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82 Cards in this Set
- Front
- Back
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Primary threats to our immunity
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Unique viruses
HIV/AIDS Hep C TB Hospital acquired & foodborne Lethal influenza |
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Infectious disease in 2011
5 culprits |
Land use patterns
Increased trade & travel Inappropriate use of antibiotics Pathogenic mutations Lifestyle change |
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INNATE IMMUNITY Characteristics
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Rapid
Invariant Limited in specificity Repeat exposures to a particular microbe do not create larger or faster responses (no memory) |
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INNATE IMMUNITY
Four types of rapid, non-specific responders |
Neutrophils
Macrophages Monocytes Natural killer cells - complement system - proteins of contact activation system |
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INNATE IMMUNITY
Neutrophils |
Process - Phagocytosis
Target - Bacteria/fungi Location - Bone marrow>Tissues Activation molecules - C3b, leukotriene, IL-8 |
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INNATE IMMUNITY
Macrophages/Monocytes |
Process - Antimicrobial; Antigen presentation to helper T cells
Target - Intracellular pathogens, mycobacterium, parasites, & fungi Location - Bone marrow > Tissues Activation molecules - Proteases, interferon, bacterial endotoxin |
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INNATE IMMUNITY
Natural killer cells |
Process - Cell lysis, cytokine release
Target - Virus & tumor cells Activation molecules - Spontaneous killers |
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INNATE IMMUNITY
Eosinophils |
Process - Release toxic proteins
Target - Parasites Location - Tissues Activation molecules - C5a, C3b, leukotrienes |
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INNATE IMMUNITY
Mast cells/Basophils |
Process - Histamine release
Target - Reactive to IgE, does not target antigens Location - Lungs, mucosa, systemic Activation molecules - IgE, C3a, C4a, C5a (lungs only) |
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INNATE IMMUNITY
Complement |
Process - Sequential activation; Cascading of events
Target - Opsonization; Smooth muscle contraction; Histamine release; Increased vascular permeability; Cell lysis; Cell death Location - Inactive in BLD; Synthesis liver Activation molecules - CLASSIC: Antigen-antibody complexes, aggregated by Ig's, C-reactive protein; ALTERNATE: C3b membrane attack |
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Complement
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1. Activation of neutrophils, Chemotaxis
2. Vasodilation, increased permeability of blood vessels 3. Mast cell degranulation 4. Opsonization, phagocytosis, lysis of bacteria |
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Phagocytosis
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1. Phagocytic WBC meets bacterium that binds to cell membrane
2. Phagocyte uses cytoskeleton to push its cell membrane around bacterium, creating lg vesicle, the phagosome 3. Phagosome containing bacterium separates from cell membrane & moves into cytoplasm 4. Phagosome fuses with lysosomes containing digestive enzymes 5. Bacterium is killed & digested within vesicle |
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INNATE IMMUNITY
Physical components |
Skin, mucous membranes, cilia, mucus
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INNATE IMMUNITY
Chemical components |
Gastric acid, lysozyme, complement, acute phase proteins
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INNATE IMMUNITY
Cells |
Phagocytes, NK cells
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ACQUIRED IMMUNITY
Characteristics |
Requires time (4 days -3 wks) for induction
Variant - unique response to each foreign substance Highly specific Repeat encounters produce larger, more rapid responses (basis for vaccines) |
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ADAPTIVE (or acquired) IMMUNITY
Types of "delayed, remembers antigens" |
Humoral component (mediated by B lymphocytes)
Cellular component (mediated by T lymphocytes) Found only in "jawed vertebrates" |
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ACQUIRED IMMUNITY
Chemical components |
Antibodies
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ACQUIRED IMMUNITY
Cellular components (There are no physical components for Acquired) |
T lymphocytes, B lymphocytes
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ACQUIRED IMMUNITY
Active method |
Vaccination
Infection |
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ACQUIRED IMMUNITY
Passive method |
Transplacental
Colostrum (first 2-3 days of breastmilk) Administration of serum |
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ACQUIRED IMMUNITY
Macrophages |
Localize antigen
Present antigen to lymphocytes Regulate lymphocytes via cytokine secretion Bind Ag-Ab complexes Remove/destroy antigen |
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ACQUIRED IMMUNITY
T lymphocytes |
Act as helper cell for some antigens
Secrete cytokines to regulate/activate macrophages/B lymphocytes Recruit other T lymphocytes Present antigen to B lymphocyte cytotoxic cell 2/3: Helper cells (CD4) which secrete cytokines 1/3: Suppressor/cytotoxic cells (CD8) which protect against virus-infected cells, reject foreign tissue grafts, immune response to tumors... and Secrete cytokines, interferon, IL-2, TNF, lymphotoxin Secrete: |
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ACQUIRED IMMUNITY
B lymphocytes |
Immunoglobulin production
Bind Ag-Ab complexes Bind Ag to T lymphocytes |
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Cytokines
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Promote cellular communication w/certain cells
Regulate inflammation, growth, & healing |
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Interferons
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Prevents cellular viral replication
Increases expression of MHCI & MHCII antigents Destroys tumor cells |
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Major histocompatibility complex (MHC)
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Required for antigen recognition by T-cells
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Chemokines
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Potent chemo-attractants
Controls cell migration into extravascular space Arthritis, glomerulonephritis, pulmonary disease, skin disorders |
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3 types of defects or alterations in immune function (for both innate & acquired)
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Injury caused by inadequate immunity
Injury caused by excessive immunity Injury caused by misdirection of immune response |
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INADEQUATE INNATE IMMUNITY
Neutropenia |
Acquired, Autoimmune, Sepsis, Idiopathic
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Acquired Neutropenia
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Chemo, AIDS Rx, Chloramphenicol, Anti-thyroid drugs, Gold salts, Acetaminophen, phenacetin, Tricyclic antidepressants, Phenothiazines
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Autoimmune Neutropenia
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Systemic lupus
Rheumatoid arthritis |
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Sepsis (Neutropenia)
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Granulocytopenia - peritonitis, pneumococcal sepsis
Net decrease in granulocyte production - Use > marrow production, Alcoholics, Folic acid deficiency |
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Idiopathic Neutropenia
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No obvious cause
Mild reduction in neutrophils Not assoc w/life-threatening infection Myeloproliferative or myelodisplastic issue if other cell types reduced |
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EXCESSIVE INNATE IMMUNITY
Neutrophilia |
>7000 per microliter - splenic leukostasis, chloromas
Symptoms at >100,000 - no brain involvement |
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EXCESSIVE ACQUIRED IMMUNITY
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Allergic reactions (atopic, anaphylaxis, anaphylactoid)
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Intraop allergic reactions
STATS |
Incidence: 6-10% of all adverse reactions
Risk: 1-3% for most drugs 1:5,000-25,000 anesthetics >90% occur within 3 min of admin Under anesthesia: Circulatory collapse most common sign |
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Atopic allergic reaction
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Increased allergic predisposition
Maintain large quantities of circulating IgE antibodies |
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Anaphylaxis allergic reaction
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Immediate, rapid release of IgE by mast cells
Generalized, systemic symptoms Within sec or as long as 60 min after trigger |
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Anaphylactoid allergic reaction
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Clinical events caused by non-IgE mediated trigger
Potentially life-threatening but may be self-limited |
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Common allergic trigger agents in OR (order from most common to least)
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NMB drugs (58%)
Latex (17%) Antibiotics (15%) Colloids (4%) Hypnotics (3.4%) Opioids (1.3%) Other agents (1.3%) |
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Sources of anaphylaxis (those relevant to us)
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Nuts, milk, eggs, seafood, fish
Latex Antibiotics (esp PCN & cephalosporins) Neuromuscular blockers Aspirin & other NSAIDs IV contrast media, blood products, IV fluids/colloids Opioids ACE Inhibitors |
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Primary treatment for anaphylaxis under GA
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Stop administration of possible antigens
Maintain airway - 100% O2 Discontinue all anesthetic agents Expand intravascular volume Epi 5-10 mcg/kg if hypotension and PRN CPR |
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Secondary treatment for anaphylaxis under GA
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Antihistamines (diphenhydramine 0.5-1 mg/kg)
Catecholamine infusion Aminophylline (5-6 mg/kg over 20 min) Corticosteroids (200 mg hydrocortisone or 1-2 g methylprednisolone esp if complement mediated) Sodium bicarb based on ABG Airway evaluation |
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Type I Hypersensitivity Reaction is...
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Anaphylaxis
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Type II Hypersensitivity Reaction is...
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Cytotoxic - autoimmune hemolytic anemia
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Type III Hypersensitivity Reaction is...
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Immune complex reactions - lupus, rheumatoid arthritis, glomerulonephritis
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Type IV Hypersensitivity Reaction is...
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Delayed hypersensitivity - contact dermatitis, host versus graft disease
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Process of Anaphylaxis (5 steps)
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1. Allergen binds with mast cell antibodies (IgE)
2. Histamine + other mediators released 3. First wave of symptoms in seconds or delayed 4. Activated mast cells produce cytokines 5. Second wave of symptoms 6-8 hrs later |
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How do anaphylactoid reactions occur?
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Classic - IgG or IgM
Alternate - Latex, drugs, endotoxins, contrast dye IV contrast, latex, narcotics Histamine release |
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MINIMIZING RISK PRE-OP
Atopic allergies or allergic rhinitis |
Contrast dye
Latex allergies |
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PRE-OP PREPARATION (for high-risk patients)
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H1 & H2 antagonists 16-24 hrs preoperatively
Maximize volume status Optional: Large steroid doses (2g hydrocortisone) should be given prior to exposing pt to high incident agents |
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MINIMIZING RISK PRE-OP
Geriatric & beta-blocked patients |
Increased risk of problems with pretreatment & anaphylaxis rx
Less responsive to treatment regimens Avoid drugs likely to trigger anaphylaxis |
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Risk factors for latex allergy
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Spina bifida
Multiple surgeries Health care workers Rubber industry workers Patient w/familial allergies Children w/urinary birth defects Allergies to: bananas, avocados, kiwi, passion fruit |
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Latex allergy Presentation & Precautions
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Presentation: delayed approx 30 min
Precautions: gloves, IV ports, med caps, foleys, drains, ventilator bellows, ETT, LMA, NGT, BP cuff, airways, syringes, ECG pads CRNA/MDA/healthcare workers - increased risk for allergic response to latex |
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Host vs. Graft Transplant Rejection - Hyperacute vs. Acute
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Hyperacute:
Complement mediated Host has preexisting antibodies (ex. ABO blood type antibodies) Humoral mediated immune response Occurs within minutes if xenotransplanted organs placed in non-immunosuppressed Acute: Takes 1 wk for donor T-cell activation to begin |
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Hydrocortisone
Prednisone Methylprednisolone Dexamethasone Betamethasone |
Hydrocortisone - Potency 1, Dose 20 mg, Duration 8-12 hrs, replacement therapy
Prednisone - Potency 4, Dose 5 mg, Duration 12-36 hrs, systemic anti-inflammatory & immunosuppressive effects Methylprednisolone - Potency 5, Dose 4 mg, Duration 12-36 hrs, systemic anti-inflammatory & immunosuppressive effects Dexamethasone - Potency 25, Dose 0.75 mg, Duration 36-72 hrs, use when H2O retention is an issue Betamethasone - Potency 30, Dose 0.75 mg, Duration 36-72 hrs, use when H2O retention is an issue |
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List of autoimmune disorders
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Addisons, Celiac, Graves, Dermatomyositis, Hashimoto's thyroiditis, MS, Myasthenia gravis, Chronic active hepatitis, Ulcerative colitis, RA, SLE, Sjogren, Rheumatic heart disease, Type 1 diabetes, Pernicious anemia, Scleroderma, Idiopathic thrombocytopenia purpura
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ANESTHETIC IMPLICATIONS
Rheumatoid arthritis |
Cervical instability
Positioning |
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ANESTHETIC IMPLICATIONS
SLE (lupus) |
Renal injury
Cardiac effects |
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ANESTHETIC IMPLICATIONS
Addison's Disease (chronic adrenal insufficiency) |
Addisonian crisis
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Primary immunodeficiency disease (3 listed)
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SCIDS
HIV/AIDS DiGeorge Syndrome |
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HIV/AIDS
Cell mediated immune defect is primary... what type of infection? |
Retroviral infection
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HIV/AIDS
Humoral immune effects also occur... which cell's function is altered? |
B lymphocyte function altered
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HIV/AIDS
Pathology? |
CD4 T-lymphocyte (helper cell) dysfunction
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HIV/AIDS
Transmission rate? |
Depends on subtype virulence, viral load, host factors, genetics
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HIV/AIDS
Acute phase |
Lymph nodes replicate virus
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HIV/AIDS
Diagnosis |
Serologic (acute phase cannot be detected clinically)
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AIDS Clinical Manifestations:
Respiratory |
Pneumocystis carinii
TB Fungal infections Kaposi's sarcoma Lymphoma Lung abcess |
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AIDS Clinical Manifestations:
Neurological |
Cerebral toxoplasmosis
Primary CNS lymphoma Multifocal leukoencephalopathy |
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AIDS Clinical Manifestations:
Cardiac |
Involvement present but clinically silent
Generalized vascular disease due to anti-retroviral drugs |
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AIDS Clinical Manifestations:
Other |
Unexplained hypotension - adrenal insufficiency with advanced HIV
Skin - lots of issues |
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HIV/AIDS
Treatment |
Nucleoside reverse transcriptase inhibitors - AZT, DDI, 3TC
Non-nucleoside reverse transcriptase inhibitors - Nevirapine, Efavirenez Protease inhibitors - Saquinavir, Indinavir, Ritonavir |
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HIV/AIDS
Anesthesia related details |
20% will require surgery
Anesthesia, surgery both decrease cell mediated immunity - modification of immune mediators GA reduces immunity more than regional Preop Eval - patient status, surgery type, anesthesia choice Continue antiretroviral meds intraop! RA better overall except local injected into CSF Avoid homologous blood transfusion Link b/t CD4 level & complications? |
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Perianesthesia stressors include....
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Stress response to surgery
Hyperglycemia Hypothermia... altered tissue perfusion Inflammatory response to surgery |
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Volatiles & IV anesthetics do what to immune function?
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Depress immune function
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Volatiles & IV anesthetics depress various aspects of stress response thus...
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the net immune effect of these drugs may not be deleterious
Evidence reveals conflicting conclusions regarding effects of anesthetic agents on immune function |
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Overall opioids are immunosuppressive to some degree... more details?
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MSO4 - suppresses NK cells, lymphocyte proliferation, & inflammatory cytokine production
Fentanyl - comparable results reversible with naloxone... limited to first 72 hrs... lower tumor burden Effects in pts without pain may be immunodepressive. Effective postop pain control & thus lack of SNS activation likely returns pt to autonomic balance & restores immune response |
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How to optimize immune function perioperatively...
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Reduce metabolic response to surgery
Avoid hyperglycemia & hypothermia Ensure adequate tissue perfusion Use minimially invasive procedures when possible Antibiotics in timely manner Limit invasive instrumentation Avoid blood transfusion if possible |
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Nosocomial infections
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Leading cause of death
35 million pts/yr = 1.75 million infections (5%) 175,000 are bloodstream infections 70% are pts with CVP catheters 90% of CVP related BSIs can be prevented w/antibiotic bonded catheters Would save 5000-9000 lives per year |
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MRSA (methicillin resistant staphylococcus aureus)
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>deaths than HIV/AIDS
32:100,000 Most resistant Young, sexually active, prisoners, pts exposed to many antibiotics Produces toxin --> skin lesions, tissue necrosis Sharing needles, towels, soap, bed linens, sports equip |
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Which antibiotics treat MRSA?
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Vancomycin, gentamycin, ciprofloxacin
(all personnel must be aware pt has MRSA) |
