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MBBS II HIS > L 16 - Immunosuppressive and immunomodulatory drugs > Flashcards

L 16 - Immunosuppressive and immunomodulatory drugs Flashcards

1
Q

Ig, antigen, effector mechanism of Type I hypersensitivity reaction?

A

IgE
Soluble antigen (e.g. allergen)
Mast cells and basophils

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2
Q

List allergens that cause type I hypersensitivity rxn?

A

 Skin contact: poison plants, animal scratches, pollen, latex

 Injection: bee sting

 Ingestion: medication, nuts, shellfish

 Inhalation: pollen, dust, mold, mildew (霉菌), animal dander

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3
Q

Define the 2 phases of Type I Hypersensitivity rxn?

A

Early phase: Within minutes of exposure to allergen (quick): Last 30-90 minutes

Late phase: 4-8 hours later: Last Several days: Often leads to chronic inflammatory disease

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4
Q

Reaction that forms histamine? Storage form of histamine?

A

histidine decarboxylase decarboxylates histidine

> > histamine + CO2

Stored in intracellular granules Complexed with acidic protein, heparin

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5
Q

Which locations in body has high amounts of mast cells?

A

Practically all tissues, but unevenly distributed

High in lung, skin, and the gastrointestinal tract

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6
Q

Describe the release of histamine from mast cell after stimulation?

A
  1. Binding of IgE primes the mast cell to respond to allergen.
  2. Allergen induces cross-linking of IgE and clustering of Fc receptors.
  3. Signal transduction to stimulate degranulaion.
  4. histamine released from granules
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7
Q

Type of receptors that get stimulated by histamine?

A

H1 / H2 / H3 / H4 seven transmembrane G-protein coupled receptors

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8
Q

Response of H1 receptor stimulation on BV and smooth muscles

A

1) Stimulates blood vessel dilation: decrease peripheral resistance
2. Increases capillary permeability: increase exudation and swelling
3. Contracts smooth muscle (other than blood vessel) (e.g. bronchioles)
4. Itch and pain

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9
Q

List some mild forms of Type I Hyersensitivity rxn?

A

skin: urticaria
eyes: conjunctivitis
nasopharynx: rhinitis
gastroenteritis

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10
Q

List some severe forms of Type I Hyersensitivity rxn?

A

asthma anaphylactic shock

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11
Q

Histamine can be stored in granules for pronlonged time. T or F?

A

False

if not stored = rapidly inactivated by amine oxidase

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12
Q

List 3 H1 antagonists.

A

Diphenhydramine
Hydroxyzine
Promethazine

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13
Q

List advantages and disadv. of H1- antogonists first gen.

A

Cheap, effective

  • Short duration of action
  • Penetrate blood-brain barrier = sedation, CNS impairment
  • Low specificity = more ADR
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14
Q

List ADRs of gen 1 H1-antagonist?

A

Not very specific: binds to other receptors

  • sedation, CNS impairment (**Gen 1 esp.)
  • Anticholinergic: dry mouth, urinary retention, blurred vision
  • Antiadrenergic: dizziness, hypotension, reflex tachycardia
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15
Q

Which allergic symptoms are relieved by Diphenhydramine ?

A

allergic rhinitis: sneezing, runny nose, itching, watery eyes

itching, allergic skin reaction

Controls coughs due to cold / allergy

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16
Q

Advantages of gen 2 H1-antagonist over gen 1?

A

1) Poor penetration into CNS system = less CNS toxicity, sedation
2) More specific/selective for peripheral H1 receptors = no/little anticholinergic / antiadrenergic side effects
3) Rapid onset
4) Longer duration of action

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17
Q

List 3 gen 2 H1 blocker?

A

Cetirizine
Fexofenadine
Loratadine

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18
Q

Explain why fexofenadine has less ADR than Gen 1 H1 blocker?

A

1) Bulky groups eliminate anticholinergic, antiadrenergic effects = increase specificity
2) Cannot cross blood-brain barrier (note the polar COOH, OH) = hydrophilicity

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19
Q

List the 3 therapeutic uses for antihistamines?

A
  1. Allergic, inflammatory conditions: allergic rhinitis, urticaria, cold or allergy
  2. Motion sickness, nausea (prophylaxis)
  3. Somnifacients (inducing sleep): insomnia
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20
Q

How does H1 blocker reduce motion sickness?

A

Block central H1 and muscarinic receptors at cerebellum&raquo_space; block activation of vomiting centre in Area Postrema of Medulla oblongata

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21
Q

D/D interactions of H1 blocker?

A

 All CNS depressants (potentiated effects)

 Monoamine oxidase (MAO) inhibitors (increased side effects)

 Cholinesterase inhibitors (decreased effectiveness in treating Alzheimer’s disease)

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22
Q

OD effects of H1 blocker?

A

CNS: hallucinations, excitement, ataxia, convulsions

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23
Q

List some indications for immunosuppressants? (think ERS, Neruo, MSS, HIS all have some autoimmune diseases)

A

1) Allograft rejection*****

2) Autoimmune diseases
•DM type 1
•MS
•Rheumatoid arthritis 
•Autoimmune hemolytic anemias 
•Idiopathic thrombocytopenia purpurea(ITP) 
•Acute glomerulonephritis 
•SLE
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24
Q

Describe the 3 signals between APC and T cells during induction phase?

A
  1. Signal 1 – MHC + TCR (CD3 receptor complex)
  2. Signal 2 – CD80/86 or B7 on APC + CD28 on T-cells
  3. Signal 3 – CD40/CD40L and ICAM-1/LFA-1 interactions enhance activation

Cytokines (e.g. IL-2 + CD25) stimulate T-cell proliferation

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25
Describe the 3 responses in effector phase of APC- T cell response?
Cytokine production Induce Cytotoxic effects Induce Antibody production
26
Describe the intracellular activation of T-cells via IL-2 ***
1) Activated T cell > increase intracellular Ca2+ 2) Activate calcineurin > dephophorylate and activate NFATc (Nuclear Factor of Activated T cells) 3) NFATc moves into nucleus > increase transcription of IL-2 4) IL-2 released > binds to CD25 (autocrine) > activate mTOR 5) mTOR cause clonal expansion
27
List 2 classes of microbial product** immunosuppresants and give 2 examples each
1. Calcineurin inhibitors ◦Cyclosporine ◦Tacrolimus | 2. mTOR inhibitors ◦Sirolimus ◦Everolimus
28
Preparation and indication of CsA?
IV or oral (poor) +/- corticosteroids and antimetabolites first-line therapy in the prophylaxis treatment of transplant rejection Treat unresponsive severe autoimmune diseases
29
MoA of CsA?
1. binds to a cytoplasmic receptor protein called cyclophilin (CpN) 2. inhibits calcineurin (CaN) phosphatase 3. prevents activation of nuclear factor (NFATc) 4. inhibits synthesis of IL2,
30
Metabolism of CsA?
metabolized by the CYP3A system Affect CYP450 = D/D rxn
31
ADR of CsA?
Nephrotoxicity *** Opportunistic infections Lymphoma *** (others: hypertension, hyperkalemia, tremor, hirsutism ...etc)
32
Preparation and indication of Tacrolimus?
prevention of rejection of solid organ +/- corticosteroids and/or an antimetabolite
33
MoA of Tacrolimus?
1. binds to FKBP 2. inhibits calcineurin phosphatase 3. prevents activation of nuclear factors 4. inhibits synthesis of IL-2 in T-cells
34
ADR of Tacrolimus?
nephrotoxicity and neurotoxicity (tremor, seizure, hallucination)*** Post-transplant, Insulin-dependent DM
35
Tacrolimus and CsA can be given together. T or F?
False share a mechanism of action and metabolic route >> never given together (additive nephrotoxicity)
36
Preparation and indication of Sirolimus/ Rapamycin
Triple: Sirolimus + Tacrolimus(/CsA) + Corticosteroids kidney / heart transplantation
37
MoA of Sirolimus?
Binds to cytoplasmic FKBP >> interferes with mTOR signal (= serine-threonine kinase controlling T cell proliferation) >> inhibits translation of mRNAs that promote transition from G1 to S phase of cell cycle >> T cells arrest in G1 phase (unresponsive to IL-2 stimulus)
38
Metabolism and ADR of Sirolimus?
Oral, Liver metabolism hyperlipidemia***, hypertension, leukopenia, thrombocytopenia infection
39
D/D rxn of Sirolimus?
