GI Step 2

What is the pathology behind liver cirrhosis and what are the causes of it? How will it manifest?

Liver fibrosis and areas of necrosis Caused by: Alcoholism, HBV, HCV, hemochromatosis, primary biliary sclerosis, primary sclerosing cholangitis, chronic bile duct obstruction, a-1 antitrypsin deficiency, NASH) Manifests initially with weakness, weight loss. Progresses to GI bleeding, varicosities, hepatosplenomegaly, ascites, peripheral edema and jaundice. Advanced disease manifests as mental status change, asterixis (flapping), testicular atrophy , gynecomastia, spider telangiectasieas (increased estrogen), palmar erythema, digital clubbing, and Dupuytren contractures Labs will show increased AST, ALT, GGT, ALP, PT, and decreased albumin, platelets, and anemia

What are the various types of gastric cancer and what is the prognosis associated with them?

Squamous cell carcinoma (rare) Adenocarcinoma (common) a. Ulcerating b. Polypoid c. Superficial spreading - good prognosis; mucosal and submucosal layers only d. Linitis plastica - poor prognosis; all layers involved

Which bacteria cause vomiting as the primary symptom of bacterial gastroenteritis?

Staph aureus (mayonaisse, custard, room-temperature food) Bacillus cereus (rice)

What are the screening guidelines for colon cancer patients?

Start at 50: 1. Colonoscopy, if normal, then every 10 years (takes 10 years for a polyp to become cancerous) 2. Another option is to do flexibly sigmoidoscopy every 5 years in addition to fecal occult blood test 3. Another option is to do annual fecal occult blood test

How do you treat anal fissures?

Stool softener and topical nitroglycerin If they're recurrent, then consider partial sphincterotomy

Highlights of cryptosporidium

Immunocompromised patients present with very watery diarrhea Can see acid-fast stain in stool Treat with nitazoxanide

Ranson criteria

Increased mortality if 3 or more of the following Upon Admission (GA LAW) Glucose > 200 AST > 250 LDH > 350 Age > 55 WBC > 16000 48 hours after admission (Calvin and HOBBeS) Calcium < 8 Hematocrit decreased > 10% O2 < 60 mmHg BUN increases > 5 Base deficit > 4 Sequestration > 6 L

Who tends to get volvulus and how do you diagnose it? How do you treat it?

Infants and elderly get volvulus Diagnosed two ways: 1. Double Bubble on AXR 2. Bird's beak on barium enema Treat by colonoscopic decompression, and if that doesn't work you have to do surgery

What is acute gastritis, how do you diagnose it and how do you treat it?

Inflammation of the gastric mucosa caused by NSAIDS, alcohol, stress, or corrosive materials It can occur ANYWHERE in the stomach Treat by d/c'ing alcohol use or problem medications. Also give PPI or H2-antagonist

Highlights of juvenile polyposis

Polyps form throughout the GI tract that frequently cause bleeding, but only slightly increase risk for colon cancer

What is the primary cause of achalasia? Secondary causes? How do you treat it?

Primary cause is the idiopathic tight lower esophageal sphincter with impaired peristalsis Secondary causes are Chaga's disease, cancer, and scleroderma Treat with balloon dilation (pneumatic dilation), myotomy, or botulinum injection. Could be treated with nitrates/Ca channel blockers but those have side effects on the heart

How do you treat Whipple's disease and what are the complications of the disease?

Treat with Bactrim or Ceftriaxone for 12 MONTHS Actually has a very high mortality if untreated

HepE: what type of virus? How do you get it? How do you treat it? What are the complications?

Calicivirus Get it from water (fecal-oral) Treatment is self-limited Can cause MATERNAL mortality in pregnancy

If you suspect a malabsorption syndrome, how do you proceed to find the diagnosis?

1. 48-72 hr stool collection with Sudan stain (sudan stain confirms steatorrhea) 2. If Sudan stain is positive, perform a D-xylose test (monosaccaride) a. If D-xylose is not found in stool, then it's probably PANCREATIC insufficiency b. If D-xylose is found in the stool, then check for Sprue, Whipple disease, or bacterial overgrowth 3. If Sudan stain is negative, then check the stool pH a. If stool pH is low, then it is a LACTASE deficiency b. If stool pH is normal, then move to the next step 4. Schilling Test (1st stage is giving oral Vitamin B12 to see if it is absorbed; 2nd stage is giving oral Vitamin B12 AND intrinsic factor a. Therefore, if you have an abnormal 1st stage and a normal 2nd stage, you have pernicious anemia b. Whereas if both stages are abnormal, then you have an problem with the ileum or simple bacterial overgrowth

What are the two different types of chronic gastritis and how does their management differ?

1. Chronic Gastritis Type A a. Occurs in the fundus b. Result of autoimmune antibodies against parietal cells c. Therefore, patient will also have pernicious anemia and a decreased gastric acid level d. Treat by replacing Vitamin B12 2. Chronic Gastritis Type B a. Occurs in the antrum b. Most commonly caused by H. pylori infection c. Increased gastric acid levels, and increased risk for ulcers and cancer d. Treat with triple therapy (PPI, clarithro, amoxicillin/metronidazole) to eradicate H. pylori

If a patient has ascites and you perform paracentesis, what does the make-up of the ascitic fluid tell you about the etiology of disease?

1. Cirrhosis - Protein <2.5, WBC < 300, normal glucose, and decreased amylase 2. Spontaneous bacterial peritonitis - PMN > 250, Protein > 1, Glucose < 50, LDH>serum LDH 3. Neoplasm - Very high albumin, LDH = 60% of serum LDH 4. Portal hypertension - Serum albumin:Ascites albumin>1.1

What does the biopsy look like on a patient with alcoholic liver disease? How do you treat it?

1. Fatty liver 2. Areas of necrosis 3. Lots of PMN's Treat with: 1. Alcohol cessation 2. Increased caloric intake, especially thiamine and folate 3. If they remain sober, liver transplantation

How do you treat a GI bleed?

1. Fluid replacement 2. Locate source of bleeding a. Small bleed - usually heals on own b. Upper GI - PPI c. Cirrhosis - antibiotics and b-blockers d. Varices - sclerotherapy e. AVM's/diverticula - vasopressin f. Surgery might be indicated if severe

How do you treat pancreatitis and what are the complications associated with it?

1. IV fluids 2. NPO 3. Drop NG tube 4. Pain control with opiods 5. Surgery may be required for necrosis/chronic pancreatitis Complications include: 1. Pseudocyst 2. Abscess 3. Necrosis 4. Fistula 5. Renal failure 6. Shock/DIC/Sepsis 7.Respiratory failure 8. Pancreatic cancer (chronic pancreatitis)

Explain the progression of liver disease in alcoholism. What labs will be increased and why?

1. Initially there are fatty deposits in the liver. At this point it is reversible with alcohol cessation 2. Next comes hepatic inflammation with some early areas of necrosis 3. Continued inflammation leads to fibrosis and more areas of necrosis (definition of cirrhosis) Labs: Increased AST, ALT, GGT, total bili, alkaline phosphatase, PT (decreased factor VII production), and increased WBC This can all lead to cirrhosis, hepatic encephalopathy, and coagulation disorders

Explain the pathophysiology of hepatorenal syndrome

1. Liver disease causes Portal HTN 2. Portal HTN leads to splanchnic release of NO, which causes SYSTEMIC VASODILATION 3. Vasodilation leads to renal hypoperfusion and pre-renal failure 4. This will manifest by increased creatinine and decreased urine sodium (<10)

What are the main causes of neonatal jaundice? Complications?

1. Physiologic - low activity of UGT initially leads to jaundice and should clear in 1-2 weeks a. Could also be breastfeeding failure 2. Hemolytic - ABO incompatibility, G6PD deficiency, or other RBC abnormalities 3. Hepatic - Gilbert's, Crigler-Najjar, biliary atresia (>15 indirect bili, >2 direct bili) Most costly complication is Kernicterus, which is bilirubin deposits in basal ganglia and hippocampus which can cause permanent damage. Therefore when levels are high, we treat with phototherapy, and if that doesn't work we'll perform exchange transfusion

What is the Charcot triad and what should you do if you see it?

1. RUQ pain 2. Jaundice 3. Fever Suspect cholangitis and perform US or HIDA scan

What are the two types of hiatal hernia and how do you treat them?

1. Sliding (95%) - Gastroesophageal junction and portion of stomach slide up through the diaphragm a. Generally just treat symptoms of GERD 2. Paraesophageal (5%) - stomach protrudes through diaphragm, but gastroesophageal junction remains below diaphragm b. Requires surgical repair because of risk of stomach incarceration T

What are the 2 types of esophageal cancer? Tell me the highlights and the treatment?

1. Squamous cell carcinoma - most commone worldwide 2. Adenocarcinoma - most common in the US; obesity is a risk factor Treat both with surgery +- chemo and radiation Both of them carry a poor prognosis because of local extension and metastasis

How do you treat liver cirrhosis and what are the complications?

1. Stop offending agent 2. Treat varices with b-blockers/sclerotherapy 3. Lactulose and Rifaximin for hepatic encephalopathy Complications include: 1. Hepatic encephalopathy 2. Portal HTN 3. Varices 4. Spontaneous bacterial peritonitis 5. Renal failure

How do you treat colon cancer?

1. Surgical resection + lymph node dissection 2. If a lymph node is positive, then adjuvant chemotherapy

What is the proper treatment of GERD?

1. Weight loss, diet modification, elevate head of bed 2. Antacids 3. If Antacids don't work, then H2 antagonist or PPI 4. If recurrent, then Nissen fundoplication or hiatal hernia repair

How do you treat pancreatic cancer and what are the complications associated with it?

1. Whipple (removal of pancreatic head, duodenum, distal stomach, proximal jejunum, common bile duct, and gallbladder) - this is indicated for cancer in the pancreatic head that hasn't metastasized 2. Adjuvant chemo Very poor prognosis (<2% 5-year survival), even with a successful Whipple (20-30%). Another complication is migratory thrombophlebitis (Trousseau syndrome)

What are the types of endocrine pancreatic cancers? How do they present and how do you treat them?

1. Zollinger-Ellison a. Gastrin-secreting tumor b. Presents as refractory PUD 2. Insulinoma - b-islet cell cancer a. Whipple triad - hypoglycemia, hypoglycemia symptoms while fasting, and carbo loading improves symptoms) b. increased fasting insulin with high C-peptide 3. Glucagonoma - a-islet cell cancer a. Refractory DM, glucagon > 500 b. Diarrhea, weight loss, mental status change, MIGRATORY NECROLYTIC ERYTHEMA c. Worst prognosis 4. VIPoma - non-B-islet cell cancer a. Watery diarrhea, weakness Treat all of them with: 1. Surgical resection 2. Octreotide, chemo, embolization for metastatic

What is Hemolytic Uremic Syndrome, what causes it, and how do you treat it?

A triad of acute kidney injury, hemolytic anemia, and thrombocytopenia Can be caused by E.coli O157:H7 and Shigella Treat by close observation, as it is usually self-limited

Pathogenesis, presentation, and treatment of Wilson's disease

AR disease that results in abnormal COPPER SECRETION. It localizes in the: 1. Liver 2. Brain 3. Cornea Patient presents with personality changes, ataxia, dysphagia (brain), jaundice, tremor, hepatomegaly (liver) and Kayser-Fleischer rings (cornea) Labs will show decreased ceruloplasmin (copper-carrying protein in blood) and increased urinary copper Treat with: 1. Trientine or penicillamine for copper chelation 2. Zinc for maintenance therapy 3. Dietary copper restriction (no organs, shellfish, chocolate, nuts, mushrooms) 4. Vitamin B6

Pathogenesis, presentation, and treatment of hemochromatosis

AR disease with increased iron absorption in the gut. The iron deposits in the: 1. Liver 2. Pancreas 3. Heart 4. Pituitary Therefore it presents with symptoms of CHF and DM, a bronze skin pigmentation (bronze diabetes), arthralgias, hepatomegaly, impotence and testicular atrophy (hypopituitarism) Treat with Regular phlebotomy (initially weekly until levels are normal, and then monthly). Have the patient avoid alcohol, and if they have a lot of iron you can chelate with deferoxamine

Explain the pathophysiology behind primary biliary sclerosis. How do you treat it?

AUTOIMMUNE disease that causes INTRAHEPATIC bile duct obstruction. This leads to an accumulation of bile acids, cholesterol, and bilirubin in the liver and blood. Since it is autoimmune, it is related to Sjogren's, RA, scleroderma, and is more common in women. It will have positive ANTIMITOCHONDRIAL ANTIBODIES Treat with ursodeoxycholic acid. You can add colchicine or methotrexate in more severe disease, and it may require a liver transplant

What are the common causes of acute and chronic pancreatitis?

Acute - BAD HITS Biliary obstruction (gallstones) Alcohol Drugs Hypercalcemia/hypertriglyceridemia Idiopathic Trauma Scorpions Chronic - Alcohol or congenital defect

When does bacterial gastroenteritis need to be treated with antibiotics? Which ones do you use?

Campylobacter can be treated with erythromycin Clostridium botulinum with botulism antitoxin C. dif with metronidazole and/or vancomycin Shigella can be treated with ciprofloxacin or Bactrim Vibrio cholera is treated with tetracycline or doxycycline

Highlights of Ulcerative Colitis

Autoimmune disease that starts in the rectum and works it's way up Isn't transmural erosion, but it does present with BLOODY diarrhea. Therefore the patient can present with orthostatic hypotension and tachycardia Associations include pyoderma gangrenosum (nasty ulcerated lesions on the legs), uveitis, ankylosing spondylitis, and primary sclerosing cholangitis Diagnose with p-anca (usually positive), lead pipe colon without haustra Signficantly increased risk of COLON CANCER Treat with mesalamine, steroids, immunosuppressives, TOTAL COLECTOMY is curative

Give me the highlights of celiac sprue

Autoimmune disorder (antiendomysial and antigliadin antibodies) Associated with Down Syndrome and Dermatitis Herpetiformis Primarily causes JEJUNAL damage

If a patient presents with dysphagia, what are the two diagnostic tests and which should you do first?

Barium Swallow and EGD Do barium swallow first because it is less invasive and carries less risk.

What drugs are used to protect the gastric mucosa in the presence of an ulcer?

Bismuth subsalicylate Sucralfate Misoprostol

Which bacteria cause bloody diarrhea as the primary symptom of bacterial gastroenteritis?

Campylobacter jejuni (poultry) E.coli O157:H7 (beef) Salmonella (MOST COMMON FOODBOURNE; eggs, milk, poultry, fresh produce) Shigella (food/water) Yersinia enterocolitica (pork and fresh produce)

What medications are antacids and what are the side effects?

Calcium carbonate - can cause constipation (3 C's) Aluminum hydroxide - Magnesium - can cause diarrhea

What labs do you look for to help diagnose stomach cancer?

CEA (carcinoembryonic antigen) Elevated 2-glucuronidase in gastric secretions

What are the roles of CXR, Barium swallow, and EGD in the diagnosis of Peptic Ulcer Disease?

CXR - used to rule out perforation Barium swallow - The barium will form pockets of collection in the area of an ulcer a. Also can help diagnose a malignant lesion associated with an ulcer. Findings will include a mass near the ulcer, irregular filling in the base of an ulcer, and abnormal mucosal folds EGD - used to detect active bleeding and perform biopsies a. If patient has symptoms > 2 month, are >40 years old, and/or have had previous ulcers need to have an EGD to rule out adenocarcinoma

What is a carcinoid tumor and how does the patient present? What will the labs show and how do you treat it?

Carcinoid tumor is a cancer of neuroECTODERMAL cells (APUD cells - amine precursor uptake and decarboxylation cells) Commonly arises in appendix, rectum ileum, or bronchopulmonary tree Usually they are asymptomatic or have belly pain, however once it metastasizes to the liver they will experience a carcinoid SYNDROME (flushing, diarrhea, bronchoconstriction) caused by release of serotonin Diagnose by urine 5-HIAA levels and CT scan Treat with resection if < 2 cm, tumors > 2 cm with surgery and IFN-alpha and octreotide

Differentiate between a small bowel obstruction and a large bowel obstruction

Cause: SBO - adhesions, hernias LBO - cancer AXR: SBO - ladderlike loops of dilated bowel LBO - HUGE distention of bowel Treatment: (both require surgery if unsuccessful) SBO - NPO, IV fluids, NG tube LBO - NPO, IV fluids, colonoscopy

Differentiate cholelithiasis, cholecystitis, and cholangitis

Cholelithiasis - gallstone in the gallbladder that can obstruct the cystic duct Cholecystitis - inflammation of GALLBLADDER, most commonly caused by obstruction of the cystic duct a. increased WBC, increased bilirubin Cholangitis - infection of the BILE DUCTS caused by duct obstruction (more severe) a. increased WBC, bilirubin, alkaline phosphatase, AST and ALT, increased amylase if pancreatic obstruction, and POSITIVE BLOOD CULTURES Treat cholecystitis and cholangitis with IV fluids, antibiotics, and cholecystecomy. Severe cholangitis may require emergency bile duct compression before patient is stable enough to perform cholecystectomy

What medications are H2 antagonists, how do they work, and what are the side effects?

Cimetidine, ranitidine They block H2 receptors, which inhibit downstream release of gastric acid These can cause headache, diarrhea, and thrombocytopenia (rare) Cimetidine can cause gynecomastia and impotence

How do you classify/stage colon cancer?

Class A (stage I) - The tumor is localized to the bowel wall Class B (stage II) - Local spread to serosa/pericolic fat Class C (stage III) - Lymph node involvement Class D (stage IV) - Distant metastases (primarily liver and lung)

How do you diagnose zollinger-ellison syndrome? Once it is diagnosed, how do you treat it?

Diagnose one of many ways: 1. Increased fasting gastrin 2. Positive secretin-stimulation test a. When you give secretin, you find an abnormally high amount of gastrin 3. Gastrin sampling in several pancreatic/abdominal veins can help localize the tumor 4. SPECT (single photon emission computed tomography) localizes the tumor by finding somatostatin receptors Treat with: 1. Surgical resection 2. PPI and H2 ease symptoms 3. Octreotide in metastatic disease (palliative measure)

If an AXR shows a calcified gallbladder, what is on your differential and what will you do next?

Differential: 1. Chronic cholecystitis 2. Gallbladder cancer (10-30%) Perform a cholecystectomy to confirm diagnosis. This is important because gallbladder cancer has a poor prognosis, and it will involve resection of part of liver, adjuvant chemotherapy and radiotherapy

Highlights of Crohn's disease

Disordered response to intestinal bacteria Lesions located ALL OVER the GI tract with TRANSMURAL thickness Since it's transmural, there is an increased risk of fistula's, abscesses, fissures, etc. COBBLESTONING on colonoscopy Primarily watery diarrhea Associations include kidney stones, erythema nodosum, arthritis, ankylosing spondylitis, uveitis, and primary biliary chonlangitis Treat with mesalamine, corticosteroids, and immunosupressives

What will the labs look like in a person with Hepatitis?

Elevated AST and ALT Increased Total Bilirubin Increased Alkaline phosphatase If it is Hep C, then you'll see anti-HCV antibodies and positive HCV polymerase chain reaction

What exactly is ileus and what causes it? How do you treat it?

Ileus is an obstruction of the bowel due to paralysis (not a mechanical obstruction Commonly caused by recent surgery, but can also be caused by infection, ischemia, opiod use, and DM You treat it by stopping opiods, making patient NPO, then decompressing the obstruction via colonoscopy

What is Necrotizing enterocolotis, what are the risk factors, how does it present, and how do you treat it?

Idiopathic necrosis of the gut mucosa Risks are preterm birth or low birth weight Presents with vomiting, abdominal distention, hematochezia, diarrhea, and poor feeding Treat with TPN, IV broad spectrum antibiotics, NG suction and surgical resection of necrotic bowel

Highlights of Turcot syndrome

FAP + CNS tumors Autosomal recessive, whereas all the others (FAP, HNPCC, Gardner) are autosomal dominant

Highlights of Gardner syndrome

FAP + bone/soft tissue tumors

HepC: what type of virus? How do you get it? How do you treat it? What are the complications?

Flavivirus (SS RNA) Primarily through blood, could also be sexual contact Treat with IFN-alpha and possibly ribavarin Chronic hepatitis (80%), cirrhosis (50%), increased risk of HCC

How do you treat diverticulitis?

If it's early and mild - antibiotics and bowel rest Advanced and/or perforation: surgical removal of necrotic bowel and closure of perforation plus broad-spectrum antibiotics. Patients often require a diverting colostomy

How does the location of gastric carcinoma influence the treatment?

If it's in the lower third (antrum area), then you can perform subtotal gastrectomy If it's in the middle or upper third, then you have to perform a total gastrectomy

HepB: what type of virus? How do you get it? How do you treat it? What are the complications?

Hepadnavirus (DNA) Primarily through sexual contact, but also through blood Treat with IFN-alpha and/or antivirals (lamivudine) Can develop chronic hepatitis (5%), HCC (3-5%), fulminant hepatic failure (1%)

Highlights of HNPCC

Hereditary Non-Polyposis Colorectal Cancer, therefore it is a cancer that arises from normal colonic mucosa, not polyps It also predisposes patients to other types of cancer, notable endometrial cancer

What is the most common cause of bowel obstruction in a child < 2?

Intussusception

What is a pseudocyst and how do you diagnose it?

It is a sac filled with pancreatic enzymes. If a patient who recently had acute pancreatitis presents with a fever and epigastric pain, then suspect it. Diagnosed by increased WBC and aspiration of fluid that shows increased amylase

What will the labs and images look like in a case of ischemic colitis? How do you treat it?

Labs: increased WBC (?) and increased serum lactate Radiology: Barium enema = "thumb printing" or diffuse submucosal changes. CT will show bowel thickening and air within bowel Treat with IV fluids, bowel rest, and removal of necrotic bowel.

What is the most common cause of chronic diarrhea in adults?

Lactase deficiency (lactose not metabolized in the jejunum)

What is diffuse esophageal spasm, how does it present, and how do you treat it?

Like it sounds, spasm of the esophagus without normal peristalsis Therefore the patient will have dysphagia/chest pain, and the barium swallow will show a CORKSCREW pattern Treat with Ca blockers, nitrates, and tricyclic antidepressants to reduce chest pain/dysphagia

What is on your differential for causes of PUD?

Most common: NSAIDS, H.pylori, alcohol, tobacco Less common: 1. Curling ulcer - side-effect of a severe burn 2. Cushing's ulcer - side effect of increased intracranial pressure 3. Zollinger-Ellison syndrome - gastrin-secreting tumor of the duodenum or pancreas

When is antibiotic treatment of bacterial gastroenteritis contraindicated and why?

Most of the time bacterial gastroenteritis is self-limited and antibiotics are not needed However, in the case of E.coli O157:H7, treatment with antibiotics can cause further release of the toxin, making the disease worse, and is therefore contraindicated

What are the 2 main causes of dysphagia and how do you tell the difference between the do from H&P?

Neuromuscular disorder (achalasia, esophageal motility, scleroderma) will have difficulty swallowing solids AND liquids Obstruction disorder (esophageal web, stricture, cancer, radiation) will only have difficulty swallowing solids

What are the common causes of viral gastroenteritis?

Norwalk virus Rotavirus in children Coxsackie A Adenovirus Echovirus Since it is a virus, there will be no fecal WBC's

Highlights of Entamoeba Histolytica

Obtained primarily from water/poor sanitation Causes mild to severe BLOODY diarrhea Treat with metronidazole and paromomycin

HepA: what type of virus? How do you get it? How do you treat it? What are the complications?

Picornavirus (SS RNA) Get from shellfish Self-limited treatment with no severe complications

Highlights of Familial Adenomatous polyposis

Patient gets HUNDREDS of polyps that will turn into cancer almost 100% of the time Therefore it's a good idea for a FAP patient to get a prophylactic colectomy

How does a patient with pancreatitis present and what will you see on labs/imaging?

Patient has pain radiating to the back, nausea, vomiting, fever, tachycardia. a. They may also have bluish discoloration of flank (Grey Turner sign) and/or discoloration of periumbilical region (Cullen sign) Labs: elevated amylase and lipase. If it is chronic pancreatitis, there will only be a mild increase, but fecal elastase will be low AXR: sentinel sign (dilated loop of small bowel near pancreass) or cutoff sign (right colon distention near pancreas) CXR: pleural effusion, hemidiaphragm elevation CT: pseudocyst/enlarged pancreas

Highlights of Peutz-Jeghers syndrome

Patients with polyps in the colon that are HAMARTOMAS (low risk of malignancy) They will also have mucocutaneous discolorations on their mouth, hands, and genitals

Highlights of Taenia solium

Protozoan found in undercooked pork Causes mild diarrhea, but severe CNS symptoms (neurocysticercosis) Treat with praziquantel for intestine, and mebendazole for neurocysticercosis

Highlights of Trichinella spiralis

Protozoan found in undercooked pork Causes myalgias, periorbital edema, and eosinophilia Treat with albendazole Can use mebendazole if they have CNS symptoms

HepD: what type of virus? How do you get it? How do you treat it? What are the complications?

RNA Get it from blood, but it requires a co-existent HepB infection Treat with IFN-alpha Can cause severe hepatitis or cirrhosis

What is the most common presentation of a benign liver mass? What are examples of benign liver masses and how do you treat them?

RUQ fullness in a woman with a history of OCP use Could be hepatic adenoma, hepatic cyst, hemangioma, or focal nodular hyperplasia Don't treat it unless it's large and could cause mass effect

What are the risk factors for hepatocellular carcinoma and how do you confirm diagnosis? How do you treat it and what are the complications?

Risks: HBV, HCV, hemochromatosis, cirrhosis, aflatoxin (Aspergillus)-contaminated food, schistosomiasis Confirm diagnosis with biopsy, but it's usually contraindicated because of high vascularity. Therefore, you perform: 1. CT, MRI, US will show liver mass 2. Labs will show increased ALPHA-FETOPROTEIN Treat with surgical resection and chemotherapy. Poor prognosis because of portal/hepatic vein obstruction and liver failure

What are the risk factors for intussusception and how do you treat it?

Risks: HSP, Meckel's diverticulum, Adenovirus, and cystic fibrosis Treat with barium enema, and if that doesn't work then surgery

What are the risk factors of pancreatic cancer? How does the patient present and how do you diagnose it?

Risks: chronic pancreatitis, smoking, DM, family history, obesity, high-fat diet Patient presents with epigastric pain radiating to back, painless jaundice, non-tender gallbladder (courvoisier sign) classically. Also other non-specific signs Diagnose with biopsy. Indications for biopsy include abnormal mass on CT, increased CA 19-9, bilirubin, and/or alkaline phosphatase. If CT scan can't locate the actual tumor, then ERCP should be able to

What do HNPCC, FAP, Gardner syndrome, and Turcot syndrome all have in common?

They are all caused by mutations of the APC gene on Chromosome 5 (Adenomatous Polyposis Coli gene)

How do PPI's work and what are the side effects?

They block the H/K ATPase, which effectively blocks the release of gastric acid Well-tolerated, but in some patients in increases the effects of warfarin, benzo's, and phenytoin

How do you differentiate between primary biliary sclerosis and primary sclerosing cholangitis?

They both have similar labs (increased alkaline phosphatase, GGT, cholesterol, bilirubin, and normal AST and ALT) and their biopsies appear very similar Therefore you have to take into account these 3 things: 1. Gender (females = primary biliary sclerosis because it is autoimmune) 2. ERCP ("pearls on a string" appearance of primary sclerosing cholangitis) 3. Antimitochondrial antibodies (positive in primary biliary sclerosis)

How does a patient with portal hypertension present and how do you treat it?

They present with varices (hematemesis), ascites, abdominal pain, change in mental status, cirrhosis symptoms, testicular atrophy, and gynecomastia Treat with: 1. Restrict salt and give diuretics 2. Vasopressin/sclerotherapy for varices 3. If renal failure: dialysis 4. Lactulose and Rifaximin 5. IV Abx for bacterial peritonitis 6. TIPS (transjugular intrahepatic portosystemic shunt)

Explain the pathophysiology behind primary sclerosing cholangitis. How do you treat it?

This is destruction of the INTRAHEPATIC and EXTRAHEPATIC bile ducts that leads to fibrosis and cirrhosis. It is commonly associated with Ulcerative Colitis and is more common in men Confirm diagnosis by ERCP, which will show "pearls on a string" appearance of the bile ducts Treat with ursodeoxycholic acid, methotrexate, and corticosteroids. You can also stent the bile duct strictures, and a liver transplant may eventually be necessary

How do you treat a pancreatic pseudocyst and what are the complications?

Treatment: 1. Mild - observe for 6 weeks 2. Initially painful, rapidly growing, or lasting > 6 weeks = drainage (surgery, percutaneous, or endoscopic) Pseudocyst could rupture, form an abscess, or cause a hemorrhage

What is the difference between Crigler-Najjar syndrome type 1 and type 2?

Type 1 = BAD a. Severe deficiency of glucuronosyl-transferase, and therefore indirect bilirubin will be > 5 and there will be persistent jaundice and CNS symptoms (kernicterus) b. Treat with phototherapy, plasmapheresis, and calcium phosphatase + orlistat c. Liver transplant may be necessary Type 2 = MILD a. Phenotypically similar to Gilbert's, but it can require some treatment b. Phenobarbital increased production of glucuronyltransferase and reduces jaundice

Explain the pathophysiology behind portal hypertension and the causes

Venous blood pools in the portal system because of some blockage, and it backs up into the systemic venous system Caused by: 1. Pre-hepatic - Portal vein thrombosis 2. Intra-hepatic - cirrhosis, schistosomiasis, granulomatous disease 3. Post-hepatic - Hepatic vein thrombosis (Budd-Chiari), right-sided heart failure

Which bacteria cause watery diarrhea as the primary symptom of bacterial gastroenteritis?

Vibreo cholera (seafood) Vibreo parahemolyticus (oysters) Clostridium Dificile (antibiotic use) E. coli (ETEC) - traveler's diarrhea

Where are the famous stomach cancer nodes?

Virchow's node - left supraclavicular node Sister Mary Joseph's node - periumbilical node Krukenberg - to the ovary

How do you treat hemorrhoids?

Warm baths, sclerotherapy, ligation, or excision. Always tell the patient to increase their fiber

What is pilonidal disease and how do you treat it?

When you have cutaneous sinus tracts in your butt crack (high up in the butt crack) Usually it's asymptomatic and you don't need to treat it, but if the sinus becomes obstructed and infected, you can I&D it then attempt to close the sinus

If someone with PUD requires NSAID use for a co-morbid condition, how do you treat them?

With a selective COX-2 inhibitor

What is Zenker diverticulum, how do you diagnose it and how do you treat it?

Zenker is an outpouching of the mucosa in the upper esophagus Patient will have bad breath and regurgitation of food, and then you'll see the outpouching on barium swallow. Treat with a diverticulectomy or a cricopharyngeal myotomy