med surge test 3 pp

ELEMENTS OF HISTORY

Past medical history Family history Genetic history Current medications Allergies to medications or other substances Lifestyle behaviors Occupation Social environment

Interventions

Patient safety Fall precautions Fluid replacement Oral fluids Drug therapy IV fluids Andidiarrheal Antimicrobial Antiemetic Antipyretics

RISK FACTORS

People from all age, socioeconomic, and racial/ethic groups can potentially have impaired immune systems - some however are at greater risk than others. Suppressed immune response- drugs Age Very young Elderly Non-immunized state Susceptible to a number of infections- diseases Rubella, measles, mumps, tetanus, hepatitis, diphtheria, etc Environmental factors Poor nutrition, exposure to pollutants, heavy metals, and other stressors Unsafe sanitary conditions, contaminations, poor hand hygiene Chronic illnesses Primary immunodeficiency conditions directly impair immune system (HIV) Diabetes, COPD, malnutrition, cancer

Introduction to Acid-Base Chemistry

Acids - release hydrogen ions when dissolved in water Bases - bind with hydrogen ions in solutions Buffers - critical in maintaining normal body fluid pH Body fluid chemistry: Bicarbonate ions (HCO3) Relationship between CO2 and hydrogen ions Calculation of free hydrogen ion level

Clinical Significance: Osmosis & Filtration

Act together at capillary membrane to maintain normal ECF and ICF volumes Thirst mechanism is example of how osmosis helps maintain homeostasis Feeling of thirst caused by activation of brain cells responding to changes in ECG osmolarity

TRANSMISSION-BASED PRECAUTIONS Airbornexl airxl

Airborne Precautions Pathogen is spread via air currents Transmission via ventilation systems, shaking sheets, sweeping Precautions include Same as those for contact, with addition of special room, special mask, and mask for patient when transported book *When to Use:* Use airborne precautions to control the spread of infections that are trans- mitted person-to-person on air currents.These include tuberculosis, varicella (chickenpox), SARS, and rubeola (measles). Pathogens spread by this method are very small and can be easily transmitted through ventilating systems as well as by any activities that stir the air, such as fanning sheets, shaking out towels, or sweeping the floor. *Patient Placement and Transport * ■ Place the patient in an airborne infection isolation room (AIIR)—one with negative pres- sure that discharges and exchanges the air outside or through a high-efficiency particulate air (HEPA) filtration system. Monitor air pressure daily (usually this is via an electronic device with an alarm). ■ If such a room is not available, transfer the patient to a facility where one is available. ■ Keep the room door closed when not required for entry and exit.To maintain the nega- tive pressure and contain the airborne organisms. ■ In the event of an outbreak involving large numbers of patients who require airborne pre- cautions, consult with infection preventionists for patient placement. ■ Limit transport of the patient outside the room to medically necessary purposes. If trans- port is necessary, cover any infectious skin lesions and have the patient wear a mask.The transporter is not required to mask if the patient is wearing a mask and infectious skin lesions are covered. Notify the receiving department.The receiving department can then take airborne precautions. ■ Ambulatory care: Triage and identify patients with suspected airborne precautions upon entry to the agency. Place the patient in an AIIR as soon as possible. If one is not available, place a mask on the patient and place him in an exam room. Do not reuse the room for at least an hour after the patient leaves it. *Personal Protective Equipment * ppexl ■ Keep airborne isolation supplies just outside the patient's room on a cart. ■ Don a mask on entering the room. Wear a special, fit-tested, approved mask (e.g., N95 respirator) if the patient is suspected of having pulmonary tuberculosis or smallpox. ■ Remove your respirator/mask outside the room after closing the door. If the respirator is not disposable, clean and store according to the manufacturer's instructions. ■ When using a respirator mask, check the seal. Hold your hands over the respirator and exhale. If you feel air around your nose, adjust the nosepiece; if you feel air at the edges, adjust the straps. ■ When the patient has rubeola, varicella (chickenpox), or disseminated zoster, the CDC makes no recommendation about use of PPE if, based on your history of vaccination or disease, you think you are presumed immune to the disease. ■ If the patient has or is suspected of having rubeola or varicella, only immune caregivers should provide care. Immune caregivers do not need to wear masks.

Hormonal Regulation

Antidiuretic hormone (ADH) Renin-angiotensin system Aldosterone Thyroid hormone Brain naturetic factor

OTHER ANTIMICROBIAL AGENTS

Antiviral Antifungal Antiprotozoal

Antibody-mediated immunity

B-lymphocyte-Becomes sensitized to foreign cells and proteins with the assistance of macrophages and helper/inducer T-cells Plasma cell-Secretes immunoglobulins in response to the presence of a specific antigen Memory cell-Remains sensitized to a specific antigen and can secrete increased amounts of immunoglobulins specific to the antigen on re-exposure

Acid-Base Regulation

Buffer systems Respiratory mechanisms Renal mechanisms

ACE Inhibitors

Disrupt renin-angiotensin II pathway by reducing amount of ACE produced With less angiotensin II, less vasoconstriction and reduced peripheral resistance Greater excretion of water and sodium in urine By locking angiotensin II receptors, blood pressure lowers

Hyperacute Rejection

Hyperacute rejection begins immediately on transplantation and is a result of antigen-antibody complexes that form in the blood vessels of the transplanted organ (Abbas et al., 2015). The recipient's blood has pre-existing antibodies to the antigens (including blood group antigens) present in the donated organ. The antigen-antibody complexes adhere to the lining of blood vessels and activate complement, which triggers small blood clots to form throughout the new organ. Widespread clotting occludes blood vessels and leads to ischemic necrosis, inflammation with phagocytosis of the necrotic blood vessels, and release of enzymes into the new organ. The enzymes cause massive cellular destruction within the transplanted organ. Hyperacute rejection occurs mostly in transplanted kidneys but is less common now with better HLA matching. Symptoms of rejection are apparent within minutes of attachment of the donated organ to the recipient's blood supply. The process usually cannot be stopped once it has started, and the rejected organ is removed as soon as hyperacute rejection is diagnosed. Acute Rejection Acute rejection first occurs within 1 week to 3 months after transplantation and sporadically after that as a result of two mechanisms. The first mechanism is antibody mediated and results in vasculitis within the transplanted organ. This reaction differs from hyperacute rejection in that blood vessel necrosis (not occlusion) leads to organ destruction. The second mechanism is cellular. The recipient's cytotoxic/cytolytic T-cells and NK cells enter the transplanted organ through the blood, penetrate the organ cells, start an inflammatory response, and cause lysis of the organ cells. Diagnosis of acute rejection is made by laboratory tests that show impaired function of the donated organ and by biopsy of the donated organ. Symptoms of acute rejection vary with each patient and with the specific organ transplanted. For example, when acute rejection occurs in a transplanted kidney, the patient usually has some tenderness in the kidney area and may have other general symptoms of inflammation. An episode of acute rejection after solid organ transplantation does not automatically mean that the patient will lose the new organ. Drug management of the recipient's immune responses at this time may limit the damage to the organ and allow the graft to be maintained. Chronic Rejection The origin of chronic rejection is related to chronic inflammation and scarring. The smooth muscles of arteries overgrow and occlude these vessels (Abbas et al., 2015). The organ tissues are replaced with fibrotic, scarlike tissue, and function is reduced in proportion to the amount of scarring. This type of reaction is long-standing and occurs continuously as a response to chronic ischemia caused by blood vessel injury. The results of chronic rejection are unique to different transplanted organs. For example, in transplanted lungs chronic rejection thickens small airways. In transplanted livers chronic rejection destroys bile ducts. In transplanted hearts this process is called accelerated graft atherosclerosis (AGA) and is the major cause of death in patients who have survived 1 or more years after heart transplantation. Although good control over the recipient's immune function can delay this type of rejection, the process probably occurs to some degree with all transplanted solid organs obtained from donors who are not identical siblings of the recipients. Because the fibrotic changes are permanent, there is no cure for chronic graft rejection. When the fibrosis increases to the extent that the transplanted organ can no longer function, the only recourse is retransplantation. Management of Transplant Rejection Rejection of transplanted solid organs involves all three components of IMMUNITY, although cell-mediated immune (CMI) responses contribute the most to the rejection process. Maintenance therapy is the continuous immunosuppression used after a solid organ transplant. The drugs used for routine therapy after solid organ transplantation are combinations of a calcineurin inhibitor, a corticosteroid, and an antiproliferative agent Corticosteroids cause a general immunosuppression, which leave the patient at greater risk for infection. Although corticosteroids remain a part of therapy, the dosages are lower than in the past. Calcineurin inhibitors and antiproliferative agents are part of "selective immunosuppressant" therapy These drugs more specifically target immunity components that are responsible for rejection. Which drugs are used depends on the transplant type and other patient-specific conditions. These are all oral agents and must be taken for the life of the transplanted organ. All are immunosuppressive to some degree, and the dosage is adjusted to the immune response of each patient. Treatment with these agents increases the risk for bacterial and fungal infections and for cancer development. Rescue therapy is used to treat acute rejection episodes. The drug categories for this purpose are the monoclonal and polyclonal antibodies Approved drugs used to manage transplant rejection are Corticosteroids Broadly inhibit cytokine production in most leukocytes, resulting in generalized immunosuppression Prednisone (Deltasone) Oral Hypertension Hyperlipidemia Osteoporosis Weight gain Cushingoid appearance Opportunistic infection Glaucoma GI ulcer formation Hyperglycemia ---- Calcineurin Inhibitors—The inhibition of calcineurin stops the production and secretion of IL-2, which then prevents the activation of lymphocytes involved in transplant rejection Cyclosporine (Sandimmune, Neoral, Gengraf) Oral Nephrotoxic Hypertension Tremor Coronary artery disease Hirsutism Gingival hyperplasia Opportunistic infections Malignancies Hyperuricemia Hepatoxicity ---- Tacrolimus (Astagraf XL, HECORIA, Prograf) -Oral, Nephrotoxic Hypertension Hyperkalemia Hypomagnesemia Hyperglycemia Opportunistic infections Malignancies ----

NURSING RESPONSE: INFLAMMATION

Ineffective thermoregulation Assess and document temperature Antipyretic drug use Cooling measures Acute pain Heat and cold therapies ■Avoid direct contact with the heating or cooling device. Cover the hot or cold pack with a washcloth, towel, or fitted sleeve. ■Apply hot or cold intermittently, leaving it on for no more than 15 minutes at a time in an area.This precaution helps prevent tissue injury (e.g., burns, impaired circulation). It also makes the therapy more effective by preventing rebound phenome- non: At the time the heat or cold reaches maximum therapeu- tic effect, the opposite effect begins. ■ Check the skin frequently for extreme redness, blistering, cyanosis (blueness), or blanching. When heat or cold is first applied, the thermal receptors react strongly, and the person feels the temperature intensely. Over about a 15-minute period, the receptors adapt to the new temperature, and the person notices it less. Caution clients not to change the temperature when this occurs because doing so can cause tissue injury. *Applying Heat Therapy* Local application of heat is used to relieve stiffness and dis- comfort associated with musculoskeletal problems. It may also be used for patients with wounds. Heat increases blood flow to an area through vasodilatation, increased capillary permeability, and reduced blood viscosity. Increased blood flow brings oxygen and white blood cells to the wound and aids in the healing process. Heat promotes the delivery of nu- trients and removal of waste products from the tissue, pro- motes relaxation, and decreases stiffness and muscle tension. -When heat is applied to a large area of the body, vasodilata- tion may cause a drop in blood pressure and a feeling of faint- ness. Warn patients to be alert for this effect if they will be administering heat at home. *Applying Cold Therapy* The application of moist or dry cold causes vasoconstriction and decreases capillary permeability. It produces local anesthesia, re- duces cell metabolism, increases blood viscosity, and decreases muscle tension. It also slows bacterial growth. Applications of cold are used to prevent or limit edema and reduce inflamma- tion, pain, oxygen requirements, and bleeding. Cold therapy is often used to treat fevers and sports injuries (e.g., sprains, strains, fractures, and contusions), and to prevent swelling after surgery (e.g., an ice bag may be applied to the perineum after childbirth; an ice collar may be applied to the throat after a ton- sillectomy). Cold applications have the following side effects: ■Elevated blood pressure. Because cold causes vasoconstriction, it may increase the patient's blood pressure. ■Shivering. Prolonged cold may cause shivering, a normal response as the body attempts to produce heat. ■Tissue damage. Prolonged exposure to cold may cause tissue damage due to impaired circulation. Cooling Baths A cooling bath is often used to treat a high fever (above 104°F [40°C]). It promotes heat loss through conduction and vaporization. Elevation Rest, immobilization, and medications

Local Complications of IV Therapy

Infiltration Phlebitis and post-infusion phlebitis Thrombosis Thrombophlebitis Ecchymosis and hematoma Site infection Venous spasm Nerve damage

Delegation

Initial assessment of a wound, as well as ongoing evaluation of a wound that requires treatment, must be done by the reg- istered nurse. You may delegate to nursing assistive person- nel (NAP) inspection of the skin for evidence of skin break- down. Instruct the NAP to notify you of redness, tissue warmth, or drainage. You may also delegate turning and position changes to the NAP. Turning and movement prevent tissue damage from ischemia, thereby preventing pressure ulcers. You may delegate turning and position changes to the NAP. Turning and movement prevent tissue damage from ischemia, thereby preventing pressure ulcers Taping a Dressing:As a nurse, you are responsible for assessing the wound and evaluating interventions. However, this procedure may be del- egated to nursing assistive personnel (NAP). Placing Skin Closure: This procedure itself may be delegated to a NAP unless it is a new wound requiring sterile technique. Assessment of the incision line or wound is a licensed professional's responsibil- ity and should not be delegated. Applying Binders/ Applying Bandages: This procedure itself may be delegated to a NAP.Assessment of the incision line or wound is a licensed professional's responsibility and should not be delegated. Removing Sutures and Staples: This procedure itself may be delegated to a NAP who has been trained in the skill. Assessment of the incision line or wound is a licensed professional's responsibility and should not be delegated. Shortening a Wound Drain/ Emptying a Closed-Wound Drainage System: This procedure may be delegated to a NAP who has been ap- propriately trained in the skill.Assessment of the incision line or wound is a licensed professional's responsibility and should not be delegated. NOOOOooo delegation Removing and Applying Dry Dressings: This procedure requires knowledge of wound healing. It should be performed by a registered nurse. Do not delegate this skill. also, do not delegate, Removing and Applying Wet-to-Damp Dressings no dele--As a nurse, you are responsible for assessing the wound and evaluating interventions.You should not delegate application of a negative pressure wound therapy device to a NAP. How- ever, you may ask the NAP to report to you any changes in the wound dressing, pressure in the unit, or alarm Applying and Removing a Transparent Film Dressing: Because assessment of the wound and knowledge of clean technique are important, you should not delegate this procedure to a NAP. Obtaining a Needle Aspiration Culture From a Wound is an invasive procedure that requires knowledge of wound healing. It should be performed by a registered nurse or an LPN trained in the correct procedure. Do not delegate this skill to nursing assistive personnel (NAP) -Performing a Sterile Wound Irrigation: This is an invasive, sterile procedure that requires nursing assessment, judgment, evaluation, and teaching during the pro- cedure. It requires knowledge of wound healing and should be performed by a registered nurse. Do not delegate this skill to nursing assistive personnel (NAP). Turning and Repositioning. Reposition the patient at least every 2 hours However, patients with very fragile skin or little subcutaneous tissue might need to be repositioned more frequently. At-risk individuals who are chair bound should be repositioned every hour or taught to shift their weight every 15 minutes. Place a turning schedule at the bedside so that all caregivers can participate in the prevention strategy. For an example of a patient turning schedule, Inspect Skin Daily Skin care begins with regular inspection of the skin—at least daily for patients at risk—and usually every 8 to 12 hours for institutionalized patients. You must have adequate light to detect subtle, early skin changes. Use a penlight to inspect bony prominences if direct sunlight is not available. Be sure to check pressure points for erythema, tenderness, or edema. Instruct family members and caregivers about the impor- tance of early detection of skin problems. In obese patients, skin damage can occur under breasts, abdominal folds, or anywhere skin contacts skin. Use the "rule of 30" to guide your positioning: Elevate the head of the bed 30° or less, and when the patient is on her side, position the patient at a 30° angle to avoid direct pres- sure on the trochanter. If the head of the bed is elevated more than 30°, limit the time in this position to minimize pressure and shear. To protect skin during turning or repositioning, use lift devices or drawsheets, heel and elbow protectors, or sleeves and stockings. Never drag a patient when pulling her up in bed. Support surfaces include specialty mattresses, integrated bed systems, mattress replacements, and overlays. These products may consist of air, gel, foam, or water, and are available in various sizes and shapes for beds, chairs, exam tables, and operating room tables

Electrolytes lab values rhyme

Little Maggie is 1.3 to 2.1 years old (Mg+). She ate 3.5 - 5.0 bananas (K+) and drank 9.0 - 10.5 oz. milk (Ca+). Then she took an 136 - 145 hour nap after swimming in the ocean (Na+).

