Exam 1 Slides Flashcards
(147 cards)
1
Q
Pharmacology
A
The study of the biological effect of drugs that are introduced into the body to cause some sort of change.
2
Q
pharmacokinetics
A
what happens to drugs in the body
3
Q
pharmacodynamics
A
- mechanism of action
- effects on the body
4
Q
chemical name
A
long and complex, used in research
5
Q
generic name
A
official name of drug, only one generic name, usually more complicated than the trade name, lower case
ex: acetaminophen
6
Q
trade name
A
brand name, given by pharmaceutical company.
easier to remember and pronounce
upper case
7
Q
prototype
A
- one drug (typically the first) that represents a group or class of medication
- new drugs in the class are compared to the prototype for effectiveness and side effects
- ex: ibuprofen/advil: represents the class of NSAID
8
Q
therapeutic effects
A
- intended effects of the drug
- what we want to happen
9
Q
adverse effects
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- unexpected reaction
- dangerous reaction
10
Q
side effects
A
-unintended effects
-unavoidable
11
Q
toxicities
A
harmful effects
12
Q
allergic reaction
A
- unexpected
- may be dangerous
- involves the immune system
13
Q
preclinical trials
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tested on lab ANIMALS for therapeutic and adverse effects
14
Q
phase I studies
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HUMAN VOLUNTEERS are used to test drug
15
Q
phase II studies
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drug is tried on patients who have the DISEASE that the drug is designed to treat
16
Q
phase III studies
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the drug is used in a VAST CLINICAL MARKET. Prescribers are informed of adverse effects and monitor their patients closely. Unexpected responses may occur and the drug may be withdrawn from the market
17
Q
phase IV studies
A
CONTINUED EVALUATION by the FDA
18
Q
schedule I controlled substance
A
- not approved for medical use, no reason to prescribe
ex: heroin, LSD, ecstasy
19
Q
schedule II controlled substance
A
used medically, but HIGH potential for abuse
ex: narcotics, amphetimines such as Dilaudid, oxycodone
NO REFILLS ALLOWED
20
Q
schedule III controlled substance
A
less potential for abuse
ex: non barbiturate sedatives, non-amphetamines, stimulants such as ketamine, testosterone, anabolic steroids
21
Q
schedule IV controlled substance
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some potential for abuse
ex: primarly sedatives, anti-anxiety medications such as xanax, valium, ambien
22
Q
schedule V controlled substance
A
low potential for abuse
ex: medications containg small amounts of certain narcotics or stimulants, usually antitussives such as cough suppressants with some codeine or ephedrine containing medications
23
Q
OTC medications
A
- over 80 classes
- prescription strength OTC - same drug available OTC but with higher dose
- consumers must be able to diagnose own condition and monitor effectiveness EASILY
- low risk of abuse or side effects
- some OTC are available behind pharmacy counter due to abuse possibility ex: sudafed containing meds
24
Q
dietary and herbal supplements
A
- can only claim affect on BODY STRUCTURE or FUNCTION (not medical condition)
ex: st. johns wort - affects emotional balance (does not treat depression) - FDA only monitors POST-MARKET
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adverse interactions (herbal medications)
- some herbals can increase the toxicity of medication or cause decreased therapeutic effects
ex: ginko biloba suppress platelet aggregation; can increase risk of bleeding in patients on blood thinners
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teratogens
substances that can cause congenital malformations in developing fetus
ex: alcohol, marijuana, and nicotine
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category a
safe for fetus
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category b
lack of studies to show benefit/risk
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category c
no studies, animal studies possible risk
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category d
drugs that have possible risk to the fetus
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category x
drugs that have a known risk
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pharmacogenomics
the study of how genes affect a person's response to drugs
- new field that combines pharmacology and genomics to develop effective, safe medications and doses that will be tailored to a persons genetic makeup
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pathophysiology
study of disease and injury
changes in the physiology of the body
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disease
disruption in homeostasis: could be physical, mental, or social
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homeostasis
tendency to maintain an equilibrium
steady state of internal chemical and physical conditions
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intrinsic factors causing disease
genes
immunity
age
gender
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extrinsic factors causing disease
bacteria
viruses
injury
behaviors
stressors
fungi
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stages of disease
exposure
onset
remission
convalescence
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idiopathic
unknown cause
- we might have ideas or theories
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latrogenic
caused by some treatment
- a medical cause
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exacerbation
worsening of a disease
- acute decline in a persons chronic disease
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hypo-
under, below
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hyper-
above, over
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-penia
lack of, deficiency
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-cytosis
refers to cells, increase
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-osis
process or condition
production or increase
invasion or infection
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-itis
inflammation
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-pathy
disease or suffering
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three phases of drug action
- pharmaceutic
- pharmacokinetic
- pharmacodynamic
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phase 1: pharmaceutic
all oral drugs must go through dissolution in order to be absorbed
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phase 2: pharmacokinetic
what the body does to the drug
four processes:
absorption
distribution
metabolism/biotransformation
excretion
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crossing cell membranes
- drugs must pass through cells that are close together to get to blood and site of action
- membrane structure is phospholipid
- drugs MUST BE lipid soluble to pass membrane
- water soluble drugs require passage through channels or pores
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first pass effect
- metabolism of drug before systemic circulation
- % of drug broken down in the liver
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bioavailability
the amount of drug left after first pass
- PO varies
- IV is 100%
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Enteral Route
by way of GI tract (oral/gastric mucosa, small intestine, rectum)
- enteric coated
- PO
- SL, Buccal, Rectal
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EC (enteric coated)
enteral absorption
- intended to break down in small intestine NOT stomach
- first pass effect
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PO
enteral absorption
- breakdown starts in stomach, absorbed in small intestine
- first pass effect
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SL, Buccal, Rectal
enteral absorption
- all highly vascularized tissue
- no first pass effect
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parenteral route
SQ, IM, IV, intrathecal (into spinal canal), epidural
IV: fastest (no barriers to absorption, often irreversible)
- does not go through first pass effect
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topical (transdermal) route
- application of meds to body surfaces
- eyes, skin, ears, nose, lungs
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pharmacokinetic phase: distribution
- movement of the drug through the body
- process by which the drug molecules leave the blood stream and arrive at the site of action
- depends largely on the adequacy of blood circulation
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disruptions in distribution
decreased blood flow = decreased distribution
- peripheral vascular disease
-abscesses
- tumors
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blood brain barrier (bbb)
- cells in the capillary wall of the brain with very tight junctions that prevent drug passages
- only drugs that have a transport system or are lipid soluble can cross
- alcohol can cross
- glucose can cross
- not fully developed in infants
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distribution: protein-binding effect
- temporary storage of drug molecules that allow for drugs to be available for a longer period of time
goal: maintain a steady free drug concentration aka steady state
*** only unbound drug is active and free to exert effects
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pharmacokinetic phase: metabolism
aka biotransformation
- method by which drugs are inactivated or biotransformed --> metabolite
- liver is the major site for this where it converts lipid-soluble drugs into water soluble metabolites
- kidney excrete these metabolites
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metabolism: CYP450
cytochrome p450: a group of isoenzymes that metabolize drugs
- about half of all drugs are metabolized by this system
- drug to drug interactions can occur when drugs metabolized by the same isoenzyme are taken concurrently
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cyp450 substrate
drug uses the cyp450 system for metabolism
- pro-drug is a substrate that uses this system to convert to an active form
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cyp450 inducer
speeds up metabolism of this system
- reduces the amount of drug in the body
-reduces the therapeutic effect
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cyp450 inhibitor
slows down metabolism of the cyp450 system
- increases the amount of drug in the body
- increases the risk of toxicity
ex: grapefruit/grapefruit juice - avoid for 2-4 hours after taking medications
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pharmacokinetics phase: excretion
elimination of drug from the body
- generally only hydrophilic drugs can be excreted effectively
kidney is the major site of excretion
- through glomerular filtration
- tubular secretion
- tubular reabsorption
Renal labs = blood urea nitrogen: BUN, creatinine
GFR (best measure of kidney function)
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elimination: half life
serum half life (T1/2) is the time required for the serum concentration of a drug to decrease by 50%
- takes about five half lives for 97% of the drug to be eliminated
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elimination
takes about 4-5 half lives for "steady state" to occur which is the GOAL
- steady state occurs when intake of drug equals amount metabolized or excreted
- T1/2 determines dosing interval
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around the clock dosing (atc)
goal is to maintain 50% concentration in the body
- used to treat chronic pain
- PRN ordered for breakthrough pain
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onset
time it takes for drug to elicit therapeutic response (latent period)
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peak
time it takes for drug to reach its maximum therapeutic effect
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duration
time drug concentration is sufficient to elicit a therapeutic response
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pharmacodynamic phase
what the drug does to the body
- drugs may increase, decrease, replace, inhibit, destroy or protect to CREATE A RESPONSE
- drugs exert MULTIPLE rather than single effects on the body (some are desired and some are not)
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metaproterenol
MOA: broncho dilator
Uses: acute asthma attack or COPD
