Type II Hypersensitivity Reaction

Type II hypersensitivity, also known as antibody-mediated cytotoxic hypersensitivity, is caused by immunoglobulin G (IgG) and IgM antibodies Antibodies Immunoglobulins (Igs), also known as antibodies, are glycoprotein molecules produced by plasma cells that act in immune responses by recognizing and binding particular antigens. The various Ig classes are IgG (the most abundant), IgM, IgE, IgD, and IgA, which differ in their biologic features, structure, target specificity, and distribution. Immunoglobulins directed against antigens on cells or extracellular materials. The reaction leads to cytotoxic processes involving antibodies Antibodies Immunoglobulins (Igs), also known as antibodies, are glycoprotein molecules produced by plasma cells that act in immune responses by recognizing and binding particular antigens. The various Ig classes are IgG (the most abundant), IgM, IgE, IgD, and IgA, which differ in their biologic features, structure, target specificity, and distribution. Immunoglobulins and the complement system. Interference with the normal cellular operation generating either stimulatory or inhibitory dysfunction is another mechanism that occurs. The inciting antigen can be intrinsic or part of the host cell. Extrinsic antigens such as blood products or medications can provoke a similar reaction. For diagnosis, laboratory tests and invasive procedures are utilized, depending on the system affected. Management of resulting disease ranges from supportive care to antibiotics, immunosuppressive medications, and surgery.

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Overview

  • Hypersensitivity reaction
    • A “hyper” or exaggerated response to what should be considered harmless environmental antigens
    • Types I, II, and III are immediate reactions occurring within 24 hours.
    • Type IV reaction develops over several days.
  • Type II hypersensitivity reaction
    • Hypersensitivity reaction mediated by immunoglobulin M (IgM) and IgG antibodies Antibodies Immunoglobulins (Igs), also known as antibodies, are glycoprotein molecules produced by plasma cells that act in immune responses by recognizing and binding particular antigens. The various Ig classes are IgG (the most abundant), IgM, IgE, IgD, and IgA, which differ in their biologic features, structure, target specificity, and distribution. Immunoglobulins (Ab) that bind to:
      • Intrinsic antigens on cell surfaces (e.g., RBCs) or extracellular materials (e.g., basement membrane)
      • Extrinsic antigens (e.g., blood products, drugs)
    • Antibody (AB)-antigen complex leads to processes resulting in cell lysis, tissue damage, and/or dysfunction.

Pathophysiology

Activation of the complement system

The following mechanisms are triggered by the binding of Ab-antigen complexes:

  • Complements: large, distinct proteins involved in a sequential enzyme cascade for host defense
  • Complement numbers (C1-4) do not indicate the order of activation; they reflect the order of discovery.
  • Pathways from C1 are mobilized by Ab-antigen complexes → C3 → cleaved to C3a and C3b → C3b cleaves C5 to C5a and C5b
  • C3a, C4a, and C5a
    • Mediators of inflammation Inflammation Inflammation is a complex set of responses to infection and injury involving leukocytes as the principal cellular mediators in the body's defense against pathogenic organisms. Inflammation is also seen as a response to tissue injury in the process of wound healing. The 5 cardinal signs of inflammation are pain, heat, redness, swelling, and loss of function. Inflammation = anaphylatoxins
    • Mast cell and basophil degranulation
    • C5a also causes neutrophil chemotaxis.
  • C5b and C6, C7, C8, C9: 
    • Membrane attack complex (MAC) 
    • Attaches to cell membrane Cell Membrane A cell membrane (also known as the plasma membrane or plasmalemma) is a biological membrane that separates the cell contents from the outside environment. A cell membrane is composed of a phospholipid bilayer and proteins that function to protect cellular DNA and mediate the exchange of ions and molecules. The Cell: Cell Membrane and creates ion-permeable channels causing osmotic changes and cell lysis
  • C3b: 
    • An opsonin (tags antigens for elimination by phagocytes = opsonization) mediating phagocytosis of target cells
  • Examples: transfusion reaction, autoimmune hemolytic anemia Autoimmune Hemolytic Anemia Autoimmune hemolytic anemia (AIHA) is a rare type of hemolytic anemia characterized by antibody production against self RBCs, leading to destruction of these cells in the spleen and other reticuloendothelial tissues. The disease is generally categorized as warm or cold, depending on the thermal reactivity of the autoantibodies. Autoimmune Hemolytic Anemia

Antibody-dependent cell-mediated cytotoxicity (ADCC)

  • Antibodies, or opsonins, bind their antigen-binding fragment (Fab) sites to antigens and tag them for phagocytosis.
  • If antigen-Ab complexes are too large to be phagocytosed, Fc-receptor–bearing effector cells, mainly natural killer (NK) cells, are recruited.
  • NK cells bind to Fc receptor of Ab → release toxic granules into cells → perforin and granzymes boreholes in membrane → cell lysis 
    • Examples: transplant rejection, immune reaction against neoplasm

Antibody-mediated cellular dysfunction

  • Non-cytotoxic; cell function impaired without cell injury Cell injury The cell undergoes a variety of changes in response to injury, which may or may not lead to cell death. Injurious stimuli trigger the process of cellular adaptation, whereby cells respond to withstand the harmful changes in their environment. Overwhelmed adaptive mechanisms lead to cell injury. Mild stimuli produce reversible injury. If the stimulus is severe or persistent, injury becomes irreversible. Cell Injury and Death or inflammation Inflammation Inflammation is a complex set of responses to infection and injury involving leukocytes as the principal cellular mediators in the body's defense against pathogenic organisms. Inflammation is also seen as a response to tissue injury in the process of wound healing. The 5 cardinal signs of inflammation are pain, heat, redness, swelling, and loss of function. Inflammation
  • Autoantibodies bind to cell-surface receptors to produce an abnormal activation/blockade of the signaling process. 
  • Examples: 
    • Myasthenia gravis Myasthenia Gravis Myasthenia gravis (MG) is an autoimmune neuromuscular disorder characterized by weakness and fatigability of skeletal muscles caused by dysfunction/destruction of acetylcholine receptors at the neuromuscular junction. MG presents with fatigue, ptosis, diplopia, dysphagia, respiratory difficulties, and progressive weakness in the limbs, leading to difficulty in movement. Myasthenia Gravis (Ab causes blockade of acetylcholine receptor)
    • Graves’ disease (Ab causes stimulation of thyroid stimulating hormone (TSH) receptor) 
    • Pernicious anemia (Ab against intrinsic factor)
Antibody-dependent cellular cytotoxicity hypersensitivity

Antibody-dependent cellular or cell-mediated cytotoxicity: antibody binds the surface antigens of the target cell. Fc-bearing effector cell (natural killer or NK cell) binds the antibody Fc region and releases cytotoxic granules leading to lysis of the target cell.

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Clinical Presentation

Type II hypersensitivity can result from the following conditions:

Transfusion reactions Transfusion reactions Transfusion-related complications occur during or after a blood product is given. These complications can be classified as immunologic, non-immunologic and acute, and delayed. Non-immunologic reactions are caused by the transmission of disease in blood products, and immunologic reactions are antigen-antibody-mediated. Transfusion Reactions (ABO or blood group incompatibility)

  • Blood group A or O recipient would react with a type AB or B donor (due to the presence of anti-B antibodies Antibodies Immunoglobulins (Igs), also known as antibodies, are glycoprotein molecules produced by plasma cells that act in immune responses by recognizing and binding particular antigens. The various Ig classes are IgG (the most abundant), IgM, IgE, IgD, and IgA, which differ in their biologic features, structure, target specificity, and distribution. Immunoglobulins)
  • Blood group B or O recipient would react with type A or AB donor (due to the presence of anti-A antibodies Antibodies Immunoglobulins (Igs), also known as antibodies, are glycoprotein molecules produced by plasma cells that act in immune responses by recognizing and binding particular antigens. The various Ig classes are IgG (the most abundant), IgM, IgE, IgD, and IgA, which differ in their biologic features, structure, target specificity, and distribution. Immunoglobulins)
  • Symptoms: fever Fever Fever is defined as a measured body temperature of at least 38°C (100.4°F). Fever is caused by circulating endogenous and/or exogenous pyrogens that increase levels of prostaglandin E2 in the hypothalamus. Fever is commonly associated with chills, rigors, sweating, and flushing of the skin. Fever, itching, urticaria Urticaria Urticaria is raised, well-circumscribed areas (wheals) of edema (swelling) and erythema (redness) involving the dermis and epidermis with associated pruritus (itch). Urticaria is not a single disease but rather is a reaction pattern representing cutaneous mast cell degranulation. Urticaria (Hives); serious reaction results in respiratory distress and hypotension Hypotension Hypotension is defined as low blood pressure, specifically < 90/60 mm Hg, and is most commonly a physiologic response. Hypotension may be mild, serious, or life threatening, depending on the cause. Hypotension
Transfusion reactions induced by type ii hypersensitivity reactions

Transfusion reactions Transfusion reactions Transfusion-related complications occur during or after a blood product is given. These complications can be classified as immunologic, non-immunologic and acute, and delayed. Non-immunologic reactions are caused by the transmission of disease in blood products, and immunologic reactions are antigen-antibody-mediated. Transfusion Reactions induced by type II hypersensitivity reactions. This diagram shows blood type groups and their corresponding antibodies Antibodies Immunoglobulins (Igs), also known as antibodies, are glycoprotein molecules produced by plasma cells that act in immune responses by recognizing and binding particular antigens. The various Ig classes are IgG (the most abundant), IgM, IgE, IgD, and IgA, which differ in their biologic features, structure, target specificity, and distribution. Immunoglobulins and antigens.

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Autoimmune hemolytic anemia (against RBCs)

  • Can be IgG-mediated (warm autoimmune hemolytic anemia Autoimmune Hemolytic Anemia Autoimmune hemolytic anemia (AIHA) is a rare type of hemolytic anemia characterized by antibody production against self RBCs, leading to destruction of these cells in the spleen and other reticuloendothelial tissues. The disease is generally categorized as warm or cold, depending on the thermal reactivity of the autoantibodies. Autoimmune Hemolytic Anemia) or IgM-mediated (cold autoimmune hemolytic anemia Autoimmune Hemolytic Anemia Autoimmune hemolytic anemia (AIHA) is a rare type of hemolytic anemia characterized by antibody production against self RBCs, leading to destruction of these cells in the spleen and other reticuloendothelial tissues. The disease is generally categorized as warm or cold, depending on the thermal reactivity of the autoantibodies. Autoimmune Hemolytic Anemia)
  • Manifested by weakness, shortness of breath, pallor from anemia to jaundice Jaundice Jaundice is the abnormal yellowing of the skin and/or sclera caused by the accumulation of bilirubin. Hyperbilirubinemia is caused by either an increase in bilirubin production or a decrease in the hepatic uptake, conjugation, or excretion of bilirubin. Jaundice, icterus, dark urine from hemolysis

Pernicious anemia (against intrinsic factor)

  1. Ab prevents absorption of vitamin B12, causing B12 deficiency anemia.
  2. B12 deficiency can lead to general symptoms of anemia, glossitis, paresthesias, gait problems.

Hemolytic disease of the fetus and newborn Hemolytic disease of the fetus and newborn Hemolytic disease of the fetus and newborn (HDFN), also known as erythroblastosis fetalis, is caused by maternal IgG antibody destruction of the fetal RBCs. Rhesus (Rh) blood group incompatibility (frequently triggered by D antigen) and ABO incompatibility are common causes. Hemolytic Disease of the Fetus and Newborn (against RBCs; RhD incompatibility)

  • First pregnancy Pregnancy Pregnancy is the time period between fertilization of an oocyte and delivery of a fetus approximately 9 months later. The 1st sign of pregnancy is typically a missed menstrual period, after which, pregnancy should be confirmed clinically based on a positive β-hCG test (typically a qualitative urine test) and pelvic ultrasound. Pregnancy: Diagnosis, Maternal Physiology, and Routine Care: Rhesus-negative woman conceives a rhesus-positive fetus.
  • Labor Labor Labor is the normal physiologic process defined as uterine contractions resulting in dilatation and effacement of the cervix, which culminates in expulsion of the fetus and the products of conception. Normal and Abnormal Labor: During labor, fetal RBCs leak into the mother.
  • Postpartum: Fetal RBCs survive long enough to elicit an IgG response.
  • Second pregnancy Pregnancy Pregnancy is the time period between fertilization of an oocyte and delivery of a fetus approximately 9 months later. The 1st sign of pregnancy is typically a missed menstrual period, after which, pregnancy should be confirmed clinically based on a positive β-hCG test (typically a qualitative urine test) and pelvic ultrasound. Pregnancy: Diagnosis, Maternal Physiology, and Routine Care: Maternal anti-D antibodies Antibodies Immunoglobulins (Igs), also known as antibodies, are glycoprotein molecules produced by plasma cells that act in immune responses by recognizing and binding particular antigens. The various Ig classes are IgG (the most abundant), IgM, IgE, IgD, and IgA, which differ in their biologic features, structure, target specificity, and distribution. Immunoglobulins cross the placenta Placenta The placenta consists of a fetal side and a maternal side, and it provides a vascular communication between the mother and the fetus. This communication allows the mother to provide nutrients to the fetus and allows for removal of waste products from fetal blood. Placenta, Umbilical Cord, and Amniotic Cavity and attack fetal RBCs of the second rhesus-positive fetus.
  • Newborns may present with self-limiting hemolytic anemia to hydrops fetalis (severe anemia, skin Skin The skin, also referred to as the integumentary system, is the largest organ of the body. The skin is primarily composed of the epidermis (outer layer) and dermis (deep layer). The epidermis is primarily composed of keratinocytes that undergo rapid turnover, while the dermis contains dense layers of connective tissue. Structure and Function of the Skin edema Edema Edema is a condition in which excess serous fluid accumulates in the body cavity or interstitial space of connective tissues. Edema is a symptom observed in several medical conditions. It can be categorized into 2 types, namely, peripheral (in the extremities) and internal (in an organ or body cavity). Edema, ascites Ascites Ascites is the pathologic accumulation of fluid within the peritoneal cavity that occurs due to an osmotic and/or hydrostatic pressure imbalance secondary to portal hypertension (cirrhosis, heart failure) or non-portal hypertension (hypoalbuminemia, malignancy, infection). Ascites, pulmonary/ pericardial effusion Pericardial effusion Pericardial effusion is the accumulation of excess fluid in the pericardial space around the heart. The pericardium does not easily expand; thus, rapid fluid accumulation leads to increased pressure around the heart. The increase in pressure restricts cardiac filling, resulting in decreased cardiac output and cardiac tamponade. Pericardial Effusion and Cardiac Tamponade).

Autoimmune thrombocytopenic purpura

  • Phagocytes destroy sensitized platelets Platelets Platelets are small cell fragments involved in hemostasis. Thrombopoiesis takes place primarily in the bone marrow through a series of cell differentiation and is influenced by several cytokines. Platelets are formed after fragmentation of the megakaryocyte cytoplasm. Platelets in the blood.
  • Increased bleeding risk: < 20,000/μL
  • Can have petechiae, purpura, epistaxis to severe hemorrhage

Acute rheumatic fever Rheumatic fever Acute rheumatic fever (ARF) is an autoimmune inflammatory process that usually follows Streptococcal pharyngitis. Acute rheumatic fever usually occurs 2-4 weeks after an untreated infection and affects the heart, skin, joints, and nervous system. Rheumatic Fever

  • Antibodies against the cell wall of Streptococcus Streptococcus Streptococcus is one of the two medically important genera of gram-positive cocci, the other being Staphylococcus. Streptococci are identified as different species on blood agar on the basis of their hemolytic pattern and sensitivity to optochin and bacitracin. There are many pathogenic species of streptococci, including S. pyogenes, S. agalactiae, S. pneumoniae, and the viridans streptococci. Streptococcus also react with the myocardium.
  • Major manifestations: arthritis, carditis, Sydenham chorea, subcutaneous nodules, erythema marginatum

Goodpasture syndrome Goodpasture Syndrome Goodpasture syndrome, also known as anti-glomerular basement membrane (GBM) disease, is an autoimmune disease characterized by circulating antibodies directed against glomerular and alveolar basement membranes. Affected individuals present with symptoms of rapidly progressive glomerulonephritis and alveolar hemorrhage. Goodpasture Syndrome

  • Antibodies attack antigens in the basement membrane of alveoli (pulmonary hemorrhage) and kidneys Kidneys The kidneys are a pair of bean-shaped organs located retroperitoneally against the posterior wall of the abdomen on either side of the spine. As part of the urinary tract, the kidneys are responsible for blood filtration and excretion of water-soluble waste in the urine. Kidneys (nephritis).
  • Initially presents with systemic complaints, followed by renal (hematuria) and pulmonary symptoms ( dyspnea Dyspnea Dyspnea is the subjective sensation of breathing discomfort. Dyspnea is a normal manifestation of heavy physical or psychological exertion, but also may be caused by underlying conditions (both pulmonary and extrapulmonary). Dyspnea, hemoptysis Hemoptysis Hemoptysis is defined as the expectoration of blood originating in the lower respiratory tract. Hemoptysis is a consequence of another disease process and can be classified as either life threatening or non-life threatening. Hemoptysis can result in significant morbidity and mortality due to both drowning (reduced gas exchange as the lungs fill with blood) and hemorrhagic shock. Hemoptysis, cough)

Graves’ disease

  • TSH-receptor antibodies Antibodies Immunoglobulins (Igs), also known as antibodies, are glycoprotein molecules produced by plasma cells that act in immune responses by recognizing and binding particular antigens. The various Ig classes are IgG (the most abundant), IgM, IgE, IgD, and IgA, which differ in their biologic features, structure, target specificity, and distribution. Immunoglobulins stimulate the thyroid gland Thyroid gland The thyroid gland is one of the largest endocrine glands in the human body. The thyroid gland is a highly vascular, brownish-red gland located in the visceral compartment of the anterior region of the neck. Thyroid Gland to produce free T4 and T3 without TSH.
  • Goiter Goiter A goiter is a chronic enlargement of the thyroid gland due to nonneoplastic growth occurring in the setting of hypothyroidism, hyperthyroidism, or euthyroidism. Morphologically, thyroid enlargement can be diffuse (smooth consistency) or nodular (uninodular or multinodular). Goiter, exophthalmos on exam with symptoms such as heat intolerance, anxiety, tremors, palpitations, weight loss.

Myasthenia gravis Myasthenia Gravis Myasthenia gravis (MG) is an autoimmune neuromuscular disorder characterized by weakness and fatigability of skeletal muscles caused by dysfunction/destruction of acetylcholine receptors at the neuromuscular junction. MG presents with fatigue, ptosis, diplopia, dysphagia, respiratory difficulties, and progressive weakness in the limbs, leading to difficulty in movement. Myasthenia Gravis

  • Antibodies inhibit the binding of acetylcholine to the nicotinic acetylcholine receptor. 
  • Antibodies also activate complement-mediated receptor destruction.
  • Fluctuating muscle weakness, worse at the end of the day or after exercise (ptosis, diplopia, fatigable chewing, limb weakness)
  • Respiratory muscle weakness leads to respiratory failure Respiratory failure Respiratory failure is a syndrome that develops when the respiratory system is unable to maintain oxygenation and/or ventilation. Respiratory failure may be acute or chronic and is classified as hypoxemic, hypercapnic, or a combination of the two. Respiratory Failure (myasthenia crisis).
Mechanism of grave's disease and myasthenia gravis

Mechanism of Graves’ disease (left) and Myasthenia gravis Myasthenia Gravis Myasthenia gravis (MG) is an autoimmune neuromuscular disorder characterized by weakness and fatigability of skeletal muscles caused by dysfunction/destruction of acetylcholine receptors at the neuromuscular junction. MG presents with fatigue, ptosis, diplopia, dysphagia, respiratory difficulties, and progressive weakness in the limbs, leading to difficulty in movement. Myasthenia Gravis (right), both caused by type II hypersensitivity mechanism.

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Diagnosis and Management

Diagnosis and management vary depending on the manifestations, organ system involved, and severity of impairment produced by the reaction.

Transfusion reactions Transfusion reactions Transfusion-related complications occur during or after a blood product is given. These complications can be classified as immunologic, non-immunologic and acute, and delayed. Non-immunologic reactions are caused by the transmission of disease in blood products, and immunologic reactions are antigen-antibody-mediated. Transfusion Reactions

  • Diagnosis: clinical; Coombs test
  • Management: cessation of transfusion, repeat of blood typing and crossmatching and supportive care ( disseminated intravascular coagulation Disseminated intravascular coagulation Disseminated intravascular coagulation (DIC) is a condition characterized by systemic bodywide activation of the coagulation cascade. This cascade results in both widespread microvascular thrombi contributing to multiple organ dysfunction and consumption of clotting factors and platelets, leading to hemorrhage. Disseminated Intravascular Coagulation ( DIC DIC Disseminated intravascular coagulation (DIC) is a condition characterized by systemic bodywide activation of the coagulation cascade. This cascade results in both widespread microvascular thrombi contributing to multiple organ dysfunction and consumption of clotting factors and platelets, leading to hemorrhage. Disseminated Intravascular Coagulation) work-up depending on severity of reaction)

Autoimmune hemolytic anemia

  • Diagnosis: hemolysis work-up; Coombs test
  • Management (first-line): glucocorticoids Glucocorticoids Glucocorticoids are a class within the corticosteroid family. Glucocorticoids are chemically and functionally similar to endogenous cortisol. There are a wide array of indications, which primarily benefit from the antiinflammatory and immunosuppressive effects of this class of drugs. Glucocorticoids; treat the underlying condition
  • Refractory cases may require immunosuppressive drugs, splenectomy.

Pernicious anemia

  • Diagnosis: CBC, B12, folate Folate Folate and vitamin B12 are 2 of the most clinically important water-soluble vitamins. Deficiencies can present with megaloblastic anemia, GI symptoms, neuropsychiatric symptoms, and adverse pregnancy complications, including neural tube defects. Folate and Vitamin B12 level with confirmatory tests if with borderline levels
  • Management: B12 supplementation

Hemolytic disease of the fetus and newborn Hemolytic disease of the fetus and newborn Hemolytic disease of the fetus and newborn (HDFN), also known as erythroblastosis fetalis, is caused by maternal IgG antibody destruction of the fetal RBCs. Rhesus (Rh) blood group incompatibility (frequently triggered by D antigen) and ABO incompatibility are common causes. Hemolytic Disease of the Fetus and Newborn

  • Diagnosis: pregnancy Pregnancy Pregnancy is the time period between fertilization of an oocyte and delivery of a fetus approximately 9 months later. The 1st sign of pregnancy is typically a missed menstrual period, after which, pregnancy should be confirmed clinically based on a positive β-hCG test (typically a qualitative urine test) and pelvic ultrasound. Pregnancy: Diagnosis, Maternal Physiology, and Routine Care history, maternal antibodies Antibodies Immunoglobulins (Igs), also known as antibodies, are glycoprotein molecules produced by plasma cells that act in immune responses by recognizing and binding particular antigens. The various Ig classes are IgG (the most abundant), IgM, IgE, IgD, and IgA, which differ in their biologic features, structure, target specificity, and distribution. Immunoglobulins, ultrasound, fetal lab tests
  • Prevention: anti-RhD at 28 weeks’ gestation and within 72 hours of birth

Autoimmune thrombocytopenic purpura

  • Diagnosis: clinical with CBC, peripheral smear, HIV, hepatitis C Hepatitis C Hepatitis C is an infection of the liver caused by the hepatitis C virus (HCV). The infection can be transmitted through infectious blood or body fluids and may be transmitted during childbirth or through IV drug use or sexual intercourse. Hepatitis C virus can cause both acute and chronic hepatitis, ranging from a mild to a serious, lifelong illness including liver cirrhosis and hepatocellular carcinoma (HCC). Hepatitis C Virus, and other tests based on history
  • Goal of management: prevent clinically important bleeding
  • If with bleeding, management may include: platelet transfusion, intravenous immunoglobulin (IVIG), glucocorticoids Glucocorticoids Glucocorticoids are a class within the corticosteroid family. Glucocorticoids are chemically and functionally similar to endogenous cortisol. There are a wide array of indications, which primarily benefit from the antiinflammatory and immunosuppressive effects of this class of drugs. Glucocorticoids

Acute rheumatic fever Rheumatic fever Acute rheumatic fever (ARF) is an autoimmune inflammatory process that usually follows Streptococcal pharyngitis. Acute rheumatic fever usually occurs 2-4 weeks after an untreated infection and affects the heart, skin, joints, and nervous system. Rheumatic Fever

  • Diagnosis: lab tests (C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), antistreptolysin O (ASO)) with Jones criteria, echocardiogram
  • Management: antibiotics for Streptococcus Streptococcus Streptococcus is one of the two medically important genera of gram-positive cocci, the other being Staphylococcus. Streptococci are identified as different species on blood agar on the basis of their hemolytic pattern and sensitivity to optochin and bacitracin. There are many pathogenic species of streptococci, including S. pyogenes, S. agalactiae, S. pneumoniae, and the viridans streptococci. Streptococcus and supportive care

Goodpasture syndrome Goodpasture Syndrome Goodpasture syndrome, also known as anti-glomerular basement membrane (GBM) disease, is an autoimmune disease characterized by circulating antibodies directed against glomerular and alveolar basement membranes. Affected individuals present with symptoms of rapidly progressive glomerulonephritis and alveolar hemorrhage. Goodpasture Syndrome

  • Diagnosis: clinical along with labs (antineutrophil cytoplasmic antibodies Antibodies Immunoglobulins (Igs), also known as antibodies, are glycoprotein molecules produced by plasma cells that act in immune responses by recognizing and binding particular antigens. The various Ig classes are IgG (the most abundant), IgM, IgE, IgD, and IgA, which differ in their biologic features, structure, target specificity, and distribution. Immunoglobulins (ANCA), anti-glomerular basement membrane (anti-GBM) Ab), renal biopsy
  • Management: plasmapheresis and immunosuppressive therapy

Graves’ disease

  • Diagnosis: TSH-receptor Ab confirms diagnosis; thyroid function tests
  • Management: symptom control (beta-blockers) and reduction of thyroid hormone synthesis (antithyroid drugs, radioiodine, or thyroidectomy)

Myasthenia gravis Myasthenia Gravis Myasthenia gravis (MG) is an autoimmune neuromuscular disorder characterized by weakness and fatigability of skeletal muscles caused by dysfunction/destruction of acetylcholine receptors at the neuromuscular junction. MG presents with fatigue, ptosis, diplopia, dysphagia, respiratory difficulties, and progressive weakness in the limbs, leading to difficulty in movement. Myasthenia Gravis

  • Diagnosis: single-fiber electromyography (most sensitive) and immunologic studies
  • Management: pyridostigmine, immunotherapies, and thymectomy

References

  1. Brodsky, R.; Mentzer, W. (Ed.); Tirnauer, J. (Ed.). (2019). Diagnosis of hemolytic anemia. UpToDate. Retrieved Aug 17, 2020, from https://www.uptodate.com/contents/diagnosis-of-hemolytic-anemia-in-adults
  2. Davies, T.; Ross, D. & Mulder, J. (Eds.). (2019). Pathogenesis of Graves disease. UpToDate.  Retrieved Aug 18, 2020, from https://www.uptodate.com/contents/pathogenesis-of-graves-disease
  3. Bird, S.; Shefner, J. & Goddeau, R. (Eds.). (2020). Pathogenesis of Myasthenia gravis Myasthenia Gravis Myasthenia gravis (MG) is an autoimmune neuromuscular disorder characterized by weakness and fatigability of skeletal muscles caused by dysfunction/destruction of acetylcholine receptors at the neuromuscular junction. MG presents with fatigue, ptosis, diplopia, dysphagia, respiratory difficulties, and progressive weakness in the limbs, leading to difficulty in movement. Myasthenia Gravis. UpToDate. Retrieved Aug 17, 2020, from https://www.uptodate.com/contents/pathogenesis-of-myasthenia-gravis
  4. Mak, T.; Saunders, M.; Jett, B. (2007). Primer to the Immune response. Elsevier.
  5. Pranay, K.; Sanghera, P.; Batuman, V. (Ed.). (2018). Goodpasture syndrome Goodpasture Syndrome Goodpasture syndrome, also known as anti-glomerular basement membrane (GBM) disease, is an autoimmune disease characterized by circulating antibodies directed against glomerular and alveolar basement membranes. Affected individuals present with symptoms of rapidly progressive glomerulonephritis and alveolar hemorrhage. Goodpasture Syndrome. Medscape. https://emedicine.medscape.com/article/240556-overview

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