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Pharmacology and Fluid Therapy > Medication Classifications (LO2) > Flashcards

Medication Classifications (LO2) Flashcards

1
Q

Drugs are organized into classifications according to

A

the body system they affect, their therapeutic use or clinical indication, and/or their physiologic or chemical action

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2
Q

13 classifications of drugs

A

Opioid antagonists

Non-narcotic  analgesics

Inhalation  anesthetics

Adrenergic agonists

Bronchodilators

Antianginal agents

Anticoagulants

Platelet inhibitors

Uterotonics

Vitamin and electrolyte
supplements

Antihypoglycemic agents

Antimicrobials

Antidotes or neutralizing agents

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3
Q

Opioid

A

binds to opioid receptors to provide analgesic effects

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4
Q

Analgesic

A

medication that relieves pain

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5
Q

Anesthetics

A

medication that makes the body less sensitive to the perception of pain

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6
Q

Bronchodilators

A

medication which increases airflow to lungs by dilating the bronchi and bronchioles

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7
Q

Antiangina

A

medication to manage or reduce the heart condition angina

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8
Q

Anticoagulants

A

medication to prevent blood clots

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9
Q

Platelet inhibitors

A

medications which reduce blood clotting by preventing platelet cohesion

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10
Q

Uterotonics

A

medication to induce contraction of uterus

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11
Q

Antihypoglycemic

A

counteracting low blood glucose  

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12
Q

Antimicrobials

A

medication to destroy or slow growth of microorganisms

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13
Q

Antidotes

A

medication to counteract poison

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14
Q

The CNS

A

which is comprised of the brain and spinal cord, receives signals from sensory receptors (e.g., pain, vision, cold, pressure, smell), processes these signals, and controls body responses to them

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15
Q

The classifications that you are going to study that affect the central nervous system are:

A

Opioid antagonists
Non-narcotic analgesics
Inhalation anesthetics

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16
Q

Opioid Antagonist

A

Narcotic medications elicit both analgesic and CNS effects

Some patients experience a feeling of well-being with their use

Opioid antagonists may be used to treat both narcotic abuse symptoms as well as therapeutic narcotic symptoms

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17
Q

Mechanism of Action of Opioid Antagonist

A

Opioid antagonists attach to opioid receptors and displace the narcotic, thereby rapidly reversing the effects of the narcotic

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18
Q

Types of Opioid Antagonists

A

Pure antagonists

Partial antagonists

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19
Q

Pure antagonists

A

Competitive blocking drugs

Occupy a receptor site so that narcotic cannot, but do not have any effect themselves

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20
Q

Partial antagonists

A

Bind with receptor sites

Produce weak narcotic-like effects in the absence of other narcotics

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21
Q

common uses of Opioid Antagonists

A

Narcotic induced respiratory depression

Narcotic addictions

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22
Q

common examples of Opioid Antagonists

A 
*Naloxone 
Nalmefene 
Butorphanol 
Nalbuphine 
Pentazocine
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23
Q

cautions of Opioid Antagonists

A

Partial antagonists may cause worsening of respiratory depression

Use caution when administering to individuals that are addicted to narcotics due to resulting withdrawal symptoms

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24
Q

Non-Narcotic Analgesics

A

Pain levels must be assessed before and after an analgesic is administered to determine its effectiveness

Analgesics inhibit the body’s reaction to pain

Non-narcotic analgesics differ from narcotic analgesics as they produce analgesia through both the CNS and peripheral mechanism of action at the site of injury

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25
Q

Mechanism of Action of Non-Narcotic Analgesics

A

provide analgesia by blocking prostaglandin stimulation in the CNS

cause fever reduction by affecting the hypothalamic center to reduce temperature, and they increase sweating and peripheral blood flow in order to increase heat loss

Select non-narcotic analgesics will also reduce inflammation by stabilizing cell membranes so that cells are less permeable, thus limiting edema formation

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26
Q

Common Uses of Non-Narcotic Analgesics

A

Mild pain management

Reduce fever

Pain from inflammation

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27
Q

Common Examples of Non-Narcotic Analgesics

A

Nonsteroidal anti-inflammatory drugs (NSAID)
*Ibuprofen
*Ketorolac
Naproxen

Salicylates
*Aspirin®

Analgesic/Antipyretic
*Acetaminophen (Tylenol®)

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28
Q

Cautions of Non-Narcotic Analgesics

A

May cause gastric erosion and ulceration, increased risk of bleeding, and renal impairment

Overdose of salicylates and acetaminophen may result in acidosis and respiratory complications

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29
Q

Anesthetics

A

An anesthetic is any drug that has the capability of causing loss of all sensations, not only the sensation of pain

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30
Q

two types of general anesthetics:

A

Inhalation  anesthetic

Injection  anesthetic

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31
Q

Mechanism of Action of general anesthetics

A

There are 4 stages to anesthesia, and mechanism of action depends on the stage that is achieved by the drug.

