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MBChB Year 1 Principles Pathology > Inflammation 1 > Flashcards

Inflammation 1 Flashcards

1
Q

What can cause inflammation?

A

Injury (infection), trauma, foreign bodies, immune reactions and necrosis

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2
Q

What is the response to injury?

A

Vascular changes and cellular changes through chemical mediators and morphologic patterns

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3
Q

What are the vascular changes that occur?

A

Changes in flow and vessel caliber (vasodilation), which first involves arterioles then capillary beds

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4
Q

What mediates vascular changes?

A

Histamine and nitric oxide

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5
Q

What is the result of vascular changes?

A

Increased heat (calor) and redness/erythema (rubor)

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6
Q

What are the 5 types of cellular changes?

A

Stasis (inhibition of cell growth), white cell margination, rolling (leukocytes slow down and adhere to the wall), adhesions and migration

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7
Q

What is the normal flow of blood?

A

Central within a vessel. With dilation the rate of flow slows and cells are able to move peripherally (especially large white cells) - also white cell margination (migration towards vessel walls)

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8
Q

Why can cells stick to vessels in inflammation and not normally?

A

Normally the vessel walls are too slippy so blood cells can’t stick, however in inflammation the vessels express proteins on the lumens surface that match a protein on the white cell surface (lock and key - ligands)

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9
Q

What specific molecules are expressed on cell walls?

A

Selectins, integrins, vascular cell adhesion molecules (VCAM) and intercellular adhesion molecule (ICAM)

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10
Q

What do integrins bind to?

A

ICAM

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11
Q

Is integrin/selectin interaction with ligands low or high affinity?

A

Low affinity (binding on AND off is fast)

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12
Q

What increases selection expression?

A

Histamine and thrombin (from inflammatory cells)

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13
Q

What increases endothelial cell expression of VCAM and ICAM?

A

Tumour necrosis factor (TNF) and interleukin-1 (IL-1)

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14
Q

What do chemokines from the site of injury bind to?

A

Proteoglycans on the endothelial cell surface (which then increase the affinity of VCAMs and ICAMs for integrins

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15
Q

What are leaky vessels?

A

The loss of proteins from inside the cell to outside, which then causes water to follow = change in the cell’s osmotic balance (swelling)

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16
Q

Why do vessels leak?

A

Endothelial contraction, direct injury, white cells, transcyotisis and new vessel formation

17
Q

What molecule makes new vessels but also increases leakiness?

A

Vascular endothelial growth factor (VEGF)

18
Q

What is chemotaxis?

A

Cells follow a chemical gradient and move along it (involves bacterial components, complement, leukotrienes and cytokines (interleukins)

19
Q

What are the 3 phases of phagocytosis?

A

Recognition/attachment, engulfment and killing/degradation

20
Q

What are the recognition receptors in phagocytosis?

A

Mannose receptors, scavenger receptors and opsonins

21
Q

Why are mannose receptors used in phagocytosis?

A

Bacterial surface glycoproteins and glycolipids contain (terminal) mannose residues but mammalian glycoproteins and glycolipids do not (they have silica acid or N-acetylgalactosamine)

22
Q

Why are scavenger receptors used in phagocytosis?

A

Similar to mechanism that phagocytes recognise low density lipoproteins

23
Q

Why are opsonins used in phagocytosis?

A

Bacteria are protein coated so they stand out from ‘self’ cells. These coats include components of the complement cascade as well as immunoglobulin (IgG)

24
Q

What happens in engulfment in phagocytosis?

A

Pseudopods are formed (fake limbs) as are vesicles (phagosomes) that join with lysosomes (phagolysosomes)

25
Q

What happens in killing and degradation in phagocytosis?

A

NAPDH oxidase helps oxygen to gain an electron from NAPDH to become superoxide. Nitric oxide synthase combines NO with superoxide to produce ONOO

26
Q

What are the 4 pillars of inflammation?

A

Rubor, tumor, calor and dolor

27
Q

What is rubor?

A

Redness caused by increased perfusion, slow blood flow and increased permeability of vessels

28
Q

What is calor?

A

Heat caused by increased perfusion, slow blood flow and increased permeability of vessels

29
Q

What is tumor?

A

Swelling due to vascular changes (eg more perfusion, slow flow and increased permeability)

30
Q

What is dolor?

A

Pain mediated by prostaglandin and bradykinin

31
Q

What is functiono laesa?

A

Loss of function (technically the 5th pillar of inflammation but not always included)

32
Q

What inflammatory cell characterises acute inflammation?

A

Neutrophil (a polymorph/many lobes to the nucleus and granulocyte with phagocytic and cytotoxic abilities)

MBChB Year 1 Principles Pathology (3 decks)

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