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Pharm Exam 4 > Pulm and Analgesic Exam 4 Pharm > Flashcards

Pulm and Analgesic Exam 4 Pharm Flashcards

1
Q

How do histamine and LT receptors initiate SM contraction?

A

They are GPCRs that activate Phospholipase C and leads to Ca2+ influx and cGMP to initiate SM contraction

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2
Q

How do Gq proteins influence the SM in airways?

A

They activate PLC leading to inc in IP3 and Ca2+ influx resulting in actin/myosin coupling = bronchoconstriction

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3
Q

How do the Gi proteins influence the SM in airways?

A

Dec adenylate cyclase activity and cAMP levels = bronchoconstriction (M2)

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4
Q

How do the Gs proteins influence the SM in airways?

A

Inc Adenylate cyclase activity and cAMP levels leading to the dissolution of actin/myosin = bronchodilation

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5
Q

What is the MOA of the Sympathomimetics?

A

They act via Gs and inc cAMP to relax SM and dec Mast cell degranulation

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6
Q

What are the impt Sympathomimetics for pulm?

A

Isoproterenol, albuterol, terbutaline, metaproterenol

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7
Q

What is one potential problem w/ beta-adrenergic agents?

A

They can vasodilate in lungs and perfuse poorly ventilated areas; give O2 to counter this effect

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8
Q

What are the long acting beta-agonists?

A

Salmeterol and Formoterol

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9
Q

What are the Methylxantines and their MOA?

A

Theophylline, Caffeine, Theobromine inc cAMP by preventing breakdown by inhibiting phosphodiesterase

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10
Q

Who should avoid methylxantines?

A

Elderly w/ heart conditions

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11
Q

How do you avoid toxicity of theophylline?

A

Closely monitor blood levels

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12
Q

What is the effect of tri-nucleotides on Mast cells?

A

Inc. GTP stimulate secretion; Inc ATP inhibits secretion

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13
Q

What is omalizumab?

A

It is a monoclonal antibody that targets the FC portion of IgE so can’t attach to Fcepsilon

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14
Q

When do you use chromolyn sodium?

A

Phophylactically to inhibit asthma exacerbations

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15
Q

What is the MOA of Zileuton?

A

It inhibits 5-lipoxygenase to inhibit LT production

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16
Q

What are the LTD4 receptor antagonists?

A

Zafirlukast and Montelukast

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17
Q

When are Leukotriene modifiers especially useful?

A

Aspirin induced asthma

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18
Q

What is useful w/ inhaled corticosteroids?

A

They don’t turn off the rest of the immune system

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19
Q

What is a risk of rapid withdrawl of corticosteroids

A

adrenal insufficiency

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20
Q

Which is special about ciclesonide?

A

It is designed to be cleaved by esterase locally

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21
Q

What is a unique risk of inhaled corticosteroids?

A

Oropharyngeal candidiasis

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22
Q

What are three benefits of airway delivery?

A
  1. Speeds delivery of active cmpds 2. Delivers medication to appropriate site 3. Minimizes systemic Side Effects
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23
Q

What Abx can be used w/ corticosteroids for acute exacerbations?

A

Doxy

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24
Q

What receptor is targeted by Antihistamines?

A

H1

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25
Q

What are 2 important decongestants and their MOA?

A

Pseudoephedrine and phenylephrine; alpha adrenergic stimulation

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26
Q

What type of pain is associated w/ breakthrough spikes?

A

Cancer Pain (compression)

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27
Q

What are Tx options for multiple sclerosis?

A

IFN-beta, Glatiramer actetate, corticosteroids

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28
Q

How does IFN-beta MOA in MS?

A

Reduce BBB penetration of immune cells

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29
Q

What drugs can be used as abortive tx of migraines?

A

Acetaminophen + Caffeine, Triptans, Ergotamine they all cause vasoconstrictions

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30
Q

What drugs can be used for migraine prevention?

A

Antidepressants, anti-seizures, and beta-blockers

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31
Q

Describe Abeta fibers

A

Non-noxious (touch and pressure) and Fastest

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32
Q

Describe Adelta fibers

A

Pain, cold; myelinated; Fast; 1st pain reflex arc

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33
Q

Describe C fibers

A

Pain, Temp, Touch, Pressure, Itch; Unmyelinated and slow

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34
Q

Where do Adelta fibers terminate?

A

Lamina 1

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35
Q

Where do C fibers terminate?

A

Lamina 2

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36
Q

What is central sensitization?

A

It is an enhanced activity of the glutamate system

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37
Q

What are the 2 types of alkaloids that Opium contains?

A

Phenanthrenes and Benzylisopuinolines

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38
Q

What are the Phenanthrenes?

A

Morphine, Codeine, and Thebaine

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39
Q

What are the Benzylisopuinolines?

A

Noscapine and Papaverine

40
Q

What determines the antagonist quality of the Phenanthrenes?

A

The bulkiness of the N-allyl group; bulkier = more antagonistic

41
Q

What does methylation at the 3 position -OH of morphine produced?

A

Codeine - which has decreased potency

42
Q

What does ketone formation at the 6th position -OH of morphine give?

A

Hydromorphone which has an increased activity

43
Q

What metabolite of morphine is still potent?

A

Morphine-6-glucuronide

44
Q

Where are phenanthrenes metabolized?

A

Liver

45
Q

How are phenanthrenes excreted?

A

Glomerular filtration; 90% in 24hrs

46
Q

What are the opioid receptors and their respective endogenous peptides that activate them the most?

A

Mu - Endorphins; Kappa - Kynorphins; Delta - Enkephalins; Orphanin Opioid Receptor/Nociceptin - Nociceptin/Orphanin FQ

47
Q

What is a reason to not use Kappa opioid receptor agonists?

A

They cause dysphoria

48
Q

What beta-endorphins act on the Mu-receptor?

A

Pro-opiomelanocortin (endogenous morphine)

49
Q

Describe Signal Transduction of the Opioid Receptor

A

Presynaptically located and is Gi linked to dec cAMP so dec Ca2+ and dec release of NT; also linked to a K+ channel so causes hyperpolarization

50
Q

Why do you use Hydromorphone post-op?

A

It is 4-5x more potent than morphine and has a >t1/2 than fentanyl

51
Q

What drug do you give if they are opioid intolerant?

A

Meperidine

52
Q

What receptors are affected by Buprenorphine?

A

Partial mu agonist, weak Kappa agonist, delta antagonist

53
Q

What is the use of buprenorphine?

A

It is used to tx opioid withdrawal

54
Q

What is the MOA of Tramadol?

A

It is a 5HT releaser and NE reuptake inhibitor, weak mu opioid agonist

55
Q

What is 4x as potent as Tramadol

A

Its O-demthylated metabolite

56
Q

What is Tapentadol?

A

A weak mu agonist and inhibits norepi reuptake

57
Q

How should buprenorphine be administered for opioid misuse?

A

Oral admin

58
Q

How should Naloxone be administered for opioid misuse?

A

IV admin

59
Q

What are the Arylproprionic Acids?

A

Ibuprofen and naproxen

60
Q

What are the Arylacetic acids?

A

Indomethacin and Diclofenac

61
Q

What are the Enolic acids?

A

Piroxicam

62
Q

What are the p-Aminophenols?

A

Acetaminophen

63
Q

Where is COX2 constitutively expressed?

A

The brain and spinal cord. This is why it is induced in setting of inflammation

64
Q

Where does ASA affect COX enzymes?

A

It acetylates Ser529

65
Q

Where is ASA absorbed?

A

Jejunum

66
Q

What is the difference b/w the t1/2 of ASA and Salicylate?

A

ASA = 15 mins; Salicylate = 12 hrs

67
Q

How do you inc the excretion of ASA?

A

Give bicarb to inc the pH of urine. ASA is passively reabsorbed from tubule so if can deprotonate it won’t diffuse through membranes

68
Q

What are the methods of metabolism for nonsalicylate NSAIDs

A
  1. oxidation, 2. Demethylation, 3. Conjugation
69
Q

What is the major difference b/w ibu and naproxen?

A

t1/2: Ibu - 2 hrs, Naproxen - 14 hrs

70
Q

What is the big risk w/ Diclofenac?

A

Peptic ulcers long term

71
Q

What is one of the most potent reversible inhibitors of PG synthesis?

A

Indomethacin

72
Q

What are the uses of Indomethacin?

A

Acute gouty arthritis, Ankylosing Spondylitis

73
Q

What is Sulindac?

A

Less toxic indomethacin derivative

74
Q

What are the uses of Sulindac?

A

RA and Ankylosing Spondylitis

75
Q

What is the risk of p-Aminophenols?

A

Acute overdose can lead to fatal hepatic necrosis

76
Q

How do you tx the gastric SE of salicylates?

A

Misoprostol a PGE1 analog

77
Q

What are the affects of Salicylate OD

A

Metabolic acidosis w/ compensatory respiratory alkalosis

78
Q

What do you give to tx salicylate OD?

A

Dextrose, Sodium Bicarbonate to inc urinary excretion

79
Q

How does Acetominophen damage the kidneys?

A

It inhibits PGE2 which induces vasoconstriction and results in papillary necrosis

80
Q

What is Leflunomide and MOA?

A

It is an antiproliferative agent that initiates G1 arrest to inhibit T-cell proliferation and B cell Ab production

81
Q

What is Anakinra?

A

Recombinant IL-1 Receptor antagonist

82
Q

What are absolute contraindications of anakinra?

A

Pre-existing malignancy and neutropenia

83
Q

What are the TNF-alpha blocking agents?

A

Etanercept, Infliximab, adalimumab

84
Q

What is Febuxostat?

A

It is a non-purine inhibitor of Xanthene oxidase

85
Q

What is the MOA of Probenacid?

A

It competes for renal tubular anion transporter of uric acid and blocks reabsorption

86
Q

What are the topical anesthetics that inhbit Na channels?

A

Lidocaine, Benzocaine, and Oxybuprocaine

87
Q

What is the difference b/w Lidocaine and Bupivicaine?

A

Lido lasts 30min-2 hrs and Bupivicaine lasts 3.5 hs

88
Q

What are the Na channel blockers that are also Tricyclic Antidepressants?

A

Amitryptiline, Carbamezipine, and Lamotrigine

89
Q

What is a big risk of Lamotrigine?

A

Steven-Johnson Syndrome

90
Q

What enzyme is impt for metabolism of TCA/SNRI?

A

CYP2D6

91
Q

Where are TCA/SNRIs excreted?

A

Renal Excretion

92
Q

Where are Ca Channels that can be affected in pain tx expressed

A

Nerve terminals

93
Q

What are the CCBs for pain tx?

A

Gabapentin, Pregabalin, Ziconotide, and Levetiracetam

94
Q

What is Qutenza?

A

It is used to desensitize a nerve and reduce expression of TRPV1

95
Q

What is a risk of TRPV1 antagonists?

A

Hyperthermia b/c of heat intolerance

Pharm Exam 4 (3 decks)

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