Step Up - GI Flashcards
What is the most common form of colorectal cancer? What is the most sensitive and specific screening tool? What cancer marker is used to track disease following treatment?
1) Adenocarcinoma
2) Colonoscopy
3) CEA
What are the risk factors for developing colorectal cancer (7)?
1) Age >60
2) Adenomatous polyps - Villous worse than tubular
3) PMHx of CRC
4) IBD - UC > Crohn’s
5) Fam Hx
6) Diet - high fat, low fiber
7) Major polyposis syndromes
Describe briefly the major polyposis syndromes (6). Focus on inheritance pattern, malignant potential, and associated symptoms.
1) Familial adenomatous polyposis (FAP) - AD, CRC risk is 100%, colectomy at 40.
2) Gardner syndrome - AD, FAP + bone/skin/soft tissue involvement, CRC risk 100%, colectomy at 40.
3) Turcot syndrome - AD or AR, polyps + CNS tumor
4) Peutz-Jeghers - AD, hamatomas, pigmented skin lesions, low malignant potential
5) Familial juvenile polyposis coli - Rare, childhood, small CRC risk
6) Hereditary nonpolyposis CRC - Lynch Syndrome
What are general clinical features for CRC (3)? What are clinical features specific to right (4)/left (3)/rectal (3)?
1) General - abdo pain, wt loss, blood in stool
2) Right - RLQ mass, occult blood, melena, anemia
3) Left - change in caliber, change in BM haboits, hematochezia
4) Rectal - hematochezia, tenesmus, rectal mass
What is the appropriate treatment and follow-up to CRC (4)
1) Surgical resection of affected bowel and lymphnodes
2) Annual CT and CXR for 5 years after
3) Colonoscopy at 1 year, then every 3 years
4) Track CEA every 3-6 months
- Radiation therapy useful in rectal cancer
Rank the malignant potential of the adenomatous polyps from most to least malignant (3).
Villous > Tubulovillous > Tubular
What are the risk factors for diverticulosis (2)? What are the clinical features (4)? What is the diagnostic test of choice? What are the complications (2)?
1) low-fiber diet, fam Hx
2) Clinically - usually asymptomatic, LLQ discomfort, bloating, diarrhea/constipation
3) Barium enema
4) Painless rectal bleeding, diverticulitis
What are the clinical features of diverticulitis (3)? What tests are indicated and contra-indicated in the work-up? What are the potential complications (4)? What are the appropriate treatments (2)?
1) Clinically - fever, leukocytosis, LLQ pain
2) CT abdo/pelvis. Contra: Barium enema and colonoscopy
3) Complications - abscess, fistula, perforation, obstruction
4) IV Abx and bowel rest. Surgery if complicated course
List and briefly describe the four types of acute mesenteric ischemia.
1) Arterial embolism - cardiac origin
2) Arterial thrombosis - occlusion over pre-existing atherosclerotic disease
3) Nonocclusive mesenteric ischemia - Splanchnic vasoconstriction due to low CO
4) Venous thrombosis - hypercoagulable state, many causes.
- typically occur in superior mesenteric vessels.
What are the clinical features of acute mesenteric ischemia (5)?
1) Pain worse than suggested by physical findings
2) Anorexia/Vomiting
3) GI bleed
4) Peritonitis
5) Sepsis/Shock
How is acute mesenteric ischemia diagnosed? What is the treatment (5)?
1) Mesenteric angiogram
2) Tx: IV fluids and broad-spectrum Abx
3) If vasoconstrictive - vasodilator intra-arterial injection
4) If embolic - thrombolytics or embolectomy
5) If venous thrombosis - Heparin
6) Surgery for dead tissue (perforation)
What vessels are affected in chronic mesenteric ischemia (3)? What activity typically precipitates an episode of pain? What is the Tx?
1) Celiac, superior and inferion mesenteric artery occlusion due to atherosclerosis
2) Eating
3) revascularization surgery
What is ogilvie syndrome? Who does it effect? What are the treatments (3)?
1) SSx of large bowel obstruction, with no mechanical obstruction present
2) The ill elderly
3) Stop offending medical agent, decompress with enema or colonoscopy, NG suction.
What are the most common offending Abx leading to pseudomembranous colitis?
1) clindamycin
2) Ampicillin
3) Cephalosporins
What is the cause of pseudomembranous colitis? What are the clinical features (3)? How is it diagnosed? How is it treated (2)?
1) C. diff
2) watery diarrhea, crampy abdo pain, toxic megacolon
3) C diff toxins in stool
4) Metronidazole > Vancomycin
Describe the types of colonic volvuli (2). What are the clinical features (3)? How are they treated (2)?
1) Sigmoid (75%) or Cecal (25%)
2) Clinically - colicky abdo pain, abdo distention, anorexia/nausea/vomiting
3) Tx:
a) Sigmoid - sigmoidoscopy is both diagnostic and therapeutic. Elective sigmoid resection as recurrence is high
b) Cecal - Emergency surgery
Liver cirrhosis leads to destruction of liver anatomical architecture. As a result portal HTN and biochemical dysfunction can result. Discuss the clinical features of portal HTN (4), and biochemical dysfunction (2).
1) Portal HTN - ascites, peripheral edema, splenomegaly, varicose veins (gastric, esophageal, anal)
2) Biochemical - reduced albumin and clotting factor synthesis
What 5 metrics are used to determine hepatic functional reserve (Child-Pugh classification)?
1) Ascites
2) Bilirubin
3) Encephalopathy
4) INR ratio
5) Albumin
What are the most common causes of cirrhosis (2)?
1) Alcoholic liver disease
2) Chronic hep B or C infections
Outline the treatment for acutely bleeding esophageal varices (4). What is the long-term therapy?
1) Variceal ligation/banding
2) Endoscopic scleotherapy
3) IV octreotide - reduces portal HTN
4) Esophageal balloon tamponade
- B-blocker for long-term care to prevent rebleed
What are the complications associated with liver failure (hint: AC, 9H) (11)?
1) Ascites
2) Coagulopathy
3) Hypoalbuminemia
4) Portal HTN
5) Hyperammonemia
6) Hepatic encephalopathy
7) Hepatorenal syndrome
8) Hypoglycemia
9) Hyperbilirubinemia
10) Hyperestrinism
11) HCC
Provide the clinical features of hepatic encephalopathy associated with liver disease (4).
1) Decreased LOC - confusion, poor concentration, coma
2) Asterixis - flapping tremor
3) Rigidity/hyperreflexia
4) Fetor hepaticus - musty odor of breath
How is hepatic encephalopathy treated (3)?
1) Lactulose - prevents ammonia absorption in GI tract
2) Rifaximin - Abx to kill gut flora, decrease ammonia production
3) Diet - limit protein to 30-40 g/day
What are the clinical features suggestive of hyperestrinism secondary to liver failure (4)?
1) Spider angiomas
2) Palmar errythema
3) Gynecomastia
4) Testicular atrophy
How are the coagulopathies of liver failure treated? What lab marker is abnormal?
1) Fresh frozen plasm
2) PT prolonged
- vit K doesn’t work as liver is diseased
What is Wilson’s disease? What organs are affected typically (4)? How is the diagnosis made (3)? What is the treatment (2)?
1) AR, dysfunction making ceruloplasmin protein, copper aggregates in liver and other tissues
2) Organs: Liver, CNS, Renal, Cornea
3) Dx: impaired LFTs, low ceruloplasmin levels, liver biopsy with high copper conc.
4) Tx: Chelating agent, Zinc (prevent absorption)
What is Hemochromatosis? What are the complications (6)? How is the diagnosis made (3)? What is the treatment (2)?
1) AR, excess absorption of iron
2) Complications: Cirrhosis, cardiomyopathy, DM, arthritis, hypogonadism, hyperpigmented skin
3) Dx:
a) High: serum iron, ferritin, transferring sat
b) Low: total iron binding capacity
c) Liver biopsy
4) Repeat phlebotomies, liver transplant if severe.
List and briefly describe 3 common benign tumors of the liver.
1) Hepatocellular adenoma - seen in women using contraceptives. Risk of rupture. D/C drugs, surgical resection if large
2) Cavernous Hemangiomas - Most common tumor of liver. Resect if mass effect present.
3) Focal nodular hyperplasia - bening, no treatment
What are the 2 pathological types of hepatocellular carcinoma? What is the most common risk factor for HCC?
1) Nonfibrolamellar - Hep B/C or cirrhosis related. Poor prognosis
2) Fibrolamellar - Not Hep B/C or cirrhosis related. Resectable, better prognosis
3) RF: Cirrhosis
What are the clinical features of HCC (3)? How is it diagnosed (2)? How is it treated (2)?
1) SSx:
a) Constitutional - anorexia, fatigue, wt loss
b) Abdo pain
c) signs of liver disease - ascites, jaundice, splenomegaly
2) Dx: Biopsy, track AFP
3) Tx: resection possible in very few cases, liver transplant, local chemo/rad. Poor outcomes.
