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ID Therapeutics :') > I'm having a immune response..(exam 1) > Flashcards

I'm having a immune response..(exam 1) Flashcards

1
Q

what is an immunomodulator?

A

agents that have the capacity for both positive and negative actions (ex- bacteria & their products on the immune system)

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2
Q

what is an immunostimulant?

A

stimulates the immune response (ex- isoprinsine, BCG- used in certain stages of bladder cancer & levamisole- stimulates T cells and macrophages in immune deficiency)

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3
Q

what is an immunoadjuvant?

A

most effective when used in combination with antigen administration

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4
Q

what is an immunosuppressant?

A

substances which have the ability to attenuate the immune response (ex- azathioprine, glucocorticoids, antilymphocyte globulin, cyclosporine)

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5
Q

naturally acquired active immunity

A

antigens enter the body naturally, body induces antibodies and specialized lymphocytes

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6
Q

artificially acquired active immunity

A
  • intentional administration of immunogens (vaccine) to develop an immune response
  • ex) live virus vaccines- attenuated or weakened form of a virus such as measles, mumps, and rubella (MMR) vaccine or the varicella vaccines
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7
Q

naturally acquired passive immunity

A

-maternal transfer of IgG to fetus in utero or via nursing

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8
Q

artificially acquired passive immunity

A
  • transfer of immunoglobulins from another host by intentional administration to prevent or treat disease
    ex) tetanus, rho-gram
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9
Q

What is measles?

A
  • a serious respiratory disease caused by measles virus manifested by a rash and fever, very contagious (4 days prior to rash and 4 days after rash)
  • spread by coughing and sneezing
  • symptoms usually appear about 10-12 days after exposure to measles
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10
Q

What are symptoms of measles?

A
  • early symptoms are often: high fever, cough, runny nose, red watery eyes, rash
  • small red spots and some slightly raised
  • spots and bumps in tight clusters give a splotchy red appearance
  • rash often appears 2-4 days after the fever, may last 5-6 days
  • begins at the hairline, moves to the face & neck, down the body, then arms and legs
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11
Q

what are koplik spots?

A

-blue-white spots on the inside of the mouth that occur 24-28 hours before the rash stage

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12
Q

What is Tetanus?

A

-characterized by muscle spasms and back muscle spasms which start in the jaw and progress to other body parts with addiotnal symptoms of fever, sweating, headaches, urinary retention, tachycardia, hypertension and impaired swallowing

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13
Q

How is tetanus caused?

A
  • caused by spores from the bacteria, Clostridium tetani, found in soil, dust and animal feces. Spores enter a deep flesh wound and can produce a serious toxin, tetanospasmin
  • it is NOT contagious
  • vaccination can reduce this disease, high mortality rates seen in unvaccinated people
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14
Q

DTAP

A
  • DtaP for all children less than 7 years of age
  • the ideal DTaP immunization schedule for children is at 2, 4, and 6 months with an additional dose at 15 to 18 months
  • a booster DTaP vaccine for children ages 4 to 6 years
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15
Q

Tdap

A

-helps protect against tetanus, diptheria, and whooping cough in preteen children and adults

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16
Q

Td

A

-older children & adults need to get a Td booster shot every 10 years to stay protected

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17
Q

what are cytokines?

A

-soluble mediators of immune response secreted by various cells and affect the activity of other cells or the secreting cells

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18
Q

examples of pro-inflammatory

A

-IL-1. TNF, Colony Stimulating factors (CSF)

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19
Q

examples of regulatory cells

A
  • interleukins (IL-1. IL-2, IL-4, IL-6, Il-12

- tumor necrosis factor: TNF-alpha, TNF-beta

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20
Q

examples of hematopoietic growth factors

A
  • granulocyte & granulocyte-monocyte CSF
  • erythropoietin
  • IL-3 multi-lineage CSF
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21
Q

macrophages, fibroblasts, endothelial cells

A

-activation of T- and B-lymphocytes, hematopoietic growth factor, and induction of inflammatory events

