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Exam 6 Flashcards

1
Q

Amino Ester Local Anesthetics

A

Tetracaine
Procaine
Cocaine
Benzocaine

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2
Q

Amino Amide Anesthetics

A

Lidocaine
Mepivacaine
Prilocaine
Bupivacaine
Articaine

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3
Q

Local Anesthetic Location of Action

A

Mostly at the spinal cord

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4
Q

A delta Nerve Fiber General Function

A

Primary pain sensors
Transmit fast signals

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5
Q

B Nerve Fiber General Function

A

Response to vasomotor, visceromotor, sudomotor, pilomotor signals

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6
Q

C Nerve Fiber General Function

A

Transmit second pain signals

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7
Q

Local Anesthetic General Structure

A

One lipophilic region and one hydrophilic region

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8
Q

Unique Feature of Amino Ester Local Anesthetics

A

Short duration of action due to endogenous esterases

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9
Q

Amino Amide Local Anesthetic Nomenclature

A

All have two “I’s” in the name

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10
Q

Local Anesthetic General Mechanism

A

Blocks Na+ channels from INSIDE THE CELL

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11
Q

Local Anesthetic General Cellular Mechanism

A

Cross the cell membrane unprotonated
Become protonated INSIDE the cell
Protonated form blocks the Na+ channel

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12
Q

Local Anesthetic Nerve Fiber Preference

A

Fast rate fibers like A and C sensory fibers
Myelinated fibers
Small nerve fibers blocked first

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13
Q

PKa of Most Local Anesthetics

A

7.8 to 9.1
Protonated and positively charged at phys pH

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14
Q

Benzocaine Unique Feature

A

PKa of 3.5

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15
Q

Local Anesthetic Administration

A

Topical
Field Block Injection
Nerve Block Injection
Spinal Block Injection

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16
Q

Weak Potency Short Duration Local Anesthetics

A

Procaine

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17
Q

Moderate Potency Intermediate Duration Local Anesthetics

A

Lidocaine
Mepivacaine
Prilocaine

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18
Q

High Potency Long Duration Local Anesthetics

A

Tetracaine
Bupivacaine
Etidocaine
Ropivicaine

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19
Q

Cocaine Unique Feature

A

Intrinsic vasoconstrictive properties

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20
Q

Local Anesthetic Degradation

A

Esters hydrolyzed by plasma butyrylcholinesterase
Amides converted to water soluble metabolites by liver CYPs

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21
Q

Local Anesthetics Adverse Effects

A

Injection Site Irritation
Hypersensitivity to Degradation Byproducts
Dose Dependent Toxicity
Methemoglobinemia

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22
Q

Local Anesthetics Associated With Methemoglobinemia

A

Benzocaine
Lidocaine
Prilocaine

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23
Q

Procaine Usage

A

Short acting
Low potency and rapid onset
Dental applications and infiltration anesthesia
Very little risk of systemic toxicity

