Acute Inflammation Flashcards
1
Q
Causes of Injury
A
- Trauma
- Infection
- Heat/cold
- Chemical
- Infarction
2
Q
Inflammation Process
A
- Injury
- Inflammation: neutrophils
- Demolition: macrophages
- Repair: angiogenesis
3
Q
Inflammation: Important Features
A
- Blood components: WBCs, proteins
- Blood vessels: deliver mediators
- Chemical mediators: drivers of inflammation
- Cellular and extracellular components of CT
4
Q
Acute Inflammation
A
- Earliest response
- Last days
- Features: neutrophils, oedematous exudate, vasodilation
- Non-specific
5
Q
Chronic Inflammation
A
- Later response
- Lasts weeks/months/yrs
- Features: macrophages, lymphocytes, plasma cells, assoc fibrosis/scaring
- Specific or nonspecific
6
Q
Aims of A. Inflammation
A
- Deliver nutrients and defence cells
- Destroy any infective agents
- Remove debris
7
Q
Features of A. Inflammation
A
- Vascular response
- Exudate
- Variable tissue necrosis
8
Q
A. Inflammation: Vascular and Cellular Response
A
- initial dilatation of focal blood vessels increasing blood flow, then blood flow slows
- Vessels become leaky and permeable, permitting the passage of water, salts and small proteins from the plasma into the damaged area (exudation)
- Circulating neutrophils are attracted to the damaged area and adhere to swollen endothelial cells (margination) and migrate through BM (emigration) into damaged area
- Later, macrophages and lymphocytes migrate to damaged area
9
Q
Exudate
A
Protein rich fluid and cells that have escaped from blood vessels due to an increase in vascular permeability
10
Q
Components of A. Inflam Exudate
A
- Fluid: carries nutrients and mediators
- Fibrin: network of fibrin prevents migration of micro-organisms and produces a scaffold for migration of neutrophils and macrophages through damaged area
- Many neutrophils: ingest and kill offending agents
- Few macrophages and lymphocytes
11
Q
Types of A. Inflam Exudate
A
- Serous
- Fibrinous
- Purulent
- Suppurative
- Hemorrhagic
12
Q
Serous Exudate
A
- Absence of prominent cellular response
13
Q
Fibrinous Exudate
A
- Contains large amounts of fibrin
- Usually if injury is quite severe
- Often in lungs
14
Q
Purulent and Suppurative Exudate
A
- Usually bacterial cause
- Contains cellular response (mainly neutrophils)
- Suppurative: purulent exudate + significant liquefactive necrosis (pus)
15
Q
Hemorrhagic Exudate
A
- Contains many RBCs from damaged and ruptured blood vessels
16
Q
Chemical Mediators of AI
A
- Cell-derived mediators
- Plasma-derived mediators
17
Q
Learn Table in Slides!!
A
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18
Q
Neutrophils
A
- Produced by maturation of precursor cells in bone marrow
- Short life span (hours)
- Motile
- Chemical mediators attract them to damaged area
- Phagocytic
- Release free radicals
- Release lysosomal enzymes to breakdown extracellular matrix when they die -> pus
19
Q
Neutrophilia
A
- Raised neutrophil count in blood
- Usually due to bacterial infection
- Cytokines (IL1 and TNF) released from macrophages and neutrophils circulate in the blood and stimulate increased neutrophil release and increased production of neutrophils in the bone marrow
20
Q
Monocytes/Macrophages
A
- Monocytes in blood
- Macrophages in tissue
- Diff functions in diff parts of the body
- Monocytes leave circulation at sites of inflammation, phagocytose tissue debris and pathogens
- Live longer and larger than neutrophils
21
Q
Signs of Acute Inflammation
A
- Redness: vessel dilatation and increased blood flow
- Heat: same as above
- Pain: pressure effects on nerve endings and chemical factors
- Swelling: accumulation of exudate
- Loss of function: direct local damage
22
Q
Types of AI
A
- Depend on site and cause of inflammation
- Purulent: large quantities of pus consisting of neutrophils, necrotic cells and oedema, abcesses
- Fibrinous: more severe injuries = greater vascular permeability and vessels more permeable to fibrin
- Serous: outpouring of thin fluid e.g. blister
23
Q
Systemic Effects of AI
A
- Fever
- Decreased appetite
- Malaide, myalgia, arthralgia
24
Q
Fever
A
