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IMMUNOLOGY- Immune Responses Flashcards

1
Q

Which are acute phase reactants?

A

Factors whose serum concetration change significantly in response to inflammation

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2
Q

When and where is produced the acute phase reaction?

A

Produced by the lieer in both acute and chronic inflammatory states

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3
Q

Who induces acute phase reactions?

A

IL-6, IL-1, TNF α and IFN γ

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4
Q

How are acute phase reactants classified?

A

Positive

Negative

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5
Q

Which is the upregulated and which is the downregulated in Acute phase phase reactants?

A

Positive (Upregulated)

Negative (Downregulated)

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6
Q

In Acute phase phase reactants which are positive regulators?

A 
Serum Amyloid A
C reactive protein 
Ferritin
Fibrinogen
Hepcidin
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7
Q

C reactive protein

A

Opsonin

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8
Q

Which is the function of Opsonin?

A

Fixes complement and facilitates complement

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9
Q

What is teh clinical meaning of C- reactive protein?

A

Sign of ongoing inflammation

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10
Q

Which is the relationship between ferritin and microbials?

A

ferritin binds ans sequesters iron to inhibit microbial iron scavenging

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11
Q

What is Fibrinogen?

A

Coagulation factor

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12
Q

What does Fibrinogen promotes?

A

Endothelial repair

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13
Q

Which lab correlates with Fibrinogen?

A

Erythrocyte sedimentation rate (ESR)

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14
Q

This is the function of Hepcidin

A

Prevents release of iron bound by ferritin

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15
Q

Which disease does Hepcidin prevents?

A

Anemia of chronic disease

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16
Q

These are Negative (Downregulators) or Acute phase reactants

A

Albumin

Transferrin

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17
Q

What is the effect of Albumin reduction?

A

Conserves amino acids for positive reactants

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18
Q

What is the effect of Transferrin?

A

Internalized by macrophages to sequester iron

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19
Q

What is the main purpose of the Complement?

A

System of interacting plasma proteins that play a role in innate immunity and inflamation

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20
Q

This is a mechanism of defense used in complement that uses the membrane?

A

Membrane Attack Complex (MAC)

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21
Q

From which bacterias does Membrane Atack complex (MAC) protects?

A

Against Gram negative bacteria

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22
Q

Which are the pathways to activate Complement?

A

Classic pathway
Alternative pathway
Lectine pathway

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23
Q

Who mediates classic pathway of complement?

A

IgG or IgM

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24
Q

Who stimulates the activation of alternative pathway of Complement?

A

Microbe surface molecules

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25
Who stimulates Lectin pathway of complement?
Mannose or other sugars on microbe surface
26
What does C3b manages?
Opsonization
27
These complements carried anaphylaxis process
C3a, C4a and C5a
28
This complement manages Neutrophil chemotaxis
C5a
29
What is the purpose of C5b-9?
Cytolysis by membrane atack complex (MAC)
30
Which complement binds bacterias?
C3b
31
Who are the primary opsonins in bacterial defense?
C3b and IgG
32
Which other function does C3b has?
Helps clear immune complexes
33
Whoare inhibitors of Complement?
Decay accelerating factor and C1 esterase inhibitor help prevent complement activation on self cells (eg RBC)
34
Which are Decay accelerating factors?
DAF, aka CD55
35
These are complement disorders
C1 esterase inhibitor deficiency C3 deficiency C5- C9 deficiencies DAF (GPI anchored enzyme) deficiency
36
What does C1 esterase inhibitor deficiency clinically cause?
Hereditary angioedema
37
Which medicines are contraindicated in C1 esterase inhibitor deficiency?
ACE inhibitors
38
Which diseases are increased in C3 deficiency?
Increase risk of Severe, recurrent pyogenic sinus and respiratory tract infections Increases Susceptibility to type III hypersensitivity reactions
39
From which bacteria is increased the susceptibility in C5- C9 deficiencies?
recurrent Neisseria bacterimia
40
What does DAF (GPI anchored enzyme) deficiency cause?
Complement mediated lysis of RBCs and paroxysmal nocturnal hemoglobinuria
41
How is consider IL-1?
An endogenous pyrogen
42
This is another name for IL-1
Osteoclast activating factor
43
These are the clinical manifestations of IL-1
Causes fever | Acute inflamation
44
Which is the mechanism of action of IL-1?
Activates endothelium to express adhesion molecules; induces chemokine secretion to recruit leukocytes
45
How is classified IL-6?
An endogenous pyrogen
46
Who else can secrete IL-6?
Th2 cells and macrophages
47
What is the effect of IL-6?
Causes fever and stimulates production of acute phase proteins
48
Major chemotactic factor for neutrophils
IL-8
49
This IL Induces differentiation of T cells into Th1 Cells
IL-12
50
Which other effect does IL-12 has?
Activates NK cells
51
Who secretes IL-12?
B cells and macrophages
52
Which cytokines are secreted by macrophages?
``` IL-1 IL-6 IL-8 IL-12 TNF α ```
53
Who mediates septic schock and activates endohtelium?
TNF α
54
What is the effect of TNF α?
Causes leukocyte recruitment, vascular leak
55
Which are the main effect of the first 6 IL?
``` IL-1 FEVER IL-2 stimulates T cells IL-3 stimulates bone marrow IL-4 stimulates IgE production IL-5 stimulates IgA production IL-6 stimulates acute phase protein production ```
56
These IL are secreted by all T cells
IL-2 | IL-3
57
Which is the effect of IL-2
Stimulates growth of helper , cytotoxic and regulatory T cells
58
Supports the growth and differentiation of bone marrow stem cells
IL-3
59
Functions like GM-CSF
IL-3
60
Who secretes interferon γ?
Th1 cells
61
Which properties does Interferon γ has?
Antiviral and antitumoral properties
62
What cells are activated by Interferon γ?
NK to kill virus infected cells
63
Which other effect does Interferon γ has?
Increases MHC expression and antigen presentation in all cells
64
Which IL are produced by Th2 cells?
IL-4 IL-5 IL-6
65
What effect does IL-4 has on Th2 cells?
Induces differentiation into Th2 cells
66
Promotes growth of B cells. Enhances class switching to IgE and IgG
IL-4
67
Which are the effects of IL-5?
Promotes differentiation of B cells Enhances class switching to IgA Stimulates the growtlh and differentiation of eosonophils
68
This IL modulates inflamatory response
IL-10
69
What does IL-10 do?
Inhibits action of activated T cells and Th1
70
Who else secretes IL-1?
Th2 cells and regulatory T cells
71
Who else has similar actions as IL-10 by inhibiting inflamation?
TNF β
72
Which is the importance of Interferon α and β?
A part of innate host defence against both RNA and DNA viruses
73
What are the interferons?
Are glycoproteins synthesized by viral infected cekks that act locally on uninfected cells "priming them" from viral defense
74
Once the Virus infects primed cells, what does Viral dsRNA activates?
RNAase L | Protein kinase
75
Which is the effect of RNAase L?
Degradation of viral/ host mRNA
76
What does Protein kinase inhibits?
Inhibition of viral/host protein synthesis
77
What are the results of Interferon α and β?
