Principle Flashcards
0
Q
Pharmacokinetics
A
The action of the body on a medication.
1
Q
Pharmacodynamics
A
The action when a medication is administered, it begins to alter a function or process of the body.
2
Q
Processes of pharmacokinetics
A
Liberation Absorption
Distribution Metabolism
Excretion
3
Q
When a medication binds to a receptor site, what 4 possible actions will occur.
A
- Channels permitting the passage of ions in cell walls may be opened or closed.
- A biochemical messenger becomes activated, initiating other chemical reactions within the cell
- A normal cell function is prevented.
- A normal or abnormal function of the cell begins.
4
Q
Two types of medications/chemicals directly affect cellular activity by binding with receptor sites on individual cells.
A
Agonist
Antagonist
5
Q
Agonist medications
A
Initiate or alter a cellular activity by attaching to receptor sites, prompting a cell response
6
Q
Antagonist medications
A
Prevents endogenous and exogenous agonist chemicals from reaching cell receptor sites and initiating or altering a particular cellular activity.
7
Q
Affinity
A
Is the ability of a medication to bind to particular receptor sites.
8
Q
What two properties determine the number of receptor sites bound by a medication?
A
Affinity and concentration.
9
Q
The minimum concentration needed to initiate or alter cellular activity is known as the?
A
Threshold level
10
Q
The concentration of medication required to initiate a cellular response is known as?
A
Potency
11
Q
Efficacy
A
The ability to initiate or alter cells activity in a therapeutic or desired manner
12
Q
Dose response curve
A
Illustrates the relationship of medication dose(or concentration) and efficacy.
13
Q
Agonist effects on
Alpha 1
A
Vasoconstriction of arteries and veins
14
Q
Agonist effects on
Alpha 2
A
Insulin restriction
Glucagon secretion
Inhibition of NE release
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
16
Q
Agonist effects on
Beta 2
A
Bronchus and bronchiole relaxation
Insulin secretion
Uterine relaxation
Arterial dilation in certain key organs
17
Q
Agonist effects on
Dopaminergic
A
Vasodilation of renal and mesenteric arteries
Numerous receptor subtypes exist
18
Q
Agonist effects on
Nicotinic
A
Present at neuromuscular junction,allowing ACh to stimulate muscle contraction
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.
20
Q
Antagonists can either be
A
Competitive or non competitive
21
Q
Competitive antagonists
A
Temporarily bind with cellular receptor sites, displacing agonist chemicals.
22
Q
Efficacy of competitive antagonist is directly related to?
A
It’s concentration near the receptor sites.
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.
24
As the competitive antagonist concentration falls or when the concentration of agonist chemicals increase...
A greater number of agonist chemicals bind with receptor sites and continue or resume cellular activation.
25
The efficacy of a competitive antagonist is related to its affinity compared to?
The affinity of the agonist chemicals present
26
Noncompetitive antagonists
Permanently bind to the receptor sites and prevent activation by agonist chemicals
27
Effects of noncompetitive antagonists continue till
New receptor sites or new cells are created
28
Efficacy of competitive antagonist is directly related to?
It's concentration near the receptor sites.
29
Partial agonist chemicals
Bind to the receptor site, but do not initiate as much cellular activity or change as do other agonists.
30
Partial agonists effectively lower?
The efficacy of other agonists that may be present at the cells.
31
What are the three primary types of body substances that medications distribute through?
Water
Lipids
Protein
32
If a medication is water soluble higher weight based doses will be administered to?
Infants rather then adults or elderly.
33
Lipid soluble medication requires higher doses for?
Elderly people
34
What types of medication may require increased initial doses to overcome widespread distribution?
Water and lipid soluble
35
Medication metabolism in the liver is affected by?
Cytochrome P-450 system
36
A decrease in liver or kidney function requires doses to be?
Decreased due to impaired elimination from e body.
37
What is paradoxical medication reactions and who are prone to it?
Pts clinical experience effects opposite from the intended effects of e medication. Pts at extremes of age.
38
Formula for ideal weight for men
Kg=50+2.3 times the pts height in inches over 5 feet
39
Ideal weight for women
Kg=45.5+2.3 times pt height in inches over 5 feet
40
How does fever affect drug metabolism?
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.
