Immunology Flashcards
(158 cards)
1
Q
what are lymph nodes?
A
1) Act with filtration of B or T cells
2
Q
What are the parts of the lymph node, and what is the use?
A
1) Follicule: B cell localization
2) Medulla: Drain lymphatics and contain reticular cells
3) Paracortex:houses T cells ( not well developped in DiGeorge syndrome)
3
Q
Which part of the body do the following lymph nodes drain? Cervical Hilar Mediastinal Axillary Celiac Superior mesenteric Inferior mesenteric Internal iliac Para-aortic Superficial inguinal Popliteal.
A
1) Cervical (head and neck)
2) Hilar (lungs)
3) Mediastinal (Trachea and esophagus)
4) Axillary: Upper limb, breast, skin, ombilical
5) Celiac: liver, stomach, spleen, pancrease
6) Superior mesenteric: lower duodenum, jejunum, ileum, colon to splenic flexure
7) Inferior mesenteric: colon from splenic flexure to upper rectum
8) Internal iliac: lower rectum to anal canal, vagina, cervix, prostate
9) Para-aortic: testes, ovaries, kidnies, uterus
10) Superficial inguinal: anal canal, skin below ombilicus, scrotum,vulva
11) Popliteal: dorsolateral foot, posterior calf
4
Q
where are T cells found within the spleen?
A
1) Periarteriolar lymphatic sheath
5
Q
Where are B cells found?
A
In the follicles in the white pulp
6
Q
What is found in the marginal zones between the red pulp and the white pulp?
A
Macrophages
Specailized B cells
Antigen presenting cells
7
Q
What is seen in blood smear after a splenectomy?
A
1) Howell-Jolly bodies (nuclear remnants)
2) Target Cells
3) Thrombocytosis: loss of sequestration and removal
4) Lymphocytosis: loss of sequestation
8
Q
What is the thymus used for?
What are changes to thymus depending on the condition?
A
1) Site of T Cell differentiation and maturation
2) Hypoplastic with DiGeorge’s syndrome
3) Enlarged if have myasthenia gravis.
9
Q
What are components of inate vs adaptive immunity?
A
1) Inate have neutrophils, macrophages, and noncytes
2) Adpative have: T cells, B cells and antibodies
10
Q
What is the resistance between inate and adaptive immunity?
A
1) Inate: perists through generations, and does not change within an organismes lifetime
2) Microbial resistance, not heritable
11
Q
Response to pathogents (inante vs adaptive)
A
1) Inate: rapid
2) Adpative: highly specific, and refined over time, the memory response is faster
12
Q
What are proteins associated with the rapid/inate?
A
1) Inate: C-reative protein
2) Adaptive: immunoglobulins
13
Q
How does recognition occur? (Innate vs adaptive)
A
1) Inate: Tollike recpetors
2) Pattern recognition receptors (LPS for gram - bacteria)
3) Adpative: Memory activated B and T cells.
14
Q
MHC 1 vs MHC 2 in terms of loci?
A
HLA-A, HLA-B, HLA-C (1 letter)
MHC-2 (HLA-DP, HLA-DQ, HLA-DR) (has 2 letters)
15
Q
MHC 1 vs MHC 2, binding?
A
1) TCR and CD8 (MHC 1)
2) TCR and CD4 (MHC 2)
16
Q
MHC 1 vs MHC 2 expression?
A
1) MHC1: on all nucleated cells (but not RBC)
2) MHC 2: On all APC
17
Q
Function of MCH 1 vs MHC 2?
A
MHC 1: endogenously synthesized antigens
MHC 2: Presents exogensously sythesized antigens
18
Q
What are associated proteins with MHC 1 and MHC 2?
A
B2-microglobulin
Invariant chain
19
Q
What are HLA subtypes associated with disease? Hemochromatosis B8 B27 DQ2/DQ8 DR2 DR3 DR4 DR5
A
A3: Hemochromatosis
B8: Addison diseasse, mysanthia gravis
B27: PSoratic arthritis, ankylosing spondylitis
DQ2/DQ8: Celiac disease
DR2: Multiple scleosis
DR4: Rheumatoid arthritis. DM
DR5: pernicious anemia (Hashimoto thyroiditis)
20
Q
What do natural killer cells do?
A
1) Use perforin and granzymes to induce apoptosis of infected cells and tumor cells
2) Activity enhanced by IL 2, Il-12, IFN- alpha
21
Q
What are the positive and negative selection of T cells?
A
Positive selection: Thymic cortex, capable of binding to self MHC are allowed to survive
Negative selection: Thymic medulla. T cells with high affinity for self antigens undergo apoptosis.
22
Q
What do helper T cells do?
A
1) TH 1 cell Secrete IFN-Gamma that activate the macs and cytotoxic T cells.
2) Th2 cells: Il-4 and IL-5 (recruits eospinophils for parasitic defense and promote IgE
23
Q
What is naive T-Cell activation?
A
Dendritic cells do the recognizing
1) Presented to MHC II (either CD4+ or CD8+)
2) Proliferation and survival
3) Cell activates cytokines and kills virus infected cells
24
Q
What is B cell activation class, switching?
A
1) B cell receptor mediated endocytosis (presented on MHC II)
2) Cell secretes cytokines that Ig Class switch of B cell, and activates the antibody production.
25
What are the structures of antibody Fab, and the Fc?
1) FaB: fragment antigen binding (determines idiotype), only 1 antigenic specificity per B cell
2) Fc (Constant): Carboxyl terminal
26
How is generation of antibody diversity accomplished?
1) Recombination of light and heavy chains
2) Random addition of nucleotides in the chains
3) Recombination of light and heavy chain genes
27
What immunoglobulin isotypes?
1) IgG: delayed response to bacterial toxins and viruses
2) IgA: prevents attachements of bacteria and virus to mucous membrane (secretory)
3) IgM: intermediate response to antigen
4) IgD: Unclear
5) IgE: immnuity to worms by activating eosinophils.
28
What are the thymus-independent antigens?
1) Weakly immunogenic (requires boosters)
2) Thymus dependent: Contain diphtheria vaccins (immnuological memory occur as a result of direct contact with B cells and Th-Cells
29
What are acute phase reactants?
Factors whose serum concentration change significantly in response to inflammation (notably IL-6)
```
C-reative protein
Ferritin
Fibrinogen
Hepcidin
Serum Amyloid A
```
30
What are negative (downregulated) during stress?
1) Albumin
| 2) Transferrin
31
What does C-reactive protein measure?
Facilitates phagocytosis, sign of ongoing inflammation
32
What does ferritin measure?
Binds and sequesters iron to inhibit microbial iron scavenging
33
What does fibrinogen measure?
1) Coagulation factor, promotes endothelial repair (goes with ESR)
34
What does Hepcidin show?
1) Decrease iron absorption, and decrease iron release
35
What does serum amyloid A show?
1) Prolonged elevation can lead to amyloidosis
36
What does transferrin show?
Internalized by macrophages to sequester
37
Which organ produces the complement system?
Hepatically synthesized plasma proteins that defend against gram - bacteria
38
How is the complement system mediated?
By IgG of IgM
39
What are the functions of complement pathway?
C3b opsonization
C3a, C4a, C5a anaphylaxis
C5: neutrophil chemotaxis.
40
Disorder associated with C1 esterase inhibitor deficiency?
1) Angioedmea (unregulated kallikrein, increased bradykinin)
41
Disorder associated with C3 deficiency?
Recurrent sinus and respiratory infection
42
Disroder associated with C5-C9 deficiency?
Increased susceptibility to Neisseria bacteremia
43
Disorder associated with DAF (GP1-anchored enzyme deficiency)?
Complement mediated lysis of RBC
44
Passive vs active immunity due to acquisition?
1) Receiving preformed antibodies vs exposure to foreign antigens
45
Passivevs active immunity due to onset?
Passive is rapid, and active is long lasting protection with memory
46
Passive vs active immunity duration?
Passive: short life span
Active: long lasting (protection)
47
Examples of passive vs active immunity?
IgA in breast milk
IgG crossing placenta
Active: natural infection
48
What are some examples of passive immunity vaccines?
1) Tetanus
2) Botulism
3) HBV
4) Varicella
5) Rabies
When there is exposure to one of these entities, then the vaccine is given, and because works rapidly, can heal.
49
Which response is activated by the live attenuated vaccine?
Cellular and humoral response
50
what are the pros and cons of live attenuated vaccine?
1) Induces lifelong immunity
| 2) cons: may revert to virulent form *cannot be given if immunocrompromised, or pregnent
51
What are some examples of live attenuated virus?
1) Influenzae
2) Measels
3) BCG
4) Polio (sabine)
5) Varicella
6) yellow fever
52
What are pros and cons of inactivated or killed vaccine?
Pro: safer then live vaccine
Cons: weaker, immune response, and needs a booster
53
What are the 5 types of hypersensitivity reactions?
1) Type 1 (anaphylactic and free antigen crosslinked IgE
(rapid reaction, because has preformed antibodies)
Test with IgE
2) Type 2 Cytotoxic (direct and indirect coombs test)
Direct: detects antibodies bound to patient's RBC
Indirect: detects serum antibodies
IgM and IgG
3) Type 3: immune complex *immune complex-antigen/antibody*, its IgG
(Vasculitis or systemic manifestations)
Examples: SLE, polyarertis nodosa, post streptococcal glomerulonephrtis
4) Type 4:Sensitized T cells encounter antigen and the release cytokines (lead to macrophage activation)
Usually this is delayed or last cell mediated, and not transferred by serum.
Examples: Contact dermatitis
Graft vs host disease
Multiple sclerosis
54
What is serum sickness?
Immune complex disease in which antibodies to foreign proteins are produced
might be deposited on membrane and can fix tissue
Can lead to arthus reaction
55
What are the causes if serum sickness?
Drugs acting as haptens
56
What are the symptoms of serum sickness?
1) Fever
2) Urticaria
3) Arthralgia
4) Proteunuria
5) Lymphadenopathy (5-10 days) after antigen exposure
57
What is Arthrus reaction?
1) Antibody medited hypersensitivity reaction
2) Intradermal injection of antigen into pre-senstized skin
3) Have immune complex on the skin leading to edema, necrosis, and activation of the complement
58
What are possible types of blood transfusion reactions?
1) Allergic Reaction
2) Anaphylactic reaction
3) Febrile nonhemolytic transfusion reaction
4) Acute hemolytic transfusion reaction
59
What is presentation and cause of allergic reaction to blood?
1) Hypersensitivity to plasma proteins: urticaria, pruritis, wheezing, fever
60
Presentation and cause of anaphylactic reaction?
IgA deficient individual
Needs to recieve blood products without IgA
Dyspnea, brochospasm, hypotension
Treatment: epinephrine
61
Presentation and cause of febrile, non hemolytic transfusion reaction?
Type 2 hypersensitivty reaction
Host antibodies against donor HLA
Fever
Headaches
Chills
Flushing
62
Causes and presentation of acute hemolytic transfusion reaction?
Type II reaction
Intravascular hemolysis
ABO incompatibility
```
Fever
Hypotension
Tachycardia
Flank pain
Hemoglobinuria
Jaunedice
```
63
Autoantibody with anti-ach?
Mysanthia gravis
64
Autoantibody with anti-basement membrane?
Goodpasture syndrome
65
Autoanotbody with anticardiolipin, lupus anticoagulant?
SLE, Antiphospholipid syndrome
66
Autodantibody with anti-centromere?
Limited scleroderma (CREST)
67
Autoantibody with anti desmosome?
Pemphigus vulgaris
68
Autoantibody with anti-dsDNA, anti-Smith?
SLE
69
Autoantibody with anti-glutamic acid and decarboxylase?
Type 1 DM
70
Antihemidesmosome?
Bullos pemphigoid
71
Anti-histone?
Drug induces lupus
72
Anti-Jo-1, anti-SRP, Anti-Mi 2?
Polymyositis, dermatomyositis
73
Antimicrosmal, and antithyroglobulin?
Hashimoto thyroiditis
74
Antimitochondrial?
Biliary cirrhosis
75
Anti-nuclear (ANA)?
SLE (non-specific)
76
Anti-parietal cell?
Pernacious anemia
77
Antiphospholipase A 2 receptor?
Membraneous nephropathy
78
Anti-Scl-70?
Scleroderma diffuse
79
Anti-smooth muscle?
Autoimmune hepatitis type 1
80
Anti SS, anti SSB?
Sjogen syndrome
81
Anti TSH receptor?
Graves disease
82
Anti-U1 RNP?
Mixed connective tissue disease
83
Voltage gated calcium channel antibodies?
Lambert-eaton
84
Anti-endomysial, IgA anti-tissue transglutaminase?
Celiac disease
85
p-ANCA?
1) Eosinophilic granulomatosis with polyangitis
| Churg-Strauss
86
C-ANCA?
Granulomatosis with polyangiitis (Wegener)
87
Rheumatoid factor (IgM antibody that targets IgG Fc)
Rheumatoid arthritis
88
Defect, presentation, and findings of X-linked Bruton agammaglobinemia?
1) NO B cell maturation
Recurrent bacterial and enteroviral infection
2) Absent B cells in peripheral blood smear
3) Absent lymph nodes and tonsils
89
Defect, presentation, findings selective IgA deficiency?
1) Very common
2) Usaully assymptomatic (have airway and GI infections), Autoimmune, atropy anaphylaxis
3) Decreased IgA, normal IgG, and IgM
90
Defect, presentation, findings associated with common variable deficiency?
1) Defect in B cell differentiation
2) Can be acquired in the 20-30
3) Increased risk of brochiectasis and lymphoma, and sinus pulmonary infections
4) Decreased plasma cells and decreasedimmunoglobulins
91
What is the complement system?
Classic system that is IgG or OgM mediated
92
What are the functions of opsonins?
Bacterial defense, to help with phagocytosis
93
What is C1 esterase inhibitor deficiency?
Hereditary angioedema due to activation of kallikrien (ACE contrindicated)
94
What is C3 deficiency?
1) Increase recurrent pyogenic sinus infections
| 2) Increase hypersensitivity III reactions
95
What are C3-C9 deficiencies?
Susceptibility to recurrent Neisseria bacteria
96
What are DAF (GP1 anchored enzyme) deficiency?
Linked to paraoxymal nocturnal hemoglobinuria
97
Why is IL-1 important?
Fever
98
IL-2 linked?
Stimulates T cells
99
IL-3 linked to?
Stimulates bone marrow
100
IL-4 linked to?
Stimulare IgE
101
IL-6 linked to?
Fever and acute phase proteins
102
TNF-alpha linked to?
Mediates septic shock
| Cachexia in malignancy
103
what are T-Cells?
TCR binds to antigen MHC complex
CD3 (Associated with signal transaction)
CXCR4/CCR5: co receptors for HIV
104
What are B cells associated with?
Ig (binds antigen)
CD 19, CD 20
Targets Epstein Barr
105
What are the hematopoietic stem cells associated with?
CD 34
106
What is anergy?
When a cell is not activated by exposure to antigen
(exposure without the costimulatory signal)
Mechanism of self tolerance
107
What are the effects of bacterial toxins?
Staph aureus and pyrogens activate CD 4+ and cause massive release of cytokins
108
How do endotoxins work?
Directly stimulare MACS by binding with endotoxin receptor TLR4/CD14
109
What are examples of antigenic variation?
1) Can be rearrangement of RNA segments
| 2) Classic examples include: Salmonella, Borrelia recurrentis, N. Gonorrhea, parasites.
110
Defect, presentation, findings Thymic aplasia?
1) 22q11 deletion
2) Failure to develop 3rd and 4th pharyngeal pouches (no thymus or parathyroids)
Presentation: Tetany, controncal Tetralogy of Fallot)
111
Defect, presentation, findings of Il-12 deficiency?
1) Decreased Th1 response
2) Mycrobial and fungal infections
3) Present after BCG
112
Defect, presentation, hyper IgE syndrome (Jobs syndrome) ?
1) Deficiciency of Th17 cells
2) Impaired of recruitement neutrophils
3) Coarse farcies, staph abcess, retained primary teeth, dermatological problems
113
Defect, presentation, findings, Chronic mucocutaneous candidasis?
1) T-Cell dysfunction
2) Non-invasive candida albicans
3) Absent T cell proliferation
114
Defect, presentation, findings with severe combined immunodeficiency?
1) Il-2R gamma chain mutation
2) Failure to thrive, diarrhea, thrush, recurrent viral, bacterial, fungal infections
3) Treatment: bone marrow transplant
4) No thymic shadow on x-ray,
115
Defect, presentation, findings of ataxia telangiectasia?
1) Defect in ATM gene (can't repair DNA)
2) Triad of cerebeller defects, ataxia, spider angiomas, IgA deficiency
3) Findings: decreased IgA, IgG, IgE
116
Defect, finding, presentation of Hyper IgM?
1) CD40L on Th cell
2) x-linked recessive
3) Severe pyogenic infections
4) pneumocytis cryptosporidium
5) Decreased IgG, IgA, IgE
117
Defect, presentation, findings with Wiskott-aldrich syndrome?
1) Mutation in WAS gene
| 2) Thrombocytopenia, Eczema, recurrent infections,
118
What are leukocyte adhesion deficiency?
1) LFA-1 integrin
| 2) Bacterial skin infection, no pus formation, delayed ombilical cord seperation
119
Defect, presentation, findings Chdiak-Higashi syndrome?
1) Defect in LYST gene
2) Recurrent pyogenic infections by staph
3) Peripheral neuropathy, neurodegeneration
4) Pancytopenia, and coagulation defects
120
Defect, presentation, findings of chronic granulomatous disease?
1) Defect in NAPH oxidase (X-linked)
2) Increased susceptibility to catalase organisms (Nocardia, Pseudomonas, Listeria)
3) Findings: abnormal dihydrorhadamine
121
What are common bacterial infections associated with immunodeficiency?
1) Pseudonomas aeruginosa
2) Strep pneumoniae
3) H. Influenzae
4) N. Meningitidis
5) E. Coli
6) Klebsiella pneumoniae
122
Common virus infection of immunodeficiency?
1) CMV
2) EBV
3) VZV
4) Enteroviral encephalitis
123
Common fungi and parasite infections in immunodeficiency?
Candida (aspergillus systemic)
| Giardiasis
124
What are the types of grafts?
1) Auto grafts (from self)
2) Syngeneic graft (from identical twin or clone)
3) Allograft: nonidentical individual of the same species
4) Xenografts: from different species
125
Onset, pathogenesis, features of hyperacute reaction?
1) Onset within minutes
2) Pre-existing antibodies react with donor antigen
3) Hypersensitivity reaction
4) Widespread thromosis of graft vessels with ischemia and necrosis (need to remove the graft)
126
Onset, pathogenesis, features of acute infection?
1) Weeks to months
2) CD8 + cells are activated against the MHC (similar to hyperacute, except the antibodies develop after transplant)
3) Vasculitis with dense interstitial lymphocyte
4) Prevent, reverse with immunosuppression
127
Onset, pathogenesis, features of chronic infection?
1) Months to years
2) CD4+ cells respond to APC (Both cellular and humoral reaction)
3) Recipient secrete cytokines, proliferation of vascular smooth muscles
4) Brpnchiolitis obliterans, accelerated atherosclerosis, chronic graft nephropathy, vanishing bile duct
128
Onset, pathogenesis, features of graft-vs. host disease?
1) Grafted immunocompetent T cells proliferate, and reject host cells as foreign
2) Severe organ dysfunction
3) Type of IV hypersensitivity reaction
4) Maculopapular rash, jaunedice, diarreha, hepatosplenomegaly
Usually in bone marrow and lvier transplant
Can be beneficial in bone marrow transplant (the graft attacks the tumor)
129
Mechanism, Use, toxicity of cyclosporin?
1) Calcineurin inhibitor (prevent IL-2 transcription)
2) Used in transplant, psoraisis, rheumatoid arthritis
3) Nephotoxic, HTN, neurotoxicity, gingival hyperplasia
130
Mechanism, use, toxicity, tacrolimus (FK506)?
1) Calcinurin (prevent IL-2 transcription)
2) Transplant rejection
3) Nephrotoxicity, diabtetes, hirutism
131
Mechanism, use, toxicity sirolimus?
1) mTOR inhibitor, prevents IL-2
2) Kidney transplant
3) Pancytopenia, insulin resistance, hyperlipidemia (NOY nephrotoxicity)
132
Mechanism, Use, toxicity daclizumab, basilixmab?
1) Blocks IL-2
2) Used in kidney transplant
3) HTN, tremor
133
Mechanism, use, toxicity, azathioprine?
1) Anti-metabolite (inhibit lymphocyte proliferation)
2) Transplant rejection, rheumatoid arthritis, Crohn, glomerulonephritis
3) Leukopenia, anemia, thrombocytopenia
134
Mechanism, use,toxicity of MMF?
1) Prevents purine synthesis of B and T cells
2) Transplant rejection, rheumatoid arthritis, lupus nephritis
3) GI upset, pancytopenia, HTN, hyperglycemia, less neurotoxic and nephrotoxic
135
Mechanism, use, toxicity of corticosteroids?
1) Suppress B and T cells, induce apoptosis of T lymphoctyes
2) Transplant rejection and prophylaxis, autoimmune and inflammatory disorders
3) Hyperglycemia, osteoporosis, central obesity, avascular necrosis of femoral head, psychosis
136
Adesleukin IL-2 (recombinent cytokines) agent and clinical uses?
1) Renal cell carcinoma, and metastatic melanoma
137
Recombinent cytokines Epoetin alfa?
Anemias
138
Filgrastin (G-CSF)?
Recovery for bone marrow
139
Sargramostim (GM-CSF)?
Recovery of bone marrow
140
IFN-alpha?
1) Chronic hepatitis B and C, Kaposi Sarcoma, malignant melanoma
141
IFN- Beta?
1) Multiple sclerosis
142
IFN-gamma?
Chronic granulomatous disease
143
Romiplostin, eltrombopage (Thrombopoietin receptor agonist)?
Thrombocytopenia
144
Oprelvekin?
Thrombocytopenia
145
Cancer therapy: Alemtuzumab?
1) Target: CD52
| 2) Clinical use: CLL, MS
146
Cancer therapy Bevacizumab?
1) Target VEGF
| 2) colorectal cancer, renal cell carcinoma
147
Cancer therapy Cetuximab?
1) Target EGFR
2) Stage IV colorectal cancer
3) Head and neck cancer
148
Cancer therapy Rituximab?
1) Targets CD 20
2) B Cell, non-hodgkin
3) Lymphoma
149
Cancer therapy Trastuzumab?
1) Her2/neu
| 2) Breast cancer
150
What are threee medications that can be used to treat IBD, rheumatoid arthritis, ankolizing spondylitis and psorarias?
1) Adalimumab, certolizumab, infliximab
| 2) Works on soluable TNF-alpha
151
Autoimmune therapy eculizumab?
1) Complement protein C5
| 2) Paroxysmal nocturnal hemoglobinuria
152
Autoimmune therapy natalizumab?
1) Alpha 4 integrin
2) Multiple sclerosis
3) Crohn's disease
153
What are other applications for abciximab?
1) Platelet glycoprotiens IIb/IIIA
| 2) Antiplatelet for prevention of ischemic complications in patients
154
What are other uses for denosumab?
1) Osteoporosis (inhibits osteoclasts)
155
What are applications for digoxin Fab?
1) Antidote for digoxin toxicity
156
Applications for omalizumab?
1) Targets IgE
| 2) Prevents allergic asthma
157
Applications for Palizumab?
1) RSV F protein
| 2) RSV prophylaxis for high risk infants
158
What medication can be used for age related macular degeneration?
1) Ranibizumab
| 2) Bevacizumab
