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PTH 509 Pharm > Exam 1 stuff > Flashcards

Exam 1 stuff Flashcards

1
Q

what are the 3 characteristics of a drug?

A
  • effective
  • safe
  • selective
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2
Q

generics vs brand names

A

if generic is FDA approved then content is equivalent

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3
Q

how long does it take on average to get a new drug on the market?

A

10 years

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4
Q

prescription vs OTC

advantages and disadvantages

A

OTC - advantages: increase access, less cost

OTC - disadvantages: self-care, drug interaction

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5
Q

Pharmacokinetics

A

study of absorption, distribution, metabolism, and excretion

USE to have better care!

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6
Q

Pharmcodynamics

A

study of drug at site of action and EFFECT on body!

USE to have max efficacy

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7
Q

Toxicology

A

study of harmful effects of chemicals

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8
Q

Zero order vs first order

A

Zero - set amount removed per time (independent on conc. i.e., alcohol)

First order - set % removed per time
(depends on conc)

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9
Q

absorption paths

A 
Oral
sublingual
rectal
inhalation
injection
topical 
transdermal
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10
Q

bioavailability

A

extent to which the drug reaches systemic circulation

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11
Q

distribution of a drug depends on what 3 things?

A
  • characteristics (solubility, size, ionized or unionized (get thru)
  • bound to plasma proteins? (inactive when bound)
  • blood flow to tissues
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12
Q

2 phases of metabolism

A

Phase I : make drug hydrophilic

Phase II : cytochrome P450 oxidases

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13
Q

Elimination

A

give them opposite (basic or acidic) to help flush it out

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14
Q

Clearance (Cl)

A

amount of blood (or other fluid) from which all drug is removed per unit of time

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15
Q

Half-life (t1/2)

A

dosing regimen to achieve steady-state concentration of drug in blood

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16
Q

Idiosyncratic

A

infrequently observed drug effect

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17
Q

hypo, hyper-reactive

A

on quantal dose curve

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18
Q

Hypersensitivity

A

allergic reaction to a drug

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19
Q

tolerance

A

time related loss of response to a drug (weeks-> months)

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20
Q

tachyphylaxis

A

tolerance that happens very quickly (mins -> hours)

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21
Q

Efficacy

A

ability to bind and activate and lead to some response.

Antagonists do not have efficacy.*

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22
Q

Competitive vs non-competitive antagonists

A

competitive: competes and can be overcome. reversible

Non-competitive: effects long lasting. not reversible. must recycle complex

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23
Q

receptor regulation

A

increase stim = decrease receptor func

decrease stim = increase receptor number and sensitivity

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24
Q

the triple response of Lewis

A

1- immediate red scratch mark
2 - red flare around scratch mark
3 - red swollen area around flare

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25
Mediators of inflammation
PROSTAGLANDINS. derived from AA from diet and stored until needed.
26
COX 1 vs COX 2
COX -1 = housekeeping. good. always on. COX 2 = inflammation. injury induced. no effect on stomach
27
Steroid MOA
1- bind receptor 2- activates complex 3- localized to nucleus 4- induction or repression - inhibit cytokines - increase annexin I = no prostaglandins
28
OA
intrinsic defect in the joint cartilage, not immune response
29
Gout
caused by deposits of urate in the joints and cartilage
30
Opiods
agents that alleviate pain INDEPENDENTLY of anti-inflammatory effect. -receptors = Mu, Kappa, delta
31
Effects of opioid agonists
Constipation cough suppression respiratory depression pupil constriction
32
Histamine involved in
- allergic reactions - tissue response to injury - mediator of gastric acid secretion - may serve in CNS neural modulation
33
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????
34
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
35
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
36
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
37
inner vs outer cortex.
``` inner = glucocorticoids outer = mineral ```
38
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)
39
Regulation of glucocorticoids
* not stored. made as needed | * controlled by ACTH
40
Regulation of mineralcorticoids
renin-angiotensis system
41
Cushing's syndrome
Excess of glucocorticoids
42
primary hyperaldosteronism
excessive secretion of aldosterone
43
adrenocortical insufficiency
- replacement therapy with corticosteroids | - gluco always required. possibly need mineral
44
addison's disease
deficiency of both gluco and mineral corticoids
45
congenital adrenal hyperplasia
deficiency of enzymes for glucocorticoid synthesis
46
Corticosteroid and acute/chronic injuries
``` Acute = no help to soft tissue Chronic = will help soft tissue injury ```
47
Steroid diabetes
taking corticosteroids can result in development of diabetes. causes an increase in blood glucose levels. need more insulin to control the increase.
48
All ganglion (neurotransmitter stuff)
ACh to Nicotinic-n
49
Parasympathetic nervous system neurotransmitter path
ACh -> Nn -> ACh -> M (various organs)
50
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)
51
Somatic motor system neurotransmitter path
ACh -> Nm (skeletal muscle) ** only place to nicotinic-m!
52
Cholinergic | what, binds
ACh binds - Nn, Nm, and muscarinic
53
Adrenergic | what, binds
Epi and NE binds - alpha 1 & 2, beta 1 & 2, dopamine
54
Beta 1 dominant in **
HEART
55
beta 2 dominant in **
LUNGS
56
**Life cycle of ACh | made and degraded
made - choline and acetyl CoA - stored until needed - broken down by AChE
57
**life cycle of NE
made - bunch of stuff | -terminated by form of re-uptake!
58
Myasthenia gravis
- fluctuating muscle weakness and rapid fatigue - drooping eyelids, difficult swallowing, weakness of muscles, difficulty breathing - autoimmune - antibodies against Nm receptors *use: Neostigmine
59
Nicotinic N and M
``` Nn= ganglion Nm= only skeletal muscle. block = relaxation ```
60
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 ```
61
MATHCING!!! ****** noncatecholamine drugs to receptors
``` Ephedrine = alpha 1 & 2, Beta 1 & 2 phenylephrine = Alpha 1 terbultaline = beta 2 ```
62
Alpha 1 uses
vasoconstriction, nasal decongestion, delay of anesthetic absorption, elevation of BP, pupil dilation
63
Alpha 2 uses
``` Peripheral = inhibit NE release CNS = reduce stim of adrenergic receptors ```
64
Beta 1 uses
HEART STUFF!
65
Beta 2 uses
LUNG STUFF! asthma | also for delay preterm labor
66
Dopamine uses
(kidney?) | Shock!
67
functional unit of kidney
nephron
68
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.

PTH 509 Pharm (7 decks)

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