Sangcha-an, MArLies P.

Endocrine Disorder

ADRENAL GLANDS Adrenal medulla- produce CATECHOLAMINES Adrenal Cortex 3 zones Zona glomerulosa- ALDOSTERONE Zona fasciculata- produces CORTISOL/GLUCOCORTICOID HYDROCORTISONE Zona reticularis-SEX HORMONES PANCREAS

ISLETS OF LANGERHANS- endocrine function Alpha Cells GLUCAGON Beta Cells INSULIN Delta Cells SOMATOSTATIN THYMUS GLAND -located below the sternum -produces THYMOSIN/THYMOPOETIN -T-cells

PITUITARY ANTERIOR LOBE

HORMONE HYPO FXN HYPER FXN

PHYSICAL ASSESSMENT
Palpation of thyroid gland- place inner and middle fingers below the cricoid cartilage, palpate the isthmus as he swallows. CHVOSTEK`S sign- tap the facial nerve, facial muscles contract toward ear, (+) hypocalcemia TROSSEAU`S sign place BP cuff on the arm and inflate, (+)carpal spasm,hypocalcemia Auscultate on enlarged thyroid for SYSTOLIC BRUITS a sign of hyperthyroidism due to hypervascularity

GH
ACTH TSH

Dwarfism young Cachexia - adult

Atrophy of adrenal cortex Atrophy depressed thyroid function Atrophy & infertility Underdevt of mammary glands

Gigantism young Acromegaly-adult

Cushings dse Graves dse

FSH PROLACTIN

Exaggerated fxn of sex organs Decreased milk production

DIAGNOSTICS
1. Serum CALCIUM NV=9 to 10 mg/dl Increased in Hyperparathyroidism Decreased in Hypoparathyroidism 2. CATECHOLAMINE assess adrenal medulla function EPINEPHRINE NV=30 to 95 pg/ml Increased in PHEOCHROMOCYTOMA 3. CORTISOL evaluate adrenocortical function NV= 8 am- 8 to 24 mcg/dl, 4pm- 2 to 15 mcg/dl > Increased in CUSHING`S DSE > Decreased in ADDISON`S DSE 4.ORAL GLUCOSE TOLERANCE TEST NV= 65 to 110 mg/dl -increased in DIABETES MELLITUS -decreased in HYPOGLYCEMIA

POSTERIOR PITUITARY LOBE

1. Oxytocin 2. ADH a. Diabetes insipidus B. SIADH Syndrome of Inappropriate ADH THYROID GLAND- 2 lobes Metabolism master-regulates body`s metabolism T3-Triiodothyronine T4-Thyroxine Calcitonin

PARATHYROID GLANDS 4 Produce Parathyroid Hormone

5. GLYCOSYLATED HEMOGLOBIN- monitor glucose in D.M. over 3 months NV= < 6% of total Hgb -increased in uncontrolled D.M. 6. TSH detect primary Hypothyroidism NV= 0.5 to 3.5 mU/ml -increased in HYPOTHYROIDISM -decreased in HYPERTHYROIDISM 7. THYROXINE (T4) RIA NV= 4 to 11 mcg/dl - increased in HYPERTHYROIDISM - decreased in HYPOTHYROIDISM 8. TRIIODOTHYRONINE (T3) NV= 75 to 220 ng/dl - increased in HYPERTHYROIDISM - decreased in HYPOTHYROIDISM 9. RADIOACTIVE IODINE UPTAKE TEST-RAIU - px ingest oral dose of radioactive iodine -decreased iodine uptake- HYPOTHYROIDISM -increased iodine uptake- HYPERTHYROIDISM * Confirm if patient has allergy to iodine/ shellfish

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.Rotate sites- may lead to Lipodystrophy localized disturbance of fat metabolism

ENDOCRINE MEDICATIONS
Classification & Examples
Sulfonylureas -Tolbutamide (Orinase) - Chlorpropamide (Diabinese) - Glipizide (Glucatrol) - Glimepiride (Amaryl) - Glibenclamide Biguanides - Metformin (Glucophage) Alpha-Glucosidase Inhibitors - Acarbose (Precose) - Miglitol (Glyset) Thiazolidinediones - Rosiglitazone (Avandia) - Pioglitazone (Actos)

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

INSULIN

ONSET

PEAK

DURATION

3 . Antithyroid meds - PTU (PROPYLTHIOURACIL) thyroid hormone antagonist, used for HYPERTHYROIDISM -can cause AGRANULOCYTOSIS, monitor CBC 4. Thyroid Replacement meds - LEVOTHYROXINE thyroid hormone, for HYPOTHYROIDISM 5. Glucocorticoids/HYDROCORTISONE used for acute ADRENAL CRISIS 6. IODINE preparations the size and vascularity of
the thyroid gland; inhibit release of thyroid hormones

Ultra rapid acting Insulin analog (Humalog)

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

15 mins.

2-4 hrs.

6-8 hrs.

-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.

1.) Lugols solution - 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 2.) Saturated solution of potassium iodide (SSKI)

..sangcha-an, Marlies P.

HYPOGLYCEMIA blood glucose <50mg/dl

ENDOCRINE DISORDERS 1.ADDISON`S dse adrenal hypofunction

ADDISONIAN CRISIS / ACUTE ADRENAL CRISIS - deficiency of mineralocorticoids/ glucocorticoids -affects the liver decreased glucose - stomach- decreased dig. Enzymes - kidneys- decreased H2O and Na S/S of Addison`s: a. Hypotension d. Hypoglycemia b. Dehydration e. hyponatremia c. Nausea and vomiting Treatment: 100 mg HYDROCORTISONE IV

S/S: tachycardia, pallor, weakness,diaphoresis TREATMENT: provide oral glucose/sucrose -bolus of 25 g. Of 50% Dextrose

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 -Diabetic Retinopathy blindness -D.Nephropathy damage kidneys

2. DIABETES MELLITUS
A. Insulin Dependent Diabetes Mellitus (IDDM) or Type I -destruction of beta cells of the pancreas little or no insulin production B. Non InsulinDependent Diabetes Mellitus (NIDDM) or Type II -probably caused by: - number of insulin receptors -INSULIN RESISTANT DISEASE -occurs over age 40 but can occur in children -common in overweight or obese S/S of DIABETES MELLITUS (TYPE1/2) - Polyuria - weakness - Polydipsia - fatigue - Polyphagia - blood sugar - weight loss - (+) glucose in urine (glycosuria) LABS: FBS : >126 mg/dl NON-FASTING: >200 mg/dl TREATMENT FOR TYPE 1 D.M. a. Insulin replacement b. Pancreas transplantation TREATMENT FOR TYPE 2 D.M. a. Insulin therapy, Weight reduction b. Oral antidiabetic drugs c. c. DIABETIC DIET 50%CHO,30%FAT,20%CHON,vit.,minerals

2. Neuropathy
-Damage to the neurons caused by vascular insufficiency and blood glucose

3.DKA (DIABETIC KETOACIDOSIS)

- life-threatening complication of D.M. - PATHOPHYSIO: Hyperglycemiaincrease blood glucose absence of insulinbody breaks down fat (lipolysis) to fatty acids and to ketones--increase ketones --lead to metabolic acidosis DKA S/S of DKA: a. Dehydration b. Rapid and deep breathing (KUSSMAUL`S) c. Fruity breath odor due to acetone d. 3 P`S e. Weight loss LABS: serum glucose >200 to 800 mg/dl increased serum ketone level positive urine acetone ABG result metabolic acidosis ECG- tall T waves- hyperkalemia TREATMENT: a. Correct dehydration using non-dextrose IVF b. Insulin c. Monitor ABG, K level

4. DIABETES INSIPIDUS
Water metabolism disorder -Deficiency of ADH / VASOPRESSIN TYPES: a.Neurogenic/Central Diab.insipidus - inadequate release/synthesis of ADH b. Nephrogenic Diab. Insipidus - inadequate renal response to ADH c. Psychogenic Diab. Insipidus - extemely large fluid intake ex. psychosis

7. SIADH (SYNDROME OF INAPROPRIATE ADH)

Caused commonly by OAT- CELL LUNG CANCER - Increased ADH production BODY RETAINS WATER S/S of SIADH: a. Anorexia b. Nausea, vomiting c. Weight gain TREATMENT: > restrict fluid intake -

5. HYPEROSMOLAR HYPERGLYCEMIC NONKETOTIC SYNDROME (HHNS)

-acute hyperglycemic crisis PATHOPHYSIO: Hyperglycemia increase blood glucose in serumcauses fluid shifts fluid shifts in the brain causes coma and death S/S of HHNS: a. Dehydration c. diaphoresis b. Hypotension d. 3 P`s LABS: serum glucose- 800 to 2,000 mg/dl glycosuria, ketones absent ABG- normal

8. THYROID STORM or THYROTOXICOSIS

- life-threatening due to surge of thyroid hormone GRAVE`S dse most common form of hyperthyroidism - increase in T3,T4 HYPERMETABOLISM S/S: tachycardia > stupor Vomiting > fever LABS: Increase T3,T4 Decrease TSH Treatment: Propylthiouracil (PTU) Avoid ASPIRIN bec. Salicylates block binding of T3,T4 Post-op care after Thyroidectomy a. O2 therapy, suction secretions b. Monitor for signs of bleeding and edema c. elevate head of bed 30o, support head and neck to avoid tension on sutures d. check dressing frequently, check behind the neck for bleeding e. assess for signs of resp. distress, hoarseness (laryngeal edema or damage) Simple goitre: they are due to hyperplasia, with eventual fibrosis separating hyperplastic areas from less active areas giving it a multinodular appearance (Multinodular goitre). Colloid goitre: accumulation of large amounts of colloid, it can even form cysts Gastrinomas (gastrin gastric acid causing peptic ulcer- Zollinger Ellison syndrome)

6. MYXEDEMA COMA
life threatening disorder that results from hypothyroidism -caused by HASHIMOTO`S dse chronic autoimmune thyroiditis S/S of Myxedema coma: a. Periorbital edema, peripheral edema b. Decrease mental ability- OBTUNDED c. Thick,dry tongue, hoarseness d. Slow,slurred speech e. Hypoglycemia f. Hypotension g. LABS: T3,T4 decreased TSH increased Treatment: a. Administration of HYDROCORTISONE IV b. LEVOTHYROXINE thyroid agent