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Pituitary
Endocrine
| Question | Answer |
|---|---|
| Hypothalamus hormones | CRH, GHRH, GnRH, TRH, DA, SS |
| Pituitary hormones | Prolactin; GH; ACTH; ADH; TSH; LH/FSH |
| Adrenal hormones | Epinephrine; Cortisol; Aldosterone |
| Control of prolactin | produced by pit; neg inhib by DA (so the more DA, less prolactin) |
| Regulation of Hypothalamus | Upper cortical inputs (CNS); Autonomic NS; environmental cues (light & temp); Peripheral endocrine FB |
| FSH: fx | Estrogen (F); Spermatogenesis (M) [if no estrogen prod: FSH increases] |
| LH: fx | regulates ovulation; stimulates testosterone in men [if no testosterone prod: LH increases] |
| TSH: fx | increases thyroid hormone production [if no TH prod: TSH increases] |
| Prolactin: fx | induces lactation |
| GH: fx | controls acral growth |
| ACTH: fx | stimulates cortisol production |
| Primary hypothyroidism | Thyroid gland fails to make T4; TSH is HIGH; FREE T4 is LOW |
| Secondary hypothyroidism: | Pituitary gland fails to make TSH; TSH is inappropriately LOW; FREE T4 is LOW; Other Pit Hormone Deficiencies; cannot follow TSH (must also follow Free T4) |
| Hypothyroid S/S | Cold intolerance; Fatigue; Heavy Menstrual Bleeding; Wt Gain; Myxedema Coma |
| Secondary hypothyroidism: incidence | Much rarer than primary |
| Secondary hypothyroidism: you cannot: | Follow TSH to adjust thyroid hormone replacement |
| Secondary hypothyroidism: poss sequela of: | panhypopituitarism |
| Secondary hypothyroidism: consider in pt with S/S of: | hypothyroidism & low normal TSH, low normal t4 |
| Secondary hypothyroidism: Do not: | replete thyroid hormone before repleting cortisol; if pt adrenal/ cortisol deficient, & replete TH first, revs up metab, can lead to adrenal crisis (wont have enough cortisol to support metabm) |
| Secondary hypothyroidism: Dx | Sx of Hypothyroidism; Low TSH; Low T4; Other Sx to suggest Pan-Hypopituitarism |
| Adrenal Insufficiency (AI) is: | Cortisol Deficiency |
| Primary Adrenal Insuff = | Addison Dz; adrenal gland does not respond to ACTH & not make adrenal hormones |
| Secondary Adrenal Insuff = | Pit does not make ACTH; adrenal is not stimulated to make cortisol |
| Tertiary Adrenal Insuff = | Suppression of CRH & ACTH by exogenous cortisol use |
| Primary Adrenal Insuff: Sx | Sx based on hypocortisolism & hypoaldosteronism: Fatigue & Hyponatremia (most important); Hypotension; Hyperkalemia; Hyperpigmentation (from ACTH); Death |
| Gold standard to dx primary Addison dz | Low morning cortisol <5 |
| Secondary Adrenal Insuff: due to: | Failure of pit to secrete ACTH; caused by the same causes of Pan-Hypopituitarism |
| Secondary AI & RAAS | b/c secondary & tertiary adrenal insuff only involve low ACTH levels, the RAAS is still intact; Only cortisol is deficient. |
| Secondary AI: Sx | Hyperkalemia & Hypotension are rarely seen; hyperpigmentation is not seen |
| Secondary AI: Dx | Low morning cortisol <5; Low ACTH in setting of low cortisol; No Response to synthetic ACTH (cortrosyn) stim test; Insulin Tolerance Test; Metyrapone Test |
| Secondary AI: synthetic ACTH (cortrosyn) stim test | baseline cortisol, then: 250 mcg IM Cortrosyn; cortisol s/b over 18 (if adrenal gland is working) |
