Pathology - Inflammation Ii

Front 1

Under normal physiologic conditions, how does hydrostatic press within vessels relate to colloid osmotic press?

Back 1

They approx balance out. Result = fluid retained in intravascular space (within vessels).

Front 2

Under what 3 conditions can increased V of fluid pass across the vascular wall?

Back 2

1. Increased hydrostatic press due to hypertension and/or Na+ retention (hypernatremia).

2. Decreased colloid osmotic press (ie decreased plasma protein conc, esp albumin).

3. Lymphatic and/or venous obstruction.

Front 3

The leakage of what fluid (transudate or exudate) is consistent with edema?

Back 3

Transudate (low cell count, few proteins).

Front 4

In acute inflammation, there is a net outflow of fluid from _____, ______, and _____ into extracellular tiss that overwhelms that capacity for resorption by postcapillary venules and lymphatics.

Back 4

Arterioles, capillaries, venules.

Front 5

The fluid that forms in extracellular tiss in inflammation is typically an _____. What characterizes this type of fluid?

Back 5

Exudate.

Increased amount of proteins and cell #s compared to transudate.

Front 6

For transudative effusion:

-appearance?

-relative amount of total protein?

-relative cell count?

Back 6

Clear, light yellow.

Low.

Low.

Front 7

For modified transudative effusion:

-appearance?

-relative amount of total protein?

-relative cell count?

-often seen in what common disease in cats?

Back 7

Clear, light yellow.

High.

Low.

FIP yields modified transudate that is high proteins but poorly cellular.

Front 8

For exudative effusion:

-appearance?

-relative amount of total protein?

-relative cell count?

Back 8

Turbid, yellow.

High.

High.

Front 9

What are the 4 main outcomes of the acute inflammatory response?

Back 9

1. Resolution

2. Healing by fibrosis

3. Abscess formation

4. Progression to chronic inflammation (often involves macrophagic granulomas).

Front 10

What is a hallmark of chronic inflammation?

Back 10

Fibrosis

Front 11

What is chronic inflammation?

Back 11

Inflammation of prolonged duration: wks, months, yrs.

Front 12

What are 3 instances when chronic inflammation can occur?

Back 12

1. Acute inflammatory response fails to eliminate initial cause.

2. Repeated episodes of acute inflammation.

3. Unique characteristics/virulent factors in inciting substance/microbe, eg mycobacterium in Johne's, fungal bacteria, bacteria hiding in urinary stones.

Front 13

What are some examples of conditions associated w chronic inflammation in animals?

Back 13

-various bacterial, fungal, and protozoan infectious agents

-autoimmune diseases, eg rheumatoid arthritis, allergic dermatitis

-foreign bodies

-lick granuloma

-EOSINOPHILIC GRANULOMAS OF CATS!!!!

Front 14

Describe eosinophilic granuloma.

Back 14

AKA rodent ulcers, linear granulomas.

Thick plaques, fibrous tiss along lips. Ropey tissue along back of legs.

Filled w macs.

Front 15

Eosinophilic granulomas and other conditions associated w chronic inflammation cause the inflammation via what 4 mechanisms?

Back 15

-persistent +/- resistant infection

-isolation

-unresponsiveness

-autoimmunity

Front 16

Chronic inflammation is maintained by ______.

Back 16

inflammatory mediators

Front 17

In chronic inflammation, inflammatory mediators lead to what 5 things?

Back 17

1. Infiltration and activation of lymphocytes, macs, plasma cells, and MNGCs.

2. Necrosis

3. Fibroplasia (proliferation of fibroblasts and deposition of collagen)

4. Granulation tiss formation (angiogenesis and neovascularization)

5. Re-epithelialization and tiss repair (initiation of wound healing)

Front 18

True or false?

An abscess may form where acute inflammation fails to eliminate the inciting cause.

Back 18

True

Front 19

An abscess is a collection of which cells?

Back 19

Predominantly neuts.

Also cell debris, macs, fibroblasts, and a variable # of lymphocytes (pus).

Front 20

Describe the role of fibroblasts in abscess formation

Back 20

Produce collagen, which forms a thin wall that can become a thicker fibrous capsule --> wall off exudate.

Front 21

Granulomatous inflammation is caused by what?

Back 21

Persistence of inciting stimulus for inflammation.

Front 22

True or false?

Granulomatous inflammation typically causes minor tissue injury.

Back 22

False. It causes extensive tiss injury and necrosis.

Front 23

In granulomatous inflammation there is a shift in inflammatory cells from neuts to what?

Back 23

Lymphocytes, macs, and MNGCs.

Front 24

When does a granuloma form?

Back 24

When cells in granulomatous inflammation organize themselves into a distinct mass/nodule.

Front 25

What are the cellular components of granulomas/nodular granulomas?

Back 25

Central area: macs, epithelioid macs, MNGCs.

Outer layer: fibroblasts, lymphocytes, plasma cells.

Front 26

How do caseating granulomas differ from non-caseating granulomas?

Back 26

Caseating have central core of necrosis

Front 27

What are 2 common causes of granuloma formation?

Back 27

Fungal infections

Myobacterium

Front 28

What is this? How do you know?

Back 28

Nodular granuloma.

Concentric layers.

Front 29

True or false?

Abscesses are typically more chronic than granulomas.

Back 29

False. Granulomas more chronic.

Front 30

What sort of inflammation is this? Taken from ileum of ruminant w Johne's.

Back 30

Diffuse granulomatous inflammation.

Note diffuse activated macs (cells w pink nuclei) and lymphocytes, bit of hemorrhage. Note normal epithelial lining vs inflammatory cell pop'n.

(Granulomatous inflammation can also be localized, ie, single granuloma.)

Front 31

What is this in a bovine lung? Could the animal have been treated effectively w antibiotics? Why/why not?

Back 31

Abscess.

Nope.

Drugs can't get in bc fibrous capsule too thick.