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Transplant Flashcards

1
Q

What are the major transplant antigens?

A

MHC and ABO blood type.

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2
Q

Which HLA types are used for kidney allocation?

A

HLA -A, -B, and -DR.

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3
Q

Which antigen is the most important in kidney donor/recipient matching?

A

HLA -DR. Better match = better long term function/less rejection.

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4
Q

What criteria are used for kidney allocation in the US?

A

Time on list, HLA matching, and panel reactive antibody.

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5
Q

What is Panel Reactive Antibody (PRA)?

A

Identical to cross match, but detects HLA.

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6
Q

How does a higher PRA affect transplant waiting time?

A

Higher PRA will move up higher on the transplant list because it is more difficult to find a match.
-Usually wait longer on list if high
-Gets percentage of cells that recipient serum reacts with

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7
Q

What factors increase PRA?

A

Transfusions, pregnancy, previous transplant, and autoimmune disease.

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8
Q

What does a positive crossmatch indicate?

A

-Lymphocyte crossmatch)
-Detects preformed recipients’ antibodies by mixing recipient serum with donor lymphocytes= termed positive crossmatch (would result in hyperacute rejection)

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9
Q

What is the most common cancer after transplant?

A

MC CA after transplant= skin (squamous cell), then Post-transplant lymphoproliferative disorder. Both of these treatment = decreasing immunosuppression

Post-transplant lymphoproliferative disorders (PTLD)
B cell lymphoma (EB virus infection)
Give ganciclovir for EB virus infection. Rituximab (anti-CD20)
Discontinuation of immunosuppression
Skin tumors: SCC more common than BCC
Average time for a SCC to form following transplant = 8 years

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10
Q

What is hyperacute rejection?

A

Hyperacute rejection (1st 24 hours) – MCC by ABO blood type incompatibility, also anti-HLA abs. Should be detected on crossmatch. Type II hypersensitivity. Organ turns blue and mottled. Tx: Remove organ, emergency re-TXP

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11
Q

What characterizes acute rejection?

A

Occurs days to 6 months post-transplant, mediated by recipient T cells to donor HLA antigens.

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12
Q

What is the treatment for acute rejection?

A

Increase immunosuppression, with pulse steroids being the best option.

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13
Q

What does acute rejection show on pathology?

A

Lymphocytes.

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14
Q

What is chronic rejection?

A

Occurs months to years post-transplant, mainly caused by MHC (HLA) incompatibility. Tx: Increase immunosuppression

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15
Q

What does chronic rejection show on pathology?

A

Fibrosis.

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16
Q

What is the mechanism of action of Mycophenolate (MMF)?

A

Inhibits purine synthesis (DNA anti-metabolite), which inhibits growth of T cells.

-Cellcept
-Don’t follow drug levels
-1000 mg BID

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17
Q

What are the side effects of Mycophenolate (MMF)?

A

Nausea, vomiting, diarrhea, and myelosuppression.

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18
Q

What is the mechanism of action of Cyclosporine?

A

Binds cyclophilin protein, inhibiting calcineurin and decreasing cytokine synthesis. Inhibits IL-2 and IL-4 -> Inhibits T cell activation

Hepatic metabolism
Undergoes enterohepatic re-circulation -> Biliary drain (T tube) can cause decreased levels-> need to increase dose

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19
Q

What are the side effects of Cyclosporine?

A

Nephrotoxicity, hepatotoxicity, tremors, seizures, HUS, nausea, vomiting, diarrhea, and gingival hyperplasia.

Does not alter wound healing

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20
Q

What is the mechanism of action of Tacrolimus?

A

Prograf/FK-506
Binds FK binding protein, inhibiting calcineurin and decreasing IL-2 and IL-4.

Hepatic metabolism but much less hepatic recirculation compared to cyclosporine
Less rejection episodes in kidney txp when compared to cyclosporine (calcineurin inhibitors)

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21
Q

What are the side effects of Tacrolimus?

A

Nephrotoxicity, increased nausea, vomiting, diarrhea, diabetes, and mood changes.

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22
Q

What is the mechanism of action of Sirolimus?

A

Sirolimus (rapamycin) – Binds FK binding protein like FK-506 but inhibits mammalian target of rapamycin mTOR → Decreases IL2,
Not a calcineurin inhibitor!!!!

Is not nephrotoxic
Associated with reduced incidence of de novo malignancies

23
Q

What are the side effects of Sirolimus?

A

ASSOCIATED WITH DRUG INDUCED HEPATIC ARTERY THROMBOSIS, avoid in early liver TXP
Issues with wound healing= avoid in early post op
SE: interstitial lung dz, pneumonitis, thrombocytopenia

24
Q

What is Anti-thymocyte globulin?

