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Immuno Block Mid Term 2 > Immunosupressants and Modulators > Flashcards

Immunosupressants and Modulators Flashcards

1
Q

phosphlipase (PLA2) in arachidonic acid synthesis

A

in charge of turning fatty acid from cell membrane into the arachidonic acid

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2
Q

COX1/2 (cyclooxygenases) role on arachidonic acid

A

turns the acid into prostaglandins and thromboxanes

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3
Q

Lipoxygenases role on arachidonic acid

A

turns the acid into leukotrienes

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4
Q

cytochrome p450 role on arachidonic acid

A

turns acid into epoxides and HETEs

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5
Q

Where are prostaglandins made?

A

made by most cells

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6
Q

Where are thromboxanes made?

A

in platelets

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7
Q

Where are leukotrienes made?

A

in leukocytes

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8
Q

NSAIDs mechanism of action

A

inhibit COX1/2 in arachidonic acid breakdown, so cells cannot make prostaglandins and thromboxanes

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9
Q

COX1 role in body

A

constitutively expressed and in charge of homeostatic functions like renal, GI mucosal, and platelet function

inhibiting cox 1 will lead to more toxicity

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10
Q

Cox-2 role in body

A

mainly in charge of the inflammatory response and is only selectively activated, so inhibitors of Cox2 are more effective in leading to a therapeutic effect

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11
Q

NSAIDs toxicity in the GI tract

A

leads to a decrease in mucosal secretions because of inhibition of the PGE2…sometimes can lead to gastric bleeding

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12
Q

PGE2 role in GI

A

is in charge of stimulating mucosal secretions

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13
Q

What can you coadminister to help the NSAIDs GI toxicity?

A

an antacid like prilosec may help avoid gastric bleeding

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14
Q

PGE2 role in kidney and toxicity with NSAIDs

A

It helps vasodilate in kidney and lead to filtration, since NSAIDs inhibit the production the vessels stay constricted and not enough is filtered and can lead to kidney damage

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15
Q

Thromboxane A2 toxicity with NSAIDs

A

NSAIDs inhibit TXA2 which are in charge of promoting platelet activation

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16
Q

Pharmacokinetics mechanism of aspirin

A

irreversibly binds COX1 through covalent modifications, so has longer lasting effects

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17
Q

When is aspirin used for ischemic conditions?

A

now only used as a medication following a stroke of MI, not suggested to give prior

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18
Q

Random disease aspirin cures?

A

kawasaki disease

maybe colorectal cancer

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19
Q

Reyes syndrome

A

viral infection..then give aspirin..leads to disease with neurological effects and is very deadly

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20
Q

Aspirin and asthma interaction?

A

can have aspirin sensitive asthma due to blocking the COX pathway and forcing arachidonic acid down the leukotriene pathway and therefore make leukotrienes that lead to bronchoconstriction

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21
Q

Two NSAIDs with extreme COX2 selectivity

A

Celebrex (celecoxib) and Vioxx (rofecoxib)

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22
Q

Problem with the COX2 selectivity drugs?

A

lead to less GI toxicity but way more cardiovascular toxicities, and inhibit PGI2 which is for anti-clotting factors

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23
Q

Two Different mechanism for Leukotrienes inhibition?

A

can inhibit the lipoxygenase (LOX) or inhibit the leukotrienes themselves

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24
Q

Luekotriene antagonist drug name

A

Montelukast

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25
Q

Lipoxygenase (LOX) inhibitor drug name

A

Zileuton

26
Q

What do corticosteroids effect?

A

they block the production of prostaglandins, thromboxanes and leukotrienes

27
Q

Main types of corticosteroids…4

A

hydrocortisone, prednisone, mehtylprednisolone, Dexamethasone

28
Q

Mechanism of corticosteroids

A

pass through membranes because of hydrophobicit and then serve to effect transcription…mainly inhibit expression of inflammatory products like TNF and induce expression of anti inflammatory like lipocortin

29
Q

Lipocortin or Annexin 1 relation to corticosteroids

A

This is the antiinflammatory product that is induced by corticosteroids

30
Q

Lipocortin mechanism of antiinflammatory effect

A

inhibits the phospholipases PLA2 in eicosanoid production

31
Q

Corticosteroid toxicity in respiratory

A

CSs are mainly adminstered orally, leads to increased risk of thrush and pneumonia

32
Q

Corticosteroid toxicity examples

A

weight gain, moon face (CS redistributes fat), skin thinning, high BP, increased bone fracture risk

33
Q

What molecule makes corticosteroids weaken the skin?

