Hypersensitivities Flashcards
Acute inflammation progresses either to…. or …….
resolution
or
Chronic Inflammation
Resolution of Acute
1) supression of neutrophil recuritment
- stop inflammatory signaling
2) increase macrophage recruitment
- to clean up dead cell debri and pathogens
3) Scavenger function
4) tissue reapir
Acute leading to chronic
1) initiation of adaptive
2) fail to resolve, leads to chronic inflammation
What occurs with chronic inflammation that has to do with your vessels
angiogenesis
Outcomes of acute inflammation
1) resolution
2) healing by fibrosis
3) chronic inflammation
Major cells involved in Acute
1) Neutrophils
2) Mononuclear cells
- monocytes
- macrophages
Primary mediators of Acute
1) Vasoactive amines
2) PGs
3) activated complement
Major cells involved in Chronic
1) mononuclear cells
- macrophages, dendritic cells, monocytes
- the reason is we need these apc cells to stimulate our naive T cell and B cell population to initiate humoral and cellular immunity
Primary Mediators of Chronic
Cytokines
1) IFN-gamma
2) TNF-alpha
3) other cytokines
4) growth factors
- so maybe for angiogenesis
5) ROS species
6) hydrolytic enzymes
Summarize primary mediators of chronic
cytokines such as
1) IFN gamma
2) TNF alapha
other cytokes
growth factors
ROS
hydrolytic enzymes
Name 4 histological patterns of chronic inflammation
1) Mononuclear
- disordered
- has fibrosis
2) Granulomatous
- foreign body rxn, TB
- ORDERED pattern of macrophages/mononuclear cells
3) Eosinophilic
- parasites
- allergic, dominated by eosinophils with FIBROSIS
4) lymphoid neogenesis
-typically autoimmune disease
-spontaneous organization of new lymphoid structures
examples
-HEV, B lymphocytefollicles/germinal centers
Disorder, accompanied by fibrosis
Mononuclear histology
Parasites
allergic dominated by eosinophils with FIBROSIS
Eosinophilic
Typically in autoimmune disease
spontaneous org of new lymphoid structures HEV, B lymph/germinal centers
Lymphoid neogenesis
Foreing body rxn TB
ordered pattern of macrophages and other mononucelar cells
Granulomatous
Mononuclear histology
disordered
accompanied by fibrosis
Eosinophilic histology
parasites
allergic dominated by EOSINOPHILS with FIBROSIS
Granulomatous histology
FB, TB
ORDERED pattern of macrophages and other mononuclear cells
Lymphoid neogenesis
typically autoimmune
spontaneous organization of NEW lymphoid structures
HEV, B lymph follicles/germinal centers
Macrophages and Dendritic Cells are derived from what stem cell?
Myeloid stem cell
Immature Macrophages and Dendritic cells that haven’t left circulation and specialized into their tissues
MONOCYTES
Monocytes and granulocytes are distinct categories of progeny from myeloid stem cell
True
Moonocyte/macrophage progression
1) blood monocyte
2) tissue monocyte
3) activated macrophage/histiocyte
4) granulomatous inflammtion
multiNUCLEATED giant cell
Different activators of macrophages induce different phenotypes
IFN-y > GRANULOMA
IL4/IL13 > FOREIGN BODY GIANT CELL
TNFalpha> DENDRITIC CELLS
Macrophage effector functions
chemokines
cytokines
GF for tissue recovery
antimicrobial like hydrogen peroxide respiratory burst
Respiratory burst
also called oxidative burst
is the rapid release of reactive oxygen species (superoxide anion and hydrogen peroxide) from different types of cells
*hypersensitivity rules
1) are disease of ANTIGEN REENCOUNTER
2) No one has hypersensitivity rxn the FIRST TIME ag is ENCOUNTER
3) too much or inappropriate adaptive immunity
4) adaptive immunity inappropriately recruits innate mech that cause damage to our own bodies
Allergy
common disease of too much immune response
an overeaction, disproprotinate reponse to th danger of antigen
list 4 igE mediated allergic rxn
1) systemic anaphylaxis
- drugs
- serum
- venoms
- peanuts
2) acute urticaria (wheel and flare)
- animal hair
- insect bites
- allergy testing
3) allergic rhinitis (hay fever)
- pollens (ragweed, timonthy, birch)
- dust mite feces
4) asthma
- danders (cat)
- pollens
- dust-mite
5) food allergy
- tree nuts
- peanuts
- shellfish
- milk
- eggs
- fish
actopic
allergy prone
non-atopic
non-allergy prone
3 factors that contribute to allergy prone
1) genetic predisposition
2) antigen disproportionately favor Th2/IgE induction
3) genetic/environment predisposition to express Th2’IgE promoting cytokines with prolonged kinetics or greater magnitude than avg
Primary effector mech in allergy
1) immediate release of mast cell granules (histamine)
2) production of chemical mediators of inflammation
only….induce T cell reponses
Proteins or Peptides
Allergens are often….
proteases
low dose allergens favors activation of …..
IL-4 producing CD4 T cells
……are of low molecular weight so it can diffuse out of particle into mucus
low molecular weigh
Allergans are ……so can be readily eluted from particle
highly soluble
Allergens contain peptides that bind host MHC class……
MHCII required for T cell priming
Allergic rxn can be divide into 2 phase
1) Immediate
- release mediators in granules
2) Late Phase
downstream casacasde from ARACHADONIC ACID
Allergic rxn immediate response
release of preformed mediators in granules
Allergic rxn late phase resposne
downstream casacade form arachadnoc acid
….stabilizes granules preventing histamine relase
sodium cromoglycate
Wheal-and-flare type I hypersensitivity
Type I allergic reactions. Called a wheal-and-flare reaction, it includes swelling, produced by the release of serum into the tissues (wheal), and redness of the skin, resulting from the dilation of blood vessels (flare)
How is allergy treated? Four ways
1) reverse TH2 and Th1 balance
2) block co-stimulation to inhibit TH2 cytokines
- inhibit CD40-L
- inhibit IL-4 or IL-13
3) inhibit IgE binding to mast cell
- block IgE receptors
4) inhibits mediator effects on specific receptors, inhibit synthesis of specific mediators
- antihistamine drugs
- LOX inhibitors
5) block cytokine and chemokine receptors that mediate eosinophil recruitmnet and cativation
Which type of Ig or T cell is associated with Type 1 hypersensitivity?
IgE
Which type of Ig or T cell is associated with Type 2 hypersensitivity?
IgG
Which type of Ig or T cell is associated with Type 3 hypersensitivity?
IgG
Which type of Ig or T cell is associated with Type 4 hypersensitivity?
TH1
TH2
CTL
What is Type I hypersensitivity?
Immediate hypersensitivity
IgE mediate atopic (allergic) and anphylactic rxn in previously exposed individuals (Sensitized)
Type I hypersensitivity mechanism
1) INITIATION: cross-linkage by antigen of IgE bound to Rc receptors on mast cells and basophils after reexposure of sensitized host to allergan
2) EFFECTOR mech: degranulation of mast cells and basophils releasing vasoactives/other mediators like histamine and SRS-A is a mixture of LTC4, LTD4, LTE4
3) clinical manifestation:
- shock, vascular collapse, respiratory collapse
- chronic localized rxn: asthma, allergic rhinitis (hay fever) and wheal and flare (hives)
4) desensitization therapy: repeated injections of increasing doses of allergen induce production of IgG which binds lalergen and prevents its binding to igE on sensitized cells
Define Type I immediate hypersensitivity
IgE-mediated atopic (allergic) and anaphylactic reactions in previously exposed (sensitized) individuals
How is Type I Immediate hypersensitivity INITIATED?
Cross-linkage by antigen of IgE bound to Fc receptors on mast cells and basophils AFTER REEXPOSURE of SENSITIZED HOST to allergens
Type I immediate hypersensitivity effector mechanism:
degranulation of mast cells adn basophils relasing numerous vasoactive and other mediators such as histamine and SRS-A (slow-reacting substance of anaphylaxis) which is LTC4, LTD4, LTE4 mixture
- vasoconstriction
- bronchospasm
- increased permeability
Type I immediate hypersensitivity clinical manifestation:
Acute: anaphylaxis shock, vascular collapse, respiratory collapse
Chronic recurrent localized rxn: asthma, allergic rhinitis (hay fever), and wheal and flare (hives)
Type I immediate hypersensitivity densensitization strategy:
repeated injections of increasing doses of ag induce PRODUCTION of IgG which binds th elalergen and prevents its binding to IgE on sensitized cells
Type I hypersensitivity is mediated by
IgE
Eosinophils possess receptors of Fc region of IgE only after….
activation
Describe Type I hypersensitivity cross linking in detail:
1) B lymphocyte recognizes allergan
2) B lymphocyte proliferates and differentiates into PLASMA CELLS
3) plasma cell produce IgE which go find Fc receptors on Mast Cells and basophils
4) Allergens cross reacting with igE on mast cell
* 5) when allergen is REINTRODUCED, it cross-links the Fab protions of igE bound to the mast cell
6) Mast cell is triggered to degranulate and release histamines and other inlammatory mediators
7) inflammatory rmediators are now able to bind dto receptors on target cells leading to vasodilation, constriction of bronchioles, excess mucus secretions, other symptoms of allergy
Late-phase response of Mast Cells
- recruitment of Th2 cells
- eosinophils
- basophils
Immediate-phase of Mast Cells
mast cell degranulation
Type I immediate hypersensitivity localized allergic rxns- symptoms depend on …..of mast cell/basophil degranulation
LOCATION
If mast cell/basophil degranulates in the skin you get
Skin > eczema
If mast celll/basophil degranulates in the GI tract?
GI tract > bomiting diarrhea (food allergies)
If mast cell/basophil degranulates in the nasal mucosa?
Nasal mucosa > allergic rhinitis (hay fever)
If mastcell/basophil degranulates in the respiratory tract?
Respiratory tract > asthma
Systemic allergic reaction: Type I define
1) systemic anaphylaxis
2) acute loss of bp due to systemic vasodilation
3) bronchoconstriction causes asphyxiation
death can occur w/in minutres
epinephrine counteracts theeffects of allergic mediators on smooth muscle and vasculature
Type I hypersensitivity, your atopicness depends on 4 things
1) exposure to infectious diseases in early childhood
2) environmental pollution
3) allergen levels
4) dietary changes
Define Type II hypersensitivity
ANTIBODY-DEPENDENT CYTOXTOXICITY
How is Type II hypersensitivity initiated:
binding of ab to cell surface antigens
Type II hypersensitivity effector mechanisms
1) COMPLEMENT ACTIVATION by cell surface antigen-antibody complex- cell lysis by MEMBRANE ATTACK COMPLEX
2) ANTIBODY-DEPENDENT CELLULAR CYTOTOXICITY (ADCC) triggered by binding of ab to Fc receptors of MACROPHAGES and NK cells -> cell destruction
3) C3a and C5a attract neutrophils and promote inflammation
Type II hypersensitivity Clinical Manifestations
1) hemolytic transfusion rxn: ab to RBC ag
2) Drug induced thrombocytopenia (low platelets in blood) and hemolytic anemia: ab to drugs absorbed on platelets and RBC
3) hemolytic disease of newborn: maternal ab to antigens on fetal RBC, especially RH antigens
4) autoimmune disease
Type II hypersensitivity is aka
antibody-dependent hypersensitivity
1) IgG-mediated destruction of cells
ANTIBODY-DEPENDENT CELLULAR CYTOTOXICITY (ADCC)
triggered by binding of ab to Fc receptors of MACROPHAGES and NK cells -> cell destruction
Type II hypersensitivity
How does Type II hypersensitivity destroy
1) complement-mediated lysis (MAC)
2) opsonization
3) antibody-dependent celluar cytotoxicity (ADCC)
Type I hypersensitivity is mediated by
IgE
Type II hypersensitivity is mediated by
IgG
Type III hypersensitivity is mediated by
IMMUNE COMPLEXES
Type IV hypersensitivity is mediated
Cell-mediated
Immediate Hypersensitivities
1) Type I > IgE
2) Type II > IgG
3) Type III > immune complexes
Delayed hypersensitivity
Type IV
Type II effector mechanism
1) complement activation by ab:ab complex (classical)
- cell lysis by MAC
2) ADCC ab:Fc receptor on MACROPHAGES and NK cells -> cell destruction
3) C3a and C5a attract neutrophils and promote inflmmation
Define Type III hypersensitivity
immune complex-induced
Type III immediate hypersensitivity Effector Mech:
activation of complement cascade by immune complexes leading to acute inflammatory rxns
Type III clinicla manifestations
1) Arthus rxn: local skin rxn (redness and swelling) induced by intradermally injected ag or insect bite
