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1

• Hypothalamus basic fxn:

o secrete hormones to ant pituitary thru portal vessels to control thyroid, adrenals, gonads, growth
o direct neural connection to post pituitary, storage for ADH and oxytocin

2

• 1st, 2nd, 3rd endocrine dos:

o 1: originates in peripheral endocrine gland
o 2: dt ↑ or ↓stim by pituitary
o 3: dt ↑ or ↓stim by HTH

3

• Hyper- and hypo-fxn of HTH:

o Hyper: ↑ stim by pituitary; hyperplasia/neoplasia of gland; ectopic hormone production (hormone-secreting neoplasia); exogenous hormone administration; auto-Abs (eg Grave’s dz)
o Hypo: ↓ stim by pituitary; AI, tumor, toxins, CA, vascular dos w/in gland; Genetic; Hormone resistance

4

• Endocrine cc hx:

o Ssx mb insidious and nonspecific! 1+ glands mb involved, broad ssx: metabolism, growth, energy, sexual fxn
o HPI, ROS: HA, heat/cold intolerance, response to exercise, Changes in menses, erectile fxn, skin, vision, weight
o FHx endo dos, CA, AI

5

• Endo cc PE, labs, image:

o PE: vitals, growth charts in kids, HEENT, genitalia exams, neuro/MSE
o Lab: peripheral & regulating hormone. Effects on circadian rhythms. Serum, urine, salivary samples. Dynamic testing (stimulation or suppression tests)
o Imaging: MRI or CT often needed, US, scans

6

• Pituitary dos:

o Anterior: empty sella, hypofxn (apoplexy, infarction/Sheehan syndrome, dwarfism), hyperfxn (hyperprolactinemia, acrmegaly & gigantism), adenoma, other masses
o Posterior: Central DI (or neurogenic), hyperfxn (SIADH)

7

• Empty Sella, 2 types

o radiographic finding; enlarged sella turcica not entirely filled w pituitary tissue
o 1st: defect diaphragm sella allows ↑CSF pressure to ↑ sella, compress and flatten pituitary (congenital or 2nd to injury); mb hormone def
o 2nd: mass (mb adenoma) enlarges the sella. →Hypopituitarism, or infarction. Pit tumor may secrete GH, prolactin, ACTH →hyperpituitarism

8

• Empty sella epidem, ssx, image:

o F > M, obese, HTN, post-injury (surgery, head trauma, ischemia after childbirth)
o SSX: mb asx, HA, visual field defects. ↑ or ↓hormonal secretion
o Imaging: x-ray skull and MRI brain. mass > 1cm requires hormonal testing for ↑ or ↓secretion

9

• Hypofunction of Ant Pit, causes

o Partial or total loss of anterior lobe fxn
o Causes: pit tumors (adenomas, CA), infiltrative lesions, cranio-pharyngiomas, sarcoidosis, arterial aneurysms, thromboses, postpartum shock (Sheehan’s), TBI, ischemic stroke, subarachnoid hemorrhage; HTH dos {mass, lung or breast CA mets, iatrogenic (radiation tx), infx like TB meningitis}

10

• AP hypofxn ssx:

o depends on hormones affected
o GH def: ↓ serum glucose, mb asx in adult; In kids: → ↓ growth, maturation
o ↓ GN (LH and FSH) → ↓ sex fxn; F: amenorrhea, oligomenorrhea, ↓ libido, infertility. M: erectile dysfxn, testicular atrophy, ↓ libido, infertility
o TSH def: facial puffiness, bradycardia, cold intolerance. Newborn: cretinism
o ACTH def (Addison’s): fatigue, hypotension, intolerance to stress

11

• AP hypofxn work-up:

o Labs: Hormones: 8am serum cortisol: > 3mcg/dl but lt 18 → measure ACTH (↓in hypopit); ↓cortisol & ↑ACTH = adrenal insuff
o ↓TSH, fT4
o GNs: M: ↓ T, LH. F: premenopausal w a/oligomenorrhea: Check FSH, LH, E2
o GH: ↓ IGF-1
o Provocative tests: GHRH, CRH, TRH, GnRH given together IV. Measure glucose, cortisol, GH, TSH, prolactin, LH, FSH, ACTH at intervals > 3 hrs
o Imag: CT or MRI
o DDX: anorexia nervosa, alcoholic liver dz, myotonia dystrophica, polyglandular AI dz

12

• Pituitary apoplexy, ssx, PE, comp, dx, px:

o =Sudden hemorrhage of pit adenoma → edema and hypofxn
o SSX: sudden onset severe HA, stiff neck, visual field defects (bitemporal hemianopsia dt pressure on optic chiasm, diplopia dt pressure on occulomotor nerves)
o PE: ↓BP; HEENT, visual fields by confrontation
o Comp: really big → coma, death, esp ACTH, cortisol def → hypotension. Less severe: sudden hypopit sxs
o Dx: MRI; mb blood in CSF
o Px: spontanteously resolve or w surgical decompression

13

• Pituitary Infarction, or Sheehan syndrome, path

o Aka: postpartum hypopituitarism or postpartum pituitary necrosis, dt hemorrhage & hypovolemic shock
o Path: 1) Hypertrophy and hyperplasia of lactotroph cells during pg → enlarged ant pit, w/o ↑blood supply
o 2) defect in ant pit ↓P portal venous system (post pit usu not affected dt direct arterial supply)

14

• Sheehan ssx, work-up:

o SSX: mb asx; Severe (life-threatening): lethargy, anorexia, weight loss, inability to lactate. Less severe: failure to lactate, menses doesn’t resume, ↓ sexual hair
o Workup: full hx, PE
o Lab: serum hormones: May affect 1+ (→ panhypopituitarism); ↓ prolactin
o Imag: x-ray sella turcica (empty sella syndrome or tumor present); uss CT or MRI

15

• Pituitary dwarfism (short stature)

o ↓ GH from pit or HTH dz. (may → ↓GH only or in panhypopit)
o Causes: Idiopathic, emotional deprivation, hereditary
o PE: plot body measurements Growth charts: ↓, w norm proportions = hallmark; ↓Height velocity; Puberty mb normal if def is GH, abn if panhypopit
o Lab/Dx: ↓ IGF-1 & GH (but st borderline norm)
o Imag: x-ray hands for bone age (delayed)
o DDX: usu genetic or dt physiological delay rather than GH def (familial, Constitutional Delay in Growth and Puberty CDGP, idiopathic short stature ISS)
o Pathologic: Undernutrition, Crohn’s, Celiac, Juvenile RA, CF, chronic kidney dz, skeletal dysplasias, hypothyroid, precocious puberty, Cushing’s

16

• Hyperfunctioning Anterior Pituitary

o Adenomas over-secrete hormones (or commonly none): PRL, GH, ACTH
o SSX depend on hormones: usu 1 affected, rest are ↓. Mb ↑intracranial P sxs if a mass (check for papilledema)

17

• Hyperprolactinemia

o Causes: mc adenomas, drugs (methyldopa, anti-depressants, cimetidine, phenothiazines, antihypertensives, opioids, methadone) stress, pg. ↑ Prolactin → inhibit LH/FSH secretion
o SSX: General: HA, visual change; Pre-m F: persistent lactation after pg, amenorrhea, menstrual abn, infertility, galactorrhea; Post-m F: HA, ↓vision; M: ↓libido, ED, infertility, gynecomastia, Osteopenia, mb galactorrhea
o PE: HEENT, visual fields, ssx of hypothyroid, hypogonad
o Lab: ↓ prolactin (N: 5-20; mb > 200ng/ml w tumors); If ↑: check E&P
o Imag: MRI (adenoma). DEXA (↓low bone mineral density)
o Tx: Depends on severity of ssx. DA agonist drugs (bromocriptine). radiation or surgery

18

• Acromegaly and Gigantism

o ↑GH secretion: usu dt pit adenoma
o SSX: Kids (rare): ↑long bone growth → ↑ height (gigantism); Adults: suspect if (slow developing) macrognathia, ↑hands and feet (shoes, gloves, rings no longer fit); coarse facial features, upper incisors separate; CVD, sleep apnea, DM 2, HA, vision loss, carpal tunnel
o PE: Organomegaly, enlarged tongue
o LAB: ↑IGF-1; OGT fails to ↓GH to lt 2 ng/ml in 2 hrs
o Imag: X-ray: thick bone, ↑ sinuses, eroded sella, tufted phalanges, thick soft tissue; MRI pit (mb mass). If norm, Chest & abd CT for extra-pit GH-secreting mass
o Tx: Somatostatin analogs meds which block GH release. Pit surgery

19

• Pituitary Adenoma

o Seen on MRI:
o Grade 0: intrapit microadenoma ( ≤ 1cm)
o Grade 1: intrapit microademoma, focal bulging of sellar wall
o Grade 2: intrasellar macroadenoma, diffusely enlarged sella, no invasion
o Grade 3: macroadenoma, localized sellar invasion
o Grade 4: macroadenoma, extensive sellar invasion/destruction
o tests for ↑ or ↓ hormones: PRL, IGF-1, fT4, Dexamethasome suppression test

20

• Other pit masses

o cysts, mets, lymphocytic hypophysitis (lymphocytic infiltration often in late pg →HA and hypopit)

21

• Central DI (or neurogenic) (vs. nephrogenic DI), etio, ssx:

o def ADH → ↑ dilute urine, ↑ thirst
o types: chronic, complete, partial, temporary; 1st or 2nd. mb ingest and excrete 5-30 L fluids/d w rapid dehydration if stop drinking!
o Causes: HTH or post pit dz (infx, tumors, vascular dos), idiopathic, familial, AI
o SSX: usu abrupt onset. Idiopathic: only polyuria ( > 3L/d), polydipsia, nocturia. 2nd: ssx of causative dz. Dry skin, dry mucus membranes, irritability

22

• Central DI work-up:

o FHx, Hx renal dos
o PE: Tachycardia, weak pulse; neuro status, dehydration status
o Labs: Water restriction test: urine volume & osmolality every hr, plasma Na and Osm every 2 hrs (4-18 hrs); Norm: ↑plasma osm → ↓volume conc urine. DI: urine more dilute ( lt 200 mOsm/kg) than plasma (↑). Psychogenic polydipsia: both very dilute
o Other labs: FBG, UA: SG lt 1.005, no glucosuria; electrolytes: Ca, BUN, creatinine
o DDX: Polyuria: renal dos (nephrogenic polyuria), BPH, hyperglycemia; psychogenic polydipsia: emotional upset, little or no nocturia or nighttime thirst

23

• SIADH (Syndrome of inappropriate secretion of ADH)

o = ADH secretion w/o appropriate stimulus
o Causes: stroke, head trauma, small cell carcinoma, drugs (SSRIs, methotrexate, opiates, NSAIDS, etc), pneumonia, HIV
o SSX: Lethargy, HA, difficult concentrate, gait disturbance, falls, N/V, coma, sz, fluid overload; Concomitant ssx of etio
o PE: Tachycardia, HTN, ↑weight
o LAB: ↓ serum Na, urine Na > 40mEq/L. U osm > serum ( U > 100mOsmol/kg). N serum K, acid-base balance, BUN, creatinine. mb screen for HIV
o Imag: CXR to r/o infx or mass, MRI to r/o CNS lesion
o DDX (↓ urine output): renal dz, urinary blockage, heart dz

24

• Adrenal cortex hypofxn dos:

o 1st adrenal def (Addison’s)
o 2nd adrenal def w ↓cortisol

25

• Primary adrenal def (Addison’s), etio, ssx, PE:

o Etio: 70% idiopathic (AI) atrophy of adrenal gland
o Other: gland destruction by viral infx, sarcoidosis, granuloma, neoplasm, amyloid, inflame, iatrogenic
o 4/100,000, all ages, sexes
o Tends to manifest w metabolic stress and trauma
o Ssx: Insidiously progressive. weak, fatigue, anorexia, N/V, diarrhea or constipation, abd pain, cold intolerance, dizzy, fainting, low resistance to infx/stress, salt craving, muscle or jt pn, gait disturbance, difficult concentrate
o PE: hypotension, ↓wt, signs of dehydration. Skin: hyperpigmentation (diffuse, mouth), vitiligo. Ear: auricular calcification (rare). Small heart in later stages

26

• Addison’s labs:

o Electrolytes: Serun: ↓ Na+ & Cl-, ↑K (→ dehydration, ↓blood vol, hypotension, circulatory collapse), ↑Ca; Urine: ↑Na, ↓K
o ↓ am serum cortisol lt 3mcg/dl (hypotension, disturbed CHO, fat, protein metabolism). → ↑ACTH → hyperpigmentation, vitiligo
o Insulin hypersensitivity, hypoglycemia (FBG)
o ↓serum ALD
o CBC: mb anemia, eosinophilia
o ↑ BUN
o ↓ urine cortisol metabolites: ↓ 17-hydroxy-ketosteroids
o ACTH stimulation test (gold standard): IV cosyntropin, cortisol measured at baseline, 30, 60 min. if lt 18 mcg/dl, measure ACTH. If ↑: 1st adrenal insuff. If N/↓: adrenal insuff 2nd to pit insuff

27

• Adrenal crisis:

o MEDICAL EMERGENCY! profound weakness, peripheral vascular collapse, renal failure/azotemia, pain in legs, back, abd
o Crisis usu dt infx, trauma, surgery, salt loss dt heavy sweating

28

• Addison’s ddx:

o renal dz, diuretic use, SIADH and salt wasting nephritis. (All can cause ↓Na, usua assoc w edema but NO hyperpigmentation or ↑K)

29

• 2nd Adrenal def w ↓cortisol:

o 2nd to ↓ACTH stim dt destructive adrenal or pit lesion or prolonged ( > 4 wks) suppression w cortisone
o SSX: like 1st, but no hyperpigmentation.
o Labs: ACTH stim test: N or ↓ ACTH. CMP (N K and BUN, mb ↓Na dt dilution). Low serum cortisol. mb ↓ thyroid and sex hormones
o Imag: MRI or CT

30

• Adrenal cortex hyperfxn, dos:

o Hypersecretion of 1+ adrenal hormones, compensatory or acquired
o Congenital Adrenal Hyperplasia (CAH)
o Cushing’s dz and syndrome
o 1st Hyperaldosteronism (Conn syndrome)
o 2nd Hyperaldosteronism