Adverse effects: tachycardia and/or palpations
Desired: dilates bronchial passage
Not Desired: tachycardia or palpitations
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pharmacodynamic: receptors
proteins located on the cell surface
- chemicals in teh body interact with drugs to produce effects
- these chemicals BIND with the drug via the drug-receptor complex
- complex initiates a physiochemical reaction (agonist vs antagonist)
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agonist
drug that has the ability to INITIATE a desired therapeutic effect by BINDING to a receptor
ex: isoproterenol is a beta1 adrenergic agonist
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antagonist
produces its action NOT by stimulating receptors but PREVENTING or BLOCKING or INHIBITING other natural substances (ligands) from binding and causing a response
ex: Zantac H2 antagonist, Benadryl H1 antagonist, propranolol beta 1 adrenergic antagonist
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antacids
work by neutralizing gastric acidity through DIRECT chemical interaction
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magnesium sulfate
works as a powerful laxative by retaining water in the intestinal lumen through the osmotic effect
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therapeutic index
measure of relative safety of drug
- narrow therapeutic index
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narrow therapeutic index
have a ratio of the
the lowest concentration at which clinical toxicity commonly occurs
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black box warning
required by the FDA for drugs that are especially dangerous
- is the strongest safety warning a drug can carry and still remain on the market
- must be on the package inset, label, and any magazine or advertising
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9 processes to prevent errors
1. restrict high alert drugs and medication routes
2. practice drug differentiation
3. use computerized systems for med admin
4. make patient info readily accessible
5. standardize and simplify
6. apply reminders
7. include the patient in therapy
8. done use trailing zeros
9. use leading zeros
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additive effect
2 drugs taken with similar MOA
ex: two antibiotics are given to treat a complicated infection
increase therapeutic effects
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synergism/potentiation
two drugs with DIFFERENT MOA but result in a combined drug effect greater than that of either drug alone
ex: coumadin and aspirin
increase therapeutic effects
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activation
of drug metabolizing enzymes int he liver --> decreases metabolism rate of the drug (cyp450 system)
increase therapeutic effects
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displacement
displacement of one drug from plasma protein-binding sites by a second drug --> increases effect of displaced drug
increase therapeutic effects
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antidote
drug given to ANTAGONIZE the toxic effects of another drug
ex: naloxone for opioid overdose
decrease therapeutic effects
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decreased intestinal absorption
applied to PO medications
decrease therapeutic effects
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inflammation
-occurs with cell injury
-protective mechanism that begins healing process
- destroy invading and harmful agents
- limit the spread of harmful agents
- prepare damaged tissue for repair
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signs of localized inflammation
redness
swelling
heat
pain
loss of function
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causes of inflammation
exogenous (surgery, trauma)
endogenous (tissue ischemia)
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types of inflammation
acute and chronic
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events of inflammation
tissue injury or bacterial antigens
- vasodilation and increased vascular permeability
- leukocyte recruitment and emigration
- phagocytosis of antigens and debris
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chemotaxis
process by which neutrophils are attracted to inflamed tissue
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exudate
fluid that leaks out of blood vessels, neutrophils and debris
serous
serosanguineous
purulent
hemorrhagic
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serous
watery, low protein, mild inflammation
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serosanguineou
pink tinged fluid, small amount of rbcs
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purulent
severe inflammation with bacterial infection, neutrophils, protein, and debris
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hemorrhagic
lots of RBCs, most severe inflammation
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cytokines IL-1, IL-6 and TNFalpha lead to:
fever
increased neutrophils
lethargy
muscle catabolism
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major histocompatibility complex (MHC)
- cluster of genes on chromosome 6
- aka human leukocyte antigen complex
- proteins made by these genes are on cell surfaces
- MHC class I and class II
- proteins used to discriminate between self and non self
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specific adaptive immunity
-recognizes foreign invaders
-destroys foreign invaders
- retaining memory of invaders
- B cells (humoral)
- T cells (cell mediated)
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B cells
humoral immunity
- memory cells: cells that remember exposure to an antigen
- plasma cells: cells that secrete antibodies
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IgG
most common, 75-80%, protects against bacterial and viral infections
- previous infection or vaccination
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IgM
10% activates compliment for cytotoxic functions
-early, recent infectionsI
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IgA
secretory functions, protects against infections
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IgD
trace amounts in serum, more on B cells, stimulates B cells to multiply and differentiate
