Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

m 2 > PHARMACOLOGY part 2 > Flashcards

PHARMACOLOGY part 2 Flashcards

1
Q

botulinum toxin prevents the release of ___

A

acetylcholine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

hemicholinium prevents the synthesis of ___

A

acetylcholine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

why is it almost impossible to enhance the destruction of acetylcholine?

A

because it is broken down almost instantaneously

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

neostigmine is a ___ inhibitor

A

cholinesterase (like physostigmine)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

___ is a synthetic atropine-like drug used to dry salivation and as an antispasmodic agent

A

propantheline (probanthine)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what is phenobarbital?

A

a barbiturate anticonvulsant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

curarine is a ___ receptor blocker that causes ___

A
  • nicotinic

- muscular paralysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

edrophonium is an anticholinesterase used to treat ___

A

myasthenia gravis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

gallamine is a long acting neuromuscular junction blocker used for ___

A

paralysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

all paralysis inducing drugs act via ___ receptor at the ___

A
  • nicotinic

- neuromuscular junction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

salivation is typically considered to be a ___ response

A

cholinergic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

cholinergic agonists are useful in treating xerostomia except in which patients?

A

those who have been subject to head and neck radiation therapy, due to nonfunctional salivary gland tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

ephedrine is a mixed acting adrenergic ___

A

agonist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what are the cholinergic stimulation effects of the eye?

A

miosis (pinpoint pupil) and reduction of intraocular pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what are the cholinergic stimulation effects of the cardiovascular system?

A
  • bradycardia
  • vasodilation, but only from injected cholinergic agents, since the muscarinic receptors on the vascular smooth muscle has no neural input
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what are the cholinergic stimulation effects of the GI tract?

A

increased spasmodic activity, increased salivation and acid secretion (overdose: nausea, vomiting, diarrhea)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what are the cholinergic stimulation effects of the urinary tract?

A

increased urination

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what are the cholinergic stimulation effects of the respiratory system?

A

bronchoconstriction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what are the cholinergic stimulation effects of the glandular system?

A

lacrimation and sweating

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what are the cholinergic stimulation effects of skeletal muscle?

A

tremor and ataxia (overdose: muscle weakness, cramps and fasciculations)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what are the anticholinergic (antimuscarninic) actions of the eye?

A

mydriasis and loss of accomodation, and increase of intraocular pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what are the anticholinergic (antimuscarninic) actions of the cardiovascular system?

A

increased heart rate (overdose: tachycardia)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what are the anticholinergic (antimuscarninic) actions of the GI tract?

A

decreased spasmodic activity, decreased salivation and acid secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what are the anticholinergic (antimuscarninic) actions of the urinary tract?

A

decreased urination

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what are the anticholinergic (antimuscarninic) actions of the glandular system?

A

decreased lacrimation, decreased sweating (overdose: hot, dry skin, hyperthermia)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

what are the anticholinergic (antimuscarninic) actions of the skeletal muscle?

A

no effects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

what are the anticholinergic (antimuscarninic) actions of the CNS?

A
  • tertiary amines such as atropine get into the brain and cause restlessness, headache, excitement, hallucinations, and delirium
  • quaternary amines like methantheline and propantheline only have peripheral actions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

a ___ blocker, since it acts by preventing ACh from stimulating nicotinic receptors at the ganglia level will have both anticholinergic and antiadrenergic effects

A

ganglionic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

what is the acronym for remembering the effects of cholinergic stimulation?

A
  • SLUD
  • increased salivation, lacrimation, urination, and defecation
  • the heart is the exception in that activity or heart rate is decreased (bradycardia)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

organophosphates kill you from too much ___ stimulation

A

cholinergic (SLUD + bradycardia)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

what is the affect of glandular secretions to atropine?

A
  • glandular secretions are generally under cholinergic control, so sweating and salivation are greatly reduced by the anticholinergic drug atropine
  • side effects of atropine could include burning dry mouth and hyperthermia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

what are examples of a cholinergic overdose?

A

nausea, vomiting, and orthostatic hypotension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

why is scopolamine used for sedation but atropine is not?

