Adrenal Gland Flashcards
Primary adrenal failure (Hypoadrenocorticism)
Dependent on which zones destroyed
Glucocorticoids (cortisol) or mineralocorticoids insufficient
What causes primary adrenal failure
Spontaneous
Iatrogenic (mitotane, ketoconazole, trilostane- medication treating hyperadreno)
Secondary hypoadrenocorticism
Pituitary failure to secrete ACTH (isolated glucocort. insufficiency)
What causes secondary hypoadrenocorticism
Idiopathic (suppression of ACTH)
Neoplasia
Genetic (standard poodles, collies)
T/F: Hypoadrenocorticism is a life threatening condition with mineralcorticoid deficiency and requires immediate life saving intervention
TRUE
Maintain Na, K and water balance
CS of hypoadrenocorticism
Lacks of gluco: depression, lethargy, anorexia, vomiting
Lack of mineral: collapse and bradyarrhthmias
When is Hypoadrenocorticism glucocorticoid tx required
Iatrogenic or spontaneous secondary hypoadren.
Primary addison’s disease without mineral deficiency
↑ with stress, illness, sx, trauma and exercise
How is the glucocorticoid tx given?
↓ or discontinuation therapy
↓ to physiologic doses slowly
Over 1-3 weeks
Hypoadrenocorticism glucocorticoid tx
Dexamethasone
Prenisolone sodium succinate
Hydrocortisone
Glucocortidoid adverse effects
Exogenous admin → adrenal cortisol suppression and atrophy
When is hypoadrenocorticism mineralcorticoid tx needed?
Only if aldosterone deficient
Not recommended until Na concentration within reference ranges
Mineralcorticoid replacement for hypoadrenocorticism
Fludocortisone (PO QD)
Desoxycorticosterone (IM monthly)
Fludocortisone
Ease of dx/ adjusting dose
Daily therapy
Expensive
Side effects of Fludocortisone
PU/PD, polyphagia, hair loss, weight gain
↑ prevalence when combined with gluco
Desoxycorticosterone
Low adverse effects if used alone
Less common tx failures
Infrequent admin
Desoxycorticosterone adverse effects
Missinga dose could be fatal
_____________ is considered an addisonian (hypoadrenocorticism) crisis
Hyperkalemia
Hyperkalemia
IVFT (↑ GFR and restores circulating blood vol)
Slow infusion of calcium gluconate (protects mycardium)
Insulin (glucose move into cell wall, K flows)
Dextrose (moves K intracellulary
Hypoadrenocorticism tx response
Occurs within 1-2 hrs
Cats takes longer
Na deficiency causes renal washout (several days diurese)
Pituitary dependent hyperadrenocorticism (cushing’s)/ PDH
85% of K9/ feline
Benign tumor secretes ACTH → ↑ release of cortisol from adrenal glands
Adrenal dependent hyperadrenocorticism
50% benign
Autonomously secretes coritsol
CS associated with hyperadrenocorticism
PU/PD, polyphagia, skin lesions (thin, non healing), anestrus
Goals of hyperadrenocorticism therapy
Eliminate hypersecretion of cortisol
Dog: medical managment
Cats: bilateral adrenalectomy (lifelong tx for hypoadren)
T/F: no drug will cure PDH
TRUE
tx focuses on mediating amount of cortisol present
Mitotane (hypoadren) MOA
Adrenolytic: causes selective necrosis of zona fasciculate and reticularis (that secrete cortisol and sex hormones)
Specfiic for hyperplastic glands
Mitotane induction and maintenance
Induction: serum cortisol levels @ normal range
Maintenance: based on dose and duration, depends on ACTH test
Mitotane uses
Patients with diabetes mellitus
Removes the cause for insulin resistance (hypocalcemia may occur)
Adverse effects of mitotane
GI: V/D, anorexia
Neurologic: weakness, ataxia
Rapid drop cortisol levels
Goal of adrenal dependent hyperadrenocorticism
Complete destruction of the tumor tissue in the adrenals
Require high doses and longer induction times
Admin predisone concurrently
Trilostane (hyperadren) MOA
Synthetic steroid analog that inhibits adreal enzyme production of cortisol and aldosterone
Adverse effects of trilostane
Mild lethargy and vomiting
Can affect aldosterone → hypoadrenocortisol crisis can occur
Ketoconazole (hyperadren) MOA
Triazole antifungal
↓ serum cortisol and testosterone
Ketoconazole uses
Dogs that can’t tolerate mitotane
Limited efficacy and expensivw
