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Transplant Hep Boards > Session II- Cholangio > Flashcards

Session II- Cholangio Flashcards

1
Q

what are risk factors for CCA?

A

In the east- parasitic infection - opisthorchis viverini and Clonorchis

In the west- PSC

intrahepatic and extra hepatic risk factors:
- cholerdocal cysts, choledocholithiasis, cirrhosis, HBV

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2
Q

What is the cause of death of most patients with CCA post resection?

A

local tumor recurrence within 2 years post resection

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3
Q

What is the most common subtype of CCA

A

perihilar –> extrahepatic (below cystic duct) –> intrahepatic

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4
Q

What is the standard of care for treatment of perihilar CCA in PSC and non PSC

A

in PSC- peri-hilar CCA should be transplant due to high risk of multifocal CCA

otherwise, perihilar CCA in non PSC should be resected. Ro or negative margin is 70-80%, 5 year OS depends on if negative margins and if negative LN

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5
Q

What are anatomical contraindications to resection for a perihilar non PSC CCA?

A
  1. Encaseement of PV- relative, as surgeons can now reconstruct PV
  2. Unilateral ductal dilation with contralateral vascular encasement
  3. unilateral atrophy with either contralateral ductal or vessel involvement
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6
Q

Can perihilar CCA be transplantable?

A

yes, per Mayo protocol (combines neoadjuvant chemo with LT), only for unresctable pCCA or all cases of pCCA in PSC

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7
Q

What is the eligibility criteria for transplant in unresectable pCCA?

A

Mayo protocol inclusino:
1. Diagnosis of pCCA (see other life)
2. unresectable tumor above cystic duct OR resectable pCCA in PSC
3. RADIAL (not longitudinal) diameter of 3 cm or less
4, no inta or extra hepatic mets
5. otherwise a LT candidate

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8
Q

What is exclusion criteria for neoadjuvant OLT in pCCA?

A

cannot be intrahepatic cya
no prior radiation or chemo
no prior biliary resection
no intrahepatic mets
no evidence of extra hepatic disease
CANNOT HAVE TRANSPERITONEAL BIOPSY (INCLUDING PERCUTANEOUS AND EUS GUIDED FNA). intraluminal via ecrp or transhepatic is ok, just not transperitoneal

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9
Q

Who does better after LT for pCCA?

A

PSC patients tend to do better compared to de novo (tend to be younger, dx at earlier stage, and less likely to have pathologic confirmation of CCA)

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10
Q

How to get MELD exception points for pCCA?

A

malignant stricture with one of the following:
1. aneuploidy
2. biopsy or cytology
3. evidence of mass that is <3cm Radial (extension of stricture does not count)
4. CA 19-9 >100 without evidence of cholangitis

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11
Q

Once transplanted for pCCA, what predicts disease free survival? What predicts recurrence

A

residual tumor. those with no residual tumor have the highest 5 year survival.

invovlement of LN predicts recurrence (which is why surgery is contraindicated and upfront chemo is prefered if LN involved)

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12
Q

you are transplanted for pCCA according to mayo protocol. but explant with high risk features. what next?

A

patients with high risk features on explant are often enrolled in adjuvant therapy protocol
- convert FK to mtor inhibitor after 4 weeks
- GEM/CIS month 4-10 post LT
-imaging month 4 and 12 post LT and then annual –> helps detect early disease to try and do resection and/or LRT since most will recur in the liver

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13
Q

What are post LT complications in pCCA?

A

PV stenosis (due to Radiation injury) - same rate in LDLT and DDT

HAT and stenosis
- Thrombosis is higher in DDLT than LDLT
- Stenosis is higher in DDLT than LDLT
This is because the time from radiation to transplant is shorter in LDLT, so can use the recipients native HA. In DDLT, the time is longer, so a jump graft is often needed

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14
Q

What is lifetime risk of CCA in PSC

A

6-13%
26% in those with dominant stricture

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15
Q

When are most patients with PSC diagnosed with CCA?

A

usually within 1-2 years of diagnosis of PSC (so early in disease)

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16
Q

How does CCA present in those with PSC?

A

-usually is multifocal
- do not need to have advanced fibrosis to develop CCA in PSC

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17
Q

When should you start to suspect CCA in those with PSC?

A

-worsening LFTs
- new dominant stricture, bile duct focal thickening/enhancement on MRCP
- CA 19-9 >100 (without cholangitis)
- bile duct obstruction

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18
Q

What is treatment for intrahepatic CCA?

A

resection with LAD
Ablation
TARE

transplant is contraindicated because survival is poor

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19
Q

What are the differences between intrahepatic CCA and HCC?

A
  • no meld exception for iCAA
  • poor prognosis with iCCA with high recurrence rate
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20
Q

How can you diagnose iCAA?

A

only be diagnosed via biopsy, not worried like you are with perihilar because everything is intrahepatic

radiologically, will see involution, bile duct dilation. If <2cm, will see early enhancement that persists. If >2cm, will see early peripheral enhancement followed by progressive enhancement of rest of lesion. LACK OF WASHOUT

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21
Q

What is considered early for iCCA?

A

single lesion <2 cm

if >2cm or more than 1 lesion –> advanced

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22
Q

How to use CA 19-9 in CCA?

A

good for prognosis, not so much for diagnosis

Can be elevated in benign biliary disease of cholangitis

Level is significantly associated with cirrhosis and LN mets

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23
Q

What are the Milan criteria for neuroendocrine tumors?

A
  1. Confirmed histology of G1 or G2 tumor
  2. Primary tumor drained by portal system (some rectal and bronchiole tumors are not drained by portal system(
  3. hepatic involvement of <50%
  4. Complete resection of primary tumor and all extra hepatic disease with stable disease od good response to therapies for at least 6 months
  5. age <60, relative contraindication
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24
Q

Where do NET metastasize to?

A

1/2 of NET patients develop liver mets and is OFTEN the only site of metastatic disease

majority fo time, these are unresectable

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25
Q

What is a hepatic angiosarcoma?
what are risk factors

A

3rd most common liver tumor

Risk factors: vinyl chloride, arsenic, cyclophosphamide, anabolic steroids, OCP

high mortality due to rupture and/or liver failure

Tx: resection + chemotherapy, OLT contraindicated due to poor outcomes

Can be mistaken for hemangioma, so if calling it hemangioma and esp if on periphery, think HEHE

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26
Q

Who does hepatic epithelial hemangioendothelioma affect?

A

women, middle aged

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27
Q

What stains should be used for hepatic epithelial hemangioendothelioma and which should be negative?

A

Factor VIII-related Ag, CD34, CD31

Negative for epithelial markers like cytokeratin and CEA

Must distinguish from adenocarcinoma or sarcoma

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28
Q

What is treatment for hepatic epitheliod hemangioendotheliuma?

A

resction

if >10 nodules or >4 involved hepatic segments –> LT, having mets is NOT a contraindication

anti-VEGF

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29
Q

What imaging is seen in hepatic epithelial hemangioendothelioma?

A

confluent mass with capsular retraction

looks a lot like hepatic hemangioma, so need to be sure

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30
Q

what does hep c cause? macro or micro steatosis?

A

macro

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31
Q

what does Wilson cause? macro or micro steatosis?

A

macro

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32
Q

what does parenteral nutrition or starvation cause? macro or micro steatosis?

A

macro

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33
Q

what does abetalipoproteinemia cause? macro or micro steatosis?

A

macro

unable to absorb fats, very low cholesterol, hepatomegaly, prob skinny, look for fat soluble vitamins deficiencies

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34
Q

what does amiodarone cause? macro or micro steatosis?

A

steatohepatiits

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35
Q

what does methotrexate cause? macro or micro steatosis?

A

macro

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36
Q

what does tamoxifen cause? macro or micro steatosis?

A

macro

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37
Q

what does steroids cause? macro or micro steatosis?

A

macro

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38
Q

what does valproate cause? macro or micro steatosis?

A

micro

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39
Q

what does antiretroviral meds cause? macro or micro steatosis?

A

micro

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40
Q

what does acute fatty liver of pregnancy? macro or micro steatosis?

A

micro

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41
Q

what does HELLP cause? macro or micro steatosis?

A

micro

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42
Q

what does inborn error of metabolism cause? macro or micro steatosis?

A

micro

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43
Q

What are the alcohol cut offs when evaluating patients with suspected NAFLD?

A

> 21 standard drinks on average per week in men

> 14 standard drinks on average per week in women

this is considered significant when evaluating patients with suspected NAFLD

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44
Q

Do you screen family members for nafld?

A

not currently

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45
Q

What helps to predict steatohepatitis in patients with NAFLD?

A

metabolic syndrome. this helps identify patients who may benefit from liver biopsy

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46
Q

What scores can help predict fibrosis in NAFLD?

A

NAFLD fibrosis score
and FIB 4 index (plt count, age, AST, ALT)

VCTE or MRE helpful in identifying advanced fibrosis in patients with NAFLD

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47
Q

Who should get a biopsy in NAFLD

A

presence of metabolic syndrome
NFS
FIB4
VCTE
MRE

if there are competing etiologies for HS

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48
Q

What should histology for NAFLD differentiate?

A

NAFL (steatosis)
NAFLD with inflammation
NASH with steatosis with lobular and portal inflammation and hepatocellular ballooning

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49
Q

When can pharmacologic treatments be used in NASH

A

in those with biopsy proven NASH and fibrosis

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50
Q

What kind of lifestyle intervention helps with NASH

A

hypo caloric diet (daily reduction by 500-1000 kcal) and moderate intensity exercise

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51
Q

what percentage of weight loss is needed to improve nash

A

3-5% of body weight to improve steatosis

7-10% to improve majority of histopathological features of NASH including fibrosis

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52
Q

Can you use metformin in NASH

A

no, does not improve histology

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53
Q

Who can pioglitazone be used in?

A

those with and without diabetes with BIOPSY PROVEN NASH. If not biopsy proven, should not be used

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54
Q

Who can vit E be given to with NASH?

A

daily dose of 800 IU/day
improves histology in nondiabetic adults with biopsy proven NASH

should not be used in diabetic patients or those with cirrhosis or those without biopsy

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55
Q

How to use omega 3 fatty acids in NASH?

