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PHAC3001 > MT3 > Flashcards

MT3 Flashcards

1
Q

Phytocannabinoids

A

derived from the Cannabis plant

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2
Q

Synthetocannabinoids

A

man made

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3
Q

Endocannabinoids

A

present naturally in the body (eg Anandamide)

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4
Q

toxic effects of soaps/detergents on cells

A

sodium and alkali kill many bacterias and viruses along with mechanical scrubbing

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5
Q

acids and alkalis toxic effect on microbes

A

prevent growth;

benzoic acid in food;

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6
Q

heavy metals - toxic effect on microbes

A

prevent growth

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7
Q

halogens - toxic effects on microbes

A

hypochlorous acid used in pools with chlorine

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8
Q

Alcohols - toxic effect on microbes

A

70% alcohol used in labs

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9
Q

Phenols - toxic effects on microbes

A

disrupts membranes;
Denature proteins;
inactivates enzymes;

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10
Q

oxidizing agents - toxic effect on microbes

A

disrupt disulphide bonds thus structure of membrane

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11
Q

alkylating agents - toxic effects on microbes

A

disrupts structure of proteins and nucleic acids

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12
Q

dyes - toxic effects on cells

A

some interfere with cell replication

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13
Q

Peptidoglycan

A

the fibrous scaffold in the wall of bacteria

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14
Q

Penicillin-binding protein (PBP)

A

the enzyme that helps to make the peptidoglycan scaffold

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15
Q

beta lactamase

A

an enzyme that causes resistance to antibiotics

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16
Q

porins

A

protein pores that pierce the membrane

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17
Q

pain

A

an unpleasant sensory and emotional experience associated with actual or potential tissue damage

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18
Q

nociception

A

the physiological processes in responses to a noxious stimulus

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19
Q

Allodynia

A

pain in response to a normally innocuous stimulus

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20
Q

hyperalgesia

A

enhanced pain to a normally painful stimulus

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21
Q

morphine

A

10% of opium
high analgesia
addictive
most prominent in plant

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22
Q

codeine

A

0.3-2% of opium
less powerful analgesia than morphine
less addictive than morphine

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23
Q

Heroine

A

Highly potent analgesia but extremely addictive.

Passes through BBB faster than morphine.

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24
Q

opiate

A

drugs derived from opium

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25
Q

opioid

A

agents with opiate-like actions

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26
Q

narcotic

A

Sleep inducing drugs producing dependence

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27
Q

naloxone

A

a non-specific opioid receptor antagonist.

28
Q

therapeutic indication for opioids

A
  • option for cancer pain
  • primary option for acute pain
  • unclear use for chronic pain (less efficacious, SEs)
  • requires continuous assessment
29
Q

negative side effects of opioids

A 
Severe constipation
Somnolescence (sleepy)
Cardioresp. depression
Tolerance
Dependence
30
Q

tolerance

A

increased doses required to achieve therapeutic level

203 weeks after frequent opioid use

31
Q

treating tolerance

A

Rotation to another opioid
RE-couple to a non-opioid adjunct.
You should start low and go slow.

32
Q

Physical dependence

A

Mild: lacrimation, sweating, yawning
Severe: anorexia, cramps, nausea, vomiting, restlessness, irritability, tremor, HR/BP changes, chills, spasms, PAIN

33
Q

psychological dependence

A

Compulsive drug-seeking behaviour.

Happens when drugs have mood-enhancing properties

34
Q

treating dependence

A

stop drug intake
naltrexone - miu antagonist
methadone - miu agonist

35
Q

methadone

A

miu-agonist for treating dependence.
Good oral bioavailability
Selective, long-lasting/slow withdrawal

36
Q

addiction

A

state of physical and psychological dependence; preoccupation with acquiring and using drugs despite knowledge of adverse health effects. occurs to detriment of other activities.

37
Q

paradoxical opioid-induced hyperalgesia

A

prolonged opioid use leads to increased pain.

  • sensitize peripheral nociceptors
  • sensitize dorsal horn neurons
  • altered descending control mechanisms

Use glutamate antagonist because glutamate receptor involvement.

38
Q

peripherally restricted opioids

A
  • future of opioid analgesia
  • Target pain at source
  • Less nociceptor sensitization
  • Don’t pass BBB –> less addictoin, CNS effects
39
Q

how to improve opioid receptor levels

A
  • inhibit B-arrestin activity
  • inhibit receptor degradation (protease inhibitors)
  • promote receptor recycling
40
Q

people with arthritis experience

A
  • reduction in quality of life
  • disability
  • loss of sleep/fatigue
  • depression
  • PAIN
41
Q

eicosanoids

A

Include prostaglandins.
Discovered via knowledge that semen’s vasomotor activity.
Uterine smooth muscle contracts/relaxes in its presence.

42
Q

prostaglandins

what is it?
how is it made?

A

involved in causing inflammation and pain.

Produced by oxygenation of arachidonic acid in cell membranes via COX1 or COX2

43
Q

Aspirin

A
  • Classic NSAID
  • Derived from bark of willow trees
  • Inhibits COX1 and COX2
  • Anti-platelet (clotting)
  • 500mg-4g/day
44
Q

Other NSAIDs

A

Ibuprofen, naproxen, diclofenac

  • COX1/2 inhibitors
  • similar pharm to aspirin (analgesic, anti-inflam, but no anti-clotting)
  • Longer half-life; more potent
45
Q

recommendations for CX2 NSAID use

A
  • select patient at low risk for thrombotic events
  • prescribe lowest dose required to control symptoms
  • add 81mg aspirin + proton pump inhibitor with increased risk of thrombotic events
46
Q

NSAID/opioid combos

A
  • can’t keep escalating NSAID doese
  • FDA requires synergy + better than placebo
  • Less likely opioid abuse
  • Ease of prescribing combo
  • effective analgesia and minimized SEs of each component
47
Q

topical NSAIDs

A
  • mostly used for arthritis pain
  • Minimized central SEs
  • Can produce irritation due to vehicle
48
Q

advantages of smoked cannabis (3)

A
  • pain relief
  • improve sleep
  • reduced anxiety
49
Q

disadvantages of smoked cannabis (3)

A
  • not appropriate for all patients
  • Psychotropic SEs
  • Smoking not safest mode of admin
50
Q

TRPs

A

Transient receptors potential channels.

  • more than 30 different TRPs and 6 families
  • molecular sensors of taste, temp and pain
  • many have dual functions
51
Q

Antibiotics

A

chemical agents produced by one organism that have some toxic or inhibitory effect on another organism or cell.

52
Q

selective toxicity

A

Idea that you can use toxic drugs, which as long as they are more toxic to your target than to normal tissues, can be useful.

  1. antimicrobial drugs
  2. anticancer drugs
53
Q

Bacterosidal

ex.

needed when?

A

druggs that kill bacteria when they are introduced.

ex. penicillin

required if the patient is immunosuppressed

54
Q

bacteriostatic drugs

ex.

A

inhibit growth of bacteria. Growth resumes when the drug was removed.

ex. sulfonamides.

Success depends on there being an effective immune response

55
Q

what to do about beta lactamases?

A

1) use a beta-lactamase-resistant antibiotics (eg. Nafcillin)
2) Combine with a beta lactamase inhibitor (Eg. clavulanate)

56
Q

benefits of newer generations of cephalosporins

A

1 - better activity against gram -ve
2 - better able to move into tissue spaces
3 - more resistant to B-lactamases

57
Q

Advantages and disadvantages of using antimicrobial drugs in combinations

A

ADVANTAGES:

  • wider spectrum for mixed infections.
  • Reduced dose for individual agents.
  • Synergism between antibiotics.

DISADVANTAGES

  • Increased possibility of adverse reactions.
  • Antagonism between antibiotics.
  • Greater risk of antibiotic resistance.
58
Q

Example of an antagonistic antibiotic combination

A

Chloramphenicol + aminoglycoside

59
Q

4 methods of antibiotic resistance

A

1) Decreased entry
2) Bypass pathway
3) Enzymatic degradation
4) Altered target gate

60
Q

Sulfonamide resistance (3)

A

May be due to

  1. Decreased permeability of cell membrane
  2. Bacteria make a diff form of DHPS that binds sulphonamide poorly.
  3. Increased production of PABA made by the bacteria.
61
Q

Trimethoprim resistance (3)

A

May be due to:

1) Decrease perm of cell mem
2) Bacteria prod a form of DHFR that binds trimethoprim poorly
3) Bacteria prod more DHFR

62
Q

Cancer definition

A

Loss in the normal control mechanisms that govern cell survival, proliferation, and differentiation

63
Q

Principles of chemotherapy

A
  • Agent must be tolerable to treatment can be completed
  • Administer max tolerable dose
  • Cyclic therapy with dose and regimen chose for max effectiveness
  • Combinations to increase efficacy
  • Surgery followed by chemo
64
Q

Modes of interfering with TK signalling

A
  • MOA against TK ligand
  • MOA against TKR
  • Small molecule inhibitors
65
Q

primary resistance to drug

A
  • drug is ineffective on first attempt

- most commonly related to impaired response to cell death signals in tumour cells

66
Q

acquired resistance

A
  • drug worked at first, then became ineffective

- related to adpatation and mutation of tumour cells

PHAC3001 (2 decks)

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