Endocrine II Flashcards
glands located on top of each kidney
adrenal glands
outer vs inner portion of adrenal gland
Outer = adrenal cortex Inner = adrenal medulla
What hormones do the adrenal cortex release? Adrenal medulla?
Adrenal cortex:
1) Mineralocorticoids (zona glomerulosa) –> aldosterone
2) Glucocorticoids (zona fasciculata) –> cortisol, corticosterone
3) Androgenic steroids (zona reticularis) –> estrogen, androgens
Adrenal medulla: secretes catecholamines (epinephrine, norepinephrine)
hormone that inhibits level of Na+ excreted into the urine and helps to maintain blood volume and BP
aldosterone
hormone that controls the body’s use of fats, proteins, and carbohydrates
hydrocortisone (cortisol)
hormone that suppresses inflammatory reactions in the body and also affects the immune system
corticosterone
Effects of epinephrine vs norepi:
Epinephrine (adrenaline)
• Increases the heart rate and force of contraction
• Facilitates blood flow to the muscles and brain
• Causes relaxation of smooth muscles
• Helps with conversion of glycogen to glucose in the liver
Norepinephrine (noradrenaline)
• Has little effect on smooth muscle, metabolic processes, and CO
• Has strong vasoconstrictive effects, increases BP
______ is normally produced by the pituitary gland to stimulate the adrenal gland to produce cortisol.
ACTH
Functions of cortisol:
o Maintains glucose (blood sugar) regulation
o Suppresses the immune response
o Released as part of the body’s response to stress
o Nonspecific cardiac stimulant that activates release of vasoactive substances
a wasting disease caused by failure of secretion of hormones by the adrenal cortex
chronic adrenocortical insufficiency
Chronic adrenocortical insufficiency causes a deficiency of which two hormones?
cortisol and aldosterone
More than 90% of cases of chronic adrenocortical insufficiency are due to one of these:
- autoimmune adrenalitis
- tuberculosis
- AIDS
- metastatic cancer
Addison disease vs Cushing disease
Addison disease = hypocortisolism
Cushing disease = hypercortisolism
Name the adrenal gland disorder: weakness, easily fatigued, weight loss, GI disturbances
Addison disease
Name the adrenal gland disorder: hyperpigmentation of skin and mucosa because increased levels of ACTH precursor hormone stimulates melanocytes
Addison disease
Common sites of hyperpigmentation (Addison disease):
face, axillae, nipples, areolae, and perineum
Name the adrenal gland disorder: decreased mineralocorticoid (aldosterone)
Addison disease
Addison disease results in decreased mineralocorticoids (aldosterone) due to what (4) things:
- potassium retention (hyperkalemia)
- sodium loss (hyponatremia)
- hypotension
- hypovolemia
Name the adrenal gland disorder: hypoglycemia may occur as a result of glucocorticoid deficiency and impaired gluconeogenesis
Addison disease
treatment for Addison syndrome
corticosteroid replacement therapy
Name the adrenal gland disorder: adrenal hyperfunction
Cushing syndrome
condition that causes the adrenal gland to produce excess cortisol
Cushing syndrome
Possible causes of the excess production of cortisol (Cushing syndrome):
Tumor in the adrenal cortex producing excess cortisol
ACTH-like hormone can be produced from cancer cells such as lung cancer
ACTH excessively produced from a pituitary tumor (pituitary adenoma) within the brain
the most common cause of Cushing syndrome
taking cortisone-like medications (Prednisone is the most common)
Manifestations of increased levels of glucocorticoids (cortisol):
Hypertension and weight gain Fat in the facial area—moon facies Fat deposition on posterior neck and back—buffalo hump Diabetes and osteoporosis Depression Hirsutism
The following do NOT usually cause Cushing syndrome:
Inhaled corticosteroid medicines for asthma
Topical corticosteroid medications
Oral corticosteroids taken every day for short periods of time or every other day for longer periods
medical emergency caused by a lack of cortisol
acute adrenal crisis
patients may experience lightheadedness or dizziness, weakness, sweating, abdominal pain, nausea and vomiting, or even loss of consciousness
acute adrenal crisis
Adrenal crisis occurs if:
Adrenal gland is deteriorating—inadequate production of cortisol
Pituitary gland injury (secondary adrenal insufficiency)—inadequate production of ACTH
primary vs secondary adrenal insufficiency
Primary = Addison's disease Secondary = pituitary gland injury
Risk factors for acute adrenal crisis:
Physical stress: infection, dehydration, trauma, surgery, adrenal gland or pituitary gland injury
Ending treatment with steroids (prednisone) too early—tapering is key
Patient taking exogenous steroids their body cannot produce extra in time of need
Name the adrenal gland disorder: can occur in patients taking exogenous corticosteroids
acute adrenal crisis
Why does acute adrenal crisis occur in patients taking exogenous corticosteroids?
