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Blood and Lymph > Immunology Test 2 > Flashcards

Immunology Test 2 Flashcards

1
Q

T Cells vs B Cells

A

T cells must be present at site of interaction with antigen presenting molecule; secretions are short range. B cells secrete antibody and don’t have to be present to see the result.

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2
Q

What activates T-Cells?

A

antiogen + Antigen presenting Molecule

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3
Q

Th0

A

is the precursor to all Helper T cells

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4
Q

Where do Th0 cells exist?

A

when presented by DC they move from afferent lymph to paracortex to show T-cells to cause them to divide and differentiate.

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5
Q

Th1

A

delayed hypersensitivity T-Cells; proliferate rapidly in lymph node; react with antigen precession cells and secretes cytokine to attract macrophages in Classically activate M1.

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6
Q

What does Th1 secrete when it encounters an APC?

A

IFN-gamma (a lymphokine and cytokine), as well as IL-2

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7
Q

IFN-gamma

A

is a pro-inflammatory cytokine that is chemotactic for macrophages

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8
Q

macrophages activated by IFNgama

A

classically activated to ingest bacteria and kill it.

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9
Q

Why does Th2 secrete IL-2?

A

help activate killer T-cells

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10
Q

What do the macrophages activated by Th1 secrete?

A

TNFalpha and IL-1

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11
Q

Th17

A

very similar to Th1, produces inflammatory IL-17 a more ferocious inflammatory agent than Th1.

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12
Q

what types of infection is Th1 involved in?

A

bacteria

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13
Q

what types of infection is Th17 involved in?

A

fungal infections, and autoimmunity

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14
Q

what method of activation does Th17 utilize for its macrophages?

A

Classic M1 macrophages

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15
Q

lymphokines are a subset of..

A

cytokines

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16
Q

Th2

A

leave node and circulate through blood and lymph to encounter antigen in tissue; secretes IL-4 t activate M2 macrophages

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17
Q

what does Th2 secrete?

A

IL-4

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18
Q

IL-4

A

chemotactic for eosinophils

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19
Q

What type of macrophages are activated by Th2?

A

Alternative activated or M2

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20
Q

M2 vs M1 activation

A

M1 = classical and it is involved in inflammtaion; M2 = healing (debris removal, scar, walling-off)

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21
Q

What does Th2 help to target?

A

Macrophages that target eosinophils

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22
Q

When does Th1 show up compared to Th2?

A

Th1 is first then Th2 takes over in repair and healing

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23
Q

Tfh

A

Follicular Helper T-Cells; migrate into follicle in cortex when activated by DC; help B cells to recognize antigen and activate into antibody secreting plasma cell

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24
Q

Two functions of Tfh

A

1) help B cells recognize antigen and activate antibody secretion 2) Class switching from IgM

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25
Q

Treg

A

Regulatory T-Cell; very small population (only 5%) that suppress activation of other T-helper cells.

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26
Q

Treg in the gut

A

Secretes IL-10 and TGF-Beta to avoid immune response to food.

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27
Q

Phenotype of regulatory T-cells

A

CD4+/CD25+

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28
Q

Cytotoxic TCells (CTL)

A

signal target cell to activate apoptosis by engaging CD95 (death receptor) and secrete lytic granules (granzymes) and Perforins to allow penetration of granzymes.

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29
Q

Granzymes

A

lytic granules secreted by CTL

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30
Q

Perforins

A

secreted by CTL to allow penetration of granzymes.

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31
Q

Viral Hepatitis

A

CTLs kill the body’s own liver cells, but not the virus itself

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32
Q

Memory Cells

A

after response to antigen, the number of T-cell declines. These cells have same attributes of stem cells in that they can rapidly replicate in response to antigen (low concentrations)

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33
Q

Subpopulation markers

A

CD3, CD4, CD8 - surface markers on T cell population; involved in Tcell activation

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34
Q

CD3 is on..

A

virtually all cells

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35
Q

CD4 is on…

A

only T-helper cells

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36
Q

CD8 is on…

A

only CTL cells

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37
Q

MHC Restriction

A

T cell will only recognize peptide antigen when it is bound to body’s own MHC molecule; A t cell is antigen specific and MHC restricted.

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38
Q

MHC

A

Major Histocompatibility Complex - fruit bowl on surface of APC that contains the epitope piece

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39
Q

Antigen Presentation - extrinsic

A

Antigen is broken down by lysosomal enzymes in DC, vesicles fuse with surface with MHC on inner surface —> fusion causes MHC on surface to express partially broken own antigen.

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40
Q

What are the antigen presenting cells?

A

Macrophages, dendritic cells, B-cells

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41
Q

Epitopes for T-cells must be

A

continuous epitopes (B cells can be continuous or discontinuous)

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42
Q

T-Cell Receptor

A

same structure as antibody, except two chains called Alpha and beta which a constant and variable region.

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43
Q

Do T-cells have variable regions?

A

Yes - they have special VDJ regions that recombine and have 3 CDRs.

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44
Q

Where does T-cell development take place?

A

Thymus

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45
Q

CD3 is associated with..

A

the TCR and it transmits signal when the Th cell binds to correct antigen and MHC

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46
Q

TCR-pMHC

A

when antigen interacts with TCRR, this becomes activated and activates a cascade of accessory molecular interaction that modify, enhance, diminish activation.

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47
Q

what CD types are on MHC Class II?

A

CD4 (shut off CD8); all Th cells

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48
Q

What CD types are on MHC class I?

A

CD8 (shut off CD4); all CTL cells

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49
Q

MCH Class II

A

used by DC, macro, B-cells; selective for Th cells; antigen presenting cleft is made up of two peptides

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50
Q

MCH Class I

A

present on all nucleated cells; antigen presenting peptide is composed of one single peptide with stabilization constant peptide. Dependent on intrinsic pathway.

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51
Q

Intrinsic APC

A

when contents uptake via the extrinsic pathway leak out of the vesicle and are put on the surface of MCH class cells.

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52
Q

what types of cells react to MCH Class i?

A

CTL

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53
Q

Cross Presentation

A

cells can bring samples in from periphery and arranged not only for Th response, but also for CTL

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54
Q

CD4

A

is on helper T cells and helps strengthen the binding between MHC class II and APC

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55
Q

B-cell as antigen presenting molecule

A

B cell binds to antigen and takes into cell and loads into Clas II MCH. Tfh recognizes MHC II and hopes B cell to release antibody. Epitope that the B cell sees is not the same as the Tfh epitope.

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56
Q

To activate B cell, is the epitope the same as the Tfh?

A

no! there is digestion in between.

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57
Q

what if you block B-cell endocytosis?

A

cannot be activated by T cells to make antibody

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58
Q

Which is a better APC DC or B cell?

A

DC because B cells don’t produce cytokines

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59
Q

T-Independent Antigens

A

don’t get help from T-cell for activation; it is a carbohydrate antigen with a large backbone. This clustered binding is enough signal for activation, but DOES NOT signal for class switching.

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60
Q

Lectin

A

proteins that recognize simple sugar sequences (mannose Binding protein) and bind to T-cell and B Cells to simulate binding to an antigen when they are not.

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61
Q

Mitogens

A

a type of lectin that causes mitosis.

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62
Q

cytokine storm

A

when a bunch of T-cells are activated at same time and leads to lethal pro-inflammatory response

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63
Q

Where does the thymus originate?

A

Epithelial from pharyngeal cleft, macrophages from marrow; thymocytes from bone marrow

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64
Q

Notch receptor

A

lymphoid cells from marrow get into cortex and interact with these receptors who guide them into the T-cell differentiation pathway

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65
Q

Pre-T cells

A

large in size, double negatives (CD4-/CD8-) that have activated Rag1 and Rag2 for VDJ rearrangement.

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66
Q

General process of T-cell maturation

A

Double negative to double positive to mature phenotype with single positive.

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67
Q

How selective is the T-cell development?

A

Very selective and the majority of T-cells are double positive; fewer than 2% are exported from thymus.

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68
Q

A T-cell must meet there requirements…

A

1) not recognize self to cause autoimmunity (MCH alone or MHC with self peptide) 2) not recognize free antigen 3) recognize antigenic peptide plus self MHC

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69
Q

Thymic Epithelial Cells

A

the cells responsible or secretion of T-cells in the thymus. The cells express on their surface MHC class I and II.

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70
Q

T-Cell selection has three options

A

Non-selection, positive selection, negative selection

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71
Q

Non-selection

A

no binding to MHC because it does not recognize self MHC and leads to apoptosis.

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72
Q

Positive Selection

A

CDR1 and CDR2 bind to alpha helices of MHC groove, but CDR3 does not interact with the endogenous peptide. This cell survives.

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73
Q

Negative Selection

A

TCR binds to MHC with self peptide with TOO high of affinity that results in T-cell activation.

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74
Q

if developing T-cell binds with all 6 CDRs…

A

it becomes an autoimmune

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75
Q

Fate of negative selection..

A

apoptosis or regulatory T-cells -(thymic or natural regulatory-Tcell)

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76
Q

Histocompatibility

A

outcome of grafts of living tissues between two individuals

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77
Q

Histocompatibility -2

A

Mouse; found on Ch17 that encodes tissue rejection factors (histocompatibility antigens).

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78
Q

What is the histocompatibility complex on human cells?

A

Human Leukocyte Antigen that has four importan loci A, B, D, and DR with incredible genetic polymophism.

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79
Q

What chromosome is HLA located on?

A

Ch6

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80
Q

What is the order of HLA?

A

closest to centromere Class II, Class III and then Class I (furthest from centromere)

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81
Q

Class II loci on HLA?

A

DP, DQ, DR (DR most important)

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82
Q

Class I loci on HLA?

A

B, C, A (most important A and B)

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83
Q

what loci do we need to know for transplants?

A

HLA A, B, DR

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84
Q

who are you more likely to match for antibodies with, your sister or your parent?

A

sister

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85
Q

Linkage disequilibrium

A

not much recombination in HLA genes!

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86
Q

anchor position

A

Sites of coordination in amino acid sequence between epitope and MHC

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87
Q

how many CDRs does T cell receptor use to bind to MHC?

A

4

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88
Q

how many CDRs does Tcell receptor use to bind to epitope?

A

2

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89
Q

Synergeic

A

isografts - grafts between genetically identical individuals

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90
Q

Allogeic

A

allografts - grafts between non-identical membrane of same species

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91
Q

Zenogeneic

A

Xencografts: grafts between members of different species

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92
Q

Hyperacute rejection of graft

A

graft is given to patient with pre-existing antibody. Antibody binds to endothelial cells on grafts blood vessel and activate complement and vasospasm. Graft never perfuses with blood.

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93
Q

Graft Rejection

A

Th1 recognizes MHC with foreign antigen (class II - DR); and secrete IFNgamma and bring in macrophages from the graft recipeient. Th1 secrets nearby CTL that is bound to MHC antigen of Class I (HLA-A and HLA-B) to kill target graft.

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94
Q

what if donor has identical Class I, but different class ii?

A

Th1 is activated, but not CTL. graft is still rejected but slower

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95
Q

What if donor is different Class I, but identical Class II?

A

no TH1 is activated, IL-2 will not be generated and few CTL is activated.

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96
Q

which match is more important Class I or II?

A

II

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97
Q

why do we respond more strongly to something that is not a pathogen (graft?)

A

receptor interacts with MHC in a slightly skewed position, and it thinks that the MHC is foreign and leads to destruction. The response is much slower if it is completely foreign (ie horse skin vs human)

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98
Q

HLA linked Diseases

A

modifications of self proteins create novel epitopes that associate strongly with MHC alleys.

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99
Q

natural, active immunity

A

immunity from exposure to a pathogen; longest lasting

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100
Q

Natural, passive immunity

A

enjoying the products of someone else immune response, pregnancy with IgG

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101
Q

Artifical Active immunity

A

immunization with vaccines, toxioid or antigen preparations

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102
Q

what does a dirty vaccine indicate?

A

more complex the mixture of molecules, the more likely to have unpleasant side effects

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103
Q

which provide better immunity - live or killed?

A

Live - infectious but attenuated.

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104
Q

Artificial, Passive Immunity

A

immune serum or purified antibodies to protect pt at risk of disease. We have antiwar for tetanus, rabies, hepatitis, chicken pox.

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105
Q

Toxoid

A

inactivate toxin that is almost always as effective at eliciting an immune response

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106
Q

Rabies Vaccine

A

active immunization with vaccine growth on human diploid cells; onset is slow so immunization can occur after exposure.

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107
Q

Diphtheria Vaccine

A

another toxoid

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108
Q

Pertussis vaccine

A

whooping cough; old vaccine was ineffective and has been replaced with acellular pertussis. But vaccine is present for strains in 1950, so not completely effective

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109
Q

Measles Vaccine

A

Rates increase significantly when immunizations go down; has extremely high heard immunization

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110
Q

Conjugate Vaccines

A

capsular carbohydrates are T-independent,b ut fail to generate an immune response. So if you couple a complex carb with a protein “carrier” to which Tfh cells could respond and aid B cell in making anti-carbohydrate IgG antibody.

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111
Q

what type of antibodies to B-cells make that are simulated by complex carbohydrates?

A

IgM only

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112
Q

what kind of antibody do the B-cells make when stimulated by conjugate vaccine?

A

IgG

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113
Q

what deos the protein antigen from a conjugate vaccine get loaded onto?

A

MHC Class II

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114
Q

Rotasheild

A

a vaccine against rotavirus that was taken off the market because it caused intussusception leading to necrosis and peritonitis due to hypertrophy of Peyer Patch.

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115
Q

Intussusception

A

telescoping of the bowel, risking blood supply loss causing necrosis and peritonitis

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116
Q

Adjuvants

A

substances added to vaccines to make them more immunogenic

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117
Q

how to adjuvants work?

A

cause an innate immune response that leads to more effect adaptive response.

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118
Q

most common adjuvant?

A

Alum

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119
Q

Alum

A

potassium aluminum sulfate adjuvant that mimics PAMPs to stimulated DC that drive Tfh.

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120
Q

Herd Effect

A

decrease in infection rate in the non-immune part of the herd.

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121
Q

Bacterial Immunity

A

extracellular bacteria are mostly combated by antibody; some are destroyed by C9 of the MAC; intracellular bacteria can survive in the macrophage but are killed if activated by Th1 cells.

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122
Q

Most important principle of immunity

A

humoral immunity may prevent illness, but once ill, T cell immunity is necessary for recovery.

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123
Q

Viral Immunity

A

local immunity (IgA) prevent the invasion of a virus; if it gets into blood it is stopped by IgG; if virus infects cells, T-Cell response is required and virus stimulates cytokine and chemokines to activate DC cells to pick up debris and process the peptides. Presented on Class II and cross-presented on Class I (for CTL)

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124
Q

what viruses are the hardest to deal with?

A

viruses that never appear in blood or lymph, but go latent (herpes)

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125
Q

Titer

A

reciprocal of the maximal diluation of patient’s serum that is still positive in some defined test.

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126
Q

DNA Vaccines

A

immunizing for the DNA that the antigen is encoded from so it would be translated in cell; advantages is quicker vaccine production, more stable faccine, and antigen would be made in body cells producing a natural, active immunity.

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127
Q

Monocytes/Macrophage - Time in marrow

A

Short time - 7 days

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128
Q

Monocytes/Macrophage - days in intravascular compartments

A

3-5 days

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129
Q

Monocytes/Macrophage - presence in tissues

A

days-months

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130
Q

Monocytes/Macrophage - histology

A

gray cyto, kidney shaped nulcues, changing morphology with tissues

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131
Q

Monocytes/Macrophage - function

A

1)move to sites of infec/inflam 2) filter (splenic macrophage) 3) processing and presenting antigens 4) clearance of apoptotic cells

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132
Q

why is clearance of apoptotic cells important

A

could cause severe inflammation and devastating tissue injury if not removed.

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133
Q

Neutrophil - Storage pool

A

10-14 days

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134
Q

Neutrophil - peripheral blood

A

6h

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135
Q

Neutrophil turnover

A

1-2 days

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136
Q

Neutrophil - function

A

innate immune system, non-specific defense against microbes, response to injury

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137
Q

what happens with neutrophils in tissue?

A

look for sights of potential infection and either kill the infection source or die themselves and get turned over my monocytes

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138
Q

what do neutrophils recognize?

A

they have no memory, but look for pattern recognition on microbes

139
Q

Eosinophil - Bone marrow

A

influenced by IL-5

140
Q

Eosinophil - histological features

A

large eosinophilic granules, bi-lobed nuclei

141
Q

where doe eosinophils reside?

A

external surfaces (tracheobronchial tree, GI tract

142
Q

how long do eosinophils survive in periphery?

A

weeks

143
Q

Eosinophil - Function

A

Phaocyte, role in allergy, paraste infection, response to tumor, immunoenhancing or immune suppressive

144
Q

Basophil - histology

A

similar size to eosinophils, bi lobed nulcue, prominent purple/blue granules

145
Q

what receptors are on basophils?

A

IgE

146
Q

Basophil - function

A

pathophysiology hypersensitivity reactions

147
Q

what cells make up cells in the progenitor compartment?

A

stem cells

148
Q

what compartment are the myeloid precursors in?

A

mitotic compartment

149
Q

what cells make up the myeloid precursors in the mitotic compartment

A

myeloblast, premyelocye, myelocyte

150
Q

Process of myeloid precursors

A

proliferation and maturation

151
Q

Percentage of myeloid precursors in mitotic compartment?

A

Myelocyte 16%>promyelocyte 4%> myeoblast 1%

152
Q

How long to myeloid precursors stay in the mitotic compartment

A

10-14 days

153
Q

what myeloid precursors are in the storage compartment?

A

Metamyelocytes, Band and sets

154
Q

what process occurs in the storage compartment?

A

maturation

155
Q

what is the % of the myeloid precursors in the storage compartment?

A

Band 30%> metamyelocyte 22% > Seg 21%

156
Q

which is larger the mitotic compartment or storage compartment?

A

storage with 73%, while mitotic has 21%

157
Q

what is the role of the myeloid precursors?

A

terminal cells of the neutrophil line. They are active and their job is not to proliferate, but finish maturing and form the storage compartment.

158
Q

what is the function of the storage pool?

A

a collection of cells that can be localized to fight infection quickly.

159
Q

Marginating pools

A

pools of neutrophils that hang on the edge of post capillary venules

160
Q

What is the ration of neutrophils in peripheral blood and marginating pool?

A

1 to 1

161
Q

how long do neutrophils live in peripheral blood

A

9-12 hours

162
Q

how long to neutrophils live in the tissue?

A

around 24 hours. Before they undergo apoptosis and are turned over by monocytes

163
Q

where are neutrophils depleted in neutropenia?

A

storage compartment

164
Q

neutropenia - definition

A

decrease in absolute neutrophil count (including band and set polymorphonuclear leukocytes) below accepted age norm

165
Q

General pattern for neutrophil count

A

greatest at newborn, but decrease after 1 week and up until 2 years, then increase during childhood to adulthood. 3000- 1,1000 — 1500

166
Q

What things affect neutrophil norms

A

ethnic and racial groups have lower norms, and altitude above 5,000 Ft lowers the norm in infants

167
Q

implications of neutropenia

A

decreased delivery of neutrophils to tissue causes inability to resolve bacterial and fungal infections and localized infection

168
Q

ANC of 1,500-1,000

A

No risk

169
Q

AND of 1,000- 500

A

moderate to mild neutropenia

170
Q

ANC 500-250

A

Moderate to severe neutropenia

171
Q

what are the symptoms of moderate to severe neutropenia

A

skin, mucous membrane infections

172
Q

ANC

A

severe neutropenia

173
Q

Symptoms of severe neutropenia

A

sepsis, pneumonia

174
Q

what sites should you focus your physical exam on in neutropenia

A

teeth and gums, lymph nodes, hepatoslenomegaly, infected sites.

175
Q

why should we look carefully at gums in neutropenia?

A

they are the only place on the body with direct penetration of mucosal barrier

176
Q

how often would you perform a CBC and why in neutropenia

A

2x a week for 6 weeks; to see if neutropenia is persistent or intermittent. If it cycles, want to see how low the cycles and evaluate their absolute risk

177
Q

What laboratory tests should you perform for neutropenia?

A

CBC (with retic), Bone marrow aspirate/biopsy, blood chemistries with LDH, uric Acid, alkaline phosphate, anti-neutrophil antibodies

178
Q

primary decreased bone marrow reserve

A

all cells have gone away as in Kostmann, Scwachman-Diamond, cyclic neutropenia

179
Q

Potions for a decreased marrow reserve?

A

primary disorders, part of complex phenotype combined with other diseases, Secondary disorders, or idiopathic

180
Q

Secondary decreased bone marrow disorders

A

decrease in marrow due to chemo, drug induced, nutritional, viral infection

181
Q

Normal Marrow Reserve

A

usually indicates an increased or normal production of neutrophils;. Due to immune or non-immune causes

182
Q

Immune - normal marrow reserve

A

chronic benign neutropenia in childhood, autoimmune, alloimmune, drug induced, infection

183
Q

Non-Immune normal marrow reserve

A

infection, hypersplenism, excessive margination

184
Q

Infection associated neutropenia

A

a secondary cause; most common cause

185
Q

Mechanisms of Infection associated neutropenia

A

Increased utilization, excessive complement mediated margination, marrow suppression/failure, unusual cytokine/chemokine induced margination, antibody production

186
Q

infections associated with neutropenia

A

viral, bacterial, fungal, protozoal, rickettsial

187
Q

clinical characteristics of antibiotics induced neutropenia

A

onset: days to weeks; acute symptoms, recurrence with small dose of antibodies; positive antibody test

188
Q

Clinical characteristics of toxin neutropenia

A

onset is weeks to months, directly toxic to cells, rechallange with high dose may relapse after latent period

189
Q

toxic drug that causes neutropenia

A

phenothiazine

190
Q

Hypersensitivity in secondary neutropenia

A

onset is weeks to months, associcated with rash, fever, lymphadenopathy, hepatitis, nephritis, rarely aplastic anemia

191
Q

drugs that cause hypersensitivity neutropenia

A

dilantin, phenobarbital

192
Q

hypersensitivity vs. Toxic neutrophilia

A

toxic is directly toxic to cells; hypersensitivity elicits are more inflammatory response in nature and less toxic.

193
Q

Mechanism of Cancer Chemo on secondary neutropenia

A

suppression of myelopoiesis

194
Q

Findings of chemo induced neutropenia

A

other cytopenias present such as anemia, thrombocytopenia

195
Q

Aplastic anemia induced secondary neutropenia mechanism

A

stem cell failure with other cytopenias present

196
Q

Vitamin B12 and folate deficienty induced secondary neutropenia mechanism

A

ineffective hematopoeisis; intramedually death secondary to effets of deficient on replication

197
Q

Vit B12 and Folate deficiency neutropenia findings

A

other cytopenias (thrombocytopenia) with megaloblast changes in marrow

198
Q

Hypersplenism induced neutropenia mechanism

A

reticuloendothelial sequestration with other cytopennia

199
Q

Causes of secondary neutropenia

A

Drug/toxin induced, chemo, aplastic anemia, Vitb12 and folate deficiency, hypersplenism

200
Q

management of Secondary neutropenia

A

withdrawal of drugs or toxins, treatment of underlying disorder, replacement of deficienty, management of infections, support care with prophylactic, G-CSF in some conditions

201
Q

G-CSF in treatment of secondary neutropenia

A

used in chemotherapy, primary cytokines to cause production in marrow

202
Q

Marrow production in immune neutropenia

A

Normal to increased

203
Q

Storage pool in immune neutropenia

A

normal to mildly decreased

204
Q

Mechanism of immune neutropenia

A

increased turnover of neutrophils, vascular compartment decreased levels

205
Q

Categories of Immune neutropenias

A

alloimmune, chronic benign childhood neutropenia, autoimmune, drug-induced

206
Q

Fe saturation under 10%

A

iron deficiency

207
Q

Anemia of Chronic inflammation iron saturation

A

10-20%

208
Q

autoimmune neutropenia clinical features

A

may find ITP, AIHA, and other hematologic antibodies, immunodeficiency states, variable ANC, normal cellularity, late maturation arrest

209
Q

Management of autoimmune neutropenia

A

treat primary autoimmune disorder, G-CSF may be helpful

210
Q

Alloimmune neutropenia - mechanism

A

maternal: to neutrophil specific antigens, transplacental passage and bidning to neonatal neutrophils

211
Q

Clinical features of alloillumine neutropenia

A

usually lasts 2-4 weeks; occasionally 3-4 months; may be asymptomatic, but could develop skin infections and rarely sepsis or meningitis. Confused with neutropenia by sepsis; myeloid hyperplasia with arrest at mature; small storage pool

212
Q

In response to EPO injections, you would expect..

A

increased reticulocyte count, fall if MCV if Fe deficient, treatment is controversial whether it makes them feel better.

213
Q

Management of alloimmune neutropenia

A

antibiotics and supportive care for infection, IVIG infusion, consider G-CSF for severe infection

214
Q

pancytopenia

A

abnormal patelets, wbc, Rbc

215
Q

MCV in sickle cell anemai

A

normal to high; except in sickle Beta than

216
Q

what cells are involved primary neutropenia

A

stem cells and neutrophil precursors

217
Q

dacryocytes

A

tear-dropped cells

218
Q

anisocytosis

A

RBC unequal in size

219
Q

polychromasia

A

bluish cells in reticulocytes

220
Q

congenital disorders of Stem cells and myeloid precurosors

A

Congenital Neutropenia (Kostmann’s Syndrome), cyclic neutropenia, Shwachman-Diamond, Glycogenosis Ib, neutropenia with metabolic disease or immune disorders

221
Q

Kostmann’s Syndrome - Mechanism

A

apoptosis of myeloid precursors associated with Elastase (ELA-2) mutations; sometimes defects in G-CSF receptor

222
Q

Kostmann’s Syndrome - inheritance

A

AD, AR, sporadic

223
Q

Kostmann’s Syndrome - Clinical Features

A

severe neutropenia in infancy, monocytosis, eosinophilia (putting out other cells, but no neutrophils), Myeloid hypoplasia in marrow; tno storage pool; recurrent purulent infections, risk of AML or myelodysplaisa

224
Q

Why does Kostmann’s not have a storage pool?

A

arrest in maturation in promyelocyte and myelocyte stage (mitotic pool)

225
Q

Treatment of Kostmann’s

A

aggressive treatment of infection, G-CSF 3-100 to keep ANC high, consider BMT for poor response to G-CSF

226
Q

Cyclic Neutropenia Mechanism

A

ELA-2 mutation and apoptosis in precursors and cyclic hematopoesis

227
Q

Inheritance of cyclic neutropenia

A

AD, Sporadic

228
Q

Symptoms of cyclic neutropenia

A

fever, pharyngitis, aphthous ulcers, gingivitis, periodontitis

229
Q

ITP

A

antibodies against platelets

230
Q

how long do cycles last in cyclic neutropenia

A

21 +/- 3 days; the rest of the time neutrophils are normal

231
Q

ANC in cyclic neutropenia

A
232
Q

Schisotcytes

A

fragmented part of red blood cell, jagged with two pointed ends and no area of central pallor

233
Q

Bone marrow in cyclic neutropenia

A

myeloid hypoplasia, arrest at myelocyte level during neutropenia

234
Q

management of cyclic neutropenia

A

aggressive antibiotics, G-CSF daily to increase the low value of ANC so risk of infection decreases

235
Q

Shwachman-Diamond Syndrome - mechanism

A

FAS associated premature apoptosis of marrow precursors; Decreased CD34+, marrow stromal defect

236
Q

Shwachman-Diamond Syndrome - inheritance/genetics

A

AR, defect in SBDC gene on Ch17

237
Q

Clinical features of sHwachman-Diamond

A

multisystem - neutropenia, pancreatic insufficiency, metaphyseal chondrodysplasia, dysmorphic features, 25% develop marrow aplasia, 25% develop MDS/AML; neutrophil dysfunction, recurrent infection

238
Q

Management of SHwachman -Diamond

A

pancreatic enzyme replacement, aggressive antibiotic therapy, BMT for severe

239
Q

Cartilage Hair hypoplasia

A

AR, short limbed dwarf, fine hair, neutropenia

240
Q

Dyskeratosis Congenita

A

X linked, nail dystrophy, hyperpigmentation, marrow hypoplasia, neutropenia

241
Q

Chronic idiopathic neutropenia mechanism

A

myeloid hypoplasia and maturation arrest at myelocyte, metamyelocyte or blast stage, no specific inheritance

242
Q

Clinical features of idiopathic neutropenia

A

mod to severe neutropenia, recurrent infections, no neutrophil antibodies

243
Q

management of idiopathic neutropenia

A

G-CSF

244
Q

leukocytosis

A

increase in total WBC risk of infection, inflammation, malignancy, Increase in neutrophils (segs and band)

245
Q

Neutrophilia causes

A

increased production, enhanced release of storage pool, decreased egress from ciruculation, reduced migration

246
Q

Eosinophilia causes

A

Allergic disorder, dematits, parasitic infections, tumor, GI disorder, Hereditary, hyperesinophilic syndromes,

247
Q

Neutrophilia definition

A

> 7,500 cells/ul

248
Q

Eosinophilia AEC

A

> 350 /ul

249
Q

Monocytosis AMC

A

> 1,000 newborn; >500 children, adults

250
Q

Causes of Monocytosis

A

hematologic disorders, collagen vascular disease, granulomatous disease, infection, malignant disease

251
Q

Causes of monocytopenia

A

glucocorticoid admin, infection with endotoxemia

252
Q

Basophilia causes

A

hypersensitivity reactions, inflammation and infection, myeloproliferative disease

253
Q

Basophilopenia causes

A

glucocorticoid admin, thyrotoxicosis

254
Q

where do lymphocytes enter the lymph node?

A

through afferent lymphatic vessels and into the sub capsular space.

255
Q

how does lymph lead the lymph node?

A

efferent lymphatic vessels

256
Q

Traveculae

A

short connective tissue in the lymph nodes that extend and divide the cortex.

257
Q

Reticular fibers

A

are located in the cortex and paracortex, used by dendritic cells to hang on as they flow through the lymph node.

258
Q

Lymphoid Follicle

A

In the cortex that houses B cells and germinal centers

259
Q

Germinal centers

A

located in the follicle; regions of active cell proliferation and apoptosis. Made up of B cells, dividing B cells, and macrophages.

260
Q

Composition of cortex vs. paracortex lymph node

A

Cortex is B cells; Parapcortex is T-Cells (with some B)

261
Q

Lymph node Medulla

A

region of loosely arranged cords of cells containing B cells, a few T cells and plasma cells.

262
Q

High Endothelial Venule

A

Vessels that have endothelial bulges that act as sites of recognition and diapedesis of lymphocytes from blood into the lymphatic node space. Notable for their rounded protrusions into the lumen

263
Q

Primary Follicle of Lymph Node

A

also called primary lymphatic nodule; not vernal in center of follicle, but tight knit cells.

264
Q

What are the different layers of the germinal center

A

inner follicle cells, mantle zone of closely packed lymphocytes and marginal zode of looser packed lymphocytes.

265
Q

What cells are in the follicle center? be specific

A

Centroblasts and centrocytes (plasma cells)

266
Q

Tingible body macrophages

A

engulf apoptotic cells

267
Q

where do most macrophages exist in the lymph node?

A

subcapsular space

268
Q

Trabeculae of the thymus

A

the bilobed thymus is ensheathed in connective tissue septa that divides the tissue into pseudo lobules

269
Q

Thymus cortex

A

located closest to the capsular sheath, more densly packed set of developing thymocytes or T-cells (appears darker with nucleus).

270
Q

where do mature thymocyte precursors reside in the thymus?

A

medulla

271
Q

What defines the cortex vs medulla of the thymus?

A

density of the T-cell packing. Cortex is densly packed with immature thymocytes. Medulla is loosely packed more mature thymocytes

272
Q

Where are the blast cells in the thymus

A

just beneath the capsular, give rise to the immature thymocytes in the cortex.

273
Q

IF T cells return to the thymus, where do they congregate?

A

Medulla

274
Q

Stromal Cells

A

Epithelioreticular cells, cells that are epithelial-like, dendritic cells, or macrophages. provide matrix and envelop developing thymocytes in large folds as T-cell matures from cortex towards medulla.

275
Q

Stromal cell Role

A

negative and positive T- cell selection, secrete cytokines and thymic hormones important for thymocyte maturation; DIFFERENTIATIO OF SELF FROM NON_SELF

276
Q

Does the thymus contain reticular fibers?

A

No, because there is no bulk flow through it. Stromal cells provide support and have Hassal’s Corpuscles

277
Q

Hassal’s Corpuscles

A

concentric layers of reticular cells in Thymus medulla. Produce thymic stromal lymphoprotin that suppressing autoimmune events.

278
Q

How does blood get into the thymus?

A

enter through small arteries through outer capsule and penetrate into thymus and spread within CT septa between lobules.

279
Q

Blood thymus barrier

A

Combined layers of ensheathed endothelioreticular cells that are connected by tight junctions in vessels

280
Q

Importances of Blood Thymus Barrier

A

so maturing thymocytes are not exposed to any molecules circulating in blood.

281
Q

what is the arteriole blood supply to the thymus?

A

internal thoracic and inferior thyroid

282
Q

Where is the blood thymus barrier in the thymus?

A

cortex, but not medulla.

283
Q

what is unique to the thymus

A

there is no afferent lymphatics

284
Q

what is unique to the spleen

A

open blood circulation through porous splenic sinuses.

285
Q

what artery supplies the spleen?

A

splenic artery

286
Q

what vein drains the sleep?

A

splenic vein.

287
Q

Blood flow in the spleen

A

in through the splenic artery and then branches to central arterioles that run deeper into the spleen, but as they get deeper then are lined with discontinuous endothelial cells, allowing platelets, RBC and leukocytes to enter sinuses that contain loosely packed arrangements of cells

288
Q

periarteriolar lymphoid sheath

A

lymphocid tissue that is arranged around central arterioles that is composed of T-cells

289
Q

Red Pulp

A

loosely-arrnaged channels/sinuses that blood flow through after leaving central arterioles. (the space)

290
Q

White pump

A

more organized lymphoid tissue in spleen, found directly outside the central arterioles.

291
Q

Reticular fibers of spleen

A

found primarily in red pump

292
Q

Macrophages in spleen location

A

in senescent red cells and platelets

293
Q

Macrophages function in spleen

A

moging senescetn RBCs and platelets, recycing iron, and converting hemoglobin in bilirubin.; removal of debris and bacteria

294
Q

Mucosal-Associated Lymphoid Tissue examples

A

tonsils (palatine, lingual), pharyngeal (adenoids), esophageal nodules, Bronchial nodes and large number of cells might increase in abundance and size as get distal.

295
Q

Peyer patch

A

nodules located in the muscosa and submucosa of the colon

296
Q

M cells

A

involved in MALT, special surface epithelial cells found in small intestine and respiratory tract and deliver antigen to underlying lymphoid tissue.

297
Q

what antibodies are involved in MALTs?

A

IgA; are secreted across mucosal epithelia and in bile. Activated B-cells that were exposed to antigen in MALT, enter lymph, undergo mitotic expansion in mesenteric lymph node, flow out thoracic duct and enter blood, and then pass through underlying CT at any region in intestine to become antibody secreting plasma cells.

298
Q

component cells of MALT

A

T and B cells, plasma cells, macrophages

299
Q

Structures of MALTs

A

lymphoid tissue is not packaged within capsule CT

300
Q

distribution of lymphocytes in MALT

A

larger, dividing immatre lymphocytes in center and smaller,, more dense lymphocytes in periphery.

301
Q

Challenged white pulp nodules

A

clearly visible germinal center in the spleen.

302
Q

Periarteriolar lymphatic sheath

A

consist of T-cells

303
Q

Unchallenged White Pulp Nodules

A

clearly visible nodule in spleen, made of B cells. Non dividing.

304
Q

General outline of innate immune system

A

Infection/tissue damage triggers through TLR receptors inflammatory mediators that case vascular dilation, permeability, and emigration of leukocytes which trigger emigration of phagocytes and monocytes in innate response and EVENTUALLY emigration of monocytes and lymphocytes in adaptive response

305
Q

Receptors in Rolling/Adherence

A

Sialyx LeX, L-Selectin, B2 integrins (CD11b/CD18)

306
Q

Biochemical process of the Rolling/Adherence Receptors

A

PM associated, granule containing store recpetors, actin cytoskeleton and accessory proteins

307
Q

Chemotaxis Receptors

A

C5a, N-formyl oligopeptides, lipid compounds, GM-CSF, IL8, TNFalpha

308
Q

Chemotaxis Receptors organlles/biochemical process

A

PM, actin and accessory proteins, granules (specific), glycolysis as energy source

309
Q

Ingestion Receptors

A

FcR1,2,3; C3b, CR-1

310
Q

Ingestion receptors organelles and biochemical process

A

PM, actin cyto and accessory proteins, glycolysis

311
Q

Degranulation/Killin Receptors

A

FcR1, 2, 3, C3b, CR-1

312
Q

Degranulation Killing Organelles and biochemical process

A

PM, actin ctyoskeleton, Azurophilic and specific granules; phagolysosomal formation, glycolysis

313
Q

Respiratory Burst

A

the processing of taking oxygen and making oxygen radicals that are toxic and can interact with phagocytosed substane for degradation

314
Q

Where do the electrons originate to make Superoxide radical?

A

NADPH

315
Q

what is protective of oxygen radicals

A

SOD catalase, GHS

316
Q

NOX2

A

Also known as GP91Phox; protein that uses NADPH to transfer electrons to make superoxide

317
Q

GP91Phox

A

works with P22phox on membrane, to interact with cytosolic PHox proteins in complex to take NADPH and electrons to make superoxide.

318
Q

Screening of Innate Immune Disorders

A

CBC, Diff, morphology, Bactericidal activity, chemotaxis activity, Expression of antibodies, DHR oxidation

319
Q

Bactericidal Activity

A

Mix cells with bacteria and see how they kill it

320
Q

Chemotaxis Assay

A

put cells above filter and in bottom chamber, put C5a and incubate and see # and distance through filter

321
Q

DHR

A

A compound that oxidizes dye to fluorescent compound. If you treat with bacteria to enlist more oxygen radicals, fluorescence should increase

322
Q

Leukocyte Adhesion Deficiency 1 - clinical

A

Soft tissue infections (skin, mucosa), gingivitis, mucositis, periodontist, delayed separation of umbilical cord, poor wound healing

323
Q

Leukocyte Adhesion Deficiency 1 - Functional Defect

A

Decreased adherence of neutrophils to endothelial surface, defect in movement of neutrophils to tissue. Neutrophilia

324
Q

Leukocyte Adhesion Deficiency 1 - molecular Defect

A

Complete or partical deficiency of CD18; AR

325
Q

Chediak-Higashi Syndrome - Clinical

A

Oculocuatenous albinism (white forelock), nystagmus photophobia (light bothers eye), recurrent infections, fever, hepatosplenomegaly, hemophagocytic disorder, neurodegenerative syndrome

326
Q

Chediak-Higashi Syndrome - Functional defect

A

Giant granules in leukocytes, defect in movement and decreased degranulation and microbicidal activity. Neutropenia

327
Q

Chediak-Higashi Syndrome - Molecular Defect

A

alterations in membrane fusion by forming leaky granules. Altered MT assembly. CHS1 gene, AR

328
Q

Myeloperoxidase Defieciency - Clinical Presentation

A

Generally healthy; increased fungal infections with diabetics

329
Q

Myeloperoxidase Defieciency - Functional Defect

A

Partial/complete deficiency of myeloperoxidase (converts Superoxide to hydrogen peroxide); defect in killing bacteria, significant defect in killing candida

330
Q

Myeloperoxidase Defieciency - Molecular Defect

A

Post translational modification defect in protein processing; AR

331
Q

Myeloperoxidase

A

enzyme that converts superoxide to hydrogen peroxide

332
Q

Chronic Granulomatous Disease - Clinical

A

Recurrent purulent infections with catalase positive bacteria, fungi on skin and mucosa. Deep infections in lung, spleen, lymph nodes, bones

333
Q

CGD - Functional Defect

A

Neutrophilia, normal adherence and chemotaxis, ingestion and degranulation. Defect in oxidase enzyme. No toxic oxygen metabolites produced, so absent or reduced ability to kill coagulase positive bacteria and fungi.

334
Q

CGD - molecular defects

A

Absent Cyto B558 (Gp91Phox complex); absent P22Phox; Absent p47 Phox; Absent p67Pox; Mild X-linked variant in G-6-PD deficiency in PMNs

335
Q

Cyto B558 absence- inheritance

A

Sex linked recessive

336
Q

p22Phox - inheritance

A

AR

337
Q

p47phox

A

AR

338
Q

Characteristics of phagocyte disorder

A

1) High rate of bacterial or fungal infections 2) infections against atypical pathogens, 3) exception severity of infection; 5) periodontal disease in children 6) infections occur at interface area, more common than deep (though those do occur)

339
Q

what activate complement system?

A

lectins, bacterial protein, surface bound IgG

340
Q

Deficiency in C1q, C2, C4 complications

A

SLE (lupus), autoimmunity, inflammatory vascular disease

341
Q

Deficiency in C3 complication

A

Recurrent bacterial infections

342
Q

Deficiency in C5-C9 complications

A

severe infection with neisseria (meningaococcus)

343
Q

Management of innate immune disorders

A

1) anticipate infection and aggressive attempts to define causative event; 2) surgical procedures to be both diagnostic and therapeutic 3) prompt broad spectrum antibiotics, switch when microbial diagnosis is made 4) some may need 3ug/kg/day 5)some need prophylactic antibiotics

344
Q

Transplantation of neutropenia

A

hematopoetic stem cell might be used to reconstitue myeloid function if good match

Blood and Lymph (6 decks)

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