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Immune system Flashcards

1
Q

What are the functions of Lymph

A
  1. Normally, filtration of fluid out of the capillaries is slightly greater than absorption of fluid into the capillaries.
  2. The excess filtered fluid is returned to the circulation via lymph.
  3. One-way flap valves permits interstitial fluid to enter, but not leave the lymph vessels.
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2
Q

Edema occurs when?

A
  • Occurs when the volume of interstitial fluid exceeds the capacity of the lymphatics to return to its circulation
  • Can be caused by excess filtration or blocked lymphatics
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3
Q

Blockage of lympatics can be due to?

A
  1. Cancer
  2. Surgery
  3. Infections
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4
Q

This bacteria can cause blockage of lympatics

A

Wuchereria bancrofti

Causes Filariasis or Elephantitis

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5
Q

The body immune system entails four deferent systems which are?

A
  1. Antibody mediated (humoral) immunity – consist of B lymphocytes
  2. Cell mediated immunity – consist of T lymphocytes
  3. Complement system
  4. Phagocytes
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6
Q

These lymphocytes make up humoral immunity

A

B lymphocytes

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7
Q

These lymphocytes make up cell mediated immunity

A

T lymphocytes

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8
Q

Humoral immunity

A

Antibody mediated immunity

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9
Q

Immune system is composed of which 2 types of cells

A
  1. White blood cells (leukocytes)
  2. Tissue cells derived from white blood cells
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10
Q

Immune cells work together by two ways

A
  1. By actually destroying invading bacteria or virus by phagocytosis
  2. By forming antibodies and sensitized lymphocytes which destroy or inactivate the invaders
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11
Q

Leukocytes are made up of 2 types of cells which are?

A

Granulocutes

Agranulocytes

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12
Q

Name 3 granulocytes

A

Basophiles, eosinophils, neutrophils

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13
Q

Name 2 agranulocytes

A

lymphocytes, monocytes

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14
Q

Mobile units of defense that seek out and destroy a foreign invader

A

Leukocytes

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15
Q

Normal leukocyte count

A

4,000 – 10,000/ mL

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16
Q

Acute inflammatory response cell “first responders”

A

Neutrophiils

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17
Q

mixture of dead neutrophils is

A

PUS

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18
Q

Normal Neutrophil count

A

40%-75% of WBCs

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19
Q

These cells contain granules with heparin , histamine and bradykinin

A

Basophils

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20
Q

Defend against worm infection e.g. pinworm

A

Eosinophils- 2%

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21
Q

Cells with Large kidney shaped nucleus that are differentiated into macrophages in tissues

A

Monocytes (5%)

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22
Q

Degranulation of mast cells leads to release of?

A

Release of histamine, bradykinin, heparin , Slow reacting substance of anaphylaxis (SRS-A)

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23
Q

These cells Involve in type I hypersensitivity

A

Mast cells

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24
Q

Neutrophils

A
  1. Acute inflammatory response cell “first responders”
  2. Phagocytic cells
  3. 40%-75% of WBCs
  4. Multilobed nucleus (polys)
  5. Contain lysosomes with hydrolytic enzymes and oxidases
  6. “PUS” is a mixture of dead neutrophils
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25
Q

Basophils- 0.5%

A
  1. Mediates allergic reaction
  2. Contain basophilic granules with heparin , histamine and bradykinin
  3. Release due to binding of IgE
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26
Q

Eosinophils- 2%

A
  1. Defense against worm infection e.g. pinworm
  2. Highly pagocytic for Ag-Ab complex
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27
Q

Monocytes (5%)

A
  1. Large kidney shaped nucleus
  2. Differentiated into macrophages in tissues
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28
Q

Mast cells

A
  1. Similar to basophils
  2. Mediates allergic reaction
  3. Degranulation =release of histamine, bradykinin, heparin , Slow reacting substance of anaphylaxis (SRS-A)
  4. Can bind IgE to membrane
  5. Involve in type I hypersensitivity
  6. Cromolyn sodium (Intal) prevents mast cell degranulation, given for exercise induce asthma
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29
Q

This drug prevents mast cell degranulation

A

Cromolyn sodium

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30
Q

an outward radial movement of leukocytes toward the capillary endothelium

A

Magination

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31
Q

movement of leukocytes out of the circulatory system and towards the site of tissue damage or infection.

A

Diapedesis

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32
Q

Slow movement of the leukocytes toward the site of infection

A

Ameboid motion

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33
Q

Atraction of leukocytes to the source of infection

A

Chemotaxis

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34
Q

Cell ingestion of bacteria, viruses, other foreign particles by powerful oxidizing agents

A

Phagocytosis

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35
Q

Name 5 actions of phagocytic cells in correct order

A
  1. Magination
  2. Diapedesis
  3. Ameeboid motion
  4. Chemotaxis
  5. Phagocytosis
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36
Q

The reticuloendothelial system is composed of which immune cells

A

Monocyte-Macrophages

Macrophages are derived from monocytes

Also called monocyte-macrophage system

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37
Q

Macrophages “Pac man” are present in?

A
  1. lymph nodes
  2. lungs
  3. liver (Kupffer cells)
  4. spleen
  5. bone marrow.
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38
Q

What are the three main functions of macrophages that provide first line defense

A
  1. Phagocytosis
  2. Antigen presentation
  3. Cytokines productions
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39
Q

Phagocytes ingest bacteria, viruses, other foreign particles by powerful oxidizing agents. Identify the oxidizing agents

A
  1. Superoxide (O2-)
  2. Hydrogen peroxide H2O2
  3. Hydroxyl OH-
  4. hypochlorite ClO-
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40
Q

TB becomes a chronic infection because?

A

bacteria have protective coat against macrophage oxidizing agents

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41
Q

Macrophage in spleen removes encapsulated bacteria namely _______, _________and ________, therefore, splenic dysfunction will lead to infection. These require Vaccination.

A
  1. s.pneumonia
  2. salmonella
  3. H.influenza
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42
Q

Describe antigen presentation as a role of macrophages

A

Invaders are ingested and broken down.

Fragments of antigen presented on surface of macrophages along with MHC.

These antigens are presented to CD4

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43
Q

Describe Cytokines productions as a role of macrophages

A

e.g. IL-1(activates T-helper cell) and TNF (tissue necrotic factor)

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44
Q

Patient’s who have spleenectomy or spleen dysfunction will require what vaccines

A
  1. Pneumococcal
  2. H. influenza
  3. Salonella (there is a vaccine for salmonella typhi/ typhoid)
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45
Q

Coating of bacteria with antibodies/ complement proteins to enhance phagocytosis

A

Opsonization

Fetus will receive these antibodies fro the mother IgG

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46
Q

Phagocytosis by macrophage is enhanced by?

A
  1. Opsonization by antibodies/CP
  2. Lack of protective coat on infected or cancer cells
  3. Rough surface of offending agent
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47
Q

Name all the labeled steps of phagocytosis

A
  1. Binding
  2. Engulfment
  3. Phagosome formation, acidification, proteolysis
  4. Lysosome fusion
  5. membrabe disruption
  6. Antigen presentation

X. MHC

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48
Q

Name 4 substances involed in inflamation

A

−Bradykinin

−Histamine

−Serotonin

−Lymphokines

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49
Q

Inflammation Events

A
  1. Vasodilation
  2. Increase capillary permeability
  3. Migration of granulocytes and monocytes
  4. Swelling of cells
  5. Substances involved (Bradykinin, Histamine, Serotonin, Lymphokines)
  6. “Walling off” of inflammation by fibrin clot −Prevent spread. E.g Staph=> localized infection
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50
Q

First line of defense

A

Tissue macrophages ; already present in tissues

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51
Q

Second line of defense

A

Neutrophil invasion

−Margination, diapedesis, chemotaxis

−Stimulation of bone marrow to release stored leukocytes, 4-5 hours

− increased count – neutrophilia

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52
Q

Third line of defense

A

Macrophage proliferation −Invasion by circulating monocytes

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53
Q

Fourth line of defense

A

Stimulation of granulocyte and monocyte production −Growth factors produced by tissue macrophages: TNF, IL-1

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54
Q

Describe the Cell-mediated Response to Inflammation

A
  1. Tissue macrophages −First line of defense ; already present in tissues
  2. Neutrophil invasion −Second line of defense; Margination, diapedesis, chemotaxis ; Stimulation of bone marrow to release stored leukocytes, 4-5 hours; Elevated count = neutrophilia
  3. Macrophage proliferation−Third line of defense; Invasion by circulating monocytes
  4. Stimulation of granulocyte and monocyte production −Fourth line of defense; Growth factors produced by tissue macrophages: TNF, IL-1
  5. Formation of pus −Composed of dead neutrophils, monocytes and tissue debries
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55
Q

Describe the control of bone marrow production of granulocytes and monocyte-macrophages in response to multiple growth factors released from activated macrophages in an inflamed tissue

A
  • Activated microphage will release G-CSF, granulocyte colony-stimulating factor; GM-CSF, granulocyte-monocyte colony-stimulating factor; IL-1, interleukin-1; M-CSF, monocyte colony-stimulating factor; TNF, tumor necrosis factor which direcly stimulate the bone marrow to produce granulocytes, monocytes/macrophages
  • TNF and IL-1 produced by macrophage will also stimulate endothelial cells to produce GM-CSF, G-CSF and M-CSF to stimulate the bone marrow
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56
Q

Innate (natural) immunity is genetically-encoded (built in) to recognize

A
  1. Common pathogenic features
  2. Against foreign substances
  3. Not acquired through contact with an antigen
  4. Non specific
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57
Q

Innate immunity includes?

A
  1. Neutrophils
  2. Macrophage
  3. Natural killer cells
  4. Complement proteins
  5. Gastric acid
  6. Skin
  7. Dendritic cells
  8. Inflammation
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58
Q

Only type of T lymphocyte (?) that plays an important role in natural immunity

A

Natural Killer (NK) Cell

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59
Q

Natural Killer (NK) Cell

A
  1. “Pit Bulls” of defense system (constant surveillance)
  2. Only type of T lymphocyte (?) that plays an important role in natural immunity
  3. Specialized killers of virus-infected cells- “enemy hideouts” and tumor cells by inserting perforins
  4. Induce apoptosis (program cell death) of virally infected cells and tumor cells
  5. They are active without prior exposure to virus. That’s why called “natural” killer
  6. They do not have to pass through thymus in order to mature
  7. Killing does NOT require recognition of MHC proteins
  8. Not specific to any virus
  9. Induce cells to undergo apoptosis (programmed cell death)
  10. IL-2 activated NK cells are being used for the treatment of certain cancers.
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60
Q

When an NK cell recognizes a cell as “non-self” it releases _____________

A

cytotoxic perforins (stab the pathogens) and granzymes

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61
Q

a substance that can induce an immune response when introduced into an healthy host and that can react with the antibody produced from that response

A

ANTIGEN
“Antibody generator”

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62
Q

Acquired (adaptive) immunity

A
  1. Occurs after exposure to bacteria, virus or toxins
  2. Specific
  3. Mediated by circulating antibodies and lymphoid cells (T and B cells)
  4. Can be active or passive
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63
Q

Active immunity

A
  1. Is resistance after contact with foreign antigen e.g. bacteria
  2. The host actively produces antibodies
  3. Long lasting protection (memory)
  4. Slow onset
  5. Examples: clinical or sub-clinical infection, immunization
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64
Q

Passive immunity

A
  1. Is resistance based on antibodies preformed in another host e.g. sheep, goats, dogs or horses
  2. Short life-span of antibody
  3. Prompt availability
  4. IgA in breast milk and IgG through placenta are examples of passive immunity
  5. Example: after exposure to Tetanus toxin , Botulinum toxin, HBV, Rabies, patients are given preformed antibodies.
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65
Q

After exposure to _______ paients are given preformed antibodies to be healed rapidly.

A
  1. Tetanus toxin
  2. Botulinum toxin
  3. HBV
  4. Rabies

Mnemonic To Be Healed Rapidly

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66
Q

IgA in breast milk and IgG through placenta are examples of?

A

passive immunity

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67
Q

Two types of acquired immunity

A

Active -resistance after contact with foreign antigen e.g. bacteria

Passive -resistance based on antibodies preformed in another host e.g. sheep, goats, dogs or horses

68
Q

These cells have small rounded densely stained nucleus. Have two look alike types and are responsible for acquired immunity.

A

Lymphocytes

T-cell and B-cell present in lymphoid tissues

69
Q

These lymphocytes are part of the humoral immunity

A

B lymphocytes

70
Q

These lymphocytes are part of the cellular immune response

A

T lymphocytes

originates from bone marrow but mature in Thymus

71
Q

These lymphocytes differentiate into plasma cells which produces antibodies and memmory cells

A

B lymphocyte

72
Q

These cells were discovered in Bursa of birds

A

B lymphocytes

73
Q

These lymphocytes only recognize antigen when presented by APC

A

T lymphocytes

74
Q

In thymus (boot camp) T cells _____________

A

undergo positive and negative selection. They are trained to differentiate between self and non-self. Only 10% graduate successfully to become immunocompetent, self-tolerant T cells. 90% are killed

75
Q

T lymphocytes are Sub-classified to CD4 and CD8 cells. Normal=_______ in AIDS= _________

A

2: 1
0. 5:1

76
Q

T lymphocytes differentiate into?

A
  1. Natural killers ( NK cells)
  2. Cytotoxic/killer (CD8) T cells
  3. T-Helper (CD4) cells
  4. T- Suppressor Cells
77
Q

These T cells Kill virus infected, neoplastic and donor graft cells

A

Cytotoxic/killer (CD8) T cells

78
Q

These T-cells activate macrophage and help B-cells

A

T-Helper (CD4) cells

79
Q

_________ destroys T-Helper cells

80
Q

A defficiency of these T- Cells will lead to autoimmune deseases

A

T- Suppressor Cells

81
Q

Compare and contrast B vs T cell functions on hypersensitivity reactions

A

B- cells

  1. Allergy (type I hypersensitivity): IgE
  2. Cytotoxic (type II) and immuncomplex (type III) hypersensitivity: IgG

T-cells

  1. Responsible for delayed cell mediated hypersensitivity (type IV)
82
Q

Compare and contrast B vs T cell functions on transplant

A

B cells are responsible for hyperacute organ rejection while T-cells play an important role in organ (allograft) rejection (acute and chronic)

83
Q

Major Functions of B and T Cells

84
Q

Antibody mediated immunity vs cell mediated immunity

85
Q

Describe the sequence of events in antibody mediated immunity

A
  1. Involves cooperation of 3 cells; macrophages, T-helper cells and B-cells
  2. Entry of bacteria into the body
  3. Ingestion by macrophage (APC)
  4. Bacteria is broken down and its fragment (antigen) appear on the surface of macrophage along with MHC II (major histocompatibility complex) proteins
  5. Antigen-MHC II complex react with T-helper (CD4) lymphocytes which then produce lymphokines (IL)
  6. These factor activates the B-cells that differentiate into Plasma cells. Plasma cells secretes large amount of antibodies specific to a particular antigen (bacteria) to kill them all
  7. Elevated Plasma cells in Multiple Myeloma
86
Q

Describe the sequence of events in cell mediated immunity

A

1-3. is same as antibody-mediated immunity

  1. Antigen-MHC II complex react with T-helper lymphocytes
  2. T-helper cells are activated by interleukin (IL-1) produced by macrophages. T-helper cells perform following functions:
  3. −Produce IL-2 and gamma-interferon: activates macrophages and cytotoxic T-cells (CD8) ; increase killing efficiency of intracellular bacteria
  4. −Help B cells to make antibodies
  5. −Convert B cell to Plasma Cells- “factories of antibodies”
87
Q

After activaton by IL-1 produced by macrophages, T-helper cells perform what 3 functions in cell mediated immunity

A
  1. Produce IL-2 and g - interferon
  2. Help B cells to make antibodies
  3. Convert B cell to Plasma Cells- “factories of antibodies”
88
Q

What is the action of IL-2 and gamma - interferon produced by T-heper cells

A
  1. Activates macrophages and cytotoxic T-cells (CD8)
  2. Increase killing efficiency of intracellular bacteria
89
Q

After reaction of T-helper cell with Antigen-MHC II complex in antibody mediated immunity, what follows

A
  1. T-helper cell produce IL
  2. IL activates B-cells
  3. B-cells defferentiate to plasma cells
  4. Plasma cells secrete large amounts of antibodies specific to the particular antigen to kill them all.
90
Q

Very high quantity of plasma cells

A

Multiple myeloma

91
Q

Describe

A

Multiple Myeloma

  1. Plasma cell tumor
  2. Punched out lesions of skull
    * Plasma cells with off-center nucleus (eccentric)*
92
Q

Deferentiate between A.Primary response (immediate) and secondary response (delayed)

A

Primary response - “immediate”

  1. First exposure of antigen gives rise of antibody within 7-10 days
  2. IgM is first to appear– Primary response

Secondary response – “delayed”

  1. Second exposure to same antigen– rapid antibody response
  2. Higher level, more robust
  3. Due to formation of ‘memory cells’ after first exposure
  4. IgG is produced in large amount
93
Q

Name labeled curves

A

A. IgM

B. IgG

C. Total

94
Q

Name labeled curves

A

A. IgM

B. IgG

C. Total

95
Q

ANTIBODIES

A
  1. Antibodies are immunoglobulins (20%) that react specifically with the antigen that stimulated their production
  2. Composed of light and heavy chains
  3. Variable portion recognizes antigen
  4. Constant portion activates compliment and binding to cell surface receptor
96
Q

Name the 5 classes of antibodies

A
  1. IgG– most abundant, opsonizes bacteria, neutralizes toxins, cross the placenta, provide immunity to infant.
  2. IgA–Main Ab in secretions, protect mucous membrane from attack by bacteria and viruses. Prevent attachment of bacteria and viruses
  3. IgM— First produce; primary response to an antigen, activate complement , does not cross placenta (largest size)
  4. IgD– unclear function
  5. IgE– “Evil” antibody , mediated immediate hypersensitivity reaction, release Histamine, SRS-A from mast cells and basophils upon exposure to allergens
97
Q

Main Ab in secretions

A

IgA

  1. ​Main Ab in secretions
  2. Protect mucous membrane from attack by bacteria and viruses.
  3. Prevent attachment of bacteria and viruses
98
Q

most abundant antibody

A

IgG

  1. most abundant
  2. opsonizes bacteria
  3. neutralizes toxins
  4. cross the placenta
  5. provide immunity to infant

IgG crosses the placenta during Gestation.

99
Q

This antibody’s function is unclear

100
Q

This antibody mediates immediate hypersensitivity reaction

A

Evil antibody IgE

  1. Mediates immediate hypersensitivity reaction
  2. Release Histamine, SRS-A from mast cells and basophils upon exposure to allergens
101
Q

This part of the antibody activates compliment and binding to cell surface receptor

A

Constant portion

102
Q

This part of the antibody recognizes antigen

A

Variable portion

103
Q

Complement System

A
  1. Series of ~ 20 proteins
  2. Activated by microorganisms
  3. Will coat the microorganisms –opsonization
  4. Adherence reaction −phagocytic cells have receptors for C3
  5. Biological active fragments −produce reactive oxygen intermediates
  6. Activate mast cells
  7. C5-C9 make membrane attack complex (MAC) to make a ‘hole’ in bacteria
104
Q

________ and _________act as antigen presenting cells (APC)

A

Macrophage and dendritic cells

105
Q

APCs present _______ along with _______ to T cells

A

antigen

Major Histocompatibility Complex proteins- MHC

106
Q

Describe 2 types of MHC proteins

A

MHC-I

−All body cells have MHC-I proteins

−Infected cells present viral antigen to cytotoxic cells (CD8)

MHC-II

−Antigen presenting cells (e.g. macrophage) have MHC-II proteins

−APC present viral antigen to helper T-cells (CD4)

−Main determinant of organ rejection

_MHC I goes with CD8 MHC II goes with CD4. Remember 18 and 24_

107
Q

The main determinant of organ rejection is

108
Q

Membrane attack complex is made of?

109
Q

What are the functions of compliment activation

A
  1. Lysis
  2. Chemotaxis
  3. Opsonization
110
Q

Acquired immunity sequnce of events in presence of antigens

A
  1. Macrophage (APC) ingests and partially digest an antigen, then present part of the antigen along with MHC-II on the cell surface
  2. An “immune synapse” forms with a naïve (immature) T helper (CD4) cells
  3. T helper (CD4) is activated by a) Cell to cell contact “signal 1” b) IL-1 secreted by APC “signal 2”
  4. Activated T helper (CD4) produces IL-2
  5. IL-2 acts in an autocrine fashion to cause the cell to multiply forming a clone
  6. The activated T helper (CD4) cell do the followings:

−Promote B cell activation and differentiating it to plasma cell. Plasma cell then produces antibodies.

−Activate a cytotoxic T cell (CD8) cell to attack and destroy virus infected cell

  1. Cytotoxic CD8 cell can also be activated by forming a synapse with an MHC-I antigen binding site on virus infected cell.
111
Q

The activated T helper (CD4) cell do the followings:

A
  1. Promote B cell activation and differentiating it to plasma cell. Plasma cell then produces antibodies.
  2. Activate a cytotoxic T cell (CD8) cell to attack and destroy virus infected cell
112
Q

T helper (CD4) is activated by

A
  1. Cell to cell contact “signal 1”
  2. IL-1 secreted by APC “signal 2”
113
Q

This is produced by activated T helper (CD4) and acts in an autocrine fashion to cause the cell to multiply forming a clone

114
Q

Cytotoxic T-helper cells can be activated in which 2 ways

A
  1. Activation by T-helper cells
  2. Formationof a synapse with an MHC-1 antigen binding site on virus infected cell
115
Q

Cytotoxic T-cells (CD8) are direct-attack killer cells “hand-to-hand combat” which can kill?

A
  1. Kill micro-organism
  2. Kill virus infected body cells by stabbing the cells with perforins – “destroying the enemy hideout”
  3. Kill cancer cells and transplant organ cells
116
Q

Cytotoxic T-Cells have_________, which binds to _______ on virus infected cell.

117
Q

What is the function of suppressor T-cells

A
  1. Suppress cytotoxic T cells and T helper cell
  2. ‘Turn off’ immune cells when infection brought under control
  3. Prevent excessive immune reaction against body’s own tissues
  4. Important role in “immune tolerance”
  5. Absence of suppressor T-cells => autoimmune disease
118
Q

Interferon

A
  1. Made and release by host cell in response to pathogens
  2. Interferon (a,b, g) interfere (inhibit) viral protein synthesis
  3. Activate NK cells to kill viral infected cell
  4. Breakdown viral mRNA
119
Q

Zileuton (Zyflo)

A
  1. 5-lipooxigenase inhibitor
  2. Prevents formation of leukotriene
  3. Adverse effects: dyspepsia, arthralgia, chest pain, fever
120
Q

Montelukast (Singulair) and Zafirlukast

A
  1. Competitive antagonist of leukotriene on cysteinyl-leukotriene 1 receptor
  2. Prevent bronchospasm, vasoconstriction and eosinophil recruitment
121
Q

slide 67

122
Q

Recombinant cytokines for clinical use in Renal cell Ca. Melanoma

A

Aldesleukin (IL-2)

123
Q

Recombinant cytokines for clinical use in anemia due to renal failure

A

Erythropoietin

124
Q

Recombinant cytokines for clinical use in recovery of bone marrow

A

Filgrastim/ Sargramostim [Granulocyte colony-stimulating factor (GCSF)]

125
Q

Recombinant cytokines for clinical use in Hepatitis Band C, Kaposi’s sarcoma, leukemias, melanoma

A

a- interferone

126
Q

Recombinant cytokines for clinical use in Multiple sclerosis

A

ß- interferone

127
Q

Recombinant cytokines for clinical use in Chronic granulomatous disease

A

g- interferone

128
Q

Recombinant cytokines for clinical use in Thrombocytopenia

A

Oprelvekin (IL-11)

129
Q

Describe the pathophysiology of type I hypersensitivity

A
  1. Anaphylactic and atopic: Antigen induces formation of IgE
  2. IgE binds with mast cells and basophils
  3. Re-exposure to same antigen result in cross linking of Ag and cell bound IgE
  4. Release of vasoactive mediators from mast cells, in minutes. (First and Fast)
  5. Anaphylaxis, asthma, itching, wheal/flare, hypotension and circulatory collapse
130
Q

In type I hypersensitivity reexposure to antigen leads to crosslinking of Ag and Cell bound IgE resulting in fast release of vasoactive mediators. What are the vasoactive mediators?

A

−Heparin

−Histamine

−PGs

−Kinin

−PAF (Platelet activating factor)

−SRS-A (slow reacting substance of anaphylaxis)

−Serotonin

131
Q

What are the moderate symptoms of type I reactions

A
  1. Pruritus,
  2. urticaria,
  3. angioedema,
  4. SOB,
  5. respiratory distress,
  6. hypotension,
  7. shock,
  8. arrhythmias,
  9. abdominal pain,
  10. severe NVD,
  11. feeling of impending doom
132
Q

The most common cause of type I reactions is?

133
Q

Causes of type I hypersensitivity include?

A
  1. Food (MCC)
  2. medications
  3. radiocontrasts
  4. blood products
  5. venoms
  6. bee stings
  7. ragweed/molds
  8. various chemicals
134
Q

What are the type 1 hypersensitivity allergic and atopic disorders?

A

−Rhinitis

−Hay fever

−Eczema

−Hives

−asthma

135
Q

What is the difference between anaphylactic and anaphylactoid reactions?

A

Anaphylaxis is IgE mediated whereas anaphylactoid reactions result from direc stimulation of mast cells and do not require IgE.

136
Q

Dextran causes anaphylaxis or anaphylactoid reaction?

A

Anphylactoid reaction

137
Q

Anphylactoid reaction are due to?

A
  • Emptying of mast cells without IgE e.g. drugs or volume expanders (dextran).
  • Direct action on mast cells
  • By activation of complement system
  • Non-immune mediated
  • S/S are same as anaphylactic reaction
138
Q

What is the treatment of anaphylaxis and anaphylactoid reactions?

A

−ABC

−Epinephrine IV or S/C

−Antihistamines

−Corticosteroids

−IV fluid , oxygen

139
Q

60% of anaphylactic reactions are from which drugs?

A

Neuromuscular blocking agents with suc being the most common

140
Q

What percentage of anaphylactic reactions is linked to latex?

141
Q

What percentage of anaphylactic reactions is linked to Antibiotics?

142
Q

What percentage of anaphylactic reactions is linked to hypnotics?

A

3-4% with propofol being the most common. Others are thiopental and midazolam

143
Q

Bruton’s Agammaglobuinemia

A
  • B-cell deficiency.
  • X-linked.
  • Associated with low immunoglobulins and recurrent Bacterial infections after 6 months of age when maternal antibodies (IgG) decline.
144
Q

Thymic Aplasia (DiGeorge’s syndrome)

A
  1. T-cell deficiency.
  2. Thymus and parathyroid fail to develop.
  3. Present with Tetany due to hypocalcemia.
  4. Recurrent viral , fungal and protozoal infections.
145
Q

Severe Combined Immune Deficiency (SCID)

A
  • Severe deficiency of both B and T-cells.
  • Recurrent bacterial , viral ,fungal and protozoal infections.
  • Patient lives in plastic ‘bubble’ to avoid any exposure.
  • Treatment: BMT (no rejection)
146
Q

Chronic Granulomatous disease

A
  1. Phagocytic deficiency due to lack of NADPH oxidase (no superoxide to kill bugs).
  2. Bacterial infections by staph and strep
147
Q

Patients with this immune disorder have defective chemotaxis and elevated IgE

A

Job’s Syndrome

148
Q

Patients with this immune disorder have a defect in DNA repair enzyme. They presents with ataxia, spider angioma and IgA deficiency

A

Ataxia-telangiectasia

149
Q

Patients with this immune disorder have microtubular dysfunction, decreased phagocytosis which leads to recurrent bacterial infections

A

Chédiak-Higashi syndrome

150
Q

Patient with this condition presents with Tetany and has T- cell deficiency with undeveloped Thymus and parathyroid

A

Thymic Aplasia (DiGeorge’s syndrome):

151
Q

Patient with this condition have recurrent Bacterial infections every 6 months and a B-cell deficiency

A

Bruton’s Agammaglobuinemia

152
Q

This patient has no no superoxide (NADPH oxidase) to kill bugs

A

Chronic Granulomatous disease

153
Q

Cytotoxic reaction are what type?

A

Type II hypersensitivity

Mo Tip

154
Q

These antibodies mediate type II reactions

155
Q

Desease in ths hypersensitivity reaction tends to be specific to tissue or site where antigen is found.

156
Q

IgG, IgM bind on Antigen on “enemy” cell, leading to lysis (by complement) or phagocytosis

A

Type II Cytotoxic

157
Q

Patient with type II hypersensitivity presents with

A

−Mismatch blood transfusion

−Autoimmune hemolytic anemia

−Rh disease (Erythoroblastosis fetalis)

−Goodpasture’s disease

−ITP

−Rheumatic fever

−Grave’s disease

−Myasthenia gravis

158
Q

Ag-Ab complexes activates which attract neutrophils; neutrophils release lysosomal enzymes Complement fixation leads to tissue damage- “collateral damage”

A

Type III hypesensitivity- Immune complex

159
Q

This type of hypersensitivity is associated with vasculitis and systemic manifestation

A

Type III hypesensitivity- Immune complex

160
Q

A patient with a type III hypersensitivity presents with?

A

−Poststreptococcal glomerulonephritis

−Serum sickness

−Arthus reaction (e.g. swelling and inflammation after tetanus vaccine)

−SLE

−Rheumatoid arthritis

161
Q

Sensitized ‘T’ Lymphocytes encounter antigen and then release lymphokines (lead to macrophage activation)

A

Type IV - Delayed (cell-mediated) type

162
Q

In this hypersensitivity immune reaction response is delayed and does NOT involve antibodies

A

Type IV: Delayed (cell-mediated) type

163
Q

What is the presentation of Type IV hypersensitivity?

A

−TB skin test

−Transplant rejection

−Contact dermatitis (e.g. poison ivy)

−Type I DM

−Multiple sclerosis

−Hashimoto’s thyroiditis

−Guillian-Barré syndrome

164
Q

Mo TIP: ACID

A

Anaphylaxis and Atopic (type I)

Cytotoxic (type II)

Immune complex (type III)

Delayed (cell mediated) (type IV)

165
Q

Identify A and B

A

A: Zileuton

B: Montelukast

166
Q

Review slide 66and 67

A
  1. Virus released by an infected cell is ingested and processed by an antigen-presenting cell (APC) e.g. a macrophage.
  2. The viral epitope (antigen) is presented in association with a class II MHC proteins to the virus specific T cell receptor (TCR) on the CD4 cells (double hand shake).
  3. The macrophage make IL-1 which help to activate CD4 ( T helper) cell.
  4. The activated CD4 makes interleukins (e.g. IL-2) which activates CD8 cell (cytotoxic T cell) to attack the virus infected cell, and the IL-4 and IL-5 which activate the B cell => plasma cells and produce antibody.
  5. The specificity of the cytotoxic response mounted by the CD8 cell is provided by TCR, which recognizes the viral epitope presented by the virus-infected cell in association with class I MHC protein.
  6. Note cell mediated (T cell) and antibody (humoral) mediated (B cell) immune responses

A&P III (6 decks)

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