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Adult Health II > Transplants > Flashcards

Transplants Flashcards

1
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2
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The Immune System

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  • Defense, homeostasis & surveillance
  • Multifaceted response to attack from outside (pathogens) and inside (neoplasms)
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3
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Three Phases - Immune systeme

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  1. Recognition of the substance as non-self
  2. Proliferation of immunocompetent cells
  3. The effector phase or action against theforeign substance
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4
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Innate Immunity

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  • What we are born with – genetically based
  • NonspecificMultiple cell types & chemical regulators
  • First line of defense against non-self
  • No memory
    • Surface barriers
    • Normal flora
    • White blood cells – leukocytes
    • Complement
    • Chemokines
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5
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WBC’s or Leukocytes

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  • 5,000 – 10,000 WBC’s per mm3
  • Act like independent single-cell organisms
    • move & can capture things on their own
  • Produced in the bone marrow
  • All recognize self & non-self
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6
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Antigen

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  • A substance capable of eliciting an immune response
  • Antigens on the surface of cells that are genetically predetermined by a series of like genes.
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7
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Lymphocytes – B Cells

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  • Responsible for the production of antibody or immunoglobulin
  • Primary purpose is to mark an antigen for destruction by the immune system.
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8
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Macrophages

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  • FIXED – concentrated in lungs, liver, lymph nodes, spleen, brain microglia, kidney mesoangial cells, synovial cells & osteoclasts
  • WANDERING – roam the blood vessels– can leave them to go to an infection site (extravasation)
  • Once they digest they place some of the proteins on their surface – antigen presentation
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9
Q

T Lymphocytes

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  • Produced in bone marrow – mature in thymus

  • All have CD3 & Ag specific T cell receptors (TCR)o
  • Cellular immunity
  • Killer T cells – CD8+
  • Helper T cells– CD4+
  • Suppressor T cells
  • Memory T cells
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10
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B Lymphocytes

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  • Produced in bone marrow & mature there
  • All have Ag specific Immunoglobulins (Ig) on surface
  • Humoral immunity – produce antibodies
  • Memory cells circulate
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11
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CD4 + T Helper Cells

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  • Recognize antigen processed & presented in association with HLA class II
  • Presentation takes place in lymphoid tissue – spleen, lymph nodes
  • Specific receptors on T helper cells bind to the Ag:HLA class II complex
  • T helper cell becomes activated
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12
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CD8 + T killer Cells

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  • Recognize Ag presented with HLA class I molecules – Ag that has been synthesized within the cell (i.e.: virus)
  • Recognition of APC by T killer cells usually results in death of the APC
  • Fulminant hepatitis (HBV) – liver damage caused by T killer cells
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13
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Cluster of Differentiation: (CD)

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  • > 160 clusters – each cluster is a different molecule that coats the surface
  • Found on lymphocytes

  • 100,000 molecules on every T & B cell
  • Huge variability in antigen receptors
  • CD4+ = T helper cells

  • CD8+ = T killer cells
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14
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15
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Human Leukocyte Antigens (HLA)

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  • Proteins found on the surface of almost every cell (except erythrocytes) o
  • Form the basis for self- recognition o
  • Bind antigen pieces for presentation to T cell receptors (TCR’s)
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16
Q

HLA Class I

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  • Found on every nucleated cell in the body
  • HLA-A, -B, and -C
  • Recognized by CD8+, T killer cells
  • Bind fragments of foreign proteins that are produced inside the cells
  • Antiviral, antitumor and acute graft rejection
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17
Q

HLA Class II

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  • Only found on antigen presenting cells
  • HLA-DR, -DQ, and -DP

  • Macrophages, dendritic cells, B cells
  • Recognized by CD4+, T helper cells and by T suppressor cells – regulators of immune response
  • Bind fragments of foreign proteins that have been proteolytically degraded by APC’s
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18
Q

B Cells

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  • B cells clone and differentiate under the influence of Th2 produced interleukins 4 and 5
  • B cells change morphology – no longer have Ig on surface
  • Become plasma cells that produce Ab in vast quantities
  • Ab binds to Ag – targeting these cells for destruction
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19
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B Cells – Humoral Immunity

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  • B cells become plasma cells which produce
  • vast quantities of antibodies specific to Ag
  • Antibodies circulate in the blood & lymph – the body’s “humors”
  • B cells can also present Ag to Th cells
  • Some return to lymph tissue to remember & wait for the next attack
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20
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Five types of antibodies

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  • IgG – the main type in circulation, binds to pathogens, activates complement, and enhances phagocytosis
  • IgM – the largest type in circulation, activates complement and clumps cells
  • IgA – found in saliva and milk, prevents pathogens from attaching to epithelial cells in digestive and respiratory tracts
  • IgD – on surface of immature B cells, its presence signifies the readiness of a B cell
  • IgE – found on basophils in blood and on mast cells in tissues. Responsible for immediate allergic response and protection against certain parasitic worms
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21
Q

Cellular immunity

A
  • CD4+ T helper cells

    • Th 1 – release –> IL-2 –> T helper & killer cells
  • CD8+ T killer cells
  • Cytokines
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22
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Hummoral Immunity

A
  • B cells – Plasma cells
  • Antibodies
  • Complement
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23
Q

Transplantation Immunology Applied

A
  • Goal is to replace diseased organs with healthy organs to save & prolong life
  • Once replaced, the goal is to protect the foreign organ from the host’s immune system
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24
Q

Panel Reactive Antibodies (PRA)

A
  • Antibodies to Class I MHC HLA antigens
    • Found on all nucleated cells
o These antibodies do not occur naturally
    • Development requires previous exposure to foreign HLA antigens
      • Multiple pregnancies
      • Blood transfusions
      • Prior transplantation
25
Q

Cross Matching

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  • Identify preformed Antibody’s in the recipient to the donor’s HLA
  • Positive cross match means the donor’s lymphocytes are killed by the recipient
  • High risk of hyperacute rejection & vascular rejection
  • Wait for a prospective negative donor- specific cross-match before transplanting organs into a patient with PRA’s > 10-15%
  • Results take 4-6 hours
  • Positive cross-match means the lymphocytes of the potential donor are killed by antibodies of the potential recipient
26
Q

Minimize PRA’s

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  • Antibodies form when recipient’s Th cells detect foreign antigens on nucleated cells 

  • RBC’s & platelets are not nucleated 

  • WBC’s are nucleated – use leukocyte 
reduction filters 

  • Leukoreduction filters also remove cells infected with CMV
27
Q

Plasmaphereis (reduce PRA’s)

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  • Reduce the concentration of cytotoxic Ab’s
  • Blood is divided into its components by centrifugation – plasma then replaced by FFP or albumino
    • Also used to treat humoral rejection
28
Q

Who should receive induction therapy?

A
  • “High-risk” recipients:
    • Re-transplants
    • Pediatric recipients
    • High PRA
    • African-American recipients
    • Long cold ischemia time
    • Recipients of kidneys from “marginal” donors
    • Pancreas transplants
29
Q

Induction Agents

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  • Anti T-Cell antibodies and
  • Il-2 Receptor Inhibitors
30
Q

Anti T-Cell antibodies induction agents

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  • Thymoglobulin
    • Nonselective depletion of T lymphocytes
  • Muromonab OKT3
    • Targets CD3 portion of TCR complex
31
Q

IL-2 Receptor Inhibitors

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  • Bind to CD25 subunit of IL-2 receptors on surface of activated Th1 lymphocytes
  • Depletion of IL-2 receptor positive cells
    • Basiliximab (Simulect®)
32
Q

Common immunosuppressive drugs:

A
  • Cyclosporine (Neoral®, Sandimmune®, Gengraff ®)
    • Formulations not interchangeable
  • Tacrolimus (Prograf®)
  • Mycophenolate mofetil (Cellcept®)
  • Mycophenolic acid (Myfortic)-enteric coated formula
  • Sirolimus (Rapamune®)
  • Corticosteriods (Prednisone/Methylprednisolone)
33
Q