A

should not be used as a specific treatment of NAFLD or NASH, but may be considered to treat hypertriglyceridemia in patients with NAFLD

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56
Q

Can statins be used in cirrhosis?

A

yes, esp NASH cirrhosis since there is high risk of CVD. But should be avoided in decompensated cirrhosis

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57
Q

Which IS drug increases risk of obesity? Which decreases risk of obesity?

A

Steroids increase risk of obesity
mTOR decreases risk of obesity

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58
Q

Which IS drug increases risk of DM

A

steroids> tac, cyclo> mTOR

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59
Q

Which IS drugs cause dyslipidemia

A

mTOR>cyclo>tac, steroids

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60
Q

which drug causes HTN

A

tac,cyclo>steroids>mTOR

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61
Q

What is the most important risk factor for NAFLD recurrence after LT

A

post LT BMI

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62
Q

What IS is absorbed in the duodenum?

A

tac and mTOR

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63
Q

where is mmm absorbed?

A

in stomach, so can be affected by sleeve gastrectomy. also lose stomach in RGY so also affected in Roux

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64
Q

what does cyclo need for absorption

A

bile salt

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65
Q

What is needed for diagnosis of iCCA?

A

biopsy/histopathological confirmation

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66
Q

How do you treat iCCA?

A

surgical resection for those with a single nodule in a resectable location without evidence of metastatic disease and who have adequate functional liver volume

transplant is not an option

no data on LR

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67
Q

What is workup for pCCA or dCCA?

A

cross sectional imaging for assessment of tumor extent

ERCP with biliary brushings for cytology and FISH anaylaisis

if tx is an option, avoid EUS FNA and percutaneous biopsy due to risk of tumor dissemination. If LT is not an option, then EUS FNA can be diagnostic

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68
Q

When should MAYO protocol be used?

A

if pCCA + PSC
or
pCCA in de novo (non PSC) but unresectable

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69
Q

What chemo is recommended in advanced CCA

A

gemcitabine plus cisplatin for newly diagnosed patients

if progression on gemcitabine and platinum, then FOLFOX for second line

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70
Q

What should you do is a lesion with arterial enhancement and portal phase washout is seen in someone without cirrhosis?

A

Diagnosis of HCC cannot be made by imaging in patients without cirrhosis, even if enhancement and washout are present.

So biopsy is required in these cases.

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71
Q

What are high risk features of HCC

A

size >/= 1 cm
arterial enhancement
washout

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72
Q

What is stage 0 BCLC

A

child Pugh A
single lesion <2 cm
ecog PS 0-1

Treatment:
resection
MWA or RFA

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73
Q

What is stage A BCLC

A

single or 2-3 nodules <3 cm
ECOG PS 0-1

Treatment:
Resection
OLT
RFA
MWA
TARE/TACE
SBRT

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74
Q

What is stage B BCLC

A

multinodular
ECOG PS 0-1
Child Pugh A-B

Treatment: TARE
Downsize –> OLT

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75
Q

What is stage c BCLC

A

portal vein invasion
ECOG PS 0-2

Treatment:
Sorafenib
Levatinib

Second line: nivolumab
cabozantinib
regorafenib

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76
Q

What is Stage D BCLC

A

child Pugh C
Any T, N, or M
ECOG PS >2

Treatment:
OLT
supportive care

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77
Q

How do you manage LR1 and LR2 lesions?

A

observation with imaging according to standard HCC screening

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78
Q

How do you manage LR3?

A

intermediate probability

repeat or alternative diagnostic imaging in 3-6 months

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79
Q

How do you manage LR4

A

multidisciplinary discussion for tailored workup that may include biopsy or repeat or alternative diagnostic imaging in

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80
Q

How do you manage LR M

A

malignancy but not definitive HCC

multidisciplinary discussion, but most cases will need biopsy and/or repeat/alternative diagnostic imaging in

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81
Q

What is eligibility for down staging to get MELD exception points?

A

a. one lesion >5 cm and <8 cm
b. 2-3 lesions; at least one >3, all <5, total diameter less than 8 cm
c. 4-5 lesions <3 cm, total diameter less than 8 cm

Have to be downstaged into MILAN in order to be eligible for meld exception points

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82
Q

What is requirement for atezo/bev

A

required to have EGD within 6 months and adequate control of varices

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83
Q

when is post transplant malignancy more common?

A

can occur early or late into transplant. Probability of death from malignancy increases over time

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84
Q

What is the most likely cancer de novo after transplant

A

non melanoma skin cancer

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85
Q

What are risk factors for solid malignancies post transplant?

A

age
male sex
smoking
LT for alcohol related cirrhosis or PSC
excess IS
sun exposure
Infections:
- HHV8 for kaposi sarcoma
- ebv for nasopharyngeal carcinoma
- hpv for cervical, vulvar, andal, and oropharyngeal
- hbv for hcc

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86
Q

Who has highest risk of CRC post transplant?

A

those transplanted for PSC. but also found that any one transplanted, had higher rate- but unclear if this should change surveillance guidelines

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87
Q

When is risk of PTLD highest?

A

in the first 12-18 months (prob because this is time when IS is highest)

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88
Q

How often should patients with PSC and IBD get colonoscopy?

