My med surg exam study guide

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2015

Med-Surg Nursing Exam Study Guide I created this study guide to study for our nursing school Med-Surg exam, as well as to help study for the HESI and NCLEX exams.

Jennifer Cook Nursing School 4/30/2015


Med-Surg Exam Study Guide Outline         

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Fluid Overload (Hypervolemia) – Pg. 1 - 2 Dehydration (Hypovolemia) and Related Lab Value – Pg. 2 – 3 Hypokalemia and Hyperkalemia – Pg. 3 – 5 o Potassium Levels – Pg. 6 – 7 DVT Management – Pg. 8 – 10 Erickson’s Stages – Pg. 10 Piaget’s Theory – Pg. 10 O2 Therapy and COPD – Pg. 11 – 12 Diabetes Insipidus – Pg. 12 - 13 Diabetes Mellitus Type I and Type II – Pg. 14 – 19 o Hypoglycemia vs Hyperglycemia – Pg. 19 o Diabetes Medications (Oral) – Pg. 20 – 24 o Insulin – Pg. 24 o Metformin – Pg. 25 o DKA – Pg. 25 – 26 Rheumatoid Arthritis – Pg. 26 – 28 Osteoporosis – Pg. 28 GERD – Pg. 29 Hiatal Hernia – Pg. 29 – 30 TB Management – Pg. 30 – 31 Asthma – Pg. 32 o Asthma Medications – Pg. 33 Heart Failure – Pg. 34 – 41 o Heart Medications ( ACE Inhibitors, ARB’s, B-Blockers, Adrenergic Antagonists Blockers, Aldosterone Antagonists) – Pg. 37 – 40 Arterial vs Venous Insufficiency – Pg. 41 – 43 Malignant Hyperthermia – Pg. 43 Anesthesia – Pg. 43 – 45 Anticoagulants, Fibrinolytics (Thrombolytics – Clot Busters), Antibrinolytics, and Platelet Inhibitors – Pg. 45 – 48 Vitamin B12 Deficiency Anemia, Sickle Cell Anemia, and Other Anemias – Pg. 48 – 50 Polycythemia Vera – Pg. 50 – 51 Hemophilia and PT/INR – Pg. 51 – 52 Hypertension and MI – Pg. 53 – 62 Page 1 of 107


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o HTN Medications (ACE Inhibitors, ARB’s, Vasodilators, B-Blockers, Calcium Channel Blockers, Antihypertensives) – Pg. 54 – 57 o Diuretic Drugs (includes ADH) – Pg. 58 – 62 UTI – Pg. 63 Blood Transfusion – Pg. 64 – 65 Chronic Renal Failure – Pg. 66 – 67 Left and Right CVA – Pg. 68 Anaphylaxis – Pg. 69 Pneumonia – Pg. 70 Emphysema – Pg. 71 Bronchitis – Pg. 71 PE: Pulmonary Embolus – Pg. 72 Pneumothorax – Pg. 73 Hypoxia – Pg. 74 – 75 AD PIE – the nursing process – Pg. 75 Fractures – Pg. 76 Hypernatremia (↑ Sodium – NA) and Hyponatremia (↓ Sodium – NA) – Pg. 77 – 79 Lab Values – Pg. 79 – 83 Electrolytes – Pg. 83 Disease Chart – Pg. 84 – 85 Acidosis vs. Alkalosis – Pg. 85 – 94 Cranial Nerves – Pg. 95 Hypocalcemia (↓ Ca) and Hypercalcemia(↑ Ca) – Pg. 96 – 98 Hypermagnesemia (↑ Mag) and Hypomagnesemia (↓ Mag) – Pg. 99 – 100 Endocrine Disorders (Hypothyroidism, Hyperthyroidism, Cushing’s Disease, Grave’s Disease) – Pg. 101 Shock – Pg. 102 Calcium – Phosphorus Relationship – Pg. 103 Bowel Obstruction – Pg. 104 Hip Fractures – Pg. 105

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Med-Surg Exam Study Guide Fluid Overload (Hypervolemia) What are clinical manifestations of fluid overload? 

Cardiovascular Changes o Bounding pulse quality o Peripheral pulses full o ↑ B/P o ↓ Pulse pressure o ↑ Central venous pressure o Distended neck and hand veins o Weight gain Respiratory Changes o ↑ Respiratory rate o Shallow respirations o Dyspnea increases w/exertion or in the supine position o Moist crackles present on auscultation Skin and Mucous Membrane Changes o Pitting edema in dependent areas as well as joints and skin around bony prominences (elbows, metacarpals, metatarsals) o Skin pale and cool to touch. Skin and puncture sites from needles sticks may “weep” as fluid tries to escape through the skin. Neuromuscular Changes o Altered LOC o H/A o Visual disturbances o Skeletal muscle weakness o Paresthesia’s Gastrointestinal Changes o ↑ motility o Enlarged liver Lab Values o Serum electrolyte values are normal o ↓ Hgb o ↓ Hct o ↓ Serum protein levels

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Dehydration (Hypovolemia) and Lab Values How does dehydration potentially affect lab values? Sodium Excess (hypernatremia) –This is sometimes caused from being dehydrated or an inadequate water intake. The person can experience red flushed skin; dry, sticky mucous membranes; increased thirst; temperature elevation; water retention; hypertension; and decreased or absent urination. However, we do still need a good deal of sodium in our diets. This is because sodium helps water to generate the electricity in our bodies. There is still a fine line here because too much sodium will require us to need more potassium to keep everything balanced out.

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Hypokalemia vs Hyperkalemia What assessment findings do you see in a patient with hypokalemia and hyperkalemia? 

Hypokalemia – Weakness, fatigue, anorexia, abdominal distention, arrhythmias, decreased bowel sounds

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Hyperkalemia – Anxiety, arrhythmias, increased bowel sounds Page 6 of 107


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Potassium Levels What is the normal potassium level of the blood and what symptoms might you see with high or low levels?  

Normal Value – 3.5 to 5.0 mEq/L (3.5 to 5 mmol/L) Hyperkalemia (High) – bilateral muscle weakness that begins in quadriceps, transient abdominal cramps, diarrhea, and potentially life-threatening cardiac dysrhythmias, and cardiac arrest; possible ECG abnormalities. Must remember to  urine output before administering IV solutions containing potassium.

Hypokalemia (Low) – bilateral muscle weakness that begins in quadriceps and may ascend to respiratory muscles, abdominal distention, decreased bowel sounds, constipation, and potentially life-threatening cardiac dysrhythmias; signs of digoxin toxicity @ normal digoxin levels.

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DVT Management

What patients are at increased risk for DVT? 

Three factors contribute to venous thrombus formation: 1.) Damage to the vessel wall (injury during surgical procedures) 2.) Alterations of blood flow (slow blood flow in calf veins associated w/bed rest) 3.) Alterations in blood constituents (change in clotting factors or increased platelet activity). These 3 factors are often referred to as Virchow’s Triad. The highest incidence is among patients who have undergone hip surgery, total knee replacement, or open prostate surgery.

Other conditions include: o Pregnancy Page 10 of 107


o o o o o o o o o o o o o o

Injury Ulcerative Colitis Immobility Inheriting a blood-clotting disorder Prolonged bed rest, such as during a long hospital stay, or paralysis Birth control pills or hormone replacement therapy Being overweight or obese Smoker Cancer Heart Failure ≥ 60 years old Sitting for long periods of time, such as when driving or flying A personal or family history of deep vein thrombosis or pulmonary embolism (PE) Inflammatory bowel disease

List interventions to minimize the risk of a DVT.               

Prevention of immobility when possible Patient Education Drink adequate fluids to avoid dehydration Elevate legs when sitting or lying in bed Exercise legs during long periods of bedrest or sitting Wear sequential or graduated compression stockings Early ambulation after surgery, etc. Use of Venous plexus foot pump Use alternatives to contraceptives Stop smoking Assessment of risk Anticoagulation (eg, LMWH, fondaparinux, adjusted-dose warfarin) Intermittent pneumatic compression IVCF In Regards to IV Therapy o Use evidenced-based venipuncture technique. o Make only two attempts to perform venipuncture. o Choose the smallest-gauge catheter in the largest vein possible. o Secure catheter adequately. o Use armboards if short peripheral catheters are placed in areas of joint flexion. o Ensure adequate hydration to avoid changes in blood composition and flexion of the extremity. Page 11 of 107


o Prophylactic low-dose warfarin

Erickson’s Stages What are Erikson's eight stages of life?        

Trust vs. Mistrust (Birth to 1 year) Autonomy vs. Sense of Shame and Doubt (1 to 3 years) Initiative vs. Guilt (3 to 6 years) Industry vs. Inferiority (6 to 11 years) Identity vs. Role Confusion (Puberty) Intimacy vs. Isolation (Young Adult) Generativity vs. Self-Absorption and Stagnation (Middle Age) Integrity vs. Despair (Old Age)

Piaget’s Theory Summarize Piaget's theory of cognitive development. It includes four periods that are related to age and demonstrate specific categories of knowing and understanding.    

Period I: Sensorimotor (Birth to 2 years) – Infants develop a schema or action pattern for dealing w/the environment. Period II: Preoperational (2 to 7 years) – During this time children learn to think w/the use of symbols and mental images. Period III: Concrete Operations (7 to 11 years) – Children now are able to perform mental operations. Period IV: Formal Operations (11 years to Adulthood) – The transition from concrete to formal operational thinking occurs in stages during which there is a prevalence of egocentric thought.

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Oxygen Therapy and COPD

What is the oxygenation device that delivers the highest concentration of O2? A nonrebreather mask w/reservoir bag. Minimum flow of 10L/min and delivers FIO2 of 60% to 80%. Which one delivers the most precise amount of O2? A Venturi Mask controls amount of specified oxygen concentration; delivers percentage of FIO2 from 24% to 60%. What liter(s) of O2 does a simple mask need to be set? Should be set @ 5 L or more to avoid rebreathing exhaled carbon dioxide retained in the mask. Which oxygen delivery method is considered low-flow? Nasal Cannula Explain the pathophysiology of why a patient with COPD should not receive high-flow O2?

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Patient’s w/COPD who are breathing spontaneously should never receive high levels of oxygen therapy because it results in a decreased stimulus to breathe. Do not administer oxygen @ more than 2 L/min unless a health care provider’s order is obtained. Hypoxia stimulates the drive to breathe in the chronic CO2 retainer patient. When applying O2, close monitoring is imperative to prevent unsafe increases in the patient's PaO2, which could result in apnea. In general, use a delivery system such as a Venturi mask or nasal cannula. Avoid routine use of a non-rebreather mask with 15 L/min of oxygen, unless the patient is not responding to lower flow rates. In some patients with chronic carbon dioxide retention, high flow oxygen may cause respiratory depression with the rapid rise in oxygen depressing the central ventilatory drive.

Diabetes Insipidus

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Diabetes Mellitus Type I and Type II   

Erectile Dysfunction – In diabetes, it is Autonomic Neuropathy. Diabetic Retinopathy Patient Teaching Concern – can cause blindness. Diabetic Exercise - ? walking.

What is the difference between Type I and Type II Diabetes? 

Type I – an autoimmune disorder in which beta cells of the pancreas are destroyed in a genetically susceptible person and no insulin is produced. o Is abrupt in onset o Requires insulin injections to prevent hyperglycemia and ketosis and to sustain health. o Represents fewer than 10% of all people who have diabetes. o Occurs primarily in childhood or adolescence but can occur at any age. o Causes patients to be thin and underweight.

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o May follow a viral infection; viral infection can trigger autoimmune antibody formation. o Can lead to ketoacidosis. Type II – a problem resulting from a reduction in the ability of most cells to respond to insulin (insulin resistance), poor control of liver glucose output, and decreased beta cell function. o Is generally slow in onset o May require oral antidiabetic drug therapy or insulin to correct hyperglycemia. o Is usually found in middle-aged and older adults but may occur in younger people. o May be part of the metabolic syndrome. o Occurs more often among obese people. o Is usually not associated with ketoacidosis. o Represents about 90% of all people who have diabetes. o May be present for years before it is diagnosed.

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Features

Age at Onset

Type I Juvenile-onset Diabetes Ketosis-Prone Diabetes Insulin-Dependent Diabetes Mellitus (IDDM) Usually younger than 30 yr. Occurs at any age

Symptoms Etiology

Abrupt onset, thirst, hunger, increased urine output, weight loss Viral infection

Former Names

Pathology Antigen patterns Antibodies Endogenous Insulin and CPeptide

Pancreatic beta-cell destruction HLA-DR, HLA-DO ICA’s present at DX

Type II Adult-onset Diabetes Ketosis-Resistant Diabetes Non-Insulin-Dependent Diabetes Mellitus (NIDDM) Peaks in 50’s; may occur earlier Frequently none; thirst, fatigue, blurred vision, vascular or neural complications Not known Insulin resistance Dysfunctional pancreatic beta cell None None

None

Low, normal, or high Page 20 of 107


Inheritance Nutritional Status Insulin Medical Nutrition Therapy

Complex Usually non-obese All dependent on insulin Mandatory

Dominant, multifactorial 60% to 80% obese Required for 20% to 30% Mandatory

Hypoglycemia vs Hyperglycemia Differentiate between signs and symptoms and treatment of hypo and hyperglycemia? 

Hypoglycemia o S/S – Cool, clammy skin; anxious, nervous, irritable, mental confusion, seizures, coma, weakness, double vision, blurred vision, hunger, tachycardia, palpitations, Glucose < 70 mg/dL, negative for ketones. o TX – Mild: treat with 10 to 15 g of carbohydrate (can use glucose tablets or glucose gel, or various types of foods like fruit juice, hard candies, saltines, etc.); Moderate: treat with 15 to 30 g of rapidly absorbed carbohydrate, take additional food, such as low-fat milk or cheese, after 10 to 15 minutes. Severe: treat by administering 1 mg of glucagon IM or Subcu, give 2nd dose in 10 minutes if person remains unconscious, call PCP immediately, if still unconscious, transport to ER, give small meal when person wakes up and is no longer nauseated. Hyperglycemia o S/S – Warm, moist skin; dehydration, Rapid, deep respirations - Kussmaul type; acetone odor (“fruity” odor) to breath, mental status varies from alert to stuporous, obtunded, or frank coma, acidosis; hypercapnia; abdominal cramps, nausea, and vomiting, decreased neck vein filling, orthostatic hypotension, tachycardia, poor skin turgor, Glucose > 250 mg/dL, positive for ketones. o TX – Regular exercise, maintain diabetes diet regimen, insulin adjustments, regular monitoring of blood glucose levels, take medication as directed.

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Diabetes Medications 

Oral Antidiabetic Drugs o Biguanide (1st line)  Mechanism of Action – works by decreasing glucose production by the liver. May also decrease intestinal absorption of glucose and improve insulin receptor sensitivity.  Side Effects – GI disturbances are the most common. Also may experience a metallic taste.  Contraindications – client’s w/renal disease or renal dysfunction. Can increase risk of lactic acidosis. Others include alcoholism, hepatic disease, heart failure, metabolic acidosis, etc.  Route/s of Administration - PO  Common Drugs  Metformin (only drug in this class and considered 1st line drug) o Sulfonylureas (2nd generation) – (Can be used w/Metformin)  Mechanism of Action – bind to specific receptors on beta cells in the pancreas to stimulate the release of insulin.  Side Effects – hypoglycemia is the most common and depends on eating habits, and presence of hepatic or renal disease. Also weight gain, skin rash, nausea, epigastric fullness, and heartburn.  Contraindications – hypoglycemia, potential for cross-allergy in patients who are allergic to sulfonamide ABT’s.  Route/s of Administration – PO  Common Drugs  glipizide – Glucotrol  glyburide – Diabeta  glimepiride – Amaryl

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o Glinides  Mechanism of Action – increase insulin secretion from pancreas w/much shorter duration.  Side Effects – hypoglycemia, weight gain  Contraindications – similar to those for the sulfonylureas.  Route/s of Administration - PO  Common Drugs  repaglinide – Prandin  nateglinide - Starlix o Thiazolidinediones (Glitazones)  Mechanism of Action – acts by regulating genes involved in glucose and lipid metabolism. Work to decrease insulin resistance by enhancing the sensitivity of insulin receptors.  Side Effects – increased risk of heart failure, peripheral edema, and weight gain.  Contraindications – clients w/New York Heart Association class III or IV heart failure and use caution in client’s w/liver or kidney disease.  Route/s of Administration - PO  Common Drugs  pioglitazone – Actos (only one in use) o Alpha-Glucosidase Inhibitors (less commonly used)  Mechanism of Action – work by reversibly inhibiting the enzyme alphaglucosidase that is found in small intestine.  Side Effects – high incidence of flatulence, diarrhea, and abdominal pain. May also elevate levels of hepatic enzymes.  Contraindications – not recommended for use in clients w/inflammatory bowel disease, malabsorption syndromes, or intestinal obstruction.  Route/s of Administration - PO  Common Drugs  Acarbose – Precose  Miglitol – Glyset

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o Dipeptidyl Peptidase IV (DPP-IV) Inhibitors  Mechanism of Action – work by delaying the breakdown of incretin hormones by inhibiting the enzyme DPP-IV.  Side Effects – most common are URI, headache, diarrhea. Hypoglycemia can also occur. Cases of pancreatitis have also been reported.  Contraindications - allergy  Route/s of Administration - PO  Common Drugs (only 3 available)  Sitagliptin – Januvia  Saxagliptin – Onglyza  Linagliptin - Tradjenta o Amylin Agonists  Mechanism of Action – work by mimicking the action of the natural hormone amylin.  Side Effects – nausea, vomiting, anorexia, and headache  Contraindications – clients w/gastroparesis or those taking drugs that alter gastrointestinal motility.  Route/s of Administration - PO  Common Drugs  Pramlintide – Symlin (only one available) o Incretin Mimetics  Mechanism of Action – enhance glucose-dependent insulin secretion, suppress elevated glucagon secretion, and slow gastric emptying.

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Side Effects – nausea, vomiting, diarrhea. Rare cases of hemorrhagic or necrotizing pancreatitis have been reported. May also experience weight loss of 5 to 10 pounds. Contraindications - allergy Route/s of Administration - PO Common Drugs (only 2 available)  Exenatide  Liraglutide

Insulin Absorbed fastest in the abdomen, followed by deltoid, buttocks, and thighs.

What is the onset and peak action of regular and NPH insulin? 

Regular – Short-Acting Insulin o Onset – 0.5 hr. o Peak - Humulin R: 2-4 hrs., Novolin R: 2.5-5 hrs. (Most Common ones) NPH – Intermediate-Acting Insulin (Most Common: includes Humulin N, Novolin N) o Onset – 1.5 hrs. o Peak – 4-12 hrs.

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Metformin What teaching would you give the client who will begin taking Metformin?     

Take drug with food. Report symptoms of lactic acidosis: malaise, unusual muscle pain, respiratory distress, increasing somnolence, and abdominal distress. Report any illness that causes severe vomiting, diarrhea, or fever. Withhold Metformin for 48 hours before use of iodinated contrast materials used in certain radiographic studies. Tablets must be swallowed whole and never crushed or chewed.

DKA Describe DKA, cause and treatment? It occurs in people with Type I DM and is most often precipitated by illness, especially infection. It is characterized by uncontrolled hyperglycemia, metabolic acidosis, and increased production of ketones. 

Cause – Lack of insulin and ketosis. Results from the combination of insulin deficiency and an increase in counter regulatory hormone release. Hormonal changes lead to increased use liver and kidney glucose production and decreased glucose regulatory hormones leads to the production of ketoacids with resultant ketonemia and metabolic acidosis. TX – (Pretty much the same as Hyperglycemia, except is an emergency situation). Blood glucose management, Fluid replacement, Electrolyte replacement, Insulin therapy, and Acidosis management (Hypokalemia is a common cause of death in the TX of DKA).

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Rheumatoid Arthritis Discuss rheumatoid arthritis and its associated management. Rheumatoid arthritis (RA) is a chronic, progressive, systemic inflammatory autoimmune disease process that damages and destroys synovial joints. Transformed antibodies (rheumatoid factors [RF’s]) attack healthy tissue, especially synovium, causing inflammation. Onset may be acute and severe or slow and insidious, and the pattern of illness progression includes remissions and exacerbations. Permanent joint changes may be avoided or mitigated when RA is diagnosed early. Early aggressive treatment to suppress synovitis may lead to a remission. Systemic means that inflammatory factors related to this disease affect more than the joints. Affected body systems include cardiovascular (vasculitis, myocarditis, pericarditis), lung (pleurisy, pneumonitis), eyes, and skin. Inflammatory factors also contribute to anorexia, weight loss, and nutritional derangements. Genetic factors combine with environmental conditions and interact to

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trigger RA. Female reproductive hormones may influence the development of RA, because the disease affects more women than men.

Management Includes: 

Drug Therapy o Disease-modifying antirheumatic drugs (DMARD’s) – slow progression of mild RA before it progresses. Ex. Plaquenil, Azulfidine o NSAID’S – Drug of choice for pain. o Biological response modifiers (BRM’s) – interfere with the action of different inflammatory mediators. Ex. Enbrel, Humira, Orencia. o Steroidal anti-inflammatory drugs o Other immunosuppressive drugs o Analgesic drugs Nonpharmacologic Management o Rest, positioning, ice, and heat o Plasmapheresis (plasma exchange) Page 29 of 107


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o Hypnosis, acupuncture, magnet therapy, imagery, or music therapy o Stress management o Nutrition o Nutritional supplements Promotion of Self-Care Management of Fatigue Enhancement of Body Image

Osteoporosis

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GERD Explain GERD, its medical management including dietary concerns. It is the most common upper GI disorder in the US. It occurs as the result of the backward flow (reflux) of GI contents into the esophagus. Reflux produces symptoms by exposing the esophageal mucosa to the irritating effects of gastric or duodenal contents, resulting in inflammation. Can lead to strictures or Barrett’s esophagus. Clinical Manifestations – Dyspepsia (heartburn), Regurgitation (may lead to aspiration or bronchitis), Eructation (belching), Flatulence (gas), coughing, hoarseness, or wheezing at night, water brash (hyper salivation), dysphagia, odynophagia (painful swallowing), epigastric pain, nausea, pyrosis (retrosternal burning), Globus (feeling of something in back of throat), pharyngitis, dental caries (severe cases). Management – Nutrition therapy, Lifestyle changes, and Drug Therapy 

Nutrition – limit or eliminate foods that decrease LES pressure, such as chocolate, alcohol, fatty foods (especially fried), caffeine, and carbonated beverages. The client should also restrict spicy and acidic foods (orange juice, tomatoes) until esophageal healing can occur. Peppermint can also aggravate symptoms. Large meals should be avoided. Eat 4 to 6 small meals per day. Do not eat for at least 3 hours before going to bed. Eat slowly and thoroughly.  Lifestyle – Elevate HOB by 6 to 12 inches for sleep. Sleep on right side-lying position. Smoking and alcohol cessation. Weight reduction. Avoid wearing constrictive clothing, lifting heavy objects or straining, and working in a bent-over or stooped position. Possibly eliminate NSAID’s, nitrates, and calcium channel blockers as they can cause reflux. Drug Therapy – Antacids, histamine blockers, and proton pump inhibitors (PPI’s).

