Treatment Rapid rehydration w/isotonic solution (1L NS) Vasopressors - plasma (for hypotension) Volume expanders d/t volume that's lost from losing aldosterone/mineralcorticoids

Polystyrene sulfonate (Kayexalate) > Kayexalate releases Na+ ions in exchange for K+ IV glucose (solution or bolus) Oxygen Steroid replacement - IV hydrocortisone 100mg bolus then Q8 for 24 hrs then tapered

Nursing Interventions Monitor VS (esp HR & BP) & orthostatic q4h Daily wts > glucocorticoid overdose & overhydration may be occurring

Monitor electrolytes (esp Na+ & K+) > elevated K+ above 6 mEq/L causes nerve & muscle irritability - numbness, tingling, tachycardia, intestinal colic & diarrhea progressing to cardiac arrest, convulsion, & flaccid paralysis, acidosis > hyponatremia - cellular swelling 1st manifested in the CNS causing irritability, apprehension, confusion, seizures & coma; cold, clammy skin; postural hypotension; n/v; abd cramping; flaccid paralysis ! if steroids too high, Na+ & water (edema) will accumulate & K+ will be lost

Secondary adrenal insufficiency r/t ACTH deficiency from the pituitary > can be from pituitary tumor > pituitary essentially sleeping d/t exogenous glucocorticoids dx'd w/low ACTH & low cortisol

treatment w/glucocorticoids only > pt to keep glucocorticoid inj adrenal crisis remains a risk factor

Adrenal & Pituitary Disorders Flashcards by Kaylie Krauzyk

Adrenal Glands

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Adrenal Hormones (“sugar, salt, sex”)

Cortex

Glucocorticoids - cortisol

Mineralcorticoids - aldosterone

Androgens - dehydroepiandrosterone & androstenedione

Medulla

Catecholamines - epinephrine & norepinephrine

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“sugar”

affects metabolism
regulates blood sugar levels, growth, anti-inflammatory action & dec effects of stress

Glucocorticoids

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“salt”

e.g., aldosterone

affects sodium absorption, loss of K+ by kidney & ultimately BP

Mineralcorticoids

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“sex”

are converted to testosterone peripherally

Androgens

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increase HR, RR, BP, & cardiac output
vasoconstrict & bronchodilate
fight-or-flight response

Catecholamines

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Adrenal Disorders: Cortical

Primary adrenal insufficiency - Addison’s Disease, Addisonian crisis

Secondary adrenal insufficiency
- hyperaldosteronism
- Cushing’s syndrome
- Cushing’s disease

Adrenal Disorders: Medullary

Pheochromocytoma

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a primary adrenal failure
- etiology: 80% autoimmune
- others incl chronic infections, CMV, lyme
- adrenals make insufficient glucocorticoids & mineralcorticoids

Addison’s disease

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Secondary adrenal insufficiency refers to the suppression of the hypothalamic/pituitary/adrenal axis

e.g.

hyperaldosteronism
Cushing’s syndrome
Cushing’s disease

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Is a catecholamine-releasing tumor located in the adrenal 85% of the time but can be found in other symptomatic tissues throughout the body (nerve)

dx based on excessive catecholamines in blood or urine
CT, MRI, or nuclear scan
treatment - surgical

Pheochromocytoma

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Normally, the pituitary gland secretes ___ throughout the day & peaks in the morning & shortly >we rise

This stimulates the adrenals to secrete their hormones

___ is also secreted when the body is stressed & elicits the fight-or-flight response (glucocorticoids are released to dec inflammation, slight sodium retention & release glucose stores in the liver for energy)

ACTH

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___ will conserve sodium to inc blood volume

___ will increase HR, RR, & bronchodilate & vasoconstrict

All of which will increase BP & cardiac output to supply our skeletal muscle w/good blood supply to run or remove the organism from the stressor

Mineralcorticoids

Catecholamines

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Addison’s (adrenal insufficiency ↓) s/s

Usually autoimmune process contributing to etiology (75%); also, AIDS, infarct, ca, bilat adrenalectomy, & TB
! has nothing to do w/ACTH or the pituitary

→ mild fatigue
→ irritability
→ wt loss
→ n/v
→ postural hypotension
→ hyperpigmentation

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Diagnostics

Blood hormonal assays -

↑ or ↓ cortisol

↑ or ↓ ACTH (in 1° adrenal insufficiency)

↑ or ↓ ACTH (in 2° adrenal insufficiency)

May see ↑ or ↓ aldosterone ?

↓ cortisol

↑ ACTH 1°

↓ ACTH 2°

↓ aldosterone

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Serum -

↑ or ↓ Na+

↑ or ↓ K+

↑ or ↓ glucose

↓ Na+

↑ K+

↓ glucose

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Imaging

xray (for bony matter)

MRI & CT (soft tissue analysis)

angiogram

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___ ___ test if hyponatremia, hyperkalemia to determine if low ACTH is the cause

cosyntropin stimulation (test)

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Treatment/Nursing

Glucocorticoid replacement
- dexamethasone (Decadron), hydrocortisone (Hydrocortone)
- monitor for hypercortisolism
- 2/3 dose in am & 1/3 dose in pm to mimic body’s natural diurnal adrenal activity
- may require 100mg cortisol inj if severely injured or incapacitated - MedicAlert badge

→ monitor for osteoporosis, glaucoma, & other sx’s of long-term glucocorticoid use

Mineralcorticoid replacement

fludrocortisone (Florinef)
→ watch BP; look for wt gain - edema
sodium & fluid replacement

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back, abdomen, or leg pain
depressed or changed mentation/loss of consciousness
volume depletion - hypotension & shock
electrolyte imbalance -
↑ or ↓ Na+
↑ or ↓ K+

Addisonian crisis

↓ Na+

↑ K+

! may progress if not treated or if pt not adequately covered by supplemental hormones during a major stressor (like surgery); added stressors equate to more supplemental steroids to prevent crisis

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Addisonian crisis

sudden profound weakness
acute renal failure
hypoglycemia
hyperthermia

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Treatment

Rapid rehydration w/isotonic solution (1L NS)
Vasopressors - plasma (for hypotension)
Volume expanders d/t volume that’s lost from losing aldosterone/mineralcorticoids

Polystyrene sulfonate (Kayexalate)
> Kayexalate releases Na+ ions in exchange for K+
IV glucose (solution or bolus)
Oxygen
Steroid replacement - IV hydrocortisone 100mg bolus then Q8 for 24 hrs then tapered

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Nursing Interventions

Monitor VS (esp HR & BP) & orthostatic q4h
Daily wts
> glucocorticoid overdose & overhydration may be occurring

Monitor electrolytes (esp Na+ & K+)
> elevated K+ above 6 mEq/L causes nerve & muscle irritability - numbness, tingling, tachycardia, intestinal colic & diarrhea progressing to cardiac arrest, convulsion, & flaccid paralysis, acidosis

> hyponatremia - cellular swelling 1st manifested in the CNS causing irritability, apprehension, confusion, seizures & coma; cold, clammy skin; postural hypotension; n/v; abd cramping; flaccid paralysis

! if steroids too high, Na+ & water (edema) will accumulate & K+ will be lost

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Monitor for hypoglycemia
Monitor u/o
> monitor for oliguria r/t shock
> pt should carry identifying info on dz, emergency #’s, MD #’s & rx’s/dosages
> pt to carry IM form of dexamethasone & MedicAlert bracelet

Minimize stressors

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Secondary adrenal insufficiency

r/t ACTH deficiency from the pituitary
> can be from pituitary tumor
> pituitary essentially sleeping d/t exogenous glucocorticoids
dx’d w/low ACTH & low cortisol

treatment w/glucocorticoids only
> pt to keep glucocorticoid inj
adrenal crisis remains a risk factor

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Cushing's ? overproduction of ACTH; endogenously in pituitary

disease

? excess glucocorticoid exposure; exogenously

syndrome

Most common cause admin of exogenous corticosteroids 85% of endogenous cases d/t ACTH-secreting pituitary tumor

Other causes include - adrenal tumors - ectopic ACTH production in tumors outside hypothalamic-pituitary-adrenal axis [usually lung & pancreas tumors]

Cushing's s/s * r/t excess corticosteroids & mineralcorticoids ! Wt gain most common feature - trunk (centripetal obesity) - "moon face" - cervical area - transient wt gain from ↑ Na+ & water retention

* Hyperglycemia > glucose intolerance assoc w/cortisol-induced insulin resistance > inc gluconeogenesis by liver

* Protein wasting > catabolic effects of cortisol leads to weakness esp in extremities > protein loss in bones leads to osteoporosis, bone & back pain * Loss of collagen