A

annual, even post transplant

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89
Q

Can checkpoint inhibitor be used post transplant

A

with caution, graft loss seen in 1/3 of patients

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90
Q

What are curative therapies for HCC

A

resection
LT
ablative techniques

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91
Q

What are non curative therapies for HCC

A

TACE
TARE
SBRT
chemo

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92
Q

What is T1 lesion

A

one nodule < 2 cm

(remember T2= milan= 1 lesion that is 2-5 cm OR 2-3 lesions =3 cm)

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93
Q

What is T2 lesion

A

one nodule 2-5 cm
or
2-3 nodules all <3, but each has to be greater than or =1

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94
Q

How should patients with child Pugh A cirrhosis and early stage (T1 or T2) HCC be treated?

A

AASD recommends resection over RFA

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95
Q

What are AFP cutoffs for MELD exception points

A

AFP>1000 regardless of tumor size cannot get MELD exception

must be <500 after LRT to be eligible

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96
Q

How do you survey for HCC recurrence in post transplant patients

A

abdominal and chest CT scan, but timing and duration is not certain

Retreat score ** not in guideline

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97
Q

When is thermal ablative technique most efficacious?

A

when tumor is <3 cm

98
Q

What is needed post ablation?

A

patients postulation are at high risk for recurrence and surveillance should be performed with contrast enhanced CT or MRI every 3-6 months

99
Q

Should adults with cirrhosis awaiting LT and T1 HCC be treated or undergo observation?

A

observation with follow up imaging over treatment. Wait until they become T2 lesion so that they can get MELD exception points

100
Q

Should adults with cirrhosis and T2 HCC awaiting liver transplant undergo transplant alone or transplant with bridging while waiting?

A

bridge to therapy (use of LRT to induce tumor death and deter tumor progression beyond Milan criteria

101
Q

Should adults with advanced HCC with microvascular invasion and/or metastatic disease be treated with systemic therapy or LRT or no therapy?

A

systemic therapy in patients with CP A/B plus advanced bcc with microvascular invasion and/or metastatic disease

102
Q

What is the MOA of CyA

A

forms complex with cylcophilin and this binds to calcineurin. So now after blocking calcineurin, there is inhibition of dephospho rylation of NFAT

Excreted in bile

half life of 8 hours

p450 metabolism

103
Q

What is MOA of tacro?

A

binds to immunophilin and forms a complex and inhibits calcineurin.

25x more potent than CyA

excreted in bile

half life of 11 hours

p450 metabolisms

104
Q

What are CNI side effects? (6)

A

nephrotoxicity (early reversible, later irreversible)

neurotoxicity (tac >cyA) ranges from seizures, Pres, HA, tremors

Diabetes (TAC.CyA)

HLD, HTN

Hair loss (TAC), gain (CyA)

HUS (Tac>cyA): low plts, hemolytic anemia, AKI

105
Q

What are renal sparing protocols?

A

reduction of CNI exposure, but typically requires antibody induction

106
Q

What is MOA of MMF

A

inhibits purine synthesis

potent inhibitor of B and T cells

Made SE: GI, marrow suppression, GVH like gut lesion

Stop if considering pregnancy

107
Q

What is MOA of sirolimus/everolimus?

A

form complex with FKBP that binds to mTOR and halts cell cycle progression

blocking mTOR inhibits vascular endothelial growth factor and angiogenesis that is needed for wound healing

108
Q

What black box warning for sirolimus

A

increased risk of HAT and death in LT recipients

109
Q

What are SE of mTOR

A

pancytopenia
HAT
Hypertriglyceridemia
oral and GI ulcer
proteinuria (usually in those with underlying CKD)
pneumonitis

side effects are usually trough dependent so sometimes can try lowering trough

sirolumus half life is 63 hours

EVL is 30 hours half life, but usually BID dosing

excreted in bile

110
Q

How are CNI, mTOR, steroids metabolized?

A

metabolized thought the cytochrome P450 3A4, 3a5.

So if a drug blocks the Cyp450, it will increase concentration

Substrates for the efflux transporter P-GP

111
Q

What drugs increase concentration of CNI and mTOR

A

any drug that blocks CYp3A4/5

macrolide: clarithromycin, azithromycin
antifungals: fluconazole, verapamil
CCB: diltiazem, nifedipine,

others: reglan, protease inhibits, grapefruit juice

112
Q

what drugs decrease CNI and mTOR?g

A

drugs that induce CYP3A4/5

antibiotics: rifampin, rifabutin
Anticonvulsants: phenytoin, carbamazepine, phenobarbital

Others: St johns wort

113
Q

When does acute TCMR occur? helpful labs?

A

generally 5-30 days post transplant

more common in those with autoimmune, young, females, retransplant

if GGT is normal, acute rejection is unlikely. but GGT is not specific for AMR

114
Q

How to differentiate between mild, moderate, and severe ACMR?

A

mild <50% portal tract involvement
moderate >50% portal tract involvement
severe: obliteration of central vein in addition to portal vein

115
Q

How do you treat mild TCMR vs moderate to severe TCMR?

A

mild- increased maintenance IS without steroids

moderate/severe: steroids. If severe histopath, consider initial ATG

116
Q

What is chronic rejection

A

progressive, obliteraly arteriopathy and intrahepatic cholangiopathy/loss

117
Q

who does chronic rejection usually involve?

