Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

General Pathology, VPTH 342 > Lecture 14: Transudates and Exudates > Flashcards

Lecture 14: Transudates and Exudates Flashcards

1
Q

True or False: Inflammation is a sign of autolysis?

  1. True
  2. False
A

True or False: Inflammation is a sign of autolysis?

  1. True
  2. False

When there’s autolysis, the body is dead and inflammation can’t happen. Inflammation is an active process, and won’t happen in an animal that’s deceased.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Which of these in an appropriate morphologic diagnosis?

  1. Caseous necrosis
  2. Lymph node, necrosis, chronic
  3. Caseous lymphadenitis, diffuse, chronic
  4. Lymphadenitis, diffuse
A

Which of these in an appropriate morphologic diagnosis?

  1. Caseous necrosis
  2. Lymph node, necrosis, chronic
  3. Caseous lymphadenitis, diffuse, chronic
  4. Lymphadenitis, diffuse

It has a location, duration, organ and process

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Pancreatitis is to pancreas as typhlitis is to:

  1. Cecum
  2. Ear
  3. Toe nail
  4. Trachea
A

Pancreatitis is to pancreas as typhlitis is to:

  1. Cecum
  2. Ear
  3. Toe nail
  4. Trachea
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

In normal microvascular flow, __________ __________ is high on the arteriole side of the capillary, and __________ __________ is high on the venule side of the capillary.

A

In normal microvascular flow, hydrostatic pressure is high on the arteriole side of the capillary, and oncotic pressure is high on the venule side of the capillary.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

During acute inflammation, what forces or factors promote the accumulation of fluid exudate in the interstitium?

A
  • Increased hydrostatic pressure in the arteriole capillary beds
  • Increased vascular pressure
  • Increased oncotic pressure outside the vascular space
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How does increased arteriole hydrostatic pressure lead to the formation of thrombus, at a site?

A

If you have increased arteriole hydrostatic pressure, that will cause protein loss through the interendothelial junctions. That increases the oncotic pressure outside of the vascular space, which the body tries to correct by fluid loss from the vasculature. Decreased fluid on the arteriole side of the capillary means that you could have stasis, because there’s decreased fluid. That can meet the criteria for the formation of a thrombus at that site.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the first reflex to hemostasis?

A

Vasoconstriction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How does vasodilation play a role in acute inflammation?

A

Vasodilation increases the flow in arterioles. The meta-arteriolar sphincter opens, the hydrostatic pressure increases, and the venules dilate.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What compound is a major player in the expansion of interendothelial junctions?

A

Histamine

Where two endothelial cells would usually meet and form a barrier, under the influence of histamine they will retract, and open up that space.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are some mechanisms of increased vascular permeability?

A
  1. Retraction of endothelial cells
  2. Endothelial injury
  3. Leukocyte-mediated vascular injury
  4. Increased trancytosis (when cells cross an intact endothelial cell)

Side note: We won’t talk about increased transcytosis much. Just be aware that it happens.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Tell me more about the retraction of endothelial cells, as a mechanism of increased vascular permeability.

A
  • Occurs mainly in venules
  • Induced by histamine, NO, other mediators
  • Rapid and short-lived (minutes)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Tell me more about endothelial injury, as a mechanism of increased vascular permeability.

A
  • Occurs in arterioles, capillaries, venules
  • Caused by burns, some microbial toxins, nearby thrombus, crushed in a traumatic event
  • Rapid: may be long-lived (hours to days)

Perhaps they’ve been overstimulated, they’ve been over activated by the presence of LPS

These cells simply cannot cover that vascular space anymore

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Tell me more about leukocyte-mediated vascular injury, as a mechanism of increased vascular permeability.

A
  • Occurs in venules, pulmonary capillaries
  • Associated with late stages of inflammation
  • Long-lived (hours)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the characteristics of a transudate?

A

Low Specific Gravity (1.012 or less)

Low protein concentration

Low cellularity

Typically a clear fluid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the characteristics of an exudate?

A

Increased Specific gravity (~1.020)

Increased protein concentration (>4g/dl)

Increased cellularity (accumulates over time)

Typically a cloudy, opaque fluid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is a modified transudate?

A

Somewhere in between a transudate and an exudate.

May have high protein concentration, but low cellularity, or vice versa

We’ll cover this more in clin path, just know it exists for now.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

In the fluidic phase of inflammation (increased vascular permeability), what happens:

A
  • Increased viscosity of blood
  • Margination of leukocytes and platelets
  • Proteins (fibrinogen and globulins) move into the interstitium
  • Possible thrombosis of small vessels and lymphatics
  • Increased lymphatic flow early, may or may not lead to later thrombosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the steps of the leukocyte adhesion cascade?

A
  • Rolling
  • Adhesion
  • Transendothelial migration
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are the steps of cellular exudation?

A
  • Margination (rolling: selectins)
  • Stable adherence (upregulation of selectins)
  • Emigration/Transmigration (actual movement of cells out of the vasculature)
  • Chemotaxis (directed locomotion via chemical stimulus)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are the proteins that play a role in stable adherence and emigration/transmigration?

A

Stable adherence: Chemokine upregulation of ICAM-1

Emigration/Transmigration: PECAM

More info on them (from wikipedia):

ICAM-1 - This protein is a type of intercellular adhesion molecule continuously present in low concentrations in the membranes of leukocytes and endothelial cells. Upon cytokine stimulation, the concentrations greatly increase. ICAM-1 can be induced by interleukin-1 (IL-1) and tumor necrosis factor (TNF) and is expressed by the vascular endothelium, macrophages, and lymphocytes.

PECAM-1 is found on the surface of platelets, monocytes, neutrophils, and some types of T-cells, and makes up a large portion of endothelial cell intercellular junctions. The encoded protein is a member of the immunoglobulin superfamily and is likely involved in leukocyte transmigration, angiogenesis, and integrin activation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Walk me through what happens when you have an acute inflammatory stimulus, like a cut or a foreign body under the skin,

A

Acute inflammatory stimulus: Sliver, maybe a cut, maybe a foreign body gets driven under the skin

Now you have antigens, maybe bacteria, maybe plant fibers. This will serve as a stimulus for neutrophil recruitment. This takes place through a variety of Inflammatory mediators: cytokines, chemokines. L-selectin is then expressed on neutrophils. When the endothelial cells are in the presences of certain cyto/chemokines, the receptor will be more strongly expressed on the endothelial cells.

This tethers the neutrophil to the endothelial cell, which allows for the expression of additional mediators. This results in the pulling of these cells through the vascular wall, towards the initial stimulation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are some chemotaxins for PMNs?

PMNs = polymorphonuclear leukocytes = neutrophils, mainly

A

C5a, Bacterial products, FDPs, Chemokines (like IL-1), LTB4 (Leukotriene B4), PAF (platelet activating factor), Dead cells (necrotaxis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are some chemotaxins for macrophages?

A

C’, Bacteria, Cationic proteins from PMNs, Chemokines (IL-8)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are some chemotaxins for Eosinophils?

A

C5a, Parasites, Mast cell products: Histamine, eotaxin, Chemokines (IL-4, IL-5, IL-13), Ag-Ab complexes

25
Q

What are the effector cells of acute inflammation?

A
  • Vascular endothelial cells
  • Mast cells
  • Neutrophils
  • Eosinophils
  • Monocytes/macrophages
26
Q

Refresh my memory about Neutrophils.

Life span?

Are neutrophils the main cellular component of acute exudation? Why?

A

Neutrophils are the first line of cellular phagocytic defense. Acute exudates are neutrophilic.

Life span: In blood - 5-10 hours. In Tissue - 1-4 days.

Neutrophils are the main cellular component of actue exudation because they are motile, they are the primary leukocyte in peripheral blood (except in cattle), and they have two forms of kiling capabilities: phagocytic and the release of granule contents.

27
Q

List some more characteristics of neutrophils.

A
  • Short-lived
  • Low protein synthesis
  • Anaerobic glycolysis (helpful in the center of an abscess)
  • Dead end cells (can’t re-enter blood stream)
  • Primary and secondary granules
  • Some species have heterophils rather than neutrophils (reduced myeloperoxidase: Avians, rabbit, guinea pig)
28
Q

What is an immature neutrophil called? When would you see it?

A

Immature neutrophils are called band neutrophils. The nuclues forms a blobby, horseshoe shape.

Band neutrophils are released into the bloodstream before they are mature; it’s not uncommon to see them in a significant inflammatory situation. Means the body is trying to keep up.

In the attached image, 1 is a band neutrophil, 2 is a normal neutrophil

29
Q

What stage of a myocardial infarct is this?

What are the arrows point to?

A

Image is showing an acute stage of a myocardial infarct

First stage would have been the transudation of fluid. There would have been a fair amount of fluid, followed rapidly by infiltration of neutrophils (what the arrows are pointing to).

How do we know we’re seeing neutrophils? The big key is that we’re seeing, in the aggregate, a very dark nuclear structure that has a squiggly appearance to it.

If you see a number of them, it’s safe to say that many/most of them are neutrophils. Consider the company that they cell is keeping.

30
Q

What stage of a myocardial infarct is this?

A

This is a sub-acute or chronic situation

The neutrophils have been recruited because there are dead and dying myocardial sites in this area. Will break down the debris so that the next stage can take place, which is the influx of macrophages to clear things up.

Starting to get some presence of fibroblasts in here as well, which is a separate mechanism

31
Q

What are some characteristics of Mast cells?

A

Large blueish-purple nuclei

Very granular

Can be a mucosal or connective tissue type of mast cell

4-12 week life span in tissue

High affinity receptors for IgE -> put to work for degranulation

Granules: Histamine, tryptase & chymase, other things that will break down the extracellular matrix

32
Q

What are some characteristics of eosinophils?

A

Eosinophils enter lesions at acute to chronic transitions

Granules: collagenase, gelatinase, other proteinases that are going to break down the extracellular matrix

Collagen degradation: eosinophilic granulomas, mast cell tumors

33
Q

What are some chemical mediators of acute inflammation?

A
  • ICAM upregulation
  • Histamine
  • Kinis (tachykinin, bradykinin)
  • Complement cascade (complement products with other effects)
  • Arachidonic acid metabolites (prostaglandins, leukotriene, PAF)
  • Cytokines
  • Interferons and chemokines
  • Antimicrobial peptides
  • Acute phase proteins
34
Q

What are some important things to remember about the previously listed Chemical Mediators of acute inflammation?

A
  • Remember that each of these mediators have short half-lives
  • Can be destroyed enzymatically and/or be scavenged by protective mechanisms
  • Can be blocked by endogenous inhibitors
  • These are very potent activators, and very capable mediators. When they are called on, they will show up and will have a strong effect. Once that effect is no longer needed, they need to be shut down.
  • There’s a series of checks and balances for severity of acute inflammatory responses
  • Can exploit them, or temper them with drugs. Otherwise, some inflammatory processes can surpass their usefulness, and cause further damage
35
Q

Macrophage characteristics, in an intermediate to chronic cell response?

A
  • Comprise the mononuclear phagocytic system: specialized by organ (kupffer cells, PAMs and PIMS, for example)
  • They are motile and phagocytic
  • Have anaerobic or aerobic glycolysis
  • Long lived cells
  • May have secretory functions and protein synthesis
  • Can form giant cells
36
Q

What are the two possible morphologies of Giant cells?

A

Langhans morphology, where the nuclei are arranged at the periphery

Foreign Body macrophage morphology, where the nuclei are gathered centrally

37
Q

What are some functions of macrophages?

A
  • Antigen processing; Antigen presenting cells (Trigger of adaptive immune response)
  • Combat and hide intracellular pathogens (true for mycobacteria and leishmania)
  • Degrade tissue debris
  • Iron metabolism (hemoglobin into hemosiderin)
  • Heme metabolism (bilirubin)
38
Q

What are some mediators of vascular permeability?

A
  • Vasoactive amines: histamine and serotonin
  • Kinins, e.g. bradykinins
  • Prostaglandins and leukotrienes (part of arachidonic acid metabolism)
  • Platelet and leukocyte products (Platelet Activation Factor (PAF) and Tumor Necrosis Factor (TNF)
39
Q

List three complement cascade functions that are relevant to this lecture.

A
  • Host defense
  • Bridging innate and adaptive immunity
  • Disposal of waste
40
Q

List three components of host defense (as part of C’) and the proteins involved

A
  • Opsonization (C3, C4 fragments)
  • Chemotaxis/activation (C5a, C3a, C4a)
  • Lysis of microbes (C5b-C9, MAC)
41
Q

Describe what is meant by “Bridging Innate and Adaptive Immunity” (as part of C’) and the proteins involved

A

Ab response assist/augment (C3b, C4b)

42
Q

Describe what is meant by “Disposal of Waste” (as part of C’) and the proteins involved

A

Ag-Ab or apoptotic cells (C1q, C3, C4)

43
Q

What mediators of inflammation is generated from the breakdown of membrane phospholipids?

A

Membrane phospholipids are broken down by phopholipase into arachidonic acid.

If the AA is broken down by lipoxygenase, the result is leukotrienes

If the AA is broken down by cyclooxygenase (COX-1, COX-2), the result is prostaglandins.

44
Q

We know that inflammatory mediators are derived from lipid membranes and inhibitors. Why are corticosteriods so effective at blocking/preventing/stopping an inflammatory process?

A

Corticosteriods are so effective because they inhibit the initial cell membrane breakdown process. They inhibit phospholipase, which cuts off the whole breakdown process at the initial stage.

45
Q

If you can’t take a corticosteriod to block inflammatory mediators, what’s your next best choice?

What are some examples of these next-best-choice drugs?

A

COX inhibitors; COX-1, COX-2

Rimadyl: COX-1

Deramaxx: COX-2

Celebrex: COX-2

Aleve: COX-1 and -2

46
Q

What do steroids inhibit?

A

Phospholipases

47
Q

What do prostaglandins help to regulate?

What can they induce if their levels are too high?

A
  • Fever
  • Tachycardia
  • ACTH response
  • Clotting/hemostasis via thromboxane
48
Q

What do leukotrienes help to regulate?

What can they induce if their levels are too high?

A
  • Increase vascular permeability
  • Chemotaxis
  • Vasocontriction
  • Exacerbate acute inflammatory response
49
Q

Is the clotting cascade separate from the kinin cascade, the fibrinolytic system and the complement cascade?

A

Nope. All these cascades are interconnected

Lots of activity on one side of this chart will have an influence on the rest of them.

50
Q

What do kinins do? What are two examples of kinins?

A

Kinins mediate inflammation; they modulate clotting and compliment cascades.

Bradykinins: vasoactive peptide

  • Proinflammatory (increased vascular permeability, vasodilation:hypotension, sensitivity to pain increased, smooth muscle contraction: bronchoconstriction)
  • Plasma pathway; tissue kinin pathway

Tachykinins: vasoactive neuropeptides

  • Substance P
  • Synthesized by sensory afferent nerves in lung, GI (vasoconstriction or vasodilation, allergic reactions and asthma)
  • Induces inflammation, released from mast cells, eosinophils, stimulated nerve fibers
51
Q

How are antimicrobial peptides involved as a chemical mediator of acute inflammation?

A
  • Alpha, beta-defensins
  • Produced by neutrophils, epithelial cells
  • Works in a specific microenvironment, is pH dependent
  • Frogs have tons of these on their skin
52
Q

How are acute phase proteins involved as a chemical mediator of acute inflammation?

A
  • C-reactive protein, haptoglobin, fibrinogen, alpha1-antitrypsin
  • Concentration increased/decreased by 25% in inflammation
  • Synthesized in liver
53
Q

How are cytokines involved as a chemical mediator of acute inflammation?

A
  • Produced by many cell types
  • Modulate functional expression of other cell types in inflammation
  • Interferons
              - Glycoprotein cytokines
          - Produced by lymphocytes, others
          - Response to viruses, virus-infected cells, parasites, neoplastic cells
54
Q

How is inflammation controlled?

A
  • Localized reaction: mediators are concentrated
  • Neutralization of the primary irritant
  • Mediators are short lived
  • Self destruct spontaneously
  • Enzymatic breakdown (e.g. kininase)
  • C’ component inactivators
  • PGs and LTs are unstable
  • Proteases
  • Antioxidants (against ROS; Vit E, Selenium, Vit C)
  • Dilution by exudates
  • Corticosteroids (endogenous)
55
Q

What are some effects you would see in an acute-phase reaction, as a mediator of inflammation?

A
  • Fever
  • Increased sleep
  • Decreased appetite
  • Increased acute-phase proteins
  • Hemodynamic effects (shock)
  • Neutrophilia
56
Q

What are some endothelial effects, as a mediator of inflammation?

A
  • Increased leukocyte adherence
  • Increased PGI synthesis
  • Increased Procoagulant activity
  • Decreased Anticoagulant activity
  • Increased IL-1, IL-8, IL-6, PDGF
57
Q

What are some fibroblast effects, as a mediator of inflammation?

A
  • Increased proliferation
  • Increased collagen synthesis
  • Increased Collagenase
  • Increased Protease
  • Increased PGE synthesis
58
Q

What are some leukocyte effects, as a mediator of inflammation?

A
  • Increased cytokine secretion (IL-1, IL-6)

General Pathology, VPTH 342 (24 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions