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DWT exam 1 > Pharmacology anti inflammatories > Flashcards

Pharmacology anti inflammatories Flashcards

1
Q

glucocorticoids clinical use

A

Most consistently effective drugs available for a wide variety of inflammatory/immune conditions
* Respiratory disease
* Dermatologic disease
* Gastrointestinal disease
* Ophthalmic disease
* Musculoskeletal disease
* Neurologic disease
* Immune-mediated and autoimmune disease

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2
Q

arachadonic acid pathway

A
  1. inflammation causes phospholipase A2 to break down phospholipids into arachodonic acid which breaks down into leukotrienes and prostoglandin H2
  2. glucocorticoids block phospholipase A2
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3
Q

glucocorticoid genomic pathway

A
  1. glucocorticoid binds to glucocorticoid receptor
  2. heat shock protein 90 is degraded
  3. glucocorticoid receptor + glucocorticoid move to nucleus and bind to and stim anti inflammatory genes, blocks expression of pro inflammatory genes
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4
Q

what cells have glucocorticoid receptors

A

a lot! almost every cell

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5
Q

mineralicorticoid affects

A

regulation of Na/K balance
use for treating adrenocortical insufficiency (addisons)

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6
Q

potency

A

Related to the affinity of the drug for the glucocorticoid receptor
Not related to plasma PK

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7
Q

duration of activity

A

Also related to receptor affinity
Also not related to plasma pharmacokinetics
* Half-life measured in minutes
* Effects measured in hours

Related to drug and formulation!

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8
Q

phosphate and succinate ester formulations

A

Highly soluble
Suitable for IV administration
Rapid onset of action
“ER” drugs
ex: sodium phosphate, sodium succinate

S= soluable

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9
Q

phosphate and succinate ester formulations

A

Highly soluble
Suitable for IV administration
Rapid onset of action
“ER” drugs
ex: sodium phosphate, sodium succinate

S= soluable

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10
Q

acetate and acetonide ester formulations

A

Poorly soluble
More lipophilic, less ionized
Onset of action is days to weeks
Prolonged absorption from injection site
Suitable for IM, SC or IA administration
ex: triamcinaline base (potencey 5, duration 24-36hr) triamcinaline acetonide (potency 30, duration 14-21 days)

act = for a long time

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11
Q

Aqueous suspension formulations

A

Rapidly absorbed after IM or SC administration
Some labeled for IA administration

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12
Q

solution formulations

A

Polyethylene glycol or alcohol vehicles
IV or IM administration
Polyethylene glycol vehicle – give slow IV, caution in cats

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13
Q

prednisone vs prednisalone

A

Prednisone is a prodrug
It is converted to prednisolone
Cats and horses have low bioavailability of prednisone (Low capacity to convert prednisone to prednisolone)

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14
Q

cats vs dogs glucocorticoid dosing

A

Cats require higher doses for the same effect
* Cats have Fewer GRs and Lower affinity GRs

Cats are more resistant to adverse effects

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15
Q

glucocorticoid effect on leukocytes

A

Affect the number of circulating immune cells
* Increased neutrophils and monocytes (Neutrophilia and monocytosis (+/-))

Decreased lymphocytes, eosinophils and basophils
* Lymphopenia, eosinopenia, basopenia
* Species differences

Affect the function as well
* Decreased release of inflammatory cytokines

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16
Q

glucocorticoid immunsuppression

A

High doses of corticosteroids= ‘Immunosuppressive dose’
* Inability to mount and immune response
* Inability to fight infection
* T cells > B cells
* Treats an overactive immune response!