A
  • atropine overdose causes CNS excitation and tachycardia

- atropine is actually useful in surgery in cases where reversal of bradycardia is necessary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

what is the immediate cause of death as a result of organophosphate toxicity?

A

respiratory paralysis, which results from the stimulation of nicotinic receptors at the neuromsucular junction, resulting in paralysis of skeletal muscles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

which drug classes have potent anticholinergic activity?

A
  • prototypes atropine and scopolamine
  • tricyclic antidepressants
  • H1 antihistamines
  • opioid analgesics
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

what is the mechanism of action of adrenergic receptor blockers?

A

alpha or beta adrenergic drugs such as prazosin or propranolol act by competitive inhibition of postjunctional adrenergic receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

what are the 4 drugs that inhibit the action of adrenergic nerves, and what is their mechanism of action?

A
  • reserpine: depletes NE by inhibiting reuptake
  • guanethidine: inhibits the release of catecholamines
  • alpha methyldopa: acts centrally as a false neurotransmitter which gets taken up into storage vesicles and released with NE, thus decreasing sympathetic activity
  • clonidine: stimulates alpha2 receptors in the CNS with a resulting decrease in sympathetic outflow
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

what are the 3 mechanisms of action of indirect acting sympathomimetic drugs?

A
  • amphetamine, tyramine, and ephedrine act by stimulating the release of stored NE
  • TCAs and cocaine block reuptake
  • MAOIs block enzymatic destruction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

what is the action of epinephrine in the presence of an alpha blocker?

A
  • “epinephrine reversal”
  • int he presence of an alpha blocker (usually prazosin, but chlorpromazine may also be given), epi causes a decrease in blood pressure rather than increased because beta mediated vasodilation predominates
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

what is the action of epinephrine in the presence of NE?

A
  • vagal reflex
  • injection of a pressor dose of NE may result in decreased heart rate due to activation of baroreceptors which stimulate vagal reflex to reduce heart rate
  • vagal reflex is blocked by atropine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

what is the result of alpha-1 receptor stimulation?

A

vasoconstriction, urinary retention, mydriasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

what is the result of beta receptor stimulation?

A

increased heart rate (B1), bronchodilation (B2), and vasodilation (B2)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

what is the result of alpha-1 block?

A

vasodilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

what is the result of beta block?

A

decreased heart rate (B1), bronchoconstriction (B2)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

parkinson’s is a result of ___ deficiency in the brain

A
  • dopamine

- therefore, the remedy is to increase dopamine in the brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

what is the treatment for parkinson’s?

A
  • levodopa with carbidopa
  • injected DA doesn’t cross the BBB, but levodopa, a precursor to DA, does
  • carbidopa is given with levodopa to block dopa decarboxylase activity in the periphery, which in the absence of carbidopa, converts levodopa to DA in the periphery, decreasing the amount of levodopa that ends up in the brain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

what are the side effects of levodopa?

A
  • levodopa is a sympathomimetic and will produce sympathetic stimulation in the periphery
  • development of abnormal facial movement, nausea and vomiting, cardiac arrhythmias, and mental disturbances are all associated with levodopa therapy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

___ and ___ are the only centrally acting antihypertensives, reducing sympathetic outflow via alpha-1 agonist action

A

methyldopa and clonidine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

what is the mechanism of action of amphetamine?

A
  • indirect-acting sympathomimetic (acts like NE)

- causes release of neurotransmitter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

what are the mechanisms of action of cocaine, TCAs, ephedrine, and MAOIs?

A
  • cocaine: reuptake inhibition and release
  • TCAs: reuptake inhibition
  • ephedrine: causes release but also acts at receptor itself
  • MAOIs: block NT degradation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

what are the affects of the injection of a sympathomimetic drug?

A
  • stimulates both alpha and beta receptors
  • alpha-receptor stimulation produces vasoconstriction, increased systolic and diastolic pressure, and reflex tachycardia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

which drug can be used in pretreatment to prevent a response from amphetamine?

