Pathopharmacology & Pathophysiology

Exam 1 Immunity
Readings:
Aschenbrenner & Venable Drug Therapy in Nursing
o Chapter 13: pages 169-175 (Epinephrine)
o Chapter 45: pages 927-932 (Acyclovir), 934-936 (Oseltamivir)
o Chapter 46: pages 944-950; Classification paragraphs on pages 950, 959,
964, 971 (HAART)
o Chapter 54: pages 1173-1178 (Interferon alfa-2a)
Giddens Concepts for Nursing Practice
o Chapter 20: pages 204-215
Lewis Medical-surgical Nursing
o Chapter 14: pages 209-211 (Type 1: IgE Mediated Reactions), 214
Collaborative Care: Anaphylaxis
o Chapter 15: pages 231-233 (HIV)
o Chapter 24: pages 436 (Herpes Zoster Virus in Table 24-5)
o Chapter 27: pages 503-504 (Influenza)
o Chapter 44: pages 1007-1015 (Hepatitis C only)
Immunity Giddens Chapter 20
Immunity: a physiologic process that provides an individual with protection or defense
from disease
Accomplished through the actions of the immune system, which is a body-wide,
complex, interrelated group of cells, tissues, and organs that work within a
dynamic communication network to protect the body from attacks by foreign
antigens, typically proteins.
Foreign antigens may include microorganisms (bacteria, viruses, parasites, or
fungi), but may also be proteins found in pollens; foods; bee, snake, or spider
venom; vaccines; transfusions; and transplanted tissues.
Innate Immunity = immunity present at birth
o Provides nonspecific response not considered antigen specific
o Has no memory of the encounters, does not remember specific foreign
antigens, and does not provide any ongoing protection against future
infection.
Acquired Immunity = immunity protection that is gained after birth either
actively or passively
o Active Acquired Immunity = develops after the introduction of a foreign
antigen resulting in the formation of antibodies or sensitized T lymphocytes
Ex: active immunity may be obtained artificially through the immune
response to an immunization or it may be obtained naturally through
the immune response to exposure to infectious pathogens such as
varicella-zoster virus
o Passive Acquired Immunity = occurs by the introduction of preformed
antibodieseither from an artificial route, such as a transfusion of
immunoglobulin (Ig), or from a natural route, such as from a mother to her
fetus through placental blood transference or through colostrum transfer
during breastfeeding

Humoral Immunity = The component of the immune response involving the

transformation of B cells into plasma cells that produce and secrete antibodies to a
specific antigen
o Cells Involved = B cells
o Products = antibodies
o Memory Cells = present
o Protection = bacteria, extracellular viruses, respiratory & GI pathogens
o Ex: anaphylactic shock, atopic diseases, transfusion reaction, bacterial
infections
Cell-Mediated Immunity = T lymphocyte response = T lymphocytes undergo
differentiation on exposure to a foreign antigen, developing into subtypes of cells
that may directly attack the antigen or stimulate the activation of other leukocytes.
Cytotoxic T lymphocytes attack and kill antigens directly with preference for
viruses or mutated cells that have become cancerous.
o Cells Involved = T cells, macrophages
o Products = sensitized T cells, cytokines
o Memory Cells = present
o Protection = fungus, intracellular viruses, chronic infectious agents, tumor
cells
o Ex = tuberculosis, fungal infections, contact dermatitis, graft rejection,
destruction of cancer cells
Optimal Immune Response: 3 functions = defense, homeostasis, and
surveillance
o 1. Protects the body from invasion of microorganisms and other antigens.
By skin boundary surfaces including mucous membranes, enzymes,
natural microbial flora, and complement proteins
o 2. Removes dead or damaged tissue and cells.
By activities of phagocytes, natural killer T lymphocytes, granulocytes,
and macrophages providing innate, nonspecific immunity
o 3. Recognizes and removes cell mutations that have demonstrated abnormal
cell growth and development.
By antibodies derived from B lymphocytes and the T lymphocytes
resulting from learned or acquired specific immunity
Altered Immunity: conditions in which immune responses are either suppressed
or exaggerated
Suppressed Immune Response: hypo-, immunocompromised or are considered
to be at a state of immunodeficiency
o Immunocompromised/Immunodeficient
o Individuals are unable to provide an adequate immune defense against the
invasion of microorganisms or foreign proteins
o Result: individual is at significant risk for infection, or if immunosuppression
occurs over time, they are at risk for cancer because of the loss or removal
of mutating cells
o Primary Immunodeficiency: occurs as a result of improperly developed
cells or an absence of cells required to execute the immune response
Born with a genetic mutation or there is a missing piece of immune
system
Primary can cause secondary

o Secondary Immunodeficiency: a loss of immune functioning (in a person

with previously normal immune function) as a result of an illness or
treatment
Loss of function of immune system (autoimmune disorder, skin grafts)
Intentional: autoimmune disorder, organ transplants, skin grafts,
cancer treatment
Adverse effect of treatment = chemo cancer
Exaggerated Immune System: hyper-, an overreaction of the immune system
o Range from allergic reactions, cytotoxic reactions, and autoimmune reactions
o Hypersensitive mostly talking about
o Autoimmune immune system starts attacking own body
o Critical component of immune system: ability to differentiate between self
and non-self
Accomplished by the presence of unique proteins on the surface of
every cell that distinguish each individual as self and are as unique
to each individual as fingerprints.
When recognition fails, immune system may begin attacking host cells
in an exaggerated immune response. This process leads to the
development of autoimmune diseases and disorders (rheumatoid
arthritis)
Cells Associated with Immune Response
B lymphocytes (B cells): A type of lymphocyte that differentiates into
plasmocytes (plasma cells) that secrete antibodies that attack foreign cells or
proteins in distant portion of the body
o Antibody immunity
o Bone marrow-derived
o Secretes antibodies
o B cells and ANTIBODIES are best at destroying bacteria and bacterial
products
o B cells can differentiate into PLASMOCYTES, which produce and secrete
antibodies that react with specific chemical targets called ANTIGENS
T lymphocytes (T cells): directly kill antigen-bearing cells, which are foreign cells
or body cells that have been infected by viruses
o Cell-mediated immunity
o Thymus-dependent
o Cytotoxic T cells attack and kill antigens directly with preference for viruses
or mutated cells that have become cancerous
o T cells are best at destroying eukaryotic cells that express surface antigens,
such as virus-infected cells and grafted and tumor cells
o Cells that migrate from the bone marrow to the thymus differentiate into T
lymphocytes (thymus-dependent cells). The thymus secretes hormones,
including thymosin, that stimulate the maturation and differentiation of T
lymphocytes.
B & T Cells:
o B cells and T cells are the main types of lymphocytes.
B cells work chiefly by secreting substances called antibodies into the
bodys fluids. Antibodies ambush foreign antigens circulating in the
bloodstream. They are powerless, however, to penetrate cells. The job
of attacking target cellseither cells that have been infected by

