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Essentials of Pathology > Acute Inflammation > Flashcards

Acute Inflammation Flashcards

1
Q

Causes of Injury

A
  • Trauma
  • Infection
  • Heat/cold
  • Chemical
  • Infarction
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2
Q

Inflammation Process

A
  1. Injury
  2. Inflammation: neutrophils
  3. Demolition: macrophages
  4. Repair: angiogenesis
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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
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4
Q

Acute Inflammation

A
  • Earliest response
  • Last days
  • Features: neutrophils, oedematous exudate, vasodilation
  • Non-specific
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5
Q

Chronic Inflammation

A
  • Later response
  • Lasts weeks/months/yrs
  • Features: macrophages, lymphocytes, plasma cells, assoc fibrosis/scaring
  • Specific or nonspecific
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6
Q

Aims of A. Inflammation

A
  • Deliver nutrients and defence cells
  • Destroy any infective agents
  • Remove debris
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7
Q

Features of A. Inflammation

A
  • Vascular response
  • Exudate
  • Variable tissue necrosis
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8
Q

A. Inflammation: Vascular and Cellular Response

A
  1. initial dilatation of focal blood vessels increasing blood flow, then blood flow slows
  2. Vessels become leaky and permeable, permitting the passage of water, salts and small proteins from the plasma into the damaged area (exudation)
  3. Circulating neutrophils are attracted to the damaged area and adhere to swollen endothelial cells (margination) and migrate through BM (emigration) into damaged area
  4. Later, macrophages and lymphocytes migrate to damaged area
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9
Q

Exudate

A

Protein rich fluid and cells that have escaped from blood vessels due to an increase in vascular permeability

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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
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11
Q

Types of A. Inflam Exudate

A
  • Serous
  • Fibrinous
  • Purulent
  • Suppurative
  • Hemorrhagic
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12
Q

Serous Exudate

A
  • Absence of prominent cellular response
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13
Q

Fibrinous Exudate

A
  • Contains large amounts of fibrin
  • Usually if injury is quite severe
  • Often in lungs
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14
Q

Purulent and Suppurative Exudate

A
  • Usually bacterial cause
  • Contains cellular response (mainly neutrophils)
  • Suppurative: purulent exudate + significant liquefactive necrosis (pus)
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15
Q

Hemorrhagic Exudate

A
  • Contains many RBCs from damaged and ruptured blood vessels
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16
Q

Chemical Mediators of AI

A
  • Cell-derived mediators

- Plasma-derived mediators

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17
Q

Learn Table in Slides!!

A

..

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
  1. Release of exogenous pyrogens from bacteria or viruses -> stimulate production of endogenous pyrogens (cytokines e.g. IL1 and TNFA) and interferons
  2. Endogenous pyrogens stimulate prostaglandin synthesis within the vascular and perivascular cells of the hypothalamus
  3. 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
  1. Luminal obstruction
  2. Continued secretion of mucus -> increased pressure
  3. Possible mucosal ischaemia
  4. Mucosal injury
  5. Acute mucosal inflammation
  6. Secondary bacterial invasion
  7. Spread of inflammation transmurally
29
Q

Stages of Acute Appendicitis

A

ESG

  1. Early acute appendicitis (mucosal inflam)
  2. Acute suppurative (pus) appendicitis (transmural inflammation)
  3. Acute gangrenous appendicitis (necrosis through muscularis externa)
30
Q
  1. Early acute appendicitis
A
  • Neutrophilic exudate in mucosa
  • Mild vasodilation
  • Dull pain
31
Q
  1. 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
  1. 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
  1. Haematogenous spread (most common)
  2. Direct implantation (traumatic)
  3. Local extension: infection in sinus, tooth or surgical site
  4. 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

Essentials of Pathology (10 decks)

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