Immunology Flashcards

1
Q

What class of lymphoid organ is a lymph node ?

A

Secondary

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2
Q

Functions of lymph node

A

Filtration by macrophages

Activation /Storage of B and T cells

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3
Q

Where are B-cells located at in the lymph node ?

A

Follicle

2nd Follicle has active germinal center

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4
Q

Where are T cells found in the Lymph node

A

Paracortex (in-between the cortex and medulla)

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5
Q

What are found in the medulla of a lymph node

A

Macrophages and reticular cells

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6
Q

What part of a lymph node may be under developed in DiGeorge Syndrome ?

A

Paracorted (where the T cells are)

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7
Q

Lymph drainage : Upper limb and Lateral breast

A

Axillary

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8
Q

Lymph drainage : Stomach

A

Celiac

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9
Q

Lymph drainage : Duodenum Jejunum

A

Superior mesenteric

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10
Q

Lymph drainage : Sigmoid colon

A

Inferior mesenteric

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11
Q

Rectum (Above the pectinate line)

A

Internal iliac

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12
Q

Lymph drainage : Anal Canal

A

Superficial inguinal

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13
Q

Testes

A

Para-aortic

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14
Q

Scrotum

A

Superficial inguinal

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15
Q

Thigh

A

Superficial inguinal

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16
Q

Lateral Side of dorsum of foot

A

Popliteal

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17
Q

Three Major Forms of MHC HLA’s

A

HLA A,B,C

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18
Q

What CD molecule on T Cells is associated with binding MHC I on nucleated cells ?

A

CD8

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19
Q

MHC I presents what kind of antigens ?

A

Intracellular Peptide (loaded in the ER)

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20
Q

What molecule does MHC I pair with to get to the cell surface ?

A

B2 Microglobulin

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21
Q

What are the three main forms of MHC II molecules ?

A

HLA DP, DQ and DR

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22
Q

What CD molecule on T-Cells is associated with binding of MHCII on APC’s ?

A

CD4

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23
Q

What are the APC’s (Only cells that express MHC II)

A

B-cells , Macrophages, Dendritic Cells

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24
Q

Where kind of antigens are loaded on MHC II ?

A

Mostly extracellular, packed in endosomes

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25
Disease associated with A3
Hemochromotosis
26
Disease associated with B27 (4)
Psoriasis , Ankylosing Spondylitis, IBD, Reiters 'PAIR'
27
Disease associated with DQ2/DQ8
Celiac
28
Disease associated with DR2 (4)
MS, Hay Fever, SLE, Goodpastures Drive 2 -- >SHaG M (SLE, Hay fever, Goodpastures, MS)
29
Disease associated with DR3 (2)
Type I Diabetes, Graves
30
Disease associated with DR4
Rheumatoid Arthritis, Diabetes Type 1
31
Disease associated with DR5
Pernicious Anemia, Hashimotos
32
What do NK cells recognize on cells that are virally infected ?
Antigen presented on MHC I | Lack of MHC I
33
How doe NK cells control viral and tumor infection ?
Use Granzyme and Perforin to cause apoptosis in infected cells
34
What Cytokines enhance the activity of NK cells /
IL-2, IL-12 , INF-1 and INF-B
35
What Ab's produced by B-cells is the main opsonizing Ab of the body ?
IgM
36
What Ab's produced by B-cells activate complement ?
IgM and IgG
37
What Ab's produced by B-cells sensitize mast cells ?
IgE
38
Type II and Type III hypersensitivites are due to which Ab ?
IgG
39
Type I hypersensitivity is due to ..
IgE
40
Role of CD4 T-Cells (helper T cells)
``` Help B-cells make Ab's (class switching) Activate cells of the immune system ```
41
Role of CD 8 Cells
Kill virally infected cells (also neoplastic) Mediate Delayed type hypersensitivity (Type IV) Mediate transplant rejection etc.
42
Where is + selection in the thymus ?
Cortex
43
What does + Selection check on T-Cells ?
abilitiy to bind MHC molecules on self molecules No binding --> No activation Too much --> Anergy
44
Where does - Selection of T-cells take place ?
Medulla of thymus
45
What does - selection of T-cells check ?
Binding of self antigen to a high affinity (if so they undergo apoptosis)
46
Once in the lymph node, what cytokine helps push a CD4 T cell to become a TH1 ?
IL-12
47
Once in the lymph node, what cytokine helps push a CD4 T cell to become a TH2 ?
IL-4
48
Naive CD -cells receive stimulation by binding of TCR to MHC I/II and Binding of what other signal ?
CD28 (on T-cell) to B7 (on APC)
49
In the CD4+ TH1, what do they secrete upon activation to activate macrophages ?
INF- gamma
50
What inhibits activation of TH1 cells ?
IL-4 and IL-10 Both are secreted by TH2 cells (IL-4 is a signal that activates TH1 cells )
51
In the CD4+ TH2, what do they secrete upon activation to activate B-cells or to recruit Eosinophils ?
IL4, IL5, IL10, and IL13
52
What inhibits activation of TH2 ?
INF-gamma
53
When a B-cell presents antigen to T-helper cell, what other stimulatory signal must occur (besides TCR/MHCII) to cause the T-h cell to release cytokines needes for class switching and Ab production ?
CD40 (Receptor on B-cells) must bind CD40 L on T-cell
54
What is the function of T-reg T-cells ?
Suppress immune response by inhibiting CD4, CD8 effector functions
55
What surface proteins do T-reg cells express ?
CD3,4 and 25.
56
What cytokines do T-reg cells produce ?
IL-10 and TGF-b (anti-inflammatory)
57
Which portion of an Ab recognizes antigen >
Fab (Variable portion of Light and heavy chain)
58
What portion of an Ab do most Ab receptors on cells recognize ?
Constant (Fc portion) Note: Fc portion of IgM and IgG fix complement
59
Heavy chain contributes to both Fab and Fc portion of Ab. What doe the Light chain contribute to ?
Just the Fab portion.
60
The variable portion of heavy chain has VDJ portion. What does the light chain have ?
Just V and J
61
What portion of the Ab determines if it is IgM, IgD , IgG etc ?
Fc portion !
62
Which Ab's are produced on the surface of mature B-cells ?
IgM and IgD
63
What cells are responsible for the secretion of IgE, IgA and IgG ?
Plasma cells with AGE comes Plasma cells.
64
What is the most abundant Ig isotope >
IgG
65
Functions of IgG
Fixes complement Crosses placenta Opsonizes bacteria Neutralizes viruses and toxins
66
Where do you typically see IgA at ?
``` Muccous membranes (stops attachment of bacteria) Found in tears, saliva and mucous ```
67
Which Ab is produced in the immediate immune ab response ?
IgM (IgG is seen in the delayed ab response) | IgM (and D) are on mature B-cell surfaces, first to be produced
68
Like Ig, IgM can... but unlike IgG , IgM cannot
Fix complement | Cross the placenta
69
Can IgM be a monomer ?
Yes ! When attached to B-cell surface, otherwise it is a pentamer.
70
What is the main function of IgE /
Crosslinking to mast cells and basophils to mediate allergic response (Type I hypersensitivity) very important in the immune response to parasites. IgE levels will be very High !
71
What type of antigen must be present to illicit memory ?
Protein antigen W/O protein, cannot be presented on MHC to T-cells
72
The release of Ig without memory is known as ..
Thymus independent
73
What antigens are considered thymus independent thus still illicit release of Ig w/o memory ?
``` LPS (Gram -) Polysaccharide capsules (SHiN SKiS) ``` This is why we conjugate capsule/toxins to proteins in vaccines. I believe only IgM will be produced though, since T-cells cannot induce class switching ?
74
Thymus dependent antigens contain
protein
75
What cause 'memory'
B-cell interaction with T-cells ( CD40L binding to CD40R on B-cells ).. Activation to 'plasma cells' which have memory.
76
Role of C3b
Opsonization
77
Role of C3a and C5a
Anaphylaxoids | C5a is also chemotactic for neutrophils
78
C5-9
MAC ! Destroys anything with outer peptidoglycan or LPS Has a hard time with Neisseria since they have LOS (Not LPS)
79
Two components of complement system that stop complement activation on self ?
DAF | C1 Inhibitor
80
The Alternative Pathway for Complenent activation is due to C3 being cleaved to C3b by ..
Spontaneous occurrences | Microbial surfaces
81
What is the make up of the C3 Covertase in the Alternative Pathway ?
C3bBb
82
What is the C5 convertase seen in the Alternative Pathway ?
C3bBb3b --> C5b
83
What is the impetice behind activation of the classical pathway ?
Anti-body antigen complexes (IgG or IgM)
84
In the Classical Pathway , C1 is activated by Ab/Ag complexes. What is the purpose of the active C1 complex ?
To cleave C2 to C2a and C4 to C4b
85
What is the C3 convertase of the Classical and MBL pathway ?
C4b2a
86
What is the C5 convertase of the Classical and MBL pathways ?
C4b2a3b --> C5b
87
Disease associated with C1 Inhibitor deficiency ?
Angioedema
88
What meds are contraindicated in C1 Inhibitor deficiency ?
ACE inhibitors
89
What infections are patients with C3 deficiency at risk for ?
Pyogenic sinus and respiratory infections
90
What kind of HS rxn's are people with C3 deficiency at risk for ?
Type III
91
MAC deficiency leads to susceptibility to
Neisseria infections
92
Why are patients with DAF deficiencies prone to Paroxysmal Nocturnal Hemoglobinuria ?
At night, hypoventilation occurs --> CO2 buildup and subsequent activation of Complement. DAF inhibits activation of complement.
93
IL-1
Pyrogen (Modulates the Temperature center in the brain) and causes inflammation Activates ICAM on endothelium to allow for neutrophil tight binding
94
IL-6
PYROGEN Secreted by TH2 cells Causes fever and acute phase proteins
95
IL-8
Major chemotactic factor for Neutrophils
96
IL-12
Differnetiation of Naive to TH1 Activates NK cells
97
TNF-a
Septic Shock Activates endothelium Leukocyte recruitment
98
IL-2
Activates T-cells
99
IL-3
Stimulates bone Marrow | Functions like GM-CSF
100
IL-4
IgE and G production (Promotes growth of B-cells, class switching) Secreted by TH2 cells to suppress TH1 differentiation
101
IL-5
IgA production (Growth of B-cells) Promotes differentiation of Eosinophils
102
Hot T-Bone stEAk
``` Hot = IL-1 T = IL-2 activation of T cells Bone= IL-3 E = IgE from IL4 A = IgA from IL5 ```
103
Secreted by Macrophages
IL-1 ,6,8,12 | TNF-a
104
Secreted by ALL T-cells
IL-2,3
105
Interferon-y
Secreted by TH1 cells to activate Macrophages | Suppresses TH2
106
Secreted by TH2 cells
IL 4,5,10 (earlier list said 13 too)
107
IL10
Modulates immune response | Inhibits T-cell (Also secreted by T-reg cells)
108
What is unregulated in an uninfected cell that undergoes stimulation via Interferon ?
Production of a Ribonuclease that inhibits viral protein synthesis by degrading viral mRNA
109
Which interferon increases MCH I and II expression and presentation of antigen to effector cells (T-cells) ?
Interferon-y
110
What cells are activated by interferons to kill infected cells ?
NK cells
111
TCR , CD3 and CD28
All T-Cells
112
TCR , CD3, CD4*, CD28 and CD40L
T-Helper Cells
113
TCR, CD3,CD28 and CD8*
Cytotoxic T cells
114
IgM/D, CD19*, CD20* , CD21* , CD40 (R), MHC II and B7
