Endocrinology Flashcards
(43 cards)
ADH release signal
Cell bodies in the supraoptic nuclei of the hypothalamus send axons to the posterior pituitary and release ADH (hypothalamic neurons synthesize ADH)
Signals that trigger ADH release
Low BP - carotid (CNIX) and aortic (CNX) baroreceptors
Decreased arterial stretch due to low blood volume
Increased osmolality - hypothalamic osmoreceptors
Sympathetic stimulation
Angiotensin II secretion
Low blood volume
Secretion of ADH is most sensitive to what trigger
Plasma osmolality changes
ADH method of action in kidney
ADH binds V2 receptors in distal tubule and collecting duct activating GPCR-cAMP-PKA sequence
This causes more aquaporin channels to be inserted in the membrane for more water uptake
Diabetes insipidus and ADH
ADH lacks its normal effect on the collecting duct
Causes frequent urination
Large volume of urine is diluted
Central vs nephrogenic diabetes insipidus (DI)
Central- lack of ADH- could be from damage to pituitary or hypothalamus. Treat with desmopressin (antidiuretic)
-will have decreased plasma ADH in labs
Nephrogenic- Kidneys unable to respond to ADH
-Can be caused by drugs like lithium, or kidney disease
-Desmopressin will not work
Water deprivation test for DI
Drink fluids over night, give breakfast w/o fluids
Weigh patient
No fluid during day, weigh patient every 1-2 hrs
Empty bladder, measure volume and osmolality of urine as well as plasma osmolality
If results suggest DI, patient drinks and desmopressin is administered
Remeasure plasma osmolality and urine osmolality/volume
Syndrome of inappropriate ADH secretion SIADH
Excessive ADH secretion
Excessive water retention
Hypoosmolality fails to inhibit ADH release
-Hyponatremia, decreased plasma osmolality, increased urinary osmolality
Factors causing aldosterone production and sequence of events
Decreased Na, Increased K+ in blood
Decreased blood volume or blood pressure
Kidney signaled to release renin
Liver releases angiotensinogen which is converted to angiotensin I by renin
AT1–>AT2 –> adrenal cortex –> Aldosterone–> water/Na+ reabsorption
Aldosterone effect on kidney
Aldosterone combines with cytosolic receptor in distal tubule
Hormone/receptor complex travels to nucleus and new protein channels/pumps are synthesized
Increased Na reabsorption and K+ secretion in ascending limb, distal tubule, collecting duct
Other effects of angiotensin II besides Aldosterone secretion
Increased sodium/hydrogen exchange causing increased sodium reabsorption along nephron
Increased thirst
Vasoconstriction
Increased ADH secretion
Primary adrenal insufficiency
Both cortisol and aldosterone secretion decreased
Secondary or tertiary adrenal insufficiency
Cortisol decreased but renin-angiontensin-aldosterone axis still exists
ANP
When atria are distended, ANP is released
Increases excretion of NaCl/water by kidneys
-vasodilation of afferent and vasoconstriction of efferent arterioles- increasing GFR and filtration load
-Inhibit renin/aldosterone secretion and ADH action on distal tubule/collecting duct
-inhibit NaCl reabsoprtion
Ventricles produce BNP (brain natriuretic peptide) that has a similar function
-both decrease total peripheral resistance
Urodilatin
Encoded by the same gene as ANP
Secreted by the distal tubule and collecting duct
Influences only the function of the kidneys
Stimulated by increased BP and ECF volume
Inhibits NaCl and water reabsorption by medullary portion of collecting duct
Sympathetic nerve activity and regulation of NaCl/water reabsorption
Catecholamines released from sympathetic nerves stimulate reabsorption of Na and water by proximal tubule, thick ascending limb, distal tubule and collecting duct
Increase renin secretion
Decrease GFR (vasoconstrict afferents)
Addisons disease
Atrophy of adrenal gland
Decreased cortisol and aldosterone secretion
Causes increased CRH release from hypothalamus
Causing increased ACTH release from pituitary
Hyperpigmentation
Response to increased sodium intake
Decreased sympathetic activity
Increased ANP
Decreased peritubular capillary osmotic pressure
Decreased renin/angiotensin/aldosterone system
Causes of K+ shifts out of cells–>hyperkalemia
Insulin deficiency B2 adrenergic antagonist a-adrenergic agonists Acidosis Hyperosmolarity Cell lysis Exercise
Causes of K+ shift into cells–>hypokalemia
Insulin B2 adrenergic agonists a-adrenergic antagonists Alkalosis Hypoosmolarity
Insulin effect on K+ balance
Stimulates K+ uptake into cells by increasing Na/K pump activity
Ensures ingested K does not remain in ECF
Deficiency of insulin like in type I diabetes causes decreased K+ uptake and hyperkalemia
Three pathways triggering aldosterone release
Hypothalamus CRH–>pituitary ACTH–> adrenal cortex aldosterone
High plasma K+–> adrenal cortex secrete aldosterone
Renin-angiotensin system
Increased ENaC: Liddle syndrome lab results (renin, aldosterone, EC volume or BP)
Low renin
Low aldosterone
High EC volume/BP
Decreased B-hydroxysteroid dehydrogenase: apparent mineralocorticoid excess, licorice lab results (renin, aldosterone, EC volume or BP)
Low renin
Low aldosterone
High EC volume or BP
