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Pathology I > Inflammation And Repair > Flashcards

Inflammation And Repair Flashcards

1
Q

A vascular reaction to injury of tissue

A

Inflammation

-provides defense against micro organisms

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2
Q

Replacement of damaged tissue

A

Repair

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3
Q

What are some common causes of inflammation?

A

Physical injury
Immune reaction
Infection

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4
Q

What is the function of inflammation to damaged tissue?

A

Prepare the damaged site for repair

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5
Q

Inflammation is characterized by what suffix?

A

“-itis”

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6
Q

What type of inflammation is characterized by circulatory, cellular, humoral and neurogenic responses with an outpouring of fluid and cells (exudation)?

A

Acute inflammation

Also characterized by a rapid course and accumulated neutrophils (PMNs)

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7
Q

What kind of inflammation is generally prolonged and characterized by scar tissue formation?

A

Chronic inflammation

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8
Q

Clinical signs are consistent and predictable in _______ inflammation and variable and less predictable in _______ inflammation

A

Acute: chronic

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9
Q

What are the benefits of inflammation?

A

Defense

  • localize and dilute damaging agents
  • transports antibiotics and therapeutic drugs to the injury site
  • promotes fibrin deposit formation
  • stimulates immune response
  • mobilizes phagocytes
  • brings oxygen and nutrients to area for resolution and repair
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10
Q

What are the potentially harmful effects of inflammation?

A
  • leukocyte products injure tissue by releasing enzymes indiscriminately
  • prolonged vascular pooling can cause hypoxia and thrombosis
  • excessive swelling (myofascial compartment, cranial cavity)
  • can increase injury, promote scarring and delay repair
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11
Q

What are the cardinal signs of acute inflammation?

A
  • heat (calor) - due to vasodilation and increased blood flow
  • redness (rubor) vasodilation with hyperemia
  • swelling (edema) - due to vasodilation and accumulated fluid
  • pain (dolor)
  • loss of function (functio laesa)
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12
Q

What are the circulatory responses to acute inflammation?

A
  • vasodilation, increased blood flow and increased vascular permeability due to structural changes
  • leukocytes, fluid and plasma proteins accumulate
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13
Q

What is the triple response of Lewis?

A

Mild, reversible vascular response to blunt stroking of skin:
- white line: from momentary arteriolar constriction (insignificant and transient)
- red line (flush): local vasodilation due to release of histamine
- flare (spread): neurogenic mechanisms and chemical factors dilate adjacent vessels and enlarge “red zone”
Wheal: pale swelling due to edema

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14
Q

What is stasis?

A

Pooling of blood as the result of vasodilation and slowed rate of flow

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15
Q

Blood pooling and dilation of venules leads to what?

A

Congestion, hemoconcentration and sludging

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16
Q

What is hemoconcentration?

A

When blood becomes thicker following pooling and dilation of venules due to plasma fluid escaping into surrounding tissue. This concentrates the blood.

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17
Q

What is sludging in relation to alternations in blood flow associated with inflammation?

A

Clumping of RBCs due to decreased blood flow, hemoconcentration and actions of inflammatory products that make RBCs sticky

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18
Q

What is an ESR?

A

Erythrocytes sedimentation rate - the rate at which RBCs sediment is influenced by inflammation and therefore can be measured to confirm systemic inflammatory response (ex: Giant Cell Arteritis)

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19
Q

Increased vascular permeability associated with acute inflammation will result in _______.

A

Exudates - consists of fluids, plasma proteins, debris and leukocytes

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20
Q

What are the reversible mechanisms of increased permeability of vessels (especially venules) in acute inflammation?

A
  • endothelial cells contract and open gaps (regulated by chemical mediators)
  • opening of trans cytoplasmic channels
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21
Q

If there is direct injury to the endothelia of vessels in acute inflammation, what will happen?

A

Detachment and necrosis of injured endothelial cells that will leave gaps until repaired

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22
Q

What is the permeability of new blood vessels that form during repair from acute inflammation?

A

They are very permeable (leaky) to plasma elements and therefore contribute to edema

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23
Q

THe pattern of exudation in acute inflammation reflects ______.

A

The severity of vascular injury

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24
Q

What pattern of exudation is generally associated with milder forms of injury with opening of inter-endothelial cell junctions?

A

Serous exudates

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25
Q

What pattern of exudation gives rise to an albuminous straw-colored fluid?

A

Serous exudates

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26
Q

In appearance, sxudates are ______ while transudates are ______.

A

Cloudy : clear

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27
Q

A blister is an example of what pattern of exudation?

A

Serous exudates

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28
Q

What pattern of exudation is associated with more severe injury to endothelium and larger gaps are formed leading to escape of fibrinogen?

A

Fibrinous exudates

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29
Q

When extensive, fibrin deposits promote the infiltration of ______ cells and contribute to the formation of _______

A

Fibroblast : collagenous scar tissue

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30
Q

What pattern of exudation is associated with extensive and severe endothelial damage that contributes to leakage of all blood components?

A

Hemorrhagic exudates

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31
Q

What are some causes of hemorrhagic exudates?

A

Bacterial meningitis and acute radiation injury

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32
Q

What are the steps of cell (leukocyte) response in acute inflammation?

A
  • margination (and rolling)
  • pavement in (adhesion)
  • emigration (diapedesis)
  • migration (chemotaxis)
  • aggregation
  • phagocytosis
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33
Q

What is margination in the cell response?

A

Leukocytes move from the center to the periphery of vessels in response to adhesive mechanisms and decreased blood flow associated with inflammation. They begin to stick to endothelium

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34
Q

What is pavementing in the cell response?

A

Leukocytes adhere to the vessel wall and line-up (like cobble stones)

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35
Q

What is emigration in the cell response?

A

Diapedesis- following adhesion of leukocytes to vessel walls, they actively squeeze through gaps in the vessels and into the tissue

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36
Q

What is migration in cell response?

A

Chemotaxis - the directed movement of leukocytes toward chemical attractants (bacterial products, complement, arachidonic acid metabolites, etc) released at the site of injury

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37
Q

What is aggregation in the cell response?

A

Leukocytes accumulate at site of inflammation

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38
Q

What are the steps of phagocytosis?

A

Adhesion
Ingestion
Killing
Digestion

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39
Q

What is involved in the adhesion step of phagocytosis?

A

Recognition and attachment

  • it is mediated by leukocyte membrane receptor
  • aided by opsonins that that coat the foreign cell and bind specific receptors on leukocytes (examples of opsonins: IgG and complement)
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40
Q

What is involved in the ingestion step of phagocytosis?

A

Engulfment

  • pseudopodia extend around foreign particle and form phagocytic vesicle
  • lysosomes and other cytoplasmic vesicles fuse with phagocytic vesicles and discharge contents to form phagolysosomes
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41
Q

What is involved in the killing step of phagocytosis?

A

Leukocytes produce noxious microbicidal (cytotoxic) agents
Some of this is done by oxygen dependent mechanisms, so it can give rise to oxygen derived free radicals
Some of this is done by oxygen independent mechanisms (lysosomal enzymes)

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42
Q

Products formed by leukocytes during phagocytosis can can injury to surrounding tissues. How?

A
  • Regurgitation through feeding
  • incomplete (frustrated) phagocytosis
  • cytotoxic release from dying leukocyte
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43
Q

What is involved in the digestion step of phagocytosis?

A

Degradation

- acid hydrolases (lysosomal enzymes) digest ingested materials within phagolysosomes

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44
Q

What is another name for neutrophils?

A

PMNs - polymorphonuclear leukocytes

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45
Q

Who are the first responders in inflammation?

A

Neutrophils

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46
Q

Which leukocytes dominate in acute inflammation?

A

Neutrophils

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47
Q

Neutrophils survive in the tissue for only a few days. Why?

A
  • lack the capacity for mitosis
  • sensitive to pHs that are common in inflammatory response
  • undergo apoptosis when “finished”
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48
Q

What cells are efficient phagocytes of bacteria?

A

Neutrophils

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49
Q

Which leukocyte cells contribute to the “first line of defense”

A

Neutrophils

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50
Q

Which leukocytes are associated with all phases of inflammation but respond more slowly and dominate in chronic inflammation?

A

Monocytes/macrophages

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51
Q

Monocytes/macrophages have prolonged survival in the tissue. WHy?

A
  • capable of mitosis and can therefore be sustained by proliferation
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52
Q

What is the primary function of monocytes/macrophages?

