[A] 1.50 Vascular changes and exudation in the acute inflammation Flashcards Preview

Pathology A - General Pathology > [A] 1.50 Vascular changes and exudation in the acute inflammation > Flashcards

Flashcards in [A] 1.50 Vascular changes and exudation in the acute inflammation Deck (31)
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1
Q

Infectious inflammation caused by…

A

Pathogens

2
Q

Non-infectious inflammation caused by…

A
  • Foreign body
  • Trauma
  • UV radiation
  • Tumour
  • Irritation
  • Allergy
3
Q

Acute inflammation: Aim

A
  • Elimination of toxic agents, necrotic tissues and cells
  • Rapid protection until an effective immune response
  • Restrict toxins & pathogenic inflammatory agents to the site of injury

Few seconds after injury

4
Q

Effective immune response =

A

Subacute inflammation

5
Q

Acute inflammation: Effect on a microscopic scale

A
  • Diluting & inactivating biologic and chemical toxins
  • Killing & sequestrating microbes and neoplastic cells
  • Degrading foreign body
  • Providing wound healing (growth) factors to ulcerated surfaces and traumatised tissue
6
Q

Modified inflammatory reactions

A

Caused by:

  • Anti-inflammatory treatments
  • Drugs
7
Q

Panniculitis

A

Inflammation of adipose tissue

8
Q

Stomatitis

A

Inflammation of oral cavity mucosa

9
Q

Typhlitis

A

Inflammation of Caecum

10
Q

Proctitis

A

Inflammation of Rectum

11
Q

Omphalitis

A

Inflammation of navel

12
Q

Pyelitis

A

Inflammation of renal pelvis

13
Q

Salpingitis

A

Inflammation of uterine tube

14
Q

The four cardinal signs of acute inflammation

A
  • Rubor (Redness)
  • Tumor (Swelling)
  • Calor (heat)
  • Dolor (pain)
  • (+ Loss of function)
15
Q

The inflammatory response consists of which two main components?

A
  • Vascular reaction
  • Cellular reaction

Parallel, coherent processes

16
Q

Identification of the inflammatory stimuli can be by…

A
  • PAMPs (Pathogen-associated molecular patterns)
  • DAMPs (Damage associated molecular patterns)
  • TLRs (Toll-like receptors) & other PRRs (pattern recognition receptors)
17
Q

PAMPs

A

Molecules associated with groups of pathogens

  • Recognised by cells of the innate immune system
18
Q

DAMPs

A

Nuclear/cytosolic proteins

  • Cellular stress, damage and necrotic cell death cause release of DAMP molecules or alarmins
19
Q

Changes in vascular flow and calibre

A
  • Begin early after injury
  • Vasodilation first involves the arterioles → opening of new capillary beds in the injured area
  • Increased blood flow (heat and redness)
20
Q

Vasodilation (cell-derived mediators)

A

Induced by the action of several mediators

  • Histamine*
  • Serotonin*
  • Prostaglandins
  • Nitric oxide

*Secreted by mast cells, basophil granulocytes & platelets

21
Q

Cytokines

A

Small proteins used in cell signalling

  • Produced by:
    • Macrophages
    • B-lymphocytes
    • T-lymphocytes
    • Mast cells
    • Endothelial cells
    • Fibroblasts
22
Q

Examples of cytokines in inflammation

A
  • Interferons
  • Chemokines
  • Interleukins
  • Lymphokines
  • Tumour necrosis factors (TNF)
23
Q

Vascular changes of microcirculation during inflammation

A
  • Haemostasis
  • Venula-hyperpermeability
  • Microvascular exsudation - Inflammatory exsudate (oedema)
24
Q

Haemostasis

A
  • Vasodilation & loss of fluid → Conc. of blood cells in the vessel of microcirculation
  • Increased viscosity of the blood & slower blood flow
25
Q

Increased vascular permeability

A

Vascular leakage

  • Hallmark of acute inflammation
  • Leads to the escape of protein-rich fluid (exudate) into the extravascular tissue
    • Increased interstitial hydrostatic pressure and endothelial dysfunction
  • Extravascular fluid = Inflammatory oedema
26
Q

Causes of endothelium becoming leaky during inflammation

A
  • Endothelial gaps form in postcapillary venules
  • Direct endothelial injury (burns/lytic bacterial infections)
  • Leukocyte mediated endothelial injury
27
Q

Acute inflammation - Cellular events

A

The critical function of the inflammation is to deliver leukocytes to the site of injury

  • Leukocytes ingest agents, kill bacteria and other microbes and remove necrotic tissue
28
Q

Acute inflammation - Cellular events

A
  1. In the vascular lumen: Leukocyte margination, rolling and adhesion
  2. Transmission across the endothelium (Leukocytadiapedesis)
  3. Migration in the interstitial tissues
  4. Leukocyte activation & phagocytosis
  5. IC degradation
29
Q

Leukocyte adhesion deficiency (LAD)

A
  • Defects in the leukocyte adhesion process
  • Marked leukocytosis and recurrent infections
  • Impaired migration of leukocytes from the blood vessels to sites of infection
    • Requires adhesion of leukocytes to the endothelium
30
Q

Leukocyte adhesion deficiency (LAD) as a congenital defect

A
  • Holstein calves (Bovine LAD (BLAD))
  • Irish setters (Canine LAD (CLAD))
31
Q

Clinical signs of BLAD

A
  • Gingivitis
  • Tooth loss
  • Oral ulcers
  • Enteric ulcers
  • Leukocytosis
  • Pneumonia

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