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Disorders oI the Posterior Pituitary


Diabetes Insipidus
Syndrome oI Inappropriate Antidiuretic
Hormone (SAIDH)
Posterior Pituitary
Posterior pituitary hormones are
actually
produced in the
hyopthalamus and
only stored in the posterior
pituitary
Posterior pituitary hormones
Antidiuretic hormone
(ADH)
Oxytocin
The hormones secreted by the
posterior pituitary are
Antidiuretic hormone
(ADH) (Also call
vasopressin)
and oxytocin.
ADH contributes to Iluid
balance by
Controlling renal
reabsorption oI Iree water
It also has potent
vasoconstrictive
properties.
Posterior Pituitary
Antidiuretic
hormone (ADH)
(Also called
vasopressin)
Disorders/diseases
resulting Irom
dysIunction
Excess: Syndrome oI
Inappropriate ADH
secretion (SIADH)
Deficiency: Diabetes
Insipidus
SIADH
Posterior Pituitary Hypersecretion
SIADH - Syndrome oI Inappropriate
Hormone Secretion
ADH (anti-diuretic hormone) is a hormone made in the pituitary
gland.
ADH does what the name says -
it stops urination - diuresis
Slowing or stopping urine production leads to Iluid retention.
That in turn causes a dilution oI body sodium
SIADH - Syndrome oI Inappropriate
Hormone Secretion
Depending on the rapidity & the extent oI the sodium drop, a
battery oI S/S appear.
Lethargy, weakness, & Ioggy thinking are common. Personality
changes can happen.
Low sodium levels oIten make pt nauseated
II the situation is not corrected, seizures, coma, & even death
can Iollow.
Syndrome oI Inappropriate Antidiuretic
Hormone Secretion - SIADH
$ADH occurs
when there is
too much vasopression (ADH)
with
inappropriate water retention
and
decreased blood Na levels
Results Irom many
diIIerent conditions and drugs
May be produced by
certain tumors such as
lung cancer
or may result Irom
chronic lung diseases.
Medicines associated with
SIADH include common
meds as antidepressants,
antianxiety agents,
antipsychotic agents, seizure
meds, and desmopressin
(DDAVP)
Syndrome oI Inappropriate Antidiuretic
Hormone Secretion - SIADH
Results Irom
Inability to produce & secrete dilute urine
Water retention
Increased extra cellular Iluid volume
Hyponatremia Diseases that aIIect the hypothalamus
Dx oI SIADH
The Iollowing criteria should be IulIilled beIore a
diagnosis oI SIADH can be made:
persistent excretion oI concentrated urine with no reason
Ior ADH release
normal renal and adrenal Iunction
no edema or hypovolaemia should be present
the urine osmolarity should be greater than the serum
osmolarity
Physical Assessment oI SIADH
Initially, S/S are R/T retention oI water.
Most common complaints
GI disturbances-loss oI appetite, N,V
Nurse
Weighs pt & documents any recent weight gain
Checks pt extremities Ior presence oI edema
Pt with SIADH have Iree water, not salt, that is retained &
edema is not usually present due to intracellular Iree water
Assessment-Clinical ManiIestations oI SIADH
ater retention, hyponatremia, & resulting fluid shifts have an
eIIect on $ function, especially when serum sodium level drops.
Normal serum Na 135-145.
S/S occur when serum Na level drops below 125,
and especially below 115
linical $$
Lethargy, headaches, hostility, uncooperativeness, disorientation
Early sign -Change in LOC
Neurological S/S can progress Irom lethargy and headaches to
decreased responsiveness, seizures, and coma.
Nurse assess deep tendon reIlexes, which are oIten or sluggish
V/S changes-tachycardia associated with increased Iluid volume &
hypothermia associated with CNS disturbance
Normal Lab Values
serum osmolality
(285-295 mOsm/kg)
sodium
(Na 135-145 mEq/L)
chloride (95-105 mEq/L)
Urine osmolality -
-24 hr specimen
500-800 mOsm/kg H20
-Random specimen:
50-1200 mOsm/kg/H20
Osmolality is measures in
milliosmoles per kilogram
oI water (mOsm/kg).