Essentially results in apoptosis, thereby interrupting viral amplification
78
Which cells possess MHC I?
All cells except mature RBCs
79
Which are the cell surface proteins that T cells have?
TCR CD3 CD28
80
This is the importance of TCR
Binds antigen -MHC complex
81
In which process is CD3 associated?
Associated with TCR fpr signal transduction
82
What is the effect of CD28?
Binds B7 to APC
83
These are the cell surface proteins on Helper T cells
CD4 and CD40 ligand
84
Which is the cell surface protein on Cytotoxic T cells?
CD8
85
Name all cell surface proteins for B cells
Ig (binds antigen) CD19, CD20, CD21, CD40 MHC II, B7
86
This is the receptor for EBV
CD21
87
For Macrophages these are the cell surface proteins
CD14, CD40 MHC II, B7 Fc and C3b receptors
88
Cell surface proteins on NK cells
CD16 | CD56
89
What is the effect of CD16?
Binds Fc of IgG
90
Unique marker for NK
CD56
91
What is anergy?
Self reactive T cells become nonreactive without constimulatory molecule
92
Can B cells become anergic?
B cells also become anergic, but tolerance is less complete than in T cells
93
Who can produce Superantigens?
S. pyogenes | S. aureus
94
Which are the habilities of superantigen?
Cross link the β region of the T cell receptor to the MHC class II on APCs
95
What are the effects of superantigen on T cells?
Can activate any T cell, leading to massive release of cytokines
96
Who can produce Endotoxins/ lipopolysaccharide?
Gram negative bacteria
97
Which cells are stimulated by Endotoxins/ lipopolysaccharide?
Macrophages
98
How can Endotoxins/ lipopolysaccharide stimulate macrophages?
Directly stimulates macrophages by binding to endotoxin receptor CD14, Th cells are not involved
99
Which bacterias show Antigen variation?
``` Salmonella (2 flagellar variants) Borrelia (relapsing fever) Neisseria gonorrhea (pilus protein) ```
100
Which is the classic virus that shows Antigen variation?
Influenza virus (major = shift, minor= drift)
101
This parasite has antigenic variation
Trypanosomes (programmed rearrangement)
102
How does passive acquisition of immunity happens?
Receiving preformed antibodies
103
How is the onset of acquiring passive immunity?
Rapid
104
How long does Passive immunity last?
Short span of antibodies (half life= 3 weeks)
105
Which are examples of Passive immunity?
IgA in breast milk Maternal IgG crossing placenta Antitoxin Humanized monoclonal antibody
106
After which microorganism exposure are given preformed antibodies?
Tetanus toxin Botulinum toxin HBV Rabies virus
107
How is active immunity acquired?
Exposure to foreign antigens
108
This is the onset of Active immunity
Slow
109
How long does Active immunity last?
Long lasting protection (memory)
110
Which are examples of Active immunity?
Natural infection Vaccines Toxoid
111
When is recommended the combined passive and active immunization?
For Hepatitis B or Rabies exposure
112
Which is the reason of vaccination?
Vaccines are used to induce an active immune response (humoral and/ or cellular) to specific pathogens
113
How are vaccines classified?
Live attenuated vaccine | Inactive or killed vaccine
114
What is a live attenuated vaccine?
Microorganism loses its pathogenicity but retains capacity for transient growth within inoculated host
115
Which kind of response does live attenuated vaccine induces?
Mainly induces a cellular response
116
Which is the advantage of administering live attenuated vaccines?
Induces strong, often lifelong immunity
117
Which disadvange do live attenuated vaccines have?
May revert to virulent form
118
When is contraindicated the use of live attenuated vaccines?
In pregnancy and immune deficiency
119
These are examples of live attenuated vaccines
``` Measles Mumps Rubella Polio (Sabin) Influenza (intranasal) Varicella Yellow fever ```
120
Which are the characterisitics of Inactivated or killed vaccines?
Pathogen is inactivated by heat or chemicals; maintaining epitope structure on surface antigen is important for immune response
121
Which immunity is induced with Inactivated or killed vaccines?
Humoral immunity induced
122
This is an advantage of Inactivated or killed vaccines
Stable and safer than live vaccines
123
This is a disadvantage of Inactivated or killed vaccines
Weaker immune response; booster shots usually required
124
Which are examples of Inactivated or killed vaccines?
``` Cholera Heàtitis A Polio (Salk) Influenza (injection) Rabies ```
125
How many types of Hypersensitivity exist?
I, II, III, IV
126
How else is Hypernsensitivity type I is known?
Anaphylactic and atopic
127
Which is the mechanism of action of Hypernsensitivity type I?
Free antigen cross links IgE on presensitized mast cells and basophilsm triggering immediate release of vasoactive aminesthat act at postcapillary venules (eg. histamine)
128
Why does the reaction develops rapidly in Hypernsensitivity type I?
Because of preformed antibody
129
Whho manages the delayed reaction in Hypernsensitivity type I?
Due to production of arachidonic acid metabolites (leukotrienes)
130
Which Hypernsensitivity types are mediated by antibodies?
Types I, II, III
131
Which test helps in Hypernsensitivity type I?
Skin test for specific IgE
132
This is the alternative name for Hypernsensitivity type II
Cytotoxic (antibody mediated)
133
How does Hypernsensitivity type II works?
IgM, IgG bind to fixed antigen on enemy cell, leading to cellular destruction
134
Which the three mechanism of Hypernsensitivity type II?
Opsonization leading to phagocytosis or complement activation Complement mediated lysis Antibody dependent cell mediated citotoxicity, ussually due to NK cells or macrophages
135
In Hypernsensitivity type II, who lead to Membrane attack complex?
Antibody and complement
136
Which lab test helps for Hypernsensitivity type II?
Direct and Indirect Coombs
137
What does Direct Coombs detects?
Detects antibodies thathave adhered to patients RBCs
138
Which is an example of Direct Coombs?
Test an Rh + infant of an Rh - mother
139
This is what indirect coombs detects
Detects antibodies that can adhere to other RBCs
140
Give an example of Indirect coombs
Test an Rh - woman for Rh + antibodies
141
This Immunity type is also known as Immune complex
Hypernsensitivity type III
142
What happens in Immune complex immunity?
Antigen- antibody (IgG) complex activate complement, which attracts neutrophils; neutrophils release lysosomal enzymes
143
Which diseases are Immune complex immunity related?
Serum sickness | Arthus reaction
144
What happens in Serum sickness?
An immune complex disease in which antibodies to the foreign proteins are produced
145
How much times does it takes for antibodies to be produced in Serum sickness?
5 days
146
How is damage produced in Serum sickness?
Immune complexes form and are deposited in membranes, where they fixed complement (leading to tissue damage)
147
Who is more common Serum sickness or Arthus reaction?
Serum sickness
148
What is Arthus reaction?
A local subacute antibody mediated hypersensitivity (type III) reaction
149
This an example of how to cause Arthus reaction
Intradermal onjection of antigen induces antibodies, which form antigen-antibody complexes in the skin
150
Which are the clinical manifestations of Arthus reaction?
Edema, necrosism and activation of complement
151
What causes most cases of Serum sickness?
By drugs acting as haptens
152
When do you suspect Serum sickness?
Fever, urticaria, arhtralgias, proteinuria, lymphadenopathy 5-10 days after antigen exposure
153
What causes Arthus reaction?
Antigen- antibody complexes
154
Which test can be used for Arthus reaction?
Immunofluorescent staining
155
Delayed type of Immunity
Hypersensitivity Type IV
156
Who mediates delayed type of immunity?
T cell mediated
157
How does Hypersensitivity Type IV works?
Sensitized T lymphocytes encounter antigen and then release lymphokines
158
Which is the final result of Hypersensitivity Type IV?
Macrophage activation; no antibody involved
159
Can Hypersensitivity Type IV be transferable by serum?
Cell mediated; therefore it is not transferable by serum
160
Which test are used for Delayed immunity?
Patch test, PPD
161
Which is the mnemonic for Hypersensitivity types?
``` ACID Anaphylactic and Atopic (Type I) Cytotoxic (Type II) Immune complex (Type III) Delayed (cell mediated, Type IV) ```
162
Which are examples Hypersensitivity type I disorders?
Anaphylaxis | Allergic and Atopic disorders
163
Bee sting, some food/drug allergies, are examples of this Hypersensitivity disorder
Hypersensitivity type I- anphylaxis
164
These are allergic and atopic disorders
``` Rhinitis Hay fever Rczema Hives Asthma ```
165
Which are the presentation of Hypersensitivity type I disorders?
Immediate Anaphylctic Atopic
166
Name examples of Hypersensitivity type II disorders
``` Autoimmune hemolytic anemia Pernicious anemia Idiopathic thrombocytopenic purpura Erytroblastosis Fetalis Acute hemolytic transfussion reactions Rheumatic fever Goodpasture syndrome Bullous pemphigoid Pemphigus vulgaris ```
