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Pharmacology: Kaplan, Uworld, FA > Drugs inflammator and relared disorder_ Eicosanoid pharmacology > Flashcards

Drugs inflammator and relared disorder_ Eicosanoid pharmacology Flashcards

1
Q

_______ are cell-regulating polyunsaturated fatty acids

A

Eicosanoids

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2
Q

Eicosanoids is synthesized from ______ and released by actions of __________ from lipid membranes

A

Arachidonic acids; phospholipase A2

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3
Q

Eiconsanoids are present in ______ concentration in most cells but synthesized and released on demand in response to stimuli

A

Low

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4
Q

Stimulus that triggers release of eicosanoids

A

IgE-mediated reactions (HSR type I); inflammatory mediators, trauma, heat; and toxins

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5
Q

eicosanoids interact with specific receptors, which are ________ effector systems

A

G-protein coupled to 2nd messenger

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6
Q

membrane phosplipids “____________” ——> arachidonic acid which gives

  1. cyclooxygenase (COX1, COX2) —->endoperoxides: giving PGI2; PGD2, PGE2, PGF2alpha
  2. Lipooxygenase (LOX) —->hydroperoxides: giving Leukotrienes
A

phospholipase A2;

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7
Q

Prostaglandins (PGs) are _________ in stomach, dilates renal vasculature, contracts uterus and maintains ductus arteriosus

A

Cytoprotective

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8
Q

TxA2 causes

A

platelet aggregation

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9
Q

GI PGs and platelets TxA2 are synthesized via

A

COX1 (constitutive)

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10
Q

________ synthesizes PGS involved in inflammation; fever, and pain

A

COX2 (inducible)

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11
Q

both enzymes _____ and ______ synthesizes renal PGs which increases RBF

A

COX1 and COX2

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12
Q

_______ are formed via hydroperoxides from LOX on arachidonic acid

A

Leukotrienes (LTs)

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13
Q

________ inflammatory mediator leading to neutrophil chemoattractant; activates PMNS(polymorphonuclear leukocytes); increase free radical formation - cell damage

A

LTB4

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14
Q

LTB4 (inflammatory mediators)

A

neutrophil chemoattractant; activates PMNS(polymorphonuclear leukocytes); increase free radical formation - cell damage

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15
Q

LTA4; LTC4 and LTD4 causes

A

anaphylaxis and bronchoconstriction (role in asthama)

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16
Q

Leukotrienes are targets for ?

A
  1. Glucocorticoids: decreases phopholipase A2 activity leading to both antiinflammatory and immunosuppressive actions
  2. Zileuton: inhibits lipooxygenase leading to decrease LTs used in Rx of asthma
  3. Zafirlukast and “lukasts” : LT-receptor antagonists used in Rx of asthma
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17
Q

inhibits lipoxygenase leading to decrease LTs used in Rx of asthma

A

Zileuton

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18
Q

ecreases phopholipase A2 activity leading to both antiinflammatory and immunosuppressive actions

A

Glucocorticoids

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19
Q

LT-receptor antagonists used in Rx of asthma

A

Zafirlukast and “lukasts”

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20
Q

__________ are formed via endoperoxides from actions of cyclooxygenases (COXs)

A

Prostaglandins

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21
Q

_______ is expressed in most tissues: platelets, stomach; and acts to synthesize TxA2 and cytoprotective PGs

A

COX1

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22
Q

_______ is expressed in brain and kidney and sites of inflammation

A

COX2

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23
Q

_______ are drugs of PGE1

A

Misoprostol: ( used previously in Rx of NSAID induced ulcers; protective action on gastric mucosa)

Alprostadil: ( maintains patency of ductus arteriosus; vasodilates, used in male impotence) - CI in preg unless used as abortifacient (misoprostol + miferprsitone combined)

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24
Q

used previously in Rx of NSAID induced ulcers; protective action on gastric mucosa

A

Misoprostol

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25
Q

maintains patency of ductus arteriosus; vasodilates, used in male impotence) - CI in preg unless used as abortifacient (misoprostol + miferprsitone combined)

A

Alprostadil

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26
Q

_______ used to close ductus arteriosus

A

Indomethacin

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27
Q

PGE2 causes

A

uterine smooth muscle contraction

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28
Q

uses of PGE2

A

dinoprostone used for “Cervical ripening” and as abortifacient

29
Q

abortifacient means

A

combination of misoprostol + miferprsitone

30
Q

used for “Cervical ripening” and as abortifacient

A

dinoprostone

31
Q

PGF2-alpha actions

A

causes uterine and bronchiolar smooth muscle contraction

32
Q

drugs of PGF2-alpha are

A

Carbopros (used as abortifacient)

latanoprost (Rx glaucoma (decrease intraocular pressure)

33
Q

_______Rx glaucoma (decreases intraocular pressure

A

latanoprost

34
Q

PGI2 (prostacyclin) uses

A

pulmonary HTN

35
Q

PGI2 actions

A

platelet stabilizer and vasodilators

36
Q

Drugs of prostacyclin (PGI2) include

A

epoprostenol

37
Q

Prostacylin

A

Vasodilator (PGI2)

38
Q

PGE2 and PGF2-alpha

A

both increases in primary dysmenorrhea

Therapeutic effects of NSAIDs may be due to inhibition of their synthesis

39
Q

Thromboxanes (TxAs) (TxA2)

A

platelet aggregator (inhibition of synthesis underlines protective role of acetylsalicylic acid (ASA) post-MI))

40
Q

Nonsteroidal anti-inflammatory drugs (NSAIDs)

A

most are non-selective inhibitors of cyclooxygenases, acting on COX 1 and COX2 isoforms to decrease formation of PGs and TxA2

41
Q

most are non-selective inhibitors of cyclooxygenases, acting on COX 1 and COX2 isoforms to decrease formation of PGs and TxA2

A

Nonsteroidal anti-inflammatory drugs (NSAIDs)

42
Q

______ are analgesic, antipyretic and antiinflammatory and have anti-platele effects

A

NSAIDs

43
Q

Acetylsalicylic acid (ASA) is prototype of ________ which includes more than 20 individual drugs

A

NSAIDs

44
Q

Platelet stabilization via PGI2

A

activation of PGI2 receptors —>stimulation of adenylate-cyclase —–>increase cAMP —> increase activity of internal Ca2+ “pumps” —> decrease free Ca2+ => platelet stabilization

45
Q

Platelet aggregation via TxA2

A

activation of TxA2 receptors —>stimulation of phospholipase C —> increase PIP2 hydrolysis —> PIP3 ——>mobilization of bound Ca2+ —-> increase free ca2+ => platelet aggregation

46
Q

Acetylsalicylic acid (ASA: Aspirin) causes

A

irreversible inhibition of COXs; covalent bond via acetylation of Serine hydroxyl group near the active site

47
Q

covalent bond via acetylation of Serine hydroxyl group near the active site

A

Acetylsalicylic acid (ASA: Aspirin)

48
Q

Actions of ASA is dose dependent:

A
  1. antiplatelet aggregation: low dose, used in post-MI prophylaxis to reduce risk of transient ischemic attack (TIAs)
  2. analgesia and antipyresis: moderate dose
  3. antiinflammatory: high doses
  4. uric acid elimination:
    • Low to moderate doses –> decreases tubular
      secretions —> hyperuricemia
    • High-doses: decrease tubular reabsorption
      =>uricosuria
  5. Acid-Base and Electrolyte balance:
    • High therapeutic: mild uncoupling of oxidative phosphorylation —> increase respiration —> decrease PCO2 —-> respiratory alkalosis —-> renal compensation —–> increase HCO3- elimination —> compensated respiratory alkalosis (pH = normal; decrease HCO3- ; decrease PCO2)
    • Adults: stable condition but in children it increases
      toxicity
    • Toxic dose: inhibits respiratory center —> decrease respiration —-> increase PCO2 —-> respiratory acidosis (decreased pH, decrease HCO3- and normalization of PCO2) plus inhibition of Krebs cycle and severe uncoupling of oxidative phosphorylation (decreases ATP)—-> metabolic acidosis, hyperthermia and hypokalemia (decrease K+)
49
Q

Side effects of ASA (aspirin)

A

GI irritation, ulcer and bleeding;
salicylism ( tinnitus, vertigo, decrease hearing —often 1st
sign of toxicity)
Brochoconstriction : exacerbates asthma
Hypersensitivity, especially “triad”: asthma, nasal polyps, rhinitis
Reye Syndrome: encephalopathy
increase bleeding time (antiplatelet)

chronic use:
   -  associated with renal dysfunction
Drug interactions: 
    - ethanol (increase GI bleeding)
    - OSUs and warfarin (increase effects)
    - uricosurics (decrease effects)
50
Q

aspirin overdose management

A

extensions of the toxic actions, + at high dose vasomotor collapse occurs, with respiratory and renal failure

management: no antidote; managed via gastric lavage (+/- activated charcoal); + ventilatory support and symptomatic manangement of acid-base/ electrolyte imbalance and hyperthermia and resulting dyhration
increase urine volume and its alkalinization facilitates ASA renal elimination; ASA follows zero-order elimination at toxic doses

51
Q

ASA follows _______elimination at toxic doses

A

zero-order

52
Q

other examples of NSAIDs that are reversible inhibitors of COX 1/2 with analgesic, antipyretic, and antiinflammatory actions include

A 
Ibuprofen
Naproxen
indomethacin
ketorolac
sulindac

comparison with ASA:
analgesia: ketorolac > ibuprofen/naproxen> ASA
GI irritation: < ASA(but still occurs use misprostol)
minimal effects on acid-base balance, no effect on uric acid elimination
allergy: common (cross HS with ASA)
Renal: chronic use, nephritis, nepheritic syndrome, acute failure (via decrease PGE2 and PGI2, which normally maintains GFR and RBF) does not occur with sulindac

53
Q

which PGs normally maintains GFR and RBF

A

PGE2 and PGI2

54
Q

toxicities of Indomethacin

A

thrombocytopenia, agranulocytosis and >CNS effects

55
Q

toxicities of sulindac

A

Steven-johnson syndrome, hematotoxcity

56
Q

Selective COX 2 inhibitors

A

Celecoxib

57
Q

_______ not as effective as antiflammatory compare to other NSIADs; less GI toxicity; less antiplatelet actions

A

Celecoxib

58
Q

may possibly exert prothrombotic effects via inhibition of endothelial cell function (MI and strokes)

A

Celecoxib

59
Q

Cross-hypersensitivity between ________ and _________

A

Celecoxib and sulfonamides

60
Q

NSAIDs are associated with _________?

A

increased risk of thrombotic events such as MI and stroke

61
Q

_________ has no inhibition of COX in peripheral tissues and lacks sign. antiinflammatory effects

A

Acetaminophen

62
Q

Equivalent analgesic and antipyretic activity to ASA due to inhibition of cyclooxygenases in CNS

A

Acetaminophen

63
Q

Comparison of Acetaminophen to ASA

A

no antiplatelet action; no Reye syndrome; no effects on uric acid; not bronchospastic (safe in NSAID HS and asthmatic) and GI distress is minimal at low-moderate dose

64
Q

Acetaminophen toxicity effects

A

Hepatotoxicity:

  • its metabolized mainly by liver glucuronyl transferase to form inactive conjugate
  • at P450 it results in formation of reactive metabolite (N-acetylbenzoquinoneimine), which is inactivated by glutathione (GSH)
  • in overdose: finite stores of GSH is depleted resulting in metabolite reacting with hepatocyte causing nausea and vomiting, abdominal pain, liver failure due to centrilobular necrosis
  • chronic use of ethanol enhances liver toxicity via induction of P450

management of hepatotoxicity: N-acetylcysteine (supplies -SH groups), preferably within 1st 12 hrs

65
Q

________ (supplies -SH groups), preferably within 1st 12 hrs in hepatotoxicity

A

N-acetylcysteine

66
Q

N-acetylcysteine also used as

A

mucolytic in CF disease

67
Q

“Tot” toxicity

A

young children are gustatory explorers; therefore compounds responsible for toxicity in children age of 3 years are : aspirin, acetaminophen (ppl know about reye syndrome), supplementary iron tablets

68
Q

aspirin, acetaminophen (ppl know about reye syndrome), supplementary iron tablets

A

“Tot” toxicity

Pharmacology: Kaplan, Uworld, FA (9 decks)

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