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Step 1 > Inmunology > Flashcards

Inmunology Flashcards

1
Q

Deficiency associated with Neisserial infections:

A

Complement factors C5-C9

Because Neisseria has a very thin wall

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2
Q

PGs, histamine, bradykinin and serotonin functions:

A

Vasodilation (arteriole)
Increased vascular permeability (post-capillary venule by perycite contraction)
Bradykinin and PGE2 contribute to pain!

PGs are released by arachidonic acid metabolism
Histamine is released by basophils, mast cells and platelets
Bradykinin is released by the kinin cascade, it dilates the arterioles but constricts the veins
Serotonin is released by the brain, GI and platelets

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3
Q

Leukotrienes function:

A

Contraction:
Vasoconstriction
Bronchospasm
Increased vascular permeability (pericyte contraction)

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4
Q

Complement functions:

A

C3a, C4a and C5a: trigger histamine release form mast cells, involved in anaphylaxis (anaphylatoxins)

C5a: attracts neutrophils

C3b: opsonin for phagocytosis and clear inmune response

C5b+C6-C9 from the membrane attack complex (hole)

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5
Q

Thromboxane A2 function:

A

Made by platelets
Platelet aggregation!!
Vasoconstriction; contributes to angina!

Opposite to PGI2 prostacyclin

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6
Q

IL4 (IL13) function and origin:

A

Made by T helper 2

Increases T helper 2 on the inflammation site

Inhibits T helper 1

Activates class switching to IgE, abundant in atopic disorders

IL13 is associated with minimal change disease!

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7
Q

INF gamma function and origin:

A

Made by T helper 1

Recruits and activates macrophages

Converts macrophages into epithelioid histiocytes in granuloma (quantiferon test)

Activates T helper 1

Inhibits T helper 2

Activates class switching to IgG

Increases expression of MHC 1 and 2 in cells

Activates NK (together with IL12)

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8
Q

Leukotriene B4 and IL-8 function and origin:

A

IL8 is made by macrophages and epithelial cells
LTB4 comes from the mb phospholipids of macrophages, neutrophils, mast cells that break and start the arachidonic acid cascade

Chemotactic, call neutrophils to go to the antigen site. Neutrophils come before (B4)

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9
Q

IL2 function and origin:

A

Made by T helper 1

Increases proliferation of lymphocytes: CD4, CD8 and NKs! and monocytes. Aldeskeukin in tto of renal cell ca. and melanoma

Induce secretion of INF gamma, abundant in granulomatous diseases

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10
Q

Tissue damage that leads to abscess formation is due to:

A

Lysosomal enzymes released by neutrophils and macrophages

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11
Q

Type 4 hypersensitivity is mediated by:

A

T helper 1 (activated by IL12 through T-bet)
T helper 17 (activated by IL23 through ROR gamma T)
It is delayed

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12
Q

IL5 function and origin:

A

Made by T helper 2 and mast cells

Helps eosinophils (type 1 hypersensitivity, atopic disorders as asthma)

Helps TGF beta to class switch to IgA

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13
Q

IL12 function and origin:

A

Made by macrophages and B cells

Promotes differentiation of T helper cells into T helper 1 (important in granuloma and psoriasis)

Activates natural killer cells (together with INF-gamma)

With IL2 activates CD8+ cytotoxic T cells

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14
Q

IL10 function and origin:

A

Made by T helper 2 and Tregs

Shuts down T helper 1: ↓IL2, INFγ, MHC2, dendritic cells and macrophages

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15
Q

TGF-beta function and origin:

A

Made by platelets, macrophages, lymphocytes and mast cells

Tissue regeneration and repair, promotes differentiation of fibroblasts into myofibroblasts (fibroblast growth factor, active after burns and during scaring, contributes to keloids)

Activates class switching to IgA (also IL-5)

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16
Q

Where is CD14 and what recognizes?

A

On all phagocytes (macrophages)

Recognizes lipopolysaccharide on gram - bacteria

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17
Q

NF-kappaB function:

A

Activates synthesis of immune mediators when toll-like receptors are activated, is a transcription factor.

Secretes: IL1, TNF-alpha, IL6, IL8 and IL12

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18
Q

PGE2 function:

A

Mediates pain and fever

Maintains the patency of the ductus arteriosus (we give alprostadil as a drug to maintain PDA that is actually PGE1)

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19
Q

PGI2 function:

A

Also called prostacyclin, made by the endothelium
Inhibits platelet aggregation!!
Vasodilation

Opposite to TXA2

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20
Q

Substances that attract neutrophils, important for migration:

A

Endogenous:
Leukotriene B4: +potent
IL8 (by macrophages, persistent acute inflammation)
C5a! the A!
Kallikrein! (SILK: C5a, IL8, LTB4, kallikrein)
Fibropeptides
5-HETE (leukotriene precursor)

Exogenous:
Bacterial products (N-formyl methionyl peptides)
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21
Q

What causes mast cell activation?

A

Trauma
C3a and C5a
Cross linking of IgE by antigen

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22
Q

Mediators of vasodilation:

A

Histamine (also swelling)
PGs
Bradykinin (it dilates the arterioles but constricts the veins)

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23
Q

Macrophages production of IL-1 and TNF-alpha causes:

A

Increases COX activity in the hypothalamus which increases PGE2 to cause fever.

TNF-alpha causes cachexia, insulin resistance and increases capillary permeability (leads to ARDS and shock in sepsis)

IL-1 activates osteoclasts

Think SYSTEMIC inflammation!!

Abundant in rheumatoid arthritis

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24
Q

IL-1 function and origin:

A

Made by monocytes, macrophages, B cells, dendritic cells, endothelium…

Neutrophils rolling and adhesion (increases endothelial ICAMs)

Actives the hypothalamus for fever

Activates T helper, B cells and NK

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25
Q

Leukocyte adhesion deficiency; cause and presentation:

A

Defect in CD18 (beta 2 chain) of LFA-1 integrin

Omphalitis, difficult wound healing, necrotic lesions, increased circulating neutrophils and no pus

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26
Q

Chediak-Higashi syndrome; cause and presentation:

A 
Microtubule defect due to CHS1/LYST protein
Pyogenic infections (no phagolysosomes)
Neutropenia (no neutrophil division)
Giant granules in leukocytes
Defective platelets
Albinism
Peripheral neuropathy 
So abnormal phagocytes, NK cells and cytotoxic T lymphocytes
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27
Q

Chronic granulomatous disease; cause and presentation:

A

NADPH oxidase defect (colorless/ yellow/ negative nitroblue tetrazolium test)
Catalase + infections: PLACES Pseudomona, Listeria, Aspergillus, mucor, Candida, cryptococcus, enterobacteriae as E. coli, S. aureus, burkholderia cepacia, serratia (osteomyelitis), nocardia

Tto: INF-gamma

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28
Q

CD4+ T cells recognize:

A

MHC class II (4*2=8)

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29
Q

CD8+ T cells recognize:

A

MHC class I (8*1=8)

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30
Q

Where is MHC II and which antigens carries?

A

Is on antigen presenting cells, carries extracellular antigens

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31
Q

Where is MHC I and which antigens carries?

A

Is on all nucleated cells and platelets, carries intracellular antigens

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32
Q

T cells flight:

A

T helper 1: intracellular
T helper 2: parasitic
T helper 17: extracellular bacteria and fungi

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33
Q

Causes of severe combined immunodeficiency:

A

IL-2 receptor defects (X-linked) 50%

JAK-STAT signaling deficit (recessive)

Adenosine deaminase deficiency (buildup of dATP that inhibits de novo deoxynucleotides synthesis) (recessive)

Rag mutations (recessive)

MHC II deficiency (CD4+ helper T cannot help maturation of B and T cells) (recessive)

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34
Q

Deficit and common infections in X-linked (Burton) agammaglobulina:

A

Btk deficiency: no B cells in blood, all Ig low, but a lot of immature preB in bone marrow

T cells are fine

They get bacterial, enterovirus and Giardia infections

Onset in kid

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35
Q

Main characteristics of common variable immunodeficiency:

