Week 5: Endocrine Flashcards
What are the 2 adrenocortical hormone disorders?
Addison’s and Cushing
What is Cushing Syndrome?
hypercortisolism (too much cortisol)
What can cause hypercortisolism?
Primary= disease of the adrenal cortex (Cushing SYNDROME)
Secondary= disease of the anterior pituitary (Cushing DISEASE)
Exogenous steroids= long term steroid use for other diseases (Cushing’s SYNDROME)
What are the s/s of Cushing syndrome?
- CNS- mood swings, insomnia, loss of libido
- Suppression of immune- impaired wound healing and risk for infection
- protein breakdown - muscle wasting, muscle weakness, thinning of skin, bone pain, thinning hair
- maintain vascular system - HTN, capillary friability
- increased glucose availability - glucose intolerance and hyperglycemia
What is the treatment for Cushings?
treat the cause; take out tumor, or stop steroids
drugs; aminoglutethimide and ketoconazole
MOA of aminoglutethimide
blocks the synthesis of all adrenal steroids
indication for aminoglutethimide
temporary therapy to decrease cortisol
S/E of aminoglutethimde
drowsiness, nausea, anorexia, and rash
MOA of ketoconazole
antifungal drug that also inhibits glucocorticoid synthesis
Indication for ketoconazole
adjunct therapy to surgery or radiation for Cushing Syndrome
S/E of ketoconazole
severe liver damage
do NOT take with ETOH, drugs, or while pregnant
What is Addison Disease?
disease of the adrenal cortex that causes HYPOsecretion of ALL 3 adrenocortical hormones
The lack of which hormone causes the most severe effects of Addisons?
Cortisol
What is the etiology of Addisons?
idiopathic, autoimmune, or other
Pathogenesis of Addisons?
adrenal gland is destroyed, most symptoms don’t show until 90% non-functional causing adrenocorticotropic hormone (ACTH) and melanocyte-stimulating hormone (MSH) are secreted in large amounts
Early s/s of Addison Disease
anorexia, weight loss, weakness, malaise, apathy, E- imbalances, and skin hyperpigmentation
Late s/s of Addison disease
Think Na and water retention problems
-hypotension, decreased cardiac output, salt craving, hyponatremia, hyperkalemia, hypoglycemia, weakness and fatigue, hyperpigmentation
What are complications of Addisons?
Addisonian (Adrenal) crisis
What causes an Addisonian crisis?
sudden loss of adrenal gland OR sudden increase in stress OR suddenly stopping steroid therapy
What is the pharmacotherapy of Addison disease?
-glucocorticoid (sometimes mineralocorticoid)
What considerations with the drug therapy of Addisons?
NEVER abruptly stop steroid therapy, take higher doses during stress, always have an emergency supply, and wear a medic alert bracelet
What is pheochromocytoma?
rare tumor of the adrenal medulla that produces excessive catecholamines (epinepherine and norepinepherine)
r/f for pheochromocytoma
young to middle age
S/S of pheochromocytoma
headache, diaphoresis, and tachycardia
What is the treatment for pheochromocytoma
preferred= surgery
drugs= alpha-adrenergic blockers (used for inoperable tumors and preop HTN)
What alpha-adrenergic is taken with pheochromocytoma?
phenoxybenzamine
What is the MOA of phenoxybenzamine?
long-lasting IRREVERSIBLE blockage of alpha adrenergic receptors
s/e of phenoxybenzamine
lowers blood pressure ,nasal congestion, reflex tachycardia, sexual s/e for men (remember IRREVERSIBLE)
What are the two Antidiuretic hormone disorders?
Diabetes Insipidus and SIADH
What is SIADH?
“Syndrome of Inappropriate AntiDiuretic Hormone”
-an abnormal production or sustained secretion of ADH
Characterization of SIADH
fluid retention, low serum osmolality, hyponatremia, concentrated urine
Etiology of SIADH
-Malignant tumors (e.g. small cell carcinoma of the lungs)
-CNS disorders (e.g. head trauma, stroke, brain tumor)
-drug therapy (e.g. morphine, SSRIs, chemo)
-Miscellaneous conditions (e.g. hypothyroidism, infection)
What is osmolality with SIADH?
Serum= LOW
NA+=LOW
UO=LOW
weight=GAIN
Urine SG= HIGH
SIADH s/s
dyspnea, fatigue, confusion, lethargy, muscle twitching, convulsions, impaired taste, anorexia, vomiting, cramps,
SEVERE= Na<100-115 causes possible irreversible neurological damage
what is the treatment of SIADH
treat the cause first
second line = demeclocycline
What class is demeclocycline?
tetracycline
MOA for demeclocycline
interferes with renal response to ADH
S/E of demeclocycline
photosensitivity, teeth staining, and nephrotoxic
What is Diabetes Insipidus (DI)?
a deficiency of ADH or a decreased renal response to ADH, characterized by excessive loss of water in urine
What two forms of DI?
