Презентация на тему Antihistamine agents. Immunopharmacology

Презентация на тему Antihistamine agents. Immunopharmacology, предмет презентации: Медицина. Этот материал содержит 29 слайдов. Красочные слайды и илюстрации помогут Вам заинтересовать свою аудиторию. Для просмотра воспользуйтесь проигрывателем, если материал оказался полезным для Вас - поделитесь им с друзьями с помощью социальных кнопок и добавьте наш сайт презентаций ThePresentation.ru в закладки!

Слайды и текст этой презентации

Слайд 1
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ANTIHISTAMINE AGENTS.
IMMUNOPHARMACOLOGY

ZSMU Pharmacology Department
Lecture № 6


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Allergic Reactions on Drugs include 4 types of Hypersensitivity Reactions:

A. Humoral type:
Type I : Anaphylactic reactions
Type II : Cytolytic reactions
Type III : Retarded reactions
B. Cell mediated (Ig-mediated):
Type IV : Delayed reactions


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ANTIALLERGIC DRUGS
1. Drugs Stabilizing Mast Cell Membrane:
Glucocorticoids: Prednisolone, Hydrocortisone
Antihistamine H1 : Ketotifen
Mast cell stabilizers: Cromolyn, Nedocromil
β-adrenomimetics: Adrenaline, Ephedrine
Methylxanthines: Euphylline (Aminophylline)
2. Antihistamine H1 agents: Dimedrol, Diprazine, Loratadine
3. Agents eliminating generalized symptoms of immediate allergic reactions:
Adrenomimetics: Adrenaline
Methylxanthines: Euphylline, Theophylline
Ca2+ preparations: Calcium chloride, Calcium gluconate
4. Agents decreasing tissue damage: Glucocorticoids


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Drugs used to treat
Delayed Type Hypersensitivity Reactions:
1. Immunosuppressants –
suppressing mainly cell-mediated immunity:
Glucocorticoids,
Cyclosporin, Tacrolimus,
Cytotoxic Drugs,
Antilymphocytic serum,
Monoclonal Antibodies (Muromonab CD3), Antilymphocytic Immunoglobulin
2. Drugs decreasing tissue damage –
Glucocorticoids
NSAIDs


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H1- and H2- Receptors exert their effects by
different pathways:
Binding of an agonist to H1- Receptors =>
stimulates the intracellular activity of
the Phosphatidylinositol Pathway
Binding of an agonist to H2- Receptors =>
↑the production of cAMP by Adenyl Cyclase

Histamine promotes vasodilation by causing
vascular endothelium to release Nitric Oxide (NO),
which diffuses to the vascular smooth muscle where
it stimulates cGMP production


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H1-Receptor Antagonists
I GENERATION (SEDATIVE):
Dimedrol (Diphenhydramine)
Diprazine (Promethazine)
Suprastine (Chloropyramine)
Diazoline
Tavegyl (Clemastin)
II GENERATION (NON-SEDATIVE):
Loratadine (Claritin)
Terfenadine
Astemizole
Phencarol (Quifenadine)
III GENERATION (ACTIVE METABOLITES):
Telfast (Fexofenadine)
Zirtek (Cetirizine)


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Pharmacodynamics of antihistamine H1 blockers
▶ Block the actions of histamine by reversible competitive
antagonism at the H1-receptor
▶ Antagonist effects at other receptors:
▶ M - Cholinoceptors
▶ α1 - Adrenoreceptors
▶ 5-Hydrohytryptamine (5-HT) receptors

Diprazin ▶ Dimedrol ▶ Suprastin ▶ Diazolin



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Dimedrol (Diphenhydramine)-Tab 0.05 g, amp 1%-1 ml
competes to H1 receptors on the smooth muscle of
the bronchi, GIT, uterus, and large blood vessels.
By binding to receptors, suppresses histamine-induced allergic symptoms, even though it does not prevent its release.
Central antimuscarinic actions is responsible for antivertigo, antiemetic, and antidyskinetic action.
Clinical uses:
▶ Allergy symptoms
▶ Motion sickness
▶ Parkinson’s disease
▶ Nonproductive cough
▶ Insomnia


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Suprastine (Chloropyramine)-Tab. 0.025 g, amp. 2% - 2 ml -
H1 receptor antagonist of I generation.
It competes to histamine H1 receptor sites on the smooth muscle of the bronchi, GIT, uterus, and large blood vessels.
It has less expressed antihistamine, M-cholinoblocker and sedative effects than Dimedrol.
Clinical uses:
▶ Allergic dermatosis
▶ Allergic rhinitis
▶ Conjunctivitis
▶ Quincke’s edema
▶ Medicamental allergy
▶ Hay (pollen) fever


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Terfenadine (Claritin)-.
● blocks cardiac K+ channels, prolongs Q-T and
has occasionally produced Polymorphic Ventricular Tachycardia.
The risk is increased in liver disease or when inhibitors of CYP3A4 are administered concurrently – because larger amounts of unchanged drug reach systemic circulation.
Erythromycin, Clarithromycin, Ketoconazole and Itraconazole
are the drugs precipitating their
cardiotoxicity as they block
microsomal CYP-450 enzymes.
Because of this risk,
Terfenadine has been withdrawn
by most manufactures.
Clinical use: allergic rhinitis


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Telfast (Fexofenadine) and Zirtek (Cetirizine)
non-toxic metabolites of Terfenadine
that do not block K+ channels in the heart –
does not prolong Q-T interval.

Telfast has plasma T1/2 11-16 hours and duration of action 24 hours.


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Drugs used to treat Delayed Type Hypersensitivity Reactions:
I. IMMUNOSUPRESSANTS - suppressing mainly
cell-mediated immunity:
1.Inhibitors of IL-2 production or action:
Cyclosporine (Sandimmune)
Tacrolimus
2.Inhibitors of cytokine gene expression:
Glucocorticoids: Prednisolone
3. Antitumor Cytotoxic Agents:
a) Alkylating agents: Cyclophosphan
b) Antimetabolites: Azathioprine, Mercaptopurine, Methotrexate
4.Blockers of the T-cell surface molecules involved in signaling - Monoclonal Antibodies: Basiliximab and Daclizumab


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Clinical uses of immunosupressants:

▶ to suppress rejection of transplanted organs
▶ to suppress graft-versus-host disease
▶ to treat diseases that are believed to have autoimmune component in their pathogenesis:
● Idiopathic thrombocytopenic purpura
● Hemolytic anemia
● Glomerulonephritis
● Myasthenia gravis
● Systemic lupus erythematosus
● Rheumatoid arthritis
● Psoriasis


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Cyclosporine amp.5% - 1 ml, caps. 50 mg –
a polypeptide antibiotic with immunosuppressive activity but no effect on the acute inflammatory reaction per se.
The main action is a relatively selective inhibitory effect on IL-2 gene transcription, though an effect on
the transcription of the genes for IFN-γ and IL-3
has also been reported:
IL-2 Release and
↓ IL-2 Receptors Expression =>
↓ Clonal Proliferation of T-cells
↓ Transcription of the genes for interferon-γ
Clonal Proliferation of cytotoxic T-cells from
CD8+ precursor T-cells


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2.Glucocorticoids
Prednisolone Beclomethasone
Hydrocortisone Betamethasone
Triamcinolone Fluocinolone (Flucinar)
Dexamethasone Fluomethasone (Lorinden)

▶ Decrease Transcription of Genes for
IL-2
TNF-α
IFNγ
IL-1
and many other INTERLEUKINS in both the INDUCTION and EFFECTOR PHASES of the immune response =>
Restrain the clonal proliferation of Th cells


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3. Antitumor Cytotoxic Drugs
Cyclophosphan (Cyclophosphamide)
Tab. 0.05 g, amp. 0.2 and 0.5 g
● is cytotoxic only after generation of
its alkylating species, following
their hydroxylation by CYP-450.

▶ Exerts its cytotoxic effects by
covalently binding to nucleophylic groups
on various cell constituents
▶ Destroys proliferating lymphoid cells
but also appears to alkylate
some resting cells.


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Methotrexate – the folate analogue –
acts as a false substrate,
inhibits enzyme activity of dihydrofolate reductase =>
↓Tetrahydrofolic acid required for the synthesis of
Purine Bases and Thymidine =>
=> Synthesis of DNA and RNA building blocks ceases.
The effect of these antimetabolites can be reversed by administration of Folic acid.


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Azathioprine – Tab. 50 mg - interferes with purine synthesis.
a prodrug metabolized to give
the antimetabolite 6-mercaptopurine,
a purine analogue that inhibits DNA synthesis.
▶ Both cell-mediated and antibody-mediated
immune reactions are depressed by azathioprine since
it inhibits clonal proliferation in the induction phase of
the Immune response by a cytotoxic action on dividing cells.
Clinical uses:
Control of tissue rejection in TRANSPLANT SURGERY
Autoimmune diseases: systemic lupus erythematosus,
rheumatoid arthritis.
Adverse effects:
bone marrow depression
skin eruptions, hepatotoxicity.


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Basiliximab (Simulect) and Daclizumab -
Monoclonal Antibodies against IL-2Rα Receptors
on Th cells
They saturate the receptors and thereby:
Block T Cells Signal Transduction Events
Prevent T cells from Replication and from Activating the B cells, which are responsible for production of antibodies.


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IMMUNOMODULATING AGENTS

I. Biogenic substances:
1. Preparations of the Thymus:
Thymosin
Thymalin
Tactivine
2. Peptides:
Thymogen
3. Inductor of Interferon:
Cycloferon


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4. Interferons:
Interferon – α: amp. 1 and 3 million IU, SC
amp. 100,000 IU – intranasally
Interferon - β: IFN β-1a, IFN β-1b
Interferon - γ 1b

5. Inerleukin-2
6. BCG

II. Synthetic compounds:
Levamisol (Decaris) – Tab. 50 mg and 150 mg


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Cycloferon (amp 12.5%-2 ml, Tab 0.15 )
- low-molecular inductor of interferon
(Acridone-Acetic Acid)
▶ Immunomodulating
▶ Antiviral
▶ Antinflammatory effects
Clinical uses:
Viral Hepatitis
Herpetic and Cytomegalovirus Infections
Chlamidiosis
HIV-infection (AIDS, stage IIA-IIIB)
Immunodeficiency conditions


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Inerferon-α (Laferon) – amp. 1 and 3 million IU or SC, amp. 100,000 IU – intranasally
Mechanism of action:
direct antiproliferative action against tumor cells or
viral cells to inhibit replication and modulation of
host immune response by:
■ enhancing phagocytic activity of macrophages
■ augmenting specific cytotoxicity of
lymphocytes for target cells.


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Clinical uses:
Neoplasms
Chronic Myelogenous Leukemia
Malignant Melanoma and Kaposi’s Sarcoma Renal Cell Carcinoma
T-cell Leukemia
Hepatitis B and C
Multiplied Sclerosis
Acute Respiratory Virus Infection


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BCG (Bacille Calmette-Guerin) vaccine
viable strain of Mycobacterium bovis
nonspecific immunostimulant
has been successful only in intravesical therapy for Superficial Bladder Cancer.

BCG appears to act via activation of macrophages
to make them more effective killer cells


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Thank you for Attention !


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