Ch_3 - Gastroenterology Flashcards
GI Bleed, Orthostatic Hypotension, Esophogeal Varices, Epigastric Pain, ZES, Diabetic Gastroparesis, GERD, Pancreatitis, Infectious Diarrhea, MALABSORPTIVE Diseases (Celiac dz, Whipple's dz, Chronic Pancreatitis, Lactose Intolerance, Carcinoid Syndrome, IBS, IBD, Constipation), DIVERTICULAR Dz (Diverticulitis), Cholecystitis, Ascending Cholangitis, LIVER dz (Viral Hep, Cirrhosis, Hemochromatosis, Wilson's dz, Primary Biliary Cirrhosis, Primary Sclerosing Cholangitis, Autoimmune Hepatitis, ESOPHO
The most important feature of GI bleed is _______, not __________.
Severity, not etiology. Cause is important but not as important as severity
If a GI bleed is severe, do what next?
First, resuscitate with FLUIDS and BLOOD
What is one easy way to determine the severity of a bleed (eg, GI bleed)
SBP <90 mmHg = Extremely severe bleeding
The following Hemodynamic findings are associated with how much volume loss?
- Blood donation
- Orthostasis
- Pulse > 100/min
- SBP < 100mmHg
- Blood donation –> ~10%
- Orthostasis –> ~15-20%
- Pulse >100 –> ~30%
- ~30%
If GI bleed is severe, how should you go about managing the situation?
Short answer: IV Fluids, CBC, Platelets, PT/INR, FFP, PPI, PRBCs
Long answer:
- Make sure IV FLUIDS have been started
- What is the BP?! If SBP is < 90 mmHg
- Make sure a TYPE and CROSS for PACKED RBCs (PRBCs) transfusion has been sent.
What does orthostatic mean?
BP and pulse is normal at rest when lying flat, but BP drops and pulse rises when standing up/sitting up.
SBP decrease >20 mmHg or Pulse increase > 10/min
T/F Orthostatic evaluation can identify who has a minor bleed and who has a severe one
True. If there’s no OS on evaluation, you can be confident that bleeding is not severe.
How long does it take to follow CBCs?
6-12 hours! An orthostatic hypotension eval is indispensable. Do it yourself!
T/F Check for orthostasis right after giving a lot of fluids
False, check BEFORE giving a lot of fluids
For severe bleeds, give ____(4)_____
- Fluids
- Blood
- Platelets
- Plasma (FFP) with PT/INR increase
Best management for Esophogeal varices (2)
- Octreotide NOW!
- Banding (call GI service! – only they can do endoscopy, which is needed for Banding)
- Sclerotherapy if Banding can’t be done
T/F 3. Beta-blockers (Propranolol or Nadolol) can be effectively used to treat an acute variceal bleed
False! They do nothing
Octreotide + Banding (or sclerotherapy)
T/F One CBC can determine the severity of a variceal bleed
False
Hematocrit drops ____ points with hydration
only 2-3 points
Patient presents with severe GI bleed, possibly secondary to esophogeal varices. You call the GI service. What will be asked of you?
Indicate why you think they have a severe bleed. Provide:
- CBC
- PT/INR
- BP
- Response to fluids
What kills a patient with a severe GI bleed?
GI bleed –> hypotension + severe ANEMIA –> Myocardial Ischemia (CHECK EKG!)
(Lightheadedness doesn’t kill you)
GI bleed –> severe, symptomatic anemia. What are the symptoms?
lightheadedness, SOB, fatigue, chest pain
GI bleed –> severe, symptomatic anemia. Best next step in management?
Blood transfusion now!
T/F Fluid replacement is more important than endoscopy for a severe GI bleed
True
GI bleed –> check Orthostasis and ask yourself the following questions: (8)
- When did the bleeding start?
- Is stool red or black?
- Vomit – bright red blood or dark “coffee grounds”?
- How many bowel movements or episodes of vomiting w/ blood or black stool?
- Sx: Lightheaded, SOB, Chest Pain?
- History of heart dz?
- Previous scope through mouth or rectum?
- Antacid use?
Lower GI bleed etiology? (4)
Diverticulosis Angiodysplasia or AVM Polyps Hemorrhoids Cancer
Lower GI bleed vs. Upper GI bleed
what color?
L-GIB - bright red blood on bowel movement
U-GIB - can be red if it’s extremely severe and fast, in about 10% of cases
T/F Hemorrhoid bleed may mimic a serious GI bleed
True, a small amount of red blood into the toilet makes the water look red and exaggerates the severity of the blood loss.
Features of a hemorrhoid bleed?
- No change in HCT w/ repeated testing
- Found on rectal exam
- Normal BP and Pulse
- Absence of orthostatic change in BP or Pulse
T/F Guaiac-positive, brown stool is severe
False, it’s not severe
Etiologies of Upper GI bleeds?
Ulcer dz - both duodenal or gastric Gastritis Esophagitis Duodenitis Varices Cancer
What question should you always ask yourself when thinking about what test to order?
Always ask, “What will I do differently based on THAT test?”
What is the most common cause of Upper GI bleed?
What is the most dangerous cause of UGIB?
MCC - Ulcer disease
MDC - Varices
What type of varices can occur in the upper GI tract?
How can you differentiate?
Why do/can they occur?
Esophogeal, Gastric; Diff via Endoscopy
d/t Portal Hypertension
The initial management of an upper GI bleed depends on what?