A

multiple TCMR bouts

severe TCMR with centriblobular necrosis

noncompliance

under IS

118
Q

What are histologic criteria for chronic rejection

A
  • need 8-10 portal tracts (so need at least a 2 cm biopsy piece)

Minimal criteria for CR are any of the following:
- bile duct loss affecting greater than 50% of the portal tracts
- presence of bile duct atrophy/pyknosis affecting a majority of the bile ducts with or without bile duct loss
- foam cell obliterative ateriopathy

119
Q

What stain can be used for chronic rejection

A

CK-19- stains for bile duct. So if use stain and don’t see bile ducts, may be sign of cr

120
Q

What is management of chronic rejection?

A

-switch cyclo to tac in early CR
- add n mTOR or MMF but little data
- consider infection prophylactic
- avoid over IS with later cases of liver synthetic dysfunction

121
Q

What is associated with graft failure in chronic rejection

A
  • bile duct loss >50%
  • severe perivenular fibrosis
  • foam cell clusters within sinusoids
  • severe hyperbole
122
Q

When to consider AMR?

A

-refractory rejection/steroid resistant
- restransplatn (sensitized)
- SLK
- unexplained chronic fibrosis or inflammation

123
Q

How to make diagnosis of AMR

A

histologic findings: portal edema, ductular reaction, neutrophilia, sinusoidal inflammatory infiltration

C4d staining (lining portal vasculature and in the SINUSOIDS)

presence of DSA

124
Q

What is management of AMR

A

antibody binding agent: IVIG

antibody removing therapy: plasmapharesis

Antibody production inhibitor: rituximab (anti CD 20)

bortezomib (proteasome inhibits - inhibits plasma cells)

eculizumab: complement inhibition (blocks injury from DSA)

125
Q

What is first line therapy for aspergillous

A

voriconazole

amp causes renal toxicity and shake and bake

itraconazole is used for dimorphic fungi like histoplasmosis but not first line for asperfillus (for the fungi that are geographic)

126
Q

How can asperillus present?

A
  1. colonization - no symptoms
  2. allergic bronchopulmonary aspergillosis (wheezing, IgE, treatment is inhaled steroids)
  3. aspergilloma, fungas ball
  4. invasive pulmonary aspergillosis
    – in sinus
    – lungs (nodules)
127
Q

What is treatment of aspergillous

A

voriconzaole. can’t use long term because of risk of skin cancer. Can use posa for prophylactic

128
Q

What is seen on biopsy for aspergillous

A

acute septae, think of two fingers

129
Q

what causes non septet hyper at 90 degree

A

mucor

130
Q

what is treatment of mucor

A

surgery (antifungals aren’t as helpful because don’t have good blood supply) + ampho

so source control + anti fungal

131
Q

what is treatment for cmv pneumonitis

A

ganciclovir
get CMV PCR- culture results are too slow

In general: start with PO valganciclovir 900 BID for induction

can use IV ganciclovir if severe disease absorptionor if bad GI disease and concerned about
Minimum 2 weeks (3 weeks for GI) if PCR is undetectable
- cidovovir or foscarnet if resistant CMV

132
Q

How can CMV present

A
  1. asymptomatic viremia
  2. CMV syndrome - mono like, fever, malaise, myelosuppresion
  3. end organ disease
    - pneumonia, hepatitis, colitis, retinitis, CNS
  4. Compartmentalized CMV- pathologic evidence of end organ disease, where serum PCR is negative, but biopsy is positive (think CMV colitis)
133
Q

Who does HEV affect and what is treatment? What do you see on biopsy

A

affects immunocompromised

can see portal inflammation with mixed lymphoplasmacytic infiltrate

Treatment is ribavirin and to decrease IS

134
Q

What is the cutoff for treating assymptomatic CMV viremia”

A

1500 IU/mL

135
Q

What are risk factors for death >1 year post LT

A

male
older age
HTN
DM
pre-transplant malignancy
renal failure = strongest predictor

136
Q

What is the most common metabolic complication post LT

A

HTN-60%
HLD and metabolic syndrome 50%
DM 30%

usually occurs 1-3 years post transplant

137
Q

Which is worse for HTN, cya or tac?

A

CYA - slight predisposition when compared to tac

138
Q

How do you treat HTN post LT

A

first line: calcium channel blocker: amlodipin
but if proteinuria is present–> start with ACE or ARB

second line: acei/arb

third line: beta blockers

first line combination: calcium channel blocker +ACEI/ARB

139
Q

What is goal BP post LT

A

BP<140/90
if proteinuria present, goal <130/80

140
Q

How to diagnose post LT HLD?

A

Fasting LDL >100
Fasting Triglycerides >200

141
Q

What drugs do you need to watch in HLD post LT

A

statins ok
do not use sirolimus as it worries HLD
prefer tac over CSA, minimize CNI (add MMF to do so)

142
Q

How do you treat hypertriglyceridemia post LT

A

Fasting TG>200
omega 3 fatty acids
gemfibrozil or fenofibrate

143
Q

When to chose tac over CyA? when to choose Cya over tac

A

Cya worsens HTN and HLD
Tac worsens DM

144
Q

What are meds to avoid in DM and renal dysfunction

A

avoid metformin
If GFR<30 –> avoid acarbose, exenatide, pramlintide, gliptins

145
Q

What are the CVD risk factors?

A

-older age at transplant
- male
history of CAD
transplanted for NASH
post LT DM
post LT HTN
obesity

146
Q

What drug should be avoided in CVD?

A

sirolimus

147
Q

What are risk factors for chronic renal failure post LT

A

-peri-transplant renal failure
pre-existing CKD
- CNI
-DM
-HTN

148
Q

How does CNI causes renal injury

A

renal vasoconstriction

149
Q

What to do if on CNI and renal injury

A

dose reduction may prevent progression of renal injury
no clear difference between tac and CSA

150
Q

What is the best strategy for renal preserving IS?

A

early adoption of low dose CNI + mmf

151
Q

Why is it hard to use mtor + mmf

A

acceptable rejection but increase side effects like leukopenia and mouth ulcers

152
Q

When does bone density worsen and improve?

A

bone density significantly declines in the 3-6 months post LT but returns to pre transplant levels by one year

153
Q

When do you treat for osteoporosis post LT

A

T score <-2.5 or if fractures occur
T score <-2.0 and other risk factors

154
Q

How do you treat osteoporosis

A

First line: bisphosphonates
- can cause harm to fetus, careful in pre-menopausal women
- increased osteonecrosis of jaw in patient with renal impairment
-aledronate good oral option
- zoldrndroic acid good infusion option

155
Q

What are the cancers in post LT for which risk is significantly increased

A

non melanoma skin cancer : sun explorer, smoking, ETOH
PTLD: >50 years old, EBV negative recipient
vulvar carcinoma:
lung/head & neck cancers: tobacco and alcohol use
colorectal cancer: IBD

156
Q

What is first line tx for PTLD

A

reduce IS

157
Q

What happens to pediatric growth post LT

A

linear growth failure is common pre tx, but may return to normal after successful LT

Catch up growth plateaus 2-3 years post LT (steroids may delay or attenuate catch up growth)

50% pediatric recipients will ultimately have lower heights than their genetic potentials

lower psychosocial function

increase in cognitive deficits

158
Q

How do you manage late HAT

A

41% require re-transplant (vs 71% for earlier HAT)
30% AC only
50% develop ischemic cholangitopathy

159
Q

In those who are retransplanted, what are outcomes compared to initial LT

A

outcomes significantly worse than for initial LT

160
Q

How do you make diagnosis of fibrosis cholestatic HCV

A

usually month 1-3
bili >6
Alk phos >5 x ULN
very high HCV RNA
absence of biliary complications

161
Q

What is seen on biopsy for fibrosis cholestatic HCV

A

ballooning of hepatocytes in perivenular zone
little inflammation
variable bile ductular proliferation without duct loss

162
Q

What are predictors of alcohol relapse post LT?

A

higher number of drinks per day (>10)
prior relapse despite treatment for AUD
drinking despite legal or medical consequences
poor social support
significant psychiatric co-morbidity
co-morbidt illicit drug use (does not include THC)
***not clear that any specific length of pre- LT abstinence predicts post LT abstinence

163
Q

Which meds contribute to steatosis post LT

A

steroids
mtor>CNI

164
Q

What is incidence of post LT steatosis at 1 and 5 years

A

1 year: 60%
5 year: 80%

165
Q

What is incidence of post LT NASH

A

1 year 50%
5 year is 40%

166
Q

What is the most important things we can do to prevent post LT death in NASH pt

A

manager CV risk factors

167
Q

How often does AIH recur post transplant

A

35%

168
Q

What are risk factors for recurrent AIH>?

A

no consistent risk factor!!!

ACR, steroid withdrawal are NOT associated with increased AIH

But acute and chronic rejection are more commonly seen in patients transplanted for AIH

those who get recurrent AIH, recurrence is even higher if re-transplanted

169
Q

What percentage and when do patients with PBC recur?

A

20-30%
at 5 years

170
Q

When does recurrent AIH usually occur

A

8-12% at 1 year post LT

36-68% at 5 years

171
Q

Which drug has been slightly associated with recurrent PBC

A

Tac in small studies has been associated with recurrence of PBC

172
Q

How often does PSC recur

A

20% at 5 years

173
Q

What do you have to be mindful of when diagnosisg recurrent PSC

A

think about ischemic cholangiopathy
so do not diagnose <90 post LT for PSC
IC occurs relatively early post transplant and then plateaus meaning they don’t develop allograft dysfunction whereas PSC typically progresses

IC doesn’t start at year 2, but PSC can

174
Q

What are risk factors for recurrent PSC

A

active IBD
ACR, especially repeated episodes
Cholagniocarcinoma before LT
younger recipient, older donor
Living donor LT increases risk of recurrent PSC

175
Q

What is protective against recurrent PSC

A

pre LT colectomy

176
Q

What are outcomes of re-transplant for recurrent PSC

A

outcomes are better than when retransplanted for other outcomes

177
Q

What are recurrent rates for HCC for those transplanted WITHIN Milan criteria

A

10-15% HCC recurrence rate after transplant
Median time to recurrence =20 months

178
Q

What are major sites of recurrence for HCC

A

lungs and liver

179
Q

What are pre LT risk factors for rHCC

A

AFP: higher AFP means higher risk of rHCC
- AFP trend upward= higher risk of rHCC

