Pharmacology, Quiz #5

Front 1

What two types of hormones are we concerned with in pharmacology?

Back 1

peptide and steroid

Front 2

What are the organs of the endocrine system?

Back 2

-hypothalamus/pituitary
-thyroid/parathyroid
-pancreas
-adrenal gland
-testes/ovaries

Front 3

When drugs are used with specific therapeutic goals in mind, how are they used?

Back 3

(1) diagnosis
(2) metabolic action
(3) effect on reproductive system

Front 4

Endocrine drugs are rarely a cure, instead, what do they do?

Back 4

Replace
Antagonize
Supplement

Front 5

Describe a peptide hormone.

Back 5

-cell signaling is quick (via increase in cAMP or IP3 secondary messengers); more rapid action
-water soluble
-given parenterally because easily degraded in the GI tract

Front 6

Describe a steroid hormone.

Back 6

-lipid soluble, therefore can co more places
-can go topically, orally or parenteral
-works on the cell nucleus to synthesize new proteins (increases mRNA)

Front 7

What affects solubility of a drug?

Back 7

the form in which an endocrine drug is prepared as a therapeutic

Front 8

What defines the route which a drug is given?

Back 8

the form

Front 9

What affects absorption of a drug?

Back 9

-route of administration
-solubility/insolubility

Front 10

What indirectly affects drug duration?

Back 10

absorption

Front 11

What is one way to change solubility of a drug?

Back 11

prepare as a salt
-insoluble salts increase rate of absorption, but also increase duration
-soluble salts - give IV

Front 12

What effect does pharmaceutics have?

Back 12

on absorption

Front 13

What are ways to alter absorption?

Back 13

-change the vehicle used
-change the size of particles (larger the size, decrease drug absorption)

Front 14

What type of hormone do you use if your therapeutic goal is diagnosis? What is your goal by injecting this hormone?

Back 14

peptide - injection (many are pituitary hormones)
Goal: to see if organ works

Front 15

Your therapeutic goal is diagnosis - why would you inject ACTH (or its synthetic derivative cosyntropin?

Back 15

to see if adrenal cortex works

Front 16

Your therapeutic goal is diagnosis - why would you inject ADH (vasoptessin)? Where is ADH normally found?

Back 16

-to diagnose and treat diabetes insipidus
-comes from posterior pituitary gland

Front 17

What are three examples of using hormones as a diagnostic agent?

Back 17

(1) ACTH
(2) TSH
(3) ADH
-if you give the drug and the endocrine organ works, then it is not a problem with that organ - more a problem of the pituitary gland

Front 18

What produces parathyroid hormone and calcitonin?

Back 18

PTH- parathyroid gland (releases Ca++)
calcitonin-thyroid gland (puts Ca++ back in)

Front 19

What would you use to increase Ca++ levels when they are low?

Back 19

-soluble Ca++ salts given IV (Ca++ gluconate)
-PTH is not readily available

Front 20

What would you do to decrease Ca++ levels in the body (like in the case of a neoplasia or rodenticide poisoning)?

Back 20

(1) dilute the body with saline
(2) calcitonin (side effects are allergies or decreased side effects)

Front 21

Why would an animal have high Ca++ levels?

Back 21

neoplasia or
toxicosis caused by the rodenticide cholecelciferol

Front 22

Name two metabolic and antimetabolic actions (ions) in vet med?

Back 22

(1) Ca++ equilibrium
(2) Iodine metabolism

Front 23

What is the role of iodine?

Back 23

Helps make thryoid hormone
-this plays a role in maintaining the:
(1) CNS
(2) skin
(3) general metabolism

Front 24

Name a T4 thyroid drug we use to treat hypothyroidism.

Back 24

levothyroxine - this is a prodrug therefore requires an active liver to become active

Front 25

Compare T3 and T4.

Back 25

T3= very short half life and is much more potent than T4 (4X) (microgram doses); dose more often
T4=has a longer half life, it is a prodrug, dose less often (mg doses)

Front 26

What species requires a higher dose of thyroid hormone and why?

Back 26

canine - due to increased clearance rate

Front 27

Describe the pharmacokinetics of thyroid hormone?

Back 27

>90% protein bound (much watch what other drugs are used with this)
-metabolized in the liver
-p/o administration
-fecal elimination
-does not have a wide margin of safety

Front 28

When would you use antithyroid drugs and what is the most common species to use it in?

Back 28

-use for diseases causing decreased weight and increased activity (hyperthyroidism)
-used in cats a lot

Front 29

What radioactive isotope could you use to treat hyperthyroidism?

Back 29

Iodine 131
-decreases both size of thyroid and release of thyroid hormone

Front 30

What compound (not radioactive) could you use to treat hyperthyroidism?

Back 30

thioamides (methimazole)
-it prevents I going to T4 and thus decreases synthesis of thyroid hormones

Front 31

Which route would you normally administer an thioamide? What are the side effects of this drug?

Back 31

PO (topical is questionable)
-side effect is vomiting, lethargy and immune mediated anemia

Front 32

What cells make insulin and glucagon?

Back 32

insulin = beta
glucagon = alpha

Front 33

What forms can diabetes mellitus be in ?

Back 33

type1: insulin dependent (usually dogs); beta cells don't work
type2: insulin independent (usually cats)

Front 34

How would a vet treat type I vs. type 2 diabetes mellitus?

Back 34

the same - treat with insulin (humans treat type 2 differently)

Front 35

What is the difference in the way diabetes mellitus is managed in humans vs. animals?

Back 35

humans - managed in a narrow range
animals - range is not as important as owner ease of care b/c animal does not live as long

Front 36

What is the difference between human insulin and vet insulin?

Back 36

Human: products are rapid absorption and short duration (for closer management); has a human protein; larger concentrations (100 U/ml)

Vet: products are long acting; porcine source; concentrations are (40 U/ml)

Front 37

What are insulin suspensions made with to make them longer acting?

Back 37

-protein and zinc
-takes longer to absorb therefore they last longer

Front 38

What is the duration of a short-acting insulin? How are these given?

Back 38

-lasts 1-5 hours
-onset to peak is 1/6 - 1.5 hours
-given IV or SubQ

Front 39

What is the duration of a intermediate-acting insulin? How are these given?

Back 39

-lasts 18-24 hours
-onset to peak is 1-12 hours
-given SC once or twice daily

Front 40

What is the duration of a long-acting insulin? How are these given?

Back 40

-lasts 20-24 hours
-onset to peak is 1-8 hours
-given SC once daily

Front 41

How is hypoglycemia treated?

Back 41

with glucagon - has quick onset (1 min)and short duration (20 min)

Front 42

What happens when an overdose of insulin is given and you have hypoglycemia?

Back 42

-rapid onset
-CNS: weakness, confusion, convulsions, psychoses
-SKIN: moist, pallid
OTHER: shallow, rapid breathing

Front 43

What happens to an animal in a diabetic coma (hyperglycemia?

Back 43

-gradual onset
-CNS: drowsy, dim vision
-SKIN: dry, flushed
OTHER: acetone breath, thirst, rapid pulse, air hunger

Front 44

Why would you give an animal glucagon?

Back 44

-used to treat hypogylcemia due to insulin overdose or shock

Front 45

What is caused by hypo activity of the adrenal gland?

Back 45

Addison's disease

Front 46

What is caused by hyper activity of the adrenal gland?

Back 46

Cushings Disease

Front 47

What are glucocorticoids used for?

Back 47

(1) membrane stabilizers
(2) Anti-inflammatory
(3) immune suppression
(4) promotion of gluconeogenesis
(5) cerebral edema
(6) neoplasia
(7) aid parturition in the bovine

Front 48

What are some adverse effects of glucocorticoids when given?

Back 48

(1) immune suppression
(2) GI irritation
(3) adrenal suppression
(4) catabolic changes - a dog that has Cushings (too much glucocorticoids) changes the way fats and proteins are used in the body
(5) behavioral effects
(6) cateracts

Front 49

How can glucocorticoids be administered?

Back 49

oral, injection, topically

Front 50

Why would you want glucocorticoids over mineralocorticoids?

Back 50

Na retention

Front 51

What are two natural glucocorticoids?

Back 51

-cortisone - the pro drug therefore need an active liver
-hydrocortisone (cortisol)

Front 52

What four things are necessities as part of the structure of glucocorticoids?

Back 52

(1) =O at (C-3)
(2) double bond at (C-4 to C-5)
(3) -OH (or =O if a prodrug) at (C-11)
(4) -OH basic steroid at (C-21)

Front 53

What are the two shot acting glucocorticoid drugs? What is their length of action? Which one is the pro-drug and what does it look like?

Back 53

hydrocortisone (C11= -OH)
cortisone - the pro-drug (C11=O)
-lasts 8-12 hours

Front 54

What does an additional bond between (C1-C2) on a glucocorticoid mean? (3 things)

Back 54

(1) increase glucocorticoid effect, decrease mineralcorticoid effect
(2) increase duration of action because it is a foreign compound
(3) increase potency (can use a lower dose)

Front 55

What drugs have an additional double bond on the glucocorticoid? What is their duration of action?

Back 55

-prednisone (with =O on C11) - Pro Drug
-prednisolone (with =OH on C11)

-duration of action is 12-36 hours

Front 56

What does adding a F on C-9 of a glucocorticoid do?

Back 56

-increases the potency, therefore you can decrease the dose

Front 57

What does adding a -CH3 on (C-16) of a glucocorticoid do - on top of the double bond between C1-C2?

Back 57

increases the action of glucocorticoids even more than the others; increases the duration of action even more

Front 58

Where would you add a F on a glucocorticoid?

Back 58

C-9

Front 59

Where would you add an CH3 on a glucocorticoid?

Back 59

C-16

Front 60

Name the two long-acting drugs we are concerned with as glucocorticoids? What is their duration of action?

Back 60

-dexamethasone
-betamethasone

-24-72 hours

Front 61

What bonds does dexamtheasone have?

Back 61

-all the bonds a glucocorticoid should have (4) with an OH at (C-11)
-a double bone at (C1-C2)
-a F at C-9
-A CH3 at (C-16)

Front 62

As the glucocorticoids get to be longer lasting, what happens?

Back 62

-duration of action increases
-potency of glucocortiocids increases
-potency of mineralcorticoids decreases

Front 63

Name two soluble salts.

Back 63

succinate and phosphate salts

Front 64

IV preparations should be in what type of form?

Back 64

solutions

Front 65

Are suspensions or solutions more slowly absorbed?

Back 65

suspensions - therefore they last longer

Front 66

How are glucocorticoids metabolized?

Back 66

-by microsomal enzymes - cytochrome P450 for oxidation to active C11-OH
-glucaronidation

Front 67

What type of salt would you use for a topical glucocorticoid?

Back 67

insoluble salt

Front 68

What are the species differences in half life for glucocorticoids?

Back 68

Horse (1/2 hr) < dog (2 hrs) < man (3 hrs) <cow (6 hrs)

Front 69

What do you use mineralcorticoids to treat? What drug would you use?

Back 69

Addision's Disease
-cortisone

Front 70

What disease would you use adrenocorticoid antagonists to treat?

Back 70

Cushings Disease

Front 71

What do adrenocorticoid antagoinists do?

Back 71

(1) decrease synthesis OR increase biotransformation
(2) cytotoxic action
(3) MAO-B inhibitor that decreases dopamine and shuts of ACTH

Front 72

What drug is often used to increase milk production in cows?

Back 72

growth hormone (somatotropin)

Front 73

What type of compounds are steroids?

Back 73

C-III

Front 74

Is testosterone highly protein bound?

Back 74

YES

Front 75

What is testosterone (steroids) mainly used for?

Back 75

debilitating diseases, but high chance for abuse by athletes

Front 76

What are some long term effects and problems associated with the use of androgens?

Back 76

-C-III record keeping, human abuse
-damage to liver and germ cells
-change in lipid metabolism and electrolyte balance (Na retention)
-dermal effects

Front 77

What are two antiandrogens.

Back 77

estrogen, GnRH