Posterior Pituitary Flashcards
Describe the pathway of ADH/Oxytocin release
1) Hypothalamic neurons synthesize oxytocin or ADH
2) Transported down axons of hypothalamic-hypophyseal tract to posterior pituitary
3) Oxytocin/ADH are stored in axon terminals in posterior pituitary
4) Hypothalamic neurons firing causing releasing of oxytocin/ADH to blood
What is the function of oxytocin?
Releases milk and uterus muscle contractions during labor, dilation of cervix
What are the actions of vasopressin?
Adjust water permeability of collecting duct in kidneys
Electrolyte handling: mild increase in reabsorption of Na and secretion of K
Vascular resistance: increase vascular resistance —> increase BP
Association with cortisol: cortisol has inhibitory effect on CRH and ADH, adrenal insufficiency leads to a persistent rise in ADH
Factor VIII and vWF release from vascular endothelium
What are the major stimuli for ADH secretion?
Hyper osmolality and effective circulating volume depletion
How is osmolality and volume sensed to release ADH?
Osmoreceptors in the hypothalamus sense sodium concentration or glucose in uncontrolled diabetes
Baroreceptors also sense volume in aortic arch and carotid sinus
Cause release of ADH —> increased water reabsorption —> increased blood volume and pressure
What factors can increase circulating ADH?
Nausea (500 fold rise)
Surgery (elevated ADH for several days after operation due to stress response)
What is the action of ADH on the kidneys?
Adds aquaporins to the collecting duct leading to dilute blood (concentrated urine)
What happens to ADH when you drink a glass of water?
Water is absorbed into blood, plasma osmolality drops—> hypothalamus sees drop and signals pituitary gland to slow release of ADH —> low ADH leads to diluted urine —> plasma osmolality is back to normal
When extracellular fluid sodium concentration rises, plasma osmolality will ___
Increase
When plasma osmolality increases, all of the following occur except:
Thirst mechanism in hypothalamus is activated, anterior pituitary decreases release of ADH, ADH causes increased water absorption in collecting ducts, ADH causes vasoconstriction to increase BP
Anterior pituitary decreases release of ADH
Based on what you know about ADH, high levels of ADH will cause
Large Volume of dilute urine, small volume of concentrated urine
Small volume of concentrated urine
Based on what you know about ADH, high levels of ADH will cause
Large volume of dilute urine, small volume of concentrated urine
Small volume of concentrated urine (high urine osmolality)
Condition defined by hyponatremia and hypo-osmolality resulting from continued secretion or action of ADH despite normal or increased plasma volume
Syndrome of Inappropriate Antidiuretic Hormone secretion
What is the most common cause of euvolemic hyponatremia in hospitalized patients?
Syndrome of Inappropriate Antidiuretic Hormone secretion
SIADH consists of __________
Hyponatremia, inappropriately elevated urine osmolality, and decreased serum osmolality in a euvolemic patient, urine sodium >30-40 mmol/L (normal is 20 on random sample)
What setting does SIADH need to be diagnosed in?
Setting of otherwise normal cardiac, renal, adrenal, hepatic, and thyroid function in absence of diuretic therapy
What is the etiology of SIADH?
Inappropriate hypersecretion from hypothalamus/pituitary or ectopic production
4 categories that stimulate ADH release, potentiate ADH action, or have uncertain mechanism:
-nervous system disorders: acute psychosis, hemorrhage, inflammatory and demyelinating diseases, mass lesions, stroke, trauma
-Neoplasms: extra thoracic, mediastinal, pulmonary
-Pulmonary diseases: hypercapnia can stimulate ADH release
Drug-induced: can stimulate release of ADH or potentiate
What is the general clinical presentation of SIADH/early symptoms?
Based on severity of hyponatremia and rate of progression (slower=less symptoms)
Anorexia, nausea, and malaise are early symptoms and may be seen when serum Na is less than 125
Further decrease in Na: headache, muscle cramps, irritability, drowsiness, confusion, weakness, seizures, and coma as osmotic fluid shift results in cerebral edema and increased ICP
What are the 3 key mild-moderate symptoms of SIADH?
Headache, disorientation/confusion, impaired memory
What are the 5 advanced symptoms of SIADH?
Confusion, disorientation, somnolence, hallucinations, acute psychosis
What are the 3 key symptoms of grave SIADH?
Seizures, severe somnolence, coma
In SIADH, the patient is normally ____ and _____ presenting as
Euvolemic, normotensive; peripheral and pulmonary edema, dry mucous membranes, reduced skin turgor, and orthostatic hypotension are usually absent
Edema in a hyponatremia patient warrants consideration of CHF, cirrhosis, or CKD
What is diagnostic criteria for SIADH?
Hyponatremia with corresponding serum hypo osmolality
Continued renal excretion of Na
Urine osmolality is increased
Absence of clinical evidence of volume depletion- normal skin turgor, blood pressure
Absence of other causes of hyponatremia ie adrenal insufficiency, hypothyroidism, cardiac failure, pituitary insufficiency, renal disease with salt wastage, hepatic disease, or drugs that impair renal water excretion
Correction of hyponatremia by fluid restriction
What labs should be ordered to diagnose SIADH and rule out other causes?
Serum Na+, potassium, chloride, and bicarbonate
Plasma osmolality
Serum creatinine
Blood urea nitrogen
Blood glucose
Urine osmolality
Serum cortisol
Thyroid-stimulating hormone
What diagnostic tests should be ordered to help in diagnosis of SIADH and rule out other causes?
Serum Na+, potassium, chloride, bicarbonate
Plasma osmolality
Serum creatinine
Blood urea nitrogen
Blood glucose
Urine osmolality
Serum cortisol
Thyroid-stimulating hormone
How is SIADH treated?
Depends on degree of hyponatremia, symptoms, and whether acute (<48 hours) or chronic
Consult with nephrologist for difficult cases
What can correcting hyponatremia too rapidly in SIADH cause?
Central pontine myelin ply’s is with permanent neurologic deficits
Neurological disease caused by severe damage of the myelin sheath of nerve cells in the brain stem, specifically the pons, and characterized by acute paralysis, dysphagia, and dysarthria, and other neurological symptoms.
Central pontine myelinolysis
What is treatment of SIADH in an emergency setting?
Aggressive management if seizures, stupor, coma, respiratory arrest:
Raise serum Na+ levels (by .5-1 mEq/h and not more than 10-12 mEq in first 24 hours)
3% hypertonic saline = fluid of choice
Neurological symptoms and serum Na+ monitoring
Furosemide increases excretion of free water and has been used along with hypertonic saline
How is SIADH treated in an acute setting?
3% hypertonic saline
Loop diuretics with saline (furosemide)
Vasopressin-2 receptor antagonists (aquaretics, such as conivaptan)
Water restriction
What is the MOA of vasopressin receptor antagonists?
Inhibition of AVP V2 receptor reduces number of aquaporins-2 water channels in the renal collecting duct and decreases water permeability of collecting duct