If out of Milan at time of transplant, higher risk of rHCC

180
Q

What are post LT risk factors for rHCC

A

AFP at transplant
Microvascular invasion
Largest size (cm)+ number of viable HCC nodules on explant

181
Q

What is treatment of recurrent HCC

A
  1. reduce IS in general. Sirolimus/mTOR does not improve recurrence free survival
  2. resection or LRT is treatment of choice if singe rhCC
  3. when disease is more widespread, then systemic therapy is appropriate
    — but avoid immune checkpoint inhibits due to risk of graft loss
182
Q

Which group has higher risk for recurrence post transplant for cholangiocarcinoma

A

de novo cholangio has higher risk of recurrence when compared to cholangio in those with PSC

LT for PSC associated perihilar CCA has significantly increased survival compared to de novo PSC

183
Q

What is post LT surveillance for HCC

A

in general it is CT Abdomen/Pelvis and chest every 6 months for three years post LT

based on RETREAT score and risk factors

184
Q

What are risk factors for recurrent pCCA?

A

peri-neural or lymphovascular invasion in explant
presence of viable tumor in explant
elevated CA 19-9 at time of transplant
encasement of portal vein

185
Q

What is cholestatic Hep A

A

protracted jaundice >3 months
T bili >10, peak levels around week 8

186
Q

What is relapsing Hep A

A

symptoms for 3 weeks
elevated LFTs up to 12 months
of those who relapse –> 20% have more than 1 relapse

187
Q

What are extra hepatic manifestations of Hep A

A

vasculitis, cryoglobulinemia, aplastic anemia

188
Q

What can you use for cholestatic liver tests in acute viral hep

A

urso 300 mg BID x 3 weeks

189
Q

What are the Hep A vaccines

A

Havrix 2 doses, 0 and 6-12 monts
VAQTA 2 doses, 0, 6-18 months
TwinRx- combined Hep A and Hep B, 0, 1, 6 months (3 doses)
or accelerated is 0,7,21,30 days + booster at 12 months (4 doses + booster)

190
Q

Can patients have anti HEV without having HEV

A

yes, prevalence of anti HEV is 6-21% in US

191
Q

How do you get HEV

A

swine, shellfish, deer board, blood transfusion

191
Q

How do you get HEV

A

swine, shellfish, deer board, blood transfusion

192
Q

How do you treat Hep E in immunocompromised patients

A
  1. Reduce immunosuppresion
  2. if HEV + after 12 weeks of reducing IS, then given ribavirin 600-1000 mg/d for for 12 weeks
  3. if still positive, then extend for 12 more weeks
  • can check HEV in serum and stool
193
Q

What mutation is most common in patients with Budd Chiari

A

JAK 2 *** normal blood counts do not rule out myeloproliferative disorder

194
Q

What must be excluded in BCS

A

a space occupying lesion - can lead to compression of the vasculature (i.e.Hepatic cysts, adenomas, cystadenomas, invasive aspergillosis)

195
Q

What malignancy can be seen with BCS

A

HCC

196
Q

What are risk factors for HCC in BCS

A

long segment IVC thrombus
combined IVC and HV thrombus
cirrhosis
older age
*** beware- large nodules (regenerative, dysplastic) may be misinterpreted as HCC

197
Q

What is SOS

A

circulatory dysfunction at the level of sinusoid, so occlusion of central venue but hepatic vein are patent

198
Q

what is criteria for SOS, early?

A

After stem cell transplant 1-21 days
2 of the following three thing:
- total bili >2
-hepatomegaly or RUQ pain
- >5% weight gain from fluid

199
Q

What is diagnostic criteria for SOS, late

A

after stem cell transplant >21 days
- Histologically proven OR
-total bili >2
- painful hepatomegaly
>5% weight gain from fluid, ascites and US evidence of SOS

200
Q

What is used for prevention and treatment of SOS

A

Urso for prevention
Defibrotide(antithrombitic, fibrinolytic) for treatment

201
Q

What chemo is associated with SOS

A

myeloablative
AZA
oxaliplatin
cyclophosphamide
Mephalan

***cirrhosis is a contraindication for myeloablative therapy

202
Q

What are the components of MELD used for Heart Transplant candidates

A

only includes cr and bili
INR is not part of it because patients undergoing heart transplant are usually on warfarin

203
Q

What is graft vs host disease and when does it occur

A

donor cytotoxic T cells against recipient tissue
occurs >1 month post OLT

204
Q

What is diagnosis of GVHD

A

liver tests are normal
look for chimerism (person’s body contains two different sets of DNA)

205
Q

What is treatment of GVHD

A

steroids/ decrease or stop IS
can do ruxolitinib or infliximab if steroid refractory

206
Q

what are symptoms of GVHD

A

fever, diarrhea, rash (that is trunk and arms compared to palms and soles in post HSCT)

207
Q

which vaccines are contraindicated post transplant

A

live
varicella (Zostavax), small pox, BCG, MMR, yellow fever, influence flu mis

208
Q

How to given pneumonia vaccine post transplant

A
  1. 15 or 20 (both of these are conjugate)
  2. If you got 15, then give 23 (poysaccradice 1 year later).
  3. IF got 20, nothing is needed
209
Q

