Inflammation and Healing Flashcards Preview

Phase 2a - Introductory Clinical Sciences > Inflammation and Healing > Flashcards

Flashcards in Inflammation and Healing Deck (94)
Loading flashcards...
31

what is the effect of histamine?

dilates vessel
increases vascular permeability

32

describe the role of tissue macrophages in acute inflammation

secrete chemical mediators that attract neutrophil polymorphs to the site

33

describe the role of the lymphatics in acute inflammation

channels dilate, and drain away the oedema fluid, limiting swelling.
antigens are carried to regional lymph nodes for recognition by lymphocytes.

34

what is the major role of neutrophil polymorphs in acute inflammation?

PHAGOCYTOSIS

35

describe the steps of phagocytosis

1. adhesion of particle to cell surface (opsonisation facilitates)
2. ingestion of particle by sending out pseudopodia
3. fusion of lysosomes with the phagosome - phagolysosome
4. intracellular killing of microorganism

36

list the five terms used to describe special macroscopic appearances of acute inflammation - as dependent on the type of tissue involved and the type of agent provoking the inflammation.

serous
suppurative (purulent) inflammation
membranous inflammation
pseudomembranous inflammation
necrotising (gangrenous) inflammation

37

describe some beneficial effects of acute inflammation

dilution of toxins - allows them to be carried away in lymphatic.
entry of antibodies - phagocytosis, toxin neutralisation.
transport of drugs (antibiotics) to inflamed area
fibrin formation impedes movement of microorganisms.

38

describe some harmful effects of acute inflammation

vascular damage.
swelling - e.g. airway obstruction
inappropriate inflammatory response - type 1 hypersensitivity reactions (e.g. hayfever)

39

what factors determine the outcome of acute inflammation?

type of tissue involved.
amount of tissue destruction.
both of these depend on nature of injuring agent.

40

what is the usual result of acute inflammation?

resolution

41

what causes acute inflammation to progress to suppuration?

excessive exudate

42

what causes acute inflammation to progress to organisation?

excessive necrosis

43

what causes acute inflammation to progress to chronic inflammation?

persistent causal agent

44

what conditions favour resolution of acute inflammation?

minimal cell death/tissue damage.
occurred in organ with regenerative capacity (e.g. liver)
rapid destruction of causal agent
rapid removal of fluid/debris - good local vascular drainage.

45

what is pus?

a mixture of living/dying/dead neutrophils and bacteria, cellular debris and possibly globules of lipid

46

what conditions favour progression of acute inflammation to organisation?

large amounts of fibrin.
lots of necrotic tissue.
exudate and debris not removed/discharged

47

what are the systemic effects of inflammation?

pyrexia.
constitutional symptoms.
weight loss.
reactive hyperplasia of reticuloendothelial system.
haematological changes.
amyloidosis.

48

what are the predominant cells seen in chronic inflammation?

lymphocytes, plasma cells and macrophages
(also fibroblasts and multinucleate giant cells)

49

list the causes of chronic inflammation

primary chronic inflammation
transplant rejection
progression from acute inflammation
recurrent episodes of acute inflammation

50

give some examples of causes of primary chronic inflammation

TB, leprosy, viral infections - resistance to phagocytosis.
endogenous - necrotic adipose tissue, bone
exogenous - silica, asbestos, sutures, prostheses
autoimmune diseases
chronic IBD eg ulcerative colitis
primary granulomatous diseases - Crohn's, sarcoidosis

51

what are the macroscopic appearances of chronic inflammation?

chronic ulcer
chronic abscess cavity
thickening of wall of a hollow viscus
granulomatous inflammation
fibrosis

52

describe the cellular infiltrate seen in chronic inflammation

lymphocytes, plasma cells and macrophages.
possibly a few eosinophil polymorphs, but no neutrophil polymorphs.
some macrophages may form neutrophil giant cells.

53

describe the differences between macrophages and neutrophil polymorphs

macrophages can ingest a wider range of materials.
neutrophil polymorphs last 3 days - destroy themself when they ingest microorganisms.
Macrophages are long-lived - if they can't kill ingest microorganisms, they will harbour them.

54

give some examples of organisms that can survive inside macrophages

mycobacteria - M tuberculosis and M leprae.
histoplasma capsulatum.

55

what are macrophages derived from? what system does this make them part of?

blood monocytes.
mononclear phagocyte system aka reticuloendothelial system.

56

define a granuloma

aggregation of epithelioid histiocytes

57

what cell types does a granuloma contain?

epithelioid histiocytes
also possible - lymphocytes and histiocytic giant cells

58

give some examples of granulomatous disease

Tuberculosis
leprosy
Crohn's disease
sarcoidosis

59

describe the morphology of an epithelioid histiocyte

vague histological resemblance to epithelial cells.
large vesicular nuclei
eosinophilic cytoplasm.
elongated.
arranged in clusters.

60

name a major secretory product of epithelioid histiocytes

angiotensin-converting enzyme
can use ACE levels as a marker for systemic granulomatous disease (e.g. sarcoidosis)