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General Pathology -- Roecker > Gen Pathology Exam 1 Section 2: Inflammation and Repair > Flashcards

Gen Pathology Exam 1 Section 2: Inflammation and Repair Flashcards

1
Q

Neutrophils

A

granulocytes; most abundant (~70% all circulating WBC’s); perform phagocytosis at site of ACUTE inflammation

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2
Q

Basophils

A

granulocytes; ~1% all WBC’s; involved in allergic reactions (asthma, anaphylaxis, atopic dermitis, and allergic rhinitis)

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3
Q

Eosinophils

A

granulocytes; ~3% all WBC’s; commonly involved with parasitic infections and allergic reactions

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4
Q

Monocytes/Macrophages

A

agranulocytes; (~10% all WBC’s); Monocytes differentiate into Macrophages when “activated” at site of CHRONIC inflammation
Macrophages–> preform phagocytosis

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5
Q

Lymphocytes

A

agranulocytes; ~25% of all WBC’s; Numerous categories (Tcells, Bcells, NK cells); at CHRONIC inflammation sites

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6
Q

T-cells

A

NOT a single type of cell; represent a group of similar but different types of cells ( cytotoxic T cells, T helper cells, and B cells)

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7
Q

B cells

A

transition into plasma cells

Plasma Cells = the primary cell involved with antibody production (adaptive immunity)

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8
Q

What cells function as sentinel cells for infection or injured tissues?

A

macrophages
dendritic cells
mast cells
—they secrete cytokines = pro-inflammatory

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9
Q

Acute Inflammation

A

initial response to injury or infection; develops with in minutes of initial stimulus; lasts hrs to days
Main cell = neutrophils
Produces–> fever, rigors, body aches, or headaches
- Unlikely to result in fibrosis

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10
Q

Cardinal Signs of Inflammation

A
  1. redness
  2. heat
  3. swelling
  4. pain
  5. loss of fxn
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11
Q

Chronic Inflammation

A

when inflammation persists past an amount of normal tissue time needed to resolve
Main cells = macrophages and lymphocytes
- they replace neutrophils ~ 48 hours post infection or injury

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12
Q

“Secondary tissue injury”

A

inadvertent injury to normal cells due to unregulated inflammation (like autoimmune conditions or allergic reactions)

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13
Q

What are the two main cellular receptors associated with Acute Inflammation?

A
  1. Toll-like receptors

2. Inflammassomes

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14
Q

Toll-like receptors

A

within sentinel cell’s plasma membrane and detect infectious pathogens–> then secrete pro-inflammatory cytokines

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15
Q

Inflammasomes

A

within sentinel cell’s cytosol and detect molecules associated with cellular injury/damage (extracellular DNA and ATP, uric acid from DNA break down, or amyloid proteins) –> then secrete cytokines

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16
Q

Inflammatory stimuli

A

infections microbes, necrosis, foreign bodies

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17
Q

Foreign bodies

A

shrapnel (grenade fragments, splinters, sutures,etc. that are traumatically introduced

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18
Q

What does acute inflammation begin with?

A

changes to blood vessel walls that allows fluid, plasma proteins and leukocytes to leave circulation and move toward target tissue

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19
Q

Vascular Changes ass. with acute inflammation

A

begin with vasoconstriction–> quick, lasts few seconds
transitions to prolonged vasodilation –> therefore vessel walls are more permeable (so intravascular fluid and plasma proteins more through vessel wall)

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20
Q

Three Mechanisms to Increase Vessel Wall Permeability

A
  1. Endothelial Cell Contraction
  2. Endothelial Injury
  3. Angiogenesis
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21
Q

Endothelial cell contraciton (Ass. w/ Vessel Wall Permeability)

A

most common; “retraction of endothelial cells”; ind. endothelial cells squeeze down and produce gaps
- mediated by HISTAMINE

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22
Q

Endothelial injury (Ass. w/ Vessel Wall Permeability)

A

less common; continue until endothelial cells been repaired
Caused by: severe burns, severe infecitons, exposure to highly toxic substances
- Endothelial cell necrosis

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23
Q

Endothelial cell necrosis

A

may cause unregulated fluid loss in inds. with severe burns; when 20% body covere din 3rd or 4th degree burns and care not provided –> ind. at risk of lethal hypovolemia shock

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24
Q

Angiogenesis (Ass. w/ Vessel Wall Permeability)

A

formation of new blood vessels– do NOT have mature vessel walls yet and therefore increase permeability; common at site of tissue repair and hallmark feature of tumor growth

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25
Q

Edema

A

fluid that accumulates with increase vessel wall permeability

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26
Q

Exudate

A

protein-rich form of edema at site of ACUTE inflammation; no pitting
Ex: sprained ankle

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27
Q

Transudate

A

protein-poor form of edema; with non-inflammatory processes; produces “pitting edema”
Ex: congested heart failure

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28
Q

How do leukocytes get recruited, related to vessel walls?

