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162 Cards in this Set
- Front
- Back
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The endocrine system is composed of:
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a series of ductless glands
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The endocrine system communicates through the use of:
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Hormones
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Hormones are:
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chemical messengers that travel though the bloodstream to their target organ
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The body’s glands are divided into two categories:
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endocrine and exocrine
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*Explain the endocrine glands:
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-ductless -release secretions directly into blood stream -secretions have regulatory function |
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*Explain the exocrine glands:
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-secrete through a series of ducts (sebaceous and sudoriferous) -their secretions are protective and functional |
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Pituitary Gland
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—“master gland”
Anterior pituitary gland Posterior pituitary gland |
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*Thyroid gland:
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-butterfly shape, with one lobe laying on either side of the trachea -very vascular gland -secretes T4 and T3 |
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*Parathyroid gland:
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-four parathyroid glands -increases the concentration of calcium in the blood -regulates the amt of phosphorus in the blood |
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*Adrenal gland:
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–Adrenal cortex (three layers that secrete hormones called steroids)
–Adrenal medulla (two hormones released during stress-epinephrine/adrenaline and norepinephrine) |
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*Pancreas:
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-very active organ composed of both exocrine and endocrine tissue -cells secrete insulin and glucagon |
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The endocrine glands are responsible for:
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regulation of numerous physiological processes in the body, including reproductive functions
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What are the female sex glands?
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Ovaries
Placenta |
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What are the functions of the ovaries?
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secrete estrogen, which is responsible for the development of secondary sexual characteristics
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*The placenta is only present in the woman during pregnancy. What are the functions of the placenta?
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during this time the ovaries become inactive and the placenta releases the estrogen and progesterone needed to maintain the pregnancy |
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*What hormones are secreted by the placenta?
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estrogen and progesterone |
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*What hormone is secreted by the testes?
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testosterone |
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*What bodily changes result from the hormone secreted by the testes?
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-the appearance of axilary, pubic, and facial hair -maturation of the reproductive organs -deepening of the voice -the development of muscle and bone mass -sperm formation in males |
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What are the male sex glands?
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Testes
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*Thymus gland:
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-produces thymosin which plays an active role in the immune system |
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*Pineal gland:
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-secretes melatonin which prevents sexual maturity from occuring until adulthood |
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What is Acromegaly ?
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-Overproduction of somatotropin (growth) hormone in the adult
-Idiopathic hyperplasia of the anterior pituitary gland -Tumor growth in the anterior pituitary gland -Changes are irreversible -a relatively rare disorder |
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Acromegaly Clinical manifestations:
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-Enlargement of the cranium and lower jaw
-Separation and malocclusion of the teeth -Bulging forehead -Bulbous nose -Thick lips; enlarged tongue -Generalized coarsening of the facial features -Enlarged hands and feet -Enlarged heart, liver, and spleen -Muscle weakness -Hypertrophy of the joints with pain and stiffness -Males—impotence -Females—deepened voice, increased facial hair, amenorrhea -Partial or complete blindness with pressure on the optic nerve due to tumor -Severe headaches |
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*The characteristic clinical manifestations of acromegaly occur throughout the body. When collecting information from patients, what subjective data should be obtained? What questions should be asked of this patient?
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includes determining the presence of headaches of visual disturbances and any precipitating factors -muscle wekness in relation to activities performed |
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*The significant changes in appearance associated with acromegaly have the potential to have psychosocial implications. What nursing diagnoses may be applicable to the psychosocial needs of the patient diagnosed with acromegaly?
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disturbed body image, related to enlargement of the hands, feet, tongue, jaw and soft tissue |
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Hyperpituitary-Acromegaly Diagnosis:
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-Increase serum Somatotropin (growth hormone)
-X-rays, -MRI -Physical Exam -Oral glucose challenge-level does not go down |
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Hyperpituitary-Acromegaly
Clinical Manifestations: |
-Enlarged pituitary gland
-HA -Visual disturbances -slanting forehead -Course facial features -Protruding Jaw -Increased BP -CHF -menstrual changes -sleep apnea -Hypertrophy of soft tissue Such as tongue, skin, and visceral organs -enlargement of small bones in the hands and feet |
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What are diagnostic tests for acromegaly?
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-History & clinical manifestations
-CT scan & MRI -Ophthalmologic exams -Labs: GH & IGF-1 (Insulin-like Growth Hormone) Definitive test is the oral glucose challenge test |
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Acromegaly: Medical management
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-Medications:
-Cryosurgery -Transsphenoidal removal of tissue -Proton beam therapy |
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*Cryosurgery:
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the use of subfreezing temperatures to destroy tissue |
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*Transsphenoidal Removal of tissue:
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the removal of tumor tissue |
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*Proton beam therapy:
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irridation procedure that uses very low doses of radiation and therefore it is much less destructive to adjacent tissues than radiation |
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Medications for Acromegaly:
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-Dopamine agonists: cabergoline
-Somatostatin analogs (inhibit GH): octreotide |
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Complications of acromegaly
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Enlargement of liver, spleen & heart, cardiac dysrhythmias, CHF, respiratory difficulty
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*The patient experiencing acromegaly will often experience 7 to 9 years between the diagnosis of the disorder and the onset of clinical manifestations. What factors could be associated with this delay in a definitive diagnosis?
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because it takes a subsequent overabuncance of growth hormone to produce the many changes throughout the patients body and in many cases it can take 7-9 yrs for these hormones to become subsequently overabundant |
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* When acromegaly is suspected, the diagnosis will be made based upon the patient’s health history, clinical manifestations, and the results of screening tests. What tests can be anticipated? What findings will support a positive diagnosis?
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the GH-suppression (also called the glucose-loading test) may be done to evaulate GH levels...GH levels will be high with gigantism |
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* After diagnosis and treatment, what prognosis can the acromegalic patient anticipate?
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even with adequate medical or surgical treatment, the physical changes are irreversible and the patient is prone to developing complications |
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Acromegaly : Nursing interventions (Supportive)
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-Assess ability of ADLs D/T weakness, stiffness & joint pain
-Assess headaches – concern for tumor progression -Soft, easy-to-chew diet – encourage chewing thoroughly -Analgesics – non-opioid as needed -Activity intolerance -Body image disturbances |
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Acromegaly: Patient teaching
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-ROM exercises to prevent muscle atrophy & loss of movement
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What is Gigantism?
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-Overproduction of growth hormone
-Caused by hyperplasia of the anterior pituitary gland -Occurs in a child before closure of the epiphyses |
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The secretion of growth hormone is responsible for what?
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the growth and development of the body’s tissues
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When growth hormone is produced in excess what can result?
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Gigantism
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*What are the role of epiphyses in gigantism and why is gigantism impacted by their development?
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when overproduction of GH occurs in a child before closure of the epiphyses, there is an overgrowth of the long bones which results in the attainment of great height, accompanied by increased muscle development. |
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Gigantism: Clinical manifestations/assessment
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-Great height
-Increased muscle and visceral development -Increased weight -Normal body proportions -Weakness |
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Gigantism: Medical management
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-Surgical removal of tumor
-Irradiation of the anterior pituitary gland |
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*Clinical manifestations associated with gigantism resemble an “overgrowth.” Despite their large size, the affected patients experience weakness. What causes this weakness?
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*
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* What nursing care will be needed for the patient diagnosed with gigantism?
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the nurse must be understanding and compassionate and accentuate the positive aspects of being tall |
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Gigantism Nursing Diagnosis & interventions:
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-Emotional support
-Chronic low self-esteem R/T irreversible body changes -Ineffective coping R/T personal vulnerability |
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Posterior pituitary hormones are actually produced in the _______ and only stored in the ________.
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Hypothalamus; posterior pituitary
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Posterior pituitary hormones:
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Antidiuretic hormone (ADH)
Oxytocin |
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The hormones secreted by the posterior pituitary are :
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Antidiuretic hormone (ADH) (Also call vasopressin)
and oxytocin |
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ADH contributes to fluid balance by:
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Controlling renal reabsorption of free water
It also has potent vasoconstrictive prope |
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Antidiuretic hormone (ADH) Also called:
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Vasopressin
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Excess ADH:
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Syndrome of Inappropriate ADH secretion (SIADH)
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Deficiency ADH:
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Diabetes Insipidus
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ADH (anti-diuretic hormone) is a hormone made in:
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pituitary gland
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ADH does what the name says:
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it stops urination – diuresis
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Slowing or stopping urine production leads to:
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fluid retention
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Fluid retention causes:
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a dilution of body sodium
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SIADH:Depending on the rapidity & the extent of the sodium drop, a battery of S/S appear, including:
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Lethargy, weakness, & foggy thinking are common. Personality changes can happen.
