ScopePhysiology
Disorders
PITUITARY DISEASES ADH DISEASES ADRENAL GLANDS DISEASES THYROID DISEASES PARATHYROID DISEASES PANCREAS DISEASES
Major Hormone Secreting Glands
“The Sequence”Hypothalamus↓Pituitary Gland or HypophysisAnterior or AdenohypophysisPosterior 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
The Pituitary Gland- Is a gland located below the hypothalamus at the base of the brain.
APGAdenohypophysis- TSH - target thyroid gland- 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)
PPGNeurohypophysis- 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
Thyroid and ParathyroidThe 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 glandsAnatomy- Located at the back of the thyroid glands- Four in number
- Follicular Cells- T3, T4- ↑BMR, and- ↑ CHON and bone turnover- T3- metabolism, growth- T4- catabolism, body heat production- C Cells- Calcitonin - ↓calcium & phosphate levels - Parathormone -calcium & phosphorus regulation, osteoclast
The PhysiologyParathyroid Hormone is released in HYPOCALCEMIA -↑ calcium level
Calcitonin is stimulated by HYPERCALCEMIA-↓calcium level
Parathyroid hormone is NOT secreted in HYPERCALCEMIA
Calcitonin is inhibited by HYPOCALCEMIA
The Adrenal GlandsAnatomy- 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 GONADSAnatomy
OvariesThese two almond-shaped glands are found in the pelvic cavity attached to the uterus by the ovarian ligament
TestesThese two oval-shaped glands are found in the scrotum
PhysiologyOvary- estrogen - affects devt of female sex organs and secondary sexual characteristics- progesterone- influences menstrual cycle, stimulates the growth of uterine wall, and maintains pregnancyTestes- testosterone- affects the devt of male sex organs and secondary sexual characteristics
Pineal GlandMelatonin (dec skin pigmentation, inhibit gonadotropic hormone)
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 hormones2. HYPO- when the gland does not secrete enough hormonesHyper 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 ICP (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 Findings1. Increased growth Gigantism or Acromegaly2. large and thick hands and feet3. Visual disturbances4. Hypertension, hyperglycemia5. Organomegaly
Pituitary TumorsBasophilic 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 ICP
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
Oral care- Monitor LOC and neurologic status- No activity that will increase ICP- Watchout Diabetes Insipidus, Monitor I & O- Observe for CSF leakage- Administer prescribed medications
DISORDERS OF THE POSTERIOR PITUITARY GLAND: ADH Abnormality SIADH DI
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 changes2. Abnormal weight gain3. DISORDERS OF the PITUITARY GLAND: Posterior gland4. ASSESSMENT findings5. Hypertension6. Anorexia, Nausea and Vomiting7. 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 Interventions1. Monitor VS and neurologic status2. Provide safe environment3. Restrict fluid intake (less than 500cc/day)4. Monitor I and O and daily weight5. Administer Diuretics and IVF carefully6. Administer 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 findings1. Polyuria of more than 4 liters of urine/day2. Polydipsia3. Signs of Dehydration4. Muscle pain and weakness5. Postural hypotension and tachycardia
Diagnostic Test1. Urinary Specific gravity very low, 1.006 or less2. Serum Sodium levels high
Management:- FVD intervention- Synthetic ADH administration (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 Interventions1. Monitor VS, neurologic status and cardiovascular status2. Monitor Intake and Output3. Monitor urine specific gravity4. Provide adequate fluids5. Administer Chlorpropamide or Clofibrate as prescribed to increase the action of ADH if decreased6. Administer 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
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 Interventions1. Monitor VS, I and O and urine sp gravity2. Monitor serum K and Na3. Provide Potassium rich foods and supplements4. Administer prescribed diuretic- Spironolactone- K sparer5. Maintain sodium-restricted diet6. Prepare patient for possible surgical interventions
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
Exaggerated functions
1. Gluconeogenesis HYPERGLYCEMIA
2. Protein breakdown OSTEOPOROSISS, delayed wound healingPurplish striae , BleedingMuscle wasting
3. Fat breakdown THIN extremity, Truncal deposition
4. Decreased WBC IMMUNOSUPPRESSION
Functions of Mineralocorticoids
Exaggerated functions
1. Sodium Retention Hypernatremia
2.Secondary water retention
Hypervolema- Hypertension
3. Potassium excretion HYPOKALEMIA
Function of androgen: Hair growth
HIRSUTISM
Assessment1. Generalized muscle weakness and wasting2. Truncal obesity3. Moon-face4. Buffalo hump5. Easy bruisability
6. Reddish-purplish striae on the abdomen and thighs7. Hirsutism and acne8. Hypertension
9. Hyperglycemia10. Osteoporosis11. Amenorrhea
Management: Diet: Low Sodium, High Potassium FVE intervention Replace potassium Insulin administration Hypertension Surgery is adrenalectomy
Critical conditions: Arrhythmias due to hypoK Hypertensive crisis Fluid overload Hyperglycemia
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 administration- Steroid medication
Nursing Interventions- Monitor VS especially BP - Monitor weight and I and O- Monitor blood glucose level and K- Administer 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,- ↑ RR, and acute hypotension - Dehydration- Arrhythmias due to hyperkalemia- Hypoglycemia- Same with DI
Nursing Interventions- Administer IV glucocorticoids, usually hydrocortisone- Monitor VS frequently- Monitor I and O, neurological status, electrolyte imbalances and blood glucose- Administer IVF- Maintain bed rest- Administer 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 DiseaseCritical Conditions- Dehydration- 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- catecholamines (nor E and E)
Sign and Symptoms:- 5 H: HPN, Headache, Hypermetabolism- Hyperglycemia, Hyperhidrosis(sweat),, n&v, anorexia, dilated pupils, weight loss, tremors, cold extremities, CHF and cerebral
bleeding.
Diagnosis - VMA vanilly mandelic acid (urine specimen)- 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)
HypothyroidismCaused 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
Assessment1. Lethargy and fatigue
2. Weakness and paresthesia3. COLD intolerance4. Weight gain5. Bradycardia, constipation6. Dry hair and skin, loss of body hair7. 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
HyperthyroidismCaused 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 INTERVENTIONS1. Provide adequate rest periods in a quiet room 2. Administer anti-thyroid medications that block hormone synthesis- Methimazole and PTU3. Provide a HIGH-calorie diet, HIGH protein4. Manage diarrhea5. Provide a cool and quiet environment6. Avoid giving stimulants7. Provide eye care
Hypoallergenic tape for eyelid closure8. Administer PROPRANOLOL for tachycardia9. Administer IODIONE preparation- Lugol’s solution and SSKI to inhibit the release of T3 and T410. Prepare clients for Radioactive iodine therapy11. Prepare patient for thyroidectomy12. 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 Storm1. HIGH fever2. Tachycardia and Tachypnea3. Systolic HYPERtension4. Delirium and coma5. Severe vomiting and diarrhea6. Restlessness, Agitation, confusion and Seizures
NURSING INTERVENTIONS1. Maintain PATENT airway and adequate ventilation2. Administer anti-thyroid medications such as Lugol’s solution, Propranolol, and Glucocorticoids3. Monitor VS4. Monitor Cardiac rhythms
5. Administer PARACETAMOL 6. ( not Aspirin) for FEVER7. 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
HypoparathyroidismCaused:- 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- +Laryngeal spasm - Severe anxiety and apprehension- Muscle cramps- Cardiac dysrhythmias
Management:- Treat the cause- IV calcium gluconate -Syringe and ampule of Ca sol. on bedside
- Oral Ca with Vit. D
HyperparathyroidismCaused:
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)- 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 insulindiseased pancreas (beta cell)
Type II NIDDMdecreased insulininadequate 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- Glycosuria- glucose level exceed renal threshold (180mg/dl)- Inc Blood Viscosity- sluggish circulation, microorganism proliferation, infection- Ketonuria- Tissue wasting- Weight Loss
Complications- Macroangiopathies
brain: CVAheart: Myocardial Infarctionperipheral arteries: peripheral vascular disease
- Microangiopathieskidneys: renal failureeyes: retinopathy/cataract
- Neuropathyspinal cord/ ANSparalysisperipheral neuropathynumbness/tingling sensationneurogenic 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 hypoglycemiaregular 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
ONSET PEAK DURATIONImmediate Acting, Lispro
5-15 min 30-90 min hours
Rapid Actingclear insulin Humulin R, Regular, Semilente Actrapid
30-60min 2-4 hours 6-8 hours
Intermediate Acting-cloudy NPH Lente, Humulin N Monotard
1-2 hours 6-8 hours 18-24 hours
Long Acting cloudy UltraLente
3-4hours 16-20hours
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 administration (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)- Administer 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/dl100 gm of sugar orally then check after 2H
- OGTT - 200 mg/dlblood 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%