viruses or cells that have been distorted by canceris left to T cells or

other immune cells
Unlike B cells, T cells do not recognize free-floating antigens. Rather,
their surfaces contain specialized antibody-like receptors that see
fragments of antigens on the surfaces of infected or cancerous cells. T
cells contribute to immune defenses in two major ways: Some direct
and regulate immune responses, whereas others directly attack
infected or cancerous cells
Major Histocompatibility Complex (MHC) = surface proteins which function to
differentiate cells of the self/host from foreign particles (self and non-self)
o A collection of glycoproteins (proteins with a carb) that exist on the plasma
membrane of nearly all body cells
o Class I: found on all cells
o Class II: found on specialized cells
Generation of Clonal Diversity: process where the specificity of lymphocytes to
a specific antigen emerges as a person is challenged by the presence of foreign
antigens throughout life
o Lymphocytes that can recognize and react to a specific antigen proliferate
o Occurs when an antigen selects those lymphocytes with compatible
receptors and expands their population
o The immunocompetent B and T lymphocytes also differentiate into mature B
and T cells
o On reexposure to same antigen = more rapid & efficient immune response,
indicating a memory capacity for the immune system (Memory B cells &
Memory T cells)
Antibody: Immunoglobulins (Ig) essential to the immune system that are
produced by lymphoid tissue in response to bacteria, viruses, or other antigens
o Plasma cells produce antibodies
o Secreted by B lymphocytes
o Formed after a B cell encounters and engulfs an antigen and then interacts
with helper T cells; B cell then begins producing identical copies of a specific
antibody
o Y-shaped proteins that circulate through the blood stream and bind to
specific antigens, thereby attacking microbes
o Immunoglobulins are primarily responsible for the body's response to
invading bacteria and viruses and provide the humoral immunity
component of an immune response
Antigen: Substance, usually a protein that causes the formation of an antibody
and reacts specifically with that antibody
Phagocytes: found throughout the body and are usually responsible for
recognizing and ingesting foreign antigens as they enter the body
o Macrophages and neutrophils are the primary phagocytic cells responsible
for this first line of defense during an immune response
o Phagocytosis is the process of ingesting cellular material and involves the
ability of phagocytes to be selective in recognizing cells that must be
ingested and discarded.
Complement system: works to enhance the immune response and to help rid the
body of antibody-antigen complexes. The complement system is comprised of 25
major proteins that circulate in an inactive form in the blood and are engaged in a

cascade of interactions when the first protein molecule (C1) encounters an

antigen-antibody complex
o Also responsible for the dilation and ultimate leaking of fluid from the
vascular system, leading to the redness and swelling during the
inflammatory process that are associated with an immune response
Dendritic Cells: recognized as potent cells in asserting control from initiation to
termination of the immune response
o Have a sentinel function throughout the body as they look for foreign
antigens and alert lymphocytes to the presence of injury or infection
o AKA antigen presenting cells; they bind to antigens and then process and
present them to both B and T lymphocytes in an immune response. They
have been found to directly activate helper and killer T cells and present
cancer cells to cytotoxic T cells, which respond by killing mutant cells
Cytokines: soluble factors secreted by WBCs and a variety of other cells in the
body) that act as messengers between the cell types
o Instruct cells to alter their proliferation, differentiation, secretion, or activity.
Populations at Risk for Altered Immunity
Age
o Young/Infant: organs and immune system are not fully developed, rely on
mother
o Elderly: thymus stops working/less productive B cells (and by extension T
cells) stop working
Body does not respond as well or as quickly
Fewer T lymphocytes, produce fewer immunoglobulins, experience a
delayed and diminished hypersensitivity response, and demonstrate an
increase in autoantibodies
Non-immunized State: body doesnt learn how to respond
Chronic Illness: body is constantly using resources to deal with chronic illness,
can get overworked = immune system spread too thin
Medical Treatments/Exposure
o Geographic region affected = Ebola outbreak in West Africa
o Chemotherapy suppresses immune system
High Risk Behaviors: unprotected sex, high adrenaline junkies
Substance Abuse: any drug, alcohol
Pregnancy: mom is splitting immune system
o Working for mother and baby = stretched too thin
Gender, Race, Ethnicity, Genetics, Environmental = HYPERSENSITIVITY
o Genetic abnormalities
o Inherited traits
o Autosomal diseases/dysfunctions
o Cardiovascular disease = females more prone
Elements of History
Past medical history = what drugs/illnesses/diseases have they had in the past
Family history
Genetic history
Current medications
Allergies to medications or other substances = can turn into exaggerated immunity
Lifestyle behaviors