Hiatal Hernia Define hiatal hernia and describe associated client teaching. A hernia is a weakness in the abdominal muscle wall through which a segment of bowel or other abdominal structure protrudes. Increased intra-abdominal pressure can contribute to hernia formation. It is also called diaphragmatic hernias; involve protrusion of the stomach through the esophageal hiatus of the diaphragm into the chest. The esophageal hiatus is the opening in the Page 31 of 107


diaphragm through which the esophagus passes from the thorax to the abdomen. Most patients with hiatal hernias are asymptomatic, but some may have daily symptoms similar to those with GERD. Client Teaching  

Nonsurgical Management – Similar to those for GERD and include drug therapy, nutrition therapy, and lifestyle changes. Surgical Management o Avoid lifting and restrict stair climbing for 2 to 6 weeks after surgical repair. o Inspect the surgical wound daily and report the incidence of swelling, redness, tenderness, or discharge to the physician. o Report S/S of infection or fever to the physician. o Avoid prolonged coughing episodes to prevent dehiscence of the fundoplication. o Stop smoking o About diet modifications, including weight loss goals if needed, eating small portions, avoiding irritating foods and liquids, and reporting recurrence of reflux symptoms to the physician. o Avoid straining and prevent constipation; stool softeners or bulk laxatives may be needed.

TB Management What are the diagnostic tests and precautions for hospitalized TB patient? 

Diagnostic Tests o NAAT (Nucleic Acid Amplification Test) – A new rapid test for tuberculosis that was developed and approved by the World Health Organization in 2010. Results are available in less than 2 hours. Widespread use of this test is endorsed and should soon replace other diagnostic methods. o Acid-Fast Bacillus Test – Not specific for TB, but it is used as a quick method to determine whether TB precautions should be started until more definitive testing can be completed w/either a two-step procedure or the QuantiFERON-TB Gold. o QuantiFERON-TB Gold o Blood Analysis – Uses QuantiFERON-TB Gold. Relatively rapid test w/results ready in 24 hours and is most useful in the acute care setting to determine whether a symptomatic patient has TB. o Sputum Culture – Confirms DX. Requires 1 to 4 weeks to determine a positive or negative result.

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o Tuberculin Test (Mantoux Test) – Most commonly used. Placed intradermally in the forearm. Does not indicate active disease, only exposure to disease. o CXR Precautions o Airborne Precautions in a well-ventilated room that has at least six exchanges of fresh air per minute. o All health care workers must wear an N95 or high-efficiency particulate air (HEPA) respirator when caring for the patient. o When hand and clothing contamination is a risk, use Standard Precautions w/appropriate contact protection (gowns and gloves). o Perform hand washing before and after patient care. o Precautions are discontinued when the patient is no longer infectious.

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Asthma 

Do PFT’s to evaluate

.

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Which inhaler medications should be used as a rescue drug for the client with asthma?

Short-Acting Beta² Agonist (SABA) o Albuterol (Proventil, Ventolin) o Bitolterol (Tornalate) o Levalbuterol (Xopenex) o Pirbuterol (Masair) o Terbutaline (Brethaire) Cholinergic Antagonist – Ipratropium (Atrovent, Apo-Ipravent) – Can relieve and prevent asthma. Does not work as well as SABA’s but can be used in place of SABAs by patients who cannot tolerate side effects of beta² agonists.

Which medications should be taken on a regular schedule to prevent exacerbation's of asthma?  

Long-Acting Beta² Agonist (LABA) o Formoterol (Foradil) o Salmeterol (Serevent) Because Singulair (monteleukast) and other leukotriene modifiers are not as effective as inhaled steroids, they are not considered a first-line treatment for asthma. However, Singulair (monteleukast) and other leukotriene modifiers can be useful if inhaled steroids alone do not control your asthma symptoms.

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Heart Failure Describe the assessment findings of right and left sided heart failure. Why are they different?

Right-Sided HF – Associated w/↑ systemic venous pressures and congestion. o Systemic venous congestion o Peripheral edema o Jugular distention o Enlarged liver and spleen o Anorexia and nausea o Dependent edema (legs and sacrum) o Distended abdomen o Swollen hands and fingers o Polyuria at night o Weight gain o Increased blood pressure (from excess volume) or decreased blood pressure (from failure) o Other Info: The heart's pumping action moves "used" blood that returns to the heart through the veins through the right atrium into the right ventricle. The right ventricle then pumps the blood back out of the heart into the lungs to be replenished with oxygen. Right-sided or right ventricular (RV) heart failure usually occurs as a result of left-sided failure. When the left ventricle fails, increased fluid pressure is, in effect, transferred back through the lungs, ultimately damaging the heart's right side. When the right side loses pumping power, blood backs up in the body's veins. This usually causes swelling in the legs and ankles.

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Left-Sided HF (Previously known as CHF, but still widely used) – Associated w/↓ cardiac output and ↑ pulmonary venous pressure.  BNP level. o Impaired tissue perfusion o Pulmonary congestion o Edema o Weakness o Fatigue o Dizziness o Angina o Acute confusion o Restlessness o Palpitations o Pallor o Weak peripheral pulses o Cool extremities o Hacking cough, worse at night o Dyspnea/Breathlessness o Crackles or wheezes in lungs o Frothy, pink-tinged sputum o Oliguria (scant urine output) o Tachypnea o S3/S4 summation gallop o Decreased blood flow to the major body organs can cause dysfunction, especially renal failure. Can occur when the patient is at rest. o The pulse may be tachycardic, or it may alternate in strength (pulsus alternans). o Other Info: The heart's pumping action moves oxygen-rich blood as it travels from the lungs to the left atrium, then on to the left ventricle, which pumps it to the rest of the body. The left ventricle supplies most of the heart's pumping power, so it's larger than the other chambers and essential for normal function. In left-sided or left ventricular (LV) heart failure, the left side of the heart must work harder to pump the same amount of blood. There are two types of left-sided heart failure. Drug treatments are different for the two types.  

Systolic failure: The left ventricle loses its ability to contract normally. The heart can't pump with enough force to push enough blood into circulation. Diastolic failure (also called diastolic dysfunction): The left ventricle loses its ability to relax normally (because the muscle has become stiff). The heart can't properly fill with blood during the resting period between each beat.

