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Pharmacology > 16/17 > Flashcards

16/17 Flashcards

1
Q

Ad fibers:

A

faster, myelinated axons response first to noxious mechanical stimuli. Produce the initial sensation of sharp pain

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2
Q

C fibers:

A

slower, unmyelinated axons respond to thermal, mechanical and chemical assaults. Dull, aching, or burning pain.

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3
Q

5x more —- fibers than —- fibers

A

C

Ad

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4
Q

Nociception = the ability to

A

feel pain

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5
Q

Nociceptors are molecular sensors. Different nociceptors respond to various noxious stimuli such as heat, cold, mechanical perburbations, or protons. Their activation leads to

A

local depolarization which in turn initiates action potentials.

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6
Q

Allodynia

A

pain from normally painlesss stimuli

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7
Q

Hyperalgesia

A

heightened sense of pain to noxious stimuli

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8
Q

Hyperalgesia

A

heightened sense of pain to noxious stimuli

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9
Q

Channels that let in Cl will

A

hyperpolarize

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10
Q

Channels that let in Na will

A

depolarize

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11
Q

Channels that let out K will

A

hyperpolarize

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12
Q

PREsynaptically: Hyperpolarization

A

diminishes Ca++ influx and neurotransmitter release

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13
Q

PREsynaptically: Depolarization

A

enhances Ca++ influx and neurotransmitter release

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14
Q

Pro-opiiomelanocortin peptides

A

beta endorphin

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15
Q

Pro enkephalin peptides

A

met-enkephalin and leu-enkephalin

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16
Q

Prodynorphin peptides

A

dyn-A, dyn-B and alpha neo endorphin

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17
Q

Three important opioid receptors

A

mu, kappa, delta. mu is important. All GPCRs, all widely in CNS, all activate Galphai

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18
Q

Opioid receptors all activate

A

Gai

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19
Q

Beta endorphin is the natural ———- of mu opioid receptor

A

agonist.

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20
Q

How opioids work: in PNS and CNSGPCRs modulate nerfve activity. Don’t act as blockers, but

A

make nerve impulses difficult to conduct

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21
Q

Activation of opioid receptors will also lead to activation of a particular type of —————-. This will ————– the cell.

A

potassium channel (via GbGg)

hyperpolarize

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22
Q

Opioids - reduction of Ca and hyperpolarization will

A

diminish generation of AP.

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23
Q

Opioids can inhibit synaptic transmission if receptros are located

A

pre or post synaptically

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24
Q

Mu receptors —— important forms

A

3

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25
Q

mu receptors found in

A

Found in periaqueductal gray region, superficial dorsal horn of the spinal cord, nucleus accumbens, amygdala, cerebral cortex. Mainly, presynaptic.
Found in GI tract (inhibit peristaltic action, cause constipation).

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26
Q

Opioid analgesics produce

A

analgesia, respiratory depression, constipation, GI spasm, dependence

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27
Q

Morphine is the prototypical full agonist of

A

mu receptor.

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28
Q

Patients also report morphine more effective against

A

dull aches as opposed to sharp pains.

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29
Q

Patients also report morphine more effective against

A

dull aches as opposed to sharp pains.

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30
Q

Adverse effects of opioids

A

constipation

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31
Q

Tolerance rate for morphine

A

seen 5-7 days of treatment. Toxic effects remains if tolnce has developed. Mech is controversial

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32
Q

Morphine is metabolized by—— very quickly in the liver. Morphine-3glucuronide (M-3-G) is the primary product Morphine-6-glucuronide (M-6-G) is the secondary product.

A

UGT2B7

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33
Q

M-3-G is

A

inactive/useless more or less

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34
Q

Morphine as a pill is

A

not very useful

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35
Q

Codeine
Substitution at —- position renders it more effective orally than morphine (probably relates to absence of 3glucuronidation in liver).