aggravates cyclosporine-induced renal dysfunction cyclosporine increases sirolimus-induced hyperlipidemia
40
List 4 Antimetabolites and Cytotoxic agents?
Azathioprine Mycophenolate mofetil Cyclophosphamide Methotrexate
41
MoA of Azathioprine?
Prodrug: converted to 6-mercaptopurine >> 6-thioinosinic acid blocks the de novo purine synthesis for lymphocyte proliferation
42
Preparation and indication of Azathioprine?
Triple: Azathioprine + CsA/ Tacrolimus + Corticosteroids Haemolytic anemia, kidney transplantation and autoimmune disorders: Crohn's, GN
43
ADR and D/D interactions of Azothioprine?
MAJOR ADR = MYELOSUPPRESSION*** especially for subjects with defective TPMT Other: increased risk of cancer, and GI irritation D/D: Allopurinol, Xanthine oxidase cause accumulation
44
Preparation and indication of Mycophenolate mofetil?
Triple: Mycopehnolate mofetil + CsA/ Tacrolimus + Corticosteroids sole agent for heart, kidney, and liver transplants
45
MoA of Mycophenolate mofetil?
GI: hydrolyze to mycophenolic acid (MPA) >> inhibit inosine monophosphate dehydrogenase (IMP Dehydrogenase ) >> blocking de novo formation of guanosine phosphate, lymphocytes cannot divide
46
ADR of Mycophenolate mofetil?
diarrhea, nausea, vomiting, abdominal pain, leukopenia, and anemia
47
List 4 Polyclonal & Monoclonal antibodies
Antilymphocyte globulins Intravenous immunoglobulins (IVIG) IL2 receptor antagonists, daclizumab/basiliximab Alemtuzumab, Rituximab etc
48
Indication and preparation of Antilymphocyte globulins?
prevent early allograft rejection, or severe rejection episodes Used with other immunosuppressive agents
49
Metabolism and MoA, admin. of Antilymphocyte globulins?
IV | ADCC - Antibody-bound cells are depleted in liver and spleen
50
ADR of Antilymphocyte globulins
Chills and fever,and skin rashes leukopenia, thrombocytopenia, infections,
51
Difference in source between Antilymphocyte globulins and Intravenous immunoglobulins (IVIG)
Antilymphocyte globulins = prepared by immunization of rabbits / horses with human lymphoid cells IVIG = prepared from human plasma pooled from many donors
52
Indication of IVIG? MoA?
autoimmune diseases, pretransplant desensitization, and treatment of antibody-mediated rejection (AMR) Unclear MoA: B-cell apoptosis and modulate B-cell signalling
53
ADR of IVIG?
Flu-like symptoms: headache, fever, chills, myalgias hypotension/hypertension, aseptic meningitis** acute renal failure and thrombotic events**
54
MoA of IL-2 receptor antagonist? Give 2 examples?
basiliximab, daclizumab anti-CD25 antibodies >> bind to the α chain of IL-2 receptor on activated T cells >> inhibit IL-2 mediated T-cell activation and proliferation
55
Indication of IL-2 receptor antagonist?
induction therapy in transplantation decreasing the incidence of acute rejection: Prophylaxis of kidney transplantation in combination with steroids or CsA
56
Administration and ADR of IL-2 Receptor antagonist?
intravenously; very well tolerated, virtually no side effects
57
Difference in composition between Basiliximab and Daclizumab?
Basiliximab = a chimeric antibody: 25% murine & 75% human sequences Daclizumab = humanized antibody: 90% human sequences
58
MoA of cortical steroids in treating organ transplant rejection?
Inhibit cytokine production by T cells and macrophages >> inhibition of nuclear factor kappa B activation >> Bind glucocorticoid response elements in the promoter regions of cytokine genes >> disrupting T cell activation and macrophage mediated tissue injury.
59
Name 2 corticosteroids and indication in organ transplant?
prednisone or methylprednisolone acute rejection + chronic graft-versus-host disease + autoimmune disease
60
ADR of corticosteroids?
Diabetogenic, hypercholesterolemia, cataracts, osteoporosis, and hypertension, Glucose intolerance, Cushing syndrome ...etc

MBBS II HIS (30 decks)

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