week 9- endo 2 Flashcards
• TSH testing:
o measures pit stim of thyroid
o ↑: thyroid doesn’t make enough T4 (1st hypo)
o ↓: 1) hyperthyroid, 2) abn pit doesn’t make TSH (2nd hypo)
• Thyroid hormone state:
o free=available for uptake
o bound=circulating storage pool
• T4 tests:
o Total T4: bound + free. ~99% on TBG (doesn’t enter tissues)
o fT4/fTI (index): Free; measured direct or calc as fTI= free/bound. helps tell if abn T4 is dt abn TBG (pg, viral hepatitis, cirrhosis, breast CA)
• Triiodothyronine (T3)
o ↑: hyperthyroid (st ↓TSH, ↑T3 & T4 mb normal)
o Hypothyroid: T3 mb normal (w ↑TSH, ↓T4)
o PG and OCPs: ↑ both total T4 & T3
• N TSH, N fT4, NT3:
o Euthyroid
• N TSH, N/↑ fT4, N/↑T3:
o Euthyroid hyperthyroxinemia
• N TSH, N/↓ fT4, N/↓ T3:
o Euthyroid hypothyroxinemia
• ↑ TSH, N fT4, N T3:
o Subclinical hypothyroid
• ↑TSH, ↓fT4, N/↓T3:
o Primary hypothyroid
• ↓TSH, N fT4, N T3:
o Sunbclinical hyperthyroid
• ↓TSH, ↑/N fT4, ↑T3:
o Hyperthyroid
• T3-Resin uptake:
o serum inc w radiolabeled T3 tracer
o insoluble resin added to trap remaining unbound radio-T3
o Result: % tracer bound to resin (inverse of # free binding sites for T3)
o Distinguish TBG excess and def from hyper/hypo-thyroid
• ↑ tT4, ↑T3RU, ↑FTI:
o Hyperthyroid
• ↑ tT4, ↓T3RU, N FTI:
o TBG excess
• ↓ tT4, ↓T3RU, ↓ FTI:
o Hypothyroid
• ↓ tT4, ↑T3RU, N FTI:
o TBG def
• Serum Reverse T3:
o rT3 = biologically inactive, dt deiodination of T4 (diff enzyme), mainly in liver
o ↓ T3 & ↑ rT3: mb ssx hypothyroid → ↑ protein synthesis and O2 consumption by all cells
o ↑ rT3: mb chronic dz, Wilson’s syndrome
• Anti-thyroid antibodies (ATA):
o a-TG: (+) in Hashimoto’s
o a-thyroperoxidase (a-TPO): catalyzes iodination of tyrosine; ↑ in Hashimoto’s
o TSH receptor (TRAb)
• TRH test:
o serum TSH measured after inj w TRH to determine if thyroid problems dt ↓ TRH (3rd hypothyroid, rare)
• Thyroglobin (Tg):
o Monitor w thyroid CA w thyroid glands removed
o =protein produced by normal thyroid cells and thyroid CA cells
• Radioactive Iodine Uptake (RAIU):
o swallow sm amt radioactive iodine
o ↑: thyroid gland is overactive
o ↓: underactive
• Thyroid Scan:
o may show diffusely high or low intake or discrete (nodular) areas of high (Hot nodule) or low (cold nodule) intake
o gets a “picture” of the gland
• Ultrasound:
o used to determine if a nodule is solid or cystic
• Goiters
o = enlarged thyroid gland; diffuse or nodular
o Mb seen in normal, hypo/hyperthyroid
o Geographical differences in incidence dt I def
o Etio: I def (endemic goiter), ↑TSH, Grave’s, Pg
o Many of no clinical significance but full assessment needed
o Ssx: often asx. Early: pressure/lump in throat, choking sensation, dyspnea, dysphagia
• Goiter staging:
o Normal: ~20g in size o 0: not visible; non-palpable o 1: possibly visible; mb palpable, ↓40 g o 2: visible; easily palpable, ~40 g o 3: visible, palpable, > 40g
• Goiter work-up:
o Labs: TFTs, ATAs
o neck x-rays, thyroid scan, US w needle bx = gold standard for dx
• Euthyroid (Simple) Goiter:
o dt ↓thyroid fxn w/o clinical dz.
o Etio: Endemic, pg, menopause, hormone effects, I
o goitrogens interfere w I uptake (Brassicas, soy, peanuts, millet, strawberries, peaches, sweet potato, etc)
o drugs (amino-salicylic acid, sulfonylureas, lithium)
o Labs: ↑TSH, ↓T4 in hypothyroid
• Thyroid nodules:
o Usu benign, scan to r/o malig
o Labs: TSH, FT4, ATA titers, serum Ca
o Thyroid US, fine-needle aspiration bx
o Thyroid scan: “hot” nodules in hyperfxn, “cold” in non-fxn, “warm” = nodule w normal fxn
• Hypothyroidism, causes:
o F > M, tends to be familial; gland mb small and fibrotic, or goiter
o Causes: inherited enzymatic defects, AI, RAI exposure, anti-thyroid drugs, dietary goitrogens, thyroidectomy, inflam, granuloma, neoplasms, congenital aplasia, pituitary failure
• Hypothyroid ssx:
o weak, fatigue, lethargy, cold intolerance, wt gain
o anorexia, constipation, hair loss, dry hair, dry coarse cold skin
o dyspnea, myalgias/arthralgia, paresthesias
o irregular menses, infertility, periorbital edema, thick tongue, ascites
o pallor, ↓reflexes, anemia, bradycardia, effusions, vitiligo, goiter
o CTS, eyelid dropp, psychosis, ↓facial expression, carotenemia
o ↑heart, hoarseness, poor memory, hypothermia, myxedema coma
• Age of onset/course of hypothyroid:
o Congenital →Cretinism: resp distress, cyanosis, poor feeding, hoarse cry, umbilical hernias, slow velocity bone growth
o Juvenile: slow growth, slow dentition, eczema, mental deficiencies, other general hypoT ssx
o older: main sign mb confusion, dementia, paranoia, depression.
• Hypothyroid work-up:
o Labs: ↓ tT4 and FTI (index). ↑TSH if 1st, otherwise ↓/N. a-TPO if suspect Hashimoto’s. Serum TG when suspect subacute thyroiditis. CBC: anemia common, ↑ lipids
o Image: MRI of pituitary if suspect 2nd
o ddx: 1st vs 2nd (other hormone systems involved). 1st: ↑TSH, ↓T4 & T3. 2nd: ↓BP, ↓lipids, SSX of other def. Causes of ↓TBG: chronic LV or renal dz, starvation, ↓CHO diet
• Hashimoto’s Thyroiditis, incidence, ssx, work-up:
o = chronic AI thyroiditis (chronic inflame)
o Mc cause hypothyroid in US
o F > M, 8:1; mc 30-50
o FHx common
o May follow hyperthyroid symptoms
o SSX: Painless goiter, nontender, smooth or nodular. mb other AI. Mb ssx hypothyroid, early hyperthyroid, or none
o Labs: early: NT4, N/↑ TSH, ↑ a-TPO. Late: ↑TSH, ↓T4. ATAs may disappear.
o RAIU usu ↓ or N
o US thyroid
• Subacute Thyroiditis (DeQuervain’s Thyroiditis):
o Acute inflame, prob related to viral (URI)
o SSX: Sudden sore throat (neck pain), shift side to side, then lateralize. Pain may radiate to ears, jaw (confuse w dental or otitis). Hyperthyroid usu → hypo. Severe lassitude and prostration.
o Usu resolves in wks-mos
o PE: Gland often painful and asymmet enlarged
o labs: ↑T4 at first and then ↓. TSH depends on what T4 is doing.
o Mb ↑WBC, ↑ESR.
o (+) ATAs uncommon
• Silent Thyroiditis
o AI: silent form of Hashimoto’s except for very ↓RAIU
o ssx: mild goiter w/o tenderness, self -limited hyperthyroid stage wks-mos, → hypothyroid, full recovery
o mb ATAs. N/↑ ESR, N WBC
• Potential complications of hypothyroidism:
o Myxedema coma: med emerg, mc cold climate; in pt w long standing hypothyroid
o ssx: coma, extreme hypothermia, areflexia, szs, CO2 retention, resp depression, ↓CBF. mb precipitated by cold, infx, trauma
o Tx: usu hormone replacement for life. Armour USP Thyroid w T4, T3, T2 and T1 or synthetic thyroxine (Synthroid, only T4). Monitor TFTs carefully
• Hyperthyroidism:
o Usu AI etio. F > M. 1% pop. Familial tendency.
o SSX: mb dramatic or subtle. Tachycardia, warm moist skin, fine tremor, eye edema, lacrimation, photophobia, sweating, nervousness, fatigue, ↑appetite, heat intolerance, ↓wt, weak, emotional lability, ↑BMs, insomnia, poor memory, thinning hair, apathy
o PE: Goiter. Cardio: Wide PP, A-fib. Eye: lid lag, lid retraction. Neuro: hyperreflexia. Skin: hyperpigmentation
• Grave’s Dz (Toxic diffuse goiter), ssx:
o Etio: AI; mc form hyperthyroid, involves ATAs, lymphocyte infiltration of gland.
o SSX: of hyperthyroid, w 1+:
o Exophthalmos = infiltration of retro-orbital tissue creates pressure, lymphatic infiltration of ocular muscles → blurred, double vision, ocular weakness. can occur any time in dz, may never go away.
o Pretibial myxedema: non-pitting infiltration of mucinous ground substance on tibia. Skin may initially appear red, later brawny
• Graves work-up, tx:
o Labs: TSH, FT4, ATA
o 24 hr RAIU scan (↑)
o Tx: Propylthiouracil (PTU) or Methimazole are two anti-thyroid agents that impair organification of iodine, ↓thyroid gland production of T4 and T3. prevents peripheral conversion of T4 to T3. Mb gland ablation w radioactive iodine (I131), surgery
• Toxic Nodular Goiter (Plummer’s Dz):
o Etio: 1+ thyroid nodules can hyperfxn autonomously, inhibit HTH and pituitary → hypofxn of rest of gland. mc elderly
o SSX: classic hyperthyroid, or not
o PE: thyroid nodules
o Labs: ↑T4, mb ↑T3, ↓TSH, ATAs rare
• T3 Toxicosis
o Hyperthyroid sxs w N T4 and FTI, but ↑ serum T3 will identify the case
• Thyrotoxicosis Factitia
o Self admin thyroid meds. no goiter.
o Check serum T3 if suspect. ↓ I uptake scan
• Thyroid Storm:
o Abrupt onset hyperthyroid ssx
o PLUS (all extreme): fever, weakness, wasting, restless, mood swings, confusion, psychosis, coma, HM w mild jaundice, CV collapse and shock from untx thyrotoxicosis
o Mb precipitated by infx, trauma, surgery, embolism, DKA, labor or discontinuation of anti-thyroid meds
o Ddx: hypoglycemia, hypoxia, sepsis, encephalo/meningitis, heat stroke, withdrawal (alcohol, benzodiazepines, opioids)
o Tx: Emerg. Propanolol helps ↓ adrenergic ssx. IV I to “stun” thyroid gland, IV glucose, hydration, electrolyte balance, cooling blanket, adrenal steroids, tx any precipitating cause (infx). mb fatal, even w tx
• Wilson’s Syndrome:
o not a thyroid dz per se; end organ sensitivity to normal thyroid hormone fxn is impaired
o Ssx ↓ thyroid fxn, normal labs, ↓body temp (↓98.3 in afternoon)
o Labs: usu N, mb ↑rT3. (may follow severe trauma, circulatory shock, CA, malnutrition)
o Tx: hormone cycling, tx underlying causes
• Thyroid CA:
o F > M (2:1). mc young
o Risk factors: Low dose radiation to neck, “down-winder” exposure to radioactive particulate matter.
o PE: Solitary nodules suspicious if hard consistency
o Lab: TFTs, serum calcitonin (↑in medullary form thyroid CA)
o Procedures: US, bx, Thyroid scan (cold nodules more suspicious than hot, yet majority of both are benign)
o Tx: usu surgical removal. Monitor Tg levels
• Diabetes Mellitus:
o Hyperglycemia is central sign, → hyperlipidemia, accelerated atherosclerosis, ketoacidosis, neuropathy, angiopathy, nephropathy, retinopathy
o Polyuria when serum glucose > 180 mg/dl, over renal threshold for glucose
o etio: environmental, hereditary and pathological (biological defect in insulin or lack of it). Mb Viral stim a-islet Abs for IDDM. Familial links in both IDDM and NIDDM.
