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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
Q

Mediators of inflammation

A

PROSTAGLANDINS.

derived from AA from diet and stored until needed.

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26
Q

COX 1 vs COX 2

A

COX -1 = housekeeping. good. always on.

COX 2 = inflammation. injury induced. no effect on stomach

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27
Q

Steroid MOA

A

1- bind receptor
2- activates complex
3- localized to nucleus
4- induction or repression

  • inhibit cytokines
  • increase annexin I = no prostaglandins
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28
Q

OA

A

intrinsic defect in the joint cartilage, not immune response

29
Q

Gout

A

caused by deposits of urate in the joints and cartilage

30
Q

Opiods

A

agents that alleviate pain INDEPENDENTLY of anti-inflammatory effect.

-receptors = Mu, Kappa, delta

31
Q

Effects of opioid agonists

A

Constipation
cough suppression
respiratory depression
pupil constriction

32
Q

Histamine involved in

A
  • allergic reactions
  • tissue response to injury
  • mediator of gastric acid secretion
  • may serve in CNS neural modulation
33
Q

Histamine receptors (H1,2,3)

A

H1= located on vascular, respiratory, and GI smooth muscle

H2= regulation of gastric acid secretion

H3= local regulation of histamine release????

34
Q

H1 vs H2

A

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
Q

Anabolic vs corticosteroids

A

Anabolic - derivatives of testosterone. used by athletes

Corticosteroids - steroid hormones, produced in adrenal cortex, athletes try to mask anabolic use with this

36
Q

Hypothalamic-pituitary interface

A

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
Q

inner vs outer cortex.

A 
inner = glucocorticoids
outer = mineral
38
Q

Physiological effects of glucocorticoids

A

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
Q

Regulation of glucocorticoids

A
  • not stored. made as needed

* controlled by ACTH

40
Q

Regulation of mineralcorticoids

A

renin-angiotensis system

41
Q

Cushing’s syndrome

A

Excess of glucocorticoids

42
Q

primary hyperaldosteronism

A

excessive secretion of aldosterone

43
Q

adrenocortical insufficiency

A
  • replacement therapy with corticosteroids

- gluco always required. possibly need mineral

44
Q

addison’s disease

A

deficiency of both gluco and mineral corticoids

45
Q

congenital adrenal hyperplasia

A

deficiency of enzymes for glucocorticoid synthesis

46
Q

Corticosteroid and acute/chronic injuries

A 
Acute = no help to soft tissue
Chronic = will help soft tissue injury
47
Q

Steroid diabetes

A

taking corticosteroids can result in development of diabetes. causes an increase in blood glucose levels. need more insulin to control the increase.

48
Q

All ganglion (neurotransmitter stuff)

A

ACh to Nicotinic-n

49
Q

Parasympathetic nervous system neurotransmitter path

A

ACh -> Nn -> ACh -> M (various organs)

50
Q

Sympathetic nervous system neurotransmitter path

A

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
Q

Somatic motor system neurotransmitter path

A

ACh -> Nm (skeletal muscle)

** only place to nicotinic-m!

52
Q

Cholinergic

what, binds

A

ACh

binds - Nn, Nm, and muscarinic

53
Q

Adrenergic

what, binds

A

Epi and NE

binds - alpha 1 & 2, beta 1 & 2, dopamine

54
Q

Beta 1 dominant in **

A

HEART

55
Q

beta 2 dominant in **

A

LUNGS

56
Q

**Life cycle of ACh

made and degraded

A

made - choline and acetyl CoA

  • stored until needed
  • broken down by AChE
57
Q

**life cycle of NE

A

made - bunch of stuff

-terminated by form of re-uptake!

58
Q

Myasthenia gravis

A
  • fluctuating muscle weakness and rapid fatigue
  • drooping eyelids, difficult swallowing, weakness of muscles, difficulty breathing
  • autoimmune - antibodies against Nm receptors

*use: Neostigmine

59
Q

Nicotinic N and M

A 
Nn= ganglion
Nm= only skeletal muscle. block = relaxation
60
Q

MATCHING!!!! ***** catecholamine drugs to receptors

A 
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
Q

MATHCING!!! **** noncatecholamine drugs to receptors

A 
Ephedrine = alpha 1 & 2, Beta 1 & 2
phenylephrine = Alpha 1
terbultaline = beta 2
62
Q

Alpha 1 uses

A

vasoconstriction, nasal decongestion, delay of anesthetic absorption, elevation of BP, pupil dilation

63
Q

Alpha 2 uses

A 
Peripheral = inhibit NE release
CNS = reduce stim of adrenergic receptors
64
Q

Beta 1 uses

A

HEART STUFF!

65
Q

Beta 2 uses

A

LUNG STUFF! asthma

also for delay preterm labor

66
Q

Dopamine uses

A

(kidney?)

Shock!

67
Q

functional unit of kidney

A

nephron

68
Q

urine filtering and exit

A
  • 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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