Term
| How do you estimate free calcium levels? |
|
Definition
| Total calcium - 0.8(grams of albumin below normal) |
|
|
Term
| How does body pH effect calcium levels? |
|
Definition
| Alkalosis increases calcium binding to albumin, potentially causing hypocalcemia. |
|
|
Term
| What are the direct actions of PTH? |
|
Definition
- Increase renal tubular reabsoption of calcium in distal tubule
- Activation of vitamin D (hydroxylation at 1 position)
- Increased phosphate excretion
- Promotes release of calcium and phosphate from bone (osteoblast --> RANKL --> osteoclast)
|
|
|
Term
| What is the difference between PTH generated in primary hyperparathyroidism and PTH administered exogenously? |
|
Definition
| Intermittant PTH promotes bone formation (prevents osteoperosis), constant PTH causes overall bone loss. |
|
|
Term
| Which organs respond to calcium? What is the mechanism of response? |
|
Definition
| Parathyroid and renal cells; calcium sensing receptor activation --> phospholipase C --> inositol-triphosphate (decreases PTH secretion, synthesis and inhibits calcium and water re-asborbption by the renal tubule) |
|
|
Term
| What is a common cause of hyhpercalcemia and bone resorption associated with cancer? |
|
Definition
| PTH Related Peptide (13aa polypeptide that activates PTH receptor) |
|
|
Term
| What is the order of activation for Vit D? Which form is an accurate predictor of calcium storage? |
|
Definition
Synthesized from 7 dehydro-cholesterol and sunlight in skin; 25 hydorxylation in live; 1 hydroxylation in kidney (active form)
25(OH) D |
|
|
Term
| What are the "moans, groans, bones and stones" of hypercalcemia? |
|
Definition
Moans- malaise, fatigue
Groans - constipation, gastritis, pancreatitis
Bones- Osteitis fibrosa cystica, osteoporosis
Stones- renal stones |
|
|
Term
| What are some of the indications for surgical treatment of primary parathyroidism? |
|
Definition
| Young age (<50), serum calcium >1mg/dl ULN, evidence of end organ damage (bone mineral density low, renal stones, elevated creatinine) |
|
|
Term
|
Definition
| Parafollicular cells in thyroid gland. Secret calcitonin (inhibits resorption of bone by osteocalsts) |
|
|
Term
| A patient has a history of a viral URI. They present with an inflamed thyroid, and pain with swallowing. A biopsy shows multinucleate giant cells and lymphocytes, but no Hurthle cells (metaplastic epithelial cells with abundant eosinophilic granules). What is the most likely diagnosis? |
|
Definition
|
|
Term
| What are the histological features of Graves? |
|
Definition
| Pseudopallilary (lacking fibrovascular cores) ingrowths into the colloid. Colloid itself contains scalloped edge. |
|
|
Term
| What are some longterm complications of multinodular goiters? Histologically, how can you distinguish them from a goiter caused by Graves? |
|
Definition
- Hemorrhage, scarring, and eventual calcification due to follicular rupture.
- No papillations
|
|
|
Term
| How can you distinguish follicular adenoma from follicular carcinoma? |
|
Definition
| Adenoma is completely encapsulated, while carcinoma shows vascular and capsular invasion |
|
|
Term
| What are the differences between follicular and papillary carcinoma? |
|
Definition
Follicular carcinoma lacks the nuclei changes associated with papillary carcinoma (longitudinal nuclear grooves and "Annie eye" nuclei)
Follicular carcinoma invades the blood, while papillary invades the lymph |
|
|
Term
| What cells are responsible for medullary carcinomas? |
|
Definition
|
|
Term
| A patient presents with history of strokes (cardiac myxoma), acromegaly, and multiple naevi. What is the most likely syndrome? |
|
Definition
|
|
Term
| What are some possible complications of thyroidectomy? |
|
Definition
- Injury to the recurrent laryngeal nerve (hoarseness)
- Accidental removal of parathyroid glands (hypocalcemia)
|
|
|
Term
| What are some of the main effects of thyroid hormone? |
|
Definition
- Increase catecholamine effect (lipolysis, glycogenolysis, gluconeogenesis)
- Increae mitochondrial action, respiratory enzymes, Na-K ATPase
- Increase oxygen consumption, basal metabolic rate
|
|
|
Term
| What is the ideal rate of iodine intake? Below what level impair thyroid gland function at puts patient at risk for a goiter? What are your concerns if you see a pregnant woman with a goiter? |
|
Definition
| >200 ug/d is ideal. Less than 50 ug/d results in elevation of TSH and goiter. Low iodine can result in cretinism in newborns. |
|
|
Term
| What is the function of TPO? In which diseases are antibodies directed against TPO observed? What is thyroglobulin? What is its clinical importance? |
|
Definition
