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Pharm > Principle > Flashcards

Principle Flashcards

0
Q

Pharmacokinetics

A

The action of the body on a medication.

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1
Q

Pharmacodynamics

A

The action when a medication is administered, it begins to alter a function or process of the body.

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2
Q

Processes of pharmacokinetics

A

Liberation Absorption
Distribution Metabolism
Excretion

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3
Q

When a medication binds to a receptor site, what 4 possible actions will occur.

A
  1. Channels permitting the passage of ions in cell walls may be opened or closed.
  2. A biochemical messenger becomes activated, initiating other chemical reactions within the cell
  3. A normal cell function is prevented.
  4. A normal or abnormal function of the cell begins.
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4
Q

Two types of medications/chemicals directly affect cellular activity by binding with receptor sites on individual cells.

A

Agonist

Antagonist

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5
Q

Agonist medications

A

Initiate or alter a cellular activity by attaching to receptor sites, prompting a cell response

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6
Q

Antagonist medications

A

Prevents endogenous and exogenous agonist chemicals from reaching cell receptor sites and initiating or altering a particular cellular activity.

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7
Q

Affinity

A

Is the ability of a medication to bind to particular receptor sites.

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8
Q

What two properties determine the number of receptor sites bound by a medication?

A

Affinity and concentration.

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9
Q

The minimum concentration needed to initiate or alter cellular activity is known as the?

A

Threshold level

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10
Q

The concentration of medication required to initiate a cellular response is known as?

A

Potency

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11
Q

Efficacy

A

The ability to initiate or alter cells activity in a therapeutic or desired manner

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12
Q

Dose response curve

A

Illustrates the relationship of medication dose(or concentration) and efficacy.

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13
Q

Agonist effects on

Alpha 1

A

Vasoconstriction of arteries and veins

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14
Q

Agonist effects on

Alpha 2

A

Insulin restriction
Glucagon secretion
Inhibition of NE release

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15
Q

Agonist effects on

Beta 1

A

Increased heart rate(chronotropic effect)
Increased myocardial contractility (inotropic)
Increased myocardial conduction(dromotropic effect)
Renin secretion for urinary retention

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16
Q

Agonist effects on

Beta 2

A

Bronchus and bronchiole relaxation
Insulin secretion
Uterine relaxation
Arterial dilation in certain key organs

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17
Q

Agonist effects on

Dopaminergic

A

Vasodilation of renal and mesenteric arteries

Numerous receptor subtypes exist

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18
Q

Agonist effects on

Nicotinic

A

Present at neuromuscular junction,allowing ACh to stimulate muscle contraction

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19
Q

Agonist effects on

Muscarinic 2

A

Present in the heart, activated by ACh to offset sympathetic stimulation, decreasing heart rate, contractility, and electrical conduction velocity.

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20
Q

Antagonists can either be

A

Competitive or non competitive

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21
Q

Competitive antagonists

A

Temporarily bind with cellular receptor sites, displacing agonist chemicals.

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22
Q

Efficacy of competitive antagonist is directly related to?

A

It’s concentration near the receptor sites.

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23
Q

As the concentration of of a competitive antagonist increases near the receptor sites,it is able to?

A

Prevent a greater number of agonist chemicals from reaching the receptor.

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24
Q

As the competitive antagonist concentration falls or when the concentration of agonist chemicals increase…

A

A greater number of agonist chemicals bind with receptor sites and continue or resume cellular activation.

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25
Q

The efficacy of a competitive antagonist is related to its affinity compared to?

A

The affinity of the agonist chemicals present

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26
Q

Noncompetitive antagonists

A

Permanently bind to the receptor sites and prevent activation by agonist chemicals

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27
Q

Effects of noncompetitive antagonists continue till

A

New receptor sites or new cells are created

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28
Q

Efficacy of competitive antagonist is directly related to?

A

It’s concentration near the receptor sites.

