Pathology Inflammation

Front 1

What are two goals of inflammation?

Back 1

Kil/Neutralize/Quarantine Damaging factors & Increase blood flow (call firemen in)

Front 2

Can you see inflammation in the dead?

Back 2

No.

Front 3

Inflammation is ____ for healing & repair.

Back 3

necessary

Front 4

Inflammation is a specific response to ____ cuasative agents

Back 4

non-specific

Front 5

What is the first "fireman" to arrive at the scene?

Back 5

PMNs

Front 6

What is the typical lifespan for a PMN

Back 6

8.2 hours

Front 7

Acute inflammation involves ____.

Back 7

PMNs & EMNs also

Front 8

Chronic inflammation involves ____

Back 8

Lymphocytes & Marcophages

Front 9

List 4 mediators of inflammation:

Back 9

Histamine, Heparin, Bradykinin, & Prostaglandin

Front 10

Give the sequence of inflammation (10 steps)

Back 10

1. Vasodilation, 2. Increased Vasclar Permeability, 3. Stagnation of Blood Flow, 4. Margination, 5. Rolling, 6. Adhesion, 7. Transmigration (diapedesis), 8. Chemotaxis, 9. Phagocytosis, 10. Sequelae (after effects: innocent bystanders, etc.)

Front 11

These three stages of inflammation are Vascular Changes:

Back 11

Vasodilation, Increased Vascular Permeability, & Stagnation of Blood flow

Front 12

The stages from ____ to ____ are Cellular Level stages of inflammation:

Back 12

(4) Margination to (10) Sequelae

Front 13

Define "Transudate"

Back 13

Fluid discharge [sudare = "to sweat"]

Front 14

What's the specific gravity of blood plasma leaking through pores?

Back 14

1.105 (water with a few protiens in it).

Front 15

The proteins on endothelial cells responsible for allowing "rolling" are:

Back 15

"Selectin Proteins"

Front 16

The proteins on endothelial cells responsible for allowing "adhesion" are:

Back 16

"Integrin Proteins"

Front 17

Selectin proteins are present due to:

Back 17

Histamine

Front 18

Integrin proteins are present due to:

Back 18

IL-1, TNF

Front 19

The proteins aiding in transmigration are:

Back 19

"PECAM Proteins"

Front 20

Chemotaxis is due to:

Back 20

C5a, C3a, LBT4, and toxins

Front 21

Phagocytosis is mediated by:

Back 21

C3b, IgM, & IgG

Front 22

Define Sequelae:

Back 22

The "sequel:" Events happening after an inflammatory response (Innocent bystander death, & healing).

Front 23

Arachidonic Acid aka

Back 23

Eicosanoids

Front 24

What are two Eicosanoid Pathway Types?

Back 24

LOX Pathways & COX Pathways

Front 25

List 5 degranulation products:

Back 25

Substnace P, Histamine, Heparin, ECF, PAF.

Front 26

Which degranulation product appears first: histamine or PGD2?

Back 26

Histamine release from stored vesicles. PGD2 must be synthesized.

Front 27

What cells are responsible for the vascular chnages in inflammation:

Back 27

Mast cells & Basophils

Front 28

Define "Exudate"

Back 28

Leakage of cellular material out of the lumen (present in stronger inflammatory responses)

Front 29

Mild inflammation shows

Back 29

Transudate

Front 30

Severe inflammation shows:

Back 30

Exudate

Front 31

Purulent exudate is associated with what type of necrosis?

Back 31

Liquefactive necrosis

Front 32

Purulent exudate in the anterior chamber is called:

Back 32

Hypopyon, causing Uveitis.

Front 33

List 3 types of Exudate Acute Inflammation:

Back 33

1. Serous, 2. Fibrinous, 3. Purulent

Front 34

List 3 lesions associated with acute inflammation:

Back 34

1. Abscess, 2. Cellulitis, 3. Ulcer

Front 35

What are the major etiologies underlying ulceration?

Back 35

Ischemia, Toxins, & Trauma

Front 36

What enzymes do glucocorticoids inhibit?

Back 36

Phospholipases

Front 37

What enzmes are affected by COX inhibitors?

Back 37

Cylcooxygenases. (NSAIDs affect them too)

Front 38

What prostaglandin cuases fever?

Back 38

PGE2

Front 39

Name 5 ways to treat asthma:

Back 39

1. H1 blocker (Benedryl), 2. Mast cell stabilizer (Cromolyn), 3. B2 agonist (Foravil), 4. Leukotriene antagonist (Singulair), Steroids (Flovent)

Front 40

What pathways does Aspirin inhibit?

