Module 8A - Immune System Flashcards
What is the immune system?
• Complex network of cells, tissues, organs, and molecules that work together to defend the body against pathogens, including viruses, bacteria, fungi, and parasites
• Plays a crucial role in recognizing and neutralizing harmful substances from the environment and fighting against the body’s
own cells when they become cancerous
What is the immune system composed of?
• Leukocytes and Immune cells and proteins and other molecules
• Adaptable and Innate Immune system
• Lymphatic System
What are the key functions of the immune system?
Defense Against Pathogens
• Recognizing and eliminating pathogens
Surveillance Against Cancer
• Identifying and destroying cells that have become cancerous
Wound Healing and Tissue Repair
• Managing the process of inflammation and healing
Maintaining Homeostasis
• Removing dead cells and renewing tissues
What are the characteristics of the innate immunity?
- Non-Specific Response
• The innate immune system provides a general defense against pathogens, meaning it does not recognize specific pathogens but rather responds to several indicators of infection - Immediate Response
• It responds to pathogens within minutes to hours of exposure and is the body’s first line of
defense - No Memory
• Innate responses do not adapt to repeated infections; the response is the same each time a pathogen invades - Components
• Physical Barriers: Skin and mucous membranes • Chemical Barriers: Stomach acid, enzymes in tears and skin oils
• Cellular Defenses: Phagocytic
• Inflammatory Response: Release of cytokines that recruit immune cells to sites of infection
Advantages
• Provides immediate protection
• Protects against all pathogens
Disadvantages
• Lacks specificity
• No immunological memory
What are the characteristics of the adaptable immunity?
- Specific Response
• The adaptive immune system can recognize specific pathogens through antigens. Each
lymphocyte recognizes a unique antigen - Slower Response
• It takes days to become fully effective; it is activated after the innate immune response - Memory
• Once an antigen is recognized, the adaptive immune system creates memory cells that
allow it to respond more rapidly and effectively upon subsequent exposures - Components:
- Lymphocytes: T cells (cytotoxic and helper) and B cells
- Antibodies: Produced by B cells that specifically bind to antigens
- Effector Mechanisms: Cell-mediated immunity (T cells) and humoral immunity (antibodies)
Advantages
• High specificity for specific pathogens
• Immune memory leads to quicker responses upon repeated exposures
Disadvantages
• Takes time to mount an initial response
• Requires prior exposure to the pathogen
What are the key differences between innate and adaptable?
Speed and Timing
• Innate immune system acts immediately
• Adaptive system takes longer to respond but develops memory for a faster response on subsequent exposures
Specificity
• Innate immunity is non-specific
• Adaptive immunity is highly specific to a pathogen’s antigens
Memory
• Innate immunity lacks memory
• Adaptive immunity develops immunological memory, leading to an enhanced and faster response to repeated
exposures to the same pathogen’s antigens
Neutrophils
• Most abundant type of WBC in humans and are a critical component of the innate
immune system
• Primarily responsible for responding to infections, especially bacterial and fungal
Eosinophils
• Involved in combating parasitic infections and mediating allergic inflammatory
responses
Basophils
• Least common WBC
Monocytes
• Differentiate into Macrophages
• Numerous roles within the immune system
T-Lymphocytes (T-Cells)
• WBC responsible for mediating cellular immunity through the direct killing of infected host cells
• Created in the bone marrow and mature in the thymus
• Can differentiate into various subsets such as cytotoxic T cells, helper T cells, and regulatory T cells
B-Lymphocytes (B-Cells)
• Create humoral immunity by producing and secreting antibodies that target specific antigens
• Created and mature in the bone marrow and differentiate into plasma cells
• Plasma cells produce antibodies and memory B cells that provide long-term immunity to a specific antigen
Helper T Cells (CD4+ T Cells)
• Assist other cells in the immune system by releasing cytokines, which can amplify
the immune response
• Helper T cells are further categorized based on the cytokines they produce: T Helper 1 Cells (TH1), T Helper 2 Cells (TH2), T Helper 17 Cells (TH17)
Cytotoxic T Cells (CD8+ T Cells)
• Cells are responsible for directly killing infected cells, primarily those infected with viruses or transformed by cancer
• Recognize antigens presented by MHC class I molecules on the surface of infected cells
Memory T Cells
• After an initial response to a specific antigen, some T cells become memory cells
• Persist long-term in the body and enable a faster response upon re-exposure to the
same antigen
What do B-Lymphocytes differentiation into?
