prominent forehead

prominent jaw

enlarged hands/feet

HTN

insulin resistance --> DM

increased random IGF-1

continued elevated serum GH following admin of oral glucose

surgical resection of pituitary adenoma usually 1st choice

Meds- octreotide/lanreotide (somatostatin analogs) 

Meds - Pegvisomant (GH receptor blocker)

1. often asymptomatic
2. 1st sx: bone pain
3. kyphosis, bowed tibias, large head, HA's, deafness, frequent fx's
4. typically involves skull, femur, tibia, pelvis, and/or humerus

1. serum alkaline phosphatase markedly elevated
2. serum C-telepeptid is high
3. serums 25-OHvitamin D (r/o vit. D deficiency)

1. x-ray - osteolytic lesions w/ focal radiolucencies
2. flame shaped lytic lesions on long bones
3. bones become thicknened & deformed
4. bone scan can indentify active lesions

• hypercalcemia leading to renal calculi
• spinal cord compressin (vertebral collapse)
• cranial n. palsy

1. asymptomatic-oversation
2. nasal calcitonin-salmon 

• not as potent as bisphosphonates 
• less SE

   3.   bisphosphonates 

• first treatment can induce pain
• alendronate - 40mg daily
• tiludronate 400 mg daily
• Risedronate 30 mg daily

generally good

prognosis worse earlier in life or w/o treatment

can lead to marked deformity & pain

• usually sporadic
• sometimes part of MEN 1
• if arise d/t MEN 1 can secrete prolactin, HG, or both and are more aggressive 

• can cause hypopituitarism
• gonadotropin difficiency - insufficiences of LH & FSH causing hypogonadism & infertility
• TSH deficiency - can cause hyperthryoidism - fatigue, weakness, weight change, hyperlipidemia
• GH deficiency- in childhood causes hypoglycemia & short stature.  In adulthood causes obesity, increased systolic BP, increased LDL and reduced CO

• hypoglycemia, hyponatremia, reduced testosterone
• low free T4, while TSH is not elevated
• ACTH deficiency

DI

hyponatremia post-op

visual field impairment 

morbid obesity

1. transsphenoidal removal of pituitary tumors can reverse hypopituitarism - hyponatremia can result, so check serum Na for 2 weeks post-op
2. endocrine substitution must be given for deficiencies - mainstay of tx
3. octreotide can prevent GH release in GH releasing tumors
4. cortisone for ACTH deficiency
5. levothyroxine to correct hypothyroidism
6. GH replacement 

1. abrupt withdrawal of steroids MCC (in pts not gradually tapered off steroids)
2. previously undiagnosed pt w/ Addison's disease subjected to stress
3. exacerbation of known Addison dz (who didn't increase steroids during stress)
4. Bilateral adrenal infarction (usually d/t hemorrhage) 

1. Shock primary manifestation (2ry to mineralocorticoid deficiency - decreased BP)
2. hypotension, hypovolemia
3. nonspecific sx: abd. pain, N/V, fever, weakness, lethargy, coma)

lab studies:

• BMP 
• hyponatremia, hyperkalemia, hypoglycemia
• cortisol levels
• ACTH
• CBC

1. IV fluids: NS to correct hypotension & hypovolemia (D5NS if hypoglycemia)
2. Steroids: dexamethasone (if undiagnosed), hydrocortisone (if known Addison's)
3. reversal of -lyte abnormalities: hyponatremia, hyperkalemia, hypoglycemia, hypercalcemia
4. fludrocortisone (Florinef)

1. Redistribution of fat: central (trunk) obesity, "moon facies," Buffalo hump, supraclavicular fat pads
2. catabolism (breakdown) of protein - wasting of extremities, skin atrophy (easy bruising, striae), increased infections, hyperpigmentation (esp w/ increased ACTH)
3. HTN, weight gain, osteoporosis, hypokalemia, acanthosis nigricans, mental (depression, mania, psychosis)
4. Androgen excess: hirsutism, oily facial skin, acneiform rash, increased libido, virilzation, amenorrhea

1. low dose dexamethasone suppression test
2. increased 24h urinary free cortisol levels
3. increased salivary cortisol levels

dexamethasone is 4x more potent that cortisol

normal response is cortical suppression

No suppression = Cushing's syndrome

24h urinary free cortisol levels

(elevated urinary cortisol = Cushing's syndrome)

1. high dose dexamethasone suppression test
2. ACTH levels

• establishes Cushing's dx from other causes
• ACTH production in Cushing dz is only partially resistant to glucocorticoid negative feedback (adrenal tumors/ACTH producing tumors are independent)
• Suppression = Cushing's dz. the other 3 major causes of Cushing's will not suppress
• No suppression = adrenal or ectopic ACTH producing tumor 

1. Cushing's dz (pituitary) - transsphenoidal sx, XRT if unresectable
2. Ectopic or adrenal tumors: tumor removal.  Ketoconazole in inoperable patients (decreased cortisol production)
3. iatrogenic steroid therapy.  GRADUAL steroid withdrawal (to prevent Addisonian crisis)

diabetic ketoacidosis (DKA) 

&

Hyperosmolar hyperglycemia syndrome (HHS)

glucose - these pts are unable to meet the demand of increased insulin requirements in response to the hyperglycemia esp during stress

older pt w/ type 2 DM 

higher mortality

insulin deficiency 

1. hyperglycemia

2. dehydration

3. ketonemia (anion gap metabolic acidosis)

4. K+ deficit

usually occurs in pts with type 2 DM & some other illness leading to reduced fluid intake (MC infection)

1. dehydration, increased osmolarity, hyperglycemia

2. potassium deficit

3. absence of severe ketosis (type II DM pts make enough insulin to prevent ketogenesis)

1. hyperglycemia: thirst, polyuria, polydipsia, nocturia, weakness, fatigue, confusion, N/V, CP
2. abd pain (in DKA)
3. AMS changes (in HHS)

1. tachycardic and tachypnic 
2. hypotensive
3. fever if infection
4. decreased skin turgor
5. DKA: ketotic breath (fruity with acetone smell) 
6. DKA: Kussmaul's respiration (deep continuous respirations as lung attempts to blow off excess CO3 to reduce acidemia)

ABC

mental status

vital signs

volume status 

screen for precipitating events

1. IV fluids: critical 1st step : isotonic 0.9% NS until hypotension/orthostasis resolves

• Then 0.45% NS
• When glucose levels reach 250 switch to D5 0.45 (1/2) NS to prevent hypoglycemia from the insulin therapy 

2.  Insulin (regular) : lowers serum glucose & switches body from catbolic to anabolic state --> decreased gluconeogenesis, reduced ketone & fatty acid production

3. Potassium (1st verify renal output).  Correction of DKA invariably will cause hypokalemia. K repletion recommended if K is low/normal (20-40mEq/L if K+ < 5.5)

women

prognosis is worse in men

incidence is rising 

9% are fatal

papillary (76%)

but least aggressive & spreads by local extension

caused by genetic mutation or translocation

16%

often metastasizes to lung, bone, brain, & liver

seen in elderly & is most aggressive

often causes dysphagia or vocal cord paralysis

• 4%
• distributed as 1/3 sporadic
• 1/3 familial
• 1/3  w/ multiple endocrine neoplasia (MEN) syndrome
• may cause sxs from their poss secretion of calcitonin, prostaglandins, serotonin, adrenocroticotropic hormoen (ACTH) and other peptides

• childhood irradiation to head & neck confers a 25 fold increase in thyroid Ca and may emerge 10-40 yrs post exposure
• other risks : fam hx, Gardner syndrome, MEN type II

• U/S routinely performed
• RAIU may be helpful to assess risk of malignancy & help plan surgical approach
• positron emission tomography (PET) scanning particularly useful in detecting thyroid CA metastases w/ limited iodine uptake

• surgical resection is indicated
• RAI ablation may be useful for residual dz
• patients require T4 replacement for life