diseases of the endocrine system

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Diseases of the endocrine system. Review hormones. Anterior pituitary GH TSH ACTH FSH LH Prolactin MSH Posterior pituitary Vasopressin (ADH) Oxytocin Thyroid T3, T4 Parathyroid PTH Adrenal cortex Aldosterone Cortisone Androgens, estrogens, progestins. Review. - PowerPoint PPT Presentation

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Page 1: Diseases of the endocrine system
Page 2: Diseases of the endocrine system

Anterior pituitary GH TSH ACTH FSH LH Prolactin MSH

Posterior pituitary Vasopressin (ADH) Oxytocin

Thyroid T3, T4

Parathyroid PTH

Adrenal cortex Aldosterone Cortisone Androgens, estrogens, progestins

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Adrenal Medulla Catecholamines: epinephrine, norepinephrine

Pancreas Insulin Glucagon

Ovaries Estrogens Progesterone

Testes Testosterone

Thymus Thymosin – promotes development of immune cells – gone

in adulthood due to atrophy Pineal gland

melatonin

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Page 5: Diseases of the endocrine system
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Mainly increase in hGH Chronic and progessive

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Increase hGH in childhood S/S

Proportional increase in size because epiphyseal closure has not occurred yet

Abnormal and accelerated growth Often caused by an adenoma (cancer) Dx: CT and blood levels of hGH Tx: radiation or surgery usually

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Increase hGH in adulthood S/S

Overgrowth of face, hands, and feet Overgrowth of soft tissues

Dx and Tx same as gigantism

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Hypopituitarism in childhood Underdevelopment of the body often

caused by lack of hGH Many causes Tx: hormone replacement when needed

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Not same as diabetes you hear about from the media

Disturbance of water metabolism S/S

Polyuria, polydipsia, signs of dehydration, such as dry mucous membranes, hypotension, dizziness, constipation, and poor skin turgor

Tx: replacement DDAVP (desmopressin acetate)

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High T3, T4 production Low TSH levels S/S

Tachycardia, nervousness, excitability, insomnia, weight loss, tremor, loss of hair.

In advanced, exophthalmos (outward protusion of eyes)

Sudden exacerbation can indicate life-threatening condition, such as thyrotoxicosis (thyroid storm)

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Dx: TSH, T3, and T4 levels. If concerns, thyroid scan

Tx: B-blocker for tachycardia PTU or Tapazole to stop thyroid production Radioactive Iodine for curative measures

Will “kill” the thyroid Will need thyroid replacement afterwards for life NEVER performed if pregnant because will

destroy mother’s and child’s thyroid

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Graves disease Form of hyperthyroidism Body produces antibodies against thyroid,

which connect and mimic TSH causing large increase.

Thyroid will eventually “burn out” over time causing hypothyroidism

Can form a goiter

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Low T3, T4 High TSH levels S/S:

Dry skin, fatigue, weakness, weight gain, loss of hair, constipation, intolerance to cold

Dx: TSH levels Tx: Levothyroxine (synthroid) for life Severe cases cause Myxedema

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Cretinism Hypothyroidism in infancy S/S

Mental and growth retardation, stocky stature with protruding abdomen, lack of muscle tone contributing to inability to stand or walk, slow to smile in infancy

Part of Metabolic screening required at birth

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Hard, painless lump or nodule on thyroid. Some exhibit dysphagia or hoarseness

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Causes high blood calcium S/S:

Muscle weakness and paralysis, heart conduction problems, kidney stones, breakdown of bones causing increase risk for fractures

Dx: High PTH, calcium, chloride, and alkaline

phosphatase. Low serum phosphorus.

Tx: depends on cause

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Causes low blood calcium S/S:

Hypocalcemia, overstimulation of skeletal muscle, numbness, tingling, muscle spasms

Dx: Low serum calcium High serum phosphate

Tx: depends on cause. Calcium and Vit D supplementation

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High cortisol levels S/S:

Fatigue, weakness, changes in body appearance, weight gain.

Fat deposits on scapular area (buffalo hump) and abdomen. Moon face. Acne

Hypertension, edema, hyperlipidemia, osteoporosis, atherosclerosis, diabetes mellitus

Increase risk of infection due to suppression of immune response

Excessive hair growth, amenorrhea, impotence

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Low to none aldosterone and cortisol Several symptoms including

hyperkalemia Tx: replacement of hormones

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Either inadequate production of insulin by the pancreas or faulty utilization of insulin by the cells.

S/S: Polydipsia, polyuria, fatigue, weight loss,

hyperglycemia Several forms including

Insulin dependent diabetes mellitus (IDDM) (Type 1)

Non-insulin dependent diabetes mellitus (NIDDM) (Type 2)

Gestational diabetes

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Insulin is secreted by the pancreas, connects to different cells on receptors causing glucose to go from the blood into the cell. As a result, blood glucose levels decrease.

If enough insulin is not released, then glucose will remain elevated in the blood

If the receptors are not working well, the insulin will not work causing the blood glucose levels to remain high

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If glucose cannot get into the cells, then another source must be used, which is fat and protein, resulting in production of waste products called ketones. Ketones increase the acidity of the blood (lower pH). They also produce a fruity odor on the breath.

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Atherosclerosis resulting in MI and CVA Retinopathy resulting in blindness Neuropathy Renal failure Delayed healing More prone to infection PVD resulting in foot ulcers

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Usually in childhood Often antibodies destroy B-cells of

pancreas resulting in no insulin production

Tx: insulin replacement

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Usually in adulthood but seen now in obese children

Patient often overweight or a family Hx Produces enough insulin but receptors

are not responding appropriately Tx: oral medications first, then insulin

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Fasting blood sugar over 126 on two separate occasions results in a diagnosis

Fasting blood sugar between 101-125 is considered glucose intolerance

A1C Blood test measures how sugars have been

running for past 3 months Depending on source, A1C should be <7.0 or

<6.5 A non-diabetic will have an A1C <6.0

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Yearly eye exams #1 cause of blindness

Foot exams #1 cause of amputations

Cholesterol Blood pressure Smoking Micro-protein in urine once/year

#1 cause of kidney failure

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Sulfonylureas Glipizide, glyburide, amaryl Increases insulin release Side effect of hypoglycemia

Metformin Increases receptor response Side effect of GI disturbance

Thiazolidinediones (TZD) Actos, Avandia Increases number of receptors Side effect of edema – not to be used in CHF

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Several different forms including long-acting and short-acting

Required to be injected Lantus most common long-acting

Lasts 24 hours Won’t cause hypoglycemia in most cases

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Diabetic education Nutritional education Education on how to use meters Regular checking sugars Weight loss for type 2

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Diabetes occurring during pregnancy Important to monitor closely Make cause large babies Usually resolves after delivery but not

always Some oral medications may be used but

not all Usually requires insulin

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S/S Sweating, nervousness, weakness, hunger,

dizziness, trembling, headache, palpitations, confusion, abnormal behavior, coma

Brain’s fuel source is glucose – cannot use fat or glycogen, so low sugar causes CNS symptoms

Most commonly drug-induced Insulin, sulfonylureas, alcohol, excessive exercise,

ect… Tx: increase glucose and correct underlying cause If idiopathic, then diet modification. No

medications for long-term Tx

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