Endocrine + Gender Affirming Hormone Flashcards
Antidiuretic Hormone (ADH)
Secreted by brain’s hypothalamus’s posterior pituitary gland
Role of vasopressin in RAAS
- Vasopressin: ADH secreted when pt’s fluid down or hypotensive ⇒ causes Na+ & Water retention + peripheral vasoconstriction
- Pts fluid down or hypotensive → body secretes antidiuretic hormone called vasopressin
- Vasopressin acts on kidney by telling it to hold onto sodium which also retain water to keep fluid volume up
- Ie. during overwhelming infection, IS causes capillaries and blood vessels to be leaky → give vasopressin which is a vascular presser to combat the pt’s vasodilation → retains fluid
Pathophysiology of Syndrome of Inappropriate AntiDiuretic Hormone (SIADH) (what, causes, results in)
- SIADH: High lvls of antidiuretic hormones (ADH)
- Posterior pituitary dysfunction
- Causes:
- Ectopic (coming from outside) non-endocrine secreting sites of ADH production
- Malignancy: tumors from neuroendocrine cells can act as ectopic site of ADH production
- Brain injury ⇒ dysregulation of hypothalamus ⇒ unregulated production of ADH
- Specific drugs can mimic ADH behavior ⇒ continuous water retention
- Ectopic (coming from outside) non-endocrine secreting sites of ADH production
- Results in: ADH acts on adrenal collecting ducts ⇒ ↑ permeability to water ⇒ ↑ water reabsorption in kidneys ⇒ extremely saturated urine + bc your body’s holding onto so much fluid (HYPERvolemic) ⇒ blood Na+/Sodium becomes diluted ⇒ blood Na+ lvls <135 mEq/L (you’re HYPOnatremic)
- If you’re hyponatremic ⇒ your blood levels are considered hypoosmolality (↓ osmolality) bc osmolality is measure of solutes in your fluids so if you have ↓ Na+ solutes ⇒ ↓ blood osmolality
- If you’re urine is super saturated however, your urine sample is considered hyperosmolality (↑ osmolality) bc your body is retaining the fluids so urine is more concentrated (urine specific gravity is extremely concentrated)
Complications of SIADH
- HYPOnatremia monitoring !!! (< 135 mEq/L)
- Seizures
- Headaches
- Muscle cramps
- Nausea
- If serum/plasma Na+/sodium lvls get < 110-115 mEq/L ⇒ irreversible neurological damage & possibly comatose
Clinical Manifestations of SIADH
- Increased fluid retention leads to →
- Edema
- ↓ urine output
- HYPERvolemic
- HYPOnatremic
- Blood lvls at HYPOosmolality state
- Urine is extremely concentrated and at a HYPERosmolality state
- Neurocognitive effects
- Mood swings
- Confusion
- Hallucinations
- Coma
Nursing Interventions for management of SIADH
- Goal: fixing Na+ deficit & not to fluid overload pt
- Instill fluid restriction first !!! before giving Na+ bc they’re alrdy retaining excessive amt of fluid (HYPERvolemic) bc if you give more then it’ll worsen electrolyte imbalance, esp causing further dilution of plasma Na+ (blood Na+ lvls <135 mEq/L (you’re HYPOnatremic))
- Fluid restriction: 800 - 1000 mEq/mL
- Treatments/Management Options:
- Fluid restriction
- Hypertonic saline: extremely strong solute solution that has high concentration of salt ⇒ treats systematic HYPOnatremia
- Rapidly increases serum Na+ concentration by pulling water out of cells and into bloodstream
- Give IV
- Remember: start slow !!! no more than 12 mEq/L within 24 hrs bc if you rapidly ↑ Na+ ⇒ can cause central pontine myolysis (locked-in syndrome): cognitively aware but physically inactive
- Vaptans: nonpeptide vasopressin receptor antagonist that causes aquaresis ⇒ excretes solute-free urine
- Differs from diuretics bc it promotes excretion of water w/o electrolyte loss (classified as an aquaretic)
- Give orally or IV
- Demeclocycline: tetracycline-like antibiotic that can cause water diuresis and restores plasma Na+ concentration lvls to norm (for resistant or chronic SIADH)
Pathophysiology of Diabetes Insipidus (DI)/Polyuria-Polydipsia Syndrome + Results in…
- DI/Polyuria-Polydipsia Syndrome: inability of kidneys to increase permeability of water due to insufficiency of ADH ⇒ excessive water excretion ⇒ large vols of dilute urine (pretty much complete volume loss) but doesn’t get rid of the electrolytes in your body so there’s ⇒ ↑ amt of plasma osmolality ⇒ drier your body is (higher plasma osmolality you have = drier you are!)
- Results in:
- Polyuria: excessive urine volume output
- Polydipsia: excessive thirst
- Primary Polydipsia: excessive fluid intake ⇒ results in polyuria even if you have appropriate amt of ADH hormone and renal response
- HYPERnatremia (> 145 mEq/mL) bc body isn’t getting rid of electrolytes
Neurogenic DI
insufficient amt of ADH bc of disruption of pituitary gland ⇒ ↓ ADH
Nephrogenic DI
insensitivity of renal collecting ducts to ADH hormone (kidneys unresponsive to ADH, even though it’s produced and released normally) ⇒ ↓ ADH
Dipsogenic DI
excessive water intake ⇒ lowers plasma osmolarity to the point it falls below threshold necessary to trigger ADH secretion from posterior pituitary gland ⇒ ↓ ADH
Central DI
inadequate production of arginine vasopressin (AVP) aka ADH due to failure in hypothalamic-neurohypophyseal system to respond to osmotic stimulation that normally plasma osmolarity (high solute concentration in the blood) triggers AVP release to reabsorb water
Acquired Central
hereditary mutations of AVP hormone responsible for fluid retention where there’s disruption in neurohypophyseal system, including hypothalamus, posterior pituitary gland, and connections between them ⇒ interferes w/ production, storage, or release of AVP/ADH
Role of iodine in diet for thyroid function
- Iodine needed for thyroid production of T3 & T4
- ↓ plasma iodine lvls ⇒ stimulates thyroid to produce…
- ↓ Triiodothyronine (T3) & Thyroxine (T4, tetraiodothyronine): regulates metabolic activity
- May cause goiter (enlarged thyroid) via…
- ↓ plasma iodine lvls ⇒ ↓ T3 & T4 ⇒ pituitary gland releases more thyroid-stimulating hormone (TSH) to signal thyroid to work harder ⇒ thyroid gland grows larger to try and capture more iodine to compensate for hormone shortage
Pathophysiology of HYPOthyroidism
- Hypothyroidism: insufficient production of Triiodothyronine (T3) & Thyroxine (T4, tetraiodothyronine) that regulates metabolic activity
- Normally:
- Hypothalamus releases thyrotropin-releasing hormone (TRH)
- TRH stimulates anterior pituitary to secrete thyroid-stimulating hormone (TSH)
- TSH stimulates thyroid gland to produce thyroxine (T4) & triiodothyronine (T3) hormones
- T3 & T4 have negative feedback on hypothalamus and anterior pituitary to regulate system
- Normally:
Dysfunction Types of HYPOthyroidism
- Tertiary Hypothyroidism: dysfunction in hypothalamus itself ⇒ ↓ thyrotropin-releasing hormone (TRH) ⇒ ↓ anterior pituitary secretion of TSH ⇒ ↓ thyroid gland secretion of T3 & T4
- You get low amts of everything: TRH, TSH, T3 & T4
- Secondary Hypothyroidism: dysfunction in anterior pituitary ⇒ ↓ TSH ⇒ ↓ thyroid gland secretion of T3 & T4
- You get low amts of TSH, T3& T4
- Primary Hypothyroidism: dysfunction in thyroid gland itself ⇒ ↓ secretion of T3 &T4
- You just have low amts of T3 & T4
