Endocrine Flashcards by Jamaira Belmes

MCC of hyperpituitarism

Associated with distinct endocrine signs and symptoms

FUNCTIONING ANTERIOR PITUITARY ADENOMA

1 cm - limit size to determine micro/macroadenoma

Prolactin cell adenoma - MC

Somatotroph adenoma - 2nd MC

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2nc MC pituitary adenoma

present with mass effects - visual disturbance

NON-FUNCTIONING ADENOMA

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Microscopic findings in pituitary adenoma

Uniform (monomorphic)

Sparse reticulin network

Few mitosis

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Sine qua non of Pituitary Carcinomas

atypical adenoma + metastases (CSF/systemic)

METASTASES (craniospinal/systemic)

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Occurs at ~75% parenchymal loss

CAUSES:
tumors/mass lesions
PITUITARY APOPLEXY
SHEEHAN SYNDROME
Empty sella syndrome

HYPOPITUITARISM

GH and gonadotropin (FSH and LH) lost FIRST –> TSH and ACTH –> prolactin (lost LAST)

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ADH DEFICIENCY

CAUSES:
CNS disorders

Central Diabetes Insipidus

serum osmolality - N - H
urine osmolality - L
serum ADH - L

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Unresponsiveness of renal tubules to ADH

CAUSES:
drugs
renal disorders

Nephrogenic Diabetes Insipidus

serum osmolality - N - H
urine osmolality - L
serum ADH - H

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ADH EXCESS

CAUSES:
SCLC
CNS disorders

SIADH

serum osmolality - L
urine osmolality - N - H
serum ADH - H

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slow-growing tumors account for 1% to 5% of intracranial tumors

suprasellar, with or without intrasellar extension

bimodal age distribution - one peak in childhood (5 to 15
years) and a second peak in adults 65 years of age or older

ADULTS - headaches and visual disturbances

CHILDREN - growth retardation due to pituitary hypofunction and GH deficiency

CRANIOPHARYNGIOMA

from vestigial remnant of RATHKE’S POUCH

Adamantinomatous - compact, lamellar
*WET KERATIN
*DYSTROPHIC CALCIFICATION

Papillary
*papillae

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MCC of primary hyperthyroidism

Autoantibodies against TSH receptor

GRAVES DISEASE

symmetrically enlarged thyroid

MICROSCOPIC:
diffuse hypertrophy and hyperplasia of thyroid follicular epithelial cells
pseudopapillary structures
pale, scalloped colloid

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MCC of congenital hypothyroidism

IODINE DEFICIENCY

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MCC of hypothyroidism in iodine-sufficient areas

AUTOIMMUNE

i.e. Hashimoto

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MCC of hypothyroidism in iodine-sufficient areas

autoimmune disease that results in destruction of the thyroid gland and gradual and progressive thyroid failure

T cell mediated injury

Autoantibodies against THYRPGLOBULIN and TPO

COMPLICATIONS:
development of neoplasms (marginal zone B cell lymphoma, papillary thyroid ca)

HASHIMOTO THYROIDITIS

PAINLESS thyroid enlargement

diffusely enlarged thyroid

HURTHLE cell changes
GERMINAL CENTERS
(+) FIBROSIS

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Autoantibodies against TPO

Family history of autoimmunity

(+) URTI

SUBACUTE LYMPHOCYTIC

thyroid grossly normal

PAINLESS thyroid enlargement

(-) fibrosis
(-) Hurthle cells

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Antigen-mediated immune damage to follicular cells

(+) URTI prior to thyroiditis

believed to be triggered by a viral infection

majority of patients have a history of an URTI just before the onset of thyroiditis

Granulomatous thyroiditis (also called De Quervain thyroiditis)

unilateral or bilaterally enlarged and firm thyroid

PAINFUL thyroid enlargement

multinucleate giant cells enclose pools of colloid

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TRIAD of GRAVES DISEASE

Hyperthyroidism
Exophthalmos - fibrosis (orbit and EOM)
Dermopathy - pretibial myxedema (dermal thickening)

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Thyroid enlargement caused by IMPAIRED THYROID HORMONE synthesis

MASS EFFECT

LOW incidence of malignancy

GOITER

iodine deficiency –> compensatory increase in TSH –> trophic effect of TSH on thyroid –> enlargement of the thyroid gland