41
Special consideration with
| Pulmonary hypertension
May have acute decompensation when vasopressors are used
42
Special consideration with
| Glucose 6 phosphate dehydrogenase deficiency
Salicylate meds such as Asa may precipitate hemolysis
43
Special consideration with
| Sickle cell
Adequate hydration and intravascular fluid volume and diuretic medications or vasoconstrictors may fatally complicate sickle cell
44
Pregnant pts have better renal function while?
Supine
45
FDA pregnancy category classification
| 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.
46
FDA pregnancy category classification
| B
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
47
FDA pregnancy category classification
| C
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
48
FDA pregnancy category classification
| D
Positive evidence of human fetal risk but benefits from use in pregnant women may be acceptable despite the risk (life threatening)
49
FDA pregnancy category classification
| X
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.
50
Administering multiple doses of the same medication to obtain a desired response or continuous administration demonstrates?
Cumulate action
51
Adverse effects are also known as
Untoward effects
52
Idiosyncratic medication reactions are when
Adverse effects occur that are completely unexpected and not previously known to occur with a particular medication
53
LD50
Median lethal dose,Weight based dose that causes death in 50% of animals tested
54
TD50
Median toxic dose,for particular adverse effect of medication 50% of animals tested had toxic effects at or above this weight based dose
55
ED50
Median effective dose, for particular use or indication
56
Therapeutic index
Is the relationship between the ld50 td50 and ed50
57
Tolerance of a medication is
Certain medications known to have decreased efficacy or potently when taken repeatedly by a pt
58
Down regulation
Mechanism that reduces available cell receptors for a particular medication causing tolerance
59
Cross tolerance
Repeated exposure to a medication with a particular class has the potential to cause tolerance to other medications in the same class.
60
Tachyphylaxsis
Repeated doses within a short time rapidly causes tolerance making medication virtually ineffective.
61
Habituation
Repeated exposure to certain medication or chemicals, abnormal tolerence to adverse or therapeutic effects associated with a substance
62
Medication Interference
Undesirable medication interactions
63
Pharmacokinetic values of medication
Onset
Peak
Duration
64
Onset and peak of a medication are generally related to?
Absorption and distribution
65
Duration of effect is generally related to?
Medication metabolism and elimination
66
Bioavailability
Is the percentage of unchanged medication that reaches circulation
67
Medication interaction
| Addition or summation
Two meds w/ similar effect combine to produce a greater effect than that of either medication individually
68
Medication interaction
| Synergism
Two meds w/ a similar effect combine, and resulting effect is greater then the sum of the medications (ie,1+1=6)
69
Medication interaction
| Potentiation
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.
70
Medication interaction
| Altered absorption
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.
71
Medication interaction
| Altered metabolism
The action of one medication increases or decreases metabolism of one medication within the body.
72
Medication interaction
| Altered distribution
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
73
Medication interaction
| Altered elimination
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
74
Medication interaction
| Physiologic antagonism
Two medications, each producing opposite effects are present simultaneously, resulting in minimal or no clinical changes.
75
Medication interaction
| Neutralization
Two medications bind together in new body creating an inactive substance
76
GI medication absorption
| GI motility
Ability of medication to pass through GI tract into the bloodstream
77
GI medication absorption
| GI pH
Perfusion of the GI system (may be decreased during systemic trauma or shock)
78
GI medication absorption
| Presence of foods, liquids, or chemicals in the stomach
Injury or bleeding in the GI system(both can alter GI motility, decreasing e time that oral medications can be absorbed)
79
IO site/ vein
| Proximal tibia
Popliteal vein
80
IO site/ vein
| Femur
Femoral vein
81
```
IO site/ vein
Distal tibia(medial malleolous)
```
Great saphenous vein
82
IO site/ vein
| Proximal humerous
Auxiliary vein
83
IO site/ vein
| Manubrium
Internal mammary and azygos veins
84
What type of medication molecules easily pass through the phospholipid bilayer?
