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Year 2 Pharmacology > Immunomodulation > Flashcards

Immunomodulation Flashcards

1
Q

When three times is immune modulation needed?

A

Immune suppression- reducing inflammatory response, reducing allergic response, supression of innapropriate immune response

Enhance host immune response- to infection, vaccination, enhance immune response against neoplasia

Future- administration of immune system elements- invoke/limit response in degenerative disease

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2
Q

What are the 4 types of hypersensitivity reactions and what causes them?

A

Type I- IgE and MCT mediated
Type II- IgG mediated
Type III- immune complex disease
Type IV- cytotoxic T cell mediated

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3
Q

What are the 2 sources of antigens which cause immune mediated disease?

A

Idiopathy/autoimmunity

Exogenous antigen

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4
Q

What is the difference between anti-inflammatories compared to immunosuppressive medications?

A

Anti-inflammatories- act to block some effector mechanism of innate immune system
Immunosuppressive- Mainly act to reduce function of adaptive immune system, reduce lymphocyte proliferation/limit effect

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5
Q

What are the three main groups of drugs in veterinary practice?

A

Drugs which:
Inhibit cytokine gene expression
Inhibit IL-2 production/action
Inhibits DNA synthesis

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6
Q

What is the ‘first’ line of immunosuppressive drugs?

A

Glucocorticoids

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7
Q

Describe the chemical features of glucocorticoids and where are they metabolised and excreted?

A

Lipophilic and highly protein bound
Metabolised by the liver
Excreted by the kidneys

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8
Q

What is the mechanism of action of glucocorticoids?

A

Bind to Glucocorticoid receptor in cytoplasm- transit to nucleus, bind to DNA influencing transcription of genes in many tissues
Stabilise mast cell membranes reducing degranulation
Reduce pro-inflammatory cytokine production- reduced IL-2- reduced lymphocyte numbers esp CD4+
Down regulate Fc receptor expression on macrophages
Reduce antigen presentation

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9
Q

What does the effect of glucocorticoids depend on?

A

Dose anf formulation

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10
Q

What are the three commonly used glucocorticoids and what are their potency compared to cortisol?

A

Prednisolone- 5x
Methylprednisolone- 7x
Dexamethasone- 35x

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11
Q

How can glucocorticoid side effects be reduced?

A

Topical administration

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12
Q

What systemic effects are caused by glucocorticoids?

A

Stimulate gluconeogenesis
Suppress inflammation
Alter fat, protein and CHO metabolism
Suppress HPA axis

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13
Q

What are the adverse effects of glucocorticoids?

A 
Skin thinning, comedones, calcinosis cutis 
Weight gain, Protein/muscle loss 
Polyphagia
Laminitis?
Panting
HPAA 
Lethargy/euphoria
PU/PD
GI bleeding
Hyper-coagulability
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14
Q

When are glucocorticoids contraindicated?

A 
Uncontrolled infections
Diabetes mellitus
Corneal and GI ulcers
Heart disease
Burns
Pregnancy
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15
Q

Why are glucocorticoids not used for long term treatment of immune diseases?

A

Balancing effective treatment against side effects can be impossible
Prolonged use suppresses HPA axis

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16
Q

Where is IL-2 produces and what does it stimulate?

A

Produced by Th (CD4+) cells
Stimulates clonal proliferation and activation of T cells
B cell proliferation
Activity of innate immune cells- macro, NK cells

17
Q

Which two IL-2 inhibition drugs are commonly used in practice?

A

Ciclosporin

Tacrolimus

18
Q

What is the mode of action of the IL-2 inhibition drugs?

A

Block calcineurin activation giving reduced IL-2 production

19
Q

How is ciclosporin administered and how can the dose be reduced?

A

Topical, oral or parenteral

Co-administration with ketoconazole can reduce the required dose

20
Q

How is tacrolimus usually administered?

A

Most commonly topical administration

21
Q

Where are are ciclosporin and tacrolimus?

A

Metabolised by liver cytochrome P450 enzymes

Excreted in bile

22
Q

What are the adverse effects of ciclosporin and tacrolimus?

A

Transient vomiting
Possible increase in risk neoplasia
Opportunistic infections

23
Q

What drugs inhibit DNA synthesis?

A

Azathioprine
Mycophenolate mofetil
Leflunomide

24
Q

What is the mode of action of azathioprine?

A

Inhibits purine synthesis, inhibition of DNA and RNA synthesis land therefore alterations in cell metabolism- reduces TH1 mediated immunity
Slow onset of actions 7-35 days

25
Q

How is azathioprine administered metabolised, excreted, why is it not used in cats?

A

Administered- oral
Metabolised- liver to active form
Excreted- in all excreta
Cats have low activity of enzyme that metabolises to active form

26
Q

What are the adverse effects of azothioprine?

A 
Hepatopathy
Myelosupression
Pancreatitis 
GI signs
Reduce dosage after 2 weeks to reduce risk of adverse effects
27
Q

What is the mode of action of mycophenolate mefoentil ?

A

Inhibits an enzyme crucial to purine synthesis in lymphocytes for proliferation of B and T cell:
Reduced T cell differentiation
Reduced antibody responses
Reduced dendritic cell maturation

28
Q

How is mycophenolate mofentil administered, metabolised, excreted?

A

Administered- orally sometimes IV
Metabolised- hepatically
Excreted- renally

29
Q

What are the adverse effects of mycophenolate mofentil?

A

Weight loss
Diarrhoea
Co-administration with ciclosporin may reduce effect

30
Q

What are the actions of human immunoglobulins in animals?

A

Saturates Fc receptors preventing antibody from binding
Binds to T and B cells inhibiting proliferation and activation
Presents Fas-FasL interactions
Short lived but rapid effect

31
Q

What are the possible adverse effects of human immunoglobulin?

A

Cost
Hyper-coagulability
Glomerulonephritis
Transfusion reactions

32
Q

What drugs are used for refractory cases and specific conditions and what are their actions?

A

Leflunomide- DNA synthesis inhibitor- T and B cell inhibition and T regulation induction
Liposomal clodronate- induces killing of splenic macrophages and dendritic cells, inhibits clearance of opsonised RBCs
High dose alkylating agents- kill lymphocytes via DNA damage

33
Q

How can rational use of immune suppression be considered?

A

1) is it an immune mediated disease
2) can a trigger factor be identified and eliminated
3) Is immune suppression required
4) What drugs are appropriate
5) Can the disease be managed with topical rather then systemic
6) potential for adverse effects
7) risk to owner of treatment
8) Do the benefits outweigh the risks

34
Q

What are second line immunosuppressives used for and what are the problems of using them?

A

Used in conjunction with steroids or when steroids are contraindicated

May increase the risk of opportunistic infections

35
Q

What is the mode of action of imiquimod, how is it applied?

A

Activates TLR7, encourages langerhans cell maturation and transit to lymph nodes
Applies to skin

36
Q

What is oncept IL-2 used for?

A

Feline vaccine associated sarcoma

37
Q

What drug might be used in the future for immune stimulation?

A

Monoclonal antibodies

Year 2 Pharmacology (11 decks)

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