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Pathobiology > Inflammation and Repair > Flashcards

Inflammation and Repair Flashcards

1
Q

What are the classical localized signs / symptoms of acute inflammation?

A

Rubor - redness
Tumor - enlarged area due to edema / swelling
Calor - Warmth
Dolor - Pain

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2
Q

What is one important feature of tissue in order for inflammation to occur?

A

Tissue must be vascularized in order for cellular / molecular reaction of inflammation to occur (involves vascular response and leukocyte influx)

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3
Q

What is the primary difference between acute / chronic inflammation in terms of cellular involvement?

A

Acute - involves neutrophils and monocytes from blood converting to macrophages

Chronic - Predominately macrophages, lymphocytes, and plasma cells

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4
Q

When does a repair process typically occur?

A

Occurs concurrently with acute inflammation but usually finishes afterwards

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5
Q

What is the vascular response of acute inflammation and how does this occur? How does this relate to edema?

A
  1. Vessels vasodilate -> increased blood flow + intravascular hydrostatic pressure
  2. Vascular permeability increases -> protein leaks out into interstitium -> fluid follows -> exudative edema
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6
Q

What leads to the intravascular stasis of blood in inflammation?

A

Plasma leaks out of the vasculature into the interstitium -> blood becomes thick and sludgy due to the formed elements of the blood being in greater concentration

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7
Q

What chemicals mediate the hyperemia of inflammation? What is their role?

A

These are the vascular vasodilators:

Histamine and NO

-> increase the intravascular hydrostatic pressure

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8
Q

What are the four mechanisms of how vascular permeability is increased in acute inflammation, and which is most common?

A
  1. Formation of gaps between endothelial cells of venules - most common
  2. Injury to endothelium of microcirculation
  3. Endothelial transcytosis
  4. Secondary to angiogenesis - forming blood vessels are immature / leaky
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9
Q

What are the two mechanisms behind forming gaps between endothelial cells? What mediates this?

A
  1. Immediate response -> endothelial cell contraction mediated by histamine, bradykinin, and leukotrienes
  2. Delayed, longer-lasting response -> retraction of endothelium due cytoskeletal changes mediated by cytokines (IL-1, TNF, and IFN-y)
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10
Q

What causes injury to endothelial cells in microcirculation?

A

Bacterial toxins, tissue necrosis, or activated leukocytes (i.e. macrophages / neutrophils)

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11
Q

What is endothelial transcytosis and how does it occur?

A

Water can leak THROUGH endothelial cells in a VEGF-mediated phenomenon, occurring mostly in endothelium of venules.

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12
Q

Where and when does leukocyte diapedesis usually occur? What initiates the process?

A

Occurs in postcapillary venules, with neutrophils entering 1-2 days after injury

Process is initiated when leukocytes are marginated due to the intravascular stasis of blood (not mediated by a receptor)

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13
Q

Where does vasodilation occur? Increased vascular permeability?

A

Vasodilation - Primarily in pre-capillary arterioles, increases the hydrostatic pressure in the capillaries + venules

Vascular permeability - primarily in the venules, but due to endothelial injury can occur anywhere in vasculature

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14
Q

What are the steps in invasion of leukocytes into the tissues?

A
  1. Margination
  2. Rolling
  3. Adhesion
  4. Transmigration (diapedesis)
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15
Q

How does rolling occur? What upregulates this

A

Leukocytes transiently attach to E-selectins on endothelium in a low affinity interaction to slow them down via their sialylated carbohydrate ligands (sialyl-Lewis) receptors.

E and P selectins are upregulated via histamine, TNF, and IL-1

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16
Q

What mediates adhesion?

A

Firm attachment, high affinity interaction between VCAM-1 and ICAM-1 (integrin ligands) of endothelial cells and ligands on leukocytes. These are upregulated via IL-1 and TNF.

ICAM = integrin cell adhesion molecule

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17
Q

What process moves integrins to a high-affinity state?