A

Equine or rabbit polyclonal antibodies against T cell antigens (CD2, CD3, CD4)
Is cytolytic → complement dependent
Used for induction and severe acute rejection episodes

Blocks the T cell activating pathway by constitutively activating it and causing it to EXPLODE.

25
Q

What are the side effects of Anti-thymocyte globulin?

A
  • cytokine release syndrome (fever, chills, pulm edema, shock) give steroids, Tylenol, Benadryl before drug to prevent this.
  • Myelosuppresion
  • PTLD!!!!!!!
26
Q

What is Basiliximab/Daclizumab?

A

Monoclonal antibody IL-2 receptor inhibitor used as induction or for refractory acute rejection.

SE = hypersensitivity reaction
-Commonly used as induction agent for kidney transplant
-No nephrotoxicity

27
Q

What is Post-Transplant Lymphoproliferative Disease (PTLD)?

A

The second most common malignancy following transplant, caused by EBV.

Fever, adenopathy, SBO.
Highest risk is small bowel TXP.
Majority occur within the first year
Caused by EBV, mediated B cell proliferation

RF:
- Cytolytic antibodies (e.g. anti-thymocyte) with pre-transplant seronegative EBV who become sero-positive EBV after transplant
- EBV negative patients are higher risk than EBV positive patients
Can convert to non-hodgkins B cell lymphoma.
Dx: FNA or biopsy.

28
Q

What is the treatment for PTLD?

A

Decrease immunosuppression; if that fails, use Rituximab + CHOP-R.

29
Q

What is the most common infection in transplant recipients?

A

CMV = MC infection in TXP recipients.
MC deadly form is CMV pneumonitis.
Transmitted by leukocytes.
Bx shows cellular inclusion bodies.
Presents as febrile mononucleosis

First month: post op infection
2 – 6 months: opportunistic infection: CMV, pneumocystis, aspergillosis
After 6 months: infections rare

30
Q

What is the treatment for CMV infection?

A

Tx: Ganciclovir, reduce immunosuppression if possible.
CMV IVIG + ganciclovir given for severe infections and after TXP for CMV negative recipient with CMV positive donor

31
Q

What is the treatment for HSV and Zoster in transplant recipients?

A

Acyclovir.

32
Q

What is the BK virus?

A

BK mole virus “polyomavirus” – 5% of renal TXP get BK virus in kidney, 80% lose graft. MCC of nephropathy leading to graft loss
Tx: reduce immunosuppression

33
Q

What is brain death?

A

Brain death
Precludes diagnosis → Temp < 32, BP < 90 (can be on pressors), intoxicants, sedatives, hypernatremia, hyperglycemia, desaturation <85% with apnea test

Must have following for 6 hours:
- Absent cervico-ocular reflex (dolls eyes) – moving head, eyes fixes on image
- Caloric reflex test – tests above as well. Warm water  nystagmus to same side, cold opposite side
- No spontaneous respirations
- No corneal, gag, reflex
- Fixed and dilated pupils
- Positive apnea

EEG shows electrical silence
MRA shows no blood flow to brain
No reflexes, can have spinal reflexesCan still have tendon reflex with brain death

Apnea test - best test and only one needed. Rest are adjuncts.
Pre-oxygenate for 10 minutes, take off vent for 8-10 minutes
- If CO2 > 60 or increased by 20 = positive for brain death
- If BP drops < 90, desaturation <85%, or spontaneous breathing → negative test, place back on vent

Brain dead patient develops hemodynamic instability
Usually happens after brain herniation: Rule out volume issue 1st
If not volume issue, then low hormone issue
Hormone replacement can improve organ procurement rate by 50%
Give these patient’s T3/T4, methylprednisolone and vasopressin

34
Q

What is Donation after Cardiac Death (DCD)?

A

Donation after cardiac death (DCD) – Occurs after devastating brain injury, usually
- does not meet brain death criteria
- Some brain reflex can be present. Family usually decides to withdraw care
- Need to withdraw support in ICU or OR to declare the patient dead
- Requires a period of 5 minutes of asystole (no blood pressure, pulse etc)  then can declare death
- After withdrawal, if does not meet criteria of death in 60-90 mins, kidney won’t be procured, 30 mins for liver and lung
- Can procure Lungs, liver, pancreas and kidneys. No heart o intestine
- DCD has inferior outcomes compared to DBD

35
Q

What is Donation after Brain Death (DBD)?

A

Donation after brain Death (DBD)- Occurs after devastating brain injury
- Meets criteria for brain death. Time of brain death = time of death
- Once brain declared dead, patient kept on vent throughout organ procurement
- Can obtain Heart, lungs, liver, pancreas, kidneys and intestine

36
Q

What is warm ischemic time?

A

Warm ischemia time - Warm ischemic time refers to the amount of time that an organ remains at body temperature after its blood supply has stopped
- This is very minimal with brain death because heart is still working
- Much longer for DCD

37
Q

What is cold ischemic time?

A

Cold ischemic time - refers to the amount of time that an organ is chilled or cold and not receiving a blood supply
- Varies widely by organ.

38
Q

Living donor

A

General living donor
Long term survival is better, when organ used from living donor vs cadaveric
Also has improved graft survival

Donors
Most donors with CA are excluded – Unless in remission for 5 years or squamous/basal cell skin cancer, and some intracranial tumors.
Donor conditions which make TXP Contraindicated:
- Cirrhosis
- Most CA types, except squamous or BCC skin cancer
- Active blood infection

Transplant is contraindicated in cancer that have a MALIGNANT potential. Cannot use ANY organ from donor

39
Q

Kidney transplant

A

MC indication is ESRD from diabetes
Can cold store kidney for 48 hours
UTI in kidney, can still use it as donor
Donor: Must have GFR > 80 to be candidate to donate
MCC of death  myocardial infarction
MCC post op oliguria  ATN (path shows dilation + loss of tubules)
MCC new proteinuria  Renal vein thrombosis, dx w/ US

5 year survival: 70% cadaver, 80% living
Median survival 15-20 years. TXP extends life 15 years
MC complication for living kidney donor wound infection
MCC of death for living kidney TXP donor – PE
Patients who receive kidney transplant before needing dialysis have lower rejection and mortality
Patients who receive a kidney from living donor have better survival

40
Q

Kidney transplant complications

A
  • Urine leak MC Cx #1 – Sx: low UOP and high Cr. Dx: Duplex, tx: IR drainage (high Cr)  place stent
  • Renal artery stenosis – Dx: duplex, (shows flow acceleration at level of stenosis) Tx: Return to OR to revise
  • Renal vein thrombosis – Dx: Duplex: no flow to vein.  To OR
  • Renal artery thrombosis – usually 2/2 to technical issue. Dx US (high flow). Tx: Nephrostomy tube???
  • renal arterial resistive index (RI) = RI = (peak systolic velocity - end diastolic velocity) / peak systolic velocity. Upper limit of normal = 0.7
  • Lymphocele – MCC of external ureter compression
  • MC occurs 3 weeks after TXP!!!!!
  • Dx: Renal US, will see hypoechoic fluid PLUS hydronephrosis from ureter compression. Good graft perfusion, normal Cr in fluid
  • Tx: 1st try PC drainage (normal Cr), If fails then need peritoneal window (intraperitoneal marsupialization
  • Acute rejection - pathology shows tubulitis or vasculitis (more severe). Tx = pulse steroids or others
  • Kidney rejection work up: Fluid challenge, duplex, biopsy, decrease CSA or FK
41
Q

Liver transplant

A

MC indication for TXP is cirrhosis from hepatitis C
MC indication for children  biliary atresia
Can cold store for 24 hours
Macrosteatosis – best predictor of primary non-function. Cut off is 60%. If >60% macrosteatosis (Fat in liver) then cannot donate
MC adult donation – right lobe, segment 5,6,7,8
MC pediatric – left lateral 2,3
Complications – start with duplex and Bx for diagnosis
- Biliary leak MC complication: Tx: IR drainage and ERCP with sphincterotomy and stent (across leak if possible)
- Biliary stenosis –Dx: US shows dilated ducts Tx: ERCP dilation and stent
- Primary non-function – emergent re-transplant
- Early hepatic artery thrombosis  Dx: duplex. Can re-operate to fix anastomosis, or PTA and stent but if fulminant hepatic failure  emergent re-transplant
- Late hepatic artery thrombosis  no fulminant failure, but has hepatic abscess and strictures.
- MCC of hepatic abscess after liver TXP – late hepatic artery thrombosis
- Cholangitis – see JUST PMNS in portal triad, not mixed
- Acute rejection – path shows portal venous lymphocytosis, endothelitis (see mixed infiltrate in portal triad, not just PMN), bile duct injury. Tx: pulse steroids
Very low chronic rejection, only 5% lifetime. Path shows disappearing bile ducts
5-year survival 70%. Median survival 15-20 years
Hepatitis B recipient tx: adefovir and lamivudine. Reduces reinfection rate to 5%
Hepatitis C recipients reinfects all grafts

