Surgically Emergent
 Medically Emergent
 Self-Limiting
Surgically Emergent
************** Case Study #2 **************
Appendicitis
Etiology/Demographics
 Obstruction of the appendiceal lumen, usually by a fecalith, but occasionally by
foreign bodies
 Most common atraumatic surgical abdominal emergency in the 10-30 year old age
group.
 Common in this age group due to having more lymph tissue that is more likely to
become hyperplastic and cause obstruction.
 Not as likely to see in the very young and the very old.
 More common in those from European and North American countries – probably
related to the relative lack of fiber in the diet. Our rate of appendicitis in this country
has actually decreased over the last 10-15 years as our intake of fiber has increased.
 Men more likely than women to be affected (1.5:1)
 2/3 of cases reported between October and May. Why? May be due to influenza
during those months that stimulates follicular hyperplasia, which can obstruct the
appendiceal lumen.
 Persons with a family history of appendicitis are also at increased risk.
 25% perforate by 24 hours, 75% by 48 hours.
8|P age
Subjective
 In classic appendicitis, the pain begins as vague and poorly localized, usually felt in
periumbilical area. As progresses, pain localizes to the right lower quadrant.
 However, need to keep in mind that appendix can have different anatomic variations
(i.e. size, position) in different people…can present differently!
 A retrocecal appendix (15%) can cause back or flank pain
 A long appendix can cause pain in the LL or RUQ
 A retroileal appendix can lead to testicular pain
 A pelvic appendix may cause suprapubic pain
 Clinical pearl – usually pain proceeds vomiting
 Characteristics of pain can be highly variable – crampy to sharp to dull. Can easily
confuse with PID
 May have obstipation
Objective
 Physical exam reveals abdominal tenderness, RLQ tenderness, abnormal bowel
sounds, +/- rebound
 Patient usually wants to hold still, not to move around
 Psoas sign/Obturator sign/Rovsing’s sign
 Pelvic, rectal exams as needed
 The 3 findings with the greatest predictive value are:
 Pain in the right lower quadrant
 Migration of that pain from the periumbilical region
 Abdominal rigidity on examination
Source: Rubin, RN (April 1, 2003). Young man with acute right lower quadrant pain. Consultant, 538-540.
************** Case Study #3 **************
Assessment/Not to be missed
 Keep in mind the presentation of appendicitis is not always straightforward,
especially in the very young and very old. Diagnosis is missed ½ of the time in
patients over the age of 60, and most of the time in patients younger than four years
old, and almost always in patients less than two years old.
 Don’t miss PID, ectopic pregnancy, ovarian cyst
Plan
 Obtain labs – CBC (be sure to pay attention to manual differential – may not see rise
in WBC’s, but may see increase in neutrophils), chemistries (if presentation unclear,
consider including amylase), C-reactive protein, urinalysis, urine HCG if child
bearing age and indicated
 No imaging necessary in typical appendicitis (but in non-straight-forward cases, a
different diagnosis is found in 15% of cases)
Source: Holden, DM, & Einstein, DM (January 2007). Imaging in practice: Which imaging test for right lower quadrant pain?
Cleveland Clinic Journal of Medicine, 74(1), 37-40.

Imaging may be useful in differentiating appendicitis from other conditions such
as Crohn’s disease, right-sided diverticulitis, right colonic neoplasm, bowel
9|P age

ischemia, acute pyelonephritis, ureteral calculus, PID, and hemorrhagic ovarian
cyst.
 Plain-film radiography of the abdomen rarely provides useful information in the
above cases (One study showed it have 0% sensitivity for appendicitis,
pyelonephritis, pancreatitis, and diverticulitis)
 Role of abdominal or transvaginal ultrasound: diagnostic accuracy of > 85%,
useful in the exclusion of adnexal disease in younger women
 Graded-compression ultrasonography is helpful in evaluating thin young children
and obstetric patients
 Overlying bowel gas can technically limit the ability of ultrasonography to
identify a normal or perforated appendix. If this occurs, CT can be used for
further evaluation.
 CT is the imaging test of choice for suspected appendicitis in adults who are
not pregnant. (NOTE: Will need to order abdominal/pelvic CT to provide
visualization of entire abdomen/pelvic area….abdominal CT alone will not
include total colon.)
 CT without contrast: lower sensitivity in thinner patients with little intraabdominal fat and in patients with early or mild appendicitis; limited ability to
show inflammatory or neoplastic processes
 CT with IV contrast: facilities recognition of appendicitis, especially in subtle
cases and in thin patient with little intra-abdominal fat; also better at showing
complications of perforation such as abscess formation as well as other
pathological entities that may cause abdominal pain. Complications: severe
allergic reaction, renal failure.
 CT with enteric (oral) contrast: oral contrast is given 1.5 to 2 hours before the
exam to opacify and distend the distal small bowel and cecum; this
visualization of anatomic landmarks helps in identifying the appendix
(differentiating it from surrounding structures). (contrast can also be given
rectally)
 Imaging (CT of abdomen/pelvis) may be useful in patients in whom the
diagnosis is uncertain
Refer to surgeon for evaluation
************** Case Study #4 **************
Obstruction
Etiology/Demographics
 Pain is caused by distention and increased wall tension of affected area
 Common causes – previous abdominal surgery with adhesions, tumor, constipation
(obstipation)
Subjective
 If acute onset of obstruction, the pain is intense, severe and colicky or wavelike,
patient is restless.
10 | P a g e



If slow onset of obstruction, pain is more vague, patient may complain of dyspepsia,
bloating, etc.
Signs of upper obstruction – vomiting
Signs of lower obstruction – no flatus, or if partially obstructed, may see diarrhea
Objective
 Abdominal distention
 Borborygmi or no bowel sounds
Assessment/Not to be missed
 Tumor or malignancy (colon cancer to be discussed later)
Plan
 Labs (CBC, chemistries, etc.)
 If concerned regarding perforation, get upright chest x-ray (check for
pneumoperitonitis)
 Flat plate of abdomen can be helpful to visualize air in small intestine, impaction, etc.
 CT of abdomen/pelvis (will often show dilated loops of bowel)
 Refer for further evaluation.
 If simple obstruction, may manage medically with decompression by tube
insertion.
 If strangulation – surgically emergent
************** Case Study #5 **************
Acute Gall Bladder (Cholecystitis, Cholelithiasis)
Etiology/Demographics
 Cholecystitis, or inflammation of the gallbladder, may be acute or chronic
 Types of acute cholecystitis
 Acute calculus cholecystitis
 Inflammation of the gallbladder that develops in the presence of gallstones
(cholelithiasis)
 95% of cases of acute cholecystitis
 Acute acalculus cholecystitis
 Inflammation of the gallbladder in the absence of gallstones
 5% of cases
11 | P a g e
Age
Body habitus
Childbearing
Drugs
Ethnicity
Family
Gender
Hyperalimentation
Ileal and other
metabolic diseases
Risk Factors for Gallstone Formation
Increasing age
Obesity, rapid weight loss
Pregnancy
Fibric acid derivatives, contraceptives, postmenopausal estrogens,
progesterone, octreotide (Sandostatin), ceftriaxone (Rocephin)
Pima Indians, Scandinavians
Maternal family history of gallstones
Females
Total parenteral nutrition, fasting
Ileal disease (Crohn’s disease), resection or bypass, high
triglycerides, diabetes mellitus, chronic hemolysis, alcoholic
cirrhosis biliary infection, primary biliary cirrhosis, duodenal
diverticula, truncal vagotomy, hyperparathyroidism, low level of
HDL cholesterol
Source: Ahmed, A, Cheung, RC, & Keeffe, EB (March 15, 2000). Management of gallstones and their complications, American
Family Physician, 61(6), 1673-1680.
Subjective
 Typically presents with RUQ pain, may radiate to mid-epigastric area, scapula.
 Pain is usually constant/steady, lasting over an hour
 Often accompanied by nausea, vomiting, and fever without jaundice
Objective
 (+) Murphy’s sign
 If can feel gallbladder, really be concerned regarding malignancy
Assessment/Not to be Missed
 Acalculous cholecystitis
 Perforation
 Be especially cautious in those with underlying health problems such as diabetes
 Pancreatitis
Plan
 Obtain CBC (once again pay close attention to manual differential), chemistries (may
or may not see increase in liver enzymes), amylase (stone obstruction of cystic duct
can lead to pancreatitis)
 Gallbladder ultrasound
 If ultrasound is negative for stones, may consider ordering HIDA scan
(administration of cholecystokinin [CCK] causes the gallbladder to contract;
allows estimation of the ejection fraction of the gallbladder (normal ejection
fraction is 35-75%)
 Refer to surgeon
 Cholecystectomy (laparoscopic vs. open)
12 | P a g e


For high surgical risk or patients refusing surgery, nonsurgical therapy
includes oral bile acid dissolution (ursodeoxycholic acid) or lithotripsy
Some patients experience post-cholecystectomy diarrhea.
 Treatment: Lomotil 1 tab after each loose stool X 1-2 months. If no relief,
cholestyramine daily (binds with bile)
Skill Check: Try out the scenario at http://meded.ucsd.edu/isp/1999/surgery/index.html
Ovarian Cyst
 Usually see rebound, unilateral adnexal pain with bimanual exam
 Usually have signs of peritoneal irritation
 Consider usual acute abdominal condition labs
 Consider pelvic ultrasound
 Refer to surgeon
Ectopic Pregnancy
 Usually with rebound, signs of peritoneal irritation
 Suspect in women of childbearing age
 Urine HCG or serum HCG in addition to usual labs
 Pelvic ultrasound
 Refer to surgeon
 Can be life-threatening
Abdominal Aortic Aneurysm (AAA)
Sources:
Almahameed, A, Latif, AA, & Graham, LM (October 2005). Managing abdominal aortic aneurysms: Treat the aneurysm and the risk
factors. Cleveland Clinic Journal of Medicine, 72(10), 877-888.
Lederle, FA (May 5, 2009). In the clinic: Abdominal aortic aneurysm. Annals of Internal Medicine, ITC5, 1-16.
Risk factors: older age, smoking, male gender, white race, family history of AAA,
occlusive atherosclerotic disease
U.S. Preventive Services Task Force recommendations
 One-time screening for abdominal aortic aneurysm (AAA) by ultrasonography in
men aged 65 to 75 who have ever smoked.
 Recommends against screening in women
 No recommendation regarding men 65-76 years old who never smoked
Aneurysm may be asymptomatic:
 If small, risk of having surgery vs. risk of bleeding if does not have surgery must
be weighed
 Are AAAs palpable?
 3-3.9 cm = palpable 29-61% of the time
 > 5 cm = palpable 76-82% of the time
 Do yearly ultrasound to check if getting larger
 3-4 cm.
Check every 12 months
 4-4.5 cm Check every 6 months
13 | P a g e




> 4.5 cm Refer to vascular subspecialist
Surgery usually recommended for aneurysms 2 inches (5.5 cm) or more in
diameter for men (5 cm in women) and for aneurysms that are enlarging quickly
(> 0.6-0.8 cm/yr)
Surgery may be a traditional (open) repair or endovascular stent grafting
(endograft)
 Endograft good for older patient or patients at higher operative risk
 Open repair for younger patients
After endograft, CT at 1, 6, and 12 months, and then yearly (AAA should
decrease in size).
If AAA leaking:
 Patients may complain of tearing pain that radiates to back; pain is severe
 Pain may radiate to groin, testicles, legs, or buttocks
 May feel pulsating mass (approximately 83% of the time)
 Hypotension present (45% of the time)
 Will need open repair (outcome usually good if repaired before it ruptures; <
40% survive a ruptured AAA)
Trauma
************** Case Study #6 **************
Medically Emergent
Acute Pancreatitis
Sources:
Amerine, E. (June 2007). Get optimum outcomes for acute pancreatitis patients. The Nurse Practitioner, 32(6), 44-48.
Etiology/Demographics
 Inflammatory breakdown of pancreatic architecture, with release of digestive
enzymes into the interstitium of the gland, leading to autolysis (= “autodigestion”)
 Two forms of acute pancreatitis
 Edematous (or interstitial) is usually mild and resolves in about 7 days
 Severe or necrotizing is associated with a high degree of complications and
mortality
 More than 80% of cases of acute pancreatitis can be attributed to ethanol abuse or
biliary stones
 Other causes: hypertriglyceridemia, tumor, mumps
 Use of some medications such as thiazide diuretics, furosemide, nitrofurantoin
[Macrobid], and GLP-1 meds used in diabetes, including Byetta, Bydureon, and
Victoza
14 | P a g e
Subjective
 Sharp, periumbilical pain
 History of alcoholism, gallbladder disease, mumps, use of meds noted above
 May complain of persistent vomiting
 Pain is worse with food, somewhat better with upright position
Objective
 Acutely ill, very uncomfortable
 May have abdominal distention, tenderness, diminished bowel sounds, fever
Assessment/Not to be Missed
 Perforation (check bowel sounds, CXR)
Plan
 CBC, CMP, amylase, lipase
 Amylase – found primarily in pancreas and salivary glands; begins to rise 3-6
hours after onset of acute pancreatitis and peaks in approximately 24 hours;
returns to normal within 2-3 days after onset
 Lipase – found only in pancreas; increases in blood within 24-36 hours after
onset; remains elevated up to 14 days longer than amylase
 Imaging
 Ultrasound: main role is to detect gallstones as the likely cause
 CT: Most useful in patient with severe or atypical presentation; may be helpful in
differentiating acute pancreatitis from conditions such as perforated peptic ulcer,
mesenteric ischemia, acute cholecystitis, and bowel obstruction or perforation.
 Mild pancreatitis requires supportive therapy
 Discontinue offending drug if acute pancreatitis drug-induced
 Pain control, antiemetic medications, IV fluids
 Diet: NPO to avoid recurrence of pain resulting from the activation of pancreatic
enzymes; begin diet after pain, tenderness and ileus have resolved (start with clear
liquids, progress to full diet
 Re-evaluate labs until normal
 Recovery usually within 5-7 days
 Pancreatitis due to obstruction from gallstones, dysfunction of the Sphincter of Oddi,
or malignancy requires endoscopic retrograde cholangiopancreatography (ERCP)
with possible stone extraction and/or sphincterotomy of the ampula, or stent
placement in the biliary duct
 Moderate to severe pancreatitis: admit to critical care unit
 Local complications include formation of pseudocyst or pancreatic abscess, requiring
percutaneous aspiration or drainage. (may take up to 4 weeks to develop)
15 | P a g e
Pyelonephritis
Etiology: Infection of the upper urinary tract/kidney
Subjective:
 Presents with complaints of flank pain, often accompanied by nausea and
vomiting
 Usually febrile
Objective:
 On exam – acutely ill, CVA tenderness
Diagnosis/Plan: What would urinalysis results likely be?
 Definitely need urinalysis and culture. Start on fluoroquinolones while awaiting
C & S results
 May need IV fluids
 May need hospitalization for fluids and IV antibiotics if unable to keep oral
antibiotics down or if pregnant
 Follow closely
Kidney Stones
Subjective:
 Pain is result of obstruction/partial obstruction of urinary tract
 Patient complains of colicky pain – usually flank
 May also report diminished urinary stream
 Patient appears restless, can’t get comfortable
Diagnosis/Plan:
 Blood noted in urine dipstick; can do CT "Stone protocol" (doesn't require
contrast media...great for folks with renal insufficiency)
 May need admission for fluids, pain control
 If manage outpatient, follow frequently, give urine strainer to hopefully catch
stone
Pelvic Inflammatory Disease
 Pain with pelvic/bimanual, may be excruciating
 Fever
 May need hospitalization
 Increased risk of infertility, scarring, ectopic pregnancy
 May say she is monogamous, but “serially” monogamous
Ischemic Bowel Disease
(See Mesenteric Ischemia later in this handout)
 Arteries that supply oxygenated blood to the large and small intestines become
narrowed or blocked.
 At risk: age > 50, smoking, obesity, high cholesterol, HTN, CVA, afib, DVT, MI
16 | P a g e
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Presentation variable
May have rectal bleeding
Self Limiting
Gastroenteritis
Viral
 Most common cause of gastroenteritis
 Patient presents with complaints of abdominal cramping, accompanied by diarrhea,
often times emesis. No blood is present in stool or emesis
 Heavy fruit syrup may help settle stomach
 Many times report someone else in family or someone exposed to is ill with same
thing
 On exam will see generalized abdominal tenderness – bowel sounds generally
hyperactive, although may be hypoactive/absent if has just thrown up
 Examine/investigate signs of dehydration – i.e. orthostatics, mucous membranes, skin
turgor, last void, etc. If dehydrated consider IV fluids (avoid fluids with dextrose for
first liter – leads to more fluid loss related to relative hypertonicity)
 Usually lasts for 24-72 hours – if longer, at least consult, if not refer
 Treatment – clear liquids, bland foods (BRAT diet = bananas, rice, applesauce, toast),
gradually adding regular foods (fatty and dairy products last), also avoid alcohol
(gastric irritant) and smoking
 If nausea is severe, consider antiemetic such as phenergan or Zofran. Otherwise,
antidiarrheals/antiemetics are not recommended.
 Wait 30 minutes after vomiting before taking something by mouth – allows reverse
peristalsis to correct itself
Food Poisoning
 Likely to have a more abrupt onset in comparison with viral gastroenteritis
 Self-limiting, need to evaluate for dehydration/need for IV fluids or other supportive
measures
 If gotten from a restaurant, report to Health Department
 Same treatment as for viral gastroenteritis
Traveler’s Diarrhea
 Prevention is the best strategy
o If traveling in North America, advise not to drink any untreated water (i.e.,
mountain streams, lakes, etc.) due to risk of Giardia or similar organisms.
o If traveling to underdeveloped countries, advise no water, drinks with ice
cubes or made with water, fresh vegetables or fruits that may have been
washed in water. Bottled water is best!
 In past, some have promoted antibiotic prophylaxis for travelers, however with
emergence of resistant strains, there is concern about this practice.
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o One option is to treat with Pepto Bismol 60 ml QID. Warn patient that stool
will turn dark. (can also get black tongue)
If acutely ill, treat with Cipro 500 mg bid for 3 days or Bactrim DS one bid for 3
days. Consideration can be given to sending antibiotics with patient to take if
becomes symptomatic while traveling.
Gastritis
 Associated with alcohol intake, smokers
 Patient complains of nausea, burning, gnawing pain
 Treat by having patient discontinue alcohol/smoking
 Also use Mylanta or OTC H2 Blocker
Chronic Abdominal Pain
Ovarian Cancer
 Need high index of suspicion since symptoms are nonspecific
 Consider ovarian cancer in the differential diagnosis of women who present with
unexplained abdominal pain, abdominal swelling, GI symptoms such as
constipation, and/or pelvic pain.
 Abdominal bloating  increased abdominal size  urinary urgency
 One study found 40% of women with ovarian cancer visited their doctor at least
once because of abdominal or pelvic symptoms between 36 and 4 months before
their cancer was diagnosed. However, only 25% of these patients received pelvic
imaging or CA-125 testing during that time. In contrast, 61% received abdominal
imaging and about 30% received GI tests.
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Source: Smith, LH et al. Ovarian cancer: Can we make the clinical diagnosis sooner. Cancer. Advanced online
publication. August 22, 2005.
To avoid delay in diagnosis, order pelvic imaging and CA-125
Pancreatic Cancer (PC)
Source: Abbruzzese, JL, Lowy, AM, Pleskow, D, & Xiong, HQ (February 2006). Update on the approaches to pancreatic disease.
Patient Care. 15-24.
Pancreatic carcinoma (August 24, 2011) accessed at http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001283/?report=printable
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4th leading cause of cancer-related mortality
Fewer than 5% of patients survive beyond 5 years
Risk factors
o Smoking
 Smoking + family history = doubles the risk of PC
o Diabetes
o Long-term inflammation of pancreas (chronic pancreatitis)
o Age
o Genetic susceptibility (BRCA2 gene, familial polyposis gene, and Lynch
syndrome
o Lynch syndrome= Hereditary Nonpolyposis Colorectal Cancer, an
autosomal dominant problem.
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Associated with increased risk of other cancers (ovarian,
endometrial, renal, gastric, hepatobiliary, small intestine)
S/S: fatigue, weight loss, anorexia, nausea and vomiting, abdominal/back pain
(from local invasion), jaundice
o If head of pancreas affected (exocrine function), frequently present with
progressive obstructive jaundice from blockage of bile drainage into the
small intestine; manifests as dark urine and pale stools
o If PC in endocrine portion of pancreas (tail), new-onset diabetes or
changes in glucose tolerance in patients with diabetes is also a frequent
finding.
o Possible Sister Mary Joseph Nodule…what is this?
Imaging: Helical CT remains the test of choice for diagnosing pancreatic masses
and extra-pancreatic metastases and for determining resectability of the tumor.
Management
o Resectable in approximately 15% of patients on initial presentation
 Whipple resection (pancreaticoduodenectomy) if PC in head of
pancreas
o Standard chemotherapy for advanced pancreatic cancer is gemcitabine
(Gemzar), but research continues.
************** Case Study #7 **************
Gastroesophageal Reflux Disease (GERD)
Source: Hart, AM (August 2013). Evidence-based recommendations for GERD treatment. The Nurse Practitioner, 38(8), 26-34.
Demographics/Etiology
 Reflux of acid into the esophagus
 Associated risk factors include obesity, pregnancy, nicotine, caffeine, and alcohol use
 Other associated risks are decrease in sphincter tone of the lower esophageal
sphincter (LES), decreased secondary peristalsis, defective mucosal resistance,
delayed gastric emptying, gastroparesis secondary to diabetes, IBS, peptic ulcer
disease, asthma, COPD, angina
 More prevalent with use of anticholinergics, nitrates, and oral corticosteroids
 Cochrane review found patients presenting with concomitant GERD and H. Pylori
infections typically experience improvement in GERD symptoms with H. Pylori
eradication.
 Prevalence rate in US 15-20%
 Occurs equally in men and women; more common in whites than non-whites
 44% of U.S. adult population have heartburn once/month
 14% have symptoms weekly; 7% have daily symptoms
 50-80% of patients with asthma have GERD (remember, bronchodilators also loosen
the LES)
 GERD is the most common cause of non-cardiac chest pain
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Clinical pearl: Patients with chronic cough have high likelihood of having GERD
and should receive a trial of antisecretory therapy.
Subjective
 Gnawing, burning, reflux sensation up the chest that is worse after large meals, lying
down, bending over
 Pain at least temporarily alleviated with the use of antacids
Objective
 Usually a normal exam
 May have mid-epigastric tenderness to palpation
Not to be Missed
 MI, PUD, cholelithiasis, scleroderma, gastric cancer
Plan
 Stool guaiac
 Weight loss if obese
 Wear loose clothing (tight clothes around the waist and abdomen put pressure on the
stomach, aggravating the symptoms)
 Avoid late evening meals
 Avoid lying down or bending right after eating.
 Elevate head of bed with bricks or blocks (simply raising head on extra pillows does
not work!)
 Avoid high fat and high carbohydrate foods
 Avoid medications that decrease lower esophageal sphincter tone, including:
 Beta2-agonists (bronchodilators)
 Alpha-adrenergic antagonist
 Nitrates
 Anticholinergics
 Theophylline
 Morphine
 Meperidine
 Barbiturates
 Avoid medications that irritate/promote breakdown of the esophageal mucosa such as
NSAIDs, steroids
 D/C nicotine, caffeine, alcohol
 Antacids after meals and at HS
 If antacids not sufficient, can try OTC H2 blocker – split into BID dose works better
(i.e. Zantac or Axid 150 mg bid) or OTC PPI (omeprazole)
 Other options would be a prescription proton pump inhibitor (such as lansoprazole
[Prevacid], rabeprazole [AcipHex], esomeprazole [Nexium], or pantoprazole
[Protonix]) or a promotility agent such as metaclopramide (Reglan, which increases
peristalsis)
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Take PPIs 30 minutes before breakfast (if bid, take before breakfast and evening
meal)
If this is not sufficient to control symptoms, referral to gastroenterology usually made
for further evaluation by EGD (esophagogastroduodenoscopy)
Two strategies for treating GERD:
 Step-up approach
 Phase I: Lifestyle modification
 Phase II: Treatment with an H2 receptor antagonist (H2RA) or promotility
agent
 Phase III: Increase in dose or frequency of H2RA monotherapy, or treatment
with H2RA combined with a promotility agent
 Phase IV: Treatment with proton pump inhibitor (PPI) or surgery
 Step-down approach – give highest dosage of PPI for symptomatic control and
step down once it is achieved
 To avoid “rebound reflux,” PPIs should be gradually discontinued over a few
weeks (halving the dose every week, until on lowest dose, then taking lowest dose
for 1 week)
Concerns regarding use of PPI’s
 Gastric acid has a protective effect against enteric infections; therefore gastric
acid suppression can permit pathogens to more readily colonize in the upper GI
tract and predispose individuals to infections, such as pneumonia and Clostridium
difficile associated diarrhea.
 Association between prolonged PPI use (> 1 year) and a moderately increased risk
of hip and vertebral factures
 Prolonged PPI use may impact vitamin B12, iron, and magnesium absorption
 Interaction of clopidogrel (Plavix) with omeprazole (Prilosec) and esomeprazole
(Nexium) use.
 Clopedogrel is a prodrug metabolized in the liver to an active form that
inhibits platelet aggregation. Cytochrome CYP2C19, an enzyme involved in
this activation process, is inhibited by PPIs, a phenomenon that can decrease
antiplatelet response and increase risk for CV events.
Complications
 Dental erosions
 Pharyngeal ulcerations
 Laryngeal damage
 Reflux esophagitis
 Esophageal ulcers and strictures (Schlotsky's ring)
 Barrett’s esophagus
o Replacement of the normal squamous epithelium of the esophagus with a
metaplastic columnar epithelium, a risk factor for developing esophageal
adenocarcinoma
o Mechanism: Barrett’s esophagus linked to repeated and prolonged
exposure of the esophageal mucosa to gastric material refluxed into the
esophagus
21 | P a g e
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o 10% of individuals with chronic GERD have Barrett’s esophagus
o 0.5-1% of Barrett’s esophagus patients develop adenocarcinoma of the
esophagus every year
o More common in those who smoke or drink alcohol.
o Mean age at diagnosis = 55, men:women 2:1
o Increased risk with longer duration of GERD symptoms
o Treatment: radiofrequency ablation of abnormal tissue
Esophageal adenocarcinoma
Refractory GERD
 In the event of failed response to a PPI, it is important to both reconfirm the
diagnosis of GERD (focusing on ruling out alarm symptoms) and ensure proper
administration of PPIs 30 minutes prior to breakfast.
 Alarm symptoms of GERD suggesting complicated disease:
o Black or bloody stools
o Choking
o Chronic cough
o Dysphagia
o Early satiety
o Hematemesis
o Hoarseness
o Iron deficiency anemia
o Odynophagia
o Weight loss
Source: Heidelbaugh, JJ, Gill, AS, Harrison, RV, & Nostrant, TT. (August 15, 2008). Atypical presentations of gastroesophageal
reflux disease. American Family Physician, 78(4), 483-488.
Dyspepsia
Source: Talley NJ, Vakil N. (2005) Guidelines for the management of dyspepsia. Am. J. Gastroenterol, 10: 2324-2337.
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Vague discomfort in the upper abdomen or chest described as gas, feeling of fullness,
gnawing, or burning
May have GERD, peptic ulcer, functional (nonulcer) dyspepsia, or (rarely)
malignancy
Patients with the onset of dyspepsia at age 56 or older or those with alarm symptoms
at any age should undergo immediate upper endoscopy.
o
Alarm symptoms: see those listed above, along with persistent vomiting,
family history of GI malignancy, previous documented peptic ulcer,
abdominal mass, or lymphadenopathy.
Patients with reflux-predominant symptoms should be treated as if they have GERD
If prevalence of H. pylori infection in the community is < 10%, a trial of a PPI is
recommended. If trial fails, a test for H. Pylori infection followed by eradication if
positive should be pursued
When H.pylori is more common, test for H. pylori first, then trial a PPI. If this fails,
may consider upper endoscopy.
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Peptic Ulcer Disease (PUD)
Etiology/Demographics
 Ulceration of the duodenal or gastric mucosa
 Number of associated factors including the interplay of acid production, pepsin
secretion, and mucosal defense mechanisms, also Helicobacter pylori infection
 Male:Female ratio 2:1
 Smoking
 Alcohol use
 Stress
 NSAID use – serves as a local irritant, but most importantly is a prostaglandin
inhibitor, which interferes with the normal synthesis of mucosa
 Long-term or high dose steroid use
 Family history (to a degree)
 Type O blood
Symptoms
 Peptic ulcer disease is typically manifested by symptoms including burning pain
or discomfort localized in the center part of the abdomen
 PUD pain is often worse when the stomach is empty, allowing gastric acid to
come in contact with the ulcer; improved when a patient consumes food to satiety.
Helicobacter pylori
Source: Saad, R, & Chey, WD (February 2005). A clinician’s guide to managing Helicobacter pylori infection. Cleveland Clinic
Journal of Medicine, 72(2), 109-124.
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H. pylori is now widely accepted as a contributing factor in peptic ulcer disease
(many feel that it is the underlying etiology of PUD)
Prevalence of H. pylori varies geographically
o It is associated with lower socioeconomic status, poor hygiene (very
prevalent in underdeveloped countries, even in children, however most are
asymptomatic)
In the US, H. pylori infection occurs in approximately 20% of those younger than
40 and in approximately 50% of those older than 60
There seems to be a decreasing incidence of H. pylori in the US due to improving
socioeconomic conditions over the century
Mode of transmission is unclear, although person-to-person fecal-oral spread is
suspected because clusters occur in families.
Gastric adenocarcinoma and gastric lymphoma have been epidemiologically
linked to H. pylori
There are a wide variety of serological tests available for screening of H. pylori
for the office to the laboratory, all with varying sensitivities/specificities
C-labeled urea breath test: Patient takes urea orally which is labeled with an
isotope. If H. pylori is present in the stomach, labeled carbon dioxide (CO) is
produced as a result of the interaction. This CO can be detected in the patient's
breath within minutes of the urea ingestion. The patient breathes into a collection
bag or onto a flat breath card. (NOTE: Patient must stop treatment for GERD for
2 weeks prior to the test, except can use antacids.)
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Number of different treatment options for H. pylori. First line regimens (14 day
duration) are:
o Clarithromycin-based triple-drug therapy used in patients who are not
allergic to penicillin
 Omeprazole 20 mg twice daily, plus amoxicillin 1 g twice daily
plus clarithromycin 500 mg twice daily
o Bismuth-based quadruple therapy used in penicillin-allergic patients
 Bismuth subsalicylate (Pepto-Bismol) 525 mg four times daily,
plus metronidazole 250 mg four times daily, plus tetracycline 500
mg four times daily, plus histamine H2
Not to be Missed
GI cancer
Plan
 If the patient has any “red flags” (i.e. sustained progressive weight loss, dysphagia,
odynophagia [pain with swallowing], persistent vomiting, nocturnal wakening,
hematemesis, melena) refer for endoscopy.
 If patient with no “red flags” and has no previous documented ulcer disease, treat
empirically with H2 blocker or PPI for at least a full 4 weeks (if large ulcer or a
gastric ulcer, may need up to 8 weeks of therapy).
 If patient does well, follow.
 If no response, refer.
 If patient has no “red flags”, but gives a history of a previously documented ulcer, test
for H. pylori and treat with one of the above mentioned therapies if positive. If H.
pylori negative, treat with H2 blocker or PPI as previously discussed. Follow up is
important with all groups!
 Strongly encourage smoking cessation if appropriate
 Avoid eating before bedtime (helps prevent increased nighttime gastric acid
production)
 Avoid medications that injure the mucosal barrier (i.e. NSAID, steroids)
 Alleviate emotional stress.
 Can try antacids
Chronic Pancreatitis
 Mild to severe recurrent epigastric pain, usually after years of alcohol abuse, however
also may be due to gallbladder obstruction
 Often times these individuals are very difficult to manage due to pain control issues.
 Refer
Chronic Cholecystitis/Cholelithiasis
 Patient gives history of recurrent episodes of biliary colic that has resolved
spontaneously. Symptoms may be worsened by fatty intake or caloric excess.
 Ultrasound is first line test of choice
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For patients that are symptomatic and have gallstones documented on ultrasound,
refer to surgeon for evaluation for elective cholecystectomy
For those patients who are asymptomatic and stones are found coincidentally (i.e. on
CT scan done for another reason): do not treat or recommend surgery. Only 20%
will develop active disease in their lifetime
Do recommend that patients with chronic disease discontinue estrogens, as they
promote gall bladder disease.
Recommend gradual weight loss for obese patients (avoid drastic diets/severe calorie
restrictions as this may actually exacerbate symptoms)
The Acute Abdomen in the Older Patient
Acute Abdomen in the Elderly
Source: Burg, MD, & Francis, L. (August 2005). Acute abdominal pain in the elderly. Emergency Medicine. 8-13.
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A common and life-threatening condition
Elderly often delay seeking health care
 Cognitive impairment?
 Decreased mentation?
 Fear of loss of independence?
 Neuropathy or chronic use of meds such as corticosteroids or pain
relievers may blunt pain perception
Presentation may be atypical…Need high index of suspicion
Consider the possibility of an intra-abdominal process in all older patients seeking
treatment for an acute illness
Many medical conditions that cause or lead to painful abdominal disorders are
more common in the elderly, such as intra-abdominal malignancies, vascular
disease, cholelithiasis, and diverticulosis
History “Have-To’s”
 Duration and location of pain
 Presence/absence of vomiting
 Whether patient is passing flatus
 What abdominal surgery has previously been performed
Physical Signs
 Physical signs are conspicuous by their absence in some older patients with acute
abdominal disease
 Peritonitis is less likely to cause rebound tenderness
 Pyrexia and tachycardia less likely to be present
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Physical Examination
 Careful inspection of inguinal and femoral areas for presence of incarcerated
hernia
 Listening for bowel sounds
 Rectal examination to rule out fecal impaction and GI bleeding
Diagnostic Tests to Consider
 CBC with differential
o WBC’s may not be elevated
o Significant left shift
o Low Hct with perforated peptic ulcer
 BUN, Creatinine
o Increased with dehydration, GI bleed
 Electrolytes
o Low K from vomiting, diarrhea
o Low Na with acute illness
 Liver function
o Increased with cholelithiasis, hepatitis, cholangitis
 ABGs
 EKG
o Inferior wall MI – abdominal pain, intractable vomiting
 Imaging
o Abdominal x-ray (erect/supine)
o Abdominal ultrasound
o Abdominal/pelvic CT
o Laparoscopy for continued diagnostic uncertainty
************** Case Study #8 **************
Cholecystitis
 Most common cause of acute abdominal pain in the older patient
 Complications
o Ascending cholangitis
o Empyema of the gallbladder
o Perforation of the gallbladder
o Pancreatitis (high amylase)
o Indications of gallstone in common duct: elevated bilirubin
Bowel Obstruction
 Responsible for 25% of acute abdomens in older patients
 Common causes
o Incarcerated hernia
o Carcinoma
o Adhesions
o Volvulus (a twisting of the bowel on itself)
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o Fecal impaction
Appendicitis
 14% of cases of acute abdomen in elderly
 Mortality rate up to 15%
o Late presentation
o Inaccurate diagnosis
o High prevalence of perforation at time of presentation
o Decreased blood flow to appendix
o Narrower lumen, thinner wall
 Signs/symptoms
o Less likely to have classic RLQ pain, fever, or elevated WBC
o More likely to have
 Diffuse abdominal pain
 Abdominal guarding
 Abdominal mass
Peptic Ulcer Disease (PUD)
 Incidence increases with age
 More likely to be taking both Rx and OTC NSAIDs
 Smoking, heavy alcohol intake
 Empirical anti-ulcer therapy without endoscopy not suggested
o Greater risk of malignant ulcer
************** Case Study #9 **************
Diverticulitis
Source: Wu, JS, & Baker, ME (July 2005). Recognizing and managing acute diverticulitis for the internist. Cleveland Clinic Journal
of Medicine, 72(7), 620-627.
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Diverticulosis increases with age (5% in the 5th decade to about 50% in the 9th
decade)
Most commonly affects sigmoid (BUT can occur anywhere in the colon…check
for recent colonoscopy results)
Associated with long-term low-fiber diets
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10-25% of patients with diverticulosis eventually develop inflammation in the
diverticula = diverticulitis
o Often found during colonoscopy with recommended treatment being highfiber diet
o
Historically, providers have recommended avoiding ingestion of seeds,
corn, popcorn, and nuts for fear that they might become entrapped in
diverticular, but no controlled studies support this dietary restriction
(Source: Salzman, H, & Lillie, D. (October 1, 2005). Diverticular disease: Diagnosis and treatment. American
Family Physician, 72(7), 1229-1234.
Common symptoms
o Classic, but may be absent in older patient:
 Pain in LLQ
 Fever
 Tender mass in LLQ
o Alternating diarrhea and constipation, rectal bleeding
 Discomfort decreased after passing stool
o Malaise, anorexia, N & V
Clinical Pearl: Tenderness tends to be focal if the process is contained and
contamination is minimal, and generalized if inflammation extends to a large area.
 Diagnosis: labs (CBC, ESR), imaging (CT abdomen/pelvis)
 CT most helpful for patients with a confusing clinical presentation, those with
a palpable LLQ mass which might be a drainable abscess, and to evaluate
patients whose condition is not responding to standard therapy for acute
diverticulitis
 If has not had a colonoscopy previously, will need one...however cannot scope
during acute diverticulitis due to risk of diverticular blowout
Treatment
o If symptoms and findings are minor: Outpatient treatment
 Rest the bowel: Liquid diet or low-residue diet
 Adequate hydration
 Oral antibiotic effective against colonic flora
 Flagyl plus fluoroquinoline X 7-10 days OR Augmentin
 NOTE: Patients usually respond fairly quickly (first day)
to antibiotic therapy. If not, may need CT and possible
admission.
o If patient cannot tolerate oral intake and/or elderly: Admit
 IV fluids
 IV antibiotics
 Bowel decompression via NG
o Surgery if abscess, peritonitis, or sepsis
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Mesenteric Ischemia
Source: Nishijima, DK. (May 1, 2012). Mesenteric ischemia in emergency medicine. Accessed at
http://emedicine.medscape.com/article/758674-overview
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A disease of old age due to atherosclerosis or clot
o > 2/3 of cases in those age 70+
Mortality rate > 80%
3 major arteries supply blood to the stomach, small intestine, and large intestine
o Significant collateral circulation provides some protection from ischemia
(able to compensate for approximately a 75% acute reduction in
mesenteric blood flow for up to 12 hours without substantial injury)
o No symptoms until 2 of 3 of these are blocked/narrowed
Causes:
o Chronic: long-standing atherosclerotic disease of 2 or more of the
mesenteric vessels
o Acute: causes include:
 arterial embolism usually from a dislodged cardiac thrombus
 arterial thrombosis due to acute worsening of ischemia in patients
who have preexisting atherosclerosis
 severe and prolonged intestinal vasoconstriction most commonly
from severe systemic illness with systemic shock secondary to
reduced cardiac output
 can also occur with cocaine ingestion, ergot poisoning,
digoxin use, and use of alpha-adrenergic agonists
Symptoms
o Chronic: severe abdominal pain (periumbilical) 30-60 minutes after
eating; decreased intake wt. loss, diarrhea, N&V, constipation
o Acute: sudden, severe abdominal pain, vomiting, diarrhea
Diagnosis is difficult; CT scan and angiography are best for diagnosing this (note:
MRI no better than CT)
Suggestive findings
o Pain more severe than expected; pain is disproportionate to physical
examination findings
o History of arteriosclerosis
o Postprandial abdominal pain
o Diarrhea (heme +)
o Leukocytosis
Treatment
o Chronic: no smoking, diet/exercise, cholesterol & BP control
o Acute: surgery
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Colon Cancer
Demographics
 Colorectal cancer (cancer of the colon or rectum) is the 2nd leading cause of
cancer-related death in the United States
 In 2003, there were an estimated 147,500 new cases and 57,100 deaths from
colorectal cancer
o Of those diagnosed, 93% are aged 50 and older
Who is at Risk?
 Risk increases with advancing age
 Inflammatory bowel disease
 Personal or family history of colorectal cancer or colorectal polyps
 Certain hereditary syndromes (Lynch syndrome – CRC; familial polyposis)
 Lack of regular physical activity contributes to risk for colon cancer, but does not
affect rectal cancer risk
 Low fruit and vegetable intake
 Low-fiber and high-fat diet
 Obesity
 Alcohol consumption
 Tobacco use
Survival
 If colorectal cancer is detected early, while the disease remains localized, the 5year survival rate can exceed 90% in men and women
 A 2012 study found about 2/3 of Americans ages 50-75 have had the
recommended screenings for colorectal cancer
 If the tumor is not detected early, morbidity and mortality increase rapidly.
o In the U.S., the current 5-year rate is only 50-55%, because, regardless of
sex, 65% of patients present with advanced stage disease
 What is needed: more aggressive screening and prevention strategies to facilitate
earlier detection and improved treatment outcomes
Pathophysiology
 Colon cancer is believed to arise from polyps, which are protrusions that extend
from the mucosal surface of the colonic wall.
 Colon polyps may be nonneoplastic, or neoplastic, based on their histopathology
o Nonneoplastic polyps include hyperplastic, inflammatory, and lymphoid
polyps
o Neoplastic polyps, which are generally called adenomas, can be further
subdivided into benign or malignant adenomas
 Malignant = polypoid carcinoma
 Benign adenomas have the potential to become malignant
 Tubular adenomas represent 75% of all neoplastic polyps
and are the least likely to progress to a malignant state.
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Villous adenomas are the mostly likely to progress to
becoming cancerous
 Tubulovillous adenomas have an intermediate potential
for becoming cancerous
Predicting the probability that an adenoma will develop into cancer
o Overall, fewer than 1% of all polyps progress to cancer
o However, from 5% to 40% of adenomas are estimated to progress to
cancer
 Generally, the smaller the polyp, the lower the likelihood of cancer
o The process by which normal mucosa is converted into an adenoma and
then cancer is gradual, occurring over approximately 5-10 years.
Clinical Presentation
 Most cases are diagnosed between the ages of 60 and 75
o At diagnosis, almost 25% of patients have distant disease, while another
40% have regional disease involving the surrounding lymph nodes, which
increases the risk for metastases.
 Most common site is on the right side of the colon, frequently involving the
ascending or transverse colon
 Without screening, early detection of colorectal cancer is difficult, because
patients with localized tumors are often asymptomatic
 Most common symptoms include:
o Appearance of blood on or around the stool
o Abdominal pain (frequently crampy and intermittent)
o A change in bowel habits (constipation, diarrhea, or a change in stool
caliber or frequency)
o Iron deficiency anemia secondary to clinically silent GI bleeding
o Unexplained weight loss (in patients with more advanced disease)
Screening and Early Detection
 With the conversion of normal mucosa to carcinoma taking up to 10 years, there
is a large window of opportunity to use screening procedures to detect polyps, the
precursors of this cancer, and to remove them before they become cancerous.
 Approximately 70-80% of all cases occur in people at “average risk,” meaning
that screening of the general population (as opposed to high-risk groups only) is
appropriate.
 US Preventive Services Task Force:
o Recommends screening for colorectal cancer (CRC) using fecal occult
blood testing (FOBT), sigmoidoscopy, or colonoscopy in adults,
beginning at age 50 years and continuing until age 75 years.
o Recommends against routine screening for CRC in adults age 76-85 years.
There may be considerations that support CRC screening in an individual
patient.
o Recommends against screening for CRC in adults older than age 85 years.
o Insufficient evidence regarding use of CT colonography and fecal DNA
testing as screening modalities for CRC.
31 | P a g e