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IgE
role in immunity against parasites and allergic reactions, signaling of mast cell degranulation
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passive immunity
-transfer of plasma containing antibodies from an immunized person to non immunized person
-mother to fetus
-injection of antibodies
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active immunity
-protected state due to bodys own immune response
-active infection
-vaccines
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traditional vaccines
inactive or killed organism
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attenuated vaccines
weakened organism
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toxoids
inactivated toxins that stimulate production of antitoxin
ex: tetanus
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conjugate vaccines
protein or toxoid from one organism attached to a disease causing organism to stimulate response
ex: H influenzae type B
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infection
colonization of a host by a MICROBIAL species
- localized or systemic
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common causes of infection
viruses
bacteria: much larger than a virus
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rare causes of infection
fungal
protozoa
helminths
prions
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modes of transmission
microorganisms must have a RESORVOIR --> habitat where organism usually lives and grows
- can be humans, animals, insects, environments
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portal of entry for orgnansims
oroparynx and nasopharynx
genitourinary tract
bodies biggest barrier = SKIN
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translocation portal of entry
movement of bacteria across the intestinal lining
- occurs frequently in the perotineal cavity
- bloodstream
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blood portal of entry
blood transfusion contamination
needle sticks
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maternal-fetal transmission portal of entry
cross the placental barrier and directly to fetus
can occur during childbirth
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infectious process: injury
initial insult to area occurs
- short period of vasoconstriction
-prolonged period of vasodilation
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infectious process: increased permeability
at site of injury
-fluid pulled out of vascular space
-fluid moves out of vessel to the place of injury
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infectious process: immigration of leukocytes
from the fluid out of the vascular space --> neutrophils attract to area of injury
- these neutrophils attach to the enothelium and move through injured tissue
- other cells involved: eosinophils, NK cells, monocytes
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infectious process: phagocytosis
once leukocytes make it to the area of injury this occurs
- neutrophils and monocytes are the specific WBCs involved
-they recognize, engulf and destroy
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infectious process: exudate
its purpose is to transport the leukocytes to injured area, dilute toxins that might be present and transport nutrients for the healing process
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infectious process: systemic symptoms
can occur if infectious process does not remain localized
-total body response stimulates the hypothalamic fever set point
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gram stain
returned within hours
-takes a STAIN of bacteria and shows gram negative or positive + shape and arrangement
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culture and sensitivity
takes at least 24 hours for basic and up to 72 for full identification
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what can you culture?
sputum
urine
blood
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superinfections
new infection that occurs during treatment for a DIFFERENT infection
-typically caused by a resistant organism
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C DIFF
treatment with PO/IV
never give antidiarrheal medications until sure patients do not have c diff
complications:
- pleudomembranous colitis
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candidiasis
can cause overgrowth of fungus
-typically occurs int he mucous membranes
- try and prevent:
- mycostatin: swish and spit antifungal meds
- nystatin: antifungal powder
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cellular adaptation
changes that your bodies cell go through to permit survival and maintenance of cellular function
- cells can change their SIZE AND FORM
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atrophy
decreased or shrinking cell size
- two types: physiologic and pathologic
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physiologic atrophy
related to a developmental issue (less common)
143
pathologic atrophy
related to decreased workload or changed environmental conditions
ex: nutritional deficiencies, blood supply decrease, hormonal problems
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atrophied cells
have decreased protein synthesis (building) and/or increased protein catabolism (breakdown)
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hypertrophy
increased in the size of the cell and can increase function of the cells
- heart and kidney most prone to this in negative adaptation
-muscle/skeletal cells do this naturally
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hyperplasia
increased number of cells results from increase rate of cellular division or repsonse to prolong injury
- skin, intestinal, and glandular cells because they have the ability to divide
- can be normal physiologic hyperplasia (pregnancy and wound healing)
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dysplasia
abnormal changes in size, shape, or organization of mature cells often related to atypical hyperplasia
often associated with neoplastic growths
- however dysplasia does not mean cancer
inflammation and chronic irritation is associated
