Gastroenterology Flashcards
recent MI, combative patient, and intestinal perforation
relative contraindication to GI endoscopy
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
EGD (esophagogastroduodenoscopy)
if patient has a possible bile duct obstruction give antibiotics before
ERCP (endoscopic retrograde cholangiopancreatography)
biliary obstruction, dx/tx pancreatic duct obstruction, dx of PSC (primary schlerosing cholangitis), tx of choledocholithiasis with cholangitis are indications for…
ERCP
further eval of abnormal biliary or pancreatic duct imaging from CT/MRCP/EUS
other indications for…
ERCP
ERCP is CONTRAINDICATED in ACUTE pancreatitis, except:
- impacted gallstones
2. ascending cholangitis (bacterial infection causing cholangitis)
bile duct obstruction, chronic pancreatitis, if acute pancreatitis doesn’t get better, and is the test of choice for PSC (primary sclerosis cholangitis)
MRCP (magnetic resonance cholangiopancreatography)
what visualizes the bile tract?
retrograde cholangiography
what visualizes the pancreatic duct?
retrograde pancreatography
staging GIT, biliary tree, and pancreatic malignancy
diagnosing chronic pancreatitis
dx/tx pancreatitis complications
providing access to pancreatic duct or biliary tree
EUS (endoscopic ultrasonography)
normal swallowing
deglutition
when swallowing doesn’t proceed appropriately for any reason
dysphagia
pain with swallowing
odynophagia
3 main causes of dysphagia
- transfer disorders (oropharyngeal)
- anatomic/structural disorders
- motility disorders
you should always work up this disorder and NOT treat it empirically
dysphagia
usually the 1st test performed to work up dysphagia
barium swallow
definitely the 1st test performed to work up dysphagia if symptoms are SEVERE, or new-onset dysphagia with LIQUIDS
barium swallow
why is barrium swallow done before endoscopy?
- 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
if a patient has h/o reflux and presents with slight-to-moderate dysphagia for solids you can do this test first
EGD
generally only done if dysphagia persists after negative barium swallow and EGD
esophageal manometry
general workup of dysphagia
- barium swallow
- endoscopy
- manometry study
chest pain, dysphagia for SOLIDS and LIQUIDS, usually years, regurgitation
achalasia
finding on barium swallow in achalasia
bird-beak narrowing distally
done to diagnose and exclude a tumor at esophagogastric junction (“pseudoachalasia”)
EGD
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
- traditional aperistalsis
- esophageal compression
- 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
- pneumatic dilation
- onabotulinum-toxin A (Botox)
- 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…
- anatomic: intermittent: solids
- anatomic: progressive: solids, THEN liquids
- anatomic: progressive: solids, THEN liquids
- motility/neurologic: longstanding: solids, AND liquids
- motility/neurologic: intermittent: solids, AND liquids (esp. COLD)
- various: progressive: solids AND liquids
disease
- Schatzki ring
- esophageal stricture
- cancer
- achalasia
- DES
- 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
- 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?
- esophageal adenocarcinoma
- squamous cell carcinoma
- 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?
- esophagitis
- stricture
- 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?
- pill-induced esophagitis
2. opportunistic infections
common causes of pill-induced esophagitis
- doxycycline (teenager with acne)
- KCl
- ASA
- NSAIDs
- iron
- bisphosphonates (alendronate)
- 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:
- Candida
- herpes simplex virus (HSV)
- 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)
- heartburn alone –> trial treatment –> improvement
- ALARM SYMPTOMS or persistent GERD symptoms –> endoscopy
- erosive esophagitis: if immunocompetent –> treat
- erosive esophagitis: if immunocompromised –> treat based on biopsy
- stricture –> treat
- 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:
- normal EGD and still have symptoms
- hoarseness, coughing, or atypical chest pain, but no sxs of GERD
- 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:
- patients REFRACTORY to medical tx
- YOUNG patients with SEVERE disease
- 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:
- 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
- discontinue NSAIDs
- test and treat if H. pylori +
- conduct a PPI treatment trial
- order EGD if alarm symptoms or failure of therapy
how is gastritis classified?
either histology or etiology
classification of gastritis by histology:
- superficial gastritis (early, neutrophils)
- atrophic gastritis (mid, lymphocytes)
- 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:
- GASTRITIS
- PUD
- GASTRIC ADENOCARCINOMA
- 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:
- h/o PUD
- EGD showing ulcer disease, erosive gastritis, or duodenitis
- MALT lymphoma
- 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
- EGD with biopsy= GOLD STANDARD
2. CLOtest and other rapid urease tests
noninvasive tests for H. pylori
- urea breath test (1st choice for treatment effectiveness)
- fecal antigen test (good for primary diagnosis)
- 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?
- h/o H. pylori-associated ulcer
- persistent dyspepsia despite test-and-treat strategy
- H. pylori MALT lymphoma
- 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)
- Helicobacter pylori infection (MCC)
- NSAIDs
- high acid secreting states (Zollinger-Ellison)
- Crohn disease of duodenum/stomach
risk factors for NSAID-induced PUD
- first 3 months of use
- high doses
- elderly patient
- history of ulcer disease or prior UGIB
- cardiac disease
- concurrent steroid use
- serious illness
- 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:
- symptoms include dysphagia or odynophagia
- UGIB
- abnormal UGI (barium swallow) or CT scan
- 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
- H. pylori treatment
- decrease acid secretion (H2 blockers, PPIs)
- 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?
- treat current bleed
2. assess risk for rebleed
EGD findings indicating INCREASED chance of rebleeding of ulcer?
- larger size of ulcer
- active bleeding during endoscopy
- visible vessels on non-bleeding ulcer
- visible clot
VERY LOW chance of ulcer rebleeding?
- NO BLEEDING
- NO CLOT
- NO VISIBLE VESSELS
what doesn’t stop bleeding peptic ulcers?
- gastric lavage
2. IV vasoconstrictors
- Osler-Weber-Rendu (hereditary hemorrhagic telangiectasia)- telangiectasias on skin, buccal/nasal mucosa, GIT, lungs, and brain
- 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
- adenocarcinoma (MOST COMMON- 95%)
- carcinoids
- lymphoma
- GIST (gastrointestinal stromal tumors; e.g. leiomyosarcoma)
2 types of gastric adenocarcinoma
- 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
- EARLY- occurs 30 minutes after eating (hyperosmolality of food and fluid shifts in small bowel)
- 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
- calcium oxalate kidney stones
- steatorrhea
- gallstones
- B12 deficiency
- hypocalcemia (from vitamin D malabsorption)
- bile acid-induced diarrhea
- 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?
- 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
- albumin
- Ca++
- cholesterol
- carotene
- serum iron (all LOW)
- PT (PROLONGED)
2 subdivisions of malabsorption
- MUCOSAL TRANSPORT (something wrong with intestinal uptake)
- 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
- evidence of malabsorption
- positive tissue transglutaminase Ab test OR antiendomysial Ab test
- positive response to gluten-free diet
- 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
- arthralgias (MOST COMMON symptom preceding diagnosis)
- abdominal pain
- weight loss
- 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
- 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
- FAP (familial adenomatous polyposis)
- Gardner syndrome
- Peutz-Jeghers syndrome
- 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
- asymptomatic diverticulosis (most common)
- painful diverticulosis
- diverticular bleeding
- 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
- ischemic colitis (MOST COMMON)
- chronic mesenteric ischemia
- acute mesenteric ischemia (70% mortality)
- 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
- abdominal pain after meals
- abdominal bruit
- 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)
- upper abdominal pain radiating through to the back
- serum amylase or lipase 3x upper limit of normal
- 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
- bowel sounds present and passing flatus/stools
- doesn’t need narcotics
- 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
- pancreatic calcification
- diabetes
- 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
- abnormal bile secretion
- accelerated nucleation of microcrystals to MACROcrystals
- 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:
- biliary colic (abdominal pain)
- fever
- jaundice
acute cholangitis
Reynold’s pentad:
- biliary colic (abdominal pain)
- fever
- jaundice
- SEPTIC SHOCK
- 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?
- inactive carrier state (asymptomatic with NORMAL liver enzymes)
- 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
- 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
- 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
- serum ceruloplasmin
- slit-lamp exam
- urine copper
treatment of Wilson disease
2-PHASE process
- chelation with PENICILLAMINE
- 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
