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234 Cards in this Set

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  • Back
Describe the food drug and cosmetic act
born 1938
empowered the food and drug administration to enforce and set premarket safety standards
when did the comprehensive drug abuse prevention and control act started
1970
Schedule 1 drugs
High abuse potential
No medical indications
Heroin, LSD, Mecaline
Schedule 2 drugs
Highe abuse
accepted medical indications
Opium, cocaine, morphine,codeine , oxycodone, methadone,
schedule 3 drugs
less abuse potential
Vicodin or tylenol with codeine
schedule 4 drugs
Low abuse potential
Diazepam, lorazepam, phenobarbital
schedule 5 drugs
lower than schedule 4 for abuse potential
includes limited amounts of opiods for cough aor diarhea
6 rights of medication
right medication
righe dose
right time
right route
right patient
right dicumentation
Pharmocokinetics
how a drug is absorbed
pharmocodynamics
how a drug interacts with the body
the Pharmocokinetic processes
Absorption
Distribution
Biotransformation
Elimination
Enteral route
delivery of a medication throug the gastrointestinal tract
Parenteral route
delivery of a medication outside of the gastrointestinal tract
( needles)
efficacy
a drugs ability to cause the expected response
summation
the additive effect
two drugs given together that have the same effect
Synergism
two drugs that both have the same effect are given together to produce a response greater than the sumof their individual responses 1+1=3
Potentiation
one drug enhances the effect of another
Factors affecting drug response relationship
age
body mass
sex
environment
time of administration
Pathology
genetics
psychology
what do alpha 1 receptors do
cause peripheral vasoconstriction
mild bronchoconstriction and stimulation of metabolism
What do the alpha 2 receptors do
stimulation of these receptors is inhibitory they serve to prevent over release of norepinephrine in the receptors
What does the Dopaminergic receptors do
vasodilation (increased blood flow at the kidney)
how do you figure an infusion rate over time (example 500 ml over one hour
Volume x drip factor
divide by Time
how do you calculate infusion rates example 2mg per
min of lidocane
Volume x drip x desired dose
divide by dosage on hand
what is the antidode for aspirn overdose
mucamist
Chemical name
describes the drugs chemical composition and molecular structure
Generic name
name given by the us adopted name council
trade name
the drug has a registered trademark , use of the name restricted by he drugs patent owner (usually the manufactruer)
Pharaceutics
the study of how various drug forms influence pharmacokinetic and pharacodynamic activities
Pharmocokinetics
the study of what the body does to the drug
-absorption
-distribution
-Metabolism
-Excretion
Pharmocodynamics
The study of what the drug does to the body
- the mechanism of drug actions in living tissues
Pharaceutical phase
disintegration of dosage form Dissolution of drug in body
Pharacodynamic phase
drug receptor interaction
Pharmacotherapeutics
the use of drugs and the clinical indications for drugs to prevent and treat diseases
-Empirical therapeutics
-Rational therapeutics
Pharmacognosy
the study of natural (plant and animal) drug sources
Pharmaceutic
Dosage form, design affects, dissoulution
pharmaceutic aid

substances which are of little or no therapeutic value, but are necessary in the manufacture, compounding, storage, etc., of pharmaceutical preparations or drug dosage forms. They include solvents, diluting agents, and suspending agents, and emulsifying agents. Also, antioxidants; preservatives, pharmaceutical; dyes (colouring agents); flavoring agents; vehicles; excipient; ointment bases.
