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Drug Action I > Block 1 - Respiratory Med Chem > Flashcards

Block 1 - Respiratory Med Chem Flashcards

1
Q

What are esters metabolized to?

A

carboxylic acid

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2
Q

How are histamine receptors similar to muscarenic?

A

Contains ionic and h-binding sites

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3
Q

Describe the SAR of 1st gen Antihistamines

A
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4
Q

What are the classes of 1st gen antihistamines?

A
  1. ethanolamine ethers
  2. tricyclic
  3. piperazine
  4. alkylamines
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5
Q

Why does ethanol amine have short half lives?

A

N-dealkylation

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6
Q

What gives doxylamine antimuscarinic effects?

A

CH3 on X and ionic binding of 3 amine

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7
Q

How does alkyl amines different from other 1st AH?

A

longer duration of action, less sedation

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8
Q

What is the primary metabolism of alkyl amines?

A

N-dealkylation

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9
Q

What are piperazine?

A

Hydroxyzine -> cetirizine
anticholinergic ADRs

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10
Q

What gives tricyclic AH LA?

A

S brings more lipophilicity to rings

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11
Q

What makes tricyclic different than antipsychotics phenothiazines?

A

Antipsychotics are unbranched and have a substituent on ring

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12
Q

What makes 2nd gen AH differ from 1st?

A
  1. Less anticholinergic
  2. Less CNS/ sedation
  3. More hydrophilic
  4. long half-life
  5. Varied structures
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13
Q

Why does Fexofenadine have less CNS activity?

A

effluxes out of BBB by the p-gp
Folds on itself to bind to H1 receptor

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14
Q

Why should you drink fruit juice with allegra?

A

Juices inhibit OAT1A2 from absorbing drug into the blood stream

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15
Q

What drug is pseudo irreversible? why?

A

Zyrtec because will strongly bind to receptor and slowly release from it

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16
Q

Why does Zyrtec not have CNS activity?

A

Folds on itself like Allegra and removed by p-gp

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17
Q

What is the difference between loratadine and desloratidine?

A

Des is more potent with a longer half-life, a metabolite of loratadine.
Both are removed by p-gp by do not fold

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18
Q

What are the characteristics of olopatadine?

A
  1. Zwitterion
  2. Topical
  3. Long duration and rapid onset
  4. Inhibits mediators and mast cell stabilizer
  5. Minimal must effect from N and COOH
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19
Q

What is the MAO of azelastine?

A
  1. Mast cell stabilizer
  2. LTC4 inhibition
  3. Antihistamine
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20
Q

What is the MOA for cromolyn?

A
  1. Mast cell degranulation inhibitor
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21
Q

Why is cromolyn polarity absorbed?

A

Contains 2- charges that must both be neutralized to pass through membrane

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22
Q

What are the endogenous steroids?

A

Hydrocortisone and cortisone

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23
Q

Out of the 2 endogenous steroids which is active?

A

hydrocortisone

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24
Q

What makes a steroid active?

A
  1. ketone on 3 and 20
  2. alkene on 4
  3. OH on 11, 17, 21
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25
Q

At what positions do steroids bind?

A

beta

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26
Q

What is the difference between glucocorticoids and mineralocorticoids?

A

G: glucose homeostasis, anti-inflammatory
M: sodium and water retention

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27
Q

Why are ketone and OH groups important for steroids?

A

to form H bond at GC receptor sites

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28
Q

What is the exception on the OH 21 on steroids?

A

Can be Cl or thioester

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29
Q

What make steroids a prodrug?

A

Ketone on 11 or 21

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30
Q

What makes a steroid more acidic?

A

F on 9a or 12a

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31
Q

What are the mechanism of inactivating a GC steroid?

A
  1. Loss of 21 OH
  2. Ring A reduction
  3. C-17 oxidation
  4. C11 keto enol isomerization
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32
Q

Why is the purpose of esterfying GC?

A
  1. increase or decrease lipophilicity
  2. Increase log P (lipo) -> longer duration of action and more local activity
  3. prodrug
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33
Q

What portion of the steroid can be esterized?

A

C21 (easiest)
C17 (slower more hindered)
C11 (highly hindered so no activity)

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34
Q

Why would diesters in steroid be beneficial?

A

Lipo enhancement and increased duration of action (slow metabolism)

35
Q

What are benefits of hydrophilic esters?

A
  1. IM/IV use
  2. Rapid onset
  3. easy excretion by kidneys
  4. wider distribution and and more ADRs
36
Q

What are the important qualities of Inhaled GC?

A
  1. fast systemic clearance following GI absorption
  2. short half-life
  3. no active metabolites
  4. high affinity for gr
37
Q

What are the endogenous agonists of adrenergics?

38
Q

What does the insertion on 16b methyl on a steroid mean?

A

decrease MC activity

39
Q

What does the insertion on 9a chloro on a steroid mean?

A

increased GC and MC activity

40
Q

What does the insertion on 9a chloro on a steroid mean?

A

increased GC and MC activity

41
Q

What does the insertion of 16,17 acetal on a steroid mean?

A

decreased MC activity

42
Q

Insertion of 6a F?

A

Increase GC

43
Q

Insertion of 9aF?

A

Increases MC and GC

44
Q

Double bond on 1?

A

slows ring A reduction (longer duration of action)

45
Q

Where are b2 receptors located?

A

skeletal muscle, lungs, live, uterus for relaxation, intestine

46
Q

how does isoproterenol differ from NE and E?

A

only b selectivity

47
Q

What metabolized E and NE?

A

COMT and MAO

48
Q

What is metabolized by COMT?

A

Catechol to methyl on O

49
Q

What is metabolized by MAO?

A

1 amine to aldehyde

50
Q

How do you slow do COMT on adrenergic?

A

Don’t have OH group on neighboring carbons

51
Q

What is SAR of adrenergic?

A
  1. 2 carbon spacer between amine and phenyl ring
  2. Ethyl group on R2 reduces MAO metabolism and increase b selectivity
  3. Positively charged amine with pKa of 8.5-10
  4. R1 increasing size -> b selectivity blocking MAO
  5. 1 H bond former in phenyl
52
Q

What provides b2 selectivity?

A

tert, but, phenyl ring substitutions, ethyl group on R2

53
Q

What is the difference between albuterol and leva?

A

AL: racemic
Leva: R isomer

54
Q

Why is salemeterol longer acting?

A
  1. resistant to MAO and COMT
  2. larger drug that anchors to protein
  3. very lipophilic with b2 selectivity
55
Q

How does formoterol differ from salmeterol?

A
  1. faster onset and great water solubility
  2. 12 hr duration
  3. B2 and resistant to MAO and COMT
56
Q

What is the MOA of Zileuton?

A
  1. Inhibits 5-LOX that produces leukotrienes
  2. N-OH chelates iron in enzyme
  3. Good absorption and high PPB
  4. Increases plasma levels of propranolol, theophylline, and warfarin
57
Q

What is the SAR of leukotriene receptor antagonists?

A
  1. acidic or negative ionizable functional group (COOH etc)
  2. H-bond acceptor function
  3. 3 hydrophobic regions
58
Q

Why does singular have high PPB?

A

lipophilic and acidic that binds to albumin

59
Q

Why can food decrease the effects of Zafirlukast?

A

Food makes the stomach more basic. Drug becomes ionized in the environment and unable to be absorbed into the blood do to its charge

60
Q

What is the difference between levorotatory and dextrotatory isomers?

A

L: are for pain (analgesic)
D: are for cough (antitussive)

61
Q

What is the opiod receptor?

A

µ
OH on 3 is the active form

62
Q

What is the structure of codeine?

A

Prodrug of mrophine contain a methyl on 3 to improve F

63
Q

How does codeine metabolize to morphine?

A

O dealkylation by CYP2D6 becoming a phenyl for activity that binds to µ

64
Q

What are the ADRs of opioids (levo isomer)?

A

Constipation, drowsiness, lightheadedness

65
Q

What make dextromethorphan differ from tradition opioids?

A

low binding to µ and more for antitussives without ADRs of levos. Parent and metabolite are actives

Antagonizes NMDA and ø-1 receptors instead

Contains a methoxy

66
Q

Describe the MOAs of Guaifenesin?

A
  1. Muscle relaxant and anticonvulsant, NMDA antagonist
  2. Increases volume and reduce viscosity of mucous
67
Q

Describe MOA of Dornase Alfa?

A

Used for CF that causes over secretion of fluid containing DNA, drug contains DNAse I to breakdown DNA

68
Q

What is the MOA of NAC?

A
  1. antioxidant and expectorant that loosens mucus
  2. reduces inflammation in tubes and lung
69
Q

What is important about benzonatate?

A

Local anesthetic
Potential OD if chewed or dissolved

70
Q

Endogenous NT of Antimuscarinics?

71
Q

Common ADRS of antimuscarinics?

A
  1. Blurred vision
  2. Dry mouth
    3, Tachycardia
  3. Urinary difficulty
  4. HA
72
Q

How does ACh bind of receptor?

A

2 H-bond with O-H
Asp-tert amine (ionic)

73
Q

What are the pharmacophores of atropine?

A

Alcohol, amides, alcohol esters, alcohol ethers

74
Q

What is the SAR of antimuscarinics?

A
  1. Carbon next to ring is more active
  2. Methyl on N is optimal
  3. Quat N is good for ionic bond but not necessary, can replace with carbon but creates lower affintiy
  4. Carbocylic or heterocyclic ring(s)
75
Q

What is the difference between ipratropium and tiotropium?

A

I: not selective for muscarinic receptors (Short DOA: 6 hr)
T: M1 and M3 selectivity (DOA: 24 hr - lipophilic)

Poor absorption from quat amine

76
Q

Describe the t1/2 of aclidinium?

A

Due to rapid hydrolysis of ester bond in plasma to acid and alcohol derivatives
M2 and M3 selectivity
t1/2: 2.4 min

77
Q

Natural PDEi?

A
  1. Caffeine
  2. Theophylline
  3. Theobromine
78
Q

How does Theophylline bind to PDEi?

A

2 hydrophobic bond
2 h-bond

79
Q

Why is theophylline problematic?

A
  1. Narrow TI
  2. Poor aqueous solubility
  3. Potent
80
Q

What is the salt form of theophylline?

A

aminophylline

81
Q

What is gives roflumilast its PDE4i activity?

A

ring with 2 ethers
Long t1/2 and active metabolite

82
Q

What are the benefits of Varenicline (Chantix)?

A
  1. reduces cravings
  2. partial agonist of nicotine receptor
  3. lower efficacy of binding
83
Q

What are the natural inhibitors of dopamine?

A

CNS stimulats

84
Q

How does bupropion differ from meth?

A
  1. No metabolites with sympathomimetic and anorexigenic properties
  2. tert but inhibits N-dealkylation that is associated with meth
  3. extensively metabolized

Drug Action I (32 decks)

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