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
chimeric IgG1 antibody against TNF-a
infliximab
Recombinant human monoclonal IgG1 antibody containing only human peptide sequences and is injected subcutaneously
Adalimumab
A pegylated form an anti-TNF Fab portion of an antibody administered SC once a month
Certolizumab
ACCENT I and ACCENT II
A crohn’s disessae clinical trial evaluating infliximab in a new long-term treatment regimen
40% of patients who experience initial response will maintain remission for at least 1 year with repeated infusions of infliximab every 8 weeks
SONIC trial
study of biologic and immunomodulator-naive patients with crohn’s disease
infliximab plus azathioprine > infliximab > azathoprine
CHARM trial
Crohn’s trial of the Fully Human Adalimumab for Remssion Maintenance
PRECISE II trial
pegylated antibody fragment evaluation in Crohn’s disease
A recobinant humanized IgG4 antibody against a4-integrin that has been shown to be effective in induction and maintenance of patients with CD
natalizumab
adverse efect of natalizumab which is the reason why it is no longer widely used
progressive multifocal leukoencephalopathy (PML)
most important risk factor for development of PML in natalizumab user
exposure to JC polyomavirus
other risk factors:
longer duration of treatment
prior treatment with an immunosuppressant medication
a monoclonal antibody directed against a4b7 integrin that has the ability to convey gut-selective immunosuppression
vedolizumab
biological product that is highly similar to the reference product not withstanding minor differences in clinically inactive components
biosimilars
nutritional therapies for IBD
bowel rest and TPN
operation of choice for UC
ileal pouch/anal anastomosis (IPAA)
major complication of surgical therapy for UC
bowel obstruction
most frequent complication of IPAA
pouchitis
the need for surgery in CD is related to (2)
duration of the disease
site of involvement
most frequently performed operation for CD
surgical resection of the disease segment
when will you do the colonoscopy after surgical procedrue for CD
after 6 months
T or F: fertility rates of patients with quiescent IBD is normal
True
part of the female reproductive system that can be scarreed by the inflammatory process of CD
right fallopian tube (due to proximity to the terminal ileum)
preferred route of delivery for patients with IBD
cesarean delivery
female patients with IBDmust be in remisiion ____ before conception
6 monhs
safest antibiotics that can be used for CD in pregnancy
Ampicillin adn cephalosporins
metronidazole - may be used in the 2nd and 3rd trimester
ciprofloxacin - contraindicated
extensive colitris is defined as involvement of
> 1/3 of the colon
risk factors for cancer in UC (7)
long duration diseae extensive disease family history of colon cancer PSC colon stricture post-inflammatory pseudopolyp (UC) bypassed colon segments (CD
Patients with CDhave increased risk of these malignancies (4)
NHL
leukemia
myelodysplastic syndrome
cancer in the lower rectum and anal canal (squamous cell carcinoma) - for those with severe perianal disease
Saclihe herniation of the entire bowel wall
True diverticulum
Protrusion of the mucosa through the muscularis propria of the colon
False or pseudodiverticulum
most common type of diverticulum affecting the colon
False or pseudodiverticulum
Where is the sitre of protrusion in False or pseudodiverticulum?
site of penetration of nutrient artery or vasa recti through muscularis propria
Common location of diverticular disease globally? among asians?
left and sigmoid colon and rectal sparing
in asian, 70% in the right colon and cecum
inflammation due to retention of particulate material within diverticular sac and formation of a fecalith
diverticulitis
complication of diverticular disease (2)
perforation
bleeding
most common cause of hematochezua i patients > 60 years
colonic diverticular henorrhage
Percentage of patients with diverticulosis who will have GI bleeding
20%
risk factors for bleeding in diverticular disease (3(
hypertension
atheroscleosis
Aspirin and NSAIDs use
best diagnostic test for localization of massive bleeding of diverticular disease in otherwise stable patients
angiography
may also used as therapeutic by occluding the bleeding using coil
for bleeding diverticular disease patients who are on anticoagulant, what is the treatment in order to eliminate risk of further bleeding
segmental resection subtotal colectomy (if bleeding sites are not localized)
inidcation for emergent surgery for bleeding diverticular disease
unstable patients
6 unit bleed within 24-hr
clinical manifestation of acute uncomplicated diverticulitis or SUDD (symptomatic uncomplicated diverticular disease) (4)
fever
anorexia
LLQ pain
obstipation
clinical manifestation of diverticular perforation
generalized peritonitis
clinical presnentation of pericolonic abscess of diverticular disease (2)
localized peritonitis
abdominal distension
Complication of diverticular disease (4)
abscess - 16%
perforation - 10%
stricture - 5%
fistula - 2%
best diagnostic test for diverticulitis
CT scan
CT scan criteria for diverticulitis (4)
sigmoid diverticula
thickened colonic wall > 4 mm
inflammation within the pericolic fat
+/- collection of contrast media or fluid
When will you do colonoscopy after an attack of diverticular diseae?
after 6 weeks to rule out sigmoid malignancy
perforated diverticular disease staging
HInchey classification system
Purpose of the Hinchey claddification system
predict outcome following surgical management of complicated diverticular disaease
best management for asymptomatic diverticular disease
lifestyle modifications
fiber-rich diet
avoid smoking
initial management of symptomatic uncomplicated diverticular disease
bowel rest
antibiotics
inications for hospitalization of divertocular disease patients (4)
unable to take oral therapy
several comorbids
fails to improve in the ourpatient therapy
complicated diverticultis
Recommended antibiotics for acute diverticulitis
3rd gen cephalosporin or ciprofloxacin + metronidazole
add ampicillin for non-responders for enterococci coverage
mainstay management for ppost acute diverticulitis episode
symptom prevention
risk factors for recurrence of diverticulitis (3)
younger age
diverticular abscess
frequent attacks (>2 per year)
poorly absorbed broad-spectrum antibiotic associated with 30% less frequent recurrent symptoms of diverticulitis
rifaximin
Hinchey stage Ia
pericolic phlegmon
Hinchey stage Ib
pericolic abscess
Indications for CT-guided percutaneous drainage of Hinchey Ib adn II diverticular disease
> 3 cm + well-defined wall
abscess < 5 cm - resolve with antibiotic therapy
Contraindications for CT-guided percutaneous draignage of diverticular abscess (3)
no percutaneous access route
pneumoperitoneum
fecal peritonitis
most common cause of fecal incontinence
obstetric injury of the pelvic floor
fecal incontinence in aduts is most common in this population
women >65 y, especially parous
in the management of fecal incontinence, this helps strengthen external sphincter muscle while training patient to relax with defecation to avoid unnecessary straining and further injury to the sphincter muscles
biofeedback
3 main hemorrhoidal complexes
left lateral
right anterior
right posterior
diagnostic technique to identify position of hemorrhoidal disease
anoscopy
description of stage I hemorrhoid
enlargement with bleeding
description of stage II hemorrhoid
protrusion with spontaneous reduction
description for Stage III hemorrhoids
protrusion requiring manual reduction
description of stage IV hemorrhoid
irreducible protrusion
managemnet for acutely thrombosed hemorrhoid
excision within 1st 72 hours
results from an infection involving the glands surrounding the anal canal
anorectal abscess
most common location opf anorectal abscess
perianal (40-50%)
other locations:
ischiorectal - 20-25%
intersphincteric - 2-5%
supralevator - 2.5%
hallmarks of anorectal abscess (2)
pain and fever
T or F: all patients with anorectal abscess must be treated with antibiotics
false
only those who are immunocompromised, have prosthetic hearrt valves, artificial joints or IBD
origin of the majority of fistula in ano
cryptoglandular
communication of an abscess cavity with an identifiable internal opening within the anal canal
fistula in ano
fistula in ano most commonly opens in
dentate line (where anal glands enter anal canal
most commpon fistula in ano based on the relation to the anal sphincter muscles
intersphincteric - 70%
transphincteric - 23%
suprasphincteric - 5%
extrasphincteric - 2%
presents as constant drainage from perianal region associated with a firm mass and increasing with defecation
fistula in ano
A posterior external fistula will enter the anal canal in the posterior midline, whereas an anterior fistula will enter the nearest crypt. this is called the
Goodsall’s rule
exception to this rule: if exiting > 3 cm from anal verge
best option of treatment for new cases of fistula in ano
placement of seton (vessel loop or silk tie placed through the fistula tract)
Surgical tretament for intersphincteric and low transphincteric fistula in ano:
siimple fistulotomy
surgical treatment for high transsphincteric fistula in ano
anorectal advancement flap in combination with drainage catheter or fibrin glue
Anal fissure commonly involves which part of the anal canal?
posterior anal cancal
but also involves the anterior
Suspected causes for anal fissure not located at the posterior or anterior anal fissure (4)
TB
syphilis
Crohn’s
CA
pathognomonic findings of anal fissure on anal manometry
increased anal resting pressure + sawtooth deformity with paradoxical contractions of the sphincter muscles
duration of chronic anal fissures
> 6 weeks
occurs when splanchnic perfusion fails to meet the metabolic demands of the intestines
intestinal ischemia secondary to ischemic tissue injury
Intestinal ischemia is classified based on etiology, which dictates management. These are (3):
(1) arterioocclusive mesenteric ischemia
(2) non-occlusive mesenteric ischemia
(3) mesenteric venous thrombosis
Risk factors for arterioocclusive mesenteric ischemia (4):
Atrial fibrillation
Recent myocardial infarction
Valvular heart disease
Recent cardiac or vascular catheterization
All of which are acute in onset and result in embolic clots reaching the mesenteric circulation
A class of intestinal ischemia also known as “intestinal angina,” that is generally more insidious and often seen in the aging population affected by atherosclerotic disease
Nonocclusive mesenteric ischemia
Causes of nonocclusive mesenteric ischemia (4)
Atherosclerotic disease
High-dose vasopressor infusions
Patients presenting with cardiogenic or septic shock,
Cocaine overdose
It is the most prevalent gastrointestinal disease complicating cardiovascular surgery.
Nonocclusive mesenteric ischemia
The incidence of ischemic colitis following elective aortic repair is
5–9%, and the incidence triples in patients following emergent repair
Risk factor for mesenteric venous thrombosis
hypercoagulable state
Collateral vessels within the small bowel are numerous and meet within the duodenum and the bed of the pancreas. This area is known as:
Griffiths’ point
Collateral vessels within the colon meet at the splenic flexure and descending/sigmoid colon. This area is known as:
Sudeck’s point
2 areas that are inherently at risk for decreased blood flow that may cause intestinal ischemia
Griffiths’ point and Sudeck’s point
the most common locations for colonic ischemia (2)
Griffiths’ point and Sudeck’s point
The splanchnic circulation can receive up to ___ of the cardiac output.
30%
Protective responses to prevent intestinal ischemia include (3)
Abundant collateralization
Autoregulation of blood flow
Ability to increase oxygen extraction from the blood
Most frequent origin of emboli that cause intestinal ischemia
Heart (in 75% of cases)
In intestinal ischemia, where does the emboli preferentially lodge?
superior mesenteric artery (SMA) just distal to the origin of the middle colic artery
T or F: Progressive thrombosis of at least 3 of the major vessels supplying the intestine is required for the development of chronic intestinal angina
false. 2
A disproportionate mesenteric vasoconstriction (arteriolar vasospasm) in response to a severe physiologic stress such as shock
Nonocclusive ischemia
Mortality rate of intestinal ischemia
> 50%
The most significant indicator of survival in intestinal ischemia
timeliness of diagnosis and treatment
Presents with severe acute, nonremitting abdominal pain strikingly out of proportion to the physical findings, associated with nausea and vomiting, transient diarrhea, anorexia, and bloody stools
Acute mesenteric ischemia
PE finding of early acute mesenteric ischemia (2)
minimal abdominal distention and hypoactive bowel sounds
The rest is normal
Later findings in acute mesenteric ischemia (2)
peritonitis and cardiovascular collapse
T or F: Diagnostic modalities are useful in diagnosis of intestinal ischemia but should not delay surgical therapy
True
Earlier features of this disease seen on abdominal radiographs include bowel-wall edema, known as “thumbprinting.”
intestinal ischemia
Progression of this disease will have the radiographic findings of air seen within the bowel wall (pneumatosis intestinalis) and within the portal venous system.
intestinal ischemia
A highly sensitive test for intestinal ischemia
CT angiography with three-dimensional reconstruction
In acute embolic disease causing intestinal ischemia, this test is best performed intraoperatively
mesenteric angiography
T or F: A negative duplex scan does not exclude the diagnosis of mesenteric ischemia
False, virtually precludes the diagnosis
One of the biggest limitations of duplex scanning is
Patients’ body habitus
The duplex imaging yields poor results in obese patients
When suspecting mesenteric ischemia involving the colon, performing this test is high yield. This is often an excellent diagnostic tool in patients with chronic renal insufficiency who cannot tolerate IV contrast.
endoscopy
The “gold standard” for the diagnosis of acute arterial occlusive disease is
Angiography
The “gold standard” for the management of acute arterial occlusive disease is
laparotomy
The goal of operative exploration in intestinal ischemia is to
resect compromised bowel and restore blood supply
Site of occlusion when the proximal jejunum is often spared while the remainder of the small bowel up to the transverse colon will be ischemic.
SMA
The surgical management of acute mesenteric ischemia of the small bowel is
embolectomy via arteriotomy
The presence of these laboratory results are useful in support of the diagnosis of advanced intestinal ischemia (4)
Leukocytosis
Metabolic acidosis
Elevated amylase or creatinine phosphokinase levels
Lactic acidosis
these markers may not be indicative of either reversible ischemia or frank necrosis
Investigational markers for intestinal ischemia include (4)
d-dimer
glutathione S-transferase
platelet- activating factor (PAF)
mucosal pH monitoring
Why do we need aggressive fluid resuscitation in intestinal ischemia?
Early manifestations of intestinal ischemia include fluid sequestration within the bowel wall leading to a loss of interstitial volume.
Intervention of choice to maintain hemodynamics in intestinal ischemia
fluid resuscitation
Ischemia of the colonic mucosa is graded as mild, moderate and severe. Describe each.
Mild - minimal mucosal erythema
Moderate - pale mucosal ulcerations and evidence of extension to the muscular layer of the bowel wall
Severe - severe ulcerations resulting in black or green discoloration of the mucosa, consistent with full-thickness bowel-wall necrosis
Degree of reversibility of mild, moderate, and severe ischemia of colonic mucosa
mild - nearly 100%
moderate - ~50%
frank necrosis - dead bowel
T or F: Primary anastomosis may be performed in patients with acute intestinal ischemia
False
The diagnosis of mesenteric thrombosis is frequently made on
abdominal spiral CT with oral and IV contrast
The goal of management of mesenteric venous thrombosis are (4)
optimize hemodynamics
correct electrolyte abnormalities with massive fluid resuscitation
Intravenous antibiotics
anticoagulation
Of all acute intestinal disorders, this is associated with the best prognosis.
Mesenteric venous insufficiency
Presents with intestinal angina, post-prandial abdominal pain, weight loss and chronic diarrhea
Chronic intestinal ischemia
associated with increased need of blood flow to the intestine following meals - hence the post prandial pain
T or F: Abdominal pain without weight loss is not chronic mesenteric angina
True
The treatment of chronic mesenteric ischemia is associated with an 80% long-term success rate
Angioplasty with endovascular stenting
Main stimulator of secretion of water and electrolytes from the pancreatic ductal cells
Secretin (lesser extent, CCK)
Evokes an enzyme-rich secretion from pancreatic acinar cells
CCK
5 causes of acute pancreatitis
Gallstone, alcohol, ERCP, hypertriglyceridemia, drugs
Type of pancreatitis where pancreas blood supply is maintained
Interstitial pancreatitis
Type of pancreatitis where pancreas blood supply is interrupted
Necrotizing pancreatitis
Accepted pathogenic theory of acute pancreatitis where proteolytic enzymes are activated in the pancreas acinar cell rather than in the intestinal lumen due to premature activation of trypsin
Autodigestion
Major symptom of acute pancreatitis
Abdominal pain
Characteristic of abdominal pain in acute pancreatitis
Steady and boring in the epigastrium or periumbilical region, and may radiate to the back, chest, flanks, and lower abdomen
3 causes of shock in acute pancreatitis
o Hypovolemia
o Increased kinin peptides – causing vasodilation
o Systemic effects of proteolytic and lipolytic enzymes
Part of pancreas that is edematous when there is occurrence of jaundice
Head of the pancreas
Location of pleural effusion in acute pancreatitis
Left-sided
Faint blue discoloration around the umbilicus
Cullen’s sign
Cause of cullen’s sign
Hemoperitoneum
Blue-red-purple or green-brown discoloration of the flanks
Turner’s sign
Cause of Turner’s sign
Due to tissue catabolism of hemoglobin from severe necrotizing pancreatitis with hemorrhage
Serum amylase in acute pancreatitis returns to normal in how many days:
3-7 days
Serum lipase in acute pancreatitis returns to normal in how many days
7-14 days
Preferred test for acute pancreatitis
Lipase
More specific test for acute pancreatitis
Lipase
Harbinger of more severe disease (i.e. pancreatic necrosis) in acute pancreatitis
Hemoconcentration (Hct > 44%)
Cause of prerenal azotemia in acute pancreatitis
Due to loss of plasma intro the retroperitoneal space and peritoneal cavity
3 causes of hyperglycemia in acute pancreatitis:
o Decreased insulin release
o Increased glucagon release
o Increased output of adrenal glucocorticoids and catecholamines
Elevated ALP, AST and bilirubins in acute pancreatitis indicates involvement of:
Gallbladder and pancreatic head
Initial diagnostic imaging modality in acute pancreatitis
Abdominal ultrasound
Criteria that categorized morphologic features of acute pancreatitis via CT scan:
Revised atlanta criteria
3 criteria for acute pancreatitis diagnosis (2 out 3)
o Typical abdominal pain in the epigastrium that may radiate to the back
o 3-fold or greater elevation in serum lipase and/or amylase
o Confirmatory findings of acute pancreatitis on cross-sectional abdominal imaging
4 markers of severity of acute pancreatitis
o Hemoconcentration (Hct > 44%)
o Admission azotemia (BUN > 22 mg/dL)
o SIRS
o Signs of organ failure
2 Differences between the biliary colic and acute pancreatitis abdominal pain
o Pain of biliary tract origin is more-right sided or epigastric than umbilical or left upper quadrant
o Ileus is usually absent
Criteria that defines phases of acute pancreatitis, outlines severity of acute pancreatitis, and clarifies imaging definition
Revised Atlanta criteria
2 phases of acute pancreatitis
o Early < 2 weeks
o Late > 2 weeks
Phase of acute pancreatitis where Severity is defined by clinical parameters rather than morphologic findings
Early phase
Most important clinical finding in regard to severity of the acute pancreatitis episode
Persistent organ failure – > 48 h
You must do CT imaging in the 1st 48 h of admission of acute pancreatitis: true or false
False
Radiographic feature of greatest importance to recognize in the late phase of acute pancreatitis
Necrotizing pancreatitis of CT
Difference between moderately severe and severe acute pancreatitis
o Moderately severe – transient organ failure (<48h)
o Severe – persistent organ failure (>48h)
Diffuse pancreatic enlargement and homogenous contrast enhancement on CT scan
Interstitial pancreatitis
Lack of pancreatic parenchymal enhancement by IV contrast on CT scan
Necrotizing pancreatitis
Most important treatment intervention for acute pancreatitis
Safe, aggressive IV fluid resuscitation
Better crystalloid for hydration in acute pancreatitis
Lactated Ringer’s
What is safe, aggressive IV fluid resuscitation in acute pancreatitis
15-20 ml/kg (1050-1400) mL as initial bolus followed by 2-3 ml/kg/hr (200-250 mL/h) to maintain UO > 0.5 ml/kg/hr
Why is Lactated Ringer’s solution a better crystalloid than NSS?
Decrease systemic inflammation
Strategy wherein there is measurement of hematocrit and BUN every 8-12 hrs to ensure adequacy of fluid resuscitation
Targeted resuscitation strategy
5 clinical and laboratory parameters in BISAP
o BUN > 25 mg/dL o Impaired mental status (GCS < 15) o SIRS o Age > 60 years o Pleural effusion
BISAP score that indicates increased risk for in-hospital mortality
≥ 3
Diet for mild acute pancreatitis (once abdominal pain resolved)
Low-fat solid diet
Preferred nutrition for more severe cases after 2-3 days of admission
Enteral nutrition (preferred than TPN)
Prophylactic antibiotics is recommended for necrotizing pancreatitis: True or false
False; broad spectrum antibiotic may be given if patient appears septic, then discontinued once with negative cultures
Definitive management of infected pancreatic necrosis
Pancreatic debridement (necrosectomy)
Persistent pancreatic fluid collections after 6 weeks
Pseudocyst
Diagnosis of pancreatic duct disruption is confirmed by what diagnostic?
MRCP or ERCP
> 90% effective at resolving the leak in pancreatic duct disruption
Bridging pancreatic stent (nonbridging are less effective)
3 perivascular complications of acute pancreatitis:
o Splenic vein thrombosis
o Gastric varices
o Pseudoaneurysm
Incidence of recurrent pancreatitis
25% of patients
2 most common etiologic factors of recurrent pancreatitis
o Alcohol
o Cholelithiasis
4 Cardinal manifestations of chronic pancreatitis
o Abdominal pain
o Steatorrhea
o Weight loss
o Diabetes mellitus
Primary cause of chronic pancreatitis
Alcohol
Independent, dose-dependent risk factor for chronic pancreatitis and recurrent acute pancreatitis
Smoking
Most frequent cause of chronic pancreatitis in children
Cystic fibrosis
Pancreatitis that has the following histopathologic findings: Lymphoplasmacytic infiltrate, storiform fibrosis, abundant IgG4 cells
Autoimmune pancreatitis
Marker for autoimmune pancreatitis
IgG4 – elevated in 2/3 of patients
Criteria used in diagnosing autoimmune pancreatitis
Mayo Clinic HISORt criteria
Parameters in Mayo Clinic HISORt criteria for AIP
o At least 1 or more of the following: Histology Imaging Serology Other organ involvement Response to glucocorticoid therapy
Treatment of AIP that has dramatic response within 2- to 4-week course
Glucocorticoids
Dose of prednisone in AIP
o Initial dose: 40 mg/day for 4 weeks
o Tapered by 5 mg/week
Very effective at inducing and maintaining remission in AIP
Rituximab
In chronic pancreatitis, patients seek medical attention predominantly because of 2 symptoms. What are these?
o Abdominal pain or maldigestion
o Weight loss
2 tests used in evaluation of suspected pancreatic steatorrhea
o Fecal-elastase-1 – abnormal (low)
o Small bowel biopsy – normal
Initial modality of choice in chronic pancreatitis
Abdominal CT imaging
Test that has best sensitivity and specificity in chronic pancreatitis
Hormone stimulation test using secretin
Radiographic findings that is pathognomonic for chronic pancreatitis
Diffuse calcifications on plain films
Arterial bleeding into the pancreatic duct
Hemosuccus pancreaticus
The cumulative risk of pancreatic carcinoma in chronic pancretitis
4% after 20 years
Cornerstone of therapy in pancreatic steatorrhea
Pancreatic enzyme replacement
Pancreatic enzyme replacement formulation must deliver sufficient amount of what substance into the duodenum to correct maldigestion and decrease steatorrhea?
Lipase
Hereditary pancreatitis is mutation on gene on what chromosome? What codons?
Chromosome 7, codons 29 and 122
Incidence of pancreatic carcinoma in hereditary pancreatitis at age 70
40%
Ventral pancreatic anlage fails to migrate correctly to make contact with the dorsal anlage
Annular pancreas
Ring of pancreatic tissue encircling the duodenum
Annular pancreas
Surgical procedure of choice for annular pancreas
Retrocolic duodenojejunostomy
Most common congenital anatomic variant of human pancreas
Pancreas divisum
Pancreas divisum does not predispose patients to pancreatitis: True or false
True
Appear as a small-caliber ventral duct with an arborizing pattern on ERCP/MRCP
Pancreas divisum
Treatment of pancreatitis with pancreas divisum
o Conservative
o Endoscopic or surgical intervention only if with recurrence
Diagnostic test for macroamylasemia
Serum chromatography
Amylase circulate in the blood in a polymer form too large to be easily excreted by the kidney
Macroamylasemia
Most common cause of UGIB
Peptic ulcers
3 high risk findings of ulcer on endoscopy
- Active bleeding
- Nonbleeding visible vessel
- Adherent clot
High-dose, constant infusion of IV PPI sustain intragastric pH of:
> 6
Rebleeding percentage of peptic ulcers within the next year if no preventive strategies done
10-50%
3 main factors in ulcer pathogenesis:
- Helicobacter pylori
- NSAIDs
- Acid
Eradication of H. pylori decrease PUD rebleeding to:
< 5%
If necessary, what NSAID would you give in patient with GIB?
COX-2 selective plus a PPI
For GIB patients with CVD who takes low-dose aspirin for secondary prevention, when will you resume aspirin?
Restart aspirin ASAP after their bleeding episode (1-7 days)
For GIB patients who take aspirin for primary prevention, when will you resume aspirin?
No need to resume
If GIB is unrelated to H. pylori or NSAIDS, until when should you give PPI to patients?
Should remain on PPI therapy indefinitely because of rebleeding rates of 42% at 7 years
Most common bleeding site of Mallory-Weiss tear
Gastric side of the GEJ
Mallory-Weiss tear stops spontaneously in how many percent of cases?
80-90%
Recurrence rate of Mallory-Weiss Tear
0-10%
Poorer outcomes than other sources of UGIB
Esophageal varices
4 treatment for Esophageal varices
- Endoscopic ligation
- IV vasoactive medications
- Non-selective beta blockers
- TIPS
2 indications of TIPS in patient with BEV:
- For patients with persistent or recurrent bleeding despite endoscopic and medical therapy
- 1st 1-2 days of hospitalization for acute BEV in patients with advanced liver disease (Child-Pugh class C with score 10-13)
Endoscopically visualized breaks that are confined to the mucosa
Erosive disease
Cause of erosive esophagitis
GERD
Most important cause of gastric and duodenal erosions
NSAID use
Watermelon stomach
Gastric antral vascular ectasia
Aberrant vessel in mucosa bleeds from a pinpoint mucosal defect
Dieulafoy’s lesion
Hereditary hemorrhagic telangiectasias
Osler-Weber-Rendu
Prolapse of proximal stomach into esophagus with retching
Prolapse gastropathy
Bleeding from the bile duct
Hemobilia
Bleeding from pancreatic duct
Hemosucus pancreaticus
Percentage of obscure GIB that originate in the small intestine
~75%
3 most common causes of small-intestinal GIB in >40 years old:
- Vascular ectasias
- Neoplasm
- NSAID-induced erosions and ulcers
Most common cause of significant small intestinal GIB in children
Meckel diverticulum
Most common cause of LGIB
Hemorrhoids
Aside from hemorrhoids and anal fissures, what is the most common cause of LGIB?
Diverticulosis
Usual location of diverticulosis
Right colon
Bleeding stop spontaneously in how many percent of diverticulosis?
~80-90%
Rebleeding rate in diverticulosis
~15-40%
Without source of GIB identified on UGIE and colonoscopy
Obscure GIB
Bleeding vascular ectasias and aortic stenosis
Heyde’s syndrome
2 most common causes of significant colonic GIB in children and adolescents
- Inflammatory bowel disease
* Juvenile polyps
Measurement of these 2 is the best way to initially assess a patient with GIB
Heart rate and BP
It may take up to how many hours for Hgb to fall in acute GIB
72 hrs
Hemoglobin does not fall immediately in acute GIB. Why?
Proportionate reductions in plasma and red cell volumes
Transfusion is recommended once Hgb is _____. And what do you call this strategy?
- ≤ 7 g/dL
* Restrictive transfusion strategy
In melena, blood has been present in the GIT for how many hours?
≥ 14 h or as long as 3-5 days
Aside from melena, what are 2 other clues of UGIB in differentiating with LGIB?
- Hyperactive bowel sounds
* Elevated BUN
3 baseline characteristics predictive of rebleeding and death in UGIB:
- Hemodynamic compromise
- Increasing age
- Comorbidities
Promotility agent to improve visualization? Dose?
Erythromycin 250 mg IV ~ 30 min before endoscopy
In what subset of UGIB patients will you give antibiotics? And what antibiotics?
- Cirrhotic
* Quinolone or ceftraixone
May improve control of bleeding in cirrhotics with UGIB in the 1st 12 h after presentation
IV vasoactive medications
When should you perform upper endoscopy? In high-risk patients?
- Within 24 hrs
* Within 12 hrs
BUN scoring in Glasgow- Blatchford score
- 18.2 to <22.4 = 2
- 22.4 to <28.0 = 3
- 28.0 to <70.0 = 4
- ≥ 70 = 6
Hemoglobin scoring in Glasgow- Blatchford score (men and women)
- 12 to <13 (men) = 1
- 10 to <12 (women) = 1
- 10 to <12 (men = 3
- <10 = 6
SBP scoring in Glasgow- Blatchford score
- 100-109 = 1
- 90-99 = 2
- <90 = 3
Heart rate scoring in Glasgow- Blatchford score
≥ 100 = 1
Scoring of other markers in Glasgow- Blatchford score
- Melena = 1
- Syncope = 2
- Hepatic disease = 2
- Cardiac failure = 2
In patients with hematochezia + hemodynamic instability, what procedure should you do first?
UGIE to rule out UGIB
Procedure of choice for LGIB, unless bleeding is too massive
Colonoscopy
Procedure for massive LGIB
Angiography
Procedure for LGIB in patients < 40 years old with minor bleeding
Sigmoidoscopy
Initial test in patients with massive bleeding from the small intestine
Angiography
Next step in patients with GIB with negative UGIE or colonoscopy
- Second-look procedure – repeat upper and lower endoscopy
* May also do push enteroscopy
Inspect the entire duodenum and proximal jejunum with a pediatric colonoscope
Push enteroscopy
If second-look procedure in GIB patient is negative, what is the next step?
Video capsule endoscopy (may also do push enteroscopy)
May be used initially instead of video capsule in patients with possible small bowel narrowing
CT enterography
If capsule endoscopy is negative, what is the next step?
Observe or do further testing with deep enteroscopy
Next step if you have a positive FOBT:
Do colonoscopy
Responsible for nearly 50% of the mortality from all cirrhosis
Chronic and excessive alcohol ingestion
Pathology of ALD consists of three major lesions:
Fatty liver
Alcoholic hepatitis
Cirrhosis
Mortality of patients with alcoholic hepatitis concurrent with cirrhosis:
nearly 60% at 4 years
World’s third largest risk factor for disease burden
Alcohol
Cause of most of the mortality attributed to alcohol
Cirrhosis
Mortality is directly related to alcohol consumption
The most important risk factors involved in the development of ALD (2)
Quantity and duration of alcohol intake
T or F. Men are more susceptible to ALD
False. Women are more susceptible.
- Develop advanced liver disease with substantially less alcohol intake
- Due to effects of estrogen, proportion of body fat, and gastric metabolism of alcohol
~12g of alcohol is equivalent to (in terms of beer, wine and spirits)?
- 1 beer
- 4 oz of wine
- 1 oz of 80% spirits
Threshold in developing ALD (women and men)
- > 14 drinks per week in men
* > 7 drinks per week in women
Beverage that has protective effect in ALD
Coffee
The initial and most common histologic response to hepatotoxic stimuli
Fatty liver
The major enzyme responsible for alcohol metabolism
alcohol dehydrogenase
Hepatocyte injury characterized by: ballooning degeneration, spotty necrosis, polymorphonuclear infiltrate, and fibrosis in the perivenular and perisinusoidal space of Disse
Alcoholic hepatitis
Critically ill patients with alcoholic hepatitis short-term (30-day) mortality rates of >50% is seen in patients with (6)
- Coagulopathy – prothrombin time increased >5 s
- Anemia
- Serum albumin <25 g/L (2.5 mg/dL)
- Serum bilirubin >137 μmol/L (8 mg/dL)
- Renal failure
- Ascites
In liver disease, discriminant function score that indicates poor prognosis is
> 32
Model for End-Stage Liver Disease (MELD) score that indicates significant mortality in alcoholic hepatitis
≥21
Based on MELD scoring, dismal prognosis of cirrhosis is seen in patients with (4)
- Ascites
- Variceal hemorrhage
- Deep encephalopathy
- Hepatorenal syndrome
the cornerstone in the treatment of alcoholic liver disease
Complete abstinence from alcohol
Glucocorticoids may be given in ALD if the DF is ___ and MELD scores is ____
For DF >32 or MELD >20
Prednisone 40 mg/day or Prednisolone 32 mg/day for 4 weeks
T or F. Women with encephalopathy from severe alcoholic hepatitis are good candidates for glucocorticoids
True
Nonspecific TNF inhibitor that may be used for severe alcoholic hepatitis
Pentoxifylline
T or F. Transplant candidacy for ALD should be reevaluated after a defined period of sobriety
Patients presenting with alcoholic hepatitis – not a transplant candidate
In men, ______ of ethanol produces fatty liver; ______ for 10–20 years causes hepatitis or cirrhosis. Only ____ of alcoholics develop alcoholic liver disease.
40–80 g/d
160 g/d
15%
T or F. When the underlying insult that has caused the cirrhosis has been removed, there can be reversal of fibrosis
True
Reversal of fibrosis is most apparent in treatment of what cause of cirrhosis?
chronic hepatitis C
Reversal of fibrosis may be observed after treatment of what underlying causes of cirrhosis? (3)
- Chronic hepatitis C
- Hemochromatosis
- Alcoholic liver disease
In terms of nodules, alcoholic cirrhosis is classified as
Micronodular cirrhosis
Nodules are usually < 3 mm in diameter
In terms of nodules, alcoholic cirrhosis after cessation of alcohol use is classified as
mixed macro- and micronodular cirrhosis
larger nodules may form after cessation
Ethanol is mainly absorbed by the
small intestine and through stomach (lesser degree)
Unique form of hemolytic anemia in severe alcoholic hepatitis with spur cells and acanthocytes
Zieve’s syndrome
Reflective of portal hypertension with hypersplenism in cirrhosis
Thrombocytopenia
AST:ALT ration in alcoholic cirrhosis
2:1
Liver biopsy is withheld until abstinence has been maintained for at least
6 months to determine residual, nonreversible disease
5-year survival rate for patients with complications of cirrhosis and continue to drink
<50%
Cornerstone of therapy of alcoholic cirrhosis
Abstinence
Percentage of hepatitis C virus that develop into chronic hepatitis C
80%
Percentage of chronic hepatitis C will develop cirrhosis over 20-30 years
20-30%
T or F. Liver damage in cirrhosis secondary to chronic hepatitis C is due to cytopathic effect of the virus
False. It is a noncytopathic virus – liver damage is probably immune-related
In terms of nodules, cirrhosis secondary to chronic hepatitis C is classified as
mixed macro- and micronodular cirrhosis
Percentage of hepatitis B virus that develop into chronic hepatitis B
5%
Percentage of chronic hepatitis B will develop cirrhosis
20%
Highly successful therapy for cirrhosis with hepatitis C
Direct-acting antiviral protocols
- Well-tolerated
- Short duration (8-12 weeks)
- Costly
T or F. Treatment of autoimmune hepatitis includes immunosuppressive therapy such as glucocorticoids or azathioprine
False. Will not benefit from immunosuppressive therapy with glucocorticoids or azathioprine because the AIH is “burned out”.
Positive autoimmune markers in autoimmune hepatitis (2)
- ANA
* Anti-smooth-muscle antibody (ASMA)
T or F. Non-alcoholic steatohepatitis can progress to increased fibrosis and cirrhosis
True
Type of biliary cirrhosis that will have no improvement with surgical or endoscopic interventions
Intrahepatic
Type of biliary cirrhosis that will benefit from surgical or endoscopic biliary tract decompression
Extrahepatic
All chronic cholestatic syndromes share the histopathologic features of chronic cholestasis, such as (4)
- Cholate stasis
- Copper deposition
- Xanthomatous transformation of hepatocytes
- Irregular biliary fibrosis
Major causes of chronic cholestatic syndromes (4)
- Primary biliary cholangitis
- Autoimmune cholangitis
- Primary sclerosing cholangitis
- Idiopathic adulthood ductopenia
T or F. Primary biliary cholangitis has strong male preponderance.
False. Female
Mostly seen in middle-aged women
Portal inflammation and necrosis of cholangiocytes in small- and medium-sized bile ducts
Primary biliary cholangitis
Antibodies present in 90% of cases of primary biliary cholangitis
Antimitochondrial antibodies (AMA)
- Not pathogenic
- Useful markers for making a diagnosis of PBC
Treatment of primary biliary cholangitis (3)
- Liver transplantation
- Ursodeoxycholic acid (UDCA)
- Obeticholic acid
Treatment of choice for primary biliary cholangitis patients with decompensated cirrhosis
Liver transplantation
The only approved treatment that has some degree of efficacy by slowing the rate of progression of the primary biliary cholangitis
Ursodeoxycholic acid (UDCA)
13-15 mg/kg/day
Slow the rate of progression of PBC, but it does not reverse or cure the disease
Approved for use in primary biliary cholangitis patients with inadequate response to UDCA
Obeticholic acid
Earliest lesion of primary biliary cholangitis
Chronic nonsuppurative destructive cholangitis
- Necrotizing inflammatory process of the portal tracts
- Medium and small bile ducts are infiltrated with lymphocytes and undergo duct destruction
In terms of nodules, cirrhosis secondary to primary biliary cholangitis is classified as
Micro- or macronodular
Most notable clinical feature of primary biliary cholangitis
Significant degree of fatigue out of proportion to what be expected for either severity of the liver disease or the age of the patient
The presence of this symptom prior to the development of jaundice indicates severe disease and poor prognosis
Pruritus
Present in 50% of cases and can be debilitating
Features that are unique to primary biliary cholangitis (3)
- Hyperpigmentation (trunk and arms; seen in areas of exfoliation and lichenification associated with progressive scratching)
- Xanthelasma
- Xanthomata
This tests are most important in the setting of AMA-negative PBC (2)
- Liver biopsy
2. Cholangiography
Cholangiography must be done in patients with AMA-negative with cholestatic liver enzymes to rule out
Primary sclerosing cholangitis
Treatment for intractable pruritus in PBC
Plasmapheresis
Chronic cholestatic syndrome characterized by diffuse inflammation and fibrosis involving the entire biliary tree
Primary sclerosing cholangitis
Final, end-stage manifestation of PSC
Biliary cirrhosis
Biopsy finding in PSC
periductal fibrosis
Helpful in making diagnosis
Antibodies that is positive in 65% of PSC
pANCA
GI condition that is present in > 50% of patients with PSC
Ulcerative colitis
Colonoscopy must be performed once PSC is established to rule out
Ulcerative colitis
Definitive diagnostic test for PSC
Cholangiography
Imaging technique of choice for initial evaluation of PSC
MRCP
ERCP is performed in PSC to determine presence of
dominant stricture
Cholangiographic findings of multifocal stricturing and beading involving both the intra- and extrahepatic biliary tree (classic beaded appearance)
Primary sclerosing cholangitis
Stricture is short and with intervening segments of normal or slightly dilated bile ducts that are distributed diffusely
PSC appearance on cholangiography associated with overall poor prognosis
High-grade, diffuse structuring of the intrahepatic bile ducts
Definitive treatment of PSC
Liver transplantation
Dreaded complication of PSC
Cholangiocarcinoma
Relative contraindication for liver transplantation
Cardiac cirrhosis is secondary to
long-standing right-sided CHF
Description of fibrosis in cardiac cirrhosis
Pericentral
Inherited disorder of iron metabolism with progressive increase in hepatic iron deposition
Hemochromatosis
Treatment of hemochromatosis
regular therapeutic phlebotomy
Inherited disorder of copper homeostasis causing failure in excretion of excess amounts of copper resulting to accumulation of copper in the liver
Wilson’s disease
Kayser-Fleischer corneal rings is seen in
Wilson’s disease
Low ceruloplasmin and elevated 24-h urine copper levels are seen in
Wilson’s disease
Treatment of Wilson’s disease
copper-chelating medications
inherited disorder that causes abnormal folding of the α1AT protein
α1AT deficiency
α1AT deficiency phenotype with greatest risk for development of chronic liver disease
ZZ phenotype
Only 10-20% develops chronic liver disease
Liver biopsy result of periodic acid-Schiff (PAS)-positive and diastase-resistant globules
α1AT deficiency
Only effective treatment in α1AT deficiency
Liver transplantation
Portal hypertension is elevation of the hepatic venous pressure gradient (HVPG) to
> 5 mmHg
Portal hypertension is caused by 2 simultaneously occurring hemodynamic processes:
- Increased intrahepatic resistance to the passage of blood flow through the liver due to cirrhosis and regenerative nodules
- Increased splanchnic blood flow secondary to vasodilation within the splanchnic vascular bed
Portal hypertension is directly responsible for 2 major complications of cirrhosis
- Variceal hemorrhage
2. Ascites
Mortality rate of BEV with each episode of bleeding
20-30%
Prehepatic causes of portal hypertension (3)
- Portal vein thrombosis
- Splenic vein thrombosis
- Massive splenomegaly (Banti’s syndrome)
Which is the most common cause of portal hypertension: pre, intra, or posthepatic?
Intrahepatic (95%)
presinusoidal, sinusoidal, or postsinusoidal
Cirrhosis is presinusoidal, sinusoidal, or postsinusoidal cause of portal hypertension?
Sinusoidal
Presinusoidal cause of portal hypertension (2)
- Congenital hepatic fibrosis
2. Schistosomiasis
Percentage of cirrhotic patients that has portal HPN
> 60%
Postsinusoidal cause of portal hypertension
Venoocclusive disease
Posthepatic causes of portal hypertension (3)
- Budd-Chiari Syndrome
- Venoocclusive disease
- Chronic right-sided cardiac congestion
Affecting the hepatic veins and venous drainage to the heart
3 primary complications of portal hypertension
- Gastroesophageal varices with hemorrhage
- Ascites
- Hypersplenism
Hepatic venous pressure gradient (HVPG) that is at risk for variceal hemorrhage
> 12 mmHg
Sinusoidal cause of portal hypertension (2)
- Cirrhosis
2. Alcoholic hepatitis
____ of patients with cirrhosis have varices. And ____ of patients with varices will develop bleeding
1/3
1/3
_____ of cirrhotics per year develop varices
5-15%
Certain endoscopic stigmata for esophageal varices (6)
- Red wale sign
- Hematocystic spots
- Diffuse erythema
- Bluish color
- Cherry red spots
- White-nipple spots
2 main categories of treatment of esophageal varices
- Primary prophylaxis
2. Prevention of rebleeding
Primary prophylaxis of esophageal varices (3)
- Endoscopy for routine screening
- Nonselective beta blockade (Nadolol and propranolol)
- Endoscopic variceal band ligation
Medications that decrease mortality related to variceal hemorrhage
Nonselective beta blockade (Nadolol and propranolol)
Prevention of rebleeding in esophageal varices is achieved by
Repeated variceal band ligation until varices are obliterated
Vasoconstricting agents used in BEV (3)
Somatostatin
Octreotide
Vasopressin
A direct splanchnic vasoconstrictor given in BEV
Octreotide 50-100 μg/h by continuous infusion
Treatment of acute BEV for patients who cannot get endoscopic therapy immediately or who need stabilization prior to endoscopic therapy
Balloon tamponade
• Sengstaken-Blakemore tube
• Minnesota tube
First-line treatment to control bleeding acutely in BEV
Endoscopic intervention
Sclerotherapy
EVBL
If with bleeding from gastric varices that cannot be controlled by EVL, what is the next step?
Transjugular intrahepatic portosystemic shunt (TIPS)
Creates a portosystemic shunt by a percutaneous approach using an expandable metal stent, which is advanced under angiographic guidance to the hepatic veins and then through the substance of the liver to create a direct portocaval shunt
Alternative to surgery for acute decompression of portal hypertension
Transjugular intrahepatic portosystemic shunt (TIPS)
Complication of TIPS (in 20% of patients)
Encephalopathy
Reserved for BEV patients who fail endoscopic or medical management or who are poor surgical risks
Transjugular intrahepatic portosystemic shunt (TIPS)
Management of recurrent variceal hemorrhage (4)
- Repeated variceal band ligation
- Beta blockade
- Portosystemic shunt surgery
- TIPS
Usually the 1st indication of portal hypertension
Hypersplenism with thrombocytopenia
Most common cause of ascites
Portal hypertension related to cirrhosis
In ascitic patients, at least ____ of fluid in the abdomen before they are aware that there is an increase
1-2 L
Hepatic hydrothorax is more common on what side
Right
Rent in the diaphragm with free flow of ascitic fluid into the thoracic cavity
Serum ascites-to-albumin gradient (SAAG) that is indicative of portal hypertension
> 1.1 g/dL
Serum ascites-to-albumin gradient (SAAG) that is indicative of infectious or malignant causes
<1.1 g/dL
Absolute PMN level of ascitic fluid that is indicative of infection
> 250/μL
Treatment of ascites secondary to cirrhosis (2)
- Dietary sodium restriction
2. Diuretic therapy
Dietary sodium restriction in ascites
< 2 g of Na per day
Dose of spironolactone and furosemide in ascites secondary to cirrhosis
Spironolactone 100-200 mg/day as a single dose; can be increased to 400-600 mg/d
Furosemide 40-80 mg/day; can be increased to 120-160 g/d
Treatment of refractory ascites secondary to cirrhosis (3)
- Repeated large-volume paracentesis with albumin
- TIPS procedure
- Liver transplantation
____ of patients survive 2 years after the onset of ascites in cirrhosis
<50%
Poor prognosis
Spontaneous infection of the ascitic fluid without an intraabdominal source
Spontaneous bacterial peritonitis
Presumed mechanism for development of SBP
Bacterial translocation
Most common organism causing SBP
Escherichia coli
Other gut bacteria
Gram-positive bacteria: S. viridans, S. aureus, and Enterococcus sp.
Secondary bacterial peritonitis is suspected if ____ organisms are identified in the culture of ascitic fluid
> 2
Most common cause of secondary bacterial peritonitis
Perforated viscus
Clinical presentation of SBP (5)
- Ascites
- Fever
- Altered mental status
- Elevated WBC
- Abdominal pain or discomfort
T or F. In patients with BEV, prophylaxis for SBP must be given
True
Treatment of SBP
3rd generation cephalosporin
T or F. Hepatorenal syndrome is a combination of liver and renal pathology.
False. HRS is a form of functional renal failure without renal pathology
Clinical feature of hepatorenal syndrome
large amount of ascites in patients who have a stepwise progressive increase in creatinine
HRS type with progressive impairment in renal function and a significant reduction in creatinine clearance within 1-2 weeks of presentation
Type 1 HRS
Type 2 HRS – fairly stable
Which HRS type has worse outcome?
Type 1 HRS
Management of HRS (5)
- Dopamine or prostaglandin analogues
- Midodrine – α agonist
- Octreotide
- IV albumin
- Liver transplantation – best therapy
Best therapy for HRS
Liver transplantation
Alteration in mental status and cognitive function in the presence of liver failure
Hepatic encephalopathy
T or F. Development of encephalopathy is a requirement to arrive at a diagnosis of fulminant hepatic failure
True
T or F. Brain edema occurs in hepatic encephalopathy
True
Sudden forward movement of the wrist when patients extend their arms and bend their wrists back
Asterixis
“liver flap”
Dietary protein used in management of hepatic encephalopathy
vegetable-based protein
Mainstay of treatment of hepatic encephalopathy
Lactulose
Non-absorbable disaccharide that causes colonic acidification and catharsis in patients with hepatic encephalopathy
Lactulose
Dose of rifaximin in hepatic encephalopathy
550 mg BID
Vitamin K Dependent clotting factors
II, VII, IX, X
Common abnormality in RBC morphology of cirrhotic patients
Macrocytosis
