Lecture 8 Blood: WBCs, Infection and Immunity (Ch. 34, 35) Flashcards

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1
Q

When do eosinophils increase?

A

during parasitic infection or allergy

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2
Q

Mast cells are the mature form of what WBC?

A

Basophils

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3
Q

What WBC type plays a role in attacking cancer cells?

A

Lymphocytes

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4
Q

What are the two types of acquired immunity?

A

cell-mediated (T cells) and humoral (B cells)

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5
Q

In T-cell epitope recognition; what do MHC I & MHC II do?

A

MHC I- binds CD8 co-receptors on cytotoxic T cells

MHC II- binds CD4 co-receptors on Helper T cells

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6
Q

State differences between CD4 and CD8.

A

CD4- bind MHCII to stimulate lymphokine production and B cell proliferation
CD8- binds MHC I to rapidly attack target

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7
Q

What are platelets in relation to megakaryocytes, and what are the approximate sizes of both types of cells?

A

platelets are fragments of megakaryocytes (~2 um) and megakaryocytes are ~100 um).

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8
Q

What are the key contents of platelets and their functions?

A

-thromosthenin: actin/myosin contractile proteins
-ER/GA for secretory granules
-mitochondria: ATP for clotting
-fibrin stabilizing factor
PDGF: capillary and blood vessel epithelium repair

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9
Q

What is a “band shift,” and what does it indicate?

A

A “band shift” is an increase in “band cells,” referring to the horseshoe shaped “band in neutrophils. It indicates a proliferate of neutrophils as a sign of disease.

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10
Q

Describe the inflammatory response cascade of tissue macrophages.

A
  1. increased local blood flow
  2. increased vessel permeability
  3. margination: capture of PMNs or macrophages
  4. Diapedesis: movement through vessel wall
  5. Chemotaxis to target
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11
Q

What are the chemotactic agents involved in the inflammatory response that we learned about?

A

histamine, bradykinin, serotonin, prostaglandins, cytokines, lymphokines, complement proteins, clotting components, debris

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12
Q

What is the role of bradykinin in the inflammatory response?

A

It increases vessel wall permeability and diameter

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13
Q

What effect do cytokines have during neutrophil invasion as part of the inflammatory response?

A

Cytokines increase selectin and ICAM-1 expression on endothelial cells. They bind PMN integrins to promote adhesion prior to migration to site of injury. Selectins trap neutrophils on endothelial cells, as they would otherwise roll throught the top of the endothelial cell.

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14
Q

Which enzymes increase the efficacy of phagocytosis of neutrophils and tissue macrophages?

A

lysozymes and lipase

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15
Q

What is the timeline of the inflammatory response?

A
  1. immediate: tissue macrophages phagocytize and release cytokine
  2. Hour 1: cytokines (TNF-alpha, IL-1) cause: release of stored PMNs from 5k to 25k/ul; neutrophilia; up-regulation of adhesion molecules (selectin, ICAM-1); induce leukocyte proliferation
  3. Hours 1 - 8: margination, diapedesis, and chemotaxis of phagocytic cells to target
  4. Hour 8 - days: secondary PMNs and macrophages become available for additional phagocytosis
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16
Q

Where do monocytes localize once they mature to macrophages in tissues?

A
  1. lymph nodes (walls of sinuses to ingest material)
  2. liver (Kupffer cells): detoxify hepatic portal blood system
  3. lung (alveolar macrophages): ingest particles and microbes in airway
  4. spleen: found in red pulp to filter blood
  5. skin (histiocytes): wound protection
17
Q

What is the difference between innate and acquired immunity?

A

Innate immunity involves a rapid response to a microbe/toxin that is intrinsic and rapid (takes minutes, hours), involving the skin, HCl in stomach, PMNs/macrophages, complement, antimicrobial agents
Acquired immunity involves an induced response that can be cell-mediated (T cells) and/or humoral (B cells)

18
Q

What are the effects of the complement system?

A
  1. Opsonization and phagocytosis
  2. Lysis (lytic complex C5b6789)
  3. Agglutination
  4. Neutralization of viruses
  5. Chemotaxis
  6. Activation of mast cells and basophils
  7. Inflammatory effects
19
Q

Describe the steps of B cell maturation

A

B cells clones proliferate in the bone marrow

  1. Antibody selection: B cell clones bind antigens
  2. Clones expand to generate array of specific antibodies; migrate to lymph nodes
  3. Antibody secretion: antigen recognition triggers pathogen destruction
20
Q

Which lymphokine(s) promote(s) proliferation of T cells?

A

Interleukin-2 promotes proliferation of CD-8 T cells (cytotoxic T cells), CD4 T-cells (T helper cells), and suppressor T cells.

21
Q

Which lymphokine(s) promote(s) proliferation of B cells?

A

Interleukin-4, -5, and -6 are B-cell growth factors (BCGFs).

22
Q

Which lymphokine promotes leukocyte proliferation?

A

GM-CSF; it enhances the phagocytic capacity of the the immune response

23
Q

Whih lymphokine acts as a macrophage activator?

A

Interferon gamma

24
Q

Which types of cells are targets of cytotoxic T cells?

A

virus-infected cells, cancer cells, and tissue transplants

25
Q

Describe the classical complement pathway.

A

Antigen-antibody complexes allow Fc domains (antibody tails) to bind C1 which complexes with C4 on C2. C4/2 activates alternative pathway protective mechanisms.

26
Q

Describe the alternative complement pathway.

A

Microbes bind Factors B and D (innate) which activates C3.

  1. C3b triggers phagocytosis (opsonization)
  2. C3a (also C5a) mast cell activator; histamine and heparin release increase local blood flow
  3. C5a chemo-attractant for PMNs and macrophages
  4. C5b + 6789 form lytic complex that ruptures bacterial cell membranes.
27
Q

What constitutes pus?

A

accumulated material (dea bacteria, PMNs, macrophages, necrotic tissue) as a result of infection

28
Q

What is the pathophysiology of rheumatic fever?

A

streptococcal antigens produce antibodies that cross-react with host tissues; may lead to post-streptococcal glomerulonephritis and/or rheumatic endocarditis

29
Q

Describe the classifications of leukemia by tissue origin

A
  • Lymphocytic: lymphoid; often metastatic

- Myelogenous: bone marrow; unlikely to spread (involving neutrophils, eosinophils, basophils, monocytes)