Disease Exam 1: Immunopathology Flashcards

Terms Definitions
Innate immunity, aka ___ or ___ immunity, are defense mechanisms are present ___ infection and have ___ to recognize microbes and protect individuals against infection.
- natural or native- before- evolved
Acquired immunity aka ___ or ___ immunity are mechanisms that are stimulated by/adapt to ____ and are capable of___ ___ and __ ___ substances.
- microbes- recognizing microbial and non-microbial substances
Most common easily recongized form of innate immunity= skin, also mucosal membranes are innate immunity.
Acquired immunity is specific and is stimulated by some substance, like metal in jewelery or microbes
Innate (non-specific) immunity involves ___ ___ cells providing the first defense against pathogens. These cells include:
- antigen- independent- Phagocytic cells (neutrophils and macrophages are always present)- natural killer cells- epithelial barriers
what are the major leukocytes in blood?
LMNEB: - lymphocytes- monocytes- neutrophils- eusinophils- basophils
Innate immunity has no ____.
no memory
innate immunity anatomical barriers:
Skin (physical barrier)epidermis - thin outer layer containing tightly packed epidermal cells and keratin (water-proofing)Mucous membranes (ciliated epithelial cells); saliva, tears and mucous secretions - GI, urogenital, respiratory tracts
Innate immunity- physiological barriers:
- temperature: normal body temp inhibits growth of most organisms, fever can effect microorgansims- pH- low pH of skin, stomach, and vagina inhibits microbial growth
Toll like receptors are part of ___ immunity. They are ___ ___ located on ___ cells. TLRs recognize ____ ____ by their ___ ___ ___ ___.
- innate- membrane proteins- inflammatory cells (WBC)- non-self antigens- pathogen-associated molecular patterns (PAMPs)
what are the 2 important cellular reactions of innate immunity?
- inflammation- anti-viral defense
Inflammation, a cellular reaction involved with innate immunity, is the process in which ____leukocytes (____, ___) are recruited and activated to kill microbes.
- phagocytic leukocytes (neutrophils and macrophages)
monocytes that enter a tissue and mature are called ____.
The anti-viral defense, a cellular response of innate immunity, is mediated by ____ cells and ___ cells. The ___ cells are ___ and anti-viral ____ and they inhibit ___ __ and ____. The ___ cells provide early protection against viruses.
- dendritic cells and NK cells- dendritic cells are interferon and anti-viral cytokines> prevent infection and replication- NK cells> early protection against viruses
Acquired (Adaptive , Specific) immunity develops later, after exposure to microbes, and is even more powerful than innate immunity in combating infections. By convention, the term “immune response” refers to adaptive immunity.
Acquired specific immunity is ___ ___ and causes lymphocyte expansion. ___ __ produce antibodies for the humoral response. While __ __ are involved in the cell-mediated immune response.
- antigen dependent- B lymphocytes> antibodies, humoral- T cells> cell mediated response
Acquired immunity can be ___ or ___.
- active or passive
___ acquired immunity means you have your own antibodies, whether that be through exposure to the infectious agent or a vaccine.
___ acquired immunity means that you acquired ready-made antibodies from your mother or other sources.
If you get maternal antibodies, they will not be ___ b/c this one is too big to cross the placenta. If baby has this, it is its own.
CD4 cells are __ ___ cells.
T helper
CD8 cells are ____ ___ __ cells.
- cytotoxic/suppressor T cells
when T cells leave the thymus they become ___ or ___ cells.
CD4 or CD8
locations of CD4 cells:
- mature in thymus- located in peripheral blood, bone marrow, thymus, paracortex lymph node, and Peyer's patches
CD8 cells: Cytotoxic T-cells kill cells that are infected with viruses or bacteria; kill neoplastic and donor graft cells. They have CD8 receptors and are sometimes called T8 cells.
Helper T-cells interact with and promote formation of antibodies by B-cells. They are characterized by a surface receptor called CD4, and the cells are sometimes called T4 cells.
mature T cells are found in the ___, where they comprise __ to ___% of lymphocytes.
- blood- 60-70%
T-cell zones of peripheral lymphoid tissues include the ___ of a ___ __.
- paracortex of a lymph node (outside of the follicle)
Each T- cell recognizes a specific ____ __ ____ by means of a ___ ___ ____ ____.
- cell bound antigen- specific T-cell receptor
B cells mature in the __ ___. Mature B cells are located in the ___ ___ and ___ ___, ___ ___ of lymph nodes, and ___ ___.
- mature in bone marrow- found in peripheral blood, bone marrow, germinal follicle of lymph nodes, and Peyer's patches
B cells differentiate into ___ ___ that produce ____.
- plasma cells- immunoglobulins
B cells are responsible for the ___ response of acquired immunity in which they make ____.
- humoral - antibodies
___ synthesis by B cells begins at birth. Prsense of this at birth may indicate a congenital infection ( ____ ).
___ synthesis begins at 2 months of age. Presence of IgG at birth is from the mother.
Mature B cells constitute 10% to 20% of the circulating peripheral lymphocyte population and are also present in peripheral lymphoid tissues such as lymph nodes, spleen, and mucosa-associated lymphoid tissues.
B cells recognize antigens via ___ ___ receptor complex.
B-cell antigen receptor complex
role of CD4 helper T cells:
- activate macrophages- inflammation- stimulate B lymphocytes
Macrophages are present in ___ ___ and ___. They are involved in ____ and ___ ___ and also act as ___ ___ cells.
- connective tissue and organs (alveolar macrophages, and lymphoid sinuses)- phagocytosis- cytokine production- antigen presenting
in lymphoid germinal centers you have __ cells, in the lymphoid paracortex you have __ cells, in the lymphoid sinuses you have ____.
- B cells- T cells- macrophages
Dendritic cells mature in ___ ___ ___ ___. They are present in ___, ___ cells, and ___ ____. They act as ___ ___ ___.
- bone marrow stem cells- skin, Langerhan's cells, germinal follicles- antigen presenting cells
natural killer cells make up 10-15% of peripheral blood lymphocytes. They do not express __ or ___ ___ ___ ___. They are __ and ___. These cells can kill a variety of infected cells or tumor cells without ___ ___ to the microbe or tumor. Thus, they are an
- do not have T or B specific lymphocyte receptors- large and granular- without prior exposure- early line of defense
Macrophages are part of the ___ ___ ___, derived from blood ___ entering tissues.
- mononuclear phagocyte system - monocytes
Tissues of the immune system:
- regional lymph nodes- mucosal lymphoid tissue: Tonsils and adenoids, Waldeyer's ring, peyer's patches, and appendix- bone marrow- thymus- spleen (white pulp)-
cat scratch disease, you will usually see a swollen ___ lymph node, though the scratch will be distal to this.
major location of B cells:
- germinal follicles in lymph nodes= main B cell home
major location for T cells:
- paracortex aka parafollicular in lymph nodes- thymus
major location for histiocytes:
- sinuses in lymph nodes- skin (Langerhan cells)
Lymph nodes consist of an outermost ___ and an inner ___. The cortex is composed of an outer cortex of ___ ___ organized into ____ ____, and deep or ____ areas made up of mostly ___ ___ and ___ ___.
- outermost cortex- inner medulla- B cells organized into lymphoid follicles- parafollicular areas- T cells and dendritic cells
When an immune response is underway in a lymph node, some of the follicles contain central areas of intense __ __ proliferation called ___ ___ and are known as ___ ___ ___. The medulla consists of strings of ____ and antibody secreting ___ ___ known as th
- B cell proliferation- germinal centers- secondary lymphoid follicles- macrophages- plasma cells
With metastatic carcinoma, what part of lymph node to you look at to see if it has spread?
lymph node sinuses
Antibody(Ab) is a ____ produced in response to an antigen that is specific to the antigen and binds to it via __ ____ interactions. Antibodies are also known as ____. We will use the term ____ to talk about any antibody. And we will use the term antibody
- glycoprotein- non-covalent interactions- immunoglobulins- immunoglobulins
Some B lymphocytes terminally differentiate in to ___ cells, which are responsible for the ___ response to an antigen via ____ production. Other B cells do not differentiate and instead become ___ cells that are responsible for the ____ response to an ant
- plasma- primary- IgM antibody- memory- secondary- IgG, IgE, IgA
___ _ ___ are responsible for long term immunity.
Memory B cells
Antibodies are made of a protein molecule with 4 protein subunits. 2 subunits are identical and are larger and called the ___ ___. The other two __ chains are also identical to each other.
- heavy chains- light chains
2 roles of immunoglobulins:
- act as plasma membrane bound antigen receptors on the surface of a B cell- act as antibodies free in cellular fluids functioning to intercept and eliminate antigenic determinents
Immunoglobulins are made of 4 polypeptide chains: 2 light chains which are ___ or ____, and 2 heavy chains which are ___, ___, ___, ___, or __.
- kappa or lambda- alpha, delta, gamma, epsilon, mu
The type of heavy chain determines the immunoglobulin isotype : IgA, IgD, IgG, IgE, or IgM
___ is the first antibody developed by baby. It is used in primary responses. Is it transferred via placenta?
IgM- NOT transferred in placenta
IgG is involved in ___, it is ___ in the placenta. There are 4 subclasses: __, __, __, __.
- opsonization- transferred- IgG1, IgG2, IgG3, IgG4
IgE binds ___ ___ and is involved in ___ ___. It is also in __ like ___ __ and ___. It is NOT transferred via placenta.
- mast cells- allergic reactions- secretions- breast milk- saliva
IgA is found as dimer in secretions and does not cross placenta.
Human Leukocyte Antigen genes (HLA genes) for ___ ___ are unique to each individual and are located on the __ arm of chromosome __. HLA genes and their subtypes are transmitted to children from their parents. These HLA proteins make up the ___ ____ ____.
- HLA proteins- short arm of chromosome 6- Major Histocompatibility Complex.
what HLA protein is associated with increased risk for ankylosing spondylitis?
HLA-B27= ankylosing spondylitis
what HLA protein is associated with multiple sclerosis.
HLA-DR2= multiple sclerosis
what HLA proteins are associated with Diabetes mellitus type 1?
purposes of HLA testing;
- transplanatation workup- determining disease risk
HLA testing Transplantation workup Close matches of HLA-A, -B, and -D loci in both the donor and graft recipient increase the chance of graft survival.
Hypersensitivity diseases= immune mediated inflammatory diseases
Type I ___ Hypersenstivity reactions are depend on ___ for the activation of ___ cells.
- Type I Immediate- IgE- mast cells
Type II ___ ___ Hypersensitivity Reactions are dependent on ___.
- Type II Antibody Mediated- antibodies
Type III ___ ___ ___ Hypersensitivity Reactions result in ___ of ___ ___ complexes.
- Type III Immune Complex Mediated- deposition of antibody-antigen complexes
Type IV ___ ___ Mediated Hypersensitivity Reactions are ____ ___ and mediated by __ ___.
