patho pharm exam 1

what is needed for safe medication administration and nursing care

KAS

knowledge

skill

attitudes toward administering: care plans, being empathetic, etc

QSEN (quality and safety education for nurses)

patient centered care, teamwork, evidence based practice, quality improvement, safety, informatics

generic

not capitalized

trade

copyright symbol, capitalized

filler ingredients = can cause problems

black box

the warning on medicines that regulates drugs

CDER

test drugs to see if they can be otc or prescription

dependance

physiological or psychologic need for substance (body cant function wo it)

usually controlled substances

physical need = physical condition without drug

withdrawal

physical discomfort when stop using

schedules

schedule 1 - most potential for abuse

schedule 5- least potential for dependance

therapeutic agent categories

drugs or meds - therapeutic or adverse response

biologics/biosimilar - make things in body that exist alr in low amounts

complementary medicine - on top of meds/biologics

three types of drug names

chemical, generic. trade

OTC

no provider needed

adverse effects if not used properly

easy to get

might not help

prescription drugs

from provider

lots more benefits = max therapy

they monitor adverse effects

phases of nursing process

assessment - look @ desired and adverse effects, collect data

analysis/diagnosis - whats wrong, what can go wrong, activity intolerance, pain, risk of falls, urinary problems

planning -goals, interventions, short long term goals

implementation - what does the nurse need to to for success? delegate care

evaluation - see if plan worked

health history general questions

chief complaint

allergies

past med hx

fam hx

drug hx

health management (when last time visit doctor?, can u sleep)

reproductive hx

personal social hx (alc, caffine, religious)

health risks

what do you need to know for all meds?

what drug

names

intended use

effects

contraindications

side effects

route

adverse events

adverse effects? (2)

side effect - non therapeutic rxn, transient

allergic/shock - serious, monitor closely

5 MAIN RIGHTS

patient, medication, dose, route of admin, time of delivery

extra rights to med administration

right reason, refuse, knowledge, documentation

THREE MAIN CHECKS WITH DRUG ADMIN

check MAR (med record)

check during prep

check before administration

stat

given immediately once

asap

within 30 mins

routine

course of treatments, regular schedule

single

given once at specific time, preordered

prn

as needed, based on condition

standing

based on circumstance, not patient condition

concentration

ex. 125mg/5ml

routes of drug admin

enteral - po, gi tract

topical - absorb in skin

parenteral - bypass gi tract, straight to blood, injections

tablets/capsules

enteral

caries with bioavailability based on pt

sublingual and buccal

enteral

rapid onset due to rich blood supply

rapid dissolving tablet and films

enteral

no need for water

NG or G tube

enteral

ng = nose to stomach

g = tube in stomach

transdermal

topical

patch

slow absorption

opthalmic

topical

treat eye

can be irrigation, etc

otic

topical

ear to break up blockages

nasal

topical

FAST

vaginal

topical

rectal

topical

bypass vomitting

SLOW

intradermal

parenteral

small volume

easy absorb due to more blood supply flow

in dermis

subcutaneous

parenteral

deeper tissue layers

insulin

intramuscular

parenteral

ventrogluteal site - no big vessels, best spot

deltoid - teens and adults

vastus lateralis - above knee slightly, for babies

IV

parenteral

rapid onset

full bioavailability

what r three types of iv

large volume infusion - matinence

intermittent infusion - another iv that is used alongside a large infusion

iv bolus/push - concentrated dose given into circulation

drug receptor

portion of tissue that drug binds to —> action

PD

pharmacodynamics

study of what drug does to body

efficacy

max potential of a drug

focus on this more

potency

amount of drug needed to have an effect

more potent means smaller dose to get effect

affinity

drug attraction to receptor, higher affiniity means more drug will reach the receptor site

agonist

attracted to receptor since is similar to substance in body (hormones, enzymes), MAKES SIMILAR REPSONSE

PERFECT KEY

full agonist - have maximum efficacy

partial agonist - less than EMAX

antagonist

key also fits in hole but doesnt make a response, just blocks it from doing anything

Competitive antagonist - high affinity but still can be knocked off

noncompetitive antagonist - not reversible

EC50

concentration of drug that gives half the max result

lethal dose

which dose will 50% of population die

toxic dose

dose that makes 50% of pop toxic resultse

effective dose

dose that produces half the max therapeutic result for 50 percent of population

ionic vs hydrogen bonds

ionic bonds - reversible

hydrogen - attraction of hydrogen atom

selectivity

is the drug able to bind to a lot of receptors?

better to high selectivity

ED50

50% of pt will respond

emax

max effect a drug can have

TI

LD50 / ED50

smaller it is, the more risk with the medicine since the effective dose is close to the lethal dose

potency

less amount of drug but max effect = potent

efficacy

what is the mex effect a drug can bring

more important than potency, most of the time choose which is EMAX

more receptors means what for a drug?

more can bind = more effects with less of a dose

4 pharmacokinetic processes?

absorption

distribution

metabolism

excretion

absoprtion

ingesting —> bloodstream

bioavailibility affected

first pass effect - how much meds taken by liver?

how long does it take to produce effect

bioavailibility

low bioavail = more drug needed to reac MEC

what affects drug absorption

dose

route

lip[id soluble? (this one can pass)

surface area of absorptive site

digestive mobility

blood flow

ph

ionized? (trouble going)

nonionized vs ionized

think of aspirin in stomach

in stomach, becomes nonionized due to acid and can cross membranes

in small intestine, goes back to ionized and cant pass thru

distribution

meds are in blood alr

based on blood flow, protein binding, acidic and basic drugs

drug protein complexes

affect distribution

protein bind to drugs = ineffective and nvr reach target

blood brain barrier/ fetal placenta barrier

prevent meds from coming in due to tight membranes

metabolism

LIVER!!!!!!!!!

prepare for excretion

PHASES of metabolism in liver

make it so that drug cant be reabsorbed

phase 1 - CYP 450 system —> inactive drug by making it polar (water soluble)

phase 2 - make it more water soluble, renal excretion

GAS stages

alarm adaptive or resistance and exhaustion

ALARM

stress triggers HPA, activate SNS

resistance

adrenal - cortisol

sns nerve fibers - nor/epinephrine (catecholamines)

exhaustion

continued stress

onset of disease

breakdown of systems combatting stress

hpa axis

alarm phase sets this chain off

stress, hypothalamas CRH, anterior pituitary ACTH, adrenal cortisol

cortisol

acth (pituitary) activates adrenal —> cortisol

lipophillic

glucogenesis

protein breaking in other tissue (not liver)

low wound healing (bc glucose lvl)

HTN, lower bone density

supress Th1 (immune cells), stimulate Th2 (inflammatory)

allostasis

allostatic load - cumulative wear and tear

how body maintains homeostasis

reactive response (stress responses)

classic stress, physical and mental stress

anticipatory response (stress responses)

worrying before it happens

conditional response

PTSD

associate stimulus with danger

catecholamines

NORepinephrine - vasoconstriction, up BP, dilate eyes, sweat glands in pits/palms, piloerection

epinephrine - (focus on heart), vasodilation (of certain tissues to supply flow to others), increase glucose

neuropeptide y (NPY)

stress mediator, growth factor, vasoconstriction

influences hunger, temp, emotion

cortisol effects on pregancy

supresses luteinizing hormone, estradiol, progesterone, hypothalamic gonadotropin hormone (releases reproductive hormones)

proinflammatory cytokines

stress ups this

decrease t cell and b cell function (immune cells)

drug therapy during pregnancy?

hold off unless treating major conditions (epilepsy, HTN, diabetes, infections, autoimmune disorders)

pregnancy and the pharmacokinetics

change all stages ADME, excretion rate may increase

teratogens

substance organism or physical agent that permanantly damages fetus or abnormality

diethystilbestrol (DES), thalidomide, methotrxate

phases of pregnancy

wk1-2 - doesnt matter, kills embryo or no effect

3-10 - teratogensmore harmful important since organs developing

11-40 - most substance trasnfer since most blood flow and thinning membranes on placenta

drug category ratings`

A - safe

B - confidently safe (no ibuprofen in 3rd trimester)

C - animals show adverse effects, avoid unless needed (ssri)

D - avoid it, alcohol

X - absolutely not, will cause lots of harm

lactation and factors that effect it

time between drug, dose, illicit drugs

infants

0-12m

have ingest all meds (think of other ways of admin)

IM routes

risks vs benefits

toddlers 1-3

short and concise language to toddler, mix with foods

vastis lateralis injection (side of upper thigh)

preschoolers

3-5

explain so they involved

school-age children

6-12

longer explanations detailed

pharmocokinetics in neonates and peds

absorption - 1-2y ph less, slow gastric emptying, lower first pass = lower dose needed, faster IM absorption

distribution - more water, lower fat, less protein binding, bloodbrainbarrier immature

metabolism - immature liver, older have faster metabolism

excretion - less excretion due to lower kidney filtration

neonates and how do you determine dose?

body surface, weight kg, ex. 1mg/kg