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PSL301 > TT1 review > Flashcards

TT1 review Flashcards

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1
Q

Types of immune responses

A
  1. Innate immunity: Rapid and non-specific immune response
    1. Adaptive immunity Slower, Specific
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2
Q

Primary vs Secondary lymphoid tissue

A

Primary - Where white blood cells are first produced

Secondary - Where the immune response actually happens (encounters the antigen)

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3
Q

Function of the lympathic system

A
  1. Return excess tissue fluid to the blood
  2. Transport pathogens/dentritic cells to lymph nodes
  3. Transport fat from digestive system to the blood
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4
Q

How much water per day is returned from lymphatic to the blood?

A

~3L

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5
Q

Structure of the spleen

A

Red pulp: Location of macrophages and blood vessels White pulp: lymphocytes

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6
Q

What does lymph nodes vs spleen monitor

A

Lymph nodes monitor pathogens in the lymph or the interstitial fluid Spleen mainly monitors the blood for pathogens

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7
Q

Types of lymphocytes

A

B cell T cell NK cells

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8
Q

Monocytes function

A
  1. Migrate into tissues and become macrophages, responsible for phagocytes that present antigens
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9
Q

What are neutrophils

A

Type of phagocytes that circulate in the blood and migrate into tissues

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10
Q

Eosinophils function

A

Found in the digestive tract, lungs, urinary and genital epithelia, defend against parasites Also participates in allergic reactions

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11
Q

Basophils and Mast cells

A

Release chemicals that contribute to inflammation and innate immune response

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12
Q

Dendritic cell function

A

Found in skin and other organs, present antigens to other cells

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13
Q

Which cells are phagocytes (immune system)

A

Monocytes (Macrophages) Neutrophils

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14
Q

Physical barriers of innate immune system

A
  1. Epithelium - skin and mucous membranes 2. Glandular secretions - Mucous, antibodies, enzymes 3. Stomach acidity - Low pH to destroy pathogens 4. Mechanical removal - coughing, sneezing, GI motility
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15
Q

What chemicals do phagocytes recognize?

A

PAMPs (Pathogen associated molecular patterns) DAMPs (Damage associated molecular patterns)

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16
Q

How do infected issue attract phagocytes into injury area? and eventually phagocytosis?

A
  1. By expressing a special adhesion protein on epithelial cell, grabbing the phagocyte into the area
    1. Diapedesis (extravasation) allows white blood cell to crawl past the epithilial cell
    1. Chemotaxis - Chemotaxins (DAMPs and PAMPs) attract phagocyte to pathogen
    1. Phagocytosis
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17
Q

What is an opsonin

A

substance that coats the pathogen, making it likely to absorb the pathogen

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18
Q

How does phagocytosis occur

A
  1. Pathogen binds to PRR (patten recognition receptor) 2. Or pathogen coated with antigen (opsonization) binds to Fc receptors
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19
Q

How do some viruses evade the immune system?

A

Blocks the host cell synthesis of MHC Class I protein, responsible for presenting viral antigens on surface This makes the cell invisible to T cells but
NK cells will look and kill any cell that doesn’t have MHC Class I on the surface

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20
Q

How does NK cells recognize normal vs viral infected cell

A

Normal cell: MHC Class I is present on the surface, NK cell’s inhibitory receptor detects and inhibits release of granules Infected cell Lack of MHC Class I means inhibitory receptor is not bound. NK releases granules of cytotoxic compounds which kill the cell

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21
Q

Interferon types and function

A

A and B (alpha and beta) - prevent viral replication in cells y (gamma) activate macrophages and other immune cells

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22
Q

What are complement proteins and types for each function

A

They are antimicrobial proteins responsible for Opsonization - C3b Inflammation - C3a Membrane attack complex C3b causes activation of C5 complexes which lyse the bacteria

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23
Q

How is C3 complement activated

A
  1. Classical pathway (Antigen - antibody complex) 2. Lectin pathway (Microorganisms cell wall polysaccharide) 3. Alternative pathway (No inhibitors on microbe surface)
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24
Q

Inflammatory response steps

A
  1. Tissue damage causes change in interstitial fluid
    1. Mast cells release histamine and heparin → Increased blood flow to form clot
    1. Histamine and heparin attracts phagocytes especially neutrophils
    1. Tissue repair processes such as specific defence activation, removal of debris by phagocytes
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25
How is temperature raised to produce fever?
Pyrogens (any chemical that alerts the immune system) change body temperature set point in hypothalamus
26
Role of fever in immune system
1. Speeds up the metabolic activity of the host 2. 2. Inhibits some pathogens (due to inability to cope with higher temperatures)
27
How do B cells and T cells acehieve specificity?
They have receptors that recognize specific shapes
28
What things do T-cell receptors recognize
Viral/Bacterial antigen, and also the MHC protein itself
29
Where do T cells undergo selection?
Thymus
30
What happens to T and B cells that recognize self (your own proteins)
They get killed off
31
How are B cells activated?
1. Antigen binds to BCR 2. Internalisation of BCR-antigen (digestion) 3. Presentation of antigen through MHC II protein, to activate T-cells
32
How does B cell produce antibodies?
1. Helper T-cell reads the MHC II and Antigen on B cell surface 2. 2. T-cell produces specific cytokines like interleukins 3. Interleukins can help B-cell differentiate
33
What happenes to the activated B cell
It divides, some daughter cells will just produce antibodies some daughter cell will turn into memory B cell
34
What is platelets made from?
Megacaryocyte cell (Type of blood cell)
35
What is special about megakaryocyte
Its a cell that has a lot of duplicates of DNA without cell division
36
Helper T-cell function
1. It binds to MHC Class II 2. Releases cytokines that activates the immune system
37
Cytotoxic T-cell function (which MHC, and function)
1. Binds to MHC Class I 2. Induces cytotoxicity to pathogens/infected/tumour cells
38
What does MHC Class II do, and where is it found
1. Present exogenous antigens 2. Found on B cells, Macrophages, Dendritic cells 3. Activates Helper T cells
39
What does MHC Class I do and where is it found
1. Presents endogenous antigen (Bacteria/Virus inside cell) 2. Found on all nucleated cells 3. Activates cytotoxic T cells
40
How do allergies occur and reexposure
1. Antigen presenting cell engulfs allergen molecule 2. Antibodies are made from B-cells, and memory cells remember the allergen 3. Reexposure causes faster immune response since antibodies are already there + memory cells 4. Rapid inflammatory response caused, servere cases may go through anaphylaxis
41
How can anti-D antigens developed (Rh-)
1. Transfusion with Rh+ people 2. Pregnancy with Rh+ baby
42
First pregnancy vs second pregnancy (Rh- mom w/Rh+ baby)
1. First pregnancy causes anti-D antibody development in maternal blood 2. Second pregnancy may cause severe immune response against baby blood 3. Causes Jaundice, Anemia, Enlarged liver and spleen (Not that important to remember)
43
What are the 3 stages of hemostasis?
1. Vascular phase 2. Platelet phase 3. Coagulation phase
44
What happens in vascular phase?
Vasoconstriction
45
What prolongs vasocontrisction?
1. Serotonin 2. Endothelin-1 3.Thromboxane A2
46
Platelet phase detailed steps
1. Exposed colagen binds and actiavtes platelets 2. Factors released from platelets 3. These factors attract more platelets 4. Platelets aggregate, and forms a plug
47
What factors are involved in platelete phase?
1. VonWillbrand to link platelets and collagens, and attracting nearby platelets 2. ADP, platelet activating factor, serotonin, thromboxane A2 *Thromboxane A2 and serotonin prolongs vacular phase
48
Where is von Willebrand factor produced and what does it do
1. Endothelial cells and platelets 2. It attracts platelets and sticks to collagen 3. Regulate levels of factor 8
49
What prevents platelet clots from forming in non-injured blood vessels?
- Prostacyclins and nitric oxide Both prevent platelet adhesion and are vasodilaters
50
What happens in coagulation cascade (Common pathway)
1. Factor X activated by Ca2+ and PL → Active factor X 2. Active factor X cuts prothrombin into thrombin via Ca2+, factor V, and PL (phospholipids) 3. Thrombin cuts Fibrinogen → Fibrin 4. Thrombin also activates factor XIII (13) via Ca2+ 5. Collection of fibrin forms the fibrin polymer/mesh
51
Extrinsic pathway for common pathway activation (Coagulation step)
1. Tissue damage releases factor III, activating factor 7 2. Factor 7 can activate factor 9 and 8, which also activates X 3. Factor III and factor 7 together activates factor X
52
Warfarin mecahnism of action
1. Blocks the vitamin K needed for synthesis of thrombin, factor 7, 9 and 10
53
Intrinsic pathway to activate common pathway
1. Collagen or other activators activate factor 12 2. Active factor 12 activates factor 11 with Ca2+ 3. Active 11 activates factor 9 4. Along with factor 8 and 9, factor 10 is activated
54
What positive feedback is there in the common pathway?
1. Thrombin - activates more factor 11, leading to more factor 9 2. Active Factor 10, activating more factor 7
55
What was the problem with the coagulation cascade model?
1. Some people despite having enough coagulation factors and enzymatic reactions, they were still bleeding too much 2. This lead to the cell-based theory where platelets were the center rather than the factors
56
What are the 3 phases in cell-based theory of coagulation?
1. Initiation phase 2. Amplification phase 3. Propagation phase
57
What happens in initiation phase of cell based theory?
*Overall idea: Small amounts of thrombin made → Thrombin spark Detailed: 1. Exposure of tissue factor to active factor 7 activates factor 10 and factor 9 2. Factor 10 activates thrombin (prothrombin → thrombin)
58
What happens in the amplification phase of cell based theory
1. Thrombin activates factors 5, 11, 8 on surface of platelets 2. Along with vonwillebrand, it will activate platelets
59
What happens in propagation phase of cell based theory?
OVERALL IDEA: Huge bursts of thrombin is made 1. Tenase is formed from active factors on surface of platelets 2. Tenase activates factor 10, → activates more thrombin
60
How is the platelet clot removed?
1. Plasminogen is converted to plasmin by tPA and thrombin 2. Plasmin breaks down fibrin into fragments *Note that tPA build up is slower than platelet clog formation thus longer the clog is there the more likely its broken down
61
Anticoagulant types
Plasminogen/Plasmin - released from liver and activated by thrombin and tPA → Breaksdown fibrin tPA - Released from many tissues, normally present (no activation), → Activates plasminogen Antithrombin III - Made in liver, activated by Heparin, blocks Factors 9,10,11,13 and thrombin Prostacyclin - released from endothelial cells, non-activated → inhibits platelet aggregation

PSL301 (5 decks)

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