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NURS 5315 Exam 2 Study Guide:
Modules 3, 4 Normal Lab Values Inflammation, Altered Immunity and Infection Immune System
- Examine the structure and function of the immune system. ▪ Natural Immunity (innate resistance/immunity ❖ Exists prior to exposure to a microbe ❖ Born with it, based on genotypes & species ❖ Skin, mucous membranes ❖ Does not improve after exposure ❖ Functions to kill invading microorganisms & activated acquired immunity ❖ Cells of innate immunity: phagocytic cells, antigen presenting cells, natural killer cells, & complement - Active acquired immunity ▪ Obtained after exposure to antigen ▪ Improves with repeat exposure, antigen or immunization - Passive acquired immunity ▪ Acquired after the transfer of antibodies or T cells ▪ Mother to fetus, antibodies cross placenta or breast milk WBC 4.5- 11 pH 7.35-7.45 PT 11-12.5 Na 135- 145 Creatinine 0.5-1. Hemoglobin 13- 16 PaCO2 35- 45 INR <1.6 K 3.5- 5 BUN 8- 22 Hematocrit 37- 49 PO2 80- 100 PTT 23- 33 Mg 1.2- 2 Serum Osmolality 285- 295 MCV 80- 100 HCO3 22- 28 Ca 8.5-10.5 Osmolar GAP < Platelet 130- 400 Glucos e 70- 100 Anion GAP < F PO4 3-4.
▪ Artificial is when antibodies are given to recipient to provide immunity ❖ Rabies, tetanus, hepatitis, & snake bites ▪ Immediate protection, but only lasts as long as the antibodies ~ 2 weeks
- Antigen – virus/bacteria - Self-antigen - Allergens
- Cell mediated immunity – governed by T cells ▪ T cells are differentiated (named) by the expression of antigens on their cell membrane called “cluster of differentiation” (CD). ▪ CD4 cells = T-helper / T4 cells ❖ Activate macrophages, B cells, cytotoxic T cells, & other CD4 cells ❖ Release lymphokines that begin the inflammatory process ❖ Mediate delayed hypersensitivity reactions (TB skin test) ❖ Functions are performed by subgroup of CD4 cells called TH1 & TH2, release lymphokines Type of T-lymphocyte Cells Function T-Helper cells Activate macrophages, B-cells, cytotoxic T cells and other CD4 cells, release lymphokines (TH1 & TH2), that being the inflammatory process. Mediate delayed hypersensitivity reactions (TB skin test) T-cytotoxic cells Kill virus infected cells, tumor cells, & allograft cells (transplant tissue) through release of cytotoxic chemicals which destroy the cell membrane or induce apoptosis. NK Killer cells Contain granules that attack & kill virus infected or cancerous cells T-Regulatory cells Slow or stop the immune response once the invader is defeated ▪ Memory T cells – allow host to remember antigens & respond quicker & more vigorously after the initial exposure. Liver for many years and can reproduce themselves ▪ Activation of T Cells:
Differentiate between the roles of B-Lymphocytes and T-lymphocytes in the recognition and processing of antigens. Type of Cell Role in the Recognition & Processing of Antigens B-Lymphocytes T-lymphocytes
- Differentiate between the role of T-Helper Lymphocytes and B-lymphocytes in the immune response. Primary and secondary immune responses.
- Primary Immune response ▪ Upon initial exposure to an antigen, the immune system will mount a response within 5-7 days ▪ Characterized by a rise in IgM antibodies, then a rise in IgG
- Secondary Immune response aka anamnestic immune response ▪ The second time the immune system is exposed to the same antigen ▪ IgM rise, but IgG rises much more than in the primary immune response Aging and the Immune System - Examine the age-related changes which occur in the immune system ▪ By middle age, thymus is only 15% of its maximum size = decreased T cell differentiation but not T cell numbers ▪ B cells produce less antibodies, less circulating memory B cells & increase circulation of autoantibodies ▪ After age 60, decreased T cell activity - Evaluate the physiologic differences in fetal and neonatal immune function. Stage of Development (^) Immune Function Differences Fetal Can mount primary immune response & produce IgM antibodies, unable to produce significant amount of IgG, unable to produce IgA. At birth IgG levels in umbilical cord blood is near adult levels but then drops off after
the cord is cut. Neonate Deficient in phagocytic activity, antibody production, & complement Inflammation
- The process of inflammation. Key Player Role and Function Mast Cell Histamine 1 Histamine 2 Cytokines Leukotrienes Prostaglandins Chemotactic Factors Platelet Activating Factor Neutrophils Monocytes Complement Kinin Coagulation Cascade a. Analyze the steps of the arachidonic acid pathway.
