ENDOCRINE PATHOPHYSIOLOGY:

ALTERATIONS IN PITUITARY FUNCTION

www.kanonhealth.org

THE POSTERIOR PITUITARY

DIABETES INSIPIDUS (DI) &

SYNDROME OF INAPPROPRIATE ANTIDIURETIC HORMONE

(SIADH)

17 MARCH 2021

POSTERIOR PITUITARY HORMONES

• ADH

• CONTROLS PLASMA OSMOLALITY VIA

OSMORECEPTORS

• AFFECTS PERMEABILITY OF RENAL

TUBULES AND COLLECTING DUCTS

• OXYTOCIN

• UTERINE CONTRACTION

• INTRAMAMMARY PRESSURE AND

MILK EXPRESSION

• SPERM MOTILITY

• Synthesized in the hypothalamus

• Stored and secreted by the posterior pituitary

ADH

• ADH

• V1 – ARTERIAL WALLS

• CONSTRICTS SMOOTH MUSCLE WITHIN THE ARTERIAL WALL

• V2 – KIDNEY COLLECTING DUCTS

• IT REGULATES FLUID BALANCE

• V3 – PITUITARY TISSUE

• INVOLVED IN ACTH RELEASE

• Synthesized in the hypothalamus

• Stored and secreted by the posterior pituitary

• Maintains fluid and electrolyte balance

DIABETES INSIPIDUS

•LACK OF ENOUGH ADH IN BLOODSTREAM OR RESISTANCE TO

ADH IN KIDNEY

•ETIOLOGY

•CENTRAL OR NEUROGENIC DIABETES INSIPIDUS (DI)

•NEPHROGENIC DI

•PSYCHOGENIC (PRIMARY POLYDIPSIA OR DIPSOGENIC)

ADH IS RELEASED IN RESPONSE TO SMALL ELEVATIONS IN

SERUM OSMOLALITY, SECONDARILY IN REACTION TO

HYPOVOLEMIA OR HYPOTENSIVE SITUATIONS

.

•NEPHROGENIC

• INABILITY OF KIDNEY TUBULES TO RESPOND TO CIRCULATING ADH

•DECREASE OR ABSENCE OF ADH RECEPTORS

•CELLULAR DAMAGE TO NEPHRON ALONG THE PROXIMAL AND DISTAL

TUBULES

•KIDNEY DAMAGE

•COMPLICATIONS OF DRUG THERAPY (LITHIUM)

•PSYCHOGENIC (PRIMARY POLYDIPSIA OR DIPSOGENIC)

•RARE FORM OF WATER INTOXICATION

•COMPULSIVE WATER DRINKING ABOUT 5L- DRINKING WATER WITHOUT

ELECTROLYTES

DI

DI PATHOPHYSIOLOGY

• INABILITY OF THE KIDNEY TO

INCREASE PERMEABILITY TO

WATER (TO REABSORB IT)

• EXCRETION OF LARGE

VOLUMES OF DILUTE URINE

AND IN INCREASE IN PLASMA

OSMOLALITY

• INCREASE IN THIRST

• DEHYDRATION –

HYPOTENSION/HYPOVOLEMIC

SHOCK

• SEVERE HYPERNATREMIA AND

HYPEROSMOLALITY

• FREE WATER EXCRETED IN

URINE

• EXTRACELLULAR

DEHYDRATION

• DECREASED CEREBRAL

PERFUSION

• LARGE QUANTITY OF

DILUTE

URINE/CONCENTRATED

BLOOD

DI ASSESSMENT• CLINICAL

MANIFESTATIONS

• POLYURIA,

NOCTURIA,

POLYDIPSIA

• LARGE BLADDER

CAPACITY AND

HYDRONEPHROSIS

• DIFFERENTIATE

FROM DM AND

OTHER POLYURIC

STATES

• DIAGNOSIS BASED ON THESE

CLINICAL MANIFESTATIONS IN

THE ABSENCE OF ANY OF THE

FOLLOWING

•DIURETICS, FLUID

CHALLENGE,

HYPERGLYCEMIA

• CENTRAL DI THAT OCCURS

BECAUSE OF ↑ ICP IS LIFE

THREATENING

• FIND AND TREAT UNDERLYING

CAUSE

• DIAGNOSIS

• LABORATORY STUDIES

• SERUM NA > 145 MEQ/L

• SERUM OSMOLALITY > 295 MOSM/KG WATER

• URINE OSMOLALITY < 300 MOSM/KG WATER

• URINE SPECIFIC GRAVITY <1.005.

