2015 gastroenterology one

1/20/2016

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GASTROENTEROLOGYPart One of Two

Rutgers, The State University of New Jersey

Dipali Yeh, M.S. PA-CRutgers Physician Assistant Program

Certification/Recertification Examination Review Course

June 2015

PANCE/PANRE Review Course

Infectious Esophagitis

• Immunocompromised

• Risks: AIDS/DM/Steroids

• Odynophagia/dysphagia

• CMV/HSV-other clinical features

• Diagnosis: endoscopyDiagnosis: endoscopy– CMV esophagitis: large ulcers

– Herpes: shallow ulcers

– Candida: white plaques

• Treatment: specific to the type of infection– CMV esophagitis: valgancyclovir/foscarnet

– Herpes: acyclovir

– Candida: Amphotericin B


Pill-induced esophagitis

• Offending agents– Tetracycline

– Doxycycline

– KCl

– NSAIDs

P t ti• Presentation– Odynophagia/dysphagia/retrosternal chest pain

– Several hrs-days after ingestion

• Endoscopy: varied findings

• Study of choice: double contrast esophagram

• Treatment: – Prevention

– Remove offending agent

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Radiation Esophagitis

• Presentation– Dysphagia several months following radiation treatment

• Acute >>> Chronic

• Mucosal edema/inflammation>>>impaired peristalsis/motility


Reflux Esophagitis

• Etiology– Lower sphincter fails as barrier to stomach contents

• Predisposing factors– GERD, PUD

– Prolonged vomiting

• Presentation– Heartburn, retrosternal burning

– Radiation into the neck

– Postprandial component

• Findings– Superficial ulcerations

– Distal esophagus

• Definitive diagnostic: endoscopy


Motility Disorders

• Achalasia

• Scleroderma

• Esophageal spasms

• Zenker’s diverticulum

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Achalasia

• Etiology unknown

• Common in adults 30-60 yrs

• Presentation– Gradual dysphagia: solids + liquids

– Cough/choking/aspiration/pneumonia

• Diagnostics– Barium swallow: Bird’s beak

– endoscopy

– Manometry: most sensitive

• Treatment– Pharmacological: Ca+ channel blockers, isosorbide, local LES botox injections

– Surgical: Dilatation, myotomy


Achalasia

http://commons.wikimedia.org/wiki/File%3AAcha.JPGBy Farnoosh Farrokhi, Michael F. Vaezi. [<a href="http://creativecommons.org/licenses/by/2.0">CC‐BY‐2.0</a>], <a href="http://commons.wikimedia.org/wiki/File%3AAcha.JPG">via Wikimedia Commons</a>


Scleroderma

• 90% patients have esophageal involvement

• Part of CREST syndrome

• Clinical: GERD, dysphagia to solids & liquids

• DiagnosisDiagnosis– Barium swallow: aperistalsis

– Manometry: most sensitive; decreased LES tone

• Treatment: proton pump inhibitors– omeprazole (Prilosec), pantoprazole (Protonix)

• Complication: GERD

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Esophageal spasms

• Etiology: not understood; possible nitric oxide deficiency

• Clinical: chest pain/dysphagia

• Diagnosis: “corkscrew” esophagus on bariumDiagnosis: corkscrew esophagus on barium

• Treatment: Ca+ channel blockers, hycosamine, tricyclic antidepressants


Esophageal spasms

http://commons.wikimedia.org/wiki/File%3ADiffuser_Oesophagusspasmus_002‐13.jpgBy Hellerhoff (Own work) [GFDL (http://www.gnu.org/copyleft/fdl.html) or CC‐BY‐3.0 (http://creativecommons.org/licenses/by/3.0)], via Wikimedia Commons


Zenker’s diverticulum

• Outpouching of posterior hypopharynx

• History: esophageal spasms, hiatal hernia

• Older patients/insidious onset

• Clinical: dysphagia/regurgitation/halitosis

• Diagnosis: Barium swallowDiagnosis: Barium swallow

• Asymptomatic = no treatment

• Symptomatic = myotomy/diverticulectomy

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Mallory-Weiss tear

• Tear in the GE junction

• Forceful vomiting/retching

• Clinical feature: hematemesis, self-limiting

• Diagnosis: generally clinically, also endoscope

• Treatment:Treatment: – Most heal w/in 48 hours

– Endoscopic epi/thermal coagulation


Esophageal neoplasms

• General Considerations– 50-70yrs old

– M:F=3:1

– Squamous cell: 95%

– Adenocarcinoma

Risk Factors– Risk Factors• Squamous Cell: tobacco and alcohol abuse

• Adenocarcinoma: Barrett’s, obesity


Esophageal neoplasms

• Clinical features– Dysphagia>solid food + wt loss

– Pneumonia/Voice hoarseness

– Chest pain

• Diagnosisi i i ll b i d– initially-barium study

– definitive-endoscopy

• Treatment: surgery

• Prognosis: 5-yr survival rate < 20%

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Esophageal strictures

• Complication of GERD/Esophagitis

• Clinical presentation– Dysphagia to solid foods over months-years

• Diagnosis-biopsy

• Treatment– Endoscopic dilatation

– Long term PPIs

– Refractory: endoscopic triamcinolone


Esophageal varices

• General considerations– Most common cause of UGIB secondary to portal HTN

• Risk factors ↑ chance of bleeding– Size

– Red wale markings

Li di i– Liver disease severity

– Active ETOH use

• Presentation– High-grade: hematemesis/hypovolemia

– Low-grade: melena + iron-deficiency anemia


Esophageal varices

Treatment• Acute

– Hemodynamic stability: fluids/blood products– Pharmacological

• Octreotide-vasoactive agent• Vitamin K-abnormal PT• Lactulose-encephalopathy• Antibiotic prophylaxis

• Endoscopic• Sclerotherapy• Mechanical tamponade• TIPS procedure

• Mortality– 30% during 1st bleeding episode– 50% within 6 weeks

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Esophageal obstructive entities

