Endocrine function disorders
Hormone Disorders
-TERTIARY: abnormality in stimulation from the HYPOTHALAMUS -SECONDARY: abnormality in stimulation from the PITUITARY -PRIMARY: abnormality in the GLAND
Goiter
-enlarged gland -does not tell if hypo or hyperfunction
Parathyroid Disorders
-hyperparathyroidism -excess PTH secretion •parathyroid tumor •bones become soft, fragile, and deformed •Ca2+ and phosphate blood levels increase •promotes renal calculi formation
Parathyroid Disorders
-hypoparathyroidism (low Ca) •surgical excision during thyroid surgery •fatal tetany in 3 -4 days due to rapid decline in blood calcium level (lack of Ca gives + charge, closer threshold for action potential, too many contractions)
Major endocrine glands
-hypothalamus -pituitary gland -pineal gland -thyroid gland -parathyroid gland
Adrenal Insufficiency
-primary; DESTRUCTION OF ADRENAL (TB, HIV, autoimmune) -secondary; FAILURE OF ACTH SECRETION -slow and insidious condition -can loose up to 90% of adrenal tissue before symptoms are seen -stress causes hypoadrenal crisis
Major endocrine glands
-thymus gland -adrenal gland -pancreatic islet -gonads
Aldosterone Functions
1. decreasing blood pressure and/or sodium ion concentration stimulate secretion of the enzyme renin into the bloodstream. renin + angiotensinogen---> angiotensin I + ACE---> angiotensin II
Aldosterone Functions
2. angiotensin II stim adrenal cortical cells to secrete aldosterone. aldosterone released into blood
Aldosterone Functions
3. aldosterone acts on kidney to conserve sodium ions and (by osmosis) water 4. blood pressure and/or sodium ion concentration return toward normal, inhibiting further secretion of renin
Pituitary Hormones
-Growth hormone -FSH and LH- stimulate gonads -ACTH- stimulate adrenal cortex -TSH- stimulates thyroid
Which hormone(s) stimulate the ovaries and testes? a.GH b.FSH and LH c.TSH d.ACTH and GH
b) FSH and LH
Adrenal Cortical Disorders
•Adrenal cortical INSUFFICIENCY: inability to make all three hormones -Primary adrenal cortical insufficiency (Addison disease) -Secondary adrenal cortical insufficiency -Acute adrenal crisis
Graves' disease
•Chemosis, Conjunctivitis and Proptosis, exopthalmoseand diplopia. Dry cornea, compression of the optic nerve. Pretibialmyxedema. Hypertrichosis. •Features in elderly: Mainly cardiac problem. Atrial fibrillation or heart failure •Features in children: excessive height or excessive growth rate, weight gain. Behavioral problem. Apathetic thyrotoxicosis (ozil eyes)
Adrenal androgen
•DHEA is a pro hormone •Converted to testosterone in the periphery •Important source of testosterone in the female •Responsible for pubertal hair growth in female
Adrenal Cortical Disorders
•EXCESSIVE adrenal secretion -Glucocorticoid hormone excess (Cushing syndrome) -Hyperaldosteronism •Congenital adrenal hyperplasia -Decreased cortisol synthesis; other hormones may be increased or decreased
Hypothyroidism Menifestations
•Early: Fatigue, Lethargy, Weakness. Weight gain, Arthralgiaor Myalgia. Muscle cramps, COLD INTOLERANCE. Dry Skin, Thin brittle nails, Headache, Constipation, bradycardia, Alopecia or dry coarse hair, Slow deep tendon reflex.
Hyperthyroidism Menifestation
•Fatigue, Weight loss, HEAT INTOLERANCE, Depression, nervousness, irritability, Menstrual irregularities, Weakness, Muscle cramp. Increase sweating. Lid lag, tachycardia, atrial fibrillation, Fine tremor, moist warm skin, Hyper reflexia, Thyroid acropacy (clubbing and swelling of finger, periosteal new bone formation)
Hyperthyroidism Pathogenesis
•Graves' disease (promote T4) •Toxic adenoma of the Thyroid •Subacute thyroiditis (autoimmune) •Jodbasedow disease
Thyroid Imbalances
•Hyperthyroidism (thyrotoxicosis) -Graves disease (gland gets bigger produce too much hormone) -Thyroid tumors
Thyroid Imbalances
•Hypothyroidism -Congenital -Acquired ºHashimoto thyroiditis (most common) ºThyroidectomy
Hypothyroidism Menifestations
•Late: Slow Speech, Absence of Sweat, PERIPHERAL EDEMA, Pallor, Decreased sense of taste & smell, Dyspnea, Deafness, Poor libido, amenorrhea / Menorrhagia, Puffiness of face and eyelid, HARD PITTING EDEMA, effusions in the pleural, peritoneal and pericardial cavity as well as joints.
Hypothyroidism Pathogenesis
•Primary failure of the thyroid •Auto immune Thyroiditis(Hashimoto's disease). (antibody against horm) •Secondary failure to the gland due to pituitary
Hypothyroidism Pathogenesis
•Prolonged Iodine deficiency (goiter) •Antithyroidtherapy •Thyroidectomy •Radioiodine therapy (thyroid disease, body over exertion)
Hypothalamus-Pituitary Axis
•Releasing hormones from hypothalamus tell the pituitary what to release into the blood •Trophic hormones from the pituitary tell specific peripheral glands to grow and produce their hormones
Thyroid Insufficiency Due to Lack of I
•T3 and T4are not made •There is no negative feedback to the hypothalamus •TRH and TSH continue to be made •If it is able, the thyroid will grow in response to the TSH
Thyroid Control
•Thyroid releases T3 and T4 •Both are carried by binding proteins •T3 stimulates metabolism •T4is inactive until converted into T3 in the tissues •Both exert negative feedback on the hypothalamus
Hyperthyroidism Pathogenesis
•ThyrotoxicosisFactitia •Struma Ovarii •TSH hypersecretionby pituitary •Pregnancy and tropoblastic tumor
Adrenal Medulla
•adrenal medulla -inner core, 10% to 20% of gland •has dual nature acting as an endocrine gland and sympathetic ganglion of sympathetic nervous system -consists of modified sympathetic postganglionic neurons called chromaffincells -when stimulated release catecholamines (EPINEPHRINE and NOREPINEPHRINE) and a trace of dopamine directly into the bloodstream
Adrenal Medulla
•effect is longer lasting than neurotransmitters -increases alertness and prepares body for physical activity - •mobilize high energy fuels, lactate, fatty acids, and glucose •glycogenolysis and gluconeogenesis boost glucose levels •glucose-sparing effect because inhibits insulin secretion -increases blood pressure, heart rate, blood flow to muscles, pulmonary air flow and metabolic rate.
Thyroid Gland
•largest endocrine gland -composed of two lobes and an isthmus below the larynx -dark reddish brown color due to rich blood supply
Thyroid Gland
•parafollicular (C or clear) cells secrete calcitonin with rising blood calcium -stimulates osteoblast activity and bone formation -calcitonin removes Ca from body
Parathyroid Glands
•secrete parathyroid hormone (PTH) -increases blood Ca2+ levels •promotes synthesis of calcitriol •increases absorption of Ca2+ •decreases urinary excretion •increases bone resorption
Adrenal Cortex
•secretes 5 major steroid hormones from three layers of glandular tissue -ZONA GLOMERULOSA (thin, outer layer) •secretes mineralocorticoid-regulate the body's electrolyte balance -ZONA FASCICULATA (thick, middle layer) •secretes glucocorticoids -ZONA RETICULARIS (narrow, inner layer) •secretes sex steroids
Thyroid Gland
•secretes thyroxine (T4 because of 4 iodine atoms) and triiodothyronine (T3) -T4 which is converted to T3 (T4 only in circulation) -increases metabolic rate, O2 consumption, heat production (calorigenic effect), appetite, growth hormone secretion, alertness and quicker reflexes
Thyroid Gland
•thyroid follicles -sacs that compose most of thyroid -contain protein rich colloid -follicular cells -simple cuboidal epithelium that lines follicles
Parathyroid Glands
•usually four glands partially embedded in posterior surface of thyroid gland -can be found from as high as hyoid bone to as low as aortic arch
Simple goiter is caused by increased production of thyroid hormone.
False Rationale:Simple goiter is the result of iodine (I) insufficiency. Since I is necessary in order to produce thyroid hormone, a deficiency results in low serum levels of T3 /T4. This causes TSH to stimulate the thyroid gland to make more hormone (which it cannot do because it needs I). The cells of the thyroid gland hypertrophy in an effort to function (make thyroid hormone).
