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Immuno Block Mid Term 2 > Immunosupressants and Modulators > Flashcards

Immunosupressants and Modulators Flashcards

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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
Lipoxygenase (LOX) inhibitor drug name
Zileuton
26
What do corticosteroids effect?
they block the production of prostaglandins, thromboxanes and leukotrienes
27
Main types of corticosteroids...4
hydrocortisone, prednisone, mehtylprednisolone, Dexamethasone
28
Mechanism of corticosteroids
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
Lipocortin or Annexin 1 relation to corticosteroids
This is the antiinflammatory product that is induced by corticosteroids
30
Lipocortin mechanism of antiinflammatory effect
inhibits the phospholipases PLA2 in eicosanoid production
31
Corticosteroid toxicity in respiratory
CSs are mainly adminstered orally, leads to increased risk of thrush and pneumonia
32
Corticosteroid toxicity examples
weight gain, moon face (CS redistributes fat), skin thinning, high BP, increased bone fracture risk
33
What molecule makes corticosteroids weaken the skin?
Keratin
34
What molecule makes corticosteroids lead to increas bone fracture risk?
osteocalcin
35
Calcineurin inhibitors mechanism
calcineurin is downstream in the TCR complex, so inhibiting it means it is unlikely the T cell will make IL-2
36
Common drugs that are calcineurin inhibitors
cyclosporin and tacrolimus
37
Calcineurin inhibitor toxicities
malignancies...non hodgkins lymphoma most common
38
Mechanism of JAK STAT inhibitors
Inhibits Jak3 and doesnt allow the cell IL-2 receptor cascade to occur, so no IL2/cytokine production
39
JAK STAT inhibitor drug name
Tofacitinib
40
cytokine antibody drugs mechanism
antibodies bind and inhibit the cytokines, especially TNF
41
common cytokine antibody drug names
adalimumab mepolizumab tocilizumab
42
Mepolizumab mechanism and use
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
Mechanism of DNA synthesis inhibitors
though different mechanisms, they all converge by not allowing production of purine nucelotides and therefore inhibit proliferation of T cells and other cells
44
Azathioprine mechanisms (2)
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
Azathioprine toxicity
if it is inserted and does not lead to cell death...can have mutagenecity acute myeloid leukemia lung adenocarcinoma
46
3 important DNA/RNA synthesis inhibitors
azathioprine mycophenolate methotrexate
47
mycophenolate mechanism of action
inhibits production of GTP which is needed for DNA/RNA synthesis
48
methotrexate mechanism of action
inhibits the dihydro folate receptor which is involved with folate and production of purines for DNA
49
can you give any DNA/RNA synthesis inhibitors when pregnant?
NO...do not give azathioprine or mycophenolate and definitely do not give methotrexate
50
leflunomide mechanism of action and use
used for inhibiting tumors and inhibits production of WBCs blocks production of nucleotide precursors
51
mTOR inhibitor mechanism of action
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
common drug for mTOR inhibitor
Sirolimus
53
Common drugs for cytokine receptor antibodies
``` Anakinra Basilixumab Benzralizumab Omalizumab Rituximab ```
54
Anakinra receptor and target cell
IL-1R, various
55
Basilixumab receptor and target cell
IL-2R, T cells
56
Benralizumab receptor and target cell
IL-5R, eosinophils
57
Omalizumab receptor and target cell
IgE, B cells
58
Rituximab receptor and target cell
CD20 and B cells
59
how do you decrease absorption of drugs as you age?
decrease SA in intestines, decrease blood flow in GI tract may want to consider increasing doses
60
mechanisms of reducing metabolism of drugs as age?
decreased hepatic metabolism and biliary excretion means you may want to reduce dosage
61
mechanisms of changing distribution as age?
decrease albumin, decrease in lean body mass and total body water may want to modify dosage
62
Mycophenolate suggestion for decreased absorption in aging?
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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