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Block A - Molecules to Global Health > Pharmacology > Flashcards

Pharmacology Flashcards

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Organic Chemistry 101 flashcards
1
Q

ß1 Receptor

A
  • Sympathetic

- Heart

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2
Q

ß2 Receptor

A
  • Sympathetic

- Bronchi in the lungs

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3
Q

α1 Receptor

A
  • Sympathetic

- Smooth muscle, periphery

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4
Q

α2 Receptor

A
  • Sympathetic

- autoreceptors

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5
Q

M1 Receptor

A
  • Parasympathetic

- Brain

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6
Q

M2 Receptor

A
  • Parasympathetic

- Heart and autoreceptors

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7
Q

M3 Receptor

A
  • Parasympathetic

- Airways and exocrine glands

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8
Q

Nicotinic Receptor

A
  • Parasympathetic

- brain and neuromuscular junction

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9
Q

Adverse effect of drugs may be :

A
  1. An extension of the desired effect: dose related

2. Unrelated to the desired effect: surprise toxicity

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10
Q

What are the criterias to be CEPA toxic?

A

CEPA toxic = persistence + bioaccumulation + toxic

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11
Q

What’s the approach of treatment of poisoning?

A
  1. Maintain vital functions: ABCD
  2. Identify poison
  3. Decontaminate – prevent further absorption
  4. Enhance elimination (like use of activated charcoal)
  5. Antidote: chelating agents, antivenins, receptor antagonists
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12
Q

Distinguish first order and zero order DRUG and KINETICS

A

DRUG:
First order drugs always follow first order kinetics (proportional to the concentration) while 0 order drug follows 0 order kinetics when saturated and then 1st order kinetic when below threshold of saturation. YOU CAN PREDICT THE CLEARANCE OF FIRST ORDER DRUGS
KINETICS:
1. First order kinetics (elimination): amount eliminated/unit time depends on the amount in the compartment and thus can be predicted.
2. In a 0 order kinetic, you can’t predict the T1/2.
(Half life T1/2 = time to decrease 50%)

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13
Q

What are factors of the drugs that influence its absorption?

A 
o	Lipid solubility (more hydrophobic, faster) 
o	pH (depends on the tissue that absorbs it and f the drug is ionized or not)
o	Blood flow to tissue (more blood flow = faster but stay less longer)
o	Bioavailability (depends on the route)
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14
Q

What are the 2 phases of drug metabolism?

A

Phase 1: drug metabolite with modified activity (lipophilic)

Phase 2: Inactive drug metabolite (hydrophilic)

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15
Q

What are the different receptor superfamilies ?

A

Receptors: recognizes a transmitter or hormone, triggers cellular response
Types:
1. Nuclear receptors
2. Catalytic receptors (they recruit proteins to do stuff, like RTK)
3. Cytokine receptors
4. Ligand-gated ion channels
5. Receptors coupled to G proteins (most targeted receptors by drugs)

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16
Q

Define the types of agonist/antagonist.

A

Categories:

  1. Full agonist (high efficacy)
  2. Partial agonist (medium efficacy)
  3. Antagonist (0 efficacy)
  4. Inverse agonist (negative efficacy)
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17
Q

True or false: The higher is a therapeutic index, the safer the drug is.

A

True !

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18
Q

List some of the factors that contribute to inter-patient variability.

A 
Age
Gender
Renal and hepatic function
Concurrent drugs
Concurrent diseases
Adverse/allergic reactions
Pharmacogenetic (phenotype, pharmacokinetics, pharmacodynamics)
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19
Q

Non-compliance is a big contributor to therapeutic failure. What are its causes ?

A 
Denial
Forgetfulness
Stubbornness
Embarrassment
Side effects/interaction with other drugs
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20
Q

Explain pharmacokinetics and pharmacodynamics.

A

Pharmacokinetics: how it gets to the site, how it is distributed (ADME: absorption, distribution, metabolism, excretion)

Pharmacodynamics: pharmacologic effect, clinical response, how it acts (toxicity/effectiveness). WHAT DRUGS DO IN THE BODY

*Distinction: pharmacology includes ALL substances and effects on living cells (properties, effects, mechanism, pharmacokinetics, therapeutic use)

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21
Q

what’s a drug potency ?

