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HCR240-Chapter24EndocrineDisorders1.pptx

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Chapter 24

Endocrine Disorders

Basic Concepts

Endocrine glands secrete chemical messengers (hormones) into bloodstream

Many endocrine processes involve several tissues

Hypothalamus

Sends signals to the pituitary gland

Anterior pituitary

Receives hormonal signals from hypothalamus

Basic Concepts (continued)

Posterior pituitary

Releases hormones synthesized by hypothalamus

End organs

Targets for pituitary hormones, may or may not secrete additional hormones

Hypothalamic-Pituitary-Hormonal Axis

Link between hypothalamus-pituitary-end organ

Pituitary (hypophysis)

Anterior pituitary (adenohypophysis)

Blood vessel connection with hypothalamus (hypothalamus-hypophyseal portal system)

Releases tropic hormones

Posterior pituitary (neurohypophysis)

Neural connection with hypothalamus

Hormones made by hypothalamus, stored and released by posterior pituitary

Pituitary as Master Gland

Growth hormone

Prolactin

Adrenocorticotropic hormone

Thyroid-stimulating hormone

Follicle-stimulating hormone

Luteinizing hormone

Posterior

Antidiuretic hormone

AKA: arginine vasopressin

Oxytocin

Endocrine Regulation

Negative feedback mechanism

End-product hormone negatively feeds back to prevent further stimulatory signals

Example: thyroid hormones suppress thyroid-stimulating hormone production

Receptor activity

Upregulation

Increased receptor sensitivity and number

Downregulation

Decreased receptor sensitivity and number

Endocrine Regulation (continued)

Three Major Types of Endocrine Conditions

Hormone deficiency

Gland destruction

Autoimmune, infection, tumor

Hormone excess

Tumor, autoimmune, genetic mutation

Hormone resistance

Usually genetic (lack hormone receptor or ability to respond)

Endocrine Dysfunction

Hypofunction

Inadequate amount of hormone

Hyperfunction

Excessive amount of hormone

Three levels of dysfunction

Primary

Endocrine gland itself

Secondary

Abnormal pituitary activity

Tertiary

Dysfunction of hypothalamic origin

Endocrine Dysfunction Causes

Autoimmune

Antibodies target endocrine gland, may cause hypofunction or hyperfunction

Neoplasia

Hypofunction or hyperfunction of gland itself or any endocrine tissue the gland affects

Some cancers: paraneoplastic disorder in which cancer cells secrete hormone-like substances

Endocrine-disrupting compounds (EDC’s)

Chemical in environment that can alter endogenous hormone functions

Diabetes Insipidus (DI)

Posterior pituitary hypopituitarism

Lack of ADH or response to ADH

Dilute, large volume urine

Plasma concentration increases

Categories of disease

Central DI

Lack ADH from the posterior pituitary

Nephrogenic DI

Kidney fails to respond to ADH

Distinguish by administering ADH to see if kidneys can respond, if so, central DI

Diabetes Insipidus (DI) (continued)

Signs and symptoms

Frequent urination, thirst, dehydration, disorientation, seizures

Blood test will show high osmolarity and hypernatremia

Urine osmolarity and specific gravity will be low

Diabetes insipidus differs from diabetes mellitus (no hyperglycemia in DI)

Treatment

ADH administration (if central DI)

Syndrome of Inappropriate ADH (SIADH)

Excessive ADH

Causes: brain injury or neurosurgery

Paraneoplastic disorder

Causes fluid retention

Concentrated urine, dilute plasma, hypervolemia

Treatment

Fluid restriction

Slow correction of hyponatremia

ADH receptor antagonists may be used

Thyroid

Triiodothyronine (T3) and thyroxine (T4)

Iodine required for synthesis

Thyroxine

Regulate body metabolism

Thyroid disorder more common in women

Primary thyroid disorders most common

Enlarged thyroid can indicate hypo- or hyperfunction

Goiter

Enlargement of the thyroid

May or may not present with thyroid dysfunction signs and symptoms

May develop with:

Excess TSH

Low iodine levels

Goitrogens

Foods or other substances that promote thyroid gland enlargement

Hypothyroidism

Hashimoto’s thyroiditis

Autoimmune disorder

Anti-thyroglobulin antibody and anti-thyroperoxidase antibody

Other causes

Drugs

Genetics

Thyroiditis (postpartum period especially high incidence)

Congenital hypothyroidism: cretinism

Hypothyroidism: Signs and Symptoms

Cold intolerance

Weight gain

Lethargy

Fatigue

Memory deficits

Poor attention span

Muscle cramps

Constipation

Decreased fertility

Puffy face

Hair loss

Brittle nails

Systemic Effects of Hypothyroidism

Hyperlipidemia

Yellow-orange skin (elevated carotene levels)

Anemia

Decreases filtration by kidney

Pendred’s syndrome: defective iodine incorporation into thyroid hormone

Myxedema: Adult severe hypothyroidism

Subclinical hypothyroidism: present in elderly

Diagnosis of Hypothyroidism

Primary: high TSH, low free T3, low free T4

Secondary: low TSH, low free T3 and T4

Hashimoto’s thyroiditis antibodies

Antithyroglobulin (anti-Tg)

Antithyroperoxidase (anti-TPO)

Ultrasound

Recommended: thyroid test in women at age 35 and every 5 years after

Treatment of Hypothyroidism

Replacement hormone: levothyroxine

Surgical intervention if necessary

Myxedema coma

Severe hypothyroid condition

Will progress to confusion and coma if untreated

Hyperthyroidism

Elevated free T3 and free T4

Graves’ disease

Most common cause

Autoimmune stimulation of the thyroid gland

Hyperthyroidism (continued)

Other causes

Subacute thyroiditis

Thyroid adenoma

Excessive TSH

Subacute thyroiditis

Toxic multinodular goiter

Excessive iodine ingestion

Jod-Basedow syndrome

Secondary to pregnancy, HCG is similar to TSH

Graves’ Disease

Thyroid-stimulating antibodies

Bind to thyrotropin receptors

Gland enlargement

Continual synthesis thyroid hormones

Graves’ Disease (continued)

Nervousness

Insomnia

Sensitivity to heat

Weight loss

Enlarged thyroid gland

Atrial fibrillation

Increased HR

Increased sympathetic nervous system sensitivity

Exophthalmos

Wide-eyed stare

Extraocular area filled with mucopolysaccharides

Graves ophthalmopathy

Periorbital edema and bulging of the eyes

Hypothyroidism vs. Hyperthyroidism

Hyperthyroidism Diagnosis

Primary: low TSH, high free T3 and T4

Secondary: high TSH, high free T3 and T4

Antibodies for Graves’ disease

Anti-thyroid peroxidase (anti-TPO)

Thyroid stimulating immunoglobulin

Ultrasound with color-Doppler evaluation

Radioactive iodine scanning and iodine uptake

Treatment of Hyperthyroidism

Antithyroid hormone medication propylthiouracil (PTU)

Radioactive iodine treatment

Surgery

If gland removed, replacement thyroid hormone (levothyroxine) needed for life

The Adrenal Gland: Cortex and Medulla

Medulla

Glucocorticoids

Cortisol

Androgens

Mineralocorticoids

Aldosterone

Cortex

Epinephrine

Norepinephrine

Adrenal Insufficiency

Secondary

Decreased ACTH

Primary

AKA: Addison’s disease

Autoimmune destruction adrenal cortex

Antibodies to adrenal cortex

Antibodies to steroid enzymes

Hypoadrenalism and Glucocorticoids

Hypoadrenalism can also be due to exogenous glucocorticoids

With prolonged glucocorticoid use, CRF-ACTH signals to adrenal cortex suppressed

Adrenal gland down regulates receptors

Steroid usage should not be abruptly stopped

Individual may be unable to respond to stressor

Smallest dosage of steroid needed should be given to patient to lessen adrenal atrophy

Adrenal Insufficiency Symptoms

Weakness

Hypotension

Easy fatigue

Emotional lability

Anorexia

Hypoglycemia

Electrolyte imbalances

Hyponatremia

Hyperkalemia

Tanned appearance due to melanocyte-stimulating hormone (MSH)

ACTH and MSH arise from same precursor molecule

Women

Loss of pubic and axillary hair

Amenorrhea

Adrenal Insufficiency (continued)

Diagnosis

Rapid ACTH test

With ACTH administration, cortisol should rise within 30 minutes

No cortisol rise: adrenal cortex insufficiency

Treatment

Daily replacement of glucocorticoid and mineralocorticoid

Parenteral steroid coverage in times of major stress, trauma, surgery

Hyperadrenalism

AKA: hypercortisolism

Cushing’s disease

Elevated ACTH, tumor in pituitary

Cushing’s syndrome

Elevated cortisol, hyperfunction of adrenal cortex

Exogenous steroids most common cause of Cushing’s syndrome

Hyperadrenalism (continued)

Causes

Pituitary adenoma

Cushing’s disease

Cushing’s syndrome

Adrenal hyperplasia, adrenal neoplasm

Carney complex

Genetic disorder

McCune-Albright syndrome

Cushing’s syndrome and precocious puberty

Secretion of ACTH from tumors

Hyperadrenalism Signs and Symptoms

Weight gain

Redistribution of body fat to the face, trunk, and abdomen

Puffy face called “moon facies”

Extra subcutaneous fat in the cervicothoracic area called “buffalo hump”

Increase in the waist-to-hip circumference ratio

Striae

Easy bruising and poor wound healing

Women

Hirsutism

Male pattern hair growth

Amenorrhea

Hyperadrenalism Signs and Symptoms (continued)

Effects of High Cortisol Levels

Block the action of insulin

Glucose intolerance and hyperglycemia

Inhibit bone formation and accelerates bone reabsorption

Osteopenia, osteoporosis

Suppress immune response

Hypertension

Diagnosis of Hyperadrenalism

Serum levels

Elevated WBCs, hyperglycemia, hypokalemia

Salivary levels of cortisol, 24-hour urine cortisol

Dexamethasone suppression test

Administer dexamethasone

Serum cortisol should be suppressed

Cushing’s syndrome: no cortisol suppression with dexamethasone

MRI, CT scan

Treatment of Cushing’s Syndrome

Surgery

Ketoconazole

Suppress cortisol

learning guide M6

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