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Patho > inflammation & wound healing > Flashcards

inflammation & wound healing Flashcards

1
Q

inflammation can only occur in…

A

A LIVING PERSON!!!! dead tissue cannot produce and inflammatory response

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2
Q

neutrophils represents ______ inflammation & lymphocytes represents __________ inflammation

A

acute & chronic

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3
Q

What are the 5 cardinal signs of inflammation?

A
  1. Calor (hot)
  2. Rubor (redness)
  3. Tumor (swelling)
  4. Dolor (pain)
  5. Functio laesa (loss of function)
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4
Q

Describe why you get redness and warmth after injury, such as burning your finger

A
  1. injury creates stimulus signaling smooth muscle
  2. smooth muscle VASOCONSTRICT so initial few seconds after injury no pain, warmth or redness
  3. then VASODILATION= warmth & redness to the injured area
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5
Q

Describe why edema occurs with injury

A

vasodilation=> increased blood flow through the capillaries which have no smooth muscle to control blood flow=> increase pressure in the capillaries.

This pressure starts forcing plasma to filter through the vessel walls = EDEMA

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6
Q

How does the blood flow slow down?

A

because the plasma is leaving the capillaries there is increased hemoconcentration which leads to congestion & eventually Rouleaux formation

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7
Q

Define Rouleaux formation, what does it do?

A

erythrocytes form stacks

this impedes the flow and circulation of blood, this allow the WBC to stay in the infected area, site of inflammation and not pass it from fast blood flow

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8
Q

What is pavementing?

A

When WBC’s marginate and become attached to the edge of the endothelium

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9
Q

What is the mechanism of pavementing?

A
  1. inflammation activates soluble mediators = INTERLUKINS
  2. Interlukins activate ADHESION MOLECULES on leukocytes & endothelial cells to STICK TO WALL
  3. platelets adhere to to capillary endothelial cells to clot and form FIBRIN STRANDS to help anchor the leukocytes
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10
Q

how long are the capillaries and venules permeable for ?

A

several hours to several days

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11
Q

in acute inflammation what are most of the cells that are present?

A

neutrophils (PMNs)

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12
Q

Fill in the blank:
As inflammation evolves, PMN’s are joined by other cells such as ____________ which becomes apparent within the first ________ hours

A

monocytes, 24

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13
Q

what is the life span of a PMN?

A

2-4 days

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14
Q

with chronic inflammation what does a PMN eventually get replaced with?

A

macrophages, lymphocytes & plasma cells

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15
Q

What are the phases for emigration of leukocytes?

A
  1. Adhesion of PMN to endothelium
  2. insertion of cytoplasmic pseudopods between the junction of the endothelial cells. AKA squeeze through endothelial membrane
  3. pass through basement membrane
  4. move away from the vessel toward to cause of inflammation
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16
Q

Define chemotaxis? What activates it?

A

active movement of PMN along a concentration gradient.

Chemotactic substances such as, bacteria or tissue destroyed by inflammation or from activated complement.

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17
Q

What occurs once the PMN’s reach their chemotatic substances?

A

they loose their mobility and start PHAGOCYTOSIS

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18
Q

What are the steps of phagocytosis?

A
  1. Recognition
  2. Attachment
  3. Engulfment
  4. Kill bacteria
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19
Q

what is attachment of the PMN to the bacteria facilitated by?

A

leukocytes have:

  • C3 receptors for COMPLEMENT
  • receptors for Fc portion of IMMUNOGLOBULINS
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20
Q

what is the substance released in the phagocytic vacuole to kill the bacteria?

A

bacteriocidal substances

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21
Q

what does pus consist of?

A

dead any dying PMN’s & tissue debris

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22
Q

define suppurative inflammations or purulent

A

inflammations dominated by pus formation

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23
Q

What are the two important clinical findings that inflammation produces?

A

fever and leukocytosis

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24
Q

What is the mechanism behind a fever?

A

bacteria => triggers PMNs & macrophages => release pyrogens (interleukin I & TNF) => act as thermoregulator center in hypothalmus & release prostaglandins to mediate fever

when the source of inflammation is gone, then interleukin I and TNF will no longer be released and therefore the fever will go down

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25
Q

how many WBCs are in nl blood

A

less than 10,000 WBC’s/mm3

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26
Q

Fill in the blank:

Mediators of inflammation act on the ______________, stimulating rapid release of _____________

A

bone marrow, leukocytes

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27
Q

leukocytosis is when the number exceeds…

A

12- 15,000

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28
Q

what areas would you look for typical signs of inflammation during a PE?

A

skin, eyes, oral mucosa, genital organs

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29
Q

What is the mildest form of inflammation?

A

Serous Inflammation: exudation of fluid that is clear like serum

[Extra info]

  • occurs in early stages
  • typical of VIRAL infections (vesicles of herpes )
  • autoimmune (SLE) serous pericarditis, pleuritis
  • 2nd degree burns-> blisters
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30
Q

Define fibrinous inflammation

A

exudate that is rich in FIBRIN

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31
Q

what is the largest plasma protein?

A

fibrinogen

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32
Q

in fibrinous pericarditis when friable fibrin between the epicardium and pericardium is separated what does it resemble?

A

spread it like BREAD & BUTTAAAA (butter) !!!!!

YUMYUMYUMYMUYMU

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33
Q

What types of infection is fibrinous inflammation seen in?

A

bacterial such as strep throat and PNA

34
Q

describe purulent inflammation

A

viscous yellow fluid composed of dead PMN and necrotic tissue from pus forming bacteria (staph & strep)

35
Q

What is a localized collection of pus with an organ or tissue ?

A

abscess

36
Q

describe an abscess

A

central portion of purulent material surrounded by a wall composed of a capsule of fibrotic granulation tissue

-tx: need to be evacuated

37
Q

what is the difference between an abscess and a sinus?

A
  • an abscess is enclosed cavity in the tissue

- a sinus is when the cavity forms a tract to the surface of the body

38
Q

large abscess can also form fistulas which are…

A

channels formed between two preexisiting cavities or hollow organs and the surface of the body.

-can be formed between two loops of bowel, fused together by inflammation

39
Q

What can cause fibrinous pericarditis?

A

infection, prior surgery

40
Q

define ulcerative inflammation & give an example

A

inflammation of the body surfaces or the mucosa of hollow organs

Ex. stomach or intestine may result in an ulcer or loss of epithelial lining. PEPTIC ULCERS

41
Q

define an ulcer

A

defect involving the epithelium but may extend into the deeper connective tissues

42
Q

what is a form of ulcerative inflammation that is combined with fibrinopurulent exudation?

A

pseudomembranous inflammation

43
Q

what forms a pseudomembrane?

A

exudate of fibrin, pus, cellular debris, and mucous forms on the surface of ulcers

-it can be scraped away to expose ulcerated defects that bleed profusely

44
Q

Give an example of pesudomembranous inflammation

A

pseudomembranous colitis from C. Diff. (Gram +)

-caused by bacteria overgrowth from broad spectrum abx

45
Q

Throw back: Best example of a fistula and fistula formation is …

A

Crohns Disease

it is transmural- it is all the way through.

so when two loops of small bowl touch it can form a fistula through each bowel

46
Q

Throw back: What is an organism that forms an abscess in the lungs?

A

gram postive cocci in grape like clusters- Staph aureus

47
Q

Define granulomatous inflammation

A

special form of chronic inflammation that typically is not preceded by an acute, PMN mediated inflammation

48
Q

Throw back: for a bleeding gastric or duodenal ulcer to form has to extend into

A

the submucosa where all the blood supply is

49
Q

TBT: What meds can you give to tx pseudomembranous colitis from C.Diff?

A

Flagel & Vancomycin

50
Q

TBT: Inside pseudomembranous colitis is not the organism but it is the…

A

Toxin (A or B) which can be tested from a stool sample

51
Q

what causes granulomatous inflammation?

A

antigens that evoke a cell mediated hypersensitivity reaction or by antigens that persist at the site of inflammation

52
Q

give an example of prototype granulomatous disease

A

TB

53
Q

acute inflammation may heal without complication except when…

A

considerable destruction of tissues

-complete healing may be postponed or never accomplished

54
Q

stable cells can enter into the cell cycle and become…

A

actively mitotic where they enter mitosis, divide and replace the loss

55
Q

The heart does not repair by functional myocytes, it heals with…

A

fibrosis

56
Q

continuously dividing cells are …

A

labile cells. divide through entire lifespan and can give rise to more differentiated cells

also known as.. STEM CELLS!!!!