A

is a measure of drug activity expressed in terms of the amount required to produce an effect of given intensity (based on EC50)
i.e. the dose that give 50% of the expected effect

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22
Q

What’s the therapeutic index ? what does it mean if high?

A
  • TI (therapeutic index) = LD50 / ED50 = lethal dose for 50% of the person / dose that does an effect on 50% of the person
  • the higher the TI, the safer the drug (increased margin of safety)
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23
Q

define compliance

A

sometimes called adherence, it’s the extent to which a patients follow treatment instruction

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24
Q

what are the 4 types of non-compliance ?

A
  • patient fails to obtain the medication
  • patient fails to take the medication as prescribed
  • patient prematurely discontinues the medication
  • patient (or another person) takes the medication innaproprietely
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25
Q

does a patient prefer to take more drugs less often in a day of less drugs more often ?

A

more drugs less often (the number of drugs doesn’t appear to be as important as the number of times a day doses must be remembered)

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26
Q

what’s a endogenous ligand ? What else can be ligand in the body ?

A
  • a substance that the body makes (neurotransmitter, hormone or other mediator)
  • drugs can also be ligands of the body’s receptor
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27
Q

what are the receptor that most drugs target ?

A

GPCR (récepteurs couplé aux protéines G)

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28
Q

do all drugs act on receptors ?

A

No.

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29
Q

what does a low dissociation constant (Kd) means ?

A

Kd = k2/k1. It reflects the affinity of a drug to a receptor.
the lower the Kd, the higher the affinity to a receptor

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30
Q

what are spare receptors ?

A

receptors where maximal effect occurs without all receptors occupied by agonist

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31
Q

what does constitutive receptor activity mean ?

A

that even without receptor activity, some receptors can be activated (do something)

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32
Q

in order for a inverse agonist to work, what does the receptors need to do when unbond ?

A

unbound receptors produce a detectable basal signal (constitutive receptor).
The response is then lower than the basal response when there’s a inverse agonist.

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33
Q

on what is based efficacy ?

A

on the maximal effect. If 2 drugs reach a 100% maximal effect, they have the same efficacy even if one takes longer to reach it.

34
Q

on what is based potency ?

A

EC50. The drugs that reach the faster its EC50 is the more potent.

35
Q

what does potency reflect ?

A

recognition of a drug to a receptor

36
Q

what does efficacy reflect ?

A

transduction of the signal

37
Q

what do surmountable antagonism reflects V?

A

competitive reversible antagonism

38
Q

what do INSURMONTABLE antagonism could reflect ?

A
  • competitive irreversible antagonism

- non competitive antagonism

39
Q

when you talk about a antagonist, what does insurmontable mean ?

A

that the antagonist is not surmountable by high agonist concentration

40
Q

allosterism is an other word for ?

A

noncompetitive antagonism

41
Q

It is true ? The more hydrophobic a drug is, the faster it’s gonna get absorb ?

A

Yes and no – CUT-OFF PHENOMENON : after a certain oil/water partition, the absorption rate goes down.

42
Q

how can the fact that the drug is ionized or not change the absorption of a drug ?

A
  • NONIONIZED ACIDS get absorbs more in low PH (stomach)

- NONIONIZED BASES get absorbs more in high PH (intestines)

43
Q

what happens if a drug is bounded to a protein carrier ?

A

if they stay bounded, they’ll never have an effect !

44
Q

what is the main goal of metabolisation ?

A

to get a drug more hydrophilic and get into the pipi (hihihi pipi caca)

45
Q

how can a drug have a bioavaibility of 100% ?

A

by intravenous dose (bypass the portal circulation)

46
Q

what is the main actor in phase 1 of metabolisation ?

A

CYP (like p450)

47
Q

what are the phase 2 reactions ?

A

conjugaison (+= h20)

48
Q

what can happen if the acetaminophen intake exceeds therapeutic doses ?

A

both normal pathways are saturated and the p450-dependant pathway becomes increasingly important. As long as there’s GSH, it’s not toxic but when none is available, it causes LIVER FAILURE.

49
Q

what do p450 inducer mean ?

