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Advanced Pathophysiology > Inflammation and Immunity > Flashcards

Inflammation and Immunity Flashcards

1
Q

What are the major organs of the immune system?

A

Tonsils and adenoids, thymus, lymph nodes, lymphatic vessels, appendix, bone marrow, spleen, Peyer’s patches

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2
Q

Name the innate and adaptive cells of humoral (antibody mediated) immunity.

A

Innate: Myeloid cells (non-host epitopes)
Adaptive: B cells (antibodies, also T helper cells, and APCs)

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3
Q

Name the innate and adaptive cells of cell mediated immunity.

A

Innate: NK cells (MHC existence)
Adaptive: T cells (MHC1-TCR)

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4
Q

What is the body’s first line of defense?

A

The skin and mucous membranes.

They act as a physical barrier as well as an antimicrobial peptide barrier

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5
Q

Review the leukocytes involved in immune function and the inflammatory process.

A

Neutrophils
Monocytes/macrophages
Eosinophils
Basophils

{Platelets and erythrocytes
(all formed from myeloid stem cell)}

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6
Q

What types of leukocytes are the first to appear after injury?

A

Neutrophils

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7
Q

What role do each of the leukocytes play in inflammation?

A

Neutrophils: first responders/begin phagocytosis
Macrophages- Ingest microbes and clean up debris after inflammatory response
Eosinophils- degranulate releasing cytotoxic chemical enzymes
Basophils/mast cells- degranulate releasing pro-inflammatory mediators

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8
Q

Describe the concept of a ‘shift to the left of normal’

A

This shows more circulating immature cells known as band cells which indicates increased neutrophil production and acute infection.

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9
Q

Outline the 3 major types of lymphocytes.

A

NK cells
T Cells- Helper CD4 and Cytotoxic CD8
B cells

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10
Q

How do the lymphocytes specifically recognize foreign pathogen?

A

NK cells- innate immunity
Helper T cells(CD4)- via APC (B cells). Helper T cells recognize sequences on the MHC II and active an immune response triggering the release of lymphocytes to respond to a foreign pathogen.
Cytotoxic T cells(CD8)- Recognize the self sequences on the MHC I, if not recognized they active and eliminate.
B cells- Receptors allow B cells to recognize foreign epitopes (specific antigen) and bind/engulf to present to helper T cell. T cells recognize protein are then activated. Exposure to antigens prompts B cells to mature into antibody secreting plasma cells and memory cells.

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11
Q

What is the difference between MHC I and MHC II?

A

MHC I are surface proteins on the body’s cells indicating the cells belongs there-‘self’. (recognized by cytotoxic T cells and NK cells)

MHC II are surface proteins that bind with antigens and display them for helper T cells. in order to active the immune system (displayed by dendritic, macrophages and B cells and recognized by helper T cells)

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12
Q

Innate and specific/adaptive immunity are different because:

A

Innate immunity is nonspecific and caused by an immediate degranulation response, while adaptive immunity is mediated by specific B and T cells based on a prior exposure.

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13
Q

Antibodies have two regions:

A 
Constant: determines the class of antibody
Variable: contains the sequence specific to the antigen/epitope
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14
Q

What does the complement system do?

A

The complement system enhances the body’s response to foreign invaders: inflammation, chemotaxis, and lysis of target cells.

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15
Q

What are the different pathways of the complement system and how are they activated?

A
  • Classical pathway- Activated by the C1 protein. Presence of an Ab is essential (IgG or IgM)=formation of antibody-antigen complex.
  • Alternative pathway- Activated by C3 protein. Ab not need-can be activated on first exposure to antigen. Triggered by lipopolysaccharide in Gram neg bac walls and bac endotoxin.
  • Lectin pathway- Activated by C2 and C4. Ab not need, can be activated on first exposure. Triggered by binding mannose on bacterial walls.
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16
Q

What are Kinins?

A

Small polypeptides that cause powerful vasodilation, increased vascular permeability and smooth muscle contraction when activated during inflammation. They are also responsible for pain.

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17
Q

How are the kinin and clotting systems linked?

A

Both the kinin and clotting system are activated by Factor XII (Hageman factor).

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18
Q

How is the complement system controlled?

A

Enzymes in plasma degrade activators and a number of inhibitory proteins are released. Ex- protein S prevents the complement membrane attack from attaching to and lysing cells.

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19
Q

Where are B and T cells produced and where do they mature?

A

B cells- Produced and mature in bone marrow

T cells- Produced in the bone marrow and mature in the thymus

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20
Q

What is clonal diversity?

A

All different types of T and B cells are randomly produced to have a receptor specific to one particular antigen. The specificity of an antigen is acquired upon formation of the cell.

21
Q

What is clonal selection?

A

The theory that illustrates the selection of T and B cells that are specific to a particular antigen. This in turn causes proliferation/differentiation of that one particular T or B cell to create an army to fight off the recognized antigen

22
Q

What is central tolerance?

A

Recognizing self antigens and not reacting to them. During the formation process in the generative organs lymphocytes are put through rigorous testing. Those that recognize self as a foreign antigen and have potential to attack self are eliminated via negative selection.

23
Q

What is peripheral tolerance?

A

This same process of negative selection of self tolerance that happens in peripheral tissues.

24
Q

What is SCID?

A

Severe combined immunodeficiency. Common lymphoid stem cell is absent=T, B, and in some case NK cells never develop. Most severe form is reticular dysgenesis. ‘boy in the bubble.’

25
Q

Describe Hypersensitivity Type I:

A
  • *IgE response to antigens (allergens)
  • immediate reaction
  • pl. B cells produce allergen specific IgE over repeated exposure IgE levels increased=increased response
  • *Mast Cells- activated by IgE antigen binding to IgE receptor site induces degranulation= histamine release, cytokines, arachidonic acid, protease, etc.
26
Q

Describe Hypersensitivity Type II:

A
  • *IgG and IgM
  • *Tissue specific- antibodies that attack antigens on the surface of specific cells or tissues.
  • Ex- bl. transfusion reactions, hemolytic disease of the newborn, IMMEDIATE significant graft rejection (host vs graft) all of these are examples of alloimmunity.
27
Q

What is Alloimmunity?

A

A condition in which the immune system reacts against antigens of tissues from other members of the same species

28
Q

Describe Hypersensitivity Type III:

A
  • *IgG and IgM (IgE)
  • *Systemic
  • *Failure of immune/phagocytic systems to effectively remove antigen-antibody complexes which are then deposited into tissues causing activation of the complement system and sustaining inflammation (immune mediated)
  • *Ab complexes carried in blood= can be distributed all over.
  • *Not immediate
  • Ex- lupus (SLE)
29
Q

Describe Hypersensitivity Type IV:

A
  • *T lymphocytes- cell mediated, no primary antibody
  • *Antigen stimulates T cells to differentiate into cytotoxic T cells and helper T cells
  • *Delayed onset
  • Ex- delayed rejection (graft vs. host), contact dermatitis
30
Q

What is a primary immune disorder?

A

Congenital phenotypes that result from abnormal development or maturation of immune cells (ex SCID) and primary disorders of immune cells (ex HIV/AIDS)

31
Q

What is a secondary immune disorder?

A

Acquired: Physical, psychosocial, nutritional, environment and pharmacological factors that negatively affect the immune system an alter its function.

32
Q

Blood types:

A

A: has A antigen and anti B Ab
B: has B antigen and anti A Ab
AB: A and B antigen and no Ab (universal recipient)
O: No antigens and both A and B Abs (universal donor)

33
Q

What is the hallmark of immunodeficiency?

A

Recurrent infections, often with opportunistic organisms.

34
Q

T cell deficiencies:

A

**Viral, fungal, and atypical microorganisms
-DiGeorge syndrome (no thymus/no func of thymus)
Chronic mucocutaneous candidiasis

35
Q

B cell and phagocyte deficiencies:

A
  • Microorganisms requiring opsonization
  • Bruton’s agammaglobulinemia (Xlinked)
  • Common variable immunodeficiency
36
Q

Complement deficiencies:

A
  • Present like Ab deficiencies
  • C3 deficiency is most severe
  • Mannose-binding lectin (MBL) deficiency
37
Q

What is the pathologic progression of disease?

A

Colonization (benign or not)
Invasion
Multiplication
Spread

38
Q

Describe the clinical progression of infectious disease:

A
  1. Invasion of pathogen
  2. Incubation period
  3. Prodromal period (subclinical or non-specific s/s)
  4. Illness period
  5. Convalescent period (s/s receding)
  6. Host eradicate disease or becomes carrier
39
Q

Gram positive bacteria:

A

Thick cell walls. Produce and release exotoxins during bacterial growth.

40
Q

Gram negative bacteria:

A

Thin cell walls and lipopolysaccharide (LPS) coat which produces endotoxins when they die)

41
Q

TRUE or FALSE: Fungal Infections are controlled by phagocytes and T lymphocytes.

A

TRUE

42
Q

Why are systemic fungal infections in humans difficult to treat?

A

Fungi have thick outer cell layer and are able to adapt. They have similar properties to the human hosts cells so the agents used to treat have serious side effects.

43
Q

Describe the viral life cycle:

A

Virion binds to a host cell receptor causing an enzyme release allowing for penetration. Once inside the cell the virion uncoats itself and enters the nucleus where it replicates and matures. Once matured it exits the nucleus and moves toward the cell surface where it causes budding and more viruses are released in the hosts system.

44
Q

DNA virus:

A

Provirus

  • Enters the host cells nucleus and becomes integrated into the chromosomal DNA
  • Is transcribed into mRNA before protein translation
  • Viral DNA that has integrated with host DNA is transmitted to daughter cells during mitosis= can pass to offspring
45
Q

RNA virus:

A

Directly produce mRNA
-Translated in viral proteins and genomic RNA, eventually packaged into new viruses
Retroviruses carry the enzyme reverse transcriptase that creates a double stranded DNA version of the virus (ex HIV)

46
Q

HIV’s entry into the cell:

A

HIV membrane fuses with the host cell membrane gaining entry to the host cell’s cytoplasm. Once inside the HIV RNA uses reverse transcriptase to form a proviral dsDNA and integrates into the host cells DNA.

47
Q

What is a plasma cell?

A

An activated B cell that can synthesize and release antibodies. This process of B cell activation is ‘helped’ by the helper T cells.

48
Q

Primary immune response Ab:

A

IgM. Forms as a pentamere= higher change to recognize Ab.

49
Q

Which Ab is often found in our ‘tracts’ (resp/GI)

A

IgA. Dimer

Advanced Pathophysiology (12 decks)

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