Drug absorption rates for PO administration
liquids
suspensions
powders
capsules
tablets
coated tablets
enteric coated tablets
Factors that effect absorption
Food and fluids
Dosage fromulation
status of the absorptive surface
rate of blood flow to the small intestine
acidity of the stomach
status of gi motility
Routes of drug administration
enteral (gigu)
parenteral
topical
Enteral route
oral
sublingual
buccal
absorbed through small intestine
First pass effet
the metabolism of a drug and its passage from the liver into the circulation, a high first pass effect would be giving an oral route med, it is processed by liver before reaching target. IV meds prevent first pass effect
Parenteral route
IV
IM
Sub q
ID
intrathecal
inraarticualr
transdermal can be parentaeral too
Topicla route
skin
eyes
ears
nose
lungs
rectum
vagina
Dustribution
the trasport of a drug in the body by the bloodstrea to its site of action
areas of rapid distribution
muscle
skin
fat
areas of rapid distribution
heart
liver
kidneys
brain
Metabolism or biotransformation
the biochemicla transformaion of a drug into an inactive metabolite, a more soluble compound or a more potent metabolite ,
liver , muscle , kidneys , lungs , plasma ,intestinal mucosa
Biologic transformation of a drug into an
inactive metabolit
more soluble compound
more potent metabolite
Factors that decrease metabolism
cardiovascular dysfuncion
renal insufficiency
starvation
obstructive jaundice
slow acetylator
erythromycin or ketaconazole drug therapy
Factors that increase metabolism
fast acetylator
barbiturate therapy
rifampin therapy
areas of rapid distribution
muscle
skin
fat
areas of rapid distribution
heart
liver
kidneys
brain
Metabolism or biotransformation
the biochemicla transformaion of a drug into an inactive metabolite, a more soluble compound or a more potent metabolite ,
liver , muscle , kidneys , lungs , plasma ,intestinal mucosa
Biologic transformation of a drug into an
inactive metabolit
more soluble compound
more potent metabolite
Factors that decrease metabolism
cardiovascular dysfuncion
renal insufficiency
starvation
obstructive jaundice
slow acetylator
erythromycin or ketaconazole drug therapy
Factors that increase metabolism
fast acetylator
barbiturate therapy
rifampin therapy
A Drug
is any chemical that can affect living processes
Therapeutics
the medical use of drugs
The ideal drug
Effectiveness
Safety
Selectivity
Seven important aspects of drug therapy
Assessment
Dosage and administration
Evaluating and Promoting effects
Minimizing adverse effects
and interactions
Prn decisions
Managing toxicity
three ways that a substance can cross cell membranes
passing throgh channels and pores for very small molecules
2, transport systems for selective carriers that may or may not use atp
3,direct penetration of the cell membrane (like dissolves like)drugs that are lipid soluble will pass through due to the phospholipid layers of the cells
Ph dependent ionization
the idea that an acid will be unionized in acidic media but will in an alkaline environment
ion trapping (ph partitioning
drugs will accumulate on whichever side of the membrane that favors their ionization. with this we can determine which environment a drug will accumulate (using Ph dependent ionization)
Factors that control Distribution
1,Blood flow to tissues
2,Exiting the vascular system at capillary beds
3,Typical capillary beds, Drugs pass between cells
4, the blood brain barrier
5,placenta -same as blood brain
6, protein binding, albumin is important drugs that bind stay in the system for a long time and can be a source of drug interaction
7,Some drugs must enter cells to reach sites of action
Concepts of metabolism
1,most drugs are metabolised in the liver
2,Metabolism makes it possible for the kidney to excrete many drugs that otherwise could not
3,Activation of prodrugs, which is a drug that is not active until conversion in the body
4,increased or decreased toxicity
Factors that influence rate of metabolism
Age, hepatic maturation doesnt occur until about a year old
2,induction of drug metabolizing enzymes, which increases the metabolism causing the need for an increased dose for that drug and other drugs given at the same time
3,First pass effect, hepati inactivation of certain oral drugs
4,Nutritional status
5, competition between drugs
Concepts of renal drug excretion
Glomerular filtration and
passive tubular reabsorption,causing drugs that are lipid soluble to undergo passive rabsorption.
2, active tubular secretion
Factors that modify renal drug excretion
Ph dependent ionization, by manipulating urine ph can promote the ionization of a drug can decrease passive rabsorption.
3,competition for active tubular transport
4,Age infants have a limited capacity to excrete drugs
5,time course of drug responses
6,plasma drug levels
Non renal routes of drug excretion
breast milk
bile, lungs, sweat, saliva
Describe the significance of drug plasma levels
used to estimate the concentration of a drug at the action site by checking plasma concentration
Therapeutic range
keeping the drug within this range is the goal, a narrow therapeutic range makes things hard
Drug half life
the time required for the amount of a drug in the body to decrease by 50%
Loading doses
used when a plateau must be reached quickly
Describe the decline from plateau
when a drug is discontinued 94% of a drug will be eliminated over an interval of 4 half lives
Maximal efficacy
the largest effects that a drug can produce
relative potency
the amount of a drug that must be given to elicit an effet
Drug receptor
any functional macromolecule in a cell to whic a drug binds to produce its effecs
what do drugs do at receptors
mimic or block the action fo the bodys own regulatory molecules
Describe drug receptors and selectivity of drug action
if drugs interact with only one kidn of receptor than effects will be limited but it can still produce a variety of effects so selectivity does not guarantee safety
simple occupancy theory
the intensity of the response to a drug is proportional to the number of receptors it occupies.