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32
Q

4 stages of Anesthetics

A

Stage 1: Analgesia
Stage 2: Involuntary movement
Stage 3: Surgical anesthesia
Stage 4: Medullary paralysis

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33
Q

Stage 1 of anesthetics

A

Stage 1: Analgesia.

 Cerebral cortex is inhibited causing a decreased response to pain, a feeling of euphoria, and possible unconsciousness.

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34
Q

stage 2 of anesthetics

A

Stage 2: Involuntary movement.
Cerebral cortex is completely depressed and the hypothalamus takes over control of bodily functions.

There is an increase in sympathetic tone which causes an increase in heart rate, blood pressure, respirations, and muscle tone.

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35
Q

stage 3 of anaesthetics

A

Stage 3: Surgical anesthesia. 
The hypothalamus is depressed, and cardiac and respiratory function returns to normal.

Spinal reflexes are blocked and skeletal muscles relax.

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36
Q

stage 4 of anesthetics

A

Stage 4: Medullary paralysis. The medulla is paralyzed, thus cardiac and respiratory centres are affected, and death may occur.

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37
Q

common uses of anesthetics

A

Surgeries
Dental procedures
Pain control (nitrous oxide’s main use)

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38
Q

Common Types of Inhalation Anesthetics

A

Volatile liquids

  • -Ether
  • -Enflurane
  • -Halothane
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39
Q

Gases

A
  • *Nitrous oxide

- *Penthrox 

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40
Q

cautions of anesthetics

A

Oxygen must be included with all inhalation anesthetics or hypoxia will result

They may cause nausea and vomiting in patients, so must monitor airway

Potentially  hepatotoxic

May cause heart to be sensitive to catecholamines (naturally occurring hormones such as dopamine or epinephrine), thus resulting in possible  dysrhythmias

Potentially fatal malignant hyperthermia may result, characterized by temperatures as high as 43° C and muscle rigidity

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41
Q

non-opiod analgesics

A

have antipyretic properties

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42
Q

3 main types of non-opiod analgesics

A

Salicylates (asprin)

Non steroidal anti-inflammatory medications (NSAIDs) (ibuprofen)

Para-aminophenol derivatives (tylenol)

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43
Q

Sedation

A

used to couteract anxiety before procedure

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44
Q

Hypnosis

A

medications that ensure they sleep through event

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45
Q

Benzodiazepines and MOA

A

seditatives used to prepare pts for invasive procedures

MOA: affect the inhibitory neurotransmitter gamma-aminobutyrate acid (GABA) in the brain causing brain activity to slow

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46
Q

Midazolam (Versed)

A

is a popular benzodiazepine

has potent amnesic effect that inhibits patients ability to recall the procedure

Onset of action is 1-3mins

has a 30-60min duration of action

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47
Q

Diazepam (Vilum)

A

moderatley longer acting benzodiazepine

30-90 min duration of action

Onset of action 5mins

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48
Q

Barbiturates and MOA

A

believed to work similarto benzo’s;

MOA: increase affinity between receptor sites and the inhibitory neurotransmitter GABA

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49
Q

Thiopental (pentothal)

A

short acting barbiturate

Onset action of 10-20secs

Duration of action 5-10mins

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50
Q

Nonbarbiturate hypnotics

A

almost identical properties to benzo’s and barbiturates

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51
Q

Etomidate(Amidate/Lipuro)

A

ultra short common choice

Onset action of 5-15 secs

Duration of action of 3-5 mins

Minimal effects on hemodynamic stability and decreases intracranial pressure and cerebral oxygen metabolism

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52
Q

Propofol (diprivan)

A

Onset of 10-20 secs

Duration lasts 10 to 15mins

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53
Q

Anticonvulsants and MOA

A

anti seizure meds

MOA: work by inhibiting the influx of sodium into cells enhancing the inhibitory GABA system reducing excitatory glutamingeric neurotransmission and reducing activity in calcium channels

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54
Q

Classes of anticonvulstants include

A

hydantoins (phenytoin [Dilantin]),

iminostilbenes (carbamazepine)

valproic acid

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55
Q

Stimulation of CNS can be acomplished in 2 ways

A

increasing excitatory neurotransmitters

by decreasing inhibatory neurotransmitters

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56
Q

Amphetamines

A

are CNS stimulants

They increase the release of dopamine and norepinephrine to increase wakefullness and awarness

Increase tachycardia, hypertension and can cause seizures and psychosis

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57
Q

Methylphenidate (Ritalin)

A

intended to allow pts to better focus and avoid distraction

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58
Q

Psychotherapeutic Medications and MOA

A

MOA: work by blocking dopamine receptors

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59
Q

Depression often treated with

A

seretonin reuptake inhibitors

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60
Q

Monoamine oxidase inhibitors

A

block the metabolism of monoamines in the brain

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61
Q

Tricyclic antidepressants (TCAs)

A

have powerful inhibitory effects:

They Block the neurotransmitters norepinephrine and serotonin from being reabsorbed in the brain

They block ACH from reaching its receptors which may lead to tachycardia

They block alpha 1 receptors which may produce orthostatic hypotension

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62
Q

CNS Agents

A

a class of drugs that produce physiological and psychological effects through a variety of mechanisms

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63
Q

specific agents

A

which bring about an identifiable mechanism with unique receptors for the agent

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64
Q

Nonspecific agents

A

which produce effects on different cells through a variety of mechanisms and are generally classified by the focus of action or specific therapeutic use

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65
Q

Stimulants

A

exert their action by excitation of the CNS

some of the specific drugs included in this group are caffeine, cocaine and various amphetamines

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66
Q

Patient may be prescribed CNS depressants which

A

slow brain activity to treat anxiety, muscle tension, pain, insomnia, stress, panic attacks and sometimes seizures

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67
Q

CNS depressant examples

A

lorazepam (Atrivan)

triazolam (Halcion),

chlordiazepoxide (Librium).

Diazepam (Valium),

alprazolam (xanax)

opiclone (Imovane)

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68
Q

the sympathetic branch of the ANS is based on…

the parasympathetic branch function is to…

A

The sympathetic branch of the ANS is based on

the parasympathetic branch function is to return the body to balance (homeostasis)

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69
Q

neurotransmitters for the adrenergic (sympathetic) response

A

epinephrine and norepinephrine

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70
Q

Medications that affect the ANS will…

A

either trigger or block an autonomic response

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71
Q

Adrenergic Agonists

A

often referred to as sympathomimetic drugs because they “mimic” the actions of the sympathetic nervous system.

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72
Q

Mechanism of Action of Adrenergic Agonists

A

are used to stimulate peripheral adrenergic receptors, alpha (α) and beta (β), and mimic the actions of the sympathetic nervous system

Drugs that act directly on the receptor are  direct-acting, and those that alter the release of norepinephrine are indirect-acting

The drug can be either  non-selective or  selective to the receptor sites they stimulate.

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73
Q

Non-selective α and β Agonists uses and action

A
  • Treatment of anaphylaxis/shock (currently only use for PCP)
  • Stimulates α1 receptors causing vasoconstriction, thus increasing blood pressure

Treatment of cardiac arrest
-Stimulates β1 receptors stimulate the heart, causing an increase in heart rate, force of contraction, and impulse contraction

Treatment of glaucoma
-Decreases intraocular pressure

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74
Q

α1 agonist uses and action

A

Decongestants

-Stimulate α1 receptors causing vasoconstriction and thereby decreasing congestion in the area

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75
Q

α2 Agonists uses and action

A

Treatment of glaucoma

-Stimulates α2 receptors causing a decrease in intraocular pressure

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76
Q

β1 Agonists: uses and action

A

Treatment of cardiac arrest and hypotension

-Stimulates β1 receptors causing an increase in heart rate, force of cardiac contraction, and cardiac conduction

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77
Q

β2 Agonists: uses and actions

A

Bronchodilators

-Stimulate β2 receptors, decreasing bronchoconstriction and causing bronchodilation

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78
Q

adrenergic drug cautions and side effects

A

CNS stimulation — anxiety, jitters, insomnia, tremors

Cardiac stimulation (β1 effect) — increase heart rate, force of cardiac contraction, and cardiac impulse conduction; palpitations and arrhythmias can occur

Increased blood pressure (α1 effect)

Urinary retention (α1 effect)

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79
Q

Beta-receptor - general
(non-specific)
ex: eye

  • effect
  • beta agonist
  • beta antagonist
A

-effect
relaxes ciliary muscle

-beta agonist
non specific agonists: isoproterenol
epinephrine

-beta antagonist
propranolol
timolol
nadolol

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80
Q

b1 selective drugs
ex: myocardium

  • effect
  • beta agonist
  • beta antagonist
A

-effect
increases contractility
increases heart rate

-beta agonist
norepinephrine

-beta antagonist
metoprolol
atenolol

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81
Q

b2 selective adrenergic drugs
ex: lungs

  • effect
  • beta agonist
A

-effect
bronchodilation

-beta agonist
bronchodilators:
fenoterol
albuterol
terbutaline
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82
Q

Alpha-receptor - general
ex: vascular smooth muscle

  • effect
  • beta agonist
  • beta antagonist
A

-effect
skin and skeletal muscle vessel constriction

-beta agonist
epinephrine
norepinephrine

-beta antagonist
phentolamine

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83
Q

a1 drugs
ex: vascular smooth muscle

  • effect
  • beta agonist
  • beta antagonist
A

-effect
vasoconstriction

-beta agonist
phenylephrine

-beta antagonist
prazosin

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84
Q

a2 drugs
ex: vascular smooth muscle

  • effect
  • beta agonist
  • beta antagonist
A

-effect
Opposes α1 vasoconstriction Inhibits NE release
Decreases adrenergic activity

-beta agonist
clonidine

-beta antagonist
yohimbine

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85
Q

Neuromuscular blocking agents

A

affect the somatic nervouse system by inducing paralysis

86
Q

Depolarizing neuromuscular blocking agents

A

stimulate depolarization of muscle cells which manifests as muscle twitches the medication then produces continuous stimulation of muscle cell which does not allow it to return to its resting state

87
Q

Nondepolarizing neuromuscular blocking agents

A

find in a competitive but non-stimulatory manner to part of the ACH receptor as a result these drugs do not cause muscle twitches

88
Q

Succinycholine

A

a depolarizing neuromuscular blocking agents that is paralytic for prehospital airway management

Rapid onset action less than 45 seconds

Short duration of action 4 to 5 mins

89
Q

Vecuronium

A

a non-depolarizing neuromuscular blocker that produces paralysis

Onset action of 30 seconds

Duration of action of 30 minutes

90
Q

Pancuronium

A

neuromuscular blocking agents that may be used in prehospital setting

Onset action of 90 to 120 seconds

Duration of action of 45 minutes to 90 minutes

91
Q

Adrenergic Agonists (sympathomimetics)

A

stimulates the adrenal medulla to release norepinephrine and epinephrin which stimulate one of two types of sympathetic receptors dopaminergic receptors and adrenergic receptors

92
Q

Dopiminergic receptors

A

produce dilation of renal, coronary and cerebral arteries there are no medication’s that specifically target these receptors

93
Q

3 categories of bronchodilators

A

β2 agonists 

Anticholinergics

Xanthines

94
Q

β2 Agonists

A

Act on the sympathetic nervous system

“Fit and act” at β2 receptors in the lungs

Stimulate bronchial smooth muscle causing bronchodilation and decreased respiratory secretions

Stabilize inflammatory cells, but do not treat inflammation

classified as short acting or long acting

95
Q

short acting β2 Agonists

A

can be used about 15 minutes prior to exercise or exposure to a known trigger as a preventative measure

common examples: *salbutamol,
terbutaline,
salmeterol

96
Q

long acting β2 Agonists

A

onset is slower but effects last 12 hours

common example: formoterol

97
Q

Anticholinergics

A

Act on the parasympathetic nervous system

Block action of acetacholine on bronchial smooth muscle resulting in bronchodilation and decreased respiratory secretions

Stabilize inflammatory cells, but do not treat inflammation

98
Q

common anticholinergics

A

*ipratropium bromide  

combined  *ipratropium bromide

salbutamol

99
Q

Xanthines

A

Act directly on respiratory muscle to cause bronchodilation

Most commonly used orally, but sometimes by injection

Not very effective for acute management, used mainly as chronic or maintenance treatment to prevent asthma symptoms

Have a narrow therapeutic range, which leads to a low safety margin

100
Q

common Xanthines

A

theophylline,

aminophylline

101
Q

common uses of all bronchodilators

A

Treat acute asthmatic episodes

  • -Short acting β2 agonists are used because they act quickly
  • -Longer acting β2 agonists are of little value for acute episodes due to the length of onset

Prevent acute asthmatic episodes

Treat chronic obstructive pulmonary disease (COPD).
–Best treatment involves anticholinergics, but other bronchodilators may be used

102
Q

bronchodilator cautions

A

Short acting β2 agonists should only be used as required; not as a regular or daily drug

103
Q

bronchodilator Side Effects

A

CNS stimulation — anxiety, insomnia, restlessness, tremors

Cardiac stimulation — tachycardia, palpitations, hypertension

May precipitate angina, myocardial infarction, and dysrhythmias

Nausea and vomiting

Abdominal cramps

104
Q

bronchodilator drug interactions

A

Beta blockers may block the effect

Monoamine oxidase inhibitors and tricyclic antidepressants may potentiate effects

105
Q

what is the preferred receptor to treat respiratory emergencies

A

beta 2 because they produce smaller increases in heart rate and force of contraction which decreases the body’s rate of oxygen consumption

106
Q

what is a well known CNS Stimulant which is also a Xanthine

A

caffeine

107
Q

common decongestants and cold products

A

pseudoephedrine
dextromethorphan
diphenhydramine

108
Q

Antianginal agents

A

are used to treat a cardiac condition called angina

109
Q

Angina

A

is an ischemic heart disease that results in a decreased blood flow to the myocardium due to a buildup of atherosclerotic plaques, or coronary artery vasospasm

110
Q

Three main classes of antianginal agents are:

A

*Nitrates (currently only class that can be administered by PCP)

Beta-blockers

Calcium channel blockers

111
Q

Nitrates

A

can relieve symptoms of ischemic heart disease, but are not a cure for it.

