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ANCC - Fitzgerald Notecards > Gastrointestinal System > Flashcards

Gastrointestinal System Flashcards

1
Q

Acute Appendicitis: Overview of clinical presentation, physical findings, and immediate treatment/referral

A
  • young adult c/o acute onset of periumbilical pain, steadily getting worse
  • Over 12-24 hrs → pain starts to localize at McBurney’s point
  • pt has no appetite (anorexia)

PE:
- low-grade fever
- RLQ pain (McBurney’s point) w/ rebound and guarding
- psoas and obturator signs are positive
- when appendix ruptures, clinical signs of acute abdomen (involuntary guarding, rebound, and boardlike abdomen)

REFER TO ED!

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2
Q

Acute Cholecystitis: Overview of clinical presentation, physical findings, and immediate treatment/referral

A
  • Overweight female c/o severe RUQ or epigastric pain, occurring within 1 hour (or more) after eating a fatty meal
  • Pain may radiate to R shoulder
  • Accompanied by N/V and anorexia

If left untreated → gangrene of gallbladder (20%)

May require hospitalization!

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3
Q

Acute Diverticulitis: Overview of clinical presentation, physical findings, and immediate treatment/referral

A
  • Elderly pt w/ acute onset of high fever
  • anorexia
  • N/V
  • LLQ abdominal pain

RF:
- ↑ age
- constipation
- low dietary fiber intake
- obesity
- lack of exercise
- frequent NSAID use

Signs of acute abdomen:
- Rebound
- positive Rovsing’s sign
- boardlike abdomen

Lab
- CBC → leukocytosis w/ neutrophilia w/ left shift (presence of band signals severe bacterial infection; bands are immature neutrophils)

Complications
- abscess
- sepsis
- ileus
- small-bowel obstruction
- hemorrhage
- perforation
- fistula
- phlegmon stricture

MAY BE LIFE-THREATENING!

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4
Q

Acute Pancreatitis: Overview of clinical presentation, physical findings, and immediate treatment/referral

A
  • Adult pt c/o acute onset of fever
  • N/V
  • associated w/ rapid onset of abdominal pain, radiating to midback (“boring”) located in epigastric region

Frequent causes:
- drugs (approx 90% of cases)
- biliary factors
- alcohol abuse

PE:
- guarding & tenderness over epigastric area or upper abdomen
- positive Cullen’s sign
- positive Grey Turner’s sign
- may have ileus
- may show s/s of shock

*** Classic pain of acute pancreatitis is severe midepigastric pain that radiates to midback

REFER to ED!

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5
Q

Cullen’s Sign

A

blue discoloration around umbilicus

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6
Q

Grey Turner’s sign

A

blue discoloration on the flanks

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7
Q

Clostridium Difficile (C. Diff) Colitis: Overview of clinical presentation, physical findings, and immediate treatment/referral

A
  • Severe watery diarrhea from 10-15 stools/day
  • accompanied by lower abdominal pain w/ cramping and fever
  • Sx usually appear within 5-10 days after initiation of antibiotics (e.g., clindamycin [Cleocin], fluoroquinolones, cephalosporins, penicillins) ← implicated as most likely causes of C. diff infection

Most cases occur in pts in hospitals + those in nursing homes

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8
Q

Colon Cancer: Overview of clinical presentation, physical findings, and immediate treatment/referral

A
  • Very gradual (years) w/ vague GI symptoms
  • Tumor may bleed intermittently
  • may have iron-deficiency anemia
  • Changes in bowel habits, stool, or blood stool
  • Heme-positive stool
  • dark, tarry stool
  • mass on abdominal palpation

Etiology/RF
- Males
- older pts (> 50 years)
- hx of multiple polyps or IBD (Crohn’s or UC)
- postmenopausal w/ iron-deficiency anemia
- African American have highest incidence of colon CA in US
- USPSTF recommends screening for colon CA between ages of 50-75

Refer to GI for colonoscopy and endoscopy

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9
Q

Crohn’s Disease: Overview of clinical presentation, physical findings, and immediate treatment/referral

A
  • an IBD that may affect any part(s) of the GI tract (from mouth [canker sores]), small intestine, rectum, and anus
  • If ileum is involved → watery diarrhea w/out blood or mucus
  • if colon → bloody diarrhea w/ mucus
  • During relapse → fever, anorexia, weight loss, dehydration, and fatigue w/ periumbilical to RLQ abdominal pain occur
  • Fistula formation and anal ds occur only with CD (NOT UC)
  • May palpate tender abdominal mass
  • Remission and relapses are common
  • Higher risk of toxic megacolon and colon CA
  • Risk of lymphoma also ↑, esp for pts treated w/ azathioprine
  • More common in Ashkenazi Jews
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10
Q

Ulcerative Colitis (UC): Overview of clinical presentation, physical findings, and immediate treatment/referral

A
  • IBD that affects the colon/rectum
  • bloody diarrhea w/ mucus (hematochezia) more common in UC than w/ CD
  • Severe “squeezing” cramping pain, located on L side of abdomen w/ bloating and gas
  • exacerbated by food
  • relapses characterized by fever, anorexia, weight loss, and fatigue
  • accompanied by arthralgias and arthritis (15-40%)
  • affect large joints, sacrum, and ankylosing spondylitis
  • may have iron-deficiency anemia or anemia of chronic ds
  • has remissions and relapses
  • ↑ risk of colon CA
  • Risk of toxic megacolon
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11
Q

Zoolinger-Ellison Syndrome

A

A gastrinoma located on the pancreas or stomach
- secretes gastrin, which stimulates high levels of acid production in stomach
- end result → multiple and severe ulcers in stomach and duodenum
- C/o epigastric to midabdominal pain
- stools may be a tarry color
- screening by serum fasting gastrin level
- Refer to GI

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12
Q

Normal Findings: Route of food or drunk from the mouth (to the anus)

A

Esophagus → stomach (hydrochloric acid, intrinsic factor) → duodenum (bile, amylase, lipase) → Jejunum → ileum → cecum → ascending colon → transverse colon → descending colon → sigmoid colon → rectum → anus

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13
Q

Normal Findings: Abdominal Contents in the following:
1. RUQ
2. LUQ
3. RLQ
4. LLQ
5. Suprapubic area

A
  1. Liver, gallbladder, ascending colon, Kidney (right), pancreas (small portion); right kidney is lower than left because of liver displacement
  2. stomach, pancreas, descending color, kidney (left)
  3. Appendix, ileum, cecum, ovary (right)
  4. Sigmoid color, ovary (left)
  5. Bladder, uterus, rectum
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14
Q

Abdominal Maneuvers (Acute Abdomen or Peritonitis): Psoas/Iliopsoas

A

POSITIVE finding if RLQ abdominal pain occurs during maneuver

  • Indicates irritation to iliopsoas group of hyp flexors in abdomen.
  • Positive finding → peritoneal irritation
  • With pt in supine position, have pt raise R leg against pressure of professional’s hand resistance
  • With pt on left side, extend right leg from the hip

** Psoas and obturator signs are positive for acute appendicitis

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15
Q

Abdominal Maneuvers (Acute Abdomen or Peritonitis): Obturator Sign

A

Supine position

POSITIVE if inward rotation of the hip causes RLQ abdominal pain
- Rotate R hip through full ROM
- POSITIVE sign is pain w/ movement or flexion of hip

** Psoas and obturator signs are positive for acute appendicitis

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16
Q

Abdominal Maneuvers (Acute Abdomen or Peritonitis): Rovsing’s Sign

A

Supine Position

Deep palpation of LLQ of the abdomen results in referred pain to the RLQ, which is a POSITIVE Rovsign’s sigh
- A sign of peritonitis
- R/O acute or surgical abdomen

** Rovsign’s and Markle maneuvers → Positive tests = acute abdomen

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17
Q

Abdominal Maneuvers (Acute Abdomen or Peritonitis): McBurney’s Point

A

Area located b/t superior iliac crest and umbilicus in RLQ
- Tenderness or pain is a sign of possible acute appendicitis

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18
Q

Abdominal Maneuvers (Acute Abdomen or Peritonitis): Markle Test

A

Heel Jar

Instruct pt to raise heels and then drop them suddenly
- An alternative is to ask pt to jump in place

POSITIVE if pain is elicited or if pt refuses to perform because of pain

** Rovsign’s and Markle maneuvers → Positive tests = acute abdomen

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19
Q

Abdominal Maneuvers (Acute Abdomen or Peritonitis): Involuntary Guarding

A

With abdominal palpation, the abdominal muscles reflexively become tense or boardlike.
- Suspect acute or surgical abdomen.
- REFER TO ED!

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20
Q

Abdominal Maneuvers (Acute Abdomen or Peritonitis): Rebound Tenderness

A

Pt c/o worsening abdominal pain when hand is released after palpation of abdomen compared w/ pain felt during deep palpation
- Suspect acute or surgical abdomen
- Refer to ED!

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21
Q

Abdominal Maneuvers (Acute Abdomen or Peritonitis): Murphy’s Maneuver

A

Press deeply on RUQ under the coastal border during inspiration
- Midinsspiraotry arrest is a POSITIVE finding (Murphy’s sign)
- Positive w/ cholecystitis or gallbladder disease

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22
Q

Abdominal Maneuvers (Acute Abdomen or Peritonitis): Carnett’s Test

A

An abdominal maneuver, used to determine of abdominal pain is from inside the abdomen or if it is located on abdominal wall

  • Pt is supine w/ arms crossed over their chest
  • Instruct pt to lift up shoulders from table so the abdominal muscles (rectus abdominus) tightens
  • If source of pain is the abdominal wall, it will ↑ pain; if source is inside abdomen, the pain will improve
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23
Q

Gastroesophageal Reflux Disease
1. Definition/Etiology
2. Clinical Presentation
3. Lab/Diagnostics
4. Treatment (first-line nonpharms)
5. Complications

A
  1. Acidic gastric contents regurgitate from stomach into esophagus d/t inappropriate relaxation of the lower esophageal sphincter
    - 40% of US adults have GERD
    - Chronic GERD causes damage to squamous epithelium of lower esophagus
    - In ~10%, chronic GERD → Barrett’s esophagus (a precancer) → ↑ risk of squamous cell cancer (cancer of esophagus)

RF:
- chronic use of NSAIDs, aspirin, or alcohol

    • middle-aged to older adult
      - chronic heartburn of many years’ duration
      - s/s associated w/ large and/or fatty meals
      - worsen when supine
      - long-term hx of self-medication w/ OTC antacids and H2 antagonists

PE:
- acidic or sour odor to breath
reflux of sour acidic stomach contents, esp w/ overeating
- thinning tooth enamel (rear molars) d/t/ ↑ hydrochloric acid
- chronic sore red throat (not associated w/ cold)
- chronic coughing

  1. Clinical diagnosis (hx and clinical sx)
    GOLD STANDARD: Upper endoscopy/Biopsy
    • FIRST-LINE (mild/intermittent GERD): life style changes
      - Avoid large and/or high-fat meals, esp 3-4 hours before bedtime
      - avoid foods or meds that relax lower esophageal sphincter or foods or meeds that irritate esophagus
      - Weight reduction if overweight (BMI >25) or obese
      - Smoking cessation; smoking ↑ stomach acid and ↓ esophageal sphincter pressure
      - combine lifestyle changes with antacids (mild GERD) taken after each meal and HS
      - If poor response → prescribe meds and continue w/ lifestyle changes
    • Barrett’s esophagus (a precancer for esophageal cancer) → Dx w/ upper endoscopy w/ biopsy
      - Esophageal cancer
      - Esophageal stricture/scarring

If worrisome sx in GERD (e.g., odynophagia [pain w/ swallowing], dysphagia [difficulty swallowing
], early satiety, weight loss, iron-deficiency anemia [blood loss], weight loss, or male >50 years) → Refer to GI

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24
Q

Foods and Medications that can worsen GERD symptoms

A

Foods:
- Peppermint- or mint-flavored gum or candy
- Chocolate
- Caffeine
- Alcoholic drinks
- Carbonated beverages
- Tomato sauce
- Citrus drinks (e.g., orange juice)
- fatty foods

Meds:
- CCB
- NSAIDs
- Nitrates
- Alpha-adrenergic receptor agonists
- Anticholinergics
-Iron supplements
- Bisphosphonates
- Quinidine
- Theophylline

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25
Q

GERD Medications

A

First line (mild-to-mod sx or mild esophagitis): H2 antagonists
- Taken at bedtime
- Ranitidine (Zantac) 300 mg HS
- Nizatidine (Axid) 300 mg HS
- famotidine 40 mg HS

Proton-pump inhibitors (PPIs): For erosive esophagitis → Refer to GI
- Omeprazole (Prilosec) 20 mg once daily
- esomeprazole (Nexium) 40 mg once daily
- lansoprazole (Prevacid) 30 mg once daily
- pantoprazole (Protonix) 40 mg once daily

  • Dose PPIs 30-60 mins before meals
  • Long-term use of PPIs associated w/ ↑ risk of osteoporosis and bone/hip fractures in postmenopausal women (interferes w/ calcium homeostasis); acute interstitial nephritis, hypomagnesemia, C. diff infection, ↓ iron absorption
  • Do not d/c PPIs abruptly d/t rebound sx (worsens symptoms); tape dose to wean

Antacids (mild symptoms):
- Aluminum-magnesium-simethicone (Myylanta, Maalox)
- calcium carbonate (tums, caltrate)
- aluminum-magnesium (Gaviscon)
- minerals can bind w/ certain meds such as tetracycline and levothyroxine (Synthroid)

If no relief after 4-8 wks, if pt is at high risk for Barrett’s esophagus (long-term GERD, white male >50 years), or experiencing worrisome sx → Refer to GI for upper endoscopy/biopsy (GOLD STANDARD)

** Start w/ H2 antagonists; if poor relief or erosive esophagitis → step up to PPIs

** For mild cases of GERD → lifestyle management and antacids or H2 antagonists
- For mod-severe esophagitis → First-line: PPIs

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26
Q

Odynophagia

A

Pain w/ swallowing

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27
Q

Barrett’s Esophagus: Important considerations

A
  • Chronic heartburn should be referred to a GI for an endoscopy to r/o Barrett’s esophagus
  • Ptt w/ Barrett’s esophagus have 30x higher risk of ca of the esophagus (adenocarcinoma type)
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28
Q

Acute Gastroenteritis:
1. Definition/Etiology
2. Clinical Presentation

A

1 & 2: Main sx: diarrhea

Most common pathogens:
- viruses (50-70%)
- bacteria (15-20%)
- protozoans (10-15%)

29
Q

Diarrhea (definition)
- Acute
- Persistent
- Chronic

A

loose, watery stool, ≥ 3 times/day

Acute diarrhea → lasts 1-2 days
Persistent diarrhea → 2-4 weeks
Chronic diarrhea → ≥4 weeks

30
Q

Acute Gastroenteritis: Viral Gastroenteritis
- Clinical presentation

A
  • Acute onset of N/V
  • accompanied by watery diarrhea, not bloody
  • self-limited and short duration, lasting 1-3 days

Most common viral pathogens:
- rotavirus
- noroviruses → can cause outbreaks in crowded areas (e.g., nursing homes and cruise ships)

31
Q

Acute Gastroenteritis: Bacterial Gastroenteritis
- Clinical presentation

A
  • Acute onset of high fever
  • bloody diarrhea
  • severe abdominal pain
  • at least x stools in 24-hours
  • incubation period ranges from 1-6 hrs d/t contaminated food (enterotoxin) or 1-3 days if bacterial infection
  • sx may resolve in 1-7 days

Antibiotics can prolong length and/or severity of disease

Bacterial Pathogens:
- Escherichia coli
- Salmonella
- Shigella
- Campylobacter
- C. diff (antibiotic use, recent hospitalization)
- Listeria (pregnant women 12x risk)

32
Q

Acute Gastroenteritis: Protozoal Gastroenteritis
1. Clinical Presentation
2. Risk Factors
3. Preventative measures