- Release of exogenous pyrogens from bacteria or viruses -> stimulate production of endogenous pyrogens (cytokines e.g. IL1 and TNFA) and interferons
- Endogenous pyrogens stimulate prostaglandin synthesis within the vascular and perivascular cells of the hypothalamus
- These prostaglandins stimulate the production of neurotransmitters to reset body temp at a high level
25
Q
Outcomes of AI
A
- Resolution
- Variable regeneration and organisation (repair)
- Chronic inflammation
26
Q
Fibrin vs Fibrosis
A
- Fibrin: Plasma protein that forms a scaffold (cleaved by enzyme - fibrinogen -> fibrin)
- Fibrosis: scar tissue formation - mainly consisting of collagen
27
Q
Acute Appendicitis
A
- Mainly a disease of adolescents and young adults
- Usually due to a luminal obstruction
28
Q
Pathogenesis of Acute Appendicitis
A
- Luminal obstruction
- Continued secretion of mucus -> increased pressure
- Possible mucosal ischaemia
- Mucosal injury
- Acute mucosal inflammation
- Secondary bacterial invasion
- Spread of inflammation transmurally
29
Q
Stages of Acute Appendicitis
A
ESG
- Early acute appendicitis (mucosal inflam)
- Acute suppurative (pus) appendicitis (transmural inflammation)
- Acute gangrenous appendicitis (necrosis through muscularis externa)
30
Q
- Early acute appendicitis
A
- Neutrophilic exudate in mucosa
- Mild vasodilation
- Dull pain
31
Q
- Acute suppurative appendicitis
A
- Inflam spreads transmurally (occurs quite quickly as wall is quite thin)
- Mucosal ulceration and purulent exudate in lumen
- Fibropurulent exudate over inflamed serosa
- Dilated congested blood vessels -> appendix appears bright red
- +/- microabscess formation in wall
32
Q
- Acute gangrenous appendicitis
A
- Necrosis through the muscularis externa due to:
- Large numbers of neutrophils releasing enzymes and free radicals and bacterial toxins
- Followed quickly by rupture and acute peritonitis
33
Q
Macroscopic Features of Appendicitis
A
- Serosa/adventitia appears red and covered in a fibrinopurulent exudate
- Mucosal ulceration and necrosis or pus
34
Q
Appendicitis: Clinical Features
A
- Abdominal pain/tenderness
- Low grade fever
- Nausea/vomiting
- Anorexia
- Neutrophilia
35
Q
Appendicitis: Complications
A
- Perforation due to transmural necrosis
-> spread of faecal organisms into peritoneal cavity
-> generalised peritonitis or localised periappendiceal abscess
(necrosis of appendix wall is caused by enzymes and oxygen derived free radicals released from neutrophils and also bacterial infection) - Generalised peritonitis
-> rapid progression to septic shock
36
Q
Septic Shock
A
- Develops as a complication of generalised acute peritonitis
- Due to gram neg bacteria (originally from GIT) entering and proliferating in the blood stream
- Inflammatory system activated in response to gram neg bacteria
37
Q
Routes of Brain Infection
A
- Haematogenous spread (most common)
- Direct implantation (traumatic)
- Local extension: infection in sinus, tooth or surgical site
- Via the PNS into the CNS: occurs with certain viruses
38
Q
Meninges
A
- DAP
39
Q
Meningitis
A
- Inflammation of the pia and arachnoid mater and SA space
- Inflam spreads rapidly because of the circulation of CFS around the brain and spinal cord
- Inflammation associated with meningitis - usually caused by infection, but it may be triggered by non-infective inflammation e.g. chemical meningitis
40
Q
Bacterial Meningitis
A
- Acute pyogenic (pus-producing) meningitis
- Symptoms: headache, photopobia, neck stiffness
- Cloudy/purulent CSF
- High neutrophil count
41
Q
Bacterial Meningitis: Complications
A
- Cerebral oedema and increased ICP
- Organisation of exudate -> adhesions which may cause:
- blockage of CSF flow -> hydrocephalus
- compression of cranial nerves -> cranial nerve palsies
- Septic shock
42
Q
Meningococcal
A
- Meningococcus replication releases large amounts of endotoxin
- Endotoxin from bacterial cell wall interacts with macrophages to release cytokines and free radicals
- Permanent damage to vascular endothelium
- Vascular disruption and petechial haemorrhages
- Multiorgan shock
