Pathology Flashcards

1
Q

What is the definition of inflammation?

A

a well organized cascade of fluid and cellular changes within vascularized tissue; host response to remove damaged/necrotic tissue or foreign invaders

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2
Q

What are the 5 cardinal signs of inflammation?

A

Heat
Redness
Swelling
Pain
Loss of function

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3
Q

How is inflammation part of the process of repair and healing?

A

destroys, dilutes or wall off injurious agents
initiates healing and tissue repair

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4
Q

How is inflammation a protective response?

A

It gets rid of pathogens
Removed nectrotic debris (phagocytosis
Repair the damage= return to normal structure/function

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5
Q

What are the types of inflammation?

A

Acute and Chronic

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6
Q

What are the characteristics of acute inflammation?

A

short duration (minutes to days)

exudation of fluid & plasma protein (edema)

emigration of leukocytes (mostly neutrophils)

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7
Q

What are the characteristics of chronic inflammation?

A

Longer duration (days to years)
Macrophages & lymphocytes
Proliferation of blood vessels & connective tissue

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8
Q

What are the 3 main components of acute inflammation?

A

1) vascular alteration leading to increased blood flow (hyperemia)
2) Changes in microvasculature permeability that allow plasma proteins & leukocytes to leave the circulation
3) Emigration of leukocytes into the perivascular area

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9
Q

What are the stimuli for acute inflammation?

A

Infections
Trauma
Physical & chemical agents
Tissue necrosis
Foreign body
Immune reactions

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10
Q

What is exudate and when does it form?

A

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

Formed when there is significant alteration in small blood vessel permeability at the site of injury (increased interendothelial spaces)

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11
Q

What is transudate and when does it form?

A

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

Formed due to an ultrafiltrate of blood from either increased hydrostatic pressure or decreased oncotic pressure

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12
Q

What is edema?

A

accumulation of fluid in interstitial or serous cavities

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13
Q

What are the 4 main mechanisms that result in edema?

A

1) increased vascular permeability
2) increased intravascular hydrostatic pressure
3) decreased intravascular osmotic pressure
4) decreased lymphatic drainage

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14
Q

What is pus?

A

a purulent exudate rich in leukocytes (mostly neutrophils) and cell debris

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15
Q

What are some vascular changes in acute inflammation?

A

Vasodilation involves arterioles first, then results in opening new capillary beds

Increased permeability of microvasculature

loss of fluid results in concentration of RBCs in small vessles, increased blood viscosity & blood stasis

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16
Q

What are the 4 mechanisms for vascular leakage?

A

1) endothelial contraction
2) direct endothelial injury
3) leukocyte-dependent injury
4) increased transcytosis

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17
Q

What are the endothelial changes involved in contraction?

A

It increases in interendothelial space

It is mediated by histamine, bradykinns, leukotrienes

Rapid and short-lived

Occurs mainly in venules

Induced by histamine and NO

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18
Q

What are the endothelial changes associated with direct injury?

A

Direct damage to endothelium causes necrosis & detachment

Starts immediately, lasts until thrombosis occurs or endothelium repaired

Rapid and may be long lived

Occurs in arterioles, capillaries, venules

Caused by burns, & some microbial toxins

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19
Q

What are the endothelial changes associated with leukocyte-mediated injury?

A

Activated leukocytes may secrete free radicals & proteolytic enzymes, leading to cell damage

Occurs in venules, pulmonary capillaries

Associated with late stages of inflammation

Long lived (hours)

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20
Q

What are the endothelial changes associated with transcytosis?

A

Increased transport of fluid & protein through endothelial cells occurs in venules

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21
Q

What are the vasoactive amines?

A

Histamine
Seratonin

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22
Q

What are the arachidonic acid metabolites?

A

Nitric oxide (NO)
Cytokines

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23
Q

What are the plasma derived mediators?

A

Complement system

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24
Q

How is histamine presented?

A

Is a performed state in mast cells, basophils & platelets in cytoplasmic granules

25
Where are chemical mediators of inflammation formed?
Preformed in secretory granules within cells Newly synthesized within cells Liver
26
What are the actions of histamines?
Dilation of arterioles Increased vascular permeability of venules which causes endothelial contraction
27
What is seratonin released in response to?
Platelet aggregation
28
How is arachidonic acid metabolites formed?
By the degradation of cell membrane phospholipids by phospholipases
29
What is a product of the arachidonic acid pathway and what do they do?
Eicosanoids which regulate inflammation and hemostasis
30
What are the two primary classes of inflammatory metabolites produced by eicosanoids?
Prostaglandins Leukotrienes
31
What do corticosteroids do to the arachidonic acid pathway?
Inhibits phospholipases & the production of arachidonic acid
32
What produce prostaglandins?
Cyclooxygenases
33
What is lipoxygenase and what does it produce?
It is an enzyme that produces leukotrienes & lipoxins from arachidonic acid
34
What synthesizes nitric oxide (NO) and what produces it?
Synthesized by nitric oxide synthase and is produced by endothelial cells, macrophages, & neurons
35
What are the 2 functions of NO?
Vasodilation Inhibits cellular inflammatory responses
36
How does NO inhibit the inflammatory response?
Inhibits leukocyte recruitment & migration
37
What can nitric oxide derivatives become and what do they do?
They become free radicals and kill microbes
38
What do cytokines primarily do?
Modulation of activities of other cells
39
What are the main cytokines involved in acute inflammation?
IL-1 & TNF
40
What are the local effects of IL-1 and/or TNF on vascular endothelium?
Expression of leukocyte adhesion molecules Production of IL-1, chemokines Procoagulation Decrease anticoagulant activity
41
What are the local effects of IL-1 and/or TNF on leukocytes?
Activation of leukocytes Production of cytokines
42
What are the local effects of IL-1 and/or TNF on fibroblasts?
Increase collagen synthesis
43
What are the systemic effects of IL-1 and/or TNF?
Fever Leukocytosis Increase acute-phase proteins Decrease appetite Increase sleep
44
How is complement used as a defense against microbes?
It forms the membrane attack protein which is like sticking a straw into a cell
45
What does the activation of complement cause?
Increased vascular permeability Chemotaxis Opsonization
46
What causes the activation of the classical complement pathway?
Reaction with IgG or IgM containing antigen-antibody complex
47
What causes the activation of the alternative complement pathway?
Contact with microbial surfaces & polysaccharides
48
What causes the activation of the lectin complement pathway?
Plasma mannose-binding lectin binds to microbes
49
What is the initial steps in complement activation lead to?
1) formation of C3 convertase which cleaves C3 2) Release of C3a 3)Covalent attachment of C3b which initiates formation of C5 convertase 4) formation of C5-9 (MAC)
50
What does C3a + C5a do?
Facilitate histamine release from mast cells (anaphylatoxins) Vasodilation, increase permeability
51
What does C3b do?
Act as opsonis when fixed to bacteria; facilitate phagocytosis by neutrophils & macrophages (receptor)
52
What are the 3 possible outcomes for acute inflammation?
Complete resolution Healing by connective tissue replacement (fibrosis) Progression to chronic inflammation
53
What are the 4 morphological patterns of acute inflammation?
Serous inflammation Fibrinous inflammation Suppuration inflammation Ulcers
54
What are the characteristics of serous inflammation?
Thin watery fluid derived from plasma mesothelioma cells These mesothelial cells line the peritoneum, pleura, & pericardium Fluid in these 3 cavities are called effusion
55
What are the characteristics of fibrinous inflammation?
Accumulation of fibrin Usually found in body cavity linings If fibrin is not removed it can lead to fibrosis
56
What are the characteristics of pus/purulent exudate?
Neutrophils, liquefactive necrosis, edema
57
What are the characteristics of ulcers?
Local defect or excavation of the surface of organ or tissue
58
What is the difference between an erosion and ulcer?
Erosion are superficial and do not go below the basement membrane Ulcers go below the basement membrane or can go straight through and make a hole