The Finny- PHARM Flashcards
What is pharmacology?
Study of drugs that alter functions of living organisms
• Includes pharmacotherapy, pharmacokinetics, pharmacodynamics
Which health care providers are involved in the management, distribution, and education of pharmacology?
Doctors
Dietitians
Pharmacists
PAs
NPs
Nurses
RTs
CNAs
4 major concepts that assist in understanding pharmacology
-Nursing management of drug therapy
-Medication
-Core drug knowledge
-Core patient variables
What is core drug knowledge
Pharmacotherapeutics
Pharmacokinetics
Pharmacodynamics
Precautions/contraindications
Drug interactions
adverse/side effects
Patient/family teaching
What are the core patient variables
Culture
Health status
Inherited traits
Life style
Diet
Life span
Environment
Habits
Gender
CHILD LEHG
What is nursing management of drug therapy
Education and safety
How do we maximize therapeutic effects
Promote absorption
Appropriate time
Lab values
How do we minimize adverse effects
Modify admin
Allergies
Contraindications
Safety checks
Assess pt
Lab values
Adverse effects
DC/withhold
MAC SALAD
Sources/ types of medications
Animal
Plant
Minerals
Synthetic
Semi-synthetic
What are the 3 classifications of drug nomenclature
therapeutic
physiologic
chemical
What classification is categorized by the disease state it is used to treat
Therapeutic classification
Which classification is categorized by the drugs MOA
Pharmacologic
Which drug names are lowercase
generic
Which drug names are uppercase
Brand-Trade names
What is the USP-NF
The United States Pharmacopeia - National Formulary
What is the purpose of the USP-NF
Sets the standards for drugs / reviews drugs
Not a government agency
What information about drugs should be included during pt teaching?
Drug name
Reason drug was prescribed
Intended effects
Adverse/ side effects
7 parts of a med order
Pt name
Order date/time
Name of drug
Dosage
Route
Frequency
HCP signature
7 rights of med administration
Right:
Pt
Med
Dose
Route
Time
Reason
Documentation
What is Pharmacotherapeutics
Achievement of the desired therapeutic goal from drug therapy
The indication for giving the drug- right reason
What is Pharmacokinetics
Effects of the BODY on the drug
absorption
distribution
metabolism
excretion
What is Pharmacodynamics
The effects of the DRUG on the body
Variables that affect drug action
Toxicology
What is enteral
By way of the intestines
What is Parenteral
By way other than the intestines
What is absorption
movement of the drug from the site of administration into the bloodstream
What factors affect absorption
Dosage
Route
GI Function
Lipid solubility
Blood flow
Surface area
pH
Food
Dr. GLBS fish food
What route is absorbed faster than IM and Subcut
IV
Geri pH is
more alkaline
Geri GI motility is
Slowed
Reduced blood flow
What is distribution
Movement of drug into cell
What factors affect distribution
Tissue availability
Blood flow
Protein binding
Solubility
Does the blood brain barrier have a low or high selectivity
Highly selective
Geris lean body mass is
Decreased
Geris fat is
Increased
Geris body water content is
Reduced
Geris protein binding sites are
Reduced
Geris BBB is
Less effective
What is metabolism
Conversion of the drug into another substance or substances
Metabolites
What effect limits drugs effect due to break down by liver
Hepatic first pass effect
What INCREASES metabolism
Inducers
What DECREASES metabolism
Inhibitors
Geris liver is
Decreased in size/ mass
Decreased blood flow- decreased metabolism
What is excretion
Removal of the drug
What is clearance
Rate of disappearance
Both renal and hepatic
Geris renal filtration is
Decreased- reduced blood flow/ decrease in nephrons
What is half life
Time it takes for 50% of drug to be eliminated
Protein binding
60-89%
Moderate
Protein binding
Above 89%
High
Protein binding
Below 30%
Low
The relation between the effective dose and lethal dose
Therapeutic index
In between peak and trough
Therapeutic index
Adverse effect can happen if there is not enough_____
for drugs to attach to
Albumin
Po drugs absorb where
small intestine
What is an agonist
Promote function
Stimulate the cell to act
What is an antagonist
Block function
Block something else from attaching to and causing an effect
Antidotes
What factors contribute to distribution
Protein binding
Blood flow
Tissue availability
Drugs ability to leave the body depends on what
Protein binding
What factors affect metabolism
First pass effect
Inducers
Inhibitors
Liver damage/aging
Name some inhibitors
Benadryl/ grapefruit
Name some inducers
Tobacco/ St. John’s wort
A damaged liver causes what
High levels of active drug / toxicity
The main mechanism drugs use to cause their effect on the body
Binding with receptors
What is the study of biological, chemical, physiologic interactions of a drug in the body
Pharmacodynamics
What is receptor theory
Drugs exert their effects by binding with receptors
What is a Physiochemical reaction
Binding either stimulates or inhibits normal cell functions
(Agonist vs. antagonist)
Direct
Describe changes in the permeability of cell membrane to one or more ions:
Ion channels open or close
(Calcium channel antagonists)
Direct
Drugs that modify the synthesis, release, or inactivation of neurohormones that regulate physiologic processes
Acetylcholine
Norepinephrine
(Indirect)
Non receptor drugs
Antacids- act chemically
Anticancer Drugs- structurally similar to nutrients required by the body; interfere with normal cell function
Osmotic diuretics- increase osmolarity
Metal chelating agents- combine with toxic metals
Variables that affect drug action
Potency
Serum drug level
Therapeutic index
Efficacy
Maintenance vs. loading dose
MEC
P STEMM
Drug-diet admin times
30 mins before or after meal
Specific drugs: 1hr before or 2 hrs after
What are additive effects
Combine to create a bigger effect than what was originally desired
What is synergism
Help each other produce the desired effect
What is displacement
When drugs that are high protein bound fight compete for protein binding
One drug displaces another
Pt related variables
Preexisting conditions
Ethnicity
Psych factors
Genetics
Weight
Age
Gender
PEP G SWAG
What occurs with to much therapeutic effect
Adverse effects
What are adverse effects
Undesired response to a drug
What drugs have adverse effects
All drugs
What is the strongest FDA warning
Black box warning
Toxicity results from what
Excessive amounts of a drug
May damage body tissue
Name different types of toxicity
cardiotoxicity
ototoxicity
ocular damage
immunotoxicity
hepatotoxicity,
nephrotoxicity,
neurotoxicity
Subcut landmarks
the upper posterior area of the arm
Anterior aspects of the thighs
abdomen 2 inches away from the navel
lateral abdomen
Subcut needle length and gauge
25-30 G
3/8” - 1”
IM landmarks
IM needle length and gauge
20-25 G
5/8”-1.5”
3 purposes for intra dermal injections
Skin testing (drug/allergy sensitivities)
Determine presence of microorganism
Local anesthesia
Intradermal landmarks
Lightly pigmented, thinly keratinized, hairless skin (thinner skin)
Ventral forearm
Outer aspect of the upper arms
Scapular area of back
Upper chest
Intradermal equipment
TB or 1mL syringe
1mL calibrated in 0.01 increments (usually 0.01 to 0.1mL injected)
TB syringe most common
26 -27 G
3/8” - 5/8”
How do you hold the skin for an intradermal injection
Taut
What angle do you insert the needle during an intradermal injection
5-15 degrees
Which way should the bevel face during an intradermal injection
Up
What should be visible during an intradermal injection
The needle should be visible under the skin
What is a bleb or wheal
The bubble that forms during an intradermal injection
How should you inject & remove the needle during an intradermal injection
Slowly
How long should you massage the area after an intradermal injection
NEVER
What is pain
A sensory and emotional experience associated with actual or potential tissue damage
Whatever the patient says it is
Pain is based on what
The individuals previous experience and social, environmental, and cultural influences
What are noiceptors
Afferent neurons
Place where the sensation of peripheral pain begins
Where are nociceptors found
Skin
Muscle
Connective tissue
What are the 2 types of nociceptors
A-Delta fibers
C-fibers
What fibers are small
A-Delta
Which fibers respond to mechanical stimuli
A-Delta
Which fibers sense dull pain
C-fibers
Which fibers sense sharp pain
A-Delta fibers
Which fibers sense burning pain
C-fibers
Which fibers respond quickly to acute pain
A-Delta fibers
Which fibers are myelinated
A-Delta fibers
Which fibers sense pinching pain
A-Delta fibers
Which fibers sense stinging pain
A-Delta fibers
Which fibers are slow
C-fibers
Which fibers are unmyelinated
C-fibers
Which fibers respond to mechanical stimuli
A-Delta fibers
Which fibers respond to mechanical chemical stimuli
C-fibers
Which fibers respond to hormonal stimuli
C-fibers
Which fibers respond to thermal stimuli
C-fibers
Which fibers sense aching pain
C-fibers
Which fibers transmit sensations with touch or temp
A-Delta fibers
What med is used for fever pain and inflammation
Ibuprofen
What med is used for fever, mild pain, and has no anti-inflammatory actions
Acetaminophen
Para-aminophenol derivative
Which med is 99% protein binding
Ibuprofen or acetaminophen
Ibuprofen
High doses of acetaminophen can cause what
Compromised renal function
What is the antidote for acetaminophen
Acetylcysteine
What can increase risk for bleeding in patients taking ibuprofen
(Drug-natural)
Ginger
Garlic
Ginko
Chamomile
What pain med is the best choice for those on blood thinners
Acetaminophen
What med is the best choice for those with hypersensitivity to aspirin, NSAIDs, and are intolerant to GI
Acetaminophen
What legislation:
Designated drugs that must be prescribed by a HCP and separated into prescription and non-prescription classes
1952
Durham-Humphrey amendment
What legislation:
Was the first law directed towards controlling addiction
1914
Harrison Narcotic Law
What legislation:
Provided regulation regarding the manufacture and distribution of certain drugs
1914
Harrison Narcotic Law
What legislation:
Regulated distribution of narcotics and categorized narcotics
1970
Comprehensive Drug Abuse Prevention and Control Act
What legislation:
Established the DEA
1970
Comprehensive Drug Abuse Prevention and Control Act
What legislation:
Established 5 categories (schedules)
1970
Comprehensive Drug Abuse Prevention and Control Act
What is schedule 1
What is schedule 2
What is schedule 3
What is schedule 4
What is schedule 5
MEDS:
Schedule 1
Heroin
LSD
weed
MEDS:
Schedule 2
Opioid analgesic
Morphine
Meperidine (Demerol)
MEDS:
Schedule 3
Tylenol with codine
Ketamine
Anabolic steroids
MEDS:
Schedule 4
Xanax
valium
Ativan
Ambien
tramadol
pentazocine
anticonvulsants
Muscle relaxers
Sedatives
MEDS:
Schedule 5
Antidiarrheal
Antitussives with small amounts of narcotics (codeine)
Nursing Implications for scheduled meds
The count: inventory must match
The record: narcotic sheet
Co-signing all discarded and wasted meds: another RN
All controlled substances locked
- narcotics double locked
Myths associated with pain
Pain increases as we age
Pain is a psych issue made up in the pts head
Taking an opioid will lead to addiction
Addiction is the most serious adverse effect
Major complication arising from morphine administration
Light headedness
Dizziness
Confused
Sedation
Hypotension
N/V
Constipation
Respiratory depression
Fall risk
What is PQRST
Provoking factor-cause
Quality- feels like
Radiate/relief- does it move? Any relief?
Severity- scale 1-10
Timing- how long? Constant? Intermittent?
