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DWT Exam 2 > Pathology > Flashcards

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
Q

Where are chemical mediators of inflammation formed?

A

Preformed in secretory granules within cells

Newly synthesized within cells

Liver

26
Q

What are the actions of histamines?

A

Dilation of arterioles
Increased vascular permeability of venules which causes endothelial contraction

27
Q

What is seratonin released in response to?

A

Platelet aggregation

28
Q

How is arachidonic acid metabolites formed?

A

By the degradation of cell membrane phospholipids by phospholipases

29
Q

What is a product of the arachidonic acid pathway and what do they do?

A

Eicosanoids which regulate inflammation and hemostasis

30
Q

What are the two primary classes of inflammatory metabolites produced by eicosanoids?

A

Prostaglandins
Leukotrienes

31
Q

What do corticosteroids do to the arachidonic acid pathway?

A

Inhibits phospholipases & the production of arachidonic acid

32
Q

What produce prostaglandins?

A

Cyclooxygenases

33
Q

What is lipoxygenase and what does it produce?

A

It is an enzyme that produces leukotrienes & lipoxins from arachidonic acid

34
Q

What synthesizes nitric oxide (NO) and what produces it?

A

Synthesized by nitric oxide synthase and is produced by endothelial cells, macrophages, & neurons

35
Q

What are the 2 functions of NO?

A

Vasodilation

Inhibits cellular inflammatory responses

36
Q

How does NO inhibit the inflammatory response?

A

Inhibits leukocyte recruitment & migration

37
Q

What can nitric oxide derivatives become and what do they do?

A

They become free radicals and kill microbes

38
Q

What do cytokines primarily do?

A

Modulation of activities of other cells

39
Q

What are the main cytokines involved in acute inflammation?

A

IL-1 & TNF

40
Q

What are the local effects of IL-1 and/or TNF on vascular endothelium?

A

Expression of leukocyte adhesion molecules
Production of IL-1, chemokines
Procoagulation
Decrease anticoagulant activity

41
Q

What are the local effects of IL-1 and/or TNF on leukocytes?

A

Activation of leukocytes
Production of cytokines

42
Q

What are the local effects of IL-1 and/or TNF on fibroblasts?

A

Increase collagen synthesis

43
Q

What are the systemic effects of IL-1 and/or TNF?

A

Fever
Leukocytosis
Increase acute-phase proteins
Decrease appetite
Increase sleep

44
Q

How is complement used as a defense against microbes?

A

It forms the membrane attack protein which is like sticking a straw into a cell

45
Q

What does the activation of complement cause?

A

Increased vascular permeability
Chemotaxis
Opsonization

46
Q

What causes the activation of the classical complement pathway?

A

Reaction with IgG or IgM containing antigen-antibody complex

47
Q

What causes the activation of the alternative complement pathway?

A

Contact with microbial surfaces & polysaccharides

48
Q

What causes the activation of the lectin complement pathway?

A

Plasma mannose-binding lectin binds to microbes

49
Q

What is the initial steps in complement activation lead to?

A

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
Q

What does C3a + C5a do?

A

Facilitate histamine release from mast cells (anaphylatoxins)
Vasodilation, increase permeability

51
Q

What does C3b do?

A

Act as opsonis when fixed to bacteria; facilitate phagocytosis by neutrophils & macrophages (receptor)

52
Q

What are the 3 possible outcomes for acute inflammation?

A

Complete resolution
Healing by connective tissue replacement (fibrosis)
Progression to chronic inflammation

53
Q

What are the 4 morphological patterns of acute inflammation?

A

Serous inflammation
Fibrinous inflammation
Suppuration inflammation
Ulcers

54
Q

What are the characteristics of serous inflammation?

A

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
Q

What are the characteristics of fibrinous inflammation?

A

Accumulation of fibrin
Usually found in body cavity linings
If fibrin is not removed it can lead to fibrosis

56
Q

What are the characteristics of pus/purulent exudate?

A

Neutrophils, liquefactive necrosis, edema

57
Q

What are the characteristics of ulcers?

A

Local defect or excavation of the surface of organ or tissue

58
Q

What is the difference between an erosion and ulcer?

A

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

DWT Exam 2 (6 decks)

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