• Esophageal Webs– Plummer-Vinson

– Proximal esophagus

– Presentation

• Schatzkiʼs ring– GERD/hiatal hernia

– Distal esophagus

– Presentation• Food impaction

– Barium swallow• shelf

• Food impaction

– Barium swallow• Lower esophageal

narrowing


GERD

• 3 mechanisms– Transient LES relaxation, increased intra-abdominal pressure, spontaneous

reflux

• Risk factors– Alcohol, caffeine, obesity, smoking

Cli i l f t• Clinical features– Heartburn

– Chest pain/halitosis/cough

• Diagnosis: – Ambulatory 24hr pH monitoring: most sensitive/gold standard

– Endoscopy• refractory to secretory therapy

• Alarm symptoms (next slide)

• Long-standing history (Barrett’s)


GERD

• Alarm symptoms– Refractory heartburn

– Dysphagia

– Unintentional Weight loss

– GI bleed/anemia

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Diagnostic testing in Upper GI Pathology

• 1. Endoscopy– Refractory to secretory therapy– Patients with alarm symptoms (next slide)– Chronic reflux – Barrett’s predisposition

• 2 ambulatory pH monitoring• 2. ambulatory pH monitoring– Confirm GERD– GERD sx + negative endoscopy– Refractory to longstanding PPI treatmetn– Refractory to antireflux surgery

• 3. Manometry– peristaltic abnormalities; – Preop antireflux surgery


GERD Treatment options

• Lifestyle/diet modifications: 20% effective– *weight loss

• Three main options– Antacids

• Maalox, mylanta, gaviscon

H2 bl k– H2 blockers• Cimetidine, ranitidine, famotidine, nizatidine

– Proton pump inhibitors• Omeprazole, lansoprazole, pantoprazole, rabeprazole, esomeprazole,

dexlansoprazole

– ..also…Prokinetics (metoclopramide)/Baclofen only after diagnostic eval

• Surgery– Nissen fundoplication

– Stretta procedure

– Endocinch


GERD Treatment approach

• Intermittent/mild symptoms: – Weight loss

– Antacids

– H2blockers twice daily

• Moderate symptoms:O d PPI 8 k h f h i– Once a day PPI x 8 weeks: therapy of choice

– If symptoms continue thereafter, maintenance PPI

– H2 blockers + PPI combination therapy

• Risks associated with PPIs– If (+)osteoporosis, can remain on PPI therapy

– Risk factor for Clostridium difficile

– short term PPIs: CAP

– No need for alteration with clopidogrel (re: adverse cardiovascular events)

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Gastritis

• Atrophic– Risk for gastric CA, pernicious anemia, autoimmune

• Hemorrhagic– ICU/Burn

• Infectious– H. pylori- most common cause

• Presentation– Nondescript abd pain, anorexia, bloating, nausea

• Treatment – Etiology-dependent


Helicobacter pylori• Gram-negative spiral-shaped bacillus

• Clinical presentation: nausea/abdominal pain

• Diagnosis: based on history– Urea breath test (most sensitive)/fecal antigen assay

– Endoscopy-but not for uncomplicated disease


Helicobacter pylori

• Treatment

• combination therapy x 14d– 1st line:

Triple therapy: PPI + amox + clarithromycin

– Quadruple therapy: PPI + bismuth + 2 antibiotics( l ith i + i illi t t li + t id l )• (clarithromycin + amoxicillin, tetracycline + metronidazole)

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PUD

• Break in the mucosa

• Duodenal > gastric

• Risks: smokers/long-term NSAID use

• 2 major causes– Chronic NSAID use

– H pylori infection- most common


PUD

• Clinical features– Hallmark: epigastric pain

– Duodenal: improves with food

– Gastric: worsens with food

• Diagnosis: upper endoscopy

• Treatment– Avoid irritating factors

– Combination therapy

– misoprostol


Gastric neoplasms

• 3 types– Adenocarcinoma: 90-95%

– Lymphoma

– Gastrinoma (Zollinger-Ellison Syndrome)

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Gastric neoplasms

• Adenocarcinoma– 50-70yrs old

– M:F = 2:1

– 5 year survival < 20%

– Risk factors• Genetic: Familial/Blood Group AGenetic: Familial/Blood Group A

• Environmental: H. pylori/smoking/low socioeconomic

• Predispositions: chronic gastritis/pernicious anemia


Gastric neoplasms

• Adenocarcinoma– Clinical features

• Early: can be asymptomatic

• Later: cachexia, dyspepsia, weight loss, GIB

• Virchow’s node

• Sister Mary Joseph nodule

• Krukenberg tumor


Gastric neoplasms

• Adenocarcinoma– Diagnosis

• endoscopy with biopsy– (>55 yrs old w/ new sx/fails antisecretory treatment)

• Malignant ulcer: irregular folds & base

– Treatment• 30% of patients-surgery=curative

• Combination chemo + radiation improves survival

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Gastric neoplasms: Lymphoma

• 95% are non-Hodgkin B cell lymphoma

• Risk factor: H pylori

• Clinical features: same as adenocarcinoma

• Diagnosis: endoscopic biopsy

• Treatment: combination chemotherapy w/without radiationTreatment: combination chemotherapy w/without radiation


Gastric neoplasms: ZES

• Zollinger-Ellison Syndrome (Gastrinoma)

• Refractory PUD

• 1/3 associated with MEN-1

• Clinical features– PUD symptoms refractory to treatmenty p y

– Heartburn 20%

– Secretory diarrhea 60-70%

– Abdominal pain 80%


Gastric neoplasms: ZES

• Diagnosis– Fasting serum gastrin level > 150pg/ml (nl 100)

– pH < 2.0

– SRS w/ SPECT: identifies 60% of gastrinomas

• TreatmentM di l PPI h d f h i– Medical: PPIs are the drug of choice

– Surgical= curative before hepatic spread

– 15-year survival rate=95% w/o hepatic mets at dx

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Cholelithiasis/Cholecystitis

• Majority: cholesterol stones

• Bilirubin stones.think SCD/IBD/Hemolytic anemias

• F>M

• Risk factors– Ageg

– Obesity

– Rapid weight loss

– Insulin resistance

– Family history



• Clinical features– Biliary colic

– Nausea, vomiting

– Murphy’s sign: inhibit inspiration

– Fever

Di i• Diagnosis– Leukocytosis; ↑ LFTs/Amylase/Lipase=pancreatitis

– RUQ sono: (+)gallstones; GB wall thickening

– HIDA: no filling in cholecystitis; most specific test

– ERCP: indicates biliary obstruction



• Treatment– Medical

• IV fluids

• Bowel rest

• Antibiotics X 7-10d» Ampicillin + aminoglycoside

» Cephalosporin + ampicillin-sulbactam

• Pain management: morphine/meperidine

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• Treatment– Surgical: laparascopic cholecystectomy

