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Principles > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

pharmacodynamics

A

effect drug has on body

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2
Q

pharmacokinetics

A

effect body has on drug

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3
Q

agonist possesses

A

efficacy and affinity

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4
Q

antagonist possesses

A

only affinity

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5
Q

define affinity

A

strength of association between ligand and receptor

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6
Q

define efficacy

A

ability of agonist to evoke cellular response

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7
Q

what axis is potency on

A

x axis, increasing potency from right to left

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8
Q

what axis is efficacy on

A

y axis, increasing efficacy from bottom to top

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9
Q

competitive antagonism has what effect on graph

A

parallel shift to right

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10
Q

non-competitive antagonism has what effect on graph

A

depresses curve as binds to different site

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11
Q

define absorption

A

process when drug enters body

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12
Q

define distribution

A

process when drug leaves circulation and enters tissues

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13
Q

define metabolism

A

process when drug converted to more polar form for excretion

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14
Q

define excretion

A

process when drug leaves body

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15
Q

factors controlling drug absorption

A

solubility, chemical stability, lipid-to-water partition coefficient, degree of ionisation

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16
Q

lower pKa or higher Ka means what type of acid

A

stronger acid

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17
Q

define oral availability

A

fraction of drug that reaches systemic circulation after oral ingestion

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18
Q

define systemic availability

A

fraction of drug that reaches systemic circulation after absorption

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19
Q

enteral routes of administration

A

oral, sublingual, rectal

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20
Q

parenteral routes of administration

A

IV, IM, inhalation, topical

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21
Q

advantages of sublingual

A

rapid absorption

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22
Q

advantages and disadvantages of inhalation

A

large surface area but requires dexterity (skills)

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23
Q

where are drugs distributed

A

one or more body fluid compartments, not evenly distributed around body

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24
Q

what are the body fluid compartments?

A

intracellular water, extracellular water (interstitial, plasma, transcellular)

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25
Q

define volume distribution

A

apparent volume in which drug is dissolved

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26
Q

for IV what does Vd = ?

A

for IV, Vd = dose / plasma concentration

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27
Q

what does Vd < 10L mean

A

drug mainly retained in vascular compartment

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28
Q

what does Vd 10-30L mean

A

drug mainly in extracellular water

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29
Q

what does Vd > 30L mean

A

drug distributed throughout whole body or accumulated in certain tissues

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30
Q

what does MEC stand for

A

minimum effective concentration

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31
Q

what does MTC stand for

A

maximum tolerated concentration

32
Q

Therapeutic ratio = ?

A

Therapeutic ratio = MTC/MEC. Higher ratio, safer the drug

33
Q

what is first order kinetics

A

rate of elimination is directly proportional to drug concentration

34
Q

what is the clearance of a drug

A

volume of plasma cleared of drug in unit time

35
Q

Rate of elimination = ?

A

rate of elimination = Clearance x Plasma concentration

36
Q

when is dosing to a steady state reached

A

after 5 half lives

37
Q

for drug dosing orally what happens to plasma concentration

A

plasma concentration fluctuates about an average steady state value

38
Q

what is the loading dose

A

initial dose higher before stepping down to lower maintenance dose. Employed to decrease time to steady state for drugs with longer half-lives

39
Q

define half life

A

time for concentration of drug in plasma to half

40
Q

what is zero order kinetics

A

initially eliminated at constant rate

41
Q

how can drug metabolism happen

A

convert drug to more polar metabolites not readily absorbed or convert drug to metabolites less pharmacologically active than parent compound

42
Q

what are the 2 phases of drug metabolism

A 
phase 1 (rhs of liver): oxidation, reduction and hydrolysis to make drug more polar. 
phase 2 (lhs of liver): Conjugation, when endogenous compounds added to increase polarity
43
Q

example of phase 1 and phase 2 drug metabolism reactions

A

CYP450 monooxygenase cycle

44
Q

3 phases of drug excretion

A
  1. glomerular filtration
  2. active tubular secretion
  3. passive reabsorption
45
Q

what does glomerular filtration achieve

A

removes unbound drugs

46
Q

what does active tubular secretion achieve

A

can secrete highly bound drugs. Organic anion transporter handles acidic drugs and Organic cation transporter handles basic drugs like morphine

47
Q

what does passive reabsorption rely on

A

urine concentration, factors influencing reabsorption include polarity, urinary pH and urinary flow rate

48
Q

what is depolarisation and hyperpolarisation

A 
depolarisation = membrane potential becomes less negative.
repolarisation = membrane potential becomes more negative
49
Q

Sodium channels

A

Na flows down conc. gradient INTO cell. but still negative anions outside so NA+ flow down electrical gradient OUT of cell. When conc gradient = electrical gradient then Ena= +61mV

50
Q

Potassium channels

A

K+ flow down concentration gradient OUT of cell. but still negative anions inside cell to K+ flow down electrical gradient INTO cell.
Ek = -90mV

51
Q

which channels are depolarising

A

Na channels = depolarising so move membrane potential towards Ena.
K+ channels = repolarising s more Em towards Ek.

