Brainscape's Knowledge GenomeTM

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


See full index

MHD Exam 1 > Acute Inflammation > Flashcards

Acute Inflammation Flashcards

1
Q

What is acute inflammation?

A

the reaction of vascularizezed tissue to injury

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

acute inflammation involves the interaction of ___

A
  • pathogen/injury
  • host inflammatory cells
  • complement and coagulation cascades
  • chemokines and cytokines
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

acute inflammation involves the accumulation of

A

fluid, plasma proteins, and innate immune cells

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

the intensity of the response of AI is determined by

A

the stimulus, the duration of the stimulus, genetics of the host local factors, and medical interventions

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

causes of inflammation

A

infections, tissue necrosis(ischemia, thermal injury, etc), foreign bodies, and immune reactions (hypersensitivity)

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

inlfammasome

A
  • multi-protien complex characterized by activation of CASPASE 1
  • it cleaves IL-1 to its active form to set the inflammatory cytokines in action
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what activates monocytes?

A

pamp and damps (pathogen and damage assoc molecular pathogens)

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

inflammatory cytokines that recruit neutrophils

A

IF-1 and TNFa

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

cellular response of GPCRs in AI

A

cytoskeletal changes and signal transduction which causes:

  • increased integrin avidity causing adhesion to endothelium
  • chemotaxis and migration into tissues
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Cellular response of Toll-like receptors

A
  • production of mediators which amplify the inflammatory reaction
  • production of reactive oxygen species and lysosomal enzymes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

cellular response of cytokine receptors

A

production of reactive oxygen species and lysosomal enzymes

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

cellular response of phagocytic receptor

A
  • phagocytosis of microbe into phagosome

- production of reactive oxygen species and lysosomal enzymes

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

vascular response to AI

A
  • NO causes vasodilation to increase flow and vascular permeability
  • cytokine/chemokine induced endothelial changes allow innate cells access to the inflammatory site
  • plasma proteins like complement and Ab access the extracellular space
  • BASIC GOAL: increase the chance that a leukocyte can respond to the signal
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

5 main signs of inflamation

A
  • rubor (redness)
  • calor (heat)
  • dolor (pain)
  • tumor (swelling/edema from incr vascularization)
  • loss of function
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Phase 1 of AI

A
  • recognition of injury and attraction of neutrophils
  • expression of surface lectins and proteoglycans cause leukocytes to stick to epithelium and roll onto different receptors. Then the WBCs enter the tissue (diapedesis) and migrate to the source of the injury
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

which cytokines increase adhesion molecules?

A

IL-1, IL-6, and TNFa

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

what is chemotaxis

A

unidirectional movement along a chemical gradient which could be:

  • bacterial peptides
  • complement components (especial C5a)
  • proinflammatory cytokine tetrad
18
Q

how does chemotaxis work?

A

the chemoattractants activae membrane receptors on the innate cells that then activate cytoskeleton (especially actin) changes that move the cell along the gradient to the site of the inflammatory stimulus

19
Q

Phase 2 of AI

A
  • recruitment of monocytes/macrophages, dendritic cells, and T cells especially by neutrophil degranulation
  • this also signals more neutrophils to stop coming
20
Q

smoking inhibits ____ in AI

A

the neutrophil turn off signal

21
Q

location of monocyte

A

blood

22
Q

location of macrophage

A

fluids in the body

23
Q

location of histiocyte

A

tissue

24
Q

which cytokines cause proliferation of WBCs in AI?

A

G-CSF, GM-CSF, and IL-3

25
Q

Which cytokines cause maturation of WBCs in AI?

A

IL-1, IL-6, and IL-8

26
Q

sequence of cell traffic in AI

A

edema–neutrophils—monocytes/macrophages

27
Q

neutrophils (or PMNs)

A
  • most numerous leukocyte in circulation
  • signature cell of AI
  • marrow capable of rapid production and release
  • segmented nuclei
  • granules which kill the offender
28
Q

Bone marrow response to AI

A
  • cytokines and growth factors signal the marrow to make more cells
  • it responds by pushing mature and slightly immature but functional neutrophils out early and in vast amounts
  • causes elevated leukocyte count in pts
29
Q

left shift in AI

A
  • bone marrow is producing immature neutrophils (cells to the left of mature) called bands
  • bands will show up in the pts peripheral blood
30
Q

actions of neutrophils at site of injury

A
  • phagocytosis
  • recognition/attachment
  • engulfment/degranulation to form the phagolysosome
  • killing/degradation via an oxidative burst that generates kililng molecules
  • NETS (neutrophil extracellular traps)
31
Q

recognition and attachment of neutrophils in AI

A

Ab and C3b coating bind the pathogen to FcR and C3bR

32
Q

NETs

A
  • chromatin spray to the outside of the cell to trap bacteria and fungi
  • its chromatin is laden with killer granules
  • causes neutrophil to die b/c it sacrifices its nucleus
33
Q

oxidative burst and killing

A
  • degranulation
  • oxidative burst
  • activation of NADPH generated H2O2
  • lysosomal enzymes donate MPO
  • MPO + halide =HOCl
  • *important- need NADPH
34
Q

monocytes/macrophages

A
  • largest leukocyte in the blood
  • has many granules, large golgi, and indented nucleus
  • some home to specific organs and take up residence as fixed macrophages
35
Q

phase 4 of AI

A
  • cleanup of debris
  • main players in cleanup = TGF-B and IL-10
  • scavenging of apoptotic neutrophils promotes macrophage growth factors and repair
36
Q

control of AI is highly dependent on _____

A

macrophages

37
Q

No TLR or phagocytic receptor activation after AI leads to ___

A
  • decreased pro-inflammatory mediator syntheis and release, which macrophages sense as they are cleaning up dying neutrophils
  • predominant cytokines are TGF-B and IL-10
38
Q

Serous/Transudate AI

A
  • least severe
  • protein poor transudate from capillary to a space- peritoneal, pericardial, or pleural
  • cells aren’t leaky, so only lose fluid and not protein
39
Q

Fibrinous AI

A
  • intermediate severity

- fluid with larger molecules dominated by fibrinogen which converts to fibrin and potential scarring

40
Q

Suppurative/Abscess/Exudate AI

A
  • most severe
  • protein rich fluid with inflammatory cells and alive and dead necrotic debris
  • high hydrostatic pressure and leaky endothelial cells so protein leaks along with fluid
41
Q

ulcerative AI

A

underlying inflammation causes excavation of a mucosal or skin surface

MHD Exam 1 (6 decks)

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