The major determinants oI
plasma osmolality are Na,
glucose, & urea
Urine speciIic gravity
1.003-1.030
1.002-1.035
Highdehydration
Lowdiabetes insipidus
concerntrated urine
~ than 50-100 mOsm/kg
with
normal vascular volume
and
normal renal Iunction
Lab Assessment in SIADH
W 97,cellular Iluid volume expansion aIIects electrolyte levels in the
serum and the urine
Lcv|'cd urine sodium levels and speciIic gravity reIlect an
3.7c|cd concentration oI the urine
Serum sodium levels are /0.70,80/, oIten as low as 110 mEq/L
(normal serum sodium 135-145 mEq/L) due to emxm<eIIwImx <<Iwre
emgmrm1<r and 3.70,80/ Na excretion
~.~ ..~..~ causes changes in both plasma and urine osmolality
Plasma osmolality is decreased, and the urine is hyperosmolar in
relation to the plasma
Osmolality
&rine osmolality -24 hr specimen 500-800 mOsmg H20
Random specimen: 50-1200 mOsmgH20
Osmolality is measures in milliosmoles per kilogram oI water
(mOsm/kg). The major determinants oI plasma osmolality are Na,
glucose, & urea.
The Kidneys are mainly responsible Ior maintaining the concentration
oI body Iluids within this range oI osmolality.
hen the plasma osmolality becomes abnormal,
changes in the level oI antidiuretic hormones (ADH)
cause the kidneys to
conserve or increase the excretion oI water
to return the osmolality to normal
Posterior Pituitury hypersecretion - SIADH
$ymptoms - fluid retention
low serum osmolality
(normal285-295 mOsm/kg)
dilutional low sodium
(normal Na 135-145 mEq/L)
low chloride
(normal95-105 mEq/L)
Causes -
Diseases eIIect the hypothalmus
pneumonia
TB
positive pressure ventilation
Trauma
concerntrated urine
(~ than 50-100 mOsm/kg)
with normal vascular volume and
normal renal Iunction
muscle cramps & weakness
cerebral edema, lethargy, anorexia,
headache, seizures, coma.
AIDs
delirium tremens
Ectopic ADH secreting
tumor
SIADH - Diagnostic Tests
Blood & Urine tests
Must have
low serum sodium
low plasma osmolality
level
Inappropriated
concentrated urine
(increased urine osmolality
level)
These tests indicate
excess oI body water
relative to the amount oI
body sodium.
In other words, ADH is
inappropriately holding onto
too much water.
Important to eliminate other
causes of a low sodium level,
such as hypothyroidism or
adrenal insuIIiciency, beIore
settling on a dx oI SIADH
Rx- removing the oIIending
drug or tumor, & treat the
underlying condition.
Posterior Pituitary: SIADH,DI
Affect kidney's ability to concentrate urine
Measured by urine speciIic gravity
Measures number and size oI particles
Normal: 1.003 - 1.030
High dehydration
Low Diabetic Insipidus 1.001-1.005
Concentrated urine: SIADH
Dilute urine: DI
Posterior pituitary: SIADH
ADH excess water intoxication
water is reabsorbed, so assess Ior
increased blood volume, Iluid retention
concentrated urine, low urine output
dilutional hyponatremia (same Na, more H20)
muscle cramps and weakness
anorexia, n/v, irritable, conIused, disorient, seizure
SIADH and Hyponatremia
Hyponatremia- a lower than normal concentration oI sodium in
the blood
Caused by inadequate excretion oI water oI by excessive water
in the circulating bloodstream
In a severe case the pt may experience water intoxication,
with conIusion and lethargy, leading to muscle excitability,
convulsions, and coma.
Treatment: Fluid and electrolyte balance may be restored by IV
inIusion oI a balanced solution or a Iluid restricted diet.
SIADH
Diagnosis & Treatment
Diagnosis
measure urine volume
and
osmolality
Treatment
II Na125
Restrict Iluids 800 - 1000
ml/day.