Severity!
Initial management of upper GI bleed ?
Depends on severity:
IV fluids
frequent checks of CBC (until it stops changing)
correction of coagulopathy (if there is one)
PPIs for ALL upper GI bleeds
Epi injection or electrocautery for ulcers w/ active bleeding
T/F Checking CBC frequently is important for a severe upper GI bleed
T/F Using a Nasogastric tube could be useful in the management of a pt w/ an upper GI bleed
True
False
With a variceal bleed, do you wait for endoscopy to confirm variceal bleed? Explain
No, start Octreotide b/c it decreases portal pressure and has no major adverse effects
Varices that bleed should be managed how? How can you prevent the next bleed?
Octreotide + Band varices that bleed; gastric varices are hard to “grab” to band
BBs (Propranolol or Nadolol) are used only to PREVENT the next bleed!
How to manage persistent bleeds?
Persistent bleed = persists despite banding and octreotide Need TIPS (Trans-jugular Intrahepatic Portosystemic Shunt)
What is TIPS?
TIPS = Transjugular Intrahepatic Portosystemic Shunt
Used for persistent bleeds
TIPS = catherer down the Jugular vein to create a “shunt” b/w the portal and hepatic veins. This replaces the need for surgical shunting.
A patient presents with an esophogeal variceal bleed that is persistent despite Octreotide and Banding therapy. What temporary method can be done to slow bleeding until TIPS can be done?
A Blakemore Tube – balloon placed in esophagus and stomach to “tamponade” or “compress” the vessels. This is a temporary method of SLOWING BLEEDING in those who need to be kept alive for a few hours until TIPS can be done.
What is “minor bleeding”?
Normal BP/pulse
No orthostasis
No recent change in HCT
Patient presents to office with minor GI bleed characterized by guaiac-positive stool. What finding may you see on CBC? If there are no localizing symptoms, what should you do next?
Guaiac = Heme
CBC –> Microcytic Anemia
Colonoscopy (even if they had one last year!)
Upper endoscopy
Rarely, pill endoscopy, in those whom endoscopy does not show the cause.
Although majority of epigastric pain is benign, your job as the interviewer is to…?
…find serious pathology by asking the right qs.
Synonym for epigastric pain
EP = pain below the xiphoid process = Dyspepsia
T/F In 50-90% of outpatients, pathology will never be found on a patient w/ epigastric pain
T
T/F Patients admitted for Epigastric pain are markedly skewed toward more serious pathology. Gastritis, Pancreatitis, and other causes form of pain do not have tenderness on exam
First sentence = True
Second sentence = False, Only pancreatitis is tender
What are some consequences of NG tubing?
An NG tube may be misplaced in a lung. That’s why X-Ray is so important before tube feeding is started, and why routine NG tube in GI bleed is a bad idea.
What is the MCC of epigastric pain in the general population?
Non-Ulcer Dyspepsia = NUD
What is nunulcer dyspepsia?
NUD = pain w/o pathology. It’s like a tension HA of your guts.
Although NUD is the MCC of epigastric pain in the general population, the inpatients on the Wards rotation will more likely have ???
Ulcer dz, Pancreatitis, GERD, Esophagitis/Duodenitis/Gastritis, and/or Cancer
What factors must you think about when trying to differentiate b/w benign from dangerous dz?
Duration, Intensity, Time of onset, and Aggravating/Relieving factors for all Pain syndromes (ie, OLDCARTS).
Specifically for epigastric pain, in addition to OLDCARTS, what other questions should you ask?
Weight changes 1. Have you experienced weight loss? 2. Have you actually weighed yourself? What is the exact amount you lost? 3. How much did you weigh ~6months ago? Swallowing 4. Is it difficult to swallow? 5. Does food get STUCK when you eat? 6. Pain w/ swallowing? Nausea/Vomiting 7. Are you nauseated? Do you actually vomit? How often? Bleeding 8. Do you have blood in your stool or when you vomit? Antacids 9. Does the pain go away w/ Antacids?
Patient comes in with epigastric pain and you remember that in addition to OLDCARTS, you have to look for “alarm symptoms”. What are these?
Weight loss
Dysphagia
Odynophagia
Bleeding (Vomit, Stool)
Any patient with epigastric pain
1) alarm Sx + Age >45-55 or
2) if alarm sx persist or worsen despite use of PPIs should get what?
Upper Endoscopy = EGD (EsophagoGastroDuodenoscopy)
Why is an EGD is used for patients over 45 with alarm symptoms associated w/ epigastric pain?
- Most accurate test of the stomach
- Allows BANDING of varices and cautery of visible vessels in an ulcer
- Needed for stomach biopsy to exclude CANCER in gastric ulcer
- To dx b/w stomach and duodenal ulcer (only EGD can do this!)
What is the only way to exclude upper GI cancer?
EGD
Compare/Contrast
EGD vs Barium contrast
EGD»_space; Ba Study
Reason? –>
EGD is far more accurate study of stomach,
can do biopsy or therapeutic procedures, and exclude Gastric cancer assoc w/ ulcer.
H. pylori can be tested w/o Endoscopy, but why would you still do an endoscopy?
4% of gastric ulcer is assoc w/ cancer and EGD could exclude cancer
H. pylori testing is best done on ???
BIOPSY!
Discuss efficacy of various H. pylori testing
- Biopsy is the best test
- It’s important to drive treatment w/ PPI, Clarithromycin, and Amoxicillin
- Helicobacter stool antigen or breath testing is not as good as biopsy
- stool antigen and breath test CAN DIFFERENTIATE b/w old vs. current infection.
- SEROLOGY is clinically useless
When should you only treat for H. pylori? In patients who experience what? If it’s not treated, what may be the consequence?
Treat only in those w/ ulcers or gastritis. Ulcers will recur if H. pylori is not eradicated.
The ONLY clear indications for stress ulcer prophylaxis are (4)
- Mechanical ventilation/intubation
- Head trauma
- Burns
- Coagulopathy
T/F NSAIDs and steroids are indications for stress ulcer prophylaxis
False
Although PPIs are generally benign, there is a slight risk of (3)
- C. diff colitis
- Osteoporosis from interference w/ Ca++ absorption
- Pneumonia: gastric acid protects against gastric colonization w/ bacteria
What is Zollinger-Ellison Syndrome (ZES) caused by?
ZES is caused by ELEVATED GASTRIC ACID and ELEVATED SERUM GASTRIN.
Look for ZES and get a gastrin level only if you see the following (4)
- Large ulcers (>1cm)
- Recurrence after eradication of H. pylori
- Distal location near the far end of the duodenum near the ligament of Treitz.
- Multiple ulcers
Why is diarrhea common in ZES?
Acid inactivates Lipase
A patient who is suspected of having ZES should have a serum _____ level tested when they are off what medications?
serum GASTRIN level when off of PPIs and all forms of antacids
ZES suspected, but equivocal levels of gastrin. Next best step?
Secretin Test
- normal response (no ZES) –> decrease in gastrin
- ZES - gastrin stays high even after giving secretin.
What is the confirmatory test for ZES?
Endoscopic ultrasound and Nuclear somatostatin receptor scan
- Confirm that ZES is local and resectable by excluding Mets w/ these 2 modalities
Patient has ZES. If local, how to treat? If Mets, how to treat?
If local –> surgical resection
If mets or unresectable –> lifelong PPIs
What is one complication for the stomach due to long-standing diabetes?
Diabetic Gastroparesis - weakening of the stomach - inability to stretch
Long-standing diabetes damages what that leads to gastroparesis? Consequence?
nerves; pts cannot feel the “stretch” of the bowel that is the main stimulant for GI motility.
How can you recognize diabetic gastroparesis?
Bloating
Nausea
Constipation
Abdominal discomfort
Patient with long-standing diabetes presents with bloating, nausea, constipation, and abdominal discomfort. You suspect diabetic gastroparesis. Next best step in mgmnt?
Look at the response to treatment with:
Metoclopramide and Erythromycin
If the diagnosis of DM Gastroparesis is equivocal, then what?
Do a nuclear gastric emptying study. Patients eat Barium-soaked bread and are monitored for the time it takes for it to leave the stomach.
GERD is d/t what?
abnormally RELAXED LES. Acid comes up out of the stomach and hits the back of the throat and vocal cords.
T/F GERD causes 25% of chronic cough.
T
What qs should you ask of someone you think has GERD?
- Does the pain/discomfort in your belly go anywhere? (like your chest)
- Do you have ‘heartburn’? Do you have pain in your chest?
- Do you have a bad taste in your mouth? Does it taste like metal, like you have pennies in your mouth?
- Is your throat sore?
- Do you feel your voice is hoarse?
- Do you cough, especially at night?
T/F The test for GERD is generally the response to PPIs.
True, 95% of those w/ GERD should respond w/in a day to tx w/ PPIs.
When should specific testing for GERD be done?
If the sx are persistent even with PPIs.
T/F Helicobacter can cause GERD
False, it cannot
How to treat GERD?
Start ANY PPI
Ask the pt later the same day if the sx have improved
If sx persist, ask your resident/attending about performing an EGD or 24-hr
T/F Surgical treatment can be given to GERD patients.
T
Surgical resection such as Nissen fundoplication is done for the small percentage (<5%) of patients NOT controlled w/ PPIs
What is a major consequence of GERD?
Barret’s Esophagus; develops from long-standing GERD (usually >5 yrs). But, it’s not always clear when to scope to screen for it. If patient presents w/ alarm sx (eg, weight loss, anemia, blood in stool, etc), SCOPE.
How is Barret’s diagnosed?
EGD and biopsy. Biopsy is the only way to confirm the metaplastic change that occurs.
How many people with Barret’s per year develop adenocarcinoma?
0.4-0.8% (less than 1%)
How to treat Barret’s?
PPIs and repeat EGD every 2-3 yrs for early detection of CA
T/F Barret’s esophagus is reversible
True! Metaplasia is reversible
Patient with GERD is scoped and biopsied. Low-grade dysplasia of the esophagus is the diagnosis. Now what?
PPI and re-scope/re-biopsy every 6 months. No resection b/c it’s reversible.
Patient with GERD is scoped and biopsied. High-grade dysplasia of the esophagus is the diagnosis. Now what?
PPI and either endomucosal resection with endoscope OR Distal esophagectomy
Why must surgery be done on high-grade dysplasia of lower esophagus?
Because of high probability of transformation into adenocarcinoma (invasive CA). Mucosal “shaves” with EGD are effective.
Pt comes in with worsening, severe epigastric pain and tenderness on palpation. Most likely Dx?
Pancreatitis
With increasing incidence of obesity, why would one expect pancreatitis to increase?
Increase incidence of gallstone dz.
Pacreatitis work-up includes elevations of what enzymes?
lipase and amylase. Lipase more specific.
What should you ask the patient if you suspect pancreatitis?
If there’s radiating pain to the BACK
N/V (if so, how many times; is there blood?)
Quantity of ALCOHOL patient drinks
History of GALLSTONES
What is the Ranson’s criteria?
Although obsolete, still asked on rounds
Ranson’s Criteria = elevated WBC, Low Ca++, Age>55, high AST, and high LDH
Ranson was a surgeon working before there were CT scans. He made these criteria to determine the need for surgical debridement.
T/F No test determines the severity of pancreatitis in first 48 hours
T
T/F CT is not necessary for confirming pancreatitis, although it is most sensitive
T
What can show the cause of pancreatitis?
CT or US can show cause – eg, stone or obstruction. Scan is used to determine if stone removal is needed
What is MRCP?
MCRP = Magnetic Resonance CholangioPancreatography = DIAGNOSTIC method that best visualizes the DUCTAL structure of the pancreas and biliary system
What is ERCP?
ERCP = Endoscopic Retrograde CholangioPancreatography = THERAPEUTIC method to remove stones and dilate structures
Compare MRCP and ERCP
MRCP finds the obstruction, while ERCP fixes it
T/F There is no medication that increased the speed of resolution of pancreatitis
T - Physicians provide “rest” of the pancreas and give a lot of fluid. Pancreatic inflammation releases a lot of mediators, which cause “leak” of capillaries.
What is the main cause of death in acute pancreatitis?
Inadequate fluid replacement. Don’t be afraid to give 150-250 mL/hr for the first day.
Treatment and management of acute pancreatitis…GO
- NPO, IV fluids in large volumes, analgesics
- PPIs are often used (not clear if they help)
- CT w/ >30% necrosis needs IMIPENEM or MEROPENEM and CT-guided BIOPSY
- Infected necrotic pancreatitis is rare, but needs SURGICAL DEBRIDEMENT
With diarrhea, what is more important, severity or etiology?
Severity, not etiology. You gotta know who needs antibiotics and IV fluids
Severity of diarrhea = ??
Volume depleted and febrile
What qs should you ask of a patient who has severe diarrhea?
- Is SBP < 90-100? Is pulse > 100/min?
- Check for orthostasis: increase in pulse >10 or drop in SBP >20 on rising
- Fever? Oral temp >100.3F
- Blood in stool?
- Abdominal pan or tenderness on exam?
What may you be asked on rounds about a patient with diarrhea?
- Duration of sx
- Frequency of bowel movements
- Blood in stool
- Fever; has a Temp been taken, or does the pt just feel warm?
- Lightheadedness
- Others that live w/ pt who have the same problem/diarrhea. Did you eat at the same place? same food?
T/F A precise microbiologic diagnosis is rarely confirmed, and decisions about treatment must be made before you have any test results back.
T
Bloody Diarrhea may be present with which major pathogens?
Campylobacter, Salmnonella, Shigella, Yersinia, or some Vibrio species.
T/F Blood may be present only in microscopic or “occult” amounts in brown stool (diarrhea), thus it is caused by invasive pathogens
true
T/F Fecal leukocytes (WBCs) have the same significance as blood
True – they mean that the organism is invasive
What is the only way to distinguish bw invasive organisms that can cause diarrhea?
Stool culture
Pt has diarrhea. What should you do if you don’t see blood in the stool?
Test for:
- Occult blood (guiac–ie heme)
- Fecal blood w/ Methylene Blue stain
- Culture
- Ova and parasite exam
Pt has diarrhea, AIDS w/ < 100 CD4+ cells. What is the most likely organism and what test would you run?
Cryptosporidium
Modified Acid-fast stain
Pt has diarhhea. hiker, camper.
Organism?
Test?
Giardia
ELISA stool ANTIGEN, Ova and Parasite test
Pt has diarrhea. Antibiotic use
Organism
Test?
C. diff
Stool TOXIN assay
Pt has diarrhea. Hemolysis, low platelets, elevated BUN and Creatinine.
Organism?
Test?
E. coli O157:H7
Sorbitol MacConkey agar
E.coli O157:H7 does NOT grow on routine media!
Pt has diarrhea. Flushing, wheezing immediately after fish eating
Organism?
Test?
Scombroid
Stool culture
T/F Majority of infectious diarrhea cases are self-limited and benign
T - i.e. they don’t require antibiotic tx
There’s much higher incidence of Ciprofloxacin use in those ADMITTED to the hospitals b/c that’s the reason they have been admitted.
What can you give a patient who is suffering from diarrhea that does not have blood or fever?
Antimotility agents (eg, Diphenoxylate [Lomotil]) or Loperamide [Imodium]
If a patient has “severe” diarrhea, how should he be treated? What does “Severe” mean?
Severe = Fever + bloody stool + Hypotension/Tachycardia + Abdominal Pain/tenderness
Treat w/ Antibiotics
Initial Tx is based on SEVERITY not etiology!
C. difficile treatment?
- Metronidazole first; Vanco only if metro fails
- Recurrences are treated w/ repeat course of Metro
- Very severe cases get both Metro and Vanco
Giardia Tx?
