types of inflammation

Question 1

shape of neutrophil nucleus

Answer 1

segmented

Question 2

shape of Macrophage nucleus

Answer 2

oval

Question 3

shape of lymphocyte nucleus

Answer 3

condensed and round

Question 4

Neutrophils characteristics

Answer 4

• irregular, multi-lobed nuclei
• no two look alike
• undergo lysis
• infiltrate tissue
• collect in spaces and on surfaces
• can for abscesses in serve cases by creating local necrotic pocket filled with neutrophils

Question 5

Macrophage characteristics

Answer 5

blood macrophages, tissue macrophages, macrophages in inflammation
-sub-acute, chronic inflammation
-granulomatous inflammation-> epithelioid cells and giant cells
lot os cytoplasm

Question 6

Lymphocyte characteristics

Answer 6

T cells

• very small, round nucleus
• almost no cytoplasm
• uniform
• viral illnesses and chronic immune reactions
• almost always seen with macrophages
• look alike

Question 7

Plasma cells

Answer 7

perinuclear pale area-> synthesis of antibodies

• “clock face” nucleus-> distributed chromatin
• chronic auto-immune reactions

Question 8

Eosinophil characteristics

Answer 8

• migrate to area due to specific, inflammatory chemotactic signals, especially from mast cells
• numerous eosinophils granules-> major basic proteins, degradative enzymes
• seen in areas of allergic or parasitic diseases

Question 9

Bacterial infection will have?

Answer 9

Neutrophils

Question 10

Viral infection will have?

Answer 10

Lymphocytes

Question 11

TB will have?

Answer 11

granuloma formation (epitheloid macrophages, lymphocyte)

Question 12

auto-immune reaction will have?

Answer 12

lymphocytes, plasma cells

Question 13

allergy or parasites will have?

Answer 13

mast cells and eosinophils

Question 14

evolution of inflammation: pre-acute

Answer 14

first few hours-> evidence of cell injury, necrosis, edema

Question 15

evolution of inflammation: Acute

Answer 15

12-24 hours-> neutrophils first to respond

Question 16

evolution of inflammation: subacute

Answer 16

neutrophils mixed with first monocytes

Question 17

evolution of inflammation: 48-72 hours

Answer 17

macrophages begin to predominate

Question 18

evolution of inflammation: chronic

Answer 18

> 72 hours

-macrophages and lymphocytes

Question 19

why do cell changes occur with inflammation?

Answer 19

changes in predominant cell type because change in adhesion and migration specific cell types
-specific adhesion molecules, specific cytokines, chemotactic molecules

Question 20

acute inflammation characteristics

Answer 20

first 6-48 hours
PRIMARILY neutrophils
-milder forms on injury or bacterial infections

Question 21

sub acute inflammation

Answer 21

24-72 hours

• goes from predominately neutrophils to predominately macrophages
• neutrophils are in the processes of undergoing apoptosis
• collections of macrophage occur both from emigrating monocytes and macrophages division

Question 22

chronic inflammation

Answer 22

• predominately lymphocytes, macrophages, and plasma cells
• could represent resolution phase of an acute inflammatory response
• may be weeks to years
• granulomas are a form of chronic inflammation
• chronic inflammation is often accompanied by fibrosis and scar formation

Question 23

how does inflammation differ from superficial layers to deeper layers?

Answer 23

• surfaces such as skin or mucosa-> superficial layers are subjected to repeated episodes of acute inflammation
• Deeper layers-> experience chronic inflammation (ulcers)

Question 24

serous inflammation

Answer 24

extracellular fluid associated with mild injury-> void of cellular infiltrates (not a of protein)

• fluid derived from blood serum due to increased vascular permeability
• seen in epidermis and mesothelium-> pleural, peritoneal, pericardial cavities
• examples: blisters, pericardial effusion secondary to viral myocarditis

Question 25

fibrinous inflammation

Answer 25

accumulation of fibrin -due to increase in vascular permeability sufficient to permit passage of fibrin molcules -greater vascular damage/change than that associated with serous inflammation Example: adhesion associated with surgical trauma

Question 26

how does resolution in fibrinous inflammation occur?

Answer 26

1.) lysis-> enzymatic digestion by plasmin, phagocytosis by macrphages 2.) organization-> fibrin not removed act as scaffolding and stimulus for fibroblast + blood vessel migration scarring

Question 27

what is fibrinous?

Answer 27

collection of fibrin which is formed from fibrinogen that enters the tissue space from the blood (increased vascular permeability) -Part inflammation process (hours to days)

Question 28

what is fibrosis?

Answer 28

implies multiplication of fibroblasts and laying down of new collagen fibers which form scar tissue -part of chronic inflammation or regeneration and healing (weeks to months to years)

Question 29

characteristics fibrinous

Answer 29

- fibrin from fibrinogen - originates in blood and enters into tissue due to increased vascular permeability - fine stringy fibers in a tissue space - acute inflammatory response - hours to days - usually disappears

Question 30

characteristics of fibrosis

Answer 30

new synthesis of collagen fibers from activated fibroblast - long dense pink fibers laid down in tissue - chronic inflammation or healing and regeneration - days to weeks to years - does not disappear - clue: if fibrosis is present it is chronic inflammation

Question 31

suppurative inflammation

Answer 31

accumulation of neutrophils (pus) +/- necrotic cells, fluid - usually associated with pyogenic bacterial infectious (strep, staph, also gram negatives) - abscess -> localized accumulation purulent material with liquefactive necrosis

Question 32

Lymphocytic

Answer 32

(non-suppurative) - accumulation of lymphocytes - usually chronic - characteristic of viral diseases - also immune-mediated and auto-immune diseases

Question 33

granulomatous inflammation/granuloma

Answer 33

persistent antigen (TB) or chronic inflammatory reaction (foreign body) - activated macrophages activate T-cells by synthesis of IL-1, IL-12, antigen presentation - activated T-H1 lymphocyte-> IFN-gamma-> activated macrophage-> epithelial macrophages-> multinucleated giant cells

Question 34

epithelioid macrophages

Answer 34

large activated macrophages - macrophages activated due to IFN-gamma produced by T-lymp - increased pahgocytosis, metabolism, and lysosomal enzymes - morphology: eosinophilic cytoplasm, large pale nuclei, "epithelial appearance"

Question 35

multinucleated giant cells

Answer 35

formed by fusion of epitheloid giant cells - can be very large (45-50) - up to 20 or more nuclei - periphery of cell-> Langhan's type immune type granulomas - center of cell foreign body-type-> responses to inert foreign material

Question 36

Ulcers

Answer 36

local excavation/defect on a mucosal surface produced by sloughing of necrotic (inflamed) epithelium +/- underlying tissue - most commonly-> mouth, stomach, intestine, genitourinary system - peptic ulcers-> stomach, intestine - Acute-> increased PMN's dilated/congested blood vessels at margins - chronic-> lymphocytes, macrophages, fibrous connective tissue at base

Question 37

Difference between erosion versus ulcer?

Answer 37

erosion: are superficial only (acute or subacute inflammation) ulcer: have loss of mucosal layers to muscularis (always associated with surrounding chronic inflammation and fibrosis)