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GI disorders Flashcards

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Family Nurse Practitioner (FNP) flashcards
1
Q

True/false: Anal fissures commonly present posteriorly

A

True - If fissure is off midline, transverse, or irregular consider alternative diagnosis

  • Consider alternative diagnosis if standard anal fissure therapy does not show improvement
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2
Q

Anal fissure treatment and management

A
  • Prevent constipation (most potent risk factor)
    • Increase dietary fluid and fiber intake (supplementation) + stool softener
      • Stool softeners → magnesium citrate, magnesium hydroxide (Mild of Magnesia), polyethylene glycol (MiraLAX)
    • Mineral oil
  • Sitz baths, cool compresses

If severe or does not respond to above treatment,

  • Intra-anal NTG or DHP CCB (nifedipine)
  • Botox
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3
Q

What type of hemorrhoids do the superior and inferior hemorrhoidal veins form (internal vs external)?

A

Superior → internal hemorrhoids

Inferior → external hemorrhoids

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4
Q

How are internal hemorrhoids graded (I to IV)?

A
  • Grade I - do not prolapse
  • Grade II - prolapse upon defecation but reduce spontaneously
  • Grade III - prolapse upon defecation and must be reduced manually
  • Grade IV - prolapsed and cannot be reduced manually
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5
Q

True/false: Reports of persistent bleeding, dark blood mixed with stool, or development of anemia r/t rectal bleeding warrants prompt referral to colonoscopy for evaluation for colorectal cancer

A

True

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6
Q

How can a patient manage chronically protruding or prolapsing hemorrhoids?

A

Manual reduction after evacuation

  • Will complain of itch, mucus leaking, staining of undergarments with streaks of stool
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7
Q

Hemorrhoids treatment and management

A

Prevention

  • Weight control, high fiber diet, fiber supplementation, regular aerobic exercise, increased fluid intake
    • 20-30 g fiber/day

Acute flare ups

  • Astringents and topical corticosteroids
  • Sitz baths
  • Analgesics
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8
Q

Acute appendicitis clinical presentation

A

Early signs → epigastric or periumbilical pain, shifts to RLQ in 12 hours, pain aggravated by walking/coughing

Late signs → N/V

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9
Q

Acute appendicitis physical examination

A
  • Rebound tenderness (indicates peritoneal irritation)
  • Positive psoas and obturator sign
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10
Q

Acute appendicitis diagnostic testing (labs)

A
  • Total WBC count (“left shift” indicates bacterial infection)
    • Leukocytosis → elevation in total WBC
    • Neutrophilia → elevation in neutrophils (ANC >7,000)
    • Bandemia → elevation in number of bands or young neutrophils
  • CRP
  • hCG to rule out ectopic pregnancy
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11
Q

Acute appendicitis diagnostic testing (imaging)

A
  • CT scan with contrast of abdomen → imaging of choice
  • Can consider US if concerned about radiation risk
    • Minimize radiation in children and women of reproductive age (can follow up with CT if needed)
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12
Q

Signs of appendices perforation

A
  • Marked leukocytosis with total WBC count >20,000-30,000
  • Fever >102 F
  • Peritoneal inflammation
  • Symptoms lasting longer than 48 hours
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13
Q

Risk factors for gallstone formation

A
  • 50+ years old
  • Female
  • Obesity
  • Hyperlipidemia
  • Rapid weight loss (including patients who have undergone bariatric surgery)
  • Pregnancy
  • Genetic factors
  • European or Native American ancestry
  • Chronic ingestion of a diet with high glycemic index
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14
Q

Cholelithiasis clinical presentation

A
  • Sudden onset pain 1 hour after eating a fatty meal
    • Pain episodes last 1-5 hours
  • RUQ or epigastrum
  • Radiates to tip of right scapula (Collin’s sign)
  • N/V (vomiting provides pain relief)
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15
Q

Cholecystitis clinical presentation

A

Results from acute inflammation of gallbladder (from gallstones)

  • RUQ or epigastric pain and tenderness to palpation (Murphy’s sign)
  • Vomiting
  • Occasional fever
  • Some degree of jaundice
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16
Q

Cholecystitis and cholelithiasis diagnostic testing

A
  • RUQ abdominal US (can be used during pregnancy)
  • HIDA scan more sensitive and specific at revealing obstructed cystic duct
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17
Q

What is the significance of ALT, AST, alkaline phosphatase (ALP), and GGT?

A

ALT → liver specific, elevated with hepatocellular damage (normal 0-31)

AST → found in liver, myocardium, skeletal muscle; elevated with hepatocellular damage (normal 0-31)

ALP → levels increase in response to biliary obstruction, intrahepatic or extra hepatic cholestasis (normal 0-125)

GGT → elevated noted in obstructive jaundice, hepatic metastasis, intrahepatic cholestasis (normal 0-45)

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18
Q

Acute cholecystitis treatment and management

A
  • Low fat diet of clear liquids
  • Analgesics
  • Antibiotics if evidence of infection
  • Consider cholecystectomy
    • If seriously ill and considered too high risk to undergo cholecystectomy, US guided gallbladder aspiration or percutaneous cholecystectomy
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19
Q

Colorectal cancer risk factors

A
  • History of IBD (ulcerative colitis or Crohn’s)
  • Personal history of neoplasia
  • 50+ years old
  • Family history
  • Familial polyposis syndrome
  • Diet high in fat, red meat, low in calcium
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20
Q

Colorectal cancer clinical presentation

A
  • Vague abdominal complaints
  • Iron deficiency anemia
  • Late signs → bowel obstruction (sudden onset vomiting, abdominal pain, distention)
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21
Q

Colorectal cancer screening recommendation and tests

A

Starting at age 45 or 50 years and continue until age 75 years while in good health (life expectancy >10 years)

  • Colonoscopy every 10 years
  • Flexible sigmoidoscopy every 5 years
  • Stool DNA test (cologuard) every 3 years
  • Fecal immunochemical test (FIT) every year
  • Guaiac fecal occult blood test (gFOBT) every year
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22
Q

Diverticulosis (symptomatic) clinical presentation

A
  • Mild left sided abdominal cramping
  • Increased flatus
  • Pattern of constipation alternating with diarrhea
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23
Q

Diverticulitis clinical presentation

A
  • Fever
  • Leukocytosis
  • Diarrhea
  • LLQ pain
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24
Q

Diverticular disease diagnostic testing

A

Usually an incidental finding after colonoscopy

  • Diverticulitis → abdominal CT w/ contrast (reveals bowel wall thickening)
    • Chest x-ray may reveal free air = perforation

NO barium enema should be administered or colonoscopy performed

  • Wait to perform colonoscopy 4-6 weeks after diverticulitis attack
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25
Q

Diverticulosis treatment and management

A
  • High fiber diet
  • Fiber supplements (bran, psyllium, methyl cellulose)
  • Regular aerobic exercise
  • Don’t necessarily need to make dietary changes
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26
Q

Diverticulitis treatment and management

A
  • Conservative management:
    • Liquid diet for gut rest
  • Antibiotics for severe and complicated cases
    • Metronidazole +
    • Ciprofloxacin or levofloxacin or TMP-SMX
      • Alternative → amoxicillin-clavulanate
    • If patient becomes worse or does not respond to therapy within 2-3 days, perform abdominal CT with surgical consultation
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27
Q

True/false: With recurrent diverticulitis episodes, surgical intervention with partial colectomy is an option to remove problematic portion of the intestines

A

True

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28
Q

What is peptic ulcer disease?

A

Includes loss of mucosal surface, extending to muscular mucosal, that is at least 5 mm in diameter

  • Imbalance between gastric protective mechanisms and irritating factors
    • Exposure to peptic juices (acid and pepsin)
  • Located in ares → duodenum, stomach, esophagus, small intestine
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29
Q

Risk factors for peptic ulcer disease

A
  • Alcohol abuse with cirrhosis
  • Frequent use of NSAIDs and corticosteroids
  • 60+ years old
  • History of PUD (especially gastric)
  • Previous of histamine1 receptor antagonist, PPIs, or antacids for treatment of GI symptoms
  • Smoking
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30
Q

Which type of peptic ulcer is more common - duodenal or gastric?

A

Duodenal

  • Risk factor: h. pylori infection
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31
Q

Peptic ulcer disease clinical presentation

  • Duodenal
A
  • Epigastric burning, gnawing pain 2-3 hours after meals
  • Relief with foods, antacids
  • Clusters of symptoms with periods of feeling well
  • Waking up at 1-2 am with symptoms common
  • Tender LUQ
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32
Q

Peptic ulcer disease (duodenal) diagnostic testing

A

If duodenal suspected → stool antigen test and/or breath testing to confirm h. pylori infection

  • Should NOT take PPI for 2 weeks before testing
  • Repeat stool antigen test >8 weeks posttreatment
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33
Q

Peptic ulcer disease (gastric) diagnostic testing

A
  • Upper GI endoscopy with biopsy → differentiate between ulcer and gastric malignancy
  • H. pylori testing
34
Q

Gastric peptic ulcer clinical presentation

A
  • Pain reported with or without meals
    • Pain worse with eating (lessens within 1 hour)
  • N/V, weight loss
35
Q

Treatment of h. pylori associated with duodenal/gastric ulcer

A

PPI + amoxicillin + metronidazole + clarithromycin x14 days

36
Q

Peptic ulcer disease treatment

A

NSAID induced duodenal ulcer and gastritis (not gastric ulcer) → H2RAs

  • Ranitidine (zantac)
  • Famotidine (pepcid)

PPIs - omeprazole (prilosec), esomeprazole (nexium)

  • Best taken on empty stomach, 30 minutes before breakfast
  • Associated with reduced absorption of iron, vitamin b12
  • Therapy should NOT extend past 8 weeks
  • Gradually taper or try every-other-day dosing to avoid rebound gastric hyperacidity
37
Q

GERD clinical presentation

A

Common → dyspepsia, chest pain at rest, postprandial fullness

Non-GI symptoms (especially with chronic disease) → hoarseness, sore throat, nocturnal cough, wheezing

38
Q

Behavioral modifications to prevent GERD symptoms

A
  • Remain upright and avoid supine position within 3 hours of a meal
  • Eat small meals
  • Eliminate occasions of overeating
  • Weight loss
  • Elevated HOB on 4” blocks
39
Q

If behavioral modifications do not help to improve GERD symptoms, what medication is considered next step?

A

Antacids - used for mild, intermittent GERD

  • Should be taken 1-3 hours after meals and at bedtime
  • Should be separated from other meds at least 2 hours apart
40
Q

If use of antacids and behavioral modifications can’t control mild, intermittent GERD, what is the next step medication?

A

HrRA at full prescription strength

  • If no improvement is seen in 6 weeks, longer term therapy with H2RA is unhelpful
41
Q

If H2RAs, antacids, and behavioral modifications don’t work against GERD, what is the next step medication?

A

PPI

  • If symptoms do not resolve after 8 week course, refer to GI w/ upper GI endoscopy
42
Q

PUD red flags that warrant immediate endoscopy and GI referral

A
  • Bleeding or anemia
  • Unexplained weight loss
  • Progressive dysphagia or odynophagia
  • Recurrent vomiting
  • Family history of GI cancer
43
Q

GERD red flags that warrant further evaluation

A
  • Dysphagia (difficulty swallowing)
  • Odynophagia (painful swallowing)
  • GI bleeding
  • Unexplained weight loss
  • Persistent chest pain
44
Q

Esophageal cancer clinical presentation

A
  • Early stages are usually asymptomatic
  • Late stage → epigastric or retrosternal pain, persistent hoarseness, cough
    • Iron deficiency anemia
    • Dysphagia
    • Weight loss
45
Q

Hepatitis clinical presentation

A

Over course of 2-3 weeks then will have return of energy, appetite, well being

  • Malaise
  • Myalgia
  • Fatigue
  • Nausea
  • Anorexia
  • Clay colored stool
  • Arthritis-like symptoms
  • Skin rash
  • Jaundice
46
Q

Hepatitis A disease markers (lab tests)

A

Active disease → HAV IgM, elevated hepatic enzymes (x10 upper limits)

Chronic disease → chronic hep A doesn’t exist

Past infection → anti-HAV

47
Q

Hepatitis B disease markers (lab tests)

A

Active disease → HBsAg, elevated hepatic enzyme (x10 upper limits)

Chronic disease → HBsAg, anti-HBC

48
Q

Hepatitis C disease markers (lab tests)

A

Active disease → anti-HCV, RNA detected, elevated hepatic enzymes

Chronic disease → anti-HCV, RNA detected, normal or slightly elevated hepatic enzymes

Past infection → Anti-HCV, no RNA

49
Q

Hepatitis A prevention

A
  • Heat food to higher than 185 degrees F (85 C) for 1 minute
  • Proper hand hygiene
  • Clean environmental surfaces with 1:100 bleach solution
  • Immunization
50
Q

Hepatitis A treatment

A

No treatment; body will clear virus

  • Rest, eat small snacks rather than large meals, eat high calorie foods
  • Avoid hepatotoxic medications (I.e. acetaminophen) and alcohol
51
Q

True/false: Hepatitis D can only occur in persons with acute or chronic hepatitis B

A

True - Hepatitis B and D acute co-infection has a course of illness similar to that of only acute hepatitis B

52
Q

Hepatitis B prevention

A
  • Limit exposure to blood and bodily fluids
  • 1:10 dilution of bleach to clean up blood spills
  • Condom use
  • Vaccination
  • After HBV exposure, should receive HBIG and hep B vaccine within 24 hours
53
Q

Hepatitis B treatment

A
  • Chronic hep B
    • interferon (interferon-alpha, pegylated interferon)
    • Nucleoside/nucleotide analog (telbivudine, adenovirus, entecavir, tenofovir, lamivudine)
54
Q

Hepatitis C risk factors

A

Spread through blood and body fluids

  • Prior to 1992, spread through blood transfusions and organ transplants
  • Tattooing, branding, piercing (poorly sanitized equipment)
    • More than 50% of HCV infections caused by injection drug use with needle sharing
55
Q

Hepatitis C treatment

A
  • Refer for expert consultation
    • Antivirals available to achieve sustained virological response (absence of detectable virus 12 weeks after completion of treatment)
  • Surveillance with serology or imaging for patients with evidence of cirrhosis
56
Q

What is irritable bowel syndrome (IBS)?

A

Functional bowel disorder characterized by abdominal pain or discomfort and altered bowel habits in the absence of detectable structural abnormalities

  • May have psych component (stress, anxiety, depression)
57
Q

IBS clinical presentation and physical exam

A
  • Protracted history of intermittent diarrhea and constipation + abdominal pain
  • Increased belching or flatulence
  • Abdominal distention
  • Dyspepsia, heartburn, nausea
  • Tenderness of sigmoid colon
58
Q

IBS diagnostic testing (Rome IV criteria)

A

Recurrent abdominal pain at least 1 day/week in the past 3 months with 2+ of the following:

  • Symptoms related to defecation
  • Change in stool frequency
  • Change in stool form or appearance
59
Q

IBS red flags that suggest more serious disease

A
  • Overt GI bleeding
  • Iron deficiency anemia
  • Nocturnal passage of stool
  • Unintentional weight loss
  • Family history of IBD or colorectal cancer
  • Recent changes in bowel habits
  • Leukocytosis
  • Presence of palpable abdominal mass or lymphadenopathy
60
Q

Is diagnostic testing indicated for IBS?

A

Diagnostic testing not required in patients whose history and symptoms are compatible with IBS

  • Further testing warranted for those who do not improve in 2-4 weeks of empiric therapy and referral to GI
61
Q

IBS management (prevention)

A
  • Adequate hydration
  • Addition of dietary fiber (at least 25-35 g with at least 4-6 glasses of water)
  • Avoidance of trigger foods
    • Coffee, disaccharides, legumes, cabbage, high carb diet, excessive fructose and artificial sweeteners
  • Moderation of caffeine intake
  • Fiber supplementation
62
Q

Pharmacotherapy treatment for IBS

A
  • Low dose TCA or SSRI
  • Loperamide (imodium) or eluxadoline (viberzi) for IBS-D
  • Lubiprostone, linaclotide, plecanatide for IBS-C
  • Prebiotics and probiotics
63
Q

What is inflammatory bowel disease (IBD)?

A

Likely involves autoimmune response in GI tract (genetic component)

  • Two major types: UC (limited to the colon), Crohn’s (involves any part of the GI tract)
64
Q

IBD clinical presentation (including imaging findings)

A
  • Bloody diarrhea
  • Tenesmus - feeling of the need to defecate even through colon is empty
  • Extraintestinal symptoms → arthritis

Crohn’s → abdominal pain, involuntary weight loss, diarrhea, intestinal obstruction, anterior and posterior anal fissures

  • Cobblestone mucosal pattern and “skip lesions” on endoscopy or CT
  • Transmural
65
Q

IBD diagnostic testing

A
  • Elevated CRP and ESR
  • Leukocytosis
  • Anemia
    • Vitamin B12 deficiency with Crohn’s
66
Q

