Immune Dysfunction Flashcards
Types of immunity (2)
Innate immunity
adaptive (acquired) immunity
What is the function of the immune system?
Functions to protect the host against micro-organisms
Innate immunity characteristics (4)
Rapid, non-specific
Recognizes common pathogens
Requires no prior exposure
No long-lasting immunity; Has no memory but response always identical
What makes up innate immunity (non-cellular) (4)
Is made up from Non-cellular elements
Epithelial and
mucous membranes
Complement
Acute phase proteins
What makes up innate immunity (cellular) (4)
Cellular elements;
-Neutrophils; Fastest response; respond first
-Macrophages; Slower but sustained response
-Monocytes
-NK (natural killer) cells
Characteristics of Complement
Complements the role of other immune cells; Both innate and adaptive
Augments phagocytes and antibodies
Marks/tags pathogens for permanent destruction
Over 30 plasma and cell surface proteins that are involved in the complement system
Where are complement elements produced?
Most elements produced in liver
Consider liver failure/ ESLD = less good protective/ complement system
How are the complement cells/elements activated
C1 or alternately C3
Most numerous of WBC’s
neurtrophils
Neutrophils migrate ____ in ____ infections and release _______ that then ______ after that they become ______
Migrate rapidly in bacterial infections that Release cytokines->phagocytize
After they phagocytize/ release cytokines they Become purulent exudate
Neutrophils 1/2 life
6hrs
What are neutrophils sensitive to?
Sensitive to acid environments of infection
largest blood cells
Monocytes
Monocytes circulate to _____ then turn into ______
Circulate to tissue specific areas then turn into macrophages when in the specific areas
Macrophages on the epidermis turn to
Langerhans
Macrophages on the liver turn into
Kupffer cells
Macrophages to the lung become
Alveolar cells
Macrophages to the CNS become
Microglia
Monocytes characteristics (4)
-Mobilize just after neutrophils
-Phagocytic destruction
-Produce NO (VD) and cytokines
-Persist at sites of chronic infection (keep working for longer)
Least common blood granulocytes
Basophils
Where to mast cells reside?
Reside in connective tissue close to blood vessels
Basophils and mast cells characteristics (4)
Express high affinity receptors for IgE
Initiators of hypersensitivity
Stimulate smooth muscle contraction
Play major role in allergies, asthma, eczema
Basophils and mast cells release…..(4)
Histamine, leukotrienes, cytokines, prostaglandins
What cells are Heavily concentrated in GI mucosa
eosinophils
Characteristics of eosinophils (2)
Protect against parasites
Degrade mast cell inflammation
Adaptive immunity Characteristics (4)
-Present only in vertebrates
-Delayed onset of activation
-Capable of memory and specific antigen response
-Derived from hematopoietic stem cells (lymphoid precursor)
Adaptive immunity humoral component
B cells
B cells produce______ that bind to ___,____,____
Produce antibodies (IGE, IGA, IGM) that bind to foreign proteins of bacteria, viruses, and tumors
Adaptive immunity Cellular component
T cells
Types of T cells
helper and cytotoxic
T cells originate in the ____ and mature in the _____
Originate in bone marrow
Mature in thymus (thymectomy = increase risk of infection)
What to T cells characteristics (4)
Produce interferon, interleukin
Role in chronic inflammation
Respond to infection
Activate IgE
Active immunity
Pathogen deliberately administered then you expect antibodies to be created
Repeat exposure if see virus/bacteria again -> quicker response
Lasts for months to years
Vaccines
Live, inactivated, recombinant
Passive immunity
Receive antibodies from another individual (not making them)
Protection lasts few weeks to months
Maternal IgA antibodies via breast milk is what type of immunity
passive
Neutropenia is what type of immune response
Inadequate immune response
Asthma or eczema is what type of immune response
Excessive (or exaggerated)
Autoimmune disorders is what kind of immune response
Misdirection
what is hypersensitivity
Reaction to a foreign antigen
What does hypersensitivity cause
Causes altered T-cell and antibody response (IGE = long memory/response)
Response varies from uncomfortable to fatal
What does hypersensitivity require
Requires prior sensitization;
Grass, latex, gluten, nuts, medications
Most common hypersensitivity
Most common: drugs
NSAIDS, antibiotics, PPI’s, NMBD
Type I allergic response
immediate hypersensitivity
T cells stimulate B cells
IgE antibodies already produced (the memory exists)
On second exposure
Antigen releases calcium
Release of histamine, heparin, inflammatory mediators
Histamine triggers causes….
bronchoconstriction, vascular permeability, vasodilation, gastric acid
anaphylaxis, asthma, angioedema, conjuctivitis, dermatitis are examples of…….
Type I allergic response/immedate hypersensitivity
Treatment of Type I responses
Prevent histamine effects:
Antihistamines
Cromolyn sodium (helps with bronchconstriction)
Bronchodilators
COX pathway inhibitors
Diagnostic tests (dx what they are allergic to)
Small doses of allergen to desensitize
Type II allergic response
cytotoxic hypersensitivity
IgG, IgM, and complement mediated
Activattion of B cells to produce antibodies
Reaction time for type 2 allergic response/ cytotoxic hypersensitivity
minutes - hrs
hemolytic anemia, myasthenia gravis, transfusion reactions are examples of _____
Type II allergic response
Treatment for cytotoxic hypersensitivity
Anti-inflammatories
Immunosuppressives
Type III allergic response
immune complex hypersensitivity
Failure of the immune system to eliminate antibody-antigen complex -> keep depositing the antigens/ antibodies and elements and are deposited in the
Joints, kidneys, skin, eyes
Also mediated by IgG and IgM
Type III allergic response response time
Take hours-weeks to develop
systemic lupus erythematosus (SLE), rheumatoid arthritis are examples of what type of response???
Type III allergic response
Treatment for Type III allergic response
Anti-inflammatories
Maybe immunosuppressives
Type IV allergic response
T lymphocyte, monocyte/macrophage mediated and Does not involve antibodies
contact dermatitis, tuberculosis, Stevens-Johnson syndrome are what type of reaction
Type IV allergic response
Cutaneous symptoms are most common in what reaction?
Type IV allergic response
Treatment for Type IV allergic response
Anti-inflammatories
immuosuppressives
Anaphylaxis prevalence
1 in 5000 to 1 in 20,000 anesthetics
Symptoms of anaphylaxis (5)
Systemic vasodilation
Hypotension
Extravasation of protein and fluid
Bronchospasm
Untreated…PEA
Anaphylaxis reaction time
Usually occurs within 5-10 minutes of exposure
Anaphylaxis pathophysiology
Previous exposure creates IgE antibodies from -> Subsequent exposure to antigen->Antigen-antibody reaction->Mast cells and basophils degranulate->Release histamine, leukotrienes, prostaglandins, eosinophil/neutrophil chemotactic factor, platelet-activating factor->Symptoms of anaphylaxis->Up to 50% of intravascular fluid extravasates -> Lifetime prevalence 5%
“Biphasic” anaphylaxis occurs in____
Occurs in 4-5% of patients
“Biphasic” anaphylaxis
Secondary anaphylactic episode that Occurs following an asymptomatic period without second exposure
“Biphasic” anaphylaxis time to response
Occurs 8-72 hours later
Risk factors for “Biphasic” anaphylaxis (2)
Severe initial response
Initial response required multi doses of epi
Risk factors for perioperative anaphylaxis (5)
Asthma
Longer duration of anesthesia
Females (not in teen yrs)
Multiple past surgeries
Presence of other allergic conditions
Diagnosis of anaphylaxis can be compromised because of …..(2)
Communication issues
Covered by surgical drapes
What kind of test can verify mast cell activation and release
Plasma tryptase concentration
1-2 hrs
To see Baseline within 60 minutes of treatment you should run what kind of test to diagnose anaphylaxis
Plasma histamine concentration
Skin testing time and response
6 weeks after reaction
Wheal and flare response
Primary treatment for anaphylaxis
Stop administration of drugs, blood, colloids
100% oxygen
Epinephrine
fluid therapy
Epinephrine dose for anaphylaxis adults and children
10mcg-1mg IVP; repeat q 1-2 minutes (adults)
1-10mcg/kg IVP; repeat q 1-2 minutes (child)
In resistant to epi anaphylaxis use…..
Resistant to epi use; vasopressin, methylene blue and they
Inhibits NO production
Fluid therapy for anaphylaxis
Crystalloid: NS 10-25 ml/kg over 20 minutes; repeat prn
Colloid: 10ml/kg over 20 minutes; repeat prn
How does Epinephrine work against anaphylaxis
Decreases degranulation of mast cells and basophils ↓ effect of degranulation (vasodilation)
Alpha1: supports BP
Beta 1: inotropic and chronotropic effects
Beta 2: bronchodilation
Secondary treatment for anaphylaxis (4)
Bronchodilators
Antihistamines
Corticosteroids
Observe for relapse
allergy
Antihistamine meds/ dose for anaphylaxis
H1: diphenhydramine 0.5-1mg/kg IV
H2: ranitidine 50mg IV
Corticosteroids meds/ dose for anaphylaxis children and adults
Hydrocortisone 250 mg IV or methylprednisolone 80 mg IV (adults)
Hydrocortisone 50-100 mg IV or methylprednisolone 2 mg/kg IV (child)
Transfusion reactions characteristics
Response to surface antigen on donor RBC
A, B, AB and O and Rh antigens
Transplant rejection
Response to antigens on donor organ
Due to preexisting antibodies
Acute or chronic
Graves disease
Most common cause of hyperthyroidism
Caused by autoantibodies to the TSH receptor
Multiple sclerosis
Immune mediated inflammation
Destroys myelin and underlying nerve fibers
Rheumatoid arthritis
Abnormal production of pro inflammatory factors that are deposited on the skin and joints and eyes
Infection thought to play a role
SLE
Autoimmune, inflammatory
Antibodies against RBC, lymphocytes nucleic acids, platelets, coagulation proteins
Affects multiple organ systems
Angioedema is what type of reaction
Type 1 hypersensitivity response
What causes Hereditary angioedema
C1 esterase inhibitor deficiency/dysfunction. Causes of the deficiency/ dysfunction caused by
menses
trauma
infection
stress
oral-contraceptives
and excessive production of bradykinin
What does excessive production of bradykinin cause
Usually limited by C1 inhibiting kallikrein and factor XIIa
Laryngeal swelling, potent vasodilator
Not responsive to antihistamines
What is the relationship between ACE and bradykinin
ACE causes the breakdown of bradykinin….ACE inhibitors block that breakdown.
ACE inhibitors
Responsible for degradation of bradykinin
Affects vascular permeability; stimulates substance P
Vasodilation and fluid extravasation
Acquired angioedema presents with…….
Lip, tongue, face swelling
Urticaria and itching are absent!
treatment of angioedema (6)
Airway maintenance
(tracheal intubation
Tracheostomy)
FFP
C1 inhibitor concentrate
Epinephrine
Antihistamines
glucocorticoids
One of the most common forms of acquired immune deficiency
HIV/AIds
What does HIV/AIDS
The virus (HIV) thru reverse transcription makes a double helix DNA with all viral genetic material
Can change amino acid sequence; new version not recognized
Destroys monocytes, macrophages, Tcells
AIDS is final stage of infection caused by HIV
Seroconversion with HIV/Aids happens in what time frame?
2-3 weeks after inoculation
Symptoms of HIV/AIds
Flu like;
Fever
Fatigue
Night sweats
Pharyngitis
Myalgias
Arthralgias
How is HIV converted to aids
Higher basal levels of virus…..more rapid conversion to AIDS
Initial symptoms of HIV conversion to aids….
Weight loss
Failure to thrive
Diagnosis of AIDs (4)
-ELISA: 4-8 weeks after infection
-Viral load
-CD4/helper T lymphocytes <200,000
-HAART agent sensitivity
What skin concerns do we have with HIV/Aids pts
Fat pad redistribution
make sure they are padded
HIV/AIDs pts metabolism consideration
Inhibition of cytochrome P-450 (prolonged effect)
Hormone synthesis
Cholesterol synthesis
Vit D metabolism
Drug metabolism
Bilirubin metabolism
Scleroderma other name and is characterized by …..
“systemic sclerosis”
Inflammation
Vascular sclerosis
Fibrosis of skin and viscera
Scleroderma Risk factors
Onset 20-40, mostly women, no cure
S/s of scleroderma
Localized, limited, diffuse
Decreasing mobility of fingers
Facial pain
Raynaud’s
*Hypo-motility of GI tract
*LES tone decreased
Cardiac dysrhythmias/conduction abnormalities
*Pulmonary fibrosis
*Renal artery stenosis
Preoperative labs for Scleroderma pts (4)
ECG
BUN/Creatinine
CBC/Platelets
CXR/PFT’s
Anesthesia implications of scleroderma
Organ system dysfunction
Arterial catheter concerns
Continue preop calcium channel blockers
Contracted intravascular volume
Aspiration risk (RSI)
Limited neck mobility/Pulmonary compliance
Inhalation agents effect on the immune system
Suppress NK cells, induce apoptosis of Tcells
Impair phagocytes
Unclear impact on tumor cells
(Sevo stimulates renal cell (bad); inhibits non-small cell (good))
Induction meds on the immune system
Midazolam decreases migration of neutrophils
Ketamine depresses NK cell activity
Propofol decreases cytokines, PROMOTES NK cells
Opioids effect on the immune system
Suppress NK cells (especially morphine and fentanyl)
NSAIDs affect on the Immune system
Beneficial; inhibit prostaglandin synthesis
