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Pathology 2220 > Week 2: Inflammation > Flashcards

Week 2: Inflammation Flashcards

1
Q

Define Inflammation:

A

The response of living tissue to injury

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2
Q

What is the goal of inflammation?

A

To bring Leukocytes and plasma proteins that normally circulate in the blood to the site of infection or tissue damage, Eliminate the agent and initiate healing

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3
Q

For Acute Inflammation what is/are the:

  1. Onset -
  2. Cells Involved -
  3. Tissue Injury, Fibrosis -
  4. Local and Systemic Signs -
A
  1. Fast, minutes/hours
  2. Mainly neutrophils
  3. Mild, self limited
  4. Prominent
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4
Q

For Chronic Inflammation what is/are the:

  1. Onset -
  2. Cells Involved -
  3. Tissue Injury, Fibrosis -
  4. Local and Systemic Signs -
A
  1. days, months, years
  2. Monocytes (Macrophages), Lymphocytes
  3. Often severe, progressive
  4. less prominent
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5
Q

Redness is the result of __________________ which is a ________ event.

A

Increased blood flow

Vascular event

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6
Q

Swelling is a result of ________ hydrostatic pressure, _________ permeability and ____________________ of WBC. This is a _________ event.

A

Increased
Increased
Active emigration of WBC
Vascular event

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7
Q

What is exudation?

A

The passage of fluid and cells from the vessels into the interstitial tissue

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8
Q

Give a brief summary of exudation:

A
  1. Chemical mediators caused endothelial contraction
  2. Gaps appear between the endothelial cells
  3. Fluid and proteins escape (Small molecules first, fibrinogen last)
  4. Tissue osmotic pressure increases causing swelling
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9
Q

Summarise the Vascular events of inflammation:

A

Changes in calibre of vessels - initial constriction (secs) followed by dilation, capillaries then arterioles

Changes in blood flow (increased at first, later slows)

Changes in permeability (leakage of fluid and protein)

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10
Q

Summarise the Cellular events of inflammation:

A

Recruitment of leukocytes to site of infection and injury

Leukocyte migration through endothelium (emigration) and to site of injury (chemotaxis)

Recognition by phagocytes of microbes and dead tissue

Removal of the offending agent

Other responses of leukocytes – initiation of repair process, leukocyte mediated tissue injury

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11
Q

What is resolution?

A

Restoration of tissue to a completely normal state after acute inflammation or other tissue damage or death

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12
Q

When is resolution most likely to occur?

A
  • When cell death and tissue damage is minimal
  • When damaged cells are capable of regeneration
  • When causative organism is rapidly eliminated
  • Where local conditions favour removal of exudate
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13
Q

Describe the process of resolution:

A
  1. Fibrin and other proteins dissolved by fibrinolysin and enzymes from neutrophils and macrophages
  2. Fluid removed in blood and lymphatic vessels
  3. Removal of all debris by phagocytes to lymph nodes
  4. Blood flow returns to normal
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14
Q

Define “Ulcer”:

A

A break in the surface (of the body or an organ) and its replacement by inflammatory tissue. Most commonly seen in skin and alimentary tract.

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15
Q

Define “Sinus”:

A

A tract leading from a chronically inflamed cavity to a surface. Usually lined by granulation tissue.

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16
Q

Define “Fistula”:

A

A tract, open at both ends, making an abnormal communication between two surfaces

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17
Q

Define “Cellulitis”:

A

The spread of inflammation in the connective tissue planes.

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18
Q

What is suppuration?

A

The formation of pus

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19
Q

What is pus?

A

An accumulation of dead and living neutrophils, dead and living bacteria ( when inflammation caused by pyogenic bacteria), protein (especially fibrin) and other particulate matter (eg cell fragments etc)

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20
Q

What is an abcess?

A

A pus-filled cavity

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21
Q

What is an Empyema?

A

An accumulation of pus in a naturally occurring body cavity

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22
Q

Explain the evolution of the abcess:

A
  1. Starts as an inflammatory exudate with many neutrophils
  2. Proteins, bacteria and polymorphs clump to form a mass
  3. Tissue death
  4. New capillaries and fibroblasts develop at edge of accumulated material
  5. Fibroblasts start to lay down scar tissue (collagen)
  6. Pus resorbed (if small amount) or can burst onto (‘point’) to external surface (sinus)or adjacent body cavity (fistula) and be discharged in this way
  7. Collagen deposition proceeds to formation of mature scar
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23
Q

Chronic inflammation endures _______ than acute inflammtaion. It can be caused by the ___________________ from the acute inflammatory response

A

Longer

Inability to removed the agent

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24
Q

What are the 2 types of healing?

A

Resolution and repair

25
Q

What is repair?

A
  • Repair occurs when resolution is impossible
  • It involves formation of granulation tissue
  • Maturation of granulation tissue to scar tissue (fibrosis)
26
Q

Define organisation:

A

The growth of new capillaries and fibroblasts into the damaged tissue together with migration of macrophages. Macrophages remove debris, fibroblasts lay down collagen

27
Q

What is granulation tissue?

A

New capillaries and fibroblast

28
Q

What is healing by primary intention?

A

Occurs in clean wounds with opposed edges (eg surgical wounds)
Results in minimal scarring
Occurs in short time
Strengthening, devascularisation continues longer

29
Q

What is healing by secondary intention?

