Brainscape's Knowledge GenomeTM

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


See full index

Pathology > Inflammation > Flashcards

Inflammation Flashcards

1
Q

What is inflammation

A

Inflammation is the response of vascularized tissue that delivers leucocyte and molecules of host from circulation to the site of infection and cell damage in order to eliminate the offending agent

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

What are the 5 R of inflammation

A

Recognition
Recruitment
Removal
Regulation
Repair

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

What are cardinal signs of inflammation

A

Calor
Rubor
Dolar
Tumour
Functional loss

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

Describe vascular events of inflammation

A

Transient vasoconstriction
Vasodilation

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

Describe vascular events of inflammation

A

Transient vasoconstriction
Vasodilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Causes of increased vascular permeability

A

Endothelial cell contraction
Endothelial injury
Increased transcytosis of protein
Leakage from new blood vessels (angiogenesis)

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

Describe cellular events of inflammation

A

Recruitment of WBC
Activation of WBC
Phagocytosis
Killing and degradation

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

Steps of leucocyte recruitment

A

Margination and rolling
Adhesion
Transmigration
Migration to interstitial tissue

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

Rolling is mediated by which adhesion molecules

A

Selectins

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

What are the 3 selectins

A

E selectin
P selectin
L selectin

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

What molecules mediate adhesion

A

Integrins join on ligand on cell endothelium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is diapedesis

A

After being arrested on the endothelial
surface, leukocytes migrate through the vessel wall primarily by squeezing between cells at intercellular junctions.
This extravasation of leukocytes, called diapedesis,

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

What is chemotaxis

A

After extravasating from the blood, leukocytes move toward sites of infection or injury along a chemical gradient by a process called chemotax

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are chemotactic agents

A

Bacterial products, particularly peptides with N-formylmethionine termini
• Cytokines, especially those of the chemokine family
• Components of the complement system, particularly C5
• Products of the lipoxygenase pathway of arachidonic
acid (AA) metabolism, particularly leukotriene B4
(LTB4)

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

Why are neutrophils abundant in acute inflammation

A
  1. They are most numerous
  2. React rapidly to cytokines
  3. Attach firmly to adhesion molecules
  4. They short lived
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Leucocyte activation enhances the following function

A

1.Phagocytosis
2.Intracellular destruction of phagocytosed microbes and dead
cells
3. Liberation of substances that destroy extracellular microbes
and dead tissues,
4.Production of mediators, including arachidonic acid metabolites and cytokines, that amplify the inflammatory reaction, by recruiting and activating moreleukocytes

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

What are steps of phagocytosis

A

(1) recognition and attachment of the particle to the ingesting
leukocyte;
(2) engulfment, with subsequent formation of a phagocytic vacuole; and
(3) killing and degradation of the ingested
material.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is opsonisation

A

material.
Leukocytes bind and ingest most microorganisms and
dead cells by means of specific surface receptors. Some of
these receptors recognize components of the microbes and
dead cells and other receptors recognize host proteins,
called opsonins, that coat microbes and target them for
phagocytosis (the process called opsonization).

19
Q

What happens during oxidative burst

A

Increased oxygen consumption
Glycogen catabolism
Glucose oxidation
Production of ROS

20
Q

What are neutrophlic extra-cellular trap NEXT

A

These are fibrillar network produced by neutrophils
These traps provide high concentration of antimicrobial substance at site of infection and prevent spread of microbes by trapping them

21
Q

Clinical examples of leucocyte induced injury

A

Acute respiratory distress
syndrome

Acute transplant rejection Lymphocytes; antibodies and
complement

Asthma Eosinophils; IgE antibodies

Glomerulonephritis Antibodies and complement;
neutrophils, monocytes

Septic shock Cytokines

Chronic

Rheumatoid arthritis Lymphocytes, macrophages;
antibodies?

Asthma Eosinophils; IgE antibodies

Atherosclerosis Macrophages; lymphocytes?

Chronic transplant rejection Lymphocytes, macrophag

22
Q

What can be the defects in leucocyte functions

A

LEUCOCYTE ADHESION DEFECT: type 1 due to defective synthesis of the CD18 β
Type 2 : due to by a defect in fucose
metabolism resulting in the absence of sialyl–Lewis X,
the oligosaccharide on leukocytes that binds to selectins
on activated endothelium.
DEFECT IN MICROBIAL ACTIVITY : eg chronic granulomatous disease
DEFECTS IN PHAGOLYSOSOME FORMATION

23
Q

What are morphological patterns of acute inflammation

A
  1. SEROUS INFLAMMATION is characterized by the outpouring of a watery, relatively protein-poor fluid that, depending on the site of injury, derives either from the plasma or
    from the secretions of mesothelial
    cells lining the peritoneal, pleural, and pericardial cavities.
  2. FIBRINOUS INFLAMMATION occurs as a consequence of
    more severe injuries, resulting in greater vascular permeability that allows large molecules (such as fibrinogen) to
    pass the endothelial barrier
  3. SUPPURATIVE (PURULENT) INFLAMMATION and abscess
    formation. These are manifested by the collection of
    large amounts of purulent exudate (pus) consisting of
    neutrophils, necrotic cells, and edema fluid.
    4.• AN ULCER is a local defect, or excavation, of the surface
    of an organ or tissue that is produced by necrosis of cells
    and sloughing (shedding) of necrotic and inflammatory
    tissue
24
Q

What are performed , cell derived inflammatory mediators

A

Histamine
Serotonin

25
Q

What are newly synthesized cell derived mediators

A

Prostaglandin
Leucotrines
Platelet activating factor
Reactive oxygen species
Nitric oxide
Cytokines
Neuropeptides

26
Q

Systemic effects of acute inflammation

A

1.Fever
2.Leucocytosis
3. Acute phase reactants- to protect normal cells, these are
•certain cellular protection factors
•some coagulation proteins
• transport proteins
•immune agent
• stress protein
• antioxidants
4. Lymphangitis
5. Septic shock

27
Q

Outcomes of acute inflammation

A
  1. resolution- complete return to normal tissue
  2. Fibrous healing - repair by fibrosis
  3. Suppuration - acute abscess
  4. Chronic inflammation
28
Q

What is granulomatous inflammation

A

Granulomatous inflammation is a distinctive type of chronic inflammation characterized by aggregates of activated macrophages and scattered lymphocytes, forming a granulomatous pattern.

29
Q

What is granulomatous inflammation

A

Granulomatous inflammation is a distinctive type of chronic inflammation characterized by aggregates of activated macrophages and scattered lymphocytes, forming a granulomatous pattern.

30
Q

What is the purpose of granulomatous inflammation

A

Type 4 hypersensitivity, it is a protective reaction by host but eventually causes tissue destruction because of persistence of poorly digestible antigen

31
Q

What are characteristics of chronic inflammation

A
  1. INFILTRATION with mononuclear including macrophages, lymphocytes, plasma cell
  2. TISSUE DESTRUCTION by inflammatory cells (hallmark)
  3. REPAIR- either by proliferation or fibrosis
32
Q

In what cases proliferation occurs
And in what cases fibrosis occurs

A

If the cells have capacity to regenerate, it heals by proliferation otherwise fibrosis

33
Q

Chronic inflammation occurs due to?

A
  1. PERSISTENT INFECTION, difficult to eradicate
    Persistent infection causes activation of t lymphocytes mediated response
  2. IMMUNE MEDIATED INFLAMMATORY DISEASE eg rheumatoid arthritis
  3. EXCESSIVE and INAPPROPRIATE activity of immune system eg rheumatoid heart disease
  4. ALLERGIC DISEASES eg bronchial asthama
  5. Disease NOT CONVENTIONALLY inflammatory
  6. Prolonged exposure to TOXIC agents like silica
34
Q

Main cells of chronic inflammation

A

Macrophages
Lymphocytes

35
Q

Precursor of macrophages

A

Monocytes get converted into macrophages
Why?
1. Size increase
2. Life time increase

36
Q

Macrophages of diff organs

A

Liver - kupffers cell
Spleen - sinus histocytes
Lungs - alveolar macrophages
Cns - microglial cells
All these together mononuclear phagocytic system

37
Q

What activates the macrophages

A

Il1 , il13
Microbial products

38
Q

t Lymphocytes types

A

Type 1 helper T cells - activates macrophages
Type 2 helper T cells - activate eosinophils and macrophages also recruitment of macrophages
Type 17 helper T cell - activating and recruiting monocytes and neutrophils

39
Q

Factors required for classical and non classical macrophages activation

A

For classical- interferon gamma
For non classical - il13
Il4

40
Q

What are the proteins involved in allergic reaction

A

Major basic protein and cationic protein
These proteins are toxic to parasites and also cause epithelial cell necrosis

41
Q

What is granulomatous inflammation

A

Distinctive type of chronic inflammation characterized by aggregate

42
Q

Where do we see granulomatous inflammation

A
  1. Prolonged inflammation
  2. Immune mediated inflammatory response eg crohn’s disease
  3. Unknown etiology eg sarcoidosis
  4. Foreign body - suture or spinctor
43
Q

Morphology of granulomatous inflammation

A

Pathology (4 decks)

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