Brainscape's Knowledge GenomeTM

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


See full index

Gen Path #2 > Inflammation 2 > Flashcards

Inflammation 2 Flashcards

1
Q

Sequence of leukocyte events

A

1.Margination, rolling, adhesion
2.Transmigration across endothelium (also called diapedesis)
3.Migration in interstitial tissues toward chemotactic stimulus (chemotaxis)
4.Phagocytosis and synthesis of biochemical mediators

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

Neutrophil margination

A

-vasodilation results in slower flow of blood which allows the neutrophils to move to the edges
-edema and stasis

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

Neutrophil rolling

A

-binding of proteins on endothelium and the neutrophils
>done by selectins. Slows the neutrophils and rolls them along the endothelium

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

Neutrophil Adhesion

A

-getting the neutrophils to stop and have firm adhesion is conducted by integrins (beta1 and beta2)

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

Leukocyte adhesion deficiencies

A

-Cattle, dogs (irish setters) and people with Leukocyte adhesion disorders that lack the expression of beta 2 integrins
>means neutrophils can slow down, but never stop and can’t get into site of infection. Therefore neutrophils high in circulation but low numbers in sites of infection
-animals typically die within a few days/weeks

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

BLAD

A

-cattle leukocyte adhesion deficiency
-develop severe gingivitis, tooth loss, oral ulcers, enteric ulcers, cutaneous ulcers, diarrhea, pneumonia (**note all things that are interacting with the outside environment)

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

Leukocyte types depending on time

A

-Early inflammation: neutrophils because there is many of them, they respond rapidly to cytokines, and they adhere strongly to adhesion molecules. But they have a short lifespan once they leave the circulatory system
-Late inflammation: neutrophils are replaced by monocytes (long life)

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

Viral infections

A

-lymphocytes predominant

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

Hypersensitivity reactions

A

-eosinophils predominant

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

Chemotaxis

A

-directed movement of cells toward a chemical attractant. They will move toward the higher amount/gradient

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

Hydrocephalis

A

-congenital or acquired
>congenital if the skull is dome shaped because no way for the skull to change afterwards
-enlarged ventricle, very large brain and dome shaped skull
-excess fluid in the brain

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

Leukocyte induced injury

A

-Eg. pus filled kidney
>leukocytes release lysosomal substances into extracellular space= Frustrated phagocytosis

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

Frustrated phagocytosis

A

-blob attached to something and neutrophils are unable to properly engulf
-when it can’t fully surround, the neutrophils will “barf” everything out (lysozymes) and destroy surrounding tissues by accident

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

Smoke induced frustrated phagocytosis

A

-Smoking results in antigens that result in neutrophils releasing elastase through frustrated phagocytosis which breaks down elastin in the alveoli, resulting in smoke induced pulmonary emphysema

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

Heave line in horse

A

-Horse is working heard to breath
-results from chronic inflammatory response to lung

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

Neutrophils release Reactive oxygen species

A

-results in damage to surrounding structures

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

Neutrophils are indiscriminate about what they target

A

**reason why you would want to minimize immune response
-occurs through NETs, reactive oxygen species, lysozymes

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

Mandible of Cow

A

-pylogranulomas inflammation in jaw resulting in lumpy jaw, chronic legion
>morphologic diagnosis: abscesses or bone growth

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

Chemical mediators of inflammation

A

-high number of them that all interact
-short lived because they can become inactivated by enzymes, scavenged, of inhibited by other proteins
-either come premade within cells or secreted in inflammatory cells, or within the liver

20
Q

Plasma derived mediators

A

-complement
-kinins
-coagulation proteins

21
Q

Cell derived mediators

A

-always present sequested in granules of cells= histamines
-sythesized within cells (not always present)= NO, cytokines, chemokines, Arachidonic acid metabolites

22
Q

Complement pathway functions

A

-induces inflammation, phagocytosis, and MAC: lysis of microbes

23
Q

C5a, C3a Complement

A

-inflammatory pathway
-induces endothelial breakage
-also activate enzymes that tend to inhibit complement

24
Q

Complement components inadvertently attached to vessel walls

A

-can also see immune reactions and damage to vessels/tissues

25
Q

Fibrin pathway

A

-When fibrinogen activates and becomes fibrin, at the same time there will be activation of pathways which results in activation of plasminogen and formation of plasmin which helps break down fibrin
**Good because don’t want excess fibrin formation and having everything stuck together

26
Q

What cells make inflammatory mediators?

A

1.platelets
2.neutrophils
3.monocytes/macrophages
4. mast cells
5.mesenchymal cells (connective tissue cells such as osteoblasts, fibroblasts, etc.)

27
Q

Histamine

A

-among the first mediators to be released during inflammation by mast cell degranulation due to physical injury, immune reactions, anaphylatoxins, cytokines

28
Q

Histamine effects

A

-causes dilation of arterioles and increases vascular permeability of venules
-redness, heat, swelling

29
Q

Arachidonic acid metabolites

A

-produced by platelets, endothelial cells and leukocytes via remodeling of plasma membranes
-involved in almost all steps of acute inflammation

30
Q

Anti-inflammatory steroids

A

-inhibit phospholipases which prevent arachidonic acid

31
Q

COX inhibitors and aspirin

A

-inhibit cyclooxygenase which inhibits prostaglandin production
-prevents clotting

32
Q

Chemotaxis

A

-linked to arachidonic acid
-when inhibited by steroids, less movement of cells

33
Q

Renal medullary infarction

A

-associated with vet intervention from animals being given NSAIDs because it results in less vasodilation and poor blood flow

34
Q

Cytokines

A

-produced by many cell types that modulate functions of other cells
-Eg. Tumor necrosis factor & interleukin-1

35
Q

Tumor necrosis factor and interleukin-1

A

-react at local level and systemic level
>change set points or modulate inflammation levels
>liver to make more acute phase proteins
>increase set point temp of hypothalamus
>increase leukocytes production in bone marrow
-can have good or bad impact (eg. Can induce thrombus formation, decrease CO)

36
Q

Chemokines

A

-family of small cytokines that act as chemoattractants for leukocytes

37
Q

NO

A

-vasodilator relaxing vascular smooth muscle
-NO free radicals are toxic to microbial and mammalian cells
-reduce platelet aggregation and adhesion

38
Q

Acute phase response

A

-an adaptive component of innate defense and consists of numerous predetermined and orchestrated local and systemic reactions to the acute phase stimuli
>mediated by IL-1, TNF, IL-6

39
Q

Clinical or pathological changes associated with acute phase response

A

-fever (triggered by things like changes in cell wall of bacteria)
-anorexia
-somnolence
-tremors, shivering
-acute phase proteins
-leukocytosis

40
Q

Fever

A

-most common sign off acute phase response
-PGE2 in vascular and perivascular cells of the hypothalamus which stimulates the production of NTs which reset the temperature set point
-can allow growth in terms of fungus or can prevent growth of bacteria

41
Q

Acute phase proteins

A

-produced by liver
-increases plasma concentration 25%
-there are positive or negative acute phase proteins
>Positive: anti-inflammatory
>negative: maintenance of homeostasis

42
Q

Fibrinogen and acute phase response

A

-increase in fibrinogen concentration measured in ruminant and horses which determine where animal is with its acute phase protein response

43
Q

Leukocytosis

A

-increased number of leukocytes in blood
-common with bacterial infection
-increased release of cells from bone marrow (younger WBCs)= left shift
-prolonged infection induced proliferation of precursors in the bone marrow

44
Q

Three choices with inflammation

A

1.damage is neutralized, and animal goes back to normal health
2.damge neutralized, but enough damage occurs that healing occurs through fibrosis and scarring
3.Chronic inflammation

45
Q

IL-8

A

-chemokine
-attracts neutrophils

46
Q

Macrophage inflammatory protein

A

-chemokine
-attracts everything except neutrophils

47
Q

Eotaxin

A

-chemokine
-attracts eosinophils

Gen Path #2 (15 decks)

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