A

Chemokines from the inflamed tissue (i.e. IL-8) are transcytosed and expressed on interior vascular surface. These also bind to the leukocytes and cause higher affinity expression of ligands on leukocyte surface which bind ICAM/VCAM more tightly

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18
Q

What CD marker mediates diapedesis of leukocytes, and what is needed to get thru the basement membrane?

A

CD31 - PECAM-1 = “peeking thru the endothelium”

-> collagenases are needed to break through the basement membrane of the endothelium

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19
Q

How does chemotaxis occur?

A

Exogenous or endogenous chemotaxic factors bind GPCRs on leukocytes, leading to actin reorganization with assembly at the front of the filopod and disassembly at the rear to move towards the stimulus, with contraction of actin / myosin

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20
Q

What receptors can mediate the activation of leukocytes?

A
  1. Toll-like receptors
  2. GPCRs - chemokines and anaphylatoxins
  3. Cytokines - IFN-y
  4. Opsonins - IgG, C3b, etc
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21
Q

What occurs once leukocytes are activated? (This can occur in the bloodstream or interstitium)

A
  1. Inflammatory response is amplified -> greater adhesion and production / secretion of chemical mediators
  2. Initiation of phagocytosis and release of toxic products like ROS both intracellularly and extracellular
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22
Q

How does recognition and engulfment in phagocytosis work?

A

Recognition - via receptors (i.e. TLRs) or opsonins

Engulfment - cytoplasmic pseudopods surround particle, form a phagosome which will be fused with a lysosome

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23
Q

What are the two mechanisms of killing in phagocytosis and which is more important? What mediators are involved in the less important pathway?

A
  1. Oxygen-dependent - most important
  2. Oxygen-independent - less important, includes proteins which increase permeability of membranes, including lysosomes, proteases, hydrolases, defensins, and major basic protein of eosinophils
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24
Q

What are the oxygen-dependent mechanisms of killing?

A
  1. Formation of superoxide anion via NADPH oxidase
  2. Formation of hypochlorite (OCl-) via myeloperoxidase
  3. Generation of peroxynitrite radicals from NO
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25
Q

What is a neutrophil extracellular trap (NET)?

A

Neutrophils go on a suicide mission and use their nuclear chromatin / antimicrobial granules to form meshworks to trap pathogens (i.e. S. aureus)

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26
Q

What are some mechanisms by which leukocytes release damaging chemicals mediating host cell damage?

A
  1. Regurgitation during feeding (of substances)
  2. Frustrated phagocytosis (too large to eat, release contents extracellularly)
  3. Membrane injury via phagocytosed material
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27
Q

How is acute inflammation typically terminated?

A
  1. Removal of initial stimulus
  2. Short-lived nature of chemical mediators + apoptosis of neutrophils
  3. Production / release of antiinflammatory agents like TGF-beta, lipoxins
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28
Q

What acute inflammatory substances are the “early responders” present in preformed stores, and what releases them? What do they do generally?

A

Vasoactive amines - cause vasodilation and increased vascular permeability

  1. Histamine - mast cells
  2. Serotonin - activated platelets
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29
Q

What are the pathways by which complement is activated?

A
  1. Classical - Binding of C1 to IgG or IgM
  2. Lectin - C1 binds sugar residues on pathogen
  3. Alternative - C3b directly binds to the pathogen and is stabilized by factor B and properdin to C3 convertase for further opsonization
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30
Q

What ultimately fixes the MAC?

A

When C4b2b3b of lectin / classical pathway or C3bBb3b of alternative pathway becomes a C5 convertase and converts / binds C5b to the cell, allowing formation of MAC from C5-9

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31
Q

What are the anaphylatoxins of the complement pathway and how do they exert their effects?

A

C3a and C5a -> cause vasodilation and increased vascular permeability by directly stimulating mast cell release of histamine

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32
Q

How does complement function to cause chemotaxis of immune mediators?

A

Primarily C5a acts as a chemoattractant directly binding leukocytes.

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33
Q

What is the kinin system and how is it activated?

