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VM722 Pharm > Exam 3 > Flashcards

Exam 3 Flashcards

1
Q

Nociception vs. pain

A
  • Nociception – reception of primary afferent AP signals from activated nociceptors that detect tissue-damaging (noxious) stimuli
  • Pain – conscious perception of a noxious stimulus
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2
Q

how do inflammatory products Bradykinin, cytokines, PG’s affect nociception/pain?

A

Active TRP’s peripherally to increase pain

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3
Q

How do glutamate agonists affect nocicpetion/pain

A

In CNS, dorsal horn: affects AMPA receptors first to stimulate pain, then stimulates windup via NMDA receptors

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4
Q

How does substance P affect nociception/pain

A

inflammatory mediator, affects G-prot linked receptors at synapse (CNS, dorsal horn)

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5
Q

How does BDNF affect nociception/pain

A

affects G-prot linked receptors at synapse

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6
Q

How do TRP receptors mediate nociception/pain

A

Transient receptor potentials (TRP’s) must be activated in to increase pain perception

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7
Q

How are TRP’s involved in nociception in periphery

A

TRP’s activate peripheral nociceptors or are activated by inflammation

PG’s, bradykinin, cytokines (TNFa, IL-1, IL-8), lipids –> activate TRPA1, TRPV1

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8
Q

How are TRP’s involved in nociception centrally

A

increase pain sensation by increasing the number of AP’s sent up to CNS via wind-up

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9
Q

How do NSAIDs act peripherally as analgesics?

A

NSAIDS ↓ prostaglandin synthesis and ↓ TRP activation via COX inhibition

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10
Q

How do local anesthetics act peripherally as analgesics?

A

Local anesthetics block APs

Work anywhere along pain pathways BUT limited use except on nerves, lower spinal cord

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11
Q

How does Capsacin act peripherally as analgesics?

A

topical analgesic from hot pepper oil - desensitizes TRPV1 (heat)

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12
Q

Where to opioids work to effect analgesia?

A

Dorsal horn, centrally
periaqueductal gray matter/raphe magnus
May inhibit or excite descending neurons

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13
Q

How does Tramodol work?

A

Serotonin/NE reuptake inhibitor
Weak mu opioid agonist
Acts in raphe magnus to inhibits dorsal horn neurons (secondary afferents) –> Fewer pain signals to brain

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14
Q

How do alpha 2 agonists act centrally as analgesics?

A

work post-synaptically at non-adreneric receptors, cause CNS inhibition & decrease pain signaling from post-synaptic neuron

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15
Q

How do NMDA antagonists act centrally as analgesics?

A

affect synapses by blocking NMDA receptors

e.g. Ketamine

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16
Q

2 major pools of histamine

A

Mast cells in connective tissue (and baso’s)

Non-mast cell tissue (lungs, skin, gastric mucosa)

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17
Q

What effect does a histamine receptor blockade have on degranulation

A

Only partially antagonizes histamine release by degranulation

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18
Q

Things that trigger histamine release

A

Immune-mediated (e.g. IGE hypersens)
Drug-induced (NMJ blockers, morphine
Plant & animal stings
Physical injury (trauma, heat, cold)

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19
Q

Class H1 histamine receptor

A

Relaxation of of vascular smooth m. –> vasodilation
Contraction of bronchial smooth m. (except cats, sheep)
Increase capillary permeability –>edema
Stims sensory nerves –> pain, itching

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20
Q

Classic sign of H1 receptor activation

A

reddening, swelling (wheal) & flare

typically due to allergy or inflammation

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21
Q

Class H2 histamine receptor

A

Histamine released from ECL (enterochromaffin-like cells) –> stim gastric acid secretion from parietal cells

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22
Q

How do H1 antagonists work

A
  • prevent action of released histamine (doesn’t prevent histamine release)
  • relax constricted bronchioles, decrease vasodilation & capillary permeability, antipruritic, pain relief
  • also prevents motion sickness
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23
Q

First generation H1 antagonist

A

enter CNS, often cause sedation, anti-muscarinic mostly

e.g. Diphenhydramine (benadryl)

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24
Q

Adverse effects of H1 antagonists

A
  • CNS depression, anti-muscarinic (anti-sludge) effects
  • Contraindicated for glaucoma (increase intra-ocular P)
  • Causes tolerance (decreases efficacy)
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25
Q

2nd generation H1 antagonist

A

enter CNS less, less sedation caused

E.g. Ioratadine (Claratin)

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26
Q

H2 antagonist

A

Used for ulcers, drug-induced gastritis, reflux
Inhibit gastric acid secretion by blocking H2 receptors
e.g. Famotidine (pepcid), anything ending in -tidine

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27
Q

Adverse effects of H2 antagonists

A

uncommon, usually well-tolerated

Cimetidine inhibits cytochome p450 - other drugs metabolized by this pathway can build up

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28
Q

What does serotonin regulate

A

gut motility, body temp, sleep, mood, behavior, pain

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29
Q

What are ergot alkaloids

A

serotonin agonists
Ergovaline - fungus in fsecue grass, SE US, causes neurotoxicity, gangrene in cattle
Blocked by ketanserin (serotonin receptor, H1 antaognist)

30
Q

Uses of serotonin modifiers in GI

A
  • Metaclop, Cisapride (receptor agonists) - Increase parasymp activity, increase gut motility
  • Receptor antagonists - appetite stim, antiemetic, anti ergovaline-induced toxicity
31
Q

SSRI’s (selective serotonin reuptake inhibitor)

A
  • increase serotonin = positive behavior effects

- May involve desens or down regulation b/c 4-6 weeks before see effects

32
Q

SSRI use in dogs

A

separation anxiety
compulsion behaviors
aggression

33
Q

SSRI use in cats

A

inappropriate urination (spraying)
compulsive behaviors
aggression
psychogenic alopecia

34
Q

When would you use NSIM’s

A
  • when NSAID not effectively managing a condition
  • when immunosuppression is desired
  • AI systemic dz
35
Q

Calcineurin inhibitors

A

Bind to certain proteins to inhibit cacineurin = no dephosphorlyation of NFAT –> no nulcear translocation, no gene exression –> no T cell activation or cell-mediated immunity
Cyclosporine & Tacrolimus

36
Q

Difference between NSAIDs and NSIMs

A

NSAIDs don’t get immunosuppression

37
Q

Calcineurin inhibitor uses

A

IMHA, IBD, IM-polyarthritis, atopic dermatitis, perianal fistulas in dogs, organ transplant regimens, dry eyes

38
Q

Adverse effects of Calcineurin inhibitors

A

Vomiting (dogs), anorexia (cats), weight loss, depression, lethargy

39
Q

Cytotoxic alkylating agents

A
  • Suppress B, T cells & rapidly dividing cells (bone marrow)
  • MOA - nitrogen mustard adds alkyl grp –> damages DNA of B, T cells (but T cells less susceptible to inhibition)
  • Cyclophosphamide, Chlorambucil (slower acting, less toxic)
40
Q

Uses for Cytotoxic alkylating agents

A

IMTP, SLE, rheumatoid arthritis, phemphigus, maybe IMHA

41
Q

Cytotoxic alkylating agent toxicity

A

Bone marrow suppression
Nausea, vomiting, diarrhea, alopecia
Sterile hemorrhagic cystitis (just Cyclophosphamide)
Chlorambucil - phemphigus, IM skin dz in cats

42
Q

Cytotoxic inhibitors of purine synth

A

Pro-drug - active metabolite disrupts purine synth = no B/T cell proliferation
MOA unclear, immunosuppression may take weeks
Azathioprine, Mycopheonlate mofetil (more $$)

43
Q

Uses for Cytotoxic inhibitors of purine synth

A

Often used in combo w/ corticosteroids

IBD, IM skin dz, IMHA, etc.

44
Q

Cytotoxic inhibitors of purine synth toxicity

A

Immunosuppression & bone marrow sup (esp. cats) - Myco may be better alternative
Less commonly causes GI distress, anorexia, pancreatitis, heptotoxicity

45
Q

Oclacitinib (aka Apoquel)

A

Manages chronic itching, chronic/severe atopic dertmatitis
JAK-1/3 inhibitor - decreases inflammatory cytokines and cytokines that cause itch (IL-31)
Causes bone marrow suppression, but good alternative if dogs not tolerating other drugs

46
Q

Cytopoint

A

Manages atopic dermatitis in dogs
Monoclonal Ab against IL-31 (itchy cytokine)
Minimal bone marrow suppression

47
Q

Types of corticosteroids

A

glucocorticoids (cortisol)

Mineralocorticoids (aldosterone)

48
Q

Glucocorticoids

A
  • zona fasiculata
  • stress –> hypothalamus releases CRG –> anterior pituitary releases ACTH –> adrenal cortex releases cortisol
  • See changes in genetic expression (slow) or see more rapid increase in metabolism
49
Q

Mineralocorticoids

A
  • zona glomerulosa

- stimm’d by ACTH, Angiotensin II –> AIP cause salt, water retention

50
Q

Metabolic changes from glucocorticoids

A

increased glu production, increased insulin secretion/resistance (can lead to diabetes)

51
Q

Cardiovascular changes from glucocorticoids

A

vasoconstriction, cardiac contraction,
angiotensin release & salt/water retention –> plasma vol expansion
Can see hypertension (dogs), CHF (cats)

52
Q

Other glucocorticoid effects in body

A

bronchodilation, skin probs, immune fx, digestive enz secretion (possibly ulceration), anti-inflammatory at higher doses

53
Q

How do glucocorticoids cause anti-inflammatory effects

A

inhibit activity of phospholipase A2 (step before cox) = no PG’s, etc.
Also suppress WBC migration, fx
Cell mediate immunity suprpessed

54
Q

How are glucocorticoids compared to eachother?

A

Everything compared against Hydrocortizone
Short duration (< 12 hrs)
Anti-inflamm potency: 1
Mineralocorticoid potency: 1

55
Q

Fludrocortisone

A

Short duration (< 12 hrs)
Anti-inflamm potency: 10
Mineralocorticoid potency: 125
Can be used systemically for cortisol AND aldosterone replacement w/ Addison’s

56
Q

Prednisone & methylprednisolone

A

Intermediate duration (12-36 hrs)
Anti-inflamm potency: 4 & 5
Mineralocorticoid potency: 0.8 & 0.5
Used systemically for long-term management of allergy, chronic inflammation (e.g. arthritis), and immunosuppression (e.g. AI dz)

57
Q

Dexamethasone

A

long duration (36 - 72 hrs)
Anti-inflamm potency: 25
Mineralocorticoid potency: 0
Used systemically for immediate relief of hypersensitivity and septic shock, long term control of allergy and immunosuppression

58
Q

Alternate-day therapy

A

Used to taper of GC’s & fix iatrogenic hypoadrenocorticism
Useful if GC’s being used for anti-inflam effects, not great if used for immunosupp effects

59
Q

Generalized seizures

A 
Can occur repeatedly or become continuous (+5 min Status epilepticus)
Grand mal (majorly motor) or petit mal (lose touch, less motor)
60
Q

MOA’s for anticonvulsants

A

Prevent initiation or spread of seizure focus
Raise seizure threshold
Inhibit excitatory neural activity
(suppress AP’s, agonize GABA)

61
Q

Anticonvulsant vs. Anesthetic

A

Anticonvulsant - suppress seizure activity but don’t produce unconsciousness

Anesthetic - suppress seizure activity but do produce unconsciousness

62
Q

Diazepam and seizures

A

commonly used, esp. for status epilepticus
rapidly distributes to CNS to inhibit neuronal activity
Increases efficacy of endogenous GABA (= neuronal inhibition)
Good for short-term stabilization tx - multiple administration methods, half life 3 hrs dogs

63
Q

Adverse effects of Diazepam

A

Tolerance developed if used chronically
Sedation, behavioral changes
Hepatic toxicosis in cats w/ chronic oral treatments

64
Q

Bromide

A

stabilization, maintenance tx if Diazepam or Pheno don’t work - or in combo
MOA unknown, hyperpolarizes activated Cl channels
Adverse - joint stiffness in rear limbs, CNS depression, coughing (cats)

65
Q

Clonazepam (benzodiazepine)

A
  • Like Diazepam but more potent
  • maybe good alternative to cats (no hepatotoxicity)
  • inhibition via GABA receptors
  • eliminated by zero-order kinetics
66
Q

Phenobarbital

A

Most widely used SA anticonvulsant for chronic maintenance tx (good 2nd line to Diazepam)
Doesn’t produce significant sedation
hepatic metabolism via cP450’s

67
Q

Phenobarbital MOA

A
  • increase seizure threshold
  • decreases electrical activity of the seizure focus
  • increases the efficacy of endogenous GABA on GABA(a) receptors
  • Bind to specific sites on GABA(a) receptors – sites distinct from benzodiazepine sites
68
Q

Phenobarbital adverse effects

A

sedation, polyphagia, PU/PD that subsides w/ tolerance, increased hepatic metab
Increased liver enz, heptocutaneous syndrome (necrolytic dermatitis)
Affects thyroid and corticosteroid metab

69
Q

Gabapentin

A
  • Structural analog of GABA but doesn’t interact with GABA receptors
  • MOA unknown - inhibits Ca channels in neurons
  • Use in combo w/ other drugs to treat refractory seizures, or when hepatic dz an issue
  • Avoid human liquid product of it (has xylitol)
70
Q

Levetiracetam

A

New, increasing use, $$
MOA unk, may influence Ca-dependent NT release, short half life
Binds exclusively in CNS
Dogs w/ refractory seizures

71
Q

Drugs to use to stabilize/stop seziures

A

Diazepam
Phenobarbital
Bromide

72
Q

Drugs used for seizure maintenance

A

Primary: Phenobarbital, Bromide

Secondary/add on: Gabapentin, Levetiracetam

VM722 Pharm (5 decks)

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