A

that’ll accélère la metabolisation = speed up drug inactivation

50
Q

what do p450 inhibitors do ?

A

inhibits metabolisation = drugs stays longer.

51
Q

example of inducers :

A
  • etanol (alcohol)
  • rifampin
  • smoking
52
Q

example of inhibitors

A
  • grapefruit juice

- quinidine

53
Q

how can the urine pH play on elimination ?

A

if the urine is more acidic, it’ll clear out more the basic substances and vice versa

54
Q

what’s the apparent volume of distribution (V) ?

A

a physical propriety of a drug : a certain drug has a higher or lower tendency to be distributed more broadly in a person’s body.
Vd = amount of drug in the body/concentration in the blood

55
Q

what’s the clearance ?

A

rate of drug elimination.

= amount of blood cleared of drug/unit of time

56
Q

how can you calculate the t1/2 of a drug ?

A

(0,693 x apparent volume of distribution) / clearance

57
Q

what’s the 2 compartment model ?

A

When you give a drug, there’s a time it’ll increase in the plasma, but then it’s start distributing = fast drop in plasma concentration. The second drop (slower) represent the elimination

58
Q

what’s a loading dose ?

A

a first higher dose because you want the steady state to be achieved faster than the 4 half live (normally it takes that time)

59
Q

what’s the LOAEL ?

A

: lowest observed adverse effect level

60
Q

NOAEL

A

No observed adverse effect concentration (looks like it has an effect, but it’s not significant)

61
Q

substances are deemed to be toxic if they enter, or may enter, the environnement in amounts that :

A
  1. have an immediate or long-term effect on the environment or its biological diversity
  2. endanger the environment upon which life depends
  3. endanger human life or health
62
Q

If exposure and hazard of a drug don’t overlap, is it CEPA toxic ?

A

No (of the exposure is too low to cause hazard, it’s not toxic)

63
Q

what post-ganglionnaire neurotransmitter is an exception in the sympathetic system ?

A

Ach in the sweat glands

64
Q

MUSCARINIC Ach receptor are mostly ?

A

parasympathetic (and sweat glands)

65
Q

NE and E receptors (adrenoreceptors) are 100%

A

sympathetic

66
Q

where can a therapeutic drug act in the CHOLINERGIC junction ?

A
  • on the release of the vesicule containing Ach
  • on the presynaptic receptors (feedback control)
  • on the postsynaptic receptors
  • on Ach esterase (AchE inhibitors)
67
Q

Ach esterase (AchE)

A

elimine l’acéthylcholine

68
Q

what’s the main difference between muscarinic and nicotinic receptor ?

A 
MUSCARINIC 
- act through G-protein 
- take minute or second for effect
NICOTINIC 
- act through ligand-gated ion channels (conformational change) 
- takes milliseconds to produce effect
69
Q

name a kind of AchE inhibitor

A

nerve gases

70
Q

where can a therapeutic drug act in the ADRENERGIC junction ?

A
  • transmitter synthesis
  • transmitter storage
  • transmitter release
  • pre or post synaptic receptors
  • transmitter reuptake
  • enzymatic inactivation
71
Q

What’s a autoreceptor ? name an example ?

A

it’s a presynaptic receptor that modulate the transmitter release
- a2 adrenergic receptor

72
Q

how does the parasympathetic slows down the heart ?

A

Ach is released from the vagus nerve onto mAChR (M2) in the sino-artrial node of the heart

73
Q

is beta2 stimulated by both epinephrine and norepinephrine ?

A

No, not by norepinephrine

74
Q

clonidine

A

a2 agonist.

-Leads to decrease in NE secretion and BP.

75
Q

prazosin

A

a1 antagonist

- inhibits peripheral vasoconstriction

76
Q

what is pheochromocytoma ? how do you treat it ?

A

a tumor secreting excessive (nor)adrenaline.

- best treated with an irreversible antagonist like phenoxybenzamine

77
Q

albuterol

A

beta1 and 2 agonist (aka HR and airways +++)

78
Q

nicotine

A

nicotinic receptor (parasympa) agonist

79
Q

atropine

A

muscarinic receptor (parasympa) antagonist

80
Q

propanolol

A

beta blocker

Block A - Molecules to Global Health (8 decks)

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