Affinit
the strength of the attraction between a drug and its receptor (high affinity makes a very potent drug)
Agonist
activate receptors,,

mimics the bodys regulatory processes
atagonist
prevent receptor activation
noncompetitive antagonist
bind irreversibly to receptors and reduce maximal response that an agonist can produce
competitive antagonist
bind reversibly to receptors competing with agonists for binding sites
partial agonists
have moderate intrinsic activity, acts as antagonists as well as agonists
types of analgesics
nsaids and opiods
what is pain
whatever the patient says it is and where the patient says it is, very unpleasant
Pain threshold
the level of stimulus needed to produce the perception of pain , a measure of the physiologic response of the nervous system
Pain tolerance
the amount of pain a patient can endure without its interfering with normal function, subjective response
classification of pain by onset and duration
Acute pain and chronic pain
classification of pain
somatic
visceral
superficial
vascular
referred
neuropathic
phantom
cancer
psychogenic
central
Pain transmission gate theory
uses the anology of a gate to describe how impulses from damaged tissues are sensed in the brain
Tissue injury causes the release of what
bradykinin
histamine
potassium
prostaglandins
serotonin, all of these stimulate nerve endings starting the pain process
what are the two types of nerves stimulated
A and C fibers
what regulates the type of apin a person feels
A and C fibers in damaged areas
where is the location of the gate in reference to pain
Dorsal horn, which is the point of spinal cord entry to the brain
What does the gate do in reference to pain and what happens when you shut the gate
regulates the flow of sensory impulses to the brain
closing it stops the impulses
What does activation of large diameter A fibers do
closes the gate and limits perception of pain
what does activation of smal diameter C fibers do.
opens the gate which allows impulse transmission to the brain and causes pain perception
What dos the nerve fibers from the brain that inervate the gate do with regards to pain perception
allows the brain to evaluate, identify and localize the pain. It controls the gate before the gate is open.
what does the body produce to inhibit transmission of a pain.
Produce Enkephalins and Endorphins that bind to the opoid receptors.
what does rubbing a painful area do
Stimulates the large sensroy fibers (A fibers) this closes the gate, pain reduced
Opioid analgesics
pain relievers that contain opium form the opium poppy
(Narcotics)
Agonist
bind to opioid pain receptor in the brain (reduction of pain)
Partial agonist
bind to pain receptor cause weaker neurologic response (mixed agonist)
Antagonist
reverse the effects of these drugs on pain (competitive antagonists)
What are the five types of opiod receptros
MU
Kappa
Delta
Sigma
Epsilon
What are some other uses for opiod anagesics
cough suppression
diarrhea
balanced anesthesia
Analgesics contraindications
allergy
asthma or resp problems
intracranial pressure
pregnance
Opioid analgesics adverse effects
pupil constriction
N/V
respiratory depression
constipation
itching
flushing
urinary retention
drugs that bind to opiod receptors and prevent a response
Naloxone
Naltrexone
opiates physical dependence and tolerance
need larger doses for same effect because of the physical adaptation of the body
Opiate psychologic dependence
the need for the drug for effect other than pain relief
Opioid withdrawal syndrom
extreme pain and irritability, like a bad flu
Acetaminophen
analgesic adn antipyretic effects,
no aniinflammatory effects
why use aetaminophen
great for people that cant have apirin
gets rid of pain by blocking prostiglandin synthisis
reduces fever
(lethal whith overdose, antidote is acetylcysteine regimen) do not excede 4000 mg per day
What are anesthetics
drugs that depress the central nervous system
muscle relazation
depression of consciousness
loss of sensory stimulation
What is anesthesia
state of depressd cns activity
General anesthetics what are the two types
inhaled (volatile liquids or gasses that are vaporized in oxygen and inhaled and injectable
What are adjunctive drugs to general anesthetics
sedative hypnotics (benzoe)
opioids (morphine)
Neuromuscular blocking drugs
Anticholinergics (atropine)
what is general anesthetics used for
surgical procedures,
unconsciousness
muscle relaxation
what are the adverse effects of general anesthetics
myocardial depresson is commonly seen also effects the peripheral circulation, liver, kidneys, respiratory tract.
could also cause malignant hyperthermia ( 104 temp and tachypnea, tachycardia and muscle rigidity)
what are local anesthetics for
block nerve impulses to a certain area
topical
parenteral
spinal
infiltration
nerve block
topical
paralysis occures in what order when using aneshtetcs
1) autonomic activity is lost
2) pain and other sensory functions are lost
3) motor activity is the last to be lost
(when the drug wears off recovery occurs in the reverse order)
what are NMBAs
prevent nerve transmission to certain muscles resulting in paralysis these are used with anesthetic during surgery
How does succinylcholine work
it isa the only depolarizing drug, works lik acetylcholine causing depolarization. but the metabolism is slower than ACh. so if it is present repolarization cannot occur
what do Nondepolarizing NMBAs do
prevent ACh form acting at the neuromuscular junctions. Nerve cell membrane is not depolarized so the muscle fibers are not stimulated and contraction does not occure
what is the order of paralysis for NMBAs
muscle weakness
paralysis of small rapidly moving muscles (fingers and eyes)
Paralysis of limbs, neck and trunk
Paralysis of intercostal muscles and diaphragm
(recovery is in reverse order)
flaccid paralysis
NMBAs indications
maintaining controlled ventilation during surgery
ET tube
reduce muscle contraciton in an area that needs surgery
Diagnostic for myasthenia gravis
adverse effects of NMBAs
hypotension due to the releaseof histamine and tachycardia due to the blockade of muscarinic receptors
describe moderate sedation or conscious sedation
combo of benzos and opiates
anxiety and sensitivity to pain are reduceed and patient cannot recal procedure, this is nice because the airway is maintained and patient can follow comands
what are some important nursing implications for a patient with sedation
teach the patient how to breath deep and talk about what they may feel or hear monitor for reacitons and vital signs make sure to orientate during recovery
Epilepsy
Chronic recurrent pattern of seizures
Seizure
episode of abnormal electrical activity in the nerve cells of the brain
Convulsions
involuntary spasmodic contraction of any or all voluntary muscles throughout the body
describe Primary or idiopathic epilepsy
the cause cannot be determined
Accounts for more than 50% of cases
Describe secondary epilepsy
Distinct cause identified
trauma, infection, cerebrovascular disorder
what is a partial seizure
short alterations in consciousness
confusion
repetitive unusual movements (chewing or swollowing)
what is simple seizures
No impaired consciousness
Face arm and leg motor movements
Sensory Hallucinations
Personality changes
What are complex seizures
Impaird consciousness
Memory impaiment
behavioral effects
Aura, chewing and swollowing movements
Tonic clonic activity
what are generalized seizures
both ceerebral hemispheres involved
brief loss of consciousness with no confusion
head drop or falling down symptoms
tonic clonic and spasm possible
patient stares off into space
Antiepileptic Drugs
Known as anticonvulsants
usuall life long treatment for control of seizures
how do the AEDs work
prevent generation of spread of electrical discharge and protect surrounding nomal cells, the idea is thought to be that they alter movement of sodium, potassium, adn calcium across neve cells in the brain,
IV phenytoin should only be used with what iv fluid
Normal Saline
What is parkinsons disease
chronic, progressive, degenerative disorder that effects the dopamine producing neurons in the brain. This is cause by an imbalane of two neurtransmitters (Dopamine and Acetylcholine) DECREASE IN DOPAMINE AND INCREASE IN ACETYLCHOLINE
When does Parkinsons diseas start showing symptoms
when about 80% of the dopamine that is stored in the substantia nigra of the basal ganglia is depleted
what is needed for Parkinsons to be controled (Partially)
Functioning nerve terminals that can take up dopamine
Symptoms of Parkinsons Disease
Bradykinesia (slowness)
Rigidity
Tremor Postural instability
Dyskinesia
Difficulty in performing voluntary movements
1 Chorea, irregualr,spasmodic involuntary movements of the limbs or facial muscles.
2.Dystonia, abnormal muscle tone leading to impaired or abnormal movements
Describe the on and off phenomenon with PD (Parkinsons Disease)
rapid mood swings in response to levdopa
PD worsens with too little dopamine
Dyskinesia occurs when too much is present
This is a progressive disease
Describe Levodopa therapy
It is a precursor of dopamine
Because of the blood brain barrier, exogenously supplied dopamine can not enter but levodopa can. It is taken up by the dopaminergic terminal and converted into dopamine, therapy nonfunctional between 5 and 10 years
What is the goal with the drug therapy for Parkinsons
1)increase levels of dopamine
2) antagonize or block the effects of ACh
3) Slow the progression of the disease
What drug catagories are used for parkinsons disease
Anticholinergic
Antihistamines
Dopamine receptor agonist that are direct acting like levodopa and indirect acting like MAO-B inhibitors and COMT inhibitors
what does MAOIs like SELEGILINE do for parkinsons disease
MAOIs break down catecholamines in the CNS
If you block one like MAO-B you get an increase in the levels of dopaminergic stimulation in the CNS (these are used as adjunct therapy) and use can delay unresponsiveness to levodopa therapy
MAOIs adverse effects
usually mild
nausea, lightheadedness, dizziness, abdominal pain, insomnia, confusion, dry mouth
(doses higher than 10 mg may cause a hypertensive crusis)
Three types of Dopaminergic therapy for parkinsons
Replacement (presynaptic)
Direct acting/replacement
indirect acting
Carbidopa
this is given with levodopa to stop the breakdown of it befor reachin the target in the brain. part of presynaptic therapy
Indirect acting Dopaminergic therapy causes what
the release of dopamin from the storage sites at the end of the nerve cells that are still intact and blocks reuptake into the nerve endings (more dopamine will than be available) SYMMETREL is a drug that does this
why is it important to use COMT inhibitors like TOLCAPONE AND ENTACAPONE
COMT is the enzyme responsible for the breakdown of levodopa
Describe direct acting Dopaminergic therapy
Directly stimulates the dopamine receptors and stimulate the production of more dopamine
What does Anticholinergic therapy do
blocks ACH
used to treat muscle tremors and rigidity
Why does ACh accumulate in PD
because of the lack of Dopamine this causes pill rolling and tremors and rigidity
Anticholinergic therapy indications
treatment of PD
treatment of drug induced extrapyramidal reaction to certain antipsychotic drugs
Anticholinergic side effects
Drowsiness, confusion, disorientation, constipation, nausea, vomiting,urinary retention,blurred vision, (DILATED PUPILS AND PHOTPHOBIA AND DRY SKIN)decreased salivation
Patient teaching with regard to PD drugs
drink plenty of fluids and watch for side effects
Avoid vit B6 in amounts greater than 10mg
If taking levodopa with MAOIs watch for hypertensive crisis
DO NOT stop drug use suddenly
Levodopa may darken the urine and sweat.
COMT inhibitor effect only take a few days
DRUG HOLIDAYS
what are sedatives
drugs that have an inhibitory effect in the cns
they reduce Nervousness
Excitability and Irritability
All of this without causing sleep
What are Hypnotics
Cause sleep
A sedative can become a hypnotic if it is given in large enough doses
Barbiturates
Introduced in 1903
used for insomnia and sedation
Habit forming
Low therapeutic index
Replaced with benzodiazepines
4 categories of barbiturates
Ultra short, for short surgery
Short, sedative or hypnotic adn control of convulsive conditions
Intermediate, same as short
Long, same as intermediate
Barbiturates mechanism of action
site is reticular formation in the brainstem
It inhibits GABA,
nerve impulses traveling in the cerebral cortex are also inhibited
Barbiturates effects
Low doses= sedative effects
Highe doses= hypnotic effects (this will lower resp rate)
They are notorious enzyeme inducers, that is they stimulate liver enzymes that cause the metabolism or breakdown of many drugs that results in a shortened duration of action.
Indications for barbiturates
hypnotics
sedatives
anticonvulsants
anesthesia for surgery
Barbiturates adverse effects
CNS depression
Respiratory depression
Upset GIGU
Agranulocytosis, hypotension
Stevens Johnson syndrome
Reduced REM sleep causing agitation and stress
what can barbiturate overdose lead to
respiratory arrest
sleep, coma, death
What can very large doses of barbiturates be used for
Anesthesia induction
Uncontrollable seizures
(phenobarbital coma)
Describe some barbiturate drug interactions
ETOH, antihistamines, benzos,opioids,tranquilizers will all have additive effects
MAOIs will prolong effects of barbiturates.
The increased metabolism will reduce anticoagulant response leading to clot formation.
What is the most frequently prescribed sedative hypnotic
Benzodiazapines because of the favorable drug effects. like not suppressing REM sleep as much and not increasing metabolism of other drugs.
Classification of Benzodiazepines
sedative-hypnotic
Anxiolytic
What are the benzodiazepine types
long acting
short acting
There are also nonbenzodiazepine hypnotics that share many characteristics of benzodiazepines, they are used to treat insomnia
Mechanism of action for benzodiazepines
Depress CNS activity affecting hypothalamic, thalmic and lmbic system.
there are benzodiazepine receptors
Benzodiazepines drug effects
calming the CNS
Inducing sleep
Induce skeletal muscle relaxation
Benzodiazepine indiations
Sedation
Sleep induction
Skeletal muscle relaxation
Anxiety relief
treatment of alcohol withdrawal
Agitation
Depression
Epilepsy
Balanced anesthesia
Moderate conscious sedation
Benzodiazepines adverse effects
Headache
Drowsiness
Dizziness
Vertigo
Lethargy
Hangover effect
rebound insomnia if for a few days if you quit
Muscle relaxants indications
muscle spasms
Multiple sclerosis,cerebral palsy
How do muscle relaxants work
CNS is the site of action
Acts directly on skeletal muscle
Closely resembles GABA
dantrolene (Dantrium)
Malignant hyperthermia crisis
Muscle relaxant adverse effects
Euphoria
Lightheadedness
Dizziness
Drowsiness
Fatigue
Muscle weakness
GABA
In vertebrates, GABA acts at inhibitory synapses in the brain
Drugs that act as agonists of GABA receptors (known as GABA analogues or GABAnergic drugs) or increase the available amount of GABA typically have relaxing, anti-anxiety and anti-convulsive effects
psychotherapeutics
the treatment of emotional and mental disorders
psychotherapeutic drug types
antianxiety drugs
antidepressants
antimanic drugs
antipsychotics
what are the three main emotional and mental disorders
Psychoses
Affective disorders
Anxiety
Affective disorders
(mood disorders)
abnormally pronounced emotions, Bipolar disorder
Psychosis
emotional disorder that impairs the mental function.
loss of contact with reality
what is anxiety
unpleasant state of mind
sense of dread and fear
response to negative situations
what are the 6 anxiety disorders
Obsessive-compulsive disorder
Posttraumatic stress disorder
Generalized anxiety disorder
Panic disorder
Social phobia
Simple phobia
Biochemical ibalance theory
mental disorders are associated with abnormal levels of endogenous chemicls such as neurotransmitters in the brain
Catecholamines
Dopamine
Norepinephrine
Indolamines
Serotonin
Histamine
biochemicals necessary for normal mental function
GABA
Acetylcholine
Sodium, potassium, magnesium
Treatment for benzodiazepine overdose
flumazenil
Drug of choice for treatment of mania
lithium
What does antimanic drugs like lithium do
Thought to potentiate serotonergic neurotransmission
Biogenic amine hypothesis
Depression and mania are due to alteration in neuronal an synaptic catecholamine concentration at adrenergic receptor sites in the brain;
Depression=deficiency of catecholamine especially norepinephrine
Mania=excess amines
Permissive hypothesis
Affective disorders are due to decreased concentrations of serotonin.