A

increase in vessel wall permeability = fluid leaves vessels = decrease fluid content of blood = blood becomes MORE viscous and flows slower at site of ACUTE inflammation–> pushes larger WBC’s to wall and RBC’s to enter

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29
Q

Steps of WBC exiting vessel

A
  1. Margination
  2. Rolling
  3. Firm adhesion
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30
Q

Margination

A

process of WBC’s accumulating near vessel wall

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31
Q

Rolling

A

WBC’s roll along vessel wall; mediated by SELECTINS

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32
Q

Firm Adhesion

A

WBC’s stop moving and tightly bond onto inside vessel wall; mediated by INTEGRINS

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33
Q

Lymphangitis

A

acute inflammatory reaction is within the lymphatic vessels; almost always result of microbial infection after trauma

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34
Q

Lymphadenopathey

A

general term; for a disease affecting the lymph nodes

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35
Q

Lymphadenitis

A

a lymph node is inflammed and commonly associated with increase in size and pain upon palpation

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36
Q

Opsonization

A

“coating” or “tagging” microbes or cellular debris with an opsonin (greatly enhances phagocytosis); adheres immunoglobulins (antibodies) or complement proteins to outside wall of infections microbes or injured tissues

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37
Q

Phagosome

A

what target is engulfed into by pseudopodia

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38
Q

Phagolysome

A

binding of phagosome lysosomes; and breaks down its contents by exposing to bursts of ROS and lysosomal enzymes

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39
Q

Leukocyte-Induced Tissue Injury or Secondary Tissue Injury

A

when leukocytes injure normal cells and harmful to body; may occur as collateral damage to tissue surrounding acute inflammation reaction ; leukocytes are indiscriminate

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40
Q

What three situations cause Leukocyte-induced Tissue injury?

A
  1. Persistent Infections
  2. Ischemia-Reperfusion injuries
  3. Hypersensitivity Reactions
41
Q

Factors that influence outcome of acute inflammation (4)

A
  1. nature of injury (i.e burn vs infection)
  2. severity of injury
  3. tissue(s) being injured
  4. Host’s responsiveness of injury –> ex. age
42
Q

What are the three main outcomes of Acute inflammation?

A
  1. Resolution
  2. Chronic Inflammation
  3. Fibrosis (scarring)
43
Q

Resolution outcome of acute inflammation

A

“complete resolution” or tissue “regeneration”; reestablishing tissue to state indistinguishable from pre-injury status; injured cells must be able to replicate (divide); most likely occurs in mild, limited, and injuries involving minimal tissue
Ex: paper cut or an aphthous ulcer

44
Q

Fibrosis outcome of acute inflammation

A

(=scarring); occurs following sig. tissue injury or in cells with NO ability to divide or repair; chronic inflammation often transitions into this

45
Q

Scar tissue

A

= non functional tissue anc cannot perform functions of cells it replaced

46
Q

Examples of Fibrosis

A
  • liver cirrhosis and loss of metabolic activity
  • scars on skin and decrease elasticity and strength
  • survive heart attack and decrease cardiac contractability and develop heart failure
47
Q

Six Morphological Patters of Inflammation

A
  1. Serous Inflammation
  2. Fibrosis Inflammation
  3. Purulent Inflammation
  4. Ulcerative Inflammation
  5. Pseudomembranous Inflammation
  6. Granulomatous Inflammation
48
Q

Serous inflammation

A 
involves serum (serous fluid) accumulating within spaces b/w epithelial cells or within body cavities; commonly triggered by viral infections, burns, or autoimmune rxns
- NOT infected and does NOT contain large amounts of leukocytes 
Ex: blister
49
Q

Large and small blister

A 
vesicle = smaller blister
bulla = large blister
50
Q

Fibrosis inflammation

A

occurs when high levels of inflammation cause a large increase in vessel wall permeability to point where large molecules (like fibrinogen) move outside of vessel lumen and become deposited on inflamed tissue

51
Q

What is fibrosis commonly triggered by?

