Lecture 19: How the Body Responds to Injury Flashcards

1
Q

what are the cells involved in acute inflammation

A

neutrophil granulocytes and polymorphs

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2
Q

what are the 5 Rs of the inflammatory process

A
Recognition 
Recruitment
Removal
Regulation
Resolution
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3
Q

what happens during vasodilation

A
  • increased amount of blood but slower blood flow

- causes stasis of blood and an increase in hydrostatic pressure beyond normal levels

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4
Q

what happens during acute inflammation

A

1) vasodilation
2) increased vascular permeability and extravasation of fluid
3) emigration of leukocytes, primarily neutrophil polymorphs

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5
Q

what are the types of oedema

A
  • exudate: high in proteins and may contain some white and red blood cells
  • transudate: mainly the leaking of fluids, low in proteins
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6
Q

how are tissues drained of fluid

A

tissues drained through lymph nodes back into venous system via thoracic duct

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7
Q

what causes increased vascular permeability

A

histamine and NO cause endothelial cells to contract

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8
Q

how do phagocytic leukocytes leave the vasculature and what are the processes mediated by

A
  • margination and rolling along the vessel wall. mediated by selectins upregulated by TNF and IL-I
  • adhesion to the activated endothelium. mediated by VCAM-I and ICAM-I integrins upregulated by TNF and IL-I
  • emigration through the vessel wall into the surrounding tissues. mediated by CD31 / PECAM-I
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9
Q

what allows amoeboid movement of the leukocytes

A

leukocyte forms processes from contractile cytoplasmic microtubules

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10
Q

what are the mediators in vasodilation

A
  • histamine
  • NO
  • prostaglandins
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11
Q

what are the mediators in increased vascular permeability

A
  • histamine
  • bradykinin
  • leukotrienes
  • complement C3a and C5a
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12
Q

what are the mediators in chemotaxis and leukocyte recruitment

A
  • TNF
  • IL-I
  • complement C3a and C5a
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13
Q

what are the mediators in fever

A
  • TNF
  • IL-I
  • prostaglandins
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14
Q

what are the mediators in pain

A
  • prostaglandins

- bradykinin

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15
Q

what are the mediators in tissue and cell damage

A
  • ROS
  • NO
  • lysosomal enzymes from leukocytes
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16
Q

what are the types of harmful inflammation and what do they look like

A
  • serous inflammation because of effusion (collection of fluid)
  • fibrinous inflammation with effusion and lots of fibrin
  • purulent inflammation because of effusion and lots of pus and neutrophils
  • ulceration (destruction of an epithelial structure due to abscess)
17
Q

causes of chronic inflammation

A
  • immune mediated inflammatory diseases, eg Crohn’s disease
  • persistent infections, eg some viral and fungal infections
  • inability to heal, eg chronic peptic ulcer of the stomach
  • prolonged exposure to toxic agents, eg silicosis of the lung
18
Q

what is a granuloma

A
  • an area of activated epithelioid macrophages
  • pallisated if surrounded by leukocytes, naked if not
  • caseating if shows central necrosis, non-caseating if not
  • may fuse to form giant multinucleated cells
19
Q

what are granulomas characteristic of

A
  • mycobacterial infection
  • sarcoidosis
  • may be idiopathic or caused by drugs
20
Q

what are the dominant cells in acute and chronic inflammation

A

acute: neutrophil
chronic: lymphocyte

21
Q

what is eosinophil accumulation mediated by

A

IgE produced by plasma cells

22
Q

what is healing by primary and secondary intention

A
  • primary: when the skin edges come together properly

- secondary: wound is too large / other factors interfere with skin edges coming together properly

23
Q

what are important examples of metaplasia

A
  • oesophagus: squamous epithelium –> columnar epithelium due to gastric content reflux (Barrett’s)
  • bronchus: pseudostratified ciliated columnar epithelium –> squamous epithelium due to smoking
  • cervix: columnar endocervical mucosa –> squamous epithelium sue to HPV infection