Recommend regular screening for all adults aged 50 years or older, including:
o FOBT every year
o Flexible sigmoidoscopy every 5 years
o Double-contrast barium enema every 5 years
o Total colon examination by colonoscopy every 10 years
NOTE: High-risk individuals (those with a genetic predisposition for colorectal
cancer, a family history of the disease, or inflammatory bowel disease) typically
begin screening at an earlier age and undergo more frequent surveillance, usually
with colonoscopy.
o With first-degree relatives with CRC, recommendation for colonoscopy
every 5 years, beginning at age 40 or 10 years than the earliest family
diagnosis (whichever comes first)
 First-degree relatives include parents, siblings, and children
Postpolypectomy surveillance strategies
according to risk of recurrent advanced adenoma
Colonoscopic Findings
Recommendation
Above Average Risk
Small, left-sided hyperplastic polyps in a
Continue average risk screening strategy
patient who does not meet criteria for
hyperplastic polyposis syndrome
1-2 small (< 1 cm) tubular adenomas
Colonoscopy every 5-10 years
High Risk
3-10 adenomas, or any adenoma > 1 cm with
Colonoscopy every 3 years
villous features or high-grade dysplasia
>10 adenomas
Colonoscopy more often than every 3 years,
consider genetic counseling for familial
syndrome
Hyperplastic polyposis syndrome
Colonoscopy, no clear recommendation on
interval, further investigation needed
Source: Bianchi, LK & Burke, CA (June 2008). Understanding current guidelines for colorectal cancer screening: A
case-based approach. Cleveland Clinic Journal of Medicine, 75(6), 441-448.

