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Term 3: Immunology/Pathology > Immune System Diseases > Flashcards

Immune System Diseases Flashcards

1
Q

Difference between primary and secondary immunodeficiency syndromes?

A
  • Primary = inherited

- Secondary = acquired

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2
Q

What are the 5 major risk groups of adults at high risk of developing AIDS?

A
  • homosexual/bisexual men (50%)
  • IV drug users (not homosexual) (20%)
  • Recipients of blood and blood components who are not hemophiliacs (1%)
  • Heterosexual contacts of members of other high risk groups (20%)
  • HIV infection of the newborn (2% under 13 y/o) =placental transmission
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3
Q

What are the two ways in which HIV viral transmission occurs?

A
  • Direct inoculation into the blood vessels by trauma

- infection of dendritic cells or CD4+ cells within the mucosa

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4
Q

Sexual transmission of HIV is _________ by coexisting sexually transmitted diseases especially those associated with genital ulceration.

A

Enhanced

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5
Q

HIV is a non-transforming human retrovirus belonging to the lentivirus family, meaning:

A

-it will not transform normal cells into cancer cells

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6
Q

What is the structure of the HIV virus?

A
  • Spherical

- electron dense core surrounded by a lipid envelope derived from host cell membrane

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7
Q

What is contained within the HIV core?

A
  • The major capsid protein p24
  • Nucleocapsid protein p7/p9
  • Two copies of viral genomic RNA
  • The three viral enzymes protease, reverse transcriptase and integrase
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8
Q

Why is research of HIV so complicated?

A

-there are a butt load of subtypes

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9
Q

What are the two main targets of HIV infection?

A
  • Immune system

- CNS

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10
Q

Describe the pathogenesis of HIV.

A
  • Profound immune deficiency, primarily cell-mediated immunity
  • results from infection and loss of CD4+ T cells and impairments of surviving Th cells
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11
Q

Describe the life cycle of HIV.

A

Consists of infection of cells, integration of the provirus into the host cell genome, activation of viral replication, and production and release of infectious virus

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12
Q

What does gp120 bind to?

A

CD4

CCR5 & CXCR4

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13
Q

Describe the process of HIV entering a cell.

A
  • gp 120 binds CD4
  • gp120 & CD4 binds CCR-5 receptor (on T cell)
  • leads to fusion to host cell
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14
Q

Why are naive T cells difficult for HIV to infect?

A
  • they contain an active form of an enzyme that introduces mutations to the HIV genome
  • they don’t express CCR5 & CXCR4
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15
Q

Can macrophages and dendritic cells also be infected by HIV?

A

-Yes

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16
Q

Why can’t B cells produce antibodies to HIV

A

-They don’t have the T cells to stimulate them

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17
Q

What are the three phases of the clinical manifestations of HIV?

A
  • An acute retroviral syndrome
  • Middle chronic phase
  • Clinical AIDS
18
Q

What is the initial clinical presentation of the initial viremia of HIV?

A
  • Acute retroviral syndrome
  • 3-6 weeks after infection
  • nonspecific symptoms including sore throat, myalgias, fever, weight loss, and fatigue similar to the flu
19
Q

Describe the middle chronic phase of HIV infection.

A
  • In the next phase of the disease lymph nodes and spleen are sites of continuous HIV replication
  • during this phase of the disease there are little or no clinical symptoms
  • However the infection is killing off T cells and over years the CD4+ T cells drop to insufficient numbers
20
Q

Describe the AIDS stage of HIV infection.

A

The final progression is to AIDS, characterized by a breakdown of host defense, a dramatic increase in plasma virus, and severe, life threating disease

21
Q

Why does it take at least 6 months (of age) for a primary immunodeficiency to show up?

A

-Momma’s antibodies

22
Q

What is the difference between Type I and Type II leukocyte adhesion defects?

A

Type I: Defect in synthesis of Beta2 chain shared by integrins

Type II: Defects in selectins

23
Q

What is Chediak-Higashi syndrome?

A
  • defective fusion of phagosomes and lysosomes, resulting in defective phagocytic function and susceptibility to infection
  • main abnormalities: neutropenia, defective degranulation, and delayed microbial killing
24
Q

Why does Chediak-Higashi syndrome result in neutropenia?

A

-need to phagocytose bacteria to create cytokine signals to attract neutrophils

25
Q

What is chronic granulomatous disease?

A

-defects in bacterial killing due to defects in gene encoding components of superozide

26
Q

What is the most common compelement deficiency?

A

-deficiency of C2

**many pts have no clinical manifesttions, probs because the alternative pathway is adequate

27
Q

What does a deficiency in C3 result in?

A
  • susceptibility to serious pyogenic (pus generating) infections
  • Increase in incidence of immune complex-mediated glomerulonephitis
28
Q

What is SCID?

A

Severe combined immunodeficiency (SCID) represents a constellation of genetically distinct syndromes, all having in common defects in both humoral and cell-mediated immune responses

29
Q

Why do infants with SCID get a rash after birth?

A

-maternal T cells that transferred across the placenta attack the fetus

30
Q

What is the treatment for SCID?

A

-Bone marrow transplant

**without this, pt will die in first year

31
Q

Describe X-linked SCID.

A
  • The most common form, accounting for 50-60% of cases and is more common in boys than girls
  • The genetic defect is a mutation in the common gamma chain subunit of cytokine receptors in T cells
  • As a result of this defect there is a profound defect in the earliest stages of lymphocyte development
32
Q

What is X-linked agammaglobulinemia?

A
  • characterized by failure of B cell precursors to develop into mature B cells = no antibodies
  • Caused by mutation in a cytoplasmic tyrosine kinase called Bruton Tyrosine Kinase (Btk)
  • when mutated, pre-B cell receptor cannot deliver signals to nucleus and maturation stops
33
Q

What is DiGeorge Syndrome?

A

-DiGeorge sysndrome is a T cell deficiency that results from failure of development of the third and fourth pharyngeal pouches (Thymus)

34
Q

Why would DiGeorge Syndrome result in tetany?

A
  • Underdeveloped thymus means no calcitonin
  • no calcitonin means blood Ca too high
  • Causes muscle contraction
35
Q

What is Common variable immunodeficiency?

A
  • Usually a diagnosis of exclusion
  • This relatively frequent but poorly defined entity encompasses a heterogenous group of disorders in which the common feature is hypogammaglobulinema, generally affecting all the antibody classes but sometimes only IgG
36
Q

What characterizes tissue transplant rejection?

A
  • a process in which T lymphocytes and antibodies produced against graft antigens react against and destroy tissue grafts
  • Recognition of graft Alloantigens by T and B lymphocytes
37
Q

What is the major antigenic difference between a donor and recipient that results i rejection?

A

-HLA differences

38
Q

What is the direct pathway of allorecognition by T cells in organ transplant?

A
  • T cells of the transplant recipient recognize allogenic (donor) MHC milecules on the surface of APCs in the graft
  • It is believed that dendritic cells carried in the donor organs are the most important APCs for initiating the antigraft response, because they not only express high levels of class I and II MHC molecules but also are endowed with costimulatory molecules
39
Q

What is the indirect pathway of allorecognition by T cells in organ transplant?

A
  • In the indirect pathway, recipient T lymphocytes recognize MHC antigens of the graft donor after they have presented by the recipient’s own APCs
  • This process involves the uptake and processing of MHC molecules from the grafted organ by host APCs.
40
Q

Acute cellular rejection is most commonly seen within the initial months after transplantation. What triggers this response?

A

-this process is an inflammatory reaction in the graft triggered by cytokines released by activated CD4+ T cells

Term 3: Immunology/Pathology (17 decks)

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