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MSK2 > Drugs > Flashcards

Drugs Flashcards

NSAIDs, Antibiotics

1
Q

Describe the mechanism of action of NSAIDs

A

Block production of prostaglanding by blocking COX conversion of arachidonic acid to PGG2

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2
Q

Compare COX 1 and 2

A
  • COX1: constitutive, always present, maintain turnover cells, required for life
  • COX2: inducible, active in response to inflammatory stimulus, invoke production of PGs that are not usually there (PGE2)
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3
Q

Where are COX1 found?

A
  • Intestines
  • Platelets
  • Stomach
  • Kidney
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4
Q

Where are COX2 found?

A
  • Macrophages
  • Leukocytes
  • Fibroblasts
  • Endothelial cells
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5
Q

Outline some equine specific problems with NSAIDs

A
  • Thrombophlebitis wih pheynbutazone if have perivascular injection
  • Prescription of phenylbutazone only done when this can be entered into passport immediately
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6
Q

Give examples of suggested equine specific effects of NSAIDs that have

A

Inhibit:

  • Inflammation
  • Pyrexia
  • Oedema
  • Endotoxaemia
  • Ileus
  • Adhesion formation (tenuous evidence)
  • Thrombosis
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7
Q

Discuss the effect of NSAIDs on wound healing

A
  • Some compromise to healing

- However pain has more significant impact on wound healing so administration of NSAIDs still positive

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8
Q

Outline the pharmacokinetics of NSAIDs

A
  • Hepatic metabolism and renal excretion
  • High protein binding, low vol of distribution
  • Significant individual variation in response and susceptibility to toxicity
  • Effects often outlive the plasma half life
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9
Q

Compare the risks of NSAIDs in ponies and horses

A

Ponies more susceptible to phenylbutazone toxicity than horses

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10
Q

Explain the adverse effects of NSAIDs regarding the kidney

A
  • Reduce renal blood flow as this is mediated by prostaglandins in the medulla
  • Hypotension + NSAID = renal damage
  • Some concern regarding pre/peri-operative use bu several NSAIDs licensed for this
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11
Q

Explain the adverse effects of NSAIDs regarding the GI system

A
  • Prostaglandins cytoprotective in the GIT
  • GI side effects most common with chronic use
  • Direct irritation and PG inhibition are the cause of these signs
  • Some require administration with food, others on empty stomach
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12
Q

List the serious GI side effects of NSAIDs

A
  • Vomiting (small animals)
  • Colic
  • Inappetance
  • Diarrhoea
  • Protein losing enteropathy (PLE), secondary anaemia
  • Ulceration
  • Death
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13
Q

Explain the role of prostaglandins in the GIT

A
  • Cytoprotective
  • Decrease volume, acidity and pepsin content in the stomach
  • Stimulate bicarbonate secretion
  • Promote mucosal blood flow and repair and turnover of cells
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14
Q

Compare the adverse effects of NSAIDs on the GI system of young and adult hoses

A
  • Young: more susceptible to gastric ulceration

- Adults: more susceptible to right dorsal colitis

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15
Q

Describe the long term adaptation of the GI system to NSAID use

A
  • Increased mucosal blood flow
  • Increased mucosa cell regeneration
  • Decreased inflammatory cell infiltrate
  • From 14 days
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16
Q

Explain the role of enterohepatic recycling in the GI safety of NSAIDs

A
  • Excretion into intestine from bile
  • Leads to repeated exposure of the duodenum to the drug
  • Directly correlates to toxicity
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17
Q

Give examples of ways in which the GI safety of NSAIDs can be improved

A
  • Protective strategy
  • Sucralfate sucrose (aluminium sulphate)
  • H2 agonists
  • Protein pump inhibitors
  • Newer coxibs
  • Different formulation of NSAIDs sometimes tolerated better by different individuals
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18
Q

How does hepatotoxicity occur as a consequence of NSAID use?

A

Type I and type III reactions

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19
Q

List the adverse effects of NSAID use in cats

A
  • Hyperthermia
  • Respiratory alkalosis
  • Metabolic acidosis
  • Methaemoglobinaemia
  • Haemorrhagic gastro-enteritis
  • Renal failure
  • Hepatic injury
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20
Q

Which NSAID is particularly dangerous in cats?

