Endocrine Problems Flashcards
Diabetes Insipidus (DI)
Deficiency of production or secretion of ADH or with decreased renal response to ADH d/t injury to neurohypophyseal system
3 types of Diabetes Insipidus (DI)
- Central 2. Nephrogenic: 3. Primary
Central Diabetes Insipidus
(Neurogenic): interference in ADH synthesis or release (brain tumor, head trauma, brain injury, CNS infection)
Nephrogenic Diabetes Insipidus
inadequate renal response to ADH (in the setting of N ADH levels) (drug therapy esp. lithium, renal damage or hereditary renal disease)
Primary Diabetes Insipidus
(aka psychogenic): excessive water intake (lesion in thirst center, psychological disorder)
Clinical Manifestations (Central and Nephrogenic) of diabetes insipidus
◦ Polydipsia, polyuria (5-20 L/day) with very low specific gravity and low urine osmolality (dilute urine) ◦ Serum osmolality is elevated d/t hypernatremia caused by pure water loss from kidneys ◦ Patients compensate by drinking water ◦ May be fatigue from nocturia, may have generalized weakness ◦ If PO intake cannot keep up with urinary losses – hypovolemia results (weight loss, constipation, poor tissues turgor, hypotension, tachycardia, hypovolemic shock) ◦ CNS manifestations – irritability, mental dullness, coma ◦ Primary DI – overhydration and hypervolemia (vs. the dehydration and hypovolemia)
Diagnostic studies of Diabetes Insipidus
◦ ID cause – Hx and PE, water deprivation test
Thyroid Function
regulates energy, metabolism, growth and development
Thyroid Hormones
thyroxine (T3) and triiodothyronine (T3)
Thyroid Disorders
enlargement benign and malignant nodule, inflammation, hyper and hypo function
Goitre
Enlargement of the thyroid gland; may be associated with hyperthyroidism, hypothyroidism, or normal thyroid function.
Most common cause of goitre
Lack of iodine
Treatment of goitre
thyroid hormones, surgical removal for large goitres
Nodules
palpable deformity, increased incidence with age
Malignant nodules
Thyroid CA – most common endocrine CA
Thyroiditis
An inflammation of the thyroid gland that may cause hyperthyroid or hypothyroid manifestations.
Causes of thyroiditis
- Viral (subacute granulomatous thyroiditis), bacterial/fungal infection (acute thyroiditis) – abrupt onset painful (T3 T4 high then decrease; TSH low then increases) 2. Chronic autoimmune thyroiditis (Hashimoto’s thyroiditis) - can lead to hypothyroidism; thyroid tissues replaced by lymphocytes and fibrous tissue – most common cause of goitorus hypothyroidism (T3 T4 low, TSH high, antithyroid antibodies present) 3. Silent thyroiditis (T3 T4 high then decrease; TSH low then increases; RAIU decreased) 4. Postpartum thyroiditis
Hyperthyroidism
A clinical syndrome characterized by a sustained increase in synthesis and release of thyroid hormones by the thyroid gland
Thyrotoxicosis
A hypermetabolic state caused by excessive circulating levels of thyroxine, triiodothyronine, or both.
Grave’s Disease
An autoimmune disease of unknown origin, marked by diffuse thyroid enlargement and excessive thyroid hormone secretion. ◦ Develop antibodies that attach to TSH receptors and stimulate the thyroid to produce T3 and/or T4 – cause manifestations/thyrotoxicosis ◦ Disease pattern characterized by exacerbations and remissions and may progress to destruction of thyroid tissue (causes hypothyroidism)
Clinical Manifestations of Grave’s Disease
◦ Related to effects/amount of excess hormones ◦ Palpable or visualized goiter – may be able to auscultate bruit d/t increased blood supply ◦ Exophthalmos - protrusion of eyeballs d/t impaired venous drainage – edema, fate deposits ◦ See Table 51-6 p. 1405 for additional manifestations of thyroid hyperfunction
Complication of Grave’s disease
Thyrotoxic Crisis ‘Thyroid Storm’ – rare – intensified manifestations of hyperthyroid – medical emergency – can be induced by stressors (trauma, infection, surgery); heart and nervous tissue more sensitive to epinephrine and norepinephrine
Diagnostic Studies of Grave’s disease
◦ Labs – decreased TSH, elevated free T4(free: unbound to protein – only free T4 is biologically available) ◦ RAIU demonstrated increased and more diffuse uptake than other forms of thyroiditis
Goal of treatment of Grave’s disease
block effects of excessive hormones and stop their oversecretion
Medications used to treat Grave’s disease
ØAntithyroid Drugs ØIodine - high dose, (with antithyroid drugs) – inhibits synthesis of T3 and T4, blocs release of hormones, decreased vascularity of thyroid gland; for use during thyroid storm or prior to surgery ØBeta Blockers: (with antithyroid drugs) symptoms relief – decreased HR, BP
Radioactive Iodine Therapy for Grave’s disease
treatment of choice (unless pregnant) – damages or destroys thyroid tissue, limiting hormone secretion; high incidence of post treatment hypothyroidism
Subtotal Thyroidectomy for Grave’s disease
surgical removal; if goiter large and/or compression of trachea, or no response to other therapies
Hypothyroidism
Insufficient circulation of thyroid hormones resulting in a hypometabolic state.
2 types of hypothyroidism
Primary and Secondary
Primary Hypothyroidism
destruction of thyroid tissue, defective hormone synthesis
Secondary hypothyroidism
pituitary disease with decreased secretion of TSH or hypothalamic dysfunction with decreased secretion of TRH
Causes of hypothyroidism
• May be transient, related to thyroiditis, or from discontinuation of thyroid hormone therapy • Worldwide – iodine deficiency is the most common cause • Canada - adult atrophy of thyroid gland (end result of Hashimoto’s thyroiditis an Grave’s disease); also as a result of treatment for hyperthyroidism – surgical removal, or radioactive iodine therapy; drugs – Amiodarone, Lithium
Clinical Manifestations of hypothyroidism
Vary depending on severity and duration of deficiency ◦ Insidious and non-specific slowing of body processes ◦ Onset is slow ◦ Fatigue, lethargy, impaired memory, depression, slowed speech, decreased initiative and concentration ◦ Decreased CO and contractility, decreased exercise tolerance and SOBOE ◦ Anemia, easy bruising, increased lipids and triglycerides ◦ Constipation, cold intolerance, dry skin, hair loss, brittle nails ◦ Menstrual abnormalities – menorrhagia, anovulation, fertility issues ◦ See Table 51-6 p. 1405 for additional manifestations of thyroid hypofunction
Myxedema
The characteristic facies of severe, longstanding hypothyroidism (i.e., puffiness, periorbital edema, and masklike affect) caused by an accumulation of hydrophilic mucopolysaccharides in the dermis and other tissues. ◦ Severe longstanding hypothyroidism ◦ Accumulation of hydrophilic polysaccharides in the tissues ◦ Characterize facies- periorbital edema, puffiness, masklike effect
Myxedema coma
The progression of the mental sluggishness, drowsiness, and lethargy of hypothyroidism to a notable impairment of consciousness or coma that is a medical emergency.
