Common Lab Values
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166 terms
Terms | Definitions |
|---|---|
 WBC | 5,000 - 10,000ul |
| RBC | 4.5 - 6 million ul |
| Platelets | 150,000 - 400,000 ul |
| Hbg | 12 - 18 grams |
| Hct | 36 - 54% |
| SEGS (neutrophils) | 54 - 62% |
| eosiniphils | 1 - 3% (if elevated, allergic reaction or parasites) |
| basophils | .75% (if elevated, inflammation) |
| monocytes | 3 - 7% (if elevated, chronic infection) |
| lymphocytes | 25 - 33% |
| sodium | 135 - 145 mEq/L |
| chloride | 97 - 107 mEq/L |
| potassium | 3.5 - 5.3 mEq/L |
| blood sugar | 80 - 120 (70 - 110) |
| serum creatinine | 0.5 - 1.5 mg/dl |
| BUN | 5 - 20 mg/dl |
| albumin | 3.50 - 5.5 g/dl |
| calcium | 4.5 - 5.5 mEq/L - 8.6 - 10.0 mg/dl |
| phosphorous | 3.0 - 4.5 mg/dl |
| magnesium | 1.3 - 2.5 mEq/L |
| amylase | 50 - 180 u/dl |
| PT | 10 - 15 seconds |
| PTT | 20 - 36 seconds |
| pH | 7.35 - 7.45 |
| PaO2 | 80 - 100 mmHg |
| PaCO2 | 35 - 45 mmHg |
| HCO3 | 22 - 26 mEq/L |
| O2 sat | 96 - 100% |
| specific gravity of urine | 1.010 - 1030 |
| creatinine clearance of urine | 600 - 2,000 mg/ 24 hours (males higher than females); 80 - 135 ml/min |
| inflammation and the immune response - surveillance - differentiates... | self cells and foreign cells in one's body |
| self cells | the regular cells in your body |
| foreign cells | invading cells "antigens" |
| inflammation and the immune response - defense... | inactivates, eliminates, or destroys foreign cells thru antibody formation or t - cell attacks |
| Human leukocyte antigens | determines tissue type of a person; key for recognition and self tolerance |
| bone marrow | source of all blood cells including immune system cells |
| stem cells | (pluripotent) undifferentiated |
| leukocytes | (WBCs) recognition vs. self tolerance, destruct foreign invaders, produce antibodies, compliment activation |
| leukocytes | produce cytokines |
| compliment | innactive proteins that attach themselves to the foreign body |
| inflammation | provides immediate protection against the effects of injury or foreign invaders/ proteins |
| inflammatory actions | important in ridding the body of harmful organisms |
| inflammation | stimulates both antibody and cell-mediated actions for full immune response |
| infection | occurs in response to tissue injury and to the invasion of organisms |
| infection | usually accompanied by inflammation |
| neutrophils | account for 50 - 75% of WBCs |
| neutrophils | belong to the granulocyte group; billions released every day |
| neutrophils | takes 12 to 14 days for maturation; once released, lives only 12-18 hours |
| segmented | mature neutrophils |
| bands or stabs | immature neutrophils |
| CBC | differentiates between mature and immature neutrophils |
| left shift | when band neutrophils outnumber segmented neutrophils in the blood stream |
| phagocytosis | when the neutrophil attatches itself to the antigen, then chews it up and spits it out (like a cow) |
| a used neutrophil | can no longer break up another foreign particle |
| macrophage | do same things as phagocytes, only can last years |
| macrophage | arise from immature monocytes released into the bloodstream |
| monocytes | from myeloid cells |
| macrophage | important in immediate inflammatory responses through phagocytosis |
| macrophage | can be used over and over again - unlike neutrophils |
| macrophage | stimulates cell and antibody mediated immunity |
| basophils | cause obvious s/s of inflammation |
| basophils | contain vasoactive amines that act on blood vessels |
| basophils - heparin, histamine, kinins, serotonin increase | capillary permeability, which leads to swelling and redness during an inflammatory response |
| eosinophils | produce inflammatory reactions when released; especially in the case of parasites or an allergic reaction |
| inflammatory reactions release vasoactive chemicals which... | help control the extent of an inflammatory response, especially during an allergic reaction |
| stage 1 vascular in sequence of inflammatory response | increase of blood flow to the area causing hyperemia (redness) and edema |
| stage 1 vascular | macrophages are most active; limited phagocytosis d/t small amt. available immediatley after injury |
| stage 1 vascular - bone marrow | stimulated to release more neutrophils and attracts the to the site of injury |
| stage 2 cellular excudate in sequence of inflammatory response | increase in neutrophils (up to 5x's more) at site of injury; pus is formed |
| exudate | pus; comes from neutrophils |
| neutrophils are produced in | bone marrow |
| if infection long term or chronic... | bands are released which won't help out with phagocytosis and chances of a microbial infection are increased |