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ACE Inhibitors o Ace Inhibitors are also used to treat heart failure (see other notes above).  o Mechanism of Action  Prevent angiotensin I from converting to angiotensin II  Angiotensin II – potent vasoconstrictor; stimulates aldosterone secretion – stimulates Na+ and H2O resorption – increases B/P  ACE inhibitors – prevent Na+ and H2O resorption by inhibiting aldosterone – diuresis-decreases blood volume and blood return to the heart – decreases preload and the workload of the heart. o Medications in this Class  See Above +  trandolapril – Mavik  perindopril – Aceon, Coversyl

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Angiotensin II Receptor Blockers – ARB’s o ARB’s are also used to treat heart failure (see other notes below). o Mechanism of Action  Potent vasodilators  Decrease systemic vascular resistance (afterload)  Angiotensin II receptor blockers help relax your blood vessels, which lowers your blood pressure and makes it easier for your heart to pump blood.  By narrowing blood vessels, can increase your blood pressure and force your heart to work harder. Angiotensin II also starts the release of a hormone that increases the amount of sodium and water in your body, which can lead to increased blood pressure. Angiotensin II can also thicken and stiffen the walls of your blood vessels and heart.  That allows blood vessels to widen (dilate). o Medications in this Class  See Above +  candesartan – Atacand Beta-Blockers o Beta Blockers are also used to treat heart failure (see other notes below). o Also used as antianginal medications. (See other notes below).

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o Mechanism of Action  Reduce sympathetic nervous system stimulation to the heart  Decrease heart rate, delay AV node conductivity, reduce myocardial contractility, and decrease myocardial automaticity.

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Aldosterone Antagonists o Mechanism of Action  Impede aldosterone to prevent retention of sodium and water.  These are potassium-sparing diuretics, which also have additional properties that may help people with severe systolic heart failure live longer. o Medications in this Class  spironolactone – Aldactone  eplerenone - Inspra o Side Effects – N & V, Stomach Cramps, and Diarrhea are the most common. o Contraindications – allergy, pregnancy, lactating women  Also in patients with anuria, acute renal insufficiency, significant impairment of renal excretory function, hyperkalemia, Addison’s disease and with concomitant use of eplerenone.

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Arterial vs Venous Insufficiency

Differentiate the clinical manifestation of arterial versus venous insufficiency. Page 43 of 107


Arterial Insufficiency – Patients w/an acute arterial occlusion describe severe pain below the level of the occlusion that occurs even at rest. The affected extremity is cool or cold, pulseless, and mottled. Small areas on the toes may be blackened or gangrenous. o Patient reports claudication after walking about 1 – 2 blocks o Rest pain usually present o Pain at ulcer site o End of Toes o Between the toes o Deep o Ulcer bed pale, w/even edges o Little granulation tissue o Cool or cold foot o Decreased or absent pulses o Atrophy of skin o Hair loss o Pallor w/elevation o Dependent rubor o When acute, neurologic deficits noted o Often presents with the “six P’s” of ischemia:  Pain  Pallor  Pulselessness  Paresthesia  Paralysis Page 44 of 107


 

Poikilothermy (coolness)

Venous Insufficiency o Chronic nonhealing ulcer o No claudication or rest pain o Moderate ulcer discomfort o Patient reports of ankle or leg swelling o Ulcer bed pink o Brown pigmentation o Ankle area o Usually superficial, w/uneven edges o Granulation tissue present o Ankle discoloration and edema o Full veins when leg slightly dependent o No neurologic deficit o Pulses present o May have scarring from previous ulcers

Malignant Hyperthermia Describe the clinical manifestations associated with Malignant Hyperthermia and give the drug of choice.  

Clinical Manifestations – Tachycardia, Skin mottling, Cyanosis, Myoglobinuria, Rise in end tidal carbon dioxide, Elevated temperature. Drug of Choice – Dantrolene (muscle relaxant). It is given intravenously until a patient has stabilized. Then, the medication typically is continued in pill form for three days.

Anesthesia What is the difference between General and Regional Anesthesia? 

General Anesthesia – A reversible loss of consciousness induced by inhibiting neuronal impulses in several areas of the central nervous system (CNS). The patient is unconscious and unaware, and has loss of muscle tone and reflexes. Agents are administered by inhalation and IV injection. Page 45 of 107


Local or Regional Anesthesia – Disrupts sensory nerve impulse transmission from a specific body area or region. The patient remains conscious and able to follow instructions. o Local – Delivered topically (applied to the skin or mucous membranes of the area to be anesthetized) and by local infiltration. o Regional – Type of local anesthesia that blocks multiple peripheral nerves in a specific body region. It includes field block or nerve block and spinal or epidural routes of delivery.

General and Local Anesthetics 

General Anesthetics o Mechanism of Action – progressive reduction of sensory and motor CNS functions. o Contraindications – drug allergy, pregnancy, narrow-angle glaucoma, and known susceptibility to malignant hyperthermia (increase temp, muscle rigidity, tachycardia) from prior experience w/anesthetics.  Drugs for Moderate Sedation (Conscious Anesthesia) o Mechanism of Action – does not cause complete loss of consciousness and does not normally cause respiratory arrest. Allows the patient to relax and have markedly reduced or no anxiety, yet still maintain his or her own open airway, and respond to verbal commands. o Side Effects – Mild amnesia (which is desired).  Local Anesthetics o Central  Spinal  Intrathecal  Epidural  Peripheral  Infiltration  Nerve Block  Topical o Mechanism of Action – work by rendering a specific portion of the body insensitive to pain by interfering w/nerve transmission.  Neuromuscular Blocking Drugs (can still hear everything, must use pain medicine or anxiety medicine w/these) o Depolarizing  Mechanism of Action – Works similarly to the neurotransmitter acetylcholine (ACh). They bind in place of ACh to cholinergic receptors at the motor endplates of muscle nerves or neuromuscular junctions. Page 46 of 107


o Non-depolarizing  Mechanism of Action – also bind to ACh receptors at the neuromuscular junction, but instead of mimicking ACh, they block its actions. Are competitive antagonists of ACh. o Side Effects – muscle damage, elevated potassium, muscle pain w/depolarizing, hypotension w/non-deploraizing.

Anticoagulants, Fibrinolytics, and Platelet Inhibitors What is the difference between Anticoagulants, Fibrinolytics, and Platelet Inhibitors? 

Anticoagulants – Work by interfering with one or more steps involved in the blood clotting cascade. They prevent new clots from forming and limit or prevent extension of formed clots. They do not break down existing clots. They are thrombin inhibitors, vitamin K antagonists, and indirect factor X inhibitors. Fibrinolytics (also known as thrombolytic drugs or “clot busters”) – Selectively break down fibrin threads present in formed blood clots. The mechanism to start fibrin degradation is activation of the inactive tissue protein plasminogen to its active form, plasmin. Plasmin directly attacks and degrades the fibrin molecule. The use of these results in the best clot breakdown with less disruption of blood clotting.

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Platelet Inhibitors (anti-platelet drugs) – prevent either platelet activation or aggregation (clumping). The most widely used drug for this effect is aspirin, which inhibits the production of substances that activate platelets, such as thromboxane. St. John’s Wort, inhibit platelet activity.

Vitamin B12 Deficiency Anemia What is the recommended diet for the client with B12 deficiency anemia? When anemia is caused by a dietary deficiency, the focus of management is to increase the intake of foods rich in vitamin B12 (animal proteins, eggs, and dairy products).  Extra Information: The Dietary Guidelines for Americans describe a healthy diet as one that: 

Emphasizes a variety of fruits, vegetables, whole grains, and fat-free or low-fat milk and milk products:

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Milk and milk products are good sources of vitamin B12. Many ready-to-eat breakfast cereals are fortified with vitamin B12.    

Includes lean meats, poultry, fish, beans, eggs, and nuts. Fish and red meat are excellent sources of vitamin B12. Poultry and eggs also contain vitamin B12. Is low in saturated fats, Trans fats, cholesterol, salt (sodium), and added sugars. Stays within your daily calorie needs.

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Polycythemia Vera What are the recommended interventions for the client with Polycythemia Vera?            

Drink at least 3 liters of liquids each day. Avoid tight or constrictive clothing, especially garters and girdles. Wear gloves when outdoors in temperatures lower than 50 F. Keep all health care-related appointments. Contact your physician at the first sign of infection. Take anticoagulants as prescribed. Wear support hose or stockings while you are awake and up. Elevate your feet whenever you are seated. Exercise slowly and only on the advice of your physician. Stop activity at the first sign of chest pain. Use an electric shaver. Use a soft-bristled toothbrush to brush your teeth. Page 52 of 107




Do not floss between your teeth.

Hemophilia Which blood product is the standard for care of the client with Hemophilia? Why? The bleeding problems of Hemophilia A are managed by either regularly scheduled infusions of synthetic factor VIII or factor VIII cryoprecipitate (highly concentrated blood product, replaces fibrinogen) or intermittent infusions as needed. Hemophilia is actually two different hereditary bleeding disorders resulting from clotting factor deficiencies. Hemophiliacs form platelet plugs at the bleeding site, but the clotting factor deficiency impairs the formation of stable fibrin clots. 

Hemophilia A (Classic Hemophilia) is a deficiency of factor VIII and accounts for 80% of cases of hemophilia. Page 53 of 107




Hemophilia B (Christmas disease) is a deficiency of factor IX and accounts for 20% of cases.

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Hypertension



Give Tylenol for pain

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Ace (Angiotensin-Converting Enzyme) Inhibitors o Mechanism of Action  Inhibit angiotensin converting enzyme. This results in decreased B/P. B/P is reduced by decreasing systemic vascular resistance (SVR).  Aids in heart failure patients due to prevention of sodium and water resorption. This leads to decreased preload and the work required by the heart. o Medications in this Class  benazepril-Lotensin  captopril-Capoten  enalapril-Vasotec  fosinopril-Monopril  lisinopril-Prinivil, Zestril  quinapril-Accupril  Ramipril-Altace o Side Effects - Dry cough, rhinorrhea, and allergic-like symptoms are the most common side effects.  Increased blood-potassium level (hyperkalemia), Fatigue, Dizziness, Headaches, Rapid heartbeat, Fainting, in rare cases — but more commonly in blacks and in smokers — ACE inhibitors can cause some areas of your tissues to swell (angioedema). If it occurs in the throat, that swelling can be life-threatening. o Contraindications - drug allergy, high potassium level, lactating women, children, and patients with unilateral renal stenosis  Nonsteroidal anti-inflammatory drugs (NSAIDs), such as ibuprofen (Advil, Motrin IB, others) and naproxen (Aleve) decrease the effectiveness of ACE inhibitors. Angiotensin II Receptor Blockers – ARB’s o Mechanism of Action  Help relax your blood vessels (dilate), which lowers your blood pressure and makes it easier for your heart to pump blood. o Medications in this Class  losartan-Cozaar  irbesartan-Avapro  olmesartan-Benicar  telmisartan-Micardis  valsartan-Diovan o Side Effects – Headache, Dizziness, Lightheadedness, Nasal congestion, Back and leg pain, Diarrhea o Contraindications – pregnancy, allergy, lactating women Vasodilators o Mechanism of Action  Open (dilate) blood vessels. They work directly on the muscles in the walls of your arteries, preventing the muscles from tightening and the walls from narrowing. As a result, blood flows more easily through your

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arteries, your heart doesn't have to pump as hard and your blood pressure is reduced. o Medications in this Class  minoxidil-Loniten  hydralazine-Apresoline  diazoxide-Hyperstat  nitroprusside-Nitropress o Side Effects - Chest pain, rapid heartbeat (tachycardia), heart palpitations, fluid retention (edema), nausea, vomiting, dizziness, flushing, headache, nasal congestion, excessive hair growth, contraindications, routes of administration. Some can increase your risk of developing lupus (connective tissue disease). o Contraindications - drug allergy, hypotension, cerebral edema, head injury, acute MI, coronary artery disease, may be contraindicated in cases of heart failure that is secondary to diastolic dysfunction. Beta-Blockers (also known as beta-adrenergic blocking agents) o Mechanism of Action  Reduce your blood pressure.  Block the effects of the hormone epinephrine, also known as adrenaline.  When taking these, the heart beats more slowly and with less force, thereby reducing blood pressure.  Also help blood vessels open up to improve blood flow. o Medications in this Class  carvedilol – Coreg  metoprolol – Lopressor, Toprol XL  atenolol - Tenormin o Side Effects – Fatigue, Cold hands, Headache, Upset stomach, Constipation, Diarrhea, Dizziness are the most common. Others include Dyspnea, Loss of Libido, Insomnia, and Depression. o Contraindications – systolic heart failure, serious conduction disturbances, DM, peripheral vascular disease.  Generally aren't used in people with asthma because of concerns that the medication may trigger severe asthma attacks. In people who have diabetes, beta blockers may block signs of low blood sugar, such as rapid heartbeat. It's important to monitor your blood sugar on a regular basis.  Beta blockers can also affect your cholesterol and triglyceride levels, causing a slight increase in triglycerides and a modest decrease in highdensity lipoprotein, the "good" cholesterol. These changes often are temporary. You shouldn't abruptly stop taking a beta blocker because doing so could increase your risk of a heart attack or other heart problems. Calcium Channel Blockers (also called calcium antagonists) o Some calcium channel blockers are available in short-acting and long-acting forms. Short-acting medications work quickly, but their effects last only a few hours. Long-acting medications are slowly released to provide a longer lasting effect. o Mechanism of Action Page 57 of 107


  

Prevent calcium from entering cells of the heart and blood vessel walls, resulting in lower blood pressure. Relax and widen blood vessels by affecting the muscle cells in the arterial walls. Some calcium channel blockers have the added benefit of slowing your heart rate, which can further reduce blood pressure, relieve chest pain (angina) and control an irregular heartbeat.

o Medications in this Class  diltiazem – Cardizem  amlodipine - Norvasc o Side Effects – Constipation, Headache, Rapid heartbeat (tachycardia), Dizziness, Rash, Fatigue, Flushing, Nausea, Swelling in the feet and lower legs o Contraindications –  Calcium channel blockers interact with grapefruit products.  Can reduce your ability to eliminate calcium channel blockers from your body, allowing the medication to build up in your body. This buildup could cause serious side effects.

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Diuretic Drugs

Helps to rid your body of salt (sodium) and water. They work by making your kidneys put more sodium into your urine. The sodium, in turn, takes water with it from your blood. That decreases the amount of fluid flowing through your blood vessels, which reduces pressure on the walls of your arteries. ANTI-DIURETIC – Vasopressin: Causes H2O Retention o Overall Side Effects Include:  Low sodium in your blood (hyponatremia)  Dizziness  Headaches  Increased thirst  Muscle cramps  Increased blood sugar  Increased cholesterol  Rash  Joint disorders (gout)  Impotence  Menstrual irregularities  Breast enlargement in men (gynecomastia)

Carbonic Anhydrase Inhibitors o Mechanism of Action Page 60 of 107


inhibit the activity of the enzyme, carbonic anhydrase, which is found in the kidneys, eyes, and other parts of the body o Medications in this Class  acetazolamide – Diamox  methazolamide - Neptazane o Side Effects - acidosis, hypokalemia, drowsiness, anorexia, paresthesia, hematuria, urticaria, photosensitivity, and melena o Contraindications - hyponatremia, hypokalemia, severe renal or hepatic dysfunction, adrenal gland insufficiency, cirrhosis o Routes of Administration – P.O. Loop Diuretics o Mechanism of Action  blocks chloride and sodium reabsorption  manage the edema associated with heart failure and hepatic or renal disease, control hypertension, and increase renal excretion of calcium o Medications in this Class  bumetanide – Bumex  furosemide – Lasix  torsemide - Demedex o Side Effects - hypokalemia, hyperglycemia, neutropenia, aplastic anemia o Contraindications - hepatic coma, severe electrolyte loss Osmotic Diuretics o Mechanism of Action  increases osmotic pressure in the glomerular filtrate, which in turn, pulls fluid into the renal tubules from the surrounding tissue o Medications in this Class  mannitol - Osmitrol o Side Effects - convulsions, thrombophlebitis, pulmonary congestion o Contraindications - severe renal disease, pulmonary edema, intracranial bleeding

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Potassium-Sparing Diuretics (also known as aldosterone-inhibiting diuretics) o Mechanism of Action  Block the resorption of sodium and water that is induced by aldosterone secretion.  interfere with sodium-potassium exchange o Medications in this Class  amiloride – Midamor  spironolactone – Aldactone  triamterene - Dyrenium o Side Effects - urinary frequency, dizziness, headache, cramps, nausea, weakness and hyperkalemia o Contraindications - hyperkalemia, severe renal and hepatic failure, anuria o Routes of Administration – P.O. Thiazide and Thiazide-Like Diuretics o Mechanism of Action  inhibits the reabsorption of sodium, potassium, and chloride, which results in osmotic water loss o Medications in this Class  Thiazide Diuretics include: Page 62 of 107


 hydrochlorothiazide – Esidrix, HydroDIURIL  chlorthiazide – Diuril  trichlormethiazide – Metahydrin  Thiazide – Like Diuretics include:  metolazone – Mykorx, Zaroxolyn o Side Effects - electrolyte imbalances, metabolic imbalances o Contraindications - hepatic coma, renal failure, anuria

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UTI

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Blood Transfusion

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Chronic Renal Failure

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Left and Right CVA

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Anaphylaxis

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Pnuemonia

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Emphysema

Bronchitis

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PE – Pulmonary Embolus

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Pneumothorax

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Hypoxia 

African American Cyanosis – check oral mucosa

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AD PIE - the nursing process

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Fractures

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Hypernatremia and Hyponatremia

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Lab Values What are the normal lab values for the following:      

Sodium – 136 - 145 milliEquivalents/liter (mEq/L). Potassium – 3.5 - 5.0 milliEquivalents/liter (mEq/L). Calcium – 9 – 10.5 mg/dL Chloride – 98 – 106 mEq/L Magnesium – 1.3 – 2.1 mEq/L Phosphorus – 3 – 4.5 mg/dL

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Electrolytes

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Diseases Chart

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Acidosis vs Alkalosis

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Cranial Nerves

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Hypocalcemia and Hypercalcemia

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Hypomagnesemia and Hypermagnesemia

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Endocrine Disorders (Hypo and Hyperthyroidism, Cushing’s, etc.)

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Shock

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Calcium Phosphorus Relationship

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Bowel Obstruction

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Hip Fractures

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