A

Keratin

34
Q

What molecule makes corticosteroids lead to increas bone fracture risk?

A

osteocalcin

35
Q

Calcineurin inhibitors mechanism

A

calcineurin is downstream in the TCR complex, so inhibiting it means it is unlikely the T cell will make IL-2

36
Q

Common drugs that are calcineurin inhibitors

A

cyclosporin and tacrolimus

37
Q

Calcineurin inhibitor toxicities

A

malignancies…non hodgkins lymphoma most common

38
Q

Mechanism of JAK STAT inhibitors

A

Inhibits Jak3 and doesnt allow the cell IL-2 receptor cascade to occur, so no IL2/cytokine production

39
Q

JAK STAT inhibitor drug name

A

Tofacitinib

40
Q

cytokine antibody drugs mechanism

A

antibodies bind and inhibit the cytokines, especially TNF

41
Q

common cytokine antibody drug names

A

adalimumab
mepolizumab
tocilizumab

42
Q

Mepolizumab mechanism and use

A

binds to IL-5 and inhibits its action… which is mainly in eosinophils…some people have eosinophil asthma and this is effective in treating it

43
Q

Mechanism of DNA synthesis inhibitors

A

though different mechanisms, they all converge by not allowing production of purine nucelotides and therefore inhibit proliferation of T cells and other cells

44
Q

Azathioprine mechanisms (2)

A

can be similar in form to a adenine or guanine and be inserted into chain…leads to cell death

or

a form that simply blocks DNA synthesis without being inserted

45
Q

Azathioprine toxicity

A

if it is inserted and does not lead to cell death…can have mutagenecity

acute myeloid leukemia
lung adenocarcinoma

46
Q

3 important DNA/RNA synthesis inhibitors

A

azathioprine
mycophenolate
methotrexate

47
Q

mycophenolate mechanism of action

A

inhibits production of GTP which is needed for DNA/RNA synthesis

48
Q

methotrexate mechanism of action

A

inhibits the dihydro folate receptor which is involved with folate and production of purines for DNA

49
Q

can you give any DNA/RNA synthesis inhibitors when pregnant?

A

NO…do not give azathioprine or mycophenolate and definitely do not give methotrexate

50
Q

leflunomide mechanism of action and use

A

used for inhibiting tumors and inhibits production of WBCs

blocks production of nucleotide precursors

51
Q

mTOR inhibitor mechanism of action

A

mTOR is mammalian target of rapamycin which is in the IL-2R cascade and when inhibited does not allow cell proliferation in response to IL-2

52
Q

common drug for mTOR inhibitor

A

Sirolimus

53
Q

Common drugs for cytokine receptor antibodies

A 
Anakinra
Basilixumab
Benzralizumab
Omalizumab
Rituximab
54
Q

Anakinra receptor and target cell

A

IL-1R, various

55
Q

Basilixumab receptor and target cell

A

IL-2R, T cells

56
Q

Benralizumab receptor and target cell

A

IL-5R, eosinophils

57
Q

Omalizumab receptor and target cell

A

IgE, B cells

58
Q

Rituximab receptor and target cell

A

CD20 and B cells

59
Q

how do you decrease absorption of drugs as you age?

A

decrease SA in intestines, decrease blood flow in GI tract

may want to consider increasing doses

60
Q

mechanisms of reducing metabolism of drugs as age?

A

decreased hepatic metabolism and biliary excretion

means you may want to reduce dosage

61
Q

mechanisms of changing distribution as age?

A

decrease albumin, decrease in lean body mass and total body water

may want to modify dosage

62
Q

Mycophenolate suggestion for decreased absorption in aging?

A

possibly increase dosage due to reduced GI blood flow and smaller SA in the SI

Immuno Block Mid Term 2 (10 decks)

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