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Pathology-1 > Chronic Inflammation and Wound Healing > Flashcards

Chronic Inflammation and Wound Healing Flashcards

1
Q

Chronic Inflammation

A

Inflammation lasting weeks to years, combining ongoing inflmmation (activity), tissue injury, and tissue repair

  • may eveolved from an acute infla process or de novo
  • contributory to malignant transformation in15% of all cancer
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2
Q

What are some causes of chronic inflammation?

A
  1. persistant/hard to eradicate infections
  2. Immune- mediated inflammatory diseases
  3. prolonged environmental exposure to toxins (asbestos, silica, hyperlipidemia)
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3
Q

What type of inflammation is this?

A

acute (bronchopneumonia)

  • neutrophilic infiltrate
  • vascular congestion
  • edema
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4
Q

What type of inflammation is this?

A

chronic (farmer’s lung)

-chronic inflammatory cells

(Lymphocytes, MO, Plasma cells)

  • tissue destruction
  • attempts at healing-fibrosis
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5
Q

What cells are involved in chronic inflammation?

A

Macrophages, Lymphocytes (“immune inflammations), Plasma Cells (secrest Abs), Eosinophils (seen in allaergic/Parasitic infections), Mast Cells (source of histamine)

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6
Q

When do the number of monocytes peak?

A

@48 hrs

-Once monocytes are extravasated–>Macrophage

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7
Q

What cells are part of the mononuclear phagocytes system?

A

Macrophages

derived from bone marrow

  • Monocytes (Intravascular, T1/2= 24hrs)
  • Macrophages (Connective Tissue, T1/2= months)
  • Kupffer Cells (Liver Sinusoids)
  • Sinus Histocytes (Spleen and LN sinusoids)
  • Alveolar Macrophages (Lung)
  • Microglia (CNS)
  • Osteoclasts (Bones)
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8
Q

Classically activated M1

A

Microbicidal

-respond to microbial Ag (via TLR), IFNgamme to make ROS/RNS, cytokines

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9
Q

Alternatively activated (M2)

A

Tissue Repair/Fibrosis, may have anti-inflammatory function

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10
Q

If a macrophage becomes stimulated by microbes, or cytokines (IFNgamma) from T cells what is it involved in?

A

Inflammation and tissue injury (Ros, Proteases, Cytokines)

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11
Q

If a macrophage becomes stimulated by IL-4, cytokines what is it involved in?

A

Repair (growth factors, fibrogenic cytokines, angiogenic factors,etc)

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12
Q

What type of cells do you see in a granulomatous inflammtion?

A
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13
Q

Epitheliod histocytes (aggregates of activated MO) w/ collae of lymphocytes and plasma cells

A
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14
Q

What does the fusion of histiocytes make?

A

Giant cells

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15
Q

What are two types of giant cells?

A
  1. Langhans’ Giant Cells: Multiple peripheral nuclei
  2. Foreign Body Giant Cells: multiple randomly scattered nuclei
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16
Q

Why do granulomas forms?

A

body’s attempt to contain difficult-to-eradicate organisms, or foreign material

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17
Q

What are 2 types of granulomas?

A

Foreign Body Granuloma-Talc, sutures, prosthetic joints, breast implants

Immune granuloma- MO acting as APC’s induce a chronic T-cell response. May be caseating or non-caseating

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18
Q

What are non-caseating granulomas?

A

Lack central necrosis

19
Q

What are common etiologies of non-caseating granulomas?

A

rxn to foreign materam saracoidosis, beryllium exposure, Crohns Disease, and cat sratch.

20
Q

What is special about the cat sratch granulomas?

A

They are stellate shaped.

21
Q

What are caseating granulomas?

A

exhibit central necrosis

22
Q

Tuberculosis and fungal infections exhibit what types of granulomas?

A

Caseating granulomas

23
Q

What are 3 ways to narrow down the DDX for infections/noninfection causes of granulomatous inflammation?

A
  1. Caseating necrosis vs non caseating
  2. stains for acid fast bacilli
  3. prominent plasma cells or neutrophils
24
Q

What are some systemic effects of inflammation?

A
  1. fever- pyrogens (LPS, IL-1 TNFa) drive fever via hypothalamic prostaglandin signaling
  2. Acute phase reactants- liver derived serrum markers of inflmmation. ex. C reactive protein (CRP), fibrinogen
  3. leukocytosis: increase WBC to 12-20,000 (nl: 4500-11,000)
    acute: neturophilia (bacterial infection)
    chronic: leukocytosis (Viral)

Allergic: Eosinophilia

25
Q

Bacteremia

A

Presence of bacteria in the bloodstream

26
Q

Sepsis

A

the systemic inflmamatory response to infection

27
Q

Systemic Inflammatory response syndrome (SIRS)

A

systemic inflammatory response to any severse clnical insult (NOT INFECTIOUS), with 2 or more of the following

  • fever >38C or <36C
  • heart rate >90
  • RR> 20 or PaCO2 <32mHG
  • WBC>12,000, <4,000 or >10% bands
28
Q

Shock

A

systemic tissue hypoperfusion

2ndary to either:

  1. decrased CO
  2. Decreased efefctive circulating blood vol
29
Q

What are 3 major forms of shock?

A
  • cardiogenic (AMI, arrhythmia, tamponade, PE)
  • hypovolemic (hemorrhage, fluid loss s/p burns)
  • septic (acterial vasodilation, venous pooling)
  • others: neurgenic shock, anaphylactic shock
30
Q

What bacteria commonly cause Septic Shock?

A

Gram + sepsis more common

31
Q

Septic Shock: Pathophysiology

A
  1. systemic arterial dilation–> hypoperfusion despite increase CO
  2. Widespread endothelial activation–> hypercoagulable state–> DIC (50% of septic pts)
32
Q

What are the contributors to the development of shock?

A
  1. inflammatory mediators- TNF, IL-1, ROS, PGs, Complement (chemoattractants, opsonins)
  2. Endothelial activation- thrombosis, increase permeability, vasodilation
  3. Metabolic abormalities-insulin resistance, hyperglycemia (suppresses PMNs)
  4. Acquired immunosuppresion
  5. Organ dysfxn- multiple organ failure (MOF)
33
Q

What are the three stages of shock?

A
  1. non progressive
    - compensatory/homeostatic reflexes

–>baroreceptors, catecholamine release, ADH, Renin-angio system, sysmpathetic activatin

–>maintain CO and BP to heart, brain

  1. progressive (Hypoperfusion, acidosis)
    - Oxphos–>Glycolysis. acidosis blunts vasomotor response–> blood stasis- hypercoagulability
  2. irreversible
34
Q

Local/reversible cell injury allows for?

A

Regeneration

35
Q

Extensive/Chronic cell injury allows for?

Replacemet by connective tissue (Scar), mostly collagen and other extracellular matrix

A
36
Q

What step does replacement of damaged tissue involve?

A
  1. Inflammation
  2. Angiogenesis
  3. Fibroblast ingrowth and proliferation
  4. scar formatoin
  5. Connective tissue remodeling
37
Q

Cutaneous Wound healing: Healing by Primary uinion

A
  1. rapid blood clot (fibrin complement)-attracts PMNs, MO, scaffold for migrating fibroblasts, keratinocyts
  2. granulation- fribroblasts and endothelial proliferation (Angiogenesis) driven by GFs
  3. Collagen Deposition: MO cleanup
38
Q

Growth Fctors and Cytokines Affecting Various Steps in Wound Healing

A

TGFa- EGF, FGF

TGFb- inportant FGF; inhibit inglammation

PDGF- endothelium, SM, FGF

EGF- angiogenesis, skeletal dev.

VEGF- angiogenesis

39
Q

Granulation tissue

A

loose, edematous

vascular proliferation

plub fibroblasts

loose collagen fibrils

scattereted inflammatory cells

40
Q

What do these picture represent?

A

Trichrome stain: Collagen content in granulation tissue vs mature scar

41
Q

How is a larger excisional wound healed?

A

By secondary intention

  • bigger inflammatory response, more granulation
  • substantial scar formatoin, prominent wound contraction (due to myofribroblast induciton via PDGF/TGFB/FGF2, or by EMT from epithelial cells)
42
Q

What factors retard wound healing?

A
43
Q

What are some systemic factors that retard wound healing

A
44
Q

What are some pathological aspects of wound healing?

A
  • deficient granulation tissue or scar deposition (predisposes to wound dehiscence)
  • ulceration secondary to insuffient vascularization or denervation (diabetes)
  • Excessive scarification (Keloid)
  • Contractures: excessive wound contraction, particularly after burns

Pathology-1 (5 decks)

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