39: Systemic Effects of Inflammation

CBC changes seen in acute/chronic inflammation

Leukocytosis → neutrophilia

CBC changes seen in inflammation that progressing towards septic shock

Can see leukocytosis (neutrophilia) or leukopenia (neutropenia) depending on the amount of tissue consumption

Left shift

Dipping into younger and immature cell populations

Mediators that cause fever

Prostaglandins

Mediators that stop fever

Neurotransmitters

Source of APPs

Do we even have to ask…(liver)

3 key APPs that increase during inflammation

• C reactive protein (CRP)

• Fibrin

• Serum amyloid A (SAA)

Cytokines that direct APP production

I present, your acute inflammatory cytokines:

• TNF

• IL-1

• IL-6

Functions of APPs

• Opsonization

• Bind chromatin

• Clear necrotic debris

• RBC rouleax formation

Clinical relevance of APPs

Easy to measure stall/cage side and assess systemic inflammation

Downside of SAA

Can cause secondary amyloidosis during prolonged inflammation

Shock

Decrease CO → decreased perfusion → cellular hypoxia → cell death

Types of shock

• Cardiogenic

• Hypovolemic

• Septic

Type of shock associated with inflammation

Septic

Inflammatory processes that are widespread in SIRS

• Vasodilation

• Leaky vessels

• Leukocyte adhesion

• Endothelial damage

Role of M1 in SIRS

Encourages inflammation to the point of wreaking havoc; also causes prostaglandin and histamine release

Cause of sepsis

Bacterial/endotoxic products running rampant systemically, causing acute inflammation everywhere

Necropsy finding that may indicate endotoxemic shock

Adrenal gland necrosis: massive cortisol release → gland gets tired → dies

End stage condition of sepsis

DIC