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SRNAPharmacology I > EXAM2-NE,Dop,Dobu,Iso,Phenyl, Amph > Flashcards

EXAM2-NE,Dop,Dobu,Iso,Phenyl, Amph Flashcards

1
Q

Caution of norepinephrine in patients with ________why?

Norepinephrine directs precursor to

A
  • Right RV Failure; because increase in PVR and decrease in Venous return not well tolerated.
  • Epinephrine
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2
Q

Norepinephrine cause

A

Increased contractility and conduction velocity

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3
Q

Norepinephrine vs. Epinephrine

A

As you titrate higher, REFLEX BRADYCARDIA even though it is a Beta 1 agonist.

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4
Q

NE leads to _____ ______ due to activation of ______ reflex.

A

Reflex bradycardia due to activation of baroreceptor reflex.

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5
Q

CYCLOPROPANE and HALOTHANE

A

Increases cardiac autonomic irritability and therefore seem to sensitize the myocardium to the action of IV epinephrine or norepinephrine.

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6
Q

Epi cause intense ___________ and may cause Extravasation and sloughing treated with ________ which is ___ ____ -___antagonist

A

peripheral vasoconstriction; PHENTOLAMINE; non-selective alpha 1 and alpha 2 antagonist.

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7
Q

Dopamine precursor to

A

Norepinephrine

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8
Q

Main clinical effects (2)
Which receptor does it stimulate?
Is is lipid soluble or polar?
CNS activity

A

1.Direct acting effects at the receptor.
beta, alpha and dopamine (BAD)
2. causes release of NE from non-adrenergive nerve terminals.

POLAR- DOES NOT CROSS BBB
LOW CNS activity

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9
Q

Endogenous work in the brain , dopamine

A

yes

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10
Q

Given as a drug, dopamine works in the brain?

A

no

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11
Q

Is dopamine administered orally?

A

NO

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12
Q

Dopamine is metabolized by which 2 enzymes? and how is it excreted ?

A

MAO and COMT

Enzymes convert it to inactive metabolites and then excreted by kidneys

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13
Q

Plasma half life of dopamine is _____Duration of action _____

A

2 minutes; less than 10 minutes

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14
Q

In plasma, liver and kidney because of abundance of

______and ______enzymes

A

MAO and COMT

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15
Q

Clinical uses of dopamine (MOHTS)

Positive _______in conditions such as

A 
Positive inotrope in condition such as 
MI
Open heart surgery
Hemodynamic imbalances
Trauma
Septicemia
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16
Q

****MEMORIZE Dopamine dosing scheme (DBA)

A

0.5 - 3 mg/kg/min (Dopamine)

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17
Q

****MEMORIZE Dopamine dosing scheme (DBA)

A

0.5 - 3 mcg/kg/min (Dopamine dose)
3 - 10 mcg/kg/min (Beta dose
10> alpha dose

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18
Q

What percentage of the dose of dopamine is taken up into specialized neuro-secretory vesicles?

A

25%

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19
Q

The predominant effects of dopamine are dose -related

A

True

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20
Q

Low dose is the _______dose
Less than _____
Stimulates ______ receptors and leading to ______ and ________ which increases _________ and _______blood flow.

A

dopamine dose : 3mcg/kg/min
vascular dopamine 1 and D2;
renal coronary and mesenteric arterial vasodilation;
Renal and splanchnic blood flow

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21
Q

With low dose of dopamine, ______ and ____ are decreased

A

Prelaod and afterload

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22
Q

Dopamine: Renal blood flow increases (with Low doses ) ___ ____ and ______

A

GFR; UO and excretion of sodium

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23
Q

At low doses of dopamine is to ______ but do not use low dose of dopamine for _______ why?

A

PROMOTE RENAL BLOOD FLOW

renal protective effects; no evidence to support.

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24
Q

Renal dose effects is antagonized by ___________ _______ such as ______, ______ , ______

A

Dopamine 2 blockers (antagonists)
Droperinol
Haloperinol
Metoclopramide

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25
Q

At beta dose, you are still stimulating ______ but the response is mediated by

A

Beta-1 receptors

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26
Q

Dopamine has little or no effect on

A

B2 adrenergic receptors

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27
Q

Lusitropic agent

A

myocardium relaxant

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28
Q

High dose Dopamine is the range of ________mcg/kg/min and the clinical effects include.? which effect predominates? but you can still see _____effects

A

10-20 ; Increases in MAP
CO
Alpha 1
beta 1

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29
Q

At very high rates of dopamine

A

Alpha 1 receptors stimulated

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30
Q

1st treatment of dopamine - STOP infusion

2nd treatment of Dopamine, administer –>

A

Phentolamine

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31
Q

Dopamine _____Prolactin, GH, thyroid hormones

A

Decreases

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32
Q

Prolonged infusion of dopamine can deplete

A

NE stores

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33
Q

Prolonged infusion of dopamine can deplete____

Indirect effect going away, need direct effect of drugs.

A

Endogenous NE stores

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34
Q

Synthetic sympathomimetic amine same thing as

A

Synthetic catecholamines

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35
Q

Isoproterenol is a

A

synthetic catecholamines

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36
Q

Isoproteronol is a___________ and it stimulates both _____ and _____

A

non-selective B-adrenergic agonist that stimulates both B1 and b2

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37
Q

When being given IV isoproterenol? why

A

HAS TO BE PROTECTED FROM LIGHT, can start to degrate

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38
Q

Isoproterenol PREDOMINANTLY METABOLIZED BY ______, primarily in the _____

A

COMT ; liver

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39
Q

Clinical uses of ISOPROTERENOL

A

SYMPTOMATIC

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40
Q

General dose of ISOPROTERENOL

A

1-10 MCG/MIN continuous IV

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41
Q

Cardio-vascular effects of ISOPROTERENOL

A

Increase HR
increases cardiac automaticity
Increase MYOCARDIAL OXYGEN CONSUMPTION
Increase Myocardial contractictily

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42
Q

Isoproterenol will ________ coronary perfusion pressure due to

A

Decreases; vasodilation in renal, mesenteric and vascular bed.

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43
Q

CO is ______with isoproterenol due to positive _____and _______effects in the face of decreased PVR

A

Increases; Inotropic; chronotropic

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44
Q

MAP is _____ or _____ with isoproterenol? why ?

A

Unchanged or decrease; PVR and DBP decreased

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45
Q

Does compensatory baroreceptor reflex occur with ISOPROTERENOL ? Yes or NO and Why or why not?

A

No; because It does NOT INCREASE MAP

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46
Q

Avoid ISOPROTENROL when potent INHALATIONAL ANESTHETICS such as _______. If you must give, ______ the dose of isoproterenol

A

HALOTHANE; decrease

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47
Q

Preload and afterload should be _______ with ISOPROTERENOL

A

DECREASED

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48
Q

DOBUTAMINE is a ________ and a ______

Recall the meaning of direct acting?

A

Synthetic catecholamine; direct acting inotropic agent

Does not rely on endogenous store of NE

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49
Q

Dobutamine is a ______ mixture.

A

Racemic

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50
Q

Dobutamine is metabolized by _______meaning?

A

COMT; Need continuous infusion to maintain therapeutic level

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51
Q

When it comes to HR increases with is better DOB or ISO?

DOB its better for ______

A

ISO

INOTROPIC

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52
Q

Clinical use of dobutamine is even better if the patient has a high

A

HR and SVR

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53
Q

CV effects of Dobutamine are due to ____which is more potent_____and possess

A

BOTH StereoISOMERS (+ and -); (+); alpha 1 antagonist properties.

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54
Q

Mild to minimal effect on _____ and _____ with dobutamine

A

HR; BP

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55
Q

ISOPROTERENOL slightly higher risk with

A

cardiac arrhythmias

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56
Q

DRASTICALLY Increased with Dobutamine

A

Contractility

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57
Q

EPHEDRINE is a________

A

mixed synthetic non-catecholamines

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58
Q

The indirect acting effect of Ephedrine is _______

A

causes release of endogenous NE from pre-synaptic terminals

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59
Q

Ephedrine is a weak direct agonist on

A

alpha 1, 2, beta 1, beta 2

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60
Q

Non catecholamines is always ______than non-catecholamines agenst

A

WEAKER

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61
Q

response is reduced or BLUNTED by prior treatment with

A

RESERPINE and GUANETHIDINE

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62
Q

EPHEDRINE is a potent CNS ______

Tell nerve endings to release

A

Stimulant; NE

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63
Q

Is ephedrine lipid soluble ? does it cross BBB and has CNS activity?

A

Yes; yes

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64
Q

EPHEDRINE IS metabolized SLOWLY by______enzyme and is not acted on by______. the slow metabolism allow

A

MAO ; COMT; oral absorption

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65
Q

Ephedrine half life is ______ and can be given _____but preferred route is _____

A

3-6 hours; IM; IV

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66
Q

Ephedrine can be eliminated _______

A

Unchanged.

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67
Q

Ephedrine use for

A

Low BLOOD PRESSURE (hypotension)

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68
Q

EPHEDRINE Resemble

A

EPINEPHRINE (weakened)

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69
Q

EPHEDRINE has similar effect but_____effects is less intense and last _____than epinephrine

A

Blood pressure; last 10X longer.

70
Q

PRINCIPAL mechanism for CV effects of ephedrine.

A

Increase myocardial contractility due to activation of Beta 1

71
Q

CLONIDINE is a________ agonist enhances :

A

alpha-2 ; Enhances the presser effects of EPHEDRINE in awake AND anesthetized

72
Q

Another alpha -2 agonist used to enhance effects of EPHEDRINE

A

PRECEDEX.

73
Q

If the patient is on CLONIDINE

A

Reduce ephedrine dose.

74
Q

Patients taking beta blockers at home, lower dose of ephedrine why?

A

Drug to drug interactions

Because you WILL HAVE AN EXAGERRATED ALPHA RESPONSE because BETA receptors are blocked.

75
Q

EPHEDRINE IS subject to _______meaning? solution is to ?

A

TACHYPHYLAXIS; smaller response to a given dose; switch to a direct acting sympatomimetic

76
Q

Heart transplant patient ______won’t work , why? you have to use ______Acting agent.

A

EPHEDRINE; DIRECT

77
Q

Uterine blood flow is not greatly altered when ephedrine is used to restore BP to normal after production of sympathetic nervous system blockade, however it can cause a ______umbilical artery pH resulting in _______ _________ at delivery, which may suggest that even though it does not alter uterine blood flow, it may be NOT be the best agent to use in this clinical setting.

A

LOW ; FETAL ACIDOSIS.

78
Q

EPHEDRINE cause in the eye

A

Mydriasis

79
Q

Norepinephrine is a potent ____-agonist with modest ______agonism and has MINIMAL TO NO activity on ______ receptors

A

Alpha 1; Beta 1; B2

80
Q

What is the main use of NE ? (PM)

A

Increased total PERIPHERAL VASCULAR RESISTANCE

Increase MAP

81
Q

An adjunct to tx of hypotension and cardiac arrest?

A

Norepinephrine.

82
Q

What is the first line initial vasopressors agent of choice in the treatment of SEPTIC SHOCK?

A

Norepinephrine.

83
Q

Dose of Norepinephrine is

A

0.01-3 mcg/kg/min

84
Q

Norepinephrine produces intense arteriole and venous _________ in all vascular beds EXCEPT of _________arteries. Venous constriction lead to _______ and _______

A

Constriction
coronary.
Increasing venous return and augment SV

85
Q

Use NE in caution for patient with _______ because PVR is ______with NE

A

Pulmonary HTN; Increased

86
Q

What is increased in NE

A

MAP
SBP
DBP
PVR

87
Q

NE: Excessive peripheral vasoconstriction lead to __________ which can cause 3 effects

A

decreased perfusion to renal splanchnic and vascular bed.
End-organ hypoperfusion
Tissue hypoxia
metabolic acidosis and ischemia

88
Q

With NE the compensatory ____ ____ activity does what ? which overcomes the ____

A

Vagal reflex slows the HR which overcomes B1 stimulation.

89
Q

What happens to CO with the administation of NE? why?

A

CO is typically unchanged or decreased slightly.

Because the increase in afterload and vascular resistance may decrease CO and increase the work of the heart.

90
Q

Is the Hyperglycemia seen in epi seen in NE? why or why not?

A

It is not seen unless large dose of NE is administered

Because NE is not as effective as hormone as epi is

91
Q

Why is the use of LEVOPHED during cyclopropane and Halothane anesthesia constraindicated?

A

because of the risk of producing VTach or Vfib.

92
Q

NE drug interaction include the caution in patients taking_______, why? what is teh action of those drugs

A

MAOIs
tryptiline or imipramide types
Because it may lead to SEVERE HYPERTENSION.
MAOIs inhibit MAO which is one of the enzymes breaking down Catecholamines.

93
Q

Dopamine is an endogenous neurotransmitter in both ___ and_____. And CNS is important in the ________

A

CNS and PNS ; regulation of movement.

94
Q

Where are the effects of EXOGENOUSLY administered dopamine?

A

In the peripheral nervous system.

95
Q

Why must dopamine always be given as a continuous infusion?

A

to maintain therapeutic concentration since its rapidly metabolized.

96
Q

Special considerations with the handling of dopamine?

A

Do not add to alkaline solution (inactivates)

PROTECT FROM LIGHT

97
Q

What makes dopamine different among catecholamine agents? ( MURGS)

A 
It simultaneously increases;
Myocardial contractility 
Renal blood flow
GFR
Sodium excretion
Urine output
98
Q

At low dose of dopamine you can see a _______ In SBP and DBP and preload and afterload are ________

A

Decreased; decreased.

99
Q

Dopamine produces greater _____ and _________ than does dobutamine

A

diuresis and natriuresis

100
Q

Moderate dose of Dopamine is _____mcg/kg/mi include stimulation of ______Receptors directly in the heart as well as some _______ in the peripheral vasculaturs, thus ___

A

3-10; beta 1; alpha 1

101
Q

The low dose of dopamine stimulate the release of NE from

A

Non-adrenergic nerve endings.

102
Q

The moderate of dopamine stimulate the release of NE from

A

Sympathetic nerve endings.

103
Q

Dopamine, at moderate dose, HR and cardiac contractility ______ which will increase ____ and ______

A

Increases; CO and SV

104
Q

At moderate doses , CO, HR, contractility and SV are________ those effects are mainly due to ________. will that release of NE be seen in patients with chronic cardiac failure? why or why not?

A

increased; direct stimulation of B1 receptors and the release of NE from sympathetic nerve endings
-no because neurotransmitters may be depleted.

105
Q

Dopamine on Beta 2 receptors?

A

no effect on B2

106
Q

Dopamine due to its beta 1 effect is considered a positive ____, _____, ____, _____ agent.

A

Chronotropi, inotropic, dromotrophic and lusitropic

107
Q

At moderate dosing dopamine what are the renal effects?

A

renal effects still evident due to the combination of D1 mediated vasodilation increased CO and altered sodium tubular reaborption.

108
Q

At high doses of dopamine stimulation of alpha 1 leads to __________leading to ________preload and afterload. And an increase in ________ and ______can attenuate further increases in CO. PVR is also ______. If SVR rises too much you may see ______

A

peripheral vasoconstriction ; increased; SVR and BP ; increased; Reflex braducard

109
Q

Dopamine at very high doses, ________Mcg/kg/min, _____Predominates and vasoconstriction effect?

A

May compromise the circulation of the limbs and override the cardiac B1 effects.

110
Q

Cardiovascular risks with DOPAMINE: can induce

A

tachyarrhythmia and MI

111
Q

More than dobutamine and or epi, DOPAMINE is associated with ________ it can also decreased myocardial blood flow due to _________ and _______ and worsening _______in patients with ________

A

Sinus tachy and ventricular arrhythmia and other cardiac abnormalities; coronary VASOCONSTRICTION , vasospasm, increased wall tension; ischemia

112
Q

Dopamin is not recommended in those cardia patients ?

A

R sided HF

113
Q

Dopamine gastrointestinal effect? why?

A

N/V ; due to stimulation of D2 receptors

114
Q

Dopamine GI In CRITICAL ILLNESS at low and high doses? why? What causes the MODS?

A

can lead to mesenteric ischemia;
it impairs GI motility in critical illness
Mucosal ischemia, and the translocation of bacteria and toxins..

115
Q

Dopamine is a______ neurotransmitter at the carotid bodies. The result is _______of ventilation in patients who are treated with dopamine for increased ______________/ Dopamine decreases arterial oxygen saturation impairing ________. Monitor

A

Inhibitory; Myocardial contractility ;

V/Q matching in the lungs; ABGs

116
Q

Dopamine ENDOCRINE RESPONSE _____can occur. Decreases ____ _____ _____ _____ hormone secretion

A

Hyperglycemia can occur

Prolactin, Growth hormone, thyroid hormone, pituitary.

117
Q

Isoproterenol is a ___________ and a potent non selective ____ and _____ agonists

A

synthetic catecholamine; B1; B2

118
Q

What is the most potent activator of all sympathomimetic at B1 and B2?
It lacks______agonism

A

Isoproterenol; alpha1

119
Q

Must be protected form light? (2 drugs)

A

Dopamine

Isoproterenol

120
Q

3 clinical uses for isoproterenol for CV

A

Heart block
Adams-Stokes Attacks
Bronchospasm during anesthesia 0.01-0.02mg

121
Q

This drug decreased PVR in patients with pulmonary HTN______

A

Isoproterenol

122
Q

Isoproterenol and Epinephrine should not be given simultaneously, why?

A

Because they are both cardiac stimulants, and the combination can lead to serious arrhythmias.

123
Q

Why is isoproterenol not desirable for patients with CAD? also a poor choice for treating?

A

It simultaneously decreased coronary artery perfusion, and increases myocardial oxygen requirements.
Septic Shock

124
Q

Never use ISOPROTERENOL in patients with

A

Low BP

125
Q

Dobutamine is a predominantly_____Agonist with mild to minimal ____ and ____activity

A

B1; beta 2 and alpha1

126
Q

Is DOBUTAMINE a pure Beta1 adrenergic agonist?

A

Not

127
Q

Onset of action of Dobutamine?

when is steady state concentration achieved?

A

within 1-2 minutes ; within 10 minutes

128
Q

Dopamine, Epinephrine and Dobutamine should all be dissolved in _____why?

A

D5W; to avoid inactivation of the catecholamine that may occur in alkaline solution.

129
Q

Dobutamine may be combined with _______ to decrease after load and optimize_____in the presence of SVR.

A

Vasodilators; CO;

130
Q

Dobutamine has ______prominent inotropic than chronotropic effects on the heart compared to isoproterenol

A

More

131
Q

Dopamine vs dobutamine concerning NE store? SA node?

A

Does not cause the release of Endogenous NE as does dopamine

Enhance conduction of SA node.

132
Q

Dobutamine: Preload and Afterload are _______and contractility is ______ and HR is either ______or ______

A

Decreased; increased; same or increased.

133
Q

Is renal flow increased with dobutamine? why?

A

Yes ; because CO is increased

134
Q

As with any inotropic agents, Dobutamine may potentially?

A

Increase the size of an MI by increasing Myocardial O2 demand

135
Q

The majority of EPHEDRINE’s effect is via the _______ action which

A

Displaced endogenous NE from the pre-synaptic sympathetic nerve which increased NE release from the nerve endings.

136
Q

What is the 2nd action of Ephedrine ?_______what results in a loss of direct sympathomimetic effect ?

A

weak direct agonist on alpha 1 and 2 and Beta 1 and 2

Loss of polar 3- & 4 OH group

137
Q

Ephedrine use to treat hypotension associated with_______ and ________why?

A

Regional anesthesia
Injected/inhaled anesthetics
Because the hypotension is cause by sympathetic NS blockade.

138
Q

Used as a nasal decongestant and has antiemetic effect similar to that of droperinol with less sedation?

A

EPHEDRINE

139
Q

What is the usual dose of EPHEDRINE?

IV and IM

A

2.5mg to 25mg IV

25mg to 50mg IM

140
Q

2 conditions in which ephedrine may not work as well?

A 
sepsis (endogenous NE depleted)
Heart transplant (endogenous NE absent)
141
Q

Ephedrine and hyperglycemia

A

Does not produce

142
Q

Epinephrine should NOT BE administered during or within 14 days following the administration of ______

A

MAO inhibitors.

143
Q

Phenylephrine is a

A

Direct acting synthetic non-catecholamines

144
Q

Use of Phenylephrine

A

Hypotension- regional and epidural Hypotension- women in labor

145
Q

Typical phenylephrine dose

A

50-200mcg/IVP

146
Q

What effect can phenylephrine may have?

A

Reflex Bradycardia

147
Q

Other clinical use of Phenylephrine

Topical?

A

Can prolong the duration of spinal anesthesia when local anesthetics.
nasal decongestants

148
Q

Phenylephrine can be use to relieve

A

Drugs induced Priaprism

149
Q

Phenylephrine has a ______onset and _______duration

A

Rapid; short

150
Q

MAP is increased and CPP is with Phenylephrine

A

increased

151
Q

Phenylephrine: CO is ________ may reflect an increase in __________ but are

A

Decreased: afterload; Baro-receptor mediated reflex.

152
Q

Premedication with _______Will augment pressure response to

A

Oral CLONIDINE

153
Q

Clonidine is a _____ (class) ; If the patient is on clonidine at home?

A

alpha 2 agonist. decrease the dose of phenylephrine

154
Q

Phenylephrine stimulation of _________Receptors in the heart. ____Constriction greater than _____constriction

A

Alpha 1 receptors ; venous; arterial

155
Q

Halothane does what to the myocardium ?

A

Sensitize myocardium to catecholamines

156
Q

Phenylephrine ________ afterload ; Contractility ________; MAP is _________

A

Increase; unaffected; increased; may help with reflex bradycardia.

157
Q

Phenylephrine :Uterine effect in the Uterus

A

Uterine blood flow slightly decreseHIGHER UMBILICAL artery pH

158
Q

Drug of choice for parturients patient

A

Phenylephrine better than ephedrine

159
Q

Amphetamine is _____agent

A

indirect-acting synthetic noncatecholamine agentt

160
Q

Mechanism of action of AMPHETAMINE

A

indirectly tell nerve to release norepinephrine, dopamine and (serotonin) 5HT from their storage sites, work in the CNS

161
Q

Amphetamine does /doesnt cross BBB? what is the MAIN MECHANISM OF ACTION?

A

Does; in the CNS

162
Q

What is common with amphetamine? _______and drug dependence is

A

Tachyphylaxis; high

163
Q

Amphetamine are all______

A

Weak bases

164
Q

Amphetamine on heart? BP and CO?

A

Increase SBP and DBP

Does not increase CO

165
Q

**CNS effects of amphetamine

A

Appetite suppression
****Enhance analgesia produced by opioids
Stimulate Respiratory center
**Additive drug to drug interaction
Feeling of wakefulness, alertness, agitation, dizziness, restlessness.

166
Q

Dose of phenylephrine?

A

50-200 mcg IV

167
Q

Phenylephrine better for when ______Constriction is needed and CO is ______ and for the hypotension in patients with ______and ________ to increase _______without ______Side effects?

A

Peripheral; adequate; CAD and Aortic stenosis; Coronary Perfusion Pressure ; chronotropic effects.

168
Q

Phenylephrine acts on _______of alpha ___receptors in the heart and my contribute to arrhythmia with

A

small number

halothane.

169
Q

Explain the effect of phenyelphrine on the heart?

A

It is a potent alpha 1 agonists which produces systemic vasoconstriction increases the work of the heart. so if the coronary circulation is impaired, the decrease in myocardial oxygen supply/demand may precipitate angina.

170
Q

Phenylephrine reflex bradycardia is due to

A

rapid increase in SBP and DBP

171
Q

What is the treatment of amphetamine OVERDOSE?

A

Is the acidification of the urine to eliminate through the kidneys.

SRNAPharmacology I (29 decks)

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