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74 Cards in this Set
- Front
- Back
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Diabetes Type 1
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-Insuling Dependent
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Diabetes Type 2
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-Insulin Independent
-Not ketosis prone -Children with sedentary life -Strong genetic predisposition -Controlled mainly with oral agents |
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Goals of Diabetes Treatment
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-Achieve and maintain normal blood glucose levels
-BG monitoring -Drug therapy -Diet -Exercise -Rest and reduce stress |
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Patient Teaching
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What is the patient's perspective
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Diabetes Diagnostic Studies
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-Blood glucose:
*fasting *random *ac or pc -Glycosylated hemoglobin:(A1C or HbA1c) normal <6 *over past three months -Oral glucose tolerance test -Urine testing for ketones especially for sick days |
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Other events indicating BG monitoring
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-Change in condition that resembles hypo/hyperglycemia
such as stroke -Use of TPN |
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S/S of Hypoglycemia
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-Weakness, fatigue
-Headache, dizziness -Sweating -Anxiety, tremors -Lack of cordination -Hunger, nausea -Impaired vision -LOC |
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S/S of Hyperglycemia
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-Thirst
-Frequent urination -Hunger -Blurred vision -Drowsiness -Nausea -Dry skin -Hyperosmolar blood serum |
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Complications of Hyperglycemia
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-Damaged blood vessels, nerves and decreased ability to fight infections
-Affects kidneys, eyes, skin, feet, heart |
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Classifications of DM
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-Type 1
-Type 2 -Gestational Diabetes -Diabetes due to drugs that raise BG -Chronic pancreatitis -Removal of pancrease -Cushings disease -Acromegaly -Pheochromocytoma (tumor in adrenal gland) |
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Defects of Type 2 DM
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-Decreased Tissue sensitivity to insulin (dysfunction at the receptor site)
-Beta cells: less repsonsive or decrease insulin production -Hepatic Insensitivity: liver continues to release glucose despite high insulin levels |
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Differential Diagnosis
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-Young/old
-Thin/obese -Ketone/non-ketotic -Abrupt/progressive onset -C-peptide: low in type 1, normal or elevated in type 2 |
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Clinical Findings Type 1
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-Polyuria
-Polyphagia -Polydipsia (increased thirst) -Rapid weight loss -Weakness -Thin -Young -Ketones |
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Clinical Findings Type 2
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-Polyuria
-Polyphagia -Polydipsia -Fatigue -Blurred vision -Older -Obese -No obvious signs, found at routine MD visit |
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Exercise Induced Hypoglycemia
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-Can occur up to 24 hours after exercising
-Test before exercising and eat a snack if necessary -Eat good diet after |
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Sulfonylureas
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-Mechansim of action: increase insulin secretion by beta cells
-Timing: give AC, QD-BID, duration 12-14 hours -Medications: *Glipizide/Glucotrol -Risks: hypoglycemia |
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Meglitinides
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-Mechansim of action: increase insulin secretion by beta cells
-Timing: give AC, QD-TID, duration unknown -Medications: *Repaglinide/prandine *Starlix -Risks: hypoglycemia (less than sulfonylureas |
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Biguanides
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-Mechansim of action: Decrease hepatic glucose production (gluconeogenesis)
-Timing: Usually BID (with food), onset: 24-48hrs duration 12-14hrs -Medications: *Metformin: Glucophage -Nursing considerations: titrate dose upward over 1-2 weeks, no risk of hypoglycemia -Risks: lactic acidosis, stop med with acute illness, renal failure, CHF, and dyes |
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Thiazolidinediones (TZDs)
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-Mechansim of action: Increase tissue sensitivity to insulin
-Timing: QD-BID, duration: long half life, can cause liver toxicity -Medications: *Pioglitazone: Actos (major ankle swelling) *Rosiglitazone: Avandia *Regal -Risks: Weight gain, edema, several weeks to be effective |
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Drawing up mixed doses
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-Inject air into long acting insulin (cloudy)
-Inject air into the short acting insulin (clear) -Draw up short acting insulin -Draw up long acting insulin (mixing vile first) -Make sure to have two licensed RNs confirm both draws of insulin |
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Acute Complications of Diabetes
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-Type 1: Diabetic Ketoacidosis (DKA)
-Type 2: Hyperglycemic hyperosmolar nonketotic syndrome (HHNKS) -Hypoglycemia/insulin shock |
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Diabetic Nephropathy
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-Damage to the renal vessels can lead to kidney failure
-1/3 of new ESRD patients are diabetic -Leading cause of kidney failure |
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Foot problems
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-60-80% of amputations are DM patients
-Causes: infections, non-healing ulcers -Increased risk due to: neuropathy, poor circulation, high BG levels impair WBC function |
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NIDDM develop HHNKS
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-Hyperglycemic Hyperosmolar Nonketotic Syndrome or Coma for Type 2
-some insulin is available, therefore ketones do not build up in the serum -hyperosmolar state leads to diuresis and decrease in LOC |
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HHNKS: Physiology
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Sever osmotic diuresis loss of water, glucose and electrolytes causes dehydration and high serum Na, decreased intervascular volume, all leading to more stress thus causing more glucose to enter the blood stream
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HHNKS: Causes
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Type 2 DM, precipitated by illness, inability to drink fluids at will
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HHNKS: S/S
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-Hyperglycemia, dehydration (HR up, BP down), neuro sx, coma (no ketosis, acidosis as some insulin present)
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HHNKS: Treatment
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-Rehydrate
-Correct electrolyte imbalance (Potassium usually needed) -Normalize BG -Treat underlying cause |
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DKA Cause
