Q: What are the causes and signs of calcium ion deficiency?
A: -Kids- rickets
A: -Adults- osteomalacia
A: -Contributes to osteoporosis
A: -Tetany
Q: What are the causes and signs of phosphate toxicity?
A: -Low serum calcium ion
A: -can cause bone loss
A: -renal stones
Q: What are the causes of chloride ion deficiency?
A: Secondary to emesis, diuretics, renal disease
Q: What are the causes of metabolic acidosis?
A: -Diabetic ketoacidosis
A: -Diarrhea
A: -Lactic Acidosis
A: -Salicylate OD
A: -Acetazolamide OD
Q: What are the causes of respiratory acidosis?
A: -COPD
A: -Airway obstruction
Q: What are the causes of respiratory alkalosis?
A: -High altitude
A: -Hyperventilation
Q: What are the characteristics of acute poststreptococcal glomerulonephritis seen with immunofluorescence?
A: Granular pattern
Q: What are the characteristics of acute poststreptococcal glomerulonephritis seen with the electron microscope?
A: Subepithelial humps
Q: What are the characteristics of acute poststreptococcal glomerulonephritis seen with the light microscope?
A: Glomeruli enlarged and hypercellular
A: neutrophils
A: 'lumpy-bumpy'
Q: What are the characteristics of rapidly progressive (crescentic) glomerulonephritis seen on LM and IF?
A: Crescent-moon shape
Q: What are the clinical features of renal cell carcinoma?
A: -Hematuria
A: -Palpable mass
A: -Secondary polycythemia
A: -Flank pain
A: -Fever
Q: What are the clinical symptoms of a nephritic syndrome?
A: I' = inflammation; hematuria, hypertension, oligouria, azotemia
Q: What are the clinical symptoms of nephrotic syndromes?
A: O = proteinuria
A: Hypoalbuminuria
A: Generalized edema
A: Hyperlipidemia
Q: What are the consequences of renal failure?
A: 1. Anemia
A: 2. Renal osteodystrophy
A: 3. Hyperkalemia
A: 4. Metabolic acidosis
A: 5. Uremia
A: 6. Sodium and water excess
A: 7. Chronic pyelonephritis
A: 8. HTN
Q: What are the factors associated metabolic alkalosis?
A: -Increased pH
A: -Increased PCO2
A: -Increased HCO3-
Q: What are the factors associated with metabolic acidosis?
A: -Decreased pH
A: -Decreased PCO2
A: -Decreased HCO3-
Q: What are the factors associated with respiratory acidosis?
A: -Decreased pH
A: -Increased PCO2
A: -Increased HCO3-
Q: What are the factors associated with respiratory alkalosis?
A: -Increased pH
A: -Decreased PCO2
A: -Decreased HCO3-
Q: What are the functions of calcium ion?
A: -Muscle contraction
A: -Neurotransmitter release
A: -Bones, teeth
Q: What are the functions of sodium ion?
A: -Extracellular fluid
A: -Maintains plasma volume
A: -Nerve/muscle function
Q: What are the functions of the chloride ion?
A: -Fluid/electrolyte balance
A: -Gastric acid
A: -HCO3/Cl shift in RBC
Q: What are the functions of the magnesium ion?
A: -Bones, teeth
A: -Enzyme cofactor
Q: What are the functions of the phosphate ion?
A: -ATP
A: -nucleic acids
A: -Phosphorylation
A: -Bones, teeth
Q: What are the functions of the potassium ion?
A: -Intracellular fluid
A: -Nerve/muscle function
Q: What are the signs of magnesium ion deficiency?
A: -Diarrhea
A: -Alcoholism
Q: What are the signs of magnesium ion toxicity?
A: -Decreased reflexes
A: -Decreased respirations
Q: What are the signs of phosphate deficiency?
A: -Kids- rickets
A: -Adults- osteomalacia
Q: What are the signs of potassium ion toxicity?
A: -EKG changes
A: -Arrhythmia
Q: What bugs cause ammonium magnesium phosphate kidney stones?
A: Urease-positive bugs such as Proteus vulgaris or Staphylococcus
Q: What calcium molecules form calcium kidney stones?
A: Calcium oxalate or calcium phosphate or both
Q: What can excess Na and water cause?
A: CHF and pulmonary edema
Q: What can the hyperkalemia associated with renal failure lead to?
A: Cardiac arrhythmias
Q: What causes metabolic alkalosis?
A: 1. Vomiting
A: 2. Diuretic use
A: 3. Antacid use
A: 4. Hyperaldosteronism
Q: What causes renal osteodystrophy?
A: Failure of active vitamin D production
Q: What characteristics of Berger's disease are seen with IF and EM?
A: Mesangial deposits of IgA
Q: What characteristics of focal segmental glomerular sclerosis are seen with the LM?
A: Segmental sclerosis and hyalinosis
Q: What characteristics of Goodpasture's syndrome are seen with IF?
A: Linear pattern
A: Anti-glomerular basement membrane antibodies
Q: What characteristics of Membranoproliferative glomerulonephritis are seen with the EM?
A: subendothelial humps
A: 'tram track'
Q: What characteristics of membranous glomerulonephritis are seen with IF?
A: Granular pattern
Q: What characteristics of membranous glomerulonephritis are seen with the EM?
A: Spike and Dome'
Q: What characteristics of membranous glomerulonephritis are seen with the LM?
A: Diffuse capillary and basement membrane thickening
Q: What characteristics of minimal change disease are seen with the EM?
A: Foot process effacement
Q: What characteristics of minimal change disease are seen with the LM?
A: Normal glomeruli
Q: What characteristics of SLE are seen with the LM?
A: Wire-loop appearance with extensive granular subendothelial basement-membrane deposits in membranous glomerulonephritis pattern
Q: What defines metabolic acidosis?
A: -pH less than 7.4
A: -PCO2 less than 40 mm Hg
Q: What defines metabolic alkalosis with compensation?
A: -pH greater than 7.4
A: -PCO2 greater than 40 mm Hg
Q: What defines respiratory acidosis?
A: -pH less than 7.4
A: -PCO2 greater than 40mm Hg
Q: What defines respiratory alkalosis?
A: -pH greater than 7.4
A: -PCO2 less than 40 mm Hg
Q: What diseases often cause uric acid kidney stones?
A: Diseases with increased cell proliferation and turnover, such as leukemia and myeloproliferative disorders
Q: What disorders can lead to hypercalcemia and thus kidney stones?
A: 1. Cancer
A: 2. Increased PTH
A: 3. Increased vitamin D
A: 4. Milk-alkali syndrome
Q: What disorders cause an increased anion gap?
A: 1. Renal failure
A: 2. Lactic acidosis
A: 3. Ketoacidosis (DM
)
A: 4. Aspirin ingestion
Q: What disorders cause metabolic acidosis and normal anion gap?
A: 1. Diarrhea
A: 2. Glue sniffing
A: 3. Renal tubular acidosis
A: 4. Hyperchloremia
Q: What disorders make up the WAGR complex?
A: Wilms' tumor
A: Aniridia
A: Genitourinary malformation
A: mental-motor Retardation
Q: What does potassium deficiency cause?
A: -Weakness
A: -Paralysis
A: -Confusion
Q: What factors are associated with transitional cell carcinoma?
A: Exposure to cyclophosphamide, smoking, phenacetin, and aniline dyes
Q: What genetic disorder and mutation are associated with renal cell carcinoma?
A: Renal cell carcinoma is associated with von Hippel-Lindau and gene deletion in chromosome 3
Q: What genetic disorder is associated with Wilms' tumor?
A: Deletion of tumor suppression gene WT-1 on chromosome 11
Q: What is a common cause of adult nephrotic syndrome?
A: Membranous glomerulonephritis
Q: What is acute renal failure often due to?
A: Hypoxia
Q: What is Berger's disease?
A: IgA nephropathy
A: -Mild disease
A: -Often postinfectious
Q: What is chronic failure due to?
A: HTN and diabetes
Q: What is the 2nd most common type of kidney stone?
A: Ammonium magnesium phosphate
Q: What is the cause of magnesium ion deficiency?
A: Secondary to malabsorption
Q: What is the cause of metabolic alkalosis?
A: Vomiting
Q: What is the cause of potassium ion deficiency?
A: Secondary to injury, illness or diuretics
Q: What is the cause of sodium deficiency?
A: Secondary to injury or illness
Q: What is the compensatory mechanism of metabolic alkalosis?
A: Hypoventilation
Q: What is the compensatory mechanism of respiratory alkalosis?
A: Renal HCO3- secretion
Q: What is the compensatory response to metabolic acidosis?
A: Hyperventilation
Q: What is the compensatory response to respiratory acidosis?
A: Renal HCO3- reabsorption
Q: What is the course of membranoproliferative glomerulonephritis?
A: Slowly progresses to renal failure
Q: What is the course of rapidly progressive (crescentic) glomerulonephritis?
A: Rapid course to renal failure from one of many causes
Q: What is the Henderson-Hasselbalch equation?
A: pH = pKa + log [(HCO3-)/(0.03*PCO2)]
Q: What is the most common cause of childhood nephrotic syndrome?
A: Minimal change disease (lipoid nephrosis)
Q: What is the most common renal malignancy of early childhood (ages 2-4)?
A: Wilms' tumor
Q: What is the most common renal malignancy?
A: Renal cell carcinoma
Q: What is the most common tumor of the urinary tract system?
A: Transitional cell carcinoma
Q: What is the primary disturbance in respiratory acidosis?
A: Increased PCO2
Q: What is the primary disturbance of metabolic acidosis?
A: HCO3- decrease
Q: What is the primary disturbance of metabolic alkalosis?
A: Increased HCO3-
Q: What is the primary disturbance of respiratory alkalosis?
A: Decreased PCO2
Q: What is the sign of calcium ion toxicity?
A: Delirium
Q: What is the sign of sodium ion toxicity?
A: Delirium
Q: What lesions are seen on the LM in diabetic nephropathy?
A: Kimmelstiel-Wilson lesions
Q: What might an elevated anion gap indicate?
A: MUD PILES
A: 1. Methanol
A: 2. Uremia (chronic renal failure)
A: 3. Diabetic ketoacidosis
A: 4. Paraldehyde or Phenformin
A: 5. Iron tablets or INH
A: 6. Lactic acidosis (CN-, CO, shock)
A: 7. Ethanol or Ethylene glycol
A: 8. Salicylates
Q: What paraneoplastic syndromes are associated with renal cell carcinoma?
A: Ectopic EPO, ACTH, PTHrP, and prolactin
Q: What severe complications may kidney stones lead to?
A: Hydronephrosis
A: Pyelonephritis
Q: What social factor increases the incidence of renal cell carcinoma?
A: Smoking
Q: What type of hypersensitivity contributes to the pathogenesis of Goodpasture's syndrome?
A: Type II hypersensitivity
Q: Where can transitional cell carcinoma occur?
A: -Renal calyces
A: -Renal pelvis
A: -Ureters
A: -Bladder
Q: Where does renal cell carcinoma originate?
A: Renal tubule cells, polygonal clear cells
Q: Which kidney stone is often secondary to cystinuria?
A: Cystine
Q: Which kidney stone is strongly associated with gout?
A: Uric acid kidney stones
Q: Which of the nephrotic syndromes are worse in HIV pts?
A: Focal segmental glomerular sclerosis
Q: Which type of kidney stones constitute the majority of kidney stones (80-85%)?
A: Calcium
Q: Why are ammonium magnesium phosphate kidney stones often associated with UTIs?
A: Ammonium magnesium phosphate stones can form large struvite calculi that can be a nidus for UTIs
Q: Why does renal failure cause anemia?
A: Failure of EPO production
Q: Why does renal failure cause metabolic acidosis?
A: Due to decreased acid secretion and decreased generation of HCO3-
Q: 3 main roles of Ig binding to bacteria
A: - opsonization
A: - neutralization
A: - complement activation
Q: A defect in phagocytosis of neutrophils owing to lack of NADPH oxidase activity or similar enzymes is indicative of what immune deficiency disease?
A: Chronic granulomatous disease
Q: After exposure to what 4 things are preformed (passive) antibodies given?
A: Tetanus toxin, Botulinum toxin, HBV, or Rabies.
Q: All nucleated cells have what class of MHC proteins?
A: class I MHC proteins
Q: Anaphylaxis, asthma, or local wheal and flare are possible manifestations of which type of hypersensitivity?
A: Type I
Q: Anti-gliadin autoantibodies are associated with what disease?
A: Celiac disease
Q: Anti-Scl-70 autoantibodies are associated with what disease?
A: diffuse Scleroderma
Q: Autoimmune hemolytic anemia, Rh disease (erythroblastosis fetalis), and Goodpasture's syndrome are examples of what kind of hypersensitivity reaction?
A: type II hypersensitivity
Q: Class I major histocompatibilty complex consists of …
A: 1 polypeptide, with B2-microglobulin
Q: Class II major histocompatibilty complex consists of …
A: 2 polypeptides, an a and a B chain
Q: Cytotoxic T cells have CD(?), which binds to class (?) MHC on virus-infected cells.
A: CD8 binds to class I MHC
Q: Define acute transplant rejection.
A: Cell-mediated due to cytotoxic T lymphocytes reacting against foreign MHCs. Occurs weeks after transplantation.
Q: Define adjuvant.
A: Adjuvants are nonspecific stimulators of the immune response but are not immunogenic by themselves.
Q: Define chronic transplant rejection.
A: Antibody-mediated vascular damage (fibrinoid necrosis)--irreversible. Occurs months to years after transplantation.
Q: Define hyperacute transplant rejection.
A: Antibody-mediated due to the presence of preormed anti-donor antibodies in the transplant recipient. Occurs within minutes after transplantation.
Q: Define Ig allotype.
A: Ig epitope that differs among members of the same species (on light or heavy chain)
Q: Define Ig idiotype.
A: Ig epitope determine by the antigen-binging site (specific for a given antigen-binding site)
Q: Define Ig isotype.
A: Ig epitope common to a single class of Ig (5 classes, determined by the heavy chain)
Q: Give 3 classic examples of bacteria with antigen variation.
A: (1) Salmonella (2 flagellar variants)
A: (2) Borrelia (relapsing fever)
A: (3) Neisseria gonorrhoeae (pilus protein)
Q: Give 3 examples of possibly causes for SCID?
A: (1) failure to synthesize class II MHC antigens
A: (2) defective Il-2 receptors
A: (3) adenosine deaminase deficiency
Q: Goodpasture's syndrome is associated with what kind of autoantibodies?
A: anti-basement membrane antibodies.
Q: Helper T cells have CD(?) which binds to class (?) MHC on antigen-presenting cells.
A: CD4 binds to class II MHC
Q: How does Bruton's agammaglobulinemia usually present?
A: as bacterial infections in boys after about 6 months of age, when levels of maternal IgG antibody decline
Q: How is active immunity acquired?
A: Active immunity is induced after exposure to foreign antigens. There is a slow onset with long-lasting protection.
Q: How is passive immunity acquired?
A: by receiving preformed antibodies from another host. Antibodies have a short life span, but the immunity has a rapid onset.
Q: IL-4 promotes the growth of B cells and the synthesis of what 2 immunoglobulins?
A: IgE and IgG
Q: In what immune deficiency do neutrophils fail to respond to chemotactic stimuli?
A: Job's syndrome
Q: In what T-cell deficiency do the thymus and parathyroids fail to develop owing to failure of development of the 3rd and 4th pharyngeal pouches?
A: Thymic aplasia (DiGeorge syndrome)
Q: Job's syndrome is associated with high levels of what immunoglobulin?
A: IgE
Q: MHC I Ag loading occurs in __(1?)__ while MHC II Ag loading occurs in __(2?)__?
A: (1) in rER (viral antigens)
A: (2) in acidified endosomes.
Q: Primary biliary cirrhosis has what kind of autoantibodies?
A: anti-mitochondrial antibodies
Q: Role of TH1 cells?
A: produce IL-2 (activate Tc cells and further stimulate TH1 cell) and g-interferon (activate macrophages)
Q: Role of TH2 cells?
A: produce IL-4 and IL-5 (help B cells make Ab)
Q: Sensitized T lymphocytes encounter antigen and then release lymphokines which leads to macrophage activation' in what hypersensitivity reaction?
A: Type IV
Q: TB skin test, transplant rejection, and contact dermatitis are examples of what type of hypersensitivity reaction?
A: Type IV
Q: The 3 kinds of MHC class I genes are…
A: A, B, and C
Q: The 3 kinds of MHC class II genes are…
A: DP, DQ, DR
Q: The Fc portion of immunoglobulins are at the __?__ terminal.
A: The carboxy terminal
Q: What 2 cytokines are secreted by macrophages?
A: IL-1 and TNF-a
Q: What 2 kinds of autoantibodies are specific for systemic lupus?
A: Anti-dsDNA and anti-Smith
Q: What 3 cytokines are classified as 'acute phase cytokines'?
A: IL-1, IL-6, and TNF-a
Q: What 3 ways do interferons interfere with viral protein synthesis?
A: (1) alpha and beta interferons induce production of a second protein that degrades viral mRNA
A: (2) gamma interferons increase MHC class I expression and antigen presentation in all cells
A: (3) activates NK cells to kill virus-infected cells.
Q: What affect do the acute phase cytokines have on fat and muscle?
A: mobilization of energy reserves to raise body temperature
Q: What affect do the acute phase cytokines have on the bone marrow?
A: Incr. Production of Colony stim. Factor (CS) which leads to leukocytosis
Q: What affect do the acute phase cytokines have on the hypothalamus?
A: increase body temperature
Q: What antibody isotype can cross the placenta?
A: IgG
Q: What are 3 types of antigen-presenting cells?
A: macrophages, B cells, and dendritic cells
Q: What are the maim symptoms of serum sickness an at what period of time following Ag exposure?
A: fever, urticaria, arthralgias, proteinuria, lymphadenopathy 5-10 days after Ag exposure
Q: What are the major symptoms of graft-vs.-host disease?
A: maculopapular rash, jaundice, hepatosplenomegaly, and diarrhea.
Q: What B- and T- cell deficiency, assoc. with IgA deficiency, presents with cerebellar problems and spider angiomas?
A: ataxia-telangiectasia
Q: What causes the tissue damage associated with Serum sickness?
A: formation of immune complexes of foreign particles and Abs that deposit in membranes where they fix complement
Q: What class of MHC proteins are the main determinants of organ rejection?
A: class II MHC
Q: What complement components can cause anaphylaxis?
A: C3a and C5a
Q: What components of the alternative complement pathway make the C3 convertase?
A: C3b, Bb
Q: What components of the alternative complement pathway make the C5 convertase?
A: C3b, Bb, and 3b
Q: What components of the classic complement pathway make the C3 convertase?
A: C4b, C2b
Q: What components of the classic complement pathway make the C5 convertase?
A: C4b, 2b, and 3b
Q: What components of the complement pathway are deficient in Neisseria sepsis?
A: The MAC complex--(C5b, C6, C7, C8, C9)
Q: What cytokines attract and activate neutrophils?
A: TNF-a and B
Q: What disease is associated with a X-linked defect in a tyrosine-kinase gene associated with low levels of all classes of immunoglobulins?
A: Bruton's agammaglobulinemia
Q: What disease is associated with anti-epithelial cell autoantibodies?
A: Pemphigus vulgaris
Q: What disease is associated with anti-microsomal autoantibodies?
A: Hashimoto's thyroiditis
Q: What does a deficiency of C1 esterase inhibitor cause (in the complement cascade)?
A: angioedema because of overactive complement
Q: What does a deficiency of C3 cause (in the complement cascade)?
A: can lead to severe, recurrent pyogenic sinus and respiratory tract infections.
Q: What does deficiency of decay-accelerating factor (DAF) in the complement cascade cause?
A: leads to paroxysmal nocturnal hemoglobinuria (PNH)
Q: What does Job's syndrome classically present with?
A: recurrent 'cold' (noninflamed) staphylococcal abscesses
Q: What does TNF-a stimulate dendritic cells to do during the acute phase response?
A: TNF-a stimulates their migration to lymph nodes and their maturation for the initiation of the adaptive immune response.
Q: What elements of the complement cascade made the Membrane Attack Complex (MAC)?
A: C5b, C6, C7, C8, and C9
Q: What Ig is found in secretions as a monomer or a dimer?
A: IgA
Q: What Ig is found in secretions as a monomer or a pentamer?
A: IgM
Q: What immune deficiency disease has an autosomal-recessive defect in phagocytosis that results from microtubular and lysosomal defects of phagocytic cells?
A: Chediak-Higashi disease
Q: What immune deficiency is associated with elevated IgA levels, normal IgE levels, and low IgM levels?
A: Wiskott-Aldrich syndrome
Q: What immune deficiency presents with tetany owing to hypocalcemia, congenital defects of the heart and great vessels, and recurrent viral, fungal, and protozoal infections?
A: Thymic aplasia (DiGeorge syndrome)
Q: What immunoglobulin isotype has the lowest concentration in serum?
A: IgE
Q: What immunoglobulin isotype is involved in type-I hypersensitivity reactions?
A: IgE
Q: What immunoglobulin isotype is produced in the primary response to an antigen and is on the surface of B cells?
A: IgM
Q: What immunoglobulin isotype mediates immunity to worms?
A: IgE
Q: What immunoglobulin isotype prevents the attachment of bacteria and viruses to mucous membranes?
A: IgA
Q: What immunoglobulins bind and activate the classic complement pathway?
A: IgG and IgM (the Fc portion)
Q: What interleukin induces naive helper T-cells to become TH1 cells?
A: IL-12
Q: What interleukin induces naive helper T-cells to become TH2 cells?
A: IL-4
Q: What interleukin stimulates the growth of both helper and cytotoxic T-cells?
A: IL-2
Q: What is Chronic mucocutaneous candidiasis?
A: T-cell dysfunction specifically against Candida albicans.
Q: What is important about the CD3 complex?
A: It is a cluster of polypeptides associated with a T-cell receptor and is important in signal transduction.
Q: What is the cellular process that causes type I hypersensitivity?
A: Ag cross-links IgE on presensitized mast cells and basophils, triggering the release of vasoactive amines.
Q: What is the cellular process that causes type II hypersensitivity?
A: IgM, IgG bind to Ag on 'enemy' cell, leading to lysis (by complement) or phagocytosis (its cytotoxic).
Q: What is the main antibody in the secondary immune response?
A: IgG
Q: What is the most abundant immunoglobulin isotype?
A: IgG
Q: What is the most common selective immunoglobulin deficiency?
A: selective IgA deficiency
Q: What is the rise in temperature during the acute phase response help do (3 things?)
A: (1) increase specific immune response
A: (2) increase antigen processing
A: (3) decrease viral and bacterial replication
Q: What is the triad of symptoms seen with Wiskott-Aldrich syndrome?
A: recurrent pyogenic infections, eczema, and thrombocytopenia
Q: What kind of autoantibodies are associated with CREST/Scleroderma?
A: anti-centromere antibodies
Q: What kind of autoantibodies are known as rheumatoid factor?
A: anti-IgG antibodies
Q: What kind of immunity (antibody-mediated or cell mediated) is involved in autoimmunity?
A: antibody-mediated immunity (B cells)
Q: What kind of immunity (antibody-mediated or cell mediated) is involved in graft and tumor rejection?
A: cell mediated immunity (T cells)
Q: What kind of transplant rejection is reversible with immunosuppressants such as cyclosporin and OKT3?
A: acute transplant rejection
Q: What kinds of adjuvants are included in human vaccines?
A: aluminum hydroxide or lipid
Q: What kinds of cells have class II MHC proteins?
A: antigen-presenting cells (e.g. macrophages and dendritic cells)
Q: What parasites have antigen variation?
A: trypanosomes (programmed rearrangement)
Q: What symptoms characterize the Arthus reaction and what causes them?
A: edema, necrosis, and activation of complement due to the Ag-Ab complexes that form in the skin following intradermal injection of Ag.
Q: What type of cell secretes IL-3?
A: activated T-cells
Q: What type of cells does gamma interferon stimulate?
A: macrophages
Q: What type of hypersensitivity reaction is the Arthus reaction?
A: type III
Q: Where does the alternative complement pathway occur?
A: On microbial surfaces
Q: Where does the classic complement pathway occur?
A: antigen-antibody complexes
Q: Where is the defect in SCID?
A: the defect is in early stem-cell differentiation, leading to B- and T-cell deficiency
Q: Which interleukin causes fever?
A: IL-1
Q: Which interleukin enhances the synthesis of IgA?
A: IL-5
Q: Which interleukin stimulates the production and activation of eosinophils?
A: IL-5
Q: Which interleukin supports the growth and differentiation of bone marrow stem cells?
A: IL-3
Q: Which is the only type of cell-mediated hypersensitivity reaction, and thus not transferable by serum?
A: Type IV
Q: Wiskott-Aldrich syndrome is a defect in the ability to mount what immune response?
A: an IgM response to capsular polysaccharides of bacteria.
Q: With what disease are anti-histone autoantibodies associated?
A: drug-induced lupus
Q: With what disease are anti-nuclear antibodies associated?
A: systemic lupus
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