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GBA Physiology > Hematology and Immune Physiology - Theoretical Questions > Flashcards

Hematology and Immune Physiology - Theoretical Questions Flashcards

1
Q

Hematopoiesis:

How much RBCs and WBCs are forming relatively out of 10^11 daily ? Why?

A

75% - WBC (Shorter life span)

25% - RBC (120, Longer life span)

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2
Q

Hematopoiesis: where? In fetus and Adult

Forms of production site?

A

Fetus - Liver
Adult - Bone marrow:
Yellow Bone marrow - Inactive (fatty)
Red Bone Marrow - Active or Hyperplastic (HSC, HC and Stromal cells)

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3
Q

Hematopoietic stem cells:

Markers, potency, function

A

c-Kit and CD34
Omnipotent to Oligopotent to Multipotent
Self renewing asymmetrical divisions

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4
Q

What is special about Multipotent progenitor cells (MPP) ?

A

The first cell formed in hematopoiesis unable of self renewal. From it the formation pathway divides to Myeloid and Lymphoid Lineages

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5
Q

What are the synonyms for the the Progenitor cells and Hematopoietic growth factors?

A

Progenitor cells - colony forming units (CFU)

Hematopoietic growth factors - Colony stimulating Factors (CSF)

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6
Q

What are CLPs? what are their outcomes?

A

CLP -Common lymphocyte precursors: Lymphoid lineage - Forming T and B-Cells (naive) and NK cells

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7
Q

What are CMPs? what are their outcomes?

A

CLP -Common Myeloid precursors: Myeloid lineage - Forming Monocytes, Mast cells and Megakaryocytes and Erythrocytes

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8
Q

What determines the life span of the blood elements?

A

RBCs - Rigidity of old cells cause clearing in hepatic circulation.
Platelets - Used up continuously by micro injuries
WBC - Used up continuously by Immune functions

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9
Q

What causes the Stress Hematopoiesis?

A

Hypoxia - HIF1-Alpha - EPO - Erythrocytes↑

Infection - Granulocytes↑

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10
Q

What Cytokines? Examples for Hematopoietic CSF?

A

Glycoproteins that cause transcription through TyrK mechanism. IL3 is a CSF for Myeloid Line.
EPO- Erythrocytes↑

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11
Q

What is the general principle for the Hematopoiesis regulation?

A

Early stage - Many factors (Overlapping)

Late stage - Fewer specific factors

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12
Q

What is an Hematopoietic Niche ?

A

Cell to cell interaction in the bone marrow for differentiation signaling - Causes the Divisional Asymmetry . Chemokines - Regulate the movement of Stem cells through these.

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13
Q

How are Thrombocytes formed?

A

Budding off the the Megakaryocytes into the vessels lumen. Cell Fragments.

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14
Q

What are the Reticulocytes?

A

Final RBCs progenitor still containing RNA for Hemoglobin synthesis (After nucleus removed)

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15
Q

Why are the kidney responsible for the EPO secretion ? (Mostly, Some is from liver)

A

They have the smallest AVDO2, Meaning their JG cells can sense with the greatest resolution the changes in O2 supply.

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16
Q

what ae the derivatives of the Monocytes developing course ?

A

Osteoclasts, Dendritic Cells, Macrophages, Kupffer cells and Alveolar Macrophages.

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17
Q

What regulates the Formation of Platelets?

A

Thrombopoietin from Liver.

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18
Q

What is necessary for Erythropoetin?

What could happen in shortage of each?

A

Folic Acid, B12 and Iron.
Iron↓ - Microlytic Anemia
Folic Acid and B12↓ -Megaloblastic Anemia

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19
Q

What are the steps of Primary hemostasis?

A

1) Vasoconstriction
2) Platelet adhesion
3) Platelet Activation and Aggregation

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20
Q

What are the steps of Secondary Hemostasis?

A

Activation of Coagulation factors and Fibrin

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21
Q

What are the steps of Fibrinolysis?

A

Activation of Fibrinolysis and Lysis of Plug

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22
Q

What causes Vasoconstriction in Injury?

A

Endothelin released from raptured Endothelial cells and Neurogenic Intermediates also released: TH5, K, THX2

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23
Q

What causes Platelets Adhesion?

A

vWF binding them to Collagen of Subendothelial tissue.. With GP4 and GP2b binding proteins.

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24
Q

What causes Activation of Platelets (6)?

A 
Collagen - Subendothelial Tissue (Gq)
TXA2 - from other platelets
5HT - from other platelets
Adrenaline - Blood and from other platelets
Thrombin - Formed in clotting 
PAF - from WBCs
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25
Q

What happens to activated platelets?

A

They form lamellipodia for interactions with other platelets and They release ADP and THX2 to cause other platelets to adhere. They also have a negative phosphatidylserine surface allowing for Coagulation factors activation.

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26
Q

What prevents Platelets aggregation?

A

NO and PGI2 coming from Uninjured Endotheliales

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27
Q

What is the role of Vitamin K in Hemostasis?

A

Gla proteins formation: Vit K in its reduced form is a cofactor for Carboxylases in the liver that react to form the Gamma-Carboxyglutamic acids residues (Gla) essential for binding to phosphatidylserine surface of Platelets and Coagulation.

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28
Q

Extrinsic Pathway of Coagulation:

A

Factor VII forms a complex with Ca and Tissue factor (F3) which is then able to cleave and Activate Factor X.

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29
Q

Intrinsic Pathway of Coagulation:

A

Factor XII is conformationally changed and activated by Activated Platelets which Cleaves Factor XI which with Ca Cleaves Factor IX which forms a complex with factor VIII and Ca to Cleave Factor X.

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30
Q

Common Pathway of Coagulation:

A

Factor X activated by Intrinsic or Extrinsic Pathway Cleavage. With Factor V and Ca forms Prothrombinase complex which is able to Cleave thousands of Prothrombins and form Active Thrombins (Amplification)

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31
Q

Which factors are cleaved by Thrombin?

A

Fibrinogen (Factor I), Factors V, VIII, XI, XIII

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32
Q

What is the job of Factor XIII?

A

Transglutaminase that crosslinks together fibrin mesh to further strengthen the structure (Ca cofactor)

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33
Q

What happens to Factor VIII if they are not active?

A

1) Get degraded

2) Bound to vWF in blood

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34
Q

What is the way Thrombin inhibits Coagulation?

A

Thrombomodulin causes changes in specificity for Thrombin that inactivate Factors V and VIII.
This happening in a complex with APC and Protein S as well.

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35
Q

What is the way Antithrombin inhibits Coagulation?

A

Potentiated intrinsically by Heparan Sulfate and Extrinsically by Heparin it directly inactivates thrombin.

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36
Q

What is the way TFPI inhibits Coagulation?

A

Activated by Xa it inhibits FVII-TF Complex

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37
Q

What are the Vit K dependent Coagulation factors?

What inhibits their formation?

A

Factors II, VII, IX, X and Protein C, because all of them have a Gla domain. Warferin and Coumadin blocks VitK reductase and lead to Gla Domain to not form.

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38
Q

What is the in vitro way to stop coagulation?

A

EDTA and other Ca Chaleators. These prevent the High Ca level needed for the Cascade to occur.

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39
Q

What are the roles of Platelets after Primary Hemostasis?

A

Clot retraction and Plasminogen-Activator Inhibiting Factor. As well as secretion of VEGF and PDGF which help Growth of Endothelial and SMCs around clot.

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40
Q

What is the job of tPA? What does it bind while it does it? Other factor is able to replace it?

A

tPA activates Plasminogen, Fibrin dependent.
Urokinase Plasmin Activating factor (uPA).
Both come from Endothelial Cells

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41
Q

What are the inhibitors of the Fibrinolytic pathway?

A

PAI-1 - Inactivates uPA and tPA
Alpha-2-Plasmin Inhibitor - Inactivates Plasmin
TAFI - a Carboxypeptidase inhibiting Plasmin action by changing Lysine residues on Fibrin.

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42
Q

What are the Patterns on Molecules signaling for Macrophages to eat them (Opsonization)?

A

PAMPs - Pathogen Associated Molecular Pattern:

Mannan, LPS, Peptidoglycan also Viral DNA or RNA

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43
Q

What helps Macrophages to recognize PAMPs?

A

PRR -pattern recognition receptors

Can cause Phagocytosis in Macrophages and Neutrophills or Signaling molecules release if Pathogen number is High.

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44
Q

What are the Most iMportant Signaling PRR? Subtypes?

A

Toll-Like Receptors:
Extracellular - types 1,2,4,5,6
Intracellular- 3,7,8,9

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45
Q

Once TLRs are activates what gets secreted? Targets?

A

They cause activation of NF-kB that allow transcription of TNF-Alpha, IL-1, IL6 which causes inflammation

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46
Q

What are the 5 Signs for Inflammation?

A

1) Fever
2) Swelling
3) Pain
4) Redness
5) Joint Immobility

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47
Q

What are the Leukocyte Migration steps? Protein factors?

A

Rollin - Selectins
Adhesion - ICAMs
Diapedesis -Integrins (Between the Endothelial cells)
Migration - Chemokine (GPCR) dependent in the CT

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48
Q

What is the Complement System?

A

A system of Circulating proteins that are integrating the Innate Immune response like Opsonization, Chemotaxis and Lysis of Bacteria. Activated by the Pathogen.

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49
Q

What are the Pathway initiations of the Complement system?

A

Classical: Pathogen-Antibody Fc portion is bound by C1 protein
Lectin: Mannose is Bound by Lectin which binds C4
Alternative:C3b binds directly to the Pathogen

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50
Q

What are the Complement system proteins? by order

A

C1 - C4 - C3b - C5b - C6…9

51
Q

What is the purpose of C3a and C5a?

A

They get activated by Mast cells and act as a chemotactic agents for Inflammation and Attracts Phagocytes

52
Q

What could form from C5b to C9?

A

MAC - Membrane attack complex:

Causes Bacteria Lysis

53
Q

What is the Purpose of C3b? How is this process happening without it?

A

It is an Opsonin - Attracts Phagocytosis by Macrophages.

Otherwise could occur by Macrophage Binding the Antibody for detection or PRR

54
Q

What is CRP?

A

C- Reactive Protein

Allows for Opsonization of Microbes and Complement system activation

55
Q

Eosinophils - Activity?

A

Major Basic Proteins produce ROS for Oxidative attack.

Efficient against Multicellular Parasites.

56
Q

Basophils - Activity?

A
  • IL6, TNF-Alpha, Histamine and Heparin Production
  • Inflammatory Response and Allergies
  • Efficient against Multicellular Parasites.
57
Q

Neutrophil - Activity?

A
  • Phagocytosis in Bacterial Infections

- Most efficient in Phagocytosis and Oxidative Burst

58
Q

Dendritic Cells? - Activity?

A
  • Capable of Phagocytosis

- “Professional” Antigen Presenting Cells for Helper T cells (Link Between Adaptive and Innate)

59
Q

Natural Killer cells - Activity?

A

They descend from similar lineage as T cells.

Kill MHC-I Negative cells. Secrete Granzymes, Perforins and Inflammatory Cytokines.

60
Q

What do we measure in PT?

A

Extrinsic Pathway

61
Q

What do we measure in PPT?

A

Intrinsic pathway

62
Q

What does the Amount of Fibrinopeptide A tells us?

A

Amount of Fibrin Formed

63
Q

What does the Amount of D-Dimers Tells us?

A

Efficiency of Thrombin, FXIII and Plasmin

64
Q

What is the function of B-Cells as part of the adaptive Immune system?

A

Immunological Memory

Stronger and more specific response

65
Q

What are the Primary Lymphoid organs?

A

Bone marrow and Thymus

This is where the B and T cells mature (RESPECTIVELY)

66
Q

What are the Secondary lymphoid organs?

A

Spleen, Lymph Nodes and MALT

These are sites of Initiation of Adaptive Immune response

67
Q

Where are B-cells found in the Lymph Nodes?

A

Primary lymphoid follicles
Lymphocyte Patrol : This is where they receive the Antigens and activate, and after the response is done washed back to blood

68
Q

What are the special features of the Immune response ?

A

1) Specificity - Epitope recognition
2) Diversity - VDJ recombination allows for different Antibodies
3) Memory - Each exposure generate more specific Memory cells
4) Clonal Expansion - allows for amplification of Plasma or Memory cells

69
Q

Antibodies different positions:

A

Antibodies are Immunoglobulins that could be membrane bound as antigen receptors of B cells or Secreted by Plasma cells to Mucus, Interstitial cells and plasma

70
Q

What are the different parts of the antibody:

What 4 type of domains are present? what is their purpose?

A
  • 2 Identical Light chains and 2 identical Heavy chains
  • These are held together by S-S Bridges
  • Variable domains for recognition: V-Heavy and V-Light
  • Constant domains for mediation: C-Heavy and C-Light
71
Q

What is left of the Antibody once cleaved by papain? what are they originally composed of?

A
  • 2 x Fab (Antigen binding): C1 and V Heavy

- 1 x Fc (Crystallizable) : C2 and C3 Heavy

72
Q

What gives us the 5 x 10^13 total receptor diversity?

A

VDJ Recombination: 50V, 25D and 6J genes

Junctional diversity: Addition/Removal of Nucleotides

73
Q

Properties of IgG:

A
  • Monomer
  • Mediate Opsonization
  • Mediate Complement sys
  • can neutralize bacterial toxins
  • CROSSES THE PLACENTAL MEMBRANE
74
Q

Properties of IgA:

A
  • Dimer

- Mucosal Immunity

75
Q

Properties of IgM:

A
  • Pentamer
  • Used as BCR (Immature and Part of Mature)
  • Mediate Complement sys
76
Q

Properties of IgE:

A
  • Monomer
  • Part of Allergic Reaction
  • defence against Parasites
77
Q

Properties of IgD:

A
  • Monomer

- Part of BCR (mature)

78
Q

What are the positive and negative selections in B cells development?

A
  • Positive: Chains Function test, if not - Apoptosis

- Negative: if Recognize self antigen - Apoptosis

79
Q

What does the BCR have other than IgD and IgM?

What is its importance?

A

IgAlpha and IgBeta that form Immunoreceptor tyrosine based activation motif) ITAM. Phosphorylated upon antigen recognition - NF-kB - Proliferation and differentiation

80
Q

What can activate B-Cells?

A

Free Antigens or Antigen presenting cells

81
Q

T-Cells dependent activation of B-Cells:

A

T dependent Antigens (More harmful in AIDS) taken and presented by T cells MHC-II molecule. BCR + Antigen Epitope + MHC-II make a sandwich and T cells now secrete IL4 that allow B-cell differentiation and growth.

82
Q

Isotype Switching:

A

A process that may occur for B-Cells as they activate.

They start producing and Secreting IgGs instead of IgM for a greater overall effect.

83
Q

T-Cells Independent activation of B-Cells:

A 
TI antigens (T Independent) are recognized by BCR.
Rapid activation but less Isotype switching in comparison with T-dependent (more IgM) so less effective.
84
Q

Plasma cells Jobs: what is the result?

A

Secreting Antibodies, Clonal expansion and becoming Memory cells. This is why after the second exposure to the Antigen activated Memory cells are able to produce a much broader stronger Response.(Acquired Immunity)

85
Q

What are the types of T-cells? What are their Markers?

What are the MHCs that they recognize? What are their jobs?

A

T Helper Cell - CD4+ - MHC-II - Activation of B cells

Cytotoxic T Cell - CD8+ - MHC-I -Destroy Tumor/Virus cells

86
Q

What is the Positive selections in T cells development?

A

At first Immature T-cells are both CD8 and CD4 Positive.
The T-Cell gets to differentiate if there is a binding of Either one of the MHC-I or MHC-II cells of the Thymoepithelial cells (Accordingly). Loose Bind= Apoptosis (FAS ligand).

87
Q

What is the Negative selections in T cells development?

A

After Positive selection, in the Medulla, Dendritic cells expose the T cell to own Antigen. Binds too tight = Apoptosis / Binds loose = differentiation. Prevention of Autoreactive cells.

88
Q

T -Cell receptors:

A
  • 1 Antigen binding site (Antibodies have 2)
  • Always bound
  • Beta+Alpha+Zeta chains (Variable +Constant)
  • ITAM for NF-kB activation
89
Q

What is MHC?

A

Major Histocompatibility Complex. Mediates recognition in the Immune response.
MHC-I: All nucleated cells (non on RBC)
MHC-II: Only on Antigen presenting cells: Dendritic, Macrophage and B cells

90
Q

Explain the function of Cytotoxic T-Cells after activation:
Infected virus/tumor cell forms a complex with -
MHC-I+Epitope+TCR

A

Release of Granzymes and Perforins.
Perforins - make a pore in the infected cell
Granzymes - come in the cell and activate Caspases and Apoptotic cascades.

91
Q

What are T-helper cells -1 doing?

A 
Activating Macrophages (Another adaptive to innate link).
Can recognize Antigen presenting cells MHC-II
92
Q

What are T-helper cells -2 doing?

A

Activating B-cells. CD4+ Most Important job.

Can recognize Antigen presenting cells MHC-II

93
Q

Peripheral Tolerance of T cells:

A

Regulatory T cells can inhibit reaction against own T cells by specific cytokines. (CD25+)

94
Q

Give examples for Autoimmune diseases: name the targets or consequences

A

Myasthenia Gravis - Nicotinic Ach receptors
Multiple sclerosis: Myelin Sheath Toughness
Graves: Goiter

95
Q

Peripheral Tolerance of B :

A

Anergic B-Cells that are unresponsive or even silence other responses of other Bs to the Epitope.

96
Q

What are common for the Innate and Adaptive Immune?

A

Fc of Antibodies
Complement system
NK cells

97
Q

What does Interferon do?

A

Inhibits replication in surrounding cells of Infected Viral cell.

98
Q

What is Cytokine Switch?

A

T helper cells type 1 Inhibit T helper Type 2 (Cross inhibition)

99
Q

What is the basis of the blood groups in Human?

A

The Presence or Absence of Carbohydrates on RBCs.

There above 30 antigens on RBCs but most are not reactive. Specific transferases carry them to surface.

100
Q

What is the H antigen?

A

Fucose (Fuc)

101
Q

What is the A antigen?

A

N-acetylgalactosamine (NaC) (On top of Fucose)

102
Q

What is the B antigen?

A

Galactose (Gal) (On top of Fucose)

103
Q

What is the O Antigen?

A

No additional Enzyme transferase activity. Meaning there is only the Fucose antigen (H)

104
Q

What is the dominance of the transferase enzymes that leads to the antigens of blood groups?

A

A, B allele - Codominant

O allele - Recessive

105
Q

What will cause an agglutination reaction with Blood Type A?

A

Since it has Anti-B (Antibodies) it will have agglutination with blood transfusion from B and AB blood types.

106
Q

What will cause an agglutination reaction with Blood Type B?

A

Since it has Anti-A (Antibodies) it will have agglutination with blood transfusion from A and AB blood types.

107
Q

What will cause an agglutination reaction with Blood Type AB?

A

Since it has no antibodies for other blood groups it will have NO agglutination with blood transfusion from ANY type.

108
Q

What will cause an agglutination reaction with Blood Type O?

A

Since it has Anti-A and Anti-B (Antibodies) it will have agglutination with blood transfusion from A, B and AB blood types. Allows Transfusion only from O type.

109
Q

What are the ABO Antibodies in the Immune system made of? Why is this important in Pregnancy?

A

IgM. Because these are Pentamers they do not cross the Placental barrier.

110
Q

What happens when there is incompatible blood type transfusion? What Immunological events?

A

Antibodies bind the foreign RBCs Antigen. Activation of Complement system and Phagocytosis - Ultimately Intravascular Hemolysis.

111
Q

What is the treatment when incompatible blood type transfusion has occurred?

A

Antihistamine, Corticosteroids and Epinephrine.

Other question on why

112
Q

What is the basis of the Rhesus system?

A 
1 D (Dominant) Antigen (Out of 6 types that are weak).
Antigen D is a protein channel not understood.
Rh positive means there is D+ on the RBC surface.
113
Q

What is the Genotype, Antigen and Antibody product of Rh positive?

A

Genotype: DD and Dd
Antigen Product: D
Antibody: No Anti-D

114
Q

What is the Genotype, Antigen and Antibody product of Rh negative?

A

Genotype: DD and dd
Antigen Product: d
Antibody Anti-D: EXPRESSED ONLY AFTER EXPOSURE

115
Q

What are the D Antibodies in the Immune system made of? Why is this important in Pregnancy?

A

Anti-D is a IgG. Means that it can cross the placental barrier! after first pregnancy to a Rh+ child the mother can be exposed and IMMUNED (Anti-D production). The second child (If Rh+) RBCs could be attacked by Anti-D .

116
Q

What could be done to prevent Rh incompatibility in pregnancy? 2 Ways :

A

1) C- Section: Prevents delivery from Mixing Maternal and Fetal blood.
2) Injecting Mother with an Inactive Anti-D before delivery neutralizing the fetal Antigens.(Pre-Emptive)

117
Q

What is the Two sided test? What is being checked in each part?

A

Checking the Compatibility before Transfusion:
Forward: RBC of Patient + Antibodies (Anti-B, Anti-A)
Reverse: Serum Patient + A/B/O blood types cells

118
Q

After seeing the results and understanding that both patient and donor are compatible, What is the next step?

A

Taking a sample from recipient and donor and check with donor in a sample tube. In reality there are patches like structures for fast checking in case of emergency.

119
Q

Anaphylactic Reaction Defenition:

A

Immediate Hypersensitivity by chemical stored in mast cells - Histamine, Leukotrienes or Heparins.
Could occur upon Incompatible blood transfusion.

120
Q

Anaphylactic Reaction 1st Exposure:

A

1st Exposure:

1) IgE by plasma cells are produced
2) IgE binds Mast cell membrane (or Basophil converted Mast cell)

121
Q

Anaphylactic Reaction 2nd Exposure:

A

2nd Exposure:

1) Same Antigen binds IgE of Mast cells.
2) Mast cells release content: Histamine, Leukotrienes or Heparins (Also ECF-A)

122
Q

Anaphylactic Reaction: what is the effect of the Histamine, Leukotrienes or Heparins (Also ECF-A) released from Mast cells?

A

Bronchoconstriction - Inability to breath
Vasodilation - Low blood pressure
Could be deadly.

123
Q

Anaphylactic Reaction: Treatment?

A

Antihistamine, Corticosteroids and in severe cases Epinephrine

124
Q

What is the distribution of the blood types?

A 
A -40%
B -20%
AB - 10%
O - 30%
Also:
Rh+ : 85%
Rh- : 15%

GBA Physiology (12 decks)

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