Infection, Inflammation, Sepsis, and Pneumonia Flashcards
1
Q
What is infection?
A
- Invasion of tissues by pathogens
2
Q
What is inflammation?
A
- Complex protective reaction
- Body’s response to invasion
- Damaging agents destroyed, diluted
- Without inflammation, survival not possible
- Process has consequences- potentially harmful (autoimmune)
- Local or systemic (e.g. sepsis)
- Acute or chronic
3
Q
What are the cardinal signs of inflammation?
A
- Rubor, calor, dolor, tumour, loss of function
- Increased blood flow- vascular dilation- redness and heat
- Increased vascular permeability gives oedema- welling
- Certain chemical mediators stimulate nerve endings- pain (also stimulated by stretching from oedema)
- Pain and swelling can result in loss of function
4
Q
What are the components of inflammation?
A
- Vasodilation- increases blood delivery, increase temp, removes toxins
- Exudate- delivers immunoglobulins, etc, dilutes toxins, fibrinogen, increase lymphatic drainage
- Increased lymphatic drainage- bugs, phagocytes and antigens to immune system
- Cells- killers, phagocytosis removes pathogenic organisms
5
Q
What are the phases of inflammation?
A
- First, dilation of vessels
- Fluid leads to interstitial due to increased permeability of vessels
- Second, cells move into interstitium
6
Q
Describe oedema fluid
A
- Transudate has low protein content
- Usually caused by alterations in hydrostatic/ oncotic pressure, implies a hydrostatic problem
- An exudate has a high protein content, caused by increased vascular permeability
- Implies inflammation
7
Q
What cells are involved in inflammation?
A
- Endothelium cells- adhesion molecules (neutrophils can stick, roll and migrate from endothelial cells)
- Neutrophils degranulate
- Interleukin and cytokines destroy- cellular damage
- Cells not entirely specific
8
Q
What are the effects of mediators of inflammation?
A
- Vasodilation- prostaglandins, NO
- Vascular permeability- histamine, serotonin, C3a, C5a, bradykinin
- Fever- IL1,6, TNF-α, prostaglandins
- Pain- prostaglandins, bradykinin
- Tissue damage- neutrophil and macrophage lysosomal enzymes, oxygen metabolites
9
Q
What is sepsis?
A
- Systemic response to infections
- Life-threatening
- Organ dysfunction= breakdown in regulation of inflammatory response
10
Q
What is SIRS?
A
- Systemic inflammatory response
- Rise in temp
- Pyrexia= clinical signs
- Tachycardia >90
- Tachypnoeic- >20 breaths/minute
- Leucocytosis- high white cell >12,000mm³ or < 4,000mm³ or >10% immature neutrophils
- Non-specific
- SIRS also caused by trauma, burns, pancreatitis, and other insults
11
Q
What is sepsis?
A
- SIRS with presumed or confirmed infectious process
- Severe sepsis- involves 1 acute organ failure
- Septic shock- severe sepsis with hypotension refectory to adequate volume resuscitation
12
Q
Describe the pathogenesis of sepsis?
A
- Injury- invading pathogens
- Local inflammatory cells
- ICAMS- intracellular adhesion molecules
- Neutrophils adhesion (activation of cytokines/coagulation)
- Amplification and systemic overspill
- Leads to SIRS/ Sepsis
13
Q
What is ATP bioenergetics?
A
- Cell survival
- Mitochondria
- Reduction in ATP–> bioenergetic failure, resulting in mitochondria failure (leads to cell death)
- Less oxygen
- Leads to sepsis
14
Q
What organisms may cause Sepsis?
A
- Only 60% have conformed infection
- Similar clinical picture with all
- Gram +ve/-ve
- Positive- thick peptidoglycan layer
- Negative- thin peptidoglycan layer
15
Q
What are important gram negatives?
A
- Medically relevant cocci- Neisseria sps, Moxarella
- Medically relevant bacilli/ coccobacilli
- Lungs- haemophilus, klebsiella, psuedomonas legionella
- Urine- E coli, enterobacter, proteus
- GIT- salmonella, helicobacter
