Phagocytosis, Complement And Oedema Flashcards Preview

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Flashcards in Phagocytosis, Complement And Oedema Deck (14):
1

What happens during phagocytosis?

• Immune cells engulf pathogen
• Phagosome forms
• Lysosomes fuse to the phagosome forming a phagolysosome
• Lytic enzymes are released by the lysosomes and digest the pathogens
• Macrophage presents antigens on cell surface membrane --> APC

2

How does a macrophage kill pathogens once they have been engulfed?

• Macrophages produce toxic chemicals, such as nitric oxide, that can kill surrounding cells.
• Phagolysosomes produce, antimicrobial peptides, and lysozyme.
• The phagolysosome is also a nutrient-limiting environment.

3

What is opsonisation?

• Anitbody Opsonization is the process by which a pathogen (virus, fungi or bacteria that causes disease) is marked of ingestion and destruction by a phagocyte (white blood cells that protects the body by ingesting harmful foreign particles)
• Involves the binding of an opsonin i.e., antibody, to a receptor on the pathogen’s cell membrane.
• After opsonin binds to the membrane, phagocytes are attracted to the pathogen.
• Summary - Opsonization is a process in which pathogens are coated with a substance called an opsonin, marking the pathogen out for destruction by the immune system.

4

What is complement?
Note = It's not necessary to know the function of all the complement factors

It is the response of a group of serum proteins to the recognition of molecular components of microorganisms. They become sequentially activated in an enzyme cascade – the activation of one protein enzymatically cleaves and activates the next protein in the cascade.

5

Describe how complement leads to activates inflammation, cell lysis and participates in oponization
Note = It's not necessary to know the function of all the complement factors

Complement can be activated via three different pathways (including classical and alternative), which can each cause the activation of C3, cleaving it into a large fragment, C3b, that acts as an opsonin, and a small fragment C3a (anaphylatoxin) that promotes inflammation.
- Activated C3 can trigger the lytic pathway, which can damage the plasma membranes of cells and some bacteria.
- C5a, produced by this process, attracts macrophages and neutrophils and also activates mast cells.

6

What is oedema?

An accumulation of an excessive amount of watery fluid in cells, tissues or serous cavities

7

What is lymphoedema?

• Lymphoedema – Swelling (especially in subcutaneous tissues) as a result of obstruction of lymphatic vessels or lymph nodes and the accumulation of large amounts of Lymph in the affected region

8

How can you distinguish between oedema and lymphoedema?

Lymphoedema does not pit (on touch) as it is protein rich, stimulates fibroblast proliferation which produces collagen

9

What happens in congestive heart failure?

In Congestive Heart Failure the right and left ventricle are not pumping properly so they dilate. Venous blood ‘dams up’ because the right ventricle cannot cope with the venous return.

10

What is the significance of starling forces?

Governs whether fluid moves into capillaries (absorption) or out of capillaries (filtration)

11

What causes capillary hydrostatic pressure?

Capillary hydrostatic pressure is caused by the force that the blood exerts on the walls of the capillaries – draws fluid out of vessels

12

What causes capillary oncotic pressure?

Capillary oncotic pressure is due to proteins in the circulating blood that draw fluid into vessel – draws fluid into vessels

13

Describe and explain the changes in pressure along a capillary

From arterial to venous end of a capillary
-Hydrostatic (blood) pressure decreases (35 -> 15mmHg)
-Oncotic pressure is constant (25mmHg)

Arterial end net filtration pressure is +10 mmHg (35-25)
Fluid exits the capillary (hydrostatic pressure > osmotic pressure)

No net movement of fluid in the middle of the capillary
(hydrostatic pressure = osmotic pressure)

Venous end filtration pressure is -10 mmHg (15-25)
Fluid re-enters capillary (hydrostatic pressure < osmotic pressure)

14

How can venous hypertension lead to skin staining?

• HighBP in venous system
• Blood backs up and the pressure increases
• Skin staining is caused by red blood cells leaking out into tissue fluid surrounding cell
• Causes haemosyderin stain, rust like in appearance
• Ferrous oxide in haemoglobin --> ferric oxide (rust)