REVIEW OF IMMUNE SYSTEM ANATOMY AND PHYSIOLOGY

Lymphoid organs Lymphoid cells Immune response Types of immunity

COMPLICATIONS OF WOUND HEALING

*Hemorrhage* Whenever a capillary network is interrupted or a blood vessel is cut, bleeding occurs. Hemostasis (cessation of bleeding) usu- ally occurs within minutes of the injury. Possible causes include a slipped suture, erosion of a blood vessel, a dislodged clot, or infection. The risk of hemor- rhage is greatest in the first 24 to 48 hours following surgery or injury. Bleeding may be internal or external. ----Internal Bleeding. Swelling of the affected body part, pain, and changes in vital signs (i.e., decreased blood pressure, elevated pulse) may indicate internal bleeding. Internal bleed- ing, in this chapter, includes hematoma, a red-blue collection of blood under the skin, which forms as a result of bleeding that cannot escape to the surface. The amount of blood in a hematoma varies. A large hematoma causes pressure on sur- rounding tissues. If it is located near a major artery or vein, it may impede blood flow. ------External Hemorrhage. Compared to internal bleeding, external hemorrhage is easier to recognize. You will see bloody drainage on the dressings and in the wound drainage devices. When there is a brisk hemorrhage, blood often pools under- neath the client as the dressings become saturated. To be sure that you recognize the full extent of the bleeding, remember to look underneath the patient. *Infection* Microorganisms can be introduced to a wound during an injury, during surgery, or after surgery. Suspect infection if a wound fails to heal. Localized swelling, redness, heat, pain, fever (temperatures higher than 38°C [100.4°F]), foul-smelling or purulent drainage, or a change in the color of the drainage may also indicate infection. The symptoms are likely to occur in a contaminated or traumatic wound within 2 to 3 days. In a clean surgical wound, you will usually not see signs and symptoms of an infection until the fourth or fifth postopera- tive day. Incisions that begin draining within 5 to 7 days of surgery are at risk for dehiscing. *Dehiscence* Rupture (separation) of one or more layers of a wound is called dehiscence. Wound dehiscence is most likely to occur in the inflammatory phase of healing, before large amounts of collagen have been deposited in the wound to strengthen it. The most common causes of dehiscence are poor nutritional status, inadequate closure of the muscles, or wound infection. Obese clients are also more likely to experi- ence dehiscence because fatty tissue does not heal readily and the patient's mass increases the strain on the suture line. Dehiscence is usually associated with abdominal wounds. Patients often report feeling a pop or tear, especially with sud- den straining from coughing, vomiting, or changing positions in bed. Usually there is an immediate increase in serosan- guineous drainage. Nursing interventions include maintain- ing bedrest with head of bed elevated at 20° and the knees flexed. To prevent evisceration, a binder may be applied and activity modified. The surgeon should be notified of the dehiscence and may visit the patient to examine the wound. *Evisceration* Evisceration is total separation of the layers of a wound in which internal viscera protrude through the incision (Fig. 36-5). Evisceration is a rare complication and is a surgical emer- gency. Immediately cover the wound with sterile towels or dress- ings soaked in sterile saline solution to prevent the organs from drying out and becoming contaminated with environmental bac- teria. Have the patient stay in bed with knees bent to minimize strain on the incision. Notify the surgeon and ready the patient for a surgical procedure (see Chapter 40 for perioperative care) *Fistula formation* A fistula is an abnormal passage connecting two body cavities or a cavity and the skin. Fistulas often result from infection. An abscess forms, which breaks down surrounding tissue and creates the abnormal passageway. Chronic drainage from the fistula may lead to skin breakdown and delayed wound healing. The most common sites where fistulas form are the gastrointestinal and genitourinary tracts. Figure 36-6 illustrates a fistula between the rectum and vagina.

COLLABORATIVE CARE: IMMUNODEFICIENCY

Monitor immune function Nutrition Prevent opportunistic infections Monitor and treat opportunistic infections Drug therapy

COMMON DIAGNOSTIC TESTS 1

*PRIMARY TESTING* Red blood cell count and white blood cell count with differential Fluorescent antinuclear antibody C-reactive protein (CRP) Erythrocyte sedimentation rate (ESR) *OTHER DIAGNOSTIC TESTS AND DISEASE-SPECIFIC TESTING* Allergy testing Genetic testing Rheumatoid factors (RFs) Western blot test TORCH antibody panel Organ function tests

Facts to remember

1 L of water weighs 2.2 lb, equal to 1 kg Weight change of 1 lb = fluid volume change of about 500 mL Daily weights is the most important intervention when evaluating the hydration of your patient.

Midline Catheter

3 to 8" long, 3 to 5 Fr, double or single lumen Inserted through vein in upper arm Used for therapies lasting 1 to 4 wk Do not use for vesicant drugs; can cause tissue damage if extravasation occurs Do not use to draw blood

CLINICAL MANAGEMENT: SCREENING

No routine screenings for general population Human immunodeficiency virus (HIV) screening for those with specific risk factors

Blood Transfusions and Other Components

Packed red blood cells Platelets Fresh frozen plasma Albumin Several specific clotting factors

Fluid Intake

Primarily through drinking fluids IOM recommendation: 2,700 mL/day women, 3,500 mL/day men 20% from food/metabolism of food Fluid intake regulated by thirst Change in plasma osmolality Hypothalamus

FUNCTION OF THE INFLAMMATORY RESPONSE

Restitution of normal, functioning cells after injury Fibrous repair when restitution of functioning cells is impossible

Inverse Relationships

Sodium & Potassium Calcium & Phosphorus

Central IV therapy

Vascular access device (VAD) placed in central circulation, specifically within superior vena cava (SVC) near junction with right atrium Chest x-ray to confirm placement

remember

Veins cannot be used in patients with: Mastectomy Axillary lymph node dissection Lymphedema Paralysis of upper extremities Dialysis graft or fistulas

Bicarbonate

Weak base Major buffer of ECF From intestinal absorption of ingested bicarbonate into ECF, kidney absorption and breakdown of carbonic acid

ALTERED IMMUNITY

What is meant by "altered" immunity? Conditions in which immune responses are either suppressed or exaggerated Suppressed responses are referred to as immunocompromised or immunodeficiency Exaggerated responses are referred to as hypersensitive

Compartment Syndrome

When increased tissue perfusion in a confined space causes decreased flow to the area Compartments of the leg in cross section.

CATEGORIES locaxl

watkins systemic- is fever, diaphoresis, chills, body ache, malaise, HIV..... *increased wbc* local- swelling. rash, redness, discharge ------------------ *Local* Some infections cause harm in a limited region of the body, such as the upper respiratory tract, the urethra, or a single bone or joint. Such infections are said to be local.--local infection evidenced by pain, redness, swelling, and warmth. Occurs in a limited region in the body (e.g., urinary tract infection, infected wound, sprained ankle, boil on the hand, an abscess of finger, Increasing or Continual Pain from Wound, pyelonephritis, cellulitis, cystitis *Duration* Acute: rapid onset of short duration (e.g., common cold) Chronic: slow development, long duration (e.g., osteomyelitis)book---, chronic infections (e.g., an abscess) develop slowly and last for weeks, months, or even years. Some chronic infections, such as relapsing fever, recur after periods of remission. Latent: infection present with no discernible symptoms (e.g., HIV/AIDS, Tuberculosis) *Systemic* Spread via blood or lymph and spread throughout the body. Affects many regions (e.g., septicemia, high blood pressure, flu, Systemic lupus erythematosus, Rheumatoid arthritis, Sarcoidosis, meningitis, headache, stiff neck, temperature higher than 101° F (38.3° C) systemic infections occur that require strong antibiotics such as methicillin. *Source* Hospital-acquired/health care-acquired infection versus community-acquired infection Primary infection versus secondary infection book A *primary infection* is the first infection that occurs in a patient. Especially in immunocom- promised patients, one or more *secondary infections* may follow a primary infection. For example, a frail client infected with pneumonia may develop herpes zoster (shingles), a viral infection related to past infection with varicella, secondary to the stress of illness. ------------- *Local Indicators* • Conversion of a partial-thickness injury to a full-thickness injury • Ulceration of healthy skin at the burn site • Erythematous, nodular lesions in uninvolved skin and vesicular lesions in healed skin • Edema of healthy skin surrounding the burn wound • Excessive burn wound drainage • Pale, boggy, dry, or crusted granulation tissue • Sloughing of grafts • Wound breakdown after closure • Odor *Systemic Indicators* • Altered level of consciousness • Changes in vital signs (tachycardia, tachypnea, temperature instability, hypotension) • Increased fluid requirements for maintenance of a normal urine output • Hemodynamic instability • Oliguria • GI dysfunction (diarrhea, vomiting, abdominal distention, paralytic ileus) • Hyperglycemia • Thrombocytopenia • Change in total white blood cell count (above or below normal) • Metabolic acidosis • Hypoxemia

Inflammation infxl macxl

watkins: what are responsible for recognizing and ingesting foreign antigens as they enter the body? phagocytes. they recognize ingest and eat ---------------------- Neutrophil-Nonspecific ingestion and phagocytosis of microorganisms and foreign protein Macrophage-Nonspecific recognition of foreign proteins and microorganisms; ingestion and phagocytosis. Assists with antibody-mediated immunity and cell-mediated immunity Monocyte-Destruction of bacteria and cellular debris; matures into macrophage Eosinophil-Releases vasoactive amines during allergic reactions to limit these reactions Basophil-Releases histamine and heparin in areas of tissue damage

WOUNDS wz

*Classification of Wounds* Open- open if there is a break in the skin or mucous membranes. Open wounds include abrasions, lacerations, puncture wounds, compound fractures (projection of bone through the skin), and surgical incisions. closed- If there are no breaks in the skin, the wound is de- scribed as closed. Contusions (bruises) or tissue swelling from fractures are common closed wounds. Acute- Acute wounds are expected to be of short duration. In a healthy person, these wounds heal spontaneously without complications through the three phases of wound healing (inflammation, proliferation, and maturation). chronic- Wounds that exceed the expected length of recovery are classified as chronic wounds. The natural healing progression has been interrupted or stalled because of infection, continued trauma, ischemia, or edema. Chronic wounds include pres- sure, arterial, venous, and diabetic ulcers. These wounds are frequently colonized with 7rl types of bacteria, and healing is slow because of the underlying disease process. Unless the wound is properly diagnosed and the underly- ing disease treated, a chronic wound may linger for months or years Clean Clean wounds are uninfected wounds with minimal inflammation. They may be open or closed and do not involve the gastrointestinal, respiratory, or genitourinary tracts (these systems frequently harbor bacte- ria). There is little risk of infection for a clean wound. Clean/contaminated wounds are surgical incisions that enter the gastrointestinal, respiratory, or genitourinary tracts. There is an increased risk of infection for these wounds, but there is no obvious infection. contaminated- include open, traumatic wounds or surgical incisions in which a major break in asepsis occurred. The risk of infection is high for these wounds. infected- Wounds are considered infected when bacteria counts in the wound tis- sues are above 100,000 organisms per gram of tissue. How- ever, the presence of beta-hemolytic streptococci, in any number, is considered an infection. Signs of wound infection include erythema and swelling around the wound, fever, foul odor, se- vere or increasing pain, a large amount of drainage, or warmth of the surrounding soft tissue. Superficial- Superficial wounds involve only the epidermal layer of the skin. The injury is usually the result of friction, shearing, or burning. partial- extend through the epidermis but not through the dermis. full-thickness extend into the subcutaneous tissue and beyond Penetrating- The descriptor penetrating is sometimes added to indi- cate that the wound involves internal organs. Wound depth is a major determinant of healing time: The deeper the wound, the longer the healing time. *Types of Wound Drainage* *Serous exudate*: straw-colored book Clean wounds typically drain serous exu- date. It is watery in consistency and contains very little cellu- lar matter. Serous exudate consists of serum, the straw-colored fluid that separates out of blood when a clot is formed. *Sanguineous*: bloody drainage book You will often see sanguineous exu- date (bloody drainage) with deep wounds or wounds in highly vascular areas. It indicates damage to capillaries. Fresh bleeding produces bright red drainage, whereas older, dried blood is a dark, red-brown color. *Serosanguineous*: mix of bloody and straw-colored fluid book In new wounds, you will most commonly see serosanguineous drainage, a combination of bloody and serous drainage. *Purulent*: yellow, contains pus book The thick, often malodorous, drainage that is seen in infected wounds is called purulent exudate. It contains pus, a protein-rich fluid filled with WBCs, bacteria, and cellular debris. It is commonly caused by infection from pyogenic (pus-forming) bacteria, such as streptococci or staphylococci. Normally, pus is yellow in color, although it may take on a blue-green color if the bacterium Pseudomonas aeruginosa is present. ■Purosanguineous Exudate. Red-tinged pus is called purosanguineous exudate. It indicates that small vessels in the wound area have ruptured.

NURSING ASSESSMENT: PRESSURE ULCERS

*Determine stage* book *Stage I Pressure Ulcer* - Localized area of intact skin with nonblanchable redness, usually over a bony prominence. - The area may be painful, firm, soft, or warmer or cooler as compared to adjacent tissue. - Discoloration will remain for > 30 min after pressure is relieved. - Dark skin may not have visible blanching; its color may differ from that of the surrounding area.Therefore, stage I may be difficult to detect. *Stage II Pressure Ulcer* -Involves partial-thickness loss of dermis. -Stage II pressure ulcers are open but shallow and with a red pink wound bed. -There is no slough. -May also be an intact or open/ruptured serum- filled blister, or a shiny or dry shallow ulcer without slough or bruising. -Do not use this stage to describe skin tears, tape burns, perineal dermatitis, maceration, or excoriation. -Do not mistake moisture-associated skin damage or fungal infections for stage II pressure ulcer. -Stage II ulcers do not involve sloughing or bruising *Stage III Pressure Ulcer* -A deep crater characterized by full- thickness skin loss with damage or necrosis of subcutaneous tissue. -May extend down to, but not through, underlying fascia. -Undermining (deeper- level damage under boggy superficial layers) of adjacent tissue may be present. -Bone/tendon is not visible or directly palpable. -Some stage III pressure ulcers can be extremely deep when located in an area with significant adipose layers. *Stage IV Pressure Ulcer* -Involves full-thickness skin loss with extensive destruction, tissue necrosis, or damage to muscle, bone, or support structures. -Exposed bone/tendon is visible or directly palpable. -Slough or eschar may be present. -Undermining and sinus tracts (blind tracts underneath the epidermis) are common. -The depth of a stage IV pressure ulcer varies by location.They can be shallow on the bridge of the nose, ear, occiput, and malleolus because these areas do not have subcutaneous tissue. -Stage IV ulcers can extend into muscle and supporting structures (e.g., fascia, tendon, or joint capsule). --Often require a full year to heal. Even once healed, the site remains at risk for future injury because the scar is not as strong as the original tissue. Stages I-IV: classified by tissue involvement Stages III and IV: involve tissue necrosis Suspected deep tissue injury- An area of skin that is intact but discolored. It might be purplish or deep red, painful, boggy, or have a blister.---Occurs due to damage of underlying soft tissue from pressure or shear.-----Findings can be subtle enough that often DTI is not recognized until after severe tissue damage has occurred.-----May heal or evolve further and become covered by thin eschar, rapidly exposing additional layers of tissue even with optimal treatment.-----In darker pigmented individuals, discoloration might go undetected. **a wound that has 100% eschar can not be staged** *Unstageable Pressure Ulcer* -Involves full-thickness skin loss. -The base of the wound is obscured by slough (tan, yellow, gray, green, or brown necrotic tissue) or eschar (tan, black, or brown leathery necrotic tissue). -Until enough slough and/or eschar is removed to expose the base of the wound, the true depth, and therefore stage, cannot be determined. -Stable eschar is dry, adherent, and intact without erythema or fluctuance. Do not remove stable eschar, as it serves as "the body's natural cover." Escharxl is thick, hard, and black or brown, also known as an unstageable pressure ulcer. Sloughxl is usually soft, stringy, and pale yellow or gra Use PUSH tool Wet → dry it Open → cover it Unclean → clean it Necrotic → don't scrub it Dry → moisten it

Fluid Imbalances dehydrationxl fluidxl

*Fluid Volume Deficit* Hypovolemia *Dehydration* Dry skin, mucous membranes blood pressure q 15 mins place 2 18-gauge iv lines WITH NS o2 at 3l via nasal cannula Nonelastic skin turgor Decreased urine output and blood pressure (hypotension); increased heart rate (tachycardia); rise in temperature *Weight loss* interventions urine output= 400-600ml if lower call dr clients need 2000ml of fluid drink 2-3l of water

FACTORS AFFECTING SKIN INTEGRITY

*Impaired circulation* Negatively affects tissue metabolism book The vascular system brings oxygen-rich blood to the tissues and removes metabolic waste products. Circulatory impairment interferes with tissue metabolism. Impaired arterial circulation restricts activity, produces pain, and leads to muscle atrophy and thin tissue that is prone to ischemia and necrosis. Impaired venous circulation results in engorged tissues with high levels of meta- bolic waste products, thereby increasing the risk for edema, ul- ceration, and breakdown. Both forms of circulatory impairment delay wound healing, and may lead to chronic wounds. *Medications* Side effects: itching, rashes book Side effects and idiosyncratic reactions to medications can affect skin integrity and wound healing. Any medication that causes pruritus (itching), dermatoses (rashes), photosensitivity, alope- cia, or pigmentation changes can result in changes that impair skin integrity or delay healing. The following are examples: ■ Blood pressure medications decrease the amount of pressure required to occlude blood flow to an area, creating a risk for ischemia. ■ Anti-inflammatory medications, such as over-the-counter (OTC) nonsteroidal anti-inflammatory drugs (NSAIDs) and steroids, inhibit wound healing. ■ Anticoagulants (e.g., heparin, warfarin) can lead to extrava- sation of blood into subcutaneous tissue. As a result, even minimal pressure or injury can cause a hematoma. ■ Chemotherapeutic agents delay wound healing because of their cellular toxicity. ■ Certain antibiotics, psychotherapeutic drugs, and chemotherapy agents for cancer increase sensitivity to sunlight, increasing the risk for sunburn. ■ Several herbal products, such as those containing lavender and tea tree oil, have a drying effect on the skin. *Moisture* Leads to maceration book Moisture leads to maceration (softening of the skin) and in- creases the likelihood of skin breakdown. Incontinence and fever are the most common sources of moisture. Bowel in- continence is particularly troublesome because feces contain digestive enzymes and microorganisms that readily lead to excoriation (denuding) of superficial skin layers, placing such a patient at risk for moisture-associated skin damage (MASD), dermatitis (inflammation of the skin), pressure ulcers, and infection. *Fever* Depletes moisture Increases metabolic rate book Fever leads to sweating, which can cause maceration. In addi- tion, it increases the metabolic rate, thereby raising the tissue demand for oxygen. An increased demand for oxygen is diffi- cult to meet if there is any circulatory impairment or tissue compression from immobility. *Infection* delay/impede healing book Contamination of a wound refers to the presence of microor- ganisms in the wound. All chronic wounds are contaminated. As bacteria begin to increase in number, a wound is said to be *colonized*, though the microorganisms are causing no harm. Wounds are colonized from the surrounding skin and local skin organisms, the external environment, and internal sources, usually from the mucous membranes of the gastroin- testinal system. A wound becomes *critically colonized* when the bacteria begin to overwhelm the body's defenses. Critical colonization may be detected by subtle signs, such as an in- crease in drainage, or by more pronounced signs such as a new foul odor, a change in color of the wound bed, new tunneling of the wound, or absent or friable granulation tissue. An *infection* implies the microorganisms are causing harm by releasing toxins, invading body tissues, and increasing the metabolic demand of the tissue. Infection of the skin makes it more vulnerable to breakdown and impedes healing of open wounds. If not stopped, bacteria can then gain access to the systemic circulation. *Lifestyle* Tanning, bathing, piercings, tattoos book The following are some lifestyle habits that affect skin integrity: ■ Tanning exposes the skin to ultraviolet radiation, thereby increasing the risk for skin cancer. ■ Hygiene habits involving either excessive or insufficient skin hygiene are not healthy for skin integrity. Frequent bathing and use of soap remove skin oils and may lead to drying, which jeopardizes the skin's barrier function. Infrequent cleansing of the skin contributes to excessive oiliness, clogged sebaceous glands, and inadequate removal of microbes on the skin, which can infect a wound or lesion. ■ Regular exercise improves circulation. ■ A nutritious diet provides the nutrients needed to maintain skin integrity. ■ Smoking compromises the oxygen supply to the tissues, mak- ing skin more prone to breakdown and delaying wound healing. It also interferes with vitamin C absorption, which is needed for collagen formation. ■ Body piercings and tattoos present a risk for infection and scar- ring. Complications, which occur in about 20% of piercings, include local infections, sepsis, endocarditis, hepatitis, and toxic shock syndrome. Intraoral and perioral piercings can result in gingivitis, damage to teeth and gums, and choking. Advise patients to become informed about the procedure and about aftercare and to find reputable piercers.

Body Fluid Compartments

*Intracellular* Within the cells *Extracellular* Interstitial Intravascular Transcellular

COMMON DIAGNOSTIC TESTS

*Laboratory tests* Complete Blood Count (with WBC differential) Culture and sensitivity C-reactive protein (CRP) Erythrocyte sedimentation rate (ESR) Serologic tests to detect specific antibodies or viruses *Radiographic studies* X-rays MRI CAT PET and indium scans

Major Electrolytes (cont'd)

*Phosphate (Phosphorus)* ICF anion Bound with calcium in teeth and bones; inverse relationship Activates vitamins and enzymes; assists in cell growth and metabolism Plasma levels of calcium and phosphorus exist in a balanced reciprocal relationship *Bicarbonate* ICF and ECF; acid-base balance Regulated by kidneys Produced by body to act as buffer

EXAGGERATED IMMUNE FUNCTIONING*

*SYMPTOMS* Allergic symptoms Pain Fatigue Fever *CLINICAL FINDINGS* Allergic response Mild allergic response Severe allergic response Autoimmune disorders Can range from vague findings to findings associated with organ failure *Note: Symptoms of autoimmune disorders tend to be vague. Clinical findings vary widely based on the severity of the problem.

Peripheral IV Therapy

*Short peripheral catheters:* Superficial veins of dorsal surface of hand and forearm Dwell for 72 to 96 hr, then require removal and insertion into another site Portable vein transilluminators available ***BD Insyte Autoguard IV catheter. With the push of a button, the needle instantly retracts, reducing the risk for accidental needle stick injuries. Needles and Sharps Do not recap, bend, break, or hand-manipulate used nee- dles. If recapping is necessary, use a one-handed scoop tech- nique. Place used sharps in puncture-resistant containers.

Acid-Base Imbalances

Acidosis Serum pH below 7.35 Respiratory cause: retention of CO2 Metabolic cause: loss of bicarbonate

Acid-Base Imbalances (cont'd)

Alkalosis Serum pH above 7.45 Respiratory cause: blowing off CO2 Metabolic cause: increase in bicarbonate

Considerations for Older Adults

At risk for most electrolyte imbalances from age-related organ changes Have less total body water than younger adults; more at risk for fluid imbalances; more likely to be taking drugs affecting fluid or electrolyte balance

Electrolyte Imbalance

Can occur in healthy people as result of changes in fluid intake and output Can be life threatening if severe; can occur in any setting

Remember...

Change lipid tubing every 24 hr Change blood tubing within 4 hr Change propofol (Diprovan) tubing every 6 to 12 hr *Check facility protocol for possible deviations

MAINTAINING A CLEAN ENVIRONMENT

Clean spills and dirty surfaces promptly Remove pathogens through chemical means (disinfect) Remove clutter Consider supplies brought to the client room as contaminated Consider items from the client's home as contaminated

CLINICAL MANAGEMENT

Clinical management of individuals with immunosuppression or hyper immune conditions varies widely depending on the type of condition, severity, and attributes variables such age: Age Health status Underlying medical conditions

Implanted Port

Consists of portal body, dense septum over a reservoir, and catheter Single or double Surgically created subcutaneous pocket houses the port body Usually placed in upper chest/extremity Not visible externally Flushing after each use and at least once per month between therapies prevents clot formation in internal chamber

Infusion System

Containers - plastic (PVC-free or DEHP-free), glass Administration sets—secondary, intermittent Add-on systems Needleless connection devices Rate-controlling infusion devices

Infusion Therapy

Delivery of medications in solutions and fluids by parenteral route IV therapy most common route IV therapy most common invasive therapy administered to hospitalized patients

Clinical Significance: Edema

Develops with changes in normal hydrostatic pressure differences Pitting edema in a patient with heart failure.

Who draws an ABG?

Doctor respiratory therapist anestielogist phlabomist *nurse interprets*

FACTORS THAT INCREASE INFECTION RISK

Developmental stage- Children frequently begin to have more infections when they start interacting with people outside their family (e.g., when they begin day care or start school). This is a natural process known as acquiring active immunity. Older adults are also susceptible hosts because the immune response declines with aging. Skin, a primary defense, becomes less elastic and more prone to breakdown with aging. Elders also tend to be less active, and their nutrition may be inadequate. Breaks in the skin- A break in the skin, whether caused by a surgical procedure, skin breakdown, an insect bite, or insertion of an intravenous device, creates a portal of entry for infectious microorganisms Illness/injury, chronic disease- Recuperation from infection or injury lim- its the physical resources available to combat a new pathogen. Smoking, substance abuse Tobacco Use. Smoking is a major risk factor for pul- monary infections. Smoking interferes with normal respira- tory functioning, including the ability to move the chest, cough, sneeze, or have full air exchange. Chemicals in tobacco paralyze cilia; thus, secretions pool in the lower airways, creat- ing a hospitable environment for bacterial growth. People exposed chronically to secondhand smoke (e.g., bartenders, children of smokers) are also at increased risk for infection. Substance Abuse. Alcohol curbs hunger. As a result, many chronic alcohol users do not consume an adequate diet. Alcohol is also toxic to the liver and to the cells lining the intes- tinal mucosa. Inhaled substances, such as marijuana and cocaine, affect respiratory cilia in a manner similar to tobacco. Any substances that affect orientation and energy level will diminish food intake, activity, rest, and hygiene—factors that support host defenses. Injecting substances leads to breaks in skin integrity, further increasing the risk of infection. Multiple sex partners- The more sexual partners a person has, the higher his risk of acquiring a sexually transmit- ted infection (STI). Medications that inhibit/decrease immune response--Some medications are given for the purpose of reducing the immune response, for example, to patients receiving organ or tissue transplants. For most patients, though, decreased immunity is an unwanted side effect of treatment. Even common medications, such as nonsteroidal anti-inflammatory agents (NSAIDs) (e.g., ibuprofen), decrease the immune response. As a side effect, some medications, such as chemotherapeutic agents, decrease the production of white blood cells or cause the cells produced to be abnormal. Even antibiotics can increase the risk for infection. For example, an antibiotic given for a respiratory infection may cause a vaginal yeast infection because it destroys colonies of normal vaginal flora, allowing the harmful microbes to thrive. These are considered *superinfections* (opportunistic growth of harmful transient pathogens that are normally kept in check), and some can be extremely challenging to treat. Nursing/medical procedures--Several procedures are associated with an increased risk of infection. For example, urinary catheterization may injure the fragile urethral mucosa, provide a direct pathway for pathogens into the bladder, and prevent the normal flushing of the urethra. Also, an IV line inserted to infuse an antibiotic may serve as a portal of entry for pathogens.

Fluid Imbalances (cont'd) fluidsxl

Fluid Volume Excess= full bounding pedal and post tibial pulse pitting edema= feet ankles,calves shallow respirs w/ crackles on auscultation Hypervolemia Overhydration Elevated blood pressure, bounding pulse Pale, cool skin Edema/ascites Crackles

Acid-Base Balance

Fluid contains equal number of positive charges, ions with negative charges Balance occurs by matching rate of hydrogen ion production with loss

IMPLEMENTING SURGICAL ASEPSIS

Includes Creation of a sterile environment Use of sterile equipment/supplies Sterilization of reusable supplies Surgical hand scrub Surgical attire Sterile gloves Sterile field Use of sterile technique

Sources of Acids

Incomplete breakdown of glucose Destruction of cells Bicarbonate *Normal ratio of carbonic acid to bicarbonate is 1:20.

EXAGGERATED IMMUNE RESPONSE exxl

Individuals who have a "hyper" or exaggerated immune response range from: Allergic reactions Autoimmune reactions Critical point to immune system: Differentiate between self and non-self Accomplished by presence of unique proteins on surface of every cell When system fails to recognize "self" - system begins to attack host cells Cytotoxic reactions This process leads to autoimmune diseases and disorders Examples: Rheumatoid arthritis or systemic lupus erythematosus

DEFINE AND DESCRIBE THE CONCEPT OF INFLAMMATION

Inflammation is an immunologic defense against tissue injury, infection, or allergy.

Nontunneled Percutaneous Central Venous Catheter

Inserted through subclavian vein in upper chest or jugular veins in neck May require insertion in femoral vein—rate of infection is high 7 to 10 inches (15 to 25 cm) long; up to 5 lumens Tip resides in superior vena cava Chest x-ray confirms placement

CONSEQUENCES OF AN EXCESSIVE OR INEFFECTIVE INFLAMMATORY RESPONSE

Local tissue damage from compression Development of chronic inflammation Systemic pathology: Atherosclerosis Chronic renal disease Neurologic disorders

REVIEW OF IMMUNE RESPONSE 1

Major histocompatibility complex (MHC) Surface proteins Divided into 2 classes Class I - found on all cells Class II - on specialized cells Function - to differentiate cells of the "self/host" from foreign protein. "non-self are capable of initiating an immune response Organs involved with immune response Are spread throughout the body - termed lymphoid organs Include: bone marrow, thymus gland, spleen, tonsils, adenoids, and appendix Lymphocytes are formed, grow, mature, and released into the body from these organs

CLINICAL MANAGEMENT: SCREENING

Most common infection screening: Sexually transmitted infection in high-risk groups Tuberculosis screening in high-risk groups General question: How do you determine who is in a "high-risk" group?

Filtration

Movement of fluid through cell or blood vessel membrane because of differences in water volume pressing against confining walls

CLINICAL MANAGEMENT: SECONDARY PREVENTION

No specific screenings are performed for the general population as it relates to this concept.

Intravenous Solutions

Normal serum osmolarity (adults) = 270 to 300 mOsm/L: Isotonic = 270 to 300 mOsm/L Hypertonic = fluids >300 mOsm/L Hypotonic = fluids < 270 mOsm/L

PHYSIOLOGIC PROCESSES AND CONSEQUENCES

OVERVIEW OF IMMUNE RESPONSE pp chart pp20

Movement of Fluids and Electrolytes

Osmosis Diffusion Filtration Active transport

CLASSIFICATION OF ANTIBIOTIC AGENTS

Penicillin Cephalosporins First, second, third, and fourth generation Fluoroquinolones Tetracyclines Macrolides Aminoglycosides

NURSING INTERVENTIONS: PRESSURE ULCER

Prevention Meticulous skin care and moisture control Adequate nutrition Frequent repositioning Therapeutic mattresses Client/family teaching

CLINICAL MANAGEMENT: PRIMARY PREVENTION

Reducing risk for injury and infection Maintaining good hygiene Properly using safety equipment Properly storing and preparing food

Clinical Application

Renin-angiotensin II pathway is greatly stimulated with shock, or when stress response is stimulated Patients with hypertension often take ACE inhibitors

NURSING RESPONSE: INFLAMMATION

Risk for fluid deficit Assessment Intake and output Careful observation Fluid administration Vital signs

NURSING RESPONSE: INFLAMMATION

Risk for infection Lab values Assessment of site Monitoring Documentation Standard precautions

Older Adult Care

Skin care Vein and catheter selection Cardiac and renal changes

Cell Types Involved in Cell-Mediated Immunity book

The WBCs with the most important known roles in CMI include several specific T-lymphocytes (T-cells) along with a special population of cells known as natural killer (NK) cells. T-cells have a variety of subsets, each of which has a specific function. Different T-cell subsets can be identified by the presence of "marker proteins" (antigens) on the cell membrane's surface. More than 200 different T-cell proteins have been identified on the cell membrane, and some of these are commonly used clinically to identify specific cells. Most T-cells have more than one antigen on their cell membrane. For example, all mature T-cells contain T1, T3, T10, and T11 proteins. The names that identify specific T-cell subsets include the specific membrane antigen and the overall actions of the cells in a subset. The three T-lymphocyte subsets that are critically important for the development and continuation of CMI are helper/inducer T-cells, suppressor T-cells, and cytotoxic/cytolytic T-cells. The natural killer cell (NK cell) also contributes to CMI. Helper/inducer T-cells have the T4 protein on their membranes. These cells are usually called T4+ cells or TH cells. The most correct name for helper/inducer T-cells is CD4+ (cluster of differentiation 4). Helper/inducer T-cells easily recognize self cells versus non-self cells. When they recognize non-self (antigen), helper/inducer T-cells secrete cytokines that can enhance the activity of other WBCs and increase overall immune function. These cytokines increase bone marrow production of stem cells and speed up their maturation. Thus helper/inducer T-cells act as organizers in "calling to arms" various squads of WBCs involved in inflammatory, antibody, and cellular protective actions. Suppressor T-cells have the T8-lymphocyte antigen on membrane surfaces. These cells are commonly called T8+ cells, CD8+ cells, or TS-cells. Suppressor T-cells help regulate CMI. Suppressor T-cells prevent hypersensitivity (IMMUNITY overreactions) on exposure to non-self cells or proteins. This action prevents the formation of antibodies directed against normal, healthy self cells, which is the basis for many autoimmune diseases. The suppressor T-cells secrete cytokines that have an overall inhibitory action on most cells of the immune system. Suppressor T-cells have the opposite action of helper/inducer T-cells. For optimal CMI, then, a balance between helper/inducer T-cell activity and suppressor T-cell activity must be maintained. This balance occurs when the helper/inducer T-cells outnumber the suppressor T-cells by a ratio of 2 : 1. When this ratio increases, indicating that helper/inducer T-cells vastly outnumber the suppressor cells, overreactions can occur, some of which are both tissue damaging and unpleasant. When the helper/suppressor ratio decreases, indicating fewer-than-normal helper/inducer T-cells, IMMUNITY is suppressed, and the person's risk for infections increases. Cytotoxic/cytolytic T-cells are also called TC-cells. Because they have the T8 protein present on their surfaces, they are a subset of suppressor cells. Cytotoxic/cytolytic T-cells destroy cells that contain a processed antigen's human leukocyte antigens (HLAs). This activity is most effective against self cells infected by parasites such as viruses or protozoa. Parasite-infected self cells have both self HLA proteins (universal product code) and the parasite's antigens on the cell surface. This allows immune system cells to recognize the infected self cell as abnormal; and the cytotoxic/cytolytic T-cell can bind to it, punch a hole, and deliver a "lethal hit" of enzymes to the infected cell, causing it to lyse and die. Natural killer (NK) cells are also known as CD16+ cells and are very important in providing CMI. These cells have direct cytotoxic effects on some non-self cells without first being sensitized. They conduct "seek and destroy" missions in the body to eliminate non-self cells. The NK cells are most effective in destroying unhealthy or abnormal self cells such as cancer cells and virally infected body cells Cytokinesxl Cell-mediated IMMUNITY (CMI) regulates the immune system by producing cytokines. Cytokines are small protein hormones produced by the many WBCs (and some other tissues). Cytokines made by the macrophages, neutrophils, eosinophils, and monocytes are called monokines. Those produced by T-cells are called lymphokines. In addition, many other body cell types can produce and respond to cytokines. Cytokines work like hormones: one cell produces a cytokine, which in turn exerts its effects on other cells of the immune system and on other body cells. Cytokines control many inflammatory and immune responses and are controlled by interactions with other systems. Cytokines include the interleukins (ILs), interferons (INFs), colony-stimulating factors, tumor necrosis factor (TNFs), and transforming growth factors (TGFs). The interleukins are the largest group of cytokines, with interleukin-33 (IL-33) being the most recently defined

DEFINE AND DESCRIBE THE CONCEPT OF IMMUNITY

The normal physiologic response to microorganisms and proteins as well as conditions associated with an inadequate or excessive immune response. Lets look deeper in to immunity definitions...

Combined Metabolic & Respiratory Acidosis

Uncorrected respiratory acidosis leads to poor oxygenation and lactic acidosis More severe than metabolic or respiratory acidosis alone Combined problem of DKA and COPD lead to this

remember

Use of IV pumps does not decrease the nurse's responsibility to carefully monitor the patient's infusion rate and site!

left shift or bandemia

When analyzing the differential of a normal WBC count, a left shift or bandemia indicates that the patient's bone marrow cannot produce enough mature neutrophils to keep pace with the continuing infection and is releasing immature neutrophils into the blood. These immature cells are of no benefit because they are not capable of phagocytosis.

Hallmark of respiratory acidosis:

watkins give o2 2 make it go up Decreased PaO2 with rising PaCO2

metabolic acidosis metaxl

watkins think lower gi: renal failure and severe diarrhea/dka *renal failure electrolyte values are high, potassium k+ etc bc kidneys are not fx so there not able to get rid of it, so they go on dialysis, hyperkalemia where going to see: 1.muscle twitching 2. muscle weakness 3. flaccid paralysis 4. arrythmias and seizures= lactic acid 5. at risk for increased respiration rate and depth WHEN YOU SEE potassium think MUSCLES/heart ------------ severe diarrhea like ibs, food poising were going to give omodium, ------------------ *Hydrogen ions* Overproduction Under-elimination *Bicarbonate ions* Under-production Over-elimination

RISK FACTORS 2 supxl

watkins which of the following is a genetic rf for having a suppressed immune system? - Fibromyalgia, supress the immune system bc of stress, pain, dx, good/bad days, depression Suppressed immune response...cont. *Medical treatments* May be implemented to specifically inhibit optimal immune response or may lead to immunosuppression as a consequence of treatment Tissue graft or tissue transplantation - need to suppress to avoid rejection Pharmacologic treatments for autoimmune hypersensitivity reactions like SLE and cancer - inhibit the immune response with treatment regimens *Genetics* fat ma Fibromyalgia- genetic Allergies Type I diabetes Multiple sclerosis asthma *High-risk behaviors and substance abuse* HIV - Hepatitis virus - shared needles - high-risk sexual behaviors) Alcoholism - compromised (innate and acquired) immunity *Pregnancy* Creates a situation where the mother is immunocompromised Fetus is in a "privileged" immunity environment

Artificial passive IMMUNITY

would be used to present disease or death from rabies, tetanus, and poisonous snakebites.

