Q: Which hormones are lipid soluble?
A: Progesterone, estrogen, glucocorticoids (and therefore can cross membrane and interact with intracellular receptors)
Q: Which hormones are made from peptides?
A: insulin, growth hormone (so it interacts with cell surface receptors)
Q: What does the Adenohypophysis (anterior pituitary) derive from?
A: Rathke’s Pouch — make up 80% of pituitary gland
Q: What does Neurohypophysis (posterior pituitary) derive from?
A: Glia (from supraoptic and paraventricular nuclei) — make up 20% of pituitary gland
Q: What are the five types of anterior pituitary cells? Are they acidophilic or basophilic? What do they produce?
Somatotrophs — Acidophilic –> GH
Lactotrophs — Acidophilic –> PRL
Corticotrophic — Basophilic –> ACTH, MCH, POMC, endorphins, lipotrophin
Thyrotrophs — Basophilic –> TSH
Gonadotrophs — Basophilic –> FSH, LH
Q: What’s unique about Somatotrophs and Lactotrophs?
A: They are only acidophilic pituitary cells (Mnemonic: “ALS”), only ones controlled by inhibitory hormones, and most common causes of pituitary adenomas.
Q: How will acidophiles and basophiles stain?
A: Acidophilic will stain pink.
Basophils will stain purple.
Q: How can you tell the difference between anterior and posterior pituitary under the microscope?
A: Anterior has a whole bunch of different types of cells, so they will be mixed pink and purple. Posterior has neural tissue (see lotsa glial cells).
Q: What is the most common cause of hyperpituitarism? What’s the least common cause?
A: Most common — Adenoma of the pituitary.
Least common — Carcinoma of the pitutiary.
Remember Adenoma is overgrowth of glandular cells… so keeps secreting stuff.
Carcinoma is just tumor of the epithelium, usually squamous. They are not glandular, so hyperpituitarism due to carcinoma is rare.
Q: Diabetes Insipidus vs. SIADH:
Diabetes Insipidus = too little ADH –> hypernatremia
SIADH = too much ADH –>hyponatremia, can’t make diluted urine.
Q: What is the most common cause of SIADH?
A: Abnormal posterior pituitary secretion regulation. Ectopic secretion of ADH by malignant tumor.
Q: What are the mass effects of pituitary adenomas?
A: when it gets massive, it compresses on optic chiasm –> bitemporal hemianopsia (lose vision of outer half visual fields on both sides)
Q: What are the most common pituitary adenomas?
A: Prolactin, GH, ACTH
Q: Are pituitary adenomas usually benign or malignant?
A: benign. They don’t spread… just either cause problems by producing too much hormones or have mass effect.
Q: What are pituitary adenomas called when they secrete active hormones?
A: Functional pituitary adenomas. Otherwise if it does not secrete hormones, it is nonfunctional.
Q: In 25% of your patients, you find small adenomas in their pituitaries. WHat is it and is it bad?
A: Microadenomas.. common and totally benign.
Q: Which two hormones work through G-protein/cAMP?
A: GH and ACTH. So a mutation in GNAS-1 (gsp oncogene) can lead to somatotroph or corticotroph cell adenomas. (Mnemonic: “GAG”)
Q: Pituitary adenomas that grow so big without any signs… is it functional or nonfunctional?
A: NONFUNCTIONAL! Because it doesn’t secrete hormones, the patient doesn’t feel the affects, and therefore the adenoma grows undetected for a long time, until the patient feels the mass effects (like bitemporal hemianopsia)
Q: Histologically, what’s the difference between pituitary adenoma and normal pituitary?
A: Pituitary adenoma has the same type of cells (monomorphism) while normal pituitary has the usual 5 types of cells. There is also no reticulin network. Usually small round cells and lots of vascularity.
Q: What is the classical clinical triad of prolactinoma?
A: Amenorrhea (no menses), Galactorrhea (spontaneous lactation), Infertility. May or may not have libido loss.
Q: What symptoms would a man with prolactinoma experience?
A: Usually little symptoms, but may have impotence, headaches, or visual loss.
Q: What is normal prolactin level?
A: Normally less than 20 ng/mL in females, and less than 15 ng/mL in males. If over 1000 ng/mL, likely a prolactinoma.
Q: Somatotroph adenoma (GH adenoma) before and after closure of epiphyses lead to what?
A: Before closure –> Gigantism
After closure –> Acromegaly
Q: What is the most common cause of acromegaly?
A: Somatotroph adenoma (Growth Hormone adenoma). Cause more than 95% of cases. The tumor produces a lot of GH, which causes hepatic and chondral secretion of IGF-1, which lead to bone growth and lean muscle mass. The rest of cases is caused by ectopic GH-secreting tumors. Remember “ectopic” means it is found somewhere where it usually is not.
Q: What are characteristics of acromegaly?
A: Organomegaly = enlarged organs
Prognathism = protruding jaw
Arthropathy = disease of joints
Macroglossia = large tongue
Hyperhidrosis = excessive sweating
Frontal bossing = prominent eyebrow ridge
Q: What can acromegaly lead to?
A: galactorrhea, carbohydrate intolerance, diabetes, headaches, visual loss (if tumor too large due to mass effect), hypertension, congestive heart failure, GI cancers.
Q: What kinda resection do you need to do to take out pituitary tumors?
A: Endoscopic endonasal transsphenoidal resection
Q: Cushing Disease vs. Cushing Syndrome:
A: Cushing Syndrome = hypercortisolism caused by anything
Cushing Disease = hypercortisolims caused specifically by ACTH-secreting pituitary adenoma.
Q:What is Nelson’s Syndrome?
A: It’s not actually a syndrome. It’s when you wrongly cut out the adrenal gland thinking it would solve Cushing syndrome, only to realize the hypercortisolism was actually caused by ACTH adenoma in pituitary gland, not adrenal gland.
Q: Why is gonadotroph adenomas difficult to diagnose?
A: Because there are no recognizable symptoms — you might get decreased libido in men or amenorrhea in premenopausal women.
Q: What is Pituitary apoplexy?
A: hemorrhage of the pituitary gland due to pituitary adenoma. This is due to nonfunctioning pituitary adenomas, which get so big because they don’t cause any major symptoms.
Q: What is Sheehan Syndrome?
A: Sheehan Syndrome = when you get necrosis of anterior pituitary shortly after giving birth, due to insufficient blood flow to enlarged pituitary, enlarged by pregnancy.
Q: What genetic mutation leadas to hypopituitarism of GH, Prolactin, and TSH?
Q: Who’s at risk for Empty Sella Syndrome?
A: OBESE MULTIPAROUS PATIENTS!!!
Q: What is Empty Sella Syndrome?
A: When CSF herniate into the sella, pushing the pituitary to the side, making the sella look like it’s “empty.”
Q: What is Diabetes Insipidus?
A: Diabetes insipidus is when you can’t concentrate your urine. It is caused by too little ADH (anti-diuretic hormone), so you pee a lot, and its all diluted, but you still have hypernatremia (too much salt in blood) because you’re peeing away all that water in the blood, concentrating the salt.
Q: What are the four causes of Diabetes Insipidus?
1.Neurogenic: Posterior pituitary ain’t releasing enough ADH
2.Nephrogenic: Kidneys ain’t responding to ADH
3.Primary Polydipsia: Mouth feels dry so constantly drinking
4.Gestational: Too much ADH being metabolized.
Q: What are the two types of suprasellar tumors?
1.Gliomas – most common – from glial cells of posterior pituitary.
2.Craniopharyngioma – from vestigial remnants of Rathke’s pouch of anterior pituitary.
Q: What are the two types of Craniopharyngiomas?
1.Adamantinomatous– more common in children. VERY HARD.
2.Papillary– more common in adults.
Q: Who gets craniopharyngioma?
A: BIMODAL AGE DISTRIBUTION! Children 5-15 and Adults 50 and up.
Q: How bad is Craniopharyngioma?
A: There is good prognosis but it can erode bone, and cause mass effects (growth retardation, vision loss, diabetes insipidus)
Q: How does thyroid migrate during embryogenesis?
A: During embryogenesis, thyroid migrates from the tongue, downward. The most common heterotopic thyroid tissue is in the tongue.
Q: What is the histological organization of thyroid tissue?
A: Follicles lined with epithelium that produce colloid (when stimulated by TSH). Follicles filled with the colloid and store thyroglobulin. In between follicles (interstitium) is C-cells that produce calcitonin.
Q: Summarize T3 and T4:
-Most thyroid hormones are bound
-T4 converts to T3
-T4 acts as a circulating reservoir for converting to T3.
-There’s a lot more T4 than T3, and T4 lasts longer too, so that’s why it acts like a reservoir.
Q: How do you measure T3?
A: Remember T4 lasts longer and a lot more of it, so it’s easier to measure and more reliable. It is in constant equilibrium with T3, so to calculate amount of T3 (to measure the physiological activity of hormones), measure T4.
Q: Are most goiters functional or nonfunctional?
Q: What is it called when you have a functional goiter that causes hyperthyroidism?
A: Plummer Syndrome
Q: Thyrotoxicosis vs. Hyperthyroidism:
A: Thyrotoxicosis = elevated free T4 and free T3 (isn’t necessarily caused by thyroid disorder, i.e. drugs, pituitary)
Hyperthyroidism = Thyrotoxicosis due to thyroid disorder (i.e. Graves Disease)
Q: What is Subclinical Hyperthyroidism?
A: When you have low TSH but normal T4 and T3.
Q: What is Apathetic Hyperthyroidism?
A: When an elderly patient has hyperthyroidism but the effects are blunted because of their age.
Q: What does Thyroid hormone do?
A: Increases BMR — so too much causes tachycardia, weight loss, heat intolerance, sweating, tremor, restless
Q: What causes the wide-eyes adn exophthalmia of hyperthyroid patients?
A: Wide-eyes: sympathetic
Exophthalmia: connective tissue build-up behind eyes.
Q: Primary vs. Secondary vs. Tertiary vs. Exogenous causes of SUSTAINED Thyrotoxicosis?
Primary: thyroid gland overactivity (MOST COMMON) — due to drugs
Secondary: pituitary overactivity
Tertiary: hypothalamus overactivity
Exogenous: taking too much thyroid hormone
Q: What causes TRANSIENT thyrotoxicosis (temporary)?
A: Subacute Granulomatous Thyroiditis, Subacute Lymphocytic Thyroiditis, and Hashimoto Thyroiditis.
Q: Is subacute granulomatous vs. lymphocytic thyroiditis painful or painless?
A: Granulomatous = painful = because forms granulomas
Lymphocytic = painless = because just t-cells.
Q: What is Struma ovarii?
A: When you have a teratoma filled with thyroid tissue (usually in ovarian teratomas)
Q: What three drugs can cause drug-induced goiter (which is primary goiter because affects thyroid gland directly)?
A: Amiodarone (anti-arrhythmia drug), Iodides, Lithium (psychiatric drugs) [Mnemonic: "AIL"]
Q: What is the only type of thyrotoxicosis that is associated with increased TSH?
A: Secondary Thyrotoxicosis. i.e. TSH-producing pituitary adenoma, Ectopic TSH-producing tumors, mutated thyroid hormone beta receptor in pituitary that can’t be inactivated by too much thyroid hormone. All others (like producing too much T3/T4) have decreased TSH because of negative feedback.
Q: What does “Iatrogenic” mean?
A: Symptoms is caused by the doctor or the treatment.
Q: What does “Factitious” mean?
A: When the disease is caused purposefully by the patient over-administering on drugs.
Q: What is another name for Graves Disease?
A: Basedow Disease (probably hear more in Europe)
Q: What is the Merseburg Triad (Graves Disease Triad)?
A: Goiter, Palpitations, Exophthalmus
Q: Who gets Graves Disease?
A: More women than men (7:1 Women to men)
Q: What antibodies do you find in Graves Disease (which is an autoimmune disease)?
A: TSI, TGI, TBII, and sometimes you see anti-TPO.
TSI — Thyroid-Stimulating Immunoglobulin — binds and triggers TSH receptor. SPECIFIC FOR GRAVES!
TGI — Thyroid Growth-stimulating Immunoglobulin — cause follicular cell proliferation
TBII — TSH-binding Inhibitor Immunoglobulin — prevent TSH from binding to receptor
Q: Histologically, what do you see with Graves disease?
A: Scalloped epithelial cells around the follicles due to resorption of colloid
SOFT TISSUE PATHOLOGY