Pancreas/Adrenal Hormones and Endocrine Pathology Flashcards
What are the subdivisions of the adrenal glands
cortex and medulla
what are the functions of the adrenal cortex
store lipids (cholesterol and fatty acids) maufacture steroid hormones (corticosteroids)
what are the functions of the adrenal medulla
production of epinephrine and norepineprhine
what are the divisions of the adrenal cortex, and what do they produce
zona glomerulosa (mineralocorticoids-aldosterone) zona fasciculata (glucocorticoids-cortisol) zona reticularis (androgens)
what is the function of aldosterone, and what causes it secretion
stimulates conservation of sodium and elimination of potassium.
it is stimulated by low Na in blood (or high K), low blood volume, and low bp
what are the actions of glucocorticoids
they accelerate glucose
what are the hormones of the adrenal medulla
epinephrine and norepinephrine
what are the actions of epinephrine and norepinephrine
mobilization of muscular glycogen and breakdown of glucose for ATP
fats are broken down into fatty acids - ATP production
glycogen breakdown in liver
increased heart rate and contractility
What are the characteristics of the exocrine pancreas
clusters of pancreatic acini and ducts that take up almost all of the pancreas and secrete alkaline into the digestive tract
What are the characteristics of the endocrine pancreas
cell clusters called pancreatic islets (islets of langerhans) with alpha, beta, delta, and F cells
What are the 4 types of cells in pancreatic islets, and what are their secretions
alpha cells - glucagon
beta cells - insulin
delta cells - hormone similar to GH-IH
F cells - pancreatic polypeptide
what does GH do in children and adults
children - muscle and skeletal development
adults - maintain blood glucose, mobilizes lipid reserves
what is the general adaptation syndrome (GAS)
the hormonal stress response
what are the phases of the general adaptation syndrome
alarm phase
resistance phase
exhaustion phase
what are the characteristics of the alarm phase of GAS
increased catacholamines from the adrenal medulla due to stress =
- increased mental alertness
- increased energy use by cells
- mobilization of glycogen and lipid reserves
- changes in circulation
- sweating
- increased heart rate
what are the characteristics of the resistance phase of GAS
increase in GH, glucagon, cortisol, aldosterone, renin due to stress
- mobilization of remaining lipids and protein (break down of tissues)
- elevation of blood glucose
- conservation of Na and water
What are the charateristics of the exhaustion phase of GAS
- lipid reserves exhausted
- damage to organs
- inability to produce glucoccorticoids
- failure to balance electrolytes
what are the three classifications of endocrine pathologies
primary, secondary, and tertiary problems
what are primary, secondary, and tertiary problems of the endocrine system
primary = issue is with the final gland secondary = issue is with the pituitary gland tertiary = issue is with the hypothalamus
how does ADH work
it places aquaporins into the collecting duct = water reabsorption
how is hypersecretion of ADH diagnosed
normal adrenal and tyroid function, water retention, hyponatremia (low Na), and hypoosmolarity
what causes ADH hypersecretion
ectopic production of ADH
surgery (stress)
drugs
cranial abnormalities
how is ADH hypersecretion treated
water restriction, removal of ADH producing tumor, ADH receptor blockers
What is hyposecretion of ADH called
diabetes insipidus (polyuria, and polydipsia - thirst) dilute urine, dehydration
what are the three types of diabetes insipidus
neurogenic - insufficient ADH
nephrogenic - insufficient ADH response
Psychogenic - drinking too much water
how do you clinically differentiate between the three types of diabetes insipidus
- restrict water if urine osmolarity increases = PSYCHOGENIC
- if it doesnt increase give them ADH
- If urine osmolarity increases = NEUROGENIC
- if it doesn’t increase = Nephrogenic
what are the treatments for the different types of diabetes insipidus
neurogenic = supplement ADH nephrogenic = drink a lot and eat NaCl psychogenic = water restriction
what causes oxytocin release
cervix stretching, breast stimulation, baby crying, stress
what is the problem with low oxytocin, and high oxytocin
hyposecretion = lack of milk, long labor, lack of compassion/bonding
hypersecretion - galactorrhea
what happens to the anterior pituitary hormones when the hypothalamus isn’t working
all pituitary hormones decrease, except prolactin, which increases because PIF (inhibits prolactin) isn’t secreted
if you have low levels of anterior pituitary hormones how do you determine if that is due to hypothalamic or anterior pituitary issues
- take a blood sample of hormones
- give them some hypothalamic releasing factor
- take another blood sample
- if the hypothalamic releasing factor increased the hormone levels then it is a hypothalamus problem, if it didn’t then its a pituitary problem
what is pan hypopituitarism, and what causes it
when all of the anterior pituitary hormones are deficient, it it caused by non specific damage to the pituitary
what are the two causes of hypopituitarism
pituitary infarction (hemorrage in the brain) empty sella syndrome
what are the 4 causes of hyperpituitarism
benign pituitary adenoma
destruction of an end organ
hypothalamic disorder
carcinoma
what is the most common hormone to be hyper expressed by the pituitary gladn
PRL
what effect does a pituitary tumor have on the visual field
as the tumor grows it increases the blind spot in each eye
what are the initial symptoms of a hyperpituitarism caused by a tumor
visual defect
headache
occulomotor palsies
What stimulates, and inhibits prolactin release from the ant. pit.
stimulated by
- TRH and Oxytocin (from hypothalamus)
- stress, high estrogen, ovulation, suckling
Inhibited by
- somatostatin and dopamine (PRL causes this - feedback)
- estrogen and progesterone (pregnancy)
what are the actions of PRL
proliferation of mammary tissue
sythesis milk proteins
calcium mobilization
stimulates immune system
what are the effects of hypersecretion of PRL
females - amenorrhea - galactorrhea - hirsutism - osteopenia males - hypogonadism - impaired libido - infertility - gynecomastia - galactorrhea
what is the main treatment for PRL hypersecretion
dopamine agonists
what is the problem with low PRL
poor milk production
decreased immune function
What stimulates and inhibits the secretion of GH
stimulated by - GHRH - Ghrelin (from stomach) - estrogen and testosterone inhibited by - somatostatin (- feedback of GH on hypothalamus) - IGF (somatomedins)
what are the actions of GH
stimulate IGF production growth of long bones (with IGF) increase protein AA incorporation (with IGF) inhibit protein breakdown (with IGF) increase lipolysis (with IGF) inhibits hepatic glucose uptake stimulates the immune system
hypersecretion of GH =
gigantism
acromegaly
how is hypersecretion of GH treated
somatostatin analogs
What stimulates and inhibits the release of TSH
stimulated by - TRH - Cold Inhibited by - T3 - Dopamine - Somatostatin - stress
what are the actions of T3
regulates the basal metabolic activity of most cells
increase mRNA synthesis
What is the difference between congenital cretinism and developmental cretinism
congenital cretinism is when a pregnant mother and the fetus both have hypothyroidism. developmental cretinism is when only the fetus has hypothyroidism (less severe, can be treated with thyroid supplements)
What is hashimoto thyroiditis
autoimmune destruction of thyroid gland, most common cause of hypothyroidism
what is dequervain thyroiditis
enlaged sore thyroid following a URI
What is silent thyroiditis
alternating hypothyroiditis and hyper thyroiditis occuring in middle age, or postpartum women
What is Reidel thyroiditis
rare hypothyroidtis with a large mass that compresses the trachea
what is graves disease
an autoimmune hyperthyroidism where anti TSH-receptors bind, and ACTIVATE TSH receptors, causing high levels of T3 and T4
(SCALLOPED COLLOID)
When do patients get goiters
too much TSH, can be normal, high, or low levels of T3 and T4
which goiter is more likely a tumor diffuse or nodular
nodular
what is the difference between cushing disease and cushing syndrome
cushing disease is elevated ACTH production due to a pituitary tumor which causes elevated cortisol. cushing syndrome is elevated cortisol caused by an adrenal tumor or taking too much cortisol
how does MCH relate to ACTH
when ACTH is synthesized, it is broken off of POMC. one peice becomes ACTH the other becomes MCH
what does high MCH cause
hyperpigmentation
What does elevated cortisol cause
insulin resistance weight gain increased blood glucose muscle wasting osteoporosis decreased immunity sensitivity to catecholectamines
how do you differentiate between causes of high cortisol levels
dexamethasone test (synthetic cortisol) if low does decreases ACTH and cortisol it is chronic stress causing it. if it takes a high does to decrease ACTH and cortisol it is a pituitary tumor if nothing decreases ACTH and cortisol it is caused by ectopic ACTH
what happens with catecholectamine hypersecretion
it is caused by adrenal medulla hyperfunction (tumors of the chromaffin cells) and it causes elevated HR, elevated BP, diaphoresis, weight loss, hyperglycemia
What is addison disease
primary adrenal insufficiency, too little cortisol and mineralocorticoids. typically caused by autoimmunity
what are the symptoms of addison disease
slow onset
weakness
hypotension
skin hyperpigmentation
What is MEN
multiple endocrine neoplasia
What is MEN 1 vs. MEN 2
MEN 1 is when most of the neoplasia is outside of the thyroid (parathyroid, pancreas, and pituitary)
MEN 2 is when most of the neoplasia is found in the thyroid
What is the main difference between MEN 2a and MEN 2b
MEN 2b includes marfan characteristics
What determines which part of the body with store fat
the areas with lipoprotein lipase LPL will gain the most fat
