ATI Unit 12 Posterior Pituitary Disorders Flashcards Preview

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Flashcards in ATI Unit 12 Posterior Pituitary Disorders Deck (23):

what does the posterior pituitary gland secrete and what does under- and oversecretion of this do?

- secretes vasopressin or ADH (antidiuretic hormone)

- oversecretion = SIADH (syndrome of inappropriate ADH) where you hold on to too much water and there's little urine outpus

- undersecretion of ADH = diabetes insipidus, always too much urine output, hypotension, thirst

(both often result in fluid/electrolyte imbalances)


what are the three types of diabetes insipidus

1) primary = hypothalamus or posterior pituitary messed up
2) nephrogenic = inherited problem in renal tubules (don't react to vasopressin/ADH)
3) drug-induced = lithium carbonate (Lithium) or demeclocycline (Declomycin)


what two drugs can induce diabetes insipidus?

1. lithium carbonate (Lithium)
2) demeclocycline (Declomycin)
- changes how kidneys respond to ADH


so what are some assessments you want to check out with diabetes insipidus?

1. are they taking lithium or demeclocycline
2. is there anything cranial related: think tumors, trauma, cranial surgery, and infection (meningitis, encephalitis)
3. dehydration/decreased thirst response
4. people with renal failure/insufficiencies
5. are they using diuretics?
6. dysphagia/poor food intake


subjective and objective findings of diabetes insipidus

- polyuria (output of 4-20 L/day of dilute urine)
- polydipsia (excessive thirst, 2-20L/day)
- nocturia
- fatigue
- dehydration EVB thirst, weight loss, muscle weakness, headache, constipation, dizzinesss

- sunken eyes
- tachycardia
- hypotension
- loss of skin turgor
- dry mucous membranes


Lab tests for diabetes insipidus

Urine (DILUTE)
Decreased urine.....
- urine specific gravity (less than 1.005)
- urine osmolality (less than 300 mOsm/L)
- pH
- Na+, K+
(as urine volume increases, osmolality decreases)

- increased everything (as serum volume decreases, osmolality increases)

Radioimmunoassay - decreased ADH


using a water deprivation test for diabetes insipidus

- basically withhold fluids and see if urine still stay diluted despite this
- if postural hypotension, dizziness, tachycardia develop, STOP, patient is dehydrated


using a vasopressin test for diabetes insipidus

- a subq vasopressin shot is given and if patient has diabetes insipidus, urine output after shot will be increased specific gravity
- differentiates nephrogenic from central DI


if a patient has diabetes insipidus what's a food to avoid?

caffeine - diuretic effect


if a patient with DI develops constipation what foods would help?

bulk food and fruit juices


what meds are given for DI?

1. ADH replacement agents (desmopressin acetate or DDAVP; aqueous vasopressin or Pitressin)
- synthetic ADH
- teachings: weight, I/O match, electrolytes, specific gravity

2. ADH stimulants - carbamazepine (Tegretol)
- anticonvulsants stimulate release of ADH
- monitor for thrombocytopenia (bruising, fever, sore throat)

3. vasopressin (Pitressin)
- the hormone
- can cause vasoconstriction so caution in clients with CAD
- water intoxication: headache, confusion
- lifelong therapy


what weight gain should a client report?

greater than 0.9kg (2lb)


what is the general change in the body that SIADH causes?

- posterior pituitary releasing too much ADH
- water is reabsorbed
- renin-angiotensin system blocked and sodium still secreted
Leads too....
water intoxification
dilutional hyponatremia
cellular edema (can cause decreased serum osmolality b/c of fluid shifts)


so what are the risk factors in a patient with SIADH?

- malignant tumors like the oat-cell lung cancer can cause hypersecretion
- another is increased intrathoracic pressure like with positive pressure ventilation
other: cranial trauma, meningitis, stroke, pain, stress, meds

diuretics can further complicate sodium losses


which meds can cause SIADH

- alcohol
- lithium carbonate
- phenytoin


major assessments in SIADH

- bad bad: confusion lethargy and Cheyne-Stokes respiration mean impending crisis; when Na+ level drop further = seizures, coma, death

- manifestations of volume excess: hypertension, tachycardia, crackles in lung, distended neck beins, taut skin, intake > output


Lab tests for SIADH

Urine (Concentrated)
increases specific gravity, Na+, osmolarity

Serum/Blood (DILUTE)


what is the first priority in nursing care for SIADH

prevent further hemodilution
- restrict oral fluids 500-1000mL/day
- comfort measures includes mouth care, ice chips, lozenges, and staggered water intake for thirst


nursing care for SIADH

a. flush tubes with NS not H2O to replace Na+ and prevent further hemodilution
- I/Os
- monitor for up BP, tachycardia, hypothermia
- weight daily (.9kg/2lbs = 1L of fluid)
- diuretic possible if fluid overload loop diuretic


medications for SIADH

1) demeclocycline (Declomycin)
- tetracycline derivative
- may cause DI
- may take week
- monitor for yeast infection
- client rinse toothbrush with diluted 10% bleach solution and increase yogurt consumption

2) lithium carbonate
- blocks renal response to ADH
- poss DI
- monitor for lithium toxicity, tremors, ataxia, NVD
- monitor blood glugose

3) furosemide (Lasix)
- causes Na+ exretion may worsen dilutional hyponatremia (nausea, decreased appetite, vomitting)

4) administer hypertonic fluids
- SOB could mean heart failure


what are the complications of SIADH

water intoxication, cerebral edema, severe hyponatremia


what are the symptoms of water intoxication

lung crackes, distended neck beins, neuro status changes, edema, decreased urinary output


what is CPM

central pontine myelinolysis
- condition from SIADH treatment characterized by nerve damage b/c of myelin sheath destruction in brainstem (pons); common cause is rapid change in Na+ levels in body (hyponatremia treated and levels rise too fast)

- when treating, monitor serum sodium levels and neuro status q2-4hrs