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22
Q

CD4+ T-lymphs

A

-activation of T-lymphs, B-lymphs, and NK cells

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23
Q

CD4+ T-lymph, mast cells, basophils, eosinophils

A

-B & T lymph growth factor, activation of macrophages, promotes IgE production, proliferation of bone marrow precursors

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24
Q

CD4+ T-lymph, macrophages, mast cells, fibroblasts

A

-T & B lymph growth factor, hematopoietic growth factor, augments inflammation

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25
Q

what are the roles of macrophages, NK cells, T-lymphs, B-lymphs, mast cells

A

-activation of neutrophils, endothelial cells, lymph and liver cells to produce acute phase proteins

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26
Q

what is the role of T-llymphs?

A

tumoricidal

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27
Q

what is the role of monocytes?

A

antiviral, activation of NK cells and macrophages, up regulation of MHC class I

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28
Q

what is the role of T-lymph, NK cells?

A

activation of macrophages, NK cells, up regulation of MHC class I

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29
Q

Granulocyte-CSF (Filgrastim)

A

stimulates proliferation of neutrophils

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30
Q

Granulocyte-Monocyte CSF or Sargramostim (Leukine)

A

promotes leukopoiesis (WBC)

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31
Q

Interleukin-2: Aldesleukin (Proleukin)

A

anti-neoplastic & immunomodulator

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32
Q

Erythropoietin & Darbepoetin alfa

A

stimulates erythropoiesis

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33
Q

Interferon-beta 1a & interferon beta 1b

A

fibroblast interferon

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34
Q

what are exogenous growth factors?

A

-substances that stimulate hematopoietic precursors: uses recombinant DNA

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35
Q

Granulocyte-monocyte colony stimulating factors - Sargramostim (Leukine)

A

-human GM-CSF exhibits a dose-dependent increase in the production of neutrophils and monocytes; may improve neutrophil and monocyte function
Indications: to treat myelosuppressive chemotherapy syndromes, HIV disease, chemotherapy-induced neutropenia

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36
Q

Sargramostim adverse effects

A

fever, diarrhea, nausea, vomiting, malaise, weakness, headache & chills

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37
Q

Filgrastim (Neupagen) or Pegfilgrastim (Neulasta)

A

affects primarily neutrophils

  • drug of choice to increase neutrophils
  • used to treat chemotherapy-induced neutropenia, bone marrow transplatation, myelodysplastic syndrome, HIV disease
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38
Q

Filgrastim (Neupagen) or Pegfilgrastim (Neulasta) Adverse effects

A

bone pain, nausea, vomiting, marked leukocytosis, increase uric acid, hypersensitivity reactions

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39
Q

what are the actions of IFN-alpha?

A
  • antiviral effect
  • growth inhibitor effect on normal and malignant cells
  • immunomodulation enhanced NK cell activity, enhanced cytotoxicity of T cells, phagocytosis of macrophages
  • multiple disease indications
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40
Q

Peginterferon alfa-2a & 2b

A
  • pegylated recombinant human interferon: inducer of innate antiviral immune response and inhibits viral replication of virus infected cells
  • suppresses cell cycle progression and proliferation; induces apoptosis and anti-angiogenic actions
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41
Q

Peginterferon alfa-2a & 2b adverse effects

A

bone pain, myalgia, HAQ, fatigue, fever, neutropenia & specific disease response parameters

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42
Q

what are antibodies?

A

humoral immune response produce antibodies from specific mature B cells called plasma cells that are sensitized to a specific AG epitope

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43
Q

what can endogenous antibodies do?

A
  • activate complement
  • facilitate opsonization
  • directly neutralize virus or toxin
  • AB dependent cytotoxicity of cell
  • Direct antimicrobial action generate oxidants
  • reduce damage of inflammation to host
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44
Q

what are polyclonal antibodies?

A
  • immune response to AG are heterogenous with different B cell lines that are sensitized to the different epitopes and then produce different ABs to same AG
  • an example of artificially acquired passive immunity - transfer of immunoglobulins made in one host (specific animal) to a patient thru intentional administration to prevent or treat disease
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45
Q

What is Intravenous Immunoglobulin (IV IG)?

A
  • an IV blood product containing at least 90% of pooled IgG AB harvested from at least 1000 pts (polyclonal formulation)
  • products = Gammagard S/D, Gamunex, Ocagam
  • approved for primary immunodeficiency, idiopathic thrombcytopenia purpura (ITP), off label use: neonatal sepsis, autoimmune disease, acute infections
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46
Q

what are the AEs of IV immunoglobulin?

A
  • myalgia, arthralgia, N/V

* do not interchange IV IG with IM IG*

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47
Q

what are monoclonal antibodies?

A
  • immunoglobulin sequences that recognizes a specific AG or proteins
  • b cells produces and secretes. specific antibody to specific AG
  • clones of B cells produces identical AB or monoclonal AB
  • hybridoma technology has overcome survival of single monoclonal cells –> most common type of MoAB is the IgG
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48
Q

what can monoclonal antibodies target?

A
  • surface AG and cause cell death

- target growth factor receptors

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49
Q

what are some limitations of monoclonal antibodies?

A
  • limited production of MoAb
  • antigenic modulation
  • chronic impact as DRUGS on immune system: infections & cancer
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50
Q

What is human Anti-mouse Antibodies (HAMAS)?

A
  • hypersensitivity & infusion reactions
  • greatest with mice source
  • careful monitoring with murine vs. human MoABs
  • premedication prior to infusions
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51
Q

what is primary (congenital) Immunodeficiency?

A
  • diagnosed in an infant/toddler
  • genetic defects resulting in impaired maturation or function of immune system components
    ex: severe combined immunodeficiency (SCID): deficits in T or B cells
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52
Q

what is secondary (acquired) immunodeficiency?

A
  • non-genetic and acquired over lifetime
  • -> in developed countries, the causes are cancer, anti-neoplastic therapy, irradiation, immunosuppression therapy
  • related to environment, advanced age, concurrent chronic diseases
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53
Q

how can functional assessment of cell mediated immunity of T lymphocytes be deterimed?

A

via intradermal. administration of common recall AG (candida albicans, mumps, tuberculin, trichophyton

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54
Q

what is anergy?

A

-if NO response to skin tests

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55
Q

what is total immunoglobulins Ig measure?

A
  • measure of B cell function by serum protein electrophoresis within 5 fractions
  • used for primary or secondary immunodeficiencies
  • gamma-globulin fraction of SPEP contains IgG, IgM, IgA, IgE, IgD
  • **active infections produce IgM, later or memory AG producing IgG-hepatitis
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56
Q

What is autoimmune disease?

A

-diseases caused by the body’s immune system initiating an immune reaction against self-antigens or auto-antigens

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57
Q

what is immunologic tolerance?

A

-a state in which an individual is incapable of developing an immune response to a specific antigen

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58
Q

what is self tolerance?

A
  • lack of responsiveness to an individuals own body “antigen”
  • self tolerance underlies our ability to live in harmony with our own cells and tissues
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59
Q

Autoimmune-Systemic Lupus Erythematosus (SLE)

A
  • systemic autoimmune disorder characterized by a large number of autoantibodies targeted again the nucleic acid, erythrocytes, coagulation proteins, lymphocytes, platelets
  • incidence found primarily in women - 10:1
  • chronic and acute inflammation ongoing
60
Q

immune actions of TNF-alpha

A
  • has a central role in inflammatory response by increasing tissue adhesion molecules and stimulation of pro-inflammatory cytokines & prostaglandins
  • these endogenous mediators continue acute & chronic inflammation
61
Q

Cytokine surface receptors

A

-found on target cells: interact with cytokines to augment immune activity

62
Q

Soluble Cytokine Receptors

A

-interact with targeted cytokines and augments OR suppresses cytokine activity (influence inflammatory action)

63
Q

what is an allergy?

A

immunologic responses to environmental or endogenous antigens that can result in disease (or hypersensitivity) and be clinically harmful

64
Q

what is autoimmunity?

A
  • disturbances in immunologic tolerance with response to auto-antigens
  • -> immune system of host often ignores auto-antigens
65
Q

what is alloimmunity?

A
  • immune system of host mounts an immunologic response to tissue of another individual
  • -> transplantation or transfusion reactions
66
Q

What are clinical features of allergic drug reactions?

A
  • no correlation with known pharmacological properties of the drug
  • requires an induction period on primary exposure but not on administration (will not happen with first exposure)
  • occurs with doses FAR BELOW therapeutic range
67
Q

what are the symptoms of allergic reactions?

A
  • rash, angioedema, serum sickness syndrome, anaphylaxis and asthma
  • occurs in small proportion of the population
  • *disappears on cessation of therapy and reappears after re-adminstration of a small dose of the suspected drugs of similar chemical structure
  • desensitization may be possible
68
Q

What are some predisposing factors to hypersensitivity reactions?

A
  • age & gender: females > males, children < adults
  • genetics: pts with hx of asthma, allergic rhinitis or atopic dermatitis may develop drug allergies that are more severe
  • associated illnesses: AIDs, Mono, lymphocytic leukemia demonstrate a higher incidence. of allergic reaction to certain drugs
  • previous drug exposure
  • drug related factors: dose, frequency of exposure, route of administration (topical has greatest risk of sensitization)
69
Q

what does hypersensitivity onset depend on? (4 factors)

A

-original immunologic insult/injury
-hosts genetics
-specific type of immunologic reaction (chronic vs acute)
-hosts risk factors:
A. primary immunodeficiency: genetic abnormality
B. secondary immunodeficiency: immunosuppressive therapy, irradiation, chronic diseases, malnutrition

70
Q

What are the drugs that are most commonly associated with allergic reaction?

A
  • beta lactam antimicrobial agents
  • aspirin and NSAIDs: 9-20% of asthmatics are sensitive to these
  • sulfonamide drugs: usually delayed hypersensitivity, cotrimoxazole & HIV
  • pharmaceutical additives: azo dyes, sulfites, parabens
  • cancer chemotherapy agents: L-asparaginase, monoclonal antibodies, immunoglobulin
71
Q

what is type 1 hypersensitivity?

A
  • immediate allergy or anaphylaxis

- a rapidly developing immunologic reaction mediated by IgE antibody release following subsequent exposure to antigen

72
Q

What is anaphylaxis?

A

-a form of type 1 hypersensitivity reaction that is life threatening manifested by respiratory depression, laryngeal edema, hypotension, and cardiovascular collapse.

73
Q

What are the steps of Immediate type 1 hypersensitivity?

A

1) first exposure to AG
2) sensitized B lymphocytes are activated, specific plasma cells form & produce IgE AB, AB binds to mast cells
3) on second exposure to AG, cross linking occurs on mast cell with degranulation = you are going to have vasodilation, increased capillary permeability, airway constriction, mucus secretion, pain & itching = needs IMMEDIATE evaluation

74
Q

Type 1 hypersensitivity primary mediators

A

-histamine, chemotactic factors (eosinophil, neutrophil), proleases

75
Q

Type 1 hypersensitivity secondary mediators

A

leukotrienes B4, C4, D4 & prostaglandin D2

76
Q

What are anaphylaxis symptoms & mechanisms?

A
  • severe anaphylaxis: cardiovascular and/or severe respiratory symptoms
  • symptoms onset is rapid after exposure to allergen- may occur within 30 minutes & up to 2 hours after allergen exposure fatality is greatest in the first few hours
  • -> usually due to asphyxia due to airway obstruction
  • needs observation for up to 12 hours after recognized allergen exposure due to “late-phase” reactions
77
Q

what are atopic allergies?

A
  • genetic tendency to develop allergic disease
  • it includes atopy (heightened immune responses to common allergins such as asthma & allergic rhinitis, reactions to food, specific drugs, insect venom
78
Q

Anaphylaxis must include 1 of 3 criteria:

A

1- acute onset of symptoms in with involvement of skin &/or mucosa –> generalized hives, flushing/pruritus, swollen tongue, lips, uvula & at least one of the following: respiratory compromise dyspnea stridor, wheezing, bronchospasm, reduced blood pressure or end organ dysfunction
2- two or more of the following that occur rapidly after exposure: involvement of skin &/or mucosa, respiratory compromise, reduced blood pressure & persistent GI symptoms
3- reduced blood pressure after allergen exposure

79
Q

Treatment of anaphylaxis (none drug)

A
  • emergency treatment to restore respiration & circulation to minimize risk of death - maintain airway
  • stop offending agent (if able to be identified)
  • place patient in recumbent position: assess airway, circulation –> elevate legs above head, call 911 or EMS or resuscitation team
80
Q

Drug treatment of anaphylaxis

A

-epinephrine 1:1000 IM or SQ & repeated every 15 to 20 minutes (primary treatment in lateral aspect of thigh) to counteract bronchoconstriction & vasodilation

81
Q

What are the different types of auto-injectors/epi-pens that are used to treat anaphylaxis?

A
  • epi pen to deliver 0.3mg/injection or epi 5mg VS

- AUVI-Q (Kaleo) dose for children based upon weight of 15 kg (0.015mg) or >30kg (0.030mg)

82
Q

What do you do if there is epinephrine resistant bronchospasm?

A

have to be in ER!
1- treat with oxygen therapy (8-10 L/min)
2- administer 25-50mg of diphenhydramine (parenteral)
3- late phase –> plus anti-H2 receptor blocker (ranitidine)
4- if hypotension, give IV fluids or colloid replacement
5- give IV hydrocortisone sodium succinate (5mg/kg) or 250mg (or 20 mg po prednisone for mild cases) to reduce recurrence risk = treat late phase manifestations

83
Q

How does penicillin cause an anaphylactic/type 1 hypersensitivity?

A
  • anaphylactic reactions characterized by urticarial eruptions & angioedema
  • if no alternative to PCN for therapy & high suspicion of allergy to PCN, then patient may undergo skin testing
84
Q

what is penicillin and cephalosporin cross reactivity?

A
  • many patients with PCN allergy show cross-reactivity. to beta-lactam antibodies with unknown incidence
  • most allergists will NOT administer cephalosporins to patients with hx of immediate hypersensitivity reaction
  • cross sensitivity is due to similarities in R1 side chains
85
Q

what is desensitization in regards to type 1 hypersensitivity reactions?

A
  • to be used in a patient with documented drug allergy that requires treatment with that specific drug - when theres no alternative available
  • process may reduce the the risk of anaphylaxis but NOT risk of other hypersensitivity reactions
86
Q

what is tissue specific hypersensitivity (type 2)?

A

-AG on target cell bind directly with AB (IgG & IgM) resulting in cellular destruction or function reduction

87
Q

what is complement mediated lysis?

A

AG attacks target cell, AB reacts with the AG present on the cell surface

  • AB-AG interaction activates complement system resulting in direct membrane damage
    ex) ABO mismatched transfusion reaction or RBC destroyed by autoimmune hemolytic anemia
88
Q

what is macrophage mediated phagocytosis?

A
  • cell destruction by macrophages once IgG & C3 opsonize target cell
    ex) erythroblastosis fetalis or hemolytic anemia of newborn (Rh incompatibility between mother and infant)
89
Q

what is neutrophil-mediated immune destruction?

A

-the AB coated cells are phagocytized by neutrophils after complement activated for chemotaxis

90
Q

what is antibody-dependent cytotoxic hypersensitivity?

A

-involves the natural killer cells & NOT AG specific. The AB on target cell recognizes Fc receptors on NK cells & release of granzymes and perforin result causing cell death

91
Q

what is malfunction of target cells?

A
  • does not destroy the cell
  • usually AB blocks the cellular receptor from completing specific physiological function: autoimmune disorder results
    ex) graves disease
92
Q

what is serum sickness?

A
  • generalized reaction
  • fever, swollen lymph nodes, arthralgias, dermatitis, vasculitis at 5 to 10 days after exposure to AG
  • often associated with antibody therapies: vaccines
93
Q

what is arthus reaction?

A
  • may be localized to an organ, joints, small blood vessels or skin
  • treatment = removal of the AG
94
Q

Drug induced lupus (type 3)

A
  • milder & more rare than SLE
  • symptoms: arthralgia, fever, malaise, myalgia, minimal organ involvement
  • see elevated ANA titer, SS-DNA & ESR
95
Q

what drugs are known to cause drug induced lupus?

A
  • slow acetylators: hydralazine, procainamide, Isoniazid, Quinidine
  • TNF-alpha inhibitors: Infliximab, etanercept, adalimumab
96
Q

Agents that are known to cause serum sickness:

A
  • animal serums
  • bee venom injections
  • cefaclor
  • Ciprofloxacin
  • Insulin (from animal sources)
  • Iron dextran
  • IV immunoglobulin
  • monoclonal antibodies
  • penicillins
  • sulfonamides
97
Q

what is cell mediated hypersensitivity?

A
  • type 4 a-d
  • the delayed hypersensitivity results when. an individual is re-exposed to an antigen
  • cell death results from cytotoxic T lymphocytes, associated cytokines and recruitment of macrophages
98
Q

what is contact dermatitis (type 4)?

A

-caused by cosmetics, drugs, clothes dye, foods, rubber, latex, poison ivy/mango
-signs: burning or stinging with erythema, swelling, peeling, blisters with oozing and crusting, itching,
**if in mouth or eyes = GO TO ER
diagnosed by: patch test for 48, 72 & 96 hrs with scores to identify response to allergen

99
Q

What is the treatment for contact dermatitis (drug vs homeo)

A
  • topical steroids
  • antihistamine: oral for sedation/sleep, avoid topical
  • topical immunomodulators: tacrolimus
  • systemic steroids- oral or parenteral
  • cold compress for acute sxs
  • calamine for oozing lesions
  • mild soaps
  • avoid known triggers and wash skin
100
Q

what is anergy?

A

absence of cell mediated immune response

101
Q

definitions of SJS and TEN (type 4 C)

A

SJS: <10% of body
TEN: >30% of body
SJS/TEN: 15-30% of body

102
Q

Clinical presentations of SJS & TEN:

A

macules rapidly spread and coalesce, leading to epidermal blistering, necrosis and sloughing

  • incidence is higher in bone marrow transplant recipients, HIV pts, pts with SLE and chronic rheumatologic diseases
  • middle age women & older are at higher risk
103
Q

What. drugs have been associated with SJS or TEN?

A
  • sulfa drugs (cotrimoxazole, sulfasalazine)
  • other antibiotics (aminopenicillins, fluoroquinolones, cephalosporins)
  • anti-epileptics ( phenytoin, carbamazepine, phenobarbital, valproate, lamotrigine)
  • others: piroxicam, allopurinol, chlomezanone
104
Q

Non-pharm associations with SJS or TEN:

A
  • infection
  • viral (herpes, HIV, Mumps)
  • vaccinations
  • graft vs host disease
  • drug hx and infection hx are essential
105
Q

Symptoms of SJS/TEN

A

-sore throat, fever, fatigue, burning eyes for 1-3 days
-rash or lesions on face, arm, trunk, legs, soles & develop blisters & erosions of confluent macules
=emergency!

106
Q

Acute generalized Exanthematous Pustulosis (AGEP)- type 4D

A
  • rare but severe reaction that occurs after drug admin or infection
  • characterized by rapid appearance of 100s-1000s of small nonfollicular subepidermal & intraepidermal sterile pustules with a background of erythemis
  • may begin on face or intertriginous areas up to 3 weeks after drug exposure
107
Q

AGEP frequent drug causes:

A
  • aminopenicilins, sulphonamides, quinolones, hydroxychloroquine, terbinafin & diltiazem
  • bacterial/viral/parasitic infections are less frequent associations
108
Q

what allergic-like reaction occurs with anticonvulsants?

A
  • drug reaction with eosinophillia & systemic symptoms

- delayed onset 3 - 8 weeks

109
Q

NSAID sensitive reactions

A
  • occur in asthmatics
  • develops in middle age, NO hx os ASA intolerance
  • presentation: rhinitis & processes to sinusitis w/nasal polyps, steroid dependent asthma can develop
110
Q

Drug induced fever

A

-often associated with hypersensitivity reaction but may be due to pharmacologic action of drug

111
Q

what is an IR Tacrolimus formulation?

A
  • Prograf

* *do not substitute with other TAC IR generics

112
Q

What are the 3 ER Tacrolimus formulations?

A
  • Astagrof XL
  • Envarsus
  • IV Prograf
113
Q

Astagrof XL

A

(TAC)

  • polymer
  • 1 mg ER = 1 mg IR
  • *not interchangeable with TAC IR
  • troughs may be lower than IR
114
Q

Envarsus

A
  • molecular drug with continuous dosing
  • 70% of IR daily dose
  • *not interchangeable with TAC IR or Astagraf
115
Q

IV Prograf

A

(TAC)

  • in castor oil
  • continuous infusion over 24 hours –> only stable for 24 hours
  • *anaphylaxis may occur, short term use
  • keep it in glass
116
Q

What are cycclosporine formulations? (4)

A
  • Neoral
  • Gengrof
  • Sandimmune
  • Sandimmue IV
117
Q

Neoral

A
  • CYA
  • BID with trough monitoring
  • may dilute modified CYA solution in apple and orange juice only
118
Q

Gengraf

A
  • CYA
  • emulsion capsules & modified emulsion solution
  • Bioequivalent to Neoral!
119
Q

Sandimmune

A

-CYA
-castor oil capsules & can flocculate or gel below 20C
-not bioequivalent or interchangeable
-QD dosing
-erratic bioavailability
may dilute with milk or OJ

120
Q

Sandimmune IV

A
  • CYA
  • anaphylaxis may occur - short term use
  • reserved for patients unable to tolerate oral route
  • discard after 24 hours
121
Q

adverse effects for cyclosporines

A
  • hyperlipidemia
  • nephrotoxicity
  • tremor, headache
  • hypertension
  • hyperglycemia
  • gingival hyperplasia
  • hirsutism
  • diarrhea, vomiting
122
Q

adverse effects from tacrolimus

A
  • diarrhea, nausea
  • nephrotoxicity
  • tremor, headache
  • insomnia
  • hyperglycemia
  • hyperlipidemia
  • hypertension
123
Q

CNI drug interactions: Inhibition of P450 & P-gp - higher troughs and AUC

A
  • CCBs: diltiazem, verapamil
  • Anti fungal: ketoconazole
  • antibiotics: erythromycin
  • protease inhibitors: indinavir, ritonavir
  • gastric acid suppressors: omeprazole
  • grapefruit juice
124
Q

CNI drug interactions: Induction of P450 & P-gp - lower troughs and AUC

A
  • antibiotics: rifampin
  • anti fungal: casofungin
  • anticonvulsants: carbamazepine, phenytoin
  • St johns wart
125
Q

TDM for CNIs

A
  • both CYA & TAC demonstrate linear kinetics
  • frequent monitoring of CNI troughs with renal function during early post transplant period
  • verify time of last dose, drug formulation and dosage regimen
126
Q

Mycophenolic acid (2)

A
  • mycophenolate Mofetil (cellcept)
  • mycophenolic acid sodium (myfortic)
  • this drug is useful to prevent proliferation of the committed T cells.
  • inhibits purine synthesis & prevents lymphocyte development
127
Q

Cellcept vs Myfolic acid dose conversion

A

1000 mg = 720 mg

128
Q

Mycophenolic acid Drug-Drug interactions

A
  • renal elimination: acyclovir & co-trimoxazole
  • combined oral contraceptives
  • alterations in drug binding to albumin
  • cyclosporine inhibits MRP2 transporter
129
Q

Mycophenolic acid adverse effects

A
  • *GI: N/V, diarrhea –> chronic symptoms
  • leukopenia, neutropenia, anemia, thrombocytopenia
  • *as renal function declines, adjust the MPA regimen to lower dose with longer interval based upon pts ADE response
130
Q

Glucocorticoid therapy drugs and doses: short acting agents

A
  • cortisone: 25 mg

- hydrocortisone: 20mg

131
Q

Glucocorticoid therapy drugs and doses: intermediate acting agents

A
  • prednisone: 5mg
  • prednisolone: 5mg
  • methylprednisolone: 4mg
132
Q

Glucocorticoid therapy drugs and doses: long acting agents

A

dexamathasone: 0.75 mg

133
Q

Principles for Glucocorticoid use

A
  • maintenance: lowest dose for shortest duration
  • single AM dose
  • taper schedule
134
Q

Drug-Drug interactions: inhibition of glucocorticoids

A
  • oral contraceptives
  • conjugated estrogens
  • macrolide antibiotics
  • enhance hypokalemia
135
Q

Drug-Drug interactions: induction of glucocorticoids

A
  • phenytoin
  • rifampin
  • tacrolimus
  • cyclosporin
  • mycophenolic acid
  • anti acids
136
Q

Adverse effects of glucocorticoids

A
  • axillary & lower abdominal striae
  • ecchymoses
  • steroid induced avascular necrosis
137
Q

what are some post transplant complications?

A
  • hypertension
  • opportunistic infection
  • diabetes
  • hyperlipidemia
  • osteoporosis
  • lymphoproliferative disorder
138
Q

what is induction therapy?

A
  • block T cell activation or other immunologic activation at the time of graft placement
  • avoid use of full dose CYA or TAC in the immediate post transplant period
  • target HIGH RISK pts
139
Q

what are advantages & disadvantages of induction immunosuppression?

A

advantage: may improve early graft function, may prevent graft rejection & improve graft survival
disadvantage: may increase costs & risk of cytomegalovirus infection & post transplantation lymphoproliferative disease

140
Q

what are the general steps of med intro for induction immunosuppression?

A

1) ONE induction agent: thymoglobulin or Alemtuzamab
2) mycophenolate mofetil or Azathioprine
3) methylprednisolone or prednisone –> at high doses with rapid tapering
4) followed by delayed use or low doses of calcinruein inhibitors such as either cyclosporin or tacrolimus

141
Q

Anti-thymocyte Globullin (ATG)

A
  • used in high risk depleting induction
  • these antibodies coat the hosts T-cells in the blood & are then destroyed by the complement system
  • admin IV infusion of 4-6 hours for 2-4 daily doses
142
Q

Anti-thymocyte Globulin adverse effects

A
  • flu like syndrome- fevers, chills, nausea, vomiting on first dose due to cytokine release syndrome –> premeditate with diphenhydramine and APAP
  • long term: leukopenia, lymphopenia, thrombocytopenia, erythema
  • serum sickness as a result of exposure
143
Q

Alemtuzumab Monoclonal AB (Campth)

A
  • use for HIGH risk only
  • acts directly against the CD52 surface AG expressed on all lymphocytes, NK cells, macrophages, monocytes and eosinophils
144
Q

KEY things to know about Alemtuzumab

A
  • 2 doses of .3mg/kg/dose OR 20-30mg IV as a single dose over 2-3 hours
  • premedication: each dose is proceeded by IV methylprednisolone 30 mins before infusion
  • anti-infective prophylaxis for at least 2 months after D/c
  • either dosing regimen results in prolonged lymphocyte depletion
145
Q

Alemtuzumab adverse effects

A
  • HAMA reaction with initial treatment –> pretreatment is required
  • profound lymphopenia
  • thrombocytopenia
  • increased risk of malignancy, infection or autoimmune reactions
146
Q

Non-depleting induction: Basiliximab (Simulect)

A
  • used for LOW risk patients
  • will prevent activated T lymphocyte proliferation since the IL-2 receptor will be resistant to IL-2 stimulation
  • minimal adverse effects
147
Q

what is Benlysta?

A

1st drug that has been directed to the B cell receptor to be able to cause B cell depletion as a therapeutic approach for SLE patients

ID Therapeutics :') (3 decks)

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