Pathophys Exam 2 (1 Of 3) - Immunology

Front 1

What is the difference between active acquired immunity and passive acquired immunity in terms of longevity of immunity?

Why is this?

Two examples of each.

Back 1

Active acquired immunity
-have the rest of your life
-It is natural exposure
-mumps / chick pox / measles / immunization
-produces memory B-cells and T-cells.

Passice acquired immunity
-last 7-10 days and are metabolized
-Performed antibodies infused into patient
-mother antibodies from milk/placenta
-antiserum (tentanus, botulism, snakebite)

Front 2

Distinguish between primary and secondary immune responses in terms of:

response time;

Back 2

Primary: 5 days

Secondary: <24hrs

Front 3

Distinguish between primary and secondary immune responses in terms of:

types of antibodies involved;

Back 3

Primary: IgM (priMary response)

Secondary: IgG (Gail has the GOOD stuff)

Front 4

Distinguish between primary and secondary immune responses in terms of:

levels of antibodies in the blood.

Back 4

Primary: IgM (pri-M-ary response) -- low levels

Secondary: IgG (Gail has the GOOD stuff) -- higher levels

Front 5

What are lymphocytic stem cells?

Back 5

naive B-cells / T-cells made in bone marrow

Front 6

Are lymphocytic stem cells immunocompetent?

Back 6

NO

Front 7

What is meant by the term “immunocompetent”?

Back 7

B-cells / T-cells that can respond to an antigen

Front 8

Where do lymphocytic B stem cells become immunocompetent?

Back 8

bone marrow

(bursal equivalent)

Front 9

Where do lymphocytic T stem cells become immunocompetent?

Back 9

thymus

(process of Pos/Neg selection)

Front 10

What types of immunocompentent T cells are produced in the thymus?

Back 10

cytotoxic T cells (T8, CD8, CTL, Tc, CTC)

T helper cells (T4, CD4, Th)

Front 11

MHC (major histocompatibility complex) Class I molecules are encoded in what region?

Back 11

HLA-A, HLA-B, HLA-C region of the MHC complex on human chromosome 6

Front 12

MHC (major histocompatibility complex) Class II molecules are encoded in what region?

Back 12

HLA-DP, HLA-DR, HLA-DQ of the MHC also on human chromosome 6

Front 13

On what cells are MHC Class I molecules found?

Back 13

ALL cells in body EXCEPT red blood cells (RBC).


(RBC have ABO/Rh+ instead of HLA/MHC I)

Front 14

On what cells are MHC Class II molecules found?

Back 14

1. B-cells

2. Antigen Presenting Cells (APC)
-macrophages
-dendritic cells.

Front 15

Know the 7 steps in the activation of the humoral arm of the immune system.

Back 15

1. APC phagocotize antigen (e.g. virus)
2. APC processes antigen --->> MHC class II
3. APC+MHC class II --->> travels to lymph node, secretes Interleukin-1
4. Th2 with CD4, binds to MHC class II
5. Th2 activated (interleukin-1/MHC class II): mitotic division + seeks out B-cell with same antigen on MHC class II
6. activated Th2 / B-cell + cytokines --->> activates B-cell
7. activated B-cell --->> Plasma cells / Memory B Cells

Memory B cells distribute throughout body

Front 16

What are the two “working ends” of an antibody?

Back 16

Fc (crystalline fragment)

Fab (antigen binding site)

Front 17

What are the three possible actions of the Fc end of the antibody?

Back 17

-Binding to surface
-PMNs (neutrophils and eosinophils)
-Mast cells
-Initiates Opsonization

-transport IgG: across placenta / Milk into fetal circulation

-activate complement system ("classic" antibody dependant, C1-complex)

Front 18

Characteristic/description of immunoglobulins

IgM

Back 18

10 binding sites

secreted EARLIER in primary immune response

does not have high affinity for antigen
(because the B-cells have not gone through affinity maturation)

Front 19

Characteristic/description of immunoglobulins

IgG

Back 19

2 antigenic binding sites

secreted LATER in the primary immune response
(after B-cells have gone through affinity maturation)

Front 20

Characteristic/description of immunoglobulins

IgA

Back 20

Secreted by B-cells on the submucosal regions of the intestine and repiratory mucosa

Has a J chain that holds two subunits

Front 21

What subset of helper T cells plays a major role in activating the cytotoxic arm of the immune system?

In the Humoral arm?

Back 21

Th1 - cytotoxic

Th2 - humoral arm

Front 22

What are the main target cells for CTLs (CD8, Tc, CTC, T8)?

Back 22

viral infected
-measles, mumps, influenza, H1N1, H5N1
bacterial infected
-reckettsiae, chlamydia, tuberculosis
protozoal parasites
-malaria
allographs
-foreign HLA I / II antigens
Cancer cells

Front 23

What are the two routes in which cytotoxic killer cells (Tc, CTC) are activated?

Back 23

1) Th1 independent:
APC presents antigen on MHC class I
+other cytokines and molecules
activates naive Tc cell

2) Th1 dependent
APC presents antigen on both MHC class I / II
Th1+MHC II --->> IL-2
naive Tc / MHC I + IL-2 --->> activated Tc

Front 24

How do CTLs recognize a cell infected with a virus?

Back 24

By “Docking “to virally infected cell that is presenting a piece of the virus on its class I antigen

Front 25

How do CTLs (Tc, CD8, CTC, T8) kill the target cells?

Back 25

A)
dock with MHC class I

B)
Perforin/Granzyme killing
FasL/Fas Killing

Front 26

Explain the process of Perforin/granzyme killing

Back 26

1. Tc CD8 binds to MHC Class I w/ antigen presenting
2. Tc release perforin / granzymes
3. perforin makes holes in target
-cell lysis
4. granzymes enter target thru perforin holes
-caspase cascade leads to apoptosis

Front 27

Explain the process of FasL/Fas killing

Back 27

1. Tc CD8 binds to MHC Class I w/ antigen presenting
2. Tc FasL binds to target cell Fas
-leads to apoptosis

Front 28

What are natural killer (NK) cells?

Back 28

Natural killer (NK) cells are:

-a lymphocyte that is neither T4, T8, nor a B-cells
-already specialized to kill certain types of
viral infected
cancer cells

Front 29

Explain how NK cells kill it’s target cell via the killer activating receptor/killing inhibitory receptor.

Back 29

NK + viral/cancer cells with:

+STRESS protein
--MHC class I (inhibits)

kills via perforin/granzyme

Front 30

List and explain the 5 major changes that occur to the immune system with aging

Back 30

Thymus shrinks (thymic involution)
Lower naive:memory T cells ratio (b/c shrinking thymus)
Decrease Receptor CD28 (T cell can't activate)
T cell: reduced IL-2 (can't make, nor respond)
less T cell function = less B cell activation

Front 31

What type(s) of antibodies are found in the serum of the following blood types:

A, B, AB, O?

Back 31

A: anti-B
B: anti-A
AB: (none) -- universal receiver
O: anti-A/anti-B -- universal donor

Front 32

When do the ABO antibodies develop within a person?

Back 32

around 6 months following birth

Front 33

What Class are the ABO blood group antibodies?

Back 33

A/B: IgM -- cannot cross placenta
O: IgG/IgM -- IgG can cross, may cause HDN

Front 34

In a paternity suit, the child is blood type AB and the mother is type A. The alleged father of the child is blood type O. Does the mother have a case

Back 34

NO, the true father must be blood type B/b (or B/O)

Front 35

The parents of a child are Rh-positive
yet the child is Rh-negative.

What must be the genotype of the parents?

Back 35

heterozygous D/d (carriers of the Rh- allele)

Front 36

Can hemolytic disease of the newborn (HDN) be caused by incompatibility of the ABO blood group?

Back 36

Yes

Front 37

What is the usual ABO blood type of the mother if a newborn suffers from HDN?

Back 37

Mother is type O, and child is A or B

Front 38

What characteristic of the Mother's "O" type blood, with infant "A" or "B", increases the risks for HDN?

Back 38

Mother's anti-A, anti-B (IgG) antibodies enters the fetal circulation, causing hemolysis of fetal RBCs

Front 39

In Rh-HDN, explain how sensitization occurs.

Back 39

HDN caused by Rh incompatibility:

1. maternal hemorrhage is common during labor
2. Rh D-negative mother may first encounter the D antigen

Front 40

At the time of this sensitization (i.e., first pregnancy), why can’t the Rh antibodies cross the placenta from the mother’s side and enter the child’s circulation?

What about 2nd pregnancy?

Back 40

Primary Response:
-Mother's anti-D (anti-Rh) are IgM... can't cross placenta

Secondary Response:
-subsequent pregnancies, produce anti-D (anti-Rh) IgG ... can cross placenta

Front 41

In subsequent pregnancies, HDN can cause the condition of kernicterus. What is it? How is it caused? Why is it not a problem during pregnancy? Why is it a problem after birth?

Back 41

Hemolysis due to HDN results in high concentrations of bilirubin within fetal circulation

In utero, bilirubin is cleared through the placenta

Following birth, bilirubin can accumulate in the fat tissue of the brain causing brain damage—a condition called kernicterus

Front 42

In subsequent pregnancies, HDN causes severe anemia in the fetus. Why? Why does this lead to hepatomegaly and splenomegaly?

Back 42

Lysis of fetal RBCs, can lead to anemia.
Liver/Spleen compensate by increasing size, producing more RBCs, and grow (hepatomegaly, splenomegaly)

Front 43

A complication of severe HDN causes fetal tissue to become swollen and is usually fatal—what is it called?

Back 43

hydrops fetalis, in which the fetal tissues become swollen (edematous). This condition is usually fatal, either in utero or soon after birth.

Front 44

When is Rh immunoglobulin (RhIG or RHOgam) given to the mother to prevent HDN? How does RhIG prevent HDN?

Back 44

RhIG or RHOgam are IgG anti-D antibodies that stick on the outside of any of the childs Rh-positive cells that have entered maternal circulation. This “hides” the Rh-positive antigen from the maternal immune system.The current standard is to administer RhIG to all unsensitized Rh-negative women at 28 week’s gestation with an additional dose administered soon after birth if the infant is Rh-positive.