Northeastern University 2350 Integrated Pathophysiology and Pharmacology Exam 1 Study Guide PDF

Northeastern University 2350 Integrated Pathophysiology and Pharmacology Exam 1 Study Guide Overview: Modules covered include 1, 2, and 3 Test Composition: 50 questions, multiple choice Study Tips: How to study Pathophysiology · There are many different diseases, illnesses and syndromes...

Northeastern University 2350 Integrated Pathophysiology and Pharmacology Exam 1 Study Guide Overview: Modules covered include 1, 2, and 3 Test Composition: 50 questions, multiple choice Study Tips: How to study Pathophysiology · There are many different diseases, illnesses and syndromes you will be learning about this semester. When you look at these different diseases a helpful structure to review is to consider the following for each disease process: o Pathophysiology: What normal process of the body is being disrupted and how? What is the course of the disease, acute vs. Chronic, etc.? Other things to consider: prognosis, morbidity and mortality. o Manifestations: What will I see/what will a person with this disease experience? Signs/symptoms o Treatments: Can this be treated? Possible medications reviewed for treatment and other nonpharm treatments. How to study Pharmacology · There are many different drugs and drug classes that are covered throughout this semester. It can be challenging to determine what is need to know versus what is nice to know. When you review different drugs and drug classes consider the following information: o Mechanism of action: how does it work o Therapeutic use: what is it used to treat o Nursing Process: What information do you need to safely give the drug? What information do you need to know if the drug is working? o Adverse Effects: What is common and what is high risk? o Off label: what else might this drug be used for? · Note on drug names: NCLEX testing will include drug names. Drugs will be listed by generic name only. Knowing generic names is important as this is the universal language of drug therapy. o Specific drugs names will be highlighted as prototypes/examples of drugs. You are expected to know these names. o Other names might be included on an exam. If this happens, you will see the drug class (broader category) included in the question prompt.  § Drug classes in some cases may be identifiable by naming norms often in the form of a common suffix. Keep an eye out for this to easily identify drugs as part of drug class. o Key take away: know example/prototype/gold standard drugs, be able to identify drug classes as the broader identifier in pharmacology. Module 1: Foundations of Pathophysiology Module Objectives: · Describe the chemical make-up and function of the cell membrane - Cell membrane is made up of a phospholipid bilayer that is selectively permeable that separates the inside from the outside. - Key function: selectively allow certain molecules to pass through and block others. This is maintaining homeostasis. · Identify basic cellular components and explain their function - Cell Membrane: controls what enters and exits the cell - Nucleus: contains DNA and genetic material, “control center” - Cytoplasm: Chemical reactions occur - Mitochondria: produces energy for the cell - Ribosomes: proteins made (protein synthesis) - ER: protein and lipid synthesis - Tissues: o Connective: support and protection o Epithelial: protection o Muscle: skeletal, smooth, cardiac o Nervous: communication · Describe the processes of energy production in the cell - Cell metabolism is the process that changes the calorie containing nutrients (carbs, proteins, fats) into ATP, providing the energy needs of the cell. o ATP is formed through 3 major ways: glycolytic pathway, citric acid cycle, and the electron transport chain. - Catabolism: break down of nutrients and body tissues to produce energy - Anabolism: building more complex molecules from similar ones - Cellular respiration: glucose is broken down into smaller molecules, releasing energy in the from of ATP  o Mainly happens within the mitochondria and there are multiple stages such as glycolysis, Krebs cycle, and oxidative phosphorylation - Anerobic respiration: NO oxygen o Glycolytic pathway in cytoplasm - Aerobic respiration: YES oxygen o In mitochondria · Compare and contrast Passive and Active transport - Passive transport: does not require energy and is moving molecules down the concentration gradient (high to low concentration) - Active transport: requires energy and is moving molecules against the concentration gradient (low to high concentration) · Compare and contrast common cellular structural adaptations - Atrophy: decrease in size of cells, tissues, or organs o Ex: bedridden clients typically have decline in muscle mass from underuse and immobility - Hypertrophy: the enlargement of an organ from the increase in size of its cells. o Ex: left ventricular hypertrophy in HF (enlarged heart muscles) o HYPER= high amounts TROPHY= big trophy (large muscles or organs) - Hyperplasia: enlargement of an organ caused by an increase in the reproduction rate of its cells o Ex: BPH- bengin prostatic hyperplasia o HYPER= high amounts PLASIA= productions - Metaplasia: change of a cell from 1 type to another type of cell o Ex: changes in the tissue of the airways in response to smoking or chronic irritation o think Metamorphosis - Dysplasia: healthy cells undergo abnormal changes. o Ex: cervical dysplasia o Dysplasia Dysfunctional production of cells (ABNORMAL) ​ -​ Neoplasia: new,abnormal growth of tissues ○​ Ex: neoplasma (tumors), malignant melanoma (skin cancer) ○​ Neo-plasia ​ ​ New production of cells · Outline two pathologic conditions related to cell alterations - · Cell Injury - Apoptosis: normal, shrink, controlled cellular turnover, allows for new cell growth o Process occurs with cell aging which limits our life span - Ischemia: lack of oxygen/ blood supply to cells/ organs o CAN BE REVERSED, depending on depth of injury o Brains, heart, gut o Causes pain o Can result in necrosis. o Myocardial Infarction- those cardiac cells being infarcted or injured due to lack of oxygen to that area - Necrosis: Cell death by loss of oxygen/ blood supply o (CAN NOT BE REVERSED) o May lose limb, organ, portions of organ o Can not feel pain - Hypoxia: reduce oxygen amount to the cells o Leads to depletion of ATP o When we move from aerobic to anerobic, sodium potassium pump stops, and cell will start to swell due to increase intracellular sodium -​ Now have glycolic pathway which produces lactic acid. -​ Damages cell membrane and degrades it · Differentiate between necrosis and apoptosis - Necrosis: cell death caused by injuries or disease; cells swell and burst o Think: N- necrosis N- not living tissue - Apoptosis: normal programmed cell death (cellular suicide), occurs as part of growth or development · Compare and contrast the inheritance patterns of altered chromosomal disorders - · Explain the relationship between genetic alterations and the individual's response to medications · Homeostasis - Stability and balancing of the biological system necessary for survival - Stabilizing body temp., bluid balance, etc. · Causes of Disease/Illness (intrinsic, extrinsic, hereditary) - Intrinsic: things we cannot change that are inside our body o Genetic, age, gender - Extrinsic: we can change outside of our body o Infectious, behaviors o Alcohol use, diet, drug use, inactivity, smoking, stressors - Hereditary: may be carried from generation to generation - Genetic: occurs due to gene variant (mutation) in genome which may/ may not be inherited · Diffusion vs. Osmosis - Diffusion: Movement of solutes from GREATER concentration to LESSER concentrations - Osmosis: movement of water across a semipermeable membrane. Moves DOWN its concentration gradient from side with lesser number of particles and greater water, to greater particles and lesser water. · Tonicity of IV fluids · Fluid volume overload and fluid volume deficit Fluid Volume Deficit: dehydration - Isotonic Dehydration- hypovolemia o Water + electrolytes equal loss o Causes: inadequate intake of fluids and solutes, excessive loss of isotonic fluids - Hypertonic Dehydration o Water loss> electrolyte loss (SHRINK) o Causes: conditions that increase fluid loss, hyperventilation, diarrhea, prolonged fevers - Hypotonic Dehydration o Electrolyte> water loss (SWELL) o Causes: chronic illness, kidney disease, chronic malnutrition - Clinical manifestations: o Increase; serum osmolality, hematocrit, BUN level, serum sodium, o Decreased; urine output, dry mouth, constipation, fever Fluid Volume Overload: - Isotonic Overload o Excessive fluid in ECF -​ Causes: inadequate controlled IV fluids, kidney disease - Hypertonic overload o RARE, excessive sodium intake -​ Causes: rapid infusion of hypertonic saline - Hypotonic Overload o Excessive fluid in ICF -​ Causes: early kidney disease, heart failure, SIADH secretion, inadequate controlled IV fluids - Clinical manifestations: o Decreased serum osmolality, hematocrit, BUN level, serum sodium level o Elevated BP, increased RR, skeletal muscle weakness, increased urine output, pale cool sin, increased motility.  · Hypernatremia and hyponatremia HYPERnatremia HYPOnatremia Fluid higher than > 145 meg/L Fluid less than 5 meg/L Potassium loss 7.5) Clinical Manifestations: Clinical Manifestations: - Slow/ irregular pulse - Weak, irregular pulse - Hypotension - tachycardia - Dysrhythmias - orthostatic hypotension - Weakened skeletal muscles - nausea/ vomiting - Muscle spasms - shallow respirations - Profound weakness - skeletal muscle weakness - Diarrhea Management/ Treatment Management/ Treatment - stop potassium sources - carefully replacing potassium - insulin/ glucose can move potassium back into - diet changes cells -​ ECF (extra cellular fluids): large amounts of sodium Na - ICF (intracellular fluids): large amount of potassium K+ (most abundant intracellular electrolyte) - When electrolytes dissolve in a solution, form charged ions o Cations: + charge o Anions: - charge VOCAB: · Etiology: cause of disease · Predisposing factor: tendency to put a person at risk for a certain disease · Pathogenesis: development of disease · Acute occurring: resolving quickly · Chronic occurring: over a lng period of time > 6 months · Manifestation: clinical effects of evidence of disease · Sign: objective (what we see) · Symptom: what a patient describes as subjective · Syndrome: group of signs and symptoms that occur together or cluster thatw e sue to help diagnose · Diagnosis · Prognosis: likelihood of full recovery · Morbidity  · Mortality · Complication: new problem that arises because of disease · Incidence · Prevalence Module 2: Core Pharmacology Module Objectives: · Differentiate between the generic and trade names of drugs -​ Generic Name: the original designation that the drug was given when the drug company applied for the approval process -​ Trade name: the name by the pharmaceutical company that developed it · Describe the phases of drug development Whole process takes 5-6 years ​ Preclinical Trials: chemicals that may have a therapeutic value are tested either vitro (outside a living organism) or in vivo (inside or on a living organism) ○​ 2 purposes: (a) to determine whether they have the presumes effects in living tissue and (b) to evaluate any adverse effects ○​ NO humans ​ Phase I studies: uses human volunteers to test the drug for safety and dosage information ○​ Tightly controlled and paid volunteers ○​ Scrutinize the drugs being tested for effects in humans; and look for adverse effects and toxicity ○​ About 70% of drugs move on ​ Phase II studies: evaluates the drug in more patients who have the disease that the drug is designed to treat ○​ Performed in hospitals, clinics, doctors offices, etc.  ○​ About 33% move on ​ Phase III studies: uses the drug in a larger sample of population, ○​ To determine the treatment benefit and to monitor side effects that may have not been apparent in other studies ○​ patient s are asked to record symptoms of their experience ○​ Researchers then evaluate the reported effects to determine whether they are caused by the disease or drug. ○​ 25-30% move on -​ Drugs that finish phase III move to FDA -​ Only drugs with FDA approval will be marketed ​ Phase IV studies: continued evaluation ○​ unexpected/ new adverse effects must be reported to the FDA · Differentiate between drug schedules and between pregnancy categories Drug Schedule -​ Schedule I (C-I): High abuse potential; no accepted medical use (heroin, LSD, cannabis) -​ Schedule II (C-II): High abuse potential w/ severe dependances liability (cocaine, methamphetamine, fentanyl) -​ Schedule III (C-III): less abuse potential than schedule II drugs and moderate dependence liability (ketamine) -​ Schedule IV (C-IV): less abuse potential that schedule III drugs and limited dependence liability (xanax, vallum, tramadol) -​ Schedule V (C-V): limited abuse potential. Primarily small amounts of narcotics (codeine) used as antitussives or antidiarrheals -​ Limited quantities could be purchase without prescription Pregnancy Categories -​ Category A: controlled studies show NO risk; pregnant women studies ( folic acid, Vit Bfi) -​ Category B: No evidence of risks shown in humans; animals may show risk (NSAIDs, PPl, H2 Blocker) -​ Category C: Risk cannot be ruled out; potential benefits outweigh potential risks; animal studies show adverse effects on fetus but no adequate studies in humans (antidepressants, MDAs) -​ Category D: positive evidence of human fetal risk, benefits may outweigh the risk (alcohol, warfarin)  -​ Category X: contraindicated in pregnancy; clearly outweighs risk (thalidomide, Vit. A) · Outline the four phases of pharmacokinetics and describe the effects on an individual's response to medication Absorption: what happens to a drug from the time it enters the body until the bloodstream; is dependent on route of administration -​ Through GI tract (oral or rectal), mucous membrane, skin, lung, muscle or subcutaneous tissues -​ Route of administration: -​ Oral: drugs are absorbed more slowly; determine empty stomach or full; pH of stomach alters the ability of the medication to break down for use. -​ Intravenously (IV); drug immediate into bloodstream; rapid onset (fastest) -​ Intramuscular (IM); drug directly into capillaries and the blood stream (second fastest) -​ Subcutaneous injection (SI); drug just under the skin where it is slowly absorbed into circulation -​ Absorption Process: -​ !Passive diffusion: no cellular energy; occurs more quickly if the drug molecule is small, in soluble water and in lipids, and has no electrical charge. -​ Active transport: uses energy; may be large or moving against concentration gradient; important in drug excretion in kidneys Distribution: movement of a drug to body tissues; places where a drug may be distributed depend on the drug's solubility, perfusion of the area, cardiac output, and binding of the drug to plasma proteins Example: areas with little blow flow have trouble delivering the drug to that area -​ Protein binding: drug must be free from the protein binding site to act on the tissue -​ Blood Brain barrier: protects CNS; drugs that are highly lipid soluble are more likely to pass by the BBB and reach CNS, drugs that are not highly lipid soluble are not able to pass BBB -​ Placenta and Human Milk: evaluate all drugs before giving to pregnant person; nurse must always check the ability of a drug to pass into human milk when giving a drug to a person who is lactating Metabolism: process by which drugs are changed into new chemicals -​ ! Liver: everything that is absorbed from GI tract first enters liver to be treated; detoxifies many chemicals and uses others to produce needed enzymes and structures -​ Liver uses cytochrome P-45o enzyme system to alter the drug and start its biotransformation -​ First Pass Effect: drugs given orally are carried directly to the liver after absorption, where they may be largely inactivated by liver enzymes before they can enter the  general circulation… large % of oral dose to be destroyed without reaching the targeted tissue. -​ Because of this, oral drug dose could be higher than injected drugs -​ Responsible for neutralizing some of the drugs -​ Enzyme induction: process by which the presence of a chemical caused increased activity of an enzyme system Excretion: removal of drug from the body; kidneys, skin, lungs, bile, feces -​ BUN and creatinine levels are often monitored to to evaluate kidney function if there is a concern regarding medication excretion -​ Many factors that change drugs effectiveness; weight, age, sex, physiological factors, pathological factors, genetic factors, -​ Half-life: the time it takes for the amount of the drug in the body to decrease to one half of its peak level (time it takes for 50% of the medication to be removed from circulation) -​ Important to follow schedule of drug administration to avoid overdose. ​ Pharmacokinetics How medications travel through body -​ Critical concentration: the amount of drug needed to cause a therapeutic effect -​ Therapeutic index: ratio of the blood concentration at which a drug becomes toxic to the concentration at which the drug is effective -​ The higher the therapeutic index, the larger the safety margin before the med becomes toxic. -​ Loading dose: a dose higher than what is usually used for treatment, administered to allow the drug to reach the critical concentration sooner. -​ Dynamic Equilibrium: the actual concentration that a drug reaches in the body results from a dynamic equilibrium ​ Pharmacodynamics The way the drug affects the body -​ Receptor sites: specific area of cell membranes that that react with certain chemicals to cause an effect within the cell -​ Selective Toxicity: ability of a drug to attack only those systems found in foreign cells · Identify two factors that influence how a drug affects the body Maximal Efficacy: highest level of effect a drug can produce Potency: how strong or powerful a drug is at producing its effect Mode of Action: helps predict how a drug will work, and what effects it will have in the body -​ Agonist: activates receptors -​ Antagonists: inhibits receptors (stops action of other drugs and chemicals) -​ Partial agonist: activates a little and blocks it from being additionally activated ​ Drug interactions Nurses must be aware that the human factor has a tremendous influence on what actually happens to a drug when it enters the body · Toxic Effects on drugs Adverse Effects -​ Undesired effects that may be unpleasant or dangerous -​ Primary Action: overdose -​ Patient suffers effects that are merely an extension of the desired effect -​ Example: Patient with kidney impairment may not be able to excrete the drug and may cumulate the drug in the body causing toxic effects -​ Nursing action: monitor patient carefully and adjusting the prescribed dose to fit that particular need -​ Secondary Action: undesired + pharmacological effects -​ Drugs can produce a wide variety effects in addition to pharmacological effects -​ Sometimes drugs can be altered to not produce secondary effects… sometimes this is not possible -​ Patient should be informed that these extra effects may occur and how to deal with them -​ Drug allergy/ Hypersensitivity: occur when the body forms antibodies to a specific drug, causing an immune response when the person is re exposed to the drug -​ Patient cant be allergic to a drug they've never taken, but can have cross allergies (ex: patient is allergic to penicillin… could also be allergic to amoxicillin) -​ Nursing action: must constantly assess for for potential rug allergies and must be prepared to intervene appropriately -​ Drug Allergies: -​ Anaphylaxis: severe and potentially life threatening -​ Immune system goes into overdrive releasing chemicals like histamine that cause various systems throughout the body (toruble breathing, swelling of face & throat, throat hives, rash, nausea, low BP) -​ Cytotoxic: when medication taken ends up hammering your bodies cells instead of helping them -​ Drug may accidentally damage body cells… nausea, vomiting, hair loss -​ Ex: chemotherapy… treats cancer cells but can harm healthy cells -​ Serum sickness: delayed allergic reactions body has to certain medications -​ Can happen after taking antibodies or injections · Drug induced tissue/organ damage Dermatologic: adverse directions involving the skin (rash- dermatitis)  -​ Assessment: hives, rash, lesions exfoliative dermatitis -​ Interventions: provide frequent skin care, avoid; rubbing, tight clothing, rough clothing, administer antihistamine when appropriate -​ Stomatitis: inflammation of mucous membrane; direct toxic reaction to drug or because the drug deposits in the end capillaries in the mucous membranes Superinfection: from several drugs (antibiotics) destroying normal flora (protective bacteria in GI tract) -​ Assessment: fever, diarrhea, black or hairy tongue, swollen tongue, mucous membrane lesions, vaginal discharge. -​ Interventions: supportive measures; frequent mouth care, skin care, access to bathroom, antifungal therapy Blood Dyscrasia: bone marrow suppression; caused when drugs that cause cell death are used -​ Assessment: fever, chills, sore throat, weakness, dark urine, anemia, low wbc (leukopenia) -​ Interventions: monitor blood levels, provide safety measures Ocular: problems with visions, double vision, blurry vision -​ Assessment: blurring of vision, color vision changes, corneal damage, and blindness -​ Interventions: monitor vision, supportive measures, monitor light Auditory: 8th cranial nerve damage -​ Assessment: dizziness, tinnitus, loss of balance, loss of hearing -​ Interventions: prevent falling injury,monitor perceptual loses/ changes. Neurological: effects of neurological functioning -​ Assessment: confusion, insomnia, parkinson like symptoms -​ Interventions: safety measures to prevent injury Drug toxicity and injury Liver Injury/ Hepatotoxicity: because of first pass effect, liver cells are exposed to full impact of drug before its broken down -​ medication levels may rise to dangerous levels if liver is unable to metabolize the medication -​ If two or more hepatotoxic medications are combined, risk of liver injury increases -​ Assessment: fever, malaise, nausea, vomiting, jaundice, ab pain -​ Intervention: notify and stop drug if needed, provide supportive measures Renal Injury/ Nephrotoxicity: some medications are excreted from the kidney, unchanged from their active form and others are modified to be metabolites; both can cause damage to nephron -​ Assessment: elevated BUN and Cr, decreased urine output, edema, electrolyte imbalances -​ Interventions: notify prescriber, apply supportive measure Teratogenicity: drugs that reach the fetus and cause harm Causes of Medication error: -​ Performance deficits (30%)- just did it wrong -​ Knowledge Deficit (14%)- do not know what your supposed to do -​ Miscalc of doses: (13%) -​ Communication mistake (15%)- handwriting, abbreviation, decimal -​ Use electronic notes Module 3: Module Objectives: · Differentiate between innate and adaptive immunity Innate Immunity: immediate nonspecific defense -​ Front line defense; always ready and respond quickly to a threat (security guard) -​ skin , mucous membrane, WBCs, neutrophils, macrophages Adaptive Immunity: targeted specific defense -​ More specific; takes longer to kick in -​ Highly skilled at targeting particular invaders (special forces) -​ WBCs, lymphocytes, t-cell, b-cell · Describe the inflammatory response -​ The bodies way of protecting itself from harmful stimuli Alarm system: tissues get damaged or infected → immune cells detect → release signaling molecules (cytokines, chemokines, histamine) → act as messengers signaling other cells to respond to the threat and promote inflammation. -​ Histamine and other inflammatory meters cause blood vessels near site of injury or infection to dilate -​ Increased blood flow brings more immune cells to oxygen and nutrients to the affected area → helps fight off pathogens and promote tissue repair. -​ Inflammatory mediators also increase permeability of blood vessel walls allowing immune cells and fluid containing proteins and nutrients to move from the bloodstream into the surrounding tissue → causing swelling, redness, and heat at site. Signs of Inflammation: -​ Erythema: redness of skin of infected area; blood flows to surface of skin -​ Heat: when blood vessels dilate= increase warm blood to area → increase of temp -​ Edema: swelling; fluid leaks into tissues -​ Pain: warning signal to protect injured or inflamed areas and avoid further damage. · Compare & contrast autoimmune disorders and immunodeficiency Immune Deficiency: absent or depressed immune system -​ Primary: bodies immune system is weakened from birth or not working as it should because of genetic factors; not working from the start -​ Genetic mutations, B cell loss, fewer T cells, Chronic Neutropenia -​ Secondary: bodies immune system becomes weekend or compromised later in life due to external factors (acquired) -​ Infections, certain meds, HIV, chemo, malnutrition Autoimmune Disorders: immune system that's supposed to protect the body, starts attacking its own cells and tissues thinking they are invaders → immune response -​ Does not recognize certain cells as their own -​ Can affect, bone, cartilage, other connective tissue · Describe the mechanisms of infectious disease Infection: when a pathogen (virus, bacterium, fungi, parasite, etc.) enter the body -​ Once in the body → attach to host cells → gains entry into tissues or cells → begins to replicate within host tissues or cells -​ Pathogens target specific organs or systems in the body depending on their tropism → as it replicates it produces toxins or trigger inflammatory response → tissue damage at the onset of symptoms → immune system defends to eliminate invader. ​ Barrier Defences: Skin: protects internal tissues and organs of the body; first line of defense Mucous Membrane: lines area of the body exposed to external influences; respiratory tract, GI, GU Gastric Acid: acidity of stomach aids digestion and distorts many pathogens Major Histocompatibility Complex: ability to distinguish between self cells and foreign cells; human ID code is carried on a chromosome called MHC. Cells and mediators of the immune system (cytokines, leukocytes, granulocytes, macrophage, dendritic cell, mast cell, histamine, b lymphocyte, t lymphocyte, cytotoxic and helper t cells, antibodies) Leukocytes: WBCs Granulocytes: release into bloodstream where they circulate until they are recruited to sites of infection or inflammation -​ Neutrophils: phagocytic- engulf and destroy bacteria and other pathogens; first responders, highly mobile -​ Basophils (1%): release histamine and other chemicals involved in allergic reactions and inflammation -​ Eosinophils: combating parasitic infections and modulating allergic responses; regulate inflammation Macrophage: clean up crew; controls and cleans up debris, dead cells, and foreign invaders constantly in body -​ Phagocytic -​ Antigen presenting -​ Releases cytokines and chemokines -​ Granuloma Dendritic Cells: essential for initiating and coordinating adaptive immune response against pathogens; shape overall immune response Mast Cells: crucial role in immune system; involvement in allergic reactions and inflammation; WBC found in connective tissue -​ Exposure to allergen or certain drugs or physical injury → release histamine into surrounding tissues → symptoms like sneezing, itching, watery eyes, difficult breathing Histamine: inflammatory mediator that causes blood vessels to dilate or widen and become more permeable → increase blood flow to affected area → leakage of fluid from blood vessels = swelling, redness,heat (inflammation) Lymphocyte: WBC and immune system; produced in bone marrow ​ T cells: matures in Thymus ○​ I attack inside the cells ○​ Crucial role in cell mediated immunity ○​ Activated by dendritic cells or macrophages ○​ Helper T cell (CD4+): help coordinate immune responses by releasing cytokines ○​ Cytotoxic cells (CD8T): directly kill virus infected cells ○​ Regulatory T cells: suppress excessive immune responses to prevent autoimmune reactions ​ B cells: matures in Bone marrow ○​ I attack outside the cells ○​ When activated by antigens → differentiate into plasma cells → produce and secrete antibodies (immunoglobulins) that can recognize and neutralize specific pathogens ○​ Activated by T cells *** once mature T and B cells circulate in bloodstream and lymphatic system ​ Natural killer cells Antibodies (immunoglobulins IG): specialized proteins produced by B-lymphocytes in response to foreign substances (bacteria, viruses, toxins) -​ Antibody binds to antigen= lock and key → triggers cascade of reactions that lead to the formation of membrane attack complexes → punch holes in membranes of pathogens causing them to burst -​ Prevents pathogen from infecting host cells by blocking its ability to attack and enter cells -​ Activates complement system- group of protein in the blood that help destroy pathogens directly and enhance inflammatory response Hypersensitivity reactions (Type 1, Type 2, Type 3, Type 4)  -​ When allergen enters the body hypersensitivity occurs -​ Damage done to the body as a result of immune reactions TYPE 1: Anaphylactic; immediate hypersensitivity reaction -​ ***When immune system overreacts to harm and substances mistaking them for dangerous invaders → allergic reaction -​ IgE antibodies bind to specific allergens - harmless, (food, dander, pollen, etc. -​ IgE binds to immune cells, mast, cells, basophils -​ Continuous exposure to same allergen → allergen binds to IgE antibodies already attached to mast cells and basophils → triggers release of histamine, leukotrienes, and cytokines in tissues → inflammation and symptoms of allergic reaction -​ Clinical manifestations: sneezing, earache, tearing, itchy nose ears and throat, rhinorrhea, congestion, HA, red eye, fatigue, chemosis -​ Potential complication: anaphylaxis- life threatening TYPE II: Cytotoxic; antibody-mediated immune reaction -​ ***immune system targets specific cells or tissues in the body; include cells with surface proteins that have been altered and appear foreign -​ Antibodies (IgG or IgM bind to antigens (proteins) on host cells → marking them for destruction → host cell destroyed -​ Cytotoxic (cell toxin): toxic substance or process that results in cell damage or death -​ IgG- alerts WBCs to kill a cell -​ Clinical manifestations: varies; Autoimmune hemolytic anemia (targets RBCs), autoimmune thrombocytopenia (targeting platelets) TYPE III: immune complex reaction -​ Immune complex = antibody (IgG or IgM) binds with antigen (microbial components, toxins, or bodies on cells/ tissues -​ When immune complex deposits in tissues → complement activation → inflammation and tissue damage -​ Disorders: rheumatoid arthritis (RA) , systemic lupus erythematosus (SLE) Rheumatoid arthritis (RA): chronic systemic anti inflammatory disease -​ attacks peripheral joints, cervical spine, and surrounding muscles tendons, ligaments, blood vessels Systemic Lupus Erythematosus (SLE): chronic autoimmune disease from dysregulation of immune system TYPE IV: cell mediated/ delayed hypersensitivity -​ Immune response mediated by T-cells (rather than antibodies) (different than type 1-3) -​ TH1 cells stimulate macrophage activity → causes tissue damage -​ TB skin test- tuberculin reaction results from a small amount of tuberculin injected into the skin of a person previously exposed from tuberculosis Bacteria Bacteria Classification -​ Broad vs. Narrow Spectrum; when infection unknown use broad; specific infection use narrow -​ Mechanism: -​ Bactericidal: antibiotics death of bacterial cells; kill bacteria directly by interfering with essential bacteria functions -​ Bacteriostatic: antibiotics inhibit the growth and replication of bacteria without necessarily killing them -​ Gram (+): cell wall retains a purple stain -​ Gram (-): cell wall retains and pink -​ Aerobic: use oxygen -​ Anaerobic: no oxygen Vaccines Prime the immune system to recognize and effectively respond to specific pathogens Reduces severity of infection → immunity against the disease -​ Cause immune response without having the full course of a disease -​ Caution: febrile seizure or cerebral injury, acute infection -​ CI: immune deficiency, received immunoglobulins or blood products within 3 months -​ ADE: fever, rash, malaise, chills, drowsiness, anorexia, vomiting, irritable, pain, redness, swelling DRUGS Immune system: -​ Immune modulating: substances that can change or regulate the activity of immune system (enhance/ suppress) Thalidomide; treats multiple myeloma and erythema nodosum  -​ Immune stimulants: assist the immune system to fight specific pathogens or cancer cells -​ Interferons (interferon alpha 2b): used to treat various cancers, hepatitis, warts -​ Interleukins: inhibits tumor growth; AE: flu like symptoms lethargy, fatigue, CNS Colony stimulating factors: filgrastim (neuropen); give after supressive chemo, leukemia, bone marrow transplants -​ MOA: increase production of neutrophils in bone marrow -​ AE: headache, fatigue, alopecia, nausea -​ CI: allergy to drug -​ Immune suppressants: Tacrolimus (prograf) and Cyclosporine: helps with organ rejection after transplants; treatment of chronic rejection and rheumatoid arthritis and psoriasis -​ AE: bone marrow suppression, liver and kidney problems, renal dysfunction, pulmonary edema Anti Inflammatory Salicylates- acetylsalicylic acid (aspirin/ ASA): -​ Anti Inflammatory and fever reducing -​ MOA: decrease prostaglandin response -​ AE: bleeding, N/V/D, tinnitus, -​ CI: no KIDS, hypersensitivity NSAIDs- ibuprofen -​ Anti Inflammatory and fever reducing (RA, OA -​ MOA: decrease prostaglandin response -​ AE: N/V/D, hypertension, constipation -​ CI: allergy, GI bleed DMARD: -​ Autoimmune disease (RA)- improvement in joint function -​ MOA: suppress inflammatory response -​ AE: site reactions, upper rep infections, HA GI -​ CI: pregnancy, bone marrow suppression, heptic/ renal diseas, anemia, alcohol use, cancer, aids Acetaminophen (Tylenol): -​ NON inflammatory- used instead of nsaids to decrease bleed risk -​ Mild joint pain, fever, peptic ulter -​ MOA: block production of prostoglandins, acts on CNS -​ AE: Liver toxicity, renal dysfunction  -​ CI: alcohol, pregnancy Epinephrine (anaphylactic): -​ Give anaphylactic reaction and cardiac arrest -​ MOA: stimulates alpha invader receptors causing vasoconstriction, increasing BP -​ Antibiotics Penicillin - amoxicillin Carbapenems Cephalosporin Tetracyclines Aminoglycosides Sulfonamides Fluoroquinolones ISoinzid (INH) Antivirals “Clovir” Antifungals Fluconazole Clotrimazole · Describe common side effects and explain nursing implications for select categories of medications (antibiotics, antivirals & antifungals) · Explain drug (antibiotic) resistance and the nurse's role in antibiotic stewardship · Describe common side effects and explain nursing implications for select categories of medications (anti-inflammatory) Key Terms/Concepts: · Inflammatory response (cardinal signs of inflammation: erythema, heat, pain, edema, pain) · Immune system key terms (aquired vs. Innate immunity) · Cells and mediators of the immune system (cytokines, leukocytes, granulocytes, macrophage, dendritic cell, mast cell, histamine, b lymphocyte, t lymphocyte, cytotoxic and helper t cells, antibodies) · Autoimmune disease · Immune deficiency (primary vs. Secondary) · Hypersensitivity reactions (Type 1, Type 2, Type 3, Type 4) · Vaccines · Infection (s/s, bacterial vs. Viral) · Key pharmacology content (immune modulating agents, immune stimulants, immune suppressants, anti-inflammatory drugs, NSAIDs, antibiotics, antivirals, antifungals) · Immune stimulant agents, colony stimulating factors (filgrastim (Neupogen)) · Medications used for treatment of anaphylactic responses (epinephrine, antihistamine/diphenhydramine) · Anti-inflammatory agents (salicylates/aspirin, NSAIDs/ibuprofen) · Acetaminophen does not have anti-inflammatory properties · Antibiotic therapy key ideas (broad v. narrow spectrum, bactericidal v. bacteriostatic, gram-positive v. gram-negative, aerobic v. anaerobic) · Antibacterial drug classes and key agents (penicillin/amoxicillin, carbapenems/ - “penem”, cephalosporin, tetracycline/ “-cycline”, aminoglycosides/gentamicin, sulfonamides/ “-azole”, fluroquinolones/Ciprofloxacin) · Antimycobacterial used for the treatment of mycobacterial infections tuberculosis and leprosy: key drugs, isoniazid (INH) · Antivirals: key drug identifiers, end in - “clovir” · Antifungals: key drugs, fluconazole Chapters Covered: Tucker: Focus on Nursing Pharmacology o Chapter 15: Introduction to the Immune Response and Inflammation o Chapter 8: Anti Infective Agents o Chapter 9: Antibiotics o Chapter 10: Antiviral Agents o Chapter 11: Antifungal Agents Norris: Essentials of Pathophysiology o Chapter 9: Inflammation, tissue repair, and wound healing (191-203) o Chapter 10: Mechanisms of Infectious Disease o Chapter 11: Innate and Adaptive Immunity o Chapter 12: Disorders of the Immune System (265-283, 286-end) o Chapter 16: Temperature Regulation (433, 434)