57
Q

What are examples of labile cells?

A

stem cells, hair follicles, skin cells, intestinal cells, endometrium, bone marrow cells

-RBC live 120 days and new ones come from bone marrow

58
Q

what are quiescent cells?

A

STABLE CELLS!

dont divide regularly, can stimulate division if necessary

59
Q

Where can stable cells be found?

A

parenchymal organs such as liver or kidneys.

partial hepatectomy stimulates remaining liver cells to enter mitosis, divide and replace the loss, once regenerated it becomes stable and stop dividing

60
Q

what are nondividing cells?

A

PERMANENT cells.

they do not have the capacity to proliferate under any circumstances

61
Q

What are examples of nondividing cells?

A

neurons, myocardial cells

62
Q

how do myocardial cells repair itself?

A

FIBROUS SCARRING!!!!

63
Q

how do brain cells repair itself?

A

gliosis

64
Q

what are the most important cells that are involved in wound healing?

whats the mechanism?

A

Leukocytes, macrophages, connective tissue cells and epithelial cells

PMN briefly scavenge the site, macrophages stay at the site and produce factors and mediators that act on connective tissue cells

65
Q

What are the steps in healing?

A
  1. myofibroblasts
  2. angioblasts
  3. fibroblasts
66
Q

myofibroblast is composed of..

A

has smooth muscle cells (contracting) and fibroblasts.

Contracts and brings margins together so proliferating epithelial cells can cover and restore epithelium

67
Q

what are angioblasts?

A

the precursors of blood vessels that proliferate like sprouts from small vessels at the margins of the wound

  • appear 2-3 days after incision
  • 5-6th day who area is covered
68
Q

fibroblasts are the….

A

cells that produce most of the extracellular matrix

69
Q

What do fibroblasts produce?

A

Fibronectin- GLUE to keep everything together, provides strength to connective matrix

Collagen- initially type III -> type I, and fills the gap. Fibrosis

70
Q

what is the most common form of collagen in the body?

A

Type I

71
Q

When does collagen acquire its full strength?

when does that occur?

A

when it is laid down in the extracellular space

several weeks after injury

72
Q

What is First Intention?

A

wound-> coagulated blood-> scab…

  • scab is invaded in PMN’s (scavenge debris)
  • 2-4 days later macrophages come and secrete growth factors and mediators
  • ingrowth of myofibroblasts, angioblasts & fibroblasts
73
Q

What is granulation tissue composed of?

A
  1. vascularized connective tissue rich in macrophages
  2. myfibroblasts
  3. angioblasts
  4. fibroblasts
74
Q

what is the final collagenous structure called?

A

SCAR!!!

SIMBAAAA RAWWRRRR

75
Q

How long does it take for the wound to transfer into the scar?

A

3-6 weeks

76
Q

What occurs in order for the scar to be remodeled?

A

collagen is replaced by collagen that is indistinguishable from nl skin

77
Q

What is Secondary Intention?

A

how the infected wound heals when there are large defects.

the myofibroblasts cant contract the wound so granulation tissue remains exposed.

may never completely heal

78
Q

What are the most important determinants of wound healing?

A
  1. site of wound: ex. skin heals well, brain does not heal at all
  2. infection: sterile wounds heal faster than infected
  3. mechanical factors: wounds heal faster if the margins can be moved together and site is immobile
  4. Age: wounds heal faster in children than adults/elderly
  5. Circulatory Status: wounds with ischemic tissue heals poorly
  6. nutritional & metabolic factors: general well being promotes wound healing
79
Q

What are complications of wound healing?

A
  1. Deficient scar formation

2. Excess scar formation

80
Q

What does deficient scar formation mean?

what can cause that?

what can result from it?

A

sluggish formation of granulation tissue

Cause: DM, ischemia, inadequate collagen due to corticosteroid hormones

Result: scars that dont have enough strength so wound margins separate

81
Q

what is excess scar formation?

A

hypertrophic scars composed by mostly Type II collagen (Keloids)

results from defective remodeling of scar tissue

Patho (6 decks)

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