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Phases of Goiter

HYPERPLASTIC
*diffuse, symmetrical enlargement
*columnar

COLLOID
*brown, glassy, translucent
*flattened and cuboidal
*abundant

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TYPES OF GOITERS

Diffuse Nontoxic (Simple)
*areas of iodine insufficiency and intake of goitrogens (cassava - thiocynate)

Multinodular
*irregular enlargement of thyroid
*repeated hyperplastic and colloid phases –> nodularity
*unencapsulated nodular architecture

Toxic Multinodular (PLUMMER SYNDROME)
*autonomous nodule in a long standing multinodular goiter
*(+) hyperthyroidism
*(-) ophthalmopathy, (-) dermopathy

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Clinical Factors Favoring Malignancy in Solitary Thyroid Nodule

Solitary nodule
Young, Male
History of radiation therapy
NON-FUNCTIONAL - COLD nodules

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Shares morphological features with ADENOMATOUS NODULE and FOLLICULAR CARCINOMAS

FOLLICULAR ADENOMA

encapsulated lesions
uniform-appearing follicles
little pleomorphism
rare mitosis

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HALLMARKS of thyroid adenoma

intact, well formed capsule encircling the tumor

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MC thyroid cancer

account for the majority of thyroid carcinomas associated with previous exposure to IONIZING RADIATION

PAPILLARY CA

(RET/PTC, BRAF)

papillary fronds with fibrovascular cores
ORPHAN ANNIE NUCLEI
PSAMMOMA BODIES - calcifications
LYMPHATIC METASTASIS

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2nc MC thyroid cancer

FOLLICULAR CA

(RAS, PAX 8, PPAR y)

invading thyroid capsule and vasculature
oncoytic type of Hurthle cells

2nc MC thyroid cancer

FOLLICULAR CA (RAS, PAX 8, PPAR y) invading thyroid capsule and vasculature oncoytic type of Hurthle cells HEMATOGENOUS METASTASIS

represent aggressive neoplasms of the thyroid follicular epithelium less than 5% of thyroid tumors, but with a high mortality rate RAPID ENLARGEMENT LARGE MASS

ANAPLASTIC CA pleomorphic GIANT CELLS SARCOMATOUS appearance - spindle shaped cells (+) CYTOKERATIN (+) PAX - 8

Neuroendocrine neoplasms derived from the parafollicular cells (C cells) (+) calcitonin

MEDULLARY RET small, polygonal to spindle shaped cells acellular AMYLOID deposits

FAVORABLE prognosis

papillary thyroid ca minimally invasive follicular ca

UNFAVORABLE prognosis

widely invasive follicular ca medullary thyroid ca anaplastic thyroid ca

Most helpful thyroid differentiation marker in anaplastic ca

PAX-8

Used to diagnose parathyroid gland pathologies

TECHNETIUM 99 radionuclide scan SCINTIGRAPHY SESTAMIBI SCANS

Clinical manifestations of symptomatic primary hyperparathyroidism

STONES, THRONES, BONES, GROANS, PSYCHIATRIC OVERTONES kidney stones polyuria and polydipsia bone pain weakness, constipation, abdominal/flank pain confusion, hallucinations, irritability

Hallmark of Severe Hyperparathyroidism

increased osteoclast activity peritrabecular fibrosis cystic brown tumor

HALLMARK of HYPOCALCEMIA

TETANY

ABSOLUTE insulin deficiency B cell destruction TYPE IV HLA - CHROMOSOME 6 antibodies against islet cells (anti-insulin, anti-GAD, anti-ICA2)

TYPE I DM

RELATIVE insulin deficiency insulin resistance B cell dysfunction genetic, environmental, proinflammatory

TYPE II DM

Acute Complications of DM

hypoglycemia DKA HHS

Macrovascular diseases in DM

Coronary Heart Disease - MI - MCC of death Peripheral Arterial Disease Cerebrovascular Disease

Microvascular diseases in DM

Retinopathy Nephropathy Neuropathy diffuse BM thickening and leaky capillaries NODULAR GLOMERULOSCLEROSIS - KIMMELSTIEL WILSON LESION pyelonephritis, necrotizing papillitis NERVES - glove and stocking pattern - MC

