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142 Cards in this Set

  • Front
  • Back
Selectively suppress FSH and LH secretion and depresses ovarian function

A. Combination contraceptives
B. Progestin-only contraceptives
A. Combination contraceptives
Causes a thickening of the cervical mucus and prevents sperm penetration. Also causes endometrial alterations that impair implantation.

A. Combination contraceptives
B. Progestin-only contraceptives
B. Progestin-only contraceptives
Describe monophasic oral contraceptive pills
- Only one (constant) dose of estrogen/progesin throughout entire pill cycle
Describe multiphasic oral contraceptive pills
- Constant dose of estrogen
- Increasing doses of progestin throughout cycle
What are the 2 possible estrogenic components of combination oral contraceptive
(OCP) pills?

A. ethinyl estradiol
B. conjugated estrogens - premarin
C. mestranol
D. diethylstilbestrol
A. ethinyl estradiol
C. mestranol
Which of the following is/are contraindications for oral contraceptives?
(select all)

A. diabetes
B. liver disorder
C. clotting disorder
D. over 35 y/o
E. smoker
A. diabetes
B. liver disorder
C. clotting disorder
D. over 35 y/o
E. smoker

(over 35 y/o AND smoker causes increased risk for MI & stroke)
Risk of venous thromboembolism may be related to increased
(select all)

A. estrogen
B. LH
C. FSH
D. progestin
A. estrogen
T/F

Oral contraceptives can reduce the risk of breast cancer
False

(Reduce risk of ENDOMETIRAL & OVARIAN cancer)
What is the mechanism of action of the pro-fertility drug CLOMIPHENE?

A. partial estrogen antagonist to interfere with negative feedback of LH/FSH = LH surge = ovulation
B. synthetic GnRH, which stimulates LH/FSH release (short-acting)
C. derived from urine of postmenopausal wome, which mainly has FSH activity
D. derived from urine of pregnant women, and has pro-LH activity
A. partial estrogen antagonist to interfere with negative feedback of LH/FSH = LH surge = ovulation
What is the mechanism of action of the pro-fertility drug GONADORLIN?

A. partial estrogen antagonist to interfere with negative feedback of LH/FSH = LH surge = ovulation
B. synthetic GnRH, which stimulates LH/FSH release (short-acting)
C. derived from urine of postmenopausal wome, which mainly has FSH activity
D. derived from urine of pregnant women, and has pro-LH activity
B. synthetic GnRH, which stimulates LH/FSH release (short-acting)
What is the mechanism of action of the pro-fertility drug MENOTROPIN (Pergonel)?

A. partial estrogen antagonist to interfere with negative feedback of LH/FSH = LH surge = ovulation
B. synthetic GnRH, which stimulates LH/FSH release (short-acting)
C. derived from urine of postmenopausal women, which mainly has FSH activity
D. derived from urine of pregnant women, and has pro-LH activity
C. derived from urine of postmenopausal women, which mainly has FSH activity
What is the mechanism of action of the pro-fertility drug hCG (Pregnyl)?

A. partial estrogen antagonist to interfere with negative feedback of LH/FSH = LH surge = ovulation
B. synthetic GnRH, which stimulates LH/FSH release (short-acting)
C. derived from urine of postmenopausal women, which mainly has FSH activity
D. derived from urine of pregnant women, and has pro-LH activity
D. derived from urine of pregnant women, and has pro-LH activity
___ in blood penetrates into the subendothelium and becomes oxidized. Oxidized ___ causes transendothelial migration of monocytes/macrophages which in turn ingest oxidized ___ to form foam cells in fatty streaks. Further proliferation of smooth muscle cells & deposition of extracellular matrix results in atherosclerotic plaque formation.

A. HDL
B. LDL
C. triglycerides
E. carbohydrates
B. LDL
Which pathway of cholesterol and triglyceride (TG) regulation is described?
- Chylomicrons (CM) degraded by lipoprotein lipase
- Uptake of TG by adipose tissue and muscle
- Transport of CM remnants to liver

A. exogenous pathway
B. endogenous pathway
C. reverse transport of cholesterol
D. de novo cholesterol synthesis
E. enterohepatic circulation
A. exogenous pathway
Which pathway of cholesterol and triglyceride (TG) regulation is described?
- Liver synthesize and secrete VLDL
- VLDL is degraded by lipoprotein lipase to form IDL and LDL
- Uptake of IDL and LDL by LDL receptor-mediated endocytosis

A. exogenous pathway
B. endogenous pathway
C. reverse transport of cholesterol
D. de novo cholesterol synthesis
E. enterohepatic circulation
B. endogenous pathway
Which pathway of cholesterol and triglyceride (TG) regulation is described?
- As cells die, cholesterol is released and trapped in HDL.
- Cholesterol in HDL is esterified by LCAT and transferred to VLDL
- VLDL is then metabolized to IDL and LDL and taken up by the liver

A. exogenous pathway
B. endogenous pathway
C. reverse transport of cholesterol
D. de novo cholesterol synthesis
E. enterohepatic circulation
C. reverse transport of cholesterol
Which pathway of cholesterol and triglyceride (TG) regulation is described?
- Bile salt is synthesized by the liver
- Bile is then released into the intestine and recycled

A. exogenous pathway
B. endogenous pathway
C. reverse transport of cholesterol
D. de novo cholesterol synthesis
E. enterohepatic circulation
E. enterohepatic circulation
Which pathway of cholesterol and triglyceride (TG) regulation is described?
- Liver is the major site of cholesterol synthesis
- HMG-CoA reductase is the rate limiting enzyme

A. exogenous pathway
B. endogenous pathway
C. reverse transport of cholesterol
D. de novo cholesterol synthesis
E. enterohepatic circulation
D. de novo cholesterol synthesis
Which of the following anti-atherogenic drugs acts as a VLDL secretion inhibitor?

A. resins
B. statins
C. niacin
D. fibrates
E. probucol
C. niacin
What is the mechanism of action of NIACIN?

A. inhibits lipase involved in lipolysis in adipose tissue = ↓ free fatty acid available for TG synthesis = ↓ production/release of VLDL
B. negatively bind bile salts = ↑ cholesterol conversion to bile acid
C. HMG-CoA reductase inhibitors = cells express more LDL receptors = decreased cholesterol
D. stimulate lipoprotein lipase = increased VLDL clearance
E. inhibits oxidation of LDL & prevents ingestion by macrophage foam cells
A. inhibits lipase involved in lipolysis in adipose tissue = ↓ free fatty acid available for TG synthesis = ↓ production/release of VLDL
What is the mechanism of action of RESINS?

A. inhibits lipase involved in lipolysis in adipose tissue = ↓ free fatty acid available for TG synthesis = ↓ production/release of VLDL
B. negatively bind bile salts = ↑ cholesterol conversion to bile acid
C. HMG-CoA reductase inhibitors = cells express more LDL receptors = decreased cholesterol
D. stimulate lipoprotein lipase = increased VLDL clearance
E. inhibits oxidation of LDL & prevents ingestion by macrophage foam cells
B. negatively bind bile salts = ↑ cholesterol conversion to bile acid
What is the mechanism of action of STATINS?

A. inhibits lipase involved in lipolysis in adipose tissue = ↓ free fatty acid available for TG synthesis = ↓ production/release of VLDL
B. negatively bind bile salts = ↑ cholesterol conversion to bile acid
C. HMG-CoA reductase inhibitors = cells express more LDL receptors = decreased cholesterol
D. stimulate lipoprotein lipase = increased VLDL clearance
E. inhibits oxidation of LDL & prevents ingestion by macrophage foam cells
C. HMG-CoA reductase inhibitors = cells express more LDL receptors = decreased cholesterol
What is the mechanism of action of FIBRATES?

A. inhibits lipase involved in lipolysis in adipose tissue = ↓ free fatty acid available for TG synthesis = ↓ production/release of VLDL
B. negatively bind bile salts = ↑ cholesterol conversion to bile acid
C. HMG-CoA reductase inhibitors = cells express more LDL receptors = decreased cholesterol
D. stimulate lipoprotein lipase = increased VLDL clearance
E. inhibits oxidation of LDL & prevents ingestion by macrophage foam cells
D. stimulate lipoprotein lipase = increased VLDL clearance
What is the mechanism of action of PROBUCOL?

A. inhibits lipase involved in lipolysis in adipose tissue = ↓ free fatty acid available for TG synthesis = ↓ production/release of VLDL
B. negatively bind bile salts = ↑ cholesterol conversion to bile acid
C. HMG-CoA reductase inhibitors = cells express more LDL receptors = decreased cholesterol
D. stimulate lipoprotein lipase = increased VLDL clearance
E. inhibits oxidation of LDL & prevents ingestion by macrophage foam cells
E. inhibits oxidation of LDL & prevents ingestion by macrophage foam cells
Which drug causes the largest decrease in LDL?

A. resins
B. statins
C. niacin
D. fibrates
E. probucol
B. statins
Which drug causes a decrease in HDL?

A. resins
B. statins
C. niacin
D. fibrates
E. probucol
E. probucol
Which drug causes the largest decrease in TG?

A. resins
B. statins
C. niacin
D. fibrates
E. probucol
D. fibrates
Which of the following drugs causes an increase in TG?

A. resins
B. statins
C. niacin
D. fibrates
E. probucol
A. resins
Which of the following antidepressant drugs acts by: blocking reuptake pumps for 5HT & NE and are negative allosteric modulators of NT uptake

A. tricyclics
B. SSRI’s
C. SNRI’s
D. MAOI’s
A. tricyclics

(block α₁, HI, and M1 receptors, and Na⁺ channels)
Which of the following antidepressant drugs acts by: inhibiting 5HT reuptake without blocking α₁, H1, M1, or Na⁺ pumps

A. tricyclics
B. SSRI’s
C. SNRI’s
D. MAOI’s
B. SSRI’s
(Selective Serotonin Reuptake Inhibitors)
Which of the following antidepressant drugs acts by: selective 5HT & NE uptake blocker without blocking α₁, HI, or M1 receptors.