– Dissolution therapies• Chenodeoxycholic acid

• UDCA


Choledocholithiasis/Cholangitis

• Common bile duct stones

• Risk factors– Infection

– Biliary stasis

– s/p cholecystectomy

• Most common cause>acute bacterial cholangitis– E. coli, Klebsiella, Enterococcus, Enterobacter



• Charcot’s triad: Cholangitis– RUQ pain, fever, jaundice in 50-70% of patients

• Reynold’s pentad– Charcot’s triad + AMS + hypotension

– Indicates development of sepsis

• Diagnosis– Initial: RUQ Sono

– Gold Standard: ERCP

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• Treatment– GB stones present: Lap chole + bile duct exploration

– Isolated CBD stones: Endoscopic therapy then lap chole


Primary sclerosing cholangitis

• Biliary system fibrosis and thickening

• Etiology: possibly autoimmune; (+)association with Ulcerative colitis

• Mean age at diagnosis: 39

• M: F = 7: 3


Primary sclerosing cholangitis

• Clinical features– Progressive jaundice

– Pruritus

– Anorexia, fatigue, indigestion

• DiagnosisEl d lk li h h– Elevated alkaline phosphatase

• Treatment– Acute: ciprofloxacin

– Liver transplant: survival rate > 80% at 1yr

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Acute Viral Hepatitis

• Acute vs chronic

• Causes– Viral: most common

– Toxins (alcohol, acetaminophen)

• Acute viral hepatitis– A&E are self-limited w/ no long-term sequelae

– (“it was something I AtE”: fecal-oral transmission)

– B/C/D are parenterally infectious


Hepatitis C

• At-risk population– Injection drug users

– Organ/blood trasnfusion before 1992

– Hemophilia w/blood product transfusion before 1987

– ESRD on HD

Children born to infected mothers– Children born to infected mothers

– HIV patients



• Clinical features– Fatigue

– Malaise

– Anorexia

– RUQ pain

PE: jaundice RUQ tenderness– PE: jaundice, RUQ tenderness

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• Diagnosis• Hepatitis A: IgM

• Hepatitis D

• Anti-HDAg, RNA

– Hepatitis E

• Anti HEV IgM antibodies• Anti-HEV IgM antibodies


Hepatitis B Serology


Hepatitis C Serology

Anti-HCV HCV RNA Interpretation

+ + (+)HCV infection

+ - Resolution/acute (low viral load)

- + Early/false + RNA

- - (-)HCV infection

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• Treatment– Hepatitis A: self-limited; no specific treatment

– Hepatitis B: tx based on HBeAg; entecavir/tenofovir/peg-IF

– Hepatitis C: peg-interferon/ribavirin• Needlestick: monitor RNA/LFTs @ 2wk, 4wk, 6mo

– Hepatitis D: no treatment has been evaluatedHepatitis D: no treatment has been evaluated

– Hepatitis E: self-limited; no specific treatment



• Prevention– Hepatitis A vaccine

• Endemic area travelers, MSM, HCPs, chronic liver dz

– Hepatitis B vaccine • Vaccinate at 0, 1, 6 months

– Hepatitis Cep s C• Follow standard precautions/ no vaccine exists

– Hepatitis D• Hep B vaccination

– Hepatitis E-public hygiene


Chronic Viral Hepatitis

• Viral infection: most common cause of chronic hepatitis

• Applies to B, C, D

• HBV/HCV=leading cause of cirrhosis/hepatocellular CA

• Clinical features– Fatigue, nausea, jaundice, RUQ paing , , j , Q p

– Advanced symptoms: dark urine, itching, wt loss

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• Diagnosis– ALT/AST 2—5x normal

– ALT>AST

– Alk phos minimally ↑ unless (+)cirrhosis

– Liver biopsy determines disease severity



• Treatment– Hep B: peg-interferon & nucleoside/tide analogues (lamivudine)

– Hep C: curable; • Current standard treatment: ribavirin + PEG IFN

– Hep D: high doses of PEG IFN

– Autoimmune: corticosteroids + azathioprineAutoimmune: corticosteroids + azathioprine


Cirrhosis

• Irreversible fibrosis & nodular regeneration

• 2 main causes– Chronic Hepatitis C

– Alcohol liver disease

• 2 main complications– Portal HTN

– Liver insufficiency

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Cirrhosis

• Clinical features– Weakness, fatigue, weight loss

– Nausea, vomiting, anorexia

– PE: hepatomegaly, muscle atrophy, palmar erythema, spider angiomata*

– Late stage disease• AscitesAscites

• Encephalitis

• Esophageal varices


Cirrhosis

• Diagnosis– Leukopenia/anemia

– ↓ albumin/↑ AST

– ↑ Alk phos/antimitochondrial abs: primary biliary cirrhosis

– Ascites: SAAG >/=1.1 g/dL=portal HTN

Low platelets (< 150 000 mm)– Low platelets (< 150,000 mm)


Cirrhosis

• Treatment– Abstinence from alcohol/hepatotoxic drugs

– Ascites• Salt restriction/bed rest/spironolactone

• If ↑K, give furosemide

– VaricesV ces• Propranolol to ↓ portal pressures

• Octreotide

• Endoscopic therapy

– Encephalopathy

– Spontaneous bacterial peritonitis

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Cirrhosis

• Treatment– Encephalopathy

• Lactulose 15-30mL twice daily

• TIPS procedure

– Surgery• Liver transplant: definitivep


Liver Neoplasms

• Benign– Cavernous hemangioma

– Hepatocellular adenoma

• Malignant-can be primary or metastatic– Liver is common site of mets from lung/breast

• Primary hepatocellular CA risk factors– Hepatitis B/C

– Cirrhosis

– Aflatoxin B1 exposure (Aspergillus)