 Occupation
Social environment = substance abuse
Common Diagnostic Tests
Primary Testing = use first**, then try other methods
o RBC count & WBC count with Differential (CBC)
High WBC possible infection
High RBC hemolytic interactions
Differential count shows count of all WBCs and can show what kind of
problem you are having
o Fluorescent Antinuclear Antibody
Shows if you are having any autoimmune disorder problem
o C-Reactive Protein (CRP)
Shows inflammation pt of immune response, but does not show
where in the body
o Erythrocyte Sedimentation Rate (ESR)
Shows inflammation pt of immune response, but does not show
where in the body
Other Testing = use after primary testing
o Allergy testing
o Genetic testing
o Rheumatoid factors (RFs) = specific test for rheumatoid arthritis (a
autoimmune disorder)
o Western blot test = tests for HIV
o TORCH antibody panel = tests for certain viruses (herpes)
o Organ function tests = kidney, liver
Clinical Management
Prevention
o Immunizations (CDC)
o Avoid high-risk behaviors
o Adequate nutrition
o Exercise
o Infection control measures
Screening
o No routine screening for general public tests are expensive and dont
always give us a great idea of what is going on unless there are s/s to go
along with it
o HIV screening for those with specific risk factors
Interrelated Concepts
Inflammation part of immune response, may or may not be visible
Infection infection precipitates (triggers) inflammation and immune response
Tissue Integrity if skin is intact, you have a good first barrier defense system
Stress alters hormone (cortisol) levels and can possibly weaken immune system
Exaggerated Immune System
Consequences:
o Acute hypersensitive reaction
Mild to severe
Localized to systemic (whole body)
Ex: bee sting pain/itchiness on arm (mild, localized to arm)

Ex: bee sting hives, respiratory system swells, feelings of death

(severe, systemic)
o Autoimmune disorders: chronic body-wide system disease
Can cause...
Destruction of body tissue
Abnormal organ growth (Chrons disease GI trouble)
Change in organ function
o Other symptoms: pain, fatigue, fever (common when you have altered
immune system)
Anaphylaxis
Type I IgE-Mediated reaction
o Type I hypersensitivity
o IgE antibodies
Occurs only in susceptible persons highly sensitized to specific allergens
o When first exposed = body is sensitized (swelling, itching)
o Next exposure = full anaphylaxis
Mediators released systemically
Reactions occur within minutes
Signs/Symptoms:
o Neurologic
Headache
Dizziness
Paresthesia = general abnormal feeling/sensation (burning, tingling)
Feeling of impending doom (death)
o Integumentary/Skin
Pruritus = itching/rash on top of skin
Angioedema = swelling under skin (common in hands/feet)
Constricts respiratory system = hard to breath
Erythema = redness color
Urticaria = hives, welts on top of skin
o Respiratory
Hoarseness
Coughing
Sensation of narrowed airway
Wheezing
Stridor = abnormal, high-pitched, musical breathing sound
Dyspnea, tachypnea = difficult breathing
Respiratory arrest
o Cardiovascular
Hypotension = veins dilate, low BP (body isnt getting enough blood)
Dysrhythmias = abnormal heart rhythm
Tachycardia = faster than normal HR (trying to keep up with
hypotension)
Can only last so long, leads to cardiac arrest
Cardiac arrest
o Gastrointestinal (GI)
Cramping, abdominal pain
Nausea, vomiting

Diarrhea

EPINEPHRINE: Nonselective Adrenergic Agonist

o Pharmacotherapeutics: anaphylactic shock, allergic reactions, possibly
asthma
o Pharmacokinetics
A: systemic (into all tissues); IM or SQ/SC (in bk: parenterally,
topically, inhalation)
D: systemic (throughout body)
E: kidneys
M: liver, rapid
Dur: 1-4 hours
Important to know duration because if penicillin is in system
longer than the duration of epinephrine, you need to give second
dose
o Pharmacodynamics: nonselective = alpha 1 and 2 (dilating), beta 1 and 2
(constricting)
Acts directly on the postsynaptic adrenergic receptors
Alpha 1 & 2 usually cardiac
Causes vasoconstriction effect is increased systolic BP and
decrease diastolic
Beta 1 & 2 usually respiratory
Causes bronchodilation by stimulation of beta-2 (asthma pt)
Dosage is important because Alpha will overcome Beta 2 (which does a
little bit of cardiac and little bit of respiratory)
o Contraindications/Precautions: hypersensitivity (allergy), sulfite
sensitivity, closed angle glaucoma, in labor, severe cardiac disorders,
glycogenesis/hyperglycemia (insulin levels can increase)
o Adverse Effects: hypertension, anxiety, cardiac arrhythmias (tachycardia),
cerebrovascular disease (cerebral hemorrhage - brain bleed)
Common: tremors, weakness, nausea, sweat, may feel heart
palpitations
o Interactions: anesthesia (cardiac arrhythmias), labor pt taking oxytocin
(hypertension); tricyclic antidepressants, beta-blockers
What if someone is taking beta-blocker? Overstimulate beta receptor
bc it is being blocked and causes the alpha receptors to dominate
cause high hypertension
o Labs to be Monitored: Kidney (BUN, creatinine); blood sugar levels, BP,
HR, oxygenation, EKG strips
o Patient Teaching: Should come from all these categories; use of
inhalers/nebulizers
o Lifespan Issues: elderly, young
o Pregnancy Category: C
Collaborative Care: Exaggerated Immune System
o Recognize s/s
o Remove exposure (if possible)
o Airway support: elevating head, laying down, sitting up (depending on
situation)
o Prevent spread with tourniquet: depends on what they have (if they have

been injected/stung bitten)

o Pharmacotherapy: give epinephrine, Benadryl or other antihistamine,
Albuterol (further dilates lungs)
o Treat for shock: depending on when it was caught - airway/volume support

Suppressed Immune System

Consequences:
o Four abnormal conditions can weaken immune system/stimulate immune
response
Transplant rejection
Neoplasms cancer tumors
Autoimmune disorder exaggerated immune response
Viral Invasion
o Two major problems occurring:
Cancer
Infection (primary or secondary)
Symptoms
o Report of frequent infections
o Report of poor wound healing
o Fatigue
o Malaise
o Weight loss
Clinical Findings
o May appear poorly nourished or have wasting syndrome
o May have chronic wounds
o May have enlarged lymph nodes
o Presence of opportunistic infection
Collaborative Care: Immunodeficiency
o Monitor immune function
o Nutrition
o Prevent opportunistic infections
o Monitor and treat opportunistic infections
o Drug Therapy
Viral Reproduction
o Adsorption: attachment to host cell
o Penetration: entrance of viral chromosome into host cell
o Uncoating: removal of protein coat/envelope from virus
o Replication
o Transcription
Herpes Zoster: acute unilateral and segmental inflammation of the dorsal root ganglia
Caused by activation of varicella-zoster virus (VZV)
Inflammation of dorsal root ganglia
Signs/Symptoms
o Lesions (groups of vesicles and pustules

o Neuralgia pain (nerve)

o Pruritus
o Fever
o Postherapetic neuralgia
o Scarring is possible
Collaborative Care
o Vaccination for adults over 50
o Antiviral agent
Puirnucleoside drug
o Mediated compresses
o Analgesics for pain
o Neuralgic symptom management

ACYCLOVIR: Purine Nucleoside Analogues

Pharmacotherapeutics: all herpes viruses
Pharmacokinetics
o A: GI system; orally (common), topically, IV
o D: systemic
o E: mostly by kidneys (drug unchanged hard on kidneys)
o M: liver (only a little)
o HL: if pt has any prior problems, it will extend HL dramatically (risk of
toxicity)
o Dur:
Pharmacodynamics: enzyme in virus (viral cell) absorbs it, inhibits viral
replication
o Must undergo phosphorylation, process by which phosphate combines with
an organic compound
Contraindications/Precautions: hypersensitivity, renal dysfunction, pre-existing
neurological condition
Adverse Effects: Tremors, involuntary muscle spasms
o Neurological side effects: lightheadedness, headaches, tremors
o Severe: hallucinations, coma
o Lack of appetite dehydration affects kidneys/renal function
o Abdominal
o Risk of nephrotoxicity (because it is so heavily excreted by kidneys)
Interactions: Valproic acid (seizure med) acyclovir makes the valproic acid
not work as well = more at risk to have seizures
Labs to be Monitored: urine output (amber, tea colored), Kidney: BUN, creatinine
Patient Teaching: Watch urine, intake/output, drink lots of water (high risk of
dehydration), watch for side effects (neurological and GI), know what other
drugs/alcohol they are taking and encourage not to, inform what to do if dose was
missed, breast feeding moms feed either right after taking drug or hours after it
was taken, regular interval administration
Lifespan Issues: elderly, repeated cases
Pregnancy Category: B
o Crosses placenta, breast milk baby gets higher dosage than mom bc serum
levels higher in breast milk than blood
Influenza

Season November April

Virus types A, B, C
Signs/Symptoms (FACTS)
o Fever, Aches, Chills, Tiredness, Sudden onset
o Pneumonia is common complication may need antibiotic to treat
Collaborative Care
o Vaccinations
o Rest, Hydration
o Respiratory support
Influenza can be very severe virus attacks lungs
Oxygen, ventilated or intubate
o Analgesics for pain
o Antipyretics medications for fever
OSELTAMIVIR: (TAMIFLU) Neuraminidase (protein on virus) Inhibitor
Nueramenidase inhibitors protein on influenza virus. So drug stops this
protein from breaking off and spreading (budding) which is why it works best
in the first 48 hours
Pharmacotherapeutics: influenza
Pharmacokinetics
o A: GI tract; oral
o D: systemic
o E: kidneys
o M: pro-drug, liver; becomes active after metabolism
o HL: effective in first 48 hours
o Dur:
Pharmacodynamics: drug stops the protein on influenza virus from breaking off
and spreading (budding) which is why it works best in the first 48 hours
Contraindications/Precautions: hypersensitivity; renal/liver dysfunctions,
chronic airway limitations (COPD, asthma); fructose sensitivity
Adverse Effects: nausea, vomiting, bronchitis, pneumonia (side effect of
influenza itself), insomnia, vertigo
Interactions: none
Labs to be Monitored: Kidney labs, urine output and color, hydration level, resp
rate, how are they breathing (easy, hard and in distress)
Patient Teaching: Pt with diabetes watch sugar levels bc of high fructose
content in liquid
Lifespan Issues:
Pregnancy Category: C
Hepatitis C (HCV): Inflammation of the liver RNA virus
Spread through blood and body fluids; complicated bc pt might not know they are
in acute phase
o Most common method of transmission: contaminated needles
Acute infection (1-4 months)
o RNA virus stimulates release cytokines which tell system to attack
liver cells
o Liver damage is mediated by cytotoxic cytokines and natural killer
cells that cause lysis of infected hepatocytes

o Most likely to spread to other people

o Liver can regenerate the damaged cells
o Lysis of infected cells damage to liver cells by cytokines
o Cholestasis interruption to bile flow; gallbladder problems
o Regeneration
o Some dont show symptoms may not be caught
Chronic infection (15-20 years)
o Fibrosis scarring of the liver
o Cirrhosis extreme fibrosis, extensive destruction of liver cells
o Liver cannot recover from these
Signs/Symptoms
o Rash comes from cytokine release
o Angioedema swelling under skin
Can cause respiratory/airway problems
o Arthritis comes from inflammation from immune response of cells
attacking liver
o Fever
o Malaise
o Jaundice liver cannot break down BILIRUBIN
Urine may darked
o Also possible:
Cryoglobulinemia abnormal proteins found in the blood
Glomerulonephritis infection and inflammation of kidney
(particularly the glomerulus) patient may have trouble excreting
Vasculitis inflammation of drug vessels
Hepatomegaly Enlargement/swelling? of liver
Collaborative Care: Hep C
o Diet modifications well balanced, tolerable
o Vitamin supplements
B complex (liver helps to synthesize B) and K (clotting)
o Rest
o Avoid alcohol
o Avoid drugs metabolized by liver
Hard to treat other diseases or problem
Wont metabolize drugs correctly high risk for toxicity
o Interferon type of drug to treat hep C
Has effects on viral replication cycle
o Anti-emetics keep from getting nauseous, headaches for hydration
purposes
INTERFERON ALFA-2A: Cytokines
Pharmacotherapeutics: Hepatitis C, Some times of cancer: pro-inflammatory,
anti-viral, anti-proliferative properties (keeps cancer cells from multiplying)
Pharmacokinetics
o A: systemic; IM, SQ
o D: systemic
o E: kidneys, primarily glomerular filtration
o M: liver, some by kidneys
Pharmacodynamics: inhibits viral replication DNA synthesis & RNA

Contraindications/Precautions: liver/renal disease, any history of cardiac

disease, any compromised neurological function
Adverse Effects:
o Common
Neuro: dizziness, confusion, lethargy, depression
GI: anorexia, nausea/vomit, change in taste
Flu-like symptoms: fatigue, malaise
o BP problems, cardiac arrhythmias, (Blood) effects (bone marrow disorders),
low platelet count issue with clotting
Interactions: Theophylline (asthma drug them together), HIV medication
(HAART) together cause neurotoxicity or hematotoxicity (blood)
Labs to be Monitored:
o Liver ALT, AST
o Kidney BUN, creatine
o Cardiovascular EKG
o CBC (complete blood count) to keep track of blood toxicity
o Psychosocial things
o Possible influenza swa
Patient Teaching: Monthly blood draw (labs), s/s of kidney/liver failure, no
pregnancy, injection technique; if given at night may be able to sleep through
s/s; needs to be refrigerated; no alcohol
Lifespan Issues: Not approved for patients under 18; Elderly watch for
kidney/liver function
Pregnancy Category: C

Human Immunodeficiency Virus (HIV)

CD4 Cells: T cells help to recognize foreign antigens and infected cells
o Activate antibody producing B cells which can induce cell-mediated immunity
Cytotoxic and natural killer cells start to destroy foreign antigens
HIV: retrovirus
o RNA with envelope is used to attach to host cells
Replicated via RNA into DNA
Replicates first as RNA and then into DNA
o Glycoproteins are used to attach to cells
o Obligate parasite
o Pathophysiology
gp120 binds to cells with a CD4+ protein receptor site on:
CD4 cells (high affinity)
monocytes
macrophages
certain nerve cells
Enzymes: integrase and protease
Uses integrase to integrate itself into the CD4 cell DNA and
becomes a permanent part of the CD4 cells structure
Fusion of viral envelope and plasma membrane
Viral RNA is transcribed into a single strand of viral DNA
Protease used to cut the strands of RNA

Provirus: virus prior to leaving cell, noninfectious in cell, replicates

and becomes infectious after leaving the cell
Replication occurs constantly, but symptoms may not be undetectable
for years
1. HIV inserts itself into DNA, 2. HIV RNA are cut into single strand DNA
by protease, 3. Integrase and protease are used to enter CD4 cell, 4.
Once virus leaves the cell it is infectious, 5. Replication always
occurring but may not be detectable for years
o Diagnosis
Initially made by a screening test followed by a confirmatory assay
Oral swab or blood test
Confirmatory assay/Western blot test
Screening tests are highly sensitive, whereas confirmatory assays are
highly specific
Western blot test (specific)
The combination use of these two types of tests produces results that
are highly accurate
o Lab Tests for HIV: want to look at all 3 before making any changes
to HAART therapy
CD4 Cell Count
Indication of current immunologic status of patient (healthy is
800-1200) 200-800 is weakened immune status. AIDS is less
than 200 (severely weakened). Allows providers to prevent any
other opportunistic infection. Predictor for disease progression
and survival. Slower decrease is good and suppressing virus
healthier longer. After therapy you should see increase in CD4
count
Viral Load HIV RNA Count
Count how well virus is suppressed by meds. Undetectable is
<50ml. Shows treatment response. Blood test. Checked at time
at diagnosis and every 3 to 4 months. GOAL IS UNDETECTABLE
LEVELS AND SUSTAIN IT AT THESE LEVELS FOR AS LONG AS
POSSIBLE
Resistance assays
Genotypic: genetic makeup for patients HIV. Presence for genes.
Determines strain
Phenotypic: takes a sample and puts it in with drugs and watches
how virus reacts. More expensive and takes longer
o Goals of HIV Therapy
Reducing complications and prolonging survival
Improving quality of life
Restoring and preserving immunologic function (increasing CD4+ cell
count)
Increased CD4+ cell count = immune system is
strengthening/improving responding well to therapy
Maximally and durably suppressing viral load
Decrease in viral load means replication of HIV has sload
Preventing perinatal HIV transmission
HAART (Highly Active Antiretroviral Therapy)