Plasma Cells
• Create and secrete large amounts of antibodies specific to the antigen they
are exposed to
• Antibodies play a key role in the immune response by neutralizing
pathogens or marking them for destruction by other immune cells
Memory B Cells
• Do not secrete antibodies but persist in the body for years or even decades
• Provide a rapid and robust response upon re-exposure to the same antigen
• Forms the basis of immunological memory.
Antigen
• Substance that the body recognizes as foreign, which can trigger an immune response aimed at attacking and eliminating it
• These substances can come from outside the body, like viruses or bacteria, or can be abnormal cells from within the body, such as cancer cells
• Can be proteins, polysaccharides, or other biochemical molecules derived from pathogens (such as viruses and bacteria) or from non-infectious sources (including pollen, food, and own body cells in cases of autoimmune
diseases)
• Basically, think of it as the SSN or SIN (for ya’ Canadians, eh)
What are the 5 Classifications of Antibodies / Immunoglobins?
IgG
• Most abundant (~80%)
• Humoral immunity
IgA
• Body secretions (saliva, tears, mucous membranes)
IgM
• First antibody produced with detection of foreign antigens
IgE
• Associated with allergies
IgD
• Found on the surface of B cells
What are Antigen-Presenting Cells (APCs)?
• Antigen-Presenting Cells (APCs) are specialized to capture microbial antigens and display these to lymphocytes
• Antigen-Presenting Cells (APCs)
• Dendritic Cells
• Macrophages
• B-Lymphocytes
• Display antigen complex with their Class II MHC molecule on their
surface
• Interact with T helper cells and B cells
What are the three classifications to immune system disorders?
• 1. Hypersensitivity
• 2. Autoimmune
• 3. Immunodeficiency
What is the pathogenesis to hypersensitivity? How are the reactions initiated? What are 4 types of immunodeficiency diseases?
It is an excessive or harmful reaction to an antigen that normally does not illicit an immunologic response
• Imbalance between effector mechanisms of immune response and control mechanisms that limit the response
Exogenous Antigens
• Microbes, chemicals, food, pollen, dust, drugs
• May range from itchy nose, runny eyes to extreme fatal situations- anaphylaxis
• Commonly referred to as allergies
Endogenous Antigens
• Our own cell antigens
• Lead to autoimmune diseases
Fo ur Types of Hypersensitivity Reactions
• Immediate (type I) hypersensitivity
• Commonly referred to as allergies
• Antibody-mediated (type II) hypersensitivity
• Immune complex-mediated (type III) hypersensitivity
• Cell-mediated (type IV) hypersensitivity
What is the pathogenesis to autoimmune?
• Disorders and diseases that are due to a failure of the body’s immune system for self-tolerance
• Immune system is unable to distinguish self-antigens from foreign antigens
• Immune system produces autoantibodies that attack the body’s own antigens
What is the pathogenesis to
immunodeficient immune disorders? What are 2 categories of immunodeficiency diseases?
• The immune system is deficient or not functioning at full capability
• Leaves the body vulnerable for the development of diseases and
disorders
• 1. Primary (congenital) immunodeficiencies
• 2. Secondary (acquired) immunodeficiencies
- Hypersensitivity reactions are when the body’s immune system
causes a deficient response to identified antigens.
• A) True
• B) False
B) False
Immunodeficient disorders can be due to a genetic abnormality or
due to a viral infection.
• A) True
• B) False
A) True
What is the other names of type 1 hypersensitive reactions?
• Immediate (Type I) Hypersensitivity
• IgE hypersensitivity reactions
• Allergies
What is the role of the key substances associated with the pathogenesis of type 1 hypersensitivity reactions?
Allergen
• Substance that causes an immune response
• Causes sensitization of the mast cells
IgE Antibodies
• Antibodies created in response to specific allergen (antigen)
Mast Cells
• Immune cells that release chemical mediators that cause the physiological changes
Predicated upon IgE antibodies binding to mast cells
• Causes the release of chemical mediators- HISTAMINE
• Responsible for the clinical and pathologic outcomes of this reaction (inflammation)
What are the steps involved with type 1 hypersensitivity reactions?
- First Exposure
• Sensitization
Dander is phagocytized by an APC
• Carries the antigen (called an allergen) to a lymph node
• APC presents allergen (antigen) to a Naïve T Helper Cell
• Naïve T helper cell is built to recognize a specific antigen, but has not been exposed to it yet
Naïve T helper cell differentiates to a Type 2 T Helper Cell (TH2)
• Becomes Primed
Primed TH2 releases Interleukin 4 (IL-4) that causes B cells to make IgE antibodies
• Specific to the cat dander
• Instead of IgM antibodies
These IgE antibodies have a HIGH affinity for receptors on mast cells
• Bind to mast cells
IgE antibodies bound to mast cells- are now sensitized
• Specifically for cat dander
- Re-Exposure
• Go back to your friend’s place with that annoying cat lol
• Re-exposure to the cat dander • Dander antigens bind to IgE antibodies on the mast cells
• Sensitized mast cells
• Mast cells go crazy and release their chemical mediators
What is the role histamine with type 1 hypersensitivity reactions?
Vasoactive Amines
• HISTAMINE is the main vasoactive amine
Causes
• Vasodilation
• Increased vascular permeability
• Smooth muscle contraction
• Increased mucus secretion
What is the role prostaglandins have with type 1 hypersensitivity reactions?
Lipid Mediators
• Prostaglandins and leukotrienes from the
arachidonic acid pathway
Causes:
• Bronchospasm (smooth muscle contraction)
• Increased mucus secretion
• Increase vascular permeability
Compare and contrast immediate and late-phase response of type 1 hypersensitivity reactions
Immediate Response
• Vasodilation, increased vascular permeability, smooth muscle contraction
• 5-30 minutes after exposure; subsides in about 60 minutes
Late-Phase Response
• Roughly 2-24 hours afterwards
• Characterized by inflammation and tissue damage
• Recruitment of leukocytes can amplify and sustain inflammatory processes
• Eosinophils, Basophils
What are the common signs/symptoms of type 1 hypersensitivity reactions?
• Urticaria / Urticaria
• Allergic Rhinitis
• Allergic Conjunctivitis
• Allergic Asthma
• Pruritus
Common Treatments
• Antihistamines
• Block the effects of histamine
• Corticosteroids
• Decrease inflammatory
What is anaphylaxis?
Life Threatening Type 1 Hypersensitivity Reaction
• Massive and intense systemic type 1 hypersensitivity reaction
• Causes immediate and severe reactions
• Mast cell mediator release and an increased intensity of reactions
What is the processes, complications, and characteristics associated with anaphylaxis?
Individuals go into Anaphylactic Shock
• Airways spasm and fill with mucus
• Major drop in blood pressure and tachycardia
• Hives, itchiness, swelling of skin
• Abdominal pain, diarrhea, vomiting
Treatment
• Epinephrine pen
Must seek medical attention!!!!!
• Symptoms may get better and then get worse
What is the role cytokines have with type 1 hypersensitivity reactions?
Cytokines
• Tumor Necrosis Factor (TNF) and Cytokines Causes
• Increased mucus secretion
• Promote leukocyte recruitment
All of the options must occur for type 1 hypersensitivity reactions, except?
• A) APCs must present antigen to T helper cells
• B) IgM antigens must bind to mast cells
• C) A person must have prior exposure to the antigen
• D) Mast cells must release histamine
B) IgM antigens must bind to mast cells
All the options are true regarding type 1 hypersensitivity
reactions, except?
• A) Urticaria is a possible outcome
• B) Corticosteroids are a treatment option
• C) A complication of anaphylaxis is high blood pressure
• D) The majority of symptoms are a result of a massive secretion of histamine
C) A complication of anaphylaxis is high blood pressure
What are the alternative names of type II hypersensitivity reactions?
AKA: Antibody-Mediated (Type II) Hypersensitivity
AKA: Cytotoxic Hypersensitivity
• Due to the mediated destruction of cells
What is the general process of type II hypersensitivity reactions?
IgG antibodies directed against target antigens on the surface of cells or other tissue components or exogenous molecules
• Basically- our own antibodies bind to our own cells’ antigens eliciting various reactions that cause disease, damage, and destruction
What is the variables that can lead to a type II hypersensitivity reaction?
IgG antibodies bind to healthy cells’ antigens or extrinsic antigens
• Intrinsic antigen
— Cell normally makes these antigens
• Extrinsic (exogenous) antigen
— A drug antigen
Compare and contrast the four mechanisms to type II hypersensitivity reactions
- Opsonization and Phagocytosis
• When a cell’s antigen are bound to antibodies or C3b complement protein
• Mark the cell to be phagocytized - Complement System Activation
• Formation of MAC- causes cell lysis - Antibody-Dependent Cell-Mediated Cytotoxicity (ADCC)
• Antibody-Antigen complex is recognized by Natural Killer (NK) cells - Antibody Mediated Cellular Dysfunction (Non-Cytotoxic)
• Antibodies bind to cell’s receptors (antigens) - Blocks the receptor from binding its target substance- hormone or neurotransmitter
- Causes activation of receptor- stimulates receptor
• Either case- cell’s function is disrupted
• Examples:
• 1. Myasthenia Gravis • 2. Graves disease
What option is TRUE regarding type II hypersensitivity reactions?
• A) It only involves self antigens
• B) It can lead to opsonization
• C) All the outcomes lead to cytotoxic processes
• D) All the options are true
B) It can lead to opsonization
What are the one outcomes of the non-cytotoxic pathway of type II hypersensitivity reactions? What are the 3 outcomes of the cytotoxic pathway of type II hypersensitivity reactions?
Antibody Mediated Cellular Dysfunction
Opsonization and phagocytosis
Complement system activation
Antibody Dependent Cell Mediated Cytotoxicity
What are the several diseases Type II (antibody-mediated) hypersensitivity reactions associated with?
• Autoimmune hemolytic anemia
• Myasthenia gravis
• Graves disease
• Pernicious anemia
• Vasculitis
• Acute rheumatic fever
• Goodpasture syndrome
All of the options are true regarding type II hypersensitivity
reactions reactions, except?
• A) Cell lysis is a possible outcome
• B) Overactivation of a cellular receptor is a possible outcome
• C) All outcomes lead to cellular death
• D) Can lead to the formation of MAC
C) All outcomes lead to cellular death
What are other names for type III hypersensitivity reactions?
AKA: Immune Complex–Mediated Diseases
What is the pathogenesis of type III hypersensitivity reactions?
Antigen-antibody complexes (called immune complexes) that are
formed in the circulation may deposit in blood vessels
• Leading to complement system activation and acute inflammation
• Causes tissue damage
Only involves antibodies bound to soluble antigens
• Not attached to a cell
Type II Hypersensitivity: Antibodies target antigens bound on cell surfaces in the blood
What are the types of antigens that can lead to type III hypersensitivity reactions?
Exogenous
• Foreign protein that is injected or produced by an infectious microbe
Endogenous
• Individual produces antibodies against self antigens (autoimmunity)
What are the main organs involved with type III hypersensitivity reactions?
• Kidney (glomerulonephritis)
• Joints (arthritis)
• Small blood vessels (vasculitis)
What are the three steps to type III hypersensitivity reactions?
- Formation of antigen
• Antibody complexes in circulation - Deposition of these immune complexes in
tissues
• Blood vessels primarily - Inflammatory reaction in various sites
• Complement system
Define the process that leads to tissue damage with type III hypersensitivity reactions
Step 1: Formation of Antigen-Antibody Complexes
• Introduction of a protein antigen triggers an immune response that results in the formation of antibodies
• Antibodies are secreted into the blood and react with the
antigen still present in the blood
• Antibody-Antigen complexes form (immune complexes)
Step 2: Deposition of These Immune Complexes
• Circulating antigen-antibody complexes are deposited in various tissues
Site where these immune complexes are deposited:
• Organs where blood is filtered at high pressure to form other fluids
• Urine and synovial fluid for example
• Like the glomeruli and joints
Step 3: Inflammation and Tissue Injury
• Immune complexes deposited in tissues initiate
acute inflammatory reactions via complement system
• Tissue damage is similar no matter where
complexes are deposited
Depending on the location, the name is different:
• Vasculitis if it occurs in blood vessels
• Glomerulonephritis if it occurs in renal glomeruli
• Arthritis if it occurs in the joints
What is true of type III hypersensitivity reactions?
• A) Involves antibodies binding to both cellular and soluble antigens
• B) When the antibody-antigen complexes are deposited, they activate the complement system
• C) A common location for the antibody-antigen complexes to be deposited is the heart
• D) None of the options are true
B) When the antibody-antigen complexes are deposited, they activate the complement system
All of the following options are common locations for the antibody-antigen
complexes to be deposited associated with type III hypersensitivity reactions, except?
• A) Kidney
• B) Liver
• C) Joint
• D) Small blood vessels
B) Liver
The difference between type II and type III hypersensitivity reactions is that type III
only binds to soluble antigens and type II only binds to cellular antigens?
• A) True
• B) False
A) True
What are the conditions with Common Immune Complex-Mediated (Type III) Hypersensitivity Diseases?
• Systemic lupus erythematosus
• Reactive arthritis
• Arthus reaction
• Nephritis (glomerulonephritis)
• Vasculitis
What is the other names of type IV hypersensitivity reactions?
• AKA: T cell-mediated (type IV) hypersensitivity
• AKA: Delayed Type Hypersensitivity
What is the immune cells involved with type IV hypersensitivity reactions?
• It is NOT antibody mediated but CELLULAR mediated reactions
• Involves the actions of two different types of T lymphocytes
• Remember where lymphocytes were also associated?
• Each type has its own outcomes and physiological changes
What is the two types of type IV hypersensitivity reactions?
- Cytokine-Mediated Inflammation
• Cytokines are produced mainly by CD4+ T cells - Direct Cell Cytotoxicity
• Mediated by CD8+ T cells
CD 4+ Cells
• AKA: Helper T Cells
• Release cytokines
CD8+ Cells
• AKA: Killer T Cells and Cytotoxic T Cells
• Kill specific targets (assassins)
What is the process of cytokine-mediated inflammation associated with type IV hypersensitivity reactions?
• CD4+ T cell-mediated Type IV hypersensitivity reactions
• When APC presents antigen to CD4+ T cells it differentiates into
• T H1 and TH17 effector lymphocytes
These effector lymphocytes release various chemical mediators to lead to:
• Increase production of effector cells
• Recruitment of macrophages
• Activates macrophages to release pro-inflammatory chemical mediators
Classic example of DTH is the tuberculin reaction
• PPD skin test (purified protein derivative)
• Mantoux test
• Tuberculosis protein antigens are injected into the dermis
• If a person has been previously exposed to this antigen, the body mounts a type IV
hypersensitivity reaction to the antigen
• Takes time for leukocytes and reactions to occur: 24-48 hours
Why does delayed-type hypersensitivity can occur?
• Contact Dermatitis and Drug Reactions are commonly DTH reactions
• Poison ivy exposure is an example
What is the process of direct cell cytotoxicity associated with type IV hypersensitivity reactions?
Direct Cell Cytotoxicity
• CD8+ T cells Type IV hypersensitivity reactions
• Cytotoxic T lymphocytes (CTLs) are created specific for a specific antigen
• DESTROY CELLS DIRECTLY (remember- think assassins)
• CTLs when bind to an antigen on a cell, it goes into KILLER MODE
• CTLs release molecules that ultimately kill the cell:
• Perforins: ”Punch” holes in plasma membrane
• Granzymes: “Enzymes that destroy/kill the cell
Compare and contrast the four types of hypersensitivity reactions
Immediate (type 1) hypersensitivity - Production of IgE antibody
Antibody-mediated (type II) hypersensitivity - Production of IgG, IgM
Immun complex-mediated (type III) hypersensitivity - Deposition of antigen-antibody complexes
Cell-mediated (type IV) hypersensitivity - Activated T lymphocytes
What option is TRUE regarding cytokine–mediated inflammation reaction?
• A) Antibodies activate CD4+ cells
• B) There is recruitment of macrophages
• C) Cells are directly destroyed
• D) There is recruitment of neutrophils
B) There is recruitment of macrophages
All of the options are true regarding type IV hypersensitivity reactions, except?
• A) Activation of cytotoxic T cells leads to cellular death via perforins
• B) Macrophages release pro-inflammatory chemical mediators with cytokine-mediated
inflammation
• C) Both versions utilize antibodies to destroy foreign antigens in the body
• D) The reason there can be delayed type hypersensitivity is due to the time it takes for
leukocytes to be recruited and activated
C) Both versions utilize antibodies to destroy foreign antigens in the body
What is the general process and characteristics to autoimmune disorders?
What are common autoimmune disorders?
What is the meaning of immunologic tolerance and self-tolerance in association with autoimmune disorders?
What are the two mechanisms for self-tolerance the body utilizes?
Compare and contrast central and peripheral tolerance
What are the variables associated with the development of autoimmunity?
Negative selection occurs with peripheral tolerance?
• A) True
• B) False
B) False
A viral infection could be a variable that leads to the development
of an autoimmune disorder?
• A) True
• B) False
A) True
What are the characteristics to systemic lupus erythematous (SLE)?
What is the primary hypersensitivity reaction it is associated with?
What is role within SLE and an anti-nuclear antibody (ANA)?
What is the risk factors to SLE?
What is the epidemiology to SLE?
Why can be challenging to diagnosis of SLE?
What the pathogenesis of SLE?
What is the clinical manifestations of SLE?
What are the signs and symptoms associated with the common clinical manifestations of SLE?
How and why is SLE treated?
SLE is characteristically associated with the production of antibodies
against DNA and DNA associated proteins.
• A) True
• B) False
A) True
All of the following are common clinical manifestations of SLE, except?
• A) Glomerulonephritis
• B) Pericarditis
• C) Retinopathy
• D) Erythematous
C) Retinopathy
Corticosteroids are a common treatment because of their ability to
activate CD4+ cells.
• A) True
• B) False
B) False
What is pathogenesis mechanisms associated with Sjogren’s Syndrome?
What are the hallmark symptoms of Sjogren’s Syndrome?
What is the epidemiology, treatment, and prognosis of Sjogren’s Syndrome?
What is the alternative name associated with systemic sclerosis?
What is the pathogenesis of systemic sclerosis?
What is the overall complication associated with the development of systemic sclerosis?
What is the epidemiology associated with systemic sclerosis?
Compare and contrast diffuse and limited scleroderma
What are the clinical manifestations of system sclerosis and their complications?
What are the effects of corticosteroids?
Why and how are corticosteroids used to treat autoimmune conditions?
All of the options are associated with Sjogren’s Syndrome, except?
• A) Xerostomia
• B) Commonly occurs in individuals older than
• C) Keratoconjunctivitis sicca
• D) Mainly affects men
D) Mainly affects men
All of the options are associated with systemic sclerosis, except?
• A) GI tract dysfunction
• B) Excessive fibrosis being deposited into tissues
• C) Damage to the salivary glands
• D) Skin is the most common location that is affected
C) Damage to the salivary glands
What is the general process and complication associated with immunodeficiency disorders?
What is the term immunocompromised?
What is the two classifications of immunodeficiency disorders?
What are the characteristics associated with primary immunodeficiency?
Compare and contrast the two mechanisms associated with primary immunodeficiency disorders
What are the characteristics to severe combined immunodeficiency (SCID)?
What are the characteristics associated with secondary immunodeficiency?
What are conditions that can lead to secondary immunodeficiency?
Compare and contrast the three mechanisms that can lead to secondary immunodeficiency
Severe combined immunodeficiency (SCID) is associated with:
• A) Viral infection that depletes the function of the immune system
• B) A genetic condition that impairs the development of T and B lymphocytes
• C) Genetic condition that only affects humoral immunity
• D) None of the options are associated with SCID
B) A genetic condition that impairs the development of T and B lymphocytes
All of the following options are mechanisms that can lead to
secondary immunodeficiency, except?
• A) Malnutrition
• B) Chemotherapy
• C) Taking a specific drug
• D) Genetic abnormality
D) Genetic abnormality
Describe the characteristics, etiology, and complications:
• DiGeorge Syndrome
Describe the characteristics, etiology, and complications:
• Goodpasture Syndrome
Describe the characteristics, etiology, and complications:
• Arthus Reaction
Describe the characteristics, etiology, and complications:
• Amyloidosis
This condition is characterized by the absence of T cells within the body?
• A) Goodpasture Syndrome
• B) Amyloidosis
• C) DiGeorge Syndrome
• D) Arthus Reaction
C) DiGeorge Syndrome
This condition is a hypersensitivity reaction associated with complications from injection of
antigens into the body?
• A) Goodpasture Syndrome
• B) Amyloidosis
• C) DiGeorge Syndrome
• D) Arthus Reaction
D) Arthus Reaction
This condition is characterized by alveolar hemorrhaging and glomerulonephritis?
• A) Goodpasture Syndrome
• B) Amyloidosis
• C) DiGeorge Syndrome
• D) Arthus Reaction
A) Goodpasture Syndrome