A

B cells ok but all Ig low and decreasing

Increased risk of autoimmune disease and lymphoma

Onset at teens-20s

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36
Q

Pathophysiology of X-linked hyper-IgM sd:

A 
The activation of naïve IgM is good but mutated CD40 LIGAND (CD154) on T cell so no class switching of B cell: you get a lot of IgM but not IgA, IgG and IgE (mucosal infections)
X-linked recessive (actually there is a rare CD40 deficiency that is AR)

Onset in kid

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37
Q

C5-C9 completament deficiency causes:

A

Neisseria (gonorrhoeae and meningitidis) infections

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38
Q

C1 inhibitor deficiency causes:

A

Edema of skin and mucosas (periorbital)

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39
Q

What type of hypersensitivity is lupus? what are it’s key plasma findings?

A

Type 3, antigen-antibody complexes that activate complement

Low lymphocytes
Low C3 and C4
Mild thormbocytopenia
Increased gamma globulin production

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40
Q

Antibodies for lupus:

A

More specific:
Anti-dsDNA: prognostic and renal disease activity indicator; in 70%
Anti-Smith: pathognomonic but just in 30%

More sensitive: ANAs; in 95-100%

Others:
Antiphospholipid
Anti-ribonucleoprotein P (psychosis)
Anti-histones (drug induced HIP)
Anti-SSA (Ro) IgG that can cause heart block in the baby
Low early complement C1q, C4 and C2
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41
Q

Which is the most common renal damage in lupus? what is its imaging? Which is the most common pulmonary damage in lupus?

A

Renal:
Type 4: diffuse proliferative glomerulonephritis (type of nephritic sd.) also the most severe

LM: Wire looping
IF: granular; IgG and C3 deposition
EM: sub-ENDOthelial (capillary loops get thick making the wire loop)

Pulmonary:
Interstitial lung disease

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42
Q

Cause of nephrotic sd. in lupus and imaging:

A

Type 5: membranous glomerulonephritis

LM: silver stain, membrane thickening
IF: granular; IgG and C3 deposition
EM: spike and dome, sub-EPIthelial

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43
Q

What type of hypersensitivity is sjögren sd?

A

Type 4, lymphocyte (cell) mediated

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44
Q

Specific antibodies and histology for Sjögren sd:

A

ANA and anti-ribonucleoprotein! (SSA form mom to baby can cause congenital heart block)

Lymphocytic infiltrates often with germinal centers (periductal in focal lymphocytic sialadenitis!!)

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45
Q

Specific antibodies for limited sclerodermia:

A

Anti-Centromere

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46
Q

Specific antibodies for diffuse sclerodermia:

A

More specific: Anti-DNA topoisomerase 1 (anti-Scl-70 antibody)

Anti-RNA polymerase 3

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47
Q

Specific antibodies and clinic in mixed connective tissue disease:

A

U1 ribonucleoprotein: most specific
ANA and rheumatoid factor

Clinic is a mixtures of SLE, systemic sclerosis and polymyositis

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48
Q

TGF-alpha function:

A

Epithelial and fibroblast growth factor for wound healing

TGF-beta is also a fibroblast growth factor

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49
Q

Name 2 angiogenic growth factors? and 4 activators of fibroblasts?

A

Angiogenic:
VEGF
Fibroblast GF!!! FGF

Fibroblasts (trichrome, reticulin staining): in chrirrosis, nodular sclerosis, sclerodermia:
IL1
TGF-β (thanks goddess for fibrosis baby)
PDGF (important for the migration of smooth m. cells into in atherosclerosis)
FGF

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50
Q

Causes of eosinophilia:

A

Allergy, asthma (type I hypersensitivity)
Parasites
Hodgkin mixed cellularity (IL5)
Chung-Strauss
Chronic adrenal insufficiency
Myeloproliferative disorders (+ basophils in CML)

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51
Q

IL-6 function and origin:

A

Made by monocytes, macrophages, T helper 2 and bone marrow

Stimulates plasma cell growth and antibody production. It is high in mieloma multiple (but it is IL1 who causes the lytic lesions in MM)