A

reserpine, because it causes depletion of NE from storage sites, and therefore NE cannot be released by amphetamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

what are the effects of alpha-1 agonists?

A

increased smooth muscle tone, so vasoconstriction leading to increased blood pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

what are the effects of alpha-2 agonists?

A

given orally they cause hypotension by reducing sympathetic outflow from the CNS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

what are the effects of beta-1 stimulation?

A

increased cardiac rate and force of contraction, thus positive inotropic and chronotropic actions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

what are the effects of beta-2 stimulation?

A

dilation of skeletal muscle blood vessels and bronchi or relaxation of bronchiolar smooth muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

what are the effects of adrenergic stimulation of the following organs: eye, heart, vascular smooth muscle, skeletal muscle vessels, bronchiolar smooth muscle, and sweat glands

A
  • eye: mydriasis or relaxation of ciliary muscle
  • heart: acceleration, increased contractility
  • vascular smooth muscle: vasoconstriction
  • skeletal muscle vessels: relaxation or dilation
  • bronchiolar smooth muscle: relaxation/bronchodilation
  • sweat glands: sweating
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

stimulation of beta-1 receptors in the cardiac muscle will increase ___ BP, and beta-2 stimulation will decrease ___ BP

A
  • systolic

- beta-2 stimulation will dilate vessels going to the liver and skeletal muscle, producing a decrease in diastolic BP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

what action does epinephrine have where it is useful in the treatment of acute bronchospasm?

A

it causes bronchodilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

injection of epi usually causes a rise in blood pressure due to what 3 things?

A
  • myocardial stimulation that increases ventricular contraction
  • an increase in heart rate
  • vasoconstriction due to alpha receptor stimulation (most important)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

why are vasoconstrictors included in local anesthetic preparations?

A
  • prolong and increase the depth of anesthesia by retaining the anesthetic in the area injected
  • reduce the toxic effect of the drug by delaying its absorption into the general circulation
  • to render the area of injection less hemorrhagic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

an asthmatic patient typically takes a drug that has bronchodilatory effects, which is effective for which receptor?

A

beta-2 agonist

63
Q

phenylephrine is an alpha-1 agonist used for ___

A

stuffy noses

64
Q

pseudoephedrine is a ___

A

decongestant

65
Q

albuterol is acts at what receptor?

A

beta-2 agonist

66
Q

how is therapeutic index calculated?

A

TI = LD50/ED50

  • LD50 is the dose that elicits a lethal response in 50% of patients
  • ED50 (or TD50) is the dose that elicits a therapeutic response in 50% of patients
  • larger therapeutic index is safer
67
Q

patients with atypical plasma cholinesterase don’t metabolize succinylcholine at the same rate, and thus show a prolonged drug action and increased sensitivity to the drug. what is this an example of?

A

idiosyncratic reaction

68
Q

benzodiazepines typically end in what suffix?

A

“pam”, “lam”, or “zam”

chlordiazepoxide is an exception

69
Q

what is the mechanism of action of benzodiazepines?

A

modulate the activity of the inhibitory neurotransmitter, GABA

70
Q

what are the advantages of benzodiazepines versus barbiturates?

A

less addition potential, less profound CNS depression, larger therapeutic index, less respiratory depression

71
Q

T or F:

many benzodiazepines form active metabolites

A

true

72
Q

IV injection of diazepam (benzodiazepine) can cause ___ due to ___

A

irritation such as thrombophlebitis, due to the solvent the BDZ is dissolved in

73
Q

what are the drug classes for sedatives?

A

benzodiazepines and barbiturates

74
Q

what is thiopental? why does it have a quick onset and short duration?

A
  • a barbiturate whose action is terminated by redistribution of the drug out of the brain - it enters the brain rapidly and exits rapidly, thus quick onset and short duration
  • therefore its duration of action is determined by redistribution away from its site of action in the brain to less well-perfused tissues
75
Q

T or F:

barbiturates are analgesic

A

false

76
Q

bartiburate overdose is lethal due to ___

A

respiratory depression

77
Q

barbiturates are contraindicated in patients with ___

A

intermittent porphyria (barbs enhance porphyrin synthesis and thus will aggravate the disease)

78
Q

why are barbiturates problematic as anesthetics?

A

they often induce excessive salivation and bronchial secretion, usually requiring the use of an anticholinergic drug to be administered to reduce these secretions

79
Q

barbiturates are always classified according to ___

A

their duration of action (thiopental: ultrashort acting; phenobarbital: long acting)

80
Q

barbiturates typically end in what suffix?

A

“barbital”, “albital”, and “pental”

81
Q

when pain is present, what affect can barbiturates have?

A

they may make the pain worse, resulting in arousal, rage, and perhaps delirium in the patient

82
Q

which class of sedatives are more popular due to their safety?

A

benzodiazepines

83
Q

why are benzodiazepines better for dental sedation than barbiturates and opioids?

A

BDZs present less risk of respiratory depression

84
Q

compare midazolam and diazepam/valium

A
  • midazolam is water soluble, and thus does not need to be dissolved in propylene glycol like valium (it is the solvent that causes thrombophlebitis seen with valium injections)
  • midazolam is short acting compared to valium because it does not have active metabolites like valium
85
Q

what is the only 1st generation antipsychotic still used to any extent?

A

haloperidol (haldol), a specific D2 receptor blocker

86
Q

what is the mechanism of action of antipsychotics?

A

blockade of dopaminergic sites in the brain

87
Q

what are the major side effects of antipsychotics?

A

anticholinergic effects and extrapyramidal stimulation resulting in tardive dyskinesia

88
Q

many 2nd generation antipsychotics block dopamine receptors but also ___ receptors

A

serotonin (5-HT)

89
Q

T or F:

2nd generation antipsychotics (like clozapine) treat negative as well as positive symptoms

A

true

90
Q

do 1st or 2nd generation antipsychotics have fewer extrapyramidal side effects like tardive dyskinesia?

A

2nd generation

91
Q

what are examples of TCAs?

A

imipramine and amitriptyline

92
Q

what medications are used for the treatment of depression?

A
  • TCAs
  • MAOIs (tranylcypromine or phenylene) are also used (not classified as antidepressants)
  • 2nd generation antidepressants (SSRIs) like fluoxetine (prozac) are most commonly used
93
Q

what is the mechanism of action of antidepressants?

A

blockade of amine reuptake or alterations of receptor number (SSRIs block serotonin reuptake selectively)

94
Q

what is the side effect of antidepressants?

A

anticholinergic or atropine side effects

95
Q

___ is the drug of choice for the manic phase of manic depression

A

lithium

96
Q

___ is the prototypic phenothiazine, an antipsychotic drug used in the treatment of schizophrenia

A
  • chlorpromazine

- other antipsychotic drugs used for this purpose are haloperidol and thioridazine, which act via dopaminergic receptors

97
Q

___ is an irreversible condition that consists of involuntary movement of skeletal muscles, a condition which may be seen following prolonged use of drugs

A
  • tardive dyskinesia
  • this is typically a dopaminergic mediated effect resulting from development of supersensitivity from chronic blockade of dopamine receptors in basal ganglia
98
Q

what main drugs cause gingival hyperplasia?

A
  • anticonvulsants (dilantin and phenytoin)
  • calcium channel blockers (nifedipine)
  • immunosuppressant (cyclosporine)
99
Q

anti-inflammatory drugs are ___ or ___ that suppress the immune system in addition to their anti-inflammatory activity. why can this be problematic?

A
  • corticosteroids or glucocorticoids
  • suppression of the immune system can cause latent infections such as tuberculosis to go systemic, or opportunistic infections such as candidiasis may become more of a problem
100
Q

what are the side effects of anti-inflammatory drugs?

A

gastric ulcers, immunosuppression, acute adrenal insufficiency, osteoporosis, hyperglycemia, and redistribution of body fat

101
Q

adrenal steroids, otherwise known as ___, cause gastric ulcers

A

corticosteroids

102
Q

the onset of anesthesia is inversely proportional to the ___ of the anesthetic in the blood

A
  • solubility
  • the more soluble the agent is in the blood, the more must be given to reach critical tension in the brain
  • the more insoluble, the faster the onset and offset of effect
103
Q

halothane is associated with what adverse side effect?

