Patho 1st unit

schedule 1

available only by prescription and provided by a pharmacist

what are the 3 categories of pharmacotherapeutics?

drugs/ medication- a chemical agent capable of producing a physiological response

biologics- a medication produced from a living organism (normally administered IV or IM)

Natural health products - sourced/ derived from plants (vitamins, calcium, etc)

what are the 3 types of drug names

1. generic: describes the drug, same name around the world (ex, ibuprofen)

2. brand/trade : name by manufactured company (ex: Advil)

3. chemical: chemical composition of the drug

what is biosimular?

cheaper version of the patent biologic but made the same with the same things.

schedule 2?

available only from a pharmacist

schedule 3?

open access only in a pharmacy

unscheduled

can by anywhere

nursing process

assessment, diagnosis

planning

implementation

evaluation

AC?

BEFORE MEALS

PC

AFTER MEALS

QD

ONCE DAILY

BID

TWICE DAILY

TID

THREE TIMES DAILY

QID

FOUR TIMES DAILY

QHS

AT BEDTIME

QAM

EVERY MORNING

QPM

EVERY EVENING

QOD

EVERY OTHER DAY

QH

EVERY HOUR

Q2H

EVERY 2 HOURS

Q3H

EVERY THREE HOURS

PRN

AS NEEDED

pharmacokinetics

what the body does to the drug (ADME)

pharmacodynamics

what the drug does to the body ( drug effects, mechanism of action)

what makes a drug easily absorbed and distributed

non ionized

lipophilic

small

what makes a drug easily excreted

ionized(polar), hydrophilic

diffusion

high concentration - low concentration

facilitated diffusion

high concentration - low concentration uesing pumps

three types of ossmosis

isotonic- equal concentration inside and out of a cell

hypotonic- higher concentration inside cell water flows inside - cell swells

hypertonic- higher concentration outside cell - water rushes out - cell shrinks

absorption

drug into circulation (bioavalibilty)

distribution

transport of drug through the body to target tissue (blood flow, tissue size, ppb, barriers— factors)

metabolism

prepares drug for excretion

activates pro drugs (liver)

excretion

filters through kidneys and excreted

blood flow percentage to parts of the body

bone marrow- 5%

brain- 18%

heart- 5%

liver-25%

kidneys- 20%

muscles -20%

skin -7 %

2 main plasma proteins

albumin— binds acidic drugs

alpha- 1 acid glycoproteins - binds basic drugs

unbound drugs vs bound drugs

unbound- active

bound - inactive

therapeutic range

amount of drug it takes to reach a state where positive effects are happening

c max

maximum concentration of a drug

timing it takes for peak concentration of intravenous

15-30 mins

timing it takes for peak concentration of intramuscular

30-60 mins

timing it takes for peak concentration of oral

60 + mins

loading dose

increased dose of something to immediately cause therapeutic range to be met

therapeutic index

how safe a drug is to be administered multiple times without reaching toxicity

TD50 (median toxic dose) / ED50(median therapeutic dose) = TI

the lower the number the more dangerous

narrow therapeutic index meds

Digitoxin (lanoxin)

warfarin (Coumadin)

phenytoin (dilantin)

tacrolimus (prograf, astagraf)

phase 1 metabolism

the liver uses enzymes ( especially the Cyp450 enzymes ) to chemically alter the drug

ex: cyp3a4 and cypia2

enzymes can be effected by inducers and inhibitors

inducers

make the enzyme work faster - drug will be broken down faster

inhibitors

slow down enzyme - make drug stay active for longer

enzymes are saturable

meaning there is no limit to how much drug they can process at once

phase 2 metabolism

conjugation: body attaches another chemical group to the drug or metabolite - makes substance more water soluble and easier to excrete ( doesn’t always go through phase 2)

metabolism of acetaminophen

phase 1 : → NAPQI (toxic) → converted by gluthione → non toxic substance

what is used in an acetaminophen overdose

N- acetylcysteine ( restores deprived glutathione stores)

pro drug

Inactive drug - active metabolite

cardiac output equation

HR X SV

normal HR= 80-100

normal SV= 70ml

Clarence

rate of elimination of a drug in an hour

elimination(total amount of urin voided in an hour/peak plasma concentration = Clearence (mg/dl/hr)

1st order elimination

elimination is proportionate to drug serum concentration

zero order elimination

rate of elimination/ clearance is constant no matter how high drug serum levels are

eg: ethanol, aspirin, phenytoin

creatinine

natural waste product of creatine ( muscle amino acid compound)

excreted by the kidneys

creatinine clearance

indication of GFR function

CRCL(ml/min) = ((140-age) x lean body weight (kg))

---

serum creatinine (mg/dl) x 72

→ whole thing times by 0.85 if female

half life

time needed for drug plasma concentration to decrease by 50%

4X half life = 90% of drug eliminated

receptor affinity

strength/ length of binding

specific, saturable, reversible

drug efficacy

effectiveness

potency

strength → how much drug is required to reach therapeutic range

lower amount = higher potency

agonist

binds easily and mimics endogenous substance

eg: morphine

partial agonist

maximum response is smaller then full agonist even if all receptors are occupied ( can interfere with agonists)

eg: buprenorphine

inverse agonist

induces the opposite effect of the naturally binding substance

eg: caffeine bonds to adenosine receptors → which normally produces calming effects

antagonist

blocks the receptor to prevent endogenous or endogenous-like receptors from binding

eg: naloxone

factors influencing patients response to drugs

clinical factors: age weight, health issues

administration: drug form, route, interactions

pharmacokinetics: ADME

pharmacodynamics: how the drug acts

issues older adults face with drug effectiveness

• decreased peristalsis, acuity, elimination, GFR(reduces 1% every year)

• decreased liver func

• lower albumin ( effects PPB)

• decreased cardiac output (effects distribution)

• polypharmacy

issues paediatric patients have with drug effectiveness

immature liver/kidney func

more adipose tissue- cation with lipophilic drugs

dose is always calculated in kg of body weight

most common toxixity’s

ASA

Tylenol

Opioids

benzodiazepines

alcohol

THC

cocaine

clinical procedure in toxicity/ overdose

Airway

breathing

circulation

disability: assessment dysfunctions and treat accordingly - ex: seizures

exposure: identify the drug/ substance and treat

ASA toxidrome

• confusion

• tachycardia

• tachypenia

• hyperthermia

• diaphorisis

• vomiting

acetaminophen toxidrome

abdominal pain

loss of appetite

nasua/vomiting

diaphoresis

somnolence

opioid toxidrome

Bradypnea/apnea

bradycardia

somnolence/coma

constricted pupils

cocaine

agitation, tremors

tachycardia

tachypenia

hyperthermia

diaphoresis

dilated pupils

adsorption

treatment for overdose

binding of drug to decrease absorption

activated charcoal→ enteral administered→ binds drug to surface carbons - eliminated via stool

inducing metabolism

restoring metabolites → increase rate of metabolism

tx of tylonal toxicity

depleted glutathione enzyme → causes low phase 2 metabolism → accumulation of NAPB

tx: NAC(n-acetylcysteine) IV or PO → inhances phase 2 metabolism

tx of ETOH toxicity

depleted dehydrogenase enzymes→ Tx by metadoxin (IV) restores depletion → increases phase 2 metabolism

• induces ADH and ALDH metabolism

tx of opioid over dose

naloxone/narcan→ MU & kappa receptor antagonist (what opioids bind too)

onset: 2-4 mins

duration of action = 45 mins (multiple doses may be needed)

Tx of benzodiazepine toxicity

flumazenil (IV) → gabba receptor antagonists→ what benzodiazepines bind too

tx of ASA overdose

sodium bicarbonate: alkalization of urin pc → indie acidic drug excretion

hemodialysis

way to treat toxicity→ filtering all blood through a mechine