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24
Q

Tetracaine Usage

A

Long acting slow onset
High Potency
Topical

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25
Cocaine Usage
Medium duration medium potency Topical and ENT Cardiotoxic
26
Benzocaine Usage
Fast onset Well absorbed thru mucous membranes Mouth and gum irritation Risk of Methemoglobinemia
27
Lidocaine Usage
Medium onset medium duration Moderate potency Neutral at phys pH for faster duration and onset Topical
28
Prilocaine Usage
Moderate onset medium duration Moderate potency Neutral at phys pH CROSSES BBB Associated with Methemoglobinemia
29
Spasm Treatment Drugs
Chlorzoxazone Cyclobenzaprine Orphenadrine Methocarbamol
30
Spasticity Treatment Drugs
Baclofen Tizanidine Benzodiazepine Botulinum Toxin Dantrolene
31
Spasms
Long lasting involuntary contraction of striated muscle Independent of posture
32
Antispasmodic Location of Action
Spinal cord Act at higher neural levels at higher doses
33
Onset and Duration of Antispasmodics
Methacarbamol 30 minutes and 1 to 2 hrs Chlorzoxazone 60 minutes and 1 hr Cyclobenzaprine 60 minutes and 12 to 24 hrs Orphenadrine 60 minutes and 2 to 4 hrs
34
Antispasmodic General Mechanisms
Chlorzoxazone generalized neural suppressant Methacarbamol generalized neural suppressant Cyclobenzaprine reduction of tonic somatic motor activity Orphenadrine anticholinergic
35
Tricyclic Like Antispasmodics
Cyclobenzaprine Methacarbamol
36
Most Common Antispasmodic Adverse Effects
Drowsiness Dizziness Constipation Addiction and physical dependence
37
Methacarbamol Unique Adverse Effect
Discolored urine
38
Spasticity Pathology
Spontaneous muscle contraction resulting from brain or spinal cord injuries Velocity dependent resistance to passive muscle stretch
39
Spasticity Associated Diseases
Brain and spinal cord damage Stroke MS Cerebral Palsy Adrenoleukodystrophy ALS PKU
40
Central Acting Spacticity Treatments
Baclofen Tizanidine Benzodiazepine Botulinum toxin
41
Muscle Acting Spasticity Treatments
Dantrolene
42
Central Acting Spasticity Treatment General Mechanisms
Baclofen GABA B receptor agonist Tizanidine alpha 2 adrenergic receptor agonist Benzodiazepine GABA A receptor agonist Botulinum Toxin direct neurotoxicity
43
Receptor Locations
Alpha 2 and GABA B presynaptic GABA A and GABA B postsynaptic
44
Baclofen Usage
Spasticity in MS and spinal cord injury Hiccups Neuropathy
45
Baclofen Adverse Effects
Drowsiness Dizziness Constipation
46
Intrathecal Baclofen Advantages
Oral effectiveness only achieved at high doses Intrathecal route requires a smaller dose and give fewer side effects
47
Baclofen Mechanism
Binds presynaptic GABA B receptors inhibiting Ca2+ influx and neurotransmitter release Binds postsynaptic GABA B receptors activating K+ channels Reduces substance P from nociceptive afferent nerve terminals
48
Tizadine Usage
Decreases spasticity in MS and spinal cord injury
49
Tizadine Mechanism
Negative feedbacks central Alpha 2 receptors
50
Tizadine Adverse Effects
Drowsiness Dizziness Dry mouth LOW BLOOD PRESSURE
51
Botulinum Toxin Usage
Decreases spasticity in cerebral palsy, stroke, TBI, and advanced MS
52
Botulinum Toxin Adverse Effects
Excessive muscle weakness Non exact muscle paralysis
53
Benzodiazepine Usage
Use with Baclofen in spinal cord injury and cerebral palsy treatment NOT useful in stroke NOT useful in Parkinson’s or Huntingtons
54
Benzodiazepine Mechanism
Binds to GABA A receptors and increases chloride conductance Results in presynaptic inhibition
55
Benzodiazepine Adverse Effects
Drowsiness Dizziness Confusion Dry mouth
56
Dantrolene Usage
Decreases spasticity in upper motor neuron lesions Decreases spasticity in stroke and spinal cord injury Malignant hyperthermia Neuroleptic malignant syndrome
57
Dantrolene Mechanism
Blocks contraction mostly in fast muscle fibers Reduces depolarization induced Ca2+ from sarcoplasmic reticulum Peaks 3 to 6 hours after oral administration
58
Dantrolene Contraindications
Causes overall muscle weakness DO NOT USE IN ALS
59
Dantrolene Adverse Effects
Hepatotoxicity Diarrhea
60
Bupivicaine Usage
Slow onset long duration High potency Hydrophobic Epidurals and nerve blocks
61
IV General Anesthetics
Methohexital Etomidate Propofol Ketamine
62
Inhaled General Anesthetics
Nitrous Oxide Halothane Sevoflurane Isoflurane Desflurane
63
IV Anesthetics General Use
Induction of general anesthesia in adults
64
Inhaled Anesthetics General Use
Induction of general anesthesia in children Maintenance of general anesthesia in adults and children
65
General Anesthesia Stage 1
Patient is conscious and drowsy with variable analgesia
66
General Anesthesia Stage 2
Excitement and delirium then patient becomes unconscious but responds with reflexes to pain Irregular respirations
67
General Anesthesia Stage 3
Surgical anesthesia with regular respirations but no spontaneous movement
68
General Anesthesia Stage 4
Medullary depression, loss of respiration and vasomotor control, and death
69
General Structure of IV Anesthetics
Lipophilic
70
IV Anesthetic Onset
Induction in one arm brain circulation time
71
Barbiturate IV Anesthetic
Methohexital
72
Propofol Mechanism
GABA A agonist Sedative and amnestic but NOT analgesia
73
Propofol Metabolism
CYP enzymes in the liver
74
Propofol Onset and Duration
40 second onset 8 min duration
75
Methohexital Mechanism
GABA A recetor agonist
76
Methohexital Metabolism
In the liver
77
Etomidate Mechanism
GABA A agonist
78
Methohexital Onset and Duration
30 second onset 10 min duration
79
Etomidate Metabolism
Plasma esterase
80
Etomidate Onset and Duration
30 second onset 4 min duration
81
Etomidate Unique Properties
Minimal cardiovascular and respiratory effects
82
Ketamine Mechanism
NMDA receptor antagonist
83
Ketamine Metabolism
In the liver
84
Ketamine Onset and Duration
Almost immediate onset 64 min duration
85
Ketamine Unique Use
Good in children Can produce trance like state
86
Ketamine Unique Properties
Dissociation Hallucinations in adults Significant analgesia Bronchodilation Minimal cardiovascular effects
87
Inhaled Anesthetic Unique Properties
Very pungent Sevoflurane not as much Halothane has none
88
Inhaled Anesthetic Pharmacokinetics
Goal to achieve equilibrium between alveoli and brain
89
Factors of Anesthetic Uptake
Partial pressure Blood solubility Alveolar blood flow
90
Partial Pressure and Water Solubility
More water soluble agents have lower partial pressure
91
Blood:Gas Partition Coefficient
Measures solubility of gas in blood
92
Blood:Gas Partition Coefficient and Induction Time
Low blood solubility gives faster induction
93
Anesthetic Gas Equilibrium
When partial pressures in various tissues are equivalent
94
Anesthetic Gas Activation Targets
GABA A Cl- Channels Glycine Receptors K+ Channels
95
Anesthetic Gas Inhibitory Targets
Acetylcholine receptors Glutamate Receptors NMDA Receptors Serotonin Receptors
96
Anesthetic Gas Potency
Alveolar partial pressure that prevents movement in 50% of 40 year old patients in response to a standard painful stimulus
97
Anesthetic Gas Potency Nomenclature
1 Minimum Alveolar Concentration
98
Relationship Between Potency and Induction Time
NO RELATIONSHIP
99
Nitrous Oxide Potency and Partial Pressure
Low Potency High Partial Pressure
100
Anesthetic Gas Standard Dosage
1.2 to 1.3 MAC prevents overt patient reactions
101
Relationship Between MACs of Coadministered Gas
Additive
102
Factors That Increase MAC and Decrease Potency
Infancy Chronic alcohol use Hyper Na+ Sympathomimetics
103
Factors That Decrease MAC and Increase Potency
Old age Acute alcohol intoxication Pregnancy Opiates and sedatives Hypothermia
104
Anesthetic Gas Cardiovascular Adverse Reactions
Systemic Vasodilation Myocardial Suppression Blunted Baroreceptor Reflex Reduced Sympathetic Tone
