Gen Surg: Endocrinology Flashcards
Describe the embyological origin of the thyroid
Originates from the foramen cecum (junction at the anterior 2/3 and posterior 1/3 of the tongue). The thyroglossal duct migrates down the midline in front of the hyoid to form most of the thyroid.
Lateral contributions from neural crest cells form the posterolateral aspect.
Congenital thyroid problems due to abnormal embryology
Thyroid duct cysts: Midline masses presenting in kids 4-5 yrs. Tend to get infected (difficult to remove). Dx w/ US.
Lingual thyroid: mass in tongue or pharynx in infant that may cause airway obstruction.
Location and function of the recurrent laryngeal nerves and superior laryngeal nerve.
Branches of the vagus nerve. Provide abduction and adduction to vocal cords. Innervate all muscles of the larynx except cricothyroid.
L nerve: loops under aortic arch then travels up to larynx.
R nerve: loops around subclavian artery and travels upward.
If one cord paralyzed, get hoarse voice. If both paralyzed, may have airway obstruction.
Superior laryngeal nerve: innervates the cricothyroid and allows tensing of vocal cords to control pitch and volume of speech.
Anatomy/function of adrenals
Cortex contains:
Zona glomerulosa: mineralcorticoid production (aldosterone)
Zona fasciculata: glucocorticoid production (CRF –> ACTH –> cortisol)
Zona reticularis: adrenal androgens.
Medulla: produces Nor/Epi
Arterial supply: superior, middle and inferior adrenal arteries.
Venous drainage: L adrenal vein goes to L renal vein, R adrenal vein goes to IVC direct.
Classification of hyperparathyroidism
Primary: increased PTH from abnormal PT gland. High Ca, high PTH. Etiology: single adenoma (85%), 4 gland hyperplasia (10%), double adenomata, cancer (<1%)
Secondary: increased PTH from Ca wasting, e.g. in renal failure, GI losses. Low Ca, high PTH. chronic state of hypocalcemia –> hyperplastic PT gland.
Tertiary: ESRD kidney transplant pts with correct secondary PTH. High Ca, High PTH. Consequence of longstanding low Ca resulting in hypertrophied PT gland that remains hypertrophied post-renal transplant.
Approach to thyroid nodule
Hx: change in size, compression symptoms (dysphagia, dyspnea, dysphonia), hypo/hyper-T4 symptoms, cancer risk factors (M>F, extremes of age, hx of radiation to head/neck, famHx).
Thyroid nodule + hoarse voice = thyroid cancer until proven otherwise.
PEx: character of mass (size, mobility, texture). feel for cervical lymphadenopathy. Voice quality, signs of hyper/po thyroid.
Investigations: CBC, lytes, BUN, Cr, PTT, INR, TSH, T4.
US should be done prior to FNA Bx to characterize nodule (cystic vs solid).
FNA biopsy: looks at cells for Betheseda classification.
Betheseda classification of thyroid nodule tissue from FNA Bx
Non-diagnostic: repeat FNA.
Benign: observe, repeat US in 6-12 months, repeat FNA if changed from previous.
Atypia: unknown significance.
Follicular neoplasm: can’t determine if there is capsular or vascular invasion, need diagnostic lobectomy to distinguish from adenoma vs carcinoma.
Suspicious for malignancy: 2/3 are malignant. OR for definitive Dx.
Malignant: total thyroidectomy +/- LN dissection.
Hypercalcemia DDx
Ca++ OD. Primary or teritiary hyperPTH (primary hyperPTH is the most common outpt cause of hypercalcemia). Immobility/iatrogenic. Metastasis. Paget's disease of the bone. Addison's disease. Neoplasm: malignancy is the most common inpatient cause of hypercalcemia. ZE syndrome. Excess vit D+A intake. Sarcoid/granulomatous process.
Symptoms of hypercalcemia
Stones: multiple kidney stones.
Bones: bony pain, fractures, osteoporosis.
Groans: abdo pain, constipation.
Psych overtones: depression, anxiety, irritability.
Also: polyuria, polydipsia, nocturia, pancreatitis, anorexia.
Hypercalcemia investigations
CBC, lytes, Ca, PTH, Cr, Vit D.
Bone density.
24 hr urine collection of Cr and Ca.
Imaging of PT gland: US. Also sestamibi scan.
HyperCa Tx
Fluids!!
Lasix.
Treat underlying cause (e.g. if due to hyperPTH, then neck exploration and removal of adenoma. If all 4 glands enlarged, remove 3.5).
Other option: bisphosphonates
Conn’s Syndrome: Etiology, symptoms, investigations, mgmt
Primary hyperaldosteronism.
Etiology: adrenal adenoma vs adrenal hyperplasia.
Symptoms: HTN, hypokalemia (Na retention, K wasting).
Investigations: aldosterone:renin ratio. Adrenal venous sampling to determine if unilateral or bilateral disease. Increased on one side -> adenoma, both sides -> hyperplasia. Do CT/MRI imaging if unilateral.
Mgmt:
Bilateral: spironolactone.
Unilateral: pre-op give spironolactone then surgically remove adenoma.
Cushing Syndrome: etiology, symptoms
Excessive cortisol production.
Etiology: Iatrogenic (most common), ACTH secreting adenoma of pituitary (true Cushings disease), adrenal adenoma/carcinoma, ectopic ACTH production.
SS: truncal obesity, hirsutism, moon face, buffalo hump, purple striae. HTN, DM, weak/fatigued/myopathy, easy bruising, depression, osteoporosis.
Cushings tests
24 hr urine free cortisol to see if high or midnight cortisol to screen (normally should be lowest at midnight).
If high cortisol but low ACTH, likely adrenal adenoma.
To determine source:
1) overnight dexamethasone suppression test: check cortisol levels in am, if low then cortisol was suppressed and Cushings was not the diagnosis. If high, check ACTH levels.
- High cortisol and LOW ACTH, then no suppression and suggests adrenal source from adenoma. Requires adrenal imaging.
- High cortisol and high ACTH despite dex, either ectopic or pituitary source.
2) Overnight high dose dexamethasone suppression: to differentiate pituitary vs ectopic source.
- If ACTH/cortisol levels are suppressed, PITUITARY (order MRI)
- If cortisol and ACTH levels STILL high, do chest CT or abdo CT to look for ectopic source.
Etiologies of hyperthyroidism (and tx of most common cause)
Grave’s: most common (hyperthyroidism with diffuse uptake of iodine on scan).
Tx w/ PTU, methimazole or thyroid ablation with radioactive iodine.
Surgical only if C/I to meds and radioactive iodine or failure of tx.
Other: toxic solitary nodule, multinodular goitre.
