Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Step 1 - Immunology > Immune responses > Flashcards

Immune responses Flashcards

1
Q

Actue-phase reactants are mainly produced by

A

liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

APR are induced by

A

IL-6

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Opsonin that fixes complement and facilitates phagocytosis

A

C-reactive protein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Function of ferritin

A

Binds and sequesters iron to inhibit microbial iron scavenging

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

APR that correlates with ESR

A

Fibrinogen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

APR that dicreases iron absorption by degrading ferroportin and iron release from macrophages

A

Hepcidin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Acute phase reactants: upregulated

A 
C reactive protein
Ferritin
Fibrinogen
Hepcidin
Serum Amyloid A
Procalcitonin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Prolonged elevation can lead to amyloidosis

A

Serum amiloyd A

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Acute phase reactants: downregulated

A

Albumin

Transferrin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

System of hepatically synthesized plasma proteins that play a role in innate immunity and inflammation

A

Complement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Membrane attack complex defends against

A

Gram - bacteria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Pathways of complement activation

A
  1. Classic pathway: IgG or IgM mediated
  2. Alternative pathway: microbe surface molecules
  3. Lectin pathway: mannose or other sugars on microbe surface
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

C3b function

A

Opsonization: C3B Binds Bacteria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

C3a, C4a, C5a function

A

Anaphylaxis: A

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

C5a function

A

Neutrophil chemotaxis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

C5bC9 function

A

Cytolisis by membrane attack complex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Opsonins

A

C3b: binds bacteria

IgG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Opsonin function

A

Greek: prepare for eating=enhance fagocytosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Secondary function of C3b

A

Clearing immune complexes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Inhibitors of complement, preventing complement activation on self cells

A

DAF: decay accelerating factor: CD55

C1 esterase inhibitor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

C3 deficiency

A
  1. Increases risk of severe recurrent pyogenic sinus and respiratory tract infections
  2. Susceptibility to type III hypersensitivity reactions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

C5-C9 deficiencies

A

Susceptibility to recurrent Neisseria bacteriemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

C1 esterase inhibitor deficiency

A

Hereditary angioedema due to unregulated activation of kallikrein that increases bradykinin
Low C4 levels
ACE inhibitors are contraindicated (bradykinin causes dry cough)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

CD55 (DAF) deficiency

A

Complement mediated lysis of RBCs and paroxysmal nocturnal hemoglobinuria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Hereditary angioedema

A

C1 esterase inhibitor deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Inerleukines: hot t-bone steak

A 
Il1: fever
IL2: stimulates T cells
IL3: stimulates bone marrow
IL4: Stimulates IgE production
IL5: Stimulates IgA production
IL6: Stimulates akute-phase protein production
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Major chemotactic factor for neutrophils

A

IL-8

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

IL-12 functions

A

Induces differentiation of T cells into Th1 cells

Activates NK cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Tumor necrosis factor alpha function

A

Activates endothelium
WBC recruiment
Vascular leak

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Causes cachexia in malignancy

A

Tumor necrosis factor alpha

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Maintains granulomas in Tuberculosis

A

Tumor necrosis factor alpha

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Cytokines secreted by macrophages

A

1, 6,8,12,TNFalpha

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

IL that funcitions like GM-CSF

A

IL.3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Secreted by T cells in response to antigen/IL-12 from macrophages; stimulates them to phagocyte pathogens; Inhibits differentiation of Th2 cells

A

Interferon gamma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Attenuate immune response

A

TGF beta

IL-10

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Enhances class switching to IgE and IgG

A

IL-4 (Th2)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q 
Enhances class switching to IgA
Stimulates eosinphils
A

IL-5

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Increases MCH expression and antigen presentation by all cells

A

Interferon gamma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Respiratory (oxidative burst)

A

Activation of phagocyte NADPH oxidase complex which utilizes 02 releasing ROS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Deficiency of NADPH oxidase

A

Chronic granulomatous disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Patients with NADPH oxidase are at risk of

A

Infection by catalase positive species:

  • S.aureus
  • Aspergillus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Protein in P aeruginosa that generates ROS to kill competing microbes

A

Pyocyanin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Part of innate host defense against RNA and DNA viruses, synthesed by virus infected cells that act locally on uninfected cells

A

Interferon alpha and beta

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Binds do B7 of APC

A

CD28 in T cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Cytotoxic T cells coreceptors for HIV

A

CXCR4

CCR5

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Co receptor for EBV in B cells

A

CD21: you can drink beer at the bar when you are 21

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Marker for NK

A

CD56

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Hematopoietic stem cells, cell surface marker

A

CD34

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

State during which a cell cannot become activated by exposure to its antigen

A

Anergy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

T and B cells become anergic when

A

Exposed to their antigen without costimulatory signal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Bacteria that can produce superantigens

A

S pyogenes

S aureus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Superantigens effect

A

Cross-link te beta region of the T cell receptor to the MHC class II on APCs: activate Cd4+: massive release of cytokines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Antigenic variation examples

A
  1. Bacteria: salmonella, Borrelia recurrentis (relapsing fever), N gonorrhoeae (pilus protein)
  2. Viruses: inflenza, HIV, HCV
  3. Parasites: trypanosomes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Receiving preformed antibodies is a form of

A

Passive immunity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Treatment in non-vaccinated After exposure to:

Tetanus toxin, Botulinum toxin , HBV, Varicella, Rabies virus, diphteria

A

Preformed antibodies (passive)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Duration of passive immunity

A

Short span of antibodies: 3 weeks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Vaccines are a for of ____ immunity

A

Active: humoral (B cells) or cellular (T cells)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Types of vaccine

A
  1. Live attenuated vaccine

2. Inactive or killed vaccine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Live attenuated vaccines that can be given to HIV patients who have a CD4 account >200/mm3

A

MMR: triple vírica

Varicella

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Examples of Live attenuated vaccine

A 
BCG: Bacilo Calmette-Guerin: tbc
Measles
Mups
Polio: Sabin
Rotavirus
Rubella
Varicella
Yellow fever
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Live attenuated vaccine induce a

A

Cellular and humoral response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Inactivated or killed vaccine induce a

A

Humoral response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Examples of inactivated vaccines

A 
Rabies
Influenza
Polio: Salk
Hepatitis A
RIP always
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Hypersensitivity types

A 
ACID
Type I: Anaphylactic and Atopic:. antigen-IgE
Type II: Citotoxic: antibody mediated
Type III: Immune complex
Type IV: Delayed, cell mediated
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Hypersensitivity antibody mediated types

A

I, II, III

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Free antigen cross links IgE on presintized mast cells and basophils

A

Hypersensitivity type I

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Antibodies bind to cell surface antigens

A

Hypersensitivity type II

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Hypersensibility type I tests

A

Skin test

Blood test: ELISA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Hypersensibility type II tests

A

Direct Coombs test

Indirect Coombs test

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Direct coombs test detects

A

Antibodies Directly attached to RBC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Indirect Coombs test detects

A

Presence of unbound Antibodies in the serum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Type II hypersensibility reactions

A
  1. Cellular destruction
  2. Inflamation
  3. Cellular dysfunction
73
Q

Examples of type II Hs cellular destruction

A

Hemolytic disease of the newborn
Immune thrombocytopenic purpura
Transfusion reactions
Autoinmune-hemolytic anemia

74
Q

Examples of type II Hs cellular inflamation

A

Goodpasture syndrome: Ab anti-GBM
Rheumatic fever
Hyperacute transplant rejection

75
Q

Examples of type II Hs cellular disfunction

A

Myasthenia gravis

Graves disease

76
Q

Immune complex antigen-antibody (IgG) are responsable for hypersensitivity reaction type

A

III

77
Q

Hypersensitivity reaction type III

A

Immune complex antigen antibody activates complemente which attrack netrophils that release lysosomal enzymes

78
Q

Examples of hypersensitivity reaction type III

A

SLE
Polyarteritis nodosa
Postestreptococcal glomerulonepfritis

79
Q

Serum sickness

A

hypersensitivity reaction type III
Antibodies to foreign proteins (drugs) are produced
Fever, urticaria, arthalgia, proteinuria, lymphadenopathy

80
Q

Arthus reaction

A

hypersensitivity reaction type III
Intradermal injection of antigen into presensitized individual leads to immune complex formation in the skin
Edema, necrosis, complement activation

81
Q

hypersensitivity reaction type IV mecanisms

A

Direct cell cytotoxicity CD8+

Delayed type hypersensitivity: CD4+

82
Q

Examples of hypersensitivity reaction type IV

A 
Type 1 DM: CD8
Contact dermatitis
Graf versus hostage
PPD and patch tests
4Ts: transplant rejections, T cells, TB skin tests, touching (contact dermatitis)
83
Q

Blood transfusion reactions

A
  1. Allergic/anaphylactic reaction
  2. Febrile nonhemolytic transfusion reaction
  3. Acute hemolytic transfusion reaction
  4. Transfusion-related acute lung injury
84
Q

Transfusion to IgA deficient individuals

A

Blood products without IgA

85
Q

Allergic anaphylactic reaction to blood transfusion

A

Type 1 hypersensitivity

86
Q

Febrile nonhemolytic transfusion reaction

A

Type 2 hypersensitivity reaction

87
Q

Acute hemolytic transfusion reaction

A

Type 2 hypersensitivity reaction

88
Q

Donor anti-leukocyte antibodies against recipient neutrophils and pulmonary endothelial cells

A

Transfusion related acute lung injury

89
Q

Autoantibody implicated in Miastenia gravis

A

Anti Ach Receptor

90
Q

Autoantibody implicated in Goodpasture syndrome

A

Anti glomerular basement membrane

91
Q

Autoantibody implicated in antiphospholipid syndrome

A

Anti beta2 glycoprotein

92
Q

Autoantibodies implicated in SLE and antiphospholipid syndrome

A

Anticardiolipin

Lupus anticoagulant

93
Q

Autoantibody implicated in CREST syndrome

A

Anticentromere

94
Q

Autoantibody implicated in penfigus vulgaris

A

Anti-desmoglein (desmosome)

95
Q

Autoantibody implicated in DM1

A

Anti-glutamic acid decarboxylase

Islet cell cytoplasmic antibodies

96
Q

Autoantibody implicated in polymiositis and dermatomyositis

A

Antisynthetase: anti Jo1
Anti SRP
Antihelicase: anti mi 2

97
Q

Autoantibody implicated in Hashimoto thyroiditis

A

Antimicrosomal
Antithyroglobulin
Anti thyroid peroxidase

98
Q

Autoantibody implicated in 1º biliary cirrosis

A

Antimitochondrial: AMA

99
Q

Autoantibody implicated in Pernicious anemia

A

Antiparietal cell

Anti intrinsic factor

100
Q

Autoantibody implicated in 1º membranous nephropathy

A

AntiPLA2 Rc

101
Q

Autoantibody implicated in Slcerodermia

A

Anti-Scl-70 (Dna topoisomerase I)

102
Q

Disease in which autoantibody Anti-smooth muscle has an active role

A

Autoimmune hepatitis type I

103
Q

Autoantibody implicated in Sjögren syndrome

A

Anti-SSA
Anti-SSB
Sjögren syndrome: SS

104
Q

Autoantibody implicated in Graves disease

A

Anti TSH receptor

105
Q

Autoantibody implicated in Lambert Eaton myasthenic syndrome

A

Anti presynaptic voltage gated CALCIUM channel

106
Q

Autoantibody implicated in Celiac disease

A

IgA anti endomysial
IgA anti-tissue transglutaminase
If IgA deficient individual: IgG

107
Q

p-ANCA diseases

A
  • Churg-strauss
  • Microscopic polyangiitis
  • Ulcerative colitis
108
Q

c-ANCA diseases

A

Wegner granulomatosis

109
Q

Autoantibody implicated in reumathoid arthitis

A

Reumatoid factor: IgM vs IgG Fc region

Anti-CCP

110
Q

Autoantibody implicated in SLE

A

ANA
Anti dsDNA
Anti Smith

111
Q

Autoantibody implicated in drug-induced lupus

A

Anti-histone

112
Q

Autoantibody implicated in mixed connective tissue disease: SLE, sclerodermia, polymyositis

A

Anti-U1 RNP

113
Q

B cell immunodeficiencies

A

Bruton (X-linked) agammaglobulinemia
Selective IgA deficiency
Common variable immunodeficiency

114
Q

X linked (Bruton) agammaglobulinemia: deffect

A

Deffect in BTK : B cell tyrosine kinase
No B cell maturation
X linked recessive: higher prevalence in boys

115
Q

Recurrent bacterial and enteroviral infections after 6 months from birth

A

X linked (Bruton) agammaglobulinemia: No more maternal IgG is left

116
Q

Absent B cells in peripheral blood
Low Ig of all isotypes
Absent/scanty lymph nodes and tonsils
Life vaccines contraindicated

A

X linked (Bruton) agammaglobulinemia

117
Q

Most common 1ary immunodeficiency

A

Selective IgA deficiency

118
Q

Presentation of Selective Ig A deficiency

A
  • Majority are asymptomatic
  • Airway and GI infections
  • Atopy
  • Anaphylaxis to IgA containing products: blood
119
Q