American Cancer Society advertising in medical journals: “Keep talking to your
patients about colon cancer screening, so you won’t have to talk to them about
colon cancer.”
Chemoprevention
 In population-based observational studies, people had lower rates of colorectal
cancer if they were taking various agents, including NSAIDs, calcium, and folate.
o Aspirin has shown a modest risk reduction, but is associated with
concomitant risks.
o COX-2 inhibitors are under study as an adjunct to endoscopic surveillance
and surgery in patients with familial adenomatous polyposis.
o Exisulind, the sulfone metabolite of sulindac (NSAID) reduces adenomas
in patients with familial adenomatous polyposis.
o Calcium and folate supplementation have been found to moderately
reduce adenoma formation without significant risk.
32 | P a g e
References regarding colorectal cancer:
 www.cdc.gov website (Center for Disease Control)
 Kamakshi, V.R., & Goodin, S. (2001). Prevention and management of colorectal
cancer in women. Journal of the American Pharmaceutical Association, 4 (4),
585-595.
 Burke, C.A., Bauer, W.M., & Lashner, B. (April 2003). Chemoprevention of
colorectal cancer: Slow, steady progress. Cleveland Clinic Journal of Medicine,
70 (4), 346-350.
Hepatic Problems
Cirrhosis and Chronic Liver Failure
Cirrhosis is a consequence of chronic liver disease, with liver tissue being replaced by
fibrosis, scar tissue, regenerative nodules, and leading to loss of liver function; final stage
of chronic liver damage/disease
Liver failure occurs when >75% of the liver is no longer able to function due to
inflammation of the liver.
 Acute liver failure: loss of function occurs within days to weeks; may be
reversible (acetaminophen overdose is leading cause)
 Chronic liver failure: damage is severe; occurring over years to decades;
generally irreversible (Hepatitis C and ETOH abuse are leading causes)
Most common ages 40-50 years; men>women; 10th leading cause of death in men; 12th in
women
Best treatment is prevention, with emphasis on:
- reducing alcohol consumption
- limiting occupational hepatotoxin exposure, and
- preventing parenteral transmission of hepatitis B and C.
The overall goal is to minimize hepatocellular injury and the risk of progressing to
chronic liver failure and cirrhosis.
Symptoms
 Most symptoms are nonspecific and may include:
o easy bruising (WHY?)
o fatigue
o malaise
o weight loss
 Other symptoms or diseases may occur as a result of the primary disorder that
caused the cirrhosis. These symptoms and diseases may be a clue to the cause
and include Addison’s disease, arthralgia, autoimmune disease, bone pain,
33 | P a g e
diabetes mellitus, heart failure, hyperpigmentation, hypothyroidism, loss of libido,
night blindness, pruritus, and steatorrhea.
Clinical Findings
 Physical examination abnormalities include:
- clubbing
- hepatomegaly
- jaundice
- lacrimal and parotid gland enlargement
- muscle wasting
- gynecomastia and testicular atrophy in men (WHY?)
- palmar erythema
- spider angioma
- splenomegaly
 Portal hypertension is suggested by abdominal collaterals (caput medusae),
ascites, encephalopathy, esophageal varices, hemorrhoids, and splenomegaly.
Staging and Treatment of Ascites
Source: Fowler, C. (April 2013). Management of patients with complications of cirrhosis. The Nurse Practitioner, 38(4),14-22.
Stage
1
2
3
Refractory