A

Occurs in open wounds (loss of tissue, necrosis or infection)
Often results in significant scarring (fibrosis)
Process may continue for months or years

30
Q

Explain the process of fibrosis:

A
  1. Fibrocytes stimulated by polypeptides from surrounding damaged cells
  2. Become active fibroblasts. Commence protein synthesis
  3. Secretion of ground substance including fibrinonectins
  4. Secretion of procollagen
  5. Condensation to fine reticulin fibres
  6. Further condensation to mature collagen fibres
  7. Binding and weaving to form scar tissue
  8. Fibroblasts revert to fibrocytes
31
Q

What local factors negatively affect healing?

A

Low blood supply
Infection
Excessive movement
Foreign Material

32
Q

What systemic factors negatively affect healing?

A

Deficiency of vitamin C, amino acids and zinc
Excess adrenal corticosteroids
Chronic disease

33
Q

How can we recognise neutrophils?

A

3 lobed nucleus

Secretory nucleus

34
Q

What impetigo?

A

An acute superficial infection of the skin that forms pustules and yellow crusty sores

35
Q

What are some predisposing factors for impetigo?

A

Minor Trauma
Poor Hygiene
Warm/Humid Climate

36
Q

The most common Impetigo causing organism is _______________.

A

Staphylococcus aureus

37
Q

What are the features of Common Impetigo?

A
  • Thin walled vesicles or pustules
  • Rupture to form a thick golden crust
  • Solitary or clustered, face or extremities
38
Q

What are the features of Bullous Impetigo?

A
  • Erosions and flaccid bullae

- Caused by an exotoxin which results in keratinocytes falling apart and blister formation

39
Q

What is the histopathology of Impetigo?

A
  • Subcorneal (ie under the stratum corneum) collection of neutrophils
  • Can see more neutrophils migrating upwards through the epidermis
  • Surface crust of serum and dying neutrophils
  • May see bacterial colonies
40
Q

What is Acne Vulgaris?

A

An inflammatory disorder of the pilosebaceous unit

hair follicle and sebaceous gland

41
Q

How does Acne Vulgaris present?

A

Lesions are variable and include:

Comedones, Papules, Pustules, Cysts, Sinuses, Scars

42
Q

What are comedones?

A

Comedones are widened hair follicles which are filled with keratin, other debris, bacteria and sebum
– Closed : “whiteheads”
– Open: “blackheads”

43
Q

What are the causes of Acne Vulgaris?

A

– Abnormal follicular keratinisation, with retention of keratin within the follicle
– Increased sebum production due to androgens
– Presence of bacteria: Propionibacterium acnes
– Inflammation

44
Q

Describe the pathogenesis of Acne Vulgaris:

A
  1. Ongoing dilation of comedo leads to the wall of the follicle becoming very thin, eventually it ruptures
  2. The keratin, sebum and bacteria incite an acute inflammatory response
  3. Predominantly neutrophils at first – pustule formation
  4. Followed by granulomatous inflammation and fibrosis (scarring)
45
Q

Superficial Folliculitis usually affects the _________ part of the hair follicle called the __________. It may be related to _________________.

A

Superficial
Infundibulum
Bacterial Infection

46
Q

What is a Furuncle?

A

A boil - caused by a deeper infectious inflammatory process centred on the pilosebaceous unit

47
Q

Where are Furuncles commonly found?

A

Areas of friction with clothing - Thighs, Back of the Neck and Buttocks

48
Q

How does a Furuncle present?

A
  • Begins as a painful papule with surrounding erythema (redness) and swelling
  • The centre becomes soft, yellow and may discharge pus
49
Q

What are the Histological features of Furuncles?

A

Neutrophils surround follicle
Follicle may be destroyed, residual shafts may be seen
Surface shows ‘crust’ of serum and dying neutrophils

50
Q

What can cause Furuncles?

A

Often Bacterial - Staphylococcus Aureus
Viral - e.g. herpes simplex
Fungal

51
Q

__________ is an acute inflammatory process within the dermis which is usually caused by _________________.

A

Erysipelas

Streptococcus pyogenes

52
Q

What are the characteristics of Erysipelas?

A
  • Oedematous, tender, hot, well demarcated red plaques
  • Often accompanied by a fever
  • Face, feet, hands and lower limbs are most affected
53
Q

What is Cellulitis?

A

Similar to Erysipelas but involves deeper tissue
Often occurs in the legs
Expanding erythema

54
Q

What is the Histology of Erysipelas/Cellulitis?

A
  • Dermal oedema and lymphatic dilatation

* Diffuse infiltrate of neutrophils

55
Q

TNF-α activates _____________ cells to up regulate cell surface adhesion molecules called __________. These bind ___________ on the surface of __________. This initiates _________ of these cells.

A 
Endothelial cells
Selectins
Integrins
Neutrophils
Emigration
56
Q

Which cytokines stimulates neutrophil generation?

A

IL-1 and IL-6

57
Q

What are the predisposing factors for cellulitis?

A 
Minor trauma
Peripheral Vascular Disease 
Diabetes 
Lympoedema
Alcohol Abuse
58
Q

What are the histological features of cellulitis?

A

Dermal oedema and lymphatic dilation

Diffuse infiltrate of neutrophils

Pathology 2220 (10 decks)

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