Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Immunology > 5 - Innate 3: Inflammation > Flashcards

5 - Innate 3: Inflammation Flashcards

1
Q

what is acute mastitis?

A

sudden dysfunction/inflammation of the mammary gland by bacteria, accompanied by swelling, heat, and obvious pain and discomfort for the cow. The halmark diagnostic feature of acute mastitis is the presence of leukocytes in the milk

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what is the economic importance of bovine mastitis?

A

lower milk production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what is the farm-side test to test for bovine mastitis?

A

California Mastitis test. higher levels of agglutination means more inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what are the five steps of acute inflammation?

A
  1. delivery of leukocytes and plasma proteins to the site of injury (vasodilation, vascular permeability, chemotaxis of leukocytes)
  2. elimination of agent (effector processes)
  3. trigger acquired immunity
  4. initiate tissue repair
  5. systemic responses (fever, leukocytosis)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what are the cardinal signs of acute inflammation?

A

redness (rubor), heat (calor), swelling (tumor), pain (dolor), and loss of function (functio laesa)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

the most common initiator of acute inflammation is:

A

sentinel cell detection of microbial or parasitic products within host tissues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Name a few triggers of inflammation:

A

trauma, physical and chemical injury, foreign bodies, inappropriate products of adaptive immunity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

many of the triggers of inflammation release ___

A

DAMPs, which, although endogenously derived, can lead to activation of macrophages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

activation of macrophages with PAMPs and DAMPs is indicative of:

A

infection and tissue injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

PAMPs and DAMPs activate inflammasomes within macrophages, leading to the release of:

A

interleukins (proinflammatory cytokines) and lipid mediators

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

give 4 examples of mediators for local vascular changes:

A
  • histamine, serotonin (mast cells)
  • nitric oxide
  • prostaglandins and leukotrienes
  • Cytokines and Chemokines

These mediators change the vascular permeability and expand the capillary beds to slow down the blood velocity for leukocytes to have more opportunity to stop the pathogen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Histamine is released from the granules of Mast Cells adjacient to blood vessels. This release is induced by:

A

-trauma/cold/heat
- immune reactions (IgE)
- C3a, C5a
- histamine releasing proteins from leukocytes
- neuropeptidies (substanceP)
- cytokines (IL1, IL8)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

histamine binds to __ receptors on endothelial cells and causes ____

A

1) H1 receptors
2) dilation of arterioles and increased permeability of venules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

nitric oxide (NO) is released from endothelial cells and macrophages. it induces:

A

relaxation of vascular smooth muscle, leading to vasodilation and increased vascular permeability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

in the short term, NO is proinflammatory, as it leads to vasodilation. in the long term, it reduces leukocyte recruitment, and therefore plays an _____ role

A

anti-inflammatory

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Leukotrienes and Prostaglandins are both local vascular mediators. How do they differ in their mechanism of action?

A

Both increase vascular permeability. Leukotrienes stimulate smooth muscle contraction and neutrophil chemotaxis, and prostaglandins induce vasodilation and hyperalgesia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How do NSAIDS stimulate an antiinflammatory response?

A

NSAIDs prevent arachidonic acid from converting into prostaglandins by inhibiting the enzymes (COX1 and 2) that catalyze the reaction.

NOTE: prostaglandins are local vascular mediators that stimulate an inflammatory response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are NSAIDs?

A

Non-steroidal anti-inflammatory drugs. They are cox 1/2 inhibitors that serve local anti-inflammatory and analgesic effects, as well as serving a central anti-pyretic effect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Cytokines and chemokines (IL-1B, IL-6, TNF-a, IL-8) serve as inflammatory mediators by:

A

activating leukocytes and endothelial cells, causing systemic reactions. Chemokines in particular activate chemotaxis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what are 4 consequences of vasodilation?

A
  • increased blood to area
  • expansion of capillary beds
  • decreased velocity of flow
  • increased permeability (fluid loss)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what are the three predominant mediators of vasodilation in the inflammatory response?

A
  • Histamine
  • Nitric oxide
  • prostaglandins
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what are four consequences of increased vascular permeability?

A
  • larger gaps between endothelial cells (due to trauma and endothelial contraction)
  • active transport of plasma through endothelial cells (transcytosis)
  • high protein fluid accumulates within the tissues, causing edema
  • edema further activates endothelial cells to produce more inflammatory mediators
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

increased vascular permeability is primary mediated by what three molecules?

A

Histamine
Leukotrienes
Prostaglandins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what does vasodilation and increased permeability (fluid loss) result in?

A

Local stasis of blood flow (AKA decreased blood velocity)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what are the four phases of leukocyte recruitment (extravasation)?

A
  1. leukocyte margination (tethering) and rolling
  2. firm endothelial adhesion (pavementing)
  3. diapedesis (transmigration)
  4. migration in intersitital tissues (chemotaxis)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

describe margination and rolling of leukocytes

A

leukocytes transiently adhere to the endothelium, allowing close interaction between them and the endothelial wall. Rolling in the presence of chemokines activates high-affinity integrins on the leukocyte that allow them to adhere

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

what is bovine leukocyte adhesion deficiency?

A

in holstein cattle, an autosomal recessive disorder impairs an integrin gene (B2-integrin), which prevents adhesion of leukocytes to the endothelium. this renders them unable to extravasate, and cattle with this disorder tend to die premature deaths due to recurrent bacterial infections due to their impaired immune response.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

describe firm adhesion (pavementing) of leukocytes

A

chemokines and rolling activate leukocytes activate the integrins on the leukocytes to bind to the endothelium through specialized endothelial receptors at the site of infection. Then the leukocytes spread out along the endothelial surface, hence the term “pavementing”

29
Q

Describe Diapedesis

A

This occurs primarily in the venules. leukocytes transmigrate through the endothelial wall into the extracellular matrix. This is possible because the basement membrane of the endothelium is compromised by leukocyte secretion of collagenases.

30
Q

where does diapedesis primarily occur?

A

the venules

31
Q

after transmigration (diapedesis), what allows the leukocytes to adhere to the extracellular matrix?

A

B1-integrins (CD44), found on the leukocytes themselves

32
Q

Describe chemotaxis

A

the recruitment of leukocytes to a specific site of insult via the establishment of a chemical gradient of chemoattractants.

33
Q

give two examples of exogenous chemoattractants used in chemotaxis

A

Bacterial proteionogenic amino acids (N-formyl-methionine, leucine, phenylalanine, fMLP)

Bacterial lipids

34
Q

give two examples of endogenous chemoattractants used in chemotaxis

A

C3a, C5a (complement)

Leukotrienes

IL-8 (chemokine)

35
Q

how do neutrophils detect a chemotactic gradient and move in the right direction?

A

Using receptors for chemoattractants
dispersed on its plasma membrane,
the neutrophil extends its pseudopod in
the region of the greatest chemotactic receptor
activation and then pulls the rest of itself
toward the stimulus.

36
Q

what are a common secondary responder to acute inflammation?

A

Monocytes, that mature into macrophages after they extravasate to the site of infection

37
Q

rank the following leukocytes in the order in which they appear during inflammation:
neutrophils, B cells, phagocytes, cytotoxic T cells, helper T cells

A
  1. Neutrophils (0-4 days)
  2. phagocytes (0- week 6)
  3. Helper T cells (day 4 - week 6)
  4. Cytotoxic T cells (day 7 - week 6)
  5. B cells (week 3 - week 6)
38
Q

what is pus?

A

necrotic neutrophils and other cells

39
Q

what is leukocyte is primarily recruited during inflammation caused by parasitic infection?

A

Parasites elicit eosinophil-dominated inflammatory responses through the recruitment of eosinophils via CCL11 (a, eotaxin)

40
Q

acute inflammation of the intestinal mucosa of a horse with strongyle infection should show what type of inflammatory response?

A

eosinophil-dominated

41
Q

There are at least 11 systemic effects of acute inflammation. Name as many as you can (or at least be able to recognize them on a multiple choice test lol)

A
  1. anorexia
  2. altered sleep patterns
  3. lethargy
  4. cachexia
  5. shock
  6. fever
  7. leukocytosis
  8. metabolic acidosis
  9. alterations to acute phase proteins
  10. decreased vascular resistance (systemic vasodilation)
  11. increased heart rate
42
Q

the majority of systemic effects of acute inflammation are mediated by the systemic release of:

A

TNF-a, IL-1, and IL-6 (proinflammatory cytokines) from the activated leukocytes at the site of infection

43
Q

what is the effect on the bone marrow during systemic acute inflammation?

A

leukocytosis

44
Q

what is the effect on the hypothalamus during systemic acute inflammation?

A

increased prostaglandin release leading to fever, as well as increased ACTH release stimulating further production of corticosteroids which in turn stimulate production of acute phase proteins from the liver

(sorry i know this is confusing, theres a good diagram of this in the slide deck)

45
Q

what is the effect on the liver during systemic acute inflammation?

A

increased production of acute-phase proteins

46
Q

what are the three main organs affected by acute inflammation?

A

bone marrow (leukocytosis)
hypothalamus (fever)
liver (production of acute phase proteins)

47
Q

describe leukocytosis

A

An increased number of leukocytes (primarily neutrophils) circulating in the blood. This is because IL-1 and TNF accelerate the release of stored neutrophils in the bone marrow.

48
Q

prolonged infection induces production of ______ and the release of __________

A
  1. Colony stimulating factors (CSFs)
  2. Immature (band) neutrophils
49
Q

what does “left shift” neutrophilia indicate?

A

neutrophils are immature when they are released from the bone marrow. This is the most common change in blood profile during acute inflammation

50
Q

Acute phase proteins (APPs) are produced by the liver. Give some examples of APPs whose serum levels INCREASE during inflammation (positive APPs)

A

C-reactive protein (CRP)
Serum amyloid A (SAA)
Haptoglobin
AGP
Ceruloplasmin
fibrinogen

51
Q

Acute phase proteins are produced by the liver. give some examples of APPs whose serum levels DECREASE during inflammation (negative APPs)

A

albumin
transferrin

52
Q

what are two clinical signs vets use to assess acute inflammation?

A

Neutrophilia (leukocytosis)
Levels of APP in blood serum

53
Q

what is the pathogenesis of fever?

A

pyrogens (TNF-a, IL-1, IL-6, LPS) stimulate the anterior hypothalamus to produce prostaglandins (PGE2), which act on thermoregulatory neurons that control the body’s temperature set point. The set point is increased, which promotes metabolic and behavioural changes that increase heat production and minimize heat loss

54
Q

during fever, what are three things that increase heat production?

A

catecholamines
thyroxine
shivering

55
Q

during fever, what are four things that minimize heat loss?

A

vasoconstriction
piloerection
postural changes
behavioural changes

56
Q

what are some proposed functions of fever?

A

induction of heat shock proteins, enhancing leukocyte response

increased leukocyte response

enhanced phagocytosis

increased T cell proliferation

increased motility and activation of some leukocytes

inhibition of some microbes

enhanced interferon-stimulated responses

induction of Fe-sequestering proteins

57
Q

Is the resolution of inflammation an active or passive process?

A

active

58
Q

failure to actively terminate acute inflammation leads to:

A

chronic inflammation and tissue destruction

59
Q

what are the four mechanisms of inflammation resolution?

A
  1. short half-life of inflammatory mediators
  2. production and release of anti-inflammatory cytokines and molecules
  3. apoptosis of proinflammatory cells
  4. desensitization of prostaglandin receptors
60
Q

how quickly after the start of an inflammatory response does the coordinated program of termination occur? (in other words, when does the resolution of acute inflammation begin)

A

within hours of starting an inflammatory response

61
Q

what do we call an inflammatory response that lasts months/years/indefinitely due to never resolving the cause of the acute inflammation?

A

chronic inflammation

62
Q

during chronic inflammation, the long term production of TNFa, IL-1 and IL-6 promotes:

A

tissue damage

63
Q

what are three examples of continual microbial invasion that can induce chronic inflammation?

A

gum disease

unhealed wounds

fungal and mycobacterial infections that arent resolved

64
Q

what is fibrosis?

A

scar-like tissue seen in cases of chronic viral infections, autoimmune diseases, and alcoholic liver diseases. It is caused by excessive fibrous connective tissue (fibroblasts) seen with cell necrosis

65
Q

what are granulomas?

A

Granulomas are organized aggregates of macrophages, often with characteristic morphological changes, and other immune cells. they form in response to persistent infection or foreign materials that individual macrophages cannot eradicate/destroy

66
Q

what is the pathogenesis of mastitis?

A

infectious bacteria ascends into the mammary gland via the streak canal, where the bacteria then proliferate. PAMPs and sentinel cells do their thing, and acute inflammation occurs. later, the systemic effects of acute inflammation also occur

67
Q

how do we diagnose mastitis?

A
  • sudden onset, typical clinical signs
  • aspect milk, CMT/cell count
  • blood: left shift neutrophilia, haptoglobin, SAA
68
Q

how do we treat mastitis?

A

intragland antibiotics and herd prevention

Immunology (18 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions