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Gen Path > Inflammation 2 > Flashcards

Inflammation 2 Flashcards

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
Q

What happens during the permeability event of inflammation?

A

Changes in the microvasculature (capillary) permeability that allow for plasma proteins and leukocytes to leave the circulation

26
Q

What are the 4 causes of edema?

A

Increased vascular permeability
Increased intravascular hydrostatic pressure
Decreased intravascular osmotic pressure
Decreased lymphatic drainage

27
Q

What protein is a huge contributor to oncotic pressure?

A

albumin

28
Q

What causes transudate?

A

Think changes in starling forces (hydrostatic and oncotic pressure)

29
Q

What is the protein and cellular content of a transudate?

A

Low protein and few cells

30
Q

What causes exudate?

A

Think changes in vascular permeability (inflammation)

– The vessel is super leaky and is letting out tons of cells and tons of proteins

31
Q

What is the protein and cellular content of an exudate?

A

High protein and lots of cells

32
Q

What are the two mechanisms that cause an increase in vascular permeability?

A

Contraction of endothelial cells and endothelial injury

33
Q

What will make endothelial cells contract? How quickly will it happen?

A

Chemical mediators like histamine

It’s an immediate transient response but only last for 15-30 minutes

34
Q

How can endothelial injury lead to an increase in permeability? How long can it last for?

A

Necrosis leads to detachment with leads to increased leakage
– Think burns and toxins

Rapid onset, but it can last hours to days

35
Q

What does histamine do?

A

Vasodilation and Increased vascular permeability

36
Q

Increased vascular permeability means that what can escape (or exude)?

A

Larger proteins like immunoglobulins (destroy microbes) and coagulation factors (fibrinogen)

37
Q

How do we get fibrin from fibrinogen?

A

Thrombin!

38
Q

What is fibrin usually associated with?

A

often associated with infectious causes, but not always!

Anything that causes enough vascular leakage can lead to fibrin

39
Q

What happens during the cellular event of inflammation?

A

Leukocytes accumulate at the site of injury and (hopefully) eliminate the offender

40
Q

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?

A

Vasodilation will cause blood flow to slow down and these cells will begin to flow near the vessel wall along the endothelium.

Margination

41
Q

What would an exudate look like?

A

Thick fluid, full of leukocytes and proteins

42
Q

What would a transudate look like?

A

It would be a thinner fluid like synovial fluid

43
Q

If an exudate is due to bacteria, what leukocyte is the main player?

A

Neutrophils - first responder

Gen Path (5 decks)

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