Acute Inflamation Flashcards

1
Q

What are the principle causes of acute inflammation? (4)

A
  • microbial infections
  • hypersensitivity reactions
  • physical agents
  • chemical agents
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2
Q

What are the physical characteristics of acute inflammation?

A
  • red - rubor
  • hot - calor
  • swollen - tumour
  • painful/tender - doll
  • loss of function
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3
Q

What causes rubor?

A

dilation of blood vessels

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4
Q

What causes calor?

A

peripheral increase in temp

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5
Q

What causes tumour?

A

due to oedema - watery fluid accumulation

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6
Q

What cause dolor?

A

stimulation of nerve endings by pressure and chemical mediators

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7
Q

What happens in the vascular phase?

A

dilation and increased permeability

  • endothelial cells well initially, then contract to increase space between them
  • process is regulated by chemical mediators
  • epithelial cells are not damaged
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8
Q

What happens in the exudative phase?

A

fluid and cells escape from permeable venues (small veins)

- net loss of fluid from vascular into interstitial space - resulting in tumour/oedema

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9
Q

What is exudate?

A

mass of cells and fluid that has seeped out of blood vessels or organs in inflammation

  • high protein content
  • proteins include immunoglobulins (antibodies)
  • continuously removed by lymphatics
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10
Q

What are the differences between exudate and transudate?

A

transudate:

  • no net flow out
  • normal vascular permeability
  • low protein content
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11
Q

What is the function of the lymphatic system in acute inflammation?

A

lymphatics are dilated - drain fluid from exudate - antigens are carried to lymph nodes - recognised by lymphocytes

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12
Q

What is lymphangitis?

A

inflammation of the lymph vessels

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13
Q

What is lymphadenitis?

A

inflammation of the lymph nodes

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14
Q

What is the diagnostic feature of acute inflammation?

A

neutrophil accumulation in the extracellular space

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15
Q

What are neutrophils?

A

the most common white blood cell

- very short lived

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16
Q

What are the functions of neutrophils?

A
  • kill organisms
  • degrade necrotic tissue
  • ingest offending agents
  • produce chemical mediators
  • produce toxic oxygen radicals
  • produce tissue damaging enzymes
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17
Q

What is chemotaxis?

A

the movement of a motile cell or organism in a direction corresponding to a gradient of increasing/decreasing concentration of a particular substance

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18
Q

What happens in neutrophil chemotaxis?

A

the neutrophils migrate towards sites of infection/inflammation

  • cell surface receptors allow neutrophils to detect chemical gradients of molecules (chemotactic compounds) - these direct the path of their migration
  • at the site of the antigen the concentration of chemotactic compounds tends to be higher
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19
Q

What do chemotactic compounds include?

A
  • bacterial products
  • some complement components
  • products of neutrophil activity
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20
Q

What are chemical mediators of acute inflammation?

A

any messenger that acts on blood vessels, inflammatory cells or any other cells to contribute to an inflammatory response
- spread of an acute inflammatory response following an injury suggests chemical substances (chemical mediators) released from injured tissue spread outwards into uninjured areas

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21
Q

Where are chemical mediators derived from?

A

exogenous (from in cells) - endotoxins

endogenous (extracellular) - plasma, leukocytes, endothelial cells, fibroblasts

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22
Q

What do endogenous chemical mediators cause?

A
  • vasodilation
  • emigration of neutrophils
  • chemotaxis
  • increased vascular permeability
  • itching and pain
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23
Q

What are plasma factors?

A

clotting factors - proteins that work together with platelets to clot blood

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24
Q

What are the 4 enzymatic cascade systems found in plasma?

A
  • complement system
  • the kinins
  • the coagulation factors
  • fibrinolytic system
25
Q

What is the complement system?

A

cascade system of enzymatic proteins - activated during inflammatory system - helps get rid of pathogens and antigens

26
Q

What are the coagulation factors function?

A

the conversion of soluble fibrinogen into fibrin - seals leaks

27
Q

What is the fibrinolytic system?

A

lysis of fibrin into fibrin degradation products

28
Q

How do neutrophils carry out their function?

A
  • movement (chemotaxis)
  • recognition of and adhesion to micro-organisms
  • phagocytosis
  • intracellular killing of micro-organisms
29
Q

What are opsonins?

A

proteins that bind to extracellular materials and make them more adherent to phagocytic cells and more amenable to engulfment or ingestion

30
Q

Why are opsonins important?

A

most micro-organisms are not recognised until they are coated in opsonins
these opsonins greatly enhance phagocytosis

31
Q

How do opsonins work?

A

they bind to specific receptors on leucocytes (WBCs) and greatly enhance phagocytosis

32
Q

What are the major opsonins?

A

Fc fragment of IgG
C3b - fragment of C3 generated by complement activation
Collectins - plasma proteins that bind to microbial cell walls

33
Q

What is phagocytosis?

A

process in which cells such as neutrophils and macrophages ingest solid particles

34
Q

What does acute inflammation look like?

A
  • serous
  • catarrhal
  • fibrinous
  • hemorrhagic
  • suppurative
  • membranous
  • pseudomembranous
35
Q

Serous?

A

protein rich fluid exudate

36
Q

Catarrhal?

A

mucus hypersecretion

37
Q

Fibrinous?

A

exudate contains plentiful fibrin

38
Q

Hemorrhagic?

A

severe vascular injury

39
Q

Suppurative?

A

production of pus

40
Q

Membranous?

A

epithelium coated by fibrin

41
Q

Pseudomembranous?

A

superficial mucosal slough

42
Q

What is suppuration?

A

formation of pus - due to mainly neutrophils also bacteria, cellular debris
- caused almost always by an infective agent

43
Q

What is an abscess?

A

a collection of puss surrounded by a membrane of sprouting capillaries, neutrophils and occasional fibroblasts

44
Q

What happens to a drained abscess?

A

the abscess cavity collapses and is obliterated by organisation and fibrosis

45
Q

How may deep seated accesses drain?

A

along a sinus tract or fistula

46
Q

What is a fistula?

A

abnormal connection between two hollow spaces (blood vessels, intestine, hollow organs)

47
Q

What is an ulcer?

A

a local defect or excavation of the surface of an organ or tissue that is produced by the sloughing of inflammatory necrotic tissue

48
Q

What is sloughing/slough?

A

dead tissue sperating from living tissue

49
Q

What is necrotic tissue?

A

death of cells or tissues due to injury/disease especially in a localised area of the body

50
Q

Where is ulceration most commonly found?

A
  • inflammatory necrosis of the mucosa - mouth, stomach, intestine
  • chronic leg ulcers in those with circulatory disturbance
51
Q

What are the beneficial effects of acute inflammation?

A
  • dilution of toxins - (then can be carried away by lymphatics)
  • entry of antibodies - (due to increased vascular permeability)
  • fibrin formation - (impedes movement of microorganisms)
  • transport of drugs - (eg antibiotics)
  • delivery of nutrients and oxygen - (aided by increased fluid flow)
  • stimulation of immune response - (fluid exudate containing antigens reaches local lymph nodes)
52
Q

What are the harmful effects of acute inflammation?

A
  • digestion of normal tissues
  • swelling - eg. brain swelling, laryngeal oedema
  • inappropriate inflammatory response - eg. type I hypersensitivity (allergic reaction)
53
Q

What are the systemic effects of acute inflammation?

A
  • pyrexia (fever) -
  • constitutional symptoms
  • reactive hyperplasia of the reticuloendothelial system
  • haematological changes
54
Q

Explain pyrexia in acute inflammation?

A

elevation in temperature may improve efficiency y of leukocyte killing and probably impairs the replication of many offending microorganisms

55
Q

What are constitutional symptoms?

A

Constitutional symptomsrefers to a group ofsymptomsthat can affect many different systems of the body. eg. weight loss, malaise, nausea …

56
Q

Explain weight loss in inflammation?

A
  • due to negative nitrogen balance - especially when there is extensive chronic inflammation
57
Q

What is reactive hyperplasia of the reticuloendothelial system?

A

?

58
Q

What haematological changes can occur as a result of inflammation?

A
  • increased erythrocyte sedimentation rate (rate at which red blood cells separate from serum)
  • anaemia (low red blood cells)
  • leukocytosis (increased white blood cells)