Exam 2 Mod 3&4 Flashcards
Posterior pituitary releases
ADH
Disorders involved if ADH is high
SIADH
Disorders involved if ADH is low
Diabetes insipidus/DI
Anterior Pituitary releases
ACTH, MSH, GH, TSH, Prolactin, LH, and FSH
Disorders involved w/ anterior pituitary
if high- gigantism, acromegalic, Cushing’s.
If low- Dwarfism, Acromicria, Simmond’s disease.
Deficiency in one or more of the anterior pituitary hormones, resulting in metabolic problems, sexual dysfunction. If it’s selective hypopituitarism only one hormone is deficient and is the most common.
Hypopituitarism
Deficiency sx of ACTH
hypoglycemia, vomiting, malaise
Deficiency sx of TSH
fatigue, constipation, cold intolerance, bradycardia
Deficiency sx of GH
hypoglycemia, short stature
Deficiency sx of ADH
polyuria, polydipsia, hypernatremia, lethargy, dehydration
Assessment of Hypopituitarism
-Gonadotropin deficiency (LH and FSH)
-Loss of sexual characteristics in men (facial and body hair, low libido, impotence)
-Loss of sexual characteristics in women ( amenorrhea, infertility, decreased libido, breast atrophy, pain during coitus, less axillary or pubic hair)
-Neurologic changes: loss of visual acuity, especially peripheral vision, temporal headaches, diplopia, ocular muscle paralysis, limiting eye movement.
-Diagnostic testing: Blood levels of pituitary hormones, hormone stimulation testing, Head CT & head MRI (brain lesions, tumor, prolactinoma), angiography -brain.
-Labs measure effects of hormones rather than actual hormone levels. Ex. T3 & T4 for TSH. Testosterone, estradiol, and prolactin.
True of False
Pts with hypopituitarism will require lifelong replacement of deficient hormones.
True
Hormone over secretion occurs with pituitary tumors or tissue hyperplasia. Tumors most often in the anterior pituitary cells: produce growth hormone, prolactin, and adrenocorticotropic hormone.
Hyperpituitarism
Hyperpituitary Disorders - Growth secreting hormone
Onset of growth hormone hypersecretion BEFORE puberty. Continues into adulthood resulting in abnormal height.
Gigantism
Hyperpituitary Disorders - Growth secreting hormone
Hypersecretion AFTER puberty. Occurs in adulthood so changes are seen in face, hands, feet, and ears.
Acromegaly
Hyperpituitarism: Assessment
Obtain info about
Family hx, change in appearance: change in hat, glove, ring, or shoe size.
Sx: fatigue and lethargy, backache, arthralgias, headaches and change in vision, menstrual changes, changes in sexual functioning.
Hyperpituitarism Diagnostic testing includes
-Hormone levels in blood and urine (any or all may be elevated; prolactin, ACTH, and GH)
-CT
-MRI
-Suppression testing (High glucose levels should normally suppress release of GH. Give 100g or oral glucose or 0.5 g/kg followed by serial GH level measurements)
Hyperpituitarism Drug therapy includes
-Dopamine agonists to stimulate dopamine receptors in the brain and inhibit the release of certain pituitary hormones (especially prolactin and GH)
Bromocriptine (Parlodel) and Cabergoline (Dostinex)
-Somatostatin analogs: Ocreotide (sandostatin) and lanreotide.
-GH receptor Blockers (For GH-secreting tumors): Pegnisomant.
What is the most common surgical management tx for hyperpituitarism?
Hypophysectomy- involves the removal of the pituitary gland along with the tumor. Goal is to decrease abnormal hormone levels, relieve HA, possible reversal of sexual dysfunction.
Concern w/ Hypophysectomy
CSF leak
-Postnasal drip - clear
-Increased swallowing
-Halo sign
-Persistent HA often means CSF leak into the sinuses
What is the post-op care for hypophysectomy?
-Monitor neuro response hourly x 24hrs, then every 4 hrs and document any changes in vision, mental status, LOC, or decreased strength in the extremities.
-Observe for complications such as DI, CSF leak, infection, & increased ICP.
-Keep HOB elevated, avoid coughing, perform deep breathing exercises hourly, avoid bending forward.
-Perform oral rinses and apply moisturizers over the lips.
-Assess for manifestations of meningitis.
-Teach patient self-administration of prescribed hormones.
Patho: H2O metabolism problem caused by ADH DEFICIENCY or inability of kidneys to respond to ADH. Excretion of large amounts of diluted urine.
Diabetes Insipidus (DRY INSIDE)
What classification of DI?
Renal tubules do not respond to ADH (severe kidney injury)
Nephrogenic
What classification of DI?
Problem in the hypothalamus or pituitary gland > lack of ADH production or release.
Primary Neurogenic DI
What classification of DI?
Caused by tumors, head trauma, infections, surgeries
Secondary Neurogenic DI
What classification of DI?
Caused by lithium and demeclocycline interfere with the kidney response to ADH
Drug-related DI
What are the assessment findings of DI?
Large amounts of very dilute urine (greater than 4L per day), causing dehydration and hypovolemia. Increased thirst but often not adequate to compensate for volume loss, which can lead to hypovolemic shock!.
Cardiac sx- hypotension, tachy (signs of hypovolemic shock), weak pulses, hemoconcentration
Skin sx- poor skin turgor, dry mucous membranes
Neuro Sx- decreased cognition, ataxia, increased thirst, irritability
Urine characteristics of DI
Dilute urine w/ low specific gravity (less than 1.005)
What is desmopressin?
Desmopressin is a synthetic hormone
Best test to diagnose central diabetes insipidus. In a water deprivation test, urine production, blood electrolyte levels, and weight are measured regularly for a period of 24 hrs, during which the person is NPO. Pt is given ADH (promotes fluid retention ) to determine if neuro or nephrogenic. If osmolarity increases, the kidneys are working so the problem is neurogenic.
Fluid deprivation test
Urine osmolality
After fluid deprivation <300
After desmopressin >800
Neurogenic DI
Urine osmolality
After fluid deprivation <300
After desmopressin <300
Nephrogenic DI
DI drug therapy
Teach them to weigh themselves daily
-Desmopressin (DDAVP), a synthetic form of vasopressin (or ADH) given intranasally in a metered spray or an oral tablet. May be lifelong with permanent conditions.
-Aqueous vasopressin: for short-term therapy or when the dosage must be changed often; given parenterally
-Chlorpropamide
Patho: Too much ADH!! Failure of negative feedback system.
ADH (vasopressin) secretes even when plasma osmolarity is low or normal. Caused by shock, trauma, stress, malignancies.
Water retention> fluid overload. Increase in kidney filtration further inhibits release of renin and aldosterone causing further increase of sodium loss.
Syndrome of Inappropriate Antidiuretic Hormone (SOAKED INSIDE)
Assessment finding of SIADH
Dilutional Hyponatremia, GI disturbances, N/V, loss of appetite, weight gain, bounding pulse, hypothermia, decreased urine volume and increased urine osmolarity.
Interventions for SIADH
-Fluid restriction 500-100 mL/24hrs. ( monitor for fluid overload)
-Drug therapy with vasopressin receptors antagonists (vaptans) and diuretics.
-Treat underlying cause
-Hypertonic saline
-Tube feedings and GI tube med administration consideration? Use saline instead of water.
Vaptans (tolvaptan, lixivaptan, satavaptan) treat
hyponatremia
Patho: Adrenal cortex production of steroid hormone may decrease as a result of inadequate secretion of adrenocorticotropic hormone (ACTH), dysfunction of the hypothalamic-pituitary control mechanism, or direct problems of adrenal gland tissue
Adrenal gland hypofunction
True or False?
Acute adrenocortical insufficiency (adrenal crisis) is life-threatening.
True
Common cause of secondary adrenal insufficiency?
Sudden cessation of glucocorticoid therapy
AKA adrenal insufficiency - illness that occurs when the body doesn’t make enough of certain hormones. In this disease, the adrenal glands make too little cortisol and, often too little of another hormone, aldosterone.
Addison’s Disease
Secondary Addison’s disease is caused by the
Sudden cessation of long-term high-dose glucocorticoid therapy
Life threatening event; need for cortisol and aldosterone is greater than available supply. Usually occurs in response to stressful events.
Sx include: profound fatigue, dehydration, Vascular collapse (low BP), renal shutdown, low serum NA+, high Serum K+. hyperpigmentation.
Acute adrenal insufficiency/Addisonian crisis
Sx of Addison’s disease
bronze pigmentation of skin, changes in distribution of body hair, GI disturbances, weakness, weight loss, postural hypotension, hypoglycemia
Hypersecretion of cortisol by adrenal cortex results in this syndrome/disease, hypercortisolism, or excessive androgen production. This can be caused by drug therapy for another health problem. Most common cause is glucocorticoid therapy. Most common non-drug cause is pituitary adenoma. Women are more effected than men.
Hypercortisolism (Cushing’s disease)
TOO MUCH STEROID
S/sx of Cushing’s disease
truncal obesity, moon face, buffalo hump. High fasting glucose. Increased androgen production (acne, more body hair, oligomenorrhea (irregular period) in women. Emotional instability is very common. Poor wound healing.
Pituitary Cushing’s, ACTH is
elevated
Adrenal Cushing’s, ACTH is
low
Hypertension due to increased aldosterone. Increased hepatic gluconeogenesis and insulin resistance. Can lead to cardiovascular disease and frequent infections/poor wound healing. Treatment depends on the etiology. If pt has surgery, they will receive corticosteroids to prevent Addisonian crisis.
Cushing’s Syndrome
What hypermetabolic adrenal disorder?
Increased secretion of aldosterone results in mineralocorticoid excess.
Primary hyperaldosteronism (Conn’s syndrome)
What hypermetabolic adrenal disorder?
Nonmalignant catecholamine-producing tumors of the adrenal medulla. Tumors produce, store, and release epinephrine and norepi.
Overproduction of catecholamines (epi and norepi/fight or flight).
Pheochromocytoma
What potential life-threatening event is a pt w/ pheochromocytoma at risk for?
Hypertensive crisis - BP 180/120 or greater
Triggered by stressful event - managing stress is VERY important
Tx for Pheochromocytoma
-Alpha-adrenergic blockers (doxazosin, tolazoline)
-Removal of tumor
S/sx of Pheochromoctyoma
Classic: hypertension, HA, sweating. Other: flushing, anxiety/panic, palpitations, abdominal pain, dizziness, blurry vision, sx of diabetes, tachy, heart failure.
Thyroid cells fail to produce sufficient levels of thyroid hormones (multiple reasons). Everything SLOWS down.
Etiology/Causes Hashimoto’s, thyroid surgery, radioactive iodine treatment.
Hypothyroidism
Hypometabolic Thyroid Disorders
Problem in the actual thyroid gland (low T3 and T4)
Primary
Hypometabolic Thyroid Disorders
Problem in the pituitary gland (low TSH, T3 and T4)
Secondary
S/sx of hypothyroidism
Sleeping 14-16 hrs a day, constipation, cold intolerance, may have difficulty in psychosocial functioning (similar to depression on a surface level).
Tx for hypothyroidism
-Replace thyroid hormone (Synthroid (levothyroxine).
Administer on empty stomach. OTC vitamins or minerals, especially calcium containing preps must be avoided for at least 4 hours. Calcium interferes with the absorption.
Why does the patient need to avoid calcium-containing supplements or preps for 4 hours before & after taking Synthroid?
Calcium interferes with the absorption.
Myxedema coma is a medical emergency. It is usually precipitated by trauma or illness. What are the s/sx?
profound lethargy, muscle weakness, mental decline, hypothermia, hypotension. Facial swelling of lips, eyelids, and tongue.
How is myxedema coma treated?
REPLACE THYROID HORMONE IMMEDIATELY. And give supportive care.
Too much thyroid hormone. Everything speeds up.
hyperthyroidism
Causes hypermetabolism and increased sympathetic nervous system activity. Can also be caused by adenoma( compresses the pituitary causing increased release of hormone), viral infection, excessive iodine or thyroid hormone intake (including long-term amiodarone use). Affects protein, fat, and glucose metabolism.
Thyrotoxicosis (thyroid storm)
Autoimmune disorder resulting from Hashimoto’s thyroiditis: immunoglobulins bind to TSH receptors on thyroid follicular cells
Grave’s disease
1st line tx for hyperthyroidism
Propylthiouracil (PTU)-1st line: Inhibits production of thyroid hormone
Other forms of tx for hyperthyroidism
*Drug therapy: Antithyroid drugs (1st line is methimazole), iodine preparations, beta-adrenergic blocking drugs
*Radioactive iodine: Destroys thyroid tissue upon uptake
*Surgical Management: Total or subtotal thyroidectomy
Post op complications of thyroidectomy
Hemorrhage, respiratory distress, hypocalcemia and tetany, laryngeal nerve damage, thyroid storm or thyroid crisis, eye and vision problems of Graves’ disease.
Post op monitoring for thyroidectomy
hoarseness or stridor, suture line pressure, hypocalcemia and tetany, thyroid storm (rare) happens during surgery.
