Medication Classifications (LO2) Flashcards
Drugs are organized into classifications according to
the body system they affect, their therapeutic use or clinical indication, and/or their physiologic or chemical action
13 classifications of drugs
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
Opioid
binds to opioid receptors to provide analgesic effects
Analgesic
medication that relieves pain
Anesthetics
medication that makes the body less sensitive to the perception of pain
Bronchodilators
medication which increases airflow to lungs by dilating the bronchi and bronchioles
Antiangina
medication to manage or reduce the heart condition angina
Anticoagulants
medication to prevent blood clots
Platelet inhibitors
medications which reduce blood clotting by preventing platelet cohesion
Uterotonics
medication to induce contraction of uterus
Antihypoglycemic
counteracting low blood glucose
Antimicrobials
medication to destroy or slow growth of microorganisms
Antidotes
medication to counteract poison
The CNS
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
The classifications that you are going to study that affect the central nervous system are:
Opioid antagonists
Non-narcotic analgesics
Inhalation anesthetics
Opioid Antagonist
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
Mechanism of Action of Opioid Antagonist
Opioid antagonists attach to opioid receptors and displace the narcotic, thereby rapidly reversing the effects of the narcotic
Types of Opioid Antagonists
Pure antagonists
Partial antagonists
Pure antagonists
Competitive blocking drugs
Occupy a receptor site so that narcotic cannot, but do not have any effect themselves
Partial antagonists
Bind with receptor sites
Produce weak narcotic-like effects in the absence of other narcotics
common uses of Opioid Antagonists
Narcotic induced respiratory depression
Narcotic addictions
common examples of Opioid Antagonists
*Naloxone Nalmefene Butorphanol Nalbuphine Pentazocine
cautions of Opioid Antagonists
Partial antagonists may cause worsening of respiratory depression
Use caution when administering to individuals that are addicted to narcotics due to resulting withdrawal symptoms
Non-Narcotic Analgesics
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
Mechanism of Action of Non-Narcotic Analgesics
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
Common Uses of Non-Narcotic Analgesics
Mild pain management
Reduce fever
Pain from inflammation
Common Examples of Non-Narcotic Analgesics
Nonsteroidal anti-inflammatory drugs (NSAID)
*Ibuprofen
*Ketorolac
Naproxen
Salicylates
*Aspirin®
Analgesic/Antipyretic
*Acetaminophen (Tylenol®)
Cautions of Non-Narcotic Analgesics
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
Anesthetics
An anesthetic is any drug that has the capability of causing loss of all sensations, not only the sensation of pain
two types of general anesthetics:
Inhalation anesthetic
Injection anesthetic
Mechanism of Action of general anesthetics
There are 4 stages to anesthesia, and mechanism of action depends on the stage that is achieved by the drug.
4 stages of Anesthetics
Stage 1: Analgesia
Stage 2: Involuntary movement
Stage 3: Surgical anesthesia
Stage 4: Medullary paralysis
Stage 1 of anesthetics
Stage 1: Analgesia.
Cerebral cortex is inhibited causing a decreased response to pain, a feeling of euphoria, and possible unconsciousness.
stage 2 of anesthetics
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.
stage 3 of anaesthetics
Stage 3: Surgical anesthesia.
The hypothalamus is depressed, and cardiac and respiratory function returns to normal.
Spinal reflexes are blocked and skeletal muscles relax.
stage 4 of anesthetics
Stage 4: Medullary paralysis. The medulla is paralyzed, thus cardiac and respiratory centres are affected, and death may occur.
common uses of anesthetics
Surgeries
Dental procedures
Pain control (nitrous oxide’s main use)
Common Types of Inhalation Anesthetics
Volatile liquids
- -Ether
- -Enflurane
- -Halothane
Gases
- *Nitrous oxide
- *Penthrox
cautions of anesthetics
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
non-opiod analgesics
have antipyretic properties
3 main types of non-opiod analgesics
Salicylates (asprin)
Non steroidal anti-inflammatory medications (NSAIDs) (ibuprofen)
Para-aminophenol derivatives (tylenol)
Sedation
used to couteract anxiety before procedure
Hypnosis
medications that ensure they sleep through event
Benzodiazepines and MOA
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
Midazolam (Versed)
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
Diazepam (Vilum)
moderatley longer acting benzodiazepine
30-90 min duration of action
Onset of action 5mins
Barbiturates and MOA
believed to work similarto benzo’s;
MOA: increase affinity between receptor sites and the inhibitory neurotransmitter GABA
Thiopental (pentothal)
short acting barbiturate
Onset action of 10-20secs
Duration of action 5-10mins
Nonbarbiturate hypnotics
almost identical properties to benzo’s and barbiturates
Etomidate(Amidate/Lipuro)
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
Propofol (diprivan)
Onset of 10-20 secs
Duration lasts 10 to 15mins
Anticonvulsants and MOA
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
Classes of anticonvulstants include
hydantoins (phenytoin [Dilantin]),
iminostilbenes (carbamazepine)
valproic acid
Stimulation of CNS can be acomplished in 2 ways
increasing excitatory neurotransmitters
by decreasing inhibatory neurotransmitters
Amphetamines
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
Methylphenidate (Ritalin)
intended to allow pts to better focus and avoid distraction
Psychotherapeutic Medications and MOA
MOA: work by blocking dopamine receptors
Depression often treated with
seretonin reuptake inhibitors
Monoamine oxidase inhibitors
block the metabolism of monoamines in the brain
Tricyclic antidepressants (TCAs)
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
CNS Agents
a class of drugs that produce physiological and psychological effects through a variety of mechanisms
specific agents
which bring about an identifiable mechanism with unique receptors for the agent
Nonspecific agents
which produce effects on different cells through a variety of mechanisms and are generally classified by the focus of action or specific therapeutic use
Stimulants
exert their action by excitation of the CNS
some of the specific drugs included in this group are caffeine, cocaine and various amphetamines
Patient may be prescribed CNS depressants which
slow brain activity to treat anxiety, muscle tension, pain, insomnia, stress, panic attacks and sometimes seizures
CNS depressant examples
lorazepam (Atrivan)
triazolam (Halcion),
chlordiazepoxide (Librium).
Diazepam (Valium),
alprazolam (xanax)
opiclone (Imovane)
the sympathetic branch of the ANS is based on…
the parasympathetic branch function is to…
The sympathetic branch of the ANS is based on
the parasympathetic branch function is to return the body to balance (homeostasis)
neurotransmitters for the adrenergic (sympathetic) response
epinephrine and norepinephrine
Medications that affect the ANS will…
either trigger or block an autonomic response
Adrenergic Agonists
often referred to as sympathomimetic drugs because they “mimic” the actions of the sympathetic nervous system.
Mechanism of Action of Adrenergic Agonists
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.
Non-selective α and β Agonists uses and action
- 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
α1 agonist uses and action
Decongestants
-Stimulate α1 receptors causing vasoconstriction and thereby decreasing congestion in the area
α2 Agonists uses and action
Treatment of glaucoma
-Stimulates α2 receptors causing a decrease in intraocular pressure
β1 Agonists: uses and action
Treatment of cardiac arrest and hypotension
-Stimulates β1 receptors causing an increase in heart rate, force of cardiac contraction, and cardiac conduction
β2 Agonists: uses and actions
Bronchodilators
-Stimulate β2 receptors, decreasing bronchoconstriction and causing bronchodilation
adrenergic drug cautions and side effects
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)
Beta-receptor - general
(non-specific)
ex: eye
- effect
- beta agonist
- beta antagonist
-effect
relaxes ciliary muscle
-beta agonist
non specific agonists: isoproterenol
epinephrine
-beta antagonist
propranolol
timolol
nadolol
b1 selective drugs
ex: myocardium
- effect
- beta agonist
- beta antagonist
-effect
increases contractility
increases heart rate
-beta agonist
norepinephrine
-beta antagonist
metoprolol
atenolol
b2 selective adrenergic drugs
ex: lungs
- effect
- beta agonist
-effect
bronchodilation
-beta agonist bronchodilators: fenoterol albuterol terbutaline
Alpha-receptor - general
ex: vascular smooth muscle
- effect
- beta agonist
- beta antagonist
-effect
skin and skeletal muscle vessel constriction
-beta agonist
epinephrine
norepinephrine
-beta antagonist
phentolamine
a1 drugs
ex: vascular smooth muscle
- effect
- beta agonist
- beta antagonist
-effect
vasoconstriction
-beta agonist
phenylephrine
-beta antagonist
prazosin
a2 drugs
ex: vascular smooth muscle
- effect
- beta agonist
- beta antagonist
-effect
Opposes α1 vasoconstriction Inhibits NE release
Decreases adrenergic activity
-beta agonist
clonidine
-beta antagonist
yohimbine
Neuromuscular blocking agents
affect the somatic nervouse system by inducing paralysis
Depolarizing neuromuscular blocking agents
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
Nondepolarizing neuromuscular blocking agents
find in a competitive but non-stimulatory manner to part of the ACH receptor as a result these drugs do not cause muscle twitches
Succinycholine
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
Vecuronium
a non-depolarizing neuromuscular blocker that produces paralysis
Onset action of 30 seconds
Duration of action of 30 minutes
Pancuronium
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
Adrenergic Agonists (sympathomimetics)
stimulates the adrenal medulla to release norepinephrine and epinephrin which stimulate one of two types of sympathetic receptors dopaminergic receptors and adrenergic receptors
Dopiminergic receptors
produce dilation of renal, coronary and cerebral arteries there are no medication’s that specifically target these receptors
3 categories of bronchodilators
β2 agonists
Anticholinergics
Xanthines
β2 Agonists
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
short acting β2 Agonists
can be used about 15 minutes prior to exercise or exposure to a known trigger as a preventative measure
common examples: *salbutamol,
terbutaline,
salmeterol
long acting β2 Agonists
onset is slower but effects last 12 hours
common example: formoterol
Anticholinergics
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
common anticholinergics
*ipratropium bromide
combined *ipratropium bromide
salbutamol
Xanthines
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
common Xanthines
theophylline,
aminophylline
common uses of all bronchodilators
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
bronchodilator cautions
Short acting β2 agonists should only be used as required; not as a regular or daily drug
bronchodilator Side Effects
CNS stimulation — anxiety, insomnia, restlessness, tremors
Cardiac stimulation — tachycardia, palpitations, hypertension
May precipitate angina, myocardial infarction, and dysrhythmias
Nausea and vomiting
Abdominal cramps
bronchodilator drug interactions
Beta blockers may block the effect
Monoamine oxidase inhibitors and tricyclic antidepressants may potentiate effects
what is the preferred receptor to treat respiratory emergencies
beta 2 because they produce smaller increases in heart rate and force of contraction which decreases the body’s rate of oxygen consumption
what is a well known CNS Stimulant which is also a Xanthine
caffeine
common decongestants and cold products
pseudoephedrine
dextromethorphan
diphenhydramine
Antianginal agents
are used to treat a cardiac condition called angina
Angina
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
Three main classes of antianginal agents are:
*Nitrates (currently only class that can be administered by PCP)
Beta-blockers
Calcium channel blockers
Nitrates
can relieve symptoms of ischemic heart disease, but are not a cure for it.
nitrates MOA
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
Vasodilation results in:
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
common uses of nitrates
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
common examples of nitrates
*Nitroglycerin
cautions of nitrates
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
drug interactions with nitrate
Viagra®
Cialis®
Levitra®
Beta Blockers
another treatment and management used for angina.
They are effective with angina pectoris, but are not effective when used for vasospastic angina.
Beta Blockers MOA
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.
common uses of beta blockers
Reducing the severity and frequency of exertional angina attacks
Post myocardial infarction
common examples of beta blockers
Metoprolol
Atenolol
Timolol
cautions of beta blockers
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
Calcium Channel Blockers
Calcium channel blockers are another treatment used to help treat and manage angina.
Calcium Channel Blockers MOA
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
Calcium Channel Blockers common uses
Angina
Variant angina (Prinzmetal’s angina and vasospastic angina)
Common Examples of Calcium Channel Blockers
Verapamil
Diltiazem
Nifedipine
cautions of Calcium Channel Blockers
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.
Chronotropic effect
Inotropic effects
Dromotropic effects
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
Cardiac glycosides
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
Antidysrhythmic medications
used to treat and prevent cardiac rhythm disorders further classified into four groups according to the fundamental mode of action on the heart
four groups of antidysrhythmic medications
Sodium channel blockers
Beta blockers
Potassium chanel blockers
Calcium channel blocker’s
Sodium channel blockers effect on heart
slow the conduction through the heart (negative dromotropic effect)
Beta blockers effect on heart
reduce the adrenergic stimulation of the beta receptors
Potassium channel blockers effect on heart
increase the heart contractility (positive inotrophy) and work against the reentry of blocked impulses
Calcium channel blockers effect on heart
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)
thrombolytics
designed to break down (lyse) the clot and improve client outcomes if given shortly after the development of the clot
Anticoagulants
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
MOA of anticoagulants
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
Common Examples of anticoagulants
*Heparin (monitor only)
Low molecular weight heparins
Warfarin
common uses of coagulants
During or after surgeries
A combination of anticoagulants may be used when a patient is first beginning oral anticoagulant therapy
anticoagulants cautions
When doses are too high the following bleeding may result:
Bleeding gums
Nosebleeds
Easy bruising
Platelet inhibitors
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.
MOA of platelet inhibitors
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
TXA2
thromboxane A2 a type of thromboxane with prothrombotic properties
Common Examples platelet inhibitors
*ASA
Dipyridamole
Ticlopidine
Clopidogrel
Common Uses platelet inhibitors
Primary prevention of a myocardial infarction
Prevention of a reinfarction in patients with previous myocardial infarction history
Prevention of thrombotic stroke
Cautions platelet inhibitors
Increased risk of gastrointestinal bleeding and hemorrhagic stroke
Increased risk of bleeding
fibrolytic agent
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
two different classifications of medications used to stop preterm labour, induce labour, or control postpartum hemorrhage
uterine stimulants and uterine relaxants.
Uterotonics
given to facilitate uterine contraction
MOA of uterotonics
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.
Common Uses of uterotonics
Induce or speed up labour
Facilitate contractions following a spontaneous abortion
Treat postpartum hemorrhage
Common Examples of uterotonics
*Oxytocin® (monitor only)
Misoprostol
Syntometrine
Ergometrine
Cautions of uterotonics
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.
oxytocin
Naturally occurring hormone that has multiple reproductive functions
it increases the force and frequency of contractions
used to reduce postpartum haemorrhage
tocolytic medication
Suppress the force and frequency metre and contractions
ex: magnesium sulfate
ex: terbutaline
magnesium sulfate
Relaxes the smooth muscles including those in the uterus
terbutaline
Beta agonist that has been used as a tocolytic agent
Vitamin and Electrolyte Supplements
The body is unable to synthesize vitamins and electrolytes and must, therefore, rely on an adequate and constant supply through diet
MOA of Vitamin and Electrolyte Supplements
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
Vitamin A
Required for production of rhodopsin which enables specialized retinal cells (rods) to adapt to dim light
Vitamin D
Regulates serum calcium levels in conjunction with parathormone and calcitonin
Vitamin E
Prevents formation and accumulation of toxic metabolites; maintenance of red blood cell membranes
Vitamin K
Synthesis of blood clotting factors II, VII, IX, X
Vitamin B
Necessary for cell reproduction and maturation
Vitamin C
Involved in formation of catecholamines, steroids, and conversion reactions
Sodium
Helps to maintain normal fluid balance
*Potassium
Maintains cell structure and function; regulates muscle function (monitor only)
Calcium
Plays role in muscle contraction, blood coagulation and bone formation
Hydrogen
Regulates acidity and alkalinity of body fluids
Cautions of Vitamin and Electrolyte Supplements
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.
Antihypoglycemic Agents
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.
MOA of Antihypoglycemic Agents
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
common uses of Antihypoglycemic Agents
Hypoglycemia
Common Examples of Antihypoglycemic Agents
- Glucagon
- D5/D10
- D50W
- Oral glucose
Cautions of Antihypoglycemic Agents
Ensure that glucose levels are monitored before and after administration
Antimicrobials
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
General Guidelines for Use of Antimicrobials
Take as directed for the full course of treatment
Space doses evenly apart
Be aware of compliance issues, reinfection, and superinfection
Antibiotics
Antibiotics or antibacterial drug classes are used to treat bacterial infections
Each antibiotic drug is generally effective for only certain pathogenic bacteria
Types of Antibiotics
Beta-lactam Sulfonamide Tetracycline Macrolide Aminoglycoside Fluoroquinolone Miscellaneous
type of Beta-lactam antibiotics
Penicillins
Cephalosporin antibiotics
Carbapenem antibiotics
MOA of antibiotics
Preventing cell wall synthesis (penicillins)
Blocking the synthesis of folic acid (sulfonamides)
Interfering with protein synthesis (tetracyclines, macrolides, aminoglycosides)
Interfering with DNA synthesis (quinolones)
common uses of antibiotics
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
cautions of antibiotics
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.
Antivirals
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
Types of Antivirals
Viral DNA Polymerase Inhibitors
Antiretrovirals
- -RNA Reverse Transcriptase Inhibitors
- -Protease Inhibitors
Viral Uncoating Blockers
MOA of antivirals
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).
Common Uses of antivirals
Treatment of herpes
Decrease HIV virus production (antiretrovirals)
Influenza A prophylaxis
Cautions of antivirals
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.
Antifungals
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.
Types of Antifungals
Azole
Nystatin
Amphotericin B
Terbinafine
MOA of antifungals
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.
Common Uses of antifungals
Skin and mucus membrane infections
Systemic fungal infections
Nail fungal infections
Cautions
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
Medications used to treat HIV
Classified as antiretrovirals
- Nucleoside reverse transcriptase inhibitors:
- Non nucleoside reverse transcriptase inhibitors:
- Protease inhibitors
Antidotes and Neutralizing Agents
Antidotes and neutralizing agents are administered in poisoning and overdose situations in an attempt to antagonize or inactivate the substance
MOA of Antidotes and Neutralizing Agents
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
Common Uses of Antidotes and Neutralizing Agents
Intentional and accidental overdose and poisonings
Common Examples of Antidotes and Neutralizing Agents
- 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
cautions of Antidotes and Neutralizing Agents
Most poisons have no specific antidote, so care must be supportive in nature, focus on prevention of further absorption, and promote poison elimination
common medication classifications that affect the gastrointestinal system
Antacids, Antiflatulents, Digestants, Antiemetics, Laxatives Antidiarrheals
Antiemetics
Antiemetic is a classification of medication used to control nausea and vomiting in patients
N/V is typically triggered by four main mechanisms:
Stimulation of the cerebral cortex and limbic system.
Stimulation of the chemoreceptor trigger zone (CTZ).
Stimulation of the vestibular system.
Stimulation of peripheral pathways.
how Stimulation of the cerebral cortex and limbic system. cause n/v
The common causes of this type of N/V are increasing intracranial pressure, irritation of the meninges and emotional stress
how Stimulation of the chemoreceptor trigger zone (CTZ). cause N/V
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.
primary neurotransmitters within the chemoreceptor trigger zone (CTZ)
Dopamine (D2), Serotonin (5HT3) and Neurokinin (NK1) are the primary neurotransmitters within this area of the brain.
How Stimulation of the vestibular system. cause n/v
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.
how Stimulation of peripheral pathways. causes N/V
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.
5-HT3 receptor antagonist
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.
H1 Histamine antagonist
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.
Some common examples of antiemetics are:
- Gravol (H1 Histamine antagonist)
* Ondansetron (5-HT3 receptor antagonist)
