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124 Cards in this Set
- Front
- Back
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immunity
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body's protection
immune memory=timing doesn't matter tolerance=eliminates what it needs to without attacking body surveillance =(concept) thinks the body is always on the look out |
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immunopathology
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study of dz resulting from dysfunctions in the immune system
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epitopes (immunogenic)
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part of the antigen molecule that functions as a antigenic determinant it permits the attachment of certain antibodies
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autoimmunity
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when the normal immune system flips on the body and attacks the host leading to TISSUE DAMAGE
as body ages tissues change and body is less able to recognize self |
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hypersensitivity
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body over responds to an antigen
-this can also be bad -often does not occur w/1st exposure -4 types -most allergic reactions type I or IV |
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gammopathies
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Immunoglobulins are over produced
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Immune Deficiencies
-Primary -secondary |
primary= problems with the cells or tissues involved with immunity most often congenital/inherited
secondary=the immune system develops normally but then there is a problem later, most acquired later in life |
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bone marrow and immunity
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-lymphoblasts generated from stem cells
-B lymphs mature in marrow then enter the blood stream -T lymphs move to the thymus were they mature into many different types of cells |
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from birth to purpose life of a B lymphocyte
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-stem cells in bone marrow=lymphoblasts
-lymphoblasts mature in marrow -into B lymphocyte -these move into the blood circulation can turn into: -memory cells or plasma cells -plasma cells-can turn into antibodies part of HUMORAL RESPONSE Remember humoral response ACTIVATES cellular response remember B=BONE and make antiBodies also think the humerus is a bone |
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from birth to purpose life of a T lymphocyte
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-stem cells in bone marrow=lymphoblasts
-lymphoblasts move to thymus -there they mature T lymphocyte can turn into: -regulator T cells =into helper T or suppressor T or -effector T cells =which can turn to cytotoxic T cells part of CELLULAR RESPONSE remember T-Thymus and aTTack antigens also think killers are in cells 60-70% of lymphocytes are in blood |
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Spleen in immunity
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acts kinda like a filter
-part of lymphiod tissues -is a RESERVE TANK red pulp=old RBCs are destroyed white pulp=conc. of lymphocytes |
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types of immunity
-Natural |
NATURAL (innate) immunity =
-present at birth -nonspecific broad spectrum coverage -1st line defense after antigen exposure -DOES NOT REMEMBER -complement system 1) cellular response- machrophages, natural killer cells, neutrophils 2) inflammatory response /fever 3)physical and chemical barriers 2 stages: -immediate=w/in 4 hours -delayed=4-96hrs after exposure |
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Granulocytes
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AKA granular leukocytes (cytoplasm)=fight by releasing cell mediators such as histamine, bradykinin, and prostoglandins or by engulfing
Nuetrophils Eosinophils Basophils PHILS |
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Nongranular leukocytes
types |
(histocytes when in tissues)
Monocytes Lymphocytes |
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Inate Factor
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-part of natural immunity
1st line of DEFENSE -no memory or antibodies 1) mechanical =skin, MM, cilia 2) physical=coughing, sneezing,etc 3) chemical=GI, tears, saliva -also cells that F in immune response like machrophages and inate inflammatory response 1) NK cells 2)Phagocytes (macrophages/neutrophils) |
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most microbial infections induce..................
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an inflammatory response mediated by T cells and cytokines if this is excessive it can cause tissue damage
so....................................... regulatory mechanisms must be there to STOP the reaction happens mostly d/t the production of cytokines and the transformation of growth factor that inhibits macrophage activity |
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types of immunity
-Acquired |
AKA as adaptive immunity
-must RECOGNIZE the antigen -ANTIGEN-ANTIBODY RESPONSE 1)Active (body makes antibodies) -natural-contact with antigen -artificial-immunizations -lasts a long time/forever 2)Passive -natural-received from mother -artificial-immunoglobulins given -only lasts a short time BOTH=use 2 mechanism 1)cell-mediated T-cells 2)effector mechanisms B-cells |
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response to invasion
3 means of defense |
1st) phagocytic immune response
-granulocytes and macrophages and eosinophils (weakly) EAT foreign and dead cells 2nd) humoral immune response AKA antibody response 3rd) cellular immune response |
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antigen
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-the part of the invading organism that stimulates antibody production
-this is also where the antibody "fits" onto the organism 2 types: 1) complete protein antigens= animal dander, pollen, horse serum -stimulates complete HUMORAL 2) haptens (incomplete antigens) -low molecular wt stuff like meds -produce a carrier complex |
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4 stages of the immune response
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1) Recognition Stage
-recognition of foreign substance is initiating event -uses lymph nodes release lymphocytes into blood for surveillance -macrophages help them process antigens 2) Proliferation Stage -lymphocytes containing the antigenic message (blueprint) return to nearest lymph node -this stimulates resident T and B lymphocytes to differentiate -node may enlarge 3) Response Stage -the differentiated lymphocyte functions in cellular or humoral response 4) antibody of humoral immunity or cytotoxic (killer) T cell of cellular immunity come into CONTACT with the antigen and the fun begins |
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Humoral response triggered by what kind of antigens
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-bacterial phagocytosis and lysis
-anaphylaxis -allergic hay fever/asthma -immune complex dz -BACTERIAL and some viral |
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Cellular response triggered by what kind of antigens
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-transplant rejection
-delayed hypersensitivity -graft-vs-host dz -intracellular infection -VIRAL, FUNGAL, PARASITIC |
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antibodies
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-large proteins called immunoglobulins
-prepare antigens for PHAGOCYTIC cells Consist of 2 subunits: -1 portion is at least 2 binding sites for antigen known as Fab fragments -the other allows participation in complement system ------------------------------------- REMEMBER-they do NOT work alone |
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types of immunoglobulins
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IgG
IgA IgM IgD IgE REMEMBER- GAMDE ordered from most to least % in body |
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IgG
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-75% of total
-in serum/tissues (interstitial fluid) -bloodborne/tissue infections -activates complement system -enhances phagocytosis -CROSSES THE PLACENTA -"ALL PURPOSE" -SECONDARY IMMUNE RESPONSE -long term MEMORY -TAKES 1-2 DAYS to respond -ACQUIRED immunity SECONDARY response= the antigen specific B-memory cells created from primary response secrete antibodes preGGers |
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IgA
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-15% of total
-blood, saliva, tears, pulmonary, GI, prostatic, vaginal secretions, and breast milk -respiratory, GI, GU infections -prevents antigen absorption from food -passes to neonate via breastmilk -'GAREKEEPERS" =protect openings -FOOD POISONING lactAtion |
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IgM
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-10% of total
-intravascular serum -1st TO RESPOND to bacterial/ viral -TAKES 4-8 DAYS AFTER -activates the complement system -Aquired immunity primary response=B cell has contact with antigen and makes antibodies and form memory cells |
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IgD
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-0.2% of total
-small amount in serum -may influence B-lymph differentiation -MAY PLAY ROLE IN RH MARKERS -FIGHTS OFF BLOOD PRODUCTS |
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IgE
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-0.004% of total
-serum -ALLERGIC/hypersensitivity reactions -combats PARASITIC infections |
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antigen determinant
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-part of the antigen that binds to the antibody
-the most efficient immunological responses occur when it fits like a "lock and key" -no response if it does not fit -poor fit or low specificity occurs when it binds with antigens it wasn't designed for and can cause unwanted damage =this is known as cross-reactivity and can be seen in rheumatic fever when antibodies made for Strep. pyogenes cross reacts to pt's heart causing valve damage |
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Helper T cells
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-CD4 is 1 on the cell surface proteins
-activated when antigen is recognized -TURN ON SYSTEM -activate B-lymphocytes and phagocytes -help B-lymphs TURN TO PLASMA cells -PLASMA cells secrete IMMUNOGLOBULINS secrete cytokines=generic term for nonantibody protein that act as intracellular mediators -starts and augment inflammation |
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Cytotoxic T cells
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-attack antigen directly by altering cell membrane and causing lysis
in cells infected w/virus -plays a role in graft rejection |
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Supressor T cells
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-CD8 is 1 of the cell surface proteins
lymphocytes that decrease B cell activity to a level at which the immune system is compatible with life/health -in other words it operates w/ NEGATIVE FEEDBACK to SHUT DOWN IMMUNE system when antigen has been killed -this does NOT happen in HYPERSENSITIVITY ?? |
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Memory cells
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type of lymphocyte
responsible for recognizing antigens from previous exposure and mounting an immune response |
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null lymphocytes
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-subpopulation of lymphocytes
-destroy antigens already coated in antibody -special receptor sites on surface allow them to connect w/antibodies known as antibody-dependant, cell mediated cytotoxicity |
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NK cells
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type of lymphocyte
-natural killer cells -recognize infected and stressed and malignant cells and kill them by secreting macrophage-activating CYTOKINES LYMPHOKINES from lymphocytes MONOKINES from monocytes |
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complement system
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-"NEIGHBORHOOD WATCH"
-circulating plasma proteins 9-16 -made in liver -activated by antibody or antigen -cause a cascading effect -RBCs/platelets have receptors for it -HUMORAL and inflammation(INATE) immunity 3 major functions: -defends against bacterial infection -bridges natural and acquired immunity -disposes of immune complexes and byproducts of inflammation -many autoimmune dz/disorders w/chronic inflammation might be caused by continued or chronic activation of this system |
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immunomodulators
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AKA biological response modifier
-affects the HOST by effecting immunoregulatory network -interferons and colony stimulating factors are the most common |
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Interferon
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type of biological response modifier/ specifically a LYMPHOKINE
CAUSE UNINFFECTED CELLS TO HAVE ANTIVIRAL QUALITIES -can activate other immune sys components -have ANTIVIRAL and ANTITUMOR properties -made by T/B lymphs and macrophages in response to antigens -supress antibody production and cellular immunity -help cytolytic role of macrophages and NK cells -used to tx immune r/t disorders and chronic inflammatory conditions |
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colony stimulating factors
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type of biological response modifier
-glycoprotein cytokines that regulate hematopoietic cells Erythropoietin=stims RBC production Thrombopoietin=growth/differentation of bone marrow cells Interleukin-5= stims growth/survival of eosinophils and basophils Stem cell factor and IL-3=stimuli for many hematopoietic cells |
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genetic engineering
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-uses recombinant DNA technology
1) combine genes from different sources 2) gene therapy=abnormal gene replaced |
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stem cells
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-capable of self renewal and differentiation
-produce RBC/WBC -totipotent=stem cells on steriods -embryonic/pluripotent=many types of cells/tissues |
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estrogen and immunity
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-estrogen enhances immunity
-so autoimmune dz more common in women -5th leading cause of death in reproductive years -androgens are immunosupresive |
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immunosenescence
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-aging process stimulates changes in immune system
-natural immunity contines to function -impaired T and B cell function -increased risk of autoimmune dz -physical/chemical barriers decline -decreased efficacy of vaccines |
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nutrition and the immune system
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Vitamin D, zinc, copper, manganese, and selenium are important
polyunsaturated fats=reduce inflammation decreased protein=atrophy of lymphoid tissue, depression of antibody response, reduced circulating T cells, impaired phagocytic function |
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what kinds of things weaken the immune system
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-immunosupression increases risk of cancer BUT cancer is immunosupressive
-radiation=destroys lymphocytes -renal failure-reduced lymphocytes -removal/transplant of some organs -burns=loss of protection/immunoglobulins -stress=cortisol release from adrenal cortex -XS exercise=causes stress -STDs or previous infections |
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medications that reduce immune system
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-lrg dose antibiotics
-corticosteriods -antineoplastics/cytotoxic agents -salicylates -lrg doses of NSAIDs -anesthetic agents |
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highest risk for HIV infection d/t contaminated blood transfusion before what year
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1985
-since then the risk is very very low |
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psychoneuroimmunology
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-bidirectional pathway between the brain and the immune system
-lymphocytes and macrophages have receptors that can respond to neurotransmitters and endocrine hormones -cells in brain (hypothalamus) can recognize prostoglandins, interferons, interleukins , histamine, and serotonin all which are released during INFLAMMATORY process -so guided imagery, humor, hypnosis, etc can help in immune conditions |
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cardinal symptoms of immunodeficiency
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-chronic or recurrent severe infections
-infections caused by unusual organism -infections from normal body flora -poor response to standard tx of infections -chronic diarrhea |
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10 warning signs of primary immune deficiency
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-8+ new ear infections in 1 year
-2+ serious sinus infections/1 year -2+ months on antibiotics w/little effect -2+ pneumonias in 1 year -failure of infant to grow/gain weight -recurrent deep skin/organ abscesses -persistent thrush after age 1 -need for IV antibiotics to tx infection -2+ deep seated(cellulitis/meningitis/sepsis) -a family hx of primary immune dz |
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2 types of IgE mediated allergic reactions
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1) atopic
-hereditary disposition and local reaction to IgE antibodies -allergic rhinitis, asthma, atopic dermatitis/eczema 2) nonatopic -lack genetic component and organ specificity |
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3 basic defenses of immune system
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-physical and chemical barriers
-inflammatory response -immune response |
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mast cells
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-contain heparin and histamine
-located in skin and MM -major role in IgE mediated immediate hypersensitivity reactions -release chemical mediators |
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types of chemical mediators
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1) primary
preformed and found in mast cells and basophils 2) secondary inactive precursors that are formed and released in response to primary mediators |
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how allergy works -BASIC
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-allergen triggers B cell to make IgE
-IgE attaches to mast cell -triggers release of chemical mediators |
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list primary mediators
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-histamine
-eosinophil chemotactic factor of anaphylaxis -platelet activating factor -prostoglandins -basophil kallikrein |
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histamine
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-preformed/released by MAST cells
-effects greatest in 1st 15 minutes -H1 receptors on bronch/vascular -H2 receptors in GI parietal cells EFFECTS: -vasodilation, wheals -contraction of bronchials-wheezing -increased vascular permeability -increased mucus secretion |
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eosinophil chemotactic factor of anaphylaxis
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AKA ECF-A
-primary mediator -preformed and released by MAST cells -attracts eosinophils to site |
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platelet activating factor
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primary mediator
-bronchoconstriction/smooth muscle -platelet aggregation and release of serotonin and histamine |
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prostoglandins
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primary mediator
-smooth muscle contraction -vasodilation=increased permeability -FEVER, PAIN w/inflammation in inflammatory response |
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basophil kallikrein
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primary mediator
-preformed in MAST cells -frees bradykinin bradykinin= -secondary mediator -bronchoconstriction -vasodilation=hypotension -nerve stimulation =PAIN |
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Serotonin
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secondary mediator
-potent vasoconstrictor -contraction of bronchial muscle |
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list secondary mediators (allergic)
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-bradykinin
-serotonin -leukotrienes |
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leukotrienes
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-secondary mediator
-initiates INFLAMMATORY response -wheal and flare skin reactions |
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List types of hypersensitivity reactions
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I-Anaphylactic
II-Cytotoxic III-Immune complex IV-Delayed Type ACID |
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I-Anaphylactic hypersensitivity
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-most severe and FAST
-edema in many tissues -hypotension/bronchospasm -can be local (insect bites) or systemic -SENSITIZED TO ALERGIN -allergen triggers B cell to make IgE -IgE attaches to mast cell -triggers release of chemical mediators -like hay fever |
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II-Cytotoxic hypersensitivity
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-mistaken identity or SELF FIGHTING
-IgM or IgG or IgA bind to antigen -attacks normal tissue/cells/RBCs (transfusions/ diabetes) |
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III-Immune complex hypersensitivity
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-immune complexes formed w/binding of antibody to antigen
-phagocytes clear complexes -but complexes may be in tissues -KIDNEY and JOINTS most common place for issues= because when an antibody and antigen bind they form a COMPLEX which are large and may CLOG SMALL VESSELS |
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IV-delayed or cellular hypersensitivity
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-occurs 1-3 days AFTER exposure
-mediated by T cells and macrophages NOT antibodies -redness and itching are common -seen w/tape,cosmetics, plants -TRANSPLANTS, CONTACT DERMATITIS |
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Lab values- Eosinophils
increased=eosinophilia?? |
-5-15%=nonspecific but may be allergy
-15-40% (moderate)=allergy counts: -obtained via specimen during s/s active allergic response if present total serum IgE levels -high levels support dx -WNL levels do NOT exclude it -not as sensitive as other tests ............ such as -PRIST/ ELISA/ EIA |
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Organs important ti immunity
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Spleen
Thymus Lymph System including Tonsils |
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Thymus and immunity
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produces/T cells untill puberty
-these are ALL the body WILL HAVE -also secrete something to make them mature in nodes -SHRINK W?AGE |
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what is the point of corticosteriods
and when are they released |
-released when body is STRESSED
-used for ENERGY -ANTI INFLAMMATORY -but DECREASE immune function |
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so what increases the immune system
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-ENDORPHINS (HUMOR)
-1# is PRAYER -sleep, culture, nutrition -LOW STRESS RESPONSE |
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Role of stress:
-negative feedback -positive feedback |
-negative=NO STRESS
-positive=STRESS must reach negative feedback again or you will DIE |
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3 stages of Stress Response
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1) Fight or Flight
-increased ACTH -increased Catecholamine= epinephrine (adrenal) -increased corticosteriods (renal) =ENERGY 2)Resistance -TSH (thyriod)= increased BMR -aldosterone (adrenal) and ADH (posterior pituitary)=increase B/P and O2 capacity 3)Exhaustion -body can't keep it up forever REMEMBER -everything speeds up except the GI tract |
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Neutrophils
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-AKA polys or pmns
-1st TO ARRIVE -SHORT LIFE OF 6 HOURS -amebode action like sperm -chemotaxis="like GPS" -LYSOSOMES=to KILL |
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Eosinophils
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-big for ALLERGIES and stress
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Basophils
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-big for TRANSFUSIONS
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Monocytes
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-"PEACE KEEPERS"
-amebode and chemotaxis -also can REPLENISH lysosomes to kill -will HANG around for MONTHS after -also phagocytes |
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Lymphocytes
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-come later
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Major Histocompatability Complex
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-FOUND ON CELLS
-use this test b4 TRANSPLANTS -tests for HLA=human luekocyte antigen HLA= -gives specifics of MHC -SET OF 6 MAJOR ANTIGENS -must have 4+ match to transplant -will hear "6 way marker" or however many matched |
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Some MAJOR autoimmune dz
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-SLE
-rheumatoid arthritis -scleroderma -hemolytic anemia -thrombocytopenia purpura -multiple sclerosis -Gullian-Barria -myasthesia gravis -rheumatic fever -Addison's dz -thyroiditis -hypothyroidism -pernicious anemia -ulcerative colitis Goodpasture's syndrome -glomerulonephritis -primary biliary cirrhosis -chronic active hepatitis -uveitis -TYPE 1 DIABETES |
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Types of primary immune deficiency
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-phagocytic defects
-B-cell defects -T-cell defects -combined B and T cell defects -complement defects (Gravley says to think B-cells that don't develop or differentiate to make antibodies) |
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primary immune deficiency
phagocytic dysfunction |
-most are genetic and effect innate sys
-characterized by dz specific infections -use nitroblue tetrazolium reductase test to help dx |
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nitroblue tetrazolium reductase test
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-indicates cytocidal (causing death of cells) activity of phagocytic cells
-used in dx of primary immune deficiency-phagocytic dysfunction |
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primary immune deficiency
B-cell Deficiencies |
1) lack of B cell differentiation=NO PLASMA cells so NO ANTIBODIES
-called X-linked agammaglobulinemia (Burton's dz) or autosomal where it will correct -NO/LOW B-cells in BLOOD 2) same as above but there is DIMINISHED ANTIBODY production= hypogammaglobulinemia where some Ig's are working or panhypoglobulinemia where they are all screwed up -MAY HAVE B-cells WNL but not normal/mature -may be tx w/IVIG or IV immunoglobulins |
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primary immune deficiency
T-cell Deficiencies |
-lead to OPPORTUNISTIC infections
-think persistent thrush -hypocalcemia and poor adrenal F -ie, DiGeorges syndrome= THYMUS gland does not develop or does not function resulting in NO IMMUNE SYSTEM -may need marrow/thymus transplant -may also need IVIG |
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primary immune deficiency
combined B and T cell |
-poor prognosis d/t many infections
-ex -severe combined immunodeficiency dz (SCID) -Wiskott-Aldrich syndrome (WAS) -stem cell/marrow transplants |
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primary immune deficiency
Complement system |
???
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Managing IV immunoglobulin infusion
(IVIG) |
-reconstituted w/a dilutent made form 1000's of donors
-dose 100-400mg/kg monthly+ ADVERSE REACTIONS: -flank and back pain (renal) -tightness of chest, headache -fever, chills -ANAPHYLACTIC reactions w/n 30-60mins -obtain HEIGHT AND WEIGHT for dose -assess VS, HOLD for FEVER -premed w/tylenol and benadryl prn 30 minutes b4 -be careful if using a NEW TYPE -infuse SLOW no more than 3mL/min -BE ALERT FOR TICKLE/LUMP in throat -STOP at 1st sign of reaction -pt w/LOW levels of Ig are HIGHER risk REMEMBER -ALL products contain SOME IgA -if pt has low IgA they have IgE antibodies to IgA and MUST GET replacement from IgA-deficient pts |
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Types of secondary immunodeficiency
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-HIV (AIDS)
-malnutrition (most common) -chronic stress/burns/trauma -DM -drugs -and the other things listed as weakening the immune system |
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Nursing Management for pt's w/immunodeficiency
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-assess hx of infections/immunizations
-assess for current infections -oral care is important -inflammatory response may be blunted -COUNT PULSE/RR for 1 MINUTE -listen to lungs -monitor labs/ cultures -good hygiene esp HANDWASHING -nutrition/stress/drugs/etc -ASPEPTIC TECHNIQUE STRICT -tell pt to report CHANGE in status -continue tx w/out interruption |
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Allergy skin tests
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-NOT DONE if bronchospasm present
-scratch/prick tests done FIRST -intradermal if negative scratch/prick -have ER EQUIPMENT available -back is best place if many tests -negative response does NOT mean no sensitivity to allergen -good for FOOD ALLERGIES -BAD for medications -AVOID corticosteriods/antihistamines 48-96hrs before the test -DOCUMENT site and allergen used -wheal is measured |
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Provocative allergy testing
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-injects allergen into tissue that is sensitive to it
-can only test 1 kind at a time -and risk for reaction INCREASES |
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RAST
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-radioallergosorbent test
-radioimmunoassay that measures alleregn specific IgE -allergens combined w/pt serum -also tells HOW much allergen is needed to produce response HOW ALLERGIC ARE YOU? -it costs a lot more and can only test some stuff but no systemic reactions |
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Most common substances that cause anaphylactic reactions
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-PENICILLIN (antibiotics)
-CONTRAST AGENTS (iodine) -nuts,shellfish,milk,soy,wheat,dairy -insect stings -NSAIDS/ vaccines/hormones/anesthetics -opiods -LATEX |
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how are anaphylactic reactions classified
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MILD: occurs w/2 hours
-warmth -fullness in mouth/throat -nasal congestion, watery eyes -periorbital edema, pruritis MODERATE: same onset as mild -flushing,warmth,anxiety -bronchospasms, cough,dyspnea SEVERE: ABRUPT ONSET -dyspnea, cyanosis, hypotension -dysphagia -abdominal cramping, N/V/D -seizures, cardiac arrest, coma CARRY AN EPI-PEN if know allergies and get to hospital in cause of a rebound reaction |
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Medical response/tx of anaphylactic reactions
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-CPR if needed
-Oxygen -epinephrine 1:1000 sq in ue or thigh follwed by IV infusion -antihistamines/corticosteriods -vasopressors/glucagon for B/P -NS IV to expand fluid volume -RX FOR EPI-PEN w/DEMO |
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How to use EPI-PEN
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-remove gray safety cap
-while holding needle down in fist -swing and jap in thigh at 90 angle -should hear a CLICK -HOLD it there for 10 seconds -massage area for 10 seconds -place back in tube -take it to ER w/you |
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Allergic Rhinitis
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-AKA Hay Fever, seasonal allergic rhinitis
-most common respiratory allergy -type I hypersensitivity reaction -can cause loss of smell, hearing, and deformities in kids -attacks begin and end at same time each year -spores die in freezing weather -so may have s/s year round in FL -sneezing w/congestion -clear runny nose w/itching -may result in sore/dry throat -headache, sinus pain -epistaxis -use of HEPA filters -keeping clean house -avoiding outdoor activity w/high count -also meds |
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Immunotherapy
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-this is what we do to Layla
-must keep in office and monitor for 30 minutes -if redness occurs may not want to increase dose -dose cannot be increased during pregnancy but may be continued |
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Contact Dermatitis
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-type IV DELAYED hypersensitive reaction
-TRUE test most common patch test used to dx |
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Atopic dermatitis
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-type I immediate hypersensitivity reaction
-AKA atopic eczema/dermatitis -lots of histamine in skin=itching -CHRONIC w/periods of remission |
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Dermatitis Medicamentosa
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(Drug Reaction)
-often appear suddenly -RASH most common -looks more intense than others -will disappear w/drug withdrawl -STOP MED IF YOU SEE THIS and report |
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Urticaria
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-AKA Hives
-type I hypersensitive reaction -hives last for hours or days then may reaper -chronic if more than 6 weeks |
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angioneurotic edema
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-involves deeper layers of skin
-more diffuse swelling than hives -DOES NOT PIT on pressure/looks red -ACE inhibitors/penicillins common cause |
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Food allergy and pregnancy
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if a pt is pregnant and has close relative w/food allergy, hay fever, eczema, etc they should avoid PEANUTS
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Latex and food allergy cross reactivity
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Latex comes from a TROPICAL tree so think of TROPICAL FRUITS
-kiwi -mango -avocado -banana -pineapple -passion fruit -chestnuts |
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ESR
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erythrocyte sedimentation rate
-increased w/inflammation of connective tissues |
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C-reactive protein test
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-shows presence of abnormal glycoprotein d/t inflammation
-elevated w/ACTIVE inflammation |
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Rheumatic Disease
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-commonly called arthritis
-but there are 100's of types CLASSIFICATION: -monoarticular or polyarticular AND inflammatory or noninflammatory -joint most often effected but can be systemic -primary inflammation d/t immune response -degradation s/t pannus (pannus=synovial fluid w/inflammatory cells) -most common symptom PAIN -observe pt during activities -ESR may be elevated |
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Rheumatoid Arthritis
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-diffuse connective tissue dz
-AUTOIMMUNE disease PATHO: -phagocytosis =enzymes w/n joint -pannus formation and degradation S/S: -pain,swelling,warmth,loss of function -starts in small joints first -often acute onset -s/s bilateral and symmetric -JOINT STIFFNESS IN THE MORNING -pt may protect joints by not moving -spongy/boggy feeling joints -lack og mobility=contractures -deformities are common -fever,wt loss, node enlargement -Raynaud's phenomenon -painless,movable nodules LATER -Sjogren's syndrome -RA factor (lab value) -synovial fluid is cloudy,milky,dark yellow -X-ray for baseline then q3yrs |
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Raynaud's phenomenon
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-may be seen w/Rheumatoid Arthritis, scleroderma
-cold and stress induced vasospasm causing episodes of digital blanching and cyanosis |
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Sjogren's syndrome
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-may be seen w/Rheumatoid Arthritis
-dry eyes and dry MM |
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SLE
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Systemic Lupus Erythematosus
-more common in women -exaggerated production of autoantibodies -genetic,hormonal(childbearing years), environmental(sunlight), and chemical/drug induced SLE -B and T cells play role but more B cells -SYSTEMIC AUTOIMMUNE DISEASE -most often musculoskeletal arthralgia and arthritis -many skin manifestations BUTTERFLY RASH MOST COMMON -oral ulcers/ pericarditis -renal issues which may cause HTN -widespread CNS involvement changes in behavior or cognition |
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Scleroderma
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-"hard skin"
PATHO: -mononuclear cells cluster on skin -stimulate lymphokines to make procollagen -insoluble collagen forms in tissues -edema =taught, shiny,smooth skin -skin becomes fibrotic and loses function -this happens systemically S/S: -starts slowly w/Raynaud's phenomenon -swelling of hands -skin cannot be pinched -sweat glands obstructed=dry skin -localized to hands/feet for years -face is mask like, immobile, rigid mouth -LEFT V of heart=HEART FAILURE -esophagus hardens=dysphagia -GI and lungs effected CREST SYNDROME -pt should avoid extreme temps -use lotions -STOP SMOKING |
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CREST SYNDROME
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s/s seen w/scleroderma
C=calcinosis (Ca deposits in tissue) R=Raynaud's phenomenon E=esophageal hardening/dysfunction S=sclerodactyly (scleroderma of digits) T=telangiectasia(capillary dilation that forms a vascular lesion) |
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Polymyositis
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-group of dz known as idiopathic inflammatory myopathies
-VERY RARE -antibodies are present but do NOT cause damage to muscle -PROXIMAL weakness often 1st sign -symmetric and diffuse muscle weakness -pt may have trouble combing hair, walking stairs -may need assistive devices |
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Inate inflammatory response
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-triggered when foreigner enters tissue
-ruptures mast cells=histamine -histamine=dilates vessels -dilated vessels are leaky -platelets leak out -injured tissue releases chemokines -chemokines attract WBC -WBC phagocytic action =pus -leaky vessels also cause=swelling, redness,heat |
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Macrophage
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cells in body that will eat antigen and then produce an antigen protein (information) that is picked up by T-helper cells and passed on to B-cells
B cells can also do something like this (engulfing and making a marker for T-cell) |
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How Antibodies Fight invaders
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-agglutination= 1 antibody causes 2+ antigens to clump/stick together to help phagocytosis
-opsonization=the antigen-antibody molecule is coated w/a sticky subsatnce to help phagocytosis -COMPLEMENT SYSTEM -may also neutralize |
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Antigen Variation
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when an antigen alters it's surface proteins (by changing RNA/DNA) so it isn't RECOGNIZED by immune system
The Flu does this and that is why we can get it every year |