PROTECTIVE ISOLATION

"Protective Environment" Patients who are immunosuppressed (e.g., receiving chemotherapy) are sometimes placed in a special form of isolation, called protective isolation or reverse isolation. However, the CDC states that standard and transmission- based precautions are adequate protection for most of those patients. They recommend a "protective environment" only for a special class of stem cell-transplant patients, who are neutropenic (have a low white blood cell count) secondary to chemotherapy. Most of the recommendations are engineering and environmental services rather than nursing measures. Protects the client from organisms Used in special situations with immune-compromised client population Precautions include Room with special ventilation and air filters; no carpeting; daily wet-dusting Avoiding standing water in the room (e.g., humidifier) Nurse not assigned to other clients with active infection Standard and transmission-based precautions, plus mask and other PPE (to protect patient) The CDC recommends and the United States Occupational Safety and Health Adminis- tration requires employers to provide personal protective equipment (PPE) for healthcare workers (e.g., gloves, gowns, face masks, and eye protection *protective isolation* being used for clients with low WBC counts, clients undergoing chemotherapy, or clients with large open wounds or weak immune systems. Protective isolation usually includes following standard precautions; placing the patient in a private room; restricting visitors; wearing a mask, gown, and gloves for patient care; and special cleaning or disposal of the patient's equipment and supplies. Some units, such as neonatal intensive care units, burn units, and labor and delivery suites, may follow some aspects of protective isolation all the time.

Hydrostatic Pressure

"Water-pushing pressure" Force that pushes water outward from a confined space through a membrane Amount of water in any body fluid space determines pressure

PICC Complications

**phlebitis** a patient's IV insertion site red, warm, and slightly edematous. The patient has classic signs of phlebitis, an inflammation of the vein. The IV line must be discontinued immediately to reduce the risk of thrombophlebitis and embolism. ------- **infiltration** Coolness is a classic sign of infiltration, along with swelling, pallor, and possibly tenderness. Infiltration is a leakage of IV solution out of the intravascular compartment into the surrounding tissue. Phlebitis Thrombophlebitis Catheter-related bloodstream infections (CR-BSI) Infiltration and extravasation rare Can accommodate all types of therapy

FACTORS AFFECTING SKIN INTEGRITY

*Age* Infants, are born with varying amounts of vernix caseosa, a creamy substance that protects their skin. Their skin is thinner and more permeable than that of adults, which predisposes in- fants to skin breakdown (e.g., diaper rash). The subcutaneous layer (brown fat) and sweat glands are not fully developed, es- pecially for preterm infants. As a result, in the first few weeks of life infants' temperature-regulating systems are immature, which is why they need be swaddled to maintain body heat. Sex hormones released during puberty increase sebaceous and sweat gland activity, which leads to perspiration odor and sometimes acne. Older adult skin: less elastic, drier, reduced collagen, areas of hyperpigmentation, more prone to injury book The activity of the sebaceous and sweat glands diminishes with aging, resulting in drier skin. *Xerosis* (itchy, red, dry, scaly, cracked, or fissured skin) is a problem for up to 85% of older adults and can be a threat to the integrity of their skin. Along with loss of lean body mass, the subcutaneous tissue layer thins, giving the normal-weight individual a sharp, angular appearance. Changes in collagen fibers decrease the elasticity of the dermal layer, thus weakening the strong bond between the epidermis and dermis. These changes make the skin prone to breakdown and prolong wound-healing time. Regeneration of healthy skin takes at least twice as long in an 80-year-old as in a 30-year-old. In addition, many older adults have chronic diseases that interfere with healing. Diabetes, for instance, predisposes to infection; and liver dysfunction inter- feres with synthesis of blood-clotting factors. *Mobility status* Increased pressure, shearing, and friction can lead to breakdown book Impaired Mobility A healthy person moves and shifts position unconsciously when he senses pressure or discomfort. However, for people who cannot move independently, the weight of the body on the bed or chair causes an increase in pressure and may lead to skin breakdown. Impaired mobility is caused by conditions that require complete bedrest or that severely limit activity (e.g., paralysis, high-risk pregnancy, sedation, casts, and altered sensory perception). *Nutrition/hydration* Poor nutrition, less regeneration -------Protein. Healthy skin requires protein to maintain in- tegrity, repair minor defects, and preserve intravascular vol- ume. If protein levels decline from excess loss or inadequate intake, minor defects cannot be repaired, fluid leaks from the vascular compartment of dependent areas, and edema (excess fluid in the tissues) develops. Edema decreases skin elasticity and interferes with the diffusion of oxygen to the cells. There- fore, the skin becomes prone to breakdown. -------Cholesterol. Abnormally low cholesterol levels predis- pose patients to skin breakdown and inhibit wound healing. Patients on low-fat tube feedings may experience deficiencies in fatty acids and linoleic acid, as well as cholesterol. Together, these fats aid in providing calories for wound healing and maintain a waterproof barrier in the stratum corneum. ----Calorie Intake. If calorie intake is inadequate, the body uses proteins for energy (catabolism). Proteins are then un- available for building and maintenance functions (anabolism) (see Chapter 28 as needed). When undernutrition is prolonged, the person experiences loss of subcutaneous tissue, and muscle atrophy. As a result, there is less padding between the skin and the bones, predisposing the skin to pressure ulcers. ------Ascorbic Acid, Zinc, and Copper. Vitamin C, or ascor- bic acid, is involved in the formation and maintenance of col- lagen, so a deficiency can delay wound healing. Zinc and cop- per are also involved in collagen formation, and deficiencies of either may impair healing. -----Hydration. Poor skin turgor may occur as a result of dehydration, whereas edema may result from overhydration. For further discussion on fluid requirements, Dehydration = poor turgor *Sensation level* Diminished sensation leads to increased risk for pressure and breakdown book Clients with peripheral vascular disease, spinal cord injury, di- abetes, cerebrovascular accident, trauma, or fractures often have diminished tactile sense. They are therefore more prone to skin breakdown. If you've ever touched a hot surface and quickly pulled back your hand, you know the importance of tactile sensation. *A client with diminished sensation* is less able to sense a hot surface and would likely suffer a burn. A cut or wound in an area with limited sensation may go unnoticed and therefore untreated. The client with diminished sensation is also unable to feel pressure in an affected area. As a result, he may not shift position to relieve pressure over bony prominences or be aware that shoes or clothing are constricting. *Clients with impaired cognition* (i.e., Alzheimer's disease, de- mentia, altered level of consciousness) are at higher risk for skin breakdown because they are not aware of the need to reposition.

HEALTHCARE-RELATED INFECTION

*An infection acquired as a result of healthcare* Cost to the healthcare system = $4.5 billion/year Leading cause of death Preventable with use of aseptic principles/techniques *Exogenous Healthcare-Related Infection:* Pathogen acquired from healthcare environment *Endogenous Healthcare-Related Infection: * Normal flora multiply and cause infection as a result of treatment book (e.g., chemotherapy or antibiotics) causes the normally harmless microbe to multiply and cause infec- tion. For example, candidal vaginitis (yeast infection) may develop in a client receiving antibiotics after surgery.

Fluid Overload: Collaborative Care

*Assessment* *Interventions* Patient safety Pulmonary edema Drug therapy Nutrition therapy Monitoring of I&O

Dehydration: Collaborative Care

*Assessment* History *Physical assessment/clinical manifestations:* Cardiovascular Respiratory Skin Neurologic- mental status Renal

Major Electrolytes (cont'd)

*Calcium* Bone health; neuromuscular function; cardiac function Insufficiency leads to osteoporosis Absorption requires active form of vitamin D Stored in bones Influenced by hormones: Parathyroid hormone Thyrocalcitonin *Magnesium* ICF; bone; many cellular functions Alcoholism leads to low levels Critical for skeletal muscle contraction, carbohydrate metabolism, ATP formation, vitamin activation , cell growth *Chloride* ECF; bound to other ions Imbalance occurs resulting from other electrolyte imbalances Treat underlying electrolyte imbalance or acid-base problem

COLLABORATIVE CARE: EXAGGERATED IMMUNE RESPONSE 3

*Clinical outcomes:* Adequate ventilation Restoration of blood pressure and pulse to pre-reaction normal levels Adequate urine output indicating adequate circulatory volume Modulation of hypersensitivity response Management of pain experience Maintenance of join and muscle mobility; self-care for ADLs where possible; restoration or maintenance of adequate levels of physical activity

INFLAMMATORY DISEASE

*Diseases that result in inflammatory process* Viruses Bacteria Pneumonia fungi Protozoa Others *Diseases that produce inflammatory effect* Antibiotic-resistant organisms Asthma Allergic disease Response to allergens and irritants *Diseases caused by inflammatory effect* Self-induced inflammatory reaction Arthritis Myocardial infarction Obesity

STRUCTURE OF THE SKIN skinxl

*Epidermis* The epidermis is the outer portion of the skin Stratum corneum: the outermost layer, is composed of numerous thicknesses of dead cells. Functioning as a barrier, it restricts water loss and prevents fluids, pathogens, and chemicals from entering the body Stratum germinativum- The sratum germinativum, the innermost layer, continu- ally produces new cells, pushing the older cells toward the skin surface. *Keratinocytes* are protein-containing cells that give the skin strength and elasticity. Deeper in the epi- dermis are *melanocytes*, which produce *melanin*, a pig- ment that gives skin its color and provides protection from ultraviolet light. *Langerhans cells* are mobile. Their func- tion is to phagocytize (engulf) foreign material and trigger an immune response. *Dermis*- The dermis lies below the epidermis and above the subcutaneous tissue. It is made of irregular fibrous con- nective tissue that provides strength and elasticity to the skin and is generously supplied with blood vessels. Within the dermis are sweat glands, sebaceous (oil) glands, ceruminous (wax) glands, hair and nail follicles, sensory receptors, elastin, and collagen. *Subcutaneous layer* - The subcutaneous layer is com- posed primarily of connective and adipose tissue. It provides insulation, protection, and a reserve of calories in the event of severe malnutrition. This layer varies in thickness in different body sites. Sex hormones, genetics, age, and nutrition also influence the distribution of subcutaneous tissue

Calcium (9.0-10.5 mg/dL)

*Hypercalcemia* *Causes*: hyperparathyroidism, thiazides, immobilization *S&S*: bones are brittle, kidney stones (majority made of calcium) muscle weakness, constipation, anorexia, nausea, vomiting, polyuria, polydipsia, bizarre behaviors, bradycardia *Treatment*: MOVE!, fluids, Phospho Soda ® & Fleet ® enema (↑PO4, Ca will ↓), steroids, add PO4 to diet, safety precautions, must have vitamin D to use Ca Phosphorus foods are protein foods avoid hctz *Hypocalcemia* *Hint*: Think muscles first *Causes*: hypoparathyroidism, radical neck, thyroidectomy *S&S*: (Same as Hypomagnesemia) Rigid muscle tone, seizures, muscle twitching, stridor/laryngospasms, + Chvostek's, + Trousseau's, Arrhythmias, ↑ DTRs, minds changes, swallowing changes (aspiration)-- cardiac dysrhythmias, increased neuromuscular excitability, muscle cramps, twitching, hyperactive reflexes, carpal and pedal spasms, tetany *Treatment*: Vitamin D, phosphate binders, Ca pills like ca citrate pill every morning, needs dairy, broccoli, spinach Food sources of calcium Milk Milk products Dark green leafy vegetables Salmon Calcium-fortified foods such as breads and cereals.

Potassium (3.5-5.0 mEq/L) Excreted by the Kidneys; if the kidneys are not working well then the serum K+ will ↑

*Hyperkalemia* *Hint*: Can cause life-threatening arrhythmias *Causes*: Kidney problems, Aldactone: Diuretic It can treat high blood pressure. It can also treat fluid retention (edema) and high levels of the hormone aldosterone *S&S*: Begins with muscle twitching → then proceeds to muscle weakness → then flaccid paralysis *Treatment*: Dialysis, Ca Gluconate (↓ arrhythmias), glucose & insulin, ***Kayexalate*****antidote --------------------- *Hypokalemia* *Hint*: Can cause life-threatening arrhythmias *Causes*: Vomiting, NG suctioning, diuretics, not eating *S&S*: muscle cramps, weakness---poor muscle contraction, FLACCID MUSCLE WEAKNESS, fatigue, skeletal muscle weakness, poor muscle tone, hyporeflexia, possibly paralysis, weakening of the respiratory muscles, decreased GI motility, anorexia, nausea, vomiting, ileus with decreased bowel sounds, parathesias, confusion, lethargy, DYSRHYTHMIAS, flattened T wave. *Treatment*: Give K+, Aldactone, eat more K+ Food sources of potassium kxl Bananas Oranges Apricots Figs Dates Carrots Potatoes Tomatoes Spinach Dairy products Meats

Magnesium (1.3-2.1 mEq/L) Excreted by kidneys and can be lost other ways (GI tract)

*Hypermagnesemia* (TOO MUCH SEDATIVE) *Hint*: Think muscles first *Causes*: Renal failure, antacids *S&S*: ↓ DTRs, ↓ muscle tone, ↓ LOC, ↓ pulse, ↓ respirations, arrhythmias, flushing, warmth, mg makes you calm & prevent seizures *Treatment*: Ventilator, Dialysis, Safety precautions *Antidote*: Calcium Gluconate (will increase respirations) *Hypomagnesemia* (NOT ENOUGH SEDATIVE) *Hint*: Think muscles first *Causes*: Diarrhea, alcoholism *S&S*: Rigid muscle tone, seizures, stridor/laryngospasms, + Chvostek's, + Trousseau's, Arrhythmias, ↑ DTRs, minds changes, swallowing changes (aspiration), low blood calcium, muscle cramps, spasms, nausea, weakness, irritability, and confusion. chxl *Treatment*: Give Mg, √ kidney fx, seizure precautions, eat magnesium

Sodium (136-145 mEq/L) Na level in your blood is totally dependent on how much H2O you have in your body

*Hypernatremia* = Dehydration Too much NA; not enough H2O *Hint*: Think Neuro Changes 1st! *Causes*: Hyperventilation, heat stroke, DI *S&S*: dry mouth, thirsty, swollen tongue *Treatment*: Restrict salt, dilute client with fluids, daily weights, I&O, monitor lab work Feeding tube clients tend to get dehydrated *Hyponatremia* = Dilution Too much H2O; not enough H2O *Hint*: Think Neuro Changes 1st! *Causes*: Drinking H2O for fluid replacement (vomiting, sweating), polydipsia (thirsty), D5W, SIADH SIADH= sodium deficit, cb retention of water Syndrome of inappropriate antidiuretic hormone secretion *S&S*: Headache, seizure, coma *Treatment*: Client needs Na, Client doesn't need H2O

RISK FACTORS: PRESSURE ULCER DEVELOPMENT

*INTRINSIC FACTORS* • Circulation • Underlying health status *Immobility *Impaired sensation *Malnourishment/ Nutrition *Aging *Fever *EXTRINIC FACTORS* Friction Friction damages the outer protective epidermal layer, decreasing the amount of pressure needed to develop skin lesions *Pressure*- (formerly called decubitus ulcers, pressure sores, and bedsores) are localized areas of injury to the skin, and possibly the underlying tissue, usually over a bony prominence. They are caused by unrelieved pressure, or pressure in combination with shearing forces, which compromises blood flow to an area, resulting in ischemia (inadequate blood supply) in the underlying Tissue ischemia leads to tissue anoxia (lack of oxygen) and cell death. The key variables in ischemia are time and pressure. Small amounts of pressure over an extended period of time or a large amount of pressure for a short period of time results in tissue ischemia. Pressure ulcers can occur in as little time as 2 hours, though it may take as long as 5 days for the full extent of tissue damage to be known. When ischemia first occurs, the skin over the area is pale and cool. When you relieve the pressure (e.g., by turning the patient), vasodilation occurs, and extra blood rushes to the area to compensate for the ischemic period. The area flushes bright red (*reactive hyperemia*). If the redness does not disap- pear quickly, tissue damage has occurred. The redness should last about half as long as the duration of the ischemia. For example, if the tissue was compressed for an hour, reactive hyperemia should not last more than about 30 minutes. Although time and pressure are the key variables, several other factors predict the likelihood of pressure ulcer formation (Fig. 36-7). Some factors are intrinsic and some are extrinsic. *Shearing* Shearing occurs when the epidermal layer slides over the dermis, causing damage to the vascular bed. It most com- monly occurs when the head of the bed is elevated and the patient slides downward, causing shear to develop in the sacral area. When shearing occurs, the amount of pressure needed to occlude circulation is cut in half. ----*Exposure to moisture* especially in the form of urine or feces, macerates the skin and also decreases the amount of pressure required to produce ulceration.

STAGES OF INFECTION

*Incubation*: from time of infection until manifestation of symptoms; can infect others book Incubation is the stage between successful invasion of the pathogen into the body and the first appearance of symp- toms. In this stage, the person does not suspect that he has been infected but may be capable of infecting others. This stage may last only a day, as with the influenza virus, or as long as several months or even years, as with tuberculosis. *Prodromal*: appearance of vague symptoms; not all diseases have this stage book The prodromal stage is characterized by the first appearance of vague symptoms. For example, a person infected with a cold virus may experience a mild throat irritation. Not all infections have a prodromal stage. *Illness*: signs and symptoms present book Illness is the stage marked by the appearance of the signs and symptoms characteristic of the disease. If the patient's immune defenses and medical treatments (if any) are inef- fective, this stage can end in the death of the patient. *Decline*: number of pathogens decline book Decline is the stage during which the patient's immune defenses, along with any medical therapies, successfully reduce the number of pathogenic microbes. As a result, the signs and symptoms of the infection begin to fade. *Convalescence*: tissue repair, return to health book Convalescence is characterized by tissue repair and a return to health as the remaining number of microorganisms approaches zero. Convalescence may require only a day or two or, for severe infections, as long as a year or more.