Nonionic(not charged)
| Lipophilic(lipid loving)
85
Lager medication molecules use
Pinocytosis
86
Facilitated diffusion
When medications bind to carrier proteins
| Requires no energy
87
Active transport is used to move medication molecules
Across a gradient
88
Three anatomic barriers that prevent passage of medication through openings in capillary walls
Blood brain
Blood placenta
Blood testes
89
Plasma protein binding
Significantly alters distribution of certain medications within the body, medication molecules temporarily attach to proteins in blood plasma
90
As a medication undergoes bio transformation it becomes
A metabolite
91
Metabolite can become either
Active or inactive
92
Active metabolizes
Remain capable of some pharmacologic activity
93
Inactive metabolite
No longer possess the ability to alter cell process or body function
94
4 effects on medications through bio transformation
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
Two patterns of metabolism and excretion
Zero order elimination
| First order elimination
96
Zero order elimination
A fixed amount of a substance is removed during a certain period of time.
97
First order elimination
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
First order elimination is quantified as a medication's
Half life
99
Half life
The time needed in an average person for metabolism and excretion of 50% of a substance in he plasma
100
Anhelmintics
Treats intestinal parasites
| Affects GI
101
Anticoagulants
Reduce the efficacy of clotting factors present in the blood
102
Antiemetic
Treat or prevent nausea and vomiting
| Affects CNS and GI
103
Antihistamine
Bock histamine receptors, dry mucus membranes, inhibit immune response in allergic reactions
104
Antihyperlididemics
Decrease blood cholesterol,sequester cholesterol chemicals in bite
105
Barbiturates
Reduce or prevent seizures, provide sedation
106
Calcium channel blockers
Reduce heart rate and bp
107
Cardiac glycosides
Decrease heart rate and improve contractility
108
Cholesterol sysntheisis inhibitors
Prevent cholesterol conversin in the liver
109
Cholinergics
Activate secretory glands in eyes and GI,improve muscle weakness in myasthenia gravis
110
Corticosteroids
Decrease inflammation,immunosuppressant
111
Glucocorticoids
Replacement or maintenance therapy, treat systemic inflammation, numerous other uses
112
Glycoprotein IIb/IIIa inhibitors
Deactivate proteins involved in platelet aggregation
113
Histamine-2 receptor antagonists
Block histamine receptors, including those responsible for gastric acid secretion
114
Immunomodulators
Inhibit or enhance functioning of the immune system
115
Immunosuppressant
Prevent rejection of transplanted organs and tissues, treat rheumatoid arthritiis
116
Insulin
Positive inotropic effects, allows cellular glucose uptake, treat hyperkalemia
117
Mineralocorticoids
Promote sodium and water retention
118
Mucolytics
Assist with elimination of mucous in the respiratory tract
119
Mydriatics
Dilate pupils for ocular diagnostic and treatment procedures
120
Narcotic analgesics
Relieve pain and relieve or suppress cough
121
Nasal decongestant
Decrease upper airway mucous secretion
122
Neuromuscular blocking agents
Provide paralysis in incubated and ventilated pts
123
Phophodiesterase inhibitors
Treat erectile disfunction
124
Protein pump inhibitors
Suppress activity or parietal cell acid secretion
125
Selective serotonin reuptake inhibitors SSRI
Treat depression, anxiety, and related conditions
126
Tocolytics
Decrease or eliminate uterine contractions during preterm labor
127
Tricyclics antidepressant
Treat depression, neuropathy, and chronic pain syndromes
128
Xanthines
Bronchodilation
129
Etomidate
| Onset, peak, duration
30 to 60 sec
Peak in 60 sec
Lasts 5 mins
130
What can happen if multiple doses of etomidate are given?
Adrenal suppression
131
Klonopin
Clonazepam
132
Restoril
Temazepam
133
Benzodiazepines have what qualities?
Potent anti seizure
Anxiolytic
Sedative properties
134
At high doses benzos can cause
Hypotension
135
Prehospital benzos are pregnany class?
D
136
Neuromuscular blockers antagonize ACh at what receptors?
Nicotenic
137
Succylcholine
| Onset, duration
Onset 30 to 60 sec
| Duration 3 to 8 min
138
Rocuronium
Onset
Duration
1 to 3 min
| 15 to 60 min
139
Beta2 receptor sites on bronchial smooth muscle causes
Muscle relaxation, and bronchial dilation when antagonized by beta 2 agonits
140
Two varieties of beta agonists
Selective, and nonselective
141
How does albuterol effect potassium in the body?