167
Which are the characteristics of Hypersensitivity type II disorders?
Disease tends to be specific to tissue or site where antigen is found
168
Give examples of Hypersensitivity type III disorders
``` SLE Polyartheritis nodosa Poststreptococcal glomerulonephritis Serum sickness Arthus reaction (swelling and inflammation following tetanus vaccine) ```
169
Which possible presentations can Hypersensitivity type III disorders have?
Can be associated with vasculitis and systemic manifestations
170
These are Hypersensitivity type IV disorders
``` Multiple sclerosis Guillian Barre syndrome Graft versus host disease PPD (test for M. tuberculosis) Contact dermatitis (poison ivy, nockel allergy) ```
171
What is a characteristic of Hypersensitivity type IV disorders?
Response is delayed and does not involve antibodies
172
Which are the possible blood transfusion reaction?
Allergic reaction Anaphylactic reaction Febrile nonhemolytic transfusion reaction Acute hemolytic transfusion reaction
173
Which is the pathogenisis of Allergic reaction to Blood transfusion?
Type I hypersensitivity reaction against plasma proteins in transfused blood
174
In case of allergic reaction to blood transfusion which could be the clinical presentations?
Urticaria, pruritusm wheezing, fever
175
How do you treat Allergic reaction to Blood transfusion?
With antihistamines
176
What is anaphylactic reaction to blood transfusion?
Severe allergic reaction
177
What happens in anaphylactic reaction to blood transfusion? and what is the solution?
IgA deficient individuals must receive blood products that lack IgA
178
Which is the clinical presentation of anaphylactic reaction to blood transfusion?
Dyspnea, bronchospasm, hypotensionm respiratory arrestm shock
179
Which kind of Hypersensitivity disorder is Febrile nonhemolytic transfussion reaction?
Type II hypersensitivity reaction
180
What happens in Febrile nonhemolytic transfussion reaction?
Host antibodies against donor HLA antigens and leucocytes
181
These are the manifestations Febrile nonhemolytic transfussion reaction
Fever, headachesm chills, flushing
182
Which kind of Hypersensitivity disorder is Acute hemolytic transfussion reaction?
Type II hypersensitivity reaction
183
How is Acute hemolytic transfussion reaction classify?
Intravascular hemolysis | Extravascular hemolysis
184
What happens in Intravascular hemolysis in Acute hemolytic transfussion reaction?
ABO blood group incompatibility
185
This is what happens in Extravascular hemolysis in Acute hemolytic transfussion reaction
Host antibody reaction against foreign antigen in donor RBCs
186
Clinical presentation of Acute hemolytic transfussion reaction
Fever, hypotension, tachypnea, tachycardia, flank pain, hemoglobinemia (intravascular), jaundice (extravascular hemolysis)
187
Which could be the complication caused by bacterias in case of No T cells?
Sepsis
188
In case of No B cells which bacterias can caused disease?
``` Encapsulated (SHiNE SKiS) S. pneumoniae H. influenzae type B Neisseria meningitidis Escherichia coli Salmonella Klebsiella pneumoniae Strep group B ```
189
We are at risk of these bacterias infection in case of no granulocyte
Staphylococcus Burkholderia cepacia Serratia Nocardia
190
Which bacteria is the principal that affects in case of no complement?
Neisseria (No membrane attack complex)
191
These viruses increased the risk of infection if No T cells
CMV, EBV, JCV, VZV | Chronic infection with respiratory/ GI viruses
192
Which vaccines are contraindicated in patients with no B cells?
Live vaccines
193
Which viruses infect in patients without B cells?
Enteroviral encephalitis | Polivirus
194
For patients with no T cells, are at higher risk for these Fungi infections
Candida | Pneumocystis Pneumoniae
195
For patients without IgA this is the most common parasite infection
GI giardiasis
196
No granulocyte patients are at higher risk of these fungi infection
Candida, Aspergillus
197
Patients with no B cells are at higher risk of recurrent infection by...
Bacterias
198
For patients with no T cells these microorganism are the most probable cause of infection
Fungal and Viral infection
199
Which are B cell disorders?
X-linked agammaglobulinemia
200
This is an alternative name for X-linked agammaglobulinemia
Bruton agammaglobulinemia
201
Which inheritance mode does Bruton agammaglobulinemia has? who are affected?
X linked recessive | Increase in boys
202
What is defective in X-linked agammaglobulinemia?
Defect in BTK, atyrosine kinase gene→ No B cell maturation
203
Which is the clinical presentation of X-linked agammaglobulinemia?
Recurrent bacterial and enteroviral infections after 6 months (Decreased maternal IgG)
204
These could beclinical findings in X-linked agammaglobulinemia
Absent/ scanty lymph nodesand tonsils
205
Which are the findings in Bruton agammaglobulinemia?
Normal CD19+ B cell count | ↓ Pro B, ↓ Ig of all classes
206
Which is the most common immunodeficiency?
Selective IgA deficiency
207
Which is the defect in selective IgA deficiciency?
Unknown
208
Which is the clinical presentation of selective IgA deficiciency?
Majority Asymptomatic Can see: Airway and GI infection. Autoimmune disease, Atopy, anaphylaxia to IgA containing products
209
These are the lab results in selective IgA deficiciency
IgA <7 mg/ dL with normal IgG, IgM levels
210
What is wrong in Common variable immunodeficiency?
Defect in B cell differentiation | Many causes
211
When can Common variable immunodeficiency be acquired?
In 20-30s
212
These could be findings in patients with Common variable immunodeficiency
Increase risk of autoimmune disease | Bronchiectasis, lymphoma, sinopulmonary infections
213
Which labs are affected in Common variable immunodeficiency?
Decreased plasma cells | Decreased Immunoglobulins
214
These are T cell disorders
Thymic aplasia IL-12 receptor deficiency Autosomal dominant hyper IgE syndrome Chronic mucocutaneous candidiasis
215
Thymic aplasia is also known as...
DiGeorge Syndrome
216
What is affected in DiGeorge syndrome?
22q11 deletion; failure to develop 3rd and 4th pharyngeal pounches→ Absent thymus and parathyroids
217
Which are the clinical manifestations of DiGeorge syndrome?
Tetany (hypocalcemia) Recurrent Viral/Fungal infections (T cell deficiency) Conotruncal abnormalities
218
Name Conotruncal abnormalities
Tetralogy of Fallot | Truncus arteriosus
219
Which are the findigs in Thymic aplasia?
↓ T cells, ↓ PTH, ↓ Ca2+ Absent Thymic shadow on CXR 22q11 deletion defected by FISH
220
What is wrong in IL-12 receptor deficiency?
↓ Th1 response
221
Which is the inheritance mode of IL-12 receptor deficiency?
Autosomal recessive
222
When can IL-12 receptor deficiency be presented?
After administration of BCG vaccine
223
This is how IL-12 receptor deficiency can manifest
Disseminated mycobacterial and fungal infections
224
What is decreased in IL-12 recetor deficiency?
↓ IFN γ
225
Also known as Job syndrome
Autosomal dominant hyper IgE syndrome
226
What is the defect in Autosomal dominant hyper IgE syndrome?
Deficiency of Th17 cells due to STAT3 mutation→ Impaired recruitment of neutrophilstp sites of infection
227
These are the clinical findings in Job syndrome
FATED | coarse Facies, cold (noninflamed) sthapylococcal Absceses, retained primary Teeth, ↑ IgE, Dermatologic problems (eczema)
228
We see this lab alteration in Autosomal dominant hyper IgE syndrome
↑ IgE, ↓ IFN γ
229
What is altered in Chronic mucocutaneous candidiasis?
T cell dysfunction. Many causes
230
This is the presentation of Chronic mucocutaneous candidiasis
Noninvasive Candida Albicans infections of skin and mucous membranes
231
What can be found in Chronic mucocutaneous candidiasis?
Absent in vitro T cell proliferation in response to Cnadida Antigens Absent cutaneous reaction to Candida antigens
232
Which are B and T cell disorders?
Severe combined immunodeficiency (SCID) Ataxia Telangiectasia Hyper IgM syndrome Wiskott Aldrich syndrome
233
How can we classified the defects in SCID?
Defective IL-2R gamma chain (most common, X linkes) | Adenosine Deaminase Deficiency (Autosomal recessive)
234
This is how SCID can be presented
Failure to thrive, chronic diarrhea, thrush | Recurrent viral, bacterial, fungal and protozoal infections
235
Which is the treatment for SCID?
Bone marrow transplant
236
Is it possible to have a Bone marrow transplant rejection in SCID?
No concern for rejection
237
These are the findings in SCID
``` ↓T cell receptor excision circles (TRECs) Absence of thymic shadow (CXR) Germinal centers (lymph node biopsy) and T cells (flow cytometry) ```
238
Which is the problem in Ataxia Telangiectasia?
Defects in ATM gene → DNA double strand breaks → cell cycle arrest
239
Which is the triad for Ataxia Telangiectasia?
``` Cerebellar Defects (Ataxia) Spider Angiomas (telangiectasia) IgA deficiency ```
240
These are the findings in Ataxia Telangiectasia
↑ AFP ↓ IgA, IgG and IgE Lymphopenia, cerebellar athrophy
241
What is the defect in Hyper IgM syndrome?
Most commonly due to defective CD40L on Th cells= class swithcing defect
242
How is Hyper IgM syndrome genetically classify?
X linked recessive
243
Which are the infection that can occur in Hyper IgM syndrome?
Severe pyogenic infections early in life | Oportunistic infection with Pneumocystis, Cryptosporidium, CMV
244
In Labs what is altered in Hyper IgM syndrome?
↑ IgM | ↓↓ IgG, IgA, IgE
245
Which is the mutation in Wiskott- Aldrich syndrome?
Mutation in WAS gene
246
Which is the inheritance mode of Wiskott- Aldrich syndrome?
X linked recessive
247
What is the problem with T cells in Wiskott- Aldrich syndrome?
T cells unable to reorganize actin cytoskeleton
248
These is the mnemonic for Wiskott- Aldrich syndrome
``` WATER Wiskott- Aldrich syndrome Thrombocytopenic purpura Eczema Recurrent infections ```
249
Which risk are higher in Wiskott- Aldrich syndrome?
Increased risk of Autoimmune disease and malignancy
250
These are the lab alterations in Wiskott- Aldrich syndrome
↑ IgE, IgA ↓ to normal IgG, IgM Fewer and smaller platelets
251
These diseases are classified as Phagocyte dysfunction
Leukocyte adhesion deficiency (type 1) Chédiak- Higashu syndrome Chronic granulomatous disease
252
Which is the defect in Leukocyte adhesion deficiency (type 1)?
Defect in LFA-1 integrin (CD18) protein on phagocytes;
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What happens if there is a defect in LFA-1 integrin (CD18) protein on phagocytes?
Impaired migration and chemotaxis
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Inheritance mode of Leukocyte adhesion deficiency (type 1)?
Autosomal recessive
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These are characteristics of clinical presentation of Leukocyte adhesion deficiency (type 1)
Recurrent bacterial skin and mucosal infections, absent pus formation, impaired wound healing, delayed separation of umbilical cord (>30 days)
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What is increased in Leukocyte adhesion deficiency (type 1) ?
Neutrophils
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Although Neutrophils are increased in Leukocyte adhesion deficiency (type 1) what is the problem with them?
Absence of neutrophils at infection sites
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In this phagocyte dysfunction there is a defect in lysosomal trafficking regultator gene (LYST)
Chediak Higashi syndrome
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Which is other problem in Chédiak Higashi syndrome?
Microtubule dysfunction in phagosome lysosome fusion
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Which is the inheritance pattern for Chédiak Higashi syndrome?
Autosomal recessive
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Who are the main bugs who cause recurent pyogenic infections in Chédiak Higashi syndrome?
Staphylococci and streptococce
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These are the clinical manifestations of Chédiak Higashi syndrome
``` Recurrent pyogenic infections Partial albinism Peripheral neurophaty Progressive neurodegeneration Infiltrative lymphohistiocytosis ```
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These lab result are altered in Chédiak Higashi syndrome
Giant granules in neutrophils and platelets Pancytopenia Mild coagulation defects
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What is the defect in Chronicgranulomatous disease?
Defect in NADPH oxidase→ ↓ reactive oxygen species (superoxide) and absent respiratory burst in neutrophils
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This is the inheritance mode in Chronic granulomatous disease
X linked recessive
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From which microorganisms are patients suceptible in Chronic granulomatpus disease?
``` ↑ Suceptibility to catalase + organisms (PLACESS) Pseudomona Listeria Aspergillus Candida E. Coli S. aureus Serratia ```
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Which lab test help in the diagnosis of Chronic Granulomatous?
``` Abnormal dihydrorhodamine (flow cytometry) test Nitrobuline tetrazolinum test is - (test out of favor) ```
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Name all types of Graft
Autograft Syngeneic graft Allograft Xenograft
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What is a autograft?
From self
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This kind of graft comes form identical twn or clone