- Oxidization of iodine and coupling of iodotyrosines to form T3/T4; anti-TPO seen in Hashimoto's thyroiditis (90%) and Graves (60%)
- Substance in colloid which provides scaffold for T3/T4; after thyroidectomy to remove cancer, presence in circulation suggests relapse
|
|
|
Term
| What is the Wolff Chaikoff effect? How is it utilized to treat thyroid disorders? |
|
Definition
Large excess of iodine ingested inhibits organification of iodine for 2-3 days. Large bolus of iodine is given to patients experiencing thyroid storm
. |
|
|
Term
| What effect would birth control have on a patient's total T4? Free T4? |
|
Definition
| Increased, due to increase in TBG. No change in free T4 (patient will be euthyroid) |
|
|
Term
| How are beta-blockers used to treate thyroid disorders? |
|
Definition
| Ameloriate the tachycardia induced by hyperthyroidism, which increases concentration of beta receptor and response. |
|
|
Term
| What does T3 resin uptake measure? Under which conditions would it be high? Low? |
|
Definition
T3 resin uptake measure how many binding sites for T3 and T4 are available.
- Low in high TGB (euthyroid), hypothyroidism
- High in low TGB (euthyroid), hyperthyroidism
|
|
|
Term
| What can cause myxedema coma? What lab values would you use to distinguish it from sick euthyroid syndrome? |
|
Definition
Prolonged hypothyroidism, precipitated by cold exposure, sepsis or other stressful conditions. Characterized by low T4, T3, T3R, and high cholesterol and TSH.
SES will have low T4 and T3, but with high T3R and low TSH. |
|
|
Term
| What are the parafollicular cells? What is their function? |
|
Definition
| Cells within the thyroid gland follicles. Also known as C-cells. Synthesize and secrete calcitonin, an inhibitor of bone resorption. |
|
|
Term
| What are the pathological characteristics of Hashimoto thyroiditis? |
|
Definition
Extensive lymphocytic infiltrate, with well-developed germinal centers. Hurthle cells (eosinophilic, metaplastic epithelial cells) are abundant
Note: Hurthle cells also found in follicular adenomas |
|
|
Term
| What is the natural history of subacute thyroiditis? What is the typical pathology? |
|
Definition
Patient typically experience a viral upper respiratory infection just before onset of thyroiditis, inducing an immune response. Patient experiences tranient hyperthyroidism followed by transient hypohtyroidism. Recovery occurs in 6-8 weeks.
Multinucleate giant cells enclosing pools of colloid |
|
|
Term
| Which thyroid complication is characterized by pseudo papillae (papillae encroaching on colloid which lacks fibrovascular cores)? |
|
Definition
|
|
Term
| How can Graves be distinguished from multinodular goiter? How can follicular adenoma be distinguished from multinodular? |
|
Definition
Grossly, Graves is more likely to be diffuse. Microscopically, goiters lack the papillations found in Graves.
Follicular adenomas are encapsulated. |
|
|
Term
| What are the pathological characteristics of follicular adenoma? |
|
Definition
| Spherical encapsulated lesions, generally cold on scintigram. Hurthle cell change is characterized by bright eosinophilic metaplastic cells. |
|
|
Term
| What are some pathological characteristics that distinguish follicular from papillary carcinoma? |
|
Definition
| Papillary has nuclear changes and is more likely due to ionizing, childhood radiation. Nuclear changes include Orphan Annie eye and longitudinally grooved nuclei. Finally, papillary tend to metastesize via lymph, not blood. |
|
|
Term
| A patient comes in complaining of amenorrhea, galactorrhea, and headache. Lab values show increased PRL. Which therapeutic regiment are you most likely to try first? |
|
Definition
For prolactinoma, primary treatment is with dopamine/bromocriptine (unless acidophil stem cell adenoma)
Surgeyr is the ultimate therapy. |
|
|
Term
| A patient comes in with prognathism, thickneing of soft tissues of face and lips, as well as various other features of acromegaly. What lab value will most likely provide a definitive diagnosis? What is the primary form of treatment? What are some genetic associations for this disease? |
|
Definition
| GH producing adenomas can be diagnosed by insulin-like growth factor I levels, which are responsible for the clinical symptoms. Primary treatment is surgery. GH is associated with MEN-1 and Carney complex. |
|
|
Term
| What are the target organs of MEN-1? Carney complex? |
|
Definition
- MEN-1 will most likely present with pituitary, parathyroid and pancreatic abnormalities (peptic ulcers from gastrin, diarrhea from VIP, hypoglycemia from insulin overproduction)
- Carney complex will present with cardiac myxoma, naevi and neural tumors.
|
|
|
Term
| A patient you're following for possible pituitary adenoma begins complaining of headache, visual impairment, cranial nerve palsies. What is your primary concern? |
|
Definition
|
|
Term
| What hormonal imbalance would you expect to find in a malnourished child? |
|
Definition
| High GH with low levels of IGF-I |
|
|
Term
| What are the regulators of prolactin? Which hormone does prolactin regulate? |
|
Definition
Estrogen and TRH stimulate prolactin, while dopamine inhibits its release. Prolactin decreases gonadotropin levels.
Prozac can induce prolactin secretion, thereby indirectly inhibit FSH/LH |
|
|
Term
| How does central adrenal insufficiency differ from primary hypoadrenalism? |
|
Definition
| Aldosterone levels are normal, since adrenal aldosterone release is mediated by AngII and not ACTH. No hyperpigmentation. |
|
|
Term
| How would you expect oral contraceptive to effect cortisol levels? |
|
Definition
| Increase in estrogen causes increase in CBG, increasing total cortisol levels but maintaining normal free cortisol levels. |
|
|
Term
| What are some factors and conditions that can skew an overnight dexamethasone test? |
|
Definition
| Alcohol, stress, as well as various medications (rifampin and phenytoin) can lead to an overnight value >5 mcg/dl (a false positive for Cushing's syndrome) |
|
|
Term
| What is the pathogenic mechanism for familial hypocalcuric hypercalcemia? What lab values would you expect to see? How could you distinguish it from primary hyperparathyroidism? What drug mimics this condition? |
|
Definition
Reduced sensitivity of calcium receptor, meaning high levels of calcium are required to induce secretion of PTH.
Patient will have high serum calcium, normal serum PTH and low urinary calcium excretion (primary hyperPTH has high calcium excretion)
Lithium |
|
|
Term
| A patient you are following has hypercalcemia but low PTH. They have marked weight loss, cachexia, dehydration and mental confusion. What is the most likely pathological mechanism of their hypercalcemia? |
|
Definition
| Malignancy-related PTH-RP produced by lung, esophageal, H&N, cervical renal or breast cancer. Could also be activated Vit. D produced by some lymphomas, or multiple myeloma-related bone reabsorption. |
|
|
Term
| How do you treat hypercalcemia? |
|
Definition
- Hydrate (replace volume lost, increase water/sodium, calcium to DCT and LoH, furosemide)
- Decrease resorption of bone: palmidronate, alendronate
- Salmon calitonin
- Glucocoriticoids
- Oral phossphate
- Dialysis
|
|
|
Term
| After checking a hypocalcemic patient's history for thyroid surgery and lab values for ionized calcium, what do you check? |
|
Definition
- Phosphorous levels (high = hypoparathyroidism, PTH deficiency or resistance; low = vitD problem)
- Magnesium levels (low = PTH secretion problems)
|
|
|
Term
| How does 21-hydroxylase deficiency present? |
|
Definition
| Patient has low aldosterone and cortisol levels, with high testosterone, leading to hyperkalemia and precocious puberty (if male) and virilization (if female) |
|
|
Term
| How does 11-hydroxylase deficiency present? |
|
Definition
| Like 21-OHase, males present with precocious puberty and females are virilized. However, the patient is also hypertensive due to generaiton of an aldosterone precursor, DOC, which acts as a potent mineralcorticoid. |
|
|
Term
| How does 17-hydroxylase deficiency present? |
|
Definition
| Sexual development is stunted (ambiguous genitalia in males), with hypertension. |
|
|
Term
| How is primary aldosteronism tested? How can one distinguish it from secondary aldosteronism? |
|
Definition
Patient is given 2L saline over 4 hrs or salt tables for 5 days. Positive test is a serum aldosterone >15 ng/mL.
Primary hyperaldosteronism has low renin. |
|
|