A
    • Sx develop within 7 days of exposure and typically last ≥ 7 days
      - usually watery diarrhea
      - Traveler’s diarrhea starts w/in 3-7 days after exposure
      - usually resolves in 5-7 days
      - usually self-limited

Protozoal pathogens:
- Giardia lamblia
- Entamoeba histolytica
- Cryptosporidium

    • Travel to developing countries
      - Recent antibiotic use
      - Immunocompromised state
      - Daycare or resides in a crowded setting (e.g., nursing homes, institutions)
    • Drink bottled water during foreign travel; avoid ice cubes
      - food and water precautions when traveling in third-world countries
      - Wash hands frequently
      - Careful food preparation, such as washing vegetables and fruits
      - Rotavirus vaccine (infants)
33
Q

Irritable Bowel Syndrome
1. Definition/Etiology
2. Clinical Presentation
3. Lab/Diagnostics
4. Treatment (nonpharm, see other cards for pharm)

A
  1. Chronic functional disorder of the colon (normal colonic tissue) marked by exacerbations and remissions (spontaneous)
    - commonly exacerbated by excess stress
    - may be classified as diarrhea-predominant or constipation-predominant
    - in some cases, may alternate b/t the two
    • young adult to middle-aged female c/o intermittent episodes of mod-to-severe cramping pain in lower abdomen, esp in LLQ
      - bloating w/ flatulence
      - relief after defecation
      - stools range from diarrhea to constipation or both types w/ ↑ frequency of bowel movements

PE:
- a complete physical exam should be performed to exclude other causes
- VS are typically normal
- Abdominal exam: tenderness in lower quadrants during an exacerbation; otherwise exam is normal
- Rectal exam: stool is normal w/ no blood or pus
- Stools are heme negative

  1. Clinical Presentation
    - Colonoscopy/Endoscopy
    • ↑ dietary fiber; supple w/ psyllium (Metamucil or Konsyl), methylcellulose (Citrucel), wheat dextrin (Benefiber); start at low dose (causes gas)
      - AVOID gas-producing foods
      - ↓ life stress; address anxiety/stress w/ pt an doffer treatment strategies
      - R/O: amoebic, parasitic, or bacterial infections; inflammatory ds of GI tract
      - Check stool for ova and parasites (esp. diarrheal stools) w/ culture

*** Do not give antidiarrheal meds if pt has acute onset of bloody diarrhea, fever, abdominal pain, pr pain what worsens w/ defecation because it may be caused by E. coli O157:H7, Shiga toxin-producing E. coli (STEC), amebiasis, Salmonella, Shigella, or other pathogens → May need to go to ED!

34
Q

Antispasmodics for abdominal pain

A

administer dicyclomine (Bentyle) or hyoscyamine PRN

35
Q

Treatment: IBS w/ constipation

A

Begin w/ a trial of fiber supplements, polyethylene glycol (osmotic laxative)

36
Q

Treatment: IBS w/ severe constipation

A

Prescribe lubiprostone or linaclotide (contraindicated in pediatric pt <6 years; has caused death from dehydration)

37
Q

Treatment: IBS w/ diarrhea

A

take loperamide (Imodium) before regularly scheduled meals

38
Q

Treatment: Severe diarrhea-predominant IBS

A

Administer alosetron (warning: ischemic colitis, which can be fatal)

39
Q

Peptic Ulcer Disease
Gastric Ulcer and Duodenal Ulcer Disease
1. Definition/Etiologyy
2. Clinical Presentation

A
    • Duodenal ulcers → more common than gastric ulcers
      - Most pts (up to 70%) are asymptomatic
      - Gastric ulcers have ↑ risk for malignancy )up to 10%) compared w/ duodenal ulcers (benign)
      - Common cause: Helicobacter pylori for both ulcers
      - Most causes occur b/t 25-64 years
      - Recurrence rate for untreated PUD ~60%

Etiology
- Most common cause: H. pylori (Gram-) infection
- Chronic NSAID and aspirin use → disrupts prostaglandin production → ↓ GI blood flow w/ ↓ of protective mucus layer + inhibits cyclooxygenase (COX 1 and COX 2) enzyme, which ↓ prostaglandin production
- Cigarette smoking and/or alcohol use
- Drug-induced PUD can result from bisphosphonates, clopidogrel, anticoagulants, potassium supplements, corticosteroids, chemotherapeutic drugs, illicit drugs (crack cocaine)

*** Worrisome sx for esophageal cancer: early satiety, anorexia, anemia (bleeding), recurrent vomiting, hematemesis, weight loss

    • recurrent epigastric pain
      - burning/gnawing pain or ache (80%)
      - pain relieved by food and/or antacids (50%) w/ recurrence shortly after meals (gastric ulcer) and 2-4 hrs after a meal (duodenal ulcer)
      - pain also recurs when hungry or stomach is empty
      - self-medicating w/ OTC antacid, H2 blocker, and/or PPI
      - May be taking NSAIDs or aspirin for chronic pain or prophylaxis against heart ds or stroke
      - Black or tarry stools (melena)
      - red/maroon blood in stool (hematochezia)
      - coffee-ground emesis
      - iron-deficiency anemia indicates GI bleeding
      - If signs of shock (hemorrhage) w/ boardlike abdomen and rebound tenderness → Call 911!

PE:
- Abdominal exam: normal or mildly tender epigastric area during flare-ups
- Hemoccult: can be positive if actively bleeding

40
Q

Worrisome sx for esophageal cancer

A
  • early satiety
  • anorexia
  • anemia (bleeding)
  • recurrent vomiting
  • hematemesis
  • weight loss
41
Q

Peptic Ulcer Disease
Gastric Ulcer and Duodenal Ulcer Disease
3. Labs/Diagnostics

A
    • CBC (iron-deficiency anemia = bleeding)
  • Fecal occult blood test (FOBT) are needed (can be negative if no active bleeding)
  • all pt diagnosed with PUD should be tested for H. pylori infection
  • Urea breath test → indicative of active H. pylori infection; commonly used to document eradication of H. pylori after treatment. Use of PPIs within 2 wks of test can interfere w/ results
  • Stool antigen → can be used to confirm infection and posttreatment to document eradication; urea breath test and stool/fecal antigen test are more sensitive for active infection than serology/titers
  • Serology (Titers): H. pylori immunoglobin (IgG) levels ↑; presence of antibodies does not necessarily indicate current infection. H. pylori antibodies can be elevated for months to years
  • GOLD STANDARD: Upper endoscopy and biopsy of gastric and/or duodenal tissue
  • Multiple severe ulcers or unresponsive to treatment: Use fasting gastrin levels to r/o Zollinger-Ellison syndrome PRN
  • Gastric ulcers: requires an endoscopy to r/o gastric cancer and document healing of ulcers
42
Q

Peptic Ulcer Disease
Gastric Ulcer and Duodenal Ulcer Disease
4. Treatment: H. pylori negative ulcers

A

H. pylori Negative Ulcers
- Stop NSAID use; if pt needs long-term NSAIDs, ulcer formation risk can be ↓ if combined w/ PPI or misoprostol
- Encourage smoking cessation and stop alcohol use
- Combine lifestyle changes with PPIs or H2 antagonists (no antibiotics); duration of therapy is from 4-8 weeks; if recurrent ulcers, poor response after 4-8 weeks, or suspect bleeding ulcer → Refer to GI

H2 Antagonists:
- Ranitidine (Zantac) 150 mg BID or 300 mg HS
- Nizatidine (Axid) 150 mg BID or 300 mg HS
- Famotidine (Pepcid) 40 mg HS

PPIs
- Omeprazole (Prilosec) 20 mg daily
- Esomeprazole (Nexium) 40 mg daily
- Lansoprazole (Prevacid) 15-30 mg daily

43
Q

Peptic Ulcer Disease
Gastric Ulcer and Duodenal Ulcer Disease
4. Treatment: H. pylori positive ulcers

A

H. pylori Positive Ulcers
* Requires antibiotics for 14 days + PPI PO BID

Triple Therapy:
- Clarithromycin (Biaxin) 500 mg BID + Amoxicillin 1 g BID or metronidazole (Flagyl) 500 mg BID if allergic to amoxicillin x 14 days + standard-dose PPI PO BID x 14 days

Quadruple therapy
- Bismuth subsalicylate tab 600 mg QID +
- Metronidazole tab250 mg QID +
- Tetracycline cap 500 mg QID x 2 weeks +
- Standard-dose PPI PO BID x 14 days

** Sequential therapy, salvage therapy, and other tx regimens for H. pylori are available for clinical use but not necessary for exam

** If high resistance of clarithromycin in your area, avoid using; eradication rates in US using traditional triple therapy <80%

** PPIs cure ulcers faster than H2 antagonists

44
Q

Acute Diverticulitis
1. Definition/Etiology (What is a diverticula?)
2. Clinical Presentation (what is acute abdomen s/s?)
3. Lab/Diagnostics

A
    • Diverticula are small pouch-like herniations on external surface of colon 2º to chronic lack of dietary fiber
      - higher incidence in Western societies
      - up to 50% of Americans ≥ 60 years have diverticula in colon
      - Majority of cases, left colon (descending colon and sigmoid) is involved
      - Diverticulitis occurs when diverticula become infected → high risk of rupture and bleeding, can be life-threatening
      - HOSPITALIZE → Mod-severe cases, dehydration, elderly, s/s of acute abdomen, high fever, comorbidities, or immunocompromised
    • elderly or older adult w/ LLQ abdominal pain
      - constant and has been present for several days
      - i bowel obstruction, may have N/V or ileus d/t peritonitis
      - Abdominal palpation → tenderness in LLQ
      - ~50% of pt have had one or more prior episodes of similar pain
      - reports hx of change in bowel habits; up to 50% will have constipation; some will have diarrhea

PE:
- Acute diverticulitis: If acute abdomen → positive fore rebound, positive Robsign’s sign, and boardlike abdomen → Refer to ED
- Diverticulosis: Physical exam is normal; no palpable mass; no tenderness; diverticula can be visualized only by colonoscopy

    • CBC w/ leukocytosis, neutrophilia >70%; left shift (band forms)
      - presence of band forms signals severe bacterial infection; bands are immature neutrophils → Refer to ED
      - FOBT positive if bleeding
      - Reticulocytosis if acute bleeding and ↓ hgb/hct
45
Q

Acute Diverticulitis
4. Treatment (uncomplicated vs complication; chronic and follow-up)
5. Complications

A

Uncomplicated mild cases: can be treated outpt
- Clear liquid diet + antibiotics should show improvement in 48-72 hrs
► Amoxicillin-clavulanate 875/125 mg PO BID or ciprofloxacin 750 mg BID + metronidazole (Flagyl) 500 mg Q6H; duration based on clinical response; usually treat for 7-10 days
- Opiates should be avoided during acute phase since they ↑ intraluminal pressure and promote an ileus
- ↑ fiber intake is not recommended in acute management of diverticulitis
- Probiotics have been used to prevent recurrences w/ mixed success

