immunology Flashcards
homeostasis
what our bodies aim to maintain
what homeostasis involves
continuous motion, adaptation, and change by the body in response to environmental factors to maintain itself in a stable state
scientific definition of homeostasis
the tendency of biological systems to maintain relatively constant conditions in the internal environment while continuously interacting with and adjusting to changes originating within or outside the system
for most body systems, homeostatic mechanisms exist to
maintain and restore stability to body functions
for most systems, when a disordered physiological process occurs that causes, results from, or is associated with a disease or injury
the various systems of the body will act to maintain or return the body to homeostasis
homeostatic imbalance
inability to maintain homeostasis
homeostatic imbalance can occur as result of
illness or injury
homeostatic imbalance may lead to
disease or death
example of diseases that result from homeostatic imbalance
diabetes dehydration hypoglycemia hyperglycemia gout hypothermia
homeostasis and aging
body’s mechanisms to maintain homeostasis may weaken with age and lead to an unstable internal environment
subjective data
what the person says about themselves during history taking
objective data
what you as the healthcare professional determines during the physical examination
analyzing data
breaking down the data to examine and better understand
identifying issues, strengths, weaknesses
developing potential nursing diagnoses
pathology
the nature of the disease and its causes, processes, development, and consequences
physiology
describes mechanisms operating within an organism; the functions and activities of organs, tissues, and cells, and accompanying symptoms/occurrences/presentations
pathophysiology
the study of the physical and biological abnormalities occurring within the body as a result of the disease
immune system
our body’s defense system
protection from foreign organisms
protective response to injury or infection presents as
inflammation warmth redness swelling pain
all immune system cells arise from
the bone marrow
immune cells travel to other parts of the body
two categories of immunity
innate = the immune system we are born with adaptive = the immune system that targets specific threats to the body
innate immunity
- First line of defense
- Rapid response
- Not specific to particular pathogen
- No memory
- No long-lasting immunity
main components of innate immunity
Skin, mucous membranes, GI tract, Respiratory tract, nasopharynx, cilia, eyelashes, body hair
•Phagocytic cells – dendritic cells, eosinophil granulocytes, neutrophils, monocytes, macrophages, Natural killer (NK) cells
•Inflammatory process cells – endothelial cells, fibroblasts, thrombocytes, keratinocytes
lab tests for immune system functioning
c-reactive protein (increased levels can indicate inflammation or bacterial infection, marker for inflammation)
immunoglobulin (measures levels of different types of immunoglobulins/antibodies)
white blood cell count
components of white blood cells
neutrophils lymphocytes monocytes eosinophils basophils
neutrophils
most common type of white blood cell
lymphocytes
two main types of lymphocytes: B cells and T cells
monocytes
foreign material, removes dead cells, and boost the body’s immune response
eosinophils
fight infection, inflammation, and allergic reactions
defend the body against parasites and bacteria
basophils
release enzymes to help control allergic reactions and asthma attacks
adaptive immunity
specific immune response stimulated by invading pathogen
t cells
originate in thymus
viral infection protection
helper cells (Th), cytotoxic cells (Tc), suppressor/regulatory cells
b cells
originate in bone marrow produce antibodies (immunoglobulins) and develop into memory cells
antigen
any substance that combines with lymphocyte to trigger immune response
antibody
protein that binds to antigen on invading pathogen to eliminate pathogen
how invaders are eliminated (opsonization)
marking “invader” for ingestion and elimination by phagocytosis
“gluing” invader/bacteria to neutrophils and macrophages to facilitate phagocytosis
how invaders are eliminated (phagocytosis)
cell uses is plasma membrane to engulf the “invader” which is then digested
apoptosis
- Physiological process of cell death
- Regulates immune response by inducing timely death of T and B cells to prevent prolonged response that can cause problems for the body
- Eliminates immune cells that target self-antigens to prevent attack on self
- Used by certain immune system cells to destroy target cells