Chronic low doses
* Effects on innate and cell-mediated immunity

Immunosuppression related to dose AND/OR duration of dosing
Cumulative dose is a factor in humans

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17
Q

glucocorticoids and metabolic effects

A

Stimulate glucose and lipid production (regional adiposity)
* Hyperglycemia
* Increase triglycerides, cholesterol, glycerol

Mobilization of amino acids from extrahepatic tissues
* Muscle breakdown

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18
Q

glucocorticoids effect on blood vessels

A

Stabilize membranes and decrease vascular permeability

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19
Q

endocrine effects glucocorticoids

A

Diabetes mellitus (cats)
* Gluconeogenic
* Antagonize insulin

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20
Q

glucocorticoids Hyper- and hypoadrenocorticism

A

when giving glucocorticoids, you can give too much and be in a hyperadrenocorticism state (cushings)
body stops producing its own cortisol because it is supplemented
drug administration stops > hypoadrenocorticism
TAPER OFF STEROIDS

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21
Q

glucocorticoid hepatopathy/hepatomegaly

A

Stimulate production of the steroid-specific isoenzyme of alkaline phosphatase (ALP) - dogs
(increased ALP)

22
Q

glucocorticoid GI ulceration effect

A

Slow turnover of enterocytes
**Inhibition of protective prostaglandins **
Potentiate the ulcerogenic effects of NSAIDs