Metronidazole, Tinidazole
Cryptosporidia tx?
Nitazoxanide
Campylobacter tx?
Azithromycin or erythromycin if confirmed as Camp
E.coli O157:H7 Tx?
AVOID antibiotics!
Scombroid Tx?
Diphenhydramine (benadryl; antihistamine)
Viral, Staph, Bacillus cereus Tx?
- Supportive Tx w/ fluids
2. Antibiotics don’t help!
What is the definition of “Severe C. difficile”?
- Fever
- WBC > 15,000-20,000/mm3
- Creatinine > 1.5 mg%
- > 10 movements a day
Which malabsorptive diseases are characterized by steatorrhea?
- Celiac dz
- Whipple’s dz
- Tropical sprue
- Chronic pancreatitis
How are the 4 malabsorptive diseases similar in their clinical presentation?
- Weight loss
- Stool described as “oily, greasy, floating, and especially foul-smelling”
- Ask, “do you bruise easily?” -Vitamin K malabsorbed; high PT
- Vitamin D deficiency/Low Calcium - look for bone disease such as Osteoporosis.
- Vitamin B12 def - macrocytic anemia
- Stool: Sudan black stain positive (fecal fat test)
Synonym for Celiac disease
Gluten-sensitive enteropathy
Sx/Sx of Celiac disease
Malabsorption Sx +
- Fe deficiency anemia (very common) d/t damage to duodenum
- Dermatitis herpetiformis (not common)
- Small bowel lymphoma
T/F Celiac disease has a strong association w/ Diabetes
T
Celiac dz treatment
Eliminate gluten from diet
Celiac disease Diagnosis
Do SEROLOGY first! - Anti-transglutaminase antibodies and anti-Endomysial antibodies - Anti-GLIADIN are imprecise BIOPSY - most accurate - flattened villi - Exclude bowel wall lymphoma
Whipple’s disease clinical presentation
Malabsorptive +
Eye, joint, neurologic manifestations
Whipple’s dz Diagnosis?
BIOPSY of bowel w/ PAS+ organisms
PCR or stool for Tropheryma whippelii
Whipple’s dz Treatment
Antibiotics for 6-12 months: Ceftriaxone, Doxycycline, TMP/SMX (Bactrim)
Define Chronic Pancreatitis
Repeated episodes of pancreatitis over a period of yearS. Debilitating abdominal pain. Fat malabsorption (loss of lipase). B12 malabsorption (no pancreatic enzymes to detach B12 from R-protein to allow for IF binding).
Pt with chronic pancreatitis who gets an X-Ray or CT is expected to have _____
Calcification
XR – 50-60%
CT - 80-90%
T/F Amylase and Lipase are elevated in chronic pancreatitis
False - they are normal or low – pancreas is “burnt out” and destroyed
What is the most accurate test for chronic pancreatitis?
IV Secretin stimulation test
Normal response = massive release of pancreatic enzymes into the duodenum
Chronic pancreatitis = no release of bicarb-rich fluid into duodenum
Treatment of Chronic Pancreatitis
- Replace pancreatic enzymes Orally (Lipase, Trypsin, and Amylase in pill form)
- Pain management w/ Celiac Ganglion block by injectionvia Endoscopic US
T/F Lactose intolerance is very common and these patients are never admitted to the hospital for it
T
Sx of lactose intolerance?
Diarrhea and Gas
How to recognize lactose intolerance?
No fever or blood in stool
No weight loss
No systemic findings
Rapid resolution 1 day after stopping milk products (except Yogurt)
Treatment of Lactose Intolerance
Avoid milk products or use LactAse replacement
Define Carcinoid syndrome
Heart becomes fibrotic b/c of chronic 5HT exposure
Clinical presentation of Carcinoid Syndrome
- Episodic, chronic diarrhea
- Flushing, Wheezing, and rarely Right-sided cardiac fibrosis
- Telangiectasia from chronic flushing
- Mets lesions to LIVER are almost always present
- Urinary 5-HIAA
Treatment of Carcinoid Syndrome
Octreotide or Lanreotide
T/F Patients with IBS are rarely admitted to the hospital, but many seek help at clinic
T
IBS = Irritable Bowel Syndrome
T/F IBS abdominal pain is specific
false, non-specific
When you see a pt with suspected IBS, what is your primary concern?
Rule out serious pathology
IBS diagnosis can only be made after testing is done. What testing?
NORMAL
- EGD
- Colonoscopy
- Abdominal CT
IBS clinical presentation
- Abdominal pain
- Diarrhea AND/OR Constipation
- Sx less severe at night
- Pain relieved by bowel movement
- No weight loss
- No blood, mucus, or fever
IBS treatment
No single effective therapy.
- Fiber and bulking agents (Metamucil, Psyllium husks, bran
- Anti-spasmodics - Hyoscyamine or Dicyclomine
- TCAs
Define Inflammatory Bowel Disease (IBD)
Crohn’s and UC are idiopathic, inflammatory IBD diseases.
CP of IBD
Abdominal pain, diarrhea, blood and mucus in stool, CD can have fever and Palpable abdominal masses
What is considered an “acute exacerbation” of IBD?
> 10-20 bowel movements a day, often w/ blood
What to treat w/ for acute episodes of IBD?
