NURS 2550 Test
Which of the following is not a medication error?
Wrong strength/concentration
Wrong infusion rate
Wrong duration of treatment
Wrong environment
90% of all medication errors are due to? Choose all that apply.
Human factors such as not having the knowledge about the medications
Communication mistakes such as miscommunciation of oral or written orders
Name confusion
Not knowing how the patient looks
Which of the following is not a category of medication errors?
Medication administration rights
System issues with the environment of where the med is being prepared, the prescribers writing and medications dispensing systems
Knowledge and understanding
Education on safety
What ways can you reduce and prevent medication errors? Choose all that apply.
Culture of safety, education and transparency
The infrastructure by using pharmacists in high risk areas and providing healthcare providers with available information
Estimating the abbreviations and the dose
The use of verbal orders
Use infusion pumps that don't have free-flow protection
Medication reconciliation is where
Medications that a patient takes at home is compared to the list of new meds being prescribed
Medications that a patient takes at home doesn't need to be compared to meds being prescribed
New medications that a patient is prescribed are compared to old medications
None of the above
What is pharmacodynamics?
The intensity and nature of response once drug gets to site
The amount of drug that gets to the site
The response of the drug once it gets to the site
The intensity of response of drug once it gets to site and the amount of drug that gets to the site
The principles of drug actions are? Choose all that apply
Interacts with receptor
Alters the physiological process
Have more than one effect
Have less than one effect
Alters psychological process
What do non-receptor mediated interactions result of?
Chemical interactions such as laxatives
Physical interactions such as antacids
Chemical and physical interactions such as laxatives and antacids
Physical, chemical and electrical interactions such as laxatives and antacids
What are the steps of the receptor process?
Receptor to ligand binding, Signal transduction, cellular responses and changes in gene expression
Receptor to ligand binding, signal transduction, changes in gene expression and cellular responses
Signal transduction, receptor to ligand binding, cellular responses and changes in gene expression
Signal transduction, receptor to ligand binding, changes in gene expression and cellular responses
How do drugs bind to receptors instead of ligand?
Drug + Receptor <--> Drug-Receptor complex -> Response
Drug -> Receptor -> Drug-Receptor complex -> Response
Drug + Receptor --> Drug-Receptor complex -> Response
None of the above
What is included in a drug interactions? Choose all that apply
Receptors are normal points of control of cell function
Receptor function is normally regulated by molecules supplied by body
Drugs mimic or block the effect of the endogenous compounds at the receptor
A drug can't make the body do something new, only help the body help itself
None of the above
Which primary receptor family is an endogenous drug that attaches to receptor site on cell membranes and effects the inside cell and on the cell to use energy?
Cell membrane
Ligand-gated ion channels
G protein-coupled receptor systems
Transcription factors
Which primary receptor family is an endogenous drug that attaches to receptor site on cell membranes and creates channels to allow movements of ions to pass in or out of the cell based on the concentration?
Cell membrane
Ligand-gated ion channels
G protein-coupled receptor systems
Transcription factors
Which primary receptor family is an endogenous drug that attaches to receptor site on cell membranes or pocket, goes through cell membrane 7 times, stimulates G protein and binding proteins stimulates defector to stimulate response?
Cell membrane
Ligand-gated ion channels
G protein-coupled receptor systems
Transcription factors
Which primary receptor family is found inside the nucleus not on the cell membrane and the endogenous hormone goes inside cell when released, penetrates cell membrane, attaches to receptors, goes through transcription and the messenger RNA goes through a process to create proteins for drug to be created?
Cell membrane
Ligand-gated ion channels
G protein-coupled receptor systems
Transcription factors
What structure does the drug receptor interaction depend on? Choose all that apply.
Drug resembles a natural ligand or receptor
Binds to receptor
Controls rate of process
Chemical and physical structure
What is simple occupancy theory? Choose all that apply.
Intensity of response to a drug is proportional to the number of receptor occupied by that drug
Maximal responses occur when all available receptors have been occupied
Doesn't explain why some drugs work better than others, therefore modified occupant theory was created
Can account the differences between efficacy and potency
Based on affinity and intrinsic activity
What is modified occupancy theory? Choose all that apply.
Accounts for the differences between efficacy and potency
Affinity is used to determine the strength of attraction and explains potency
Intrinsic activity is used to determine the activation once bound to receptor and explain efficacy
Intensity of response to drug is proportional to the number of receptors occupied by drug
Maximal responses occur when all available receptors have been filled
The lock is ______ and the key is ______ in the lock and key theory.
Drug, receptor
Receptor, drug
Drug, cell membrane
Cell membrane, drug
In the lock and key theory, affinity is ______ and intrinsic activity is _______.
Open, fit
Fit, open
Closed, fit
Fit, closed
What happens with the long-term use of drugs with the dynamic receptors?
Increase or decrease the number or sensitivity of receptors
Increase the number or sensitivity of receptors
Increase the sensitivity and action of receptors
Decrease the number and action of receptors
What is down regulation?
Occurs with an agonist that causes loss of effect/tolerance
Occurs with an agonist and due to increased sensitivity causes withdrawal
Occurs with an antagonist that causes loss of effect/tolerance
Occurs with an antagonist and due to increase in sensitivity causes withdrawal
What is up-regulation?
Occurs with an agonist that causes loss of effect/tolerance
Occurs with an agonist and due to increased sensitivity causes withdrawal
Occurs with an antagonist that causes loss of effect/tolerance
Occurs with an antagonist and due to increase in sensitivity causes withdrawal
What is the selectivity of drug receptor interactions? Choose all that apply.
Each receptor participates in only a few physiologic processes
More selective, more desirable
More selective, less desirable
One drug or ligand may act at more than one receptor
One drug or ligand may act at less than one receptor
What does an agonist do?
Mimics natural ligand and uses affinity and intrinsic activity
Mimics natural ligand and uses affinity only
Blocks natural ligand and uses affinity and intrinsic activity
Blocks natural ligand and uses intrinsic activity only
What is the difference between partial and full agonist?
Partial agonist is more active than natural ligand and full agonist is less active than natural ligand
Full agonist is more active than natural ligand and partial agonist is less active than natural ligand and can act as either agonist or antagonist
Partial agonist is more active than natural ligand and can act as antagonist and full agonist are less active than natural ligand
Partial agonist is less active than natural ligand and full agonist are more active than natural ligand and can act as antagonist or agonist
What does an antagonist do?
Blocks natural ligand and uses affinity and no intrinsic activity
Blacks natural ligand and uses affinity only
Mimics ligand and uses affinity and intrinsic activity
Mimics ligand and uses intrinsic activity only
What is the first phase in the dose of a drug and the physiological response (dose—response relationship)?
Large increase dose, small increase effect
Small increase dose, large increase effect = Therapeutic range
Increase dose, no effect = Maximal efficacy
None of the above
What is the second phase in the dose of a drug and the physiological response (dose—response relationship)?
Large increase dose, small increase effect
Small increase dose, large increase effect = Therapeutic range
Increase dose, no effect = Maximal efficacy
None of the above
What is the third phase in the dose of a drug and the physiological response (dose—response relationship)?
Large increase dose, small increase effect
Small increase dose, large increase effect = Therapeutic range
Increase dose, no effect = Maximal efficacy
None of the above
What is the difference between efficacy and potency?
Potency is max effect of drug and efficacy is the amount of drug to achieve specific effect
Efficacy is the max effect of the drug and potency is the amount of drug to achieve specific effect
What is the standard therapeutic dose?
ED50 - Effective dose in half of population
ED25 - effective dose in quarter of population
LD50 - Effective dose in half of population
LD25 - effective dose in quarter of population
What is the therapeutic index of a drug? (LD is from animals and ED is from humans)
LD25/ED25
LD50/ED50
ED25/LD25
ED50/LD50
What is the measure of safety for the therapeutic index of a drug?
Room between therapeutic and dangerous dose
Rooms between maximal efficacy and dangerous dose
When the therapeutic dose and dangerous dose overlap
When the maximal efficacy and dangerous dose overlap
According to DSM-V what are the top 2 clinical features of major depressive disorder? Choose all that apply.
Depressed mood
Lost of interest or pleasure in daily activities for more than 2 weeks
Suicidal
None of the above
What is the pathogenesis of MDD? Choose all that apply.
Complex and not understood
Completely understood
Factors come from genetics, self esteem and up bringing of child
Factors come from environment, siblings and friends
Comes from reason or triggered by life events
Triggered by life events but doesn't come from reasons
What is monoamine deficiency? Choose all that apply.
Deficiency in monoamine neurotransmitters
Type of endogenous compound that act as neurotransmitters
Are a neurotransmitters
Examples are NE, Epinephrine, Serotonin and Dopamine
Examples are NE, Epinephrine and RE
What are the steps in order of a deficiency in monoamines?
When there aren't enough monoamines there aren't as many released into the synaptic cleft, decrease in monoamines binding to specific receptors located on post synaptic neuron and less reuptake by a dopamine or serotonin transporter & less monoamines sitting on receptors will affect response
When there aren't enough monoamines there aren't as many released into the synaptic cleft, less monoamines sitting on receptors will affect response & decrease in monoamines binding to specific receptors located on post synaptic neuron and less reuptake by a dopamine or serotonin transporter
Decrease in monoamines binding to specific receptors located on post synaptic neuron, when there aren't enough monoamines there aren't as many released into the synaptic cleft & less monoamines sitting on receptors will affect response
None of the above
What is true about Dopamine? Choose all that apply.
The precursor is L-DOPA
Their is no precursor
Two pathways that release dopamine are VTA (frontal lobe and amygdala) and substantial nigra (corpus callosum)
The VTA is the only pathway that release dopamine
Affects perception and mood & rewards motivation and pathway
Initiates movement
Schizophrenia is an increase in dopamine and parkinsons is a decrease in dopamine
Schizophrenia is a decrease in dopamine and parkinsons is a increase in dopamine
What is true about Serotonin? Choose all that apply.
The precursor is L-DOPA
The precursor is 1-trytophan
Another names for Serotonin is 5-hydroxytrytophan
Effects mood, sexual feelings, processing memories, sleep, eating patterns, cognition and serotonergic pathways
Effects the way you move, your dreams, cognition, sleep, physical activity, memory
What are the 3 treatment for MDD?
Medications
Injections
Somatic therapies such as electroconvulsive therapy (ECT) and transcranial magnetic stimulation (TMS)
Psychotherapy specific for depression
Out of the 5 major classes what does Fluoxetine fall into?
Selestive serotonin reuptake inhibitors (SSRIs)
Serotonin/NE reuptake inhibitors (SNRIs)
Tricyclic antidepressants (TCAs)
Monoamine oxidase inhibitors (MAOs)
Atypical antidepressants
Which of the following is NOT a basic consideration for antidepressants?
Timing for a therapeutic response
Dosing for efficacy
Treatment regimens
Suicidal risks
Safety of environment
Which of the following is not a risk for suicidal tendencies on antidepressants?
Increased risk at beginning
Induce suicide
When dosage changes
Making sure you give large amounts out at a time so they don't have to continually refill
Observe patients for checking or squirrelling
What is SSRIs mechanism of action?
Blockade of serotonin reuptake by fluoxetine which can lead to serotonin being more available to bind to and activate post synaptic receptors
Mimic serotonin reuptake by fluoxetine which can lead to serotonin being more available to bind to and activate post synaptic receptors
Blockade of dopamine reuptake by fluoxetine which can lead to serotonin being more available to bind to and activate post synaptic receptors
Mimic dopamine reuptake by fluoxetine which can lead to serotonin being more available to bind to and activate post synaptic receptors
Which of the following is not a therapeutic use for Fluoxetine?
MDD
Bipolar
Panic disorder
Bulimia nervosa
Premenstrual dysphoria
Anxiety
Which of the following is not a pharmacokinetic for Fluoxetine?
Well absorbed with or without food and bound to plasma protein
Metabolized by liver, excreted in urine
Short half life
Takes 4 weeks for plasma levels to reach therapeutic range
4 weeks for drug or metabolite not to be seen in blood
Which adverse effect of Fluoxetine is an increase in serotonergic transmission in brain stem and spinal cord?
Neonatal adverse effects
Extrapyramidal side effects
Serotonin syndrome
Bruxism
Hyponatremia
Which of the following are drug interactions of Fluoxetine? Choose all that apply.
Monoamine oxidase drugs
Tricyclic antidepressants
Anti platelet drugs
Anticoagulants
Ibuprofen
Acetaminophen
Who has a higher risk of ADHD and when do symptoms start?
Boys, 3-7 yrs
Girls, 3-7 yrs
Young adult, 19+
Teenagers, 10-16
What is the pathogenesis of ADHD? Choose all that apply.
Only partially understood
Structural and functional changes in brain
Neuronal pathways which use monoamines to communicate and send signals to nerve cells has difficulty with regulation
Genetics don't play a role
Fully understood
Where in the brain are the structural and functional changes for people with ADHD? Choose all that apply.
Frontal lobe
Basal ganglia
Brainstem and cerebellar
Hippocampus
Occipital lobe
Medulla oblongata
Which is NOT a symptom of inattention?
Failure to give close attention to detail
Difficulty sustaining attention and following instructions
Can organize tasks efficiently
Has a hard time listening
Easily distracted and often forgetful
Which is NOT a symptom of hyperactivity?
Fidgets
Climbs
On the go
Can play with others without problems
Talks excessively
What is NOT a symptom of impulsivity?
Interrupts
Blurts out
Is able to wait their turn
Makes important decisions without thinking of long term consequences
Accident prone
How is ADHD managed? Choose all that apply.
Pharmacological therapy - CNS stimulants (Methylphenidate)
Therapy for child - family, parental education, behavioural
Counsellor
PNS stimulants
Which of the following is not a pharmacological effect of Methylphenidate?
CNS
CVS
Tolerance
Abuse
Physical dependence
Chemical dependence
Which of the following is not a adverse effect of Methylphenidate?
CNS stimulation
CVS
Acute toxicity
Overdose
Chronic toxicity
What is schizophrenia and psychosis?
Disorganized thinking and inability to comprehend
Disorganized thinking and ability to comprehend
Organized thinking and ability to comprehend
Organized thinking and inability to comprehend
Parts of brain associated with Schizophrenia. Choose all that apply.
Positive - occipital, temporal, basal ganglia and auditory system
Positive - limbic system
Negative - limbic system
Postive - occipital, temporal, basal ganglia and auditory system
Cognitive - hippocampus and frontal lobe
Cognitive - hippocampus and occipital love
Which of the following symptoms of Schizophrenia has problems with thinking?
Cognitive
Positive
Negative
Which of the following symptoms of Schizophrenia has exaggerated perception and function base?
Cognitive
Positive
Negative
Which of the following symptoms of Schizophrenia has loss of function and emotion based?
Cognitive
Positive
Negative
What of the following does not relate to first generation antipsychotics for low potency?
Dementia patients can take them
Chlorpromazine
Mechanism of action is to block receptors for D2, NE, Ach and H1
Effects can cause serious movement disorders- extrapyramidal symptoms
Administered 30% orally, 10x higher IM
Hepatic metabolism and excreted in urine
What of the following does not relate to first generation antipsychotics for high potency?
Haloperidol
Different mechanism of action from low potency
Same effects of low potency
Administered 60% oral or IM
Hepatic metabolism and excreted in urine
What do extrapyramidal symptoms cause?
D2 blockade when taking antipsychotics
Mimic D2 when taking antipsychotics
Serotonin blockade when taking antisychotics
Mimic serotonin when taking antipsychotics
Which of the following are symptoms of acute dystonia?
Severe spasms of head muscles
Oculogyric crisis - upward eyes
Opisthotonus - trunk forward and head/lower limbs thrust forward
You can't break joints from muscle spasms
Can impair breathing
Treatment - give anticholinergics to relax muscles
Which of the following are symptoms of Parkinsonism?
Bradykinisia
Mask faces
Drooling, ridgidy
Shuffled gate
Posture is upright
Treatment - giver anticholinergics
Don't give Levodopa - can counteract
Which of the following are symptoms of akathisia
Pacing
Constant squirming
Treatment - Beta blockers, benzodiazepines, anticholinergics, decrease dose of FGA or lower potency
Can develop for first 2 years of treatment
Which of the following are symptoms of Tardive dyskinesia?
Involuntary choreoathetoid - worm like movements of tongue
Does not consist of lip smacking
Overtime, limbs, trunk, toes, fingers are affected
Treatment - none, can decrease anticholinergic drugs or FGA
What are some other side effects of 1st generation antipsychotics? Choose all that apply.
Anticholinergic effects
Neuroleptic malignant syndrome
Orthostatic hypotension
Sedation
Agranulocytosis
Seizures
Sexual dysfunction
Mood disorder
Neuroendocrine effects
Anxiety
Depression
Which of the following is not a drug interactions with first generation antipsychotics?
Anticholinergics
CNS depressants
Levodopa
Dopamine agonists
Dopamine antagonists
Which of the following dos not relate to 2nd generation antipsychotics?
Not for elderly with dementia
Olanzapine
The mechanism for actions blocks receptors for 5HT, D2, ACh, H1and NE
More at risk for developing metabolic effects such as weight gain, diabetes, dyslipidemia and low risk for causing extrapyramidal symptoms
Tardive deskinesia is an early effect risk
Administered rapidly orally, IM95% drug bound to plasma protein, 1/2 life approx 12 hrs
Excreted in urine and feces
Which of the following is not another side effect of 2nd generation antipsychotics?
Sedation
Seizures
Orthostatic hypotension
Agranulocytosis
Anticholinergics effects
Neuroendocrine effects
What is Apripiprazol? Choose all that apply.
Dopamine system stabilizer - partial agonist at 5HP and D2
Fewer adverse effects - metabolized by CYP3A4
Indications - Schizophrenia, bipolar, MDD, agitation, irritability
More adverse effects - metabolized by CYP3A4
Which of the following does not fall under sedative hypnotics?
Depress the CNS
Express/excite the CNS
Used for anxiety and insomnia
Large dose = effects more sedative
Small dose = effects directed to lessen anxiety
Benzodiazepines
What is the physiology of sedative hypnotics?
Limbic system, prefrontal cortex and Gamma-Aminobutyric acid (GABA)
Frontal cortex, limbic system, GABA
Occipital lobe, frontal lobe and GABA
None of the above
What is the pathophysiology of sedative hypnotics?
Anxiety, anxiety disorders and sleep disorders
Anxiety, depression and sleep disorders
Anxiety, anxiety disorders and depression
Anxiety, anxiety disorders and schizophrenia
Which of the following is benzodiazepines not used for?
Primary - anxiety and insomnia
Secondary - anesthesia, manage seizures, manage muscle spasms, help with alcohol with drawl
Tertiary - all of the extrapyramidal effects
What is the mechanism of action of benzodiazepines?
Enhance actions of GABA - GABA binds at receptor chloride, BDZ binds to another receptor to increase channel opening, Cl influx is created from those and flows in cell and cent fire, No GABA no effect
Enhance actions of non inhibitory neurotransmitter - binds at receptor chloride, BDZ binds to another receptor to increase channel opening, Cl flows in cell and cent fire
None of the above
All of the above
What are the effects of Benzodiazepines? Choose all that apply.
Increase GABA activity - decrease CNS activity
Increase dose = different response - low dose affects just brain, increase dose affects more areas and high dose affects CNS in general
General = high dose
Cerebellum = decrease dose
RAS = decrease dose
Limbic = low dose
Which of the following is not an adverse effect for CNS?
Sedation
Sleep related behaviours
Anterograde amnesia
Paradoxical stimulation
Circulatory depression
Which of the following is not an adverse effect for abuse?
Sleep and anxiety
Tolerance
Withdrawl
Non-dependence
Which of the following is not an adverse effect/contraindication?
IV use
Pregnancy, lactation
Sexually active
What is a drug-drug interaction for Benzodiazepines? Choose all that apply.
CNS stimulants
Ex. alcohol
Ex. sugar
Antagonist - flumazenil
Agonist
What happens when the elderly have access to benzodiazepines? Choose all that apply.
Increased risk of dementia
Increased risk of falls and fractures
Helps with dementia
Makes them more stable
None of the above
What is cyclooxygenase (COX)? - over the counter pain medications inhibitors
An enzyme that normally converts arachidonic acid into prostanoids (prostaglandins) and related compounds (prostacyclin)
A neurotransmitter that converts arachidonic acid into prostanoids (prostaglandins) and related compounds (prostacyclin)
An endogenous hormone that converts arachidonic acid into prostanoids (prostaglandins) and related compounds (prostacyclin)
All of the above
What is the process of over the counter pain medications?
Injury to tissues --> phospholipids released --> arachidonic acid --> cyclooxygenase (COX) --> prostanoids, prostacyclin and thromboxane A2
Injury to tissues --> arachidonic acid -->phospholipids released --> cyclooxygenase (COX) -->prostanoids, prostacyclin and thromboxane
Injury to tissues --> phospholipids released --> cyclooxygenase (COX) --> arachidonic acid --> prostanoids, prostacyclin and thromboxane
None of the above
What site does COX cause synthesis of prostaglandins E2 (PGE2) and prostaglandin I2 (prostacyclin/PGI2), promoting inflammations and making receptors in area sensitive to painful stimuli?
Sites where tissues have been injured
Stomach
Platelets
Blood vessels
Kidney
Brain
Uterus
What site does COX promote the synthesis of prostaglandins E2 (PGE2) and prostaglandins I2 (prostacyclin/ PGI2) helping to protect gastric mucosa by: decreasing gastric acid secretion, increase bicarbonate and cytoprotective mucus & maintains blood flow to submucosa
Sites where tissues have been injured
Stomach
Platelets
Blood vessels
Kidney
Brain
Uterus
What site does COX promote synthesis of thromboxane A2 (TXA2) which stimulates platelet aggregation (to form clots)
Sites where tissues have been injured
Stomach
Platelets
Blood vessels
Kidney
Brain
Uterus
What site does COX promote synthesis of PGI2 causing vasodilation
Sites where tissues have been injured
Stomach
Platelets
Blood vessels
Kidney
Brain
Uterus
What site does COX promote synthesis of PGE2 and PGI2 promoting vasodilation
Sites where tissues have been injured
Stomach
Platelets
Blood vessels
Kidney
Brain
Uterus
What site does COX derive prostaglandins mediating fever and helping with the perception of pain
Sites where tissues have been injured
Stomach
Platelets
Blood vessels
Kidney
Brain
Uterus
What site does COX derive prostaglandins help promote contraction of the uterus
Sites where tissues have been injured
Stomach
Platelets
Blood vessels
Kidney
Brain
Uterus
What are the two forms of cyclooxygenase (COX)? Choose all that apply
COX 1, COX 2
COX 2, COX 3
COX 1, COX 3
COX 3, COX 4
Which of the following describes what COX 1 (mostly good) does? Choose all that apply.
Found in most tissues
Protects gastric mucosa
Supports renal function
Promotes platelet aggregation (clotting)
Mediates inflammation
All of the following are negative outcomes of COX 1 except which? (it will be the positive one)
Gastrointestinal erosion & ulceration
Bleeding tendencies
Renal impairment
Risk of developing acute myocardial infarction and stroke
Which of the following are drugs that block COX 1 and 2?
NSAIDs (aspirin, ibuprofen, naproxen)
Acetaminophen
Antidepressants
None of the above
Which drug in Cox 1 can decrease the risk of developing acute myocardial infarction (AMI) and stroke?
Aspirin
Acetaminophen
Ibuprofen
Naproxen
Which of the following describes what COX 2 (mostly bad) does? Choose all that apply.
Mediates inflammation
Makes receptors more sensitive to pain
Produced at sites where tissue has been injured
Mediates fever and pain perception in brain
Supports renal function
Found in tissue
Protects gastric mucosa
Promotes clotting
Promotes vasodilation blood vessels
Can contribute to colon cancer
All of the following are positive outcomes of COX 2 except which two? (It will be negative) Choose 2 answers
Surpasses inflammation
Alleviates pain
Decreases fever
Protects against colon cancer
Renal impairment
Can increase the risk of developing AMI and stroke
All of the following drugs have anti -inflammatory properties in the 1st generation (conventional or traditional) except one which is in 2nd generation (selective). Which is it?
Acetylsalicylic acid (Aspirin/ASA)
Ibuprofen (Motrin/Advil)
Naproxen (Aleve)
Celecoxib (Celebrex)
Which of the following drugs have NO anti-inflammatory properties?
Acetylsalicylic acid (Aspirin/ASA)
Ibuprofen (Motrin/Advil)
Naproxen (Aleve)
Celecoxib (Celebrex)
Acetaminophen (Tylenol)
What is correct about 1st and 2nd generation? Choose all that apply.
1st generation inhibits both COX 1 & 2
2nd generation blocks only COX 2
1st generation only blocks COX 2
2nd generation inhibits both COX 1 & 2
Suppress pain and inflammation
Dont suppress pain and inflammation
1st generation poses serious side effects except which of the following (which would be 2nd generation adverse effect)?
Gastrointestinal erosion and ulceration
Increase the risk of developing AMI and stroke
Bleeding tendencies
Renal impairment
All of the following are uses for Aspirin expect?
Relief of mild-moderate pain
Decrease fever
Decrease inflammation
Dysmenorrhea (painful periods)
Protects against thrombolytic disorders (AMI) and colon cancer in low doses
Relief of severe pain
What is the mechanism of action for Aspirin for when it inhibits COX 1 and COX 2? Choose all that apply.
When inhibits COX 1: decreases risk of AMI and stroke
When inhibits COX 2: decrease pain, fever and inflammation
When inhibits COX 2: decreases risk of AMI and stroke
When inhibits COX 1: decrease pain, fever and inflammation
Which of the following is not a major adverse effect (with long term use) of Aspirin due to inhibition of COX 1?
Increased risk of GI ulceration when: increased secretion of HCL acid and pepsin, decrease cytoprotective mucus, decreased submucosal blood flow and direct irritant action on GI mucosa
Bleeding
Renal impairment
Toxicity
Reyes Syndrome with influenza or chicken pox --> encephalopathy and fatty liver degeneration
Pregnancy complications in third trimester --> premature closure of ductus arterioles in utero
Lukemia (Cancer)
Through pharmacokinetics how is aspirin absorbed?
Well and quickly
Bad and slow
Well and slow
Bad and quickly
Through pharmacokinetics how is aspirin metabolized? Choose all that apply.
Very short half life because acetylsalicylic acid quickly converts to salicylic acid
Very long half life because acetylsalicylic acid converts to salicylic acid slowly
Low therapeutic doses half life for salicylic acid is 2 hours and high dose is 20 hours
Low therapeutic doses half life of salicylic acid is 20 hours and high dose is 2 hours
Through pharmacokinetics how is aspirin distributed?
Bound to plasma protein --> widely distributed to all body tissues and fluids
Not bound to plasma protein --> low distribution to body tissues and fluids
Bound to fatty acid --> widely distributed to body tissues and fluids
Not bound to fatty acids --> low distribution to body tissues and fluids
Through pharmacokinetics how is aspirin excreted?
Kidneys -->more alkaline the pH the more H+ ions are excreted
Kidneys --> more acidic the pH the more H+ ions that are excreted
Liver -->more alkaline the pH the more H+ ions are excreted
Liver --> more acidic the pH the more H+ ions that are excreted
What are the correct plasma drug levels in Aspirin? Choose all that apply
Low therapeutic dose = <100mcg/mL
High therapeutic dose = 150-300mcg/mL (for severe inflammation)
Signs of toxicity = >200mcg/mL and severe toxicity is >400mcg/mL
Severe toxicity is >400mcg/mL
Which of the following is not a drug interaction for Aspirin?
Anticoagulants
Glucocorticoids
Alcohol
Other NSAIDs
Angiotensin-converting enzyme (ACE) inhibitors or Angiotensin II receptor blockers(ARBs)
Vaccines
Grapefruit
Which of the following are contraindications of Aspirin? Choose all that apply.
Bleeding disorder
Peptic ulcer disease
Hypersensitivity to NSAIDs
Pregnancy (3rd trimester)
Children with chicken pox or influenza
Lukemia (Cancer)
Which are the two most common alerts for Aspirin? Choose 2.
Low dose used to prevent preeclampsia (pregnancy complications)
Withdraw 1 week prior to surgery date
Withdraw 2 weeks prior to surgery date
High dose used to prevent preeclampsia (pregnancy complications)
What is the difference between aspirin and non-aspirin?
In non-aspirin, NSAIDs cause reversible inhibition of cyclooxygenase
In Aspirin - NSAIDs cause reversible inhibition of cyclooxygenase
None of the above
What is NOT true about non-aspirin?
Work as an anti-inflammatory, analgesic and anti-pyretic
Does not protect against acute myocardial infraction and stroke
Those hyper sensitive to aspirin are likely to be hypersensitive to non-aspirin
Does not treat fevers, pain or arthritis
What is not true about Ibuprofen?
Inhibit cyclooxygenase
Has anti-inflammatory, analgesics and antipyretic actions
Used for fever, mild to moderate pain and arthritis
Used for severe pain
Better for treating dysmenorrhea (period problems)
Produce the increase in gastric bleeding, decrease platelet aggregation and increases risk for acute myocardial infraction
What is not true about naproxen?
Highly sleeve for COX 1
Long half life - should be given less often
Short half life
Used for arthritis, burritos, tendonitis, dysmenorrhea, fever and mild-moderate pain
Adverse effects are GI disturbances, renal function compromise, prolonged bleeding time, risk of AMI and stroke
What is not true about Ketorolac?
Potent analgesic with minimal anti-inflammatory actions
Pain relief equivalent to opioids but without as many adverse effects
Only for short term, acute pain of moderate-severe intensity (post op)
Suppress prostaglandin synthesis
Given orally or paternally (IV/IM), onset 30 min, peak 1-2 hours and duration 4-6 hours
Adverse reactions are different from NSAIDs
What is not true about Celecoxib?
Used for osteoarthritis, rheumatoid arthritis, ankylosing spondylitis, acute pain, dysmenorrhea, familial adenomatous polyposis (inherited cancer of large intestine)
Not long term management because it can cause CV risks
COX 2 inhibitors don't have CV benefits
Don't inhibit COX 1 therefore do not decrease platelet aggregation (increase risk of AMI and stroke), do not protect the stomach (increase risk for user and bleeding) and don't protect renal function
Good choice for long term management as it prevents CV disease
Interactions may: decrease diuretic effect of furosemide (treat build up of congestive heart failure), decrease antihypertensive effect of ACE inhibitors, warfarin, increase levels of lithium and celecoxib levels may increase by fluconazole (treat fungal infections)
What does Acetaminophen not have? Choose all that apply
Analgesics and antipyretic properties
Inhibits prostaglandin synthesis in CNS
Decrease fever and pain
Inflammatory properties
Suppress platelet aggregation
Decrease renal blood flow or cause impairment
What is the metabolic major pathway for Acetaminophen?
Conjugates with glucuronic acid and other compounds to form non-toxic metabolites & almost all of drug is metabolized at therapeutic doses
Conjugates with glucuronic acid and other compounds to form toxic metabolites & almost all of drug is metabolized at therapeutic doses
Conjugates with glucuronic acid and other compounds to form non-toxic metabolites & only a little bit of the drug is metabolized at therapeutic doses
Conjugates with glucuronic acid and other compounds to form toxic metabolites & only a little bit of the drug is metabolized at therapeutic doses
What is the metabolic minor pathway for Acetaminophen?
Oxidized by cytochrome P450 (enzyme) into a reactive toxic metabolite (only small amount of drug converted into toxic metabolite then converts to non-toxic)
Oxidized by cytochrome P450 (enzyme) into a reactive non-toxic metabolite (large amount of drug converted into toxic metabolite then non-toxic)
None of the above
What is the overdose process?
Large amount of drug is processed by minor pathway --> increase the amount of toxic metabolite as glutathione converts the toxic metabolite to non-toxic form --> it becomes depleted & detoxification stops --> results in increase toxic metabolites --> liver damage
Large amount of drug is processed by major pathway --> increase the amount of toxic metabolite as glutathione converts the toxic metabolite to non-toxic form --> it becomes depleted & detoxification stops --> results in increase toxic metabolites --> liver damage
Large amount of drug is processed by minor pathway --> increase the amount of toxic metabolite as glutathione converts the toxic metabolite to non-toxic form --> it becomes depleted & detoxification stops --> results in increase toxic metabolites --> kidney damage
Large amount of drug is processed by major pathway --> increase the amount of toxic metabolite as glutathione converts the toxic metabolite to non-toxic form --> it becomes depleted & detoxification stops --> results in increase toxic metabolites --> kidney damage
What happens if you overdose on Acetaminophen? Choose all that apply.
Causes liver injury
Cause kidney injury
Signs and symptoms of coma, death and hepatic failure
No signs and symptoms
Symptoms of nausea, vomiting, diarrhea, sweating and abdominal pain
Treatment: Acetylcysteine
No treatment
What are the drug interactions for acetaminophen? Choose all that apply
Alcohol (increase toxic metabolite)
Warfarin (increase bleeding)
Vaccines (decrease immune response)
Marijuana (Increase toxic metabolite)
Anticoagulants (increase bleeding)
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