Pharm Exam Iii

Front 1

What controls appetite?

Back 1

-ventral and lateral nuclei of the hypothalamus

Front 2

Neurtransmitters in control of appetite?

Back 2

-norepi (through alpha 2 receptors)
-dopamine (through D1 receptors)
-GABA (controversial)
-serotonin is inhibitory (5-HT)

Front 3

Vitamin B is an appetite stimulant and a supplement for what species?

Back 3

-monogastrics

Front 4

Why do we give vitamine B to monogastrics?

Back 4

-improve general physical conditions and thus appetite

Front 5

What are three examples of an anabolic steroid?

Back 5

-Nandrolone decanoate
-stanozolol
-boldenone undecyclenate

Front 6

This drug is used to stimulate erythropoiesis in cats and dogs, thus it is believed to enhance RBC counts and possibly stimulate a dogs appetite?

Back 6

nandrolone decanoate

Front 7

What anabolic steroid is not approved for vet med?

Back 7

-dandrolene decanoate

Front 8

Stanozolol has a ___________ anabolic effect, but a _________________ androgenic effect.

Back 8

high anabolic, weak androgenic

Front 9

The tablet form of stanozolol is only used in what specie(s), but not in what specie(s).

Back 9

-only used in dogs and cats
-not used in horses

Front 10

This drug is used for anemia of chronic disease, to improve appetite, promote weight gain and increase strength and viability.

Back 10

-stanozolol

Front 11

Can you use stanozolol in cats?

Back 11

-no. hepatotoxic

Front 12

What is boldenone undecyclenate?

Back 12

-anabolic steroid

Front 13

what is boldenone derived from?

Back 13

-testosterone

Front 14

what drug has an androgenic effect and can suppress endogenous testosterone and stimulate erythropoeisis like dandrolene?

Back 14

-boldenone

Front 15

when would you want to use boldenone?

Back 15

-adjunctive therapy treating debilitated horses when improvement in weight, haircoat or general physical condition is desired

Front 16

Is boldenone a long acting or short acting steroid?

Back 16

-long acting steroid

Front 17

We use boldenone extra label for?

Back 17

-cats to stimulate appetite

Front 18

In general what do we use anabolic steroids for?

Back 18

-to improve general physical conditions

Front 19

What are the two benzodiazepines?

Back 19

-diazepam (valium)
-oxazepam

Front 20

Are benzodiazepines long or short acting?

Back 20

-only short term
-the effect is gone after 2-3 treatments

Front 21

What is the mechanism of action of benzodiazepines?

Back 21

-not know
-antagonism of serotonin and increased release of GABA have been postulated

Front 22

You have a dog home in suffering from anxiety, the owner just wants to sedate him to get hime home. When you palpate him he has very tense muscles and the owner tells you that he has a history of seizures. What do you want to give him?

Back 22

diazepam or oxazepam
-they have anxiolytic, hypnotic, sedative, skeletal muscle relaxation and anticonvulsant effects

Front 23

what drug is frequently used orally to stimulate appetites in cats and occasionally in dogs?

Back 23

-oxazepam

Front 24

This drug can be used orally, IV or IM in cats and dogs and is used IV in horses and goats to stimulate appetite.

Back 24

-diazepam

Front 25

If you have a dog with decreased appetite, would you give him diazepam, why/why not?

Back 25

-no. it doesn’t stimulate appetite as well in dogs as in cats

Front 26

What are the adverse effects of benzodiazepines?

Back 26

-sedation
-ataxia
-excitement
-HEPATOTOXICITY IN CATS IS UNPREDICTABLE

Front 27

This is a second generation antihistamine and a potent antagonist of serotonin.

Back 27

-cyproheptadine

Front 28

What is cyproheptadine used orally for?

Back 28

-appetite stimulant in cats
-antihistaminic
-antipuriritic in cats and dogs

Front 29

Can cyproheptadine be given orally?

Back 29

-yes, good bioavailability

Front 30

Where is cyproheptadine metabolized?

Back 30

-liver and eliminated in the urine

Front 31

what are the major side effects of cyproheptadine?

Back 31

-sedation and anticholinergic effects
-constipation
-decreased exocrine gland thus constipation?
-these effects are not that significant they are for first generation antihistamines though

Front 32

20% of cats following oral administration of cyproheptadine experience?

Back 32

-CNS stimulation (aggressive behavior) in some cats

Front 33

This is a tetracyclic antidepressant?

Back 33

-mirtazapine

Front 34

Mirtazapine works how?

Back 34

-antagonist of central pre-synaptic alpha 2 receptors thus is increases NE and thus it is an appetite stimulant

Front 35

Mirtazapine is an antagonist of what serotonin receptor?

Back 35

-5 HT3

Front 36

When you have a animal with poor appetite and emesis together, what drug would you want to use?

Back 36

-mirtazapine

Front 37

How often do you use martazapine in cats vs. dogs?

Back 37

-cats-twice/week
-dogs-once daily

Front 38

What are the major side effects of mitrazapine?

Back 38

-sedation, vocalization, hypotension and tachycardia

Front 39

This is a synthetic progestin used occasionally as an appetite stimulant.

Back 39

-megestrol acetate

Front 40

How does megestrol acetate work?

Back 40

-has anti-estrogen and glucocorticoid activity (causes adrenal suppression)

Front 41

You have a dog that has been diagnosed with benign prostatic hypertrophy and dermatologic and behavior related conditions, what drug do you give him?

Back 41

-megestrol acetate

Front 42

why should you use caution when you give megestrol acetate to cats?

Back 42

-adrenal suppression, adrenal atrophy, diabetes mellitus

Front 43

this is a catabolic drug that requires that the owner provide increased protein.

Back 43

-glucocorticosteroids

Front 44

What are two examples of glucocorticosteroids?

Back 44

-prednisolone and dexamethasone

Front 45

How often do you give prednisolone or dexamethasone in small or large animals?

Back 45

-daily basis or every other day in small and large animals

Front 46

What is the mechanism of action of glucocorticosteroids?

Back 46

-not know
-may result from glucocorticoid –induced euphoria

Front 47

What cells types and systems do glucocorticosteroids affect?

Back 47

-almost all cell types and sytems in animals

Front 48

Adverse effects from glucocorticosteroids are generally associated with?

Back 48

-long term use, esp at high doses

Front 49

Short term drug usage of glucocorticosteroids is associated with what risks?

Back 49

-short term is unlikely to cause adverse reactions even in very high doses

Front 50

Why would you want to use glucocorticosteroids short term?

Back 50

-as an appetite stimulant

Front 51

which species, cats or dogs, generally need a higher dose of glucocorticosteroids?

Back 51

-cats for efficacy without adverse effects

Front 52

Where is the emetic center?

Back 52

-medulla oblongata
-chemoreceptor trigger zone=close to emetic center

Front 53

what is the point of emetics?

Back 53

-vomiting reflex and general consideration

Front 54

who can/can’t vomit?

Back 54

-carnivores, pigs and primates=vomit

Front 55

What are six things that can induce vomiting?

Back 55

1. GI irritations
2. middle ear disorders
3. motion sickness (CN 8)
4. drugs/toxins and metabolic disorders
5. increased intraocular pressure
6. pain

Front 56

What are some disadvantages of emetics?

Back 56

-dehydration, acid/base balance problems, electrolyte imbalances, aspiration pneumonia, ruptured stomach

Front 57

The vomiting reflex may be triggered by input from what four types o stimuli?

Back 57

1. stimulation of vagus nerve cause by irritation of tissues or organs innervated by the vagus nerve (GI tract, peritoneum)
2. stimulation of higher centers of brain (cerebral cortex) by emotional stimuli
3. direct stimulation of CRTZ (not protected by blood-brain barrier)
4. stimulation of inner ear nerves involved with balance (motion sickness stim inner ear can cause emesis in vet patients)

Front 58

What are the two groups of emetics?

Back 58

1. central emetics
2. local (peripheral) emetics

Front 59

What do central emetics work on?

Back 59

-act at receptors in chemoreceptor trigger zone (CTZ) or vomiting center

Front 60

what do peripheral (local) emetics work on?

Back 60

-act at receptors in esophagus, stomach, pharynx, and small intestines and stimulate vomiting centers with afferent pathways

Front 61

What are some examples of central emetics?

Back 61

1. apomorphine HCl
2. xylazine

Front 62

This drug is a dopamine receptor AGONIST in the CTZ.

Back 62

-apomorphine

Front 63

Apomorphine is a ___________ derivative.

Back 63

-morphine derivative with marginal depressant activity

Front 64

What is the emetic of choice in dogs?

Back 64

-apoporphine

Front 65

If you give apomorphine orally, will you have the desired response easily?

Back 65

-no! it is unpredictable orally (slowly absorbed, also low oral bioavailability)

Front 66

If you give subsequent doses of apomorphine will they work as well as the initial dose?

Back 66

-the are less likely to induce emesis if emesis does not occur after the first dose

Front 67

Is apomorphine stable in solution?

Back 67

-no.

Front 68

If you give apomorphine IV, how quickly will vomiting occur?

Back 68

-within one minute

Front 69

If you give apomorphine IM, how quickly will vomiting occur?

Back 69

-within 5 minutes

Front 70

Can you give apomorphine SQ to the conjunctival sac and get desired effects?

Back 70

-yes, you stimulate emesis in 2-10 minutes

Front 71

Is apomorphine effective in swine?

Back 71

-no.

Front 72

Can you use apomorphine in cats?

Back 72

-NO! Causes CNS stimulation and thus possible seizures

Front 73

For emesis in cats you should use what drug over apomorphine?

Back 73

-naloxone

Front 74

what are some major side effects of apomorphine?

Back 74

-depression in dogs
-seizures, CNS stimulation in cats
-respiratory depressant effect can be reversed by naloxone but not emetic effects

Front 75

How can you reverse emetic effects of apomorphine?

Back 75

-use phenothiazine tranquilizers?

Front 76

This is an alpha 2 adrenergic receptor agonist, it is the preferred emetic in cats (IV or IM), emesis occurs in 3-5 minutes and emesis is induced when administration below doses in cats recommened for sedation.

Back 76

-xylazine

Front 77

To prevent aspiration pneumonia, what should you do after you give xylazine or any other emetic?

Back 77

-wait 3-5 minutes for all the vomiting, then induce further anesthesia

Front 78

What are some examples of a local emetics?

Back 78

-sodium chloride
-powdered mustard
-1% copper sulfate (dogs and pigs)
-1% zinc sulfate solution
-3% hydrogen peroxide
-syrup of ipecac (contains alkaloid emetine)

Front 79

What is the drawback to using sodium chloride?

Back 79

-not reliable
-can cause salt poisoning

Front 80

Why would you use centrally acting and locally acting emetics?

Back 80

1. eliminate poison in the GI tract (central emetics are preferred)
2. following emesis use activated charcoal

Front 81

Why would you prefer to use central emetics to eliminate poison in the GI tract?

Back 81

-bc local emetics are slower

Front 82

When would you not want to use emetics?

Back 82

-if ingestion of corrosive acids and alkalis is suspected
-animals ingested volatile liquids such as gasoline and most oils
-comatose, depressed and unconscious animals (use gastric lavage)
-animals with bloat, gastric torsion, or esophageal damage (megaesophagus) or recent abdominal surgery
-animals having seizure
-animals with shock or dyspnea

Front 83

What should you be aware of before you give emetics?

Back 83

1. fatal aspiration of hydrogen peroxide is possible in cats and dogs
2. syrup of ipecac vs. extract of ipecac
a. extract is 10x more cardiotoxic than syrup of ipecac
3. if repeated syrup of ipecac fails to induce emesis, gastric lavage is indicated to remove potentially toxic doses (cardiotoxic)
4. Powder and syrup of ipecac can induce severe toxicity including death in cats

Front 84

What kind of ipecac should you never use?

Back 84

-EXTRACT OF IPECAC

Front 85

If you just gave a full dose of syrup of ipecac and no vomiting has happened for 30 minutes, what should you do?

Back 85

-use gastric lavage bc it can be cardiotoxic

Front 86

what is a group of a centrally acting antiemetic?

Back 86

-phenothiazines
-butyrophenone derivatives
-metoclopramide

Front 87

What are some drugs that fall under the group of phenothiazines?

Back 87

1. acepromazine
2. chlorpromazine
3. promazine
4. prochlorperazine
5. mepazine
6. perphenazine
7. trifluoperazine
8. promethazine

Front 88

How does acepromazine work?

Back 88

-broad spectrum anti-emetic
-antagonizes the CNS stimulatory effects of dopamine

Front 89

How do you give acepromazine?

Back 89

orally or parenterally

Front 90

What are some of the actions of acepromazine?

Back 90

-antidopaminergic
-antihistaminergic
-anticholinergic effects

Front 91

You are seeing a dog that is vomiting and you determine that it is vomiting as a result of parasympathetic impulses entering the vomiting center from the GI and peritoneal tracts, can you use acepromazine to make it stop vomiting?

Back 91

-no! Acepromazine is a weak inhibitor of cholinergic responses and thus cannot be used to prevent vomiting caused by parasympathetic impulses entering the vomiting center from GI, or peritoneal areas.

Front 92

What are some side effects of using acepromazine?

Back 92

1. sedation
2. hypotension

Front 93

why do you see hypotension with the use of acepromazine?

Back 93

-due to peripheral alpha blockage

Front 94

What can you do to avoid hypotension with the administration of acepromazine?

Back 94

-fluid replacement therapy if necessary before use of phenothiazines

Front 95

Why would it be ok to give a dog that is traveling acepromazine?

Back 95

-you get sedation with the antiemetic effects which can be good for cats or dogs that are being transported

Front 96

Can you use acepromazine in epileptic patients? Why/why not?

Back 96

-no! not to be used in epileptic patients, because it lowers the seizure threshold

Front 97

If you don’t see sedation in an animal from acepromazine would could be happening?

Back 97

-excitement (instead of depression in 15-20% of animals)

Front 98

Why can’t you use acerpromazine in a dehydrated animal?

Back 98

-always rehydrate patients before using phenothiazine tranquilizers bc they can cause hypotension, and they may already be depressed just from being dehydrated

Front 99

What are the two butyrophenone derivatives?

Back 99

1. haloperidol
2. droperidol

Front 100

Why are haloperidol and droperidol considered major tranquilizers and antiemetics?

Back 100

-due to antidopaminergic activity

Front 101

are butyrophenone derivatives commonly used as antiemetics?

Back 101

-no due to their side effects (similar side effects as phenothiazines)

Front 102

what is butorphanol?

Back 102

-opioid agonist/antagonist (it is mixed!)

Front 103

Why can butorphanol be used as an antiemetic?

Back 103

-due to blockage of opioid receptors in emetic center

Front 104

When is butorphanol commonly used?

Back 104

-in dogs for chemotherapy-induced emesis

Front 105

Butorphanol is an agonist at what receptors and an antagonist at what receptors?

Back 105

-agonist at kappa receptors
-antagonist at mu receptors

Front 106

Metoclopramide is a derivative of what?

Back 106

-procainamide

Front 107

What kind of emetic activity does metoclopramide have?

Back 107

-both central and peripheral antiemetic activities

Front 108

Where does metoclopramide have its effects and what does it do there?

Back 108

-central-potent antidopaminergic activity in CTZ

Front 109

What does metoclopramide do to serotonin?

Back 109

-inhibits serotonin

Front 110

What does metoclopramide do peripherally?

Back 110

-increases gastric contraction
-speeds up gastric emptying
-increases esophageal sphincter tone
-promotes peristalsis in duodenum and jejunum

Front 111

Is metoclopramide a prokinetic?

Back 111

-yes

Front 112

where does metoclopramide have its prokinetic effect?

Back 112

no effect on motility in the distal part of small intestines and the colon

Front 113

what can be used to antagonize apomorphine induced emesis besides phenothiazide tranquilizers?

Back 113

-metoclopramide

Front 114

If metoclopramide more potent as an antiemetic or prokinetic?

Back 114

more potent as an antiemetic

Front 115

You have a dog that has come in and you determine that it has obstruction in the proximal portion of the duodenum and it is vomiting as a result. The owner is distraught that her animals is vomiting, so you decide to give it metoclopramide. Is this a good idea or a bad idea?

Back 115

-BAD idea! Metoclopramide is contraindicated in animals with GI obstruction bc it has some prokinetic effects!!

Front 116

Can you give metoclopramide to epilepsy patients?

Back 116

-no! it decreases the seizure threshold

Front 117

Can you use metoclopramide with pheonothiazine tranquilizers?

Back 117

-no.

Front 118

Does metoclopramide have a long or short half life?

Back 118

-short half life
have to give it 4x/day or constant rate IV infusion

Front 119

what is the most common side effect of metoclopramide?

Back 119

-CNS disorders
-restlessness, hyperactivity, tremors

Front 120

In what species will you see CNS disorders as a result of metoclopramide administration?

Back 120

-horses and cats

Front 121

what are three antagonists of serotonin?

Back 121

1. odansetron
2. ganesetron
3. granisetron

Front 122

What kind of receptors do odansetron, ganesetron and granisetron work on?

Back 122

-central and peripheral receptors

Front 123

When would you want to use antagonists of serotonin as antiemetics?

Back 123

-effective for cancer-chemotherapy-induced and radiation-induced vomiting
-effective for post operative vomiting

Front 124

Can you use antagonists of serotonin for motion sickness?

Back 124

-no! they are ineffective for motion sickness

Front 125

Odansetron, ganesetron and granisetron are used primarily in what species?

Back 125

-dogs
-use in cats is controversial

Front 126

what receptors does maropitent (cerenia) work on?

Back 126

-central and peripherally mediated emesis

Front 127

What does maropitent do in the CNS?

Back 127

-neurokinin-1 receptor antagonist in CNS by inhibiting substance P

Front 128

Maropitent is approved for use in what species?

Back 128

-dog

Front 129

What is the most popular antiemetic in dogs?

Back 129

maroptitent bc it is FDA approved for that use

Front 130

How should you administer maropitent?

Back 130

-orally for acute vomiting and motion sickness
-SQ for acute vomiting

Front 131

What are some side effects of maropitent?

Back 131

-hypersalivation
-diarrhea
-anorexia
-swelling and pain at the injection site

Front 132

What is the most potent antiemetic drug when vomiting is caused by motionsickness or car problems?

Back 132

-antihistamines (histamine H1 receptor antagonists)

Front 133

Do antihistamines have potent or weak anticholinergic and antimuscarinic actions?

Back 133

-potent

Front 134

How do antihistamines have an antiemetic action?

Back 134

-inhibition of cholinergic and histaminergic input from vestibular apparatus with the cerebellum to vomiting center

Front 135

Why are antihistamines so good as antiemetics in dogs with inner ear problems?

Back 135

-bc dogs have more alpha 2 adrenergic receptors than cats do (that is why xylazine works better in cats)

Front 136

Can you use antihistamines in horses?

Back 136

-no! it reduces GI motilitycolic
-you can try them at low doses to make sure you don’t cause colic

Front 137

With therapeutic doses of antihistamines, what happens to the CNS?

Back 137

-depression (sedation)

Front 138

Since antihistamines have antimuscarinic effects what are some of the side effects of their administration?

Back 138

-urinary retention or frequency
-dysuria
-constipation
-dry mouth
-blurred vision
(blocks SLUD)

Front 139

why should you use caution when you are giving antihistamines to pregnant animals?

Back 139

-teratogenic effect

Front 140

What is the antimuscarinic prototype drug?

Back 140

-ATROPINE

Front 141

Antimuscarinic agents are modest, strong, or weak antiemetic drugs?

Back 141

modest antiemetic drugs

Front 142

How can antimuscarinics induce vomiting?

Back 142

-by reducing GI motility they can promote vomiting in vet med
-that is why their usage is contraindicated in vet met patients

Front 143

You have a dog that has IBS and is vomiting as a result of this, what can you give it?

Back 143

-antimuscarinic agents

Front 144

What is the mechanism of action of antimuscarinic agents?

Back 144

-muscarinic receptors in GI tract are blocked and so are cholinergic afferents to the vomiting center
-block muscarinic receptors in the emetic centers (central and peripheral)

Front 145

What do antimuscarinics do in the GI tract?

Back 145

-anitspasmodic effects (antidiarrheal)
-remember they block SLUD response

Front 146

Do glycopyroolate, propenthaline, methoscopolamine and isopropamide cross the BBB?

Back 146

-no!

Front 147

Does aminopentamide cross the BBB?

Back 147

-yes

Front 148

How do antacids work?

Back 148

-they neutralize the HCl secreted by gastric parietal cells and reduce the emetogenic effect of gastric hyperacidity

Front 149

Why are antacids useful as antiemetics?

Back 149

-alkalinization tends to increase gastric motility (local)

Front 150

How do antacids work?

Back 150

-they neutralize the HCl secreted by gastric parietal cells and reduce the emetogenic effect of gastric hyperacidity

Front 151

Will alkalinization increase, decrease or not change gastric motility?

Back 151

-alkalinization tends to increase gastric motility (local)

Front 152

Why are antacids useful as antiemetics?

Back 152

-by alkalinizing the stomach they increase gastric motility so it isn’t coming back up the other way as vomit

Front 153

How do corticosteroids work as antiemetics?

Back 153

-mechanism is unknown
-used IV with central antiemetics against emetogenic cancer chemotherapy or inflammatory gastritis (central)

Front 154

What are some sedatives that can be used at antiemetics?

Back 154

-barbituates (Phenobarbital)
-benzodiazepines (diazepam)
-also used to control psychogenic and behavioral vomiting (central)

Front 155

In animals suffering from GI disorders why would it not be out of line to use antiemetics?

Back 155

-if you reduce GI motility you can promote vomiting, so by using drugs that promote GI motility (ie prokinetics) you can reduce vomiting esp in those suffering from GI disorders

Front 156

What are two antiulcer agents?

Back 156

1. antacids
2. gastric antisecretory drugs
3. cytoprotective drugs

Front 157

What are three examples of gastric antisecretory drugs?

Back 157

1. anticholinergics
2. H2 receptor antagonists
3. proton pump inhibitors

Front 158

What are the three major types of receptors on gastric parietal cells?

Back 158

1. muscarinic Ach receptors (stimulated by vagus)
2. gastric receptors (stimulated by gastrin)
3. histaminergic 2 receptors (stimulated by histamine released from enterochromaffin-like cells)

Front 159

Can you use histaminergic 2 receptors for control of allergies?

Back 159

-allergy has nothing to do with histamine 2 receptors!!! They are only located on gastric parietal cells
-if you want to control allergies for analphylactic you have to use H1 receptor antagonists

Front 160

What species is extremely prone to ulcers?

Back 160

-horses

Front 161

What species are frequently diagonised with ulcers?

Back 161

-dogs, ulcers are less frequently diagonised in cats

Front 162

Where will you find ulcers in ruminants, but they are hard to diagnose?

Back 162

-abomasal ulcers

Front 163

Physiological stimulation of gastric acid secretion from a meal involves the release of ___________ from ______________ cells and the release of ________ from ________ enteric neurons.

Back 163

-gastrin from G-cells
-acetylcholine from gastric enteric neurons

Front 164

Both gastrin and acetylcholine act via specific receptors on the ______ ________-Cells to release histamine that finally stimulates the parietal cells via activation of their _______-receptors.

Back 164

-specific receptors act on the mucosal ECL-cells to release histamine that finally stimulates the parietal cells via activation of their H2-receptors.

Front 165

Blocking of receptors for gastrin (CCK2), acetylcholine (M3) or histamine inhibits?

Back 165

-gastric acid secretion

Front 166

The most potent inhibitors of gastric acid secretion are?

Back 166

-hstimaine H2-receptor blockers and proton pump inhibitors, but antacids only neutralize the secreted acid into the gastric lumen, they do not inhibit the production of gastric acid

Front 167

Why are antacids called cytoprotective drugs?

Back 167

-they increase the synthesis of prostaglandin in the GI tract, so they are called cytoprotective drugs

Front 168

what are some major antacids used in vet med?

Back 168

1. aluminum salts (basaljel, amphojel)
2. magnesium salts
3. calcium carbonate

Front 169

What are two types of aluminum salts used at antacids?

Back 169

1. hydroxide and carbonate
2. silicates and phosphates

Front 170

What are two types of magnesium salts?

Back 170

1. hydroxide
2. oxides, silicates

Front 171

Calcium and aluminum preparations of antacids cause?

Back 171

-constipation

Front 172

Magnesium salts as antacids also cause?

Back 172

-they are laxatives

Front 173

What do antacids do?

Back 173

-neutralize gastric HCl
-increase gastric pH above 4, which inhibits pepsin secretion

Front 174

How long do carbonate preparations last?

Back 174

-they are fast acting, NOT prolonged. We have to give them very often
-this is why they are not used commonly in vet med

Front 175

How fast/long do magnesium preparations last?

Back 175

-slow to moderate, prolonged action

Front 176

How long do aluminum preparations last?

Back 176

-slow acting, prolonged action

Front 177

Why would you choose to use antacids?

Back 177

1. adjunctive treatment of gastric hyperacidity, peptic ulcers, gastritis, reflux esophagitis

Front 178

If you have a hyperphophatemic cat and a renal failure dog, but is one drug that you can use to treat both of these animals?

Back 178

-aluminum salts (antacids)

Front 179

How do aluminum phosphates work?

Back 179

-decreases phosphate absorption by forming insoluble aluminum phosphates in the intestines

Front 180

when would you use antacids in a ruminant?

Back 180

-grain overload, rumen acidosis

Front 181

What is the major side effect of magnesium?

Back 181

-up to 20% of magnesium can be absorbed, hypermagnesia in animals with renal disease (not to be used in animals with kidney disease)
-not clinically significant unless they are suffering from kidney disease

Front 182

Should you use drugs that contain magnesium in animals with kidney disease?

Back 182

-no!

Front 183

Calcium antacids can cause what undesirable effects with chronic usage?

Back 183

-can cause metabolic alkalosis, gastric acid rebound, hypercalcemia, calcuria urolithiasis, hypophosphatemia, and constipation with chronic usage

Front 184

If antacids alkalinize the urine, what can happen?

Back 184

-increase the rate of elimination of weak acids (NSAIDS, Phenobarbital)

Front 185

Antacids can do what to oral absorption of drugs?

Back 185

-may alter the oral absorption of drugs either by changing the gastric pH or by directly binding to drugs

Front 186

Why should sodium bicarbonate not be used as an antacid?

Back 186

-systemic absorption causes alkalosis and overuse may generate CO2 and lead to gastric distention

Front 187

When you make the stomach pH alkaline, does gastrin production increase, decrease or stay the same?

Back 187

-increases

Front 188

If you are giving antacids and making the stomach pH alkaline, there will be increased production of gastrin, but what happens after you take the animal off of antacids?

Back 188

-gastrin production continues to stay high, this is called GASTRIC ACID REBOUND

Front 189

What are three examples of gastric antisecretory drugs?

Back 189

1. anticholinergics
2. H2 receptors antagonists
3. Proton pump inhibitors

Front 190

Even though we have anticholinergic drugs will they have any efficacy for the treatment of gastrointestinal ulceration?

Back 190

-no!

Front 191

Are anticholinergic drugs proven to be effective for the control of gastrointestinal ulceration in animals despite the role of muscarinic receptors in gastric acid secretion?

Back 191

-no!

Front 192

What are four examples of H2 receptor antagonists?

Back 192

1. cimetidine
2. ranitidine
3. famotidine
4. nizatidine

Front 193

What do H2 receptor antagonists do?

Back 193

-inhibit gastric acid secretion by blockage of H2 receptor on parietal cells (competitive antagonist) (also known as systemic antacids)

Front 194

H2 receptor antagonists are used for?

Back 194

the treatment of ulcers (gastric, duodenal and abomasal), esophageal reflux and duodenal gastric reflux

Front 195

What is cimetidine used for experimentally?

Back 195

-as an immunomodulator (ie for the treatment of melanomas)

Front 196

What are two H2 receptor antagonists that are prokinetic drugs?

Back 196

-nizatidine and ranitidine are used as prokinetic drugs

Front 197

Is cimetidine potent or weak cytochrome p450 inhibitor or stimulator?

Back 197

-potent cytochrome p450 inhibitor

Front 198

Is ranitidine a potent or weak cytochrome p450 inhibitor or stimulator?

Back 198

-weak cytochrome p450 inhibitor

Front 199

With cimetidine and ranitidine given with other drugs, will you see an increase, decrease or not change in the metabolism of the other drugs?

Back 199

-reduced metabolism of the other drugs (ie phenytoin, warfarin, Phenobarbital)

Front 200

Is the potency of cimetidine as a cytochrome p450 inhibitor clinically significant?

Back 200

-yes

Front 201

What is a disadvantage of cimetidine?

Back 201

-least potent drug and has to be administered 3 to 4 times/day

Front 202

How often do you have to give ranitidine?

Back 202

-twice a day (famotidine and nizatidine once a day)

Front 203

What is the order of potency of H2 receptor antagonists?

Back 203

Famotidine>ranitidine=nizatidine>cimetidine

Front 204

Are H2 receptor antagonists rapidly absorbed orally?

Back 204

-yes and excreted in urine as metabolites and in parent form

Front 205

What are some therapeutic usages of H2 receptor antagonists?

Back 205

-used in dogs and cats with gastritis, gastric ulcers, esophagitis, mastocytosis and gastrinomas

Front 206

In animals with exocrine pancreatic disease what do we use H2 receptor antagonists for?

Back 206

-used to prevent destruction of replacement pancreatic enzymes by gastric acid in dogs and cats

Front 207

What do we use H2 receptor antagonists for in horses?

Back 207

-gastritis and gastric erosions

Front 208

What is an example of a proton pump inhibitor?

Back 208

omeprazole

Front 209

When omeprazole used as a prodrug?

Back 209

-when it is given prodrug when given orallycomes back to stomach get protonated and becomes activated

Front 210

What is the mechanism of action of omeprazole?

Back 210

-activated in parietal cells
-covalently bind to with hydrogen-potassium ATPase enzyme to inhibit the end stage of gastric acid formation
-it takes 4-5 days for synthesis of new hydrogen-potassium ATPase enzymes

Front 211

Does omeprazole have a long or short duration of action?

Back 211

-long duration of action, only have to give it once a day

Front 212

How long does it take omeprazole to have its effects?

Back 212

-3 to 4 days

Front 213

If you want omeprazole to have its effects sooner than 3 to 4 days, what can you do?

Back 213

-give it IV and it will have immediate effects
-this is very expensive though bc there is no vet med formula of omeprazole for IV administration

Front 214

what is the overall effect of omeprazole?

Back 214

-increase stomach pH thus decreasing gastric acid production

Front 215

Is omeprazole stable in gastric pH?

Back 215

-no.

Front 216

Is omeprazole a prodrug?

Back 216

-yes, it has to be metabolized in the body to be activated

Front 217

Can omeprazole be given orally?

Back 217

yes, rapidly absorbed orally, but bioavailability is variable (dose, gastric pH)

Front 218

Does bioavailability of omeprazole increase, decrease or stay the same with repeated administration?

Back 218

-may reach 70% with repeated administration

Front 219

where is omeprazole metabolized and excreted?

Back 219

-metabolized by the liver and excreted in urine

Front 220

Does omeprazole enhance or inhibit cytochrome p450s?

Back 220

-inhibits cytochrome p450s

Front 221

What drug would you want to use to treat GI ulcers, reflux esophagitis, gastric producing tumors (ie gastrinomas), mastocytosis, prophylaxis of NSAIDs induced ulcers?

Back 221

-omeprazole is the most commonly used drug for these

Front 222

What are some side effects of omeprazole?

Back 222

-diarrhea, colic, vomiting, hematologic abnormalities

Front 223

For GI ulcers what is the general group of drugs that you would want to use?

Back 223

-use proton pump inhibitors

Front 224

what is a cytoprotective drug?

Back 224

-sucralfate (aluminum sucrose sulfate)

Front 225

what is the mechanism of action of sucralfate?

Back 225

-forms a sticky past-like complex in acid gastric juice (pH<4)
-also binds to and inactivates acids and pepsin
-binds to the surface of ulcerated tissue and forms a cytoprotective layer
-other proposed mechanisms: reduces pepsin action, stimulates prostaglandin synthesis, locally stimulates epidermal growth factor

Front 226

When does sucralfate work best?

Back 226

-in an acidic environment

Front 227

How is sucralfate primarily administered?

Back 227

-orally

Front 228

What should you remember about sucralfate?

Back 228

NEVER give it rectally!!

Front 229

Is absorption of sucralfate minimal or extensive?

Back 229

-minimal

Front 230

what are some adverse reactions of sucralfate?

Back 230

absorbs and reduces bioavaialability of other drugs

Front 231

What is misoprostol?

Back 231

-a methyl ester analogue of prostaglandin E1

Front 232

why are prostaglandins very good for the gut?

Back 232

-they inhibit acid secretion and stimulate mucus and bicarb production and enhance the mucosa and increase mucosal blood flow so they are good for the stomach

Front 233

Is mesoprostol rapidly absorbed orally?

Back 233

-yes

Front 234

What should you remember about misoprostol and its effects?

Back 234

-first pass effect is significant, converted to misoprostol acid that is active

Front 235

What drug is used as an adjunct in treating/preventing gastric ulceration, most useful for prevention of NSAIDS induced GI lesions?

Back 235

-misoprostol

Front 236

NSAIDs do what do prostaglandin?

Back 236

-block the synthesis of prostaglandin
-since prostaglandins are good for the gut, by blocking then NSAIDS commonly cause ulcers

Front 237

what are the major side effects of misoprostol?

Back 237

-diarrhea
-colic
-potential abortifacient in the pregnant animal (since it is a prostaglandin analogue)

Front 238

What is another drawback to misoprostol besides it possibly causing abortions and diarrhea or colic?

Back 238

-it is expensive

Front 239

What do prokinetics promote?

Back 239

1. Gastric and intestinal motility
2. useful in functional motility disorders
3. esophagus
4. stomach
5. intestines

Front 240

You have a horse that has just had abdominal surgery, besides pain killers, what else would you want to supply that horse with?

Back 240

prokinetics!

Front 241

What stimulates and what inhibits gastric motility?

Back 241

-stimulates: cholinergic-increase GI motility or use adrenergic ANTAGONISTS aka dopaminergic antagonists
-inhibits: adrenergic

Front 242

Modulation of enteric nervous sytem is _______________ and _________________.

Back 242

-dopaminergic and serotoninergic

Front 243

What is motilin?

Back 243

-a GI peptide with prokinetic action

Front 244

What antagonists to what receptors stimulate gastric motility?

Back 244

-antagonists of D2 and 5HT-3

Front 245

Receptor agonists of 5HT-4 can do what to gastric motility?

Back 245

stimulate gastric motility

Front 246

what kind of analog is erythromycin?

Back 246

-motilin analog

Front 247

what receptors does erythromycin stimulate?

Back 247

-motilin receptors

Front 248

What is a prokinetic antibiotic for equine medicine?

Back 248

-erythromycin

Front 249

What can you use for gastric reflux inhorses?

Back 249

-lidocain-1/10th of the dose is the prokinetic drug dose

Front 250

Why are cholinomimetics not commonly used in vet med?

Back 250

-bc of side effects

Front 251

What are bethanocol, carbachol and neostigmine again?

Back 251

-indirect inhibitors of acetylcholinesterase
-they are reversible
-can be used as prokinetics

Front 252

Metoclopramide is most potent as an?

Back 252

-antiemetic

Front 253

Metoclopramide is structurally related to?

Back 253

-procainamide

Front 254

How does metoclopramide have its effects?

Back 254

-central antidopaminergic (antiemetic effect), additionally, acts peripherally as both an antidopaminergic and as a direct and indirect stimulator of cholinergic receptors

Front 255

Can metoclopramide be given orally?

Back 255

-well absorbed orally but has a significant first pass effect

Front 256

What is the best way to administer metoclopramide as far as availability?

Back 256

-parenterally is better than oral

Front 257

Why don’t we use bethanechol, carbachol and neostigmine as prokinetics?

Back 257

-bc of their side effects

Front 258

In what form is metoclopramide excreted?

Back 258

-excreted as conjugated metabolites (urine and bile) and pass parent form (urine)

Front 259

What can you give to antagonize the prokinetic effect of metoclopramide?

Back 259

-atropine or opioid antagonists

Front 260

What should you remember about where metoclopramide has its effects?

Back 260

-improves GI motility but not in the distal part of the intestine. It doesn’t stimulate motility in the colon.

Front 261

What can metoclopramide do in horses and cats?

Back 261

-crosses the BBB and causes excitement

Front 262

Does metoclopramide have a long or short half life?

Back 262

-short, so give as a constant rate IV

Front 263

What is domperidone?

Back 263

dopaminergic antagonist with similar prokinetic properties of metoclopramide

Front 264

Does domperidone have cholinergic activity?

Back 264

-no

Front 265

Can you use atropine to inhibit domperidone?

Back 265

-no! bc it has no cholinergic activity

Front 266

This drug is used in horses with fescue toxicity.

Back 266

-domperidone

Front 267

This drug is commonly used to induce lactation in small animals and mares?

Back 267

-domperidone

Front 268

What is dexpanthenol a precursor of?

Back 268

-coenzyme A

Front 269

What does coenzyme A do?

Back 269

-aids in the production of Ach

Front 270

This drug is used in animals with intestinal atony, postoperative retention of flatus and feces, prophylaxis and treatment of paralytic ileus, and equine colic?

Back 270

-dexpanthenol

Front 271

You would not want to use what drug in animals with ileus secondary to obstruction, and colic caused by treatment of cholinergic anthelmintics?

Back 271

-dexpanthenol

Front 272

Why shouldn’t you use dexpanthenol in animals with GI ileus caused by GI obstruction or colic?

Back 272

-bc it improves GI motility (it is a prokinetic drug)

Front 273

Is dexpanthenol a relatively safe drug?

Back 273

-yes

Front 274

What is cisapride?

Back 274

-5HT-4 receptor agonist on cholinergic myenteric neurons to enhance Ach release

Front 275

How potent is cisapride compared to metoclopramide?

Back 275

cisapride is 8 times more potent than metoclopramide

Front 276

What does cisapride do that is like metoclopramide?

Back 276

increases lower esophageal peristalsis and sphincter pressure and accelerates gastric emptying
=stimulates motility in the distal parts of the small intestine including the colon

Front 277

What are cisaprides antiemetic effects due to?

Back 277

due to blockade of 5HT-3 receptors in CTZ (chemoreceptor Trigger Zone) and also due to prokinetic effect

Front 278

What is unique about cisapride?

Back 278

-increases motility in the distal portion of the small intestine including the colon, unlike metoclopramide

Front 279

Does cisapride have any affect on D2 or H1 receptors?

Back 279

-no!

Front 280

What are the side effects of cisapride?

Back 280

-no adverse effects at therapeutic dosages, may cause diarrhea and abdominal pain

Front 281

Why is cisapride not available for humans anymore, and how do we get it for vet med now?

Back 281

-it causes fatal cardiac toxicity in humans
-we order it from a compounding pharmacy now

Front 282

What drug has been used in dogs to reduce regurgitation associated with megaesophagus (dilated esophagus) and to treat cats with chronic constipation or frequent vomiting from hairballs, which causes gastric statis and megacolon?

Back 282

-cisapride

Front 283

What drug can you use in horses for GI stasis?

Back 283

-cisapride

Front 284

Can you use metocholopramide for megacolon?

Back 284

no! you can use cisapride for megacolon though

Front 285

How should you administer cisapride for gastrointestinal stasis in horse?

Back 285

-rectally

Front 286

What are two H2 receptor antagonists?

Back 286

-ranitidine
-nizatidine

Front 287

How do H2 receptor antagonists such as ranitidine and nizatidine have their effect?

Back 287

-they have significant cholinesterase inhibition

Front 288

Will ranitidine increase, decrease or not change GI motility?

Back 288

-increases GI motility by inhibiting cholinesterase

Front 289

What do ranitidine and nizatidine do to the small intestines and colon motility?

Back 289

-stimulate gastric emptying and small intestine/colonic motility

Front 290

Can H2 receptor antagonists be given orally?

Back 290

-yes, they have good oral bioavailability

Front 291

Are H2 receptor antagonists safe drugs?

Back 291

-yes

Front 292

What drug is used in dogs and cats for gastric and duodenal ulcers (ie gastrinomas)?

Back 292

-ranitidine or nizatidine

Front 293

What are the three classes of antidiarrheal drugs?

Back 293

1. narcotic analgesic
2. anticholinergics/antispasmodics
3. protectants/absorbents

Front 294

What are three opioid agonists aka narcotic analgesic?

Back 294

-paregoric, diphenoxylate, loperamide, opium

Front 295

What do you have to remember about animals that come into your office with diarrhea?

Back 295

-before you give an antidiarrheal drug you should determine the underlying cause of the diarrhea

Front 296

What drugs decrease propulsive motility, GI secretion and increase rectal sphincter tone?

Back 296

-narcotic analgesic

Front 297

What is considered to be the drugs of choice in dogs for diarrhea?

Back 297

-narcotic analgesic aka opioid antagonist

Front 298

What antidiarrheal drug poorly penetrates the CNS in cats?

Back 298

-loperamide

Front 299

Why should you be careful about the use of loperamide?

Back 299

-it is a neurotoxic drug for p glycoprotein so you should be careful when you use it in collies and crosses the BBB

Front 300

What are three anticholinergic/antispasmodics?

Back 300

1. aminopentamide
2. methscopolamine
3. propantheline

Front 301

Why should you use anticholinergic/antispasmodics with caution in the treatment of diarrhea?

Back 301

-bc of hypomotility rather than hypermotility associated with most cases of diarrhea

Front 302

What are the four effects of anticholinergic/antispasmotic drugs such as aminopentamide, methscopolamine and propantheline?

Back 302

1. anticholinergic
2. antiemetic
3. antidiarrheal
4. antiarrhythmic effects

Front 303

Why is atropine not commonly given as an antidiarrhea med?

Back 303

-bc of its short half life

Front 304

Why should you be careful when you use anticholinergic drugs for diarrhea?

Back 304

-bc hypermotility associated with most cases of diarrhea. Anticholinergic drugs decrease GI motility

Front 305

Difference bt protectants and absorbants?

Back 305

-protectants: have coating action and protect the inflamed mucosa from further irritation
-absorbants: bind to bacteria and their toxins

Front 306

What are kaolin/pectin suspensions?

Back 306

-protectant antidiarrheals

Front 307

Where is bismuth subsalicylate metabolized?

Back 307

-metabolized in the colon

Front 308

What two effects do bismuth have?

Back 308

1. coating
2. antibacterial effects

Front 309

What effects does salicylate have?

Back 309

anti-inflammatory effect and reduces secretions by inhibiting prostaglandins

Front 310

Activated charcoal is an absorbent that is used to treat?

Back 310

-poisonings

Front 311

How should you treat toxicities?

Back 311

1. emesis
2. activated charcoal

Front 312

Why should bismuth subsalicylate be used with caution in cats because of?

Back 312

-conversion to aspirin

Front 313

What antidiarrheal interferes with GI radiographic examinations?

Back 313

-bismuth

Front 314

What are substances that loosen the bowel contents and promote defecation?

Back 314

-laxatives/cathartics

Front 315

What are cathartics or purgatives?

Back 315

laxatives with a strong or harsh effects

Front 316

What are laxatives/carthartics used for?

Back 316

-maintenance of soft feces and prevention of straining to defecate
-cleansing of the bowel before radiographic procedures
-elective surgery or colonoscopy
-elimination of unabsorbed toxins in cases of acute poisonings
-reductions of fecal impactions
-facilitation of defection in patients with painful anorectal conditions
-facilitate passage of trichobezoars (hairballs)

Front 317

what are some contraindications for the use of laxatives or cathartics?

Back 317

-vomiting and regurgitation disorders
-undiagnosed abdmoninal pain
-colic
-conditions susceptible to intestinal perforation
-intestinal obstruction (not constipation)

Front 318

What are lubricants?

Back 318

-oils or other hydrocarbon derivatives

Front 319

Should you use heavy oil or light oil for colics?

Back 319

heavy oil

Front 320

Why should you use a stomach tube when you administer oil to a ruminant?

Back 320

-to prevent aspiration pneumonia
-some prefer to use it rectally to prevent aspiration too

Front 321

What is the principle ingredient of many oral laxatives for hairball treatment in cats?

Back 321

-petrolatum

Front 322

Chronic usage to oils or petroleum can lead to?

Back 322

malabsorption of fat soluble vitamins and drugs

Front 323

How do bulk laxatives work?

Back 323

-bind to water in the colonic lumen, thereby soften fecal mass

Front 324

When do bulk laxatives become effect?

Back 324

-effective within 24 hours and reach a maximum effect after several days of repeated administrations

Front 325

What are bulk laxatives used for in general?

Back 325

-used for relief of constipation and for relief of certain types of impaction in horses

Front 326

What can fresh pineapple chunks or fresh juice for?

Back 326

-acts as a bulk laxatives

Front 327

What can you use for sand colic in horses?

Back 327

-raw linseed oil

Front 328

Osmotic cathartics contain?

Back 328

-magnesium or phosphate anions

Front 329

Osmotic cathartics are well or poorly absorbed from the GI tract?

Back 329

-poorly absorbed from the GIT

Front 330

Non-saline type osmotic cathartics contain?

Back 330

-lactulose (unabsorbed carbohydrates) and prolyethylene glycol electrolyte solutions

Front 331

How do osmotic cathartics work?

Back 331

-retain water in the GI tract due to somotic pressure and softens the stool and stimulates stretch receptors in the gut wall to enhance peristalsis (increase GI motility)

Front 332

What is used in dogs by stomach tube to evacuate the colon prior to GI exam or surgery?

Back 332

-polyethylene glycol 350

Front 333

What is the primary use of lactulose?

Back 333

-used for hepatic encephalopathy to reduce absorption of ammonia from the GIT

Front 334

Lactalose is metabolized by bacteria to form?

Back 334

-formic, acidic and lactic acid!!!

Front 335

Lactalose is metabolized by bacteria to form?

Back 335

-These are also osmotically active (attract water into the colon) make the pH of the colon more acidic, this will increase motility of the colon. This why we use lactalose for the treatment of megacolon in the cat, but this tastes terrible, they hate the taste of lactalose. So by making the pH more acidic they cause the movmeent of ammonia from blood itnot he colon and ammonia-->ammonium and is excreted in the feces, so this increases the excretion of ammonia as ammonium.

Front 336

What is milk of magnesia?

Back 336

-magnesium hydroxide

Front 337

what is Epsom salt?

Back 337

-magnesium sulfate

Front 338

What species do we use sodium phosphate salts in?

Back 338

-horses and dogs

Front 339

Why shouldn’t you use phosphate containing enemas in cats?

Back 339

-cats are susceptible to electrolyte imbalances (hyperphosphatemia or hypocalcemia)

Front 340

What is docusate sodium and calcium and poloxamers?

Back 340

-surfactants/stool softeners

Front 341

How to surfactants/stool softeners have their effect?

Back 341

-anionic compounds, they have detergent-like action that promotes the mixing of water, lipids and other fecal materials (wetting agents). Might also stimulate intestinal water and electrolyte secretion.

Front 342

What is the most important group of surfactants/stool softeners?

Back 342

-docusate

Front 343

What do you use docusate for?

Back 343

-small animals for treatment of hard, dry feces, after anal surgery, impaction in horse and digestive upsets in ruminants (bloat release, enema-DSS, therabloat, Docu-soft, etc)

Front 344

What do you use to treat acute forgage or frothy bloat in ruminants?

Back 344

-formulations of docusate and poloxamers

Front 345

What should you not use surfactants with and why?

Back 345

-surfactants should not be used with mineral oil, other laxatives or drugs because they can enhance the intestinal absorption of many compounds

Front 346

How do irritant cathartics work?

Back 346

-irritate gut wall, causing stimulation of GI smooth muscle and increased peristalsis

Front 347

Are irritant cathartics often used in vet med?

Back 347

-no. they are used short term if they are used at all

Front 348

Are cathartics considered to be prodrugs?

Back 348

-yes, all are prodrugs and plant derivatives

Front 349

what are diphenylmethane derivatives?

Back 349

-cathartics for humans

Front 350

What are anthraquinone derivatives?

Back 350

-human OTC cathartics

Front 351

How does caster oil have its effects?

Back 351

-due to ricinoleic acid

Front 352

How do all NSAIDs work?

Back 352

-they inhibit cyclooxygenase enzyme acitivity

Front 353

Non-steroidal anti-inflammatory drugs can be divided into what two groups?

Back 353

1. NSAIDs that inhibit cyclooxygenase
2. NSAIDS that do not inhibit cyclooxygenase

Front 354

What are the three eicosanoids?

Back 354

1. prostaglandins
2. thromboxanes
3. leukotrienes

Front 355

What is inflammation?

Back 355

-the body’s response to injury

Front 356

what is the ultimate goal of inflammation?

Back 356

-to promote the healing process

Front 357

Why would you choose to use anti-inflammatory agents?

Back 357

-pain (relief of pain)

Front 358

what are eicosanoids derived from?

Back 358

polyunsaturated fatty acids and arachidonic acid

Front 359

How is arachidonic acid released from membrane phospholipids?

Back 359

primarily released by phospholipase A2 in response to physical, chemical, hormonal, and neurotransmitter stimuli

Front 360

How are prostaglandins different from other autacoids?

Back 360

-they are not localized or stored in tissue pools

Front 361

What makes prostaglandins?

Back 361

-cyclooxygenase enzyme synthesizes prostaglandins

Front 362

What make leukotriens?

Back 362

-lipoxygenase

Front 363

What are the two cyclooxygenase isozymes?

Back 363

1. COX-1
2. COX-2

Front 364

Which cox is constitutive and which isn’t?

Back 364

-COX-1=constitutive
-COX-2=inducible; inflammatory states

Front 365

Which cyclooxygenase isozyme is considered to be the “good enzyme”?

Back 365

-COX-1

Front 366

Which cyclooxygenase isozyme forms compounds for pathogenesis?

Back 366

-COX-2 forms prostaglandins for pathogenesis

Front 367

If the ratio of COX-2/COX-1 is less than one what does that mean?

Back 367

-safety and efficacy, the smaller the ratio, the more specific the drug is for inhibiting COX-2. Smaller ratio tells you that you need less conc of the drug to inhibit COX-2.

Front 368

Why are most of the NSAIDs used in vet med often accompanied by side effects?

Back 368

-bc most NSAIDs used in vet med inhibit cox1 and cox2 enzymes and that is why we observe their side effects.

Front 369

What do prostaglandins do to vascular smooth muscle?

Back 369

-vasodilate thus hypotension

Front 370

TXA2 and PGF2 alpha mostly act as vasodilators or vasoconstrictors?

Back 370

-vasoconstrictors

Front 371

What do prostaglandins do to gastrointestinal smooth muscle?

Back 371

-mixed effects (they can increase or decrease GI motility)
-can cause GI cramps or diarrhea
-PGI2 exerts antidiarrheal effects

Front 372

What prostaglandins relax respiratory smooth muscle?

Back 372

-E2, I2

Front 373

What prostaglandins constrict respiratory smooth muscle?

Back 373

contracted by TXA2, PGF2 alpha (bronchoconstriction)

Front 374

Why should you be careful if you are a female using TXA2 and PGF2alpha?

Back 374

-it can be absorbed through the skin or resp tract and causes uterine smooth muscle contraction
-ie abortion

Front 375

which prostaglandin inhibits platelet aggregation?

Back 375

-PGI2

Front 376

which prostaglandin facilitates platelet aggregation?

Back 376

-TXA2

Front 377

Which NSAID irreversibly inhibits TXA2?

Back 377

-aspirin, thus we can use it for old people who have hypercoagulative blood bc it blocks TXA2 which is present to facilitate platelet aggregation

Front 378

Do PGE2 and PGI2 increase, decrease, or not change GFR?

Back 378

-increase GFR bc they vasodilate (thus they are naturetics and diuretics too)

Front 379

You have a patient with congestive heart failure, should you give her NSAIDs for pain?

Back 379

-NO! prostaglandins are diuretics. So don’t use NSAIDs in congestive heart failure patients bc you will block the effects of prostaglandins (either endogenous or exogenous) and cause decrease in peeing thus you are not getting rid of the excess fluid present because of heart failure. You will also cause decreased blood flow to the kidney and cause renal failure

Front 380

Are prostaglandins good, bad, or otherwise for the GI tract?

Back 380

-they are good for the GI tract

Front 381

Why are PGs good for the GIT?

Back 381

decrease gastric acid secretion and increase mucus and bicarbonate production

Front 382

What are the two most potent inhibitors of gastric acid secretion?

Back 382

-ranitidine and proton pump inhibitors (omeprazole)

Front 383

What do PGs do in the CNS?

Back 383

-fever (PGE2)
-that is why we used NSAIDS as antipyretics

Front 384

Does PGE2 increase, decrease or not change the release of norepinephrine from the sympathetic neurons?

Back 384

-PGE2 inhibits the release of norepi from sympathetic neurons

Front 385

What does PGE2 do to the neuroendocrine system?

Back 385

-stimulates the release of various hormones such as growth hormone, prolactin, TSH, ACTH, FSH, LH

Front 386

What is one of the most potent chemoattractant for neutrophils?

Back 386

-LTB4

Front 387

which leukotrienes are potent bronchoconstrictors?

Back 387

-LTC4 and LTD4

Front 388

What compounds increase microvascular permeability, plasma exudation, and respiratory mucus secretion, and are slow reacting substances of Anaphylaxis (SRSA)?

Back 388

-leukotrienes

Front 389

What effect do leukotriens have on the heart?

Back 389

-reduce myocardial contractility and coronary blood flow leading to cardiac depression and hypertension

Front 390

What are the four cardinal signs of inflammation?

Back 390

-heat, redness, swelling and pain

Front 391

Glucocorticoids inhibit the activity of?

Back 391

-phospholipase 2

Front 392

Cyclooxygenase inhibitors are all weak acids or weak bases?

Back 392

-weak acids

Front 393

What is the mechanism of action for NSAIDs?

Back 393

-some inhibit cyclooxygenase and this inhibit prostaglandin biosynthesis

Front 394

Which COX do you want to inhibit with NSAIDs?

Back 394

-COX-2=prostaglandin=NSAIDs block production of prostaglandins

Front 395

What are the pharm actions of NSAIDs?

Back 395

-antipyretic
-anti-inflammatory
-analgesia
-anti-platelets

Front 396

You are at a farm and seeing a mare that is suffering from severe visceral pain because she is colicing and she has broken on of her slint bones while she was thrashing around in her stall because of her discomfort. You come out to see her and decide you have to treat her pain. Her owner suggests that she has aspirin tablets that she gives to the old barn dog and asks if she can use those as a pain killer for her mare. What do you say?

Back 396

-NO! NSAIDs do not provide analgesia for colic or broken bones
-give banamine and send her to U of I you can’t walk her and get her comfortable again

Front 397

You have a client that has sheep with foot rot. To make the sheep more comfortable you leave him with a bottle of banamine. The producer calls you back in a couple of days pissed at you because the banamine isn’t working. You talk to him and find out he has also been giving another drug to his sheep. What drug is probably reversing the effects of the flunixin? (it probably isn’t likely that this farmer will have this drug, but lets say he is a heroin addict and his doctor gave him this drug and since he is drugged out of his mind he decides to share it with his beloved sheep)

Back 397

-naloxene-it is an opioid antagonist, it is often used to reverse heroin or morphine toxicity

Front 398

What cells make cox enzymes?

Back 398

-most cells

Front 399

Once the body inhibits cox enzymes in platelets what has to happen to platelets?

Back 399

-the body has to produce new platelets

Front 400

Almost all NSAIDs are weak acids or weak bases?

Back 400

-weak acids

Front 401

Are NSAIDs well absorbed by the gut?

Back 401

-yes. They are weak acids and the gut is acidic, so it stays in its unionized form and can be well absorbed

Front 402

Is oral bioavailability of NSAIDs good?

Back 402

-it varies with drugs and species and whether it was given with food or not

Front 403

Most IV preparation of NSAIDs are alkaline or acidic?

Back 403

-alkaline, so perivascular leakage can cause inflammation or necrosis

Front 404

You are giving phenobutazone and find that I has leaked out of the vessel you were giving it into, should you be worried?

Back 404

-yes, it could cause inflammation or necrosis bc of its perivascular leakage

Front 405

Do NSAIDs have a small or large volume of distribution?

Back 405

-small volume of distribution
-bc albumin binds with NSAIDs

Front 406

You have a dog come in that has been hit by a car on a hot day. The owner tells you that the dog seemed a little lethargic and dehydrated before she left for work that morning and concluded that she must have been trying to cross the highway to get to a pond and some trees to relax and get a drink when she was hit. Can you give this dog NSAIDs to make her more comfortable after you have her stabilized?

Back 406

-no. since you have a dehydrated dog you could have a higher concentration in the ECF and could cause toxicity (same thing would happen with protein losing enteropathy-bc you wouldn’t have protein to bind NSAIDs so more active drug would be in the system)

Front 407

Why is the half life of NSAIDs so short in horses?

Back 407

-horses have alkaline urine (NSAIDs are weak acids, ionized form-gets peed out)

Front 408

Can you use the plasma concentration of NSAIDs and pharmaceutical response to determine the duration of clinical response?

Back 408

-no. clinical duration of response is related more to nature of the binding and complexing of the drug with cyclooxygenase than with half lives (there is no good correlation bt plasma drug concentrations and pharmaceutical response)

Front 409

How are NSAIDs eliminated?

Back 409

-by phase II conjugation by forming with glucuronic acid and primarily eliminated in the urine

Front 410

Why should you be careful when you use NSAIDs in geriatrics and pediatrics?

Back 410

-these patients have lower GI and liver functions which are necessary to conjugate and eliminate the drug

Front 411

If you make the pH of a patients urine more alkaline and at the same time you are giving NSAIDs, will you have to increase, decrease or not change the frequency with which you give the drug in order to maintain pharm actions?

Back 411

-increase bc if you make the urine more alkaline and NSAIDs are weak acids, then more of the NSAID is going to be in the ionized form and get peed out

Front 412

NSAIDs undergo enzyme induction by what two drugs?

Back 412

-phenylbutazone and aspiring bc they both enduce p450s

Front 413

NSAIDs undergo enzyme inhibition by what drug?

Back 413

-phenylbutazone

Front 414

What is the most common and severe side effect associated with NSAIDs?

Back 414

-GI ulceration

Front 415

What drugs should you never ever mix with NSAIDs? And why?

Back 415

-glucocorticosteroids bc they increase gastric acid secretion and increase gastric acid production and delay mucosal healing

Front 416

There are several reasons why you shouldn’t give NSAIDs to a patient in congestive heart failure, but what property of NSAIDs make them contradict what you might be treating an NSAIDs patient with for their congestive heart failure?

Back 416

-NSAIDs cause sodium and fluid retention, thus if you are giving lasix to an animal in congestive heart failure you may be contracting yourself and not getting the best results possible.

Front 417

Why shouldn’t you use NSAIDs in animals with haematological disorders?

Back 417

-NSAIDs increase bleeding time, bc they prevent formation of thromboxane A2
-aka bc they inhibit platelet aggregation

Front 418

Are NSAIDs bad for the liver?

Back 418

-they are hepatotoxic

Front 419

What do you have to keep in mind when you give an NSAID with other drugs?

Back 419

-they are highly bound acidic drugs and can displace or be displaced by other drugs from their protein binding sites this can lead to complications
-ie phenobutazone with warfarin

Front 420

NSAIDs may diminish the cardiac effects of what drug and how?

Back 420

-furosemide (lasix) bc they reduce preload through prostaglandins, and since NSAIDs block prostaglandin, then they are diminishing the cardiovascular effects of furosemide…once again, don’t use NSAIDs in CHF patients

Front 421

Most NSAIDs are inactivated by?

Back 421

-conjugation with glycine, glucuronic acid, sulfate or glutathione

Front 422

Why are NSAIDs more toxic in neonates?

Back 422

-bc kidney function is not fully developed yet in neonates and NSAIDs are inactivated by conjugation with glycine, glucuronic acid, sulfate or glutathione

Front 423

What are three angiotensin-converting enzyme inhibitors?

Back 423

-captopril
-enalapril
-benazapril

Front 424

What are fluoroquinolones and what do they have to do with NSAIDs?

Back 424

-baytril is an example
-when given with NSAIDs fluoroquinolones reduce the efficacy of GABA leading to seizures (this effect has not been confirmed in vet med)

Front 425

What are three types of agents that can interfere with the oral bioavailability of NSAIDs?

Back 425

-antacids
-mucoprotective agents
-absorbent antidiarrheal drugs

Front 426

What are the three major therapeutic uses of NSAIDs?

Back 426

1. musculoskeletal disorders (DJD, osteomyelitis, navicular disease, laminitis)
2. adjunct therapy for septic and endotoxic shock
3. to control pain and inflammation

Front 427

Practical tip for NSAIDS:

Back 427

you need to educate the client and the staff about the side effects of these drugs. If you use one NSAID and the drug seems to not be working, try another one. Good idea before putting them on NSAIDS try to determine CBC, urinalysis and baseline chem. If the animal is young and you are using them short term you don’t have to do this. If they are old and you are going to use them chronically, do this every three to four weeks.

Front 428

Can you give aspirin to a cat?

Back 428

-with extreme caution. Baby aspiring every 2-3 days can be given-the dose is extremely important

Front 429

What is the most effective NSAID for anitplatelet therapy?

Back 429

-aspirin

Front 430

Why would you even try to give aspirin to a cat?

Back 430

-it can be useful to treat feline thromboembolism

Front 431

Why would you give aspirin to a horse?

Back 431

-equine laminitis
-equine verminous arthritis

Front 432

What state that we talked about with coagulation in path would aspirin be good for?

Back 432

-DIC

Front 433

Why do we not commonly use aspirin in horse?

Back 433

-bc of its short half life

Front 434

What NSAID is known to cause GI and bone marrow hyperplasia (mainly in cats), pulmonary edema (sheep) and acidosis (resp and metabolic) in severe toxicosis?

Back 434

-aspirin

Front 435

How can you treat for aspirin toxicosis?

Back 435

1. gastric emptying (emesis or lavage)
2. then use oral activated charcoal
3. sodium bicarbonate IV to correct acidosis and enhance excretion
4. for dehydration dextrose 5% in water

Front 436

What is naproxen used for?

Back 436

-orally in horses
-treats soft tissue pain (myositis) in race horses

Front 437

Can you use naproxen in dogs?

Back 437

-no. just horses

Front 438

What is meclofenamic acid?

Back 438

-old drug, not used anymore. Don’t use it.

Front 439

What is a very potent analgesic NSAID that is used for horses and cattle, dogs, cats, ferrets, rabbits, rodents, pocket pets, and birds?

Back 439

-banamine! Flunixin meglumine

Front 440

Why is flunixin meglumine such a potent analgesic?

Back 440

-prostaglandins sensitize pain nociceptors to bradykinin.
-banamine inhibits bradykinin synthesis

Front 441

Why shouldn’t you use banamine in dogs for more than three days?

Back 441

-vomiting
-GI and renal side effects
-there are safer drugs to use for pain

Front 442

If you give one dose of banamine and find that it is ineffective for pain control, can you give another dose to get an increased effect?

Back 442

-no! subsequent doses are unlikely to be of benefit and may result in increase chances for toxicity

Front 443

What is a rare side effect of banamine IV in horses and cattle?

Back 443

-anaphylaxis

Front 444

When would you want to give flunixin to a horse?

Back 444

-visceral pain and inflammation=colic!

Front 445

What do you use banamine for in cattle?

Back 445

-control of pyrexia associated with bovine respiratory disease and endotoxemia and to control inflammation with endotoxic shock

Front 446

This drug is approved for dogs and horses and used also in cattle and swine. It can be given orally or parenterally (IV) but should not be administered injectable. It is metabolized in the liver to its active metabolite and is used to treat musculoskeletal disorders in dogs and horses for treatment of lameness. What drug is this?

Back 446

-phenylbutazone

Front 447

What is the active metabolite of phenylbutazone?

Back 447

-oxyphenbutazone

Front 448

Why should the use of phenylbutazone be avoided in dogs?

Back 448

-there are newer and safer drugs that do the same thing for them

Front 449

Oral toxicity of phenylbutazone may cause?

Back 449

-protein losing enteropathy resulting in shock and death

Front 450

Why should you use caution when you give phenylbutazone to ponies and foals?

Back 450

-high incidences of hypoproteinemia and GI ulceration

Front 451

What are some contraindication for phenylbutazone?

Back 451

patients with serious heart, liver, or kidney pathology

Front 452

Is acetomenophen approved for vet med?

Back 452

-no

Front 453

This NSAID is an antipyretic and analgesic, but has not anti-inflammatory and antiplatelet activity and doesn’t cause GI ulceration but does cause hepatotoxicity.

Back 453

-acetaminophen

Front 454

Can you use acetameniphen in cats?

Back 454

-no! its Tylenol, cats lack glucuronyl transferase enzyme

Front 455

acetameniphen toxicity can cause?

Back 455

-methemoglobinemia, hemolytic anemia (Heinz body anemia), and dark colored urine
-icterus, facial edema, lethargy

Front 456

What is the primary site for toxicity of acetaminophen?

Back 456

-the liver-centrolobular hepatic necrosis

Front 457

What can you do to treat acetaminophen toxicity

Back 457

-gastric lavage, activated charcoal or the specitic antidote, oxygen therapy against anemia

Front 458

What is the specific antidote for acetaminophen toxicity?

Back 458

-specific antidote=N-acetylcysteine
-cimetidine for hepatoxocity?

Front 459

Why do you not want your cat to eat OTC cold preparations?

Back 459

-some contain phenacetin, toxic in cats bc it is metabolized into acetaminophen

Front 460

This NSAID is approved for dogs and used in cats, rabbits, rodents, pocket ptes, horses and birds for relief of pain and inflammation (osteoarthritis). Contraindications can be bleeding disorders (Von Willebrand’s disease). Recent reports show that this drug could be associated with hepatotoxicity?

Back 460

-carprofen (rimadyl)

Front 461

This NSAID is approved for IV use for horses. Some consider this drug to be the NSAID of choice for use in cats. Is not labeled to be used IM in horses, but is gives the longest effect with the lowest dose possible. It can cause gastric ulcers in cats and dogs.

Back 461

-ketoprofen

Front 462

This drug is used in musculoskeletal disorders and pain. Very useful in the management of pain and inflammation of cats with feline lower urinary tract disease.

Back 462

-ketoprofen

Front 463

Which NSAID is safer than flunixin or bute for horses?

Back 463

-ketoprofen

Front 464

This drug is approved for dogs, and recently for cats. It is the first approved NSAID for cats.

Back 464

-meloxicam

Front 465

What is the only safe way to give meloxicam?

Back 465

-SQ injection

Front 466

Meloxicam is related to what drug?

Back 466

-piroxicam, but with a much greater safety

Front 467

What are the side effects of meloxicam? You have to know these!

Back 467

1. vomiting
2. soft stool
3. diarrhea

Front 468

This drug is used for dogs. It is a dual inhibitor of arachidonic acid metabolism. It is believed that tepoxalin inhibits both the cyclooxgenase enzyme and 5-lipoxygenase enzyme activities.

Back 468

-tepoxalin

Front 469

Does tepoxalin inhibit lipoxygenase involved in leukotriene synthesis?

Back 469

-no!

Front 470

Will you see leukotriens persisting after you administer tepoxalin?

Back 470

-yes. It doen’st inhibit lipoxygenase, it just inhibits cyclooxygenase

Front 471

This drug is approved for oral use in dogs for the relief of pain associated with inflammation. Toxicity includes vomiting, soft-stool diarrhea, tachycardia, bradycardia, cough, lethargy, weakness, seizures, hematuria, polydipsia, polyuria, fever, urticaria, dermatitis.

Back 471

-deracoxib

Front 472

This drug is to be used in dogs orally and NOT to be used in cats. It is used for the relief of pain and inflammation associated with osteoarthritis. Toxicity is associated with vomiting, anorexia, soft-stool/diarrhea, hypoproteinemia, lethargy

Back 472

-etodolac

Front 473

This drug is use in horses. It is applied topically. It is well tolerated by animals, might cause weight loss, gastric ulcers, diarrhea, and uterine discharge.

Back 473

-diclofenac aka surpass

Front 474

This drug is approved for dogs to be used orally and also was approved in horses recently. It is use for relief of pain and inflammation associated with
Osteoarthritis.

Back 474

-firocoxib

Front 475

This drug is used in dogs as adjunctive treatment of transitional cell carcinoma of the bladder. It is also used in squamous cell carcinomas, mammary adenocarcinomas and transmissible veneral tumor.

Back 475

-piroxicam

Front 476

This drug can be used in cats for its antitumor effects, but it should be used with extreme caution since it hasn’t been evaluated in them yet. (you should know it hasn’t been evaluated in cats yet)

Back 476

-piroxicam

Front 477

Why should you think twice about giving piroxicam to a dog?

Back 477

-dose of the drug that has effect is very close to the dose that causes toxicity

Front 478

This NSAID is an anti-leukotriene drug, not a bronchodilatory, cannot be used for acute bronchoconstriction and is currently being used in cats for feline asthma and for atopic dermatitis in dogs.

Back 478

-zafirlukast

Front 479

What are some NSAIDs that do not inhibit cyclooxygenase?

Back 479

-orgotein
-dimethyl sulfoxide
-polysulfonated glycosaminoglycan
-glucosamine/chondroitin sulfate
-hyaluronic acid

Front 480

This is a metaloprotein approved drug for dogs and horses and has superoxide dismutase activity. It also has bovine protein in it. It is used in horses with soft tissue inflammation and dogs for spondylitic syndromes or vertebral disease.

Back 480

-orgotein

Front 481

What are some adverse reactions to orgotein?

Back 481

-urticaria/purities in horses and anaphylaxis in dogs

Front 482

This is a medical grade solvent approved for horses and dogs. It penetrates biological membranes without causing damage. And has anti-inflammatory and analgesic effects by scavaging free radicals. It is a diuretic and causes vasodilation by increasing histamine release. Additionally it has a weak antimicrobial effect. It is FDA approved for vet med in reducing swelling due to musculoskeletal trauma.

Back 482

-DMSO aka dimethyl sulfoxide

Front 483

What do you have to be careful not to cause when you use DMSO?

Back 483

-ethylene glycol poisoning-essentially antifreeze poisoning

Front 484

When would you not want to use DMSO?

Back 484

-concurrently with anticholinesterases
-some are using DMSO as an adjunctive treatment of myasethenia gravis

Front 485

What should you remember for sure about DMSO being an industrial grade solvent?

Back 485

-it is available as an industrial grade solvent, but you should never use this form for vet med

Front 486

What can be derived from DMSO commercially?

Back 486

-MSM (neutroceutical NSAID)

Front 487

This NSAID is approved for horses and dogs and is similar to mucopolysaccharides of cartilaginous tissue. Horses with non-infectious and/or traumatic joint dysfunction and associated lameness of the carpal and hock joints may benefit from this drug.

Back 487

polysulfated glycosaminoglycan. Adequan.

Front 488

Adequan has been used anecdotally in the treatment of?

Back 488

-indolent corneal ulcers in dogs and horses

Front 489

What are the five effects of PSGAG aka adequan aka polysulfated glucosaminoglycan?

Back 489

1. bind to damage cartilage
2. inhibit catabolic processes
3. sitmulates synthesis of new cartilage
4. improves viscosity and elasticity of synovial fluid
5. improves PGE2 synthesis

Front 490

What are five contraindications for the use of PSGAG?

Back 490

1. previous hypersensitivity to PSGAG
2. joint sepsis
3. use of non-sterile technique (intra-articular)
4. post-injection inflammation
5. use with caution during pregnancy and in breeding

Front 491

This is a nutritional supplement, and there is no veterinary approved products as pharmaceuticals. It is an amino sugar synthesized in vivo from glucose and glutamine. It is also an acid found in normal cartilage.

Back 491

-glucosamine

Front 492

Glucosamine is used by cartilage cells to produce what two products and stimulates the production of what two products?

Back 492

Produces:
1. glycosaminoglycans
2. hyaluronic acid
stimulates production of:
1. glycosaminoglycans
2. proteoglycans
-also scavenges free radicals which is always a plus

Front 493

What are some drawbacks to using glucosamine?

Back 493

-minor GI disturbances (such as stool softening) and hypersensitivity reactions are possible.

Front 494

This drug is chemically identical regardless of species. It can be given orally for joint dysfunction due to non-infectious synovitis not associated with severe DJD in horses. It also has an ophthalmic preparation.

Back 494

-hyaluronic acid

Front 495

What are the four desired effects of using hyaluronic acid?

Back 495

1. joint lubrication
2. shock absorbing effect
3. anti-inflammatory effect by scavenging free radicals and suppressing prostaglandins
4. articular cartilage nutrition is improved

Front 496

This NSAID is naturally occurring in synovial fluid.

Back 496

-hyaluronic acid

Front 497

Where are glucocorticoids made?

Back 497

-adrenal gland

Front 498

Where are glucocorticoids specifically made in the adrenal gland?

Back 498

-zona fasciculate
-zona reticularis

Front 499

If you give exogenous glucocorticoids what are you doing?

Back 499

prednisone, etc. you are basically shut down the pituitary gland and the hypothalamus so you will decrease CRH and ACTH. If you give glucocorticoid for a long time, adrenal glands with atrophy! Know that!

Front 500

Do animals or humans have diurinal rhythms of cortisol?

Back 500

-humans

Front 501

Do animals have episodic events of cortisol?

Back 501

-yes

Front 502

What does that adrenal gland do?

Back 502

1. regulates the HPA axis
2. episodic secretion of ACTH
3. negative feedback by cortisol at pituitary and hypothalamic level

Front 503

What is the general action of glucocorticoids?

Back 503

-maintenance of fluid homeostasis by regulation of volume and composition of body fluids

Front 504

What do glucocorticoids do to glucose metabolism?

Back 504

-increase gluconeogenesis

Front 505

What do glucocorticoids do to proteins?

Back 505

-decrease protein synthesis

Front 506

What do glucorticoids do to lipid metabolism?

Back 506

-alter it (antiinsulin effect)

Front 507

How do glucocorticoids have anti-inflammatory effects?

Back 507

-maintain microcirculation and normal vascular permeability; stabilize lysosomal membranes, inhibit production of prostaglandins; inhibits free radical formation

Front 508

How do glucocorticoids have their antiinflammatory effects?

Back 508

-Glucocorticoids work through nuclear receptors and cytosolic receptors

Front 509

Lipocorticoids?

Back 509

Lead to inhibition of phospholipase A2 (breaks down membrane phospholipids and you end up with arachidonic acid) form the arach acid you can make prostaglandins, leukotrienes, thromboxanes, etc.

Front 510

What are the two main effects of glucocorticoids in pharm?

Back 510

1. anti-inflammatory effects
2. metabolic effects

Front 511

What are the long term effects of glucocorticoids on energy metabolism?

Back 511

-antiinsulin action
-increased glucose production from amino acid=muscle wasting
-reduced incorporation of amino acids into protein (catabolic action)
-diabetes mellitus

Front 512

Why can glucocorticoids lead to diabetes mellitus ( a diminished insulin secretory capacity)?

Back 512

-bc glucocorticoids are gluconeogenic

Front 513

What effects do glucocorts have on water and electrolyte balance?

Back 513

-inhibition of ADH thus PU/PD, increased ECF volume=increased GFR=increased peeing

Front 514

Excessive administration of glucorts does what to blood pressure and electrolyte balance?

Back 514

-may lead to exacerbate hypertension and may induce hypokalemia

Front 515

Most glucocorticoids not only affect glucocorticoid receptors but also affect mineralicorticoid effects. What do mineralicorticoids do?

Back 515

induce hypokalemia, so they have an increased loss of K, so what stays in? Sodium stays in and it is an osmotic agent, which draws water in. This is how you can get hypertension.

Front 516

What are glucs effects on the immune system?

Back 516

-suppress both the cells and the action of the immune system

Front 517

CBC of an animal on glucocorticoids for a long time will look like what?

Back 517

Lymphopenia
Eosinopenia
Increase in segmented neutrophils bc they don’t leave the blood stream to go to sites of infection

Front 518

What do we call the CBC pattern caused by long term use of glucocorticoids?

Back 518

-a stress glucogram
-can see with stress or exogenous glucocorticoids, it doesn't matter whether the animal is making them or they are being given.

Front 519

What effects, in general, do glucocorticoids have in low and high doses?

Back 519

A lower dose=antiinflammtory
Higher dose=immunosppressive effects

Front 520

What are the cardiovascular effects of glucs?

Back 520

-increases blood volume=increases CO=positive chronotropic and inotropic actions
-necessary for max catecholamine sensitivity
-Need to have normal glucocorticoids to have normal blood pressure. Catecholamines are blocked to. With adensonian patients you have to not only give catecholamines but you have to give glucocorticoids too.

Front 521

In shock, how might glucocorticoids cause more problems?

Back 521

-the production of the vasoactive products of lipid peroxidation (arachidonic acid cascade) such as vasoconstrictor thromboxane A2, may be decreased by glucocorticoids, but primarily only in the early stage of disruption

Front 522

what are the endocrine effects of glucocorticoids?

Back 522

-suppression of ACTHA, TSH and GH
-lowered concs of thyroid hormones and cortisol

Front 523

How do glucocorticoids reduce inflammation?

Back 523

-antagonize toxins and kinins reducing the resultant inflammation

Front 524

REMEMBER!! The most beneficial effects of glucs are

Back 524

nonspecific, ie: they have effects regardless of intitial insult

Front 525

What are some therapeutic usages of glucs?

Back 525

1. physiological replacement
2. intensive short term and shock
3. anti-inflammatory and antiallergy
4. immunosuppressive
5. chronic palliative: decrease disease expression, but don’t cure
6. special: alternate day therapy

Front 526

REMEMBER: there is not right dose of glucocorticoid in a given clinical situation:

Back 526

however you should use guidelines that are available.

Front 527

What is an endocrine side effect of gluc therapy?

Back 527

-iatrogenic cushing’s adrenal insufficiency on withdrawal unmasking or exacerbation of diabetes, PU/PD, hypertension

Front 528

How can glucs have an effect on the CNS?

Back 528

-behavioral changes and decrease the seizure threshold

Front 529

How can glucs cause hepatopathy?

Back 529

-caused by an increase in glycogen

Front 530

How can glucs cause ulcers?

Back 530

-blocking PGE= which is important for mucus production in the stomach

Front 531

If you give glucs to a growing animal, what should you worry about?

Back 531

-growth retardation; catabolism

Front 532

Why do glucs cause osteoporosis?

Back 532

-inhibit calcium absorption from GIT

Front 533

What it the major dermatological effect of the use of glucs?

Back 533

-poor wound healing

Front 534

How can glucs immunologically cause problems?

Back 534

-they can exacerbate infectious disease

Front 535

What are the two chemical forms of glucs?

Back 535

-steroid base acitivity
-ester

Front 536

What does the steroid base of glucs determine?

Back 536

1. anti-inflammatory potency
2. mineralcorticoid potency
3. duration of action once at site of action

Front 537

Ester forms of glucs determine?

Back 537

1. duration of action
2. mode of administration (ie water/lipid solubility)

Front 538

what are some examples of gluc ester forms?

Back 538

1. phosphate and hemisuccinate
2. acetate, diacetate, tebutate
3. acetonide
4. pivalate

Front 539

Ability of a formulation to suppress the HPA axis is determined by?

Back 539

1. dose
2. potency of base
3. duration of action of formulation (base + ester)

Front 540

What are some applications for parenteral glucs?

Back 540

emergency situation: hemorrhagic shock, analphylaxis

Front 541

What is a gluc with rapid onset that is cheap and commonly use?

Back 541

-dexamethasone

Front 542

What is a gluc with slow onset but long duration?

Back 542

-triamcinolone acetonide
-methylprednisolone acetate (depo-medral)

Front 543

What should you always do before you use steroids on an animal?

Back 543

-diagnose what there problem is first! Then use steroids if you want

Front 544

Why should you always get a diagnosis before you administer steroids?

Back 544

-steroids are not a cure they are just masking signs

Front 545

How do you determine the dose of glucocorticoids?

Back 545

you have to use trial and error to determine the dose

Front 546

why should you use intermittent glucocorticoids where you can?

Back 546

-to avoid shutting down the HPA axis as much as possible

Front 547

You have a dog that comes in with an infectious disease on its back leg and you think you want to use glucocorticoids in conjunction with antibiotics, can you?

Back 547

-you should avoid using steroids in the presence of infectious disease

Front 548

why should you avoid using glucocorticoids in diabetic patients?

Back 548

-because glucocorticoids are gluconeogenic, so they will cause more glucose production and the animal is already in a state of too much glucose with too little insulin, so you make it worse

Front 549

why should you avoid glucocorticoids in epileptic patients?

Back 549

-it lowers the seizure threshold?

Front 550

Why are steroids with mineralcorticoid activity contraindicated in heart failure and renal disease?

Back 550

-mineralcorticoids cause the retention of Na which then causes retention of water which is contraindicated in heart failure and renal disease

Front 551

what questions should you ask before you administer glucocorticoids?

Back 551

1. how serious is the underlying disorder
2. how long will therapy be required
3. is the patient predisposed to any of the complications of steroid therapy
4. what is the anticipated steroid dose
5. which glucocorticoid preparation should be used?
6. have other methods of therapy been used? (ie to min the dose, to min side effects)
7. is an alternate day regimen indicated

Front 552

what are the four classes of therapeutic usages of glucocorticoids?

Back 552

1. physiologic replacement
2. intensive shorterm and shock
3. anti-inflammatory and antiallergy
4. immunosuppressive

Front 553

which glucocorticoid therapy would you use in addison’s disease? Why?

Back 553

which glucocorticoid therapy would you use in addison’s disease? Why?
-physiological replacement-“low dose”
-addison’s is an adrenal dysfunction, so you have mineral corticoid and glucocorticoid therapy needed

Front 554

why should you provide an animal with physiological doses of glucocorticoids when you are weaning them off of them?

Back 554

why should you provide an animal with physiological doses of glucocorticoids when you are weaning them off of them?
-bc physiologic doses have iatrogenic HPAA suppression

Front 555

If you take the adrenal gland out of a dog, what dose of glucocorticoids should you use?

Back 555

If you take the adrenal gland out of a dog, what dose of glucocorticoids should you use?
-physiological dose:
Hydrocortisone: 0.2 to 1 mg/kg
Prednisone: 0.1 to 0.2 mg/kg

Front 556

Why can you give a smaller dose of prednisone than hydrocortisone or cortisone for physiologic dose?

Back 556

Why can you give a smaller dose of prednisone than hydrocortisone or cortisone for physiologic dose?
-prednisone is more potent than hydrocortisone or cortisone (look back at the chart to see what is more potent than another)

Front 557

How often and when should you administer glucocorticoids in physiologic dose therapy?

Back 557

-once daily, usually in the AM

Front 558

If you have an addisonian patient that is brought in because it has just been hit by a car and you want to take xrays and then maybe do surgery, what should you keep in mind before you do all of those things?

Back 558

-you should give exogenous glucocorticoids first because this animal can’t deal with stress at all, otherwise it might die
-you should give 2-5 tiems the basal dose in moderate stress
-5-20x in the severe stress

Front 559

Glucocorticoids are gluconeogenic, so why do we find increse glycogen in the liver of animals on glucocorticoids for a long time?

Back 559

-it is a way to store glucose-glucose gets phosphorylated in the liver and travels to areas that need it (ie the brain)
-If you make too much glucose, then you have more insulin and that stimulates glycogen synthesis in the liver. That is why we have glycogen formation. Only works if there is an excess and insulin is high.

Front 560

What are lazaroids?

Back 560

-the metabolic effects of glucocorticoids are minimized with this type of glucocorticoids

Front 561

What are “soft” steroids?

Back 561

-loteprednol etabonate: developed on the basis of the retrometabolic drug design
-used in ophthalmology
-ciclesonide: pro-drug soft steroid used for asthma and hayfever

Front 562

Why would you use intensive short term and shock therapy with glucocorticoids?

Back 562

-don’t see long term side effects
-beneficial effects of glucocorticoids in all forms of shock are still controversial

Front 563

when you use intensive shock therapy with glucocorticoids, what should you be sure to do with the glucocorticoid administration?

Back 563

-give aggressive fluid therapy and in suspicion of endotoxic shock include bactericidal broad spectrum antibiotic, regardless of whether steroid therapy is chosen or not

Front 564

when would you give antiiflammatory and antiallergy therapy of glucocorticoids?

Back 564

-as symptomatic therapy of pruritic dermatoses
-allergic pulmonary disease
-allergic gastroenteritides

Front 565

You must remember this! What is the dose anti-inflammatory dose of prednisolone?

Back 565

-1.1 mg/kg divided by BID (meaning you give half the dose in the AM and the other half the dose in the PM)

Front 566

what is the antiiflammatory maintenance dose of glucocorticoids?

Back 566

-.55-2.2 mg/kg every 2 days

Front 567

remember: what is a rule of thumb for the anti-inflammatory dose of glucocorticoids in cats?

Back 567

-double the dose

Front 568

why should you use caution when you give glucocorticoids to obese cats?

Back 568

-you could very easily make them diabetic

Front 569

What is the dosage for injectable methylprednisolone acetate in dogs?

Back 569

-1.1 mg/kg SQ or IM for 1-3 weeks

Front 570

Before you give prednisolone, dexamethasone, triamcinolone or betamethasone what should you consider?

Back 570

-that they will last a long time and after you give them you have to deal with all of the PU/PD and other side effects that come along with glucocorticoids

Front 571

when would you use immunosuppressive therapy with glucocorticoids?

Back 571

-in immune mediated thrombocytopenia
-in autoimmune hemolytic anemia
-other autoimmune disease

Front 572

what is the induction dose for immunosuppressive therapy using glucocorticoids?

Back 572

-induction: 2.2-6.6 mg/kg prednisolone divided BID until you get the desired effect (this is why you have to consider what effect you are looking for before you give glucocorticoids)

Front 573

what is the maintenance dose of immunosuppressive therapy using glucocortoids?

Back 573

-1.2 to 2.2 mg/kg for 2 days in the AM (which is alternative day therapy)

Front 574

what is a downside to dexamethasone even though it is cheap?

Back 574

-you can’t do alternative day therapy because it lasts longer than 1 day (this could be a benefit in livestock though too)

Front 575

How long should you use the highest dose possible of glucocorticoids?

Back 575

-use highest does for a period until signs abate, then decrease in increments
-keep decreasing the dose until you get to 1.1 mg/kg of prednisolone (which is the anti-inflammatory dose) on alternate day therapy; few long term side effects this way and rarely need to decrease them further

Front 576

when should you discontinue therapy with glucocorticoids?

Back 576

2-3 months in remission; otherwise more likely for the situation to recur

Front 577

why would you have to increase the dose of glucocorticoids?

Back 577

-in long term use bc of tachyphylaxis

Front 578

when would you use chronic palliative therapy of glucocorticoids?

Back 578

-with chronic arthritis; hip dysplasia

Front 579

When do you give glucocorticoids for chronic palliative therapy?

Back 579

-dose may be intermittent or on ADT basis

Front 580

why would you not want to withdraw glucocorticoids erratically?

Back 580

-it may lead to “pseudorheumatism”

Front 581

What can you use on “off” days of glucocorticoid therapy for chronic palliative therapy?

Back 581

use nonsteroidal analgesics on off days

Front 582

what are the advantages of alternative day therapy (ADT)?

Back 582

-less suppression of HPAA side effects decrease: this means that animals can still respond to stress

Front 583

If the ADT is short you may go to what kind of schedule?

Back 583

-no therapy on the off day

Front 584

If you are using ADT and you notice that the animal is still having signs on the off day, what can you do?

Back 584

-supplement with replacement dose on those dose, or add nonsteroidal therapy

Front 585

If relief is not maintained by ADT, what can you do?

Back 585

give single dose in the AM

Front 586

What are some common pitfalls of ADT?

Back 586

1. using ADT as primary therapy
2. using long acting steroid preparations
3. changing too quickly from daily Rx to ADT at high steroid doses
4. failure to use supplemental therapy

Front 587

what are some signs of glucocorticoid withdrawal?

Back 587

1. dullness
2. mental depression
3. increased fatiguability
4. incoordination
5. unthriftiness and weight loss
6. loose stools
7. behavioral changes

Front 588

Normal animal we would like an see an increase in cortisol after it has been given ACTH.

Back 588

If you have an addisonian animal or one that you have made to have atrophied adrenals, then you should see the hypoadrenocorticism situation…there would be no stimulation after you give ACTH. If you want to use this animal in surgery, then this will tell you that you need to help the animal out with the stress associated with the surgery. If an addisonian animal you would get no response from ACTH.

Front 589

What are considered to be mild stresses?

Back 589

-anethesia, minor illness, minor surgery, visit to the vet

Front 590

what are considered to be severe stresses?

Back 590

-severe illness, major surgery

Front 591

Remember with all topical therapy,

Back 591

Remember with all topical therapy, regardless of what type of steroid you use regardless of acute or chronic conditions you still affect the HPA axis just as if you gave it parenterally or orally.

Front 592

Does intra-or sublesional admin of glucocorticoids have systemic effects?

Back 592

-yes

Front 593

Does intraarticular administration of glucocorticoids have systemic effects?

Back 593

-yes and can cause steroid arthropathy

Front 594

Are glucocorticoids used for ophthalmology?

Back 594

-yes. Frequently used. Topical or subconjunctival preparations are used
-used in therapy for retinitis, choroiditis, optic neuritis, orbital cellulites

Front 595

In the cushanoid animal: microadenomas that will lead to an increase in ACTH secretion
In those cases what would you see in an ultrasound of the abdomen?

Back 595

-ACTH stimulates the adrenal glands and thus an increase in the size of the adrenal glands and an increase in cortisol. ACTH is a trophic hormone=it leads to growth
-This is called "pituitary dependent cushings"
-if you have a problem in the adrenal glands, what would you expect?
-the other adrenal would atrophy
-what would you expect to happen at the pitutitary level?
-very little ACTH
If you have a tumor in both adrenal glands then you would have two enlarged adrenals, but they wouldn't be bilaterally symmetrically enlarged-this means it has to be an increase in ACTH secretion
Majority of ACTH dysfunctions are pituitary dependent

Front 596

What is the etiology of a cushanoid animal?

Back 596

pituitary micro- or macroadenomas; carcinomas

Front 597

what species most commonly is afflicted with hyperadrenocorticisim aka cushings?

Back 597

-dogs, it is rare in cats

Front 598

what are some historical findings of animals with cushings?

Back 598

-PU/PD
-Polyphagia
-Weight loss
-lethargy

Front 599

Explain why you would expect to see PU/PD, polyphagia, weight loss, and lethargy in a cushings animal?

Back 599

-PU/PD: you have an animal with too much cortisol just like if you were giving exogenous glucocorticoids which leads to diabetic like effects
-polyphagia: the animal is not responding to insulin, just like diabetic so it is eating more to try to keep up, also glucocorticoids would be catabolic, so the animal is mobilizing lots of fat and protein the body
-weight loss-basically the same as above
-lethargy: the animal has high cortisol levels

Front 600

Why do you see potbellied abdomen in cushings?

Back 600

-

Front 601

What is cushing’s in cats associated with?

Back 601

-spontaneous alopecia
-skin falls apart when you touch it; it is so fragile it will break

Front 602

Most cushingoid cats also have?

Back 602

-diabetes mellitus

Front 603

what does cortisol do to insulin?

Back 603

-it antagonizes it which leads to insulin resistance

Front 604

when you do an ACTH test on a cushingnoid animal, what would you expect to see?

Back 604

-a hyperresonse to ACTH
-the post adrenal cortisol levels are still very high

Front 605

What do we use the ACTH test for?

Back 605

-to assess how good our treatment for cushings it working

Front 606

what are the steps to performing an ACTH test?

Back 606

-take a blood sample
-give an IV injection of ACTH
-wait 60 minutes
-take another blood sample and measure cortisol levels

Front 607

What are the surgical treatment options for cushings in dogs and cats?

Back 607

-cats: surgical removal of adrenal glands or pituitary mass
-dogs: mostly medical; surgical treatment is same as in the cat

Front 608

What are the four drugs that can be used to treat hyperadrenocortical animals?

Back 608

1. op’DD (lysodren)
2. ketoconazole
3. L-deprenyl
4. trilostane

Front 609

How does lysodren work?

Back 609

-it causes selective necrosis of the zona fasciculate and reticularis of the adrenal cortex

Front 610

Does op’DDD effect the zona glomerulosa?

Back 610

-rarely

Front 611

Do you get mineralicorticoid deficiencies with op’ddd?

Back 611

-rarely

Front 612

why do we generally start an animal off with getting 50mg/kg/day of op’ddd?

Back 612

-it is a “loading period”: it decreases the capacity of the adrenal cortex to a degree where cortisol secretion becomes minimal and the animal is unable to respond to exogenous ACTH with an increase in cortisol secretion

Front 613

How do you know your loading dose of op’ddd has been successful?

Back 613

-do your ACTH stimulation test after 7 to 10 days
-you would want to see no response!
-your baseline cortisol should be low and your post ACTH cortisol should also be low. That means you have been successful

Front 614

After you have given a loading dose of op’ddd why should you just give it once weekly?

Back 614

-bc during your loading period you do not kill all of the cells in the adrenal gland and you want to keep them suppressed an in line after the initial time to knock them back

Front 615

How can you create a diabetic when you are giving op’ddd?

Back 615

As you take away the corisol with your treatment, you take away the insulin resistance factors bc cortisol counteracts insulin, so if you have the animal on insulin, you probably have to decrease the insulin day by day so the animals doesn't get hypoglycemic after/during treatments.
-basically serum cortisol levels decrease with op’ddd and the animal becomes more sensitive to insulin

Front 616

How do you know you have had a successful loading dose of op’ddd?

Back 616

-the ACTH stimulation test indicates little or no response to the drug and cortisol concentrations are low-now the same dose is given once weekly only

Front 617

How can you reduce the side effects of a loading dose of op’ddd?

Back 617

-divide the dose and give it over a 2 day period

Front 618

what is an unsuccessful loading period with op’ddd?

Back 618

-if after the loading period the ACTH stimulation test indicates a normal or exaggerated response to treatment, then op’ddd is continued and the dog is retested at 5 day intervals until you get the desired response
ACTH still shows an increase in cortisol still. Then what? Increase the dose, increase by 25% initially, give another 5 days then do another ACTH, then do another ACTH test then increase to 50% and continue on. This can get expensive though. Treat until you see your response, then take that dose that you have been giving daily and then give that dose once per week.

Front 619

What are some side effects of treatment with op’ddd?

Back 619

-lethargy, weakness, vomiting and anorexia
These side effects are the same as animal with mineralicorticoid deficiencies. Any animal that you send home on OP prime DDD, that owner should have glucocorticoids on hand. If they see side effects they should give a small amount of glucocorticoids before they come in to see you. You don't want an addison's animal to come into your practice and not be able to handle stress (they have too little or no cortisol)
-if you get a previously cushanoid, no well controlled animal, cannot respond to stress. Don’t do anything to them without giving them glucocorticoids so they can cope with the stress of being in your office!

Front 620

In some dogs treated with op’ddd, the use of what other drug can be beneficial, but may seem counter intuitive?

Back 620

-maintenance therapy with glucocorticoids becomes necessary to minimize or eliminate adverse effects of the drug
-if adverse signs persist, then the drug should be evaluated for other medical problems

Front 621

If you need to give a dose of glucocorticoids after you have given op’ddd, what dose should you give?

Back 621

-physiological replacement dose ie: 0.2 mg/kg/day for prednisolone and 1.0 mg/kg/day of cortisone
Give the physiological replacement dose if you need to give glucocorticoids. Better to divide it BID
-doses are different bc of the difference of potency of the drugs

Front 622

Will some animals that were previously cushingnoid still need glucocorticoids the rest of their lives?

Back 622

-yes. And some dogs do well without anything. It just depends

Front 623

All dogs that have been on op’ddd need what in times of stress?

Back 623

-5-10 times the physiological replacement dose in times of stress

Front 624

You just treated a dog with op’ddd and you are sending it home, what MUST you make sure that owner has in her hand when she leaves?

Back 624

-glucocorticoids in case the animals starts to be addisonian
This is a toxic treatment. Somebody should call these owners on a daily basis and ask how the dog is doing that day.

Front 625

How often should you re-evaluate your dose of op’ddd in a dog?

Back 625

-every 3 months

Front 626

When a dog comes in after 3 months for a re-evaluation on its cushingnoid status, but tests should be run?

Back 626

ACTH
-complete physical exam, CBC, chemical profile and urinalysis

Front 627

If an animal comes in for re-evaluation of its cushingnoid status after 3 months and you do an ACTH test and see that cortisol levels are __________, then the animal can be examined very __________.

Back 627

-see cortisol levels are very, very low or don’t respond at all then see the animal every 6 months

Front 628

What should you keep in mind after you have treated a dog with op’ddd?

Back 628

-it is not a cure. You are not treating the underlying cause for increased amounts of ACTH and thus cortisol. You also must keep in mind that you did not kill all adrenal cells, so there are still come that can come back, some animals can become resistant to op’ddd and you must then re-evaluate
You have not eliminated the high ACTH level. You have taken the negative feedback away with your treament so you ACTH can come back an stimulate the cells that are remaining and then cortisol levels can go sky high again.

Front 629

If an animal goes into remission for cushings after op’ddd treatment, what should you do?

Back 629

-“loading” again with op’ddd for 3-10 days
-in some cases you might have to increase the dose of op’ddd by more than 50% to get a response

Front 630

What is ketoconazole?

Back 630

-antifungal drug that does inhibit steroid and sterol synthesis in animals. It needs to be given daily, but it will inhibit steroid synthesis. You can use this drug as an alternative to the other drugs. Anorexia and vomiting can occur with this and a hair coat change can occur.

Front 631

How should administer ketoconazole?

Back 631

-orally with food, divide dose BID
-it is very expensive
-can cause anorexia and vomiting

Front 632

Can you reverse the inhibition of steroidogenesis as a result of ketoconazole administration?

Back 632

-yes

Front 633

when you would want to use ketoconazole?

Back 633

-in dogs that have adverse effects from op’ddd
-dogs showing resistance to drugs
-before surgery
-not effective in cats

Front 634

why would you want to give ketoconazole before a surgery?

Back 634

-you don’t want to do surgery on a cushings animal because remember high cortisol means that you don’t heal well

Front 635

what is L-deprenyl therapy for PDH?

Back 635

-This drug has been approved by FDA for cushings but is not very effective
L-deprenyl is metabolized to amphetamine which means the dogs is running around and feeling better, but it doesn't affect cortisol very effectively.

Front 636

How does Trilostane work?

Back 636

-competitively inhibits the enyme 3 beta hydroxysteroid dehydrogenase
-few develop clinical signs and biochemical evidence of hypoadrenocorticism

Front 637

With trilostane administration would you expect to see an increase, decrease or no change in the size of the adrenal glands?

Back 637

Will be increased in size because you have not changed ACTH which is a trophic hormone. So you will actually see larger adrenals and they will look lumpy.

Front 638

After you give trilostane, how often do you want to monitor for ACTH stimulation test?
-every 4-6 hours post pill

Back 638

Don’t want to see a complete suppression, but you do want to see a decrease for sure.
With Op prime DDD you want to see no increase. With both you want to see a dramatic decrease. Monitor serum K values (they increase mildly and have no clinical significance)-but if you see a dramatic increase of K associated with a dramatic decrease in Na, then you know you have an emergency on your hands.

Front 639

Is efficacy higher in trilostane or lysodren?

Back 639

-lysodren (85%), trilostane (70%)

Front 640

what are some side effects of trilostane?

Back 640

-lethargy
-decreased appetite
-10% mild hyperkalemia
-addisonian crisis uncommon

Front 641

In the adrenal cortex, what are the layers and what is made in each?

Back 641

-glomerulosa: mineralicorticoids
-fasciculata: glucocorticoids, sex steroids (few)
-reticularis: glucocorticoids, sex steroids (many)

Front 642

What do mineralicorticoids do?

Back 642

-increase reabsorption of Na from urine, sweat, GI tract
-thus causing the expansion of ECV

Front 643

What is Addison's disease anyway?

Back 643

Let's start with a brief overview of Addison's disease. It is the common name for hypoadrenocorticism, or adrenal insufficiency. It is a disease with symptoms that are common in many other ailments, making diagnosis difficult and sometimes a process of elimination. But once Addison's is correctly diagnosed, a properly treated dog can live a normal active life.

Front 644

Regulation of aldosterone synthesis occurs through?

Back 644

-renin via rennin-angiotensive II
-rise in plasma K
-ACTH

Front 645

What are the signs of addisons disease?

Back 645

-increased sodium loss
-increased K and H ion retention
-dehydration, hypotension, hemococentration, cardiovascular disturbances
-hypo or hyperglycemia

Front 646

When you run an ACTH test what should the outcomes be in normal and abnormal?

Back 646

-Normal stimulation: post ACTH 6-15 ug/dl
-animals with hypoadrenocorticism (addisons): post ACTH results <2ug/dl in 98%

Front 647

Do you get a response in iatrogenic cushingoid animals when you do an ACTH test?

Back 647

-no

Front 648

Do you get a response when you do an ACTH test on secondary hypoadrenocorticism animals?

Back 648

-no

Front 649

What does the term addisonean mean?

Back 649

-it means you are both mineralicorticoid and glucocorticoid deficient

Front 650

If you don’t have desoxycorticosterone pivalate on your shelf, what can you give?

Back 650

-give fluid (w/o Na) and glucocorticoids that would also have mineralicorticoids too, these animals will survive and get the pivalate.
How would you monitor for this?
-you have electrolyte changes (high K is toxic to the heart)
-you would monitor an animal with pivalate by measuring electrolytes in a blood samples. In some animals it will last 18 days before you have to inject again and in some animals it will last 40 days. Have the owner come back in 20 days, check electrolytes again.

Front 651

Chronic management of hypoadrenocorticism (Addison’s disease):

Back 651

-Tx: pivalate, prenisone or prednisolone
-give the physiological dose unless the animal is stress, then you need to give them more so they can cope with stress

Front 652

With ADT what two steroids can you use?

Back 652

-cortisones or prednisones

Front 653

Why do you commonly see prednisolones used in dogs and cats?

Back 653

-because in smaller animals it is easier to dose prednisolone

Front 654

How is insulin released from the beta cells in the pancreas?

Back 654

as proinsulin

Front 655

What is the structural makeup of insulin?

Back 655

-A chain and B chain at equimolar ration produce peptide the A and B chain are held together by a disulfide bond

Front 656

Is insulin anabolic or catabolic?

Back 656

-anabolic. It tries to make things ie. Glucose uptake, amino acid uptake, DNA synthesis, inhibits the catabolic things like gluconeogenesis and protein breakdown

Front 657

Which type of diabetes do we commonly see in animals and what is going on with this type?

Back 657

-type I, there is an absolute deficiency in insulin and destruction of beta cells which is part of an autoimmune problem, thus you have to give back what the animal is missing=insulin

Front 658

In Type I diabetics if you do a glucose stimulation test, what would you expect to see?

Back 658

no rise in insulin with the administration of glucose
-normally beta cells should immediately respond with an increase in insulin

Front 659

What is the pathology of diabetes mellitus in the dog?

Back 659

-degeneration of islets or no islets
-vacuolarization/glycogen deposits
-lymphocytic infiltration of islets is rare

Front 660

when do animals get type II diabetes?

Back 660

-with obesity
-relative deficiency of insulin initially
-defect in insulin secretion-the biphasic response is NOT normal
-insulin resistance!!! Ie tissues do not respond to insulin appropriately
-increased glucose output in the liver but decreased glucose uptake by tissues
-if insulin receptor doesn’t work right, then decreased glucose uptake into tissues

Front 661

Other types of diabetes can be associated with what conditions?

Back 661

-endocrinopathies
-pancreatitis
-associated with drugs=glucocorticoids

Front 662

What are four risk factors for diabetes in cats?

Back 662

1. age
2. obesity
3. neutering
4. gender

Front 663

Which form of diabetes are cats likely to have?

Back 663

-type II

Front 664

With most dogs and cats, you should treat with____________ because we don’t have other good treatments available.

Back 664

-insulin

Front 665

What are some of the signs upon clinical presentation with of diabetic dogs and cats?

Back 665

-PU/PD, polyphagia/anorexia, weight loss/obesity, weakness, vomiting, cataract in the dog, neuropathy (pantigrade stance in the cat)

Front 666

What are the pharmacological treatment options in the dog and cat for diabetes?

Back 666

-Insulin for both!
Others: dog=acarbose, cat=glipizide, acarbose

Front 667

How does acarbose work?

Back 667

-delays glucose uptake after eating, but is more for people, not animals, bc glucose in animals after eating does not rise very quickly or very much like it does in humans

Front 668

When you are considering insulin use, what are some of your options?

Back 668

-insulin preparations, dosage, time of injection, time of feeding, type of food, amount of food

Front 669

If you give insulin to a starving animal would you expect to see an increase, decrease or no change in glucose levels?

Back 669

-glucose wouldn’t really change bc they have no glucose to take up

Front 670

If you were to feed a starving animal and give it insulin, would you expect to see an increase, decrease or no change in glucose levels?

Back 670

-increase in glucose and it would stay high

Front 671

What are the two different strengths of insulin and what do they mean?

Back 671

-U 100=means 100 units/mL
-U 40=means 40 units/mL

Front 672

What is the only type of insulin that can be given IV?

Back 672

-regular insulin (human recombinant insulin)

Front 673

If you have a diabetic animal that is not eating or is vomiting, what insulin would you want to use and why?

Back 673

-short acting=human recominbant insulin (regular) it can be given IV

Front 674

what are the three main sources of insulin?

Back 674

1. recombinant human insulin (regular, neutral protamine hagedorn)
2. recombinant human insulin analogues (mutated insulins)
3. animal source insulins

Front 675

With respect to efficacy, is there really any difference between the different types of insulin?

Back 675

-no. every animal reacts slightly differently to the insulin given
-only exception is if you have a sick diabetic, use regular insulin-that is the recombinant human insulin (regular)

Front 676

How can the duration of action of insulins be defined?

Back 676

-short acting (human R) and all the rest. There is really no intermediate acting and long acting bc it just depends on the animal

Front 677

If you give other insulins IV, besides regular insulin, what can happen?

Back 677

-the proteins in those can lead to anaphylactic response

Front 678

What are the two types of human recombinant insulins?

Back 678

-NPH, and PZIR

Front 679

what makes a mutated human recombinant insulin?

Back 679

-one or two AA have been changed

Front 680

If you have a diabetic animal that is still eating and not sick, what insulin would you give?

Back 680

-NPH (neutral protamine hagedorn)

Front 681

Glargine has become popular for use in what species?

Back 681

-cats

Front 682

What makes glargine different than all other insulin preparations?

Back 682

-no proteins in the buffer, aqueous, clear solution
-it forms micro-precipitates when injected SQ
-the microprecipitate formation and slow absorption are dependent on the pH of the glargine, so it cannot be mixed with other insulins or DILUTED!

Front 683

What is the one animal source of insulin that is still available?

Back 683

-pork insulin

Front 684

T/F. The use of pork insulin is much better for very sick diabetic patients bc it is more similar to the kind of insulin that animal would make on its own.

Back 684

-false. Just because it is animal insulin does not mean the animal will respond better to it than to human insulin

Front 685

How often does an owner typically have to give insulin?

Back 685

-twice daily

Front 686

Will an animal die of hyperglycemia?

Back 686

-no. but they will die of hypoglycemia which is why it is important to give insulin

Front 687

What are the recommended initial dose of insulin?

Back 687

-.5 units/kg SQ in dogs
-0.2 to 0.5 units/kg SQ in cats

Front 688

Why should you always start cats at a lower dose of insulin than dogs?

Back 688

-they seem to be more sensitive to insulin than dogs
-Start with this dose (conservative dose), send O home and O needs to know watch dog…why?
Animal might become weak, seizure: hypoglycemia; need to make sure animal eats
Come back after week and do glucose curve (measure glucose in response to insulin)
Takes a week or two b4 see response to insulin, they need to be able to recognize insulin again; that’s why start out w/conservative dose
Animals don’t generally die from hyperglycemia, but do from hypoglycemia

Front 689

All human insulins, w/one exception, need U100 syringes

Back 689

All of insulins on market, one Vetsulin, will have 40 units/mL
This is important b/c if client runs out of U40 syringes that go with the U40 vet formulation, then goes to pharmacy and say need insulin syringes will get U100 synringes and could overdose (if you use u100 syringes instread of u40 you will overdose the animal)

Front 690

Can you dilute insulin?

Back 690

-yes. Use diluent of the company, other diluents change the pharmacokinetics and pharmacodynamics

Front 691

What is the one insulin that you cannot dilute?

Back 691

-glargine insulin

Front 692

If you do an insulin test and plot it out, what should it look like?

Back 692

-like a bowel. Insulin would wear off in the middle and then rise on each eand
-this is why you give it in 12 hour intervals

Front 693

What is it called when you have a fairly rapid decrease in blood glucose and go down to about 50 (hypoglycemic) and then have a rapid rise in blood glucose?

Back 693

-somogyi rebound

Front 694

What is a somogyi rebound due to?

Back 694

-due to counter insulin regulatory hormones-do not want to see this

Front 695

When should you feed an animal relative to insulin injections?

Back 695

-feed them before an insulin injection and feed them the same amount every time. That way you know that you are feeding enough and given enough insulin to have a balanced effect. If you see weight loss in an animal, then this can tell you that your insulin isn’t working bc you know you have been feeding the same amount the whole time.

Front 696

What do you need in blood to counteract the effect of insulin?

Back 696

-glucose

Front 697

What kind of food should you put a diabetic cat or dog on?

Back 697

-cat: high protein, low carb
-dog: nutritionally balanced diet works fine

Front 698

What are the three major classes of oral medications for diabetic animals?

Back 698

1. thiazolidinediones
2. sulfonylureas-don’t work in animals
3. alpha-glucosidase inhibitors-aren’t needed in animals

Front 699

What are the two oral treatment options for the diabetic cat?

Back 699

1. glipizide
2. acarbose

Front 700

Oral antidiabetics such as glipizide can only be used in what species?

Back 700

-cats, not dogs

Front 701

What are some side effects of glipizide?

Back 701

-vomiting, hypoglycemia, increased liver enzymatic activity

Front 702

How does glipizide work?

Back 702

Binds to Beta receptor-->leads to secretion of insulin
w/insulin, another hormone amylin is secreted
If hyperstimulate B cells w/this drug, then what you are doing is taking normal islet (like next slide) and make it into the next next slide

Front 703

How does thiaxolidinedione have its effects?

Back 703

-changes glucose and lipid metabolism
-increase insulin sensitivity aka sensitizes tissue to insulin

Front 704

If insulin is chronically given as a slight overdose, will you see an increase, decrease or no change in weight of the diabetic animal?

Back 704

-increase in weight because the higher level of insulin drives more nutrients into cells where they are stored (primarily as fat).

Front 705

If there is not enough insulin being given to a diabetic animal, will you see an increase, decrease, or no change in the weight of the animal?

Back 705

-decrease. You will see weight loss

Front 706

How can a client treat for hypoglycemia at home?

Back 706

-karo syrup (orally or rectally)

Front 707

How does thiaxolidinedione have its effects?

Back 707

-changes glucose and lipid metabolism
-increase insulin sensitivity aka sensitizes tissue to insulin

Front 708

If insulin is chronically given as a slight overdose, will you see an increase, decrease or no change in weight of the diabetic animal?

Back 708

-increase in weight because the higher level of insulin drives more nutrients into cells where they are stored (primarily as fat).

Front 709

If there is not enough insulin being given to a diabetic animal, will you see an increase, decrease, or no change in the weight of the animal?

Back 709

-decrease. You will see weight loss

Front 710

How can a client treat for hypoglycemia at home?

Back 710

-karo syrup (orally or rectally)

Front 711

2 reasons for using L-T4 rather than T3 for treatment of hypothyroidism?

Back 711

1. transfer of T4 to T3 is regulated process in each tissue, so we really don't have control over that. Each tissue makes the decision about how much hormone they make
2. Because there are two deiodinative pathways of metabolism of thyroid hormone, T4 can go through either pathway:
a. it can go through the 5-prime deiodinase: ID I or ID II
b. it can go through the 5-deiodinase: ID I or ID III pathway
-this way the body can still decide which tissues need more T3 and which ones don't

Front 712

3 reasons for the high dosage requirement of for T4 in dog vs. man?

Back 712

1. glucuronidation: most important in liver. protects animal from oral overdosages
2. human elimination of thyroid hormone is much slower than dogs
3. bioavailability of most T4 products is low in the dog and variable

Front 713

Key clinical and biochemical ways to monitor thyroid replacement therapy in dog. Describe 2 endocrine tests with recommended sampling regimens for serum monitoring

Back 713

1. Serum T4: monitor once daily or twice daily
2. Monitoring TSH: evidence for body's response

Front 714

Compare and contrast the mechanisms of the antithyroid drugs methimazole, propylthiocuracil, and radiocontrast agents like iopanoic acid

Back 714

methimazole: inhibits thyroidal thyroid peroxidase enzyme
carbimazole: prodrug: less GI irritation
propylthiouracil: causes AIHA and ITP
radiocontrast agents:

Front 715

2 reasons for using L-T4 rather than T3 for treatment of hypothyroidism?

Back 715

1. transfer of T4 to T3 is regulated process in each tissue, so we really don't have control over that. Each tissue makes the decision about how much hormone they make
2. Because there are two deiodinative pathways of metabolism of thyroid hormone, T4 can go through either pathway:
a. it can go through the 5-prime deiodinase: ID I or ID II
b. it can go through the 5-deiodinase: ID I or ID III pathway
-this way the body can still decide which tissues need more T3 and which ones don't

Front 716

3 reasons for the high dosage requirement of for T4 in dog vs. man?

Back 716

1. glucuronidation: most important in liver. protects animal from oral overdosages
2. human elimination of thyroid hormone is much slower than dogs
3. bioavailability of most T4 products is low in the dog and variable

Front 717

Key clinical and biochemical ways to monitor thyroid replacement therapy in dog. Describe 2 endocrine tests with recommended sampling regimens for serum monitoring

Back 717

1. Serum T4: monitor once daily or twice daily
2. Monitoring TSH: evidence for body's response

Front 718

Compare and contrast the mechanisms of the antithyroid drugs methimazole, propylthiocuracil, and radiocontrast agents like iopanoic acid

Back 718

methimazole: inhibits thyroidal thyroid peroxidase enzyme
carbimazole: prodrug: less GI irritation
propylthiouracil: causes AIHA and
ITP
Radiocontrast agents:
a. iopanoic acid: T3 falls and T4 stays the same
b. iodinated radiocontrast dyes:inhibit both type I and type II peirpheral tissue prime deiodinases

Front 719

3 major side effects of methimazole in cats, and list pharmaceutical stragegies which have been attempted to reduce these effects?

Back 719

-GI effects appear more limited via both NOT avoided by TD route
-no reduction in side effects of neutropenia, hepatotoxicity, or facial excoriations
-questions about PLO preparation and reproducibility
-ruling out some oral ingestion in poorly observed clinical cases is difficult

Front 720

Def opiates:

Back 720

-alkaloids derived from opium including morphine and codeine

Front 721

Def opioids?

Back 721

-all naturally occuring and synthetic compounds which act as agonists or antagonists at opioid receptors

Front 722

Def narcotic?

Back 722

-drug capable of inducing sleep (ie narco-leptic)
-now used in legal rather than pharm context to refer to a variety of drugs of abuse

Front 723

Describe anatomical sites of central nervous system inhibition and one peripheral site of inhibition of pain perception by opioids.

Back 723

-NSAIDs work in periphery
-opioids interact at the site of transmission neurons and are important at stimulating the inhibitory pathays through the presynaptic pathways. Opioids can suppress the perception of pain by inhibiting the stimulatory pathways

Front 724

list three families of opioids and three opioid receptor subtypes which have been molecularly cloned.

Back 724

opioid families: enkephalin, endorphins, and dynorphins
opioid receptor subtypes:
mu, kappa, delta