Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

DWT exam 2 > pathology acute inflammation > Flashcards

pathology acute inflammation Flashcards

(58 cards)

Start Studying
1
Q

inflammation definition

A

A well organized cascade of fluid and cellular changes within vascularized tissue

Host response to remove damaged/necrotic tissue or foreign invaders

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

5 cardinal signs of inflammation

A
  1. heat
  2. redness
  3. swelling
  4. pain
  5. loss of function
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

purpose of inflammation

A

Inflammation is part of the process of repair and healing
* destroys, dilutes, or walls off injurious agents
* initiates healing and tissue repair

Fundamentally a protective response
* Get rid of pathogens
* Remove necrotic debris (phagocytosis)
* Repair the damage = return to normal structure/function

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

acute inflammation

A

Rapid
Short Duration
minutes to days
Characterized by exudation of fluid and plasma protein (edema) and emigration of leukocytes (mostly neutrophils)

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

chronic inflammation

A

Longer duration: days to years
Macrophages and lymphocytes **
Proliferation of blood vessels and connective tissue (fibrosis**)

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

3 main components of acute inflammation

A

1) Vascular alteration (vasodilation) leading to increased blood flow (hyperemia)

2) Changes in microvasculature permeability (leaky) that allow plasma proteins and leukocytes to leave the circulation

3) Emigration of leukocytes into the perivascular area

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

exudate

A

Inflammatory extravascular fluid with
* high protein concentration (>5 g/dL)
* high cell content (>5000 leukocytes/mL)
* high specific gravity >1.020

Formed when there is significant alteration in small blood vessel permeability at the site of injury
ex: pus

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

transudate

A

Extravascular fluid with
* low protein concentration (<2 g/dL)
* low cell content (<1500 leukocytes/mL)
* low specific gravity <1.012

An ultrafiltrate of blood
Increased hydrostatic pressure (ie. congestive heart failure)
Decreased oncotic pressure (hypoproteinemia)

looks like serum (clear, straw colored)

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

effusion

A

fluid accumulates in body cavity

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

edema

A

An accumulation of fluid in interstitial or serous cavities

Increased vascular permeability
Increased intravascular hydrostatic pressure
Decreased intravascular osmotic pressure
Decreased lymphatic drainage

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

pus

A

Pus - a purulent exudate rich in leukocytes (mostly neutrophils) and cell debris
purrulent = adjective!!

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

vascular changes with acute inflammation

A
  1. Vasodilation – involves arterioles first, then results in opening new capillary beds; mainly induced by histamine and nitric oxide acting on vascular smooth muscle
  2. Increased permeability of microvasculature – protein rich fluid pours out into extravascular tissue
  3. Loss of fluid results in concentration of red cells in small vessels, increased blood viscosity and blood stasis
  4. Stasis – allows leukocytes to accumulate along the endothelium and stick to it (leukocyte emigration/diapedesis)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

4 mechanisms for vasular leakage:

A
  1. endothelial contraction: Endothelial cells contract –> increase in interendothelial space (mediated by histamine, bradykinins, leukotrienes), Rapid and short-lived (15-30 minutes)
  2. direct endothelial injury: Direct damage to endothelium causes necrosis and detachment (burns, lytic bacteria), Starts immediately, lasts until thrombosis occurs or endothelium repaired
  3. leukocyte-dependent injury: Activated leukocytes may secrete free radicals and proteolytic enzymes, leading to cell damage
  4. Increased transcytosis: Increased transport of fluid and protein through endothelial cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

endothelial contraction

A

1st mechanism for vasular leakage
Endothelial cells contract –> increase in interendothelial space
mediated by histamine, bradykinins, leukotrienes

Rapid and short-lived (15-30 minutes)

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

endothelial direct injury

A

2nd mechanism for vasular leakage
Direct damage to endothelium causes necrosis and detachment (burns, lytic bacteria)
Starts immediately, lasts until thrombosis occurs or endothelium repaired

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

leukocyte mediated injury endothelial changes

A

3rd mechanism for vasular leakage
Activated leukocytes may secrete free radicals and proteolytic enzymes, leading to cell damage

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

transcytosis

A

4th mechanism for vasular leakage
Increased transport of fluid and protein through endothelial cells

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

Leukocyte Extravasation Stages

A
  1. Margination, rolling, and adhesion: in normal blood flow endothelium does not “catch” cells, it must be activated by cytokines to do so
  2. Transmigration across endothelium (mainly venules), also called diapedesis
  3. Migration – in interstitial tissue toward a chemotactic stimulus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

selectins

A

initiate low affinity rolling of leukocytes
binds and releases like velcro

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

Margination, Rolling, and Adhesion in leukocyte extravasation

A

Blood stasis
* helps leukocytes stack up at periphery (against vessel wall)

Rolling
* leukocytes adhere transiently to endothelium
* roll until becoming firmly attached to endothelium

Neutrophils, monocytes, eosinophils, basophils, lymphocytes all use the same method described above

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

integrins

A

high affinity binding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

low affinity binding of leukocytes extravasation

A

Mediated by selectins expressed on surface of endothelium and leukocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

high affinity binding of leukocyte extravasation

A

Integrins on leukocytes bind to immunoglobulin family receptors on endothelial cells

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

genetic deficiencies in leukocyte adhesion

Study These Flashcards
A

Heritable deficiencies in type and amount of adhesion molecules (selectins/integrins) can inhibit leukocyte transmigration and acute inflammation

This may result in poor inflammatory response to pathogens and dead tissue

Causes recurrent infections

25
transmigration of leukocyte extravasation
Leukocyte inserts a **pseudopod into the junction between endothelial cells and squeezes through** **Made possible by adhesion molecules** located on leukocytes and endothelial cells
26
chemotaxis of leukocyte extravasation
Movement of leukocytes in tissue along a **chemical gradient** can be due to: * Exogenous products – bacteria * Endogenous products – complement system components (C5a, leukotriene B4, cytokines) Cell moves by extending a filopodia that pulls the back of the cell forward.
27
steps of phagocytosis
1. Recognition and Attachment 2. Engulfment 3. Killing or degradation of ingested material
28
recognition and attachment in phagocytosis
microbe binds to phagocytic receptor
29
engulfment in phagocytosis
phagocyte membrane zips up around membrane and makes pseudopods **Pseudopods flow around particle to form a phagosome** **Phagosome fuses with lysosome** in cell creating the **phagolysosome**
30
killing and degredation in phagocytosis
**Reactive oxygen species (ROS)** * Produced within the lysosome * Respiratory burst – rapid oxidative reaction * **Primary mode of microbial killing** Lysosomal enzymes
31
Release of Leukocyte Products During Killing (phagocytosis)
Collateral damage when neut dies while killing in a phagolysosome **Release of lysosomal enzymes and ROS into extracellular space** Cytotoxic release – crystals (eg. urates) can puncture the cell during phagocytosis and lead to leakage of enzymes and other leukocyte products
32
Neutophil extracellular traps (NETs)
Produced by neutrophils in response to infectious pathogens and inflammatory mediators Mechanism of killing microbes Extracellular fibrillar network composed of: * **Meshwork of nuclear chromatin** * **Antimicrobial peptides and enzymes**
33
genetic defects in leukocyte function
Inherited defects in leukocyte **adhesion** * Leukocyte Adhesion Deficiencies (LAD) Inherited defects in **phagolysosome fusion** * Chediak–Higashi syndrome Inherited defects in **microbicidal activity** **ALL CAUSE RECURRENT INFECTIONS**
33
genetic defects in leukocyte function
Inherited defects in leukocyte **adhesion** * Leukocyte Adhesion Deficiencies (LAD) Inherited defects in **phagolysosome fusion** * Chediak–Higashi syndrome Inherited defects in **microbicidal activity** **ALL CAUSE RECURRENT INFECTIONS**
34
Cell derived mediators
Vasoactive amines (Histamine, Seratonin) Arachidonic acid metabolites Nitric oxide (NO) Cytokines
35
Plasma derived mediators
complement system
36
histamine
* vasoactive amine * Present in a **PREFORMED state in mast cells**, basophils and platelets in cytoplasmic granules * can be released instantly, as needed * mast cells typically are found in connective tissue near blood vessels
37
Histamine is released in response to:
* physical injury (heat, cold, trauma) * immune reactions (IgE binding, type 1 hypersensitivity) * presence of complement fragments C3a and C5a (anaphylatoxins)
38
Actions of histamine
vasoactive amine * dilatation of arterioles * increases vascular permeability of venules * causes endothelial contraction in venules
39
serotonin
vasoactive amine also known as 5-hydroxytryptamine **preformed** in platelets Released **in response to platelet aggregation** actions are similar to histamine in acute inflammation
40
Arachidonic acid metabolites
The **degradation of cell membrane** phospholipids by phospholipases yields AA Eicosanoids * Products of AA metabolism * regulate inflammation and hemostasis Two primary classes of inflammatory metabolites * **prostaglandins** * **leukotrienes**
41
Eicosanoids
* Products of AA metabolism * regulate inflammation and hemostasis
42
Arachidonic acid cascase
1. cell membranes broken into arachidonic acid by phospholipase (glucocorticoids inhibit) 2. arachidonic acid turned into prostaglandin by cyclooxygenase (NSAIDS inhibit) 3. lipooxygenases cleave arachidonic acid into leukotrienes
43
lipoxygenase
Enzyme that produces leukotrienes and lipoxins from AA
44
leukotrienes
Chemotactic for leukocytes Vascular effects: vasoconstriction, ↑ vascular permeability produced from arachidonic acid by lipoxygenase
45
lipoxins
produced from arachidonic acid by lipoxygenase Lipoxins inhibit inflammation Inhibit leukocyte recruitment and cellular components of inflammation
46
Nitric oxide
* Produced by **endothelial cells, macrophages, neurons** * Synthesized by **nitric oxide synthase** NO: 2 functions in inflammation * **Vasodilation** (contributes to vascular reaction) * **Inhibits cellular inflammatory response** * **reduces platelet aggregation** and adhesion (anti-inflammatory) * **inhibits leukocyte** recruitment (anti-inflammatory) As a free radical **kills microbes**
47
cytokines
polypeptides produced primarily by **macrophages and lymphocytes** Primary action is **modulation of activities of other cells** The main cytokines involved in acute inflammation are **IL-1** (interleukin-1) and **TNF** (tumor necrosis factor)
48
The main cytokines involved in acute inflammation
IL-1 (interleukin-1) and TNF (tumor necrosis factor)
49
TNF/IL-1 actions
vascular: * leukocyte adhesion molecules * procoagulant activity leukocytes: * activate * produce cytokines fibroblasts * proliferate, repair * increase collagen synthesis systemic * fever * leukocytosis * decrease appetite * increase sleep
50
complement
Defense against microbes * formation of **MAC** - membrane attack complex Complement activation causes * **↑ vascular permeability** * **Chemotaxis** * **Opsonization** Main components are present as inactive plasma precursors (C1-9)
51
complement activation pathways
alternate: microbe antigens directly activate c3 convertase classical: antibodies bind to antigens activating c3 convertase lectin: mannose-binding lectin binds to antigen activating c3 convertase c3b causes: * recruitment lymphocytes * phagocytosis * formation of MAC
52
classical complement pathway
reaction with IgG or IgM containing antigen-antibody complex
53
alternate complement pathway
contact with microbial surfaces and polysaccharides (cobra venom, endotoxin)
54
lectin complement pathway
plasma mannose-binding lectin binds to microbes
55
C3 convertase
The **initial steps in complement activation** lead to formation of an enzyme - C3 convertase - which cleaves C3 C3 cleavage leads to: * release of C3a (anaphylatoxin) * covalent attachment of C3b (initiates formation of C5 convertase) * formation of C5-9 (**MAC**)
56
C5a
facilitate **histamine release** from mast cells (vasodilate, increase permeability) **activates lipoxygenase pathway** of AA metabolism in neutrophils and monocytes **chemotactic** for neutrophils, monocytes, eosinophils, basophils | complement
57
C3b
act as **opsonins** when fixed to bacteria; facilitate **phagocytosis** by neutrophils and macrophages (receptor) | complement

DWT exam 2 (22 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions