GI disorders Flashcards
(82 cards)
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
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
- Increase dietary fluid and fiber intake (supplementation) + stool softener
- Sitz baths, cool compresses
If severe or does not respond to above treatment,
- Intra-anal NTG or DHP CCB (nifedipine)
- Botox
3
Q
What type of hemorrhoids do the superior and inferior hemorrhoidal veins form (internal vs external)?
A
Superior → internal hemorrhoids
Inferior → external hemorrhoids
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
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
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
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
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
9
Q
Acute appendicitis physical examination
A
- Rebound tenderness (indicates peritoneal irritation)
- Positive psoas and obturator sign
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
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)
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
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
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)
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
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
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)
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
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
20
Q
Colorectal cancer clinical presentation
A
- Vague abdominal complaints
- Iron deficiency anemia
- Late signs → bowel obstruction (sudden onset vomiting, abdominal pain, distention)
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
22
Q
Diverticulosis (symptomatic) clinical presentation
A
- Mild left sided abdominal cramping
- Increased flatus
- Pattern of constipation alternating with diarrhea
23
Q
Diverticulitis clinical presentation
A
- Fever
- Leukocytosis
- Diarrhea
- LLQ pain
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
25
Diverticulosis treatment and management
* High fiber diet
* Fiber supplements (bran, psyllium, methyl cellulose)
* Regular aerobic exercise
* Don't necessarily need to make dietary changes
26
Diverticulitis treatment and management
* 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
27
True/false: With recurrent diverticulitis episodes, surgical intervention with partial colectomy is an option to remove problematic portion of the intestines
True
28
What is peptic ulcer disease?
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
29
Risk factors for peptic ulcer disease
* 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
30
Which type of peptic ulcer is more common - duodenal or gastric?
Duodenal
* Risk factor: h. pylori infection
31
Peptic ulcer disease clinical presentation
* Duodenal
* 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
32
Peptic ulcer disease (duodenal) diagnostic testing
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
33
Peptic ulcer disease (gastric) diagnostic testing
* Upper GI endoscopy with biopsy → differentiate between ulcer and gastric malignancy
* H. pylori testing
34
Gastric peptic ulcer clinical presentation
* Pain reported with or without meals
* Pain worse with eating (lessens within 1 hour)
* N/V, weight loss
35
Treatment of h. pylori associated with duodenal/gastric ulcer
PPI + amoxicillin + metronidazole + clarithromycin x14 days
36
Peptic ulcer disease treatment
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
GERD clinical presentation
Common → dyspepsia, chest pain at rest, postprandial fullness
Non-GI symptoms (especially with chronic disease) → hoarseness, sore throat, nocturnal cough, wheezing
38
Behavioral modifications to prevent GERD symptoms
* 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
If behavioral modifications do not help to improve GERD symptoms, what medication is considered next step?
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
If use of antacids and behavioral modifications can't control mild, intermittent GERD, what is the next step medication?
HrRA at full prescription strength
* If no improvement is seen in 6 weeks, longer term therapy with H2RA is unhelpful
41
If H2RAs, antacids, and behavioral modifications don't work against GERD, what is the next step medication?
PPI
* If symptoms do not resolve after 8 week course, refer to GI w/ upper GI endoscopy
42
PUD red flags that warrant immediate endoscopy and GI referral
* Bleeding or anemia
* Unexplained weight loss
* Progressive dysphagia or odynophagia
* Recurrent vomiting
* Family history of GI cancer
43
GERD red flags that warrant further evaluation
* Dysphagia (difficulty swallowing)
* Odynophagia (painful swallowing)
* GI bleeding
* Unexplained weight loss
* Persistent chest pain
44
Esophageal cancer clinical presentation
* Early stages are usually asymptomatic
* Late stage → epigastric or retrosternal pain, persistent hoarseness, cough
* Iron deficiency anemia
* Dysphagia
* Weight loss
45
Hepatitis clinical presentation
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
Hepatitis A disease markers (lab tests)
Active disease → HAV IgM, elevated hepatic enzymes (x10 upper limits)
Chronic disease → chronic hep A doesn't exist
Past infection → anti-HAV
47
Hepatitis B disease markers (lab tests)
Active disease → HBsAg, elevated hepatic enzyme (x10 upper limits)
Chronic disease → HBsAg, anti-HBC
48
Hepatitis C disease markers (lab tests)
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
Hepatitis A prevention
* 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
Hepatitis A treatment
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
True/false: Hepatitis D can only occur in persons with acute or chronic hepatitis B
True - Hepatitis B and D acute co-infection has a course of illness similar to that of only acute hepatitis B
52
Hepatitis B prevention
* 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
Hepatitis B treatment
* Chronic hep B
* interferon (interferon-alpha, pegylated interferon)
* Nucleoside/nucleotide analog (telbivudine, adenovirus, entecavir, tenofovir, lamivudine)
54
Hepatitis C risk factors
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
Hepatitis C treatment
* 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
What is irritable bowel syndrome (IBS)?
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
IBS clinical presentation and physical exam
* Protracted history of intermittent diarrhea and constipation + abdominal pain
* Increased belching or flatulence
* Abdominal distention
* Dyspepsia, heartburn, nausea
* Tenderness of sigmoid colon
58
IBS diagnostic testing (Rome IV criteria)
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
IBS red flags that suggest more serious disease
* 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
Is diagnostic testing indicated for IBS?
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
IBS management (prevention)
* 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
Pharmacotherapy treatment for IBS
* Low dose TCA or SSRI
* Loperamide (imodium) or eluxadoline (viberzi) for IBS-D
* Lubiprostone, linaclotide, plecanatide for IBS-C
* Prebiotics and probiotics
63
What is inflammatory bowel disease (IBD)?
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
IBD clinical presentation (including imaging findings)
* 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
IBD diagnostic testing
* Elevated CRP and ESR
* Leukocytosis
* Anemia
* Vitamin B12 deficiency with Crohn's
66
IBD conservative management
* 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
IBD pharmacotherapy
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
Celiac disease clinical presentation
Often misdiagnosed as having IBS
* Diarrhea
* Bloating
* Abdominal pain/discomfort
* Anemia
* IgA deficiency
* Flatulence
69
Celiac disease → foods that do NOT contain gluten
* Rice
* Corn
* Millet
* Potato
* Buckwheat
* Soybeans
70
Pancreatitis risk factors
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
Diagnosis criteria for acute pancreatitis
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
Acute pancreatitis clinical presentation
* 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
Two ominous signs of acute pancreatitis
* Grey-Turner sign → ecchymosis around the flanks
* Cullen's sign → periumbilical ecchymosis with superficial edema
74
Acute pancreatitis diagnostic testing
* Abdominal CT scan
* Abdominal US to rule out contributing gallbladder disease
* Serum amylase and lipase
75
Acute pancreatitis treatment
* 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
What are pancreatic pseudocysts?
Benign pockets of fluid lined with scar or inflammatory tissue
* Typically occurs after an episode of pancreatitis
77
Abdominal pseudocyst clinical presentation
* Often asymptomatic
* Persistent abdominal pain that radiates to the back
* N/V
* Palpable upper abdominal mass
78
Pancreatic pseudocyst diagnostic testing
* 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
Pancreatic pseudocyst treatment
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
Pancreatic cancer risk factors
* History of chronic pancreatitis
* Tobacco use
* DM
* Genetics
81
Pancreatic cancer clinical presentation
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
Pancreatic cancer diagnostic testing
* Endoscopic US, MRI, PET scan
