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Test # 5

Hypothalmus Consist of Posterior Pituitary (Anti-Diuretic Hormone) & Anterior Pituitary (Releasing Hormones)
Posterior Pituitary Stores ADH & Oxytocin
ADH Comes from the posterior Pituitary
ADH Is stimulated by: dehydration and Low B/P.
ADH (Action) The Kidneys reasorbs the water
ADH (Result) Increase B/P & Increase the blood volume
Oxytocin Comes from the posterior pituitary
Oxytocin Stimulated by dilation of the cervix, & stimulation of the breast
Oxytocin (Action) Uterine contracts
oxytocin (results) The letdown reflex (milk is released)
Hypothalmus Produces releasing hormones leading into the Anterior Pituitary
Anterior Pituitary Releases Prolactin, ATCH, LH, TSH, GH, FSH
Prolactin (Anterior Pituitary Releases) Stimulates milk production
FSH (Anterior Pituitary Releases) Stimulates sperm & ova production
GH (Anterior Pituitary Releases) Stimulates Growth
LH (Anterior Pituitary Releases) Stimulates release of sex hormones & Ovalation
ATCH (Anterior Pituitary Releases) stimulates adrenal cortex & Adrenal Medulla
Adrenal cortex (ATCH) consist of 3 hormones: sex hormone, Aldostrone, Cortisol
Aldostrone hormone is stimulated by low B/P, Low sodium, and increase potassium.
Aldosterone action Increases sodium & water absorption and increase B/P.
Cortisol Action Decrease inflammation, and stimulated glucongenosis, "glycogen to glucose"
Adrenal Medulla (ATCH) Stimulated by stress, and flight or fight response
Adrenal Medulla (ATCH) 2 Hormones Epinephrine & Norepiephrine
Epinephrine (Adrenal Medulla (ATCH)) Increases HR & B/P, Dilates bronchioles= Action Increase O2, Liver converts glycogen in to glucose= "Burst of energy"
Norepiephrine (Adrenal Medulla (ATCH)) Action is vasocostriction= increase B/P
TSH (Anterior Pituitary Releases) Thyroid Simulating Hormone, has 2 main hormones (Tyroid & Parathyroid)
Thyroid Hormone (Thyroid Simulating Hormone) Has 3 hormones within itself (Calcitonin, T3, & T4)
Calcitonin (Thyroid Hormone)Stimulated calcium in the blood.
Calcitonin (Thyroid Hormone) action Action is to help reabsorb calcium into the bone
T3 & T4 (Thyroid Hormone) Regulates metabolism
Parathyroid (Thyroid Simulating Hormone) Pulls calcium from the bone, increases calcium in the blood for re-absorption by the kidneys.
Parathyroid (Thyroid Simulating Hormone) Intervention to keep calcium in the blood weight bearing activities, eating calcium rich foods, keeps calcium in the blood.
TSH levels TSH levels will be high if T3 and T4 is low
Hypothalmus structure above the pituitary gland, translates nervous system impulses into the endocrine system
Pituitary gland Produces hormones that regulate the secretion of the other glands.
Pineal body produces the hormone melatonin
Thyroid produces the hormones that regulate body metabolism
Parathyroid secretes parathyroid hormone which affects the amount of calcium in the blood
Thymus Produces the hormone thymosin that stimulates the lymphoid organs to produce T-lymphocytes or antibodies in newborns and young children.
Pancrease produces the hormones insulin and glucagon. Insulin regulates transportation of sugar, fatty acids, and aminoacids into the cells.
Adrenal glands produces 30 hormones
Gonads The primary sex gland
Function of the Endocrine System Effects almost every cell, organ, and function of the body. The endocrine system is closely linked with the nervous system and the immune system, Negative feedback mechanism
Hormones Chemical messengers of the body Act on specific target cells
Effects of Aging Secretions decrease with age but does not lead to serious hormones deficiencies or illness unless specific pathological conditions develop
Assessment (Health History)1 Neuromuscular changes: spasms, twitching, signs of neuropathy, Weight, Excessive Thirst , Urination, Change in energy level Heat or Cold Tolerance Mood and Memory: mood swings, agitation, confusion,
Assessment (Health History)2 Family Hx: diabetes mellitus, diabetes insipidus, goiter, obesity, Addison’s disease, infertility. Sexual history: changes, characteristics, menstruation, menopause, hormone replacement therapy
Assessment(Physical Exam)1 Vital Signs: changes in P/T may be seen in Thyroid disorders; changes in BP may be seen in Adrenal disorders Weight: changes seen in Thyroid & Adrenal disorders in addition to diabetes
Assessment(Physical Exam) 2 Skin Changes: hyperpigmentation seen in Addison’s disease; dry scaly skin seen in hypothyroid; dusky lower extremities with weak pulses seen in DM Tremor: seen in hyperthyroidism, hypoglycemia, & pheochromocytoma
Assessment(Physical Exam)3 Affect: depression seen in hypothyroidism; nervousness seen in hyperthyroidism & pheochromocytoma; agitation may be seen in hypoglycemia Exophthalmos(bulging eyes): seen in Graves Disease [Fat deposits & edema behind the eyes]
Assessment(Physical Exam)4 Fat Pads: seen in Cushing’s Syndrome [commonly seen on back on neck (buffalo hump), shoulders & ‘moon’ face] Enlarged Thyroid: Excessive stimulation by TSH in both type of thyroid diseases
Thyroid Tests 1 TSH: secreted by the Pituitary; increases in HYPOthyroidism because the pituitary is sending out MORE of this hormone trying to STIMULATE the thyroid to function better.
Thyroid Tests 2 Decreases in HYPERthyroidism because the pituitary senses that the thyroid is overactive. T3 and T4: directly secreted from the thyroid so they decrease in Hypothyroid and increase in Hyperthyroid.
Parathyroid Tests 1 PTH (Parathyroid Hormone): Increases in hyperparathyriodism; decreases in hypoparathyroidism Calcium: Increases in Hyperparathyroidism; decreases in hypoparathyroidism
Parathyroid Tests 2 Phosphorus: opposite of calcium (see/ saw effect); decreases in hyperparathyroidism, increases in hypoparathyoidism
Pituitary Tests 1 GH (Growth Hormone): Increased in Acromegaly; decreased in small stature or dwarfism ADH (Antidiuretic Hormone/ Vasopressin): increased in SIADH; decreased in diabetes insipidus
Pituitary Tests 2 Urine Specific Gravity: decreased in diabetes insipidus ACTH (Adrenocorticotropic Hormone): Increased in Addison’s; Decreased in Cushings & long term steroid therapy
Adrenal Tests 1 Cortisol: Increased in Cushing’s Syndrome & stress; Decreased in Addison’s disease & steroid withdrawal 24-Hour Urine for VMA: Increased in Pheochromocytoma Pancreatic Function Tests (Diabetes)
Pancreatic Function Tests (Diabetes)1 Fasting Blood Glucose: Increased in Cushing’s & Diabetes; Decreased in hypoglycemia & Addison’s Glycosylated Hemoglobin (HbA1c): 7% or greater seen in poor diabetes control
Pancreatic Function Tests (Diabetes)2 Fructosamine (glycated albumin): increased in poor diabetes control; decreased in severe hypoproteinemia
Endocrine Disorder Result From Insufficient Hormone Activity Hypofunction of a gland Insensitivity of the target tissue
Endocrine Disorder Result Excessive Hormone Activity Hyperactive Gland Ectopic Hormone Production Self Administration of Too much Replacement Hormone
Endocrine Disorder Primary Disorder Problem within the gland that is out of balance
Endocrine Disorder Secondary Disorder Caused by Problems outside the Gland Imbalance in a tropic hormone Drugs Trauma Surgery Problem in Feedback Mechanism
ADH Disorders Too Little = Diabetes Insipidus
ADH Disorders Too Much = SIADH (Syndrome of Inappropriate Antidiuretic Hormone)
Diabetes Insipidous Pathophysiology Insufficient ADH (AntiDiuretic Hormone: responsible for reabsorption of water in the kidneys) If ADH is lacking reabsorption is prevented, leading to diuresis. Patients urinate 3–15 L per Day
Diabetes Insipidous Causes Pituitary Tumor, Surgery or Trauma to the Pituitary gland Drugs such as glucocorticoids or alcohol
Diabetes Insipidous Causes Psychogenic (patient drinks large amounts of drugs in the absence of disease) Nephrogenic (occurs mostly in males) diagnosed when kidneys do not respond to ADH often caused by kidney disease
Diabetes Insipidous Signs & Symptoms 1 Polyuria & Polydipsia (extreme thirst) Nocturia Dilute Urine (Urine specific gravity decreased) Dehydration (Increased serum osmolality resulting in concentrated blood)
Diabetes Insipidous Signs & Symptoms 2 Hypotension, poor skin turgor & weakness Hypovolemic Shock Decreased LOC Death
Diabetes Insipidous Diagnosis Urine Specific Gravity <1.001 Plasma Osmolality Increased CT or MRI done to determine Cause Urine Glucose may also be checked to rule out Diabetes mellitus.
Diabetes Insipidous Diagnosis Water Dep Test 1 Water Deprivation Test (patient deprived of H2O for 6 hrs; body wt & urine osmolality are tested hourly. If urine continues to be & patient is losing weight as a result of volume depletion, Diabetes Insipidous is suspected.
Diabetes Insipidous Diagnosis Water Dep Test 2 In the second stage of the test the patient receives an injection of ADH with a final urine test 1 hour later. If Diabetes Insipidous is nephrogenic, the kidneys will not repsond to the ADH.
Diabetes Insipidous Diagnosis ADH levles ADH levels can be measured in the blood or urine following administration of hypertonic saline or fluid restriction. Normal response would be elevated ADH. If it is not elevated Diabetes Insipidous is suspected.
Diabetes Insipidous Interventions & Nursing Care 1 Hypotonic IV Fluids & Encourage PO Fluids IV or SQ Vasopressin (synthetic form of ADH) Intranasal DDAVP (Desmoopressin) used for long term therapy Diabinese used to help the kidneys respond better to ADH
Diabetes Insipidous Interventions & Nursing Care 2 Thiazide Diuretics Decrease urine flow in the absence of ADH Hypophysectomy required if Pituitary Tumor is Involved Monitor Daily weight, I&O, vital signs & Urine Specific Gravity Report significant drop in BP or increase in Pulse to RN or MD
SIADH (Syndrome of Inappropriate Diuretic Hormone)Pathophysiology Too Much ADH (opposite effect of diuretic) Excess water is reabsorbed by the kidney, leading to decreased urine output & fluid overload Decreased Serum Osmolality (blood becomes diluted
SIADH (Syndrome of Inappropriate Diuretic Hormone)Causes Some Cancers may be ectopic sites for production of ADH like substance Drugs: some antidepressants, Chemo, Anesthesia Brain Tumors or Infections
SIADH (Syndrome of Inappropriate Diuretic Hormone Signs & Symptoms Weight Gain Without Edema Dilutional Hyponatremia Serum Osmolality <275 mOsm/kg Concentrated Urine Muscle Cramps and Weakness d/t electrolyte imbalance Brain Swelling, Lethargy, Confusion, Seizures, Coma, Death
SIADH Diagnostic tests Serum/Urine Sodium Serum/Urine Osmolality Serum ADH will be High Testing to locate ADH secreting tumor
SIADH Diagnostic tests (Water Load Test) Water Load Test: administer a specific amount of water, then measure blood & urine sodium & osmolality hourly for 6 hours; Patients with SIADH retain water instead of secreting it
SIADH Interventions & Nursing Care 1 Eliminate Cause Surgical Removal of Tumor Fluid Restriction of 800-1000 ml/ 24 hrs; offer small amounts of fluids in high sodium Offer hard candy to reduce sensation of thirst Provide ice chips but must count as part of fluid restriction
SIADH Interventions & Nursing Care 2 Oral Sodium encouraged to maintain Serum Sodium levels Hypertonic Saline IV Lasix or Declomycin used to block action of ADH in the kidney if the cause is inoperable Cancer Monitor daily weight, I & O, VS. Lung sounds & lab values
SIADH Interventions & Nursing Care 3 Report Change in Level of Consciousness immediately Monitor for Seizures Encourage the use of a Medic Alert Bracelet Instruct patient to report any weight gain of greater than 2lbs in 1 day, change in urine output or acute thirst
Growth Hormone Imbalance Too Little = Short Stature/ Dwarfism
Growth Hormone Imbalance Too Much = Gigantism, Acromegaly
Growth Hormone Deficiency Pathophysiology Deficient GH in Childhood results in short stature Growth Not Affected in Adults
Growth Hormone Causes Tumor, Surgery, or Trauma to the Pituitary or Hypothalmus Failure of Pituitary to Develop Psychosocial: severe neglect or emotional stress Malnutrition most common cause worldwide
Growth Hormone Signs & Symptoms in Children Grow Only to 3 to 4 Feet with normal body proportions Slowed Sexual Maturation May Have Mental Retardation Other Symptoms, Depending on Other Pituitary Hormones Involved
Growth Hormone Signs & Symptoms in Adults Fatigue, Weakness, Excess Body Fat, Hypercholesterolemia, Decreased Muscle and Bone Mass. Sexual Dysfunction, Risk for CVD, Headaches, Mental Slowness, Psychological disturbances, Decreased Quality of Life, Growth Hormone Imbalance
Growth Hormone Deficiency Diagnosis GH Stimulation test: Measures GH in Response to Induced Hypoglycemia MRI for presence of Pituitary Tumor
Growth Hormone Deficiency Interventions & Nursing Care Administer Synthetic GH (Somatropin) SQ Surgery to remove Pituitary Tumor
Acromegaly Pathophysiology Excess Growth Hormone in Adults Bones Grow in Width, Not Length Organs and Connective Tissues Also Enlarge Impaired Tolerance to Carbohydrates leads to Elevated BG
Acromegaly Causes Pituitary Hyperplasia (excess growth) Benign Pituitary Tumor Hypothalamic Dysfunction
Acromegaly Signs & Symptoms Change in Shoe or Ring Size Nose, Jaw, Brow, hands & Feet Enlarge Teeth May Be Displaced causing difficulty chewing or dentures do not fit Difficulty Speaking and Swallowing Sleep Apnea develops
Acromegaly Signs & Symptoms Headaches & Visual Changes result from pressure of the tumor Diabetes Mellitus may develop d/t increased workload on the pancreas Osteoporosis & Arthritis Erectile dysfunction in men & Amenorrhea in women
Acromegaly Diagnosis GH Level & GH Response to Oral Glucose (normally glucose suppresses GH release) CT Scan or MRI to locate Pituitary Tumor Example of Acromegaly
Acromegaly Interventions & Nursing Care 1 Treat Cause Hypophysectomy: Lifelong TH, Steroids, Desmopressin, & Sex Hormone Replacement Sandostatin: decreases GH levels (injectable); Parlodel decreases GH levels (PO) Pegvisomant (Somavert) blocks the effects of GH on receptor sites
Acromegaly Interventions & Nursing Care 2 Acknowledge patient ‘s feelings of anger or depression r/t body image changes Provide Information regarding support groups Assess for increased risk for injury; maintain safe environment Request swallowing eval; Observe for sleep apnea
Acromegaly Undergoing Hypophysectomy Baseline Neurological Assessment Preoperative Teaching Deep Breathing, Incentive Spirometry Avoid Coughing, Sneezing, Straining Postop Let patient know symptoms will be relieved but bone growth & visual changes may not reverse
Acromegaly Undergoing Hypophysectomy Post-Op Care Neurologic Assessment Urine for Specific Gravity (Risk for DI) Nasal Packing and Mustache Dressing if surgery was done transsphenoidal (Do not remove)
Acromegaly Undergoing Hypophysectomy Post-Op Care Monitor & Report Cerebrospinal Fluid Drainage (use glucose test strips to check drainage) No Coughing, Sneezing, Blowing, Straining, Bending HRT with Target Hormones
Acromegaly Undergoing Hypophysectomy Education Blow Nose Gently Take Stool Softeners and Antitussives prn Brush Teeth Carefully Take Hormones as Prescribed Call if Fever, Drainage, Frequent Urination, Excessive Thirst
Thyroid Hormone Imbalance Hypothyroidism Pathophysiology: primarily occurs in women over 50; if occurs in Infants severe G&D problems occur
Thyroid Hormone Imbalance Hypothyroidism Primary Not Enough TH even though enough TSH is being secreted by the pituitary gland
Thyroid Hormone Imbalance Hypothyroidism Secondary = Not Enough TSH from the pituitary gland to stimulate TH
Thyroid Hormone Imbalance Hypothyroidism Tertiary = Not enough Throtropin releasing Hormone (TRH) secreted by the Hypothalmus
Thyroid Hormone Imbalance Hypothyroidism Most cases of Hypothyroidism are Primary All result in Slowed metabolism and in severe cases Myxedema (nonpitting edema throughout the body)
Thyroid Hormone Imbalance Hypothyroidism Causes Congenital Defect, Inflammation of the Thyroid, Iodine Deficiency Autoimmune (Hashimoto’s Thyroiditis) destroys thyroid tissue & leads to hypothyroidism Pituitary or Hypothalmic lesion; Thyroidectomy
Thyroid Hormone Imbalance Hypothyroidism S&S Fatigue, Bradycardia, Hypoventilation Constipation, Weight Gain Mental Dullness Cold Intolerance Dry Skin and Hair Heart Failure, Hyperlipidemia
Thyroid Hormone Imbalance Hypothyroidism S&S Myxedema 1 develops in advanced disease Hypothermia: temp less than 95 Decreased respirations, mental function and lethargy Decreased BG, decreased Cardiac Output, decreased kidney perfusion resulting in nonpitting edema of the face, hands & feet
Thyroid Hormone Imbalance Hypothyroidism S&S Myxedema 2 Patient needs intubation, ventilation, warming blankets, IV Synthroid
Hypothyroidism Diagnosis T3 and T4 Low TSH High in Primary in attempt to stimulate TH TSH Low in Secondary Serum Cholesterol and Triglycerides
Hypothyroidism Interventions & Nursing care 1 Hormone Replacement: Levothyroxine/Synthroid; monitor labs for therapeutic levels Assess for Fatigue Monitor elderly for orthostatic hypotension Monitor for constipation: encourage fiber, water & ambulation
Hypothyroidism Interventions & Nursing care 2 Obtain order for stool softner if needed Assess skin for dryness, apply lotion, assist with transfer q2hrs
Hypothyroidism Interventions & Nursing Care for Myxedema Coma Monitor VS hourly Warming Blanket Ensure patent airway & Mechanical Ventilation as needed IV Levothyroxine (Synthroid) IV Fluids w/ Glucose
Hypothyroidism Interventions & Nursing Care for Myxedema Coma Administer corticosteroids as ordered Monitor changes in LOC hourly Aspiration precautions
Hyperthyroidism Pathophysiology: All forms cause Increased Metabolic Rate & number of Beta-Adrenergic receptor sites, which increases activity of norepinephrine increasing fight or flight response and resulting symptoms
Hyperthyroidism Primary Too Much TH
Hyperthyroidism Secondary = Too Much TSH from pituitary overstimulates the thyroid gland
Hyperthyroidism Tiertiary = Excess TRH from the hypothalmus
Hyperthyroidism Causes Autoimmune (Grave’s Disease) Multinodular Goiter or Toxic Adenoma Thyroiditis or tumor Pituitary Tumor (Secondary) Synthroid Overdose
Hyperthyroidism S&S 1 Hypermetabolic State: Heat Intolerance, Increased, Appetite, Weight Loss, Frequent Stools, Nervousness, Tachycardia, Palpitations, Tremor, Heart Failure can result from inefficient heart pump, Warm Smooth Skin,
Hyperthyroidism S&S 2 Exophthalmos: bulging of eyes (Grave’s Disease) Photophobia, blurred or double vision Mania & Psychosis in long term untreated disease Elderly often present with heart failure, A-fib, fatigue, Apathy, & depression
Hyperthyroidism Diagnosis 1 Elevated T3 and T4 TSH Low in Primary TSH High in Secondary (Pituitary cause) TSI (Thyroid Stimulating Immunoglobulin) is present in Graves
Hyperthyroidism Diagnosis 2 Radioactive Iodine uptake test or thyroid scan can be done to determine hyperactivity of the gland or locate a nodule or tumor
Hyperthyroidism Complications 1 Thyrotoxic Crisis (Thyroid Storm): sever hyperthyroid state that can occur in patients that are untreated or who develop another illness or stressor.
Hyperthyroidism Complications 2 . May also occur after thyroid surgery in patients who were not adequately prepared with antithyroid medication d/t manipulation of thyroid during surgery Can result in death in just 2 hours if not treated immediately
Hyperthyroidism Complications 3 S&S= Thyroid Storm Tachycardia, Hypertension Fever, Dehydration Restlessness, Delirium Coma & Death
Hyperthyroidism INT & N/C Thyrotoxic Crisis IV Fluids, Cooling Blanket, & Acetaminophen for Fever (Avoid ASA: it increases T4 in circulation) Propranolol (Inderal) for Tachycardia Elevate HOB & Administer Oxygen
Hyperthyroidism INT & N/C Hyperthyroidism PTU & Tapazole inhibit synthesis of Thyroid Hormone; must be taken for 12-18 months Propranolol (Inderal) relieves sympathetic nervous system symptoms High doses of Oral Iodine suppress the release of thyroid hormone
Hyperthyroidism INT & N/C Hyperthyroidism Radioactive Iodine (I 131) used to destroy part of the thyroid (given PO) Keep skin clean & dry; apply barrier cream as needed Monitor weekly weights Provide quiet, restful environment; Promote relaxation with music, massage etc
Hyperthyroidism INT & N/C Hyperthyroidism Thyroidectomy: removal of the thyroid may be needed if other measures do not work; antithyroid meds must be given first to calm the thyroid before surgery and prevent thyroid storm which can occur due to the manipulation of the thyroid during surgery.
Hyperthyroidism INT & N/C Hyperthyroidism Antithyroid meds slow heart rate & reduce vascularity of the gland, to decrease the risk of bleeding during surgery. Patient will probably need thyroid replacement hormone after surgery even if some thyroid gland is left.
Hyperthyroidism INT & N/C Hyperthyroidism Monitor VS, especially Temperature; administer tylenol as ordered; cooling blanket as needed; prevent shivering; offer fluids; Monitor for Dehydration; Report changes in VS to RN/ MD
Hyperthyroidism INT & N/C Hyperthyroidism Provide low fiber, low sodium, bland, high calorie diet in small, frequent meals; Monitor electrolytes especially K+ & Na+
Hyperthyroidism INT & N/C Hyperthyroidism Administer Lubricating eye drops as needed; encourage use of dark, tight fitting sunglasses to protect eyes from light; Tape eyes shut for sleeping; Elevate HOB at night to reduce edema behind the eyes notify MD ASAP if eye pain or vision changes
Nursing Care of the Patient Receiving Radioactive Iodine Hospital In Hospital (usually given to patients with thyroid CA in high dose) Limit Time Spent with Patient; maintain safe distance when caring for patient Glove and Gown; Avoid caring for patients if Pregnant
Nursing Care of the Patient Receiving Radioactive Iodine Hospital Take Precautions with Urine, Emesis, Body Fluids; Double Flush Toilet Call Radiation Specialist can be called for specific precautions
Nursing Care of the Patient Receiving Radioactive Iodine Home At Home (patients given lower doses are often sent home after given the Iodine) Avoid Close Contact w/ family for a Week (often told to be quarantined from other family x 3 days) Sleep Alone Wash Hands Carefully After Urinating
Nursing Care of the Patient Receiving Radioactive Iodine Home Avoid Oral Contact Wash eating utensils thoroughly with soap & water Avoid Pregnancy for at Least a Year
Side Effects of Radioactive Iodine Rare but may include sore throat, dry mouth or eyes & nausea Teach patient symptoms of hypothyroidism and encourage them to report any symptoms to MD; can occur up to 15 years after treatment Long term side effects are still not known
Goiter Pathophysiology Enlarged Thyroid Gland May enlarge in response to Elevated TSH or d/t an autoimmune process such as in Graves’ disease
Goiter Pathophysiology May also increase d/t Iodine deficiency or some medications Once the cause of the Goiter is removed the gland often returns to normal size or surgery may be required
Goiter S&S Enlarged Thyroid Gland or swelling at the base of the anterior neck If gland is enlarged posteriorly can cause difficulty swallowing or breathing Patient may have a sensation of fullness in the neck S&S HYPO/HYPER Thyroid or Norm
Goiter Diagnosis Ultrasound or Thyroid Scan done to evaluate type & size of growth TSH, T3, and T4 measured to determine thyroid function
Goiter IVT& N/C Treatment aimed at Cause: Avoid Goitrogens (certain foods & Meds); Given Iodine supplements if appropriate Treat Hypo or Hyperthyroidism if indicated
Goiter IVT& N/C Synthroid may be given to reduce TSH levels via negative feedback Radioactive Iodine or Thyroidectomy if Size is Causing Symptoms Monitor Breathing (Stridor); Swallowing Evaluation
Cancer of the Thyroid Gland Tumor of the Thyroid Gland: Usually Benign; More Common in Women
Cancer of the Thyroid Gland S&S Hard Painless Nodule; TH levels Usually Normal Dysphagia; Dyspnea; Persistent cough & changes in voice
Cancer of the Thyroid Gland Diagnosis Thyroid Scan Shows “Cold Spot”; “hot spot” indicates a benign tumor Biopsy by fine needle aspiration confirms the diagnosis
Cancer of the Thyroid Gland Interventions Radioactive Iodine, Chemotherapy, Thyroidectomy (Partial or Total)
Thyroidectomy Preoperative Monitor Breathing and Swallowing; Monitor Vital Signs & voice quality for baseline to compare post-op Antithyroid Drugs to Achieve Euthyroid State; reduces size & vascularity of thyroid, reduces risk of bleeding Routine pre-op teaching
Post Operative Thyroidectomy Monitor Vital Signs, O2 sat, drain & dressing Q15 minutes X4, Q30 min x4, Q1h x4, Q4h Monitor dressing for potential bleeding and hematoma formation; check posterior dressing
Post Operative Thyroidectomy Monitor respirations; potential airway impairment; Encourage IS or CDB; Q1h; Humidified oxygen, Yaunkers suction available; Trach set at bedside; notify MD immediately for any respiratory distress
Post Operative Thyroidectomy Assess pain and provide pain relief measures; Pain meds; AVOID aspirin Semi-Fowler’s position, Support head; Avoid tension on sutures Assess voice for changes but discourage talking; hoarseness common
Post Operative Thyroidectomy Monitor for hypocalcemia related to injury or removal of parathyroid glands AEB tetany (numbness/ tingling, muscles spasms around the mouth) First fluids: cold/ice, tolerated best, then soft diet; IV Fluids; monitor I & O
Post Operative Thyroidectomy Ensure Patient knows they will need Synthroid medication for life
Hypoparathyroidism Pathophysiology Decrease in PTH Calcium Stays in Bones Hypocalcemia & Hyperphosphatemia (sea / saw effect)
Hypoparathyroidism Causes Heredity Accidental Removal of Parathyroids During Thyroidectomy
Hypoparathyroidism S&S Tetany: + Chvostek’s & Trousseau’s sign Numbness and Tingling of Fingers and Peri-oral Area; Muscle Spasms Cardiac Dysrhythmias
Hypoparathyroidism Diagnosis PTH & Serum Calcium Low
Hypoparathyroidism INVT & N/C Acute: IV Calcium Gluconate Long Term Oral Calcium with Vitamin D Thiazide Diuretics reduces calcium excreted in the urine
Hypoparathyroidism INVT & N/C Monitor for Signs of Tetany & report to RN/ MD Keep Trach set at bedside High Calcium Diet Parathyroid Imbalances
Hyperparathyroidism Pathophysiology Parathyroid Overactivity Increased PTH Hypercalcemia Hypophosphatemia
Hyperparathyroidism Causes Parathyroid Hyperplasia Benign Parathyroid Tumor Heredity
Hyperparathyroidism S&S Fatigue Depression Confusion Nausea and Vomiting Kidney Stones Joint Pain Pathologic Fractures Dysrhythmias Coma Cardiac Arrest Parathyroid Imbalances
Hyperparathyroidism Diagnosis Serum Calcium Elevated 24-Hour Urine for Calcium Phosphate Decreased PTH Elevated X-Rays for Bone Density
Hyperparathyroidism INVT & N/C IV NS to Dilute Calcium Furosemide (Lasix) Calcitonin, Alendronate (Helps pull calcium out of the blood and into the bone) Estrogen Therapy (Women) Parathyroidectomy
Hyperparathyroidism INVT & N/C Monitor Calcium levels Encourage Oral Fluids Encourage Strengthening & weight bearing exercises Provide a safe environment for ambulation; Assist with ambulation as needed Encourage smoking cessation (smoking causes bone loss)
Adrenal Pathophysiology Tumor of Chromaffin Cells of Adrenal Medulla; Usually Benign Secretes Epinephrine and Norepinephrine
Adrenal Cause: Unknown
Adrenal S&S Fight or Flight Hypertension, Tachycardia, Palpitations Tremor, Diaphoresis Hyperglycemia Headache, Vision Changes Risk for Stroke & Organ Damage
Adrenal Diagnosis 24-Hour Urine for Metanephrines and VMA No Caffeine or Medications Before Test CT or MRI to Find Tumor
Adrenal INVT & N/C Beta Blockers (Propranolol [Inderal]) Alpha Blockers (Phenoxybenzamine [Dibenzyline]) Adrenalectomy
Adrenal INVT & N/C Risk for Injury Related to Hypertensive Crisis Monitor VS Quiet, Calm Environment; No Caffeine Replacement Corticosteroids Postop
Adrenal Cortex Hormone Imbalances Hyposecretion Addison’s Disease
Adrenal Cortex Hormone Imbalances Hypersecretion Cushing’s Syndrome
Addison’s Disease Patho Pathophysiology: Deficient Cortisol and/or Aldosterone and/or Androgens
Addison’s Disease Causes Autoimmune AIDS CA Pituitary or Hypothalamus Problem Abrupt Discontinuance of Steroids
Addison’s Disease S&S Hypotension Sodium Loss Potassium Retention Hypoglycemia Weakness Fatigue Bronze Skin Nausea and Vomiting
Addison’s Disease Diagnosis Serum and Urine Cortisol Level Blood Glucose Electrolytes BUN/HCT ACTH Stimulation Test
Addison’s Disease Complication: Adrenal Crisis S&S Profound Dehydration Hypotension Hypoglycemia Shock, Coma, Death
Addison’s Disease INVT & N/C Glucocorticoids and Mineralocorticoids Daily for Life Two-thirds in AM, One-third in PM Double or Triple in Times of Stress May Be Placed on High Sodium Diet Assess fluid balance
Addison’s Disease INVT & N/C Monitor VS closely Good skin assessment Limit activity; Provide quiet, non-stressful environment Crisis Prevention: NEVER ABRUPTLY DISCONTINUE STEROIDS!
Cushing ’s syndrome Pathyphysiology Excess Adrenal Cortex Hormones Cortisol Aldosterone Androgens
Cushing ’s syndrome Causes: Hypersecretion of ACTH Hypersecretion of Cortisol Prolonged Use of Exogenous Glucocorticoids
Cushing ’s syndrome S&S Salt and Water Retention Hypokalemia Thin, Fragile Skin Acne Facial Hair in Women Amenorrhea
Cushing ’s syndrome Diagnosis Based on Appearance Plasma and Urine Cortisol ACTH Dexamethasone Suppression Test Adrenal Disorders
Cushing’s Syndrome INV & N/C Surgery if Tumor (Adrenalectomy) Reduce Dose of Steroid Change Schedule of Administration Symptom Control Diabetes Treatment Low-sodium, High-potassium Diet
Cushing’s Syndrome INV & N/C Prevent injury; establish a protective environment; assist as needed Increased protein, calcium and vitamin D in diet Meticulous skin care and frequent, careful skin assessment. Monitor blood glucose
Cushing’s Syndrome INV & N/C Plan activity with rest periods; Provide restful environment Decrease risk of infection; avoid exposure to infections, assess patient carefully as corticosteroids mask signs of infection.
Cushing’s Syndrome INV & N/C Reinforce teaching to patient & family about causes of emotional instability.
Adrenalectomy Nursing Care Preoperative Care Monitor Electrolytes, Glucose Preoperative Teaching
Adrenalectomy Nursing Care Postoperative Care Monitor for Adrenal Crisis Lifelong Hormone Replacement
Diabetes Mellitus Pathophysiology A disorder caused by decreased production of insulin, or by decreased ability to use insulin. Insulin is a hormone produced by the pancreas that is necessary for cells to be able to use blood sugar.
Diabetes Mellitus Patho The cause of diabetes mellitus is unknown, but heredity and diet are believed to play a role in its development. Diabetes results when the pancreas produces insufficient amounts of insulin to meet the body’s needs.
Diabetes Mellitus Patho pancreas produces insulin, but the cells are unable to efficiently use it (insulin resistance). Insulin isneeded for blood sugar (glucose) to go from the blood the cells, and unless the sugar gets into the cells, the body cannot use it.
Diabetes Mellitus Patho The excess sugar remains in the blood and is then removed by the kidneys. Symptoms of excessive thirst, frequent urination, and hunger develop. The (metabolism) of carbohydrates, fats, and proteins is altered.
Type 1 Diabetes IDDM, Juvenile (Old Names); Autoimmune Response to Virus; Destruction of Beta Cells Pancreas Secretes NO Insulin; More Common in Young, Thin Patients; Prone to Ketosis Requires insulin injections to live.
Type 2 Diabetes Reduced Tissue Sensitivity to Insulin; Insulin is produced in inadequate amounts or could be High but due to insulin resistance, hyperglycemia results. Eventually pancreas wears out & insulin production decreases.
Type 2 Diabetes NIDDM, Adult Onset (Old Names); Decreased Beta Cell Responsiveness to Glucose; Reduced Number of Beta Cells
Type 2 Diabetes Largest Risk Factor is Obesity; Accounts for 90% of all persons with DM Gradual on set with slow progression of symptoms. Non dependent on insulin injections (may need to take at certain times in their life.
Type 2 Diabetes Treatment includes diet and exercise. Studies show with 10-20% weight loss these patients will no longer be diabetic. Not Ketosis-Prone
Latent Autoimmune Diabetes of Adulthood (LADA) Variation of Type 1 diabetes Many Initially diagnosed with Type 2 found to have Islet Cell Antibodies Like Type 1 Blood glucose often not controlled with oral medications
Latent Autoimmune Diabetes of Adulthood (LADA) Beta Cell destruction occurred more slowly than with type 1 diabetes Patient may also be classified as thin or obese because the disorder has slightly different characteristics depending on the patient’s body fat.
Metabolic Syndrome: 3 or more met There is a link between Prediabetes & metabolic syndrome: Metabolic Syndrome is diagnosed when 3 of the following criteria are met. Elevated Waist Circumference (> 40’ in men & 35’ in women) Elevated Triglycerides (150 or >)
Metabolic Syndrome: 3 or more met Low HDL Cholesterol (40 or < in men & 50 or < in women) Elevated Blood Pressure (130/85 or higher) Elevated Fasting Blood Glucose (110 or greater)
Metabolic Syndrome: 3 or more met Other risk factors include physical inactivity, aging, hormonal imbalance and genetic predisposition. Patient’s fitting this profile should be monitored closely for the development of Type 2 diabetes & heart disease
Diabetes Mellitus S&S The 3 Ps Polyuria (excessive urination) Polydipsia (excessive thirst) Polyphagia (excessive hunger) Fatigue Blurred Vision Infection Prone Abdominal Pain Headache Ketosis/Acidosis
Diabetes Mellitus Diagnosing Fasting Blood Glucose ≥ 126 mg/dL Casual Blood Glucose ≥ 200 mg/dL Glucose Tolerance Test > 200 mg/dL after 2 Hr Urinalysis showing glucose and ketone bodies in the urine
Diabetes Mellitus Diagnosing Glycohemoglobin (HbA1c): Normal 4% to 6%; HbA1c >7% indicates poor BG control over past 2-3 months Over 6% indicates diabetes Inaccurate in patient’s with anemia
Diabetes Mellitus Prevention of Type 2 Lose 5% to 10% Body Weight 30 Minutes of Exercise 5 Days per Week Reduce Fat and Calories
Diabetes Mellitus Goals of Treatment Preprandial (premeal) Glucose 90 to 130 mg/dL; Peak Postprandial (aftermeal) Glucose < 180 mg/dL Glycohemoglobin < 7%; Blood Pressure < 130/80 Mm Hg
Diabetes Mellitus Goals of Treatment Immediate goals of treatment: stabilize the metabolism, restore normal body weight, and eliminate the symptoms of high blood-glucose.
Diabetes Mellitus Goals of Treatment Long-term goals of treatment: Prolong life, improve the quality of life, relieve symptoms, and prevent long-term complications through education, careful dietary management and weight control, medication, physical activity, self testing, and foot care.
Diabetes Mellitus INT & N/C Medical Nutrition Therapy (MNT): Patient Education ADA Exchange Lists, Carbohydrate Counting, Glycemic Index Low Fat, Low Sodium, Limit Simple Sugars, Use Complex Carbohydrates
Diabetes Mellitus INT & N/C Eat at regular intervals, Consistent Day-to-day, REMEMBER CULTURAL DIETARY NEEDS Healthy, well balanced meal plan anyone can eat
Diabetes Mellitus INT & N/C Exercise: Patient Education Lowers Glucose up to 24 Hours, Lowers Blood Lipids Best Done Regularly to prevent fluctuations in BG; Avoid Exercise During Acute Hyperglycemia
Diabetes Mellitus INT & N/C Monitor Blood Glucose, Carry Fast Sugar, Educate patient to obtain Medic Alert Bracelet
Diabetes Mellitus INT & N/C MEDS Insulin for Type 1 or 2 Action: Insulin lowers blood sugar by allowing it to leave the blood stream and enter the cell Helps glucose convert to glycogen Inhibits tissue breakdown of fat and protein
Diabetes Mellitus INT & N/C MEDS Insulin for Type 1 or 2 Action: Promotes intake of amino acids into muscles Promotes utilization of glucose- energy Insulin pump: provides all day, ‘tighter’, glucose control without frequent BG sticks and injections (video)
Oral Hypoglycemics for Type 2 Action Depends on Medication: usually taken once daily 30 minutes before breakfast Stimulate Pancreas to produce more insulin Increase Tissue Sensitivity to Insulin Slows Carbohydrate Digestion and Absorption
Oral Hypoglycemics for Type 2 New Developments Exenatide (Byetta): taken along with oral hypoglycemic meds; stimulates insulin secretion, lowers glucagon production, slows gastric emptying and promotes weight loss.
Oral Hypoglycemics for Type 2 New Developments Pramlintide (Symlin): injectable drug used with insulin; reduces glucose levels following meals; may also promote weight loss in individuals who are overweight. Patient’s have increased risk of hypoglycemia.
Insulin Pump Diabetes Mellitus INT& N/C Monitoring of Blood Glucose: Patient Teaching Test AC and HS Record Results Analyze Meaning of Results Know Target Glucose Levels Teach Patients to Call MD if Out of Range Urine Testing for Ketones If Blood Sugar Greater than 300
Alterations in Blood Glucose Hyperglycemia: Blood Glucose >126 mg/dL Causes Overeating Stress Illness Not Enough Insulin or Oral Medication
Symptoms of Hyperglycemia 3 Ps Blurred Vision Fatigue, Lethargy Headache Abdominal Pain Ketonuria Coma
Treatment of Hyperglycemia Check Blood Glucose Use Sliding Scale Insulin If Blood Glucose is Greater Than 300, Check Ketones Determine Cause and Eliminate If Blood Glucose is Greater Than 180 for 2 Days, Call MD Call MD if Ill or Vomiting
Hypoglycemia Hypoglycemia (Insulin reaction): Blood Glucose less Than 50
Reactive Hypoglycemia: BG less than 70 often a complication of diabetes treatment, but can occur without DM & may be a warning of impending DM.
Reactive Hypoglycemia: Patho May occur as an overreaction of the pancreas to eating. The pancreas senses the blood glucose level increasing & produces more insulin than needed resulting in low BG.
Reactive Hypoglycemia: Patho Can also be d/t low levels of glucagon or high levels of insulin from the pancreas or activation of the sympathetic nervous system.
Causes of typical hypoglycemia Too Much Insulin, Exercise, Not Enough Food
Signs & Symptoms of all forms of hypoglycemia Headache; Hunger Fight or Flight: Tremor, Cold Sweats, Palpitations Neuroglycopenia: Irritability, Confusion, Seizures, Coma CAUTION: Elderly patients with Autonomic Neuropathy = No Symptoms of hypoglycemia & need to be monitored closely
Hypoglycemic Treatment Recheck in 15 Min; Repeat until BG of 70 is reached. Do not over treat to prevent hyperglycemia Snack if Greater Than 1 Hr Until Meal; snack should contact complex carb & protein Acute Treatment if patient unable to swallow IV D50 or SQ Glucagon
Hypoglycemic Treatment If S&S of Hypoglycemia are observed check BG before treating For Reactive Hypoglycemia do not give fast sugars or simple sugars. Give complex carb & Protein and encourage small, frequent meals. Ensure patient avoids fasting and eats high fiber foods.
Hypoglycemic Treatment Administer 15 to 20 G Fast-Acting CHO: 4 oz OJ, 6 oz Soda, mini box raisins, 6-8 lifesavers, glucose tab
Diabetic Ketoacidosis (DKA)patho Mainly occurs with type 1 diabetes Insulin Deficiency & Glucose is very high Cells Starving due to insufficient insulin to allow glucose into the cells
Diabetic Ketoacidosis (DKA)patho Fat Breaks Down for the body to use for energy instead of glucose Byproduct of Fat Breakdown is Ketones, which are Acidic and results in Ketoacidosis; a type of Metabolic Acidosis
Diabetic Ketoacidosis (DKA)Causes High Blood Glucose due to undiagnosed type 1 or uncontrolled BG Stress or Illness causing severe increases in BG
Diabetic Ketoacidosis (DKA)S&S Flu-like Symptoms Symptoms of Hyperglycemia: 3 P’s Kussmaul’s Respirations: Body’s attempt to compensate for acidosis w/ deep respirations; Fruity Breath
Diabetic Ketoacidosis (DKA)S&S Electrolyte Imbalance: hypokalemia Dehydration, Tachycardia, Hypotension, Shock Coma & Death when BG gets too high
Diabetic Ketoacidosis (DKA)INT& N/C IV Fluids; Glucose added when BG drops to 180 to prevent hypoglycemia; Potassium also added to stimulate insulin release from the pancreas IV Insulin Drip
Diabetic Ketoacidosis (DKA)INT& N/C Frequent Glucose Monitoring to determine when Glucose needs to be added to IV or when Insulin needs to be D/C’d Electrolyte Monitoring for Potassium levels
Diabetic Ketoacidosis (DKA)INT& N/C Prevention: Careful monitoring of BGs; Check urine for Ketones if Blood Sugar is >300: if present Drink Fluids, Check Again, Call MD if Still Present; NEVER stop or change Insulin dose w/o MD supervision!
Hyperosmolar Hyperglycemia Patho also know as HHNK ( Hyperosmolar Hyperglycemic NonKetotic Syndrome) Mainly Occurs in Type 2 Diabetes
Hyperosmolar Hyperglycemia Patho Blood Glucose Elevated often from stress or illness but can be due to poor diet or medication control
Hyperosmolar Hyperglycemia Patho Type 2 patients produce some insulin so cells do not starve, Ketoacidosis does not result, patient does not feel as ill as patients w/ DKA and symptoms are slower to develop causing delay in seeking treatment
Hyperosmolar Hyperglycemia S&S Polyuria; Profound Dehydration; Extreme Thirst Lethargy, mental confusion Blood Glucose may be 1,000 to 1,500 mg/dL Electrolyte Imbalance Shock, Coma & Death
Hyperosmolar Hyperglycemia INT& N/C IV Fluids; Glucose added when BG drops to 180 to prevent hypoglycemia; Potassium also added to stimulate insulin release from the pancreas IV Insulin Drip
Hyperosmolar Hyperglycemia INT& N/C Frequent Glucose Monitoring to determine when Glucose needs to be added to IV or when Insulin needs to be D/C’d Electrolyte Monitoring for Potassium levels
Hyperosmolar Hyperglycemia INT& N/C Prevention Prevention: Careful monitoring of BGs; Drink Fluids of BG is rising, especially during stress or illness; Call MD with HIGH BG results; NEVER stop or change Insulin dose w/o MD supervision!
Macrovascular Changes: Circulatory System (excess blood sugar damages blood vessels & increases platelet aggregation resulting in the following:
Macrovascular Changes: Circulatory System (excess blood sugar damages blood vessels & increases platelet aggregation resulting in the following: Atherosclerosis & Ateriosclerosis; HTN; Stroke CAD, MI; Peripheral Vascular Disease Patients need to avoid smoking, maintain normal weight and exercise regularly
Macrovascular Changes: Circulatory System (excess blood sugar damages blood vessels & increases platelet aggregation resulting in the following: Patients should be receiving aspirin or other antiplatelet medication, ACE inhibitors for BP & statins for cholesterol control
Microvascular Changes: Tiny blood vessels in the eyes and kidneys become damaged leading to chronic health issues Retinopathy, Nephropathy:
Macrovascular Changes: Retinopathy: small hemorrhages can occur, which can cause blindness if not corrected. Patients need to have an annual eye exam to monitor for changes.
Macrovascular Changes: Nephropathy: damage to tiny blood vessels in the kidneys will eventually result in renal failure; ACE inhibitors & angiotensin receptor blockers can slow the development of kidney problems.
Macrovascular Changes: Monitor urine tests for albumin; if + patient should be on low protein diet to delay nephropathy development
Neuropathy: Damage to nerves from chronic hyperglycemia Results in numbness & pain in extremities, erectile dysfunction in men, sexual dysfunction in women, gastroparesis (delayed stomach emptying) and other problems.
Neuropathy: Damage to nerves from chronic hyperglycemia Pain from neuropathy cannot be successfully treated with analgesics; antidepressants & anticonvulsants can be helpful. Lyrica is a new drug that can be helpful for some to reduce painful nerve impulses.
Neuropathy: Damage to nerves from chronic hyperglycemia Improved control of Blood Glucose levels is helpful.
Neuropathy: Damage to nerves from chronic hyperglycemia Infection: Healing from injuries is slow d/t impaired circulation; also WBC are not as effective at fighting infection. In addition, Periodonatal (gum) disease also occurs more frequently in patients with diabetes.
Neuropathy: Damage to nerves from chronic hyperglycemia Diabetic Foot Care Debridement of Diabetic Foot Ulcer Long Term Complications
Foot Problems & Care Combination of PVD, neuropathy & increased risk of infection makes patients with diabets more prone to foot wounds and infections.
Foot Problems & Care Prevention is #1: patients need a daily routine of checking & caring for feet Inspect feet daily; report sores, changes & signs of infection. Wash feet daily with lukewarm water & mild soap; dry thoroughly.
Foot Problems & Care Soften dry skin with lotion or petroleum jelly. Protect feet with comfortable, well-fitting shoes. Exercise daily to promote good circulation. See a podiatrist for foot problems & to have corns or calluses removed.
Foot Problems & Care Remove shoes/socks during visits to MD to remind them to examine feet. Discontinue smoking which decreases blood flow to feet.
Care of Patient Undergoing Surgery Frequent Glucose Monitoring Sliding Scale Insulin or Insulin Drip Maintain Glucose 140 to 180 mg/dL in Critically Ill Check with Surgeon regarding whether patient should receiving insulin prior to surgery
Brand: Glucophage Generic: metformin Keeps liver from makimg glucose
Brand: Precose, Glyset Generic: acarbose, meglitol Blocks sugar getting out of intestines
Brand: Rezulin, Avandia, Actos Generic:troglitazone, rosiglitazone, pioglitazone Helps muscles use insulin better only useful in type 2 diabetes. Need contious use of insulin not good for Type 1 Diabetics
Brand: Amaryl, Glucotrol, Glucotrol XL, Diabeta Generic: Glimepiride, glipizide, glyburide Helps pancreas make more insulin
Brand: Prandin Generic:repaglinide Helps pancreas make more insulin
rapid Acting insulin Brand: Novolog Generic Insulin Aspart Brand: humalog Generic: Insulin Lispro
rapid Acting insulin Onset Within 15 MINS
rapid Acting insulin Peak 1-1.5 hours
rapid Acting insulin Duration 2-4 Hours
Short Acting Brand: Humulin R Generic:Regular R Brand: Novolin R Generic:Regular R
Short Acting Onset Within 30 MINS
Short Acting Peak 2-3 Hours
Short Acting Duration 3-6 HOURS
Intermediate -Acting Brand: Humulin N Generic: NPH (N) Brand: Novolin N Generic: NPH (N)
Intermediate -Acting Onset 2-4 hours
Intermediate -Acting Peak 4-12 HOurs
Intermediate -Acting Duration 12-18 Hours
Long Acting Brand: Levemir Generic: Insulin detemir Brand: Lantus Generic: Insulin Glargine
Long Acting Onset 6-10 Hours
Long Acting Peak None
Long Acting Duration 24 Hours
Pre mixed NPH (Intermediate, Regular, short-acting) Brand: 70/30 Generic: 70% NPH & 30% REG Brand: Novolin 70/30 Generic:70% NPH & 30% R Brand:Humulin 50/50 Generic: 50% NPH & 50% R
Pre mixed NPH (Intermediate, Regular, short-acting)ONSET 30 MIN
Pre mixed NPH (Intermediate, Regular, short-acting)Peak 2-4 Hours
Pre mixed NPH (Intermediate, Regular, short-acting)Duration 14-24 Hours
Premixed Lispro Protamine (Rapid acting) Brand: Humalog Mix 75/75 Generic 75%Lispro 25% Brand: 50/50 Generic 50%/50%
Premixed Lispro Protamine ONSET 15-30 mins
Premixed Lispro Protamine Peak 30 min-2.5 hours
Premixed Lispro Protamine Duration 16-20 hours
Premixed Lispro Protamine 50/50 onset 10-15 mins
Premixed Lispro Protamine 50/50 peak 30 mins-2.5 hours
Premixed Lispro Protamine 50/50 Duration 10-16 hours
Premixed Aspart Protamine Rapid acting Brand: Novolog70/30 Brand Novolog 50/50
Premixed Aspart Protamine Rapid acting onset 10-30min
Premixed Aspart Protamine Rapid acting peak 1-4 hours
Premixed Aspart Protamine Rapid acting Duration 24 hours
Created by: kvoltaire