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Pharm 2 (3rd Quarter) > Final > Flashcards

Final Flashcards

1
Q

Work only by synergistic spontaneous recovery from NMB

A

Anticholinesterase (neostigmine/edrophonium)

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2
Q

Anticholinesterase MOA

A

Inactivate acetyl-cholinesterase in NMJ synaptic cleft

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3
Q

Neostigmine

Dose

Onset

Peak

Duration

A

0.04-0.07 mg/kg

Onset 1 min

Peak 9 min

Duration 20-30 min

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4
Q

Neostigmine metabolism and excretion

A

Metabolized in liver

80% excreted in urine in 24 hr

50% excreted unchanged

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5
Q

Muscarinic side effects of anticholinesterases (8)

A 
NV
Bradycardia
Prolong QT
Bronchoconstriction
Salivary gland stimulation
Miosis
Increased GI tone
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6
Q

Ability to maintain head lift requires TOF ratio of

A

0.6

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7
Q

Ratio of TOF recovery required

A

0.9

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8
Q

Significant risk to pt recovery with NMB

A

Residual paralysis

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9
Q

Increase in NMB after a period of recovery

A

Recurarization

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10
Q

Recurirarization risk increased with

A

Respiratory acidosis and renal insufficiency

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11
Q

Sugammadex MOA

A

Encapsulates rocuronium rendering it unavailable to bind at NMJ

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12
Q

Sugammadex is a (chemical makeup)

A

G-cyclodextrin compound

Gamma cyclodextrin- 8 member sugar ring

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13
Q

Sugammadex is ineffective with

A

Benzylisoquinoliniums

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14
Q

Mechanism for ions and molecules bonding to metals and other ions

A

Chelation

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15
Q

Sugammadex properties (4)

A

Highly water soluble

PH 7.5

Osmolality 300-500mOsmol kg

Molecular wt 2178

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16
Q

Sugammadex metabolism and excretion

A

Not metabolized and renal excreted unchanged

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17
Q

Sugammadex can bind with drugs other than NMBs

Highest affinity after Roc for

A

Remifentanil

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18
Q

To re-establish NMB after reversal with sugammadex

A

Recommend benzylisoquinolinium

Roc will have less profound effect

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19
Q

Sugammadex and coags

A

limited (<1hr) increase in PTT and PT

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20
Q

Naturally occurring catecholamines

A

Epi

NE

Dopamine

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21
Q

Synthetic catecholamines

A

Isoproterenol

Dobutamine

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22
Q

Synthetic non-catecholamines

A

Ephedrine

Amphetamines

Phenylephrine

Methoxamine

Mephentermine

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23
Q

Alpha 1 couples to a Gq resulting in

A

Increased intracellular Calcium

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24
Q

Alpha 2 couples to Gi results in

A

Decreased cAMP activity

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25
Q

Beta receptors couple to Gs results in

A

Increase cAMP activity

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26
Q

Sympathomimetic drugs effects on adrenergic receptors where

A

Post ganglionic SNS

Preganglionic adrenergic neurons

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27
Q

Adrenergic receptors specifically bind to

A

Epi and NE for activation

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28
Q

Alpha 1 agonists

A

NE, phenylephrine, methoxamine

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29
Q

Alpha 1 antagonists

A

Phenoxybenzamine

Phentolamine (regifting)

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30
Q

Alpha 1 post synaptic effects

A 
Vasoconstriction 
Mydriasis
GI relaxation
Contraction of GI and bladder 
    Sphincters
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31
Q

Alpha 2 agonists

A

NE and epi

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32
Q

Selected agonist actions alpha 2

A

Smooth muscle contraction

NTS inhibition (can lead to sedation)

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33
Q

Alpha 2 agonists

A

Dexmedetomidine

Clonidine

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34
Q

Alpha 2 antagonists

A

Yohimbine

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35
Q

Where does alpha 2 work

A

Presynaptic- inhibition of NE

Post synaptic- plt aggregation
Hyperpolarization of CNS cells
Sedation

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36
Q

Beta 1 selected agonist actions

A

Increased myocardial contractility

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37
Q

Beta 1 agonists

A

Isoproterenol

Dobutamine

Epi

NE

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38
Q

Beta 1 antagonists

A

Metoprolol

Atenolol

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39
Q

Beta 2 selected agonist actions

A

Smooth muscle relaxation

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40
Q

Beta 2 agonists

A

Albuterol

Terbutaline

Isoproterenol

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41
Q

Beta 2 antagonists

A

Propanolol

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42
Q

Non-selective beta blocker

A

Propanolol

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43
Q

Beta 3 selected agonist actions

A

Lipolysis

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44
Q

6 steps of adrenergic transmission

A

Synthesis

Storage

Release (Ca mediated exocytosis)

Binding

Degradation

Recycling

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45
Q

Catecholamines are metabolized by

A

MAO and COMT

46
Q

Majority of inhibition of catecholamines is due to

A

Reuptake

47
Q

Direct acting sympathomimetic MOA

A

Act at post synaptic receptors

48
Q

Indirect sympathomimetic MOA

A

Presynaptic release of NE

49
Q

Do not require endogenous catecholamines to produce effects (even if catecholamines are depleted)

A

Direct acting adrenergic

50
Q

Indirect acting adrenergics elicit mostly

A

Alpha and beta 1 effects

51
Q

Require endogenous catecholamines to produce effects

A

Indirect acting adrenergics

52
Q

Alpha 1 agonists used to tx

A

Hypotension
Ophthalmic- mydriasis
Cough and cold preparations

53
Q

Alpha 2 agonists used for

A

Antihypertensive, sedative, tx of opiate and ETOH withdrawal

54
Q

Precedex is

A

Selective alpha 2 adrenergic agonist

55
Q

Precedex sedation MOA

A

Decreased activity in locus ceruleus of brain stem

Increasing activity of GABA in ventrolateral preoptic nucleus

56
Q

Most common adverse event of precedex CNS

A

NV

Agitation

57
Q

Direct acting beta 1 agonists

A

Dopamine

Dobutamine

Epinephrine

Isoproterenol

58
Q

Beta 1 agonist uses

A

CHF

Cardio genie shock

59
Q

Beta 1 agonists result in

A

Increased conduction, automaticity and contractility

60
Q

Beta 2 agonist action

A

Vasodilation, bronchodilation, GI relaxation, uterine and bladder relaxation

61
Q

Beta 3 agonist actions

A

Glycogenolysis

Lipolysis

62
Q

Example of selective beta 2 agonists

A

Albuterol

63
Q

Epi binds to hepatic alpha 1 resulting in

A

Breakdown of glycogen

64
Q

Epi binds to cardiac beta 1 receptors resulting in

A

Increased CO, HR, conduction, contractility

65
Q

Epi binds to renal beta 1 receptors results in

A

Increased renin secretion from juxtaglomerular renal cells

66
Q

Epi activates beta 2 receptors of liver and muscle results in

A

Increasing glycogenolysis by activating adenylate cyclase signaling pathway

67
Q

Epi activates beta 2 receptors in skeletal muscle BV results in

A

Vasodilation

68
Q

Epi formation

A 
Tyrosine >
DOPA >
Dopamine >
NE >
Epi
69
Q

Enzyme found in adrenal medulla that converts NE to epi

A

PNMT

70
Q

Epi is drug of choice for anaphylaxis due to

A

Suppressive effects on the immune system

71
Q

Epi dose 1-2 mcg/min results in

A

Stimulation of beta 2 in peripheral vasculature

72
Q

Epi 4 mcg/min stimulates

A

Beta 1 in heart

73
Q

Epi 10-20 mcg/min stimulates

A

Beta 1 and beta 2 with alpha predominating in vascular beds

74
Q

Adding epi to LA that is inherent vasodilator results in

A

Increase duration

75
Q

Epi for CPR

Why?

A

Increase PVR and CO via alpha 1 and beta 1 activation

76
Q

NE increases BP by

A

Increasing SVR

77
Q

2 major urinalysis metabolites of NE

A

VMA and MOPEG

78
Q

Dopamine works on what receptors (adrenergic)

A

Beta > alpha

79
Q

Dopamine at 3-10 mcg/kg/min

A

Beta 1 receptors

80
Q

Dopamine at > 10 mcg/kg/min

A

Alpha 1 receptors

81
Q

Dopamine inactivated by

A

Reuptake via DAT

82
Q

Dopamine at 2-5 mcg/kg/min

A

D1 receptors- vasodilation (increased renal BF, coronary artery vasodilation, mesenteric vasodilation)

83
Q

Most potent activator of beta receptors

A

Isoproterenol

84
Q

Increase BP with Isoprel due to

A

Increased CO (directly increases BP)

85
Q

No alpha effects with isoprel leads to

A

Lower MAP and decreased DBP r/t decreased SVP

86
Q

Primary use of isuprel

A

Bradycardia and heart block

87
Q

Usual dose of isuprel

A

0.2-2 mcg/kg/min

88
Q

Dobutamine uses

A

CHF and cardiogenic shock

89
Q

Primary action of dobutamine

A

Direct stimulation of beta 1 receptors

90
Q

+ isomer of dobutamine is

A

Potent beta 1 agonist

91
Q
  • isomer of dobutamine is
A

Alpha 1 agonist

92
Q

Dobutamine infusion

A

Start at 0.5-1 mcg.kg.min

Infusion 2-10 mcg/kg/min

93
Q

Infusion rate of phenylephrine

A

Initial 100-180 mcg/min

Maintenance 20-60 mcg/min

94
Q

Beta 2 agonist used for Treatment of asthma and slow uterine contractions

A

Terbutaline

95
Q

Beta 2 agonist used for acute bronchospasm

A

Albuterol

96
Q

Primary vasopressin receptor

A

ACPR1A

97
Q

Vasopressin dose

A

0.5-20 units IVP

Infusion 0.01-0.04 units/min

98
Q

Most often used LA

A

Cocaine, teracaine, lidocaine

99
Q

What determines the amount of LA that exists in active non-ionized form

A

PKA

100
Q

Neostigmine dose

A

25-70 mcg/kg

NO MORE THAN 5 MG

101
Q

Pyridostigmine dose

A

0.1-0.3 mg

102
Q

Edrophonium dose

A

0.5-1 mg/kg

103
Q

Phyostigmine dose

A

15-60 mcg/kg

104
Q

How much atropine and glyco with neostigmine?

A

1/2 as much atropine

1/4 as much glyco

105
Q

Large doses of anticholinesterase drugs administered with minimal NMB can produce

A

NM dysfunction

106
Q

Neostigmine and pyridostigmine metabolism

A

Metabolized by liver microsomal enzymes.

Plasma cholinesterases

107
Q

More lipophilic anticholinesterase

Means?

A

Phyostigmine

Crosses BBB

108
Q

Onset edrophonium

A

1-2 min

109
Q

Onset neostigmine

A

7-11 min

110
Q

Pyridostigmine onset

A

16 min

111
Q

Hepatic metabolism % of
Neostigmine
Edrophonium
Pyridostigmine

A

Neo 50%

Edr 30%

Pyridostigmine. 25%

112
Q

Anticholinesterase drugs MOS

A

Competitive cholinesterase inhibitors

Reduces breakdown of Ach = increase Ach to compete with NMBDs at binding site = reverse NMB

Pharm 2 (3rd Quarter) (6 decks)

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