Liver Neoplasms

• Clinical features– Anorexia, cachexia, abd pain, weight loss

– (+)bruit/friction rub on auscultation

• Diagnosis– Leukocytosis

T k AFP 200 / l– Tumor marker: serum AFP: > 200 ng/ml

– If hx cirrhosis, surveillance u/s q6mo

– CT/MRI with contrast =imaging modality of choice

– Needle bx not recommended for resectable tumors

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Liver Neoplasms

• Treatment– Benign: only treat if risk of rupturing hepatic capsule

– Early stage w/ no liver dysfunction: surgical resection

– Local tumor ablation

– Liver transplant

P i• Prognosis– 5yr-survival w/ surgical resection: 50-70%

– Liver transplant w early disease at detection 5-year survival: 70-80%


Acute Pancreatitis

• Most common causes: gallstones and alcohol abuse

• Also serum triglycerides >1K mg/dl, neoplasm, idiopathic

• Atlanta Revisions (2013)– mild (absence organ failure/local complications)

– Moderate (local complications and/or transient organ failure)

– Severe (organ failure >/= 48hrs)

• Clinical features– Hallmark: abdominal pain, nausea, vomiting

– Tachycardia, hypotension in severe cases

– Grey-Turner sign: flank ecchymosis

– Cullen sign: umbilical ecchymosis


Acute Pancreatitis

• Diagnosis– Lab tests

• ↑ serum amylase/lipase<<more sensitive/specific

• Leukocytosis

• Elevated LFTs with biliary obstruction

– Ranson’s Criteria • Increased mortality with each additional factor

– Imaging• CT more accurate than u/s to confirm dx

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Acute Pancreatitis: Ranson Criteria

On admission

• Age > 55 years

• WBC > 16,000/uL

• Glucose >200 mg/dL (>11

After 48 hours of admission

• Fall in hematocrit >10%

• Increase in BUN to > 5 mg/dLg (

mmol/L)

• LDH > 350 IU/L

• SGOT (AST) > 250 IU/L

• Calcium < 8 mg/dL

• PO2 < 60 mmHg

• Base deficit > 4 meq/L

• Fluid sequestration > 6 Liters


AP risk assessment

• >55 yrs

• BMI >30

• AMS

• Comorbid disease

SIRS i i (2/3)

• BUN > 20

• Rising BUN

• HCT > 44%

• Rising HCT

El d i i• SIRS criteria (2/3)– HR>90bpm

– RR>20 or PaCO2>32

– T>38 or <36

– WBC <4 or >12K or >10% bands

• Elevated creatinine

• Pleural effusions

• Pulmonary infiltrates

• Extrapancreatic collections


Acute Pancreatitis

• Treatment– Keep NPO

– Hydromorphone (Dilaudid)

– AGGRESSIVE Fluid resuscitation (achieve urine output 0.5ml/kg/hr)• Crystalloids

• Most beneficial in the first 12-24 hoursMost beneficial in the first 12 24 hours

– Nausea/Vomiting• promethazine (Phenergan), ondansetron (Zofran)

• NG suction if intractable

– When to progress to a solid diet

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Chronic pancreatitis

• 80% of cases secondary to alcohol abuse in the US

• Also: cholelithiasis, PUD, hyperlipidemia

• ? Evidence cigarette smoking alone as etiology

• Classic triad: – pancreatic calcification/steatorrhea/DM-20% of patients

• Clinical features– Abdominal pain


Chronic pancreatitis

• Diagnosis– ↑ fecal fat due to exocrine pancreatic insufficiency

– DM due to endocrine insufficiency

– Pancreatic calcifications on abd x-ray: 20-30%

• TreatmentD fi i i d l i– Definitive: treat underlying cause

– Analgesics: tramadol (Ultram)

– Pancreatic enzyme therapy

– Steroids if autoimmune etiology


Pancreatic neoplasms

• 4th most common cause of CA in the US

• Risk factors– Age, tobacco use, etoh abuse, previous abd radiation

– Genetic predisposition

• 75% occur in the pancreatic head

• Clinical features– Abd pain, nausea, vomiting

– Diarrhea

– Weight loss, jaundice

– Courvoisier’s sign: palpable GB

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Pancreatic neoplasm

• Diagnosis– Labs

• Anemia, impaired glucose tolerance, steatorrhea

– Imaging• CT scan with contrast: preferred imaging

– Tumor markersu o e s• CA 19-9

• Treatment– No mets: surgery, then chemo= 5yr survival 20%

– Unresectable tumor: chemo + radiation

– Mets: manage pain/complications

End of Part One

GASTROENTEROLOGY


End of Part OnePlease go on to Part Two

1/20/2016

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GASTROENTEROLOGYPart Two of Two


Dipali Yeh, M.S. PA-C

Rutgers Physician Assistant Program Certification/Recertification Examination Review

Course

June 2015


Appendicitis

• Most common acute surgical emergency

• Fecalith in < 30% of patients

• Usually between 10-30 yrs old

• Clinical manifestations– Early: periumbilical pain, then localize to RLQy p p , Q

– Associated: nausea, vomiting, anorexia

– Psoas sign

– Obturator sign


Appendicitis

• Diagnosis– Leukocytosis in 80% of cases

– Preferred imaging: CT scan

• Treatment– Laprascopic appendectomy

Ab f / i illi l l (Ti i )– Abx: cefotetan/ticarcillin-clavulanate (Timentin)

– If perforation: ceftriaxone (Rocephin) & metronidazole (Flagyl)

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Celiac disease

• Inflammatory condition of small intestine

• Precipitation foods: wheat, rye, barley

• Immunological response to gluten

• High-risk groups– 1st degree relativesg

– Type I DM

– Autoimmune thyroid disorder

• HLA-DQ2/DQ8(+) patients

• Clinical features: wt loss, diarrhea, abd distention

• Dermatitis herpetiformis


Celiac Disease

• Diagnosis– IgA endomysial antibody

– IgA tTg antibody

– Confirmation: small intestine biopsy

• TreatmentI i l f di– Institute gluten-free diet

– Supplementation: vitamin D, calcium, B12, folate

– Bone density studies (70% patients have osteopenia/osteoporosis)


Constipation

• Occurs in 10-15% of adults

• More common in women• 1st step in eval: what is “constipation”• Most common causes