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29
Q

Partial agonist chemicals

A

Bind to the receptor site, but do not initiate as much cellular activity or change as do other agonists.

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30
Q

Partial agonists effectively lower?

A

The efficacy of other agonists that may be present at the cells.

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31
Q

What are the three primary types of body substances that medications distribute through?

A

Water
Lipids
Protein

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32
Q

If a medication is water soluble higher weight based doses will be administered to?

A

Infants rather then adults or elderly.

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33
Q

Lipid soluble medication requires higher doses for?

A

Elderly people

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34
Q

What types of medication may require increased initial doses to overcome widespread distribution?

A

Water and lipid soluble

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35
Q

Medication metabolism in the liver is affected by?

A

Cytochrome P-450 system

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36
Q

A decrease in liver or kidney function requires doses to be?

A

Decreased due to impaired elimination from e body.

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37
Q

What is paradoxical medication reactions and who are prone to it?

A

Pts clinical experience effects opposite from the intended effects of e medication. Pts at extremes of age.

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38
Q

Formula for ideal weight for men

A

Kg=50+2.3 times the pts height in inches over 5 feet

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39
Q

Ideal weight for women

A

Kg=45.5+2.3 times pt height in inches over 5 feet

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40
Q

How does fever affect drug metabolism?

A

Initially it will increase metabolism of drugs in the liver due to tachycardia and reducing the amount of drug returned to circulation by the liver.
*fever also suppresses function of the cytochrome p450 system, ultimately decreasing rate of metabolism in certain classes of medications.

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41
Q

Special consideration with

Pulmonary hypertension

A

May have acute decompensation when vasopressors are used

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42
Q

Special consideration with

Glucose 6 phosphate dehydrogenase deficiency

A

Salicylate meds such as Asa may precipitate hemolysis

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43
Q

Special consideration with

Sickle cell

A

Adequate hydration and intravascular fluid volume and diuretic medications or vasoconstrictors may fatally complicate sickle cell

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44
Q

Pregnant pts have better renal function while?

A

Supine

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45
Q

FDA pregnancy category classification

A

A

Controlled studies fail to demonstrate risk to fetus in first trimester(no evidence of a risk in later trimesters) and possibility of fetal harm is low.

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46
Q

FDA pregnancy category classification

B

A

Either animal reproduction studies have not demonstrated a fetal risk but there are no controlled studies in pregnant women or animal studies have shown an adverse effect(other then a decrease in fertility) at was not confirmed by studies in women in first trimester(no evidence in of risk in later trimesters

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47
Q

FDA pregnancy category classification

C

A

Either animal studies revealed adverse effects on fetus and no controlled studies in women or studies in women and animals not available
Drugs should only be given if potential benefit justifies the potential risk to the fetus

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48
Q

FDA pregnancy category classification

D

A

Positive evidence of human fetal risk but benefits from use in pregnant women may be acceptable despite the risk (life threatening)

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49
Q

FDA pregnancy category classification

X

A

Fetal abnormalities
Evidence of fetal risk
Risk of drug in pregnant women outweighs any possible any possible benefits. Contraindicated in women who are or may become pregnant.

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50
Q

Administering multiple doses of the same medication to obtain a desired response or continuous administration demonstrates?

A

Cumulate action

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51
Q

Adverse effects are also known as

A

Untoward effects

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52
Q

Idiosyncratic medication reactions are when

A

Adverse effects occur that are completely unexpected and not previously known to occur with a particular medication

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53
Q

LD50

A

Median lethal dose,Weight based dose that causes death in 50% of animals tested

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54
Q

TD50

A

Median toxic dose,for particular adverse effect of medication 50% of animals tested had toxic effects at or above this weight based dose

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55
Q

ED50

A

Median effective dose, for particular use or indication

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56
Q

Therapeutic index

A

Is the relationship between the ld50 td50 and ed50

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57
Q

Tolerance of a medication is

A

Certain medications known to have decreased efficacy or potently when taken repeatedly by a pt

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58
Q

Down regulation

A

Mechanism that reduces available cell receptors for a particular medication causing tolerance

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59
Q

Cross tolerance

A

Repeated exposure to a medication with a particular class has the potential to cause tolerance to other medications in the same class.

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60
Q

Tachyphylaxsis

A

Repeated doses within a short time rapidly causes tolerance making medication virtually ineffective.

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61
Q

Habituation

A

Repeated exposure to certain medication or chemicals, abnormal tolerence to adverse or therapeutic effects associated with a substance

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62
Q

Medication Interference

A

Undesirable medication interactions

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63
Q

Pharmacokinetic values of medication

A

Onset
Peak
Duration

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64
Q

Onset and peak of a medication are generally related to?

A

Absorption and distribution

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65
Q

Duration of effect is generally related to?

A

Medication metabolism and elimination

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66
Q

Bioavailability

A

Is the percentage of unchanged medication that reaches circulation

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67
Q

Medication interaction

Addition or summation

A

Two meds w/ similar effect combine to produce a greater effect than that of either medication individually

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68
Q

Medication interaction

Synergism

A

Two meds w/ a similar effect combine, and resulting effect is greater then the sum of the medications (ie,1+1=6)

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69
Q

Medication interaction

Potentiation

A

The effect of one medication is greatly enhanced by the presence of snore medication, which does not have the ability to produce the same effect.

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70
Q

Medication interaction

Altered absorption

A

The action of one medication increases or decreases the ability of another medication to be absorbed by the body.ie medications at increase or decrease GI pH or modality may increase or decrease the absorption of other medications that are taken orally.

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71
Q

Medication interaction

Altered metabolism

A

The action of one medication increases or decreases metabolism of one medication within the body.

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72
Q

Medication interaction

Altered distribution

A

The presence of one medication alters the area available for distribution of anywhere medication, which becomes important when both medications are bound to the same site.if proteins are already occupied by one medication
Toxic levels of the other medication may develop

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73
Q

Medication interaction

Altered elimination

A

Medications may increase or decrease the functioning of the kidneys or other route of elimination,influencing the amount of or duration of effect of another medication in the body

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74
Q

Medication interaction

Physiologic antagonism

A

Two medications, each producing opposite effects are present simultaneously, resulting in minimal or no clinical changes.

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75
Q

Medication interaction

Neutralization

A

Two medications bind together in new body creating an inactive substance

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76
Q

GI medication absorption

GI motility

A

Ability of medication to pass through GI tract into the bloodstream

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77
Q

GI medication absorption

GI pH

A

Perfusion of the GI system (may be decreased during systemic trauma or shock)

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78
Q

GI medication absorption

Presence of foods, liquids, or chemicals in the stomach

A

Injury or bleeding in the GI system(both can alter GI motility, decreasing e time that oral medications can be absorbed)

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79
Q

IO site/ vein

Proximal tibia

A

Popliteal vein

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80
Q

IO site/ vein

Femur

A

Femoral vein

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81
Q 
IO site/ vein
Distal tibia(medial malleolous)
A

Great saphenous vein

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82
Q

IO site/ vein

Proximal humerous

A

Auxiliary vein

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83
Q

IO site/ vein

Manubrium

A

Internal mammary and azygos veins

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84
Q

What type of medication molecules easily pass through the phospholipid bilayer?

A

Nonionic(not charged)

Lipophilic(lipid loving)

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85
Q

Lager medication molecules use

A

Pinocytosis

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86
Q

Facilitated diffusion

A

When medications bind to carrier proteins

Requires no energy

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87
Q

Active transport is used to move medication molecules

A

Across a gradient

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88
Q

Three anatomic barriers that prevent passage of medication through openings in capillary walls

A

Blood brain
Blood placenta
Blood testes

89
Q

Plasma protein binding

A

Significantly alters distribution of certain medications within the body, medication molecules temporarily attach to proteins in blood plasma

90
Q

As a medication undergoes bio transformation it becomes

A

A metabolite

91
Q

Metabolite can become either

A

Active or inactive

92
Q

Active metabolizes

A

Remain capable of some pharmacologic activity

93
Q

Inactive metabolite

A

No longer possess the ability to alter cell process or body function

94
Q

4 effects on medications through bio transformation

A
  1. inactive substance can become active
  2. An active metabolite can be changed into another active medication
  3. an active medication can be completely or partially inactivated
  4. A medication can be transformed into a substance that is easier for the body to eliminate.
95
Q

Two patterns of metabolism and excretion

A

Zero order elimination

First order elimination

96
Q

Zero order elimination

A

A fixed amount of a substance is removed during a certain period of time.

97
Q

First order elimination

A

The rate of elimination is directly influenced by plasma levels of the substance.
In essence, the more substance in the plasma, the more the body works to eliminate the substance.

98
Q

First order elimination is quantified as a medication’s

A

Half life

99
Q

Half life

A

The time needed in an average person for metabolism and excretion of 50% of a substance in he plasma

100
Q

Anhelmintics

A

Treats intestinal parasites

Affects GI

101
Q

Anticoagulants

A

Reduce the efficacy of clotting factors present in the blood

102
Q

Antiemetic

A

Treat or prevent nausea and vomiting

Affects CNS and GI

103
Q

Antihistamine

A

Bock histamine receptors, dry mucus membranes, inhibit immune response in allergic reactions

104
Q

Antihyperlididemics

A

Decrease blood cholesterol,sequester cholesterol chemicals in bite

105
Q

Barbiturates

A

Reduce or prevent seizures, provide sedation

106
Q

Calcium channel blockers

A

Reduce heart rate and bp

107
Q

Cardiac glycosides

A

Decrease heart rate and improve contractility

108
Q

Cholesterol sysntheisis inhibitors

A

Prevent cholesterol conversin in the liver

109
Q

Cholinergics

A

Activate secretory glands in eyes and GI,improve muscle weakness in myasthenia gravis

110
Q

Corticosteroids

A

Decrease inflammation,immunosuppressant

111
Q

Glucocorticoids

A

Replacement or maintenance therapy, treat systemic inflammation, numerous other uses

112
Q

Glycoprotein IIb/IIIa inhibitors

A

Deactivate proteins involved in platelet aggregation

113
Q

Histamine-2 receptor antagonists

A

Block histamine receptors, including those responsible for gastric acid secretion

114
Q

Immunomodulators

A

Inhibit or enhance functioning of the immune system

115
Q

Immunosuppressant

A

Prevent rejection of transplanted organs and tissues, treat rheumatoid arthritiis

116
Q

Insulin

A

Positive inotropic effects, allows cellular glucose uptake, treat hyperkalemia

117
Q

Mineralocorticoids

A

Promote sodium and water retention

118
Q

Mucolytics

A

Assist with elimination of mucous in the respiratory tract

119
Q

Mydriatics

A

Dilate pupils for ocular diagnostic and treatment procedures

120
Q

Narcotic analgesics

A

Relieve pain and relieve or suppress cough

121
Q

Nasal decongestant

A

Decrease upper airway mucous secretion

122
Q

Neuromuscular blocking agents

A

Provide paralysis in incubated and ventilated pts

123
Q

Phophodiesterase inhibitors

A

Treat erectile disfunction

124
Q

Protein pump inhibitors

A

Suppress activity or parietal cell acid secretion

125
Q

Selective serotonin reuptake inhibitors SSRI

A

Treat depression, anxiety, and related conditions

126
Q

Tocolytics

A

Decrease or eliminate uterine contractions during preterm labor

127
Q

Tricyclics antidepressant

A

Treat depression, neuropathy, and chronic pain syndromes

128
Q

Xanthines

A

Bronchodilation

129
Q

Etomidate

Onset, peak, duration

A

30 to 60 sec
Peak in 60 sec
Lasts 5 mins

130
Q

What can happen if multiple doses of etomidate are given?

A

Adrenal suppression

131
Q

Klonopin

A

Clonazepam

132
Q

Restoril

A

Temazepam

133
Q

Benzodiazepines have what qualities?

A

Potent anti seizure
Anxiolytic
Sedative properties

134
Q

At high doses benzos can cause

A

Hypotension

135
Q

Prehospital benzos are pregnany class?

A

D

136
Q

Neuromuscular blockers antagonize ACh at what receptors?

A

Nicotenic

137
Q

Succylcholine

Onset, duration

A

Onset 30 to 60 sec

Duration 3 to 8 min

138
Q

Rocuronium
Onset
Duration

A

1 to 3 min

15 to 60 min

139
Q

Beta2 receptor sites on bronchial smooth muscle causes

A

Muscle relaxation, and bronchial dilation when antagonized by beta 2 agonits

140
Q

Two varieties of beta agonists

A

Selective, and nonselective

141
Q

How does albuterol effect potassium in the body?

A

Promotes cellular uptake of potassium

Can be used as a temporary treatment for hyperkalemia

142
Q

How is levabuterol different then albuterol?

A

It is structurally similar but without many of the reported beta 1 effects

143
Q

Ipatropium bromide antagonizes what receptors?

A

Muscarinic receptors

144
Q

Corticosteroids are administered in respiratory emergencies to?

A

Reduce airway inflammation, and ultimately improve oxygenation and ventilation

145
Q

Antidysrhythmic medication target

A

Cells within the heart or suppresses ectopic foci

146
Q

Antidysrhythmics are grouped by what classification scheme?

A

Vaughn williams

147
Q

Cardiac phases in order

A

4,0,1,2,3,4

148
Q

Cardiac cycle begins at what phase

A

4

149
Q

Phase 4

A

Cardiac cells are at rest
Waiting for spontaneous impulse from within(automaticity) or transfer of an impulse from an adjacent cardiac cell
Coincides with diastole of the heart.

150
Q

Phase 0

A

Begins with rapid influx of sodium ions through channels in the cardiac cells, potassium ions slowly begin to exit the cell, and depolarization occurs, altering the electrical charge present in the cell.

151
Q

Phase 1

A

Sodium influx decreases while potassium continues to exit the cell slowly.

152
Q

Phase 2

A

Begins the movement of calcium into the cell while potassium leave the cell

153
Q

Phase 3

A

Calcium movement ceases with continued outflow of potassium

Depolarization and myocardial contraction are occurring through phase 2 and 3

154
Q

Absolute refractory period

Effective refractory period

A

During phases 0,1,2, and 3
No additional depolarization may occur because of external stimuli.

Limits the potential the maximum heart date by ensuring that a certain amount of time elapses between myocardial contraction.

155
Q

Immediately after the absolute refractory period the brief period where an unusually powerful stimulious can initiate depolarization known as

A

Relative refractory period

156
Q

Class 1 anti dysrhythmic

A

Slow the movement of sodium brought channels in certain cardiac cells
Procainmide
Lidocaine

157
Q

Antidysrhythmic class 1a

A

Suppresses activity of ectopic foci and slow conduction velocity. This has the potential to prolong QRS and QT interval.
Effective for a variety of atrial and ventricular dysrhythmias,

158
Q

Antidysrhythmic class 2b

A

Blocks sodium channels in the purkinje fibers and ventricle, effectively resolving various ventricular dysrhythmias and suppressing ectopic foci.
Quickly metabolized by the liver.
Use caution with pts with kidney or liver disease

159
Q

Class II antidysrhythmic

A

Beta adnergic blocking agent

Beta blockers competitively inhibit catecholamine activation of beta receptors

160
Q

Precautions/toxic effects of beta blockers

A

Toxic effects include bradycardia,hypotension,conduction delays, and a variety of cardiovascular effects.
Use extreme caution in pts with reactive airway disease
Also may cause massive conduction abnormalities when given simultaneously or other medications that slow av node conduction.

161
Q

Metoprolol MOA in ami and ischemia

A

Reduces rate during myocardial ischemia and certain atrial tachycardias w/ modest drop in BP
Reduces rate resulting in lower myocardial oxygen consumption

162
Q

Class III antidysrhythmic

A

Increases duration of phases 1,2, and 3 of the cardiac cycle by extending the cellular action potential, these medications prolong the absolute refractory period, treating atrial or ventricular tachycardias.

163
Q

Class III antidysrhythmic amiodarone

A

Useful in treating atrial and ventricular tachycardias
Controversial uses in treatment of wow
Widely distributed throughout the body.

164
Q

Class IV antidysrhythmic

A

Calcium channel blockers
Reduce BP and control hr and may increase myocardial oxygen delivery during periods of ischemia.
May be used to inhibit uterine contractions during preterm delivery, long term management of migraines, and treatment of cardiomyopathy.

165
Q

Class IV MOA

A

Slow conduction through the av node, decrease automaticity of ectopic foci within e heart, and decrease the velocity of the heart.
Cardiac workload and oxygen consumption are decreased by lowering PVR(afterload) while simultaneously reducing cardiac output.

166
Q

Class IV antidysrhythmic in prehospital use

A

Diltiazem verapamil

Control of heart rate in pts with a flutter or a fib.

167
Q

Class V antidysrhythmic

A

Adenosine
Psvt
Adenosine decreases cardiac conduction velocity and prolongs the effective refractory period, producing a several second pause in cardiac activity.

168
Q

Alpha blockers

A

Prevents endogenous catecholamines from reaching alpha receptors, primarily in smooth muscle of blood vessels

In general these medications lower bp(diastolic primarily) and decrease systemic vascular resistance.

169
Q

Nonselective blockade of alpha 2 receptors causes

A

A reflex tachycardia by allowing an increase of NE secretion by the sympathetic nervous system

170
Q

Pts taking alpha blocking medications are prone to?

A

Postural hypotension and tachycardia

171
Q

Alpha adnergic receptor antagonists re prescribed for pts with?

A

Hypertension, an enlarged prostate gland, and glaucoma

172
Q

Clonodine catapres is primarily

A

Alpha 2 receptor agonist often given for emergency treatment of HTN
By activating alpha 2 receptors clonodine suppresses the release of NE, causi vasoconstriction

173
Q

Labatalol (trandate)

A

Alpha 1,beta 1, and beta 2 antagonism properties

IV form has far greater effect on beta 1 and 2 then alpha 1

174
Q

Pts at risk for Unopposed alpha stimulation, such as pheochromocytoma or cocaine overdose should…?

A

Receive another alpha adnergic antagonist before receiving labatolol for HTN crisis.
In this case the decreasing CO due to beta 1 antagonism prompts secretion of endogenous catecholamines potentially causing uncontrolled hypertension.

175
Q

Vagus nerve controls

A

Parasympathetic stimulation of receptor sites in the heart,lungs,digestive system, and throughout the chest and abdomen.

176
Q

Vagus nerve releases ACh that acts on…?

A

Muscarinic 2 receptors in he heart to decrease inotropic,chronotropic, and dromotropic effects.

177
Q

Excessive activation of Muscarinic 2 receptors by ACh causes…?

A

Bradycardia and conduction delays in e heart.
Other receptors: increased salivation,bronchi constriction, pulmonary secretions,vomiting, emesis,diarrhea,tearing, and a vast array of unwanted clinical effects.

178
Q

AChE inhibitors in pesticides and nerve agents permits excessive release of ACh and leads to elevated levels of ACh in the body. This Is treated by

A

Atropine sulfate

179
Q

Atropine is classified as an

A

Competitive muscarinic receptor blocker

180
Q

During AChE inhibitor toxicity, atropine is continuously administered until respiratory and hemodynamic status improve, but atropine does not…?

A

Bind to nicotinic receptors so consequentially it will not improve muscle weakness,fasciculations, or paralysis from cholinergoc poisoning.

181
Q

Vagus nerve controls

A

Parasympathetic stimulation of receptor sites in the heart,lungs,digestive system, and throughout the chest and abdomen.

182
Q

Vagus nerve releases ACh that acts on…?

A

Muscarinic 2 receptors in he heart to decrease inotropic,chronotropic, and dromotropic effects.

183
Q

Excessive activation of Muscarinic 2 receptors by ACh causes…?

A

Bradycardia and conduction delays in e heart.
Other receptors: increased salivation,bronchi constriction, pulmonary secretions,vomiting, emesis,diarrhea,tearing, and a vast array of unwanted clinical effects.

184
Q

AChE inhibitors in pesticides and nerve agents permits excessive release of ACh and leads to elevated levels of ACh in the body. This Is treated by

A

Atropine sulfate

185
Q

Atropine is classified as an

A

Competitive muscarinic receptor blocker

186
Q

During AChE inhibitor toxicity, atropine is continuously administered until respiratory and hemodynamic status improve, but atropine does not…?

A

Bind to nicotinic receptors so consequentially it will not improve muscle weakness,fasciculations, or paralysis from cholinergoc poisoning.

187
Q

Vagus nerve controls

A

Parasympathetic stimulation of receptor sites in the heart,lungs,digestive system, and throughout the chest and abdomen.

188
Q

Vagus nerve releases ACh that acts on…?

A

Muscarinic 2 receptors in he heart to decrease inotropic,chronotropic, and dromotropic effects.

189
Q

Excessive activation of Muscarinic 2 receptors by ACh causes…?

A

Bradycardia and conduction delays in e heart.
Other receptors: increased salivation,bronchi constriction, pulmonary secretions,vomiting, emesis,diarrhea,tearing, and a vast array of unwanted clinical effects.

190
Q

AChE inhibitors in pesticides and nerve agents permits excessive release of ACh and leads to elevated levels of ACh in the body. This Is treated by

A

Atropine sulfate

191
Q

Atropine is classified as an

A

Competitive muscarinic receptor blocker

192
Q

Vagus nerve controls

A

Parasympathetic stimulation of receptor sites in the heart,lungs,digestive system, and throughout the chest and abdomen.

193
Q

Vagus nerve releases ACh that acts on…?

A

Muscarinic 2 receptors in he heart to decrease inotropic,chronotropic, and dromotropic effects.

194
Q

Excessive activation of Muscarinic 2 receptors by ACh causes…?

A

Bradycardia and conduction delays in e heart.
Other receptors: increased salivation,bronchi constriction, pulmonary secretions,vomiting, emesis,diarrhea,tearing, and a vast array of unwanted clinical effects.

195
Q

AChE inhibitors in pesticides and nerve agents permits excessive release of ACh and leads to elevated levels of ACh in the body. This Is treated by

A

Atropine sulfate

196
Q

Atropine is classified as an

A

Competitive muscarinic receptor blocker

197
Q

Vagus nerve controls

A

Parasympathetic stimulation of receptor sites in the heart,lungs,digestive system, and throughout the chest and abdomen.

198
Q

Vagus nerve releases ACh that acts on…?

A

Muscarinic 2 receptors in he heart to decrease inotropic,chronotropic, and dromotropic effects.

199
Q

Excessive activation of Muscarinic 2 receptors by ACh causes…?

A

Bradycardia and conduction delays in e heart.
Other receptors: increased salivation,bronchi constriction, pulmonary secretions,vomiting, emesis,diarrhea,tearing, and a vast array of unwanted clinical effects.

200
Q

AChE inhibitors in pesticides and nerve agents permits excessive release of ACh and leads to elevated levels of ACh in the body. This Is treated by

A

Atropine sulfate

201
Q

Atropine is classified as an

A

Competitive muscarinic receptor blocker

202
Q

Atropine is used for bradycardia when

A

Vagal stimulation of maucarinic-2 receptors is suspected

203
Q

When atropine is administered for bradycardia ACh activation is

A

Prevented of muscarinic 2 receptors is prevented allowing underlying sympathehtic stimulation to predominate.

204
Q

Atropine is unlikely to be effective for treatment of bradycardia caused by

A

Blocked cardiac conduction such as in second and third degree AV blocks

205
Q

Pts exposed to pesticides and nerve agents (AChE inhibitor toxcitity)are to

A

Receive atropine continuously until respiratory and hemodynamic status improves regardless of total dose required.

206
Q

In AChE inhibitor exposure atropine does not

A

Bind to nicotinic receptors so it will not improve muscle weakness, fasciculations, or paralysis from cholinergic poisoning.

207
Q

Catecholamines

A

Are naturally occurring chemicals in the body that stimulate receptor sites in the sympathetic nervous system.

208
Q

Two structures of catecholamines

A

The catechol group

The monoamine oxidase group

209
Q

Endogenous catecholamines include

A

Epinephrine , norepinephrine , and dopamine.

These chemicals stimulate alpha, beta, and dopaminergic receptor sites.

210
Q

Catecholamines are rapidly metabolized by?

A

Catecholamines are rapidly metabolized by monoamine oxidase and catechol O-methyltransferase( an enzyme), resulting in brief duration of action after admin

211
Q

Sympathomemtic chemcicals are not

A

Found naturally in the body

212
Q

Sympathyomemetic mimic

A

Catecholamines and do not undergo the same metabolism as catecholamines thus allowing longer duration of action.

213
Q

Epinephrine stimulates

A

Alpha, beta 1 and beta 2 receptors causing potent vasoconstriction, a marked increase of inotropic ,dromotropic , and chronotropic,CO and powerful bronchodilation.

214
Q

Epinephrine infusion drips are used for

A

Profound hypotension, shock, and refractory bradycardia.

215
Q

Norepinephrine

A

Stimulates beta 1 amped alpha receptors causing increase in BP, contractility(inotropic), and chronotropic (heart rate)
Vasoconstrictor(alpha effects) are usually greater then cardiac (beta1 effects )

216
Q

Dopamine has an affinity to

A

For dopaminergic receptor sites that is greater than the affinity for beta receptor and a greater affinity to beta receptors the alpha sites.

217
Q

Dopamine activation by dose

A

Dopaminergic receptors are activated at 2.5 to 5 causing mesinteric and renal artery vasodilation
5-10 activates beta 1 causing inotropic and chromotropic effects
10-20 alpha 1 effects predominate(dopaminergic receptors not activated)

218
Q

Dobutamine

A

Synthetically manufactured catecholamine similar to dopamine.
It activates beta1 and to lesser degree beta 2 and alpha1 receptor sites. Dopaminergic receptors are not activated.
Slight +chromotropic, while providing significant +inotropic

219
Q

When combined with a vasodilator medication, dobutamine for cardiogenic shock…

A

Increases inotropic while decrease in afterload, resulting in improved cardiac output

220
Q

Neo synephrine (phenylephine)

A

Almost pure alpha 1 agonist
Minimal beta 1 effects
Potent vasoconstrictor w/ longer duration the. Catecholamines
May cause reflex tachycardia, and tachyphylaxis

221
Q

Vasopressin(pitressin, ADH)

A

Has emerged as a potent vasopressor medication recommended in ACLS
Secreted in response to plasma hyperosmolerity(elevated concentration of glucose and plasma proteins) or intravascular volume depletion.
Clinically is administered for treatment of GI bleeding, diabetes insipidus, shock,and cardiac arrest.

Pharm (2 decks)

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