Immune system Flashcards
(166 cards)
1
Q
What are the functions of Lymph
A
- Normally, filtration of fluid out of the capillaries is slightly greater than absorption of fluid into the capillaries.
- The excess filtered fluid is returned to the circulation via lymph.
- One-way flap valves permits interstitial fluid to enter, but not leave the lymph vessels.
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
3
Q
Blockage of lympatics can be due to?
A
- Cancer
- Surgery
- Infections
4
Q
This bacteria can cause blockage of lympatics
A
Wuchereria bancrofti
Causes Filariasis or Elephantitis
5
Q
The body immune system entails four deferent systems which are?
A
- Antibody mediated (humoral) immunity – consist of B lymphocytes
- Cell mediated immunity – consist of T lymphocytes
- Complement system
- Phagocytes
6
Q
These lymphocytes make up humoral immunity
A
B lymphocytes
7
Q
These lymphocytes make up cell mediated immunity
A
T lymphocytes
8
Q
Humoral immunity
A
Antibody mediated immunity
9
Q
Immune system is composed of which 2 types of cells
A
- White blood cells (leukocytes)
- Tissue cells derived from white blood cells
10
Q
Immune cells work together by two ways
A
- By actually destroying invading bacteria or virus by phagocytosis
- By forming antibodies and sensitized lymphocytes which destroy or inactivate the invaders
11
Q
Leukocytes are made up of 2 types of cells which are?
A
Granulocutes
Agranulocytes
12
Q
Name 3 granulocytes
A
Basophiles, eosinophils, neutrophils
13
Q
Name 2 agranulocytes
A
lymphocytes, monocytes
14
Q
Mobile units of defense that seek out and destroy a foreign invader
A
Leukocytes
15
Q
Normal leukocyte count
A
4,000 – 10,000/ mL
16
Q
Acute inflammatory response cell “first responders”
A
Neutrophiils
17
Q
mixture of dead neutrophils is
A
PUS
18
Q
Normal Neutrophil count
A
40%-75% of WBCs
19
Q
These cells contain granules with heparin , histamine and bradykinin
A
Basophils
20
Q
Defend against worm infection e.g. pinworm
A
Eosinophils- 2%
21
Q
Cells with Large kidney shaped nucleus that are differentiated into macrophages in tissues
A
Monocytes (5%)
22
Q
Degranulation of mast cells leads to release of?
A
Release of histamine, bradykinin, heparin , Slow reacting substance of anaphylaxis (SRS-A)
23
Q
These cells Involve in type I hypersensitivity
A
Mast cells
24
Q
Neutrophils
A
- Acute inflammatory response cell “first responders”
- Phagocytic cells
- 40%-75% of WBCs
- Multilobed nucleus (polys)
- Contain lysosomes with hydrolytic enzymes and oxidases
- “PUS” is a mixture of dead neutrophils
25
Basophils- 0.5%
1. Mediates allergic reaction
2. Contain basophilic granules with heparin , histamine and bradykinin
3. Release due to binding of IgE
26
Eosinophils- 2%
1. Defense against worm infection e.g. pinworm
2. Highly pagocytic for Ag-Ab complex
27
Monocytes (5%)
1. Large kidney shaped nucleus
2. Differentiated into macrophages in tissues
28
Mast cells
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
29
This drug prevents mast cell degranulation
Cromolyn sodium
30
an outward radial movement of leukocytes toward the capillary endothelium
Magination
31
movement of leukocytes out of the circulatory system and towards the site of tissue damage or infection.
Diapedesis
32
Slow movement of the leukocytes toward the site of infection
Ameboid motion
33
Atraction of leukocytes to the source of infection
Chemotaxis
34
Cell ingestion of bacteria, viruses, other foreign particles by powerful oxidizing agents
Phagocytosis
35
Name 5 actions of phagocytic cells in correct order
1. Magination
2. Diapedesis
3. Ameeboid motion
4. Chemotaxis
5. Phagocytosis
36
The reticuloendothelial system is composed of which immune cells
**Monocyte-Macrophages**
Macrophages are derived from monocytes
Also called monocyte-macrophage system
37
Macrophages “Pac man” are present in?
1. lymph nodes
2. lungs
3. liver (Kupffer cells)
4. spleen
5. bone marrow.
38
What are the three main functions of macrophages that provide first line defense
1. Phagocytosis
2. Antigen presentation
3. Cytokines productions
39
Phagocytes ingest bacteria, viruses, other foreign particles by powerful oxidizing agents. Identify the oxidizing agents
1. Superoxide (O2-)
2. Hydrogen peroxide H2O2
3. Hydroxyl OH-
4. hypochlorite ClO-
40
TB becomes a chronic infection because?
bacteria have protective coat against macrophage oxidizing agents
41
Macrophage in spleen removes encapsulated bacteria namely \_\_\_\_\_\_\_, \_\_\_\_\_\_\_\_\_and \_\_\_\_\_\_\_\_, therefore, splenic dysfunction will lead to infection. **These require Vaccination**.
1. s.pneumonia
2. salmonella
3. H.influenza
42
Describe antigen presentation as a role of macrophages
Invaders are ingested and broken down.
Fragments of antigen presented on surface of macrophages along with MHC.
These antigens are presented to CD4
43
Describe Cytokines productions as a role of macrophages
e.g. IL-1(activates T-helper cell) and TNF (tissue necrotic factor)
44
Patient's who have spleenectomy or spleen dysfunction will require what vaccines
1. Pneumococcal
2. H. influenza
3. Salonella (there is a vaccine for salmonella typhi/ typhoid)
45
Coating of bacteria with antibodies/ complement proteins to enhance phagocytosis
Opsonization
Fetus will receive these antibodies fro the mother IgG
46
Phagocytosis by macrophage is enhanced by?
1. Opsonization by antibodies/CP
2. Lack of protective coat on infected or cancer cells
3. Rough surface of offending agent
47
Name all the labeled steps of phagocytosis
1. Binding
2. Engulfment
3. Phagosome formation, acidification, proteolysis
4. Lysosome fusion
5. membrabe disruption
6. Antigen presentation
X. MHC
48
Name 4 substances involed in inflamation
−Bradykinin
−Histamine
−Serotonin
−Lymphokines
49
Inflammation Events
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
50
First line of defense
Tissue macrophages ; already present in tissues
51
Second line of defense
**Neutrophil invasion**
−Margination, diapedesis, chemotaxis
−Stimulation of bone marrow to release stored leukocytes, 4-5 hours
− increased count – neutrophilia
52
Third line of defense
**Macrophage proliferation** −Invasion by circulating monocytes
53
Fourth line of defense
**Stimulation of granulocyte and monocyte production** −Growth factors produced by tissue macrophages: TNF, IL-1
54
Describe the Cell-mediated Response to Inflammation
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
55
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
* 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
56
Innate (natural) immunity is genetically-encoded (built in) to recognize
1. Common pathogenic features
2. Against foreign substances
3. Not acquired through contact with an antigen
4. Non specific
57
Innate immunity includes?
1. Neutrophils
2. Macrophage
3. Natural killer cells
4. Complement proteins
5. Gastric acid
6. Skin
7. Dendritic cells
8. Inflammation
58
Only type of T lymphocyte (?) that plays an important role in natural immunity
Natural Killer (NK) Cell
59
Natural Killer (NK) Cell
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.
60
When an NK cell recognizes a cell as “non-self” it releases \_\_\_\_\_\_\_\_\_\_\_\_\_
cytotoxic perforins (stab the pathogens) and granzymes
61
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
ANTIGEN
“**Ant**ibody **gen**erator”
62
Acquired (adaptive) immunity
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
63
Active immunity
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
64
Passive immunity
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.
65
After exposure to _______ paients are given preformed antibodies to be healed rapidly.
1. **T**etanus toxin
2. **B**otulinum toxin
3. **H**BV
4. **R**abies
## Footnote
*Mnemonic **T**o **B**e **H**ealed **R**apidly*
66
IgA in breast milk and IgG through placenta are examples of?
passive immunity
67
Two types of acquired immunity
**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
These cells have small rounded densely stained nucleus. Have two look alike types and are responsible for acquired immunity.
**Lymphocytes**
T-cell and B-cell present in lymphoid tissues
69
These lymphocytes are part of the humoral immunity
B lymphocytes
70
These lymphocytes are part of the cellular immune response
**T lymphocytes**
originates from bone marrow but mature in Thymus
71
These lymphocytes differentiate into plasma cells which produces antibodies and memmory cells
B lymphocyte
72
These cells were discovered in Bursa of birds
B lymphocytes
73
These lymphocytes only recognize antigen when presented by APC
T lymphocytes
74
In thymus (boot camp) T cells \_\_\_\_\_\_\_\_\_\_\_\_\_
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
T lymphocytes are Sub-classified to CD4 and CD8 cells. Normal=\_\_\_\_\_\_\_ in AIDS= \_\_\_\_\_\_\_\_\_
2: 1
0. 5:1
76
T lymphocytes differentiate into?
1. Natural killers ( NK cells)
2. Cytotoxic/killer (CD8) T cells
3. T-Helper (CD4) cells
4. T- Suppressor Cells
77
These T cells Kill virus infected, neoplastic and donor graft cells
Cytotoxic/killer (CD8) T cells
78
These T-cells activate macrophage and help B-cells
T-Helper (CD4) cells
79
\_\_\_\_\_\_\_\_\_ destroys T-Helper cells
HIV
80
A defficiency of these T- Cells will lead to autoimmune deseases
T- Suppressor Cells
81
Compare and contrast B vs T cell functions on hypersensitivity reactions
**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
Compare and contrast B vs T cell functions on transplant
B cells are responsible for hyperacute organ rejection while T-cells play an important role in organ (allograft) rejection (acute and chronic)
83
Major Functions of B and T Cells
84
Antibody mediated immunity vs cell mediated immunity
85
Describe the sequence of events in antibody mediated immunity
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
Describe the sequence of events in cell mediated immunity
1-3. is same as antibody-mediated immunity
4. Antigen-MHC II complex react with T-helper lymphocytes
5. T-helper cells are activated by interleukin (IL-1) produced by macrophages. T-helper cells perform following functions:
1. −Produce IL-2 and gamma-interferon: activates macrophages and cytotoxic T-cells (CD8) ; increase killing efficiency of intracellular bacteria
2. −Help B cells to make antibodies
3. −Convert B cell to Plasma Cells- “factories of antibodies”
87
After activaton by IL-1 produced by macrophages, T-helper cells perform what 3 functions in cell mediated immunity
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
What is the action of IL-2 and gamma - interferon produced by T-heper cells
1. Activates macrophages and cytotoxic T-cells (CD8)
2. Increase killing efficiency of intracellular bacteria
89
After reaction of T-helper cell with Antigen-MHC II complex in antibody mediated immunity, what follows
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
Very high quantity of plasma cells
Multiple myeloma
91
Describe
Multiple Myeloma
1. Plasma cell tumor
2. Punched out lesions of skull
* Plasma cells with off-center nucleus (eccentric)*
92
Deferentiate between A.Primary response (immediate) and secondary response (delayed)
**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
Name labeled curves
A. IgM
B. IgG
C. Total
94
Name labeled curves
A. IgM
B. IgG
C. Total
95
ANTIBODIES
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
Name the 5 classes of antibodies
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
Main Ab in secretions
**IgA**
1. ****Main Ab in secretions
2. Protect mucous membrane from attack by bacteria and viruses.
3. Prevent attachment of bacteria and viruses
98
most abundant antibody
**IgG**
1. most abundant
2. opsonizes bacteria
3. neutralizes toxins
4. cross the placenta
5. provide immunity to infant
*Ig**G** crosses the placenta during **G**estation.*
99
This antibody's function is unclear
IgD
100
This antibody mediates immediate hypersensitivity reaction
**Evil antibody IgE**
1. Mediates immediate hypersensitivity reaction
2. Release Histamine, SRS-A from mast cells and basophils upon exposure to allergens
101
This part of the antibody activates compliment and binding to cell surface receptor
Constant portion
102
This part of the antibody recognizes antigen
Variable portion
103
Complement System
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
\_\_\_\_\_\_\_\_ and \_\_\_\_\_\_\_\_\_act as antigen presenting cells (APC)
Macrophage and dendritic cells
105
APCs present _______ along with _______ to T cells
antigen
Major Histocompatibility Complex proteins- MHC
106
Describe 2 types of MHC proteins
**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 CD**8** MHC **II** goes with CD**4**. Remember **18** and **24***_
107
The main determinant of organ rejection is
MHC II
108
Membrane attack complex is made of?
C5-C9
109
What are the functions of compliment activation
1. Lysis
2. Chemotaxis
3. Opsonization
110
Acquired immunity sequnce of events in presence of antigens
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
7. Cytotoxic CD8 cell can also be activated by forming a synapse with an MHC-I antigen binding site on virus infected cell.
111
The activated T helper (CD4) cell do the followings:
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
T helper (CD4) is activated by
1. Cell to cell contact “signal 1”
2. IL-1 secreted by APC “signal 2”
113
This is produced by activated T helper (CD4) and acts in an autocrine fashion to cause the cell to multiply forming a clone
IL-2
114
Cytotoxic T-helper cells can be activated in which 2 ways
1. Activation by T-helper cells
2. Formationof a synapse with an MHC-1 antigen binding site on virus infected cell
115
Cytotoxic T-cells (CD8) are direct-attack killer cells “hand-to-hand combat” which can kill?
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
Cytotoxic T-Cells have\_\_\_\_\_\_\_\_\_, which binds to _______ on virus infected cell.
CD8
MHC-I
117
What is the function of suppressor T-cells
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
Interferon
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
Zileuton (Zyflo)
1. 5-lipooxigenase inhibitor
2. Prevents formation of leukotriene
3. Adverse effects: dyspepsia, arthralgia, chest pain, fever
120
Montelukast (Singulair) and Zafirlukast
1. Competitive antagonist of leukotriene on cysteinyl-leukotriene 1 receptor
2. Prevent bronchospasm, vasoconstriction and eosinophil recruitment
121
slide 67
review
122
Recombinant cytokines for clinical use in Renal cell Ca. Melanoma
Aldesleukin (IL-2)
123
Recombinant cytokines for clinical use in anemia due to renal failure
Erythropoietin
124
Recombinant cytokines for clinical use in recovery of bone marrow
Filgrastim/ Sargramostim [Granulocyte colony-stimulating factor (GCSF)]
125
Recombinant cytokines for clinical use in Hepatitis Band C, Kaposi’s sarcoma, leukemias, melanoma
a- interferone
126
Recombinant cytokines for clinical use in Multiple sclerosis
ß- interferone
127
Recombinant cytokines for clinical use in Chronic granulomatous disease
g- interferone
128
Recombinant cytokines for clinical use in Thrombocytopenia
Oprelvekin (IL-11)
129
Describe the pathophysiology of type I hypersensitivity
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
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?
−Heparin
−Histamine
−PGs
−Kinin
−PAF (Platelet activating factor)
−SRS-A (slow reacting substance of anaphylaxis)
−Serotonin
131
What are the moderate symptoms of type I reactions
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
The most common cause of type I reactions is?
Food
133
Causes of type I hypersensitivity include?
1. Food (MCC)
2. medications
3. radiocontrasts
4. blood products
5. venoms
6. bee stings
7. ragweed/molds
8. various chemicals
134
What are the type 1 hypersensitivity allergic and atopic disorders?
−Rhinitis
−Hay fever
−Eczema
−Hives
−asthma
135
What is the difference between anaphylactic and anaphylactoid reactions?
Anaphylaxis is IgE mediated whereas anaphylactoid reactions result from direc stimulation of mast cells and do not require IgE.
136
Dextran causes anaphylaxis or anaphylactoid reaction?
Anphylactoid reaction
137
Anphylactoid reaction are due to?
* 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
What is the treatment of anaphylaxis and anaphylactoid reactions?
−ABC
−Epinephrine IV or S/C
−Antihistamines
−Corticosteroids
−IV fluid , oxygen
139
60% of anaphylactic reactions are from which drugs?
Neuromuscular blocking agents with suc being the most common
140
What percentage of anaphylactic reactions is linked to latex?
17%
141
What percentage of anaphylactic reactions is linked to Antibiotics?
15%
142
What percentage of anaphylactic reactions is linked to hypnotics?
3-4% with propofol being the most common. Others are thiopental and midazolam
143
Bruton’s Agammaglobuinemia
* **B**-cell deficiency.
* X-linked.
* Associated with low immunoglobulins and recurrent **B**acterial infections after 6 months of age when maternal antibodies (IgG) decline.
144
Thymic Aplasia (DiGeorge’s syndrome)
1. **T**-cell deficiency.
2. **T**hymus and parathyroid fail to develop.
3. Present with **T**etany due to hypocalcemia.
4. Recurrent viral , fungal and protozoal infections.
145
Severe Combined Immune Deficiency (SCID)
* 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
Chronic Granulomatous disease
1. Phagocytic deficiency due to lack of NADPH oxidase (no superoxide to kill bugs).
2. Bacterial infections by staph and strep
147
Patients with this immune disorder have defective chemotaxis and elevated IgE
Job’s Syndrome
148
Patients with this immune disorder have a defect in DNA repair enzyme. They presents with ataxia, spider angioma and IgA deficiency
Ataxia-telangiectasia
149
Patients with this immune disorder have microtubular dysfunction, decreased phagocytosis which leads to recurrent bacterial infections
Chédiak-Higashi syndrome
150
Patient with this condition presents with **T**etany and has **T**- cell deficiency with undeveloped **T**hymus and parathyroid
Thymic Aplasia (DiGeorge’s syndrome):
151
Patient with this condition have recurrent **B**acterial infections every 6 months and a **B**-cell deficiency
Bruton’s Agammaglobuinemia
152
This patient has no no superoxide (NADPH oxidase) to kill bugs
Chronic Granulomatous disease
153
Cytotoxic reaction are what type?
Type II hypersensitivity
## Footnote
***Mo Tip***
154
These antibodies mediate type II reactions
IgG
IgM
155
Desease in ths hypersensitivity reaction tends to be specific to tissue or site where antigen is found.
Type II
156
IgG, IgM bind on Antigen on “enemy” cell, leading to lysis (by complement) or phagocytosis
Type II Cytotoxic
157
Patient with type II hypersensitivity presents with
−Mismatch blood transfusion
−Autoimmune hemolytic anemia
−Rh disease (Erythoroblastosis fetalis)
−Goodpasture’s disease
−ITP
−Rheumatic fever
−Grave’s disease
−Myasthenia gravis
158
Ag-Ab complexes activates which attract neutrophils; neutrophils release lysosomal enzymes Complement fixation leads to tissue damage- “collateral damage”
Type III hypesensitivity- Immune complex
159
This type of hypersensitivity is associated with vasculitis and systemic manifestation
Type III hypesensitivity- Immune complex
160
A patient with a type III hypersensitivity presents with?
−Poststreptococcal glomerulonephritis
−Serum sickness
−Arthus reaction (e.g. swelling and inflammation after tetanus vaccine)
−SLE
−Rheumatoid arthritis
161
Sensitized ‘T’ Lymphocytes encounter antigen and then release lymphokines (lead to macrophage activation)
Type IV - Delayed (cell-mediated) type
162
In this hypersensitivity immune reaction response is delayed and does NOT involve antibodies
Type IV: Delayed (cell-mediated) type
163
What is the presentation of Type IV hypersensitivity?
−TB skin test
−Transplant rejection
−Contact dermatitis (e.g. poison ivy)
−Type I DM
−Multiple sclerosis
−Hashimoto’s thyroiditis
−Guillian-Barré syndrome
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**Mo TIP: ACID**
**A**naphylaxis and Atopic (type I)
**C**ytotoxic (type II)
**I**mmune complex (type III)
**D**elayed (cell mediated) (type IV)
165
Identify A and B
A: Zileuton
B: Montelukast
166
Review slide 66and 67
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
