Module 7 - Immunity

Question 1

Protection from infectious disease by a collective, coordinated response of the cells and molecules of the immune system

Answer 1

Immunology

Question 2

Innate

Answer 2

-AKA Natural or native
-First line of defense
-Early, rapid
-Recognizes self vs. non-self, prevents establishment of infection
-Includes:
Skin, Mucous membranes, Phagocytic leukocytes, natural killer cells, plasma proteins (complements)

Question 3

Adaptive

Answer 3

-AKA specific or acquired
-Second line of defense
-Slower, more effective
-Recognition, plan, attack
Two types of responses:
-Humoral: B lymphocytes antibodies
-Cell-mediated: T lymphocytes activate phagocytes or kill host cells

Question 4

Antibodies

Answer 4

IgG (most abundant - crosses placenta)
IgA
IgM (first circulating Ig to appear in response to an antigen and it the first antibody type made by a newborn)
IgD
IgE

Question 5

Adaptive: Humoral

Answer 5

• Defend in blood and mucous
• B lymphocytes produce antibodies
• B cells recognize antigen –> into plasma cells, then secrete antibodies
• Antibodies bind to microbes before they invade tissue and mark microbe for destruction

Question 6

Adaptive: Cell-Mediated

Answer 6

• Inside the cell where antibodies can’t get to
• T lymphocytes recognize APC
• Helper T Cells: Help out B cells w/ antibody production and phagocytes destroy their contents
• Cytotoxic T Cells: Kill intracellular microbes

Question 7

Factors Affecting Immune Response

Answer 7

• Age (Newborn/Elderly)
• Nutritional Status (Malnutrition, Excess Adipose Tissue - chronic inflam response)
• Stress

Question 8

Rapid reaction to exposure to antigen, can be within minutes, range in severity from rhinitis to anaphylaxis

Answer 8

Immediate Hypersensitivity (IgE
0

Question 9

Inflammatory response that takes 24-72 hours to develop in response to activated mononuclear lymphocytes; exemplified by the tuberculin skin test

Answer 9

Delayed (Type IV) Hypersensitivity

Question 10

Life-threatening hypersensitivity manifested by widespread edema, bronchospasms, and vascular shock secondary to vasodilation (histamines)

Answer 10

Systemic Anaphylaxis

• previous exposure to antigen creates IgE
• Level of severity dependent on level of sensitization to antigen

Question 11

Symptoms of Anaphylaxis

Answer 11

Hives, itching, difficulty breathing, vomiting, cramps, diarrhea, edema, and obstruction of the airway

Question 12

Common Antigens in Systemic Anaphylaxis

Answer 12

Food
Insects
Drugs
Latex

Question 13

_____ are potent vasodilators that respond to antigen exposure within 5-30 minutes, increasing capillary permeability and smooth muscle contraction and bronchoconstriction

Answer 13

Histamines

Question 14

___________ block histamine release and treat symptoms such as edema, rhinitis, hives, etc.

Answer 14

Antihistamines

ex. Benadryl, Claritin, Zyrtec
- caution pt about drowsiness

Question 15

• Breakdown in the body’s ability to differentiate b/w self and non-self antigens
• Specific cause is unknown, could be genetic and/or environmental (includes infectious agents)

Answer 15

Autoimmune Disorders

-can affect almost any type of cell or tissue in the body

Question 16

Treatments of Autoimmune Disorders

Answer 16

Immunosuppressive agents

Steroids

Question 17

Work by preventing DNA synthesis in immune cells, preventing replication and eventually causing cell death

Answer 17

Immunosuppresive Agents

Question 18

• Works by suppressing inflammatory response that characterizes disorders such as rheumatoid arthritis and lupus
• Can have severe side effects depending on dosage and length of therapy

Answer 18

Steroids

Question 19

Primary Immunodeficincies

Answer 19

• Congenital/inherited
• Etiology: Genetic (recessive, X-linked or autosomal mutations)
• Patho: mutations affect signaling pathways that dictate immune cell development/symptoms of A.I disorders
• Clinical consequences: early detection is critical, types of infection help diagnose, family trees are important, can be fatal in early childhood

Question 20

Secondary Immunodeficincies

Answer 20

• Acquired (AIDS is the most common)
• Etiology: pathogen, aging, malignancies, malnutrition, drugs
• Patho: IgG loss, T cell deficit, wbc dysfunction
• Clinical consequences: no cure, immunosuppressed, congenital transmission is possible

Question 21

HIV develops into Acquired Immune Deficiency Syndrome in the presence of a CD4 count below ___ and /or an ______ ______

Answer 21

below 200

opportunistic infection

Question 22

HIV is transmitted through ____, _____, _____ ____, _____

Sexual contact is the most common method

Answer 22

Blood
Semen
Vaginal Fluid
Breastmilk

Question 23

HIV is a _______ that infects certain cells (CD4 T Cells, macrophages, dendritic cells)

The death of these types of cells create decreased immune response even if the person is asymptomatic, creating susceptibility to many illnesses

Answer 23

Retrovirus

Question 24

Stages of HIV

Answer 24

• Primary Infection
• Latency (Chronic, asymptomatic)
• AIDS (HIV, CD4 below 200 +/ opportunistic infection)

Question 25

Antiretrovirals

Answer 25

- Decrease the amount of virus in the body | - 5 classes: each class attempts to interrupt the life cycle of the virus at different points

Question 26

Combination therapy is ideal, usually at least 3 drugs called:

Answer 26

HAART Highly Active AntiRetroviral Therapy Goal is undetectable viral load and increasing CD4 count