NHI Module III Exam PDF

Nursing Health & Illness Module III Exam Chapter 8: Nursing Care of Patients with Infections (15 questions) ❖ Process of Infection o Infectious agent (table 8.1 on page 85) ▪ Microbiota: microbes occurring naturally in a body part ▪ Pathogen: disease causin...

Nursing Health & Illness Module III Exam Chapter 8: Nursing Care of Patients with Infections (15 questions) ❖ Process of Infection o Infectious agent (table 8.1 on page 85) ▪ Microbiota: microbes occurring naturally in a body part ▪ Pathogen: disease causing microbe ▪ Bacteria: single-celled; might depend on hosts but can live and reproduce outside of host Aerobic: need oxygen to live; found on skin Anaerobic: can live without oxygen; found in GI tract Rod-shaped: thick-walled spores; example includes c. diff., needs to be disinfected with bleach Rickettsiae: vectors include living organisms; examples include typhus, scrub typhus, rocky mountain spotted fever ▪ Virus: smaller than bacteria; depend on host cells to live and reproduce; antiviral drugs only decrease symptoms ▪ Fungi: yeasts and molds; normal flora of mouth, vagina, intestinal tract; antifungal medications are available although serious fungal infections are rare ▪ Protozoa: single-celled parasitic organisms with flexible membranes and live in the soil ▪ Helminths: wormlike parasites; trichinosis is a disease transmitted by eating raw or undercooked meat of pigs or wild animals with the larvae ▪ Prion: proteins found mainly in the brain; long incubation periods, no inflammatory response; progress is rapid and can lead to death; example includes creutzfeldt-jakob disease o Reservoir: environmental home for infectious agent ▪ Animate: people, insects, animals, plants (living things) ▪ Inanimate: water, soil, medical devices (not living) o Portal of exit: path by which infectious agent leaves its reservoir o Mode of transmission ▪ Direct: direct contact or droplet spread through touching, kissing, or sex; examples include scabies, mononucleosis, pertussis, influenza, and STIs PPE: gloves, surgical masks, goggles, gowns, shoe covers ▪ Indirect: can be vehicle-borne, vector-borne, or airborne Vehicles: biologic procedures (blood/organs), soiled bedding, food, surgical instruments, toys, water, and wound dressings; examples include influenza, norovirus, hepatitis B; to prevent-  hand hygiene, cleaning patient equipment per protocols, clean food and water Vectors: through living source other than humans (fleas, mice, rats, mosquitos, and ticks); examples include lyme disease, malaria, plague, zika virus; to reduce- avoid infested areas, using insect repellants, and rodent control Airborne: can be inhaled and deposited on host membranes; examples include measles, chickenpox, tuberculosis; to prevent- use a HEPA filter to filter tiny particles most efficiently o Must wear n95 mask o Portal of entry: respiratory tract, skin, mucous membranes, GI tract, GU tract, placenta ▪ Determining factors: host’s condition and virulence (ability to produce an infection o Susceptible host: occurs from defense breakdown; burns, chronic diseases, immunocompromised, invasive procedures, malnourishment, stress, very young or very old ▪ Watch for atypical signs of infection in older adults: behavioral changes, may not have a fever ❖ Body’s Defense Mechanisms o Skin and mucous membranes (1st line): pH is less than 7; body also has an abundance of microflora o Cilia: hairlike structures that line the mucous membranes of upper respiratory tract, trap dust, mucous, pus, and foreign particles and then push them up to pharynx with wavelike movements to be expectorated (coughing) o Gastric acid: pH of 1-5 destroys most organisms that enter stomach o Immunoglobulins: also called antibodies; protein particles made by plasma cells; antigens are markers on cell surface o Leukocytes and macrophages: 5 different types (page 88) ▪ Phagocytosis: when neutrophils and macrophages engulf and digest the foreign antigens o Lysozymes: bactericidal enzymes found in WBCs, tears, saliva, and sweat o Interferons: group of antiviral proteins that help destroy infected cells and may inhibit tumor cell growth o Inflammatory response: caused by pathogens, trauma, or other injuries to tissue; may or may not present with infection ▪ Vascular response: first step; local vasodilation (increased blood flow), redness and heat at injury which brings more plasma to area to nourish the tissue  ▪ Inflammatory exudate: second step; increased permeability of blood vessels; possible swelling which can cause pain on nerve endings ▪ Phagocytosis and purulent exudate: final step; destruction of pathogen and their toxins by leukocytes through phagocytosis; pus may form which contains protein, cellular debris, and dead leukocytes o Immune system: body’s final defense; immune cells and lymphoid tissue ❖ Infectious diseases (infection: results when immune system protection fails) o Risk factors for infection: age, chronic diseases, dysphagia, environment, immobility, immunocompromised, instrumentation, incontinence, invasive procedures, malnutrition, medications o Localized infection: microbes in one specific area; pain, redness, swelling, warmth at site o Sepsis: “life threatening organ dysfunction caused by dysregulated host response to infection”; possible septic shock ▪ Watch for a decrease in blood pressure o Laboratory assessment: use of gram staining, C&S, antibody tests, CBC with differential, ESR ▪ Gram positive: will turn purple ▪ Gram negative: will turn pink ▪ Erythrocyte sedimentation rate: early screening test for inflammation o Immunity: ability of body to protect itself from diseases ▪ Natural: species specific ▪ Innate: hereditary/genetics ▪ Acquired: active or passive through exposure to organisms, vaccines, immunoglobulin injection o Disease examples ▪ Infectious mononucleosis: epstein-barr virus is usual cause (a herpes virus also known as the “kissing disease”) Very contagious Extreme fatigue, anorexia, chills, red sore throat, headache, high fever, enlarged lymph nodes, tonsils may have white coating Important to intervene with symptom management and teaching about importance of resting ▪ Ebola: direct contact transmission Use hand hygiene and special PPE S/S: appear in 2-21 days (fever, headache, diarrhea, vomiting, abdominal pain, muscle pain, unexplained bruising and bleeding) Complications: joint and vision problems Supportive care only ▪ Zika virus: transmitted by infected mosquitos  Use hand hygiene and contact precautions S/S include fever, headache, rash, muscle/joint pain, conjunctivitis Supportive care: acetaminophen, fluids, rest Complications: Guillain-Barre syndrome, birth defects ❖ Infection control in health-care agencies o HAI: infection from care in a health agency ▪ Risk factors: host’s condition, multiple antibiotic therapy, high risk units, immunocompromised, ▪ Common pathogens: Escherichia coli, staphylococcus aureus, pseudomonas aeruginosa o Hand hygiene: with any patient contact, and always after glove use ▪ Lather for 20 seconds (hum happy birthday song 2 times) ▪ Interlace fingers, scrub nails against palms, rinse with fingers downward ▪ Dry with paper towels and turn off faucet with paper towel o Asepsis: freedom from organisms ▪ Medical asepsis: clean technique; reduce number of pathogens ▪ Surgical asepsis: sterile technique; area is free of microorganisms and spores; used with surgery and sterilization o Ultraviolent light: disinfects patient care areas and rooms after traditional cleaning; UV lights bounce and reflect light waves in minutes o Infection prevention (precautions- table 8.3 on page 94) ▪ Standard: use with all patients; blood, body fluids, body substances; hand hygiene always; may include gloves, gowns, goggles, masks, face shields ▪ Transmission-based: specific infectious diseases; use with standard precautions ▪ Vancomycin-resistant enterococci (VRE): private room, gloves, gowns, always decontaminate equipment o Prevention of respiratory tract infections ▪ Risk factors: invasive tubes (endotracheal, nasotracheal, tracheostomy) ▪ Prevention: oral hygiene, coughing and deep breathing, VAP bundles o Prevention of GI tract infections (most common HAI) ▪ Risk factors: foley catheter ▪ Prevention: appropriate use, remove is unnecessary, intermittent catheterization, strict aseptic technique, secure tubing, closed system, keep bag below bladder level o Prevention of surgical wound infections o Prevention: sterile technique for dressing changes, monitor wound ❖ Antibiotic-resistant infections o Methicillin-resistant staphylococcus aureus (MRSA) ▪ Difficult to treat which leads to high mortality rate  ▪ Treatment: vancomycin hydrochloride; will end up needing PICC ▪ Use contact precautions ▪ S/S: warm red bumps, fever, drainage o Vancomycin-resistant enterococci (VRE) ▪ Direct/indirect transmission ▪ Prevention: proper hand hygiene, restricting vancomycin use, teach about wiping front to back, isolating at home (having own toilet and not sharing it), flushing twice ▪ Difficult to treat ▪ Treatment: combo antibiotic therapy ▪ Isolation when hospitalized ❖ Treatment of infections: antibiotics, antivirals, antifungals o Monitor peak/trough levels (especially with vancomycin) ❖ Antibiotic-associated diarrhea: upset of natural gut microbiota which can be harmful after normal microflora is destroyed; inflammation due to toxin release; watery stools; usually resolves when antibiotic is stopped o Meds: ampicillin, cephalosporins, and clindamycin o Clostridium Difficile: gram positive; overgrowth with imbalanced gut; transmitted fecal-oral route ▪ Possibly leads to pseudomembranous colitis which is life-threatening ▪ Nursing care: hand washing with soap and water; stopping antibiotic ▪ Treatment: metronidazole (Flagyl) or vancomycin (Vancomycin) Possible fecal microbiota transplant (when other treatment has failed) ❖ Nursing Process o Risk for infection r/t external factors: watch for fever if inflammatory response cannot be noted, monitor WBCs ▪ Respiratory: encourage fluids, deep breathing and pain relievers, provide oral care or suction, use sterile water, elevate HOB at least 30 degrees ▪ GI tract: encourage fluid intake to replace loss during fever or vomiting or diarrhea, teach hand hygiene with antimicrobial soap and water ▪ GU tract: only place foleys if completely necessary, use sterile technique for inserting and clean it 2x daily o Deficient knowledge r/t infection and treatment: educate about how to control the risk for infect and how to use antibiotics correctly, educate about side effects and adherence to treatment Chapter 18: Immune System Function, Assessment & Therapeutic Measures (6 questions) ❖ Immune system o Lymphoid organs, lymphocytes and WBCs, chemicals, lymphatic system (lymph, vessels, nodes, and spleen)  o Antigens: chemical markers that identify cells ▪ Human cells have “self-antigens” ▪ If they’re foreign, they will not match and instead be destroyed o Lymphocytes ▪ Natural killer cells: patrol body and produce a quick attack; blood, bone marrow, lymph nodes, spleen; destroy pathogens and tumor cells ▪ T and B cells: specific immune responses; both come from red bone marrow then the T cells migrate to thymus and B cells mature in bone marrow then migrate to lymphatic tissue T cells: thymus-derived B cells: bone marrow-derived; memory cells ▪ Antibodies: immunoglobulins or gamma globulins; glycoproteins produced by plasma cells in response to foreign antigens; specific to one antigen IgG: in blood and extracellular fluid or lymph; provides long-term immunity after vaccine or illness recovery; can cross placenta to provide passive immunity IgA: in external secretions such as tears or saliva or other mucous membranes; provides passive immunity when breastfeeding IgM: in blood or lymph; produced first during infection (IgG production follows) IgD: B cells; antigen specific receptors on B lymphocytes IgE: mast cells or basophils; important with allergic reactions as mast cells release histamine ▪ Immunity Cell-mediated: against intracellular pathogens, malignant cells, and grafts of foreign tissue o Recognition of foreign antigen by helper T cells (CD4), killer T cells lyse cells (CD8), memory T cells remember specific antigens, suppressor T cells limit immune response Humoral: “antibody-mediated”; against extracellular pathogens o B cells proliferate and differentiate, plasma cells produce antibodies that circulate forming an antigen-antibody complex, memory B bells, antibodies label antigen for phagocytosis o Antigen-antibody complex stimulates complement fixation, enzyme complex lyses cells and labels foreign antigens for phagocytosis ❖ Antibody responses o First exposure to foreign antigen stimulates antibody production in small amts  o Second exposure causes memory cells to make large amounts of antibody o Vaccines are based on this principle o Allergic response: when antibodies respond to foreign but harmless antigens ▪ Teach about always carrying an epinephrine autoinjector and making sure it’s not out of date ❖ Types of immunity: o Passive: temporary; antibodies obtained outside person ▪ Naturally: placental transmission; antibodies in breastmilk ▪ Artificially: injection of performed