– Inadequate fluid/fiber intakeq

– Poor bowel habits

• Primary etiology: slow transit time

• Secondary etiology: medication SE/systemic disorders

• Diagnosis: if refractory to treatment, colonic transit studies

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Constipation

• Treatment– Dietary/lifestyle measures

• 30g fiber/d, fluids, discontinue meds precipitating

– Osmotic laxatives• Magnesium hydroxide, lactulose, polyethylene glycol

– Stimulant laxativeS u ve• Bisacodyl, senna, cascara


Constipation→Fecal Impaction

• Complication: Fecal Impaction– Decreased appetite, abd pain, distention

– Clinical presentation• Firm feces palpable on DRE

– Treatment• Initial: saline/mineral oil enemaInitial: saline/mineral oil enema

• Subsequent: digital disimpaction

– Long-term goal: maintain soft stool/regular BMs


Diverticular disease

• Diverticulosis– Uncomplicated mucosa/submucosa herniations

– 50-80% of patients > 80yrs old

– Western diet

– Most common: sigmoid colon

Asymptomatic/uncomplicated=no imaging– Asymptomatic/uncomplicated=no imaging

– Recommended: high fiber diet/fiber supplements

– 10-25% patients develop diverticulitis

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Diverticular disease: Diverticulitis

• Clinical manifestations– Anorexia, LLQ pain, fever

– LLQ tenderness on PE

– 5% have diverticular bleeding

• DiagnosisL k i 70 80% f i– Leukocytosis: 70-80% of patients

– CT scan: inflammation

– Barium study: not in acute setting; risk perforation

– Colonoscopy: after acute syndrome has resolved


Diverticular disease: Diverticulitis• Treatment

– Uncomplicated w/mild symptoms• 1st line:

• ciprofloxacin/levofloxacin + metronidazole x 7-10d

• TMP/SMX + metronidazole x 7-10 days

• 2nd line • amox/clavulanic acid or moxifloxacin

• Clear liquid diet & advance as tolerated

– Unresponsive to outpatient treatment/unable to tolerate PO• Admit + IV antibiotics

• 1st line • piperacillin/tazobactam, ampicillin/sulbactam

• 2nd line • Ampicillin + metronidazole + quinolone or aminoglycoside


Diverticular disease: Diverticulitis

– Surgery: perforation/obstruction

– Abscess formation > 4cm: CT-guided drainage, then surgery in 6wks

– Avoid nuts/seeds/popcorn? Recent studies negate this

– Maintain high-fiber diet (>30 g/d)

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Inflammatory bowel disease

• Ulcerative colitis & Crohn’s disease

• Common in developed countries

• M=F

• Peak incidence 15-30, 2nd peak 7th decade

• Risk factor: Fam hx/Ashkenazi Jew descentRisk factor: Fam hx/Ashkenazi Jew descent

• Cigarette smoking: bad for Crohn’s/good for UC



CROHN’S

• Poor prognosis

• Esophagus>anus• (rectal sparing)

UC

• Improved course

• Colon (rectal involvement)

Smoking

Sites of GI involvement

• “Skip lesions”

• (+)

• RLQ pain/diarrhea/fatigue

• Not curative

• Continuous disease

• (-)

• Abd pain/hematochezia

• Can be curative

Lesions

Transmural involvement

Symptoms

Surgery



• Skin

• Eyes

• Pyoderma gangrenosum• Erythema nodosum (pretibial)• Vasculitis

• Iritis• Conjunctivitis

• Joints-most common

• Liver

j• Uveitis

• Arthritis• Ankylosing spondylitis

• Sclerosing cholangitis• Hepatitis

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• Diagnosis– Colonoscopy: preferred imaging except with peritoneal signs

– Biopsy: determine histopathology

– Crohn’s: cobblestone appearance/skip lesions

– UC: diffuse erythema rectum→proximally

Avoid endoscopy in acute disease→perforation/toxic megacolon– Avoid endoscopy in acute disease→perforation/toxic megacolon


Crohn’s Disease

http://commons.wikimedia.org/wiki/File%3ACD_colitis.jpgBy Samir at en.wikipedia [GFDL (http://www.gnu.org/copyleft/fdl.html) or CC‐BY‐SA‐3.0 (http://creativecommons.org/licenses/by‐sa/3.0/)], via Wikimedia Commons


Inflammatory bowel disease: Treatment

• 5-ASA-for maintenance– Sulfasalazine (Azulfide)

– Mesalamine (Asacol, Pentasa)

• Corticosteroids-for acute attacks– Prednisone/methylprednisone

• Immunomodulators-for refractory disease– 6-mercaptopurine

– Methotrexate

– Cyclosporine

– WBC/LFTs<<monitor

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Inflammatory bowel disease: Treatment

• Antibiotics-for acute infectious flare-ups– metronidazole (Flagyl)

– ciprofloxacin (Cipro)/levofloxacin (Levaquin)

• Surgery– Crohn’s: reserved for complications-segmental resection

UC i l l– UC: curative, total proctocolectomy

• Cancer: UC/Crohnʼs patients– Screening colonoscopy q1-2 yrs 8-10 yrs after dx


Intussusception

• Invagination of proximal into distal segment

• 95% cases>children• Risk factors: viral enteritis, CF, Meckelʼs• Risk factors in adults: Neoplasm

• Clinical featuresClinical features– Currant jelly stool, palpable mass

– Adult: abdominal pain, nausea, vomiting, diarrhea

• Diagnosis– barium enema in children, CT in adults

• Treatment– barium enema in children, surgery in adults


Irritable Bowel Syndrome

• Recurrent abd pain associated with defecation/∆ bowel habits

• It is the most common cause of chronic/recurrent abd pain in the US (affects up to 20% of adults)

• F>M

• Symptoms associated with menses/stressy p

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• Clinical features– Symptoms vary widely

– Lower abd pain relieved with defecation

– Alarm features• Anemia

• Weight lossWeight loss

• FH colon CA

• Major symptom ∆/1st symptom after age 50

– PE: usually normal



• Diagnosis– Diagnosis of exclusion

– Colonoscopy if alarm features

• Treatment– Strong provider-patient relationship & reassurance

Fib h– Fiber therapy

– Antispasmodics

– Antidepressants

– Psychological cognitive therapy/hypnosis


Intestinal ischemia

• Predisposing conditions– Older age

– Arterial embolus conditions (arrhythmias, heart failure, valve disease)

– Arterial occlusion conditions (trauma, vasculitis, AAA)

– Low-flow states (sepsis, dialysis)

Extensive surgery>esophagus/stomach/duodenum– Extensive surgery>esophagus/stomach/duodenum

– Most common site: SMA

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Intestinal ischemia

• Clinical presentation– Acute: pain out of proportion to exam

– Chronic: postprandial abdominal angina

– Also: fever, nausea, vomiting, diarrhea

– PE: hypotension, tachycardia, ↓ bowel sounds

Di i• Diagnosis– Labs: leukocytosis, hemoconcentration, metabolic acidosis

– Plain film: air-fluid levels, thumb-printing sign

– MDCT Angiography: 95% s/s


Intestinal ischemia

• Treatment– Initial: volume replacement, optimize cardiac output

– Antibiotics: broad-spectrum• ciprofloxacin (Cipro) + metronidazole (Flagyl)

• piperacillin & tazobactam (Zosyn)

– Evidence of gangrene: to the ORv de ce o g g e e: o e O


Colonic polyps

• Classifications– Nonadenomatous=benign

– Adenomatous=malignant potential

• Types: sessile, flat, pedunculated

• Nonadenomatous– Account for 90% of large bowel

– Found in 50% of patients > 60 yrs old

• Adenomatous– Have malignant potential

– Malignancy risk increases with size (>2cm=highest risk)

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Colonic polyps

• Clinical features– Generally asymptomatic

• Diagnosis– Preferred method: colonoscopy

– Flex-sig detects 50-60% of polyps

• Treatment– Endoscopic polypectomy: ↓ mortality/incidence of colorectal CA

– Surgical resection when endoscopic resection is not possible


Colorectal cancer

• 3rd most common cancer in the US/2nd leading cause of cancer death

• 95% are adenocarcinoma arising from adenomas

• Sites of development: 38% cecum, 35% sigmoid, rectal

• Risk factors– Age: 90% occur in patients >50yrs oldg p y

– (+)FH

– Hx IBD (Ulcerative colitis/Crohns)


Colorectal cancer

• Clinical features– Slow-growing-no symptoms for years

– Asymptomatic-detected by FOBT

– Fatigue/weakness>iron-deficiency anemia

– ∆ bowel habits circumferentially

Hematochezia/tenesmus/urgency– Hematochezia/tenesmus/urgency

– Proximal lesions: bleeding

– Distal: obstruction/perforation

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Colorectal cancer

Diagnosis/Screening

• Procedure of choice: colonoscopy

• Barium enema/CT– Colonoscopy unable to reach cecum

– Nearly obstructing tumor; prevents passage of scope


Colorectal cancer

• Colonoscopy

• Flex sig

• CT colography

• Q10 yrs

• Q5yrs

• Q5yrs

Screening options beginning at age 50 for average‐risk individuals

• Barium enema

• FOBT/FIT

• CEA

(CEA> 5ng/ml=poor prognosis)

• Q5yrs

• Annually

• to monitor patients; not detection


Colorectal cancer

• Single first-degree relative diagnosed >/= 60– Begin screening at age 40

– Guidelines as average-risk individual

– Preferred: colonoscopy q10 years

• Single first-degree relative diagnosed </= 60 or 2 first-degree l tirelatives

– Begin screening at age 40 or 10 years younger than age at diagnosis of youngest affected relative

– preferred: colonoscopy q5 years

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Colorectal cancer: Treatment

• Primary treatment: Surgery

• Chemotherapy• Metastatic disease

• Adjuvant with Stage III (node +)

• 5-flourouracil

• Capecitabine

• Irinotican

• Oxaliplatin

• Radiation• Peritoneal/rectal involvement

• Rare for disease with mets


Colorectal cancer

• Chemoprevention– NSAIDS including aspirin

• Dietary prevention– More fruits/vegetables/fiber

– No reduction on 3 randomized trials on 3-8 yr follow up


Small Bowel Obstruction

• Causes– 60% adhesions

– 10% hernias

– Others: neoplasms, IBD, volvulus

• Clinical featuresE l– Early

• diffuse, crampy colicky abd pain

• Vomiting, hyperactive BS

– Late• Steady abd pain, better localized

• (-)BS, quiet abdomen

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Small Bowel Obstruction

• Diagnosis– Abdominal X-ray

• Dilated bowel loops

• (+)air-fluid levels

– CT• Help determine etiologyp gy

• Gas in the wall>>strangulation

• Treatment– NGT

– IV fluids, opioid pain medication, antiemetics

– Surgery: for strangulated source , avoid in paralytic ileus


Large Bowel Obstruction

• Slower, less dramatic in presentation

• Most common cause: neoplasm

• Other: strictures, hernias, volvulus, fecal impaction

• Clinical features– Abd distention, anorexia, nausea, vomiting, , , g

– Late stage: feculent vomiting, no BS


Large Bowel Obstruction

• Diagnosis– Abdominal x-ray: free air, bird’s beak volvulus

– CT scan: confirm etiology

• Treatment– Surgery more likely with LBO

E d d l l– Endoscopy to reduce any volvulus

– Surgery: ostomy very likely; temp vs permanent

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Toxic megacolon

• TRUE EMERGENCY

• Extreme dilatation & immobility of colon

• Complication– UC, Crohn’s, pseudomembranous colitis

• High risk of perforationg p

• Clinical features– Fever, abd cramps, distention

– (+)rigid abdomen & rebound tenderness

– (+)shock, hypovolemia


Toxic megacolon

• Diagnosis– Abdominal x-ray: colonic dilatation > 6cm

• Treatment– Broad-spectrum antibiotics

– NG suctioning & colonic decompression

IV fl id– IV fluids

– Surgery: possible colectomy/colostomy


http://commons.wikimedia.org/wiki/File%3AToxisches_Megacolon_bei_Colitis_ulcerosa.jpgBy Hellerhoff (Own work) [CC‐BY‐SA‐3.0 (http://creativecommons.org/licenses/by‐sa/3.0)], via Wikimedia Commons

