Immune Flashcards
Active vs Passive Immunity
Definition and Examples
ACTIVE
-Pathogen deliberately admin
-Repeat exposure…quicker response
-Ex: Vaccines
PASSIVE
-Receive antibodies from another
-Protection lasts few weeks to months
- Ex: Maternal IgA antibodies via breast milk
Types of Cells
1.) Neutrophils
2.) Monocyptes/ Macrophages
3.) Basophils/Mast
4.) Eosinophils
Neutrophils
-#
-How it works?
-How long it lasts?
-Works in what environ?
-Most numerous of WBC’s
-Migrate rapidly in bacterial infections
-Release cytokines
–>phagocytize
–>Purulent exudate
½ life 6 hours
Sensitive to acid environments of infection
Monocytes and Macrophages
Size?
What tissues does it work on?
Skin, liver, lung, CNS
How does it work? (2)
Where does it usually work at?
Monocytes: largest blood cells
Circulate to tissue specific areas…macrophages
TO DIFFERENT LOCATIONS:
Langerhans (epidermis)
Kupffer (liver)
Alveolar cells (lung)
Microglia (CNS)
Mobilize just after neutrophils
-Phagocytic destruction
-Produce NO and cytokines
-NO DILATE = more BF for better response
-Persist at sites of chronic infection
Basophils and Mast
Common?
Where do they both reside in?
High affinity receptors for ___?
Functions? Releases (4)
Stimulates : ____
Plays major roles in: _____ (3 disease)
Basophils
=Least common blood granulocytes
Mast cells
–>Reside in connective tissue close to blood vessels
They BOTH:
-Express high affinity receptors for IgE
-Initiators of hypersensitivity
-Histamine, leukotrienes, cytokines, prostaglandins
-Stimulate smooth muscle contraction
-Play major role in allergies, asthma, eczema
Eosinophils
Heavily resides in _____
Helps protect against: _____
Function: _____
-Heavily concentrated in GI mucosa
-Protect against parasites (we get in GI)
-Degrade mast cell inflammation
Innate vs Adaptive Immunity
Type of memories?
Components?
Non-cellular elements
Type of cells? Humoral components of each?
INNATE:
Rapid, non-specific and no antibodiy
Requires no prior exposure
No memory/ No long-lasting immunity
• response always identical
Non-cellular elements
• Epithelial and mucous membranes
• Complement
• Acute phase proteins
• Neutrophils
• Macrophages
• Monocytes
ADAPTIVE
Present only in vertebrates
Delayed onset WITH memory and specific antigen response
Derived from hematopoietic stem cells
Humoral component
• B cells= antibodies
• T cells (helper and cytotoxic)
o –>Originate in bone marrow; Mature in thymus
• Produce interferon, interleukin
• Role in chronic inflammation
• Respond to infection
• Activate IgE
Type 1 Allergic Response
AKA:______
What cells stimulated: !!
Ig__?
Second exposure response, what happens?? Whats released? (4)
Examples: (5)
Treatments??
aka: “immediate hypersensitivity”
(ADAPTIVE IMMUNITY)
T cells stimulate B cells
IgE antibodies produced
IgE =IMMEDIATE
On second exposur:
-Antigen releases calcium
-Release of histamine,heparin, inflammatory mediators
**Histamine triggers:
Bronchoconstriction
vascular permeability,
Vasodilation
Gastric acid
Example:
Anaphylaxis, asthma, angioedema, conjuctivitis, dermatitis
Treatment Type I:
Prevent histamine effects:
Antihistamines
Cromolyn sodium
Bronchodilators
COX pathway inhibitors
Diagnostic tests
Small doses of allergen to desensitize
Type 1 Allergic Response Treatment
Types of meds?
Types of Test?
Prevent histamine effects:
-Antihistamines
-Cromolyn sodium
-Bronchodilators
-COX pathway inhibitors
-Diagnostic tests
-Small doses of allergen to desensitize
Type II Allergic Response (DELAYED)
AKA:
Ig__
Ig__
What type of cell activated? Antibodies or no?
Examples? (3)
Treatment? (2)
Aka: cytotoxic hypersensitivity
-IgG, IgM, and complement mediated
-Activate B cells to produce antibodies
Presentation and severity vary (DELAYED)
–>Reaction time: minutes-hours
Examples:
hemolytic anemia, myasthenia gravis, transfusion reactions
Treatment:
Anti-inflammatories
Immunosuppressives
Type 3 Allergic Response
AKA:
Works when:
Complexes deposits in:
(4)
Mediated by/ Immediate or Delayed?? How long does it take?
Ig__
Ig___
Examples: (2)
Treatment (2)
What class of meds?
Aka: immune complex hypersensitivity
-Failure of the immune system to eliminate antibody-antigen complex
Complexes deposited in
-Joints, kidneys, skin, eyes
Also mediated by IgG and IgM (DELAYED)
–>Take hours-weeks to develop
Examples:
* Systemic lupus erythematosus (SLE), rheumatoid arthritis
Treatment:
Anti-inflammatories
Maybe immunosuppressives
Type 4 Allergic Response
What types of cells mediated? (3)
Does it involve any anti-bodies?
What types of symptoms? Examples?? (3)
Treatment: (2)
What types of meds classes?
Mediated by:
-T lymphocyte
-Monocyte
-macrophage
Does NOT involve antibodies
Cutaneous symptoms most common
Examples:
* Contact dermatitis
* Tuberculosis
* Stevens-Johnson syndrome (ASA/Tylenol)
Treatment:
Anti-inflammatories
Immuosuppressives
Hypersensitivity:
What type of response?
Prior sensitization?
Examples?
Response to what common drugs? (3)
-Causes altered T-cell and antibody response
-Requires prior sensitization to foreign antigen
–>Grass, latex, gluten, nuts,
Most common: drugs
–>NSAIDS, antibiotics, PPI’s
Complements
Role of immune cells: innate vs adaptive
How many plasma and cell surface proteins? Most produced in the ____.
Activated by ____ or ____ pathways
Both innate and adaptive
-Augments phagocytes and antibodies
-Marks pathogens for permanent destruction
Over 30 plasma and cell surface proteins –>Most elements produced in LIVER
LIVER FAILURE = WORSE IMMUNE SYSTEM
Activated by C1 or alternately C3
Anaphylaxis
Occus within ____ mins of exposure
Symptoms?? <3 and resp?
Risk factors?? (4)
5-10 mins exposure
-Systemic vasodilation
-Hypotension
-Extravasation of protein& fluid
-Bronchospasm
-Untreated…PEA
- Longer duration of anesthesia
- Females (Not in teen years)
- Multiple past surgeries
- Presence of other allergic conditions (ex: Asthma, Type 2/3)
Bi phasic anaphylaxis?
occurs in % pt?
occurs in ___ hours later?
Risk factors (2):
“Biphasic” anaphylaxis
-Occurs in 4-5% of patients
Secondary anaphylactic episode
-Occurs following an asymptomatic period
Without second exposure
Occurs 8-72 hours later
Risk factors
-Severe initial response
-Initial response required multi doses of epi
Diagnosis of Anaphylaxis:
Plasma tryptase concentration
-Within__ hrs
-To check for what?
Plasma histamine concentration
-to get a baseline within ___ mins?
-What kind of testing?
-How long to test after rx?
¢ Compromised by
Communication issues
Covered by surgical drapes
Plasma tryptase concentration
-1-2 hours
-Verifies mast cell activation & release
Plasma histamine concentration
-Baseline within 60 minutes of treatment
Skin testing
-6 weeks after reaction
-Wheal and flare response
Primary Treatment for anaphylaxis?
–> Epi doses for adult
–> Epi doses for peds?
–> Backup?
Fluid Therapy
Crystalloid dose:
Colloid dose:
Secondary Treatment for anaphylaxis? What types of meds?
Primary:
1.) STOP drugs, blood, colloids
2.) 100% O2
3.) Epi
Adult: 10mcg-1mg IVP q 1-2 mins
Peds: 1-10 mcg/kg IV q 1-2 mins
Vasopression/Methylene Blue
-use if resistent to epi
-Inhibits NO production
Fluid Therapy:
-Crystalloid dose: NS 10-25 ml/kg over 20 mins PRN
-Colloid dose: 10 ml/kg over 20 mins PRN
Secondary Treatment:
-Blood sample/ allergy testing
-Bronchodilators
-Antihistamines
-Corticosteroids
Secondary Treatment for anaphylasis:
Diphenhydramine dose:
Ranitidine dose:
ADULT
Hydrocortisone dose: ___ mg
OR
Methylpredinosolone dose: ____ mg
PEDS
Hydrocortisone dose: ___ mg
OR
Methylpredinosolone dose: ___ mg/kg
Diphenhydramine dose: 0.5-1 mg/kg IV
Ranitidine dose: 50 mgIV
ADULT
Hydrocortisone: 250 mg IV
OR
Methylpredinosolone:80 mg IV
PEDS
Hydrocortison: 50-100 mg IV
Methylpredinosolone: : 2 mg/kg IV
EPINEPHRINE
How does it work??
Alpha1:
Beta1:
Beta2:
-Decreases degranulation of mast cells and basophils
-↓ effect of degranulation….vasodilation
-Alpha1: supports BP
-Beta 1: inotropic and chronotropic effects
-Beta 2: bronchodilation
CAUSES IN ANGIOEDEMA
Hereditary Angio-edema
Deficient in: ______
Causes:
Excess in: _____ (causes?)
Symptoms??
Acquired Angio-edema
What meds cause?
Degradation of: ____
L> Symptoms
What if the patient is itching???
C1 esterase inhibitor deficiency/dysfunction
Menses (period)
oral-contraceptives
trauma
infection
stress
Excessive production of bradykinin
-Usually limited by C1 inhibiting kallikrein and factor XIIa
-Laryngeal swelling, potent vasodilator
-Not responsive to antihistamines
Involves legs, hands, face, upper respiratory tract
Acquired
–> ACE INHIBITORS (responsible for degradation of bradykinin
–> L> Lip, tongue, face swelling
**NO urticaria and itching –> Itching = anaphylactic
Treatment for Angio-edema (3)
TYPE ___ SENSITIVITY
Airway maintenance:
DRUGS?
Airway maintenance
-Tracheal intubation/Tracheostomy
Drugs
-FFP
-C1 inhibitor concentrate
-Epinephrine
-Antihistamines, glucocorticoids? (wont really work for angioedema)
Specific Immune Responses
Transfusion reactions Rx to:
Transplant rejection Rx to:
Graves disease causes:
Multiple sclerosis causes what:
(destroys ___)
Rheumatoid arthritis
(abnormal production of: )
SLE
Transfusion Rx:
-Response to surface antigen on donor RBC
A, B, and Rh
Transplant rejction:
-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 proinflammatory factors
-Infection thought to play a role
SLE
-Autoimmune, inflammatory
Antibodies against RBC, lymphocytes nucleic acids, platelets, coagulation proteins
Affects multiple organ systems
HIV
One of the most common forms of acquired immune deficiency
How does HIV work?
Destroys ____ (3) cells
How to diagnosis?
CD4/ helper T Lymphocytes: <_____
How long after infection?
-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
Diagnosis
-ELISA: 4-8 weeks after infection
-Viral load
-CD4/helper T lymphocytes <200,000
-HAART agent sensitivity