COLLABORATIVE CARE: SUPPRESSED IMMUNE RESPONSE

*Infection* Clinical management of infection and opportunistic diseases are important part of clinical care (antibiotics) - more next week** *Gastrointestinal Dysfunction* Pharmacologic treatment of diarrhea, candidiasis, and fluid and electrolyte loss *Skin Disorders* Pharmacologic treatment of skin rash *Nutrition* Multiple vitamin and mineral supplements Dietary supplements such as Ensure or equivalent Evaluation of weight and BMI

Intravenous Solutions

*Isotonic Infusate* Water does not move into or out of body's cells Risk for fluid overload, especially older adults *Hypertonic Infusate* Corrects fluid, electrolyte, and acid-base imbalances by moving water out of body's cells, into bloodstream Parenteral nutrition is example *Hypotonic Infusate* Moves water into cells and expands them

COMMON DIAGNOSTIC TESTS 2

*Laboratory tests* CBC WBC with differential CRP ESR Serologic tests to detect specific antibodies or viruses *Radiographic studies* MRI CAT PET scans colonoscopy

PREVENTING INFECTION: IMPLEMENTING MEDICAL ASEPSISxl

*MEDICAL ASEPSIS* ("clean technique") "A STATE OF CLEANLINESS THAT DECREASES THE POTENTIAL FOR THE SPREAD OF INFECTIONS" refers to procedures that decrease the potential for the spread of infections. You probably already practice medical asepsis in other settings without realizing it. For example, at home you wash your hands before and after han- dling foods. Before chopping food, you make sure the cutting board and utensils you use are clean. After using it, you wash the board with hot, soapy water. In the healthcare setting, *medical asepsis includes hand hygiene, environmental clean- liness, standard precautions, and protective isolation*. The effectiveness of these measures, and the patient's safety, de- pend on nurses' rigorously and consistently following the principles of asepsis. **Protective Isolation. If a client is in protective isolation, be sure that equipment has been disinfected before it is taken into the room. Take linen and dishes directly to the protec- tive isolation room, and hand them to someone wearing the required protective garb. jargon**Transmission-Based Isolation. If the client is in transmission- based isolation, disinfect the equipment on removal from the room. When removing linen or nondisposable items from a room with contact, droplet, or airborne isolation, place them in special isolation bags.-----This process requires two healthcare workers. The worker inside the room wears protec- tive clothing and handles only contaminated items. The second worker stands at the door and holds the isolation bag open. The first worker places items inside the bag without touching the outside of the bag. If the bag contains linens, the isolation bag is closed and placed in a laundry hamper. Securely close the isolation trash bag, and place it in a special isolation trash container. *PROMOTED THROUGH* Maintaining a clean environment--- A clean environment includes the surfaces in a patient's room, as well as supplies, equipment, and other objects brought into the room. An object is said to be contaminated if it becomes unclean—that is, if you suspect it may contain pathogens. *The floor, soiled dressings, used tissues, sinks, commodes, and bedpans are other examples of contaminated items.* Agency policies determine whether a reusable item is cleaned, disinfected, or sterilized, based on how the item is used. Maintaining clean hands-based on the amount of contact you have with patients or con- taminated objects, as well as the patient's infection status and susceptibility to infection.-- Handwashing involves five key factors: time, water, soap, friction, and drying. Following Centers for Disease Control (CDC) guidelines

LINES OF DEFENSE AGAINST INFECTION

*Primary Defenses* pg 610 bn Anatomical features, limit pathogen entry and prevent organisms from entering the body. Intact skin- skin surface normal flora The respiratory tree. The nares, trachea, and bronchi are cov- ered with mucous membranes that trap pathogens. The nose contains hairs that filter the upper airway; the nasal pas- sages, sinuses, trachea, and larger bronchi are lined with cilia, tiny hairlike cells that sweep microorganisms upward from the lower airways. Coughing and sneezing forcefully expel organisms from the respiratory tract. Mucous membranes The mouth- contains lysozyme and continually washes microbes from the teeth and gums.---In addition, normal flora of the mouth compete for nutrition with invading organisms, thereby limiting the number of pathogens. eyes- Tears: contain lysozyme, an antimicrobial enzyme. Normal flora in GI tract Normal flora in urinary tract many different white blood cells (WBCs) and their products??? *Secondary Defenses* Biochemical processes activated by chemicals released by pathogens Phagocytosis-Phagocytic WBCs include neu- trophils, monocytes, and eosinophils. Complement cascade- triggers the release of chemicals that attack the cell membranes of pathogens, causing them to rupture. Complement also sig- nals basophils (WBCs), to release histamine, which prompts inflammation. Inflammation-The inflammatory process begins when histamine and other chemicals are released either from dam- aged cells, or from basophils being activated by complement. With inflammation, blood vessels dilate and become more permeable, which increases the flow of phagocytes, antimicro- bial chemicals, oxygen, and nutrients to the affected area. The classic signs and symptoms of inflammation are localized warmth and erythema (redness), which develop as blood flow is increased. In addition, fluid leaking from the more perme- able blood vessels accumulates in the surrounding tissue, causing edema, which in turn prompts pain as pressure is exerted on nerve endings. Fever-many clinicians do not treat a fever unless it's greater than 102°F (38.9°C).

WOUND HEALING PROCESSES wz

*Regeneration* In epidermal wounds No scar book When a wound affects only the epidermis and dermis, regenerative/epithelial heal- ing takes place. No scar forms, and the new (regenerated) epithelial and dermal cells form new skin that cannot be distin- guished from the intact skin. Partial-thickness wounds heal by regeneration. *Primary intention* Clean surgical incision/edges approximated Minimal scarring book When a wound involves minimal or no tissue loss and has edges that are well approxi- mated (closed), primary (first) intention healing takes place (Fig. 36-2A). Little scarring is expected. A clean surgical incision heals by this method. *Secondary intention* Wound edges not approximated -Tissue loss -Heals from inner layer to surface book Healing by secondary (second) intention occurs when a wound (1) involves exten- sive tissue loss, which prevents wound edges from approxi- mating, or (2) should not be closed (e.g., because it is infected). Because the wound is left open, it heals from the inner layer to the surface by filling in with beefy red granulation tissue (a form of connective tissue with an abundant blood supply) (Fig. 36-2B). Epithelial tissue may appear in the wound as small pink or pearl-like areas. Do not mistake this as a sign of infection. Wounds that heal by secondary intention heal more slowly, are more prone to infection, and develop more scar tissue. Pressure ulcers (discussed later) and infected wounds are examples. *Tertiary intention* Granulating tissue brought together -Delayed closure of wound edges book A wound heals by tertiary (third) intention, also called delayed primary closure, when two surfaces of granulation tissue are brought together (Fig. 36-2C). This technique may be used when the wound is clean-contam- inated or contaminated. Initially the wound is allowed to heal by secondary intention. When there is no evidence of edema, infection, or foreign matter, the wound edges are closed by bringing together the granulating tissue and suturing the sur- face. Such wounds require strict aseptic technique during all dressing changes because they are prone to infection. Tertiary intention healing creates less scarring than does secondary, but more than primary intention healing.

Major Electrolytes

*Sodium* Extracellular fluid (ECF): regulates fluid volume Kidney reabsorbs "Where sodium goes water follows" *Potassium* Intracellular fluid (ICF): muscle contraction; cardiac conduction Kidneys eliminate Regulates protein synthesis, glucose use and storage

CLINICAL MANAGEMENT: PRIMARY PREVENTION

*Vaccinations* Vaccinations are administered to people across the lifespan; visit the CDC website at www.CDC.gov for recommended vaccination schedules. *Hygiene* Personal hygiene Food hygiene Patient care hygiene Hand hygiene Infection control practices

Scope of Concept

*acidotic* pH < 7.35 *optimal* pH 7.35-7.45 PaCO2 HCO3 normal *alkalotic* pH> 7.45 Acid-base balance can be viewed as on a continuum; optimal balance is seen in the middle and extremes of imbalance are on each end of the spectrum.

Assistive Personnel (APs) uap

ADLs Bathing Positioning every 2 hrs Ambulating oral care 3-4 hrs- with warm saline....mothwash not encouraged bc of alcohol Feeding (without swallowing precautions) Specimen collection Intake and output Vital signs (for stable patients)

IMMUNITYxl

Adaptive internal protection resulting in long-term resistance to effects of invading microorganisms Body must learn to generate specific immune responses when infected by or exposed to specific organisms Book IMMUNITY is protection from illness or disease that is maintained by the body's physiologic defense mechanisms. This protection requires the interaction of immunity and inflammation IMMUNITY with inflammation is critical to maintaining health and preventing disease. immunity plays a role in repair of damaged tissues. evolve is an adaptive internal protection that results in long-term resistance to the effects of invading microorganisms. This means that the responses are not automatic.

FACTORS THAT SUPPORT HOST DEFENSES

Adequate nutrition- To manufacture cells of the immune system-*protein, vitamins, minerals, and water*.-- maintain production of white blood cells, and to repair damaged tissues. Balanced hygiene -Sufficient to decrease skin bacterial count -Not overzealous; causes skin cracking Rest/sleep Rest and sleep conserve energy needed for healing. Sleep needs vary, and there is really no "correct" amount or pattern of sleep. However, sleep of 6 to 9 hours per night is considered fully restorative for most people. Exercise and Activity. Research demonstrates that exer- cise is just as important as rest and sleep. Too little activity causes circulation to slow and the lungs to supply less oxygen. Excessive exercise leads to fatigue and joint injury. Reducing stress Whether physical or mental, stress decreases the body's immune defenses. Numerous studies demonstrate a correlation between stress and disease. Laughing, in contrast, increases oxygenation, promotes body movement, and increases immune responses. Immunization Immunization via vaccination can pro- tect against several infectious diseases (e.g., measles, mumps, and other childhood diseases; pneumonia, influenza, small- pox, and shingles). Unfortunately, some pathogens, such as the virus that causes the common cold, mutate too rapidly for an immunization to be developed. Encourage clients to follow recommendations for immunizations. For most diseases, at least 85% of the population must be immunized in order to protect the entire population from the disease. If you need specific recommended immunizations throughout the life span and their role in health promotion

CLINICAL MANAGEMENT: COLLABORATIVE INTERVENTIONS

Antimicrobial therapy Rest and comfort care measures Nutritional support Fluids Disinfection of physical environment

NURSING INTERVENTIONS RELATED TO WOUND CARE

Applying negative pressure wound therapy Dressing a wound Gauze/transparent film Hydrocolloids/hydrogels Supporting/immobilizing a wound Binders Binders may be used to keep a wound closed when there is danger of dehiscence, or to immobilize a body part to aid in the healing process. They are typically used on large areas of the body and are designed for a specific body part. They may be made of cloth or elasticized material and fasten with straps, pins, or Velcro. The most common binders are the following: ■ A triangular arm binder or sling is used to support the upper extremities. Because commercial slings are readily available, you will use the triangular sling infrequently. ■ A T-binder is used to secure dressings or pads in the perineal area. ■ An abdominal binder is used to provide support to the ab- domen. It is often ordered when there is an open abdominal wound that is healing by secondary intention. The binder decreases the risk of dehiscence. Abdominal binders may be straight or multitailed. bandages A bandage is a cloth, gauze, or elastic covering that is wrapped in place. With the exception of a sling, most bandages come in rolls and in various widths, commonly 1.5 to 7.5 cm (0.5 to 3 in.). Use a narrow width on small body parts, such as a finger, and wider bandages on arms and legs. ■Cloth bandages are most commonly used as slings to im- mobilize an upper extremity or to hold large abdominal dressings in place. ■ Gauze is the most frequently used type of bandage. It is available in many sizes and forms and readily conforms to the shape of the body. It may also be impregnated with med- ications for application to the skin or with plaster of Paris, which, when dried, hardens to form a cast. ■ Elastic bandages are used to apply pressure and give support (e.g., to improve venous circulation in the legs). Ace bandages are the most common form of elasticized bandage. ■A rolled bandage is a continuous strip of material (gauze, stretchable gauze, or elastic webbing) that you unroll as you apply it to a body part. To apply a rolled bandage, hold the free end in place with one hand, and use the other hand to pass the roll around the body part. Exert equal tension on each pass (or turn). Each turn should overlap the last one- half to two-thirds the width of the bandage, except for the circular turn. There are five basic turns for rolled bandaging Applying heat and cold Local application of heat or cold has been used for therapeu- tic purposes for centuries. Temperature-sensitive nerve end- ings respond readily to temperatures between 59°F and 113°F (15°C and 45°C). Response to heat or cold depends on the area being treated, the nature of the injury, duration of the treatment, age, physical condition, and the condition of the skin

Alkalosis: Patient-Centered Collaborative Care

Assessment (same for metabolic and respiratory alkalosis) Hypocalcemia Hypokalemia CNS changes—positive Chvostek's and Trousseau's signs Neuromuscular changes—tetany Cardiovascular changes Respiratory changes

RECOGNIZE WHEN AN INDIVIDUAL HAS ALTERED IMMUNITY

Assessment of immune disorders and dysfunction begins with a thorough health history and physical examination Basic laboratory and diagnostic testing procedures Followed by more specific tests depending on the individual's history and current s/s Genetic testing may also be important to confirm a diagnosis Determine appropriate counseling concerning a persons prognosis Make reproduction recommendations

Normal Blood pH

Balance of acids and bases in body fluids *Normal for:* Arterial blood = 7.35 to 7.45 Venous blood = 7.31 to 7.41 *Changes can affect:* Shape of hormones and enzymes Distribution of other electrolytes (fluid and electrolyte imbalance) Excitable membranes Effectiveness of hormones and drugs

Significance of Fluid Balance: Renin-Angiotensin II Pathway

Blood (plasma) volume and intracellular fluid most important to keep in balance Kidneys are major regulator of water and sodium balance; maintain blood and perfusion pressure to all tissues/organs poor perfusion= flattened neck veins supine position, normal veins are distended When the kidneys sense a low parameter, they secrete renin

Infection Control

CDC recommends aseptic preparation and technique including: Hand hygiene Clip hair; do not shave Ensure skin is clean Wear gloves Prepare skin with 70% alcohol or chlorhexidine

Catheter-Related Bloodstream Infection (CR-BSI)

CR-BSI one of several preventable hospital-acquired infections (Institute for Healthcare Improvement) www.ihi.org

Cell-mediated immunity

Cell-Mediated Immunity Whereas the humoral immune response acts directly against antigenic cells, the cell-mediated immune response destroys microorganisms (usually viruses). Four types of T cells are responsible for the cell-mediated immune response: ■Cytotoxic (killer) T cells directly attack and kill pathogens and infected body cells. ■Helper T cells help regulate the action of cytotoxic T cells, as well as that of B cells in humoral responses. ■Memory T cells. The first time an antigen invades the body, T cells form that respond to that specific antigen. The mem- ory T cells are able to increase the speed and amount of the T-cell response with subsequent invasions by that antigen. ■Suppressor T cells are thought to stop the immune response when the infection has been contained. *Helper/inducer T-lymphocytes (T-cells)-Enhances immune activity of all parts of general and specific immunity through secretion of various factors, cytokines, and lymphokines *Cytotoxic/cytolytic T-cell Selectively attacks and destroys non-self cells, including virally infected cells, grafts, and transplanted organs *Natural killer cell Nonselectively attacks non-self cells, especially body cells that have undergone mutation and become malignant; also attacks grafts and transplanted organs book Cell-mediated IMMUNITY (CMI), or cellular immunity, involves many white blood cell (WBC) actions and interactions. CMI also is adaptive or acquired true immunity that is provided by lymphocyte stem cells that mature in the secondary lymphoid tissues of the thymus and pericortical areas of lymph nodes (see Fig. 17-7). Certain CMI responses influence and regulate the activities of antibody-mediated immunity (AMI) and innate immunity (inflammation) by producing and releasing cytokines. For total or full immunity, CMI must function optimally. Protection Provided by Cell-Mediated Immunity Cell-mediated IMMUNITY (CMI) helps protect the body through the ability to differentiate self from non-self. The non-self cells most easily recognized by CMI are cancer cells and self cells infected by organisms that live within host cells, especially viruses. CMI watches for and rids the body of self cells that might potentially harm the body. CMI is important in preventing the development of cancer and metastasis after exposure to carcinogens.

REVIEW OF IMMUNE RESPONSE 2

Cells associated with immune response All cells are derived from stem cells in the bone marrow and begin as either myeloid progenitor or lymphoid progenitor cells Myeloid - neutrophils, monocytes, eosinophils, basophils, and mast cells Lymphoid -B lymphocytes, mature T lymphocytes, and natural killer cells B and T lymphocytes As person is challenged by foreign antigens during life, specifity of lymphocytes to a specific antigen emerges process called "clonal selection" Re-exposure to same antigen the person will have more rapid and efficient immune reponse indicating a "memory" capacity for the immune system During fetal development produced in large numbers B-lymphocytes - Preprocessing and maturation occurs in the liver T-lymphocytes - maturation occurs in the thymus gland

EXAGGERATED IMMUNE RESPONSE / CONSEQUENCES 2

Chronic body-wide system disease Autoimmune disorder occurs when immune system attacks and destroys healthy cells of the "self" following a breakdown of what has ben termed "self tolerance" 80 autoimmune disorders identified - may have more than 1 simultaneously 3 potential outcomes for autoimmune disorder Destruction of body tissue Abnormal organ growth Change in organ function

Systemic Complications of IV Therapy

Circulatory overload Speed shock Allergic reaction Catheter embolism

NURSING INTERVENTIONS RELATED TO WOUND CARE

Cleansing/irrigating *Caring for a drainage device* Jackson-Pratt; Hemovac *Débriding a wound* Sharp Mechanical Chemical Enzymatic Autolysis

COLLABORATIVE CARE: SUPPRESSED IMMUNE RESPONSE

Clinical outcomes: Normal GI transit time Resolution of infection Adequate hydration Adequate nutrition Resolution of skin rash Restoration of adequate nutrition, body weight, and BMI

Fluid Balance

Closely linked to/affected by electrolyte concentrations Fluid intake Fluid loss Minimum urine amount needed to excrete toxic waste products = 400 to 600 mL Insensible water loss - through skin, lungs, stool

REVIEW OF IMMUNE RESPONSE 5

Complement system Works to enhance the immune response and help rid the body of antibody-antigen complexes Comprised of 25 proteins - circulate in an inactive form in the blood Engage in a cascade of interactions when the first protein molecule (C1) encounters an antigen-antibody complex Cascade is responsible for the dilation and ultimate leaking of fluid from the vascular system, leading to the redness and swelling during the inflammatory process

TRANSMISSION-BASED PRECAUTIONS Contactxl contxl

Contact Precautions Pathogen is spread by direct contact Sources of infection: draining wounds, secretions, supplies Precautions include Possible private room Clean gown and glove use Disposal of contaminated items in room Double-bag linen and mark book When to Use: Use contact precautions when direct contact with the patient or the patient's environment can lead to spread of the pathogen.This is the most common form of transmission. Draining wounds, dressings, patient supplies, and secretions are sources of infection. Indirect contact, or contact with fomites, can also transmit pathogens that spread by this method. *Patient Placement and Transport* ■ Ideally, consult with an infection preventionist for patient placement. ■ Place in a private room, if available. Private room provides the most effective protection. ■ If no private room is available, place patient in a room with a patient with an active infec- tion caused by the same organism and no other infections. ■ When transporting the patient, ensure that infected or colonized areas of the body are contained and covered. ■ Ambulatory care: Place the patient in an exam room or cubicle as soon as possible. Personal *Protective Equipment (PPE)* ppexl ■ Wear clean nonsterile gloves when touching the patient's intact skin. Don gloves on entry to the room. ■ Wear a clean gown if you anticipate your clothing may contact the patient or any contam- inated items in the room. ■ Remove PPE and observe hand hygiene before leaving the room.Take care that your skin and clothing do not contact environmental surfaces on the way out of the room. *Equipment, Supplies, and Environment* ■ Keep contact precaution supplies just outside the patient's room on a cart. ■ Double bag all linen and trash (or use a single waterproof bag), and clearly mark them contaminated. ■ Use disposable equipment (e.g., blood pressure cuffs) if possible; otherwise, clean and disinfect the equipment per institutional policy before removing them from the room and before use on another patient. ■ Ensure that the patient room is cleaned and disinfected at least daily. ■ Home care: Limit the amount of nondisposable equipment brought into the home. If possible, leave the equipment in the home until discharge from home care. ■ Home care: If equipment cannot remain in the home, clean and disinfect items before taking them from the home, or place them in a plastic bag for transport to a reprocessing area.

REVIEW OF IMMUNE RESPONSE 7

Dendritic cell function in an immune response Discovered 35 years ago; recognized as potent cells in asserting control from initiation to termination of the immune response; have "sentinel" function throughout the body as they look for foreign antigens and alert lymphocytes to the presence of injury or infection; they bind to antigens and then process and present them to both B and T Lymphocytes in an immune response. Found to directly activate helper and killer T cells Present cancer cells to cytotoxic T cells

TRANSMISSION-BASED PRECAUTIONS Dropletxl dropxl

Droplet Precautions Pathogen is spread via moist droplets Coughing, sneezing, touching contaminated objects -Precautions include Same as those for contact Addition of mask and eye protection within 3 ft of client book *When to Use*: Use droplet precautions when the pathogen can be spread via moist, large droplets (e.g., sneezing, coughing, talking). Droplets can spread infection by direct contact with mucous membranes or through indirect contact, for example, suctioning or touching a bedside table that was contaminated with moist droplets and then rubbing your eyes. *Patient Placement and Transport* ■ If no private room is available and the patient must be placed with patients who have a different infection, ensure that the patients are physically separated by more than 3 ft. Keep the privacy curtain closed.This minimizes contact between patients. Ideally, consult with an infection preventionist for patient placement.A private room provides the most effective protection. ■ Limit transport outside the room to medically necessary purposes; if transport is neces- sary, the patient should wear a mask.The transporter is not required to mask. *Personal Protective Equipment* ppexl ■ Keep droplet precaution supplies just outside the patient's room on a cart. ■ Wear a mask when working within 3 ft of the patient. Don the mask on entry into the room.Whether to wear goggles is an unresolved issue. Follow agency policy. ■ Change PPE and perform hand hygiene between contact with patients in the same room, regardless of whether one or both patients are on droplet precautions.

RISK FACTORS 3

Exaggerated immune response Gender, race, ethnicity SLE occurs more often in women than men by a 10:1 ratio and African Americans are 8 times more likely to contract the disease tan Caucasians/non-Hispanics Genetics May be minor and just an annoyance or may lead to destruction of normal tissue, loss of organ function, or death Environmental or food allergies (minor to severe) Environmental or medication exposure Foods, drugs, pollens, dust, molds, bee venom, vaccines, or serum may evoke a reaction (types I, II, or III) Generally does not happen with first exposure but with re-exposure However genetic predisposition by exposure by mother during fetal development may cause an exaggerated response on first exposure

Clinical Significance: Blood Pressure

Example of hydrostatic filtering forces, moving whole blood from the heart to capillaries where filtration occurs to exchange water, nutrients, and waste products between the blood and tissues

Interventions: Respiratory Acidosis Respiratory Acidosisxl

Focus is on improving ventilation and oxygenation, maintaining patent airway *Drug therapy* Bronchodilators Anti-inflammatories Mucolytics Oxygen therapy Pulmonary hygiene Ventilation support Prevention of complications

NURSING ASSESSMENT: SKIN AND WOUNDS

Focused skin assessment *Braden scale* (based on sensory perception, moisture, activity, mobility, nutrition, and friction or shear) Numeric value for six risk factors related to impaired skin integrity Total score <18 = risk book n scales. The Braden scale is used to identify persons at risk for developing pressure ulcers. The Braden scale evaluates six major risk factors: sensory perception, moisture, activity, mobility, nutrition, and friction and sheer (see the Focused Assessment box, The Braden Scale for Predicting Pressure Sore Risk). The final score reflects the patient's risk; the lower the score, the more likely the patient will develop a pressure ulcer. A score of 18 or less for hospitalized patients indicates risk. Interventions should be based on the individ- ual risk factors, as well as the total score. You should use this scale to assess the patient on admission to the facility and again in 48 to 72 hours. Studies have shown the second score to be more predictive, probably related to increased aware- ness of the patient's status. The Braden Q is a modified scale used in children. *Wound assessment* Location Size Appearance Drainage Redness Swelling

Clinical Significance: Diffusion

Free movement of particles (solute) across permeable membrane from area of higher to lower concentration Important in transport of most electrolytes; other particles diffuse through cell membranes Sodium pumps Glucose cannot enter most cell membranes without help of insulin

Hypotonic Solutions D2.5W, ½ NS, 0.33% NS aka 1/3

Go into the vascular space then shift out into the cells to replace cellular fluid (solutions cause fluid to move into the cells, leading to swelling and in some instances, bursting of cells). **ADMINISTER SLOWLY TO PREVENT CELLULAR EDEMA!! They rehydrate the client without causing HTN *Examples*: D2.5W, ½ NS, 0.33% NS aka 1/3 (**Hypo=hippo = solution >30%**) *Uses*: Client with HTN, cardiac or renal disease and needs fluid replacement due to N/V, burns, hemorrhage, etc. Also, for dilution when a client has hypernatremia( excessive na) or cellular dehydration-shrunk, so we need increase the volume inside of the cell. **Alert**: Watch for cellular edema find balance

Isotonic Solutions NS, LR, D5W, D5 ¼ NS

Goes into the vascular space and stays there Solution causes no fluid shift between compartments but rather expands circulating volume in the body. *Examples*: NS, LR, D5W, D5 ¼ NS *Uses*: Client has lost fluids through N/V, burns, sweating, trauma NS is the basic solution when administering blood products ***Alert*: DO NOT use these solutions in clients with HTN, cardiac disease, or renal disease ***Alert*These solutions can cause increase NA levels (when administering solutions that contain NA) and fluid volume excess--more fluid volume, that would increase our bp, which will increase the cardiac workload if they have renal dz and we are already retaining fluid on the body theyre not going to be able to get that fluid out

Acidosis: Patient-Centered Collaborative Care

History CNS changes *Neuromuscular changes* ↓ muscle tone, deep tendon reflexes *Cardiovascular changes* Early: ↑ heart rate, cardiac output changes Worsening: hyperkalemia; ↓ heart rate; T wave peaked and QRS widened; weak peripheral pulses; hypotension

Interventions: Metabolic Acidosis

Hydration *Drug therapy* Bi A Bicarbonate (only with low serum level) Insulin to treat DKA Antidiarrheals

Fluid & Electrolytes iv Solutions fluidsxl

I*sotonic (normal) Solutions* "Stay where *I* put it!" *Hyp*O*tonic Solutions* "DILUTE"- swollen rbc "Go *O*ut of the vessel" *Hyp*E*rtonic Solutions* "concentrated" "*E*nter the Vessel" shrunken rbc crenated

Types of Infusion Therapy Fluids

IV solutions (including parenteral nutrition) Blood and blood components Drug therapy

Remember...

If osmolarity is >600 mOsm/L, best infused in central circulation where greater low provides adequate hemodilution TPN has osmolarity >1400 mOsm/L TPN should never be infused in peripheral circulation—can damage blood cells and endothelial lining of vein

NURSING RESPONSE: INFLAMMATION

Imbalanced nutrition (less than body requirements) Caloric intake and protein Oxygenation Enteral nutrition

INFECTIOUS PROCESS

Immune responses to bacterial invasion: B lymphocytes are activated, resulting in the production of antibodies. T lymphocytes are activated, resulting in phagocytosis. Complement system is activated to enhance overall response. Bacteria release endotoxins or exotoxins, which damage the cells of the host and initiate an inflammatory response.

CLINICAL MANAGEMENT: PRIMARY PREVENTION

Immunizations Avoid high-risk behaviors Adequate nutrition Exercise Infection control measures

COLLABORATIVE CARE: EXAGGERATED IMMUNE RESPONSE 2

Immunosuppression Pharmacotherapy Corticosteroids Chemotherapeutic agents NSAIDs immunomodulators Pain Management Pharmacotherapy NSAIDs corticosteroids Hypothermia or hyperthermia treatments as appropriate Maintenance of mobility and physical activity

SUPPRESSED IMMUNE RESPONSE

Individuals who have a "hypo" or suppressed immune system are referred to as: Immunocompromised In a state of immunodeficiency Types of immunodeficiency primary - occurs as a results of improperly developed cells or an absence of cells required to execute immune responses Secondary - loss of immune functioning as a result of an illness or treatment Individuals are unable to provide adequate immune defense against invasion Leaves them at significant risk for infection Leaves them at risk for cancer if immunosuppression occurs over time due to loss or removal of mutating cells

DEFINE AND DESCRIBE THE CONCEPT OF INFECTION.

Infection is the invasion and multiplication of microorganisms in body tissues, which may be unapparent or the result of local cellular injury caused by competitive metabolism, toxins, intracellular replication, or antigen-antibody response. Simply put... When microorganisms capable of producing disease invade the body

RISK FACTORS: POPULATIONS AT GREATEST RISK

Infections potentially affect all individuals, regardless of age, gender, race, and socioeconomic status. Populations at greatest risk are the: Very young Poor Uninsured Residents of geographic areas where an infection is prevalent

RISK FACTORS: POPULATIONS AT GREATEST RISK

Inflammation can affect all individuals, regardless of age, gender, race, and socioeconomic status. The populations at risk for a severe or ineffective inflammatory response are the: Very young Very old Uninsured

Infection

Inflammation occurs in response to tissue injury as well as to infection by organisms. Infection is usually accompanied by inflammation; however, inflammation can occur without infection. Inflammation without infection includes joint sprains, myocardial infarction, and blister formation. Inflammation caused by noninfectious invasion includes allergic rhinitis, contact dermatitis, and other allergic reactions. Inflammations from infection include otitis media, appendicitis, and viral hepatitis, among many others. Inflammation does not always mean that an infection is present.

Remember...

Interventions to reduce infection risk: Clean needleless system connections before use with antimicrobial for 30 seconds Do not tape connections between tubing sets Use evidence-based hand hygiene guidelines from CDC and OSHA

Alternative Sites for Infusion

Intra-arterial therapy Intraperitoneal (IP) infusion Subcutaneous infusion Intraspinal infusion Intraosseous therapy

OPTIMAL IMMUNE RESPONSE

Involves the three protective functions: Protects the body from invasion of microorganisms and other antigens Removes dead or damaged tissue and cells Recognizes and removes cell mutations that have demonstrated abnormal cell growth and development To accomplish these functions system reacts with three lines of defense First: skin boundary surface includes (mucous membranes, enzymes, natural microbial flora, and complement proteins.) Second: activities of phagocytes, natural killer T lymphocytes, granulocytes, and macrophages Third: antibodies derived from B lymphocytes and the T lymphocytes

Diffusion

Is the free movement of particles (solute) across a permeable membrane from an area of higher concentration to an area of lower concentration (down a concentration gradient) This action controls the movement of solute particles in solution across various body membranes.

Osmosis

Is the movement of water only through a selectively permeable (semipermeable) membrane. In order for osmosis to occur, a membrane must separate two fluid spaces and one space must have particles that cannot move through the membrane (this membrane is impermeable to these particles). Isotonic fluids Hypertonic fluids Hypotonic fluids

Hemodialysis Catheter

Large lumens accommodate hemodialysis or pheresis procedure (harvests specific blood cells) Catheter-related bloodstream infections (CR-BSI), vein thrombosis are common problems Do not use for administering other fluids/medications (except in emergency)

Peripherally Inserted Central Catheter (PICC)

Length of 18 to 29 inches (45 to 72 cm) Chest x-ray determines placement *Power ICCs used for contrast * injection; can also attach to transducers for CVP monitoring

REVIEW OF IMMUNE RESPONSE 6

Lymphocyte function in an immune response B Lymphocyte response Plasma cells Memory cells Ig cells Immunoglobulins are primarily responsible for the body's response to invading bacteria and viruses and provide the humoral immunity component of an immune response T Lymphocyte response Undergo differentiation on exposure to a foreign antigen, developing into subtypes of cells that may directly attack the antigen or stimulate the activation of other leukocytes Cytotoxic T lymphocytes attack and kill antigens directly with preference for viruses or mutated cells that have become cancerous This process is termed "cellular or cell-mediated immunity" 7rl types of T lymphocytes (T cells) - 3 primary groups Helper T cells - (CD4) - helps in functions of the immune system by regulating most of the system's functions via the protein mediators, lymphokines. They direct and encourage other T cells and also help to activate B lymphocytes Cytotoxic T cells - "killer cells" - directly kill foreign antigens and may kill cells of the self supxl Suppressor T cells - suppress the function of both helper and cytotoxic T cells in order to prevent hyperimmune responses evolve Suppressor T-cells prevent hypersensitivity (allergy) (IMMUNITY overreactions) on exposure to non-self cells or proteins preventing the formation of antibodies directed against healthy self cells, which is the basis for many autoimmune diseases. Complement system response 25 primary proteins Amplifying and increasing the efficiency and efficacy of the other components of the immune system Contributes to the inflammatory response

REVIEW OF IMMUNE SYSTEM ANATOMY AND PHYSIOLOGY

Lymphoid tissues Leukocytes (WBCs) Neutrophils-.62% is a normal segmented neutrophil- 55%-70% of total WBCs- and refers to mature neutrophils, which, along with macrophages, eliminate invaders (infection) by phagocytosis. *function*Phagocytize pathogens- *Granular WBCs* Monocytes-3%-8% of total WBCs- *function* Able to phagocytize directly as well as to differentiate into macrophages, which help clean up damaged tissue, infection, and cellular debris. Percentage increases in tuberculosis, protozoal, and rickettsial infections. *Agranular WBCs* Eosinophils-1%-3% of total WBCs- most active against infestations of parasitic larvae and also limits inflammatory reactions. Some eosinophil granules contain enzymes that degrade the vasoactive chemicals released by other leukocytes. This is why the number of circulating eosinophils increases during an allergic response. *function* Bind to helminthes and release toxins to destroy them; mediate allergic reactions; have limited role in phagocytosis. Percentage increases in parasitic infections. *Granular WBCs* Basophils- 0.5%-1% of total WBCs; an elevated count indicates inflammation--cause the signs and symptoms of inflammation.---Basophil function acts on blood vessels with heparin, histamine, serotonin, kinins, and leukotrienes. *** *function* Release histamine and heparin granules as part of the inflammatory response. Percentage normal during infections.---*Granular WBCs* Lymphocytes-28% is a normal count in the differential-Lymphocytes are the cells needed for long-lasting antibody-mediated immunity (AMI) and cell-mediated immunity (CMI).- 20%-35% of total WBCs *function* T cells—responsible for cell-mediated immunity; recognize, attack, and destroy antigens. B cells—responsible for humoral immunity; produce immunoglobulins to attack and destroy antigens. Percentage of total lymphocytes increases in viral infection and chronic bacterial infection; decreases in sepsis.---*Agranular WBCs* Immune response Types of immunity evolve For bands, 4% is a normal count. Bands are elevated only when an infection is present and the bone marrow cannot keep up with mature segmented neutrophils.

Vascular Access Devices

Major types: Short peripheral catheters Midline catheters Peripherally inserted central catheters (PICC) Nontunneled percutaneous central venous catheters (CVC) Tunneled catheters Implanted ports Hemodialysis catheters

Closing....Keys to success

Make sure that you have reviewed your lecture notes, PPT, handouts, case studies Make sure you have reviewed the objectives at the beginning of the chapter. Make sure to have reviewed the key points at the end of the chapter. Make sure that you have reviewed the ATI skill modules

Administering iv Medications

Medication safety Rapid therapeutic effect Never assume IV administration is same as giving that drug by other routes Prescribing infusion therapy

Practical Nurses (PNs) lpnxl

Monitoring findings (as input to the RN's ongoing assessment) Reinforce client teaching from a standard care plan Performing tracheostomy care Suctioning Checking NG tube patency Administering enteral feedings Inserting a urinary catheter Administering medications

self-tolerance

Non-self proteins and cells include infected body cells, cancer cells, cells from other people, and invading organisms. Recognizing self versus non-self is called self-tolerance. This action prevents IMMUNITY from harming healthy body cells. Self-tolerance is possible because of the different proteins present on cell membranes. • WBCs are the only body cells able to recognize non-self cells and to attack them.

iv solutions

Normal serum osmolarity (adults) = 270 to 300 mOsm/L: Isotonic = 270 to 300 mOsm/L Hypertonic = fluids >300 mOsm/L Hypotonic = fluids < 270 mOsm/L

A WOUND FOR SPECIAL CONSIDERATION: PRESSURE ULCER

Nurses play a major role in prevention and treatment Pressure ulcers affect 15% of hospitalized clients They are caused by unrelieved pressure to an area, resulting in ischemia

CONSEQUENCE OF UNCONTROLLED INFECTION

Once the body's compensatory mechanisms (e.g., vascular, renal, nervous, respiratory) are overcome, the following process occurs.

REVIEW OF IMMUNE RESPONSE 4

Phagocytes Found throughout the body Responsible for recognizing and ingesting foreign antigens as they enter body Macrophages and neutrophils are primary phagocytes - first line of defense - macrophages are more effective than neutrophils Macrophages stored in connective tissues, spleen, liver, and lining of respiratory and GI tracts Neutrophils stay circulating n the blood Phagocytosis is the process of ingesting cellular material and involves the ability of phagocytes to be selective in recognizing cells that must be ingested and discarded. "self" cells - smooth and covered with smooth proteins "non-self" - antibody-antigen complexes are rougher surfaces and are particularly susceptible to phagocytic functioning book To protect without causing harm, immune system cells exert actions only against non-self proteins and cells. Immune system cells can distinguish between the body's own healthy self cells and non-self proteins and cells.

Tunneled Central Venous Catheter

Portion lies in subcutaneous tunnel Used for frequent and long-term infusion therapy Has cuff of antibiotic-containing material to help reduce infection

Interventions: Alkalosis

Prevent further losses of hydrogen, potassium, calcium, chloride ions Restore fluid balance Monitor changes, provide safety Modify or stop gastric suctioning, IV solutions with base, drugs that promote hydrogen ion excretion

SUPPRESSED IMMUNE RESPONSE 2

Primary immunodeficiency (PI) Situation wherein the entire immune defense system is inadequate and the individual is missing some or all of the components necessary for a complete immune response NIH identified 70 types of immunodeficiencies 10 warning signs - consider PI if 2 or more are present 4 or more new ear infections w/in 1 year 2 or more serious sinus infections w/in 1 year 2 or more months taking antibiotics with little effect 2 or more pneumonias w/in 1 year Failure of an infant to gain weight or grow normally Recurrent, deep skin or organ abscesses Persistent thrush in mouth or fungal infection on skin Need for IV antibiotics to clear infections 2 or more deep-seated infections including septicemia Secondary immunodeficiency Other health problems develop for immunocompromised patients Increase in incidence of infection by bacteria and viruses Development of super-infections (MRSA, C-Diff) Development of treatment-resistant fungal infections secondary to antibiotic treatment for primary bacterial infections

Acidosis: Patient-Centered Collaborative Care

Respiratory changes Kussmaul respiration Skin changes (metabolic and respiratory acidosis) Warm, dry, and pink (vasodilation) Psychosocial assessment

CLINICAL MANAGEMENT: COLLABORATIVE INTERVENTIONS

Rest, ice, compression, elevation (RICE) Most helpful after sprain, strain, or trauma- Wounds caused by trauma have a greater risk of infections and slower healing Helps minimize swelling Most beneficial for the first 24 to 48 hours after injury General discussion questions What is the best method for applying ice? What should the nurse monitor? After applying a compression device, the nurse should monitor for what developments? How high is "high enough" when elevating an extremity?

Electrolytes normal lab labsxl values

Sodium 136-145 mEq/L Potassium 3.5-5.0 mEq/L Calcium 9.0-10.5 mg/dL Magnesium 1.3-2.1 mEq/L Chloride 96-106 mEq/L Phosphate 3.0-4.5 mg/dL

Specialized Infusion Team

Specially trained nurse initiates and maintains infusion therapy Teams promote cost savings, patient satisfaction, patient outcomes

Specific Immunity

Specific IMMUNITY is an adaptive protection that results in long-term resistance to the effects of invading microorganisms. This means that the responses are not automatic, which is why specific immunity is also known as acquired immunity. The body has to learn to generate specific immune responses when it is infected by or exposed to specific organisms. Lymphocytes develop actions and products that provide true immunity. These cells develop specific actions in response to specific invasion (Fig. 17-7). The two divisions of specific immunity are antibody-mediated immunity and cell-mediated immunity. As indicated by Fig. 17-4, activation of both types of specific immunity require interactions with actions and cells of innate immunity.

Foods High in Magnesium magxl

Spinach Mustard Greens Summer Squash Broccoli Halibut Turnip Greens Pumpkin Seeds Peppermint Cucumber Green beans Celery Kale Sunflower Seeds Sesame Seeds Flax Seeds

IMPLEMENTING CDC GUIDELINES

Standard Precautions Protects healthcare workers from exposure Decreases transmission of pathogens Protects clients from pathogens carried by healthcare workers

LINES OF DEFENSE AGAINST INFECTION

Tertiary Defenses *specific immunity*: the process by which the body's immune cells "learn" to recognize and destroy pathogens they have encountered before. The cells involved in specific immunity are the *lymphocytes*, WBCs produced from stem cells in the red bone mar- row. B lymphocytes, or B cells, grow to maturity in the bone marrow, whereas T lymphocytes, or T cells, mature in the thy- mus. After maturing, most B cells and T cells travel to the lymph nodes, spleen, and other sites of lymphatic tissue. Some circulate in blood and lymph. From all of these loca- tions, lymphocytes seek out foreign cells and other matter to target for destruction. Lymphocytes recognize foreign substances by the molecules present on their surfaces. These molecules that trigger a specific immune response are called antigens. Humoral immunity- pg 611 bn book Antibody-mediated immunity (AMI) (also known as humoral immunity) can be transferred from one person or animal to another.==Circulating antibodies can be transferred from one adult to another and provide the receiving adult with immediate short-term immunity. B-cell production of antibodies in response to an antigen Cell-mediated immunity The cells and actions of cell-mediated immunity control and coordinate the entire inflammatory and immune responses. Cell-mediated IMMUNITY (CMI) protects the body through differentiation of self from non-self. These are important in preventing the development of cancer and metastasis after exposure to carcinogens. Direct destruction of infected cells by T cells

Acid-Base Control Action& Mechanisms: Kidneys

Third line of defense against pH changes Stronger for regulating acid-base balance; take longer than chemical and respiratory Kidney movement of bicarbonate, kidney is seen by ct scan. Formation of acids Formation of ammonium

STEPS IN AN ACUTE INFLAMMATORY RESPONSE

Tissue injury and the release of chemical mediators Vasodilation and increased blood flow Swelling and retraction of activated endothelial cells Increased vascular permeability and leakage of small plasma proteins "Walling off" Movement of immune response cells to the site of injury Exudate formation Movement of glucose and oxygen to the site needing repair Release of chemical repair factors from activated endothelial cells

Transplant Rejection

Transplant rejection is caused by general and specific immunity functions of a host directed against tissues and organs transplanted from other people. Host natural killer (NK) cells and cytotoxic/cytolytic T-cells are the major cells responsible for the destructive attacks on transplanted organs (grafts) leading to host rejection of these helpful tissues. Because the solid organ transplanted into the recipient (host) is seldom a perfectly identical match of human leukocyte antigens (HLAs) (unless the organ is obtained from an identical sibling) between the donated organ and the recipient host, the patient's immune system cells recognize a newly transplanted organ as non-self. Without intervention, the recipient's immune system starts immunologic actions that destroy these non-self cells, leading to rejection of the transplanted organ. Rejection is a complex series of responses that change over time and involve different components of IMMUNITY. Rejection can be hyperacute, acute, or chronic.

Fluid Output

Urine: 1,500 mL/day Minimum 30ml/day - acknowledge kidney function Skin: perspiration Lungs: exhalation Feces: 100-200 mL/day

Hypertonic Solutions--- D10W, 3% NS, 5% NS, D5LR, D5 ½ NS, D5 NS, TPN, Albumin

Volume expanders that will draw fluid into the vascular space from the cell (solutions cause fluid to move out of the cells, resulting in shrinkage of the cells). *Examples*: D10W, *3%* NS, *5%* NS, D5LR, D5 ½ NS, D5 NS, TPN, Albumin (***hyper people are skinny, skinny people = tiny #'s <30%***) *Uses*: Client with hyponatremia or a client who has shifted large amounts of vascular volume to a third space3rd or has severe edema, burns, or ascites *Alert* Must watch for fluid volume excess, monitor in an ICU setting with frequent monitoring of BP, P, and CVP especially if they are receiving *3% NS or 5% NS*

HAND WASHING GUIDELINES

Wash for at least 15 seconds in nonsurgical setting; 2-6 minutes in surgical setting. Remove jewelry and clean beneath fingernails. Use a bactericidal solution or use water if hands are visibly soiled. Use warm water, not hot Apply soap to wet hands Use friction Rinse soap Towel or hand dry

Body Fluid

Water is the primary body fluid Water content varies with age, sex, adipose tissue Water contains solutes Electrolytes Nonelectrolytes Homeostasis - proper functioning of all body systems; requires fluid and electrolyte balance

Sources of Acids & Bicarbonate

When acid is present, free hydrogen ions dissociate and must be controlled for pH balance Body continuously generates acids and hydrogen ions as metabolism waste products

Acid-Base Control Actions & Mechanisms: Respiratory

When chemical buffers alone cannot prevent blood pH changes, respiratory system is second line of defense: Hyperventilation Hypoventilation

WASH YOUR HANDS birthday

When you arrive in the unit Use soap and water if there is potential for exposure to Bacillus anthracis (or other spore-producing bacteria such as C. difficile). Alcohol-based solutions are not effective against spores. When you leave the unit Before and after restroom use Before and after client contact Before and after contact with client belongings Before gloving After glove removal Before and after touching your face Before and after eating After touching a contaminated article When you see visible dirt on your hands

labsxl--- Common Tests for Evaluating the Presence of or Risk for Infection

White blood cell (WBC) count with differential- 5,000-10,000/mm3. Leukocyte (WBC) count-4,500-11,000/mm3 func Usually done as a part of a complete blood count (CBC) but may be ordered as an independent test.WBCs may increase when a wound develops; continued elevation may signal infection.A lowWBC count may delay wound healing. Leukocytes are responsible for an inflammatory reaction at the wound site, phagocytosis of bacteria and cellular debris, and the creation of antibodies. --Serum protein- 6.0-8.0 g/dL --Serum albumin- 3.4-4.8 g/dL ----Serum prealbumin- 12-42 mg/dL func Low serum levels indicate limited nutritional stores that delay wound healing or place the patient at high risk for pressure ulcers. Serum protein may be monitored as an indicator of the ability to heal a wound or prevent a pressure ulcer. Serum protein and albumin levels are closely related. However, both fluctuate slowly.A more accurate measure of a patient's immediate protein stores is reflected in prealbumin level. Coagulation studies: Partial thromboplastin time, activated (aPTT)- Varies with respect to equipment and reagents used. Critical values: >70 sec or <53 sec Prothrombin time (clotting time)- Critical values: >20 sec (uncoagulated) or 3 times normal control (anticoagulated) International normalized ratio (INR)- < 2.0 for patients not receiving anticoagulation therapy; 2.0-3.0 for those receiving coagulation therapy Blood cultures- A sample of blood placed on culture media and evaluated for growth of pathogens. Normally, should show no growth of infectious microorganisms. Urine cultures- Urine is normally sterile with no microorganism growth. Throat cultures, wound cultures-Presence of microorganisms is normal, but there should be no growth of infectious microorganisms.To yield the most reliable results, blood cultures should be obtained from peripheral sites, using venipuncture by trained phlebotomists, unless a culture is specifically ordered from a central catheter or peripherally inserted central catheter. Disease titers- Blood tests for specific disease immunity (e.g., to rubella) Panels to evaluate specific disease exposure-Blood tests to evaluate exposure to specific diseases (e.g., HIV, hepatitis) Immunoglobulin (IgG, IgM) levels- Blood tests to evaluate humoral immunity status C-reactive protein (CRP)- A blood test to measure inflammatory change or bacterial infection Agglutinins, warm or cold- Used to diagnose atypical infections by detecting antigens in the blood Erythrocyte (red blood cell) sedimentation rate (ESR or sed rate)- A measure of inflammatory changes. Sed rate increases with inflammation. Normally it is at 15 mm/hr for men and < 20 mm/hr for women. Erythrocyte sedimentation rate (ESR) -Younger than 50 yr: 0-15 mm/hr; -older than 50 yr: 0-20 mm/hr Iron level- Normally 60-90 g/100 mg. Lower in chronic infection.

Laboratory Assessment: metabolic acidosis

pH < 7.35 Bicarbonate < 21 mEq/L PaO2 normal PaCO2 normal or slightly decreased Serum potassium high

Respiratory Alkalosis

watkins cause of Respiratory Alkalosis is respiratory. *panic attack s/s- anxious* light headed, tingling around there mouth(numb) aka peri-oral numbness, also numbness in finger and feet bc they are not taking in alot of o2, so it goes to the major organs 1st and the furthest away is hands and feet, less oxygenated bld to hands and feet, wants to get oxygenated bld to hand/heart first *Hyperventilation* ct breathing too fast, and removing co2. pts do this when they are having a panic attack. if we start having Respiratory Alkalosis, we have them breath into a paper bag to bring back co2. try and get them to slow down there breathing, good breaths in nose out of mouth to slow it down. if they cant calm down and theyre still hyperventalating, they may have to be sedated. *another cause is acute aspirin overdose/ antidote is acetylsalic acid mucomyst/monitor there abg's* ----------------- *Hyperventilation*—anxiety, fear, improper vent settings, stimulation of central respiratory center due to fever, DNS lesion, salicylates

Respiratory Acidosisxl decrease o2 increased co2 acidxl

watkins cause of respiratory acidosis is respiratory. Respiratory function is impaired, causing problems with O2 and CO2 *hypoventilation* co2 is being RETAINED bc bad lungs bc of pneumonia post-op, pt at risk for pneumonia, we teach them cough and deep breath/ incentive spirometer. if the pt is 2 yrs they can blow bubbles expands lungs. car wreck= collapsed lungs/pneumothorax, pneumothorax treatment is with chest tube put in by physician mid-abdominal incision- shallow breathing, keeping in co2...s/s for retaining co2= lethargic, dizzy, confused, h.a, sleepy, worst case scenario comatose, unconscious. decrease o2 increase co2 leading to unconscious *2 early signs s/s of hypoxia* tachycardia, restlessness,... anxiety ---1st thing we do is assess for a patent airway= give o2. 6 things to do for pneumonia? 1. mucolytics- mucinex 2. deep breathing exercises 3.give fluids/water, 4. postural drainage to put them into position to help drain aka percussion 5. suctioning 6. high fowlers -------------------------- *Retention of CO*: *Respiratory depression bc opiods/narcotics/chronic users of sleeping pills* *air*xl Airway obstruction Inadequate chest expansion Reduced alveolar-capillary diffusion

COLLABORATIVE CARE: EXAGGERATED IMMUNE RESPONSE 1 abc

watkins client is having an anaphylaxis reaction,what would u do 1st? -assess for a patent airway *Anaphylaxis* Support of airway, breathing, and circulation Subcutaneous epinephrine if type 1 reaction Other bronchodilators Intubation and ventilator support Circulatory volume expanders Vasopressors (raises bp) to maintain blood pressure and circulating volume *Pharmacotherapy* Subcutaneous epinephrine if type 1 reaction Other bronchodilators *Education:* Avoiding contact with pathogen initiating anaphylactic response, proper use of an EpiPen for self-administration of epinephrine

laboratory assessment respiratory acidosis

watkins give o2 2 make it go up *ps ps ps* pH < 7.35 Serum potassium levels elevated (if acute acidosis) PaO2 low Serum potassium levels normal or low (if renal compensation present) PaCO2 high Serum bicarbonate variable

Compensation

watkins kidneys remove acid through urine, filter excrete waste and absorb stuff we want. kidneys work slow. hours-days lungs work faster than kidneys ------------------------------- Body attempts to correct blood pH changes pH < 6.9 or >7.8 usually fatal Respiratory system more sensitive to acid-base changes; can begin compensating in seconds to minutes Kidneys more powerful; result in rapid changes in ECF composition; fully triggered for imbalance of several hours to days

breaking the chain of infection

watkins the biggest way to prevent infection is: 1.educating pts to wash there hands 2. proper ppe 3. keep areas dry and clean ■Reduce exposure to pathogens through the use of aseptic technique (discussed shortly). Make sure your healthcare providers clean their hands before they touch you.This is one of the most important infection prevention and control measures. Wash your hands often with soap and water.Wash for 15 to 30 seconds, or as long as it takes to sing the "Happy Birthday" song. Handwashing involves five key factors: time, water, soap, friction, and drying. Use alcohol-based hand sanitizer if soap and water are not available or hands are not visibly soiled. Sanitizer should contain at least 60% alcohol. ■Maintain skin integrity and support natural defenses against infection. ■Reduce stress. ■Promote immune function through collaborative care. ■Provide supportive measures to decrease the length of time that a patient needs invasive devices, such as intravenous lines and urinary catheters. other stuff Specific nursing activities will be based on the unique situa- tion of the client, as described in the etiology of the diagnostic statement. For example: For clients who have had surgery and general anesthesia or who are at risk for pneumonia, promote coughing and deep breathing on a regular basis *For clients being mechanically ventilated, provide special oral care designed to prevent ventilator-associated pneumonia.* (See the accompanying QSEN box for an example.) *For clients who have breaks in the skin or incision sites, provide regular assessment for infection status* and follow appropriate medical or surgical asepsis guidelines. For all clients at risk for infection, provide care that is based on principles of medical asepsis. For all clients at risk for infection, provide care that is based on principles of medical asepsis Community health nurses can limit disease transmission through surveillance of the community, tracking of disease patterns, and initiation of prompt treatment *For clients who are at risk for disease* based on age, debili- tated state, congregate living arrangement, or employment in healthcare facilities, facilitate participation in *vaccination programs*, which can *help* them *acquire immunity* from some communicable diseases. Other preventive *nursing activities* are discussed in the following sections. They *include providing client teaching, supporting host defenses, and practicing medical and surgical asepsis*.

Metabolic Alkalosis alkxl

watkins upper, loss of upper gi content. emesis, irritation from too many antacids/tums. 1. observe for a level of consciousness, 2. throwing up or ng tube ngxl 3. level k+ would be *low*. 4. low potassium causes muscles cramps, 5. arrthymias, 6. charley horse, if potassium is low it needs to be replaced. iv fluids, pills, capsules, --------------- Base excess—excessive intake bicarbonates, carbonates, acetates, citrates Acid deficit—prolonged vomiting, excess cortisol, hyperaldosteronism, thiazide diuretics, prolonged NG suction

REVIEW OF IMMUNE RESPONSE 3 iggxl

watkins which immunogoblin is responsible for allergic symptoms? ige the primary immunogoblin that crosses the placenta barrier is? igg ---------------- *watkins* *Antibody production is Secreted by B lymphocytes* t-helper cells B-lymphocyte-Becomes sensitized to foreign cells and proteins with the assistance of macrophages and helper-inducer T-cells wbc- fight the infection rbc- carry o2 --------------- Antibodies or immunoglobulins (Ig) - formed after encounter and engulfing of an antigen and then interacts with helper T lymphocytes *mega d* *IgM* - remains in the blood and efficiently kill bacteria; largest of the immunoglobulins; first antibody produced with an initial immune response-- ■ IgM is the first antibody to appear when an antigen is encountered. *IgE* - responsible for allergy symptoms and increased in the presence of parasitic worms; normally found in trace amounts- *IgG* - primary immunoglobulin; may enter tissue spaces, selectively crosses the placenta, coats antigen for more effective and effcient presentation for an immune response; *binds to macrophages and neutrophils for increased phagocytosis*- ■ IgG is the most common immunoglobulin in the body. It takes at least 10 days for IgG to be produced in response to an initial infection. *IgA* - protects entrance to the body; found in high concentrations in body fluids (*tears, saliva, secretions of the respiratory and GI tracts*)- IgA antibodies are secreted by mucous membranes around body openings, providing additional protection for these portals of entry. *IgD* - found within the cell membrane of B lymphocytes- IgD antibodies form on the surface of B cells and trap potential pathogens.