five primary classes of antibodies
IgG IgM IgA IgD IgE
IgG antibodies
major type (~75%) in plasma
prominent in memory response to antigens already encountered
crosses placenta from mother to fetus
IgA antibodies
prominent in secretions and significant in first-line defense
IgM antibodies
main antibody synthesized by B cells in primary/initial antibody response
IgE antibodies
significant in allergic responses and worm infestations
IgD antibodies
significant in primary/initial response to new pathogens
immune response activation
immune system activated when a foreign organism/molecule/vaccine is recognized by circulating phagocytic cells (such as macrophages or dendritic cells) that capture and break it down, presenting antigens to B cell lymphocytes
•B cell produces specific antibody against specific antigen to eliminate foreign pathogen
immune response regulation
regulatory T cells control immune response by suppressing activity to prevent damage to self
•Regulatory T cells factor in preventing autoimmune responses and anaphylaxis
immune system resolution
immune response resolves when foreign antigen eliminated
•T and B cells have differentiated into memory cells for this specific pathogen pending future invasion
adaptive immunity naturally acquired
active = antigens enter the body naturally; body induces antibodies and specialized lymphocytes passive = antibodies pass from mother to fetus via placenta or to infant via the mother's milk
adaptive immunity artificially acquired
active = antigens are introduced in vaccines; body produces antibodies and specialized lymphocytes passive = preformed antibodies in immune serum are introduced by injection
pediatric differences with immunity
Newborns have some antibody protection from mother for first few months
Newborns are susceptible to infections as immune system is immature and developing
Newborns have low immunoglobulin concentrations
Newborns have less responsive Natural Killer cells
Newborns have immature monocytes and macrophages
older adult differences with immunity (immunosenescence)
immune system function declines with age
Increased susceptibility to infectious diseases and cancer:Macrophages destroy bacteria and cancer cells more slowly
T cells respond less quickly to antigens
Poorer response to vaccinations: Binding affinity of antibody to antigen decreased
Older adults may have an increase in autoimmune responses as immune system less able to distinguish self from nonself
general signs and symptoms of infection
•Fever •Chills and sweats •Change in cough or a new cough •Sore throat •Shortness of breath •Nasal congestion stiff neck burning or pain with urination redness, soreness, or swelling diarrhea vomiting new onset of pain
4 phases of clinical process of infection
incubation period
prodromal stage
invasion period
convalescence
factors that influence the capacity of a pathogen to cause disease
communicability immunogenicity infectivity mechanism of action pathogenicity portal of entry toxigenicity virulence
incubation period
initial contact with infectious pathogen to the presentation of first symptoms
pathogen multiplying at portal of entry
ranges from 2-30 days depending on host resistance, virulence, and distance from entry to target organ
prodromal stage
first presentation of symptoms
1-5 days
non-specific symptoms such as malaise, fever, muscle aches
invasion stage
presentation of more specific prominent symptoms
pathogen multiplying and establishing in target organ
convalescent stage
recovery
pathogen eliminated by immune system cells
memory cells developed
epidemic
new cases of a disease exceed the normal occurrence during a given period of time
•An increase, often sudden, in the number of cases of a disease above what is normally expected in that population in that area
•Outbreak refers to epidemic for a limited geographic area; localized
endemic
the steady presence of a disease in a defined geographic area or population
•The baseline of the disease in a community
pandemic
when disease spread affects a large number of populations worldwide
bacteria
- One-celled
- Multiply by simple division
- Cause respiratory infections such as otitis media, tonsillitis, pneumonia, bronchitis, sinusitis, pharyngitis, whooping cough
- Treat with antibiotics
viruses
some of the smallest organisms known
•Invade cell, take over cell’s machinery, and force cell to reproduce virus
•Cause most respiratory infections such as influenza, the common cold/rhinovirus, some pneumonias and bronchiolitis/respiratory syncytial virus
•Treat with antiviral
viruses can only replicate
inside the cell of the host invaded
no ability to metabolize on own
basic structure of virus
consists of nucleic acid protected by a protein shell, the capsid
some may have additional envelope of fat
viruses are classified by
format of nucleic acid in the virion (ribonucleic acid [RNA] or deoxyribonucleic acid [DNA])
Single stranded (ss) or double stranded (ds)
Presence of the reverse transcriptase (RT) enzyme Present in retrovirusesUsed to make complementary DNA from RNA (reverse of usual normal process of making RNA from DNA)
pathologies of the immune system result from
increased or decreased white blood cells or immune system cells
increased white blood cells
expected when fighting an infection
overactivity- hypersensitivity (can result in autoimmunity and allergies)
decreased white blood cells
immunodeficient- predisposition to infections
secondary to decreased production- bone marrow problem or congenital disease
secondary to loss- infection of white blood cells
human immunodeficiency virus (HIV)
caused by infection with HIV1 or HIV2 which are retroviruses in the retroviridae family lentivirus genus
HIV produces
cellular immune deficiency characterized by the depletion of helper T lymphocytes (cd4 cells)
the loss of cd4 cells results in the development of opportunistic infections and neoplastic processes
virus pathway
Virus attaches to target cell
Penetrates the host cell membrane
Viral RNA is transcribed into the host cell DNA (reverse transcription)
Viral genetic material is integrated into the host cell chromosome
Production of new viral components and assembly of new virions
Virions exit from host cell and maturation occurs
HIV pathogenesis
Decrease in number of CD4 + Th cells due to infection and destruction by HIV
Glycoprotein gp120 on HIV facilitates entry into cell
HIV infected cells shed gp120 to induce apoptotic cell death of uninfected T lymphocytes, altering immune system response and impeding clearance of HIV
HIV infected CD 4 +Th cells fuse leading to formation of multinucleated cell (syncytium)
With fusion there is death of the uninfected cell
characteristics of HIV
Can kill host in a short period of time (relatively rare)
Can be completely eliminated from body Or can enter a state of latency
Retrovirus with ability to convert own RNA to DNA with the aid of an enzyme (reverse transcriptase)
Retroviruses are very fragile – easily inactivated by mild detergent, gentle heating, drying or moderately high or low pH
Transitions from acute to chronic infection with persistent replication – HIV unique among viruses
Two primary types of HIV: HIV 1 (most common) and HIV 2 (less virulent; lower viral loads and slower decrease of CD4)
three stages of HIV
acute seroconversion/acute HIV infection
clinical latency/asymptomatic or chronic HIV infection
acquired immunodeficiency syndrome (AIDS)
acute seroconversion/acute HIV infection
2-4 weeks post HIV infection flu like symptoms such as fever, malaise, generalized rash HIV multiplies and destroys cd4 cells body producing HIV antibodies HIV level (viral load) high risk of HIV transmission high
clinical latency/asymptomatic or chronic HIV infection
generalized lymphadenopathy common
may have no symptoms
HIV multiplies at low levels
acquire immunodeficiency syndrome (AIDS)
most severe phase of HIV infection HIV level (viral load) high risk of transmission high cd4 cells low risk of opportunistic infections high prognosis approximately 3 years
clinical manifestations of HIV
Patients may manifest one of several different conditions:
Serologically negative (no detectable antibodies)
Serologically positive (positive for antibodies against HIV )
Early stages of HIV disease
Early stages of AIDS illness
Early symptoms are nonspecific to HIV and include fatigue, fever, muscle aches, and headaches (flu like symptoms)
Early stages of HIV are asymptomatic and may last as long as 10 years in untreated people, during which viral load increases and numbers of CD4+ cells progressively decrease
over time (8-15 years) chronic infection by HIV causes
a depletion in function cd4 T helper cells leading to compromised immune system
HIV stimulates systemic immune activation
accelerates decline in overall immune competence - increase in dysfunction of T cells and inflammation
what percentage of cd4 cells are lost in the early stages of an acute HIV infection
80%
HIV infection leads to increased gut permeability
GI tract major site of HIV replication
transmission of HIV
blood transfusion condomless sex needle sharing mother to child accidental exposure
HIV can directly damage the
brain (causes cognitive impairment)
gonads (causes hypogonadism)
kidney (causes renal insufficiency)
heart (causes cardiomyopathy)
range of HIV manifestations
asymptomatic to AIDS
AIDS is defined by
serious opportunistic infections or cancers or a cd4 count of <200/mcL
how can HIV be diagnosed
antibody, nucleic acid, or antigen testing
nucleic acid tests
check blood for presence of the virus’ RNA
determine how much virus is present (viral load)
antibody and antigen tests
test for presence of HIV antibodies and antigens
HIV produces antigen p24 (before body starts producing antibodies to HIV)
antibody tests
test for HIV antibodies
venous blood for better detection
can use oral fluid or finger prick blood (later detection)
opportunistic fungal infections
Oropharyngeal candidiasis Candida esophagitis Vulvovaginal candidiasis Cryptococcus- meningitis/ pneumonia Pneumocystisis jiroveci pneumonia (PJP)
opportunistic protozoal infections
Cryptosporidium
Toxoplasmosis
Isosporiasis
opportunistic bacterial infections
Mycobacterium avium complex (MAC) Tuberculosis Pneumonia Bacillary angiomatosis Listeria monocytogenes Pelvic inflammatory disease Salmonellosis
opportunistic viral infections
Cytomegalovirus (CMV) Herpes simplex Herpes zoster Oral hair leukoplakia (EBV) Progressive multifocal leukoencephalopathy (PML) Castleman’s disease
opportunistic cancers
Karposi’s sarcoma
Invasive cervical cancer
Lymphoma
other opportunistic infections
Cellulitis
Osteomyelitis
Endocarditis
clinical manifestations of AIDS
Fatigue
Unexplained weight loss: greater than 10%
Fever
Lymphadenopathy
Skin or mucous membrane lesions: purplish-red nodules
Cough
Persistent diarrhea
Tongue/mouth “thrush”
Perianal vesicular and ulcerative lesions of herpes simplex infection
AIDS related cancer-Kaposi’s sarcoma
Cytomegalovirus retinitis
common signs of AIDS in pediatrics
Oral candidiasis
Bacterial infections
Failure to thrive
Lymphadenopathy
how neonates get AIDS
transmission may be placental
contact with maternal blood at birth
postnatal exposure to parent who is exposed (eg. breastfeeding)
systemic lupus erythematosus
when the immune system attacks the body’s own tissues and organs
systemic autoimmune disease
chronic, inflammatory, connective tissue disease of unknown origin
lupus involves
many organs and body systems including skin, joints, kidneys, lungs, CNS, hematopoietic system
lupus is characterized by
remission and exacerbations
lupus ranges from
a mil episodic disorder to rapidly fatal disease process
3 major classifications of lupus
discoid lupus erythematosus (affects skin only), systemic lupus erythematosus (affects one or more organs), and drug-induced.
suspected triggers of lupus
exposure to ultraviolet lights
estrogen
pregnancy infections
medications
autoantibodies
antibodies that react to the client’s own tissues
autoantibody production results from
hyperreactivity of B cells because of disordered T cell function
drugs that can cause drug induced lupus
Procainamide (used to treat heart arrhythmia)
Hydralazine (used to treat hypertension)
Quinidine (used to treat heart arrhythmia and malaria)
pathophysiology characteristics of lupus
Large variety of autoantibodies are produced
Autoimmune reaction is targeted at components of the cell nucleus
Production of pathogenic autoantibodies by T and B cells which attack own tissues and organs
Immune complexes containing antibodies against DNA deposit in the membranes of the:
Kidneys
Heart
Brain
Joints
Skin
Results in multiorgan inflammation: Joints, skin, kidneys, blood cells, brain, heart, lungs, GI
clinical manifestations of lupus
arthralgia or arthritis vasculitis and rash renal disease hematological abnormalities cardiovascular disease photophobia fever weight loss excessive fatigue
involved body systems with lupus
Dermatological Musculoskeletal Cardiopulmonary Renal Disease Nervous System Hematological
lupus nephritis
Inflammatory complication
Complexes of autoantibodies and complement accumulate in the glomerulus, causing cell proliferation, inflammation, and injury
Clinical manifestations include:
Proteinuria, edema and signs of nephrotic syndrome (hypoalbuminemia, hypolipidemia, lipiduria, decreased vitamin D levels, hypothyroidism)
Disease progression may be silent or may progress to end-stage kidney failure
nervous system manifestations of lupus
Generalized or focal seizures
Cognitive dysfunction (disordered thought processes, disorientation, memory deficits, and psychiatric symptoms such as severe depression and psychosis)
Stroke or aseptic meningitis
Headaches
hematological manifestations of lupus
Anemia
Mild leukopenia
Thrombocytopenia
Increased or decreased coagulopathy
does a patient have increased or decreased coagulopathy with antiphospholipid antibody syndrome?
increased
integumentary and lupus
Alopecia Dry, scaly scalp Keratojunctivitis Malar butterfly rash Palmar or discoid erythema Urticaria Periungal erythema Purpura, Petechiae Leg Ulcers
diagnosing lupus
Fulfillment of at least four criteria–
with at least one clinical criterion AND one immunologic criterion
OR 2) Lupus nephritis as the sole clinical criterion in the presence of ANA
or anti-dsDNA antibodies.
SOAP BRAIN MD for lupus
serositis oral ulcers arthritis photosensitivity blood renal ANA immunologic neurologic malar rash discoid rash
specific labs to assess for lupus
Antibody titers (i.e. anti-DNA, anti-Sm, ANA)
Anti-Sm = anti-Smith antibodies have high specificity for SLE
LE cell preparation
Serum complement levels
Urinalysis
Positive LE preparation, anti-DNA antibody or antibody to Sm nuclear antigen
Proteinuria or cellular casts
Hemolytic anemia, leukopenia, lymphopenia, or thrombocytopenia
Antinuclear antibodies
*Specific tests to address system clinical manifestations
signs and symptoms of rheumatoid arthritis
Inflammation and swelling of joint synovium with subsequent destruction of articular structures.
Systemic inflammation of any other organ systems, leading to associated comorbidities such as cardiovascular disease, pleural effusions, etc. (which can increase morbidity and mortality)
Pain, fatigue, and disability—decrease quality of life
the synovitis, swelling, and joint damage that characterize active RA are
the end results of complex autoimmune and inflammatory processes that involve components of both the innate and adaptive immune systems.
pathophysiology for RA
The “trigger” causes the body to create autoantibodies that aim for joint linings
Autoantibodies include rheumatoid factor (RF) and anti-cyclic citrullinate peptide antibody (anti-CCP).
Autoantibodies bind with their target antigens in blood and synovial membranes, forming immune complexes [antibody-antigen complexes] such as RF binds with IgG forming an immune complex.
Immune complexes deposited in synovial membrane attract white blood cells (ie. granulocytes) and activate inflammatory process
T cells activated to secrete inflammatory cytokines [including tumour necrosis factor alpha (TNF-α), Interleukin (IL)-1, IL-6, IL-8, transforming growth factor beta (TGF-β), fibroblast growth factor (FGF) and platelet-derived growth factor (PDGF)]
Cytokines stimulate immune and inflammatory response. Impaired clearance of immune complexes leads to sustained inflammatory response.
Now activated, B and T lymphocytes increase production of rheumatoid factors and enzymes that, in turn, increase and continue the inflammatory response.
Synovial membrane is damaged by the inflammatory and immune process.
Inflammation then spreads and involves synovial blood vessels (become occluded).
As blood flow decreases, metabolic needs increase, and hypoxia and metabolic acidosis occur.
Acidosis stimulates synovial cells to release hydrolytic enzymes into surrounding tissues
Inflammation causes coagulation, and deposits of fibrin on the synovial membrane, in the intracellular matrix, and the synovial fluid.
Fibrin develops into granulation tissue (pannus) over denuded areas of the synovial membrane.
Neutrophils are attracted to the site
Proteolytic enzymes are released
Thickening of synovial lining occurs and cartilage is damaged
Chronic inflammation causes hypertrophied synovial membrane which invades cartilage, ligaments, tendons and joint capsule
lab tests for RA
Rheumatoid factor (RF) Cyclic Citrullinated Peptide (CCP) Erythrocyte Sedimentation Rate (ESR) C-Reactive Protein (CRP) Antinuclear Antibody (ANA)
None of these tests can singularly conclude that a patient has rheumatoid arthritis
The combined results from all, alongside a number of other criteria including physical symptoms and genetics, are used to reach a rheumatoid arthritis diagnosis.
clinical manifestations of RA
onset = usually gradual, may be abrupt
course = generally progressive, characterized by remission and exacerbations
pain and stiffness = predominant on arising lasting > 1 hour, also occurs after prolonged inactivity
affected joints = appear red, hot, swollen, “boggy” and tender to palpation, decreased range of motion, weakness
systemic manifestations = fatigue, weakness, anorexia, weight loss, fever, rheumatoid nodules, anemia
deformities of chronic advanced RA
swan neck deformity
boutonniere deformity
ulnar deformity
hallux valgus
swan neck deformity
flexion of the distal interphalangeal and metacarpophalangeal joints, hyperextension of proximal interphalangeal joint
boutonniere deformity
avulsion of extensor hood of the proximal interphalangeal joint
ulnar deformity
ulnar deviation of the fingers at the metacarpophalangeal joint
hallux valgus
displaced toes, lateral angulation
rheumatoid nodules
Subcutaneous nodes
Firm, non-tender
Often found on fingers and elbows
sjorgen’s syndrome
Decreased lacrimal and salivary gland secretion
Decreased tearing and photosensitivity
felty’s syndrome
Inflammatory eye disorders
Splenomegaly, lymphadenopathy, pulmonary disease, blood dyscrasias (i.e. anemia)
complications of RA
Joint destruction Flexion contractures Hand deformities- difficulty grasping Nodular myositis Cataracts- loss of vision Nodules on vocal chords Carpal tunnel syndrome Cardiac complications
signs and symptoms of juvenile idiopathic arthritis (JIA)
Arthritis present for at least 6 weeks before diagnosis (mandatory for diagnosis of JIA)
Either insidious or abrupt disease onset, often with morning stiffness or gelling phenomenon and arthralgia during the day
Complaints of joint pain or abnormal joint use
History of school absences or limited ability to participate in physical education classes
Spiking fevers occurring once or twice each day at about the same time of day
Evanescent rash on the trunk and extremities
Psoriasis or more subtle dermatologic manifestations
JIA differs from RA
Large joints are most commonly affected
Chronic uveitis
Serum tests may be negative for rheumatoid factor, if rheumatoid factors are positive the child will have a worse prognosis
Subluxation and ankyloses may occur in the cervical spine if disease progresses
JIA that continues through adolescence can have severe effects on growth and adult morbidity
pediatric severe combined immunodeficiency (SCID)
Severe combined immunodeficiency, SCID, is a rare genetic disorder characterized by the disturbed development of functional T cells and B cells caused by numerous genetic mutations that result in differing clinical presentations.
Life-threatening syndrome of recurrent infections, diarrhea, dermatitis, and failure to thrive
Most patients present before age 3 months; With no intervention, SCID leads to severe infection and death by age 2 years
SCID results from and causes changes in
Results from mutations in at least 13 different genes
Causes changes in lymphocyte development and function which blocks differentiation and proliferation of T cells and sometimes, B and NK cells
pathophysiology of SCID
X-linked recessive that affects more males than females
Combined deficiency that affects both T and B cells with little to no antibody production
Few detectable lymphocytes in the circulation and secondary lymphoid organs
clinical manifestations of SCID
Susceptibility to infections occurs most commonly in the first month of life
Suffers from chronic infections and fails to completely recover from infections
FTT is a consequence of persistent illnesses