| stage 3 tissue repair and replacement | starts during the onset of an injury |
| stage 3 tissue repair and replacement | leukocytes stimulate nearby healthy tissue to divide and help replace the injured tissue and stimulate new blood vessel growth and scar tissue formation |
| innate immunity | native immunity/ natural immunity |
| inflammatory response includes | skin, mucous, complement, and natural killer cells |
| inflammatory response begins... | when a large number of antigens enter the body and avoid detection and elimination by natural immune defenses |
| adaptive immunity | "acquired immunity"; the body learns to make it |
| active immunity | body takes active role when antigens enter; produced by host after antigens enter |
| natural active immunity | most effective and longest lasting - the best! |
| artificial active immunity | vaccination or immunization |
| passive immunity | PREformed antibodies or T - cells are injected or passes person to person - from an outside source |
| natural passive immunity | antibodies passed from mother to fetus through breast milk, placenta... |
| artificial passive immunity | antibodies injected from another source, like rabies, tetanus, snake venom, etc... |
| unsensitized | B - lymphocytes must recognize the antigen as non-self |
| macrophages | assist B-lymphocytes by helping to recognize the antigen, then attaching itself to the antigen. It then get handed off to the Helper T-cell |
| the macrophage and helper t cell... | process the antigen and expose the antigen's recognition sites |
| the helper t cell... | delivers the antigen to the B-lymphocytes so that recognition can occur |
| once recognition of an antigen occurs... | the B-lymphocyte becomes sensitized to the angtigen - this can only happen once, but once sensitized, ALWAYS sensitized |
| B-lymphocyte divides into | Plasma cells and memory cells |
| plasma cells | immediately begin forming antibodies; has short life span |
| memory cells | remain dormant until the next antigen exposure |
| antibodies are produced by the | plasma cells |
| antibodies are released into the... | blood stream and other extracellular fluids as antibodies; circulate for 30 days; can be transferred person to person for immediate immunity with short duration |
| IgG | most abundant; crosses placenta & from breast milk; provides sustained immunity against bacterial and viral infections |
| IgA | protectiv mechanism; inhibits bacteria and viruses from adhering to skin and mucous membranes; protects internal environment; more skin diseases |
| IgD | helps to identify; serves as an activated receptor on B-lymphocytes |
| IgM | mediates autoimmune reactions; mediates ABO incompatibility reactions in blood transfusions |
| IgE | degranulation of basophils and mast cells during inflammatory responses; especially active in allergic reactions; assist in clearance of parasites; prevents pulmonary infections |
| sustained immunity- memory | provides humans with long - lasting immunity to a specific antigen |
| memory cells respond to a re-exposure by... | dividing into plasma and blast cells, where blast cells continue to divide and create more plasma cells |
| plasma cells secrete... | large amts. of the antibody specific for the sensitizing antigen; response so rapid person does not become ill |
| cell mediated immunity | CMI; "cellular immunity"; involves many WBC actions and interactions |
| four types of leukocytes are important for the development and continuation of CMI | Helper/ inducer t-cells, suppressor t-cells, cytotoxic/ cytolytic t-cells, natural killer cells |
| helper/inducer t-cells | "T4" or "CD4" cells; secrete lymphokines that regulate the activity of other leukocytes; increase bone marrow production; speed up maturation of cells of myeloid and lymphoid origin. A "calling to arms" |
| suppressor t-cells | "T8" or "CD8" cells; prevent continuous overreactions/ hypersensativity reactions to exposure of non-self cells, preventing the formation of autoantibodies directed against healthy self-cells |
| suppressor t-cells | secrete lymphokines that have an inhibitory action on cells of the immune system; inhibit growth and activation of immune system cells; |
| suppressor t-cells | balance of 2 helper: 1 suppressor cell needs to occur to help revet overreaction or infection |
| increased helper t-cells | overreaction of immune system |
| increased suppressor t-cells | will suppress the immune system and not allow it to function |
| cytotoxic/ cytolytic t-cells | "Tc-cells"; subset of suppressor cells b/c they have T8 proteins; destroy cells that contain a processed antigen major histocompatibility complex protozoa |
| cytotoxic t-cells | bind with the MHC of the organism, causing cell death (d/t puncturing holes in membrane) |
| natural killer cells | direct cytotoxic effects on target non-self cells; no sensitization process; actions unrelated to WBC attacks or other leukocyte activity |
| natural killer cells | conduct seek and destroy missions; most effective against destroying abnormal or unhealthy self cells like viral or cancer cells |
| cells responsible for transplant rejection | natural killer cells and cytotoxic/ cytolytic cells |
| hyperacute stage of rejection | begins immediately on transplantation; an antibody - mediated response; host blood has pre-existing antibodies to donor's antigens; antibody/ antigen complexes adhere to lining of blood vessels, causing blood clotting> microcoagulation throughout the organ> leading to ischemic necrosis, inflammation with phagocytosis of necrotic blood vessels, release of lytiv enzymes into organ, causing graft loss |
| peope at risk for hyperacute rejection | organ wrong ABO type, recieved multile blood transfusions prior to transplant, multiple pregnancies, underwent previous transplant- must have transplanted organ removed! |
| acute rejection | increase of immunosuppressants; occurs w/in 1 week to 3 months; r/t antibody mediated vasculitis w/in transplanted organ OR, cytotoxic t-cells and nk cells enter transplanted organ through blood, infiltrate organ cells, and cause lysis of organ cells - doesn't mean client will lose the organ! |
| chronic rejection | functional tissue of transplanted organ replaced with fibrotic, scar-like tissue; ability of organ funtioning depends on how much organ tissue is damaged; longstanding problem as a response to blood vessel injury and ischemia; once there is enough organ damage that it can no longer function, pt. must have re-transplant |
| immunosuppressants used for t/x of transplant rejection | Cyclosporin (Sandimmune) - commonly used |
| immunosuppressants used for t/x of transplant rejection | Azathioprine (Imuran) |
| immunosuppressants used for t/x of transplant rejection | Mycophenolate mofetile (Cell-Cept) |
| corticosteroids used for t/x of transplant rejection | Prednisone - not on for as long as other meds d/t side effects |
| monoclonal antibodies used for t/x of transplant rejection | Basiliximab (Simulect) - started 2 hours pre-surgery; doesn't allow t-cells to grow or become activated |
| monoclonal antibodies used for t/x of transplant rejection | Daclizumab (Zenapax) - started 2 hours pre-surgery; doesn't allow t-cells to grow or become activated |
| Cyclosporin (Sandimmune) | nephrotoxic, hepatotoxic, neurotoxic; increases BG; causes gingival hyperplasia; EXPENSIVE!; taken daily for life |
| hypersensativity (allergy) and autoimmunity - type 1 | rapid hypersensativity - most common; results from increased production of IgE antibodies; acute inflammatory reaction occcurs and causes release fo histamine and other vasoactive amines from basophils, eosinophils, and mast cells |
| hypersensativity (allergy) and autoimmunity - type 1 caused by... | inhalation of pollen, fungal spores, dander, dust, grass, ragweed; injestion of foods, food additives, drugs; injection of bee venom, drugs, contrast dyes, adrenocorticotropic hormone; contact with pollen, food, environmental proteins (latex, etc...) |
| allergic rhinitis "hay fever" | affects 10%; IgE binds to basophils and mast cells which release vasoactive amines when stimulated; primary phase - binding causes cell degranulation ane release of amines (histamine), causing an allergic reaction of itchiness and redness; secondary phase - other vasoactive amines draw WBCs to the area, stimulating an inflammatory reaction |
| allergic rhinitis management | find out pt's h/x (what season are s/x worst? etc...); rhinorrhea (clear or white drainage), itchy watery eyes, sinus pressure, scratchy throat; CBC - increased eosinophils, RAST (radioallergosorbent test), serum IgE levels |
| allergy testing - scratch test | d/c corticosteroids and antihistamines 5 days PRIOR to testing; small drops of sera scratched into skin; positive result occurs w/in 20min - cleanse site after testing |
| allergy testing - oral food challenge | client eliminated suspected food 7-14 days prior to testing; client eats one type of food /day; monitor for s/s |
| decongestants | vasoconstricts inflamed tissue, reducing edema |
| antihistamines | compete for histamine sites and block it from binding to the receptor |
| corticosteroids | decrease inflammatory and immune responses |
| decongestant meds | PO and nasal sprays; Ephedrine/ Pseudophedrine |
| antihistamine meds | diphenhydramine/ Benadryl - generation 1, makes you drowsy; Claritin, Allegra, Zyrtec |
| corticosteroid meds | Solumedrol |
| mast cell stabilizers | preventative, NOT abortive; prevent mast cell membranes from opening when an allergen binds to IgE; DON'T help during an acute episode |
| mast cell stabilizer meds | take a week or so before; cromolyn sodium/ Accolate |
| desensitization therapy | sub-Q allergy shots (increasing increments of allergen per shot) |
| anaphylaxis | most dramatic and life-threatening example of a type 1 hypersensativity; effects multiple organs w/in seconds to minutes of exposure; can be fatal |
| assessment of anaphylaxis | uneasy/ anxious, decreased BP, apprehensive, weak, impending doom, generalized pruritis, urticaria (hives), erythema, angio edema, bronchoconstriction, mucosal edema, congestion, rhinorrhea, wheezes, lump in throat, stridor, hypoxemia, hypercapmia (increased CO2), HTN, rapid weak pulse, increased HR, loss of conciousness |
| stridor | priority! indicative of laryngio or bronchospasm; don't delegate someone else except RN or above! |
| penicillin | #1 anaphylactic - PRODUCING drug if person is allergic! |
| medication used w/ anaphylaxis | epinephrine - vasoconstrictor; (1:1000) 0.3 to 0.5 mL sub-Q |
| medication used w/ anaphylaxis | antihistamines - diphenhydramine/ Benadryl - IV |
| medication used w/ anaphylaxis | aminophylline - treats bronchospasms - IV 6mg/kg over 20 to 30 minutes |
| medication used w/ anaphylaxis | aerosol t/x - Alupent or Proventil |
| anaphylaxis interventions | emergency respiratory management - may require O2 by NC, mask, or ET tube<(intubation) |
| prevention and t/x of anaphylaxis | avoid allergens, wear medic allert bracelet, carry emergency anaphylaxis kit (EpiPen), inform Dr. of all allergies, have precaution equipment available if allergic med is necessary > trach kit or airway |
| latex allergy | type 1 sensitivity; foods r/t latex= bananas, kiwi, avocado, chestnuts, papaya, mango; comes from a tree |
| latex allergy management | avoid latex products, use latex-free health care products, don't chew gum around latex allergic client; clients w/ spina bifida are almost always allergic! |
| hypersensativity (allergy) and autoimmunity - type 1 includes... | allergic rhinitis "hay fever", anaphylaxis, and latex allergies |
| hypersensativity (allergy) and autoimmunity - type 2 | cytotoxic reactions - things that have to do w/ blood; an antigen - antibody complex forms and the self - cell is destroyed by phagosytosis |
| hypersensativity (allergy) and autoimmunity - type 2 includes... | blood transfusions, hemolytic anemias, Goodpasture's syndrome, and thrombocytopenic purpura; t/x = d/c offending drug or blood product and do plasmapheresis |
| hypersensativity (allergy) and autoimmunity - type 3 | immune complex reactions - not directed to a particular site, you need to remove the source! - soluble immune complexes are formed, deposited on walls of small blood vessels on the kidney, skin, and joints and activates complement |
| hypersensativity (allergy) and autoimmunity - type 3 includes... | Rheumatoid arthritis, lupus, serum sickness - after receiving serum or certain drugs, PCN, animal - based drugs |
| hypersensativity (allergy) and autoimmunity - type 4 | delayed hypersensitivity - sensitized T - lumphocytes from a previous exposure respond to an antigen by producing and releasing certain lymphokines and recruit, retain, and activate macrophages to destroy antigen; occurs w/in hours or days |
| hypersensativity (allergy) and autoimmunity - type 4 includes... | PPD skin test, poisoned ivy, contact dermatitis, organ donation rejection |
| 5 cardinal signs of inflammation | warmth, redness, swelling, pain, and decreased function |
| hypersensativity (allergy) and autoimmunity - type 4 management... | remove offending agent, monitor reation site and distally check for circulation |
| hypersensativity (allergy) and autoimmunity - type 4 meds... | corticosteroids - reduce inflammation; DON'T use Benadryl - won't work b/c histamine is NOT main mediator |
| hypersensativity (allergy) and autoimmunity - type 5 | stumulatory reactions - excessive stimulation of normal cell surfaces - focus on one organ only - not generalized! |
| hypersensativity (allergy) and autoimmunity - type 5 includes... | Grave's disease - autoantibody attatches to TSH to over-produce thyroid hormones> hyperthyroidism |
| hypersensativity (allergy) and autoimmunity - type 5 t/x... | reducing production of autoantibodies with immunosuppression; surgical or radiation of thyroid tissue |
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