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Module 5

NRSG 2872 Adult Health

This Week in Adult Health

Mon. 13 Oct.

Wed. 15 Oct.

Fri. 17 Oct.

Exam 2 – covering modules 3 & 4

Clinical #5 0630-1900

Lab #5 1000-1530 – Blood Administration

Module 5 – Hematologic & Immune System •Chapter 33: Assessment of Hematologic System•Chapter 34: Concepts of Care for Patients with Hematologic Systems

Finish Module 5 0830-1000•Chapter 16: Concepts of Inflammation & Immunity•Chapter 18: Concepts of Care for Patients with Hypersensitivity & Autoimmunity

All assignments due by midnight

Mon. 13 Oct.

Fri. 17 Oct.

Sun. 19 Oct.

Hematologic System & Immune System

Hematologic

•Brief review of hematologic system & its components •Brief review of hematologic assessment •Types of anemia including iron deficiency & sickle cell•Blood transfusion & reactions •Leukemia

Infection & Immunity

•Brief review of inflammation, infection, & immunity•Brief review of assessment •Types of allergic reactions, including anaphylaxis & angioedema •Systemic lupus erythematosus (SLE)

Module Objectives

Perform a focused assessment of a client with hematological concerns

Implement appropriate nursing care procedures for patients with hematological concerns

Assessment of the Hematologic System

Chapter 33

Physiology

  • Components
  • Plasma – no cellular elements
  • Clear, straw-colored liquid
  • About 90% water
  • 6-8% protein
  • Albumin most abundant
  • Globulins
  • Fibrinogen – needed for clot formation
  • Prothrombin – needed for coagulation
  • Normal body nutrients – carbs (glucose), proteins (amino acids), fat (lipids)
  • Metabolic waste products
  • Formed elements (cells)
  • Erythrocytes (RBCs)
  • Leukocytes (WBCs)
  • Thrombocytes (platelets)

Erythrocytes (RBCs)

  • Formed in the bone marrow  erythropoiesis
  • Need vitamin B12 & folic acid
  • Early childhood, all bones contain red marrow which is replaced with fatty, yellow marrow as child grows
  • In adult, only specific bones contain red marrow (flat & irregular bones)
  • Primary function is transport of O2 & CO2
  • Hemoglobin is primary component of RBC
  • Serves as buffer in acid-base balance
  • Hemoglobin combines easily with O2 to form oxyhemoglobin
  • Iron major component of hemoglobin & is necessary for O2 transport
  • Hematocrit is percentage of the blood occupied by erythrocytes
  • If exposed to hypotonic solutions, water enters RBC = cell wall rupture & destruction/hemolysis
  • Hemolysis also occurs when membranes are damaged (trauma & burns)
  • Primary work of WBCs is accomplished when cells leave circulating volume & enter body tissue to remove pathogens
  • Types
  • Granulocytes – originate in bone marrow
  • Neutrophils, eosinophils, & basophils
  • Primary function to destroy bacteria
  • Agranular leukocytes – originate primarily in lymphatic tissue
  • Consist of lymphocytes & monocytes
  • Assist in removal of broken-down tissue cells
  • Primarily involved in activating immune response

Leukocytes (WBCs)

  • Primarily involved with hemostasis – when a vessel wall is damaged, platelets adhere to the area & eventually form a platelet plug to decrease bleeding
  • Hemostasis – 3 phases
  • 1st tissue injury causes release of platelet factor; thromboplastin formed
  • 2nd prothrombin is converted to thrombin
  • 3rd phase thrombin converts soluble fibrinogen to insoluble fibrin (looks like a fine network of thread like a mesh or web)
  • Fibrinolysis – the process by which clots are formed

Thrombocytes (Platelets)

Blood Classification

  • Blood types: A, B, AB, O
  • Antigens on RBCs
  • A type  A antigen
  • B type  B antigen
  • AB type  A&B antigens
  • O type  No antigens (universal donor)
  • Plasma antibodies
  • A type  Anti-B
  • B type  anti-A
  • AB type  None (universal recipient)
  • O type  Anti-A & Anti-B
  • Transfusion risk – mismatched blood causes clumping (agglutination) & destruction (hemolysis)
  • Rh+  D antigen present
  • RH-  No D antigen
  • RH- person can form antibodies if exposed to Rh+ blood

Rh System

Assessment

  • History – any diseases of bone marrow or RBC-producing organs, treatments (chemo, radiation), family history, prior blood transfusions
  • Bleeding problems during pregnancy/labor
  • Presence of chronic disorders
  • Effects of aging
  • Nutritional status – especially iron, folic acid, protein
  • Current blood values – complete blood count (CBC)
  • Focused exam – skin, lymph nodes, liver & spleen enlargement
  • Assess for pallor, jaundice, cyanosis – do not rely on skin alone
  • Tongue changes with anemia
  • Look for bleeding gums, bruising

Concepts of Care for Patients with Hematologic Conditions

Chapter 34

Anemias

  • Low RBC count & decreased levels of hemoglobin & hematocrit
  • Defect in bone marrow
  • Loss of RBCs
  • Hereditary disorders
  • Inadequate nutritional intake of iron, folic acid
  • The more rapid an anemia occurs, the more severe the symptoms
  • Healthy term infants have adequate iron stores for first 5-6 months
  • Common goal of treatment is to identify origin and correct underlying problem
  • Pale skin, delayed wound healing
  • Brittle, thinning hair
  • Generalized lymphadenopathy
  • SOA, dyspnea on exertion, tachypnea
  • Tachycardia, palpitations, postural hypotension
  • Chronic fatigue, weakness, apathy
  • Anorexia, nausea, weight loss, constipation, diarrhea
  • Beefy red tongue, stomatitis, hematemesis
  • Headache, dizziness, tingling in extremities

General Clinical Manifestations

Iron Deficiency Anemia

  • Inadequate intake of dietary iron or excessive loss of iron
  • Risk factors
  • Common in adolescent d/t rapid growth
  • Vegetarians & lacto-ovo vegetarians
  • Occurs in infants who primarily consume milk
  • May occur in pregnancy
  • Heavy menstrual bleeding
  • Other blood loss states
  • Older adults more prone d/t poor intake & decreased absorption
  • Diagnostics – decreased iron, Hgb and Hct
  • Manifestations – may be asymptomatic in early stages, then general symptoms of anemia
  • Pallor, glossitis, cheilitis – most common findings
  • Treatment
  • Supplemental iron
  • Dietary supplementation
  • Inability to absorb vitamin B12 (cobalamin)
  • May be associated with a loss of intrinsic factor (gastrectomy, gastric bypass) or an autoimmune problem
  • Risk factors – typically not associated with diet; most common in adults older than 60
  • Familial tendency
  • May be precipitated by gastrectomy, gastritis, Crohn disease, or chronic alcoholism
  • Long-term use of PPIs and H2 histamine receptor blockers prevent release of intrinsic factor
  • Gastric atrophy
  • Diagnostics
  • Homocysteine, cobalamin, serum folate levels
  • Reduced number of RBCs and presence of abnormal RBCs
  • Gastric analysis for free hydrochloric acid
  • Manifestations – general symptoms of anemia, confusion
  • Paresthesia in the extremities, weakness, reduced vibratory sense
  • Loss of balance, ataxia
  • Smooth, beefy, red tongue (glossitis)
  • Treatment – injections of vitamin B12 or intranasal may be required for life; maintain good nutrition

Pernicious Anemia

  • Characterized by pancytopenia – decreased bone marrow production – RBCs, WBCs, platelets
  • Risk factors – exposure to certain meds & chemicals can precipitate
  • Chemotherapeutic agents, radiation
  • Anticonvulsant meds
  • Benzene, insecticides, arsenic
  • Radiation therapy
  • Up to 70% of cases are idiopathic, thought to be autoimmune
  • Diagnostics – bone marrow biopsy
  • Clinical manifestations – general symptoms of anemia, fever, infections associated with thrombocytopenia
  • Treatment
  • Remove causative agent
  • Hematopoietic stem cell transplant
  • Immunosuppressive therapy

Aplastic Anemia

  • Associated with decreased dietary intake of folic acid
  • Risk factors – origin very similar to that of B12
  • Poor nutrition – decreased folic acid intake, alcoholism, anorexia
  • Malabsorption syndromes
  • Deficiency may occur with increased demands for folic acid – infancy, adolescence, pregnancy
  • Drugs – anticonvulsants, methotrexate, oral contraceptives
  • Hemodialysis
  • Clinical manifestations
  • Slow, insidious onset
  • Weight loss, emaciated
  • May appear ill with malnourishment
  • Diagnostics – differentiate between folic acid and vitamin B12 deficiency
  • Treatment – oral replacement, encourage increased dietary intake

Folic Acid Deficiency Anemia

  • All patients with anemia
  • Decrease body O2 needs
  • Assess tolerance to activities
  • Cluster care
  • Supplemental O2 as needed
  • Prevent infection
  • Frequent hand hygiene
  • Limit visitors
  • Watch for signs & symptoms, elevated WBC, neutrophil
  • Assess for complications
  • Make sure heart can maintain adequate CO
  • Evaluate for symptoms of hypoxia
  • Teach implications of disease and how to maintain health
  • Explain medical regimen; benefits & side effects
  • Discuss importance of follow up
  • Identify foods high in vitamin B12, iron, folic acid

Anemia Nursing Interventions

Sickle Cell Disorder

  • Genetic disorder causes mutation in gene for hemoglobin
  • Causes chronic anemia, pain, disability, organ damage, increased infection & early death due to poor blood perfusion
  • RBCs become sickle shaped, rigid, clump together sticky and fragile RBCs
  • Block blood flow & perfusion (vaso-occlusive event) – leads to further tissue hypoxia & more sickle-shaped cells
  • Hypoxia is the most common trigger for RBCs to sickle
  • Other triggers include dehydration, high altitudes, infection, smoking, stress, weather changes, strenuous exercise, blood loss
  • Sickled cells usually go back to normal shape when trigger is removed, but some Hgb remains twisted
  • Average lifespan of a sickle cell is 10-20 days compared with the 120-day lifespan of a normal RBC  hemolytic anemia

SCD Vaso-occlusive Crises (VOCs)

  • Sudden onset
  • Can occur as often as every few weeks or as seldom as once a year
  • Many are in good health most of the time with crises only in response to triggers
  • Repeated crises & impaired perfusion cause long-term damage to tissues & organs
  • Development of small infarcted areas & scar tissue formation
  • Eventually organ failure results
  • Spleen, liver, heart, kidney, brain, joints, bones, & retina most often affected
  • Average life expectancy of adults with SCD is 22 years less

SCD Etiology & Genetic Risk

  • Autosomal recessive pattern of inheritance
  • Specific mutation in the Hgb gene leads to formation of HbS instead of HbA
  • Patient with SCD have two HbS gene alleles, one from each parent
  • Sickle cell trait (SCT) when one abnormal gene is inherited
  • Can pass to any children
  • Can occur in all races & ethnicities
  • More common in people from certain regions
  • About 1 in 13 (8%) of African Americans have SCT
  • Cannot be prevented, genetic counseling for family planning if desired
  • SCT usually have no symptoms or abnormal findings other than presence of hemoglobin S
  • Adult with SCD usually has long-standing diagnosis
  • Ask about previous crises, factors that preceded, degree of severity, management
  • Explore any recent sick contacts & assess for signs & symptoms of infection
  • Review all activities & events in the past 24 hours including food & fluid intake, exposure to extreme temps, drugs taken, exercise, trauma, stress, etc.
  • Assess perceived energy level by using a scale ranging from 0 to 10
  • Ask about changes in sleep patterns & rest, ability to climb stairs, activity that induces SOA

SCD History

  • Pain – most common
  • Other symptoms vary depending on site of reduced perfusion & tissue damaged
  • CV – look for SOA, general fatigue, weakness, murmurs, S3 heart sound, increased jugular venous distention
  • Compare peripheral pulses, temp, cap refill in all extremities
  • Extremities distal to blood vessel occlusion are usually cool to touch, have slow cap refill, may have reduced or absent pulses
  • HR is usually rapid & BP may be low to normal
  • Respiratory - pulmonary HTN over time; increased risk of pneumonia; acute chest syndrome
  • \Skin changes – pallor/ash gray or cyanosis (look at conjunctivae, palms, soles, etc.); jaundice; ulcers on the legs
  • Musculoskeletal – arms and legs often the site of blood vessel occlusion. Joints may be damaged. Inspect for swelling, temp, or color difference. Assess ROM.
  • CNS – look for cognitive & behavioral changes as early signs of cerebral hypoxia

SCD Manifestations

  • Lab
  • High performance liquid chromatography (HPLC) detects hemoglobin variants
  • Preferred method for diagnosis of SCD
  • Part of newborn screening in some states
  • Sickle cell screen
  • Other labs indicate complications of disease, especially during crises
  • WBC count usually high r/t chronic inflammation
  • Imaging
  • Bone changes d/t chronically stimulated marrow & low bone oxygen levels
  • Joint x-rays may show necrosis & destruction
  • Ultrasound, CT, PET, MRI may show soft tissue & organ changes
  • Other
  • ECG may show cardiac infarcts & tissue damage changes r/t area of heart damaged
  • Echos may show cardiomyopathy and decreased CO

SCD Diagnostics

  • Pain management
  • IV opioids – morphine, hydromorphone
  • Warm compresses, hydration, relaxation
  • Hydration – oral fluids & IV
  • Medications
  • Hydroxyurea (increases fetal Hgb)
  • L-glutamine (decreases sickling)
  • Infection prevention
  • Watch CBC, inspect mouth, lungs, urine
  • VS q4h
  • Oxygen & transfusion
  • O2 during crises
  • RBC transfusions to dilute HbS as necessary
  • Monitor for side effects
  • Hydroxyurea – teratogenic, bone marrow suppression

SCD Nursing

  • Drink 3–4 L fluids daily
  • Avoid cold, heat, high altitudes
  • No cold packs
  • Dress appropriately for weather
  • Avoid overheating & overexposure to sun
  • No smoking, alcohol, or drugs
  • Mild exercise; avoid contact and/or strenuous sports
  • Get vaccines & regular checkups
  • Use auto-injector at first sign of crisis
  • Notify providers of SCD diagnosis

SCD Patient & Family Education

Blood Transfusions

  • Whole blood or components of blood for replacement
  • Packed RBCs (PRBCs)
  • Excessive blood loss
  • Anemia (Hgb <6 or 6-10)
  • Kidney failure
  • Fresh frozen plasma (FFP)
  • Coagulation factor deficiencies (hemophilia)
  • Albumin – burns, hypoproteinemia
  • Clotting factors
  • Cryoprecipitate – hemophilia A
  • Platelets
  • Platelets less than 20,000 or 50,000 & actively bleeding

Blood Transfusion – Preprocedural

  • Verify labs & provider order
  • Confirm blood type & Rh
  • Get crossmatch sample
  • Check past reactions
  • Record baseline vitals
  • Use 18–20G IV
  • Prime tubing with NS
  • Inspect blood
  • Two RN check
  • Start within 30 min
  • Stay with patient 15–30 min

Blood Transfusion – During Procedure

  • Remain with the patient for first 15-30 minutes
  • Monitor VS & rate of infusion per facility policy
  • Complications
    • Acute hemolytic
    • Febrile
    • Allergic
    • Bacterial
    • Circulatory overload
  • Alert provider immediately if any indications of reaction

Blood Transfusion - After

  • Obtain VS upon completion
  • Dispose of blood administration set according to facility policy
  • Document patient’s response

Acute Hemolytic Reaction

  • Occurs immediately or during subsequent transfusions
  • Incompatible blood products
  • Can occur following transfusion or with as few as 10 ml of blood
  • Ranges from mild to life threatening
  • Findings – fever, chills, low-back pain, tachycardia, flushing, hypotension, CP, tachypnea, nausea, anxiety, hemoglobinuria, impending sense of doom
  • STOP the transfusion
  • Remove blood tubing from IV access
  • DO NOT CONTINUE INFUSING NS
  • Change out the tubing down to the hub and start a new infusion of NS
  • Monitor VS & fluid status
  • Send blood bag & administration set to lab for testing

Febrile Reaction

  • Occurs within 2 hours of starting transfusion
  • Development of anti-WBC antibodies
  • Seen when client has received multiple transfusions
  • Findings include – chills, hypotension, tachycardia
  • Increase of 1 degree F (0.5 degrees C) or greater from pretransfusion
  • Use WBC filter for administration
  • Stop transfusion to give antipyretics
  • Initiate infusion of NS using new tubing

Allergic Reaction

  • Occurs during or up to 24 hours after transfusion
  • Sensitivity to a component
  • Findings are usually mild – itching, urticaria, flushing
  • May develop anaphylactic reaction
  • Mild rection
  • Stop transfusion
  • Initiate NS using new tubing
  • Give antihistamine (e.g. diphenhydramine) as ordered
  • Restart transfusion slowly if prescriber orders
  • Anaphylactic reaction
  • Stop transfusion
  • Give epi, O2, or CPR as indicated
  • Remove blood tubing
  • Start NS infusion with new tubing

Bacterial Reaction

  • Occurs during or up to several hours after transfusion
  • Contaminated blood products
  • Findings include wheezing, dyspnea, chest tightness, cyanosis, hypotension, shock
  • STOP the transfusion
  • Give antibiotics & IV infusion of NS using new tubing
  • Send blood culture specimen to lab for analysis

Circulatory Overload

  • Can occur at any time during transfusion
  • Transfusion rate too rapid for client
  • Older clients or those with preexisting increased circulatory volume at increased risk
  • Findings – crackles, dyspnea, cough, anxiety, JVD, tachycardia
  • Can progress to pulmonary edema
  • Slow or stop transfusion depending on severity of symptoms
  • Position client upright – feet lower than heart level
  • Give O2, diuretics, morphine as ordered
  • Chronic disorder – proliferation of all red marrow cells owing to chromosomal mutation
  • Risk factors – usually during middle age (median age 60), more common in males
  • Diagnostics
  • CBC – increased RBC, WBC, platelets, & hemoglobin
  • Erythropoietin level
  • Bone marrow biopsy
  • Manifestations
  • Early – HTN which can cause HA, vertigo, tinnitus, pruritus, visual disturbances
  • Ruddy complexion
  • Hepatosplenomegaly; peptic ulcer dyspepsia
  • Complications – stroke secondary to thrombosis
  • Treatment
  • Phlebotomy
  • Myelosuppressive agents
  • Symptom management
  • Nursing – help patient understand dietary implications and disease

Polycythemia Vera

Leukemia

  • Uncontrolled proliferation of abnormal WBCs
  • Eventual cellular destruction occurs because of the infiltration of the leukemic cells into the body tissue
  • Highly vascular organs are primarily affected – spleen, liver, lymph nodes show marked infiltration, enlargement, fibrosis
  • Invasion of bone marrow by the leukemic cells can precipitate pathologic fractures
  • 3 primary consequences of leukemia
  • Anemia from RBC destruction & bleeding
  • Infection associated with neutropenia
  • Bleeding tendencies caused by decreased platelets

Types of Leukemia

Acute lymphocytic leukemia (ALL)

•Peak occurrence around 4; then again around 65 years •Favorable prognosis with chemo •Leukemic cell infiltrate the meninges, precipitating increased ICP; leukemic meningitis

Acute myelogenous leukemia (AML)

•Most common in older adults •Peak incidence age 60-70 years

Chronic myelogenous leukemia (CML)

•Uncommon before age of 20 years; peak incidence at age of 45 years •Onset generally slow •Symptoms less severe than those in acute stages of disease

Chronic lymphocytic leukemia (CLL)

•Common malignancy of older adults; rare before age 30 years•More common in men •Frequently asymptomatic; often diagnosed in a chronic fatigue workup

Leukemia Manifestations

  • Anemia, fever, bleeding tendencies occurring together
  • Anorexia, weight loss, cough
  • CNS involvement – headache, confusion, increased irritability
  • Fatigue, lethargy
  • Petechiae, bruises easily, epistaxis
  • Complaints of bone & joint pain
  • Hepatomegaly & splenomegaly

Leukemia Diagnostics

  • Bone marrow aspiration & biopsy
  • CBC
  • Studies to evaluate liver function
  • ALT
  • AST
  • BUN
  • Serum creatinine
  • Medications
  • Corticosteroids
  • Antineoplastics
  • Xanthine-oxidase inhibitor – allopurinol decreases uric acid levels in clients receiving antineoplastics
  • Chemo – usually involves induction, consolidation, and maintenance phase
  • Combo used to promote remission
  • Hematopoietic stem cell transplantation
  • Radiation therapy
  • Remission characterized by absence of leukemic cells & disappearance of all symptoms

Leukemia Treatment

Leukemia – Nursing

  • Prevent or limit
  • Infection
  • Bleeding episodes
  • Renal complications associated with chemo
  • Adverse effects of chemo
  • Stomatitis
  • Soft toothbrush
  • Avoid lemon-glycerin swabs, sodium lauryl sulfate in toothpaste, mouthwash with alcohol
  • Provide pain relief
  • Use smallest needle possible
  • Limit venipunctures & injections
  • Soft toothbrush, no flossing
  • Avoid alcohol-based mouthwash
  • Electric razor only
  • Prevent constipation
  • Avoid aspirin & NSAIDs
  • No catheters, enemas, or suppositories
  • Monitor for bleeding signs
  • Handle gently to prevent injury

Bleeding Precautions

  • No aspirin or aspirin-containing products
  • Caution with NSAIDs
  • Discourage pets, fresh flowers, houseplants
  • Teach how to stop bleeding
  • Teach importance of good handwashing & other infection prevention measures
  • Teach early signs of infection
  • Community resources

Leukemia – Home Care

Concepts of Inflammation & Immunity

Chapter 16

  • Functions
  • Defense
  • Homeostasis
  • Surveillance
  • Antigens
  • Foreign to the body – think bacteria, viruses, or other pathogens
  • Elicit an immune response
  • Allergens are antigens that produce allergic response
  • Antibodies
  • Proteins produced by B Cells in response to antigens
  • Help recognize & gi9ght off future infections by the same pathogen
  • Active & passive immunity

Physiology of Immune System

Humoral & Cell-Mediated Response

  • Humoral response
  • Antibodies produced by plasma cells circulate through the blood
  • Bind to & inactivate antigens or infectious agents
  • Cell-mediated responses
  • A response is initiated by recognition of antigens by T cells
  • T cells then differentiate into specific cells that react directly with the antigen
  • Provides cellular immunity, delayed hypersensitivity
  • Humoral & cellular responses are not independent, but interdependent

Properties of Immunologic Response

  • Specificity
  • Formation of specific antibody for each antigen
  • Does not protect against other antigens
  • Memory
  • Both responses are capable of “remembering” the antigen
  • Responds more rapidly if exposed to the same antigen again
  • Self-recognition
  • IS has capability of distinguishing self or self-antigens from non-self or foreign antigens
  • Self-antigens do not illicit an immune response
  • Early response – self-limiting innate resistance or natural barrier
  • Responds to site of tissue injury
  • Results in redness, heat, swelling & pain d/t vasodilation, increased vascular permeability, WBC migration to injury
  • Destroys injurious agents & removes them, confines agents to the area, stimulates immune response, promotes healing
  • Chronic inflammation lasts 2 weeks or longer
  • Frequently preceded by an unsuccessful acute response
  • Infiltration of lymphocytes & macrophages occur in attempt to protect body
  • Area may be walled off by a granuloma

Inflammatory Response

  • Infants protected at birth by maternal antibodies that cross placenta
  • Infants' immune system begins to function around 6 months
  • With aging, diminished response of cell-mediated immunity and decline in efficiency of humoral immunity
  • Older patients at increased risk for impaired inflammation & wound healing secondary to chronic diseases & meds that impair the inflammatory response

Effects of Aging on Immune Response

Concepts of Care for Patients with Hypersensitivity & Autoimmunity

Chapter 17

  • Inflammation & immunity are protective when directed against appropriate targets with time-limited response
  • When response is excessive, widespread, or directed against normal body tissue = damage
  • Excessive responses underlie problems with hypersensitivity (aka allergy)
  • Allergen = an antigen that triggers excessive inflammation or immunity overreactions
  • Inhaled
  • Ingested
  • Injected
  • Contacted via skin or mucous membranes
  • Can cause minor inconvenience (itchy, watery eyes, sneezing) to life-threatening reactions
  • Classified into 4 basic types depending on timing, pathophysiology, and symptoms
  • Predisposition to allergies is genetic, but specific allergies are NOT inherited

Hypersensitivities/Allergies

  • Occurs when a person has previously been sensitized to a specific antigen
  • Results from increased production of IgE antibody which causes release of histamine
  • Smooth muscle contraction (spasms of bronchial muscles & airway obstruction)
  • Capillary vasodilation & increased capillary permeability leading to vascular collapse (decreased BP)
  • Increased nasal stuffiness & bronchial secretions
  • Usually occurs minutes after exposure
  • Conditions associated with type I
  • Anaphylaxis (most severe)
  • Latex allergy (within minutes)
  • Atopic reactions (most common)

Hypersensitivity Type I

  • Antibodies destroy the cell on which the antigen is bound = tissue injury
  • Normal process of phagocytosis accelerated & begins to damage healthy tissue
  • Conditions associated with Type II
  • Hemolytic disease of newborn (Rh factor)
  • Leukopenia & thrombocytopenia
  • ABO blood incompatibility (hemolytic reaction)
  • Goodpasture syndrome

Hypersensitivity Type II

Hypersensitivity Type III

  • Cause: Immune complexes deposit in tissues
  • Affected Areas: Kidneys, skin, joints, lungs, blood vessels
  • Symptoms: Inflammation & tissue damage
  • Examples:
  • Persistent infections (strep)
  • Systemic Lupus Erythematosus (SLE)
  • Rheumatoid Arthritis (RA)
  • T cells are sensitized to an antigen from a previous exposure; occurs 24-48 hours after exposure
  • May take 72 hours to reach max intensity
  • Sensitized T cells initiate inflammatory response, leads to cellular damage & damage to surrounding tissue
  • Conditions associated with type IV
  • TB, skin testing
  • Contact dermatitis (poison ivy)
  • Transplant rejection
  • Latex allergy

Hypersensitivity Type IV

  • Occurs in clients highly sensitized to a specific allergen
  • Antigen-antibody response causes release of histamine
  • Histamine causes allergic reaction  hives & itching
  • Causes vasodilation & increased capillary permeability
  • Risk factors
  • History of exposure to allergen
  • Amount of allergen
  • Absorption of ingested allergen
  • Antibody levels from previous exposure
  • Occupational, social, environmental factors
  • The more rapid the onset of symptoms, more severe the reaction

Anaphylactic Reaction

Manifestations

  • Depends on level of prior sensitivity & amount of allergen
  • Mild to moderate
  • Peripheral tingling
  • Pruritus, urticaria
  • Sensation of warmth
  • Edema of lips & tongue
  • Nasal congestion
  • Flushing
  • Anxiety
  • May rapidly progress to
  • Acute anxiety
  • Difficulty breathing (bronchospasm, laryngeal edema), GI cramping, cyanosis, hypotension

Anaphylaxis Treatment

  • Type I hypersensitivity reaction
  • involves all blood vessels & bronchiolar smooth muscle
  • Causes widespread blood vessel dilation, decreased CO, bronchoconstriction within seconds to minutes after exposure
  • Occurs rapidly & systemically and can be fatal
  • Major factor in fatal outcomes is delay in giving epinephrine!
  • Can be fatal even with appropriate intervention – prevention is KEY
  • Epi – first line of treatment for severe reactions – repeat q5-15 minutes
  • O2 high concentrations
  • IV fluids, vasopressors, volume expanders to maintain circulatory status
  • Maintain patent airway – intubation or trach may be needed
  • Corticosteroids to reduce inflammation
  • In hospital – drugs & injectable imaging contrast media (dyes); food & insect stings or bites in community settings
  • ID clients with predisposition to a reaction
  • Evaluate all client history regarding reactions to meds, foods, insect bites, vaccines (esp. egg-cultured), blood products, diagnostic agents)
  • If a hypersensitivity is suspected, a localized skin test may be done
  • Prevention is priority
  • Maintain adequate ventilation
  • Bed rest, low Fowler position with legs elevated
  • High O2 concentration as needed
  • Use of airway adjuncts as needed
  • Medications to reverse bronchospasm (albuterol, corticosteroid, epinephrine)
  • Restore adequate circulation
  • IV fluids (NS or LR), carefully titrate with VS
  • Vasopressors & volume expanders
  • Closely monitor all patients for early signs
  • If you suspect anaphylaxis, immediately notify rapid response team
  • Give epi as soon as possible

Anaphylaxis Nursing

Patient Education – Auto Epinephrine Injectors

  • Practice with trainer device
  • Carry 2 injectors at all times
  • Store in case, avoid heat/light
  • Use at first sign of reaction
  • Inject into outer thigh at 90°
  • Hold for 3 seconds, then massage
  • Call 911 immediately

Angioedema

  • Severe type I hypersensitivity reaction - emergency
  • Sudden localized swelling of the deeper layers of the skin
  • Can occur in any part of the body – arms, hands, legs, feet, genitals
  • Most often seen in lips, face, tongue, larynx, & neck
  • Intestinal angioedema can also occur
  • Drugs most associated include ACE inhibitors & NSAIDs including aspirin
  • Greatest risk from ACEIs within the first 24 hours after starting

Angioedema Manifestations

  • Swelling of lips – can also include face, throat, or extremities
  • Itching also common
  • Difficulty breathing & muscle weakness in severe cases – requires medical attention

Angioedema – Nursing

  • Obtain history – need to know all drugs taken on a regular basis, especially for BP
  • No specific test can diagnose
  • Interventions focus on maintaining airway & stopping reaction
  • O2 by NC
  • Administer epinephrine & corticosteroids as ordered
  • Indications for intubation – stridor & inability to swallow
  • If intubation not possible, emergency trach needed (must be below level of edema)
  • Autoimmune condition occurs when IS no longer recognizes normal tissue
  • Reacts against self-antigens & begins to destroy host tissue
  • Autoimmune response & disease occurrence
  • Direct action of the antibody on the cell surface
  • Causes cell destruction & may activate inflammatory response
  • An alteration of both B cells and/or T cells can produce auto-sensitized T cells & cause tissue damage
  • Definitive genetic component to autoimmune diseases
  • Affect women 3x more often than men

Autoimmune Conditions

Autoimmune Response

  • Systemic
  • Connective tissue disorders – SLE
  • Rheumatic disorders – RA
  • Chronic pain & progressive immobility
  • Organ specific
  • Myasthenia gravis, MS, Guillain-Barre
  • Hyperthyroid, celiac
  • Addison
  • T1DM, pernicious anemia
  • Multisystem inflammatory autoimmune disorder
  • Affects multiple organs
  • Characterized by diffuse production of auto-antibodies that attack & cause damage to body organs & tissue
  • Tissue injury caused by deposition of immune complexes through the body – activates immune response
  • Severity varies greatly; periods of remission & exacerbation
  • Risk factors
  • Women 20-40 years of age
  • Familial tendency
  • More prevalent in Black Americans, Asian Americans, Hispanics, Native Americans
  • Maybe triggered by environmental stimulus, infections, & meds – sun exposure most common

Systemic Lupus Erythematosus

SLE Manifestations

  • General: Fatigue, fever, weight loss
  • Skin: Butterfly rash, sun sensitivity, mouth ulcers, hair loss
  • Joints: Pain, swelling, arthritis
  • Kidneys: Proteinuria, nephritis
  • Heart/Lungs: HTN, pericarditis, pleurisy
  • Neuro: Seizures, confusion
  • Blood: Anemia, low WBC/platelets
  • Other: Raynaud’s, emotional changes

SLE Diagnostics

  • No specific test is diagnostic – assess symptoms
  • Presence of antinuclear antibody (ANA), high levels of anti-DNA, and presence of anti-Smith (Sm)
  • C-reactive protein (CRP), ESR – monitor inflammation & therapy effectiveness
  • Most important problems – persistent pain, chronic inflammation, fatigue, possible loss of tissue integrity, decreased self-esteem
  • NSAIDs
  • Corticosteroids for exacerbations
  • Immunosuppressants
  • Antimalarial agents (hydroxychloroquine)
  • Steroid-sparing drugs (methotrexate)

SLE – Treatment

  • Prevent exacerbations
  • Maintain good nutrition; low-cholesterol diet
  • Avoid exposure to infections
  • Teach about skin problems – discoid lesions, hair loss
  • Avoid exposure to sunlight – SPF 30 minimum
  • Maintain adequate perfusion
  • Assess for numbness, tingling, weakness of hands & feet
  • Prevent injury to extremities, especially fingers
  • Watch fluid status – cardiac status, fluid retention, weight gain
  • Pain control
  • Establish schedule to conserve energy, still maintain activity
  • NSAIDs
  • Non-pharmacologic therapy to supplement analgesics
  • Maintain renal function
  • Watch for peripheral edema, HTN, hematuria, decreased output
  • Monitor BUN and creatinine
  • Watch for UTI & teach good hygiene to prevent UTI
  • Maintain psychological equilibrium

SLE – Nursing

Human Immunodeficiency Virus (HIV)

  • Caused by a retrovirus that causes immunosuppression
  • Infection causes increased susceptibility to infection d/t diminished response of the IS
  • Transmission
  • Blood
  • Sexual
  • Perinatal
  • CD4 T helper cells are regulating cells in the IS; level of CD4 T cell sis used to monitor stages & progression of virus
  • Normal T cell count at least 800 cells
  • Higher viral load = greater risk of transmission

Stage I – Acute HIV

  • Intense viral replication & dissemination of HIV throughout the body
  • Symptoms are mild, ranging from no symptoms to flulike symptoms
  • Window of seroconversion – period from when person is infected until HIV antibodies can be detected (average 1-3 weeks)
  • May have vague, nonspecific symptoms for years
  • High viral load and CD4 count falls, but only temporarily

Stage II – Chronic HIV

  • Asymptomatic - CD4 count greater than 500 & low viral load
  • Chronic vague symptoms persist – fever, fatigue, headache, night sweats
  • Persistent generalized lymphadenopathy
  • Symptomatic – CD4 count between 200 & 500 & increased viral load
  • Exacerbation of symptoms
  • Localized infections, increased lymphadenopathy, and neurologic manifestations
  • Candida is a common problem
  • Hairy oral leukoplakia – may be indication of progression of disease
  • Shingles, oral, or genital herpes lesions
  • Kaposi sarcoma
  • Cutaneous skin lesion – looks like a bruise; later will turn dark violet or black
  • Invades body organs, extremities, skin, torso
  • May become painful

Stage III – Acquired Immunodeficiency Syndrome (AIDS)

  • CD4 T-cell count less than 200 & viral load increased
  • Diagnosis made when HIV-positive client develops at least one of the following disease
  • AIDS dementia complex
  • At least one opportunistic cancer
  • Invasive cervical cancer
  • Kaposi sarcoma
  • Burkitt lymphoma
  • Immunoblastic lymphoma
  • Primary lymphoma of the brain
  • At least one opportunistic infection – viral (cytomegalovirus), fungal, bacterial, or protozoal infection
  • Diseases & infections that occur in clients with AIDS
  • Take advantage of suppressed immune system
  • Type of infection & extent varies with each client, depending on extent of immunosuppression
  • Single opportunistic infections are rare
  • May be delayed or prevented with antiretroviral therapy, vaccines, and disease-specific prevention
  • Specific strains of pneumonia, TB, fungal infections, Kaposi sarcoma, candidiasis, etc.

HIV – Opportunistic Diseases

HIV Testing

  • Antibody/antigen testing – highly sensitive test
  • 4th generation testing algorithm includes confirmatory testing with HIV viral load testing for any indeterminate results
  • If negative testing but continued risky behavior, should retest in 4-6 weeks
  • If positive, assist in finding follow-up care
  • Rapid tests – ready within 20 minutes
  • Results preliminary & must be confirmed
  • Must return for standard assay if positive
  • In-home testing kids available
  • Serum monitoring after diagnosis
  • CD4 count & plasma assays
  • Evaluation for drug resistance

HIV Treatment

  • Meds – antiretroviral therapy (ART)
  • Prescribed according to viral load & CD4 count
  • Combo of at least 3 or more ART drugs
  • Women should begin ART even if pregnant
  • Combo drug therapy attacks virus at different stages
  • OTC drugs & herbals may cause reactions (especially St. John wort)
  • Meds don’t cure, but decrease viral replication & slow disease process
  • Adherence to drug schedule is critical
  • Nonadherence can lead to mutations of the virus & increased resistance
  • Educate regarding transmission
  • Safe sex
  • Don’t share needles
  • Monitor for & prevent opportunistic infection
  • Antimicrobials given in high doses for extended period, may cause neutropenia
  • Protect from iatrogenic infections or HAIs
  • Teach client symptoms
  • Persistent unexplained fever, night sweats
  • Thrush
  • Persistent diarrhea & weight loss
  • Maintain adequate nutrition
  • Teach regarding nutrition & calories – high calorie, protein to correct deficiencies
  • Encourage several small meals
  • Avoid foods that cause irritation
  • Maintain fluid & electrolyte status
  • Evaluate for weight gain & loss
  • Assess for chronic diarrhea
  • Encourage fluids

HIV Nursing

  • Home care for immunocompromised
  • Maintain personal hygiene & practice standard precautions
  • Do not share personal items (toothbrushes, razors.)
  • Teach how to prevent infection
  • Cook all veggies & meats
  • Peel fruits before eating
  • Avoid contact with animal waste (litter boxes, bird cages, fish)
  • Avoid crowds & people with respiratory tract infections
  • Do not get pregnant

HIV – Teaching