A

A system of plasma proteins which are activated in inflammation (much like complement)

Activated when Hageman factor (Factor 12) contacts collagen, which facilitates its conversion to 12a

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34
Q

What does Hageman factor do once activated?

A

12a will convert prekallikrein to kallikrein

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35
Q

What are the four functions of kallikrein?

A

Kallikrein - 4 functions

  1. Chemotactic agent like C5a or IL-8
  2. Converts HMW kininogen to bradykinin
  3. Converts plasminogen to plasmin
  4. Increases conversion of 12 (Hageman factor) to 12a (with HMWK as cofactor) -> positive feedback loop
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36
Q

What does bradykinin do?

A
  1. Histamine-like effects -> increases vasodilation and vascular permeability
  2. Pain!! sensitization of nociceptors
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37
Q

How does thrombin contribute to inflammation?

A

In addition to converting fibrinogen to fibrin, Thrombin (2a) binds to receptors on many cell types, increasing the inflammatory response by causing expression of adhesion molecules, production of cytokines, and generation of prostaglandins.

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38
Q

What activates plasmin, and is it pro-inflammatory / antiinflammatory? How does it exert its effects?

A

Activated by kallikrein, it is pro-inflammatory

Although it destroys fibrin clots, it also increases the inflammatory response by cleavage of C3 to C3a -> increased alternate pathway activation

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39
Q

What is the difference between COX-1 and COX-2, and what is the signal for their activity to increase?

A

COX-1 - constitutively active
COX-2 - inducible in inflammation

They both become active when Ca+2 in cytoplasm increases, increasing PLA2 activation to process arachidonic acid to make prostaglandins.

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40
Q

What are the general functions of the prostaglandins?

A
  1. Bradykinin-like -> vasodilation, increased vascular permeability, pain
  2. Inhibit platelet aggregation
  3. Fever
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41
Q

What COX product is the exception to the prostaglandin functions?

A

Thromboxane A2 (TXA2)

  • > causes vasoconstriction and platelet aggregation
  • > COX product which is the target of aspirin, as COX-1 is expressed mostly in platelets
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42
Q

What leukotriene is a chemoattractant for neutrophils and where is it produced?

A

LTB4 - produced by neutrophils only as a chemoattractant for other neutrophils

-> made by lipoxygenases

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43
Q

What are the general functions of the other leukotrienes and why are they not synthesized in neutrophils alone?

A

LTC4,D4,E4 (CDE)

Cause vasoconstriction, bronchospasm, and increased vascular permeability (good target for anti-asthma drugs)

Lipoxygenases are not present in all tissues -> require co-metabolism via neutrophils and platelets

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44
Q

What are lipoxins?

A

A product made by lipoxygenases in platelets, which are anti-inflammatory to the acute response

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45
Q

How are glucocorticoids anti-inflammatory?

A

Downregulation of phospholipase A2, among other things

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46
Q

How is PAF made and what does it do?

A

Platelet activating factor (PAF)

Made from phospholipids (not A2) in many cell types

  1. Stimulates leukocyte (WBC) as well as platelet activation
  2. Increases vascular permeability
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47
Q

What are the important inflammatory cytokines mediating local effects and what do they do?

A

TNF and IL-1, produced primarily by macrophages

  1. Endothelial cell activation
  2. Leukocyte stimulation (increased cytokine secretion)
  3. Stimulation of fibroblasts transition into repair phase
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48
Q

What cytokines have acute systemic effects and what are these effects?

A

TNF, IL-1, and IL-6

Causes fever, anorexia, fatigue, increased neutrophil count, APP production (IL-6)

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49
Q

What cytokines have chronic systemic effects and what is this effect?

A

TNF, IL-1, IL-6

-> cachexia (primarily mediated by TNF) -> increased lipid and protein mobilization leading to wasting

50
Q

Give two selective chemokines.

A
  1. IL-8 - selective for neutrophils

2. Eotaxin - eosinophilic chemotaxic factor

51
Q

Is nitric oxide considered proinflammatory or anti-inflammatory, and how does it work?

