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BIOM3200 > immunity > Flashcards

immunity Flashcards

1
Q

what are the levels of the wound healing

A
  1. homostasis and coagulation
  2. inflammation
  3. proliferative and migration
  4. remodeling
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2
Q

What is the role of the circulatory system?

A

TRANSPORTATION

REGULATION

PROTECTION

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3
Q

what kinds of transportations are exist in the body

A
  • Respiratory (RBCs)
  • Nutritive (digestive)
  • Excretory (wastes)
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4
Q

how circulatory system regulate the body

A

Hormonal

• Temperature

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5
Q

how circulatory system protect the body

A

Hormonal

• Temperature

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6
Q

how much blood is in the human body

A

5 LITRES = 169.07 fluid ounces or 10.57 pints

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7
Q

what is the blood made of

A

Blood plasma: Fluid portion (55%)
Formed elements: Cellular portion (45%)
• White blood cells, platelets (<1%)
• Erythrocytes (RBCs; >99%)

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8
Q

what is the blood plusma made of

A
  1. Water (92%)
  2. Proteins (7%)
  3. Solutes (1%)
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9
Q

what is the role of the plasma in keeping the presure inside the capillaries

A

Plasma plays a role in maintaining plasma
colloid osmotic pressure (pressure “pulls”
fluid from interstitial space into capillaries)

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10
Q

how much of the blood plasma is water

A

92% of the plasma is water which is the fluid portion

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11
Q

how much of the plasma is protein

A

7%

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12
Q

which proteins are presentint in the plasma

A

Albumins
- Globulins
- Fibrinogen
Complement proteins

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13
Q

what is the role of the albumin in the plasma

A

Smallest and most numerous proteins; transports hormones

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14
Q

what is the role of the plasma protein in the body

A

Exert plasma colloid osmotic pressure; regulates blood volume

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15
Q

what is the role of the Globulins

A

Transport iron, hormones, lipids

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16
Q

what is the role of the Fibrinogen

A

Essential for blood clotting

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17
Q

what is the role of the Complement proteins

A

Activated by presence of pathogens

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18
Q

what are the other solutes in the blood plasma

A

Electrolytes

  • Nutrients
  • Gases
  • Regulatory substances
  • Waste products
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19
Q

which Electrolytes are present in the plasma

A

Na+, K+, Ca2+, etc.

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20
Q

which nutrients are present in the plasma

A

Amino acids, glucose, fatty acids, vitamins, minerals

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21
Q

which gasses are present in the plasma

A

O2, CO2, N2

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22
Q

what are the Regulatory substances in the plasma

A

Hormones, enzymes

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23
Q

what are the waste products in the plasma

A

Urea, creatinine, ammonia, etc

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24
Q

what are the main component of the circulatory system (Formed Elements)

A

Erythrocytes (RBCs): Transport oxygen from the lungs to the body
Leukocytes (WBCs): Immune cells; protect the body from foreign
invaders
Platelets: Cellular fragments that promote blood clotting

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25
Q

what is the blood cell formation process

A

Hematopoiesis

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26
Q

where Hematopoiesis happens

A

Hematopoiesis occurs in the bone marrow

in adults

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27
Q

what are the process of the Hematopoiesis

A 
Hematopoietic stem cells (HSCs) become… 
…Progenitor cells, which become…
• Precursor cells that give rise to…
• WBCs
• RBCs
• Megakaryocytes 
(precursor cell to platelets)
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28
Q

what does Precursor cells need for the differentiation

A

Require CYTOKINES

for differentiation!

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29
Q

explain the RBC Formation – Erythropoiesis

A
  1. HSCs differentiate into myeloid progenitor
    cells (see previous slide), which develop into
    proerythroblasts
  2. Erythroblasts and normoblasts are formed
    and begin synthesizing hemoglobin
  3. Further in its development, the cell ejects its
    nucleus and becomes a reticulocyte
  4. Further maturation occurs in the blood
    (erythrocyte)
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30
Q

how long is the Lifespan of an RBC

A

120 days

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31
Q

why the hemoglobin is red

A

Each RBC contains 280m hemoglobin molecules that give blood its red colour

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32
Q

what is the hemogllobin made of

A

Hemoglobin: 4 globin proteins, each with a heme group that contains an iron core

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33
Q

what is the role of the heme iron

A

Heme iron (Fe) combines with oxygen to transport it to tissues

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34
Q

what is the proces of the stimulation of erythropoiesis

A

A decrease in blood oxygen stimulates erythropoiesis

  1. The kidneys sense this drop in blood oxygen and release erythropoietin (EPO)
  2. EPO acts within the bone marrow to stimulate maturation of reticulocytes
  3. Newly formed erythrocytes can now transport oxygen (attached to hemoglobin) to tissues as needed (including kidneys)
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35
Q

how much iorn do men need

A

Adult men of all ages: ~9 mg/day

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36
Q

how much iron wome need

A

Pre-menopausal adult women: ~18 mg/day

• Post-menopausal women: ~9 mg/day

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37
Q

what is the anemia

A

Anemia: Low RBC and/or hemoglobin concentration

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38
Q

what are the WBC Myeloid lineage:

A
  • Eosinophils, basophils, and neutrophils

* Monocytes

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39
Q

which factor differentiate the WBC Myeloid lineage:

A

• colony-stimulating factor (CSF) to

differentiate

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40
Q

what Myeloid progenitors give rise to

A

Myeloid progenitors also give rise to
megakaryocytes, which become
platelets thanks to thrombopoietin (TPO)

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41
Q

what are the WBC Lymphoid lineage

A

:
• T lymphocytes
• B lymphocytes
• Natural killer (NK) cells

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42
Q

what is the most used type of the stem cell

A

HSCs are the most clinically used

type of stem cell in medicine!

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43
Q

which cancer is treated by the HSC

A

Used to treat certain blood cancers

like leukemia

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44
Q

what is the leukemia

A

Leukemia: Cancer of the progenitor
cells that become leukocytes
Cellular constituents of the
IMMUNE SYSTEM

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45
Q

what is the immune system

A

The immune system includes all of the cells,
tissues, and processes involved that defend
against potential pathogens

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46
Q

what are the two defense mechanism

A

innate ( non-specific ) defense machanism

adaptive ( specific ) defense mechanism

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47
Q

what is the first line of the defense

A

non specific
skin
mucouse membrane
secration of skin and mucouse membrane

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48
Q

what is the second line of the defense

A 
non specific
phagocytic cells 
natural killers 
anti microbial proteins 
the inflammatory response
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49
Q

what is the third line of the defense

A

lymphocytes
anti bodies
macrophages and other antigen presenting cells

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50
Q

what is the relationship between the antigen and the antibody

A

Antigens found on the surface
of all cells can be detected by
certain molecules (antibodies)
secreted by immune cells

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51
Q 
Antigen recognition (or lack 
thereof) classifies that antigen 
as either being:
A

:
• SELF (non-foreign)
• NON-SELF (foreign

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52
Q

what are the blood types

A 
Type O+ (39% of Canadians)
• Type O- (7% of Canadians) – UNIVERSAL DONOR
• Type A+ (36% of Canadians) 
• Type A- (6% of Canadians) 
• Type B+ (7.6% of Canadians)
• Type B- (1.4% of Canadians)
• Type AB+ (2.5% of Canadians) – UNIVERSAL 
ACCEPTOR
• Type AB- (0.5% of Canadians)
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53
Q

what is the blood types based on

A

Blood types are based on antigens present on erythrocytes among different individuals

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54
Q

what is the type A blood

A

A antigen

anti-B antibody

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55
Q

what is the type B

A

B abtigen

anti-A antibody

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56
Q

what is the type AB

A

both A and B antigen

neither the antibody

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57
Q

what is the type O blood

A

neither antigen A or B

anti-A and anti-B antibody

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58
Q

what is the AGGLUTINATION when type A is transfered to type B

A

• Individuals with Type B blood carry anti-A antibodies
• Anti-A antibodies recognize A antigens on the transfused
blood and mark them as FOREIGN
• Anti-A antibody binding to antigen causes clumping of the erythrocytes (agglutination)
• Antigen-antibody complexes form and activate complement proteins in the recipient’s plasma
• Causes hemolysis of erythrocytes

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59
Q

what is the • Rh factor (Rh):

A

• Rh factor (Rh): Another antigen that is

commonly present on erythrocytes

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60
Q

what is the rh positive and rh negative

A

If Rh antigen is present (~85% of Caucasians): Rh positive

• If Rh antigen is not present: Rh negative

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61
Q

what is the difference between the antigen A and antigen B and antigen rh

A

Unlike anti-A or anti-B antibodies, anti-Rh antibodies are not normally present in Rh- individuals UNLESS they have been previously exposed to Rh antigen