* Wound healing delayed * Mood disturbances, insomnia * Irrationality, psychosis

* HTN > Mineralcorticoid excess may cause HTN 2° to fluid retention * Acne > Adrenal androgen excess may cause pronounced acne, virilization in women, femininization in men

- Seen more commonly in adrenal carcinomas * Women: menstrual disorders & hirsutism * Men: gynecomastia & impotence * Purplish red striae on abd, breasts, or buttocks

Diagnostics * 24-hr urine for free cortisol > levels of 50-100 mcg/day in adults indicates Cushing syndrome * False positives can occur w/depression, stress, or alcoholism * Plasma cortisol levels may be elevated

* CT & MRI of pituitary & adrenal glands

↑ or ↓ Na+, blood glucose ↑ or ↓ Ca+, K+, lymphocytes ↑ or ↓ salivary cortisol levels

↑ ↓ ↑

Associated findings that are not diagnostic of Cushing's - Leukocytosis - Lymphopenia - Eosinopenia - Hyperglycemia - Glycosuria - Hypercalciuria - Osteopenia/porosis

Diagnostics High or normal ACTH levels indicate ACTH-dependent ___ ___ (pituitary or ectopic tumor)

Cushing's disease

Low or undetectable ACTH levels indicate an adrenal or exogenous etiology

Treatment * Primary goal is to normalize hormone secretion; depends on cause

* If the issue is r/t exogenous steroids, these can be tapered down as much as possible

Surgical removal of tumor and/or radiation for __ __

pituitary adenoma

An adrenalectomy for __ __ or __

adrenal tumors; hyperplasia

For inhibition of ___ production * Cyproheptadine (Periactin) * Bromocriptine * Somatostatin

ACTH

For inhibition of ___ function * mitotane (Lysodren) * aminoglutethimide (Cytadren) * trilostane (Modrastane)

adrenal

Common s/e's of drug therapy ! anorexia, n/v ! GI bleeding ! depression ! vertigo ! skin rashes ! diplopia

* If Cushing syndrome develops during use of corticosteroids, gradually discontinue therapy, decrease dose; convert to an alternate-day regimen * Gradual tapering avoids potentially life-threatening adrenal insufficiency

Nursing Interventions: Pre-op care * Control HTN & hyperglycemia * Hypokalemia must be corrected w/diet & K+ supplements

* High protein diet helps correct protein depletion > Low in cal, carbs, & Na+ * No salt added diet to 2 g/day > Reassure pt physical sx's will resolve when hormone lvls return to normal

Nursing Interventions: Post-op care * Risk of hemorrhage is inc b/c high vascularity of adrenal glands * Manipulation of glandular tissue may release hormones into circulation * BP, fluid balance, & electrolyte lvls tend to be unstable b/c hormone fluctuations

* High doses of corticosteroids administered by IV during & several days >surgery * Report significant changes in BP, RR, HR * Bed rest until BP is stabilized >surgery

* Adrenal insufficiency develops if corticosteroid dosage tapered rapidly * Indications of hypocortisolism > vomiting > inc weakness > dehydration > hypotension

* Meticulous care should be taken when accessing skin, circulation, or body cavities to avoid infection > Normal inflammatory responses are suppressed

? Tumor in medulla - excess catecholamines (epi/norepi) s/s - paroxysm stimulated by smoking, urinating, abdominal displacement, rx's sympathetic overactivity - hyperglycemia, hyperthyroidism, psychoneurosis, high BP in excess of 250/150, pounding HAs, apprehension (feeling of impending doom), n/v, sweating > can progress to stroke, blindness, & death Inc BP can worsen w/stress or surgery or manipulation of tumor

Pheochromocytoma

Pheochromocytoma * Alpha-adrenergic blocking agents or nitroprusside - stabilize BP

* Adrenalectomy once stable

Diagnostics * Urinary catecholamines & metanephrine are direct & conclusive tests * Serum epinephrine & norepinephrine will be elevated * Urinary vanillymandelic acid in urine also diag

! Must avoid coffee, tea, bananas, chocolate, vanilla, ASA, nicotine, amphetamines, decongestants <24h urine testing * Clonidine suppression test - in normal individual, would block catecholamine release * Imaging studies

* Post-op: monitor & treat for adrenal insufficiency, hypotension, hemorrhage, & shock > Poss hypotension r/t adrenal insufficiency treated w/vasopressors, volume expanders, IV fluids, dopamine (keep in mind when giving pain rx's) * ICU hemodynamic monitoring

* Monitor for paralytic ileus - hematoma * Corticosteroid replacement - bilat adrenalectomy

Pituitary Disorders ? Diabetes insipidus (DI) Syndrome of Inappropriate Antidiuretic Hormone (SIADH)

Posterior Pituitary

? Gigantism/acromegaly Hyperprolactinemia Hyperthyroidism

Anterior Pituitary

? Pituitary hypersecretion of growth hormone (GH) S/S - HA, vision difficulties, very tall (before cartilage growth plates ossify) - enlarged hands, feet, nose, tips, tongue, joint pain, prominent cheekbones, jaw, forehead, sleep apnea, snoring, perspiring * Atherosclerosis, DM, HTN

Gigantism/acromegaly

Diagnostics GH levels ↑ GH level after ingestion of a glucose tolerance test (GTT) > Excess GH inc insulin lvls > GTT measures the rate of insulin secreted by the beta cells

xray can show changes in the bony sella turcica region CT/MRI to rule out/in soft tissue lesions Angiography will rule out/in vascular malformations

Treatment * excision of tumor * radiation * octreotide & bromocriptine

? a dopamine agonist-GH suppressant Inhibits GH & prolactin secretion & anti-parkinsonism s/e's - HA, lightheadedness - vomiting, abd cramps, fatigue - GI hemorrhage, peptic ulcer

bromocriptine (Parlodel)

? a GH suppressant Can be given IV, IM, SC May decrease effectiveness of insulin, glucagon, oral antidiabetics Monitor GH lvls, weigh q2-3d, & report >5lb gain/wk; watch for dec u/o, periph edema, stool consistency (prolongs intestinal transit)

octreotide (Sandostatin)

Nursing Interventions for hypophysectomy surgery * Protection of oral/gingival incision site * Freq oral hygiene - no brushing; keep lips moist

* Nasal drip pad monitored for bleeding & CSF * Monitor s/s for inc ICP ! elevated BP, widening PP, low pulse, pupil changes, alt resp pattern, dec LOC ! Inc pressure inc risk CSF leak (halo sign) clear w/yellow around perimeter ! inc swallowing may indicate CSF leak > no bending over & straining during BM * Check CSF for glucose if pos → is CSF

* Avoid blowing nose, cough, or sneezing * Monitor graft donor site * Monitor for transient diabetes insipidus (DI) > polyuria 2-15L/day > specific gravity of 1.005 or less, notify MD if >200 mL/hr, polydipsia

* Pre-operative neuro & ophthalmological exam to compare to post-op

? Excessive ADH secretion > retain fluids (hypervolemia) & develop a dilutional hyponatremia * Etiology: bronchogenic carcinoma, vasopressin overuse from DI

Syndrome of Inappropriate Antidiuretic Hormone (SIADH)

Risk factors - disorders of the CNS like head injury, brain surgery, tumors, infections, or rx's like vincristine (an antineoplastic), phenothiazines, or thiazide diuretics

Rx's can either affect the pituitary or inc sensitivity to renal tubules to ADH

Manifestations Serum: low sodium, low osmolality, hypervolemia w/o edema, fatigue, HA, anorexia, nausea, JVD, dec DTRs ↑ or ↓ BUN Urine: high Na+, high osmolality ! seizures & coma r/t hyponatremia

↑ BUN

Management - eliminate cause > wt may inc w/o edema r/t hypervolemia - JVD - give diuretics (Lasix), demeclocycline [to facilitate free water clearance - interferes w/ADH action - monitor for nephrotoxicity) - PO fluid restriction - I&O, daily wt

- lab electrolytes > hyponatremia - confusion, lethargy, irritability, seizures, coma, dec DTRs, fatigue, HA, anorexia, nausea - serum osmolality low > urine high in Na+ - urine osmolality high - restoration of electrolytes must be gradual; may use IV hypertonic sol'n (3% NaCl)

? A deficiency of ADH, vasopressin; can be central, nephrogenic, dipsogenic, gestational

Diabetes Insipidus (DI)

? ADH secretion or synthesis affected, complete DI - no ADH secreted Can occur 2° brain tumors, head trauma, infections of the CNS, & surgical ablation or radiation or centrally-acting rx's

Central DI

? Relates to failure of the renal tubules to respond to ADH Can be r/t hypokalemia, hypercalcemia, & to rx's (lithium, ETOH, glucocorticoids, phenytoin) - vasopressin resistant

Nephrogenic DI

? Only during pregnancy ADH isn't produced efficiently during pregnancy or water diuresis results from destruction of ADH by the placental enzyme, vasopressinase

Gestational DI

? C/b a defect to the thirst mechanism in the hypothalamus C/b abn thirst & excess fluid intake then ADH is suppressed r/t hypovolemia

Dipsogenic DI

Manifestations/Diagnostics * Polydipsia - dry lips, skin * Elevated serum sodium/plasma osmolarity - elevated serum Na+ d/t drop in BP from hypovolemia & inc aldosterone to reabsorb Na+

* Polyuria/low sodium/diluted urine > urinary SG of 1.001-1.005 > Polyuria from few to 18 L/day, nocturia & dec sleep; dilute & clear 24hr urine can be done to monitor for electrolytes, osmolality, & total vol > Upper limit of normal for a 24hr urine vol for an adult is 50mL/kg body wt * Dehydration - hypovolemic shock

* 24 hr fluid intake & output u/o <4L & greater than intake - urine is dilute w/a low SG (<1.005) & low osmolarity (50-200 mOsm/kg) * ADH levels

* Imaging studies > to view pituitary, hypothalamus, & renal defects

? A synthetic pituitary antidiuretic hormone Increases reabsorption of water by inc permeability of collecting ducts in the kidneys dec u/o intranasal, PO, IV, SC Monitor for water intoxication, hyponatremia, confusion, rapid wt gain, seizures

Desmopressin (DDAVP)

DDAVP Challenge Test - inject 2 mcg of DDAVP SC - ask pt to empty bladder @ 1 & 2 hrs >the injection & measure the osmolality of these samples

- if either sample has an osmolality >50% higher than the value immediately before DDAVP was given, pt probably has **complete (severe) neurogenic DI** - if the rise in urine osmolality >DDAVP is <50%, then **complete (severe) nephrogenic DI is very likely**

Fluid deprivation test * withhold fluids for 8-12 hrs * Weigh pt freq * Inability to slow down the u/o & fail to concentrate urine are diagnostic

* Stop test if pt is tachycardic or hypotensive Sweat test - gold standard test for cystic fibrosis (CF) may show elevated chlorine levels

Pharmacologic & Nursing Management * DDAVP - PO or intranasal > Can be given IM if dehydration is severe

* Can also use chlorpropamide (Diabinese) in mild dz as they potentiate the action of ADH & stimulate production

* In the case of **pituitary (central/neurogenic) DI**, the treatment of choice is usually a synthetic form of ADH known as DDAVP * Taken by inj, nasal spray, or tablet at whatever dose and/or freq is necessary to completely eliminate the inc in urination, thirst, & drinking w/o allowing periodic "breakthrough" or "escape"

* Only 'toxic' s/e is water intoxication & it's rare provided the pt remembers to drink fluids only when they're truly thirsty * Occasionally, other treatment like chlorpropamide may be used in preference to DDAVP

* Pts w/**dipsogenic DI** or other forms of primary polydipsia can't take DDAVP in usual way b/c they invariably develop water intoxication during treatment

* Only thing that can be done here is to voluntarily limit fluid intake as much as poss & sometimes take a single small dose of DDAVP @ bedtime to reduce freq of awakenings to urinate

* Maintain adequate hydration * Educate pt about actions of rx's, how to admin rx's, wear MedicAlert bracelet * Monitor polydipsia/polyuria - may need to inc dose of vasopressin or desmopressin

* Nephrogenic - HCTZ or indomethacin (Indocin) in pts w/nephrogenic DI; treatment w/DDAVP or chlorpropamide is ineffective * If the underlying cause of the DI can't be eliminated, s/s of DI can be reduced by dec amt of salt in the diet & taking certain diuretics which have a paradoxical effect in this dz

* Monitor I&O & daily wt gain > Weights normally trend down w/dehydration * Monitor serum & urine electrolytes, SG of urine > Too much medication can inc water retention

Adrenal & Pituitary Disorders Flashcards

- Hypopituitarism / Hyperpituitarism - Diabetes Insipidus - Syndrome of Inappropriate Antidiuretic Hormone (SIADH) - Adrenal Insufficiency - Hypercortisolism (Cushing’s) - Hyperaldosteronism