Pharm Exam 3

Front 1

Objs of neoplastics

Back 1

Inc patient survival time
Improve quality of life
Dec tumor size
Dec/prevent metastasis

Front 2

Uses of chemotherapy

Back 2

Adjunct to surgery/radiation or sole therapy
Must balance with toxicity to cancer cells vs. normal cells

Front 3

Chemotherapy decisions based on:

Back 3

Tumor type, malignancy, patient conditions, tumor responsiveness, constraints of owner (money, time, emotional strain)

Front 4

Cell cycle

Back 4

G0=resting
G1=RNA/protein synthesis
S=DNA synthesis
G2= pre-miotic interval
M-mitosis

Front 5

Neoplastic therapeutic index

Back 5

Narrow

Front 6

Calculating neoplastic drug doses

Back 6

Body surface area vs. body weight
Body weight for cats & dogs <10kg
Surface area otherwise

Front 7

Primary toxicities of neoplastics

Back 7

Bone marrow suppression, gi disturbances, alopecia
Acute: gi, allergic reactions/anaphylaxis
Delayed: myelosuppression, tissue damage- alopecia, extravasation
Don't breed animals bcuz neoplastic drugs are teratogenic

Front 8

Neoplastic drugs that cause extravasation

Back 8

Extravasation=tissue necrosis if miss vein
Doxorubicin, vincristine, vinblastine

Front 9

Neoplastic drugs that cause mild bone marrow suppression

Back 9

L-asparine, vincristine

Front 10

Neoplastic drugs that cause severe bone marrow suppression

Back 10

Carmustine, lomustine

Front 11

Reasons for antineoplastic therapy failure

Back 11

Resistance, incorrect dose/drug, slow growing tumor, inability to reach all cancer cells, patient toxicity

Front 12

Reasons for antineoplastic resistance

Back 12

Altered ADME, tumor blood flow, low drug conc., drug inactivation, changes in target receptor, repair of drug induced damage, inc. drug efflux

Front 13

Handling of chemo therapeutic agents

Back 13

Teratogenic
Exposure via: inhalation, ingestion, absorption
Prepare in hood and use chemo pins to prevent exposure

Front 14

Antineoplastics: alkylaying agents

Back 14

Non-cell cycle specific
Alkylation of DNA-->changes structure-->not copied
Types: nitrogen mustards, nitrosureas, platinum coordination complexes

Front 15

Nitrogen mustards

Back 15

Cyclophosphamide, chlorambucil
Moa: alkylation of DNA, forms adducts w/ DNA
Tox: myelosuppression, sterile necrotizing hemorrhagic cystitis(only cyclophosphamide)

Front 16

Nitrosureas

Back 16

Carmustine, lomustine
Moa: form DNA-DNA & DNA-protein adducts
Good for mast cell tumors, crosses BBB bcuz lipid soluble
Tox: severe myelosuppression

Front 17

Platinum coordination complexes

Back 17

Cisplatin, carboplatin
Moa: alkylation of DNA
Tox: nephrotoxicity:
cisplatin->ci in cats
Carboplatin-> less nephrotoxic, can be used in cats, myelosuppression

Front 18

Cyclophosphamide

Back 18

Nitrogen Mustard: alkylation of DNA, forms adducts w/DNA
non-cell cycle specific
Tox: myelosuppression, sterile necrotizing hemorrhagic cystitis

Front 19

Chlorambucil

Back 19

Nitrogen Mustard: alkylation of DNA, forms adducts w/DNA
non-cell cycle specific
Tox: myelosuppression, sterile necrotizing hemorrhagic cystitis(cyclophosphamide only)

Front 20

Carmustine

Back 20

Nitrosureas: form DNA-DNA and DNA-protein adducts
tox: severe myelosuppression

Go to drug for mast cell tumors, lipid soluble-->can cross BBB

Front 21

Lomustine

Back 21

Nitrosureas: form DNA-DNA and DNA-protein adducts
tox: severe myelosuppression

Go to drug for mast cell tumors, lipid soluble-->can cross BBB

Front 22

Cisplatin

Back 22

Platinum coordination complexes: Alkylation of DNA
Tox: nephrotoxicity
CI in cats

Front 23

Carboplatin

Back 23

Platinum coordination complexes: Alkylation of DNA
Tox: nephrotoxicity but less than Cisplatin can be used in cats

Front 24

Antimetabolites

Back 24

Cell cycle specific-->S phase
MOA: inhibit DNA synthesis
Folic Acid analogs, pyrimidine analogs

Front 25

Folic Acid analogs

Back 25

Methotrexate
MOA: inhibit dihydrofolate reductase(pyrimidine synthesis inhibition)
tox: myelosuppression; can precipitate in renal tubules at high doses
other: must be actively transported

Front 26

Pyrimidine analogs

Back 26

5'flurouracil,
MOA: inhibits thymidylate synthase (alters DNA/RNA synthesis)
tox:myelosuppression, crosses into CNS-->tox to cats
cytarabine
inhibit DNA sythesis, bm suppression

Front 27

Methotrexate

Back 27

Folic Acid Analog
MOA: inhibit dihydrofolate reductase(pyrimidine synthesis inhibition)
tox: myelosuppression; can precipitate in renal tubules at high doses
other: must be actively transported

Front 28

5' flurouracil

Back 28

antimetabolites: S Phase specific, pyrimidine analog
MOA: inhibits thymidylate synthase (alters DNA/RNA synthesis)
tox: myelosuppression, crosses into CNS--> toxic to cats

Front 29

Cytarabine

Back 29

antimetabolites: S Phase specific pyrimidine analog-> inhibits DNA synthesis
tox: bm suppression

Front 30

antineoplastics: Natural products

Back 30

variable affects on cell cycle
vinca alkaloids: anti-miotic; inhibit function of microtubules--> M phase specific
Anthracyclines: antineoplastic antibotics-->not cycle specific
Enzymes:G1 specific->deanimates

Front 31

vinca alkaloids

Back 31

Vincristine sulfate, Vinoblastin sulfate
natural antineoplastic
MOA: anti-miotic; inhibit function of microtubules--> M phase specific

tox:myelosuppression, extravasation, perph neuropathy (vincristine)

Front 32

Vincristine sulfate

Back 32

natural antineoplastic: vinca alkaloids
MOA: anti-miotic; inhibit function of microtubules--> M phase specific

tox: mild myelosuppression, extravasation, perph neuropathy (rare, more of a ppl thing)

Front 33

Vinoblastin sulfate

Back 33

natural antineoplastic: vinca alkaloids
MOA: anti-miotic; inhibit function of microtubules--> M phase specific

tox: myelosuppression (more than vincristine), extravasation,

Front 34

Anthracyclines

Back 34

Doxorubicin
natural antineoplastic
MOA:topisomerase inhibitors--> prevents religation of DNA
toxicity: extravasation, dose related cardiotoxicity

Front 35

Doxorubicin

Back 35

natural antineoplastic: Anthracycline
MOA:topisomerase inhibitors--> prevents religation of DNA
toxicity: extravasation, dose related cardiotoxicity

Front 36

Antineoplastic Enzymes

Back 36

L-asparaginase
natural antineoplastic enzyme
cell cycle specific --> G phase
MOA: catalyzes hydrolysis (deanimation) of asparagine
tox: anaphylxis from foreign proteins, minimal myelosuppression

Front 37

L-asparaginase

Back 37

natural antineoplastic enzyme
cell cycle specific --> G phase
MOA: catalyzes hydrolysis (deanimation) of asparagine
tox: anaphylaxis from foreign proteins, minimal myelosuppression

Front 38

Piroxicam

Back 38

NSAID: cyclooxygenase inhibitors but also works as an anti-neoplastic drug against transitional cell carcinoma tumors of the bladder
MOA: unknown, no certain cell phase affected
tox: GI effects; nephrotoxicity