Description
Minimal ascites; only detectable by ultrasound
Moderate ascites with abdominal distension
Massive ascites with marked abdominal distention
Ascites that is unresponsive or inadequately
responsive to diuretics or excessive adverse reactions
from diuretics
Treatment
Sodium restriction
Sodium restriction and diuresis
Sodium restriction, diuretics,
therapeutic paracentesis, and
TIPS (transjugular intrahepatic
portosystemic shunt)
Therapeutic paracentesis and
TIPS
Palpation of the liver reveals variable findings:
o Enlarged and easily palpable liver
o Regenerating macronodules along the liver border (micronodules are
nonpalpable)
o In advanced stages the liver is often small and hard.
Hepatocellular carcinoma should be suspected in patients demonstrating a RUQ
bruit or friction rub, especially if blood ascitic fluid is aspirated.
Other signs may occur as a result of the primary disorder that caused the cirrhosis.
They therefore may be a clue to the cause. They include arthropathy, dermatitis,
Dupuytren’s contracture, dysrhythmia, ecchymosis, glossitis, hyperpigmentation,
Kayser-Fleisher ring (pigmented ring at the outer margin of the cornea seen in
Wilson’s disease), neurologic abnormality, xanthelasma/xanthoma.
Laboratory Tests
 Generally, the following tests are ordered:
 albumin
 ALT
 Alkaline phosphatase
34 | P a g e



 AST
 bilirubin
 globulins
 5’-nucleotidase
 prothrombin time (WHY?)
Laboratory abnormalities are often nonspecific.
Certain disease processes are associated with more specific laboratory alterations that
may suggest the diagnosis (such as checking a hepatitis panel for Hepatitis B, C, D).
Liver biopsies may identify histology unique to a given diagnosis. Unfortunately, in
late-stage cirrhosis, the histology no longer differentiates the cause.
Differential Diagnosis
While most cases of cirrhosis occur secondary to alcohol abuse or viral hepatitis, the
following are also implicated:
 Alcohol
 Biliary obstruction
 Cardiovascular (right-sided heart failure, tricuspid insufficiency)
 Drugs and toxins (amiodarone, carbon tetrachloride, isoniazid, methotrexate,
methyldopa, oral contraceptives)
 Infection (Hepatitis B/C/D, schistosomiasis, tertiary syphilis)
 Malnutrition (gastroplasty, jejunoileal bypass)
 Metabolic/Inherited (antitrypsin deficiency, hemochromatosis, Wilson’s disease)
Treatment
 Therapy of cirrhosis is usually supportive and aimed at improving nutritional status,
treating complications, and avoiding factors that may accelerate hepatic insufficiency.
 When cirrhosis occurs as a result of a treatable condition, therapy should be directed
at the primary disorder.
 In a limited number of disorders, a drug or therapy of choice does exist.
 Alcoholic liver disease: Abstinence is the only established therapy.
 Alpha1-antitrypsin deficiency: Liver transplantation is curative.
 Hemochromatosis: Iron removal by phlebotomy is the therapy of choice.
Chelation therapy with deferoxamine (Desferal) and ascorbic acid is an
alternative.
 Primary biliary cirrhosis: Liver transplantation is curative. Ursodeoxycholic
acid (Ursodiol or Actigall) may offer limited benefit.
 Secondary biliary cirrhosis: Relief of biliary obstruction by endoscopy or
surgery serves a preventive and therapeutic role.
 Wilson’s disease: Penicillamine (Cuprimine) chelates copper and is the drug of
choice. Trientine hydrochloride (Cuprid) and zinc sulfate are alternative
medications. Transplantation is curative.
Diet
 Patients require a well-balanced diet high in calories.
 Limiting protein intake is important when encephalopathy is present.
35 | P a g e




The use of branched-chain amino acids also may benefit patients with
encephalopathy.
Appropriate mineral and vitamin (fat-soluble) intake is especially important when
cholestasis is present.
Sodium restriction is indicated if sodium retention occurs.
Copper restriction is important in Wilson’s disease and diseases that involve biliary
obstruction. Patients should restrict their intake of copper-rich food such as
chocolate, dried beans, organ meat, peas, shellfish, and whole wheat.
Patient Education
 Patients should be made aware of factors (drugs, toxins, infections) that may
exacerbate their liver disease.
 Alcohol counseling benefits patients and family members.
 Family planning and screening are important in a few diseases such as
hemochromatosis and Wilson’s disease.
 The correct use, need for compliance, and possible side effects of medications should
be emphasized.
 Making patients aware of disease complications encourages them to see prompt
medical attention, allowing for early diagnosis and treatment.
Follow-Up
 Monitor medication efficacy and side effects as well as disease progression.
 Complications include ascites, spontaneous bacterial peritonitis, portal
hypertension and variceal bleeding, hepatic encephalopathy, hepatic failure, and
hepatorenal syndrome (a life-threatening medical conditions involving rapid
deterioration of kidney function in individuals with cirrhosis or liver
failure. Usually occurs when liver function deteriorates rapidly due to an acute
injury such as infection, GI bleed or overuse of diuretics. Usually fatal without
liver transplant. Dialysis may help short term. Occurs in 18% of patients with
cirrhosis within 1 year of diagnosis; in 39% within 5 years of diagnosis.)
References:
Heidelbaugh, JJ, & Bruderly, M. (September 1, 2006). Cirrhosis and chronic liver failure: Part I. Diagnosis and evaluation.
American Family Physician, 74(5), 756-762.
Heidelbaugh, JJ, & Sherbondy, M. (September 1, 2006). Cirrhosis and chronic liver failure: Part II. Complications and treatment. .
American Family Physician, 74(5), 767-776.
References for following Hepatitis content:
Centers for Disease Control and Prevention, National Center for Infectious Diseases
Elgouhari, HM, Abu-Rajb Tamimi, TI, & Carey, W. (January 2009). Hepatitis B: A strategy for evaluation and management.
Cleveland Clinic Journal of Medicine, 76(1), 19-35.
Gardenier, D. & Alfandre, D. (September 2006). Primary care of the patient with chronic hepatitis C. The Journal for Nurse
Practitioners, 517-524.
Wilson, TR. (June 2005). The ABCs of hepatitis. The Nurse Practitioner, 30(6),12-21.
www.HepatitisFoundation.org
36 | P a g e
************** Case Study #10 **************
The ABC’s of Hepatitis
What is it?
Incubation
Period
How is it
Spread?
Symptoms
Treatment
of Chronic
Disease
Hepatitis A
(HAV)
HAV is a virus
that causes
inflammation of
the liver. It does
not lead to
chronic disease.
Hepatitis B
(HBV)
HBV is a virus that
causes inflammation
of
the liver. It can cause
liver cell damage,
leading to cirrhosis
and
cancer.
Hepatitis C
(HCV)
HCV is a virus
that causes
inflammation of
the liver. It can
cause liver cell
damage,
leading to
cirrhosis and
cancer.
2 to 25 weeks.
Average 7 to 9
wks.
Contact with
infected blood,
contaminated
IV needles,
razors, and
tattoo and
body-piercing
tools, Infected
mother to
newborn. Not
easily spread
through sex.
Hepatitis D
(HDV)
HDV is a virus
that causes
inflammation of
the liver. It only
infects those
persons with
HBV.
Hepatitis E
(HEV)
HEV is a virus
that causes
inflammation of
the liver. It is
rare in the U.S.
There is no
chronic state.
2 to 7 weeks.
Average 4
weeks.
Transmitted by
fecal/oral
(anal/oral sex)
route, close
person to
person contact
or ingestion of
contaminated
food and water.
Hand to mouth
after contact
with feces,
such as
changing
diapers.
Children may
have
none. Adults
usually
have light
stools, dark
urine, fatigue,
fever, nausea,
vomiting,
abdominal pain,
and
jaundice.
Not applicable
6 to 23 weeks.
Average 17 weeks.
2 to 8 weeks.
Contact with
infected blood,
contaminated
needles. Sexual
contact with
HDV
infected person.
2 to 9 weeks.
Average 40
days.
Transmitted
through
fecal/oral
route.
Outbreaks
associated with
contaminated
water
supply in other
countries.
May have none.
Some
persons have mild flu
like symptoms, dark
urine, light stools,
jaundice, fatigue and
fever.
Same as HBV
Same as HBV
Same as HEV
Interferon and
nucleoside/nucleotide
analogues (tenofovir,
entecavir, adefovir,
telbivudine,
lamivudine) control
replication of
virus with varying
success.
Also vaccinated
against hepatitis A if
not immune to it.
Alcohol rehab
Smoking cessation
Surveillance for
hepatocellular
Pegylated
Interferon alfa
2a or 2b plus
ribavirin with
varying success.
Interferon with
varying success.
Not applicable
Contact with infected
blood, seminal fluid,
vaginal secretions,
contaminated
needles,
including tattoo and
body-piercing tools.
Infected mother to
newborn. Human
bite.
Sexual contact.
37 | P a g e
None
HBV vaccine
prevents HDV
infection.
None
Infants born to
infected mother,
having sex with an
infected person
or multiple partners,
injection drug users,
emergency
responders,
healthcare
workers, persons
engaging in anal/oral
sex, and
hemodialysis
patients.
Blood
transfusion
recipients
before 1992,
healthcare
workers,
injection
drug users,
hemodialysis
patients, infants
born to infected
mother, multiple
sex partners.
Injection drug
users, persons
engaging in
anal/oral sex
and those
having sex
with an HDV
infected patient.
Travelers to
developing
countries,
especially
pregnant
women.
Vaccination.
Vaccination provides
Immune
protection for 20 plus
Globulin within
years. Hepatitis B
2 weeks of
Immune Globulin
exposure.
within 1 week of
Washing
exposure. Clean up
hands with soap infected blood with
and
household bleach and
water after
wear protective
going to the
gloves. Do not share
toilet. Use
razors,
household
toothbrushes, or
bleach (10 parts needles. Safer sex.
water
to 1 part
bleach) to
clean surfaces
contaminated
with feces, such
as changing
tables. Safer
sex.
HEPATITIS FOUNDATION INTERNATIONAL
504 Blick Drive, Silver Spring, Maryland 20904-2901
Tel: 301-622-4200 or 1-800-891-0707
Fax: 301-622-4702
Email: [email protected]
Website: www.HepatitisFoundation.org
Grid 2005
Clean up spilled
blood with
household
bleach.
Wear gloves
when touching
blood. Do
not share razors,
toothbrushes, or
needles with
anyone. Safer
sex.
Hepatitis B
vaccine
to prevent
HBV/HDV
infection.
Safer sex.
Avoid drinking
or using
potentially
contaminated
water.
Vaccine
Who is at
Risk?
Prevention
Two doses of
vaccine to
anyone over 2
yrs of
age
Household or
sexual contact
with an infected
person or living
in an area with
HAV outbreak.
Travelers to
developing
countries,
persons
engaging in
anal/oral sex
and injection
drug users.
carcinoma via liver
ultrasound and
alpha fetoprotein
measurement every
6-12 months.
Three doses may be
given to persons of
any age.
38 | P a g e
Serologic Features of Viral Hepatitis
Serologic Markers
Interpretation
IgM anti-HAV
Acute disease
IgG anti-HAV
Remote infection and immunity
HBsAg
Acute or chronic disease
HBeAg
Active replication
IgM anti-HBc (high titer)
Acute disease
IgG anti-HBc:
- HBsAg positive
Chronic disease
- HBsAg negative
Prior exposure
Form of Infection
Hepatitis A
Hepatitis B
Hepatitis C
Anti-HCv
Acute, chronic, or resolved disease
Hepatitis D
HBsAg and anti-HDV
Acute disease
Co-infection
Superinfection
- IgM anti-HBc positive
- IgG anti-HBc positive
Hepatitis E
None
Key: Anti-HAV = antibody to hepatitis A virus Anti-HCV = antibody to hepatitis C virus Anti-HDV = antibody to hepatitis D virus
HBeAg = hepatitis B e antigen
HBsAg = hepatitis B surface antigen
Anti-HBc = antibody to hepatitis B core antigen
Anti-HBs = antibody to hepatitis B surface antigen (HBsAg)
Serological Interpretation for Hepatitis B
(Centers for Disease Control and Prevention, National Center for Infectious Diseases)
Tests
Results
Interpretation
Susceptible
HBsAg
Negative
Anti-HBc
Negative
Anti-HBs
Negative
HBsAg
Negative
Immune due to natural infection
Anti-HBc
Positive
Anti-HBs
Positive
HBsAg
Negative
Immune due to hepatitis B
vaccination
Anti-HBc
Negative
Anti-HBs
Positive
HBsAg
Positive
Acutely infected
Anti-HBc
Positive
IgM anti-HBc
Positive
Anti-HBs
Negative
HBsAg
Positive
Chronically infected
Anti-HBc
Positive
IgM anti-HBc
Negative
Anti-HBs
Negative
HBsAg
Negative
Four interpretations (see below)
Anti-HBc
Positive
Anti-HBs
Negative
Four interpretations:
1. May be recovering from acute HBV infection.
2. May be distantly immune and test is not sensitive enough to detect very low level of anti-HBs in
serum.
3. May be susceptible with a false positive anti-HBc.
4. May be an undetectable level of HBsAg present in the serum and the person is actually a carrier.
39 | P a g e
Other types of hepatitis:
Autoimmune hepatitis
 Age: 30-60 years of age
 Sex: F > M
 Risk factors: associated with autoimmune conditions such as Type 1 DM, thyroid
disease, RA, vitiligo, family history, environmental exposure
 Treatment: Prednisone, Azathioprine
o Monitor LFT’s monthly
o Therapy for at least 12-18 months
o Relapse in 50%; may need lifetime maintenance therapy
Alcoholic hepatitis
 Age: 40-50 years of age
 Sex: M > F 2:1
 Risk factors: Hispanic, poor nutrition, obesity, drinking multiple types of alcohol
 Associated with 160 g/d ETOH for 10-20 years
 Treatment: diet, alcohol avoidance, corticosteroids
Drug-induced hepatitis
 Age: middle aged
 Sex: M = F
 Risk factors: psych history, history of suicide, dementia, regular ETOH intake
 Tylenol overdose most common
 Check toxicology screen
 Treatment: antidote for medication
Nonalcoholic Fatty Liver Disease (NAFLD)
Sources:
Bayard, M, Holt, J, & Boroughs, E. (June 1, 2006). Nonalcoholic fatty liver disease. American Family Physician, 73(11), 1961-1968.
Sublett, L. (August 2007). Deconstructing nonalcoholic fatty liver disease. The Nurse Practitioner, 32(8), 12-17.





