Med Surg Exam 2 Study Guide PDF

lOMoARcPSD|48573418 Med surg exam 2 study guide Medical/Surgical Nursing Concepts (Galen College of Nursing) Scan to open on Studocu Studocu is not sponsored or endorsed by any college or university Downloaded by Maggie C. (403.e...

lOMoARcPSD|48573418 Med surg exam 2 study guide Medical/Surgical Nursing Concepts (Galen College of Nursing) Scan to open on Studocu Studocu is not sponsored or endorsed by any college or university Downloaded by Maggie C. ([email protected])  lOMoARcPSD|48573418 Med surg exam 2 study guide Chap 11 Fluid compartments Intracellular 60% Contained within the cell body About 25L Veins, arteries, capillaries, heart, etc Extracellular 33% Most important area of homeostasis, area outside of cells Divided into intravascular space and interstitial space Extracellular fluid volume is about 15L In-between the cells Fluid Balance Closely linked to/affected by electrolyte concentrations Fluid intake 2.3-3L a day Fluid loss Minimum urine amount needed to excrete toxic waste products= 400-600 mL/day Insensible water loss-through skin, lungs, stool. Usually 500 to 1L a day This increases during a fever, tachypnea and extreme stress Facts to remember Any fluid imbalances that occur=continuous assessment of UOP Urine output Dehydrated pts, CHF, RF, Fluid volume deficient, and fluid volume overload IV fluids, diuretics Daily weights 1L of water weighs 2.2lb, equal to 1kg Weight change of 1lb= fluid volume change of about 500 mL Fluid volume deficit: Dehydration Fluid intake/retention does not meet bodys fluid needs; results in fluid volume deficit Assessment Thread and increased pulse rate; decreased BP; lethargy; decreased UOP; dry mucous membranes; constipation; thirst Increased H&H (hemoconcentration), BUN, sodium, and urine specific gravity Causes-vomiting, diarrhea, ileostomy, laxatives, burns, fever, diuretics, GI suctioning, and NPO Interview/risk factors Inquire about recent dietary habits Use of OTC diuretics Outdoor activities Weight gain and weight loss Who at risk: hemorrhage, vomiting, diaherra, excessive sweating, NPO, sustained burn wounds, GI suction, Diuretics, uncontrolled diabetes, Poor intake Downloaded by Maggie C. ([email protected])  lOMoARcPSD|48573418 Flat neck and hand veins, increased RR, skin tenting, tongue wrinkles, dehydration, fever, UOP concentrated, Urine specific gravity concentrated (the higher the dryer) BUN and Creatinine BUN and Creatinine are kidney markers and are sensitive to decreased blood flow BUN (10-20) and Creatinine (06-1.2) rise when nitrogenous wastes are found in the blood indicating kidney impairment GFR (>65) typically has an inverse relationship (increased BUN and Creatinine with a decreased GFR)- chronic renal failure Elevations can be caused by dehydration Fluid volume overload Assessment Bounding and increase pulse; elevated BP; dyspnea, crackles on lung auscultation; edema; decreased Hematocrit (hemodilution), decreased serum sodium and urine specific gravity (dilute urine). Weight gain is the best indicator Causes- ESRD, CHF, water intoxication, SIADH, corticosteroid therapy, and rapid fluid replacement Drug therapy Diuretics (loop diuretics) Nutrition therapy Fluid restriction ( 1200 ml/day) Salt restriction Monitoring of intake and output Daily Weight!!!! ESRD= End stage renal disease SIADH= syndrome of inappropriate ADH Edema- while standing ankles, feet, while laying down sacrum, back Extreme cases it will be everywhere Electrolyte imbalances: etiology Hyponatremia Due to sodium loss, water gain, or inadequate intake Sodium loss: drugs; diuretics, anticonvulsants, SSRIs, antipsychotics, cancer meds Hypernatremia Dehydration, excessive Na intake (sodium polystyrene, sodium bicarb, renal issue) Hypokalemia Not enough in too much out, depleting drugs, medical conditions Not enough in: inadequate K intake Too much out: GI fluid losses Depleting drugs: diuretics, corticosteroids, insulin, excessive laxative use, albuterol Black licorice-acts like aldosterone Hyperkalemia Too much intake, blood products, drugs, not enough excreted, crush injury Downloaded by Maggie C. ([email protected])  lOMoARcPSD|48573418 Too much intake: increased dietary intake,, salt substitutes, potassium supplements Donated blood Drugs: K sparing diuretics, ACE inhibitors, ARBs, NSAIDs Not enough excreted: renal failure ( low Na, K, protein diet) Crush injury: intracellular K released Hypocalcemia Inadequate intake, malabsorption, calcium loss, others Inadequate intake: calcium and vitamin D (sunlight) Malabsorption: post menopausal women, diseases that affect the small bowel, drugs (anticonvulsants) Calcium loss: loop diuretics Others: renal failure, hypoparathyroidism, low magnesium, multiple blood transfusions, alkalosis, low albumin levels Hypercalcemia Increased resorption from the bone Hyperparathyroidism Cancer Thiazide diuretics Hypomagnesemia Poor intake, poor GIT absorption, excessive GIT loss, excessive urinary losses Poor intake; alcoholics, patients on TPN or enteral feeding Poor absorption: IBD, celiac disease GIT loss: diarrhea, laxative use, NGT drainage Urinary loss: diuretics (loop and thiazide) Hypermagnesemia Excessive intake, impaired excretion Excessive intake: magnesium containing antacids/laxatives Impaired excretion: renal dysfunction Rare Sodium imbalances: affect CNS Hyponatremia Common: headache, irritability, disorientation/confusion, tired, abdominal cramping, muscle twitching/weakness, crave salt Worst case scenario (critical low): psychosis, seizures, ataxia, airway issues Treatment Mild: fluid restriction (safest), oral sodium supplements Critical: hypertonic 3% saline-----SLOWLY!!! Nursing implications: Monitor neurologic status, seizure/fall precautions, strict I/Os, implement fluid restriction, monitor labs Hypernatremia Common: Downloaded by Maggie C. ([email protected])  lOMoARcPSD|48573418 restlessness or agitation, anorexia, N/V, weakness, lethargy, confusion, crave water Worst case scenario: decreased LOC< seizures, coma Treatment: fluids PO/IV, what type (initially isotonic fluid, increase BP, switch then to hypotonic fluid (D5W) (less salt more water!!!) Nursing implications Frequent v/s, monitor neurologic status, seizure/fall precautions, strict i/os, assess skin/mm, oral care, monitor labs Give fluids if dehydration present Potassium imbalances: affect heart/muscles/GI tract Hypokalemia Common Cardiac arrhythmias, leg cramps (hallmark), muscle weakness, decreased GI motility (decreased BS, constipation, n/v), decreased DTRs, muscle weakness, alkalosis Worst case scenario Life threatening cardiac arrhythmias/cardiac arrest Hypokalemia may potentiate dig toxicity*** Treatment Increase dietary intake of potassium, k supplementation, Give IV potassium slowly!!!! 20mEq/hr Nursing implications Frequent V/s, cardiac monitoring, patent IV, monitor labs (recheck after supplementation), NEVER GIVE POTASSIUM IVP OR BOLUS!!!!! Very dangerous Remember suction S= skeletal muscle weakness, U= U WAVE, C= constipation, T= toxic effect of dig, I= irregular pulse, o= orthostatic hypotension, N=numbness Hyperkalemia Common Cardiac arrhythmias, muscle weakness (which may lead to flaccid paralysis), increased GI motility, decreased DTR’s, acidosis Worst case scenario Life threatening cardiac arrhythmias/ cardiac arrest Treatment Potassium restricted diet, if critical/symptomatic will require drug therapy (CBIGKD) which stand for: C= calcium, B= bicarb, I= Insulin (regular, IV push), G= glucose, K= kusulate (sodium poly), D= dialysis Nursing implications Cardiac monitoring, frequent labs, VS, monitor for hypoglycemia if insulin IVP given Calcium imbalances: affect neurological/neuromuscular system (9-10.5) Downloaded by Maggie C. ([email protected])  lOMoARcPSD|48573418 Hypocalcemia (over stimulation ) Common Anxiety, irritability, confusion, paresthesia’s of toes, fingers, face, around mouth, severe muscle cramping, trousseau’s and Chvostek’s sign, increased DTR’s alkalosis Worst case scenario: Seizures, high risk for fractures Treatment Calcium/vitamin d supplements; if acute or symptomatic IV calcium gluconate or IV calcium chloride Nursing implications If at high r/f hypocalcemia, assess carefully for s/s, vs, patent IV, assess for Chvostek’s and trousseau’s signs, monitor labs (esp after multiple transfusions), teach about dietary sources of calcium Hypercalcemia (under stimulation) Common Lethargy, confusion, memory loss, AMS, personality changes ( neuropsychiatric), decreased DTR’s, muscles weakness Worst case scenario Coma Treatment Reduce dietary intake of calcium, IVF, loop diuretics, bisphosphonates Nursing implications Vs, assess neurologic and neuromuscular function frequently, monitor electrolytes, maintain patent IV, strict I/Os, monitor for fractures Hypocalcemia/hypomagnesemia Palmar flexion indicating a positive trousseaus sign in hypocalcemia Facial muscle response indicating a positive Chvostek’s sign in hypocalcemia Magnesium imbalances: affect cardiac/neurological system Hypomagnesemia (not relaxed) Common Altered LOC, confusion, hallucinations, nystagmus, leg and foot cramps, Chvostek’s and trousseau’s signs, hyperactive DTRs, tachycardia, muscles cramps, spasms Worst case scenario Seizures, life threatening cardiac arrhythmias!!! Treatment Change in diet, PO or IV supplementation Nursing implications Assess mental status frequently and report changes, evaluate NM status, seizure precautions, VS, cardiac monitoring, patent IV, check electrolytes Hyper magnesemia (too relaxed) Common Drowsy, lethargic, decreased LOC, vasodilation (will decrease BP), muscle weakness (decreased muscle and nerve activity) and nerve activity, bradycardia, decreased DTR’s, occasional n/v Downloaded by Maggie C. ([email protected])  lOMoARcPSD|48573418 Worst case scenario Bradycardia, heart blocks, cardiac arrest Treatment Calcium gluconate/calcium chlorite is antidote Nursing interventions Monitor VS, and cardiac rhythm, monitor electrolytes, maintain patent IV Fluid tonicity Isotonic 0.9% NS Lactated ringers Useful for fluid resuscitation Hypertonic 3% NS 5% NS D5 or 0.9% nacl D5% lactated ringers TPN Caused for cerebral edema Used for hyponatremia Assess for fluid volume overload D5W- isotonic in bag, hypotonic in the body Normal ABG value pH 7.35-7.45 CO2 35-45 HCO3 22-26 pO2 80-100 Acidosis Hyperkalemia Hypercalcemia Hydrogen ions Overproduction Under-elimination Bicarbonate ions Under production Over elimination Metabolic acidosis Causes InsufÏcient supply of insulin (DM or DKA), excessive intake of ASA, high fat diet, renal insufÏciency, lactic acidosis, malnutrition, severe diarrhea Manifestations InsufÏcient supply of insulin (DM or DKA), excessive intake of ASA, high fat diet, renal insufÏciency, lactic acidosis, malnutrition, severe diarrhea Interventions Hydration, insulin, anti-diarrheal, sodium bicarb-as prescribed Downloaded by Maggie C. ([email protected])  lOMoARcPSD|48573418 Respiratory acidosis Causes Hypo-ventilation, asthma, brain, trauma, atelectasis, CNS depressants, PNA, pulmonary edema or emboli, COPD, sleep apnea, Drug OD Manifestation Drowsiness, confusion, hypoxia Interventions Encourage the client turn, cough, deep breath, incentive spirometry, look at the use of CNS depressants. Antidote considerations, bipap, intubation Alkalosis Hypokalemia Hypocalcemia Hydrogen ions Underproduction Bicarbonate ions Excess is released from kidneys Metabolic alkalosis Causes Diuretics, excessive vomiting and NGT suctioning, excessive sodium bicarbonate intake Manifestations Muscles cramping, paresthesia around mouth and on toes, hypotension (falls), tetany, decreased respiratory effort Interventions IVF, anti-emetics as prescribed Respiratory alkalosis Causes Hyperventilation, hysteria, fever, pain, cns stimulants Manifestations Tachypnea, dizziness, lightheadedness, perioral numbness, paresthesia’s Interventions Coach breathing, consider cns depressants (if needed), ensure airway patency (suction, as needed) ***GIVE OXYGEN*** Acid/Base imbalances pH: 7.35-7.45 (phil) CO2: 35-45 (resp. Lonnie lungs) loonie doesn’t follow phil- always opposite HCO3: 22-28 (galen lab values) (Sydney kidney-metabolic) syndey follows phil SpO2: 95-100% ROME: respiratory, opposite, metabolic, equal Co2=respiratory and acid HCO3=metabolic and base/alkaline Different sources of acid/base in the body Acids H ions Downloaded by Maggie C. ([email protected])  lOMoARcPSD|48573418 Ketoacids Carbon dioxide Lactic acid Base Bicarbonate D1-metabolic ketoacidosis don’t make insulin and insulin is used to break Lactic acid- exercise, sepsis, gout Kidney produces bicarbonate pH is a measure of the body’s free hydrogen ion level. Acid are substances that released hydrogen ions when dissolved in water, increasing the amount of free hydrogen ions in the solution. The strength of an acid is measured by how easily it releases a hydrogen ion in solution. As the pH increases then K decreases. Acidosis causes potassium to move from cells to extracellular fluid (plasma) in exchange for hydrogen ions. General acidosis symptoms Confusion Bradycardia Hypotension Muscle weakness NUGGET*** Causes of acidosis Hypoventilation OD Mechanical ventilation or neuromuscular disease DKA Salicylate overdose shock Airway obstruction-CO2 can’t get out Pulmonary edema-no gas exchange CO2 building Diaherra-acidosis (ASSidosis)-K increase pH goes down Renal failure-no production of bicarb Body is holding on you will be in the state of acidosis Treatment of respiratory acidosis Medications Oxygen Mechanical. Ventilation Treat the cause Always an underlying factor of why pt is acidosis Symptoms of respiratory acidosis Hypoventilation-> hypoxia Rapid, shallow repsirations Labored shallow breathing Decreased BP w/vasodilation Dyspnea Headache Downloaded by Maggie C. ([email protected])  lOMoARcPSD|48573418 Hyperkalemia Dysrhythmias Drowsiness, dizziness, disorientation AMS Muscle weakness Hyperreflexia Causes Respiratory stimuli (anesthesia, drug OD) COPD Pneumonia Atelectasis Treatment of metabolic acidosis Treat the cause (stop diarrhea, provide oxygen, insulin drop) Give sodium bicarbonate pH less than 7.2 NUGGET** Kidney pH goes down diabetic type 1-DKA- experience kussmaul resp. metabolic acidosis headache decreased BP hyperkalemia muscle twitching warm, flushed skin nausea, vomiting diarrhea changes in LOC kussmaul respirations causes DKA severe diarrhea Renal failure Shock Alkalosis pH greater tthan 7.45 NUGGET*** Resp breathing off CO2 breathing to fast Metabolic-loss of gastric juices rid of K puts you in a state of alkalosis Respiratory alkalosis Hyperventilation Anxiety High altitude Pregnancy Fever Initial stages of pulmonary emboli Metabolic alkalosis Downloaded by Maggie C. ([email protected])  lOMoARcPSD|48573418 Loss of gastric juice Overuse of antacids Potassium wasting diuretics Causes of respiratory alkalosis Fever Hyperventilation Hypoxia Overventilation by mechanical ventilator Overstimulation of the respiratory system Respiratory alkalosis NUGGET** Brown paper bag to treat hyperventilating Metabolic Alkalosis NUGGET** NG tubes Alkalosis symptoms Dizziness, confusion, hyperreflexia, numbness/tingling (mouth and toes), cramps/twitching, tachycardia Treating alkalosis Treat the cause Fall precautions Rebreather mask (respiratory alkalosis) Fluid and electrolytes imbalances IV fluid types Hypotonic The solute concentration is low Fluids move from intravascular space into intracellular fluid Cells swell and burst Solution lower than salt, lower osmolarity than body fluids (less salt) Isotonic Equal solute concentration within solution Hypertonic Higher solute concentration Water moves from intracellular space to intravascular space Higher concentration than the solutes in the body NUGGET** Hypovolemia (fluid volume deficit) Anything that causes blood or fluid loss or poor fluid intake Bleeding (hemorrhage) Vomiting/GI suctioning Diarrhea (laxatives) Diaphoresis/ excessive sweating Long-term NPO status Trouble swallowing or eating/drinking Downloaded by Maggie C. ([email protected])  lOMoARcPSD|48573418 Excessive urination (diuretics) Fever Hypovolemia: what am I looking for? s/s HTN WT.Loss Tented, dry skin Increased RR, Increased PR Cool skin Flat neck veins Oliguria Lethargy NUGGET*** Oral mucosa-dry Oliguria-low urine, amber color Sucken eyes NUGGET** Assessing for dehydration (laboratory & diagnostic exams) Hemoglobin increased Hematocrit increased Serum osmolarity increased BUN increased Urine specific gravity increased Electrolyte imbalances Treating dehydration Offer oral fluids and ensure intake at least q2hrs Assess pt Q2 hrs during rehydration (pulse rate/quality, urine output) IV fluids Treat the cause Assess Q2hr for dehydration BE AWARE OF FLUID OVERLOAD WHEN ON FLUIDS Tx underlying cause NUGGET** Fluid Volume Excess Anything that causes the body to retain fluid or excessive fluid intake Excessive IV fluids or water intake Blood transfusion Kidney failure Heart failure Long-term steroid use (paper thin skin) Hypervolemia: what am I looking for Lung sounds-crackle Dilution happens with electrolytes Bounding pulse compensates Downloaded by Maggie C. ([email protected])  lOMoARcPSD|48573418 JVD (jugular vein distended) Presence of s3 heart sound indication of heart failure (lub dub suishh-backflow of blood happening) PitÝng edema come back in secs. Fluid overload labs and diagnostic exams Hemoglobin decreased Hematocrit decreased Bun decreased Protein decreased Treating fluid overload Assess q2hr for worsening symptoms, electrolyte imbalances Diuretics Keep HOB 30-45 degrees PT teaching Low salt diet Possible fluid restriction Spironolactone- high K (it is sparing medication ) Furosemide low K HOB up so pt can breath-fluid overload can cause wet lungs Lab Values Sodium 135-145 Potassium 3.5-5 Calcium 8,6-10 Magnesium 1.6-2.6 Sodium Major positive cation in fluid outside of cells Excess sodium is secreted in the urine Sodium regulates the amount of water in the body If affects the brain, nervous system and muscles It helps with the body’s electrical signal for communication The movement of sodium is important to generate electrical signals Causes of hyponatremia Prolonged diuretic therapy Excessive diaphoresis InsufÏcient Na intake Kidney disease Hyponatremia and hypernatremia similar symptoms CHECK LABS TO KNOW IF HYPER OR HPO- KNOW LABS Hyponatremia Clinical manifestations Due to cellular swelling LOC changes/confusion Seizures (severe) Coma/death (severe) Due to decreased cell membrane excitability Downloaded by Maggie C. ([email protected])  lOMoARcPSD|48573418 Muscle weakness Diminished DTR’s Hyponatremia: what am I looking for Muscle weakness Tachycardia Fatigue Apathy Dry skin, pale mucus membranes Confusion Headache n/v, abdominal cramps orthostatic hypotension treatment of hyponatremia treat the underlying cause discontinue diuretics hypertonic IVF #% or 5% saline tolvaptan seizure and fall precautions (pad fails) pt teaching high salt, decrease fluid intake decrease fluids to avoid dilutions of electrolytes replace sodium because when you continue fluids you losing sodium Hypernatremia causes/risk factors Kidney failure Corticosteroids Excessive PO or IV sodium intake Dehydration s/s Vomiting diarrhea Diaphoresis Some drugs Hypertonic fluids/tube feeding Major burns MODEL (medications, meals, osmotic diuretics, diabetes insipidus, excessive H2o loss, low H2O intake) Hypernatremia assessment Confusion Dry membranes Low UOP Muscle twitching Muscle weakness Decreased deep tendon reflexes FRIED (fever (low grade), flushed skin, restless, increased fluid retention and increase BP, edema, decreased urine output, dry mouth) Downloaded by Maggie C. ([email protected])  lOMoARcPSD|48573418 Treatment of hyernatremia Treat the underlying cause 0.9% NS or D5 w/ 0.45% NS IV Diuretics: furosemide &bumetanide Pt teaching: encourage fluids, low salt diet Bumetanide-kidney disease Hyper-hold off on salt and drink water Potassium imbalances Plentiful in the GI tract A serum K level below 2.5 or above 7.0 can cause cardiac arrest 80-90% excreted through the kidney Hypokalemia Prolonged diuretic therapy Inadequate intake Severe diaphoresis Gastric suctioning, laxative use, vomiting Excess insulin K jumps on insulin and goes into cell Hypokalemia-s/s Anorexia N/v Drowsiness, lethargy, confusion Leg crams Muscle weakness Weak pulses Hypotension Cardiac dysrhythmias Constipation NUGGET*** Hypo-look at resp (decrease) Thread pulse Cardiac Muscle weakness Treatment of hypokalemia Treat the underlying cause Discontinue diuretics Fall precautions (muscle weakness) Potassium supplements Respiratory and cardiac assessments Increase potassium intake Treating hypokalemia with IV potassium Dilution: no >1 mEq K per 10ml solution Rate 5-19 mEq/hr No >20 mEq per hour*** Downloaded by Maggie C. ([email protected])  lOMoARcPSD|48573418 Note monitor pts IV site hrly for phlebitis and infiltration Must run over 1 hr (DON’T PUSH K) powder 40oz of water/juice PO pill don’t crush. Hyperklemia Greater than 5.0, ekg changes, decreased pH Results form impaired renal function Metabolic acidosis Acts as myocardial depressant (decreased HR & cardiac output) Muscle weakness GI hyperactivity Hyperkalemia causes Increase dietary intake Excessive administration of K Excessive use of salt substitutes Administration of larger quantities of blood that is old Hyponatremia Renal failure Low sodium=high K Hyperkalemia: what am I looking for Ekg changes Bradycardia Hypotension Muscle twitching Tingling followed by numbness Diarrhea Hyperkalemia treatment Medications D5w and regular insulin to facilitate movement into the cells Administer sodium polystyrene sulfonate (kayexalate) (oral or rectal) Dialysis Cardiac monitoring Treat underly8ing cause Diuretics Causes of hypocalcemia Decreased calcium and vitamin D intake Lactose intolerance Malabsorption Kidney disease Diarrhea Hypocalcemia: what am I looking for Muscle cramps Numbness/tingling Twitching/spasms Downloaded by Maggie C. ([email protected])  lOMoARcPSD|48573418 Paresthesia of fingers, toes, and face Weakness pulse Tetany Postivie troussea’s sign/Chvostek’s sign Abdominal cramping/diarrhea NUGGET** Positive trousseau’s sign- but bp cuff on any hand starts twitching Chvostek’s sign- touch cheek slightly you start winking Hypocalcemia treatment Calcium gluconate PO calcium supplements Minimize stimulations Hypercalcemia Excessive intake Excessive use of antacids with phosphate binding Excessive vitamin D intake Thiazide diuretics Cancer Hypercalcemia: s/s Increased hr Increased bp Blood clots in poor flow areas Decreased DTR’s Decreased GI peristalsis Bone pain Arrhythmias Cardiac arrest Kidney stones Excessive urination Hypercalcemia treatment Loop diuretics (laxis/bumex) IV fluids (0.9% NS) Calcitonin Phosphorus Discontinue all medications that contain or raise Ca Cardiac monitoring Hypomagnesemia Often mistaken for hypokalemia Malnutrition Diarrhea Malabsorption issues Diuretics Alcoholism Not sure draw labs Downloaded by Maggie C. ([email protected])  lOMoARcPSD|48573418 Hypomagnesemia: what am I looking for Hypertension, dysrhythmias, increased DTR’s, numbness&tingling, seizures and confusion, decreased GI motility NUGGET** Safety bed low position, padded rails Deep tendon reflex-hit knee and suppose to jerk Treatments of hypomagnesemia Treat the cause Discontinue magnesium-depleting meds Magnesium sulfate IV Hypermagnesemia causes Increased mag intake Meds IV mag replacement Hypermagnesemia s/s Lethargy and drowsiness Depressed neuromuscular activity Depresses respirations Sensation of warmth throughout the body Hypoactive deep tendon reflexes Hypotension Bradycardia Cardiac arrest Treatment of hypermagnesemia d/c all mg supplements iv fluids diuretics calcium gluconate/calcium chloride magnesium rich foods almonds, spinach, soybeans, avocados, potatoes, brown rice, cashews Care of the client w/diabetes mellitus Types of diabetes Type 1 Cause is autoimmune destruction of beta cells in pancreas Earlier onset/younger pts Tends to occur in children, but can have onset in adulthood ALWAYS requires insulin Absence of insulin Type 2 Adult onset Tends to occur in chronically overweight and obese pts (increase in nonwhites, Gestational diabetes, baby greater than 9lbs, increase LDL, decrease HDL, increase BP 140/90, increase A1C, fasting glucose of greater than 100 Downloaded by Maggie C. ([email protected])  lOMoARcPSD|48573418 Often controlled by appropriate diet and exercise, usually requires oral medication in addition to lifestyle changes Pathophysiology 1 deficits in insulin secretion 2 deficits in insulin action 3 decrease uptake of glucose by the cells results in hyperglycemia Symptoms 3 Ps (polyuria, polydipsia, Polyphagia), weight loss (start breaking down fat for energy), blurred vision, paresthesia, yeast infections (balanitis in men) Pathophysiology type 1 Produces no insulin Pathophysiology type 2 Insulin resistance Pancreas isn’t producing enough insulin Diabetes assessment History Weight and weight changes Family history; mother versus father with type 1 DM Frequent fungal infections (yeast) Delayed healing: poor LE blood flow Vision changes Peripheral neuropathy, gastropathy (due to damage of vagus nerve) 3 p’s polyuria, polydipsia, polyphagia Frequent infections Age/race: type 2 higher prevalence among non-whites and age over 40 Physical exam Acanthosis nigricans- darker skin folds Yeast infections-under breast or skin folds Decreased sensation Type 1 may present with DKA Type 2 obesity and hypertension, may present with HHS (rare) Severe Hyperglycemia Elevated serum ketones (fat by products) Hypovolemia (dehydrated) Acidosis (ketones are acidic) Kussmual respirations (deep labored rapid breathing) Fruity breath Electrolyte imbalances ( hyponatremia, hyperkalemia) DKA symptoms Cells stop responding to glucose or no glucose available Start breaking down fat which release ketones IV insulin drip required Diabetes: diagnosis Diagnostic blood tests Downloaded by Maggie C. ([email protected])  lOMoARcPSD|48573418 Fasting plasma glucose >/=126 Random BG >200 A1C>/= 6.5% (past 3 months) 75 g two hr glucose tolerance test with plasma glucose >200 Results should be confirmed with repeat testing Have to have 2 tests to confirm!!! Less than 5.8% is normal A1C levels Once diagnosed A1C less than 7% is good control!!! *****Glucometer: steps for BG monitoring****** Assessment equipment: monitor, testing strips, lancet, gauze Ensure that hands are clean before testing. Wash hands and make sure they are thoroughly dry Load new lancet (do not reuse) Prick finger at side (less painful than tip) Squeeze finger (not too hard) Touch tip against drop of blood Clean finger, remove test strips Dispose of lancet in sharps Diabetes: medical management Metformin: drug of choice for monotherapy Decreases amount of glucose produced by the liver Increases body’s response to insulin Metformin can cause lactic acidosis in pts with kidney impairment and should not be used by anyone with kidney disease Creatinine > 1.5 for men Creatinine > 1.4 for women More recent recommendation target GFR as more accurate representation of renal function (GFR of 46) Contrast media guidelines: metformin should be temporarily discontinued at the time of or prior to the procedure, and withheld 48hrs subsequent to the procedure and reinstituted only after renal function has been re-evaluated and found to be normal Pharmacology Center Sulfonylureas: stimulate insulin release from beta cells Glipizide, glyburide, glimepiride Generation Give with or just before meals Falling out if favor d/t r/f hypoglycemia Notoriously known for causing weight gain (reduces compliance) Thiazolidinediones (TZDs) decrease liver glucose production, increase sensitivity of insulin Pioglitazone, rosiglitazone, Contraindicated for pts with HF Cause liver disturbances pts have to get liver panels checked every 3 months Downloaded by Maggie C. ([email protected])  lOMoARcPSD|48573418 GLP-1 agonists: works at the level of the beta cells, agonist for a protein that increases secretion of insulin Exenatide, liraglutide Weight loss Injectable Expensive Advise pt to stop if they develop symptoms of pancreatitis DPP-4 inhibitors block destruction of hormone incretin; incretin augments secretion of insulin and decrease hepatic glucose production Sitagliptin, linagliptin n/v, warn pt in advance pancreatitis risk taken orally weight neutral newly diagnosed type 2; diet and exercise plus oral meds 9 and has signs of complications Pts who fail maximal anti-hyperglycemic therapy Insulin regimens Once daily (generally with some type of anti hyperglycemic) Twice daily basal ( morning and evening ) Basal-bolus (before meal, before bed) Sliding scale: used in hospitals Rapid acting insulin (logs) Aspart, lispro, glulisine Should be given within 10mins of meal time**** Peaks within 1hr gone in 3-5 hrs Tray must be infront of them Onset: 10-30mins Peak 30min-3hrs Duration 3-5hrs Short acting insulin (lins R) Regular insulin Should be given 20-30 mins before meal time Peaks within 2-4 hrs following administration Mixing (w/NPH) Only one able to give IV Onset 30min-1hr Peak 2-5hr Duration 5-8hrs Intermediate-acting (lins N) Downloaded by Maggie C. ([email protected])  lOMoARcPSD|48573418 NPH 70/30, 50/50, 75/25 (mixing types, regular/NPH) Peaks within 4-12hrs following administration Roll the vial of insulin Mix with regular only!! Onset 1.5hr-4hrs Peak 4-12hrs Duration 12-18hrs Long acting Insulin glargine (lantus) No peak** Insulin detemir (Levemir) Peak 6-8 hrs, duration 5-24 Onset 0.8-4hrs Peak no pronoused peak Duration 24hrs Air into cloudy, air into clear, draw clear, draw cloudy**** Insulin administration: other considerations Insulin storage: refrigerate insulin not in sue to maintain potency May be kept at room temperature for 28 days** Mixing: do not mix any other insulin types with insulin glargine or detemir (long acting), or with any pre-mixed formulations Rapid and short acting insulins can be mixed with NPH Air into cloudy Air into clear Draw up clear Draw up clody Give subcutaneous injection Abdomen is preferred injection site, at least 2 inches from the naval Rotate injection sites Rotation within one anatomic site is preferred to prevent variability in absorption Do not massage injection site!!!!! Injection sites Upper outer arm Abdomen Buttocks Upper outer thighs Complications of diabetes: hypoglycemia ‘ Definition: normal level 70-120, symptoms usually appear under 50. However no real correlation between symptoms and glucose level. Seizures when glucose reaches 20-40 Treat pt not # Symptoms due to SNS activation: the body thinks its starving due to lack of glucose Sweating, tremors, tachycardia, palpitation, anxiety, blurred vision, altered LOC, behavior changes, slurred speech, hunger, tingling around the mouth Downloaded by Maggie C. ([email protected])  lOMoARcPSD|48573418 Hypoglycemia: causes Medications: injected/given at wrong time, wrong dose Missed meals Missed tube feed TPN Alcohol: prevents liver form generating glucose (gluconeogenesis), drink with a meal or close to a meal Hypoglycemia: treatment Mild 40 in men >35in women Hyperglycemia FBG > or =100 Hypertension BP > or = 130/80 Hyperlipidemia Trig > or = 150 HDL 240mg/dL Care of the pt with common (renal) problems Polycystic kidney disease (PKD) Pathophysiology Genetic: familial disease, autosomal dominant Genetic mutations lead to formation of cysts in kidney. Cysts fill with fluid leading to kidney enlargement Presents in childhood or adulthood Clinical manifestations Abdominal/flank/back pain-palpate lightly (uncomfortable) Abdominal distension Hypertension Nocturia-early sign, sodium and water wasting Increased abdominal girth Constipation (enlarging kidneys) Bloody or cloudy urine: cyst rupture Edema Passed from family member to family member Extrarenal manifestation: cerebral aneurysm, aneurysm may rupture leading to subarachnoid hemorrhage; multisystemic Early states excessive urgency Cardiac problems; increased valve problems Cysts also be found in the liver, pancreas, and spleen Polycystic kidney disease: dx/tx Dx Kidney US: multiple bilateral cysts and renal enlargement UA: shows protein and hematuria, s/s infection Elevated bun/ creatinine: PKD leads to slow, progessive renal failure Tx: control complication** HTN: controlling htn can help preserve kidney function (ACE, ARD, BB,CCB) Priority ACE/ARBs Restrict sodium once CKD present (water follows salt) If renal failure: hemodialysis; 50% by 60yrs old Present constipation: if adequate UO fluid intake should be 2-3L daily to prevent constipation, increase dietary fiber, exercise regularly, FFF (fluid, fitness, fiber) Pain management: AVOID NSAIDs!!! May use opioids (first line of treatment), acetaminophen. Positioning, relaxation, dry heat to flank area Infections of kidney and urinary tract Downloaded by Maggie C. ([email protected])  lOMoARcPSD|48573418 Cystitis: bladder infection (lower UTI) Pyelonephritis: ascending infection, infection and inflammation of the renal pelvis (upper UTI) Women for susceptible Etiology and risk factors # 1 cause e-coli 80% of cases Predominantly women; if men look for underlying causes ( BPH, catheters, prostatitis, STDs) Instrumentation (caths, procedures) Immunosuppression (diabetes, cancer, AIDS) Obstruction (stone, tumor, or prostate) Urethral or urethral stones Sexual intercourse (contamination) Poor hygiene (wrong way wipers) Pyelonephritis Kidney infection Causes Reflux of contaminated urine into ureter and kidneys Men >65 are at higher risk due to prostate issues Diagnostics UA KUB shows inflammation, fluid, and abscesses NUGGET** BPH KUB Abscesses UTI symptoms Cystitis Dysuria Burning Frequency Urgency Suprapubic tenderness NO fever (usually) or flank pain Older adults become confused Foul, cloudy, sediment urine Pyelonephritis Same as cystitis plus Pt looks sick Fever n/v flank pain; side middle back CVA tenderness (costovertebral angle) (examined by MD), (12th rib vertebrae) (signs of kidney stone or pyelonephritis) Downloaded by Maggie C. ([email protected])  lOMoARcPSD|48573418 Nocturia Recent cystitis UTI dx/tx DX UA is gold standard test and WBCs, Leukocyte esterase,nitrates Assess the need for the catheter d/c ASAP!!! Prompt treatment is needed because it can lead to urosepsis Kidney, ureter,bladder (KUB)/CT for pyelonephritis: may identify cause Collect urine first then start ABX Nursing care Collect UA/ C&S Administer ABX as prescribed Bactrim, cephalosporin, fluoroquinolone Client teaching Increase hydration 2-L daily Avoid alcohol and caffeine Complete ABX therapy Prevent reoccurrence Hygiene (wiping front to back) Deodorants, soaps Loose fitÝng clothing, cotton underwear Empty bladder before and after intercourse Do not delay urination (go ever 3-4hrs) Cranberry pills (juice Prevent bacteria from sticking to bladder Urethritis Inflammation of urethra caused by sexually transmitted pathogens Etiology: gonorrhea, chlamydia Sx: purulent discharge from urethra (gonorrhea), white, grey or clear discharge (chlamydia), painful urination Dx: endourethral or endocervical smear Tx: antibiotics Acute glomerulonephritis (acute nephritic syndrome) Etiology Risk factors: recent strep infections!!, syphilis, chlamydia, toxoplasmosis, varicella, CMV, Mona. MOST common infectious cause is group A beta-hemolytic strep (strep pyogenes)*** Pathophysiology Recent infection that results in injury and inflammation to the nephron Clinical manifestations Hematuria Edema or SOB; peripheral or periorbital Low UOP Downloaded by Maggie C. ([email protected])  lOMoARcPSD|48573418 Tea, cola colored urine, brown, Smokey (cause by gross hematuria) Hypertension Will see blood and protein urine Most common is bacterial Diagnostic workup Urinalysis Proteinuria Hematuria 24hr urine for protein Red cell casts Antibody testing (antistrepolysis-O) CMP (comprehensive metabolic panel) Elevated bun/creatinine Decreased GFR Kidney BX NUGGET** After kidney biopsy you place pt supine When moving them log roll Assess for bleeding Coca-cola or tea colored urine in the pt who recently had strep is the giveaway!!! Acute glomerulonephritis: TX No magic cure. Supportive. Tx bp, edema Interventions Managing infections ABX Preventing complications Assessment for fluid volume overload & pulmonary edema (life threatening) Diuretics Sodium and water restricitons Restrict potein, potassium Antihypertensive meds Plasmapheresis Dialysis (severe cases) 85-95% normal renal functions resume Urolithiasis Urolithiasis- present of calculi (stones) anywhere in the urinary tract, including kidney, or bladder Nephrolithiasis-formation of stones in the kidneys Ureterolithiasis-formations of stones in the ureter Etiology Metabolic risk factors (obese,gout) High intake of calcium, vitamin D and vitamin C Dehydration Downloaded by Maggie C. ([email protected])  lOMoARcPSD|48573418 Family history Meds: indinavir, acyclovir, sulfadiazine, triamterene (cause urine to crystalize) UTI Acidic urine pH (