Unit 2- Inflammation Flashcards

1
Q

What occurs internally when there is heat/ redness in an inflammatory response?

A

dilation of blood vessels/ arterioles (redness) leads to increased blood flow (heat)

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2
Q

What is Vasodilation?

A

widening of blood vessels resulting from relaxation of smooth muscle cells affected by mediators (chemicals) released by immune cells and nervous activity in the peripheral nervous system

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3
Q

What happens internally when the body swells in an inflammatory response?

A

Oedema- protein concentrate of the exudate is less than that of the blood.
Epithelial cells increase permeability of capillary walls in response to specific mediators (histamines/ cytokines)- they contract and allow fluid into the extracellular space.

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4
Q

What are Nociceptors?

What are the three types?

A

Nerve endings that react to damaging stimuli and send signals to the spinal cord and brain (leads to perception of pain)

  1. Mechanosensitive- stimulated by mechanical stress/ damage to tissues
  2. Thermosensitive- stimulated by extremes of heat and cold
  3. Chemosensitive- stimulated by chemicals, pH etc
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5
Q

What are the benefits of Nociceptors?

A
  • transmitted rapidly in sensory A nerve fibres
  • Accurately localised- tells you a specific area in a small receptive field
  • Affected by mediated released by immune cells
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6
Q

Briefly describe the steps to Trans- endothelial cell migration?

A
  1. Injury- Macrophages become activated & produce chemokines
  2. Chemokines diffuse from the centre of cell activation to the capillaries- effecting blood flow and permeability
  3. Neutrophil will change its shape & start sticking to epithelial cells in a process called ‘rolling’.
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7
Q

What is trans endothelial cell migration?

A

where leukocytes move out of blood vessels in a well orchestrated series of steps in the absence of an endothelial cell injury

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8
Q

Which cells activate platelets?

A

Thrombin (Part of coagulation cascade)
Phosphatidylserine (damaged cells)
Collagen exposed following endothelial cell damage

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9
Q

What is the first line of defence in Acute Inflammation?

A

Tissue resident cells- degranulation of

mast cells at mucosal surfaces leads to release of histamine

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10
Q

What is the second line of defence in Acute Inflammation?

A

Infiltration of Polymorphs
e.g. Neutrophils, Eisonphils, Basophils
highly phagocytic, contain preformed proteases

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11
Q

What is the third line of defence in Acute Inflammation?

A

Monocytes
Clear dead host cells, highly phagocytic but also release mediators such as cytokines.
Express MHC molecules to kickstart adaptive immune response

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12
Q

What is the fourth line of defence in Acute Inflammation?

A

Increased production- stimulation of progenitor cells in bone marrow by colony stimulating factors (CSFs)

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13
Q

What is Systemic Inflammation and what is it caused by?

A

Chronic activation of immune system

Caused by cytokines being released into the circulation causing elevation of the set point of the hypothalamus

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14
Q

What can Systemic Inflammation lead to?

A

Cytokine Storm- hyperproduction of cytokines leading to shock

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15
Q

What are the three stages of wound healing?

A
  1. Inflammatory- substrate [1-7 days]
  2. Proliferative - repair phase [3014 days]
  3. Maturation- remodelling phase [14+ days]
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16
Q

What happens in the decline of the Inflammatory phase?

A
  • loss of stimulus (therefore altered cell signalling)

- fewer inflammatory factors are secreted and macrophages are reduced at the wound site

17
Q

How do Macrophages aid in the Proliferation stage of wound healing?

A

secret growth factors
cytokines attract cells involved in proliferation
produce factors that induce angiogenesis

18
Q

What is Angiogenesis and what is it stimulated by?

A

formation of capillary buds to produce new blood vessels
stimulated by TGF-beta (transforming growth factor), FGF (fibroblast growth factor), and PDGF (platelet derived growth factor)

19
Q

How are Fibroblasts involved in tissue repair?

A

Migration & Proliferation of Fibroblasts via growth factors- fibroblasts synthesise the extracellular matrix and collagen (structural frameworks)

20
Q

What is Purulent/ Suppurative Inflammation?

A

persistent or excessive necrosis- normally induced by bacteria

21
Q

What can tissue necrosis lead to?

A

accumulation of pus in the cavity leading to granuloma formation

22
Q

What types of Granuloma are formed during necrosis?

A
  1. Foreign body granuloma
  2. Immune Granuloma
  3. Abscess
23
Q

What are the consequences of Chronic Inflammation? (2)

A
  1. Tissue Dysfunction- persistent infection leads to constant stimulation of immune system leading to Cortisol release (stress hormone) which affects metabolism
  2. Neurodegenerative diseases- cytokines in the brain can affect neurotransmission