Back 40

COX-1 & COX-2

Front 41

What does a COX-1 inhibitor affect?

Back 41

TXA2

Front 42

What do COX-2 inhibitors affect?

Back 42

PGI2 and PGD2/PGE2/PGF2

Front 43

What is the only way to inhibit the LOX pathway?

Back 43

Use steroids!

Front 44

Name things involved with the LOX pathway:

Back 44

LTB4 → chemotaxis (* inflammation), LTC4/LTD4/LTE4 (aka SRS-A) (* inflammation), Lipoxin → endogenous antagonist to LTB4/SRS-A

Front 45

Give 3 IL-1/TNF activated Marophage Local effects:

Back 45

Activate WBCs, Produce integrins, increase fibroblast activity (produce collagen for repair)

Front 46

List 6 systemic effects of Macrophage activation:

Back 46

Fever, Malaise (Punk), Anorexia (appetite loss), Cachexia (weakness), Increased acute phase ptns., Leukopoiesis.

Front 47

What does DIC stand for?

Back 47

Disseminated Intravascular Coagulation (a big clot usually causing death)

Front 48

What form of inflammation is Bullous Pemphigoid?

Back 48

Acute Serous Inflammation

Hint 48

None

Front 49

Pseudomembrane is found in what manner of inflammation?

Back 49

Acute Fibrinous Inflammation

Front 50

Purulent (aka ____) Inflammation involves what kind of enzymes?

Back 50

Purulent (aka Suppurative) Inflammation involves pyogenic enzymes (c.f. pyrogenic)

Front 51

I say "bread and butter" inflammation, you say:

Back 51

Fibrinous pseudomembrane.

Front 52

Pyogenic enzymes are around. Etiology? "Think ____"

Back 52

"Think Microbes" (e.g. Staph Aureus, Streptococcus, Gonococcus, etc.)

Front 53

Purulent exudate aka ____?

Back 53

Suppurative exudate

Front 54

Where are abscesses commonly discovered?

Back 54

In the tonsils.

Front 55

I say "bread and butter" inflammation, you say:

Back 55

Fibrinous pseudomembrane.

Front 56

Pyogenic enzymes are around. Etiology? "Think ____"

Back 56

"Think Microbes" (e.g. Staph Aureus, Streptococcus, Gonococcus, etc.)

Front 57

Purulent exudate aka ____?

Back 57

Suppurative exudate

Front 58

Where are abscesses commonly discovered?

Back 58

In the tonsils.

Front 59

What is one thing that will you see in Chronic inflammation that you won't find (as much) in Acute inflammation?

Back 59

Lymphadenopathy

Front 60

Name 4 common etiologies associated with Chronic inflammation:

Back 60

Intracelluar inflection (Virus, things escaping phagosomes), Persistent Pathogens (TB, syphilis, Fungi.), Prolonged exposure (coal, tattoo, autoimmune), Foreign Bodies (Glass, Bullets, sutures, etc.)

Front 61

List 3 Persistent Pathogen Types:

Back 61

TB, Syphilis, Fungi

Front 62

Autoimmune disorders can be an etiology for ____ inflammation.

Back 62

Chronic Inflammation.

Front 63

Give some examples of Foreign Bodies, please.

Back 63

Suture from surgery, Glass, Bullets, Splinters, etc.

Front 64

What does the phrase "cellular involvement in chronic inflammation with macrophages" remind you of?

Back 64

Epitheliod Histocytes

Front 65

Name 3 cellular aspects involved in Chronic Inflammation:

Back 65

Macrophages, Lymphocytes, Eosinophils

Front 66

What is in the center of a granuloma?

Back 66

The causative agent & some necrosis

Front 67

What's the inner layer of a granuloma made of?

Back 67

Activated Macrophages

Front 68

What's the second layer of a granuloma made of?

Back 68

Multinucleated Giant Cells

Front 69

What is the outer layer of a granuloma made of?

Back 69

Fibroblasts with Collagen

Front 70

What substances can be found inside the first layer of a granuloma?

Back 70

Lysozyme, ROS, Proteases, FGF (Fibroblast Growth Factor, a cytokine), Frustrated Macrophages.

Front 71

What's the #1 cause of death worldwide (not in the USA though)?

Back 71

TB.

Front 72

Give two characteristics of Dormant TB:

Back 72

Inside Macrophages & Contagious

Front 73

What two signs will be seen in the lungs with TB?

Back 73

Cavitation, & Granulomas (caseating necrosis)

Front 74

Granulomas require a lot of oxygen, so in the area one will commonly find:

Back 74

Angiogenesis