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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 = ADH insufficency: cannot concentrate urine. Polyuria, polydipsia (esp night). UOP 5-20 L/day, urine spec grav <1.0006. Hypernatremia, normal glucose
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 wont respond, urine remains dilute; Central: give AVP, later serum osm changes?
DI: DDx DM; Primary Polydipsia; CHF; Prostate Hypertrophy; Cushing syn (Excess Glucocorticoids); Other Osmotic Load (Calcium); Lithium; Parkinson Dz
Causes of DI 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
Diabetes Insipidus causes: Central/Neurogenic (2/2 autoimmune destruction of ADH (AVP) secreting cells. Nephrogenic (less common) 2/2 kidney dz (abnormal receptors). SCDz, Lithium tx
SIADH sxs Weakness, anorexia, N/V, HA, mx cramps, lethargy, seizure, coma, death. NO edema despite water retention.
Created by: Adam Barnard Adam Barnard