Promotes cellular uptake of potassium
| Can be used as a temporary treatment for hyperkalemia
142
How is levabuterol different then albuterol?
It is structurally similar but without many of the reported beta 1 effects
143
Ipatropium bromide antagonizes what receptors?
Muscarinic receptors
144
Corticosteroids are administered in respiratory emergencies to?
Reduce airway inflammation, and ultimately improve oxygenation and ventilation
145
Antidysrhythmic medication target
Cells within the heart or suppresses ectopic foci
146
Antidysrhythmics are grouped by what classification scheme?
Vaughn williams
147
Cardiac phases in order
4,0,1,2,3,4
148
Cardiac cycle begins at what phase
4
149
Phase 4
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
Phase 0
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
Phase 1
Sodium influx decreases while potassium continues to exit the cell slowly.
152
Phase 2
Begins the movement of calcium into the cell while potassium leave the cell
153
Phase 3
Calcium movement ceases with continued outflow of potassium
| Depolarization and myocardial contraction are occurring through phase 2 and 3
154
Absolute refractory period
| Effective refractory period
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
Immediately after the absolute refractory period the brief period where an unusually powerful stimulious can initiate depolarization known as
Relative refractory period
156
Class 1 anti dysrhythmic
Slow the movement of sodium brought channels in certain cardiac cells
Procainmide
Lidocaine
157
Antidysrhythmic class 1a
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
Antidysrhythmic class 2b
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
Class II antidysrhythmic
Beta adnergic blocking agent
| Beta blockers competitively inhibit catecholamine activation of beta receptors
160
Precautions/toxic effects of beta blockers
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
Metoprolol MOA in ami and ischemia
Reduces rate during myocardial ischemia and certain atrial tachycardias w/ modest drop in BP
Reduces rate resulting in lower myocardial oxygen consumption
162
Class III antidysrhythmic
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
Class III antidysrhythmic amiodarone
Useful in treating atrial and ventricular tachycardias
Controversial uses in treatment of wow
Widely distributed throughout the body.
164
Class IV antidysrhythmic
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
Class IV MOA
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
Class IV antidysrhythmic in prehospital use
Diltiazem verapamil
| Control of heart rate in pts with a flutter or a fib.
167
Class V antidysrhythmic
Adenosine
Psvt
Adenosine decreases cardiac conduction velocity and prolongs the effective refractory period, producing a several second pause in cardiac activity.
168
Alpha blockers
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
Nonselective blockade of alpha 2 receptors causes
A reflex tachycardia by allowing an increase of NE secretion by the sympathetic nervous system
170
Pts taking alpha blocking medications are prone to?
Postural hypotension and tachycardia
171
Alpha adnergic receptor antagonists re prescribed for pts with?
Hypertension, an enlarged prostate gland, and glaucoma
172
Clonodine catapres is primarily
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
Labatalol (trandate)
Alpha 1,beta 1, and beta 2 antagonism properties
| IV form has far greater effect on beta 1 and 2 then alpha 1
174
Pts at risk for Unopposed alpha stimulation, such as pheochromocytoma or cocaine overdose should...?
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
Vagus nerve controls
Parasympathetic stimulation of receptor sites in the heart,lungs,digestive system, and throughout the chest and abdomen.
176
Vagus nerve releases ACh that acts on...?
Muscarinic 2 receptors in he heart to decrease inotropic,chronotropic, and dromotropic effects.
177
Excessive activation of Muscarinic 2 receptors by ACh causes...?
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
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
Atropine sulfate
179
Atropine is classified as an
Competitive muscarinic receptor blocker
180
During AChE inhibitor toxicity, atropine is continuously administered until respiratory and hemodynamic status improve, but atropine does not...?
Bind to nicotinic receptors so consequentially it will not improve muscle weakness,fasciculations, or paralysis from cholinergoc poisoning.
181
Vagus nerve controls
Parasympathetic stimulation of receptor sites in the heart,lungs,digestive system, and throughout the chest and abdomen.
182
Vagus nerve releases ACh that acts on...?
Muscarinic 2 receptors in he heart to decrease inotropic,chronotropic, and dromotropic effects.
183
Excessive activation of Muscarinic 2 receptors by ACh causes...?
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
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
Atropine sulfate
185
Atropine is classified as an
Competitive muscarinic receptor blocker
186
During AChE inhibitor toxicity, atropine is continuously administered until respiratory and hemodynamic status improve, but atropine does not...?
Bind to nicotinic receptors so consequentially it will not improve muscle weakness,fasciculations, or paralysis from cholinergoc poisoning.
187
Vagus nerve controls
Parasympathetic stimulation of receptor sites in the heart,lungs,digestive system, and throughout the chest and abdomen.
188
Vagus nerve releases ACh that acts on...?
Muscarinic 2 receptors in he heart to decrease inotropic,chronotropic, and dromotropic effects.
189
Excessive activation of Muscarinic 2 receptors by ACh causes...?
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
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
Atropine sulfate
191
Atropine is classified as an
Competitive muscarinic receptor blocker
192
Vagus nerve controls
Parasympathetic stimulation of receptor sites in the heart,lungs,digestive system, and throughout the chest and abdomen.
193
Vagus nerve releases ACh that acts on...?
Muscarinic 2 receptors in he heart to decrease inotropic,chronotropic, and dromotropic effects.
194
Excessive activation of Muscarinic 2 receptors by ACh causes...?
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
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
Atropine sulfate
196
Atropine is classified as an
Competitive muscarinic receptor blocker
197
Vagus nerve controls
Parasympathetic stimulation of receptor sites in the heart,lungs,digestive system, and throughout the chest and abdomen.
198
Vagus nerve releases ACh that acts on...?
Muscarinic 2 receptors in he heart to decrease inotropic,chronotropic, and dromotropic effects.
199
Excessive activation of Muscarinic 2 receptors by ACh causes...?
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
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
Atropine sulfate
201
Atropine is classified as an
Competitive muscarinic receptor blocker
202
Atropine is used for bradycardia when
Vagal stimulation of maucarinic-2 receptors is suspected
203
When atropine is administered for bradycardia ACh activation is
Prevented of muscarinic 2 receptors is prevented allowing underlying sympathehtic stimulation to predominate.
204
Atropine is unlikely to be effective for treatment of bradycardia caused by
Blocked cardiac conduction such as in second and third degree AV blocks
205
Pts exposed to pesticides and nerve agents (AChE inhibitor toxcitity)are to
Receive atropine continuously until respiratory and hemodynamic status improves regardless of total dose required.
206
In AChE inhibitor exposure atropine does not
Bind to nicotinic receptors so it will not improve muscle weakness, fasciculations, or paralysis from cholinergic poisoning.
207
Catecholamines
Are naturally occurring chemicals in the body that stimulate receptor sites in the sympathetic nervous system.
208
Two structures of catecholamines
The catechol group
| The monoamine oxidase group
209
Endogenous catecholamines include
Epinephrine , norepinephrine , and dopamine.
These chemicals stimulate alpha, beta, and dopaminergic receptor sites.
210
Catecholamines are rapidly metabolized by?
Catecholamines are rapidly metabolized by monoamine oxidase and catechol O-methyltransferase( an enzyme), resulting in brief duration of action after admin
211
Sympathomemtic chemcicals are not
Found naturally in the body
212
Sympathyomemetic mimic
Catecholamines and do not undergo the same metabolism as catecholamines thus allowing longer duration of action.
213
Epinephrine stimulates
Alpha, beta 1 and beta 2 receptors causing potent vasoconstriction, a marked increase of inotropic ,dromotropic , and chronotropic,CO and powerful bronchodilation.
214
Epinephrine infusion drips are used for
Profound hypotension, shock, and refractory bradycardia.
215
Norepinephrine
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
Dopamine has an affinity to
For dopaminergic receptor sites that is greater than the affinity for beta receptor and a greater affinity to beta receptors the alpha sites.
217
Dopamine activation by dose
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
Dobutamine
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
When combined with a vasodilator medication, dobutamine for cardiogenic shock...
Increases inotropic while decrease in afterload, resulting in improved cardiac output
220
Neo synephrine (phenylephine)
Almost pure alpha 1 agonist
Minimal beta 1 effects
Potent vasoconstrictor w/ longer duration the. Catecholamines
May cause reflex tachycardia, and tachyphylaxis
221
Vasopressin(pitressin, ADH)
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.
