patho pharm II -exam 2 - Endocrine Disorders 9 points
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- Syndrome of Inappropriate ADH
- Overproduction of ADH secretion without normal stimuli.
Ectopic ADH =
and usual sources:
- Ectopic ADH= Not from the pituitary
- Usual sources are cancer cells- (Small cell adenocarcinoma is most common)
- Less common causes:
- CNS disorders (brain tumor)
- Pulmonary disorders (pneumonia, TB)
- Drugs (Chemo)
- psychosis, myxedema
SIADH results in inappropriate _____ of water at distal tubules leading to water ______ or _______.
SIADH results in inappropriate reabsorption of water at distal tubules leading to water overload or intoxication.
SIADH results in what clinical manifestations?
- 1. Decreased urine output
- 2. Edema - Water intoxication
- 3. Hyponatremia- serum/ Hypernatremia- urine
- 4. Hyposmolality- serum/ hyperosmolality -urine
- 5. Fatigue, confusion, convulsions - twitches
- 6. Anorexia, Abd cramps, N/V
- 7. Dyspnea, HTN
SIADH- diagnostic findings:
Serum= Hyponatremia (dilutional), Hyposmolality
Urine= Hypernatremia, Hyperosmolality, High urine specific gravity
SIADH - nursing considerations/Interventions
- Fluid volume excess
- 1. Correct causitive problem- if possible
- 2. Monitor of electrolyte/osmolality
- 3. Fluid restricion (<800-1000cc/day)
- 4. Diuretics
- 5. Sodium replacement - Hypertonic saline IV
- 6. Pharm- lithium, demeclocycline interfere w. ADH action, Dilantin interfere w. ADH release
** Assess CNS changes, distention, BP, HR, UO, I&O
Diabetes Insipidus =
Deficient ADH secretion
Diabetes insipidus makes the body unable to _____ water resulting in ____ ____ _____ and tissue ______.
Diabetest insipidus makes the body unable to conserve water resulting in large volume diuresis and tissue dehydration.
What is the most common type of Diabetes insipidus?
- Neurogenic: insufficient amounts of ADH
- - idiopathic
- - posttraumatic
- - post-surgical
Other uncommon types: nephrogenic: insuff response of kidneys to adh; and Psychogenic (rare): compulsive water drinking
What is the cause of neurogenic diabetes insipidus?
Lesions of the hypothalamus, pituitary stalk, posterior pituitary.
- May develop due to:
- *brain tumor or head trauma
- *cerebral -aneurysms, thrombosis, infetions
- *Immunologic disorders
Pathophysiology of diabetes insipidus:
- Excretion of large amounts of dilute urine -->
- Inrease in serum osmolality --> Hypernatremia --> Dehydration --> Polydipsia
Clinical manifestations of Diabetes insipidus
- Polyuria, Polydipsia, Nocturia
- Hypernatremia - blood
- Hyperosmolality - blood/ hyposmolality - urine
Diagnostic findings for Diabetes Insipidus
Serum = hyperosmolality, hypernatremia
Urine= low specific gravity, hyposmolality, hyponatremia.
Diabetes Insipidus - Nursing considerations/treatment
- (Fluid volume deficit)
- 1. Administer hypotonic fluids (0.45 NS).. or oral 40-50 glasses/day (9-10 L)
- 2. ADH replacement- Synthetic vasopressin (DDAVP) or drugs that potentiate endogenous ADH
- 3.Monitor: I&O, daily wt, urine specific gravity measures, VS OFTEN
- 4. Provide Skin and oral care
Abnormal pituitary function results in ...
- Abnormal ADH production=
- 1. SIADH
- 2. Diabetes Insipidus
What is Acromegaly?
Late onset overproduction of growth hormone
What is gigantism?
Early onset overproduction of growth hormone.
Complications of Acromegaly
- 1. Bony proliferation
- 2. Peripheral nerve entrapment
- 3. Insulin resistance
- 4. HTN and heart failure
Acromegaly is characterized by ...
- Enlarged jaw, forehead, hands, feet and tongue
- Increased sebaceous and sweat glands
- Barrel chest
- Weakness, muscular atrophy, footdrop, and sensory changes in the hands.
Treatment for Acromegaly
Surgical removal or radiation of tumor (the cause)
Purpose of thyroid hormones and types
- ◦Affects growth and maturation of tissues
- ◦Helps regulate serum calcium
- ◦Thyroxine (T4) and Triiodothyronine (T3)
- ◦Calcitonin - affects serum calcium levels
Abnormal thyroid function results in...
- 1. Graves disease
- 2. Nodular Thyroid Disease
- 3. Thyrotoxic Crisis (aka thyroid storm)
- 1. Primary
- 2. Hashimoto
- 3. Myxedema
Definition of Graves Disease
Familial auto-immune disorder that causes hyperthyroidism because of negative feedback.
*Generalized acceleration of body processes
Pathophysiology of Graves disease:
Thyroid autoantibodies (TSI) stimulate thyroid gland --> also decreases thyroid regulators TSH and TRH --> Hyperthyroidism
Graves disease is characterized by one or more of the following...
- Goiter (visible enlargement of thyroid gland)
- Opthalmopathy (eye disease)
- Dermopathy (skin disease)
Treatment for Graves disease=
- Drugs to suppress thyroid activity (PTU)
- Radioactive Iodine
- Surgery (thyroidectomy)
What are some clinical manifestations of hyperthyroidism?
- 1. Fine hair/Hair loss
- 2. Exopthalmos - bulging eyes , Goiter
- 3. Sweating
- 4. Tachycardia, HTN
- 5. Weight loss with INCREASED appetite
- 6. Decreased libido and irregular menstration
- 7. Tremors, Muscle wasting
- 8. decreased attention span, nervousness, insomnia
Nodular Thyroid disease =
Goiter , Visible enlargement of the thyroid gland due to hyperthyroidism
Causes of Nodular thyroid disesase:
- Normal increases in TH (puberty, pregnancy)
- Iodine deficiency
- Viral Infection
- Immunologic disorder
Thyrotoxic Crisis causes =
- "Thyroid Storm"
- -Under-treated hyperthyroidism
- -Excessive stress
- - Infection
- -Pulmonary or cardiac disorders
- -Inadequate treatment for thyroid surgery
Clinical manifestations of thyrotoxic crisis =
- Tachycardia, Hypertension
- Heart failure (High output)
- N & V, Diarrhea, Dehydration
Treatment and prognosis of thyrotoxic crisis
- Propylthiouracil (PTU) -(Thyroid antagonist)
- ◦Inhibits synthesis of T3 and T4
- ◦Inhibits iodine uptake in thyroid gland
Prognosis: Fatal within 48 hours if untreated.
Definition of hypothyroidism:
= Everything slows down.
- 1. Primary hypothyroidism – Decrease in amount of circulating TH
- ◦Etiology: Non-bacterial inflammation, Viral infection, Thyroidectomy, Toxic effect of medications (Lithium, Amiodarone), Age
- 2. Hashimoto Disease (Autoimmune Thyroiditis)
- ◦Synthesis of thyroid hormone decreased
- ◦Etiology: thyroid antibodies and infiltrating lymphocytes destroy thyroid tissue, Genetic disposition
What is the most severe form of hypothyroidism?
Myxedema - occurs secondary to altered composition of dermis and other tissues, and edema.
Clinical manifestations: Non-pitting edema, especially around eyes, Thickening of tongue, Hoarseness
Labs: Hyponatremia, Hypoglycemia, anemia, bradycardia, decreased o2, increased CO2 and pH
Clinical manifestations of hypothyroidism:
- Symptoms are proportional to degree of TH deficiency
- All body systems affected
- - Decreased metabolic rate
- - Goiter may develop (Decreased TH à Increased TSH à Hypertrophy of thyroid cells àGoiter)
- **LOOK UP- Tissues become water logged due to separation connective tissue by increased amounts of protein and mucopolysaccharides (p. 637).
Ionizing radiation (Chernobyl – 1986)
- ◦Thyroid nodule on palpation
- ◦Needle aspiration of nodule
- ◦Near-total thyroidectomy
- ◦Total thyroidectomy
- ◦Post-op radio-active iodine
Adrenal Cortical Hyperfunction =
= Cushings syndrome: exaggerated actions of gluticosteroids cause excessive secretion of cotisol from adrenal cortex
What is the cause of Cushingings syndrome?
- 1. Adrenal Tumor
- 2. Corticosteroid medications such as prednisone, solu-medrol
What are some clinical manifestations of Cushing Syndrome?
- Weight gain (fat redist./water retention)
- Moon Face
- Buffalo hump (kyphosis)
- Truncal Obesity (wt in abdomen)
- Glucose intolerance (Hyperglycemia)
- Muscle wasting (protein catabolism)
- Osteoporosis (protein wasting)- fractures, reduced height
- Renal stones (HYPERCALCEMIA)
- Collagen loss- fragile skin and capillaries, easy bruise, striae
- Immunosuppression- Poor wound healing
- Mood changes
- Elevated androgens (Sx in women)- facial hair, acne, irreg .
Diagnosis of Cushing syndrome
- Complicated and challenging!
- Labs: Hyperglycemia*, Glycosuria, Hypokalemia, Metabolic alkalosis
- Elevated serum ACTH & cortisol levels
- MRIs, etc.
Adrenal Cortical Hypofunction=
- = Addison's Disease
- Hyposecretion of cortisal from adrenal cortex
What is the cause of Addison's disease?
- exogenous glucocorticosteroids
- ACTH hyposecretion
Clinical manifestations of addisons disease:
- (due to low cortisol & aldosterone)
- Weakness and fatigue
- GI dist- pain, diarrhea, anorexia
- Hyperpigmentation with areas of vitiligo -loss of pigment
- Decreased tolerance of stress
How is Addison's disease diagnosed?
- Hypoglycemia, Hyperkalemia, Hyponatremia
- decreased cortisol in blood and urine
- Altered ACTH levels
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