A

Mixture, although production is increased during inflammation by macrophages / endothelial cells

Proinflammatory properties:

  1. Vasodilation
  2. Antimacrobial activity - production of peroxynitrite free radicals

Anti-inflammatory:
Reduction of platelet and leukocyte adhesion

52
Q

What are “essential inactivators”? Give an example.

A

Proteins present in serum or tissue (antioxidants or antiproteases) which protect the ECM and neighboring cells for damage

-> example: alpha-1-antitrypsin, neutralizes neutrophil elastase

53
Q

What is substance P?

A

A pro-inflammatory neuropeptide, increases pain response in CNS / PNS

(along with bradykinin and prostaglandins)

54
Q

What substance is thought to mediate the invasion of the immune system into hypoxic tissue?

A

Hypoxia-induced factor 1alpha

55
Q

Why is uric acid considered pro-inflammatory?

A

Derived from dead cells as purine breakdown product

-> leads to production of inflammasome in phagocyte, which stimulates IL-1 release

56
Q

How can lymphatic drainage be a problem in inflammation? What are lymphangitis and lymphadenitis?

A

It is a potential source for movement of pathogens from a localized source into the systemic circulation by draining into venous circulation + tends to increase response by moving pathogens to regional lymph nodes for antigen presentation

Can cause:

  • > lymphangitis = inflammation of lymph vessels (can inflame the tract on a way to regional lymph node)
  • > lymphadenitis = inflammation of lymph nodes
  • > bacteremia
57
Q

What are the three main possible outcomes of acute inflammation? When do these occur?

A
  1. Complete resolution -> back to normal morphology and function, in tissues capable of regeneration
  2. Organization -> healing with fibrosis, if damage is significant and regeneration is limited in these tissues
  3. Persistent inflammation -> sustained tissue injury
58
Q

What is serous inflammation?

A

A type of acute inflammation in which sparsely-cellular fluid accumulates at site of trauma (i.e. blister / mild burn)

59
Q

What is fibrinous inflammation? How does it appear histologically?

A

Acute inflammatory proess where extravascular fibrin deposition predominates -> often on tissue surfaces in body cavities

Appears very eosinophilic due to fibrin buildup, and is sparsely cellular

60
Q

What is suppurative inflammation and what causes it?

A

Also called purulent inflammation, often caused by pyogenic bacteria

It is a dense collection of inflammatory cells with exudative edema and cell debris (does not always destroy tissue structure to cause necrosis)

61
Q

What is an abscess? Why can it not be treated without incision and drainage?

A

A specific type of suppurative inflammation which leads to localized liquefactive necrosis

-> will have a fibrous capsule if persistent

Not treated without drainage because the liquefactive necrosis destroys the vascularization and hence plasma drug delivery

62
Q

What is ulceration?

A

Erosion of an organ’s epithelial surface and destruction of subjacent tissue which forms a crater that is like a half-abscess.

Can develop fibrosis or chronic inflammation at the base if untreated.

63
Q

What is the most common cause of chronic inflammation, and what is the strange exception?

A

Most common: persistent tissue injury due to untreated infection or autoimmune process

Exception: Intracellular pathogens like viral infections are grouped under chronic inflammation even if they are acute -> require cell-mediated immunity like cytotoxic T cells and NK cells (appear like a chronic infiltrate)

64
Q

What are the components of the chronic immune infiltrate?

A

Primarily macrophages, lymphocytes (T cells and NK), and plasma cells

Macrophages will recruit involvement of fibroblasts

65
Q

What are the two broad categories of macrophages? How are they activated and what is their function?

A

M1 - classically activated - via TH1 cells and IFN-y, function in inflammation and microbial killing

M2 - alternatively activated - via TH2 cells, release anti-inflammatory factors like IL-10 and TGF-beta, and stimulate fibrosis / tissue repair via growth factors

66
Q

What chronic inflammatory process would not be associated with fibrosis?

A

Viral infection response

67
Q

What is granulomatous inflammation and what characterizes it?

A

A type of chronic inflammation characterized by distinct aggregates of activated macrophages + tissue injury and fibrosis

68
Q

Give two general causes of granulomatous inflammation.

A
  1. Organisms resistant to killing which will cause a Type 4 hypersensitivity: i.e. TB, histoplasmosis
  2. Particulate material which cannot be degraded -> nonabsorbable sutures, uric acid crystals
69
Q

What mechanistically occurs to form granulomas? WHat is the diagnostic cell type?

A

Persistant infection leads to enlargement, adherence, and coalescence of macrophages -> can form giant cells

T lymphocytes become activated and produce IFN-y to further activate macrophages, and IL-2 further strengthen’s T cell response

70
Q

What typically does NOT occur in particuate material granulomas which does in TB granulomas?

A

Central caseous necrosis

71
Q

What are the two primary etiologies of eosinophilic-predominant inflammation?

A

This is a subset of chronic inflammation

  1. IgE-mediated - Type 1 hypersensitivity
  2. Parasitic infections - major basic protein is useful
72
Q

What is SIRS and what is its primary etiology?

A

Systemic Inflammatory Response Syndrome (SIRS)

  • > common in bacterial infections
  • > mediated by activated macrophages secreting TNF, IL-1, and IL-6
73
Q

What are the systemic changes which occur with SIRS?

A

Nonspecific symptoms like fatigue, anorexia, myalgia

Fever -> increased prostaglandins in hypothalamus

Leukocytosis -> total WBC increased

74
Q

What are the early / late sources of WBC in leukocytosis?

A

Early - Release of reserve leukocytes from bone marrow

Late - production of colony stimulating factors, increasing formation

75
Q

What does a left shift indicate and what can cause it?

A

Reactive neutrophilia -> increased peripheral neutrophil count with increased production of neutrophils which are often in band form

-> Can be due to tissue injury, but most dramatic in bacterial infection

76
Q

What is a leukemoid reaction?

A

A marked left shift which is so drastic it looks like leukemia, but actually just caused by infection

77
Q

What are Dohle bodies and toxic granulation and what does this indicate?

A

Dohle bodies - pieces of rough ER in basophilic cytoplasm of neutrophils

Toxic granulation - dark, course granulation

-> indicates very severe infection

78
Q

What typically causes reactive lymphocytosis and what types of lymphocytes are present (one of these is abnormal and common)

A

Most common in viral infections

  • > polyclonal lymphocytes with unique surface antigen receptors
  • > atypical lymphocytes - activated CD8 cells which are large and amorphous
79
Q

When is reactive monocytosis seen?

A

Chronic inflammatory conditions like TB

80
Q

When is reactive eosinophilia seen?

A

IgE-mediated allergy, and parasitic infections

81
Q

When is reactive basophilia seen?

A

Rare -> usually a result of a bone marrow malignancy

82
Q

What are positive vs negative acute phase proteins?

A

Positive:
Proteins which are upregulated in acute inflammation

Negative:
Proteins which are downregulated in acute inflammation

83
Q

What is the function of C-reactive protein? Is it a positive or negative APP?

A

+

Opsonization of damaged cells, activation of complement
-> fairly sensitive marker for inflammation

84
Q

What is the function of serum amyloid A protein? Is it a positive or negative APP?

A

+

Levels increase rapidly in acute inflammation, probably mobilizes cholesterol to repair cell membranes

85
Q

What is the erythrocyte sedimentation rate (ESR)? Does this increase or decrease in inflammation and why?

A

Distance that RBCs settle in a vertical column of anticoagulated blood in one hour

Increased in inflammation because of elevated fibrinogen levels (+APP), leading to increased thombosis risk.

Fibrinogen helps RBCs settle faster by making RBCs stick together and form Rouleaux stacks which are higher density and reach the bottom faster.

86
Q

Is alpha-1-antitrypsin + or - APP?

A

+, protects tissues from inflammation as an inhibitor of serine proteases

87
Q

What are the functions of haptoglobin, ferritin, and hepcidin and are they positive or negative APPs?