Analyze disorders which affect immune function.
- Identify the etiology, pathophysiology and clinical manifestations of an allergic immune response. - Type I (Immediate Hypersensitivity) – immediate hypersensitivity response to an environmental allergen. ▪ Usually good, medication, pollen, etc. ▪ Poison ivy is not an IgE mediated response ▪ Occurs within minutes – hours from exposure to the allergen ▪ Begins with antibody IgE, primes the stage for a reaction to occur later ▪ Antigen then binds to the previously formed antigen-IgE complex mast cell detects the complex & begins to degranulate releases histamines & triggers inflammatory cascade ▪ Clinical manifestations are dependent on the route of allergen entered the body ❖ Urticaria, rhinitis (inflammation of the membranes of the nose), conjunctivitis, asthma/bronchoconstriction ▪ Examples: ❖ Environmental allergies, asthma exacerbation, food, drug, animal, insect venom allergies ❖ Angioedema – idiopathic or related to medications, lips, eyes, & larynx ❖ Anaphylaxis – most severe reaction - Itching, urticaria (hives), angioedema, N/V/D, abdominal cramps, wheezing, dyspnea, laryngeal edema, hypotension, shock, & death - Treated with epinephrine (dilates bronchial smooth muscle), steroids & hydration - Steroids and hydration given as necessary ❖ Atopic disorders – hay fever, asthma, eczema, & urticaria - Strong genetic disposition Autoimmunity / Autoimmune diseases - Develops when an igniting event occurs in a person who is genetically predisposed to autoimmunity - Results in immune system mounting a response against person’s own cells - Familiar tendency & more common in women - Ex: SLE & rheumatoid arthritis
Systemic Lupus Erythematosus Etiology
- Chronic, multisystem, inflammatory disease - Affects primarily women between ages 20- 40 - African Americans > Caucasians Clinical Manifestations - Butterfly rash (localized to cheek), photosensitivity, nonerosive arthritis of at least 2 peripheral joints, serositis (inflammation of serous sacs i.e. pericardial & pleural sacs), arthralgias, pulmonary hemorrhage, proteinuria, seizures, anemia, leukopenia, & thrombocytopenia Pathophysiology - Antibodies are formed against nucleic acids, erythrocytes, coagulation proteins, phospholipids, lymphocytes, platelets, & other self-components - Most antibodies are formed against DNA, RNA, histones & other components of cellular nucleus - Antibody antigen complexes are deposited in a variety of tissues (kidneys, lungs, joints, skin, blood vessels (vasculitis). Results in activation of complement, inflammatory response, & ultimately causes tissue damage Rheumatoid Arthritis Etiology - Chronic inflammation of connective tissues, primarily joints - 1-2% of adults, more common in women - Incidences increases after age 30, highest > age 60 - Nulliparity (never given birth), Children whose mother smoked (double risk) - Smoking, low socioeconomic status, obesity - HLA-DRB1 gene has increased risk of developing RA - Lower risk in women who breast fed Clinical Manifestations
Coloniz atio n Invasion Multiplication Spread Concept Definition Incubation period Pathogen beings active replication, does not experience clinical manifestations yet, highly dependent on microorganism. Prodromal stage Initial appearance of clinical manifestations, normally mild in nature Invasion period Rapid multiplication of organism & activation of the immune & inflammatory responses. Begin having organism specific clinical manifestations & inflammation. Convalescence Containment of infection, resolution of clinical manifestations. Communicability Immunogenicity Infectivity Pathogenicity Portal of entry Toxigenicity Virulence Endemic Epidemic Pandemic
- Differentiate between the structure, pathogenic properties and mechanisms by which bacteria,
viruses and fungi cause disease. Virus Structure