A

Carprofen

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21
Q

Outline the dosing and frequency of administration of NSAIDs in cats

A
  • Titrate to lowest effective dose
  • Dose to lean/ideal body weight in obese animals
  • Reduce dose but maintain frequency when titrating down
  • Intermittent therapy i.e. 2-3 times a week rather than daily better than nothing
  • Liquids more easily measured
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22
Q

Describe the screening recommended prior to commencing treatment with NSAIDs in cats

A
  • Thorough history and physical examintion esp. looking at conditions that may impact on NSAID therapy e.g. blood pressure
  • Blood biochem to asses renal and hepatic function
  • Plasma proteins and haematocrit may be markers of GI bleeding and/or mucosal damage
  • Abnormalities may not preclude NSAID use but must be evaluated and discussed with owner
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23
Q

List the NSAIDs licensed for systemic use in cats

A
  • Caprofen (once only)
  • Ketoprofen
  • Meloxicam
  • Robenacoxib
  • Tolfenamic acid
  • Acetylsalicyclic acid
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24
Q

Describe the suggested minimum monitoring parameters for long term NSAID use in cats

A
  • History
  • Full clinical exam
  • Haematocri
  • Urea, creatinine, ALT, ALP
  • Specific gravity
  • Dipstick biochem
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25
Q

Out;line guidelines for the safe use of NSAIDs in chronic MSK disease

A
  • Ensure no hypovolaemia
  • No concurrent administration of another NSAID or steroid
  • No hepatic or renal insufficiency
  • Regular (every 3-6 months) monitoring with serum biochem and haematology
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26
Q

Explain the risk of paracetamol use in cats

A
  • OD and toxicity common
  • Low feline capacity for glucoronidation of paracetamol, rely on sulfation
  • When saturated, switches to P450 door detox, creates highly reactive metabolite NAPQI
  • overwhelms glutathione availability and result is oxidative injury
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27
Q

For which species is paracetamol particularly useful?

A
  • Dogs: adjunct in refractory long term arthritis
  • Rodents/rabbits
  • Pigs
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28
Q

Discuss the use of Mavacoxib

A
  • 1 month duration in dogs
  • Good for some owners
  • No additional risk of problems in surgery over other NSAIDs
  • May need to consider addition of gastroprotectants
29
Q

Outline a therapeutic plan for the use of NSAIDs

A
  • Initial course of NSAIDs, re-check 4 weeks later
  • Improvement: continue and reassess q1-2 months
  • Little or no improvement: check owner compliance
  • Poor compliance: consider reason, consider different formulation
  • Good compliance: switch to another NSAID while observing wash out period
  • Improvement after switch: continue and reassess q1-2 months
  • No/little improvement after switch: reassess diagnosis, consider individual variation, re-evaluate complementary techniques, consider additional of adjunct, seek referral
30
Q

Outline other therapies other than NSAIDs used in the treatment of OA

A
  • Exerise management
  • Weight control and diet
  • Modification to lifestyle e.g. ramps
  • Hydrotherapy and physio
  • Chrondroprotectives
  • Joint replacement
  • IRap (interleukin-1 receptor antagonist protein)
  • Stem cell therapies
  • Other “drugs”: isoxsuprine hydrochloride, vegetable tablets, PLT
  • Neutraceuticals
31
Q

Discuss the use of NSAIDs vs opioids in the treatment of MSK pain

A
  • NSAIDs good, if not better option for MSK pain, but less good for
  • NSAIDs used more in horses as opioids can have severe side effects in horses
32
Q

Outline the practical considerations for NSAIDs

A
  • Non-scheduled but are POM-V
  • Cheaper than opioids
  • Little long term decrease in efficacy
  • longer duration of action
  • Side effects
  • Complaince
  • Co-morbidities
33
Q

List the groups of antibiotics used for MSK disease

A
  • Beta-lactams
  • Aminoglycosides
  • Tetracyclines
  • Fluoroquinolones
  • Sulfonamides
  • Diaminopyrimidines (trimethoprim)
  • Macrolides
  • Phenicols
  • Lincosamides
  • Metronidazole
34
Q

Which antibiotics used for MSK diseases have the highest priority?

A
  • 3rd and 4th gen cephalosporins
  • Fluoroquinolones
  • Macrolides
35
Q

State whether beta-lactams are bacteriocidal/static and time/concentration dependent

A
  • Bacteriocidal

- Time dependent

36
Q

State whether aminoglycosides are bacteriocidal/static and time/concentration dependent

A
  • Bacteriocidal

- Concentration dependent

37
Q

State whether Tetracyclines are bacteriocidal/static and time/concentration dependent

A
  • Bacteriostatic

- Time dependent

38
Q

State whether fluoroquinolones are bacteriocidal/static and time/concentration dependent

A
  • Bacteriocidal

- Concentraton dependent

39
Q

State whether sulfonamides are bacteriocidal/static and time/concentration dependent

A
  • Bacteriostatic

- Time dependent

40
Q

State whether trimethoprim is bacteriocidal/static and time/concentration dependent

A
  • Bacteriostatic

- Time dependent

41
Q

State whether metronidazole is bacteriocidal/static and time/concentration dependent

A
  • Bacteriocidal

- Concentration dependent

42
Q

What is the mechanism of action of beta-lactams? Give examples

A
  • Interfere with cell wall synthesis

- Examples: penicillins, cephalosporins, amoxyclav, vancomycin

43
Q

What is the mechanism of action of aminoglycosides? Give examples

A
  • Act on 50s and 30s ribosome subunits to interfere with protein synthesis
  • Amikacin, gentaycin, tobramycin, neomycin, streptomycin, kanamycin
44
Q

What is the mechanism of action of amphenicols? Give examples

A
  • Act on 50s subunit to interfere with protein synthesis

- Chloramphenicol, florfenicol

45
Q

What is the mechanism of action of macrolides? Give examples

A
  • Act on 50s subunit to interfere with protein synthesis
  • Erythromycin
  • Acythromycin
46
Q

What is the mechanism of action of lincosamides? Give examples

A
  • Act on 50s subunit to interfere with protein synthesis

- Lincomycin, clindamycin, pirlimycin

47
Q

What is the mechanism of action of sulphonamides? Give examples

A
  • Act on 30s subunits to interfere with protein synthesis, interfere with metabolic pathways
  • Sulfamethoxazole
48
Q

What is the mechanism of action of dyaminopyrimidines? Give examples

A
  • Act on 30s subunits to interfere with protein synthesis, interfere with metabolic pathways
  • Trimethoprim, pyremethamine
49
Q

Which antibiotics are DNA synthesis inhibitors? State how

A
  • Fluroquinolones (DNA gyrase inhibitors)

- Metronidazole (free radical disruption of bacterial DNA)

50
Q

Which antibiotics are RNA synthesis inhibitors? State how

A

Rifamycin only - inhibit DNA dependent RNA synthesis

51
Q

Which antibiotics are cell membrane inhibiting?

A
  • Polymyxin B

- Bacitracin

52
Q

What is the difference in use between time dependent and concentration dependent antibiotics?

A
  • Concentration: only needs to be given SID (usually)

- Time: frequent admin, 2/3/4 times a day

53
Q

Give examples of antagonistic antibiotic combinations?

A
  • Bacteriostatic + bacteriocidal usually antagonistic
  • Chloramphenicol + beta lactams
  • Tetracycline + quinolones
  • Erythromycin + aminoglycosides
54
Q

List the key side effects of penicillins

A
  • Anaphylaxis
  • Cardiac arrythmias
  • Transient hypotension
  • Autoimmune haemolytic anaemia
55
Q

List the key side effects of aminoglycosides

A
  • Nephrotoxic
  • Neuromuscular blockade
  • Ototoxic
56
Q

List the key side effects of metronidazole

A
  • Inappetance/anorexia

- Enterocolitis

57
Q

List the key side effects of tetracyclines

A
  • Nephrotoxic
  • Gastric ulceration
  • Erupting teeth and urine discolouration
58
Q

List the key side effects of chloramphenicol

A

Reversible aplastic anaemia (humans)

59
Q

List the key side effects of fluoroquinolones

A

Oral ulceration

60
Q

List the key side effects of TMPS

A

Enterocolitis

61
Q

What are the contraindications for TMPS?

A
  • Pus (natural source of PABA)
  • Gestation (blocks folic acid production)
  • Bioavailability decreased by feed
  • Sudden death when used with IV alpha 2
62
Q

What are the contraindications for use of fluoroquinolones?

A

<3yo - causes cartilage disorder

63
Q

What are the contraindications for use of tetracyclines?

A

IM administration (high risk of necrotic reaction)

64
Q

Which antibiotics are concentrated in urine?

A
  • Fluroquinolones
  • Aminoglycosides
  • Beta-lactams
  • Sulfonamides/potentiated sulfonamides
65
Q

Which antibiotics are concentrated in leukocytes?

A
  • Clindamycin
  • Erythromycin
  • Fluoroquinolones
  • Rifampicin
66
Q

Which antibiotics will always cross the BBB?

A
  • Chloramphenicol
  • Doxycycline minocycyline
  • Fluoroquinolones
  • Metronidazole
  • Rifampicin
  • Sulphonamides/trimethoprim
67
Q

Which antibiotics will cross the BBB when there is inflammation?

A
  • Penicillins
  • Some cephalosporins (ceftriaxone, ceftazidime, cefotaxime)
  • Vancomycin
68
Q

Which antibiotics used in horses have protected status?

A
  • Ceftiofur
  • Cefquinone
  • Enrofloxacin

MSK2 (29 decks)

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