D&t: Necrosis & Acute Inflammation

Front 1

Define 'pathology'

Back 1

study of structural and functional abnormalities expressed as diseases of organs and systems

Front 2

Etiological agent --> ______ --> functional consequences

Back 2

morphological changes

Front 3

What is pathogenesis?

Back 3

The mechanism of disease development, particularly over time.

Front 4

What are the morphological alterations caused by a cellular response to stress? (6)

Back 4

atrophy, hypertrophy, hyperplasia, metaplasia, dysplasia, intracellular storage

Front 5

Classic example of atrophy?

Back 5

Renal artery stenosis

Front 6

Atrophy is:

Back 6

decrease in cell size and function

Front 7

Hypertrophy:

Back 7

increase in cell size accompanied by augmented functional capacity

Front 8

Hyperplasia? Often concurrent w/ ?

Back 8

increase in the number of cells in an organ or tissue

Hypertrophy

Front 9

Metaplasia is:

Back 9

a conversion of one differentiated cell type to another

Front 10

Replacement of glandular epithelium by squamous is an example of what?

Back 10

metaplasia

Front 11

Is Metaplasia reversible?

Back 11

Usually if the stimulus is removed in time.

Front 12

What is Dysplasia? Often associated with what? Dysplasia Reversible?

Back 12

an alteration in size shape, and organization of cellular components of tissue.

squamous metaplasia

Yes, in certain instances.

Front 13

What is hemochromatosis?

Back 13

iron deposition in liver

Front 14

Irreversible cell injury --> ? Why?

Back 14

Death b/c exceeds cell's ability to adapt

Front 15

What is Necrosis?

Back 15

Structural manifestations of cell death in a living tissue or organism.

Front 16

Types of Necrosis (5)

Back 16

Coagulative, Liquefactive, Enzymic fat, Caseous, Fibrinoid

Front 17

What is a denaturation of proteins with preservation of cell outline and nuclear dissolution, charac of hypoxic cell death (excl brain).

Back 17

coag. necrosis

Front 18

What is cellular digestion into a liquid viscous mass, characteristic of focal bacterial or occasionally fungal infections

Back 18

liquefactive necrosis

Front 19

what is descriptive of focal areas of fat destruction, frequently associated with release of activated pancreatic enzymes into pancreatic tissues during acute pancreatitis?

Back 19

Fat necrosis

Front 20

a distinctive form of coagulative necrosis often associated with tuberculous infection and granulomatous inflammation.

Back 20

Caseous Necrosis

Front 21

an alteration of injured blood vessels with insudation and accumulation of plasma proteins causing the vessel wall to stain intensely with eosin.

Back 21

Fibrinoid necrosis

Front 22

Hyaline appearance of vessel walls is characteristic of what morphological type of necrosis?

Back 22

Fibrionoid necrosis

Front 23

Apoptosis is defined as:

Back 23

Programmed cell dead

Front 24

Histological features of apoptosis?

Back 24

shrinkage blebbing, nuclear fragmentation, cell fragmentation with formation of membrane-bound APOPTOTIC Bodies.

Front 25

How is apoptosis resolved? Involve inflammation?

Back 25

Phagocytic/macrophages... No, b/c it's a normal process.

Front 26

Acute inflammation is characterized by...

Back 26

increased blood flow & vessel permeability, edema, and effusion

Front 27

Edema is...

Back 27

accumulation of fluid w/i extravascular compt & interstitium

Front 28

Effusion is...

Back 28

excess fluid w/i body cavity

Front 29

What are the etiologies of increased vascular permeability in acute inflammation? (3) What are the speeds of these effects? Which is the most common?

Back 29

cells contract in response to chem. inflamm. mediators (fast)
- endothelial contraction results in transient gaps b/t cells and increased permeability to plasma proteins
**MOST COMMON**

Direct injury to endothelial cells (hours to days)

Leukocytes-dependent injury of endothelial cells (late response, long-lived)

Front 30

Transudate is...

Back 30

... edema fluid w/ LOW protein count

Front 31

Exudate is...

Back 31

... edema fluid w/ HIGH protein count

Front 32

_____ vasoactive mediators are derived from interrelated major enzyme cascades composed of series of sequentially activated proteases.

Back 32

Plasma-derived

Front 33

C4a, C3a, C5a are vasoactive mediators called _______ that enhance ________?

Back 33

anaphylatoxins, vascular permeability

Front 34

what are cell-derived vasoactive mediators derived from? Examples?

Back 34

Arachidonic acid; prostaglandins, thromboxanes, leukotrienes

Front 35

What pathway does asprin block? Prevents formation of what?

Back 35

Cyclooxygenase Pathway; prostaglandins & thromboxanes

Front 36

______ is the reaction of living tissue and it's microcirculation to pathogenic insult.

Back 36

Inflammation

Front 37

Are acute and chronic inflammation mutually exclusive?

Back 37

No.

Front 38

_____ cells predominate in Acute inflammation.

Back 38

neutrophils (PMNs)

Front 39

______ cell types predominate in Chronic Inflammation

Back 39

mononuclear inflammatory cells, lymphocyte, plasma cell, & monocyte

Front 40

Foreign body intrusion is associated with which type of inflammation? Tissue necrosis? Immune-mediated hypersensitivity? Autoimmune disorders?

Back 40

Chronic, acute, acute,chronic

Front 41

What are the outcomes of inflammation? (4)

Back 41

Resolution, Abscess, Persistent inflammation, fibrosis

Front 42

Phagocytosis and intracellular killing is a major manifestation of which type of inflammation?

Back 42

Acute

Front 43

Inflammatory edema in affected tissues is associated w/ which type of inflammation?

Back 43

acute

Front 44

Vascular dilation, increased flow, and rapid vascular response with altered microvasculature is associated with which which type of inflammation?

Back 44

Acute

Front 45

PMN margination, adhesion, emigration & chemotaxis are associated with which inflammation?

Back 45

Acute

Front 46

Put the following in one category above: Histamine, Chemokines, Formylated peptides, Anaphylatoxins, C5a, Bradykinin, Serotonin, Histamine, NO, Platet activating factor, Leukotrienes/Prostaglandins, Lipoxygenase products (LTB4)

Back 46

see the picture, 'foo

Front 47

What is the difference between fibrous and fibrinous?

Back 47

fibrous implied collagen involvement; fibrinous involves fibrin - a clotting factor that shows up in exudate along with PMNs --> fibropurulent exudate

Front 48

What is Hageman factor? It is plasma derived or cell-derived? What general things does it do/begin once activated? (4)

Back 48

f.XII re: clotting
Plasma derived.
(1) Fibrinolysis (2) complement/anaphylatoxin (3) kinin generation (4) co-ag system

Front 49

Place the following into either the "plasma-derived" category, or the "cell-derived" category:
Endothelium (NO, Platelet activating factors, prostaglandins)
Inflammatory cells
platelets
complement system activation (C3a, C5a)
mast cell/basophil degranulation
hageman factor actv.

Back 49

only plasma are f.XII and Complement cascade (C3a, C5a)

Front 50

What is opsonization? What are opsonins?

Back 50

the coating of pathogen w/ molecule that enhances phagocytosis, in this case by leukocytes.
C3b molecules

Front 51

What is the mediator for the classical pathway of the complement sys? lectin binding pathway? Alternative pathway?

Back 51

C1q

Mannose binding protein (MBP)

C3

Front 52

What is the most important role of platelet activating factor?

Back 52

stimulates synthesis of arachidonic acid derivatives.

Front 53

Initial neutrophil recruitment is dependent on the chemotaxins ___ and ____.

Prolonged recruitment dependent on...

Back 53

C5a and LTB4

Chemotactic cytokines.