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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
NSAIDS and synovial fluid
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
25
Non-PGE mediated mechs of NSAID activity
- decreased chemotaxis - down regulation of IL-1 (Hot) - decreased ROS production - interference with Ca mediated events
26
NSAID nephrotoxicity
Pretty much all. Probably a result of interference PGE that regulates blood flow in renal tubules.
27
General NSAID SE (per katzung)
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
28
Non-acetylated salicylates
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
Celecoxib (highly selective) meloxicam (preferentiall selective)
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
Diclofenac
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
Diflunisal
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
Etodolac
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
Flurbiprofen
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
Ibuprofen
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
Indomethacin
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
Ketoprofen
propanoic acid derivative Inhibits both COX (non-selectively) and lipoxygenase - major SE are in GI and CNS
37
Ketorolac
Analgesic, non-anti inflammatory - can replace morphine (TORO: bull:strong med:morphine) - similar common toxicity
38
Naproxen
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
Oxaprozin
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
Piroxicam
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
Sulindac
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
Tolmetin (non-selective COX inhibitor)
Can't treat gout | Can cause TPP (JD was a tool (toolamitin) for diagnosing dr. Coxs pt with TTP)
43
DMARDs (only 1st TL)
Disease modifying antirheumatic drugs; immunosuppressive - abaracept - azathiopine - chloroquine (+ hydroxy) - cyclophosphamide - cyclosporine - leflunomide - methotrexate - mycophenolate mofetil
44
Abaracept
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
Azathiopine
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
Chloroquine/hydroxychloroquine
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
Cyclophosphamide
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
Cyclosporine
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
Leflunomide
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
Methotrexate
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
NSAID SE: CNS- 3
Tinnitus, dizziness, HA
52
NSAID SE: Cardiovascular - 5
Fluid retention, HTN, edema, Myocardial infarction (rare), CHF (rare)
53
NSAID SE: gastrointestinal - 5
Abdominal pain, dysplasia, nausea, vomiting, ulcers/bleeding (rare)
54
NSAID SE: hematologic - 3
Thrombocytopenia (rare), neutropenia (rare), aplastic anemia (rare)
55
NSAID SE: hepatic - 2
Increased liver enzymes, liver failure (rare)
56
NSAID SE: pulmonary - 1
Asthma
57
NSAID SE: skin - 2
Rashes, pruritis
58
NSAID SE: renal - 4
Renal insufficiency, renal failure, hyperkalemia, proteinuria
59
CYP2A/CYP3C
Primary metabolism of NSAIDs
60
ROSCaILCh
Non-PG mediated effect if NSAIDs - ROS burst modification - Ca med processes down reg - IL-1 altar ion (anti pyrogenic) - chemotaxis alteration
61
Probenacid
Increases the efficacy of some NSAIDs by inhibiting clearance
62
ductus arteriosis closure
Ibuprofen and indomethacin | iBID
63
Na NSAIDs
NAproxen and NAbumetone - both can result in pseudoporphyria - bums with bad vision: photosensitivty in NAbumetone use - proximal limb: vasculitis with naproxen use
64
Betamethasone
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
Isoproterenol
Potent broncodilator - dangerous due to its ability to induce arrythmias - IsoproTERRORnol....cause it can kill you
66
Rol, Nol, but
Albuterol, terbutaline, metaproterenol, pirbuterol - B2 selective agonists - most RS mixes that are inhaled - terbutaline is available IM - 3-4 hour activation time
67
Salmeterol, formotorol (formoterol)
Long acting B2 selective agonists (12hours) | - (keeps your motor running)
68
Roflumilast
Methylxanthine trt for COPD
69
Caffeine, theophylline, theobromine
Decrease inflammation by decreasing PDEs -> increased cAMP | - PDE4 has been implicated in inflammatory cells
70
N-acetylcystine
Antidote to acetaminophen OD. Original dose dependent | No acetylation
71
Cyclosporine
Anti-necrotic process drug: retards swelling of mitos by inhibiting mito trans pores. (Spore:Pores)

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