105
Anesthetic Gas Respiratory Adverse Reactions
Need assisted ventilation Lost gag and cough reflex Reduced lower esophageal tone
106
Anesthetic Gas Body Temperature Adverse Reactions
Hypothermia
107
Anesthetic Gas Effects After Emergence
Nausea and vomiting Tachycardia and hypertension Shivering
108
Diffusion Hypoxia
Diffusion of some gases back into the lung can result in hypoxia
109
Anesthetic Gas Metabolism
Generally Minimal Halothane metabolized by CYP enzymes Halothane metabolites can bind and modify liver proteins Immune system attacks the modified liver proteins
110
Malignant Hyperthermia Causative Agents
Halogenated anesthetic gas Succinylcholine
111
Carbonic Anhydrase Inhibitor Diuretics
Acetazolamide
112
Na+ K+ 2Cl- Symport Inhibitor Diuretics
Furosemide
113
Na+ Cl- Symport Inhibitor Diuretics
Hydrochlorothiazide Chlorothiazide
114
Epithelial Na+ Channel Inhibitor Diuretics
Amiloride Triamterene
115
Aldosterone Antagonist Diuretics
Spironolactone Eplerenone
116
Osmotic Diuretics
Mannitol
117
Locations of Na+ Reabsorption
70% Proximal Tubule 20% Thick Ascending Limb 5% Distal Tubule 5% Collecting Duct
118
Na+ Reabsorption Compensation
When upstream Na+ reabsorption is blocked, downstream locations increase their reabsorption
119
Concentrated and Dilute Nephron Areas
Locations of water absorption are concentrated Locations of ion absorption are dilute
120
Carbonic Anhydrase Inhibitor Site of Action
Proximal Tubule
121
Carbonic Anhydrase Inhibitor Efficacy
Moderate due to downstream compensation
122
Carbonic Anhydrase Inhibitor Mechanism
Competitive inhibition of carbonic anhydrase Prevents conversion of Water and CO2 to H2CO3 and back H2CO3 cannot then give up an H+ No H+ to power Na+ transporter prevents Na+ reabsorption
123
Carbonic Anhydrase Inhibitor Uses
Rarely as a diuretic Open angle glaucoma Epilepsy Altitude sickness
124
Carbonic Anhydrase Inhibitor Adverse Effects
Hypo K+ Metabolic Acidosis Calcium phosphate renal stones in alkali urine
125
Na+ K+ 2Cl- Symport Inhibitor Site of Action
Thick ascending limb of Loop of Henle
126
Na+ K+ 2Cl- Symport Inhibitor Mechanism
Block Na+ K+ 2Cl- luminal transporter Inhibits reabsorption of Na+ into blood
127
Na+ K+ 2Cl- Symport Inhibitor Vascular Effects
Vasodilation
128
How do diuretics get to their site of action?
OAT1 transport to luminal membrane
129
Na+ K+ 2Cl- Symport Inhibitor Uses
Severe Edema Oliguric acute renal failure Hyper Ca2+ Increased renal drug elimination in overdose
130
How do diuretics get to their site of action?
OAT1 transport to luminal membrane for most OCT for K+ sparing amiloride and triamterene
131
Na+ K+ 2Cl- Symport Inhibitor Adverse Effects
Hypo K+ Mild hypo Ca2+ Hyperglycemia REVERSIBLE OTOTOXICITY
132
Na+ Cl- Symport Inhibitor Drug Class
Thiazides
133
Thiazide Site of Action
Distal convoluted tubule Only moderately effective compared to Na+ K+ 2Cl- Symport Inhibitor Loop medications
134
Thiazide Efficacy Note
Reduced efficacy in low GFR that happens with heart failure
135
Thiazide Mechanism
Blocks Na+ Cl- Symporter in Distal Tubule Enhances TRPV5 Ca2+ transporter which increases Ca2+ reabsorption
136
Thiazide Uses
Mild hypertension Mild edema Calcium kidney stones Osteoporosis
137
Thiazide Adverse Effects
Hypo K+ Hypo Na+ Hyperglycemia Hyperlipidemia Erectile Disfunction
138
Thiazide Drug Interactions
NSAIDS reduce efficacy through OAT1 inhibition
139
Collecting Duct Drugs
Epithelial Na+ Channel Inhibitors Aldosterone Receptor Antagonists
140
Epithelial Na+ Channel ENaC Inhibitor Mechanism
Blocks epithelial Na+ channel in lumen Does not impact K+ reabsorption
141
ENaC Inhibitor Uses
Used with loops and thiazides to prevent hyper K+ Treatment of Liddle Syndrome Treatment of CF
142
ENaC Inhibitor Adverse Effects
Hyper K+ VERY DANGEROUS WITH ACE INHIBITORS AND NSAIDS
143
Aldosterone Receptor Antagonist Mechanism
