Exam 1 stuff Flashcards
what are the 3 characteristics of a drug?
- effective
- safe
- selective
generics vs brand names
if generic is FDA approved then content is equivalent
how long does it take on average to get a new drug on the market?
10 years
prescription vs OTC
advantages and disadvantages
OTC - advantages: increase access, less cost
OTC - disadvantages: self-care, drug interaction
Pharmacokinetics
study of absorption, distribution, metabolism, and excretion
USE to have better care!
Pharmcodynamics
study of drug at site of action and EFFECT on body!
USE to have max efficacy
Toxicology
study of harmful effects of chemicals
Zero order vs first order
Zero - set amount removed per time (independent on conc. i.e., alcohol)
First order - set % removed per time
(depends on conc)
absorption paths
Oral sublingual rectal inhalation injection topical transdermal
bioavailability
extent to which the drug reaches systemic circulation
distribution of a drug depends on what 3 things?
- characteristics (solubility, size, ionized or unionized (get thru)
- bound to plasma proteins? (inactive when bound)
- blood flow to tissues
2 phases of metabolism
Phase I : make drug hydrophilic
Phase II : cytochrome P450 oxidases
Elimination
give them opposite (basic or acidic) to help flush it out
Clearance (Cl)
amount of blood (or other fluid) from which all drug is removed per unit of time
Half-life (t1/2)
dosing regimen to achieve steady-state concentration of drug in blood
Idiosyncratic
infrequently observed drug effect
hypo, hyper-reactive
on quantal dose curve
Hypersensitivity
allergic reaction to a drug
tolerance
time related loss of response to a drug (weeks-> months)
tachyphylaxis
tolerance that happens very quickly (mins -> hours)
Efficacy
ability to bind and activate and lead to some response.
Antagonists do not have efficacy.*
Competitive vs non-competitive antagonists
competitive: competes and can be overcome. reversible
Non-competitive: effects long lasting. not reversible. must recycle complex
receptor regulation
increase stim = decrease receptor func
decrease stim = increase receptor number and sensitivity
the triple response of Lewis
1- immediate red scratch mark
2 - red flare around scratch mark
3 - red swollen area around flare
Mediators of inflammation
PROSTAGLANDINS.
derived from AA from diet and stored until needed.
COX 1 vs COX 2
COX -1 = housekeeping. good. always on.
COX 2 = inflammation. injury induced. no effect on stomach
Steroid MOA
1- bind receptor
2- activates complex
3- localized to nucleus
4- induction or repression
- inhibit cytokines
- increase annexin I = no prostaglandins
OA
intrinsic defect in the joint cartilage, not immune response
Gout
caused by deposits of urate in the joints and cartilage
Opiods
agents that alleviate pain INDEPENDENTLY of anti-inflammatory effect.
-receptors = Mu, Kappa, delta
Effects of opioid agonists
Constipation
cough suppression
respiratory depression
pupil constriction
Histamine involved in
- allergic reactions
- tissue response to injury
- mediator of gastric acid secretion
- may serve in CNS neural modulation
Histamine receptors (H1,2,3)
H1= located on vascular, respiratory, and GI smooth muscle
H2= regulation of gastric acid secretion
H3= local regulation of histamine release????
H1 vs H2
H1 = allergies, common cold, motion sickness, sedative
H2 = inhibit gastric acid secretion, reduce volume of gastric acid secretion, relief symptoms of peptic ulcers, GERD
Anabolic vs corticosteroids
Anabolic - derivatives of testosterone. used by athletes
Corticosteroids - steroid hormones, produced in adrenal cortex, athletes try to mask anabolic use with this
Hypothalamic-pituitary interface
1 - environment stim hypothalamus to release CRH
2- goes to anterior pituitary to inc. or dec. ACTH
3- anterior pituitary releases hormone into systemic circulation. travels to adrenal gland.
4- target gland results in corticosteroid production.
**feedback inhibition
inner vs outer cortex.
inner = glucocorticoids outer = mineral
Physiological effects of glucocorticoids
1) protein breakdown
2) fat breakdown
3) maintain fx of vascular system
4) increase RBC and hemoglobin
5) support function of striated muscles
6) affect mood and CNS excitability
7) respond to stress
8) immunosuppression
9) anti-inflammatory activity (stops release of phospholipase A2)
Regulation of glucocorticoids
- not stored. made as needed
* controlled by ACTH
Regulation of mineralcorticoids
renin-angiotensis system
Cushing’s syndrome
Excess of glucocorticoids
primary hyperaldosteronism
excessive secretion of aldosterone
adrenocortical insufficiency
- replacement therapy with corticosteroids
- gluco always required. possibly need mineral
addison’s disease
deficiency of both gluco and mineral corticoids
congenital adrenal hyperplasia
deficiency of enzymes for glucocorticoid synthesis
Corticosteroid and acute/chronic injuries
Acute = no help to soft tissue Chronic = will help soft tissue injury
Steroid diabetes
taking corticosteroids can result in development of diabetes. causes an increase in blood glucose levels. need more insulin to control the increase.
All ganglion (neurotransmitter stuff)
ACh to Nicotinic-n
Parasympathetic nervous system neurotransmitter path
ACh -> Nn -> ACh -> M (various organs)
Sympathetic nervous system neurotransmitter path
ACh -> Nn -> NE -> alpha or beta (various organs)
ACh -> Nn -> ACh -> M (sweat glands)
ACh -> Nn (adrenal medulla) -> Epi -> alpha or beta (various organs)
Somatic motor system neurotransmitter path
ACh -> Nm (skeletal muscle)
** only place to nicotinic-m!
Cholinergic
what, binds
ACh
binds - Nn, Nm, and muscarinic
Adrenergic
what, binds
Epi and NE
binds - alpha 1 & 2, beta 1 & 2, dopamine
Beta 1 dominant in **
HEART
beta 2 dominant in **
LUNGS
**Life cycle of ACh
made and degraded
made - choline and acetyl CoA
- stored until needed
- broken down by AChE
**life cycle of NE
made - bunch of stuff
-terminated by form of re-uptake!
Myasthenia gravis
- fluctuating muscle weakness and rapid fatigue
- drooping eyelids, difficult swallowing, weakness of muscles, difficulty breathing
- autoimmune - antibodies against Nm receptors
*use: Neostigmine
Nicotinic N and M
Nn= ganglion Nm= only skeletal muscle. block = relaxation
MATCHING!!!! ***** catecholamine drugs to receptors
Epi = alpha 1 & 2, beta 1 & 2 NE = alpha 1 & 2, beta 1 Isoproterenol = Beta 1 & 2 dobutamine = Beta 1 dopamine = alpha 1, beta 1, dopamine
MATHCING!!! **** noncatecholamine drugs to receptors
Ephedrine = alpha 1 & 2, Beta 1 & 2 phenylephrine = Alpha 1 terbultaline = beta 2
Alpha 1 uses
vasoconstriction, nasal decongestion, delay of anesthetic absorption, elevation of BP, pupil dilation
Alpha 2 uses
Peripheral = inhibit NE release CNS = reduce stim of adrenergic receptors
Beta 1 uses
HEART STUFF!
Beta 2 uses
LUNG STUFF! asthma
also for delay preterm labor
Dopamine uses
(kidney?)
Shock!
functional unit of kidney
nephron
urine filtering and exit
- PCT - isotonic urine - dilute
- Loop of henle = descending loop (water permeable, concentrated urine) and ascending loop (not water permeable, returns to isotonic urine)
- DCT - water follows Na and Cl
- Late DCT and collecting duct - Na and K exchange. ADH concentrates urine.