B-cell Note: CD21 = Epstein Barr
115
CD14*, CD40(R), MHC II, B7, Fc and C3b Receptors
Macrophage
116
CD16, CD56*
NK cell
117
Explain how 'Super-antigen' bacterial toxins work (Exotoxins)
Work by increasing the cross link time between T-Cells and the APC (TCR -MHCII). As long as their is linkage the T-cell will release cytokines
118
What bacterial molecules can activate Macrophages w/o the need for T-h cells ?
Endotoxin, LPS Bind to CD14 directly. (Endotoxin receptor)
119
Which is more detrimental: Antigenic shift or drift ?
Drift --> Pandemic
120
List two ways in which passive immunity is aquired ?
``` Preformed Antibodies are injected Mothers milk (IgA in the secretions) ```
121
How does active Immunity occur ?
Exposure to foreign antigens (body takes care of the rest
122
Does passive immunity result in memory ?
NO ( lasts for up to 3 weeks)
123
What kind of immunity is vaccination ?
Active
124
After exposure to which pathogens, are pre-formed Ab's given ?
Rabies (virus) Tetanus Botulinum HBV (virus)
125
What is a live attenuated organism ?
Still living, capable of growing but does not retain the pathogenic factors that would lead to serious disease NOTE : Strong, often life long immunity Live vaccines 'may' revert back to pathogenic form
126
Examples of Live Attenuated Vaccination
MMR Nasal Chicken Pox Polio (Sabin) Yellow Fever
127
What kind of response is seen with Live Attenuated vaccines ?
Cellular
128
Inactivated or killed vaccines many induce what kind of response ?
Humoral
129
Inactivated or killed vaccines show a __________ immune response and ________ require a booster.
Weaker | Do
130
Examples of Inactivated or killed vaccines
Cholera Hepatitis A Rabies Polio (Salk)
131
What must first occur for a Type I hypersensitivity to occur ?
Sensitization to the offending antigen
132
What is present on the surface of presensitized mast cells ?
IgE
133
What is releases upon binding of Mast cellIgE with Antigen ?
Release of Histamine
134
Where in the capillary bed does histamine work ?
Post capillary membrane (according to FA) but in reality it also leads to vasodialtion of the arterioles --> rub or and valor Venule vasodialtion increases the permeability leading to edema (tumor)
135
What Ab's mediate Type II Hypersensitivity ?
IgM or IgG
136
Type II Sensitivity is Cytotoxic. What 3 mechanisms lead to cell death in Type II HS ?
Opsonization --> Phagocytosis Complement mediated lysis (IgM and IgG activate complement) Antibody Dependent Cell Mediated Cytotox (ADCC) via NK cells
137
How would you test for Type II cytotox ?
Direct and Indirect Coombs test
138
Type III HS is mediated by which Ab class ?
IgG
139
What is the mode of tissue damage in Type III HS ?
Immune complexes settle out and activate complement. Complement causes Neutrophil chemotaxis (C5a).Neutrophils release lysosomal enzymes which cause damage
140
What are the two main forms of Type III HS ?
Serum Sickness and Arthus Rxn
141
Serum sickness occurs when Ab/Ag complexes are deposit in the membranes of endothelial linings leading to
Activation of complement
142
How long does a type III rxn leading to serum sickness often take ?
Up to 5 days | Must make the Ab's
143
Arthus rxn
Same thing as Serum sickness but occurs in the skin
144
What is the main cause of type III hypersensitivity (Delayed type) ?
DRUGS
145
What are the mediators of Type IV HS ?
T-cells (Pre-sensitized, release cytokines on upon encountering antigen. Leads to activation of Macrophages (INF-y) .. NO Ab IS SEEN IN THIS !
146
Two examples of Type I HS
Anaphylaxis | Allergic Rxn
147
SLE Post Streptococcal Glomerulonephritis Polyarteritis Nodosa
Type III HS
148
Multiple Sclerosis PPD Guillan Barre
Type IV HS
149
``` Pernicious Anemia Goodpastures Disease Rheumatic Fever ITP Auto-immune hemolytic Anemia ```
Type IV
150
Type II HS | Host anti-bodies against donor HLA and antigens
Febrile Non-hemolytic Transfusion Rxn
151
``` Type II HS Intravascular hemolysis (Hemoglobinemia) or Extravascular (jaundice) ```
Acute Transfusion RXN
152
Anti-dsDNA and Anti-Smith Ab's are _________ for SLE
Specific DR2
153
ANA is _________ for SLE
Non-specific
154
Drug Induced Lupus (Hydralazine, Procainamide etc) specific antibody....
Anti-histone
155
Anti-CCP
Rheumatoid (Also, Rheumatoid Factor. DR4 association also)
156
Anti-Centromere
Sceleroderma of CREST
157
Anti-Scl70
Sceleroderma (diffuse)
158
IgA endomysial, IgA anti-tissue Transglutamase
Celiac
159
Anti-Basement Membrane
Goodpastures ( Type II , DR2
160
Anti-desmoglein
Pemphigus vulgaris
161
Anti-thyroglobulin
Hashimotos (Type IV , although it looks like Type II. DR5)
162
Anti-SSA and SSB
Sjogrens Disease
163
Anti-Glutamate Decarboxylase
Type I Diabetes
164
c-ANCA
Granulomatosis with Polyangiitis (Wegners)
165
p-ANCA
Microscopic Polyangiitis , Churg Strauss
166
What immune cells are needed to clear Encapsulated organisms ?
B-cells (opsonization is key !) SHiNE SKiS
167
What bacterial infections are prevalent in those w/o proper complement activation ?
Neisseria
168
Staphylococcyl, Serratia and Burkolderia infection are common in patients with inadequate
Granulocytes ( Organism are Catalase + ?)
169
Deficiency in which cells leads to a contraindication in administering Live Vaccines ?
B-cell deficient
170
What fungal infections are common in T-cell deficient patients ?
well, pretty much all of them.. PCP , Candida, Cryptococcus etc.
171
Which fungal infections occur if granulocytes are deficient ?
Candida, Aspergillus (Catalase + organism)
172
In X-Linked agammaglobulinemia, what molecular is affected that leads to lack of B-cell maturation and decreased globulins of all classes ?
Brutons Tyrosine Kinase (Needed for B-cell Maturation)
173
When will begin to see signs of X-Linked agammaglobulinemia
Six months post birth when maternal IgG is decreased.
174
What occurs when you give IgA containing blood to a person with Selective IgA deficiency ?
ANAPHYLAXIS
175
What kind of infections are often increased in X-Linked agammaglobulinemia ?
Sinus and Pulmonary
176
In Common Variable Immunodeficiency, you will see a regular number of B-cells but decrease...
Plasma cells ( IgA, G and E will be decreased)
177
What is the deletion associated with Thymic Aplasia (DiGeorge) ? What does this cause ?
22q11 Failure of the 3rd branchial pouch to form (thus thymus does not form. May also see the parathyroid is absent --> Hypocalcemia , Tetany.
178
Deficiency of what receptor would lead to lack of maturation of TH1 cells ? Activation of what other cell may be lessened ?
IL-12 | Macrophages (IFN-y release by TH1 --> macrophage activation)
179
What bacterial species if more prevalent in IL-12 deficiency ?
Mycobacterium (TB)
180
Job Syndrome is also known as ..
Hyper IgE Syndrome
181
What do the TH1 cells fail to produce in Job Syndrome ?
INF-y (apparently this inhibits their ability to attract neutrophils. Also, this would affect their ability to activate macrophages)
182
Job Syndrome: FATED
``` Facies Abscesses Teeth (Retained primaries) E (IgE) Dermatologic problems ```
183
What is deficient in Chronic Mucocutaneous Candidiasis ?
T-Cells
184
What is the most common defect that leads to SCID ?
X-linked defect in IL-2 receptors (remember that IL-2 is needed for the activation of T-cells)
185
What defect leads to a death of T-cells due to a build up of metabolites and leads to SCID ?
Defect in Adenosine Deaminase ( Adenosine can be Toxic to lymphocytes)
186
What will occur to B-cells in SCID ?
Innability to activate B-cells without TH2 cells. ( Need CD40L on TH2 and cytokines B-cells that may exist will not be able to class switch w/o IL-4/5 from the TH2 cells.
187
Treament for SCID ?
Bone Marrow Transplant
188
Ataxia Telangiectasia
Defect In ATM gene (codes for DNA repair enzymes)
189
Triad of Ataxic Telangiectasia
Cerebellar defects Spider angiomas IgA deficiency
190
Labs for Ataxic Telangiectasia
Increased Alpha fetoprotein
191
What is the most common cause of Hyper IgM syndrome ?
Defective CD40L on TH2 cells !!!
192
Without CD40, what will B-cells be unable to do in Hyper IgM Syndrome ?
Class Switch (IgM and D are made by B-cells IgA,G,E made by plasma cells
193
X-linked Defect in WAS gene. T-cells unable to recognize actin skeleton.
Wiskott Aldrich Syndrome
194
Triad of Wiskott Aldrich Syndrome
TIE : Thrombocytopenic purpura, Infections (immunodeficiency), Ecxema
195
What will you see in terms of Ig production in Wiskott Aldrich Syndrome ?
Increased IgE and IgA
196
Defect in LFA-1 integrin CD18 leading to increase in bacterial infections, absent pus formation and delayed separation of umbilical cord and Neutrophilia
Leukocyte Adhesion Deficiency See neutrophilia due to lack of adherence, body doesn't think you are making any. Large amount in the blood, none in the tissues.
197
Autosomal Recessive Defect in Lysosomal Traffic Regulator (LYST) Failure of Phago-lysosome fusion
Chediak Higashi Syndrome
198
What organisms willy you see recurrent infections with in Chediak Higashi
Strep and Staph
199
What is unique about the pigmentation of patients with chediak higashi ? What is seen on microscopy ?
Partial albinism | Giant granules and neutrophils
200
What is deficient in Chronic Granulomatous disease ?
NADPH Oxidase. NADPH oxidase makes ROS which is then converted to H2O2 by Superoxide Dismutase and Finally Turned into Bleach by Myeloperoxidase
201
What organismal infections will be recurrent in patients with Chronic Granulomatous Disease ?
Catalase + PLACESS for Cats (catalase +) ``` Pseudomonas Listeria Aspergillus Candida E.coli Staph Serratia ```
202
What test is typically the choice for diagnosis?
Nitroblue tetrazolium ( NADPH oxidase metabolizes dye to a deep color. if not then they are NADPH negative.
203
autograft
From self
204
Syngenic graft
From identical twin or clone
205
Allograft
from nonidentical individuals of same species
206
Xenograft
from different species
207
Hyperacute rejection
within minutes Preformed anti-bodies to donor tissue (must have sensitization) Type II Occluding graft vessels, causing ischemia and necrosis
208
ACute rejections
Weeks later Cell mediated due to CTL's. Treated with immunosuppressants Vasculitis of graft with denst interstitial lymphocytic infiltrate
209
Chronic rejection
Months to years Non sels MHC molecules are seen as Self MHC's presenting non-self antigen. Irreversible Ab' mediated vascular damage
210
Graft Versus Host
Only occurs in grafts that are immunocompetant (aka bone marrow) The graft cell attacks the host cell (T-cell proliferation causes this)
211
Signs of GVH
Maculopapular rash Jaundice Hepatosplenomegaly Diarrhea
212
MOA of Cyclosporine
Binds cyclophilins thus inhibiting calcineurin Calcineurin is needed for T-cell differentiation and activation as it regulates production of IL-2 and its receptor (IL-2 is the main stimulatory cytokine for T-cell development)
213
Toxicity associated with Cyclosporine
Nephrotoxicity, hypertension, hyperlipidemia, hyperglycemia, tremor, gingival hyperplasia (like phenytoin ?), hirsutism.
214
MOA for Tacrolimus
Binds FK-binding protein which effectively inhibits calcineurin Without calcineurin IL-2 will not be produced
215
Toxicity of Tacrolimus
Same as cyclosporine, but no gingival hyperplasia or hirsutism
216
MOA of Sirolimus (Rapamycin)
Inhibits mTOR which is needed for T-cell response to IL-2 (w/o IL-2 T-cell cannot mature, As seen in SCID)
217
What are the uses for Sirolimus (Rapamycin)
Immunosuppression after kidney transplantation in combo with cyclosporine
218
Toxicity of Sirolimus
Hyperlipidemia, thrombocytopenia, leukopenia
219
MOA of Azathioprine
Anti-metabolite of 6-mercaptopurine Interferes with metabolism and synthesis of nucleic acids Toxic to proliferating T-cells
220
Azathioprine toxicity
Bone marrow suppression | Interacts with Allopurinol since (azathioprine is metabolized by xanthine oxidase) , may increase effect.
221
MOA of Muromonab CD3
An that binds to CD3 of T-cells . Makes it so that T-cells cannot transduce signals
222
Toxicity of Muromonab CD3
Cytokine release syndrome, hypersensitivity run
223
Aldesleukin is a recombinant cytokine similar to _______ used for ________
IL-2 | Renal Cell Carcinoma and Metastatic Melanoma
224
Epoetin Alfa is a recombinant cytokine similar to _______ used for ________
Erythropoietan | Anemias
225
Alpha interferon is used to treat
Hep B,C Kaposi Sarcoma Leukemias Malignant melanoma (Virally infected cells, induces state of awareness. Stop cells from producing viral ribonuclease)
226
B-interferon is used for
MS
227
Interferon -y is used for
Chronic granulomatous disease.
228
Antidote for Digoxin intoxication
Digoxin Immune Fab
229
What does Infliximab target ?
TNF-a Used in Crohns, Rheumatoid arthritis
230
Adalimumab targets
TNFa (just like infliximab)
231
What does Abciximab target
GP IIB/IIIA Used to prevent ischemia in unstable angina
232
Trastuzumab targets
HER2 Used in breast cancer
233
Rituximab targets
CD20 Used for B-cell non-hodgkins lymphoma
234
Omalizumab targets
IgE Used for severe asthma