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Patho > L1 > Flashcards

L1 Flashcards

1
Q

Inflammation is?

A

the local vascular, lymphatic, and
cellular reaction of the living tissue against an irritant or causative agent.

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2
Q

The aim of Inflammation?

A

to localize, destroy, remove the irritant or causative agent and repair the damaged tissue.

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3
Q

Inflammation is a….. response

A

protective

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4
Q

Inflammation Can be….. harmful

A

potentially

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5
Q

Inflammation … Can It Be Harmful?

A

YES, although inflammation is a protective process, it may cause cell injury by itself due to:
* Strong reaction: as in large infarction.
* Prolonged inflammation: usually if the causative agent can not be eliminated.
* Inappropriate reaction: as in allergy or autoimmune
diseases.

This may lead to scar, permanent loss of function, or even death as in hypersensitivity disorders.

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6
Q

Causes of inflammation: ? they are Two and their eg. ?

A

 Living irritant (Microbial):
– Bacterial: staphylcocci & streptococci
– Viral: measles & influenza viruses
– Parasitic: Entamoeba histoltica & bilharzial worms
& their ova.
– Fungal: actinomyces bovis.

Non living irritant :
Physical agent: excesss heat, cold, radiation. Chemical: strong acid & alkali.
Mechanical: trauma, burns, foreign body.

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7
Q

Acute versus chronic inflammation are distinguished by ? 2

A

the duration
and
the type of infiltrating inflammatory cells

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8
Q

The inflammation is induced & regulated by ?

A

chemical mediators that produced by host cells
near the injury site in response to the injury.

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9
Q

The main cells that secrete chemical mediators are? 3

A

macrophages, mast cells, and dendritic cells.

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10
Q

Cardinal signs of (acute) inflammation ?

A

• Rubor = redness
• Calor = heat (hotness)
• Dolor = tenderness / pain
• Tumor = swelling
( described by Celsus 1st. Century AD)
• Functio laesa = loss of function
(added by R. Virchow)

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11
Q

What is the Cellulitis ?

A

acute skin infection commonly caused by
Streptococcus pyogenes or Staphylococcus aureus

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12
Q

Cardinal signs of (acute) inflammation occur as a consequence of ?

A

vascular and cellular changes

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13
Q

Two….. phases of inflammation occur
simultaneously explain the cardinal signs ?

A

overlapping

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14
Q

Inflammatory Phases ? 2

A

A. Vascular changes: (dilatation, increased
permeability, formation of exudates and
slow blood flow)

B. Cellular changes: influx of cells and their exit
from vessels into interstitial tissue

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15
Q

In the Inflammatory Phase what is the Vascular changes ? 4

A
  1. Alteration of vascular caliber
    following very brief vasoconstriction
    (seconds), vasodilation leads to increased
    blood flow and blood pooling creating
    redness and warmth (hotness)
  2. Increased vascular permeability for
    plasma proteins and cells + fluid creating
    swelling (tumor).
  3. Formation of inflammatory fluid exudates
  4. Vascular stasis: Fluid loss leads to
    concentration of red blood cells and
    slowed blood flow.
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16
Q
  1. Changes of vascular caliber
    • Brief vasoconstriction
    (seconds), followed by:
    • Vasodilatation leads to
    increased blood flow and blood pooling creating redness and hotness.
    • By the effects of chemical
    mediators as: ?? 3
A

Prostaglandins, nitric oxide, histamine

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17
Q

How ↑ vascular permeability occur?

A

Endothelial cells become “leaky”

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18
Q

Six mechanisms known to cause vascular
leakiness: ?

A
  1. Endothelial cell contraction
  2. Junctional retraction
  3. Direct endothelial injury (immediate
    sustained response)
  4. Leukocyte-dependent endothelial injury
  5. Increased transcytosis of fluid
  6. Leakage from new blood vessels.
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19
Q

Steps of Inflammation:

A

Recognition

Recruitment

Removal

Regulation

Repairing

20
Q

Elimination the Causative Agent:?

A

Destroying

Dilution

Neutralization

21
Q

Control of Inflammation: ?

A

The inflammation is normally under control because host cells & chemical mediators that involved in this processare:
-Activated only if needed(if there stimulus)
-Activated for short period
-Inactivated once its job is finished by anti-inflammatory mechanisms

22
Q

Dose the cardinal signs are present in each case of inflammation?

A

The cardinal signs are NOT present in each case of
inflammation, for examples:
* Pain (NOT present in inflammation of the lung)
* Heat (NOT present in inflammation of internal organs)

23
Q

What is the Systemic manifestations of inflammation ?

A

Fever-Headache-Malaise-Loss of Appetite-Lethargy-Nausea & Vomiting

Occur as a result of chemical mediators gain entrance to the circulatory system (acutephaseresponse).

This response also leads to elevated CRP and ESR
levels.(Why?and How?)

24
Q

Stimulus of Inflammation: ?

A

Infection-Trauma-Foreign Necrosis
bodies- tissue Necrosis-Immune reactions

25
Q

How can we recognition of the Causative Agent?

A

By circulating proteins (as complements)
&/or
cells including phagocytes, dendritic cells and epithelial cells.

The cells express receptors that have been designated to
sense the presence of harmful agents.

There are TWO major families of these receptors:
* Toll-like receptors. * Inflammasomes.

26
Q

Toll-like Receptors:

A

Cell Membrane: Detect Extracellular Agents
Endosome: Detect Ingested Agents

27
Q

Activated Toll-like receptors → Transcription →
Translation → Increase protein synthesis that will act
as:

A

-Inflammatory Mediators
-Anti-microbial Proteins

28
Q

Inflammasomes

A

cytoplasmic protein that recognize the harmful agents in the cytoplasm → Activate
Caspase-1 →ActivateIL-1 → ActivateWBCs.

29
Q

The best example for Inflammasomes ? and it’s a treated with?

A

The best example of this type is Gout which treated by
IL-1 antagonist.

30
Q

Types of Inflammation
ارجعي للجدول راجعيه يا ملكة

A
31
Q

Acute Inflammation:
 This type of inflammation will bring ….?

A

WBCs & plasma proteins RAPIDLY to the site of injury.

32
Q

Acute inflammation has2 components?

A

Vascular-Cellular changes

33
Q

Vascular Changes in Acute inflammation ?

A

-Transient Vasoconstriction
-Vasodilation
-↑ Vascular Permeability
-Activation of Endothelial Cells

All of these changes aiming to bring leukocytes and plasma proteins to the injured site

34
Q

What is the purpose of vasodilation in inflammation?

A

-To increase the amount of blood
-To slowing the blood flow
-To lose the axial stream

35
Q

How vasodilation happen?

A

By the effects of chemical mediators as:
Prostaglandins
Nitric oxide
Histamine

36
Q

Slowing of the blood flow allows to how?? And what it do??

A

Slowing of the blood flow allows WBCs to fallout from the axial stream and touch the vessel wall. This is how the cellular events of inflammation start.

37
Q

How ↑vascular permeability occur?

A

Endothelial cells become “leaky”

Several mechanisms areinvolved:
- Endothelial cell contractionand
- junctional retraction.
- Endothelial cell damage.
-leukocyte dependent endothelial injury
-↑ Transcytosis.
-Leakagefrom angiogenesis(new blood vessels)

38
Q

How ↑vascular permeability occur, Endothelial Cell Contraction:

A

 Endothelial cell contraction → intercellular gap.
 It is the commonest type of mechanism lead to increase
permeability.
 Occur as a result of the effect of histamine, kinin, &
other mediators.
 These mediators cause changes in the cell cytoskeleton.
 fast and short-lived (minutes)
 venules

39
Q

How ↑vascular permeability occur, Endothelial cell junction retraction how it’s happened?

A

– Through cytoskeleton reorganization.
– Induced by cytokine mediators (TNF, IL-1).
– 4 – 6 hrs post injury, lasting 24 hrs or more.

40
Q

How ↑vascular permeability occur, Endothelial Cell Damage what happens in this stage?

A

Endothelial damage →leakage of cells &proteins.
The leakage will continue until the damaged blood
vesselis repairedor thrombosed.
The cause of endothelial cell damage can be divided
into:
* Direct:by causative agentas physical or chemical agents.
* Indirect:by the effectof leukocytes.

41
Q

How ↑vascular permeability occur, Transcytosis how it happend?

A

Two ways
 Cell is engulfed → transported to the opposite side → released → transcytosis.
OR
 Multiple intracellular vesicles → fused together → canal formation → transcytosis.

42
Q

How ↑vascular permeability occur, Angiogenesis what is it and how happend?

A

New blood vessels will leak until the proliferating
endothelialcellsform intercellularjunction.

43
Q

Angiogenesis occur as a result of some mediators as…?

A

VEGF

44
Q

Lymphatic Vessels:?

A

↑ lymphatic flow → drain the inflamed area (edema,microbes, debris, & WBCs).
 It may lead to lymphangitis or lymphadenitis.

45
Q

Vascular changes, 3-Exudation of protein rich fluid (inflammatory fluid exudates)?

A

• Fluid, proteins, red blood cells and white blood
cells escape from the intravascular space as a
result of:
1. Increased vascular permeability (mainly in inflammation)
2. Decreased osmotic pressure intravascularly.
3. Increased hydrostatic pressure intravascularly.

46
Q

Vascular changes, 4. Vascular stasis?

A

• Slowing of the blood in the blood stream due to fluid exudation & increased viscosity.
• Allow inflammatory cells to collect in periphery to be in contact with endothelial cells and respond to the stimulus……..cellular events of inflammation.

47
Q

Differences between transudates and exudates
اارررجعي اخر سلايده بالمحاضره

A

Patho (11 decks)

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