Blocks cytoplasmic aldosterone receptor
144
Aldosterone Receptor Antagonist Use
Used with K+ wasting diuretics Primary hyperaldosteronism Hepatic Cirrhosis Treatment of Severe CHF
145
Aldosterone Receptor Antagonist Adverse Effects
Hyperkalemia USE CAUTION WITH ACE INHIBITORS AND NSAIDS Anti androgenic effects with Spironolactone
146
Eplerenone Structural Effects
9 11 epoxide structure reduces affinity for progesterone and androgen receptors
147
Osmotic Diuretic Site of Action
Proximal Tubule Loop of Henle Collecting Duct
148
Osmotic Diuretic Mechanism
Increases osmolality of tubular fluid Reduces passive reabsorption of NaCl in ascending loop
149
Osmotic Diuretic Pharmacokinetics
Given IV only in a hospital setting
150
Osmotic Diuretic Uses
Elevated intracranial pressure Removal of toxins
151
Osmotic Diuretic Adverse Effects
Extracellular Volume Expansion Dehydration Hyper K+ Hyper Na+ Acute Renal Failure
152
Antithrombotic Medications
ADP Receptor Antagonist Clopidogrel GPIIb IIIa Antagonist Abciximab PAR1 Antagonists Antagonist Vorapaxar
153
Primary Hemostatis
Platelets shape change and activation Platelet adhesion Platelet aggregation
154
Secondary Hemostasis
Activation of coagulation cascade to synthesize thrombin
155
Platelet Phase Resting Steps
PGI2 Stimulates its Gs receptors Adenylyl Cyclase converts ATP to cAMP CAMP activates PKA PKA suppresses platelet activation
156
Platelet Phase Activation Steps
ADP activates Gi receptor which inhibits conversion of ATP to cAMP cAMP cannot activate PKA which inhibits homeostatic inhibition
157
ADP Receptor Antagonist
Clopidogrel
158
ADP Receptor Antagonist Mechanism
Prodrug converted to active thiol form by CYP 2C19 Binds irreversibly to platelet P2Y12 ADP receptor Prevents activation of GPIIb IIIa receptors RESTING PLATELETS CANNOT ACTIVATE
159
ADP Receptor Antagonist Pharmacokinetics
Orally effective Maximal efficacy occurs 8 to 11 days after starting use
160
ADP Receptor Antagonist Use
Similar to low dose aspirin but slightly more effective Reduces rate of stroke MI and death in atherosclerotic patients with recent vascular event Combination with aspirin in stent patients
161
ADP Receptor Antagonist Pharmacogenomics
Wide variability in drug response Loss of function in CYP 2C19*2 allele SNP leads to therapeutic failure
162
ADP Receptor Antagonist Adverse Effects
GI Upset Rash 5 DAY BLEEDING RISK TTP
163
ADP Receptor Antagonist Drug Interactions
NO NSAIDS in patients with bleeding disorders CYP 2C19 inhibitors
164
GPIIb IIIa Antagonist
Abciximab
165
GP IIb IIIa Antagonist Mechanism
Block platelet aggregation Fab fragments of monoclonal antibody blocks fibrinogen binding
166
GPIIb IIIa Pharmacokinetics
Given IV Short half life Long duration
167
GP IIa IIIb Antagonist Use
Very effective but very expensive Given in combo with aspirin and heparin to prevent clots during stent placement
168
GPIIa IIIb Adverse Effects
BRAIN BLEEDS Anaphylaxis Thrombocytopenia
169
PAR 1 Receptor Antagonist
Vorapaxar
170
PAR 1 Receptor Antagonist Mechanism
Blocks PAR 1 receptor DOES NOT EFFECT THROMBIN CONVERSION OF FIBRINOGEN TO FIBRIN
171
PAR 1 Receptor Antagonist Pharmacokinetics
100% Protein Bound Onset within 1 Week Effects Persist 4 Weeks After Cessation
172
PAR 1 Antagonist Use
Reduce thrombotic events post MI or with PAD
173
PAR 1 Antagonist Adverse Effects
Intracranial Bleeding
174
Drugs for Prevention of Arterial Thrombus
Antiplatelet drugs
175
Drugs for Prevention of Venous Thrombus
Anticoagulant Drugs
176
Indirect Thrombin Factor Xa Inhibitor Anticoagulants
Heparin Enoxaparin Fondaparinux
177
Vitamin K Antagonist Anticoagulants
Warfarin
178
Direct Thrombin Factor Xa Inhibitor Anticoagulants
Bivalirudin Dabigatran Rivaroxaban
179
Thrombolytics
TPA
180
Common Clotting Factor
Factor X
181
Factors Inhibited by Heparin
Activated clotting factors
182
Factors Inhibited by Warfarin
