Week 1- Intro to Pharmacology + Intro to Pathophysiology + Pharm Principles Flashcards
dPharmacology (Def)
The study of the biological effect of drugs (chemicals) that are introduced into the body to cause some sort of change
Pharmacokinetics (Def)
What happens to drugs in the body
Pharmacodynamics (Def)
- Mechanism of action
- Effects on the body
Chemical name
(N-acetyl-para-aminophenol)
- long and complex
- used in research
-often when it is getting created
Generic name
(acetaminophen)
- This is the name you really need
- Official name of drug
- Only 1 generic name, usually more complicated, lower case letter.
Trade name
(Tylenol)
- Brand name, given by pharmaceutical company
- Easier to remember and pronounce
-Upper case
Prototype
- One drug, typically the first, that represents a group or class of medication.
- New drugs in the class are compared to the prototype (effectiveness/ side effects). Other manufactures of ibuprofen get compared to the prototype
- Ex: ibuprofen/ Advil- represents class NSAIDS
Therapeutic effect (Def)
Intended effect of the drug and what we want to happen
Side effect (Def)
Unintended effect, often unaviodable
Adverse effects (Def)
Unexpected reaction, dangerous reaction
Toxicities (Def)
Harmful effects
Allergic reaction
Unexpected, may be dangerous, involves an immune response to the drug
What do you need to know about each drug?
1) Name: trade and generic –> only generic on test
2) Classification (drug class): given to describe a group of medications that usually work similarly
3) Mechanism of action: how the drug works in the body
4) Indications: Why are we giving the med? What is it used to treat?
5) Common/Serious Adverse Effects: most common ones
6) Contraindications
7) Nursing indications: what to worry about when giving the med? Prior assessments? CYP?
New drugs are approved though:
FDA- chemical identified, strict testing (5 in 100,000 will be marketed)
Preclinical Trials
Tested on animals for therapeutic adverse effects
Phase I studies
Human volunteers are used to test
Phase II studies
Drug is tested on patients who have the disease that drug is designed to treat
Phase III studies
Vast clinical market. Prescribers informed of adverse effects and monitor patients closely. Can still be withdrawn from market
Phase IV studies
Continued evaluation by FDA
Schedule 1 drugs
Not approved for medical use, no reason to prescribe (Heroin, LSD)
Schedule 2 drugs
Used medically, but HIGH potential for abuse. NO refills allowed. Narcotics. (Hydromorphine, oxycodone)
Schedule 3 drugs
Less potential for abuse but still some (Non barbiturate sedatives, non-amphetamines, stimulants (Lortab, Vicodin)
Schedule 4 drugs
Some potential for abuse. Primarily sedatives, anti-anxiety (Xanax, valium)
Schedule 5 drugs
Low potential for abuse. Medications containing small amounts of certain narcotics or stimulants usually antitussives (cough suppressants with codeine, ephedrine containing meds)
Over the Counter Meds
Criteria: consumers must be able to dx. own condition and monitor effectiveness EASILY
- Over 80 classes of OTC
-Prescription strength OTC- same drug available OTC but with higher dose. Abuse potential available behind the pharmacy counter
Dietary and Herbal Supp.
- Can only claim effect on body STRUCTURE or FUNCTION (no medical conditions). Can’t say the treat anything, no MOA, or how it works.
- Not FDA approved
- Ex: St. John’s Wort - affects emotional balance (not treat depression)
- !! Some herbals can increase the toxicity of rx. meds and cause decreased therapeutic effects !!
Example of adverse interaction b/w drugs and herbals
Ginko biloba suppresses platelet aggregation (therefore can increase risk of bleeding)
Teratogens
Can cause congenital malformations in developing fetus (alcohol, marijuana, nicotine)
Teratogens: Category A
Safe for fetus
Teratogens: Category B
Lack of studies to show benefit v. risk
Teratogens: Category C
No studies, animals studies possible risk, talk to OB
Teratogens: Category D
Drugs that have possible risk to the fetus. Discussion with OB about risk to fetus
Teratogen: Category X
Drugs that have KNOWN RISK that CAN’T be outweighed by possible benefit (Thalidomide, chemo agents, isotretinoin/ retin A)
Pharmacogenomics
Study how genes affect a person’s response to the drug. Combines pharmacology and genomics to develop effective, safe meds and doses that will be tailored to person’s genetic makeup
Three disruptions of homeostasis
- physical, mental, and social
Cause of disease
- Intrinsic: autoiminne disorder
- Extrinsic: bacteria/ virus
- For disease to occur: pathogen, conducive environment, susceptible host
Intrinsic factors
Genes, immunity, age (very old/ very young), gender
Extrinsic factors
Bacteria, viruses, injury, behaviors, stressors, fungi
Process of Disease
- Identification - signs/symptoms
- Occurrence - how often/ when
- Diagnosis - identify
- Etiology - cause
- Prognosis - likelihood of recovery
Stages of disease
- Exposure
- Onset
- Remission
- Covalescence
Types of Onset
- Sudden
- Insidious- slow and gradual, chronic disease process (GI bleed)
- Latent- not active but can be (Chickenpox)
- Prodromal- pre sickness
- Manifestations- true signs/ symptoms
Types of disease: Idiopathic
We don’t know what cause it. Unknown, we might have ideas or theories
Types of disease: Iatrogenic
Caused by some treatment. A ‘medical’ cause. Ex: getting a colonoscopy and intestinal lining cut
Types of disease: exacerbation
Worsening of a disease, acute decline in a person’s chronic disease
Hypo___
under
Hyper___
above, over
____penia
lack of, deficiency
____cytosis
refers to cells, increase
____osis
process or condition, production or increase, invasion or infection
____itis
inflammation
____pathy
disease or suffering
Three phases of drug action
1) Pharmaceutic
2) Pharmacokinetic
3) Pharmacodynamic
Pharmaceutic Phase
The dissolution phase occurs
In the pharmaceutical phase all oral drugs must go through ____ in order to be absorbed.
dissolution
Tablet –> granules –> smaller particles –> solution in GI tract –> drug absorbed
Four processes of pharmacokinetic phase
1) Absorption (small intestines)
2) Distribution (in blood)
3) Metabolism/ Biotransformation (think about liver)
4) Excretion (kidneys, a little excreted in liver)
What phase of the pharmacokinetic phase do IV medications start at?
Distribution
What do meds go through between distribution and absorption
Phospholipid layer
What types of medications go through the first Pass Effect
Anything orally/ PO
First Pass Effect
Alters the amount of drug that becomes absorbed. This is occurring in the absorption phase in the liver during the pharmacokinetic process.
_______is the amount of drug left after the first pass
bioavailability
How much of a drug is bioavailable after going in an IV
100- does not go through liver
Three Routes of absorption
1) Enteral
2) Parenteral - cath
3) Topical
Enteral absorption
By way of GI tract (oral/gastric mucosa, small intestine, rectum)
- EC (enteric coated) intended to break down in small intestine NOT stomach. Still goes through first pass effect
-PO break down starts in stomach, absorbed in small intestine, first pass effect
- SL, buccal, rectal all highly vascularized tissue. NO first pass effect, by-pass liver
Parenteral absorption
- SQ, IM, IV, intrathecal (into spinal canal), epidural. IV is the fastest, no barriers to absorption. No first pass effect
Topical (transdermal)
Application of meds to body surface. Eyes, skin, ears, nose, lungs
What effects distribution?
Blood flow
Blood brain barrier
Protein- Binding effect
Pharmacokinetic: distribution
Process by which the drug molecules leave the blood stream and arrive at site of action.
Depends a lot of adequacy of blood circulation.
Decreased blood flow, decreased distribution
Blood brain barrier
Cells in the capillary wall in the brain with very tight junctions that prevent drug passage
Only drugs that have a transport system or aare
What drugs can cross the BBB? & what two substances
Alcohol + Glucose
- Have the specific transport system OR are lipid-soluble that can cross BBB
It is a protective mechanism
Protein-Binding Effect
Temporary storage of drug molecule that allows drug to be available for a longer period of time
-Drug ratio of bound to unbound molecules varies
- Binding is reversible (a rapid process)
Goal of protein-binding effect
Maintain a steady free drug concentration (Steady State)
What do protein-binding drugs bind to in our blood?
Albumin
Pharmacokinetic phase: Metabolism
When the drug is no longer in action and becomes broken down (inactivated). New structure is called a metabolite
Also called biotransformation
Where is the major place that metabolism takes places
Liver. Converts lipid-soluble drugs into water soluble metabolites. Uses Cytochrome P-450 enzymes
What is Cytochrome P450?
A group of isoenzymes that metabolize drugs .
About 1/2 drugs are metabolized by this.
Be aware of drug-drug interactions
Three ways drugs work through CYP450
1) Substrate
2) Inducer
3) Inhibitor
Substrate CYP450
If a drug uses the CYP450 system for metabolism. Pro-drug is a substrate that uses the CYP450 system to convert to an active form.
Inducer CYP450
Speeds up metabolism of the CYP450 system. Reduces the amount in the body, reduces therapeutic effect
Inhibitor CYP450
Slows down metabolism of CYP450. Increases the amount of drug in body, increases toxicity
Pharmacokinetic: excretion
Elimination of drug from the body, generally only hydrophilic drugs can be excreted effectively
Three ways the kidney excretes
1) Glomerular filtration
2) Tubular secretion
3) Tubular reabsorption
What to assess regarding kidney function and excretion
Renal labs (blood urea nitrogen (BUN), creatinine
GFR (glomerular filtration rate). Best measure of kidney function, calculated from the creatinine level, age, body size and gender.
GFR is related to free drug concentration in plasma
Elimination: Half life
Serum half life is time required for the serum concentration of a drug to decrease by 50%
Takes ____half-lives for ____% of the drug to be eliminated
5 half-lives for 97%
Elimination goal
Get to steady state. Takes about 4-5 half lives.
Steady state occurs when intake of drug equals amount metabolized/ excreted
Around the Clock Dosing
Goal to maintain 50% concentration in body. Used to treat chronic pain
Onset of drug
time it takes for drug to elicit therapeutic response (latent period)
Peak of drug
Time it takes to reach its maximum therapeutic effect
Duration of drug
Drug concentration is sufficient to elicit a therapeutic response
What is phase 3 of drug action and what does it do?
Pharmacodynamic phase- it is what the drug does to the body
Pharmacodynamic Phase
-Drugs may increase/decrease/replace/inhibit/destroy/protect or irritate to create a response
-Drugs exert multiple rather than single effects on the body (desired or not)
Pharmacodynamics: receptors
- receptors are protein located on cell surfaces
-chemicals in the body interact with drugs to produce effects (Hormones and neurotransmitters)
-these chemicals bind with the drug = drug receptor complex
Receptor Theory of Drug action: Agonist
Drug that has the ability to INITIATE a desired therapeutic effect by BINDING to a receptor. Typically what we want
Receptor Theory of Drug action: Antagonist
A drug that produces its action NOT by stimulating receptors but PREVENTING or BLOCKING or INHIBITING other natural substances from binding and causing a response
What is it called when drugs act through simple physical or chemical interactions with small molecules
Receptor-less activation
Narrow therapeutic Index (NTI)
-The measure of relative safety of drug
-NTI have a ratio of lowest concentration at which clinical toxicity commonly occurs
Black Box Warning
Required by the FDA for drugs that are especially dangerous. Strongest safety warning a drug can carry and still be on market
Where does the black box warning need to be?
- package insert
-product label
-magazine or advertising
Who created high alert medication standards and when?
1995 Institue for Safe Medication Practices (ISMP)
High alert drugs
- insulin
-heparin
-opioids
-injectable potassium chloride
-neuromuscular blocking agents
-chemotherapy drugs
Drug-drug interactions
- may be intended/unintended
-increased risk with polypharmacy - narrow therapeutic index drugs
-drug-food
-drug-herb
-drug-disease
What are the four drug interactions that INCREASE therapeutic effects
1) additive
2) synergism/potentiation
3) activation
4) displacement
Additive effect
2 drugs taken with similar MOA
Synergism/potentiation
2 drugs with DIFFERENT MOA but result in a combined drug effect greater than that of either drug alone
Activation
of drug- metabolizing enzymes in the liver –> decreases metabolism rate of the drug (CYP450)
Displacement
Displacement of one drug from plasma protein- binding sites by a second drug –> increases effect of displaced drug
Three drug interactions that DECREASE therapeutic effect
1) Antidote
2) Decreased intestinal absorption
3) Activation
Antidote
Drug given to ANTAGONIZE the toxic effects of another drug
Decreased intestinal absoption
Applied to PO meds
Activation
of drug-metabolizing enzymes in the liver –> enzyme inducers
— increase metabolism rate of the drug (quicker out of the system)
— CYP450 system
Older adults and pharmacokinetic consequnces
1) Hepatic changes
2) Cardiac and circulatory changes
3) GI changes
4) Renal changes