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Hernias

• Protrusion of organ/structure from itʼs proper cavity

• Classifications– Reducible: able to return contents

– Incarcerated: contents cannot be returned

– Strangulated: incarcerated hernia w/ compromised blood supply

• Types– Umbilical: congenital/pregnancy/obesity

– Hiatal: causes GERD

– Incisional: vertical incisions: F:M=2:1

– Inguinal: Direct & Indirect

– Femoral: increased strangulation rate


Hernias

• Clinical features– If strangulated, localized sharp, intense abd pain

– (+)anorexia/vomiting

• Diagnosis– Leukocytosis

CT/US b d– CT/US can be done

• Treatment– surgery


Anal fissure

• Frequently affects young adults; M=F

• Most at posterior midline

• Any off “midline”=red flag– Crohn’s, neoplasm, syphilis, HIV

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Anal fissure

• Clinical features/diagnosis– Based on HX & PE (severe anal pain s/p BM)

– Diagnostic triad• Fissure, sentinel tag, hypertrophied anal papilla

• TreatmentFib fl id i t k– Fiber, fluid intake

– Sitz baths

– Topical NTG/diltiazem gel to reduce sphincter tone

– Lateral internal sphincterotomy: failed medical management


http://commons.wikimedia.org/wiki/File%3AAnal_fissure_1.jpgBy Bernardo Gui (Own work) [Public domain], via Wikimedia Commons


Perianal abscess/fistula

• Causes– Most by infections of anal glands

– Also: trauma, anorectal surgery, malignancy

• Fistula: complication of chronic perianal abscess

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• Clinical features/Diagnosis– Abscess

• Perianal pain/swelling

• Local erythema, swelling, fluctuance

– Fistula• Recurrent abscess in same location

• Persistent purulent drainage from non-healing abscess



• Treatment– Abscess

• Local incision and drainage

• Antibiotic therapy alone w/o I&D-inadequate

• Antibiotics: immunocompromised, ↑ risk of infection

• Antibiotics not usually indicated after I&D

– Fistula: surgical


Pilonidal disease

• Abscess in the sacrococcygeal cleft

• Associated with subsequent sinus development

• M:F=4:1

• Clinical features: painful, fluctuant area

• TreatmentTreatment– Surgical drainage

– Antibiotic supplements

– Subsequent: follicle removal/unroof sinus tract

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Hemorrhoids

• Varices of hemorrhoidal plexus

• Causative factors– Constipation, diarrhea, pregnancy, prolonged straining

• Internal: above dentate line

• Clinical features– Internal: painless BRBPR

– External: pain & swelling when thrombosed


Hemorrhoids

• Treatment– External

• Analgesics

• Sitz baths/fiber intake

• Stool softeners

• Severe cases: excision


Thrombosed external hemorrrhoid

http://commons.wikimedia.org/wiki/File%3APerinanalthrombose_01.jpgBy Ole Gebbensleben, York Hilger and Henning Rohde [CC‐BY‐2.0 (http://creativecommons.org/licenses/by/2.0)], via Wikimedia Commons

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HemorrhoidsFindings

• Bleed, but (-)prolapse

• Prolapse but reduce spontaneously

Treatment

• High fiber diet, increased water intake, rubber band ligation, sclerotherapy

• Dietary modification, rubber band ligation, sclerotherapy

Grades

Grade I

Grade II

• Protrude and require digital reduction

• Chronically protrude; irreversible; risk strangulation

g py

• Dietary modification, rubber band ligation, sclerotherapy,

• surgical hemorrhoidectomy

• Urgent/surgical hemorrhoidectomy

Grade III

Grade IV


Anal Cancer

• 80% related to HPV

• Most: squamous cell CA

• Clinical: bleeding, pain, palpable mass

• Diagnosis: CT/MRI-look for mets/LN involve– Need biopsyNeed biopsy

• Treatment– First line: chemotherapy

– <3cm tumor: wide local excision

– Tumors not responsive to CT/recur• Abdominoperineal resection


Diarrhea

• Classifications– Acute vs Chronic

• Acute: < 2weeks

• Chronic>4weeks

– Infectious vs noninfectious• Infectious more common

– Inflammatory vs noninflammatory• Inflammatory: (+)blood diarrhea

• Noninflammatory: (-)blood

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Acute Diarrhea

• Inflammatory– Campylobacter

– Entamoeba

– Salmonella

• Noninflammatory– Cryptosporidium

– Escherichia coli

– Giardia lamblia

– Shigella

– Yersinia

– Norovirus

– Rotavirus

– Vibrio cholera


Acute Diarrhea Organism Etiology Diagnosis Clinical Features/ Treatment

Campylobacter jejuni

Raw poultry,unpasteurized milk

Stool culture

azithromycin or floroquinolone for severe disease; associated with Guillain-Barre

Entamoebaspecies

Tropical regions w/crowding and poor

Stool culture

Metronidazoletinidazole

sanitations

Salmonella species

Eggs, poultry,unpasteurized milk

Stool culture

No antimicrobials unless high risk or systemic disssemination, in which case: florquinolone

Shigellaspecies

Food/water contaminated w/human feces

Stool culture

Often mild & self-limited. If needed, fluoroquinolones. Do not give opioids

Yersinia enterocolitica

Undercooked pork, contaminated water

Stool culture

Present with appendicitis-like symptoms; in children: polyarthritis or erythema nodosum. Self-limited. If severe, treat with tetracycline or fluoroquinolone.


Acute Diarrhea

Organism Etiology Diagnosis Clinical Features/Treatment

cryptosporidium Recreational drinking water; resistant to chlorineSwimming pools; daycare

Stool culture Primarily fluid-hydration. Nitazoxanide FDA-approved

E. coli Undercooked ground beef; unpasteurized milk

Stool culture/toxin Usually self-limited; associated with hemolytic-uremicsyndrome in childrensyndrome in children

Giardia lamblia Recreational water/wilderness travel

Cysts/trophozoites in stool Acute diarrhea: watery, profuseChronic diarrhea: greasy, malodorousMetronidazole, Tinidazole

Norovirus Shellfish; food handled with fecal contamination

Clinical Limited disease 12-48 hours; diarrhea in adults, nausea and vomiting in children; supportive care

Rotavirus Undercooked pork, contaminated water

Immunoassay on stool Watery diarrhea x 1 week; supportive care

Vibrio cholerae Contaminated water/shellfish, foodvendors

Stool culture Prompt hydration; tetracycline and azithromycin shorten excretion of vibrios

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Chronic Diarrhea

• Osmotic

• *Symptoms ↓ w/fasting– Lactulose

Antacids

• Secretory

• *little ∆ w/fasting– VIPoma

– Gastrinoma

– Laxative abuse– Antacids

– sorbitol

Laxative abuse

Inflammatory Conditions: UC/Crohn’s DiseaseMotility Disorders

-scleroderma-IBS-DM -Hyperthyroidism

Malabsorption-Celiac Disease-Chronic Pancreatitis

Chronic infections: Giardia, cryptosporidium, CMV


Diarrhea

• Clinical features– Greasy, malodorous stool: malabsorption disorder

– Dysentery (w/ blood/pus): inflammatory disorder

– (+)abd pain: IBS/IBD

– (+)hx community outbreaks: viral/food source etiology


Diarrhea

• (+)heme pos stool + fecal leukocytes=IBD

• (+)fecal fat=malabsorption condition

• Send stool culture for bacterial agents/parasites/toxins

• Mucosal bx may be required to r/o inflammatory process

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DiarrheaTreatment

• Antidiarrheal agents– Reserved for mild-mod disease

– 1st line: Loperamide (Immodium) 4mg/d then 2mg/d s/p BM

• Opioids– ↓ urgency and fecal liquidity

Indication: chronic intractable diarrhea– Indication: chronic, intractable diarrhea

– Contraindication:• Bloody diarrhea

• High fever

• Systemic toxicity

• Antibiotics– Not indicated in acute diarrhea

– Immunocompromised/dehydration

– Antibiotics for specific organisms


Diarrhea: PEARLS

– Giardia: Metronidazole

– E. histolytica: Metronidazole

– Shigella: TMP/SMX (Bactrim DS) or ciprofloxacin

– Campylobacter: Erythromycin or ciprofloxacin

– C. difficile: Discontinue antibiotics if possible. Consider metronidazole if diarrhea persistsp

– Traveler's diarrhea: Ciprofloxacin or TMP/SMX (Bactrim DS)


Diarrhea: PEARLS

• Contraindications:– Antibiotics are contraindicated in Salmonella infections unless caused by S.

typhosa or the patient is severely ill.

– Avoid alcoholic beverages with metronidazole due to the possibility of a disulfiram reaction.

– Antibiotics are not indicated in foodborne toxigenic diarrhea– Antibiotics are not indicated in foodborne toxigenic diarrhea.

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Diarrhea: PEARLS

• Precautions:– loperamide should be used with caution in patients suspected of having

infectious diarrhea (especially if E. coli 0157:H7 suspected) or antibiotic-associated colitis.

– Antiperistaltic agents may speed recovery from traveler's diarrhea when used in combination with an antibiotic.co b o w b o c.

– Doxycycline, TMP/SMX, and ciprofloxacin may cause photosensitivity; use sunscreen.


Phenylketonuria

• Rare, autosomal recessive

• Unable to metabolize phenylalanine and convert it to tyrosine

• Screen patients at birth

• Diagnosis s/p age 3>brain damage

• Complications if untreatedComplications if untreated– Developmental delay

– Movement disorder

• Management: low phenylalanine diet


Lactose intolerance

• Lactase-enzyme produced in small intestine to digest lactose

• Clinical features, bloating, flatulence, diarrhea s/p ingestion of dairy products

• Result: osmotic diarrhea

• Managementg– Avoid milk/dairy products

– Use OTC lactase enzyme tablets/drops

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Vitamin/Nutritional Deficiencies

Vitamin Function Deficiency Toxicity

A Vision/antioxidant Night blindnessDry, scaly skin

Skin disordersHair lossHip fractures

D Calcium and h h

Rickett’s: hild

HypercalcemiaR lphosphate

regulationchildrenOsteomalacia: adults

Renal stones

E Cellular aging and vascular integrity

Areflexia, gait disturbances, loss of vibration sense

*least toxicInhibits Vit K, so can result in bleeding, GI discomfort

K Clotting Bleeding Anemia/jaundice

PANCE/PANRE Review CourseVitamin/Nutritional DeficienciesVitamin Function Deficiency Toxicity

Niacin Energy/fat metabolism Pellagra (3 D’s)-diarrhea-dermatitis-dementia

flushing

B1 (Thiamine) Carbohydrate metabolism

Beriberi(Dry) w/neuropathy and poor coordination(Wet) w/cardiac dysfunction and Wernicke’s

Lethargy, ataxia

encephalopathy

B6 (Pyroxidine) Protein metabolism Dermatitis/cheilosis Photosensitivity/pheripheral neuropathy

B12 (Riboflavin)

Oxidation-reduction Cheilosis/glossitisAnemia, leukopenia

N/A

Folate DNA synthesis Megaloblastic anemia N/A

Vitamin C (ascorbic acid)

Antioxidant/collagen synthesis

ScurvyFatigue, depression, poor wound healing

Renal stones, diarrhea

PROPERTIES

On passing, 'Finish' button: Goes to Next SlideOn failing, 'Finish' button: Goes to Next SlideAllow user to leave quiz: At any timeUser may view slides after quiz: At any timeUser may attempt quiz: Just Once

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Thank you and good luck!Thank you and good luck!

PANCE/PANRE Review CourseReferences• A Guide to Physical Examination and History Taking, 11th Ed.,

Barbara Bates. J.B. Lippincott Co.• Cecil Textbook of Medicine, (2012), Goldman and Ausiello.

Saunders• Current Medical Diagnosis & Treatment 2015, McPhee and

Papadakis. Lange, McGraw Hill• www.cdc.gov• http://commons.wikimedia.org/wiki/File%3AToxisches_Megacol

on bei Colitis ulcerosa jpgon_bei_Colitis_ulcerosa.jpg• http://commons.wikimedia.org/wiki/File%3AAnal_fissure_1.jpg• http://commons.wikimedia.org/wiki/File%3APerinanalthrombose

_01.jpg• http://commons.wikimedia.org/wiki/File%3ADiffuser_Oesophag

usspasmus_002-13.jpg• http://commons.wikimedia.org/wiki/File%3AAcha.JPG• 5-minute Clinical Consult (2013) Lippincott Williams and

Wilkins• Conn’s Current Therapy 2014 1st ed. (2013) Bope and Kellerman

2015 gastroenterology one

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