Brainscape's Knowledge GenomeTM

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


See full index

SP1 General Pathology > Lecture 9 2/8/24 > Flashcards

Lecture 9 2/8/24 Flashcards

1
Q

What is inflammation?

A

reaction within a living vascularized tissue to local injury

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

What types of injury can occur that cause inflammation?

A

-infectious microbes
-mechanical trauma
-heat
-cold
-radiation
-cancerous cells

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

What is the purpose of inflammation?

A

-to dilute, isolate, and eliminate cause of injury
-to repair tissue damage resulting from the injury

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

What are the basics of inflammation?

A

-requires a stimulus
-major players are in circulation/blood
-only in living tissue
-allied with healing and repair
-can be harmful

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

What are the benefits of inflammation?

A

-dilutes/inactivates biological and chemical toxins
-kills/sequesters microbes and neoplastic cells
-degrades foreign material
-provides growth factors to help with healing phase

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

What are the harms of inflammation?

A

-can destroy normal tissue
-cardinal signs of inflammation

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

What are the cardinal signs of inflammation?

A

-heat
-redness
-swelling
-pain
-loss of function

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

What descriptors should be included in a morphologic diagnosis?

A

-severity
-duration
-distribution
-modifiers
-process
-organ

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

Which terms can be used to describe the severity of a diagnosis?

A

-minimal
-mild
-moderate
-marked
-severe

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

Which terms can be used to describe the chronicity of a diagnosis?

A

-peracute: hours
-acute: hours to days
-subacute: many days
-chronic: weeks to years
-chronic-active: ongoing acute stimulus

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

How can a process be determined to be acute vs. chronic?

A

based on the type(s) of inflammatory cells and other gross changes

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

Which terms can be used to describe distribution of a diagnosis?

A

-focal
-multifocal
-locally/regionally extensive
-diffuse
-multifocal to coalescing
-segmental
-unilateral/bilateral
-cranioventral (lungs)

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

Which terms can be used when having to provide a modifier for an inflammatory process?

A

-suppurative
-necrotizing
-ulcerative
-hemorrhagic
-lymphoplasmacytic
-granulomatous
-eosinophilic

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

What are some examples of terms that can be used when providing a modifier for a specific location?

A

-bronchopneumonia
-interstitial pneumonia
-glomerulonephritis
-portal hepatitis

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

Which leukocytes are involved with inflammation?

A

-neutrophils
-monocytes/macrophages
-lymphocytes
-plasma cells
-eosinophils
-basophils
-mast cells

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

Which non-leukocytes are involved with inflammation?

A

-endothelial cells
-platelets
-fibroblasts

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

What are the characteristics of inflammatory mediators?

A

-derived from cells or plasma
-can be produced as needed or pre-formed and stored
-short-lived

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

What are the master cytokines?

A

-IL-1
-TNF

19
Q

What part of the arachidonic acid pathway is inhibited by steroids?

A

phospholipase function

20
Q

What part of the arachidonic acid pathway is inhibited by leukotriene receptor antagonists?

A

leukotrienes

21
Q

What part of the arachidonic acid pathway is inhibited by COX-1/2 inhibitors?

A

cyclooxygenase

22
Q

How is it possible for some membrane lipids to not form arachidonic acid (omega 6 fatty acid)?

A

-dietary omega 3 fatty acids insert into cell membrane
-insertion of dietary omega 3 fatty acids decreases arachidonic acid

23
Q

What are the impacts of increased omega 3s in the cell membrane?

A

-less inflammation
-less pain
-less-free radical-mediated damage

24
Q

What are the characteristics of histamine?

A

-pre-formed
-released in response to trauma, cytokines, etc.

25
Q

What are the effects of histamine?

A

-vasodilation
-increased vascular permeability
-pain and itching
-eosinophil attraction

26
Q

What are the steps of inflammation?

A

-initiation
-vasodilation
-increased vascular permeability
-activation of leukocytes
-diapedesis
-chemotaxis
-phagocytosis

27
Q

What are examples of potential stimuli for inflammation?

A

-infectious agents
-trauma
-abnormal cells
-necrotic cells
-foreign material

28
Q

Why do stimuli trigger inflammation?

A

PRRs on epithelial cells and leukocytes recognize PAMPs and DAMPs

29
Q

How do resident macrophages initiate inflammation?

A

-recognize non-self or DAMPs
-release IL-1

30
Q

How do lymphocytes initiate inflammation?

A

-recognize non-self
-release IL-1

31
Q

How does direct damage to cells initiate inflammation?

A

-damage to mast cells leads to mast cell degranulation/histamine release
-release of IL-1

32
Q

How does indirect damage initiate inflammation?

A

-sunburn irritates keratinocytes
-keratinocytes release IL-1

33
Q

How does amplification of signaling initiate inflammation?

A

-IL-1 can trigger mast cell degranulation
-histamine triggers more IL-1 release

34
Q

What occurs during vasodilation?

A

-increased blood flow to area causes heat and redness
-slowing of blood leads to margination of neutrophils

35
Q

What effect does histamine, IL-1, and TNF have on the blood vessels?

A

makes endothelial cells contract, causing leaky vessels

36
Q

How does increased vascular permeability result in edema and an increase in marginated neutrophils?

A

-fluid leaks out of vessels, resulting in hemoconcentration
-increased viscosity of blood leads to blood “sludging”
-sludging of blood results in more marginated neutrophils

37
Q

What is lost due to increased vascular permeability?

A

-fluid
-proteins/fibrinogen

38
Q

What happens when fibrinogen is exposed to collagen outside of the vessels?

A

triggers the clotting cascade, leading to fibrin formation

39
Q

How do IL-1 and TNF play a role in increased vascular permeability?

A

increase expression of adhesion molecules, increasing the number of marginated neutrophils

40
Q

Which adhesion molecules are present on vessel endothelial cells?

A

-E-selectin
-P-selectin
-ICAM-1

41
Q

How do IL-1 and TNF increase leukocyte binding, in terms of the leukocyte?

A

increase the expression and avidity/stickiness of integrins on leukocyte surface

42
Q

How are histamine, TNF, and IL-1 involved in leukocyte activation?

A

-upregulation of adhesion molecules
-increase in cytokine and prostaglandin production

43
Q

What are the characteristics of diapedesis?

A

-movement of leukocytes out of vessels
-primarily neutrophils
-depends on upregulation of adhesion molecules
-mediated by PECAM-1

SP1 General Pathology (20 decks)

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