Path And Pharm 2

Front 1

Inflammation defined

Back 1

automatic responses to all forms of injury

protective response to foreign invasion and cell injury

Front 2

Inflammation is beneficial in the sense that it _____.
Inflammation can be harmful in the sense that it _____.

Back 2

prevents or limits disease
can cause cell injury/disease

Front 3

other names for white blood cells

Back 3

inflammatory cells
leukocytes
immune cells

Front 4

Name the 4 different types of leukocytes

Back 4

Neutrophils (PMN)
Macrophages
Lymphocytes
Mast Cells

Front 5

Many-shaped nucleus...most common type of white blood cell

Back 5

Neutrophils

Front 6

Round dark nucleus; found in lymph, blood, and other cells

Back 6

lymphocyte

Front 7

Lots of blue granules in cytoplasm

Back 7

mast cells

Front 8

typical onset & resolution time for acute inflammation

Back 8

onset: minutes to hours
resolution: hours to days

Front 9

Acute inflammation etiologies

Back 9

infectious agents
physical agents
necrosis
(immune)

Front 10

Acute inflammation S/S

Back 10

Redness pain heat swelling

Front 11

Body's response in acute inflammation

Back 11

acute inflammation

Front 12

Outcomes of acute inflammation

Back 12

Resolves to normal
Abcess
Chronic Inflammation
Repair

Front 13

_____ is what acute inflammation is best designed to deal with

Back 13

Bacteria

Front 14

What phase includes the etiology and the pathologic response? What phase includes the S/S and the outcomes?

Back 14

Vascular Phase
Cellular Phase

Front 15

Phase 2
Chemical mediators that promote vasodilation

S/S that result

Back 15

histamines, prostaglandins, bradykinin

Redness & Heat

Front 16

Phase 3
Chemical mediators that promote an increase in permeability

S/S that result

Back 16

Histamines, Leukotrienes, & Bradykinin

Edema/Pain

Front 17

Plasma (water & proteins) seeping out of the blood vessels during phase 3... a process called

Back 17

Transuation

Front 18

Chemical mediators that promote the migration of PMNs from the blood vessel.

This process is called

Back 18

Leukotrienes

chemotaxis

Front 19

Lots of PMNs together

Back 19

purulent exudate/pus

Front 20

Phase 5:
There is now plasma & PMNs outside the blood vessel, but we also need more macrophages. Name the 2 methods

Back 20

Macrophages go through mitosis
Macrophages summon more macrophages via chemotaxis

Front 21

Name the 2 phagocytic cells

Back 21

Macrophages & PMNs

Front 22

Besides phagocytic cells, what's the other way to deal with etiologies in acute inflammation?

Resulting S/S

Back 22

PMNs releasing lytic enzymes.

Collateral damage to surrounding area (pain)

Front 23

Final step in acute inflammation

Back 23

Macrophages cleaning up all the dead cells

Front 24

Backup plan for acute inflammation

Back 24

chronic inflammation

Front 25

Purpose of plasma coming out of the blood vessel

Back 25

fibrim is one of the blood proteins released. Macrophages & PMNs cling to this

Front 26

Chemical mediators are synthesized...

Back 26

in a variety of cells (leukocytes, blood vessels, liver, etc.)

Front 27

Some chemical mediators act locally (examples include...)
Some chemical mediators act systemically (examples include...)

Back 27

redness, pain, heat, swelling
fever, lethargy, loss of appetite

Front 28

Histamines: Function & Medication

Back 28

vasodilation; inc. permeability

antihistamines

Front 29

Bradykinin: Function & Medication

Back 29

Pain; vasodilation; inc. permeability

Anti-Histamines

Front 30

The cyclooxygenase pathway creates

Back 30

Prostglandins

Front 31

Another name for chemical mediators

Back 31

cytokines

Front 32

Prostaglandins function & medication

Back 32

Pain, fever, vasodilation

Glucocorticoids

Front 33

Leukotrienes Function & Medication

Back 33

Increase in permeability; chemotaxis

Glucocorticoids

Front 34

Reactive Oxygen Species funciton

Back 34

Kills microbes, damages neighborhood

Front 35

Interleukin 1 (IL 1)
TNF

These are involved in _____. Functions include...

Back 35

Chronic Inflammation
Fever, lethargy, loss of appetite

Front 36

Another name for glucocortacoids

Back 36

corticosteroid

Front 37

3 Main medications used to treat chemical mediators

Back 37

NSAIDS
Glucocorticoids
Antihistamines

Front 38

The chemical mediators cause the _____, which make the patient _____. Therefore, medicines are aimed at _____ of the chemical signals

Back 38

S/S
uncomfortable
decreasing production

Front 39

COX = _____

Back 39

cyclooxygenase enzyme

Front 40

Cyclooxygenase Metabolic Pathway 1 for Prostaglandin (PG) synthesis

Back 40

Precursor PG in healthy cells

COX1

Beneficial PGs (some of which help protect the stomach lining)

Front 41

Cyclooxygenase Metabolic Pathway for Prostaglandin (PG) synthesis 2

Back 41

Precursor PG in injured and inflammatory cells

COX 2

Inflammatory PGs
(Causes pain, fever, vasodilation)

Front 42

NSAIDS stands for

Back 42

Non-steroidal anti-inflammatory drugs

Front 43

4 Effects of NSAIDS

Back 43

Anti-Inflammatory
Anti-pyretic (anti-fever)
Analgesia (anti-pain)
Anti-coagulation (decreases clotting)

Front 44

NSAIDS drugs do not include

Back 44

tylanol

Front 45

Non-selective Cox inhibitors
These are _____ drugs.

Back 45

Aspirin
Ibuprofen
Indomethacin
Naproxen

NSAIDS

Front 46

Bextra & Vioxx (selective COS-2) inhibitors) were taken off the market due to _____

Back 46

thrombosis

Front 47

Selective COX-2 Inhibitors

These are _____

Back 47

Celebrex

NSAIDS

Front 48

NSAIDS can also inhibit the production of _____ by inhibiting _____. (_____ are the other PG inhibitor)

Back 48

Prostaglandins
COX (the enzymes)
Glucocorticoids

Front 49

Nonselective COX inhibitors inhibit _____. Thus, you don't get _____. You should take these NSAIDS with _____. Chronic usage probably results in ______ unless you take antiacids

Back 49

both COX-1 & COX-2.
the bad inflammatory prostaglandins nor the good stomach lining.
food
ulcers

Front 50

Side effect of both the selective and non-selective COX inhibitor

Back 50

Slows bone healing

Front 51

Side effects of non-selective COX inhibitors

Back 51

stomach lining damage

Front 52

Side effective of selective COX-2 Inhibitors

Back 52

Promotes thrombosis (blood clotting...stroke/myocardial infarction)

Front 53

How do we diagnose acute inflammation? (consider superficial & deep)

Back 53

Superficially, S/S = redness, pain, heat, & swelling.

Deep, we use diagnostic tests to check for PMN
Complete Blood Count w/ Differential

Front 54

Lots of PMNs in blood. What's the technical terms?

Back 54

Leukocytosis (a lot of white) = neutrophilia