Micro 2 Lecture 16

Front 1

Allergy, Hypersensitivity:

Back 1

Exaggerated, misdirected immune responses that damage self-tissues.

Front 2

Autoimmunity:

Back 2

Abnormal responses to self Ag; immune system is attacking self tissues.

Front 3

Immunodeficiency:

Back 3

Deficiency or loss of immunity.

Front 4

Cancer results from:

Back 4

A lack of Surveillance.

Front 5

What are the two main possibilities for problems with the immune system?

Back 5

Overreaction or Underreaction by the immune system that causes problems.

Front 6

Allergy aka:

Back 6

Hypersensitivity

Front 7

How many types of Hypersensitivity reactions are there?

Back 7

4; l - lV

Front 8

Autoimmunity is a type of:

Back 8

Hypersensitivity

Front 9

Describe the different Hypersensitivity Reactions:

Back 9

l - Hay Fever & Anaphylaxis
ll - Blood type Incompatibilities
lll - Rheumatoid Arthritis & Serum Sickness
lV - Contact Dermatitis & Graft Rejection

Front 10

The B Cells are responsible for which types of Hypersensitivity reactions?
Which ones are the T Cells are responsible for?

Back 10

B Cells are responsible for l - lll, because they are all antibody mediated responses.
The T Cells are responsible for type lV Hypersensitivity reactions.

Front 11

Autoimmunity falls under which type:
Overreaction or
Underreaction?

Back 11

Overreaction:
Hypersensitivity Reactions l - IV

Front 12

Describe Type l Hypersensitivity Reactions:
-What's involved?
-Severity?
-How many exposures?

Back 12

Type l Hypersensitivity Reactions are: Hay Fever & Anaphylaxis.
-Involves IgE Antibodies and Mast Cells.
-Reaction can be Localized or Systemic
-Requires two exposures to the allergen.

Front 13

The two exposures to a Type l Hypersensitivity Reaction are:

Back 13

The Sensitizing Dose &
The Provocative Dose.

Front 14

Describe the Sensitizing Dose:

Back 14

The Sensitizing Dose is the first exposure to the allergen. IgE antibodies are produced that bind to mast cells.

Front 15

Describe the Provocative Dose:

Back 15

The Provocative Dose is the subsequent exposure to the allergen where Mast Cells release chemical mediators. Chemical mediators cause various allergy symptoms.

Front 16

Define Allergen:

Back 16

An Antigen that doesn't affect non-allergic people.

Front 17

To have a Type l Hypersensitivity Reaction, you have to be exposed to the Allergen at least:

Back 17

Twice

Front 18

During the Sensitizing Dose, the B Cells produce Plasma cells that release:

Back 18

IgE antibodies instead of IgM.

Front 19

The Constant region of IgE binds to the surface of:

Back 19

Mast Cells.

Front 20

Describe the binding process involved during the Provocative Dose:

Back 20

In the subsequent exposure (Provocative Dose) to the Allergen, the Allergen binds to the IgE on the Mast Cells surface, which causes it to release chemical mediators. The chemical mediators then lead to symptoms associated with Type l Hypersensitivity Reactions.

Front 21

What are some of the Chemical Mediators released by the Mast Cells?

Back 21

-Chemokines
-Histamine

Front 22

What are the symptoms of a Type l Hypersensitivity Response?

Back 22

-Tear & mucous production
-Bronchiole constriction, coughing, wheezing
-Red, itchy rash

Front 23

Localized =

Back 23

Atopic

Front 24

What are some Localized allergic reactions?

Back 24

-Hay Fever/ Allergic Rhinitis
-Asthma
-Eczema
-Food & Drug Allergies

Front 25

Allergic Rhinitis is characterized by:
And is usually caused by:

Back 25

Breathing issues, Coughing, and Mucus & Tear production
Caused by: Inhaling an Allergen.

Front 26

Asthma is characterized by:
And is usually caused by:

Back 26

Characterized by: Severe Bronchiole constriction.
Caused by: An Inhaled or Ingested Allergen.

Front 27

Eczema is characterized by:
And is usually caused by:

Back 27

Characterized by: inflammation on the skin; Painful, Itchy Rashes.
Caused by: Direct Contact with or Ingestion of Allergen.

Front 28

Describe the genetic link to being allergic:

Back 28

If your parents have allergies, is is more likely that you will have allergies, but not necessarily to the same things.

Front 29

Describe the hormone link to allergies:

Back 29

It appears that there is a hormone link since allergies can come and go after:
-Growing up
-Going through puberty
-Menopause

Front 30

Anaphylaxis is a Type __ allergic response.

Back 30

Anaphylaxis is a Type l allergic response.

Front 31

Define Systemic Anaphylaxis:

Back 31

A systemic, often explosive reaction that involves airway obstruction and circulatory system collapse.

Front 32

Describe a systemic Anaphylaxis Response:

Back 32

Chemical mediators cause bronchiole constriction and system wide vasodilation that can cause a fatal drop in Blood pressure (shock) .

Front 33

Systemic Anaphylaxis can be deadly within:

Back 33

Minutes.

Front 34

Common Causes of a systemic Anaphylaxis Response are:

Back 34

Common causes are: Things that get injected into the circulatory system, insect stings, antibiotics or serum injections.

Front 35

What are the treatments for Type l Hypersensitivity Reactions (allergies)?

Back 35

-Avoidance of Allergen
-Steroids
-Antihistamines

Front 36

What do steroids do?

Back 36

They keep B Cells from producing IgE Antibodies & they inhibit T cells.

Front 37

What do Antihistamines do?

Back 37

They block Histamine receptors on target tissue.

Front 38

What antibodies are involved in Type ll Hypersensitivity reactions?

Back 38

IgG & IgM

Front 39

Do Type ll Hypersensitivity Reactions involve IgE?

Back 39

NO!

Front 40

IgE is only found in:

Back 40

Type l Hypersensitivity reactions.

Front 41

What is the hallmark of the Type l Hypersensitivity reaction?

Back 41

IgE.

Front 42

Describe the Type ll Hypersensitivity reaction:

Back 42

It involves IgG & IgM binding to a foreign cell which activates complement and leads to the destruction of that cell.

Front 43

What are some examples of Type ll Hypersensitivity reactions:

Back 43

Transfusion Reactions:
-ABO blood groups
-Rh Factor: Hemolytic Disease of the Newborn.

Front 44

The protein markers on RBCs are called:

Back 44

A or B antigen

Front 45

People with the A antigen on their RBCs have Type ___ blood.

Back 45

People with the A antigen on their RBCs have Type A blood.

Front 46

People with the B antigen on their RBCs have Type ___ blood.

Back 46

People with the B antigen on their RBCs have Type B blood.

Front 47

People with A and B antigens on their RBCs have Type ___ blood.

Back 47

People with A and B antigens on their RBCs have Type AB blood.

Front 48

People without the A and B antigens on their RBCs have Type ___ blood.

Back 48

People without the A and B antigens on their RBCs have Type O blood.

Front 49

People with Type A blood have Anti __ Antibodies.

Back 49

People with Type A blood have Anti-B Antibodies.

Front 50

People with Type B blood have Anti __ Antibodies.

Back 50

People with Type B blood have Anti-A Antibodies.

Front 51

People with Type O blood have Anti __ Antibodies.

Back 51

People with Type O blood have Anti-A and Anti-B Antibodies.

Front 52

People with Type AB blood have Anti __ Antibodies.

Back 52

People with Type AB blood don't have either Anti-A or Anti-B Antibodies.

Front 53

What happens if you have a patient that is Type B blood and you gave them Type A blood?

Back 53

The patients Anti-A antibodies will agglutinate the foreign RBCs and complement will destroy them leading to massive hemolysis → Hemolytic shock, kidney failure, & death within minutes.

Front 54

People with Rh Factor are said to be:
People without Rh Factor are said to be:

Back 54

Rh+
Rh-

Front 55

Most humans (85%) are Rh__?

Back 55

85% of humans are Rh+

Front 56

Rh protein on the RBC is a _____ genetic trait.

Back 56

Dominant

Front 57

Do humans already have anti-Rh antibodies floating around in their blood?

Back 57

NO; Anti-Rh antibodies are only formed after exposure to Rh+ blood by someone who is Rh-

Front 58

The only person who has Anti-Rh antibodies is:

Back 58

A Rh- person that has been exposed to Rh+ blood.

Front 59

Describe Hemolytic Disease of the Newborn:

Back 59

A Rh- mom gives birth to a Rh+ baby. She develops anti-Rh antibodies due to exposure to babies Rh antigen when blood mixes during birth. If she is ever pregnant again with an Rh+ baby, her Anti-Rh antibodies will attack the babies blood since they are small enough to pass through the placenta.

Front 60

Babies with Hemolytic Disease of the Newborn usually die, but those that survive are born without:

Back 60

any mature RBCs.

Front 61

What is done to prevent Hemolytic Disease of the Newborn?

Back 61

Rh- moms with Rh+ babies are given anti-Rh antibodies at birth to kill any fetal RBCs and prevent mom's development of Anti-Rh Antibodies.

Front 62

Type lll Hypersensitivity Reactions deal with what antibodies?

Back 62

IgG & IgM

Front 63

What is the difference between Type ll Hypersensitivity Reactions and Type lll Hypersensitivity Reactions?

Back 63

Type ll Hypersensitivity Reactions are against cellular antigens;
Type lll Hypersensitivity Reactions are against soluble antigens

Front 64

Describe Type lll Hypersensitivity Reactions:

Back 64

Antibodies bind to soluble Antigens and these immune-complexes deposit in the tissues triggering an inflammatory response that damages the tissues.

Front 65

What are some Type lll Hypersensitivity Reactions?

Back 65

Arthus Reactions & Serum Sickness

Front 66

What is an Arthus Reaction?

Back 66

When a patient gets a second injection of a vaccine at the same site, Tiny particles in the vaccine stimulate a Type lll Hypersensitivity Reaction.

Front 67

What is Serum sickness?

Back 67

The stimulation of a Type lll Hypersensitivity Reaction due to exposure to blood serum from a foreign species.
-Reaction against Proteins in Horse's Serum
-Vaccines in the past used Horse Serum
-Anti-Venom treatments use Horse Serum nowadays.

Front 68

Describe the Type lll Hypersensitivity Reaction mechanism:

Back 68

Immune complexes form that are so large they fall out of solution and get deposited in the tissue wherever they have formed and stimulate inflammation.

Front 69

Type lV Hypersensitivity Reactions deal with:

Back 69

T Cells

Front 70

Describe Type lV Hypersensitivity Reactions:

Back 70

A delayed response to Antigen involving activation of, and damage by, T Cells.

Front 71

What are some examples of Type lV Hypersensitivity Reactions:

Back 71

-Delayed allergic response
-Graft Rejection

Front 72

Describe the Delayed Allergic response & Graft Rejection of Type lV Hypersensitivity Reactions:

Back 72

Delayed Allergic response - skin response to allergens
Graft Rejection - reaction of Cytotoxic T Cells directed against the foreign cells of a grafted tissue; involves recognition of foreign MHC.

Front 73

What are some allergens that cause a delayed allergic skin response seen in Type lV Hypersensitivity Responses?

Back 73

Poison Ivy, Poison Oak, Poison Sumac, Elastic, Metal Jewelry.

Front 74

Contact Dermatitis reactions require __ reactions.

Back 74

2; the Sensitizing Dose and Provocative Dose.

Front 75

Describe the process of Contact Dermatitis reaction:

Back 75

Step 1 = Sensitizing Dose:
1) Chemical Antigens are absorbed into the skin.
2) Dendritic Cells pick up the Allergen, process it and display it on MHC Class ll to T Helper Cells. T Helper Cells are differentiated into T Helper 1 Cells and CD4+ T Memory Cells.

Step 2 = Provocative Dose:
3) Second exposure re-activates T Memory Cells which release cytokines. Cytokines attract Macrophages, activate Cytotoxic T Cells, and Trigger Inflammation.

Front 76

Describe the Graft Rejection Reaction:

Back 76

Host Cytotoxic T Cells recognize foreign MHC on the graft and recruit other immune cells. An intense immune reaction is directed against the graft tissue.

Front 77

When you take tissue from someone's own body and put it somewhere else.

Back 77

Autograft

Front 78

If an autograft isn't possible, the next best thing is an:

Back 78

Isograft

Front 79

What is an Isograft?

Back 79

When they take tissue from a twin. (Twin has same MHC)

Front 80

A graft of tissue taken from the same species.

Back 80

Allograft

Front 81

A graft of tissue taken from a different species.

Back 81

Xenograft

Front 82

When some Cytotoxic T Cells from the Donor come along with the graft and attack the new host:

Back 82

Graft Versus Host Disease (GVHD) Cytotoxic T Cells go around the hosts body attacking ALL tissues.

Front 83

Given the danger of Graft Versus Host Disease, what would be some bad organs to transplant?

Back 83

Organs that harbor Cytotoxic T Cells:
-Bone Marrow
-Thymus

Front 84

The immune system attacking self-tissue:

Back 84

Autoimmunity

Front 85

Describe what happens in Autoimmunity:

Back 85

Autoantibodies & sometimes T Cells attack self-tissue.

Front 86

What are some possible causes for an Autoimmunity malfunction:

Back 86

-lost ability to determine self vs non-self (B or T cell maturation is broken)
-mutations to TCR and BCR (after maturation)
-appropriate antigen is similar to self tissue
-Viral infection (statistical link)

Front 87

If B Cell maturation is broken you get:
If T Cell maturation is broken you get:

Back 87

If Clonal Deletion is broken you get: Autoantibodies
If Negative Selection is broken you get: T Cells that attack self-tissue

Front 88

Autoimmune diseases are much more common among:

Back 88

Females (hormone link)

Front 89

Autoimmune diseases can be _________ or _________.

Back 89

organ-specific or systemic

Front 90

What are some Systemic Autoimmune diseases?

Back 90

Systemic Lupus Erythematosus (SLE) & Rheumatoid Arthritis (RA)

Front 91

Describe Systemic Lupus Erythematosus (SLE):

Back 91

Lupus patients are making antibodies against DNA.
-Lupus Damages multiple organs
-Butterfly Rash (across nose & cheeks)

Front 92

90% of Lupus patients are:

Back 92

Women of child-bearing age = strong hormonal link to Lupus.

Front 93

Describe Rheumatoid Arthritis:

Back 93

Patients are making Antibodies against Joint Tissue.
-Causes damage all over the skeleton.

Front 94

Damage in Rheumatoid Arthritis usually starts in the:

Back 94

Hands, wrists, knees, & hips.

Front 95

Rheumatoid Arthritis is closely associated with the ________ virus.

Back 95

Epstein-Barr Virus

Front 96

Describe Type 1 Diabetes Mellitus:

Back 96

Type 1 Diabetes Mellitus patients are making antibodies that attack the Islet cells of the pancreas which make insulin. Without insulin, the cells of the body cannot take in glucose from the bloodstream.

Front 97

List the Autoimmune Diseases:

Back 97

-Systemic Lupus Erythematosus (SLE)
-Rheumatoid Arthritis (RA)
-Type 1 Diabetes Mellitus
-Multiple Sclerosis (MS)
-Myasthenia Gravis

Front 98

Describe Multiple Sclerosis:

Back 98

Patient is making antibodies against the myelin sheath around nerves. T Cells contribute to the destruction of nerves.

Front 99

Describe Myasthenia Gravis:

Back 99

Patient is making antibodies against Ach receptors which prevents neural signals from reaching muscles.
-Muscle paralysis ensues.

Front 100

What virus has been associated with Myasthenia Gravis?

Back 100

Herpes Virus 6

Front 101

Define Immunodeficiency:

Back 101

Components of the Immune response system are absent or not functioning.

Front 102

What are the two types of Immunodeficiency:

Back 102

Primary immunodeficiency or Secondary immunodeficiency

Front 103

What is the difference between Primary immunodeficiency and Secondary immunodeficiency?

Back 103

Primary immunodeficiency is a genetically based lack of immunity.
Secondary immunodeficiency is acquired; due to damage after birth:
-Infections (HIV)
-Cancer (bone marrow, thymus)
-Drugs (Chloramphenicol)
-Radiation

Front 104

What are some examples of Primary immunodeficiencies:

Back 104

-DiGeorge Syndrome: No thymus develops=no T cells
-Agammaglobulinemia: patient can't make antibodies
-Severe Combined Immuno-Deficiency (SCID): lack of stem cells that produce B and T Cells = No Specific Immunity (bubble boy)

Front 105

What are some examples of Secondary Immunodeficiencies?

Back 105

HIV & Cancer

Front 106

Define Cancer:

Back 106

When a cell divides repeatedly in an uncontrolled manner forming a tumor.

Front 107

A mass of cancerous cells:

Back 107

a tumor

Front 108

Tumors can be:

Back 108

Benign or Malignant

Front 109

Benign means:
Malignant means:

Back 109

Benign means: Tumor doesn't impede tissue function.
Malignant means: Tumor does impede tissue function.

Front 110

Define Metastasis:

Back 110

When little pieces of a tumor break off and form new tumors in new locations.

Front 111

The loss of cell cycle control in a cancerous cell can occur because of:

Back 111

-Gene expression in the cell (Genetic factors)
-Viral infections (HPV = cervical cancer, Hepatitis = liver cancer)
-Environmental factors (acrylamide, asbestos, smoking)

Front 112

What is the normal process for cancer in the body?

Back 112

The Cell-Mediated immune system does surveillance around the body and normally, Cells with cancerous proteins are destroyed.

Front 113

Why does the risk for cancer increase dramatically for Immune compromised patients?

Back 113

Because immunocompromised patients lack adequate surveillance.