23
Q

fluid/electrolyte balance glucocorticoid effects

A

Sodium and fluid retention and hypokalemic alkalosis

24
Q

Polyuria/polydipsia

A

Glucosuria
glucose in urine from hyperglycemia

25
glucocorticoids mood/behavioral changes
"roid rage"
26
glucocorticoids and laminitis
Recognized clinically * Temporal relationship * Unable to reproduce experimentally **Most likely related to insulin dysregulation** Horses may need to be predisposed * Fat horses with cresty necks (EMS) Osteopenia
27
alternate day therapy of glucocorticoids
with Intermediate-acting glucocorticoids give a higher dose every other day body produces its own cortisol every other day
28
glucocorticoids tapering the dose
When discontinuing treatment To prevent signs of hypoadrenocorticism Not necessary with short-term (< 2 wk) GC therapy Necessary after long-term (>2 wk) GC therapy * Allow for recovery of the HPA axis * Takes 2 weeks after cessation of daily therapy * Takes 1 week after cessation of alternate day therapy * Based on prednisone/prednisolone in dogs
29
if you can continue a glucocorticoid completely:
Lowest possible dose at the longest possible dosing interval
30
when to administer glucocorticoids
morning
31
using alternative routes of exposure to mitigate glucocorticoid effects
Local therapy results in less systemic exposure Intra-articular Inhalant Topical (Includes ocular)
32
NSAID pathway
1. inflammation causes phospholipase A2 to break down phospholipids into arachodonic acid 2. **cyclooxygenase 1 and 2** convert arachidonic acid to prostaglandin H2 3. NSAIDS block COX 1 and/or 2
33
PGI2 prostanoid
antiplatelet, vasodilatory
34
TXA2 prostanoid
pro platelet, vasoconstriction
35
PGE2 prostanoid
pro inflammatory, pain, vasodilation, GI motility, fever
36
PGF 2alpha prostanoid
vasocontriction, smooth muscle constriction (uterus, GIT)
37
COX 1 vs COX 2
COX 1 * Constitutively expressed (expressed constantly) * Cytoprotective to the GI tract (decrease acid and increase mucus) COX 2 * induced by inflammation * pro inflammatory effects (heat, swelling, pain, fever)
37
COX 1 vs COX 2
COX 1 * Constitutively expressed (expressed constantly) * Cytoprotective to the GI tract (decrease acid and increase mucus) COX 2 * induced by inflammation * pro inflammatory effects (heat, swelling, pain, fever)
38
Wht cant we only block COX 2 and have no adverse effects?
Not that simple A lot of overlap btwn COX 1 and 2 COX-2 constitutively expressed in kidney COX-2 is needed for mucosal healing Specificity of most drugs is overcome at high doses
39
COX selectivity
**Varies by drug and species** (Don’t extrapolate between species!) Carprofen is not selective in people Appears to be selective in dogs Another drug, the opposite may be true
40
clinical uses of NSAIDS
**Antipyresis** * Including fevers caused by infection * Not all fevers need treatment **Analgesia** * Pain associated with inflammation (chronic osteoarthritis, soft tissue injury, post-operative pain) * Pain independent of inflammation = Less effective **Endotoxemia/sepsis** * Prostaglandins are responsible for many of the clinical signs **Anticoagulant (platelet) activity** * Low dose aspirin is best understood * All NSAIDs affect coagulation * Clinical significance varies with species * COX-2 and thrombosis
41
NSAIDS are not appropriate for treating:
* Immune-mediated diseases (IMHA/IMTP) * Autoimmune diseases (Pemphigus, Systemic Lupus Erythematosus) * Allergic diseases (atopy) * Inflammatory respiratory diseases (asthma, chronic bronchitis) | Need steriods or alternative drugs
42
NSAID pharmacokinetics
**High bioavailability** (active transport) Small volume of distribution (0.15 - 0.3 L/kg) High protein binding (70-99%) therefore: **Hepatic metabolism** predominates * Capacity-limited – nonlinear PK * Species differences * Neonates Dosing in one species is UNLIKELY correct for another
43
human NSAIDs for animals
“Human NSAIDs will make your pet die a horrible death” Tylenol (acetaminophen) * Atypical NSAID * Cats * Dogs – OK up to a point * Horses - OK Ibuprofen * TOXIC to Dogs and Cats
44
NSAIDS and GI ulcers
Weak acids trapped in the basic environment of the gastric surface epithelial cells resulting in cell death **GI tract part depends on species** * Dogs & cats – stomach and SI * Horses – stomach and colon * Ruminants - abomasum PGE2 effects * NOT about oral administration – injections can cause * PGE2 is necessary for healing with pre-existing damage * COX-2 inhibitors can **delay healing or cause progression of disease** * COX2 ARE SAFER BUT NOT ENTIRELY SAFE!!!
45
nephrotoxicity with NSAIDS
Inhibition of PGE2 and PGI2 * Causes vasoconstriction, **decreased renal BF**, possible toxicity Effects greatly exacerbated in dehydrated patients * Already compromised renal blood flow PGE2 constitutively expressed in the kidney * COX-2 inhibitors probably not safer Lesions are characterized by **medullary crest or papillary necrosis** * Normally receive less blood flow =More vulnerable to insult * Areas that concentrate urine
46
NSAIDs hemorrhage
Effect on platelets * Drugs that inhibit COX-1 activity * Thromboxane A2 Aspirin irreversibly binds COX-1 * Effects last for the life of the platelet (7-10 days) Most NSAIDs can induce prolonged bleeding * Less of an issue in large animals
47
hepatotoxicity and NSAIDs
**ALL NSAIDS**, fairly low incidence – mainly dogs Toxic principle (mechanism) is not clear * **Idiopathic** * Not reproducible **Anorexia, vomiting, icterus** Hepatomegaly Increased bilirubin, ALT, ALP, AST
48
IMHA/IMTP and NSAIDS
Up to 12% of drug-induced IMHA/IMTP cases in humans attributed to NSAIDs **RARE in animal species** 1 published case report in a dog with carprofen Second exposure 48 hours after initiating therapy
49
Blood dyscrasias and NSAIDs
Pancytopenic marrow failure **Non-regenerative anemia and thrombocytopenia** People and **dogs** Not used in either species anymore
50
NSAIDs and injection site reactions
* Heat, pain, swelling * Abscess formation * Tissue necrosis * Clostridial myositis (anaerobic injection) Prevention * Both the injectable formulations of phenylbutazone and flunixin can be given orally * Bioavailability similar to commercially available preparations * Tastes terrible and can be irritating * Mix with corn syrup and rinse mouth with water

DWT exam 1 (13 decks)

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