Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

spanish > Capstone - Ex 3 > Flashcards

Capstone - Ex 3 Flashcards

You may prefer our related Brainscape-certified flashcards:
Spanish flashcards Medical Spanish flashcards AP® Spanish flashcards
1
Q

How does inflammation cause pain? (peripheral)

A

Activates TRP channels

- PGs, bradykinin, cytokines, lipids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

How is pain increased (centrally)?

A

Increased Abs through pain pathways to brain

- e.g. “wind up”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

NSAIDs and Analgesia

A

MOA: dec PG synthesis and dec TRP activation

- COX inhibition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Local anesthetics and Analgesia

A

MOA: block APs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Ketamine and Analgesia

A

MOA: glutamate antagonist

- NMDA antagonist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Opioids and Analgesia

A

MOA: work at many synaptic sites (e.g. mu and kappa agonists)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

A2 agonists and Analgesia

A

MOA: work postsynaptically on non-adrenergic neurons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Two classes of endogenous steroids produced in adrenal cortex - Corticosteroids

A
  1. Cortisol (glucocorticoid)
    - zona fasciculata
  2. Aldosterone (mineralocorticoid)
    - zona glomerulosa
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Glucocorticoid Summary

A
  • production of inflammatory mediators
  • dec PGs via phospholipase A inhibition
  • WBC migration and fxn is suppressed
  • Cell-mediated immunity is suppressed
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

NSAIDs

A

MOA: inhibit COX

- dec PG synthesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Hydrocortisone (cortisol)

A

MOA: dec PGs via Phospholipase A inhibition

Use: topically for pruritus and inflammation assoc’d with allergy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Fludrocortisone

A

MOA: dec PGs via Phospholipase A inhibition

Use: systemically for cortisol and aldosterone replacement during adrenal insufficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Prednisone & methylprednisolone

A

MOA: dec PGs via Phospholipase A inhibition

Use: systemically for LONG-term management of allergy, chronic inflammation, and immunosuppression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Prednisone vs prednisolone

A

Prednisone:
- Pro drug that is metabolized to prednisolone

(Methyl)prednisolone:

  • cats/horses have less conversion from prodrug to this
  • hepatic failure has less conversion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Dexamethasone

A

MOA: dec PGs via Phospholipase A inhibition

Use: systemically for immediate relief of hypersensitivity and septic shock, long-term control of allergy, and immunosuppression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How can the adverse effects of long-term GC use be reduced?

A

Alternate-day therapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Mitotane

A

MOA: eliminate or dec availability of adrenal steroids except aldosterone

  • related to the insecticide DDT; cytotoxic

Use: hyperadrenocorticism (Cushing’s) or steroid-secreting tumors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

How do NSAIDs effect pain and inflammation?

A

MOA: inhibit PG synthesis via blocking COX

Pain: PGs inc intensity and duration of firing from nociceptors - blocking them exerts analgesic effect

Inflammation: PGs dilate small arterioles which enhance edematous actions of histamine and bradykinin - blocking them exerts anti-edematous effect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the most-commonly reported adverse effect following NSAD therapy?

A

GI issues!!

Renal and hepatic toxicities are reported with much lower frequency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Species-specific activity and COX Selectivity

A

Cannot extrapolate between species!

E.g. Carprofen is COX2 selective in dogs, COX1 selective in horses, and may be more non-selective in horses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Which COX-selective drugs have less GI effects?

A

COX-2

Aspirin, ibuprofen are COX1 selective, which is why they have worse effects in dogs!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

NSAIDs and Cats

Which are good?

A

Most are cleared via glucuronidation in the liver (cats aren’t good at this)

Meloxicam and piroxicam are better! metabolized by oxidation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are the primary reasons NSAIDs are used in animals?

A

anti-inflammatory

Anti-pyretic

Analgesic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

At what point in the nociceptive pathways do NSAIDs exert their predominant effect?

A

Nociceptors at TRP channels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What are the risks of NSAiDs and GC use concurrently

A

GI ulcers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What organ system is of most concern when giving an NSAID to adult cat

A

Kidney (esp with ahminoglycosides, ACEi, Beta-blockers, diuretics)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What are the pros and cons of using aspiring for chronic pain in the dog?

A

Pro: inexpensive, effective, easy to use

Con: GI, tolerance, blood thinning

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Why do NSAIDs fail to control pain in some patients?

A
  • pain not due to PGs (inflammation)
  • pain is too strong/intense
  • tolerance
  • individual variation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What can you give with NSAID to enhance post-op analgesia?

A

opioids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Why do we choose NSAIDs over GC for post-op pain control?

A

NSAIDs don’t suppress immune function and fewer side effects

31
Q

How do NSAIDs work?

A

Block COX and dec PGs

32
Q

Why do we use opioids in animals?

A

Analgesia for severe pain and sedation

33
Q

Why are clinically available opioids scheduled (controlled) by the DEA?

A

Misuse and abuse by humans

34
Q

How common is opioid addiction in vet patients?

