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Immunology > Exam 3 > Flashcards

Exam 3 Flashcards

1
Q

Cyclosporine mechanism of action

A

Cyclosporine forms a complex with cyclophilin A, which bind to calcineurin to inhibit Ca2+ stimulated dephosphorylation (normally takes place via a phosphatase) of cytosolic NFAT, so NFAT can’t translocate to the nucleus.
Cyclosporine also increases the expression of transforming growth factor β (TGF-β), a potent inhibitor of IL-2 stimulated T cell proliferation and generation of cytotoxic T cells.

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2
Q

Tacrolimus mechanism of action

A

Binds to FK506 binding protein 12 (FKBP-12), which is structurally related to cyclophilin. The complex binds to calcineurin, calcium, and calmodulin to inhibit calcineurin phosphatase activity.

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3
Q

Rapamycin mechanism of action

A

Inhibits T cell activation and proliferation of downstream of IL-2R (where IL-2 binds) and other T-cell growth factor receptors. The action of rapamycin is also initiated by binding to the immunophilin, FKBP-12, but the complex does not bind to calcineurin. Instead, it binds and inhibits the kinase mammalian target of rapamycin (mTOR), which is important in T cell proliferation.

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4
Q

Everolimus mechanism of action

A

Binds to FK506 binding protein 12 (FKBP-12), which is structurally related to cyclophilin. The complex binds to calcineurin, calcium, and calmodulin to inhibit calcineurin phosphatase activity.

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5
Q

Azathioprine mechanism of action

A

In the presence of nucleophiles, azathioprine is cleaved to 6-mercaptopurine. 6-mercaptopurine is converted to 6-mercaptopurine nucleotides that inhibit DNA biosynthesis. It can also be converted to 6-thioinosine 5’-phosphate (T-IMP) that inhibits de novo purine biosynthesis. Normal cells utilize purine salvage reactions, which recycle purine bases from nucleic acids and nucleotides but lymphocytes don’t so azathioprine targets the immune system and not normal cells.

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6
Q

Mycophenolate mechanism of action

A

Selectively inhibits proliferation of lymphocytes by inhibition of IMPDH (inosine monophosphate dehydrogenase), which is the rate limiting enzyme in GMP biosynthesis. GMP is a precursor of GTP and deoxy-GTP for RNA and DNA synthesis. Mycophenolate is more selective against Type II isoform of IMPDH (which is expressed more in lymphocytes) than Type I isoform (which is expressed in most cell types).

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7
Q

Corticosteroids mechanism of action

A

HSP90 is connected to the glucocorticoid receptor in the cytosol, which has a hormone binding domain and a DNA binding domain. Cortisol binds to the hormone binding domain and HSP90 leaves so that the cortisol-glucocorticoid receptor complex can form a diner and move to the nucleus where the glucocorticoid receptor binds to the glucocorticoid response element (GRE) and triggers the expression of anti-inflammatory proteins. The glucocorticoid receptor can also bind to AP-1 responsive element, negative GRE, and NFKB responsive element, which lead to gene repression.

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8
Q

Corticosteroids effects

A

Suppression of T cells by interfering with production of cytokines. Suppression of B cells by interfering with the binding of interleukins to B cells. Suppression of neutrophils by inhibiting adhesion, chemotaxis, phagocytosis, release of toxic substances, etc. Suppression of macrophages by down-regulating the expression of Fc receptors on macrophages so macrophages are less able to phagocytose opsonized particles. Diminish production of prostaglandins and leukotrienes by inhibiting cyclooxygenase and phospholipase A2, which decreases the production of pro-inflammatory arachidonic acid metabolites.

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9
Q

What are eicosanoids and why are they important?

A

Eicosanoids are fatty acids produced by three classes of enzymes: cyclooxygenases, lipoxygenases, and cytochrome P450 epoxygenase. They are important to biological functions including inflammatory (and therefore immune) responses, pain, and fever.

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10
Q

Main role of phospholipase A

A

The release of arachadonic acid from membrane phospholipids.

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11
Q

PGI2 location and function

A

PGI2 is in endothelial cells and causes vasodilation and decreases platelet aggregation

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12
Q

TXA2 location and function

A

TXA2 is in platelets and causes vasoconstriction and platelet aggregation

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13
Q

PGF2 location and function

A

PGF2 is in the uterus and causes vasoconstriction.

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14
Q

PGE2 location and function

A

PGE2 is in most cell types and causes erythema, edema, pain, and fever

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15
Q

PGD2 location and function

A

PGD2 is located in the mast cells and in the brain and causes erythema, edema, pain, and decreased platelet aggregation.

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16
Q

What are the active sites in the COX binding pocket and what do they do

A

Arg120: interacts with the carboxylate of the fatty acid
Ser530: the residue acetylated by aspirin
Tyr385: abstracts the pro-S hydrogen to initiate the COX reaction

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17
Q

What COX is found throughout the body?