A

hepatotoxicity

104
Q

what are the 4 stages of anesthesia?

A
  • stage I: analgesia
  • stage II: delirium
  • stage III: surgical anesthesia
  • stage IV: medullary paralysis
105
Q

is nitrous oxide soluble in the blood?

A

it is very insoluble in the blood, and therefore works fast and leaves the body quickly once administration is stopped

106
Q

which drug is commonly administered prior to halothane to reduce salivation and bronchial secretions caused by halothane?

A

atropine

107
Q

what are the uses for H1 antihistamines?

A
  • treating dermatologic manifestations of an allergic response (chlorpheniramine, cyclizine, dimenhydrinate)
  • preoperative medication for sedation, antiemetic properties, anticholinergic effects (promethazine)
  • controlling symptoms of parkinsonism (diphenhydramine)
108
Q

what are the uses for H2 antihistamines?

A

reduce gastric acid secretion (cimetidine), now available OTC for heartburn

109
Q

which antihistamine is used for vertigo and motion sickness?

A

meclizine

110
Q

in the treatment of parkinsonism, which drugs are often the first drug tried (before levodopa/carbidopa)?

A

drugs with anticholinergic activity

111
Q

are antihistamines cholinergic?

A

no, they are anticholinergic

112
Q

H1 antihistamines are ___ histamine receptor blockers

A

competitive

113
Q

what are the two main drugs used to treat trigeminal neuralgia?

A

carbamazepine and phenytoin

114
Q

what does epinephrine do to blood glucose levels?

A

increases it

115
Q

what are the two major side effects associated with oral contraceptives?

A

suspected carcinogenicity and the tendency to produce thromboembolisms

116
Q

___ has been postulated to inhibit GABA effects, the major inhibitory transmitter in the CNS, especially in the cortex

A

alcohol

117
Q

what are the effects of alpha agonists vs beta agonists vs muscarinic agonists on insulin release?

A

alpha agonists decrease insulin release, beta agonists increase it, and muscarinic agonists increase it

118
Q

sulfonylureas cause insulin release by ___ and are the primary oral antidiabetic agents used therapeutically

A

direct stimulation of pancreatic beta cells

119
Q

what is dicoumarol? what is its mechanism of action?

A

an oral anticoagulant, which prevents blood clotting by preventing the conversion of vitamin K to prothrombin

120
Q

what is the drug-drug interaction of warfarin and phenylbutazone?

A

phenylbutazone enhances the toxicity of warfarin by displacing it from plasma protein binding sites

121
Q

diabetes medications can be organized into 3 groups based on their onset and duration of action. what are they?

A
  • fast acting: insulin injection
  • intermediate acting: isophane insulin suspension
  • long acting: protamine zinc insulin suspension
122
Q

describe the relationship between coumarin and protein binding sites

A
  • coumarin is extensively protein bound, meaning 97% of it is protein bound (unable to get to its real receptor site of action), and only 3% is left to reach effective sites
  • this can be combated by administering with another drug that is also extensively plasma protein bound that will displace the drug that is already on these sites via competition, and thus effectively increasing the level of drug that can now get to an active receptor site
123
Q

___ disease results from failure of the adrenal cortices to produce adrenocortical hormones such as aldosterone

A
  • addison’s disease

- lack of aldosterone results in electrolyte imbalances, with the major problem being hyponatremia (sodium loss)

124
Q

___ is a mineralocorticoid that controls sodium retention and potassium excretion

A

aldosterone

125
Q

patients with suppressed adrenal function (like in addison’s disease) can’t respond to stressful situations (such as dental procedures) adequately, and an adrenal crisis may occur. what is the recommended treatment?

A

100mg of hydrocortisone hemisuccinate

126
Q

most cancer chemotherapy drugs cause cell death by ___

A

affecting the ability of cells to divide

127
Q

what is the main function of parathyroid hormone?

A

maintaining the concentration of calcium in extracellular fluid by regulating the deposition and mobilization of calcium from bone, absorption from the GI tract, excretion, etc.

128
Q

___ concentrations regulate the synthesis and release of ___

A

calcitonin (aka thyrocalcitonin)

129
Q

___ is a pancreatic hormone that stimulates glucose production

A

glucagon

130
Q

___ refers to some alteration of receptors that leads to diminished response to the drug, and is really a mechanism whereby tolerance may occur

A

desensitization

131
Q

what is salicylism?

A
  • a mild toxic reaction to aspirin (acetylsalicylic acid), usually occurring after prolonged treatment with large doses
  • nausea, tinnitus, vomiting, and GI bleeding are all symptoms
132
Q

what are side effects of aspirin which result from a single large dose?

A

disturbances of acid-base imbalance (acidosis or alkalosis), fever, and hypoglycemia

133
Q

what is methylphenidate?

A

ritalin, an indirect acting sympathomimetic that acts similar to amphetamine in the CNS as a stimulant

134
Q

are nonionized forms of drugs more or less lipid soluble? what about ionized forms of drugs? which are more rapidly excreted?

A
  • nonionized forms of drugs cross membranes more readily and are highly lipid soluble, and tend to get stored in fat tissue from where they are only slowly released
  • thus, highly ionized drugs, which are less lipid soluble, don’t get stored in fatty tissue and are subject to more rapid excretion
135
Q

why is atropine contraindicated in patients with glaucoma?

A

it is an anticholinergic drug that increases intraocular pressure, which is already the problem with glaucoma patients

136
Q

platelet aggregation is controlled by what two factors?

A
  • prostacycline, which decreases platelet aggregation

- thromboxane, which enhances platelet aggregation

137
Q

what is the sign you should look for to tell if a patient is adequately sedated with IV benzodiazepines?

A

upper eyelid ptosis (drooping of eyelid, verill’s sign)

138
Q

what is the primary advantage of IV drug administration?

A

ability to titrate the drugs

139
Q

the purpose of drug metabolism (biotransformation) is to change the drug into an excretable form, which is ___ and ___

A
  • water soluble and ionized

- this is why lipid soluble, nonionized drugs stay longer in the body

140
Q

why do patients with cirrhosis have increased postoperative bleeding after multiple extractions?

A

vitamin K is stored in the liver, which is decreased by cirrhosis, resulting in deficiencies in prothrombin dependent coagulation factors

141
Q

angina pectoris is heart pain caused by ___

A

lack of oxygen

142
Q

what are the side effects of polymixin (antibiotic that treats bacterial infections)?

A

renal necrosis

143
Q

what are the side effects of chloramphenicol (antibiotic)?

A

bone marrow depression

144
Q

what is the side effect of amphotericin B?

A

nephrotoxicity

145
Q

hydralazine (aprezoline) is a direct acting ___

A

vasodilator

146
Q

verapamil (calan) is a ___

A

type I calcium channel blocker

147
Q

thiazides may require supplemental administration of potassium. why?

A

so the patient doesn’t get hypokalemia

148
Q

which opioid receptors are involved in analgesia?

A

mu and kappa (mu at the supraspinal level, kappa at the spinal level)

149
Q

are amides or esters cross allergenic?

A

only esters are

150
Q

why do patients who use corticosteroids for arthritis often develop ulcers?

A

because these drugs block prostaglandin action in the stomach, thereby increasing acid secretion while decreasing the protective mucosal barrier of the stomach

151
Q

what are signs that a patient is getting too much nitrous?

A

nausea, euphoria, giddiness

152
Q

T or F:

sedation can decrease the amount of local anesthetic required

A

false, the patient will still feel pain and therefore require the same local anesthetic as if they weren’t receiving sedation

153
Q

sedatives, with the exception of ___, have no analgesic effect

A

nitrous oxide

154
Q

only ___ are classified as antianxiety drugs

A

benzodiazepines

m 2 (35 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions