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Immunity . Trisha Economidis, MS, ARNP Spring, 2012. WAR DECLARED…. We are at war with our environment Troops are prepared to fight from every sector of the body to keep us safe (and healthy) Regiments on the ready include: Antibodies Immunoglobulins White Blood cells

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Trisha Economidis, MS, ARNP

Spring, 2012

war declared
  • We are at war with our environment
  • Troops are prepared to fight from every sector of the body to keep us safe (and healthy)
  • Regiments on the ready include:
    • Antibodies
    • Immunoglobulins
    • White Blood cells
    • Immune Response Teams: Humoral and Cell-Mediated Immunity
    • And others…….
immune system review public enemy number one
Immune System Review: Public Enemy Number ONE
  • Antigen – a protein that stimulates an immune reaction, causing production of antibodies.
  • Viruses
  • Bacteria
  • Fungi
  • Parasites
  • Etc…..
immune system review
Immune System Review
  • Antibody – a globulin (PRO) produced by B cells as a defense mechanism against foreign materials. Combines in a lock and key style with antigens
first line of defense primary defenses
First Line of Defense: Primary Defenses
  • Prevent organisms from entering the body
  • Skin
  • Respiratory Tree
  • Tears/Saliva
  • Gi Tract – acidic environment, peristalsis
  • Bile - antimicrobial
  • GU tract – mucous membranes
secondary defenses
Secondary Defenses
  • Phagocytosis
    • White blood cells
      • TO THE RESCUE!
secondary defense 2
Secondary Defense #2
  • Complement Cascade
    • Set of proteins called complement that trigger release of chemicals that attack the cell membranes of pathogens causing them to rupture
secondary defense 3 inflammation
Secondary Defense #3: Inflammation
  • Begins when histamine and other chemicals are released directly from damaged cells or from basophils in response to complement
  • Histamine/chemical release

Dilation and increased

Permeability of blood vessels

flow of phagocytes,

antimicrobials, O2,

& nutrients to area of


secondary defense 4
Secondary Defense #4
  • Fever
  • Increases metabolism
  • Inhibits pathogen multiplication
  • Triggers specific immune responses
tertiary defenses specific immunity
Tertiary Defenses: Specific Immunity
  • Body recognizes and destroys pathogens encountered before
  • Lymphocytes – WBCs that mature to either T cells or B cells
2 types of specific immunity
2 Types of Specific Immunity
  • 1. HumoralImmunity– B (lymphs) cells stimulated to become plasma cells and produce antibodies (immunoglobulins) to the antigens.
  • Antibodies bind to and destroy antigens.
specific immunity no 2
Specific Immunity No. 2:
  • Cell-Mediated Immunity: Acts to destroy body cells that have become infected.
  • T Cells are responsible for cell-mediated immunity:
    • Cytotoxic (Killer) T cells
    • Helper T cells
    • Memory T cells
    • Suppressor T cells
wbc s name rank serial number
WBC’s – Name, Rank & Serial Number
  • Reported in the WBC Differential with a CBC
  • Basophils 0.5-1% - Release histamine and heparin granules
  • Eosinophils 1-3% - Destroy helminths, mediate allergic reactions
  • Monocytes – 3-8% - Phagocytize directly
  • Lymphocytes (20-35%) – T lymphs – recognize, attack and destroy antigens; B lymphs – produce immunoglobulins to attack and destroy antigens
  • Neutrophils – 55-70%. First to arrive – Phagocytize!
    • Bands – Immature neutrophils (normally 3-5% of total WBCs)
    • Segmented (Segs) – Mature neutrophils –( normally 50-65T of total WBCs)
shift to the left
Shift to the Left??????
  • In an acute infection more lymphocytes are produced
  • A “shift to the left” occurs when there are more bands (immature or baby neutrophils) in circulation than there are segs (mature or grownup neutrophils)
shift to the left1
“Shift to the left”
  • Higher number of bands than segs (usually when bands reach 6%) in circulation called bandemia.
  • Indicates body is responding to an acute infection, usually bacterial, or to Stress (i.e. women in childbirth)
immunoglobulins ig the special agents of humoral immunity
Immunoglobulins (Ig) – the Special Agents of Humoral Immunity
  • IgM – Goes after “first time offenders”
  • IgG – most common one. (AKA: Gamma Globulin) – Active against bacteria and viruses
  • IgE – primarily responsible for allergic response and parasitic infections
  • IgA – secreted by mucous membranes around body openings. Provides more protection for points of entry.
  • IgD – found of surface of B cells. Trap potential pathogens
what are the weapons of the immunoglobulin agents
What are the “weapons” of the Immunoglobulin Agents???
  • Phagocytosis
  • Neutralization
  • Agglutination
  • Activation of complement and inflammation
two types of immunity
Two Types of Immunity

Innate (Native)

Adaptive (Acquired)

  • Present at birth
  • First line of defense
  • Non-specific response
  • Neutrophils first on the site
  • Cannot be developed or transferred
  • Body can make it or receive it
  • Specific response
  • Results from adaptive response to invasion by an antigen (antibody formation)
  • Can be passive or active
  • Can be naturally produced or artificially acquired
assessment of the immune system
Assessment of the Immune system
  • Chief complaint – subjective data
  • Review biographic data: age, gender, race, ethnic background, family history
  • Comprehensive health history
  • Physical Assessment
immune system diagnostics
Immune System Diagnostics
  • Allergy testing (will discuss with allergies)
  • Cd4-T cell counts (Helper T’s) – reflection of immune status (normal: 500-1600 cells/mm3)
  • Viral Load testing – measures the presence of HIV viral genetic material in the patient’s blood rather than the body’s response to the virus
  • ELISA/Western Blot
  • Antibody testing
  • ANA antinuclear antibody
immune system diagnostics1
Immune System Diagnostics
  • Rheumatoid Factor
  • Serum Complement
  • ESR (erythrocyte sedimentation rate)
  • HLA testing – Human Leukocyte Antigen
health promotion and the immune system boosting your immunity
Health Promotion and the Immune System – Boosting your Immunity
  • Diet – Balanced diet
  • Exercise – Regular, moderate work-outs
  • Stress relief
  • Get enough sleep
  • Use sun exposure protection
  • Quit smoking or Don’t Start
  • Avoid Excess alcohol
  • Immunizations up-to-date
pharmacologic management of immune disorders
Pharmacologic Management of Immune Disorders
  • Antibiotics (anti-infectives)
  • Use: treatment/prophylaxis of bacterial infections
  • Cautions: Can depress bone marrow; Superinfections
    • Cephalosporins
    • Penicillins
    • Fluoroquinolones
    • Macrolides
    • Sulfonamides
    • Tetracyclines
pharmacological interventions
Pharmacological Interventions
  • Antivirals – Destroy viruses either directly or by inhibiting the ability to replicate
  • acyclovir (Zovirax); HSV-1, HSV-2, VZV
  • osetamivir (Tamiflu), zanamivir (Relenza); Influenza Types A & B
pharmacological interventions1
Pharmacological Interventions
  • Antifungals
    • Kill or stop growth of fungal infections of skin, mucus membranes, & systemic
    • Topical
      • Clotrimazole, ketoconazole, miconazole, nystatin
    • Systemic
      • Amphotericin B, fluconazole, ketoconazole
pharmacological interventions2
Pharmacological Interventions
  • Anti-inflammatory
    • Corticosteroids
      • Used for anti-inflammatory and immunosuppressive properties
      • Topical, inhaled, intranasal, opthalmic, IV, PO, IM
      • Long, intermediate, and short-acting
pharmacological interventions3
Pharmacological Interventions
  • Antihistamines
    • Relief of symptoms associated with allergies, rhinitis, urticaria
  • 1st generation-sedating
    • Chlor-trimeton (chlorpheninamine)
    • Dramamine (dimenthydrinate)
    • Benadryl (dephenhydramine)
    • Atarax, Vistaril (hydroxyzine)
  • 2nd generation-non-sedating
    • Allegra (fexofenadine)
    • Claritin (loratadine)
    • Zyrtec (cetirizine)
pharmacological interventions4
Pharmacological Interventions
  • Adrenergic sympathomimetic - Epinephrine
    • Inhibits release of hypersensitivity mediators
    • Inhibits reaction from mast cells
    • Produces bronchodilation, vasoconstriction
    • Epinephrine (Adrenalin)
        • 0.3mg-0.5 mg subcutaneously or IM (Adults)
pharmacological interventions5
Pharmacological Interventions
  • Immunotherapy
    • SC injections weekly/biweekly of allergen extracts
    • Goals of Therapy
      • Stimulate IgG levels for allergen binding
      • Decrease IgE levels
pharmacological interventions6
Pharmacological Interventions
  • Biologic Response Modifers (BRMs)
  • Broad class of drugs that alter the body’s response to diseases such as cancer and autoimmune, inflammatory and infections diseases
  • Immune Modulators – either enhance or reduce immune responses (some can do both)
    • Interferons
    • Monoclonal antibodies
    • Interleukins
    • Disease-modifying antirheumatoid arthritis drugs
pharmacological interventions7
Pharmacological Interventions
  • Immunosuppressant Drugs – Decrease or prevent an immune response
  • cyclosporine (Sandimmune, Neoral, Gengraf)

Used to prevent organ rejection in liver, kidney, and heart transplants; treatment of RA and psoriasis. Off-label use in rejection prevention of pancreas, bone marrow, heart/lung transplants.

muromonab-CD3 (Orthoclone OKT3)

Only one indicated to treat acute organ rejection in kidney, liver and heart transplant

pharmacological interventions8
Pharmacological Interventions
  • Antimalarial (What’s this doing HERE?)
  • Plaquenil (hydroxychloroquine) – used to decrease joint and muscle pain in early or mild Rheumatoid Arthritis or Lupus (SLE)
  • Gold Therapy – Rarely used in the U.S. because of toxicities, but may see in patients from other countries.
  • Antigout –
    • Acute: colchicine and an NSAID
    • Chronic: allopurinol (Zyloprim), probenecid (Benemid)
organ donation transplant one boy s story
Organ Donation/Transplant:One Boy’s Story year old, Nicholas Green

nursing management of clients with organ transplants
Nursing Management of Clients with Organ Transplants
  • Transplant success tied to matching tissue antigens, HLA (Human Leukocyte Antigens)
  • Autograft
  • Allograft
  • Xenograft
  • Histocompatibility – ability of cells and tissues to survive transplantation without immunologic interference by the recipient
host versus graft transplant rejection
Host-versus-Graft Transplant Rejection
  • Complex process involving both antibody-mediated and cell mediated responses
  • Hyperacute Rejection – Begins immediately and can’t be stopped once it begins
  • Acute rejection – occurs 1-3 mo post-transplant. Most common rejection and is treatable.
  • Chronic rejection – occurs from 4 mos to yrs post-transplant. No cure. Once organ cannot function, another transplant is only course.
treatment of transplant rejection
Treatment of Transplant rejection

