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MHD - Exam 1 > Lecture 3 & 4: Chronic Inflammation & Wound healing > Flashcards

Lecture 3 & 4: Chronic Inflammation & Wound healing Flashcards

1
Q

What are the 3 hallmarks of chronic inflammation?

A
  1. Accumulation of lymphocytes and macrophages
  2. Proliferating blood vessels
  3. Formation of connective tissue (fibrosis/scar)

Clinically, the process is of longer duration
Days, weeks or months

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2
Q

What are the 3 potential results of acute inflammation?

A
  1. resolution
  2. pus formaiton
  3. Chronic inflammation
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3
Q

What is the lack of resolution usually the result of? (5)

A
  1. Inability to get rid of the pathogen
  2. Pathogen resistance to antimicrobials
  3. Degradation resistant foreign body
  4. Persistent exposure to an autoantigen
  5. Genetic inability of the host to mount the appropriate response to the pathogen (lysosomal, oxidase system, etc….)
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4
Q

Which is the signature cell of chronic inflammation, M1 or M2 macrophage?

What do chronic high levels of inflammatory cytokines cause? (3)

A

M1 macrophage (ROS, No & lysozymes)
(Il-1, 12, and INF-Y)
- pro-inflammatory cytokines

The innate immune system senses the persistent threat and increases innate protein and cell production to thwart it

  1. Increased rates of hepatic production of defense proteins
  2. Increase HEPCIDIN (can result in iron deficiency and anemia)
  3. Increased growth factors for platelets, monocytes,
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5
Q

What cytokines are associated with anti-inflammatory effects?

A

IL-10 TGF - B

and M2 macrophages

IL-13 and IL-14

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6
Q

What type of inflammation does the following describe:

  1. Distinct form associated with persistent T-cell activation
  2. Common with persistent microbial intracellular infection
    - 3. Common with macrophage uptake of poorly degradable foreign bodies

Where is this inflammation pattern commonly found?

A

GRANULOMATOUS INFLAMMATION

  1. Sarcoidosis (non-caseating)
  2. IBD (Crohn’s disease)
  3. TB –> caseaous or necrotizing
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7
Q

What type of cells are found in granulomatous inflammation?

  1. Central portion
  2. Periphery?
  3. What type of T cells?
  4. Entire granuloma is rimmed by proliferating _____
A
  1. Necrotic debris
    (caseous)
  2. Active EPITHELIOD macrophages & giant cells
  3. CD3/CD4+ (T & B cells in periphery as well)
  4. Fibroblasts

ORGANISM IS WALLED OFF

-Collateral damage caused by progressive tissue necrosis and fibrosis can be extensive

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8
Q

An unregulated ____response or scenario when macrophages cannot kill effectively can be expressed as granulomatous inflammation

A

Th-1

  • over-expressing of INF-Y and frustrated macrophages
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9
Q

Pathophysiological effects of inflammation based on ____ activation and release of pro-inflammatory cytokine and inflammation provoked growth factors

Clinical differences are based solely upon ____ and ____ of the stimulus

The biochemical changes are ____ and reflect hepatic adjustments to inflammation

A
  1. macrophage
  2. intensity, duration
  3. “acute phase reactants”
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10
Q

What biochemical changes are caused in inflammation:

Increased the hepatic production of what 3 things?

Reciprocal decrease in ____ synthesis.

Increased hepatic production of ______ which can cause anemia due to sequestering of Fe2

growth factors which stimulate the bone marrow to increase what 2 things?

A

Increase:

  1. Fibrinogen (coagulation)
  2. Ceruloplasmin (copper regulator)
  3. Complement components (C3)

Decrease in ALBUMIN synthesis
(hypoalbuminemia)
- liver has to shunt energy for production of the acute phase reactants (fibrinogen, ceruloplasmin, and complement)

Increased HEPCIDIN

  1. increase leukocyte production
  2. Increase platelet production
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11
Q

There is a rough correlation between the decrease in albumin and what?

A

Intensity and duration of inflammatory process.

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12
Q

CRP production is stimulated by inflammation and is tightly linked to levels of what cytokine?

Why is it good to use?

What can cause a false elevation of CRP?

A
  1. IL-6
  2. Can be measured rapidly, reliably and relative low cost (CHEAP)

Can be used in semi-quantitative fashion for level of inflammation
when normal can exclude significant inflammation being present

3.
Obesity is the one morbidity that can cause a “false” elevation of CRP

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13
Q

What is the erythrocyte sedimentation rate?

What coats erythrocytes and causes them to fall rapidly through the column of plasma? (2)

Why is this becoming obsolescent?

A

Chronic inflammation causes clinically detectable antibody synthesis expressed as polyclonal increase in IgG

  1. IgG
  2. Fibrinogen

False elevation
–> when increase of IgG
myeloma, age

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14
Q

What are acute phase reactants?

A

An increase in serum proteins associated with chronic inflammation

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15
Q

A 56-year-old man has experienced severe chest pain for the past 4 hours. On physical examination he is tachycardic. Laboratory studies show a serum troponin I of 9 ng/mL. A coronary angiogram is performed emergently and reveals acute thrombosis of the left anterior descending coronary artery. In this setting, an irreversible injury to myocardial fibers will have occurred when which of the following cellular changes occurs?

A.	Blebs form on cell membranes 
B.	Cytoplasmic sodium increases 
C.	Glycogen stores are depleted 
D.	Intracellular pH diminishes 
E.	Nuclei undergo karyorrhexis
A

E. nuclei undergo karyorrhexis

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16
Q

What are the possible outcomes when cell is injured?

A
  1. adaptation
  2. Repair
  3. Death
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17
Q

When does repair get initiated?

How does “healing occur” (2)

A
  1. when inflammation begins

Healing occurs via:
1. Regeneration
-
Replacement of damaged cells by replicating cells of the same type

  1. Scar formation
    - Replacement by connective tissue (fibrous/collagen – all interchangeable)

** BOTH MAY OCCUR TOGETHER**

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18
Q

In regeneration, what remains intact and serves as scaffolding?

What must cells have the capacity of?

A

Tissue framework (extracellular matrix)

Capacity to DIVIDE
either labile or stable

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19
Q

What are the two structures within the ECM?

What 3 proteins?

A
  1. Interstitial matrix
  2. Basement membrane
  3. Fibrous structural proteins
    Collagens, Elastins
  4. Water hydrated gels
    (Proteoglycans, hyaluronan)
  5. Adhesive glycoproteins
    linking cells to each other and
    underling BM & other structure
20
Q

The following describes what type of tissues:

-Continuously dividing
- Lost cells replaced by
maturation from stem cells
- proliferation of mature cells

What are some examples?

A

LABILE TISSUES

  1. Hematopoietic cells of bone marrow
  2. Squamous epithelium of skin, oral cavity, cervix, vagina
  3. Columnar epithelium of GI tract

stratum basal of skin, crypts of intestine

21
Q

The following describes what type of tissues:

  1. Low, no level of replication
    (stuck in G0 cell cycle)
  2. Rapidly divide when stimulated

–> G1 cell cycle and beyond
(into active mitosis/replication)

EXAMPLES?

A

STABLE TISSUES

ex:

  1. Liver
  2. kidney
  3. pancreas
  4. smooth muscle cells
  5. fibroblasts
22
Q

The following describes what type of tissues:

Terminally differentiated, non-proliferative in postnatal life

Examples?

A

PERMANENT tissues

1. Brain
2. Heart
some skeletal muscle can regenerate so falls out of this category

23
Q

The following describes which growth factor
(EGF, TGF-a, VEGF, PDGF, FGs, TGF- B)

  1. Mitogenic for keratinocytes, fibroblasts; stimulates keratinocyte migration
  2. Stimulates proliferation of hepatocytes, other epithelial cells
  3. Chemotactic for leukocytes, fibroblasts; stimulates ECM synthesis; suppresses acute inflammation (suppresses acute inflammation)
  4. Stimulates proliferation of endothelial cells; increases vascular permeability

5.Chemotactic, mitogenic for fibrobasts; stimulates angiogenesis,
ECM protein synthesis

6.Chemotactic; activates and stimulates proliferation of fibroblasts, endothelial cells; stimulates ECM proteins synthesis

A

1 EGF

  1. TGF-a
  2. TGF_ B
  3. VEGF
  4. FGFs
  5. PDGF
24
Q

What is the replacement of damaged tissue with fibrous connective tissue?

Why does this occur? (2)

A

SCAR formation

  1. Injurd tissues incapable of regeneration (MI)
  2. Supporting structures (ECM) severely damaged, stem cells lost
25
Q

What is the pro and con of scar formation?

A

pro:

  • enough structural stability for injured tissue to continue fx.
  • fx. may be somewhat compromised

con:
- fibrous tissue cannot perform fx. of lost parenchymal cells

26
Q

What are the steps in repair by scar formation? (4)

A
  1. Angiogenesis
  2. Migration & proliferation of fibroblasts
  3. Formation, deposition of extracellular matrix by fibroblasts
  4. Maturation, organization of fibrous tissue elements
27
Q

What factor is responsible for the following:

  1. Promote angiogenesis
  2. Increase vascular permeability
  3. Stimulate endothelial cell migration, proliferation
A

VEGF

Roles in healing, development of collaterals at sites of ischemia, tumor growth

28
Q

When is VEGF low levels?

(what 2 areas is it high in)

hat is an important inducer of VEGF?

A

Most adult tissues,

higher levels only in PODOCYTES in glomerulus and PIGMENT EPITHELIUM of retina

  1. HYPOXIA induces angiogenesis
29
Q

Fibroblasts synthesize _____ tissue proteins

A

connective

-Recruitment, activation driven by many growth factors (PDGF, FGF, TGF-b)

30
Q

What is granulation tissue?

What 3 things does it consist of?

(what lays down immature connective tissue)

When is it present?

A

Specialized tissue that fills in defects in organs when non-regenerative cells and/or connective tissue framework is destroyed

  1. Proliferating fibroblasts laying down immature connective tissue (type III collagen)
  2. Proliferating new blood vessels
  3. tissue is red and edematous to naked eye

Present only during healing or attempt to heal destroyed tissue
*****

31
Q

What is the Process of transforming granulation tissue into a dense scar?

With time, blood vessels become less prominent, collagen matures into which type?

ultimately results in ____

A
  1. Organization
  2. TYPE I
  3. final SCAR
32
Q

What does the trichrome stain?

A

Stains mature collagen blue!

very little seen in granulation tissue, a lot in the mature scar

33
Q

What are the 8 steps of healing skin wounds from the laceration (1) to wound acquiring strength? (8)

A
  1. Laceration – defect in skin
  2. Inflammatory reaction incited
  3. Blood clot (fibrin, fibronectin) forms
  4. Epithelium regenerates to cover defect (stem cells recruited)
  5. Cells proliferate and migrate into defect
    a) Macrophages remove debris, secrete cytokines
    b) Fibroblasts produce extracellular connective tissue matrix
    c) Myofibroblasts contract the wound
    modified fibroblasts with functional features of contractile smooth muscle cells
  6. Simultaneously capillaries (endothelium) at edge of defect proliferate and extend into the defect under the influence of chemical mediators
  7. Over weeks to month defect filled with granulation tissue, becomes remodeled into mature collaged (scar)
  8. Wound acquires strength through the process
34
Q

What cells remove debris and secrete cytokines once cells migrate to the defect?

What produce the ECM matrix?

What contract the wound?

What proliferates to the edge of the defect?

A
  1. macrophages
  2. Fibroblasts
  3. Myofibrils

CAPILLARIES

35
Q

What is the difference between healing by first and second intention?

Which one shows minimal contraction my myofibroblasts?

A

First intention:

  1. Clean, uninfected surgical incision approximated by surgical sutures (brought together)
  2. Epithelial regeneration principle mechanism of repair
  3. Small scar
  4. Minimal contraction of wound

Second intention:

  1. Large skin wound
    - Extensive destruction, - contaminated,
    - infected
  2. Edges are not approximated (not brought together)
  3. Larger clot, more intense inflammation (lymphocytes)
  4. Wound granulates in without closing gap with sutures
  5. Process of healing SAME but takes longer because of the size of the defect
  6. Wound contraction by myofibroblasts
36
Q

The following describes first intention or second intention healing:

Mitoses & keritinocytes 
form granulation tissue:
1. fibroblasts
2. new blood vessels
3. macrophage
A

FIRST

37
Q

When is wound strength at about 70-80% of normal?

A

3 months

38
Q

Deposition of collagen is part of normal wound healing

T or F?

A

TRUE

39
Q

What refers to EXCESSIE deposition of collagen and other ECM components?

What can drive this?

A

FIBROSIS

  • can be driven by TGF-B
40
Q

What are some factors that may influence wound repair?

A 
Infection
Nutrition (vitamin C, iron, copper)
Glucocorticoids
Anti-inflammatory, inhibit TGF-b production  inhibit growth factors & ends acute inflammation
Poor perfusion
Diabetes mellitus
Foreign bodies
Stable or labile cells vs permanent cells
Location of injury

Vascular supply: Inflammation and healing can take place
only when there is an adequate blood supply. Devitalized tissue will not heal. Tissue with poor vascularity may heal with difficulty or be more prone to infection (example: abscess, fat).
Infection: The presence of bacteria will continue to incite an inflammatory reaction, preventing or prolonging healing.

41
Q

A 68-year-old man with diabetes mellitus, type 2 undergoes a below-knee amputation for wet gangrene (ischemic necrosis of leg). The patient’s postoperative course is complicated by severe depression and anorexia. The healthcare team is concerned that dietary deficiencies will result in impaired wound healing.
Supplementation of which of the following would be most appropriate?

A.	Copper and Vitamin D
B.	Folate and Zinc
C.	Iodine and vitamin E
D.	Vitamin C and Vitamin E
E.	Vitamin C and Zinc
A

Vitamin C and Zinc

vitamin C which is essential for collagen cross-linking (lysine and proline)

copper which is a cofactor for lysyl oxidase which cross-links lysine and hydroxylysine to form stable collage;

zinc which is a cofactor for collagenase

c. Hormones: steroids inhibit the inflammatory process, impairing healing

(example; steroid medication, Cushing’s syndrome).

42
Q

What 3 nutrients are important for wound healing?

A
  1. Vitamin C
  2. Zinc
  3. Copper
43
Q

What are some complications of wound healing? (2)

A
  1. wound dehiscence (rupture of wound),
  2. Excessive scar formation:

a. Hypertrophic scar – Excess production of scar tissue localized
to the wound; may regress

b. Keloid – Accumulation of exuberant amount of collagen;

44
Q

What is a keloid?

What is it probably driven by? (which growth factor)

How does it look?

most common in?

A
  1. Accumulation of collagen
  2. TGF - B
  3. Raised scar that grows beyond wound boundaries
  4. African Americans
45
Q

What does the following describe:

Excess production of scar tissue localized to the wound

May regress

A

Hypertrophic Scar

46
Q

31-year old firefighter suffers extensive third-degree burns over his arms and hands. This patient is a high risk for the development of which of the following complications of wound healing?

A. Contracture
B. Dehiscence (rupture of wound)
C. Keloid
D. Squamous cell carcinoma

A

Contracture

47
Q

State where the 4 types of collagens are commonly found:

A

Type 1 = bone (one)
high tensile strength

Type 2 = cartilage (cartwolage)

Type 3 = PLIABLE granulation tissue, embryonic tissue, uterus = PLIABLE

Type 4= BASEMENT MEMBRANE ( 4 on the floor)

MHD - Exam 1 (13 decks)

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