- Have cytoplasm, ribosomes, lipid plasma membrane, & outer rigid wall of peptidoglycan. - Peptidoglycan ▪ Made of sugar & peptides ▪ Provides protection against osmotic pressure. ▪ Only produced by bacteria & is the site of action for some antibiotics - Single chromosome of DNA coiled in center of cytoplasm & RNA that functions to produce protein - Polysaccharide capsules that surround bacteria & provides extra protection against phagocytosis - Plasmids are extra chromosomal DNA molecules that multiply independent of DNA. Carries the genes for antibiotic resistance & toxin production - Pili – hair like filaments that assist with attachment of the bacteria to cell surface (N. gonorrhea) - Glycocalyx – slime layer secreted by bacteria to assist with adherence to structures like skin, heart valves, or catheters. Streptococcus Mutans (located in mouth) attaches to teeth via glycocalyx formation of plaque & carries - Shapes ▪ Cocci – strep/staph. Chains of cocci – Strep, Cluster like grapes – Staph ▪ Rod – Bacilli/E. Coli ▪ Spirochetes (helical) – Treponema Pallidum (syphilis) ▪ Pleomorphic (no particular shape) – Mycoplasma Pneumoniae ▪ Intracellular parasites (rod, spherical, or pleomorphic) – Rickettsia (ticks) ▪ Diplococci (pairs) ▪ Spore – Clostridium – can become dormant & impervious to host defenses. Pathogenic Properties - Gram Negative Bacteria – thin cells walls prevent retention of stain ▪ Cell wall contains endotoxins which are released when the bacteria is lysed ▪ Endotoxins cause fever, hypotension, DIC, & septic shock and are not neutralized by antibiotics. ▪ Covered with extra membrane outside cells, more resistant than gram positive to antibiotics ▪ Neisseria (gonorrhea, meningitis), Salmonella, Shigella, & Klebsiella
- Gram Positive Bacteria ▪ Release exotoxins 3 different toxins: Type I, II, III ▪ Examples – Staph, Strep, Bacillus (Anthrax), & Clostridium (tetanus) ▪ Some secrete teichoic acid, helps protect from complement mediated lysis ▪ Type I – interact with MCH class II proteins & stimulate the over production & release of proinflammatory cytokines ❖ Food poisoning or toxic shock from staph aureus, scarlet fever from strep pyogenes ▪ Type II – cause damage to cell membranes ❖ Strep. Penumoniae, C. perfringes gangrene ▪ Type III – enter the cell & cause damage ❖ Clostridium ❖ Shigella - Acid Fast Bacilli – extremely thick cell walls composed mainly of lipids, which allow it to take up the acid- fast stain ▪ Grow extremely slow d/t lack of nutrients being able to penetrate their thick cell walls ▪ Antibiotic therapy must be given months to years to be effective ▪ Cultures takes about 8 weeks to get a final report ▪ Examples – M. Tuberculosis (TB), M. Leprae (Leprosy), M. Avium (Mycobacterium Avium Complex) - Aerobic vs. Anaerobic bacteria can be gram negative/positive - Obligate aerobes must have oxygen to maintain metabolic processes to live - Pseudomonas ▪ Gram-negative, aerobic bacillus ▪ Nosocomial infections & chronic respiratory diseases ▪ Found mainly in soil & water - Gram positive bacilli are spore forming bacteria ▪ Bacillus Anthracis (Anthrax)
❖ Gram-positive Bacteria ❖ Group A Beta Hemolytic Streptococci (Streptococcus Pyogenes) – most virulent strep
- Cause fevers
- Strep throat, Scarlet fever, Rheumatic fever, Post strep glomerulonephritis
- Can be diffuse & rapidly spreading infection that involves the tissues & extends along lymphatic channels. Can become blood borne from lymphatic pathways
- Produce capsules composed of hyaluronic acid resistant to phagocytosis
- Some contain special virulence factors
- M protein protrudes from cell wall & protects the bacteria from phagocytosis
- Streptolysin O – protein that destroys RBCs & WBCs o Immune system can develop antibodies against the protein o ASO titer can be used to diagnose infection
- Streptokinase is an enzyme that activates plasmin which dissolves clots o Allows bacteria to escape from blood clots o Exotoxins are produced by this bacteria ❖ Group B Beta-Hemolytic Streptococcal – carried vaginally & lower GI tract in ~25% of women
- Can cause neonatal meningitis – therefore pregnant women should be screen for this bacteria & treated if present
- Now causing infections in the elderly & immunocompromised
- Risk factors for acquisition of this infection include diabetes, cancer, advanced age, cirrhosis, corticosteroid therapy & HIV
- Mainly causes – bacteremia, skin & soft tissue infections, respiratory infections, and GU infections ❖ Enterococci
- 2 types – faecalis & enterococcus faecium
- Both are nosocomial infections & part of normal flora