Formerly called nonalcoholic steatohepatitis (NASH)
o Now refers to a spectrum of liver diseases ranging from steatosis (fatty
infiltration of the liver) to NASH to cirrhosis
Most common cause of elevated liver enzymes in adults in the US
Most common cause of cryptogenic cirrhosis, which is cirrhosis that cannot be
explained by hepatitis, alcohol abuse, toxin exposure, autoimmune disease,
congenital liver disease, vascular outflow obstruction, biliary tract disease
Prevalence in US: 16-23%
o Prevalence becomes greater with increasing body weight
 2/3 of those with BMI of 30 or greater
 90% of those with BMI > 39
Two types of NAFLD
o Primary NAFLD is related to metabolic syndrome-associated conditions
 Obesity
 Diabetes
 Hypertriglyceridemia
40 | P a g e








o Secondary NAFLD occurs after:
 Bariatric surgery
 Rapid weight loss in obese patients
 Total parenteral nutrition
 Hepatotoxic medications
 Lipodystrophy
 Wilson’s disease
Increased risk of cardiovascular events
Differential diagnosis: diagnosis of NAFLD requires exclusion of alcoholic liver
disease and viral hepatitis
o Requires that daily alcohol intake be < 2 drinks/day for men, <1.5
drinks/day for women
Clinical findings: most are asymptomatic; may complain of fatigue and RUQ
abdominal fullness or pain
o Up to 50% have hepatomegaly
Laboratory evaluation:
o Elevated ALT and AST, usually 1-4X the upper limits of normal (although
some have normal ALT, AST)
o Ratio of AST/ALT usually is < 1 (This ratio is usually >2 in alcoholic
liver disease)
o Alkaline phosphatase may be elevated X2 the upper limit of normal
o GGT may be elevated
Imaging: Ultrasound of liver (CT is no more sensitive and is more expensive, but
can identify other liver pathology such as masses more effectively)
American Gastroenterological Association recommendation for diagnostic
approach
o Question patient carefully about alcohol use
o Obtain ALT, AST, alkaline phosphatase, serum bilirubin, and albumin
levels, prothrombin time, and hepatitis panel
o Order imaging (ultrasound or CT)
Treatment
o Focuses primarily on risk factors for atherosclerotic heart disease (Weight
loss, exercise)
 Advise patients to avoid rapid weight loss. A study found that
liver histological findings worsened when weight loss exceeded
1.6 kg (3.5 lb) per week.
o Treat insulin resistance: metformin
o Treat hyperlipidemia:
 Modest elevation of liver enzyme levels should not preclude the use
of statins in patients for whom they are otherwise indicated.
 The National Cholesterol Education Program states that there is no
evidence that statins are harmful in patients with fatty liver caused
by obesity.
Prognosis: depends upon the extent of liver damage
o Steatosis alone generally has a benign course, and progression to cirrhosis
is rare.
41 | P a g e
Other GI Problems
Common anorectal conditions
Source: Fargo, MV, & Latimer, KM. (March 15, 2012). Evaluation and management of common anorectal conditions. American
Family Physician, 85(6), 624-630.





Pruritus ani: perianal itching
 Most patients self-treat for 12 months before seeking care
 Many causes (dermatologic, dietary irritants [beer, caffeine, chili peppers, citrus,
milk, tomatoes], fecal soilage, infections, malignancy, medications, systemic
disease, topical irritants)
 Treatment: address the underlying cause
o Proper hygiene, avoid perfumes, dyes, dietary irritants, and tight clothing
o Keep area dry, avoid itch-scratch cycle (scratching exacerbates the
inflammation, causing an irresistible urge to scratch even more)
o Sedating antihistamine such as hydroxyzine at night
o May need topical steroids for 2-4 weeks max (low-potency to minimize
skin atrophy)
Anorectal pain
 May be caused by a fissure, an abscess, thrombosed external hemorrhoids,
proctitis, perineal sepsis, or proctalia fugax.
o Anal fissures: most common site is posterior midline; treat with stool
softeners, fiber, sitz baths, topical analgesics
o Thrombosed external hemorrhoids: Sudden onset of pain caused by a clot
in the external hemorrhoidal vein. Pain is most intensive during the first
24-48 hours after the clot forms and then it resolves rapidly, even with no
treatment. If pain is beginning to diminish, treat with topical
corticosteroids, warm soaks, and stool softeners.
Anorectal masses
 May be condyloma (anogenital warts), abscess, polyp, prolapse, hemorrhoid, or
anal cancer
o Risk factors for anal cancer: HPV, 15+ sexual partners during a lifetime,
tobacco smoking, long-term corticosteroid use, receptive anal intercourse,
and in HIV-infected men and women, age < 30 or male homosexual
contact
 Can do anal pap screening in men with HIV
Anorectal fistulas
 Suspect in any patient with discharge, pain, swelling, or bleeding
 Treatment: sitz baths, high-fiber diet, analgesics (referral to surgeon for
nonhealing or complex fistulas)
Anorectal bleeding
 Due to hemorrhoids, fissures, polyps, diverticular disease, inflammatory bowel
disease, or colorectal cancer
42 | P a g e

Hemorrhoids
Etiology
 Hemorrhoidal disease may be produced by anything that increases pressure in the
hemorrhoidal veins.
 Common etiologies are thought to include:
- constipation
- straining at stool
- Valsalva maneuver during other activities such as lifting
- lesions of the rectum and distal sigmoid colon that produce venous obstruction
 Because the internal hemorrhoidal venous plexus is one of the several areas of
anastomosis of the systemic and portal circulation, internal hemorrhoids may also
develop secondary to portal hypertension produced by hepatic cirrhosis.
Symptoms
Internal hemorrhoids are commonly associated with complaints related to:
 painless rectal bleeding
 anal pruritus (itching)
 perianal soiling (secondary to mucosal secretions)
Clinical Findings
Internal hemorrhoids are graded on the basis of their anatomic presentation:
Grade
Description
Diagram
Picture
Grade I
The hemorrhoidal mass is
swollen and projects into the
anal canal (do not prolapse)
Grade II
The hemorrhoidal mass is
pendulous (prolapses) on
defecation but reduces
spontaneously.
Grade III
The hemorrhoidal mass
prolapses on defecation and
recedes only following
manual reduction.
Grade IV
The hemorrhoidal mass is
permanently prolapsed.
Source of above diagrams/photos: http://en.wikipedia.org/wiki/Hemorrhoid
43 | P a g e
Tests
Before any type of operative hemorrhoidal therapy is undertaken, a digital rectal and
flexible sigmoidoscopic examination should be performed and appropriate
coagulation studies (PT and PTT) should be obtained if clinically indicated.

Treatment
 Contrary to popular belief, there is no role for suppositories in the management of
hemorrhoidal disease.
 The treatment of grade I and grade II internal hemorrhoids consists of stool
softeners and/or surface tension-decreasing agents, warm sitz baths, and improved
bowel habits. This noninvasive protocol may reduce the need for more aggressive
intervention in the majority of patients.
 Grade III and IV hemorrhoids usually require surgery.
 Stubborn itching and inflammation respond well to topical corticosteroids;
hydrocortisone cream (1%) is adequate, relatively inexpensive, and available
OTC. Should be used 3-4 times/day.
 Caution with long term use: can permanently damage or cause ulceration
of the perianal skin
Fecal impaction and incontinence
 Fecal impaction is a partial or complete blockage of the colon by hard, dry
stool; presents as constipation or overflow incontinence
 Fecal incontinence is the involuntary loss of bowel function
 Remove physical barriers to the bathroom; institute scheduled
defecation schedules for patients with dementia
 Biofeedback, antidiarrheal medication
 PT for pelvic floor dysfunction; surgery
Hernias
Source: Amid, PK, Graham, M, & Selwyn, CA. (May 2005). Abdominal hernia: Emerging trends in diagnosis and management.
Patient Care. 43-55.
Hernia: a defect in the normal musculofascial continuity of the abdominal wall that
permits the passage of structures not normally passing through the wall.
 Incarcerated hernias are those that cannot be reduced and the contents of the
hernial sac cannot be returned to the peritoneal cavity.
 Strangulated hernias are those which occur when the blood supply to the viscera
lying within the hernial sac is obliterated or cut off.
Several types:
Inguinal hernias (75% of all abdominal hernias are inguinal)
 Direct: portions of the bowel and/or omentum protrude directly through the floor
of the inguinal canal and emerge at the external inguinal ring
 Indirect: pass through the internal abdominal ring, traverse the spermatic cord
through the inguinal canal and emerge at the external inguinal ring (8-10 times
more common in men than in women)
Femoral hernias (protrusion of omentum through the femoral canal) (3-5 times more
common in women than in men)
44 | P a g e
Ventral hernias
 Incisional hernias (develop in the scar of a previous laparotomy or in a drain site)
 Umbilical hernias (pass through the umbilical ring; often close spontaneously by
age 4 or 5 years)
 Epigastric hernias (occur through the linea alba between the xiphoid process and
the umbilicus; may produce symptoms that mimic peptic ulcer disease or biliary
colic)
History: Ask about:
 groin pain
 swelling
 ability to reduce the hernia
 circumstances of onset
 aggravating and alleviating factors, such as exacerbation on standing, straining, or
coughing
 Acute onset of colicky abdominal pain, nausea, and vomiting suggest entrapment and
strangulation in a patient with a known hernia.
 An incarcerated inguinal hernia presents gradually with scrotal pain.
Clinical Findings (inspection/palpation/maybe auscultation)
 Bowel palpable in the scrotum or in the inguinal canal.
 Bowel sounds may be audible in the scrotum if the hernia is incarcerated. If
strangulation has occurred, bowel sounds are not audible in the scrotum, and the
abdomen is likely to be tender, distended, and without bowel sounds.
When examining male:
o With a direct inguinal hernia, when the finger is inserted through the external
canal, a bulge will be felt striking the side of the finger.
o With an indirect inguinal hernia, when the finger is inserted through the external
canal, the bulge will be felt at the fingertip when the client coughs or strains.
When examining female:
o It is more difficult to establish the diagnosis of inguinal hernia; locate the external
inguinal ring by identifying the inguinal ligament and os pubic; place hand over
inguinal ring and palpate for bulge when client coughs or strains.
Differential Diagnosis of Inguinal Hernias
 Hydrocele
 Varicocele
 Spermatocele
 Epididymal cysts
 Epididymitis
 Testicular tumor
 In children, undescended testes
45 | P a g e
Differential Diagnosis of Femoral Hernias
 Enlarged lymph node
 Lipoma
 Direct inguinal hernia
 Saphenous varix
Diagnostic Tests
Often none needed, may order ultrasound if uncertain about abdominal mass
Clinical Pearls:
 If diagnosis is difficult, try having the patient change position from sitting to standing
and having him or her cough or strain. The next best diagnostic tool after a thorough
history and physical exam is a CT scan, with referral to a surgeon an option at any
point in the process.
 Pain does not equal hernia. Pain without a bulge is more likely to be something other
than a hernia.
Management
Hernias should have referral to a surgeon.
 A hernia that reduced spontaneously could become incarcerated and
strangulated
 Lack of symptoms does not necessarily mean that a hernia is harmless and can
be left alone.
 Unless a defect is very large—with a decreased risk of the herniated sac
becoming trapped outside the abdominal wall—it should be surgically
repaired.
 Femoral hernias need to be repaired as soon as possible because of the
increased risk of incarceration and strangulation.
Follow-Up
Examine annually for recurrences
Acute Diarrhea
Source: Helton, T, & Rolston, DDK (October 2004). One minute consult: Which adults with acute diarrhea should be evaluated?
What is the best diagnostic approach? Cleveland Clinic Journal of Medicine, 71(10), 778-785.
Definition: An increase in the frequency of stools with a decrease in consistency
compared with the patient’s baseline pattern. Acute is diarrhea that has lasted < 14 days;
chronic diarrhea has a duration greater than 1 month. (14-29 days = persistent acute
diarrhea)
For most cases, a brief history and treatment with oral hydration and OTC loperamide,
kaopectate, or Pepto-Bismol usually suffice.
A full H&P and diagnostic testing is needed for a patient with any of the following:
 Fever (38.5oC and above)
 Dysentery (passage of blood and mucus in the stool)
46 | P a g e






Symptoms of dehydration, particularly postural lightheadedness, decreased urine
output, and excessive thirst)
Worsening diarrhea after 48 hours
Six or more stools in 24 hours
Advanced age (70 years and older)
Compromised immune system
Age greater than 50 with severe abdominal pain
History
 Travel
 Sexual practices
 Antibiotic use within 2 months (concern for Clostridium difficile)
 Other medications (laxatives, antacids, digoxin, immunosuppressive drugs)
 Ill contacts
 Group gatherings after which other attendees also developed similar illness
 Recent surgeries or procedures
 Recent meals
 Water source
 Pets (particularly turtles)
 The onset and duration of the illness
Diagnostic Testing
 Stool for occult blood
o If (+), obtain stool cultures
 Consider empiric antibiotics if traveler’s diarrhea is suspected
 Testing stool for ova and parasites should be done if recent foreign travel, if
homosexual who is immunocompromised, if community outbreak of parasite, or
if dysentery
 Fecal leukocyte testing – if (+) suggests an inflammatory cause and would
support obtaining stool cultures
 CBC, BMP, plain film of abdomen
Chronic Diarrhea
Source: Juckett, G, & Trivedi, R. (November 15, 2011). Evaluation of chronic diarrhea. American Family Physician, 84(10), 11191126.
Definition: a decrease in stool consistency continuing for more than 4 weeks.
Categories: (may overlap)
 Watery
o Osmotic (water retention due to poorly absorbed substances)
o Secretory (reduced water absorption
o Functional (hypermotility)
 Fatty (malabsorption)
 Inflammatory (with blood and pus)
47 | P a g e
History and Physical Examination
 Determine exactly what the patient means when saying he/she has diarrhea
o It may be incontinence due to fecal impaction rather than diarrhea
 Ask about stool volume, frequency, and consistency
 Travel history
 Check regarding recent weight loss
 Examine eyes, mouth, check lymphadenopathy, abdomen, skin, rectal exam
Differential Diagnoses: Includes hundreds of conditions, but most common causes are:
 Celiac disease
 Clostridium difficile infection
 Drug-induced diarrhea
 Endocrine diarrhea (hyperthyroidism)
 Giardiasis
 Infectious enteritis or colitis: bacterial or viral gastroenteritis, amebic dysentery
 Inflammatory bowel disease
 Irritable bowel disease
 Ischemic colitis
 Microscopic colitis
Diagnostic Testing
 CBC, albumin level, ESR, liver function testing, TSH, electrolytes
 Fecal leukocyte level and fecal occult blood test
 Fecal calprotectin (to identify inflammatory bowel disease)
 If travel risk factors, stool C&S, stool ova and parasite examination, Giardia and
Cryptosporidium stool antigen tests.
Treatment: Depends on cause found
 Empiric therapy may be justified if a specific diagnosis is strongly suspected, for
example metronidazole for a traveler with possible giardiasis or bile acid resins
for bile acid malabsorption.
************** Case Study #11 **************
Chronic Constipation
Source: American Gastroenterology Association (2008). Guidelines: Managing chronic constipation.
Definition: unsatisfactory defecation resulting from difficult stool passage and/or
infrequent defecation
Clinical subgroups of constipation
 Normal transit constipation (functional constipation)
o Most common form (59% prevalence rate)
o Colonic transit time is normal
48 | P a g e



Slow transit constipation (colonic inertia)
o 13% prevalence
o Delayed colonic transit
Pelvic floor dysfunction (disorder defecation) – 25% prevalence
Combination (slow transit + pelvic floor dysfunction)
Clinical Evaluation
 History: determine predominant symptom (infrequent defecation, straining, hard
stool), duration and severity of symptoms, response to prior or current therapy
Source:
http://www.bing.com/images/search?q=bristol+stool+form+scale&id=8BFE32FF9B003C09452EAE6D5C814962C88A6276&FORM
=IQFRBA#view=detail&id=8BFE32FF9B003C09452EAE6D5C814962C88A6276&selectedIndex=0


Physical exam: rectal exam, check anal reflex, anal sphincter, look for rectocele
Diagnostics: colonoscopy if age > 50, alarm signs or additional symptoms
present
Management
 Patient education about diet (including fiber and hydration)
 Lifestyle modifications
o Encourage patients to avoid postponing defecation
o Monitoring bowel habits with a daily diary
o Moderate exercise
 Choice of therapeutic agent
o Polyethylene gycol 3350
o Milk of magnesia
o Chloride channel activator (Amitiza [lubiprostone])
o 5-HT4 (tegaserod [Zelnorm]) no longer available
 Biofeedback for pelvic floor training
************** Case Study #12 **************
49 | P a g e
Irritable Bowel Syndrome (IBS)
Source: Wilson, JF (July 3, 2007). In the clinic: Irritable bowel syndrome. Annals of Internal Medicine. ITC7-1 – ITC7-16.
Definition
IBS is characterized by abdominal pain or discomfort associated with abnormal bowel
habits (diarrhea, constipation, or alternation between the two), and associated with
symptoms of bloating, distention, straining, feelings of incomplete evacuation, and
urgency.
Epidemiology
Affects as many as 1 in 5 US adults, occurs more often in women than in men, and begins
before the age of 35 in about half of all people who develop the disorder
Pathophysiology
Certain motility and sensory abnormalities are found in IBS patients as a group, and these
distinguish them from healthy individuals:
 Various stimuli including stress, meals, and peptides alter colonic or small
intestinal motor response.
 It is presumed that pain symptoms in patients with IBS are due to hyperactivity.
 These patients also have reduced sensory thresholds for stimuli such as rectal and
ileal distention.
IBS, especially in women, overlaps with other GI disorders, non-GI pain disorders, and
affective disorders. These include painful menstruation, history of abuse, fibromyalgia
and other rheumatologic symptoms, and chronic pelvic pain.
Symptom criteria for IBS: Rome III
Recurrent abdominal pain or discomfort at least 3 days per month in the past 3
months associated with 2 or more of the following:
1. Improvement with defecation
2. Onset with change in frequency of stool
3. Onset associated with a change in the form and appearance of stool
* Criteria must be fulfilled for at least the past 3 months with symptom onset at
least 6 months before diagnosis
Symptoms
History
Physical Findings
Alarm Features that Suggest Possible Organic Disease
Weight Loss
Frequent nocturnal awakenings due to gastrointestinal symptoms
Fever
Blood mixed in stool
New onset, progressive symptoms
Onset of symptoms after age 50
Recent antibiotic use
Family history of colon or ovarian cancer or inflammatory bowel disease
Abdominal mass
Stool positive for occult blood
Enlarge lymph nodes
50 | P a g e
Clinical Findings
 The physical examination in most IBS patients is generally normal.
 Physical examination may reveal tenderness in the area of the colon in patients with
the spastic colon variety of IBS. In patients with small bowel involvement, pressure
over the umbilicus or epigastrium may precipitate symptoms.
Differential Diagnoses
Constipation-predominant symptoms
 Strictures due to inflammatory bowel disease, diverticulitis, ischemia, or cancer
 Colonic inertia
 Pelvic floor dysfunction
 Neurologic disease (Parkinson disease, MS)
 Medications (opioids, CCBs, anticholinergics)
 Hypothyroidism
 Hypercalcemia
Diarrhea-predominant symptoms
 Crohn’s disease
 Ulcerative colitis
 Microscopic colitis
 Parasites (check on travel, drinking water from streams, etc.)
 Clostridium difficile
 Other bacteria
 Small bowel overgrowth
 Sprue (gluten-sensitive enteropathy)
 Lactose intolerance
 Postgastrectomy syndrome
 HIV enteropathy
 GI endocrine tumor (carcinoid, gastrinoma)
 Laxative abuse
Laboratory Tests
 Laboratory studies are generally normal in IBS. The diagnosis should be
suspected based on the patient’s symptoms and by excluding organic diseases.
 A minimal evaluation would consist of a CBC, CMP, ESR, antibody for celiac
disease
 If diarrhea is a predominant symptom, stool samples for leukocytes, culture for
enteric pathogens, and examination for ova and parasites should be pursued.
 X-ray studies of the small bowel or colon are generally not indicated with typical
IBS symptoms. If the patient has had symptoms for more than 3 months or is
over age 50, a barium enema or colonoscopy should be performed.
51 | P a g e
Treatment
Dietary modification
 Reasonable to consider in cases in which specific foods seems to trigger
symptoms
 Review dietary habits to:
o Evaluate for lactose intolerance
o Evaluate consumption of caffeine, fructose, or artificial sweeteners
(laxative effects)
o Inquire about laxative-containing herbal products
o Determine whether drinking excess carbonated beverages, drinking with a
straw, or chewing gum, all of which can lead to swallowing too much air
and result in gas and bloating
o Advise against excess intake of fats (cause gas retention)
o Advise avoidance of certain carbohydrates such as beans, cabbage,
broccoli, and cauliflower, if they trigger symptoms (may be difficult to
digest and lead to fermentation and gas in the colon)
 Fiber is helpful for relief of constipation but not for relief of pain
Other nonpharmacologic interventions
 Reassurance
 Education with advice about trigger avoidance
 Stress management
o Patients with IBS are more likely to have had early life or current trauma,
including losses or abuse, and are more likely to have generalized anxiety
disorder and worry.
 Exercise
Pharmacologic therapies
Constipation predominant
 Increase fiber (start with one tablespoon psyllium per day or twice a day).
Alternatives include polycarbophil or methylcellulose.
 Osmotic laxative
 Stool softener
 Zelnorm (tegaserod) – binds to 5-HT4 receptors, stimulating GI peristalsis and
decreasing visceral sensitivity (Withdrawn from US Market)
 Amitiza (lubiprostone) -- activates chloride channels, increasing intestinal fluid
secretion and motility
Diarrhea predominant
 Antidiarrheals
o Loperamide (Imodium), 2-4 mg every 6-8 hours
o Diphenoxylate (Lomotil), 2.5-5 mg every 4-6 hours
 alosetron HCL tablets (Lotronex) – selective 5-HT3 receptor antagonist (inhibits
activation of non-selective cation channels which results in the modulation of the
enteric nervous system)—Withdrawn from US Market in 2000/Returned to
market in 2002.
52 | P a g e
o Now “Restricted Access in US”: In order to prescribe, you must enroll in
GlaxoSmithKline’s Prescribing Program for Lotronex
(www.lotronex.com)
Pain/gas/bloat predominant
 Antispasmodics (Anticholinergics) (dicyclomine[Bentyl], 10-20 mg. 30-45
minutes between meals four times a day; hyoscyamine [Anaspaz, Levbid, Levsin,
NuLev])
 Antidepressants (amitriptyline HCl/Elavil, or doxepin/Sinequan, starting with 2550 mg at hour of sleep and gradually increased to 75-150 mg at hs as tolerated.
Fluoxetine/Prozac, 20 mg, as single daytime dose is less sedating.)
Referral
Consultation with gastroenterology is warranted when patients do not fit Rome criteria,
when patients have alarm symptoms, and when patients do not respond to initial
management.
Celiac Disease
Source: Crowe, SE (2011). In the clinic: Celiac disease. Annals of Internal Medicine. ITC5-2 – ITC5-16.



