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PCOL > Exam 3-Paracrine > Flashcards

Exam 3-Paracrine Flashcards

1
Q

examples of paracrines

A

PGs TLs and histamine

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2
Q

main intermediate to the eicosanoids pathway

A

arachidonic acid

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3
Q

NSAIDs inhibit

A

COX1 and 2, also called PGH Synthase 1 and 2

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4
Q

Costricosteroids inhibit

A

COX 1 and 2 as well as phospholipase A2 (PLA2)

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5
Q

eicosanoid antagonists work to block

A

leukotrienes

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6
Q

prostanoids

A

PGs and TXA

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7
Q

uses for eicosanoids and analogs

A

limited by kinetics, natural forms not orally available, short systemic half life

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8
Q

eicosanoid drugs for abortion

A

dinoprostone (facilitate labor) carboprost (stop hemorrhage) misoprostol (prevent ulcers)

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9
Q

eicosanoid drugs for ED or ductus arteriosus

A

alprostadil

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10
Q

eicosanoid drugs for pulm htn

A

epoprostenol, treprostinil, iloprost

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11
Q

eicosanoid drugs for glaucoma

A

lantanprost, travoprost, bimaprost, unoprostone

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12
Q

eicosanoid drugs for constipation

A

lubiprostone (activates Cl channels in the intestine to increase fluid)

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13
Q

prostanoid synthesis: arachidonic acid makes

A

PGG2 and PGH2

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14
Q

PGH2 makes

A

proaggregants and antiaggregants

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15
Q

proaggregants

A

TXA2 works at TP receptor

PGE2 works at P1-4 receptor

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16
Q

prostanoid for glaucoma

A

PGF2alpha at the FP receptor

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17
Q

antiaggregants

A

PGI2 (prostacyclin) at IP receptor
PGD2 at DP1-2 receptor
15 deoxy at DP2 receptor

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18
Q

Overall eicosanoids do the following

A

contract uterine muscle
vasoconstrict (pp hem)
decrease IOP
hypertricosis

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19
Q

PGF2alpha analogs for glaucoma: latanoprost, travoprost, tafluprost, bimatroprost. MOA/SE

A

MOA: reduce IOP by increasing aqueous humor outflow via activation of FP receptors.
SE: eye irritation, melanogenesis, hypertrichosis.
EACH should be combined with timolol

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20
Q

PGE2 eicosanoids in general do the following

A

contract uterine muscle
inhibit gastric acid
tx ED
maintain patent ductus arteriosis

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21
Q

PGE2 eicosanoids in general have these SE

A

vasoconstrict or dilate
contract GI smooth muscle
decrease pain threshold
stimulate Bicarb

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22
Q

These delay onset of labor because they can inhibit uterine contraction

A

NSAIDS

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23
Q

Dinoprostone (PGE2)
Prepidil gel
Prostin E2 supp
Cervidil insert

A

inducing abortion, facilitate labor, fetal death, hydatidiform mole
MOA: contraction of uterine smooth muscle via EP1 or EP3.
SE: NVD, change in BP

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24
Q

carboprost (15 PGF20)

hemabate IM

A

induce abortion, pp hemorrhage.
MOA: contraction of uterine smooth muscle via FP receptors
SE: NVD, change in BP

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25
Q

misoprostol (PGE1)

cytotec PO

A

induce abortion, prevent NSAID induced ulcers
MOA: EP1 or EP3 increase mucus or decrease H
SE: NVD, change in BP

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26
Q

alprostadil (PGE1)

A

for ED
MOA: relaxes corpora cavernosa sm muscle and dilates arteries via EP2 or EP4 receptors
SE: pain or priapism
[can be injected with phentolamine (alpha1/2 antagonist) or papaverine (vasodilator)]

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27
Q

alprostadil (PGE1) for fetal circulation

A

maintains patent ductus arteriosus
MOA: replaces endogenous PGI2 which keeps ductus open via IP receptors
SE: apnea, brady, hypoTN, hyperpyrexia
(indomethacin used to tx delayed closure)

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28
Q

PGIs effects in general

A

vasodilation (pulm htn), inhibit plt aggregation

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29
Q

PGIs SE in general

A

vasodilation of vasculature, contract GI, decrease pain threshold

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30
Q

Epropostanol (Flolan) (prostacyclin analog)

A

for pulm HTN, given through central line, half life minutes
MOA: vasodilation via IP receptors
SE: NV, HA, hypoTN, flushing, inj pain, inf site infections
interaction: anti-hypertensives and anticoags

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31
Q

Treprostinil (Remodulin) (prostacyclin analog)

A

for pulm HTN, given through central line or SQ, half life hours.
MOA: vasodilation via IP receptors
SE: NV, HA, hypoTN, flushing, inj pain, inf site infections
interaction: anti-hypertensives and anticoags

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32
Q

Iloprost (ventavis TM) (prostacyclin analog)

A

for pulm HTN inhaled, half life 20-30min.
MOA: vasodilation via IP receptors
SE: NV, HA, hypoTN, flushing, inj pain, inf site infections
interaction: anti-hypertensives and anticoags

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33
Q

TXA2s in general

A

no useful effects for analog drugs but physiological effects include: vasoconstrict, contract bronch sm muscle, contract GI, contract non preg uterine muscle. NSAIDs and ASA help with decreased pain threshold and the plt aggregation

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34
Q

Leuko pathway: Zafirlukast and Montelukast inhibits

A

CysLT2 and CysLT1/2

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35
Q

Leuko pathway: zileuteon inhibits

A

5LOX

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36
Q

Leuko LTC4 and LTD4 (cysteinyl leuks) MOA

A

act at receptor CysLT1/2 and signal Gq pathway to increase Ca and cause airway smooth muscle contraction

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37
Q

Leuko LTB4

A

act at BLT1 receptor through Gi an G16 second messenger to increase Ca and stimulate immune cell attraction

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38
Q

reversal of bronchospasm

A

epi or short beta 2 agonists (albuterol and levalbuterol)

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39
Q

prevent bronchospasm

slow/long act beta 2

A

agonists (salmeterol and formoterol)

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40
Q

prevent bronchospasm anticholinergic

A

ipratropium bromide, ipratropium and albuterol

41
Q

prevent bronchospasm xanthines

A

theophylline, dyphylline

42
Q

prevent inflammation in asthma

A

corticosteriods: beclomethasone, fluticasone, budesonide

43
Q

prevent of inflammation and bronchospasm in asthma: mast cell stabilizer

A

cromolyn, neocromodil

44
Q

prevention of inflam and bronchospasm in asthma: LTC4/D4 blockers

A

zileuton, zafirlukast, montelukast

45
Q

prevention of inflam and bronchospasm in asthma: IgE neutralizer

A

omalizumab

46
Q

high camp

A

low Ca and relaxation

47
Q

low camp

A

high Ca and contraction

48
Q

Xanthines: theophylline, dyphylline

A

bronchospasm prophylaxis
MOA: inhibition of PDE
SE:anx, HA, NV, low bp, tachy, seiz, arrythmia-death.
interactions-(p450 inducers) dilantin and barbs increase clearance. (p450 inhibitors) cimetidine and erythromycin decrease clearance.

49
Q

Mast Cell stabilizers: cromolyn anything

A

generally preferred in kids with asthma over corticosteroids.
MOA: blocks histamine and eicosanoid release by mast and basophils.
SE: bad taste, then very rare: bronchospasm, cough, edema, pain, HA, Nausea

50
Q

Zileuton (zyflo)

A

leuk blocker for asthma prophylaxis. reversible inhibition of 5 lox.
SE: mild heptox
Interaction: theophylline and warfarin

51
Q

Zarfirlukast (accolate)

A

leuk blocker for asthma prophylaxis. competitve antagonist of CysLT1 receptor.
Interaction: warfarin

52
Q

Montelukast

A

comp antag of cystLT1 receptor. leuk blocker for asthma prophylaxis

53
Q

Omalizumab (xolair)

A

for asthma prophylaxis. dose based on IgE levels-prevent from binding to its receptor. SE: rash, bleeding, GI events

54
Q

COX

A

converts arachidonic acid to PGH2

55
Q

COX 1 locations

A

GI, plt, kidney, CNS

56
Q

COX 1 has what function

A

cytoprotection, aggregation, blood flow, pain and pyrexia

57
Q

inhibit COX 1 would help with

A

ulcers, chemoprevention, drug interactions, analgesia, decrease fever

58
Q

COX 2 locations

A

uterus, kidney, vasculature, inducible, CNS

59
Q

COX 2 functions

A

contraction, increase blood flow, decrease aggregation (PGI2), pain, inflamm, pyrexia

60
Q

COX 2 effects of inhibition

A

delay labor, MI or stroke, analgesia, decrease fever or decrease inflamm

61
Q

COX 1 versus 2: NSAIDS

A

both

62
Q

COX 1 versus 2: ASA

A

1

63
Q

COX 1 versus 2: celcoxib

A

2

64
Q

general NSAID interactions

A

protein bound
slowed elim by probenecid
slow elim of MTX and Li
lasix and thiazides decreased effects

65
Q

ASA

A

chemoprevention. alone or with dipyridamole.
MOA: irreversible inhibition of COX1, also some COX2
interact: uriosurics
contraindications: sx, kids, hemophilia, heptox

66
Q

Salicylates: sulfasalazine, olsalazine, mesalamine

A

for inflamm bowel disease

67
Q

diflunisal (dolobid)

A

a salicylate for musculoskeletal strains and sprains or OA. SE: less GI and less anti plt than ASA

68
Q

Propionic acids: ibuprofem naproxen, flurbiprofen, ketoprofen, fenoprofen, oxaprozin

A

NSAIDs

69
Q

Indole and Indene Acetic Acids: indomethacin, sulindac

A

NSAID. most potent so higher risk for ulcers. Tx for delayed closure of ductus arteriosus, stop pre-term labor and symptoms of gout

70
Q

Heteroaryl Acetic Acids: Tometin, Ketorlac, Diclofenac

A

NSAIDS. many formulations of diclofenac. anthrotec (diclofenac and misoprostol) a PGE1 drug and is antiulcer

71
Q

Fenamates: Mefenamic acid and meclofenamate

A

NSAIDS. SE: diarrhea and hemolytic anemia, visual disturbance

72
Q

Enolic acids: Meloxicam and piroxicam

A

mel-COX2 selective (antiulcer)

73
Q

Alkanone: nabumetone(relafen)

A

NSAID

74
Q

Pyranocarbox acid: etodolac

A

NSAID. COX2 selective (antiulcer)

75
Q

Celecoxib

A

COX2 selective inhibitor. for arthritis or uncontrolled pain or FAP. MOA: inhibit COX2
SE: NSAID renal effects, risk of CV events
Interaction: same as NSAIDS plus metab by 2C9
contraindicated: NSAID or sulfa hypersensitivity, cardiac disease or CV risks

76
Q

block COX2 and CV risk

A

increase risk for clot formation

77
Q

Tylenol

A

analgesia, NO INFLAMM BENEFIT.
MOA:?
SE: heptox d/t cyp2E1 and 1A2 convertion to NAPQI
interact: etoh, imatinib, isoniazid and rifampin upreg liver enz, tobacco.

78
Q

DMARDS

A

slow damage, more toxic than NSAID, slow onset

79
Q

alternative therapies for arthritis

A

lovaza, capsaicin, sativex, glucosamine and chondroitin

80
Q

DMARD immunosupp: MTX, lefludomide, azathioprine, cellcept, cyclosporine

A

MOA: inhibit enz to DNA synthesis or Tcell function, suppress DNA synthesis. SE: immunosupp, GI, heptox, CA. cyclosporin is nephrotox, hirsutism
contraind:ID, hep impairment, cyclo-inhibitos of 3A4

81
Q

MTX (DMARD)

A

folate analog, inhibits AICA transformylase and thymidylate synthase. stops making DNA

82
Q

Lefluomide (DMARD)

A

inhibits DHODH

83
Q

Azathioprine (DMARD)

A

purine antagonist, converted to 6 thioguanine.

84
Q

Cellcept (DMARD)

A

inhibits IMPDH/GMP/GDP/GTP production. more cell use alt pathway but T and B cells cannot

85
Q

Anti-malarial DMARD: hydroxychloroquine (plaquenil)

A

MOA:? may involve inhibition of DNA/RNA synthesis.
SE: visual dist, allergic rxn, psoriasis, heme, CNS
Contraind: hypersensitive of ocular disease***
interact: inhibits 2D6, antacids, reduces MTX clearance.

86
Q

Gold DMARD: aruanofin, aurothiomalate

A

MOA:?
SE:stomatitis, proteinuria, heme, aplastic anemia. auranofin-less efficatious and GI worse.
CAUTION-black box-heme or renal issues, stomatitis.

87
Q

Penicillamine DMARD: cuprimine, depen

A

MOA?
SE: bone marrow supp, lung/hep/renal tox, skin rxn, GI, stomatitis
contraind:preg, breast feeding, renal
caution: bone marrow supp ***
interaction: gold, cytotoxic drugs, Al or Mg antacids or Fe supp.

88
Q

Sulfasalazine DMARD

A

MOA: metab mesalamine and sulfapyridine by colon bacteria
SE:rash, GI, NV, heptox, orange yellow skin and urine, decreased male fertility

89
Q

TNF blockers DMARDs: etanercept, infliximab, adalimumab, golimumab, certolizumab

A

MOA: antagonize TNF activity by binding TNF alpha
SE: inj site rxn, immunosupp, increase Ab form, HA, GI, rash, fatigue.
Caution: CA***
interact: immunosupp, vaccines and TNF/IL blockers

90
Q

Interleukin blockers DMARDs:anakinra (kineret), tocilizumab (actemra)-IL6R, canakinumab (iaris)-IL1Beta

A

MOA: antagonize IL1R or IL6R receptors or binds IL1beta preventing interleuk mediated immune activation.
SE: inj site rxn, inf, decreased WBC/plt, GI.
Contraind:anakinra-ecoli or latex allergy
Caution: BB for toxilizumab (infection)***
interact:TNF/IL blockers, rituximab, abatacept

91
Q

Tofacitib (xeljanz) DMARD

A

nib means its a signal transduction inhibitpr (STI) or kinase inhibitor. MOA: inhibits Janus kinase (JAK) proteins.
SE: myelosupp, URI, HA, diarrhea.
caution: don’t use with other biologic DMARDs

92
Q

Rituximab (rituxan) DMARD

A

human/mouse Ab to CD20 protein, Ca channel reg cell cycle, diff in B cells
MOA: binds CD20, kills B cells.
SE: 1st inf rxn, pulm and CV efx, myelosupp
cautions: exfoliative derm **BB.

93
Q

Abatacept (orencia) DMARD

A

used for failure of other DMARDs like MTX and anti-TNF drugs.
MOA: binds CD80/86 receptor preventing full act of T cells which are central in RA path.
SE: inf rxn, URI
interaction: TNF or IL blockers or other immunosupp, live virus vaccines

94
Q

Glucocorticoids DMARDs:prednisone, prednisolone

A

MOA: decrease PLA2 and COX2 expression, decrease WBC count.
SE: limit long term use, frax, cataracts, cushing, DM, htn.
can give intraarticular

95
Q

Capsaicin DMARD

A

mediator of hot sensation from chili peppers. MOA: depletes substance P and act TRPV1 channels. SE: burn, sting.

96
Q

Gout drugs: colchicine

A

alkaloid from autumn crocus.
MOA: prevent polymerization of tubulin, inhibit cell migration and phagocyt of crystals.
SE:diarrhea, VN, alopecia, immunosupp, neuritis, myopathy.
OD tox: burning throat, bloody diarrhea, shoc, fatal ascending CNS depression

97
Q

Uricosurics:probenecid and sulfinpyrazone

A 
Gout drugs.  
MOA: inhibit reabs of uric acid in prox tube of kidney
SE: GI irritation, rash, kidney stones
Contraind:kidney stones
interact: NSAIDs may decrease effects
98
Q

Xanthine Oxidase Inhibitors: allopurinol and febuxostat

A

used in pts with very high urate, prior kidney stones, renal impairment***
MOA: competitively inhibits xanthine oxidase
SE:initial increase in attachs, rash, CV events with febux
interact:inhibits metab of probenecid, meraptopurine and azathioprine

99
Q

pegloticase (krystexxa)

A

use for refractory gout.
MOA: enzymatic degredation of uric acid to allantoin.
SE: inf rxn, anaphylaxis, initial increase in attacks, NVD
Contraind:G6PD def-causes hemolysis and malig hyperthermia***
caution in preg/breastfeeding. must have special caregiver to administer

PCOL (9 decks)

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