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PB+T > Anti-inflammatory/glucocorticoid Pharmacology > Flashcards

Anti-inflammatory/glucocorticoid Pharmacology Flashcards

0
Q

H1 - anti histamines

A

Inverse/neutral agonist against H1 receptor
1st gen: 12 hour H/L; generally sedative
- many first gens can also treat nausea
2nd gen: 12-24 hour H/L; don’t cross into CNS -> non sedative (generally)

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1
Q

Histamine: general info

A

Vasoactive amine stored in granules of mast cells (tissue specific) and basophils. Responsible for type 1 HSN, i.e. allergic response

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2
Q

Diphenhydramine

A

1st gen, not a histamine “blocker”: inverse agonist

  • sedation, muscarine inhibition (dry mouth)
  • crosses into CNS readily so lots of other side effects
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3
Q

2nd gen Anti-histamines

A

Loratidine: Claritin
Fexofenadine: Allegra
Cetirizine: Zyrtec
- generally don’t cross BBB

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4
Q

Corticosteroids: MOA, indication, administration, contraindications

A
  • Block all known eicosenoid synthesis pathways.
  • Anti inflammatory * not effective against acute asthma attacks
  • oral administration has highest rate of side effects
  • used as maintenance
  • contraindicated in: peptic ulcers, HTN, CHF, psychosis, diabetes, osteoporosis and glaucoma
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5
Q

Inhaled corticosteroids

A

MDI: metered dose inhaler (much more common); DPI: dry powder inhaler

  • local SE: dysphonia, thrush and throat irritation
  • systemic SE: glaucoma, cataracts, skin change and bruising, infections, psych effect
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6
Q

Fluticasone propionate (Flovent)

A

Medium potency, medium acting, synthetic corticosteroid
Anti-vasoactive, antipyretic and vasoconstrictive activity
- high lipophilicity
- increased tissue retention
- 14 hour H/L

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7
Q

Budesonide (pulmicort)

A

Synthetic, non- halogenated form of prednisone
High potency and first past effect, weak mineralocorticoid
2-3.6 hour H/L

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8
Q

Prednisone

A

Commonly prescribed oral corticosteroid
Metabolized in liver to active form (prodrug)
Hydrocortisone < prednisone < dexamethasone

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9
Q

Adverse side effects of inhaled corticosteroids: short term (2), long term (1)

A

Short term: hoarseness, oral candidiasis

Long terms: inhibits growth in kids

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10
Q

Adverse side effects of oral corticosteroids: short term and long term

A 
Short term: minimal, behavioral, acute peptic ulcers
Long term (14+ days): 
- adrenal suppression
- altered sugar metabolism
- infections 
- skin atrophy
- osteoporosis
- cataracts
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11
Q

Inhibiting cox enzymes regularly

A

Can push the eicosenoid pathway towards leukotrienes contributing to asthma

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12
Q

Cox-1

A

Constitutively produced
Housekeeping, gastric mucosal protection
Maintenance of renal and GI blood flow
Anti-thrombogenic

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13
Q

Cox-2

A 
Inducible enzyme (injury/stress) 
- inflammation and cancer
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14
Q

NSAIDs: general

A

Cox inhibitors; commonly used analgesics
- inhibit pro inflammatory cox generated eicosenoids
- also inhibit homeostatic cox generated eicosenoids
Very high albumin binding: underrepresented Vd

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15
Q

Aspirin

A

Acetylates Serine residues on both cox-1 and 2 (irreversible)
- low dose preferentially inhibits cox-1 (PGE/TXA) reduces platelet activation
- H/L 3-5 hours @ < 300 Mg/day; 1500+ H/L jumps t 15 hrs
SE:
- rapidly absorbed via stomach/upper small bowel (pKa 3.5) and is rapidly hydrolized.
- alkalinization of urine increases excretion
- low dose: GI irritation/bleeding (systemic cause not enteric)
- high dose: salicylism, N/V, hyperventilation, vertigo/tinnitus, metabolic alkalosis
- contraindicated in asthma

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16
Q

Selective COX-2 inhibitors:4

A

Celecoxib (contraindicated in sulfa allergic and asthma), meloxicam (only partially preferential)* protective against colon polyps

  • increased risk of thrombotic event
  • hepatotoxic, renal failure
  • telomanin
  • paroxicam
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17
Q

Key NSAID SE

A 
Non-selective AND COX-2
GI upset/bleed
Renal dysfunction
Na retention (probably 2dnary to renal dysfunction) 
Bleeding in general

Non-selective > COX-2 -> GI bleeding
- addition of PPI/H2 receptor blocker can mitigate

COX-2 > no selective -> thrombolytic events.