Also known as gluten-sensitive enteropathy, celiac sprue, nontropical sprue
Affects 1% of U.S. population
Results from an inappropriate T-cell-mediated immune response to ingested
gluten that causes inflammatory injury to the small intestine in genetically
predisposed persons. Damage to the proximal small intestinal mucosa results in
the malabsorption of nutrients.
Source: Harrison, MS, Wehbi, M., & Obideen, K. (March 2007). Celiac disease: More common than you think. Cleveland Clinic
Journal of Medicine, 74(3), 209-216.



Strong genetic component: 90-95% of patients with celiac disease possess the
HLA-DQ2 allele, and the other 5-10% possess the HLA-DQ8 allele.
Classic GI manifestations: diarrhea, flatulence, abdominal distention, weight loss,
malaise, steatorrhea, and recurrent aphthous ulcers
Associated conditions
o Dermatitis herpetiformis, a skin disorder exclusive to celiac disease
Photo source:
http://www.bing.com/images/search?q=dermatitis+herpetiformis&id=4F0A2782A9719743B8A9529FA7F4AB2BA549D03D&FOR
M=IQFRBA#view=detail&id=AB818BA0D1D7D736E482BB13FBC64E5E053EDDD8&selectedIndex=36
o Enteropathy-associated T-cell lymphoma
53 | P a g e
o Other malignancies (small-bowel adenocarcinoma, oropharyngeal and
esophageal adenocarcinoma, liver cancer, melanoma, non-Hodgkin’s
lymphoma)
o Autoimmune disorders (type 1 diabetes mellitus and autoimmune
thyroiditis)
o Down syndrome, Turner syndrome, Williams syndrome
Source: Presutti, RJ, Cangemi, JR, Cassidy, HD, & Hill, DA (December 15, 2007). Celiac disease. American Family Physician,
76(12), 1795-1802.



Testing:
o Anyone with chronic diarrhea, malabsorption, weight loss, and persistent
abdominal distention should be tested.
 Also consider in patients with premature osteopenia or
osteoporosis, unexplained iron deficiency anemia or unexplained
liver abnormalities
o Testing must be done while on a gluten-containing diet
o Serology: IgA endomysial antibodies and IgA tissue transglutaminase
antibodies
o Because serologic markers may have false-positive or false-negative
results, they cannot be relied on for the diagnosis of celiac disease.
However, positive serologic markers can indicate the need for further
evaluation with small bowel biopsy, particularly in patients at increased
risk.
o A small bowel biopsy is required to confirm the diagnosis of celiac disease
for most patients.
Treatment
o Avoidance of food products that contain gluten proteins (wheat, rye,
barley)
 Can be extremely difficult
 May produce considerable psychological, emotional, and economic
stresses
 Need formal consultation with dietician
o Correction of nutritional deficiencies associated with malabsorption (iron,
folic acid, vitamin B12, and fat-soluble vitamins
o Check thyroid function, DEXA
Follow-up
o Serologic markers may be used to monitor compliance with a gluten-free
diet
 Antibody levels typically return to normal within 3-12 months of
starting a gluten-free diet
Inflammatory Bowel Diseases (IBD): Crohn’s Disease & Ulcerative Colitis
Source: Abraham, C & Cho, JH. (November 19, 2009). Mechanisms of disease: Inflammatory bowel disease. N Engl J Med,
361(21), 2066-2078.



Evidence suggests that IBD results from an inappropriate inflammatory response
to intestinal microbes in a genetically susceptible host.
At risk for primary sclerosing cholangitis, ankylosing spondylitis, and psoriasis
IBD affects 1.4 million Americans
54 | P a g e

Peak onset is in persons 15-30 years of age
Source of following table: Buch, KE (July 2007). Inflammatory bowel disease: A clinical review of Crohn’s disease and ulcerative
colitis. Advance for Nurse Practitioners, 57-60.
Location
Common symptoms
Crohn’s Disease
Anywhere in GI tract, usually
ileocecal region
RLQ pain, diarrhea, weight loss,
low-grade fever
Radiologic appearance
Skip lesions, strictures, fistulas
Colonoscopic appearance
Ulcers separated by normal mucosa,
fistulas, strictures
Rare
Common
Common
Less common
Smokers at increased risk
Rectal Involvement
Fistulas
Strictures
Bleeding
Cigarette smoking affect*
Ulcerative Colitis
Rectum and colon, beginning distal
and extending proximal
Bloody diarrhea, crampy LLQ
abdominal pain, fecal urgency,
tenesmus, weight loss
Fine, granular mucosa, pseudopolyps,
ulceration
Continuous proximal extension of
mucosal inflammation
Always
Rare
Rare
Common
Former smokers and nonsmokers at
greater risk
++++
Colon Cancer Risk**
++
* Source: Abraham, C & Cho, JH. (November 19, 2009). Mechanisms of disease: Inflammatory bowel disease. N Engl J Med,
361(21), 2066-2078.
** Source: Wilkins, T, Jarvis, K, & Patel, J. (December 15, 2011). Diagnosis and management of Crohn’s disease. American Family
Physician, 84(12), 1365-1375.
Crohn’s disease
Source: Wilkins, T, Jarvis, K, & Patel, J. (December 15, 2011). Diagnosis and management of Crohn’s disease. American Family
Physician, 84(12), 1365-1375.


Diagnostic testing
o Initial: CBC, BUN, creatinine, liver enzymes, C-reactive protein, ESR,
stool culture and testing for C. difficile
o Subsequent testing: iron, ferritin, TIBC, vitamin B12, folate, albumin,
prealbumin, calcium, vitamin D
o Colonoscopy with ileoscopy and biopsy
Treatment
o Traditional “step-up” approach begins with corticosteroids or mesalamine
products and advances to immunomodulators or anti-tumor necrosis factor
(TNF) agents based on severity of disease
 Mesalamine products: sulfasalazine (Azulfidine) and 5aminosalicylic acid (5-ASA)
 Immunomodulators: 6-mercaptopurine, azathioprine (Imuran),
budesonide (Entocort EC), methotrexate, prednisone
 TNF agents: adalimumab (Humira), infliximab (Remicade),
certolizumab pegol (Cimzia)
o A “top-down” approach begins with anti-TNF agents
55 | P a g e
Ulcerative Colitis (UC)
Source: Langan, RC, Gotsch, PB, Krafczyk, MA, & Skillinge, DD. (November 1, 2007). Ulcerative colitis: Diagnosis and treatment.
American Family Physician, 76(9), 1323-1330.


Diagnostic testing
o Stool examinations for ova and parasites, stool culture, and testing for C.
difficile toxin
o ESR and C-reactive protein may be elevated
o CBC (may show anemia), BMP (may show electrolyte abnormalities such
as hypokalemia from persistent diarrhea)
o Colonoscopy and biopsy = tests of choice to diagnose UC
Treatment
o Therapeutic approach determined by severity of symptoms and degree of
colonic involvement
 Proctitis: 5-ASA suppositories
 Mild to Moderate UC
 Left-sided: 5-ASA suppositories
 Extensive: Oral 5-ASA and if no response, oral steroids
 Moderate to Severe UC
 Oral steroids
 If no response hospitalize to receive IV corticosteroids
 If no response to IV steroids, consider referral for therapy
with cyclosporine (Sandimmune) or infliximab (Remicade)
 Steroids are tapered when possible and 5-ASA used as
prophylaxis/maintenance
o Increased risk of developing colon cancer
 American Cancer Society guidelines:
 Initial colonoscopy 8 years after disease onset of pancolitis,
12-15 years for left-sided disease
 Follow-up colonoscopy every 1-2 years (risk of colon
cancer increases the longer patient has UC)
Obesity
Source: Meires, J, & Christie, C. (September 2011). Contemporary approaches to adult obesity treatment. The Nurse Practitioner,
36(9), 37-46.
A transdisciplinary approach to adult obesity including NP, MD, and RD (registered
dietician)
 Assess anthropometrics (RD)
o Wait-to-hip ratio
o Waist circumference
o Height and weight
o Calculate BMI
o Frame size
 Screen to rule out organic causes and make appropriate referrals (NP/MD)
o Pituitary dysfunction
o Thyroid disease
o Polycystic ovary disease
o Hypothalamic disorders
56 | P a g e


o Genetic disorders
o Others
Assess comorbid conditions (NP/MD)
o Hypertension
o Dyslipidemia
o CVD
o Hyperinsulinemia
o Diabetes
o Metabolic syndrome
o Sleep apnea
o GERD
o Osteoarthritis
o Breast, endometrial, and/or colon cancer
o Depression
o Others
Assess health risk (NP/MD/RD)
BMI
< 25
25-<27
27-<30
30-<35
35-<40
40 and above





No comorbidities
Minimal
Low
Moderate
High
Very high
Extremely high
One or more comorbidities
Low
Moderate
High
Very high
Extremely high
Extremely high
R/O weight loss contraindications (NP/MD)
o Pregnancy/lactation
o Medical/mental conditions such as eating disorders, psychosis, bipolar
disorder, severe depression
Assess readiness for weight loss (RD/NP/MD)
o Is client ready?
 If not, discuss prevention of further weight gain; reevaluate readiness
at future visits
Discuss treatment options (RD/NP/MD)
Implement weight loss protocol – Goal is to lose 5-10% body weight
o Individualized lifestyle changes including sleep recommendations
(RD/NP/MD)
o 500 calorie deficit below calculated need to result in one pound weight
loss/week
 Personalized meal plan (RD)
 Self-management training (RD/NP/MD)
 Exercise prescription (NP/MD)
 Reinforce physical activity (RD/NP/MD)
When goal weight is achieved, implement weight maintenance protocol
 Personalized meal plan (RD)
 Self-management training (RD/NP/MD)
57 | P a g e

 Exercise prescription (NP/MD) {See below}
When goal weight is NOT achieved, discuss possible adjunctive therapy (NP/MD)
o Pharmacotherapy (BMI > 27 with high health risk and no contraindications)
 Medical surveillance required (NP/MD)
 Personalized meal plan and lifestyle change (RD)
o Bariatric surgery (BMP > 30 with comorbidities)
 Medical surveillance required (NP/MD)
 Preoperative lifestyle change (NP/MD)
 Postoperative personalized meal plan and lifestyle change (RD)
Guidelines for activity prescription:
Source: Mcinnis, KJ, Franklin, BA, & Rippe, JM. (March 15, 2003). Counseling for physical activity in overweight and obese
patients. American Family Physician, 67(6), 1249-1256.
Frequency
Intensity
Time
Type of
exercise
The FITT Principle
3-5 days/week. More frequent exercise is desirable, but care should be taken to first
establish a regular exercise habit before recommending levels that may not be sustainable
in the long term
To avoid musculoskeletal injuries and promote compliance, start at a low to moderate
intensity and gradually progress over the course of several weeks or months to more
vigorous efforts (if desired by the patient)
30-60 minutes, using a gradual progression
Multiple short bouts produce similar benefits as a single long bout of the same total
duration
Low-impact activities (e.g., walking, cycling, low-impact aerobics, water exercise) that
are convenient, accessible, and perceived as enjoyable by the participant
Also: American Society of Bariatric Physicians (ASBP) Obesity Algorithm: Adult
Adiposity Evaluation and Treatment 2013 available at:
http://www.asbp.org/images/ADV-COPY_ASBPObeistyAlgorithmOctober2013.pdf


Overall management goals
o Improve patient health
o Improve quality of life
o Improve body weight and body composition
5 A’s of Obesity Management
o Ask
 Ask for permission to discuss body weight
 Explore readiness for change
o Assess
 Assess body mass index, waist circumference, and obesity stage
 Explore drivers and complications of excess weight
o Advise
 Advise the patient about the health risks of obesity, the benefits of
modest weight loss, the need for a long-term strategy, and
treatment options
o Agree
 Agree on realistic weight-loss expectations, targets, behavioral
changes, and specific details of the treatment plan
58 | P a g e
o Arrange/Assist
 Assist in identifying and addressing barriers
 Provide resources
 Assist in finding and consulting with appropriate providers
 Arrange regular follow-up
************** Case Study #13 **************
***Additional case studies to be discussed in class as time permits***