112
Q

nitrates MOA

A

is to relax vascular smooth muscles

the vascular endothelium converts nitrates to nitric oxide (NO) which causes vasodilation

Dilation of veins is greater than arteriolar dilation at the lower dosage ranges of these drugs

113
Q

Vasodilation results in:

A

Decreased amount of blood returning to the heart (preload); therefore, less blood for the heart to pump out

Decreased pressure for the heart to pump against (afterload)

Decreased afterload and preload decreases the hearts work; therefore, the heart requires less oxygen

114
Q

common uses of nitrates

A

To prevent angina attacks
–May be used as acute or long-term prophylaxis of angina

To relieve acute angina attacks

Treatment of myocardial infarctions

To help decrease blood pressure
–May be combined in hospital with other medications to control blood pressure

115
Q

common examples of nitrates

A

*Nitroglycerin 

116
Q

cautions of nitrates

A

Vasodilatation may cause headaches or orthostatic hypotension (resulting in weakness, dizziness, or fainting)

Alcohol potentiates the effects of nitrates

Drug loses its effects when exposed to light or air

Do not shake the spray as can affect dosage by displacing air in the bottle

Tolerance can be developed if used 24 hours a day

117
Q

drug interactions with nitrate

A

Viagra®
Cialis®
Levitra®

118
Q

Beta Blockers

A

another treatment and management used for angina.

They are effective with angina pectoris, but are not effective when used for vasospastic angina.

119
Q

Beta Blockers MOA

A

in treatment of angina is to block beta 1 receptors in the heart, thus decreasing heart rate and contractility

This in turn will help reduce oxygen demand by causing a decrease in afterload.

120
Q

common uses of beta blockers

A

Reducing the severity and frequency of exertional angina attacks

Post myocardial infarction

121
Q

common examples of beta blockers

A

Metoprolol
Atenolol
Timolol

122
Q

cautions of beta blockers

A

May produce bradycardia, decreased atrioventricular (AV) conduction, and reduced cardiac contractility

Should not be administered to patients with sick sinus syndrome or an AV block. Use with caution in patients with heart failure

Asthmatics should only receive beta blockers that are beta1 selective to reduce risk of bronchoconstriction

May mask signs of hypoglycemia

123
Q

Calcium Channel Blockers

A

Calcium channel blockers are another treatment used to help treat and manage angina.

124
Q

Calcium Channel Blockers MOA

A

The mechanism of action of calcium channel blockers is to block calcium channels, primarily in arterioles, resulting in arteriolar dilation and reduction in peripheral resistance (afterload)

They can also result in relaxation of coronary vasospasm, thus resulting in increased oxygen supply

Select calcium channel blockers may also block calcium channels in the heart, causing a decrease in heart rate, AV conduction, and contractility

125
Q

Calcium Channel Blockers common uses

A

Angina

Variant angina (Prinzmetal’s angina and vasospastic angina)

126
Q

Common Examples of Calcium Channel Blockers

A

Verapamil
Diltiazem
Nifedipine 

127
Q

cautions of Calcium Channel Blockers

A

Dilation of peripheral arterioles can cause hypotension and a resultant tachycardia.

Use caution with administration of calcium channel blockers that cause depression of the heart to patients taking beta blockers or that have bradycardia, heart failure, or an AV block.

128
Q

Chronotropic effect
Inotropic effects
Dromotropic effects

A

Chronotropic effect: medications that affect the heart rate

Inotropic effects: are changes in the force of contraction

Dromotropic effects: when a drug alters the velocity of the conduction of electricity through the heart

129
Q

Cardiac glycosides

A

our class of medications that are derived from plants

These medication’s block certain ionic pumps in the heart cells membranes which increases calcium concentration

130
Q

Antidysrhythmic medications

A

used to treat and prevent cardiac rhythm disorders further classified into four groups according to the fundamental mode of action on the heart

131
Q

four groups of antidysrhythmic medications

A

Sodium channel blockers
Beta blockers
Potassium chanel blockers
Calcium channel blocker’s

132
Q

Sodium channel blockers effect on heart

A

slow the conduction through the heart (negative dromotropic effect)

133
Q

Beta blockers effect on heart

A

reduce the adrenergic stimulation of the beta receptors

134
Q

Potassium channel blockers effect on heart

A

increase the heart contractility (positive inotrophy) and work against the reentry of blocked impulses

135
Q

Calcium channel blockers effect on heart

A

block the inflow of calcium into the cardiac cells decreasing the force of contraction in automaticity and may decrease the conduction velocity (negative dromotropic effect)

136
Q

thrombolytics

A

designed to break down (lyse) the clot and improve client outcomes if given shortly after the development of the clot

137
Q

Anticoagulants

A

may also be called  antithrombotics

most effective at preventing venous thrombosis, and are used to prevent formation of clots in veins and to stabilize an existing clot so it does not break off into circulation

Anticoagulants do not dissolve existing clots

138
Q

MOA of anticoagulants

A

anticoagulants disrupt the coagulation cascade and prevent the production of fibrin

They block the action of certain clotting factors, which cause platelets to stick together and form blood clots, but the method of action differs for each anticoagulant as each one works at different points in the clotting cascade

After addition of antiplatelet drugs, the formation of blood clots is reduced

Anticoagulants may be given to patients undergoing surgery to prevent blood clots from forming and decrease the risk of embolism

139
Q

Common Examples of anticoagulants

A

*Heparin (monitor only)

Low molecular weight heparins

Warfarin

140
Q

common uses of coagulants

A

During or after surgeries

A combination of anticoagulants may be used when a patient is first beginning oral anticoagulant therapy

141
Q

anticoagulants cautions

A

When doses are too high the following bleeding may result:
Bleeding gums
Nosebleeds
Easy bruising

142
Q

Platelet inhibitors

A

also called  antithrombotics 

inhibit the normal functioning of platelets

most effective for preventing  arterial thrombosis (blood clot in artery)

taken by people with a tendency to form clots in the heart and arteries where blood flow is fast

they are used to prevent clot formation after certain types of surgery (clots can lead to myocardial infarctions, strokes, etc.).

Platelet inhibitors do not dissolve existing clots.

143
Q

MOA of platelet inhibitors

A

Platelet inhibitors act at the level of platelets to prevent clots in arteries

They decrease the ability of platelets to stick together (therefore decreasing platelet aggregation) by inhibiting TXA2 or ADP.

reduce the tendency of platelets to stick together when blood flow is disrupted and prevent clot formation

144
Q

TXA2

A

thromboxane A2 a type of thromboxane with prothrombotic properties

145
Q

Common Examples platelet inhibitors

A

*ASA
Dipyridamole
Ticlopidine
Clopidogrel

146
Q

Common Uses platelet inhibitors

A

Primary prevention of a myocardial infarction

Prevention of a reinfarction in patients with previous myocardial infarction history

Prevention of thrombotic stroke

147
Q

Cautions platelet inhibitors

A

Increased risk of gastrointestinal bleeding and hemorrhagic stroke

Increased risk of bleeding

148
Q

fibrolytic agent

A

Once a blood clot has formed it may be administered to dissolve the thrombus and prevent it from breaking off and entering the bloodstream

Promote the digestion of fibrin

149
Q

two different classifications of medications used to stop preterm labour, induce labour, or control postpartum hemorrhage

A

uterine stimulants and uterine relaxants.

150
Q

Uterotonics

A

given to facilitate uterine contraction

151
Q

MOA of uterotonics

A

is stimulation of uterine contractions and compression of maternal blood vessels at the placental site in an attempt to induce labour and control postpartum hemorrhage.

152
Q

Common Uses of uterotonics

A

Induce or speed up labour

Facilitate contractions following a spontaneous abortion

Treat postpartum hemorrhage

153
Q

Common Examples of uterotonics

A

*Oxytocin® (monitor only)
Misoprostol
Syntometrine
Ergometrine

154
Q

Cautions of uterotonics

A

Ergometrine is contraindicated in women with a history of hypertension, pre-eclampsia, eclampsia, or heart disease.

Overstimulation of the uterus could result in uterine rupture, trauma to both mom and baby due to the fetus being forced through an incompletely dilated cervix, and decreased uterine perfusion.

155
Q

oxytocin

A

Naturally occurring hormone that has multiple reproductive functions

it increases the force and frequency of contractions

used to reduce postpartum haemorrhage

156
Q

tocolytic medication

A

Suppress the force and frequency metre and contractions

ex: magnesium sulfate
ex: terbutaline

157
Q

magnesium sulfate

A

Relaxes the smooth muscles including those in the uterus

158
Q

terbutaline

A

Beta agonist that has been used as a tocolytic agent

159
Q

Vitamin and Electrolyte Supplements

A

The body is unable to synthesize vitamins and electrolytes and must, therefore, rely on an adequate and constant supply through diet

160
Q

MOA of Vitamin and Electrolyte Supplements

A

Vitamins and electrolytes are equally as important for the body to maintain normal function.

If the demand is not met, body function will be compromised.

Depending on what component is lacking will determine the body function that is affected

161
Q

Vitamin A

A

Required for production of rhodopsin which enables specialized retinal cells (rods) to adapt to dim light

162
Q

Vitamin D

A

Regulates serum calcium levels in conjunction with parathormone and calcitonin

163
Q

Vitamin E

A

Prevents formation and accumulation of toxic metabolites; maintenance of red blood cell membranes

164
Q

Vitamin K

A

Synthesis of blood clotting factors II, VII, IX, X

165
Q

Vitamin B

A

Necessary for cell reproduction and maturation

166
Q

Vitamin C

A

Involved in formation of catecholamines, steroids, and conversion reactions

167
Q

Sodium

A

Helps to maintain normal fluid balance

168
Q

*Potassium

A

Maintains cell structure and function; regulates muscle function (monitor only)

169
Q

Calcium

A

Plays role in muscle contraction, blood coagulation and bone formation

170
Q

Hydrogen

A

Regulates acidity and alkalinity of body fluids

171
Q

Cautions of Vitamin and Electrolyte Supplements

A

There is specific balance that is required when administering certain electrolytes and vitamins, blood levels must be monitored as too much can be sometimes as detrimental as too little.

