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Endocrine Thyroid, Adrenal, ADH

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Lori Crawford

on 8 November 2013

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Transcript of Endocrine Thyroid, Adrenal, ADH

Dr. Lori D. Crawford, PharmD, BCPS
Endocrine Lecture
Produces 90% T4 & 10% T3
Affects endo, repro,GI, CV, pulmonary
Primary hyperthyroidism
increase thyroid hormone is synthesized
Secondary hyperthyroidism
Clinical Manifestations
Thyroid gland normally enlarges in response to an increase secrection of TSH may occur in puberty, preganancy, or idodine deficiency
When condition resolves, TSH secrection subsides and thyroid gland returns to size
Irreversible changes may have occurred in some follicular cells
So that such cells then function autonomously and produce excessive thyroid hormone
Hyperfunctioning nodules is toxic multinodular goiter
One nodule is toxic adenoma
Nodular thyroid disease
Graves Disease

Subacute thyroiditis
Nonbacterial inflammation of the thyroid often preceded by viral infection Accompanied by fever, tenderness, and enlargement of the thyroid
Iatrogenic hypothyroidism
Radioiodine thyroid ablation
Medications (lithium and amiodarone)
Postpartum thyroiditis
Occurs within 6 months of delivery
Autoimmune disease that results in stimulation of thyroid gland
T lymphocytes are sensitized to thyroid antigens
This stimulates B cells to produce immunoglobulins G antibodies or thyroid-stimulating immunoglobulins
Bind to TSH receptors in the thyroid
Cause synthesis and secretion of thyroid hormone
Graves Disease
Thyroid storm death can occur within 48 hours
Most often in individuals who have undiagnosed or partially treated severe hyperthyroidism
Hyperthermia, tachycardia, heart failure, agitation, vomiting or diarrhea
Thyrotoxic Crisis
Hashimoto disease
Results in gradual inflammatory destruction of thyroid tissue
Infiltration of lymphocytes and circulating thyroid autoantibodies (antithyroid peroxidase and antithyroglobulin antibodies)
Autoreactive T lymphocytes, antibody activation of natural killer cells, cytokines, induction of apoptosis involved in tissue destruction in Hashimoto thyroiditis
Occurs in genetic predisposed individuals associated with high iodine intake, selenium deficiency, smoking, & chronic hepatitis C
Cushing disease
Excessive anterior pituitary secretion of ACTH
Cushing syndrome
Excessive level of cortisol, regardless of cause
Disorders of the adrenal cortex
Primary adrenal insufficiency (Addison disease)
Secondary hypocortisolism
Adrenocorticol Hypofunction
Addison Disease
Anorexia, Vomiting, Nausea
Vitiligo (white patchy areas of depigmented skin
Addisonian crisis - hypotension and vascular collapse
Adrenal medulla hyperfunction
Caused by tumors derived from the chromaffin cells of the adrenal medulla
Secrete catecholamines on a continuous or episodic basis
Disorders of the adrenal medulla
Hypersecretion of ADH
Enhanced renal water retention
Increases permeability to water thus increasing water reabsorption by the kidneys
Results in expansion of extracellular fluid volume that leads to dilutional hyponatremia, hypoosmolarity, more concentrated urine
Ectopic secretion of ADH by tumor cells
Pulmonary disorders
CNS such as meningitis & trauma
Medications such as chlorpropamide, antidepressants, NSAIDS
•Insufficiency of ADH
Neurogenic DI
Insufficient amounts of ADH
Inadequate response to ADH
•Both lead to inability of the kidney to increase permeability to water
•Leads to excretion of large volumes of dilute urine and increase in plasma osmolality
Diabetes Insipidius
T4 and T3
Transported in the bloodstream primarily by three proteins
i. thyroxine-binding globulin
ii. transthyretin (TTR)
iii. albumin
T4 is secreted solely from the thyroid gland
Less than 20% of T3 is produced in the thyroid
Majority of T3 is formed from the breakdown of T4 catalyzed by the enzyme 5-monodeiodinase found in extrathyroidal peripheral tissues
Primary hypothyroidism
Thyroid function test
Serum TSH concentration
Serum total T4 concentration
Serum total T3 concentration
Serum free T4 (or T3) free hormone that is unbound
Thyroid stimulating antibodies
Thyrotropin receptor antibodies
Thyroid biopsy
Thyroperoxidase antibodies
Laboratory Tests
A midnight plasma cortisol
Late-night salivary cortisol
24-hour urine free cortisol
Cushing Disease Clinical Manifestation
Disorders of the adrenal cortex
Primary hyperaldosteronism (Conn disease)
Secondary hyperaldosteronism
Hyperaldosteronism Clinical Presentation
muscle weakness, fatigue, paresthesias, and headache.
Tetany/paralysis/polydipsia/nocturnal polyuria
Laboratory Tests
A plasma-aldosterone–to–plasma-renin-activity ratio (PA:PRA), or aldosterone-to-renin ratio (ARR) greater than 20 is suggestive of primary aldosteronism
Lab findings
Suppressed renin activity, elevated plasma aldosterone concentrations, hypernatremia (>142 mEq/L), hypokalemia, hypomagnesemia, elevated bicarbonate concentration (>31 mEq/L), and glucose intolerance

Characterize the manifestations of hypothyroidism and hyperthyroidism including basal metabolic rate, sympathetic nervous system response, weight, temperature tolerance, GI function, cardiovascular function, respiratory function, muscle tone and reflexes, general appearance, and general behavior.
Compare the disorders of hyperthyroidism to include cause, manifestations and complications: Graves disease, nodular goiter disease, and thyrotoxic crisis.
Discuss the similarities and differences of the disorders of hypothyroidism: subacute thyroiditis, Hashimoto disease (autoimmune thyroiditis), painless thyroiditis, postpartum thyroiditis, myxedema, myxedema coma.
Describe the etiology, pathogenesis, and manifestations of hyperfunction and hypofunction of the adrenal cortex: Cushing disease, Cushing syndrome, primary hyperaldosteronism, secondary hyperaldosteronism, and Addison disease.
Describe the cause, clinical manifestations, and adrenal medulla hyperfunction.
Compare and contrast the similarities and differences of SIADH and diabetes insipidus, including causative factors, pathophysiology, and manifestations.
Learning Objectives
The major homeostatic function of the posterior pituitary is the control of plasma osmolality as regulated by ADH
ADH acts on vasopressin (V2) receptors of the renal tubular cells to increase their permeability
Increased permeability causes water reabsorption into the blood and concentrated urine
ADH is also called vasopressin because at high doses it can cause vasoconstriction and result in increase in arterial blood pressure
SIADH Clinical Manifestations
Clinical Manifestations related to the severity and onset of the hypotonic hyponatremia

Na decreases from 140mEq/dL to 130mEq/Dl
Thirst, impaired taste, anorexia, fatigue

Na decreases from 130mEq/dL to 120 mEq/dL
GI- vomiting, abdominal cramps,

Na falls below 115mEq/dL
Confusion, lethargy, muscle twitching, and convulsions
SIADH Diagnosis
Serum hypoosmolality < 280 mOsm/kg
Hyponatremia <135 mEq/l
Urine hyperosmolarity
Urine sodium excretion that matches sodium intake
Normal adrenal and thyroid function must exist
Absence of conditions that can alter volume status
DI Clinical Manifestations
continuous thirst
DI Diagnosis
Low urine specific gravity <1.010
Urine osmolality <200 mOsml/kg
High serum osmolality greater or equal to 300mOsm
Continued diuresis despite a serum sodium of 145mEq/L
Which of the following statements is true regarding the pathophysiology of type 2 diabetes mellitus?
a. Insulin secretion increases glucose hepatic production
b. Glucagon-like activity 1 (GLP-1) secretion is decreased
c. Glucagon secretion decreases glucose hepatic production
d. Amylin activity is decreased
Mr. Johnson has polyuria and polydipsia. His hemoglobin A1C is 8% and he has a fasting blood glucose of 130 mg/dl. He serum sodium (Na) is 142 mg/dL . He states that he has been excessively eating more despite losing weight. These are indications of:
a. Diabetes Insipidus
b. Hyperthyroidism
c. Diabetes Mellitus
d. Addison disease
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