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Path - Immunology > Immune Mod Therapies 2 > Flashcards

Immune Mod Therapies 2 Flashcards

1
Q

What are corticosteroids?

A

Synthetic glucocorticoids based on naturally occurring steroids
NO mineralocorticoid axrtivity

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2
Q

What structures do corticosteroids have an effect on?

A

Prostaglandins
Phagocytes
Lymphocytes

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3
Q

What is corticosteroid effect on prostaglandins?

A

Corticosteroids inhibit phospholipase A2
Phospholipase A2 is usually converts phospholipids into arachidonic acid
AA is then converted to eicosainoids (prostaglandins, leukotrienes) by COX
Therefore by blocking phospholipase, no prostaglandins are produced, reducing inflammation

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4
Q

What is corticosteroid effect on phagocytes?

A

Decreases phagocytes to inflamed tissue (due to reduced signals to phagocytes)

Decreased phagocytosis

Decreased proteolytic enzymes

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5
Q

What is corticosteroid effect on lymphocyte function?

A

Lymphopoenia (sequestration of lymphocytes in lymphoid tissue)
Blocks cytokine gene expression
Decreased antibody production
Promotes apoptosis

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6
Q

What are side effects of corticosteroids?

A

Metabolic - central obesity, moon face, diabetes, lipid disorders, osteoporosis, hirsutism, adrenal suppression

Others - cataracts, glaucoma, peptic ulceration, pancreatitis, avascular necrosis

Immunosuppression

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7
Q

What do anti proliferative agents do?

A

Inhibit lymphocyte proliferation

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8
Q

What are examples of anti proliferative agents?

A

Cyclophosphamide
Mycophenolate
Azathioprine
Methotrexate

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9
Q

What is the MOA of antiprolif agents?

A

Inhibit DNA synthesis (Cells with rapid proliferation are most targeted)

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10
Q

What is the MOA of cyclophosphamide?

A

Alkylates guanine bases of DNA
Damages DNA and prevents cell replication
Affects B cells > T cells
At high dose, affects all cells with high turnover

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11
Q

What are major indications for cyclophosphamide=

A

Multisystem connective tissue disease
Vasculitis with severe end organ involvement
Anti-cancer agents

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12
Q

What are side effects of cyclophosphamide?

A
  • Toxic to proliferating cells (bone marrow suppression, sterility, hair loss)
  • Haemorrhagic cystitis (as ACROLEIN in excreted in urine)
  • Malignancy (bladder cancer, harm cancer, non-melanoma skin cancer)
  • Teratogenic
  • PCP
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13
Q

What is the mechanism of Azathioprine?

A

Metabolised by liver to 6 mercaptopurine
Blocks de novo purine synthesis
Prevents DNA replication
Preferentially inhibits T cell activation and prolif

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14
Q

What are indications of azathioprine

A

Transplant
AI disease
Autoinflamm disease e.g. Chrons, UC

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15
Q

What are side effects of azathioprine?

A

Bone marrow suppression
Hepatotoxicity
Infection

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16
Q

Individuals with what polymorphism are susceptible to bone marrow suppression?

A

Thiopurine Methyl Transferase

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17
Q

What is MOA of mycophenolate mofetil?

A

Blocks de novo nucleotide synthesis
Prevents DNA replication
Prevents T cell> B cell proliferating

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18
Q

What is indications of mycophenolate mofetil?

A

Transplantation

AI diseaase

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19
Q

What are side effects with mycophenolate mofetil?

A

Bone marrow suppression
Teratogenic
Infection (HSV, mrogressive multifocal leukoencephalopathy)

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20
Q

What is the aim of plasmapheresis?

A

PLASMA EXCHANGE aka remove pathogenic antibodies

21
Q

What occurs in plasmapheresis?

A

Patient’s blood is passed through a separator
Own cellular components are reinfused
Plasma is treated to remove Ig and then reinfused

22
Q

What is the issue with plasmapheresis and how do you solve it?

A

Rebound antibody production (because even if you get rid of the antibodies, the plasma cells are still there)

GIVE anti proliferative agent to avoid this

23
Q

What are Indications for plasmapheresis?

A

Severe antibody-mediated disease

e.g. good pastures, Myasthenia graves, transplant rejection

24
Q

What is the MOA of calcineurin inhibitors?

A

Inhibit calcineurin > prevent T cell signalling > block IL2 production

25
Q

What are examples of calcineurin inhibitors?

A

Ciclosporin

Tacrolismus

26
Q

What are SE of calcineurin inhibitors?

A 
nephrotoxicity 
HTN
neurotoxic 
diabetogenic 
dysmorphic features
27
Q

What should you monitor with calcineurin inhibitors=?

A

BP

Renal function

28
Q

What is an example of a JAK inhibitor?

A

Tofacitinib (JAK1, JAK3)

What do

29
Q

What does Tofacitinib do?

A

Interferes with JAK-STAT signalling
Influences gene transcription
Inhibits production of inflammatory molecules

30
Q

What disease is Tofacitinib good for?

A

RA

31
Q

What is an example of PDE4 inhibitor?

A

apremilast

32
Q

What is MOA of PDE4 inhibitors?

A

PDE4 works in metabolism of cAMP

PDE4 inhibitors upregulate cAMP

cAMP activates PKA, which prevents activation of transcription factors
This leads to a decrease in cytokine production

33
Q

What is anti-thymocyte globulin used for?

A

Allograft rejection

As it causes T cell depletion

34
Q

What is basiliximab?

A

an antibody directed at CD25

35
Q

What is basiliximab used for?

A

For prophylaxis of graft rejection

36
Q

What does basiliximab target?

A 
IL2 receptor (called CD25), alpha chain 
Leads to inhibition of T cell proliferating
37
Q

Side effects of basiliximab

A

Infusion reaction
Infection
Concern of long term malignancy

38
Q

how does methotrexate work

A

ANTI-FOLATE

inhibits dihydrofolate reductase, stopping DNA synthesis

39
Q

what must you give with methotrex

A

folate supplement

40
Q

what must you always measure before you prescribe azathioprine

A

Thiopurine methyl transferase aka TPMT

because people with this variant will be unable to metabolise azathioprine

41
Q

what does rituximab do

A

blocks CD20 > depletion of mature B cells

42
Q

how does natalizumab work

A

against a4 integrin

43
Q

what disease does natalizumab work against

A

MS

44
Q

list some Anti-TNFalpha antibodies

A

infliximab
adalimumab
certolizumab
golimumab

45
Q

what is the MOA of etanercept

A

TNF alpha antagonist - mops up TNF alpha > ihibits TNF alpha

46
Q

WHAT IS MOA of denosumab

A

antibody against RANKL

Normally, osteblasts produce RANKL. RANKL binds to RANK > osteoclast differentiation and function > increase bone resorption

So denosumab stops osteoclast function > reduces bone resporption

47
Q

what are indications for denosumab

A

osteoporosis

give subcut every 6 months

48
Q

what is a side. effect of denosumab

A

avascular necrosis of jaw

Path - Immunology (11 decks)

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