Week 2 Flashcards
1
Q
The immune response is part of the defense system of the body and occurs after the
A
inflammatory response
2
Q
The immune response differs from the inflammatory response in that it is
A
programmed to defend against a specific target
3
Q
In the immune response, Any nonself proteins are subject to attack (bacteria, viruses, parasites) and are termed
A
ANTIGENS
4
Q
Function of macrophages in the immune response
A
Macrophages scavenge and digest antigen during the inflammatory response
Macrophages have receptors on their surface that hold and present foreign antigen to lymphocytes in near by lymph nodes
This stimulates lymphocytes to travel to injury site seeking out antigen
5
Q
Two types of monocytes
A
Dendritic cells and macrophages
6
Q
Types of leukocytes
A
Neutrophils
Eosinophils
Basophils
Lymphocytes
Monocytes
7
Q
Principal cells of the of the immune system are the
A
lymphocytes
8
Q
Types of lymphocytes
A
Two major types of lymphocytes, B and T cells
Third type are the Natural Killer cells that act more like PMNs and Macrophages, they are NOT specific in what they attack
9
Q
Lymphocytes are derived from
A
stem cells in the bone marrow
10
Q
Lymphocytes make up how much of WBCs
A
Make up about 20 - 25% of
WBC
11
Q
Lymphocytes are located in the
A
lymph nodes, Mucosa-associated lymph tissue (Gl, respiratory, and
GU tracts), spleen, and bone marrow
12
Q
T cells mature in the
A
Thymus
13
Q
B cells are developed by
A
Developed by the fetal bone marrow and then spread to other lymph tissue
14
Q
B cells are effective against what kind of infectious agents?
A
Bacterial infections (including perio) and viruses
15
Q
2 types of B cells
A
- 1st type becomes a
PLASMA CELL when stimulated by antigens and make antibodies specific for that antigen, - 2nd type is the B MEMORY CELL which linger in the body and react quickly if the antigen appears again
16
Q
Process of B cell activation stimulates plasma cells to
A
divide and become more numerous, increasing amount of antibodies produced
Bone marrow is also stimulated to make more B cells to help with antibody production
17
Q
It generally takes about how long to build up enough antibodies to neutralize antigen
A
2-3 weeks
18
Q
Plasma cells lifespan
A
Plasma cells only live a few days
19
Q
Purpose of memory cells after death of plasma cells
A
Memory cells created as the primary response terminates
20
Q
How long can memory cells last?
A
Memory can last up to several decades in the body
21
Q
5 types of immunoglobulins, each with a different molecular structure and role
A
- IgG are the most common(75%), small molecule in tissue and circulation. Can cross the placenta. Can confer life time immunity
- IgA (15% of total) are found in saliva, tears, Gl mucosa, respiratory tract, and breast milk. Protects from inhaled and ingested antigens
IgM (10% of total) are large molecules and form quickly after antigen challenge. Provide quick, short-term protection and are replaced by IgG antibodies
IgD and IgE (less than 1% do not circulate. IgD is found on the surface of B cells and serves as a receptor and IgE binds to receptors on Mast cells during allergic reactions
22
Q
Antibodies combine with antigen forming
A
an immune complex.
23
Q
After forming the immune complex, the antibody Renders antigen
A
inactive
24
Q
Antibodies are effective against what type of antigens
A
free antigen, cannot interact with host cells that are infected T cells do that
25
Function of t cells
Two main roles
- Programmed to recognize and attack specific antigen (Cytotoxic-CD8)
- Modulate B cell antibody production by either encouraging or restraining it (T Helper - CD4 and T Suppressor-CD8)
• Produces T Memory cells which will mount a rapid response next time antigen appears
26
T cells are responsible for which type of response
Cell mediated
27
Bcells are responsible for which type of response
Humoral
28
Humoral Response
involving B cells reacting directly with freely circulating antigen
Antibodies secreted into the circulation where they bind
29
Cell-mediated or Cellular Immunity
involves the T cells
• T cells only react to antigen presented to them by Macrophages, not to freely circulating antigen like the B cell does
• T cells are then programmed to attack antigen directly (no antibodies)
• This takes a little longer than the B cell reaction (few days) so also called Delayed Immunity
30
Passive and active immunity
• Passive Immunity
- Uses antibodies produced by another
Natural or Acquired or Artificial
• Active Immunity
- Body makes its own antibodies
Natural or Acquired or Artificial
31
Microscopic view of immune response
◦ Cells:
‣ The primary cells involved in the immune response are lymphocytes B and T.
• There are three types of lymphocytes B, T and NK.
◦ B cells originate from hematopoietic stem cells in the bone marrow and mature in lymphoid tissue like in the spleen, lymph nodes and tonsils. If confronted with a free moving antigen, the B cell will be stimulated to go to the site of injury and either make B memory cells or plasma cells. The B memory cells will remember the antigen and present it to the T cell the next time. (APC) The plasma cells will be stimulated by the T cell by cytokines to produce antibodies that will form an immune complex with the antigen rendering it inactive. B cell activation also increases production of bone marrow.
◦ T cells originate from hematopoietic stem cells in bone marrow but mature in thymus and then moves to spleen. T cells have receptors that respond to antigens. Three types of T cells: T helper, T cytotoxic, T suppressor. TCR and CD3 complex essential to T cell activity. T helper (CD4 receptor) stimulate B cells plasma cells to produce more antibodies and more bone marrow. T suppressor cells suppress B cells (CD8) and T cytotoxic (CD8) kills any neoplastic or compromised cells. CD4 and 8 also determine how many T helper, T cytotoxic, T suppressor cells need to be in blood. T memory cells also function like B memory cells and store memory to respond to a previously encountered antigen.
◦ NK cells play a role in innate immune response because without reading a cells antigen it automatically kills any foreign cells. Also originates in bone marrow but unlike the other lymphocytes that are found in tissue, NK cells are found circulating the blood. Uses granules in cytoplasm to attack foreign cells.
• Make up 20-25% of WBCs.
‣ The monocytes macrophages and dendrites are also involved in the immune response.
• Macrophages also involved in immune response by phagocytizing MO and presenting the antigen to T cells. The T cells will stimulate the B cells to either become plasma cells that will produce antibodies or memory cells. The lymphocytes release lymphokines during this process to help macrophages focus on the target. But they can not remember like lymphocytes
• Dendritic cells are APC; take antigenic substances and present to lymphocytes to kick off immune response. Is a link between innate and acquired immunity. Present in tissues exposed to outside of body and present in blood immaturely. Takes antigenic substances to lymph tissue once activated. Example would be langerhans cells in oral mucosa stratum spinosum.
◦ Cytokines:
‣ Cytokines are proteins that help cells of the immune system communicate with each other and also signals (immunomodulating agents) . B and T cells produce lymphokines, monocytes produce monokines dendritic cells also produce cytokines. Cytokines also responsible for some aspects of systemic inflammatory response.
32
Immunopathology: the study of the diseases (tissue destruction) caused from the malfunctioning of immune system. Types: hypersensitivity, autoimmune, immunodeficiency
• Autoimmune disease is when the body is attacking its own antigen
• Immunodefiency is when the body no longer responds to a certain foreign antigen
• Hypersensitivity is when the body over responds to a foreign antigen; uses normal mechanisms in the immune response but exaggerates it causing immunopathologic condition and tissue damage. Antigens causing it are called allergens (encountered previously) . Sometimes too small so they have to bind with carriers (larger weight proteins in blood and skin) which are larger molecules that will help them illicit the response.
33
Type 1 hypersensitivity
What is it?
What does it do?
What it can cause?
Treatment?
‣ Type 1 (anaphylactic) immediately after exposure to a previously encountered antigen plasma cells produce IgE antibodies that bind to mast cells that will produce histamine and cause blood vessels to dilate and bronchioles to constrict. Also can cause uticaria, asthma, and hives. Need antihistamine and a corticosteroid to treat
34
Type 2 hypersensitivity
What type of antibody are seen?
What does it do?
Examples?
‣ Type 2 (cytotoxic) antibodies (Ig and IgM) binds to harmless tissue cells like red blood cells. Complement and antibodies lead to tissue damage. Example: Rh in blood incompatibility in blood transfusions, certain drug reactions, hemolytic disease of a newborn
35
Type 3 hypersensitivity
What is it?
What does it do?
Where deposits are usually found?
In what conditions or cases would we see HS #3?
What does it play a role in when it comes to periodontal tissues?
‣ Type 3 (immune complex) antibodies bind to free-floating MO antigens and make complexes that are deposited into tissues.
Complexes release tissue damaging enzymes; PMNs release lysosomal enzymes
Intitiates an acute inflammatory response via complement that attracts neutrophils, neutrophils phagocytize and die and lysozomal enzymes continue to destroy tissue
Deposits often end up in kidneys, joints, heart and small blood vessels
Fixed drug eruptions, lupus, rheumatoid arthritis, erythema multiform
Plays a role in periodontal disease
36
Type 4 hypersensitivity
What is it also called?
What does it do?
When is it seen?
What lesions can it cause?
‣ Tissues 4 (cell mediated or delayed hypersensitivity ) T cells encounter previously encountered antigen and either in response damaged tissue or recruits other cells to damage tissue. Used in tuberculosis skin test
• Called delayed because it takes 24-72 hours
• Occurs in two phases
◦ Sensitization phase:
‣ Antigen enters thru skin and is taken to nearest lymph node where memory cells are made and become localized to site
◦ Elicitation phase:
‣ subsequent exposure activations memory T cells that will then form an inflammatory response
• Seen in TB test, poison ivy, graft or organ rejection
• Can cause aphthous ulcers aka canker sores on lining mucosa
•Can cause contact dermatitis
37
Autoimmune disease definition
Can be due to___
Can be induced by__ (give specific names)
Immune system ability to distinguish self from foreign breaks down and is now attacking its own antigens. Can attack specific cells, tissue, organs and even multiple organs.
◦ Can be due to genetic factors
◦ Can be induced by microbes
‣ Streptococcal infections
‣ Epstein Barr
38
Immunodeficiency
Primary and secondary and examples
• Compromised or absent part of immune function. Infections and neoplasms develop undeterred.
◦ can be due to congenital (primary immunodeficiency) or acquired factors (secondary immunodeficiency)
‣ Primary immunodeficiency: congenital abnormality
• Results in defective functioning of at least one part of inflammatory or immune process.
• Brutons disease: the B cells don’t mature. Treated with injection of antibodies.
• Digeorge syndrome: 3rd and 4th pharyngeal pouches absent. T cells absent or diminished, lack of activity with B cells. Treatment can be with bone marrow transplant
‣ Secondary immunodeficiency : acquired after birth; conditions that weaken or stop the immune response and allow for opportunistic infections.
• diabetes, cancer, malnutrition, immunosuppressive drugs (corticosteroids, radiation and chemo) TB, HIV
39
Diseases with Immunologic Pathogenesis (10)
• Recurrent Aphthous ulcers
• Erythema Multiforme
• Lichen planus
• Reiter's syndrome
• Langerhan's cell disease/ Histiocytosis I
• Sjogren's syndrome
• Lupus Erythematosus
• Pemphigus vulgaris
• Mucous Membrane Pemphigoid
• Bullous Pemphigoid
• Bechet syndrome
40
Other autoimmune diseases (5)
41
Aphthous ulcers
What are they also called?
What precipitates outbreak?
What kind of cell are seen causing this lesion?
Where are the lesions found?
How long do they take to heal?
What are the three types?
42
Erythema Multiforme
What causes it?
What type of lesions? Where on the body are the lesions usually found? What is the common name for them?
Symptoms? (3)
Precipitating factors? (5)
Severe form name? Where lesion are found?
Treatment?
43
Lichen planus
Chronic disease affecting what part of the body?
Prevalence in the US is about __%
Most common in (what age, what gender?)
Etiology?
How are the lesions formed?
When is diagnosis made?
Charactistic lesion name and what it is (what type of lichen planus is this?)
What are some other types of lichen planus you will see?
44
Reiter’s syndrome
45
Langerhans cell disease
What it is?
What is it also called?
Usually seen in what age group?
Categories of LD
46
Other common autoimmune symptoms
47
Sjogren syndrome
48
Pemphigus vulgaris
What does it affect?
*causes what lesions?
What age range does it affect?
What sign is useful in diagnosis?
49
Mucous membrane pemphigoid
50
Bullous pemphigoid
51
Behcet syndrome
52
Difference between emerging and reemerging diseases
53
Bacteria description, metabolism, dependence on host, secretions, sensitivities, and how they are classified
54
Group A streptococci virulence, what it does to tissues, diseases it causes, sequelae possibilities
55
Impetigo type of infection, causative agent and where it comes from, how it becomes pathogenic, what kind of lesions it makes, treatment
56
Strep throat infectious agent and what is found in tonsillar region, causes, symptoms and signs, cell count?, amount of time experienced, what it can lead to, *what happens with lymph nodes
57
Scarlet fever infective agent, symptoms, type lesions and how it happens, and what it can turn into
58
Rheumatic fever infectious agent, when and why it occurs, what happens and what it leads to
59
MRSA infection what it stands for, the two types, type of lesions, what the lesions can lead to, and best way to prevent
60
Tuberculosis causative agent, how it is spread, where it lives in the body, innate defenses that are not effective, type of lesions associated, symptoms, type of hypersensitivity reaction that halts the infection, percentage of progression, when reactivation occurs, rarity of oral lesions, type of oral lesions seen and where, how to test for prior infection, test results, what is used as a follow up to test, and treatment and duration
61
Actinomycosis infectious agent, where IA comes from, how it creates disease, what it forms and lesion associated, treatment
62
Syphillis causative agent (include shape), how it is contracted, how it progresses if left untreated
63
Primary syphillis common lesion and how it happened and when, its level of infectiousness, other signs, what happens at this stage of syphillis, lesion healing with or without treatment
64
Secondary syphillis when it arises, lesions it makes on skin, oral lesions, infectiousness, when symptoms are resolved
65
Tertiary syphillis
Disease enters latency after ____phase
May last____
At this stage, can produce irreversible _______damage
Localized and destructive lesions called __occur almost anywhere
_________and ______ often sites _____ can be come perforated
Are lesions infectious?
66
Congenital syphillis How it is transmitted, what it can result in
67
Screening test for syphillis, when it is strongly positive, medicine of choice, how infectious agent reactions may react to medicine, and if and when recurrence is possible
68
Gonorrhea infectious agent, its occurrence, how it is spread, what percentage affects oralpharyngeal region and what symptoms occur in that region, what it can lead to and what treatment to prevent, and what treatment for gonorrhea in general
69
Sinusitis how common, why it occurs, treatment
70
Fungi are simple organism similar to plants but without ____
Fungi can or can’t make their own food?
Are fungi parasites?
Where do most fungi live on the human body?
Fungal infection are also called___
71
Candidiasis (moniliasis or thrush) where it is part of, what type of infection it is and under what factors is it that type of infection (10)
72
Classification of oral candidiasis (6)
73
Treatment for candidiasis
74
Deep fungal infections type of infection and where, caused by what, type of oral lesions, treatment, endemic areas for infections (include infectious agents)
75
What is the inflammatory response?
A nonspecific response to injury.
76
does the inflammatory response change based on where the injury has occured?
No, It occurs the same way no matter where in the body the injury has occurred.
77
Does the inflammatory response improve with repeated exposure?
No, it does not improve with repeated exposure.
78
What are the types of inflammatory responses? What are two types of inflammatory responses that indicate duration?
The response may be local or systemic, and it may be acute or chronic.
79
The inflammatory response is transitional. How?
changing from acute to chronic to the immune response
80
How is a inflammatory response happening in a certain tissue named?
It is named by adding 'itis' after the tissue involved.
81
What are the clinical signs of acute inflammation?
The clinical signs of acute inflammation include Pain, Heat, Redness, Swelling, and Loss of Function.
82
What is the duration of bacterial infection associated with acute inflammation?
Acute inflammation is associated with bacterial infection of 2 weeks or less.
83
What are the symptoms of chronic inflammation?
Chronic inflammation typically presents with no symptoms.
84
What is the duration of bacterial infection associated with chronic inflammation?
Chronic inflammation is associated with bacterial infection longer than 2 weeks.
85
Microscopic Events of Inflammation
1. Injury
2. Constriction of microcirculation
3. Dilation of microcirculation
4. Increase in permeability of the microcirculation
5. Transudate formation
- Transudate - Plasma w/ low protein content leaves the microcirculation
6. Increased blood viscosity
7. Decreased blood flow through the microcirculation
8. Margination (movement towards the blood vessel wall) &
pavementing (adherence to the blood vessel wall) of the
WBC
9. Emigration (WBC leave circulation & enter tissue)
10. WBC ingest foreign and dead material
11. Exudate formation
86
What percentage of blood is plasma?
55%
87
What is the water content of blood plasma?
Approximately 90-92% of blood plasma is water.
88
What percentage of blood is made up of red blood cells (RBC)?
45%
89
What percentage of blood is made up of white blood cells (WBC) and platelets?
<1%
90
What is exudate?
Fluid + Proteins from blood + Dead & Injured cells = EXUDATE
91
Why is knowing types of exudate important?
Type of exudate signals type of inflammation
92
What are the types of exudate?
1. Serous - mainly plasma fluid + proteins, clear, associated with mild injury
2. Purulent - contains lots of WBC (PMNs) and tissue debris, associated with acute inflammation (abscess and fistula)
3. Mucinous - contains lots of mucous secretions
4. Fibrinous - composed of large amounts of fibrin
93
What are chemical mediators?
Substances that start or amplify the inflammatory response.
94
Where do chemical mediators come from?
They come from the blood, endothelial cells, WBC, platelets, and microorganisms.
95
What is Histamine?
A chemical mediator released from Mast Cells.
96
What is Serotonin?
A chemical mediator released from platelets that acts like Histamine.
97
What is the Kinin System?
A system where Bradykinin acts like Histamine and causes pain.
98
What role does the Fibrinolytic System play?
Plasmin activates the clotting mechanism and the Kinin system.
99
What are Prostaglandins and Leukotrienes?
Chemical mediators released from WBC that cause continued dilation, pain, and production of MMP enzymes.
100
What are Cytokines?
Substances like Interleukin-1 (IL-1), IL-6, IL-8, and Tumor Necrosis Factor (TNF) released from WBC that cause continued movement of WBC to the area.
101
What is the first cellular component to arrive during acute inflammation?
Neutrophils (PMN) are the first to arrive during acute inflammation.
102
What types of infectious agents are neutrophils effective against?
Neutrophils are effective against bacterial and fungal infections.
103
Which cells are seen in hypersensitivity reactions?
Eosinophils are seen in hypersensitivity reactions.
104
What cellular components are involved in chronic inflammation?
Chronic inflammation involves macrophages, giant cells, lymphocytes (T & B), fibroblasts, and endothelial cells.
105
What is tissue repair?
The injured tissue undergoes repair in its attempt to restore injured tissue to its original state.
106
What must happen before the tissue repair process can be completed?
The source of injury must be removed or the injurious agents must be destroyed.
107
Do all tissue types have the ability to undergo repair?
Some tissue types have the ability to undergo repair, while other tissue types do not.
108
What happens if the source of the injury is removed?
The repair process for both types of tissue is usually completed within 2 weeks.
109
What are the three phases of the repair process?
The three phases are inflammation, proliferation, and maturation.
110
What forms the clot during healing?
A clot forms from a mesh of fibrin, platelets, and RBC. PMNs migrate to the area.
111
What is the role of macrophages in healing?
Macrophages function to debride the area and also secrete cytokines (IL-1) to stimulate growth of fibroblasts and endothelial cells.
112
What are the types of healing intentions?
Healing can be by PRIMARY, SECONDARY, or TERTIARY intention.
113
Where does healing take place?
Healing takes place in epithelium and connective tissue simultaneously.
114
What are systemic factors affecting healing?
Age, Nutritional status, Immune status, Smoking
115
What are local factors affecting healing?
Secondary infection, Tissue necrosis, Poor blood supply to area
116
What is Repair?
Repair refers to the process of restoring normal structure and function.
117
What is Regeneration?
Regeneration is the process of restoring all destroyed tissue.
118
When does Regeneration occur?
Regeneration occurs if destruction was not extensive and cells are capable of regeneration.
119
What is Fibrous Repair?
Fibrous Repair is the process of repair that involves scarring.
120
What are the stages of tissue response to injury?
Injury, Inflammation, Repair
121
What tissues are not capable of regeneration?
Brain (neurons), Cardiac muscle, Skeletal muscle
122
What is repair by regeneration?
Regeneration of normal anatomy
123
What is partial regeneration?
Partial regeneration and scarring (fibrous repair)
124
What does scarring (fibrous repair) only refer to?
Scarring (fibrous repair) only
125
Keloids
Keloid formation is a complication of the repair process that results in excessive scar tissue formation.
