Pathology-Endocrine Lecture Flashcards
What is the function of the hormones released by the hypothalamus on the pituitary?
GHRH = GH release, SST = inhibit GH release, GnRH = FSH/LH release, TRH = TSH & PRL release, DA = inhibit PRL release and CRH = ACTH release
Hormones released by the posterior pituitary
ADH and oxytocin
Etiologies of panhypopituitarism
Most common = benign craniopharyngioma. Additionally ischemia (Sheehan), tumor (metastatic or pit. adenoma), inflammation (sarcoid), trauma, infection (Tb) or surgery.
What etiologies of panhypopituitarism can arise in the hypothalamus?
Tb and sarcoidosis.
A 30 year old woman presents with headache and loss of vision. Imaging reveals a mass compressing the pituitary gland in the sella turcica. What are two variants of the most likely etiology?
Craniopharyngiomas have an adamantinomatous variant (common in children with peripheral palisading squamous epithelium and wet keratin) and a papillary variant (common in adults with solid sheets & papillae lined by squamous epithelium without keratin)
Where do hypothalamic nerves release ADH and oxytocin?
Herring bodies in the posterior pituitary.
2 causes of diabetes insipidus
Central (head trauma, surgical, tumor) or nephrogenic (renal tubule ADH insensitivity)
Characteristic presentation of diabetes insipidus
Life-threatening dehydration from excessive urination
Characteristic presentation of SIADH
Hyponatremia, cerebral edema (can lead to uncal herniation and death), total body water increase
What cells are acidophils and what hormones do they produce?
Somatotrophs (GH) and lactotrophs (PRL)
What cells are basophils and what hormones do they produce?
Corticotrophs (ACTH), gonadotrophs (FSH/LH) and thyrotrophs (TSH)
Most common pituitary adenomas
Prolactinomas (30%) and null adenomas (20%). ACTH, thryotrophic and FSH/LH adenomas are all rare.
How can you tell you are looking at an adenoma under the microscope?
There is only one cell type and no mixture of basophils and acidophils.
Manifestations of GH adenomas
Acromegaly (after epiphysis have fused), gigantism (younger people)
Typical presentation of prolactinomas in men and women?
Women: amenorrhea and galactorrhea. Men: lack of symptoms until mass effect
Simple (euthyroid) diffuse nontoxic goiter complication
Airway obstruction and difficulty breathing
A patient presents with cold intolerance, bradycardia, heart failure, high lipids and lethargy. What are some causes of this condition?
Hypothyroidism. Loss of thyroid tissue (surgery, radiation), hypothalamic failure, cretinism (infantile iodine deficiency), Hashimoto thyroiditis and granulomatous thyroiditis.
Other conditions that are associated with Hashimoto thyroiditis
Type I diabetes mellitus, SLE, lymphomas (Non-Hodgkins lymphoma, marginal zone lymphomas, MALT)
What are the types of hypersensitivities associated with Hashimoto thyroiditis?
II (plasma cells produce Abs) and IV (CD8+ cytotoxic reaction)
Histologic features of early vs. late granulomatous thyroiditis.
Early: patchy microabscesses Late: damaged follicles, lymphocyte aggregates, multinucleate giant cells and fibrosis
Histologic features of Graves disease
Tall columnar follicular cells w/papillary infolding and scalloping
Why do multi nodular goiters cause hyperthyroidism?
10% of the time one autonomous toxic nodule is produced that releases large amounts of T4. Remember that <5% of the time these can develop into a neoplasm
How do you determine if it is a multi nodular goiter or a malignancy?
Nodule has absence of a prominent capsule. Malignancies often have a thick capsule.
What tumors can be derived from the different cells in the thyroid?
Follicular cells: follicular adenoma, follicular carcinoma and papillary carcinoma. C-cells: Medullary carcinoma
Mutations that cause papillary carcinoma
RET/PTC fusion gene and BRAF.
Mutations that cause follicular and anaplastic carcinoma
RAS, P13K, and PTEN. Follicular also has PAX8:PPARG
Key item to diagnose papillary carcinoma
Optically clear nuclei
Key item in distinguishing follicular adenoma from follicular carcinoma
Capsular invasion = carcinoma
4 C’s of medullary carcinoma
Derived from C-cells, makes calcitonin, Congo red (amyloid) and carcinoembryonic antigen (CEA).
Causes of primary hyperparathyroidism
1) Adenoma (90%). Hyperplasia and parathyroid carcinoma can also cause it. FHH, MEN1 and MEN2 are familial causes.
Causes of secondary hyperparathyroidism
1) Chronic renal failure = low vitamin D and decreased Ca absorption = increased PTH.
Histologic analysis of parathyroid adenoma
Monomorphic chief cell population
Clinical symptoms of hyperparathyroidism
Painful bones, renal stone, abdominal groans and psychic moans.
Causes of hypoparathyroidism
Surgery, congenital absence (DiGeorge), Autoimmune Polyendocrine Syndrome Type 1 (APS1)
A patient presents with adrenalitis, hypoparathyroidism, hypogonadism and candidiasis. What is causing his condition?
APS1, an AR mutation in the AIRE gene on 21q22.3
A patient presents with adrenal insufficiency, hypothyroidism and type 1 diabetes. What is causing his condition?
APS2, associated with HLA-DQ or HLA-DRB
Most common causes of primary hyperaldosteronism
1) Idiopathic hyperaldosteronism 2) Adenoma of zona glomerulosa (Conn syndrome)
Etiologies of Cushing’s syndrome
Pituitary adenoma, adrenal adenoma, adrenal hyperplasia, paraneoplastic and iatrogenic (most common).
Most common cause of overactivity of the zona reticularis
21-hydroxylase deficiency shunts all cholesterol intermediates toward androgen synthesis and you get virilization.
Acute loss of adrenal glands due to infection
Waterhouse-Friderichsen Syndrome.
Chronic loss of adrenal glands with hyperpigmentation, weight loss and hypotension
Addison disease
How would an adrenal carcinoma typically present?
Virilization, adenomas typically present with Cushing’s.