Front 39

Prednisone

Back 39

glucocorticoid used in treatment of cancer

Front 40

Toceranib

Back 40

antineoplastic: multi-kinase inhibitor
phosphorylation important for cell to proliferate--> inhibit kinase so can't be phosphorylated--> tumor cell does not proliferate

Front 41

cancer drugs in food animal

Back 41

Do not use chemotherapeutics in food animal

Front 42

Gastrointestinal drugs:
Alteration = motion sickness

Back 42

Antihistamine or NK-1 blocker
Diphenhydramine (anti-hist)
Maropitant (NK-1 blocker)

Front 43

3 mediators of gastric acid secretion

Back 43

Gastrin, histamine, acetylcholine

Front 44

Antiemetics types

Back 44

Antihistamines, phenothiazines, antiserotonins, NK-1 receptor blockers, other

Front 45

Diphenhydramine

Back 45

Antiemetics and combats motion sickness
MOA: Antihistamine = Blocks histamine-1 receptors
OTC Benadryl causes sedation

Front 46

Acepromazine

Back 46

Antiemetics
Antiemetic
MOA: phenothiazines = dopamine antagonist (Main antiemetics effect) also alpha 1 blocker, hist/musc blocker

Front 47

Ondansetron

Back 47

Antiemetic
MOA: anti-serotonin = 5-HT3 antagonist

Front 48

Marcopitant

Back 48

Antiemetics
MOA: NK-1 receptor blockers (substance P antagonist)
NK=neurokinin, non sedative

Front 49

Metoclopramide

Back 49

Antiemetic, pro-kinetic
MOA: dopamine (D2 agonist); 5HT-4 agonist (stimulate GI motility), 5HT-3 antagonist
Location of kinetic action: stomach, early int

Front 50

pro kinetics CI

Back 50

never use with GI blockage

Front 51

Cisapride

Back 51

pro-kinetic
MOA: 5HT-4 agonist, 5HT-3 antagonist
Loc: entire intestine, not stomach

must be compounded

Front 52

Bethanecol

Back 52

pro-kinetic
MOA: Cholinergic agonist
Loc: entire GI (and elsewhere b/c non-specific so increased side effects!)

Front 53

Lidocaine

Back 53

pro-kinetic
MOA: local anesthetic (sodium channel blocker), but unknown how it increases GI motility
Loc: non-specific
used in house to resotre motility in colic pts

Front 54

Domperidone

Back 54

pro-kinetic
MOA: Dopamine antagonist
Loc: early GI

Front 55

histamine receptors in relation to GI drugs

Back 55

H1 = CTZ (central trigger zone)
H2= stomach

Front 56

CTZ receptors

Back 56

stimulate vomiting

D2, 5HT3, M1, H1, opiod (mu), NK1

Front 57

Acid suppressant drugs

Back 57

3 types: H2 blockers, proton pump inhibitors, antacid (acid neutralizer)

Front 58

H2 blockers

Back 58

Cimetidine (least potent), Ranitidine, Famotidine (most potent)
Acid suppressant
MOA: block H2 receptors (acid producing)--> still leaves 2 pathways to make acid

Front 59

Proton pump inhibitors

Back 59

Omeprazole
Acid suppressant
MOA: Inhbit proton pump at luminal surface of parietal cells; most potent b/c can become trapped in acid environment of parietal cell – continues working even after blood levels have declined
takes a few weeks to work but once inhibited = permanent--> must make new pump

Front 60

Magnesium hydroxide

Back 60

antacid
MOA:neutralizes acidic pH in stomach

Front 61

Misoprosotol

Back 61

protective GI drug
MOA: synthetic PGE-1 analog (prostaglandins protect gastric wall)
used to prevent ulcers w/chronic NSAID use
ADE: abortion

Front 62

Sucralfate

Back 62

MOA: coats stomach, protects from acid; coats edges of ulcers to promote healing, needs acidic env’t to work
very chalky so hard to give
leave a few hours between this drug and the next one given

Front 63

Drugs used to dec GI motility

Back 63

antimuscarinics: atropine, Glycopyrrolate, n-butylscoammonium bromide

Front 64

atropine

Back 64

antimuscarinic: can be given to dec. GI motility. also, antispasmotic

crosses BBB

Front 65

Glycopyrrolate

Back 65

antimuscarinic: can be given to dec. GI motility. also, antispasmotic

does not cross BBB

Front 66

n-butylscoammonium bromide

Back 66

antimuscarinic: can be given to dec. GI motility. also, antispasmotic

often used in horse's w/colics

Front 67

Anti-Diarrheal

Back 67

Opioids
MOA: mu receptor agonists

Front 68

Diphenoxylate

Back 68

Opioids used for anti-diarrheal
MOA: mu receptor agonists

can cross to CNS;
contains atropine to prevent abuse (constipation occurs before high does)

Front 69

Loperamide

Back 69

Opiod: OTC: used for anti-diarrheal
MOA: mu receptor agonists

Front 70

Wheat bran

Back 70

increases fecal bulk and stimulates defecation

used to relieve constipation

Front 71

Mineral oil

Back 71

lubricant used to relieve constipation

Front 72

Bisacodyl

Back 72

stimulant laxative
stimulates GI to relieve constipation

Front 73

castor oil

Back 73

stimulant laxative
stimulates GI used to relieve constipation

Front 74

Magnesium sulfate

Back 74

saline laxative (increases fecal water); also a stimulant laxative
used to relieve constipation

Front 75

Docusate

Back 75

stool softener
used to relieve constipation

Front 76

appetite cntl

Back 76

stimulated by GABA
inhibited by serotonin

Front 77

Mirtazapine

Back 77

appetite stimulant
MOA: anti-depressant

patient dependent: don't always work

Front 78

Cyproheptadine

Back 78

appetite stimulant
MOA: Anti-serotonin & antihistamine

patient dependent: don't always work

Front 79

Benzodiazepenes

Back 79

appetite stimulant
MOA: potentiate effects of GABA

Front 80

Apomorphine

Back 80

Emetics
MOA: Mu agonist, stimulate dopamine receptors in CRTZ

Front 81

how emetics induce vomiting

Back 81

affect vomiting center via vestibular center (H1, M1 receptors) or CTZ

Front 82

Apomorphine

Back 82

emetic
MOA: Mu agonist, stimulate dopamine receptors in CRTZ

Front 83

Xylazine

Back 83

emetics
MOA: alpha 2 agonist
Used mostly in cats, not consistent in dogs

Front 84

3% Hydrogen peroxide, Salt

Back 84

emetics
MOA: direct irritant effects on oropharynx/gastric lining

Front 85

Silymarin

Back 85

milk thistle
holistic remedy to treat liver disease

Front 86

Thyroid functions

Back 86

Maintains metabolic homeostasis
Normal development
Regulates myocardial gene expression
Stimulates metabolism of cholesterol to bile acids
Stimulates synthesis of proteins
Stimulates increased cellular demand for oxygen

Front 87

HPT axis

Back 87

Hypothal releases TRH--> ant. pit releases TSH--> Thyroid releases T3, T4 which inhibit TSH and TRH

somatostatin inhibits ant pit from releasing TSH

Front 88

T3 and T4

Back 88

T3 is active form
T4 is the most stable form
T4 is converted into T3

iodine is necessairy to create Thyroid hormone

Front 89

Thyroid Peroxidase

Back 89

enzyme catalyzing iodine/globlin into T4 and T3

Front 90

5' Deiodinase enzyme

Back 90

catalyzes T4--> T3 in cells

Front 91

Hypothyroidism signs

Back 91

usually dogs
Lethargy, Weight gain, Alopecia, Cold intolerance, Bradycardia, Hypercholesterolemia

