Pharm Final 2

Front 1

Glucocorticoids...Secretion

Back 1

Feed back mechanism, stress

Front 2

Glucocorticoids...MOA

Back 2

Bind to cytosolic receptors, bind to glucocorticoid response elements (GREs) in DNA, alter gene expression and protein synthesis, also acts on memebrane receptors

Front 3

Glucocorticoids...Pharmacologic effects...Energy metabolism

Back 3

catabolic except liver, carbo/protein/lipid/bone

Front 4

Glucocorticoids...Pharmacologic effects...Water and Electrolytes

Back 4

inhibits release of action of ADH causing PU/PD

Front 5

Mineralocorticoids...Pharmacologic effects...Water and Electrolytes

Back 5

retention of Na and water, excretion of K, Ca, PO

Front 6

Glucocorticoids...Pharmacologic effects...Immune and Hematologic

Back 6

AntiIF effects, Inhibit phospholipase A2 and COX2 leading to inhibition of PG, LT, PAF, cytokines, and complement components, Immunosuppressive effects

Front 7

Glucocorticoids...Pharmacologic effects...Cardiac

Back 7

direct positive inotropic and chronotropic effect, indirectly on water and electrolyte metabolism

Front 8

Glucocorticoids...Pharmacologic effects...Respiratory

Back 8

Increase the number and affinity of Badrenergic receptors (up regulation)

Front 9

Glucocorticoids...Pharmacologic effects...CNS

Back 9

mental and physical dependence mainly in humans

Front 10

Glucocorticoids...Pharmacologic effects...Endocrine

Back 10

inhibit hypothalamic-pituitary-adrenal-axis (HPAA), inhibit ACTH, TSH, FSH, LH, prolactin, GH synthesis and section

Front 11

Glucocorticoids...Pharmacologic effects...Endocrine in humans

Back 11

large doses stimulate excessive acid and pepsin in the stomach which may cause peptic ulcers

Front 12

Glucocorticoids...short acting (<24 hrs) [gluco potency, mineral potency]

Back 12

Hydrocortisone (1, ++), Cortisone (.8, ++), Prednisone (4, +), Prednisolone (4,+), Methyl-predisolone (5, +)

Front 13

Glucocorticoids...intermediate acting (24-48 hrs) [gluco potency, mineral potency]

Back 13

Triamcinolone (5, 0) **least likely mineralo tox** Used in heart failure and hypertensive

Front 14

Glucocorticoids...long acting (>48 hrs) [gluco potency, mineral potency]

Back 14

Flumethasone (15, 0), Dexamethasone (30, 0), Betamethasone (30,0)[most potent AntiIf, contra in diabetic]

Front 15

Glucocorticoids...Most potent gluco

Back 15

Betamehtasone (30,0)[most potent AntiIf, contra in diabetic]

Front 16

Glucocorticoids...Least potent gluco

Back 16

cortisone

Front 17

Glucocorticoids...Most potent mineralo

Back 17

Hydrocortisone

Front 18

Glucocorticoids...Least potent mineralo

Back 18

Triamcinolone

Front 19

Glucocorticoids...preparations

Back 19

Aqueous solutions (w/salt to make soluble, IV, ER), alcohol, suspensions(insoluble ester), topical (acetate ester), inhalation (bronchial asthma and respir. dz), oral

Front 20

Glucocorticoids...Pharmacokinetics

Back 20

readily absorbed orally, skin, and mm, widely destributed (including brain), bind extensively to plasma proteins (CBG), metabolized by conjugatin to glucoronides and sulfates then excreted in urine

Front 21

Glucocorticoids...Clinical uses

Back 21

AntiIF and antiallergic, bronchial asthma and allergic rhinitis, chonic arthritis, otitis externa, hemorrhagic and septic shock, cerebal edema, *immunosuppressive in autoimmune dz, *malignant lymphoma, multiple myeloma, mast cell tumors, hypercalcemia, bovine ketosis, appetite stimulant, prophlaxis in sx, induction of parturition in cows, replacement therapy in hypoadrenocortisim (IDDM)

Front 22

Glucocorticoids...Clinical uses...bronchial asthma

Back 22

beclomethasone, triamcinolone, dexamethasone

Front 23

Glucocorticoids...Clinical uses...immunosurppressives

Back 23

in IMthrombocytopenia and autoIMHA

Front 24

Glucocorticoids...adverse effects and toxicity

Back 24

read them in your notes....WAY TOO LONG TO TYPE :o)

Front 25

Mineralocorticoids Secretion

Back 25

*aldosterone is mainly under the control of angiotensin 2, desoxycorticosterone is mainly under the control of ACTH

Front 26

Mineralocorticoids Drugs

Back 26

Desoxycorticosterone pivalate (DOCP), Fludrocortisone

Front 27

DOC to tx hypoadrenocorticism aka Addison's Dz

Back 27

Desoxycorticosterone pivalate (DOCP), inj 3-5wk

Front 28

Mineralocorticoids Characterisitics (gluco potent, mineralo potent)

Back 28

cortisol (1,1), DOCP (0,20), Fludrocortisone (3,125)

Front 29

Have to give a glucocorticoid with....

Back 29

DOCP

Front 30

Can cause serious hypokalemia

Back 30

Fludrocortisone

Front 31

ACTH

Back 31

used IM to differentiate between primary and secondary adrenocortical insufficiency.

Front 32

ACTH cortisol levels

Back 32

It doesnt cause increase cortisol levels in 1* adrenocortical insufficiency and it produces increased cortisol secretion in 2* adenocortical insufficiency.

Front 33

Adrenocortical Dysfunction...hypoadrenocorticism- 1*

Back 33

primary due to destruction of the adrenal cortex (addison's dz)

Front 34

Adrenocortical Dysfunction...hypoadrenocorticism- 2*

Back 34

secondary due to ACTH deficiency (uncommon)

Front 35

Adrenocortical Dysfunction...hyperadrenocorticism

Back 35

Pituitary-dependent hyperadrenocorticism (PDH,
Adrenal-dependent hyperadrenocorticism (ADH)

Front 36

Tx of Primary Hypoadrenocorticism..Acute

Back 36

Normal saline, glucocorticoid replacement (a rapid-acting glucocorticoid IV such as hydrocortisone sodium phosphate or sodium succinate

Front 37

Tx of Primary Hypoadrenocorticism..Chronic

Back 37

Mineralocorticoid replacement (DOCP, Fludrocortisone, serum Na and K should be monitored), Glucocorticoid replacement such as prednisone or prednisolone, sodium chloride oral supplementation

Front 38

DOC for tx of primary hypoadrenocorticism...chronic

Back 38

Desoxycorticosterone pivalate (DOCP) IM or SC (IV may cause acute shock) every 25 (21-30) days

Front 39

Tx of Secondary Hypoadrenocorticism

Back 39

Glucocorticoids

Front 40

DOC Tx of Pituitary Dependent Hyperadrenocorticism (PDH)

Back 40

Mitotane (o,p'-DDD)

Front 41

Mitotane (o,p'-DDD)MOA

Back 41

causes selective destruction of zona fasciculata and zona reticularis (but not zona glomerulosa)

Front 42

Mitotane (o,p'-DDD) initial tx

Back 42

given orally with food daily for 6-14days

Front 43

Mitotane (o,p'-DDD) maintenance of tx

Back 43

weekly oral administration

Front 44

Tx of Pituitary Dependent Hyperadrenocorticism (PDH)

Back 44

Mitotane (o,p'-DDD), Ketaconazole,Trilostane, Selegiline, Cyproheptadine, Radiotherapy, Surgery, Pergolide mesylate

Front 45

Ketaconazole

Back 45

causes reversible inhibition of glucocorticoid synthesis with insignificant effect on mineralocorticoids, 75% efficiacy

Front 46

Ketaconazole...adverse effects

Back 46

GI irritation (anorexia, vomiting, diarrhea) and liver damage and jaundice

Front 47

Trilostane MOA

Back 47

*Inhibits the enzyme 3Bhydroxysteriod dehydrogenase which converts pregnenolone to progesterone reducing glucocorticoid levels

Front 48

Trilostane use

Back 48

short term tx of PDH, has few side effects

Front 49

Selegiline (l-deprenyl) MOA

Back 49

*Inhibits monoamine oxidase B enzyme inhibiting inactivation of dopamine, dopamine inhibits ACTH (parkinson's dz, low levels)

Front 50

Selegiline use

Back 50

Tx of PDH in dogs, Cognitive Dysfunction Syndrome (CDS) in dogs

Front 51

Selegiline Adverse Effects

Back 51

has about 50% efficiacy and should not be used for dogs with PDH and DM, pancreatitis, renal insufficiency or heart failure, should not be admin with other MAOI, tricyclic, antidepressants or opioid analgesics

Front 52

Cyproheptadine MOA

Back 52

inhibits serotonin inhibiting ACTH, has little effect

Front 53

Pergolide mesylate

Back 53

an ergot derivative

Front 54

Pergolide mesylate MOA

Back 54

potent D1 and D2 receptor agonist

Front 55

Pergolide mesylate use

Back 55

pituitary pars intermedia dysfunction (PPID) in horses (equine cushing's dz)

Front 56

tx of adrenal-dependent hyperadrenocorticism (ADH)

Back 56

surgical adrenalectomy, drug therapy (Mitotane)