IBD conservative management

A
  • Keep diet diary
  • Smoking cessation
  • Gut rest during treatment of Crohn’s
  • Mental health and social support
  • After 8-10 years of disease, need surveillance colonoscopy every 2 years
67
Q

IBD pharmacotherapy

A

Both UC and Crohn’s

  • Aminosalicylates → sulfasalazine, mesalamine (first line)
  • Immune modulators
  • Biologica (anti-TNF alpha)
  • Anti-inflammatory meds (corticosteroids)

UC

  • If limited to distal colon → mesalamine and corticosteroid rectally

Crohn’s

  • Metronidazole and ciprofloxacin for perineal disease or inflammatory mass noted
68
Q

Celiac disease clinical presentation

A

Often misdiagnosed as having IBS

  • Diarrhea
  • Bloating
  • Abdominal pain/discomfort
  • Anemia
  • IgA deficiency
  • Flatulence
69
Q

Celiac disease → foods that do NOT contain gluten

A
  • Rice
  • Corn
  • Millet
  • Potato
  • Buckwheat
  • Soybeans
70
Q

Pancreatitis risk factors

A

Most common: biliary tract disease (gallstones, excessive alcohol use, elevated TGs, idiopathic causes)

  • Less common → use of opioids, use of select medications including systemic corticosteroids and thiazide diuretics, viral infection, blunt abdominal trauma
71
Q

Diagnosis criteria for acute pancreatitis

A

At least two of the following three criteria:

  • Severe abdominal pain
  • Serum amylase and/or lipase exceeding three times the upper limit of normal
  • Abdominal imaging findings
72
Q

Acute pancreatitis clinical presentation

A
  • Band-like abdominal pain across abdomen to the back
  • N/V
  • Anorexia
  • Fever
  • Dehydration
  • Diaphoresis
  • Hypoactive bowel sounds
  • Abdominal distention
  • Epigastric tenderness with or without rebound
  • History of significant alcohol consumption and/or heavy meal immediately preceding attack
73
Q

Two ominous signs of acute pancreatitis

A
  • Grey-Turner sign → ecchymosis around the flanks
  • Cullen’s sign → periumbilical ecchymosis with superficial edema
74
Q

Acute pancreatitis diagnostic testing

A
  • Abdominal CT scan
  • Abdominal US to rule out contributing gallbladder disease
  • Serum amylase and lipase
75
Q

Acute pancreatitis treatment

A
  • Discontinue underlying cause (I.e. alcohol, corticosteroids, thiazide diuretics, hypertriglyceridemia, gallbladder disease)
  • Parenteral hydration
  • Anagelia
  • Gut rest (NPO)
  • Use Ranson criteria to determine need for admission
76
Q

What are pancreatic pseudocysts?

A

Benign pockets of fluid lined with scar or inflammatory tissue

  • Typically occurs after an episode of pancreatitis
77
Q

Abdominal pseudocyst clinical presentation

A
  • Often asymptomatic
  • Persistent abdominal pain that radiates to the back
  • N/V
  • Palpable upper abdominal mass
78
Q

Pancreatic pseudocyst diagnostic testing

A
  • Abdominal CT scan - preferred method
  • MRI to better determine fluid collections and debris within cysts
    • Both help differentiate cyst from cancer
  • If cancer, CEA and CEA-125 will be elevated
  • Normal amylase, lipase, liver enzymes
79
Q

Pancreatic pseudocyst treatment

A

Management decision made with GI specialist, surgeon, and radiologist

  • Most resolve over time without intervention
  • Can be drained if becomes bothersome (via endoscopic US guided FNA)
80
Q

Pancreatic cancer risk factors

A
  • History of chronic pancreatitis
  • Tobacco use
  • DM
  • Genetics
81
Q

Pancreatic cancer clinical presentation

A

Early signs (nonspecific)

  • Anorexia
  • Nausea
  • Fatigue
  • Epigastric or mid back pain

Later signs

  • Unintentional weight loss
  • Worsening abdominal pain (especially at night)
  • Painless jaundice

Others: thrombophlebitis, diffuse lymphadenopathy, St. Mary Joseph’s nodule (umbilical nodule)

82
Q

Pancreatic cancer diagnostic testing

A
  • Endoscopic US, MRI, PET scan

FNP boards (20 decks)

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