Induces synthesis of acute phase reactants

Increases hepcidin that binds to ferroportin to trap iron in macrophages (ferritin increases) and decrease absorption

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52
Q

Important T lymphocyte marker:

A

CD3 (important for signal transduction)

Also CD2, CD4, CD8

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53
Q

Important B lymphocyte markers:

A

CD19, CD20 and CD21

Also CD40

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54
Q

Important macrophage markers:

A

CD14 (binds to TLR-4 in LPS of gram negative bacteria). Is in all phagocytes

CD16 (Fc receptor for Fc of IgG). On macrophages, NKs and neutrophils

Macrophages are tennagers

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55
Q

What is secreted by T helper 2 cells as in asthma (type 1 hypersensitivity), parasitic infection or lepromatous leprosy?

A

IL4 and IL13: IgE class switching

IL5:eosinophils and helps INF-beta to IgA class switching

IL10: shuts down T helper 1 and activates T helper 2

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56
Q

Functions of the three subtypes of CD4+ T cells:

A

T helper 1: intracellular; secrete INF-gamma and activate macrophages and IgG class switching (antibody-dependent)

T helper 2: parasitic; secrete IL5 to activate eosinophils and IgA class switching (with INF-beta), IL4 and 13 for IgE class switching (antibody-dependent)

T helper 17: bacteria and fungi; secrete IL17 and IL22 to call neutrophils and increase cell binding to contain infection

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57
Q

Live viral vaccines examples and what inmune response do they activate:

A

MMR (measles, mumps and rubella)
Varicella
Rotavirus
…

Activate both humoral (B cells) and cell mediated (T cells) responses

58
Q

Killed viral vaccines examples and what inmune response do they activate:

A

Rest In Piece Always:

Rabies
Influenza
Polio
Hepatitis A

Activate just humoral (B cells) response because there is no peptide to present in MHC 2 to T cells so the B cell activation is T-independent: IgM

59
Q

What type of hypersensitivity is poststreptococcal glomerulonephritis and imaging:

A

Type III, inmune complexes

LM: hyper-cellular
IF: lumpy-bumpy; granular starry sky; IgG, C3 and ¡¡IgM!! deposition
EM: sub-epithelial

60
Q

What type of hypersensitivity is type I diabetes?

A

Type IV, beta cell destruction by T lymphocytes

61
Q

Characteristics of hyperacute graft rejection:

A

Happens within min-hours
Due to preformed IgG ANTIBODIES (previous transplant, multiple pregnancies)
Antibodies activate COMPLEMENT causing fibrinoid necrosis, thrombosis and ischemia
Predominant neutrophils

62
Q

Characteristics of accelerated graft rejection:

A

Happens within days
Due to previously sensitized T cells (memory)
Parenchymal damage and endothelialitis

63
Q

Characteristics of acute graft rejection:

A

Happens within weeks-up to 1 year
Due to T cells and antibodies activated by MHC1 and 2 mismatch (nr celular and humoral immunity)

Celular:
Predominant lymphocytes
Endotheliitis, tubulitis
Patchy infiltrates if lung
Treat with cyclosporin, basilizumab...

Humoral: Do not choose it unless very obvious
Necrotizing vasculitis
Complement deposition, low Cd4
Treat with rituximab

DD in kidney:
Neutrophils and fever: pyelonephritis, prevent with TMP-SMX
Acute kidney failure with no inflammatory cells: cyclosporin toxicity, take cyclosporin out

64
Q

Characteristics of chronic graft rejection:

A

Happens within months-years; gradually
Smooth m. proliferation, FIBROSIS!!!! and mononuclear infiltration

Heart: accelerated aterosclerosis
Lung: bronchiolitis obliterans (small airway obstruction)
Liver: vanishing bile duct sd. (loss of ducts)
Kidney: nephropathy with interstitial fibrosis, atrophy, vascular thickening and therefore luminal narrowing, can show basement membrane splitting

65
Q

Cells affected by Chediak-Higashi sd:

A

Phagocytes
NK cells
Cytotoxic T lymphocytes

66
Q

Treatment of chronic granulomatous disease:

A

INF-gamma

67
Q

Examples of type 1 hypersensitivity:

A 
Allergic rhinitis 
Anaphylaxis 
Food allergies 
Wheal and flare: allergy test 
Asthma
68
Q

Examples of type 2 cytotoxic hypersensitivity:

A 
Acute hemolytic anemia (as erythroblastosis fetalis)
Acute rheumatic fever
Goodpasture
Transfusion reaction!!! transtwosion
Autoimmune thrombocytopenic purpura
Pemphigoid
69
Q

Examples of type 2 non-cytotoxic hypersensitivity:

A

Myasthenia
Graves
Type 2 DM
Pernicious anemia

70
Q

Examples of type 3 hypersensitivity:

A

Vasculitis, nephritis, arthritis

SLE
Post strep glomerulonephritis 
Arthus reaction!!! Arthree
Serum sickness 
Polyarteritis nodosa
71
Q

Examples of type 4 hypersensitivity:

A 
Stevens-Johnson
Tuberculin test, intracellular organisms
Contact dermatitis (nickel, poison ivy) 
Hashimoto
MS
Rheumatoid arthritis
Type 1 DM
Guilliam-Barré
Crohn
72
Q

What does TLR-2 recognizes?

A

Peptidoglycan

73
Q

What does TLR-4 recognizes?

A

LPS of gram negative

74
Q

TLR that recognize extracellular targets:

A

TLR-1,2,4,5,6

75
Q

TLR that recognize intracellular targets:

A

TLR-3,7,8 (DNA and RNA form viruses) 9 (intracellular/non-cleared bacteria)

76
Q

Therapeutic functions of INF:

A

INF-alpha: hepatitis, hairy B cell leukemia, CML, kaposi sarcoma

INF-beta: MS

INF-gamma: chronic granulomatous disease

77
Q

Major criteria for rheumatic fever:

A

J❤️NES:

Joint, arthritis 
❤️ carditis 
Nodules, subcutaneous 
Erythema marginatum 
Sydenham chorea
78
Q

Cytokines overproduced in toxic shock sd:

A

INF-gamma and IL2 form T helper 1

IL1, TNF-alpha and IL6 form macrophages

79
Q

Wiskott-Aldrich sd; cause and presentation:

A

WAS mutation so cells can’t recognize actin cytoskeleton

X linked
Thrombocytopenia: few small platelets causing purpura
Eczema
Immunodeficiency: low IgM high IgE and IgA
Increased risk of non-Hodgkin lymphoma

80
Q

Selective IgA deficiency; cause and presentation:

A

Unknown. Most frequent

Low IgA and high IgE
Atopy
Giardia infections
Risk for blood transfusion reaction (IgE anti IgA antibodies→ anaphylaxis)
Can give false positive beta-hCG

Onset in 20-30s

81
Q

IL-7 function and origin:

A

Made by marrow and thymus

Induces differentiation into lymphocytes (NK, T helper and T cytotoxic)

82
Q

IL-3 function and origin:

A

Made by T helper and NK cells

Induces differentiation into myeloid precursors with GMCSF

83
Q

Which part of the complement pathway is activated in the presence of inmune complexes?

A

Classical; activated when IgM and IgG bind to C1

C3b removes the immune complexes

84
Q

Test used to determine HLA-1 expression for transplant:

A

Microcytotoxicity test

85
Q

What is Arthus reaction and what type of hypersensitivity is it?

A

Swelling after a vaccine (protein inoculation for which there are pre-existing antibodies)

Type 3 (even if it is localized)

86
Q

How does the body react to parasitic infection?

A

IL4 —> GATA3 —> T helper 2 —> IL4, IL13 —> Class switching to IgE —> mast cell degranulation, basophils and eosinophils (through IL5) attack

87
Q

Name B cells immunodeficiencies:

A

Burton
Selective IgA deficiency
Common variable immunodeficiency

88
Q

Name T cell immunodeficiencies:

A

Thymic aplasia
IL-12 deficiency
Job sd (AD hyper-IgE)
Chronic mucocutaneous candidiasis

89
Q

Which Coombs is for the mom and which for the baby?

A

Direct for the baby. Antigen

Indirect for the mom. Antibody

90
Q

Splenectomy is a risk factor for which type of pathogens?

A 
Encapsulated 
Blood parasites (babesia)
91
Q

Important Treg marker:

A

CD25

92
Q

Important NK markers:

A

CD56
CD16

All NK markers have 6 on them

93
Q

Name 3 important opsonins:

A

Fc portion of IgG
C3b
Collectins= mannose-binding lectin

C reactive protein

94
Q

Deficiency associated with encapsulated infections:

A

Complement factor C3

No spleen

95
Q

Antibodies for antiphospholipid syndrome:

A 
Lupus anticoagulant (long PTT)
Anticardiolipin (false VDRL)
Anti-beta2 glycoprotein 1

If you see a long PTT in someone with lupus think about antiphospholipid syndrome, they will actually be at risk of thrombosis not of bleeding!!

96
Q

Type I hypersensitivity is mediated by:

A 
T helper 2 (activated by IL4 through GATA 3)
IL4 and IL13 induce class switching to IgE
97
Q

Cosignal needed to activate T cells and B cells:

A

B7(CD80/CD86)-CD28 (Antigen presenting - T cell): needed to activate T cells
B7 for T cells!

CD40 Ligand-CD40 (T cell - B cell): needed to activate B cells for class switching and memory Abs

98
Q

Specific antibodies for polymyositis and dermatomyositis:

A

Anti-Jo-1 (tRNA synthase)
Anti-SRP (signal recognition particle)
Anti-Mi2 (helicase)

99
Q

What does seroconversion mean?

A

Class-switching, you test for this with western blot to look for antibodies

100
Q

Specific antibodies, HLAs and histology for Hashimoto:

A

Anti-thyroid peroxidase (antimicrosomal), hypo
Antithyroglobulin
DR3, DR5
Hürthle cells and germinal centers; lymphocytic infiltration!!!

Does not hurt vs de Queravain (Queravain=pain)

101
Q

Specific antibodies, HLAs and histology for Graves:

A

Thyroid-stimulating immunoglobulin (TSI) also called Long-acting Thyroid Stimulator antibodies (LATS), hyper
DR3, B8
Crowded follicles and scalloped colloid

102
Q

Specific antibodies and HLAs for Celiac disease:

A

IgA anti-tissue transglutaminase (enz that deaminates gliadin)
anti-endomysial
anti-deaminated gliadin peptide
DQ2, DQ8, DR3

103
Q

Specific antibodies and HLAs for DM1:

A

Anti-glutamic acid decarboxylase (anti-GAD)
DR3, DR4, DR3/4, DQ (DR3+DM1=DR4)

DR2 is associated with less DM1!

104
Q

Which immunodeficiencies are X-linked?

A

Burton agammaglobulina (no B cells)
Hyper-IgM (a lot of IgM but not the other Igs)
SCID due to IL-2 receptor defects (↓NK ↓T cells)
Wiskott-Aldrich (thrombocytopenia+ezema)
Chronic granulomatous disease (catalase +)

105
Q

Which cytokines cause vascular leak, DIC, insulin resistance and cachexia? how can your treat it?

A

Insulin resistance and cachexia because it reduces utilization of FA (also IL-1 and INF-gamma); you can give megestrol acetate to stimulate appetite

Vascular leak leads to septic shock and ARDS

Hypercoagulability because it kills tumors by causing coagulation and necrosis; hypercoagulability can lead to DIC

106
Q

Specific antibodies and histology for primary biliary cholangitis:

A

Anti-mitochondrial

Lymphocytic inflammation of the bile ducts+granulomas

107
Q

Specific antibodies and HLAs for rheumatoid arthritis:

A 
More specific: Alpha-cyclin citrullinated peptide (alpha-CCP)
Rheumatoid factor (IgM against the Fc portion of IgG). Big one eats the small one!

DR4!!!

108
Q

Difference between papain, pepsin and monoclonal antibodies:

A

Papain: can bind to antigen but cannot cross-link (agglutinate) or activate complement. Fab + Fcx2

Pepsin: can bind to antigen and cross-link (agglutinate) because of the F(ab’)2. Fc is digested so it cannot activate complement. F(ab’)2 + digested Fc

Monoclonals can cross-link (agglutinate = precipitate)

109
Q

IL-11 function:

A

Helps megakaryocytes to differentiate into platelets

Oprelvekin is IL-11 for myelosuppression due to QT

110
Q

Substances secreted by mast cells and basophils:

A

Basophils: heparin, histamine and leukotrienes

Mast cells: heparin, histamine, eosinophil chemotactic factor and tryptase

111
Q

Specific antibodies for pemphigus vulgaris:

A

Pemphigus: Ab against DESMOsomal DESMOsglein 1 and 3 (a cadherin)

Pemphigoid: BPAg1 and 2 Ab against hemidesmosomal dystonin

112
Q

Specific antibodies for autoimmune hepatitis? What is the pathology?

A

Anti smooth muscle antibodies
Hypergammaglobulinemia

Micro: portal and periportal lymphocytic and plasma cell infiltration

113
Q

What is the main mediator of cirrhosis?

A

TGF-β secreted by stellate cells

114
Q

What are the consequences of a defect in TAP1?

A

TAP are transporter associated with antigen processing proteins, if they do not work you cannot load peptides in MHC class 1!!! so you will have ↓CD8 and nr CD4 as in bare lymphocyte sd type 1

115
Q

Name positive and negative acute phase reactants:

A 
Positive: More FFiSH in the C
FIBRINOGEN
Ferritin
Serum Amyloid A
Hepcidin
CRP

Alos ceruloplasmin, haptoglobin, vWF, complement, erythrocyte sedimentation rate

Negative:
ALBUMIN, prealbumin (transthyretin)
transferrin

PROCALCITONIN is + in BACTERIAL infections and - in viral!!!

116
Q

Immunologic changes with age:

A

↓ NAIVE B and T cells: ↓ memory to NEW antigens
Phagocytosis and antigen presentation: ↓ memory to NEW antigens
Immune response to previously exposed antigens is intact because old memory cells remain ok bur can be some ↓ in preformed antibodies as ↓ IgM ABO antibody synthesis ↓ response to transfussions
↓ ability of neutrophils to cause apoptosis: delayed healing
↑ marrow fat and ↓ mass ↓ cell diversity and response to cytokines ↓ capacity of making new RBCs

117
Q

Factor 12 Hageman function:

A

Coagulation and fibrinolysis activation (makes and breaks cloths, DIC)
Complement activation
Kinin cascade activation that ↑bradykinin

118
Q

Which cells express CD4 on their surface?

A

Same ones attacked by HIV:

T helper cells (HIV uses CXCR4 and CCR5 as coreceptors)
Macrophages (HIV uses CCR5 as coreceptor, it hides in macrophages) and langerhans
Dendritic cells

R5 viruses use CCR5 and X4 viruses use CXCR4 so cannot infect macrophages
R5 is the one that is typically transmitted then mutates to X4 and progresses in the body

119
Q

IL important in psoriasis:

A

IL12

IL23

120
Q

IL important in rheumatoid arthritis:

A

IL1 (fx ↓ by anakinra)
TNF-alpha (fx ↓ by adalimumab, etanercept)

Choose them when you don’t know!

121
Q

Receptors needed for margination (endothelium ↔ leukocyte):

A

Selectins (E,P -prefromed 1st to show up-) ↔ Sialyl Lewis

122
Q

Receptors needed for adhesion (endothelium ↔ leukocyte):

A

ICAM-1 ↔ Integrin 18 β2 (CD11=LFA-1=Mac-1)

VCAM-1 ↔ Integrin VLA-4

123
Q

Receptors needed for diapedesis (endothelium ↔ leukocyte):

A

PECAM-1 (CD31) ↔ PECAM-1 (CD31)
Vascular marker

If the Passport (Pecam) matches you can go in

124
Q

Which diseases are associated with HLA-B8 and DR3?

A

Addison and graves

B8 is associated with Addison, myasthenia and graves (don’t Be late8 Dr. ADDISON or you will send MY patient to the GRAVE)

125
Q

Which particle is associated with signal transduction in T helper cells?

A

CD3: signal transduction!! in both helper and cytotoxic T cells
CD4 and CD8 are to interact with MHCs

126
Q

Define inmune privilege and give an example:

A

Inmune privileged organs (eyes and testes) are separate form the rest of the body and have some self antigens. After trauma they can release their antigens and this will cause an T cell response against those organs called sympathetic ophthalmia.

Even if the trauma is unilateral (for example one eye) the inmune response is bilateral (in both eyes).

127
Q

DD. between lepromatous and tuberculoid leprosy:

A

Forget about the clinical signs
Tuberculoid: positive lepromin, induration! Th1, M1
Lepromatous: acid fast bacilli on lesions negative lepromin! Th2, M2

128
Q

Large ovoid cells with eccentric nuclei refer to:

A

Plasma cells

129
Q

Function of epidermal growth factor, fibroblast growth factor and platelet derived growth factor:

A

EGF: growth by TK, expressed by tumor cells
FGF: angiogenesis FA!
PDGF: fibroblasts and vascular remodeling

130
Q

Why don’t we need the thymus in adults?

A

Because the lymphocytes that mature in the thymus are long lived

131
Q

How do you differentiate between drug side effect, acute rejection or infection as cause of a complication after transplant rejection?

A

Renal hypoperfusion, HT, tubular vacuolization!!!, no inflammatory cells: drug

Lymphocytes, tubulitis: acute rejection

Neutrophils (PMNs): infection

132
Q

How do you make a conjugate vaccine?

A

Polysaccharide conjugated with protein fragment (to induce T dependent immune response)

Polysaccharide is a starch not a protein

133
Q

What do CCR5 and CXCR-4 stand for? What is their fuction

A

CD4 is the HIV receptor CCR5 and CXCR-4 are the coreceptors

CCR5: Cysteine-cysteine chemokine receptor 5, also known as CD195 (Maraviroc is a chemokine receptor antagonist)
CXCR-4: C-X-C chemokine receptor type 4, also known as fusin or CD184

They are CHEMOKINE receptors and act as CORECEPTORS, they allow the conformation change in pg120 to show gp41 for FUSION (enfuvirtide blocks gp41)

134
Q

What is the mechanism of Hep B vacccine? and the mechanism of the flu shoot?

A

Hep B vaccine: it is recombined HBsAg that allows the body to make anti-HBs antibodies so they IMPAIR VIRION ENTRY into hepatocytes

Flu vaccine: Stimulates the formation of neutralizing antibodies against hemagglutinin so they IMPAIR VIRION ENTRY into cells

135
Q

Name two markers or mast cell activation:

A

Histamine

Tryptase

136
Q

What is the function of the peyer patches?

A

Place of presentation of antigens to the B cells

137
Q

In which infections can you use passive immunization?

A

Tetanus, botulism, hep B, varicella and rabies

138
Q

What is high at the early and late stage of an allergic reaction?

A

Early: mast cells
Late: eosinophils

Mast cells degranulate, producing histamine which attracts eosinophils. The early stage of an allergic reaction is mast cell mediated, but the late stage (including mucus production) is mediated by eosinophils

139
Q

How would you explain that a recombinant or live vaccine does not generate IgG on certain healthy people?

A

MHCs of those individuals cannot recognize the polypeptides presented, this is possible because MHCs do not undergo somatic hypermutation

140
Q

Specific HLA for narcolepsy:

A

DQB1

tto: sodium oxybate, modafinil, amphetamines

141
Q

What is CD95 and where is missing?

A

CD95 (Fas) receptors are death receptors that activate the extrinsic pathway of apoptosis
They are missing in autoimmune lymphoproliferative syndrome (autoimmunity)

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