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102 Cards in this Set
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examples of type II autoimmune diseases
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autoimmune hemolytic anemia
autoimmune thrombocytopenia purpura goodpasture's syndrome pemphigus vulgaris acute rheumatic fever graves disease myasthenia gravis insulin-resistance diabetes (type II) hypoglycemia |
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examples of type III autoimmune diseases
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subacute bacterial endocarditis (glomerulonephritis)
mixed essential cryoglobulinemia (systemic vasculitis) SLE (glomerulonephritis, vasculitis, arthritis) |
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examples of type IV autoimmune diseases
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insulin-dependent DM (beta cell destruction)
rheumatoid arthritis (joint inflammation and destruction) MS (brain degeneration, paralysis) celiac disease (gluten issues - malabsorption of nutrients ; atrophy of intestinal villi) |
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least likely to be autoimmune?
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type I
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ANCA (anti-neutrophil cytoplasmic antigen)
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Wegener's granulomatosis
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tests of inflammatory response and phagocytic cell function
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GROUP: - NON-SPECIFIC (PRIMARY) IMMUNE RESPONSE
WBC count and differential Sedimentation rate C-reactive protein Complement activity Rebuck skin window technique Quantitative or histochemical NBT test Chemilunimescence Chemotactic assay Phagocytic index Bacterial activity Phagocytic cell adherence Measurement of specific WBC enzymes |
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SPECIFIC (SECONDARY) IMMUNE REPSONSE
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Enumeration of B Lymphocytes
(EA and EAC rosette, SMIg, monoclonal antibodies) Enumeration of T Lymphocytes and subtests (E rosettes, monoclonal antibodies) Tests of Humoral (Antibody) Function Quantitation of immunoglobulins and IgG subclasses Specific antibody responses: prior sensitization, isohemagglutinins (IgM), DPT, poliovirus, or measles (IgG) Shick and dick tests (IgG) Specific antibody responses: de novo sensitization, Salmonella O (IgM); H (IgG) Tests of Cell-Mediated (Delayed Hypersensitivity) Function In vivo Skin test (prior sensitization), Candida, Trichophyton Skin tests (de novo sensitization), DNGB In vitro Lymphocyte stimulation: nonspecific (PHA); specific (antigen) Measurement of effector molecules (MIF) Mixed lymphocyte culture (MLC) Natural killer (NK) cell activity Antibody-dependent cellular cytotoxicity (ADCC or killer (K) cell activity Lymph Node Biopsy |
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Enumeration of B Lymphocytes
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(EA and EAC rosette, SMIg, monoclonal antibodies)
specific (secondary) immune response) |
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Enumeration of T Lymphocytes and subtests
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(E rosettes, monoclonal antibodies)
(specific (secondary) immune response) |
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Tests of Humoral (Antibody) Function
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Quantitation of immunoglobulins and IgG subclasses
Specific antibody responses: prior sensitization, isohemagglutinins (IgM), DPT, poliovirus, or measles (IgG) Shick and dick tests (IgG) Specific antibody responses: de novo sensitization, Salmonella O (IgM); H (IgG) specific sec, immune response |
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Tests of Cell-Mediated (Delayed Hypersensitivity) Function
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In vivo
Skin test (prior sensitization), Candida, Trichophyton Skin tests (de novo sensitization), DNGB In vitro Lymphocyte stimulation: nonspecific (PHA); specific (antigen) Measurement of effector molecules (MIF) Mixed lymphocyte culture (MLC) Natural killer (NK) cell activity Antibody-dependent cellular cytotoxicity (ADCC or killer (K) cell activity specific (secondary) immune response |
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Tissue-Damaging (Tertiary) Immune Response
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Tests of Reagin (IgE)Hypersensitivity
Direct measurement of total IgE globulins (PRIST) IgE specific antibody (RAST) Immediate-hypersensitivity skin tests Histamine release Tests of Cytotoxic Injury Red cell agglutinins Antiglobulin test (COOMBS) Tests of Ag-Ab Complex Injury Rheumatic factor (RF) Antinuclear factor (ANF) Serum complement C1q, C3, C5) Tissue biopsy (localization of IgG and C components by immunofluorescence) Tests of Injury Due to Delayed Hypersensitivity Tissue biopsy, infiltration of lymphocytes in areas of injury Skin tests (patch) in contact hypersensitivity |
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Tests of Reagin (IgE)Hypersensitivity
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Tissue-Damaging (Tertiary) Immune Response
Direct measurement of total IgE globulins (PRIST) IgE specific antibody (RAST) Immediate-hypersensitivity skin tests Histamine release |
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Tests of Cytotoxic Injury
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Tissue-Damaging (Tertiary) Immune Response
Red cell agglutinins Antiglobulin test (COOMBS |
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Tests of Ag-Ab Complex Inj
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Tissue-Damaging (Tertiary) Immune Response
Rheumatic factor (RF) Antinuclear factor (ANF) Serum complement C1q, C3, C5) Tissue biopsy (localization of IgG and C components by immunofluorescence) |
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Tests of Injury Due to Delayed Hypersensitivity
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Tissue-Damaging (Tertiary) Immune Response
Tissue biopsy, infiltration of lymphocytes in areas of injury Skin tests (patch) in contact hypersensitivity |
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Complement ACTIVITY is a ____ , BUT serum complement (C1q, C3, C5) is a _____
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non-specific (primary) test
TERTIARY test. |
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Ordinary blood count is also a
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non-specific test of immune function.
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NBT test is
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another non-specific test of immune system.
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Lymphocyte count is ___ ), but **WBC count is ____
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Lymphocyte count is secondary (specific), but **WBC count is primary (non-specific).
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total lymphocyte count for:
newborn |
For a newborn, 3500-9000.
At 6 mos, 6500-12,000. A 1 yr old, 3000-7000 A 4 yr old, 2000-4000. |
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total lymphocyte count for:
at 6 mos |
For a newborn, 3500-9000.
At 6 mos, 6500-12,000. A 1 yr old, 3000-7000 A 4 yr old, 2000-4000. |
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total lymphocyte count for:
at 1 yr |
For a newborn, 3500-9000.
At 6 mos, 6500-12,000. A 1 yr old, 3000-7000 A 4 yr old, 2000-4000. |
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total lymphocyte count for:
at 4 yr |
For a newborn, 3500-9000.
At 6 mos, 6500-12,000. A 1 yr old, 3000-7000 A 4 yr old, 2000-4000. |
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E-rosette will count ___ (E-A or E-AC will count B cells). Secondary response test.
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T cells
secondary response test |
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Best way to test integrity of the humoral arm is thru
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immunoelectrophoresis. Tests FUNCTION of humoral arm (also secondary response).
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Tuberculin reaction mediated by
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TH1 cells (CD4)
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Type IV reaction
Can do biopsy to see LOTS of mononuclear cells in Type IV rxn (a test of what?). Would assess what? integrity/FUNCTION of cell-mediated arm. |
(a secondary test of immune function
ntegrity/FUNCTION of cell-mediated arm. |
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MIF (macrophage inhibitors test) of what type of function
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T - cell
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a mixed lymphocyte culture - shows fucntion of what?
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cell-mediated arm of immune system
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immature lymph node shows us what
what type of test? |
LN biopsy tells us about immune functioning (secondary test)
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a RIST test is what type of test?
it determines what? what type of rxn? |
Tertiary test of immune function (tissue-damaging). Determines IgE – high level causes tissue damage (RIST). Test of Type I rxn.
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a haemagglutination test is what type of rxn?
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Test for Type II rxn with hemagglutination (autohemolytic anemia or hemolytic dz of newborn)
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a fANA test for SLE is what type of rxn?
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type III
SLE – Type III reaction – test for Anti-nuclear factor (w/ fANA) |
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rheum factor is what type of test?
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(not shown - Rheum Factor test is also a tertiary response)
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Skin testing can be
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Skin testing can be Type III (Arthus), Type I (immediate), or Type IV (patch testing). – all TERTIARY tests.
Skin testing can also be used to assess T cell function (recall Ags), which is a SECONDARY test. |
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TB test is mediated by what
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TH1 (CD4) cells.
secondary test |
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patch test is type ..
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Patch Test – Type IV rxn w/ tissue damage
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which passive immunization use pooled human immune gamma globulin
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HepA/B, Measles, and Rabies (and Tetanus, kind of)
Others – gammaglobulin from animal (less safe; more likely to see rxn, because the source is “less” human, and thus more foreign). |
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active vs. passive
source ANTIBODY-MEDIATED IMMUNITY |
active - self
passive - some other human or lower animal |
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active vs. passive
effectiveness ANTIBODY-MEDIATED IMMUNITY |
active - high
passive - moderate to low |
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active vs. passive
method ANTIBODY-MEDIATED IMMUNITY |
active -
1- disease itself, clinical or subclinical 2 - immunization (vaccines - killed or attentuated ; toxoids) passive - administration of antibody by -maternal transplacental transfer -injection |
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active vs. passive
time to develop ANTIBODY-MEDIATED IMMUNITY |
active - 5-14 days
passive - immediate on injection |
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active vs. passive
duration ANTIBODY-MEDIATED IMMUNITY |
active - relatively long (perhaps years)
passive - relatively short (days - weeks) |
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active vs. passive
ease of reactivation ANTIBODY-MEDIATED IMMUNITY |
active - easy by booster
passive - dangerous (possible anaphylaxis) |
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active vs passive
use ANTIBODY-MEDIATED IMMUNITY |
active - prophylactic
passive - prophylactic and therapeutic |
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why do shots have sequences / schedule?
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you wait for IgM to go up and then down
then you wait for IgG to go up and then down then you give booster shot! this way, you always keep a maximum resistance to disease |
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what is the only vaccine that we use that duplicates "real world"
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Poliovirus (Sabin) oral vaccine -- bc it mimics the natural portal of entry (GI TRACT)
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route vs natural portal of entry
vaccine route - IM natural portal - RESP TRACT |
rubeola, rubella, influenza
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route vs natural portal of entry
vaccine route - IM natural portal - skin |
rabies
yellow fever |
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route vs natural portal of entry
vaccine route - intradermal natural portal - resp tract |
small pox
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talk about poliovirus
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vaccine route for SABIN - oral just like real
vaccine for SALK - IM even tho natural portal is GI |
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what is the source of the MMR, polio and varicella vaccines
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attenuated
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what is the source of the tetanus vaccine
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toxoid
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what is the source of the meningitis vaccine
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purified capsule
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what is the source of the pertussis vaccine
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it comes from killed bacteria
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what is the source that leads to the max effect
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attenuated virus
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what is the source of the flu vaccine
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inactivated virus
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when do babies get hteir first shot
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at birth - hep B
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when do babies get DTaP
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2,4,6 mos; booster at 15 mos and 4-6 yrs, then every 10 after that.
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when do babies get MMR
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first given at 12 mos
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when do babies get varicella
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once, if 1 year old
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when is giving a live virus CONTRAINDICATED
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Do NOT give a live virus to a pregnant woman or an immunocompromised host (ex: cancer). Can develop a FULL-BLOWN case of the given dz.
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if you see 25-30% eosinophiles what is going on
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In an allergic dz, see LOTS of eosinophils (maybe ~10%). If see 25-30%, it is NOT an allergic rxn; it may be a parasite or malignancy.
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in a person with allergic conjunctivitis
what will you see in secretion? |
present would be eosinophils in secretion, pruritis, and conjunctival erythema.
Will NOT see vascularity of the cornea! |
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What is the best way to confirm allergic disease?
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Intradermal test
The best way to confirm an allergic dz. |
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when does immediate/late response to intradermal testing show up?
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Immediate response occurs within seconds.
Late phase (NOT delayed-type HS/type IV) rxn occurs several (~5-6) hours later; it is IgE mediated! |
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what is ample diagnostic test to determine food allergy
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history and PE!!
then selected skin tests tx is elim and food challenge DO NOT DO IgE and RAST - NOT NECESSARY |
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when testing someone for allergies what can they/ can't they take before hand
why? what blocks for primary and secondary immune response |
they CAN take corticosteroids
they CANNOT take antihistamines Histamine blocks PRIMARY response, but not the secondary. Corticosteroids blocks the SECONDARY response, but not the primary. Sodium cromoglycate blocks both (but not that effectively). |
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tree pollen - when do ppl react?
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MARCH to MAY/EARLY JUNE
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grass pollen - when do ppl react?
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MID-MAY to JULY
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ragweed - when do ppl react?
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MID-AUGUST to FIRST FROST (octoberish)
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dust mites - when do ppl react?
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Dust mite – perennial allergic rhinitis
People are allergic to eggs, droppings, and the mite itself. Present in carpets, pillows, mattress, etc. Lives off your dander (leading cause of dust allergy). |
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what looks like a snow shoe?
when are ppl allergic to it? |
Alternaria - all year round
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examples of distinctive aeroallergens
usually outside regional with flora usually seasonal usually difficult to avoid |
pollens, larger fungus spores
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examples of unrecognizable aeroallergens
usually in enclosed spaces determines by domestic practices often all year round often avoidable |
house dust, dander, minute fungus spores
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when do ppl get hay fever?
in spring - what causes in "early" - what causes in "late" - what causes |
spring - trees - march 10-15 - early june
early - grasses - may 1 to middle or end of july (english plantain, weed - mdmay to early or mid september) late - ragwee/march elder - aug 1 - oct 1 / first frost |
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what are important trees to think about with allergies in NYC
when? |
elm, oak, birch, cottonwod (march - may)
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what are important grasses in think about with allergies
when? |
june/kentucky blue, orchard, red top, tomothy, fescue, meadow (midmay - july)
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what are important weed to think about with allergies in NYC
when? |
ragweeds (SHORT) -- not so important are the cocklbur lambs quarter pigweed and english plaintain
radweed - mid augst to frost plantain - midmay to august |
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with pollen allergies, when are symptoms bad?
time of day? type of weather? |
time of day - morning and evening
SUNNY, WINDY DAYS |
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with mold allergies, when are symptoms bad?
time of day? type of weather? |
with molds just worry about weather - rainy misty days - bc they live up in the sky and come down with the rain
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how many ppl are affected by allergic rhinitis
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20-40 mil americans - older adolescents and young adults - 5th most COMMON CHRONIC ILLNESS
significant impact on quality of life, productiveity , healthcare costs prevalence is increasing |
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which IL's are involved in cell-mediated immunity
(humural?) how does a Th0 cell choose which way to go? |
cell: IL 12 --> 2
humeral: IL 4,5,13 With a naïve T-cell, an allergen uses IL-4 to stim TH-2 cell, which then uses IL-4,5, and 13 to stimulate humoral immunity. Meanwhile, a pathogen uses IL-12 to stim TH-1 cell, which then uses IL-2 and IFN-(gamma) to stim cell-mediated immunity. TH-0 cells have no markers. There is a balance between the two; more of one is less of the other. Patients with parasitic infections tend to have fewer allergies. |
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what type of rxn is allergic rhinitis?
when does congestion occur? |
A 2-Phase Reaction
Early manifestations include sneezing, itching, rhinorrhea, and congestion. Congestion may be present early, but MOST congestion occurs in the LATER stage (constant pounding of respiratory tract). |
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15 year old child
eye symptoms watery secretions positive skin tests lots of eosinophils antihistamines work well for him and so do steroids and immunotherapy - what is dx? |
SEASONAL ALLERGIC RHINITIS
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15 year old child
some eye symptoms mucoid secretions variable skin tests lots of eosinophils antihistamines work well for him and so do steroids and immunotherapy - what is dx? |
PERENNIAL ALLERGIC RHINITIS
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50 year old man
no eye symptoms mucoid secretions negative skin tests lots of eosinophils antihistamines work okay for him and steroids work great - what is dx? |
PERENNIAL NONALLERGIC RHINITIS
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50 year old man
no eye symptoms watery secretions negative skin tests few eosinophils antihistamines dont work at all for him and neither do steroids - what is dx? |
VASOMOTOR RHINITIS!
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how to differentiate differnt types of rhinitis?
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Keys are Response to Tx (esp. steroids) and Age of Onset
ADULT: Vasomotor usu due to non-specific agents, like smoke, odors, temperature, and humidity. Has POOR response to Tx, no polyps, few eosinophils, and watery secretions (while perennial non-allergic has good/fair response to Tx, polyps, lots of eosinophils, and mucoid secretions). CHILDHOOD: Seasonal vs. Perennial – Seasonal has WATERY secretions, frequent eye symptoms, and moderate congestion; perennial has MUCOID secretions, occasional eye symptoms, and marked congestion |
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talk about eosinophile counts with allergic rhinitis
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In an allergic dz, see LOTS of eosinophils (maybe ~10%). If see 25-30%, it is NOT an allergic rxn; it may be a parasite or malignancy.
A higher count (still NOT near 25%) would be present in allergic rhinitis combined with eczema and asthma. |
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differ the percutaneous test and the intradermal test
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Percutaneous/scratch/prick test – drop of allergen on skin, puncture the outer layers and get rxn. Allergen has a HIGHER concentration. More False Negatives, less False Positives
Intradermal – inject into skin (deeper layers); more false positives, less false negatives. |
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how to dx allergic rhinitis
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Symptoms of allergic rhinitis
Temporal pattern of symptoms (e.g. 3 weeks each fall) Spatial pattern of symptoms (e.g. worse when around animals) Personal/family history of atopic disease Allergic rhinitis Asthma Atopic dermatitis Food allergy |
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what is important to keep in differential with rhinitis
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NARES - *NARES – non allergic rhinitis with eosinophilia; unusual bc pts dev high eosinophil count in tissue, but it is NON-allergic. Most common type is coupled with asthma and Aspirin.
Indiv with Aspirin sensitivity and rhinits (and possibly asthma) is typical of NARES. Allergic : seasonal, perennial Infectious: viral, bacterial Nonallergic, noninfectious Vasomotor rhinitis Rhinitis medicamentosa NARES Hormonal rhinitis Gustatory rhinitis Atrophic rhinitis Anatomic rhinitis |
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antihistamines will releive ___ but do very little for ___
how to solve this problem? what is DOC |
Anti-histamines will relieve itching, sneezing, and runny nose, but do very little for congestion. Solve that problem by using decongestants w/ Antihistamines.
However, DOC is topical steroids and NOT oral steroids. |
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what adverse food rxns are due to...
test for food allergy with what? |
Most adverse food reactions (which can be any of Type I-IV) are due to intolerance, as opposed to “allergy”. HS rxn can involve ANY Ig.
Allergies can lead to anaphylaxis (which are much more serious), but their incidence is much lower. Test for food allergy with skin prick test. |
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examples of food intolerance
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“physiologic”
Toxicity (poisoning) Pharmacologic Metabolic Idiosyncratic |
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examples of food hypersensitivity
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(allergy) – “immunologic”
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food allergy is due to a...
(what are the main problem?) |
Allergy is due to a peptide, somewhere along the breakdown pathway, being presented to a TH2 cell. Allergen crosses the epithelium, binds IgE, releasing mediators, inc vascular permeability -> cramps/diarrhea, etc.
**Proteins are the main problem (as compared to carbs, etc.) |
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which foods are biggest "offenders"
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Only a FEW of the foods we eat are “offenders”.
For adults, “big four” – fish, shellfish, tree nuts, and peanuts (which are a bean/legume, NOT a nut) For kids, add egg, soy, milk, and wheat. These are the things drs take pts off of if suspecting a food allergy. Peanuts and shellfish are especially scary because they can cause life-threatening anaphylaxis. **Crazy rxn: oral allergy syndrome, due to X-reactivity between fruits/vegs and pollens. Ingestion of these fruits causes pruritis of the lips, tongue and palate w/o other signs of systemic rxn. Seen w/ apple/carrot and birch tree, melon/banana and ragweed, and **latex-fruit syndrome – latex, with avocado/banana/kiwi/papaya |
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when do most people "get" food allergies
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You do not grow out of allergy/atopy (that’s genetic), but you can grow out of symptoms.
The highest incidence of food allergy occurs before the age of 3-4. Pts will rarely have food allergies in teen years. Food allergy and atopic dermatitis work together, as do asthma and allergic rhinitis. |
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symptoms of reaginic - IgE and non-reaginic - non-IgE
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Reaginic (IgE) shows mostly dermatological manifestations (and anaphylaxis, vomiting, etc) – and is acute.
Non-reaginic (non-IgE) usually leads to enteropathies. Though urticaria may arise, it is FAR MC in reaginic types. reaginic - IgE Anaphylaxis Angioedema Rhinitis Abdominal pain Rash Asthma Vomiting Urticaria Diarrhea Allergic dermatitis Not Reaginic – non-IgE Enteropathies Urticaria Pneumonitis Vomiting Allergic dermatitis Hemosiderosis Asthma Diarrhea Occult bleeding Protein losing Malabsorption |