A

Haptoglobin - binds free hemoglobin
Hepcidin - decreases iron absorption and transport (kills da iron)
Ferritin - binds free iron

  • > decreases microbes ability to take up free iron
  • > positive APPs
88
Q

What is ceruloplasmin?

A

A positive APP, a major copper carrier enzyme which scavenges free radicals and oxidizes iron to Fe+3 so it can be carried by ferritin

89
Q

List a few negative APPs and why these exist?

A

Albumin, transferrin, retinol-binding protein -> reduced levels can shuttle more substrates into positive APP synthesis

Hormone-binding globulins like transthyretin and cortisol-binding globulin

90
Q

Why are transthyretin and cortisol-binding globulin negative APPs?

A

Decreased levels reduce hormone binding capacity -> temporary increase in action of free hormone (T4 and cortisol)

91
Q

What are the general features of septic shock?

A

Multisystem organ failure -> decreased cardiac output, decreased systemic blood pressure, disseminated intravascular coagulation, ARDS

92
Q

What is a labile vs stable vs permanent tissue? Give examples of each.

A

Labile - composed of cells being continuously replaced, like epithelial cells or bone marrow

Stable = quiescent - cells resting in G0 which can proliferate like hepatocytes, smooth muscle cells, and fibroblasts

Permanent tissue - cells with very limited regen capacity like neurons, cardiomyocytes, SM cells

93
Q

What cell types serve to replace cells in stable, labile, and permanent tissues?

A

Stable tissues - parenchymal tissue cells (i.e. hepatocytes divide to replace hepatocytes)

Labile tissues - stem cell pools

Stable - very limited stem cell pools, i.e. satellite cells of skeletal muscle

94
Q

What are the two types of stem cell pools and which one is utilized most commonly for tissue expansion? What is their primary difference?

A
  1. Tissue stem cells -> most common
    - Restricted differentiation capacity, i.e. basal cells of epithelium, base of intestinal crypts
  2. Multipotent adult progenitor cells
    - broad differentiation capacity
    - identified in many tissues, including bone marrow
95
Q

What are the growth factors which stimulate the proliferation of epithelial cells?

A

Epidermal growth factor (EGF)

Hepatocyte growth factor (HGF)

96
Q

What two factors are needed for angiogenesis as well as tissue regeneration and healing?

A

Vascular endothelial growth factor (VEGF)

Fibroblast growth factor (FGF)

97
Q

What two growth factors are used for the stimulation of proliferation of mesenchymal cells? What cell types would these be?

A

Platelet-derived growth factor (PDGF)
Fibroblast growth factor (FGF)

Includes fibroblasts, smooth muscle, and endothelium

98
Q

What produces the majority of growth factors? How do they signal?

A

Mesenchymal and inflammatory cells, especially activated macrophages, fibroblasts, and endothelial cells

They signal in a paracrine fashion for the most part

99
Q

What is the function of TGF-beta?

A

Transforming growth factor beta

  • > strong stimulus for fibrosis (induces fibroblast motility, proliferation, and ECM production)
  • > terminates the inflammatory response
100
Q

What path are most cytokine receptors?

A

They are receptors without intrinsic kinase activity

Note: most growth factor receptors are tyrosine kinases

101
Q

What is tissue regeneration vs compensatory hyperplasia?

A

Tissue regeneration - complete restoration of a tissue back to its original state

Compensatory hyperplasia - restoration of functional mass, but not the original anatomy

102
Q

What is the primary determining factor of whether tissue regeneration can occur?

A

After the insult, is the ECM framework intact? If so, tissue regeneration can occur. Otherwise the cells will grow back by mass, but not the same way they were before.

103
Q

What type of insult would produce an injury that requires healing with fibrosis?

A
  1. Severe injury - damage to SCM or deep structures
  2. Chronic inflammation
  3. Involvement of permanent cell types
104
Q

What is granulation tissue?

A

The first stage of healing with fibrosis, named for its gross granular appearance

105
Q

What are the three components of granulation tissue?

