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IS LEC
Hypersensitivity
Study
1
Question
What is hypersensitivity?
Answer
An exaggerated response to a typically harmless antigen that results in injury to the tissue, disease, or even death.
2
Question
What is the Gell and Coombs Classification System?
Answer
A classification system that categorizes hypersensitivity reactions into four types: Type I, Type II, Type III, and Type IV.
3
Question
What is Type I Hypersensitivity?
Answer
An immediate hypersensitivity reaction where exposure to an antigen induces the production of specific IgE antibodies, leading to degranulation of mast cells and basophils.
4
Question
What is Type II Hypersensitivity?
Answer
An immediate hypersensitivity reaction where IgG or IgM antibodies react with antigens on host cells, leading to cell damage by complement-mediated lysis or other mechanisms.
5
Question
What is Type III Hypersensitivity?
Answer
An immediate hypersensitivity reaction where IgG or IgM antibodies react with soluble antigens, forming small complexes that activate complement and cause an inflammatory response.
6
Question
What is Type IV Hypersensitivity?
Answer
A delayed hypersensitivity reaction where sensitized T cells, rather than antibodies, are responsible for inducing inflammation and tissue damage.
7
Question
What is the distinguishing feature of Type I Hypersensitivity?
Answer
A short time lag (usually minutes) between exposure to the allergen and the onset of clinical symptoms.
8
Question
What is passive cutaneous anaphylaxis?
Answer
An experiment conducted by Carl Wilhelm Prausnitz and Heinz Kstner, where serum from patients with allergic hypersensitivity reactions was shown to produce a large amount of IgE antibody in response to a small concentration of allergen.
9
Question
What are allergens in type I hypersensitivity?
Answer
Antigens that trigger type I hypersensitivity, such as peanuts, eggs, and pollen.
10
Question
What is the distinguishing feature of type I hypersensitivity?
Answer
Short time lag, usually minutes, between exposure to allergen and onset of clinical symptoms.
11
Question
Who provided the first clue about the cause of type I hypersensitivity?
Answer
Carl Wilhelm Prausnitz and Heinz Kstner.
12
Question
What is passive cutaneous anaphylaxis?
Answer
Occurs when serum from an allergic individual is transferred to a non-allergic individual who is later challenged with the specific allergen, resulting in redness and swelling.
13
Question
What does atopy refer to in type I hypersensitivity?
Answer
An inherited tendency to develop classic allergic responses to naturally occurring inhaled or ingested allergens.
14
Question
What are the key immunologic components in type I hypersensitivity?
Answer
IgE antibody, mast cells, basophils, and eosinophils.
15
Question
What initiates the transcription of the gene that codes for the epsilon heavy chain of immunoglobulin molecules in type I hypersensitivity?
Answer
IL-4 and IL-13, among other cytokines.
16
Question
What happens in the sensitization phase of type I hypersensitivity?
Answer
IgE antibody attaches to high affinity receptors, allergens are processed in lymphoid tissue, and binding of IgE to cell membranes increases antibody half-life.
17
Question
What triggers degranulation of mast cells and basophils in type I hypersensitivity?
Answer
Subsequent binding of allergen to IgE-sensitized cells.
18
Question
What is the role of mast cells in type I hypersensitivity?
Answer
Principal effector cells of immediate hypersensitivity.
19
Question
What are the preformed substances released during degranulation of mast cells in type I hypersensitivity?
Answer
Histamine, heparin, eosinophil chemotactic factor of anaphylaxis, and proteases.
20
Question
What are the primary mediators responsible for the early phase symptoms in allergic reactions?
Answer
Histamine and other preformed substances released during degranulation.
21
Question
What are some of the secondary mediators synthesized by mast cells and basophils in the late phase of type I hypersensitivity?
Answer
Platelet activating factor (PAF), prostaglandin (PG) D2, leukotrienes (LT) B4, C4, and E4, and cytokines.
22
Question
What are some of the primary preformed mediators of Type I Hypersensitivity reactions?
Answer
Histamine, Heparin, Eosinophil chemotactic factor of anaphylaxis (ECF-A), Neutrophil chemotactic factor of anaphylaxis (NCF-A), Proteases
23
Question
What are some of the secondary or newly synthesized mediators of Type I Hypersensitivity reactions?
Answer
Prostaglandin (PGD2), Leukotrienes (LTB4, LTC4, LTD4, LTE4), Platelet activating factor (PAF), Cytokines (IL-1, IL-3, IL-4, IL-5, IL-6, IL-9, IL-13, IL-14, IL-16, TNF, GM-CSF)
24
Question
What are the actions of primary preformed mediators like histamine, heparin, ECF-A, NCF-A, and proteases in Type I Hypersensitivity reactions?
Answer
Smooth muscle contraction, vasodilation, increased vascular permeability, chemotactic for eosinophils and neutrophils, conversion of C3 to C3b, stimulation of mucus production, activation of cytokines
25
Question
What are the actions of secondary or newly synthesized mediators like prostaglandin, leukotrienes, PAF, and cytokines in Type I Hypersensitivity reactions?
Answer
Vasodilation, increased vascular permeability, chemotactic for neutrophils and eosinophils, platelet aggregation, increase in inflammatory cells, increase in IgE production
26
Question
How do genetic and environmental factors influence the development of Type I Hypersensitivity reactions?
Answer
IgE responses and allergies depend on complex interactions between genetic factors and environmental triggers. Stress, physical factors, and environmental pollutants can intensify allergic reactions in susceptible individuals.
27
Question
What are the clinical manifestations of Type I Hypersensitivity reactions like anaphylaxis, rhinitis, asthma, and food allergies?
Answer
Anaphylaxis can range from localized skin reactions to severe systemic responses. Rhinitis presents with sneezing, runny nose, congestion, and itching. Asthma is characterized by airflow obstruction. Food allergies lead to symptoms like cramping, vomiting, and skin reactions.
28
Question
What is the clinical definition of a condition that reaches the lower respiratory tract and causes recurrent airflow obstruction, intermittent sneezing, breathlessness, and occasional cough with sputum production?
Answer
Asthma
29
Question
What are the causes of airflow obstruction in the lower respiratory tract?
Answer
Bronchial smooth muscle contraction, mucosal edema, and heavy mucus secretion
30
Question
What are the symptoms of food allergies that may include cramping, vomiting, and diarrhea?
Answer
Symptoms of food allergies may also include the spread of antigen through the bloodstream, leading to hives, angioedema, asthma, rhinitis, or anaphylaxis.
Autoimmunity
Study
1
Question
What is horror autotoxicus?
Answer
Horror autotoxicus is a phenomenon observed by Paul Ehrlich where the immune system attacks the host it is meant to protect, leading to autoimmune diseases.
2
Question
What are autoimmune diseases characterized by?
Answer
Autoimmune diseases are disorders in which immune responses target self-antigens, resulting in damage to organs and tissues in the body. This can be caused by T-cell-mediated immune responses or autoantibodies directed against host antigens.
3
Question
What is self-tolerance in the context of the immune system?
Answer
Self-tolerance is the ability of the immune system to accept self-antigens and not initiate a response against them. It is a state of immune unresponsiveness directed against specific self-antigens.
4
Question
What is central tolerance and where does it occur?
Answer
Central tolerance occurs in the thymus and bone marrow, the primary lymphoid organs. T cells mature in the thymus encounter self-antigens, and those with high affinity are deleted through negative selection by apoptosis.
5
Question
What is peripheral tolerance and how is it achieved?
Answer
Peripheral tolerance refers to lymphocytes in secondary lymphoid organs being rendered incapable of reacting to self-antigens. This can occur through anergy from a lack of costimulatory signals, inhibition by Tregs or apoptosis.
6
Question
How do self-reactive B cells in the bone marrow undergo tolerance mechanisms?
Answer
Self-reactive B cells in the bone marrow are eliminated through apoptosis if they recognize self-antigens strongly. Some are stimulated to rearrange their immunoglobulin genes to become non-antigen specific (receptor editing) or downregulate receptor expression (anergy).
7
Question
Why are autoimmune diseases often more prevalent among family members and genetically identical twins?
Answer
Autoimmune diseases show higher prevalence among family members and monozygotic twins due to genetic factors. Examples include HLAB27 allele for ankylosing spondylitis, TPN22 gene, IL2RA gene, and CTLA4 gene.
8
Question
How can B cells in the periphery be deleted?
Answer
B cells in the periphery can be deleted by apoptosis, rendered anergic after repeated stimulation with self-antigens, or receive inhibitory signals through receptors such as CD22.
9
Question
What are some factors that contribute to the prevalence of autoimmune diseases among family members and twins?
Answer
Autoimmune diseases are more prevalent among family members and monozygotic twins than among unrelated individuals or dizygotic twins. Examples include HLAB27 allele, TPN22 gene, IL2RA gene, CTLA4 gene, and BLK gene.
10
Question
How does hormonal influence affect the immune system in women?
Answer
Women are more likely to acquire autoimmune diseases than men. Estrogens tend to direct the immune system in favor of a Th2 response, leading to more B cell activation and antibody production. Androgens favor a Th1 response with activation of CD8 T cells.
11
Question
What is immunologic ignorance and how can it lead to autoimmune responses?
Answer
Immunologic ignorance occurs when cryptic self-antigens are hidden within tissues and are later released due to inflammation or tissue trauma, triggering an immune response. This may be caused by factors like infections, environmental toxins, or physical injury.
12
Question
What is molecular mimicry and how can it contribute to autoimmune disease development?
Answer
Molecular mimicry refers to microbes containing antigens that resemble self-antigens, leading to autoimmunity. For example, Streptococcus pyogenes in rheumatic fever. It is a principal means by which microbes trigger autoimmune diseases.
13
Question
What are epigenetics and Modification of Self-Antigens?
Answer
Refers to modifications in gene expression that are not caused by changes in the original DNA sequence, stable, and can be inherited.
14
Question
What triggers epigenetic changes?
Answer
Exposure to environmental toxins, ingestion of harmful foods or drugs, or the aging process can induce epigenetic changes by increasing or decreasing methylation of cytosine bases, modifying histones, and causing abnormal regulation by microRNAs.
15
Question
What biochemical processes are involved in posttranslational modifications as a result of exposure to environmental factors?
Answer
Acetylation, lipidation, citrullination, and glycosylation may occur, where, for example, citrullination of collagen might play a role in rheumatoid arthritis (RA) pathogenesis and glycosylation of myelin may be involved in the pathology of multiple sclerosis.
16
Question
What interactions can lead to systemic autoimmune diseases?
Answer
Interactions between factors like exposure to environmental toxins, ingestion of harmful foods or drugs, and the aging process can contribute to the development of systemic autoimmune diseases.
17
Question
What are the associated autoantibodies in systemic lupus erythematosus (SLE)?
Answer
Antibodies to double-stranded DNA, phospholipid antibodies, antibodies to RBCs, platelets, lymphocytes, ribosomal components, endothelium, and rheumatoid factor are associated with SLE.
18
Question
What are the target cells and tissues affected by systemic lupus erythematosus (SLE)?
Answer
SLE affects multiple cells and organs throughout the body, including the skin, joints, kidneys, brain, heart, and lungs.
19
Question
What are the clinical signs and symptoms of systemic lupus erythematosus (SLE)?
Answer
Nonspecific symptoms like fatigue, weight loss, malaise, fever, and anorexia, joint involvement (symmetric arthritis in small joints), skin manifestations (erythematous rash), and systemic effects like cardiac involvement and drug-induced lupus.
20
Question
What are the clinical criteria for systemic lupus erythematosus (SLE)?
Answer
Clinical criteria include acute and chronic cutaneous lupus, oral ulcers, synovitis, serositis, renal involvement, neurological symptoms, hemolytic anemia, leukopenia, and thrombocytopenia.
21
Question
What is the Latin term for 'wolf-like', from which the term 'cheeks o lupus' is derived?
Answer
Lupus means wolf-like in Latin.
22
Question
What are some systemic effects of lupus, specifically in cardiac involvement?
Answer
Systemic effects of lupus in cardiac involvement may include pericarditis, tachycardia, and ventricular enlargement.
23
Question
Which drugs are commonly implicated in drug-induced lupus?
Answer
Common drugs implicated in drug-induced lupus include procainamide, hydralazine, chlorpromazine, isoniazid, quinidine, anticonvulsants such as methyldopa, and possibly oral contraceptives.
24
Question
What are the 11 clinical criteria for diagnosing lupus?
Answer
The 11 clinical criteria for diagnosing lupus include acute cutaneous lupus, chronic cutaneous lupus, oral ulcers, nonscarring alopecia, synovitis, serositis, renal involvement, neurological symptoms, hemolytic anemia, leukopenia, and thrombocytopenia.
25
Question
What are the 6 immunologic criteria for diagnosing lupus?
Answer
The 6 immunologic criteria for diagnosing lupus include elevated antinuclear antibody titer, elevated anti-dsDNA titer, presence of antibody to the Sm nuclear antigen, presence of antiphospholipid antibody, low complement levels, and positive direct Coombs test.
26
Question
What is the key to successful treatment of lupus?
Answer
The key to successful treatment of lupus is to prevent organ damage and achieve remission.
27
Question
What are some skin manifestations of lupus and their respective treatments?
Answer
Skin manifestations of lupus may be treated with antimalarials such as hydroxychloroquine or chloroquine and topical steroids.
28
Question
What are some laboratory tests used in the diagnosis of systemic lupus erythematosus?
Answer
Laboratory tests used in the diagnosis of systemic lupus erythematosus include complete blood count, platelet count, urinalysis, erythrocyte sedimentation rate, C-reactive protein level, quantification of complement proteins, and detection of specific autoantibodies.
29
Question
What are antinuclear antibodies (ANAs) and why are they significant in the diagnosis of lupus?
Answer
Antinuclear antibodies (ANAs) are autoantibodies directed against antigens in the nuclei of mammalian cells. They are significant in the diagnosis of lupus as they are present in over 95% of patients with active lupus and are used as a major marker for the disease.
30
Question
What are extractable nuclear antigens (ENAs) and why are they important in the diagnosis of lupus?
Answer
Extractable nuclear antigens (ENAs) are a group of nuclear antigens associated with uridine-rich RNA ribonucleoproteins. They are important in the diagnosis of lupus as they represent a family of small nuclear proteins that are commonly targeted by autoantibodies in the disease.
Autoimmunity Maam Nicole
Study
1
Question
What is autoimmunity?
Answer
Conditions wherein autoantibodies and autoreactive cells result in organ or tissue damage.
2
Question
What is self tolerance in autoimmunity?
Answer
The ability to recognize own cell antigens and not react to self antigens.
3
Question
What is central tolerance in autoimmunity?
Answer
Destruction of potentially self-reactive cells during maturation of T cells in the thymus and B cells in the bone marrow.
4
Question
What is peripheral tolerance in autoimmunity?
Answer
Maintained by a balance between Th1 and Th2 cells, regulatory T cells, and T helper subsets in secondary lymphoid organs like lymph nodes and spleen.
5
Question
Explain the balance between regulatory T cells and effector T cells in autoimmunity.
Answer
In a healthy individual, there is a balance between regulatory T cells and effector T cells. An imbalance can lead to autoimmune diseases due to an increase in effector T cells and inflammation production.
6
Question
How does Major Histocompatibility Complex (MHC) influence autoimmunity?
Answer
MHC can influence autoimmunity through inheritance of specific MHC genes, expression of Class II molecules, and playing a vital role in self-tolerance.
7
Question
What is tissue injury in the context of autoimmunity?
Answer
Exposure of antigens, usually not encountered by the circulation, due to trauma or infection can lead to autoimmune responses, such as the production of antibodies against self-antigens.
8
Question
What is molecular mimicry in autoimmunity?
Answer
Molecular mimicry refers to similarities in the molecular structure between human/self antigens and viral/bacterial agents, which can trigger the production of antibodies with similar structures.
9
Question
What is polyclonal B cell activation in autoimmunity?
Answer
Activation of two or three subsets of antibodies against different kinds of structures, leading to a more diverse immune response compared to monoclonal activation.
10
Question
What triggers the production of antigens with similar molecular structures?
Answer
Exposure to antigens like Poliovirus VP2, Acetylcholine ACH, Measles Virus P3, Myelin Basic Protein, Papilloma Virus E2, Insulin Receptors
11
Question
What are the possible defects that may include abnormalities in the immune system?
Answer
1. Abnormal expression or function of key signaling molecules 2. Dysregulation of cytokines 3. Changes in B cell development subsets
12
Question
Which organisms can enhance immune system defects?
Answer
Gram negative bacteria, Cytomegalovirus, EBV (Epstein Barr virus)
13
Question
How does EBV infection lead to immune system defects?
Answer
EBV infects B cells, causing their proliferation and overproduction of antibodies, leading to an imbalance in regulation and potential autoimmunity.
14
Question
What are some other mechanisms of defects in the immune system?
Answer
Defects in natural killer cells surveillance, secretion of cytokines, apoptosis, and complementary components
15
Question
What age group is usually affected by SLE?
Answer
20-40 years old
16
Question
Which gender is more susceptible to SLE?
Answer
Women
17
Question
Which ethnicities are more commonly affected by SLE than Caucasians?
Answer
African Americans and Hispanics
18
Question
Which ethnic group has a higher possibility of remission in SLE?
Answer
Asians
19
Question
What genetic loci are associated with SLE susceptibility?
Answer
HLA A1, B8, DR3, and DQ
20
Question
What deficiencies of complement proteins are associated with SLE?
Answer
C1q, C2, and C4
21
Question
What abnormalities in immune cells are linked to SLE?
Answer
Abnormalities of Fcy receptors on B cells, macrophages, dendritic cells, and neutrophils
22
Question
What environmental factors can contribute to SLE development?
Answer
Exposure to UV light, certain medications, microbial infections
23
Question
How do hormones influence SLE development?
Answer
Hormones regulate transcription of genes that may influence autoimmunity, with women having higher estrogen levels
24
Question
What is the role of regulatory T cells in SLE?
Answer
Deficiency in regulatory T cells causes uncontrolled autoreactivity of T cells and B cells, leading to autoantibody formation
25
Question
Which autoantibody is commonly found in SLE patients?
Answer
Anti-double stranded DNA
26
Question
What is the average number of autoantibodies in a typical SLE patient?
Answer
3
27
Question
How does abnormal apoptosis contribute to SLE?
Answer
Abnormal apoptosis releases cellular constituents such as DNA and RNA, contributing to immune response
28
Question
How do inherited HLA genes contribute to SLE susceptibility?
Answer
Inherited HLA genes cause increased susceptibility to respond to self antigens, leading to increased apoptosis of cells
29
Question
What triggers polyclonal activation of B cells in SLE?
Answer
Constant presence of antigenic material due to improper clearance of cellular debris
30
Question
Why are immune complexes not cleared properly in SLE?
Answer
Due to defects in complement receptors in phagocytes, defects in the FC portion of immunoglobulins, and deficiencies of early complement components C1q, C2, C4