Adrenal Disease Flashcards

1
Q

when does cortisol peak

A

4-8am

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1
Q

what feedback system is hpa axis

A

negative feedback

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2
Q

adrenal medulla releases…

A

catecholamines which release epi and norepi

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3
Q

what does adrenal cortex release

A

cortisol
aldosterone
androgens

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4
Q

what does aldosterone do

A

increase na and h20 renal absorption
promotes exretion of k+

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5
Q

what does cortisol do

A

Glucocorticoids (Cortisol)
 Increase blood glucose
 Impacts metabolism
 Increase vasomotor tone
 Excitability of CNS & Mood
 Reduce lymphocytic activity
 Immunosuppression
 Anti-inflammatory response

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6
Q

what do androgens do

A

precursors to testosterone and estrogen

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7
Q

hyposecretion of adrenal gland is…

A

addison’s disease

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8
Q

hypersecretion of adrenal gland is…

A

cushings and pheochromocytoma

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9
Q

what does addisons look like

A

bronze skin
change in distribution of body hair
gi disturbacnes
weakness
hypoglycemia
postural hypotension
wt loss

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10
Q

adrenal crisis

A

proufound fatigue
dehydration
vascular collapes
renal shut down
decreased na
increased k

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11
Q

primary causes of addisons

A

Idiopathic/Autoimmune
 Cancer, TB, HIV
 Gram neg. sepsis (some types)
 Abdominal Radiation
 Adrenal toxic drugs
 Adrenalectomy

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12
Q

secondary causes of addisons

A

Pituitary tumor
 Hypophysectomy
 Brain/Pituitary
radiation
 Abrupt
withdrawal of
exogenous
glucocorticoids

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13
Q

what does primary causes of addisons mean

A

adrenal gland problem

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14
Q

what does secondary causes of addisons mean

A

acth problem

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15
Q

s/s of addisons

A

Hypovolemia  Orthostatic hypotension
 Electrolyte imbalances,  Crave salt
 Lethargic, depressed, confused, forgetful
 Weakness & fatigue
 Wt loss & loss of appetite
 N/V/D & abdominal pain, or constipation
 Menstrual changes
 Loss of body hair, axilla & pubic hair
 Skin pigmentation changes (Primary Dz only)

16
Q

lab findings for addisons

A

Decreased serum cortisol
 Hypoglycemia
 Decreased Na+
 Increased K+
 Increased Ca+
 Increased BUN/Cr

17
Q

what is acth stimulation test

A

Infuse ACTH
 Check cortisol levels
 Primary = no change in cortisol levels
 Secondary = cortisol levels rise

18
Q

what can increase demand of cortisol

A

surgery
trauma
infetion

19
Q

treament of addisons

A

Rapid IV Normal Saline or D5NS (acute)
 IV Steroids (acute) taper to PO (chronic)
 Hydrocortisone (Solucortef) IV
 Prednisone PO
 Treat Electrolyte/Glucose imbalances:
 Correct elevated K+-
 Correct decreased sodium
 Correct decreased glucose-
 If decreased aldosterone- fludrocortisone (Florinef)

20
Q

nsg considerations addisons

A

Fluid volume deficit
 Risk For Injury
 Fatigue
 Monitor cardiac function (K+)
 Diet teaching
 Increased sodium may be needed
 High carb, high protein diet
 S&S of hypoglycemia & treatment

21
Q

primary causes of cushings

A

adrenal tumor
hyperplasia

22
Q

secondary causes cushings

A

Pituitary adenoma that secretes ACTH  Bilateral adrenal
hyperfunction/hyperplasia

23
Q

other causes cushings

A

Ectopic ACTH syndrome (tumors)

24
Q

assessment findings cushings

A

Truncal obesity
 Buffalo hump/Moon face
 Hirsutism/acne
 Thin skin/striae/bruising
 Osteoporosis/Fractures
 Decreased muscle mass
 Cataracts
 HTN/edema/weight gain

25
Q

s/s of cushings

A

Increased appetite
 Insomnia  Fatigue
 Depression
 Oligomenorrhea
 Decreased libido
 Labile emotions- “steroid psychosis”
 Suppressed inflammatory & immune
response
 Peptic ulcers`

26
Q

cushings lab findings

A

ncreased blood glucose
 Increased Na+
 Decreased K+
 Decreased Ca++
 Decreased immune response
 Low antibodies, lymphocytes, eosinophils,
macrophages & cytokines

27
Q

where can increased cortisol levels be found

A

blood
urine
saliva

28
Q

how to diagnose cushings

A

Increased cortisol levels:
 Blood / Urine / Salivary
 Dexamethasone Suppression test
 Should make cortisol go down
 If Cushing’s- remains elevated
 Can also measure plasma ACTH levels
 Decreased with adrenal tumor
 Increased with pituitary tumor
 CT Scan/MRI to r/o tumors

29
Q

treatmnet of cushings

A

Dependent on cause
 Reduce/taper steroids
 Surgical excision
 Adrenalectomy
 Hypophysectomy (pituitary)
 Medications that inhibit adrenal function
 Radiation Therapy

30
Q

nsg considerations cushings

A

Excess Fluid Volume
 Electrolyte imbalance
 Risk for infection
 Risk for injury
 Altered Protection
 Imbalance Nutrition: More Than Body
Requirements
 Disturbed Body Image
 Fatigue/Sleep Deprivation

31
Q

diet recommendations cushings

A

High protein
 High K+
 Low carbohydrate
 Low fat
 Low Na+/fluid restrict
 High Ca++/Vitamin D
 Avoid caffeine/alcohol

32
Q

what os pheochronocytoma

A

Catecholamine producing tumor of the
adrenal gland
 Increased epinephrine & norepinephrine

33
Q

s/s of pheochromocytoma

A

Severe HTN
 HA, pallor with facial flushing, diaphoresis,
palpitations, tachycardia, hyperglycemia

34
Q

how to diagnose pheochromocytoma

A

24 hour urine collection (Metanephrine/Catecholamines)
 Oral Clonidine suppression test
 MRI/CT Scan

35
Q

treament pheochromocytoma

A

Surgery- Adrenalectomy
 Give adrenergic blocking agents before
 Adequate hydration/fluid balance
 Post-op steroids, aldosterone
 Short vs. long-term

36
Q

nsg care pheochromocytoma

A

Monitoring- risk for hypotension and hypoglycemia
 Reduced stress environment
 Education- risk for recurrence, teach clients how to
check/monitor BP

37
Q
A