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Pharm Exam 4 > Inflammation Buzzwords > Flashcards

Inflammation Buzzwords Flashcards

1
Q

Platelet function is a balance between which 2 final COX products

A

PGI2 (inhibit aggregation) & TxA2 (promote aggregation)

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2
Q

celecoxib (celebrex) rofecoxib parecoxib are in which category of NSAIDs?

A

Selective COX-2 inhibitors the “coxibs”

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3
Q

Uses for selective cox-2 inhibitors

A

1) osteoarthritis and Rheumatoid arthritis! 2) effective for acute pain *not recommended in 3rd trimester

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4
Q

What are 2 strategies to overcome GI irritation from NSAIDs?

A

1) proton pump inhibitor co-administration (to regulate acid secretion) 2) Selectively block COX2

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4
Q

anti-inflammatory drug that inhibits synthesis of pyrimidines and therefore decreases proliferation of lymphocytes (very actively dividing cells)

A

Leflunomide (“mide) just like pyri”mid”ine

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5
Q

This drug acts by mimicking a TNF-a receptor, binds TNF-a with high affinity to prevent it from binding its real receptor and causing inflammation

A

Etanercept (Enbrel)

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5
Q

CTLA4Ig; CD28 co-stimulatory antagonist therefore blocks the 2nd signal required for naive t-cell activation resulting in anergy… therefore a treatment against autoimmune diseases… approved for RA treatment that is not responsive to TNF blockers

A

Abatacept

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6
Q

Name some ways steroids counteract inflammation (2 major ways)

A

1) Largely immunosuppressive - decrease number of circulating leukocytes -decrease adherence of neutrophils - inhibit lymphocytes 2) ALSO by inhibiting arachindonic acid metabolites -THEY INDUCE LIPOCORTIN which inhibits phospholipase A2 AND inhibit transcription of COX *also inhibit cytokine production/release, reverse increase in vasc. permeability, inhibit acute phase reactants

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7
Q

Adverse side effects of propionic acids

A

not recommended for preggo or breast-feeding Causes tinnitus, rash, and *peripheral edema*

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8
Q

mAb IL-6 receptor antagonist

A

Tocilizumab

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9
Q

ibuprofen naproxen flurbiprofen ketoprofen All fall into which category of NSAIDs

A

Priopionic Acid Derivatives the “en”s Mnemonic “P-en”… propionic acid for “ens”

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9
Q

endogenous cyclic neuropeptide; binds to immune cells

A

Cortistatin

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9
Q

drug treatment of gout that acts by inhibiting migration/activation of leukocytes… D.O.C. for actually treating acute gout USED with caution in pts with renal, hepatic, CV diseases *contraindicated during pregnancy

A

Colchicine

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10
Q

What is the most widely prescribed analgesic/antipyretic/antiinflammatory drug?

A

ASPIRIN! (acetyl salicylic acid)… it is the gold standard NSAID

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11
Q

what category of NSAIDs does aspirin fall into?

A

SALicylates… anything with “sal” in it also falls into this category

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13
Q

why would you use an NSAID in a neonate?

A

to close the ductus arteriosus

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14
Q

Adverse side effects of acetaminophen and what is NOT an adverse side effect that is typically in other NSAIDs?

A

allergic rxns skin rash **Hepatic necrosis because MANY different “drugs” incorporated acetaminophen as an active ingredient… so people often accidentally overdose Chronic use has also resulted in renal failure BUT… unlike the NSAIDs… it does NOT cause GI irritation, effect platelets, or increase bleeding time!!!

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15
Q

anti-inflammatory drug that inhibits synthesis of purines

A

Azathioprine “prine” sounds like “purine”

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17
Q

In general, what 2 important things do NSAIDs do to counteract inflammation?

A

1) Inhibit COX enzymes (thus no PGs or Tx formed) 2) Decrease activity of NFkB which is responsible for driving gene expression of many pro-inflammatory genes namely cytokines and adhesion molecules

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17
Q

MOA of priopionic acids

A

Reversible inhibition of COX

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19
Q

Explain the mechanism of how selective COX-2 inhibitors might cause CV probs

A

During vascular smooth muscle injury, platelets are promoted to aggregate by COX1 (TxA2 synthesis)… this is usually kept in check by COX2 which produces PGI2 to inhibit platelet aggregation… Thus by selectively blocking COX2, you leave platelet aggregation un-opposed to potentially result in thrombotic/embolic events in heart

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21
Q

Name 4 therapeutic uses of salicylates

A

1) antipyretic 2) antithrombotic 3) mild analgesic 4) anti-inflammatory (RA, osteoarthritis, inflam bowel disease)

22
Q

What are “-sones”

A

Steroids (glucocorticoids)

24
Q

Which adhesion molecules aid in inflammation?

A

Selectins for rolling Integrins for firm adhesion Followed by extravasation (usually by neutrophils in an acute response)

25
Q

enzyme is constitutively expressed; more important for cytoprotective/housekeeping functions such as maintaining gastric mucosa integrity

A

COX-1

25
Q

MOA of acetaminophen (tylenol

A

para-aminophenol derivative that inhibits COX activity Is only a WEAK COX inhibitor in presence of peroxides

26
Q

How might aspirin be used to decrease colon cancer?

A

It prevents PGE2 formation which normally would result in growth stimulation, angiogenesis, migration/invasion, and inhibition of apoptosis (all characteristics of cancer cells)

26
Q

Indomethacin sulindac etodolac tolmetin* (exception to the rule) ketorolac diclofenac fall into what category of NSAIDs?

A

ACetic acid derivatives the “ac”s

27
Q

MOA of salicylates?

A

COVALENTLY modifiy COX1 & 2… to IRREVERSIBLY inactivate COX (aka a permanent cock block)… this is unique among all other NSAIDs

28
Q

Name the main use of acetic acid derivatives + Adverse side effect

A

inflammation… not so much for fever, pain Used for RA but offer no advantage over aspirin Adverse side effects = severe headaches

29
Q

directed against IgE; inhibits immune system response to allergens

A

omalizumab

30
Q

Name 4 adverse side effects of salicylates

A

1) CNS stimulation followed by depression 2) Tinnitus & hearing loss 3) Reye’s Syndrome/lethal drug poisoning in kids 4) SALICYLISM (salicylate poisoning)

31
Q

MOA of salicylism

A

uncoupling of oxidative phosphoryation… results in hyperventilation/ resp alkalosis At large doses in children, can result in depression of medullary respiration center… All with concurrent metabolic acidosis

32
Q

MOA of acetic acid derivates (2 of em)

A

1) Reversibly inhibit COX 2) Inhibit neutrophil migration

33
Q

MOA of steroids

A

travel in serum bound to albumin, detach and cross plasma membrane, bind to cytosolic receptor, move into nucleus and effect transcription

34
Q

How does PGE2 modulate pain?

A

Peripheral nerve sensitization Specifically effects Na+ channels to increase resting membrane potential and decrease neuron firing threshold…. the result being that a smaller concentration of stimulus is required to reach nociceptor threshold and evoke pain sensation

35
Q

Which two PGs generally relax smooth muscle?

A

PGI2 & PGE2

36
Q

Most important eicosanoid for fever and pain

A

PGE2!!!

37
Q

Uricosuric agent drugs for gout that act as competitive inhibitors at the uric acid transporter (90% of uric acid is typically recycled) *NOT to be used with salicylates or renal compromised… just the opposite of allopurinol & febuxostat *NOTE- acute gouty arthritis may be induced during initial therapy with these drugs and do NOT alter course of acute attacks

A

Sulfinpyrazone & Probenicid

38
Q

Adverse side effects of sulfinpyrazone

A

inhibition of platelet function

40
Q

Therapeutic uses of acetaminophen AND what is it NOT used for?

A

1) analgesic – as effective as aspirin for pain 2) antipyretic *NOT used as an anti-inflammatory!!! therefore not in the NSAID group

41
Q

Name 2 problems with abrupt withdrawal of steroids

A

1) flare-up of underlying disease 2) acute adrenal insufficiency (we don’t make endogenous glucocorticoids when exogenous ones are supplied… so removal of them causes an abrupt drop)

42
Q

How can PGH2 lead to so many different PGs/Tx?

A

The product of further PGH2 metabolism depends on the tissue specific enzyme!!! ie platelets have Tx synthase to result in thromboxane A2 (for vasoconstriction/promote platelet aggregation), whereas endothelial cells have PGI synthase to make PGI2 (for vasodilation/inhibition of platelet aggregation)

43
Q

inflammatory enzyme is mostly inducible and considered to be “more important” in inflammatory responses, fever, and pain

A

COX-2

44
Q

Adverse side effects of steroids

A

-disturb fluid/electrolyte balance -hypertension -hyperglycemia -increase susceptibility to infection -cause growth retardation in children -peripheral edema (just like propionic acids) *Delay wound healing *cause muscle wasting, thinning of skin

45
Q

These 2 PGs cause increase in uterine tone/frequency/intensity

A

PGE2 & PGF2a

46
Q

Why can NSAIDs also lead to GI irritation?

A

Because they block COX1 and COX2, thus they block the cytoprotective actions of COX1 at the intestinal mucosa

47
Q

These mAb’s target TNF with high affinity and specificity

A

certolizumab, infliximab, adalimumab (CIA mAb’s) Potentially cause fungal infections or TB

48
Q

Adverse side effects of selective COX-2 inhibitors (2 of em)

A

1) Skin reactions (stevens-johnsons rashes & toxic epidermal necrolysis) 2) Cardiovascular probs

49
Q

Ductus arteriosus is sensitive to the vasodilatory effects of these 2 PGs

A

PGE2 & PGI2

50
Q

Drugs that treat gout by inhibition of xanthine oxidase and therefore prevent further uric acid synthesis *do NOT affect acute case of gout *CAN be used in renal compromised pts/those using salicylates

A

Allupurinol & febuxostat

52
Q

Which final COX pathway product generally contracts smooth muscle?

A

Thromboxane A2

53
Q

simulates myelin basic protein to compete with real myelin antigens for presentation to T-cells… thus a treatment for multiple sclerosis

A

Glatiramer acetate

54
Q

3 Therapeutic uses of priopionic acids, name an advantage over aspirin

A

1) antipyretic 2) analgesic 3) anti-inflammatory (RA, OA etc) *Note– NOT used for anti-thrombotics like aspirin It is better tolerated than aspirin

Pharm Exam 4 (3 decks)

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