A. tricyclics
B. SSRI’s
C. SNRI’s
D. MAOI’s
C. SNRI’s
(Serotonin/Norepinephrine Reuptake Inhibitors)
Which of the following antidepressant drugs acts by inhibiting enzymes which metabolize 5HT and NE

A. tricyclics
B. SSRI’s
C. SNRI’s
D. MAOI’s
D. MAOI’s
(Monoamine Oxidase Inhibitors)
Which of the following are side effects of TRICYCLIC antidepressants?
(select all)

A. weight gain
B. drowsiness
C. dry mouth
D. sexual dysfunction
E. blurred vision
F. dizziness
G. increased blood pressure
H. insomnia
A. weigth gain
B. drowsiness
C. dry mouth
E. blurred vision
F. dizziness
Which of the following are side effects of SSRI antidepressants?
(select all)

A. weight gain
B. drowsiness
C. dry mouth
D. sexual dysfunction
E. blurred vision
F. dizziness
G. increased blood pressure
H. insomnia
D. sexual dysfunction
What makes mechanisms of action of LITHIUM unique from other antidepressants?
Act intracellularly, instead of at receptors

(block inositol phosphatase to ↓ inositol)
What are the mechanisms of action of ANTICONVULSANTS?
- ↑ GABA
- ↓ Ca²⁺
- ↓ Na⁺
- ↓ glutamate release
GABA is the major ____ NT in the CNS

A. stimulatory
B. inhibitory
B. inhibitory
Most drugs bind to GABA-A receptor to ____ ability of GABA to bind, which triggers Cl⁻ channels to ____, and causes a ____ in Cl⁻ conductance. This causes a small hyperpolarization to _____ formation of an AP. This leads to sedation.

- increase
- decrease

- opening
- closing

- increase
- decrease

- stimulate
- inhibit
- increase (GABA binding)
- open (Cl⁻ channels)
- increase (Cl⁻ conductance)
- inhibit (AP formation)
What are the effects of benzodiazepines (BZDs) on the following:

- Stage 1 sleep
- Stage 2 sleep
- Stage 3 sleep
- Stage 4 sleep
- REM sleep
- Stage 1 sleep = ↓
- Stage 2 sleep = ↑
- Stage 3 sleep = ↓
- Stage 4 sleep = ↓
- REM sleep = ↓ amount & ↑ latency
What are the major BZP sedatives/hypnotics?

A. triazolam
B. diazepam
C. oxazepam
D. temazepam
E. alprazolam
F. flurazepam
G. lorazepam
A. triazolam
D. temazepam
F. flurazepam
T/F

Non-BZP sedatives/hypnotics are GABA-B receptor allosteric modulators
False

(GABA-A receptor allosteric modulators)
(act at same site as BZP, just different structure)
The major side effects of Zopiclon are:
(select all)

A. dry mouth
B. amnesia
C. drowsiness
D. dizziness
A. dry mouth
C. drowsiness
D. dizziness

(Zopiclon = cyclopyrrolone = Non-BZD)
The major side effects of Zolpidem are:
(select all)

A. dry mouth
B. amnesia
C. drowsiness
D. dizziness
B. amnesia
C. drowsiness
D. dizziness

(zolpidem = imadazopyridine = Non-BZD)
Alcohol:
(select all)

A. disrupts normal sleep cycle
B. ↑ stage 3/4 sleep
C. ↓ stage 1 sleep
D. withdrawal causes insomnia & REM rebound
A. disrupts normal sleep cycle
D. withdrawal causes insomnia & REM rebound

(↑ stage 1)
(↓ stage 3/4)
What are the effects of cyclopyrrolones (zopiclon) on the following:

- sleep latency
- total sleep time
- REM rebound (yes/no)
- sleep latency = ↓
- total sleep time = ↑
- REM rebound = no
What are the effects of imadazopyridines (zolpidem) on the following:

- sleep latency
- total sleep time
- REM rebound (yes/no)
- sleep latency = ↓
- total sleep time = ↑
- REM rebound = no
1st generation antipsychotics block/antagonize:
(select all)

A. D2 receptors
B. 5HT-2A receptors
A. D2 receptors
2nd generation antipsychotics block/antagonize:
(select all)

A. D2 receptors
B. 5HT-2A receptors
A. D2 receptors
B. 5HT receptors

(antagonizing 5HT allows greater release of Dopamine)
Antagonism of 5HT causes ____ release of dopamine

A. increased
B. decreased
A. increased
Increased DA in the mesolimbic pathway is associated with positive symptoms. 2nd generation antipsychotics therefore:

A. reduce positive symptoms
B. increase positive symptoms
C. increase negative symptoms
A. reduce positive symptoms

- more D2 receptors blocked than 5HT receptors in mesolimbic pathway
Decreased DA in the mesocortical pathway is associated with negative symptoms. 2nd generation antipsychotics therefore:

A. reduce negative symptoms
B. increase positive symptoms
C. increase negative symptoms
A. reduce negative symptoms

- more 5HT receptors blocked in mesocortical pathway
- ↑ DA
Decreased DA in the nigrostriatal pathway is associated with movement disorders & tardive dyskinesia. 2nd generation antipsychotics therefore:

