Adrenal Flashcards

1
Q

what are the adrenocortical hormone disorders

A

cushings and addisons

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2
Q

what is cushing syndrome

A

a collection of s/s associated with HYPERcortisolism

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3
Q

what causes cushing syndrome

A

primary hyperfunction: disease of adrenal cortex
secondary hyperfucntion: disease of anterior pituitary
exogenous steroids: used in management of various diseases

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4
Q

what is the difference between cushing syndrome and disease

A

syndrome: inc in hormone level itself
disease: inc in the triggering hormone

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5
Q

what is the function of cortisol

A

raised blood sugar
protects against physiological effects of stress
suppresses immune and infalmmatory porcess
breaks down proteins and fats
inc cholesterol
maintain vascular system by keep BP up

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6
Q

clinical manifestations of cushings: inc glucose

A

glucose intolerance, hyperglycemia

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7
Q

clinical manifestations of cushings: maintain vascular system

A

HTN, capillary friability (ecchymoses)

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8
Q

clinical manifestations of cushings: protein breakdown

A

muscle wasting, muscle weakness, thinning of skin, osteoporosis, bone pain

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9
Q

clinical manifestations of cushings: fat breakdown

A

redistribution of fat to the abdomen, shoulders, face

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10
Q

clinical manifestations of cushings: supper of immune and inflammatory response

A

impaired wound healing and immune response, risk for infection

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11
Q

clinical manifestations of cushings: CNS excitability

A

mood swings, insomnia

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12
Q

other clinical manifesations of cushings

A

hirsutism, buffalo hump, thinning hair, thinning extremites, striae (stretch marks), moon face

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13
Q

drug therapy for cushings

A

remove tumor with surgery, taper off steriods

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14
Q

what drugs help suppress the synthesis of steroids

A

aminoglutethimide
ketoconazole
should not be used by themselves, not primary treatment

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15
Q

aminoglutethimide moa

A

blocks the synthesis of all adrenal steroids

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16
Q

aminoglutethimide indications

A

temporary therapy to dec cortisol production
- typically for ppl waiting for surgery

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17
Q

aminoglutethimide effects

A

reduces cortisol by 50%
does not affect underlying disease process

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18
Q

aminoglutethimide adverse effects

A

drowsy
N
anorexia
rash

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19
Q

ketoconazole moa

A

antifungal drug that inhibits glucocorticoid steroid synthesis

20
Q

ketoconazole indications

A

adjunct therapy to surgery or radiation

21
Q

ketoconazole adverse effects

A

severe liver damage

22
Q

ketoconazole nursing considerations

A

do not take with ETOH or other liver harmers
no for pregnancy (fetal thyroid damage)
monitor liver function tests

23
Q

what is addison disease

A

disease of the adrenal cortex that causes HYPO secretion of cortisol, aldosterone, androgen (male sex hormoes)
* more severe is low cortisol *

24
Q

cause of addison disease

A

idiopathic
autoimmune
other

25
pathogenesis of addison disease
- adrenal gland is destroyed by disease (primary insufficiency) - adrenal gland stops secreting cortisol, causes lack of negative feedback - anterior pituitary continues to secrete ACTH and MSH to stimulate cortisol production
26
when do symptoms of Addison become evident
when adrenal cortex is about 90% destroyed
27
clinical manifestations of addison: early
anorexia wt loss weakness, malaise, apathy electrolyte imbalances hyperpigmentation of skin
28
clinical manifestations of addison: broad
hypoaldosteronism --> hypoTN, salt cravings hypocorticolism --> hypoglycemia, weakness, fatigue,
29
what does hypoaldosterone cause and why
hypotension for dec vascular tone, CO, circulating blood volume salt cravings: dec serum Na levels, inc serum K levels, and dehydration *fluid volume deficit*
30
what does hypocortisol cause
dec in sugar so hypoglycemia, weakness, fatigue, unsuppressed ACTH production resulting in hyper-pigmentation
31
what is a major complication of addison disease
addisonian crisis --> acute adrenal insufficiency * body has no cortisol to combat stress *
32
cause of addisonian crisis
sudden insufficiency of serum corticosteroids resulting from - sudden loss of adrenal gland - sudden inc in stress in chronic condition - sudden cessation of corticosteroid drug therapy
33
addison pharm in general
replacement of corticosteroids - glucocorticoid: hydrocortisone (drug of choice), prednisone, dexamethasone - some need mineralocorticoid: fludrocortisone
34
steroid replacement therapy information
- dosing needs to mimic natural release of hormones so timing is important and doses are small - never abruptly stop - doses will need to be inc durign times of stress - always maintain emergency supply - wear a medical alert bracelet
35
what is the 3x3 rule
inc dose for 3 days by 3x then taper back down when stress is no longer present
36
what is pheochromocytoma
rare tumor of the adrenal medulla that produces excessive catecholamines (norep, epi) - benign most of the time
37
who is at risk for pheochromocytoma
young to middle age
38
pheochromocytoma pathogenesis
tumor cells secrete catecholamines in response to SNS stimulation (on top of adrenal medulla)
39
what does epi stimulate
alpha and beta recpetors of heart and lungs and vessels
40
what does norepi stimulate
alpha receptors in the vessels
41
clinical manifestations of pheochromocytoma
HTN leads to headache, diaphoresis, tachycardia *can be intermittent of persistent*
42
drug therapy for pheochromocytoma
prefer surgery, but can use alpha adrenergic when tumors are inoperable or preop to reduce HTN
43
what cause HTN in pheochromocytoma
activation of alpha 1 receptors on blood vessels
44
phenoxybenzamine HCL moa
long lasting irreversible blockage of alpha adrenergic receptors to lower BP - alpha 1 and 2 - irreverisble --> so will only be free again once new receptors are made
45
pheochromocytoma adveres effects
orthostatic hypotension reflex tachycardia nasal congestion sexual side effects in men (inability to ejaculate)