GI Flashcards
1
Q
What can cause ALTs and ASTs in the 1000s?
A
- Drugs/toxins
- Auto-immune hepatitis
- Viral hepatitis (A,B,D,E)
- Vascular
- Shock liver
- Budd-Chiari
- Acute stone within 24hrs
- Wilson’s (rarely)
2
Q
What can cause ALTs and ASTs in the 100s?
A
- Viral hepatitis (B,C) CMV, EBV
- Alcoholic hepatitis
*
3
Q
What can cause ALTs ASTs <100
A
- Autoimmune hepatitis (caeliacs)
- NASH
- HH
- Wilson’s
- A1AT
4
Q
What are causes of increased ALP (predominantly)
A
- Extrahepatic
- Stones
- Strictures
- PSC
- Benign obstruction
- IgG4
- AIDS cholangiopathy
- Malignant obstruction
- Intrahepatic
- Rx
- Antibiotics
- TPN
- estrogens
- MTx
- PBC
- Infections
- IHCP
- Infiltrative disease
- Rx
5
Q
What is the workup for cholestasis?
A
- U/S, CT, MRCP, EUS (R/O stones)
- ERCP not for diagnosis
- Liver Bx
6
Q
How is Hepatitis A transmitted?
A
Fecal-Oral
7
Q
What is the diagnostic test for hepatitis A?
A
Anti HAV IgM
8
Q
How is hepatitis A treated
A
- Self-limited infection
- Treatment is supportive
- Transplant for fulminant hepatitis
9
Q
Who should be vaccinated against Hep A?
A
- Travellers to Hep A endemic countries
- Chronic liver disease
- MSM
- IVDU
- Recurrent plasma-derived clotting factors
- Zoo-keepers
- Vets handling non-human primates
10
Q
Who should get hep a post-exposure proophylaxis
A
- Household contacts of hep a infected individuals
- Co-workers and clients of infected food handlers
- Contacts in childcare or junior and senior kindergarten
11
Q
How are hepatitis B serologies interpreted
A
12
Q
What is the natural history of hepatitis B
A
- <5% progress to chronic HBV
- <1% progress to liver failure
13
Q
How is acute hepatitis B treated
A
- Mainly supportive
14
Q
Which contacts of hepatitis B patients should get vaccinated and get immunoglobulins?
A
- Household contacts
- Sexual contacts
15
Q
What factors increase the risk of developing cirrhosis in hepatitis B patients?
A
- Host factors
- Older age
- male
- immunocompromised
- Co-infection with HIV/HCV/HDV
- EtOH
- Metabolic syndrome
- Disease factors
- High DNA/ALT
- Prolonged time to eAg seroconversion
- eAg negative mutant
- Genotype C
16
Q
What factors increase the risk of developing HCC in hepatitis B patients?
A
- Host factors
- Older age
- Male
- immunocompromised
- Family History
- Born in sub-saharan africa
- Co-infection with HIV/HCV/HDV
- EtOH
- Metabolic syndrome
- Aflatoxin ingestion
- Smoking
- Disease factors
- High DNA/ALT
- Prolonged time to eAg seroconversion
- eAg negative mutant
- genotype C
- Cirrhosis
*Not for cirrhosis
17
Q
What workup should be sent on diagnosis of Hep C?
A
- CBC
- Cr
- ALT
- HBV DNA
- HBe serology
- Fibroscan or Biopsy
- In high risk groups: HIV+Hep D
18
Q
What investigations should be done every 6 months in patients with HBV?
A
- ALT
- HBV DNA
If both persistently elevated, repeat fibroscan
- US for HCC screening if indicated
- NOT AFB
ALL every 6-12 months
19
Q
Who should get US screening for HCC in the HCV population
A
- Asian M>40
- Asian F>50
- Africans > 20
- All cirrhotics
- Family Hx HCC (first degree relatives)
- All HIV coo-infected starting at age 40
20
Q
Who should be treated for chronic HBV?
A
- Cirrhosis
- Liver transplant workup if decompensated, MELD>15
- Fibrosis > stage 1 with HBV DNA >2000 regardless of HBeAg status (even with normal ALT)
- Extrahepatic manifestations
- HBeAg +, elevated ALT, HBV DNA >20 000
- HBeAg - , elevated ALT, HBV DNA > 2000
-
Pregnancy
- 3rd Trimester + high DNA levels (HBV DNA >200 000) to prevent fetal transmission
- Baby should also get HBIG (and vaccines) after birth
Do not treat:
- Immune tolerant phase or inactive CHB phase (normal ALT)
- Acute infection
21
Q
What is the goal of chronic HBV treatment?
A
- Suppress virus
- eAg seroconvert
- Only applies to eAg +
- sAg seroconvert
22
Q
What will the treatment of chronic HBV accomplish
A
Prevent cirrhosis and HCC
23
Q
How is chronic HBV treated (what meds)
A
- PEG interferon
- Nucleotide analogues
- tenofovir
- entecavir
- lamivudine
24
Q
How should chronic HBV in the 3rd Trimester of pregnancy be treated
A
Tenofovir
25
List pros and cons of peg-interferon for the treatment of HBV
* _Pros_
1. Finite therapy
2. Generally more durable response
* _Cons_
1. ++ Side effects
2. Only specific patients benefit
1. Low DNA, high ALT
2. Non-cirrhotic HBeAg + (practically not used anymore)
3. **Unable to use in decompensated cirrhotics**
26
List pros and cons of nucleotide analogues
* _Pros_
1. Potent viral suppression
2. Well tolerated
3. Tenofovir/entecavir very high barrier to resistance, considered first line
* _Cons_
1. Generally many years to lifelong therapy (esp. in eAg negative)
2. Expensive
3. Unlikely to seroconvert sAg
27
Who should be screened for HCV?
1. Hx of current or past IVDU
2. Recieved healthcare or personal services where there is a lack of infection control and prevention practices
3. Recieved blood transfusions, blood products or organ transplant before 1992 in canada
4. Hx of or current incarceration
5. Born or resided in a region where Hep C prevalence is \>3%
6. such as
1. Central, east and south asia
2. Australasia and oceania
3. Eastern europe
4. Subsaharan africa
5. North Africa or the middle east
7. Born to a HCV positive mother
8. Hx of sexual contact or sharing of personal-care items with someone who is HCV-infected
9. HIV infection, particularly in MSM
10. Chronic HD treatment
11. Elevated ALT
12. Born between 1945 and 1975
28
Interpret HCV serologies
29
What is the natural History of HCV?
30
What workup should be sent on diagnosis in HCV?
1. HCV genotype testing
2. HCV RNA level
3. HIV, HBV
4. Liver enzymes
5. Liver function testing
6. Abdominal US
7. Fibrosis assesment
1. Fibroscan
2. Fibrotest
3. APRI
4. Biopsy
31
Which factors increase the risk of cirrhosis in chronic HCV?
1. Older age
2. Male sex
3. HIV/HBV co-infection
4. Obesity/DM/fatty liver
5. EtOH
32
What factors increase the risk of HCC in patients with chronic HCV?
Cirrhosis or co-existing liver disease which may accelerate fibrosis
33
Who should get treatment for chronic HCV
ALL infected patients, except:
* Short life expectancy from comorbidities
* Priority to patients with cirrhosis, advanced fibrosis or extrahepatic manifestations
* Sometimes if decompensated, may treat after transplant (Avoid MELD purgatory)
34
Give an approach to HCV treatment
1. Get information
1. Check HCV RNA and genotype and check for co-infections
2. Fibrosis/cirrhosis assessment
1. If cirrhosis, consider transplant assessment
2. Treat
1. Consider in all patients especially if fibrosis, cirrhosis or extrahepatic manifestations
2. Chose Tx regimen
3. Re-assess
1. Check viral load 12-weeks post treatment completion
2. If negative, likely cure
35
What is the typical LFT pattern in alcoholic hepatitis?
* AST/ALT \>2
36
If you suspect alcoholic hepatitis and the liver enzymes are over 300, what should you do?
Consider alternalte diagnosis Or get Bx
37
What should you do to confirm alcoholic hepatitis in a patient with underlying confounding liver disease?
Get a Bx
38
How should alcoholic hepatitis be treated?
1. Calculate MELD or Maddrey discriminant function
1. MELD\>20 or Maddrey \>32: Prednisone 40mg PO daily x28 days then taper
NO role for pentoxifylline (possible benefit in HRS)
Can consider NAC in addition to steroids
39
Name the contraindications to steroids in Alcoholic hepatitis
1. Infection
1. SBP
2. Active HBV
3. TB
4. +/- HCV
2. GI bleeding (relative)
40
Once a patient with alcoholic hepatitis is on steroids, how do you decide to continue or stop the steroids?
* Calculate Lille score
* \>0.45: Not responding. Stop
* \<0.45: Responding. Continue full course
* If patient has no improvement at 4-7 days, consider stopping prednisolone since unlikely to help
41
When should transplant be considered in alcoholic hepatitis
* If hepatic failure, refer:
* MELD≥21
* CP-c
* Typically requires 6 months of abstinence but there are exceptions
42
Name 2 _vital_ non-pharmacological strategies to prevent recurrent alcoholic hepatitis
* Nutrition
* EtOH abstinence
43
What is the difference between NAFL and NASH?
* NAFL: no hepatocellular injury
* NASH: + hepatocellular injury
44
What is NAFLD?
NAFL+NASH
45
What is required to diagnose NAFLD
1. Evidence of steatosis
1. NASH can can only be diagnosed definitively on Bx
2. liver enzymes may or may not be elevated
2. Ruled out secondary causes
46
List conditions associated with NAFLD
1. Obesity
2. T2DM
3. DLP
4. Metabolic syndrome
47
What is the most common cause of death in NAFLD
Cardiovascular
48
How is NAFLD treated
1. Weight loss
1. ≥ 3-5% of body weight to improve steatosis, ≥7-10% to improve fibrosis
2. Dietary changes + moderate-intensity exercises
2. Pharmacotherapy
1. Pioglitazone + Vitamin E (for Bx proven NASH)
2. Bariatric surgery
3. Identify + manage CV risk factors
1. Statins are OK in NAFLD/NASH and compensated NASH cirrhosis. Avoid in decompensations
49
List the causes of cirrhosis
1. Viral
2. EtOH
3. NASH
4. A-I
5. Metabolic
6. ...
50
How is the child-pugh score calculated?
51
What is the MELD criteria required to refer a patient for transplant
MELD≥15
52
What are the complications of cirrhosis?
1. Varices
2. Ascites/SBP
3. Encephalopathy
4. HRS, HPS, porto-pulmonary hypertension
5. HCC
53
What councilling should be given to cirrhotic patients?
1. Abstinence from alcohol
2. Andequate nutrition
3. In NAFLD: Weight loss
4. Limit acetaminophen to \<2g/day
5. Avoid sedatives, NSAIDS, ACEI/ARBs
6. Get vaccinated for HAV, HBV, flu
54
What should be done in primary prophylaxis to prevent bleeding in patients with varices?
55
What should be done in secondary prophylaxis to prevent bleeding in patients with varices?
Beta blocker AND banding
56
How is the SAAG interpreted?
* SAAG\>11: transudate
* SAAG\<11: Exudate
57
How should ascites related to portal hypertension be managed?
1. Initial management
1. Treat underlying liver disease
2. Salt restriction (\<2g/88mmol/day)
1. Water restriction not necessary unless Na\<125
3. Diuretics
1. Start with spironolactone 100 and lasix 40 then titrate
2. Failing medical therapy
1. Regular therapeutic paracentesis
1. Give albumin 6-8g/L of fluid removed if removing \>4L
2. Can consider TIPS if no contraindications (Encephalopathy, HCC)
3. Liver transplant
58
How can compliance to Na restricted diet be assessed?
* 24hrs urine sodium collection
* Na\<78mmol: Compliant
* Na\>78mmol: non-compliant
Diuretics should be started if ongoing ascites or unable to comply
59
How can diuretic effectiveness and compliance to a low sodium diet be assessed in patient with ascites on diuretics?
* 24hrs urine Na:
* If Na\<78: Diuretic resistant. Increase dose
* If Na\>78 **AND** not losing weight: non-compliant with low sodium diet. Reinforce diet
* If Na\>78 **and** losing weigh: Compliant with diet and diuretic sensitive. Stay the course
60
Who should get a diagnostic paracentesis to rule out SBP?
When suspected
All patients with new ascites
All cirrhotic patients with ascites presenting to hospital
61
List the classic symptoms of SBP
* Abdominal pain
* fever
Can also present with encephalopathy, hypotension, AKI, worstening liver function
62
How can a diagnosis of SBP be posed?
* Neutrophils in ascitic fluid\>250 or positive cultures
* Culture negative still requires full treatment course
63
Name one thing that should be ruled out before diagnosing a patient with SBP
Secondary causes of peritonitis (i.e perf, recent surgery...)
64
How is SBP treated
* Ceftriaxone IV x 5 days
* Fluoroquinolone if pen allergy
* Albumin
* if Cr\>88, BUN\>10.7, bili\>68 (in practice everyone)
* 1.5g/kg on day 1, 1g/kg on day 3
65
Who should get prophylaxis for SBP
* Patients who previously had SBP
* Patient with cirrhosis who present with GI bleeding
* In hospital
* Not necessary too have ascites
* Cirrhosis where ascitic fluid protein in \<15g/l and at least 1 of:
* Impaired renal function (Cr≥106, BUN≥8.9, Na≤130)
* Impaired liver function (CP≥9, bili ≥51)
66
What are the clinical manifestations of HH
1. Deposition of iron in various organs
1. Liver
1. Cirrhosis
2. Elevated liver enzymes
2. Skin
1. Bronze hyperpigmentation
3. Endocrine
1. Hypopituitarianism (impotence amenorrhea)
2. DM (islet cell destruction)
4. MSK
1. Arthropathy
1. Osteophytes in 2nd and 3rd MCP
5. Fatigue
6. Increased risk of infection
1. Yersinia enterolitica
2. Listeria monocytogenes
3. E. Coli
4. Vibrio Vulnificus
67
Give a DDx for iron overload
* Frequent blood transfusions
* SS
* Thalassemias
* Other chronic liver disease
* **NAFLD**
* HCV
* EtOH misuse
68
Give an approach to the diagnosis and treatment of HH
69
How is HH treated. Give 1st and second line
1. 1st Line: Phlebotomies, target ferritin 50-100
2. 2nd Line: Iron chelation
1. Desferoxamine
2. deferiprone
3. deferasiroox
70
What side-effects/risks are associated with iron chelation?
1. Retinal/auditory toxicity (Desferroxamine)
2. Agranulocytosis (deferiprone)
3. Liver/renal toxicity (deferasirox)
71
What foods/supplements should be avoided in HH?
1. Vitamin C supplements
2. Uncooked seadfood
No need to limit red meat/dietary iron
72
List risk factors for caeliac disease
1. Northern European descent
2. + Family History
3. T1DM
4. AI thyroid disease
5. Down and turner syndrome
6. 1st degree relative
7. IgA deficiency
73
List symptoms and signs of caeliac disease
1. Diarrhea
2. Weight loss
3. anemia
4. osteooporosis + enamel defects
5. elevated transaminitis
6. infertility
7. Vitamin + mineral deficiencies
1. B12
2. D
3. Fe
4. Calcium
8. **Dermatitis herpetiformis**
74
Give the workup for caeliac's disease
75
When should HLA DQ2/DQ8 testing be considered?
Negative test effectively rules out celiac's disease:
1. Equivocal histology in seronegative patients
2. Evaluation in patients on a gluten free diet
3. Discordant histology and serology
4. Suspicion of refractory celiac or when diagnosis is in question
5. Patients with Down syndrome
6. Patients with a history diagnosis of celiac
76
How is celiac treated
Lifelong gluten free diet
77
What food items contain gluten?
1. BROW acronym
1. **B**arley
2. **R**ye
3. **O**ats (often contaminated)
4. **W**heat
78
What should be done on follow-up after a diagnosis of celiac's
* Diet history
* Follow-up serologies 6 and 12 months post Dx then annually
* Expect reducing Ab titers and improvement of histology
\*Persistent Sx despite negative serology - repeat Bx
79
What further workup should be considered _after_ a diagnosis of Celiac's disease?
1. Micronutrient deficiencies
1. Fe
2. Folate
3. Vit D
4. B12
2. BMD per guidelines
80
List complications of celiac's disease
1. Nutritional deficiencies and anemia
2. Osteopenia/osteoporosis
3. Elevated liver enzymes
4. Dermatitis herpetiformis
5. Enteropathy associated T cell lymphoma
81
How is dermatitis herpetiformis treated
Dapsone and gluten free diet
\*R/O G6PD deficiency
82
Who should be screened for celiac disease?
1. +FHx
2. DM-1
3. Autoimmune thyroid disease
4. Down's and turners synrdrome
83
List clinical manifestations of Chrohn's disease
1. Abdominal pain
2. Diarrhea
3. Weight loss
4. fever
5. peri-anal symptoms
84
List common lab findings in Crohn's disease
1. Increased CRP
2. Low iron
3. Anemia
4. B12 deficiency
85
How is Crohn's disease diagnosed?
1. Ileocolonoscopy + Biopsy
1. Patchy inflamation
2. Skip lesions
3. aphtous ulcers
4. cobblestone mucosa
5. Rectal involvement + circumferential continuous inflammation less common in CD vs UC
2. Small bowel imaging +/- OGD
1. CT/MR enterography
2. capsule endoscopy
86
How is crohn's disease treated?
1. Induction treatment
1. Mild disease
1. Sulfasalazine
2. Budesonide
3. \*No role for 5ASA or other thiopurine
2. Moderate to severe
1. Budesonide
2. Prednisone/methylpred
3. MTX
4. Anti-TNF
1. Infliximab
2. Adalimumab
5. Anti-integrin
1. Vedolizumab
6. Anti IL12/23
1. Ustekimumab
2. Maintenance & remissionn
1. Mild
1. Thiopurine
2. Moderate to severe
1. Thiopurine
2. MTX
3. Anti-TNF
4. Anti-integrin
5. Anti IL12/23
\*When starting an anti-TNF, combine with thiopurine
87
What are markers of crohn's disease severity?
1. High CRP
2. symptoms affecting lifestyle
3. low albumin
4. deep ulcerations on endoscopy
5. complications
88
What is the prefered agent in fistulizing crohn's
Anti-TNF
89
How is perianal disease treated in crohn's disease?
1. Charracterize the fistula with EUS or MRI
2. Anti-TNF for induction and maintenance
3. +/- antibiotics if concern for infection
1. Cipro+Flagyl
4. Surgical consultation for drainage up front if abscess (drain prior to anti-TNF), complex fistula or medical failure
90
If a patient is failing all therapies for crohn's disease, what are 2 last agents that can be attempted before moving on to surgery?
1. Vedolizumab
2. Ustekinumab
91
Name intra-abdominal complications of crohn's disease
1. Strictures
1. Cold stricture
2. Hot stricture
2. fistula
3. abscess
92
How are intra-abdominal complications of Crohn's disease diagnosed?
CT/MR enterography
93
How are intra-abdominal fistulas secondary to crohn's disease treated?
Biologics or surgery
94
How are intraabdominal abscesses secondary to crohn's disease treated?
1. Drainage (IR or surgery)
2. Antibiotics (cipro/flagyl) Before immunosupression
95
How are strictures 2/2 Crohn's disease treated
* Cold strictures
* Conservative management
* Endoscopic dilation
* Surgery
* Hot strictures
* Steroid bridge to maintenance therapy (usually biologics)
96
List perianal complications of Crohn's
* Fistula
* Abscess
97
How are perianal crohn's disease complications diagnosed?
* MR pelvis
* EUS
* Examination under anesthesia
98
Which part of the GI tract is affected by UC?
Proctitis (within 18cm of anal verge)→ Left sided colitis (sigmoid to splenic flexure) → Pan-colitis (beyond splenic flexure)
99
List clinical manifestations of UC
1. Proctitis
1. Small volume + frequent BM with blood
2. tenesmus
3. urgency
4. cramping
5. Abdo pain
2. Fever
3. fatigue
4. weight loss
5. Anemia
6. Increased CRP/ESR
100
How is UC diagnosed?
1. Illeocolonoscopy + Bx
1. Continuous inflammation from rectum proximally
2. Granular, friable mucosa
3. Bx: Crypt abscesses, lamina propria cellularity
101
List the truelove/witt criteria for severe UC
1. \>6 BM/day
2. visible blood in stool
3. Pyrexia T\>37.8
4. Pulse \>90
5. Anemia Hb\<105
6. ESR \> 30
102
How is UC Treated?
1. Induction
1. Mild
1. **5ASA**
1. PO if extensive
2. PR if proctitis
1. suppository \<10cm
2. Enema if to splenic flexure
2. Budesonide
2. Moderate to severe
1. Budesonide
2. Prednisone/methylpred
3. Anti-TNF
1. Infliximab
2. Adalimumab
3. **Golimumab**
4. Anti-integrin
1. Vedolizumab
5. Anti IL12/23
1. Ustekinumab
6. **JAK inhibitors**
1. **Tofacitinib**
2. Maintenance
1. Mild
1. **5ASA PO/PR**
2. Moderate to severe
1. Thiopurine
2. Anti-TNF
3. Anti-integrin
4. Anti IL12/23
5. **JAK inhibitor**
103
How should a toxic megacolon 2/2 UC be managed
SURGICAL CONSULT!
104
What should be added when starting an antti-tnf
Thiopurine
105
What is the treatment target in IBD?
Mucosal healing and steroid free remission
106
What should you check before starting AZA/6MP
TMPT
107
How can fecal calprotectin be used in IBD
As a marker of disease severity
108
What workup should be sent in patients presenting with an IBD flare requiring admission?
1. Labs
1. CBC
2. LBC
3. Extended lytes
4. LFTs
5. bilirubin
6. albumin
7. ESR/CRP
2. Stool tests
1. C&S
2. C. diff
3. O&P
4. +/- fecal calprotectin
3. Imaging
1. AXR
2. +/- CT abdo
3. +/- CT/MR enterography
4. Endoscopy
1. For diagnosis, to assess disease severity, rule out mimics (ischemia, CMV)
2. Can send aspirates for microbiology
109
How should an IBD flare be managed in inpatients?
1. IVF, Bowel rest, DVT Prophylaxis
2. Once infection ruled out, start steroids
3. Minimize narcotics and NSAIDS
4. If minimal response after ˜72 hrs of steroids → infliximab
1. Elevated CRP and low albumin = poor response to infliximab rescue
5. Genral surgery consultation for treatment of refractory colitis, toxic megacolon, perianal/intra-abdominal abscess. complex fistulizing Crohn's
110
What are the indications for collectomy in fulminant UC?
1. **Toxic megacolon**
2. Colonic perforation
3. Severe refractory hemorrhage
4. **Refractoriness to medical therapy after 3-5 days**
111
How is a toxic megacolon defined?
1. Radiographic megacolon (\>6cm)
2. PLUS at least 3 of
1. Fever (\>38)
2. HR (\>120)
3. Neutrophils \>10.5
4. Anemia
3. PLUS at least one of:
1. Dehydration
2. Altered sensorium
3. Electrolyte disturbance
4. Hypotension
112
What workup should be done to rule out infection and when in IBD flare?
1. Rule out C.Diff if worstening diarrhea (all patients, even if no recent ABx)
2. Rule out abscess in Crohn's patients with _fever_ and _abdominal/perianal pain_
1. Use imaging
\*Immunosuppression should be withheld until risk of infection adressed
113
In patients with bloody diarrhea from an IBD flare, should DVT prophylaxis be withheld?
No
Risk of VTE \> Risk of bleed
114
What other causes of diarrhea can be considered in patients with IBD
* CMV colitis
* Bile-salt diarrhea
115
Why should NSAIDS be avoided in active IBD
Can agravate diarrhea
116
What is the maximal delay to perform endoscopy in UGIB patients with liver disease/without liver disease?
* 12h
* 24h
117
What antibiotic regimen should be given to variceal GI bleeds?
Ceftriaxone 1g IV daily x 7 days
118
List the forrest clasification of ulcers
* High risk
* 1A: Spurting vessel
* 1B: oozing vessel
* 2A: Visible vessel
* 2B Adherent clot
* Remove clot and reassess
* In unable, treat as high risk
* Low risk
* 2C: Pigmented ulcer base
* 3: Clean based ulcer
119
How should high-risk ulcers be treated after endoscopy?
* IV PPI x 72hrs
120
What workup shuld be sent in non-variceal UGIB
* CBC
* LBC
* Cross and type
* PTT INR
* Liver enzymes and function test
121
What are the transfusional targets for non-variceal UGIB
* Hb\>70
* Plt\>50
122
How should non-variceal UGIB be manages
* Reverse Anticoagulation (weigh risks and benefits)
* IV PPI
* Endoscopic management
* Erythromycin infusion pre-endoscopy
* Perform within 24hrs
* Within 12 hrs if variceal or high risk
* Endoscopic therapy to high risk ulcers only (FOrest IIa or higher)
123
If a patient has recurrent bleeding after endoscopy, what should be the next step?
* Repeat EGD
* IR embolisation
* Surgical management
* If tumor bleeding: consider radiation
124
How should bleeding gastric ulcers be managed post-endoscopy
* High risk : IV PPI x 72hrs then oral _BID_ PPI dor at least 2 weeks post endoscopy
* Low risk: Oral PPI
* Restart anti-platelets and anticoagulation as soon as possible
* Not associated with increased re-bleed but is associated in reduced all cause mortality
* Timing depends on multiple factors
* Manage risk fators
* Biopsy for H. Pilori
* Treat if positive
* Confirm eradication after treatment, if eradicated can stop PPI
* Stop unnecessary NSAIDS, stop ASA if for primary prevention
* In CV patients requiring ongoing antiplatelets consider _indefinate PPI prophylaxis_
* If unclear cause of PUD consider _indefinate PPI_ (*conditional recommendation*)
125
Who should be tested for H. Pilori
1. PUD
2. MALT lymphoma
3. Gastric cancer
4. Long term NSAID/ASA
5. Otherwise unexplained iron deficiency
6. ITP
Do not test all GERD patients without another indication
126
How is MALT lymphoma treated
H. Pilori eradication
127
What are the diagonostic tests for H. Pilori?
1. Stool antigen
2. **Histology**
3. Biopsy culture
4. **Urea breath test**
5. Serology
1. Sensitive but not specific for active infection
1. + in prior infection
128
How is H. Pilori treated?
* 1st line
* PPI/bismuth/metronidazole/tetracycline
* PPI/amoxicillin/metronidazole/clarithromycin
* 2nd line (if Tx failure)
* If they had triple therapy, then PBMT
* Otherwise PPI/amoxicillin/Levofloxacin
129
How should H.Pilori eradication be tested
* Urea breath test
* Bx
* Fecal antigen test
## Footnote
**Test everyone for eradication**
130
How should GERD be managed
1. Alarm symptoms
1. EGD
2. No alarm symptoms
1. Non-pharm management
2. Trial of PPI (30min before meal daily) x 8 weeks
1. Symptoms improve? Try to wean. If unable, then use lowest dose
2. Symptoms refractory?
1. Ensure optimization of PPI therapy
2. EGD off PPI
3. If normal, reflux monitoring
4. If negative, D/C PPI and consider other causes
* Recommendations against other medical therapies in PPI non-responders except:
* Sulcrate in pregnancy
* H2RA at night if objective nocturnal acid reflux on pH monitoring
131
What are the alarm symptoms in GERD?
* Dysphagia
* Weight loss
* GI bleed
132
List non-pharmacological management options in GERD
* Weight loss
* Avoid trigger foods
* Quit smoking
* Elevate head of bed
133
What can be considered for extra-oesophageal symptoms of GERD (coughm asthma, chest pain)? What should be done before?
1. Do usual workup first
2. Then consider PPI 8-12 weeks
3. If fail, EGD
134
How is Barrett's esophagus diagnosed?
1. Salmond colored metaplastic mucosa extending ≥1cm proximal to the GE junction
2. Biopsy confirmation of columnar interstitial metaplasia +/- goblet cells
135
List risk factors for Barrett's esophagus
1. Chronic GERD (\>5 years)
2. Age\>50
3. Male gender
4. Tobacco use
5. Central obesity
6. Caucasian race
7. NOT alcohol
136
Who should be screened for Barrett's Esophagus
1. Do not screen patients with chronic GERD
137
How should non-nodular Barrett's Esophagus be managed?
138
What are the steps to investigating and managing dysphagia?
1. **_Step 1:_** H+P
1. Oropharyngeal vs esophageal
2. Structural vs motility
3. Alarm features?
2. **_Step 2:_** Imaging and or endoscopy
1. Oropharyngeal: Video swallowing study
2. Esophageal:
1. Alarm features: endoscopy
2. No alarm features and age \<50, Sx GERD
1. Trial of PPI
3. Manometry\>barium swallow for esophageal motility disorders
4. OGD\>Barium swallow for esophageal dysphagia
139
List alarm symptoms in Dysphagia
* Weight loss
* Anemia
* Vomiting
140
What are the signs and symptoms used to differentiate Oropharyngeal from esophageal dysphagia
* Oropharyngeal
* Predisposing neuromuscular condition
* Choking
* Drooling
* Surgery/rads to head and neck
* Sx above the sternal notch
* Esophageal
* Regurgitation
* Sensation of material getting "stuck" below sternal notch
141
What are the signs and symptoms used to differentiate structural vs motility dysphagia?
142
List symptoms of achalasia
1. Progressive solid and liquid dysphagia
2. Regurgitation + reflux symptoms
3. Chest pain
4. weight loss
5. Sx refractory to PPI Tx
143
What is the typical epidemiology for achalasia
* M=F
* Age 30-60
* all ethnicities
144
What are the complications of achalasia?
1. Megaesophagus \>6cm
2. Sigmoid esophagus
3. **SCC**
145
What are the steps to posing a diagnosis of achalasia?
* **Step 1:** OGD
* R/O pseudoachalasia and obstruction
* Puckered GE junction
* Dilated, fluid-filled esophagus as disease progresses
* **Step 2:** High resolution manometry +/- barium swallow
* Manometry
* Gold standard for diagnosis
* Impaired relaxation of LES and abnormal peristaltism are diagnostic
* Barium swallow
* Bird beak esophagus
146
How is achalasia managed?
1. Good surgical candidate
1. Pneumatic dilation
1. 1st line
2. Tear/perf risk
2. Laparoscopic heller myotomy
1. 1sr line
2. Often performed with fundoplication
3. Peroral endoscopic myotomy
1. 1st line option
2. Often complicated by GERD
4. Esophagectomy
1. For patients with megaesophagus, sigmoid esophagus, failure of above treatments
2. Poor surgical candidate
1. Endoscopic botox 1st line
2. Smooth muscle relaxants
1. CCB, nitrates
2. \*Least effective
147
What is the definition of eosinophilic esophagitis?
* Esophageal disorder characterised by esophageal symptoms and esophageal eosinophilia (\>15 eos/HPF) and absence of secondary causes
148
What are the risk factors for Eosinophilic esophagitis?
1. M\>F
2. Age 20-30
3. Ass with atopy, allergy, asthma, eczema, chronic rhinitis
149
What are the clinical manifestations of Eosinophilic esophagitis?
* Solid dysphagia
* Food bolus obstruction
150
What are the endoscopic findings in eosinophilic esophagitis
1. Trachealisation of the esophagus
2. Strictures
3. Linear furrows
4. White papules (eos)
5. Crate paper esophagus
151
What is the treament goal in eosinophilic esophagitis
Complete resolution of symptoms and patholoogy
152
How is eosinophilic esoophagitis treated?
1. Dietary elimination
1. 6 food elimination diet
1. eggs
2. soy
3. cow's milk
4. wheat
5. tree nuts
6. seafood
2. Pharmacological
1. Topical steroids (fluticasone/budesonide)
2. Prednisone if topical fails
3. endoscopic
1. Consider dilation if symptomatic strictures
153
List secondary causes that may mimic eosinophilic esophagitis
1. GERD
2. Achalasia
3. CTD
4. Hypermotility syndromes
5. pill esophagitis
6. pemphigus
7. Hyper IgE syndrome
154
What are the diagnostic criteria for pancreatitis?
1. Abdo pain constant with the disease
2. Lipase/Amylase ≥3x ULN
3. Characteristic findings on imaging
155
List the etiologies of pancreatitis
1. Stones
2. EtOH
3. Others
1. Triglycerides
2. hypercalcemia
3. drugs
1. GLP- Receptor agonists
2. 5-ASA
3. thiazides
4. azathioprine
4. Autoimmune
5. Post-ERCP
6. Trauma
7. viruses
8. Malignancy
9. hereditary
10. smoking
11. scorpion bites
12. vasculitis
156
What are the 2 scores used to define severity in acute pancreatitis?
APACHE II and SIRS
157
How is acute pancreatitis generally managed?
* IVF
* 250-500 cc/hr of isotonic cristaloid (RL)
* Avoid RL if hypercalcemic
* Analgesia
* NPO, start clear fluids or low fat diet early, advance as able
* If unable to take PI, consider enteral nutrition
158
What should be done in a patient with pancreatitis if they deteriorate after 48-72hrs
159
How should acute gallstone pancreatitis be managed?
1. No urgent ERCP unless:
1. Cholangitis
2. Persistant biliary obstruction
3. severe ongoing pancreatitis
2. ERCP can be considered \>48 hours if not clinically improving with evidence of persistent stone
3. Ideally CCK before discharge
160
How is hypertriglyceridemic pancreatitis treated
1. If sick:
1. Strict NPO
2. IV insulin
3. apheresis where available
2. Long term
1. Fibrates
2. treat other causes of hyperTG (DM, ETOH)
161
List the atlanta classification for complications of pancreatits
1. Early (\<4 week)
1. Interstitial edematous pancreatitis
2. Acute peripancreatic fluid collection
3. Pancreatic necrosis
4. Acute necrotic collection
5. Infected pancreatic necrosis
1. Usually after 1 week
2. Late (\>4 weeks)
1. Pseudocyst
1. Can cause biliary or GI obstruction
2. Can become infected, requiring endoscopic/surgical drainage
2. Pancreatic abscess
3. Walled off pancreatic necrosis
162
What are the 2 types of auto-immune pancreatitis?
1. Type I
1. Part of IgG4 related diseases
2. Also can have Biliary, salivary, pulmonary, renal, thyroid, LN involvement
2. Type II
1. Isolated to the pancreas and associated to IBD
163
What is the workup for autoimmune pancreatitis?
1. CT/MRCP/EUS
1. Sausage pancreas
2. Biliary strictures
2. Serum IgG4 level
1. \>2x ULN suggestive of type I AIP
164
How is auto-immune pancreatitis treated?
1. Prednisone 40mg PO daily x 4-6 weeks then taper
1. If relapse retrial steroids or ritux or AZA
2. Look for radiographic improvement
165
List the etiologies of Chronic pancreatitis?
1. **T**oxic/metabolic: _chronic_ alcohol use, HyperTG, smoking, hyperCa, medications, toxins,CF
2. **I**diopathic
3. **G**enetic -- CF, others (PRSS1, CTRC...)
4. **R**ecurrent acute pancreatitis
5. Obstructive: Pancreatic divisium, sticture, stone, tumor
166
What are the clinical manifestations of chronic pancreatitis?
1. Severe abdo pain
2. Fat soluble vitamin deficiency
3. Exocrine pancreatic insufficiency
1. Steatorrhea
2. Maldigestion
3. Weight loss
4. Endocrine pancreatic insufficiency
1. DM
167
How is chronic pancreatitis diagnosed?
1. 1st line: CT or MRI
1. EUS if uncertain
2. Role of pancreatic exocrine function testing unclearr
168
What workup should be done once chronic pancreatitis is diagnosed?
* Ca, Triglycerides
* Med review
* IgG subcless
* In recurrent acute
* Consider MRCP, R/O divisium, stricture, tumor, stone
* Consider genetic workup "if etiology unclear, especially in young patients"
169
How is chronic pancreatitis treated?
1. Lifestyle modifications
1. EtOH and smoking cessation for all
2. Pancreatic enzymes
1. No evidence for relieving pain
2. Use if _exocrine pancreatic insufficiency_
3. Increase weight and vitamin absorption
3. Pain management
1. Antioxidants (limited benefit)
2. Opioids (if other pain control methods exhausted)
3. Celiac plexus block
4. If obstructive cause
1. Trial of ERCP, EUS, endoscopic procedures
2. If chronic pain failing endoscopic therapy, consider surgical intervention
1. Caution in EtOH
5. In highly selected patients
1. Total pancreatectomy + islet cell autotransplant
170
What are the risks associated with PPIs?
1. C. Diff
2. PNA
3. HypoMg
4. Low B12
5. AIN, CKD
6. Dementia
7. Low BMD
8. Gastric cancer
9. Death?
Based on observational data
171
For which conditions is there a clear benefit to PPIs?
* GERD
* PUD
* ZES
* H. Pilori
172
How often should PPI use be reassessed as per choosing wisely?
At least yearly
173
List a DDx for rectal bleeding
1. Painless
1. Diverticular bleed
2. hemorrhoids
3. angiodysplasia
4. cancer
5. polyps
6. radiation
7. proctitis
2. Painfull
1. Ischemic colitis
1. Needs workup for cause
2. Thrombosed hemorrhoids
3. Fissure
3. Others
1. IBD
2. Infectious
174
List causes for ischemic colitis
1. Cardioembolic
2. atheroembolic
3. Shock/low-flow
4. segmental, think vasculitis/PAN
175
How should a lower GI bleed be managed?
1. ABC-MOIF
2. Consider EGD if suspected rapid UGIB
1. Can be ruled IN with NG tube, cannot Rule-out
3. Rapid prep for colonoscopy within 24hrs
1. Recurrent bleeding -- consider repeating colonoscopy
4. Early surgery/IR referral if unstable or unable to tolerate prep
5. Stop NSAIDS or primary prevention ASA
176
When should small bowel bleeding be suspected?
In any patient with overt GI bleeding and normal EGD and colonoscopy
177
How can small bowel bleeding be diagnosed?
1. Options:
1. Repeat EGD + push enteroscopy (to proximal jejunum) and repeat colonoscopy
2. Video capsule endoscopy followed by CT enterography
1. Consider CT enterography first if concerns surrounding tumors, SB crohn's, strictures or other obstructive process that the capsule could get stuck in
3. Intraoperative enteroscopy
4. CTA if brisk active bleeding, tagged RBC scan if slow bleed
5. Conventional angiography in IR suite for massive unstable bleeding
178
How can small bowel bleeding be treated?
1. Double baloon enteroscopy
2. Surgery
3. IR embolisation
4. Supportive management with transfusions and iron replacement
179
What serology can be positive in crohn's?
ASCA
180
What serology can be positive in UC
ANCA
181
List side effects of 5-ASA
1. Headache
2. Diarrhea
3. nausea
4. pancreatitis
5. Interstitial nephritis
182
List side effects of azathioprine
1. Hepatotoxicity
2. Leukopenia
3. Lymphoma
\*do not use in TPMT deficiency
183
What are side effects of MTX
1. Cytopenias
2. hepatotoxicity
3. ILD
\*Do not use in women of childbearing age
184
What are side effects of anti-TNF
1. Infections
2. Lymphoma
3. other malignancies
4. Tb, HBV reactivation
185
What are the side effects of tofacitinib
1. Infections
2. lymphoma
3. other malignancies
4. leukopenia
5. anemia
6. HZV,Tb reactivation
7. GI perforation
186
What are the side effects of cyclosporine
1. AKI
2. HyperK
3. hirsutism
4. infection
187
List etiologies of obstruction in cholangitis?
1. Stones
2. Strictures (benign or malignant)
3. Clot
4. Masses/tumors
1. Pancreatic head
2. klatskin tumor
3. mets
5. PSC, HIV cholangiopathy
6. Biliary stent obstruction
7. Worms
1. Ascaris lumbricoides
2. tapeworm
188
What is the clincal presentation of cholangitis?
1. Charcot's triad
1. Fever
2. Abdo pain
3. Jaundice
2. Raynaud's pentad
1. Charcot's triad
2. Hypotension
3. Confusion
3. Labs
1. WBC \>10 or \<4
2. ALT/GGP \>1.5x ULN, ALT \>1.5x ULN
3. Bilirubin \>34
4. Imaging
1. Biliary dilation +/- stones
1. US CT MRCP EUS
5. Predisposition
1. PSC
2. Stricture
3. Stent
4. recent ERCP
189
What are the two types of microscopic colitis?
1. Lymphocytic
2. Collagenous
190
Who gets microscopic colitis (epidemiology)
1. Older women (\>65)
2. Comorbid autoimmune disease
1. Thyroid
2. celiac
3. RA
191
What are the symptoms of microscopic colitis?
1. Relapsing/remitting watery, non-bloody diarrea. Can be severe
2. Weight loss, abdo pain
192
How is microscopic colitis diagnosed?
* Normal appearing colonoscopy
* Bx to confirm diagnosis
193
How is microscopic colitis treated?
* Immodium
* Stop NSAIDS and offending meds
* Budesonide PO
194
How is acute cholangitis managed
1. Empiric antibiotics
1. Cover common pathogens
1. CTX + Flagyl
2. pip-tazo
3. cipro+flagyl
4. carbapenem
2. Source control
1. ERCP + Stone removal +/- sphincterotomy +/- stent placement
1. High bleed risk, ensure INR\<1.5 PLT\>50, hold Anticoagulants
2. Percutaneous transhepatic biliary drainage
1. IR guided if failed ERCP or ++ comorbidities
3. Surgical biliary drainage -- rarely necessary
195
What is the epidemiology of IgG4 related disease
* Mostly older men (age\>60)
* In coontrast Type II AIP diagnosed at age \>40 M=F
196
What are the manifestations of IgG4 related disease
1. Auto-immune pancreatitis
2. billiary sclerosis
3. retroperitoneal fibrosis
4. chronic sclerosing aortitis
5. thyroiditis
6. interstitial pneumonitis
7. tubulointerstitial nephritis
197
How is IgG4 related disease screened for and diagnosed?
1. Mesure IgG 4 levels (can help but not diagnostic)
2. Imaging of affected organ and R/O other causes
3. Gold standard: tissue Bx of affected organ
198
How is IgG4 related disease treated?
* Prednisone 40mg daily x 2 weeks them taper over 2 months
* If unable to taper consider Ritux, AZA, MMF
* Follow response to treatment symptomatically and radiologically
199
How does PSC present clinically?
1. Jaundice
2. Pruritis
3. Fatigue
4. Elevated ALP
200
Who gets PSC
* Men
* Strongly associated with UC
201
What imaging test should be ordered in suspected PSC and what will be found?
1. MRCP
1. Beading of CBD
2. strictures
\*R/O cholangiocarcinoma with ERCP and brushing of dominant stricture
202
Give 2 differentials to PSC
* IgG4 related disease
* PSC-Autoimmune overlap syndrome
203
How is PSC treated?
1. PRN ERCP for symptomatic strictures
2. MRCP q1year, screen for gallbladder cancer and cholangiocarcioma
3. If cirrhosis, screen for HCC/EoV
4. **no benefit to URSO**
5. Transplant for liver failure
204
what are the manifestations of PBC?
* Jaundice
* Pruritis
* Fatigue
* Elevated ALP
205
What is the epidemiology of PBC?
* Middle aged women
206
What diseases are associated with PBC?
1. Sjogren
2. Celiac
3. AI thyroid disease
207
How is PBC diagnosed?
1. Diagnosis requires 2/3:
1. Persistant elevation in ALP\>6 months
2. AMA Ab titers \>1:40
3. Liver Bx (if Dx unclear)
208
How is PBC managed?
1. Bone density testing, lipid profile, monitor for cirrhosis
2. URSO
3. Liver transplant for liver failure
209
Compare PBC and PSC
210
How is hepatic encephalopathy diagnosed?
1. Clinically
1. Confusion
2. asterixis
2. Look for precipitant
1. Rx
2. GI bleed
3. Lyte abnormality
4. HCC
5. SBP
211
How is hepatic encephalopathy treated
Treat precipitant
Lactulose +/- rifaximin
212
When should hepatorenal syndrome be suspected?
* Liver patients with AKI
* Oliguric
* Benign urinary sediment
213
How is hepatorenal syndrome diagnosed?
* R/O other causes of AKI
* Low urinary sodium
* Refractory to albumin 1g/kg x 2 days after stopping diuretics
214
How is hepatorenal syndrome treated?
* In this order of escalation
1. Treat underlying liver disease
2. Albumin +
1. Midodrine + octreotide
2. Terlipressin
3. Norepi (if in ICU)
3. Transplant
215
When should hepatopulmonary syndrome be suspected?
* Liver patients with dyspnea, platypnea/orthodeoxia, or hypoxemia otherwise
* PaO2\<80, A-a\>15
216
How is hepatopulmonary syndrome diagnosed?
1. TTE bubble study: showing shunt
2. R/O other causes of hypoxemia
217
How is hepatopulmonary syndrome treated
1. Supportive
2. Transplant
218
How is HCC treated?
* Curative
* Transplant
* Surgery
* Palliative
* TKI/chemo
* XRT
* TACE
219
What are the 2 types of hepatorenal syndrome
* _Type 1:_ Acute, doubling of Cr to \>221 in less than 2 weeks
* _Type 2:_ More subacute, AKI + diuretic resistant ascites
220
What can provoke a portal/mesenteric thrombus?
1. Hypercoagulable state
1. Malignancy
2. Heme disorder
1. MPN
2. PNH
3. Thrombophilias
3. Pregnancy
4. OAC use
2. Injury to portal, mesenteric vein
1. Acute intra-abdominal process
1. Pancreatitis
2. IBD flare
3. Appendicitis
4. Cholecystitis
2. Abdo surgery or trauma
3. Sluggish blood flow
1. Portal HTN
1. Cirrhosis
2. CHF
221
What workup should be sent for Portal/mesenteric VTE?
1. Thrombophila w/u + JAK2 testing IF:
1. No Hx Cirrhosis
2. Prior Hx thrombosis
3. Unusual thrombosis site
4. FHx thombosis
2. Imaging
1. 1st line US + doppler
2. Contrast CT/MR
1. Can help rule out tumor thrombus in setting of cirrhosis +/- HCC
3. Endoscopy
1. Screening OGD, R/O esophageal/gastric varices
222
How should portal and mesenteric thrombosis be managed?
1. No cirrhosis
1. Acute, symptomatic: Anticoagulate
2. Chronic: Anticoagulate if
1. Thrombophilia
2. Progression of clot into mesenteric veins
3. bowel ischemia
3. Duration: 6 months if provoked, indefinite if unprovoked/thrombophilia
4. Can use UFH/LMWH, Warfarin, DOACs off label
1. Monitor therapy
2. Cirrhosis: *Decision to treat less clear*
1. Treat: Acute complete main PVT, MVT or progression of PVT into mesenteric veins
1. At least 6 months
2. Treat chronic PVT/MVT if:
1. Inherited thrombophilia
2. Progression of thrombosis
3. bowel ischemia
4. awaiting liver transplant
3. Weight risk of clot and risk of bleeding
1. Plt count, fall risk, etc...
4. Non-selective beta blockers \> EVL if high risk varices
1. If considering EVL, hold anticoagulation periprocedurally
223
