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VTNE Review > Pain Control & Anesthetic Drugs (Overview) > Flashcards

Pain Control & Anesthetic Drugs (Overview) Flashcards

1
Q

T/F: Analgesics causes loss of consciousness

A

False

Anesthetics do this. Analgesia is pain relief without loss of consciousness and without total loss of feeling or movement.

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2
Q

T/F: NSAIDs are more effective if taken before pain.

A

True

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3
Q

T/F: NSAIDs can be used as analgesics for broken bones

A

False

NSAIDS block the formation of pain mediators in peripheral NS. They do not produce sufficient analgesia to counteract severe pain that is associated with broken bones.

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4
Q

T/F: NSAIDs are commonly used for patients with osteoarthritis.

A

True

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5
Q

T/F: Reversal agents for opioids active opioid receptors.

A

False

they bind to the receptor but DO NOT activate it.

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6
Q

What are the 5 pillars of pain?

A 
Heat
Redness
Swelling
Pain
Loss of Function
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7
Q

When would you use an Opioid over an NSAID? Why?

A

If you need strong pain relief
b/c opioids work at the brain regardless of # of signals being sent to the brain, while NSAIDs and steroids only decrease the # of pain signals being sent to the brain

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8
Q

What are the 4 parts of the nociceptive pathway?

A

Transduction
Transmission
Modulation
Perception

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9
Q

Def. transduction

A

stimulus of a nociceptor that converts physical trauma to a nerve signal

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10
Q

Def. transmission

A

the impulse is sent up sensory nerves to the spinal cord

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11
Q

Def. Modulation

A

sensory impulses in spinal cord are either inhibited or amplifed

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12
Q

Def. Perception

A

sensory impulse arrives in the brain and is perceived as pain

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13
Q

What part of the arachidonic pathway will NSAIDs inhibit?

A

NSAIDs inhibit COX and LOX from acting on arachidonic acid. This prevents arachidonic acid from being trnasformed into PGs, Thromboxanes, and Leukotrienes

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14
Q

What part of the arachidonic pathway will corticosteroids inhibit?

A

Inhibits phospholipase A2

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15
Q

Which COX is which?

Compare COX-1 to COX-2.

A

COX-1 = good enzyme
-produces PGs involved in normal physiological processes and is normally always present in different systems throughout the body

COX-2 = bad enzyme
-produces PGs that are primarily involved with physiological changes associated with inflammation

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16
Q

Why is the amount of protein in the bloodstream important when talking about NSAIDs and their power?

A

NSAIDs bind to proteins in the bloodstream, and when they do that they stay in the bloodstream in higher concentration. When there are fewer proteins for them to bind to, then the NSAID will slip out of the capillary and you won’t have as high a drug concentration.

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17
Q

What conditions can cause hypoproteinemia?

A
  • Liver disease (b/c the liver produces proteins)
  • Enteropathy (GI Dz, where the protein leaks into the bowel
  • Nephropathy (renal Dz, where the protein leaks out in the urine)
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18
Q

Differentiate between classic NSAIDs and “COXIBs”

A
  • Classic NSAIDs are not COX specific, so they bind to COX 1 & COX 2
  • COXIBs are “selected COX-2 inhibitors” meaning they target primarily COX-2
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19
Q

What side effects can be seen when COX-1 is targeted?

A
  • decreased mucus production
  • decreased GI tissue perfusion
  • decreased cell turnover
  • increased acid production as a result
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20
Q

List 3 classic NSAIDs

A

Aspirin
Flunixin Meglumaine (banamine)
Phenylbutazone

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21
Q

Why is aspirin dangerous? Why is it used?

A
  • dangerous b/c it prevents platelets from clumping

- only used in cats with saddle thrombus

22
Q

Name selective COX inhibitors

A 
carprofen
etodolac
deracoxib
meloxicam
firocoxib (Previcox)
rebenacoxib (Onsior)
23
Q

DO NOT use ____________ NSAIDs on _____ patient simultaneously.

A

multiple

one

24
Q

What are the two types of steroids produced by the adrenal gland?

A

mineralocorticoids

glucocorticoids

25
Q

Why do mineralocorticoids do? What is a natural mineralocorticoid and what does it do?

A
  • regulated electrolyte and water balance
  • Aldosterone –> causes the body to reabsorb Na from the urine back into the body; water usually follows Na, so blood volume also increases
26
Q

What do glucocorticoids do? What is the natural glucocorticoid?

A
  • antiinflammatory effect
  • inhibit phospholipase A2 in arachidonic acid pathway
  • cortisol is the natural drug
27
Q

Briefly describe how cortisol is regulated in the body

A
  • a stress signal enters the hypothalamus
  • hypothalamus releases CRF (corticotropin releasing factor) which acts on pituitary
  • pituitary produces ACTH (adrenocortioctropic hormone) which acts on the adrenal gland
  • adrenal gland produces cortisol
  • cortisol production negative feedback on pituitary gland and hypothalamus, but positive feedback on metabolic effect
28
Q

List the intermediate lasting glucocorticoids (12-36hrs)

A

Prednisone
prednisolone
methylprednisolone
triamcinolone

29
Q

What do the long-acting glucocorticoids end in (48+hr)

A

“-methasone”

Dexamethasone
Betamethasone
Flumethasone

30
Q

Impact of glucocorticoids on…

PG and Leukotriene formation

31
Q

Impact of glucocorticoids on…

capillary integrity

A

decrease b/c no PG or LK present to cause capillary swelling

32
Q

Impact of glucocorticoids on…

fibroblast activity

33
Q

Impact of glucocorticoids on…
healing time
scar formation

A

HT increase

SF decrease

34
Q

Impact of glucocorticoids on…

collagen fiber synthesis

35
Q

Impact of glucocorticoids on…

T and B cells

A

impairs T-cells making P more susceptible to bacterial/fungal infections, but does NOT impair B cells at antiinflammatory dosages

36
Q

Impact of glucocorticoids on…
Cell mediated immunity
humoral immunity

A

cell med = impair

humoral = does NOT impair at antiinflammatory lvls

37
Q

Impact of glucocorticoids on…

Lymphocytes, eosinophils, neutorphils

A

Lymphocytes & Eosinophils –> decrease b/c they’re taken up by tissues
Neutrophils –> increase b/c they jump off the blood vessel wall and into circulation

38
Q

Impact of glucocorticoids on…
Gastric acid production
Gastric mucus production

A

acid increases

mucus decreases

39
Q

Impact of glucocorticoids on…
skin thickness
hair growth
skeletal muscle mass

A

all decrease due to catabolism

40
Q

Why should you not abruptly stop giving steroids?

A
  • the adrenal gland has been suppressed because you’ve essentially been providing cortisol via the glucocorticoid
  • because it hasn’t been used, the adrenal gland has started to atrophy
  • ACTH production will start up again, but ACTH won’t have a usable adrenal gland to stimulate to produce cortisol
  • the patient becomes Addisonian and dies because cortisol is essential to life and the pet can’t produce it if you cold turkey stop the steroid
41
Q

What are the 3 opioid receptors called?

A

Mu- produces the most analgesia
kappa- produces some analgesia
delta- minor role; much unknown

42
Q

How do opioids effect GI, respiratory function, and HR?

A

GI- decreased secretions & motility
Respiratory Function- may depress it, but not huge concern in vet med
HR- bradycardia

43
Q

Name some pure mu agonists

A 
Fentanyl
Hydromorphone
Methadone
Morphine
Oxymorphone
Meperidine
44
Q

List the partial mu agonist drug

A

Buprenorphine

45
Q

List the partial antagonist drug

A

butorphanol

46
Q

What is the opioid antagonist (reversal)

47
Q

Why is DMSO and how does it help reduce pain?

A

Dimethyl Sulfoxide

inactivates or traps free radicals the destroy tissue

48
Q

What is a chondroprotective agent?

A

a class of drugs that don’t have a direct antiinflammatory effect but that decrease inflammation by decreasing damage to cartilage/protect cartilage

49
Q

What are some examples of chondroprotective agents?

A
  • polysulfate glycosminoglycans (PSGAGs)
  • Hyaluronic acid
  • Glucosamine and chondroitin sulfate
50
Q

What “pain killers” are toxic?

A

Ibuprofen (motrin, advil)
Naproxen (aleve)
Acetaminophen

51
Q

What is the treatment for acetaminophen toxicosis?

A

acetylcysteine

VTNE Review (10 decks)

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