2) intrapulmonary arthus -type rxn can be induced by inhalation of bacterial spores /fungi (farmer’s lung)
3) SERUM SICKNESS generalized rxn developing 1 or 2 weeks after a second adminstration after second adminstration of Ig of another species
- fever, rahses , glmerulonephritis due to immuen complex deposition in kidneys, vasculitis deposition in arteries, or arthritis deposition on synovial joints
Type I hypersensitivity is mediated
IgE
Type II hypersensitivity is mediated by
IgG
Type III hypersensitivity is mediated by
Immune complexes
Type IV hypersensitivity
Cell Mediated
Immediate Hypersensitivity
Type 1, 2, 3
Delayed Hypersensitivity
Type IV
Type III hypersensitivity binds antibody to
SOLUBLE ANTIGEN creates immune complexes
**IMmune complexes are remvoed from circulation b C3b binding to receptors on erthrocytes
- high lvls of immune complexes bad bc of complement activation and localized inflrmmation
Localized Type II reaction
Arthus reaction
1) injection of ag into skin with high lvsl of ab to the ag
2) intese localized inflammatory rxn characterized by influx of nuetrophils
Type III generalized reactions
- sytemic lupus erthematosus
- rheumatoid arthritis
- serum sickness
depositions in several body parts nephrons of kidney, vasculitis in arteris, arthritis - damge of tissue due to enzyme from angry cells
Define Type IV delayed type hypersensitivity
- delayed inflammatory response and cell-mediated cytotoxicity
How is Type IV hypersensitivity initiated
-ag stimulated relase of cytokines from sensitized CD4 Th1 cells
Which T cells are associated with the initiation type IV sensitivity
CD4 Th1 cells
Effector mech of TYpe IV
1) primary inflammatory response
- recruitment and activation of MACROPHAGES
2) secondary cytolytic response: activation of CD8 T cells and subsequent killing of target cells bearing antigen associated with class I MHC molecules
Exampes of Type IV hypersensitivities
1) contact dermatitis
Which of the following is the type of cell largely responsible for type I hypersensitivity responses?
a. erythrocyte
b. mast cell
c. T lymphocyte
d. antibody
B. mast cell
Type I hypersensitivities require which of the following initial priming events to occur?
a. sensitization
b. secondary immune reposne
c. cellular trauma
d. degranulation
a. sensitiziation
Which of the following are the main,ediators/initiators of type II hypersensitivity reactions
a. antibodies
b. mast cells
c. erthrocytes
d. histmaines
a. antibodies
Inflammatory molecules are released by mast cells in type I hypersensitivities; type II hypersensitivities, however, are characterized by which of the following?
a, cell lysis (cytotoxicity)
b. strong ab rxn against antigens
c. LT release upon stimulation
d. localized tissue rxn, such as hives
a. cell lysis (cytotoxicity)
A immune complex is an aggregate of which of the following
a. ab molecule
b. antigen moelcules
c. ag and ab molecules
d. histmine molecules
c. ag and ab molecules
WHich of the following is acommon tx for type II Hypersensitivity rxn?
anti-inflammatory steroid treatments
antihistamine treatments
hyposensitization injections of allergens
RhoGAM injections
anti-inflammatory steroid treatments
Which of the following induces a type III hypersensitivity?
release of inflammatory molecules from mast cells
accumulation of immune complexes in tissues and small blood vessels
destruction of cells bound by antigens
destruction of cells bound by antibodies
accumulation of immune complexes in tissues and small blood vessels
Which one of the following is not an example of a type IV hypersensitivity?
latex allergy
Contact dermatitis (e.g., contact with poison ivy)
a positive tuberculin skin test
hemolytic disease of the newborn
hemolytic disease of the newborn
Antibodies involved in type I hypersensitivities are of the ________ class.
IgE
Allergy shots work by shifting antibody responses to produce ________ antibodies.
IgG
A person who is blood type A would have IgM hemagglutinin antibodies against type ________ red blood cells in their plasma.
B
The itchy and blistering rash that develops with contact to poison ivy is caused by a type ________ hypersensitivity reaction.
IV
The thyroid-stimulating immunoglobulin that acts like thyroid-stimulating hormone and causes Graves disease is an antibody to the ________.
. thyroid-stimulating hormone receptor
For a transplant to have the best chances of avoiding rejection, the genes coding for the ________ molecules should be closely matched between donor and recipient.
MHC
. Because it is a “transplant” that can include APCs and T cells from the donor, a bone marrow transplant may induce a very specific type of rejection known as ________ disease.
graft-versus-host
Diseases due to ________ abnormalities are termed primary immunodeficiencies.
genetic
A secondary immunodeficiency is ________, rather than genetic.
acquired
A ________ cancer vaccine is one that stops the disease from occurring in the first place.
preventive
A ________ cancer vaccine is one that will help to treat the disease after it has occurred.
therapeutic
A 21-year-old woman is stung by a bee. Within 5 minutes she develops severe dyspnea. On her skin are blotchy areas of erythema. She is given an injection of epinephrine and improves over the next 30 minutes. She receives therapy over the next year in which she receives small injections of bee venom. The most likely goal of this therapy is replacement of which of the following forms of immunoglobulin on her mast cells?
a. IgA
B IgD
C IgE
D IgG
E IgM
C IgE
She has type I hypersensitivity. She has increased amounts of IgE bound to perivascular mast cells in her airways. Upon encounter with a specific antigen, the antigen binds to IgE and the mast cells degranulate, releasing vasoactive amines which mediate the symptoms through edema. By ‘desensitizing’ her with injection of small amounts of the allergen, it is hoped that there will be gradual replacement of the IgE with IgG, so that subsequent antigen encounters will not be life-threatening.
A 33-year-old woman has had increasing fatigue for the past 5 months. On physical examination there are no abnormal findings. Laboratory studies show Hgb 9.3 g/dL, Hct 28%, MCV 96 fL, platelet count 173,400/microliter, and WBC count 6090/microliter. Her direct Coombs test is negative and her indirect Coombs test is positive. Her antinuclear antibody test is positive. Which of the following immunologic mechanisms is most likely to cause her findings?
A CD8 lymphocyte-mediated cell lysis
B Extravascular hemolysis in the spleen
C Immune complex-mediated complement activation
D Intravascular hemolysis with membrane attack complex formation
E Mast cell degranulation with release of cytokines
reacall M hgb 12.3-16.3 g/dL
recall W hgb 11.5-14.6g/dL
HCT w 34-42.1%
MCV 79- 95fl
plt 143-398x 10^3/microleiter
Wbc 3.28 - 9.29 x10^3 microliter
B Extravascular hemolysis in the spleen
She has an autoimmune hemolytic anemia of the ‘warm’ variety, typical for systemic lupus erythematosus, which is marked by a positive antinuclear antibody test. The RBCs become coated with IgG antibody reactive at 37 C. The opsonized RBCs are phagocytized by splenic macrophages.`
A 7-year-old child has developed a fever and increasing dyspnea for the past month. On physical examination her temperature is 38 C. She has inspiratory wheezes on auscultation of the chest. A chest radiograph shows marked hilar lymphadenopathy and a peripheral right middle lobe granuloma. Her tuberculin skin test is positive. Which of the following forms of immunologic hypersensitivity reaction is she most likely to have?
A I
B II
C III
D IV
TYPE IV
Granulomatous inflammation is a form of type IV hypersensitivity reaction, with participation by CD4 and CD8 lymphocytes and recruitment and transformation of macrophages.`
A 38-year-old woman has had pain of her hands and feet for the past month. On physical examination there is warmth with swelling and pain on movement most marked in proximal interphalangeal joints and metacarpo- and metatarsophalangeal joints. She has remissions and exacerbations of her joint pain over the next 10 years. She undergoes plastic repair with prosthetic joint placement in her right thumb and forefinger. The excised synovial tissue is examined microscopically and shows extensive inflammation. Which of the following cell types is likely to be most numerous within this inflamed synovium?