Low sodium levels often make pt nauseated If the situation is not corrected, seizures, coma, & even death can follow. |
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SIADH:Depending on the rapidity & the extent of the sodium drop, a battery of S/S appear, including:
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Lethargy, weakness, & foggy thinking are common. Personality changes can happen.
Low sodium levels often make pt nauseated If the situation is not corrected, seizures, coma, & even death can follow. |
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SIADH occurs when there is:
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too much vasopression (ADH) with inappropriate water retention and decreased blood Na levels
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SIADH Results from:
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–Inability to produce & secrete dilute urine
–Water retention –Increased extra cellular fluid volume –Hyponatremia Diseases that affect the hypothalamus -many different conditions and drugs |
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SIADH May be produced by:
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certain tumors such as lung cancer
chronic lung diseases. |
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Medicines associated with SIADH include common meds :
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–Antidepressants
–antianxiety agents, –antipsychotic agents, –seizure meds –desmopressin (DDAVP) |
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Physical Assessment of SIADH:
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Initially, S/S are R/T retention of water.
Most common complaints GI disturbances-loss of appetite, nausea & vomiting |
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Nursing Interventions SIADH:
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-Weighs pt & documents any recent weight gain
Checks pt extremities for presence of edema |
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Pt with SIADH have:
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free water, not salt, that is retained & edema is not usually present due to intracellular free water
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Water retention, hyponatremia, & resulting fluid shifts have an effect on:
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-CNS function, especially when serum sodium level drops.
-Normal serum Na 135-145. -S/S occur when serum Na level drops below 125, and especially below 115 |
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Clinical S/S SIADH:
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-Lethargy, headaches, hostility, uncooperativeness, disorientation
-Early sign -Change in LOC -Neurological S/S can progress from lethargy and headaches to decreased responsiveness, seizures, and coma. -Nurse assess deep tendon reflexes, which are often < or sluggish |
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V/S changes with SIADH
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tachycardia associated with increased fluid volume & hypothermia associated with CNS disturbance
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Normal lab values for serum osmolality:
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(285-295 mOsm/kg
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Osmolality is:
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is measures in milliosmoles per kilogram of water (mOsm/kg). The major determinants of plasma osmolality are Na, glucose, & urea
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Urine osmolality:
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24 hr specimen
500-800 mOsm/kg H20 -Random specimen: 50-1200 mOsm/kg/H20 |
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Urine specific gravity:
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1.003-1.030
1.002-1.035 High=dehydration Low=diabetes insipidus |
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concentrated urine :
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> than 50-100 mOsm/kg with normal vascular volume and normal renal function
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Extracellular fluid volume expansion affects:
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electrolyte levels in the serum and the urine
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Elevated urine sodium levels and specific gravity reflect an increased:
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concentration of the urine
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With SIADH, Serum sodium levels are decreased, often as low as 110 mEq/L (normal serum sodium 135-145 mEq/L) due to:
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extracellular volume expansion and increased Na excretion
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Fluid retention causes changes in:
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both plasma and urine osmolality
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In SIADH, Plasma osmolality is:
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Decreased
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In SIADH, the urine is _________ in relation to the plasma
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hyperosmolar
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The major determinants of plasma osmolality are
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Na, glucose, & urea.
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The _______ are mainly responsible for maintaining the concentration of body fluids within this range of osmolality.
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Kidneys
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When the plasma osmolality becomes abnormal, changes in the level of antidiuretic hormones (ADH) cause:
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the kidneys to conserve or increase the excretion of water to return the osmolality to normal
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ADH excess =
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water intoxication
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When water is reabsorbed assess for
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increased blood volume, fluid retention
concentrated urine, low urine output dilutional hyponatremia (same Na, more H20) muscle cramps and weakness anorexia, n/v, irritable, confused, disorient, seizure |
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Hyponatremia-
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a lower than normal concentration of sodium in the blood
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Hyponatremia Caused by
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by inadequate excretion of water of by excessive water in the circulating bloodstream
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In a severe case of hyponatremia the pt may experience
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water intoxication, with confusion and lethargy, leading to muscle excitability, convulsions, and coma.
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Treatment for hyponatremia
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Fluid and electrolyte balance may be restored by IV infusion of a balanced solution or a fluid restricted diet.
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SIADH: Diagnosis
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measure urine volume
and osmolality (Na < 134mmol/L se osmol >280mmol/kg SG>1005 low BUN, creatinine, Hb, Hct). |
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SIADH: Treatment
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If Na<125:
Restrict fluids 800 - 1000 ml/day. Daily weight Monitor 3% - 5% Saline solution IV Lasix if Na<105 (cardiac symptoms) |
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SIADH Diagnostic Study includes:
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Hyponatremia
Decreased plasma osmolality Urine sodium and urine osmolality elevated Elevated ADH levels++++++ Normal renal, adrenal, & thyroid functions |
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SIADH Nursing assessment
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Headache
Personality change, Confusion Irrritability Dysarthria(difficult, poorly articulated speech) Lethargy Impaired memory Restless Weakness Fatigue, Gait disturbances Weight gain+++++ |
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What is the cornerstone of SIADH treatment?
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Water restriction
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The maximum amount of water that pt with SIADH are allowed to drink is:
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just slightly more that the amount of urine they produce
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Nursing Interventions for SIADH
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-Restrict fluid intake (800-1000 cc/day)
-Daily weight Strict I & O -Monitor urine specific gravity -0.9 NS infusion(to raise the serum Na level if water intoxication is severe) -Monitor for hyponatremia -Lasix may be admin to block circulatory overload -Drugs-demeclocyclin HCL & lithium-may be admin to block renal response to ADH, intereferes with action of ADH -Drugs - Phenytoin - inhibits ADH release -Surgery & Chemo -to remove or destroy neoplasms that may be the underlying cause of this syndrome |
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What is the role of lithium in SIADH?
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Inhibits ADH action in kidney
Blocks renal response to ADH, interferes with action of ADH |
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What is the Therapeutic outcome of Lithium when a pt has SIADH?
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Decreased urine specific gravity
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Whar is Diabetes Insipidus?
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Transient or permanent metabolic disorder of the posterior pituitary
Deficiency of antidiuretic hormone (ADH) Primary or secondary Uncommon syndrome of posterior pituitary hypofunction |
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S/S of diabetes insipidus:
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Increased thirst - polydipsia
Increased urination - polyruia |
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What are the results of diabetes insipidus?
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ADH (Vasopression) deficiency, which prevents the kidneys from reabsorbing water
Inability to conserve water |
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Decreased ADH =
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diuresis
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With Diabetes Insipidus, water is lost, so assess for
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Kidneys produce large amts of dilute urine (5L-10L in 24hrs)
low urine specific gravity (1.001-1.005) polyuria (>urine output), polydipsia (>thirst) fluid deficit weight loss, turgor,dehydration, hypotension, constipation, shock |
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Vasopressin (Pitressin) :
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is ADH
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Vasopressin (Pitressin) Classification:
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Hormone (antidiuretic)
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Vasopressin (Pitressin) Uses:
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Treatment of diabetes insipidus due to deficient antidiuretic hormone
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Vasopressin (Pitressin) Route/Dose
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IM, sc, nasal spray
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Vasopressin Nsg Implications
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replace fluid: saline and glucose
monitor I & O check specific gravity observe electrolytes Monitor adverse reactions-abdominal cramps, angina, MI |
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Diabetes insipidus treatment:
Desmopressin (DDAVP) CLASSIFICATION |
Hormone (andiuretic)
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Diabetes insipidus treatment:
Desmopressin (DDAVP) INDICATION |
Management of primary nocturnal eneuresis unresponsive to other treatment modalities
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Diabetes insipidus treatment:
Desmopressin (DDAVP) ROUTE |
po, sc, IV, Intranasal
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Diabetes insipidus treatment:
Desmopressin (DDAVP) ACTION |
An anologue of naturally occuring vasopressin (antiuretic hormone). Primary action is enhanced reabsorption of water in the kidneys
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Diabetes insipidus treatment:
Desmopressin (DDAVP) THERAPEUTIC EFFECTS |
Prevention of nocturnal enuresis. Maintenance of appropriate body water content in diabetes insipidus
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Diabetes insipidus treatment:
Desmopressin (DDAVP) Nsg Implication: |
: Monitor urine & plasma osmolality & urine volume frequently. Assess pt for symptoms of dehydration (excessive thirst, dry skin & mucous membranes, tachycardia, poor skin turgor) Weigh pt daily & assess for edema
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ADH excess =
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water intoxication
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Diabetes insipidus
Clinical manifestations/assessment |
Polyuria; polydipsia
May become severely dehydrated Lethargic Dry skin; poor skin turgor Constipation |
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Diabetes insipidus
Medical management/nursing interventions |
ADH preparations
Limit caffeine due to diuretic properties |
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TSH excreted by the
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anterior pituitary gland
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What happens when TSH is excreted?
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Works as a negative feedback with T3 & T4 made in the thyroid gland
When T3 & T4 are high, TSH is low |
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Hyperthyroidism
Etiology/pathophysiology |
-Also called Graves’ disease
-Overproduction of the thyroid hormones -Exaggeration of metabolic processes -Exact cause unknown |
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Hyperthyroidism occurs more commonly in
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women than men
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Hyperthyroidism:
Clinical manifestations/assessment |
-Edema of the anterior portion of the neck
-Exophthalmos -Inability to concentrate; memory loss -Dysphagia -Hoarseness -Increased appetite -Weight loss -Nervousness Insomnia Tachycardia; hypertension Warm, flushed skin Fine hair Amenorrhea Elevated temperature Diaphoresis Hand tremors |
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Hyperthyroidism:
Medical management/nursing interventions |
Medications
Propylthiouracil Methimazole Radioactive iodine Subtotal thyroidectomy |
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When hyperthyroidism is suspected, a full diagnostic workup is warranted. What tests can be anticipated? What findings will support a positive diagnosis for the condition?
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* P. 1770 box 51-1 in book
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Hyperthyroidism can be managed with the use of medications as well as surgical intervention. When medications are prescribed, what is their mode of action?
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* p. 1770 table 51-1
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Hyperthyroidism:
Medical management/nursing interventions |
Postoperative
Voice rest; voice checks Avoid hyperextension of the neck Tracheotomy tray at bedside Assess for signs and symptoms of internal and external bleeding Assess for tetany Chvostek’s and Trousseau’s signs Assess for thyroid crisis |
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During the postoperative period of a patient with hyperthyroidism the patient’s environment is monitored. What characteristics are desired for the patient’s care environment? Why?
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keeping the bed in semi-fowlers position with pillows supporting the head and shoulders -pt should be cautioned about hyperextending the head -suction and trach equip should be available -cool mist humidifier |
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Hypothyroidism
Etiology/pathophysiology |
-Insufficient secretion of thyroid hormones
-Slowing of all metabolic processes -Failure of thyroid or insufficient secretion of thyroid-stimulating hormone from pituitary gland |
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Hypothyroidism is a common disorder. What populations are affected most?
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*
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What conditions can cause hypothyroidism?
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*
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Hypothyroidism:
Clinical manifestations/assessment |
-Hypothermia; intolerance to cold
-Weight gain -Depression -Impaired memory; slow thought process -Lethargic -Anorexia -Constipation -Decreased libido -Menstrual irregularities -Thin hair -Skin thick and dry -Enlarged facial appearance -Low, hoarse voice -Bradycardia -Hypotension |
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Hypothyroidism can affect both:
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newborns and adults
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What medical terminology is used to refer to the condition of hypothyroidism in newborns? In adults?
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*
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Hypothyroidism (continued)
Medical management/nursing interventions |
Medications
Levothyroxine (T4) Symptomatic treatment Keep patient warm Extra time for physical care so patient does not feel rushed Accurate records of stools & give stool softeners as ordered High protein, high fiber, low carbohydrate diet Fluids encouraged Watch for cardiac symptoms – chest pain, dyspnea, HR & rhythm Teach not to stop medication – will be taking for life Be aware of increased risk for adverse effects of sedatives, hypnotic, ad anesthetics |
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Hyperparathyroidism
Etiology/pathophysiology |
-Overactivity of the parathyroid, with increased production of parathyroid hormone
-Hypertrophy of one or more of the parathyroid glands -Chronic renal failure, pyelonephritis, glomerulonephritis -Parathyroid carcinoma is very rare with rapid progress and grave prognosis |
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Hyperparathyroidism affects:
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women between the ages of 30 and 70 years of age.
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Hyperparathyroidism
Clinical manifestations/assessment |
-Hypercalcemia
-Skeletal pain; pain on weight-bearing -Pathological fractures -Kidney stones -Fatigue -Drowsiness -Nausea -Anorexia -Constipation -Personality changes – even paranoia -Disorientation |
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What is the primary manifestation of hyperparathyroidism?
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Hypercalcemia is the primary manifestation
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Why is there pain associated with hyperparathyroidism?
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*
because calcium leaves the bnones and accumulates in the bloodstream and as a result the bones become demineralized causing skeletal pain, pain on weight bearing, and pathologic fractures. High level of Ca can also result in kidney stones |
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The cardiovascular system may be impacted by hyperparathyroidism. What will occur if this system becomes involved?
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*
hypertension and cardiac dysrhythmias may be present -changes in the serum calcium level may cause bradycardia and other cardiac irregularities |
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Hyperparathyroidism
Medical management |
-Removal of tumor
-Removal of one or more parathyroid glands |
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Hyperparathyroidism: Nursing Interventions
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Pre-op is help restore F&E balance
Strain urine for possible stones Cranberry juice help promote acidic urine Assess pain and medicate as needed per orders Post-op – same as thyroidectomy Careful I&O – tend to retain fluid and may have low UOP Assess for signs of hypocalcemia Good body mechanics to prevent pathologic fractures |
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When hyperparathyroidism is suspected, a series of diagnostic tests will be performed. A radiographic examination of the skeleton might be ordered. What results would be anticipated to support a positive diagnosis?
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*
x-rays may reveal skeletal decalcification PTH levels are increased alkaline phosphate levels are increased serum calcium levels are increased serum phosphorus is decreased |
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Hypoparathyroidism
Etiology/pathophysiology |
-Decreased parathyroid hormone
-Decreased serum calcium levels -Inadvertent removal or destruction of one or more parathyroid glands during thyroidectomy |
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A reduction of parathyroid hormones will result in hypoparathyroidism.
What will cause this disorder to occur? |
*
when there is a decrease in the parathyroid hormones there are decrease levels of serum calcium |
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Hypoparathyroidism
Clinical manifestations/assessment |
-Neuromuscular hyperexcitability
-Involuntary and uncontrollable muscle spasms -Tetany -Laryngeal spasms -Stridor -Cyanosis -Parkinson-like syndrome -Chvostek’s and Trousseau’s signs |
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Hypoparathyroidism
Diagnostic testing |
-Decreased serum calcium & increased urine calcium
-Increased serum phosphorus & decreased urine phosphorus |
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Hypoparathyroidism
Medical management/nursing interventions |
-Calcium gluconate or calcium chloride IV (slow) – if out of vein leads to tissue extravasation
-Vitamin D given orally to increase absorption and blood level of calcium |
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The management of hypoparathyroidism involves
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the administration of calcium gluconate or calcium chloride
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When developing a plan of care for hypoparathyroidism, what dietary recommendations should be made?
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*
contain foods high in calcium such as dairy products, dark green vegetables, soybeans, and canned fish with bones included |
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Hypoparathyroidism
Nursing Interventions |
-Monitor for signs of hypercalcemia
-Assess for respiratory distress, renal involvement and adverse reactions to calcium therapy such as bradycardia, syncope, and hypotension -Risk for injury R/T hypocalcemia |
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hypoparathyroidism
Client Teaching |
-Know S&S of early hypocalcemia
-Teach pt to monitor pulse for changes -Teach proper fluid balance – intake/output but mostly daily weight -Proper diet -Take calcium supplements as ordered |
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Hypercalcemia S/S
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N, vomiting, disorientation, anorexia, abdominal pain, and weakness
Assess for respir |
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Hyperparathyroidism
Etiology/pathophysiology |
-Overactivity of the parathyroid, with increased production of parathyroid hormone
-Hypertrophy of one or more of the parathyroid glands -Chronic renal failure, pyelonephritis, glomerulonephritis -Parathyroid carcinoma is very rare with rapid progress and grave prognosis |
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Hyperparathyroidism affects:
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women between the ages of 30 and 70 years of age.
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Hyperparathyroidism
Clinical manifestations/assessment |
-Hypercalcemia
-Skeletal pain; pain on weight-bearing -Pathological fractures -Kidney stones -Fatigue -Drowsiness -Nausea -Anorexia -Constipation -Personality changes – even paranoia -Disorientation |
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What is the primary manifestation of hyperparathyroidism?
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Hypercalcemia is the primary manifestation
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Hyperparathyroidism
Medical management |
-Removal of tumor
-Removal of one or more parathyroid glands |
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Hyperparathyroidism: Nursing Interventions
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Pre-op is help restore F&E balance
Strain urine for possible stones Cranberry juice help promote acidic urine Assess pain and medicate as needed per orders Post-op – same as thyroidectomy Careful I&O – tend to retain fluid and may have low UOP Assess for signs of hypocalcemia Good body mechanics to prevent pathologic fractures |
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Hypoparathyroidism
Etiology/pathophysiology |
-Decreased parathyroid hormone
-Decreased serum calcium levels -Inadvertent removal or destruction of one or more parathyroid glands during thyroidectomy |