Insulin deficiency sufficient to develop KETOACIDOSIS <7.25 (+) KETONES usually VISCERAL (nausea, vomiting, abdominal pain)

DKA

Insulin deficiency insufficient to develop KETOACIDOSIS >7.30 usually NEUROLOGIC (altered mental status)

HHS

MC Pancreatic Neuroendocrine Tumor

INSULINOMA

Hyperinsulinism WHIPPLE TRIAD hypoglycemia (<50 mg/dl) neuroglycopenic symptoms relief upon parenteral glucose administration

INSULINOMA pancreas BENIGN (+) amyloid deposition

Hypergastrinemia pancreatic islet tumor hypersecretion of gastric acid severe peptic ulceration

GASTRINOMA (Zollinger Ellison Syndrome) gastrinoma (Passaro) triangle usually MALIGNANT

Ovoid, spherical, laminated nodules of matrix observed in diffuse and nodular diabetic glomerulosclerosis

KIMMELSTIEL-WILSON DISEASE

Hallmark of macrovascular disease in DM

ACCELERATED ATHEROSCLEROSIS MI - MCC of death in diabetes

Abdominal striae, obesity, dorsocervical fullness (buffalo hump), moon facies LAB FEATURES: increased 24 hr urine free cortisol ACTH-independent - increased cortisol --> decreased ACTH ACTH dependent - increased ACTH --> increased cortisol pituitary (Cushing disease) or ectopic (SCLC) - increased ACTH

CUSHING SYNDROME Exogenous steroids - MCC overall ACTH secreting pituitary adenoma (Cushing disease) - MC endogenous cause

Crisis in patients with CHRONIC adrenocortical insufficiency Rapid withdrawal of steroids in patients maintained on steroids MASSIVE ADRENAL HEMORRHAGE - Waterhouse Friedrichsen syndrome

Primary Acute Adrenocortical Insufficiency

MCC of primary hyperaldosteronism (CONN DISEASE) INCREASED ALDOSTERONE PRIMARY - increased aldosterone -- decreased renin SECONDARY - increased aldosterone and renin

Bilateral idiopathic hyperaldosteronism

Primary Chronic Hypoaldosteronism (ADDISON DISEASE)

(-) mineralocorticoid (-) glucocorticoid (+) HYPERPIGMENTATION - secondary to collateral increase in MSH that accompanies the increase in ACTH to low adrenal cortisol output NO response to ACTH stimulation test

Bilateral adrenal hemorrhage as a complication of DISSEMINATED bacterial infection N. meningitidis

WATERHOUSE-FRIEDRICHSEN SYNDROME

Eosinophilic, laminated cytoplasmic inclusions in aldosterone secreting adenomas

SPIRONOLACTONE BODIES

Morphology of Addison Disease

irregular shrunken glands with LYMPHOID INFILTRATES

Chronic adrenal insufficiency (Addison Disease) in the developed world

secondary to autoimmune adrenalitis

Other important causes of chronic hypoadrenalism

Tuberculosis and infections due to opportunistic pathogens associated with the human immunodeficiency virus and tumors metastatic to the adrenals

TRIAD diaphoresis headaches palpitations from CHROMAFFIN cells of MEDULLA releases catecholamines INCREASED urinary excretion of free catecholamines and metabolites (VANILLYLMANDELIC ACID (VMA) and METANEPHRINES)

PHEOCHROMOCYTOMA Rule of 10's 10% - extra-adrenal 10% - bilateral 10% - biologically malignant 10% - NOT associated with HPN 25% - have germline mutations

Histologic findings in Pheochromocytoma

ZELLBALLEN - clusters of polygonal or spindle shaped chromaffin or chief cells surrounded by sustentacular cells (like paraganglioma) METASTASIS - only reliable criterion for malignancy lymph nodes liver lungs bone

MEN 1 (WERMER SYNDROME)

3PS pituitary - prolactinoma - MC parathyroid pancreas

MEN 2 (SIPPLE SYNDROME)

2A pheochromocytoma parathyroid hyperplasia medullary thyroid ca 2B pheochromocytoma medullary thyroid ca neuromas ganglioneuromas marfanoid habitus