Endocrine System Flashcards
Hyperpituitarism causes and common symptom
Caused by adenomas (too many cells, too many hormones)
- The pituitary is right above a set of optic nerves. So a larger pituitary will “stomp out” the optic nerves beneath it.
- This reduces outer peripheral eyesight In general for the endocrine system: if know hormone, can guess the symptoms
Hyperpituitarism caused by three types of adenomas
Prolactinoma
Somatotroph Adenoma
ACTH-producing adenoma
Hyperpituitarism
-histopathology
- usually pituitary has diverse cells
- can tell if an adenoma cuz things will look uniform
- CANT tell what type of adenoma by looking at the cells
Prolactinoma
“prolactin, milk, breasts, sex characteristics”
with too much prolactin:
- Amenorrhea and spontaneous release of milk (galactorrhea) in women
- Loss of libido/impotency in males
Somatotroph Adenoma produce what?
“somatic, body, body builders, Growth Hormone”
- Growth Hormone producing adenomas
- GH stimulates insulin-like growth factor 1 (ILGF-1)
Somatotroph Adenoma clinical
GH symptoms:
-Gigantism (if adenoma happens before epiphyses close) -Acromegaly (if after epiphyses close)
Insulin like growth factor 1 symptoms:
-Can cause diabetes mellitus/abnormal glucose tolerance
ACTH-producing Adenoma produce what?
Too much ACTH which activates adrenocorticoid production
This will make the adrenal produce too much cortisol
ACTH-producing Adenoma manifestations clinical
manifestations:
-hypercortisolism manifests itself as cushing disease
clinical:
- cortisol has a feedback loop to turn off ACTH production. So if take out adrenal to Tx Cushings feedback lost and cells will make more ACTH, causing adenoma to grow faster and become more aggressive
- Hyperpigmentation may also occur, as ACTH is derived from a melanin regulator precursor
Hypopituitarism Causes
Not enough hormones
-why?
Usually something is cramping the pituitary’s space causes:
- Tumors (Pit. tumors, craniopharyngiomas, gliomas)
- Ischemic pituitary necrosis (hypotension from post partum hemorrhage)
- or, if not a ceiling over pituitary, brain will crush it (called Empty Sella Syndrome)
hypopituitarism -clinical
clinical:
- pallor (no melanin production)
- hypothyroidism (no TSH)
- Failure of lactation (no prolactin)
- Adrenal insufficiency (no ACTH)
- ovarian failure w/amenorrhea (no LH)
Posterior Pituitary Syndrome
Diabetes Insipidus
post. pituitary makes ADH (which acts to retain water)
Too little ADH = lack of water retention Na still retained and this coupled with water loss leads to an increased sodium concentration
posterior pituitary syndrome clinical
clinical:
- polyuria (urinating often)
- Thirst
- Polydipsia (excessive thirst)
Hyperthyroidism
Too much metabolism
- bulging eyes, sweaty, hot, bad tempered etc
- Graves disease:
Ab-mediated hyperthyroidism
Hypothyroidism -two causes
- can be caused by dietary iodine deficiency
- Or can be autoimmune (Hashimoto’s)
symptoms opposite to hyperthyroidism (tend to be overweight, cold etc)
Hashimoto’s Thyroiditis -mechanism -at risk for
Mechanism:
-humoral and cellular immunity
At risk for:
- Thyroid follicles being destroyed which lets thyroid hormone precursor spew out everywhere, putting patient at risk for thyrotoxicosis
- B cells overproliferating creates risk for B-cell non-Hodgkin Lymphoma
Goiter
- Reflects inadequate synthesis of thyroid hormone
- may seem contradictory
- the idea is that the thyroid is storing a lot of thyroid precursor which builds up, causing the goiter
Hyperparathyroidism -Three Types
- Primary
- spontaneous hypersecretion of PTH -mainly due to parathyroid adenomas - Secondary
- Enlargement/hypersecretion in response to hypocalcemia - Tertiary
- Enlargement from secondary remains after the cause is gone
Hyperparathyroidism -clinical manifestations (same for all three types)
Clinical
- PTH normally demineralizes bone to increase blood calcium levels
- so blood calcium will be raised, patient will make more stones and this will mess with conduction in the heart
Papillary Carcinoma
-What is it?
The most common form of Thyroid Cancer
Papillary Carcinnoma
- Pathogenesis
- Histopathology
Pathogenesis:
-activation of MAP Kinase pathway involved in most cases
Histopathology:
- Psamomma bodies -concentric calcified structures which look like onions
- “Orphan Annie Eye” Nuclei -Nuclei look empty due to finely dispersed chromatin
Adrenals:
- Adrenal Cortex:
- Adrenal Medulla:
Adrenal cortex:
- makes Glucocorticoids which control carb, fat and protein metabolism
- Makes mineralcorticoids which control the amount of water and electrolytes present in the body
Adrenal medulla:
-makes catecholamines
Cushing Syndrome
- Where is it?
- How to remember?
Cushing Syndrome
-In the adrenal cortex
“c for cushing, c for corticosteroid”
Cushing Syndrome
-Causes
- Administration of exogenous steroids
- Pituitary Adenoma (Increased ACTH)
Cushing Syndrome
-Clinical
Corticosteroids increase blood sugar in any way possible. This sugar will inevitably be stored as fat
Signs:
- Obesity (extremities unaffected)
- Moon Face (obesity of the face)
- Buffalo Hump (obesity of the neck)
Addison Syndrome
- Where is it?
- How to remember?
- Adrenal Cortex
- If Cushing is too much corticosteroid, addison is too little (its the opposite of Cushings)
Addison syndrome
-Causes
- Autoimmune Adrenalitis
- TB
- AIDS
- Metastatic Cancers
- Withdrawal of long term corticosteroid Tx
Addison syndrome
-Clinical
Things associated with not enough corticosteroids:
- weakness
- weight loss
- GI symptoms
- HYPERPIGMENTATION*
*Adrenal insufficiency will lead pituitary to produce more ACTH and, consequently, more POMC (melanin precursor)
Pheochromocytoma
- Where is it
- How to remember?
- Are most cases unilateral or bilateral?
- In the Adrenal Medulla
- Pheochromocytoma looks like it can be abbreviated as PCC with CC corresponding to CateCholamines
- It is a neoplastic condition springing from a single cell so most cases are unilateral
Pheochromocytoma
- Histopathology
- Dx
- Clinical
Histopathology:
-“Cell Ballin”–> forms Zell Ballen, or circumscribed nests of neoplastic cells
Dx:
-Increased levels of catecholamine metabolites, particularly vanillylmandelic acid (VM acid)*
*mandelic looks like medulla
Clinical:
- Catecholamines cause hypertension and the antsy behavior associated with nervousness
- Hypertension -Tachycardia -nervousness
