Pain Control & Anesthetic Drugs (Overview) Flashcards

(51 cards)

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.

24
Q

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

A

mineralocorticoids

glucocorticoids

25
Why do mineralocorticoids do? What is a natural mineralocorticoid and what does it do?
- 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
What do glucocorticoids do? What is the natural glucocorticoid?
- antiinflammatory effect - inhibit phospholipase A2 in arachidonic acid pathway - cortisol is the natural drug
27
Briefly describe how cortisol is regulated in the body
- 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
List the intermediate lasting glucocorticoids (12-36hrs)
Prednisone prednisolone methylprednisolone triamcinolone
29
What do the long-acting glucocorticoids end in (48+hr)
"-methasone" Dexamethasone Betamethasone Flumethasone
30
Impact of glucocorticoids on... | PG and Leukotriene formation
Decrease
31
Impact of glucocorticoids on... | capillary integrity
decrease b/c no PG or LK present to cause capillary swelling
32
Impact of glucocorticoids on... | fibroblast activity
decrease
33
Impact of glucocorticoids on... healing time scar formation
HT increase | SF decrease
34
Impact of glucocorticoids on... | collagen fiber synthesis
decrease
35
Impact of glucocorticoids on... | T and B cells
impairs T-cells making P more susceptible to bacterial/fungal infections, but does NOT impair B cells at antiinflammatory dosages
36
Impact of glucocorticoids on... Cell mediated immunity humoral immunity
cell med = impair | humoral = does NOT impair at antiinflammatory lvls
37
Impact of glucocorticoids on... | Lymphocytes, eosinophils, neutorphils
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
Impact of glucocorticoids on... Gastric acid production Gastric mucus production
acid increases | mucus decreases
39
Impact of glucocorticoids on... skin thickness hair growth skeletal muscle mass
all decrease due to catabolism
40
Why should you not abruptly stop giving steroids?
- 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
What are the 3 opioid receptors called?
Mu- produces the most analgesia kappa- produces some analgesia delta- minor role; much unknown
42
How do opioids effect GI, respiratory function, and HR?
GI- decreased secretions & motility Respiratory Function- may depress it, but not huge concern in vet med HR- bradycardia
43
Name some pure mu agonists
``` Fentanyl Hydromorphone Methadone Morphine Oxymorphone Meperidine ```
44
List the partial mu agonist drug
Buprenorphine
45
List the partial antagonist drug
butorphanol
46
What is the opioid antagonist (reversal)
naloxone
47
Why is DMSO and how does it help reduce pain?
Dimethyl Sulfoxide | inactivates or traps free radicals the destroy tissue
48
What is a chondroprotective agent?
a class of drugs that don't have a direct antiinflammatory effect but that decrease inflammation by decreasing damage to cartilage/protect cartilage
49
What are some examples of chondroprotective agents?
- polysulfate glycosminoglycans (PSGAGs) - Hyaluronic acid - Glucosamine and chondroitin sulfate
50
What "pain killers" are toxic?
Ibuprofen (motrin, advil) Naproxen (aleve) Acetaminophen
51
What is the treatment for acetaminophen toxicosis?
acetylcysteine