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Pharm II - Exam 2 - Steven's Questions
Terms in this set (172)
Alcohol, sedative hypnotics and anxiolytics
1. What are the ways that alcohol is metabolized?
a. ADH (alcohol dehydrogenase)
b. MEOS (Microsomal-ethanol oxidizing system)
2. Is alcohol an inducer of cytochrome?
a. Yes, it induces CYP2E1 which is also the one that metabolizes it down
3. What order kinetics does alcohol follow when broken down?
a. Zero order kinetics, 1 drink per hour
4. What drug is used to inhibit aldehyde dehydrogenase and will lead to a buildup of acetaldehyde, causing the individual to be sick?
a. Disulfiram (Antabuse)
5. What are the pharmacodynamics of alcohol?
a. Down regulation of GABA receptors due to an overactivation
b. Up-regulation of NMDA receptors
c. Withdrawal due to pharmacodynamic tolerance
6. What are the other drugs classes to be aware of that can alcohol can cause cross tolerance in?
c. All three of these are CNS depressants
7. What is the mechanism of action for alcohol?
a. Binds to GABAA receptors to increase Cl- influx and enhance inhibitory GABA transmission
8. What effects does alcohol have in smooth muscle?
a. It can have a vasodilatory effect and lead to hypothermia
9. What effect is seen in the kidneys with alcohol?
10. If seizures occur with acute alcohol toxicity what drugs would you use to treat it?
a. Lorazepam- benzodiazepine
b. Phenytoin- anticonvulsant
11. What are the common nutritional deficiencies seen in alcoholics?
a. Folate and thiamine deficiencies
12. Wernicke-Korsakoff syndrome can be seen in chronic alcohol abusers, what are the signs and symptoms of this?
a. Paralysis of eye muscles, ataxia, confusion, coma and death
13. What other CNS effects can you see in chronic alcoholics?
a. Korsakoff psychosis: memory loss
b. Peripheral neuropathy
14. What is the mechanism of action for naltrexone?
a. Opioid receptor antagonist, blocks the ability of alcohol to stimulate the reward pathway
b. No more happy no more drinkie
15. What drug is a structural analogue of GABA and is used to restore the normal GABA and glutamate balance?
16. What patient would naltrexone be contraindicated in and what could you give this patient instead?
a. Liver damage patient contraindicated
b. Give them Acamprosate (excreted by kidneys, no lover damage)
17. What would be the DOC for preventing seizures in an alcoholic patient?
18. What are the drugs to give an alcoholic that has seizures and what one is first or better?
a. Lorazepam first
b. Phenytoin second
19. What class of drugs would be used to treat acute anxiety?
a. Benzodiazepines DOC
20. What class of drugs would be used to treat general anxiety?
a. Benzodiazepines DOC
21. What class of drug would be used to treat phobias, panic disorders, and obsessive compulsive?
22. What is the mechanism of action for barbiturates?
a. Binds GABA receptor, stimulate Cl- influx
b. Produces inhibition independent of GABA
c. Causes euphoria
23. What is our short acting barbiturate that is used to induce anesthesia?
24. What barbiturate is used as an anticonvulsive for seizures?
25. Where are barbiturates metabolized?
a. Liver, by CYP450
26. What are some side effects of barbiturates to be aware of?
a. CNS depression: drowsiness, impaired motor skills and judgment, can last 10-22h
b. Paradoxical excitement
c. Severe physiological and psychological dependence
27. What are the two contraindications for barbiturates?
a. Enhance porphyrin synthesis: abnormal heme synthesis
b. Pulmonary insufficiency: respiratory depression
28. Do barbiturates have a ceiling effect?
a. No they do not!
b. These are a supra-additive class especially when combined with alcohol
29. Are benzos dependent or independent of GABA?
30. Do benzos have a large or small margin of safety?
a. Large, because they have a ceiling effect
31. What would be the benzo of choice for insomnia?
32. What benzo would be used for status epilepticus patients?
33. What drugs will be given to a patient that is having withdrawal from alcohol and/or barbiturates?
34. What are some of the side effects to be aware of for benzos?
a. CNS depression: dizzy, drowsy, sedation
b. Paradoxical excitement: dis-inhibition of suppressed behavior
d. Sleep related behavior: sleep driving, eating, walking
35. What are the contraindications for benzodiazepine use?
a. Do not give during pregnancy
i. Unless absolutely necessary: category D
b. Sleep apnea
36. What are the DOC for insomnia?
c. Think ZZZZZ for sleep
37. What drug resets the sleep wake cycle and acts as a melatonin analogue?
38. What drug can be given to treat anxiety but not produce sedating symptoms?
i. Partial agonist for postsynaptic 5-HT1A receptor (serotonin receptor)
ii. Full agonist for presynaptic 5-HT1A receptor
Lecture 2 Anticonvulsants
39. What kind of seizures fall under partial seizures?
a. Simple: focal, brief 20-90 seconds, no loss of consciousness
b. Complex: longer <2 min, altered or loss of consciousness, hallucinations
c. Partial with secondary generalized tonic-clonic: loss of consciousness
40. What seizures are considered generalized?
a. Absence: sudden, 10-30s, loss of awareness
b. Tonic clonic: tonic rigidity (15-30s), clonic jerking (60-120s), loss of consciousness
c. Myoclonic: brief spasm or rigidity
d. Atonic: sudden loss of postural tone, fall
41. What is the mechanism of action for most anticonvulsant drugs via GABA?
a. Inhibit GABA metabolism
b. Stimulate GABA receptors
c. Binds synaptic vesicular protein, SV2A
42. What is the anticonvulsant mechanism in regard to glutamate?
a. Decrease activation of glutamate receptors (NMDA)
b. Common targets: voltage gates Na+ and Ca++ channels
c. SV2A, K+ channels, NMDA and AMPA receptors can be other targets
43. What is the most likely anticonvulsant drug to cause stevens-johnson syndrome?
44. You are treating a patient for generalized tonic clonic seizures with a drug that prolongs the inactivation of a Na+ channel. The patient comes back with complaints of
What drug are they likely on?
45. You are treating a patient with the DOC for
but will also help with their
Another doctor wants to put the patient on phenytoin or phenobarbital as well, but you know that this will increase the metabolism of your drug. What drug did you originally put them on?
46. What is the mechanism of action for phenobarbital?
a. Prolongs opening of Cl channel at GABA receptor
47. What drug is used as an adjunct for partial and generalized tonic clonic seizures, and can also be used for neuropathic pain?
b. Remember this is also excreted by the kidney
48. What is the mechanism of action and the seizure for use of lamotrigine?
a. Inactivation of Na+ channel, decrease glutamate activity
b. Used for partial seizures
49. What drug can be used for migraine prevention but has side effects that include acute myopia/ glaucoma?
50. What drug binds SV2A and appears to decrease glutamate and increase GABA release?
51. What is the DOC for absence seizures?
b. This is the drug that has hiccups as a side effect
52. What is the mechanism of action for valproic acid?
a. Blocks Ca2+ channels and Na+ channels
b. This is hepatotoxic
53. Benzodiazepines such as diazepam and lorazepam are the DOC for what seizure?
a. Status epilepticus
Lecture 3 Local anesthetics
54. How do esters differ from amides in regard to duration of action and systemic toxicity?
a. Esters have shorter duration of action
b. Esters have increased systemic toxicity
55. What anesthetic drug has a pKa of 3.5 and therefore will always be in the non-ionized form in the body?
56. Absorption of a drug is affected by what factors?
b. Site of injection
c. Drug-tissue bonding
d. Chemical properties of the drug
e. Local blood flow
f. Vasoconstricting agents
57. How are amide drugs metabolized?
a. By the liver, CYP450
58. How are esters metabolized?
a. Rapidly by butyrylcholinesterase in the plasma
59. What is the order of sensitivity to anesthetic drugs?
a. Sympathetic > sensory > touch > motor
60. What anesthetic drugs are likely to have cardio side effects?
a. Bupivacaine: more potent sensory blocker than motor blocker
61. An allergic reaction to anesthetics is more likely with an ester or an amide?
a. Ester because of PABA metabolite
62. What anesthetic would we use for diagnostic testing due to its short duration of action?
63. What ester type drug would we use if we wanted a longer duration of action and is 16X more potent than procaine?
64. How is benzocaine given?
a. Topical only
65. What drug is least preferred for spinal blocks due to its risk of TNS?
66. What amide anesthetic is largely limited to the dental field but has a risk of causing methemoglobinemia?
67. What is the preferred drug as an epidural during labor and childbirth?
68. What drug is used in peripheral and epidural blocks, it also has vasoconstricting effects at clinical doses?
69. What is mepivacaine not preferred in and what type of anesthetic is it?
a. Not used in labor or topically
b. Amide type drug
70. What drug may cause motor block but nor sensory block?
71. What is the amide type anesthetic drug that also has an ester group, allowing it to be metabolized in the plasma and have a decreased systemic toxicity?
Lecture 4 Antidepressants
72. What is the biogenic amine hypothesis of depression?
a. Abnormal neurotransmission of dopamine, norepinephrine, and serotonin
73. What are the antidepressant targets when treating for TCAs, SSRIs, SNRIs, DA reuptake and MAOIs?
a. TCAs: inhibit reuptake of NE and 5-HT, also block other things, very dirty drug
b. SSRIs: selective inhibition of 5-HT reuptake
c. SNRIs: inhibit the reuptake of NE and 5-HT
d. MAOIs: inhibit metabolism of NE, DA, 5-HT, binds irreversibly
74. Compare amitriptyline to nortriptyline.
a. Amitriptyline: tertiary amine, inhibits 5-HT reuptake
b. Nortriptyline: secondary amine, inhibit NE reuptake
75. What antidepressant classes can be used during pregnancy?
76. What is a major side effect that is associated with TCA toxicity?
a. Torsades de pointes
77. What are the SSRI drugs?
78. What SSRI would be used in a patient with obsessive-compulsive disorder?
79. What SSRI is most likely to inhibit CYP450 enzymes and lead to sexual dysfunction?
80. What SSRI is preferred in elderly patients?
81. What is the DOC for depression?
82. What effect should we be aware of when patients add St. John's Wort when they are of SSRIs?
a. Serotonin syndrome
83. What effect does fluoxetine have on opioids?
a. Inhibits the conversion to the active compound
84. Why might a MAOI that selectively inhibits MAO-B be more beneficial for a patient than one that inhibits MAO-A?
a. MAO-B selectively metabolizes DA and tyramine in the CNS but not he GI tract
85. What MAOI is most likely to cause hypertensive crisis?
i. This is the drug of last choice, it interacts with MAO-A and B
86. What MAOI is selective for MAO-B and has fewer side effects?
87. What antidepressant is least likely to cause sexual dysfunction?
88. What antidepressant blocks presynaptic alpha 2 receptors and is the preferred drug in patients with depression and insomnia/anxiety?
Lecture 5 Antipsychotics and moor stabilizers
89. What re the positive and negative symptoms of schizophrenia?
a. Positive: hallucinations and delusions, disorganized speech and thinking, due to over-active dopamine pathway in limbic system (mesolimbic)
b. Negative: apathetic, withdrawn, anti-social, depression, due to underactive dopamine pathway in frontal cortex (mesocortical)
90. What dopamine pathway consists of the VTA to limbic system and has effect of euphoria, emotions, and reward?
91. What are the four dopamine pathways?
92. What dopamine pathway is in charge of prolactin release?
93. What is the mesocortical pathway in charge of?
a. Cognition and emotion
94. What is the nigrostriatal pathway control?
a. Movement and motor control
95. What antipsychotic drug has an antiemetic effect with it as well?
96. What antipsychotics are least likely to cause tardive dyskinesia?
97. What effect would we see drug interaction wise if we combined an antipsychotic with a sedative hypnotic?
a. Increased sedation
98. What is the mechanism of classical antipsychotics?
a. Block DA D2 receptors, have effect in mesolimbic region primarily
99. What drug may cause retinal deposits and browning of the vision? This drug also has the potential for EPS, TD, and neuroleptic malignant syndrome.
100. What is the DOC for acute psychosis situations?
101. what classical drug is most likely to give Parkinson like syndrome?
102. What is the mechanism of action for the atypical antipsychotics?
a. Blocks 5-HT2A receptors and DA D2/D4 receptors
b. This will treat both negative and positive symptoms
103. What atypical is most likely to cause agranulocytosis and makes it the drug of last choice?
b. This also has a side effect of hypersalivation
104. What drug is like clozapine but does not have agranulocytosis? This drug can cause hyperglycemia and type II diabetes.
105. What antipsychotic can quite the patient due to its very sedating effects, making it good for insomniacs?
106. What is the DOC for psychosis?
b. This drug has no significant effect on DA neurotransmission in nigrostriatal pathway
107. What antipsychotic is a partial agonist for D2, 5-HT1 and a antagonist for 5-HT2A, but doesn't have an increase in prolactin?
108. What is the DOC for bipolar disorder?
109. If Na+ levels decreases, then what would happen to lithium absorption?
a. Increase and lead to toxicity
b. Lithium has a small therapeutic window
110. What would be a good option to replace lithium as long as the patient is not pregnant but may be having rapid cycling manic/depressive phases?
a. Valproic acid
b. Remember this drug was used in anticonvulsants too
111. Other than lithium what drug can be given to treat refractory bipolar disorder but has a high chance of causing SJS?
Lecture 6 opioids and antagonists
112. What effects do you see when activating the Mu receptor for opioids?
d. Other side effects like inhibition of cough
e. This receptor opens K+ channels hyperpolarizing and inhibiting signal
113. What opioid can suppress cough but is not an analgesic?
114. What opioid is an analgesic but cannot suppress cough?
115. What would we not want to give an opioid to a patient who has BPH?
a. Because a side effect of opioids is urinary retention, and this is made worse with BPH
116. What effects of opioids do not develop a tolerance?
117. If a patient is going through opioid withdrawal symptoms what can be given to reduce these?
118. If someone overdoses on opioids what drug are you going to give them and what else will you do?
a. Give opioid antagonist: naloxone
b. Support respirations
119. What opioid is primarily used in surgery due to its short duration of action?
120. What strong agonist opioid can cause seizures if given for more than 48 hours?
121. For chronic pain patients what long acting strong opioid would they be on?
122. What drug is commonly given with acetaminophen and therefore you have to warn your patient about acetaminophen toxicity when using other drugs?
a. Hydrocodone or oxycodone
123. Would the dose needed for codeine to act as a cough suppressant need to be higher or lower than the dose for analgesia?
124. What may happen if tramadol is combined with antidepressants, and what would happen with MAOIs, TCAs, SSRIs?
a. Antidepressants: may produce seizures
b. MAOIs, TCAs, SSRIs: serotonin syndrome
125. What opioid is commonly abused by teenagers due to the blockage of NMDA receptors?
126. What are the opioid antagonist drugs?
a. Naloxone: injected
b. Naltrexone: oral
Lecture 7-8 Analgesic, NSAIDs
127. What is the mechanism of action for acetylsalicylic acid, aspirin?
a. Nonselective, irreversible inhibitor of COX-1 and COX-2
128. Which COX enzyme is inducible?
129. What is the distribution of ASA?
a. Throughout the body tissues and extracellular compartments
b. Readily crosses placental barrier
c. Slowly crosses BBB
d. Binds to plasma binding proteins
130. Patient scenario: 60 yr. female, being treated with warfarin for her heart. She sprains her ankle and takes a drug for the pain. 2-3 days later she starts bleeding and is unable to clot, why is this and what drug did she take?
a. She took aspirin and it competed with the plasma binding protein with warfarin, not there is more free warfarin in the blood causing increased bleeding, and ASA has antiplatelet effects
131. ASA, NSAIDs, and acetaminophen all have the same general effects on the body, what one also has antiplatelet effects?
a. ASA, aspirin
132. What respiratory adverse effects do we see with ASA overdose?
a. Respiratory alkalosis, then metabolic and respiratory acidosis
133. How long can the antiplatelet effects of ASA last?
a. 8-10 days
b. This is why you need to stop ASA therapy 1 week before surgery
134. What effect does low level aspirin therapy have on uric acid excretion?
a. Decreases uric acid excretion and elevates plasma levels
b. Remember this for gout section, you will not treat with ASA
135. What effects happen in the lungs with ASA treatment?
a. Aspirin asthma
136. What effect does aspirin have on pregnancy?
a. It is not teratogenic
137. What is our DOC for children with Reye's syndrome?
138. What is the mechanism of action for celecoxib?
a. Selective reversible COX-2 inhibitor
139. What adverse reaction should you watch out for with celecoxib?
a. Increased risk for cardiovascular disease
140. What is our first choice NSAID because of the low incidence of side effects?
141. What drug inhibits phospholipase A and reduces PMN migration?
142. What drug is most likely to be given post-surgical for pain and can be combined with opiates?
143. What drug is a potent COX inhibitor and decreases arachidonic acid bioavailability and is often combined with misoprostol to decrease GI side effects?
144. What NSAID has a mean plasma half-life of 13 hours and is excreted in the urine, it also has strong binding to plasma binding proteins?
145. What drug is often preferred to aspirin because it is tolerated better, it has no anti-inflammatory effects or COX inhibition?
146. An overdose is this drug can cause fatal hepatic necrosis.
147. What is the treatment for acetaminophen overdose?
Lecture 9.1 Gout
148. What drugs would we use for acute management of gout?
a. NSAIDS except ASA and salicylates
149. What drugs would be used for chronic prevention of gout?
a. Uricosuric agents: probenecid
b. Xanthine oxidase inhibitor: allopurinol, febuxostat
c. Enzyme converting uric acid to allantoin: rasburicase and pegloticase
150. What is the primary NSAID used in gout?
151. If a patient with gout has a history of PUD but it is not active what can be given to them?
152. If a patient with gout has a history of PUD but it is active what can be given to them?
a. Acetaminophen and or opioids
153. What is the mechanism of action for colchicine?
a. Binds to tubulin and inhibits microtubule formation
b. This inhibits leukocyte migration and phagocytosis
c. Reduces pain and inflammation of acute attack
154. What are the adverse effects seen with colchicine?
b. Nausea, vomiting
c. Abdominal pain
155. What is the mechanism of action for the uricosuric agents?
a. Blocking the active reabsorption of uric acid
b. Be on the lookout for kidney stone formation
156. Why would we want to do colchicine prophylaxis before we start a patient on allopurinol or febuxostat?
a. These drugs can provoke acute gouty attack when initiated so the prophylaxis will inhibit this.
157. What is the enzyme converting uric acid to allantoin agent that can only be given once to the patient because it can lead to anaphylactic shock if given again?
a. Rasburicase: this is non-endogenous to humans
158. What is the mammalian urate oxidase enzyme?
Lecture 9.2 Migraine
159. What phase of migraines can you get aura symptoms?
a. First: vasoconstrictive
160. What is our DOC for migraine treatment?
161. What are the contraindication for treating with sumatriptan?
a. Breast feeding
b. Cardiac disease
c. Cerebrovascular disease
d. Coronary artery disease
e. Diabetes mellitus
g. Peripheral vascular disease
j. Renal impairment
162. Other than sumatriptan what is another drug that acts on 5-HT receptors with less specificity and is only effective in 50% of the patients?
163. What drugs are used for migraine prophylaxis?
a. Beta blockers: propranolol
b. CCB: verapamil
c. Antidepressants: amitriptyline, fluoxetine
e. Valproic acid
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