Pathology: Test 1: 4/5. Inflammation

Front 1

1) Describe the general “goals” of the process of inflammation

Back 1

Respond to injurious insult
Eliminate “initiator” (cause)
Contain
Remove injured cells / tissues

Allow for repair / restoration
of injured tissues
Stop the inflammatory process

Front 2

2) List six (6) common initiators of the inflammatory process

Back 2

Infections: organisms/agents, toxins --Part of innate immunity
Trauma
Physical or chemical agents
Tissue necrosis
Foreign bodies
Immune reactions: hypersensitivity

Front 3

3) Describe the five (5) cardinal signs (historical perspective) of inflammation

Back 3

Calor – heat
Rubor – redness
Tumor – swelling
Dolor – pain

Functio laesa – loss of function

Front 4

4) Describe the four (4) general components of the inflammatory process

Back 4

a) Vascular: deliver components of inflammatory process to site if injury
i) Hemodynamics & vascular permeability
b) Activation of chemical mediators
i) Plasma-derived, cell-derived, ECM
c) Migration and activation of WBCs
d) Termination / resolution

Front 5

5) Acute vs Chronic: onset

Back 5

a) Acute: rapid (sec/min)
b) Chronic: slower

Front 6

6) Acute vs Chronic: duration

Back 6

a) A: short (min/days)
b) C: long, sustained

Front 7

7) Acute vs Chronic: cell type

Back 7

a) A: PMN (neutraphil) primary cell type
b) C: lymphocytes, macrophage, plasma cell

Front 8

8) Acute vs Chronic: sequential or not?

Back 8

a) A: sequential- fluid, cells, destruction, resolution
b) C: not sequential

Front 9

9) Acute vs Chronic: Granulation?

Back 9

a) A: no
b) C: yes

Front 10

10) Acute vs Chronic: tissue damage/loss of function?

Back 10

a) A: no
b) C: yes

Front 11

11) What are the 3 components of inflammation

Back 11

a) Vasculature: Fluid, Chemicals,Cells
b) Connective tissue: Matrix, Cells,
c) Parenchyma

Front 12

13) After vasoconstriction occurs in response to inflammation, what happens to blood vessels? What do you see on a patient? What net effect does this have (leading to pathology)?

Back 12

a) Vasodilation
b) See redness and heat
c) Net effect: increase hydrostatic pressure --> increased interstitial fluid (edema)

Front 13

12) What is the first vascular response to inflammation?

Back 13

a) Vasoconstriction
i) To limit blood loss

Front 14

14) In the inflammatory response what happens to the vascular structure?

Back 14

a) It is altered
i) Contraction of endothelial cells --> increased vascular permeability --> increased interstitial fluid and cells from vessels

i) Contraction makes the cells further apart from each other, so stuff can leak

Front 15

what is transudate edema?
is it inflammatory?
Protein content low or high?
what type of fluid?

Back 15

-increased hydrostatic pressure or decreased plasma oncotic pressure
-Predominantly plasma fluid
-Low protein content (low specific gravity, sg <1.015)

NOT inflammatory

Front 16

what is exudate edema?
is it inflammatory?
protein content?

Back 16

increased vascular permeability
Higher protein content (specific gravity)
Contains inflammatory cells (WBCs) in variable numbers


YES! it is inflammatory

Front 17

edema term Effusion

Back 17

excess fluid in body cavities
Peritoneal, pericardial, pleural

Front 18

edema term Serous

Back 18

yellow, straw-like color, few cells

Front 19

edema term Serosanguinous

Back 19

RBC’s (red tinge)

Front 20

edema term Fibrinous

Back 20

large amounts of fibrin due to activation of coagulation cascade

Front 21

edema term Purulent

Back 21

large numbers of PMNs (neutraphil)

Front 22

edema term Suppurative inflammation

Back 22

purulent exudate with large amount of pus (liquefactive necrosis)

Front 23

17) List the major chemical mediators of involved in inflammation, and identify which are plasma derived vs. cell-derived

Back 23

a) Plasma: Complement system and Factor XII activation
b) Cell: either newly synthesized or preformed (prostaglandins, luekotrienes, histamine, 5HT, etc.)

Front 24

18) What is the major source of plasma derived proteins?

Back 24

a) Liver

Front 25

19) What are the 2 (or 3) pathways of the complement system? Is this a plasma or cell derived response?

Back 25

a) Plasma!
b) Classical: Ab-Ag complexes
c) Alternative: triggered by complex molecules (bacterial lipospolysaccharide)
d) Lectin

Front 26

20) What is the job of the complement system? (3)

Back 26

a) Phagocytosis / Destruction
i) Opsonization (coating of bacteria for phagocytosis)
ii) MAC: membrane attack complex

b) Vascular effects
i) Anaphylatoxins: increased vascular permeability / vasodilatation

c) WBC adhesion, activation, chemotaxis

Front 27

In the complement system, what are the 2 division of the phagocytotic response?

Back 27

i) Opsonization (coating of bacteria for phagocytosis)
ii) MAC: membrane attack complex

Front 28

21) Other than the complementation system, what works to cause inflammation that is plasma mediated?

Back 28

Coagulation & Kinin Systems
Hageman Factor (clotting factor XII)

Front 29

22) What does Hageman Factor (clotting factor XII) initiate? (4 systems in inflammatory process)

Back 29

Kinin system: vasoactive
Coagulation: more on this later
Fibrinolytic system: more on this later
Complement system

Front 30

23) what are the 2 vasoactive amines (cell derived inflammatory response)? how are each individually released?

Back 30

a) Histamine & serotonin: released from storage vacuoles within mast cells (histamine) & platelets (5-HT)

Front 31

24) Arachidonic acid (AA) metabolites is cell derived or plasma? How is it generated? Releases?

Back 31

a) cell derived
b) Generated from cell membrane phospholipids
c) Prostaglandins, Leukotrienes, and Lipoxins

Front 32

25) Is Platelet activating factor (PAF) cell derived or plasma? How is it generated?

Back 32

a) Cell
b) Generated from membrane phospholipids
c) Broad-ranging effects of inflammation

Front 33

26) Cytokines are cell or plasma derived chemical mediators? 2 examples?

Back 33

a) Cell
b) Include: Tumor necrosis factor (TNF) and Interleukins (IL)

Front 34

27) Nitric Oxide (NO), cell or plasma derived? Job?

Back 34

a) Cell, potent vasodilator

Front 35

28) What do TNF and IL do? (remember what are they?)

Back 35

a) They are cell derived chemical mediators: more specifically Cytokines
b) Endothelial effects
c) Fibroblast effects
d) Leukocyte effects
e) Acute-phase reactions

Front 36

29) What are the 3 cells of acute inflammation? Which is major

Back 36

a) Neutrophils (PMN)-MAJOR
b) Eosinophils
c) Mast cells

Front 37

30) What are the 5 cells of chronic inflammation? 3 major?

Back 37

a) Lymphocytes -MAJOR
b) Macrophages (Mf) - MAJOR
c) Plasma cells- MAJOR
d) Eosinophils; mast cells
e) Fibroblasts: prominent fibrosis

Front 38

31) What are the 3 outcomes of inflammation?

Back 38

Resolution, healing by fibrosis, or ongoing chronic inflammation

Front 39

32) 3 causes of chronic inflammation? Example of each

Back 39

a) Persistent infection or injurious stimulus: Relatively low virulence but resistant to destruction
ii) E.g., tuberculosis, sutures


b) Prolonged exposure to injurious stimulus
i) Exogenous (e.g., silicosis)
ii) Endogenous (e.g., atherosclerosis)

c) Autoimmunity
i) E.g., rheumatoid arthritis, Hashimotos thyroiditis, lupus

Front 40

33) 3 processes of chronic inflammation and typical result?

Back 40

a) Tissue infiltration by mononuclear cells
i) Macrophages, lymphocytes, plasma cells
(1) Histiocytes: longstanding resident Mf in tissues
b) Tissue destruction
c) Tissue repair
i) Angiogenesis
ii) Fibrosis
d) Typically results in loss of function!

Front 41

34) What is a histiocyte?

Back 41

a) Longstanding resident Monocyte in tissue

Front 42

35) What characterizes granulomatous inflammation? Is this chronic or acute?

Back 42

a) CHRONIC
b) Aggregates of activated macrophages assume an epithelioid appearance
c) Some of the Mf coalesce to form a syncytium: multinucleated giant cells

Front 43

36) If you have Necrosis with granuloma what do you call it? What if there is no necrosis?

Back 43

a) With necrosis: caseating granuloma
b) No necrosis: noncaeseating granuloma

Front 44

37) What is the job of a granuloma?

Back 44

a) Wall off the foreign substance
b) Can’t get rid of it, so just tries to protect the rest of the body from it

Front 45

BE ABLE TO RECOGNIZE STEATOSIS IN THE LIVER AND CASEATING GRANULOMA

Back 45

if you were given a picture you better know it

If anyone wants to pitch in money I will buy an account so I can make picture flashcards...until then..grab your notes!

Front 46

38) when you see Caseating granuloma what should you think?

Back 46

TB!

Front 47

What is the cause of cat-scratch fever? tissue rxn?
THIS WILL BE ON THE TEST

Back 47

Gram-negative bacillus

tissue reaction: rounded or stellate granuloma containing central granular debris and recognizable neutrophils: giant cells uncommon

Front 48

Is sarcoidosis caseating or non caseating?

Where does it occur?

Back 48

NONcaseating granuloma with abundant activated macrophages

lung and lymph nodes

Front 49

40) Identify some of the major systemic signs of inflammation (3)

Back 49

--Fever
--Elevated plasma "acute phase reactants"
--Leukocytosis

Front 50

What are the 2 types of pyrogens associated with fever? examples?

Back 50

exogenous (bacteria)
endogenous (ILs, TNF)

Front 51

Increased PMN is known as what? caused by what? what is meant by left shift?

Back 51

granulocytosis: bacterial; left shift (when body makes white blood cells, it starts off producing immature ones that mature, when they go into systemic flow; when you have an increased need you start to pump out more neutraphils, but they instead are released early and are immature)

Front 52

Increased lymphocytes is known as? what is caused by?

Back 52

lymphocytosis; viral

Front 53

1. If you have a purulent drainage, what cell type should you be thinking? ***

Back 53

a. Neutrophils

Front 54

2. If you see opsinization what should you be thinking as far as mediators of inflammation? **

Back 54

a. Complement protein

Front 55

what do you find in granulation tissue?**

Back 55

Fibroblasts and endothelial cells