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POS - Box 3 > Transplant > Flashcards

Transplant Flashcards

1
Q

Acute phase proteins made by liver (9)

A
  1. fibrinogen
  2. haptoglobin
  3. CRP
  4. C3
  5. ceruloplasmin
  6. alpha-antitrypsin
  7. alpha-antichymotrypsin
  8. alpha-acid glycoprotein
  9. amyloid A
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2
Q

Lab findings with hepatocellular injury

A

Increased AST/ALT

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3
Q

Lab findings with liver obstruction (5)

A

Increased ALP, GGT, Bili (D), 5-nucletidase, leucine amino peptidase

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4
Q

Lab findings of decreased liver function (5)

A

Decreased albumin, transferrin, coag factors (=Increased INR)
Hypoglycemia
Altered glucose metabolism

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5
Q

What are MHC antigens?

A

Surface antigens, aka HLA (human leukocyte antigens)
Reason for organ rejection as molecules involved in antigen presentation to Tcells

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6
Q

What are class I MHC?

A

HLA-A,B,C
ALL CELLS have these on surface
same internal contents of cell and bring to surface for presentation
Recognized by CD8 = cell death
Expression increased by cytokines and interferons

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7
Q

What are Class II MHC?

A

Expression of HLA DR, DQ, DP, DM
Only on antigen presenting cells - present to CD4 cells
Leads to B-cell antibody development and presenting cell damage
Leads to macrophage activation

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8
Q

What is indirect antigen recognition?

A

Conventional antigen presentation. Antigens taken up and then presented in MHC to t-cells

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9
Q

What is direct antigen recognition?

A

In solid organ transplant, antigen presenting cells present themselves = rejection

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10
Q

Role of antibodies? (4)

A

Target for phagocytosis
Activate complement
Neutralize toxins
Block attachments of pathogens to cells or tissue

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11
Q

5 classes of immunoglobulins

A

Ig A,D,E,G,M

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12
Q

What is the structure of immunoglobulins?

A

4 peptide chains
heavy x 2
light x 2

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13
Q

What does IgD do?

A

On surface of B cells, function unknown

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14
Q

What does IgA do?

A

low levels blood, most abundant at mucosal surfaces (i.e. gut)

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15
Q

What does IgM do?

A

Surface of B cells. Secreted as pentamer (5 molecules).
Activates complement
First antibody produced at time of infection

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16
Q

What does IgE do?

A

Low amount in blood. Bound to mast cells and basophils.
Responsible for type I hypersensitivity.
Increased in parasitic infections

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17
Q

What does IgG do?

A

Most abundant AB
Production depends on cytokines
Leaves bloodstream and enters tissues
ACTIVELY TRANSPORTED ACROSS PLACENTA (the only one)
Activates complement
neutralizes toxins

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18
Q

Contraindications to transplant donation (4)

A

Sepsis - start abx before taking
Viral infection (HTLV1, HIV, HBV, HCV, EBV, CMV, HSV)
Cancer
No consent

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19
Q

What are contraindications to receiving transplant? (7)

A

HIV (actually not an absolute indication if lvls are controlled)
Malignancy
Irreversible brain damage
Irreversible infxn
Irrreversible multiple organ faiilure
Irreversible significant cardiopulmonary dz
Inability to comply with medical therapy

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20
Q

Contraindications specific to liver transplant? (8)

A

Inability to have procedure
Recent intracranial hemorrhage
Irreversible neurologic impairment
Active substance abuse
Intractable hypotension
Evidence of systemic infection
Extrahepatic malignancy
Inability to comply with followup/meds

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21
Q

Contraindications specific to renal transplant (3)

A

Recurrent renal dz (FSGS, hemolytic uremia syndrome, MPGN)
Liver transplant contraindications
psychosocial

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22
Q

What does blood transfusion effect refer to in context of organ rejection?

A

Improved graft survival believed to be secondary to suppression of rejection mechanisms in patients who receive blood before their transplant

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23
Q

What is hyper acute rejection?

A

Minutes to hours
can happen across ABO groups
preformed IgG antibodies
TYPE AND SCREEN

24
Q

What is acute rejection?

A

1-3 weeks but most common 3-6 months
T cells
2 types - vascular and cellular
Treat with methylprednisolone –> taper

25
Q

What is chronic rejection?

A

All organs:
Atherosclerosis
Obliteration
FIbrosis

26
Q

Risk factors for chronic organ rejection (6)

A

Donor issues (age, HTN, etc)
Poor organ harvest
Delayed graft function
Recipient issues (HTN, diabetes, infection)
Inadequate immunosuppression
Previous acute rejection episodes

27
Q

What is the typical immunosuppressive regime for low-risk pts?

A

Induction: IL2 inhibitor (intra-op), steroids (first 4 days)
Maintenance: Calcineurin inhibitor OR sirolimus… AND antimetabolite +/- steroids
All patients on CCB to decrease nephrotoxicity of calcineurin
Valganciclovir for CMV ppx

28
Q

What is the typical immunosuppressive regime for high-risk patients?

A

Same as low risk PLUS
thymoglobulin OR OKT3 to induction drugs and definitly on steroids for maintenance

29
Q

What are induction agents for immunosuppression for transplant?

A

anti-lymphocytic globulin
monoclonal antibody OKT3 (4)
IL2 receptor inhibitor
Radiation

30
Q

How does anti-lymphocytic globulin work for immunosuppression?

A

Targets Tcells
Can be given ppx, early transplant, or to reverse rejection
most common complication is allergic rxn
Anemia and TCP can also occur

31
Q

How does OKT3 work for immunosuppression?

A

Blocks Tcells
can elicit immune reactions
Cytokine release = chills, rigours, fever
Increased incidence of lymph proliferative disorders

32
Q

How do IL2 receptor inhibitors work for immunosuppression?

A

Basiliximab and daclizumab
Prevents IL2 from binding and propagating immune responses. IL2 is powerful cytokine

33
Q

How does radiation work for immunosuppression?

A

Decreases response of immune system
More often done before bone marrow transplant

34
Q

What are immunosuppression maintenance agents? (6)

A

Steroids
Azathioprine (imuran)
MMF
Cyclosporin
Tacrolimus
Sirolimus

35
Q

What is the MOA of adrenal corticosteroids?

A

Decreases lymphocyte counts
Decreases macrophage activity
Inhibits cytokines
Suppresses prostaglandin synthesis

36
Q

What are the side effects of adrenal corticosteroids? (11)

A

HTN
Weight gain
GI bleeding
peptic ulcers
Euphoric personality changes
Cataracts
Hyperglycemia
Pancreatitis
Muscle wasting
Osteoporosis
Avascular necrosis

37
Q

What is the MOA of azathioprine?

A

Blocks DNA, RNA synthesis
Inhibits humeral and cellular immunity
Decreases neutrophil production
Decreases macrophage activation

38
Q

What are the side effects of azathioprine (3)

A

Marrow suppression –> leukopenia
Hepatotoxicity and leukopenia
GI upset

39
Q

What is the MOA of cyclosporine?

A

Inhibits IL-1
Inhibits IL2 production
Inhibits mitogen activation
Inhibits T cell activation
** T-cell inhibition big part of it

40
Q

What are the side effects of cyclosporine? (3N 7H)

A

Nephrotoxicity (dose dependent)
Neoplasia
Neurotoxic
Hyperuricemia
HTN
Hyperglycemia
HyperK
Hyperplasia of gingiva
Hepatotoxic
Hirsutism

41
Q

What is the MOA of mycophenolate mofetil?

A

Inhibits purine metabolism
Inhibits T and B lymphocytes
**similar to azathioprine, but preferred

42
Q

What are the side effects of mycophenolate mofetil? (2)

A

Leukopenia
GI upset (diarrhea)

43
Q

What is the MOA of tacrolimus?

A

Calcineurin inhibitor
Leads to decreased IL2 production
Inhibits T helper and killer cells

44
Q

What are side effects of tacrolimus? (7)

A

Nephrotoxic
Neurotoxic
Hyperglycemia
HyperK
HTN
Hepatotoxic
Alopecia

45
Q

What is the MOA of sirolimus?

A

Binds same receptor as tacrolimus
Does NOT block T cell cytokine gene expression
Inhibits transduction of signals from IL2R to nucleus
calcium-independent pathway

46
Q

What drugs interact with cyclosporin?

A

Rifampin (decrease)
Steroids (increase)
CCBs (decrease)
Nephrotoxins (additive effect)

47
Q

What drugs increase cyclosporin levels?

A

H2 antagonists
Cephalosporins
Thiazides
Lasix
Androgenic roids
Acyclovir
Warfarin

48
Q

Which drugs decrease cyclosporine levels?

A

Rifampin
Anticonnvulsants
Sulfinpyrazone

49
Q

Which drugs increase nephrotoxicity of cyclosporine?

A

NSAIDs
Cipro

50
Q

What are post-transplant complications?

A

Infection
Neoplasia
Post-renal transplant HTN

51
Q

What ppx drugs are used to prevent post-transplant infection?

A

Acyclovir/Ganciclovir (CMV)
Septra (pneumocystis)
Nystatin/clotrimazole/fluconazole (fungus)

52
Q

Post-trransplant opportunistic infections (bugs)

A

Aspergilis
Blastomycosis
Nocardiosis
Toxoplasmosis
Cryptococcosis
Pneumocystis

53
Q

Causes of post-renal transplant hypertension

A

Graft rejection
Renal transplant artery stenosis
Native nephrectomy
Corticosteroids
Cyclosporine

54
Q

What cause renal transplant artery stenosis?

A

Improper anastomotic technique
Kinking of vessel
Damage of artery
Atherosclerotic disease
Fibrosis

55
Q

How is renal transplant artery stenosis diagnosed?

A

Imaging (MRA or angiogram)
Peripheral renin (elevated)
Captopril stimulation test (BP falls more and renin rises more)
Differential renal vein renin sampling

56
Q

What is the treatment for renal artery transplant stenosis?

A

Perc. angioplasty #1
Open surgical correction #2

POS - Box 3 (6 decks)

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