Acute Tissue Injury And Infection

Question 1

Outcomes of acute inflammation

Answer 1

Chronic inflammation, resolution, organisation (to scar/adhesion), dissemination (sepsis, shock, death)

Question 2

Resolution of inflammation

Answer 2

Elimination of injury, complete restitution of the architecture , danger signals wane, anti-inflammatory signals predominate

Question 3

Anti-inflammatory signals

Answer 3

Neutrophil apoptosis triggers inflammatory cytosine synthesis

Anti-inflammatory mediators derived from lipids promote activities such as scavenging for debris - combined with complement inhibitors result in reduction in inflammatory environment

Neuroendocrine inhibition

Stress hormones: cortisol and catecholamines (anti-inlammatories), vagus nerve effects (releases sympathetic inhibitors which create an anti-inflammatory environment

Anti-inflammatory cytokines inhibits sickness behaviours

Question 4

Danger signals

Answer 4

Extravasation diminishes - fewer leukocytes so less exudate

Neutrophil apoptosis increases

Pro-inflammatory mediators are broken down

Question 5

Steps of resolution

Answer 5

Fluid drains into the lymphatic so vascular permeability normalises

Cells either drain into lymphatic or are degraded by macrophages

Recovery of tissue depends on site of inflammation and anatomy

Question 6

Macrophages

Answer 6

Key cell secretes anti-inflammatory cytokines and clear debris

Question 7

Dissemination

Answer 7

Host response to infection causing widespread inflammatory response —> via a cytokine storm

Body reacts to infection by hyperactivity immune response - causing a depletion of inflammatory proteins, resulting in individual becoming immunosuppressed

Question 8

Sepsis

Answer 8

Life threatening organ dysfunction caused by disregulated host response to infection

Question 9

Septic shock

Answer 9

Sepsis with high serum lactase and refractory low blood pressure due to vasodilation

Production of lactic acid sign of necrosis due to tissues undergoing anaerobic glycolysis

Question 10

Immune system checkpoints

Answer 10

Assesses whether a inflammatory response should be triggered

Question 11

Immune system checkpoints in vital tissues

Answer 11

Fewer checkpoints ca trigger inflammation -> resulting in greater risk of inflammation causing damage

Question 12

Types of immune system checkpoints

Answer 12

Virulence - system surveillance e.g. altered phosphorylation

Viability - bacteria/viral nuclei acid present

Extent of cell injury and resident macrophage density

Soluble vs particle

Question 13

Plasma protease systems

Answer 13

Are mutually activating —> if you activate a compliment cascade you will also activate a clotting cascade

If one becomes dysregulated they all become dysregulated

Question 14

Immunothrombosis

Answer 14

Coagulation as inflammation

Question 15

Immunothrombosis pathway

Answer 15

DAMP recognised -> monocytes deliver tissue factor -> fibrin coats bacteria -> complement C3a and C5a activates platelets -> platelets migrate, scavenge and bundle up bacteria for neutrophils -> neutrophils activate and undergo NETOSIS -> Net trap intravascular microbes

Question 16

Immunothrombosis in sepsis

Answer 16

Many micro clots occur to try trap pathogen -> depleting clotting factors -> so circulation cannot be repaired resulting in bleeding through capillaries into soft tissue

Question 17

Tissue ischaemia

Answer 17

Tissues not receiving adequate oxygen -> usually as not receiving enough blood

Question 18

Foreign bodies

Answer 18

Cause immunosuppressive in the area as phagocytes are distracted - resulting in depleted response to other pathogens

Question 19

Phagocytosis can be undermine if

Answer 19

Bacteria have slimy capsules, decoy foreign bodies (sutures), slime, pathogens using intracellular organisms to evade