Thyroid Gland

Thyroid Disorders
Thyroid Gland produces

three hormones: Thyroxine (T4) Triiodothyronine (T3) Calcitonin T3 + T4 are referred to collectively as thyroid hormone.

Thyroid-iodine connection
Iodine is used by the thyroid to produce its

hormones

T4 - thyroxine T3 - triiodothyronine Calcitonin

Calcitonin
Secreted by the thyroid gland.
Secreted in response to high plasma levels of

calcium Decreases circulating plasma Ca++ levels by increasing its deposition in bone

Hypothyroidism

underactive state of the thyroid gland hyposecretion of thyroid hormone most common in women, middle-age

Causes : thyroidectomy pituitary / hypothalamic dysfunction iodine deficiency autoimmune thyroiditis (Hashimotos disease) immune system attacks the thyroid gland idiopathic (unknown) DX: decreased T3, T4 Elevated TSH, cholesterol

Cretinism severe physical and mental retardation resulting

from severe deficiency of thyroid function in infancy or childhood (congenital hypothyroidism) requires lifetime hormone replacement Myxedema occur from prolonged severe disease accelerated devt. of coronary artery disease coma rapid devt. of impaired consciousness and suppression of vital functions Pathophysiology inadequate secretion of thyroid hormone general slowing of all physical and mental process metabolic rate oxidation of nutrients for energy heat production

Med. Mgt. thyroid replacement therapy Levothyroxine (Synthyroid) , liothyronine Expected effects: diuresis, puffiness, improved reflexes and muscle tone, PR Nsg. Interventions provide a warm environment, conducive to rest avoid use of all sedatives assist client in choosing calorie, cholesterol diet fluid and fiber to relieve constipation physical activity and sensory stimulation gradually as condition improves monitor cardiovascular response to increased hormone levels carefully provide info. about prescribed medications (name, dosage, side effects) and importance of lifelong medical supervision

Hyperthyroidism
over-secretion of the thyroid gland also called thyrotoxicosis, tissues are stimulated by excessive thyroid hormone a recurrent syndrome, may appear after emotional stress or infection occurs mostly in women 20-50 yrs old Causes : adenoma, goiter, viral inflammation, autoimmune glandular stimulation, graves disease - most common cause

Hyperthyroidism (cont.)
DX: > elevated T3, T4 values abnormal findings in the thyroid scan Goiter enlargement of the thyroid gland due to stimulation of the thyroid gland by TSH Simple goiter enlarged thyroid gland due to iodine deficiency, intake of goitrogenic foods cabbage, turnips, soybeans may be hereditary

Thyroiditis
Inflammation of the

thyroid gland Hashimotos Disease Chronic thyroiditis Reaction of the immune system against the thyroid gland

Graves Disease
disorder char. by one or more of the ff: diffuse goiter

hyperthyroidism
infiltrative opthalmopathy exophthalmos seen in females under age 40 result from stimulation of the thyroid gland by thyroid-stimulating immunoglobulins (TSI) cause is unknown, may be hereditary, gender-related, often occurs after severe emotional stress or infection

Thyroid Storm or Crisis

a medical emergency pts. develop severe manifestation of hyperthyroidism temp., tachycardia, dysrhythmias worsening tremors, restlessness delirious or psychotic state or coma abdominal pain BP and RR Precipitated by a major stressor: infection trauma or surgery (thyroidectomy) inadequate treatment

Complications :
cardiovascular disease (HPN, Angina, CHF) Exophthalmos abnormal protrusion of the eyeballs - caused by abnormal deposits of fat and fluid in the retroocular tissue Corneal abrasion Thyroid storm or crisis life-threatening hypermetabolism and excessive adrenergic response (HR, RR, BP)

Pathophysiology:
hypertrophy and hyperplasia of the thyroid gland excessive secretion of thyroid hormone hypermetabolic condition exaggeration of all metabolic processes metabolic rate, excessive heat production appetite neuromuscular and CVS activity hyperactivity of sympathetic NS personality changes

Assessment Findings

Anxiety Flushed, smooth skin Heat intolerance Mood swings Diaphoresis Tachycardia Palpitations Dyspnea Weakness Wt. loss

Medications Propylthiouracil (PTU) antithyroid drug - blocks thyroid hormone production - can cause agranulocytosis - monitor pt. CBC Methimazole (Tapazole) blocks TH prod. Iodine preparations the size and vascularity of the thyroid gland; inhibit release of thyroid hormones 1.) Lugols solution

2.) Saturated solution of potassium iodide (SSKI)

can be given with milk or fruit juice should be taken with a straw may stain the teeth complications : brassy taste in the mouth, sore teeth and gums

Medications Propanolal (Inderal) and other adrenergic blockers relieve the adrenergic effects of excess thyroid hormone (sweating, palpitations, tremors) Radioactive iodine limits the secretion of the hormone by damaging or destroying thyroid tissue Surgical intervention (performed only when pt. is in a euthyroid state) subtotal thyroidectomy (large goiter) total thyroidectomy (if carcinoma is present)

Nsg. Interventions:

Provide calm, restful envt.

Provide adequate nutrients

1. physical comfort, cool envt. temp., bathe frequently w/ cool water 2. provide adequate rest, avoid muscle fatigue 3. stressors in the envt. noise and lights 4. relaxation techniques 1. calorie, protein, balanced diet (4,000-5,000 cal/day) 2. fluid intake 3. Restrict stimulants (tea, coffee, alcohol) 4. small, frequent feedings if hypermotility is present 5. Daily wt.

Nsg. Interventions: Provide emotional support Provide eye care 1. eye drops, dark glasses, patch eyes if necessary 2. elevate head of bed for sleep 3. restrict dietary sodium 4. assess adequacy of lid closure Be alert for complications

Post-op care after Thyroidectomy O2 therapy, suction secretions Monitor for signs of bleeding and excessive edema elevate head of bed 30o, support head and neck to avoid tension on sutures check dressing frequently, check behind the neck for bleeding assess for signs of resp. distress, hoarseness (laryngeal edema or damage) keep tracheostomy set in patients room for emergency use

Post-op Complications: be alert for the possibility of:

1. Tetany (due to hypocalcemia caused by accidental removal of parathyroid glands) assess for numbness, tingling or muscle twitching Chvosteks sign and Trousseaus sign Ca+ gluconate IV

2. Hemorrhage WOF: hypotension, tachycardia, other signs of hypovolemia WOF: irregular breathing, swelling, choking--possible hemorrhage and tracheal compression WOF: early signs of hemorrhage: repeated clearing of the throat, difficulty swallowing

Post-op Complications: be alert for the possibility of:

3. Thyroid storm - life-threatening - sudden release of thyroid hormone - fever, tachycardia, increasing restlessness and agitation, delirium

administer food and fluid with care (dysphagia is common) encourage client to gradually ROM of neck teach about medications, frequent follow-up total thyroidectomy life long replacement medication (T3, T4) subtotal thyroidectomy careful monitoring of return of thyroid function

Parathyroid Glands

Parathyroid Glands
Secretes parathormone

(PTH) PTH regulates calcium and phosphorous

Parathyroid and Calcium Regulation

Calcium most closely regulated element in our bodies!
important in conduction of electrical impulses in nervous and

muscular systems

ONLY element / mineral that has its own regulatory system

the parathyroid glands

Hyperparathyroidism
Increase in the production of PTH
Due to a benign growth of 1:4 parathyroid

glands

Induces:

abnormally high serum Ca++ levels bone decalcification development of kidney stones

Hyperparathyroidism

Fatigue Apathy muscle weakness Vomiting Hypertension Bone demineralization kidney stones

Symptoms of have become known as: "moans, groans, stones, and bones...with psychic overtones".

Hypoparathyroidism
Accidental removal

of parathyroid glands during thyriod surgery Symptoms r/t hypocalcemia & hyperphosphatemia
Neuromuscular

Tetany Numbness, tingling, cramps Bronchospasm, laryngeal spasm, carpopedal spasm

irritability

Ca+ Gluconate

 Trousseaus Sign of latent tetany

Hypoparathyroidism

Compression of the forearm in clients

having undue neuromuscular excitability due to hypocalcaemia produces spasm in the hand and wrist.

Hypoparathyroidism
Chvosteks sign of latent tetany

contraction of the muscles of the eye,

mouth or nose, elicited by tapping along the course of the facial nerve. The examiner taps gently over the facial nerve in front of the ear.

Nursing care of parathyroid dysfunction

Subjective & objective

data similar to thyroid dysfunction

Nursing Diagnosis
Altered metabolism Altered cardiac

Blood level >10 or

< 3 very significant

output Anxiety Altered comfort Impaired memory

Corticosteroid Therapy Steroids

Used to treat adrenal insufficiency Suppress inflammation & autoimmune reactions,

control allergic reactions & reduce organ transplant rejection

Side effects of high doses over long-term turned

steroid use into scare-oids

Steroids - How do they work?

Cortisol controls salt & water balance in the body Stress pituitary gland releases

adrenocorticotropic hormone (ACTH) which stimulates adrenals to produce cortisol Extra cortisol allows body to cope with stress of infections, trauma, surgery, or emotional problems When stressful situation resolves, adrenal hormone function returns to normal

Corticosteroid Therapy
Block production of substances that trigger allergic

and inflammatory actions (i.e. prostaglandins).

Impede the function of WBCs which help keep the

immune system functioning properly

Undesirable side effect: susceptibility to infection

Overview of endocrine pancreatic hormones and glucose Homeostasis

The endocrine pancreas produces hormones

necessary for metabolism and cellular utilization of carbohydrates, proteins, and fats. The cells that produce these hormones are clustered in groups of cells called islets of of Langerhans. These islets have different type of cells: Alpha Beta delta

 Alpha cells produce the hormone glucagon, which

stimulates the breakdown of glycogen in the liver, the formation of carbohydrates in the liver, and the breakdown of lipids in both the liver and adipose tissue. The primary function of glucagon is to decrease glucose oxidation and to increase blood glucose levels.

 Through glycolysis (the breakdown of liver

glycogen and gluconeogenesis ( the formation of glucose from fats and proteins), glucagon prevents blood glucose from decreasing below a certain level when the body is fasting or in between meals. The action of glucagon is initiated in most people when blood glucose level falls below 70mg/dl.

 Beta cells secrete the hormone insulin, which

facilitates the movement of glucose across cell membranes into cells, decreasing blood glucose levels. Insulin prevents the excessive breakdown of glycogen in the liver and in muscle, facilitates lipid formation while inhibiting the breakdown of stored fats and helps move amino acids into cells for protein synthesis.

 After secretion by the beta cells, insulin enters

the portal circulation, travels directly to the liver and is then released in the general circulation. Circulating insulin is rapidly bound to receptor sites on the peripheral tissues (especially muscle and fat cells) or destroyed by the liver or the kidneys. Insulin release is regulated by blood glucose; it increases when blood glucose levels increase and decreases when blood glucose levels decreases. When a person eats food, insulin levels begin to rise in minutes, peak in 30 to 60 minutes and return to baseline in 2-3 hours.

 Delta cells produce somatostatin, which believed

to be a neurotransmitter that inhibits the production of both glucagon and insulin

Diabetes Mellitus
is a chronic disorder of carbohydrate, protein, and fat metabolism resulting from insulin deficiency or abnormality in the use of insulin Predisposing factors: exact cause of diabetes mellitus remain unknown genetic / hereditary predisposition viruses pancreatitis pancreatic tumor autoimmune disorder obesity (overweight people require more insulin
to metabolize the food they eat or the number of insulin receptor sites in cells is decreased)

Types 1.Insulin Dependent Diabetes Mellitus (IDDM) or Type I destruction of beta cells of the pancreas little or no insulin production requires daily insulin admin. may occur at any age, usually appears below age 15 2.Non InsulinDependent Diabetes Mellitus (NIDDM) or Type II probably caused by: disturbance in insulin reception in the cells number of insulin receptors loss of beta cell responsiveness to glucose leading to slow or insulin release by the pancreas occurs over age 40 but can occur in children common in overweight or obese w/ some circulating insulin present, often do not require insulin

Clinical Manifestations ( Signs and Symptoms)

- Polyuria - weakness - Polydipsia - fatigue - Polyphagia - blood sugar / glucose level - weight loss - (+) glucose in urine (glycosuria) - nausea / vomiting - changes in LOC (severe hyperglycemia) (sleepiness, drowsiness coma) - recurrent infection, prolonged wound healing - altered immune and inflammatory response, prone to infection (glucose inhibits the phagocytic action of WBC resistance) - genital pruritus (hyperglycemia and glycosuria favor fungal growth : candidal infection resulting in pruritus, common presenting symptom in women)

1.

Fasting Blood Sugar (FBS)

2.

Postprandial blood sugar

NPO for 12 hours Normal value= 80-120 mg/dl 140 mg/dl or more diagnostic of DM Blood is withdrawn 2 hrs. after a meal N value = < 120mg/dl 200 mg/dl or more is diagnostic of DM NPO 12 hrs, no smoking, coffee or tea, minimize activity, minimize stress obtain FBS, administer 100 gm. Glucose by mouth diluted in juice; obtain blood and urine specimen after 1, 2 and 3 hrs. N value = blood glucose rise to 140 mg/dl in the 1st hour and returns to normal by 2nd and 3rd hrs. Abnormal = blood glucose does not return to normal by 2nd and 3rd hrs.; all urine specimen positive for glucose

3.

Oral Glucose Tolerance Test (OGTT)

4. Glycosylated hemoglobin
Provides information about blood glucose level during the previous 3 months bec. glucose in the bloodstream attaches to some of the hemoglobin and stay attached during the 120-day lifespan of the RBC

Interventions for Diabetes Mellitus A.Dietary Management

1. Follow individualized meal plan and snacks as scheduled Balanced diabetic diet 50% CHO, 30% fats, 20% CHON, vitamins and minerals diet based on pts. size, wt., age, occupation and activity 2. Pt. must have adequate CHO intake to correspond to the time when insulin is most effective 3. Routine blood glucose testing before each meal and at bedtime is necessary during initial control, during illness and in unstable pts. 4. Do not skip meals 5. Measure foods accurately, do not estimate 6. Less added fat, fewer fatty foods and low-cholesterol

Interventions for Diabetes Mellitus A.Dietary Management

7. Advise use of complex carbohydrates to help stabilize blood sugar. Meal should include more fiber and starch and fewer simple or refined sugars. 8. Avoid concentrated sweets, high in sugar (jellies, jams, cakes, ice cream) 9. If taking insulin, eat extra food before periods of vigorous exercise 10. Avoid periods of fasting and feasting 11. Keep weight at normal level, obese diabetics should be on a strict weight control program and should lose weight.

B. Teach pt. on correct administration of insulin and other hypoglycemic agents. 1. insulin in current use may be stored at room temp., all others in ref. or cool area 2. avoid injecting cold insulin lead to tissue reaction 3. roll insulin vial to mix, do not shake, remove air bubbles from syringe 4. press (do not rub) the site after injection (rubbing may alter the rate of absorption of insulin) 5. avoid smoking for 30 mins. after injection (cigarette smoking absorption) 6. Rotate sites Failure to rotate sites may lead to Lipodystrophy Lipodystrophy localized disturbance of fat metabolism Ex. Lipohypertrophy thickening of subcutaneous tissue at injection site, feel lumpy or hard, spongy result to absorption of insulin making it difficult to control the pt.s blood glucose

Factors that influence the bodys need for insulin

1. need : trauma, infection, fever, severe psychological or physical stress, other illnesses 2. need : active exercise

Hypoglycemia

S/Sx: 1. Sweating, tremor, pallor, tachycardia, palpitations and nervousness caused by release of epinephrine from the CNS when blood glucose falls rapidly 2. Headache, light-headedness, confusion, numbness of lips and tongue, slurred speech, drowsiness, convulsions and coma caused by depression of the CNS because of glucose supply of brain cells

low blood glucose (usually below 60mg/dl) results from too much insulin, not enough food, and/or excessive physical activity may occur 1-3 hrs after regular insulin injection

Management of Hypoglycemia 1. Give simple sugar orally if pt. is conscious and can swallow orange juice, candy, glucose tablets, lump of sugar 2. Give Glucagon (SQ or IM) if pt. is unconscious or cannot take sugar by mouth 3. As soon as pt. regains consciousness, he should be given carbohydrate by mouth 4. If pt. does not respond to the above measures, he is given 50 ml of 50% glucose I.V. or 1000 ml of 5%-10% glucose in water I.V.

Preventing Hypoglycemic Reactions Due to Insulin Instruct the pt. as follows: 1. Hypoglycemia may be prevented by maintaining regular exercise, diet and insulin 2. Early symptoms of hypoglycemia should by recognized and treated 3. Carry at all times some form of simple carbohydrate (orange juice, sugar, candy) 4. Extra food should be taken before unusual physical activity or prolonged periods of exercise 5. Between-meal and bedtime snacks may be necessary to maintain a normal glucose level.

Classification & Examples

Sulfonylureas -Tolbutamide (Orinase) - Chlorpropamide (Diabinese) - Glipizide (Glucatrol) - Glimepiride (Amaryl) - Glibenclamide

Mechanism of Action
stimulate beta cells of the pancreas to secrete insulin improve binding bet. insulin and insulin receptors no. of insulin receptors

Biguanides - Metformin (Glucophage)

Alpha-Glucosidase Inhibitors - Acarbose (Precose) - Miglitol (Glyset) Thiazolidinediones - Rosiglitazone (Avandia) - Pioglitazone (Actos)

body tissues sensitivity to insulin glucose uptake inhibit glucose prod. by the liver
delay absorption of glucose in the intestine enhance insulin action at the receptor sites

Oral Antidiabetic Agents

Teach pt. to estabilish and maintain a pattern of regular exercise Benefits of exercise : promotes use of CHO & enhances action of insulin blood glucose levels need for insulin the no. of functioning receptor sites for insulin perform exercise after meals to ensure an adequate level of blood glucose carry a rapid-acting source of glucose during exercise excessive or unplanned exercise may trigger hypoglycemia take insulin and food before active exercise

Teach pt. to practice good personal hygiene and positive health promotion to avoid diabetic complications 1. teach pt. about diabetic foot care 2. teach pt. the adjustments that must be made in the event of minor illness (e.g. colds, flu) continue taking insulin or oral hypoglycemic agents maintain fluid intake frequency of blood testing or urine testing 3. help pt. identify stressful situations in lifestyle that might interfere with good diabetic control 4. encourage good daily hygiene 5. advise regular eye exams 6. teach aggressive care for minor skin cuts and abrasions

Diabetic Ketoacidosis (DKA) Coma S/Sx: polyuria, thirst nausea, vomiting, abdominal pain -- due to acidosis weakness, headache, fatigue --- due to acidosis and F/E imbalance dim vision, flushed face dehydration, hypovolemic shock (PR, BP, dry skin, wt. loss) hyperpnea (Kussmauls breathing) acetone breath (fruity odor) lethargy COMA Blood glucose level > 250-350 mg/100 ml.

Hyperglycemic, Hyperosmolar, Non-Ketotic Coma (HHNC) can occur when the action of insulin is severely inhibited seen in pts. w/ NIDDM, elderly persons w/ NIDDM Precipitating factors: infection, renal failure, MI, CVA, GI hemorrhage, pancreatitis, CHF, TPN, surgery, dialysis, steroids

S/Sx: polyuria oliguria (renal insufficiency) lethargy temp, PR, BP, signs of severe fluid deficit Confusion, seizure, coma Blood glucose level > 600 mg/100 ml.

Interventions for DKA and Hyperosmolar Coma

Regular insulin IV push or IV drip 0.9% NaCl IV 1 L during the 1st hr, 2-8 L over 24 hrs. administer sodium bicarbonate IV to correct acidosis Monitor electrolyte levels, esp. serum K+ levels administer K+, monitor UO hourly (30ml/hr)

Long-term Complications of DM 1. Vascular Changes a. ) Macroangiopathy hardening and damage of the walls of large arteries Coronary Artery Disease CVA (Stroke) Peripheral vascular disease foot ulcers and gangrene b. ) Microangiopathy destruction of small blood vessels Retinopathy damage to retinal capillaries; hemorrhage, blindness Nephropathy damage microcirculation of kidneys; CRF 2. Neuropathy Damage to the neurons caused by vascular insufficiency and blood glucose Sensory and motor impairment Numbness, tingling, pain in extremities Painless neuropathy Impotence

INSULIN
Ultra rapid acting Insulin analog (Humalog)

ONSET
15 mins.

PEAK
2-4 hrs.

DURATION
6-8 hrs.

Rapid acting: Regular (Semilente) Intermediate: NPH (Lente) Long acting: Protamine Zinc (Ultralente)

-1 hr

2-4 hrs.

6-8 hrs.

1-2 hrs.

7-12 hrs.

24-30 hrs.

4-6 hrs.

18 + hrs

30-36 hrs.

Disorders of the adrenal gland

Addisons disease

Cushings syndrome

Hyperpituitarism with cushings disease

Hyperaldosteronism (Conns Syndrome

Pheochromocytoma

Syndrome of Inappropriate ADH

attention
Thanks for your attention