o Peak 5-11 T1, adulthood T2
o mc females, African Americans, Hispanics
o 2x Risk type II DM w 20% ↑ wt and w each decade of life
• Type I DM (IDDM= insulin-dependent)
o 5-10% o kids: usu non-obese, less common; dt relative or absolute insulin def. AI w islet cell Abs. ssx: severe hyperglycemia, ↓ or absent insulin, ↑circulating stress hormones. → alt fat metabolism, ketoacidosis o adults (aka T1.5, Latent AI DM in Adults (LADA) or Slow Onset type 1 DM). AI destruction islet cells, usu no ssx until 30s. Often longer period of sx (polyuria, polydipsia, fatigue weight loss) before dx
• type 2 DM (NIDDM):
o >90%
o Usu adult onset. Varying degrees of insulin resistance or def; usu obese, > 40, but now endemic in children. Usu no ketoacidosis.
o Often asx, ↑glucose on screening lab
• Gestational diabetes (GDM):
o Develops during pg (not previously dx), usu 24-28 wks (late 2nd, early 3rd tri)
o Comps/risks: Short term: pre-eclampsia, macrosomia, intrauterine fetal demise
o Long term: For child: obesity, metabolic syndrome. For mother: later development of DM
• Ddx of hyperglycemia, ssx:
o Ddx: pancreatic CA, pancreatitis, trauma to pancreas, acromegaly (and other endo), drugs (prednisone, dilantin, phenothiazides, sympathomimetics, OCPs, ERT). “stress hyperglycemia” (transient) dt ↑ cortisol, catecholamines, glucagon
o Ssx: Often abrupt onset in kids, more gradual in adults
o Earliest: polyuria, polydipsia, polyphagia
o ↓wt (T1), ↑wt (T2).
o Recurrent skin, ear, vag yeast infx, aphthous ulcers, ↓ wound healing
o Poorly controlled type 1 (or 1.5): ketosis, acidosis, air hunger, N/V, coma, death if untx
• Hyperglycemia sequelae:
o Large vessel dz: ↑incidence, earlier onset, ↑severity atherosclerosis
o Microvascular dz: regional thickening of basal lamina
o Renal damage: diabetic nephropathy: proteinuria, hematuria, sterile pyuria, renal failure
o Nerve damage: diabetic neuropathy: BL symmetrical polyneuropathies: first in feet and hands (stocking and glove neuropathy), plantar ulcers, nerve pain, impotence, GI dysfxn such as diabetic gastroparesis, C/D. PE: loss DTRs, (+) Romberg, abn monofilament foot test
o Retinal dz: diabetic retinopathy: retinal hemorrhages, cotton wool spots, neovascuralization. ↑ risk glaucoma, cataracts, blindness
o **DR = mc cause reversible blindness in US. Retinal neovascularization tx by laser photocoagulation
• DM work-up:
o PE: HEENT w fundoscopic, microfilament foot testing, full neuro exam
o Lab: BG. Dx criteria for DM:
o Normal: fasting ↓110, non-fast ↓140, GTT ↓140, HbA1c ↓5.5%
o Impaired (pre): F 110-125, NF 140-199, GTT 140-199, HbA1c 5.6-6.4
o DM: F > 126, NF > 200, GTT 1 hr > 199, 2 hr > 165, 3 hr > 145, HbA1c > 6.5
• Tests for AI dz in DM:
o C-peptide: level of insulin secretion. ↓ in DM1
o Auto-Ab Panels: Islet cell Abs (ICA): a-cytoplasmic IgG; a-Complement Fixing; a-Glutamic acid decarboxylase; a-Insulin
• Emergencies w DM:
o Ketoacidosis and Hyperosmolar coma: confusion or coma, air hunger, acetone breath, N/V, abd tenderness, extreme thirst and dry membranes, ↓wt, diabetic hx
• Ketoacidosis ssx:
o Hx: N/↑ food intake, ↓insulin, gradual (d) onset, common preceding febile illness/stress
o PE: appear ill, dry flush skin, infx, fever
o GI: dry mouth, intense thirst, hunger common, V, abd pn
o Resp: exaggerate, air hunger
o Acetone breath
o ↓BP
o Pulse: weak, rapid
o ↑ urine: glucose, ketones,
o ↑blood: glucose, ketones
o ↓ serum HCO3, ↓ 10 meq/L
o Gradual tx response: 6-12 hr p insulin
• Insulin shock (hypoglycemia) ssx:
o Hx: ↓food intake, ↑insulin, sudden onset o PE: very weak, moist pale skin, no fever o GI: drooling o Resp: N/shallow o N BP o BG: ↓ 60 mg/dL o Serum HCO3: >22 meq/L o Reponse to tx: rapid after CHO meal
• Hypoglycemia, types, causes:
o Reactive: mc, sxs 2-4 hrs after eat, dt rapid absorb glucose → ↑insulin. mb first sign of developing DM.
o “Fxnal”: idiopathic
o Causes: ↑ carb meals, ↑insulin or defective regulation, Post-gastrectomy, Specific nutrient hypersensitivities (fructose intolerance, leucine hypersensitivity)
o Meds: insulin, hypoglycemics, tetracycline, EDTA, propanolol w insulin, Dicoumerol, Phenylbutazone, EtOH, salicylates, aminobenzoic acid, haloperidol, propoxyphene and chlorpromazine.
o Spontaneous: neonates of DM mom, HDN, ↑exercise w ↓nutrition, insulinoma, def glucagon, cortisol, GH, epinephrine
• Hypoglycemia ssx, work-up:
o Pattern 1: Hunger, light-headed, weak, tremble, palpitation, diaphoresis
o Pattern 2: CNS sxs: HA, confusion, visual disturb, motor weak, palsy, ataxia, personality change → LOC, convulsions, coma
o Lab: FBG ↓50mg/dl relieved w food. C-peptide to eval insulinoma
o ***If normal glucose, but still sxs, need to determine cause
o Sxs 2-4 hrs after CHO meal: usu reactive hypoglycemia
o Sxs w fasting: need to r/o insulinoma
• Insulin Resistance (Syndrome X or Metabolic Syndrome)
o CHO sensitivity →central obesity, CVD, NIDDM, HTN, atherosclerosis
o ↑ in Mexican-American, African-American, F > M
o Other factors: post-menopausal, smokers, ↓income, ↑CHO diet, ↓exercise
• Insulin resistance work-up:
o PE: BP > 130/86 mmHg, Waist circumference M > 40 in, F >35 in
o Eyes: retinopathy, refraction changes, cataracts, keratosis, blindness
o Skin: necrobiosis lipoidica diabeticorum, red maculopapular rash or purple plaques w atrophy and ulcers, shin spots, bullae, fungus, eruptive xanthomas, herpes zoster
o Neuro: paresthesias, CN palsies, autonomic nerve palsies, orthostatic hypotension, ↓ pain and temp sensation, mb muscle weakness
o Lab: TGs > 150 mg/dl, HDL M ↓40mg/dl, F ↓50 mg/dl; FBG > 100; ↑ CRP, IL-6
o DDX: Cushing’s
• Male gonadal fxn, endocrine dos:
o Testes make and secrete T. LH (ICSH) stim interstitial cells, FSH stim spermatogenesis. Interstitial cells produce T, DHT, ↓ E2
o ↓T in developing M fetus → F phenotype
o ↓T at puberty → delayed plate closure, eunuchoidal body proportions, no puberty, poor muscle development, psychosocial immaturity
o ↓T after puberty → ↓libido, potency, ejaculate; mb hot flashes
• Primary Hypogonadism:
o Causes: BL orchitis, post surgical trauma, BL testicular torsion, post radiation, chromosomal abn, testicular agenesis
• Klinefelter’s Syndrome:
o Extra X chromosome →small testes, no sperm. Gynecomastia, eunuchoidal proportions. Usu infertile, or only ↓fertility w mosaicism
o Lab: ↓T, LH, FSH. Buccal smear for abn karyotype
• Testicular agenesis:
o Normal phenotypic M w/o testes; destruction of testis during fetal development
• Sertoli cell only syndrome:
o essentially normal M w small testes, infertility
o No sperm in semen or testicular bx
o Serum T usu normal
• Noonan syndrome
o = “male version” of Turner’s
o Normal XY karyotype, w some features of Turner’s:
o hypertelorism, short, epicanthal folds, right-sided heart dz. Mb cryptorchidism
o Often mental retardation
• Delayed puberty in Males:
o Full workup if no testicular maturation at 18
o Avg onset 12+/-2, delayed if not by 14
o Check for possible underlying dz causing puberty delay
• Normal maturation in the male:
o Testes enlarge: 11.5 yrs o Pubic hair: 12.5 o Penis enlarges: 13 o Peak height velocity: 14 o Voice changes: 14 o Horizontal pubic hair: 15
• Tanner stages in males:
o I- no pubic hair, pre-pubertal
o II- downy pubic hair, large pigmented scrotum
o III- coarse dark pubic hair, penis lengthen
o IV- pubic hair in genital pattern, wider longer penis
o V- adult pubic hair pattern, full maturation of genitalia
• 2nd hypogonadism:
o Causes: general panhypopituitarism, Kallman’s syndrome, hyperprolactinemia
o Ssx: depend on age onset. mb ↓libido, impotence, small penis, testes. 2nd sex characteristics regress, ↓muscle development, ↑pitch voice if before puberty, gynecoidal fat distribution, eunuchoidal stature
o Post pubertal changes more subtle
o Labs: ↓T, ↑FSH in testicular failure, ↓ in HTH/pit problems
• Panhypopituitarism:
o → Hypogonadotropic hypogonadism
o Destruction of pituitary or tumor → ↓production and release of pituitary hormones → hypogonadism, tumors that secrete PRL will suppress T
o Labs: serum T, ↓ LH & FSH
• Kallman syndrome:
o →Hypogonadotropic hypogonadism
o “Congenital GnRH Deficiency” (originates in HTH)
o AD, variable penetration
o ↓FSH & LH, anosmia, midline skeletal defects, mental developmental delay
o Micropenis, cryptorchidism. Boys remain prepubescent unless give T
• Precocious puberty
o Usu process of puberty is normal, but early age; a variation of normal development
o Central: triggered by a dz (intracranial neoplasm, infx, trauma, hydrocephalus)
o Concerns: mb adverse effects on social behavior and psychological development; mb ↓adult height potential, lifelong health risks
o Peripheral: 2nd sexual development induced by sex steroids from abn sources. Causes: congenital adrenal hyperplasia, adrenal tumors, gonadal tumors, germ cell tumors
• Precocious puberty dx criteria: M & F
o M: Breast development in boys before pubic hair or teste enlargement. Pubic hair or genital enlargement (gonadarche) ↓9.5
o F: Pubic hair (pubarche) ↓8 or breasts (thelarche) ↓7. menarche ↓10
• Precocious puberty ssx, work-up:
o SSX: hypotension, premature growth plate closure → short stature
o LAB: ↑androgens, ↓cortisol. electrolyte abn on CMP. Check 24 hr urine for 17-KS and serum LH and FSH
o Mb CT scans of head or adrenals
• Gynecomastia:
o Common in puberty, can cause stress; enlarge duct and alveolar tissue from adipose in elderly male
o Pathological: drugs (many!!), cirrhosis, hypogonadism, neoplasms (testicular, adrenal), hyperthyroidism, renal dz
o DDX breast CA (firm to hard mass, nipple d/c, dimpling, LA)
• Male Infertility:
o Causes: cryptorchidism, small testes: insufficient tubules to mature sperm, testicular trauma, varicocele, pelvic irradiation, chronic epididymitis, smoking
o PE: teste exam for normal descent and development of testes
o Labs: Sperm count and semen analysis, mb testicular bx, STD check. Check for hyperprolactinemia
• Endocrine Neoplasia (MEN) Syndromes
o Several endocrine tumors, usu adenomatous hyperplasia, in several glands in same individual. AD. classic types: 1, 2a, 2b o Ssx: any age. Depend on glands involved. Overlap bw types o 1 (Wermer’s): > 90% parathyroid adenomas, 60-70% entero-pancreatic tumors, 15-42% pit adenomas o 2a (sipple syndrome): 10-20% parathyroid, > 90% medullary thyroid carcinoma, 50% pheochromocytoma o 2b: > 90% medullary, 60% pheochromocytoma, 100% mucosal neuromas, 100% marfanoid habitus
• MEN 1 syndrome
o “3 Ps”
o Hyperparathyroidism: hypercalcemia, renal stones, osteoporosis
o Pituitary adenoma: hypo- or hyperfxn, HA, vision changes
o Pancreatic/GI adenoma: gastric ulcers, diarrhea
o Dx: CT or MRI, DNA testing for MEN1 gene mutation
• Polyglandular Deficiency Syndromes
o AI on mult glands (inflam tissue, attracts lymphocytes → complete or partial destruction) → mult endo gland failures
o Type I: onset childhood, earliest sign hypoparathyroid →adrenal failure often have chronic mucosal Candidiasis; assoc HLA
o Type II: adults, peak 30. Usu adrenal cortex, st thyroid, pancreatic islets →IDDM. Auto-Abs. →Poor cell mediated immunity (fungal and Candidal infx). HLA → susceptible viruses
o Type III: adults, thyroid probs, IDDM, pernicious anemia, vitiligo, alopecia (adrenals not affected)
o SSX: dt def affected hormones
o LAB: auto-Abs