A CD4 cells
B Eosinophils
C Mast cells
D Neutrophils
E NK cells
CD4 cells
She has rheumatoid arthritis, a chronic inflammatory process targeting synovium, typically involving small joints of the hands and feet, whichc is mediated by T cells.
A 14-year-old boy has had nasal stuffiness for the past month. On examination he has swelling with erythema of nasal mucosal surfaces. A corticosteroid-containing nasal spray improves his nasal breathing. He has recurrent rhinitis, and 5 years later polypoid excresences are excised from his right nasal cavity. On microscopic examination of this tissue there is marked stromal edema with numerous eosinophils. Which of the following cytokines released by mast cells is most likely to cause these eosinophilic infiltrates?
A Interleukin-4
B Leukotriene B4
C Prostaglandin D2
D Transforming growth factor-beta
E Tumor necrosis factor-alpha
IL-4
He has allergic rhinitis with inflammatory nasal polyps. This is a form of type I hypersensitivity. The IL-4 attracts eosinophils, which is a late phase reaction to allergen interaction with mast cells coated with IgE.
A 44-year-old woman has had increasing malaise for the past month. On physical examination she has 1+ pedal and presacral edema. Laboratory studies show her serum creatinine is 4.6 mg/dL. A urinalysis shows proteinuria and hematuria. Urine microscopic examination shows RBC and WBC casts. Her antinuclear antibody test is positive. Which of the following forms of immunologic injury is most likely producing her renal disease?
A CD8 lymphocyte-mediated cell lysis
B Glomerular basement membrane antibody
C Immune complex-mediated complement activation
D Macrophage activation by interferon-gamma
E Mast cell degranulation with release of cytokines
Immune complex-mediated complement activation
She has systemic lupus erythematosus with lupus nephritis, an immune complex-mediated form of glomerulonephritis. This is a form of type III hypersensitivity. The antigen-antibody complexes can activate complement.
A 29-year-old man enjoys a seafood dinner with fresh grouper from Appalachicola Bay. Three hours later he experiences extensive itching of his skin. He has a mild diarrhea. On physical examination there are areas of erythema and slight swelling of his skin from 1 to 7 cm in size on his extremities and torso. He is given diphenhydramine and the itching and urticaria subside in an hour. Which of the following substances is most likely to mediate the appearance of his signs and symptoms?
A Bradykinin
B Complement C3b
C Complement C5a
D Histamine
E Interleukin-1
F Leukotriene B4
G Prostaglandin D2
Histamine
He has localized anaphylaxis, a form of type I hypersensitivity, with the allergens in seafood absorbed in the GI tract and reacting with IgE coated mast cells, causing mast cell degranulation with release of vasoactive amines such as histamine. Antihistaminic drugs aid in treating these acute manifestations of hives, itching, and diarrhea.
A 45-year-old woman develops skin bullae over the past 5 days. On physical examination she has 1 to 4 cm flaccid bullae most prominent in her axillae and groin regions. The bullae rupture easily. A skin biopsy is performed and on immunofluorescence microscopy shows a net-like pattern of immunoglobulin deposition between keratinocytes. Which of the following forms of immunoglobulin is most likely to be deposited in her skin?
A IgA
B IgD
C IgE
D IgG
E IgM
IgG
She has pemphigus vulgaris, a form of type II hypersensitivity with antibody directed against epidermal cadherin. The loss of keratinocyte adhesion leads to bulla formation.
A 30-year-old man has become more irritable and restless over the past 4 months. He has experienced mild diarrhea. He has lost 4 kg without dieting. On physical examination there is diffuse enlargement of his thyroid gland. Which of the following immunologic mechanisms is most likely to cause his findings?
A Anti-receptor antibody
B CD8 lymphocyte-mediated cell lysis
C Immune complex-mediated complement activation
D Macrophage activation by interferon-gamma
E Mast cell degranulation with release of cytokines
A Anti
-receptor antibody
He has Graves disease of the thyroid. There is antibody directed against TSH receptor which stimulates the TSH receptor to cause increased production and release of thyroxine, with resultant features of hyperthyroidism.
A family of four goes camping for the weekend. The children play in the woods near camp, discovering new flora such as plants with compound, pointed leaves growing in clusters of 3. On Wednesday night, the two children begin to complain of ‘itchy red bumps’ on their skin. On examination there are 0.1 to 0.3 cm raised indurated erythematous nodules, often clustered, on their hands, forearms, and lower legs. A corticosteroid cream alleviates much of the itching. These lesions subside over the next week. Which of the following immunologic mechanisms is most likely to produce their skin lesions?
A Antibody-dependent cell-mediated cytotoxicity
B Anti-receptor antibody binding
C Arthus reaction
D Delayed-type hypersensitivity
E Localized anaphylaxis
F Systemic anaphylaxis
D Delayed-type hypersensitivity
They have contact dermatitis. Plants such as poison oak or poison ivy have antigens (urushiol oil) that elicit delayed-type hypersensitivity from 1 to 3 days following contact. Only one nanogram of urushiol oil found in poison ivy can cause a rash!.
A 62-year-old woman has felt increasingly fatigued with nausea for the past year. On physical examination there are no abnormal findings. Laboratory studies show Hgb 9.2 g/dL, Hct 28.1%, MCV 119 fL, platelet count 242,800/microliter, and WBC count 5920/microliter. An upper GI endoscopy is performed and she has loss of gastric rugal folds. Which of the following serologic laboratory tests is most likely to be positive in this woman?
A Acetylcholine receptor antibody
B Anti-DNA topoisomerase antibody
C Anti-microsomal antibody
D Anti-mitochondrial antibody
E Anti-nuclear antibody
F Anti-parietal cell antibody
G Glycoprotein IIb/IIIa antibody
F Anti-parietal cell antibody
She has pernicious anemia with atrophic gastritis and loss of gastric parietal cells that form intrinsic factor that complexes with B12 for absorbtion in the terminal ileum.
INTEREFERE WITH B12 absorbtion in the terminal ileum
A 24-year-old woman has experienced episodes of dyspnea with non-productive cough and fever over the past 3 months. These episodes only occur at work. On physical examination there are no abnormal findings. Investigation of her work environment reveals an air conditioner with mold growing in the outflow duct. If a lung biopsy were performed during one of these episodes, it would show focal inflammation of alveoli with neutrophils and macrophages. Which of the following immunologic mechanisms is most likely to cause her illness?
A Anti-receptor antibody
B CD8 lymphocyte-mediated cell lysis
C Hypergammaglobulinemia
D Immune complex-mediated complement activation
E Mast cell degranulation with release of cytokines
Immune complex-mediated complement activation
This is a form of type III hypersensitivity with antibody attaching to mold spore antigens in the local environment of the pulmonary alveoli. The classic form of this disease is ‘farmer’s lung’ and this variant is ‘air conditioner lung’.
A 47-year-old man with a 3 day history of fever and cough is diagnosed with pneumonia. He is started on intravenous antibiotic therapy with a cephalosporin. Within 5 minutes of starting the therapy, he develops sudden severe dyspnea. Release of which of the following chemical substances is most likely to act in small airways to exacerbate his dyspnea?
A Interleukin-1
B Leukotriene D4
C Nitric oxide
D Prostaglandin E2
E Thromboxane A2
F Tumor necrosis factor
Leukotriene D4
He has systemic anaphylaxis from a drug allergy. Cephalosporins, as well as penicillins, can have this complication. The mast cells degranulate when the allergen (in this case the drug) cross-links IgE fixed to mast cells, with release of a variety of substances. Leukotrienes can cause bronchoconstriction. He may also have marked vasodilation and edema in upper airways.
A 16-year-old girl has noted passing dark coloured urine for the past 2 days. On physical examination she has periorbital edema. A urinalysis reveals proteinuria and hematuria. A renal biopsy is performed and shows irregular deposition of immune complexes containing IgG and complement. The glomeruli have many neutrophils. Which of the following is the most likely diagnosis?
A Anti-glomerular basement membrane disease
B Food allergy
C Post-infectious glomerulonephritis
D Pulmonary tuberculosis
E Type 1 diabetes mellitus
Post-infectious glomerulonephritis
A recent infection, often with an organism such as group A streptococcus with pharyngitis, can lead to antibody production with cross-reactivity of antibodies to glomerular antigens and immune complex formation. The immune complexes attract neutrophils via complement activation and Fc receptors on the immune complexes.