172
Q

Antihypoglycemic Agents

A

The brain requires a certain level of glucose in order to sustain life; if the blood sugar drops below that level, coma, or death can result

Antihypoglycemic agents are used when blood sugar levels drop and the patient’s needs are no longer met.

173
Q

MOA of Antihypoglycemic Agents

A

Antihypoglycemic agents work in one of two ways to increase plasma glucose levels:

Break down glycogen stores from the liver

Supply usable glucose directly to the patient’s blood stream

174
Q

common uses of Antihypoglycemic Agents

A

Hypoglycemia

175
Q

Common Examples of Antihypoglycemic Agents

A
  • Glucagon
  • D5/D10
  • D50W
  • Oral glucose
176
Q

Cautions of Antihypoglycemic Agents

A

Ensure that glucose levels are monitored before and after administration

177
Q

Antimicrobials

A

Bacteria have only a few strategies to fight these drugs. However, bacteria often have the upper hand because of their high numbers and their ability to adapt and reproduce

Antibiotics, antiviral, and  anti-fungal  agents  are used to treat a variety of infections

178
Q

General Guidelines for Use of Antimicrobials

A

Take as directed for the full course of treatment 

Space doses evenly apart

Be aware of compliance issues, reinfection, and superinfection

179
Q

Antibiotics

A

Antibiotics or antibacterial drug classes are used to treat bacterial infections

Each antibiotic drug is generally effective for only certain pathogenic bacteria

180
Q

Types of Antibiotics

A 
Beta-lactam 
Sulfonamide 
Tetracycline 
Macrolide 
Aminoglycoside 
Fluoroquinolone 
Miscellaneous
181
Q

type of Beta-lactam antibiotics

A

Penicillins

Cephalosporin antibiotics

Carbapenem antibiotics

182
Q

MOA of antibiotics

A

Preventing cell wall synthesis (penicillins)

Blocking the synthesis of folic acid (sulfonamides)

Interfering with protein synthesis (tetracyclines, macrolides, aminoglycosides)

Interfering with DNA synthesis (quinolones)

183
Q

common uses of antibiotics

A

Skin and soft tissue infections

Dental infections

Respiratory tract infections

Eye, ear, nose, and throat
infections

Urinary tract infections

Gastrointestinal infections

Some sexually transmitted diseases

184
Q

cautions of antibiotics

A

Stopping too early can cause a relapse of symptoms, or it may cause the bacteria to become resistant to the medication, which could lead to ineffectiveness of the antibiotic at a later date.

Dairy products, antacids, and iron preparations containing minerals such as calcium, iron, aluminum, and magnesium may interact with some antibiotics and prevent them from being properly absorbed into the body (tetracycline, ciprofloxacin, norflaxacin)

May interfere with effectiveness of oral contraceptives

Disruption of normal flora can be disrupted causing the bacteria Clostridium difficile to over grow. This results in pseudomembranous colitis that can cause bloody diarrhea, abdominal pain, fever, and cramps.

185
Q

Antivirals

A

Antibiotics are not effective against viruses

Antivirals are a type of antimicrobial drug used to treat viral infections. Their mechanism of action is to inhibit, not destroy, the growth of the virus.

Since viruses insert themselves into a cell’s DNA, it is very difficult to make antiviral drugs that are effect against the virus, but do not harm the healthy cells

186
Q

Types of Antivirals

A

Viral DNA Polymerase Inhibitors

Antiretrovirals

  • -RNA Reverse Transcriptase Inhibitors
  • -Protease Inhibitors

Viral Uncoating Blockers

187
Q

MOA of antivirals

A

Antiviral drugs work by:

Preventing virus from replicating, but do not destroy the virus.

Inhibit reverse transcriptase, an enzyme used by RNA viruses to build their DNA (RNA Reverse Transcriptase Inhibitors).

Inhibit protease, an enzyme used by RNA viruses in the final stages of creating new virus particles (Protease Inhibitors).

Prevent the virus from incorporating into the host cells (Viral Uncoating Blockers).

188
Q

Common Uses of antivirals

A

Treatment of herpes

Decrease HIV virus production (antiretrovirals)

Influenza A prophylaxis

189
Q

Cautions of antivirals

A

Since viruses reproduce very quickly, treatment must be started immediately

Possible adverse effects are nausea, headache, dizziness or drowsiness 

Antiretrovirals may have harmful side effects, so regular blood tests are required to monitor effects on the liver, pancreas, and bone marrow.

190
Q

Antifungals

A

Fungi exist as yeasts or molds and can invade mucous membranes and the skin.

