Pharm Notes Pre Midterm 1

pharmacokinetics

what the body does to drugs (ADME)

Pharmacodynamics

study of what the drug does to the body

adverse effect

response to drugs that results in undesirable effects

toxicity

serious adverse effects, can be extension of drugs therapeutic effects

prototype drug

gold standard for medication classification of drugs

drugs made based off of prototype are called variance

prophylaxis

used to prevent illness or other undesirable outcomes

tolerance

decreasing response to repeated drug dosages

dependance

physical or psychological need for drug

synergistic effect

when 2 drugs work together to optimise effect

P formulary

antagonistic effect

2 drugs work against each other to produce the opposite of a therapeutic response

incompatability

chemical deterioration when 2 drugs are mixed

teratogenic, mutagenic and carcinogenic

causes harm to fetal development, to genetic composition or to cells- causes cancer

pharmokinetic steps

ADME

Absorption, distribution, metabolism, excretion

what affects the absorption of a drug

dosage, chemical make up of drug, route, food or fluids, acidity in the stomach, status of GI mobility/blood flow, warmth or coldness of body, surface area and contact time

bioavailability

fraction of medication that is absorped into circulatory system after first pass effects, ex- more med will be given orally vs iv for the exact same dose

first pass effect

oral med- drug metabolised in liver, some of the drug will be deactivated before it can reach the general circulation and its sites of action, reduces bioavailability to less than 100%

factors effecting distribution

water solubility (hydrophilic)- these meds are able to be dissolved in blood, lipid solubility (lipophilic) distribution slows down because these drugs do not dissolve in blood , degree it which drug is protein bound (ex- most common is albumin (allows med to go across cell membrane), unbound drug is called free drug, if someone doesn’t have enough protein or nutrition in their body- amt of unbound drug increases- toxicity or increased risk of adverse effects

factors affecting metabolism

liver function (measured by liver enzymes- AKA LFTs), drug interactions (P450 inhibitors or inducers), genetic makeup, nutrition (starvation, jaundice, fast vs slow acetylator), age, disease process (cardiovascular, kidney diseases)

cytochrome P450 enzymes

most drugs are metabolised by these enzymes, different ppl have different amts of these enzymes in their body, cause of many drug interactions

drugs that stimulate P450 enzymes- enzyme inducers (ex- barbiturates)

drugs that slow activity of these enzymes- enzyme inhibitors (ex- erythromycin)

biotransformation

transformation of substances into something beneficial to the body

types: oxidation, reduction, hydrolysis

substrates- other substances that help the above processes

Prodrug

when drug is inactive (sitting on shelf) becomes active after it goes through body (usually liver)

excretion

process through which drugs are removed from the body, primary organ is kidney

• renal excretion

• measured by GFR which declines with age and illness

• less excretion = more retention = more toxicity

liver and bowel

• biliary excretion

can also be secreted from lungs, salivary and mammary glands, skin and sweat

half life

amt of time required for half of drug to be eliminated, most drugs removed from body after abt 5 half lives

short half life- needs drug more frequently

long half life- needs drug less frequently

helps calculate steady state

additivity

combined effects of drugs

potentiation

presence of one thing largely increases effect of the effect

synergism

drugs work together to produce combined and increased effect

onset, peak and duration

onset- time it takes for drug to start working

peak- max therapeutic effect of drug

duration- time that drug produces effect in body

peak level, trough level, steady state

peak- highest blood level of drug, toxicity can occur if peak blood level of drug is too high

trough level- lowest blood level of drug

plateau/steady state- state in which amt of drug eliminates is equal to amt absorbed per each dose

steady state

having the right amt of drug in body to produce a consistent effect on the body

therapeutic index

TI = toxic dose (TD50) / effective dose (ED50)

ways that drugs exert their actions (3)

• drug receptor interactions

• enzyme interactions

• non selective interactions

drug receptor interactions

• drugs act by forming chemical bond with specific receptor sites (lock and key)

• better the fit (affinity), better the response, drugs that attach completely are called agonists

• drugs that attach but do not form a response are called antagonists

• drugs that attach, elicit some response and block other responses are called partial agonists or agonist antagonists

enzyme interactions

drugs either inhibit or enhance action of specific enzyme called selective interaction

ex- angiotensin coverting enzyme (ACE) and angiotensin coverting enzyme inhibitor (ACEI)

non selective interactions

drugs that target cell membranes or cellular processes (ex- antibiotics)

medication classifications for pregnancy or breasfeeding

medications for children

organ immaturity- reduced first pass, renal excretion

contraindications/increased risk of toxicity because of decrease in stomach acidity

greater body water, lower body fat

blood brain barrier is immature

medication for older adults

• pharmacokinetic actions become slower and distribution becomes more unpredictable

• polypharmacy

• absorption and distribution affected by

  • slower blood circulation

  • slower absorption of oral meds through intestines

• metabolism and excretion are affected mainly by liver and kidney dysfunction

• cautious of side effects, toxicity, and unusual effects of drugs

CNO medication practice standard

authority, safety and competence

best possible medication history

• any and all meds, include natural and otc

• alcohol, caffiene and tobacco intake

• past and present health history

• family history

• racial, ethnic and cultural assessment

• unusual responses to medications (allergies, sensitivities, adverse reactions)

• growth and development

• functional assessment (cognitive and psychomotor)

• lifestyle (socioeconomic, education, schedule)

med recon

• continuous assessment and updating of patient medication information to prevent medication errors

• during admission, transfer, status change, discharge

• verification, clarification, reconciliation

polypharmacy

regular use of atleast 5 meds

• increased risk for falls

• increased mortality

• increased length of stay and readmission to hospital

• risk due to decreased renal and hepatic function in older adults

• risk due to reduced hearing, vision and cognition

medication documentation

• document delivery, details, health teaching and refusals ASAP

• do not document medication delivery in advance

• observe client taking medication

• accept written orders as much as possible, do not accept verbal orders unless emergency

• question incomplete or confusing orders

med errors

any preventable adverse drug event involving inappropriate med use by patient or hcp that may or may not cause patient harm

high alert meds (HAMs) are medications with the greatest potential for error, often due to looking or sounding like another medication (ISMP)

nurse’s professional responsibility to respond to, report and document errors as well as advocate for change to prevent future re occurrence

types:

• near miss

• no harm event

• errors that cause harm

• critical incidents

• sentinel event (patient dies)

adverse drug reactions

• adverse effects

• allergic reactions

• idiosyncratic reactions

ISMP

institute for safe medication practice

• chart of do not use, dangerous abbreviations, symbols and dose designators

types of adverse drug reactions

drug-drug or drug-food interactions

practice math calculation questions

substances and antidotes

nervous system

adrenergic drugs

drugs that stimulate sympathetic nervous system

aka adrenergic agonists or sympathomimetics

• mimic effects sns neurotransmitters (catecholamines) - norepinephrine, epinephrine, dopamine

adrenergic receptors

• located throughout the body

• receptors for sympathetic neurotransmitters

• α--adrenergic receptors

• ß-adrenergic receptors

• dopaminergic receptors

  • only respond to dopamine

α-adrenergic receptors

divided into α1 and α2 receptors

differentiated by their location on nerves

α1- located on post synaptic effector cells (cell, muscle, organ the nerve stimulates)

α2- located on pre synaptic nerve terminals (nerve that stimulates effector cells), controls release of neurotransmitters

α adrenergic agonist responses

• vasocontriction

• cns stimulation

ß-adrenergic receptors

all are located on post synaptic effector cells

ß1- located primarily in the heart

ß2- located in lungs- smooth muscles of bronchioles, arterioles and visceral organs

ß adrenergic agonist responses

• bronchial, GI and uterine smooth muscle relaxation, glycogenolysis, cardiac stimulation

dopaminergic receptors

additional adrenergic receptors, stimulated by dopamine, cause dilation of the following blood vessels- increased blood flow

• renal

• mesenteric

• coronary

• cerebral

catecholamines

substances that can produce sympathomimetic response

endogenous

• epinephrine, norepinephrine, dopamine

synthetic

• dobutamine, phenylphrine hydrochloride

***depending on dose, MOA can be altered, vasodilation can become vasoconstriction in large doses

direct acting sympathomimetic

ex- epinephrine

indirect acting sympathomimetic

ex- amphetamines

mixed acting sympathomimetic

• directly stimulates receptor by binding to it

• indirectly stimulates the receptor by causing the release of stored neurotransmitters from vesicles in the nerve endings

• ex- ephedrine

physiological response to mixed acting sympatheomimetics

increased hr and bp

increased bronchodilation

drug effects- stimulation of α adrenergic receptors on smooth muscle

drug effects- stimulation of ß1-adrenergic receptors on the myocardium,
atrioventricular (AV) node, and sinoatrial node results in cardiac
stimulation.

drug effects- Stimulation of ß2-adrenergic receptors on the airways results in
bronchodilation (relaxation of the bronchi).

indications- treatment of asthma and bronchitis

indications- treatment of nasal congestion

indications- temporary relief of conjunctival congestion (eyes)

indications- reduction of intraocular pressure and dilation of pupils, treatment of open angle glaucoma

indications- cardiovascular

ADD IMAGE FROM SLIDES

vasoactive sympathomimetics (pressors, inotropes)

aka cardioselective sympathomimetics

• used to support the heart during cardiac failure or shock, various α- and ß-receptors affected, treats shock or low circulation

• stabilises pressure

• ex: dobutamine, dopamine, midodrine (good for those with weak renal), epinephrine, phenylphrine, norepinephrine

inotropes: increase contractivity (increases HR)

pressor: increase vasocontritction (increase pressure)

dobutamine hydrochloride

• problems with cardiac function

• selective vasoactive Beta 1 adrenergic drug similar to natural catecholamine dopamine

• stimulates Beta 2 receptors on heart muslces, increases cardiad output by increasing contractility (positive inotropy), increases stroke volume, esp useful in pts with heart failure

• given IV by continous infusion usually as picc line or central line

dopamine hydrochloride

• naturally occuring catecholamine

• potent dopeminergic, activates beta 1 and alpha 1 receptors

• low dose: dilate blood vessels in braine, heart, kidneys, mesentery (increased blood flow)

• high infusion rate: improve cardiac contractility and output (beta 1 adrenergic activity)

• highest doses: vasoconstriction (alpha 1 adrenergic receptor activity)

midodrine hydrochloride

• to stabilise bp, for treatment of symptomatic orthostatic hypotension

• prodrug: medication that becomes active in the body (converted in liver)

• converted by liver to active form: desglymidodrine

• alpha 1 adrenergic receptor stimulation

• front loading of doses to prevent supine hypertension (more drug initially and then drop the dose throughout the day, this is to prevent high bp when they are asleep)

epinephrine hydrochloride (adrenalin)

• endogenous vasoactive catecholamine

• acts on both alpha and beta receptors of tissues innervated by sympathetic nervous system

• improves vascular collapse (helps with shock or allergy that causes vasodilation)

• prototypical nonselective adrenergic agonist

• for emergency

• one of the primary vasoactive drug in advanced cardiac life support protocols

norepinephrine betartrate (Levophed)

stimulates alpha adrenergic receptors

• one of the first drug used for septic shock, for shock and hypotension

• causes vasoconstriction

• direct stimulation of beta adrenergic effects on the heart (Beta 1 adrenergic receptors not beta 2 for lungs)

• administered by continous infusion

phenylphrine hydrochloride (neo-synephrine)

• alpha receptor

• short term treatment to raise bp, for disarrythmias, control of supraventricular tachycardias, for vasocontriction in regional anasthesia, topical opthalmic drug (causes mydriases - make pupils bigger), nasal decongestant

α-Adrenergic Adverse Effects

• cns: headache, restlessness, excitement, insomnia, euphoria

• cv: palpitations or dysrhythmias, tachycardia, vasoconstriction, hypertension

• other: loss of apetite, dry mouth, nausea, vomiting, taste changes (rare)

  • raa system is activated with this medication, causes your heart to work harder as well as sodium and water retention, causes dryness in other areas

ß-Adrenergic Adverse Effects

cns: mild tremors, headache, nervousness, dizziness, insomnia, euphoria

cv: chest pain, increased HR, palpitations or dysrhythmias, hypertension, vasoconstriction

other: sweating, nausea, vomiting, muscle cramps aka klondikation

drug interactions of adrenergic drugs

• anasthetic drugs

• digoxin (bc its a positive inotrope)

• tricyclic antidepressants

• monoamine oxidase inhibitors (MAOIs) (with prev, slight impact on bp will interact with adrenergic drugs)

• antihistamines (both will cause vasoconstriction)

• thyroid preparations (same as prev, impacts bodys cellular metabolism)

nursing implications of adrenergic drugs

• comprehensive health history

• assess for allergies and athma, hypertension, other cv diseases

• assess renal, hepatic and cardiac function pre treatment

• baseline assessment of vitals, peripheral pulses, skin color, temp, cap refill, postural pressure and pulse

• follow admin guides of medication

• salmeterol xinafoate is indicated for the prevention of bronchospasms, not management of acute symptoms

• avoid otc and other meds for interactions

• administeration of 2 adrenergic drugs may precipitate severe cv effects such as tachycardia or hypertension

nursing implication of adrenergic drugs for iv admin

• check iv site for infiltration

• use clear iv solution

• use infusion pump

• infuse slowly to avoid dangerous cv effects

• monitor cardiac rhythm

nursing implications of adrenergic meds for pts w chronic lung diseases

• instruct pt to avoid factors that cause excacerbation

• encourage fluid intake (up to 3000mL per day)

• educate pt on proper dosing, use of equipment and equipment care

nursing implications- monitoring therapeutic effects of adrenergic drugs (cv uses)

• decreased edema

• increased urinary output

• return to normal vital signs

• improved skin colour and temp

• pedal pulse intact and strong to palpation

nursing implications- monitoring therapeutic effects of adrenergic drugs (asthma)

• normal resp rate

• improved breath sounds, fewer crackles

• increased air exchange

• decreased cough

• less dyspnea

• improved blood gases

• increased activity tolerance

TRANSFER P FORMULARY TO PAPER

Adrenergic Blockers

• binds to adrenergic receptors but they block stimulation of SNS

• have opposite effect of adrenergic drugs

• inhibit sympathetic stimulation

• aka adrenergic antagonists, sympatholytics, a blockers, b blockers and a b blockers

drug effects and indications of α- Blockers

• cause arterial and venous dilation which reduces peripheral vascular resistance and bp

• used to treat hypertension, used to control and prevent hypertension in pts with phenochromocytoma, raynaud’s disease, acrocyanosis and frostbite

• effect on receptors on prostate gland and bladder decreases resistance to urinary outflow, reducing urinary obstruction and relieving the effects of benign prostatic hyperplasia

• phentolamine

• competitive is stronger and works faster than non competitive which is slower but lasts longer

• common a blockers: phentolamine mesylate (rogitine), prazosin hydrochloride (minipress), tamsulosin (flomax)

Phentolamine

• phentolamine: antidote for adrenergic medication quickly reverses potent vasoconstrictive effects of extravasated vasopressors such as norepinephrine and epinephrine, restores blood flow and prevents tissue necrosis

• a blocker

• reduces systemic vascular resistance, used to treat hypertension

• establish diagnosis of phenochromocytoma (tumour of adrenal glands- causes massive amts of catecholamines which causes adverse effects- hypertension)

• most commonly used to treat exasveration of vasoconstrictive drugs (dopamine, norepinehrine and epinephrine)

adverse effects of a blockers

cv: palpitations, orthostatic hypotension, tachycardia, edema, chest pain

cns: dizziness, headache, anxiety, depression, weakness, numbness, fatigue

gi: nausea, vomiting, diarrhea, constripation, abdominal pain

other: incontincence, dry mouth, pharyngitis

Tamsulosin (flomax)

• a blocker used for bening prostatic hyperplasia, exclusively for male pts

• contraindications: allergy, concurrent use of erectile dysfunction drugs such as sildenafil

• AE: headache, abnormal ejaculation, rhinitis

B blockers

• block stimulation of B receptors in SNS

• compete with norepinephrine and epinephrine

• selective or nonselective

  • act on B1- called cardioselective

  • nonselective work on b1 and b2

B receptors: moa of cardioselective b blockers (B1)

• reduce sns stimulation of the heart

• decrease HR

• prolong SA node recovery

• slow conduction rate through the AV node

• decrease myocardial contractility, thus reducing myocardia oxygen demand

B Receptors: moa for non selective B blockers (B1 and B2)

• same cv effects ad cardioselective b blockers

• constricts bronchioles, results in narrowing of airways and shortness of breath

• produces vasoconstriction of blood vessels

Beta blockers indications

decrease demand for myocardial oxygen: angina, MI, hypertension

inhibit stimulation from catecholamine: cardioprotective

also dysrhythmias

beta blockers AE

cv: av block, bradycardia, heart failure

cns: dizziness, fatigue, depression, drowsiness, unusual dreams

gi: nausea, vomiting, constipation, diarrhea

hematologic: agranulocytosis, thrombocytopenia

metabolic: hyperglycemia or hypoglycemia, dyslipidemia

other: erectile dysfunction, alopecia, bronchospasm, wheezing, dry mouth

non selective b blockers: interferes with normal responses to hypoglycemia (tremor, tachycardia and nervousness), can mask symptoms, use with caution in diabetes pts

atenolol/metoprolol

• cardioselective B blocker

• commonly used to prevent future heart attacks of pt has had 1

• for hypertension and angina

• management of thyrotoxicosis to help block excessive thyroid activity symptoms

• IV use and switched to a higher dose oral dose at home

carvedilol

• non selective B blocker, a1 blocker, calcium channel blocker and possible antioxidant

• uses: heart faulure, hypertension and angina

• used as combination or adjunct drug, added to digoxin, furosemide and angiotensin converting enzyme inhibitors when used to treat heart failure

• slows progression of heart failure

• 
  

cardioselective B blockers

• atenolol (Tenormin) (NOT FOR PREGNANT WOMEN)

• esmmolol (Brevibloc)

• metoprolol (lopressor)

adrenergic blocking drugs: nursing implications

• assess for allergies and perform thorough cardiac assessment

• remember that a blockers may precipitate hypotension

• remember that b blockers may precipitate bradycardia, hypotension, heart block, heart failure and bronchoconstriction

• avoid use of otcs

• encourage pt to take med as prescribed, never to stop taking these meds abruptly, tell them to report constipation, development of urinary hesitancy or bladder distension, palpitations, dyspnea, nausea, vomiting

• teach pts to change positions slowly, and avoid caffiene

• avoid alcohol, hazardous activities until blood levels become stable

• monitor for adverse effects

when would you not use adrenergic blockers

• allergy

• can pt tolerate additional vasodilation and drop in bp?

  • peripheral vascular disease

  • liver or kidney dissease

  • coronary artery disease

  • peptic ulcer

  • sepsis

adrenergic blocking drugs therapeutic effects to monitor

• decreased chest pain in pts with angina

• return to normal bp and heart rate

• other specific effects depending on drug