52
Q

define action potential

A

a brief electrical signal at which the polarity of the membrane is momentarily reversed

53
Q

why is the membrane potential -70mV, thus closer to Ek of -90mV

A

at resting potential the membrane is 100x more permeable to K= ions than Na, but there’s a slight difference due to slight inward leak of Na ions

54
Q

What are the Nernst and Goldman- Hodgkin-Katz equations for

A 
Nernst = calculates membrane potential for single ion
Goldman = calculates overall membrane potential
55
Q

how do voltage activated Na and K channels work

A

depolarisation causes Na channels to open. Depolarisation is maintained by positive feedback which causes Na channels to enter inactivated state. K+ channels then open to cause repolarisation which causes Na channels to enter closed state

56
Q

define absolute refractory period and relative refractory period

A 
Absolute = no stimulus, cannot elicit a second action potential.
Relative = stronger than normal stimulus may elicit a second AP
57
Q

why don’t passive signals spread far from their site of origin

A

‘leaky’ nerve cell membrane. To increase conductance then increase axon diameter, or coat in conductive layer of myelin. Oligodendrocytes produce myelin in CNS. Schwann cells for PNS

58
Q

Sympathetic ANS

A

flight or fight.
preganglionic neurotransmitter is ACh.
postganglionic neurotransmitter is noradrenaline.
Thoraco-lumbar outflow (T1-L2)

59
Q

Effects of sympathetic stimulation

A
  • increases HR, force of contraction
  • relaxes bronchi, decrease mucus production
  • vasoconstriction but relax skeletal muscle
  • ejaculation
60
Q

Parasympathetic ANS

A
  • coordinates body’s basic homeostatic functions
  • preganglionic and postganglionic are ACh
  • cranial nerves 3,7,9,10
61
Q

Effects of parasympathetic stimulation

A
  • decrease HR
  • bronchconstriction, stimulates mucus production
  • no effect on blood vessels
  • erection
62
Q

t1/2 half life =

A

0.69/kel

63
Q

what is EC50

A

The conc. of agonist that results in a half maximal response (i.e. 50% of receptors are occupied)

64
Q

What are the lengths of the ganglions in para and sympathetic ANS

A 
Sympathetic = short preganglion, long post ganglion
Parasympathetic = long preganglion and short post ganglion
65
Q

what happens in neurochemical transmission

A
  • AP from CNS
  • Travels to presynaptic terminal of preganglion which triggers calcium entry and ACh release.
  • synthesis and storage of ACh opens ligandgated channels in postganglion neurone
  • causes depolarisation of AP, calcium entry and then release of noradrenaline or ACh
  • Noradrenaline activates adrenocrptors
  • ACh activates Muscarinic ACh receptors
66
Q

how are ANS signals terminated

A

degradation of ACh to choline and acetate by AChE terminates transmission.
- reuptake and reuse of choline

67
Q

structure of nicotinic ligand gated ACh receptors

A

5 glycoprotein subunits forming a central, cation conducting channel

68
Q

G protein structure and activation

A
  • receptor =7 transmembrane spans, 3 extracellular loops.
  • G p = 3 subunits (a,b,y)
  • Agonist activates receptor so it couples with G protein
  • GDP dissociates and GTP binds to alpha subunit
  • alpha subunit dissociates with GTP attached, these are signalling molecules
  • turned off by alpha hydrolysing GTP > GDP and re-joining with subunits
69
Q

M1 receptor coupled to Gq does what

A

stimulates phospholipase C, increases stomach acid secretion

70
Q

M2 receptor coupled to Gi does what

A

inhibits adenylyl cyclase and decreases HR

71
Q

M3 receptor coupled to Gq does what

A

stimulates phospholipase C, increases saliva secretion and bronchoconstriction

72
Q

B1 adrenoceptor in heart does what

A

stimulates adenylyl cyclase, increases HR/force

73
Q

B2 adrenoceptor in airways does what

A

stimulates adenylyl cyclase, bronchodilation

74
Q

A1 adrenoceptor coupled to Gq does what

A

stimulates phospholipase C, bronchoconstriction

75
Q

A2 adrenoceptor coupled to Gi does what

A

inhibits adenylyl cyclase, inhibits noradrenaline release

Principles (10 decks)

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