Gastroenterology Flashcards by Mina Sourial

Q

recent MI, combative patient, and intestinal perforation

A

relative contraindication to GI endoscopy

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Q

procedure of choice for: evaluation of odynophagia, finding PUD, before PUD surgery, if GERD treatment fails, alarm signals, UGI bleeds, dysphagia AFTER barium swallow, foreign body removal, small bowel disease, persistent dysphagia, placement of feeding or drainage tubes

A

EGD (esophagogastroduodenoscopy)

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Q

if patient has a possible bile duct obstruction give antibiotics before

A

ERCP (endoscopic retrograde cholangiopancreatography)

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Q

biliary obstruction, dx/tx pancreatic duct obstruction, dx of PSC (primary schlerosing cholangitis), tx of choledocholithiasis with cholangitis are indications for…

A

ERCP

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Q

further eval of abnormal biliary or pancreatic duct imaging from CT/MRCP/EUS
other indications for…

A

ERCP

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Q

ERCP is CONTRAINDICATED in ACUTE pancreatitis, except:

A

impacted gallstones

2. ascending cholangitis (bacterial infection causing cholangitis)

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Q

bile duct obstruction, chronic pancreatitis, if acute pancreatitis doesn’t get better, and is the test of choice for PSC (primary sclerosis cholangitis)

A

MRCP (magnetic resonance cholangiopancreatography)

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Q

what visualizes the bile tract?

A

retrograde cholangiography

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Q

what visualizes the pancreatic duct?

A

retrograde pancreatography

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Q

staging GIT, biliary tree, and pancreatic malignancy
diagnosing chronic pancreatitis
dx/tx pancreatitis complications
providing access to pancreatic duct or biliary tree

A

EUS (endoscopic ultrasonography)

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Q

normal swallowing

A

deglutition

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Q

when swallowing doesn’t proceed appropriately for any reason

A

dysphagia

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Q

pain with swallowing

A

odynophagia

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Q

3 main causes of dysphagia

A

transfer disorders (oropharyngeal)
anatomic/structural disorders
motility disorders

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Q

you should always work up this disorder and NOT treat it empirically

A

dysphagia

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Q

usually the 1st test performed to work up dysphagia

A

barium swallow

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Q

definitely the 1st test performed to work up dysphagia if symptoms are SEVERE, or new-onset dysphagia with LIQUIDS

A

barium swallow

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Q

why is barrium swallow done before endoscopy?

A

avoid risk of PERFORATION if there’s DIVERTICULA or OBSTRUCTION
may not need endoscopy if barium swallow is enough
gives endoscopist idea of what to expect

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Q

if a patient has h/o reflux and presents with slight-to-moderate dysphagia for solids you can do this test first

A

EGD

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Q

generally only done if dysphagia persists after negative barium swallow and EGD

A

esophageal manometry

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Q

general workup of dysphagia

A

barium swallow
endoscopy
manometry study

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Q

chest pain, dysphagia for SOLIDS and LIQUIDS, usually years, regurgitation

A

achalasia

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Q

finding on barium swallow in achalasia

A

bird-beak narrowing distally

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Q

done to diagnose and exclude a tumor at esophagogastric junction (“pseudoachalasia”)

A

EGD

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done to confirm dx of achalasia before tx

esophageal manometry

absence of normal peristalsis, and non-relaxing LES

manometry findings in achalasia

3 distinct subtypes of achalasia seen using high resolution manometry

1. traditional aperistalsis 2. esophageal compression 3. generalized spasm

if you're thinking of achalasia and see the following: RAPID onset of symptoms, patient older than 60 years, PROGRESSIVE symptoms, and profound WEIGHT LOSS you should worry about this...

cancer! pseudoachalasia or secondary achalasia

3 treatment options for achalasia

1. pneumatic dilation 2. onabotulinum-toxin A (Botox) 3. surgical myotomy (done via laparoscope)

how effective is Botox for achalasia, and how often do you need to repeat therapy?

- works 65% of cases - need to repeat every 6-12 months - not the greatest, but a decent alternative in patients who are high-risk for surgery

simultaneous, nonperistaltic concentration of esophagus, worse with COLD or CARBONATED liquids

diffuse esophageal spasm (DES)

causes esophageal spasms even without typical reflux symptoms

OCCULT REFLUX

barium swallow for DES shows what?

generally normal, but can show CORKSCREW pattern

Type 3 achalasia, with excess, simultaneous (nonperistaltic) contractions in distal esophagus with NORMAL LES relaxation

high resolution manometry findings of DES

what test is not helpful in DES workup?

EGD

what should be done if REFLUX is considered a possible cause of DES?

- 24-hour esophageal pH recording, OR | - PPI BID for 3 months

most important part of DES tx

REASSURANCE

if reassurance isn't enough, treat DES with these:

1st line: DILTIAZEM or IMIPRAMINE 2nd line: isosorbide or sildenafil 3rd line: botulinum toxin injection

SLOWLY PROGRESSIVE dysphagia- INITIALLY TO SOLIDS, then liquids

anatomic obstruction - Schatzki ring in YOUNGER patients - CANCER, or STRICTURE in OLDER patients

main problem: sxs are...: sxs precipitated by... 1. anatomic: intermittent: solids 2. anatomic: progressive: solids, THEN liquids 3. anatomic: progressive: solids, THEN liquids 4. motility/neurologic: longstanding: solids, AND liquids 5. motility/neurologic: intermittent: solids, AND liquids (esp. COLD) 6. various: progressive: solids AND liquids

disease 1. Schatzki ring 2. esophageal stricture 3. cancer 4. achalasia 5. DES 6. systemic sclerosis

common cause of dysphagia, YOUNGER patients

lower esophageal ring or Schatzki ring

very slowly progressive, INTERMITTENT, SOLID FOOD dysphagia (meat and bread)

lower esophageal ring or Schatzki ring

lower esophageal ring or Schatzki ring is ALWAYS associated with...

HIATAL HERNIA

treatment for lower esophageal ring or Schatzki ring

1a. dilation (with bougie method), 1b. or (through-the-scope) hydrostatic balloon 2. THEN PPIs

slowly progressive, CONSTANT (not intermittent) dysphagia for SOLID FOODS

esophageal stricture

esophageal strictures are commonly d/t

ACID REFLUX

other causes of esophageal strictures

1. PROLONGED NASOGASTRIC TUBE placement | 2. LYE INGESTION

barium swallow for esophageal stricture shows what?

narrowing at esophagogastric junction

how do you treat esophageal stricture?

dilation

what are the 3 causes of malignant esophageal obstruction?

1. esophageal adenocarcinoma 2. squamous cell carcinoma 3. extrinsic compression from NONesophageal primary cancers

this PROGRESSION of symptoms: SOLID food dysphagia to SOFT food, finally dysphagia with LIQUIDS is what until proven otherwise?

esophageal malignancy

a rare d/o that causes dysphagia d/t UPPER esophageal web

Plummer-Vinson syndrome

what type of dysphagia is found in POSTMENOPAUSAL WOMEN, is associated with IRON-DEFICIENCY ANEMIA, and has a slightly increased risk of squamous cell esophageal cancer?

Plummer-Vinson syndrome

dysphagia to both SOLIDS AND LIQUIDS from time of onset

some sort of neurologic dysfunction

examples of neurological dysfunctions causing dysphagia

- STROKE - PARKINSONISM - BULBAR PALSY (lower motor neuron- ALS, MS) - PSEUDOBULBAR PALSY (upper motor neuron- ALS)

if you suspect aspiration d/t neurologic dysfunction, what's the next best step?

BARIUM SWALLOW to confirm dx

more than 80% of what patients have involvement of esophagus?

diffuse SSc (systemic sclerosis)

what is the LES pressure in patients with dysphagia d/t systemic sclerosis?

"wide-open" with low or NO tone/pressure | causes severe acid reflux

what are the 3 possible causes of dysphagia in systemic sclerosis? and what is the workup?

1. esophagitis 2. stricture 3. impaired motility barium swallow then EGD (to look for all 3)

if you have esophagitis in a SSc patient what do you do?

- aggressive PPI tx | - FOLLOW-UP endoscopy at 2-3 MONTHS to make sure it's working and/or dilate strictures if any

what rheumatological diseases can present with dysphagia like SSc?

polymyositis and dermatomyositis

immune-mediated chronic eosinophil-predominant inflammatory d/o of esophagus

eosinophilic (allergic) esophagitis

pathogenesis involves interleukin-5 (IL-5) and eotaxin

eosinophilic (allergic) esophagitis

occurs most commonly in MEN age 20-40 years

eosinophilic (allergic) esophagitis

strong association with ALLERGIES; environmental, food, asthma, and atopy

eosinophilic (allergic) esophagitis

IgE is elevated in 2/3 of patients

eosinophilic (allergic) esophagitis

leading symptom is recurrent attacks of dysphagia with food impaction, and usually goes undiagnosed for 4-5 years

eosinophilic (allergic) esophagitis

if you have PERIPHERAL eosinophilia symptoms are _____, and is found in what percentage of patients?

WORSE | ~ 30% of patients

SCALLOPED APPEARANCE with ridges or rings (trachealization) in esophagus

"classic" EGD finding of EoE

how do you confirm dx of EoE?

esophageal biopsies showing dense eosinophilic infiltration of esophageal epithelium (> 15 eos/HPF)

which patients also have increased eosinophils?

GERD patients

EoE tx?

- allergy testing - avoid potential allergens - fluticasone (BID) or viscous budesonide (usually results in a response within 1 week)

for patients with EoE, and concomitant reflux, or PPI-responsive eosinophilic esophagitis, what medication, in addition to steroids, can be added to help with tx?

PPI

odynophagia (painful swallowing) is usually d/t what?

1. pill-induced esophagitis | 2. opportunistic infections

common causes of pill-induced esophagitis

1. doxycycline (teenager with acne) 2. KCl 3. ASA 4. NSAIDs 5. iron 6. bisphosphonates (alendronate) 7. quinidine

dx and tx of pill-induced esophagitis

- made solely on history | - sit in upright position and drink plenty of water

opportunistic infections (OIs) occur in these patients:

- immunocompromised: HIV, or diabetes | - immunocompetent taking corticosteroids

common OIs are:

1. Candida 2. herpes simplex virus (HSV) 3. cytomegalovirus (CMV)

what to do with esophagitis with thrush in the mouth?

- treat Candida empirically with FLUCONAZOLE | - if it doesn't get better, EGD with biopsy

what is a genetic variable that affects PPI efficacy? and which gives the best results?

- slow, moderate, and fast metabolizers | - slow metabolizers have MUCH better results than fast metabolizers

short term adverse effect of PPI

COMMUNITY-ACQUIRED PNEUMONIA (CAP) | more likely within 30 days, especially within 48 hours of initialization

long term adverse effects of PPI

- FRACTURE risk is increased | - HYPOMAGNESEMIA (muscle spasms, arrhythmias, seizures)

what happens when you stop PPIs abruptly after several months?

REBOUND ACID HYPERSECRETION (especially in H. pylori-NEGATIVE patients)

should you use a PPI long-term? | when is long-term use of PPIs necessary?

no, it's discouraged Barrett esophagus

PPIs DECREASE absorption and serum levels of

THYROXINE and ITRACONAZOLE/KETOCONAZOLE

PPIs INCREASE absorption and serum levels of

DIGOXIN

can you give clopidogrel with omeprazole?

YES, benefits outweigh risk | more studies needed for slow metabolizers of clopidogrel

gastroesophageal reflux is a result of...

transient relaxation of lower esophageal sphincter (LES)

motilin, acetylcholine, and maybe gastrin INCREASE...

LES pressure

progesterone (pregnancy increases GE reflux), chocolate, smoking, some medications (anticholinergics, especially) DECREASE...

LES pressure

persistent, nonproductive cough, hoarse voice, clearing of throat, fullness of throat, suspect...

gastroesophageal reflux disease (GERD)

most common non-cardiac chest pain (70%) cause

GERD

``` nocturnal cough frequent sore throat hoarseness, laryngitis, clearing of throat loss of dental enamel exacerbation of asthma VCD (vocal cord dysfunction) ```

extraesophageal manifestations of GERD

what should you always ask about in the w/u of GERD patients?

ASTHMA SYMPTOMS; especially if they occur at night

w/u of suspected GERD depending on situation (6 scenarios)

1. heartburn alone --> trial treatment --> improvement 2. ALARM SYMPTOMS or persistent GERD symptoms --> endoscopy 3. erosive esophagitis: if immunocompetent --> treat 4. erosive esophagitis: if immunocompromised --> treat based on biopsy 5. stricture --> treat 6. normal= nonerosive reflux disease (NERD) (62% of patients) --> do NOTHING

spasm of vocal cords with associated INSPIRATORY stridor

vocal cord dysfunction (VCD)

associated with increased incidence of both GERD and asthma

increased body mass index (BMI)

if you're thinking Barrett esophagus in a GERD patient...

do an EGD if patient has obstructive symptoms, do a barium swallow first

do a 24-hour esophageal pH MONITOR for atypical cases with impedance if:

1. normal EGD and still have symptoms 2. hoarseness, coughing, or atypical chest pain, but no sxs of GERD 3. treatment failure to PPIs

MILD-TO-MODERATE GERD treatment

INITIAL: - RAISE HEAD OF BED - WEIGHT LOSS OF > 10LB if overweight ANTISECRETORY drugs if unsuccessful

healing of esophagitis (not necessarily GERD) based on treatment

placebo= 25% H2 blockers= 50% PPIs= 80-95%

tx for SEVERE GERD

PPIs, indefinitely

fundoplication indications:

1. patients REFRACTORY to medical tx 2. YOUNG patients with SEVERE disease 3. ALTERNATIVE to PPIs

patients with worse GERD symptoms (GERD-related cough, hoarseness) need...

stronger and longer treatment

Barrett esophagus is...

change from esophageal SQUAMOUS to columnar epithelium with goblet cells

SCREENING for Barrett's is...

CONTROVERSIAL

recommended guidelines for Barrett screening

white males > 50 long-standing GERD elevated BMI

Barrett esophagus is associated with kind of cancer?

ADENOCARCINOMA ONLY | not squamous cell carcinoma

incidence of adenocarcinoma in Barrett esophagus

30x normal rate

antireflux meds and surgery do what for Barrett esophagus?

they don't reverse epithelial changes or eliminate cancer risk, but help with sxs

if Barrett esophagus is found, f/u endoscopies should be done based on findings

- no dysplasia: 3-5 years - low-grade dysplasia: 6-12 months - high-dysplasia without eradication therapy: 3 months

for HIGH-GRADE dysplasia in Barrett esophagus you should do ERADICATION therapy, which is...

radiofrequency ablation (RFA) or endoscopic mucosal resection (EMR)

what other eradication therapy can be done for HIGH-GRADE dysplasia in Barrett esophagus?

esophagectomy, but has HIGHER MORBIDITY | should be done in centers that SPECIALIZE in them

2 types of esophageal cancer:

``` 1. adenocarcinoma, now more common occurs in DISTAL 1/3 2. squamous cell generally occurs in PROXIMAL 2/3 caused by SMOKING and ALCOHOL (especially hard liquor) ```

smoking and alcohol have what effect on squamous cell carcinoma of esophagus?

SYNERGISTIC (multiplicative, NOT additive) carcinogenic effect

squamous cell cancer of esophagus is strongly associated with...

geographic location, DIET, and ENVIRONMENT

usual presenting symptom of esophageal cancer

DYSPHAGIA

treatment of esophageal cancer, if: small and localized, then... large or metastasized, then...

surgical resection combination chemotherapy (cisplatin and 5FU) PLUS radiation PRIOR to surgery

Zenker diverticulum is

outpouching of UPPER esophagus

common symptoms of Zenker diverticulum

FOUL-SMELLING BREATH | REGURGITATION of food eaten several days earlier

MCC of TRANSFER DYSPHAGIA (trouble initiating swallowing)

Zenker diverticulum

treatment of Zenker diverticulum

surgery

ENDOCRINAL stimulus for gastric acid release

gastrin (released by G cells in pylorus)

most important for postprandial gastric acid production

gastrin

PARACRINE stimulus for gastric acid release

histamine (released by ECL (enterochromaffin-like) cells in corpus)

neurocine effect, stimulation vagus nerve releases what onto G cells?

gastrin-releasing peptide

what decreases production of gastrin (and therefore gastric acid)

somatostatin and secretin

secretin is made by the duodenum when stomach is acidified causing:

1. DECREASE in GASTRIN production | 2. stimulates output of BICARBONATE from pancreas

serum gastrin level skyrockets, when?

patients with achlorhydria (autoimmune gastritis), or pernicious anemia

upper abdominal pain or discomfort especially after meals

dyspepsia

symptoms of dyspepsia

epigastric fullness, belching, bloating, gnawing pain, and heartburn (generally not severe pain)

causes of dyspepsia

PUD, gastritis, GERD, biliary colic, gastroparesis, pancreatitis, and cancer

classification of dyspepsia by symptoms:

GERD-LIKE, ULCER-LIKE (improves on anti-ulcer therapy) | DYSMOTILITY-TYPE (improves on promotility drugs, such as metoclopramide)

recurrent upper abdominal pain with NORMAL EGD

NON-ULCER dyspepsia

treatment plan for dyspepsia

1. discontinue NSAIDs 2. test and treat if H. pylori + 3. conduct a PPI treatment trial 4. order EGD if alarm symptoms or failure of therapy

how is gastritis classified?

either histology or etiology

classification of gastritis by histology:

1. superficial gastritis (early, neutrophils) 2. atrophic gastritis (mid, lymphocytes) 3. gastric atrophy (late, gastropathy aka metaplastic atrophic gastritis)

classification of gastritis by etiology:

type A: Autoimmune, Atrophic, pernicious Anemia, Achlorhydria type B: MOST COMMON form chronic gastritis (80%)

what part of the stomach does type A gastritis affect?

PROXIMAL stomach (fundus and corpus only)

autoantibodies against BOTH intrinsic factor and parietal cells cause what?

pernicious Anemia and Achlorhydria, and secondary hypergastrinemia (> 1000 pg/mL)

common cause of type B gastritis

H. pylori infection

itraconazole, ketoconazole, and thyroxine require what?

GASTRIC ACID for optimal absorption | fluconazole does NOT

causes of erosive gastropathy (with subepithelial hemorrhage)

NSAIDS, ALCOHOL, or SEVERE PHYSIOLOGIC STRESS

onset of erosive gastropathy in the ICU suggests

STRESS-RELATED MUCOSAL DAMAGE (SRMD) a. major surgery b. burns c. severe CNS injuries d. being on a ventilator e. coagulopathy

MOST EFFECTIVE treatment for SRMD

H2 receptor antagonist gtt or PPI gtt

H. pylori infection can cause:

1. GASTRITIS 2. PUD 3. GASTRIC ADENOCARCINOMA 4. GASTRIC B-CELL (MALT) LYMPHOMA

who gets treated in chronic gastritis?

only SYMPTOMATIC patients | h/o gastric/duodenal ulcer, personal/family h/o gastric cancer, personal h/o MALT lymphoma

test for H. pylori when:

1. h/o PUD 2. EGD showing ulcer disease, erosive gastritis, or duodenitis 3. MALT lymphoma 4. family h/o gastric cancer

how is dyspepsia treated?

- discontinue NSAIDs - test and treat if H. pylori + - conduct PPI trial - order EGD if alarm symptoms or PPI treatment failure

invasive tests for H. pylori

1. EGD with biopsy= GOLD STANDARD | 2. CLOtest and other rapid urease tests

noninvasive tests for H. pylori

1. urea breath test (1st choice for treatment effectiveness) 2. fecal antigen test (good for primary diagnosis) 3. serologic test (not a good test)

what interferes with urease test (CLOtest)?

PPIs, stop for 2 weeks before

which test has poor PPV for H. pylori?

serologic tests

is H. pylori treatment different for gastritis or PUD?

no, it's the SAME

H. pylori treatment

triple-drug therapy | O-CLAM (omeprazole 20mg + clarithromycin 500mg + amoxicillin 1G; all BID x 10-14 days)

should you test for H. pylori after treatment?

NOT recommended

in what situations do you test for H. pylori after treatment?

1. h/o H. pylori-associated ulcer 2. persistent dyspepsia despite test-and-treat strategy 3. H. pylori MALT lymphoma 4. resection of early gastric carcinoma

how soon should you test for H. pylori after treatment?

no sooner than 4 weeks

4 causes of peptic ulcer disease (PUD)

1. Helicobacter pylori infection (MCC) 2. NSAIDs 3. high acid secreting states (Zollinger-Ellison) 4. Crohn disease of duodenum/stomach

risk factors for NSAID-induced PUD

1. first 3 months of use 2. high doses 3. elderly patient 4. history of ulcer disease or prior UGIB 5. cardiac disease 6. concurrent steroid use 7. serious illness 8. concurrent ASA use

is smoking a risk factor for NSAID-induced PUD?

- exacerbates ulcer in gastric/duodenal ulcer disease | - decreases healing rate and increases recurrence/perforation rate in non-H. pylori ulcers

is ALCOHOL ulcerogenic?

NO

are CORTICOSTEROIDS alone ulcerogenic?

NO, but they DOUBLE the risk | may be 10-FOLD

how do you diagnose PUD in YOUNGER/HEALTHY PATIENTS?

- NO diagnosis needed; treat empirically (H2 blocker or PPI) | - or you can test and treat for H. pylori

how do you diagnose PUD in ALL OTHER PATIENTS?

EGD | especially with melena, heme + stool, early satiety, or IDA

you always do EGD in PUD w/u if:

1. symptoms include dysphagia or odynophagia 2. UGIB 3. abnormal UGI (barium swallow) or CT scan 4. family h/o duodenal ulcer disease

PERFORATED gastric or duodenal ulcers will show what on upright abdominal x-ray?

free air in peritoneal space

what are CONTRAINDICATED if a perforated ulcer is suspected?

EGD and UGI

pain of ulcer vs perforated ulcer

gnawing vs usually severe

treatment of PUD

1. H. pylori treatment 2. decrease acid secretion (H2 blockers, PPIs) 3. stop exacerbating processes (smoking, NSAIDs)

when is sucralfate effective, but why is it not preferred?

- treatment of NON-H. pylori PUD | - has to be taken QID (PPI is once daily)

in which patient is sulcrafate the SHORT-TERM DOC?

renal patients, because it binds PO4, but shouldn't be used long term because of aluminum accumulation and metabolic bone disease

when should you do surgery in PUD?

- UGI bleed (most common)- EGD can't stop the bleed - gastric outlet obstruction- initial treatment is balloon dilation - perforation- laparoscopic repair - recurrent/refractory ulcers- rare - Zollinger-Ellison syndrome- remove underlying gastrinoma

MCC of duodenal ulcers

H. pylori and NSAIDs only 1-3% d/t ZES

what's better in preventing NSAID-induced ulcers?

PPIs and MISOPROSTOL

how long do you treat non-H. pylori gastric ulcers?

3 months

do gastric ulcers increase gastric cancer risk?

NO, but NONHEALING gastric ulcers should be scoped and biopsied to rule it out

leading cause of BLEEDING ulcers in the US?

NSAIDs bleeding risk is DOSE-RELATED

NSAID-related ulcer risk is higher in...

females and any patient > 70 years of age

what type of NSAIDs have DECREASED GI SIDE EFFECTS?

COX-2 inhibitors (celecoxib, meloxicam)

signs of SEVERE peptic ulcer bleed/high risk of rebleed

- hemodynamic instability | - recurrent hematemesis or hematochezia

diagnostic and treatment procedure of choice for UGIB?

EGD

emergent EGD should be done in UGIB if?

1. treat current bleed | 2. assess risk for rebleed

EGD findings indicating INCREASED chance of rebleeding of ulcer?

1. larger size of ulcer 2. active bleeding during endoscopy 3. visible vessels on non-bleeding ulcer 4. visible clot

VERY LOW chance of ulcer rebleeding?

1. NO BLEEDING 2. NO CLOT 3. NO VISIBLE VESSELS

what doesn't stop bleeding peptic ulcers?

1. gastric lavage | 2. IV vasoconstrictors

1. Osler-Weber-Rendu (hereditary hemorrhagic telangiectasia)- telangiectasias on skin, buccal/nasal mucosa, GIT, lungs, and brain 2. Peutz-Jeghers syndrome (PJS)- dark melanin spots on lips, buccal mucosa, and hands and feet

2 non-ulcer causes of UGIB

GASTRINOMA, continuous gastrin production, refractory ulcers, and DIARRHEA +/- STEATORRHEA

Zollinger-Ellison syndrome

MC presentation of ZES?

diarrhea

initial w/u of ZES?

serum gastrin level (while off PPI therapy)

treatment of newly diagnosed ZES?

exploratory surgery with RESECTION OF PRIMARY TUMOR

DRUG OF CHOICE for ZES?

PPI

persistently high gastrin levels can cause?

gastric CARCINOIDS

gastric carcinoids are caused by?

CHRONIC HYPERGASTRINEMIC STATES

types of gastric carcinoids

- type 1 (70-80%)= AUTOIMMUNE GASTRITIS/PERNICIOUS ANEMIA - type 2 ( 5%)= ZES as MEN1 - type 3 (30%)= SPONTANEOUS (most aggressive)

sometimes gastric carcinoids occur in?

patients with VITILIGO

do gastric carcinoids cause carcinoid syndrome?

yes, but ALMOST NEVER (they are very slow growing)

4 malignancies of stomach

1. adenocarcinoma (MOST COMMON- 95%) 2. carcinoids 3. lymphoma 4. GIST (gastrointestinal stromal tumors; e.g. leiomyosarcoma)

2 types of gastric adenocarcinoma

1. PROXIMAL DIFFUSE | 2. DISTAL INTESTINAL

DISTAL gastric cancer has strong association with?

ENVIRONMENTAL factors, especially: - little fruits and vegetables, a lot of dried, smoked, and salted foods - nitrates and nitrites

what is most often associated with GASTRIC CANCER?

ACANTHOSIS NIGRICANS

what don't cause gastric cancer?

ALCOHOL nor GASTRIC ULCERS

diagnostic procedure of choice for nonhealing ulcer

endoscopy with multiple biopsies

should you use tumor markers, such as CEA and AFP, for gastric cancer?

NO, they are NOT USEFUL

treatment of gastric cancer

- remove cancer and adjacent LNs | - adjuvant combination chemoradiation

what are symptoms of dumping syndrome postprandial vasomotor?

PALPITATIONS, SWEATING, and LIGHTHEADNEDESS

2 types of dumping syndrome

1. EARLY- occurs 30 minutes after eating (hyperosmolality of food and fluid shifts in small bowel) 2. LATE- occurs 90 minutes after eating (probably d/t hypoglycemia)

treatment of dumping syndrome

- restrict sweets - separate liquids and solids - eat frequent small meals - high protein - complex carbohydrates

what is blind loop syndrome?

- BACTERIAL OVERGROWTH leading to FAT and B12 MALABSORPTION | - LOW D-XYLOSE ABSORPTION TEST

what is afferent loop syndrome?

- ABDOMINAL BLOATING and PAIN 20-60 minutes after eating | - vomiting relieves symptoms

gastroparesis

- delayed gastric emptying (early satiety) | - N/V/abdominal pain

gastroparesis in diabetics

highly VARIABLE gastric emptying

w/u for delayed gastric emptying

- RULE OUT obstruction first | - CONFIRM with radiolabeled solid meal (gastric emptying study)

metoclopramide FDA WARNING for LONG-TERM USE

extrapyradmidal side effects

can erythromycin be used for gastroparesis?

NOT VERY USEFUL (can be used acutely)

family members at increased risk of IBD and patient has increased risk of GI cancer in?

BOTH, Crohn disease (CD) and ulcerative colitis (UC), | but much higher in UC

complication in both CD and UC, and barium enema is CI in acute exacerbation

TOXIC MEGACOLON

more likely to get CD

SMOKERS

split by bacteria in COLON into MESALAMINE (active component) and SULFAPYRADINE

sulfasalazine

INEFFECTIVE for CD of SMALL BOWEL

sulfasalazine (because it won't be split into active metabolite)

is the cause of adverse effects of sulfasalazine

SULFAPYRIDINE

treats perianal abscesses and fistulas in CD

metronidazole

enteric-coated corticosteroid with FEWER SYSTEMIC SIDE EFFECTS than prednisone, used for small bowel CD and colon (mild-to-moderate) UC

budesonide

PREDNISONE-SPARING, used in both CD and UC, take 3-4 MONTHS to show effect

6-mercaptopurine (6-MP) and azathioprine (metabolizes to 6-MP)

CD and UC treatment with bone marrow suppressive effects

6-mercaptopurine (6-MP) and azathioprine (metabolizes to 6-MP) MONITOR CBC MONTHLY

- monoclonal antibodies to TNF-a | - given for MODERATE-TO-SEVERE CD, FISTULOUS CD, and REFRACTORY UC

infliximab certolizumab pegol adalimumab

infliximab, certolizumab pegol, adalimumab concerns:

TB REACTIVATION, but MOST COMMON side effect is URI | check for TB and hepatitis B

drugs proven to decrease relapse rate in CD

6-mercaptothioprine, azathioprine, methotrexate, and infliximab

- lesions: focal, SKIP, deep - course: indolent - less responsive to prednisone in acute flares - granulomas are pathognomonic - rectal sparing in 50% - abscesses, fistulas - small bowel involvement in > 50%

Crohn disease (CD)

- lesions: shallow, CONTINUOUS - course: more acute - very responsive to prednisone in acute flares - NO granulomas - rectum ALWAYS involved - NO perianal disease - backwash ileitis in

ulcerative colitis (UC)

drugs that decrease relapse in UC

ALL standard drugs

CD age of presentation

20's or 30's but can be any age (70's-80's smaller peak)

long-term (> 8 years) CD should be screened how often for cancer?

every other year

common in patients with Crohn disease

osteoporosis (abnormal bone density, vitamin D deficiency d/t malabsorption, and/or steroids)

STRING SIGN

"string" of contrast going through lumen of terminal ileum in CD if seen elsewhere in colon, it's called APPLE-CORE lesion, suggests CANCER

serologic marker for UC

p-ANCA

serologic marker for CD

ASCA

extraintestinal manifestations of IBD usually seen in patients with?

COLITIS - so usually associated with UC, but can be seen in CD that involves the colon

terminal ileum problems in CD usually NOT found in UC

1. calcium oxalate kidney stones 2. steatorrhea 3. gallstones 4. B12 deficiency 5. hypocalcemia (from vitamin D malabsorption) 6. bile acid-induced diarrhea 7. nutrient malabsorption

CD gallstone type?

PIGMENT

when does B12 MALABSORPTION occur?

> 60cm terminal ileum resection

when does bile acid-induced diarrhea occur?

treatment for bile acid-induced diarrhea

BILE ACID SEQUESTRANTS (cholestyramine, colestipol)

when does steatorrhea occur? | d/t DECREASED proximal gut concentration of bile salts

> 100cm of distal ileum resection

treatment for steatorrhea in CD patients

LOW-FAT DIET

treatment for MILD CD with COLON disease only

5-ASA

treatment for FLARES of CD

prednisone

1st line drug for mild-to-moderate CD of ileum or ileocecal disease

budesonide

helpful with fistulas and getting off steroids

infliximab

can develop POSITIVE ANA, SEVERE FUNGAL INFECTION, LYMPHOMA, and MS from this CD medication

infliximab

incidence of RECURRENCE AFTER SURGERY in CD depends on what?

1. site- ileocolic is highest | 2. nature of complication- obstruction, perforation, and abscesses have higher rate of recurrence

treatment scenarios for CD: COLON ONLY

sulfasalazine or mesalamine

treatment scenarios for CD: ANY ILEUM or SMALL BOWEL

slow-release mesalamine

treatment scenarios for CD: ONLY ILEUM or SMALL BOWEL

slow-release mesalamine or budesonide

treatment scenarios for CD: FISTULA or PERIANAL

- infliximab (or other immunomodulators), metronidazole, or ciprofloxacin - 6-MP also used

treatment scenarios for CD: incomplete acute small bowel obstruction

corticosteroids

screen CD patients for?

OSTEOPOROSIS

inflammation ALWAYS starts in RECTUM, extends proximally, ALWAYS confined to COLON

ulcerative colitis (UC)

INFECTIOUS causes of colitis

- E. coli O157:H7 (EHEC) - Shigella - Salmonella - Yersinia - Campylobacter - C. difficile - E. histolytica (amebiasis)

how is UC diagnosed?

colonoscopy or sigmoidoscopy

UC patient that develops jaundice, itching and cholestatic LFTs

PRIMARY SCLEROSING CHOLANGITIS (PSC) "JSEM" mnemonic - Joints - Skin - Eyes - Mouth (this mnemonic leaves out primary sclerosing cholangitis; PSC)

PANcolitis for 8 YEARS or LEFT-SIDED colitis for 15 YEARS should have...

a colonoscopy every 1-2 years

treatment for UC?

CURED with SURGERY (but difficult to do)

for MILD DISEASE of UC, treatment

- sulfasalazine PO - mesalamine PO - rectal mesalamine - hydrocortisone enema

for MODERATE-to-SEVERE DISEASE of UC, treatment

prednisone PO

treatment of fulminant UC

- hospitalize | - IV corticosteroids, infliximab, or cyclosporine

treatment of fulminant UC if symptoms persist for > 48 hours

colectomy

IBD buzzwords tenesmus

UC

IBD buzzwords rectal bleeding

UC

IBD buzzwords fecal soiling

think fistula= CD

IBD buzzwords hydronephrosis without stones

obstruction from inflammatory mass= CD

IBD buzzwords pneumaturia

think fistula to the bladder= CD

definition of diarrhea

> 200-250 g/day of stool

normal average daily stool output

150-180 grams/day

diarrhea duration

- acute = 1 month

etiology of acute diarrhea

commonly INFECTIOUS

diagnosis of acute diarrhea

check diet and travel history guaiac test and fecal WBCs

distinction between infectious diarrhea and IBD

BOTH can have crypt abscesses, but crypt distortions ONLY in IBD

treatment for INVASIVE diarrhea

- quinolones (especially ciprofloxacin) | - macrolides for Campylobacter (high quinolone resistance)

should you treat Salmonella with antibiotics?

NO, PROLONG infection

should you use antibiotics for E. coli O157:H7 (EHEC) infection?

NO! CONTRAINDICATED!

3 mechanisms of chronic diarrhea

OSMOTIC SECRETORY INCREASED MOTILITY

stool osmalality calculated=

2 x (stool [Na+] + stool [K+])

stool osmolar gap=

290 - stool osmolality calculated

SOG > 50

osmotic diarrhea | added osmoles are present causing diarrhea

SOG

normal stool, OR secretory diarrhea

in secretory diarrhea, patient is at risk of?

ELECTROLYTE DEFICIENCY (> 1L stool/day, meaning increased secretion of electrolytes)

does a 24-48-hour fast decrease secretory diarrhea?

NO, except in fatty acid- and bile acid-related diarrheas

does a 24-hour fast help with osmotic diarrhea?

YES

MOST COMMON cause of osmotic diarrhea

lactase deficiency

causes of dysmotility diarrhea

- antibiotics - hyperthyroidism - carcinoid - irritable bowel syndrome

disease with both osmotic and secretory diarrhea

CELIAC disease (malabsorption of carbohydrates= osmotic malabsorption of fat= secretory)

disease with osmotic, secretory, and dysmotility

EXUDATIVE diarrhea ``` (inflammation= causes altered motility malabsorption= causes osmotic and secretory diarrhea) ```

diarrhea and weight loss in AIDS patient WITHOUT FEVER BUT HAS LOW CD4 COUNT, suspect

``` noninvasive organisms: Cryptosporidia (usual cause) E. histolytica Giardia Isospora Strongyloides AIDS enteropathy ```

diarrhea and weight loss in AIDS patient WITH FEVER, think

``` Mycobacterium Campylobacter Salmonella Cryptococcus Histoplasma CMV ```

VOLUME: > 1L diarrhea/day in AIDS patient

AIDS-associated diarrhea

chronic bloody stools, think

UC

chronic loose stools, chronic RLQ abdominal cramping, think

CD

with GI tumors, when does carcinoid syndrome occur?

ONLY when it metastasizes to the liver

PAROXYSMAL FLUSHING; crampy, explosive DIARRHEA; and HYPOTENSIVE TACHYCARDIA

carcinoid syndrome

can cause NIACIN DEFICIENCY (pellagra)

carcinoid syndrome

diagnosis of carcinoid

check 24-hour urine for 5-HIAA (5-hydroxyindoleacetic acid); > 25mg/d

microscopic colitis (both COLLAGENOUS and LYMPHOCYTIC colitis)

chronic secretory, watery diarrhea | normal colonoscopy, only seen on microscopic biopsy

diagnosis of chronic diarrhea

stage 1: labs stage 2: more diagnostic tests stage 3: EGD and colonoscopy

"BIG 6" blood tests for malabsorption

1. albumin 2. Ca++ 3. cholesterol 4. carotene 5. serum iron (all LOW) 6. PT (PROLONGED)

2 subdivisions of malabsorption

1. MUCOSAL TRANSPORT (something wrong with intestinal uptake) 2. DIGESTION (not enough digestive enzymes)

what is celiac disease?

autoimmune gluten-sensitive enteropathy (small bowel villous atrophy and crypt hypertrophy causing malabsorption)

celiac disease can cause what in children?

GROWTH RETARDATION

deficiencies caused by celiac disease

``` iron folic acid calcium vitamin D vitamin B12 (rarely) vitamin K ```

dermatologic manifestation of celiac disease

dermatitis herpetiformis (vesicopapular rash)

4 diagnostic criteria of celiac disease

1. evidence of malabsorption 2. positive tissue transglutaminase Ab test OR antiendomysial Ab test 3. positive response to gluten-free diet 4. abnormal small bowel biopsy

treatment of celiac disease

LIFETIME GLUTEN-FREE DIET

what test to order in the following patient? a 16-year-old presents with a diagnosis of bipolar disorder

tissue transglutaminase Ab or IgA antiendomysial Ab for celiac disease

what test to order in the following patient? a 33-year-old presents with bone pain in his spine and legs

tissue transglutaminase Ab or IgA antiendomysial Ab for celiac disease

what test to order in the following patient? a 28-year-old presents with a pruritic papulovesicular eruption on her extensor elbows and knees

tissue transglutaminase Ab or IgA antiendomysial Ab for celiac disease

what test to order in the following patient? a 30-year-old presents with heme-negative stool and low Hb, MCV, and FERRITIN

tissue transglutaminase Ab or IgA antiendomysial Ab for celiac disease

what is tropical sprue?

malabsorption with partial villous atrophy | maybe caused by infectious organism

treatment of tropical sprue

tetracycline or doxycycline for 3-6 months

cause of whipple disease?

Tropheryma whipplei

cardinal tetrad of symptoms of whipple disease

1. arthralgias (MOST COMMON symptom preceding diagnosis) 2. abdominal pain 3. weight loss 4. diarrhea

diagnostic procedure of choice for whipple disease

EGD with small bowel biopsy

small bowel biopsy finding in whipple disease

FOAMY MACROPHAGES that are POSITIVE for PAS staining

treatment of whipple disease

- CEFTRIAXONE or IV PCN for 14 days | - THEN TMP/SMX FOR 1 YEAR

RELAPSE of whipple disease manifests with

CNS SYMPTOMS

short bowel syndrome happens when?

complications of short bowel syndrome

- CALCIUM OXALATE kidney stones (2/2 steatorrhea) | - gastric acid hypersecretion

treatment of short bowel syndrome

low-fat diet small frequent meals vitamin supplements TPN if needed

eosinophilic gastroenteritis can mimic

INTESTINAL LYMPHOMA and REGIONAL ENTERITIS

2 main causes of malabsorption d/t decreased digestion

1. pancreatic insufficiency | 2. bile acid deficiency

causes of pancreatic insufficiency

- chronic pancreatitis - pancreatic cancer - cystic fibrosis

determine pancreatic insufficiency with

qualitative stool exam

what must be ruled out if there is evidence of pancreatic insufficiency in patients > 55 years of age?

``` PANCREATIC CANCER (do a CT scan) ```

causes of bile acid deficiency

- ileal resection (> 100cm) (reuptake of bile acids) - severe liver disease (liver produces bile acids) - Zollinger-Ellison syndrome (increased acidity causes precipitation of bile acids - bacterial overgrowth (causes breakdown of bile acids)

best indicator of malabsorption

STEATORRHEA

"gold standard" for determining steatorrhea

3-day, quantitative fecal fat measurement steatorrhea if > 14g/d of fecal fat

best SCREENING test for steatorrhea

Sudan stain test

steatorrhea from what causes the MOST fecal fat? (can be > 50g/d)

PANCREATIC INSUFFICIENCY

first step in diagnosing malabsorption

determine if small bowel MUCOSAL problem or DIGESTIVE problem test for celiac disease or chronic pancreatitis

requires normal transmucosal transport, and doesn't need pancreatitic enzymes to be digested

D-xylose

NORMAL D-xylose test indicates

NORMAL mucosal transport | and PANCREATIC INSUFFICIENCY is MORE LIKELY

LOW D-xylose test indicates

NOT SPECIFIC, but if patient has STEATORRHEA, then small bowel disease

if LOW D-xylose test, next step?

SMALL BOWEL BIOPSY

moderate STEATORRHEA, but presenting c/o ABDOMINAL DISTENTION

bacterial overgrowth

macrocytosis with HIGH folate and LOW B12 levels

bacterial overgrowth (they make more folate, but decrease B12 absorption)

conditions causing bacterial overgrowth

- structural abnormalities (AFTER ILEOCECAL RESECTION) - motility disorders (DIABETES, and SCLERODERMA) - achlorhydria - immune disorders

bacterial overgrowth is associated with

ROSACEA

diagnosis of bacterial overgrowth?

LACTULOSE HYDROGEN BREATH TEST and sometimes a C14-glycocholate test

TREAT bacterial overgrowth EMPIRICALLY with

RIFAXIMIN (nonabsorbable antibiotic) for 2 weeks, then off for 1 week, and repeat indefinitely

> 60cm of terminal ileum resected

B12 deficiency

bile acid uptake is DECREASED | bile acid makes it to colon, causing bile acid-induced diarrhea

> 100cm of terminal ileum resected

bile acid uptake is LOST synthesis can't keep up with LOSS --> bile acid deficiency --> fat malabsorption

majority of causes of constipation

IDIOPATHIC

RECENT ONSET of constipation NO CHANGES TO DIET NO NEW MEDICATIONS

suggests OBSTRUCTING lesion

ACQUIRED MEGACOLON

- traumatic sacral nerve damage - MS - Chagas disease - aganglionic megacolon (Hirschsprung's)

what causes CHAGAS DISEASE and where is it found?

Trypanosoma cruzi Central and South America

Trypanosoma cruzi infection causes

- ACHALASIA - cardiomyopathy - acquired megacolon

common drugs that cause constipation

many, but ANTIcholinergics, and ESPECIALLY most NARCOTICS

one of the most common causes of constipation

dehydration

endocrine disorders that can cause constipation

DIABETES MELLITUS | HYPOTHYROIDISM

who gets worked up for constipation?

patients that also have: | WEIGHT LOSS, RECTAL BLEEDING, or ANEMIA

w/u for constipation with other symptoms

- colonoscopy (to r/o cancer, or strictures) | - serum Ca++ and TSH (to exclude hyper/hypocalcemia and hypothyroidism; DM comes from the history)

test for intractable constipation

colonic transit function with 24 radiopaque markers ("Sitz markers")

abnormal colonic transit function test

more than or equal to 5 markers if markers spread THROUGHOUT colon = GENERALIZED COLONIC INERTIA CLUSTERING of markers in RECTOSIGMOID colon = pelvic floor dysfunction

treatment of constipation

dietary fiber > 20g/day and fluid intake

what kind of constipation does increased fiber and water help with?

colonic inertia, but NOT pelvic floor dysfunction

presentation of fecal impaction

sudden onset watery stools/incontinence in a person with chronic constipation

treatment of fecal impaction

REMOVE impaction

in patients > 50 years of age with new-onset IBS-like symptoms, you should?

check for other causes

characteristic IBS symptoms

- abdominal relieved by defecation - change in stool frequency/consistency - NO NOCTURNAL SYMPTOMS

treatment of IBS

REASSURANCE

colon cancer risk factors

``` age > 50 adenomatous polyps UC and CD BRCA1 mutation acromegaly obesity smoking diets high in calories and animal fat ```

hereditary risk factors for colon cancer

1st degree relatives with colon cancer OR adenomatous polyps FAP HNPCC

endocarditis caused by either Streptococcus bovis or Clostridium septicum is associated with

COLON CANCER

most GI cancers arise from

ADENOMAS

adenomas with "ADVANCED" features "ADVANCED" means likely to develop cancer

high-grade dysplasia villous histology size > 10mm

do HYPERPLASTIC polyps have malignant potential?

NO | contain NO features of dysplasia

1 OR 2 small tubular ADENOMAS with low-grade dysplasia

repeat colonoscopy 5-10 years after initial polypectomy

3-10 ADENOMAS

repeat colonoscopy in 3 years

1 adenoma > 1cm

repeat colonoscopy in 3 years

any adenoma with VILLOUS features or HIGH-GRADE dysplasia

repeat colonoscopy in 3 years

> 10 ADENOMAS

repeat colonoscopy

SESSILE adenomas that are removed piecemeal

repeat colonoscopy in 2-6 MONTHS

genetics of FAP

AUTOSOMAL DOMINANT (AD)

4 types of familial polyposis syndromes in DECREASING cancer potential

1. FAP (familial adenomatous polyposis) 2. Gardner syndrome 3. Peutz-Jeghers syndrome 4. juvenile polyposis

HUNDREDS OF ADENOMAS in the COLON | 100% RISK OF CANCER

FAP

REQUIRE PROPHYLACTIC PROCTOCOLECTOMY by AGE 20!

FAP

giant stomach tumors in FAP patients are

BENIGN

variant of FAP with multiple OSTEOMAS

Gardner syndrome

patient has multiple osteomas found incidentally on an x-ray | what do you do?

colonoscopy!

variant of FAP with multiple hamartomatous polyps in small bowel, and freckles on lips and buccal mucosa

Peutz-Jeghers syndrome

variant of FAP with > 10 juvenile polyps

juvenile polyposis

hereditary nonpolyposis colon cancer a.k.a.

Lynch syndrome

colorectal, endometrial, small bowel, ureter, or renal pelvis cancer in: 3 FIRST DEGREE relatives, over at least 2 generations, with at least 1 person diagnosed

hereditary nonpolyposis colon cancer (HNPCC)

women in families with HNPCC have an increased incidence of

OVARIAN and ENDOMETRIAL cnacer

screening of patient with HNPCC risks starts at

age 25

colorectal cancer screening ASYMPTOMATIC MORE THAN OR EQUAL TO 50 YEARS of age NEGATIVE FAMILY HISTORY

colonoscopy every 10 years

USPSTF recommends AGAINST screening for colorectal cancer in which patients

> 85 years of age

colorectal cancer screening increased-risk patients

start at age 40 or 10 YEARS before age of index cancer was diagnosed, WHICHEVER IS FIRST

screening procedure of choice in patient with ANY 1st degree relative with colon cancer or an adenomatous polyp

COLONOSCOPY

test that can be done if you can't do a colonoscopy

CT colonography

screen for what in OLDER patients after episode of DIVERTICULITIS

SIGMOID COLON CANCER

where does colon cancer almost always metastasize to?

LIVER (via portal circulation)

where does colon cancer metastasize to if it only involves the RECTUM?

lung, bone, and brain WITHOUT liver mets (bypasses portal circulation)

1st treatment option for colon cancer and potentially curative

SURGICAL RESECTION

what is the adjuvant chemotherapy protocol for colon cancer?

FOLFOX - FOlinic acid (leucovorin) - 5-FU - OXaliplatin

adjuvant chemo effective in colon cancer only when?

stage 3 or locally advanced stage 2

radiation therapy prior to surgery only helpful in colon cancer for?

RECTAL lesions

4 types of diverticular disease

1. asymptomatic diverticulosis (most common) 2. painful diverticulosis 3. diverticular bleeding 4. diverticulitis

luminal narrowing of colon pencil-thin stools bouts of colicky pain relieved by BM

symptomatic diverticulosis

treatment of symptomatic diverticulosis

BULKING AGENTS (psyllium or methylcellulose)

MOST COMMON cause of colonic bleeding

diverticular bleeding

2nd most common cause of colonic bleeding (more severe bleeds)

ANGIODYSPLASIA

PAINLESS, MAROON STOOL

diverticular bleeding

treatment for diverticular bleeding

IVF, PRBCs if needed, r/o UGI, colonoscopy if bleeding doesn't stop

UGI bleed is suggested by

BUN/Cr ratio > 30:1

cause of diverticulitis

MICROPERFORATIONS

``` LLQ pain fever high WBC LLQ tenderness NO BLEEDING ```

diverticulitis

look for what on physical exam in diverticulitis

SIGMOID MASS (palpable, tender sigmoid)

most useful test in assessing diverticulitis

CT scan

AVOID what in diverticulitis

COLONOSCOPY (d/t risk of perforation)

treatment of diverticulitis should cover which organisms?

AEROBIC and ANAEROBIC GRAM-NEGATIVE organmisms

treatment of MILD diverticulitis

METRONIDAZOLE (gram-negative ANaerobic coverage) plus CIPROFLOXACIN OR TMP/SMX (gram-negative aerobic coverage) as outpatient

treatment of MODERATE-to-SEVERE diverticulitis

DUAL-drug therapy (BEST!) - aminoglycoside or ciprofloxacin (gram-negative aerobic) PLUS - clindamycin or metronidazole (gram-negative anaerobic) or single-drug therapy that has both gram-negative aerobic and anaerobic coverage

can present similarly to diverticulitis | and patients > 50 years of age need flex-sig/colonoscopy in 4-8 weeks

PERFORATION from sigmoid COLON CANCER

angiodysplasia = vascular ectasia = AVM

2nd most common cause of lower GI bleeding in elderdly

hereditary condition with multiple AVMs

hereditary hemorrhagic telangiectasias (Osler-Weber-Rendu)

recurrent melanotic stools, with NEGATIVE EGDs and colonoscopies, you should

video capsule endoscopy (VCE)

most common cause of SMALL INTESTINE obstruction

postoperative ADHESIONS

most common causes of COLONIC obstruction (in decreasing frequency)

CARCINOMA --> DIVERTICULITIS --> VOLVULUS

persistent vomiting, obstipation, and constipation

suggest obstruction

confirm diagnosis of obstruction with

flat and upright abdominal film

fluid levels SAME HEIGHT on either side of loop

PARALYTIC ILEUS

4 types of intestinal ischemia

1. ischemic colitis (MOST COMMON) 2. chronic mesenteric ischemia 3. acute mesenteric ischemia (70% mortality) 4. mesenteric venous thrombosis

ABDOMINAL PAIN and MAROON stools

ischemic colitis

areas affected by nonocclusive ischemia

splenic flexure descending colon sigmoid colon (inferior mesenteric circulation)

ischemic colitis cause

most often, NO SPECIFIC CAUSE found

possible ischemic colitis causes

- LOW-FLOW CONDITIONS (CHF) - medications/cocaine - HYPERCOAGULABLE states

sudden LLQ pain with urge to defecate, followed by passage of RED-TO-MAROON stool w/i 1 day

ischemic colitis

what do you see on abdominal x-ray (KUB) in ischemic colitis?

submucosal hemorrhage and edema (mildest injury)

what do you see with barium enema in ischemic colitis?

"THUMBPRINTING"

1st diagnostic test done for ischemic colitis

CT scan

do this with peritoneal signs in setting of suspected ischemic colitis

COLONOSCOPY withOUT bowel prep

is angiography done for ischemic colitis?

usually NOT

another name for chronic mesenteric ischemia

INTESTINAL ANGINA

classic triad of chronic mesenteric ischemia

1. abdominal pain after meals 2. abdominal bruit 3. weight loss (from tolerating only smaller meals)

pain in chronic mesenteric ischemia (intestinal angina) is d/t episodes of what?

INADEQUATE blood FLOW brought on by DIGESTION

suspect what if ABDOMINAL PAIN is OUT OF PROPORTION to physical findings

mesenteric vascular ischemia

1-3 HOURS OF DULL, GNAWING abdominal pain about 30 minutes after eating

chronic mesenteric ischemia

diagnosis of chronic mesenteric ischemia

based on SYMPTOMS

tests that can be done to help in the diagnosis of chronic mesenteric ischemia

MRA or CT ANGIOGRAM

most severe and life-threatening form of intestinal ischemia (MORTALITY RATE OF 70%- even with treatment!)

ACUTE MESENTERIC ISCHEMIA

etiology of acute mesenteric ischemia

thromboembolus in a mesenteric artery --> loss of blood flow to corresponding SMALL INTESTINE and/or ASCENDING COLON

symptoms of acute mesenteric ischemia

ACUTELY ILL with vomiting, diarrhea, and rectal blood

bowel infarction leads to

LACTIC ACIDOSIS

diagnostic test for acute mesenteric ischemia

CT ANGIOGRAPHY unless there is evidence of PERFORATION

treatment of acute mesenteric ischemia

possible embolectomy, or surgery for dead-bowel resection

mesenteric VENOUS thrombosis (MVT) is associated with

hypercoagulable states

mesenteric VENOUS thrombosis (MVT) may be

ACUTE, SUBACUTE, or CHRONIC

diagnostic procedure of choice for mesenteric VENOUS thrombosis (MVT)

CT

treatment of ACUTE MVT

THROMBOLYTICS and LONG-TERM ANTICOAGULANTS

treatment of CHRONIC MVT

sclerotherapy or portosystemic shunts

most common causes of acute pancreatitis

ALCOHOL ABUSE and GALLSTONES

diagnostic test that can cause acute pancreatitis in 2-5% of patients

endoscopic retrograde cholangiopancreatography (ERCP)

``` acidosis (eg, DKA) hyertriglyceridemia hypercalcemia trauma obstruction of ampulla of Vater (eg, pancreatic cancer) ```

other causes of acute pancreatitis

biliary microlithiasis cystic fibrosis hereditary pancreatitis hypertriglyceridemia

possibly overlooked causes of acute pancreatitis labeled as "idiopathic"

elevated enzymes in acute pancreatitis

amylase and lipase (> 3x normal)

may cause spuriously NORMAL amylase level!

acute pancreatitis with high triglyceride levels

triglyceride levels > 1,000 mg/dL can cause

pancreatitis

classification for acute pancreatitis (2 out of 3 must be present to make the diagnosis)

1. upper abdominal pain radiating through to the back 2. serum amylase or lipase 3x upper limit of normal 3. cross sectional imaging consistent with acute pancreatitis

severity of acute pancreatitis directly related to

degree of pancreatic NECROSIS (10-25% have necrosis) and if necrotic tissue is INFECTED

mortality of acute pancreatitis if necrotic tissue is NOT infected

10%

mortality of acute pancreatitis if necrotic tissue IS infected

30%

overall mortality rate for acute pancreatitis

5-10%

severe pancreatitis causes

shock and MULTIORGAN FAILURE

hemoconcentration SBP 130 bpm PO2

indicators of severe pancreatitis

most COMMON skin finding in severe pancreatitis

ERYTHEMA of flanks | extravasated pancreatic exudates

faint blue discoloration around umbilicus (includes HEMOPERITONEUM)

Cullen sign

bluish-reddish-purple or greenish-brown discoloration of flanks

Turner sign

characteristic, but NOT pathognomonic for acute pancreatitis

Cullen and Turner signs

severity scoring systems for acute pancreatitis

APACHE II and BISAP

BISAP scoring for MORTALITY

``` BUN > 25 impaired mental status SIRS age > 60 years pleural effusion ```

SIRS criteria

temperature 100.4 HR > 90 RR > 20 OR pCO2 12 OR 10% bands

current AGA recommendations for acute pancreatitis

if APACHE II score greater than or equal to 8 OR organ failure at 72 hours; get a CT to check for necrosis

associated with 2x increase in mortality in acute pancreatitis

morbid obesity (BMI > 30)

pancreatic necrosis best confirmed by

CT SCAN or MRI

pancreatic necrosis is severe if?

GREATER THAN OR EQUAL TO 30%

do this daily for acute pancreatitis

SIRS evaluation

occurs within 48 HOURS of PAIN onset in acute pancreatitis

ACUTE FLUID COLLECTION

occurs in first 1-2 weeks of acute pancreatitis (may resemble pseudocyst)

NECROTIC TISSUE

diagnosis and treatment of infected pancreatic necrosis

endoscopic or CT-guided aspiration

may occur after A MINIMUM OF 4 WEEKS after acute pancreatitis

pseudocyst

what size pseudocyst probably won't resolve on its own?

> 5cm

if pancreatic pseudocyst persists > 3-6 months and causes symptoms, then what?

drain it

may occur 4-6 WEEKS after acute severe pancreatitis with severe pancreatic necrosis

ABSCESS

pancreatic abscess on upright abdominal x-ray

"SOAP BUBBLE sign"

diagnosis of pancreatic abscess

CT-GUIDED PERCUTANEOUS ASPIRATE (90% accurate)

diagnosis of acute pancreatitis

gallbladder US to r/o gallstones

treatment of acute pancreatitis

supportive care: NPO, LR, NGT feeds (in protracted acute pancreatitis patients)

when do you give systemic antibiotics in acute pancreatitis?

ONLY if there is ESTABLISHED infection

IVF protocol for acute pancreaitis

LR is crystalloid of choice (decreased incidence of SIRS) - 20mL/kg bolus - then continuous infusion at 3mL/kg/hr for 6-8 hours - if fluid responsive: 1.5mL/kg/hr - if fluid refractory: give another 20mL/kg bolus and continuous infusion at 3mL/kg/hr - recheck at 16 hours

if amylase is still elevated after 10 days, think of

leaking pseudocyst

recurrent acute pancreatitis with NO evidence of gallstones or alcohol abuse may be d/t

MICROLITHIASIS | do elective cholecystectomy

gastric varices WITHOUT esophageal varices

ONLY happens with splenic vein thrombosis

complication of both severe ACUTE pancreatitis and CHRONIC pancreatitis

splenic vein thrombosis

criteria for resumption of oral feeds in acute pancreatitis

1. bowel sounds present and passing flatus/stools 2. doesn't need narcotics 3. patient is hungry and wants to eat

``` acute pancreatitis acute cholecystitis intestinal infarction diabetic ketoacidosis perforated ulcer salpingitis ectopic pregnancy ```

can cause elevated AMYLASE

common cause of chronic pancreatitis

chronic alcohol ingestion, > 10 years

fecal fat/day in chronic pancreatitis

> 40g/day | late stage may be > 100g/day

late chronic pancreatitis patients develop

STEATORRHEA and DIABETES MELLITUS

diagnostic triad for CHRONIC pancreatitis

1. pancreatic calcification 2. diabetes 3. steatorrhea

PROCEDURE OF CHOICE for diagnosis of chronic pancreatitis

CT scan of abdomen

diagnosis of chronic pancreatitis on CT of abdomen is made IF

- calcified pancreas, OR - dilated pancreatic duct, OR - atrophic pancreas

best test to diagnose chronic pancreatitis, BUT requires a skilled gastroenterologist

endoscopic ultrasound

if initial tests are negative, but you still suspect chronic pancreatitis do this

MRCP (NO risk of causing pancreatitis)

only advantage of ERCP over MRCP in chronic pancreatitis

endoscopic removal of CALCIFIC STONES

pancreatic duct has stenoses and dilations seen on MRCP and ERCP visualized as

"CHAIN OF LAKES"

most sensitive test for pancreatic exocrine function

SECRETIN TEST

how diabetes in chronic pancreatitis different?

decrease in insulin AND glucagon

low glucagon in chronic pancreatitis can lead to?

HYPOglycemia

do patients with diabetes from chronic pancreatitis develop retinopathy and nephropathy?

NO, usually NOT

treatment of chronic pancreatitis

alcohol and tobacco cessation pancreatic enzymes supplementation decreasing dietary fat antioxidants

SERUM IGG4 level greater than or equal to 2x normal

autoimmune pancreatitis

JAUNDICE, (unexplained upper) ABDOMINAL PAIN, and/or WEIGHT LOSS

pancreatic cancer

pancreatic cancer: HEAD of pancreas

painLESS jaundice, present early

pancreatic cancer: BODY and TAIL of pancreas

PAIN and WEIGHT LOSS, more advanced

helical CT, CTA, EUS-guided FNA biopsy, and laparoscopy to diagnose

pancreatic cancer

treatment of pancreatic cancer

RESECTION

most common reasons for tumor unresectability of pancreatic cancer

- distant metastases | - local invasion of major vessel

surgical candidate + mass in HEAD of pancreas + appears resectable

do a pancreaticoduodenectomy (Whipple resection)

serum marker for pancreatic cancer

CA 19-9

if pancreatic cancer has already metastasized

AVOID surgery | place STENT with ERCP to palliate biliary obstruction

ONLY time you use ERCP for pancreatic cancer

to place a STENT to help with biliary obstruction

glucagon-secreting, alpha-cell tumor of pancreas

glucagonoma

``` scaly NECROLYTIC ERYTHEMA weight loss anemia diarrhea persistent HYPERglycemia plasma glucagon > 1,000pg/dL ```

GLUCAGONOMA

insulin-secreting, beta-cell tumor of pancreas

insulinoma

serum gastrin > 500 in patient who is able to secrete gastric acid (not on PPI, no prior peptic ulcer)

gastrinoma

tumor that secretes vasoactive intestinal peptide (VIP)

VIPoma

VIPomas cause

PROFUSE SECRETORY DIARRHEA ("pancreatic cholera")

is cholelithiasis associated with hypercholesterolEMIA?

NO

pathophysiology of cholelithiasis

1. abnormal bile secretion 2. accelerated nucleation of microcrystals to MACROcrystals 3. defective GB emptying

cholelithiasis associated with

obesity OCPs clofibrate treatment ileal disease/resection

75% of gallstones are composed of

radioLUCENT CHOLESTEROL (pure or mixed) | the rest are bile pigment gallstones

cholelithiasis symptoms

RUQ pain (20-60 minutes, especially after fatty meal)

diagnose cholelithiasis

ULTRASOUND (90% sensitive)

best test for confirming acute CYSTIC duct obstruction (ie, ACUTE CHOLECYSTITIS)

HIDA SCAN (cholescintigraphy)

treatment of cholelithiasis, if patient has gallstones and SYMPTOMATIC

elective cholecystectomy

ACALCULOUS cholecystitis

occurs only in SERIOUSLY ILL patients; eg, major trauma, burns, after major surgeries

alkaline phosphatase and bilirubin in typical gallbladder cases

NOT elevated

INCREASING LEVELS of ALP and bilirubin (> 4mg/dL) suggest

COMMON DUCT STONE | choledocholithiasis

post-cholecystectomy patient with PERSISTENT PAIN

COMMON DUCT STONE | choledocholithiasis

treatment for common duct stones

ERCP

OBSTRUCTIVE (common duct stones) or HEPATOCELLULAR

cholestasis

Charcot's triad: 1. biliary colic (abdominal pain) 2. fever 3. jaundice

acute cholangitis

Reynold's pentad: 1. biliary colic (abdominal pain) 2. fever 3. jaundice 4. SEPTIC SHOCK 5. AMS

suppurative cholangitis (ascending cholangitis)

treatment acute cholangitis

PARENTERAL ANTIBIOTICS IV HYDRATION BILIARY DRAINAGE

best procedure for diagnosis and treatment of suppurative cholangitis (ascending cholangitis)

ERCP WITH ENDOSCOPIC SPHINCTEROTOMY

treatment for EMPHYSEMATOUS cholecystitis

emergent laparotomy with cholecystectomy AND antibiotics

antibiotics for suppurative cholangitis and emphysematous cholecystitis must cover

GRAM-NEGATIVE and ANAEROBIC organisms

do NOT use this antibiotic for suppurative cholangitis and emphysematous cholecystitis

CEFTRIAXONE (can cause biliary sludge; NO anaerobic coverage)

X-ray showing GB with CALCIFIED OUTLINE

"porcelain gallbladder" | suggests CANCER

treatment for porcelain gallbladder

OPEN cholecystectomy

nonsuppurative, progressive, destructive cholangiolitis SLOW onset, 95% ARE WOMEN- MIDDLE-AGED

primary biliary cholangitis (PBC)

florid duct lesion on liver biopsy

pathognomonic for primary biliary cholangitis (PBC)

90% of primary biliary cholangitis (PBC) have positive

ANTIMITOCHONDRIAL ANTIBODY test (> 1:40) degree of elevation does NOT correlate with severity of disease

PBC patient who present with symptoms have

ADVANCE disease

FATIGUE HIGH ALKALINE PHOSPHATASE ITCHING (first on palms and soles, then throughout body)

primary biliary cholangitis (PBC)

PBC course

indolent, but RELENTLESSLY PROGRESSIVE

ALKALINE PHOSPHATASE 2-5x above normal

PBC

hallmark test for PBC

ANTIMITOCHONDRIAL ANTIBODY test

NOT a good indicator of severity of PBC

antimitochondrial antibody test

antimitochondrial antibody test can be positive in PBC, and?

autoimmune hepatitis, and drug-induced chronic hepatitis

diagnosis of PBC is confirmed ONLY with

LIVER BIOPSY

PBC patients also have a high hepatic level of?

COPPER | as do patients with primary sclerosing cholangitis and Wilson disease

treatment of biliary cirrhosis

URSODIOL (ursodeoxycholate- a synthetic bile acid)

what SLOWS progression of primary biliary cirrhosis?

URSODIOL

BIOCHEMICAL RESPONSE to ursodiol leads to

DRAMATIC SLOWING of progression of PBC

treatment has what effect on LATE disease of PBC?

NO EFFECT

what is recommended for late disease of PBC?

liver transplantation

AAAABCs of PBC

Antimitochondrial Antibody Attack INCREASES Alk phos and CAUSES obstructive Biliary lesions and liver Cirrhosis

indolent, 70% males, average age of 45

primary sclerosing cholangitis (PSC)

PSC is strongly associated with

COLITIS (MAINLY UC [up to 75% of PSC patients have UC])

ALL PSC patients should have a

COLONOSCOPY

any UC patient with persistent, greater than or equal to 2x increase in ALKALINE PHOSPHATASE should be screened for

PSC

cause of PSC?

unknown

pathophysiology of PSC

intra- and extrahepatic biliary tract sclerosis leading to OBSTRUCTIVE JAUNDICE and CIRRHOSIS

elevated BILIRUBIN and ALKALINE PHOSPHATASE elevated hepatic COPPER but NEGATIVE antimitochondrial antibody test

primary sclerosing cholangitis (PSC)

8-15% of PSC patients develop

CHOLANGIOCARCINOMA | suspect if PSC patients abruptly worsen

diagnose PSC

MRCP

MRCP, ERCP, or transhepatic cholangiography shows what for PSC?

"BEADED" appearance

liver biopsy shows what for PSC?

"onion skin" fibrosis in portal triads | establishes the diagnosis

treatment of sclerosing cholangitis

LIVER TRANSPLANTATION

should you use ursodeoxycholic acid (UDCA) in PSC?

no, recommend AGAINST UDCA, and if on it in the past, recommend DISCONTINUING it

jaundice, increased alk phos, h/o chronic diarrhea or IBD, ESPECIALLY UC, must rule out?

PSC with MRCP or ERCP

sclerosing CHOLangitis, COLitis, high CHOLestatic bili, and alk phos; negative antimitochondrial Ab, cirrhosis, and liver failure abnormal MRCP or ERCP

PSC

female, no IBD, cancer is rare, UDCA is effective

PBC (primary biliary cholangitis

male, IBD, (UC) 8-15% risk of cholangiocarcinoma, UDCA is NOT effective

PSC (primary sclerosing cholangitis)

enzyme more liver-specific than AST

ALT (Liver)

alcoholic hepatitis AST:ALT ratio

AST:ALT ratio is about 3:1 | alcohol damages MITOCHONDRIA

viral hepatitis AST:ALT ratio

ALT > AST | ALT is more liver-specific

nonalcoholic fatty liver disease (NAFLD)2 hepatitis ALT:AST ratio

ALT:AST ratio is > 2:1 | NAFLD is also more liver-specific

alkaline phosphatase comes from

LIVER and BONES

check this when elevated alkaline phosphatase, but normal bilirubin and tranaminases

GGT (gamma glutamyl transpeptidase)

if transaminases are elevated order this: | and if still elevated:

- reorder labs to confirm - order hepatitis panel (A, B, C) - iron and ferritin (r/o hemochromatosis)

if alk phos and GGT are elevated, next test

abdominal ultrasound (look for dilated biliary ducts or metastatic liver lesions)

what type of virus is hepatitis A?

RNA

hepatitis A is easily transmitted by?

fecal-oral route (food or water) or sexually transmitted NO transplacental transmission!

NO carrier or persistent states, but can cause PROLONGED CHOLESTASIS (increased bili and alk phos) up to 4 months

hepatitis A

diagnosis of acute hepatitis A infection

high titers of anti-HAV IgM in serum | IgG indicates previous infection

- high-risk sexual behavior - IV drug use - recommended for all > 1 year of age - chronic liver disease

indications for HAV vaccine

patients with hepatitis B and C need

HAV vaccine (can be fulminant)

onset of jaundice with hepatitis A

3 WEEKS

onset of jaundice with hepatitis B

3 MONTHS

means you're producing hepatitis B virus

HBsAg

indicates past exposure to EITHER: hepatitis B VIRION, or vaccine

HBsAb | usually indicates IMMUNITY

what HB antigen DOES NOT CIRCULATE in the serum?

HBcAg

best marker for PREVIOUS exposure to HBV

HBcAb IgG

HB antigen IS secreted from hepatocytes and circulates in serum

HBeAg

correlates with the QUANTITY OF INTACT VIRUS and, therefore, INFECTIVITY and liver INFLAMMATION

HBeAg

indicates active virions and high infectivity

HBsAg AND HBeAg

only hepatitis virus composed of DNA

hepatitis B

hepatitis is strongly associated with

POLYARTERITIS NODOSA (PAN)

HBsAg + anti-HBc - anti-HBs -

acute infection

HBsAg + anti-HBc + anti-HBs -

3 possibilities: 1) acute infection (IgM anti-HBc) 2) chronic Hep B (high ALT, IgG anti-HBC) 3) inactive carrier (normal enzymes, IgG anti-HBc)

HBsAg - anti-HBc - anti-HBs +

2 possibilities: 1) remote infection 2) immunized

HBsAg - anti-HBc + anti-HBs +

remote infection

HBsAg - anti-HBc + anti-HBs -

3 possibilities: 1) window disease 2) remote infection 3) false positive

HBsAg + anti-HBc + anti-HBs +

more than 1 infection; | eg, IVDA or renal dialysis patient with both ACUTE and CHRONIC hepatitis B (infected with different strains)

SERUM SICKNESS-LIKE symptoms of hepatitis B

fever, arthritis, urticaria, and angioedema

hepatitis B prodromal symptoms constitutional get better when?

onset of jaundice

what do you give a newborn of a mother with hepatitis B?

BOTH hep B immune globulin (HBIG) and hepatitis B vaccination

asymptomatic patient has HBsAg | EITHER patient is a carrier OR has early hepatitis B

initially, follow closely

what do you give sexual contacts and infants cared for by a patient with acute HBV infection?

HBIG AND HBV vaccinations

what do you give pregnant patient with acute HBV infection?

HBIG AND HBV vaccinations

how is likelihood of developing CHRONIC HBV related to AGE?

INVERSELY | 90% chance in infants; 25-50% chance in children 1-5 years; 5% chance in older children and adults

what are 2 types of hepatitis B carrier states?

1. inactive carrier state (asymptomatic with NORMAL liver enzymes) 2. chronic active hepatitis B

how do you confirm chronic hepatitis B diagnosis?

LIVER BIOPSY

what happens to patients with INACTIVE carrier states if they become IMMUNOCOMPROMISED?

CAN develop severe exacerbations

chronic hepatitis B progresses to

CIRRHOSIS

chronic hepatitis B strongly associated with

HEPATOCELLULAR CARCINOMA (HCC)

in chronic hepatitis B, screen for HCC every?

6 months with abdominal ULTRASOUND

should you use alpha-fetoprotein (AFP) to screen for HCC?

NO, not sensitive or specific enough

when do you treat chronic active hepatitis B?

HBV DNA > 20,000 and ALT > 2x ULN

when do you treat chronic active hepatitis B with CIRRHOSIS?

treat compensated cirrhosis when HBV DNA > 2,000 treat DEcompensated cirrhosis when HBV DNA > 200

only treatment for end-stage liver disease

liver transplantation

what type of virus is hepatitis C?

single-strand RNA virus

most common liver disease in the US

NAFLD (nonalcoholic fatty liver disease)

2nd most common liver disease in the US

hepatitis C

most common HCV GENOTYPE in the US

GENOTYPE 1 (> 70%) LESS responsive to treatment

risk factors for hepatitis C

drugs, sex, blood, needles

porphyria cutanea tarda (PCT) is associated ONLY with

hepatitis C | not B

what should you do within 2-4 months after exposure to hepatitis C?

RECHECK for loss of HCV RNA (PCR) to make sure it's not chronic

how do you check for immunity to hepatitis C?

HCV RNA HCV Ab does NOT confer immunity (just means prior infection)

what percentage of HCV infections become CHRONIC?

70-80%

what percentage of chronic HCV develop end-stage cirrhosis?

25% of the 70-80% that develpp chronic HCV after 20-25 years

in chronic hepatitis C, screen for HCC every?

6 months with abdominal ULTRASOUND

#1 reason for liver transportation in the US

chronic HCV infection

MIXED cryoglobulinemia is STRONGLY associated with?

chronic hepatitis C

treat CHRONIC hepatitis C and elevated liver enzymes

COMBINATION of: pegylated INF-a ribavirin (RNA polymerase inbibitor) telaprevir or boceprevir (protease inhibitors)

adverse effect of ribavirin

HEMOLYTIC ANEMIA

what can worsen when a patient is on INF-a?

depression

what type of virus is hepatitis D?

RNA

hepatitis D needs what?

COEXISTENT hepatitis B virus infection

suspect what if sudden decompensation in patient with chronic hepatitis B?

hepatitis D

what type of virus is hepatitis E?

single-strand RNA

how is hepatitis E transmitted?

fecal-oral route (food or water) commonly after monsoon flooding

carries very high risk for fulminant hepatitis in 3rd trimester of pregnancy (20% fatality rate)

hepatitis E

TRAVELER with acute hepatitis and NEGATIVE STANDARD SEROLOGY (hep A, B), think of?

hepatitis E

does HGV cause chronic liver disease?

no evidence that it does

differential diagnoses of chronic hepatitis | A, B, C, D, F

``` A= autoimmune B= hepatitis B C= hepatitis C D1= hepatitis D (only with hep B) D2= drugs D3= diseases F= NAFLD ```

MOST SENSITIVE and LEAST SPECIFIC for autoimmune hepatitis

ANA

about 80% sensitive and MORE SPECIFIC than ANA for autoimmune hepatitis

anti-SMA antibody (smooth muscle antibody)

more SPECIFIC and SENSITIVE for autoimmune hepatitis

anti-actin antibody (AAA)

MOST SPECIFIC, but NOT SENSITIVE

anti-SLA (soluble liver antigen)

confirm diagnosis of autoimmune hepatitis

LIVER BIOPSY

treatment of autoimmune hepatitis

PREDNISONE or BUDESONIDE | +/- AZATHIOPRINE

CONTRAINDICATED and EXACERBATES autoimmune hepatitis

IFN-a

is there a cure for autoimmune hepatitis?

NO CURE

toxic, intermediate compound NAPQI, and glutathione depletion

acetaminophen toxicity

2-FOLD effect - increased P-450 system - an already decreased glutathione supply

alcohol-acetaminophen syndrome

long-term users of moderate-to-heavy alcohol should be cautious of? and, are at risk for?

taking NORMAL or higher levels of acetaminophen | at risk for SEVERE HEPATIC TOXICITY or LIVER FAILURE

can develop liver toxicity by not eating for 3-4 days and taking

THERAPEUTIC doses of acetaminophen

most common cause of FULMINANT hepatitis in the US

acetaminophen toxicity

alcoholic liver disease results in?

MACROvesicular fat accumulation

this enzyme is DISPROPORTIONATELY HIGH in alcoholic liver disease

GGT

AST is virtually always

alcoholic liver injury

can cause indolent, asymptomatic liver disease that progresses to cirrhosis

methotrexate (MTX)

young woman on OCPs who has a mass in her liver

ADENOMA

EXCLUSIVELY occurs in children

Reye syndrome

viral illness, CONCURRENT ASA use, progressive encephalopathy

Reye syndrome | MIRCROvesicular fat accumulation (50% mortality)

looks just like alcoholic liver disease, but NO h/o alcohol abuse

NASH aka NAFLD

75-80% of "CRYPTOGENIC" cirrhosis is d/t

NAFLD

DROP is a metabolic syndrome with:

Dyslipidemia insulin Resistence Obesity increased blood Pressure

treatment of NAFLD

weight loss, DM and hyperlipidemia control

treatment for biopsy-proven NASH

vitamin E

associated with CHRONIC LIVER DISEASE of ANY type and AFLATOXIN exposure

hepatocellular carcinoma (HCC, "hepatoma")

MOST COMMON cause of HCC in the US

ALCOHOLIC liver disease, with CONCURRENT HEPATITIS C (75%)

``` tender hepatomegaly BRUIT in RUQ bloody ascites high alk phos very high AFP ```

HCC

hypercalcemia (PTHrP) hypoglycemia (high demand) watery diarrhea FUO

HCC-associated PARANEOPLASTIC syndrome

- esophageal variceal hemorrhage - hepatic encephalopathy - hepatorenal syndrome - prolonged PT

complications of cirrhosis

SIZE of varices correlates with

risk of bleeding

should be prescribed to ALL patient with medium to large varices- whether or not they have had bleeding

nonselective beta-blockers propranolol or nadolol

should you perform sclerotherapy to prevent a 1st hemorrhage in medium to large varices?

NO, appear to make things worse

what do you do for a patient with cirrhosis and small esophageal varices?

NOTHING- only BIG varices bleed!

primary therapy of actively bleeding varices

ENDOSCOPIC BANDING or SCLEOTHERAPY preferably with somatostatin

give all cirrhotic patients with bleeding or ascites prophylactic PO or IV what? to prevent what?

antibiotics (3rd generation cephalosporin or quinolones) SBP (spontaneous bacterial peritonitis) AKI decrease mortality

should be prescribed to ALL patients who have had bleeding varices to decrease the chance of rebleeds

B-blocker propranolol or nadolol

only used for varices that REbleed

TIPS (transjugular intrahepatic portosystemic shunt)

``` GI bleed hypovolemia hypoxia hypokalemia sedatives tranquilizers portal venous obstruction infections alkalosis (which, increases ammonia/ammonium ratio) ```

things that can cause hepatic encephalopathy or make it worse

signs of hepatic encephalopathy

fetor hepaticus hyperreflexia asterixis altered mental status

treatment of hepatic encephalopathy

lactulose (goal of about 3 BM/day) rifaximin, metronidazole, rifampin, or vancomycin acarbose probiotics

diagnosis of hepatorenal syndrome

diagnosis of exclusion

urine sodium in hepatorenal syndrome is

very low (commonly

treatment of hepatorenal syndrome

albumin midodrine (a1 agonist) octreotide (stimulates fluid absorption from GI tract)

if prothrombin time (PT) in alcoholic is prolonged

EASILY CORRECTED with IM vitamin K

accumulation of fluid in peritoneal cavity

ASCITES

lymphatic blockage (trauma, tumors- especially primary lymphona, TB, and filariasis), NOT cirrhosis or CHF

CHYLOUS ascites

bloody ascitic fluid suggests

tumor

cloudy ascitic fluid suggests

infection

milky ascitic fluid suggests

lymphatic obstruction

what do you do if ascitic cell count is > 250 PMNs?

C&S and start antibiotics

a serum-to-ascites albumin gradient (SAAG) > 1.1 g/dL indicates

portal hypertension

definition of SAAG

albumin (serum) - albumin (ascites)

high albumin in ascites and NO portal HTN

SAAG

used to treat refractory ascites caused by cirrhosis

TIPS (transjugular intrahepatic portosystemic shunt)

common complication of TIPS

ENCEPHALOPATHY

peritoneal fluid with > 250 PMN/mL in patient with ascites

SBP (spontaneous bacterial peritonitis)

- ascites protein

risk factors of SBP

patient with SBP risk factors should receive either

INTERMITTENT (preferred) or continuous PROPHYLACTIC PO antibiotics (usually PO quinolone)

2 other possibilities that must be ruled out before assuming diagnosis of SBP

1. neutrocytic ascites | 2. primary bacterial peritonitis (PBP)

PMNs > 250/mL with NO evidence of SBP and negative cultures

neutrocytic ascites

d/t perforated viscus protein > 1 g/dL, frequently > 3 g/dL glucose 5,000 ascites fluid LDH > serum LDH

(PBP) primary bacterial peritonitis

treatment for active SBP

cefotaxime or other 3rd generation cephalosporin AND IV ALBUMIN

do NOT diurese more than this amount in treatment of ascites

> 1 L/d

okay to do what daily during INITIAL TREATMENT of recent-onset ascites or severe REFRACTORY ascites

daily paracenteses

okay to do daily paracenteses IF patient's renal function is normal AND there is:

- NO GI bleeding - NO sepsis - NO portosystemic encephalopathy (PSE)

with large-volume paracentesis (5 L or more)

replace 6-8 grams albumin for each liter of fluid removed

main finding in hereditary liver diseases

hyperbilirubinemia

only this type of bilirubin passes the glomeruli and is excreted in the urine

CONJUGATED

bilirubinRUIA results only come from

CONJUGATED hyperbilirubinemia

bilirubinRUIA is an indication of

cholestasis (because bilirubin is conjugated in liver)

very common, benign, chronic disorder resulting in mild, UNconjugated hyperbilirubinemia

Gilbert syndrome

UNCONJUGATED bilirubin

INDIRECT = WITHOUT BILIRUBINURIA

jaundice may come and go, typically brough on by

physical stress (surgery, exertion, and infection), alcohol, and alcohol

Gilbert syndrome genetics

AUTOSOMAL DOMINANT with variable penetrance

diagnosis of Gibert syndrome

increased UNconjugated bilirubin after prolonged fasting

treatment of Gilbert syndrome

NO treatment needed

increased CONJUGATED bilirubin after major surgery

BENIGN POSTOPERATIVE CHOLESTASIS

a1-antitrypsin deficiency treatment

liver transplant (or both, liver and lung transplant)

2 types of hemochromatosis

1. genetic | 2. acquired

GENETIC form of hemochromatosis

HFE gene autosomal recessive (AR)

ACQUIRED form of hemochromatosis

2/2 blood transfusions

abnormally increased intestinal iron absorption leading to tissue deposition

BOTH genetic and acquired hemochromatosis

suspect this in a thin 50-year-old with new onset DM

secondary diabetes, "bronze diabetes" 2/2 hemochromatosis

25-30% risk of HCC in patients with cirrhosis caused by | higher than any other cause

hemochromatosis

diagnosis of hemochromatosis is SUGGESTED by

high serum IRON, FERRITIN, and TRANSFERRIN

CONFIRMS diagnosis stages fibrosis of hemochromatosis

liver biopsy

confirm diagnosis for hereditary type of hemochromatosis

assay for HFE gene

initial treatment of hemochromatosis

weekly phlebotomy

treatment of hemochromatosis

phlebotomy 4x/year with goal ferritin between 50-100ng/mL

liver disease OR neurologic/psychiatric dysfunction in ADOLESCENTS

Wilson disease

impaired excretion of copper into bile --> excess copper in body tissues (especially liver)

Wilson disease

LOW serum ceruloplasmin and URINARY copper level is HIGH

Wilson disease

pathognomonic for Wilson disease

Kayser-Fleischer rings with slit-lamp exam

what CONFIRMS Wilson disease diagnosis?

liver biopsy

what also has a high liver copper level, besides Wilson disease?

PBC and PSC

screen for Wilson disease in?

adults (especially

3 screening test for Wilson disease

1. serum ceruloplasmin 2. slit-lamp exam 3. urine copper

treatment of Wilson disease

2-PHASE process 1. chelation with PENICILLAMINE 2. maintenance chelation and low-copper diet

CURE for Wilson disease

liver transplant

only treatment of fulminant Wilson disease (severe hemolytic anemia and high serum copper)

liver transplant

liver disease during pregnancy 1st trimester

mild increase in AST and ALT

liver disease during pregnancy 2nd trimester

best time for surgery for symptomatic gallstone patients

liver disease during pregnancy 3rd trimester

fulminant hepatitis d/t HEPATITIS E

MICROvesicular fat deposition modest elevation of AST/ALT/bili associated with encephalopathy, hypoglycemia, preeclampsia, pancreatitis, DIC, and renal failure

fatty liver of pregnancy

HELLP syndrome | SEVERE VARIANT OF PREECLAMPSIA

Hemolysis Elevated Liver enzymes Low Platelets

ITCHING and increased AP/bili/AST/ALT

intrahepatic cholestasis of pregnancy

Model for End-stage Liver Disease (MELD) scale predicts

MORTALITY risk

MELD > 20

candidate for transplant

NOT a contraindication to liver transplant

TIPS procedure

jaundice in those

acute viral hepatitis (MCC; 85-90%)

jaundice in those 40-60 years old

chronic cirrhosis (50-70%)

obstructive jaundice in those 60-80 years old

common duct stone or pancreatic cancer (80%)

outside of USA jaundice eosinophilia

ascariasis

US results determine next test to be done: DILATED common bile duct AND STONES

ERCP

US results determine next test to be done: DILATED common bile duct and NO stones

CT (think pancreatic cancer) or EUS

US results determine next test to be done: dilated intrahepatic ducts

CT

US results determine next test to be done: dilated ducts and testing to exclude PSC

MRCP

US results determine next test to be done: if NO dilated ducts

liver BIOPSY

vitamin deficiencies time until onset of symptoms weeks

WATER-SOLUBLE VITAMINS MAGNESIUM ESSENTIAL FATTY ACIDS

vitamin deficiencies time until onset of symptoms months

COPPER | VITAMIN K

vitamin deficiencies time until onset of symptoms year

VITAMINS A and D SELENIUM CHROMIUM

vitamin deficiencies time until onset of symptoms several years

IRON | COBALT

vitamin deficiencies time until onset of symptoms many years

B12

major cause of blindness in developing countries | earliest symptom is night blindness

vitamin A deficiency

BERBERI

vitamin B1 (THIAMINE) deficiency

2 major manifestations of thiamine deficiency

wet and dry beriberi

heart failure, ascites, and peripheral edema

wet beriberi

(confined to the nervous system) peripheral neuropathy, Wernicke encephalopathy, and Korsakoff syndrome

dry beriberi

closet drinker who develops ophthalmoplegia or nystagmus post-surgery

Wernicke encephalopathy

always give this to an alcoholic before IV dextrose infusion

thiamine (B1)

PHENOTHIAZINES and TRICYCLIC ANTIDEPRESSANTS increase tendency to develop

riboflavin (B2) deficiency

isoniazid, cycloserine, and pencillamine cause

pyridoxine (B6) deficiency

MACROcytic anemia, smooth tongue, and peripheral neuropathy

cobalamin (B12) deficiency

PELLAGRA (3 D's: dermatitis, diarrhea, and dementia) | seen in CARCINOID syndrome, and INH usage

niacin (B3) deficiency

vitamin C deficiency causes

SCURVY

PETECHIAL hemorrhages and ECCHYMOSES | perifollicular hemorrhage

scurvy

rickets in children | osteomalacia in adults

vitamin D deficiency

older patient with musculoskeletal pain/weakness, especially if h/o fat MALABSORPTION or VEGETARIANISM

consider vitamin D deficiency

areflexia and decreased vibration and position sense

vitamin E deficiency

causes of hypervitaminosis A

eating polar bear liver | vitamin supplements

symptoms of hypervitaminosis A

headache and flaky skin

symptoms of hypervitaminosis B6 (pyridoxine)

peripheral neuropathy with NORMAL motor and sensory function, but ABSENT positional and vibratory sensation

can cause marked POTENTIATION OF ORAL ANTICOAGULANTS

vitamin E hypervitaminosis

vitamin C hypervitaminosis

increase incidence of OXALATE renal stones

can cause acanthosis nigricans and cholestatic jaundice

niacin (B3) hypervitaminosis

helps MAINTAIN THE INTEGRITY OF THE SMALL INTESTINAL WALL (the loss of which is associated with the onset of multisystem failure)

ENTERIC feeding

chronically malnourished patients (especially those with resting bradycardia, hypotension, or body weight

REFEEDING SYNDROME d/t rapid refeeding

monitor what in refeeding syndrome

phosphate and potassium

what are GERD ALARM SYMPTOMS?

- nausea/emesis - chronic GI bleeding - family h/o PUD - weight loss - anorexia - IDA - abnormal physical exam - long duration of frequent symptoms - tx failure with full dose PPI - dysphagia/odynophagia

w/u of suspected esophageal cancer

- barium swallow may be done - EGD is ALWAYS done to confirm via BIOPSY - CT scan and endoscopic US are used for staging

- RF-negative peripheral polyarthritis - ankylosing spondylitis - erythema nodosum - pyoderma gangrenosum - iritis/episcleritis/uveitis - venous thrombosis - pericholangitis - primary sclerosing cholangitis - aphthous ulcers

extraintestinal manifestations of IBD