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Pharm 2 (3rd Quarter) > Final > Flashcards

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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
Beta receptors couple to Gs results in
Increase cAMP activity
26
Sympathomimetic drugs effects on adrenergic receptors where
Post ganglionic SNS Preganglionic adrenergic neurons
27
Adrenergic receptors specifically bind to
Epi and NE for activation
28
Alpha 1 agonists
NE, phenylephrine, methoxamine
29
Alpha 1 antagonists
Phenoxybenzamine Phentolamine (regifting)
30
Alpha 1 post synaptic effects
``` Vasoconstriction Mydriasis GI relaxation Contraction of GI and bladder Sphincters ```
31
Alpha 2 agonists
NE and epi
32
Selected agonist actions alpha 2
Smooth muscle contraction NTS inhibition (can lead to sedation)
33
Alpha 2 agonists
Dexmedetomidine Clonidine
34
Alpha 2 antagonists
Yohimbine
35
Where does alpha 2 work
Presynaptic- inhibition of NE | Post synaptic- plt aggregation Hyperpolarization of CNS cells Sedation
36
Beta 1 selected agonist actions
Increased myocardial contractility
37
Beta 1 agonists
Isoproterenol Dobutamine Epi NE
38
Beta 1 antagonists
Metoprolol Atenolol
39
Beta 2 selected agonist actions
Smooth muscle relaxation
40
Beta 2 agonists
Albuterol Terbutaline Isoproterenol
41
Beta 2 antagonists
Propanolol
42
Non-selective beta blocker
Propanolol
43
Beta 3 selected agonist actions
Lipolysis
44
6 steps of adrenergic transmission
Synthesis Storage Release (Ca mediated exocytosis) Binding Degradation Recycling
45
Catecholamines are metabolized by
MAO and COMT
46
Majority of inhibition of catecholamines is due to
Reuptake
47
Direct acting sympathomimetic MOA
Act at post synaptic receptors
48
Indirect sympathomimetic MOA
Presynaptic release of NE
49
Do not require endogenous catecholamines to produce effects (even if catecholamines are depleted)
Direct acting adrenergic
50
Indirect acting adrenergics elicit mostly
Alpha and beta 1 effects
51
Require endogenous catecholamines to produce effects
Indirect acting adrenergics
52
Alpha 1 agonists used to tx
Hypotension Ophthalmic- mydriasis Cough and cold preparations
53
Alpha 2 agonists used for
Antihypertensive, sedative, tx of opiate and ETOH withdrawal
54
Precedex is
Selective alpha 2 adrenergic agonist
55
Precedex sedation MOA
Decreased activity in locus ceruleus of brain stem Increasing activity of GABA in ventrolateral preoptic nucleus
56
Most common adverse event of precedex CNS
NV Agitation
57
Direct acting beta 1 agonists
Dopamine Dobutamine Epinephrine Isoproterenol
58
Beta 1 agonist uses
CHF Cardio genie shock
59
Beta 1 agonists result in
Increased conduction, automaticity and contractility
60
Beta 2 agonist action
Vasodilation, bronchodilation, GI relaxation, uterine and bladder relaxation
61
Beta 3 agonist actions
Glycogenolysis Lipolysis
62
Example of selective beta 2 agonists
Albuterol
63
Epi binds to hepatic alpha 1 resulting in
Breakdown of glycogen
64
Epi binds to cardiac beta 1 receptors resulting in
Increased CO, HR, conduction, contractility
65
Epi binds to renal beta 1 receptors results in
Increased renin secretion from juxtaglomerular renal cells
66
Epi activates beta 2 receptors of liver and muscle results in
Increasing glycogenolysis by activating adenylate cyclase signaling pathway
67
Epi activates beta 2 receptors in skeletal muscle BV results in
Vasodilation
68
Epi formation
``` Tyrosine > DOPA > Dopamine > NE > Epi ```
69
Enzyme found in adrenal medulla that converts NE to epi
PNMT
70
Epi is drug of choice for anaphylaxis due to
Suppressive effects on the immune system
71
Epi dose 1-2 mcg/min results in
Stimulation of beta 2 in peripheral vasculature
72
Epi 4 mcg/min stimulates
Beta 1 in heart
73
Epi 10-20 mcg/min stimulates
Beta 1 and beta 2 with alpha predominating in vascular beds
74
Adding epi to LA that is inherent vasodilator results in
Increase duration
75
Epi for CPR Why?
Increase PVR and CO via alpha 1 and beta 1 activation
76
NE increases BP by
Increasing SVR
77
2 major urinalysis metabolites of NE
VMA and MOPEG
78
Dopamine works on what receptors (adrenergic)
Beta > alpha
79
Dopamine at 3-10 mcg/kg/min
Beta 1 receptors
80
Dopamine at > 10 mcg/kg/min
Alpha 1 receptors
81
Dopamine inactivated by
Reuptake via DAT
82
Dopamine at 2-5 mcg/kg/min
D1 receptors- vasodilation (increased renal BF, coronary artery vasodilation, mesenteric vasodilation)
83
Most potent activator of beta receptors
Isoproterenol
84
Increase BP with Isoprel due to
Increased CO (directly increases BP)
85
No alpha effects with isoprel leads to
Lower MAP and decreased DBP r/t decreased SVP
86
Primary use of isuprel
Bradycardia and heart block
87
Usual dose of isuprel
0.2-2 mcg/kg/min
88
Dobutamine uses
CHF and cardiogenic shock
89
Primary action of dobutamine
Direct stimulation of beta 1 receptors
90
+ isomer of dobutamine is
Potent beta 1 agonist
91
- isomer of dobutamine is
Alpha 1 agonist
92
Dobutamine infusion
Start at 0.5-1 mcg.kg.min Infusion 2-10 mcg/kg/min
93
Infusion rate of phenylephrine
Initial 100-180 mcg/min Maintenance 20-60 mcg/min
94
Beta 2 agonist used for Treatment of asthma and slow uterine contractions
Terbutaline
95
Beta 2 agonist used for acute bronchospasm
Albuterol
96
Primary vasopressin receptor
ACPR1A
97
Vasopressin dose
0.5-20 units IVP Infusion 0.01-0.04 units/min
98
Most often used LA
Cocaine, teracaine, lidocaine
99
What determines the amount of LA that exists in active non-ionized form
PKA
100
Neostigmine dose
25-70 mcg/kg NO MORE THAN 5 MG
101
Pyridostigmine dose
0.1-0.3 mg
102
Edrophonium dose
0.5-1 mg/kg
103
Phyostigmine dose
15-60 mcg/kg
104
How much atropine and glyco with neostigmine?
1/2 as much atropine 1/4 as much glyco
105
Large doses of anticholinesterase drugs administered with minimal NMB can produce
NM dysfunction
106
Neostigmine and pyridostigmine metabolism
Metabolized by liver microsomal enzymes. | Plasma cholinesterases
107
More lipophilic anticholinesterase Means?
Phyostigmine Crosses BBB
108
Onset edrophonium
1-2 min
109
Onset neostigmine
7-11 min
110
Pyridostigmine onset
16 min
111
Hepatic metabolism % of Neostigmine Edrophonium Pyridostigmine
Neo 50% Edr 30% Pyridostigmine. 25%
112
Anticholinesterase drugs MOS
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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