- Transmission direct contact (mainly hands of healthcare workers)
- Most common sites of infection are urinary tract, wounds, biliary tract, & blood
- Contains penicillinase grants resistance to PCN
- Intrinsically resistant to cephalosporins, PCN & monobactams
- Usually requires combination of drug therapy for treatment: ampicillin & an aminoglycoside
- Vancomycin Resistant Enterococci (VRE) ▪ Common cause of nosocomial infections, can be life-threatening ▪ # of different phenotypes ▪ Risk factors – recent use of vancomycin, cephalosporin, or fluroquinolones, ICU admission, prolonged hospitalization, or the critically ill
- Staphylococcus Aureus ▪ Gram-positive bacterium, commonly causes HAI, skin & soft tissue infections ▪ Part of normal flora, transmitted through direct contact, hand/stethoscopes, can be found on nares & skin ▪ Has surface proteins which enable it to attach to endothelium & tissues to cause infection ▪ Produces protein A which binds with IgG antibody and masks the bacteria from the antibody ▪ Produces a coagulase which produces clotting on the exterior portion of the bacteria hiding it from the immune system ▪ Additional proteins produced by the bacteria provide it protection from complement mediated lysis ▪ Methicillin resistant staphylococcus Aureus is resistant form of the bacteria ❖ Resistance if conferred by β-lactamase ▪ Risk factors – recent antibiotic use (cephalosporin, fluoroquinolones), prolonged hospitalization, nursing home residents, invasive medical devices, dialysis - Escherichia Coli – gram negative rod, part of normal flora in gut ▪ Most significant enteric bacteria & causes disease in many different organs! ▪ Diarrhea, hemolytic uremic syndrome, most common cause of UTIs
▪ Resistant to aminoglycosides by producing aminoglycoside-modifying enzymes (AMEs) ▪ Produces excessive para-aminobenzoic acid through spontaneous mutation of rRNA which has a lower affinity to antibiotics ▪ VanA gene provides resistance to vancomycin by decreasing the binding sites of the peptidoglycan for vancomycin
- Other mechanisms of resistance ▪ Change in cell wall permeability which prevents the entry of antibiotics ▪ Some bacteria develop an altered structural target for antibiotics ▪ Altered metabolic pathway that bypasses the reaction inhibited by the drug ▪ Developed altered enzyme that can still perform its metabolic function but is much less affected by the drug - Identify the clinical manifestations associated with infectious diseases. - Differentiate between exogenous and endogenous pyrogens. - Examine the pathological effects and properties of streptococci, staphylococcal, VRE, E coli, and candida infections. - Analyze coronavirus characteristics. - Evaluate the etiology, clinical manifestations and pathophysiology for influenza, measles, and HIV infection. - Differentiate between the incubation, etiology, and modes of transmission for influenza, measles, HIV infection, and COVID-19. Viral Infection Incubation Etiology Modes of Transmission Influenza 3- 5 Measles 6- 19 HIV Infection COVID- 19
i. Differentiate between clinical manifestations and pathophysiology of influenza, measles, and COVID-19. Viral Infection Clinical Manifestations Pathophysiology Influenza Measles COVID- 19 ii. Analyze the HIV viral structure, the process by which it infects the CD4 cells and viral replication:
- the clinical significance of the CD4 cell
- how antiretroviral medications impede viral replication
- the effects of the genetic mutation which alters the expression of the CCR5 cell receptor and its clinical significance iii. Differentiate between the difference in the diagnoses of HIV Infection and AIDS. iv. Evaluate the clinical manifestations which indicate a compromised immune system in a person with HIV infection. v. Evaluate the diagnostic tests used to screen for HIV infection.
- HIV EIA ( rd generation immunoassay)
- 4 th Generation immunoassay vi. Differentiate between the etiology, clinical manifestations and pathophysiology of the following opportunistic infections common in AIDS:
- pneumocystis jiroveci pneumonia (PCP)
- mycobacterium avium complex (MAC)
- cytomegalovirus (CMV) Type of Etiology Clinical Pathophysiology