Front 92

hyperthyroidism signs

Back 92

usually cats
Weight loss, polyphagia, Hyperactivity, Tachycardia, Vomiting
tachycardia can mask kidney disese

Front 93

Thyroid hormone replacements

Back 93

L-thyroxine (t4)
if not responsive to above use L-triiodothyronine (T3)

Front 94

L-thyroxine

Back 94

T4 used for hypothyroid animals
more physiological (in the body, T4 is released by the thyroid and then converted to T3)
gives better serum balance of T3/T4
less expensive
More consistent in bioavailability

Front 95

L-triiodothyronine

Back 95

T3 given to hypothyroide animals when non-responsive to T4

less desirable than T4 b/c less physiologic, active immediatly

Front 96

Methimazole (MMI)

Back 96

Anti-thyroid
MOA: Blocks incorporation of iodine into thyroglobulin; prevents coupling of iodotyrosil groups; inhibits thyroid peroxidase
ADE: vomiting, GI signs, excoriations, liver toxicity

Front 97

Propylthiouracil (PTU)

Back 97

Anti-thyroid
MOA: Blocks incorporation of iodine into thyroglobulin; prevents coupling of iodotyrosil groups; inhibits thyroid peroxidase
not used much anymore b/c autoimmune prob in cats; also inhibits 5’ diodinase
ADE: vomiting, GI signs, excoriations, liver toxicity

Front 98

Radioactive Iodine

Back 98

Anti-thyroid
MOA: selectively destroys thyroid tissue after take up by thyroid gland
Emits gamma rays and beta particles; most local tissue destroyed by beta particles
Given orally
animals mst be isolated, cannot be monitored, be careful w/ hair and waste products

Front 99

Drug interactions on Thyroid axis

Back 99

Glucocorticoids
Phenobarbital
NSAIDS

Front 100

Glucocorticoids and thyroid hormone

Back 100

act on pituitary to decrease TSH release, so decrease T3/T4; interferes with 5’ deiodinase to decrease T3

Front 101

Phenobarbital and thyroid hormone

Back 101

increases metabolism of T3/T4 because induces liver enzymes

Front 102

NSAIDS and thyroid hormone

Back 102

interfere with binding of T3/T4 to serum proteins so can’t act

Front 103

HPA axis

Back 103

adrenocorticism and friends

hypothalamus releases Cortisol releasing horomone-->ant. pit. releases ACTH--> adrenal cortex (fasiculata cells) release cortisol--> negative feedback on above and

Front 104

receptors on hypotalamus that affect HPA axis

Back 104

inhibits CRH = NE, GABA
increase CRH= Ach, 5-HT, NE

Front 105

signs of hypoadrenocorticism

Back 105

nausea, vomiting, dec Na/inc K (due to aldosterone), lethargy, dehydration

Front 106

where is aldosterone produced

Back 106

Zona glomerulosa

Front 107

how do you treat hypoadrenocorticism

Back 107

replace glucocorticoids (cortisol) and mineralocorticoids (aldosterone)

Front 108

signs of hyperadrenocorticism

Back 108

PU/PD, pohyphagia, lethargy, pot belly/wt gain, thin skin, alopecia, muscle wasting

Front 109

Desoxycorticosterone pivalate (DOCP)

Back 109

mineralocoricoid given every 25 d;
approved for use in dogs
Acts like aldosterone to retain Na+ and secrete K+

Front 110

Fludrocortisone acetate

Back 110

mineralocorticoid given every day
Acts like aldosterone to retain Na+ and secrete K+
Can see GCC side effects

Front 111

What drugs do yo use to treat Pituitary and Adrenal dependant hyperadrenocorticism

Back 111

Trilostane: inhibits synthesis of adrenal steroids
Mitotane:selective destruction of zona fasciculate/reticularis
Ketoconazole:inhibits enzyme that converts cholesterol

Front 112

Trilostane

Back 112

use to treat Pituitary and Adrenal dependant hyperadrenocorticism
MOA: Inhibit 3-Beta, hydroxysteroid dehydrogenase -->blocks synthesis of adrenal steroids (pregnenolone -->progesterone doesn’t happen)
FDA Approved in dogs
Action in adrenal gland--> pituitary hormones affected by negative feedback
CI: Pregnant animals - affects sex hormones
ADE: vomiting, diarrhea, lethargy

Front 113

Mitotane

Back 113

use to treat Pituitary and Adrenal dependant hyperadrenocorticism
MOA: selective destruction of zona fasciculate/reticularis (less effect on glomerulosa – aldosterone)
Contra: pregnant animals
ADE: GI signs, hypoglycemia, CNS depression, liver damage, electrolyte imbalances

Front 114

Ketoconazole

Back 114

use to treat Pituitary and Adrenal dependant hyperadrenocorticism
MOA: prevents conversion of lanosterol -> cholesterol by inhibiting CYP450 enzymes
Used in animals that don’t respond well to trilostane/mitotane
Important because cholesterol is a precursor to glucocorticoids
Used in combination with other drugs to decrease dose because inhibits CYP450 enzymes, preventing metabolism of drug in liver
Drug interactions: any drug metabolized by CYP450
ADE: vomiting, diarrhea

Front 115

drugs used to treat pituitary dependent Hyperadrenocorticism only

Back 115

Selegiline (L-Deprenyl): Increases dopamine, decreases ACTH, decreases cortisol
Pergolide: dopamine agonist--> decreases ACTH, decreases cortisol

Front 116

Selegiline (L-Deprenyl)

Back 116

used to treat pituitary dependent Hyperadrenocorticism only
MOA: Monoamine oxidase B inhibitor--> dopamine breakdown is inhibited so increases dopamine--> decreases ACTH--> decreases cortisol
*Alters clinical signs, not disease process*
ADE: generally safe, vomiting/diarrhea

Front 117

Pergolide

Back 117

used to treat pituitary dependent Hyperadrenocorticism only
MOA: Dopamine agonist @ D1 & D2 receptors
No longer formulated because of human cardiovascular effects --> must compound
Used in horses
ADE: Dopamine suppresses prolactin --> inhibits lactation in pregnant or nursing animals

Front 118

insulin production

Back 118

Insulin is produced in Beta cells of islets of langerhans as preproinsulin then is systematically cleaved into-->proinsulin and then-->insulin

Front 119

actions of insulin

Back 119

mitogenesis, Glucose storage, protein synthesis, glycogen synthesis

Front 120

signs associated with diabetes mellitus

Back 120

PU/PD, Polyphagia, Weight loss, Lethargy, Hyperglycemia, Glycosuria

Front 121

goals of treatment of diabetes mellitus

Back 121

reduce blood glucose to normalish but avoid hypoglycemia (very bad! much worse than hyperglycemia)

monitor glucose with administration (glucose/time curve should look like shallow bowl), have owner look for lethargy, ataxia, anorexia

Front 122

glucose nadir

Back 122

lowest point on [glucose] per time curve

Front 123

insulin replacer MOA

Back 123

all bind to insulin receptor--> autophosphorylation, other proteins are phosphorylated/ dephosphorylated

Front 124

insulin actions:

Back 124

facilitate glucose uptake and metabolism of glucose, promote glycogen/protein/fat synthesis, uptake of ions into cell

Front 125

fast acting insulin replacers

Back 125

used for complicated diabetes (not eating, emergency, diabetic ketoacidosis); act quickly but don’t last long
Regular human insulin, Lispro, Aspart

Front 126

Aspart

Back 126

fast- acting insulin
synthetic human recombinant

Front 127

Lispro

Back 127

fast- acting insulin
synthetic human recombinant

Front 128

regular human insulin

Back 128

fast acting insulin

Front 129

Intermediate to long acting

Back 129

used for long term care
NPH (isophane)
Protamine zinc (pork insulin) = vetsulin
Glargine
Detemir

Front 130

NPH (isophane)

Back 130

intermediate to long acting insulin
human insulin recombinant

Front 131

Protamine zinc

Back 131

intermediate to fast acting insulin
pork insulin

Front 132

Glargine

Back 132

intermediate to fast acting insulin
synthetic, used in cats

Front 133

Detemir

Back 133

intermediate to fast acting insulin
synthetic, used in cats

Front 134

vetsulin

Back 134

Protamine zinc (intermediate to fast acting inslin)
pork insulin (PZ) w/ protamine added – takes longer to break down; pulled from market

Front 135

Sulfonylureas

Back 135

to treat diabetes mellitus
Glipizide
MOA: inhibit ATP dep K+ channels, resulting in depolarization of beta cells and release of insulin
Oral hypoglycemic agent so must be capable of secreting insulin from beta cells--> will not work for type I
ADE: amyloid deposition in cats

Front 136

Glipizide

Back 136

treatment for diabetes mellitus
MOA: inhibit ATP dep K+ channels, resulting in depolarization of beta cells and release of insulin
Oral hypoglycemic agent so must be capable of secreting insulin from beta cells--> won't work for type I
ADE: amyloid deposition in cats

Front 137

oral hypoglycemic agents efficacy

Back 137

don't work well for glucose cntl in animals

Front 138

drugs that are oral hypoglycemic agents

Back 138

Metformin, Acarbose, Sulfonylureas (glipizide)

Front 139

Metformin

Back 139

treatment for diabetes mellitus
improves periph. utilization of insulin
not effective in cats, severe side effects

Front 140

Acarbose

Back 140

treatment for diabetes mellitus
alpha glucosidase inhibitor (inhibits digestion of starch)

Front 141

theurapeutic goals of repro drugs

Back 141

prevent/enhance/ manipulate normal cycling or pregnancy
prevent/ terminate pregnancy
treat infertility

Front 142

endogenous hormones that deal with repro:
from hypothal

Back 142

GnRH
oxytocin(stored in pituitary but made in hypothal)= uterine contraction and milk ejection

Front 143

endogenous hormones that deal with repro: from pituitary

Back 143

FSH= follicle/sperm development
LH= follicle development + stimulation of CL to secrete progesterone, or stimulates androgen synthesis
Prolactin = stimulates postpartum lactation
oxytocin(stored in pituitary)= uterine contraction and milk ejection

Front 144

endogenous hormones that deal with repro: from uterus/ placenta

Back 144

PGF2alpha= regulatre estrus cycle in rum.; causes luteolysis and thus dec in progesterone levels
hCG (LH like)=induce ovlation
eCG/PMSG (FSH like, some LH)= induce ovlation

Front 145

endogenous hormones that deal with repro: from ovary/uterus/testes

Back 145

progesterone= helps regulate estrus cycle; hormone of pregnancy
estrogen= helps regulate estrous cycle; responsible for ovulation
testosterone= spermatogenesis--> very rarely manipulated

Front 146

GnRH drugs

Back 146

Gonadorelin
used to induce ovulation, infertility treatment

Front 147

Gonadotropin drugs

Back 147

PG600: induce ovulation, infertilty treatment
Prolactin: no therapy use
Metoclopramide: prolactin enhancer
Domperidone: prolactin enhancer

Front 148

Oxytocin drugs

Back 148

used to induce parturition and milk letdown

Front 149

Gonadorelin

Back 149

GnRH drugs
used to induce ovulation, infertility treatment

Front 150

PG600

Back 150

(hCG & eCG) – induce ovulation; infertility therapy
ADE: potential for Antibody formation --> inefficacy
used to be used to cycle sows

Front 151

prolactin

Back 151

Gonadotropin
no therapeutic uses
use prolactin enhancers instead

Front 152

Metoclopramide

Back 152

Gonadotropin, prolactin enhancer (dopamine antagonist)
No oral admin
ADE: related to dopamine antag; rare rxn in humans --> tardive dyskinesia

Front 153

Domperidone

Back 153

gonadotropin, prolactin enhancer (dopamine antagonist)
No oral admin; approved in gel form for fescue grass toxicity in mares
Does not cross BBB so no CNS effects in horses
ADE: Premature lactation (& FPT); undesirable prokinetic effect

Front 154

Oxytocin

Back 154

ecbolic agent
induce parturition and milk letdown, enhance uterine contractions
ADE: after repeated dosing --> aggressive uterine contractions

Front 155

what in tar-nation is an ecbolic agent?

Back 155

promotes labor by inc. uterine contractions

Front 156

-gest

Back 156

progesterone like drug

Front 157

-prost

Back 157

prostaglandin drug

Front 158

-prostayl

Back 158

prostaglandin drug

Front 159

Fescue toxicity

Back 159

in mares causes abortion/weak foals, prolonged gestation

treat with dopamine antagonist Domperidone

Front 160

prostaglandings

Back 160

don't handle if asthmatic or pregnant
PGF2alpha= induce parturition in sows/goats, abortion in others
Dinoprost – PGF2alpha analog
Cloprostenol – PGF2alpha analog

Front 161

PGF2 alpha

Back 161

prostaglandin
Induce parturition in sows and goats; will induce abortion in other species

Front 162

Dinoprost

Back 162

PGF2alpha analog
Used to synchronize estrus (not pigs); stimulate luteolysis (abortion) or stimulate parturition (pig and goat)
ADE: abortion, other smooth muscle contractions --> diarrhea, sweating
Pregnant women should not handle --> miscarriage!

Front 163

Cloprostenol

Back 163

PGF2alpha analog
Used to synchronize estrus (not pigs); stimulate luteolysis (abortion) or stimulate parturition (pig and goat)
Has slightly longer half life than Dinoprost
human effects: abortion, other smooth mm. contractions

Front 164

steroid hormones

Back 164

may be given orally
estrogen: illegal in FA
progestins: prevent of sync estrus
androgens: regulate spermatogenesis, abused by ppl

Front 165

Estradiol

Back 165

estrogen
Illegal in food animals!
ADE: Bone marrow suppression --> aplastic anemia & pyometria in dogs

may now be given for female incontinence to tighten urinary sphincter

Front 166

PGF2 alpha works in sows/ doe b/c?

Back 166

they are CL dependent during pregnancy

Front 167

DES

Back 167

estrogen
prohibited in FAs b/c inc risk of cervical cancer in humans
used for spay incontinence in dogs sometimes
ADE: human risks

Front 168

Progesterone - CIDR

Back 168

progestin
used to prevent or synchronize estrus; vaginal insert approved in sheep, goats and cattle

Front 169

Altregenost

Back 169

progestin
Used to prevent or synchronize estrus in mare and pig; approved in horses
ADE: High doses --> fetal abnormalities

Front 170

Metengestrol acetate

Back 170

progestin
Used to prevent or synchronize estrus; feed additive often used for feedlot heifers

Front 171

Megestrol acetate

Back 171

progestin
Used to prevent or synchronize estrus

Front 172

Syncro-Mate

Back 172

progestin
Progesterone + estrogen
Used to prevent or sync estrus; not available in US b/c contains estradiol

Front 173

Testosterone

Back 173

androgen (injectable)
Regulates spermatogenesis
ADE: negative feedback on gonadorelins/gonadotropins

Front 174

anabolic steroids

Back 174

stenozolol, boldenone, trenbelone, nandrolone
androgen
misused in ppl (used to treat HIV, burns for anabolic effect in medicine)
Not approved in animals
ADE: hepatotoxicity in cats; weight gain & Na+ retention; undesirable androgenic effects

Front 175

Finasteride

Back 175

antiandrogen
MOA: Inhibits conversion of testosterone to active form (5 alpha dihydrotestosterone)
May be used for benign prostatic hypertrophy in dogs
ADE: impotence

Front 176

Metacoparine

Back 176

stimulates GI, dopamine antagonist to inc. milk via prolactin

Front 177

corticosteroids

Back 177

split into mineralocorticoids-->affect electrolyte and fluid imbalance

Front 178

glucocorticoids

Back 178

affect carbohydrate metabolism

Front 179

Physiological actions of corticosteroids

Back 179

-fluid homeostasis (mineralocorticoids)
-inc. gluconeogenesis
-dec. protein synthesis
-inc. lipolyisis ( w/ release of glycerol and free fa)
-maintain microcirculation and normal vascular permeability
-development of pulmonary surfactant in near-term fetus

Front 180

indications for administration of glucocorticoids

Back 180

endocrine: replacement therapy (addisons)
non-endocrine: shock therapy(controversial), anti-inflammatory & anti allergic, immunosuprresive therapy, chronic palliative therapy

Front 181

indictions not acceptable for glucocorticoids

Back 181

laminitis, snake bite, lack of appetite

Front 182

glucocorticoids mechanism of action

Back 182

Genomic mechanisms: cytosolic glucocorticoid receptor (cGCR) translocates to nucleus
non-genoic effects associated with cGCR, membrane bound GCR
non-genomic/non-specific effects caused by interactions with cell membranes

Front 183

glucocorticoids genomic MOA

Back 183

cytosolic glucocorticoid receptor (cGCR) translocates to nucleus:
-inhibits pro-inflammatory transcription factors (NF-Kappa B, STAT)
-suppresses transcription of inflammatory genes (IL-1,2)
-induces transcription of immunosuppressive genes (lipocortin 1)

Front 184

adverse effects of glucocorticoids

Back 184

Hypothal. Pitu. Adrenal axis supression--> why dose must be tapered off
thin skin, potbelly, cushingoid appearance, fluid retention, weight gain, muscle wasting, Na retention/K loss
can induce parturition in last trimester
potential for congenital abnormalities

Front 185

contraindications for glucocorticoids

Back 185

joint injection: fracture, infection

all admin routes: corneal ulcers, GI ulcers, Hyperadrenocrticism,infections (esp. at immunosuppressive doses),

Front 186

all Glucocorticoids act the same way but...

Back 186

have different mineralocorticoid effects, different duration of action and different hypothal. pituit. adrenal axis suppression

Front 187

Glucocorticoids: low dose response

Back 187

used for replacement/low maintenence/ anti-inflammatory

Front 188

Glucocorticoids:high dose response

Back 188

immunosuppressive

Front 189

Glucocorticodis: pulse/shock therapy

Back 189

immunosuppressive or initial lymphocytolytic (cancer treatment)

Front 190

Glucocorticoids: parental preparations

3 types

Back 190

Rapid onset <1 min, short duration 1- hr--> ER uses for shock, anaphylaxis
Rapid onset 5-45 min, middle duration 3-4 hr--> ER use
Slow onset and long duration-->skin disease, arthritis, topical, intralesional

Front 191

Glucocorticoids: parental preparations

rapid onset, short duration

Back 191

Rapid onset <1 min, short duration 1- hr--> ER uses for shock, anaphylaxis

any GCC sodium succinate, sodium phosphate

Front 192

Glucocorticoids: parental preparations

rapid onset, intermediate duration

Back 192

Rapid onset 5-45 min, middle duration 3-4 hr--> ER use

dexamethasone SP or in propylene glycol

Front 193

Glucocorticoids: parental preparations

Slow onset and long duration

Back 193

Slow onset and long duration-->skin disease, arthritis, topical, intralesional

triamcinolone, methylprednisolone acetate, flumethasone

Front 194

Glucocorticoids: oral preparations

3 types

Back 194

rapid onset/short duration: acute and chronic conditions (alternate day therapy), replacement therapy

rapid onset/short to intermediate duration

slow onset/long duration

Front 195

Glucocorticoids: oral preparations

rapid onset/short duration

Back 195

rapid onset/short duration: acute and chronic conditions (alternate day therapy), replacement therapy

hydrocortisone, cortisone, prednisolone, prednisone, methylprednisone

Front 196

Glucocorticoids: oral preparations

rapid onset/short to intermediate duration

Back 196

rapid onset/short to intermediate duration

triamcinolone base

Front 197

Glucocorticoids: oral preparations

slow onset/long duration

Back 197

slow onset/long duration

dexamethasone, betamethasone, flumethasone

Front 198

most common glucocorticoids for cattle

Back 198

dexamethasone (injection)

anti-inflammatory, induce abortion/parturition

Front 199

most common glucocorticoids for cats

Back 199

methylpredisolone, prednisolone

Front 200

most common glucocorticoids for dogs

Back 200

prednisone

Front 201

most common glucocorticoids for horses

Back 201

dexamethasone, methylprednisolone*, triamcinolone*

*=jt injection

Front 202

new glucocorticoids

Back 202

budenoside- oral for IBD
Ciclesonide- not common
fluticasone- nasal spray

Front 203

budenoside

Back 203

new glucocorticoid used for IBD

Front 204

Ciclesonide

Back 204

new glucocorticoid - not commonly used

Front 205

fluticasone

Back 205

new glucocorticoid- nasal spray

Front 206

Hydrocortisone

Back 206

short acting <24 hours GCC
good mineralocorticoid, mild HPAA suppression, alternate day therapy not possible

oral, used for acute/chronic conditions or for replacement therapy

Front 207

Cortisone

Back 207

short acting <24 hours GCC
good mineralocorticoid, mild HPAA suppression, alternate-day therapy possible but not ideal

oral: rapid onset/ short duration--> acute/chronic conditions & replacement therapy

Front 208

Prednisone

Back 208

short acting <24 hour GCC
okay mineralocorticoid, mild HPAA suppression, alternate-day therapy possible

used for acute/chronic conditions, replacement therapy

most common GCC for dogs

Front 209

Prednisolone

Back 209

short acting <24 hour GCC
okay mineralocorticoid, mild HPAA suppression, alternate-day therapy possible

used for acute/chronic conditions, replacement therapy

commonly used in cats

Front 210

methylprednisolone

Back 210

short acting <24 hour GCC
okay mineralocorticoid, mild HPAA suppression, alternate-day therapy possible
parental has slow onset and long duration
oral has rapid onset and short duration-->replacement therapy, and acute/chronic conditions
commonly used in horse joints and cats

Front 211

Triamcinolone

Back 211

intermediate duration GCC 24-48 hr
no mineralocorticoid activity, inc. HPAA suppression, no alternate-day therapy potential
parenteral: slow onset used for skin disease/arthritis, topical
oral: rapid onset w/ short to intermediate duration

commonly used in horses for jt injections

Front 212

Flumethasone

Back 212

long acting GCC >48 hr
no mineralocorticoid activity, SUPER HPAA suppression, no alternate-day therapy potential

parental: slow onset w/long duration--> used for skin/arthritis
oral:slow onset/long duration

Front 213

Dexamethasone

Back 213

ong acting GCC >48 hr
no mineralocorticoid activity, SUPER HPAA suppression, no alternate-day therapy potential

parental: rapid onset/intermediate duration
oral: slow onset/long duration

commonly used in cattle(anti-inflam & induce parturition/abortion) & horses

Front 214

Betamethasone

Back 214

long acting GCC >48 hr
no mineralocorticoid activity, SUPER HPAA suppression, no alternate-day therapy potential

oral: slow onset/long duration

Front 215

immunosuppressants used for what alterations

Back 215

immune mediated diseases, inappropriate/overzealous immune response

example: immune mediated hemolytic anemia, lupus, pemphigus, IMT

Front 216

types of immunosuppressants

Back 216

glucocorticoids, calcineurin inhibitors, antiproliferative, antimetabolites,

Front 217

major adverse effects of immunosuppressants

Back 217

bone marryow suppression-cyclo

Front 218

glucocorticoids

Back 218

immunosuppressant
MOA: dec. gene expression of genes that affect neutrophil trafficking, suppress macrophage function, lowered lymphocyte activity, esp T-cells

Front 219

Calcineurin inhibitors

Back 219

Cyclosporin, Tacrolimus
Immunosuppressant
MOA: inhibit normal T-cell transduction
-blocks calcineurin phosphatase activity
-normally, dephosphorylates NFAT- allowing it to move to nucleus
-NFAT induces cytokine genes s/a IL-2 (T-cell growth and differentiation factor)
Adverse effects: cyclosporine- GI effects, gingival hyperplasia

Front 220

Antiproliferative (cytotoxic)

Back 220

Cyclophosphamide, Chlorambucil

MOA:alkylating agents- prevents cell from reproducing

adverse: bone marrow suppression

Front 221

Antimetabolites

Back 221

Azathioprine:
MOA: purine analog, inhibits purine synthesis leading to dec. lymphocyte proliferation
adverse: bone marrow suppression
Mycophenolate
MOA: inhibits enzyme involved in purine synthesis leading to dec. lymphocyte proliferation
adverse: GI effects

Front 222

immunosupressants w/ unknown mechanism

Back 222

Danazol, Gold, Dapsone
dapsone adverse effects: bone marrow suppression
Gold adverse effects: nephrotoxicity

Front 223

Cyclosporine

Back 223

Calcineurin inhibitors

immunosuppressant
adverse effects: GI effects, gingival hyperplasia

Front 224

Tacrolimus

Back 224

Calcineurin inhibitors

immunosuppressant

Front 225

Cyclophosphamide

Back 225

antiproliferative (cytotoxic)

immunosuppressants

Front 226

Chlorambucil

Back 226

antiproliferative (cytotoxic)

immunosuppressants

Front 227

Azathioprine

Back 227

Antimetabolite
immunosuppressant

antimetabolites immunosuppressant
MOA: purine analog, inhibits purine synthesis leading to dec. lymphocyte proliferation

adverse: bone marrow suppression

Front 228

Mycophenolate

Back 228

antimetabolites immunosuppressant
MOA: inhibits enzyme involved in purine synthesis leading to dec. lymphocyte proliferation

adverse: GI effects

Front 229

Danazol

Back 229

immunosuppressant
mechanism not well known

Front 230

Gold

Back 230

immunosuppressant
mechanism not well known

adverse: nephrotoxicity

Front 231

Dapsone

Back 231

immunosuppressant
mechanism not well known

adverse: bone marrow suppression

Front 232

Immunostimulants used for what alteration

Back 232

inadequate immune response

Front 233

temporary and correctable need for immunostimulants

Back 233

neonates w/o colostrum

correct by supplementing w/ colostrum supplement

Front 234

examples of immunostimulants

Back 234

hyperimmune serum, tetanus antitoxin

Front 235

NSAID mechanism

Back 235

blocks COX (cyclooxygenase)-->prevents formation of prostaglandins (inflammatory mediators that inc. intensity of pain perception); PGs come from metabolism of arachidonic acid

classical NSAID: non-selective inhibits COX 1 &2
COX 2 is the one expressed by infective processes-->inhibition leads to less inflammation

Front 236

NSAID uses

Back 236

acute pain/inflammation
chronic pain
fever
antihemostatic actions
endotoxemia
atherosclerosis, cancer, neurodegenrative disease, mastitis/metritis/endotoxemia, resp. diseases, calf and piglet scours

Front 237

NSAID: acute pain/inflammation

Back 237

causes inc. expression of COX (usually COX2) which inc. production of PGs

Front 238

NSAID: chronic pain

Back 238

block production of PGs (which cause inc. bradykinin) reduce inflammation

Front 239

NSAID: fever

Back 239

PGE2 acts in hypothalamus to inc. the thermoregulatory set point

Front 240

NSAID: antihemostatic actions

Back 240

thromboxane is product of AA metabolism by COX; dec. thromboxane--> dec. hypercogulability

Front 241

NSAID: endotoxemia

Back 241

LPS/endotoxin stimulates the production of cytokines by monocytes and macrophages, which stimulates production of prostaglandins and leukotrienes
*does not treat endotoxemia directly--> not an antiendotoxin
Flunixin in horses

Front 242

NSAID adverse effects general

Back 242

erosions, ulcers, GI upset, melena- block good PGs
nephrotoxicity: by blocking good PGs
Cats- repeated doses can lead to acute renal failure and death

Front 243

NSAIDS specific adverse effects

Back 243

phenylbutazone- hematopoietic; right dorsal colitis in horses
Etodoloc- KCS (dry eye)
Carprofen + others: hepatotoxicity
carprofen: bone marrow necrosis

Front 244

NSAID toxicity

Back 244

species specific
-due to differing degrees of protein binding (horses)
-sensitivity to GI effects (dogs w/chronic aspirin, flunixin, naproxen, ibuprofen)
-COX-2 vs COX-1 activity in dogs

Front 245

COX 2 dogs and NSAIDS

Back 245

Dogs have higher levels of COX-2 in the kidneys
non-selective inhibition by naproxen results in reduced renal blood flow and urinary Na retention-->renal papillary necrosis

Front 246

NSAID contraindications

Back 246

acetaminophen and cats
ibuprofen and phenylbutazone in dogs

Front 247

acetaminophen vs. cats

Back 247

lack of glucuronyl transferase--> toxic phase 1 metabolites which overwhelm the detoxifying glutathione scavenging system--> methemoglobinemia;
treatment w/ n-acetylcysteine--> allows oxidized glutathione to be reduced and reused

Front 248

ibuprofen and phenylbutazone vs. dogs

Back 248

GI effects

Front 249

How to avoid NSAID toxicity

Back 249

select drug w/ fewest adverse effects in species of interest
use w/gastroprotective drugs s/a misoprostol, omeprazole
smallest duration/ dose possible
don't use in dehydrated/ vascular compromised animls
avoid use in liver/kidney disease patients
avoid concomitant use of other drugs w/similiar actions/similiar toxicities example: GCC + NSAIDs potentiate GI effect

Front 250

NSAID elimination

Back 250

half-life vary btn species b/c of clearance differences btn species

consider this when dosing animals

Front 251

Selective COX-1 Inhibitors:

Back 251

NSAIDs
Aspirin – not approved in animals, but still marketed
Ketoprofen
Peroxicam
Phenylbutazone

Front 252

Selective COX-2 Inhibitors

Back 252

NSAIDs
Deracoxib
Firocoxib – highly selective!

Front 253

less specific cox inhibitors

Back 253

Acetominophen
Carprofen
Diclofenac
Etodolac
Flunixin
Flurbiprofen
Ibuprofen
Meloxicam
Naproxen
Piroxicam
Tepoxalin

Front 254

Tepoxalin

Back 254

NSAID: less specific cox inhibitors
works to decrease PGs and leukotrienes – COX & LOX blocker

Front 255

Piroxicam

Back 255

NSAID: less specific cox inhibitors
used to treat transitional cell carcinoma – not antineoplastic; not used as anti-inflammatory drug

Front 256

Naproxen

Back 256

NSAID: less specific cox inhibitors
not approved in animals

Dog ADE: GI sensitivity, reduced renal blood flow and urinary sodium retention-->renal papillary necrosis

Front 257

Meloxicam

Back 257

NSAID: less specific cox inhibitors
approved for use in cats

Black box warning: assoc w/ kidney disease

Front 258

Ibuprofen

Back 258

NSAID: less specific cox inhibitors
not approved in animals

GI ADE in dogs, ferrets very sensitive-->neuro and GI signs

Front 259

Flurbiprofen

Back 259

NSAID: less specific cox inhibitors
not approved in animals; human ophthalmic preparation – pH balanced; non-irritating

Front 260

Acetominophen

Back 260

NSAID: less specific cox inhibitors
not approved in animals by FDA

toxic in cats

Front 261

Carprofen

Back 261

NSAID: less specific cox inhibitors
1st NSAID approved for dogs; anti-inflammatory, analgesic

adverse: hepatotoxicity, bone marrow necrosis

Front 262

Diclofenac

Back 262

NSAID: less specific cox inhibitors

– “ac” – anti-inflammatory, acetic acid derivative

Front 263

Etodolac

Back 263

NSAID: less specific cox inhibitors

– “ac” – anti-inflammatory, acetic acid derivative

Keratoconjuctvitis Sicca = KCS (dry eye)

Front 264

Flunixin

Back 264

NSAID: less specific cox inhibitors

approved in cattle; no chronic use in dogs due to GI sensitivities, used for endotoxemia in horses

Front 265

NSAID stems:

Back 265

‘-ac’, ‘-butazone’, ‘-coxib’, ‘-fenamic’, ‘-icam’, ‘-metacin’, ‘-nixin’, ‘-profen’, ‘sal-, -sal, o-sal’

-ac- =anti-inflammatory, acetic acid derivative

Front 266

Aspirin

Back 266

NSAIDs Selective COX-1 Inhibitors:

not approved in animals, but still marketed

Front 267

Phenylbutazone

Back 267

NSAIDs Selective COX-1 Inhibitors:

ADE: hematopoietic, right dorsal colitis in horses
Illegal to use in dairy cattle
lower protein binding in horses (compared to humans) so much lower theurapeutic serum concentrations; efficacy of lower [ ] may be due to inc. in inflammatory exudates

GI effects in dogs

Front 268

Peroxicam

Back 268

NSAIDs Selective COX-1 Inhibitors:

Front 269

Ketoprofen

Back 269

NSAIDs Selective COX-1 Inhibitors:

Front 270

Deracoxib

Back 270

NSAID: Selective COX-2 Inhibitors

Front 271

Firocoxib

Back 271

NSAID; Selective COX-2 Inhibitors

– highly selective!

Front 272

Drug COX-1 COX-2
Aspirin ++++ -
Carprofen + +++
Diclofenac ++ ++
Flunixin +++ +
Ketoprofen +++ +
Meloxicam + +++

Back 272

...meh

Front 273

NSAIDs most used in ruminants

Back 273

Flunixin

Front 274

NSAIDs most used in porcine

Back 274

Flunixin

Front 275

NSAIDs most used in horses

Back 275

Phenylbutazone (#1)
Flunixin (#2)

Front 276

NSAIDs most used in dogs

Back 276

Carprofen (#1)
Meloxicam (#2)

Front 277

NSAIDs most used in cats

Back 277

Meloxicam

Front 278

NSAIDs most used in avian and exotics

Back 278

Meloxicam

Front 279

NSAID elimination

Back 279

Half life varies btn species mostly due to differences in clearance--> don't extrapolate doses based on other species
High bioavailability, does penetrate BBB, usually highly protein bound (exception phenylbutazone and horses)
Metabolized and then eliminated via kidney

Front 280

Legal constraints

Back 280

Amduca regulations: have label for everything including human OTC meds given to animals
Label should include: if lose appetite stop NSAID and call vet
Phenylbutazone illegal to use in dairy cows

Front 281

Fluid therapy is used for what alterations in the patient

Back 281

Dehydration, hypovolemia, electrolyte imbalances (Na, K, Cl, Ca), Acid/base imbalance, hypoproteinemia

Front 282

Fluid therapy: therapeutic goals

Back 282

Replace intravascular volume--> increase tissue perfusion
replace intersitial volume-> correct dehydration
meet maintence needs and replace ongoing losses

Front 283

To calculate fluids, need to know:

Back 283

Replacement
Maintenance
Ongoing losses

Front 284

how to estimate ongloing fluid losses

Back 284

estimate from clinical observation (vomiting, diarhea etc)

Front 285

how to calculate replacement for fluids

Back 285

%dehydrated x BW

Front 286

Crystalloids

Back 286

several types: replacement, maintence, hypertonic, dextrose in water
may contain Ca, Mg, or be alkalinizing

Front 287

types of fluids

Back 287

Crystalloids, Colloids, Blood products, Parenteral nutrition

Front 288

Replacement crystalloids

Back 288

similar solutes to plasma water;
20-25% remains in IV space after 1 hr;
have >er Na+ than maintenance; generally isotonic

Front 289

examples of replacement crystalloids

Back 289

acidifying: Ringer’s, .9% saline, LRS
alkalinizing: Norm-R, Plasma-Lyte

Front 290

examples of maintence crystalloids

Back 290

Acidifying:
2.5% dextrose in .45% saline + KCl;
Norm-M w/5% dextrose;
Plasma-lyte M w/5% dextrose

Front 291

maintence crystalloids

Back 291

similar solutes to extracellular fluid;
<10% remains in IV space after 1 hr;
generally isotonic

Front 292

which crystalloids have Ca++

Back 292

Any with LRS, Plasma-Lyte M w/5% dextrose

Front 293

which crystalloids have Mg

Back 293

Norm-R, Plasma-lyte A, Norm-M, Plasma-lyte M

Front 294

Alkalinizing crystalloid fluids contain

Back 294

more acetate, lactate or gluconate

Front 295

which crystalloid fluids are hypertonic

Back 295

Norm-M w/5% dextrose,
Plasma-lyte M w/5% dextrose;
Additives – 50% dextrose, 7.5% saline, NaHCO3, KCl

Front 296

Ringer's

Back 296

crystalloid
replacement, acidifying

Front 297

2.5% dextrose in .45% saline + KCl

Back 297

crystalloid
maintence, acidifying,

Front 298

.9% saline

Back 298

crystalloid
replacement, acidifying

Front 299

LRS;

Back 299

crystalloid
replacement, acidifying
contains Ca

Front 300

Norm-R,

Back 300

crystalloid
replacement, alkalinizing:
contains Mg

Front 301

Plasma-Lyte A

Back 301

crystalloid
replacement, alkalinizing:
contains Mg

Front 302

Norm-M w/5% dextrose

Back 302

crystalloid
maintence, acidifying, contains Mg, hypertonic

Front 303

Plasma-lyte M w/5% dextrose

Back 303

crystalloid
maintence, acidifying, contains Ca + Mg, hypertonic,

Front 304

What concentration of dextrose is isotonic?

Back 304

About 5%

Front 305

additives to make solutions hypertonic

Back 305

50% dextrose, 7.5% saline, NaHCO3, KCl

Front 306

Colloids

Back 306

fluids containing high molecular weight compounds that stay in IV space

Front 307

example of colloids

Back 307

Plasma, Human serum albumin, Hetastarch, Dextrans, Modified gelatins

Front 308

Oxyglobin, polyheme

Back 308

compounds sometimes included with colloids
hemoglobin bases O2-carrying compounds

Front 309

fluid therapy: Blood products

Back 309

RBCs, plasma proteins, platelets, coagulation factors

Front 310

Parental nutrition

Back 310

3 types
supplement (aas/electrolytes) up to 25% of basal metbolic needs
PPN 50% of need
TPN 100% of need

Front 311

ions and where they are in fluid compartments

Back 311

Na, Cl highest [ ] in ISF slightly higher in Ca

K, A-, Mg highest [ ] in cell

Front 312

define anesthesia

Back 312

insensible or without feeling

Front 313

Blood/gas partition coefficient

Back 313

ratio of an anesthetic in the safe phase (blood & gas), basically how it will partition itself between the two phases (affinity)
low= does not want to stay in blood--> more in CNS--> induced faster
high=wants to stay in blood--> longer induction

Front 314

path of gas anesthetic

Back 314

vaporizer-->lung--> blood-->CNS

Front 315

minimal alveolar concentration (ED50)

Back 315

dose at which 50% of animals don't respond to noxious stimuli
ED50 aka "inhalent anesthetic potency" b/c 1/MAC = potency
low MAC = more potent

Front 316

how many stages of anesthesia

Back 316

1 --> 4 with stage 3 having 4 different planes

Front 317

stage 1 anesthesia

Back 317

voluntary mvt, drug admin--> loss of consciousness

Front 318

stage 2 anesthesia

Back 318

stage of delirium/involuntary movement; loss of voluntary control (excitement stage)

Front 319

stage 3 anesthesia

Back 319

surgical anesthesia; unconsciousness w/progressive depression of reflexes

Has different planes – want to stay b/w planes 2-3 for most surgeries

Front 320

stage 4 anesthesia

Back 320

CNS extremely depressed & respiration ceases

Front 321

hypoventilation effects inhalent anesthetics how?

Back 321

increases induction time

Front 322

occupation exposure of inhalant anesthetics

Back 322

leaks, etc --> in study > 8 hours/wk exposure--> miscarriages/ abortions in preg women

Front 323

general characteristics of inhalant anesthetics

Back 323

 Reversible CNS depression
Absence of awareness (unconsciousness)
No recall of events at conscious level (amnesia)
Analgesia
Muscle relaxation
Decreased motor response to noxious stimuli (immobility)

Front 324

MOA of inhalant anesthetics

Back 324

MOA: unknown

Front 325

is iso or sevo more potent

Back 325

isoflurane

Front 326

isoflurane

Back 326

inhalent anesthetic
CNS/Resp – depression
Cardio – arrhythmias
Liver/kidney – minor

Front 327

sevoflurane

Back 327

inhalent anesthetic
CNS/Resp – depression
Cardio – mionr, some arrhythmias
Liver – minor
kidney- compound A when combined w/ soda lime is nephrotoxic to rats
more $$$

Front 328

Which has a shorter induction time: Iso or sevo

Back 328

sevoflurane has lower B/G coeff

also has faster equilibrium and a faster wake up

Front 329

only inhalant anesthetic approved for animals

Back 329

sevoflurane

Front 330

Halothane

Back 330

inhalant anesthetic that has been phased out
good anesthetic but caused hepatotoxicity and malignant hyperplasia

Front 331

barbiturates

Back 331

injectable anesthetics that proceed more rapidly through stage 2 anesthesia

inhalant anesthesia lasts longer than barbiturates

Front 332

adv/ disadv of using barbiturates

Back 332

Adv: easier to use on fractious animals; still have access to airway for sx; can use outside clinic

Disadv: Not as easy to control – once its give, its given; metabolized quicker (if liver working properly), most are not reversible

Front 333

general effects of barbiturates

Back 333

Sedation
Hypnosis
Anesthesia
Coma
Death
All are controlled substances --> must have DEA license

Front 334

barbiturates MOA

Back 334

MOA: Potentiate GABA, bind to barbiturate binding spot, increase Cl concentration --> hyperpolarization of cell, inhibition of APs
All are controlled substances

Front 335

barbiturates ADE

Back 335

All are controlled substances

ADE: outside of vein could cause tissue irritation--> sloughing

Front 336

barbiturates elimination

Back 336

Elimination via Blood -->brain (and other organs w/inc blood flow) --> muscle & adipose
So animals with decreased body fat or decreased muscle mass have longer duration of action, because drug stays in brain/CNS (ex. greyhounds)

Front 337

Systemic effects of barbiturates:

Back 337

CNS – depression, inhibition, dec seizures
Cardio – minor effects; some arrhythmias
Resp – depression! Most impt – want to be able to intubate quickly if depressed too much
Musc – relaxation
GI/Kidney – minor
Liver – induced enzymes
***Analgesia – NONE (so not considered general anesthetics)***

Front 338

Does barbiturates cause analgesia

Back 338

no! used for induction prior to intubation

Front 339

barbiturates: uses and CIs

Back 339

Use: usually for induction prior to intubation
Contra: avoid use in pregnant animals b/c fetus can have respiratory depression

Front 340

Thiopental

Back 340

Barbiturate
not in US now b/c used for capital punishment
shortest duration

Front 341

Pentobarbital

Back 341

Barbiturate
commonly used for euthanasia

Front 342

Phenobarbital

Back 342

Barbiturate
seizure management
longest duration

Front 343

adv/ disadv of giving 2 drugs at same time in same syringe

Back 343

1 stick to pt
must change needle prior to drawing up each drug (otherwise contamination occurs)
don't know which caused ADE
drug can cause other drug to precipitate

Front 344

Dissociative anesthetics: general effects

Back 344

Produce dose related unconsciousness and analgesia
Analgesia greater for somatic pain than visceral

Front 345

Ketamine

Back 345

Dissociative anesthetic, class III cntled
MOA: NMDA Receptor antagonist
least potent
Usually given in combo w/ other drugs: Benzodiazepenes + ketamine; GKX
Can use in darts b/c non-irritating to skin
No antagonist for OD, so just provide supportive care

Front 346

Ketamine: systemic effects, metabolization, CI

Back 346

CNS – hallucinations, dissociate CNS from rest of body, increase CNS blood flow, Increase intraocular pressure
Cardio – increase HR/BP (stimulate symp NS)
Resp – apneustic pattern of breathing (holding breath); intubate! Increased secretions/salivation
Musc – tremors/myoclonus
Ocular – eyes open, increased intraocular pressure
Analgesia – somatic > visceral

Metab: wake up b/c drug moves from CNS to tissues – metab in liver; excreted in kidney

Contra: head trauma, cardio dz, liver/kidney dz (prolongs effects b/c not eliminated)

Front 347

often given with ketamine to dec. side effects

Back 347

Can give w/atropine/glycopyrrolate to dec secretion side effects

Front 348

Tiletamine

Back 348

Dissociative anesthetic, Schedule III controlled drug
Same effects as Ketamine + muscle relaxant
Metab: as 2 diff drugs with different half live

Front 349

Telazol

Back 349

=Tiletamine + Zolazepam (BZD)

Dissociative anesthetics

Front 350

Phencyclidine (PCP)

Back 350

First dissociative anesthetic used in vet med
Most potent
No therapeutic use
schedule II drug
causes: mania, delirium, hallucinations

Front 351

Ketamine + benzodazepine (diazepam/ midazalam)

Back 351

ketamine causes mm. tremors maybe seizures so add BZD as a mm. relaxant

Front 352

Ketamine + benzodazepine (diazepam/ midazalam) + opoid

Back 352

ketamine causes mm. tremors maybe seizures so add BZD as a mm. relaxant

opiod dec amt of inhalent needed

Front 353

Ketamine + benzodazepine (diazepam/ midazalam) + opoid + anticholinergic

Back 353

ketamine causes mm. tremors maybe seizures so add BZD as a mm. relaxant

opiod dec amt of inhalent needed

anticholinergic dec secretions, atropine has CNS ADE, glycopyrollate is longer acting

Front 354

ketamine + alpha 2 agonist + BZD

Back 354

more relxed

Front 355

ketamine + acepromazine

Back 355

more calm, sedate prior to ketamine but may wake up enraged