A
  • Phagocytosis of bacteria and debris (cell clean up)

- produce cytokines and other active agents (IL-1, TNF, NO, components of complement, etc)

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53
Q

What are the functions of the cytokines and other active agents (IL-1, TNF, NO, components of complement, etc) that are secreted by monocytes/macrophages?

A
  • activate inflammation
  • recruit other leukocytes
  • activate fibroblast and promote collagen formation
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54
Q

What cells often appear in response to viral infections and increased response to allergies?

A

Lymphocytes and plasma cells

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55
Q

What cells are chiefly seen in hypersensitivity conditions such as allergies

A

basophils

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56
Q

WHat cells are chiefly seen in parasitic infections?

A

Eosinophils

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57
Q

PHagocytic leukocytes that produce MBP (major basic protein) which is a cytotoxic agent designed to destroy parasites but also injures tissue in the process?

A

Eosinophils

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58
Q

“Circulating mast cells” whose numbers are increased in peripheral blood in allergies?

A

Basophils

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59
Q

What is the main actions of chemical mediators in inflammation?

A
  • Initiate and regulate inflammation (both vascular and cellular steps)
  • modify actions of other mediators
  • contribute to systemic manifestation of pain and fever
  • bind to specific receptors on target cells
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60
Q

What is the origin of chemical mediators involved in inflammation?

A
  • Locally from cells such as leukocytes and endothelium at the side of injury: They can be preformed elements that are released (histamine) or synthesized on demand (prostaglandins)
  • components present in the blood such as plasma proteases (require activation)
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61
Q

Where do plasma factors used as chemical mediators in inflammation come from?

A

They are synthesized and activated in the liver and then transported to the tissue via the blood.

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62
Q

What are some examples of plasma factors used as chemical mediators in inflammation?

A
  • coagulation proteins (thrombin, fibrin, etc)
  • kinins
  • components of complement
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63
Q

WHat are some preformed mediators that are present in secretory vessels of local cells involved in inflammation?

A

Histamine
Serotonin
Lysosomal enzymes

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64
Q

Serotonin is formed from ____

A

Platelets

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65
Q

Vasoactive amines include ____ and _____

A

Histamine : serotonin

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66
Q

Histamine and serotonin mediate what in the inflammatory response?

A

Immediate increased vascular permeability and vasodilation

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67
Q

Histamine is synthesized and stored in

A

Mast cells, basophils and platelets.

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68
Q

What factors stimulate histamine release?

A
  • trauma
  • thermal factors
  • IgE mediated reactions with sensitized mast cells
  • C3a and C5a (components of complement)
  • lysosomal proteases
  • interleukin-1
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69
Q

What are the derivative of arachadonic acid in the inflammatory process?

A

Prostaglandins, thrombocytes and leukotrienes

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70
Q

The derivatives of arachadonic acid participate in every step of ______

A

Acute inflammation

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71
Q

Where is arachadonic acid found?

A

In the phospholipid bilayer of most cell types (endothelium, platelets, leukocytes)

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72
Q

How is arachadonic acid released due to cell injury?

A

Cell injury activates phospholipase A2 which releases arachidonic acid which in turn is used in synthesis of biologically active agents bu the cyclooxygenase and lipoxygenase pathways

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73
Q

The cyclooxygenase pathway of arachadonic acid produces what?

A

Prostaglandins, Prostacyclins and thromboxanes

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74
Q

What does NSAIDs inhibit?

A

Cyclooxygenase, so prostaglandins. Prostacyclins and thromboxanes are not produced

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75
Q

The lipoxygenase pathway of arachadonic acid produces what?

A

Leukotrienes

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76
Q

What do steroids inhibit?

A

Phospholipase A2, so arachadonic acid is not released from the cell membrane and therefore leukotrienes, prostaglandins, prostacyclins and thromboxanes are not produced

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77
Q

What is the function of leukotrienes?

A

They are chemotactic for neutrophils.

They also increased vascular permeability and vasoconstriction

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78
Q

What is the function of thromboxane A2? And where is it derived from?

A

Platelet aggregation and constriction of blood vessels
Promotes hemostasis
Derived from platelets

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79
Q

What is the function of prostacyclin and where is it formed?

A

Formed in endothelium
Prevent platelet aggregation and is a vasodilator
Beneficial when hemostasis is not required

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80
Q

What is the function of prostaglandin E?

A

Potent vasodilator
Potentiates the affect of bradykinin to cause pain
Mediator of fever by acting on thermoregulatory centers of the hypothalamus

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81
Q

Aspirin and most NSAIDs inhibit ______ and therefore synthesis of all ______ which functions as treatment for pain and fever

A

Cyclooxygenase : prostaglandin

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82
Q

There are 2 forms of cyclooxygenase inhibitors. What are they and how do they work?

A

COX1 - expressed in gastric mucosa so while they do diminish inflammation, they also contribute to increased gastric ulcerations
COX2 - selectively decrease inflammation but minimize stomach affects. Pulled from market due to cardiovascular side effects

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83
Q

SRS or slow reacting substance is another name for what arachadonic acid derivative?

A

Leukotrienes

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84
Q

How does Fish Oil inhibit inflammation?

A

They inhibit the production of leukotrienes (and to a lesser extent, prostaglandins), because it is structurally similar to arachadonic acid and will be metabolized by cyclooxygenase and lipoxygenase to less biologically active products

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85
Q

The other cell derived mediators of inflammation include:

A
  • lysosomal agents
  • oxygen derived radicals
  • cytokines
  • substance P (neurokinin)
  • nitric oxide
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86
Q

A group of circulating molecules that are converted to inflammatory mediators by a series of sequential enzymatic reactions

A

Plasma factors (proteases)

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87
Q

What are some examples of plasma factors?

A
  • the kinin system
  • components of the complement system
  • components of the clotting system
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88
Q

Mini ovens are converted to kinins in the presence of ______

A

Kallikrein

89
Q

Bradykinin contributes to _____ and _____

A

Vascular responses and elicits pain

90
Q

Kallikrein is a plasma protease that is also chemotactic for _____

A

Neutrophils

91
Q

What initiates the kinin system?

A

Contact of blood with collagen, exposure to endotoxins or basement membrane proteins

92
Q

What are some factors that lead to activation of complement?

A

Antigen-antibody complexes, tissue necrosis, products of kinin, coagulation systems, exotoxins, venom

93
Q

Agents of the complement system participate in _____ and _____

A

Inflammatory and immune reactions

94
Q

What is the classic pathway of compliment activation?

A

Exposure to Ag-AB complexes (ex: uric acid in gout)

95
Q

What is the alternate pathway of complement activation?

A

Exposure to endotoxins, viruses, venom, tumor cells and foreign materials

96
Q

What are the components of the clotting system?

A

Fibrinopeptides
Plasmin
Thrombin

97
Q

What functions in lysis of fibrin clots?

A

Plasmin

98
Q

What promotes vasodilation, pavementing, fibroblast proliferation and synthesis of platelet activating factor?

A

Thrombin

99
Q

What are fibrinopeptides?

A

They are formed during fibrinogenesis and fibrinolysis and participate in chemotaxis for leukocytes and permeability alterations

100
Q

What pattern of acute inflammation is common in mild injury, peaks early and resolves quickly?

A

Immediate-transient response

101
Q

Immediate-transient response is associated with the release of _____.

A

Histamine

102
Q

What pattern of acute inflammation appears hours or days after injury and results in delayed release of cytokines?

A

Delayed-prolonged response

103
Q

What pattern of acute inflammation is associated with damage to endothelium and causes include strong thermal or chemical injury?

A

Immediate-sustained response

104
Q

When inflammation leads to rapid neutralization of the injurious agent, tissue injury is minimal and normal structure and function is usually preserved. If inflammation is prolonged, what happens?

A

It can exaggerate tissue damage and promote scarring

Considered to be proliferative

105
Q

WHat are common causes of chronic inflammation?

A
  • persistent agents such as resistant infections or ineffective inflammatory responses
  • recurrent infections such as cholecystitis causing episodic exacerbations
  • primary response to low grade infections
  • prolonged exposure to non-degrading substances such as silica
  • autoimmune conditions such as RA
106
Q

What morphologic pattern of inflammation is characterized by watery, albuminous exudates and is often associated with mild injury

A

Serous

Ex: joint effusion in arthritis or a skin blister

107
Q

What morphologic pattern of inflammation is characterized by being rich in fibrin and is often associated with more sever injury?

A

Fibrinous

Ex:trauma and severe burn, bacterial infection, thematic fever and other hypersensitivity conditions

108
Q

What morphologic pattern of inflammation is characterized by a combination of serous exudates and mucus secretions and occurs in mucus membranes of the upper respiratory and GI?

A

Catarrhal

Ex: common cold, colitis

109
Q

What morphologic pattern of inflammation is characterized by a mixture of neutrophils, enzymes, debris, etc. that forms pus?

A

Pyogenic

Ex: bacteria and chemical agents that are highly chemotactic for neutrophils

110
Q

What morphologic pattern of inflammation is characterized by a collection of pus (neutrophils, enzymes, debris) developing in solid tissue and often resulting in a scar?

A

Abscess

111
Q

What is an abscess called if it has a localized, single point of discharge?

A

Furuncle

112
Q

What is an abscess called that has multiple points of discharge?

A

Carbuncle

113
Q

What kind of pyogenic lesion is characterized by pus(neutrophil, enzymes, debris) in a hollow organ or space?

A

Empyema

Ex: gall bladder lumen, pleural space

114
Q

WHat kind of pyogenic inflammation is associated with acute, diffuse, watery, spreading inflammation seen in subcutaneous tissues and fascial planes?

A

Cellulitis

Commonly caused by type A beta hemolytic strep and staph aureus

115
Q

What is cellulitis known as when it is in the face?

A

Erysipelas

116
Q

What is cellulitis called when it involves oral and pharyngeal infection that extends into the neck and mediastinum?

A

Ludwig’s angina

117
Q

What morphologic pattern of inflammation that is associated with accumulation of indigestible material and hypersensitivity giving rise to small modular lesions?

A

Granulomatous

118
Q

Granulomas associated with granulomatous inflammation consist of lymphocytes, giant cells and modified macrophages called _______

A

Epithelioid cells

119
Q

What are some common examples of granulomas?

A
  • foreign bodies: indigestible materials such as uric acid and silica
  • caseation: common in fungal and mycobacterial infections such as TB and leprosy
  • autoimmunity/hypersensitivity: RA, rheumatic fever, Crohn’s disease, sarcoidosis
120
Q

What morphologic pattern of inflammation is a local surface defect (excavation) caused by sloughing of
inflammatory necrotic tissue

A

Ulcer

121
Q

What are common locations for ulcers?

A

All epithelial surfaces:
- Skin- “bed-sores”, “stasis ulcers” (with severe varicosities
of saphenous veins), etc.
- Gastro-intestinal tract- “canker sores”, peptic ulcers, etc.
- Genito-urinary system- cystitis, cervicitis, etc.

122
Q

What is another name for a canker sore?

A

Aphthous stomatitis

123
Q

What are the stages of evolution of an ulcer?

A

Erosion - shallow and small, focal necrosis
Acute ulcer - larger erosion but still a able of complete restoration
Chronic ulcer - enlarged and deeper, often difficult to repair and may scar

124
Q

What morphologic pattern of inflammation is characterized by the formation of a membranous structure that consists of fibrin, necrotic cells and debris on a mucosal surface (common in upper respiratory and lower digestive tracts)?

A

Pseudomembranous inflammation

125
Q

What are some common causes of pseudomembranous inflammation?

A

(1) Diphtheria: lesions of larynx and pharynx
(2) Inhalation of noxious fumes or hot gases (thermal
injury) to respiratory tract

126
Q

Terminal lymphatics (capillaries) consist of _______ tubules

A

Blind ended

127
Q

What is the effect of inflammation on terminal lymphatics?

A

Inflammation leads to edema with increased lymphatic flow. This causes distention of lymphatic capillaries. The endothelial junctions in these capillaries will open and increase drainage of fluids

128
Q

What is it called when lymphatics have been invaded by streptococci and other pyogenic organisms from a primary infection?

A

Acute lymphangitis

-basically an inflamed lymph node

129
Q

What is the classic finding of acute lymphangitis due to a primary infection?

A

Red streak under skin from primary infection to inflamed lymph node

130
Q

Lymph nodes provide a second line of defense and when they become inflammed it is called ______

A

Lymphadenitis

131
Q

What are the symptoms of lymphadenitis?

A

Enlarged and tender lymph nodes

Severe infections may lead to necrosis and abscesses of lymph nodes

132
Q

Systemic manifestations of inflammation are sometimes called ______

A

“Acute phase” reactions

133
Q

What are some examples of systemic manifestations of inflammation?

A 
Fever
Sleepiness (somnolence)
Malaise
Change in appetite
Change in circulating WBCs
Alteration in plasma proteins
134
Q

An elevated ESR is likely due to what?

A

Elevated fibrinogen, a plasma protein associated with systemic manifestation of inflammation

135
Q

What plasma proteins would be elevated in systemic inflammation?

A
  • protease inhibitor
  • amyloid associated protein
  • complement
  • fibrinogen
  • CRP
  • ESR
136
Q

Normal temperature of the body are regulated by the _______ to maintain a balance between heat loss and gain

A

Hypothalamus

137
Q

What is another word for fever?

A

Pyrexia

138
Q

What are the most common causes of fever?

A
  • infection
  • non-infectious inflammatory conditions
  • tissue necrosis
  • CNS lesion
  • certain neoplasms
139
Q

What is the pathogenic mechanism of fever?

A

Actions of cytokines (IL-2, TNF-alpha) and PGE (pyrogens) will up regulate the hypothalamic thermoregulatory center

140
Q

What are the effects of fever?

A

Increased metabolism and oxygen consumption
Increased respiratory and heart rate
Dehydration

141
Q

Except for nerve cells, most cells tolerate temperature up to ______

A

105-106 degrees F

142
Q

Fever increases cardiac rate by ____ beats/minute for each degree F rise in body temperature

A

7

143
Q

What are the benefits fo fever?

A
  • stimulates proliferation of lymphocytes and production of antibodies due to action of cytokines
  • inhibits growth and leads to decreased survival of pathogenic bacteria
144
Q

What are the stages of fever?

A
  • prodrome: no fever but feeling of sick and achy
  • cold: cutaneous vessels constrict to conserve body heat and skin feels cold
  • Flush: heat production and heat loss because cutaneous vessels dilate from time to time
  • crisis: fever breaks, cutaneous vessels dilate and sweating promotes cooling
145
Q

Elevation in circulating white blood cells is called ______

A

Leukocytosis

146
Q

What leukocytes are usually affected in leukocytosis?

A

Neutrophils (in bacterial infection)

147
Q

What is “shift to the left” during leukocytosis?

A

WBC are produced at higher rates and results in immature cells being released at higher rates

148
Q

What is it called when there is a reduction in circulating leukocytes?

A

Leukocytopenia

149
Q

What are common causes of leukocytopenia?

A
  • overwhelming infection
  • marrow dysfunction
  • debilitating/immune compromising disease
150
Q

Severely reduced WBC # of less than _______ results in increased vulnerability for infection.

A

1000/ cu mm

151
Q

The ideal outcome of inflammation that prepares the site of injury for repair and completely restores tissue to normal

A

Resolution

152
Q

What are the mechanisms involved in resolution of inflammation?

A
  • reversing inflammatory process by inactivating inflammatory stimulus and reversing vascular changes
  • remove inflammatory debris and exudates
153
Q

What are the factors that favor resolution of inflammation?

A
  • limited cell death and tissue damage
  • rapid destruction of bacteria or other causative agent
  • adequate blood supply for removal of debris and fluids
  • adequate capacity for regeneration of affected tissues
154
Q

Replacement of damaged or destroyed cells by parenchyma cells and stroma (CT) is referred to as ______

A

Regeneration

155
Q

What are the three actions of tissue regeneration?

A

Resolution
Parenchymal regeneration
Repair of CT

156
Q

when damaged cells are replaced by cells of the SAME type

A

Regeneration

157
Q

What are factors influencing regeneration of tissue?

A
  • capacity for mitosis
  • # of surviving cells
  • preservation of the underlying CT stroma
158
Q

Regeneration is promoted when the tissue architecture is maintained, therefore a disruptions in ______ and _____ deposits interfere with regeneration

A

Basement membrane : scar tissue

159
Q

Tissue can be classified according to their capacity for mitosis and regeneration. Continuous replicators are classified as ______. What are some examples?

A

Labile tissues

Ex: epithelium and marrow

160
Q

Tissue can be classified according to their capacity for mitosis and regeneration. Discontinuous replicators that proliferate only when needed or stimulated are classified as ______. What are some examples?

A

Stable tissues

Ex: bones, CT, glands

161
Q

Tissue can be classified according to their capacity for mitosis and regeneration. Non-replicators are classified as ______. What are some examples?

A

Permanent tissues

Ex: neurons, striated muscle

162
Q

Repair by CT

A

Replacement of the damaged tissues with collagenous (scar, fibrous) tissue

163
Q

An immature or early form of scar consisting of connective tissue that is characteristically cellular, vascular and edematous in nature?

A

Granulation tissue

164
Q

repair by replacement of connective tissue with

“granulation tissue”

A

Organization

165
Q

Organization is favored by:

A
  • Large “persistent” fibrin deposits
  • Large areas of tissue necrosis
  • Accumulated exudates and debris
166
Q

What are the components of granulation tissue?

A
  • presence of macrophages cleaning up debris
  • presence of fibroblasts that are laying down scar tissue
  • formation of new blood vessels
167
Q

______ replace neutrophils (first responders) as clean up crew to remove debris

A

Macrophages

168
Q

Activated macrophages, in addition to removing debris in granulation tissue, produce:

A
  • proteases
  • chemotactic factors
  • coagulation factors
  • arachadonic acid metabolites
  • nitric oxide
  • platelet derived growth factor to attract platelets
  • angiogenesis factors
  • promote proliferation of fibroblasts and collagen synthesis
169
Q

What is the function of fibroblasts in granulation tissue?

A
  • migrate into site of injury and proliferate

- Produce matrix and collagen fibers

170
Q

How do fibroblasts decrease the size of wound defect and contribute to deformity of scarring?

A

Fibroblasts contain contractile fibers

171
Q

What are the two patterns of wound healing?

A
  • first intention

- second intention

172
Q

The ideal pattern of wound healing that occurs when the margins of the wound are clean such as a surgical wound that has been sutured.

A

First intention

173
Q

What are the stages of primary union in first intention wound healing?

A
  • immediate: fibrin rich blood clot appears
  • 24-48 hours: neutrophils appear and epithelium begins to regenerate
  • 3 days: macrophages are well established and granulation tissue forms
  • 5 days: granulation tissue fills wound, collagen fibrils bridge incision and blood vessels maximally formed
  • 1 month: blood vessels continue to involute, collagen content and strength increases
174
Q

How can collagen deposition in wound repair limit function?

A

The collagen is laid down somewhat ununiformly and can limit flexibility of the tissue. Things can be done to break up those adhesions and encourage collagen deposition that is more linear

175
Q

Repair of large open wounds with separated edges occurs by ______.

A

Secondary union/intention

176
Q

Tissue defect in secondary union is filled with ______

A

Granulation tissue

177
Q

What pattern of wound healing has more intense and prolonged inflammation?

A

Secondary union

178
Q

What pattern of wound repair is delayed and often results in deformity?

A

Secondary union

179
Q

What are some examples of secondary union/intention?

A

Repair of ulcers, cutaneous burns and non-sutured skin wounds

180
Q

Well placed sutures will provide ______% of original tensile strength of the tissue

A

70

181
Q

A week after initial injury, the wound strength (without sutures) is _____% original tensile strength of tissue

A

10

182
Q

3 months after initial injury, the wound strength (without sutures) is _____% original tensile strength of tissue

A

80, this is maximum repaired wound strength for skin

183
Q

What factors contribute to increased wound strength?

A
  • Type and quantity of collagen (Type 3 is initially deposited and later replaced by type 1 collagen)
  • orientation and size of collagen fibers (more strength if in the direction of tensile forces)
  • cross-linkages between collagen fibrils
184
Q

What are local factors that affect inflammation and repair?

A
  • nature and severity of injury
  • tissue type
  • adequate blood supply favors repair (skin has more blood than ligaments)
  • infections intensify tissue damage
  • movement can disrupt repair in early stages but break up adhesions in later stages
  • radiation injures blood vessels and proliferating cells
185
Q

What are host factors that affect inflammation and repair?

A
  • age (young repair quicker)
  • nutrition (more proteins are needed for would repair, vitamin C helps with collagen synthesis, zinc helps with nuclei acid synthesis)
  • hematological and circulatory disturbances (cardiovascular disease, anemia, leukocytopenia, clotting disturbances)
  • steroids and hormone levels
  • concurrent diseases (cancer, diabetes)
  • foreign bodies (bone fragments, thrombin, sutures, etc)
186
Q

How does cardiovascular disease affect wound repair?

A

Reduced perfusion results in poor wound repair and increased risk for infection

187
Q

How does anemia affect would repair?

A

Contributes to tissue hypoxia and poor repair

188
Q

How does leukocytopenia affect wound repair?

A

The dysfunctional or low leukocytes count impair immune defenses

189
Q

How does clotting disturbances affect wound repair?

A

Clotting deficiencies, hemorrhage and excessive thrombosis complicate inflammation and repair

190
Q

How do steroids affect wound repair?

A

They inhibit collagen synthesis and decrease inflammation by blocking arachadonic acid

191
Q

How do growth and thyroid hormones affect wound repair?

A

They favor and promote repair

192
Q

How do terminal stages of debilitating disease affect wound repair?

A

Disrupts normal inflammation and repair

193
Q

How does cancer affect wound repair?

A

May alter immune responses and contribute to anemia

194
Q

How does diabetes affect wound repair?

A

Gives rise to complex problems including arteriosclerosis disease, sensory neuropathy and inhibited leukocyte responses

195
Q

How do foreign bodies such as bone fragments or thrombi affect wound repair?

A

Exaggerate and prolong inflammation and interfere with repair

196
Q

Pathological complication of wound healing include:

A
  • inadequate scar tissue formation - “weak scars”
  • excessive proliferation/scarring (keloids)
  • large wounds, especially burns and ulcers give rise to contracture and scarring deformities
197
Q

What are some contributing factors to inadequate scar tissue formation?

A
  • circulatory insufficiency
  • steroid excess
  • dietary deficiencies
  • infections
198
Q

What is wound dehiscence?

A

Break down of surgical wound likely due to inadequate scarring or poor surgical technique

199
Q

Nodular masses of hyper plastic scar tissue that occurs when the wound healing process runs unchecked

A

Keloids

200
Q

What kind of wounds commonly give rise to contracture and scarring deformities once wound repair is complete?

A

Burns and large wounds such as ulcers

201
Q

Tissue repair and regeneration is regulated by _____ and ______ factors

A

Soluble and insoluble

202
Q

In regeneration and repair, normal tissue responds to signals associated with ECM component and growth factors. Initially, what is the response of the normal tissue?

A

proliferation of cells in tissue undergoing repair

203
Q

In regeneration and repair, normal tissue responds to signals associated with ECM component and growth factors. Later and as repair is completed, what is the response of the normal tissue?

A

As the normal tissue densities are reestablished in regeneration and repair, mitosis is inhibited in the tissue

204
Q

In subcutaneous bruising due to tissue trauma, _____ is common

A

Swelling (when in restricted space, may cause compression

205
Q

Therapies for tissue damage to musculoskeletal structure are directed to:

A
  • control bleeding and edema
  • minimize inflammation
  • prevent fibrous adhesions
  • promote repair
206
Q

What tissue type is highly vascular and therefore hemorrhage is commonly seen with trauma?

A

Muscle

207
Q

Tendons, when “healthy”, will more likely tear/avulse in what location due to trauma?

A
  • bony attachments and muscle-tendon junctions
208
Q

Regeneration of epithelium (mucosal tissue) of the GI is usually _______.

A

Rapid

209
Q

What is the regeneration capacity of the liver?

A

Excellent when tissue (stromal) framework is preserved.

210
Q

Scarring of the liver leads to _____

A

Cirrhosis

211
Q

What is the healing capacity of the kidneys?

A

Epithelium regenerates well but glomeruli are limited in their capacity for regeneration

212
Q

What is the healing capacity of the lungs?

A
  • trachea and chronic have excellent capacity for regeneration
  • alveoli regenerate well only if underlying architecture is maintained
213
Q

Capacity of regeneration of the alveoli after bacterial pneumonia

A

Very good

214
Q

Repair fo necrosis of the myocardium is limited due to________

A

Fibrous scarring

215
Q

The capacity for regeneration of skeletal muscles is fairly good, especially when ______ is preserved.

A

Sarcolemma

Repair of large areas of necrosis is limited

216
Q

Smooth muscle regeneration capacity after wound?

A

Fairly good

217
Q

What is the capacity for regenration of the CNS

A

Necrotic neurons or destroyed fiber tracts do not regenerate

218
Q

What is the regeneration capacity of the PNS?

A

Regenerate when neurolemma is preserved

219
Q

Fractures are usually accompanied by _____ and/or ____.

A

soft tissue damage and/or

hemorrhage.

Pathology I (10 decks)

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