Transcript Immunity - Lake-Sumter State College | Home

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
 Antigen – a protein that stimulates an immune
reaction, causing production of antibodies.
 Viruses
 Bacteria
 Fungi
 Parasites
 Etc…..
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
 Prevent organisms from entering the body
 Skin
 Respiratory Tree
 Tears/Saliva
 Gi Tract – acidic environment, peristalsis
 Bile - antimicrobial
 GU tract – mucous membranes
Secondary Defenses
 Phagocytosis
 White blood cells
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TO THE RESCUE!
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
 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
damage
Secondary Defense #4
Fever
 Increases metabolism
 Inhibits pathogen multiplication
 Triggers specific immune responses
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
 1. Humoral Immunity– 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:
 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
 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??????
 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 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
 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???
 Phagocytosis
 Neutralization
 Agglutination
 Activation of complement and
inflammation
Two Types of Immunity
Innate (Native)
Adaptive (Acquired)
 Present at birth
 Body can make it or receive it
 First line of defense
 Specific response
 Non-specific response
 Results from adaptive
 Neutrophils first on the site
response to invasion by an
antigen (antibody formation)
 Can be passive or active
 Can be naturally produced or
artificially acquired
 Cannot be developed or
transferred
Adaptive Immunity
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
 Allergy testing (will discuss with allergies)
 Cd4-T cell counts (Helper T’s) – reflection of immune
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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 Diagnostics
 Rheumatoid Factor
 Serum Complement
 ESR (erythrocyte sedimentation rate)
 HLA testing – Human Leukocyte Antigen
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
 Antibiotics (anti-infectives)
 Use: treatment/prophylaxis of bacterial infections
 Cautions: Can depress bone marrow; Superinfections
 Cephalosporins
 Penicillins
 Fluoroquinolones
 Macrolides
 Sulfonamides
 Tetracyclines
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 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 Interventions
 Anti-inflammatory
 Corticosteroids
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Used for anti-inflammatory and
immunosuppressive properties
Topical, inhaled, intranasal, opthalmic, IV, PO,
IM
Long, intermediate, and short-acting
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 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 Interventions
 Immunotherapy
 SC injections weekly/biweekly of allergen
extracts
 Goals of Therapy
 Stimulate IgG levels for allergen binding
 Decrease IgE levels
 ALWAYS EXPECT ADVERSE REACTIONS!!!
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 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 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
http://www.youtube.com/watch?v=yA8671CyM7w
7 year old, Nicholas Green
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
 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 posttransplant. No cure. Once organ cannot function,
another transplant is only course.
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?
 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
 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?
 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
 Type I reaction – occurs when the already
sensitized person (see previous slide) is reexposed 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
 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?
 Respiratory – bronchospasm, laryngeal
edema, wheezing, cough
 Cardiovascular – hypotension, tachycardia,
palpitations, syncope
 Skin – urticaria, angioedema, pruitus,
erythema
 GI – N/V/D/, abdominal pain
Emergency Care
1.
2.
3.
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)
-Oxygen
-Antihistamines
-Bronchodilators
History of Anaphylaxis?
 Obtain Medical Alert Bracelet
 Carry Epi-pen
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
 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.
 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
 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 (Radioallergosorbent)
RAST testing
 Shows the blood level of IgE (antibody) directed
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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
 Therapy-induced immunodeficiency
disorders
Drug induced:
 Cytotoxic Drugs
 Corticosteroids
 Cyclosporin
Radiation Induced Immunodeficiency
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
 Defect in one or more immune components
 Present at birth
 Classified by type of immune function that
is impaired
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
 Skin: Butterfly rash
 Raynaud’s Phenomenon
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/Symptoms
 Cardiac System
 Pericarditis - most common cardiac
manifestation
 Myocarditis
 Anemia
 Leukopenia
 Thrombocytopenia
Lupus: Signs/Symptoms
 Respiratory System
 Pleuritis – Inflammation of the pleura
 Pleural Effusions – Fluid build-up between pleura and
chest cavity
 Pneumonia
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/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/Symptoms
 Neurologic System
 Neuropathies
 Psychoses, depression
 Seizures, migraine headaches
 CNS vasculitis
 Peripheral neuropathies
CNS Vasculitis
Lupus: Signs/Symptoms
 Constitutional Symptoms
 Fatigue
 Weight changes/loss or gain
 Fever
 Arthralgias
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
 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
 Pharmacologic Management
 NSAIDS
 Antimalarials (Plaquenil)
 Corticosteroid Therapy
 Immunosuppressive ages (methotrexate or
Imuran)
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
 Importance of skin care
 Monitor body temp and other warning signs of a flare:
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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)
 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
 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
 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/Symptoms
 Early Disease Manifestations:
 Joint stiffness, swelling, pain
 Systemic:
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Low-grade fever
Fatigue
Weakness
Anorexia
Paresthesias
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/Symptoms
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Late Disease Manifestations – Systemic
Osteoporosis
Anemia
Weight loss
Subcutaneous nodules
Peripheral neropathy
Vasculitis
Pericarditis
Sjogren’s syndrome
Renal disease
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
 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 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 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)
 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
 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
 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/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
 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
 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
 Corticosteroids & immunosuppressants – tried to slow
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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
 http://www.youtube.com/watch?v=Lf8NihhvGhg
Gout
 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
Gout
 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
 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 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
 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
 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
 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/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/Symptoms
 Stage III (months to years after the tick bite)
 Chronic recurrent arthritis
 Chronic fatigue
 Cardiac complications
 Thinking/memory issues
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
 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.
Fibromyalgia
 Common Rheumatic pain syndrome with widespread 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
 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
 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 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)
 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
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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
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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
Spring 2012
 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
Transmission
Sexual Transmission
 Most common mode
Blood and Blood Products
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Sharing of needles
Transfusions
Occupational exposures
Perinatal Transmission
 Can occur during pregnancy, at delivery or
breastfeeding
Modes of Transmission
 Discovered 1983
 A ribonucleic virus (RNA)
 Called Retroviruses because they
replicate backwards
 Can’t replicate unless in living cell
Pathophysiology
 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
THEN
HIV-RNA to HIV-DNA
Genetic material replicated during cellular
division
so
All new cells infected
and
cell’s genetic codes direct cells to
make HIV
Long strands of HIV-RNA cut to length with
assist of enzyme protease
 Rapid
 Many errors and mutations
HIV Replication
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
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Protect viruses from contact with drugs
Support viral replication
 HIV damages lymph system and virus spills into blood
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
 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 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
 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
 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
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
 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
 Screening Tests
 Detect HIV antibodies
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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)
Diagnostic Studies
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
Lab Studies to evaluate response to
treatment
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
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
 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
 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
 Nucleoside Reverse Transcriptase Inhibitors
(NRTI’s)
 HIV DNA chain left incomplete by blocking chain
development
 Nonnucleoside Reverse Transcriptase Inhibitors
(NNRTI’s)
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Block conversion of HIV RNA to HIV DNA
 Nucleotide Reverse Transcriptase Inhibitors
Drugs that work by inhibiting activity of reverse
transcriptase
Identify Risk behaviors
Blood transfusions (esp. before
1985)/clotting factors
Shared needles
Sexual practices
STD’s
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 status
Health History
 Route of infection, TB, STD’s frequent
infections
 Meds
 Perception of Health
 Nutrition
 Alcohol / drug use
 Elimination
 Cognitive
 Role/relationships
 Sexuality
Nursing Assessment for clients
with HIV Infection
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
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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
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 Risks of Perinatal
Transmission
 Follow Standard Precautions
/Transmission based precautions
 Post exposure prophylaxis (PEP) with
combination ART
 Base on type of exposure
 Volume of exposure
 Status of source
Decreasing Occupational
Risks
 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
Early Intervention Health Promotion to
improve immune function