42
Q

Heart transplant

A

Can cold store for 6 hours
Indications: life expectancy < 1 year
Persistent pulmonary HTN after heart TXP associated with early mortality.
MCC of early mortality (<1 year) – infection
MCC of late mortality (>5 years) and overall: Chronic allograft vasculopathy
Acute rejection: perivascular infiltrate with increasing myocyte inflammation and necrosis
Median survival 10 years

43
Q

Lung transplantation

A

Can cold store for 6 hours
Indications: life expectancy < 1 year
Exclusion criteria for using lungs: aspiration, large contusion, infiltrate, purulent sputum, PO2 < 350 on 100% FIO2
MCC of early mortality (<1 year) – reperfusion injury (primary graft failure)
MCC of late mortality (>1 year) and overall: bronchiolitis obliterans
Acute Rejection: perivascular lymphocytosis
Chronic rejection: bronchiolitis obliterans
Median survival 5 years

44
Q

Pancreas transplant

A

Pancreas transplantation
MC indication is type I DM and ESRD. Usually combined with kidney
Indications
- Diabetic with imminent or established ESRD, who had or plan to have kidney TXP
- Patients meeting all 3: metabolic issues with DM (hypoglycemia, ketoacidosis, hyperglycemia), emotional problems with insulin therapy that is incapacitating, and consistent failure of insulin management
Need donor celiac, SMA and portal vein which is attached to recipient iliac vessels
Most use “Enteric drainage” Take 2nd portion of duodenum from donor along with ampulla, then anastomose donor duodenum to recipient bowel
Can also have pancreas drain into bladder
- Advantage of this is to check pancreatic function with urinary amylase. Amylase is more sensitive marker for pancreatic function than glucose. But this is associated with higher morbidity.
Successful pancreas/kidney TXP  results in
1. Stabilization of retinopathy
2. Decreased neuropathy
3. Decreased autonomic dysfunction (gastroparesis)
4. Decreased orthostatic hypotension.
5. No reversal of vascular disease.

45
Q

What are the components of the MELD score?

A

Model for end-stage liver disease.
Bilirubin, INR, and creatinine.

46
Q

What are the types of immune cells involved in the immune response?

A

B cells (humeral) antibodies – plasma and memory cells
IgM first to appear, but later changes to more specific IgG or IgM
IgA is the mucosal immune antibody – found in intestinal cells
IgE for mast cell mediated immunity

T cells (lymphoid) killer, cytotoxic and helper cells

Most immunosuppression drugs used target T cel activation signaling pathways.
B cell suppression: IVIG and plasmapheresis.

47
Q

What characterizes hyperacute rejection?

A

Secondary to preformed antibodies and is seen immediately when you release your cross-clamp. Only way to treat is prevention. The final cross-match checks for preformed IgG against HLC I

48
Q

What characterizes acute rejection?

A

Seen after 5 days post-transplantation. See an acute decline in graft function. T cell mediated (when the organ is biopsied, generally see an infiltration of T cells). Treated with steroids initially with good success rates.

49
Q

What characterizes chronic rejection?

A

It occurs 1-2 years after transplantation and is characterized by gradual decline in organ function and fibrosis.
- Lung: bronchiolitis obliterans
- Heart: endarteritis obliterans
- Liver: vanishing bile duct syndrome
- Kidney: interstitial fibrosis and tubular atrophy

50
Q

What are common maintenance immunosuppression regimens?

A

Old: azathioprine + prednisone
80s: cyclosporine + azathioprine + prednisone
90s: tacrolimus + cellcept (MMF) + prednisone.

51
Q

Calcineurin Inhibitors:

A

Tacrolimus (FK506) and cyclosporine
Dosed by levels:
Tacrolimus: 5-15
Cyclosporine: 150 – 400
Side Effects: renal, hyperkalemia, hyperglycemia, HTn
Tacrolimus: tremors and seizures
Cyclosporine: gingival hypertrophy, hirsutism

52
Q

Antiproliferatives:

A

Antiproliferatives: blocks de novo purine synthesis pathway, cell cannot cycle
Mycophenolate (MMF) and azathioprine
Toxicity: leukopenia, pancytopenia, GI toxicity
**Remember that the B/T cells lack the salvage pathway to create purines. Enterocytes also lack this pathway, which is why you get GI toxicity: nausea/vomiting, diarrhea

53
Q

OKT3

A

Monster ATG
Used in refractory rejection.
Side effects: monster ATG side effects. Also can get aseptic meningitis.

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