MAJOR DISORDERS OF THE ENDOCRINE SYSTEM Nio C. Noveno, RN, MAN
HORMONE REGULATION:
NEGATIVE FEEDBACK MECHANISM If the client is healthy, the concentration of hormones is maintained at a constant level. When the hormone concentration rises, further production of that hormone is inhibited. When the hormone concentration falls, the rate of production of that hormone increases.
HORMONE REGULATION:
NEGATIVE FEEDBACK MECHANISM
DISORDERS OF THE ENDOCRINE SYSTEM Primary Problem in the target gland; autonomous
Secondary Problem in the pituitary
Tertiary Problem in the hypothalamus
ANTERIOR PITUITARY DISORDERS
HYPERPITUITARISM May be due to overactivity of gland or the result of an adenoma Characterized by: Excessive serum concentration of pituitary hormones (GH, ACTH, PRL) Morphologic and functional changes in the anterior pituitary
GROWTH HORMONE HYPERSECRETION Gigantism
Acromegaly
Prior to closure of the epiphyses; proportional growth
After closure of the epiphyses; disproportional growth
HYPERPITUITARISM:
CLINICAL MANIFESTATIONS
Arthritis Chest: barrel-shaped Rough facial features Odd sensations: hands and feet Muscle weakness & fatigue Enlargement of organs Growth of coarse hair Amenorrhea; breast milk production Loss of vision; headaches Impotence; increased perspiration Snoring
HYPERPITUITARISM:
CLINICAL MANIFESTATIONS
HYPERPITUITARISM:
MANAGEMENT Medication
Radiation
BromocriptineCabergoline (dopamine agonists) GH hypersecretion and prolactinoma
Indicated for larger tumors
Ocreotide (somatostatin) GH hypersecretion
Surgery Trans-sphenoidal hypophysectomy
TRANS-SPHENOIDAL HYPOPHYSECTOMY Post-surgery nursing care
Semi- to high- Fowler’s position Protect from infection and stressful situations Hormone replacement Constant neurologic checks MIOW to check for DI WOF CSF leak Encourage deep-breathing, but not coughing Institute measures to prevent constipation [straining increases ICP]
HYPOPITUITARISM Deficiency of one or more anterior pituitary hormones Causes Infections / Inflammatory disorders Autoimmune diseases Congenital absence Tumor Surgery / Radiation therapy
HYPOPITUITARISM Simmonds' disease
[Panhypopituitarism] Complete absence of pituitary hormones Cachexia: most prominent feature Follows destruction of the pituitary by surgery, infection, injury, or a tumor
Sheehan’s syndrome [Post-partum pituitary necrosis] A complication of delivery Results from severe blood loss and hypovolemia Pituitary ischemia
HYPOPITUITARISM:
CLINICAL MANIFESTATIONS
Hypo -thermia, -glycemia, -tension
Loss of vision, strength, libido, &
secondary sexual characteristics
HYPOPITUITARISM:
MANAGEMENT Medication
Radiation
Hormonal substitution [maybe for life]
Indicated for larger tumors
Corticosteroids Levothyroxine Androgen / Estrogen Growth hormone
Surgery Trans-sphenoidal hypophysectomy
POSTERIOR PITUITARY DISORDERS
DIABETES INSIPIDUS Characterized by massive polyuria due to either lack of ADH or renal insensitivity Central DI
Due to a deficiency in ADH production Nephrogenic DI
Due to a defect in the kidney tubules that interferes with water absorption Polyuria is unresponsive to ADH, which is secreted normally.
DIABETES INSIPIDUS:
DIAGNOSTICS
Fluid deprivation test Administration of desmopressin 24-hour urine collection for volume, glucose, and creatinine
Serum for glucose, urea nitrogen, calcium, uric acid, potassium, sodium
DIABETES INSIPIDUS:
MANAGEMENT Central DI: Desmopressin, Lypressin [intranasal] Vasopressin tannate in oil [IM] Nephrogenic DI: Indomethacin-hydrochlorothiazide -desmopressin -amiloride Clofibrate, chlorpropamide
SYNDROME OF INAPPROPRIATE ADH Disorder due to excessive ADH release Clinical Manifestations Persistent excretion of concentrated urine Signs of fluid overload Hyponatremia LOC changes No edema
SIADH: DIAGNOSTICS
Low serum sodium [<135 mEq/L] Low serum osmolality High urine osmolality [>100 mOsmol/kg] High urine sodium excretion [>20 mmol/L] Normal renal function: low BUN [<10 mg/dL]
SIADH: MANAGEMENT Maintain fluid balance MIOW Fluid restriction Loop diuretic
Maintain Na balance Increased Na intake
[If with evidence of fluid overload]
Lithium or demeclocycline [Chronic treatment]
Emergency treatment of 3% NaCl, followed by furosemide [If serum Na <120, or if patient is seizing] Excessively rapid correction of hyponatremia may cause central pontine myelinolysis!
THYROID DISORDERS
THYROID FUNCTION TESTS Serum TSH
Single best screening test [high sensitivity] 0.38 – 6.15 mcU/mL If TSH is normal, fT4 should be normal. Screening required beginning 35 years, then q 5 years thereafter Also used for monitoring thyroid hormone replacement therapy
THYROID FUNCTION TESTS
Serum fT4
A direct measurement of free thyroxine, the only metabolic fraction of T4 0.9 to 1.7 ng/L (11.5 to 21.8 pmol/L) Used to confirm an abnormal TSH
THYROID FUNCTION TESTS
Total serum T3 and T4 T3 70 to 220 ng/dL (1.15 to 3.10 nmol/L) T4 4.5 to 11.5 mcg/dL (58.5 to 150 nmol/L)
T3 levels appear to be a more accurate indicator of hyperthyroidism.
THYROID FUNCTION TESTS T3 resin uptake test
Indirect measurement of unsaturated thyroid-binding globulin (TBG) 25 – 35% uptake Thyroid antibodies
5 – 10% of the population Grave’s: 80% Hashimoto’s: 100%
THYROID FUNCTION TESTS
Thyroid scan / Radioscan / Scintiscan
Utilizes a gamma camera and radioisotopes 123 I, thallium, americium, technetium-99m [99m Tc] pertechnetate Results Hot areas: increased activity Cold areas: decreased activity
THYROID FUNCTION TESTS Radioactive iodine uptake (RAIU)
Measures the proportion of administered tracer dose of ¹²³I present in the thyroid gland at a specific time after administration Results Hyper: high uptake Hypo: low uptake
THYROID FUNCTION TESTS Fine-needle aspiration biopsy
Sampling of thyroid tissue to detect malignancy Initial test for evaluation of thyroid masses Results Negative [benign] Positive [malignant] Indeterminate [suspicious] Inadequate [non-diagnostic]
THYROID FUNCTION TESTS Nursing Implications
Determine whether the patient has taken medications or agents that contain iodine [antiseptics, multivitamins, cough syrup, amiodarone]
because these may alter the test results.
Assess for allergy to iodine or shellfish.
For scans, tell patient that radiation is only minimal.
HYPERTHYROIDISM Increased basal metabolic rate (BMR) Causes Grave’s disease (autoimmune) Initial manifestation of thyroiditis TSH-screening pituitary tumor Toxic adenoma Factitious thyrotoxicosis Amiodarone therapy
HYPERTHYROIDISM:
CLINICAL MANIFESTATIONS GI hypermotility Rapid weight loss Apprehension [tremors, tachycardia, palpitations] Volume deficit; voracious appetite Exophthalmos; erratic menses Systolic BP elevated; sweating in primary disease TSH in secondary disease
HYPERTHYROIDISM:
CLINICAL MANIFESTATIONS
THYROID STORM / THYROTOXIC CRISIS Occurs in patients with existing Marked delirium but unrecognized Severe tachycardia thyrotoxicosis, Vomiting Diarrhea stressful illness, Dehydration thyroid surgery, RAI High fever
Increased systemic adrenergic activity: Severe hypermetabolism
HYPERTHYROIDISM:
MANAGEMENT Anti-thyroid drugs Propylthiouracil (PTU); methimazole Blocks thyroid hormone (TH) synthesis Used for pregnant women and patients who have refused surgery or RAI treatment During pregnancy, PTU is DOC. 1% of infants born to mothers on antithyroid therapy will be hypothyroid. WOF agranulocytosis.
HYPERTHYROIDISM:
MANAGEMENT RAI (¹³¹I), K or Na iodide, SSKI (Lugol’s) Adjunct to other anti-thyroid drugs in preparation for thyroidectomy Treatment for thyrotoxic crisis Inhibit release and synthesis of TH Decrease vascularity of the thyroid gland Decrease thyroidal uptake of RAI
HYPERTHYROIDISM:
MANAGEMENT Medications to relieve the symptoms related to the increased metabolic rate: Digitalis, propranolol (Inderal), phenobarbital Well-balanced, high-calorie diet with vitamin and mineral supplements Subtotal or total thyroidectomy
RAI THERAPY:
NURSING IMPLICATIONS
NPO post-midnight prior to administration [Food may delay absorption]
After initial dose: Urine and saliva slightly radioactive x 24H Vomitus highly radioactive x 6-8H Institute full radiation precautions.
Instruct the patient to use appropriate disposal methods when coughing and expectorating.
K OR NA IODIDE, SSKI (LUGOL’S):
NURSING IMPLICATIONS
Dilute oral doses in water or fruit juice and give with meals to prevent gastric irritation, to hydrate the patient, and to mask the very salty taste. Give iodides through a straw to avoid teeth discoloration. Force fluids to prevent fluid volume deficit. Warn patient that sudden withdrawal may precipitate a thyrotoxic crisis. Store in a light-resistant container.
HYPOTHYROIDISM A state of low serum TH levels or cellular resistance to TH
Autoimmune Developmental Dietary
Iodine deficiency Oncologic Drugs Iatrogenic Non-thyroidal Endocrine
HYPOTHYROIDISM
Causes Chronic autoimmune [Hashimoto’s] thyroiditis Hypothalamic failure to produce TRH Pituitary failure to produce TSH Inborn errors of TH synthesis Thyroidectomy / Radiation therapy Anti-thyroid therapy Iodine deficiency
HYPOTHYROIDISM Classified according to the time of life in which it occurs
Cretinism In infants and young children Lymphocytic thyroiditis Appears after 6 years of age and peaks during adolescence; self-limiting Hypothyroidism without myxedema Mild thyroid failure in older children and adults Hypothyroidism with myxedema Severe thyroid failure in older individuals
HYPOTHYROIDISM:
CLINICAL MANIFESTATIONS Dry, brittle hair; dry, coarse skin Edema (periorbital) Reduced BMR [bradycardia, bradypnea] Apathy; anorexia; anemia Increased weight; intolerance to cold Lethargy; loss of libido Enlarged tongue Drooling in primary disease TSH in secondary disease
MYXEDEMA COMA Hypotension Precipitating Factors Bradycardia Acute illness Hypothermia Rapid withdrawal of thyroid medication Hyponatremia Anesthesia / Surgery Hypoglycemia Respiratory failure Hypothermia Comause Opioid
HYPOTHYROIDISM:
MANAGEMENT Prevention Prophylactic iodine supplements to decrease the incidence of iodine-deficient goiter Symptomatic cases Hormonal replacement Levothyroxine (Synthroid) Liothyronine (Cytomel) Liotrix (Thyrolar) Dosage increased q 2-3 weeks especially in elderly patients
HYPOTHYROIDISM:
MANAGEMENT Tell patient to WOF: Chest pain, palpitations, sweating, nervousness, and other S/S of overdosage Instruct the patient to take TH at the same time each day to maintain constant hormone levels. Suggest a morning dosage to prevent insomnia. Monitor apical pulse and BP. If pulse >100 bpm, withhold drug.
HYPOTHYROIDISM:
NURSING INTERVENTIONS Diet: high-bulk, low-calorie Encourage activity Maintain warm environment Administer cathartics and stool softeners To prevent myxedema coma, tell patient to continue course of thyroid medication even if symptoms subside.
Maintain patent airway Administer medications: Synthroid, glucose, corticosteroids IV fluid replacement Wrap patient in blanket Treat infection or any underlying illness
PARATHYROID DISORDERS
HYPERPARATHYROIDISM Primary
Single adenoma Genetic disorders Multiple endocrine neoplasias Secondary
Rickets Vitamin D deficiency Chronic renal failure Phenytoin or laxative abuse
HYPERPARATHYROIDISM:
CLINICAL MANIFESTATIONS Constipation Apathy Lordosis Cardiac dysrhythmias Upset GIT Low energylevels Increased BP PTH Calcium Alkaline phospatase
PO4
HYPERPARATHYROIDISM:
MANAGEMENT Surgery to remove adenoma Force fluids; limit dietary calcium intake For life-threatening hypercalcemia: Furosemide Bisphosphonates [Etidroanate (Didrodinel), pamidronate] Calcitonin (Cibacalcin, Miacalcin)
Plicamycin (Mithracin) + glucocorticoid Mithramycin
HYPOPARATHYROIDISM Causes Congenital absence or malfunction of the parathyroids Autoimmune destruction Removal or injury to one or more parathyroids during neck surgery Massive thyroid radiation therapy Ischemic parathyroid infarction during surgery
HYPOPARATHYROIDISM:
CLINICAL MANIFESTATIONS Dyspnea; dysrhythmias Extremities: tingling Fotophobia Increased bone density Chvostek sign; cramps Irritability Trousseau sign; tetany PTH Calcium Alkaline phospatase
PO4
HYPERTHYROIDISM:
MANAGEMENT IV Ca chloride or gluconate [emergency treatment] DOC post-thyroidectomy Oral Ca salts (Ca carbonate or gluconate) Vitamin D supplementation Increase intestinal Ca absorption Dihydrotachysterol, ergocalciferol
Trousseau’s & E levated serum PO4; low Chvostek’s 2+ T ingling Ca Alkalosis; Arrhythmias Narrowing of airway Irritability Cramps
HYPOPARATHYROIDISM
Parathormone injections [in acute attacks] WOF allergies Diet: High-calcium [spinach], lowphosphate [milk, cheese, egg yolks] Al(OH)2, Gelusil, Amphogel
p.c.
Pentobarbital (Nembutal) [calm environment]
T C
ETANY
AKE RACHEOSTO MY
ALCIUM GLUCONATE
ARE
ALCIUM 8.6 – 10.6 mg / dL
PHEOCHROMOCYTOMA
ADRENAL GLANDS
ADRENAL MEDULLA
Release cathecholamines Epinephrine Norephinephrine
Released during “fight or flight” situations (sympathetic effect)
PHEOCHROMOCYTOMA
Adrenal tumor Increased Epi and NEpi
Heredity
PHEOCHROMOCYTOMA
Headache Anxiety Nausea Eye disturbances Severe hypertension
PHEOCHROMOCYTOMA
BP HR Diaphoresis BMR VMA Glucose
PHEOCHROMOCYTOMA Adrenalectomy Steroid treatment Antihypertensive and antidysrhythmic nitroprusside (Nipride) propranolol (Inderal) phentolamine (Regitine)
PHEOCHROMOCYTOMA
MBP / MIO Fluid replacements Decrease environmental stimulation Maintenance doses of steroids Follow-up check up 24-hour urine specimens [VMA and catecholamine studies]
Avoid: coffee, chocolate, beer, wine, citrus fruit, bananas, and vanilla 24h before test
ADDISON'S DISEASE
ADRENAL CORTEX HORMONES Glucocorticoids Cortisol,
corticosterone Increase blood glucose levels by increasing rate of gluconeogenesis Increase protein catabolism Increase mobilization of fatty acids Promote sodium and water retention Anti-inflammatory effect Aid the body in coping with stress
ADRENAL CORTEX HORMONES Mineralocorticoids Aldosterone,
Corticosterone, Deoxycorticosterone Regulate fluid and electrolyte balance Stimulate reabsorption of sodium, chloride and water Stimulate potassium excretion Under
the control of Renin-AngiotensinAldosterone system (RAAS)
ADRENAL CORTEX HORMONES Sex
hormones
Androgens,
Estrogens Influences the development of sexual characteristics
ADDISON'S DISEASE
Hyposecretion of adrenocortical hormones Destruction of the cortex Idiopathic atrophy
ADDISON'S DISEASE
Weakness Excess stress A/N/V/D K & ACTH elevation; Low Na, BP, cortisol, glucose
ADDISON'S DISEASE
Replacement of hormones Hydrocortisone; Fludrocortisone PNSS (0.9 NaCl) Dextrose Diet: High-CHO & CHON Low potassium, high sodium
ADDISON'S DISEASE
VS, weight, and serum glucose level 24-hour urine specimens [LOW 17- hydroxycorticosteroids & 17-ketosteroids] Electrolyte levels: K; Na Bronze-skin Changes in energy or activity
ADDISON’S DISEASE
ADDISON'S DISEASE
MVS [4x / day] Infection, Addisonian crisis, dehydration MIOW / MBP / MBG Give steroids with milk or an antacid Avoid: Contacts & Stress
CUSHING'S SYNDROME
CUSHING'S DISEASE
Adrenal hyperplasia / tumor Cushing’s disease Tumor-secreting ACTH Hypothalamic
Buffalo hump Unusual behavior (depression, personality changes, fatigability)
Facial features (moonface, hirsutism in women)
Fat (truncal obesity) ACTH and cortisol in blood
elevated; Loss of muscle mass Overextended skin (abdominal striae with easy bruisability)
Hypertension, hyperglycemia, hypernatremia Urinary cortisol elevated Menstrual irregularities Porosity of bones (osteoporosis)
CUSHING’S SYNDROME
CUSHING'S SYNDROME
Remove exogenous steroids Hypophysectomy or irradiation Adrenalectomy
CUSHING'S SYNDROME
Cyproheptadine (Periactin) Metyrapone Mitotane (Lysodren) Aminoglutethamide (Cytadren) Potassium supplements High-CHON; Low Na
CUSHING'S SYNDROME
MVS, MIOW, MBP, MBG Electrolyte levels: Na & K Urine specimens [LOW 17- hydroxycorticosteroids & 17ketosteroids] Physical appearance Changes in coping & sexuality [verbalization] Stress reduction
DIABETES MELLITUS
DIABETES MELLITUS
Insulin resistance [GDM, age] Failure in production Blockage of insulin supply Autoimmune response Excess body fat Heredity
DIABETES MELLITUS
Type I [juvenile ]/IDDM Type II [adult- onset type]/ NIDDM gradual onset
diet and exercise obesity Pancreatectomy, Cushing's syndrome, drugs
DIABETES MELLITUS
Low insulin leads to: to Hyperglycemia Glucosuria Polyuria Gluconeogenesis
DIABETES MELLITUS
Complications Microvascular Retinopathy & Renal failure Macrovascular CV and PVD Peripheral neuropathy
ruritu aresthes s oor ia oor healing
olyuri aolydipsi a olyph agia
Normal
FBS
Impaired
DM
<110mg/dl 110-125mg/dl ≥126mg/dl
2H <140mg/dl OGTT
≥140; <200mg/dl
≥ 200 mg/dl
DIABETES MELLITUS
Diet complex CHO [50% to 60%] water-soluble fiber oat, bran, peas, beans, pectin-rich FV CHON [12% to 20%] 60 and 85 g CHOO [<30%] 70 to 90 g/day / MUFA
DIABETES MELLITUS
Insulin dose adjustments depend on:
physical and emotional stresses specific type of insulin condition and needs of the client
Insulin
Onset
Peak
Duration
Ultra rapid acting insulin analog (humalog)
10-15 min
1H
3H
SAI (humulin regular)
½-1H
2-4 H
4-6 (8) H
IAI (humulin lente, Humulin NPH)
3-4 H
4-12 H
16-20 H
LAI (Protamine zinc, humulin ultralente)
6-8 H
12-16 H
20-30 H
Premixed insulin (NPH-regular [80-20, 70-30, 50-50])
½-1 H
2-12 H
18-24 hrs
Insulin glargine (Lantus )
Slower than NPH
No Peak
24 H
DIABETES MELLITUS
Somogyi effect Epinephrine & Glucagon Glycogenolysis [iatrogenically-induced hyperglycemia]
Lowering insulin dosage at night
MBG
DIABETES MELLITUS Insulin pump 1) Basal doses of regular insulin delivered every few minutes bolus doses delivered pc 2)
Appropriate amount of insulin for 24 hours plus priming is drawn into syringe
3)
The administration set is primed and needle inserted aseptically, usually into abdomen
DIABETES MELLITUS
Client teaching points: 1. Proper insulin preparation using aseptic technique 2. When to remove the pump (e.g., before showering or sexual relations) 3. MBG at home
INSULIN ADMINISTRATION Increases the hypoglycemic effects of insulin
Aspirin, alcohol, oral anticoagulants, oral hypoglycemics, beta blockers, tricyclic antidepressants, tetracycline, MAOIs Increases blood glucose levels Glucocorticoids, thiazide diuretics, thyroid agents, oral contraceptives Increase the need for increased insulin dose
Illness, infection, and stress
ORAL HYPOGLYCEMIC AGENTS
Sulfonylureas
Promotes increase insulin secretion from pancreatic beta cells through direct stimulation First Generation Agents: Acetohexamide Tolbutamide (Orinase) Tolzamide (Tolinase) Chlorpropamide (Diabenese) Second Generation Agents: Glipizide (Minidiab, Glucotrol) Glyburide (DiaBeta, Glynase, Micronase) Glimepiride (Amaryl)
ORAL HYPOGLYCEMICS
Biguanides
Reduces hepatic production of glucose by inhibiting glycogenolysis Decrease the intestinal absorption of glucose and improving lipid profile
Agents: Phenformin
Metformin (Glucophage, Glucophage XR) Buformin
ORAL HYPOGLYCEMICS
Alpha-glucosidase inhibitors
Inhibits alpha-glucosidase enzymes in the small intestine and alpha amylase in the pancreas Decreases rate of complex carbohydrate metabolism resulting to a reduced rate postprandially Agents: Acarbose (Precose, Gluconase, Glucobay) Miglitol (Glyset)
ORAL HYPOGLYCEMICS
Thiazolidinediones Enhances insulin action at the cell and postreceptor site and decreasing insulin resistance Agents:
Pioglitazone (Actos) Rosiglitazone (Avandia) Rosiglitazone + Metformin (Avandamet)
DIABETES MELLITUS
Other therapies include: 1. pancreas islet cell grafts 2. pancreas transplants 3. implantable insulin pumps 4. cyclosporin [Sandimmune, Neoral]
DIABETES MELLITUS
MBG [done pc and hs] + HbA1C MBP + weight Renal function + MIO Eye examination
GLYCOSYLATED HEMOGLOBIN (HBA1C )
Reflects effectiveness of treatment < 7.5% (good control) 7.6% - 8.9% (fair control) > 9% (poor control)
DIABETES MELLITUS
diet & weight ketonuria note infection legs / feet / toenails check [keep in between toes dry] acceptance & understanding
DIABETES MELLITUS
Administer insulin sterile technique rotating injection sites dosage / types / strengths / peak CHO source Avoid: Avoid tight shoes; smoking; heat
DIABETES MELLITUS
hypoglycemia Headache Nervousness Diaphoresis Rapid, thready pulse Slurred speech
THE CLIENT IS TIRED!
T Irritability Restlessnes remors achycardia
Hypoglycemia: <50 mg/dL
Causes: Overtreated hyperglycemia Increased exercise sxcessive hunger β-blockers Gastric paresis xcitability Alcohol intake Erratic insulin absorption iaphoresis
E D
Rx: Mild: Shakiness 10-15 gm carbohydrate Tremors 2 oz. (1 small tube of) cake icing Excessive 4 oz. orange juice hunger 6 oz. regular soda Paresthesias 6-8 oz 2% skim milk (4 to) 10 pieces of hard Pallor candy Diaphoresis
Moderate: Drowsiness Impaired judgment Double or blurred vision Headache Inability to concentrate Mood swings Irritability Slurred speech
Rx: 20-30 gm carbohydrate Glucagon 1 mg SQ/IM
Severe:
Rx:
Seizures Unconsciousnes 25 gm D s
Disorientation
50
dextrose IV
Glucagon 1 mg IM/IV
DIABETES MELLITUS
diabetic coma Restlessness Hot, dry, flushed skin Thirst Rapid pulse Nausea Fruity odor to breath
Ketoacidosis Urinary changes Sunken eyeballs Skin is warm &
Rx:
Regular insulin drip 0.9% or 0.45% NSS 1:1 [100U:100cc] flushed Membranes are dry Nursing care: Check glucose Arrhythmias 250-300 mg/dL Upset GI system [q30-60mins] Low BP 250 mg/dL DC the drip Saline solution
NON Ketosis is absent Electrolyte imbalance [K+
decrease] Thirst Obtundation Treat with regular insulin drip Initiate diet Correct hyperglycemia
Normal creatinine? Erythrocyte sedimentation rate [ESR: 0-20 mm/hr]
Poor glycemic control Hemodialysis Restrict: Na+, CHON, K+, weight Output & input (MIO) No symptoms
Reduced O2 in the eye Elevated sugar & BP Tension is high in the retina Increased lens opacity NO eyesight Annual eye exam [every 6-12 months]
MAJOR DISORDERS OF THE ENDOCRINE SYSTEM THANK YOU!
Nio C. Noveno, RN, MAN