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43 Cards in this Set

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The adrenal cortex produces 2 classes of steroids
1) corticosteroids (glucocorticoids and mineralocorticoids)
2) androgens
Natural functions of glucocorticoids
1) protect glucose-dependent functions
2) promote lipolysis
3) decrease protein synthesis
Natural functions of mineralocorticoids
1) maintain fluid and electrolyte balance (enhance Na reabsorption, expand EC fluid volume, increase in GFR)
Major glucocorticoid
cortisol
Major mineralocorticoid
aldosterone
Therapeutic use of glucocorticoids
1) nonadrenal disorders principally involving the immune system
2) neoplasia
3) replacement therapy for hypoadrenocorticism
Mechanism of Action
Glucocorticoid effects result from their interaction with cellular glucocorticoid receptors
Effects of glucocorticoid therapy
1) exert direct effects in many tissues
2) physiologic/pharmacologic effects are difficult to separate
3) adverse effects can be produces by prolonged duration of steroid administration and/or high doses
Glucocorticoid effect on energy metabolism
1) enhance carb metabolism
2) protects critical glucose-dependent serebral and cardiac functions (via enhancement of gluconeogenesis and peripheral anti-insulin effects)
3) gluconeogenesis via mobilization of FFA from adipose and reduced protein synthesis
GC effects on energy metabolism: Adverse effects
1) excessive GC-induces gluconeogenesis can cause increased protein catabolism--> muscle wasting
2) delayed wound healing and thinning of skin via reduces collagen synthesis
3) glucose intolerance, insulin resistance and overt diabetes mellitus and redistribution of body fat
GC Effects and Water and Electrolyte Balance
1) aldosterone most important mineralocorticoid in fluid and electrolyte balance
2) PU/PD in dogs (rarely cats) via: a) inhibition of ADH release and action and b) direct effects on renal distal tubules to prevent water reabsorption
GC effects on water and electrolyte balance: Adverse effects
1) salt retention and potassium losses
2) vary w/ differing GC agents
3) bring on or exacerbate hypertension
4) calcium stores are reduced through
GC effects on the cardiorespiratory systems
1) enhance vascular reactivity to other vasoactive substances; thereby maintaining blood pressure
GC effects on the cardiorespiratory systems: Adverse effects
1) promote or exacerbate hypertension or congestive heart failure via mineralocorticoid effects to: a) increase fluid volume, b) reduce endothelial-derived dilator substances, c) enhance other vasoconstrictors
GC effects on the endocrine system
1) show anti-insulin effects and increasing PTH
2) suppress the hypothalamic-pituitary adrenal axis (HPAA) resulting in reduction of synthesis and release of several stimulation hormones including: ACTH, TSH, GH, FSH
GC effects on the endocrine system: Adverse effects
1) unmasking or exacerbation of diabetes mellitus or iatrogenic hyperadrenocorticism adre possible with excess glucocorticoids
2) Induction of parturition with high doses of steroids in late prognancy resulting in abortion can occur in the horse and ruminant
GC effects on the CNS
1) reduce CSF production--> decreased intracranial pressure
2) sense of euphoria/dependence in humans (animals?)
3) may protect against hypoxic-ischemic brain damage by decreasing CNS energy requirements
GC effects on the CNS: Adverse Effects
1) polyphagia and obesity in dogs
2) abrupt discontinuation--> withdrawl (animals?)
3) may reduce threshold for seizure
GC Effects in the digestive tract
1) hepatomegaly from enhanced storage of precursors in liver
2) increased fat mobilization--> pancreatitis
GC effects in the digestive tract: Adverse effects
1) increased risk of GI ulceration
2) increased gastric acid and pepsin secretion coupled w/ reduced mucus production and mucosal cell renewal
GC effects on Immune and hematologic systems
1) anti-inflammatory and immuno-suppressive effects
2) immunosuppressive effects occur preferentially on CMI over humoral immunity
3) Capable of inducing apoptosis in lymphoid cells
4) inhibit cellular arachidonic acid production and subsequent proinflammatory mediators (analgesia)
GC effects on immune and hematologic systems: Adverse effects
1) reduced ability to mount CMI responses to virus
2) bacteria and fungi are pronounced w/ excessive GCs
3) leads to increased risk of serious infection
GC Agents: Steroid Bases
1) Determines (a) anti-inflammatory potency, b) mineralocorticoid potency, c) duration of action/biologic half-life)
2) GCs categorized as: a) short-acting, b) inermediate-acting, c) long-acting
3) Steroid hormones are metabolized by the liver then excreted by the kidney
GC Agents: Formulations
1) Oral: tablets w/ free steroid base--> rapid uptake and plasma half-life similar to biologic half-life
2) Parenteral: esterification of steroid base w/ different moieties--> affects water solubility, route of administration, and plasma half-life
3) Topical: opthalmic, otic, and derm use; free steroid base or ester
GC Agents: Formulations: Sodium phosphate, hemisuccinate/succinate esters, free-steroid solutions
1) very soluble
2) rapid availability of steroid
3)plasma drug half-life similar to biologic half-life
4) IV, IM, SQ, topical
GC Agents: Formulations: Acetate and acetonide steroid esters
1) poorly water soluble resulting in steroid deptos w/ long plasma drug half-lifes
2) SQ, IM, intralesional, intraarticular, topical
Properties of good synthetic GC agents
1) minimal mineralocorticoid properties (salt-retaining)
2) maximal anti-inflammatory capacity
Short-acting steroids
1) Hydrocortisone: topical
2) Cortisone: prodrug converted to cortisol in the liver; similar properties/uses to hydrocortisone
Intermediate-acting steroids: Prednisone/prednisolone
1) Prednisone (prodrug) is metabolized by the liver--> prednisolone
2) Prednisone use not an issue unless fulminate liver disease exists
3) Oral and parenteral administration
4) intermediate half-life ideal for alternate day therapy
5) moderate anti-inflammatory potency and little to no mineralocorticoid effects
Intermediate-acting steroids: Isoflupredone
1) greater anti-inflammatory properties compared to others in this category
2) IM, intraarticular, intralesional
Intermediate-acting: Triamcinalone
1) oral and parenteral as acetonide form
2) intermed half-life and GC potency
3) suppression of HPAA limites use to intralesional and intraarticular routes
4) not ideal for alternate day therapy
Long-acting
Betamethasone, dexamethasone, and flumethasone
1) increased anti-inflammatory potency
2) no mineralocorticoid effects
3) longer biologic half-lives
4) significant HPAA suppression
5) indicated less frequently than other preps
6) used for specific conditions
7) used more commonly in large animals due to convenience and cost issues
GC Usage: 5 categories
1) Replacement therapy
2) Intensive short-term or emergency therapy
3) Anti-inflammatory and anti-allergic therapy
4) Immunosuppressive therapy
5) Treatment of certain neoplasias
GC Usage: Physiological replacement Therapy
1) limited to GC deficiencies (Addison's) in small animals
2) animal makes ~ 1mg/kg of cortisol daily-- should be met in replacement therapy
3) less potent, short-acting or intermediate-acting steroids daily orally
4) not ideal for alternate day therapy
GC Usage: Intensive short-term or emergency therapy
1) beneficial in CNS: injury, shock, heat, stroke, allergic emergencies, bovine ketosis
2) long-acting and potent injectable GCs w/ a rapid onset of action (dex, flumeth)
3) Intermediate-acting: pred; should be used IV at shock dosages (10x immunosuppressive doses)
4) required for 48 hr when cessation of GC therapy or reduction of GC dosage occurs
5) improve hemodynamics in cerebral trauma and shock
GC Usage: Anti-inflammatory and Anti-allergic therapy
1) Most common use in vet med
2) Conditions where GCs are used: pruritic dermatoses, allergic pulmonary disease, allergic and inflammatory gastroenteritis, inflammation associated w/ eye, liver, gingiva, joints
3) Oral therapy: start w/ induction dosing regimen followed by a maintenance dosing regimen
4) dosage/frequency of side effects vary btwn species
5) anti-inflam doses ~5-10x the physiologic dose
6) given for 7-14 days, followed by decreased maintenance dose of variable duration
7) maintenance: use lowest effective dose possible to minimize HPAA suppression and adverse effects; use alternate day therapy
GC Usage: Immunosuppressive therapy
1) Diseases: IMHA, thrombocytopenia, immune-mediated arthritis
2) use protracted courses to prevent recurrence of clinical signs
3) Initial oral immunosuppressive dose for induction, then lower maintenance dose (pred, dex)
4) alternate day therapy best
5) therapy usually lasts 2-3 months or life to prevent recurrence of clinical signs
GC Usage: Neoplasia
1) oral pred used for its cytotoxic effects on lymphoid cells to treat lymphoma; also used for anti-inflammatory effects in mast cell tumors
2) GC used in combination w/ other anti-neoplastics, due to rapid development of tumor resistance
GC Usage: Topical/Intraarticular and Intralesional GC therapy
1) high concentrations can be delivered to the disease site w/ minimal systemic effects through: topical preparations, intralesional, intraarticular
2) inflammation at admin site will increase systemic absorption
3) Intraarticular admin of GCs for treatment of join conditions; most commonly used in large animals. Concerns include infection and articular cartilage damage
GC Usage: Special Considerations: Alternate day GC therapy and withdrawl of therapy
1) GC therapy w/ steroids > 2 wks duration = chronic therapy
2) Chronic GC therapy accompanied by suppression of HPAA
3) HPAA suppression occurs w/ short-term use of higher doses of GCs, adverse effects not of great concern
4) 2 guidelines for GC therapy: alternate day therapy; w/d from GC therapy
GC Usage: Special Considerations: Alternate day GC therapy
1) reduces adverse effects by allowing HPAA time to recover on "off" days
2) limited to small animals (not practical in large)
3) not effective alone
4) use as maintenance after initial cessation of clinical signs
5) use steroids w/ low potency, minimal mineralocorticoid effect, and intermediate biologic half-lives (preds)
GC Usage: Special Considerations: Withdrawal from GC therapy
1) HPAA suppression and adrenal atrophy-- reversible
2) abrupt cessation can cause recurrence of clinical signs or precipitate adverse effects associated w/ adrenal insufficiency
3) "Steroid withdrawal syndrome" more common in humans
4) tapering dose gradually + alternate day therapy allows for restoration of HPAA and reduces chances of adverse effects
GC Usage: Special Considerations: Contraindications/precautions w/ GC therapy
1) Infection: generally contraindicated unless replacement therapy in Addison's disease; don't want to suppress CMI which is needed in virus and fungal infections especially; use bactericidal antibiotic if steroid needed
2) Vaccines: antibody production not affected by GCs; avoid attenuated-live vaccines
3) Endocrine: avoid steroid use in diabetes mellitus as hyperglycemic effects interfere w/ diabetic regulation; abortions, and teratogenic effects also
4) GI: avoid steroids in pancreatitis due to worsening secondary to increased FA circulation; ulceration; no NSAIDs w/ steroids
5) Misc: can exacerbate hepatic disease; use caution in cases of congestive heart failure or hypertension; may increase seizure episodes in epileptic animals