What travel vaccines are contradicted in post

A

cholera, live thyroid, yellow fever

*** there is a inactivated typhoid that can be given

210
Q

When should patients with IBD and PSC get colonoscopy after post transplant

What about PSC alone

A

annually

PSC alone: first year and then q5 years

211
Q

What is the national organ transplant act

A

1984- established framework for transplantation. UNOS, OPTN, SRTR

212
Q

What is the final rul

A

2000
established regulatory framework for OPTN (which allocates organ

he Final Rule dramatically changed the way organ donations were allocated in the United States, moving away from a system that favored geographic areas with large donor banks towards a system that prioritized a patient’s need for organ transplant over their proximity to the donor. This move reflects increased ability to successfully preserve and transfer organs for organ transplantation farther than was previously possible. This move was controversial among areas with larger donor banks because there were concerns that the rule would disincentivize organ donation. Donor banks believed donors would be less likely to donate if the organs were being transferred out of state

213
Q

What did the declaration of Istanbul say

A

illegal to buy or sell organs, 2008

214
Q

What are the five components of ethics

A
  1. beneficence- moral obligation to act for the benefit of others
  2. autonomy
  3. non maleficence- obligation not to inflict harm
  4. justice
  5. utility- benefit to most individuals
215
Q

What ethics are seen in LDLT

A

candidate: beneficence (moral obligation to act for the benefit of others)

Donor: nonmaleficence, autonomy

216
Q

What ethics are seen in organ allocation

A

jsutice
utility (benefit to most individuals)

217
Q

What is the order of surrogate decision making

A
  1. POA
  2. if no POA, then spouse –> children –> family
218
Q

HOw to make a diagnosis of pCCA?

A

positive biliary biopsy or positive cytology

if no biopsy available, either of these can be used to define pCCA
1. malignant appearing stricture + CA 19-9>100 (with no biliary obstruction)
2. malignant apeparing stricture + suspicious cytology +/- aneuploidy on FISH
3. perihilar mass with imaging features of CCA

219
Q

What is Mayo protocol

A

only for periphilar CCA in unresectable denovo or in pCCA in PSC

  1. IV5FU followed by external beam radiation and brachytherapy
  2. Capecitabiline until transplant
  3. abdominal explorationfor staging right before transplant to sasess for regional LN invovlement and peritonael mets
  4. Liver transplant
220
Q

at is chemo regiment for advanced cholangio

A

cis/gem
- if progresses on gem/cis, then FOLFOX

221
Q

WHAT genetic alteration is associated with less aggressive tumor biology in iCCA

A

FGFR

KRAS- poorer prognosis

222
Q

k67 in net is associated with what

what about pancferatic NET vs GI NET

A

worse prognosis

pancreatic NET is worse prognosis

223
Q

What is basiliximab

A

IL2 receptor antagonist

224
Q

What drugs are metabolized by p450

A

tacro
cyclo
mtor
steroids

225
Q

What is considered prolonged WIT and prolonged CIT

A

WIT>40 min
CIT >12 hours

226
Q

What is considered too much steatosis

A

> 30%

227
Q

What is considered older donor age

A

> 70 years

228
Q

What are the ways liver can sbe split for transplant

A

child or small adult: LLS (segment 2/3)
adult: extended RL or triage (1,4-8)

229
Q

What is criteria for living donor tx

A

adult age 18-60
BMi <30
minimal hepatic steatosis <10%
graft size
- big enough for recipient GRWR >0.8 (graft to recipient weight)
-not too big for the donor (RLV>/= 30%

230
Q

What is reperfusion syndrome

A

right when unclamping occurs
drop in MAP >30% within first 5 minutes after reperfusion, lasting 1 minutes

associated with high er renal dysfunction, and major CVD events

risk factors are CIT, donor age

231
Q

define early allogradt dysfunction

A

EAD factors (>/= 1)
-bili >10 on POD 7
-INR >1.6 on POD 7
-ALT or AST >/= 2000 within first 7 days

232
Q

What is Primary graft non function

A

irrecersible extreme result of EAD not compatible with survivial without retransplant

233
Q

What is a consequence of EAD

A

AKI

234
Q

Do we care about macro or micro when thinking about grafts

A

only care about macro

235
Q

How to calculate GWRW?
recipient weight is 78.8 kg
right lobe is 960 cc or mL

A

960/1000 =0.96
(0.96/78.8)*100 = 1.21%
and since this is >0.8, would be acceptable if RLV is >30%

236
Q

Galactomannan tells you what

A

aspergillous, tx vori

237
Q

What is acyvlovir for and what is gancicylvir for

A

HSV- acylovir (pneumonitis rare)
CMV- gancivlori

238
Q

what is HEV mistaken forand what can it lead to

A

mistaken for rejection
can lead to cirrhosis

239
Q

Can you use hepatin for BCS

A

can cause HIT

240
Q

what hvpg is indiciative of SOS

A

HVPG >10

241
Q

is biopsy needed for ddx of SOS

A

no, not required, because it can be patchy, but rememeber HVPG >10 high specificity for

Transplant Hep Boards (7 decks)

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