A. reduce EPS
B. increase EPS
C. increase negative symptoms
A. reduce EPS

- blockage of 5HT receptors
- ↑ DA
In the nigrostriatal pathway, DA blocks release of prolactin, and 5HT causes release of prolactin. 2nd generation antipsychotics therefore:

A. reduce prolactin
B. increase prolactin
C. no change on prolactin
C. no change on prolactin

- block D2 receptors = prolactin release
- block 5HT receptors = blocks prolactin release
- cancels out action of each
What are common side effects of 1st generation antipsychotics?
(select all)

A. dry mouth
B. agranulocytosis
C. drowsiness
D. weight gain
E. increased positive symptoms
F. blurred vision
G. increased prolactin
A. dry mouth
C. drowsiness
D. weight gain
F. blurred vision
The amount of gas disolved in a fluid

A. partial pressure
B. Minimum Alveolar Concentration (MAC)
C. Blood/Gas Partition coefficient
D. Oil/Gas Partition coefficient
A. partial pressure
The alveolar concentration of an anesthetic that prevents movement in 50% of patients in response to a noxious stimulus

A. partial pressure
B. Minimum Alveolar Concentration (MAC)
C. Blood/Gas Partition coefficient
D. Oil/Gas Partition coefficient
B. Minimum Alveolar Concentration (MAC)
The amount of anesthetic in the blood divided by the amount of anesthetic in the gas phase, after an anesthetic is allowed to equilibrate b/t equal volumes of gas & blood

A. partial pressure
B. Minimum Alveolar Concentration (MAC)
C. Blood/Gas Partition coefficient
D. Oil/Gas Partition coefficient
C. Blood/Gas Partition coefficient
The amount of anesthetic in oil divided by its concentration in gas, at equilibrium


A. partial pressure
B. Minimum Alveolar Concentration (MAC)
C. Blood/Gas Partition coefficient
D. Oil/Gas Partition coefficient
D. Oil/Gas Partition coefficient
A measure of the potency of an anesthetic
(select all)

A. partial pressure
B. Minimum Alveolar Concentration (MAC)
C. Blood/Gas Partition coefficient
D. Oil/Gas Partition coefficient
B. MAC
D. Oil/Gas Partition coefficient

(↓ MAC = ↑ potency = ↑ oil/gas partition
A low MAC =

A. more lipophilic
B. less lipophilic
A. more lipophilic

(low MAC = more potent)
(less gas required to enter blood = easier to enter cell)
Indicates blood solubility:

A. partial pressure
B. Minimum Alveolar Concentration (MAC)
C. Blood/Gas Partition coefficient
D. Oil/Gas Partition coefficient
C. Blood/Gas Partition coefficient

(high value = low equilibration rate)
(no relation to potency)
Oil/Gas Partition coefficient directly correlates with:
(select all)

A. partial pressure
B. potency
C. solubility
D. MAC
E. equilibration rate
B. potency


(inversely with MAC)
(↓ MAC = ↑ potency = ↑ oil/gas partition)
What are the 4 potential targets for the action of general anesthetics?
1) lipid bilayer
2) lipids at protein/lipid interface
3) protein site bounded by lipid
4) protein site exposed to aqueous environment (most likely)

OR

1) GABA-A receptor
2) K⁺ channel
3) Glycine
4) NMDA (block release of glutamate)
Blood/Gas Partition coefficient is _____ related to rate of anesthetic induction

A. directly
B. inversely
B. inversely

(low blood/gas partition coefficient = more rapid equilibration)
(prefer to stay as gas & get transported rather than be absorbed)
Cardiac output is _____ related to rate of anesthetic induction

A. directly
B. inversely
B. inversely

(breathe in same amount)
(↑ CO = expose anesthetic to more blood)
(equilibrates slowly)
Ventilation is _____ related to rate of anesthetic induction

A. directly
B. inversely
A. directly

(More anesthetic breathed in)
(more taken up by blood)
(increases equilibration rate)
T/F

The driving force for equilibration of inhaled anesthetics is blood concentration
False

(driving force = PARTIAL PRESSURE GRADIENT)
The more soluble an anesthetic is, the ____ rapid it will become ELIMINATED

A. more
B. less
B. less

(solubility = blood/gas partition coefficient)
(more soluble = wants to stay in tissues longer)
The more soluble an anesthetic is, the ____ rapid it will become INDUCED

A. more
B. less
B. less

(solubility = blood/gas partition coefficient)
(more soluble = wants to stay in tissues before reaching brain)
Increasing ventilation causes ____ rapid ELIMINATION of an anesthetic

A. more
B. less
A. more

(↑ ventilation = ↓ conc. in lung = moves from blood to lung = exhaled)
Increasing CO causes ____ rapid ELIMINATION of an anesthetic

A. more
B. less
B. less

(↑ CO = breathe same amount = less diffused out of blood)
What are the common pharmacological effects of inhaled anesthetics on the following:

- blood pressure
- respiratory rate
- tidal volume
- cerebral blood flow
- renal blood flow, GFR, urinary output
- hepatic blood flow
- Malignant hyperthermia
- blood pressure = ↓ (not N₂O)
- respiratory rate = ↑
- tidal volume = ↓
- cerebral blood flow = ↑
- renal blood flow, GFR, urinary output = ↓
- hepatic blood flow = ↓
- Malignant hyperthermia = (not N₂O)
Which inhaled anesthetic is MOST POTENT?