Best practice for analgesic dosing:
Morphine
-Assess pain
-Re-assess frequently
-PRN- best if dosed routinely around the clock to ensure constant blood levels of analgesia (joint decision between pt and RN)
Best practice for analgesic dosing:
Codine
Assess respiratory function
When would you not give codine
When a pt needs to cough to clear airway because it depress cough reflex
Education for a pt who is fearful that they will become addicted to pain meds
Educate pt that their chances of becoming addicted if they take the pain med as prescribed are slim to none
How is the nervous system divided
Central nervous system (CNS)
Peripheral nervous system (PNS)
What system deals with the nerves of the brain and spinal cord
CNS
What system deals with the nerves OUTSIDE of the brain and spinal cord
PNS
How is the PNS subdivided
Afferent
Efferent
What are Afferent neurons
Carry impulses from the periphery to the CNS
What are efferent neurons
Carry impulses from the CNS to the periphery
How are efferent neurons divided
Somatic
Autonomic
Describe somatic
Voluntary
Skeletal muscle control
innervates skeletal muscles and controls voluntary movements
Describe autonomic (ANS)
Involuntary
Automatic
controls involuntary activity in smooth muscle, secretory glands and the visceral organs of the body (heart, stomach, kidneys, fallopian tubes)
How is the autonomic (ANS) divided
SNS
PSNS
What is the main function of the autonomic (ANS)
maintain constant internal environment
respond to stress
repair body tissues
Involuntary control of smooth muscle, heart, exocrine
glands (Glands that produce secretions for the surface of
an organ. Ex. Sweat glands, salivary glands)
Adrenergic refers to what
SNS
Cholinergic refers to what
PSNS
What are neurotransmitters
transmitters of nerve impulses
chemicals that transmit signals from a neuron to a target cell (across a synapse)
neurotransmitters bind with what
receptors on an effector organ/tissue to bring about an action of respective NS
What is an effector organ
an organ or cell that carries out a response from a nerve impulse
Are neurotransmitters exogenous or endogenous
Endogenous
chemicals that originate inside the body
The primary neurotransmitters in the SNS
norepinephrine (NE)
epinephrine (Epi)
The primary neurotransmitters in the PSNS
acetylcholine (ACh)
Most common NT of SNS
Norepinephrine
Mainly made in adrenal medulla
(made from norepi)
Epinephrine
Both NT & hormone
Epinephrine
Norepinephrine
Acts more like a hormone
(although sm. amounts made in nerve)
Epinephrine
Mostly made inside nerve axons
Norepinephrine
Synthesized from dopamine and released into blood as hormone
Norepinephrine
Acts mostly on alpha receptors
Norepinephrine
Acts on both alpha and beta receptors
Epinephrine
Only released during times of stress
Epinephrine
continually released into circulation at low levels as hormone
Norepinephrine
used for treating:
low BP assoc w/ septic shock
ER tx of allergic reactions
eye surgery to maintain dilation
Epinephrine
Most prevalent NT in body
Acetylcholine
NT Dominated by the PSNS
Acetylcholine
NT Crucial for arousal, learning, memory and motor function
Acetylcholine
Binds to muscarinic receptors
parasymp response
Acetylcholine
acts as an excitatory NT in skeletal muscle
Acetylcholine
Names for adrenergic drugs
adrenergic neurotransmitter (NE)= Norepinephrine
sympathomimetics
adrenergic agonists
alpha or beta adrenergic agonists
adrenergic
Names for Cholinergic drugs
Cholinergic neurotransmitters= Acetylcholine
parasympathomimetics
cholinomimetic
cholinergic agonists
cholinergic
What receptor does Acetylcholine attach to to bring about a PSNS response
muscarinic
What receptor does Acetylcholine attach to to bring about excitatory muscle contraction
Nicotinic
Direct acting drugs do what
directly stimulate receptor
Indirect acting drugs do what
stimulate neurotransmitter to be released and attach to receptor site
Adrenergic Receptors: action
Alpha 1 receptors
Vasoconstriction
Adrenergic Receptors: action
Alpha 2 receptors
Stop norepinephrine
Adrenergic Receptors: action
Beta 1 receptors
Tachycardia
Adrenergic Receptors: action
Beta 2 receptors
bronchodilation
alpha 2 agonist do what
lower blood pressure
Because the function of the alpha 2 receptor is
to stop NE (a vasoconstrictor).
So, in alpha 2 receptors, you would want an agonist to
promote the function of vasodilation which in
turn will then lower blood pressure.
Adrenergic Agonist Drugs:
Are absorbed how?
Rapidly after injection
In ER situations Adrenergic Agonist Drugs are given how
IV for rapid onset
Adrenergic Agonist Drugs can not be given by what route
PO
Adrenergic Agonist Drugs duration
Short
Can Adrenergic Agonist Drugs pass the BBB
No
Adrenergic Agonist Drugs lose effectiveness if given with what type of drug
Adrenergic Antagonists
Adrenergic Agonist Drugs cause increased risk of HTN if given with what meds
meds that increase HTN including OTC and herbal therapies (caffeine)
Nursing implications for Adrenergic Agonist Drugs
establish baseline status
(pulse, BP, lung sounds, RR, urine output, lab tests)
Monitor pt response closely
Nonselective adrenergic agonist
Epinephrine
Beta 2 agonist
Albuterol
Alpha 2 adrenergic agonist
Clonidine
What does it mean if a drug is nonselective
All receptors can be activated
Epinephrine Pharmacotherapeutics
Shock
Cardiac emergencies
Asthma
Used for tx low BP assoc w/ septic shock, ER tx of allergic reactions, & also used during eye surgery to maintain dilation
Epinephrine stimulate which adrenergic receptors
ALL
Epinephrine causes what
increased BP
increased HR & force of contraction
hyperglycemia
bronchodilation
vasoconstriction of arterioles in the skin mucosa and most viscera
Adverse effects of epinephrine
nervousness
restlessness
tremors
insomnia
angina
arrhythmias
HTN
tachycardia
Classification of epinephrine
nonselective adrenergic agonist
Trade name for norepinephrine
Levophed
Classification of norepinephrine
adrenergic agonist
With predominate alpha agonist effects
Pharmacotherapeutics of norepinephrine
Severe hypotension
Pharmacodynamics of norepinephrine
Has predominate alpha agonist effects and results in potent peripheral arterial vasoconstriction.
Results in increased BP (more than it increases HR, contraction or CO) Causes reduced renal blood flow (which limits long term use)
Pt teaching for adrenergic agonists
If you are receiving IV adrenergic drugs to stimulate
your heart or raise BP:
frequent cardiac monitoring,
HR, BP, urine output are necessary.
Pt teaching for diabetic pts taking adrenergic agonists
monitor your glucose levels carefully because adrenergic medication may elevate them
Adverse effects of adrenergic agonists
diminished renal perfusion and decreased
urine output
decreased liver perfusion with subsequent liver damage due to vasopressor action
cardiac dysrhythmias due to beta1 activity
Hyperglycemia, hypokalemia due to beta1 activity
Severe hypertension and reflex bradycardia
Limb ischemia due to profound vasoconstriction
Beta-Adrenergic Antagonists do what
Prevent stimulation of SNS by inhibiting catecholamines (epi & norepi)
How are Beta-Adrenergic Antagonists grouped
according to their selectiveness
(selective or nonselective)
Nonselective Beta-Adrenergic Antagonists affect what
Beta 1 receptor sites (mainly in heart)
Beta 2 receptor sites (bronchi, blood vessels, uterus)
[(blocks) Bronchodilation]
Selective Beta-Adrenergic Antagonists affect what
Specific receptor site
Primarily affect beta 1
Tachycardia, inotropy (increased force of contraction)
Beta-Adrenergic Antagonists end in what
-lol
Beta-Adrenergic Antagonists Pharmacotherapeutics
Angina
MI
HTN
Heart failure
Dysrhythmias
Beta adrenergic antagonists action
Antagonizes (blocks) beta receptor sites
Selective Beta adrenergic antagonists what happens with higher doses
cardioselectivity is diminished
May block beta 2 receptors
Beta adrenergic antagonists cause what
Decreased
HR
Force of contractions
Rate of a-v conduction
Side effects
Lethargy
CHF
Decreased BP
Depression
metoprolol is a what
Selective beta 1 adrenergic antagonists
metoprolol Pharmacotherapeutics
Treatment of arrhythmias, HTN, chronic angina, controlled HF.
metoprolol does what
Decreases HR & contractility, slows conduction, suppresses automaticity, and decreases cardiac output.
May block beta 2 receptors in high doses
metoprolol contraindications
Abrupt cessation of med will cause an exacerbation of angina. MI may occur
Maximizing therapeutic effects of Beta adrenergic antagonists
Do not abruptly stop medication
Minimizing adverse effects of Beta adrenergic antagonists
Prior to dose: check the apical and peripheral
pulses.
– Monitor blood pressure, cardiac rhythm
Teaching for diabetic pts taking Beta adrenergic antagonists
Check blood sugar because Beta adrenergic antagonists can mask signs of hypoglycemia
Indirect acting cholinergic agonists drug
Neostigmine
Cholinergic antagonist
Atropine
When Acetylcholine attaches to a receptor, that receptor is always a what
A cholinergic receptor
Either muscarinic or nicotinic
2 types of cholinergic receptors
Muscarinic
Nicotinic
What are muscarinic receptors
Stimulated by Ach & muscarine (alkaloid substance from mushrooms)
bethanechol chloride
Vasodilation & perfusion of organs.
What are nicotinic receptors
Stimulated by nicotine (plant alkaloid) but will
respond to ACh
Nicotinic-N (neuronal-type) receptor stimulation results in what
the release of Epinephrine
Nicotinic-M stimulation results in what
muscle contraction
What NS dominates, maintains homeostasis/internal environment
parasympathetic
Which NS dilates pupils
SNS
Which NS causes tears to flow
PSNS
Which NS constricts pupils
PSNS
Which NS thickens saliva
SNS
Which NS increases HR
SNS
Which NS increases watery saliva
PSNS
Which NS constricts bronchioles and increases secretions
PSNS
Which NS dilates the coronary artery
SNS
Which NS dilates the trachea and bronchioles
SNS
Which NS slows HR
PSNS
Which NS causes the coronary artery to constrict
PSNS
Which NS causes the GI to produce more secretions
PSNS
Which NS increases GI motility
PSNS
Which NS produces sweat
SNS
Which NS constricts blood vessels in the skin and mucous membranes
SNS
Which NS decreases GI tone and mobility
SNS
Which NS causes ejaculation in men
SNS
Which NF contracts the lower colon
PSNS
Which NS contracts the bladder and ureters
PSNS
Which NF stimulates erection in men
PSNS
Which NS contracts sphincters
SNS
Which NS relaxes the uterus and bladder
SNS
Neurotransmitters transmit signals from ___ to ____
Neurons to target cells
What is the most prevalent NT in the body
ACh
Which NT is dominated by the PSNS
ACh
Which NT is crucial for arousal, learning, memory, and motor function
ACh
Which NT transmits parasympathetic signals to end organs
ACh
Which NT will act as excitatory NT in skeletal muscle (nicotinic)
ACh
What are the muscarinic receptors
M1-M5
What do muscarinic receptors do
vasodilation and perfusion of organs
decrease BP
Which receptors are stimulated by nicotine but will respond to ACh
Nicotinic
What are the 2 nicotinic receptors
Nicotinic-N (neuronal type)
Nicotinic-M (muscle type)
Nicotinic-N stimulation results in what
The release of epinephrine
Nicotinic-M stimulation results in what
Skeletal muscle contraction
What do Adrenergic Agonists do
Stimulate all adrenergic receptors
Increase:
BP
HR
Inotropy
Hyperglycemia
Bronchodilation
Vasoconstriction of arterioles in skin
To low BP in association with septic shock
Asthma
Cardiac emergencies
ER tx of anaphylactic shock
Eye surgery to maintain dilation
What is the sub classification of epinephrine
Nonselective adrenergic agonists
What is the sub classification of norepinephrine
Adrenergic agonist with predominant alpha agonist effects
What does norepinephrine do
Helps with severe hypotension
Predominant alpha agonist effects result in potent peripheral arteriole vasoconstriction
Results in:
Increase BP
Can cause reduced renal blood flow
What is metoprolol sub classification
Beta adrenergic antagonist (Beta Blocker)
Selective to Beta 1
What does metoprolol do
Antagonizes beta receptor sites
Cardioselectivity is diminished with higher doses and will cause activity at Beta 2 receptors
- causing lung constriction
Tx:
Arrhythmias
HTN
Chronic angina
Controlled HF
Decreases HR and contractility
Slows conduction
Suppresses
Automaticity
Decreases cardiac output
What is propranolol
Adrenergic antagonist
Is propranolol selective or nonselective
Nonselective
What does propranolol do
Antagonizes beta receptor sites
What is neostigmine
indirect acting Cholinergic agonist
What is the sub classification of neostigmine
Indirect acting cholinergic agonist
What is bethanechol chloride
Direct acting cholinergic agonist
What does bethanecol chloride do
TX:
Urinary retention- increase muscle tone in bladder to allow for bladder emptying
Helps you pee
What is atropine
Cholinergic antagonist
What does atropine do
Helps clear secretions
specifically targets muscarinic cholinergic receptors
Antidote for overdose of cholinergic agonist:
Strong inhibitor of cholinergic receptors
-Brings pt back to baseline
Increases HR
Decrease secretions
Enlarged pupils
Contracts bladder and GI
Decrease GI motility
Drowsiness
What happens when you stimulate cholinergic receptors in the eye
Pupils constrict
What happens when you stimulate cholinergic receptors in the GI
Increase secretions
Increase motility
Lower colon contracts
What happens when you stimulate cholinergic receptors in the GU
Ureters and bladder contract
Increased urine output
Erection in men
What causes cholinergic crisis
Too much cholinergic stimulation (agonists)
What is an issue in cholinergic crisis
Respiratory compromise
S/S of cholinergic crisis
Muscle weakness - prolonged contraction
Slows breathing
Other parasympathetic effects
What is the antidote for cholinergic agonists
Atropine
What are excessive effects of atropine
Mad as a hatter- confusion/ delirium
Blind as a bat- pupils constrict
Red as a beet- flushed face, tachycardia
Dry as a bone- decreased secretions, thirsty
How do small doses of atropine effect the body
Bradycardia
Decreased secretions
- gets rid of death rattle, but can cause mucus plug
How do high doses of atropine effect the body
Tachycardia
Beta adrenergic antagonist inhibit what
Catecholamines
How are beta adrenergic antagonists grouped
By their selectiveness
Adverse side effects of metoprolol
Common:
bradycardia
Hypotension
Depression
Serious:
Bronchoconstriction
Bronchospasm
Common side effects of any cholinergic antagonist
Dry mouth
Constipation
Urinary retention
Blurred vision
Cholinergic antagonist prototype
Atropine
What herbal/ OTC medications increase the effectiveness of atropine
Senna (herbal laxative)
Aloe
What do you assess for in Geri’s taking atropine
Cholinergic antagonists
Increased temp - Due to suppression of perspiration and heat loss
Nervousness
Weakness
Confusion
Excitement
What do you assess for in kids taking cholinergic antagonists
Increased temp
Hyperpyrexia
Due to suppression of perspiration and heat loss
Atropine teaching
Avoid high temps
Drink water frequently
Rinse mouth frequently
Hard candy- dry mouth
Void before taking medication
Visit ophthalmologist regularly
Notify HCP- for fever or severe weakness