A

1

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18
Q

What COX is inducible?

A

2

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19
Q

What COX has the larger active site?

A

2

20
Q

What is COX 3?

A

COX-3 is a controversial/proposed cyclooxygenase that has been found in the brain of dogs and may be a target of acetaminophen.

21
Q

What is aspirin’s mechanism of action?

A

irreversibly acetylates Ser530 in the active sites of cyclooxygenase. It also alters the catalytic activity of COX-2 to make epi-lipoxins (have gastrointestinal effects and modulate vascular tome to affect regional blood flow during inflammation)

22
Q

What are the complications from aspirin?

A

Reye’s syndrome, salicylism, aspirin hypersensitivity

23
Q

What do nitrogen-containing salicylates treat?

A

irritable bowel syndrome

24
Q

Why are the 5-p-fluorophenyl derivatives more potent than aspirin?

A

They’re bulky and a better competitor

25
Q

Arylacetic and arylpropionic acid derivatives mechanism of action

A

compete with arachidonic acid at the active site of the cyclooxygenase

26
Q

Arylacetic and arylpropionic acid derivatives examples

A

sulindac, ketorolac, tolmetin, diclofenac, etodolac

27
Q

What is distinctive about the arylproprionic acid analogs?

A

They all have an alpha-methyl group (at the second carbon)

28
Q

Does stereochemistry matter for the arylproprionic acids

A

The S isomer is the active form and the R isomer is inactive. The R isomer is converted to the S isomer in vivo due to metabolism

29
Q

Which COX are arylpropionic acid analogs selective for?

A

Non-selective

30
Q

What drugs are in the arylpropionic acid analogs class?

A

Ibuprofen and naproxen

31
Q

Oxicam mechanism of action

A

enolic hydroxyl group that presumably interacts with Tyr385 and Ser530

32
Q

What is distinctive about oxicams?

A

They have very long half lives

33
Q

Oxicam examples

A

meloxicam and piroxicam

34
Q

Examples of N-arylanthranilic acids

A

mefenamic acid, flufenamic acid, and meclofenamic acid

35
Q

What happens in an acetaminophen overdose?

A

In acute overdose the normal pathway is saturated and a second metabolic pathway takes over to give rise to a reactive species (arylating intermediate) that reacts rapidly with and completely depletes GSH. The sulfur from GSH makes it extremely reactive and acetylcysteine is administered to react with it instead of the liver.

36
Q

NSAID side effects

A

GI, cardiovascular, renal, hypersensitivity, neurological, hematologic

37
Q

Explain the differences between NSAIDs

A

binding affinity, selectivity, actions on cytokines, epi-lipoxins

38
Q

Mechanism for NSAID anti-inflammatory effects

A

block prostaglandin production that mediate inflammation

39
Q

Mechanism for NSAID analgesia effects

A

prostaglandins sensitize nociceptive pathways and NSAIDs prevent this

40
Q

Mechanism for NSAID antipyresis effects

A

PGE2 interacts with EP3 receptors in the hypothalamus causing signaling that results in heat generation and decrease of heat loss from the body. NSAIDs stop the production of PGE3

41
Q

Mechanism for aspirin antiplatelet effects

A

COX-1 is in platelets and COX-2 is in the endothelial cells lining blood vessels. Platelets do not have cellular machinery and endothelial cells do so they can create more COX enzymes after aspirin acetylates them. COX-1 makes TXA2 and COX-2 makes PGI2. TXA2 causes platelet aggregation and PGI2 causes decreased platelet aggregation. PGI2 wins after the aspirin knocks the COX-1/platelets out so decreased platelet aggregation is the result.

42
Q

Zileuton mechanism of action

A

Inhibits the 5-lipoxygenase that converts arachidonic acid to 5-HPETE, preventing formation of subsequent leuokotrienes

43
Q

Zafirleukast mechanism of action

A

reversible and competitive inhibitor of the cysteinyl-leukotriene receptor

44
Q

Montelukast mechanism of action

A

reversible and competitive inhibitor of the cysteinyl-leukotriene receptor

45
Q

Cromolyn and Nedocromil sodium mechanism

A

Likely inhibits chloride channels, which may in turn inhibit calcium availability

46
Q

Cromolyn and Nedocromil sodium pharmacologic result

A

inhibits release of mediators from several cell types involved in inflammation, can reverse increased functional activation in leukocytes obtained from the blood of the asthmatic patient, can suppress release of chemotactic peptides (chemokines), and decreases neuronal sensation related to increased reactivity airways

47
Q

Lodoxamide and olopatadine ophthalmic mechanism of action

A

prevention of the antigen-stimulated release of histamine and other inflammatory mediators, may also prevent calcium influx into mast cells, blocks the action of histamine not the creation of it

Immunology (4 decks)

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