Individualized based on lifestyle, comorbidities, and other medications

Cocktail of drugs to disrupt HIV virus replication at multiple stages
o Multiple drugs used at multiple different locations
o At least 3 drugs, pt is not resistant to proven to suppress viral load
Compliance with drug treatment is essential
o Stopping therapy can lead to mutations in the virus and the medications that
were once effective can stop bring effective in suppressing your viral load
o No guarantee the drug will work again to suppress viral load
Drug Classifications
o Nucleoside/Nucleotide Reverse Transcriptase Inhibitors (NRTIs)
First class
Chemically similar to nucleotides
Once metabolized and converted into active form, inhibits reverse
transcriptase of viral DNA and becomes incorporated into viral DNA
and becomes a stumbling block for replication
Works inside the cell
o Nonnucleoside Reverse Transcriptase Inhibitors (NNRTIs)
2nd class
Treat one strain of HIV
Prevent conversion of viral RNA to DNA
Less toxic to humans because not as structurally similar to human
nucleotides
Work inside the cell
o Protease Inhibitors (PIs)
3rd class
Work inside the cell
Prevent maturation of the HIV virus into the core and cell of the HIV
virus
Most potent
Cross-resistance can occur
Very serious adverse effects
o Integrase Inhibitors
Newest class
Block enzyme integrase HIV DNA cant enter into host cell DNA
Cannot produce new genetic material to produce new viruses
Works inside the cell
o Entry Inhibitors
Fusion Inhibitors
Prevent HIV virus from binding to, fusing to, and entering the human
cell
Cant start RNA to DNA transcription
Occurs outside of the cell
Given subcutaneously, all others are given orally
HAART Side Effects
o GI upset: nausea vomiting
o Fever, Chills
o Sore throat
o Fatigue

Myalgia = muscle pain

Rash, Itching
Dizziness, Headache
Elevated Liver Enzymes = several of these meds are metabolized through
liver
HAART Adverse Effects
o Bone marrow suppression
o Anemia
o Neutropenia
o Black Box Warnings
HAART Patient Education
o Labs to be monitored
CD4 cell count, viral load, resistance assays, liver and kidneys labs,
lipids (cholesterol), electrolytes (hydration), insulin
o Follow up routines
Appointments (medical and psychosocial)
o Medication regimen
Discussing what meds are, how they work, how to take and store them,
side effects
o Any new medications
Call doctor about other prescribed, OTC, or herbal medications
o Adherence
Mutation leading to resistance
o Risk of transmission

Individualized
Duty to warn
Nervous System
o
o
o
o

Central Nervous
System (CNS) [brain
and spinal cord]

Peripheral Nervous
System (PNS) [neurons
outside brian and spinal
cord]
Efferen
t

Autonomic
nervous system

Sympathetic
nervous sytem
(adrenergic)

Alpha-1

Alpha-2

Beta-1

Afferen
t

Somatic nervous
system

Parasympathetic
nervous sytem
(cholinergic)

Beta-2

Cells
Involved
Products
Memory
Cells
Protection

Examples

Humoral Immunity
B lymphocytes
Antibodies
Present
Bacteria
Viruses (extracellular)
Respiratory and GI
pathogens
Anaphylactic shock
Atopic diseases
Transfusion reaction
Bacterial infections

Cell-Mediated Immunity
T lymphocytes,
macrophages
Sensitized T cells, cytokines
Present
Fungus
Viruses (intracellular)
Chronic infectious agents
Tumor cells
Tuberculosis
Fungal infections
Contact dermatitis
Graft rejection
Destruction of cancer cells