Endocrine System 126a3c

Scope Physiology Disorders • • • • • •

PITUITARY DISEASES ADH DISEASES ADRENAL GLANDS DISEASES THYROID DISEASES PARATHYROID DISEASES PANCREAS DISEASES

Major Hormone Secreting Glands

“The Sequence” Hypothalamus ↓ Pituitary Gland or Hypophysis Anterior or Adenohypophysis Posterior or Neurohypophysis ↓ Target Glands

The ANATOMY of the Endocrine System The Hypothalamus - This part of the DIENCEPHALON is located below the thalamus and is connected to the pituitary gland by a stalk

Physiology Secretes RELEASING HORMONES for the pituitary gland - Releasing hormones= hypothalamus

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The Pituitary Gland - Is a gland located below the hypothalamus at the base of the brain.

APG Adenohypophysis - TSH - target  thyroid gland

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ACTH - target  adrenal gland ICSH - target  testes (maturation of spermatozoa) GH - target  epiphyseal plate (bone growth) FSH target  ovary-estrogen (maturation of graafian follicles to release mature ovum) LH target  graafian follicle (formation of corpus luteum to maturation of ova) MSH → skin (pigmentation) PROLACTIN → (maturation of mammary gland and production of milk)

PPG Neurohypophysis - ADH - target kidney tubules (H2O reabsorption) - OXYTOCIN – uterine contraction and ejection of milk Pituitary Gland and Its Hormones

Target Glands • Thyroid

• • • • • • • •

Adrenal Mammary Skin Bone plates Ovaries Testes Kidney tubules Uterus

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Thyroid and Parathyroid The THYROID gland Anatomy - Located in the anterior neck lateral to the trachea - Contains two lobes connected by the isthmus - Microscopically composed of thyroid follicles where the hormones are produced and stored

The PARAthyroid glands Anatomy - Located at the back of the thyroid glands - Four in number

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Follicular Cells- T3, T4- ↑BMR, and

↑ CHON and bone turnover - T3- metabolism, growth - T4- catabolism, body heat production

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C Cells- Calcitonin - ↓calcium & phosphate levels - Parathormone -calcium & phosphorus regulation, osteoclast

The Physiology Parathyroid Hormone is released in HYPOCALCEMIA -↑ calcium level Parathyroid hormone is NOT secreted in HYPERCALCEMIA

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Calcitonin is stimulated by HYPERCALCEMIA -↓calcium level Calcitonin is inhibited by HYPOCALCEMIA

The Adrenal Glands Anatomy - Located above the kidneys - Composed of two parts- the outer Adrenal Cortex and the inner Adrenal medulla

Cortex

Mineralocorticoid:Aldosterone -Na & water reabsorption, K loss Glucocorticoid: Cortisol - blood glucose regulation Androgen: DHEA - sex hormones – testosterone Medulla (catecholamines)  stress or sympathetic effect  Epinephrine and Nor-epinephrine - neurotransmitters •

The GONADS Anatomy Ovaries These two almond-shaped glands are found in the pelvic cavity attached to the uterus by the ovarian ligament Testes These two oval-shaped glands are found in the scrotum Physiology Ovary - estrogen - affects devt of female sex organs and secondary sexual characteristics - progesterone- influences menstrual cycle, stimulates the growth of uterine wall, and maintains pregnancy Testes - testosterone- affects the devt of male sex organs and secondary sexual characteristics Pineal Gland Melatonin (dec skin pigmentation, inhibit gonadotropic hormone)

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The Pancreas - This retroperitoneal organ has both endocrine and exocrine functions Anatomy

- The endocrine function resides in the ISLETS of Langerhans - The islets have three types of cells- alpha, beta and delta cells Physiology - The ALPHA cells secrete GLUCAGON - The BETA cells secrete INSULIN - The DELTA cells secrete SOMATOSTATIN

Placenta - HCG- maintains pregnancy - estrogen, progesterone, human placental lactogen

Pancreas: Islet of langerhans

Alpha- glucagon- ↑blood sugar (hyperglycemia) by stimulating glycogenolysis & gluconeogenesis

Beta- insulin - ↓blood sugar (hypoglycemia) by facilitating transport of glucose across cell membranes of muscle, liver, adipose tissue, inhibits breakdown of proteins

DISORDERS OF THE ENDOCRINE GLAND Disorders are generally grouped into: 1. HYPER- when the gland secretes excessive hormones 2. HYPO- when the gland does not secrete enough hormones Hyper and Hypo can be classified as PRIMARY when the Gland itself is the problem or SECONDARY when the pituitary or the hypothalamus is causing the problem PITUITARY GLAND DISORDERS  HYPOPITUITARISM  HYPERPITUITARISM  PITUITARY TUMORS • Hypopituitarism - Hypofunction of the pituitary gland Caused by: - trauma, tumor at the hypothalamus or pituitary gland - complication from radiation therapy (head and neck) - Panhypopituitarism (Simmonds’ Disease)- total absence of pituitary secretions - Sheehan’s Syndrome – postpartum pituitary necrosis (bleeding) Manifestations: - Related to hypofunction of:  thyroid – hypometabolism  gonads – amenorrhea, impotence

adrenal glands - adrenal insufficiency  growth hormone – dwarfism, hypoglycemia - Hemianopsia and headache – (if due to tumor) - Increased I (if due to tumor)

Assessment Findings - Retarded physical growth due to decreased GH dwarfism - Low intellectual development - poor development of secondary sexual characteristics Management: - Surgical removal of tumor - Radiation - HRT hormonal replacement therapy • Pituitary Tumors - Usually benign - 3 Types  Eosinophilic Tumors  Basophilic Tumors  Chromophobic Tumors (most common) Eosinophilic Tumors - Gigantism (before puberty) - Acromegaly (after puberty) - Visual disturbance (compression from tumor) • Hyperpituitarism - hyper-secretion of the gland - ACROMEGALY-after 15-16 yo - Gigantism-before 15-16 yo Causes: tumor, congenital disorder

Assessment Findings 1. Increased growth Gigantism or Acromegaly 2. 3. 4. 5.

large and thick hands and feet Visual disturbances Hypertension, hyperglycemia Organomegaly

• Pituitary Tumors Basophilic Tumors - Cushing’s Syndrome

- Musculinization and amenorrhea (female) Chromophobic Tumors (COMMON) - Destroy the rest of the pituitary gland - No hormones except for prolactin (galactorrhea) - Blindness - Increased I

Diagnostic: - CT scan - MRI - Assessment Findings Management: - Drug Bromocriptine (Parlodel) – to lower GH and Prolactin - Radiation - Surgery (transsphenoidal hypophysectomy) Octreotide (Sandostatin) = preop drug to reduce tumor

Post op Care: HYPOPHYSECTOMY - Head elevation for 2 weeks/ Semi- Fowlers position - Nasal packing, Avoid sneezing, coughing

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Oral care Monitor LOC and neurologic status No activity that will increase I Watchout Diabetes Insipidus, Monitor I & O Observe for CSF leakage ister prescribed medications

DISORDERS OF THE POSTERIOR PITUITARY GLAND: ADH Abnormality  SIADH  DI

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SIADH Syndrome of Inappropriate Anti Diuretic Hormone - Increased secretion of ADH - Increased tubular reabsorption of water = water intoxication and increased blood volume (hypervolemia): (low Hct, hypoosmolality, edema) - Decreased urine output = concentrated urine (high S.G., dark urine)

- Watch out for manifestations of Fluid Volume Excess - Cause: over medication of vasopressin and benign pituitary tumor ASSESSMENT findings - Signs of Hypervolemia 1. Mental status changes 2. Abnormal weight gain 3. DISORDERS OF the PITUITARY GLAND: Posterior gland 4. ASSESSMENT findings 5. Hypertension 6. Anorexia, Nausea and Vomiting 7. HYPOnatremia Diagnostic Test - Urine specific gravity is increased (concentrated) - Hyponatremia - CBC shows hemodilution - SIADH Management: - FVE intervention - Stop vasopressin - Surgery (tumor excision) Critical conditions: - Pulmonary edema - Cerebral edema - Heart failure - Hypertension - Renal Failure Nursing Interventions 1. Monitor VS and neurologic status 2. Provide safe environment 3. Restrict fluid intake (less than 500cc/day) 4. Monitor I and O and daily weight 5. ister Diuretics and IVF carefully 6. ister prescribed Demeclocycline to inhibit action of ADH in the kidney • DI Diabetes Insipidus - Decreased ADH secretion - Decreased tubular reabsorption of water = decreased blood volume (high Hct, hyperosmolality, thrombosis) - Increased urine output = diluted urine (low S.G., clear urine) - Watch out for manifestations of Fluid Volume Deficit - Cause: trauma or injury to pituitary gland, resection of hypophysis, insensitivity of kidney to ADH

Assessment findings

1. 2. 3. 4. 5.

Polyuria of more than 4 liters of urine/day Polydipsia Signs of Dehydration Muscle pain and weakness Postural hypotension and tachycardia

Diagnostic Test 1. Urinary Specific gravity  very low, 1.006 or less

2. Serum Sodium levels  high Management: - FVD intervention

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Synthetic ADH istration (vasopressin) Desmopressin (DDAVP) spray intranasal OD or BID Vasopressin tannate in oil = IM OD or every 4 days

Critical conditions: - Thrombosis – thromboembolism – pulmonary embolism - Ischemia - Infarction - Necrosis (CVA, MI, RF) Nursing Interventions 1. Monitor VS, neurologic status and cardiovascular status 2. Monitor Intake and Output 3. Monitor urine specific gravity 4. Provide adequate fluids 5. ister Chlorpropamide or Clofibrate as prescribed to increase the action of ADH if decreased 6. ister VASOPRESIN. Desmopressin or Lypressin are given intranasal. Pitressin is given IM Abnormalities of Adrenal Gland  Conn’s  Cushing’s Disease  Cushing’s Syndrome  Addison’s Disease  Pheochromocytoma

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Conn’s Disease or Primary Hyperaldosteronism - Adrenal cortex disorder - Over secretion of aldosterone or mineralocorticoid - Increased Na and H2O reabsorption=FVE - Increased K urinary excretion=hypokalemia - Watch out for manifestations of:  SIADH  Hypervolemia or FVE / Hypertension

 Hypokalemia (arrhythmias)  Hypernatremia Caused: - tumor and trauma of the adrenal cortex Conn’s Management: - FVE intervention - Stop sodium intake - Critical conditions: - Arrhythmias - Hypertension - Same with SIADH Nursing Interventions 1. Monitor VS, I and O and urine sp gravity 2. Monitor serum K and Na 3. Provide Potassium rich foods and supplements 4. ister prescribed diuretic- Spironolactone- K sparer 5. Maintain sodium-restricted diet 6. Prepare patient for possible surgical interventions

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Cushing’s Disease (Primary)  Adrenal cortex disorder/ tumor, pituitary tumor  Over secretion of  Mineralocorticoid: Aldosterone = Na and H2O retention, K excretion  Glucocorticoid = hyperglycemia  Androgen

Female: hoarseness of voice, hirsutism, ↑ clitoris  Steroids = buffalo neck, trunkal obesity Pathophysiology Normal functions of Glucocorticoids: Cortisol 1. Gluconeogenesis 2. Protein breakdown

3. Fat breakdown 4. Decreased WBC

Exaggerated functions HYPERGLYCEMIA OSTEOPOROSISS, delayed wound healing Purplish striae , Bleeding Muscle wasting THIN extremity, Truncal deposition IMMUNOSUPPRESSION

Functions of Mineralocorticoids 1. Sodium Retention

Exaggerated functions

2.Secondary water retention 3. Potassium excretion

Hypervolema- Hypertension

Function of androgen: Hair growth

HIRSUTISM

Hypernatremia

HYPOKALEMIA

Assessment 1. Generalized muscle weakness and wasting 2. Truncal obesity 3. Moon-face 4. Buffalo hump 5. Easy bruisability

6. 7. 8.

Reddish-purplish striae on the abdomen and thighs Hirsutism and acne Hypertension

9. Hyperglycemia 10. Osteoporosis 11. Amenorrhea

Management:

Diet: Low Sodium, High Potassium FVE intervention    

Replace potassium Insulin istration Hypertension Surgery is adrenalectomy

Critical conditions:  Arrhythmias due to hypoK  Hypertensive crisis  Fluid overload  Hyperglycemia

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Cushing’s Syndrome (Secondary) - Pituitary gland disorder - Same with Cushing’s Disease - Surgery is hypophysectomy

• Addison’s Disease - Adrenal cortex disorder/ tumor, idiopathic - Hyposecretion of:  Mineralocorticoid: Aldosterone=Na and H2O excretion (hyponatremia, hypovolemia, hypotension), K reabsorption (hyperkalemia)  Glucocorticoid=hypoglycemia  Androgen=decreased libido ↑ MSH=bronzing of the skin (primary) Management - FVD intervention - Increase potassium excretion - Glucagon or simple sugar istration - Steroid medication Nursing Interventions - Monitor VS especially BP - Monitor weight and I and O - Monitor blood glucose level and K - ister hormonal agents as prescribed

- Observe for ADDISONIAN crisis - Educate the client regarding lifelong treatment, avoidance of strenuous activities, stress and seeking prompt consult during illness - Provide a high-protein, high carbohydrate and increased sodium intake Addisonian crisis - A life-threatening disorders caused by acute severe adrenal insufficiency Causes: - Severe stress - infection - trauma or surgery Pathophysiology - Overwhelming stimuli  mobilize body defense  decreased stress hormones  inadequate coping ASSESSMENT Findings for Addisonian Crisis= “severe lahat” - Severe headache - Severe pain - Severe weakness - Severe hypotension - Signs of Shock - Addison’s Disease Critical Conditions: - Addisonian crisis – cyanosis, with signs of circulatory shock: pallor, apprehension, rapid and weak pulse,

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↑ RR, and acute hypotension Dehydration Arrhythmias due to hyperkalemia Hypoglycemia Same with DI

Nursing Interventions - ister IV glucocorticoids, usually hydrocortisone - Monitor VS frequently - Monitor I and O, neurological status, electrolyte imbalances and blood glucose - ister IVF - Maintain bed rest - ister prescribed antibiotics Steroid - Dose is variable - Best time to give between 7-8 AM (active gland) to prevent side effects - Steroid-induced adrenal insufficiency = TAPERING the DOSE - Pituitary adrenal suppresion = DOSAGE CONTROL -

Steroid Hypertension, thromboembolism Prone to infection Glaucoma, corneal ulceration Muscle wasting, poor wound healing Osteoporosis, Hyperglycemia Weight gain, moon face, trunkal obesity, buffalo hump Acne MEDIC-ALERT CARD

• Addison’s Disease Critical Conditions - Dehydration

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Arrhythmias due to hyperK Hypovolemic shock Hypoglycemia Same with DI inc ACTH, inc cortisol = pituitary problem (benign tumor) normal ACTH, inc cortisol = adrenal problem (benign tumor) dec ACTH, dec cortisol = atrophy of the pituitary gland normal ACTH, dec cortisol = atrophy of the adrenal gland

• Pheochromocytoma - Hyperfunction of adrenal medulla - Cause: Tumor usually benign

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↑catecholamines (nor E and E)

Sign and Symptoms: - 5 H: HPN, Headache, Hypermetabolism

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Hyperglycemia, Hyperhidrosis(↑sweat),, n&v, anorexia, dilated pupils, weight loss, tremors, cold extremities, CHF and cerebral bleeding.

Diagnosis - ↑VMA vanilly mandelic acid (urine specimen)

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↑catecholamines (blood specimen) ↑blood sugar and glycosuria Monitor VS esp BP Give antihypertensive drugs:Phentolamine Provide high calorie foods Prepare pt forSurgical Intervention (adrenalectomy)

Abnormalities of the Thyroid Gland

• GOITER - Iodine-deficient - Goitrogenic = cabbage, beans - Compensatory hypertrophy - No s/sx, compression of the trachea - SSKI to suppress pituitary’s TSH secretions - Less than 40 fg/day of iodine = goiter - Iodized salt = 1:100,000 - PREVENTION = iodized salt  Hypothyroidism  Hyperthyroidism Note:  inc T3, inc T4, dec TSH = thyroid problem  inc T3, inc T4, inc TSH = pituitary tumor (benign) • Hypothyroidism Caused by: - Autoimmune Disease (Hashimoto’s Thyroiditis) - Use of radioactive iodine - Destruction or removal of thyroid tissue - Overtreatment of antithyroid drug  MYXEDEMA- Adults  CRETINISM- Children 3 Basic Concepts: - Decreased metabolic rate due to hyposecretion of T3 - Decreased body heat production due to hyposecretion of T4 - Hypercalcemia due to hyposecretion of calcitonin

Assessment 1. Lethargy and fatigue 2. Weakness and paresthesia 3. COLD intolerance 4. Weight gain 5. Bradycardia, constipation

6. Dry hair and skin, loss of body hair 7. Generalized puffiness and edema around the eyes and face

Con’t of s/sx - SQ swelling, puffy skin, puffy eyelids - Thinning of hair, loss of lateral 1/3 of the eyebrow - Menorrhagia or amenorrhea, decreased libido, abortions - Myxedema = severe complication leads to coma Management - Symptomatic - Monitor VS and daily weights - Provide warm environment - Diet: low calorie, high fiber - Thyroid hormone replacement - T4 Synthroid, Levothyroid - T3 Cytomel - T3 & T4 Proloid - T3 given NGT, faster than T4 - T4 given parenterally(S.E. adrenal insuf.) - Note: 3-12 wks S/Sx must disappear • Hyperthyroidism Caused by:  Grave’s Disease: Autoimmune  TSAb thyroid stimulating antibody duplicate

TSH, which increases thyroid hormone secretion ( ↑T3 and T4)  Toxic nodular goiter (benign, hot spot)  Overmedication of thyroid hormone  Severe emotional stress 3 Basic Concepts:  Increased metabolic rate due to hypersecretion of T3  Increased body heat production due to hypersecretion of T4

Hypocalcemia due to hypersecretion of calcitonin

Manifestations:  Nervousness, tremors, emotional lability  Weight loss, emaciated  Flushed skin, warm and moist  Increased temp and palpitation to atrial fibrillation  Heat intolerance  Hypertension  Difficulty in sitting quietly  Thyroid gland may be palpable and a (+) bruit  Diarrhea  Bulging eyes (exophthalmus), startled expression  Amenorrhea, oligomenorrhea, decreased libido  Delirium, disorientation, extreme nervousness  Arrhythmias  Thyroid storm = hyperpyrexia, diarrhea, dehydration,  tachycardia, arrhythmias, delirium, coma, shock, death Exophthalmus

Thyroid Scan

MANAGEMENT  Beta blockers- Metoprolol: Inderal  to control tachycardia and hypertension  Thiomides- PTU (propylthiouracil) and Tapazole ( Methimazole)

to inhibit synthesis of thyroid hormone side effects: Agranulocytosis and neutrpenia  Radioactive Iodine – isolation for a few days, body secretions are radioactive contaminated  Surgery:Thyroidectomy: 5/6 of the gland is removed  SSKI (Lugol’s) is given preop to dec thyroid vascularity & to inhibit release of thyroid hormone  Given with juice to disguise taste  Given with straw to prevent staining of teeth  Postop:  Position: Semi-fowlers, neck at the midline  Monitor for bleeding, prevent hemorrhage by placing ice collar over the neck  Monitor blood pressure- to assess for TROUSSEAU’S Sign ( hypocalcemia)  Check for tetany and monitor for signs of hypocalcemia (parathyroid gland is severed)  give calcium gluconate  Hoarseness of voice-laryngeal nerve damage- ask the client to speak every hour  Watchout thyroid crisis THYROIDECTOMY  Removal of the thyroid gland

NURSING INTERVENTIONS 1. Provide adequate rest periods in a quiet room 2. ister anti-thyroid medications that block hormone synthesis- Methimazole and PTU 3. Provide a HIGH-calorie diet, HIGH protein 4. Manage diarrhea 5. Provide a cool and quiet environment 6. Avoid giving stimulants 7. Provide eye care  Hypoallergenic tape for eyelid closure 8. ister PROPRANOLOL for tachycardia 9. ister IODIONE preparation- Lugol’s solution and SSKI to inhibit the release of T3 and T4 10. Prepare clients for Radioactive iodine therapy 11. Prepare patient for thyroidectomy 12. Manage thyroid storm appropriately

DISORDERS OF the THYROID GLAND Thyroid storm  An acute LIFE-threatening condition characterized by excessive thyroid hormone CAUSE: Manipulation of the thyroid during surgery causing the release of excessive hormones in the blood ASSESSMENT Findings for Thyroid Storm 1. HIGH fever 2. Tachycardia and Tachypnea 3. Systolic HYPERtension 4. Delirium and coma 5. Severe vomiting and diarrhea 6. Restlessness, Agitation, confusion and Seizures

NURSING INTERVENTIONS 1. Maintain PATENT airway and adequate ventilation 2. ister anti-thyroid medications such as Lugol’s solution, Propranolol, and Glucocorticoids 3. Monitor VS 4. Monitor Cardiac rhythms 5. ister PARACETAMOL 6. ( not Aspirin) for FEVER 7. Manage Seizures as required. 8. Provide a quiet environment

Parathyroid Gland Abnormalities  Hypoparathyroidism  Hyperparathyroidism

Parathyroid Gland - produce parathyroid hormone/parathormone which regulates calcium and phosphorus balance dec serum Ca level ↓ PTH release ↓ withdraws Ca from bones ↓ ↑ serum Ca levels Therefore: Hyperparathyroidism: Hypercalcemia Hypoparathyroidism: Hypocalcemia • Hypoparathyroidism Caused: - Accidental removal or destruction of parathyroid gland - Thyroidectomy - Radical neck dissection - Idiopathic - Autoimmune Diagnostic: - Decreased PTH - Decreased serum Ca (7.5 mg/100 ml) - Increased PO4 Manifestation: - Hypocalcemia - Tetany - Numbness of fingers - +Chvostek’s sign - +Trousseau’s sign

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+Laryngeal spasm Severe anxiety and apprehension Muscle cramps Cardiac dysrhythmias

Management: - Treat the cause

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IV calcium gluconate -Syringe and ampule of Ca sol. on bedside Oral Ca with Vit. D

• Hyperparathyroidism Caused:  Primary  Tumor/adenoma  hyperplasia Diagnostic: - Increased vit D - Increased PTH - Increased serum Ca (11 mg/100 ml) - Decreased PO4 Manifestation: - Hypercalcemia - Decalcification of bone - Fracture - Deep bone pain - Depression of neuromuscular function - Generalized fatigue - Memory loss - Dec LOC, stupor coma Management: - Treat the cause - Hydration (IV saline)

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Diuretics (Ca excretion) Calcitonin (inhibits bone resorption) Dietary Ca restriction Avoid thiazide and vit D (may increase Ca) Dialysis Digitalis is withdrawn (may increase Ca)

Pancreas: Islet of langerhans Alpha- glucagon- ↑blood sugar (hyperglycemia) by stimulating glycogenolysis & gluconeogenesis Beta- insulin- ↓blood sugar (hypoglycemia) by facilitating transport of glucose across cell membranes of muscle, liver, adipose tissue, inhibits breakdown of proteins, requires Na for transport of CHO and requires K for production

• Diabetes Mellitus

- DM is a disorder of glucose intolerance caused by a deficiency in insulin production and action resulting in hyperglycemia and abnormal CHO, CHON and fat metabolism.

Types  Type I or IDDM no insulin diseased pancreas (beta cell)  Type II NIDDM decreased insulin inadequate insulin • IDDM- Juvenile Onset DM, Brittle DM, Unstable DM - Genetic and hereditary - Zero insulin - Coxsackie virus - Onset: Young age before 30 y/o - 5-10% of persons with diabetes - 3 P’s with weight loss - Thin - DKA Management - Diet - Activity/Exercise - Insulin • NIDDM- Maturity Onset DM, Stable DM, Ketosis Resistant DM - Adult onset - Genetic - 90-95% of persons with diabetes - Insulin resistance - Obesity - 3 P’s - HHNK Coma or HONK Coma Manifestations - Polyuria- glucose exert high osmotic pressure w/in the renal tubules, osmotic diuresis occurs, hypovolemia, ECF/ICF dehydration - Polydipsia- results from ECF/ICF dehydration - Polyphagia- the cells are starved

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Glycosuria- glucose level exceed renal threshold (180mg/dl) Inc Blood Viscosity- sluggish circulation, microorganism proliferation, infection Ketonuria Tissue wasting Weight Loss

Complications - Macroangiopathies  brain: CVA  heart: Myocardial Infarction peripheral arteries: peripheral vascular disease - Microangiopathies  kidneys: renal failure  eyes: retinopathy/cataract - Neuropathy  spinal cord/ ANS  paralysis  peripheral neuropathy  numbness/tingling sensation  neurogenic bladder Management - Diet - Activity/Exercise - Oral Hypoglycemic Agents - Insulin- in case of stress, surgery, infection, pregnancy---these conditions trigger stress response and stimulate the secretion of epi, norepi, glucocorticoids thereby causing hyperglycemia - DIET- CHO 50%, Fats 30%, CHON 20% - ↓ calorie specially if obese - ACTIVITY/EXERCISE- ↑ CHO uptake by the cells, ↓ insulin requirements, maintains ideal body weight  done 1-2 hours after meals to prevent hypoglycemia  regular pattern - MEDICATIONS: Oral Hypoglycemic Agents- indicated only in type II DM - INSULIN OHA = oral hypoglycemic agents - Sulfonylureas - stimulates insulin secretions and increases tissue sensitivity to insulin (Glipizide, Euglucon) - Biguanides – decreases intestinal uptake and hepatic production of glucose and increases tissue sensitivity (Glucophage) Alpha - Glucosidase Inhibitor – slows CHO carbohydrate absorption (Glucobay) - Thiazolidinediones – insulin sensitizer, increases tissue sensitivity to insulin (Avandia) TYPES OF INSULIN Immediate Acting, Lispro Rapid Acting clear insulin Humulin R, Regular, Semilente Actrapid

ONSET

PEAK

DURATION

5-15 min

30-90 min

hours

30-60min

2-4 hours

6-8 hours

Intermediate Actingcloudy NPH Lente, Humulin N Monotard Long Acting cloudy UltraLente

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1-2 hours

6-8 hours

18-24 hours

3-4hours

1620hours

30-36 hours

Mixture of NPH and Regular Humulin 70/30 Novolin 70/30 Humulin 50/50 Onset 2 hours Peak 8-12 hours Duration 12-16 hours

About Insulin! - Hyperinsulinism – tremors, hunger and diaphoresis will manifest - Somogyi Phenomenon – rebound hyperglycemia after insulin istration (gradual reduction of insulin is the key to manage it) - Lipodystrophy is a complication if the site of injection is not rotated properly, it can also alter the rate of insulin absorption. - Insulin Pump – external battery operated, needle is inserted SQ that delivers regular insulin (monitor hypokalemia) Nursing Interventions - Site – abdomen (best site), upper arms, upper buttocks- rotate the site of injection - Route – SQ, only REGULAR insulin can be given as IV bolus esp in case of DKA (flush the line first it will absorb insulin) - IV bolus – mixed with D5W if hypoglycemic, or PNSS ideal for DKA and HONKS - Subcutaneous-Pinch or 45° for thin patient, 90° for regular client - Good site must be supple skin. - Mixed Insulin – regular (clear) first to be drawn followed by NPH (cloudy) - ister at room temp- cold insulin leads to lipodystrophy - Refrigerate after use.

Diagnostic Evaluation - Fasting Blood Sugar –80-120mg/dl ≥ 140 mg/dl for 2 readings - 2H Postprandial Blood Sugar Test – ≥ 200 mg/dl 100 gm of sugar orally then check after 2H - OGTT -≥ 200 mg/dl blood is withdrawn initially 150-300 gm of CHO/sugar PO every hour bloos specimen is taken (1H,2H,3H after)

done when results of FBS and 2H PPBS are borderline

- Random Blood Sugar – ≥ 200 mg/dl for 2x + 3 P’s blood is withdrawn anytime - Glycosylated Hg A1C can detect average serum glucose level over preceding 2-3 months (most reliable) Adult 2.2%-4.0% Children 1.8%-4.0%