Pharm Final Exam Flashcards
Peak level
- Peak is taken when drug is at highest level in bloodstream – allows dr to make sure patient medication level is within safe ranges
o With IV infusion, 30-60 mins after infusion given
o Drawn 1-2 hour afterwards if medication given orally
Trough level
- Trough level is lowest level of medication in bloodstream
o Drawn right before next administration of medication
Drug half-life
- Length of time required for the plasma concentration to decrease by half after administration
- Drugs with short half-lives stay in the body for a shorter period of time, vice versa with longer half-lives
Loading dose
- Loading dose – giving a higher dose of a drug to prime the bloodstream to more quickly reach the plateau
Maintenance dose
- Maintenance dose – given before the plasma level drops (aka the normal dose)
How to minimize drug-drug interactions
- The more drugs a patient receives – the greater the risk for interactions
o Encourage nonpharm alternatives and avoid copious use of OTC and herbal preps - Imperative to obtain thorough drug history
- When possible interactions – careful attention to dosage and timing
- Patients must be monitored for potential signs of interactions
o Especially when taking a drug with narrow therapeutic range
Potential results of drug-food interactions and what are the nursing implications
- Potential results of drug-food interactions – may decrease the rate or extent of absorption. Absorption of other drugs is increased in the presence of food. Some drugs must be taken with food in order to reach the therapeutic range (e.g., orange juice and iron).
o Example – to avoid
MAOI – no foods rich in tyramine
Theophylline and caffeine
Potassium sparing diuretics and salt subs
Aluminum containing antacids and citrus beverages
Vitamin K – warfarin (unless being used as antidote for warfarin) - Nursing implications – Administration with food is with or shortly after a meal. Empty stomach – 1 hour before or 2 hours after meal
What is the effect of grapejuice on some drugs?
- Effect of grapefruit juice on some drugs – inhibits metabolism of drugs, leading to increased peaks and possible toxicity
o Patients need to avoid grapefruit juice or grapefruit ENTIRELY (they can’t have 1 hour after they take med, etc)
Inotropic effects
- Force of contraction, not rate – all about strength and force
- Can be positive or negative
Chronotropic effects
- Heart rate
- Can be positive or negative (positive increases, negative decreases)
Examples of inotropic/chronotropic, because hey, why not?
- Calcium channel blockers – negative inotrope, negative chronotrope
- Beta blockers – negative inotrope, negative chronotrope
- Digoxin (cardiac glycosides) - positive inotrope, negative chronotrope
- Dopamine, dobutamine positive inotrope (dopamine also positive chronotrope)
- ACE inhibitors – negative inotrope, negative chronotrope
First-dose effect
- Profound orthostatic hypotension with the first dose of an alpha adrenergic or diuretic
- Common, especially in patients: with hypertension, on diuretics, or volume-depleted, those taking ACE inhibitors
- Patients should be given assistance when getting up
First-pass effect
- Many drugs pass through the hepatic system without incident, but some get completely metabolized before they can travel further in the body
- Larger doses may be needed, or avoiding oral route
Black box warning
- Warning issued by the FDA and notifies health professionals and consumers of extremely dangerous (and possibly fatal) risks with medication
- Strongest warning a drug can have while allowed to be on the market still
- E.g., Celebrex is only Cox-2 inhibitor on market today
Ototoxicity – what is it and what groups of drugs are most likely to cause this? What are early signs of ototoxicity?
- What is ototoxicity – rare but adverse effect that is usually (but not always) reversible – hearing loss can be transient or permanent
- Can occur when serum levels exceed therapeutic range – increased chance when other ototoxic drugs are given concurrently
- Drugs most likely to cause this – vancomycin, ferosemide, aminoglycosides
- Early signs – high-pitched tinnitus, vertigo, dizziness
Stevens-Johnson syndrome - what is it?
- Complex hypersensitive reaction (rare medical emergency) that can occur following exposure to some drugs
o Examples of drugs: penicillin, barbiturates, cocaine, dilantin, sulfonamides - Also following exposure to infections: viral, bacterial, fungal; and malignancies
- Can take weeks or months to recover from
- Discontinue any medications that could be causing it
Red man syndrome
- Anaphylactic-like adverse reaction from administration of vancomycin too quickly
- S/S: hypotension, flushing, tachycardia, redness (HENCE THE NAME), angioedema
- Usually appears within 5-10 min of infusion
- If it happens, slow the infusion rates (stop if severe)
- Can treat symptoms with antihistamines
Extrapyramidal effects – what are they? What drug most likely to see them with?
- What are they – movement disorders from effects of antipsychotics on extrapyramidal motor system
- S/S: acute dystonia (spasms of tongue/face/neck), parkinsonism, akasthisia, tardive dyskinesia
- With which drugs most likely to see – antipsychotic drugs
Stevens-Johnson syndrome - S/S?
o First symptoms – flu-like (fever, malaise, etc)
o Involves a rash that can develop into bullae that eventually rupture; the rupture of the bullae makes person susceptible to infection
o Can affect mucous membranes of eye, oral, GI, GU, and respiratory tracts
o Can lead to
Necrosis of GI or respiratory
Blindness if eyes involved
o Pt may be hypotensive, tachycardic, CNS changes (seizures, decreased LOC)
Extrapyramidal effects – How are they treated?
o Acute dystonia
Onset: few hours – 5 days
Spasms of muscles of tongue, face, neck and back; opisthotonus (body arched into dorsiflexion)
Mgmt: anticholinergic drugs (e.g., benzotropine) IM or IV
o Parkinsonism
Onset: 5-30 days
Bradykinesia, mask-like facies, tremor, rigidity, shuffling gait, drooling, cogwheeling, stooped posture
Mgmt: Anticholinergics, amantadine, or both
• Severe symptoms: switch to 2nd gen antipsychotic
o Akathisia
Onset: 5-60 days
Compulsive, restless movement; symptoms of anxiety, agitation
Mgmt: Reduce dosage or switch to low-potency antipsychotic.
• Treat with benzodiazepine, beta blocker, or anticholinergic
o Tardive dyskinesia
Onset: Months to years
Oral-facial dyskinesias, choreoathetoid movements
Mgmt: best approach is prevention; no reliable treawtment
• Discontinue all anticholinergic drugs.
• Give benzodiazepines
• Reduce antipsychotic dosage
• For severe TD – switch to 2nd gen antipsychotic
What are opioid effects?
o Respiratory depression, excessive sedation, nausea, vomiting, urinary retention, orthostatic hypotension, biliary colic, euphoria, myosis (pupillary constriction), itching, decreased GI motility, cough suppression
Tolerance
o Tolerance – biological condition in which higher doses of drug are needed to achieve same effect
Natural consequence of regular opioid use
Patients do not develop a tolerance to myosis or constipation (might develop tolerance to respiratory depression etc)
Physical dependence
o Physical dependence – Results in abstinence of symptoms if the drug is stopped abruptly
Symptoms of physical withdrawal include sweating, tremors, irritability, rhinorrhea, sneezing, N/V, diarrhea, dilated pupils
Addiction
o Addiction – psychological dependence
The individual has strong craving or need for drug
Continues to use despite possibly having issues at home, work, interpersonal relationships
What are anticholinergic drugs used for?
o Used for overactive bladder, eye disorders (to dilate pupil), bradycardia, intestinal hyperactivity, muscarinic agonist muscle poisoning
What are anticholinergic effects?
o Vasodilation, tachycardia, dilation of pupils, decreased secretions, decreased GI motility, urinary retention, increased sweating
o Can’t see, can’t shit, can’t pee, can’t spit
What are beta-agonists used for?
o Used for bronchodilation (beta 2), heart failure, increased force of contractions seen in beta-1, used in shock to increase rate and contraction strength, AV block, cardiac arrest, asthma, delay of preterm labor, management of cardiac arrhythmias, MI, hypertension
What are beta-blockers used for?
o Decreased contractility, decreased workload, slow down heart
o Hypertension, anxiety, tachycardia, angina pectoris, heart failure, myocardial infarction
What are alpha-blockers used for?
o Prevent stimulation of adrenergic receptors
o Hypertension, vasodilation, treat BPH, reverse toxicity of alpha-1 agonists, Raynaud’s disease
o Biggest thing is decrease BP
Digoxin
- Used for slowing heart rate
- Generates forceful contractions
- Assess apical pulse for 1 min, hold if less than 60
Diuretics (loop, thiazide, potassium-sparing) – what are the major differences in these?
- Loop diuretic block reabsorption of potassium and they are potassium wasting
o Have greatest potential to cause F&E imbalances because they act quickly and cause large amounts of fluids to be excreted in short time
o Can potentially cause ototoxicity - Thiazide block sodium absorption and increase water and potassium excretion – potassium wasting
o First-line for hypertension
o Don’t work as fast as loop - Potassium-sparing – I have a feeling these spare potassium (!!), block aldosterone (which blocks the exchange of sodium and potassium)
Calcium channel blockers
o What it does – block calcium channel entry ways (which would cause vasoconstriction)
vasodilates, negative inotrope, negative chronotrope
o Primary uses – hypertension, angina, dysrhythmias (except drugs mentioned below)
o Adverse effects – headache, dizziness, potential for peripheral edema
o Can have reflex tachycardia and increased contractile force with lodapine, niphedipine, nicardipine (beta blocker to treat reflex tachycardia)
Those 3 not useful in treating dysrhythmias
ACE inhibitors
o What it does - Increase cardiac output by lowering BP, and decrease fluid volume
o Primary uses – hypertension, decreased symptoms and prolonged survival in heart failure, myocardial infarction, decreased risk of stroke in patients with hypertension or left ventricular hypertrophy
o Adverse effects
Mainly hypotension
Occasionally angioedema.
Nonproductive hacking cough – 5-10% - common reason for discontinuing therapy
Hyperkalemia (so don’t give with potassium sparing)
First-dose effect – PROFOUND orthostatic hypotension
Statins
o What it does – lower LDLs and total cholesterol, raise HDLs, reduction of triglyceride levels
Also improve clinical outcomes – lower risk of heart failure, MI, sudden death
o Primary uses: hypercholesterolemia, primary and secondary prevention of CV events, primary prevention in people with normal LDL levels (rosuvastatin), post-MI therapy, diabetes
o Administered orally
Only small dose reaches system as most is absorbed on first pass through liver
o Most effective when given in evening because cholesterol synthesis normally happens at night
o If statin therapy stopped – cholesterol will return to pretreatment levels within weeks-months
Treatment should be lifelong, unless serious contraindications (esp pregnancy or muscle damage)
o Adverse effects:
Myopathy/Rhabdomyolysis – muscle aches, tenderness, weakness localized to certain muscle groups
• Mild injury myositis rhabdomyolysis (fatal)
Hepatotoxicity
What is the baroreceptor reflex? (when is it activated and what are its effects?)
- What is it – feedback loop of autonomic nervous system
- When is it activated – when blood pressure goes up and heart rate decreases OR when BP decreases and HR increases
- What are its effects – causes vasodilation or constriction based on necessary response
Anticoagulant and antiplatelet drugs
- If there are antidotes, what are they?
o Protamine sulfate antidote to heparin
o Vitamin K antidote to warfarin
Anticoagulant and antiplatelet drugs
- If there are related lab tests, what are they?
o Heparin therapy measured by aPTT, normal value is 30-40 seconds
o Warfarin measured with PT – normal 10-15 seconds – with results expressed in INR
INR 2-3 is best; used to adjust warfarin doses
PT measures time to clot – so higher value means less likely to clot, more likely to bleed
What is heparin-induced thrombocytopenia?
o Allergic reaction to heparin in which patient’s body reacts to heparin as if it’s foreign pathogen
o Symptoms: fever, fatigue, malaise
o Heparin immediately discontinued – patient should never receive again
o Unexpected drop in platelet count often an early sign
Glucocorticoids
- When are they used? (In high doses? In low doses?)
o Low doses: to treat adrenocortical insufficiency
o High doses: used to treat inflammatory disorders (e.g., asthma, rheumatoid arthritis), certain cancers, and suppresses immune responses in organ transplant recipients
Glucocorticoids
- What are glucocorticoid effects?
o Metabolism and electrolytes
Elevation of blood glucose
Suppress synthesis of proteins (can reduce muscle mass, decrease protein matrix of bone, thinning of skin)
Fat redistribution (leading to potbelly, moon face, buffalo hump characteristic of Cushing’s) – long-term, high-dose therapy
In rare cases, significant sodium retention or potassium loss
o Anti-inflammation
o Immunosuppression
o Adverse: adrenal insufficiency, osteoporosis, infection, glucose intolerance, myopathy, fluid and electrolyte disturbance, growth retardation (children), psychologic disturbances, cataracts, glaucoma, PUD, iatrogenic Cushing’s syndrome
