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Diagnosis And Management > Pharmacology > Flashcards

Pharmacology Flashcards

lecture 1

1
Q

The Study of how the body handles drugs

A

Pharmacokinetics (PK)

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2
Q

What the drugs do to the body and how they do it

A

Pharmacodynamics (PD)

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3
Q

What are the 4 stages of drug disposition?

A

Administration/ Absorption
Distribution
Metabolism
Excretion

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4
Q

movement from the site of administration into the plasma

A

absorption

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5
Q

Factors that affect the rate and degree of absorption? (6)

A
  • lipid solubility (molecular weight ad pKA)
  • surface area
  • gut content
  • GI transit time
  • Blood flow to site of administration
  • drug interaction
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6
Q

Where are most drugs absorbed?

A

small intestine

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7
Q

Approximately 75% of a drug given orally is absorbed ….?

A

1-3 hours

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8
Q

Main routes of drug administration

A 
-Oral(po)
― Sublingual
― Rectal
―Application to the epithelial surfaces (e.g. skin, cornea and vagina)
― Inhalation(pulmonary)
― Injection
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9
Q

Factors that affect the movement of drugs (equilibrium pattern of distribution between the compartments):

A 
-Permeability across tissue barriers
― Bindingwithincompartments
― pHpartition
― Fat:waterpartition
― Blood flow to the tissue
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10
Q

Factors affecting drug distribution:

A

Plasma protein binding

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11
Q

in plasma protein binding… what is found in mainly acidic drugs?

A

albumin

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12
Q

in plasma protein binding… what is found in mainly basic drugs?

A

α1-acid glycoprotein

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13
Q

What fraction of drug exerts pharmacological effects

A

only the free or unbound drug fraction

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14
Q

process of chemical modification of drugs by enzymatic reaction within the body.

A

Drug Metabolism or biotransformation

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15
Q

What is the primary site of drug metabolism?

A

liver

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16
Q

The fraction (F) of the dose which proceed unaltered from the site of administration to the systemic circulation (blood plasma)

A

bioavailability

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17
Q

Interindividual variability that is not related to drug preparation is mainly caused by change in:

A

― Enzymatic activity of gut wall or liver (first- pass metabolism)
― Gastric pH
― Intestinalmotility

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18
Q

What profoundly reduces bioavailability of a drug (that’s taken orally)

A

first-pass metabolism

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19
Q

T or F: bioavailability neglects the rate of absorption

A

True

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20
Q

T or F: Bioavailability only considers the total fraction of a drug that reaches the systemic circulation

A

True

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21
Q

Most drugs are excreted through the…

A

kidneys

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22
Q

Why can urine tests use to detect drugs?

A

because 20-30% of drugs are mainly excreted in the active form and are unchanged (such as drugs illicit)

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23
Q

Time taken for drug concentration(Cp) to decrease by half

A

Elimination half-life (t1/2)

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24
Q

The longer the half life….the longer the

A

plasma concentration in the therapeutic range

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25
Q

t1/2 is directly proportional to…

A

volume of distribution and inversely proportional to total clearance

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26
Q

flowchart of oral administration (pharmacokinetics)

A

1) oral administration
2) GIT absorption: active transport/ passive diffusion
3) portal circulation (first pass metabolism)
4) blood vessels bioavailability (distribution)
5) renal excretion

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27
Q

What the dugs do to the body and how they do it

A

pharmacodynamics (PD)

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28
Q

COORDINATE THE FUNCTION AND RESPONSES OF ALL DIFFERENT CELLS IN THE BODY

A

receptors

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29
Q

protein molecules that when activated by transmitters/hormones/drugs mediate a biological effect.

A

receptors

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30
Q

What are receptors important for?

A

chemical signaling between/within cells

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31
Q

4 types of receptor types

A

1) ligand-gates ion channels (ionotropic)
2) G protein-coupled receptors (metabotropic)
3) kinase-linked receptors
4) nuclear recepts

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32
Q

The most common protein targets

A

a) receptors
b) ion channels
c) enzymes
d) transporters

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33
Q

drugs that occupy receptors and activate them

A

agonists

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34
Q

Drugs that occupy receptors but do not activate them (can block agonists)

A

antagonists

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35
Q

maximal response a drug can produce

A

Emax (efficacy)

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36
Q

concentration needed to produce a 50% maximal response

A

EC50 (potency)

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37
Q

the lower the potency of a drug the higher….

A

the dose needed

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38
Q

how is a drugs safety determines?

A

therapeutic index (TI)

39
Q

What is compared in therapeutic effect?

A

therapeutic effective dose to the toxic dose of a pharmaceutical agent

40
Q

drug dose that produces a therapeutic response in 50% of the population

A

ED50

41
Q

Drug dose that produces a toxic response in 50% of the population

A

TD50

42
Q

therapeutic index (ratio)

A

TD50/ ED50

43
Q

The higher the number on the therapeutic index=?

A

less toxic

44
Q

What are predictable adverse drug reactions?

A
  • overdose
  • side effect
  • withdrawal effect
45
Q

Consequence of the main pharmacological • effect of the drug or its known PK. (low therapeutic effect)

A

predictable adverse effects

46
Q

Examples of predictable adverse effect drugs?

A
  • anticoagulants
  • lithium
  • hypoglycaemic
47
Q

Unrelated to the known pharmacological action of the drug (off-target)-more serious and unique to an individual

A

unpredictable adverse drug reactions

48
Q

What are the underlying mechanisms for drug to drug interactions?

A
  • behavioral (altered compliance)
  • pharmacokinetic (altered concentration)
  • pharmaceutic (outside the body)
  • pharmacodynamic (altered effect)
49
Q

What are drugs able to interact with?

A
  • drugs
  • food
  • supplements
  • medical conditions
50
Q

Drugs with similar actions

ex) alcohol and benzodiazepine (CNS depressant)

A

additive effects

51
Q

change is concentration leading to clinical consequences

A
  • altered bioavailability

- altered metabolism (prodrugs)

52
Q

any substance, including any drug, that has the capacity to harm a living organism

A

poison

53
Q

What are the stages of drug development?

A
  • drug discovery
  • preclinical development
  • clinical development (phase I-III)
  • regulatory approval
  • phase IV
54
Q

Who is checking your medicines?

AUS:
USA:

A

TGA IN AUSTRALIA (therapeutic goods Administration)

  • FDA IN USA
55
Q

Two categories of medicine?

A
  • registered medicine

- listed medicine

56
Q
  • higher risk medicines that are registered on the ARTG • evaluated for quality, safety and efficacy
  • Product Information is approved by the TGA
A

registered medicines

57
Q
  • lower risk medicines that are listed on the ARTG
  • contain pre-approved, low risk ingredients
  • Evaluated for quality and safety
  • can only make limited claims and cannot imply that they will be useful in the treatment or prevention of serious illnesses
A

listed medicines

58
Q

Are these a registered medication:

  • prescription medicines
  • OTC medicines
  • complementary medicines
A
  • prescriptions (All)
  • OTC (Most)
  • complementary (some)
59
Q

is the legal process used to restrict safe and effective use

A

Scheduling

60
Q

The higher the # of the schedules, the _______ restricted

A

more restricted

61
Q

pharmacy only medicine (large pack of paracetamol)

A

Schedule 2

62
Q

pharmacist only medicine (proton pump inhibitors)

A

Schedule 3

63
Q

prescription only medicine (blood pressure medications)

A

Schedule 4

64
Q

controlled drug (strong analgesics)

A

Schedule 8

65
Q

Generic medicines contain ________________ as the existing medicine, and they must be bioequivalent

A

the same active ingredient

66
Q

refers to whether the generic medicine releases the active ingredient into the bloodstream at the same rate and to the same extent as the original medicine

A

bioequivalent

67
Q

Australian Government program that benefits all Australians by making medicine more affordable

A

Pharmaceutical Benefits Scheme (PBS)

68
Q

Components to inflammation

A
  • heat
  • redness
  • swelling
  • pain
  • loss of function
69
Q

how is inflammation triggered?

A

Inflammatory mediators (e.g.; prostaglandins and cytokines) are released from damaged tissues and immune cells and can stimulate nociceptors (“pain receptors”) directly

70
Q

process where reduce the activation threshold of nociceptors so that the stimulation required to cause activation is less

A

primary sensitization

71
Q

What are examples of mediators?

A

histamine, prostaglandin, leukotrienes, cytokines

72
Q

What to analgesic medications help?

A

Pain!

73
Q

What do anti-inflammatory medications reduce?

A
  • swelling
  • heat
  • redness
74
Q

Where do local anesthetics and NSAIDs work?

A

nerve endings and primary afferent nerve

75
Q

Where do local anesthetics and alpha 2 agonists work?

A

dorsal root ganglion

76
Q

Where do opioids, ketamine, gabapentinoids work?

A

dorsal horn

77
Q

What tracts are analgesic medications work on?

A

ascending spinothalamic fibers

78
Q

What are facilitators of pain signaling pathway?

A
  • increase in substance P
  • glutamate and excitatory amino acids
  • serotonin
  • increase in nerve growth factor
79
Q

what inhibits the pain signaling pathway?

A
  • descending anti-nociceptive pathways
  • norepinephrine-serotonin, dopamine decrease
  • increase in poi’s
  • GABA
  • cannabinoids
80
Q

pain that affects bones, joints, connective tissue, muscles

A

somatic (nociceptive pain)

81
Q

a high threshold sensory receptor of the peripheral somatosensory nervous system that is capable of transfusing and encoding noxious stimuli

A

nociceptor

82
Q

pain due to a stimulus that does not normally provoke pain

A

allodynia

83
Q

Why are anti-inflammatory drugs used in virtually all branches of medicine?

A

This is because inflammation forms a significant component of many, if not most, of the diseases encountered in the clinic.

84
Q

Despite diversity all the NSAIDs possess ____________ properties

A

analgesic, antipyretic and anti-inflammatory

85
Q

how does the body create analgesic effect?

A

Decreased production of prostaglandin: less sensitisation of nociceptive nerve ending

86
Q

How does the body create anti-inflammatory action?

A

Reduces vasodilation and, indirectly, oedema by decreasing prostaglandin E2 and prostacyclin synthesis.

87
Q

How does the body create an antipyretic effect?

A

NSAIDspreventsthereleaseof prostaglandins by interleukin-1 in the CNS, where they elevate the hypothalamic set point for temperature control. Therefore preventing fever.

88
Q

How can you inhibit synthesis of prostaglandins?

A

inhibit COX enzymes (COX1 and COX2)

89
Q
  • impaired gastric protection
  • antiplatelet effects
  • reduction in glomerular filtration rate
  • reduction in renal flow
A

COX-1 inhibition

90
Q
  • anti-inflammatory action
  • analgesis action
  • reduction in glomerular filtration rate
  • reduction in renal flow
A

COX-2 inhibition

91
Q

indications for NSAID usage in clinic

A
  • pain due to inflammation and tissue injury
  • fever
  • osteoarthritis
  • acute gout
  • rheumatoid arthritis
92
Q

adverse effects of using NSAIDs

A
  • nausea, diarrhea, headache
  • dyspepsia, GI ulceration
  • raised liver enzymes
  • dizziness
  • salt and fluid retention
  • hypertension
93
Q

paracetamol is a form of…?

A

acetaminophen

Diagnosis And Management (8 decks)

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