Treatment of fungi is directed at destroying the fungal cell wall

Antifungal medications are used to treat fungal infections such as athlete’s foot, diaper rash, and thrush. They can be administered either topically or systemically.

191
Q

Types of Antifungals

A

Azole
Nystatin
Amphotericin B
Terbinafine

192
Q

MOA of antifungals

A

Inhibiting ergosterol synthesis in fungal cell membranes, thus inhibiting fungal cell membrane synthesis

When fungal cell membrane synthesis does not occur, the membrane becomes permeable and cell contents leak out, causing the fungal cell to die.

193
Q

Common Uses of antifungals

A

Skin and mucus membrane infections

Systemic fungal infections

Nail fungal infections

194
Q

Cautions

A

Amphotericin B is very potent and has a narrow therapeutic range, so dose must be closely monitored and blood tests must be performed to monitor drug levels

Some azole antifungals need an acidic environment in order to absorb, so no stomach acid neutralizing medications can be taken for two hours after taking it

All systemic azoles are hepatotoxic, therefore patients must be monitored with blood tests

195
Q

Medications used to treat HIV

A

Classified as antiretrovirals

  • Nucleoside reverse transcriptase inhibitors:
  • Non nucleoside reverse transcriptase inhibitors:
  • Protease inhibitors
196
Q

Antidotes and Neutralizing Agents

A

Antidotes and neutralizing agents are administered in poisoning and overdose situations in an attempt to antagonize or inactivate the substance

197
Q

MOA of Antidotes and Neutralizing Agents

A

Depending on the drug or poison they are working against, there are several ways that antidotes and neutralizing agents work. They may:

  • Compete and displace drug from receptor sites
  • Use a different cellular mechanism to overcome effects of poison
  • Prevent biotransformation
  • Bind and inactivate the poison
198
Q

Common Uses of Antidotes and Neutralizing Agents

A

Intentional and accidental overdose and poisonings

199
Q

Common Examples of Antidotes and Neutralizing Agents

A
  • Antidotes
  • Narcan (Naloxone) for opioid overdose

N-acetyl-L-cysteine for acetaminophen overdose

Chelating agents for metal ion poisoning

Glucagon for beta blocker overdose

Flumazenil for benzodiazepine overdoses

  • Neutralizing agents
  • Activated charcoal
200
Q

cautions of Antidotes and Neutralizing Agents

A

Most poisons have no specific antidote, so care must be supportive in nature, focus on prevention of further absorption, and promote poison elimination

201
Q

common medication classifications that affect the gastrointestinal system

A 
Antacids, 
Antiflatulents, 
Digestants, 
Antiemetics, 
Laxatives
Antidiarrheals
202
Q

Antiemetics

A

Antiemetic is a classification of medication used to control nausea and vomiting in patients

203
Q

N/V is typically triggered by four main mechanisms:

A

Stimulation of the cerebral cortex and limbic system. 

Stimulation of the chemoreceptor trigger zone (CTZ).

Stimulation of the vestibular system. 

Stimulation of peripheral pathways. 

204
Q

how Stimulation of the cerebral cortex and limbic system. cause n/v

A

The common causes of this type of N/V are increasing intracranial pressure, irritation of the meninges and emotional stress

205
Q

how Stimulation of the chemoreceptor trigger zone (CTZ). cause N/V

A

The CTZ is an area within the ventricle of the brain that is outside of the blood brain barrier that is directly exposed to substances in the blood and Cerebral Spinal Fluid (CSF).

Common causes of this type of N/V are metabolic abnormalities, toxins and medications.

206
Q

primary neurotransmitters within the chemoreceptor trigger zone (CTZ)

A

Dopamine (D2), Serotonin (5HT3) and Neurokinin (NK1) are the primary neurotransmitters within this area of the brain.

207
Q

How Stimulation of the vestibular system.  cause n/v

A

This is part of the inner ear that controls balance.

Stimulation of this system is mediated by Histamine.

Common causes of this type of N/V are movement related, i.e. motion sickness, vertigo.

208
Q

how Stimulation of peripheral pathways.  causes N/V

A

This pathway is triggered by stimulation of receptors in the GI tract, heart and kidneys.

Common causes of this type of N/V are toxins in the GI tract, blockage or decreased motility within the bowels.

209
Q

5-HT3 receptor antagonist

A

This type of antiemetic drug blunts or blocks the effects of Serotonin.

It is the most effective in controlling N/V associate with stimulation of the CTZ.

210
Q

H1 Histamine antagonist

A

This type of antiemetic drug blunts or blocks the effects of H1 Histamine and blunts the vestibular inputs. 

this mechanism is effective in treating N/V associated with simulation of the vestibular system.    

211
Q

Some common examples of antiemetics are:

A
  • Gravol (H1 Histamine antagonist)

* Ondansetron (5-HT3 receptor antagonist)

Pharmacology and Fluid Therapy (12 decks)

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