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UNIT SIX

ALTERATION IN ENDOCRINE FUNCTION


Introduction
Glands of the endocrine system secrete various
hormones

Hormones play a key role in maintaining normal


homeostasis as well allowing the body to deal with
periods of physiologic stress.

Abnormalities of endocrine glands generally fall into one


of the several categories:
 Hypersecretion

 Excess activity of a specific hormone or hormones


 May be due to overproduction of a hormone due to abnormal
glandular function, glandular hypertrophy/hyperplasia or the
presence of tumors that secrete hormone
 2. Hyposecretion
 Reduced activity of a specific hormone or hormones
 May be due to atrophy of glandular tissue or damage from
autoimmune attack, infection or neoplasia
 3. Altered responsiveness of a tissue to a specific hormone
 Tissue no longer responds to a specific hormone
 May involve downregulation of receptors or altered
receptor/secondary messenger function
 Circulating levels of hormone may be normal or even elevated
(example: type II diabetes)
Alteration of thyroid function
There are two main hormones produced by the thyroid
gland:
 Thyroxin (T4) and

 Triiodothyronine (T3).

Both hormones are derived from the amino acid


tyrosine and contain iodine that is extracted from the
blood.
The release of thyroid hormones from the anterior
pituitary is regulated by TRH secreted from the
anterior pituitary gland.
Hypothyroidism
 May be a primary condition resulting from a defect within the

thyroid itself or can be secondary to a lack of stimulation by TSH.


 Dietary deficiency of iodine may lead to hypertrophy of the thyroid

gland that presents as agoiter


 The most common cause of hypothyroidism is an autoimmune

condition called Hashimoto’s thyroiditis in which antibodies are


produced against the tissue of the thyroid.
 Although the exact etiology of this autoimmune disorder is

unknown, it can lead to progressive destruction of the thyroid


gland and loss of thyroid function.
Etiology:
 Hashimoto's thyroiditis

 hypopituitarism

 iodine deficiency

 enzyme deficiency

Manifestations
 Cretinism
 Hypothyroidism that occurs during fetal development
 May occur as a result of a congenital defect in thyroid
development
 Severe mental retardation due to poor development of the brain
 Poor overall development and growth retardation
 Etiology:
 maternal hypothyroidism before development of the fetal
thyroid gland,
 enzyme or iodine deficiency,
 maternal use of drugs that block hormone synthesis
(e.g., propylthiouracil)

 Clinical findings:
 mental retardation, increased weight and short stature

Myxedema
 Hypothyroidism in the adult

 May result from autoimmune destruction of the

thyroid or thyroid injury or removal


 Presents with signs of hypometabolism including:

 Cold intolerance
 Weight gain
 Fatigue
 Bradycardia
 Cool, dry skin
 Anorexia
 Constipation
 Edema of the face (swelling around the eyes), hands and
ankles;
 drooping eyelids
Possible long-term complications of untreated

hypothyroidism, including
 cardiac hypertrophy,
 heart failure, and
 myxedema coma,which presents with hypothermia,
seizures and respiratory depression
Hyperthyroidism
Increased synthesis and release of T3 and T 4

Hyperthyroidism may be
a primary condition that results from an

overactive thyroid gland or


it may occur as a result of excessive

stimulation of the thyroid by TSH from


thepituitary
 Cuase
 Grave's disease

 Toxic multinodular goiter

 Toxic adenoma

 Hypersecretion of TSH

 Iodine-induced hyperthyroidism

 Grave’s disease
 Patients with Grave’s disease produce antibodies

that bind TSH receptors on the thyroid and mimic


the actions of TSH leading to excess productionof
thyroid hormones.
 Manifestations
 The manifestations of hyperthyroidism are essentially the

same regardles of the cause of the hyperthyroidism


 they include the following:

 Increased basal metabolic rate


 Increased heat production, patient always feels “hot”
 Tachycardia
 Increased catecholamine sensitivity; patients are at risk for
cardiac arrhythmias
 Increased appetite
 Weight loss
 Enhanced bowel activity
 Behavioral changes including possible nervousness and
hyperactivity
Disorders of the adrenal glands
 The adrenal glands are small, triangular structures that lie on top of
the kidneys.
 Anatomically, the adrenal glands may be divided into two parts,
 The adrenal medulla and

 The adrenal cortex

 The adrenal medulla contains cells that secrete the catecholamines


 epinephrine and

 norepinephrine.

 Cells of the adrenal cortex secrete


 The Glucocorticoids (mainly cortisol),

 The mineralcorticoids (mainly aldosterone) and

 Some testosterone
Addison’s disease
A primary condition associated with atrophy of the
adrenal glands.
The majority of cases arise from autoimmune
destruction of the adrenal glands.
Some cases may occur as a result of adrenal gland
injury as a result of infection or tumors.
Destruction of the adrenal cortex, leading to a
deficiency of glucocorticoids, mineralocorticoids, and
androgens
 Etiology
 Autoimmune adrenalitis

 Tuberculosis

 Metastatic cancer

 PATHOLOGY:
 Atrophic, shrunken adrenal cortex, overlying a normal medulla
 Presentation
 Gradual onset of weakness

 Skin hyperpigmentation

 Hypotension

 Hypoglycemia

 Poor response to stress

 Loss of libido
Cushing’s disease

Characterized by excess circulating levels of cortisol.

Etiology
 Iatrogenic (exogenous corticosteroids)

 Pituitary corticotroph adenoma (Cushing disease)

 Adenoma produces ACTH

 Elevated ACTH

 Cortisol suppression with high-dose dexamethasone

 Adrenocortical adenoma

 Adenoma produces cortisol .

 DecreasedACTH .

 No cortisol suppression with dexamethasone


 Paraneoplastic syndrome
 Small-cell lung cancer producing ACTH

 ElevatedACTH
 No cortisol suppression with dexamethasone

 Pathology:
 Diffuse Adrenal Hyperplasia: 75% of cases

 Nodular Adrenal Hyperplasia: 25% of cases, grossly visible


nodules.

 Manifestations
 The effects of Cushing’s syndrome are primarily those of

excess
 cortisol.

 Characteristic “moon face” and “buffalo hump” patterns of

fat distribution.
 Glucose intolerance and possible diabetes mellitus.

 Thin skin, poor wound healing, impaired immune function.

 Hypertension due to increase in mineralocorticoids.

 Muscle weakness and wasting.

 Reduced bone density, hypercalciuria with possible


development of renal calculi.
 Alterations in mental function and personality.

 Increased androgen levels in females with possible


“virilization.”
 Mortality is approximately 50% within 5 years if left
untreated.
Pheochromocytoma
A tumor (usually benign) that arises in the

chromaffin cells of the adrenal medulla that


produce the catecholamines.
Symptoms are those of excess catecholamine

production and can be life-threatening.


Excess catecholamine production may be

continual or occur in episodes (“bursts”).


Clinical presentation
Hypertension

Tachycardia

Severe headache

Nausea and vomiting

Excess sweating (diaphoresis)

Palpitations

Anxiety

Risk of stroke due to marked hypertension


Diabetes Mellitus

 Definition:
 Chronic systemic disease characterized by insulin deficiency or

peripheral resistance, resulting in hyperglycemia and


nonenzymatic glycosylation of proteins

 Diagnosis:
 Fasting (overnight) venous plasma glucose concentrations of 126

mg/dL or greater on more than one occasion


 Clinical symptoms of diabetes and a random glucose level of 200

mg/dL or greater
 After ingestion of 75 g of glucose, a 2-hour venous plasma glucose

concentration of 200 mg/dL or greater


Insulin-dependent diabetes mellitus (IDDM)
Synonyms:
type I, juvenile onset diabetes, brittle diabetes

Epidemiology
Represents 10% of cases of diabetes

Affects children and adolescents usually younger than 20


Risk factors
Northern European ancestry
HLA-DR3, DR4, and DQ
Pathogenesis

 Lack of insulin due to autoimmune destruction of

betha cells
 Absolutely dependent on insulin to prevent

ketoacidosis and coma

Etiology:
 Thought to be caused by an autoimmune

reaction triggered by an infection (Coxsackie B


virus) in a genetically susceptible individual
 Morphology
 Lymphocytic inflammation of the islets of Langerhans (insulitis)

 Loss of ~cells

 Fibrosis of the islets

 Presentation
 Polydipsia, polyuria, and polyphagia

 Dehydration and electrolyte imbalance

 Metabolic ketoacidosis , accumulation of acidic ketone bodies in

the blood due to a lack of insulin-stimulated fatty acid utilization


 Coma and potentially death
Non-insulin-dependent diabetes mellitus (NIDDM)
 Synonyms:
 type II, adult onset diabetes

 Epidemiology
 Represents 90% of cases of diabetes

 Affectsobese adults usually older than 30 years

 Incidence increases with age.

 Affects 10 million in the United States (half are undiagnosed)

 Risk factors:
 obesity, increasing age, and genetic predisposition
 Pathogenesis
 Relativelyreduced insulin secretion

 Peripheral insulin resistance: reduced tissue sensitivity to

insulin due to decreased numbers of insulin receptors on


the cell membranes
 Morphology
 Nonspecific changes

 May have focal atrophy and amyloid deposition in islets

(hyalinization)
 Presentation
 Frequently asymptomatic

 Polydipsia, polyuria, and polyphagia

 Hyperosmolar nonketotic diabetic coma

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