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PATHOPHYS > 3Inflammation and phagocytosis > Flashcards

3Inflammation and phagocytosis Flashcards

1
Q

Define Inflammation

A

A nonspecific but predictable response of living tissue to injury

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2
Q

What causes injury?

A

Chemical agents, physical forces, living microbes and many other endogenous and exogenous pathologic stimuli that can disturb the normal steady state of the body

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3
Q

What kind of a process is inflammation?

A

A dynamic process evolving through several phases which lasts from a few minutes to days or even months or years

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4
Q

What kind of inflammation has a sudden onset and short duration?

A

Acute Inflammation

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5
Q

What kind of inflammation last a long time?

A

Chronic Inflammation

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6
Q

What kind of a role does inflammation play?

A

It has a protective role and is generally beneficial, but side effects may be noxious(fever). Process may become uncontrollable, producing more harm than good.(pulmonary TB elicits a protective tissue reaction that can erode pulmonary vessels, causing massive bleeding.

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7
Q

What do dead and dying neutrophils produce?

A

Pus

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8
Q

In what kind of tissue does inflammation occur?

A

Living ONLY! If inflammation is found during an autopsy this indicates the injury occurred before death

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9
Q

Five cardinal signs of inflammation

A
  1. Calor(heat)
  2. Rubor(redness-erythema)
  3. Tumor(swelling)
  4. Dolor(pain)
  5. Functio laesa(loss of function)
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10
Q

Pathogenesis of Inflammation:

Circulatory Changes

A 
Changes in blood flow=first response to injury
mechanical stimuli(burn) signals smooth muscles cells on pre-capillary arterioles, which act as sphincter regulating inflow of blood into the capillaries 
arterioles vasoconstrict for first few seconds after initial injury 
relaxation of smooth muscle(vasodilation) allows blood to rush into capillaries=redness, swelling and warmth
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11
Q

What causes the warmth during inflammation process?

A

Arterial blood is warm and is pumped into the area in large quantities, so the inflamed tissue also becomes warm(hyperemia)

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12
Q

Is the influx of blood during inflammation regulated?

A

No. The capillaries and venules are only an endothelial layer and basement membrane and cannot actively regulate the incoming bloodflow

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13
Q

What do erythrocytes do during the inflammation process?

A

sludged erythrocytes form stacks, called Rouleaux formation, which impedes and slows down the circulation even more

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14
Q

What do WBC do during the inflammation process?

A

They marginate and become attached to the edge of the endothelium(pavementing: stick to edges)

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15
Q

What allows WBC’s to adhere?

A

Leukocytes develop elongated protrusions(present but in an inactive form normally) on their surface cytoplasm and become sticky, which allows them to adhere to the endothelial cells lining the capillaries and venules
Best known activators: Interleukins

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16
Q

Where is the greatest concentration of interleukins?

A

At the site of inflammation. Derived in part from platelets and in part from leukocytes

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17
Q

What is one of the most important triggers for the release of mediators of inflammation?

A

The adhesion of leukocytes to the endothelial cells

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18
Q

What initiates clotting?

A

Platelets. Ultimately leads to the formation of fibrin strands that anchor the leukocytes to the vessel wall and prevent them from moving away

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19
Q

How long does the permeability of the vessel walls of the capillaries and venules last?

A

Several hours to several days and is usually accompanied by leakage of fluid from the vessels into the interstitial spaces

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20
Q

what cells are most common in acute inflammation?

A

Neutrophils(PMN’s)

Joined by other cells like monocytes within the first 24 hours

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21
Q

What happens to PMN’s as inflammation proceeds into chronic stages

A

PMN’s have a life span of 2-4 days only, they become less prominent and are replaced by macrophages, lymphocytes and plasma cells

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22
Q

Emigration of Leukocytes

A

Active process that occurs in phases

  1. Adhesion of PMN’s to the endothelium
  2. Insertion of cytoplasmic pseudopods between the junction of the endothelial cells
  3. passage through the basement membrane
  4. ameboid movement away from the vessel toward the cause of the inflammation(bacteria)
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23
Q

Define Chemotaxis

A

Active movement of PMN’s along a concentration gradient. The chemoattractant being derived from bacteria or tissues destroyed by inflammation, or from activated compliment
-Chemotactic substances stimulate PMN’s to move along this gradient until they reach their source or site of inflammation

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24
Q

What happens to PMN’s that reach the bacteria or other chemotactic substances?

A

They lose their mobility and begin acting as scavengers by the process of “Phagocytosis”.

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25
Q

How do PMNs recognize a bacterium as foreign?

A

A PMN encounters and recognizes a bacterium as foreign by the pseudopods extending from the surface of the PMN

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26
Q

What happens after phagocytosis?

A
  • The attachement of the cell membrane of the PMN to the bacterial cell wall.
  • Attachment can be facilitated by immunoglobulins or complement which act as opsonins
  • A PMN encounters and recognizes a bacterium as foreign by the pseudopods extending from the surface of the PMN
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27
Q

Define Phagocytosis

A

Engulfment of the bacterium is a process by which the cytoplasm of the PMN surrounds the foreign particle and encloses it into an invagination of the cell membran

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28
Q

What happens inside the phagocytic vacuole?

A

the bacterium is killed by bacteriocidal substances released from the cytoplasm of the PMN.

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29
Q

What is discharged into the lumen of phagocytic vacuoles?

A

The contents of the specific granules from PMN’s. Many die in their fight with bacteria

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30
Q

What causes pus?

A

Dead and dying PMNs, admixed with tissue debris, form the viscous yellow fluid

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31
Q

What is an inflammation dominated by pus formation called?

A

Purulent or suppurative inflammation

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32
Q

Inflammations typically produce what two important clinical findings?

A

Fever

Leukocytosis

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33
Q

Define Fever

A

Elevation in body temp exceeding 37 degrees centigrade. typical response to inflamm caused by endogenous pyrogen. Substances called interleukin-I and tumor necrosis factor (TNF) act on the thermoregulator centers in the hypothalamus(thermostat)
threshhold raised= increased body temp
*they will stop once source of inflammation is eradicated

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34
Q

Where do pyrogens come from?

A

they are released from the PMN’s and macrophages during inflammation

35
Q

What is leukocytosis?

A
  • WBC’s exceed 12-15,000, this is leukocytosis and in acute inflammation, the neutrophils predominate.
  • normal blood <10,000. mediators of inflammation act on the bone marrow, stimulating a rapid release of leukocytes
36
Q

What are the types of inflammation?

A 
Serous Inflammation
Fibrinous inflammation
Purulent inflammation
Ulcerative Inflammation 
Pseudomembranous Inflammation
Granulomatous inflammation
37
Q

what is serous inflammation?

A

Considered to be the mildest form, characterized by the exudation of fluid that is clear like serum, and occurs in the early stages of inflammation

38
Q

Give examples where you would see serous inflammation?

A

Typical of viral infections: Herpesvirus(filled with serous fluid)

Autoimmune disorders: SLE,, can affect the serosal surfaces and cause a serous pericarditis, pleuritis, peritonitis

2nd degree burns

39
Q

What is fibrinous inflammation?

A

Characterized by an exudate that is rich in fibrin, formed from long strands of polymerized fibrinogen, which is one of the largest plasma proteins.

40
Q

In what infections do you see fibrinous inflammation?

A

Bacterial: strept throat or pneumonia

41
Q

Best example of fibrinous inflammation?

A

Fibrinous pericarditis:
The surface of the heart is covered with shaggy, yellowish layers of fibrin that bridges the space between the two layers of the pericardial sac, obliterating the cavity. When the friable fibrin strands are separated, the epicardium and pericardium resemble bread and butter taken apart.

42
Q

What is purulent inflammation?

A
  • Typically caused by pus-forming bacteria, such as Staph and Strept.
  • A viscous, yellow fluid composed of dead and dying PMN’s and necrotic tissue debris.
  • Pus may accumulate on the mucosa, skin, or in the internal organs. A localized collection of pus with an organ or tissue is called an Abscess.
43
Q

What is an abscess?

A

consists of a central portion of purulent material surrounded by a wall composed of a capsule of fibrotic granulation tissue. They do not heal spontaneously and must be evacuated.
*typically caused by staph aureus

44
Q

What can happen to large abscesses?