Cyclosporine

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  • Prevents cytotoxic T cells from responding
  • Patients susceptible to viral infections
  • Major Side Effects
    • Nephrotoxic: Monitor renal values
34
Q

Corticosteroids

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  • Protects the organ from permanent damage
  • Impair the sensitivity of T cells to antigen
  • Major side effects
    • Increase risk of infection
    • Usual long term steroid effects
35
Q

Imuran

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  • Interferes with purine synthesis
  • Prevents the activation and rapid proliferation of antibodies
  • Major side effects
    • Leukopenia, thrombocytopenia, anemia
36
Q

Orthoclone (OKT3)

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  • Interferes with T cell recognition of foreign antigen
  • Massive destruction of T cells results in fever, malaise
  • Used to treat acute rejection
  • Administered for 14 days and then stoppedBody develops antibodies to this drug
37
Q

Monitoring Blood Levels

A
  • Trough level:
    • Tacrolimus-FK506
    • Cyclosporine-CYA level
      • C2 level is peak level drawn 2 hours after administration of medication
  • Sirolimus- Rapa level
  • Maintaining a consistent blood level is critical Strict medication schedule
38
Q

Important to remember:

A
  • Trough levels should be drawn at 0530
  • Always give the medication after drawing trough levelIf trough level drawn in AM, results should be available in the afternoon on that same day. If a trough level has been drawn in the morning, the level should be verified before giving the PM dose.
  • Notify MD for elevated trough levels.
  • DO NOT hold any anti-rejection medication without first notifying the transplant physician/s, even if NPO for a test/procedure.
  • NO NSAIDS - INCLUDING TORADOL
    • majority of anti-refjection medications are highly nephrotoxic
  • Sirolimus and Cyclosporine CAN BE administered concurrently.
39
Q

Why give immunosuppressive agents?

A

Hyperacute, acute, and chronic rejection

40
Q

Hyperacute Rejection

A
  • Occurs immediately
    • Previous Ag exposure – most class I HLA on donor vascular endothelium
    • Ab’s bind to cell surface – intense inflammatory response & fibrin cascade – complement fixation & clot formation
    • Rapid (minutes to hours) tissue destruction & vascular clotting
    • Rarely occurs because of pre-transplant screening
41
Q

Acute Rejection

A
  • Occurs within a week to 4 months
    • Recipient T cells exposed to class I HLA antigens on all cells of graft & class II HLA antigens of donor APC’s
    • Donor APC’s migrate to recipient lymph nodes
    • Th cells activated & produce cytokines – activate Th, Tk, B cells, macrophages
    • Attracted to graft by locally produced chemokines
42
Q

Chronic Rejection

A
  • Chronic rejection – usually occurs beyond 6 months after transplantation
    • Slow deterioration in graft function
    • T & B cell response
    • Constant production of cytokines
    • Thickening & fibrosis of vasculature is common
43
Q

Treatment of Rejection

A
  • Prevent SPECIFIC immune response
    • Remove all Th cells (OKT3 ®, Thymoglobulin ®)
    • Prevent recognition of allograft (cross-match)
    • Prevent costimulation (induce tolerance)
  • Prevent NON-SPECIFIC immune response
    • Inhibit IL-2 production (CyA, FK506)
    • Inhibit IL-2 action (Rapamycin)Inhibit T cell proliferation (Imuran, Mycophenolate mofetil)
    • Inhibit inflammation (Corticosteroids)
    • Inhibit T cell proliferation (Imuran, Mycophenolate mofetil)
    • Inhibit inflammation (Corticosteroids)
44
Q

Treatment of Humoral Rejection

A
  • Plasmapheresis
    • Reduce the concentration of Ab’s and complement proteins
  • Rituximab (Rituxan®)
    • Monoclonal antibody
    • Selectively binds to CD20 – found on the surface of B cells
45
Q

History of Heart Transplantation

A
  • Historically:
    • Radical
    • Experimental
    • Controversial
  • Early years plagued with:
    • Poor Graft Survival
  • Obstacles to success:
    • Organ Rejection
    • Inadequate healing
    • Infection
46
Q

Indications for Heart Transplant

A
  • Cardiogenic shock requiring continuous IV inotropes or mechanical circulatory support
  • NYHA class IV refractory to medical therapy
  • ACC/AHA stage D- (End stage Heart Disease)
  • Poor 1 year survival ≤50%
  • Intractable angina with CAD not amendable to surgical or percutaneous revascularization
  • Refractory, life-threatening arrhythmias unresponsive to medical therapy, catheter ablation and/or ICD implantation
47
Q

Absolute Contraindication for Heart Transplantation

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  • Malignancy
  • Hepatic Cirrhosis
  • Severe COPD
  • Major Psychiatric Illness
48
Q

Relative Contraindications

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  • Age>70
  • HIV+
  • CVA
  • Active Substance AbuseI
  • Insulin-dependent diabetes
    • With end-organ damage or poor glycemic control
  • Active Infection
  • Advanced renal disease
    • Creatinine Clearance <40
  • Non-compliance
  • Mental illness
  • Multi-organ system failure
  • Absence of a caretaker
  • Absence of financial resources
  • BMI > 35 or BMI <18
  • Pulmonary HTN
49
Q

UNOS ListingAdult Heart Transplant Candidates

A

Status1A, Status 1B, Status 2, Status 7

50
Q

STATUS1A

A
  • Hospitalized
  • Mechanical circulatory support-acute hemodynamic decompensation
  • Device related complication
  • Continuous infusion of inotrope(s)
  • Mechanical Ventilation
  • Life Expectancy without transplant <7 days
51
Q

Status 1B

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Patient has one of the following therapies: VAD or Continuous infusion of IV inotropes

52
Q

Status 2

A

Patient does not meet the criteria for Status 1A or 1B

53
Q

Status 7

A
  • The patient is temporarily unsuitable to receive a heart transplant
  • *** VAD patients are currently given a free 30 days at status 1A ***
54
Q

Transplant Procedure

A

Donor heart replaces recipient heart and is anastomosed using either the biatrial or bicaval technique

55
Q

Biatrial Technique

A
  • Donor & recipient’s hearts
    • Removed at the mid-atrial level
    • Recipient maintains a portion of native atria, aorta, & PA
  • Donor heart:
    • Denervated (parasympathetic & sympathetic nervous system fibers severed)
  • Shorter surgical time
  • Disadvantages:
    • Large anatomically abnormal atria
    • ↑ risk of tricuspid/mitral regurg
    • Permanent pacemaker may be required with persistent SA node dysfunction
56
Q

Bicaval Technique

A
  • Preferred Method!!
  • Recipient receives intact donor atrium Anastomoses at:
    • Recipients inferior & superior vena cavaAtrial cuff reduced to smaller size around pulmonary veins
  • Advantage:
    • SA Node preserved
    • ↓ SA node dysfunction
    • ↓ atrial dysrhythmias
    • ↓ risk of mitral/ tricuspid regurg.
  • Disadvantage:
    • Longer surgical time
57
Q

Allograft rejection

A
  • Hyperacute
    • Antibody mediated:
      • Proir antibodies to ABO, HLA, or endothelial antigens
  • Acute
    • Cell mediated primarily (3-6 months)
  • Chronic
    • Mostly humoral response
    • Coronary Allograft Vasculopathy
58
Q

Coronary Artery Vasculopathy

A
  • Rapid & progressive form of CAD leading to vessel lumen obliteration
  • Believed to be a form of chronic rejectionPTCA & CABG palliative but not recommendedRe-transplant only definitive treatment
  • Due to denervation patients often do not experience chest pain
  • Coronary Angiography only method of early detection
    • Prevention involves: Early treatment of hyperlipidemia, infection, & rejection

Adult Health II (4 decks)

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