Steroids
What to use for long-term control of IBD
Mesalamine
CD may result in fistulae. Any fistulae needs to be treated w/ what? (medically)
TNF drugs like Infliximab
What’s an important preventive measure for someone diagnosed w/ IBD?
Screen for Colon Cancer after 10 years of colon involvement
Both UC and CD have what? (4)
- Joint pain
- Erythema nodosum/pyoderma gangrenosum
- Uveitis/Episcleritis
- Sclerosing Cholangitis (more so w/ UC)
Manifestations more common w/ Crohn’s are? (3)
- Fistulae (from transmural GRANULOMAS): they can come through the skin or connect b/w loops of bowel or into the bladder
- Peri-anal disease
- Oral, esophogeal, and small bowel disease (anywhere in the GIT!)
Diagnosis of IBD
- Lower or upper endoscopy is first – depends on sx
2. Small bowel series is sometimes needed for CD
Acute, severe exacerbations of IBD are managed with what?
Steroids
Chronic control of UC is treated with what?
Mesalamine derivatives: Asacol (Ass; colon), Rowasa (Rectal; limited distal/rectal involvement)
Chronic control of Crohn’s dz is treated with what?
Mesalamine derivatives: Pentasa (entire 5 ‘units’ of bowel - M, E, S, SI, LI)
M = mouth
Why are Azathioprine/6-MP used for IBD?
to wean pts off steroids and for chronic control
What is one worrisome adverse effect of 6-MP? hint: GI related
Drug-induced pancreatitis
Pt with CD has fistulae. Treat with what? What must be checked before administration?
Anti-TNF meds - eg, Infliximab, Etanercept, Adalimumab
TB reactivation risk: check PPD and give INH if PPD+
Pt with perianal involvement (Crohns). Treat with? Explain
Ciprofloxacin and Metronidazole
Besides being abx, these meds have a primary anti-inflammatory effect
What is a way to cure UC?
Surgery is curative of UC, but not so effective for CD
Both UC and CD can lead to Colon CA. Risk is based mainly on what?
DURATION of colonic involvement. 10 years with either CD or UC has same risk. Must do COLONOSCOPY after 8-10 years of colonic involvement of IBD.
What’s a very common cause of Constipation in the elderly? Advise them what?
Simple Dehydration. Advise more FIBER in their diet.
Common iatrogenic causes of constipation (5)
- CCBs
- Hypothyroidism
- Opiates
- CaCO3 replacement (Calcium replacement)
- TCAs (anticholinergic)
Compare the various modalities that can screen for Colon CA
Nothing is superior to COLONOSCOPY.
Stool guiac lacks specificity and precision.
Barium is worthless and impractical.
Sigmoidoscopy would miss 40% of cancers that occur proximal to the sigmoid colon.
The general population should be screened for colon cancer when?
Age>50 every 10 years
If one family member has/d Colon CA, what are the screening recommendations?
Age>40 or 10 years earlier than family member
Every 10 years
If patient has HNPCC, 3 family members, 2 generations, 1 premature (before 50)
Screen >25 q 1-2 years
Pt w/ FAP should be screened when?
Screen w/ Sigmoidoscopy q 1 yr
CP/history of someone you suspect has Diverticular dz
Abdominal pain in LLQ Age >50-60 Blood in stool Fever Vegetarian diet (protective) Previous colonoscopy (risk for Div Dz)
Diverticulosis diagnosed by?
Endoscopy (Colonoscopy)
CP of Diverticulitis
LLQ pain, Fever, Leukocytosis, Acute onset
Diverticulitis diagnosed with?
CT scan. Avoid scoping – increased risk of perforation (weak wall!)
Therapy for diverticulosis
No specific Tx. Avoid meat and increase fiber.
Vegetarian diet is seemingly protective as they rarely get it.
Nothing can reverse it, however
Therapy for diverticulitis
Antibiotics -
- Ciprofloxacin and Metronidazole
- Ceftriaxone and Metronidazole
- Ampicillin/Sulbactam (Unasyn)
- Piperacillin/Tazobactam (Zosyn)
- Any carbapenem (eg, ertapenem, meropenem, doripenem)
CP of Cholecystitis
- RUQ pain and tenderness; fever
Lab findings of Cholecystitis
- (Fever) Leukocytosis
- Normal bilirubin and LFTs in almost all pts
Diagnosis of Cholecystitis
Clinical = RUQ pain, fever, increased WBCs, normal bili and LFTs
ULTRASOUND is best first test
CT misses some small stones
Get a SURGICAL evaluation for Laparoscopic cholecystectomy
Treatment of Cholecystitis
Unasyn (Ampicillin/Sulbactam)
Zosyn (Piperacillin/Tazobactam)
Any carbapenem (eg, ertapenem, meropenem, doripenem)
What is worse, Cholangitis or Cholecystitis?
Cholangitis is much more severe
What is ascending cholangitis?
Obstructive jaundice w/ severe infection of both the biliary tree and the liver.
Ascending cholangitis findings
- Biliary tract obstruction –> jaundice
- Increased DIRECT bilirubin
- Alkaline Phosphatase and GGTP increased
- AST and ALT may be up as well
RUQ pain/tenderness + jaundice = ??
Ascending cholangitis
Pt presents w/ RUQ pain, jaundice, and has now developed “shaking chills”. What is the ML diagnosis and what is the significance of the last symptom?
Ascending cholangitis
Shaking chills = Bacteremia
Diagnostic testing for Ascending cholangitis?
