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Mechanisms of Disease > Acute Inflammation > Flashcards

Acute Inflammation Flashcards

0
Q

What are the features of acute inflammation?

A
  • innate
  • immediate
  • stereotyped (same response every time/every case)
  • short (min/hrs)
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1
Q

Define inflammation.

A

Response of living tissue to injury, initiated to limit tissue damage

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2
Q

What are some of the causes of acute inflammation?

A
  • microbial infections e.g. pyogenic organisms
  • hypersensitivity reactions
  • physical agents e.g. trauma
  • chemicals
  • tissue necrosis
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3
Q

What are the clinical signs of inflammation?

A 
Local:
RUBOR (redness)
TUMOR (swelling)
CALOR (heat)
DOLOR (pain/loss of function)

+ exudate of oedema & infiltrate of cells

Systemic:
Fever
Tachycardia

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4
Q

Describe the sequence of events in the vascular phase of acute inflammation.

A
  1. Transient vasoconstriction of arterioles (secs)
  2. Vasodilatation of arterioles -> vasodilatation of capillaries (increased blood flow -> rubor & calor) (+histamine)
  3. Increased permeability of blood vessels -> exudation of protein-rich fluid into tissues (+histamine)
  4. Increased RBCs in small vessels and increased viscosity of blood (stasis) -> slowed circulation

note: histamine also causes pain to enforce rest (preventing further damage)

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5
Q

Describe the sequence of events in the exudation phase of acute inflammation.

A

Arteriolar dilatation -> increased hydrostatic pressure
& increased permeability -> loss of protein into interstitium
= flow of fluid out of vessel -> OEDEMA

Delivers plasma proteins to site of injury (IGs, inflamamtory mediators, fibrinogen)
Dilutes toxins
Increases lymphatic drainage (delivers microbes to phagocytes and antigens to immune system)

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6
Q

What causes the increased permeability of blood vessels during the exudation phase of acute inflammation?

A
  • endothelial contraction creates gaps (+histamine & leukotrienes)
  • cytoskeletal reorganisation creating gaps (IL-1 & TNF)
  • direct injury e.g. toxins, burns, chemicals
  • leukocyte-dependent injury due to toxic oxygen species & enzymes released
  • increased transcytosis (channels across endothelial cytoplasm) (VEGF)
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7
Q

What is the difference between exudate and transudate?

A

EXUDATE = fluid loss in inflammation with a high protein content

TRANSUDATE = fluid loss due to increased hydrostatic pressure with a low protein content
e.g. cardiac failure, venous outflow obstruction

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8
Q

Describe the sequence of events in the cellular phase of acute inflammation.

A

Infiltration of neutrophils (polymorphs) removes pathogens and necrotic debris. Attracted by bacterial products.

  1. Margination: Stasis causes neutrophils to line up at edge of blood vessels along endothelium
  2. Rolling: neutrophils stick to receptors on endothelium intermittently, causing them to “roll” along the endothelium
  3. Adhesion: neutrophils fully adhere to endothelium
  4. Emigration: neutrophils move through endothelium (diapedesis) by chemotaxis
  5. Extravasation: neutrophils now outside blood vessels
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9
Q

List some chemical mediators of acute inflammation.

A

Proteases e.g. kinins, complement system (C3a & C5a), coagulation/fibrinolytic system

Prostaglandins/leukotrienes (arachidonic acid metabolites)

Cytokines/chemokines e.g. interleukins, TNF-alpha

note: increased blood flow (histamine & prostaglandins)
increased vascular permeability (histamine & leukotrienes)
neutrophil chemotaxis (C5a, LTB4, bacterial peptides)
phagocytosis (C3b)

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10
Q

What are some local complications of acute inflammation?

A
  • swelling -> blockage of tubes e.g. bile duct, intestine
  • exudate -> compression of soft organs where there is little space e.g. cardiac tamponade
  • > serositis: infection of serous cavity due to exudate on surface of organ (e.g. ascites, pleural effusion, pericardial effusion) -> localised fibrin deposits, respiratory/cardiac impairment
  • > loss of fluid e.g. burns
  • pain & loss of function (dolor)
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11
Q

What are some systemic effects of acute inflammation?

A
  • fever: endogenous pyrogens produced (e.g. IL-1, TNF-alpha) & prostaglandins
  • leukocytosis:
    = IL-1 & TNF-alpha accelerate release of leukocytes from bone marrow
    = macrophages & T-lymphocytes produce colony-stimulating factors

note: bacterial infections = neutrophils (Acute)
viral infections = lymphocytes (Chronic)

  • acute phase response: reduced appetite (anorexia), increased heart rate, altered sleep patterns
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12
Q

What is the definition of shock, and what can it be caused by?

A

SHOCK = circulatory collapse when the arterial blood pressure is too low to adequately perfuse tissues

  • hypovolaemic: reduced circulatory volume
  • cardiogenic: reduced activity of heart
  • septic: widespread dilatation of blood vessels due to sepsis
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13
Q

What are some of the possible results of acute inflammation?

A
  • complete resolution: vascular changes stop, exudate drains to lymphatics, fibrin degraded by plasmin/proteases, neutrophils die and are carried away/phagocytosed, damaged tissue may regenerate
    note: not possible if tissue architecture has been destroyed
  • continued acute inflammation with chronic inflammation -> abscess
  • progresses to chronic inflammation -> fibrous repair and tissue regeneration
  • septic shock
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14
Q

What is the definition of an abscess? How can you treat it?

A

Localised collection of pus and necrotic tissue in solid tissue surrounded by damaged, inflamed tissue e.g. boil

note: inflammatory exudate forces tissue apart -> extreme pain due to increased pressure (therefore invariably some tissue destruction around an abscess)

Incise and drain to relieve pressure

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15
Q

How are mediators of inflammation inactivated?

A
  • short half lives
  • degraded e.g. heparinases
  • inhibited e.g. anti-proteases
  • unstable e.g. arachidonic acid derivatives
  • diluted in exudate e.g. fibrin exudation products
  • specific inhibitors e.g. endothelin, lipoxins
16
Q

Describe appendicitis. What are the causes? What are the complications?

A

Inflammation due to obstruction of appendiceal lumen

Causes:

  • inflammatory bowel disease causing lymphoid hyperplasia
  • infection
  • faecal stasis & faecaliths (hard mass of faeces within colon/appendix due to chronic constipation)
  • foreign bodies
  • neoplasms

Increased WBCs due to increased intestinal bacteria (obstruction)/stagnated mucus (increased mucus secretion)
-> pus formation -> further increase in pressure -> venous outflow obstruction ——->

-> ischaemia -> loss of epithelial integrity -> invasion of bacteria

OR: -> thrombosis of appendicular blood vessels -> perforation (disrupted continuity causing leakage of contents) -> gangrene -> peritonitis/periappendicular abscess (faeces entering peritoneal cavity)

17
Q

What is the definition of an ulcer?

A

ULCER = permanent loss of epithelium on a mucosal surface

18
Q

What is the difference between sepsis, septic shock, and septicaemia?

A

SEPSIS = putrefactive destruction of tissues by disease-causing bacteria and their toxins

SEPTIC SHOCK = widespread dilation of blood vessels so that there is insufficient blood to fill them due to severe sepsis, with resultant systemic inflammatory response associated with disseminated intravascular coagulation and multiple organ failure

SEPTICAEMIA = widespread destruction of tissues due to absorption of disease-causing bacteria or their toxins into the bloodstream (“blood-poisoning”)

19
Q

What are some long-term complications of meningitis?

A
  • septicaemia -> gangrene
  • cognitive impairment
  • hearing problems
  • seizures/epilepsy
  • neuromotor disability
  • visual disorders
20
Q

What is the link between gallstones and hepatic abscesses?

A

Obstructed bile duct -> infection of bile duct (ascending cholangitis)

21
Q

Describe the sequence of events following the inhalation of Streptococcus pneumoniae.

A

Bronchopneumonia (bronchi -> alveoli):
Alveoli filled with exudate -> consolidation in alveoli only -> fibrosis of lung tissue -> RESOLUTION

Lobar pneumonia (alvoli -> alveoli): 
Alveoli filled with exudate - consolidation in whole lobule -> fibrosis of lung tissue -> RESOLUTION
22
Q

What is inherited angio-oedema?

A

Absence of C1-esterase inhibitor -> increased bradykinin (formed from kiniogen) which increases vascular permeability

Increased capillary leakage -> widespread oedema

Laryngeal oedema -> asphyxiation

23
Q

What is chronic granulomatous disease?

A

Reduced NADPH oxidase

Ineffective phagocytosis (no oxidative burst) and unregulated neutrophil activity -> vulnerable to infection -> recurrent infections & areas of granuloma e.g. bones, bowel

24
Q

What causes inflammation to stop?

A
  • fibrinolysis of clots
  • scarring
  • granuloma formation
25
Q

Can neutrophils respire anaerobically?

A

Yes

26
Q

What is hyperaemia (increased blood flow) initiated by?

A

Capillary relaxation

27
Q

What would cause sputum to appear creamy or yellow?

A

Creamy = presence of neutrophils/inflammatory cells

Yellow = presence of bacterial debris/other WBCs (i.e. infection)

Mechanisms of Disease (8 decks)

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