NUR 2349: Professional Nursing I Exam 3 Study Guide, Exams of Health sciences

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Exam 3 Study Guide

NUR 2349: Professional Nursing I

MODULE 6: IMMUNITY

Chapter 17: Inflammation and Immunity  Allergies  True allergic reaction vs. side effects:  A true allergic reaction occurs when your body sees something as harmful and rejects it.  You can have pruritis, urticaria, redness, rhinorrhea, sneezing, itchy and watery eyes, crackles, wheezes, hoarseness, stridor, blood vessel dilation, decreased cardiac output, bronchoconstriction, and anaphylaxis.  Adverse reaction.  A side effect is a sensitivity and is not life-threating.  It can include nausea, decreased energy, muscle aches, coughing, constipation, diarrhea, easy bruising, ringing in the ears, or stuffy nose.  Angioedema may occur which is edema in lips, face, tongue, larynx, neck. Generally caused by ACE inhibitors or NSAIDs.  Something that isn’t detrimental.  Anaphylactic shock (definition, care, etc.):  Anaphylaxis is life-threatening reaction to a Type 1 hypersensitivity reaction which occurs rapidly and systemically.  Common causes are drugs, dyes, food, and insects.  Nursing interventions include maintaining the airway, administering epinephrine, and education on avoiding of allergen exposure and use of epinephrine.  The patient may need more than one shot of epinephrine.  Remove and prevent allergen exposure if possible.  Pharmacologic:  Diphenhydramine/Benadryl  Corticosteroids  Epinephrine  Antihistamines  Leukotriene inhibitors  Mast cell stabilizers  Decongestants  Allergy Shots  Inflammation  Pathophysiological process: (Cause of tissue damage.)

 Stage 1: Vascular response with blood vessel changes. Constriction of small veins and dilation of arterioles. Redness and warmth. Increased blood flow to the affected area which leads to edema and capillary leak. Macrophage is the major cell type involved and releases cytokines that stimulate more WBC production.  Stage 2: Cellular exudate. Exudate (pus) forms which contains dead WBCs, necrotic tissue, and fluids. Neutrophils secondary to cytokines from macrophages. Basophils and mast cells sustain and continue initial responses. This stage may occur for several days.  Stage 3: Tissue repair and replacement. WBCs induce the remaining healthy cells to divide. Scar tissue is formed. Blood vessels grow.  Signs and Symptoms (localized and systemic):  Localized inflammation symptoms are pain, redness, warmth, decreased function, and welling.  System symptoms are fever, increased WBC count (normal WBC values are 4,500-10,000).  Nursing care:  When wrapping the affected extremity, start distal and work proximal to promote return towards the heart. Never wrap down because it will inhibit venous return.  Medical treatment (medications, procedures, etc.):  RICE – Rest, Ice, Compression, Elevated.  Treatment includes resting the affected extremity.  Applying cold/ice for 15-20 minutes every 2-3 hours.  Utilizing compression devices to limit harmful swelling and promote blood return to the heart.  Elevating the affected extremity to promote blood and fluid return to the heart.  Immunity  Types of immunity (acquired, innate, passive, etc.):  Active immunity occurs when antigens enter a human and he/she responds by making antibodies.  Natural – Antibody formation without human assistance. o Example would be contracting a disease.  Artificial – Antibody formation with vaccination or immunization. o Example would be receiving a vaccination.  Passive immunity is the transfer of antibodies to another human from human or an animal.  Natural – Passage from mother to fetus/infant via the placenta or breast milk. o Example would be breast milk.  Artificial – Used for exposure to rabies, tetanus, or poisonous snake bites to prevent disease or death. o Example would be rabies.