Neurogenic, Nephrogenic
Etiology of Neurogenic DI
hypothalamus or pituitary gland damage
Sometimes associated with stroke, TBU, brain surgery or cerebral infections
Is Neurogenic DI onset sudden or slow?
SUDDEN
Is Neurogenic DI permanent?
Usually
What is the etiology of Nephrogenic DI?
loss of kidney function, often drug related (e.g Lithium for bipolar)
Is nephrogenic DI onset sudden or slow?
SLOW
Is nephrogenic DI acute or progressive?
progressive
What is the osmolality for DI?
serum= HIGH
sodium=HIGH
UO=HIGH
Urine SG= LOW
Weight= LOSS
s/s of DI
polyuria, polydipsia, dehydration, electrolyte imbalance, hypovolemic shock
Treatment for NEUROgenic DI
synthetic ADH replacement
Treatment for NEPHROgenic DI
thiazide diuretics
What drug is a synthetic ADH?
Desmopressin
S/E of desmopressin
small dose= none
nasal spray=irritation
large dose= hyponatremia, water intoxication
What does thyroxine (T4) do?
regulate the bodies metabolism that influences almost every body system
What is the flow for the release of thyroxine?
hypothalamus
| (TRH)
anterior pituitary
| (TSH )
thyroid gland
|
increased thyroxine
What does thyroxine inhibit?
the hypothalamus from releasing TRH, and the anterior pituitary from releasing TSH
Negative Feedback
What are the most common thyroid disfunctions?
primary thyroid disorders
What can occur with thyroid disorders?
goiter (thyroid enlargement)
What is hypothyroidism?
insufficient levels of thyroid hormones (T3 and T4)
What happens in primary hypothyroidism?
increase in release of TSH from pituitary
What is the most common cause of hypothyroidism?
Hashimoto’s thyroiditis (an autoimmune disorder)
R/F for hypothyroidism
female, age>50, Caucasian, pregnancy, hx of autoimmune disorder, family hx, medications, treatments for hyperthyroidism
Early hypothyroidism s/s
cold intolerance, WEIGHT GAIN, lethargy, fatigue, memory deficits, poor attention span, increased cholesterol, muscle cramps, raises carotene levels, constipation, decreased fertility, puffy face, hair loss, and brittle nails
Late hypothyroidism s/s
below normal temp, bradycardia, weight gain, decreased LOC, thickened skin, and cardiac complications
How does hypothyroidism affect the body?
-raises cholesterol
-raises carotene levels (yellow skin)
-causes anemia
-decreased filtration by kidney (risk of med toxicity)
-can cause hoarse voice)
What are the labs with a primary hypothyroidism diagnosis?
-high TSH levels
-Low T3 and T4
What are the labs associated with a secondary hypothyroidism diagnosis?
-high TSH levels
-high T# and T4
What is the MOA of levothyroxine?
T4-synthetic thyroid hormone, that is converted to T3 in the body
What are the three types of hyperthyroidism?
- Primary = thyroid problem
- Secondary= pituitary problem
- Tertiary = hypothalamus problem
R/F for hyperthyroidism
family hx of graves, age>40, women, Caucasian, medications, excessive iodine intake, pregnancy
What is graves’ disease
autoimmune disorder causing excess levels of T3 and T4
S/S of Graves’ disease
nervousness, insomnia, sensitivity to heat, weight loss, thyroid is enlarges, an audible bruit over thyroid, afib, myexedma, exophthalmos
What is exophthalmos?
a wide eyed stare associated with increased sympathetic tone and infiltration of the extraocular area with lymphocytes and mucopolysaccharides
labs for diagnosis of Graves’ disease?
low TSH
high T3 and T4
Treatments for Graves’ disease
antithyroid hormone medication (propythiouracil), radioactive iodine, or surgery (and then used levothyroxine)
What considerations are needed when taking propylthiouracil?
hepatotoxic and only used in 1st trimester with caution
What is a thyrotoxic crisis or thyroid storm?
overwhelming release of thyroid hormones that exerts an intense stimulus of metabolism
life threatening
What typically triggers a thyrotoxic crisis?
surgery, trauma, or infection
What causes all the symptoms of hypoparathyroidism?
hypocalcemia from insufficient PTH
S/S of hypocalcemia
muscle cramps, irritability, tetany, convulsions
What is the treatment for hypoparathyroidism?
replace PTH, normalize Ca and Vitamin D level, possible surgery (PTH are then lifelong)
S/S of hyperparathyroidism (high Ca)
muscle weakness, poor concentration, neuropathies, HTN, kidney stones, metabolic acidosis, osteopenia, fractures, constipation, depression, confusion, or subtly cognitive defects
treatment of hyperparathyroidism
reduce levels of calcium, diuretics, calcitonin, bisphosphonates, Vitamin D, and surgical interventions
