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Therapeutics 1 Kappa Epsilon Version > Inflammation/NSAIDs/DMARDs > Flashcards

Inflammation/NSAIDs/DMARDs Flashcards

1
Q

Acute or Chronic inflammation?

Accumulation of fluid & plasma proteins

A

Acute

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2
Q

Acute or Chronic inflammation?

Exudation occurs

A

Acute

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3
Q

what is exudation

A

accumulation of fluids/plasma proteins

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4
Q

Acute or Chronic inflammation?

Accumulation of Neutrophils

A

acute

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5
Q

Acute or Chronic inflammation?

TNF, IL-1, Chemokines

A

Acute

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6
Q

Acute or Chronic inflammation?

Tissue destruction by inflammatory cells

A

chronic

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7
Q

Acute or Chronic inflammation?

vascular proliferation and fibrosis

A

chronic (this is also known as scarring..)

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8
Q

Acute or Chronic inflammation?

Influx of lymphocytes and macrophages

A

chronic

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9
Q

Acute or Chronic inflammation?

IFN-gamma by T cells

A

Chronic

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10
Q

Acute or Chronic inflammation?

IL-12 released by macrophages

A

chronic

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11
Q

Main 4 Steps of Inflammation

A

1 - Vascular Changes
2 - Leukocyte Recruitment
3 - Leuckocyte Activation
4 - Leuckocyte induced tissue injury

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12
Q

Leuckocyte Recruitment:
Loose attachment/Rolling is done by _______
and
Adhesion is done by ________

A

selections; integrins

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13
Q

Which chemical mediators on inflammation are vasoactive amines

A

histamine/serotonin

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14
Q

what do vasoactive amines do

A

cause vasodilation

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15
Q

what chemical mediators of inflammation are eicosaniods

A

prostaglandins, leukotrienes, lipoxins

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16
Q

Lipoxin _________ inflammaiton

A

suppress

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17
Q

Eicosanoids are (short or long ) lived mediators that do autocrine AND paracrine signaling

A

short!

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18
Q

Eicosanoids bind to _________ receptors

A

G-coupled

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19
Q

what are the chemical mediators of inflammation for the coagulation/kinin systems

A
  • bradykinin
  • thrombin
  • fibrinopeptides
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20
Q

what are the chemical meditors of inflammation for cytokines

A

TNF and IL-1 and IFN-gamma

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21
Q

IFN- gamma for acute or chronic inflammation

A

chronic

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22
Q

TNF for acute or chronic inflammation

A

acute

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23
Q

IL-1 for acute or chronic inflammation

A

acute

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24
Q

chemical mediators for inflammation that are complement components

A

C3a, C5a

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25
Q

Role of PGE(2) in the body

A
  • dilates blood vessels
  • dilates uterus (oxytoxic)
  • dilates bronchi
    (E = Expand = Dilate!)
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26
Q

Role of PGE(F2a) in the body

A
  • constricts blood vessels
  • constricts bronchi
    (F = Fasten = constrict!)
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27
Q

Role of PGI(2)

A
  • inhibits aggregation of platelets
  • dilates
    (I = inhibit = if you no platelets — airway more open = dilated)
28
Q

Role of TXA(2)

A
  • promotes aggregation of platelets
  • constriction
    (A = aggregate = less room in vessel = constrict)
29
Q

Where does Arachidonic acid come from

A
  • released form membrane phospholipids by PLA (phospholipase A2)
30
Q

Corticosteroids and Arachidonic Acid relationship

A

if corticosteroids are given - it will suppress the production of PLA2 –> no arachidonic acid is made –> reduction in eicosanoid production

31
Q

PGH Synthase pathway in Oxygenation of Arachidonic acid is also known as _______

A

COX pathway!

32
Q

COX pathway results in _________

A

prostaglandins and thromboxanes

33
Q

Lipoxygenase pathway results in __________

A

leukotrienes (5HPETE, Lipoxins)

34
Q

COX 1 or COX 2:

aka PGH Synthase 1

A

COX 1

35
Q

COX 1 or COX 2:

Constitutively expressed in various tissues

A

COX 1

36
Q

COX 1 or COX 2:

Does gastric cyroprotection as a part of its “Housekeeping” functions

A

COX 1

37
Q

COX 1 or COX 2:

Expressed upon stimulus in inflammatory/immune cells

A

COX 2

38
Q

COX 1 or COX 2:

stimulated by growth factors, tumor promoters, and cytokines

A

COX 2

39
Q

Final Product in COX pathway - the “non-specific” product

A

going for the answer PGH-2

not prostaglandin or thromboxane since those are made specifically at different tissues

40
Q

Corticosteroids: block (some or all) pathways of eicosanoid synthesis

A

ALL! - because it inhibits PLA2 via making lipocortins

41
Q

do NSAIDs block production of leukotrienes?

A

NAH - only prostaglandins and thromboxanes (aka the products from the COX pathway)

42
Q

Eicosanoid Drugs:

Alprastodil what kind of prostaglandin drug

A

PGE1

43
Q

what does Alprastodil do

A
  • relaxes smooth muscle/expands blood vessels
    aka
    is used for erectile dysfunction by injection or suppository
44
Q

Eicosanoid Drugs:

Misoprostol is what kind of prostaglandin drug

A

PGE1 derivative

45
Q

what does Misoprostol do?

A

its cytoprotective/prevents peptic ulcer

  • also used to terminate early pregnancy if used with mifepristone
46
Q

Eicosanoid Drug:

Latanprost is what kind of prostaglandin durg

A

PGF(2) derivative/Prodrug

47
Q

what is lantanprost used for

A

it constricts blood vessels - aka used to treat high pressure in the eye (aka glaucoma)

48
Q

Eicosanoid Drug:

Prostacyclin - is what kind of prostaglandin drug

A

PGI2

49
Q

Eicosanoid Drug:

Prostacyclin is used for what?

A

well it inhibits aggregation of platelets –> is powerful vasodilator –> used to Treat pulmonary arterial HTN

aka dont use w/ anticoagulants

50
Q

What are the pharmacological activities of NSAIDs

A
  • anti-inflammatory
  • anti-pyretic
  • analgesic
51
Q

MOA of NSAIDs

A

inhibit PGH synthase (aka COX enzymes - most NSAIDs inhibit both cox 1 and 2) –> less prostaglandins are important

52
Q

MOA of aspirin that makes it inhibit blood coagulation

A

aspirin irreversibly inhibits of platelets COX -1

53
Q

What is Reye’s Syndrome

A

rara acute life threatening condition characterized by vomiting/delirium/coma due to salicylates -

54
Q

who should not get aspirin when trying to prevent Reyes Syndrome

A

kids under 12 who have a fever

55
Q

Common Drug Interaction w/ NSAID

A

anticoagulants and NSAIDs because they both to compete for albumin

56
Q

what is the role (structure activity) of alpha-methyl in arylpropionic acids

A

the alpha methyl separates the acidic ring from the aromatic ring which tends to increase activity

57
Q

How does MOA for APAP differ from NSAIDs

A

APAP does NOT inhibit archidonic acid from binding to PGHS

APAP DOES scavenge peroxynitrites required for PGHS activity

58
Q

How do we have selective COX 2 Inhibitors (structure wise)

A

the NSAID binding site in COX 1 and COX 2 are different

COX 2 has larger binding site (has valine in there instead of COX1 has isoleucine which is more bulky)

59
Q

MOA of Methotrexate -

A

inhibits ribonucleotide transformylase and thymidylate synthetase

60
Q

Why do COX 2 inhibitors have CV risk side effects

A

COX 2 inhibitors lead to an imbalance of prostaglandins and thromboxanes which leads to more platelet aggregation

61
Q

MOA for Leflunomide

A

prodrug for pyrimidine synthesis inhibitor - will deplete pyrimidines/inhibit T cell proliferation

62
Q

MOA for Hydroxychloroquine

A

accumulates in lysosomes and inhibits protein secretion

63
Q

MOA of Sulfasalazine

A

Suppress release of cytokines from macrophages

64
Q

MOA of Abatacept

A

has CTLA-4 domain to inhibit co-stimulation of T-Cells by APCs

65
Q

MOA of Rituximab

A

induces apoptosis of CD20+ - will reduce inflammation by reducing activation of T cells

Therapeutics 1 Kappa Epsilon Version (17 decks)

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