Lecture 14: Endocrine System (Exam 3) Flashcards
(45 cards)
What endocrine organs did we focus on in the endocrine lecture?
Hypothalamus and pituitary
Thyroid
Parathyroid
- Phosphate and Calcium metabolism
Adrenal gland
What is homeostasis?
-multiple layers of control with feedback
-balance
Briefly describe hormone interaction
Hypothalamus
GHRH affects GH
Somatotostain affects TSH and GH
TRH affects TSH and PRL
dopamine effects dopamine
GnRH affects LH/FSH
Adenohypophysis
GH affects multiple organs
TSH affects thyroid
PRL affects reproductive organs
LH/FSH affects reproductive organs
Target of Organs
Multiple
thyroid (can feedback hypothalamus)
reproductive organs
What endocrine diseases are covered in this lecture?
Hypothalamus/Pituitary
-Diabetes Insipidus
-SIADH (syndrome of inappropriate ADH secretion)
-Sheehan Syndrome
Thyroid
-Goiter
-Thyroiditis
-Graves Disease
Adrenal Gland
-Addison Disease
-Cushing Syndrome
-Pheochromocytoma
Parathyroid
-Osteomalacia
-Hypercalcemia
Describe the interactions of the hypothalamus
Hypothalamus
-releasing hormones act on adenohypophysis
-Neurohypophysis is the end of neurons that are in the hypothalamus
Neurohypophysis (posterior pituitary)
-Diabetes Insipidus decrease
-SIADH
Adenohypophysis (anterior pituitary) (through the blood, acidophils, and basophils)
-Adenomas increase
-Sheehan syndrome decreases
What is Diabetes insipidus?
Deficient ADH production
-by the neurohypophysis
-results in excess water excretion
-serum Na+ and osmolarity increase
-caused by head trauma, tumors, inflammation of the hypothalamus/pituitary
ADH and oxytocin are hormones that accumulate in the neurohypophysis
Two types:
- insufficient ADH–>Central DI
-ADH insensitivity –> Nephrogenic DI
Describe CDI clinically
Sx:
Frequent Urination
-Extreme thirst
-Can cause life-threatening dehydration
Treatments
-Mild CDI
-drink more water
More severe
-Vasopressin can be prescribed
What is SIADH?
Syndrome of inappropriate (comes from outside the pituitary) ADH secretion
-more frequently by ADH-secreting tumors (SCLC)
-also certain drugs, CNS disorders
Excess ADH
-Excessive water resorption
-Dilutes blood –> hyponatremia
Clinically:
-Hyponatremia
-Cerebral edema (blood volume does not change, so no peripheral edema)
-neurologic dysfunction (think water intoxication)
What is water intoxication?
Water poisoning or fatal hyponatremia
-urine excretion can be increased to 16ml/min when large quantities of hypotonic fluid are ingested
-if ingestion exceeds this, or continues for too long, cells will swell due to water uptake to cope with hypotonic ECF
Symptoms
-swelling of CNS neurons
-Convulsions, coma (can kill)
What is water intoxication?
Water poisoning or fatal hyponatremia
-urine excretion can be increased to 16ml/min when large quantities of hypotonic fluid are ingested
-if ingestion exceeds this, or continues for too long, cells will swell due to water uptake to cope with hypotonic ECF
Symptoms
-swelling of CNS neurons
-Convulsions, coma (can kill)
What is Sheehan Syndrome?
During pregnancy, the anterior pituitary (where FSH and LH are produced) undergoes hypertrophy
-Will nearly double in size
-Hormones of pregnancy
-Progesterone produced by corpus luteum
-blocks the development of additional follicles
-HCG stimulates the production
LH and Prolactin-adenohypophysis
-Support function of the corpus luteum
-Prolactin inhibits GnRH release; inhibited by estrogen and progesterone until parturition
-Prolactin release stimulated by estrogen
What is Ischemic Necrosis of the adenohypophysis?
-excessive cell numbers without increased blood flow causes minor anoxia
-more sensitive to low blood pressure
-Hypovolemic shock due to hemmorrage
-infarct will develop in the anterior pituitary
-Necrosis leading to fibrosis
What are symptoms of Sheehan symptoms?
Ischemic tissue is replaced by fibrosis nodules
-Causes postpartum hypopituitarism
Symptoms include:
-Amenorrhea (FSH/LH)
-Infertility (FSH/LH)
Lactation failure (Prolactin)
-Hypothyroidism (Thyroid-stimulating hormone)
Pallor (loss of melanocyte stimulation) POMC (MSH)
Describe how adrenal hormones move/work
-release into nearby blood vessels
-steroid hormones in the cortex
-peptide hormones (catecholamines) in the medulla
-Release induced by nerve signal
What are the diesease that are focused in the adrenal gland?
Addison Disease
-primary chronic adrenocortical insufficiency
Cushing Syndrome
-aka hypercortisolism
-exogenous and endogenous causes
Pheochromocytoma
-medullary tumor
What is Addison’s disease?
_progressive destruction of the adrenal cortex
-extensive mononuclear infiltrate
-Loss of most of the cortical cells
-60%-70%: autoimmune adrenalitis
-infections: tuberculosis or fungal
-AIDS
-Metastatic cancer
-Gross appearance of gland varies
-Autoimmune: shrunken
-Infection: inflammatory reaction
-Cancer: enlarged with tumor
Sx: 90% of the adrenal gland is lost still noticed
First: progressive weakness and easily fatigued
- Lack of aldosterone (aldosterone increases Na+ reabsorption, increases K+ secretion, and H+ secretion) increase leads to loss of sodium and retention of potassium
-Volume depletion and hypotension
**Lack of glucocorticoids (glucocorticoids produce hyperglycemia, glucosuria, secondary diabetes, and suppress the immune system) leads to hypoglycemia and lack of gluconeogenesis
-Cortisol increases gluconeogenesis
-Stress causes an adrenal crisis that can be fatal
-Adrenal crisis: continuous vomiting, abdominal pain, hypotension, vascular collapse, and coma
GI disturbances (cortisol helps break down fat, carbohydrates, and protein)
-Anorexia, nausea, vomiting, weight loss, diarrhea
Skin hyperpigmentation
-increase in POMC due to lack of cortical hormones
-Trying to make more ACTH (no negative feedback)
-POMC contains MSH fragments
-Stimulate melanocytes to produce melanin
What is Autoimmune adenalitis?
The immune system destroys steroid-producing cells in the adrenal cortex
-Autoantibodies to enzymes involved in steroid synthesis
-Associated with autoimmune polyendocrine syndromes (APS)
-Multiple diseases that involve the destruction of endocrine tissue (multiple organs)
-Best understood is APSI
-Autoantibodies to IL-7 and IL-22 (produced by T helper cells)
-Mutation is in a single gene on chromosome 22
-gene product (AIRE) is involved in protein expression in the thymus needed to remove T cells reactive to adrenal cortex antigens
What is Cushing’s Syndrome?
Pituitary adenoma
-monoclonal microadenomas
-excessive ACTH secretion will produce bilateral adrenal hyperplasia
Chronic exposure to high blood glucocorticoid levels
-most common cause is excess ACTH secretion by the adenohypophysis
-tumor in the anterior pituitary
Iatrogenic
- medial administration of glucocorticoids to treat the non-endocrine disorder
-immune suppression for autoimmune, transplant patients
-see adrenal atrophy
Endogenous (non-iatrogenic)
4 types
Pituitary Cushing Syndrome
-adrenal hyperplasia
Adrenal Cushing syndrome
-Tumor or nodular hyperplasia
Paraneoplastic Cushing syndrome
-see adrenal hyperplasia
Iatrogenic Cushing syndrome
neg. feedback: High GC/Low ACTH
What are the possible changes you will possibly see in the adrenal gland?
depending on the cause:
1.) cortical atrophy (iatrogenic Cushing syndrome)
-exogenous GC decreases ACTH
-lack of stimulation results in atrophy
2.) Diffuse hyperplasia (Cushing’s Disease)
3.) Nodular hyperplasia (ACTH-independent)
-adrenal gland is not dependent on ACTH but the adrenal gland secretes its own ACTH
4.) Adenoma/carcinoma
-causative; tumors that produce cortisol
Treatment:
removal of the adrenal gland if in one
eliminate the cause
What are the possible changes you will possibly see in the pituitary gland?
-regardless of the cause
-corticotropic basophils become paler, and fill with keratin filaments (Crooke hyaline change)
What is endogenous Cushing’s
ACTH dependent
-Cushing’s Disease
-ACTH-secreting pituitary adenoma
-Ectopic ACTH syndrome
-spontaneous
-most often-small cell lung carcinoma or bronchial carcinoid tumors
ACTH independent
-Adrenocortical tumor (produce ACTH or ACTH-like peptide)
What is the effect of high cortisol levels?
-Suppress CRH secretion (hypothalamus)
-Suppress ACTH secretion (pituitary)
-also inhibit GH, TSH, and gonadotropin release
-affects insulin production and gluconeogenesis in the liver
What are the symptoms of Cushing’s Disease?
-Hypertension
-Weight gain
-centralized (trunk, posterior neck)
-Selective atrophy of fast-twitch muscle fibers, resulting in proximal limb weakness
Glucocorticoids produce
-Hyperglycemia, glucosuria, secondary diabetes (induce gluconeogenesis, decrease glucose uptake)
-Suppress the immune system
What is Cushing’s Catabolism?
Promotes catabolism of
-Collagen
-Inhibits fibroblast function
-Bone
Leads to
-Fragile skin with poor wound healing
-Striae on the skin (especially the abdomen)
-Similar to stretch marks
-Osteoporosis