Close follow-up → if no response in 48-72 hrs or sx worsens (high fever, toxic) → Refer to ED; mod-severe cases → hospitalize
** Can be life-threatening if abscess ruptures → peritonitis, bacteremia, and septic shock

Chronic Therapy for Diverticulosis
- High-fiber diet w/ fiber supplementation such as psyllium (Metamucil) or methylcellulose (Citrucel)
- Avoidance of nuts, seeds, and popcorn is not evidence-based

    • Abscess, perforation w/ peritonitis and bleeding
      - Ileus, sepsis, death
46
Q

Acute Pancreatitis
1. Definition/Etiology
2. Clinical Presentation
3. Lab/Diagnostics
4. Treatment
5. Complications

A
    • Acute inflammation of pancreas 2º to many factors, such as alcohol abuse, gallstones (cholelithiasis), ↑ triglyceride, infections
      - Pancreatic enzymes become activated inside pancreas → autodigestion
      - Varies in severity from mild to life-threatening/death
      - Gallstones (includes microlithiasis) are responsible for 40-70% of cases; 25-35% caused by alcohol
      - ↑ triglycerides (>800 mg/dL) at very high risk for acute pancreatitis
    • acute onset of fever, N/V
      - associated w/ rapid onset of abdominal pain
      - radiates to midback
      - located in epigastric region
      - Abdominal exam reveals guarding and tenderness over epigastric area or upper abdomen
      - positive Cullen’s and Grey Turner’s sign
      - may have ileus and s/s of shock

PE:
- Cullen’s sign: bluish discoloration around umbilicus (hemorrhagic pancreatitis)
- Grey Turner’s sign: bluish discoloration on flank area (hemorrhagic pancreatitis)
- Hypoactive bowel sounds (ileus), jaundice, guarding, and boardlike upper abdomen if peritonitis

    • ↑ pancreatic enzymes (serum amylase, lipase, and trypsin)
      - ↑ AST, ALT, gamma glutamyl transferase (GGT), bilirubin, leukocytosis
      - Abdominal US and CT
      ** Amylase and lipase are sensitive tests used for pancreatic inflammation (pancreatitis)
  2. Refer to ED!
    • Serious complications such as ileus, sepsis, shock, multiorgan failure, death
      - Diabetes
47
Q

Clostridium Difficile-Associated Diarrhea
1. Definition/Etiology
2. Clinical Presentation
3. Lab/Diagnostics

A
  1. C. diff is a gram+, spore-forming anaerobic bacillus → releases toxins that produce clinical disease
    - Most cases occur in hospitalized pts
    - may also occur in institutionalized pts (nursing facilities)
    - spread: fecal-oral contact
    - C. diff colities: high recurrence rate (25%)
    - Ask about previous episodes

RF:
- Prior or current systemic antibiotic therapy
- Advanced age
- Hospitalization
- CA chemotherapy

    • classic sx: watery diarrhea a few days after antibiotic treatment d/t changes in intestinal flora (e.g., clindamycin [Cleocin], fluoroquinolones, cephalosporins, and PCN)
      - currently on abx or recently completed a course of abx
      - hx of hospitalization
      - acute onset of diarrhea w/ lower abdominal cramping and pain
      - anorexia
      - nausea
      - low-grade fever
    • Nucleic acid amplification testing (NAAT) for C. diff of a single stool sample
      - CBC w/ leukocytosis (>15,000 cells/uL)
      - metabolic profile + electrolytes
      - serum creatinine + serum BUN
      - Stool assay (by enzyme-linked immunosorbent assay) for C. diff toxins
      - Repeat stool testing for test of cure is not recommended. C. diff toxin may persist despite clinical response to treatment. Testing ant x of asymptomatic pt is not recommended
48
Q

Clostridium Difficile-Associated Diarrhea
4. Treatment
5. Complications

A
  1. Mild Disease Initial Episode Treatment
    - First line: vancomycin 125 mg PO QID x 10 days
    - Anticipate relapse in 20-25%; consider fecal microbiota transplant in recurrent disease
    - Avoid antimotility agents (loperamide) in pt w/ bloody diarrhea or antibiotic-associate colitis
    - mod evidence that probiotics are effective for those w/ intact immune systems
    - Rehydration (Naturalyte, Rehydralate), ↑ fluids, eat foods as tolerated
    - Early oral refeeding is encouraged, regular diet; restricted diets such as BRAT (bananas, rice, applesauce, toast) not necessary
    - Contact precautions!