Selective Ig A deficiency has increased susceptibility to

A

Giardiasis

120
Q

Defect in B cell differentiation

A

Common variable immunodeficiency

121
Q

Low count of plasma cells and immunoglobulins

A

Common variable immunodeficiency

122
Q

Increased risk of autoimmune disease, bronchiectasis, lymphoma and sinopulmonary infections

A

Common variable immunodeficiency

123
Q

T cell immunodeficiencies

A
  1. Thymic aplasia: DiGeorge syndrome
  2. IL-12 receptor deficiency
  3. Autosomal dominant hyper-IgE syndrome: Job syndrome
  4. Chronic mucocutaneous candidiasis
124
Q

22q11 deletion

A

DiGeorge syndrome: Di=22

125
Q

DiGeorge syndrome

A

Failure to develop 3rd and 4th pharyngeal pouches: absent thymus and parathyroids

126
Q

DiGeorge findings

A 
T disease:
Tetany: hipocalcemia
T cell deficiency: recurrent infections
ConoTruncal abnormalities: Tetralogy of Fallot, truncus arteriosus
Chromosome Twenty Two
Thymic aplasia
Hypertelorism
127
Q

IL-12 Rc deficiency: consequence and inheritance

A

Low Th1 response

Autosomal recessive

128
Q

Autosomal dominant hyperIgE syndrome: Job syndrome: deficiency

A

Deficiency of Th17 cells due to STAT3 mutation: impared recruiment of neurophils

129
Q

isolated Low IFN gamma (immunodeficiency)

A

IL12 receptor deficiency

130
Q 
Coarse Facies
Cold staphlococcal abscesses
Retained primary teeth
High IgE
Dermatologic problems
Bone fractures from minor trauma
A

Autosomal dominant hyperIgE syndrome: Job syndrome: deficiency

131
Q

High IgE
Low IFN gamma
High Eosinophils
Immunodeficiency

A

Autosomal dominant hyperIgE syndrome: Job syndrome: deficiency

132
Q

Absent in vitro T cell proliferation in response to Candida agents

A

Chronic mucocutaneous candidiasis

133
Q

B and T cell immunodeficiencies

A
  1. Severe combined immunodeficiency
  2. Ataxia telangiectasia
  3. Hyper IgM syndrome
  4. Wiskott-Aldrich syndrome
134
Q

Severe combined immunodeficiency defect

A

Deffective IL-2R gamma chain (X linked, most common)

Deffective adenosine deaminase (AR)

135
Q

Treatment of Severe combined immunodeficiency

A

Avoid live vacines
Antimicrobial prophylaxis and IVIg
Bone marrow transplant curative with no concern for rejection

136
Q

Absence of thymic shadow in CXR, germinal centers (lymph node biopsy) and T cells (flow citometry)

A

Severe combined immunodeficiency

137
Q

low T cell receptor excision circles (TRECs)

A

Severe combined immunodeficiency

138
Q

Failure to thrive, chronic diarrea and thrush

Recurrent viral, bacterial, fungal and protozoal infections

A

Severe combined immunodeficiency

139
Q

Deffect in ataxia telangiectasia

A

ATM gene: failure to repair DNA double strand breaks: cell cycle arrest

140
Q

ataxia telangiectasia triad

A
  1. Ataxia
  2. Angiomas: telangiectasia
  3. Ig A deficiency
141
Q

high AFP in immunodeficiency

A

ataxia telangiectasia

142
Q

High risk of lymphoma and leukemia in immunodeficiency

A

ataxia telangiectasia

143
Q

Defective CD40L on Th cells

A

HyperIgM syndrome: class switching deffect

144
Q

HyperIgM syndrome inheritance

A

X linked recessive

145
Q

Wiskott Aldrich syndrome: defect

A

WASp gene: leucocites and platelets unable to reorganise actin cytoskeleton: deffective antigen presentation

146
Q

Wiskot Aldrich syndrome presentation

A 
WATER
Wiskott aldrich
Thrombocytopenia
Eczema
Recurrent pyogenic infections
147
Q

Wiskott Aldrich syndrome inheritance

A

Xlinked recessive

148
Q

X linked recessive immunodefficiencies

A

Xlinked Bruton Agammaglobulinemia
Severe combined immunodeficiency IL-2R gamma chain
Hyper IgM syndrome
Wiskott Aldrich syndrome

149
Q

Phagocyte disfunction diseases

A
  1. Leukocyte adhesion deficiency type 1
  2. Chédiak.-Higashi syndrome
  3. Chronic granulomatous disease
150
Q

Defect in Leukocyte adhesion deficiency

A

LFA 1 integrin (CD18)

151
Q

Findings in Leukocyte adhesion deficiency

A

high neutrophils

Absence of neutrophils at infection sytes (impaired migration and chemotaxis)

152
Q

Delayed separation of umbilical cord

A

Leukocyte adhesion deficiency

153
Q

Chédiak-Higashi syndrome defect

A

LYST: lysosomal trafficking regulator gene: microtubule disfunction in phagosome-lysosome fusion

154
Q

Partial albinism

A

Chédiak-Higashi: melanosoma

155
Q

Giant granules in granulocytes and platelets
Pancytopenia
Coagulation defects

A

Chédiak-Higashi

156
Q

Chronic granulomatous disease defect

A

Defect of NADPH oxidase: less reactive oxigen species and less respiratory burst in neutrophils

157
Q

Nitroblue tetrazolium dye reduction test fails to turn blue

A

Chronic granulomatous disease

158
Q

Abdnormal dihydrodamine test: less green fluorescence

A

Chronic granulomatous disease

159
Q

Bacterial infections in B cell immunodeficiency

A

Encapsulated: Some Killers Have Pretty Nice Capsules

  1. Streptococcus pneumoniae, Group B streptococcus, Salmonella
  2. Klebsiella pneumoniae
  3. Haemophillus influenzae type B
  4. Pseudomonas aeruginosa
  5. Neisseria meningitidis
  6. Criptoccoccus neoformans
160
Q

Bacterial infections in T cell immunodeficiency

A

Sepsis

161
Q

Bacterial infections in patents with low granulocytes

A
  1. Staphylococcus
  2. Burkholderia cepacia
  3. Pseudomonas aeruginosa
  4. Serratia
  5. Nocardia
162
Q

Bacterial infections in complement deficiency

A
  1. Early complement deficiencies: Encapsulated

2. C5-C9 deficiency: Neisseria

163
Q

B cell deficiencies tend to produce recurrent _____ infections

A

Bacterial

164
Q

T cell deficiencies tend to produce recurrent ___ and ____ infections

A

Viral

Fungal

165
Q

Syngenic graft (isograft)

A

From twin or clone)

166
Q

Allograft

A

From nonidentical individual of the same species

167
Q

Xenograft

A

From different species

168
Q

Types of transplant rejection

A
  1. Hyperacute: type II HS
  2. Acute: type IV HS (cellular/humoral)
  3. Chronic: type IV and II HS
  4. Graft vs host disease: tupe IV
169
Q

Pathogenesis of hyperacute transplant rejection

A

Pre existing recipient antibodies react to donor antigen (type II hypersensitivity reaction), activate complement

170
Q

Features of hyperacute Transplant rejection

A

Widespread thrombosis of graft vessels: ischeima/necrosis

Graft must be removed

171
Q

Types of acute transplant rejection

A

Type IV hypersensitivity reaction:

  1. Cellular: T cells CD8+ against donor MHC
  2. Humoral: B cells: similar to hyperacute, except antibodies develop after transplant
172
Q

Features of acute transplant rejection

A
  1. Vasculitis of graft vessels with dense intersticial lympocytic infiltrate
  2. Prevent or reverse with immunosupressants
173
Q

Pathogenesis of chronic transplant rejection

A

CD4+ T cells respond to recipient APCs presenting donor peptides, including allogenic MHC

174
Q

Features of chronic transplant rejection

A

Recipient T cells react and secrete cytokines: proliferation of VSM, parenchymal atrophy and intersticial fibrosis
Atteriosclerosis

175
Q

Organ-specific examples of Chronic transplant rejection

A
  1. Lung: bronchiolitis obliterans
  2. Heart: accelerated atheriosclerosis
  3. Kidney: Chronic graft nephropathy
  4. Liver: Vanishing bile duct syndrome
176
Q

Grafted immunnocompetent T cells proliferate in the immunocompromised host and reject host cells with foreign proteins

A

Graft vs host disease

177
Q

In what situation is graft vs host disease considered beneficial?

A

Bone marrow transplant for leukemia

178
Q

Graft vs host disease is more frequent in ____ and ____ transplants

A

Bone marrow
Liver
(more lymphocytes)

Step 1 - Immunology (4 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions