Question | Answer |
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 |