A

not common

35
Q

General anesthesia vs Analgesia

A

GA:

  • amnesia (loss of consciousness)
  • analgesia (loss of pain)
  • immobilization (mm relaxation)

Analgesia:
- loss of sensitivity pain

36
Q

Tolerance and efficacy?

A

Higher tolerance, lower efficacy

37
Q

Can pts develop tolerance to resp depressants or constipation effects of opioids?

A

Resp depression: patients develop tolerance quickly

Constipation: dogs tolerate well, other spp not so much

38
Q

Can animals become dependent on opioids?

A

Yes, physically - their body no longer regulates nociceptive signals

39
Q

How do we avoid withdrawal in patients?

A

Taper dose

40
Q

MOA of endogenous/exogenous opioids - Nociceptive signals

A

MOA: Mu or kappa agonist –> opiates bind and hyperpolarize the membrane –> dec NT release

41
Q

Why is the affinity of an opiod to the opiate receptor important to know?

A

affinity relates to DOA

42
Q

Which opioid is difficult to reverse due to high binding affinity?

A

Buprenorphine - a partial mu agonist, binds with high affinity

43
Q

Is butorphanol (potency = 5 ) more or less effective than morphine for the treatment of severe, acute pain in the dog? why?

A

Butorphanol - kappa agonist and mu antagonist

Butorphanol is less effective because its not a mu agonist (like morphine)

  • only a partial agonist
  • short DOA
44
Q

Resp depression effects of butorphanol vs fentanyl

A

Butorphanol: ceiling effect
Fentanyl: lose dose - no effect; high dose - profound effect

45
Q

opioids and GI motility in horses

A

DEC GI stasis!

46
Q

How do high doses of hydromorphone affect body temperature in cats?

A

Cats = hyperthermia

other spp = hypothermia

47
Q

MOA for analgesia with tramadol

A

Weak mu agonist, 5HT and NE reuptake inhibitor

48
Q

How could you treat opioid-induced excitement in a dog?

A

Naloxone or sedative

49
Q

Common way clients administer buprenorphine to cats

A

trans mucosal

50
Q

Why is fentanyl administered as an IV infusion or a transdermal patch?

A

short DOA

51
Q

What are some consequences of morphine-induced histamine release?

A
  • vasodilation (hypotension)
  • bronchoconstriction
  • pruritus, sweating
52
Q

Are opioids used to treat pain in animals with a hx of seizures?

A

Yes, not contraindicated in therapeutic doses

Seizures only seen with OD’s

53
Q

Whats the predominant CV effect of hydromorphone in the dog?

A

Bradycardia

54
Q

How would you characterize the sedative effects of opioids?

A

Drowsiness/sleepiness without amnesia (only in ill or old animals)

55
Q

Which opioid is likely to induce vomiting in the dog and the cat?

A

morphine

*see vomiting with pre-meds

56
Q

How can you completely reverse the effects of hydromorphone or butorphanol? what about buprenorphine?

A

Naloxone!

You cannot completely reverse bup - time and naltrexone can be attempted

57
Q

What is the rationale for giving buprenorphine and meloxicam to a cat following dental sx?

A

Pain relief for 6-8 hours post-op with opioid

NSAID to reduce inflammation and pain

58
Q

MOA of Diazepam

A

Benzodiazepines - enhance GABA inhibition

59
Q

Is diazepam effective in young, healthy animals?

A

NO! its better used in old or ill animals

60
Q

Why is diazepam combined with ketamine and xylazine to induce anesthesia in the horse?

A

muscle relaxation, anticonvulsant, sedation

61
Q

Diazepam vs midazolam

A

Midazolam is water soluble and shorter acting

62
Q

Flumazenil

A

Benzodiazepine antagonist - give it to reverse sedation/fear/anxiety/not waking up fast enough

63
Q

Primary use of ACE

A

tranquilizer (anxiolytic)

64
Q

Can you reverse Ace?

A

NO!!!

65
Q

effects of Ace on CV

A

Depresses CV - vasodilation/hypotension = reflex tachycardia

66
Q

How can you enhance sedative effects of ace in a dog or cat/

A

give opioids or alpha 2

67
Q

Can you give ace in patients with hx of seizures?

A

Yes, hasn’t been proven to induce seizures BUT you can’t reverse ace so there is that risk

68
Q

Alpha2 agonists MOA of analgesic and sedative effects

A

They inhibit excitatory NT release

69
Q

Alpha 2 agonist effects on CV system?

A

BIG drop in CO, vasoconstriction/hypertension, reflex bradycardia

70
Q

Alpha 2 agonist effects on resp system

A

Mild resp depression, increases CO2 threshold

71
Q

Adv and dis-advantages of giving atropine with alpha2 agonists

A

Adv: counteracts bradycardia/hypotension

DA: doesn’t inc CO
- not advised to give anticholinergic with alpha2

72
Q

How do you reverse dexmedetomidine?

A

yohimbine or atipamezole

73
Q

what are the potential adverse effects of atipamezole?

A

profound hypotension, reflex tachycardia, excitement/pain

spanish (5 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions