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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
Bacteremia
Presence of bacteria in the bloodstream
26
Sepsis
the systemic inflmamatory response to infection
27
Systemic Inflammatory response syndrome (SIRS)
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
Shock
systemic tissue hypoperfusion 2ndary to either: 1. decrased CO 2. Decreased efefctive circulating blood vol
29
What are 3 major forms of shock?
- cardiogenic (AMI, arrhythmia, tamponade, PE) - hypovolemic (hemorrhage, fluid loss s/p burns) - septic (acterial vasodilation, venous pooling) - others: neurgenic shock, anaphylactic shock
30
What bacteria commonly cause Septic Shock?
Gram + sepsis more common
31
Septic Shock: Pathophysiology
1. systemic arterial dilation--\> hypoperfusion despite increase CO 2. Widespread endothelial activation--\> hypercoagulable state--\> DIC (50% of septic pts)
32
What are the contributors to the development of shock?
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
What are the three stages of shock?
1. non progressive - compensatory/homeostatic reflexes --\>baroreceptors, catecholamine release, ADH, Renin-angio system, sysmpathetic activatin --\>maintain CO and BP to heart, brain 2. progressive (Hypoperfusion, acidosis) - Oxphos--\>Glycolysis. acidosis blunts vasomotor response--\> blood stasis- hypercoagulability 4. irreversible
34
Local/reversible cell injury allows for?
Regeneration
35
Extensive/Chronic cell injury allows for? Replacemet by connective tissue (Scar), mostly collagen and other extracellular matrix
36
What step does replacement of damaged tissue involve?
1. Inflammation 2. Angiogenesis 3. Fibroblast ingrowth and proliferation 4. scar formatoin 5. Connective tissue remodeling
37
Cutaneous Wound healing: Healing by Primary uinion
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
Growth Fctors and Cytokines Affecting Various Steps in Wound Healing
TGFa- EGF, FGF TGFb- inportant FGF; inhibit inglammation PDGF- endothelium, SM, FGF EGF- angiogenesis, skeletal dev. VEGF- angiogenesis
39
Granulation tissue
loose, edematous vascular proliferation plub fibroblasts loose collagen fibrils scattereted inflammatory cells
40
What do these picture represent?
Trichrome stain: Collagen content in granulation tissue vs mature scar
41
How is a larger excisional wound healed?
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
What factors retard wound healing?
43
What are some systemic factors that retard wound healing
44
What are some pathological aspects of wound healing?
- 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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