Depression results from decreased serotonin and catecholamine levels
Mania results from increased catecholamin but decreased serotonin levels
Dysregulation hypothesis
Depression and other affective disorders result from a failure in the regulation of catecholamine activity
How do selective serotonin reuptake inhibiters work
increase serotonin concentrations at nerve endings, no cardio effect
New gereration antidepressants indications
Depresson
Bipolar disorder
Obesity
eating disorders
OCD
anxiety disorders
Newer generation antidepressants adverse effects
H/A, dizziness, tremor, nervousness, insomnia, FATIGUE
GIGU problems
WEIGHT GAIN AND WEIGHT LOSS
sexual dysfunction
Serotonin Syndrome causes
Delirium
agitation, Tachycardia, sweating, hyperreflexia, muscle spasms, shivering, course tremors, Hyperthermia, seizures, renal failure, rhabdomyolysis, Dysrhythmias, DIC
Newer generation antidepressant drug interactions
bound to plasma proteins
Compete with other protein binding drugs.
inhibition of cytochrome p-450 system
MAOIs
Mechanism of action of tricyclics
block reuptake of neurotransmitters, causing accumulation at the nerve endings. It is thought that increasing concentrations of neurotransmitters will correct abnormally low levels that lead to depression
increasing norepinephrine when you block the reuptake of it will cause
antidepressant effect and tremors, tachycardia etc
increasing serotonin when you block the reuptake of it causes
antidepressant effect and H/A anxiety, nausea, sexual dysfunction
An overdose of first generation antidepresants )(cyclics)results in what
death CNS and cardio systems are affected death results from seizures or dysrhythmias
there is no specific antidote, just BLS and charcoal
MAOIs
considered second line treatment for depression not responsive to cyclics but has potential to cause hypertensive crisis when taken with tyramine
MAOIs mechanism of action
inhibit the MAO enzyme system in the CNS, because of this amines like dopamine, serotonin, and norepinephrine are not broken down. which may help depression
MAOIs adverse effects
ORTHOSTATIC HYPOTENSION
tachy, dizziness, insomnia, blurred vision, nausea, drowsiness,
MAOIs overdose treatment
symptoms appear 12 hours after ingestion,
tachycardia, shock, seizures, coma.
Protect brain and heart with gastric lavage, urine acidification, hemodialysis
What should you avoid when taking MAOIs
Tyramine, it can cause a hypertensive crisis...
Some foods to avoid
mature cheese
smoked meat
yeast
red wines
italian broad beans
what could concurrent use of MAOIs and SSRIs lead to
Serotonin syndrome
How do you avoid serotonin syndrome
there should be a 2 to 5 week wash out period
Antipsychotics
drugs used to treat serous mental illness
behavioral problems or psychotic disorders
How do Antipsychotics work
they block dopamine receptors in the brain(limbic system, basal ganglia) areas associated with emotion, cognitive function, motor function.
Because of the lower Dopamine levels in the CNS a tranquilizing effect is caused
What do newer antipsychotics do
block specific dopamine receptors, D2
Block specific serotonin receptors S2
this improves the safety profile and efficacy
Antipsychotics indications
serious mental illnesses
Movement disorders (tourettes
Nausea
intractable hiccups
Adverse effects, for antipsychotics
sedation, delirium
orthostatic hypotension
syncope, dizziness, EKG changes, photosensitivity, skin rash, hyperpigmentation, pruritus. Dry mouth, constipation, leukopenia and agranulocytosis.
Neuroleptic malignant syndrome, regarding antipsychotics
High fever, unstable BP
myoglobinemia
Extrapyramidal symptoms, regarding antipsychotics
involuntary muscle symptoms similar to parkinsons.
Akathisia(muscle restlessness)
Dystonia (painful muscle spasms)
Tardive dyskinesia, (involuntary contractins of oral and facial musles)
Choreoathetosis(wavelike movements of extremities)
When taking tricyclics what may you need to do before surgery
be weaned and discontinue due to the possible reactions with anesthetic drugs
when should you wear sunscreen
when taking anipsychotics
Stimulants are
sympathomimetic drugs
Analeptics are used for
CNS stimulant
appetite suppressant (anorexiant)
treatment of ADHD
Narcolepsy
Migraine H/A
Adverse effects of stimulants include
palpitations, nausea, dry mouth, urinary frequency, insomnia
Uses for caffeine
Neonatal apnea
respiratory depression in adults
enhance effects of analgesics and migraine medications
CNS stimulation
Rules for taking drugs for ADHD
should be given at least 6 hours before bedtime to reduce insomnia
may cause dry mouth
take on empty somach 45 min before meals
may need drug holidays
keep jounal of response
Rules for serotonin agonist
avoid food cntaining tyramine