A
  1. Residual inflammation - probably acute, sometimes chronic infiltrate of immune cells from insult
  2. Growth of new capillaries / significant angiogenesis
  3. Migration and proliferation of fibroblasts into the tissue
106
Q

How does angiogenesis in granulation tissue commence, and how does this relate to fibroblast proliferation?

A

VEGF and FGF cause migration and proliferation of endothelial cell precursors from bone marrow, as well as sprouting off of existing blood vessels (most common).

Since primitive vessels are leaky prior to maturation -> exudative edema occurs. The edema serves as a good matrix for fibroblasts to migrate in develop connective tissue.

107
Q

What growth factors promote fibroblast growth and maturation in granulation tissue? How will the nearby endothelial cells appear?

A

PDGF, FGF, and TGF-beta

(these were mentioned on previous cards)

Nearby endothelial cells appear very plump because they are immature

108
Q

When does a scar form and what is the most important cytokine in its formation?

A

Forms following the granulation tissue

Most important cytokine: TGF-beta

109
Q

What are the hallmarks of scar formation (vs granulation tissue)

A
  1. Decreased number of proliferating endothelial cells and fibroblasts
  2. Increased deposition and development of ECM, especially fibrillar collagens (will be much more blue than granulation tissue on trichrome)
  3. Connective tissue remodeling
110
Q

How does connective tissue remodeling happen in a scar?

A

ECM synthesis is balanced with degradation. Metalloproteases (primarily made by macrophages) like collagenases, elastases, etc degrade some ECM while more ordered ECM is synthesized

111
Q

What is healing by first intention vs second intention?

A

1st intention - narrow skin wound with minimal tissue damage

2nd intention - larger skin defect with more extensive damage

112
Q

What is the primary functional difference in healing by first vs second intention?

A

Healing by second intention simply takes longer, with acute inflammation lasting longer and re-epithelialization taking longer

113
Q

How does scarring compare to pre-wound strength, and what is one process that often needs to occur in scars of second intention vs first intention?

A

Tissue tensile strength is never completely back to pre-wound strength.

In second intention, wounds are much bigger so often myofibroblasts will do significant “wound contracture” to pull the sides of the wound together to make it heal better. Almost like internal stitching.

114
Q

What is a scab essentially, externally?

A

Dried out blood clot

115
Q

What is the most common factor to impede wound healing?

A

Infection - local or systemic

116
Q

What other factors might be in play to impede wound healing?

A
  1. Inadequate circulating or drainage
  2. Decreased immune response due to immunosuppressive drugs or immundeficiency
  3. Malnutrition (protein or vitamin C deficiency (needed for collagen))
  4. Wound disruption - i.e. mechanical stress or foreign bodies present
117
Q

What process can result in wound dehiscence following surgery?

A

Insufficient granulation tissue and scar formation

-> improper wound healing before the dissolvable sutures fade away

118
Q

What is “proud flesh”?

A

A form of excessive wound repair in which granulation tissue extends far above the skin surface, preventing the skin from being re-epithelialized

119
Q

What is a hypertrophic scar and how does it differ from keloid?

A

Hypertrophic scar - exaggerated collagen in the dermis, resulting in a raised scar. stays within the margins of the original wound, often resolves spontaneously, and rarely recurs

Keloid - thick, abberant collagen in the dermis as well. extends beyond the margins of the original wound, does not resolve spontaneously, and often recurs

120
Q

Who are keloids most common in?

A

Individuals with darker-colored skin

-> typically see in African-American women with ear piercings

121
Q

If not given proper wound care and skin grafting for massive body burns, what can occur which is very detrimental?

A

Contracture - a form of aberrant wound healing where tissue is pulled together where it shouldn’t be and causes deformities.

-> think of the burnt child

122
Q

What body parts are most likely to have the end result be fibrosis rather than scar formation?

A

Organs after persistent tissue damage

-> pulmonary fibrosis, cirrhosis, chronic pancreatitis, etc

Pathobiology (20 decks)

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