pharmacology GRM week #5 (brief)

Week 5-Chapter 12

1. Compare sedatives and hypnotics.
a. sedatives reduce nervousness, excitability, and irritability without causing sleep in small amounts. Hypnotics have a more potent effect on the CNS and cause sleep.

2. In terms for barbiturates, what is meant by a “low therapeutic index?”
a. there is only a narrow margin where the drug is effective and beyond that margin the drug is rapidly toxic

3. Since GABA is an inhibitory amino acid, what happens to the CNS when it is potentiated?
a. inhibit nerve impulse transmission

4. What does it mean to raise the convulsive or seizure threshold?
a. decreases the threshold a patient has to convulse or have a seizure

5. What do barbiturates do to the respiratory rate?
a. decrease repiratory rate

6. By stimulating the action of enzymes that are responsible for the metabolism of many drugs, how do barbiturates affect the duration of action of these other drugs?
a. shortens their duration time

7. What are the 4 indications of barbiturates?
a. ultra-short acting, short acting, intermediate acting, and long acting

8. Which bodily system is most affected by barbiturates?
a. the CNS

9. What is the most frequent response to barbiturate overdose?
a. respiratory depression leading to respiratory arrest

10. What are the mainstays of treatment of barbiturate overdose?
a. maintenance of adequate airway, assisted respiration, and oxygen administration if needed

11. What is meant by “pressor support?”
a. drugs that cause vasoconstriction and therefore, raise the blood pressure.

12. How does activated charcoal cause the elimination of a drug from the body?
a. assists in pulling the drug from circulation then eliminating it through the GI tract

13. Know that Phenobarbital (Luminal) is the prototype barbiturate.
a. Luminal is the prototype barbiturate

14. What is the most commonly prescribed class of sedative-hypnotics?
a. benzodiazepines because they have favorable adverse effect profiles, efficacy and safety

15. What are the two classifications of benzodiazepines?
a. anxiolytics and sedative-hypnotics

16. How do benzodiazepines depress the CNS?
a. inhibit stimulation of the brain

17. Why are benzodiazepines used to prevent the symptoms of alcohol withdrawal?
a. their receptors in the CNS is the same area or alchohol addiction

18. What are the 4 most common uses of benzodiazepines
a. sedation, sleep induction, anxiety relief, and musculo-skeletal relaxation

19. What are the most commonly reported undesirable effects of benzodiazepines?
a. headaches, dizziness, paradoxical excitement or nervousness, drowsiness, vertigo, lethargy, and cognitive impairment

20. Why should benzodiazepines be avoided in the elderly?
a. create a significant fall hazard

21. What are the manifestations of a benzodiazepine overdose?
a. somnelence, confusion, coma, and diminished reflexes

22. What two substances should benzodiazepines not be combined with?
a. alcohol and analgesics

23. What is the reason for not inducing vomiting in an unconscious patient?
>?

24. How does flumazenil work as a benzodiazepine reversal agent?
>?

25. What are the pharmacologic properties of the nonbenzodiazepine hypnotics such as zolpidem (Ambien) and eszoplicone (Lunesta)?
a. anxiolytic, sedative, muscle relaxant, and anticonvulsive effects

26. How long should the nonbenzodiazepine drugs be used to treat insomnia?
a. 7-10 days

27. Which class of hypnotics has the shortest half-life, benzodiazepines or nonbenzodiazepines?
a. benzodiazepines

28. Which would you guess would have the greater “hangover” effect?
a. nonbenzodiazepines

29. How does the group of muscle relaxants act?
a. act within the CNS to relieve pain associated with skeletal muscle spasms

30. What are the two classes of muscle relaxants
a. central acting skeletal muscle relaxants and direct acting skeletal muscle relaxants

31. What is the antidote or reversal drug for muscle relaxant overdose?
a. no specific antidote

32. What may barbiturates undesirably cause in children and the elderly?
>?

33. What happens if a barbiturate is given too rapidly IV?
a. profound hypotension and marked respiratory depression

34. What is the normal blood level for phenobarbital?
>?

35. What standard safety precautions should be used on someone taking hypnotics?
>?

36. Should zolpiedem (Ambien) be taken with a mealtime snack or on an empty stomach?
a. empty stomach


Week 5-Chapter 16

37. How do most CNS stimulant drugs act?
a. stimulate the excitatory neurons in the brain

38. What are the 3 excitatory neurotransmitters?
a. dopamine, norepinepherine, and epinepherine

39. What do amphetamines stimulate?
a. areas of the brain associated with mental alertness like the cerebral cortex and thalamus

40. What is the pharmacologic action of amphetamines?
a. mood elevation or eupohoria, increased mental alertness and capacity for work, decreased fatigue and drowsiness, prolonged wakefulness, relaxation of bronchial smooth muscle, increased respiration, and dilation of pulmonary arteries

41. How do serotonin receptor agonists reduce migrane headache pain?
a. stimulate serotonin receptors in cerebral arteries and cause vasoconstriction

42. What is the original prototype SSRA?
a. sumatriptan (Imitirex)

Week 5-Chapter 17

43. What are adrenergics?
a. synthetic and naturally occurring substances

44. Why are adrenergics also called sympathomimetics?
a. mimic the effects of the SNS neurotransmitters of norepinepherine, epinepherine, and dopamine

45. You must know Table 17-1 on page 270 and what happens when alpha 1, beta 1 and beta 2 receptors are stimulated.
Adrenergic Receptor Responses to Stimulation

Body System --> Location --> Receptor --> Response

Cardiovascular:
*Blood Vessels
Alpha 1: Constriction
Beta 2: Dilation

*Cardiac Muscle
Beta 1: Increased Contractility

*Atrioventricular Node
Beta 1: Increased Heart Rate

*Sinoatrial Node
Beta 1: Increased Heart Rate

Endocrine
*Pancreas
Beta 1: Decreased Insulin Release

*Liver
Beta 2: Glycogenolysis

*Kidney
Beta 2: Increased Renin Secretion

Gastrointestinal
*Muscle
Beta 2: Decreased Motility

*Spinchters
Alpha 1: Constriction

Genitourital
*Bladder Spinchter
Alpha 1: Constriction

*Penis
Alpha 1: Ejaculation

*Uterus
Alpha 1: Contraction
Beta 2: Relaxation

Respiratory
*Bronchial Muscles
Beta 2: Dilation

Ocular
*Puppilary Muscles of Iris
Alpha 1: Mydriasis

46. What happens when a dopaminergic receptor is stimulated by dopamine?
a. cause vessels of renal, mesenteric, coronary, and cerebral arteries to dilate, increasing blood flow to these tissues

47. What happens when adrenergic drugs stimulate alpha 1 receptors?
a. vasoconstriction occurs on sites located on smooth muscle

48. What happens when adrenergic drugs stimulate beta 1 receptors?
a. increase force of contraction, increase in heart rate, and increase in the conduction of cardiac electrical nerve impulses through atrioventricular node

49. What happens when adrenergic drugs stimulate beta 2 receptors?
a. relaxation of bronchii, increased glycogenolysis, and increased renin secretion

Week 5-Chapter18

50. What is another name for an adrenergic blocker?
a. sympatholytic or adrenergic antagonist

51. What does alpha 1 adrenergic blockade lead to?
a. vasoconstiction of arterioles

52. What do ergot alkaloids cause?
a. peripheral and cerebral vasoconstriction as well as constriction of dilated arteries

53. What is an ergot alkaloid such as ergotamine (Ergostat) used for?
a. migraines and cluster headaches

54. What are the alpha blockers doxazosin, prazosin, terazosin, and tamsulosin used for?
a. venous and arterial vasodilation which lowers blood pressure

55. What are the two reasons prazosin is used?
a. treat hypertension and reduce urinary obstruction in men

56. What do beta adrenergic blocking drugs do?
a. lower HR, lower heart contractility, vasocontriction in the heart, and bronchoconstriction

57. Where are beta 1 receptors primarily located?
a. heart

58. Where are beta 2 receptors primarily located?
a. bronchioles

59. Distinguish cardioselective from nonselective beta blockers.
a. cardioselective beta blockers only block the beta receptors on the heart and nonselective beta blockers block receptors on the heart, bronchioles, and blood vessels

60. What is the effect of cardioselective beta blockade?
a. lowers HR, vasoconstriction, and lowers heart contractility

61. What happens to the bronchioles when beta 2 receptors are blocked?
a. bronchoconstriction

62. What happens to blood vessels when beta 2 receptors are blocked?
a. vasoconstriction

63. How might beta 2 blockade cause elevation of blood glucose?
a. impairs glycogenolysis

64. How does beta blockade raise blood triglyceride levels?
a. release free fatty acids from adipose tissue

65. How are some beta blockers useful in the treatment of angina?
a. lowers HR and contractility which leads to less oxygen consumption and relieves angina pain related to lack of oxygen

66. What is the mechanism for some beta blockers being cardioprotective?
a. inhibit stimulation of the heart muscles by circulating catecholamines

67. How might a beta blocker reduce the blood pressure?
a. lowers heart rate, contractility, and vasoconstriction

68. Page 291, right column under Assessment, the dotted bullets are very important information.
a. alpha blocking: cause block of the sympathetic stimulation of blood vessels which results in vasodilation and decrease in blood pressure
b. beta 1 blocking: cause block in sympathetic effects leading to lower HR, contractility and conduction which helpts treat dysfunctional irregularities in heart rate
c. beta 2 blocking: cause block in sympathetic effects on bronchial smooth muscle resulting in bronchoconstriction

69. When giving beta blockers, what SBP and HR measurements should the nurse use in determining when to notify the provider?
a. lower than 100 mm Hg or 60 bpm


Week 5-Chapter 19

70. What are the other terms for cholinergics?
a. cholinergic agonists and parasympathomimetics

71. What is the neurotransmitter responsible for transmission of effector cells in the PSNS?
a. acetycholine (Ach)

72. What are the two types of cholinergic receptors and what is it that stimulates them?
a. nicotinic receptors are stimulated by alkaloid nicatine and muscarinic receptors are stimulated by alkaloid muscarine

73. What does cholinesterase do?
a. enzyme responsible for breaking down acetylcholinesterase (AchE)

74. When cholinergic receptors are stimulated, what happens in the body?
a. permeability of cells changes and calcium and sodium are permitted to flow into the cell depolarizing the cell membrane to stimulate the effector organ

75. What are the indications or uses of cholinergic drugs?
a. reduce intraocular pressure for glaucoma patients or ocular surgery, treat various GI and bladder disorders, diagnose and treat myasthenia gravis, treat Alzheimer’s disease, and treat excessively dry mouth from Sjogren’s syndrome

76. How might cholinergics improve patient performance in Alzheimer’s?
a. replenish the brain of Ach for normal brain function

77. Page 302, right column under Assessment, the dotted bullets are very important information.
a. effects of cholinergic drugs:
-decrease in heart rate
-increase in GI and GU tone through increased contractility of the smooth muscle
-increase in the contractility and tone of bronchial smooth muscle
-increased respiratory secretions
-miosis (pupillary constriction)

Week 5-Chapter 20

78. What are the other terms for cholinergic blockers?
a. anticholinergics, parasympatholytics, and antimuscarine drugs

79. What do cholinergic blockers do?
a. block or inhibit actions of acetylcholine in the PSNS

80. What other class of ANS drugs do cholinergic drugs share the same effects with?
a. adrenergics

81. What are the major sites of action for anticholinergics?
a. heart, respiratory tract, GI tract, urinary bladder, eye, and exocrine glands

82. What do cholinergic blockers do to the eye?
a. causes pupil dilation and increased intraocular pressure
-Remember, cholinergic blockers might be detrimental to persons with glaucoma (abnormally high IOP) because they increase the IOP.

83. What is the effect of cholinergic blockers on the GI tract?
a. decreased GI motility, secretions, and salivation

84. What do cholinergic blockers do to the HR?
a. increase heart rate

85. What do they do to the bladder?
a. decrease bladder contraction leading to urine retention

86. What do they do to the skin?
a. reduce sweating

87. What do they do to the respiratory system?
a. dry mucous membranes and cause bronchial dilation

88. How do low doses of cholinergic blockers slow the HR?
a. effects cardiac center in the medulla

89. Table 20-1 on page 307 is important.
Cholinergic Blockers: Drug Effects

*Cardiovascular
Small Dose: decrease HR
Large Dose: increase HR

*Central Nervous
Small Dose: decrease muscle rigidity and tremors
Large Dose: cause drowsiness, disorientation, and hallucinations

*Eye
Dilate pupils, decrease accomodation by paralyzing ciliary muscles

*Gastrointestinal
Relax muscle tone, decrease intestinal and gastric secretions, decrease motility and peristalsis

*Genitourinary
Relax detrusor muscle of bladder, increase constriction of internal spinchter; may result in urine retention

*Glandular
Decrease broncial secretions, salivation, sweating

*Respiratory
Decrease bronchial secretions, dilate bronchial airways