Elevated LFTs
US - stones and/or ductal dilation
CT scan
MR-CP - most accurate test of the biliary and pancreatic ductal system.
What is the most accurate test for ascending cholangitis?
MRCP
Therapy of ascending cholangitis
Mechanical obstruction must be removed/released.
How? – ERCP can remove stones and dilate strictures
Antibiotics (Unasyn, Zosyn, or any Carbapenem); abx alone will not fix an obstructive stone
For all patients who have elevated/abnormal LFTs suggestive of liver disease should get what? (5)
- Repeat LFTs
- Abdominal US
- PT time: all clotting factors are made in liver except factor VIII/vWF
- Albumin level
- Hep B and Hep C testing
As you pre-round, you notice that your patient has abnormal LFTs, what must you make sure you know about?
Any Liver-toxic meds, alcohol are being used!
Patient’s history: contact private doctor if records not in chart! The patient may already have documented chronic hepatitis or something!
When AST is abnormal, you should think of ??
Drug toxicity, alcohol use
When ALT is abnormal, you should think of ??
Viral hepatitis
When Alk Phos is abnormal, you should think of ??
Biliary tract obstruction, bone disease, pregnancy
When GGTP is abnormal, you should think of ??
Biliary tract obstruction
Goes up immediately after binge drinking
When Albumin is abnormal, you should think of ??
SYNTHETIC dysfunction of liver
Can be down from malnutrition and nephrotic syndrome
Must be missing 70-80% of liver before it drops
When PT time is abnormal, you should think of ??
Best test of SYNTHETIC function of liver
Normal PT = liver is working, no matter how high the AST/ALT
Patient comes in with acute onset of jaundice, dark urine, extreme fatigue, and weight loss. What is the ML diagnosis?
Viral Hepatitis (dark urine = bilirubin)
T/F Hepatitis makes one feel totally “out of gas”. It also enhances one’s hunger.
True and
False (it shuts of hunger)
Diagnostic LAB findings of Viral Hepatitis
- Markedly elevated DIRECT bilirubin and ALT
2. Alk phos may be slightly elevated
Diagnostic imaging finding(s) of viral hepatitis
US - exclude obstruction
What is the most accurate test of Chronic Hepatitis
Biopsy - rarely needed
What is the specific test for Hepatitis A, D, and E?
IgM acutely, IgG upon resolution
What is the specific test for Hepatitis C?
- Antibody test first
- PCR RNA viral load confirms level of activity
- Genotype predicts response
What is the specific test for acute Hepatitis B?
- Surface Ag (HB-sAg)
- ‘e’ antigen (HB-eAg)
- Core antibody IgM (not IgG!)
What is the specific test for chronic Hepatitis B?
- Persistence of HB-sAg >6 mo
- HB-eAg either +/-
- Core antibody IgG (not IgM!)
How would you test to see if patient is vaccinated to Hepatitis B?
ONLY HB-surface ANTIBODY +
How would you test to see if patient has resolved (past) Hepatitis B infection?
HB-surface ANTIBODY and Core Antibody IgG
What indicates whether active Hepatitis C infection is present?
Hep C PCR DNA
T/F the only form of acute viral hepatitis that is treated is Hepatitis C
T
How do you treat acute Hep C? How long?
Interferon + Ribavirin + Boceprevir (or telaprevir).
T/F Hepatitis C rarely presents in its acute form
T
When do cases of Hepatitis C come up?
Most show up years later either on evaluation of abnormal LFTs done for another reason or on development of liver dz.
Generally, how long does treatment for chronic Hep C take?
6-12 months; use same drugs as acute hepC (IFN, Ribavirin, -Previr)
Adverse effect of Interferon?
IFN = hepC med; flu-like sx, arthralgia, myalgia, depression
Adverse effect of Ribavirin?
Anemia
What determines the likelihood of response to treatment against Hep C?
Genotype
What determines if a response to Hep C therapy has occurred?
PCR DNA
What is the only way to determine the extent of inflammation, fibrosis, or presence of cirrhosis secondary to HepC?
BIOPSY
T/F if Hep C viral load is up and you end up treating, a biopsy will change a little
T
What is the goal of Viral Hepatitis (B or C) treatment?
To drive the viral load to undetectable levels and get the pt feeling better
T/F Biopsy is needed for Hepatitis B diagnosis and prognosis
False, Although biopsy determines extent of disease, it adds little if you are going to use meds anyway
T/F Combination therapy is clearly better than monotherapy for treating Hepatitis B
False, combo therapy is not clearly useful for Hep B. Monotherapy is used
T/F Genotyping determines the likelyhood of response to treatment
False, genotyping is not used for hepB
What are the treatment options for HepB?
Not clear which drug has greater efficacy:
- -vudine’s (Lamivudine, Telbivudine)
- -fovir’s (Adefovir, Tenofovir)
- Entecavir
- IFN is by injection and has more adverse effects (flu-like sx)
What are the common manifestations of Cirrhosis? (10)
- Edema
- Ascites
- Encephalopathy
- Low Albumin
- High PT/coagulopathy
- Gynecomastia
- Varices
- Splenomegaly
- Hemorrhoids
- Thrombocytopenia
Cirrhosis –> Edema –> Tx w/ ?
Spironolactone, Lasix
Cirrhosis –> Ascites –> Tx w/ ?
Spironolactone, Lasix
Cirrhosis –> Encephalopathy –> Tx w/ ?
Lactulose, Rifaximin
Cirrhosis –> Low albumin –> Tx w/ ?
No tx
Cirrhosis –> High PT/coagulopathy –> Tx w/ ?
FFP if bleeding
Cirrhosis –> Gynecomastia –> Tx w/ ?
no Tx
Cirrhosis –> varices –> Tx w/ ?
Propranolol, nadolol (prevent next bleed)
Banding if they bleed
(Octreotide)
Cirrhosis –> Splenomegaly–> Tx w/ ?
None
Cirrhosis –> Hemorrhoids –> Tx w/ ?
None
Cirrhosis –> Thrombocytopenia –> Tx w/ ?
If bleeding, use platelets
Why do all patients w/ Ascites need a paracentesis?
to confirm the etiology as portal HTN (d/t Cirrhosis) causing a transudate and to, at times, exclude spontaneous bacterial peritonitis (SBP).
Pt has ascites, you do a paracentesis and the protein level is low (s your next step?
Prophylaxis against the first episode of spontaneous bacterial peritonitis is given w/ OFLOXACIN or TMP/SMX (bactrim).
Patient w/ ascites is paracetesed and the cell count is > 250 PMNs. What does the patient ML have and what is your best next step in mgnmt?
> 250 PMNs = SBP –> Tx w/ Ceftriaxone or Cefotaxime (both 3rd gen)
Why is the level of Albumin low in ascitic fluid in patients who have cirrhosis induced portal HTN?
Ascitic fluid d/t portal HTN is transudate (no protein or cells) based on hydrostatic forces.
SAAG > 1.1 means what?
Serum albumin > Ascitic albumin, which means…
Portal HTN and/or SBP
SAAG < 1.1 means what?
Ascitic albumin is not as low as you would think as compared to as serum albumin.
Found in Cancer or intra-abdominal infection excluding SBP
What is the MCC of Hemochromatosis?
genetic defect (HFE) resulting in the OVERABSORPTION of Iron from the DUODENUM. Fe builds up n Liver –> Cirrhosis –> MCC of death
MCC of death in Hemochromatosis
Fe in liver –> Cirrhosis –> death
Untreated hemochromatosis pts may develop what (other than cirrhosis)?
20% of untreated will develop Hepatoma
What other sites are affected by hemochromatosis?
Joints - pain, CaPP deposits (pseudogout)
Diabetes and skin darkening (“bronze diabetes”)
Infertility
Pituitary insufficiency
Best initial tests for hemochromatosis?
- Elevated Fe and Ferritin
2. Decreased TIBC
Confirmatory tests for hemochromatosis?
Most accurate - Biopsy
HFE gene and MRI can spare the need for liver biopsy
Treatment of Hemochromatosis?
Phlebotomy (if genetic cause)
Chelators (Deferasirox or Deferoxamine) - if d/t overtransfusion
Phlebotomy is more effective at removing Fe
CP of Wilson’s dz
Psychosis, paranoia, neuro abnormalities
Movement disorder
Kayser-Fleischer rings on SLIT-LAMP exam
Lab findings of Wilson dz
Coombs negative hemolysis
Ceruloplasmin level decreased
KF ring on slit-lamp exam
Most accurate test for Wilson’s dz
Biopsy
Treatment of Wilson’s dz
Penicillamine
Zinc
Trientine
CP of Primary Biliary Cirrhosis
Women 40-60
Itching and Xanthelasma
Labs of PBC
AMA
Alk Phos elevation
Treatment of PBC
Ursodeoxycholic Acid and sometimes Cholestyramine
CP of Primary Sclerosing Cholangitis
History of UC in 80%
Itchy, fatigue
Labs of PSC
High Alk phos
High Bili
No AMA!!!
Most accurate test for PSC
MR-CP or ER-CP
Treatment of PSC
Ursodeoxycholic acid and sometimes cholestyramine
CP and lab findings of Autoimmune hepatitis
Young women \+ANA elevated LFTs Anti-SMOOTH muscle antibody increased Anti-Liver-Kidney MICROSOMAL antibody
Most accurate test for Autoimmune hepatitis
Biopsy
Treatment of Autoimmune hepatitis
Steroids
CP of most esophogeal disorders?
Dysphagia and weight loss
T/F outpatient esophogeal studies – start w/ Barium; inpatient do endoscopy
Pretty much
Pt w/ progressively worse dysphagia over several months and weight loss. Long history of smoking and drinking alcohol. Stool is positive for blood. What is the ml diagnosis?
Esophogeal Cancer
Diagnosis of Esophogeal CA?
- Upper endoscopy - biopsy
- Chest CT - evaluate extent of disease
If cancer seems clear, Ba will not be enough
Treatment of Esophogeal CA
Surgical resection
Rads and chemotx
“Stent” for unresectable cases to keep esophagus open
Patient has substernal chest pain at any time. It’s not related to eating. Sometimes it’s provoked by drinking cold liquids. What is the best next step in management?
EKG and Cardiac enzymes first!
if negative for cardiac cause, do Manometry to diagnose suspected Esophogeal Spasm
Patient has substernal chest pain at any time. It’s not related to eating. Sometimes it’s provoked by drinking cold liquids. EKG/enzymes are negative for MI or angina. Manometry is positive for esophogeal spasm. What is the next best step in management?
CCBs and Nitrates