A

inflammation on body cavities; pericardium, pulmonary pleura, or meninges
Examples:
- survive heart attack and fibrinogen leaves circulation and deposits on inside of pericardium –> overtime will lead to scarring–> adds friciton to beating of heart–> accelerate heart failures

52
Q

Purulent Inflammation

A

AKA suppurative inflammation; occurs when pus is present at site of acute inflammation; most likely indicates that pyogenic bacteria have infected tissue

53
Q

Pus

A

collection of liquefied cellular tissue, protein-rich exudate, and several leukocytes (like neutrophils)

54
Q

Pyogenic

A

pus-forming

55
Q

Abscess

A

a localized collection of pus

56
Q

Ulcerative Inflammation

A

development of an ulcer, which is a local tissue defect on surface of tissue or organ; superficial cells slough off following tissue necrosis
Examples:
- canker sore (aphthous ulcer) affects ~ 50% pop.
- peptic ulcer disease, diabetic ulcers, or pressure ulcers (bed sores)

57
Q

Pseudomembranous Inflammation

A

infections microbe secretes a necrotizing toxin that causes necrtoic tissue and WBC’s to accumulate on surface
Example:
- present in tonsils of patients with diphtheria
- present in colon of patients with pseudomembranous colitis

58
Q

Granulomatous Inflammation

A

pattern of CHRONIC inflammation; a collection of macrophages, and some T-cells, and may have central region of necrosis; usually develops due to presence of foreign bodies or persistent immune reaction
- associated with tuberculosis
Also present in: Crohn’s disease, sarcoidosis, syphilis, leprosy, persistent fungal infections, and cat-scratch disease

59
Q

Noncaseating granuloma

A

commonly used to indicate the granulomatous inflammation is unlikely to be from tuberculosis

60
Q

Granuloma

A

a site of granulomatous inflammation; descirbed as a “giant cell” or Langhans giant cells b/c marcophages pack together; also described as epitheloid cells b/c the collection of macrophages also described as rambling layered appearance of epithelial cells

61
Q

Pain and Acute Inflammation is signaled by what two things?

A
  1. Prostaglandins

2. Substance P

62
Q

Prostaglandins

A

produced by mast cells, macrophages, and endothelial cells–> signal pain and fever

63
Q

Fever

A

any body temp above normal 98.6 F (37 C); most common greater than 100.4 F (38 C); produced when prostaglandins interact with hypothalamus to increase body’s temp. set point

64
Q

Substance P

A

is a neuropeptide (NT) produced by various leukocytes and sensory neurons
- involved with transmission of pain signals

65
Q

What does suffix “-oid” mean?

A

means resembling something else

66
Q

Two main processes of tissue repair

A
  1. Regeneration

2. Fibrosis (scarring)

67
Q

Regeneration

A

when tissues return to a “pre-injury” state; involves growth (proliferation) of uninjured cells at area of inflammation; ONLY possible if normal tissue not obliterated and is regular dividing or high capacity for cell division

68
Q

Examples of tissue that can regenerate

A

skin or gastrointestinal mucosa
Hepatocytes–have unique ability to regenerate; after partial heptectomy the liver may regrow to normal size following up to 90% of its mass

69
Q

Fibrosis (scarring)

A

involves deposition of fibrous connective tissue– collagen fibers; during tissue repair; serves as a “patch” rather than restoring normal tissue structure and function; occurs in tissue incapable of dividing or follow severe tissue damage

70
Q

Examples of tissue that undergoes fibrosis

A

cardiac myocytes, skeletal muscle, or CNS neurons, lungs, kidneys
and any tissue following severe tissue damage (i.e. severe abrasion)

71
Q

What is the relationship between damage to ECM and scarring?

A

Increase damage to ECM; increase scarring

72
Q

Fibroblasts

A

are recruited to site within 3-5 days by macrophages being alternatively activated and secrete growth factors and stimulate new blood vessel formation and recruit the fibroblasts

73
Q

Steps in Scar Formation

A
  1. angiogenesis
  2. fibroblast migration and proliferation
  3. collagen deposition –> scar
  4. remodeling (occurs over lifetime)
74
Q

Matrix Metallopretoeinase (MMPS)

A

breakdown tissue–collagen; they are produced by: fibroblasts, macrophages, neutrophils, and epithelial cells
Cofactor = zinc ion

75
Q

Keloids

A

scarring beyond boundaries of wound; excessive granulation tissues and excessive collagen; raised and flesh colored lesion; won’t regress and if remove it comes back worse

76
Q

Where can keloids occur?

A

any cutaneous surface; injury to dermis increase risk
- possible pain or itching
- more common in African Decent
Ex: Cauliflower Ear

77
Q

Cauliflower Ear

A

irregular collagen formation; auricular hemotoma; trauma disrupts blood vessels; shearing forces seperate anterior perichondrium from the underlying cartilage

78
Q

Treatment for Cauliflower ear

A

drainage within 7 days

79
Q

Factors influencing repair

A
  1. infection
  2. nutritional deficiency
  3. gluccorticoids (steroids)
  4. poor perfusion
  5. Etc. increase age; mechanical pressure/distortion, anemia, foreign bodies, UV light
80
Q

The Phases of healing skin wounds

A
  1. inflammation
  2. formation of granulation tissue (3-5 days)
  3. ECM deposition and remodeling
    (all overlap)
81
Q

What 4 things does Chronic Inflammation develop from

A
  1. Persistent infection
  2. prolonged injury
  3. hypersensitivity reactions
  4. immunosuppression
82
Q

Persistent infection (leading to chronic inflammation)

A

some infectious microbes = difficult to eradicate

Examples: Hepatities B and C, tuberculosis, or Clostridium difficile (C-Diff)

83
Q

Prolonged Injury (leading to chronic inflammation)

A

may be do to daily exposure that continually causes injury to tissue
Examples:
-tobacco smoke cont. injury respiratory tract and cause chronic bronchitis
- harness that continually rubs

84
Q

Hypersensitivity reactions (leading to chronic inflammation)

A

involve allergies and autoimmune conditions

85
Q

Immunosuppression (leading to chronic inflammation)

A

inadequate immune response (may allow inf. to persist longer); ass. with age related redcutions in immune function
Examples:
- AIDS
- medically- induced in ind. receiving tissue/organ transplant

86
Q

Cells involved with chronic imflammation

A

macrophages*, lympocytes (T cells, B cells, NK cells), and plasma cells

87
Q

Classically Activated Macrophages

A

perform phagocytosis of microbes and cellular debris; secrete cytokines–> promote cont. inflammation

88
Q

Stimuli that activate Classically Activated Macrophages

A

microbes, crystalline substances, or particles from tissue necrosis

89
Q

Alternatively Activated Macrophages

A

secrete Growth Factors and stimulate repair by increase angiogenesis and recruit fibroblasts

90
Q

Fibroblasts

A

cells that secrete collagen and found at CHRONIC inflammation when scar tissue deposition occuring or about to occur

91
Q

Angiogenesis

A

ingrowth of new blood vessels; also body’s way to attempt to heal area

92
Q

Systemic Effects of Inflammation

A
  1. Fever
  2. Acute-phase proteins
  3. Leukocytosis
  4. Leukemoid Reactions
  5. other effects of acute-phase reaction–anorexia, somnolence, and malaise
93
Q

Acute-phase proteins

A
  1. C-Reactive Protein (CRP)

2. Erythrocyte Sedimentation rate (ESR)

94
Q

C-Reactive Protein (CRP)

A

are elevated in inflammation response, (nonspecific lab findings for inflammation); increase CRP levels is a marker for heart attack risks; progression of coronary artery disease

95
Q

Erythrocyte Sedimentation Rate (ESR)

A

the rate that RBC’s fall out of suspension with in 1 hour (nonspecific test, marker for body-wide inflammation)
- Fibrinogen brins RBC’s together and increase ESR
(increase fibrinogen proteins, ass. with increase inflammation, and increased ESR)

96
Q

Leukocytosis

A

elevated WBC inside ciruclation
Normal Range = 4,000 - 10,000 cells per microliter
Leukocytosis = 15,000-30,000

97
Q

Bacterial infections are more likely to produce elevation of what cells?
Viral infections?

A

bacterial infections–> elevated neutrophils

viral infections–> elevated lymphocytes

98
Q

Leukemoid reactions

A 
extremely elevated WBC counts
40,000-100,000 cells per mL
Mimic elevate WBC levels ass. with leukemia
Conditions that produce this:
- infectious mononucleosis ("Mono")
- tuberculosis
- C-Diff infection

General Pathology -- Roecker (7 decks)

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