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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)
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2
Q

What can cause ALTs and ASTs in the 100s?

A
  • Viral hepatitis (B,C) CMV, EBV
  • Alcoholic hepatitis
    *
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3
Q

What can cause ALTs ASTs <100

A
  • Autoimmune hepatitis (caeliacs)
  • NASH
  • HH
  • Wilson’s
  • A1AT
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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
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5
Q

What is the workup for cholestasis?

A
  • U/S, CT, MRCP, EUS (R/O stones)
  • ERCP not for diagnosis
  • Liver Bx
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6
Q

How is Hepatitis A transmitted?

A

Fecal-Oral

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7
Q

What is the diagnostic test for hepatitis A?

A

Anti HAV IgM

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8
Q

How is hepatitis A treated

A
  • Self-limited infection
  • Treatment is supportive
  • Transplant for fulminant hepatitis
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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
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10
Q

Who should get hep a post-exposure proophylaxis

A
  1. Household contacts of hep a infected individuals
  2. Co-workers and clients of infected food handlers
  3. Contacts in childcare or junior and senior kindergarten
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11
Q

How are hepatitis B serologies interpreted

A
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12
Q

What is the natural history of hepatitis B

A
  • <5% progress to chronic HBV
  • <1% progress to liver failure
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13
Q

How is acute hepatitis B treated

A
  • Mainly supportive
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14
Q

Which contacts of hepatitis B patients should get vaccinated and get immunoglobulins?

A
  • Household contacts
  • Sexual contacts
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15
Q

What factors increase the risk of developing cirrhosis in hepatitis B patients?

A
  1. Host factors
    1. Older age
    2. male
    3. immunocompromised
    4. Co-infection with HIV/HCV/HDV
    5. EtOH
    6. Metabolic syndrome
  2. Disease factors
    1. High DNA/ALT
    2. Prolonged time to eAg seroconversion
    3. eAg negative mutant
    4. Genotype C
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16
Q

What factors increase the risk of developing HCC in hepatitis B patients?

A
  1. Host factors
    1. Older age
    2. Male
    3. immunocompromised
    4. Family History
    5. Born in sub-saharan africa
    6. Co-infection with HIV/HCV/HDV
    7. EtOH
    8. Metabolic syndrome
    9. Aflatoxin ingestion
    10. Smoking
  2. Disease factors
    1. High DNA/ALT
    2. Prolonged time to eAg seroconversion
    3. eAg negative mutant
    4. genotype C
    5. Cirrhosis

*Not for cirrhosis

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17
Q

What workup should be sent on diagnosis of Hep C?

A
  1. CBC
  2. Cr
  3. ALT
  4. HBV DNA
  5. HBe serology
  6. Fibroscan or Biopsy
  7. In high risk groups: HIV+Hep D
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18
Q

What investigations should be done every 6 months in patients with HBV?

A
  1. ALT
  2. HBV DNA

If both persistently elevated, repeat fibroscan

  • US for HCC screening if indicated
    • NOT AFB

ALL every 6-12 months

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19
Q

Who should get US screening for HCC in the HCV population

A
  1. Asian M>40
  2. Asian F>50
  3. Africans > 20
  4. All cirrhotics
  5. Family Hx HCC (first degree relatives)
  6. All HIV coo-infected starting at age 40
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20
Q

Who should be treated for chronic HBV?

A
  1. Cirrhosis
    1. Liver transplant workup if decompensated, MELD>15
  2. Fibrosis > stage 1 with HBV DNA >2000 regardless of HBeAg status (even with normal ALT)
  3. Extrahepatic manifestations
  4. HBeAg +, elevated ALT, HBV DNA >20 000
  5. HBeAg - , elevated ALT, HBV DNA > 2000
  6. Pregnancy
    1. 3rd Trimester + high DNA levels (HBV DNA >200 000) to prevent fetal transmission
    2. Baby should also get HBIG (and vaccines) after birth

Do not treat:

  • Immune tolerant phase or inactive CHB phase (normal ALT)
  • Acute infection
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21
Q

What is the goal of chronic HBV treatment?

A
  • Suppress virus
  • eAg seroconvert
    • Only applies to eAg +
  • sAg seroconvert
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22
Q

What will the treatment of chronic HBV accomplish

A

Prevent cirrhosis and HCC

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23
Q

How is chronic HBV treated (what meds)

A
  • PEG interferon
  • Nucleotide analogues
    • tenofovir
    • entecavir
    • lamivudine
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24
Q

How should chronic HBV in the 3rd Trimester of pregnancy be treated

A

Tenofovir

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25
Q

List pros and cons of peg-interferon for the treatment of HBV

A
  • 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
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26
Q

List pros and cons of nucleotide analogues

A
  • 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
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27
Q

Who should be screened for HCV?

A
  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
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28
Q

Interpret HCV serologies

A
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29
Q

What is the natural History of HCV?

A
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30
Q

What workup should be sent on diagnosis in HCV?

A
  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
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31
Q

Which factors increase the risk of cirrhosis in chronic HCV?

A
  1. Older age
  2. Male sex
  3. HIV/HBV co-infection
  4. Obesity/DM/fatty liver
  5. EtOH
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32
Q

What factors increase the risk of HCC in patients with chronic HCV?

A

Cirrhosis or co-existing liver disease which may accelerate fibrosis

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33
Q

Who should get treatment for chronic HCV

A

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)
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34
Q

Give an approach to HCV treatment

A
  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
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35
Q

What is the typical LFT pattern in alcoholic hepatitis?

A
  • AST/ALT >2
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36
Q

If you suspect alcoholic hepatitis and the liver enzymes are over 300, what should you do?

A

Consider alternalte diagnosis Or get Bx

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37
Q

What should you do to confirm alcoholic hepatitis in a patient with underlying confounding liver disease?

A

Get a Bx

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38
Q

How should alcoholic hepatitis be treated?

A
  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

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39
Q

Name the contraindications to steroids in Alcoholic hepatitis

A
  1. Infection
    1. SBP
    2. Active HBV
    3. TB
    4. +/- HCV
  2. GI bleeding (relative)
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40
Q

Once a patient with alcoholic hepatitis is on steroids, how do you decide to continue or stop the steroids?

A
  • 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
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41
Q

When should transplant be considered in alcoholic hepatitis

A
  • If hepatic failure, refer:
    • MELD≥21
    • CP-c
  • Typically requires 6 months of abstinence but there are exceptions
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42
Q

Name 2 vital non-pharmacological strategies to prevent recurrent alcoholic hepatitis

A
  • Nutrition
  • EtOH abstinence
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43
Q

What is the difference between NAFL and NASH?

A
  • NAFL: no hepatocellular injury
  • NASH: + hepatocellular injury
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44
Q

What is NAFLD?

A

NAFL+NASH

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45
Q

What is required to diagnose NAFLD

A
  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
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46
Q

List conditions associated with NAFLD

A
  1. Obesity
  2. T2DM
  3. DLP
  4. Metabolic syndrome
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47
Q

What is the most common cause of death in NAFLD

A

Cardiovascular

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48
Q

How is NAFLD treated

A
  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
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49
Q

List the causes of cirrhosis

A
  1. Viral
  2. EtOH
  3. NASH
  4. A-I
  5. Metabolic
  6. …
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50
Q

How is the child-pugh score calculated?

A
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51
Q

What is the MELD criteria required to refer a patient for transplant

A

MELD≥15

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52
Q

What are the complications of cirrhosis?

A
  1. Varices
  2. Ascites/SBP
  3. Encephalopathy
  4. HRS, HPS, porto-pulmonary hypertension
  5. HCC
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53
Q

What councilling should be given to cirrhotic patients?

A
  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
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54
Q

What should be done in primary prophylaxis to prevent bleeding in patients with varices?

A
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55
Q

What should be done in secondary prophylaxis to prevent bleeding in patients with varices?

A

Beta blocker AND banding

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56
Q

How is the SAAG interpreted?

A
  • SAAG>11: transudate
  • SAAG<11: Exudate
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57
Q

How should ascites related to portal hypertension be managed?

A
  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
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58
Q

How can compliance to Na restricted diet be assessed?

A
  • 24hrs urine sodium collection
    • Na<78mmol: Compliant
    • Na>78mmol: non-compliant

Diuretics should be started if ongoing ascites or unable to comply

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59
Q

How can diuretic effectiveness and compliance to a low sodium diet be assessed in patient with ascites on diuretics?

A
  • 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
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60
Q

Who should get a diagnostic paracentesis to rule out SBP?

A

When suspected

All patients with new ascites

All cirrhotic patients with ascites presenting to hospital

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61
Q

List the classic symptoms of SBP

A
  • Abdominal pain
  • fever

Can also present with encephalopathy, hypotension, AKI, worstening liver function

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62
Q

How can a diagnosis of SBP be posed?

A
  • Neutrophils in ascitic fluid>250 or positive cultures
    • Culture negative still requires full treatment course
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63
Q

Name one thing that should be ruled out before diagnosing a patient with SBP

A

Secondary causes of peritonitis (i.e perf, recent surgery…)

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64
Q

How is SBP treated

A
  • 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
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65
Q

Who should get prophylaxis for SBP

A
  • 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)
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66
Q

What are the clinical manifestations of HH

A
  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
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67
Q

Give a DDx for iron overload

A
  • Frequent blood transfusions
    • SS
    • Thalassemias
  • Other chronic liver disease
    • NAFLD
    • HCV
    • EtOH misuse
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68
Q

Give an approach to the diagnosis and treatment of HH

A
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69
Q

How is HH treated. Give 1st and second line

A
  1. 1st Line: Phlebotomies, target ferritin 50-100
  2. 2nd Line: Iron chelation
    1. Desferoxamine
    2. deferiprone
    3. deferasiroox
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70
Q

What side-effects/risks are associated with iron chelation?

A
  1. Retinal/auditory toxicity (Desferroxamine)
  2. Agranulocytosis (deferiprone)
  3. Liver/renal toxicity (deferasirox)
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71
Q

What foods/supplements should be avoided in HH?

A
  1. Vitamin C supplements
  2. Uncooked seadfood

No need to limit red meat/dietary iron

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72
Q

List risk factors for caeliac disease

A
  1. Northern European descent
    • Family History
  3. T1DM
  4. AI thyroid disease
  5. Down and turner syndrome
  6. 1st degree relative
  7. IgA deficiency
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73
Q

List symptoms and signs of caeliac disease

A
  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
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74
Q

Give the workup for caeliac’s disease

A
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75
Q

When should HLA DQ2/DQ8 testing be considered?

A

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
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76
Q

How is celiac treated

A

Lifelong gluten free diet

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77
Q

What food items contain gluten?

A
  1. BROW acronym
    1. Barley
    2. Rye
    3. Oats (often contaminated)
    4. Wheat
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78
Q

What should be done on follow-up after a diagnosis of celiac’s

A
  • 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

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79
Q

What further workup should be considered after a diagnosis of Celiac’s disease?

A
  1. Micronutrient deficiencies
    1. Fe
    2. Folate
    3. Vit D
    4. B12
  2. BMD per guidelines
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80
Q

List complications of celiac’s disease

A
  1. Nutritional deficiencies and anemia
  2. Osteopenia/osteoporosis
  3. Elevated liver enzymes
  4. Dermatitis herpetiformis
  5. Enteropathy associated T cell lymphoma
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81
Q

How is dermatitis herpetiformis treated

A

Dapsone and gluten free diet

*R/O G6PD deficiency

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82
Q

Who should be screened for celiac disease?

A
  1. +FHx
  2. DM-1
  3. Autoimmune thyroid disease
  4. Down’s and turners synrdrome
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83
Q

List clinical manifestations of Chrohn’s disease

A
  1. Abdominal pain
  2. Diarrhea
  3. Weight loss
  4. fever
  5. peri-anal symptoms
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84
Q

List common lab findings in Crohn’s disease

A
  1. Increased CRP
  2. Low iron
  3. Anemia
  4. B12 deficiency
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85
Q

How is Crohn’s disease diagnosed?

A
  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
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86
Q

How is crohn’s disease treated?

A
  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

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87
Q

What are markers of crohn’s disease severity?

A
  1. High CRP
  2. symptoms affecting lifestyle
  3. low albumin
  4. deep ulcerations on endoscopy
  5. complications
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88
Q

What is the prefered agent in fistulizing crohn’s

A

Anti-TNF

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89
Q

How is perianal disease treated in crohn’s disease?