Syngeneic graft
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What is a Allograft?
From nonidentical individual of same species
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This type of Graft comes from different species
Xenograft
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These are all the Transplant rejection types
Hyperacute Acute Chronic Graft versus host disease
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How long does it take for rejection to be categorized as Hyperacute?
Within minutes
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Which is the pathogenesis in Hyperacute rejection?
Pre-existing recipient antibodies react to donor antigen (Type II reaction)
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What is activated in Hyperacute reaction?
Activates complement
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These are the results of Hyperacute reaction
Widespread thrombosis of graft vessels → Ischemic/necrosis
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Which are the alternatives if treatment in Hyperacute transplant reaction?
Graft must be removed
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In this kind of Trasnplant rejection it takes weeks to months for the onset
Acute rejection
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Which are the types of Acute transplant rejection?
Cellular | Humoral
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What happens in the cellular Acute Rejection?
Cytotoxic T lymphocites activated against donor MHCs
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Which is the difference between Hyperacute and Acute Humoral rejection?
Humoral is similar to Hyperacute, except antibodies develop after transplant
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Which is the pathogenisis in Acute Transplant rejection?
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate
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How do you manage Acute transplant rejection?
Prevent/ reverse with immunosupressants
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How long does it takes for Chronic transplant rejection to onset?
Months to years
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Recipient T cells perceive donor MHC as recipient MHC and react against donor antigens presented
Chronic Transplant rejection
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Does Chronic Transplant rejection has cellular or Humoral components?
Both
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How do you manage chronic transplant rejection?
Irreversible. T-cell and antibody mediated damage
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Which organs could be the main affected by Chronic Transplant rejection
Heart Lungs Liver Kidney
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This is the main damage in chronic transplant rejection to the heart
Atherosclerosis
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How is manifested the chornic transplant rejecetion in Lungs?
Bronchiolitis obliterans
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What is the effect of Chronic transplant rejection in Liver=
Vanishing bile ducts
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Which are the main features in Kidneys during chronic transplant rejection?
Vascular fibrosis | Glomerulopathy
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How much times does Graft versus host disease takes to onset?
Varies
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What happens in Graft versus host disease?
Grafted immunocompetent T cells proliferate in the immunocpromised host and reject host cells with foreign proteins
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Which is the result of Graft versus host disease?
Severe organ dysfunction
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Which are the clinical features of Graft versus host disease?
Macupapular rash Jaundice Diarrhea Hepatosplenomegaly
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In which kind of transplants is more common to see Graft versus host disease?
Usually in bone marrow and liver transplant (rich in lymphocytes)
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When is beneficial Graft versus host disease?
Potentially beneficial in bone marrow transplant for leukemia (Graft versus tumor effect)

IMMUNOLOGY (5 decks)

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