- Type IV T Cell Mediated- antibody-independent- T cells
During the Type I Immediate, Sensitization phase ___/___ cell activation by ___ ___ produces an ___ ___.
- mast/effector- IgE antibody- inflammatory reaction
Sensitization aka ___ ___ is ___ ___ production.
- first exposure- IgE antibody
Steps in sensitization. Allergens are first processed by ___ __ ___, which are ___ and ___ cells. Then the ___ ___ ___ interact with ___ ___ cells causing ___ to stimulate ___ ___ maturation. Then ___ causes plasma cells to switch from ___ to ___ synthesi
- antigen presenting cells, macrophages or dendritic cells- antigen presenting cells- CD4 helper cells- interleukins- B cell maturation- IL-4- IL-5
with sensitization/first exposure the allergen is processed by APCS (macrophages or dendritic cells)> APCs interact with CD4 helper cells> interleukins stimulate B cell maturation> IL-4 causes plasma cells to switch from IgM to IgE production> IL-5 stimu
what role do CD4 helper cells play in sensitization?
- interact with allergen bound APCs which causes interleukins to stimulate B cell maturation
what role does IL-4 play in sensitization?
- causese plasma cells to switch from IgM production to IgE production
what role does IL-5 play in sensitization?
- stimulates production and activation of eusinophils
With Type I Immediate Reexposure to antigen phase, there is already ____ __ ___ ___ on ___ cells. When this memory __ binds the specific allergen, the __ cell releases preformed ___, such as ___, ___ ___ for eusinophils ,and ___. This is an early phase re
- memory allergen-specific IgE- mast - IgE- mast- mediators- histamine- chemotactic factors- proteases- tissue swelling- bronchoconstriction
So Type I Immediate Sensitization is known as ___ ___ production, while Type I Reexposure is known as ___ __ ___.
- IgE antibody production- mast cell activation
Type I reexposure immediate response is initially characterized by ___, ___ __, and depending on location, ___ ___ spasm or glandular ____. These occur within _ to __ minutes of exposure to an allergen and subside within ___ minutes.
- vasodilation- vascular leakage- smooth muscle spasm- secretions- 5-30 minutes- 60 minutes
Antigen binding to IgE on mast cells leads to amplication of ___ production.
Mast cells are the tissue phase of ___. The granules in both of these cells are made of ___.
- basophils- histamine
In Type I Re-exposure late/prolonged phase reaction, ___ cells synthesize and release ___ and ___, which enhance and prolonge the ___ ___ reaction.
- mast- prostaglandins and leukotrienes- acute inflammatory reaction
___ and ___, parts of the complement system, are stimulated during allergic reactions.
C3a and C5a
With Type I Hypersensitivity reactions, it is convenient that ___ cells are bone-marrow derived cells that are found predominantly near ___ __, ___ , and ____sites, where local immediate hypersensitivity reactions tend to occur.
- mast- blood vessels - nerves- subepithelial sites
Mast cells have ____ membrane bound ___ that contain biologically active ___. Mast cells and basophils are activated by the cross-linking of high affinity ___ _ __ receptors, __, and ___ (anaphylatoxins). These act by binding their receptors on mast cell
- cytoplasmic - granules- mediators- IgE Fc- C5a - C3a
Mast cells may be triggered by other stimuli such as exercise, emotional stress, chemicals (photographic developing medium, calcium ionophores, codeine, anaphytoxins C4a, C3a, C5a. These reactions, mediated by agents without IgE-allergen interaction, are
Anaphylactic Hypersensitivity is a ___ __ ____. A biopsy of the reaction site would show mostly ___ and ___ cells. This reaction may effect ___, ___ ___, and the ____ tract.
- Type I Hypersensitivity- eusinophils and mast cells- nasopharynx (rhinorrhea, rhinitis)- bronchopulmonary tissues (asthma)- GI tract (gastroenteritis)
Allergic conjunctivitis is a ___ ___ ___ reaction. List the symptoms.
- Type I Hypersensitivity Reaction- red,itchy, watery eyes- sneezing, congestion, runny nose- itchy/sore throat, post-nasal drip, cough- itchy ears/buzzing sound
Urticaria is a ___ ___ ___ reaction referring to a group of disorders in which skin ____ occurs. The release of histamine and other chemicals causes increased vascular permeability and tissue edema. The weal's can be a few vary in size, white or red, oft
- Type I Hypyersensitivity- wealing
Attacks of eczema are associated with erythema, itchy dry papules, and pustules that lead to areas of inflamed and scratched skin ('excoriation') with crusting.  Eczema is divided into two main types…
1. Atopic Eczema2. Contact Dermatitis
Atopic eczema arises because of an ___ ___ which starts in infancy or childhood. Pts with this tend to have other allergies.This can worsen after eating certain foods or being exoposed to certain allergens. Atopic Dermatitis is a ___ __ ___ ___ hypersensi
- inherited tendency- Type I IgE mediated
Its not the first wasp sting that gives you trouble it’s the second one.
In wasp stings, most deaths occur within 1 hour, with most severe reactions occurring within 10 minutes of the wasp sting. The systemic reaction is more related to the pre-existing level of circulating IgE rather than to the number of wasp stings.
With many Type I Immediate Hypersensitivities, there will be a __ __ phase that sets in 2-24 hours after without additional exposure to the antigen. This may last several days. (allergic rhinitis and bronchial asthma). This late-phase reaction is characte
- second late phase- eusinophils, neutrophils, basophils, monocytes, CD4 cells- destruction
Skin scratch testing, puncture testing, and prick testing are used to assess presence of ___ ___ ___ ___. This more sensitive and specifice and less expensive than ___ ___. A series of tiny punctures/pricks made in the skin. Small amounts of suspected all
Blood allergy testing measures total ___ level- an estimate of IgE contained within patient's serum to a specific substance. A low total IgE is NOT adequate enough to rule out sensitization to commonly inhaled allergens.patients with a high total IgE have
blood allergy testing with a high IgE means:
- pt is more prone to allergy sensitization but more tests needed for specifics
Angioedema is an extreme allergic reaction caused by ____ ___ stimulating the release of ___ from __ cells, resulting in increased vascular permeability and swelling of face and larynx. Inspiratory stridor is a symptom of upper airway obstruction.
- anaphylatoxins directly- histamine- mast cells
There is a form of hereditary angioedema where pt has a __ deficiency in the ___ system.
- C2- complement
Hereditary angioedema is an ___ ___ disease characterized by a deficiency of ___ ____ ____. Thus the continuted activation of C1, results in a deficiency of ___ and ___ in the classic pathway and means that their are increased cleavage products, __ and __
- autosomal dominant- C1 esterase inhibitor- deficiency of C2 and C4- increase C2a and C4a- anaphylactic- no activation of C3
Allergic reaction can be provoked by skin contact with poison plants, chemicals and animal scratches, as well as by insect stings. Ingesting or inhaling substances like pollen, animal dander, molds and mildew, dust, nuts and shellfish, may also cause alle
Type II Antibody Dependent Cytotoxic Reactions are usually mediated by ___ or ___ antibody classes and in same but not all complement.____ may also play a role.
- IgM or IgG- phagocytes
How to test for a Type II Antibody Dependent reaction?
- detection of circulating antibody against the tissue invovled- and/or complement in the lesion biopsy by immunoflourescense
Type II Cytotoxic Antibody Dependent reactions may be ___ ___ or ____ ___.
- complement dependent- complement independent
Type II Antibody dependent Complement dependent reaction involve ___ like with ___ ___, ______ ____, and ___ ___ ___. They also can involve ____ like with ___ __ ____ ___ ___, and __ and ___ ___ ___ in newborns.
- lysis like with ABO mismatch, Goodpasture's syndrome, and hyperacute transplantation rejection- phagocytosis like with warm (IgG) autoimmune hemolytic anemia, and ABO and Rh hemolytic disease in new borns.
Type II Antibody Dependent Complement Independent reactions involves ___ (__,__) dependent cell mediated toxicity, ___ ___ destruction of neoplastic or virus infected cells, and helminth destruction of eusinophils. In these situations, antibodies are dir
- antibody (IgG, IgE)- natural killer- against cell surface receptors- Myasthenia Gravis- Grave's Disease
The complement system is a component of ___ immunity that consists of multiple ___ ___ which fight infection by ____ pathogens, inducing ____ ___, enhancing ___ ___, and ____ some pathogens directly.
- innate- plasma proteins- opsonization- inflammatory responses- antibody responses- attacking
Activation of the complement cascade relies on cleavage of a ___ to yield an active enzyme that in turn cleaves and activates the next enzyme.
opsonization enhances ____.
In Type II Antibody dependent Complement dependent reactions, cells tagged with the antigen-antibody complex can be removed by ___ or ___, both of which are mediated by the ____ ___. ____ by ___ enhances ____. The ___ ___ ___ made of C5b, C6, C7, C8, C9 c
- phagocytosis or lysis- complement system- Opsoninzation by C3b enhances phagocytosis- membrane attack complex causes lysis
For the complement system to be able to form the components for opsonization and the membrane attack complex, you must have ___ ____.
C3 convertasae
C5b initiates the construction of a ___ ___. Then the membrane attack complex forms and is devastating to the cell b/c it disrupts the ___ ____. Loss of ___ ___ and ____ ___ ultimately lead to ___ and ___ of the cell.
- membrane pore- disrupts the membrane integrity- loss of chemical gradient and selective permeability
With type II antibody dependent complement dependent reactions, lysis occurs b/c an antibody, either __ or __, directed against the antigen activates the ___ ___leading to lysis by the membrane attack complex. Phagocytosis occurs by the __ __ in the splee
- IgG or IgM- complement system- fixed macrophages in the spleen- IgG or C3b
Activation of the complement cascade relies on generation of a C3 convertase. Cleavage of C3 is the most important step in the activation pathway. Large numbers of opsonizing proteins, primarily C3b, are generated and coat pathogen surfaces to facilitate
Immune mediated hemolytic anemia is a type __ ___ __ __ ___ reaction with ___. It is more common in ___. 70% are __antibodies. ___ ___ ___ is most common cause of this condition. It can also be drug induced or caused by alloimmune (mismatch blood transfus
- type II antibody dependent complement dependent- phagoctyosis - women- IgG- Systemic lupus erythematous
immune mediated hemolytic anemia pathogenesis:
Pathogenesis IgG-mediated hemolysis RBCs coated by IgG are phagocytosed by splenic macrophagesComplement-mediated hemolysis RBCs coated by C3b alone are phagocytosed by liver macrophages (extravascular hemolysis). RBCs coated by C5-C9 undergo intravascular hemolysis. RBCs coated by IgG and C3b are phagocytosed by liver and splenic macrophages
Hemolytic Disease of the Newborn (HDN) is a type ___ __ __ ___ ___ reaction. It is caused by ____ passage of maternal ___ __, like ___ _ or ___ __ antibodies in a type O mother (just example). This causes ____hemolytic anemia in the fetus.
- type II antibody dependent complement dependent- transplacental- IgG antibodies- (anti-D, or anti-AB antibodies from a type O mom for example)- extravascular
Rh is aka as :
D antigen
Rh hemolytic disease of the newborn occurs if the mother is __/__ __ ___ and the fetus is __/__ __ ___. Then if mother is exposed to fetal ___ __ blood due to a fetomaternal bleed, the mother will develop _____ ___ . FIRST RH INCOMPATIBLE PREGNANCY DOES N
- Rh/D antigen negative- Rh/D antigen positive- Rh positive - anti-D-IgG antibodies
With Rh hemolytic disease of the newborn, if the second child is ___ __, this is the newborn that will have extravascular hemolytic anemia b/c the ______ ___ cross the placenta.
- Rh positive- anti-D-IgG antibodies
for the child that has hemolytic disease of the newborn, how does it manifest itself:
Fetal splenic macrophages phagocytose RBCs, causing severe anemia. Fetus may develop high-output cardiac failure leading to hydrops fetalis and death. Hydrops fetalis is a combined left- and right-sided heart failure with ascites and edema.
With Acute Hemolytic Transfusion reaction (HTR)there is ___ hemolysis, this is type II antibody dependent complement dependent reaction.
intravascularjaundice commonly occurs
Example-group B patient receives group A donor blood. Anti A-IgM attaches to A positive donor RBCs producing intravascular hemolysis.
Rh positive means you have the __ __ but do not have ____.
- have the D antigen - do not have antibodies
worst kind of acute hemolytic transfusion reaction?
- giving blood type AB or type A to a type O recipient
Tests used to evaluate type II hypersensitivity include the ___ __ and the ___ ___.
- direct coombs - indirect coombs
The Direct Coomb's test detects ___and/or___ ___ to ____.
The indirect Coomb's test detects ___ in the ___.
- antibodies in the serum
Direct coombs used to determine blood type. Antigen=blood type. AB blood type has AB antigens. Now if want to determine antigens on red blood cells, you put reagent with antiA and antiB and then mix it with cells> cells glutonated > add antiglobulin reage
Say I'm type A blood, and want to see test the antibodies in my serum. I would mix my serum with ___ ___ __ cells. This would be the ___ Coombs.
- artificial B blood (contain the B antigen)- Indirect
indirect coombs is used to detect ___ antibody meaning that person would by Rh ___.
With Type II Antibody Dependent Complement Independent reactions, either __ or ___ antibodies have tagged something they shouldn't have. Thus, leukocytes with recptors for __ or ___ __ but do not ___ cells coated with these antibodies. This does not requi
- IgG or IgE- IgG or IgE- lyse- do not phagocytose- does not require complement system
type II hypersensitivity reactions are involved in destruction of helminthes, virus infected cells, and neoplastic cells.
Examples of Type II Antibody Dependent Complement Independent Reactions:
- antibody (IgG or IgE) dependent cell-mediated cytotoxicity, natural killer cell destruction of neoplastic and virus infected cells, helminth destruction by eusinophils- antibodies directed against cell surface receptors : Myasthenia Gravis, Grave's Disease
With Myasthenia Gravis, there are ___ against ___ ____. This is a ___ __ ___ ___ reaction. These antibodies are made in the ___ so you will see __ ___ with ___ ___.
- autoantibodies- acetylcholine receptors- type II complement independent reaction- thymus- thymus hyperplasia- germinal follicles
With Myasthenia Gravis the autoantibodies destroy the acetylcholine receptors on the ___ ___ ___ of ___ and block binding of the neurotransmitter to its receptor, thus ___ ___ is blocked and ____ ___ results.
- motor end plates of muscle- muscle activation is blocked- muscle weakness
Graves' disease Most common cause of increased TSH synthesis (hyperthyroidism) and thyrotoxicosis (hormone excess regardless of cause) Female dominant autoimmune disease HLA-Dr3 association Thyroid-stimulating (IgG) antibodies against TSH receptor Cause
clinical findings in all causes of thyrotoxicosis (including Grave's disease):
- weight loss with good appetite- fine tremor in hands- heat intolerance- diarrhea- anxiety- lid stare- due to increased sympathetic stimulation of eyelid muscles
Type III immunocomplex reactions activate the ___ system by ___ ___ ___ ___.
- complement system- circulating antigen-antibody complexes
Type III immunocomplex reactions:
Arise with soluble antigen; pathology is caused by the deposition of antigen-antibody aggregates or immune complexes in tissue.Larger aggregates fix complement and are readily cleared from the circulation by the mononuclear phagocytic system. The small complexes that form at antigen excess, however, tend to deposit in blood vessel walls. There they can bind receptors on leukocytes, leading to leukocyte activation and tissue injury.
with type III reactions, larger aggregates get fixed by the complement system and are readily cleared by the ___ ____ system. But the small complexes form at antigen excess and tend to deposit in blood vessels and cause tissue damage by binding to and act
mononuclear phagocyte
With type III immunocomplex reactions, upon first expsure to the antigen, synthesis of ____ occurs.
With type III immunocomplex reactions, second exposure to the antigen causes ___ of the ___ ___ ___ and ____ ____, producing ___, which attracts ____ that damage the tissue.
- deposition of the antigen-antibody complexes- complement activation- C5A- neutrophils
Receptors for C3a and C5a are on the surface of ___ cells, ___ cells, and ____. Binding of the peptide ligands to the cells causes the ___ ___. ___ ___ and ___ ___ are increased and ___ __ are expressed to facilitate migration of __ and ___ to infected ti
- endothelial cells- mast cells- phagocytes- inflammatory response- blood flow and vascular permeability increase- adhesion molecules- neutrophils and monocytes
In inflammation caused by type III immunocomplex reaction, you will likely find what cells?
- neutrophils and monocytes
C3b role:
C3a and C5a role:
mediators in local inflammation
c3a and c5a:
peptide medators of inflammation, recruit phagocytes
- binds to complement receptors on phagoctyes> opsonizes pathogens
___ is the most potent peptide mediator of inflammation. It also serves as a chemoattractant to recruit more ___ to site of infection.
Type III Immunocomplex Arthus reaction:
- localized immunocomplex reaction- Example-farmer's lung from exposure to thermophilic actinomycetes, or antigens, in air
examples of diseases caused by type III reactions:
- systemic lupus erythmetosus (DNA-anti-DNA)- rheumatoid arthritis (IgM-Fc receptor IgG)- Serum sickness (horse antithymocyte globulin-antibody)
Systemic Lupus Erthymetosus is a Type III hypersensitivity. It is a ___ __ disease that mostly effects the blood, joints, skin, and kidneys. It causes ___ ___ ___, ____, and ____. Immunocomplex deposition occurs along the ____ of the skin and may cause th
- connective tissue- hemolytic anemia, thrombocytopenia, leukopenia- basement membrane
how to test for SLE:
Positive serum antinuclear antibody (ANA) (almost all cases) Anti-double-stranded DNA antibodies and anti-Sm antibodies Used to confirm the diagnosis of SLE, because they are highly specific for the disease (few false-positive results)
screening test for SLE:
- serum antinuclear antibody test (ANA)
diagnostic test for SLE:
- anti-double stranded DNA- anti-SM antibodiesthese are very specific for the disease and give few false positives
With SLE, there is ____ serum complement b/c it got used up with ____ of the complement system. There would also be ____ at the dermal epidermal junction in skin biopsies.
- decreased - activation- immunocomplexes
With Rheumatoid arthritis, there are a series of ___ ___. __ cells in the joints produce ___ __ ____ that are ___ antibodies against the __ receptor of ___. RF complexes are also present in the serum in 70-90% of cases. This is a type ___ reaction.
- inflammatory responses- B cells- rheumatoid factor (RF) complexes that are IgM autoantibodies against the Fc receptor IgG- type III
With RA, RF complexes activate the ___ which attracts ____. The ___ produce the acute inflammation of synovial fluid and ___the RF complexes.
- complement- neutrophils- neutrophils- phagocytize
With RA, inflammation in the ___ leads to dense accumulation of __ and __ cells, ___ cells, ___ cells, ___ ___, and ___. This is known as ___ b/c its an apron of inflammation. As this increases, erosions develop at the peri-articular bone within the synov
- synovium- B and T- CD4 cells- plasma cells- lymphoid follicles- neutrophils- pannus
what cells make up panus of inflammation in RA?
- B and T cells- CD4 cells- plasma cells- lymphoid follicles- neutrophilssynovium thickens> cartilage erodes
with chronic inflammation in RA, ___ are released and destroy the articular cartilage, the end result is ___ ___ and __ ___.
- cytokines- reactive fibrosis- joint fusion
What are the two subtypes of Type IV hypersensitivity reactions:
- delayed reaction hypersensitivity- cell mediated cytotoxicity
Type IV antibody independent T-cell mediated reactions aka ____ immunity can be either ___ __ hypersensitivity with __ cells, or ____ ___ cytotoxicity with __ cells.
- cellular- delayed reaction with CD4 cells- cell mediated with CD8 cells
With type IV antibody dependent T-cell mediated Delayed hypersensitivity ___ cells interact with ____ resulting in ___injury to tissue. give example of this:
- T cells interact with macrophages (APCs with MHC class II antigens)- cytokine- example: Tuberculous granuloma
With type IV t cell mediated cell-mediated cytotoxicity, ___ _ cells interact with altered ___ ___ __antigens on ___, ___ __, or ___ __ cells, causing lysis. Give example of this:
- CD8 T cells interact with altered MHC class I antigens - neoplastic- virus-infected- donor graft cells- killing of tumor cells or virus infected cells, contact dermatitis
what type of reaction is contact dermatitis/poison ivy?
- type IV antibody independent cell-mediated cytotoxicity
granulomatous inflammation:
Specialized type of chronic inflammation Causes Infections Examples-tuberculosis and systemic fungal infection (histoplasmosis) Usually associated with caseous necrosis Caseation is due to lipid released from the cell wall of dead pathogens. - can also occur with fungal infections and histoplasmosis
Formation of a tuberculosis granuloma:
The tubercle bacillus Mycobacterium tuberculosis undergoes phagocytosis by alveolar macrophages (processing of bacterial antigen). Macrophages present antigen to CD4 T cells in association with class II antigen sites. Macrophages release interleukin (IL) 12 (stimulates formation of TH1 class cells) and IL-1 (causes fever; activates TH1 cells).TH1 cells release IL-2 (stimulates TH1 proliferation), γ-interferon (activates macrophages to kill tubercle bacillus; epithelioid cells), and migration inhibitory factor (causes macrophages to accumulate). Lipids from killed tubercle bacillus lead to caseous necrosis. Activated macrophages fuse and become multinucleated giant cells.
alveolar macrophages phagocytize TB> macrophages present antigen to CD4 cells with class II antigen sites> macrophages release IL12 (formation of TH1 cells) and IL-1(fever,activates TH1 cells)> TH1 cells release IL-2(stimulates proliferation of TH1 cells)
cell types in a TB granuloma:
- epitheloid cells (activated macrophages)- mononuclear round CD4 cells infiltrate- multinucleated giant cells formed by fusion of epitheloid cells> nuclei located at periphery
Tuberculin Reaction (Purified Protein Derivative, PPD): The classic example of delayed hypersensitivity is the tuberculin reaction, which is produced by the intracutaneous injection of tuberculin, a protein-lipopolysaccharide component of the Mycobacteri
the TB PPD + reaction is a type ___ ___ reaction characterized by accumulation of ___ cells, increased microvascular permeabiltiy, resulting in plasma proteins escaping and giving rise to dermal edema and deposition of ___ in the interstitium (induration)
- type IV delayed- mononuclear- fibrin> induration- CD4 cells
example of contact dermatitis type IV delayed reaction:
- poison ivy- reaction to nickel
The etiology of contact dermatitis is either allergic contact dermatitis (20% of cases) or irritant contact dermatitis (80% of cases).The skin reaction to poison ivy or poison oak is a classic example of allergic contact dermatitis.Contact dermatitis is a
An irritant produces direct local cytotoxic effect on the cells of the epidermis, with a subsequent inflammatory response in the dermis. The most common site is the hand.
Contact dermatitis is a ___ ___ type __ reaction results from specific ___ penetrating the ___ ___ __. The ___ combines with a ___ __ and travels to the dermis, where __ ____ ___ cells become _____. On the ___ exposure, the reaction takes place.
- cell-mediated type IV reaction- specific antigens- epidermal skin layer- antigen combines with a protein mediator- T lymphocytes CD4 cells- sensitized- subsequent
Contact dermatitis is caused by an cell mediated reaction to something with which the patient is in regular contact.
Common allergen is Rhus toxicodendron ("poison ivy")
Type IV hypersensitivity contact dermatitis info:
- reaction: 24-48 hours- looks like eczema- cells: lymphocytes, followed by macrophages, edema of epidermis- antigen site: epidermal (organic chemicals, poison ivy, heavy metals)
Type IV Hypersensitivity Tuberculin reaction info:
-reaction time: 48-72 hours- appearance: local induration- histology: lymphocytes, monocytes, macrophages- antigen site: intradermal
granuloma information:
- reaction time 21-28 days- hardened appearance- macrophages, epitheliod and giant cells, fibrosis- antigen site: persistent antigen or foreign body presence
The definitive treatment of both irritant contact dermatitis (ICD) and allergic contact dermatitis (ACD) is the identification and removal of any potential causal agents.
With infectious mononucleosis, ___ ___ is mediated by ___ ___ _ cells and ___ ___ cells. There will be ___ lymphocytes in the blood. Characteristic of this disease is mainly ___ ___ cells. The reactive ___ of T cells is largely centered in lymphoid tissue
- cellular immunity - cytotoxic CD8 Tcells and natural killer cells- atypical lymphoctyes- CD8 cytotoxic T cells- reactive proliferation
With type I anaphylactic hypersensitivity reactions, the antibody is ___, the antigen is __, the appearance is a __ or ___, the hisology reveals ___ and ___. examples include ___ ___ and ___ ___.
- IgE- exogenous antigen- weal or flare- basophils and eusinophils- allergic asthma, hay fever
with type II cytotoxic hypersensitivity reactions the antibodies are __ and __, the antigen in on the __ ___.
- IgG and IgM- cell surface
type III has __ and ___ antibodies. Type IV has __ antibodies.
- IgG and IgM- no antibodies
Rejection is the consequence of the recipient's alloimmune response to the nonself antigens expressed by donor tissues.
factors enhancing graft viability:
- ABO blood compatibility between donor and recipient- absense of preformed anti-HLA cytotoxic antibodies in recipients (people must have previous exposure to blood products to develop anti-HLA cytotoxic antibodies)- close matches of HLA-A, HLA-B, and D-loci between recipients and donors
With hyperacute transplant rejection, the recipient is ____ ___ to ____, meaning they recognize the graft antigens as non-self. This manifests itself within ___ to ___ of graft transplantation. This is __ since the introduction of routine pretransplantati
- serologically presensitized to alloantigens - minutes to hours - rare - antidonor antibodies
With acute rejection, the graft antigens are recognized by __ ___. ___ are released and eventually cause ___ ___, __ __, and __ ___. This occurs within __ hours of transplantation and over period of days to weeks.
- T cells- cytokines- tissue distortion, vascular insufficiency, and cell destruction- 24
Chronic transplant rejection results from ___ ___ and ___ ___ ___. Changes occur within __ and __ ____, and to a lesser extent, within the __ of the graft. Leukocyte infiltration is usually __ or ___. All of these changes result in __ __ __ with subsequen
- peri-transplant and post-transplant trauma- large and medium arteries- veins- mild or absent- reduced blood flow- tissue ischemia, fibrosis, and cell death
Graft versus Host Reaction (GVHD) occurs when ___ ___ ___ recognize ___ ___ ___. These diffrences are governed by genetic polymorphisms of __ ___ __ (HLA)- ___ factors, like major and minor ___ antigens and ___ ___ ___factors.
- donor immune cells- recognize disparate host antigens- human leukocyte antigen-dependent factors, like major and minor histocompatibility antigens- non-dependent HLA factors
GVHD is common with ___ __ transplants.
bone marrow
GVHD develops in the course of:
BMT or peripheral blood progenitor (hematopoietic stem cell) transplantation; Transfusion of unirradiated blood products (transfusion-associated GVHD), especially in immunocompromised individuals; or Solid organ transplantation involving organs containing lymphoid tissue.
Recognize these diseases are immune mediated- Addison’s disease (adrenal gland), pernicious anemia (stomach), Systemic lupus erythematosus (systemic), and rheumatoid arthritis (joints, but systemic).
Screen for SLE: serum ANAConfirm SLE: anti-dsDNA and anti-Sm antibodies
screening tests need to be very ___. with diagnostic tests need to be very ___.
screening needs sensitivitydiagnostic needs specificity
auto-antibody involved with pernicious anemia- an autoimmune disorder:
- anti-intrinsic factor or anti-parietal cell antibodies
antibodies with SLE:
- antinuclear antibody- anti ds DNA antibody- anti smith antibody
Grave's disease autoantibody:
- anti-TSH autoantibody
Goodpasture's syndrome antibody:
- anti-basement membrane
myasthenia gravis antibody:
- anti- acetylcholine receptor antibody
Clinical presentations of SLE are all immune mediated somehow, list some:
- vasculitis- immune mediated inflammatory changes in blood vessels- glomerulonephritis- DNA/anti-DNA complexes, hematuria, proteinuria- skin butterfly rash- joints (pain and inflammation)- CNS vasculitis, hemorrhage, infarct- pericardial and pleural changes (inflammatory changes and effusions)- endocarditis- hematologic (autoantibodies against RBCs, platelets, and/or WBCs)
RA: RF combines with IgG to produce immunocomplexes that activate the complement system immunocomplexes (type III hypersensitivity). Immunocomplexes activate the complement system to produce C5a, a chemotactic agent for neutrophils and other leukocytes to
rheumatoid factor (RF) an IgM autoantibody that has specificity for the Fc portion of IgGDescribe the type III hypersensitivity injury in RA.
Bruton's agammaglobulinemia is a failure of ___ ___ to become ___ ___ ___. There is a mutated ___ ___. This is a __ ___ ___ disorder. During the first 6 months of life, the mother's antibodies protect the child, but after that there is decreased ____.
- failure of B cells to become mature B cells- tyrosine kinase- x-linked recessive- immunoglobulins
With IgA deficiency there is a failure of ___ __ cells to mature into ___ cells. This will result in ___ if pt is exposed to ___ ___ that contain ___. Findings are decreased IgA and secretory IgA.
- failure of IgA B cells to mature into plasma cells- anaphylaxis- blood products that contain IgA
With Bruton Agammaglobulinemia in the absense of mature B cells, pts lack ___ ___ and fail to develop ___ ___ so they cannot manufacture ____. Germinal centers are poorly developed in all lymphoid tissue in these patients. Tonsils, adenoids, peripheral ly
- lymphoid tissue- plasma cells- antibodies
name the two B cell disorders:
- Brutons agammaglobulinemia- IgA deficiency
A T-cell disorder called ___ ___ is the failure of the ___ and ___ ___ ___ to develop, thus the ___ and ___ ___ fail to develop. This results in ____ manifested by ___, absent thymic shadow on radiograph, PCP, and danger of ____.
- DiGeorge syndrome- third and fourth pharyngeal pouches- thymus and parathyroid glands- hypoparathyroidism, tetany- GVHD
Severe combined immunodeficiency (SCID) is a T and B cell disorder. 15% have a ___ ___ deficiency. This is an ___ ___ disorder. ___ is toxic to the B and T cells. There is a decrease in deoxynucleotide triphosphate precursors for DNA synthesis. Also may h
- adenine deaminase
- autosomal recessive
- adenine
- gene therapy
- bone marrow transplant
The central role of CD4+ T cells in immune defense is illustrated when the human immunodeficiency virus cripples the immune system by selective destruction of this T-cell subset.The human immunodeficiency virus (HIV) binds to CD4 molecules and thus is able to invade and infect CD4+ T cells.As the disease progresses, the number of CD4+ T cells declines below its normal level of about 1000 per microliter (µl). A partial explanation for this may be the unceasing efforts of the patient's CD8+ T cells to destroy the infected CD4+ cells.
___ __ ___ __ is used to monitor immune status of AIDS patients. It is good for determining when to initiate HIV treatment and when to give prophylaxis against infections. It is NOT a confirmatory test for HIV.
CD4 T-cell count
___ ___ ___ is used to detect actively dividing viruses in AIDs patients and is also used as a marker of disease progression. It is the most ___ test for acute HIV diagnosis before seroconversion.
HIV viral loadsensitive
The ___ ___ test on HIV patients is used as an indicator of active __ ___. It is present before anti-gp120 antibodies are developed in the patient. It is positive at two different times in HIV infections—prior to seroconversion and when AIDS is diagnose
- p24 antigen- viral replications
Amyloids are insoluble fibrous protein aggregates sharing specific structural traits. Abnormal accumulation of amyloid in organs may lead to amyloidosis, and may play a role in various neurodegenerative diseases.
Elisa is the screening test for HIV b/c high sensitivity. Western Blot is diagnostic test for HIV b/c high specificity.
early and in remote stage of disease you will see __. Later in disease process you will see ___.
- early IgM- later IgG
autoimmune pernicious anemia is what kind of hypersensitivity reaction?
type II antibody dependent complement dependent reaction
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