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NUR 202 Week 5 > Adrenal & Pituitary Disorders > Flashcards

Adrenal & Pituitary Disorders Flashcards

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

1
Q
A

Adrenal Glands

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2
Q

Adrenal Hormones (“sugar, salt, sex”)

Cortex

Glucocorticoids - cortisol

Mineralcorticoids - aldosterone

Androgens - dehydroepiandrosterone & androstenedione

A

Medulla

Catecholamines - epinephrine & norepinephrine

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3
Q

?

“sugar”

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

A

Glucocorticoids

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4
Q

?

“salt”

e.g., aldosterone

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

A

Mineralcorticoids

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5
Q

?

“sex”

are converted to testosterone peripherally

A

Androgens

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6
Q

?

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

A

Catecholamines

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7
Q

Adrenal Disorders: Cortical

Primary adrenal insufficiency - Addison’s Disease, Addisonian crisis

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

A

Adrenal Disorders: Medullary

  • Pheochromocytoma
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8
Q

?

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

A

Addison’s disease

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9
Q

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

A

e.g.

  • hyperaldosteronism
  • Cushing’s syndrome
  • Cushing’s disease
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10
Q

?

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
A

Pheochromocytoma

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11
Q

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)

A

ACTH

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12
Q

___ 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

A

Mineralcorticoids

Catecholamines

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13
Q

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

A

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

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14
Q

Diagnostics

Blood hormonal assays -

?

↑ or ↓ cortisol

↑ or ↓ ACTH (in 1° adrenal insufficiency)

↑ or ↓ ACTH (in 2° adrenal insufficiency)

May see ↑ or ↓ aldosterone ?

A

↓ cortisol

↑ ACTH 1°

↓ ACTH 2°

↓ aldosterone

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15
Q

Serum -

↑ or ↓ Na+

↑ or ↓ K+

↑ or ↓ glucose

A

↓ Na+

↑ K+

↓ glucose

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16
Q

Imaging

xray (for bony matter)

MRI & CT (soft tissue analysis)

angiogram

A
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17
Q

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

A

cosyntropin stimulation (test)

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18
Q

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

A

Mineralcorticoid replacement

  • fludrocortisone (Florinef)
    → watch BP; look for wt gain - edema
  • sodium & fluid replacement
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19
Q

?

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

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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20
Q

Addisonian crisis

  • sudden profound weakness
  • acute renal failure
  • hypoglycemia
  • hyperthermia
A
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21
Q

Treatment

  • Rapid rehydration w/isotonic solution (1L NS)
  • Vasopressors - plasma (for hypotension)
  • Volume expanders d/t volume that’s lost from losing aldosterone/mineralcorticoids
A
  • 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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22
Q

Nursing Interventions

  • Monitor VS (esp HR & BP) & orthostatic q4h
  • Daily wts
    > glucocorticoid overdose & overhydration may be occurring
A
  • 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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23
Q
  • 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
A
  • Minimize stressors
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24
Q

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
A
  • treatment w/glucocorticoids only
    > pt to keep glucocorticoid inj
  • adrenal crisis remains a risk factor
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25
Q

Cushing’s

?

overproduction of ACTH; endogenously in pituitary

A

disease

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26
Q

?

excess glucocorticoid exposure; exogenously

A

syndrome

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27
Q

Most common cause admin of exogenous corticosteroids

85% of endogenous cases d/t ACTH-secreting pituitary tumor

A

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

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28
Q

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

A
  • Hyperglycemia
    > glucose intolerance assoc w/cortisol-induced insulin resistance
    > inc gluconeogenesis by liver
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29
Q
  • 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
A
  • Wound healing delayed
  • Mood disturbances, insomnia
  • Irrationality, psychosis
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30
Q
  • HTN
    > Mineralcorticoid excess may cause HTN 2° to fluid retention
  • Acne
    > Adrenal androgen excess may cause pronounced acne, virilization in women, femininization in men
A
  • Seen more commonly in adrenal carcinomas
  • Women: menstrual disorders & hirsutism
  • Men: gynecomastia & impotence
  • Purplish red striae on abd, breasts, or buttocks
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31
Q

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
A
  • CT & MRI of pituitary & adrenal glands
32
Q

↑ or ↓ Na+, blood glucose

↑ or ↓ Ca+, K+, lymphocytes

↑ or ↓ salivary cortisol levels

A

↑

↓

↑

33
Q

Associated findings that are not diagnostic of Cushing’s

  • Leukocytosis
  • Lymphopenia
  • Eosinopenia
  • Hyperglycemia
  • Glycosuria
  • Hypercalciuria
  • Osteopenia/porosis
A
34
Q

Diagnostics

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

A

Cushing’s disease

35
Q

Low or undetectable ACTH levels indicate an adrenal or exogenous etiology

A
36
Q

Treatment

  • Primary goal is to normalize hormone secretion; depends on cause
A
  • If the issue is r/t exogenous steroids, these can be tapered down as much as possible
37
Q

Surgical removal of tumor and/or radiation for __ __

A

pituitary adenoma

38
Q

An adrenalectomy for __ __ or __

A

adrenal tumors; hyperplasia

39
Q

For inhibition of ___ production

  • Cyproheptadine (Periactin)
  • Bromocriptine
  • Somatostatin
A

ACTH

40
Q

For inhibition of ___ function

  • mitotane (Lysodren)
  • aminoglutethimide (Cytadren)
  • trilostane (Modrastane)
A

adrenal

41
Q

Common s/e’s of drug therapy

! anorexia, n/v
! GI bleeding
! depression
! vertigo
! skin rashes
! diplopia

A
  • 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
42
Q

Nursing Interventions: Pre-op care

  • Control HTN & hyperglycemia
  • Hypokalemia must be corrected w/diet & K+ supplements
A
  • 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
43
Q

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
A
  • 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
44
Q
  • Adrenal insufficiency develops if corticosteroid dosage tapered rapidly
  • Indications of hypocortisolism
    > vomiting
    > inc weakness
    > dehydration
    > hypotension
A
  • Meticulous care should be taken when accessing skin, circulation, or body cavities to avoid infection
    > Normal inflammatory responses are suppressed
45
Q

?

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

A

Pheochromocytoma

46
Q

Pheochromocytoma

  • Alpha-adrenergic blocking agents or nitroprusside - stabilize BP
A
  • Adrenalectomy once stable
47
Q

Diagnostics

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

! 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
48
Q
  • 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
A
  • Monitor for paralytic ileus - hematoma
  • Corticosteroid replacement - bilat adrenalectomy
49
Q

Pituitary Disorders

?

Diabetes insipidus (DI)
Syndrome of Inappropriate Antidiuretic Hormone (SIADH)

A

Posterior Pituitary

50
Q

?

Gigantism/acromegaly
Hyperprolactinemia
Hyperthyroidism

A

Anterior Pituitary

51
Q

?

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
A

Gigantism/acromegaly

52
Q

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

A

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

53
Q

Treatment

  • excision of tumor
  • radiation
  • octreotide & bromocriptine
A
54
Q

?

a dopamine agonist-GH suppressant

Inhibits GH & prolactin secretion & anti-parkinsonism

s/e’s
- HA, lightheadedness
- vomiting, abd cramps, fatigue
- GI hemorrhage, peptic ulcer

A

bromocriptine (Parlodel)

55
Q

?

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)

A

octreotide (Sandostatin)

56
Q

Nursing Interventions for hypophysectomy surgery

  • Protection of oral/gingival incision site
  • Freq oral hygiene
  • no brushing; keep lips moist
A
  • 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
57
Q
  • 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
A
  • Pre-operative neuro & ophthalmological exam to compare to post-op
58
Q

?

Excessive ADH secretion
> retain fluids (hypervolemia) & develop a dilutional hyponatremia

  • Etiology: bronchogenic carcinoma, vasopressin overuse from DI
A

Syndrome of Inappropriate Antidiuretic Hormone (SIADH)

59
Q

Risk factors

  • disorders of the CNS like head injury, brain surgery, tumors, infections, or rx’s like vincristine (an antineoplastic), phenothiazines, or thiazide diuretics
A

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

60
Q

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

A

↑ BUN

61
Q

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
A
  • 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)
62
Q

?

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

A

Diabetes Insipidus (DI)

63
Q

?

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

A

Central DI

64
Q

?

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

A

Nephrogenic DI

65
Q

?

Only during pregnancy

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

A

Gestational DI

66
Q

?

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

A

Dipsogenic DI

67
Q

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+
A
  • 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
68
Q
  • 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
A
  • Imaging studies
    > to view pituitary, hypothalamus, & renal defects
69
Q

?

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

A

Desmopressin (DDAVP)

70
Q

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
A
  • 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
71
Q

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
A
  • Stop test if pt is tachycardic or hypotensive

Sweat test - gold standard test for cystic fibrosis (CF) may show elevated chlorine levels

72
Q

Pharmacologic & Nursing Management

  • DDAVP - PO or intranasal
    > Can be given IM if dehydration is severe
A
  • Can also use chlorpropamide (Diabinese) in mild dz as they potentiate the action of ADH & stimulate production
73
Q
  • 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”
A
  • 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
74
Q
  • 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
A
  • 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
75
Q
  • 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
A
76
Q
  • 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
A
  • 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

NUR 202 Week 5 (2 decks)

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