• MEASUREMENT OF ADH

( NORMAL 1-5 PICOGRAM/ML(PG/ML)

• WATER DEPRIVATION TRIAL

• LOSS OF >3% IS RISKY

• RISK FOR CIRCULATORY COLLAPSE AND SHOCK

DI

DI MEDICAL MANAGEMENTMEDICAL

MANAGEMENT

• BASED ON EXTENT OF

ADH DEFICIENCY AND

PATIENT VARIABLES

• AGE

• ENDOCRINE AND

CARDIOVASCULAR

STATUS

• FLUID REPLACEMENT-

ORAL OR IV (CONSIDER

HYPOTONIC)

• REPLACE ADH

• TREATMENT OF

UNDERLYING CAUSE

MEDICATIONS

• MEDICATIONS USED FOR CENTRAL DI

• (DESMOPRESSIN-DDAVP GIVEN

INTRANASALLY OR ORAL)

• MEDICATIONS USED FOR NEPHROGENIC

DI

• THIAZIDE DIURETICS USED TO

REABSORB SALT AND WATER IN

PROXIMAL TUBULES

• THEREFORE LESS IS

AVAILABLE IN THE ADH

SENSITIVE SITES IN THE DISTAL

TUBULES RESULTING IN LESS

WATER BEING EXCRETED.

• STOP ANY MEDS THAT COULD INDUCE

RESISTANCE TO ADH

• FLUID RESUSCITATION

• NURSING MANAGEMENT

• ADMINISTRATION OF FLUIDS AND MEDICATIONS

• HEMODYNAMIC MONITORING

• MONITORING OF HR, BP, CVP, AND PULMONARY ARTERY

PRESSURES PROVIDES EARLY INDICATIONS OF RESPONSE

TO FLUID VOLUME REPLACEMENT.

• EVALUATION OF RESPONSE TO THERAPY

• I&O, FOLEY, DAILY WTS.,SKIN TUGOR, THIRST & TEMP

• SURVEILLANCE FOR COMPLICATIONS

• SIDE EFFECTS OF MEDICATIONS

• HTN, VASOSPASMS, SEIZURES

DI

DI

SIADH

• EXCESS ADH SECRETED INTO BLOODSTREAM IN THE ABSENCE OF

NORMAL PHYSIOLOGIC STIMULUS FOR ITS RELEASE

• ETIOLOGY

• CENTRAL NERVOUS SYSTEM INJURY OR DISEASE

• MALIGNANT DISEASES – AUTONOMOUS PRODUCTION

• NEUROGENIC STIMULI

• PULMONARY DISEASES

• ENDOCRINE DISTURBANCES

• MEDICATIONS

SIADH PATHO

•PATHOPHYSIOLOGY

•EXCESSIVE ADH

• INCREASED KIDNEY TUBULE PERMEABILITY TO WATER (WATER-

LOGGED)

• INCREASED WATER REABSORPTION

• DECREASED ALDOSTERONE – ADRENAL GLAND RELEASE

SUPPRESSED

• DECREASED URINE VOLUME

• HYPEROSMOLAR URINE (INCREASED URINE SODIUM)

• INCREASED BLOOD (VASCULAR) VOLUME

• SERUM HYPOOSMOLALITY

SIADH PATHO (CONT.)

• PATHO (CONT.)

• DILUTIONAL HYPONATREMIA

• NA <120 – CONFUSION, SEIZURES

• DESPITE HYPONATREMIA, THE SIADH CONTINUES TO

PROMOTE SODIUM LOSS THROUGH THE KIDNEYS

• ALDOSTERONE PRODUCTION SUPPRESSION

• HYPO-OSMOLARITY= FLUID SHIFT (ECS-ICS)

• H2O RETENTION, ↓ UOP,↑ URINE OSMOLARITY, ↑ URINE NA

SIADH

• ASSESSMENT AND DIAGNOSIS

• CLINICAL MANIFESTATIONS

• CLINICAL PRESENTATION IN SIADH RELATES TO WATER

AND SODIUM IMBALANCE

• WEIGHT GAIN WITHOUT EDEMA

• LETHARGY

• ANOREXIA

• MENTAL CONFUSION

• SEIZURES, COMA, DEATH

DIAGNOSTICS

• FOR DIAGNOSIS, NORMAL ADRENAL AND

THYROID FUNCTION MUST EXIST

• SERUM LABS

• SERUM OSMOLALITY <275MOSM/KG H2O

• SERUM SODIUM <135MEQ/L

• URINE LABS

• URINE HYPEROSMOLALITY >1200 MOSM/KG H2O

• URINE SODIUM >30 TO 40MEQ/L

• URINE SPECIFIC GRAVITY >1.030

SIADH

• MEDICAL MANAGEMENT

• CORRECTION OF UNDERLYING PROBLEM

• FLUID RESTRICTION – 800-1000 ML/DAY

• HYPERTONIC SALINE- 3%NS

• RISK FOR CENTRAL PONTINE MYELINOLYSIS/ OSMOTIC DEMYLEINATION

• ∆ NA BY NO MORE THAN 8-12 MEQ/L OVER 24 HOURS

• MEDICATIONS (IF FLUID RESTRICTION DOESN’T WORK/ EUVOLEMIC

HYPONATREMIA)

• CONIVAPTAN (VAPRISOL) INPATIENT USE ONLY (NON SELECTIVE ANTAGONIST V1 AND V2)-

MORE WATER IS EXCRETED, CAREFUL TO AVOID HYPOTENSION

• DEMECLOCYCLINE (DECLOMYCIN)- DECREASES RESPONSIVENESS OF COLLECTING DUCT TO

ADH

SIADH

• NURSING MANAGEMENT

• CORRECT HYPONATREMIA- 3% FLUID

• RESTRICTION OF FLUIDS

(ACCURATE I & O, DAILY WT, MOUTH CARE)

• SEIZURE PRECAUTIONS

• PATIENT EDUCATION PT/FAMILY ABOUT DISEASE PROCESS

• COLLABORATIVE MANAGEMENT

• *** TELL RT, TECHS, ANYONE ABOUT WHY WE ARE RESTRICTING FLUIDS***

SIADH

SIADH

CHECK ON LEARNING

A PERSON IS ADMITTED TO THE UNIT WITH A DIAGNOSIS

OF LUNG CANCER AND SYNDROME OF INAPPROPRIATE

ADH. THE NURSE EXPECTS THE PERSON TO HAVE:

A. DILUTE URINE.

B. A HYPO-OSMOLAR STATE.

C. HYPERNATREMIA.

D. REDUCED EXTRACELLULAR VOLUME.

DI VERSUS SIADH

Serum

Osmolality

275-295

Urine

Osmolality

300-1200

Na (Sodium)

Serum

135-145

Specific

Gravity Urine

1.005-1.030

DI

“Dehydrated” ↑ ↓ ↑ ↓

SIADH

“Waterlogged” ↓ ↑ ↓ ↑

SUMMARY POSTERIOR PITUITARY

• SIADH OCCURS WHEN EXCESS ADH IS

RELEASED.• THIS STIMULATES KIDNEY TUBULES TO RETAIN WATER,

RESULTING IN FLUID OVERLOAD AND HYPONATREMIA

MANIFESTED BY ALTERATIONS IN SERUM AND URINARY

LABORATORY VALUES.

• CENTRAL DI OCCURS WHEN ADH IS NOT

RELEASED FROM THE POSTERIOR PITUITARY

GLAND. • EXCRETION OF LARGE QUANTITIES OF HYPOTONIC URINE

CREATES ALTERATIONS IN SERUM AND URINARY LABORATORY

VALUES.

CHECK ON LEARNING

Which of the following disorders can cause

hypernatremia?

A. DI

B. SIADH

C. CSWS

D. Diabetes mellitus

CHECK ON LEARNING

Which of the following laboratory findings would

indicate a diuresis following a brain tumor resection

as a result of DI?

A. low serum osmolality

B. Low urine osmolality

C. Hyponatremia

D. High urine specific gravity

REFERENCES

• MCCANCE, K. L., HUETHER, S. E. , BRASHERS, V.L., & ROTE, N. S. (2014). STRESS AND DISEASE

IN PATHOPHYSIOLOGY: THE BASIS FOR DISEASE IN ADULTS AND CHILDREN (7TH ED.) (PP.

717-724). ST. LOUIS: MOSBY

• URDEN, L.D, STACY, K.M. & LOUGH, M.E. (2014). NEUROLOGIC ANATOMY AND PHYSIOLOGY IN

CRITICAL CARE NURSING: DIAGNOSIS AND MANAGEMENT (7TH ED.). (PP.802-803; 831-

839). MOSBY: ST. LOUIS

• MORTON, P., & FORTAINE, D. (2018). CRITICAL CARE NURSING: A HOLISTIC APPROACH. (11TH

ED.) WOLTERS: PHILIDELPHA, PA