ACQUIRED IMMUNITY acqxl

watkins: acquired immunity is gained through? after birth ------------------ *watkins:* passive immunity is gained through? passive meaning passed from one person to another, colustrum is the term for the 1st breast milk that comes in from mom. that is what she is going to pass on that has the most antibodies and pass on to the baby. if a baby is preterm this is where we try to educate moms to really get that colostrum to the babies, so they can breastfeed, or pump and give it in a bottle or syringe *the colostrum is full of antibodies that we want baby to get* -------------- *ACQUIRED IMMUNITY acqxl* Refers to immunity protection that is gained after birth either actively or passively *Actively* actxl Develops after the introduction of a foreign antigen resulting in the formation of antibodies or sensitized T lymphocytes Examples: Immune response to an immunization (artificial) Exposure to infectious pathogens like chicken pox (natural) *Passively* Occurs by the introduction of preformed antibodies either from an artificial or natural routes Examples: Transfusion of immunoglobulin (IgG) From mother to fetus thru placental blood transference or colostrum transfer during breastfeeding book Natural passive IMMUNITY occurs when antibodies are passed from the mother to the fetus via the placenta or to the infant through colostrum and breast milk. evolve With passive IMMUNITY, the body receives antibodies that were developed in another person's body. These antibodies are recognized as foreign and are eliminated quickly. For this reason, *passive immunity is only an immediate, short-term protection* against a specific antigen. book Passive IMMUNITY occurs when the antibodies against an antigen are transferred to a human after first being made in the body of another human or animal. Because these antibodies are foreign to the receiving human, they are recognized as non-self and eliminated quickly. For this reason *passive immunity provides only immediate, short-term protection* against a specific antigen. It is used when an adult is exposed to a serious disease for which he or she has little or no actively acquired immunity. Instead the injected antibodies are expected to inactivate the antigen.

artificial immunity artxl

watkins: artificial immunity is gained through? immunizations immunizations is something that someone does into the lab and makes, so they are artificially gained, but we gain immunity from them ----------- Vaccinations cause artificial active IMMUNITY and require boosters for best long-term effects. Because the antigens used have been processes to make them less likely to grow in the body (attenuated), this exposure usually does not cause the disease. book Artificial active IMMUNITY is the protection developed by vaccination or immunization. This type of immunity is used to prevent serious and potentially deadly illnesses (e.g., *tetanus, diphtheria, polio*). Small amounts of specific antigens are placed as a vaccination into your body. Your immune system then responds by actively making antibodies against the antigen. Because antigens used for this procedure have been specially processed to make them less likely to grow in the body (attenuated), this exposure usually does not cause the disease. Artificial active immunity lasts many years, although repeated but smaller doses of the original antigen are required as a "booster" to retain the protection.

SUPPRESSED IMMUNE RESPONSE 1 supxl

watkins: identify the person at risk for having a suppressed immune function. -older adults, post-op if we have a 22 year old post-op and a 69 marathon runner, my post-op is going to over top my age. *post-op supersedes* Marathon running can suppress immune system and break it down and weaken it. when u get to that point where ur in shape and doing it all the time, when training, it can suppress ur immune system, but it does not precede a post-op pt have to look at what type of sx. laparoscopic sx compared to an open heart sx that going to make a big difference *Laparoscopy is an operation performed in the abdomen or pelvis through small incisions with the aid of a camera. The laparoscope aids diagnosis or therapeutic interventions with a few small cuts in the abdomen -------- Inadequately functioning immune system leaves the individual immunocompromised - all body systems are affected The two major types of problems that result from suppressed immune response are Infection Cancer - a depressed immunce system may be created with medications in order to avoid rejection of transplanted tissue or it may be induced as a result of treatment for various types of cancer. Assess client for cancer - use mnemonic CAUTION **'C.A.U.T.I.O.N.' : *C*: Change in bowel or bladder habits. *A*: A sore that does not heal. *U*: Unusual bleeding or discharge. *T*: Thickening or lump in the breast or elsewhere. *I*: Indigestion or difficulty in swallowing. *O*: Obvious change in a wart or mole. *N*: Nagging cough or hoarseness. In treatments of some leukemia: destruction of the bone marrow before healthy stem cells may be reintroduced and a health immune system regrows During process immune system is partially destroyed leaving individual immunocompromised In multiple myeloma, Hodgkin's disease and non-Hodgkin's lymphomas: Directly lead to immune system dysfunction and immunocompromise

INNATExl IMMUNITY innxl

watkins: innate immunity is present at birth innate immunity is what you're born with. so it comes from mom. we do not have alot of immunity when we are first born, someone who is preterm is going to have less immunity than someone who goes to term bc they havent had time to get all of that immunity from mom. *innate immunity is in the womb* Also referred to as natural or native evolve *Natural, active IMMUNITY is the most beneficial and long lasting type of immunity.* book natural active IMMUNITY occurs when an antigen enters your body naturally without human assistance and your body responds by actively making antibodies against that antigen (e.g., influenza A virus). Usually the invasion that triggers antibody production also causes the disease. However, processes occurring in your body at the same time as infection create immunity to that antigen so illness does not occur again after a second exposure to the same antigen. *Natural active immunity is the most effective and the longest lasting*. ---Active immunity occurs when antigens enter a human and he or she responds by making specific antibodies against the antigen. This type of IMMUNITY is active because the body takes an active part in making antibodies. Innate, native IMMUNITY is any natural protective feature of a person. It can be a barrier to prevent organisms from entering the body or can be an attacking force that eliminates organisms that have already entered the body. -- This is immunity present at birth Provides non-specific response not considered antigen specific Any natural protective feature of a person Provides immediate protection against effects of tissue injury and foreign proteins—critical to health and well-being Causes visible symptoms and can rid body of harmful organisms; tissue damage may result from excessive response

General Immunity: Inflammationxl infxl natxl

watkins: natural immunity is gained through? having the disease our body is developing the immunity, we have the disease, ans were naturally making those antibodies, people who had chicken pox, gained natural immunity from chicken pox. people who had the chicken pox vaccine, have artificial immunity having the disease ur making the antibodies urself bc ur exposed to it * placenta is the same as innate means ur getting it from mom*, so u r not making ur own immunity, ur getting what ur mom has, so it comes from mom---> placenta---> to baby ------------------ *The inflammatory responses, the skin, mucosa, antimicrobial chemicals on the skin, complement, and natural killer cells compose general immunity*. *the leukocytes (white blood cells [WBCs]) involved in inflammation are neutrophils, macrophages, eosinophils, and basophils. An additional cell type important in inflammation is the tissue mast cell. Neutrophils and macrophages destroy and eliminate foreign invaders. Basophils, eosinophils, and mast cells release chemicals that act on blood vessels to cause tissue-level responses that help neutrophil and macrophage actions.* ****General immunity is nonspecific and is also called innate-native immunity or natural immunity. With inflammation, general immunity provides immediate protection against the effects of tissue injury and invading foreign proteins. Innate-native immunity is any natural protective feature of a human. It is a barrier to prevent organisms from entering the body and can attack organisms that have already entered the body. This type of IMMUNITY cannot be transferred from one adult to another and is not an adaptive response. *The inflammatory responses, the skin, mucosa, antimicrobial chemicals on the skin, complement, and natural killer cells compose general immunity*. Inflammation is critical for health. General immunity and inflammation differ from specific immunity in two ways: • Inflammatory protection is immediate but short term. It does not provide true immunity on repeated exposure to the same organisms. • Inflammation is a nonspecific body defense to invasion or injury and can be started quickly by almost any event, regardless of where it occurs or what causes it. So inflammation triggered by a scald burn to the hand is the same as inflammation triggered by bacteria in the middle ear. How widespread the symptoms of inflammation are depends on the intensity, severity, and duration of exposure to the initiating event. For example, a splinter in the finger triggers inflammation only at the splinter site, whereas a burn injuring 50% of the skin leads to an inflammatory response involving the entire body. Inflammation starts tissue actions that cause visible and uncomfortable symptoms that are important in ridding the body of harmful organisms. However, if the inflammatory response is excessive, tissue damage may result. Inflammation also helps start both antibody-mediated and cell-mediated actions to activate full IMMUNITY. *The inflammatory responses, the skin, mucosa, antimicrobial chemicals on the skin, complement, and natural killer cells compose general immunity*. *the leukocytes (white blood cells [WBCs]) involved in inflammation are neutrophils, macrophages, eosinophils, and basophils. An additional cell type important in inflammation is the tissue mast cell. Neutrophils and macrophages destroy and eliminate foreign invaders. Basophils, eosinophils, and mast cells release chemicals that act on blood vessels to cause tissue-level responses that help neutrophil and macrophage actions.*

OPTIMAL IMMUNE FUNCTIONING optxl

watkins: what does it mean to have an optimal immune function? it protects the body from invasion of microorganisms abnormal cell growth is cancer which is not the optimal response ---------- Clinical indicators of optimal immune functioning reveal an individual who: Generally appears well - and well nourished Vital signs WNP for age Lymph nodes are soft, movable, non-tender Older adults may not have palpable ones Wounds are healing within a timeframe of "normal" for type of wound

EXAGGERATED IMMUNE RESPONSE / CONSEQUENCES 1 exxl

watkins: what is an ex of an exaggerated immune response? anaphylaxis ------------ Four types of exaggerated immune response - hypersensitivity reactions *Type 1* - IgE-mediated or atopic "allergic" Seasonal allergies rhinitis, bee sting Systemic anaphylactic reactions (bee sting) *Type 2* - tissue-specific or cytotoxic Autoimmune thrombocytopenic purpura, Graves' disease, autoimmune hemolytic anemia *Type 3* - immune complex-mediated Systemic lupus erythematosus *Type 4* - cell-mediated or delayed hypersensitivity Contact sensitivity to poison ivy and metals (jewelry)

SUPPRESSED IMMUNE FUNCTIONING * supxl

watkins: which s/s may a ct complain of suppressed immune system? malaise ------------ SYMPTOMS Report of frequent infections Report of poor wound healing Fatigue Malaise Weight loss *CLINICAL FINDINGS* May appear poorly nourished or have wasting syndrome May have chronic wounds May have enlarged lymph nodes Presence of opportunistic infection *Note: Symptoms and clinical findings vary widely based on the severity of the problem.

THE SPREAD OF INFECTION: SIX LINKS

watkins: 2chains infectious agent can be infected by different things. bacteria,virus,fungi and thats going to determine how we tx them. they all do not get antibiotics! I will do a culture, to see what kind of drug. like a broad spectrum antibiotics to make sure were getting the right thing for that agent *INFECTIOUS AGENTS* Pathogens Normal flora that become pathogenic book-Infectious Agent Some microorganisms live on or in the human body without causing harm. For instance, the Staphylococcus bacteria growing on human skin are usually harmless. Other microorgan- isms are beneficial or even essential for human health and well-being. They are referred to as normal flora. *Normal flora* in the intestine aid in digestion; synthesize vitamin K; and release vitamin B12, thiamine, and riboflavin when they die. In addition, they limit the growth of harmful bacteria by compet- ing with them for available nutrients. There are two types of normal flora: transient and resident. *Transient flora* are normal microbes that a person picks up by coming in contact with objects or another person (e.g., when you touch a soiled dressing). You can remove these with hand- washing. *Resident flora* live and multiply harmlessly deep in skin layers. They are permanent inhabitants of the skin, and cannot usually be removed with routine handwashing. *Pathogens* are microorganisms capable of causing disease. In fact, the precise accepted definition of the term *infection* is successful invasion of and multiplication in the body by a pathogen). The largest groups of pathogenic microorganisms are bacteria, viruses, and fungi (which include yeasts and molds). Less common pathogens are protozoa, *helminths* (commonly called worms), and *prions*, which are infectious protein particles that cause certain neurological diseases. In addition, normal flora may become pathogenic when a patient is especially vulnerable to disease, or if they enter the deep tissues or body regions they do not normally inhabit. For instance, rupture of the bowel through trauma or disease allows intestinal microbes to enter the abdominal cavity or bloodstream, where they cause infection. Once a pathogen gains entry into a host, four factors determine whether the person develops infection: ■*Virulence* of the organism (its power to cause disease) ■Ability of the organism to survive in the host environment ■Number of organisms (the greater the number, the more likely they are to cause disease) ■Ability of the host's defenses to prevent infection --------------------- watkins: 2chains the Susceptible host is going to pick on people that have a poor immune system. our post-op, age (very young/old/premature babies) immune suppressed. chemo pts, our hiv, diabetes, dialysis, steroid use, disease processes esp ppl who have chronic dz. stress, lack of sleep, nutrition-protein, vitamin c, zinc *Susceptible Host* Person with inadequate defense Four determining factors Virulence Organism's ability to survive in the host's environment Number of organisms Host's defenses book Susceptible Host A susceptible (or compromised) host is a person who is at risk for infection because of inadequate defenses against the invading pathogen. Various factors can increase susceptibility to infection, among them: age (the very young or very old), compromised immune system (as in those receiving immune suppression for organ transplantation or treatment of cancer or chronic illness), and immune deficiency conditions (e.g., HIV, leukemia). -------------------- watkins: 2chains incision wound-pressure ulcer iv site Foley catheter/jp drains-tubes inhalation ingestion membranes- mouth,nose,mouth *Portal of Entry* Eye, nares, mouth, vagina, cuts, scrapes Wounds, surgical sites, IV or drainage tube sites Bite from a vector book Portal of Entry Pathogens can enter the body through various portals of entry. Normal body openings, such as the conjunctiva of the eye, the nares (nostrils), mouth, urethra, vagina, and anus are potential portals of entry, as are abnormal openings, such as cuts, scrapes, and surgical incisions. Vectors, such as mosqui- toes, create portals of entry when they bite through the skin. In healthcare settings, common portals of entry include wounds, surgical sites, and insertion sites for tubes or needles. ------------------- watkins 2chains how it gets from one place to another vectors-animals that carry it; tick(lyme disease), mosquito fomite- inanimate objects. doorknob, money, stethoscope, scrubs, shoes, cellphone, pens, tables, countertop direct contact- something on my hands and i touch somebody indirect contact- airborne, droplet 2chains *Mode of Transmission* Contact Direct - touching, kissing, sexual contact Indirect - contact with a fomite Droplet: cough, sneeze Airborne: via air conditioning, sweeping book Mode of Transmission Contact, either direct or indirect, is the most frequent mode of transmission of infection. *Direct contact* between two people usually involves touching, kissing, or sexual intercourse. Animals commonly transmit infection via scratching and biting as well. *Indirect contact* involves contact with a *fomite*, a contaminated object that transfers a pathogen. For example, suppose that while you are charting you begin to sneeze or cough. If you cover your nose and mouth with your hand and then resume charting, you may transmit pathogens to the pen, paper, and chart (or keyboard). Shoes, eyeglasses, stetho- scopes, and other items we wear also commonly serve as fomites, as do contaminated needles. Some microbes can live only a few seconds on fomites; others can live for years. It depends on the type of microorganism and the environment. *Droplet transmission* occurs when the pathogen travels in water droplets expelled as an infected person exhales, coughs, sneezes, or talks. It may also occur during suctioning and oral care. The usual method of transmission is for the droplet to be inhaled or enter the eye of a susceptible person. Although droplets can travel only a few feet from the infectious person, within that distance they may readily contaminate fomites that then transmit the organism by contact. *Airborne transmission* occurs with much smaller organ- isms that can float considerable distances on air currents. Airborne pathogens can travel through heating and air condi- tioning systems to infect large numbers of people. Sweeping a floor or shaking out contaminated bed linens can stir up air- borne microorganisms and launch them on air currents—think of a flying magic carpet (of pathogens). The agents of measles and tuberculosis, as well as many fungal infections, are com- monly transmitted in this manner. A *vector* is an organism that carries a pathogen to a suscep- tible host, typically by biting or stinging, creating another portal of entry into the body. The mosquito is a common vec- tor for diseases, including malaria, yellow fever, and the West Nile virus. Ticks, fleas, mites, and other insects also carry various diseases. ------------------- watkins 2chains how does it get out of a person. ex- coughing, sneezing, emesis, bm, urine, semen, blood *Portal of Exit* Via Bodily fluids Coughing, sneezing, diarrhea Seeping wounds Tubes, IV lines book Portal of Exit A contained reservoir is only a potential source of infection. For infection to spread, a pathogen must exit the reservoir. In the case of human or animal reservoirs, the most frequent portal of exit is through body fluids, including blood, mucus, saliva, breast milk, urine, feces, vomitus, semen, or other secretions. The body's natural response to foreign materials, including pathogens, is to try to expel them. If you have a pathogen in the respiratory system, you cough and sneeze. If it is in the gastrointestinal system, you vomit or experience intestinal cramping and diarrhea. Microbes responsible for sexually transmitted infections can exit via semen, vaginal secretions, or blood that is present during sex. Cuts, bites, and abrasions also provide an exit for body fluid. Blood and pus seeping from a wound help transport pathogens away from the broken skin but become a portal by which infection may be transmitted to others. In healthcare- related infections, puncture sites, drainage tubes, feeding tubes, and intravenous lines commonly serve as routes for pathogens to exit the body. -------------------- watkins 2chains bacteria like to grow in warm, dark, moist, ex- stagnant water has bacteria *RESERVOIR* Where pathogens live and multiply May be living Humans, animals, insects May be nonliving Food, floors, equipment, contaminated water Most pathogens prefer a warm, moist, dark environment. book A reservoir is a source of infection: a place where pathogens survive and multiply. The human body is the most common reservoir for pathogens. Animals and insects are other living reservoirs. Nonliving reservoirs include soil, water, food, and environmental surfaces. Examples include con- taminated water, garbage, soiled diapers, and wound dressings. In healthcare facilities, many surfaces act as reser- voirs. Microorganisms have mass, and they eventually fall to the floor or onto bedside tables, chairs, or equipment. Other surfaces, such as sinks, toilets, bed rails, and bed linens, may also become reservoirs because of their proximity to patients, family members, and healthcare providers harbor- ing pathogens. carriers are capable of defending themselves from active disease but harbor the pathogenic organisms within their bodies. They have no symptoms, yet they serve as reservoirs and can pass the disease to others