Pituitary Gland - Posterior pituitary Flashcards
Posterior pituitary
- aka
- function
- blood supply
- main consequence of disease
- neurohypophysis
- nervous tissue: storehouse for hormones made in hypothalamus (ADH and oxytocin)
- inferior hypophyseal arteries
- disordered water homeostasis
Posterior pituitary
- innervation
Directly innervated by hypothalamic neurons
- Supraoptic nucleus: ADH
- Paraventricular nucleus: oxytocin
Posterior pituitary
- what might cause neuronal damage?
lesions that affect pituitary stalk or hypothalamus
Oxytocin
stimulates postpartum milk letdown in response to suckling
ADH
- released when
- action
- low bp/volume, high plasma osmolality, pain, emotional stress
- action: concentrates urine by increasing water reabsorption in the kidney
Describe osmoreceptors that are related to ADH
- located in supraoptic nucleus
- aid in ADH release and thirst regulation
What inhibits ADH
- high bp
- low plasma osmolality
- alcohol
Diabetes insipidus
- etiology
- no association with DM
- damaged pituitary gland or hypothalamus
- disrupts nl production, storage, release of ADH
- pass abnl large volume urine that is “insipid”
Diabetes insipidus
- ADH changes
- loss of ADH secretion OR action
- decreased ADH = less water reabsorption
- increased dilute urine output
- increased serum concentration
- Euvolemic hypernatremia
4 types of Diabetes insipidus
- central
- nephrogenic
- disogenic
- gestational
Diabetes insipidus
- central
- primary: genetic abnormality of ADH gene or idiopathic
- secondary (MC): Sx, skull base fx/cranial injury, suprasellar/intrasellar tumor, infection
Diabetes insipidus
- nephrogenic
kidneys do not have normal response to ADH, usually dt tubule defect (inherited or CKD)
Diabetes insipidus
- disogenic
problem with thirst mechanism, often associated with mental illness
Diabetes insipidus
- gestational
- placenta breaks ADH down and produces prostaglandins, reducing kidney’s sensitivity to ADH
Diabetes insipidus
- signs and sx
- abnl large volume dilute urine
- polyuria, enuresis, nocturia
- thirst, polydipsia
- dry skin, dizzy, nausea, confusion
- low bp, hypernatremia
Diabetes insipidus
- dx
- History and PE
- verify polyuria with 24h urine output collection (>50 ml/kg/day)
- check osmolarity
- check sodium
- water deprivation test
- MRI: not diagnostic but can help visualize tumor
Osmolarity in Diabetes
> 300 due to solute diuresis, pt should be eval for DM or other causes of excessive solute excretion
< 300: due to water diuresis, should be evaluated for type of DI
Diabetes insipidus
- how to distinguish between central and nephrogenic
- administer desmopressin (synthetic ADH)
- measure urine osmolality at timed intervals, an increase of >50% indicates central DI
- smaller/absent response suggests nephrogenic
Diabetes insipidus
- tx of central
- mild: increase fluid
- otherwise: desmopressin (DDAVP)
Diabetes insipidus
- tx of nephrogenic
- NO desmopressin
- low salt diet to reduce urine production
- increase fluids
- HCTZ
Diabetes insipidus
- tx of gestational
- DDAVP
- deliver baby
Diabetes insipidus
- tx of disogenic
- no tx…
- decrease fluid intake
SIADH
- describe
- MC cause euvolemic hyponatremia in hospitalized pts
SIADH
- define
hyponatremia and hyposmolality resulting from inappropriate and continued secretion/action of ADH despite normal/increased plasma volume
(retain too much water)
SIADH
- urine
concentrated, impaired water secretion
SIADH
- pathophysiology
- excessive ADH production = decreased volume of highly concentrated urine
- water retention
- elevated urine osmolality
- decreased serum osmolality
- hyponatremia dt excess water, not deficient sodium
SIADH
- etiology
CNS - lesions, inflammatory dz - trauma, psychosis Drugs - nicotine, phenothiazines, TCAs, SSRIs and others Pulmonary - infection - mechanical/ventilatory issue
SIADH
- signs and sx
Acute: - water intoxication - HA, confusion - Ataxia - Nausea, vomiting - anorexia - Coma, convulsions Chronic - may be asymptomatic
SIADH
- Dx
- PMH: trauma, drug use, etc.
- PE: euvolemic, normotensive
- hyponatremia and hypoosmolality
- renal excretion of na
- concentrated urine
- no volume depletion
- no other causes of hyponatremia
- fluid restriction corrects hyponatremia
SIADH
- Tx goal
- correct hyponatremia at a rate that does not cause neurologic complications
- increase serum na 0.5-1.0 mEq/h
- no more than 10-12 mE in first 24 hours
- rule of sixes (6 in 6 hours for severe sx and then stop)
SIADH
- Acute tx
- fluid restriction
- hypertonic saline (3%)
- vasopressin receptor antagonists
- furosemide (diuretic)
SIADH
- chronic tx
- fluid restriction
- vasopressin receptor antagonists
- loop diuretics