A

3

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36
Q

Codeine
Substitution at —- position renders it more effective orally than morphine (probably relates to absence of 3glucuronidation in liver).

A

3

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37
Q

Codeine better when administered

A

orally, not intramuscularly

38
Q

Codeine better when administered

A

orally, not intramuscularly

39
Q

Fentanyl

A

pain meds with other meds. Super fast onset and offset. Effects last less than an hour or so.

40
Q

Fentanyl danger factors

A

The two factors are: (1) Fentanyl is more lipid soluble than morphine or heroin. (2) Fentanyl binds tighter to the m opioid receptor than morphine or heroin.

41
Q

Fentanyl produces more

A

prolonged respiratory depression than other opioids

42
Q

mu receptor antagonists

A

reverse effect of opioid potentially

43
Q

Mixed antagonists/agonists

A

Since activation of all the opioid receptors produce analgesia, might it be possible to produce drugs that act on kor d receptors and don’t have the major adverse effects (i.e. respiratory depression) and/or don’t produce dependence.

44
Q

Injured cells release certain chemicals called

A

alarmins preceding inflammation

45
Q

The alarmin IL-33 can produce

A

‘degranulation’ of resident immune cells called mast cells.

46
Q

Histamine acts through a ——– to produce local ————–and render the capillaries ‘leaky’. This will allow more immune cells to enter the injury site and also produce ———

A

G protein coupled receptor

vasodilation

edema.

47
Q

Histamine-H1 receptor activity on vascular endothelium increases intracellular Ca++ - 2 effects

A
  1. NO production in endothelial cells (relaxation)

2. MLCK mediated contraction of capillary endothelium (rendering it leaky)

48
Q

Prostaglandins

A

mediate pain, accumulate inflammation.

49
Q

Cyclooxygenases responsible for converting

A

arachidonic acid to prostaglandins

50
Q

The action of the enzymes —— sends the arachidonic acid down the path leading to production of the prostaglandins

A

COX1 and COX2

51
Q

4 diff

A

prostaglandins, 8 diff GPCRs.

52
Q

Prostaglandins act through

A

GPCRs

53
Q

Prostaglandins (via their G protein coupled receptors) act at

A

peripheral nerve endings to sensitize pain responses.

54
Q

The NSAIDS all work by inhibition of the ——, diminishing production of ——–.

A

COX enzymes

prostaglandins

55
Q

COX 1 if inhibited

A

will lead to bad effects. Goal is to inhibit cox 2, leaving cox 1 alone.

56
Q

Platelet aggregation is mediated in part through the

A

autocrine production of thromboxane (TXA2 in the picture).

57
Q

COX enzymes inhibit ——— production.

A

Thromboxane A2 production

58
Q

No Advantage to Giving Preemptive NSAIDs to Improve Success of the Inferior Alveolar Nerve Block in Patients With

A

Symptomatic Irreversible Pulpitis.

59
Q

Advese effect of cox enzyme inhibitors

A

disruption of mucosal defense in the stomach, because prostaglandins stimulate mucus and bicarbonate secretion that helps comprise mucous gel.

60
Q

Adverse effects of cox enzyme inhibitors

A 
Increases in bleeding time (acetylsalicylic acid) Kidney problems (water, Na+ retention) Increased BP
Heart failure (rare)
61
Q

Adverse effects of cox enzyme inhibitors

A 
Increases in bleeding time (acetylsalicylic acid) Kidney problems (water, Na+ retention) Increased BP
Heart failure (rare)
62
Q

Most effective analgesia:

A

optimum dose of NSAID + additional opioid

63
Q

OSteoarthritis

A

hyaline cart breakdown in joints.

64
Q

——– contributes to tissue damage in OA

A

Inflammation

65
Q

Chondrocytes of inflammed cartilage:

A

Anabolic and catabolic activities are not balanced, the catabolic activities dominate. The extracellular matrix is not maintained in a healthy state.
One sees decreased production of collagen. Increased production of proteolytic enzymes such as matrix metalloproteases.

Inflammatory mediators produce this change. IL-1b and TNFa are particularly important

66
Q

Proinflammatory cytokines (e.g. IL- 1b, TNFa) lead to

A

Reduced collagen expression, increased MMP expression, increased expression of other proteases, increased iNOS, COX-2, PEG-2

67
Q

 Esters are hydrolyzed in the plasma and liver by pseudocholinesterase into

A

PABA

68
Q

Hyaline cartilage matrix is mostly made up of

A

type II collagen, and chondroitin sulphate, both of which are also found in elastic cartilage. It also includes keratin sulphate.

69
Q

Synovitis is characterized by proliferation of cells of the synovial lining, increased vascularization, and infiltration by

A

inflammatory cells (especially lymphocytes and macrophages).

70
Q

Eventually, synovitis leads to ——–. This overgrowth is called the ——.

A

extension of the inflammatory tissue mass to the articular cartilage

pannus

71
Q

Pannus is an abnormal layer of

A

fibrovascular tissue or granulation tissue. Common sites for pannus formation include over the cornea, over a joint surface (as seen in rheumatoid arthritis), or on a prosthetic heart valve.

72
Q

T helper 17 cells (Th17) are a subset of

A

pro-inflammatory T helper cells defined by their production of interleukin 17 (IL- 17). Th17s are developmentally distinct from Th1 and Th2 lineages. Th17 cells play an important role in maintaining mucosal barriers and contributing to pathogen clearance at mucosal surfaces, but they have also been implicated in autoimmune and inflammatory disorders.

73
Q

Of course, Th17 cells secrete other cytokines that affect the immune response -

A

One of these (TNFa) is a really, really, really important therapeutic target in auto immune disorders.

74
Q

Cardiolipin is a phospholipid that is an important component of the ———-, where it constitutes about 20% of the total lipid composition.

A

inner mitochondrial membrane

75
Q

Calpastatin is an ——- (calcium- dependent cysteine protease) inhibitor.

A

endogenous calpain

76
Q

Antiperinuclear factor antibodies

A

Stain around nucleus of neutrophils

77
Q

Detection of — is an important diagnostic for RA

A

RF

78
Q

Cardiolipin is a phospholipid that is an important component of the ———-, where it constitutes about 20% of the total lipid composition.

A

inner mitochondrial membrane

79
Q

Antibodies directed against citrullinated proteins are

A

frequently discovered in RA

80
Q

Anti-citrullinated Protein Antibodies (ACPA) recognize a diverse set of proteins and are

A

highly cross reactive

81
Q

Interestingly, citrullination of proteins itself might be important in the context of

A

tissue destruction

82
Q

ACPAs bind and induce ——– by ——

A

bone resorption

osteoclasts

83
Q

Citrullinated fibrinogen and collagen are ——- in mouse models of arthritis

A

arthrogenic

84
Q

Citrullinated fibrinogen activates ———

A

macrophages

85
Q

Drugs to treat Rheumatoid Arthritis

A

NSAIDS, Disease-Modifying Anti-Rheumatic Drugs

3) Glucocorticoids (covered in asthma section)
4) Pain medications that aren’t NSAIDS

86
Q

Disease-Modifying Anti-Rheumatic Drugs (DMARDS)

A

traditional small molecule drugs

biologics (generally monoclonal antibodies)

87
Q

Methotrexate: Enzyme inhibitor of

A

dihydrofolate reductase

This interference with folate metabolism is the mechanism by which methotrexate acts as a chemotherapeutic agent

88
Q

If you Inhibit DHFR, you inhibit

A

nucleic acid (and amino acid) synthesis

89
Q

TNFa is a

A

“pleotropic cytokine” that plays a major role in the immune/inflammatory response

90
Q

TNFa is heavily implicated in the pathogenesis of

A

autoimmune diseases

Pharmacology (19 decks)

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