Daily weigh
Monitor
3 - 5 Saline solution IV
Na 134mmol/L
se osmol ~280mmol/kg
SG~1005
low BUN, creatinine, Hb, Hct.
Lasix iI Na105
(cardiac symptoms)
SIADH
Diagnostic Study
Hyponatremia
Decreased plasma
osmolality
Urine sodium and urine
osmolality elevated
Elevated ADH
levels
Normal renal, adrenal, &
thyroid Iunctions
Nursing Assessment
Headache,Personality change,
ConIusion,Irrritability,
Dysarthria(diIIicult, poorly
articulated speech),
Lethargy,Impaired memory
Restless, weakness, Iatigue,
gait disturbances
Weight gain
SIADH Treatment
Water Restriction is the cornerstone oI treatment
Decreased water intake allows serum sodium level to rise normally.
The maximum amount oI water that pt with SIADH are allowed to
drink is just slightly more that the amount oI urine they produce
Pt must have regular serum sodium measurements to ensure that the
water restriction has been eIIective
Dehydration- The most concerning potential side eIIect Irom
treatment is dehydration.
SIADH treatment
Restrict Iluid intake (800-1000 cc/day)
Daily weight $trict I & O
Monitor urine speciIic gravity
0.9 NS inIusion(to raise the serum Na level iI ater
intoxication is severe)
Monitor Ior hyponatremia
Lasix may be admin to block circulatory overload
Drugs-demeclocyclin HCL & lithium-may be admin to
block renal response to ADH, intereIeres with action oI ADH
Drugs - Phenytoin - inhibits ADH release
Surgery & Chemo -to remove or destroy neoplasms that may
be the underlying cause oI this syndrome
SIADH treatment
Demeclocycline (Declomycin)
Lithium
Used Ior:
Excess secretion oI ADH or SIADH
Action:
Inhibits ADH action in kidney
Blocks renal response to ADH, interIeres with action oI ADH
Therapeutic outcome:
Decreased urine speciIic gravity
Analysis - Nursing Diagnosis - SIADH
1. Fluid Volume Excess R/T compromised regulatory
mechanism, excess ADH
2. High Risk Ior Injury R/T an altered level oI
consciousness, conIusion, & the possibility oI seizures
3. Altered Nutrition: Less than Body Requirements R/T
an inability to ingest or digest Iood or absorb nutrients
because oI biologic Iactors (ex-anorexia, N/V)
4. Altered Thought Processes R/T physiologic changes
within the central nervous system
Planning & Implementation
!lanning: !t Goals
The primary goal is that the pt`s
Iluid balance will be restored
nterventions to treat $ADH
(!t are !lan) consists of
Restriction water intake
Using diuretics to promote the
excretion oI water
Administering drugs that
interIere with the action oI
ADH
Replacing lost sodium
Fluid Restriction
Any excessive Iree water intake
will Iurther dilute the serum
sodium concentration
Strict I&O, daily weights,
guides the determination oI the
degree oI Iluid restriction
necessary. A wt gain oI 2
pounds (or 1 Kg) or more per
day or a gradual increase during
several days is cause Ior
concern.
A 1 Kg weight increase is
equivalent to 1000ml Iluid
retention (1Kg 1 L)
Planning &
Implementation
Drug Therapy
Diuretics are sometimes
used to treat pt with
SIADH, to rid the body
oI excessive Iluid,
especially iI CHF
results Irom Iluid overload
II diuretics are used, be
aware oI potential eIIect
oI electrolyte losses;
sodium loss can be
potentiated, which Iurther
contributes to the clinical
picture oI SIADH
Hypertonic saline (3 NaCl) may be
used to treat SIADH
Helps correct serum sodium level
Raises Na osmolality in the blood
Removes excess intracellular Iluid
Cells shrink in hypertonic solution
IV saline is given cautiously because it
may contribute to the Iluid overload
already present & precipitate an episode
oI CHF.
II the pt needs routine IV Iluids, the MD
orders a solution in saline (5 dextrose
in saline) rather than a solution in water.
Planning & Implementation
High Ris for njury
Promote saIety
Monitor pt neuro status
Subtle Changes, such as muscle
twitching beIore neuro S/S
progress to seizures or coma.
Check LOC to time, place, &
person because disorientation
may be present.
ConIusion is another neuro
sign. Nurse reduces
environmental stimuli & explain
interventions in simple terms.
Flow sheets contain ongoing
inIo about LOC, motor &
sensory neuro assessment, &
pertinent lab data helpIul in
detecting trends.
Decreased LOC and seizures
are complications oI the low
serum sodium level R/T SIADH
ursing issues
Moniforing fIuid boIonce(s/s fIuid refenfion):
Cordioc probIems (wofer reobsorbed so bId voIume):
MeuroIogicoI probIems (heodoche sei;ures,cerebroI edemo,
como,):
Energy Iimifofions (muscIe cromps, weokness):
AIIied heoIfh probIems (onorexio):
Pisk for injury: (confusion, muscIe fremors, efc.)
ursing issues
Fluid Volume Excess R/T inability to excrete water
Hyponatremia with plasma hypo-osmolality
eight gain
!otential for njury
Institute seizure precautions and saIety measures
Reorient conIused pt
!revent complications of immobility
Recognize decreased gastric motility due to hyponatremia,
combined with Iluid restriction and decreased mobility - ~constipation
Diabetes Insipidus
Posterior Pituitary
Diabetes Insipidus
Uncommon syndrome
oI posterior pituitary hypoIunction
S/S
Increased thirst - polydipsia
Increased urination - polyruia
Results Irom
ADH (Vasopression) deIiciency, which prevents the kidneys
Irom reabsorbing water
Inability to conserve water
Posterior pituitary : DI
Diabetes insipidus: 'to pass through
Decreased ADH diuresis
Water is lost, so assess Ior:
Kidneys produce large amts oI du'c urine
(5L-1L in 24hrs)
low urine speciIic gravity (1.1-1.5)
polyuria (~urine output), polydipsia (~thirst)
Iluid deIicit
weight loss, turgor,dehydration, hypotension, constipation,
shock
Posterior Pituitury hyposecretion
Diubetes Insipidus
Symptoms-
Thrist & polyuria 5 - 20Lday
$G < 1005
&rine osmol < 100 mmolL
$e osmol > 295 mmolg
Nocturia
eaness > weight loss,
hypotension, tachycardia,
constipation, shoc
$leep deprivation-due to interrupted
by need to drin fluids & urinate
Urine speciIic gravity low
(1.001-1.005)
Urine osmolality decreased
(50-200 mOsm.kg)
Urine less concentrated than
plasma
Plasma osmolality elevated
(~295 mOsm/kg)
Hypernatremia in -lood
Diabetes Insipidus
Etilogy
Familial or idiopathic
Head injury
Neuorsurgery
Damage to the
hypothalamic areas that
produce ADH
uuse
Lesion of hypofhoImus
inferferes wifh ADH
synfhesis/fronsporf/reIeo
se
broin fumour
pifuifory/cronioI surgery
heod froumo
CMS infecfion
voscuIor diseose.
Diabetes Insipidus
Etilogy
Drug Related
Ethanol &
Phenytoin (ClassiIication: Antiarrhythmic, Anticonvulsant):
Inhibit ADH secretion
Lithium (ClassiIication: Antimanic) &
Demeclocycline(ClassiIication:anti-inIective-Tetracycline):
Inhibit ADH action in kidney
4 Types oI Diabetes Insipidus
eurogenic -oIso known os
- cenfroI
- hypofhoIomic
- pifuifory
- neurohypophyseoI
- uused by o deficiency of fhe
Anfidiurefic hormone,
vosopressin
Z ephrogenic-oIso known os
- Vosopressin - resisfonf
- uused by insensifivify of fhe
kidneys fo fhe effecf of fhe
onfidiurefic hormone,
vosopressin
3) 0esfogenic-oIso known
os
- 0esfesfionoI
- uused by o deficiency of
fhe onfidiurefic hormone,
vosopressin, fhof occurs
onIy during pregnoncy
4) Dipsogenic, o form of
primory poIydipsis
- uused by
AbnormoI fhirsf ond fhe
Excessive infoke of wofer
or ofher Iiquids
Diagnosis & Rx
Diabetes Insipidus
Diugnosis D,I,
History and examination
Water deprivation test
(see next slide)
Vasopressin challenge test
(see next slide)
24 hours urine
84/:2 in -44/
MRI oI pituitary, hypothalmus
and skull to see damaged areas
%reutment
Intravenous Iluids
Hypertonic saline IV-
Extracellular solution to pull
Iluid Irom outside the cell to
inside the cell
Vasopressin SC/IM/IV, nasal
prep
Long term DDAVP
(Desmopression) nasal prep.
