33 YO female comes to office with occasional diplopia and ptosis. Symptoms becaeom prominent when looks above her head. ALso complains of fatigue in her hands and leg muscles after exercising such as swimming. What is the level of the lesion in the disease that is being described?
NMJ 2/2 myasthenia gravis - seen in females in 30-40s or males in >60yo
-fatigue and weakness of skeletal muscles
-there are no reflex, sensory or coordination abnormalitis
-characteristic feature is that the symptoms are typically seen on eertion and resolve with rest.
-weakness of eyes are dead giveaways
-bulbar movement can lead to myasthenic snarl, nasal speech and difficultiy chewing or swallowing
-AI in whih autoAB against the ACh receptors block the available mech of muscle contraction at the NMJ.
-decreased ACh receptors and simplification of postsynaptic clefts with widening synaptice space and normal presynaptive nerve terminal is MG
Extrathyroid symptoms of HYPERTHYROIDISM?
1. Proptosis, 2/2 edema of EOM and retroorbital tissue
2. Irritation and tearing are common due to corneal exposure
3. Lid retraction or lidlag
4. Cardiovascular effects = tachycardia, AFIBB PVC, elevated BP
5. Skin changes: warm and moist
What is the treatment for hyperprolactinemia?
1. TREAT CAUSE - stop the medication inducing the symptoms, for ex: hypothyroid then administer levothyroxine.
2. If prolactinoma is cause and patient is symptomatic - then treat with BROMOCRIPTIVE (DA-agonist that decreases the production of prolacting)
-continue for 2 years
-try cabergoline - better tolerated
3. Surgical intervention if bromocriptine is not effective. Recurrence rates after surgery is HIGH.
1. Elevated concentration of PTH and a low or low-normal serum calcium level
2. Chronic renal failure (#1 cause) - Vitamin D definiciency and renal hypercalcuria
3. Treatment depends on cause = if vitamin d def; give supplement; if RF give calcitriol and oral Ca2+ supplements + dietyary phosphorus restriction.
edema over tibial surface D/T dermal accumulation of mucopolysacchararides?
Pretibial myxedema seen in skin changes of HYPERTHYROID
Thyroid hormones T3 v. T4 and TBG
T4 converted to T3 by deiodination outside of the thyroid
T3 is more biologically active than T4
Most T4 and T3 is reversibly bound to TBG and is inactive
Increased TBG seen in increased T4 levels, liver dz, pregnancy, OCP, and ASA
1. Polyuria = 5-15L daily (colorless)
2. Thirst and polydypsia = hydration maintained if pts conscious with H2O access
3. Hypernatremia = mild unless pt impaired thirst drive
Paget's disease of the Bone has which dominating features?
pattern of "mosaic" on lamellar bone
elevated alk phos levels
decreased hearing bilaterally
FEMORAL BONE BOWING
bone and joint pain
What is the most common cause of death in patients wih ACROMEGALY?
CV disease --> hypertrophic CM
-IGF-1 (Somatomedin C) should be elevated; oral glucose suppression test - a glucose load without lowering GH and confirms diagnosis if ICF-1 level equilvolent.
-MRI of pituitary
-Random GH level is NOT useful
-Lab abnormalities = INC prolactin, INC glucose, INC triglycerides, INC PO4^3-
Diagnosis of hyperthyroidism
Initial test: serum TSH level (will be low) -if normal/HI then not hyperTHY
Next, order: T3/T4 levels = T4 should be HIGH (consider assay)
May order: T3 level if normal TSH and T4 and still think hyperthyroid
May order: radioactive T3 uptake - gives info of TBG; radioactive T3 can bind to either TBG or "resin" (will only bind to resin if no space of TBG which is seen in hyperthyroid) - where T4 bound to TBG. Then measure how much radioactive T3 is taken up by the resin. Importance of T3 uptake differes between elevation in T3/T4 2/2 increased TBG from the hyperthyroid due to increased free T4.
-consider hyperTHY is ecress T4, all TBG will have T4 bound so RT3 uptake increases
Next: free thyroid index (FTI)
FTI = RT3uptake x Serum total T4 / (100)
normal values = 4-11) (as T4 decreases, RT3U increases)
1. End organ resistance to ACTION of PTH
2. Laboratory value = HYPOCALCEMIA, HYPERPHOS, HIGH PTH, LOW URINARY cAMP
1. Hypovolemic hyponatremia
2. Hypervolemic hyponatremia
1. Volume contracted (dehydration)
2. Volume expanded with edema
3. Volume expanded without edema
1. Head and neck surger acct for majority of cases - thyroidectomy, parathyroidectomy, radical durgery for head and neck malignancies
2. Nonsurgical hypoparathyroidism is RARE
Papillary CA is the most common type of thyoid CA to develop after ________ exposure
MICROADENOMA < 10 MM/MACROADENOMA > 11MM
-hormonal effects 2/2 hypersecretion of: PROLACTIN (hyperprolactinemia), GH (acromegaly); ACTH (cushings); TSH (hyperthyroid)
-hypopituitary = HP stalk compression, GH dec and hypogonadotrpoic hypogonadism is the most common problem!
-headaches, visual change; bitemporal hemianopsia due to compression of optic chiasm
-excess ADH secreted from posterior pititary or an extropic source
-elevated levels lead to H2O retention and excretion of ceoncetrated urine
-although there is an increased in volume, there is no edema due to natriuresis (excretion of excessive Na+) in urine.
Graves disease or ( ___ ______ _____) is the most commone cause of hyperthyroidism. Pathophysiology and diagnosis?
Diffuse toxic goiter
Patho: thyroid stimulating IgG antibody binds to TSHR on the thyroid cells and increases the syn of excess thyroid hormone
Dx: Radioiodide scan would show diffuse uptake bc every thyroid cell is hyperfunctioning.
Treatment of pituitary adenoma?
1. Transphenoidal surgery (unless prolactinoma, then attempt medical management first)
2. Radiation therapy + rx used as adjuncts
Clinical features of decreased action (hypopituitarism)
1. Dec GH = growth failure, dec muscle mass in adults
2. Dec Prolactin = failure to lactate
3. Dec ACTH - adrenal insufficiency (Addisons)
4. Dec TSH = hypothyroidism (weight gain, dec BMR, cold intolerance, dec bone/brain maturation)
5. Dec GnRH = LH, FSH: infertility, amenorrhea, decreased 2ndary sex characteristics
6. ADH (hypothalamic lesion) = diabetes insipidus
7. Dec MSH = dec skin and hair pigmentation
WHAT IS TAO - thyroid associated opthalmopathy?
TAO - AI attack on the periorbital connective tissue and EOM.
-lid retraction, "THYROID STARE"
-proptosis, eyelid edema, diplopia
-hypothyroid, hyperthyroid (graves) or euthyroid
-TAO self limited but can require surgery
GOOD RX prior to surgical intervention: ORAL STEROIDS GOOD
Diagnosis of THYROID CA =
T3/T4 levels = normal
calcitonin - if med
Papillary = lobectomy with isthmusectomy; total if tumor > 3cm/bilateral and advanced/distant mets are present
-TSH suppression therapy, 131 - I if large
Follicular = total thyroidectomy with post op iodine ablation
Medullary = totoal thyroidectomy with post op iodine ablation
Anaplastic = chemo
Treatment types for hyperthyroid
-thionamides: Methimazole and PTU
-BB for acute management of symptoms
-sodium ipodate or iopanoic acid
2. radioiodide 131
-destruction of throid folicular cells
-most common therapy for graves
3. surgical subtotal thyroidectomy
2 forms of diabetes insipidus?
A (causes, Dx, Rx)
B (causes, Dx, Rx)
A. Central DI
-causes: idiopathic (50%), trauma, destructive diseases involving hypothalamus = tumors, sarcoid, TB, syphilis, hand schueller DZ, eosinophilic granuloma
-diagnosis: no increase in urine osmolarity with dehydration; increased response to ADH
-treatment: DDAVP = primary therapy by spral, oral, injection///OR can administer chlorpropramide = increases ADH secretion and increases the effect of ADH.
B. Nephrogenic - hypokalemia; hypercalcemia; pyelonephritis
-treatment: lithium; demeclocycline, HCTZ,
-diagnosis: doesn't INC with H2o dep and doesnt change with increased ADH.
Treatment of ACROMEGALY?
1. Transphenodal resection of pituitary adenoma
2. Radiation therapy if IGF-1 is elevated after surgery
3. Octreotide to suppress GH secretion
Fibrous thyroiditis (REIDELS)
Fibrous tissue replaces thyroid tissue leading to firm thyroid. Surgery may be necessary if complications arise
If hypothyroid too - repalce with SYNTHROID
Cold v. HOT nodules of thyroid
COld - dec IODIDE uptake - hypofunctioning nodule. Significant risk of malig. 20% malig, scanning can dec risk of malig in a warm/hot nodule.
Hot: elevated IODIDE uptake - hyperfunction. Rarely malig
RF: head and neck radiation; GARDNERS SYNDROME and COWDENS syndrome for papillary CA; medullary CA with men II.
1. Papillary carcinoma (70-80%)
-leads to aggressive, slow growth, spread
-distant mets rare
-positive iodide uptake
2. Follicular carcinoma - 15%
-15% of all thyroid CA
-prognosis worse than for all thyroid CA because spreads early to brain lung breast bone liver
-HURTHE CELL TUMOR = VARIANT OF FOLLICULAR BUT MORE AGGRESSIVE
3. Medullary CA
-3% of all thyroid CA
-33% sporative, 33% family, 33% associated with MEN II - always screen pheo
-production of calcitionin
-more malignant than follicular but less than anaplastic CARCINOMA
4. Anaplastic carcinoma - 5%
-seen in elderly
insidious onset, goes un-diagnosed for years
causes: primary hypothyroidism is the failure of thyroid to produce sufficient thyroid hormone - 95% of all cases
-HASIMOTOS disease (chronic)
-IATROGENIC (second most common cause)
---> medications *lithium
secondary hypothyroidism = pituitary TSH
tertiary hypothyroidism = hypothalamus TRH
Hashimotos thyroiditis is also associatd with?
1. LUPUS (AI DISEASE)
2. PERNICIOUS ANEMIA (AI BLOOD DISORDER)
What is myxedema coma?
Rare condition presenting with depressed state of consciousness, hypothermia, respiratory depression
-develops years post untreated hypoT3/T4
-medical emergency (50-75% mortality)
administer: IV thyroxidine and HYDROCORTISONE
Symptoms of hypothyroid:
1. Fatigue, lethargy, malaise, weakness
2. Menorrhagia-wt gain (10-30 punds)
3. Cold intolerance, decreased concentration
1. Dry skin, coarse hair, thickened face
3. nonpitting edema (glycosaminoglycan) in tissues, not Na+/H20
4. CT syndrome: GIOTER
Dx: HIGH TSH level is most sensitive; LOW TSH level (secondary hypothyroid); LOW T4 free and increase anti-mb AB
Causes of hyperthyroidism
2. Plummers dz
3. Toxic thyroid adenoma
4. Hashimotos and subacute granulmatous thyroiditis
5. Postpartum thyroiditis iodine induced hyperthyroisism with excess levothyroxine (T3)
Treatment of SIADH if:
Asymp: H2o restriction; use NS and loop diuretic, lithium carbonate-demeclocycline to inhibit the effect of ADH on the kidney
Symp: restrict H2O; administer isotonic saline. Hypertonic saline may be occasionally indicated
Parasellar signs are more prevalent in men than women - why?
Because early (impotence) sypmtoms in males will be attributed to psychollogical causes and medical evaluation is delayed - allowing for larger tumor growth
General: one or more glands produce inappropriately high amounts of PTH relative to serum CA2+ levels. most common cause of hypercalcemia
-adenoma (80%) cases - usually one gland
-hyperplasia (15-50%) - all 4 glands
Features: STONES BONES GROANS PSYCHIATRIC OVERTONES
Subacute lymphocytic thyroiditis
Painless and silent
1. Transient thyrotxic phase 2-5 months followed with hypothyroid phase that is self-limited and ONLY Manifestion of disease if the HYPERTHYROID PHASE BREIF.
2. LOW RADIOACTIVE iodide uptake will differentiate from GRAVES if during thyrotoxic phase
3. Similar to subacte thyroiditis (viral)
Medial compartment OA presents with?
pain at the medial joint line in patients older than 40 - other clinical features include morning stiffness of lesss than 30 minutes, crepitus and bony tenderness on examination. XRAY of the knee shows narrowing of joint space and steophyte formation.
1. All/some hormones released from ant pituitary may be absent; loss unprediatable (LH, FSH, GH) lost before TSH and ACTH
2. Hypothalamic/pituitary tumor = most common cause
-Infiltrative process (sarcoid/hemochromatosis)
-Head trauma, cavernosus sinus thromb
What is patellofemoral syndrome?
overuse pain syndrome of the knee. Pateints present with peripatellar pain worsened by activity or prolonged sitting 2/2 sustained flexsion and may also complain of crepitus with motion of the patella
Diagnosis of hypopituitarism is made by?
1. Dec levels of target hormones with low/normal levels of trophic hormones
2. MRI of BRAIN (misses microadenomas, unfortunately)
MCL ligament injury presents with? Stress test that aggravates tear?
pain along the medial joint line and is aggreavated by walkin. caused by valgus stress applied on the later aspect of the knee when partially flexed
Test: valgus stress test
Treatment of hypothyroid?
Levothyroxine (T4) = synthroid
-admin 2-4 weeks before actually effective
-1x/day morning dose
What is prepatellar bursitis?
pain with swelling directly over the patella. Examination will show swelling over the patella with cariable signs of inflammation - most common cause being trauma
Thyroiditis (subacute) viral thyroiditis
Features: prodromal flu like phase - weeks; causes TRANSIENT hyperT3/T4 2/2 leaking of hormone from inflammed thyroid. Followed with euthyroid then hypothyroid states. THESE ARE PAINFUL tender glands
-Radioactive iodide uptake will be LOW because thyroid follicular cells are damaged and cannot "trap"iodide for production of T3/T4.
-LOW tsh 2/2 depression by the increased T4/T3 levels with HIGH ESR
Rx: NSAIDS, ASA, 1 full mo of thyroid fcn
Thyroid cells are the only cells in the body that ABSORB IODIDE. Thus administration of _____ will destroy thyroid cells only.
-IF the 1st dose doesnt control hyperthyroidism then 6-12 mo later admin another dose
Hyperthyroidism in the elderly patient?
4. Weight loss, weakness and AFIBB
Subtotal thyroidectomy is the number 1 treatment in patients with?
LARGE GOITERS WHO ARE ALLERGIC TO PTU OR DRUGS.
-watch for hyperglycemia/calcemia postsurgically due to parathyroid inflammation/removal.
Features of hyperthyroid:
Symptoms: nervousness, nsomnia, irritible
-hand tremor, hyperactivity, tremulousness
-excessive thirst, sweating/heat intolerance
-wt loss despite increase appetitie
-Graves: diffusely enlarged thyroid (but SYMMETRIC), nontender thyroid gland; +/- bruit.
-subacute thyroiditis: a tender diffuse and enlarged thyroid (2/2 viral illness)
-Plummers disease/hashimotos: if multinodular bumby, ireegular, assympetric
-Toxic adenoma = single nodule with ATROPHIC gland 2/2 decreased amount of TSH
Treatment for INCREASED PTH:
Indications for surgery in primary hyperparathyroidism:
Indications for medical therapy:
Surgery: Age < 50, marked dec bone mas, nephrolithiasis, renal insuffiencieny, increases serum Ca2+, urinary Ca2+ > 400 mg in 24 hours
If d/t hyperplasia = remove all 4 glands and placement of paarathyroid tissue in forearm muscle.
If d/t adenoma = remove tumor, is cure
If carcinoma = get tumor, ipsilateral thyrid lobe and lymph
Medical therapy: fluids, furosemide to increase Ca2+ excretion - do not use HCTZ (retains Ca2+)
1. Hyponatremic; concentrated urine, plasma osmolarity <270 mmol/kg
2. Decreased uric acid
3. Decreased BUN and dec Cr
4. Measurement of plasma and urine ADH level
Water load test: If drinks H2O, urine output check hourly, if large amount of water excreted in urine, >65% in 4 hours - consider SIADH
Reasons for natriuresis in SIADH?
1. Volume expansion causes increase in ATRIAL NATRIURETIC PEPTIDE (increases that of urine sodium excretion)
2. Volume expansion leads to decrease in proximal tubular sodium resorption
3. RAAS inhibited 2/2 volume expansion
Primary polydypsia is seen in patients with ____ _______ and when deprived of H2O, urine, urine oSmo will increase appropriately.
4> Psychiatric overtones
1. Nephrolithiasis, nephrocalcinosis
2. Bone aches and pains; osteitis fibrosa cystica (brown tumors)
3. Muscle pain, weakness, pancreatitis, GOUT, consipation
4. Depression, fatigue, anorexia, anxiety
What is plummers disease (15% of all cases) - multinodular toxic goiter
Patho: hyperfunctioning areas producing increased T3 and T4 levels and thus have decreased TSH levels - as a result - the remainder of the thyroid is not functioning (atrophy due to decreased TSH 2/2 neg feedback with elevated T3 and T4)
Dx: patchy uptake with radio iodide scan common to elderly
1. Acute hyponatremia
2. Chronic hyponatremia
Acute: brain swelling, increase ICF volume, lethargy, weakness, coma, death, seizures
Chronic: asymptomatic, anorexia, nausea, vomiting, CNS symptoms not as common because chronic loss of sodium and potassium from cells in brain decreases brain edema due to 2ndary H2O shifts
Cl-/Phosphorus ratio of >33 or (33:1 rule) is diagnostic for?
What is the formula for serum calcium (Ca2+) ionized:
-Cl(-) is high secondary to renal HCO3- wasting (direct effect of PTH)
Ionized Ca2+ = Total Ca2+ - (serum alb x 0.8)
Suprasellar region from remnants of RATHKE's POUCH
-20-25% all pituitary lesions
Bitemporal hemoanopsia due to compression of optic chiasm - headaches, papilledema, change in mentation
MRI = diagnostic
Total/partial resection +/- radiation therapy
2. Males v. Women
1. PROLACTINOMA = #1 cause and most common type of pituitary adenoma
2. Medications = psychiatric, H2 blockers, metoclopromide, verapamil (CCB), estrogen
3. Pregnancy, renal failure, suprasellar mass, hypoT, idiopathic
If males: hypogonadism, dec libido, dec fertility, impotence, galactorrea, gynecomastic. Parasellar signs
If females: premenopausal = irregularities, oligomenorrea, amenorrhea, anovulation, infertility, decreased libido and vaginal dryness. Bitemporal hemianopsia
Diagnosis: increased serum prolactin; ORDER PREG test/TSH; CT scan and MRI
Diagnosis of primary HYPERPARATHYROIDISM
1. Ca2+ levels: hypercalcemia
-when calculating ca2+ levels, watch albumin
-calculate the ionized fraction or get ionized Ca2+
2. PTH levels: should be relative to serum Ca2+
-hypercalcemia, a normal PTH is "abnormal" because increased Ca2+ should produce negative feedback and as such (DEC PTH)
3. Hypophosphatemia, hypercalcuria, increase cAMP urine
Diagnosis of DI
***-low specific gravity of urine, low osmolarity
-normal = 250-290 mOsm/jkg
-primary polydypsia = 255-280 mOsm/kg
-DI = 280-310 mOsm/kg
Test for DI: H2O Dehydration test
1. Withhold fluids and meausre urine osmolarity/hr
2. When urine oSmo stable (<30 mOxo/kg) increases for 3 horus, inject 2 g demopressin subQ then measure urina oSmo 1 hour later.
ADH level is lOW in CENTRAL DI
ADH level is HIGH in NEPHROGENIC DI
When is a thyroid scan performed? Thyroid US?
Scan if FNA biopsy is indeterminant - good to identify decreased ("cold") or increased ("hot") accumulation of radiactive iodide.
-cold (hypofunction), "warm" = normal, "hot" (hyperfunction)
-cold lesions *thyroid lobectomy recommended
Thyroid US- differentiates a solid from a cystic node; cancers are solid (1-3mm) in diameter to be detectable. If > 4cm, not malig if cystic
-cancer in 10-20%
-solitary nodule can be CA/adenoma
-on palpation must be ICM in diameter
-malignancy if = fixed; firm/irregular nodule; nodule is SOLITARY; hx of radiation to neck; rapid development; laryngeal nerve paralysis *hoarse
Dx: #1 == FNA #2 == THYROID SCAN #3 === THYROID US
What is the only test that can reliably differentiate between BENIGN v. MALIGNANT thyroid nodule?
Hyperthyroidism and thyrotoxicosis are interchangeable as both = hyperfunctioning thyroid gland.
Why is a "thyroid storm" a medical emergency??
1. Acute exacerbation of hyperT3/T4 secondary to infection, DKA, stress (trauma, childbirth, surgery)
2. Symptoms = fever, elevated HR, psychosis, GI symptoms
3. Rx = glucose, cooling blankets, IV fluids, give PTU x 2hrs with iodide to decrease T3 release, PROPRANOLOL controls the BP and dexamethasone decreases the T3 -->T4
cardiac arrhythmias; ricketts, osteomalacia (dec calcium, inc phos, dec vitamin D)
-inc NM irritability due to hypocalcemia
--> numbeness tingling, finger/toes
--> trousseus sign = carpel spasms/chvosteks sign (tapping facial nerve)
-->grand mal seizures
--> basal ganglia calcifications
-->prolonged QT on ECG
Dx: decreased serum Ca2+, increased serum phos, decreased PTH, decreased urine cAMP
Both ____ + ______ _______ are on differential for hyperprolactinemia, thus should order?
Preg test/TSH level
Once the diagnosis of RA is certain, therapy with disease modigying anti-rheumatic drugs is and should be indicated (DMARDS). These are used ______ in course of the disease as RA is a chronic meidcal issue and the goal of therapy is induction of a remission followed by maintenance of that remission.
First line of DMARD
First line: Methotrexate due to its long hx of efficacy and safety when used weekly
other rx: hydroxychloroquine, sulfasalazine, leflunomide, etanercept, infliximab, and AZA
-broadened skeleton results from exces secretion of pituitary GH post ephipheseal closure
-GH secreting pituitary adenoma
-growth promotion (large hands/feet, organomegaly, and hypertrophic cardiomyopathy)
-metabolic changes = glucose interance, and DM, hyperhidrosis.
-parasellar manifestations: superior = bitemporal hemoanopsia; lateral cavernonsis sinus compression of inferior growth leading to sphenoid sinus inversion.
Hyperthyroid with adrenergic symptoms treatment -
Graves disease and no pregnancy -
Graves disease and pregnancy -
Radioactive iodide therapy -
1. BB - propranolol
2. Start methimazole or PTU with BB. Taper BB 4-8 weeks once methimazole starts. Continue 1-2 years. Measure TS-IgG ab @ 12 mo. If absent then dc use; if relapse then restart meds.
3. Endocrine consult b4 treatment; PTU preferred
4. Leads to hypothyroid so cnsider 131-Iodide if
-elderly + graves
-solitary toxic nodule
-pt with graves and treatment doesnt work
Treatment for hypoparathyroid?
Keep serum Ca2+ between (8.0-8.5 mg/dL)
-IV Calcium gluconate (if severe to replenish Ca2+ in mild-moderate cases)
-Vitamin D supplementation (calcitriol) both Ca2+ and Vitamin D can increase urinary Ca2+ excretion - precipitating kidney stones. Thus admin with caustion to avoid hypercalciuria and admin with fluids
(2) causes of transient hyperthyroidism:
2. Subacute granulomatous thyroiditis (transient hyper)
3. Postpardum hyper
SERIOUS SIDE EFFECTS of PTU and Methimazole (if patient is HypERthyroid)
Agranulocytosis (no neutro, eos, basos)
Anserine bursitis presents as?
Sharp pain over the anteromedial part of the ribial plateau just below the joint line of the knee. Valgus stress test failts to reporduce the pain and thus rules ot damage to MCL and radiographs are normal
Chronic LYMPHOCYTIC thyroiditis (hashimotos, lymphothyroiditis)
1. Most common cause of AI thyroid disorder; more common in females
2. Genetic = family history; anti-thyroid AB = present
3. Clinically = GOITER, hypothyroid in 20% cases when first diagnosed
3. Dx: TFT normal, antithyroid AB/antiperoxidase AB; irregular 131-I on scan
Causes of SIADH
1. Neoplasms: SCLC, pancreas, prostate, bladder; lymphoma, leukemia
2. CNS d/o (stroke, head, trauma)
3. Pulmonary disorder (TB)
4. Ventilator with PEEP
5. MEDS: Vincristine, SSRI, Chlopromide, SSRI, Oxytocin
6. Post-operative state
Hyperthyroidism and thyrotoxicosis are interchangeable as both = hyperfunctioning thyroid gland.
Why is thyroid storm a medical emergency?
1. Acute exacerbation of hyper t3 and t4 secondary to infection, DKA, stress (trauma, childbirth, surgery)
2. Symptoms = fever, increased HR, psychosis, GI symptoms
3. Rx: glucose, cooling blankets, IV fluids give PTU x 2 hrs with iodide to dec T3 release. Propranolol to control HR and dexamethasone to decrease the change of T3 to T4.