316 Exam 3 Study Guide PDF

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Fluid & Electrolyte Balance 1. Isotonic alterations • Total body water change with proportional electrolyte and water change (no change in concentration) • Isotonic fluid loss—hypovolemia • Isotonic fluid excess—hypervolemia 2. Hypertonic alterations • Increased osmolality • Hypernatremia • Water deficit in ECF (dehydration) • Hypernatremia • Serum sodium >145 mEq/L • Related to sodium gain or water loss • Manifestations • Brain cell shrinkage • Altered membrane potentials • Increased blood pressure • Isovolemic • Deficit of free water and normal sodium • Hypovolemic • Loss of sodium and greater loss of body water • Hypervolemic • Increase of body water with greater increase in sodium • Hyperchloremia often occurs with hypernatremia 3. Hypotonic alterations • Decreased osmolality • Hyponatremia • Water excess in ECF • Hyponatremia • Isovolemic • Loss of sodium with normal water • Hypervolemic • Increased body sodium causes increased body water • Hypovolemic • Loss of body water with greater loss in sodium • Dilutional • Intake of large amounts of free water which dilutes sodium • Hypochloremia often occurs with hyponatremia

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Potassium (K+)

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Major intracellular cation Concentration maintained by Na+/K+ ATPase pump Regulates intracellular electrical neutrality in relation to Na+ and H+ Roles:  Glycogen/glucose deposition  Normal cardiac rhythms  Skeletal and smooth muscle contraction (K+ for cardiac) Changes in pH affect K+ balance +  Hydrogen ions accumulate in the ICF during states of acidosis; K shifts out to maintain a balance of cations across the membrane; result is hyperkalemia Aldosterone, insulin, and epinephrine influence serum potassium levels Kidney is most efficient regulator Potassium adaptation  Slow changes tolerated better than acute Hypokalemia  Potassium level 5.5 mEq/L  Hyperkalemia is rare because of efficient renal excretion  Caused by increased intake, shift of K + from ICF into ECF, decreased renal excretion, insulin deficiency, or cell trauma  Manifestations  Depend on severity  Mild attacks  Increased neuromuscular irritability  Restlessness, intestinal cramping, and diarrhea  Severe attacks  Decreases the resting membrane potential  Muscle weakness, loss of muscle tone, and paralysis

Acid-Base Imbalances  Changes in H+ concentration lead to acid-base imbalances  Acidosis

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 Systemic increase in H+ concentration or decrease in bicarbonate (base) Alkalosis  Systemic decrease in H+ concentration or increase in bicarbonate Renal compensation – +  Kidneys resorb HCO3 into the plasma and excrete H into the urine Respiratory compensation  Lungs breath deeply and rapidly to rid the body of CO2 Metabolic acidosis  Low pH, normal or low PaCO2  Example, diabetic ketoacidosis Metabolic alkalosis  High pH, high HCO3–  Result of excessive loss of metabolic acids Respiratory acidosis  Low pH, high PaCO2  Result of alveolar hypoventilation Respiratory alkalosis  High pH, low PaCO2  Result of alveolar hyperventilation

Furosemide (Lasix): Most frequently prescribed loop diuretic • Mechanism of action • Acts on ascending loop of Henle to block reabsorption • Pharmacokinetics • Rapid onset (PO 60 min; IV 5 min) • Indications • Edema • Hypertension • Pulmonary edema • Adverse effects • Hypokalemia • Hyponatremia, hypochloremia, and dehydration • Hypotension • Loss of volume • Relaxation of venous smooth muscle • Ototoxicity • Hyperglycemia Thiazides and Related Diuretics • Also known as benzothiadiazides • Effects similar to those of loop diuretics • Increase renal excretion of sodium, chloride, potassium, and water • Elevate levels of uric acid and glucose • Maximum diuresis is considerably lower than with loop diuretics • Not effective when urine flow is scant (unlike with loop diuretics) • hydrochlorothiazide [HydroDIURIL] • Most widely used • Action: Early segment distal convoluted tubule • Peaks in 4-6 hours • Therapeutic uses • Essential hypertension • Edema • Diabetes insipidus • Adverse effects • Hyponatremia, hypochloremia, and dehydration • Hypokalemia • Use in pregnancy and lactation • Hyperglycemia • Hyperuricemia • Impact on lipids, calcium, and magnesium Potassium-Sparing Diuretics • Modest increase in urine production • Substantial decrease in potassium excretion

Rarely used alone for therapy Aldosterone antagonist • Spironolactone • Nonaldosterone antagonists • Triamterene • Amiloride • Mechanism of action • Blocks aldosterone in the distal nephron • Retention of potassium • Increased excretion of sodium • Therapeutic uses • Hypertension • Edematous states • Heart failure (decreases mortality in severe failure) • Primary hyperaldosteronism • Premenstrual syndrome • Polycystic ovary syndrome • Acne in young women • Adverse effects • Hyperkalemia • Benign and malignant tumors • Endocrine effects • Drug interactions • Thiazide and loop diuretics • Agents that raise potassium levels Osmotic Diuretic: mannitol [Osmitrol] • Promotes diuresis by creating osmotic force within lumen of the nephron • Pharmacokinetics • Drug must be given parenterally • Therapeutic uses • Prophylaxis of renal failure • Reduction of intracranial pressure • Reduction of intraocular pressure • Adverse effects • Edema • Headache • Nausea • Vomiting • Fluid and electrolyte imbalance • •

Thermoregulation

Types of Heat Transfer  Conduction  Touching an object  Cold exam table, hot pavement  Convection  To air or water  Cold or warm air from HVAC  Humidified oxygen (cold)  Evaporation  As water changes from liquid to gas  Wet clothing, sweating  Radiation  From one object to another without physical contact  Cold x-ray machine near the patient  Radiant infant warmer

Hyperthermia  Hypothalamic TRC set point unchanged

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Mechanisms that control body temperature ineffective at maintaining temp within normal range Occurs with excessive heat production or exposure to high ambient temperatures Several types  Accidental Hyperthermia  Heat exhaustion  Heat stroke  Heat cramps  Malignant Hyperthermia  Heat exhaustion (Temp between 37.8C (100F) and 40C (104F))  Results from prolonged high core or environmental temperature +  Develops to loss of Na and H2O through profuse sweating, dehydration, hypotension, blood volume, hypotension, decreased cardiac output, and tachycardia  Symptoms include weakness, dizziness, confusion, nausea, and fainting  Treat with cooling and rehydration  Heat stroke  Life threatening, results from an overstressed thermoregulatory center  Excessive rise in body core temp (>40C, 104F) AND CNS involvement  Loss of consciousness, delirium, ataxia, absence of sweating, rapid pulse rate, coma  Common in elderly in non-air-conditioned settings (extremely hot summer days)  Common with excessive physical training/exertion on hot days  Treatment includes:  Cold IV fluids, cooling blanket, ice water immersion,  Ice packs to groin, axilla, neck if other interventions unavailable  Treat shivering Malignant hyperthermia  Lethal, complication from a rare inherited muscle disorder triggered by depolarizing muscle relaxants  Most common in children and adolescents  Symptoms include uncoordinated muscle contractions, absent reflexes, coma,

Stages of Fever Development 1. Prodrome • Nonspecific complaints: mild HA, fatigue, malaise, aches/pains 2. Chill • Coincides with introduction of pyrogen into circulation • Temp  until it reaches new hypothalamic TRC set point • Sensation of being chilled and onset of general shaking • Vasoconstriction and piloerection preceded shivering • New set point reached = shivering stops and feeling of warmth begins 3. Flush • Cutaneous vasodilation, warm/red skin, temp begins to fall 4. Defervescence  Characterized by sweating

Hypothermia  Core temp 45 years of age, every 3 years Obese - BMI ≥ 25 kg/m2 or ≥ 23 kg/m2 in Asian Americans with ≥ 1 of the following:  First degree relative with DM  Sedentary lifestyle  Those with hypertension, hyperlipidemia (esp. TG > 250)  High risk race/ethnicity: African American, American Indian, Latinx, Asian American, Pacific Islander  History of CVD  Women who are pregnant or have polycystic ovary syndrome  Other clinical conditions associated with insulin resistance (e.g., severe obesity, acanthosis nigricans) Signs & Symptoms  Gradual onset – months/years  Blurred vision  Fatigue  Poor wound healing, prone to infections  Symptoms of neuropathy  3 P’s not as pronounced  Client adjusts to symptoms – denial !!

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Gestational diabetes mellitus (GDM):  Diabetes diagnosed during the second or third trimester of pregnancy (not present prior to gestation)  Screening: All pregnant women  High risk:  Family hx of type 2 DM, obesity, glycosuria, PCOS (polycystic ovarian syndrome), prior hx of GDM, or previous large-for-gestational-age infant.  If high risk: test ASAP  Low risk:  Screen at 24-28 weeks of gestation  Test using 1- or 3-hour OGTT: normal < 140 mg/dL at 1-2 hours  Threshold is lower for GDM!  All hyperglycemia is detrimental to maternal and fetal health!!  Test for persistence at 4-12 week follow-up appointment with OB provider  +GDM -> increased risk of T2DM within 5 years

Lispro (Humalog) & Aspart (NovoLog)    

Rapid-acting Structure nearly identical to natural human insulin Routes: SQ injection or SQ infusion (pump) Clear solution  Onset 0.25 hours  Peak 1 hour  Duration 3 –4 hours

Regular (Humulin-R, Novolin-R)   

Short-acting Can be administered: SQ injection, SQ infusion, IV infusion Clear solution  SQ Onset – 0.5 – 1 hour

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SQ Peak 2 –3 hours SQ Duration 3 – 6 hours

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Intermediate acting Cloudy solution – Zinc added to prolong onset and duration of activity SQ injection only  Onset – 2-4 hours  Peak – 4 –10 hours  Duration – 10 –16 hours

Glargine (Lantus) & Detemir (Levemir)   

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Long-acting Clear solution SQ injection only  Onset – 1 –2 hours  Peak – none  Duration – 24 + hours Do Not Mix with other insulins! New – Tresiba (insulin degludec) – similar to Lantus.  Comes in U-100 and U-200 strengths (U-100 = 100 units/ml; U-200 = 200 units/ml)

Insulin Therapy  

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Insulins are often combined to achieve optimal blood glucose control Common regimens:  Regular + NPH  Rapid-acting + NPH  Lantus (daily) + short acting (Regular or Rapid-acting) with meals Usually administered SQ  Review mixing technique, administration sites  Store in refrigerator (unopened)  Vials stable after opened for 30 days (label) Pre-filled syringes stable up to 1 week in refrigerator

Biguanide: metformin (Glucophage) 

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Reduces glucose production by liver Enhances insulin sensitivity at tissue level

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Does not promote weight gain Withhold preoperatively or if IV contrast used and for 48 hours after Not to be used in those with renal impairment Good effect on plasma lipids (cholesterol) SE: GI (decreased appetite, nausea, diarrhea), vitamin B12 deficiency (test for this occasionally), lactic acidosis (rare, but life-threatening)

Sulfonylureas: glipizide (Glucotrol)    

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MOA: Increase insulin production from the pancreas PO First generation (used less now)  May cause hypoglycemia Second generation (used widely)  Give 30 min. before meal  Less risk of hypoglycemia  Glipizide (Glucotrol, Glucotrol XL) SE: hypoglycemia; flushing, palpitations, nausea when combined with alcohol (a disulfuram-type reaction), beta-blockers diminish effectiveness of drug

Thiazoledinediones (TZDs): pioglitazone (Actos) 

MOA: Decreases insulin resistance by promoting glucose uptake by skeletal muscle and adipose tissue, & may decrease glucose production in liver  Mainly an add-on to metformin therapy  Not started much anymore d/t risk of MI, sudden death  SE: Headache, sinusitis, myalgia, URI  AE: Heart failure d/t renal fluid retention DPP-4 Inhibitors: sitagliptin (Januvia) 

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MOA: Enhances incretin hormone system  Inhibits DPP-4: an enzyme that inactivates the incretin hormones  Stimulates release of insulin from pancreas  Suppresses post-prandial release of glucagon Oral medication No weight gain SE: well-tolerated, rare pancreatitis

Incretin mimetic (GLP-1 RA): exenatide (Byetta, Bydureon); semaglutide (Ozempic) 

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Stimulate incretin hormone (GLP-1 receptor agonist) Decreases glucagon production

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 Increased satiety, slows gastric emptying SQ injection (daily; semaglutide weekly) Not used with insulin therapy Can be used with oral agents SE: May cause nausea, vomiting – start with low dose, hypoglycemia, pancreatitis, renal impairment

Sodium-glucose Co-transporter 2 (SGLT-2) Inhibitors: canaglifozin (Invokana)   

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Newest class of antidiabetic drug Oral medication MOA:  Reduces the amount of glucose reabsorbed in renal tubules.  Increases amount of glucose in urine (glucosuria)  Promotes osmotic diuresis – polyuria may occur SE: weight loss may occur, orthostatic hypotension, GU yeast infections

Research Update (EMPA-REG Trial):  Reduces risk of major adverse cardiac events (MACE) by 11% if established CV disease  Reduced risk of progression of kidney disease by 45%  Reduced risk of CV death or hospitalization for HF by 23%

Hyperglycemic Hyperosmolar State (HHS)  Similar to DKA, but T2DM, acute pancreatitis, severe infection  Profound hyperglycemia (> 600 mg/dL)!!  No ketoacidosis – some glucose uptake into muscle cells  Hyperosmolar state  mental confusion  profound glycosuria and water loss  Treatment:  IV fluids  IV regular insulin  electrolyte replacement  close observation for cerebral edema with fluid replacement  ….mortality high Hypoglycemia  Alert Value: BG < 70 mg/dL  Clinically Significant BG < 54 mg/dL  Causes:  Too much insulin

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too little food too much exercise Symptoms: hunger, confusion, belligerence  May or may not have SNS Sx: tachycardia, sweating, trembling  Hypoglycemia Unawareness Syndrome Treatment: 15 g Carbohydrate – 4-6 oz. Juice or regular soda, 8 oz low-fat milk  IV 50% dextrose per provider’s order (preferred)  1 mg glucagon IM if unable to swallow  Repeat blood glucose after 15-20 minutes (Rule of 15: 15 g carbohydrates, 15 minutes)...