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VM722 Pharm > Exam 3 > Flashcards

Exam 3 Flashcards

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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
2nd generation H1 antagonist
enter CNS less, less sedation caused | E.g. Ioratadine (Claratin)
26
H2 antagonist
Used for ulcers, drug-induced gastritis, reflux Inhibit gastric acid secretion by blocking H2 receptors e.g. Famotidine (pepcid), anything ending in -tidine
27
Adverse effects of H2 antagonists
uncommon, usually well-tolerated | Cimetidine inhibits cytochome p450 - other drugs metabolized by this pathway can build up
28
What does serotonin regulate
gut motility, body temp, sleep, mood, behavior, pain
29
What are ergot alkaloids
serotonin agonists Ergovaline - fungus in fsecue grass, SE US, causes neurotoxicity, gangrene in cattle Blocked by ketanserin (serotonin receptor, H1 antaognist)
30
Uses of serotonin modifiers in GI
- Metaclop, Cisapride (receptor agonists) - Increase parasymp activity, increase gut motility - Receptor antagonists - appetite stim, antiemetic, anti ergovaline-induced toxicity
31
SSRI's (selective serotonin reuptake inhibitor)
- increase serotonin = positive behavior effects | - May involve desens or down regulation b/c 4-6 weeks before see effects
32
SSRI use in dogs
separation anxiety compulsion behaviors aggression
33
SSRI use in cats
inappropriate urination (spraying) compulsive behaviors aggression psychogenic alopecia
34
When would you use NSIM's
- when NSAID not effectively managing a condition - when immunosuppression is desired - AI systemic dz
35
Calcineurin inhibitors
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
Difference between NSAIDs and NSIMs
NSAIDs don't get immunosuppression
37
Calcineurin inhibitor uses
IMHA, IBD, IM-polyarthritis, atopic dermatitis, perianal fistulas in dogs, organ transplant regimens, dry eyes
38
Adverse effects of Calcineurin inhibitors
Vomiting (dogs), anorexia (cats), weight loss, depression, lethargy
39
Cytotoxic alkylating agents
- 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
Uses for Cytotoxic alkylating agents
IMTP, SLE, rheumatoid arthritis, phemphigus, maybe IMHA
41
Cytotoxic alkylating agent toxicity
Bone marrow suppression Nausea, vomiting, diarrhea, alopecia Sterile hemorrhagic cystitis (just Cyclophosphamide) Chlorambucil - phemphigus, IM skin dz in cats
42
Cytotoxic inhibitors of purine synth
Pro-drug - active metabolite disrupts purine synth = no B/T cell proliferation MOA unclear, immunosuppression may take weeks Azathioprine, Mycopheonlate mofetil (more $$)
43
Uses for Cytotoxic inhibitors of purine synth
Often used in combo w/ corticosteroids | IBD, IM skin dz, IMHA, etc.
44
Cytotoxic inhibitors of purine synth toxicity
Immunosuppression & bone marrow sup (esp. cats) - Myco may be better alternative Less commonly causes GI distress, anorexia, pancreatitis, heptotoxicity
45
Oclacitinib (aka Apoquel)
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
Cytopoint
Manages atopic dermatitis in dogs Monoclonal Ab against IL-31 (itchy cytokine) Minimal bone marrow suppression
47
Types of corticosteroids
glucocorticoids (cortisol) | Mineralocorticoids (aldosterone)
48
Glucocorticoids
- 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
Mineralocorticoids
- zona glomerulosa | - stimm'd by ACTH, Angiotensin II --> AIP cause salt, water retention
50
Metabolic changes from glucocorticoids
increased glu production, increased insulin secretion/resistance (can lead to diabetes)
51
Cardiovascular changes from glucocorticoids
vasoconstriction, cardiac contraction, angiotensin release & salt/water retention --> plasma vol expansion Can see hypertension (dogs), CHF (cats)
52
Other glucocorticoid effects in body
bronchodilation, skin probs, immune fx, digestive enz secretion (possibly ulceration), anti-inflammatory at higher doses
53
How do glucocorticoids cause anti-inflammatory effects
inhibit activity of phospholipase A2 (step before cox) = no PG's, etc. Also suppress WBC migration, fx Cell mediate immunity suprpessed
54
How are glucocorticoids compared to eachother?
Everything compared against Hydrocortizone Short duration (< 12 hrs) Anti-inflamm potency: 1 Mineralocorticoid potency: 1
55
Fludrocortisone
Short duration (< 12 hrs) Anti-inflamm potency: 10 Mineralocorticoid potency: 125 Can be used systemically for cortisol AND aldosterone replacement w/ Addison's
56
Prednisone & methylprednisolone
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
Dexamethasone
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
Alternate-day therapy
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
Generalized seizures
``` Can occur repeatedly or become continuous (+5 min Status epilepticus) Grand mal (majorly motor) or petit mal (lose touch, less motor) ```
60
MOA's for anticonvulsants
Prevent initiation or spread of seizure focus Raise seizure threshold Inhibit excitatory neural activity (suppress AP's, agonize GABA)
61
Anticonvulsant vs. Anesthetic
Anticonvulsant - suppress seizure activity but don't produce unconsciousness Anesthetic - suppress seizure activity but do produce unconsciousness
62
Diazepam and seizures
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
Adverse effects of Diazepam
Tolerance developed if used chronically Sedation, behavioral changes Hepatic toxicosis in cats w/ chronic oral treatments
64
Bromide
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
Clonazepam (benzodiazepine)
- Like Diazepam but more potent - maybe good alternative to cats (no hepatotoxicity) - inhibition via GABA receptors - eliminated by zero-order kinetics
66
Phenobarbital
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
Phenobarbital MOA
- 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
Phenobarbital adverse effects
sedation, polyphagia, PU/PD that subsides w/ tolerance, increased hepatic metab Increased liver enz, heptocutaneous syndrome (necrolytic dermatitis) Affects thyroid and corticosteroid metab
69
Gabapentin
- 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
Levetiracetam
New, increasing use, $$ MOA unk, may influence Ca-dependent NT release, short half life Binds exclusively in CNS Dogs w/ refractory seizures
71
Drugs to use to stabilize/stop seziures
Diazepam Phenobarbital Bromide
72
Drugs used for seizure maintenance
Primary: Phenobarbital, Bromide | Secondary/add on: Gabapentin, Levetiracetam

VM722 Pharm (5 decks)

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