Immune System Flashcards
Type 4 hypersensitivity**
Delayed
Cell mediated
Caused by activated T cells NOT ANTIBODIES
Th1, Th2, CTL
24-72 hrs
Contact dermatitis/TB lesions/graft rejection/chronic asthma
Innate immunity self-vs-nonself discrimination
Based on self-vs-nonself
So it needs to be perfect
What exacerbates SLE?
Infection
Pregnancy
Surgical stress
Drugs (procainamide, hydralazine, captopril, enalopril, isoniazid, methyldopa, d-penicillamine)
SLE effects (high risk)
Seizure Stroke Dementia Neuropathy Psychosis Pericardial effusion >50% pts Tamponade rare
Mast cells**
Immediate hypersensitivity responses
Tissue fixed (perivascular spaces of skin/lung/intestine)
IgE receptors on surface (bind to antigens)
Activation=release of mediators important to immediate hypersensitivity rxns
Mononuclear cells**
Ingestion and destruction of damages and neoplasticism cells and bacteria
Effector cell-migrates to inflammation areas
Agranulocyte
Phagocytosis
Release cytokines
Present pieces of pathogens to t-lymphocytes
Hypersensitivity acronym
A (allergic/anaphylaxic/atopic)
C (cytotoxic)
I (immune complex)
D (delayed)
Adaptive immunity specificity
Highly specific! Can discriminate b/t pathogen and non-pathogen structures and minute differences in molec. structures
HIV/AIDS most common opportunistic pathogen
Pneumoncystic carinii
Pneumonia responsible for most deaths
Strict aseptic technique
Innate immunity response time
Fast (mins-hrs)
Adaptive immunity key components**
Antibodies (antigens interact with lymphocytes to form antibodies)
Innate immunity specificity
Only specific for molecules and molecular patterns associated with general pathogens or foreign particles
Anaphylaxis treatment**
Standard
EARLY!!
Standard (non-life threatening):
- Epi - 100-500 mcg subq or IM, repeat q 10-15 min for adults, kids 10 mcg/kg q 15min x2 then q 4 hrs
- Benadryl - 1-2 mg/kg or 25-50 mg IV
- Corticosteroid - questionable
- H2 blocker - Pepcid
Adaptive immunity memory
Memory good- when used can lead to faster response to recurrent or subsequent infections
Innate immunity diversity and customization
Limited- receptors are standard and only recognize antigen patterns. No new receptors are made to adapt the immune response
HIV/AIDS common comorbidities
CV - abnormal EKG 50%
Pericardial effusions 25%
Wasting syndrome - malabsorption/metabolism changes, <10% wt loss, eval fluid status
Neurological - dementia, peripheral neuropathy, autonomic abnormalities
Hematologic - platelet stability and f(x) impairment, steroid therapy or splenectomy
Cancer - non-hodgkin lymphoma (space occupying lesions in CNS), Kaposi’s sarcoma (endothelial tissue)
Type 2 hypersensitivity**
Cytotoxic
(Autoimmune hemolytic anemia)
Antibodies specific to antigens attach to cell surface
Antibody mediated/ IgG
5-8 hrs
PCN/chronic urticaria/BLOOD TRANSFUSION/ autoimmune hemolytic anemia
HIV/AIDS assessment
Current physical exam
Labs
Xrays
Type 3 hypersensitivity**
Immune complex
Antibodies bind antigens and release enzymes that cause tissue damage
IgG/ immune complex mediated
2-8 hrs
Serum sickness/arthus/glomerulonephritis/RA/systemic lupus/erythematosus
High risk latex allergy people**
Healthcare workers Neural tube defects Multiple surgeries Spina Bifida GU tract defects
Innate immunity memory
None
HIV/Aids anesthetic concern
Non-nucleoside reverse transcriptase inhibitors (NNTIs)
Induce CYP450
Adaptive immunity self-vs-nonself discrimination
Worse than innate system
But still pretty good
When it has problems causes autoimmune disease
Allergic Tendency people**
Genetic
Large IgE quantity
Innate immunity major cell types
Natural killer cells, neutrophils, macrophages, basophils, eosinophils, dendritic cells
Anaphylaxis vs. Anaphylactoid**
Anaphylaxis= IgE mediated
(Requires prior exposure)
Anaphylactoid= NOT IgE mediated (May occur with 1st exposure)
nearly identical
HIV/AIDS = ____ branch
Retrovirus invades cell-mediated branch of immune system
SLE treatment
Corticosteroids
Antimalarial
Immunosuppressants
What to do after HIV exposure
Wash and clean area
Immediate baseline test you & pt
Empirical treat with 2 or more antiretrovirals (w/in 1-2 hrs/1-2 weeks)
Periodic testing for 6 months
Anaphylaxis secondary treatment**
1-7
- Antihistamines (.5-1 mg/kg Benadryl)
- Catecholamines
- Bronchodilators
- Corticosteroids
- NaBicarb
- Eval airway before extubation
- Vasopressin for refractory shock
Antigen activity w/in adaptive immunity**
B lymphocytes have millions of distinctive antigen-specific receptors inherent to organism’s DNA
T lymphocytes can only recognize antigens bound to receptor molecules MHC1 and MHC2
Natural killer cells**
No specific tumor cell and antibody-dependent cytotoxicity
Adaptive immunity major cell types**
T cells (cell mediated) B cells (humoral) And other antigen-presenting cells
Neutrophils**
Phagocytosis, cytokine release, secretion of hydrolytic enzymes, secretion of reactive oxygen species
Effector cell-migrates to inflammation areas
Granulocyte (most numerous WBC)
6 hr 1/2 life, 1st on scene in inflamm. rxn.
Fight bacteria/fungus
Contain acid hydrolases, neutral proteases, and lysosomes. After activation produce hydroxyl radicals, superoxide, and hydrogen peroxide
RhoGAM**
To Rh NEG mom to prevent immune sxs from developing antibodies fetal Rh antigen
-after exposed once mom develops Rh antibodies (next child would cause reaction)
Innate immunity key components
Antimicrobial peptides and proteins (such as toxic granules)
Anaphylaxis initial therapy**
(1-5)
- Stop drug
- Maintain airway/ 100% FiO2
- D/C anesthetic agents
- Fluids (2-4 L crystalloid / colloid)
- Epi (5-10 mcg IV)
HIV occupational exposure** Most common needle type \_\_\_ Risk after percutaneous exposure \_\_\_ Risk after mucous membrane exposure \_\_\_ Non intact skin to infected fluid other than blood \_\_\_
Open bore most common
Perc exposure O.3%
Muc meme exposure 0.09%
Non-intact skin & not blood 0%
Macrophages**
Process/present antigens to effect inflamm., tumoricidal, and microbicidal functions
Arise from ciculating monocytes-may be confined so specific organ
Recruited/activated in response to microorg. or tissue inj.
Ingest antigens before they interact with lymphocyte receptors
HIV/AIDS two major concerns
Infection of patient
Infection of staff
-look at regional or laparoscopic options
Polymorphonuclear cells**
Ingestion or phagocytosis; killing of microorganisms; facilitation is bodily clearance of dead cells
Plasma cells**
Active in protein synthesis for formation of immunoglobulins
Platelets**
Facilitation of coagulation, influence tissue reactivity to injury
SLE presentation
Polyarthritis and dermatitis
Malar rash in 1/3 pts
Renal disease in <50% (most common cause of death, 10-20% require dialysis)
HIV/AIDS Prevent exposure
Ensure everyone is aware Highest risk with open bore needles DO NOT RECAP PPE (mask/eye ware/gloves/gowns) Hand washing Clean machines regularly
B lymphocytes**
Humoral immunity
Transformation into plasma cells which react to foreign substances by producing antibodies and immunoglobulins, active in circulatory system, cytokine release
Agranulocyte
Produces antibodies!!!
Basophils and mast cells**
Sources of histamine and heparin, which combat insult by increasing vasc. permeability/ smooth musc. contractility (bronchospasm)/ and inflamm responses
Granulocyte (least common type)
Hypersensitivity rxns
Release histamine/leukotrienes/cytokines/prostaglandins
IgE receptors on surface
Increase if given blood causing immune resp.
Active immunity diversity and customization
Very diverse!
Customized by genetic recombination do epitomes and antigenic determinants
Active vs passive immunity
?both types of adaptive/acquired?
Active= given pathogen (vaccines)
Passive=given antibodies from someone immune (Immediate but short effect)(fetus, IgA breast milk, RhoGAM)
What are antibodies?
Immunoglobulins
Each specific for particular antigen
Protect by direct attack or activation of complement system
Histidine action
Stimulates gastric secretion (H2) Contracts smooth muscle (other than blood vessels) Cardiac stim (H2) Vasodilation (H1) Inc vasc perm (H1)
High risk for autoimmune**
Female African Americans Native American Hispanics Child bearing years Working age
T lymphocytes**
Recognize/react to foreign material inside fixed tissues and to harmful organisms like neoplasticism and TB cells
Impt. in transplant rejection
Cytokine release
Agranulocyte
Cell-mediated immunity
Does NOT produce antibodies!!!!
Rank Drug reaction culprits**
- Muscle relaxants (60%)
- Roc
- females more
- Latex (15%)
- ABX (5-10%)
{“4” Hypnotics}
- Opioids (<5%)
{“5” colloids}
SLE Anesthesia concerns
Prone to PE/pneumonitis/alveolar hemorrhage/pulm HTN
1/3 pts cricoarytenoid arthritis & RLN palsy
May require corticosteroids
Cyclophosphamide (inhibits plasma cholinesterase, :. Impacts ester LA & succs)
Eosinophils**
Phagocytosis, combating parasitic diseases; defense in allergic response
Effector cell-migrates to inflammation areas
Granulocyte Heavy in GI, resp, and urinary mucosa Can cause esophagitis ?f(x) Collect at site of parasite infect., tumors, and allergic rxns
Type 1 hypersensitivity rxn**
Anaphylaxis
(Allergic/atopic)
IgE Mediated
20-30 mins
Mast cell activation
Anaphylaxis treatment**
Life threatening/Anaphylaxis
- Airway maintenance
- 100% O2
- Epi IV (50-100 mcg or more, repeat prn) - restores normal cap perm/relaxes smooth musc
- CPR, pressors, fluids
- bronchodilators
- H1 & H2 blockers
- corticosteroid
Adaptive immunity response time
Slow (days)
Systemic Lupus Erythmatous (SLE)**
type of disease and what it produces
Chronic inflammatory disease
Production of antinuclear antibodies