Describe the two most common liver abscesses in terms of their pathophys, diagnosis, and treatment.
1) Pyogenic liver abscess
a) Due to obstruction and ascension up biliary tree.
b) Dx: U/S or CT
c) IV Abx, percutaneous drainage
2) Amebic Liver abscess
a) fecal-oral transmission, intestinal amebiasis
b) dx: U/S or CT, stool O+P
c) Percutaneous drainage, IV metronidazole
- both life threatening if not treated
What is Budd-Chiari Syndrome? What is seen clinically (4)? How is it treated?
1) Patho: occlusion of hepatic outflow leading to congestion
2) Clinical: looks like cirrhosis, ascites, abdo pain, jaundice
3) Surgery - balloon angioplasty and stent
Discuss the impact of hyperbilirubinemia on urine - how does this change with conjugated vs unconjugated billis?
1) Conjugated - loosely bound to albumin, excreted in urine - thus urine is dark
2) Unconjugated - bound to albumin and not water soluble, does not exit in urine - thus no change.
- unconjugate billi can cross BBB, thus toxic
What are the causes of unconjugated billirubinemia (4)?
1) Increased production - hemolytic anemia
2) Impaired conjugation
a) Gilbert Syndrome - AD, benign
b) Crigler-Najjar Syndrome - severe, toxic
3) Drugs - sulfa drugs, radiocontrast
Which liver enzyme is most specific? What is anticipated in the lab work-up of alcoholic cirrhosis? What is indicated by mild/moderate/severly elevated ALT and AST levels?
1) ALT - specific to liver
2) AST : ALT ratio greater than 2
3)
a) Mild - chronic viral or alcoholic hep
b) mod - acute viral hep
c) Severe - severe viral hep, acetaminophen toxicitiy, ischemia, shock liver
What is the DDx for elevated ALT and AST values (hint: ABCDEFGHI) (9)
1) Autoimmune hep
2) Hep B
3) Hep C
4) Drugs
5) Etoh
6) Fatty liver
7) Growths (tumor)
8) Hemodynamic disorder (CHF)
9) Iron, copper, A1AT
What is suspected with very high ALP values? What is the value of an elevated GGT when ALP is only moderately high?
1) Biliary tree obstruction
2) Confirms the reason for ALP elevation is hepatic in origin
What clotting factors are synthesized by the liver (8).
I, II, V, VII, IX, X, XII, XIII
- reflected in PT.
What is cholelithiasis? What are the 3 types?
1) stones in gallbladder
2) Cholesterol stones - associated with obesity, DM, hyperlipidemia
3) Pigmented Stones - associated with hemolysis, alcoholic cirrhosis, or biliary tract infection
4) Mixed stones - most common
What are the clinical features of cholelithiasis (4)? What are the complications (4)? How is cholelithiasis diagnosed and what is the treatment?
1) Clinical: may be assymptomatic, RUQ/epigastric pain, pain after meals (biliary colic), Boas sign (subscapular pain)
2) Complications: cholecystitis, choledocholithiasis, gallstone ileus, malignancy
3) Dx - U/S, CT/MRI
4) Tx - none if asymptomatic, otherwise elective cholecystecomty
What are the clinical features of acute cholecystitis (6)? How is it diagnosed (3)? How is it treated (2)?
1) Clinical: constant pain in RUQ/epigastrium with radiation to shoulder, N/V+anorexia, RUQ tenderness with guarding, Murphy sign, hypoactive bowel sounds, fever and leukocytosis
2) Dx: U/S, CT, HIDA
3) Treatment:
a) conservative - NPO, IV fluids, analgesics, IV Abx
b) Cholecystectomy
What is acalculous cholecystitis? How is it treated?
1) Cholecystitis with out stone
2) Emergent cholecystectomy
What is choledocholithiasis? What are the types (2)? What are the clinical features (2)? What is seen on lab work (2)? How is it diagnosed? How is it treated?
1) Stone in CBD
2) Primary or secondary
3) High ALP and billis (direct)
4) ERCP
5) ERCP with sphincterotomy or stone extraction
With respect to cholangitis, what is Charcot’s triad? What is Reynolds pentad? How is cholangitis diagnosed (3)? What is the appropriate treatment (2)?
