PathEndocrine Flashcards
3 classic symptoms of prolactinoma
Galactorrhea, amenorrhea (females) Impotence (males)
A typical complication of prolactinoma
Fracture/osteopenia
Secondary complication of growth cell adenoma (besides growth) and its mechanism
Diabetes Mellitus, because growth hormone is gluconeogenic
Diagnostic test for GH adenoma
Failure of glucose to suppress GH
bone condition seen in women with prolactinoma and its mechanism
Osteoporosis Prolactin inhibits GnRH = no estrogen = increased osteoclast activity
Lab findings of GH cell adenoma GH: Glucose, IGF1, OGTT test
Elevated GH, elevated glucose, high IGF-1 in serum and impaired OGTT test
cell of origin in prolactinoma
acidophilic cells of ant. pituitary
Woman gives birth, begins breast feeding and then a week later she notices loss of pubic hair and difficulty with breast feeding
Sheehan syndrome
Sheenan syndrome pathogenesis
During pregnancy, pituitary swells 2x but doesn’t increase blood flow. If blood is lost during labor, pituitary infarcts (coagulative necrosis)
Empty sella syndrome defect
Herniation of arachnoid and CSF into the sella, destroying the pituitary
Sudden onset severe headache and bitemporal hemianopsia and diplopia
Pituitary apoplexy
Major cause that central DI
Null cell adenoma, hypothalamic injury, etc
Lab findings of nephrogenic DI (serum ADH, urine sp. gravity)
high, low
Most common site of ectopic ADH production
Small Cell Lung Cacner/oat cell carcinoma
2 lab values that distinguish SIADH from DI
Sodium and serum osmolality SIADH is hyponatremic, low osmolality, the others are hypernatremic, high osmolality
Midline anterior neck mass in a child
Thyroglossal duct cyst
Graves disease defect (name one antibody)
IgG stimulates TSH receptor
3 PE findings of Graves
Goiter Exophthalmos Myxedema and skin pigmentation
mechanism of exopthalmos and pretibial myxedema
T cells stimulate Fibroblasts release to glycosaminoglycans –> increases osmotic swelling and adipocyte size –> exopthalmos
3 major cell types involved in exophthalmos
Fibroblasts T cells Fat cells
Histology of graves
Tall follicular cells, papillary processes with colloid scalloping Scalloped colloid looks like little tombstones –> like…GRAVES
Patient with hyperthyroidism undergoes a surgery under general anesthesia. When they wake up they develop severe hyperthermia, Delerium, tachycardia and arrhythmias
Diagnosis?
Thyroid Storm
Are hot nodules (with I131 thyroid scan) benign or malignant
Benign (mostly)
Infant with pot bellly, swollen face, protruding umbilicul, tongue falling out of mouth
Cretinism –> congential hypothyroid
6 Ps of cretinism
Pot belly Protruding umbilicus Protouding tongue Pale Puffy Face Poor brain development
Myxedema cause
accumulation of glycosaminoglycans in skin and soft tissue
Patent states they’ve been gaining weight despite not eating more, feels fatigued and has noticed deepening of voice and feels like their tongue is larger than normal
Hypothryoidism
Hashimoto defect (3 Ab)
IgG ab against thyroid peroxidase, IgG against thyroglobulin, Antimicrosomal Ab
HLA association with hashimoto
HLA DR5
classic paradox in lab findings in Hashimoto
Patients initially present with elevated T4 levels and SSx of hyperthyroid, then come back and have SSx of hypothyroid
Why do T4 levels initially increase in Hashimoto
follicle damage causes release of T4
2 unique histology findings of Hashimoto
1- Germinal center formation (appears like a lymph node), with plasma cells 2- hurthle cells
hurthle cell description
Eosinophlic metaplasia that lines the follicles
which cancer does hashimotos increase risk for? why?
Diffuse large B cell lymphoma b/c germinal cells are being formed
Patient has an upper respiratory infection, then develops periodic episodes of tachycardia, sweating, increased appetite. C/o Jaw pain and anterior neck pain.
Subacute granulomatous Thyroiditis
Subacute granulomatous thyroiditis labs
Elevated ESR
SGT clinical course
Hyperthyroidism that may progress to hypothyroid
SGT biopsy
Granulomatous inflammation w/ giant cells
20-year-old presents with dysphagia and wheezing. The thyroid is firm when palpated but not painful, and it doesn’t move when palpated.
Diagnosis?
Riedel fibrosing thyroiditis
how does I 131 uptake help distinguish hyperthyroid/toxic goiter from cancer
Cancer is a cold nodule (doesn’t take up I 131)
5 classic cancers of the thyroid
Follicular Adenoma Follicular Carcinoma Papillary carcinoma Medullary carcinoma Anaplastic carcinoma
Hallmark of follicular adenoma on gross exam/histology
Follicles are surrounded by a thick fibrous capsule
CLassic risk factor for developing papillary carcinoma of thyroid
Radition to the head and neck area as a child
Papillary carcinoma histology (2 unique features)
Empty nuclei with central clearing (orphan annie cells), Psammoma bodies Papillary = Psammoma and Pupils (eyes)
Most common pituitary adenoma
Prolactinoma
Follicular carcinoma mutation and mechanism of invasion
RAS, capsular and vascular invasion by collagenase
Follicular carcinoma spread and prognosis
HEMATOGENOUS SPREAD. it forgot its a carcinoma Good prognosis
Dexa test result in pituitary corticotrophic adenoma
1.0 mg and 8.0 mg
- 0 mg- no change in serum/urine ACTH and cortisol level (remain high)
- 0 mg- lower level of serum and urine ACTH and cortisol level
Medullary carcinoma is a malignancy of
Calcitonin secreting parafollicular C cells
medullary carcinoma labs and inheritance
Hypocalcemia w/ hypercalciuria (b/c calcitonin increases renal excretion of Ca), Autosomal dominant (MET protooncogene)
Classic medullary carcinoma histology
sheets of cells in an amyloid (pink) stroma
Medullary carcinoma mutation
RET mutation (MEN2a 2b)
What should be done if pt has RET mutation?
Prophylactic thyroidectomy
What is the amyloid made of in medullary carcinoma?
Calcitonin deposition
Patient presents with asymptomatic hypercalcemia
Primary hyperparathyroidism
histology of papillary carcinoma
the papillary process, hypochromatic nuclei, psammoma bodies
4 main symptoms of hypercalcemia
“Stones, bones, groan, psychiatric overtones” Kidney stones Osteitis fibrosis cystica Constipation, abdominal pain, pancreatitis Depression
serum alk phos level in primary hyperPTH. Why?
Elevated b/c PTH activates osteoblasts, which secrete alk phos b/c it needs an alkaline environment to make bone
Osteitis fibrosa cystica (OFS) cause
excessive bone resorption by overactive osteoclasts
OFC gross and Xray appearance
Cysts full of brown fibrous tissue Multiple cystic spaces on Xray
Why is the cyst in OCF is brown?
Hemosiderin form macrophages
2 most common causes of secondary hyperPTH
chronic renal failure Hypovitaminosis D Really, anything that causes low Ca or high Phos
Muscle effects of hypocalcemia
Muscle spasms and fatigue
2 PE findings for hypocalcemia
Chovestek sign (tap on facial nerve = twitch) Trousseau (occlude brachail artery = carpal spasm)
3 most common causes of hypoparathyroidism
Lab findings in this case:
Surgical excision of thyroid Autoimmune DiGeorge!
Low serum PTH, low calcium and high K
If ostitis fibrosa cystica like abnormality is seen in a patient in renal failure- the condition is known as:
Renal Osteodystrophy
inheritance of MEN syndromes
Autosomal dominant. “MEN are Dominant”
MEN1 SSx
Pituitary adenoma Pancreatic tumor (ZE, gastrinoma, insulinoma) Parathyroid adenoma
MEN2a SSx
Parathyroid adenoma Pheochromocytoma Medullary Carcinoma of thyroid
MEN2b SSx
Pheochromocytoma Medullary carcinoma of thyroid Mucosal neuromas Marfanoid habitus- A TALL PERSON
MEN2 defect and pathogenesis
RET mutation, which codes for receptor tyrosine kinase
embryonic origin of the cells affected Craniopharyngioma
Rathke’s pouch
MCC (most common cause) of primary hyperaldosteronism
Bilateral adrenal hyperplasia, Adrenal adenoma (conn)
MCC of secondary hyperaldosteronism
Renal artery stenosis, CHF
How to differentiate b/w primary and secondary hyperaldo
Primary = Low Renin w/o edema Secondary = High Renin + Edema
Mechanism of striae in cushing
Cortisol inhibits fibroblast prolferation and collagen production
Classic triad of symptoms that aren’t related to physical appearance in cushings
HTN, hypokalemia and metabolic alkalosis
The basis for high dose (8.0 mg overnight) dexa suppression test
Pituitary cushings is suppressed with high dose dexa, Ectopic cushings is not
imaging findings for exogenous steroid induced cushings
bilateral adrenal atrophy
2 causes of bilateral adrenal hypertrophy
Pituitary Cushings, Ectopic Cushings (Oat cell lung carcinoma)
major cause of unilateral adrenal hypertrophy and atrophy of the opposite gland
Adrenal adenoma
major way to distinguish b/w 21OH and 11OH deficiency
21OH = hypotension , hyponatremia, hyperkalemia 11OH= Hypertension, hypernatremia, hypokalemia
21OH vs 17OH def (sexual appearance)
21OH is precocious puberty in males, ambiguous in females; 17OH is amenorrhea in females and ambiguous in males
screening test of choice for any type of congenital adrenal hyperplasia
ACTH- will be high
SSx of acute adrenal insufficiency
acute drop in BP to the point they can’t perfuse organs
2 MCC of Addison disease
autoimmune destruction of the gland (with polyglandular syndrome, TB and AIDS
how to differentiate primary vs secondary adrenal insufficiency
Primary causes hyperpigmentation due to high ACTH Secondary doesn’t affect skin b/c ACTH is low
which cancer can cause adrenal insufficiency?
Lung cancer! remember, lung cancers met to the adrenals; and also RCC
Pheochromocytoma is a tumor of
chromaffin cells
Classic presentation of pheo.
EPISODIC Anxiety/panic palpitations headaches sweating
screening test for pheo
Most common catecholamines in the urine and serum
the buzzword for the facial appearance of hyperthyroidism
“frightened appearance” Refers to staring gaze with lid lag (eyes wide open)
Histology of orbital muscles in exophthalmos will show what 2 features?
Inflammation (T cells) Increased Adipocytes
4 Tx for thyroid storm
PTU Prednisone Propanolol Potassium Iodine
High Intact PTH, low calcium, dwarfism, blunting of the fourth and fifth knuckles of the hand
Pseudohypoparathyroidism (Albright hereditary dystrophy)
What is the specific defect in PsHP (Pseudohypoparathyroidism (Albright hereditary dystrophy))?
Defective Gs protein in the renal tubular cells –> kidney doesn’t respond to PTH (PsHP is to PTH as Nephrogenic DI is to ADH)
Pseudopseudohypoparathyroidism presentation
Look like albrights (short stature, short 4th/5th digits) but don’t have end organ PTH resistance…PTH and Ca levels are normal
Familial Hypocalciuric Hypercalcemia defect
Defective Ca Sensing receptor in the PTH means body can’t respond to high Ca
Pseudohypoparathyroidism (Albright hereditary dystrophy) Labs (serum Ca, PTH)
Low serum Ca High intact PTH
Relationship of Prolactinoma and Bone in a woman
Increases risk for osteoporosis Prolactin inhibits GnRH = low estrogen = increased osteoclastic activity and fracture
Sodium levels in primary vs secondary adrenal insufficiency. Why?
Low in Primary b/c entire adrenal is dead
Normal in secondary b/c ACTH doesn’t directly stimulate the zona glomerulosa!!
Basis for CRH stimulation test in adrenal insufficiency
If CRH stimulates the production of new cortisol, the Dx is Secondary/tertiary adrenal insufficiency (b/c the pituitary wasn’t releasing ACTH) This is the same logic as in pituitary cushings vs ectopic ACTH production
Sheehan’s which hormone functions return after a few months
ADH
The earliest symptom of Sheehan’s
difficulty breastfeeding or an inability to breastfeed.
Prolactinoma cell of origin
acidophilic cells
Stalk effect
all pituitary hormones are low, but prolactin is high
Cause of these findings (visual field defect)
Prolactinoma- mass effect- compression on optic optic chiasm superiorly
Which hormone defect is seen with the associated image
Excess GH
Diseases associated with the attached image
McCune – Albright syndrome
- Female patient common
- Polyostotic Fibrous Dysplasia
- Café au lait spot
- Precocious puberty
- Endocrine abnormality (Gigantism, Hyperthyroidism, Cushing syndrome)
Likely diagnosis?
Probably prolactinoma- macroadenoma
- Blood and urine samples will be sent to measure the concentration at 0900, 1200, 1500 and 1600.
- 3/4th samples are taken after vasopressin infection.
•
•< 10% increase in urine osmolality following injection vasopressin during the test-? diagnosis
nephrogenic DI
- Blood and urine samples will be sent to measure the concentration at 0900, 1200, 1500 and 1600.
- 3RD/4th samples are taken after vasopressin infection.
- > 50% increase in urine osmolality following injection vasopressin during the test-? diagnosis
complete neurogenic DI
