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Med Surg 3 (theory class) > NURS 444 Week 9 > Flashcards

NURS 444 Week 9 Flashcards

1
Q

Anterior Pituitary Gland

A

-Tropic hormones- controls hormones secreted by other glands (TSH, ACTH, FSH/LH)

  • Growth hormone
  • Prolactin
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2
Q

Posterior Pituitary gland

A
  • Antidiuretic hormone
  • Oxytocin
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3
Q

SIADH

A

abnormal or sustained secretion of ADH (antidiuretic hormone)

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4
Q

SIADH s&s

A
  • fluid retention
  • serum hypo- osmolality
  • dilutional hyponatremia
  • hypochloremia
  • concentrated urine in presence of normal or increased intravascular volume or renal function
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5
Q

common causes of SIADH

A

most common is malignancy (small cell lung cancer?)

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6
Q

Low osmolality
high osmolality

A

low- low particles (electrolytes)

high- high particles

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7
Q

Clinical manifestations of SIADH
(dilutional hyponatremia)

A

> muscle cramping/ twitching
weakness/ fatigue
thirst
dyspnea on exertion
low UOP
increased weight
vomiting
abdominal cramps
seizures
lethargy
confusion
headache
comaa

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8
Q

SIADH diagnostic studies

A

urine and serum osmolality

  • serum osmolality < 280 mOsm/kg
  • specific gravity > 1.005

Serum sodium levels < 120 mEq/L

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9
Q

For mild symptoms and Na >125

A

restrict fluid intake to 800 - 1,000 mL/day

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10
Q

symptomatic and < 120 with symptoms

A
  • IV hypertonic fluids (3% saline)- slow infusion
  • loop diuretic (Lasix)- only when Na is 125
  • fluid restriction of 500 mL/day
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11
Q

Nursing management of SIADH

A

monitor
- VS
- I&O
- daily weights
- LOC
- urine specific gravity
- signs of hyponatremia

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12
Q

Nursing management of SIADH cont.

A
  • Restrict fluids as ordered (500-1000 mL/day)
  • HOB flat or no more than 10 degrees
  • protect from injury
  • seizure precautions
  • oral hygiene
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13
Q

Diabetes Insipidus

A

DEFICIENCY of production or secretion of ADH.

  • decreased renal response to ADH
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14
Q

Classifications of DI

A
  • Central DI: neurogenic DI.
  • nephrogenic DI
  • Primary DI (psychogenic DI)
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15
Q

Central DI (neurogenic DI)

A

most common
associated with a lesion of the hypothalamus, infundibular stem, or posterior pituitary. Interferes with ADH synthesis, transport, or release.
- Can also be caused by brain surgery, injury or infection

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16
Q

Nephrogenic DI

A

adequate ADH but decreased response in kidney.
- hypokalemia and hypercalcemia may lead to nephrogenic DI

-lithium causes drug-induced nephrogenic DI

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17
Q

Primary DI (psych)

A

less common
associated with excessive intake of water intake

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18
Q

DI

A

increased serum osmolality (hypernatremia)

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19
Q

DI clinical manifestations

A

< polydipsia and polyuria
< excretion of a lot of urine (5-20 L/day)
< generalized weakness
< nocturia
< weight loss
< constipation
< poor skin turgor
< hypotension
< tachycardia
< shock
< irritability
< mental dullness
< coma

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20
Q

DI labs

A

5-20 L/day urine output
- low specific gravity < 1.005
- low urine osmolality < 100 mOsm/ kg
- elevated serum osmolality > 295 mOsm/kg

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21
Q

Diagnostic studies for central DI

A

water restriction test
- obtain baseline weight, pulse, BP, plasma, osmolality, and urine specific gravity
- patient withholds fluids for 8-16 hours before test.

22
Q

Primary DI association

A

associated more with overhydration and hypervolemia

23
Q

DI management

A

early detection
maintenance of adequate hydration
patient teaching

24
Q

Central DI management

A
  • fluid and hormone replacement is the cornerstone for treatment!

+ hypotonic saline or D5W
+ desmopressin acetate (DDAVP)- analog of ADH
(given orally, iV, subcutaneuous, nasal spray)
+ aqueous vasopressin, vasopressin tannate, lysine vasopressin
+ Chlorpropamide (Diabenese)
+ Carbamazepine (Tegretol)

25
Q

Management of neurogenic DI cont.

A

dietary measures- low sodium diet (no more than 3g/day)

  • thiazide diuretics
  • Indomethacin (Indocin)- when above not affective. Helps increase renal response to ADH
26
Q

Adrenal Cortex hormones

A
  • glucocorticoids
  • mineralocorticoids
  • androgen
27
Q

Glucocorticoids

A

regulate metabolism, and increase blood glucose

critical to psychologic stress response

28
Q

mineralocorticoids

A

regulate;
-sodium balance
-potassium balance

29
Q

androgen

A

contributes to;
- growth and development in both genders
- sexual activity in adult women

30
Q

Problems associated with adrenal cortex

A

Excess glucocorticoids- most common is administration of exogenous corticosteroids

85% of endogenous cases are due to an adrenocorticotropic hormone (ACTH)- secreting pituitary tumor
Cushing’s Disease (mainly in women 20s-40s)

31
Q

Problems associated with adrenal cortex cont.

A

other causes;
-Adrenal tumors (more common in women 20-40)

  • ectopic ACTH production in tumors outside hypothalamic- pituitary- adrenal axis

usually lung and pancreas tumors
more common in men

32
Q

Cushing’s Syndrome causes

A

> prolonged use of steroids
ACTH-secreting pituitary disease (Cushing’s disease)
Carcinoma/ adenoma- cortisol-secreting in the adrenal cortex
excess secretion of ACTH of neoplasm outside the pituitary/adrenal glands (lung)

33
Q

Clinical manifestations of excess corticosteroids

A
  • weight gain (trunk, face, cervical spine)
  • thinning of hair
  • purplish-red striae on abd, breast, buttocks
  • easy bruising
  • hyperglycemia
  • muscle wasting/ weakness in extremities
  • delayed wound healing
  • mood disturbances; irritability, anxiety
  • insomnia
34
Q

clinical manifestations of excess mineralocorticoid

A

hypertension

unexplained hypokalemia (low K)

35
Q

clinical manifestations of excess androgen

A

menstrual disorders and hirsutism in women

gynocomastia and impotence in men

severe acene

36
Q

Diagnostic studies for adrenal (excess) problems

A

^ 24-hour urine for free cortisol
^ low-dose dexamethasone suppression test used for borderline 24-hr urine cortisol
^ CT/ MRI of pituitary and adrenal glands
^ hypokalemia and alkalosis (ectopic ACTH syndrome and adrenal carcinoma)
^ plasma ACTH may be low, normal, or elevated

37
Q

24-hour urine
Cortisol levels

A

levels above 80-120 mcg/day = Cushing syndrome

38
Q

adrenal (excess) disorder GOAL

A

normalize hormone secretion

39
Q

adrenal (excess) disorder TREATMENT depends on cause

A
  • pituitary adenoma
  • adrenal tumors or hyperplasia
  • ectopic ACTH-secreting tumors: managed by treating primary neoplasm

DRUGS ARE INDICATED WHEN SURGERY IS CONTRAINDICATED OR AS ADJUNCT TO SURGERY. CAN BE TOXIC

40
Q

What to do when Cushing’s syndrome develop from use of corticosteroids

A
  • discontinue
  • taper
  • decrease dose
  • convert to alternate-day regimen

tapering prevents potential life-threatening adrenal insufficiency

41
Q

acute interventions for adrenal excess problems

A

assessment of s&s of hormone and drug toxicity

  • complicating conditions;
    cardiovascular disease DM
    `infection
42
Q

Nursing management for excess adrenal hormones

A
  • monitor: Vs, daily weight, glucose, infection
  • monitor s&s
    abnormal thromboembolic phenomena
  • pre-op and post-op care

TEACH
- wear medic alert bracelet
- avoid exposure to stress, extreme temps., infection
- lifetime corticosteroid replacement is required

43
Q

Adrenocortical insufficiency

A
  • primary cause: Addison’s disease.
  • secondary cause: lack of pituitary ACTH secretion (rarely decrease in mineralocorticoids)
44
Q

Addison’s disease

A

most common cause is autoimmune response

most common in white females

all three classes of corticosteroids are decreased

45
Q

Clinical manifestations of adrenal insufficiency

A

disease usually advanced before diagnosis

** progressive weakness
** fatigue
** weight loss
** anorexia
** skin hyperpigmentation (typically in Addison’s)
- orthostatic hypotension
- hyponatremia
- hyperkalemia
- n&v
- diarrhea
- irritability, depression

46
Q

Addisonian crisis

A

life-threatening
- insufficient adrenocortical hormones

  • sudden, sharp decrease in hormones triggered by;
    ` stress
    ` withdrawal of hormone replacement
    ` after adrenal surgery
    ` following sudden pituitary gland destruction
47
Q

Severe manifestations of glucocorticoid and mineralocorticoids

A

– hypotension
– tachycardia
– dehydration
– hyponatremia
– hyperkalemia
– hypglycemia
– fever
– weakness
– confusion

48
Q

Adrenal insufficiency diagnostic studies

A

subnormal levels of cortisol

  • levels fail to rise over basal levels with ACTH stimulation test;
    latter indicates primary adrenal disease. positive response to ACTH stimulation indicates functioning adrenal gland
  • other abnormal lab tests
  • ECG
  • CT or MRI
49
Q

adrenal insufficiency treatment

A

+ hydrocortisone: both glucocorticoid and mineralocorticoid properties. Used as replacement commonly
+ glucocorticoids must be increased in times of stress
+ mineralocorticoid replacement with fludrocortisone (Florinef) with increased salt in diet

50
Q

Addisonian crisis care

A

Tx directed at;
shock management

high-dose hydrocortisone replacement

51
Q

Acute care for adrenal insufficiency

A

! frequent assessment
! Assess VS
! signs of electrolyte and fluid imbalance every 30 min to 4 hr for first 24 hr
! daily weights
! corticosteroid therapy DILIGENTLY
! protect against infection
! assist w/ daily hygiene
! protect from extremes: light, noise, temp.

52
Q

Instructions for replacement of hormones

A

glucocorticoids given in divided doses

mineralocorticoids given once in the mornign; mimic circadian rhythm, decrease SE of corticosteroids

Med Surg 3 (theory class) (13 decks)

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