Final review from discussion questions Flashcards
How does alcohol affect the CYP450 system?
alcohol is an inducer, meaning it increases the speed of metabolism
How does grapefruit juice affect the CYP450 system?
Grapefruit juice acts as an inhibitor, slowing metabolism, leading to drug accumulation.
How are drugs excreted from the kidney
-glomerular filtration (for unbound drugs), tubular reabsorption (lipid soluble drugs reenter the blood),
active tubular secretion into the urine).
List all the ways you can think of that one drug might interact with another (hint: pharmacokinetically and pharmacodynamically).
Y-port (both added into the same IV could cause precipitate).
Altered metabolism: induction/inhibition of CYP450
agonist/antagonist
Prior use causing downregulation or upregulation
Altered absorption: antacids, laxatives,
Combined toxicity (both bad for liver, now v bad)
Altered distribution (protein binding inhibitors, pH alterers)
Altered excretion
List some comorbidities of a patient that may result in varied drug responses
Kidney disease, liver disease, intellectual disabilities (ability to remember to take drug), variations in absorption with diarrhea/constipation, nutritional abnormalities leading to lower albumin (higher free drug for protein-bound drugs)
How are drug responses different in neonates?
- Absorption: slower and irregular gastric emptying, lower gastric pH (increased absorption esp of low pK drugs)
- Lower protein binding – higher concentration of free drugs
- immature cyp450, increased drug accumulation (until age 1)
- Lower renal blood flow, GFR and active tubular secretion, accumulation due to less excretion
- More body water, increased Vd
- Less developed BBB, more can reach the brain.
- Cant report early signs of toxicity
How are drug responses different in older adults? (physiologic)
*decreased renal function can lead to accumulation
- Rate of absorption slowed bc of decreased splanchnic circulation (so even though motility is slowed, there isn’t more blood flow to absorb the med so only the rate of absorption is slowed)
- Increased body fat, larger Vd, greater variance in the amount of drug that reaches the site of action
- Decreased albumin, more free drug (@ site of action)
- Prolonged drug effect: Decreased hepatic blood flow (slowed metabolism) and CYP450 activity, decreased 1st pass metabolism (increased effect of PO drugs)
- Changes to receptor # and affinity for receptors
What are two body compartments where ion trapping can be significant (one we can use to our advantage and another can be dangerous).
One place where this is significant is in the fetus, since it has a slightly lower pH (7.3), meaning that substances (basic) which would normally not ionize in the plasma (pH of 7.4) become ionized in the fetus and can lead to a fetal overdose/drug accumulation.
This could be advantageous in the urine where basic drugs (because the urine is acidic) are excreted more easily since they cannot be reabsorbed. Additionally, we could give a drug to make the urine more basic, so more drug would get excreted.
How do we overcome the BBB when giving drugs that we need to reach the CNS?
Inorder to reach the CNS a drug must be able to go thru the cells of the capillary walls, by being lipid soluble or having a transport system
What is the difference between a toxic effect and a side effect?
Toxic effects: negative effects due to excessive drug dose. Side effect: nearly unavoidable effect at therapeutic dosage
Which populations are particularly sensitive to drugs? (select all that apply)
- older adults
- neonates
-teens
- pregnant women
older adults and neonates
While pregnancy does have many considerations for drugs (like increased GFR, increased hepatic metabolism (more drug clearance, may need lower doses), increased GI transit time (increased absorption, may need lower doses), they are not considered sensitive because normal drug doses don’t necessarily (although they can) have an increased effect (or adverse effects)
Can we give epinephrine PO? Why or why not?
No, since it has a short half life, and since it is a catecholamine, it is degraded in the liver, meaning most of it would never enter the bloodstream if given PO
Where are MAO and COMT located?
MAO: Mostly presynaptic terminal
COMT: Mostly liver, some free
What is the difference between Catecholamines and noncatecholamines?
The half life of catecholamines is much shorter due to COMT and MAOs, so they cannot be given PO. Non-catecholamines can be given PO and can cross the BBB while catecholamines cannot. Catecholamines are reuptaken into the presynaptic cleft (MAO here, some COMT), while non-catecholamines are broken down in the liver
Which receptors does Dobutamine interact with? Does it agonize or antagonize these receptors? What are the major pharmacologic effects?
B1, A1 at high doses
Inotrope - increases cardiac contractility w/o increasing HR or BP much- used in CHF
dilates coronary arteries
Synthetic catecholamine
Agonist
Which receptors does Isoproterenol interact with? Does it agonize or antagonize these receptors? What are the major pharmacologic effects? What are cautions for this medication?
“Chemical pacemaker”
Synthetic catecholamine
Agonist of beta 1 and 2 equally
effects of increased HR and contractility, when combined with CAD can lead to an MI
Which receptors does Dopamine interact with? Does it agonize or antagonize these receptors? What are the major pharmacologic effects? Main indication
dopaminergic, also B1 in high concentrations and B2 in even higher concentrations, in highest concentrations a1 agonist
Dose dependent actions:
low renal dose: dilation of renal, splanchnic and cerebral arteries
slightly higher dose: increased contractility without increased HR, vasodilation (and renal dose effects)
high dose: vasoconstriction (main indication is hypotension)
Which receptors does Ephedrine interact with? Does it agonize or antagonize these receptors? What are the major pharmacologic effects? How is this one different?
blocks NE reuptake, A1, A2, B1,
indirect acting agonist, can cross the BBB
Which receptors do Labetalol and Carvedilol interact with? Do they agonize or antagonize these receptors? What are the major pharmacologic effects?
“Adrenergic antagonist”
B1=B2, also hits alpha receptors in large doses
Antagonist
Vasodilation, decreased HR, decreased BP, CO uneffected
Which receptors does Phentolamine interact with? Does it agonize or antagonize these receptors? What are the major pharmacologic effects?
A1=A2
Antagonist
HTN emergencies – causes vasodilation, decrease BP and increased HR
Extravasation – help reverse extreme constriction if norepinephrine extravates
Which receptors does Prazosin interact with? Does it agonize or antagonize these receptors? What are the major pharmacologic effects/side effects?
A1 antagonist selective
Effects: vasodilation, prostate relaxation
Orthostatic hypotension, reflex tachycardia d/t lower BP
Also treats BPH!
What are the pharmacologic effects of drugs that:
antagonize M
ACh inhibitors
antagonize and agonize Nm
M antagonists and Ach inhibitors block PSNS activity
Muscarinic antagonists to control overactive bladder
Drugs that both antagonize and agonize Nm don’t have a lot of clinical application
Drugs that antagonize Nm and their effects
rocuronium, vecuronium; prevent muscle contraction, flaccid paralysis
What receptors does Scopolamine act on? Agonize or antagonize?
Major pharmacologic effects
difference from other drugs in class
muscarinic antagonist
sedation???, mydriasis, sea sickness prevention
What receptors does Glycopyrrolate act on? Agonize or antagonize?
Major pharmacologic effects
difference from other drugs in class
muscarinic antagonist, does not cross BBB, so only peripheral effects (quaternary ammonium)
What receptors does Ipratropium act on? Agonize or antagonize?
difference from other drugs in class/indications
muscarinic antagonist,
used in the treatment of asthma/COPD
What is the difference between Neostigmine and Pyridostigmine?
While both are Ach inhibitors, used for myasthenia gravis, and NMB reversal, Neostigmine can also be used to increase gut motility and Pyridostigmine can be used for glaucoma.
How do a transdermal birth control patch and the vaginal contraceptive ring work?
It works the same as oral birth control by inhibiting ovulation and thickening cervical mucus. Vaginal contraceptive ring can also cause some local irritation
How does the subdermal etonogestrel implant work?
It lasts for 3-5 years and has only progesterone, can cause some irregular vaginal bleeding
What is Depot medroxyprogesterone acetate? How does it work? Warnings?
Birth control given by IM or sub q injection, works by inhibiting FSH/LH secretion. It can cause bone loss, so it is not recommended for more than 2 yrs
Copper IUD vs levonorgestrel IUD
Both IUDs work by creating local inflammation. The copper IUD can be used as emergency contraception up to 5 days after fertilization), and can last for up to 10 yrs. levonorgestrel is a hormonal IUD that thickens cervical mucus, inhibits ovulation and alters the endometrium
emergency contraceptives
progestin only: decreases pregnancy btwn 84-89%, will not terminate existing pregnancies or harm fetus, adverse effects of heavy bleeding, or GI upset
Progestin agonist/antagonist or copper IUD can be used up to 5 days after fertilization
Blood is hypotonic: meaning, what is given
meaning: low solutes in blood, fluid going into cells,
give: hypertonic fluids (3% or 5% NaCl, 10% dextrose water (D10W)
Blood is isotonic: meaning, what is given
meaning: blood = same as cells about 280-300
give: isotonic (NS (0.9%), D5W)
Blood is hypertonic: meaning, what is given
Meaning: blood has high solutes (>300), risk for cellular dehydration
give: hypotonic (1/2 NS 0.45% NaCl)
Can we give desmopressin (DDAVP) for hemophilia A? Why or why not? Describe the mechanism of action of the drug.
This drug releases factor 8 clotting factors from the vasculature into the blood, it can be given for hemophilia A because the issue is producing/releasing these factors, so it increases the amount of factor 8 in the blood. It is preferred for mild forms
Understand the general ACC/AHA guidelines for the management of blood cholesterol. (In general, I don’t need you to memorize little details).What is the purpose of these guidelines?
The purpose of the guidelines is how to decide who to treat and to what intensity they need to be treated. It separates patients into two categories (high and very high risk), and subdivides high risk by age to determine who should receive the most aggressive statins
Who should be screened
Who is at risk (ASCVD 10 yr risk assessment)
Treatment: lifestyle modifications + low/med/high drug therapy
How should your patient’s HMG-CoA reductase inhibitor dosing be adjusted with acute renal failure?
Their CK should be checked, if it is elevated (which it will be) the drug should be discontinued
Discuss HMG-CoA reductase inhibitors and myopathy. What are the s/s? What are the risks? What can happen in severe cases? How do you educate your patients to monitor for this?
s/s: aches, tenderness, weakness, can progress to myositis, with increased CK and K+
Risks: female, old age, low BMI, chronic liver or kidney disease, higher statin dose, CYP34A inhibitors, OATP1B1 inhibitors, specific genetics
Watch for s/s: measure CK upon start of therapy and again if symptomatic
What is the difference in mechanism of action between warfarin & heparin? Why do you think a patient would be prescribed one over the other?
Heparin works by binding anti-thrombin → suppresses fibrin mesh formation. Heparin works relatively quickly, and can only be given via IV or sub Q injection, so it is typically only given inpatient.
Warfarin inhibits activation of vitamin K so clotting factors 2, 7, 9, and 10 are decreased, leading to lessened clots (decreased fibrin formation). Warfarin can take a while to work, and is oral so it is a medication patients are sent home on to prevent future clots.
Name the 4 classes of antidysrhytmics and describe how they work
1 - na+ blockers
A = increase AP, ERF, QT interval
B = decrease AP, ERF
C= increase ERF only in AV node
2 - beta blockers
3 - k+ blockers, delayed repolarization, increased AP duration, increased ERP, prolongs QT,
4 - decrease HR, contractility, conduction thru AV node
Other
Adenosine - hyperpolarizes by opening K+ channel,
Digoxin - na+/k+ inhibitors, increasing ca2+, thus increased contractility,
Name the 4 classes of antidysrhythmics and what they are used for
1 - na+ blockers
A = Atrial and ventricular arrhythmias,
B = Post MI and other ventricular arrhythmias
C= SVT and afib
2 - beta blockers - SVT, VT, post MI
3 - Ventricular tachy
4 - SVT
Other
Adenosine - tachycardias where pt is unstable
Digoxin - heart failure and supraventricular dysrhythmias
What is the difference in mechanism of action between the nondihydropyridines and dihydropyridines? How does this difference alter their clinical effects?
dihydropyridines only affect the vasculature, can cause reflex tachycardia, contractility increase, while nondihydropyridines affect both the vasculature and the heart rate, decreased contractility and AV node conductivity
-grel
P2Y12 ADP agonists
-teplase
thrombolytics
-stim
leukopoetic growth factors
-dipine
dihydropyridines
-xaban
factor 10 inhibitors
-parin
anticoagulants that activate antithrombin (like heparin)
-sartan
ARB
-pril
ACE inhibitor
-fibr-
fibric acid derivatives
What is the half life of thrombolytics
5 mins
-gline
MAO-B inhibitors
-Phylline
methylxanthines
-dronanate
bisphosphonates
does sodium nitroprusside cause reflex tachycardia
no
Hypo/hyper kalemia with digoxin
hypo: toxic
hyper: subtheraputic
Q
nursing considerations for Calcitonin gene related peptide receptor antagonist
high fat meal can delay aborption by as much as 2 hours
How do inhalation anesthetics reach their site of action? Where is their therapeutic site of action
They reach their site of action through the lungs (concentration, solubility, blood flow and ventilation all play a role in their absorption)
Their therapeutic site of action is the CNS
Go through each body system and describe the effects that opioid agonists have. How are these adverse effects managed? (i.e. cough suppression can be managed by teaching your patient to deep breath & cough at intermittent intervals to clear secretions & prevent PNA)
Constipation - fiber, fluid, activity, stool softener, laxative
Miosis – usually not a problem
Respiratory depression – monitor, if needed stop opiods and give narcan. Elderly, young and those with respiratory disease are especially at risk
Decreased heart rate – stand up slowly to help avoid and limit orthostatic hypotension
Urinary retention – monitor I/Os
Orthostatic hypotension – educate pts
Cough suppression – educate pts to breath deep and cough, auscultate for crackles
Euphoria, emesis, birth defects, tolerance, neurotoxicity
Why do we avoid ergot alkaloids & triptans together?
We avoid ergot alkaloids and triptans together because they can cause excessive vasospasm
What phramacologic measures can be used to treat heart failure
REDUCE PRELOAD (Diuretics ACEi, ARBs, aldosterone antagonists, Venodilation)
REDUCE AFTERLOAD (ACEi, ARBs, BB (controversial, use w/ caution), Arteriole vasodilators)
INCREASE INOTROPY (CONTRACTILITY) (Cardiac glycosides (digoxin), Dopamine/dobutamine (sympathomimetics)
What are the differences between cardiac beta1 blocker action and cardiac calcium channel blocker action?
Calcium channel blockers cause arteriole vasodilation, while beta blockers cause decreased renin release. Both BB and nondihydropyridines decrease HR, AV node conductivity and decreased contractility
List absolute contraindications for nondihydropyridines
Drug interactions: beta blockers, digoxin
Don’t want to use with anything that would cause low contractility
Why does digoxin cause increased urine output?
Increased cardiac output = improved tissue perfusion = improved renal blood flow = more glomerular filtration = increased UOP!
When giving any medications that suppress immune responses, what are points of patient education? (hint: re: illness, infection, vaccines)
Before starting treatment, patients should become up to date on vaccines, since once the immune system is suppressed, it will be hard for the immune system to create new antibodies, and person will need increased immunity because they have less of an ability to fight infections
Once treatments are started the person is considered immunocompromised, so they should avoid sick people and encourage loved ones to get vaccinated to prevent giving them illnesses
Avoid concurrent administration of multiple immunosuppressants
These meds can also be very expensive, and are sometimes not covered by insurance
List the three MAJOR adverse effects of mitoxantrone.
Myelosuppression (neutropenia, anemia, thrombocytopenia)
Irreversible cardiotoxicity, can occur years after drug has been stopped
Fetal injury (even in low doses, r/o pregnancy before each dose)
Knowing that Na+ channel receptors have 3 states (open, inactivated, and closed) how do these types of antiseizure drugs prevent neuronal transmission on some neurons, but not all neurons?
Slows progression from inactive to closed, so action potential only in hyperactive neurons are suppressed
Discuss PK variances of antiseizure medications
Phenobarbital – CYP450 inducer
carbamazepine – CYP 450 inducer, is metabolized by CYP450
Oxycarbemazepine – Induces CYP450, can increase metabolism of oral contraceptives
Lamotrigine – estrogen lowers drug levels
topiramate w/ phenytoin – lowered drug levels of both
tiagabine – metabolized by CYP 450
What is ethosuximide used for?
Absence seizures
nursing considerations for oxcarbazepine
avoid alc and other hypo Na+ drugs
How does memantine work?
regulates glutamate at NMDA receptors causing more normal Ca2+ influx (in neuron that still work)
What are Beta-a drugs (endogenous inteferon B) used for? What do they do?
these immunomodulators are used in MS to modify immune responses (including B and T cells)
cautions with interferon beta
antibody stimulation against the drug itself can occur, rxns can range from mild to anaphylaxis
They also require special handling, esp for pregnant RNs
Mechanism, effects and PK of Marijuana
mechanism: activation of cannabinoid receptors
Effects: pleasure, memory, thinking, concentration, appetite, sensory and time perception
PK: CYP450 inhibitor
Approved uses of marijuana
supression of emisis (esp in CA chemo)
appetite stimulation in AIDS
Tx of sz in Lennox-Gastuat and Davet syndrome
Relief of neuropathic pain in MS (not approved in the US yet)
What are extrapyramidal symptoms (EPS)? Describe the four types.
Akinesias –restlessness, foot tapping, trouble standing still, pacing, feet in constant motion, rocking back and forth
Pseudoparkinsonism – stooped/shuffled gait, rigidity, bradykinesia, pill-rolling motion of the hands slight tremor at rest
Acute dystopia – facial grimacing, involuntary upward eye movement, muscle spasms of the tongue, face, neck and back (trunk arching forward)
Tardive dyskinesias – protrusion and rolling of tongue, chewing or sucking motion, facial dyskinesia, involuntary movements of the body and extremities
s/s serotonin syndrome
hyperactive bowel activity, tremor, hyperreflexia, dilated pupils (hyperthermia, altered LOC, ANS instability too)
tx serotonin syndrome
d/c med, supportive care, give serotonin receptor blockers
Why do you think it’s so important to differentiate between the two prior to initiating pharmacologic treatment?
It is particularly important to differentiate between the two because the treatment for serotonin syndrome could worsen neuroleptic malignant syndrome if misdiagnosed.
Contraindications for SGAs
avoid with other drugs that suppress bone marrow
List some atypical antidepressants
Bupropion
Esketamine
How does esketamine work
Esketamine – NMDA receptor antagonist, thus can increase glutamate (excitatory)
How does bupropion work?
Bupropion – unclear, may be d/t DA/NE reuptake
How does Na+ levels affect plasma drug levels of lithium?
Excretion is affected by Na+ concentration, the lithium goes where the sodium goes, so hyponatremia poses a risk for toxicity, while hypernatremia causes a risk for subtherapeutic drug levels
AE of lithium at theraputic dosages
N/V/D
Thirst, polyuria (block of ADH)
Lethargy, slurred speech, fine hand tremor,
renal toxicity
Hypothyroidism and goiter
Teratogenesis (avoid in first trimester, unless benefits outweigh risks)
Classes of drug interactions with lithium
Diuretics (na+ loss)
NSAIDs (increase renal artery vasoconstriction, increasing lithium levels)
anticholinergic (urinary hesitancy)
ACE inhibitors (Na+ loss)
Who should receive RSV antibodies?
Preterm infants
Congenital heart disease less than 2 yrs
Bronchopulmonary dysplasia (less than 2 yrs)
all vaccines pose a risk for anaphylaxis because
of preservatives, like neomycin, gelati
Vaccines requiring only one dose
Hep A (2nd dose only if live in high risk areas)
AE MMR
localized lymphadenopathy, joint stiffness, transient thrombocytopenia
AE DTaP
high fever, febrile seizure, encephalopathy
AE polio
polio-like syndrome only w/ oral (rare)
AE varicella
mild rash
Unique CI for MMR
pregnancy
Unique CI for DTaP
after previous dose fever above 105, febrile seizure, encephalopathy
unique CI for varicella
pregnancy, blood cancer
Unique considerations for hep B
if mom is hep B+, give immunoglobulin with first dose
unique CI for rotavirus
uncorrected GI malformation, severe vomiting or diarrhea (can’t keep in gut long enough to develop antibodies)
Antidote for overdose of AChE inhibitors
Atropine
Antidote for OD of Anticholinergic drugs
AchE inhibitor
Classes used to treat insomnia
benzos
benzo-like drugs
melatonin agonists
orexin antagonist (both sleep onset and maintenance)
barbs
What is Miralax especially good for decreasing absorption of
iron, lithium, lead
Contraindications/nursing considerations with 1st gen H1 antagonists
Sedation more prevalant in first generation, means they should not be used concurrently with other CNS depressants and alcohol. Educate to use only as directed, many ODs because people see as “safe” and are more lax about dosing
Uses of H1 antagonists
mild allergy
adjunt to severe allergy
Motion sickness (some have antagonizing pathways to vestibular apparatus in inner ear responsible for motion sickness)
Insomnia (1st gen)
How do IL-5 receptor antagonists work?
inhibit IL-5, causing decreased eosinophils
AE of IL-5 receptor antagonists
HA, pharyngitis, fatigue, hypersensitivity rxns,
How do IL-4 receptor alpha antagonists work?
decreased cytokine-induced inflammation
AE of IL-4 receptor alpha antagonists?
injexn site rxns, oral herpes, conjunctivitis, antibody development against the drug
Montelukast is the most commonly prescribed leukotriene receptor blocker. In comparing its adverse effects with the other two leukotriene receptor blockers, why do you think it’s more highly prescribed?
Minimal side effects, no CYP450 inhibition or liver injury, only rare neuropsych effects
What is the purpose and mechanism of action of drugs to treat allergic rhinitis
Intranasal glucocorticoids: suppress immune response to allergens, prevention and treatment (not PRN)
Antihistamines: block histamine, less effective than intranasal glucocorticoids, can relieve some symptoms, but not nasal congestion
Sympathomimetics: cause local vasoconstriction, so less fluid can leak out to become snot, a1 agonism, only to relieve congestion
List three drugs used for cough (antitussives). Which can cause CNS depression? Which have abuse potential?
Codeine – small abuse potential when with something to deter abuse, CNS depression
Hydrocodone – CNS depression, small abuse potential when formulated with other drugs to deter abuse
Dextromethorphan – CNS actions, high doses can cause euphoria, thus abuse potential exists
How do all glaucoma drugs except prostaglandin analogs work?
decreased production of aqueous humor
AE of Beta blockers for glaucoma
systemic beta blockade
AE of Prostaglandin analogs for glaucoma
A2 agonists: dry mouth, ocular hyperemia
ocular hyperemia (enlarged vessels)
AE of A2 agonists for glaucoma
dry mouth, ocular hyperemia
Pt education for antibiotic treatment of H. Pylori
important to take all types and complete entire 10-14 days course, they should be taken 2-3 times a day and combined with an antisecretory agent (H2RA, PPI)
For each class of antiemetics, describe a patient you would NOT administer the drug to
Serotonin receptor antagonists: pt w/ a prolonged QT or on SSRIs
SubP/NK receptor antagonists: pt on warfarin, or on oral BC not using another method of contraception
Haloperidol: prolonged QT
Cannabinoids: psychiatric disease
Scopolamine: an elderly person who is particularly prone to disorientation
Discuss opioid use in diarrhea: how do they work? What drug category are they? Why are they not schedule II like many of the other opioids?
Loperamide, and other similar drugs agonize Opioid receptors, which decreases bowel motility, they are either schedule IV or unscheduled because they are poorly absorbed (no euphoria) and they are formulated with drugs (atropine) which create unpleasant side effects if the dose is increased
How does sulfasalazine work?
Sulfasalazine is metabolized by intestinal bacteria, and converted into 2 substances, one of which (5-ASA) suppresses prostaglandin synthesis and local inflammation, the other is sulfapyridine and causes the AE associated with the drug
What is Alosteron used for
IBS-D in women
AE of alosteron
well-tolerated to severe, including death d/t ischemic colitis
What are the differences in H1 and H2 receptor agonism? What drugs do we use for each?
H1 receptor agonism causes:
Vasodilation, increased vascular permeability,
Hypotension, reflex tachy
Bronchoconstriction
itching/pain (stim of nerves)
CNS: cognition, memory, sleep/wake
Drugs: diphenhydramine (benadryl), promethazine (phenergan)
H2: gastric secretion
Drugs H2RAs: cimetidine, famotidine
Pt education for immunosuppressants
Toxic: nephrotoxicity, hepatotoxicity
AE: bone marrow suppression, infection, depression, flu-like symptoms, injection site reactions, decrease vaccine effectiveness
Don’t use with other immunosuppressants
Encourage family members to get vaccinated, avoid live vaccinations
Avoid with other nephrotoxic drugs, metabolized by CYP450 – be careful with inducers and inhibitors
mTOR inhibitors with high fat foods → increased absorption and possible toxicity
Indication for LABAs
preferred in COPD
fixed dose scheduling (not PRN)
when used alone in asthma increased mortality (USE W/ GLUCOCORTICOID)
Indication of glucocorticoid + LABA
Symbicort and advair are used for asthma
Indication B2 antagonist + anticholinergic
Combivent is used in COPD
Caution/contraindications of theophylline
Slow IV admin to avoid fatal CV events
highly variable metabolism (CYP450), requires plasma monitoring
Caffeine (also a methylxanthine) – increase AE, compete for metabolizing enzymes
tobacco/marijuana – induces CYP450
CYP450 induces – subtherapeutic lvls
CYP450 inhibitors – supratherapeutic (even toxic levels)
Interactions of Cimetidine
H2RAs are CYP450 inhibitors (toxic doses of other meds metabolized by CYP450)
antacids can decrease the absorption of Cimetidine (give 1hr apart)
Drug interactions of PPIs
increased pH causing decreased absorption of some HIV drugs and antifungals
Who are antacids contraindicated for?
All antacids contain lots of Na+, so caution with HTN, HF, or renal d. (careful electrolyte balancing)
Compare and contrast the two drugs used to increase defensive factors in the treatment of PUD
Misoprostol and sucralfate have different mechanisms of action (see 31). Misoprostol cannot be given to pregnant women, can cause dose-related diarrhea, abdominal pain, and spotting/dysmenorrhea. Sucralfate, on the other hand, has minimal side effects (some experience constipation), but can increase the absorption of some other drugs, so it should be given at least 2 hrs apart from other meds.
What’s the difference between HHS & DKA? How are they treated? What will you monitor as the bedside nurse while treating these acute issues?
DKA: rapid onset, usually in type 1, ketoacidosis, shock, glycosuria and water loss, cerebral dehydration
tx: decrease blood glucose by approximately 50mg/dL/hr, correct dehydration, correct acidosis
HHS: VERY high glucose levels, glycosuria and water loss, concentrated plasma electrolytes
tx: blood glucose by approximately 50mg/dL/hr, correct dehydration, correct acidosis
List topics of patient education when the patient is first prescribed levothyroxine.
since absorption is reduced by food it should be taken on an empty stomach, a rare adverse effect d/t high dosing is s/s of hyperthyroidism. Drug interactions should be checked as many drugs increase absorption or metabolism of this drug
The mom of your pediatric patient really wants her son to take somatropin so he grows taller – she doesn’t want him to be the “short kid” in class. What are you going to teach her about exogenous growth hormone therapy in pediatrics?
We only use it in extremely necessary cases, more than 2 SD below the mean, it is more to help kids reach the height they were genetically predisposed to
If your patient has a pituitary adenoma that results in hypersecretion of ACTH, what effects do you expect to see? What hormone is unaffected?
higher cortisol levels, increased glucocorticoids and and androgens. I would expect that mineralocorticoids (aldosterone) would remain unaffected
Your patient comes into the ER with a HR of 150, BP 80/40, dizziness, confusion, lethargy. She is close to unconsciousness and cannot really tell you anything about her medical history or medications but she is wearing a medic alert bracelet communicating that she has Addison’s Disease. What is your course of action? (Assessments, interventions, medications to prepare to administer)
She is likely having a hypotensive crisis, caused by primary adrenocortical insufficiency. She likely needs glucocorticoids (and mineralocorticoids) like cortisol to help increase her blood pressure
Provide teaching for your 55 year old patient that has been prescribed bazedoxifene to help with her severe hot flashes & night sweats.
there is some endometrial cancer risk, and she should come back if hot flashes worsen. She should also be aware it can cause blood clotting
Difference btwn Sildenafil, Vardenafil, Tadalafil
and Avanafil
Sidenafil is preferred. Vardenafil prolongs QT, Tadenafil long lasting 36 hrs, and can be used for BPH as well by relaxing the prostate
Avanafil fastest onset
Describe the pathophysiologic difference between mechanical obstruction vs. dynamic obstruction of the urethra in BPH. How does the pharmacologic treatment differ?
epithelial = mechanical
smooth muscle = dynamic
What are the pros of administering a selective alpha 1a blocker over a nonselective agent for BPH? What are the cons?
selective would just treat prostate, non selective could also help with HTN
If your patient is in a stable tachycardic rhythm and it’s going so fast that you can’t tell what the rhythm is, what is the best drug to give in this scenario?
A beta blocker, specifically a cardioselective one to decrease their heart rate.
“You are going to give a beta blocker. If it is occurring because of something above the ventricles, it will slow the heart rate so you can look at the EKG, but if it is from the ventricles, it won’t due anything and then you will know it’s Vtach”
What drugs are COX inhibitors? What is the end result of inhibition? Do these drugs inhibit COX1 or COX2 or both? What happens if we just inhibit COX2?
Preventing COX 1 and 2 Both – NSAIDs, aspirin, ibuprofen
inhibits: gastric ulceration and erosion, bleeding tendencies, leads to decreased platelet aggregation (MI, CVA protection)
COX 2- Celecoxib, more CV events
Inhibits inflammation, pain, fever, renal impairment, suppression of vasodilation (more CV events)
Discuss drug interactions with COX inhibitors.
anticoagulants –> bleeding risk
gluccocorticoids –> gastric ulceration risk
alc –> gastric bleeding risk
ACE inhibitors and ARBS –> increased impairment of renal function
vaccines –> response can be blunted d/t decreased immune response
What is different about acetaminophen than the rest of the COX inhibitors? What does this mean for the patient?
It is different from other COX inhibitors because it is mainly active through the CNS. This means it is safer for those with GI issues, and older patients but will not be protective towards CV events. On the other hand, it is less safe for those with liver disease
What is unique about a few of the local anesthetics we talked about in class: benzocaine, cocaine, chloroprocaine?
benzocaine has the adverse effect of methemoglobinemia, so it is contraindicated in those under 2
Cocaine in addition to blocking na+ channels, cocaine also blocks NE reuptake causing CNS and CV stimulation
Chloroprocaine is special because it is not effective topically (injection only) and has a short duration of action
How does ketamine work?
NMDA transmission
A few opioids are different from the rest in either adverse effects or how they are metabolized. Describe these differences with methadone, meperidine, and codeine
Methadone has pain relief properties without euphoria, so it can be used for addiction, very long half life, can prolong QT
Meperidine toxic metabolites can build up with repeated use, interacts with MAO receptors = excitation/seizures
Ccodeine – some people don’t have a response to it based on genetic variation in the CYP450 enzyme that metabolizes it
A few opioids are different from the rest in either adverse effects or how they are metabolized. Describe these differences with methadone, meperidine, and codeine
Methadone has pain relief properties without euphoria, so it can be used for addiction, very long half life, can prolong QT
Meperidine toxic metabolites can build up with repeated use, interacts with MAO receptors = excitation/seizures
Ccodeine – some people don’t have a response to it based on genetic variation in the CYP450 enzyme that metabolizes it
s/s, Cause, tx of neuroleptic malignant syndrome
Cause: DA receptor blockade from antipsychotic medications
S/s: rigidity, very high fever, coma, seizures, sweating, ANS instability (BP changes/dysrhythmias
Treatment: d/c FGA, possibly switch to SGA, supportive care
Abortive drug therapies for migraines
asprin-like drugs
seratonin receptor agonists (triptans)
seratonin 1 F receptor agonists
ergot alkloids
Calcitonin gene related peptide receptor antagonist
What are the adverse effects in general of H1 receptor blockers? What AE are more prevalent in 1st generation? What does this mean for nursing? (i.e. inpatient monitoring and outpatient education?)
Sedation*, dizziness, fatigue, N/V, loss of appetite, constipation, anticholinergic effects, respiratory effects (esp young/old pts)
*more prevalent in first gen, which means they should not be used concurrently with other CNS depressants and alcohol. Educate to use only as directed, many ODs because people see as “safe” and are more lax about dosing
6 drug classes are used in the treatment of glaucoma: beta blockers, prostaglandin analogs, alpha2 agonists, carbonic anhydrase inhibitors. List any major SYSTEMIC adverse reactions that the nurse needs to be aware of when administering these drugs.
Beta blockers : systemic beta blockade
Prostaglandin analogs: ocular hyperemia (enlarged vessels)
A2 agonists: dry mouth, ocular hyperemia
Carbonic anhydrase inhibitors : not super effective, but few AE
How does vomiting occur? What are the two MAIN pathways that we attempt to inhibit when providing antiemetics? Which drug classes inhibit each one? What is an advantage of having such a complex receptor system for vomiting?
Vomiting occurs thru either direct acting stimulation in the cortex, inner ear, or other sensory organs or thru activation of the Chemoreceptor trigger zone (CTZ) which is caused by signals from the gut
We can inhibit the CZT or the afferent GI nerves (block signal or receptor)
Block NTs in CZT: serotonin antagonists, substance P/neurokinin1 antagonists, dopamine antagonists,
Block in neuronal pathway to CTZ: anticholinergics, antihistamines
Other: glucocorticoids, cannabinoids
Benzos: sedation, suppression of anticipatory emesis
An advantage of having so many different triggers for vomiting is that there are many different ways to detect and remove food that is unsafe?
What are the AE of COX inhibitors? What about of COX2 selective inhibitors? In which patient populations would each be used? In which patient populations would each be contraindicated?
Non selective: Gi ulceration, increased bleeding risk rey syndome (No peds), toxic to fetus, not during pregnancy
More CV events bc no vasodilation → anyone with CV history,
Both can cause renal impairment so aren’t great for people where this is already an issue
CI of methotrexate
blood dyscrasias, immunodeficiency, liver disease, pregnancy
Describe how each type of biologic DMARD works (there are 3).
TNF antagonists → directly bind TNF receptor causing decreased infiltration of RBCs into joints
B lymophocyte depleting agent → acts against antigen on B cells causing cell death
T cell activation inhibitor → prevents T cell activation
What symptoms of gout are not aided with long term preventative therapy?
They lack anti inflammatory/analgesic properties so can’t help with flare ups
Describe when hormone replacement therapy might be indicated for a patient. What are some concerns with estrogen replacement therapy? What benefits do SERMs like raloxifene offer (specifically)? For which patients would therapy be contraindicated?
Hormone replacement therapy involves taking an estrogen and/or progesterone replacement. It is used often for women who have particularly bad symptoms with menopause, especially those with osteoporosis. Some concerns of hormone replacement therapy include increased blood clots and endometreal cancer (although this risk is signifcantly lower in post menopausal women). SERMs often help prevent (or slow the progression) of osteoporsis.
Raloxofene is especially good because it can ptotect against Brest cancer, doesn’t cause endometrial cancer, lowers LDL
CI: CV disease, pregnancy
Give these therapies when benefits outweight risks
What is the interaction between aminoglycosides and PCNs?
Synergistic effect → PCNs weaken cell walls, aminoglycosides enter to site of action
If mixed in the same syringe/IV line → inactivation
How are most antibiotics excreted? What does that mean for drug dosing? Does severe organ disease preclude us from administering these drugs at all?
Most antibiotics are excreted renally, which means that drug dosing should be decreased in pts with severe renal disease
We can still give these drugs, just at a lower dose, although they may need to be stopped if any s/s of renal damage occur. Generally, antibiotic courses are brief, so we can still do it
List all the antibiotics that affect (either inhibit or induce) CYP50.
Macrolides – inhibit
Isoniazid – inhibit
Rifampin – inducer
Azoles – inhibit
Which antibiotic is metabolized by the liver (not excreted unchanged by the kidneys)
ceftriaxone
Which drug classes interact with the DNA-dependent enzymes DNA gyrase & topoisomerase IV? What does this result in?
Fluoroquinolones, causes destruction of bacterial DNA
What is tetrahydrofolate (THF)? Which drug classes inhibit this substance? Why are host cells not affected by THF inhibition? List two drugs that inhibit the THF pathway. Is the combination of the two synergistic or antagonistic? What is this combination drug called?
THF is a type of folate that needs to be made for production of bacterial proteins, DNA and RNA it is only present in bacteria.
Sulfonamides and Trimethoprim inhibit the pathway, the combination of these two medications has a synergistic effect, causing less bacterial resistance and killing bacteria more effectively. The combination of these 2 meds is call bactrim
List the drugs to avoid in the patient with G6PD deficiency.
Avoid sulfonamides and tafenoquine in pts with a G6PD deficiency as they can cause hemolytic anemia
4 major first line drugs are used in the treatment of TB
Isoniazid
Rifampin
Pyrazinamide
Ethambutol
Outline the major toxicities of anti-cancer drugs. Discuss why each of these toxicities makes sense.
Immunosuppression, GI, fertility, alopecia – all are also rapidly dividing cells
Urinary stones – as cells die they spill DNA → uric acid
Extravasation → local injury
Promotion of secondary cancers d/t DNA damage, immune suppression
