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Pathology > Chapter 3 - Inflammation: Reaction to Injury > Flashcards

Chapter 3 - Inflammation: Reaction to Injury Flashcards

1
Q

Inflammation

A

Local reaction to vascularized tissue to injury

  • Acute
  • Chronic
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2
Q

Acute inflammation

A

Usually a rapid response with a short duration

  • Shows neutrophils and edema
  • Associated with bacterial infection
  • Inflammation continues until repair or scar replace is damaged tissue
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3
Q

Chronic inflammation

A

Usually a later response with a long duration

  • Acute inflammation may not proceed
  • Usually shows lymphocytes and macrophages
  • Often associated with viral or fungal infections
  • Injury is ongoing: injury, inflammation and repair coexist
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4
Q

Inflammatory cells

A

White blood cells or leukocytes; involved in immunity

  • Granulocytes
  • Mononuclear cells
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5
Q

Granulocytes

A

Polymorphonuclear leukocytes

  • Contain granular cytoplasm
  • Involved mainly an acute inflammation
  • Neutrophils
  • Eosinophils
  • Basophils
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6
Q

Neutrophils

A

65% of WBC’s

  • Also called “polys” or “PMNs” (polymorphonuclear neutrophils), “segs” (for segmented, referring to two - five segmented nuclei)
  • First to gather at damage site
  • Motile: can respond to chemotaxis
  • Phagocytosis: canon golf extracellular material (main task of neutrophils)
  • Bacteriocidal: have specific bacteriocidal enzymes to kill bacteria
  • Release chemical factors which stimulate the inflammatory response, including attracting more WBCs, stimulate bone marrow to produce neutrophils, and act on brain to increased body temperature and cause malaise
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7
Q

Eosinophils

A

3% of WBCs

  • Main cell in parasitic infection (worms, rarely protozoa or fungi)
  • Only slightly motile or phagocytic
  • Important in allergies (hay fever) attracted by basophils; roll not clear
  • Microphage: neutrophils and eosinophils
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8
Q

Basophils (in blood) > mast cell (in tissue)

A

< 1% WBCs

  • Release histamine, one of the chemical factors of inflammation and allergies
  • Cause swelling, itching, congestion, and mucus production
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9
Q

Mononuclear cells

A

Agranulocytes. Contain no granules with nonsegmented nuclei
- Important in chronic inflammation

  • Monocytes
  • Lymphocytes
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10
Q

Monocytes (in blood) > macrophages (in tissue)

A

5% of WBCs

  • Most prominent in later stages of acute inflammation and chronic inflammation
  • Motile: slower than neutrophils
  • Phagocyte: scavengers of body; only neutrophils and monocytes are highly phagocytic
  • Release inflammatory chemical factors
  • Release and science which helped agreed and clear away debries
  • Fixed macrophage - Kupffer cells (liver); microglia (brain); Langerhan cells (skin)
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11
Q

Lymphocytes

A

About 23% of WBCs

  • Appear very late in acute inflammation and chronic inflammation
  • Main cells of immune system: B and T cells according to their origin
  • Activated B cells are called plasma cells and produce antibodies and are present in chronic inflammation
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12
Q

Molecular mediators of inflammation

A
  • Plasma derived mediators

- Cell-derived molecular mediators

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13
Q

Plasma derived mediators

A
  • Clotting system
  • Complement system
  • Kinin system
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14
Q

Clotting system

A
  • About 12 proteins that cause blood clotting

- Stimulates complement and kinin systems

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15
Q

Complement system

A

Initiated by immune system or microbial products

  • About 24 proteins
  • Cause vasodilation
  • Attract WBCs
  • Directly attack and destroy microbes
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16
Q

Kinin system

A

Closely related to clotting system

  • About 12 proteins that generate molecules
  • Cause vasodilation
  • Cause increased endothelial cell permeability
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17
Q

Cell derived molecular mediators

A

Most cause vasodilation

  • Vasoactive Amines
  • Cell membrane factors
  • Cytokines
  • Prostaglandins
  • Reactive oxygen compounds
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18
Q

Vasoactive amines

A

Preformed molecule stored in granulocyte lysosomes

  • Cause local capillaries to vasodilate and become “leaky”
  • Histamine: released from mast cells, basophils, platelets
  • Serotonin: released from platelets
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19
Q

Cell membrane factors

A

From phospholipids and cell membrane of injured cells

  • Paracrine factors (local hormones) : attractive WBCs and cause vasodilation
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20
Q

Cytokines

A

Paracrine factors that attract WBCs, cause vasodilation and stimulate phagocytosis

  • Chemokines: cytokines that cause chemotaxis to site of injury
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21
Q

Prostaglandins

A

Paracrine factors that enhance vasodilation and vascular permeability

  • Fever: increases body temperature
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22
Q

Reactive oxygen compounds

A
  • Nitric oxide: causes vasodilation and is bacteriocidal

- Oxygen superoxide: bacteriocidal

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23
Q

Acute inflammation causes

A
  • Microbial infection: especially bacteria
  • Physical or chemical injury: thermal or chemical burns
  • Immune injury: poison ivy or oak dermatitis
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24
Q

*** Note on most immune injuries

A

Produces chronic inflammation

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25
Q

Phases of acute inflammation

A
  • Vascular phase: occurs first

- Cellular phase: occurs second

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26
Q

Vascular phase

A
  • Vasoconstriction
  • Vasodilation
  • Increased vascular permeability
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27
Q

Vasoconstriction

A
  • Limits spread of injurious agents

- Lasts only a short time: seconds to minutes

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28
Q

Vasodilation

A
  • Results in increased blood flow in arterioles

- Creates the redness and heat of the four cardinal signs

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29
Q

Increased vascular permeability

A

Due to histamine

  • Results in protein rich fluid moving into intravascular tissue
  • Edema: swelling
  • Loss of fluid from vessels makes blood more concentrated, slowing blood flow
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30
Q

Cellular phase

A

Migration of WBCs (mainly neutrophils) to extra vascular tissue

  • Margination
  • Extravasation
  • Chemotaxis
  • Phagocytosis
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31
Q

Margination

A

Neutrophils stick to lining a blood vessel

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32
Q

Extravasation

A

Neutrophils squeeze between endothelial cells

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33
Q

Chemotaxis

A

Neutrophils move towards injured area

34
Q

Phagocytosis

A

Neutrophils eat foreign substances

  • Opsonin: complement the coats foreign material making it easier to swallow
35
Q

Clinical signs of acute inflammation

A
  • Cardinal signs: “rubor, calor, tumor, dolor”

- Inflammatory exudates

36
Q

Redness

A

Due to vasodilation “hyperemia”

37
Q

Heat

A

Due to vasodilation

38
Q

Pain

A

Due to irritation of nerve endings, increased tissue tension or prostaglandins

39
Q

Inflammatory exudated

A
  • Serous
  • Fibrinous
  • Purulant
  • Catarrhal
40
Q

Serous

A

Contains albumin, very little fibrinogen, relatively few WBCs

  • Blister following a burn
41
Q

Fibrinous

A

High protein fluid with fibrinogen, which becomes fibrin

  • Scab and skin injuries; uremic pericarditis
42
Q

Purulent

A

Numerous neutrophils and debries and fibrinous exudates “pus”
- Neutrophils give white color to puss; also called pyogenic and suppurative exudates

  • Staphylococcus aureus: prone to form puss
  • Empyema: collection of pus and body cavity (pleural empyema)
  • Abscess; bacterial pneumonia
43
Q

Catarrhal

A

Large quantities of mucus, but relatively few cells

  • Common cold
44
Q

Consequences of acute inflammation

A
  • Repair
  • Scarring
  • Abscess
  • Chronic inflammation
45
Q

Repair

A

Short term injury results and regeneration of tissue

  • Sunburn
46
Q

Scarring

A

From severe or repeated acute inflammatory episodes

  • Severe sunburn
47
Q

Abscess

A

Local accumulation of edema, necrotic debries and dead WBCs

  • Results when pace of local inflammation and liquefactive necrosis outstrips the inflammatory process to remove the material (cellulitis)
48
Q

Causes of Chronic Inflammation

A
  • Persistent infection
  • Autoimmune disease
  • Persistent exposure to injurious agents
49
Q

Persistent infection

A

Caused by microbes

  • Syphillis: treponema pallidum
  • Tuberculosis: myobacterium tuberculosis
50
Q

Autoimmune disease

A

Immune system accidently attacks self, it’s own tissues

  • All autoimmune disease is chronic
  • If you Alyssa acute inflammation (arteritis)
  • Rheumatoid arthritis: immune system attacks ones own joints
51
Q

Persistent exposure to injurious agent

A
  • Starts acute, then becomes chronic
  • Silica exposure: rock dust
  • Smoking: cigarettes
52
Q

Clinical signs of chronic inflammation

A

Less intense than acute inflammation

  • Decreased intensity
  • Chronic inflammatory cells
  • Granulomatous inflammation
53
Q

Decreased intensity

A

Less than an acute inflammation

  • Not as red, swollen, hot and tender
  • Shrunken by scar, atrophy or necrosis
54
Q

Chronic inflammatory cells

A

Mononuclear cells (misnomer: due to multinuclear appearance of neutrophilic nuclear lobes, which are technically mono nuclear too)

  • Macrophages
  • Lymphocytes
55
Q

Macrophages

A

Very important thousand and chronic inflammation

  • Derived from blood monocytes
  • Migrate to tissues and it reside for months to years
  • Known by various names in different tissues (Kupffer, microglia)
  • Phagocyte: ingest and either digest or present it to lymphocytes
56
Q

Lymphocyte

A

The principal reactive cell in chronic inflammation

  • T lymphocytes
  • B lymphocytes
57
Q

T lymphocytes

A

Originate in thymus, cellular immunity, attack directly

58
Q

B lymphocytes

A

Originate in bone marrow

  • Humeral immunity
  • Secrete anti-bodies that circulate and blood as immunoglobulin
  • When stimulated by antigens they change appearance and are known as plasma cells
59
Q

Granulomatous inflammation

A
  • Granuloma
  • Epitheloid cell
  • Giant cell
  • Tuberculosis
60
Q

Granuloma

A

Collection of chronic inflammatory cells, especially epitheloid cells or giant cells, and often surrounded by a rim of lymphocytes

61
Q

Epitheloid cells

A

Modified macrophages

  • Long oval nuclei and abundant cytoplasm
  • Not epithelial cells, but look like them
62
Q

Giant cells

A

Large cells with multiple nuclei

  • Form by the fusion of macrophages
63
Q

Tuberculosis

A

The most common cause of granulamotous inflammation

  • Other disease associated with this include: syphilis, leprosy, fungal infections, foreign body reactions, parasites
64
Q

Consequences of chronic inflammation

A
  • Resolution to a scar

- Persistent chronic inflammation

65
Q

Distant effects of inflammation

A
  • Lymphatic system

- Systematic effects

66
Q

Lymphatic system

A

One way dream from tissue to blood for inflammatory fluid, microbes and debris

  • Lymphangitis
  • Lymphadenitis
67
Q

Lymphangitis

A

Inflamed lymphatic vessels due to infection

  • Causes red streak’s up from infection site, but not dangerous as in blood poisoning
68
Q

Lymphadenitis

A

Lymph nodes draining an injured or infected site may become infected

  • Lymph nodes and large and are tender due to infection
  • Reactive hyperplasia
  • Lymphadenopathy
69
Q

Reactive hyperplasia

A

Often lymph nodes are not infected, but rather reacting to inflammatory products draining away from infection or injury

70
Q

Lymphadenopathy

A

Enlarged and tender lymph nodes irrespective (don’t know the cause) of suspected diagnosis, Biette infection, malignancy or other benign reactions

71
Q

Systematic effects of inflammation

A

Seidel cans can find their way into the blood to induce systematic effects on the:
• Brain
• Liver
• Leukocytes

72
Q

Brain

A
  • Fever:
    • body temperature regulated by hypothalamus
    • Set point change to a higher temperature
    • Increased phagocytosis and interferon production
  • Malaise, drowsiness and decreased appetite
73
Q

Liver

A

Chronic inflammation causes increased production of:
• Reactant proteins: C – reactive protein CRP – elevates with even minor inflammation; systematic
- Associated with atherosclerosis, cancer, obesity and Alzheimer’s disease
• Fibrinogen: increased fibrinogen cause RBCs to settle rapidly measured by ESR (erythrocyte sedimentation rate) ; RA – have high ESR (sed rate)

74
Q

Leukocytosis

A

Increased WBC count in peripheral blood

  • Specific type of WBC gives clues as to cause of inflammation:
    • Neutrophils: increased neutrophils, bacterial infection
    • Lymphocytosis: increased lymphocytes, viral infection
    • Eosinophils: increased eosinophils, helminth (worms) infection
75
Q

Abscess

A

Localized collection of pus

76
Q

Pustule

A

Small elevation of the skin containing pus

77
Q

Boil

A

Deep infection of S. aureus associated with hair follicles that produce pus
- Neck, axilla, buttocks, thigh, eyelid (stye) or furuncle

78
Q

Carbuncle

A

Same as boil, except coalescing infections produce drainage sinuses: usually the neck

79
Q

Pyo, py

A

Prefix meaning pus

80
Q

Ulcer

A

Open sore on the skin or mucous membranes (decubitus ulcer)

81
Q

Fistula

A

Abnormal tube or passage from a normal cavity to a free surface or another cavity

Pathology (6 decks)

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