1) Charcot’s - RUQ pain, jaundice, fever
2) Reynolds - Charcot + shock and altered LOC
3) Dx - U/S, ERCP, labs - high billi, leukos, LEs
4) Tx - IV fluids and Abx until stable, ERCP decompression
What is Primary Sclerosis Cholangitis? What disease is it associated with? What are the clinical features (3)? How is it diagnosed? What is the treatment?
1) Idiopathic disease of intra or extra-hepatic bile ducts with associated wall thickening, leading to cirrhosis, portal HTN, liver failure
2) UC
3) jaundice, pruritis, high cholestatic LEs
4) ERCP - bead-like dilatations
5) Liver transplant
What is Primary Biliary Cirrhosis? What are the clinical features (5)? What is detected on labs (4)? How is it diagnosed? How is it treated (3)?
1) Autoimmune destruction of intra-hepatic bile ducts
2) Clinical: Pruritis, jaundice, RUQ pain, xanthomas, portal HTN
3) Labs: high ALP+GGT, positive AMAs, high cholesterol, high IgM
4) Dx: liver biopsy
4) Tx: Cholestyramine and ursodeoxycholic acid, liver transplant
What is biliary dyskinesia? How is it diagnosed? How is it treated?
1) motor dysfunction at sphincter of Oddi leading to biliary colic without gallstone
2) HIDA scan shows incomplete emptying from gallbladder of radionuclide
3) ERCP sphincterotomy
What are the main causes of appendicitis (2)? What are the clinical features (7)? How is it diagnosed (3)? How is it treated?
1) Obstruction of lumen due to hyperplastic lymph tissue or fecalith
2) Clinical: RLQ pain with guarding and rebound, N/V, anorexia (always), fever, positive: rovsign, obturator, psoas signs.
3) Dx - clinical Dx, supported by labs, CT if unsure
4) Tx - appendectomy
What are the 3 main causes of acute pancreatitis? What are the clinical feature of pancreatitis (5)?
1) gall stone, alcohol, post-ercp
2) Clinical: Steady and dull epigastric pain that radiates to back, N/V, anorexia, decreased bowel sounds. If hemorrhagic - Grey Turner, Cullen, and Fox signs
Describe the Ranson criteria used to determine the prognosis of acute pancreatitis on admission (GA LAW) and after 48 hours (CHOBBS)
1) GALAW
a) glucose > 200, Age > 54, LDH > 350, AST > 250, WBC > 16,000
2) CHOBBS
a) calcium under 8, hematocrit drop > 10%, PaO2 under 60, BUN increase > 8, Base deficit > 4, fluid sequestration >6L
How is acute pancreatitis diagnosed (3)?
1) Labs - high amylase and lipase
2) CT - most sensitive
3) ERCP - useful for gallstone pancreatitis and Tx
How is acute pancreatitis treated (hint: dependent on severity) (2)?
1) Mild - NPO, IV fluids, analgesia, NG tube
2) Severe - ICU admission, 72hr enteral feed with NJ tube
What is the most common cause of chronic pancreatitis? What are the clinical features (4)? What are some complications (6)? How is it treated (2)?
1) Alcoholism
2) Clinical: constant abdo pain, N/V, wt loss due to malabsorption
3) Complications: Steatorrhea, pseudocyst, CBD obstruction, DM, Effusions, carcinoma
4) Tx:
a) Non-Op: analgesia, NPO, pancreatic enzymes and H2 blocker, insulin, alcohol abstinence, small-meals
b) Op: pancreaticojejunostomy, Whipple
What are the clinical features (6) of pancreatic cancer? How is it diagnosed ()? How is it treated ()?
1) Clinical: Abdo pain, jaundice, wt loss, DM, migratory thrombophlebitis, Courvoisier sign (palpable gallbladder)
2) Dx: CT, ERCP, tumor markers Ca 19-9 and CEA
3) Tx: Whipple if resectable, stent if not resectable
Provide a DDx for upper GI bleed (8)
1) PUD
2) Reflux Esophagitis
3) Esophageal/Gastric varices
4) Gastric erosions
5) Mallory-Weiss tear
6) Hemobilia
7) Aortoenteric fistula
8) Neoplasm
Provide a DDx for lower GI bleed (8)
1) Diverticulosis
2) Angiodysplasia
3) IBD
4) Colorectal carcinoma
5) Colorectal adenomatous polyps
6) Ischemic colitis
7) Hemorrhoids
8) Anal fissures
Match the clinical signs of hematemesis, coffee ground emesis, melena, hematochezia, and occult blood in stool with either Upper GI bleed, Lower GI bleed, or both. Comment on the rate of bleeding if appropriate.
1) Hematemesis - Upper
2) Coffee Ground Emesis - Upper, lower rate
3) Melena - Upper (90%). May be from jejunum, ileum, or right colon
4) Hematochezia - Lower, or massive Upper
5) Occult blood - Lower or Upper
With respect to melena, what other sources can cause dark stool and must be considered on the DDx (5)?
Bismuth, carcoal, licorice, iron, spinach
What laboratory value is elevated in an Upper GI bleed?
BUN-Cr ratio (urea-creatinine).
What are the indications to proceed with surgery on a GI bleed (5)?
1) Hemodynamically unstable non-reponsive to fluid, transfusion, or endoscopic intervention
2) Recurrence of bleed after endoscopic treatment
3) Continued bleed >24 hours
4) Visible vessel at base of ulcer
5) Ongoing transfusion requirement
What are the two types of esophageal cancer? Comment on their prevalence, risk factors, and typical location in the esophagus.
1) SCC
a) prev: 50% of cases
b) RF: Etoh, smoking
c) location: upper and mid esophagus
2) Adenocarcinoma
a) prev: 50% of cases
b) RF: GERD, Barrett’s
c) location: lower esophagus
What are common clinical features of esophageal cancer (8)?
Dysphagia (solids, then liquid), Wt loss, anorexia, odynophagia, hematemesis, aspiration pneumonia, fistula formation, chest pain
How is esophageal cancer diagnosed (3)? What is the appropriate treatment (3)?
Dx - upper endo with biopsy, transesophageal U/S for local staging, CT for met work-up
Tx - Palliation, surgery if stage 2A or less, neo-adjuvant chemo/rad for surgical candidates
Describe achalasia, what are the clinical features of the disease (5)?
- LES failure to relax, abnormal peristalsis of esophageal body
1) Dysphagia (liquids and solids)
2) Regurgitation
3) Chest Pain
4) Wt loss
5) Pulmonary complications due to aspiration
How is achalasia diagnosed (3)? How is it treated (5)?
Dx: a) Barium swallow - bird's beak finding b) Upper GI endoscopy - r/o other causes c) Manometry - confirms Dx Tx: a) Adaptive measures (chew food) b) Meds - antimuscarinic, long-acting nitrates, CCB c) Botulinum toxin injection d) Forceful dilatation e) Surgical myotomy
What are the general characteristic of Diffuse esophageal spasm(2), what are the clinical features (2), how is it diagnosed (2), and how is it treated (3)?
1) Character: spontaneous contraction of esophageal body, sphincter function is normal
2) Clinical: noncardiac chest pain, dysphagia
3) Dx: manometry, barium swallow
4) Tx: Nitrates, CCB, TCAs
Describe the character, clinical features (5), diagnosis, and treatment (3) of a type 1 hiatal hernia
1) Character: GE junction and stomach herniate into thorax
2) CF: heartburn, dysphagia, chest pain, GERD, Barrett’s
3) Dx: Endoscopy
4) Tx: Medical (PPI, antacid), Nissen fundoplication
Describe the character, clinical features (5), diagnosis, and treatment of a type 1 hiatal hernia
1) Character: Only stomach herniates into thorax
2) CF: heartburn, dysphagia, chest pain, incarceration, obstruction
3) Dx: Endoscopy
4) Tx: Elective surgery
Differentiate a Mallory-Weiss tear from Boerhaave syndrome. What is associated with M-W tears? How is it treated (2)?
1) M-W: mucosal tear at or near GEJ. B-S: transmural involvement (perforation).
2) Bringe drinking and vomitus
3) 90% self-resolve, surgery
Provide the location and cause for the following exophageal diverticuli: Zenker, Traction, Epiphrenic. What is the treatment for Zenker and Epiphrenic?
1) Zenker - Upper third, criocopharyngeal muscle dysfunction, surgery (myotomy)
2) Traction - Middle third, due to inflammatory process of mediastinum
3) Epiphrenic - Lower third, due to esophagea dysmotility (achalasia), surgery (esophagomyotomy)
What are the common causes of peptic ulcer disease (4)? What are the common clinical features (5)? How is it diagnosed (4)?
1) Causes: H. Pylori, NSAIDs, Zollinger-Ellison, smoking/EtOH/coffee/stress
2) Clinical: epigastric pain, GI bleed, N/V, early satiety, wt loss
3) Dx: Endoscopy (biopsy), Urea breath test, Serology for H. Pylori antibody (does not confirm active infection), Serum gastrin for Zollinger-Ellison
Describe the management of PUD (4).
1) Directives - stop NSAID, stop coffee/EtOH/smoking, no nocturnal eating
2) Acid suppression - H2RB, PPI, antacid
3) Eradicate H. pylori - triple or quad therapy
4) Cytoprotection - Misoprostol
Describe triple and quadruple therapy for H. Pylori eradication in PUD. When is either used?
1) Triple - PPI, amoxicillin, clarithromycin
2) Quad - PPI, Bismuth subsalicylate, metronidazole, tetracycline.
- Use triple in first infection, quad in recurrence
Comment on the pathogenesis, H. pylori prevalence, malignant potential, location, age distribution, associated blood type, and risk factors for duodenal ulcers.
1) Pathogenesis - increased acid into duodenum
2) H.Pylori - 70-90%
3) Malignant potential - low
4) Location - 1-2cm distal to pylorus
5) Age - less than 40
6) Blood type - O
7) RF: NSAIDs
Comment on the pathogenesis, H. pylori prevalence, malignant potential, location, age distribution, associated blood type, and risk factors for gastric ulcers
1) Pathogenesis - decreased GI defense
2) H.Pylori - 60-70%
3) Malignant potential - high
4) Location - 4 locations
5) Age - >40
6) Blood type - A
7) RF: Smoking
What is the most common cause of gastritis? What is concerning with respect to long term outcomes? How is it treated?
1) H. Pylori
2) Risk of gastric cancer and MALT
3) Tx - if symptomatic, H. pylori eradication (Triple, Quad therapy)
What are the three characteristics to consider when investigating a suspected small bowel obstruction? What are the main clinical features (5)?
1) Partial vs. Complete - pass gas?
2) Closed loop vs Open loop
3) Proximal vs Distal - level of distension on CXR, amount of vomiting clinically
4) Clinical: Dehydration (hypochloremic, hypokalemic metabolic acidosis), abdo pain, N/V, Obstipation, abdo distension
How are small bowel obstruction treated (4)?
1) Conservative (if no peritoneal signs)
a) IV fluids to correct electrolyte imbalance
b) NG tube for decompression
c) Abx
2) If peritoneal signs present - surgery
What is seen on AXR of a paralytic ileus? How is it treated (4)?
- Gas throughout small and large bowel
1) Tx: IV fluids, NPO, NG tube, decompress if necessary.
What are the clinic signs of celiac sprue (4)? What are the complications (3)? What is the associated dermatologic condition? How is it diagnosed?
1) Clinical: diarrhea, wt loss, bloating, fatigue
2) Complications: Low vit D (Osteo), K (clot), B12 (p.anemia)
3) Dermatitis herpetiformis
4) Dx: biopsy of small bowel shows flattening of villi.
What are the major characteristics of Crohn’s disease (6)?
1) Terminal ileum typically (terminal ileum > small intestine > colon > mouth/esophagus/stomach)
2) skip lesions
3) Transmural
4) Fistulae
5) Noncaseating granulomas
6) Luminal strictures
What are the clinical features of Crohn’s disease (5)? Provide some common extra-intestinal manifestations (5)?
1) Diarrhea (non-bloody), wt loss, abdo pain, fever, extra-intestinal manifestations
2) EIM: episcleritis, uveitis, erythema nodosum, pyoderma gangrenosum, monarticular arthritis, ank spond, VTE, ITP, OA, gallstones
How is Crohn’s treated (7)?
1) Medical:
a) Sulfasalazine (5-ASA) - PG blocker
b) Metronidazole
c) Systemic corticosteroid
d) Immunosuppressant - azathioprine
e) Bile acid sequestration
2) Surgical - for complications, high recurrence
3) Nutritional supplementation
What are the general characteristics of ulcerative colitis (5)?
1) involves mucosa and submucosa only
2) Always involves rectum
3) Small bowel typically spared
4) No skip lesions
5) PMNs accumulate in crypts of colon
What are the clinical features of ulcerative colitis (6)?
1) Hematochezia
2) Abdo pain
3) frequent, small BMs
4) F, wt loss
5) Tenesmus
6) Extaintestinal symptoms
What are some common complications of UC (5)?
1) Iron def anemia
2) Hemorrhage
3) Electrolyte disturbance
4) Strictures
5) CRC
6) Sclerosing cholangitis
7) Toxic megacolon
8) Growth retardation
How is UC treated ()?
1) Acute flare - systemic corticosteroids
2) Sulfasalazine - 5-ASA (anti-inflammatory)
3) Immune suppression agents
4) Surgical - colectomy (curative)