Diagnostic studies of hypothyroidism
Labs: TSH and free T4 (correlated with Hx and PE); increased TSH = defect in thyroid, decreased TSH – defect in pituitary or hypothalamus
Goal of treatment of hypothyroidism
restoration of erythroid state
Hormone replacement therapy of hypothyroidism
levothyroxine – doses adjusted based on TSH value
Acromegaly
A condition caused by excessive secretion of growth hormone and characterized by an overgrowth of the bones and soft tissue
Acromegaly in children (Gigantism)
over growth of bones and soft tissues (epiphyses open) Gigantism
Acromegaly in adults
thickening of bones and soft tissues (epiphyses closed) rare Acromegaly
What usually causes acromegaly
Usually caused by benign pituitary tumor (adenoma)
Clinical manifestations of acromegaly
◦ Slow onset, 3rd-4th decade ◦ enlarged hands and feet with associated joint pain, potential arthritis; enlargement of bones and soft tissues of face and head; ◦ Dysphasia d/t enlarged tongue ◦ Voice deepened d/t hypertrophy of the vocal cords ◦ Sleep apnea d/t narrowed airway ◦ Skin thick, leathery, oily ◦ Peripheral neuropathy and muscle weakness ◦ Menstrual disturbances ◦ Colon CA and polyps ◦ Enlarged pituitary – pressure on surrounding structures – can impact vision, headaches ◦ Mobilizes free fatty acids – atherosclerosis ◦ GH antagonizes insulin – hyperglycemia – DM ◦ Cardiomegaly, ventricular hypertrophy, angina, HTN
Drugs used to treat acromegaly
- somatropin analogue (decreases GH levels) - dopamine agonists (suppress GH secretion) - GH receptor agonist ( directly blocked GH action)
Prolactinoma
Prolactin secreting adenoma– most frequently occurring pituitary tumor
Prolactinoma manifestations in women
ovulatory and menstrual abnormalities, decreased libido, hirsutism
Prolactinoma manifestations in men
ED, decreased libido and sperm density
Visual problems in prolactinoma due to:
tumor pressure
Prolactinoma therapies
drug therapy (dopamine agonists); surgery, radiation (last resort)
Hypopituitarism
A rare disorder that involves a decrease in one or more of the pituitary hormones. Ant Pit (ACTH, TSH, FSH, LH, GH, prolactin; Post Pit (ADH, Oxytocin)
Hormones of the pituitary gland
Ant Pit (ACTH, TSH, FSH, LH, GH, prolactin; Post Pit (ADH, Oxytocin)
Causes of Hypopituitarism
autoimmune disorders, infections, pituitary infarction (Sheehan’s syndrome), trauma, radiation, surgery
Hypopituitarism diagnostics
Labs to measure hormone levels; CT/MRI
Hypopituitarism treatment
directed at cause, hormone replacement therapy
Syndrome of inappropriate antidiuretic hormone (SIADH)
a condition characterized by fluid retention, serum hypo-osmolality, dilutional hyponatremia, hypochloremia, and concentrated urine in the presence of normal or increased intravascular volume; results from an abnormal production or sustained secretion of antidiuretic hormone despite normal or low plasma osmolarity.
Clinical Manifestations of SIADH
◦ Dependent on severity ◦ S & S hyponatremia ( cramps, muscle weakness, vomiting, abdominal cramps, muscle twitching, seizures) ◦ Low urinary output and increased body weight ◦ Decreases serum Na and plasma osmolality levels – cerebral edema, headache, seizure, coma
SIADH Diagnostic Studies
◦ Urine and serum osmolality (increased urine specific gravity, decrease serum osmolality), ◦ Serum Na level (< 134 mmol/L)
Collaborative care of SIADH
◦ Treatment is directed at cause and based on severity ◦ Goal – restore normal fluid volume and osmolality ◦ Fluid restriction 800-1000mL/24H (mild symptoms, Na > 125 mmol/L) ◦ Hypertonic IV saline carefully, gentle diuresis(severe, neuro S&S, Na <120 mmol/L ) ◦ Chronic – fluid restriction, medications ◦ See Table 51-2 for Nursing Assessment/Management of SIADH
Collaborative care in Diabetes Insipidus
◦ Based on cause, restoration of fluid and hormonal replacement ◦ Acute DI – hypotonic saline to replace urine output ◦ Hormone replacement – Desmopressin (analogue of ADH) , PO, IV, nasal spray