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-DM Type 1
-Failure to take insulin, not enough insulin, infection, stress -Potassium is outside the cells |
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DKA Physiology
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-Lypolysis, fatty acids converted to energy by liver (Ketones byproduct), acid pH, cellular dehydration
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DKA S/S
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-BG > 300-800
-3Ps -Weak, lethargic -Kussmaul resp -N/V, anorexia -Headache -Abdominal pain -Fruit breath |
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DKA Treatment
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-Normalize BG (regulare insulin given IV)
-Replace fluids -Replace Potassium (unless hyperkalemia or no urine output) |
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Intravenous Regular Insulin
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-Keep it continuous and monitor BG often
-Only use Regular insulin -If ir is add to IV bag, it can adhere to tubing, so flush insulin through new tubing |
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Adrenal Glands
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-Adrenal Cortex
-Adrenal Medulla |
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Adrenal Cortex
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-Glucocorticoids: cortisol
-Mineralcorticoids: aidosterone -Sex Hormones |
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Adrenal Medulla
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-Epinephrine
-Norepinephrine |
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Addison's Disease
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-Atrophy of adrenal cortex
-Hyposecretion of cortisol -Anterior pituitary increases ACTH -Causing increase excretion of Na and H20 (dehydration) -Hypotension, weak & irregular pulse, wght loss, anemia, hypoglycemia, mood changes, inability to handle stress, dark pigmentation of mucous membranes |
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Addison's Disease Treatment
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-Lifelong cortisol replacement therapy
-Dose needs to be increased for physical and emotional stessors -High Na intake |
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Addison's Crisis
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-Sudden life-threatening exacerbation triggered by a stressor
-Low Na, low BG, high K, dehydration, extremely low BP, tachycardia Treatment: IV cortisol, Aggressive IV NS fluid, glucose admin, B/P meds and Na retention |
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Cushing's Syndrome
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-Excessive secretion of corticosteroids, hyperplasia
-S/S: muscle wasting, weakness, protein depletion, *moonface, buffalo hump and trunk obesity*, Na and H20 retention, *decreased inflammatory response* -Treatment: *Medications to supress adrenal glands: Lysodrem, Cytadren* |
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Administration of Steroids
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-May raise Na and lower K
-Increase fluid volume -Indications: suppress inflammatory and immune response (COPD, arthritis, lupus) -Treat addison's -Treat allergic reactions |
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Precautions for Steroid Use
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-Increase BG levels
-Elderly: raises Na and BP, lowers K -Always give (orally) with food(raises HCL production in stomach) - Never abruptly D/C: need to taper off (check meds in pts transferred from ICU or CCU) -Wear Medic-alert ID bracelet |
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Side Effects of Steroids
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-PVD
-Steroid induced DM -Decrsd immune response -Inflammation -Osteoporosis -HTN, edema -Buffalo hump & moon face -Acne -Bruising -Mood changes -Hirsutism (extra hair) -amenorrhea (no period) |
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Mineralcorticoids: Hyperaldosteronism
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-Increase reabsorption of Na and H2O
-Hypernatremia (maybe edema) -Leads to increased urinary output -Leads to *hypokalemia* causing muscle weakness, cramping, fatigue, tetany, and paresthesia (alkalosis with loss of H+) -Women 7x more than men |
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Adrenal Medulla Disorder: Pheochromocytoma
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-Tumor %80 benign/Malifnant 10%
-Tumors located in other sites of adrenal tissue (aorta, ovaries, spleen) -Genetic predisposition -Secretes excessive catecholemines (epi and nor) |
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Physiology of Pheochromocytoma
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-*Flight or Fight*
-Increase HR -HTN -Na and fluid retention -Increased glucose during stress |
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S/S of Pheochromocytoma
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-HTN (220/140)
-Tachycardia, palpitations -Headache -Tremors -Hyperhidrosis (excessive sweating) -Dx: 24 hour urine to test for catecholamines |
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Posterior Pituitary
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-ADH or vasopressin
-Oxytocin |
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Vasopressin
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-Regulates Reabsorption of H2O in kidneys
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Hypersecretion of Vasopressin
-SIADH |
-Syndrome of inappropriate antiduretic Hormone secretion
-Excessive ADH production -Causes: oat cell lung cancer, CNS infection, tumor, head trauma -anything that lowers cardiac output stimulates ADH production -Serum hyponatremia -I>O -*Interstitial edema (puffy eyes, hands, face) -Tx: Fluid restriction, diuretic, replace K, albumin (osmotic diuretic) |
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Hyposecretion of Vasopressin
-Diabetes Insipidus |
-Lack of ADH
-Increased urine output (polyuria) -Increased thirst -Dilute urine -Urine Specific Gravity < 1.005 -Tx: nasal spray: desmopresin |
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Anterior Pituitary Gland
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-ACTH: acts on the adrenals
-TSH: acts on the thyroid -FSH: acts on the ovaries and testes -GH: Somatotropin |
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Growht Hormone
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-Somatotropin
-Hypersecretion: giantism/acromegaly -Hyposecretion: Dwarfism/Simmonds |
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Dwarfism
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-Hyposecretion of GH by the ant pituitary gland
-Causes: inherited, tumors, surgical removal, idiopathic -S/S: slowed growth of skeletal and soft tissues during childhood -Tx: growth hormone (only effective in children) |
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Simmond's
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-Causes: hypopituitarism: total absence of all pituitary secretions
-Rare |
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Gigantism
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-Hypersecretion of GH by the ant pituitary gland
-Excessive amounts of GH during childhood |
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Acromegaly
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-Excess of GH in adults
-Hyperplasia -Huge lower jaw -Headache -Increased pressure in head that can lead to blindness d/t pressure on the optic nerve |
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Thyroid
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-T3 & T4 secretion is controlled by TSH from the ant pit.
-T3 and T4 regulate the metabolism rate |
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Grave's Disease
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-Excessive output of Thyroid hormones by stimulation of the thyroid gland by immunoglobins
-S/S: nervousness, tachycardia, bulging eyes (exephtalmos), increased appetite, increased wght loss, muscle weakness and fatigue, increased BP, A-fib, goiter Tx: *irradiation by iodine isotope *medications that interfere with hormone production sa: propythioracil (Propacil) thimazole (Tapazole) Methimazole, PTU |
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Thyroid Storm
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Thyrotoxicosis
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Hypothyroidism
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-Insufficient thyroid hormone
-d/t: *Primary: thyroid dysfunction (low T3 & T4, high TSH0 *Secondary: ant. pit./ hypothalmic dysfunction (low T3 & T4, low TSH) -Causes: tx for hyperthyroidism -S/S: *weakness and lethargy *slowed speech, thick tongue *flat affect *memory loss *decreased heart rate *poor appetite *intolerance to cold - hypothermia *dry skin, brittle nails *wght gain *myxedema -Tx: leve-thyroxine = synthroid, Levoxyl |
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Myxedema Coma
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Severe, end-stage hypothyroidism
-Tx: maintain airways, meds, corticosteroids (for suppressed adrenal gland), correct BG and electrolyte levels, conserver body heat |
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Special Considerations for HRT
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-May takes weeks to feel better
-Take medications daily -Tx can speed up body functions causing problems for pts with: *Corinary Artery Disease *DM *Adrenal insufficiency |
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Radioactive Iodine
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-Destruction of all or part of the gland
-Given orally 3-5mos for effect -May cause hypothyroidism -Can damage parathyroid |
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Tyroidetomy
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-Post-op care: monitor for airway obstruction, sauna mask
-Keep intubation/tracheostomy equip at bedside |
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Thyroid Storm
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-AKA Thyrotoxic
-Extreme exacerbation of severe hypermatoblism -Undx or untreated hyperthyroidism -High mortality rate |
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S/S Thyroid Storm
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-High temp 102-106
-Severe tachycardia, high CHF hypoxia -Manic/psychotic behavior -Extreme diaphoresis, vomiting, diarrhea -Coma |
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Endemic Goiters
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-Non-toxic
-Iodine deficiency -Defect in thyroid hormone synthesis of T3 & T4 -Increases TSH which causes hyperplasia of gland -Firm or soft, enlarged -May have difficulty swallowing -Can progress to toxic goiter -Tx: may shrink with Thyroid hormone replacement therapy |
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Parathyroid Hormone
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-Acts on bone, intestine, kidney, to regulate calcium and phosphate metabolism
-Fosters normal excitability of nerves and muscles |
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Hypoparathyroidism
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-Equals hypocalcemia
-Causes: accidental removal with thyroidectomy, Surgery or radiation of throat or head, Autoimmune destruction -Dx: low calcium, high phosphorus |
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S/S Hypoparathyroidism
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-Same as hypocalcemia
-Paresthesia (tingling fingers) -Tetany/neuromuscular irritability *+ trousseau's sign (upper arm compression spasm) *+ chovstek's sign (tap on facial nerve produces twitch) *laryngeal spasm (crowing respirations) -EKG changes -Digitalis resistance |
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Tx Hypoparathyroidism
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Sever Case:
-IV Calcium gluconate (not given IM, can damage tissue) Mild Case: -PO calcium and vitamin D -Amphogel (binds phosphorus) |
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Hyperparathyroidism
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-Primary: Excessive secretion of PTH by para
-Secondary: seen in pts with CRF due to retention of phosphorus causing the para to increase stimulation of PTH |
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S/S Hyperparathyroidism
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-Hypercalcemia
-Muscle weakness -Constipation -Osteoporosis -Arrhythmias |