Precursor factors or non activated factors
183
Intrinsic Pathway Test
PTT aPTT
184
Extrinsic Pathway Test
PT
185
Heparin Mechanism
Indirectly inhibits factors IIa and Xa
186
Heparin Structure
Very large About 40 kDa Negatively charged
187
Low Molecular Weight Heparin
Enoxaparin Same as heparin but only 17 saccharides
188
Fondaparinux Structure
Pentasaccharide Minimal number of heparin SO4- groups to bind antithrombin factor II
189
Heparin Drug Selectivity
Heparin inactivates thrombin factor II and factor Xa equally Low Molecular Weight Heparin inactivates Xa well but thrombin factor II poorly Fondaparinux inactivates factor Xa only
190
Heparin Pharmacokinetics
Must be given IV Cleared by reticuloendothelial system macrophages Binds to plasma proteins and cells Levels vary greatly and require consistent monitoring
191
Enoxaparin LMWH and Fondaparinux Pharmacokinetics
Given SubQ at home Do not require monitoring Longer half life Cleared by the kidneys
192
Heparin Uses
Initial treatment for PE and DVT Prevents thrombosis in surgery and stent placement Often given with antiplatelet drugs
193
Heparin Adverse Effects
Bleeding Lower risk in LMWH and Fondaparinux
194
Antidote for Heparin Bleeding
Protamine Sulfate DOES NOT WORK WITH FONDAPARINUX
195
Protamine Sulfate Adverse Effects
Allergies particularly in vasectomized men
196
Heparin Induced Thrombocytopenia Mechanism
The body can develop antibodies in the first 5 to 10 days Antibodies bind platelets together and mimic platelet deficiency
197
Heparin Induced Thrombocytopenia Drug Alternatives
Fondaparinux has a VERY SMALL risk
198
Warfarin Mechanism
Vitamin K antagonist Inhibits VKORC1 in liver to deplete vitamin K dependent clotting factors Decreases formation of fibrin Delayed onset of action
199
Vitamin K Cycle
Reduced form vitamin K from diet Vitamin K is oxidized when used to activate clotting factors Oxidized vitamin K is reduced back to its active form by VKORC1
200
Warfarin Pharmacokinetics
Oral 99% bound to plasma proteins Long Half Life Metabolized by CYP 2C9 Drug activity measured with PT INR test target between 2 and 3
201
Warfarin Use
Prevention of thrombosis Transition therapy after initial course of heparin NOT USEFUL FOR EMERGENCIES
202
Warfarin Pharmacogenomics
CYP 2C9*2 and *3 SNP have reduced warfarin clearance VKORC1 Haplotype A requires substantial dose reduction
203
Warfarin Adverse Effects
Bleeding Teratogen Tissue Necrosis Purple Toe Syndrome of Microemboli
204
Warfarin Antidote
Vitamin K 4 Factor Prothrombin Complex Concentrate Transfusion for Life Threatening Bleeding
205
Warfarin Drug Interactions That Increase Efficacy
CYP 2C9 and 3A4 Inhibitors Broad Spectrum Antibiotics Anything That Promotes Bleeding
206
Warfarin Drug Interactions That Reduce Efficacy
CYP Inducers Vitamin K
207
Direct Thrombin Inhibitor General Mechanism
Factor IIa Inhibition
208
Parental Direct Thrombin Inhibitors
Bivalirudin
209
Bivalirudin Mechanism
Binds tightly to catalytic and substrate recognition site of thrombin
210
Bivalirudin Pharmacokinetics
Given IV Monitored by aPTT Short Half Life Excreted by kidneys
211
Bivalirudin Special Use
Same as heparin Good for people who have developed HITT
212
Oral Direct Thrombin Inhibitors
Dabigatran Etexilate
213
Dabigatran Mechanism
Prodrug metabolized to competitive thrombin inhibitor
214
Dabigatran Pharmacokinetics
Oral 2 to 3 hour onset Shorter Half Life \
215
Dabigatran Uses
Warfarin Replacement NO MONITORING REQUIRED
216
Dabigatran Antidote
Idarucizumab
217
Direct Factor Xa Inhibitor
Rivaroxaban
218
Rivaroxaban Mechanism
Bind and inactivates circulating and clot bound factor Xa
219
Rivaroxaban Pharmacokinetics
Oral Half Life 5 to 9 hours
220
TPA Use
Given in first 3 hours after ischemic event Given IV Half life of 5 minutes
221
Hematopoietics
Ferrous Sulfate Iron Dextran Folic Acid Cyanocobalamin Epoetin Alfa Filgastran Oprelvekin
