Post Midterm Veterinary Pharmacology

Front 1

What is the result of H1 receptor activation?

Back 1

Bronchoconstriction, vasodilation or arterioles and venules, increased capillary permeability, itchiness and pain. They are also important in memory, sleep and wake cycle and seizure suppression

Front 2

What is the result of H2 receptor activation?

Back 2

Secretion of gastric acid by parietal cells, minor heart and blood vessel effects

Front 3

Is histamine itself used as a drug?

Back 3

no- only antihistamines

Front 4

The use of the word antihistamines refer to H1 antagonists, H2 antagonists or both?

Back 4

H1 antagonists

Front 5

What are the main differences between first generation and second generation antihistamines?

Back 5

First generation cross BBB, less selective, variable efficacy with sedation and anticholinergic effects, first generation are generally OTC.
Second generation don't cross BBB, selective, devoid of anticholinergic effects, more expensive

Front 6

H1 antagonists work best if they are given before or after reaction?

Back 6

Before - they block the histamine receptor not the release of histamine so it is important to block before any massive release

Front 7

What are some adverse effects of H1 antagonists?

Back 7

sedation, dizziness, incoordination, fatigue.....like 5 million more that i am not going to list....really just say anything dammit

Front 8

What are the 6 main uses of antihistamines in Vet Med?

Back 8

1. mild allergies
2. decrease use of glucocorticoids
3. motion sickness
4.sedation
5. feline appetite stimulant (cyproheptadine)
6. photic head shaking in horses

Front 9

What are a few 1st generation antihistamines used in vet med?

Back 9

diphenhydramine, diphenhydrinate, meclizine, cyproheptadine

Front 10

What are 2 second generation antihistamines used in vet med?

Back 10

Ioratadine and fexofenadine

Front 11

Would you treat anaphylaxis with epinephrine or an antihistamine?

Back 11

Epinephrine as antihistamines only have a minor role in bronchoconstriction, hypotension and edema of the glottis in anaphylaxis

Front 12

Would you use an antihistamine for asthma?

Back 12

no, not caused by histamine and can cause mucus to thicken

Front 13

What are some properties of DMSO?

Back 13

Anti-inflammatory, analgesic, inhibits PGN production, weak antibacterial and antifungal, diuretic and has some anticholinesterase activity.

Front 14

What is DMSO generally used for in vet med?

Back 14

Equine medicine for laminitis, pneumonia, synovitis, intestinal ischemia and some nervous system injuries.

Front 15

Has DMSO been proven effective?

Back 15

No, not scientifically

Front 16

What is the common mode of DMSO administration?

Back 16

Oral, by use of feed grade DMSO metabolite called MSM (methylsulfomethane). Can cause hemolysis if given IV at 100% strength

Front 17

What is Polysulfated glycosaminoglycan used as?

Back 17

Anti-arthritic agent for dogs and horses.

Front 18

Where is Polysulfated glycosaminoglycan derived from?

Back 18

Bovine trachea which is sulfated.

Front 19

What is the function polysulfated glycosaminoglycans?

Back 19

They delay the progression of osteoarthritis catilagionous lesions by preventing pro-inflammatory mediators, inhibiting lysosomal release and acts as replacement for glycosaminoglycans as well as increasing synovial membrane production.

Front 20

What are oral glucosamine/chondrotin sulfate used for?

Back 20

Stimulate synovial fluid synthesis, inhibit degradation and improve healing of articular cartilage.

Front 21

When would you use sodium hyaluronate, during chronic severe arthritis or mild arthritis?

Back 21

Mild, horses have been shown to be less lame and have less thinning cartilage

Front 22

What are some side effects of Sodium hyaluronate administration?

Back 22

Septic or aseptic synovitis

Front 23

What are the main zones of the adrenal gland and what is produced in each?

Back 23

Cortex: Zona glomerulosa: mineralocorticoids
Zona fasiculata: glucocorticoids
Zona reticularis: adrenal androgens
Medulla: catecholamines

Front 24

Glucocorticoids are steroid hormones produced from _________.

Back 24

Cholesterol

Front 25

Glucocorticoid receptors in cells throughout the body are kept stabilized by binding to ___________ proteins.

Back 25

heat shock

Front 26

What is the general timeline of glucocorticoid effects seconds, minutes or hours?

Back 26

hours, gene transcription must be altered.

Front 27

What is the primary mineralocorticoid?

Back 27

aldosterone

Front 28

What is the main activity of mineralocorticoids?

Back 28

Regulate electrolyte concentrations and water volume by altering reabsorption of Na+, Cl- and passive water absorption and excretion of K+

Front 29

Aldosterone stimulates ____ secretion by intercalated cells in the collecting ducts.

Back 29

H+

Front 30

_______ receptors are concentrated in the kidneys while ______ receptors are throughout the body. (Glucocorticoids)

Back 30

mineralocorticoids, cortisol

Front 31

What significance is it that renal cells contain 11-Beta hydroxysteroid dehydrogenase type 2.

Back 31

catabolizes cortisol which prevents it from binding to mineralocorticoid receptors, this is significant as cortisol is found in basal levels in circulation without this enzyme the renal cells would be constantly activated.

Front 32

Corticosteroids increase or decrease available energy?

Back 32

Increases by increasing gluconeogenesis and antagonizing insulin which decreases glucose uptake by cells

Front 33

Corticosteroids increase or decrease protein catabolism?

Back 33

Increase

Front 34

Does corticosteroids promote glycogenesis, gycogenolysis or both?

Back 34

glycogenesis

Front 35

Corticosteroids antagonize Vit D3 which accelerates bone ___________ and decreases bone _________.

Back 35

resorption, formation

Front 36

Can glucocorticoids improve mood and behaviour?

Back 36

yes- creates a euphoric state

Front 37

Glucocorticoids increase or decrease gastic acid, pepsin and trypsin secretion?

Back 37

increases

Front 38

Glucocorticoids increase or decrease mucosal cell proliferation?

Back 38

Decrease

Front 39

Glucocorticoids _________ vascular integrity and __________ permeability by antagonizing mediators.

Back 39

increase, decrease

Front 40

Glucocorticoids ______ mast cell degranulation, _________ in neutrophils in circulation and ________ in macrophage phagocytosis.

Back 40

decrease, increase and decrease

Front 41

Name the three major cytokines whose production is decreased by glucocorticoids.

Back 41

IL-2, IL-1 and TNF

Front 42

T/F Glucocorticoids do not treat underlying disease, they modifiy the body's inflammatory response to the disease.

Back 42

True

Front 43

What are the main therapeutic uses for glucocorticoids?

Back 43

Anti-inflammatories, immunosuppressives, respiratory diseases, microvascular integrity and neoplasia.

Front 44

What are the three main categories of Corticosteroids?

Back 44

Short, intermediate and long acting

Front 45

Name 3 adverse effects of Corticosteroid use out of the 6,000,000,000 she listed in our notes

Back 45

polyphagia (weight gain), euphoria, osteoporosis, myopathy, fibroblast inhibition, GI ulceration, pancreatitis, hyperlipidemia, lipolysis, protein catabolism, fatty infiltration of liver, steroid hepatopathy, hyperglycemia, anti-insulin-effect, HPA axis suppression causing adrenal atrophy, immune suppression, increased risk of septicemia, recurrent septic cystitis, decreased response to infection or injury (Avoid concurrent use of high doses with vaccination), poor fracture healing, decreased healing and repair, laminitis in horses, induction of parturition during last trimester in horses, cow, and sheep; possible fetal resorption, abortion, or premature parturition in bitch and queen, teratogenic in dogs in first trimester, PU/PD- use with caution in patients with protein-losing enteropathy, nephropathy or congestive heart failure, decreased calcium absorption alters the Ca balance which is a concern with long-term use in young (↓ bone growth) and old (osteoporosis) animals, can lower seizure threshold, increase, iatrogenic (clinician-induced) hyperadrenocorticism , can get muscle wasting, delayed wound healing, thinning of the skin, thin hair (dog) or hirsutism ( horse)

Front 46

What is the duration of action of short acting glucocorticoids and give two examples?

Back 46

8-12 hours
hydrocortisone, cortisone

Front 47

What is hydrocortisone generally used for?

Back 47

topical preperations

Front 48

What is the duration of action of intermediate acting glucocorticoids and give two examples?

Back 48

12-36 hours
Prednisolone, prednisone, methylprenisolone

Front 49

What are intermediate acting glucocorticoids generally used for?

Back 49

Anti-inflammatories and immunosupressive therapy.

Front 50

What is the duration of action of long acting glucocorticoids and give an example of one?

Back 50

36-72 hours
Dexamethasone

Front 51

What is Dexamethasone generally used for?

Back 51

Used to test hypothalamic-pituitary-adrenal function. "dexamethasone supression test"

Front 52

Do short acting, intermediate acting or long acting have mineralocorticoid activity?

Back 52

Short and intermediate do while long do not.

Front 53

What is the purpose of alternate day therapy using intermediate acting corticosteroids?

Back 53

Minimize adrenal atrophy

Front 54

What is the Antipruritc dose of Corticosteroids? Anti-inflammatory? Immunosupressive dose? Dose for Shock?

Back 54

Antipruritic dose: 05-1 mg/kg
anti-inflammatory: 1-2 mg/kg
Immunosuppressive dose: 2-4 mg/kg
Shock: 5-60 mg/kg

Front 55

When stopping corticosteroid treatment after more than 2 weeks of use, weaning off the drug is necessary, why is this?

Back 55

To minimize adrenal atrophy

Front 56

What formulation (functional group addition) of corticosteroid would you use for IV emergency situation?

Back 56

Phosphate and succinate esters make the CS very water soluable and has rapid onset

Front 57

What formulation (functional group addition) of corticosteroid would you use for acute but not life threatening conditions?

Back 57

Steroid alcohols

Front 58

Which formulation (functional group addition) of corticosteroid is used for absorption over several weeks?

Back 58

Acetate and acetonide esters are poorly water soluable, persistant.

Front 59

What is the most common method for corticosteroid administration on small animals?

Back 59

Oral formulations

Front 60

What is the action of Mineralocorticoids?

Back 60

Act on distal renal tubule to increase Na+ reabsorption and K and H secretion.

Front 61

What is the main use of Mineralocorticoids in dogs?

Back 61

Addison's disease (Hypoadrenocorticism)

Front 62

What are two Mineralocoricoid drugs used for Addisons?

Back 62

Fludrocortisone acetate and deoxycorticosterone pivalate (DOCP)

Front 63

What are the two main pathways of arachadonic acid metabolism?

Back 63

Lipoxygenase pathway
Cyclooxygenase pathway

Front 64

What is the main product of the lipoxygenase pathway?

Back 64

Leukotrienes and the HETES

Front 65

What is the main product of the cyclooxygenase pathway?

Back 65

Prostaglandins

Front 66

Glucocorticoids inhibit the production of _______________ which inhibits both arachadonic pathways.

Back 66

Phospholipase A2

Front 67

Of COX-1 and COX-2 which is inducible and which is constitutive?

Back 67

COX-1 is Constitutive
COX-2 is inducible

Front 68

Which COX enzyme is referred to as the "housekeeping cyclooxygenase enzyme"?

Back 68

COX-1

Front 69

COX-1 is responsible for production of ____________ which are involved in the maintenance of normal physiological activity.

Back 69

Prostaglandins

Front 70

What induces COX-2 production?

Back 70

cytokines, trauma, endotoxins or mitogens, ischemia, seizures, neurodegenrative disorders or oxidative stress.

Front 71

All NSAIDs have what qualities?

Back 71

Analgesic, anti-inflammatory and antipyretic

Front 72

What are the 5 main therapeutic indications for NSAID use?

Back 72

1. Anti-inflammatories
2.Analgesics
3.Antipyretics
4.Antithrombotic
5.Anticancer

Front 73

Why are NSAIDs preferred over glucocorticoids as anti-inflammatories?

Back 73

NSAIDs have fewer adverse effects

Front 74

Are NSAID antiinflammatory effects as effective as glucocorticoids?

Back 74

No- GCs inhibit many more mediators

Front 75

Name 2 anti-inflammatory effects of NSAIDs.

Back 75

inhibit PGE2 production, stabilize lysosomal membranes, inhibit complement, ↓ phagocytosis, ↓leukocyte accumulation and ↓synthesis of histamine , antagonize bradykinin and histamine effects, induce free radical scavengers and uncouple oxidative phosphorylation so there is less energy for inflammatory reactions

Front 76

Why are NSAIDs prefered over opiates as analgesics?

Back 76

NSAIDs do not induce dependence or tolerance

Front 77

Do NSAIDS have an effect on normal body temperature?

Back 77

No- they just inhibit the ability of the hypothalamus to respond to pyrogens

Front 78

How do NSAIDs act as antithrmobotic agents?

Back 78

NSAIDs block COX-1 production of thromboxane(TxA2) by platelets which normall yincreases platelet aggregation.

Front 79

NSAIDs have a _______ onset of action than glucocorticoids.

Back 79

Faster

Front 80

NSAIDs are ______ acids?

Back 80

weak

Front 81

NSAIDs are metabolized by Phase 1, phase 2 or both in liver?

Back 81

Both

Front 82

Are NSAIDs bound to albumin in plasma?

Back 82

Yes

Front 83

Which domestic animal is most sensitive to NSAIDs?

Back 83

Cats due to poor glucuronidation abilities

Front 84

Is aspirin reversible or irrevesible binding drug?

Back 84

Irreversible

Front 85

Inhibition of COX-1 or COX2 has more adverse reactions?

Back 85

COX-1

Front 86

What are some adverse reactions due to COX-1 inhibition?

Back 86

Decreased platelet aggregation, decreased renal perfusion and increased GI ulcers

Front 87

COX-2 inhibitors induce ulcers where instead of the stomach?

Back 87

Colon

Front 88

What is the mechanism by which COX-1 inhibition leads to ulceration?

Back 88

Blocking COX-1 leads to decreased production of Prostaglandin E2 and F2alpha coupled which are cytoprotective of the gastric mucosa. Couple this with increased gastric acid.

Front 89

What is the mechanism by which COX-1 leads to decreased platelet activity?

Back 89

Blocks thromboxane production, which normally activates platelets and increases aggregation. Most severe in apirin as it irreversible binds and platelets lack organelles to produce new enzymes (permanent in platelet replaced)

Front 90

What is the mechanism by which NSAIDs cause renal toxicity?

Back 90

Inhibition of normal vasodilatory prostaglandins wich mediate renal blood flow. Blocks normal renal vasodilation which promotes natriuresis and diuresis which are important in dehydration situations

Front 91

Would you ever use NSAIDs and glucocorticoids at the same time?

Back 91

No, high risk of GI ulceration

Front 92

Should you use NSAIDs with aminoglycosides? why or why not?

Back 92

No, AG are nephrotoxic, compounded by NSAIDs

Front 93

What is the trade name of Acetylsalicylic acid?

Back 93

Aspirin

Front 94

How much time before surgery should you discontinue use of ASA?

Back 94

1 week

Front 95

What is the main side effect of using ASA?

Back 95

GI irritation with blood loss

Front 96

What is Phenylbutazone?

Back 96

An IV or oral nonselective COX-1and COX-2 inhibitor.

Front 97

What species is Phenylbutazone generally used in and what is its main use?

Back 97

Used mainly in horses for musculoskeletal pain.

Front 98

What is Flunixin?

Back 98

Nonselective COX-1 and COX-2 inhibtor that can be injectable or orally administered.

Front 99

What species is Flunixin usually used in and what are 2 of the main uses for it in these animals?

Back 99

Horses and Cattle, used for colic, colitis, rhabomyolysis, endotoxic shock, respiratory disease, post surgery and laminitis.

Front 100

Which NSAID is considered the best choice for visceral pain?

Back 100

Flunixin - has extra analgesic effects at spinal cord

Front 101

What species is Ketoprofen normally used in?

Back 101

Cats, dogs, horses and cattle

Front 102

What is the meat and milk withdrawl for Ketoprofen in cattle?

Back 102

1 day for meat and no milk withdrawal

Front 103

Name the 4 Main COX-2 selective drugs used in Vet med.

Back 103

Carprofen, meloxicam, deracoxib and firocoxib

Front 104

Which COX-2 selective inhibitor has been associated with idiosyncratic hepatotoxicity?

Back 104

Carprofen

Front 105

Is acetaminophen an NSAID?

Back 105

No dammit

Front 106

What are some adverse effects of acetaminophen use in dogs and cats?

Back 106

hepatic degeneration, methemoglobin and hemolysis

Front 107

Name 2 NSAIDs not used in Vet Med and give the main reason why they aren't used.

Back 107

Ibuprofen and indomethacin. Both have narrow therapeutic margins in dogs and in cats cause renal failure

Front 108

What are the 5 general guidelines for using NSAIDs?

Back 108

1. Don't use with glucocorticoids
2. Avoid in animals with renal dysfunction
3.Avoid if possible gastric ulceration or disease
4.Avoid with bleeding disorders
5.Only use prior to surgery if you have checked to see if its ok

Front 109

Name 8 NSAIDs used in Vet Med.

Back 109

1.Aspirin
2.Phenylbutazone
3. Flunixin meglumine
4.Ketoprofen
5.Carprofen
6.Meloxicam
7.Deracoxib
8.Firocoxib

Front 110

Name 2 NSAIDs that are specifically not used in Vet Med.

Back 110

1. Ibuprofen
2. Indomethacin

Front 111

What are the 5 hallmarks of inflammation?

Back 111

Pain, heat, redness, swelling and loss of function

Front 112

What are the two possible outcomes of acute inflammation?

Back 112

healing with repair or chronic inflammation

Front 113

What are the two components of inflammation?

Back 113

Vascular and cellular components

Front 114

What are the 8 steps in the process of acute inflammation?

Back 114

1. Vasodilation
2.Increased vascular permiablility
3. Leukocyte extravasation and phagocytosis
4.Neutrophils predominance shifts to monocytes
5. Endogenous chemoattractants released
6.Leukocytes become activated
7.Secretion of cytokines
8.Termination of acute phase

Front 115

During acute inflammation there are 3 stages of increased vascular permiability what are they and what causes them?

Back 115

1.Immediate transient response of venules is due to histamine and leukotrienes which causes contraction pushing fluid extracellularly
2. Delayed response due to kinins, complement and cytokines
3. Prolonged respnose due to direct endothelial damage

Front 116

In plasma form mediators of inflammation circulate in _________ form. If the mediators are cell derived they are stored in ________ or newly synthesized.

Back 116

Precursor, granules

Front 117

Name 2 inflammation mediators that cause vasodilation.

Back 117

PGNs, NO, histamine

Front 118

Give 2 inflammation mediators that cause increased vascular permiablility.

Back 118

Vasoactive amines, bradykinin, PAF, Substance P and leukotrienes

Front 119

Give 2 inflammatory mediators that cause chemotaxis (leukocyte recruitment and activation).

Back 119

C5a, leukotrienes, chemokines, IL-1, TNF and bacterial products

Front 120

Give 2 inflammatory mediators that cause fever.

Back 120

IL-1, TNF and PGNs

Front 121

Name 2 inflammatory mediators that cause pain.

Back 121

Substance P, PGNs and bradykinin

Front 122

Give 2 examples of inflammatory mediators that cause tissue damage.

Back 122

Leukocyte lysosomal enzymes, NO, free radicals

Front 123

What are the two general mechanisms of action of anti-inflammatory drugs?

Back 123

Blocking action of inflammation and blocking the synthesis of mediators.

Front 124

What is known as the SLEDGEHAMMER OF DRUGS?

Back 124

Glucocorticoids- DO EVERYTHING