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Adult Health II > Transplants > Flashcards

Transplants Flashcards

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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
Q

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
Q

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
Q

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
Q

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
Q

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
Q

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
Q

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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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

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  • CD4+ T helper cells

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

Hummoral Immunity

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

Transplantation Immunology Applied

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  • 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)

Study These Flashcards
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
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Cross Matching
* 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
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Minimize PRA’s
* 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
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Plasmaphereis (reduce PRA's)
* 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
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Who should receive induction therapy?
* “High-risk” recipients: * Re-transplants * Pediatric recipients * High PRA * African-American recipients * Long cold ischemia time * Recipients of kidneys from “marginal” donors * Pancreas transplants
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Induction Agents
* Anti T-Cell antibodies and * Il-2 Receptor Inhibitors
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Anti T-Cell antibodies induction agents
* Thymoglobulin * Nonselective depletion of T lymphocytes * Muromonab OKT3 * Targets CD3 portion of TCR complex
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IL-2 Receptor Inhibitors
* Bind to CD25 subunit of IL-2 receptors on surface of activated Th1 lymphocytes * Depletion of IL-2 receptor positive cells * Basiliximab (Simulect®)
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Common immunosuppressive drugs:
* **Cyclosporine** (Neoral®, Sandimmune®, Gengraff ®) * Formulations not interchangeable * **Tacrolimus** (Prograf®) * **Mycophenolate** **mofetil** (Cellcept®) * **Mycophenolic** **acid** (Myfortic)-enteric coated formula * **Sirolimus** (Rapamune®) * **Corticosteriods** (Prednisone/Methylprednisolone)
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Cyclosporine
* Prevents cytotoxic T cells from responding * Patients susceptible to viral infections * **Major Side Effects** * Nephrotoxic: Monitor renal values
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Corticosteroids
* 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
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Imuran
* Interferes with purine synthesis * Prevents the activation and rapid proliferation of antibodies * **Major side effects** * Leukopenia, thrombocytopenia, anemia
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Orthoclone (OKT3)
* 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
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Monitoring Blood Levels
* 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
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Important to remember:
* 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.
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Why give immunosuppressive agents?
Hyperacute, acute, and chronic rejection
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Hyperacute Rejection
* 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
Acute Rejection
* 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
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Chronic Rejection
* 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
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Treatment of Rejection
* 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)
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Treatment of Humoral Rejection
* **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
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History of Heart Transplantation
* **Historically**: * Radical * Experimental * Controversial * **Early years plagued with:** * Poor Graft Survival * **Obstacles to success:** * Organ Rejection * Inadequate healing * Infection
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Indications for Heart Transplant
* 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
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Absolute Contraindication for Heart Transplantation
* Malignancy * Hepatic Cirrhosis * Severe COPD * Major Psychiatric Illness
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Relative Contraindications
* 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
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UNOS ListingAdult Heart Transplant Candidates
Status1A, Status 1B, Status 2, Status 7
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STATUS1A
* Hospitalized * Mechanical circulatory support-acute hemodynamic decompensation * Device related complication * Continuous infusion of inotrope(s) * Mechanical Ventilation * Life Expectancy without transplant \<7 days
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Status 1B
Patient has one of the following therapies: **VAD** or **Continuous infusion of IV inotropes**
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Status 2
Patient does not meet the criteria for Status 1A or 1B
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Status 7
* The patient is temporarily unsuitable to receive a heart transplant * \*\*\* VAD patients are currently given a free 30 days at status 1A \*\*\*
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Transplant Procedure
Donor heart replaces recipient heart and is anastomosed using either the biatrial or bicaval technique
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Biatrial Technique
* **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
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Bicaval Technique
* **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
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Allograft rejection
* 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
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Coronary Artery Vasculopathy
* 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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