222
Ferrous Sulfate Use
Iron deficiency anemia Therapy for 1 to 2 months Prophylactic in pregnancy and heavy menstrual bleeding
223
Ferrous Sulfate Drug Interactions
Antacids reduce absorption Decreases absorption of tetracycline
224
Iron Dextran Use
Same as iron dextran IV and used when oral prep is unavailable
225
Iron Poisoning Antidote
Deferoxamine
226
Vitamin B12 Deficiency Anemia Consequences
Megaloblastic anemia Neurological Damage
227
B12 Deficiency Anemia Treatment
Cyanocobalamin B12
228
Cyanocobalamin B12 Use
Oral which requires intrinsic factor
229
Cyanocobalamin B12 Adverse Effects
Well tolerated Low K+
230
Folic Acid Use
Treatment of folic acid deficiency anemia Must be converted to active form by B12 Good for B12 deficiency anemia
231
Erythropoietic Growth Factors
Epoetin Alpha
232
Epoetin Alpha Mechanism
Stimulates receptors on erythroid precursors in bone marrow
233
Epoetin Alpha Usage
Give IV or Sub Q Anemia of chronic renal failure HIV Patients on Zidovudin Chemotherapy anemia
234
Epoetin Alpha Adverse Effects
Hypertension and cardiovascular effects Requires monitoring of Hb levels
235
Myeloid Growth Factor General Mechanism
Act on myeloid precursors to stimulate production of myeloid cells like NEUTROPHILS
236
Myeloid Growth Factors
Filgrastim
237
Filgrastim Uses
Severe Chronic Neutropenia Reduces risk of infection in patients undergoing myelosuppressive chemo and bone marrow transplant
238
Filgrastim Adverse Effects
Bone pain
239
Thrombotic Growth Factor General Mechanism
Stimulates proliferation of megakaryocyte proginators and maturation of megakaryocytes Overall increases platelets
240
Thrombotic Growth Factors
Interleukin 11 Oprelvekin
241
Oprelvekin Uses
Bring up platelets in chemo patients Platelets recovery in 5 to 9 days of treatment
242
Oprelvekin Adverse Effects
Fluid retention Peripheral Edema Arrhythmias
243
Full Agonist Opiates
Morphine Codeine Fentanyl Methadone Heroin
244
Most Commonly Abused Opiates
Heroin Methadone Oxycodone Hydrocodone
245
True Opiate
Purified from opium poppy resin
246
Opioids
Synthetic or endogenous compounds with similar actions to opiates
247
Opiate General Mechanism
Stimulation of G protein coupled opioid receptors
248
Mu Opioid Receptors
Morphine like action Anti anxiety and euphoria Expressed in CNS, spinal cord, and periphery
249
Mu Opioid Receptor Agonists
Morphine Beta Endorphin
250
Kappa Opioid Receptors
Mediate Pentazocine like Actions Dysphoria and hallucination Expressed in CNS and spinal cord
251
Kappa Opioid Receptor Agonists
Butorphanol Dynorphin
252
Delta Opioid Receptors
Expressed in CNS and spinal cord
253
Delta Opioid Receptor Agonists
No good selective drugs yet Enkephalins Beta Endorphin
254
NOP Receptors
Newly discovered opioid receptor family No agents yet
255
Tolerance
Decreased drug effects with repeated administration Associated with receptor desensitization and downstream post receptor mechanisms
256
Tolerance Greatly Impacts These Effects
Analgesia Euphoria Sedation Respirator Depression
257
Tolerance Minimally Impacts These Effects
Miosis Constipation
258
Dependence
Induced requirement of a drug for a patient to feel “normal” Withdrawal symptoms upon drug discontinuation
259
Substance Use Disorder
Very similar to dependence Involves strong psychological dependence Often included societal norms
260
Four Opium Poppy Extracts
Morphine Codeine Thebaine Papavarine
261
Morphine Pharmacokinetics
Administered through multiple routes Readily absorbed 5 to 15 minute onset 60 to 90 minute max effect 4 to 5 hour duration
262
Morphine Metabolism
Glucuronidated in liver Excreted by the kidneys Caution in patients with liver and kidney function
263
Morphine Dose and Tolerance
10mg normal effective dose 120 to 200mg toxic dose 300 to 60omg in substance use disorder 500mg in chronic pain patients
264
Morphine Mechanism
Blocks pain transmission at peripheral and spinal levels Blocks pain response in higher brain levels
265
Morphine Major Adverse Effects
Central respiratory depression Tolerance can develop to this effect First dose nausea Long term constipation
266
Other Morphine Adverse Effects
Miosis Skin itch due to histamine release
267
Morphine Contraindications
Caution in lung disease Caution in pregnancy DO NOT USE IN HEAD INJURIES OR CNS TUMORS
268
Morphine Drug Interactions
Sedatives and CNS depressants Ethanol can dissolve extended release coating which can lead to dangerous rapid release
269
Codiene Structure
Methyl group makes it a prodrug that is converted to morphine Less potent than morphine
270
Codeine Pharmacokinetics
Oral only Metabolized by CYP 2D6 Some patients metabolize codeine very quickly
271
Codeine Uses
Mild pain relief Additive with aspirin and acetaminophen Antitussive
272
Fentanyl Structure
Different from morphine, codeine, and methadone Synthetic analog that binds opioid receptors VERY WELL Lipophilic and crosses the BBB
273
Fentanyl Potency
100X more potent than morphine
274
Fentanyl Uses
Analgesia Sometimes Useful for Anesthesia
275
Fentanyl Pharmacokinetics
Highly available through all routes Rapid absorption and penetration into brain Duration depends on route of administration
276
Fentanyl Patch Use
Chronic Pain
277
Fentanyl Lozenge, Film, Tablet, or Nasal Spray Use
Acute pain in chronic pain patients
278
Other Difference Between Fentanyl and Morphine
No histamine release Fewer cardiovascular effects Truncal rigidity
279
Heroin Structure
Acetylated morphine prodrug 2 to 4 times more potent than morphine More lipid soluble
280
Methadone Structure
Completely different from other opiates
281
Methadone Pharmacokinetics
Orally very effective Long half life Metabolized slowly by CYP 3A4 and 2B6
282
Other Differences Between Methadone and Morphine
Long QT Torsades VERY LONG DURATION OF ACTION
283
Methadone Use
Methadone maintenance therapy for opioid substance use disorder Satisfies dependence and prevents withdrawal but provides no high Patients function normally
284
Partial Mixed Opioid Agonists
Nalbuphine Buprenorphine
285
Partial Opioid Agonist General Properties
Agonist when given alone Antagonist when given with full agonists
286
Mixed Agonist Antagonist Properties
Agonist at one receptor but antagonist at another Generates partial drug response
287
Nalbuphine Mechanism
Kappa receptor agonist gives analgesia Mu receptor antagonist prevents euphoria and respiratory depression
288
Nalbuphine Pharmacokinetics
IV, IM, SubQ Similar potency to morphine 15 min onset 4 to 5 hour duration
289
Buprenorphine Mechanism
Kappa receptor antagonist Mu receptor partial agonist Can still precipitate withdrawal
290
Buprenorphine Uses
Opioid substance use disorder Cocaine substance use disorder
291
Non Analgesic Opioids
Loperamide Diphenoxylate Dextromethorphan
292
Loperamide Use
Anti diarrheal Full agonist but only in GI tract DOES NOT ENTER THE BRAIN
293
Diphenoxylate Use
Anti diarrheal High doses can produce opioid effects
294
Dextromethorphan Use
Cough suppression Similar to opiates but not technically an opiate Sigma opioid antagonist
295
Opiate Antagonists
Naloxone Naltrexone Methylnaltrexone
296
Naloxone Use
Competitively blocks opioid receptors More effective for full agonists than mixed partial agonists Prevents respiratory depression in opioid overdose
297
Naloxone Pharmacokinetics
IV or Nasal Spray Rapid acting Short duration
298
Naltrexone Pharmacokinetics
Orally Effective Long duration of action
299
Naltrexone Use
Treatment of opioid dependence Triggers withdrawal but prevents opioid action with subsequent dosage
300
Methylnaltrexone Use
Treatment of opioid induced constipation Injected SubQ
301
Malignant Hyperthermia Mechanism
Uncontrolled release of Ca2+ from SR

PHARM (7 decks)

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