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18
Q

Leukotrienes

A

Produced by lipooxengase

  • Moderates SRS-A (slow reactive substance of anaphylaxis)
  • effectors of asthmatic bronchoconstriction
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19
Q

Leukotriene inhibitors

A

Montelukast, Zafirlukast, zileuton

  • reduce exacerbations
  • prevent activity induced, antigen, and aspirin induced bronchoconstriction
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20
Q

Nabumetone

A

Only prodrug NSAID; ketone that is metabolized to acidic active drug.

  • 24 hour H/L
  • often requires high dose
  • less GI symptoms
  • expensive
  • can cause pseudoporphyria and photosensitivty
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21
Q

Glucuronidation/sulfination

A

Two mechanism of conjugating NSAIDS to non-toxic forms

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22
Q

NSAID metabolism/excretion

A

Mostly unaffected by food intake (bioavailability)
Metabolized mostly by CYP3A/2C (P450 family)
Mostly renal excretion, almost all have slight biliary, excretion/resorption

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23
Q

Naproxen

A

One of the few NSAIDs that is not a racemic mix

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24
Q

NSAIDS and synovial fluid

A

Repeated usage results in synovial deposition: short half life drugs are typically present in amounts greater than their H/L would predict. Longer H/L drugs are found in proportion to their H/L

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25
Q

Non-PGE mediated mechs of NSAID activity

A
  • decreased chemotaxis
  • down regulation of IL-1 (Hot)
  • decreased ROS production
  • interference with Ca mediated events
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26
Q

NSAID nephrotoxicity

A

Pretty much all. Probably a result of interference PGE that regulates blood flow in renal tubules.

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27
Q

General NSAID SE (per katzung)

A

CNS: HA, tinnitus, dizziness
CV: HTN/edema (rarely MI/CHF)
GI: pain, dysplasia, N/V, bleeding/ulcers
Hematologic: (Rare) Tcytopenia, Npenia possibly aplastic anemia
Hepatic: abnormal liver tests, (rare) liver failure
Skin: rash
Renal: insufficiency, failure, hyperkalemia, proteinuria

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28
Q

Non-acetylated salicylates

A

Sodium/magnesium salicylate, salicyl salicylate

  • all effective, non-platelet inhibiting
  • indicated in PTs. with asthma or bleeding conditions
  • administered in much higher doses (3-4 g vs 100-200 Mg)
29
Q

Celecoxib (highly selective) meloxicam (preferentiall selective)

A

Selective COX-2 inhibitor: (celebate people are more choosey) non-platelet inhibiting, GI SE incidence about 1/2 non selective inhibitors. (Black box: warfarin interaxn)

  • non- cardioprotective
  • normal renal toxicity
  • celecoxib is a sulfonamide; allergies
30
Q

Diclofenac

A

Phenylacetic acid derivative
Non-selective COX inhibitor: typically less GI symptoms (especially in combined preparation with omeprazole/misoprostol) (loaf is a solid poo) but renal effects were common in high risk PTs.
- useful in eye surgical cases in gel prep.

31
Q

Diflunisal

A

salicylate derivative
Not metabolized to salicylate, enterohepatic glucuronidates it where upon second pass its active moiety is cleaved. (Lun:moon: tide:second pass -> metabolically active)
- especially useful in bone pain (cancer, oral lesions)
- clearance depends on renal function

32
Q

Etodolac

A

racemic acetic acid mix
Doesn’t undergo chiral conversion in the body
- 200-400mg TID/QID
- black box: cardiovascular risk, MI and GI bleeding

33
Q

Flurbiprofen

A

propanoic acid derivative
Most complex MOA of any NSAID: inhibits COX non-selectively, but also alters TNFa, and NO (flub, how about NO)
- it undergoes extensive hepatic metabolism (fat with a big liver)
- topical ophthalmic formula, HEENT perioperative analgesic, lozenge
- associated with movement deficits (fat and uncoordinated)

34
Q

Ibuprofen

A

phenylpropanoic acid derivative
2.4 g = 4 g aspirin (Ib proven: proves itself better, multi tier dosing effect)
- lower incidence of fluid retention relative to indomethacin
Analgesic has lower dose threshold than anti inflammatory effect
- effective at closing a patent ductus arteriosis
- contraindicated in PTs. with nasal polyps, aspirin allergies, and angioedema
- antagonistic action to aspirin
- rarely aseptic meningitis (typically with SLE PTs)

35
Q

Indomethacin

A

indole derivative
Non-selective COX inhibitor, and potentially phoslip A/C, neutrophil migration, and B/T cell proliferation
- useable includes, PDA closure, diabetes insipidus, juvenile RA, urticarial vasculitis et al.
- GI symptoms common, but HA (25%) along with cognitive effects including depression, psychosis and hallucination can occur.
- renal papillary necrosis
- probenacid increases its activity by decreasing excretion

36
Q

Ketoprofen

A

propanoic acid derivative
Inhibits both COX (non-selectively) and lipoxygenase
- major SE are in GI and CNS

37
Q

Ketorolac

A

Analgesic, non-anti inflammatory

  • can replace morphine (TORO: bull:strong med:morphine)
  • similar common toxicity
38
Q

Naproxen

A

napthylpropanoic acid
Only single enatiomer NSAID
- free fraction sig. higher in women but same half life (women use napkins more then men)
- GI bleeding not common, but double that of OTC ibuprofen
- can cause pneumonitis, leukocytoklastic vasculitis

39
Q

Oxaprozin

A

propanoic acid derivative
- among subgroup (flurbiprofen, Ibuprofen) it has the longest H/L (50-60 hrs)
(Ox plowed like a pro for 60 hours)

40
Q

Piroxicam

A

NON-selective COX inhibitor
At high doses it can inhibit PMN migration, and ROS production
- higher incidence of peptic ulcer and bleeding
- (P-cam: pooper camera can cause bleeding: higher incidence of bleeding, Ox that doesn’t have pro in it)

41
Q

Sulindac

A

sulfoxide drug
Reversibly metabolized to active sulfa metabolite. Enterohepatic circulation
- protective agains some colon, breast and prostate cancers
- can be assoc with Stevens-Johnson’s syndrome and cholestatic liver damage

42
Q

Tolmetin (non-selective COX inhibitor)

A

Can’t treat gout

Can cause TPP (JD was a tool (toolamitin) for diagnosing dr. Coxs pt with TTP)

43
Q

DMARDs (only 1st TL)

A

Disease modifying antirheumatic drugs; immunosuppressive

  • abaracept
  • azathiopine
  • chloroquine (+ hydroxy)
  • cyclophosphamide
  • cyclosporine
  • leflunomide
  • methotrexate
  • mycophenolate mofetil
44
Q

Abaracept

A

MOA: T-cell activation inhibitor (inhibits CD24 binding) (excep T cells)
Kinetics: loading dose @ 0,2,4 weeks then monthly. H/L 13-16 days
Indications: severe RA that has been unresponsive to other DMARDs
ES: increased risk of infection, (IRI) HSN I, possible lymphoma

45
Q

Azathiopine

A

MOA: 6-thioguanine inhibits inosinic acid, B/T cell function Ig and IL-2 production
Kinetics: dependent on TPMT activity
Indications: RA, potentially; psoriatic arthritis, reactive arthritis, polymyositis
SE: bone marrow suppression, GID, IRI, potential lymphomas

46
Q

Chloroquine/hydroxychloroquine

A

MOA: unknown. Potentially Tcell suppression reducing chemotaxis, stabilization of lysosomal enzymes, inhibition of DNA, RNA and trapping of free radicals
Kinetics: rapidly absorbed, extensively tissue bound in melanin containing tissues (50% free) H/L up to 45 days.
Indications: RA but not very effective. Useful for trt of skin manifestations
SE: ocular toxicity at high doses (hydroxy more potent), dyspnea, N/V, abd. Pain. Nightmares

47
Q

Cyclophosphamide

A

MOA: phosphoramide mustard cross links DNA-> B/Tcell suppression 30-40%.
Kinetics: Katzung ch54.
Indications: RA ORALLY. SLE and other RA diseases
SE: Katzung ch 54

48
Q

Cyclosporine

A

MOA: alters gene txn, and suppresses IL-1 and IL-2, inhibits macs -T cell interaxn. B cell function is also effected.
Kinetics: absorption is incomplete and erratic. Grapefruit juice increases absorption up to 62%.
Indications: RA, retards bony erosions
SE: leukopenia, tcytopenia, anemia, cardiotoxicity, sterility, bladder cancer (rare)

49
Q

Leflunomide

A

A77-1726 inhibits dihydroorate dehydrogenase -> decreased RNucleotide synthesis, decreased IL-10, NF-kB (roughly equal efficacy to methotrexate)
Kinetics: completely absorbed with a 19 day H/L, can enter enterohepatic circulation. Cholestyramine can increase H/L by 50%.
Indications: RA, stopping bony erosions, synergistic with methotrexate
SE: diarrhea, liver enzyme elevation, mild alopecia, weight gain and BP increase.

50
Q

Methotrexate

A

First line DMARD for RA
MOA: at lower (sub chemo levels) AICAR transformylase and thymadylate synthetase is inhibited -> increases AMP -> converted to Adenosine which is a potent anti inflammatory agent. Also effects chemotaxis
Kinetics: 70% absorbed after oral admin. H/L 6-9 hours (up to 24 hours. Renal excretion = 70%, biliary excretion = 30%
Indications: RA with boney erosions, lots of other AA itis conditions
SE: Nausea, mucosal ulcers common. Leukopenia, anemia, hepatotoxicity, lung HSN possible. NOT for preggers.

51
Q

NSAID SE: CNS- 3

A

Tinnitus, dizziness, HA

52
Q

NSAID SE: Cardiovascular - 5

A

Fluid retention, HTN, edema, Myocardial infarction (rare), CHF (rare)

53
Q

NSAID SE: gastrointestinal - 5

A

Abdominal pain, dysplasia, nausea, vomiting, ulcers/bleeding (rare)

54
Q

NSAID SE: hematologic - 3

A

Thrombocytopenia (rare), neutropenia (rare), aplastic anemia (rare)

55
Q

NSAID SE: hepatic - 2

A

Increased liver enzymes, liver failure (rare)

56
Q

NSAID SE: pulmonary - 1

A

Asthma

57
Q

NSAID SE: skin - 2

A

Rashes, pruritis

58
Q

NSAID SE: renal - 4

A

Renal insufficiency, renal failure, hyperkalemia, proteinuria

59
Q

CYP2A/CYP3C

A

Primary metabolism of NSAIDs

60
Q

ROSCaILCh

A

Non-PG mediated effect if NSAIDs

  • ROS burst modification
  • Ca med processes down reg
  • IL-1 altar ion (anti pyrogenic)
  • chemotaxis alteration
61
Q

Probenacid

A

Increases the efficacy of some NSAIDs by inhibiting clearance

62
Q

ductus arteriosis closure

A

Ibuprofen and indomethacin

iBID

63
Q

Na NSAIDs

A

NAproxen and NAbumetone

  • both can result in pseudoporphyria
  • bums with bad vision: photosensitivty in NAbumetone use
  • proximal limb: vasculitis with naproxen use
64
Q

Betamethasone

A

Lung development in premature (34 weeks) infants. Betamethasone is preferred because maternal proteins don’t bind it as much so higher dose gets to baby
(beta for Bebes)

65
Q

Isoproterenol

A

Potent broncodilator

  • dangerous due to its ability to induce arrythmias
  • IsoproTERRORnol….cause it can kill you
66
Q

Rol, Nol, but

A

Albuterol, terbutaline, metaproterenol, pirbuterol

  • B2 selective agonists
  • most RS mixes that are inhaled
  • terbutaline is available IM
  • 3-4 hour activation time
67
Q

Salmeterol, formotorol (formoterol)

A

Long acting B2 selective agonists (12hours)

- (keeps your motor running)

68
Q

Roflumilast

A

Methylxanthine trt for COPD

69
Q

Caffeine, theophylline, theobromine

A

Decrease inflammation by decreasing PDEs -> increased cAMP

- PDE4 has been implicated in inflammatory cells

70
Q

N-acetylcystine

A

Antidote to acetaminophen OD. Original dose dependent

No acetylation

71
Q

Cyclosporine

A

Anti-necrotic process drug: retards swelling of mitos by inhibiting mito trans pores.
(Spore:Pores)

PB+T (20 decks)

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