(analog ADH)
Diagnosis - Fluid Deprivation Test
(To identiIy cause oI polyuria)
Baseline VS, then check hourly-allows RN to detect changes,
esp postural hypotensin & tachycardia
Deprive pt oI Iluid-Observe Ior compliance with Iluid restriction
Hourly- urinary output, speciIic gravity, & osmololity
Urine test results determine whether testing can proceed.
Testing can proceed iI urinary osmolality stabilized Ior 3 samples
and 3 wt loss is noted
Dx- Vasopressin challenge
Order Ior 5 Units oI aqueous vasopressin sc
Continue hourly urinary measurements
Vasopressin triggers and ongoing assessment detects
anges in urinary specific gravity and osmolality
SpeciIic gravity & osmolality decrease with primary
and secondary diabetes insipidus
No response is seen with nephrogenic diabetes
insipidue
Diabetes insipidus treatment
Vasopressin (!itressin) : is ADH
lassification: Hormone (antidiuretic)
&ses: Treatment oI central diabetes insipidus sue to deIicient
antidiuretic hormone.
RouteDose: IM, sc, nasal spray
Nsg mplications:
replace Iluid: saline and glucose
monitor I & O
check speciIic gravity
observe electrolytes
Monitor adverse reactions-abdominal cramps, angina, MI
Diabetes insipidus treatment
Desmopressin (DDAV!)
lassification: Hormone (andiuretic)
ndication: Management oI primary nocturnal eneuresis unresponsive
to other treatment modalities
po, sc, IV, Intranasal
Action: An anologue oI naturally occuring vasopressin (antiuretic
hormone). Primary action is enhanced reabsorption oI water in the
kidneys
Therapeutic Effects: Prevention oI nocturnal enuresis. Maintenace
oI appropriate body water content in diabetes insipidus.
Nsg mplication: Monitor urine & plasma osmolality & urine volume
Irequently. Assess pt Ior symptoms oI dehydration (excessive thirst,
dry skin & mucous membranes, tachycardia, poor skin turgor)
Weigh pt daily & assess Ior edema
Observe Ior Water Intoxication
with all agents
ADH excess water intoxication
water is reabsorbed, so assess Ior
increased blood volume, Iluid retention
concentrated urine, low urine output
dilutional hyponatremia (same Na, more H20)
muscle cramps and weakness
anorexia, n/v, irritable, conIused, disorient, seizure
Diabetes Insipidus
Fluid Volume DeIicit R/T inability to conserve water
Thirst, dry mucous membranes
Decreased skin turgor
Hypotension, tachycardia
Hemoconcentration, plasma hyperosmolality, hypernatremia
Increased urine output
Dilute urine-monitor speciIic gravity
ursing Issues
FIuid ond eIecfroIyfe imboIonce:
P/T >diuresis,
monifor urine ond pIosmo osmoIorify
monifor specific grovify (usuoIIy wiII be Iow wifh diuresis)
monifor urine voIume (usuoIIy wiII be high b-I0L in Z4 hr)
Theropy successfuI when urine oufpuf ond specific grovify begin fo
refurn fo normoI
monifor s/s dehydrofion
weighf pf doiIy & ossess for edemo
FIuid voIume deficif
Murse wiII monifor for hypofension, consfipofion, shock
SIeeping probIems: P/T nocfurio & increosed fhirsf

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