| ACTH & 11-deoxycortisol | ACTH stims adrenal to make 11-deoxycortisol (which makes cortisol); Nml pit will drive up 11-d, if 11-d goes up & ACTH goes up, then pt has nml pit-adrenal axis; |
| Metyrapone Test: | Give metyrapone: blocks cortisol prodn, cortisol goes down, FB to hypo-pit, if pit working, more ACTH to inc cortisol |
| Hypogonadotropic Hypogonadism = | F: Amenorrhea/Infertility; M: Erectile Dysfunction/ Infertility; Inappropriately Low FSH/LH for low estrogen or testosterone |
| Hypogonadotropic Hypogonadism: Eval | Hx (congenital or acquired); MRI Pituitary to assess for cause; Labs (prolactin; Iron/TIBC (Hemachromotosis); other Hormonal Work-Up; if estrogen level low, do Provera challenge); Give Hormone Replacement |
| Diabetes Insipidus definition | ADH insufficency: cannot concentrate urine. |
| DI: Water Deprivation Test | Follow every 1-2 hrs: Na; UOP, Urine Osmo; Wt; BP & HR (Lying / Standing); Once serum osmo >300 & urine osmo has not increased, give 10 ug of vasopressin and follow urine osmo |
| Water Deprivation Test: purpose | distinguish btw central and (nephrogenic) DI. Nephrogenic: give AVP, kidney will not respond, urine remains dilute; Central: give AVP, later serum osmo changes? |
| Diabetes Insipidus: DDx | DM; Primary Polydipsia; CHF; Prostate Hypertrophy; Cushing syn (Excess Glucocorticoids); Other Osmotic Load (Calcium); Lithium; Parkinson Dz |
| Causes of Diabetes Insipidus | Panhypopituitarism (often have intact ADH secretion with deficient ant pit hormones); Sarcoidosis/ Infiltrative Dz; Tumor; Trauma; Image Pituitary to Dx |
| Sx of Hypopituitarism | Secondary Hypothyroidism; Hypocortisolism (secondary adrenal insuff); Amenorrhea, Menopause, Erectile Dysfunction, Infertility; Polyuria/Polydipsia |
| Management of Panhypopituitarism | Investigate / Tx Underlying Cause (MRI pit); Replace Hormones (unless CI); Cortisol First; Thyroid Hormone; Sex Steroids: Estrogen (unless postmenopause); Testosterone |
| Hyperprolactinemia: Sx (Women) | Galactorrhea; Amenorrhea; Infertility |
| Hyperprolactinemia: Sx (Men) | ED; Infertility; HA; Mass Effect (eg, from tumor in head); Galactorrhea |
| Pathognomonic for hyperprolactinemia in men: | Galactorrhea |
| Prolactin >200: due to: | Hyperprolactinemia; Pit Adenoma; Renal Fail; PG |
| Prolactin = 20-100: poss due to: | Hyperprolactinemia; Pit Adenoma; Renal Fail; PG; Drugs; Other Pit Tumors; Hypothal Tumors; Chest Wall Stimulation |
| Drugs that cause Hyperprolactinemia | Anti-DA (Anti-psychotics; Reglan); TCAs; SSRI; Verapamil; Alcohol, esp Beer; Heroin; Cocaine |
| Prolactinoma: Mgmt | dopamine agonist (bromocriptine) often replaces need for surgery. |
| Prolactinoma: Mgmt | Dopaminergic Drugs if: Macroadenoma; Mass Effect; Visual Field Deficit; Fertilty Desired |
| Prolactinoma: Mgmt: Hormone Replacement if: | No Fertility Desired; Microadenoma; Visual Field Full; No Mass Effect; Estrogen or Testosterone is low |
| Prolactinoma: Medical Management | Tx w/ Dopaminergic Drugs; DA inhib fx on prolactin; shrink tumor; Cabergoline / Bromocriptine; AE: nausea, hypotension |
| Acromegaly vs Gigantism | Acromeg: pit tumor secreting GH in adulthood; Gigantism: pit tumor secreting GH during puberty before epiphyseal plate fusion; rapid linear growth, heights up to 8ft 11 |
| Risks of LT exposure to GH include: | Arthropathy, neuropathy, CVD; HTN; resp dz; malig; CHO intol/DM |
| When to Suspect Acromegaly | MEN-1 / other FH; Prominent Brow; Enlarged soft tissue of hands / ft; Teeth Splaying; DM; HTN/ LVH; Can be Subtle |
| Acromegaly diagnostic testing | Elevated insulin-like growth factor I (IGF-1). Glucose suppression test: GH Fails to suppress <2 ng/mL after 75 g CHO load |
| Acromegaly Tx | Surgical; Somatostatin Analogs: Sandostatin; XRT |
| Cushing syndrome | Too much Cortisol Prodn; Exogenous (Use of synthetic Glucocorticoids); Endogenous = Cushing Dz |
| Cushing syndrome: Sx | DM; HTN; Osteoporosis; Psychosis; Easy Bruising; Truncal Obesity; Hyponatremia; Moon Facies; Buffalo Hump; Mx Wasting; Hirsutism; Purple Striae; Supraclavicular Fat; Infections |
| Cushing Dz = | Pit ACTH overprodn; Ectopic ACTH Prodn; or Pit/Adrenal Adenoma producing cortisol; 75-80 % of cases with endogenous cortisol excess; elevated cortisol levels do not suppress hypothalamic & ant pit secretion of CRH & ACTH |
| Ectopic ACTH production = | Nonpituitary Tumors secrete ACTH and do not respond to negative inhibition of high cortisol levels |
| Ectopic ACTH production poss d/t: | Small Cell Lung Ca; Carcinoid Tumors; Pheochromocytoma; Thymoma; Pancreatic Cell tumors; Medullary Ca of the Thyroid |
| Adrenal Hypercortisolism | ACTH & CRH are suppressed; Caused by: Adrenal Adenomas; Adrenal Ca; Micronodular or Macronodular Hyperplasia |
| Hypercortisolism: Dx | 24 hr urine for free cortisol (if >100, prob Cushing, if >300, def Cushing; Check Cortisol at night; Suppressing Cortisol with oral dex; checking ACTH levels |
| Hypercortisolism: Dx: why suppress cortisol w/Dex | if suppress to <2, then do not have Cushing (dex provided enough glucocorticoid to pit, signals need not prod cortisol); if ACTH >2, prob has tumor that does not respond to dex |
| Hypercortisolism: Dx: radiography | Do not do radiographic studies prior to lab studies (poss Incidental Tumors, False Negative Scans) |
| Hypofunction of endocrine gland d/t: | destn of primary gland: auto-immune (addison, thyroiditis) or surgical removal |
| Lack of stimulating hormone: causes | Pituitary (PanHypopituitarism); Hypothalamus (Stress, Tumor) |
| Hyperfunctioning of Endocrine Gland | Autonomous Fn of Primary Gland (Thyroid Toxic Adenoma); Autonomous Fn of Gland making Stim Hormone (Cushing Dz: ACTH); Ab’s that Stim Hor Receptor (Graves / TSI); Ectopic Prod Stim Hormone (Ectopic ACTH) |
| Imaging test of choice for sellar lesions: | MRI |
| Tx of choice for all pituitary tumors | surgery (except prolactinoma) |
| Tx for surgically untreatable cases of Cushing dz | ketoconazole |
| Central Diabetes Insipidus causes: | Neurogenic: 2/2 autoimmune destruction of ADH (AVP) secreting cells. |
| SIADH sxs | Weakness, anorexia, N/V, HA, mx cramps, lethargy, seizure, coma, death. NO edema despite water retention. |
| Diabetes insipidus clinical findings | Polyuria, polydipsia (esp at night). UOP 5-20 L/day, urine spec grav <1.0006. Hypernatremia, normal glucose |
| Peripheral (nephrogenic) Diabetes Insipidus causes: | Less common than central DI. Vasopressin insensitivity 2/2 kidney dz (abnormal receptors). Sickle cell dz, Lithium tx |
Created by:
Abarnard
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