A
  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
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90
Q

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?

A
  1. Vedolizumab
  2. Ustekinumab
91
Q

Name intra-abdominal complications of crohn’s disease

A
  1. Strictures
    1. Cold stricture
    2. Hot stricture
  2. fistula
  3. abscess
92
Q

How are intra-abdominal complications of Crohn’s disease diagnosed?

A

CT/MR enterography

93
Q

How are intra-abdominal fistulas secondary to crohn’s disease treated?

A

Biologics or surgery

94
Q

How are intraabdominal abscesses secondary to crohn’s disease treated?

A
  1. Drainage (IR or surgery)
  2. Antibiotics (cipro/flagyl) Before immunosupression
95
Q

How are strictures 2/2 Crohn’s disease treated

A
  • Cold strictures
    • Conservative management
    • Endoscopic dilation
    • Surgery
  • Hot strictures
    • Steroid bridge to maintenance therapy (usually biologics)
96
Q

List perianal complications of Crohn’s

A
  • Fistula
  • Abscess
97
Q

How are perianal crohn’s disease complications diagnosed?

A
  • MR pelvis
  • EUS
  • Examination under anesthesia
98
Q

Which part of the GI tract is affected by UC?

A

Proctitis (within 18cm of anal verge)→ Left sided colitis (sigmoid to splenic flexure) → Pan-colitis (beyond splenic flexure)

99
Q

List clinical manifestations of UC

A
  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
Q

How is UC diagnosed?

A
  1. Illeocolonoscopy + Bx
    1. Continuous inflammation from rectum proximally
    2. Granular, friable mucosa
    3. Bx: Crypt abscesses, lamina propria cellularity
101
Q

List the truelove/witt criteria for severe UC

A
  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
Q

How is UC Treated?

A
  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
Q

How should a toxic megacolon 2/2 UC be managed

A

SURGICAL CONSULT!

104
Q

What should be added when starting an antti-tnf

A

Thiopurine

105
Q

What is the treatment target in IBD?

A

Mucosal healing and steroid free remission

106
Q

What should you check before starting AZA/6MP

A

TMPT

107
Q

How can fecal calprotectin be used in IBD

A

As a marker of disease severity

108
Q

What workup should be sent in patients presenting with an IBD flare requiring admission?

A
  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
Q

How should an IBD flare be managed in inpatients?

A
  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
Q

What are the indications for collectomy in fulminant UC?

A
  1. Toxic megacolon
  2. Colonic perforation
  3. Severe refractory hemorrhage
  4. Refractoriness to medical therapy after 3-5 days
111
Q

How is a toxic megacolon defined?

A
  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
Q

What workup should be done to rule out infection and when in IBD flare?

A
  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
Q

In patients with bloody diarrhea from an IBD flare, should DVT prophylaxis be withheld?

A

No

Risk of VTE > Risk of bleed

114
Q

What other causes of diarrhea can be considered in patients with IBD

A
  • CMV colitis
  • Bile-salt diarrhea
115
Q

Why should NSAIDS be avoided in active IBD

A

Can agravate diarrhea

116
Q

What is the maximal delay to perform endoscopy in UGIB patients with liver disease/without liver disease?

A
  • 12h
  • 24h
117
Q

What antibiotic regimen should be given to variceal GI bleeds?

A

Ceftriaxone 1g IV daily x 7 days

118
Q

List the forrest clasification of ulcers

A
  • 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
Q

How should high-risk ulcers be treated after endoscopy?

A
  • IV PPI x 72hrs
120
Q

What workup shuld be sent in non-variceal UGIB

A
  • CBC
  • LBC
  • Cross and type
  • PTT INR
  • Liver enzymes and function test
121
Q

What are the transfusional targets for non-variceal UGIB

A
  • Hb>70
  • Plt>50
122
Q

How should non-variceal UGIB be manages

A
  • 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
Q

If a patient has recurrent bleeding after endoscopy, what should be the next step?

A
  • Repeat EGD
  • IR embolisation
  • Surgical management
  • If tumor bleeding: consider radiation
124
Q

How should bleeding gastric ulcers be managed post-endoscopy

A
  • 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
Q

Who should be tested for H. Pilori

A
  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
Q

How is MALT lymphoma treated

A

H. Pilori eradication

127
Q

What are the diagonostic tests for H. Pilori?

A
  1. Stool antigen
  2. Histology
  3. Biopsy culture
  4. Urea breath test
  5. Serology
    1. Sensitive but not specific for active infection
        • in prior infection
128
Q

How is H. Pilori treated?

A
  • 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
Q

How should H.Pilori eradication be tested

A
  • Urea breath test
  • Bx
  • Fecal antigen test

Test everyone for eradication

130
Q

How should GERD be managed

A
  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
Q

What are the alarm symptoms in GERD?

A
  • Dysphagia
  • Weight loss
  • GI bleed
132
Q

List non-pharmacological management options in GERD

A
  • Weight loss
  • Avoid trigger foods
  • Quit smoking
  • Elevate head of bed
133
Q

What can be considered for extra-oesophageal symptoms of GERD (coughm asthma, chest pain)? What should be done before?

A
  1. Do usual workup first
  2. Then consider PPI 8-12 weeks
  3. If fail, EGD
134
Q

How is Barrett’s esophagus diagnosed?

A
  1. Salmond colored metaplastic mucosa extending ≥1cm proximal to the GE junction
  2. Biopsy confirmation of columnar interstitial metaplasia +/- goblet cells
135
Q

List risk factors for Barrett’s esophagus

A
  1. Chronic GERD (>5 years)
  2. Age>50
  3. Male gender
  4. Tobacco use
  5. Central obesity
  6. Caucasian race
  7. NOT alcohol
136
Q

Who should be screened for Barrett’s Esophagus

A
  1. Do not screen patients with chronic GERD
137
Q

How should non-nodular Barrett’s Esophagus be managed?

A
138
Q

What are the steps to investigating and managing dysphagia?

A
  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
Q

List alarm symptoms in Dysphagia

A
  • Weight loss
  • Anemia
  • Vomiting
140
Q

What are the signs and symptoms used to differentiate Oropharyngeal from esophageal dysphagia

A
  • 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
Q

What are the signs and symptoms used to differentiate structural vs motility dysphagia?

A
142
Q

List symptoms of achalasia

A
  1. Progressive solid and liquid dysphagia
  2. Regurgitation + reflux symptoms
  3. Chest pain
  4. weight loss
  5. Sx refractory to PPI Tx
143
Q

What is the typical epidemiology for achalasia

A
  • M=F
  • Age 30-60
  • all ethnicities
144
Q

What are the complications of achalasia?

A
  1. Megaesophagus >6cm
  2. Sigmoid esophagus
  3. SCC
145
Q

What are the steps to posing a diagnosis of achalasia?

A
  • 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
Q

How is achalasia managed?

A
  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
Q

What is the definition of eosinophilic esophagitis?

A
  • Esophageal disorder characterised by esophageal symptoms and esophageal eosinophilia (>15 eos/HPF) and absence of secondary causes
148
Q

What are the risk factors for Eosinophilic esophagitis?

A
  1. M>F
  2. Age 20-30
  3. Ass with atopy, allergy, asthma, eczema, chronic rhinitis
149
Q

What are the clinical manifestations of Eosinophilic esophagitis?

A
  • Solid dysphagia
  • Food bolus obstruction
150
Q

What are the endoscopic findings in eosinophilic esophagitis

A
  1. Trachealisation of the esophagus
  2. Strictures
  3. Linear furrows
  4. White papules (eos)
  5. Crate paper esophagus
151
Q

What is the treament goal in eosinophilic esophagitis

A

Complete resolution of symptoms and patholoogy

152
Q

How is eosinophilic esoophagitis treated?

A
  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
Q

List secondary causes that may mimic eosinophilic esophagitis

A
  1. GERD
  2. Achalasia
  3. CTD
  4. Hypermotility syndromes
  5. pill esophagitis
  6. pemphigus
  7. Hyper IgE syndrome
154
Q

What are the diagnostic criteria for pancreatitis?

A
  1. Abdo pain constant with the disease
  2. Lipase/Amylase ≥3x ULN
  3. Characteristic findings on imaging
155
Q

List the etiologies of pancreatitis

A
  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
Q

What are the 2 scores used to define severity in acute pancreatitis?

A

APACHE II and SIRS

157
Q

How is acute pancreatitis generally managed?

A
  • 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
Q

What should be done in a patient with pancreatitis if they deteriorate after 48-72hrs

A
159
Q

How should acute gallstone pancreatitis be managed?

A
  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
Q

How is hypertriglyceridemic pancreatitis treated

A
  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
Q

List the atlanta classification for complications of pancreatits

A
  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
Q

What are the 2 types of auto-immune pancreatitis?

A
  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
Q

What is the workup for autoimmune pancreatitis?

A
  1. CT/MRCP/EUS
    1. Sausage pancreas
    2. Biliary strictures
  2. Serum IgG4 level
    1. >2x ULN suggestive of type I AIP
164
Q

How is auto-immune pancreatitis treated?

A
  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
Q

List the etiologies of Chronic pancreatitis?

A
  1. Toxic/metabolic: chronic alcohol use, HyperTG, smoking, hyperCa, medications, toxins,CF
  2. Idiopathic
  3. Genetic – CF, others (PRSS1, CTRC…)
  4. Recurrent acute pancreatitis
  5. Obstructive: Pancreatic divisium, sticture, stone, tumor
166
Q

What are the clinical manifestations of chronic pancreatitis?

A
  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
Q

How is chronic pancreatitis diagnosed?

A
  1. 1st line: CT or MRI
    1. EUS if uncertain
  2. Role of pancreatic exocrine function testing unclearr
168
Q

What workup should be done once chronic pancreatitis is diagnosed?

A
  • 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
Q

How is chronic pancreatitis treated?

A
  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
Q

What are the risks associated with PPIs?

A
  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
Q

For which conditions is there a clear benefit to PPIs?

A
  • GERD
  • PUD
  • ZES
  • H. Pilori
172
Q

How often should PPI use be reassessed as per choosing wisely?

A

At least yearly

173
Q

List a DDx for rectal bleeding

A
  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
Q

List causes for ischemic colitis

A
  1. Cardioembolic
  2. atheroembolic
  3. Shock/low-flow
  4. segmental, think vasculitis/PAN
175
Q

How should a lower GI bleed be managed?

A
  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
Q

When should small bowel bleeding be suspected?

A

In any patient with overt GI bleeding and normal EGD and colonoscopy

177
Q

How can small bowel bleeding be diagnosed?

A
  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
Q

How can small bowel bleeding be treated?

A
  1. Double baloon enteroscopy
  2. Surgery
  3. IR embolisation
  4. Supportive management with transfusions and iron replacement
179
Q

What serology can be positive in crohn’s?

A

ASCA

180
Q

What serology can be positive in UC

A

ANCA

181
Q

List side effects of 5-ASA

A
  1. Headache
  2. Diarrhea
  3. nausea
  4. pancreatitis
  5. Interstitial nephritis
182
Q

List side effects of azathioprine

A
  1. Hepatotoxicity
  2. Leukopenia
  3. Lymphoma

*do not use in TPMT deficiency

183
Q

What are side effects of MTX

A
  1. Cytopenias
  2. hepatotoxicity
  3. ILD

*Do not use in women of childbearing age

184
Q

What are side effects of anti-TNF

A
  1. Infections
  2. Lymphoma
  3. other malignancies
  4. Tb, HBV reactivation
185
Q

What are the side effects of tofacitinib

A
  1. Infections
  2. lymphoma
  3. other malignancies
  4. leukopenia
  5. anemia
  6. HZV,Tb reactivation
  7. GI perforation
186
Q

What are the side effects of cyclosporine

A
  1. AKI
  2. HyperK
  3. hirsutism
  4. infection
187
Q

List etiologies of obstruction in cholangitis?

A
  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
Q

What is the clincal presentation of cholangitis?

A
  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
Q

What are the two types of microscopic colitis?

A
  1. Lymphocytic
  2. Collagenous
190
Q

Who gets microscopic colitis (epidemiology)

A
  1. Older women (>65)
  2. Comorbid autoimmune disease
    1. Thyroid
    2. celiac
    3. RA
191
Q

What are the symptoms of microscopic colitis?

A
  1. Relapsing/remitting watery, non-bloody diarrea. Can be severe
  2. Weight loss, abdo pain
192
Q

How is microscopic colitis diagnosed?

A
  • Normal appearing colonoscopy
  • Bx to confirm diagnosis
193
Q

How is microscopic colitis treated?

A
  • Immodium
  • Stop NSAIDS and offending meds
  • Budesonide PO
194
Q

How is acute cholangitis managed

A
  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
Q

What is the epidemiology of IgG4 related disease

A
  • Mostly older men (age>60)
    • In coontrast Type II AIP diagnosed at age >40 M=F
196
Q

What are the manifestations of IgG4 related disease

A
  1. Auto-immune pancreatitis
  2. billiary sclerosis
  3. retroperitoneal fibrosis
  4. chronic sclerosing aortitis
  5. thyroiditis
  6. interstitial pneumonitis
  7. tubulointerstitial nephritis
197
Q

How is IgG4 related disease screened for and diagnosed?

A
  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
Q

How is IgG4 related disease treated?

A
  • 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
Q

How does PSC present clinically?

A
  1. Jaundice
  2. Pruritis
  3. Fatigue
  4. Elevated ALP
200
Q

Who gets PSC

A
  • Men
  • Strongly associated with UC
201
Q

What imaging test should be ordered in suspected PSC and what will be found?

A
  1. MRCP
    1. Beading of CBD
    2. strictures

*R/O cholangiocarcinoma with ERCP and brushing of dominant stricture

202
Q

Give 2 differentials to PSC

A
  • IgG4 related disease
  • PSC-Autoimmune overlap syndrome
203
Q

How is PSC treated?

A
  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
Q

what are the manifestations of PBC?

A
  • Jaundice
  • Pruritis
  • Fatigue
  • Elevated ALP
205
Q

What is the epidemiology of PBC?

A
  • Middle aged women
206
Q

What diseases are associated with PBC?

A
  1. Sjogren
  2. Celiac
  3. AI thyroid disease
207
Q

How is PBC diagnosed?

A
  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
Q

How is PBC managed?

A
  1. Bone density testing, lipid profile, monitor for cirrhosis
  2. URSO
  3. Liver transplant for liver failure
209
Q

Compare PBC and PSC

A
210
Q

How is hepatic encephalopathy diagnosed?

A
  1. Clinically
    1. Confusion
    2. asterixis
  2. Look for precipitant
    1. Rx
    2. GI bleed
    3. Lyte abnormality
    4. HCC
    5. SBP
211
Q

How is hepatic encephalopathy treated

A

Treat precipitant

Lactulose +/- rifaximin

212
Q

When should hepatorenal syndrome be suspected?

A
  • Liver patients with AKI
    • Oliguric
  • Benign urinary sediment
213
Q

How is hepatorenal syndrome diagnosed?

A
  • R/O other causes of AKI
  • Low urinary sodium
  • Refractory to albumin 1g/kg x 2 days after stopping diuretics
214
Q

How is hepatorenal syndrome treated?

A
  • 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
Q

When should hepatopulmonary syndrome be suspected?

A
  • Liver patients with dyspnea, platypnea/orthodeoxia, or hypoxemia otherwise
    • PaO2<80, A-a>15
216
Q

How is hepatopulmonary syndrome diagnosed?

A
  1. TTE bubble study: showing shunt
  2. R/O other causes of hypoxemia
217
Q

How is hepatopulmonary syndrome treated

A
  1. Supportive
  2. Transplant
218
Q

How is HCC treated?

A
  • Curative
    • Transplant
    • Surgery
  • Palliative
    • TKI/chemo
    • XRT
    • TACE
219
Q

What are the 2 types of hepatorenal syndrome

A
  • Type 1: Acute, doubling of Cr to >221 in less than 2 weeks
  • Type 2: More subacute, AKI + diuretic resistant ascites
220
Q

What can provoke a portal/mesenteric thrombus?

A
  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
Q

What workup should be sent for Portal/mesenteric VTE?

A
  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
Q

How should portal and mesenteric thrombosis be managed?

A
  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
Q
A

rcpsc (14 decks)

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