GASTRO Flashcards
Which causes caustic ingestion more often? Alkali or acid substance
Alkali
Glucocorticoids si recommended in the treatment of corrosive esophagitis: true or false
false
Most common location for pill to lodge?
mid-esophagus, nearing the crossing of the aorta or carina
Typical symptom of Pill-induced esophagitis
sudden onset of chest pain and odynophagia developing over hours or awaken patient from sleep
Manifestation of scleroderma esophagus
hypotensive LES adn absent esophageal peristalsis
The pre-epithelial barrier of the mucosal defense of the stomach is composed of (2):
Mucous gel
Bicarbonate
Bicarbonate is secreted into the mucous gel of the stomach by the epithelial cells to maintain a pH gradient of
pH 6-7
Migration of the gastric epithelial cells to restore a damaged region following breach of the preepithelial barrier
restitution
Play a central role in gastric epithelial defense/repair by regulating release of mucosal HCO3 and mucus, inhibit parietal cell secretion, and maintains mucosal blood flow and epithelial cell restitution
Prostaglandin
2 prinicipal gastric secretory products capable of inducing mucosal injury
HCl
Pepsinogen
Which occurs later in life? gastric ulcer or duodenal ulcer?
Gastric ulcer
95% of duodenal ulcers are located in the:
1st portion of duodenum,
90% is located within 3 cm from the pylorus
Type of gastric ulcer that is located in the gastric body, tend to be associated with low gastric acid production
Type I
Type of gastric ulcer that occr in the antrum; gastric acid can vary from low to normal
Type II
Type of gastric ulcer that occur within 3 cm from the pylorus, commonly accompanied by DUs, normal or inc gastric acid production
Type III
Type of gastric ulcer that is found in the cardia, with low gastric acid production
Type IV
Description of H. pylori
Gram negative, microaerophilic rod
At what part of the stomach does the H. pylori typically resides?
Antrum
Dormant form of H. pylori that facilitates survival in adverse conditions
Coccoid form
Factors that are essential deteminants of H-pylori-mediated pathogenesis and colonization (3):
- outer membrane protein (Hop protein)
- urease
- vacuolating cytotoxin (Vac A)
First step in infection by H. pylori is dependent on (2):
- bacteria’s mobility
2. ability to produce urease
In the developing countries, how many percent of the population may be infected with H. pylori by age 20? How about in industrialized countries?
developing countries - 80%
industrialized countries - 20-50%
2 factors that predispose to higher colonization rates of H. pylori.
- poor socioeconomic status
2. less education
Risk factors for H. pylori infection (5):
- Birth or residence in a developin country
- Domestic crowding
- Unsanitary living conditions
- Unclean food or water
- exposure to gastric contents of an infected individual
Lipopolysaccharide of this organism has low immunologic activity compared to that of in other organisms
H. pylori
may promote a smoldering chronic inflammation
Antral-predominant gastritis is seen in: DU vs GU
DUs
Corpus-dominant gastritis is seen in: GU vs DU
GU
also in gastric atrophy and gastric carcinoma
How many percent of serious NSAID-related PUD complication is not preceeded with dyspepsia?
> 80%
Pathophysiology of NSAID-inducecd ulcer?
Interruption of prostaglandin synthesis impairing mucosal defense and repai
Blood groip that has increased susceptibility to H. pylori infection?
Blood group O
H. pylori preferentiaally binds to group O anyigen
Abdominal pain occurs 90 min to 3 hours after meal. DU vs GU
DU
Frequently relieved by food or antacids: DU vs GU
DU
Most discriminating symptom of DU
Pain that wakes up patient from sleep
seen in 2/3 of DU, and 1/3 in NUD
Pain is precipitated by food. GU vs DU
GU
Nausea and weight loss is most common. GU vs DU
GU
When do you suspect that ulcer penetrated the pancreas?
