Inflammation 2 Flashcards

(43 cards)

1
Q

What is an endotoxin?

A

LPS = Lipopolysaccharide

Part of the cell wall, thus it is associated ONLY with gram-negative bacteria

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2
Q

What is an exotoxin?

A

Proteins produced by bacteria

Generally, gram-positive bacteria; however, gram-negative bacteria are also capable

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3
Q

What can both endotoxin and exotoxin lead to?

A

Sepsis

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4
Q

What does reddened serosa indicate?

A

Hyperemia

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5
Q

What does omphalophlebitis mean?

A

Umbilicus vein inflammation

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6
Q

What does polyserositis mean?

A

Multiple serosal (outside visceral) layers have inflammation

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7
Q

What are some associated findings with sepsis?

A
Suppurative meningitis
Hypopyon
Congested vessels
Fibrinous arthritis
Vertebral abscess
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8
Q

Define suppurative meningitis

A

Pus and inflammation of the brain

- will see pus on the ventral aspect (gravity)

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9
Q

Define hypopyon

A

Pus in the anterior chamber of the eye

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10
Q

What is fibrinous arthritis?

A

Fibrin and/or pus in the joint space(s)

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11
Q

What is a vertebral abscess and what can it lead to?

A

Bacteria get lodged in the physis of growing animals and forms an abscess
Leads to hind limb paresis/paralysis

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12
Q

Who is the the silver fox? What is he known for?

A

Rudolf Virchow

He created Virchow’s triangle and is considered the father of modern pathology

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13
Q

What are the three components of Virchow’s triangle? What are all three related to?

A

Stasis, vessel wall injury, and hypercoagulability

All three are related to thrombosis

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14
Q

What are the five cardinal signs of inflammation?

A

Heat, redness, swelling, pain and loss of function

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15
Q

Why do we get heat in areas of inflammation?

A

Inflammation results in hyperemia.

Vascular dilation results in increased warm blood flow to the area of the cause of inflammation

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16
Q

Why do we see redness in inflammation?

A

The hyperemia (increased blood flow)

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17
Q

Why do we see swelling with inflammation?

A

It’s due to edema

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18
Q

What are the two phases of edema?

A

Fluid phase - accumulation of fluid in the extravascular space
Cellular phase - accumulation of inflammatory cells migrating to the area)

19
Q

Define edema

A

Exudation of fluid and plasma protein

20
Q

Why do we get pain with inflammation?

A

Stretching of the region due to edema and increased inflammatory cells.
We also get chemical mediators
- Prostaglandins (induce pain)

21
Q

Why do we get loss of function with inflammation?

A

Movement of the inflamed area is reduced either due to pain (conscious or by reflex) and physical swelling

22
Q

What are the three main events of inflammation?

A

Hemodynamic events, permeability events, and cellular events

23
Q

What happens in the hemodynamic event of inflammation?

A

Vasodilation (causes hyperemia) which is induced by HISTAMINE

24
Q

What are chemical mediators involved in vasodilation?

A

Mainly histamine, but also prostaglandins and nitric oxide

25
What happens during the permeability event of inflammation?
Changes in the microvasculature (capillary) permeability that allow for plasma proteins and leukocytes to leave the circulation
26
What are the 4 causes of edema?
Increased vascular permeability Increased intravascular hydrostatic pressure Decreased intravascular osmotic pressure Decreased lymphatic drainage
27
What protein is a huge contributor to oncotic pressure?
albumin
28
What causes transudate?
Think changes in starling forces (hydrostatic and oncotic pressure)
29
What is the protein and cellular content of a transudate?
Low protein and few cells
30
What causes exudate?
Think changes in vascular permeability (inflammation) | -- The vessel is super leaky and is letting out tons of cells and tons of proteins
31
What is the protein and cellular content of an exudate?
High protein and lots of cells
32
What are the two mechanisms that cause an increase in vascular permeability?
Contraction of endothelial cells and endothelial injury
33
What will make endothelial cells contract? How quickly will it happen?
Chemical mediators like histamine It's an immediate transient response but only last for 15-30 minutes
34
How can endothelial injury lead to an increase in permeability? How long can it last for?
Necrosis leads to detachment with leads to increased leakage -- Think burns and toxins Rapid onset, but it can last hours to days
35
What does histamine do?
Vasodilation and Increased vascular permeability
36
Increased vascular permeability means that what can escape (or exude)?
Larger proteins like immunoglobulins (destroy microbes) and coagulation factors (fibrinogen)
37
How do we get fibrin from fibrinogen?
Thrombin!
38
What is fibrin usually associated with?
often associated with infectious causes, but not always! Anything that causes enough vascular leakage can lead to fibrin
39
What happens during the cellular event of inflammation?
Leukocytes accumulate at the site of injury and (hopefully) eliminate the offender
40
RBCs and WBCs normally flow in the center of the vessel (axial flow). What do they have to do during inflammation? What is this process called?
Vasodilation will cause blood flow to slow down and these cells will begin to flow near the vessel wall along the endothelium. Margination
41
What would an exudate look like?
Thick fluid, full of leukocytes and proteins
42
What would a transudate look like?
It would be a thinner fluid like synovial fluid
43
If an exudate is due to bacteria, what leukocyte is the main player?
Neutrophils - first responder