A
  • They tend to rupture, forming a sinus (a cavity usually occupied by a previous abscess that drains through a tract to the surface of the body)
  • May also form fistulas
45
Q

What is a fistula?

A

channels formed between two preexisting cavities or hollow organs and the surface of the body. A fistula can be formed between two loops of bowel, fused together by inflammation

46
Q

What is the best example of a fistula?

A

Crohns disease

47
Q

What is ulcerative inflammation

A

Inflammation of body surfaces or the mucosa of hollow organs, like the stomach or intestines, may result in ulceration, or a loss of epithelial linings.

48
Q

What is an ulcer and what are some complications associated with them?

A

An ulcer is defined as a defect involving the epithelium, but may extend into the deeper connective tissues as well (i.e. peptic ulcer)
Complications: perforations, neoplastic transformation

49
Q

What is pseudomembranous inflammation?

A

A form of ulcerative inflammation that is combined with fibrinopurulent exudation.

The exudate of fibrin, pus, cellular debris and mucous forms a pseudomembrane on the surface of ulcers that can be scraped away to expose ulcerated defects that bleed profusely.

50
Q

What causes pseudomembranous colitis?

A

Clostridium difficile: caused by a bacterial overgrowth secondary to intake of broad-spectrum antibiotics.
AKA antibiotic associated colitis
*can kill if not treated

51
Q

What is Granulomatous Inflammation?

A

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

52
Q

What may cause Granulomatous Inflammation?

A

may be caused by antigens that evoke a cell-mediated hypersensitivity reaction, or by antigens that persist at the site of inflammation.

53
Q

What is the best example of Granulomatous Inflammation

A

Tuberculosis is the prototype granulomatous disease, as are certain fungal diseases.

TB is an acid fast bacteria can only be seen on AFB(acid fast bacillus)stain

54
Q

When is TB activated?

A

TB is contained in granulomas in a healthy person, will release with immunodeficiency (chemo, AIDS)

55
Q

What are the 3 classes of cells in relation to their capacity to proliferate?

A

Continuously Dividing Cells
Quiescent Cells
Nondividing Cells

56
Q

What is the term used for how the brain repairs itself?

A

Gliosis

57
Q

What is the term used for how the heart repairs itself?

A

Fibrosis

58
Q

What are continuously dividing cells?

A

AKA Labile Cells, are cells that divide throughout the entire lifespan. These cells divide at a regular rate and give rise to more differentiated cells
AKA “stem cells”

59
Q

What is an example of a continuously dividing cell?

A

RBC’s live 120 days and the division of their bone marrow precursors is paced to allow continuous compensated for their programmed loss

60
Q

continuously dividing cells and repair

A

Can easily repair a defect in skin wounds or mucosal ulcers that can heal readily under appropriate conditions as the superficial layers are replenished from the descendants of cycling stem cells in the basal layer or the intestinal crypts.
*fast repair

61
Q

Quiescent cells

A

AKA Stable Cells, do not divide regularly, but can be stimulated to divide if necessary

62
Q

Best example of Quiescent cells?

A

Kidneys and liver:
Loss of liver parenchyma following a partial hepatectomy stimulates the remaining liver cells to enter mitosis and, by dividing, replace the loss. Once the liver has regenerated, the cells become stable again, and stop dividing.

63
Q

Nondividing cells

A

AKA Permanent Cells, do not have the capacity to proliferate under any circumstances.

64
Q

Examples of nondividing cells

A

neurons and myocardial cells. A loss of myocardial cells repairs itself by fibrous scarring. A loss of brain cells, also irreversible, repairs by Gliosis

65
Q

What cells are involved in wound healing?

A

The most important cells that are involved in wound healing are the Leukocytes, Macrophages, connective tissue cells and Epithelial cells.

66
Q

What are the roles of PMN’s and macrophages in wound healing?

A

PMN’s play a brief role in scavenging the initial site of injury, and macrophages stay at the site of injury and healing and produce certain factors and mediators that act on certain connective tissues cells.

67
Q

Cells in healing: Myofibroblasts

A

Have hybrid properties of both smooth muscle cells and Fibroblasts. This enables them to contract, which occurs within the first few days of healing, reducing the defect, holding the margins of tissue in close approximation. This enables the proliferating epithelial cells to cover the surface defect and also restores the integrity of the surface epithelium.

68
Q

Cells in healing: Angioblasts

A

Are the precursors of blood vessels that proliferate like sprouts from the several small blood vessels at the margins of the wound. These appear 2-3 days after incision, and by the 5th-6th day, the entire field is permeated by these newly formed blood vessels that will allow the influx of blood and it’s accompanying oxygen and nutrients.

69
Q

Cells in healing: fibroblasts

A

Fibroblasts: are the cells that produce most of the extracellular matrix, including :

- Fibronectin:  important in providing tensile strength to the connective tissue matrix and also has the ability to “glue” other substances and cells together.
- Collagen:  the wound initially consists of Type III collagen that is immature or young collagen laid down by fibroblasts
70
Q

What is type 3 collagen replaced by in healing?

A

Type III collagen is replaced by Type I collagen, which is the most common form of collagen in the body, providing increased strength for all tissues

71
Q

When does collagen acquire its full strength?

A

When it is laid down in the extracellular spaces. This occurs several weeks after injury, when the collagen fibers are cross-linked with each other, forming a dense meshwork.

72
Q

Describe the process of a scab

A
  • Healing of sterile surgical wounds occurs by First Intention. The incision site initially contains coagulated blood that forms a scab.
  • The scab is invaded in PMN’s whose function is to scavenge debris. These are replaced 2-4 days later by macrophages. The growth factors and mediators secreted by the macro-phages promote the ingrowth of myofibroblasts, angioblasts, and fibroblasts
73
Q

What is the vascularized connective tissue that is rich in macrophages, myofibroblasts, angioblasts, and fibroblasts

A

Granulation tissue

74
Q

What is granulation tissue?

A

a temporary, makeshift structure that changes over time. Initially it contains many myofibroblasts, which contract the wound and then disappear. The wound that was initially filled with extravasated blood will become edematous and filled with granulation tissue

75
Q

How is a scar developed?

A

the composition of the matrix changes from Fibronectin and Collagen Type III to predominantly Collagen Type I.
These changes in the dermis on skin wounds are accompanied by a proliferation of epithelial cells from the margins of the wound. These cells cover the defect within 3-7 days.

76
Q

How long does the transformation of granulation tissue to scar typically take?

A

Under ideal circumstances, the granulation tissue filling the skin defect in the wound is transformed into a scar within 3-6 weeks.

77
Q

Define first intention

A

orderly sequence of events that characterizes the healing of sharp, sterile, surgical wounds

78
Q

What heals as a secondary intention?

A

large defects and essentially all infected wounds

-Large defects cannot readily be bridged, and the surgeon cannot juxtapose the gaping tissue margins.

79
Q

Why does the granulation tissue remain exposed in secondary intention?

A

-The wound contraction cannot be accomplished by the myofibroblasts, and in such cases, the granulation tissue remains exposed to the external surface.

80
Q

Is secondary intention healing fast or slow?

A

Wound healing by secondary intention is usually prolonged, and some wounds never completely heal.

81
Q

What are the most important determinants of wound healing?

A
  1. Site of the wound: skin heals better than brain
  2. Infection: sterile heal faster than infected
  3. Mechanical factors: movement may slow healing, having clean edges that come together easily decreases healing time.
  4. Age: adults heal slower than children
  5. Circulatory status: Ischemic tissues heal poorly(diabetes)
  6. Nutritional and metabolic factors: general well-being promotes wound healing(vit C vital for healing)
82
Q

Complications of wound healing:

A
  1. Deficient scar formation: slow formation of granulation tissue occurs in diabetics(diabetes and metabolism disturbances)
    (inadequate collagen prod. in pt using corticosteroid hormones)
    *both above result in scars that may not have sufficient tensile strength and dehiscence may occur
  2. Excess scar formation: Keloids
83
Q

Define Dehiscence

A

Separation of the wound margins

84
Q

What are keloids?

A

hypertrophic scars composed predominantly of Type III collagen, and results from defective remodeling of scar tissue, with a resultant immature scar.

PATHOPHYS (5 decks)

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