Maintenance therapy – Ongoing immune suppressants Ex. cyclosporin, Imuran & a corticosteroid (prednisone)

Rescue therapy – treats acute rejection. Ex: ALG , murononab-CD3. Most effective during first course of treatment

what is an allergy
What is an allergy?
  • Allergy is an exaggerated immune response to an antigen (foreign or allergen) to which the patient has been previously exposed.
  • Also called hypersensitivity
allergy terminology
Allergy Terminology
  • Allergen – an antigen that causes an allergic sensitization
  • Mast cell – a tissue cell that contains granules filled with chemical mediators such as histamine and heparin. Play a major role in allergies as well as immune system function.
  • Atopic – relating to a hereditary predisposition toward developing certain allergic reactions
why does an allergic reaction occur
Why does an allergic reaction occur?
  • 1. First time exposure to an allergen, our body responds by making “antigen-specific” IgE
  • 2. The antigen-specific IgE binds to the surface of mast cells and basophils (both have granules containing chemical mediators including histamine that will be released when stimulated)
  • 3. Once the IgE is formed, we are sensitized to that allergen
hypersensitivity allergic reactions
Hypersensitivity (allergic) Reactions
  • Type I reaction – occurs when the already sensitized person (see previous slide) is re-exposed to the allergen (IgE mediated)
    • Histamine and other chemicals are released from the cells
    • Inflammatory response occurs from other proteins released from the cells that draw more WBC’s to the area
anaphylaxis serious type i reaction
Anaphylaxis – Serious Type I Reaction
  • Immediate life-threatening systemic reaction
  • Can occur in seconds to minutes
  • Not common
  • Life-threatening and can be fatal
  • What can cause it: allergy shots, insect bites/stings, foods (peanuts, eggs, shellfish, etc.) medications, blood products, contrast media, exercise, skin testing.
anaphylaxis what does it look like
Anaphylaxis – What does it look like?
  • Respiratory – bronchospasm, laryngeal edema, wheezing, cough
  • Cardiovascular – hypotension, tachycardia, palpitations, syncope
  • Skin – urticaria, angioedema, pruitus, erythema
  • GI – N/V/D/, abdominal pain
emergency care
Emergency Care
  • Recognize symptoms
  • A, B, Cs
  • Administer drugs

-Epinephrine 1:1000

0.3-0.5 mL SQ or Epi-pen 0.3 mL IM (adults), 0.15 mL IM (children)




history of anaphylaxis
History of Anaphylaxis?
  • Obtain Medical Alert Bracelet
  • Carry Epi-pen
did i inherit my allergies
Did I inherit my allergies?
  • Yes, and no….
  • The tendency to produce IgE to certain antigen exposure is based on genetic inheritance.
  • Allergic tendencies are inherited (atopy); specific allergies are NOT inherited
other hypersensitivity reactions
Other Hypersensitivity Reactions
  • Type II: Cytotoxic – involve IgG. Body makes antibodies that attack self cells resulting in death of the cell.
  • Ex. Hemolytic anemias, hemolytic transfusion reactions (person gets wrong blood type in a transfusion)
hypersensitivity reactions cont
Hypersensitivity Reactions, cont.
  • Type III: Immune Complex Reactions – too many circulating antigens form large antigen-antibody complexes that lodge in small blood vessel walls; triggering inflammation and tissue damage.
  • Type IV: Delayed Hypersensitivity Reactions – Sensitized T cells react to antigens by triggering macrophages to destroy the antigen.
  • Type V: Stimulatory Reactions - autoantibodies constantly stimulate reaction from normal cells resulting in a “turned on” state continuously
allergy testing
Allergy Testing
  • Method-Apply to arms or back
    • Cutaneous scratch or prick
    • Intradermal (the most accurate)
    • **Patch (for contact dermatitis)
  • Response
    • Produces localized response (wheal & flare)
    • Diagnostic for allergies to specific antigen
    • Positive reaction within minutes
      • Lasts 8-12 hours
rast testing
RAST testing
  • Shows the blood level of IgE (antibody) directed against a specific antigen
  • Advantages-can be used in people with extensive eczema or dermatitis who cannot undergo skin testing.
  • Disadvantages-Results must be interpreted in the light of your symptoms and history: A positive response to an allergen indicates only a potential allergic reaction that may not be the cause of your symptoms.
  • Twice as expensive as skin testing.
  • Results are not immediately available.
immunodeficiency disorders
Immunodeficiency Disorders
  • Therapy-induced immunodeficiency disorders

Drug induced:

        • Cytotoxic Drugs
        • Corticosteroids
        • Cyclosporin

Radiation Induced Immunodeficiency

therapy induced immunosuppression treatment
Therapy Induced Immunosuppression Treatment
  • Improve the immune function – possibly give biologic response modifiers
  • Protect from infection
    • Good hand washing
    • Limit number of people entering room
    • Careful and regular assessments
    • Low bacterial diet
    • No fresh flowers or potted plants
congenital primary immune deficiencies
Congenital (Primary Immune Deficiencies
  • Defect in one or more immune components
  • Present at birth
  • Classified by type of immune function that is impaired
system lupus erythematosus sle
System Lupus Erythematosus (SLE)
  • Chronic, multi-system, autoimmune disease
  • Affects more women than men
  • Affects more African American women than European American women
  • SLE thought to be a combination of environmental and genetic factors
lupus signs and symptoms
Lupus: Signs and Symptoms
  • Skin: Butterfly rash
  • Raynaud’s Phenomenon
lupus signs symptoms
Lupus: Signs/Symptoms
  • Musculoskeletal System
  • Muscle and joint pain very common with exacerbations and remissions
  • Arthritis – affects primarily distal joints: hands, wrists, fingers, toes, ankles, knees, etc.
  • May have tendon involvement and rupture
  • Knees and hips can have treatment related osteonecrosis from steroid therapy
lupus signs symptoms1
Lupus: Signs/Symptoms
  • Cardiac System
  • Pericarditis - most common cardiac manifestation
  • Myocarditis
  • Anemia
  • Leukopenia
  • Thrombocytopenia
lupus signs symptoms2
Lupus: Signs/Symptoms
  • Respiratory System
  • Pleuritis – Inflammation of the pleura
  • Pleural Effusions – Fluid build-up between pleura and chest cavity
  • Pneumonia
lupus signs symptoms3
Lupus: Signs/Symptoms
  • Gastrointestinal/Hepatic Systems
  • Can affect any area of the GI system as well as pancreas, spleen, or liver
  • Ex: oral ulcers, peptic ulcers, abdominal pain/N/V/D, pancreatitis, hepatomegaly, GERD, ulcerative colitis
lupus signs symptoms4
Lupus: Signs/Symptoms
  • Renal System
  • Lupus Nephritis – leading cause of death among patients diagnosed with SLE (Lupus)
  • s/s to monitor for: fluid retention (edema, wgt gain), hematuria, proteinuria, changes in urine output, hypertension
lupus signs symptoms5
Lupus: Signs/Symptoms
  • Neurologic System
  • Neuropathies
  • Psychoses, depression
  • Seizures, migraine headaches
  • CNS vasculitis
  • Peripheral neuropathies

CNS Vasculitis

lupus signs symptoms6
Lupus: Signs/Symptoms
  • Constitutional Symptoms
  • Fatigue
  • Weight changes/loss or gain
  • Fever
  • Arthralgias
lupus s s
Lupus: S/S
  • Psychosocial Issues
  • Altered body image/poor self-concept
  • Chronic fatigue/weakness may prevent being as socially active as previously
  • Fear and anxiety may occur due to the unpredictability of flares or the progression of the disease, necessity of life style changes, etc.
lupus diagnosis
Lupus: Diagnosis
  • Lab tests:

Antinuclear antibody

ESR (sed rate)

Serum complement

Various antibody titers

CBC – looking for pancytopenia

Specific testing for body system involvement

Urinalysis/24 hr urine

Diagnostic Imaging: CXR, Hand x-rays, CT OR MRI

lupus treatment
Lupus: Treatment
  • Pharmacologic Management
    • NSAIDS
    • Antimalarials (Plaquenil)
    • Corticosteroid Therapy
    • Immunosuppressive ages (methotrexate or Imuran)
lupus treatment1
Lupus: Treatment
  • Non-pharmacologic Management
    • Avoid direct exposure to sunlight
    • Use sunscreen with SPF of 30 or higher
    • Some physicians recommend avoiding use of oral contraceptives
    • Careful skin and hair care with mild soaps/shampoos
lupus important patient education
Lupus: Important Patient Education
  • Importance of skin care
  • Monitor body temp and other warning signs of a flare: increased fatigue, pain, abdominal discomfort, rash, headache, dizziness
  • Reproductive impact
  • Avoid exposure to infection
  • Need to follow treatment plan, including follow-up appointments and prompt reporting of a flare
  • Preventive health care
  • Medic Alert bracelet
rheumatoid arthritis ra
Rheumatoid Arthritis (RA)
  • Chronic, progressive, systemic, inflammatory, autoimmune disease that affects joints and other tissues or organ systems.
  • Most prevalent in European Americans
  • Affects 0.5% to 1% of the population worldwide; women more frequently than men
ra pathophysiology
RA Pathophysiology
  • Cause: believed to be genetic and environmental
  • Autoantibodies (rheumatoid factors) attack healthy tissue, especially synovial membranes, causing inflammation. Immune processes activated
  • Activation of the inflammatory and immune response damages the synovial membrane.
ra signs symptoms
RA Signs/Symptoms
  • Onset may be acute and severe (usually precipitated by a stressor such as surgery or an infection)
  • Or onset may be insidious
  • Joints primarily affected are hands, wrists, knees and feet
  • Joint involvement usually bilateral and symmetric.
  • Disease symptoms described as early or late and joint (articular) or systemic (extra-articular)
ra signs symptoms1
RA Signs/Symptoms
  • Early Disease Manifestations:
    • Joint stiffness, swelling, pain
    • Systemic:
      • Low-grade fever
      • Fatigue
      • Weakness
      • Anorexia
      • Paresthesias
ra signs symptoms2
RA Signs/Symptoms
  • Late Disease Manifestations
  • Joint deformities (swan neck and ulnar deviation)
  • Moderate to severe pain and morning stiffness

Swan neck deformity

Ulnar deviation

ra signs symptoms3
RA Signs/Symptoms
  • Late Disease Manifestations – Systemic
  • Osteoporosis
  • Anemia
  • Weight loss
  • Subcutaneous nodules
  • Peripheral neropathy
  • Vasculitis
  • Pericarditis
  • Sjogren’s syndrome
  • Renal disease
ra diagnosis
RA Diagnosis
  • Based on patient’s hx, physical assessment, and diagnostic tests
  • Lab tests: Rheumatoid factor
    • ESR and C-reactive protein
    • CBC
    • Synovial fluid exam
    • X-rays of affected joints
ra treatment
RA Treatment
  • Surgical Management:
  • A synovectomy to remove inflamed synovium may be necessary for knee or elbow
  • Total joint arthroplasty may be necessary for joint deformity and destruction
  • Arthrodesis (joint fusion) to stabilize joints such as cervical vertebrae, wrists, and ankles.
ra treatment1
RA Treatment
  • Pharmacological Management:
    • NSAIDS
    • Antimalarials
    • Corticosteroids, oral or intra-articular for temporary relief
    • Disease-Modifying Antirheumatic Drugs (DMARDS) to reduce disease activity: methotrexate, Imuran, Cytoxan or BMR’s: Humira, Enbrel, Remicade
ra treatment2
RA Treatment
  • Non-pharmacological treatment
  • Balanced program of rest and exercise – energy conservation
  • Physical and Occupational therapy
  • Heat and cold
  • Assistive devices and splints
  • Balanced nutrition
scleroderma systemic sclerosis
Scleroderma (Systemic Sclerosis)
  • Autoimmune disorder of connective tissue
  • Characterized by hardening(sclero) and thickening of the skin (derma), blood vessels, synovium, skeletal muscles, and internal organs
  • Approximately 300,000 people in the US have Scleroderma
  • Affects women more than men by 3:1
  • Affects more African Americans than Caucasians
scleroderma pathophysiology
Scleroderma - Pathophysiology
  • Early stages very similar to SLE – often misdiagnosed
  • Can be limited or diffuse
  • May have CREST syndrome:
    • Calcinosis
    • Raynaud’s phenomenon
    • Esophageal dysmotility
    • Sclerodactyly
    • Telangiectasia
scleroderma signs symptoms
Scleroderma Signs/Symptoms
  • Musculoskeletal - Joint pain
  • GI: Dysphagia and reflux, esophagitis, diarrhea or constipation, abdominal cramping and malabsorption
  • Skin: Bilateral, symmetric swelling of hands and sometimes feet. After edematous phase, the skin becomes hard and thick.
  • Facial changes – skin tightening leads to loss of skin lines, appearance of disappearing lips
scleroderma signs symptoms1
Scleroderma Signs/Symptoms
  • Facial skin symptoms:
  • Tightening of the skin
  • Disappearing lips
  • Decreased mobility of eyelids
  • Evolving process

Body image and psychosocial issues

scleroderma signs and symptoms
Scleroderma Signs and Symptoms
  • Cardiovascular: Raynaud’s Syndrome, Myocardial fibrosis, Pericarditis and dysrhythmias
  • Pulmonary: Lung fibrosis, pulmonary hypertension, exertional dyspnea
  • Renal – proteinuria, hematuria, hypertension, and renal failure
scleroderma diagnosis
Scleroderma Diagnosis
  • ANA: of at least 1:40
  • Lab tests/results similar to SLE: ESR – elevated; CBC- may show anemia, RF – elevated in about 30%
  • Barium swallow – may show esophageal dysmotility
  • X-ray of hands & wrists – muscle atrophy, osteopenia
  • No single diagnostic test – overlap with other autoimmune diseases so diagnosis may initially be difficult
scleroderma treatment
Scleroderma Treatment
  • Corticosteroids & immunosuppressants – tried to slow the progression
  • Identify early organ involvement and treat aggressively
  • Skin protection and careful ongoing assessments
  • Gastric secretion blockers for esophagitis/reflux. Avoid spicy foods, caffeine, alcohol
  • NSAIDS for joint pain
  • Be aware that the side effects from many of the pharmacological treatments can worsen symptoms of the disease
  • Metabolic d/o characterized by an acute inflammatory arthritis triggered by crystallization of urate within the joints.
  • May be caused by an inborn error of metabolism or as the result of another disease process or factor; i.e. crash diets, renal insufficiency
  • Affects approximately 3 million Americans each year, and over twice that man have been affected at some time.
  • Occurs more often in men. More common in women who are post-menopausal or taking diuretics
  • 3 clinical stages
  • 1. Asymptomatic – not detected unless a uric acid level is checked.
  • Acute - Extremely painful joint inflammation, usually in the great toe, called podagra
  • Chronic – After repeated episodes of acute gout, urates are deposited in various other connective tissues: synovial fluids (gouty arthritis); subcutaneous tissue (tophi) and kidneys(can form kidney stones and result in kidney failure)
gout treatment
Gout treatment
  • Pharmacological Management
  • Acute Gout: NSAID (Indocin) or ibuprofen; and colchicine. Taken until symptoms subside
  • Chronic gout: Prevention is key. Zyloprim (allopurinol) lowers uric acid levels. Benemid(probenecid) promotes excretion of uric acid. May be given one or the other or a combination.
gout treatment1
Gout treatment
  • Non-pharmacological Management
  • Dietary restrictions on high-purine meats (red and organ meats) and seafood (shellfish and oily fish with bones) may be recommended
  • No alcohol
  • Avoid aspirin and diuretics
  • Drink enough fluid to maintain daily urine output of 2000 mL or more
lyme disease
Lyme Disease
  • Most common tick-borne illness in North America
  • Carried by the infected deer tick (black-legged tick)
  • Occurs most often in children and young adults living in rural areas
  • Risk factors:

Spending time in wooded or grassy areas

Having exposed skin

Not removing ticks promptly or properly

lyme disease pathophysiology
Lyme Disease: Pathophysiology
  • After an incubation period of 3-30 days after the bite, the spirochete migrates outward into the skin
  • Forms a characteristic erythema migrans (bull’s eye rash)
  • May spread to other skin sites, organs, or nodes
lyme disease signs symptoms
Lyme Disease: Signs/Symptoms
  • Stage I:
  • Skin: Bull’s eye rash
  • Musculoskeletal: pain and stiffness in muscles and joints
  • Constitutional: flu-like symptoms, fever, chills, fatigue, body aches
  • If not treated or treatment is unsuccessful, progresses to Stage II
lyme disease signs symptoms1
Lyme Disease Signs/Symptoms
  • Stage II:
  • Migratory musculoskeletal pain and swelling; especially in the knees
  • Carditis with dysrhythmias, dyspnea, palpitations
  • CNS disorders: meningitis, Bell’s palsy, numbness or weakness in limbs, impaired muscle movement
  • If not diagnosed and treated can progress to Stage III
lyme disease signs symptoms2
Lyme Disease Signs/Symptoms
  • Stage III (months to years after the tick bite)
  • Chronic recurrent arthritis
  • Chronic fatigue
  • Cardiac complications
  • Thinking/memory issues
lyme disease treatment
Lyme Disease: Treatment
  • Antibiotic therapy: doxycycline, tetracycline, amoxicillin, cefuroxime, erythromycin. May be given for 3-4 weeks
  • Aspirin or another NSAID for relief of arthritic symptoms
  • May need assistive devices (splints/crutches)
  • Prevention is the Key
preventing lyme disease
Preventing Lyme Disease
  • When walking in wooded or grassy areas:
  • Wear long pants tucked into socks, long sleeves, hat, gloves, shoes
  • Use insect repellents (10-30% DEET)
  • Check yourself, your children and your pets for ticks
  • Remove a tick with tweezers by

pulling straight out. Clean with

alcohol other antiseptic.

  • Common Rheumatic pain syndrome with wide-spread musculoskeletal pain, stiffness, and tenderness
  • Women affected 9 times more often than men
  • Genetic and environmental factors are thought to contribute
  • Requires a hx of widespread pain in all 4 quadrants of the body for a minimum duration of 3 months and pain in at least 11 of 18 trigger points
fibromyalgia signs symptoms
Fibromyalgia Signs/Symptoms
  • Fatigue, moderate to severe
  • Sleep disorders
  • Problems with cognitive function (Fibro Fog)
  • Irritable Bowel Syndrome
  • Headaches and migraines
  • Anxiety and depression
  • Environmental sensitivities
fibromyalgia treatment
Fibromyalgia Treatment
  • Pharmacological Management is symptomatic:
  • 3 drugs approved as of 2009 to reduce pain levels and improve sleep: Lyrica, Cymbalta, and Savella
  • Tricyclic antidepressants such as amitryptyline may help with pain and sleep as well
  • SSRI’s - treat depression and anxiety
fibromyalgia treatment1
Fibromyalgia Treatment
  • Non-pharmacological Management
  • Physical therapy
  • Regular exercise routine
  • Alternative therapies: Massage, acupuncture, chiropractic, yoga
  • Stress management
  • Therapy to assist with depression/anxiety
chronic fatigue syndrome or chronic fatigue and immune dysfunction syndrome cfids
Chronic Fatigue Syndrome or Chronic Fatigue and Immune Dysfunction Syndrome (CFIDS)
  • Complicated disorder characterized by extreme fatigue unexplained by any underlying medical condition
  • May worsen with activity, but doesn’t improve with rest
  • No single test to confirm a diagnosis
  • Risk factors: Age (40’s and 50’s), female, overweight and inactive, stress
chronic fatigue syndrome signs symptoms
Chronic Fatigue Syndrome Signs/Symptoms
  • Fatigue
  • Loss of memory or concentration
  • Sore throat
  • Enlarged lymph nodes in neck or axilla
  • Unexplained muscle pain
  • Multiple joint pain
  • Headache of a new type, pattern or severity
  • Unrefreshing sleep
  • Extreme exhaustion lasting more than 24 hrs after physical or mental exercise
chronic fatigue syndrome treatment
Chronic Fatigue Syndrome Treatment
  • Pharmacological Management is symptom focused
  • Antidepressants
  • NSAIDS may help with body aches and pain
  • Non-pharmacological Management:
  • Gentle exercise program
  • Psychological counseling
  • Lifestyle changes: reduce stress, improve sleep habits, pacing
  • Alternative medicine: acupuncture, massage, yoga, or tai chi
  • Support groups may be helpful
  • Can be transmitted to others within few days of becoming infected
  • Large enough amount of virus must enter body of a susceptible host
  • Factors that determine whether infection occurs after exposure
    • Duration of contact
    • Frequency of contact
    • Volume of fluid
    • Virulence & concentration of organism
    • Host immune status
modes of transmission
Modes of Transmission
  • Sexual Transmission
    • Most common mode
  • Blood and Blood Products
      • Sharing of needles
      • Transfusions
      • Occupational exposures
  • Perinatal Transmission
    • Can occur during pregnancy, at delivery or breastfeeding

Discovered 1983

A ribonucleic virus (RNA)

Called Retroviruses because they replicate backwards

Can’t replicate unless in living cell

hiv rna to hiv dna
  • HIV infects cells with CD4 receptors on surface
    • Lymphocytes, monocytes/macrophages, etc.
  • Targets CD4 T-cells as have more CD4 receptors
  • Viral genetic material enters cell
  • Viral RNA produces viral DNA with help of reverse transcriptase (enzyme made by HIV)
  • Strand of DNA copies itself
  • Viral DNA enters cell nucleus & becomes permanent part of cell’s genetic structure



Genetic material replicated during cellular division


All new cells infected


cell’s genetic codes direct cells to

make HIV

  • Long strands of HIV-RNA cut to length with assist of enzyme protease
hiv replication
HIV Replication
  • Rapid
  • Many errors and mutations
immune response to hiv
Immune Response to HIV
  • B-cells make antibody specific to HIV
    • They reduce viral load in blood
  • Activated T-cells mount cellular response to viruses in lymph nodes
  • CD4 T-cells attracted to lymph nodes where HIV concentrated
    • Once CD4 cells infected virus replicates and spreads throughout body
    • Lymph nodes are reservoir for HIV
      • Protect viruses from contact with drugs
      • Support viral replication
    • HIV damages lymph system and virus spills into blood
cd4 t lymphocytes
CD4 T-Lymphocytes
  • Normally have 800-1200/microliter blood
    • >500 for healthy immune system
    • Immune problems 200-499
    • Severe problems <200
      • Immune suppression leads to opportunistic infections
  • Normal life span ~ 100 days
    • HIV infected CD4 cells dies after 2 days
    • HIV destroys 1 billion CD4 T-cells every day
  • Bone marrow and Thymus normally produce enough CD4 cells for years but…
    • Eventually HIV destroys more than body can reproduce
    • Decline in CD4 T-lymphocytes (T-helper cells) impairs immune function.
destruction of cd4 t cells
Destruction of CD4 T-cells
  • Budding
    • Leaves small holes in cell membrane
    • Cell contents leak out and cell dies
  • Fusion
    • Infected cells clump with other cells into mass that destroys all cells
  • Binding
    • Antibodies against HIV bind to surface of infected cells, activate complement system which destroys infected cells
hiv infection of monocytes
HIV infection of Monocytes
  • HIV infects monocytes by:
    • Attaching to CD4+ receptors on monocytes or…
    • Phagocytic ingestion of monocytes
  • Infected monocytes go to body tissues and differentiate into macrophages
  • HIV replicates in infected macrophages
    • No budding occurs so….
    • Cell remains intact and becomes HIV factory
clinical manifestations acute infection
Clinical Manifestations- Acute Infection
  • Acute Retroviral Syndrome
    • Flu like symptoms
      • Fever
      • Swollen lymph nodes
      • Sore throat
      • Headache
      • malaise
      • Nausea
      • Muscle and joint pain
      • Diarrhea
      • Rash
  • 1-3 weeks after infection
  • Last 1-2 weeks (or months)
  • High level of HIV in blood, CD4+ T cell count down but quickly returns to normal
clinical manifestations early chronic hiv infection
Clinical ManifestationsEarly Chronic HIV Infection
  • HIV infection to diagnosis AIDS ~ 10 years
  • Asymptomatic …but can have
    • Fatique, headaches, low fever, night sweats, lymphadenopathy
  • Not aware of infection
  • Can transmit to others
  • CD4 count >500
clinical manifestations intermediate chronic infection
Clinical ManifestationsIntermediate Chronic Infection
  • Symptoms become worse
    • Persistent fever
    • Drenching night sweats
    • Diarrhea
    • Severe fatique
  • Localized infections
    • Thrush, shingles, vaginal candidiasis, oral/genital herpes, Kaposi’s Sarcoma, oral hairy leukoplakia
  • CD4 count 200-499
  • Lymphadenopathy
  • Viral Load rises
clinical manifestations late chronic infection
Clinical ManifestationsLate Chronic Infection
  • See Diagnostic Criteria for AIDS CDC
    • HIV positive
    • And CD 4 cell count < 200 cells/mm3
    • Or an opportunistic infection
  • Decrease absolute # of lymphocytes
  • All factors = increased risk for opportunistic diseases
diagnostic studies
Diagnostic Studies
  • Screening Tests
    • Detect HIV antibodies
      • Not useful first few months of infection because of Window period
      • All infants of HIV infected Moms will test positive up to 18 months as antibodies cross placental barrier. (instead test for HIV antigens or do viral cultures)
      • ELISA (enzyme immunoassay)(EIA)
      • Western Blot (IFA)
lab studies to evaluate response to treatment
Lab Studies to evaluate response to treatment
  • Tests used to
    • Determine when to start treatment
    • Determine efficacy of treatment
    • Determine if clinical goals are being met
  • Monitor CD4 T-cell lymphocyte counts
  • Viral load (viral burden) counts (the best indication)
  • Tests for resistance to ART
goals of care
Goals of Care

Monitoring disease progression and immune function

Initiating and monitoring drug therapy

Preventing opportunistic diseases

Detecting and treating opportunistic diseases

Managing symptoms

Preventing or minimizing complications of treatment

initial visit
Initial Visit
  • Gather baseline data
    • Complete H&P
    • Immunization hx
    • Psychosocial hx
    • Dietary evaluation
  • Establish rapport
  • Initiate Education
    • HIV treatment
    • Preventing transmission
    • Improving health
    • Family planning
  • Report to state health department
goals of drug therapy
Goals of Drug Therapy

Decrease viral replication & delay progression of disease

Prevent viral resistance to drugs

Decrease HIV RNA levels to < 50 copies/microliter

Increase CD4+ T-cells to >200 (800-1200 preferred)

Delay development of HIV related symptoms

antiretroviral drugs
Antiretroviral Drugs
  • Work at various points in HIV replication cycle; decrease chance of drug resistance
  • 3 primary groups of drugs
    • Inhibit ability of HIV to make DNA copy early in replication
    • Inhibits ability of virus to reproduce in late stages of replication
    • Prevents entry of HIV into cell
drugs that work by inhibiting activity of reverse transcriptase
Drugs that work by inhibiting activity of reverse transcriptase
  • Nucleoside Reverse Transcriptase Inhibitors (NRTI’s)
    • HIV DNA chain left incomplete by blocking chain development
  • Nonnucleoside Reverse Transcriptase Inhibitors (NNRTI’s)
      • Block conversion of HIV RNA to HIV DNA
  • Nucleotide Reverse Transcriptase Inhibitors
nursing management for client with unknown status
Nursing Management For client with unknown status
  • Identify Risk behaviors
    • Blood transfusions (esp. before 1985)/clotting factors
    • Shared needles
    • Sexual practices
    • STD’s
nursing management for client with unknown status1
Nursing Management For client with unknown status
  • Identify Risk behaviors
    • Blood transfusions (esp. before 1985)/clotting factors
    • Shared needles
    • Sexual practices
    • STD’s
nursing assessment for clients with hiv infection
Nursing Assessment for clients with HIV Infection
  • Health History
    • Route of infection, TB, STD’s frequent infections
    • Meds
    • Perception of Health
    • Nutrition
    • Alcohol / drug use
    • Elimination
    • Cognitive
    • Role/relationships
    • Sexuality
patient education
Patient Education
  • Health Promotion
    • Prevent disease
    • Detect early so early intervention
  • Prevention
  • Develop safer, healthier, less risky behaviors
  • Education about Safe activities vs. Risk reducing activities
    • Abstinence
    • Outercourse
    • Monogomous partners
    • Condoms
    • Plastic wrap/latex dental dams
    • Do not use drugs – if you do don’t share equipment
    • Don’t have intercourse when under the influence of drugs/slcohol
decreasing risks of perinatal transmission
Decreasing Risks of Perinatal Transmission
  • Prevent HIV in women

Treat HIV infected pregnant women with Zidovudine

    • Decreases rate of transmission
    • Minimal side effects for baby
  • Combination therapy
    • Can decrease risk to <2%
decreasing occupational risks
Decreasing Occupational Risks
  • Follow Standard Precautions /Transmission based precautions
  • Post exposure prophylaxis (PEP) with combination ART
    • Base on type of exposure
    • Volume of exposure
    • Status of source
early intervention health promotion to improve immune function
Early Intervention Health Promotion to improve immune function
  • Nutritional support to maintain lean body mass, levels of vitamins & micronutrients, fluid balance
    • Eat nutrient dense foods
  • Eliminate alcohol, smoking, illicit drugs
  • Adequate rest and exercise
  • Stress reduction
  • Avoid exposure to infections
  • Mental health counseling / support groups