Pharm7 Flashcards

1
Q

Inflammation

A

Body’s response to injury
• Intended to be a protective mechanism to remove or neutralize the cause of the damage
Lead to repair of any damage

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2
Q

What can cause Inflammation?

A

Trauma,
infection,
burns

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3
Q

External clinical signs of inflamation

A

o Redness and heat =vasodilation
o Swelling and edema =increased vascular permeability- can dilute irritating chemical
o Pus =WBC’s that remove bacteria, debris, and devitalized tissue
Can be painful

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4
Q

Two types produced by the adrenal gland

A

 Mineralocorticoids-regulate mineral levels in the body

 Glucocorticoids-exert an anti-inflammatory effect, but also have many other effects in the body

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5
Q

Mineralocorticoids

A

regulate mineral levels in the body

Aldosterone- Sodium/ water

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6
Q

Biologic effects of glucocorticoids in the body

A
o	Decrease inflammation
o	inhibit scar tissue formation
o	Suppress the body’s immune system
o	Affect the cellular blood count
o	Increase gastric acid secretion and decrease mucus production in GIT
o	Increase protein breakdown
o	Can induce parturition
o	Increase blood glucose levels
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7
Q

Aqueous solutions of glucocorticoids

A
  • the glucocorticoid is combined with a salt and dissolved in water
  • can be given in large doses intravenously w/ less risk of an adverse reaction
  • examples: dexamethasone sodium phosphate (Azium), prednisolone sodium succinate (Solu-Delta Cortef)
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8
Q

Alcohol solutions of glucocorticoids

A
  • glucocorticoid is dissolved in alcohol
  • the label lists the glucocorticoid as the only active ingredient
  • increased risk of an adverse reaction if given IV
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9
Q

Suspensions of glucocorticoids

A
  • the glucocorticoid is suspended in a liquid vehicle(e.g. acetate, diacetate, pivalate, acetonide, valerate)
  • store at room temperature
  • must be shaken before use
  • glucocorticoid is absorbed gradually over a period of days
  • should never be administered IV
  • examples: methylprednisolone acetate (Depo-Medrol), triamcinolone acetonide (Vetalog)
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10
Q

Guidelines for safe use of glucocorticoids

A

o Use another drug if it can accomplish the same result
o Use the smallest dose possible
o Avoid continuous use
o Be cautious when using glucocorticoids with long-lasting effect
o When discontinuing, reduce dose over a period of days
o Use may be contraindicated in some patients

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11
Q

Parenteral formulations

A

Aqueous solutions
Alcohol solutions
Suspensions

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12
Q

Dosage forms available

A

topical preparations,
oral and
injectable products

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13
Q

Short-acting

A

biologic effect lasts < 12 hrs.

• hydrocortisone, cortisone- usually topically

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14
Q

Intermediate-acting

A

effect lasts 12-36 hrs.
• prednisone, prednisolone, triamcinolone, methylprednisolone
Orally, at least once a day

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15
Q

Long-acting

A

effect lasts more than 48 hrs.
• dexamethasone, betamethasone, flumethasone
injectable or oral

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16
Q

Nonsteroidal Anti-inflammatory Drugs

A

(NSAIDs)
• Exert their effect by blocking enzymes in the inflammatory cascade
Interfere of arachidonic acids, and with
• Produce fewer side effects than glucocorticoids
• Highly bound to plasma proteins

17
Q

Adverse effects of Nonsteroidal Anti-inflammatory Drugs include:

A

o GI tract- anorexia, diarrhea, melena (blood in the feces- digested), ulcer formation
 effect due to decreased protective prostaglandin production (PGE, PGI2)
o Kidney- renal tissue necrosis
 effect due to decreased protective prostaglandin production (PGE2)

18
Q

Things PGI, PG12 do

A

o Decrease volume and acidity of gastric secretions- acid favors ulcers
o Increase NaCO3 secretion in intestinal tract- protect from ulcers
o Increase gastric and intestinal mucus production- prevent ulcers
o Increase turnover and repair of GI epithelial cells- prevent ulcers

19
Q

NSAID list

A
o	Phenylbutazone 
o	Flunixin Meglumine 
o	Ibuprofen, Ketoprofen, Naproxen-
o	Acetylsalicylic Acid
o	Caprofen, Meloxicam, Deracoxib Etodolac, Firocoxib
20
Q

Phenylbutazone

A

• Phenylbutazone
o Used mostly in horses
o Available in tablet, paste, and injectable forms

21
Q

General characteristics of Phenylbutazone

A
	Inhibits cyclooxygenase
	Metabolized by the liver
	Highly protein bound
	Adverse effects include GI ulceration, renal  necrosis, retention of water and sodium, bone marrow suppression
	Cats have a very low tolerance
22
Q

Flunixin Meglumine

A

• Flunixin Meglumine
o Mostly used in horses
o Available as an injectable, paste and granules for oral administration

23
Q

General characteristics of Flunixin Meglumine

A

 Has potent analgesic properties
 Used to relieve severe pain in horses
 Adverse effects include GI ulceration after 3-4 days of use in dogs

24
Q

Ibuprofen, Ketoprofen, Naproxen

A

o Commonly used in humans, ketoprofen (Ketofen) and naproxen (Equiproxen) sometimes used in animals

25
Q

General characteristics of Ibuprofen, Ketoprofen, Naproxen

A

 All derived from propionic acid, have similar qualities
 Inhibit cyclooxygenase and lipooxygenase
 Adverse effects include GI ulceration after days of use in dogs

26
Q

Acetylsalicylic Acid

A

o Commonly used human drug
o Decreases platelet aggregation by decreasing thromboxane production
o Metabolized in liver by binding it w/ glucuronic acid for elimination
o Safer than most older NSAIDs

27
Q

Carprofen (Rimadyl), Meloxicam (Metacam), Deracoxib (Deramaxx), Etodolac (Etogesic) Firocoxib (Previcox)

A

o Newest group of NSAID agents
o Referred to as COX-2 inhibitors
o Less likely to cause adverse effects than other NSAIDs
 selectively inhibit production of prostaglandins associated w/ inflammation
 minimal effect on GI tract and kidney
o A low incidence of liver disease, renal disease, hematologic abnormalities, and serious GI disease reported

28
Q

Galliprant

A

o Belongs to a new drug class
o Blocks prostaglandin receptor associated within inflammation (EP4) ONLY
Different target- alternative to COX2
Bind receptor in tissue to prevent the binding of inflammatory prostoglandics
Acts like an antagonist

29
Q

Acetaminophen

A

o (Tylenol)
• Provides analgesia, fever reducer
• No GI ulceration, no anti-inflammatory effect
• Metabolized by liver
• *Toxic metabolite produced which is bound to glutathione rendering nontoxic
• Adverse effects seen w/ overdose
• *Methemoglobinemia, Heinz body formation, liver tissue destruction

30
Q

Chemical mediators of inflammation

A

Prostaglandins,
thromboxanes,
leuktrienes

31
Q

Corticosteroids

A

Hormones produced by the adrenal gland

o Corticosteroid production is regulated by a feedback inhibition mechanism

32
Q

Glucocorticoids

A

exert an anti-inflammatory effect, but also have many other effects in the body
produced by adrenal gland -Cortisone, Hydrocortisone (cortisol)

33
Q

The adrenal gland produces:

A

Cortex- hormones, androgens, mineralocorticoids

Medulla- epinephrine, norepinephrine

34
Q

CRF

A

Corticotrophin Releasing factor

hypothalamus

35
Q

Cushings Disease

A

too much glucocrodicoids

usually pituitary related

36
Q

Iatrogenic

A

when we overssuppulent with glucocrodicoids, and cause cushings

37
Q

PGE2

A

help to main normal blood flow to the kidney it is low, such as dehydration, shock
- when there is decreased blood flow to the kidney –>PGE2-> dilate arteries to the kidney

38
Q

Methemoglobinemia

A

oxidation of the iron in the hemoglobin molecule- affect oxygen carrying capacity

39
Q

Phenacetin

A

converted into acetaminophen in the body