A. nitrous oxide
B. halothane
C. isolurane
D. sevoflurane
E. desofurane
B. halothane
Which inhaled anesthetic is LEAST POTENT?

A. nitrous oxide
B. halothane
C. isolurane
D. sevoflurane
E. desofurane
A. nitrous oxide
Which inhaled anesthetic has the FASTEST INDUCTION/RECOVERY RATE?

A. nitrous oxide
B. halothane
C. isolurane
D. sevoflurane
E. desofurane
A. nitrous oxide

(less soluble, stays in blood, gets to brain faster...and leaves brain faster)
Which inhaled anesthetic has the SLOWEST INDUCTION/RECOVERY RATE?

A. nitrous oxide
B. halothane
C. isolurane
D. sevoflurane
E. desofurane
B. halothane

(it is the most soluble = stays in tissues longer)
Which inhaled anesthetic is the MOST SOLUBLE?

A. nitrous oxide
B. halothane
C. isolurane
D. sevoflurane
E. desofurane
B. halothane
Which inhaled anesthetic is the LEAST SOLUBLE?

A. nitrous oxide
B. halothane
C. isolurane
D. sevoflurane
E. desofurane
A. nitrous oxide
Which inhaled anesthetic provides the MOST ANALGESIA?

A. nitrous oxide
B. halothane
C. isolurane
D. sevoflurane
E. desofurane
A. nitrous oxide
Which inhaled anesthetic provides the LEAST ANALGESIA?

A. nitrous oxide
B. halothane
C. isolurane
D. sevoflurane
E. desofurane
B. halothane
What are 2 major concerns with using halothane?
1. cardiac arrhythmia
2. halothane hepatitis
Benzodiazepines (as injectable anesthetics) are primarily used for:
(select all)

A. anti-anxiety
B. analgesia
C. inducing anesthesia for short procedures
D. inducing anesthesia for patients with cardiovascular problems
E. sedation/anesthesia for children
A. anti-anxiety
Opioids (as injectable anesthetics) are primarily used for:
(select all)

A. anti-anxiety
B. analgesia
C. inducing anesthesia for short procedures
D. inducing anesthesia for patients with cardiovascular problems
E. sedation/anesthesia for children
B. analgesia
Propofol (as injectable anesthetics) are primarily used for:
(select all)

A. anti-anxiety
B. analgesia
C. inducing anesthesia for short procedures
D. inducing anesthesia for patients with cardiovascular problems
E. sedation/anesthesia for children
C. inducing anesthesia for short procedures
Etomidate (as injectable anesthetic) is primarily used for:
(select all)

A. anti-anxiety
B. analgesia
C. inducing anesthesia for short procedures
D. inducing anesthesia for patients with cardiovascular problems
E. sedation/anesthesia for children
D. inducing anesthesia for patients with cardiovascular problems
Ketamine (as injectable anesthetics) are primarily used for:
(select all)

A. anti-anxiety
B. analgesia
C. inducing anesthesia for short procedures
D. inducing anesthesia for patients with cardiovascular problems
E. sedation/anesthesia for children
D. inducing anesthesia for patients with cardiovascular problems
E. sedation/anesthesia for children
What are the major ADVANTAGES of Benzodiazepines (as injectable anesthetics)?
(select all)

A. cardiovascular stimulant
B. profound analgesia
C. cause amnesia
D. anti-convulsant
E. cardiovascular stability
C. cause amnesia (anterograde amnesia)
D. anti-convulsant
What are the major ADVANTAGES of Opioids (as injectable anesthetics)?
(select all)

A. cardiovascular stimulant
B. profound analgesia
C. cause amnesia
D. anti-convulsant
E. cardiovascular stability
B. profound analgesia
E. cardiovascular stability
What are the major ADVANTAGES of Etomidate (as injectable anesthetics)?
(select all)

A. cardiovascular stimulant
B. profound analgesia
C. cause amnesia
D. anti-convulsant
E. cardiovascular stability
E. cardiovascular stability
What are the major ADVANTAGES of Ketamine (as injectable anesthetics)?
(select all)

A. cardiovascular stimulant
B. profound analgesia
C. cause amnesia
D. anti-convulsant
E. rapid onset
F. cardiovascular stability
G. short duration
H. anti-emetic
A. cardiovascular stimulant
B. profound analgesia
C. cause amnesia
What are the major DISADVANTAGES of Ketamine (as injectable anesthetics)?
(select all)

A. not analgesic
B. long acting
C. nausea
D. respiratory depression
E. decreased blood pressure
F. involuntary muscular movement
G. emergence reactions
H. pain on injection
G. emergence reactions

(not in children <15 or adults >65)
What are the major DISADVANTAGES of Etomidate (as injectable anesthetics)?
(select all)

A. not analgesic
B. long acting
C. nausea
D. respiratory depression
E. decreased blood pressure
F. involuntary muscular movement
G. emergence reactions
H. pain on injection
A. not analgesic
F. involuntary muscular movement
H. pain on injection
What are the major DISADVANTAGES of Propofol (as injectable anesthetics)?
(select all)

A. not analgesic
B. long acting
C. nausea
D. decreased blood pressure
E. involuntary muscular movement
F. emergence reactions
G. pain on injection
D. decreased blood pressure
E. involuntary muscular movement
G. pain on injection
What are the major DISADVANTAGES of Barbituates (as injectable anesthetics)?
(select all)

A. not analgesic
B. long acting
C. nausea
D. decreased blood pressure
E. involuntary muscular movement
F. emergence reactions
G. pain on injection
A. not analgesic
D. decreased blood pressure
What are the major DISADVANTAGES of Opioids (as injectable anesthetics)?
(select all)

A. not analgesic
B. long acting
C. nausea
D. decreased blood pressure
E. involuntary muscular movement
F. emergence reactions
G. pain on injection
C. nausea

(biggest disadvantage = respiratory depression)
What are the major DISADVANTAGES of Benzodiazepines (as injectable anesthetics)?
(select all)

A. not analgesic
B. long acting
C. nausea
D. decreased blood pressure
E. involuntary muscular movement
F. emergence reactions
G. pain on injection
A. not analgesic
B. long acting
T/F

Non-BZDs can cause anterograde amnesia
False

(BZDs can)
Anti-anxiety drugs mainly target:
(select all)

A. Dopamine
B. 5HT
C. GABA-A
D. Histamine
C. GABA-A

Dopamine = antipsychotics & antidepressants
GABA-A = antianxiety & anticonvulsants
Anti-psychotic drugs mainly target:
(select all)

A. Dopamine
B. 5HT
C. GABA-A
D. Histamine
A. Dopamine

(some also block 5HT, which controls dopamine)

Dopamine = antipsychotics & antidepressants
GABA-A = antianxiety & anticonvulsants
What is the mechanism of the post-coital contraceptive, MIFEPRISTONE?
Progesterone antagonist

forces shedding of uterine lining

(used with MISOPROSTOL)
Misoprostol is a ______ used with mifepristone

A. estrogen antagonist
B. progesterone antagonist
C. synthetic prostaglandin
D. synthetic GnRH agonist
C. synthetic prostaglandin
What are the possible causes of seizures?
(select all)

A. ↓ activity of voltage-gated ion channels
B. ↓ GABA activity
C. ↑ glutamate activity
D. alteration of intracellular ion concentration
B. ↓ GABA activity (↓ inhibitory neurotransmission)
C. ↑ glutamate activity (↑ excitatory neurotransmission)

(A. INCREASED activity of voltage-gated ion channels)
(D. alteration of EXTRAcellular ion concentration)
Antiseizure drugs work by affecting the following factors in which way?

- Na⁺ channels
- Ca²⁺ channels
- GABA transmission
- Glutamate transmission
- Na⁺ channels = prolong inactivation state
- Ca²⁺ channels = inhibit Ca²⁺ influx
- GABA = ↑ GABA transmission or ↓ metabolism
- Glutamate = ↓ glutamate transmission (block Na⁺ channels)
T/F

Anti-seizure drugs treat the symptoms AND the underlying cause
False

(treat symptoms, NOT the cause)
What are the drugs of choice for PARTIAL SEIZURES?
(select all)

A. ethosuximide
B. valproic acid
C. phenytoin
D. lorazepam
E. carbamazepine
F. diazepam
B. valproic acid
C. phenytoin
E. carbamazepine

(prolong Na⁺ channel inactivation state)
What are the drugs of choice for GRAND MAL SEIZURES (generalized tonic-clonic)
(select all)

A. ethosuximide
B. valproic acid
C. phenytoin
D. lorazepam
E. carbamazepine
F. diazepam
B. valproic acid
C. phenytoin
E. carbamazepine
What are the drugs of choice for PETIT MAL SEIZURES (absence)?
(select all)

A. ethosuximide
B. valproic acid
C. phenytoin
D. lorazepam
E. carbamazepine
F. diazepam
A. ethosuximide
What are the drugs of choice for MYOCLONIC SEIZURES?
(select all)

A. ethosuximide
B. valproic acid
C. phenytoin
D. lorazepam
E. carbamazepine
F. diazepam
B. valproic acid
What are the drugs of choice for STATUS EPILEPTICUS?
(select all)

A. ethosuximide
B. valproic acid
C. phenytoin
D. lorazepam
E. carbamazepine
F. diazepam
D. lorazepam
F. diazepam
What are the 3 major types of drug interactions seen with anti-seizure drugs?
1) induce hepatic drug-metabolizing enzymes
(↓ plasma conc. of other drugs)

2) Compete for same drug-metabolizing enzyme
(↑ plasma conc. of other drugs)

3) Displacement of drugs bound to plasma proteins
(↑ plasma conc. of other drugs)
Which of the following drugs work by prolonging Na⁺ channel inactivation state?

A. ethosuximide
B. valproic acid
C. phenytoin
D. phenobarbital
E. carbamazepine
F. diazepam
G. felbamate
H. clonazepam
I. primidone
J. lamotrigine
K. gabapentin
Optimal =
B. valproic acid
C. phenytoin
E. carbamazepine

Alternative =
G. felbamate
J. Lamotrigine
Which of the following drugs works by enhancing GABA transmission?

A. ethosuximide
B. valproic acid
C. phenytoin
D. phenobarbital
E. carbamazepine
F. diazepam
G. felbamate
H. clonazepam
I. primidone
J. lamotrigine
K. gabapentin
Optimal =
B. valproic acid (↓ metabolism)
F. diazepam (↑ Cl⁻ influx)

Alternative =
D. phenobarbital (↑ Cl⁻ influx)
G. felbamate
H. clonazepam
Which of the following drugs works by reducing Ca²⁺ transmission through Ca²⁺ channels?

A. ethosuximide
B. valproic acid
C. phenytoin
D. phenobarbital
E. carbamazepine
F. diazepam
G. felbamate
H. clonazepam
I. primidone
J. lamotrigine
K. gabapentin
A. ethosuximide
B. valproic acid
Which of the following drugs works by decreasing glutamate transmission?

A. ethosuximide
B. valproic acid
C. phenytoin
D. phenobarbital
E. carbamazepine
F. diazepam
G. felbamate
H. clonazepam
I. primidone
J. lamotrigine
K. gabapentin
Optimal =
B. valproic acid (block Na⁺ channel)
C. phenytoin (block Na⁺ channel)
E. carbamazepine (block Na⁺ channel)

Alternative =
G. felbamate (block Na⁺ channel & glutamate receptor)
J. lamotrigine (block Na⁺ channel)
K. gabapentin (blocks Ca²⁺ channel)
Which of the following opioids are STRONG agonists?
(select all)

A. codeine
B. morphine
C. naloxone
D. pentazocine
E. methadone
F. naltrexone
G. fentanyl
H. propoxyphene
I. meperidine
B. morphine
E. methadone
G. fentanyl
I. meperidine
Which of the following opioids are MODERATE agonists?
(select all)

A. codeine
B. morphine
C. naloxone
D. pentazocine
E. methadone
F. naltrexone
G. fentanyl
H. propoxyphene
I. meperidine
A. codeine
H. propoxyphene
Which of the following opioids are MIXED agonist/antagonists?
(select all)

A. codeine
B. morphine
C. naloxone
D. pentazocine
E. methadone
F. naltrexone
G. fentanyl
H. propoxyphene
I. meperidine
D. pentazocine
Which of the following opioids are ANTAGONISTS?
(select all)

A. codeine
B. morphine
C. naloxone
D. pentazocine
E. methadone
F. naltrexone
G. fentanyl
H. propoxyphene
I. meperidine
C. naloxone
F. naltrexone
Which of the following opioids are derived from precursor peptides by proteolytic cleavage of POMC?
(select all)

A. enkapalin
B. propoxyphene
C. morphine
D. endorphin
E. dynorphin
F. butorphanol
G. endomorphin
A. enkapalin
D. endorphin
E. dynorphin
G. endomorphin
All opioid receptors are G-protein coupled receptors. They decrease K⁺ efflux
(hypopolarization) and increase Ca²⁺ entry.

A. Both statements are true
B. Both statements are false
C. The first statement is true, the second statement is false
D. The first statement is false, the second statement is true
C. The first statement is true, the second statement is false


(cause an INCREASE in K⁺ efflux = HYPERpolarization)
(DECREASE Ca²⁺ entry)
Match the opioid receptor to it's site of expression:

- dorsal horn of spinal cord
- hypothalamus
- periaqueductal gray, nucleus of solitract, parabrachial nucleus...

A. Mu (m)
B. Kappa (k)
C. Delta (d)
- Mu (m) = periaqueductal gray, nucleus of solitract, parabrachial nucleus...

- Kappa (k) = hypothalamus

- Delta (d) = dorsal horn of spinal cord
What are two pharmacologic actions of opioids that are cause for concern?

A. sedation
B. respiratory depression
C. biliary tract spasm
D. ventricular arrhythmia
E. bronchoconstriction
F. miosis
B. respiratory depression
C. biliary tract spasm

(NO EFFECT ON HEART)
Which of the following are NOT pharmacologic actions of opioids on the CNS?
(select all)

A. respiratory depression
B. constipation
C. biliary tract spasm
D. increased heart rate
E. suppress cough reflex
F. miosis
D. increased heart rate

(NO EFFECT ON HEART)
Which of the following are CONTRAINDICATIONS for opioid use?
(select all)

A. low respiratory reserve
B. chronic pain
C. myocardial infarction
D. head injury
E. biliary colic
F.liver insufficiency
A. low respiratory reserve
D. head injury
E. biliary colic
F.liver insufficiency
Opioid tolerance develops to:

A. analgesia
B. euphoria
C. respiratory depression
D. sedation
E. miosis
F. constipation
G. lethal dose
H. nausea
A. analgesia
B. euphoria
D. sedation
G. lethal dose
H. nausea
Opioid tolerance DOES NOT develop to:

A. analgesia
B. euphoria
C. respiratory depression
D. sedation
E. miosis
F. constipation
G. lethal dose
H. nausea
C. respiratory depression (partial)
E. miosis
F. constipation
Withdrawal symptoms of long-term heroine use can be reduced by using:

A. morphine
B. methadone
C. codeine
D. naloxone
B. methadone
Which opioids have ANTITUSSIVE effects?
(select all)

A. codeine
B. fentanyl
C. sufentanil
D. dextromethorphan
A. codeine
D. dextromethorphan

(antitussive = cough suppressant)
Which opioids have ANESTHETIC effects?
(select all)

A. codeine
B. fentanyl
C. sufentanil
D. dextromethorphan
B. fentanyl
C. sufentanil
Coma and respiratory depression due to heroine overdose can be reversed by using:

A. morphine
B. methadone
C. codeine
D. naloxone
D. naloxone
Which opioid receptor antagonist has a longer duration of action?

A. naloxone
B. naltrexone
B. naltrexone
All of the following are pharmacological effects of STRONG opioid agonist drugs EXCEPT

(A) Activation of the chemoreceptor trigger zone
(B) Decreased intestinal peristalsis
(C) Decreased arterial pCO2
(D) Suppression of cough reflex
(E) Constriction of biliary tract smooth muscle
(C) Decreased arterial pCO2
Death from overdosage of strong opioid-analgesics usually results from

(A) Cardiac arrest
(B) Respiratory depression
(C) Seizures
(D) Shock
(E) Hypertensive crisis
(B) Respiratory depression
Which ONE of the following will prevent development of an absentinence syndrome in a herion user?

(A) Naloxone
(B) Propoxyphene
(C) Phenobarbital
(D) Acetyl salicyclic acid
(E) Methadone
(E) Methadone

(because methadone is long-acting)
All of the following statements concerning methadone are correct EXCEPT:

(A) It has less potent analgesic activity than that of morphine
(B) It has longer duration of action than that of morphine
(C) It is effective by oral administration
(D) It causes a milder withdrawal syndrome than morphine
(E) It has its greatest action on μ receptor
(A) It has less potent analgesic activity than that of morphine
Which of the following statements about pentazocine is INCORRECT?

(A) It is a mixed agonist-antagonist
(B) It may be administered orally or parenterally
(C) It produces less euphoria than morphine
(D) It is often combined with morphine for maximal analgesic effects
(E) High doses of pentazocine increase blood pressure
(D) It is often combined with morphine for maximal analgesic effects

(never mix 2 opioids)
Which of the following statements about morphine is INCORRECT?

(A) It is used therapeutically to relieve pain caused by severe head injury
(B) Its withdrawal symptoms can be relieved by methadone
(C) It causes constipation
(D) It is most effective by parenteral administration
(E) It rapidly enters all body tissues, including the fetus of a pregnant woman
(A) It is used therapeutically to relieve pain caused by severe head injury

(head injury = contraindication)
Morphine is used therapeutically

(A) To suppress the withdrawal syndrome associated with the chronic use of alcohol
(B) To induce miosis
(C) To treat severe constipation
(D) To relieve pain associated with heart attack
(D) To relieve pain associated with heart attack

(NO EFFECT ON HEART)
Match each of the descriptions below with the appropriate drug

(A) Codeine
(B) Naloxone
(C) Methadone
(D) Dextromethorphan

- Weak–to-moderate opioid agonist with a higher ratio of oral to parenteral activity than morphine
- Antitussive with no dependence liability
- Opioid-receptor anatgonist
- Strong opioid agonist that has a longer duration of action and produces less intense withdrawal syndrome than morphine
(A) Codeine = Weak–to-moderate opioid agonist with a higher ratio of oral to parenteral activity than morphine

(B) Naloxone = Opioid-receptor anatgonist

(C) Methadone = Strong opioid agonist that has a longer duration of action and produces less intense withdrawal syndrome than morphine

(D) Dextromethorphan = Antitussive with no dependence liability
Most clinically used opioid analgesics are selective for which type of opioid receptor?

A. kappa (κ)
B. alpha (α)
C. beta (β)
D. mu (μ)
E. delta (δ)
D. mu (μ)
Codeine has a greater oral bioavailability compared with morphine because of which reason?

A. codeine undergoes less first-pass metabolism
B. morphine is conjugated more quickly
C. morphine directly passes into systemic circulation
D. codeine is only available in liquid formulation
E. codeine is metabolized more by hepatic enzymes
A. codeine undergoes less first-pass metabolism
In the case of an opioid overdose, naloxone can be given in repeated doses because of which property of naloxone?

A. may have a shorter half-life than the opioid agonist
B. is only effective at high cumulative doses
C. is needed to stimulate the respiratory center
D. is safe only in extremely small doses
E. is only a partial opioid agonist
A. may have a shorter half-life than the opioid agonist