High doses CCSs may affect response of pituitary
• Pituitary gets used to higher levels of CCSs, so it might not produce enough ACTH in response to stress
• Not enough ACTH = no stimulation of the adrenal cortex to produce cortisol in a time of need
The adrenals may also atrophy because they are not having to make cortisol as patient is taking it artificially
Name the adrenal gland disorder: occurs if rapid withdrawal of steroids
acute adrenal crisis
Dental management of patients taking CCSs:
Any dental procedure that causes an elevated level of physical stress can be expected to challenge the adrenal gland
• Restorations (for a patient with dental anxiety)
• Endodontic therapy
• Oral surgery
• Emotional stress—fear
Send a medical consult to patient’s MD
• Patient may need to increase the normal daily dose on the day of the procedure 2-4x
• If pain is anticipated, may also double dose the next day
• Monitor BP during treatment
Name the adrenal medulla tumor: malignant tumor arising in the adrenal medulla or within sympathetic ganglia
neuroblastoma
40% of cases of neuroblastoma develop in the _______.
adrenal gland
Name the adrenal medulla tumor: accounts for 7-10% of all childhood cancers
neuroblastoma
Name the adrenal medulla tumor: peak incidence is 3 yo
neuroblastoma
Symptoms of neuroblastoma:
Enlarging abdomen Firm, irregular non-tender mass Metastasizes to liver and bones Respiratory distress Bowel obstruction Elevated catecholamines
Name the adrenal medulla tumor: develops from the chromaffin cells that secrete catecholamines
pheochromocytoma
Name the adrenal medulla tumor: sustained or episodic hypertension
pheochromocytoma
Name the adrenal medulla tumor: tachycardia, palpitations, headache, sweating, tremor
pheochromocytoma
Name the adrenal medulla tumor: increased levels of catecholamines in the urine
pheochromocytoma
rule of 10s
Pheochromocytoma:
- 10% are bilateral, malignant, extraadrenal
- 10% no hypertension
Name the adrenal medulla tumor: 25% of cases occur in people with a germ-line mutation in one or at least six known genes
pheochromocytoma
Name the adrenal medulla tumor: 25% of cases occur in people with a germ-line mutation in one or at least six known genes
pheochromocytoma
25% of cases of pheochromocytoma occur in people with a germ-line mutation in one or at least six known genes:
RET—MEN II syndromes
NF1—type I neurofibromatosis
VHL—von Hippel-Lindau disease
sole purpose of the PTH glands
control Ca2+ within the blood in a very tight range
Name the parathyroid gland disorder: results from decreased secretion of PTH
hypoparathyroidism
most common cause of hypoparathyroidism
removal of the parathyroids during thyroidectomy
Symptoms of hypoparathyroidism:
Hypocalcemia
• Causes increased neuromuscular excitability (mild tingling of hands and feet, paresthesia, muscle cramps/spasms
• Dental related changes (if during tooth formation, pitting enamel hypoplasia, failure of teeth eruption)
• Mental effects (hyperirritability, fatigue, anxiety, mood swings/personality disturbances)
treatment for hypoparathyroidism
oral calcium and vitamin D precursor
increased PTH resulting from intrinsic PTH disease
primary hyperparathyroidism
Three things that cause primary hyperparathyroidism:
1) Adenoma of parathyroid gland (80%) –> dramatic enlargement of 1 of the 4 glands
2) Hyperplasia of parathyroid glands (15-20%) –> all 4 glands enlarged
3) Carcinoma of parathyroid gland (< 1%)
Clinical manifestations of increased PTH production:
1) painful bones
2) renal stones
3) abdominal groans
4) moans
*bones, stones, groans, moans
painful bones (primary hyperparathyroidism)
- Osteitis fibrosa cystica
- Bone resorption (fingertips)
- Generalized loss of the lamina dura
renal stones (primary hyperparathyroidism)
- Renal tubules absorb more calcium
- PTH stimulates those tubules to produce active vitamin D
- Active vitamin D promotes more calcium absorption from the intestines
abdominal groans (primary hyperparathyroidism)
duodenal ulcers, gallstones
moans (primary hyperparathyroidism)
depression, lethargy
disorder associated with an intrabony lesion called a “Brown tumor”
primary hyperparathyroidism
tumor that is well-demarcated, multilocular radiolucency
Brown tumor
locations of Brown tumor
mandible, clavicle, pelvis, ribs
excess secretion of PTH as a response to chronically low calcium levels—hypocalcemia
secondary hyperparathyroidism
Five things that can cause secondary hyperparathyroidism:
- Kidney failure requiring dialysis—most common
- Stomach or intestine bypass surgery
- Celiac disease
- Chron’s disease
- Severe vitamin D deficiency
Why do all 4 glands become enlarged with secondary hyperparathyroidism?
because there is not enough calcium, the parathyroids go into overdrive and become hyperplastic
Excess PTH production results = calcium resorbed from bones
In patients with renal failure, this is called?
renal osteodystrophy
Symptoms of renal osteodystrophy:
- Bone and joint pain
- Bone deformation and fractures at late stages
- Can lead to enlargement of the jaws
generalized loss of the lamina dura, blurring of the trabecular pattern leads to “ground glass” appearance
secondary hyperparathyroidism
Treatment for secondary hyperparathyroidism:
Optimize levels of serum calcium and phosphate (dietary restriction of phosphorous and phosphate binders)
Control PTH and vitamin D by use of vitamin D analogues
Surgical removal of the glands
Renal transplant if cause is renal failure