*** Handwashing w/ soap and water is more effective again C. diff than alcohol-based hand wipes

49
Q

Viral Hepatitis: Hepatitis Serology
IgM Antibody Hepatitis A Virus (IgM Anti-HAV)

A
  • acute infection; pt is contagious
  • Hepatitis A virus still present (infectious); no immunity yet
  • Screening test for hepatitis A
50
Q

Viral Hepatitis: Hepatitis Serology
IgG Antibody Hepatitis A Virus (IgG Anti-HAV)

A
  • Presence means lifelong immunity
  • No virus present and pt is not infectious
  • Can remain detectable for decades
  • How: Hx of native hepatitis A infection or vaccination w/ hepatitis A vaccine (Havrix)
51
Q

Viral Hepatitis: Hepatitis Serology
Hepatitis B Surface Antigen (HBsAg)

A
  • Screening test for hepatitis B
  • If positive, pt has virus and is infectious
  • How: Presence of antigen means either an acute infection or chronic hepatitis B infection
52
Q

Viral Hepatitis: Hepatitis Serology
Hepatitis B Surface Antibody (Anti- HBs)

A
  • Antibodies present and pt is immune
  • Presence may be d/t either a past infection or vaccination w/ hepatitis B vaccine
53
Q

Viral Hepatitis: Hepatitis Serology
Hepatitis B “e” Antigen (HBeAg)

A
  • Marker for actively replicating hepatitis B virus; highly infectious
  • Persistence of the “e” antigen indicates chronic hepatitis
54
Q

Viral Hepatitis: Hepatitis Serology
Total Hepatitis B Core Antibody (Anti-HBc)

A
  • Appears at onset of symptoms in acute hepatitis B and persist for life
55
Q

Viral Hepatitis: Hepatitis Serology
Hepatitis C Virus Antibody (Anti-HCV)

A
  • Screening test for hepatitis C
  • Up to 85% of cases become carriers
  • Unlike Hep A and B, a positive anti-hepatitis C virus (HCV; antibody) does not always mean pt has recovered from infection and developed immunity; it may instead indicate current infection because up to 85% of cases become carriers

If test is positive:
- Order HCV RNA to r/o chronic infection
- If positive, then pt has hepatitic C → Refer to GI for liver biopsy/treatment

56
Q

Viral Hepatitis: Hepatitis Serology
Antibody Hepatitis D Virus and/or Hepatitis D Virus RNA (HDV RNA)

A
  • Hepatitis D tests by antibody hepatitis D virus (anti-HDV) or hepatitis D virus RNA test
  • Requires presence of hepatitis B to get infection
  • can be acute or chronic infection
  • Infection w/ both Hep B and Hep D ↑ risk of fulminant hepatitis, cirrhosis, and severe liver damage; low prevalence in US
  • Transmission by sex, sharing needles, birth to an infected mother, needle sticks, semen, saliva
  • Suspect HDV infection in any person w/ positive Hep B antigen (HBsAg) who has severe sx of hepatitis or acute exacerbations

** A person must have Hep B to become infected with Hep D; there is no vaccine for Hep D, but Hep B vaccination will prevent Hep D acquisition

57
Q

Liver Function Tests (LFTs)

A

AST, ALT, alkaline phosphatase, and bilirubin are biomarkers of hepatic injury

58
Q

Liver Function Tests (LFTs): Aspartate Aminotransferase (AST)

A
  • AKA serum glutamic oxaloacetic transaminase (SGOT)
  • Normal: 0-35 U/L
  • Present in liver heart muscle, skeletal muscle, kidney, and brain
  • ↑ in hepatitis, cirrhosis, nonalcoholic fatty liver disease, alcohol abuse, drugs (e.g., acetaminophen, statins), MI, mononucleosis
59
Q

Liver Function Tests (LFTs): Alanine Aminotransferase (ALT)

A
  • AKA serum glutamic pyruvic transaminase (SGPT)
  • Normal: Males: 10-40 U/L; Females: 8-35 U/L
  • Found mainly in liver; positive finding indicates liver inflammation
  • More specific for hepatocellular injury than AST
  • Rapid ↓ in AST and ALT levels together w/ ↑ of serum bilirubin and prolongation of PT

** ALT is more sensitive to liver damage than AST; AST is also found in other orangs such as heart and skeletal system
** AST and ALT may be ↑ and reflect acute liver injury or inflammation; however, these levels may be normal in chronic liver ds (cirrhosis)

60
Q

Liver Function Tests (LFTs): Aspartate Aminotransferase/Alanine Aminotransferase Ratio (AST:ALT ratio)

A

A ratio of 2.0 or higher may be indicative of alcohol abuse

61
Q

Liver Function Tests (LFTs): Gamma-Glutamyl Transferase (GGT)

A
  • Indicator of continuous heavy drinking for several weeks or longer (~70 drinks/week)
  • found in many organs of body but mainly on live,r kidneys, and pancreas
  • Can ↑ w/ medications (phenytoin, barbiturates), biliary disease, liver cancer, or metastases, pancreatitis
  • During alkaline phosphatase ↑, check GGT, and if elevated, source is liver

** GGT ↑ in liver disease and biliary obstruction
** A “lone” ↑ = sensitive indnicator of possible alcoholism

62
Q

Liver Function Tests (LFTs): Alkaline Phosphatase (ALP)

A
  • Enzyme derived from bone, liver, gallbladder, kidneys, GI tract, and placenta
  • Highest amounts come from bones and liver; during 3rd trimester of pregnancy, ↑ levels come from placenta
  • ALP vary with age; in gen, higher levels are seen during growth spurts (physiologic osteoblastic activity) in children and teens
  • ↑ in biliary obstruction, cholestasis, bone malignancy/metastasis, healing fractures

** Normally ↑ during teen years d/t bone growth. May also be ↑ in bone disorders such as vit D deficiency, Paget’s disease, and bone CA
** A GGT, which would be elevated with liver ds may be drawn to differentiate b/t liver disease and bone disorder

63
Q

Viral Hepatitis: Hepatitis A Virus (HAV)
1. Transmission
2. Clinical Presentation
3. Labs
4. Treatment

A

No chronic or carrier state exists for Hep A
- Self-limiting infection
* Reportable to public health department

    • Transmitted via fecal or oral route from contaminated food or drink, households, sex
    • Acute onset of fever
      - headache
      - malaise
      - anorexia
      - nausea
      - vomiting
      - diarrhea
      - abdominal pain
      - dark urine
      - jaundice
    • Bilirubin >3 mg/dL
      - ALT >200 IU/L
      - IgM anti-hepatitis A virus (HAV) or
      - NAAT/polymerase chain reaction (PCR) test for hep A virus RNA
  4. -Treatment is symptomatic
    - Vaccine available (Havrix); recommended for travelers to areas where Hep A is endemic
    - Advise pt to avoid drugs and foods that can damage liver, such as acetaminophen, alcohol/ethanol, statins, isoniazid, and herbal teas
    - Avoid working in food-related jobs for 1 wk after infection onset
64
Q

Viral Hepatitis: Hepatitis B Virus (HBV)
1. Transmission
2. Clinical Presentation
3. Labs
4. Treatment

A
    • Horizontal transmission via sexual activity (semen, vaginal secretions, and saliva), blood, blood products, organs; vertical transmission occurs from mother to infant
      - can be acute and self-limiting, or chronic infection

2 & 3.

    • Vaccination: 3 total doses given during infancy (at birth, 1 month, 6 months); adults require 3 doses
      - Acute Hep B → administer injection of Hep B immune globulin (HBIG) and give first dose of Hep B vaccine ASAP (if no previous hx of vaccination x 3 doses)
      - Refer chronic Hep B to GI
      First-line agents for chronic Hep B: Antiviral agents and pegylated interferon alfa (PEF-IFN-a)
65
Q

Viral Hepatitis: Hepatitis C Virus (HCV)
1. Transmission
2. Clinical Presentation
3. Labs
4. Treatment

A
    • sharing needles
      - blood transfusions before 1992
      - mother to infant (vertical transmission)
      - needle-stick injuries in healthcare settings
      - Less common: spread by sexual contact, sharing personal items (razors or toothbrushes)
      - ~75-85% of people will develop chronic infection
      - Disease is most common cause of liver CA and liver transplantation in US
      - Highest chronic hepatitis infection and cirrhosis (30%); Cirrhosis markedly ↑ risk of liver CA or failure **Hep C has highest risk of cirrhosis and liver CA
      → Refer to GI for management

High-risk Groups:
- IV drug users
- Hemophiliacs
- Anyone with hx of frequent transfusions
- persons born b/t 1945-1965
** USPSTF recommends routine one-time HCV screening for ALL adults 18-79 years

2 & 3.

  • Screening test for Hep C is called HCV antibody (anti-HCV); if positive, next step → HCV RNA test; if positive, pt has Hep C
    • Refer to GI! High effective oral antiviral regimens available; the vast majority of Hep C pts can be treated
      - Advise pt not to share razors, toothbrushes, and nail clippers and to cover cuts and sores
      - Report acute cases to health department
66
Q

Acute Hepatitis
1. Definition/Etiology
2. Clinical Presentation
3. Labs/Diagnostics
4. Treatment

A
  1. An acute liver inflammation w/ multiple causes, including viral infection, hepatoxic drugs (e.g., statins), excessive alcohol intake, meds, and toxins
    • new onset of fatigue
      - anorexia
      - nausea
      - malaise
      - dark-colored urine for several days
      - sclera jaundice (icteric)
      - skin is jaundice
      - may have clay-colored stools
      - may have RUQ abdominal pain

PE
- Skin and sclerae have a yellow tinge (jaundiced or icteric)
- Liver; Tenderness over liver occurs w/ percussion and deep palpation

    • ALT and AST: ↑ up to 10x normal during acute phase
      - Other LFTs: ↑ bilirubin and GGT
    • Remove and treat cause (if possible)
      - Avoid hepatotoxic agents (alcoholic drinks, acetaminophen, and statins [e.g., pravastatin (Pravachol)])
      - Treatment is supportive
      - Chronic Hep B and C → managed by GI
67
Q

Case Study: Patient A
- Hepatitis B surface antigen (HBsAg): Negative
- Anti-HBs: Positive
- Hepatitis B “e” antigen (HBeAg): Negative
- Results:

A
  • Results: indicative of either:
  • Immune to Hep B; presence of Hep B surface antibodies can be d/t hx of Hep B vaccination or recovered from native Hep B infection
  • Not a carrier of Hep B (HBeAg negative, HBsAg negative)
68
Q

Case Study: Patient B
- HBsAg: Positive
- HBeAg: Positive
- Anti-HBs: Negative
- Anti-HAV: Positive
- Anti-HCV: Negative
- Results

A
  • Results: indicative of either:
  • Current Hep B infection (HBsAg positive)
  • Chronic carrier of Hep B (both HBsAg and HBeAg are positive)
  • Presence of antibodies to Hep A (anti-HAV); pt either had a previous Hep A infection or received the Hep A vaccine (has immunity)
  • Pt is a carrier of Hep B virus; if HBeAg is positive and higher reactive → pt is contagious

*** There will be serology questions. You will have to figure out what type of viral hepatitis the patient has (A, B, or C); it is usually Hep B. HBs Ag-positive status always means an infected pt (new infection or chronic)

69
Q

Viral Hepatitis: PCRs

A

PCR tests are not antibody test
- test for presence of viral RNA
- Positive = virus is present
- can be performed for diagnosing ds such as Hep C or HIV

ANCC - Fitzgerald Notecards (27 decks)

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