 Acquired immunity is an adaptive protection that results in long- term resistance to the effects of invading microorganisms. The responses are not automatic. The body has to learn to generate specific immune responses when it is infected or exposed to specific organisms. o Example would be  Innate immunity is something already in the body. o Example would be WBC fighting bacteria.  Adaptive immunity is created in response to exposure to a foreign substance. o Example would be the Varicella vaccination to prevent chickenpox. The adaptive immunity system has remembered the foreign body.  Persons at risk for compromised immunity:  Patients with an autoimmune disease, cancer patients, renal patients, HIV/AIDs patients, infants, geriatric patients, long-term steroid use, disease, injury, surgery, and immunosuppressants.  Age-related changes in immunity:  Changes in normal flora.  Lower WBC count.  Altered nutritional intake and absorption.  Decreased infection response (less fever).  Lower T-cell and B-cell function.  Need for repeat vaccinations.  Increased risk for autoimmune disease (decreased self vs. non-self- recognition).  Immunoglobulins (what do they do? Etc.):  All antibodies are immunoglobulins (gamma globulins).  Globular proteins that provide immunity.  IgA – Responsible for preventing infection in the respiratory and GI tract.  IgD – Present in low blood concentrations in conjunction with IgM.  IgE – Associated with hypersensitivity and allergic reactions.  IgG – May be related to Guillain-Barre. 75% of circulating antibodies which activate complete pathways and provide. Crohn’s patients have infusions of IgG.  IgM – 10-15% of circulating antibodies. 1 st^ antibody formation by newly sensitized B-lymphocytes.  Vaccinations (purpose, recommendations, etc.):  Provide artificial active immunity.  Require “boosting” for long-term effects. Chapter 20: Care of Patients with Hypersensitivity and Autoimmunity  Nursing care for autoimmune disorders and reduced immune function:

 Autoimmune disorders have no cure.  Infection prevention.  Pharmacological.  Selective Immunosuppressive therapy.  Antiproliferative drugs.  Calcineurin inhibitors.  Disease modifying antirheumatic drugs (DMARDs).  General immunosuppressive therapy.  Corticosteroids.  Cytotoxic drug.  Transplants  Stages of rejection:  Hyperacute:  Begins immediately after the transplant secondary to antigen-antibody complexes in the blood vessels of the transplanted organ.  Usually recognized within minutes and the organ is removed.  Most commonly seen in kidney transplants.  Becoming less common because of better HLA (receptors/fingerprints of cell matching).  Acute: o Occurs within 1 week to 3 months after the transplant secondary to antibody mediated vasculitis within the organ or cytotoxic T-cells and NK cells cause lysis of the organ through inflammation. o May be diagnosed via impaired organ function or biopsy. o Can be managed with drugs and limit organ damage.  Chronic: o Rejection secondary to chronic inflammation and scarring o Occurs to some degree in all transplant patients, but it is delayed by good control of immune function. o Retransplantation indicated when organ no longer functions secondary to fibrosis.  Immunosuppressant therapy:  Rescue Therapy  Use of monoclonal and polyclonal antibodies to treat acute rejection episodes.  Education  Drugs must be taken for life.  Doses should not be missed.  Learn the signs and symptoms of an infection.  Increased risk of cancer and infection.  Antiproliferative Agents  Azathioprine/Imuran

 Calcineurin Inhibitors  Cyclosporine/Sandimmune  Tacrolimus/Prograf  Corticosteroids.  Prednisone  Prednisolone Chapter 25: Care of Patients with Skin Problems  Wound assessment  Stages of pressure ulcers:  Stage 1 – Intact skin with non-blanchable redness.  Stage 2 – Partial thickness skin loss (epidermis/dermis)  Stage 3 – Full thickness skin loss. Subcutaneous damage or necrosis.  Stage 4 – Full thickness skin loss with exposed muscle, tendon, or bone.  Unstageable – Full thickness with skin loss, slough, or eschar (obscure true depth of the wound).  Braden Scale:  Score of 15-16 = mild risk of pressure ulcer.  Score of 12-14 = moderate risk of pressure ulcer.  Score of <11 = severe risk for pressure ulcer.  Evaluates: Sensory perception, Moisture, Activity, Mobility, Nutrition, Friction and Sheer.  Wound care & prevention  Cleaning wounds:  Daily inspections.  Avoid dryness and excess moisture.  Clean and dry skin (soap & water or wound cleaner) after incontinence episodes.  Use barrier creams if Stage II or higher.  Wet-to-Dry saline-moistened gauze – Necrotic debris is mechanically removed.  Continuous wet gauze – Continuous bathing of wound with a wetting agent to remove exudate and eschar.  Topical enzyme preparation – Enzyme helps to breakdown eschar to rid necrotic tissue.  Moisture-retentive dressing – Autolysis of wound (slow process, as it is the patient’s own healing process).

MODULE 7: INFECTION

Chapter 23: Care of Patients with Infection

 Types of infection (bacterial, viral, fungal, protozoal/parasite) o Common causes of each o Common diseases produced  Disease transmission o Principles of disease transmission (Mode of transmission, reservoir, susceptible host, portal of entry, portal of exit, etc.):  There are 3 factors of disease transmission: Reservoir, Susceptible Host, Mode of Transmission.  You need to have a portal of entry to become the host.  Reservoir – Animate (people, animals, insects) or Inanimate (soil, water, devices, objects)  Susceptible Host – Influenced by age, immunological status, EtOH and substance abuse, number of sexual partners, toxin exposure, nutritional deficiencies, disease process (chronic or acute), surgeries or trauma (breaks in skin), and medications.  Modes of Transmission – Respiratory tract (droplet or airborne illness), GI tract (foodborne illness), GU tract (indwelling catheter, urinary retention), Breaks in skin (surgery or injury), Bloodstream (CVCs, insects, UTI). o Tuberculosis care and transmission precautions:  Diagnosed by chest x-ray and blood test.  Multiple drug treatments – Isoniazid, Rifampin, Ethambutol, Pyrazinamide  Airborne Precautions – Negative pressure isolation room, N- respirators or powered air-purifying respirator masks at all times. o Transmission precautions (standard vs. droplet vs. contact vs. airborne):  Standard Precautions  All body secretions, excretions, and mucous membranes are potentially infections (NOT perspiration).  Involves the use of PPE: Gloves, Isolation Gown, Face Protection.  No more latex in USA/Canada.  Banana, kiwi, avocado allergies are associated with latex allergies.  Airborne Precautions  Negative pressure isolation room, N-95 mask or powered air- purifying respirator mask.  TB, measles (Rubeola), chickenpox (Varicella).  Droplet Precautions  Used for known or suspected infection with disease spread by droplets.  Influenza, mumps, pertussis, meningitis.  Wear mask when in contact with patient.  Must stay 6 feet away if not masked.  Contact Precautions  Used for patients known or suspected to have infections transmitted by direct or indirect contact.  Multi-Drug Resistant Organisms (MRDOs)

o Methicillin-resistant Staphylococcus aureus (MRSA) o Vancomycin-resistant Staphylococcus aureus (VRSA) o Vancomycin-intermediate Staphylococcus aureus (VISA) o Vancomycin-resistant Enterococcus (VRE) o Carbapenem-resistant Enterobacteriaceae (CRE) o Clostridium difficile (C-diff) o Lice o Scabies o RSV  PPE donning and removal:  ON o Perform hand hygiene. o Don gown. o Don face mask. o Don face mask. o Don hair cover. o Don show cover. o Don gloves.  OFF o Remove gloves. o Remove gown and roll up. o Remove goggles. o Remove mask. o Remove hair covering. o Remove shoe covering. o Perform hand hygiene. o Stages of disease (incubation, prodromal, illness, decline, convalescence):  Incubation  Invasion – Appearance of symptoms - Contagious  Prodromal  1 st^ appearance of mild symptoms  Illness  Appearance of characteristic symptoms  Decline  # of pathogens decreases due to immune response  Convalescence  Tissue repair and return to health  Pathogen exposure to health care workers (what should the nurse do if exposed to a bloodborne or other pathogen?): o Immediately wash exposed area with water. o Report exposure to appropriate personnel. o Contact employee health and seek medical attention. o Complete an incident report or injury report.

o Attend counseling.  Principles of clean vs. sterile technique: o Clean:  Ensures reduction in level of disease-causing organisms.  Does NOT kill spores. o Sterilization:  Destroys all living organisms and bacterial spores.  Sterile technique required for many surgeries and procedures.  1-inch border around and 1 foot away.  Close door and limit traffic.  Open sterile field away from you.  Front of body is the only sterile if wearing a gown.  Never turn your back.

MODULE 8: FLUID, ELECTROLYTE, AND ACID-BASE BALANCE

Chapter 11: Assessment and Care of Patients with Fluid and Electrolyte Imbalance  Interstitial vs. extracellular vs. intracellular fluid: o Interstitial  Third Space.  Part of the Extracellular Compartment.  Blood, Lymph, Bone, Connective Tissue, Cerebrospinal Fluid, Synovial Fluid, Peritoneal Fluid, Pleural Fluid. o Extracellular  Fluid outside the cells.  1/3 of the total body water. o Intracellular  Fluid inside the cells.  Hypovolemia & Hypervolemia: o Primary problem:  Hypovolemia: Circulating blood volume is decreased and leads to reduced perfusion.  Hypervolemia: Fluid Overload. o Common causes/Etiology  Hypovolemia: Dehydration.  Hypervolemia: Heart failure, Cirrhosis, Kidney Failure, Nephrotic Syndrome, Premenstrual Edema, Pregnancy. o Signs and Symptoms  Hypovolemia: Elevated HGB and HCT (secondary to fluid loss). Osmolarity. BG. Protein. BUN. Electrolyte Levels. Tachycardia, Hypotension, Faintness, Blacking Out, Decreased Urine Output, Confusion, Tachypnea

 Hypervolemia: Edema, Cramping, Headache, hypertension, shortness of breath, tachycardia or bradycardia. o Nursing care and medical treatment  Hypovolemia: Replace fluids (PO or IV), blood products, crystalloids, colloids. Strict I & O’s. Improve Blood Pressure (Last Resort Vasopressors: Norepinephrine, Epinephrine, Vasopressin, Dopamine, Phenylephrine, and Dobutamine. Oxygen.  Hypervolemia: Monitor Weight, I & O’s, Fluid Restrictions, Decreased Sodium. o Complications  Hypovolemia: Hypovolemic Shock.  Hypervolemia: Pericarditis, Heart Failure, Delayed Wound Healing, Tissue Breakdown, Decreased Bowel Function.  Electrolyte imbalances (K+, Mg++, Ca++, Na+) o Normal range:  Potassium: 3.5 – 5.5 Book (3.5 – 5.0)  Magnesium: 1.5 – 2.5 Book (1.8 – 2.6)  Calcium: 8.5 – 10.9 Book (9.0 - 10.5)  Sodium: 135 – 145 Book (136 - 145) o Primary body system involved with imbalance:  Potassium:  Magnesium:  Calcium:  Sodium: o Common causes/Etiology:  Potassium:  Hypo: o Inappropriate or excessive use of diuretics, digitalis- like drugs, or corticosteroids. o Increased secretion of aldosterone. o Cushing’s Syndrome. o Diarrhea. o Vomiting. o Wound drainage (especially GI). o Prolonged nasogastric suction. o Heat-induced excess diaphoresis. o Kidney disease impairing reabsorption of K+. o NPO.  Hyper: o Increased ingestion of salt substitutes, potassium chloride, or IV infusion containing K+. o Transfusion of whole or packed cells. o Adrenal insufficiency. o Kidney failure. o Potassium-sparing diuretics.

o Angiotensin-converting enzyme inhibitors (ACEIs).  Magnesium:  Hypo: o Alcohol Use. o Burns. o Crohn’s Disease. o Celiac Disease. o Chronic Diarrhea. o Polyuria. o Hypercalcemia. o Hyperaldosteronism. o Malabsorption Syndrome. o Malnutrition. o Diaphoresis.  Hyper: o Kidney Failure. o Use of PPIs. o Malnourishment. o Alcoholism. o Lithium Therapy. o Hypothyroidism. o Addison’s Disease o Drugs containing Magnesium: Laxatives and Antacids.  Calcium:  Hypo: o Renal Failure. o Hyperphosphatemia. o Hypoalbuminemia. o Vitamin D Deficiency. o Magnesium Deficiency. o Pancreatitis. o Hypoparathyroidism.  Hyper: o Overactive Parathyroid Gland. o Cancer. o Heredity. o Immobility. o Severe Dehydration. o Medications: Lithium. o Supplements: Calcium with D.  Sodium:  Hypo: o Excessive Diaphoresis. o Diuretics. o Wound drainage (especially GI). o Decreased secretion of aldosterone. o Hyperlipidemia.

o Kidney disease. o NPO. o Low-Salt Diet. o Cerebral Wasting Syndrome.  Hyper: o Hyperaldosteronism. o Kidney Failure. o Corticosteroids. o Cushing’s Syndrome. o Excessive Oral Sodium Ingestion. o Excessive Administration of IV containing sodium. o Signs and Symptoms:  Potassium:  Hypo: o Weakness. o Fatigue. o Muscle Cramps. o Constipation. o Arrythmias.  Hyper: o Muscle Fatigue. o Weakness. o Paralysis. o Arrythmias. o Nausea.  Magnesium:  Hypo: o Abnormal Eye Movement (Nystagmus) o Convulsions. o Fatigue. o Muscle Spasms and Cramps. o Muscle Weakness. o Numbness.  Hyper: o Nausea. o Vomiting. o Neurological Impairments. o Hypotension. o Flushing. o Headache.  Calcium:  Hypo: o Numbness in extremities and digits. o Muscle cramps. o Seizures. o Facial twitching. o Muscle weakness.

o Lightheadedness. o Bradycardia. o Anxiety. o Depression. o Hallucinations.  Hyper: o Excessive Thirst. o Frequent Urination. o Nausea. o Vomiting. o Constipation. o Confusion. o Lethargy. o Palpitations. o Cardiac Arrythmias. o Depression.  Sodium:  Hypo: o Nausea and Vomiting. o Headache. o Confusion. o Loss of Energy/Fatigue. o Restlessness. o Muscle weakness and cramping. o Seizures. o Coma.  Hyper: o Hypertension. o Resistant Hypertension. o Hypokalemia. o Weakness. o Cardiac Arrhythmias. o Muscle Cramping. o Excessive Thirst. o Nursing care and medical treatment:  Potassium:  Avoid high K+ foods (organ meat, dried fruit, bananas, cantaloupe, kiwi, avocadoes broccoli, beans, potatoes).  Drug therapy.  Magnesium:  IV Fluids.  Magnesium PO or IV.  Medications.  Dialysis.  Calcium:  Monitoring.  Surgery of Parathyroid Gland.

 Medications: o Calcitonin. o Calcimimetics. o Bisphosphonates. o Denosumab. o Prednisone. o IV Fluids with Diuretics.  Sodium:  Treat associated conditions.  Take precautions during high-intensity exercise programs.  Assess I & O’s.  IV Fluids.  Medications. o Complications:  Potassium:  Elevated – Hyperkalemia, Dehydration, Kidney Disease, Acidosis, Adrenal Insufficiency, Crush Injuries.  Low – Hypokalemia, Fluid Overload, Diuretic Therapy, Insulin Administration, Hyperaldosteronism.  Magnesium:  Elevated – Hypermagnesemia, Kidney Disease, Hypothyroidism, Adrenal Insufficiency.  Low – Hypomagnesemia, Malnutrition, Alcoholism, Ketoacidosis, Ventricular Arrythmia, Coronary Vasospasm, Death.  Calcium:  Elevated – Hypercalcemia, Hyperthyroidism, Hyperparathyroidism. Osteoporosis. Kidney Stones. Kidney Failure. Abnormal Hearth Rhythm.  Low – Hypocalcemia, Vitamin D Deficiency, Hypothyroidism, Hypoparathyroidism, Kidney Disease, Excessive Intake of Phosphorus-Containing Foods and Drinks.  Sodium:  Elevated – Hypernatremia, Dehydration, Kidney Disease, Hypercortisolism, CVA, MI, Death, HF.  Low – Hyponatremia, Fluid Overload, Liver Disease, Adrenal Insufficiency. Chapter 12: Care of Patients with Problems of Acid-Base Imbalance  How does the buffer system work (HCO3 and CO2): o Solution in the body that aims to bring fluid as close as possible to normal pH of (7.35 – 7.45). o Critical to maintaining pH at normal levels. o Binds to acidic fluid. o Releases H- ions if basic fluid. o Primary Buffers are:  Bicarbonate – HCO3 (Base)

 Carbonic Acid – H2CO3 (Acid) o What body systems are involved?  Respiratory.  Metabolic (Kidney).  Arterial blood gas interpretation o Normal values:  pH: 7.35 - 7.  Acidosis: < 7.  Alkalosis: > 7.  CO2: 35 – 45 mm Hg  Acidosis: > 45  Alkalosis: < 35  HCO3: 21 – 28 mEq/L  Acidosis: >  Alkalosis: <  PaO2: 80 – 100 mm Hg  Hypoxia: < 80 o What does compensation look like in an ABG (fully compensated vs. partially compensated vs. uncompensated)?  Uncompensated:  pH out of range and either CO2 or HCO3 will be out of range and one normal which indicates not attempt to compensate.  Partially:  pH, CO2, HCO3 all out of range which indicates an attempt to compensate.  Fully:  pH 7.35-7.45 (normal) / CO2 & HCO3 out of range. o Acid-base imbalances (Metabolic/Respiratory Acidosis/Alkalosis): o Metabolic Acidosis:  Compensation: CO2 decreases to lower pH.  Overproduction of hydrogen ions secondary to breakdown of fatty acids.  Caused by diabetic ketoacidosis, lactic acidosis (shock/hypoxia), excessive acid intake of alcohol or aspirin. starvation, severe diarrhea, renal tubule acidosis, renal failure, GI fistulas, shock  Manifestations: Headache, Hypotension, Hyperkalemia, Muscle Twitching, Flushed Skin, Nausea, Diarrhea, Vomiting, Changes in LOC, Kussmaul Respirations (compensatory hyperventilation).  Caused by diabetic ketoacidosis, severe diarrhea, renal failure, shock.  Care: Correct underlying cause. Bicarbonate administration. Fluid Replacement (PO or IV). Correct DKA, Lactic Acidosis, or Determined Cause. o Metabolic Alkalosis:  Compensation: CO2 increases to raise pH.

 Caused from severe vomiting, excessive NG suctioning, diuretic therapy, hypokalemia, excess licorice intake, excessive NaHCO use, excessive mineral corticoids.  Manifestations: Increased heart rate, dysrhythmias secondary to hypokalemia, hypotension, hypoventilation, dizziness, irritability, nervousness, tetany, seizures, paresthesia in fingers and toes, tremors, confusion. o Respiratory Acidosis:  Compensation: HCO3 increases to raise the pH.  Caused by impaired respiratory function leading to retention of CO2.  Respiratory Depression, Opiates, Head Trauma, Inadequate Chest Expansion, Flail Chest, COPD, Obesity, Airway Obstruction, Asthma, Pulmonary Edema, Sedative or barbiturate overdose, chest wall abnormalities, pneumonia, atelectasis, respiratory muscle weakness, hypoventilation.  Manifestations:  Hypoventilation turns to hypoxia.  Respiratory rate increases and becomes shallow. Attempt to blow off CO2. Decreased BP with vasodilation. Dyspnea, Headache, Hyperkalemia, Dysrhythmias, Drowsiness, Dizziness, Muscle Weakness, Hyperreflexia.  Causes decreased respiratory stimuli (anesthesia, drug overdose), COPD, Pneumonia, Atelectasis.  Care: Correct Underlying Cause. Bicarbonate Administration. Improve Ventilation and Oxygenation. Bronchodilators. Oxygen Therapy. Encourage Coughing and Deep Breathing. Elevated Head of Bed. o Respiratory Alkalosis:  Compensation: HCO3 decreases to lower the pH.  Alkalosis caused by excessive loss of CO2 through hyperventilation.  Caused by hyperventilation from hypoxia, fear, fever, pain, exercise, anxiety, pulmonary embolus, mechanical overventilation, septicemia, brain injury, encephalitis, salicylate poisoning.  Manifestations: Increased heart rate, dyspnea, chest tightness, dizziness, anxiety, tetany, panic, seizures.  Care: Reverse the cause. Prevention of further hydrogen loss. Electrolyte replacement. Administer IVF. Antiemetics. Fall Prevention.