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62
Q

is offspring genetically as same as the mother in terms of the rh antigen

A

Offspring are genetically different from

their mothers, so a mother may be Rh- while their fetus rh +

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63
Q

what is the role of the plecenta in the exposure of the fetus blood to the maternal blood

A

Placenta normally shields fetal blood from maternal blood (see Repro section), but exposure may occur during parturition

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64
Q

what is the eryththroblastosis fetalis

A

Next pregnancy: If the fetus is Rh+,
eryththroblastosis fetalis can result
• Hemolysis of Rh+ RBCs in the fetus

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65
Q

what is the anti body and what is its role

A

Antibodies are part of the adaptive (specific) immune system

• This system is built and trained to recognize and destroy specific antigens

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66
Q

what are some of the innate immune barriers and what are their responses

A

Skin/mucous membranes»» Physical barrier for pathogens
Digestive tract&raquo_space;»High acidity of stomach
Inflammatory response&raquo_space;»>Histamine release, fever
Phagocytosis&raquo_space;»>Cells that engulf foreign material
Interferons»»> Produced by cells infected by viruses
Complement system&raquo_space;»>Promote phagocytosis with the help
of antibodies (adaptive immunity)

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67
Q

what is the mechanism of the anti body

A

Antibodies target pathogens (bacteria, viruses, foreign RBCs), but binding alone does
not destroy them
• Antibodies serve as “flags” for immunological attack by:
1. Innate immune cells like macrophages and neutrophils
(next couple of lectures)
2. Complement proteins present in the plasma

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68
Q

what is the The Complement System

A

• Serves as a LINK between the innate and adaptive immune system!
• Liver produces complement proteins and release them into circulation (9 inactive
proteins labeled C1-C9)

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69
Q

what is the complement activation leads to

A

Complement activation leads to the

eventual destruction of the pathogen

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70
Q

what are the two ways of the Complement protein activation

A

Classical Pathway
Alternative Pathway
in both cases, activation of complement proteins involves sequential modifications to the proteins to generate proteolytic enzymes

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71
Q

what is the classical pathway

A

Involves antibody recognition followed by a cascade of complement protein modifications
Starts off with…
1. Antibody binding to antigen on membrane of bacterial cell
2. C4 binds to antibody-antigen complex; activated C1 hydrolyzes C4 into C4a and C4b (C4b becomes “fixed” in the membrane)
3. C3 is then split into C3a and C3b via a C3 convertase (C4b + C2a)
4. C3b converts C5 into C5a and C5b, which attract other immune cells to the site
5. C5-C9 are inserted into the cell mb to form a membrane attack complex (MAC

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72
Q

what is the mechanism of the Alternative Pathway

A

No antibodies required!
• Involves surface protein recognition by complement proteins
Low levels of C3 are constantly monitoring for and binding to
surface proteins
If C3 binds to LPS on a bacterial cell, it is then activated

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73
Q

what are the differences between alternative and the classic pathway

A 
The production of C3 convertase is where both pathways converge
• In both cases, cleavage of C3 results in C5 activation and subsequent MAC 
production
• Classical pathway:
• C3 convertase = C4b and C2a
• Alternative pathway:
• C3 convertase = C3b and factor B 
(another serum protein)
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74
Q

what is the final result of the complement system

A 
Formation of MAC (resulting in 
hemolysis)
2. Chemotaxis:
3. Opsonization:
4. Stimulation of histamine release:
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75
Q

what is the chemotaxis

A
  1. Chemotaxis: Free complement
    fragments attract phagocytic cells to
    site of infection
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76
Q

what is the opsonization

A
  1. Opsonization: Complement proteins

recruit phagocytic cells to eat bacteria

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77
Q

free complements induce which cells to release the histamine in the body

A
  1. Stimulation of histamine release:
    Free complement fragments induce
    mast cells and basophils to release
    histamine
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78
Q

what are the physical and cellular barrier of the lungs

A

– Respiratory secretions

– Resident macrophages

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79
Q

what are the Alveolar macrophages and what they do

A

Alveolar macrophages are phagocytic cells; they
recognize bacterial antigens and can either…
– Engulf bacteria (phagocytosis) and destroy them via
lysosomal enzymes
– Recruit other innate immune cells to the site via
chemotaxis

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80
Q

what are the cytokines

A

– IL-1β (Interleukin-1)

– TNF-α (Tumour necrosis factor)

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81
Q

what is the role of the CYTOKINES:

A

Increase vascular permeability
• Increase vasodilation
• Increase expression of endothelial adhesion proteins

82
Q

what is the CHEMOKINES and what is its role

A

CHEMOKINES: CXCL8

– Help attract other immune cells to the site of infection

83
Q

which cells released histamine and what is its role

A

Histamine released by mast cells and basophils further increase vasodilation and vascular permeability

84
Q

which cells release the prostaglandis and what is its role

A

– Prostaglandins released by damaged cells to intensify the effects of histamine

85
Q

which cells release the Leukotrienes and what is its role in the body

A

Leukotrienes released by mast cells and basophils further increase vascular
permeability

86
Q

what is the role of the Complement proteins,

A

Complement proteins, in addition to their direct role in killing bacteria, also stimulate histamine release, attract neutrophils by chemotaxis, and promote phagocytosis

87
Q

how neutrophis arrive on the scene

A

As the battle continues, neutrophils arrive on the scene thanks to
chemokines secreted by macrophages (chemotaxis)

88
Q

do monocytes arrive after or before the neutrophils

A

Monocytes (macrophage and dendritic cell

precursors) arrive later

89
Q

how Neutrophils and monocytes enter the tissue

A

Neutrophils and monocytes from the
blood enter the tissue at the site of
infection thanks to extravasation (also
called diapedesis)

90
Q

what is THE INFLAMMATORY RESPONSE:

A

Inflammation is characterized by classic or cardinal signs

91
Q

what are the responses of the inflammetory

A

Rubor (redness): Increased vasodilation
– Calor (heat): Increased vasodilation (fever covered in next
slide)
– Tumor (swelling): Increased vascular permeability
– Dolor (pain): Increased cytokine release stimulates pain receptors
– Functio laesa (loss of function): Tissue health is suboptimal; not in homeostasis

92
Q

what does ibuprofen do

A

Anti-inflammatory medications such as ibuprofen (a nonsteroidal anti-inflammatory drug [NSAID]) BLOCK the formation
of prostaglandins

93
Q

what is the prednison and what is its role

A

Prednisone, acting like cortisol, suppresses the immune
system by BLOCKING the formation of prostaglandins
AND leukotrienes

94
Q

why y BLOCKING the formation of prostaglandins

AND leukotrienes is bad

A

Reduced vascular permeability = fewer immune cells

at the site of infection = infection persists

95
Q

how fever happens

A

FEVER: Monocytes and macrophages, upon interaction
with bacteria, secrete cytokines that act as pyrogens
• Pyrogens affect the preoptic area of the hypothalamus,
raising body temperature

96
Q

what is the worst and best senario of the fever

A 
At worst, high fevers can lead to 
organ damage and spread of 
infection. At best, fevers are 
uncomfortable and temporary, and 
assist with recovery from infection.
97
Q

what are the GRANULOCYTES

A

neutrophils
eosinophils
basophils

98
Q

what are the AGRANULOCYTES

A

lymphocytes

monocytes

99
Q

what is the basophils

A

Contains granules that stain blue with hematoxylin dye
• Has a bilobed nucleus
• Low #’s in circulation; <1% of WBCs

100
Q

what is the function of the basophils

A

FUNCTIONS:
– Releases histamine (vasodilator)
– Releases heparin (slows down blood clotting)

101
Q

which cell is similar to the basophils

A

• MAST CELLS: similar to basophils, but located in

tissues instead of the blood

102
Q

what is the neutrophil

A

Neutrophils
• Contains granules that stain very slightly pink with eosin
• Has a multilobed nucleus
• Most abundant leukocyte; 54-62% of WBCs

103
Q

what is the function of the neutrophils

A

– First responders to infections
– Phagocytose bacteria; ~5-20 bacterial cells during
their short lifespan (1-2 days)

104
Q

what is the Eosinophils

A
  • Contains granules that stain bright red with eosin
  • Has a multilobed nucleus
  • ~1-3% of WBCs
105
Q

what is the function of the eosinophils

A

FUNCTIONS:
– Defend against parasites
– Also help against viral infections, allergic responses,
and certain types of bacteria
– Higher number of eosinophils correlates with
increased severity of asthma

106
Q

what is the Monocytes

A

• Agranulocyte: no granules; 2-3x larger than an RBC
• Has a kidney-shaped nucleus
• ~3-9% of WBCs; but only stay in the blood for ~8 hrs
before differentiating

107
Q

what is the Monocytes are precursors to:

A

– Monocytes are precursors to:
• Tissue resident macrophages
• Dendritic cells

108
Q

which Tissue resident macrophages:

A

All tissues; spleen, lymph nodes, bone marrow

109
Q

what are the microphages in the liver , brain and lungs

A

Kupffer cells: Liver
• Microglia: Brain
• Alveolar macrophages: Lungs

110
Q

what is the function of the macrophages

A 
Phagocytose bacteria (100 bacterial
cells per lifespan) AND act as antigen-presenting cells
111
Q

what is the dendritic cells

A

Dendritic cells: Antigen-presenting cells

112
Q

what is the second function of the macrophages

A

“tissue clean up crew

Remove debris: Old RBCs, dead neutrophils, cells undergoing apoptosis

113
Q

what is the lymphocytes

A

Agranulocyte: no granules; only slightly larger than
an RBC
• Has an “eccentric” nucleus
• ~25-33% of WBCs; ~5% circulating, the rest in
tissues until they encounter pathogens

114
Q

what are the type of the lymphocytes

A

– T lymphocytes (adaptive immune system)
– B lymphocytes (adaptive immune system)
– Natural killer cells (innate immune system)

115
Q

what are the function of the natural killers

A

Protect against viral infections
and some types of cancer
• Unlike B and T lymphocytes, natural killer cells
respond very quickly (within a few to several
hours) upon stimulation

116
Q

how natural killers distroy the target cells

A

Destroys target cells by cell:cell contact through

granzymes

117
Q

what doe the natural killer secregate

A

• Can release interferons (IFNs) and other cytokines to warn uninfected cells AND/OR enhance immune response mediated by other cell types

118
Q

what are the B and T lymphocytes

A

B and T Lymphocytes

• Part of the adaptive immune system (both humoral and immune-mediated immunity)

119
Q

what is the adaptive defense

A

• A subset of WBCs are conditioned to respond and attack

pathogens

120
Q

how does adaptive defense work

A

• While some of their comrades remain at the site of infection, other macrophages/dendritic cells transport antigens to a lymph node
. Neutrophils release free antigen into the bloodstream,
where these molecules can eventually reach a lymph
node

121
Q

what are the lymph nodes

A

• Lymph nodes are part of the lymphatic system (next lecture) and are home to B lymphocytes and T lymphocytes

122
Q

what are the NAÏVE LYMPHOCYTES

A

Mature lymphocytes that have not yet encountered antigen

123
Q

why lymphocytes need training

A

Lymphocytes must be trained and cloned to mount an immune response to a specific antigen

124
Q

where doe B and T lymphocytes mature in the body

A

Immature B lymphocytes stay and mature in the bone marrow

• Immature T lymphocytes leave and mature in the thymus (gone in adults)

125
Q

what is the Immunocompetence

A

Immunocompetence: Ability to carry out adaptive immune

responses

126
Q

what happens to the lymphocyte beofore moving to the lymphoid organs

A

Gain antigen receptors on their
membranes before moving to
lymphoid organs

127
Q

two major type of the T- Lymphocytes

A

• Two major types of mature, immunocompetent

T cells thus exit the thymus: – Helper T cells (CD4+ T cells) – Cytotoxic T cells (CD8+ T cells)

128
Q

what is the difference between the mature T cells and the non-mature T cells

A

• Mature T cells now have antigen receptors that can respond to antigen presented by antigen presenting cells

129
Q

do we have a lot of the lymphocytes when the pathogen enters the body

A

• Initially, when a pathogen first enters the body,
there are only a few lymphocytes that have the
correct antigen receptor to respond to that
antigen

130
Q

what is the CD4+ T Lymphocytes ( the antigen-presenting cell)

A

(cell mediated immunity
Antigen presenting cells (macrophages, dendritic cells, etc.) are “professional” cells that can present antigen on a complex called MHC II (major histocompatibility complex)

131
Q

how does the CD4+ T lymphocytes is activated

A

Antigen presented by MHC II molecules on antigen
presented cells will activate CD4+ T lymphocytes
(helper T cells)

132
Q

where re the immunocompetent helper T cells are located

A

Some immunocompetent helper T cells in the
lymph node will have antigen receptors that can
recognize the “presented” antigen

133
Q

how does the clonal selection is related to the cd+4 cells

A

ACTIVATION: Results in the clonal selection of
that helper T cell that correctly responded to the
antigen

134
Q

for the proper activation what has to happen between the antigen receptor and co- receptor

A 
For proper activation and clonal selection to occur, the 
antigen receptor (T cell receptor) and a co-receptor (CD4)
must BOTH bind to the MHC II molecule
135
Q

how do the active helper t-cells respond ? buy secreting which enzyme

A

Active helper T cells respond by secreting cytokines that
enhance the immune response of cytotoxic T cells and
activation of B cells

136
Q

are all of the t cells able to recognize the specific antigen

A

Not every immunocompetent helper T cell that leaves the thymus will recognize our specific antigen
• The ones that do will become activated, will proliferate, and become “effector” versions (help!!) or “memory” versions that can easily become effectors if infection occurs again

137
Q

how does MHC 1 works in other tissue’s cells

A

• RECAP: Antigen presenting cells (macrophages, dendritic cells, etc.) have MHC II molecules on their membrane that they can use to activate helper T cells
• ALL nucleated cells also have MHC I molecules on their membrane too
• If a tissue cell (not an APC) is infected with a virus, it can present antigen on MHC I molecules on its membrane
By presenting antigen in this way, the infected tissue cell acts
like a martyr, signaling to cytotoxic T cells that it should be
destroyed

138
Q

how is the cytotoxic T cell activate

A

• Cytotoxic T cell activation occurs in a similar manner to

helper T cell activation

139
Q

what happens if the cytotoxic T cell encounters a target cell with a foreign antigen that it can recognize on the MHC I molecule

A

If a mature, immunocompetent cytotoxic T cell encounters a target cell with a foreign antigen that it can recognize on the MHC I molecule, the T cell will kill it
• Similar to helper T cells, cytotoxic T cell activation requires a co-receptor to bind to MHC I → CD8

140
Q

why does cytotoxic T cell require the co- receptor

A

• Similar to helper T cells, cytotoxic T cell activation requires a co-receptor to bind to MHC I → CD8

141
Q

what is the destroying mechanism of the cytotoxic

A

Once activated, cytotoxic T cells release perforin to make pores in the cell membrane
• Following pore creation, granzymes(protease enzymes) are released into the cell to destroy it from the inside
• Cytotoxic T cells can also stimulate apoptosis in the affected cell

142
Q

which cytotoxic leave the lymph nodes and which one stay

A

Unlike cytotoxic T cells that leave lymph nodes to seek out and destroy foreign antigens, B cells stay put

143
Q

what happens tothe B cells when they mature and gain immunocompetence in bone marrow

A

When B cells mature and gain immunocompetence in bone marrow, they move to lymph nodes where they can produce certain types of antibodies

144
Q

when naive B cells ungergo clonal selection

A

• When certain naïve B cells are exposed to a particular antigen which binds to their B cell receptor, they undergo clonal selection

145
Q

what is the other name of the B cells

A

humoral immunity

146
Q

what will activated B cell become after the proliferate

A

– Plasma cells (effector cells) that serve as antibody factories (short-lived)
– Memory B cells (continue to proliferate; long
lived)

147
Q

how doe sthe memory B cells action during the re-exposure to the same antigen

A

Upon re-exposure to the same antigen, memory B
cells rapidly expand to produce more plasma cells
and memory B cells

148
Q

what is the role of the helper T cell in B cell activation

A

• Helper T cells also aid in B cell activation, AND B
cells can reciprocate by acting like APCs (antigen
presentation via MHC II)

149
Q

what is the role of the Neutralizing antigen

A

Antibodies block or neutralize bacterial toxins and can prevent viral attachment to body cells

150
Q

what is the role of the Agglutinating antigen

A

Antibodies cause “clumping” of pathogens (see Immune lecture 1)

151
Q

why Precipitating antigen happens

A

Antibodies cross-link soluble antigens into complexes that are too
large to stay in solution

152
Q

what is the role of the Activating complement

A

Initiate the classical pathway of the complement system (see
Immune lecture 1)

153
Q

what is the role of the Opsonization

A

Coat” the microbe for easier recognition and phagocytosis by
phagocytes

154
Q

which function of the lymphocytes has a long lasting effect of antibodies

A

• Due to the presence of long-lasting antibodies and lymphocytes thanks to clonal selection of lymphocytes

155
Q

which response of the immune system is slower and which one is faster

A

Primary responses mediated by the immune
system tend to be slower and less
intense than secondary responses

156
Q

how do we train our immune system

A 
Natural infection
• IgG antibodies received through 
placental circulation or breast milk
• Vaccination
• Immune serum: gamma globulin 
(antibody) transfer
157
Q

explain the passive and active naturally acquired immunity

A

naturally: infaction , contact with the pathogen

passive : antibodies passes from the mother to the fetus via pacenta or passes through her milk

158
Q

explain passive and active artificial immunity

A

passive injection of an immune serum

active :vaccine dead or attenuated pathogens

159
Q

how lymphocytes become self- tolerance

A

When lymphocytes undergo maturation, they are trained to recognize self-antigens in a process called self-tolerance
The non-reactive lymphocytes get to stay, while reactive lymphocytes are weeded out

160
Q

what is the Autoimmune disorders

A

Autoimmune disorders: this mechanism fails, leading to the development of autoantibodies

161
Q

what is the allergy

A

Allergies are abnormal responses by B lymphocytes or T

lymphocytes

162
Q

what are the Immediate and intermediate allergic reactions

A

– APCs present antigen to helper T cells that eventually help
recruit eosinophils to the site
– Helper T cells also stimulate B lymphocytes, which
become plasma cells that secrete IgE antibody

163
Q

how does the igE acts during the alergy

A

IgE binds to mast cells and basophils which release

histamine & other cytokines

164
Q

what is the Delayed allergic reactions

A

– Cell-mediated T lymphocyte response; symptoms are
caused by the release of cytokines
– Antihistamines provide no relief

165
Q

what is the Anaphylaxis

A

: If the antibodies/chemicals/cytokines produced
by the immune system are in large quantities, they may
reach systemic circulation and cause anaphylactic shock

166
Q

how does Anaphylactic shock happens and how does the epinephrin works

A

Anaphylactic shock causes extreme
vasodilation, low blood pressure/volume,
and bronchoconstriction
Epinephrine injection allows for near
immediate relief of these life-threatening
symptoms

167
Q

what is the mechanism of the epinephrin

A

• Epinephrine, acting as a hormone, travels
to adrenergic receptors on the blood
vessels, heart, and bronchioles

168
Q

what is the difference between the IgG and IgM

A

IgG and IgM are types of antibodies; IgG is most abundant in the blood, and IgM antibodies cause issues during mismatched blood transfusions.

169
Q

what is the purpose of the lymphatic system

A

Drain excess interstitial fluid
• Return filtered plasma proteins to the blood
• Carry out immune responses
• Transport dietary lipids

170
Q

what is the interstitial fluid

A

Interstitial fluid (water + salts, nutrients, and
wastes) is formed from filtration out of blood
tissue capillaries

171
Q

how does The Lymphatic System Draining interstitial fluid

A

Lymphatic capillaries within tissues have a
porous junctions within their endothelial cells,
allowing them to soak up:
• Excess interstitial fluid + proteins
• Microbes, antigens & immune cells
• Lipids

172
Q

how is the Lymphatic Circulation

A

• Lymph fluid picked up from interstitial space is transported
to lymph nodes
• Lymph fluid containing APCs or free antigen will subsequently
activate lymphocytes in lymph node (Immune lecture 2)
• Lymph fluid will continue to lymphatic duct where it will drain
into a major vein

173
Q

how does the lymphatic capillaries act like

A

• Lymphatic capillaries act like a “sponge”
to soak up interstitial fluid (lymph fluid)
• Series of one-way valves move the fluid
through circulation
• “Squeezed” through movement!

174
Q

why feet/legs feel swollen after airline travel?

A

Prolonged periods of sitting can cause blood to pool in the veins
• Excess blood in lower limbs = more fluid leaking out into interstitial space
• Without movement, lymphatic circulation cannot bring fluid back up to the heart
• Harmless for short periods of time!

175
Q

what are the name of the other lymphoid tissues

A

Tonsils: Trap and destroy pathogens that enter the throat
• Thymus: Site of maturation for T lymphocytes (before adulthood)
• Spleen: Filters blood and removes bacteria and viruses as well as worn out RBCs
• Peyer’s patches: Prevent bacteria from penetrating through the intestinal wall
• Appendix: Functions similarly to other intestinal lymphoid tissue

176
Q

why all of the homeostaic processes can take place in the circulatory system

A

• All homeostatic processes can take place in the circulatory system because it is a CLOSED SYSTEM

177
Q

what is the role of the blood clothing in the hemostasis

A

Sequence of responses that results in wound repair

178
Q

what is the goal of the coagulation during the blooding

A

The goal of hemostasis is to stop the bleeding that results from a break in a blood vessel via coagulation thanks to the action of platelets

179
Q

why coagulation happens concurrently with the activation of the local innate defense

A

This often happens concurrently with the activation of local innate defense mechanisms (resident macrophages) to protect against potential infection

180
Q

does stopping of bleeding help us maintain circulatory homeostasis

A

Hemostasis (stopping of bleeding) helps

us maintain circulatory homeostasis

181
Q

how does the platelets form

A

Formed from the breakdown of megakaryocytes in a process called thrombopoiesis

182
Q

does platelets enter main circulation

A

Platelets enter main circulation

•

183
Q

what is the shape of the platelets

A

Disc shaped, no nucleus

184
Q

what is the function of the platelets

A

Stop blood loss from damaged blood vessels and promote coagulation

185
Q

what happens to the platelets in the absent of the injery

A

In the absence of injury…
• Circulating platelets are inactive
• Intact endothelial cells release a type of prostaglandin and nitric oxide; both inhibit platelet aggregation

186
Q

what are the steps of the blood clothing

A

Vascular spasm causes vasoconstriction
2. Exposed collagen fibers causes platelets to stick, forming a plug
3. Coagulation: Fibrin is formed, trapping the platelets and some
RBCs, forming a clot
4. Clot dissolves once tissue damage is repaired

187
Q

how does the vascular spasm occurs

A

Vascular spasm occurs by…
• Damaged endothelial cells release a cytokine that signals to surrounding smooth muscle to contract
• If the smooth muscle is damaged, they will intrinsically contract as well
• Pain receptors stimulated by inflammatory cytokines cause contraction

188
Q

what are the process of the Formation of a platelet plug

A

Platelet adhesion: VWF is now exposed and binds to platelets

• “Stuck” platelets now secrete ADP, thromboxane A (TxA2), and serotonin to recruit other platelets to the site

189
Q

how does the platelet plug is strengthened

A

The platelet plug is strengthened by an insoluble mesh of protein called fibrin, which together with the platelet plug form a blood clot

190
Q

what does the fibrin is converted from

A

Fibrin is converted from fibrinogen through a series of enzymatic activation of blood factors

191
Q

conversion occur through which pathways

A

Conversion may occur through:
• Intrinsic pathway (damaged vessel wall)
• Extrinsic pathway (extravascular damage)

192
Q

where doe sthe most coagulation factors are produced

A

Most blood coagulation factors (proteins) are
produced in the liver, and are inactive within
circulation

193
Q

which factor is activated by the damage to the endothelial cells

A 
• Damage to the endothelial cells reveals collagen, 
which activates Factor XII 
• Factor XII activates Factor XI 
• Factor XI activates Factor IX
• Factor IX activates Factor X
194
Q

what is the Extrinsic pathway:

A

• Damaged extravascular cells release Tissue
Factor (TF) into the bloodstream
• TF activates Factor VII
• TF-Factor VIIa activates Factor X

195
Q

what is the Expedited pathway

A

Expedited pathway that leads to the activation of

the factor needed to produce fibrin

196
Q

what is the mechanism of the common pathway

A

Common pathway:
• Factor X is needed to convert prothrombin into thrombin
• Prothrombin is a Vitamin k dependent glycoprotein; Vit K
deficiency = bleeding tendencies
• Thrombin converts fibrinogen to
fibrin

197
Q

what happens once the tissue has repaired

A

Fibrinolysis
• Once tissue has repaired, Factor XIIa AND/OR tissue plasminogen activator (tPA)
convert plasminogen to plasmin in the bloodstream
• Plasmin breaks down (lyses) fibrin proteins (fibrin degradation products; FDPs)
• Clot is dissolved and blood can flow normally within this repaired blood vessel

198
Q

what is the Thrombosis

A

Thrombosis: Inappropriate formation of blood clots which can eventually occlude a blood vessel
• Clot is now called a thrombus

199
Q

what cause the thrombosis

A

Caused by endothelial injury, abnormal blood

flow, or hypercoagulability, Atherosclerosis, high BP, high blood glucose

200
Q

how does the Heart attack, stroke, or pulmonary embolism result

A

If the clot forms in a coronary artery, in the brain,
the lung, or if a clot moves from a peripheral
vessel to these organs…
• Heart attack, stroke, or pulmonary
embolism can result

201
Q

what are the Fibrinolytics/thrombolytics

A
  • Heparin
  • Inhibits the activity of thrombin
  • Warfarin
  • Inhibits activation of vitamin K (factors VII, IX, and X)
  • Aspirin
  • Inhibits release of TxA2

BIOM3200 (3 decks)

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