antibodies o Active: production of own antibodies ▪ Naturally: recovery from disease; memory cells specific to pathogen ▪ Artificially: vaccines stimulate production of antibodies and memory cells; may allow lifelong immunity Vaccines: provide artificially acquired immunity, stimulates production of small amounts of antibodies, stimulates production of memory cells ❖ Aging and the immune system o Immunosenescence: decline in immune system seen with older population ▪ Thymus gland decreases in size, increased production of immature T cells, decreased antibody response, higher incidence for cancer ❖ Microbiota: collection or community of microbes, essential for immune function o Ongoing research to better understand o Disruption and lack of diversity are possibly causing diseases: CV disease, anorexia, IBS, lupus, and rheumatoid arthritis ❖ Laboratory tests o Table 18.4 (pg 271-274) ❖ Diagnostic tests o Gene testing: genome mapping data; noninvasive o Biopsy: examined through microscope; invasive o Skin testing: only with intact immune system; invasive ❖ Therapeutic interventions o Immunotherapy: desensitization of person with anaphylactic reaction or chronic allergic symptoms; inject small amounts of extracted allergen until hyposensitivity is reached; recognize anaphylactic reaction can occur o Medications (pg 275) o Surgeries: splenectomy; monoclonal antibodies; recombinant DNA technology Chapter 19: Nursing Care of Clients with Immune Disorders (14 questions) ❖ Hypersensitivity reactions: exaggerated response o Type I hypersensitivity reactions: release of histamine ▪ Allergic rhinitis: most common form of allergy; yearly is called “perennial allergic rhinitis” and seasonally is called “hay fever” Patho: results from antigen-antibody reaction; vasodilation and local edema occur S/S: sneezy, itchy nose, profuse watery rhinorrhea, itchy/red eyes Dx: skin tests Therapeutic measures: antihistamines and nasal decongestants, corticosteroids o Use nasal decongestants cautiously with elderly ▪ Atopic Dermatitis: “eczema”; chronic inflammatory response Patho: mediated by IgE antibodies; or could be a defect in epithelial cells S/S: pruritis, edema, extremely dry skin, red weeping lesions that crust and scale over, lichenification (when skin thickens) Dx: serum IgE levels Therapeutic measures: antipruritics, diluted bleach in lukewarm baths, cool soaks, oatmeal baths, topical corticosteroids, systemic antibiotics Nursing care o help prevent dryness- wear cottons clothing, cool soaks to decrease pruritis ▪ Anaphylaxis: severe; widespread histamine release Patho: IgE antibodies produced from previous antigen sensitization are attached to mast cells throughout body S/S: capillary permeability increases, generalized smooth muscle spasms, stridor, wheezing due to bronchial narrowing, dyspnea, laryngeal edema, hypotension, tachycardia, erythema/redness, and warmth of skin o Neuro: drowsiness, possible seizures Dx: ABGs may reveal hypoxemia, ECG, hypercarbia, and acidosis Therapeutic measures: epinephrine, IV vasopressor, oxygen therapy, possible tracheotomy or endotracheal intubation, mechanical ventilation, antihistamines or corticosteroids Nursing care: maintain airway, emotional support, education o Laryngeal edema: place patient in high- or semi-fowler to improve ventilations and decrease upper airway edema ▪ Urticaria: due to meds, stress, chemicals, cold environment Patho: triggered by antigen-stimulated reaction of IgE which leads to mast cells released, especially histamine  S/S: raised lesions are pruritic, nontender, and erythematous wheal-like structures; usually on trunk of body Dx: physical exam Therapeutic measures: chronic urticaria may require IgE monoclonal antibody therapy ▪ Angioedema: most common type of allergic reaction; form of urticaria Patho: swelling from temporary vascular permeability withing subcutaneous and submucosal layers S/S: local swelling, with or without hives, non-pruritic, painless o Life threatening when upper airway is involved Dx: skin testing; H&P Therapeutic measures: antigen or allergen desensitization o Type II hypersensitivity reactions: destruction of cell or substance that has antigen attached to cell membrane; antigen is sensed as either IgG or IgM; can be beneficial if bacteria but not beneficial when RBCs are sensed as foreign (causes blood to be destroyed) ▪ Hemolytic transfusion reactions Patho: RBCs with foreign antigens rapidly lysed, occludes blood vessels; agglutination (clumping) occurs o Type O are universal donors o Type AB are universal recipients o Type is only 2% of population (very rare) S/S: ischemia, necrosis; life threatening Dx: antihuman globulin is added to see if agglutination occurs Therapeutic measures: prevention is key; antihistamines, corticosteroids, sympathomimetics o Rhogam: For Rho (D) negative patients who accidentally receive positive blood; can be form fetus by delivery, miscarriage, abortion, amniocentesis, or intra-abdominal trauma Nursing care: two nurses must double check all blood administration, stay at bedside for first 15 minutes, stop immediately if reaction is noted o If reaction occurs, keep vein patent with normal saline infusion, contact HCP, and stay with patient monitoring vitals and symptoms o Type III hypersensitivity reaction: immune complexes formed by antigens and antibodies within blood vessels, usually IgG type; leads to blood vessel damage (caused by neutrophils), red edematous lesion, bleeding, and necrosis  ▪Serum sickness: very rare; brief and self-limiting; antigen-antibody complexes cause symptoms of inflammation; 7-10 days after penicillin/sulfonamide S/S: severe urticaria and angioedema Dx: sedimentation rate, and c-reactive protein elevate due to inflammation; increased IgG and IgM Therapeutic measures: antipyretics, analgesics, and anti- inflammatories antihistamines, arthralgia o Type IV hypersensitivity reaction: delayed reaction; sensitized T lymphocyte contacts antigen; cell-mediated immune response; necrosis ▪ Contact dermatitis: when you change soaps, detergent, or when other chemicals come in contact with skin before they’re absorbed and binded to haptens (special proteins); T memory cells are creased within 7-10 days and help with second exposure Etiology: poison ivy, poison oak, latex rubber o If patient’s are allergic to latex they may also be allergic to avocados, bananas, kiwis, and tomatoes S/S: red, pruritic, fragile vesicles Dx: observations Therapeutic measures: antihistamines, topical drying agents, corticosteroids, aveeno baths, use brown soap (fels-naptha), avoid scratching skin ▪ Transplant Rejection Patho: transplanted tissue is senses as foreign; lymphocytes are sensitized immediately after transplant during induction phase Complications: total failure and loss of transplanted tissue/organ; the biggest cause of death post-transplant; immunosuppression therapy is known to lead to infections Therapeutic measures: lifelong immunosuppression therapy; supportive care based on failing organ (for example hemodialysis may be needed if kidney rejection occurs) o Observe for signs of injection as rejection can occur weeks, months, or years after (with decreasing risk) ❖ Autoimmune disorders: immune system cannot recognize itself and instead recognizes them as foreign and in response destroys the cells o Pernicious anemia: antibodies against gastric parietal cells and intrinsic factor; vitamin b12 deficiency; RBC production decreases; may be caused by gastric or bowel resections ▪ S/S: weakness, loss of appetite, glossitis, pallor, irritability, confusion, peripheral neuropathy  ▪ Therapeutic measures: corticosteroids, lifelong vitamin b12 o Idiopathic autoimmune hemolytic anemia: autoantibodies attach to RBCs by agglutinating or lysing; if lysing, RBC fragments circulate blood; if agglutination occurs, occlusions in blood vessels lead to tissue ischemia ▪ S/S: mild fatigue, pallor, hypotension, dyspnea, jaundice ▪ Dx: direct antiglobulin test (coombs test) determines cause ▪ Therapeutic measures: immunosuppressive medications, oxygen, corticosteroids, folic acid, transfusion, erythrocytapheresis, splenectomy (for severe cases) o Hashimoto Thyroiditis: common in females, middle age, down syndrome, and turner’s syndrome ▪ Patho: thyroid gland enlarges as result of overstimulation (hyperthyroidism); different autoantibodies then appear that destroy thyroid cells and hypothyroidism occurs overall ▪ S/S: enlarged thyroid gland (goiter), hypotension, dyspnea, anorexia, constipation, dry skin, weight gain, sensitivity to cold, facial puffiness, slowed mental processes ▪ Dx: TSH levels will be elevated; thyroid scan ▪ Therapeutic measures: lifelong thyroxine is required Soft diet for goiters Compression stockings to help prevent venous stasis Daily weights would be beneficial o Lupus Erythematosus (3 different types) ▪ Discoid lupus erythematosus (DLE): skin lesions; patchy, crusty, sharply defined skin plaques; on face and sun exposed areas ▪ Drug-induced systemic lupus erythematosus (DILE): after certain medication use; pleuropericardial inflammation, fever, rash, arthritis ▪ Systemic lupus erythematosus (SLE): chronic, inflammatory, multisystem disorder; most common Etiology: young women, 1st degree relatives, African Americans, Hispanics S/S: o Fatigue and fever are early vague signs o Dermatological: butterfly rash (usually flat and not pruritic), bruises, photosensitivity, alopecia, pain, pruritis o Musculoskeletal: arthralgia, arthritis o Hematological: anemia, leukocytopenia, thrombocytopenia o Cardiopulmonary: pericarditis, myocarditis, myocardial infarction, vasculitis, pleurisy, valvular disease  Therapeutic measures: symptom management, NSAIDs, immunosuppressants, corticosteroids, antimalarials, IV immunoglobulin Complications: osteronecrosis, kidney disease, thrombocytopenia, emboli, myocarditis, vasculitis, mesenteric intestinal vasculitis, sepsis th ▪ 4 type deals with neonatal infants; very rare o Ankylosing Spondylitis: chronic progressive inflammatory disease (sacroiliac, costovertebral, large peripheral joints) ▪ S/S: lower back stiffness, pain, lordosis, kyphosis, spasms, fatigue, anorexia, weight loss ▪ Therapeutic measures: no cure, just supportive care and possible surgery Educate about ROM exercises ❖ Immune deficiencies: when one or more components of immune system are either absent or insufficient o Hypogammaglobulinemia: absence/deficiency of one or more of 5 immunoglobulins from defective B cell function ▪ S/S: recurrent infections ▪ Therapeutic measures: minimize infections, IgG injections, fresh frozen plasma Good nutrition, hydration, hygiene Chapter 20: Nursing Care of Patients with HIV & AIDS (13 questions) ❖ HIV: chronic, retrovirus that only has ribonucleic acid (RNA); untreated HIV causes AIDS o HIV-1: primary and worldwide o HIV-2: primarily west africa o Patho: binging (CD4 receptor of host), fusion, reverse transcriptase (RNA to DNA), integrase (HIV DNA into host cell DNA), replication (host cell makes HIV proteins), packaging (viral envelope for new HIV), budding (release and protease cutting of HIV proteins) ▪ HIV hides out in reservoirs for infection flare-ups which leads to progressive impairment of body’s immune response; can remain inactive for years and then lay dormant in small number of cells (viral reservoirs) o Progression: initial infection, clinical latency period (symptom-free), CD4 T lymphocytes decrease, 8-12 years until symptoms appear, symptoms are due to weakened immune system o Mode of transmission: through blood, breast milk, semen, vaginal secretions o Routes of transmission: sexual, parenteral, perinatal o S/S: fatigue, headache, fever, lymphadenopathy, diarrhea, sore throat  ▪ Late s/s: SOB, weight loss, night sweats, persistent diarrhea, oral and vaginal candidiasis, dry skin or skin lesions, peripheral neuropathy, shingles, seizures, dementia ▪ Final stage: AIDS diagnosis; no sure and is fatal o Complications ▪ AIDS wasting syndrome: weight loss, chronic weakness or fever or persistent diarrhea (for more than 30 days) ▪ AIDS dementia complex: memory impairment, personality changes, hallucinations, loss of balance, slow responses, safety important ▪ Opportunistic infections: candida albicans, cytomegalovirus, pneumocystis pneumonia, tuberculosis ▪ Cancer: kaposi sarcoma o Dx: HIV antigen/antibody combo test, nucleic acid test, CBC and lymphocyte count, CD4 T lymphocyte count, viral load testing, genotyping o Therapeutic measures: no cure, begin antiretroviral therapy (ART) ▪ ART: early and aggressive, each drug acts on different stage of HIV; reduces viral load to undetectable level ▪ Goal: prevent/delay opportunistic diseases ❖ Nursing process o Ineffective protection o Ineffective coping o Risk for injury o Deficient knowledge o Impaired gas exchange o Diarrhea o Fatigue: alternate activity and rest; prioritize activities o Imbalanced nutrition- less than body requirements: weigh, monitor intake and calories, possible dietician, small and frequent meals, use antiemetics o Impaired oral mucous membrane integrity o Impaired skin integrity o Risk for situational low self esteem o Social isolation o Acute or chronic pain: complementary therapy ***2 dosage calculations***