dyspepsia becomes constant, NOT relieved by food or antacids, and radiates to the back
Ulcer complication characterized by sudden onset of severe generalized abdominal pain
Perforation
Ulcer complication characterized by worsening of pain with meals, nasuea, and vomiting of undigested food
Gastric outlet obstruction
Most frequent PE finding in PUD but with low predictive value
epigastric tenderness
PE finding of severely tender, board-like abdomen in PUD patients indicates
perforation
PE finding of succussion splash in PUD patients indicate
Gastric outlet obstruction
Most common complication of PUD
Bleeding
30-day mortality rate of GI bleeding
2.5-10%
80% of the mortality in PUD-related bleeding is due to nonbleeding causes, most commonly (3):
multiorgan failure (24%) Pulonary complication (24%) Malignancy (34%)
2nd most common complication of PUD
perforation
30-day mortality rate of PUD perforation
> 20%
Form of perforation in which the ulcer bed tunnels into an adjacent organ
penetration
Duodenal ulcer penetrates most commonly in:
pancreas, causing pancreatitis
Gastric ulcer penetrates most commonly in:
left hepatic lobes
may also cause gastrocolic fistulas
Least common PUD complication
gastric outlet obstruction
2 subcategories of functional dyspepsia:
Postprandial distress syndrome
Epigastric pain syndrome
In what subset of patients with PUD will you test for H. pylori and give antibiotic therapy before any diagnostic evaluation?
in otherwise healthy patients and < 45 y.o
Most sensitive and specific examination of the upper GIT
Endoscopy
Biopsy urease test has a sensitivity and specificity of:
> 90-95%
Mainstay of treatment of PUD (2):
Eradication of H. pylori
Therapy/prevention of NSAID-induced disease
Give 3 examples of antacids:
AlMg
Calcium carbonate
Sodium bicarbonate
Antacid that has a side effect of milk-alkali syndrome
calcium carbonate
Give the 4 H2-receptor antagonists:
Cimetidine
Ranitidine
Famotidine
Nizatidine
Inhibit the basal and stimulated acid secretion
H2-receptor antagonists
Gynecomastia and impotence are adverse effects of this drug used for treatment of PUD:
Cimetidine
Mode of action of PPI
Irreversibly inhibit the H,K-ATPase thus inhibiting all phases of gastric acid secretion
Most potent acid inhibitory agents
PPI
Repeated daily dosing of PPI leads to _____, with basal and secretagogue-stimulated acid production being inhibted by ______ after _______ of therapy
progressive acid inhibition
>95%
1 week of therapy
Anemia that is a side effecr of PPI
Vitamin B12-deficiency anemia (due to inhibition of IF production (uncommon)
Adverse effect of PPI that will interfere the absorption of certain drugs
Hypochlorydia
PPI that inhibit hepatic CYP450 (2):
Omeprazole
Lanzoprazole
Not with newer PPIs
Drug that is converted to a viscous paste within stomach and duodenum and bound to active ulcers
Sucralfate
Most common side effect of sucralfate
constipation
adverse effects of short-term use of bismuth=-containing preperations (3):
black stools
constipation
darkening of tongue
Adverse effect of long-term use of bismuth-containing preparations
neurotoxicity
Prostaglandin analogue that is used as cytoprotective agents as treatment of PUD
Misoprostol
Most common adverse effect of prostaglandin analogue
diarrhea
Greatest influence of H. pylori therapy in the management of PUD
prevent recurrence of PUD
According to teh American College of Gastoenterology clinical guidelines, the indications for testing and treating H. pyllori are (4):
- Inidviduals aged < 60 with uninvestigated dyspepsia
- with prior history of PUD ad will be given an NSAID
- Undergone resection of early gastric cancer
- Unexplained IDA and ITP
In H. pylori treatment, aim an initial eradication rate of :
85-90%
First effective triple regimen fo H. pylori
Bismuth + metronidazole + tetracycline
Salvage therapies for treatment of patients with failure of H. pylori eradication with triple thearpy (4)
- Quadruple therapy (PPI, Bismuth, tetracycline, metronidazole or clarithromycin) for 14 days
- PPI + amoxicillin + rifabutin for 10 days
- Levofloxacin + amoxicillin + PPI for 10 days
- Furazolidone + amoxicillin + PPI for 14 days
Usually used triple therapy for H. pylori eradication:
PPI BID
Clarithromyci 500 mg BID
Amoxicillin 1g BID or Metronidazole 500 mg TID
for 14 days
If there is still failure of eradication of H. pylori even with salvage therapy, what is your next step?
Do culture and sensitivity
For patients with dyspepsia, if teh non-invasive H. pylori testing revealed negative, how will you treat the patient?
empiric treatment with H2 blocker or refer to gastroenterologist
How will you confirm eradication of H. pylori?
Urea breath test
If gastric ulcer biopsy is negative, what diagnostic procedure will you do next? Include rationale
repeat endoscopy at 8-12 weeks after to document healing. if still with ulcer, do repeat biopsy
70% of GUs are eventually found malignant
Refractory ulcer is GU that fails to heal after _____ and a DU that does not heal after _____ of therapy
12 weeks
8 weeks
Tests you should do to exclude ZES (2):
fasting gastrin
secretin stimulation test
90% of refractory ulcer heal after this treatment (include duration)
high dose PPI for 8 weeks
Necessary component for surgical operations for duodenal ulcer
vagotomy
Truncal or selective vagotomy preserve these branches
celiac and hepatic branches
Type of vagotomy that has higher ulcer recurrence but with lowest overall complication rates
Highly selective vagotomy
Type of procedure that has lowest rates of ulcer recurrence but has the highest complication rate
vagotomy + antrectomy
Gastroduidenostomy is a reanoastomoses post-antrecctomy that is also known as
Billroth I
Gastrojejunostomy is a reanoastomoses post-antrecctomy that is also known as
Billroth II
Surgical procedure for antral ulcer
antrectomy (including the ulcer) with a Billroth I anastomosis
Surgical procedure for ulcer located at the esophagogastric junction
subtotal gastrectomy with Roux-en-Y esophagogastrojejunostomy (Csende’s procedure
Ulcers developing at the site of anastomosis after partial gastric resection
stomal or marginal ulcer
Most frequent presenting complaint of recurent ulcer
epigastric abdominal pain, with severity and duration more progressive than observed with pre-surgical DUs
Medical therapy for postoperative ulceration
H2-receptor antagonists (effective in 70-90% of patients)
Afferrent Loop Syndrome is associated with what type of anastomosis?
Billroth II
2 types of afferent loop syndrome
- bacterial overgrowth in the afferent limb secondary to stasis (most common)
- severe abdopminal pain and loating
What type of post-op complication causes post=prandial abdominal pain, bloating, diarrhea with malabsorption of fats and vitamin B12
afferent loop syndrome
What post op complication causes severe abdominal pain and bloating 20-60 min after meals, often followed by nausea and vomiting of bile-containing material, with improvemnt of symptoms after emesis?
afferent loop syndrome
Causes series of vasomotor and GI signs and symptoms and occurs in patients who have undergone vagotomy and drainage?
Dumping syndrome
Early dumping opccurs how many minutes after meals?
15-30 mins
Late dumping syndrome occurs how many minutes after meals?
90 min to 3h
Post-op complication manifested as crampy abdominal discomfort, nausea, diarrhea, belching, tachycardia, palpitations, diaphoresis, light headedness, and rarely syncope?
Early dumping syndrome
Post-op compl;ication that is causd by rapid emptying of hyperosmolar gastric contents into the smalal intestine causing fluid shift into the gut lumen with plasma volume contraction and acute intestinal; distention and release of vasoactive GI hormones
Early dumping syndrome
Post-op complication that is predominated by vasomotor symoptoms such as ;light-headedness, diaphoresis, palpitations, tachycardia, syncope.
Late dumping syndrome
What is the mechanism of the late dumping syndrome?
hypoglycemia from excessive insulin release
What precipitates dumping syndrome? (3)
- meals ricjh in simple carbohydrates
- high osmolarity
- large fluids
Cornerstone therapy for dumping syndrome
dietary modification
Alpha-glucosidase inhibitor that may be beneficial in late phase of dumping
Acarbose
Dietary modification for dumping syndrome
small, multiple (6) meals free of simple carbohydrates + NO liquid during meals
Post-vagotomy diarrhea most commonly follows what type of procedure?
truncal vagotomy
Post-op complication causing intermittent diarrhea occuring 1-2 h after meals
Post-vagotomy diarrhea
Treatment of post-vagotomy dirrhea (3)
Diphenoxylate or loperamide for symptom control
cholestyramine for severe cases
surgical reversal of a 10-cm segment of jejunum
Complication post-partial astrectomy with abdominal pain, early satiety, nausea, vomiting with only mucosal erythema of the gastric remnant
Bile reflux gasrtopathy
treatment of bile reflux gastropatrhy (3)
prokinetic agents
cholestyramine
sucralfate
This type of cancer increases in incidence in gastric stump 15 years after rsection, 4-5x increase risk 20-25 years post-resecryion
Gastric adenocarcinoma
Gastric acid hypersecretion due to unregulated gastrin release from a non-beta cell well-differentiated neuroendocrine tumor that is curable by surgical resection in ~40% of patients
Zollinger-Ellison Syndrome
ZES is associated with what type of neuroendocrine tumor?
Multiple endocrine neoplasia (MEN) type I
Hypergastrinemia with gastrin-stimulated acid hypersecretion and histamine release
Zollinger-Ellison Syndrome
Gastrinoma triangel is composed of:
- confluence of systic and common bile duct
- junction of 2nd and 3rd portions of the duodenum
- junction of the neck and body of the pancreas
Most common non-pancreatic lesion in ZES
duodenal tumors (50-75% of gastrinomas)
Most common clinical manifestation of ZES
PUD
2nd most common clinical manifestation of ZES
Diarrhea
3 involved organs in MEN I syndrome
- parathyroid
- pancreas
- pituitary
First diagnostic step for evaluation of ZES
obtain a fasting gastrin level
Prior to serum gastrin levels, when should you stop PPI, H2-receptor antagonist and antacids prior to testing?
PPI - 7 days prior
H2-receptor antagonist - 24 hrs prior
Antacids - 12 hours prior
During endoscopy pH measurement, what pH suggests gastrinoma?
pH < 3
for pH > 3, need a formal gastric acid analysis
In the presence of hypergastrinemia, what level of BAO is considered pathognomonic for ZES?
> 15 mEq/h
BAO/MAO ratio that is highly suggestive of ZES
> 0.6
Test that is used to differentuate between the causes of hypergastribnemia and useful in patients with indeterminate acid secretory studies
Gastrin provocative tests
Most sensitive and specific provocative tests for diagnosis of gastrinoma
Secretin stimulation test
Secretin stimulation test result that is suggestive of ZES
Gastrin of >/= 120 pg within 15 min of secretin injection
When should you stop PPI prior to a secretin stimulation test?
1 week before
2 gstrin provicative tests
- secretin stimulation test
2. calcium infusion study
Functional imaging study of choice for ZES tumor localization
PET-CT with Ga-DOTATATE (if available)
Goals for treatment of ZES (3):
- ameliorate signs and symptoms related to hormone overproduction
- curative resection of the neoplasm
- control tumor growth in metastatic disease
Treatment of choice for ZES
High dose PPI
Omeprazole or lanzoprazole 60 mg in divided doses in 24-h
Treatment of ZES that inhibits effects of gastrin release from receptor-bearing tumors and inhibits gastric acidsecretion to some extent
Octreotide
Adjunct to PPI in the treatment of ZES
Octreotide
Definitive cure for ZES
Surgery
When do yopu treat patients wioth metastatic gastrinoma?
therapy may be delayed until with evidence of tumor progression or refractory symptoms with PPI
Favorable prognostic indicators for ZES (4):
- Primary duodenal wall tumors
- Isolated lymph node tumor
- Undetectable tumor upon surgical exploration
- Presence of MEN 1
Poor outcome indicators for ZES (6):
- shorter disease duration
- higher gastrin levels (>10,000 pg/mL)
- large pancreatic primary tumor (>3 cm)
- metastatic fisease (to lymph node, liver, bone)
- Cushing’s syndrome
- rapid growth of hepatic metastases
Acute erosive gastric mucosal changes or frank ulceration with bleeding in patients suffering from shock, sepsis, massive burns, severe trauma, head injury
Stress-imduced gastritis or ulcers
Usual location of stress-induced gastritis or ulcers
fundus and body - acid-producing portions of the stomach
UGIB occur at what hour after acute injury or insult in stress-induced gastritis or ulcer?
48-72 hours
Ulcer that occur after head trauma
Cushing’s ulcer
Ulcer that occur after severe burns
Curling’s ulcer
Mortality rate of UGIB due to stress ulcer if with clinically important GI bleeding
> 40%
Preventive measure for stress ulcer is only given for patients who are high-risk such as with (4)
- mechanical ventilation
- coagulopathy
- multiorgan failure
- severe burns
Prophylaxis of choice for stress ulcer
PPIs
Most common cause of acute gastritis
infection
Rare, potentially life-threatening disorder caused by bacterial infection of the stomach
phlegmonous gastritis
High risk groups for phlegmonous gastritis (3)
- elderly
- alcoholics
- AIDS
Type of chronic gastritis with inflammatory changes limited to lamina propria of the surface mucosa
Superficial gastritis
Type of chronic gastritis where inflammatory infiltrate extends deeper into the mucosa, progressive distortion and destruction of the glands
Atrophic gastritis
Final stage of chronic gastritis with loss of glandular structures, paucity of inflammation, thinned-out mcuosa
Gastric atrophy
Morphologic transformation of gastric glands in gastric atrophy
intestinal metaplasia
type of chronic gastritis that is an important predisposing factor for gastric cancer
gastric atrophy
type of chronic gastritis that is predominantly involve the fundus and body with antral sparing
Type A gastritis
Autoimmune gastritis is what type
Type A gastritsi
Type of gastritis that is traditionally associated with pernicious anemia in the presence of circulating antibodies against parietal cells and IF
Type A gastritis or autoimmune gastritis
2 types of antibodies presnt in autoimmune gastritis and what is more specific?
anti-IF antibodies - more specific
Parietal cell antibodies
Associated diseases in type A gastritis (2):
Addison’s
Vitiligo
More common form of chronic gastritis (based on involvement)
Type B gastritis
Type of chronic gastritis that commonly involve the antrum
tyep B gastritis
Type of chronic gastritis that is caused by H. pylori infection
Type B gastritis
Type of chronic gastritis that convert to pan-gastritis
Type B gastritis
H. pylori infection can lead to cancer. Give 2 example
gastric cancer
MALT lymphoma
If chronic gastritis has signs of intestinal metaplasia, how often will you do surveillance endosccopy?
every 3 years
Treatment for eosinophilic gastritis
glucocorticoids
Gastritis that is associated with several systemic disease and Crohn’s diseae
Granulomatous gastritis
Rare disease characterized by large tortous gastric mucosal folds with male predominance
Menetrier’s disease
Menetrier’s disease commonly involves mucosal folds of:
body and fundus, with antral sparing
Pathology of this disease is massive foveolar hyperplasia replcing most of the chief and parietal cells, and is not considered as gastritis
Menetrier’s disease
Etiology of Menetrier’s disease
unknown in adults, CMV in children
First-line therapy for Menetrier’s disease
Cetuximab or anti-EGFR
Surgical procedure for menetrier’s disease
total gastrectomy
Age of onset oof UC and CD
2nd to 4th decade and 7th to 9th decade
UC vs CD: smoking prevents disease
UC
Causes disease in CD
UC vs CD: Oral contraceptive increase risk of disease
Crohn’s disease
UC vs CD: Appendectomy is protective
UC
UC vs CD: Vitamin D supplementation hasprotective effect
CD
If a apatient has IBD the lifetime risk that a first-degree relative will be affected is ___
~10%
Most common CD phenotype in East Asia
Ileocolonic CD
X-linked recessive disorder that is associated with colitis, immunodeficiency, severely dysfunctional platelets, and thrombocytopenia
Wiskott-Aldrich syndrome
Severe, refractory IBD that is caused by deficient IL-10 and IL-10 receptor function
Early-onset IBD
A state of commensal microbiota inpatients with both UC and CD
Dysbiosis - presence of microorganism that drive disease to which the immune response is directed and/or loss of microorganisms that hinder inflammation
UC vs CD: Usually involves the rectum
UC
In UC, ____ of patients have disease limited to the rectum and rectosigmoid, ____have disease extending beyond thesigmoid but not involving the whole colon, and ____ have total colitis
40-50%
30-40%
20%
UCvs CD: mucosa is erythematous and has a fine annualr surface that resembles sandpaper
mild UC
in severe diseae, hemorrhagic, edematous, adn ulcerated
UC vs CD: complications are tpoxic colitis or megacolon, and perforation
UC
UC vs CD: The process is limited to the mucosa and superficial submucosa, with deeper layers unaffected except in fulminant disease
UC
UC vs CD: the neutrophils invade the epithelium, usually in the crypts, giving rise to cryptitis and, ultimately, to crypt abscesses
UC
In CD, ____ of patients have small bowel disease alone, ____ have disease involving both the small and large intestines, and ___ have colitis alone
30-40%
40-55%
15-25%
IN the 75% of patients with small intestinal CD, 90& involve the
terminal ileum
UC vs CD: rectum is usually spared
CD
UC vs CD: segmental with skip areas
CD
UC vs CD: rarely involve the liver and pancreas
CD
UC vs CD: transmural process
CD
UC vs CD: endoscopically, apthous or small superficial ulcerations characterize mild disease
CD
UC vs CD: in more active disease, stellate ulcerations fuse longitudinally and transversely to demarcate islands of mucosa that frequently are hstologically normal resulting to cobblestone appearance
CD
UC vs CD: focal inflammation and formation of fistula tracts occur
CD
UC vs CD; Granulomas are characteristic feature
CD
Major symptoms of UC (5):
diarrhea rectal bleeding tenesmus passage of mucus crampy abdominal pain
Diarrhea in UC is often
nocturnal and postprandial
Specific marker for dtecting iintestinal inflammation
fecal lactoferrin
Marker that dtects relpse of IBD and detect pouchitis
Fecal calprotectin
Differentiate mild, moderate adn severe UC in terms of: Bowel movement
Mild: < 4/day
Moderate: 4-6/day
Severe: > 6 per day
Differentiate mild, moderate adn severe UC in terms of: blood in stool
Mild: small
Moderate: moderate
Svere: severe
Differentiate mild, moderate adn severe UC in terms of: fever
mild: none
moderate: <37.5
severe: >37.5
Differentiate mild, moderate adn severe UC in terms of: tachycardia
mild: none
moderate: <90
severe: >90
Differentiate mild, moderate adn severe UC in terms of: anemia
mild: mild
Moderate: > 75% of normal Hgb
Severe: <75% of normal Hgb
Differentiate mild, moderate adn severe UC in terms of: ESR
Mild: <30 mm
Severe: > 30mm
Differentiate mild, moderate adn severe UC in terms of: endoscopic appeaance
Mild: erythema, decreased vascular pattern fine granularity
Moderate: marked erythema, coarse granularity, absent vascular markings, contact bleeding, no ulcerations
Severe: spontaneous bleeding, ulcerations
In massive hemorrhage due to UC, when is colectomy indicated?
when a patient required 6-8 u of blood within 24-48 hrs
Defined as a transverese or right colon with a diameter of > 6 cm
Toxic megacolon
Toxic megaccolon involves what segment of colon in UC? diameter?
transverse and righ colon
> 6 cm
Most dangerous complication of UC
Perforation
In the presence of intestinal stricture, when is surgery indicated?
when the stricture prevents passage of the colonoscope
2 patterns of CD
fibrostenotic obstructing pattern
penetrating fistulous pattern
this factor influences the clinical manifestion of D
site of disease
Most common site of inflammation in the ileocolitis CD
terminal ileum
usual presentation of ileocolic CD
chronic history of recurrent episodes of right lower quadrant pain and diarrhea, pain is usually colicky and preceds and relived by defecation
Seen as “string sign” on barium studies due to severely narrowed loop of bowel, which makes the lumen resemble a frayed cotton string
ileocolic CD
Characteristic features of jejunoileitis CD
malabsorption and steatorrhea, with nutritional deficiencies
diarrhea
Clinical manifestations of CD colitis (5):
low-grade fever malaise diarrhea crampy abdominal pain hematochezia (sometimes)
Signs and symptoms of gastroduodenal disease in CD
nauea
vomiting
]epigastric pain
H. pylori - negative
Most commonly involved site in gastroduodenal CD
2nd portion of the duodenum
markers that are used to distinguish IBD from IBS (2)
fecall lactoferrin and calprotectin levels
The earliest macroscopic findings of colonic CD
apthous ulcers
Perforation in CD usually involves what site?
ileum
UC vs CD: intraabdominal and pelvic abscess occur in 10-30% of patients
CD
UC vs CD: increased titers of anti-saccharomyces cerevisiae antibodies
CD
UC vs CD: increased p-ANCAs levels
UC
Term for IBD wherein UC and CD are initiialy impossible to differentiate
indeterminate colitis
Infectious disease that mimic the endoscopic appearance of severe UC and can cause a relapse of established UC
campylobacter colitis
UC vs CD: blood and mucus in stool is more common
UC
UC vs CD: systemic symptosms are more common
CD
UC vs CD: pain is more common
CD
UC vs CD: abdominal mass is more common
CD
UC vs CD: significant perineal disease
CD
UC vs CD: small intestinal and colonic obstruction are more common
CD
UC vs CD: responds to antibiotics
CD
UCvs CD: recurrence after surgery is common
CD
UC vs CD: continuous disease
UC
UC vs CD: stricture is more frequent
CD
Similar to CDbut the mucosal abnormalities are limited to the sigmoid and descending colon
Diverticular-associated colitis
A differential diagnosis of IBDcharacterized by sudden onset of left lower quadrat pain, urdency to defecate, and the passage of bright red blod per rectum
ischemic colitis
Differential diagnosis of IBD that is caused by impaired evacuation and failure of relaxation of the puborectalis muscle
Solitary rectal ulcer syndrome
2 common drugs used in a hospital setting that mimic IBD
ipilimumab
mycophenolate mofetil
etanercept (case reports only)
2 atypical colitides
Collagenous colitis
lymphocytic colitis
completely normal endoscopic appearance
Inflammatory process that arises in segments of the large intestine that are excluded from the fecal stream, and usually occurs in patients with ileostomy or colostomy
diversion colitis
Difference of diversioon colitis from UC
crypt architecture is normal
Percentage of IBD patients that have at least one extraintetsinal disease manifestation
1/3
Extraintestinal manifestation of IBD that is characterized by hot, red, tender nodules measuring 1-5 cm in diameter and are found on the anterior surface of the lower legs, ankles, calves, thighs, and arms
eyrthema nodosum
Extraintestinal manifestation of IBD characterized by lesions that begin as pustules and spreads concentrically to rapidly undermine healty skin in the on the dorsal surface of the feet and legs, but may occur on the arms, chest, stoma, and even face.
Pyoderma gangrenosum
UC vs CD: -perianal skin tags in 75-80% of patients
CD
UC vs CD: pral mucosal lesions are more common
CD
UC vs CD: peripheral arthritsi is more common
CD
Characteristics of peripheral arthritis in IBD
asymmetric, polyarticular, and migratory, most often affecting the large joints, and worsens with exacerbations of bowel activity
UC vs CD: Aknylosing spondylitis is more common
CD
IBD with ankylosing spondylitis is associated with this antigen
HLA-B27 antigen
UC vs CD: uveitis is more common
equal
UC vs CD: episcleritis is more common
CD
An extraintestinal manifestation of IBD that is characterized by both intrahepatic and extrahepatic bile duct inflammation and fibrosism frequently leading to biliary cirrhosis and hepatic failure
primary sclerosing cholangitis
UC vs C: primary sclerosing cholangitis is more common
UC
Antibodies present in both IBD and PSC
pANCA
Gold standard diagnostic for PSC
ERCP - gold standard
MRCP - sensitive, specific and safer
Priamry scclerosing cholangitis increase risk of what cancer? IBD and PSC will increase risk of what cancer?
cholangiocarcinoma
colon cancer
Variant of PSC with normal cholangiography, and sometimes referred to as pericolangitis, and with better prognosis than classic PSC
small-duct PSC
Nephrolithiasis seen in CD is composed of what stone?
calcium oxalate
UC vs CD: nephrolithisis is more common
CD
UC vs CD: nephrolithisis is more common
CD
Medcal therapy for IBD (8)
5-ASA Glucocorticoid Antibiotics (for CD) Azathioprine and 6-MP Methotexate Cyclosporine Tacrolimus Biologic therapies
Active ingredient of sulfasalazine
5-ASA and mesalamine
Supplements that should be given along with sulfasalazine
folic acid
A once-a-day formulation of mesalamine that is designed to release mesalamine in the colon
Lialda
A once-a-day formulation containing encapsulated mesalamine granules that delivers mesalamine to the terminal ileum and colon via proprietary extended release mechanism
Apriso
Mesalamine formulation that uses an ethylcellulose coating to allow water absorption into small beads containing the mesalamine
pentasa
Most common side effects of 5-ASA (4)
headaches
nauseas
hair loss
abdominal pain
Dose of glucocorticoid for moderate to severe UC that is unresposve to 5-ASA
Prednisone 40-60mg/day
hydrocortisone 300mg/d
methylprednisolone 40-60 mg/d
A new glucocorticoid for IBDthat is released entirely in the colon and has minimal to no glucocorticoid side effects. include dose
Budesonide 9 mg/d for 8 weeks with no tapering for UC
ileal-release budesonide 9mg/d for 2-3 months and then tapered
Pouchitis in UC, which occurs in about 30-50% of UC patients after colectoy and IPAA usually responds to these 2 antibiotics (with dosage)
metronidazole 15-20 mg/kg per day in 3 divided doses
ciprofloxacin 500mg BID
active end product of azathioprine and 6-MP
thioinosinicc acid
adverse effect of azathioprine and 6-MP that occurs on 3-4% of patient, typically presenting within the 1st few weeks of therapy, and is completely reversible when the drug is stopped
pancreatitis
Methotrexate inhibits what enzyme
dihydrofolate reductase
it also decrease production of IL-1
lipophilic peptide with inhibitory effects on both the cellular and humoral immunity, blocks production of IL-2, and inhibits calcineurin
cyclosporine
Common side effects of cyclosporine (7):
hypertension gingival hyperplasia hypertrichosis paresthesias tremors headaches electrolyte abnormalities
A macrolide antibiotic with immunomodulatory properties similar to cyclosporine, nut is 100 times more potent than CSA and not dependent on bile or mucosal integrity for absorption
Tacrolimus
the first biologic therapy approved for oderate to severely active IBD
infliximab
