Lecture 10 Flashcards

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1
Q

What are signs of inflammation?

A

pain, redness, immobility, swelling (edema), heat

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2
Q

What kind of defense response is inflammation?

A

local defense response
- second line of defense

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3
Q

Why is inflammation good?

A
  • destroys injurious agent or limits its effects on the body
  • repairs and replaces tissue damaged by the injurious agent
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4
Q

Why does pain happen when inflamed? Redness? Swelling? Heat?

A
  • pain: release of certain chemicals
  • redness: more blood goes to affected area
  • swelling: accumulation of fluids
  • heat: increase in blood flow
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5
Q

What is acute inflammation?

A
  • signs develop rapidly and last a few days or weeks
  • mild and self limiting
  • principal defense cells aren’t neutrophil
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6
Q

What are examples of acute inflammation?

A
  • sore throat
  • cold
  • flu
  • scratch on the skin
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7
Q

What is chronic inflammation?

A

signs develop more slowly and can last for up to several months or years

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8
Q

What are examples of chronic inflammation?

A
  • tuberculosis
  • rheumatoid arthritis
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9
Q

What happens in early inflammation? Give an example.

A

microbial structures stimulate toll-like receptors on macrophages, triggering cytokine production
- tumor necrosis factor-alpha (TNF-alpha)

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10
Q

What are examples of microbial structures?

A
  • flagellin
  • lipopolysaccharides
  • bacterial DNA
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11
Q

What are acute phase proteins?

A
  • liver synthesizes acute phase proteins in response to TNF-alpha
  • C-reactive protein (CRP), mannose-binding lectin, fibrinogen are activated during inflammation
  • they induce local and systemic responses, aiding in blood clotting and vasodilation
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12
Q

What cells are involved in inflammation? How?

A

TNF-alpha receptors, producing more TNF-alpha
- amplifies the inflammatory response

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13
Q

What happens with excess TNF-alpha?

A
  • can lead to rheumatoid arthritis
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14
Q

How do we treat excess TNF-alpha?

A

monoclonal antibodies

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15
Q

What does inflammation activate?

A

acute-phase proteins by the liver that cause vasodilation and increased permeability of blood vessels

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16
Q

What is vasodilation responsible for?

A

redness and heat associated with inflammation

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17
Q

What are examples of vasoactive mediators?

A
  • histamine: (chemical) causes blood vessels to widen, leading to inflammation and allergy symptoms
  • kinins: (proteins) promotes inflammation, vasodilation, and pain during immune responses
  • prostaglandins: (lipids) cause inflammation, pain, fever by increasing blood flow to affected areas
  • leukotrienes: (chemicals) cause inflammation by attracting white blood cells to the site of infection or injury
  • cytokines: (proteins) regulate and communicate between cells, coordinating immune and inflammatory responses
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18
Q

What is margination?

A

sticking of phagocytes to blood vessels in response to cytokines at the site of inflammation as the flow of blood gradually decreases

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19
Q

What do cytokines do in margination?

A

alter cellular adhesion molecules on cells, lining blood vessels, causing the phagocytes to stick to the side of inflammation

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20
Q

What happens during diapedesis?

A

where phagocytes squeeze between endothelial cells of blood vessels
- ameboid movement

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21
Q

What happens during phagocytosis?

A

phagocytes began to destroy invading microorganisms

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22
Q

When can tissue repair occur?

A

once all harmful substances are removed and neutralized

23
Q

What is the stroma?

A

supporting connective tissue that is repaired
- scar tissue will form

24
Q

What is the parenchyma?

A

functioning part of the tissue that is repaired
- more active in repair

25
Q

What is the most frequent cause of a fever?

A

infection from bacteria

26
Q

What is the hypothalamus?

A

body thermostat
- 37C

27
Q

How do cytokines affect the hypothalamus?

A

release prostaglandins that reset the hypothalamus to a higher temperature
- body maintains higher temperature until cytokines are eliminated

28
Q

What is crisis?

A

when the body undergoes the infection, vasodilation, and sweat

29
Q

What is the complement activation?

A
  • working together in a cascade
  • serum proteins produced by the liver enhance the immune system in destroying microbes
30
Q

What is the classical pathway?

A

1) antibodies attached to the antigens forming antigen-antibody complex
- these complexes bind to and activate C1
2) Activated C1 activates C2 and C4 by splitting each of them into their respective alpha beta complexes
3) C2a and C4b combine and is responsible for splitting C3 into alpha beta

31
Q

What is C3a for?

A

participates in inflammation

32
Q

What is C3b for?

A

functions in cytolysis and opsonization

33
Q

Why is the alternative pathway named that?

A
  • doesn’t involve antibodies
  • activated by contact between certain complement proteins and pathogens
34
Q

What is the alternative pathway?

A

1) C3 combines with complement proteins (factor B, factor D, and factor P)
2) Complement proteins attach to microbial cell surface materials
3) C3 splits into alpha beta
- C3a and C3b have the same function as classical pathway

35
Q

What are lectins?

A

proteins and carbohydrates

36
Q

When is the lectin pathway used?

A

when macrophages, bacteria, viruses, and other foreign matters go through phagocytosis to release stimulated cytokines to produce lectins

37
Q

What is the lectin pathway?

A

1) mannose-lectin binds to mannose (carbohydrate)
2) MBL functions as opsonin and enhances phagocytosis, activating C2 and C4
3) C2a and C4b activate C3 and splits it.

38
Q

Why does MBL bind to many pathogens?

A

they recognize a distinctive pattern of carbohydrates

39
Q

What are the outcomes of complement activation? Give a short description of each.

A
  • cytolysis: activated complement proteins to create a membrane attack complex (MAC)
  • opsonization: promotes attachment of a phagocyte to a microbe
  • inflammation: activated complement proteins bind to mast cells, releasing histamine
  • regulation of complement: regulatory proteins break down complement proteins, minimizing host cell destruction
  • complement and disease: lack of complement proteins causes susceptibility to infections
  • evading the complement system: capsules prevent complement activation
40
Q

How do capsules prevent complement activation?

A

they prevent binding of complement proteins = avoiding opsonization and making it more difficult for immune cells to target and destroy microbes

41
Q

What are interferons and their function?

A

key signaling molecules that help protect cells from viral infections and activate immune cells to eliminate both viruses and bacteria
- alerts neighboring cells and coordinating immune responses to maintain a strong and effective defense system in the body

42
Q

What are IFN-alpha and IFN-beta?

A

produced by cells in response to viral infections
- cause neighboring cells to produce antiviral proteins that inhibit viral replication

43
Q

What is IFN-gamma?

A

causes neutrophils and macrophages to kill bacteria

44
Q

What is the importance of iron-binding proteins?

A

regulating availability of iron

45
Q

Why is iron a double-edged sword?

A

cells need it for functions but bacteria needs it to grow and replicate

46
Q

Where is transferrin found?

A

found in blood and tissue fluids

47
Q

Where is lactoferrin found?

A

milk, saliva, mucus

48
Q

Where is ferritin found?

A

liver, spleen, red bone marrow

49
Q

Where is hemoglobin found?

A

red blood cells

50
Q

What are siderophores for?

A

compete with iron-binding proteins

51
Q

What are antimicrobial peptides?

A

short peptides produced in response to protein and sugar on microbe

52
Q

What is the function of antimicrobial peptides?

A
  • inhibits cell wall synthesis
  • forms pores in the plasma membrane
  • acts as first line of defense against invading pathogens
53
Q

Why are antimicrobial peptides effective?

A

targets broad range of microbes

54
Q

What are other factors of nonspecific immunity?

A
  • genetic resistance
  • age
  • observing healthy protocols