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Path2201 > Topic 1: Acute Inflamation > Flashcards

Topic 1: Acute Inflamation Flashcards

1
Q

What are the cardinal clinical signs of inflammation?

A
  • redness
  • swelling
  • fever
  • pain
  • loss of function
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2
Q

What is Orbital Callulitis?

A
  • Diffuse inflammation of subcutaneous tissue
  • eyelid is red, hot swollen and tender
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3
Q

What is the framework of knowledge? (8)
who, where, why, what, how

A
  • Definition
  • Epidemiology
  • Aetiology
  • Pathogenesis
  • Morphology (Micro/ Macro)
  • Clinical Manifestations (Signs and symptoms)
  • outcomes (natural history and complications)
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4
Q

Definition of acute inflamation

A

The process by which cells and exudate accumulate in irritated tissues and usually tends to protect them from further injury

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5
Q

What did Metchnikoff contribute to the scientific field in 1882? How did this contradict Paul Ehrlich’s humoral theory?

A

1882 Methinkoff - described phagocytosis
Paul Ehrlich - said inflammation brought factors from serum to neutralise (not engulf) infectious agents
- Both shared noble prize in 1908

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6
Q

What are 2 hallmarks of inflammation?

A

vasodilation and increased permeability

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7
Q

How is inflammation regulated?

A

by chemical mediators

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8
Q

Provide an example of excessive and inappropriate inflammatory responses.

A

Excessive - anaphylaxis (type 1 hypersensitivity) to a bee sting
Inappropriate - rheumatoid arthritis

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9
Q

What are some causes of inflammation? (CHINPIG)

A

Chemical - acid, alkali, histamine

Hypoxia - leading to release of HIF-1, necrosis with release of uric acid or ATP from cells

Infectious - bacterial, fungi, vial, rickettsial, mycoplasma, protozoa

Nutritional - niacin (b3) deficiency which may lead to pellagra

Physical agents - heat, trauma, cold, radiation

Immunological - allergy or autoimmune

Genetic - HGPRTase deficient leading to gout

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10
Q

What occurs during the vascular response of inflammation?

A
  • change in blood vessel size (calibre)
  • change in permeability and blood flow
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11
Q

What occurs during swelling and exudation of inflammation?

A
  • fluid exudate
  • cellular emigration
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12
Q

What are the benefits of exudation?

A
  • dilution of irritant
  • extravasation of plasma proteins (immunoglobins, complement proteins, coagulation proteins including fibrinogen)
  • nutrition for tissue cells and leucocytes
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13
Q

Describe the histopathology of a fibrinous exudate

A
  • fenestrated endothelium in capilaries
  • high molecular weight proteins exude
  • fibrin (eosinophilic, adherent protein)
  • dilation and congestion of blood vessels
  • clear spaces in interstitium caused by oedema
  • inflammatory cells
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14
Q

Describe the macroscopy of fibrinous pericarditis

A

Inflamed heart
- fibrin appears as a strandy, off-white material
- dark red areas of haemorage

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15
Q

What are the harmful effects of exudation?

A
  • swelling (pain due to stretching, glottis, in fixed bone compartment increased pressure leads to ischemia, in fixed cranial compartment of meninges increase intracranial pressure)
  • microbe may be spread by exudate
  • stasis and endothelial injury may lead to thrombus and ischaemia
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16
Q

How do cells exit during swelling and exudation?

A
  • margination
  • adherence
  • emigration
  • chemotaxis
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17
Q

Compare the histology of neutrophils, monocytes and lymphocytes

A
  • multilobed nuclei
  • 10 - 12 um
  • predominant in early acute inflammation

monocyte
- 12-20um
- kidney-shaped nucleus
- abundant cytoplasm
- major role in later stages of inflammation

lymphocytes
- 8-10um
- uniform round/ oval nucleus
- thin rim of basophilic cytoplasm
- important in chronic inflammation and acute cause by intracellular microorganisms

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18
Q

Explain margination

A

As inflammation progresses, exudation of plasma causes increased viscosity of blood, slowing blood flow (stasis)

erythrocytes stack together, leucocytes fall to the perimeter

eventually, nearly all plasma has exuded from the vessel

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19
Q

What is pavementing?

A

A phenomenon when neutrophils cover the endothelium of a vessel

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20
Q

Explain emigration of leucocytes in inflammation

A
  • occurs via the projection of a pseudopod between endothelial cells
  • via rearrangement of the leucocyte cytoskeleton
  • under the influence of chemotactic molecules
  • after penetrating the vascular basement membrane by enzymatic digestion, move toward the site of greatest chemotactic factors
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21
Q

What is chemotaxis?

A
  • a directional movement of a cell in response to a chemical gradient
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22
Q

What is the morphology of exudate dependant upon, provide examples.

A
  • nature and dose of irritant
  • organ or tissue involved
  • nature of host response

e.g.
- serous
- mucous
- fibrinous
- purulent / suppurative (pus)
- pseudomembranous
- ulcerative
- haemorrhagic

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23
Q

What is diphtheria - pseudomembranous exudate

A
  • bacteria that causes produce toxins that injure tracheal epithelial cells
  • necrotic debris of these cells combines with fibrin to form a tenacious pseudomembrane which can obstruct the airway
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24
Q

what are the 3 steps of phagocytosis?

A
  1. recognition and attachment - opsonins
  2. engulfment - phagosome
  3. killing/ degradation - phagolysosome
25
Q

What is opsonisation?

A
  • when a microorganism is coated by opsonins (igG and C3b), to facilitate recognition and engulfment
26
Q

What are phagosomes?

A
  • facilitate engulfment
  • cytoplasmic pseudopods enclose a foreign particle in a membrane-bound phagasome
27
Q

What is a phagolysosome?

A
  • facilitates killing/degradation
  • formed by fusion of phagosome membrane with lysosomal granule
  • allows discharge of lysosomal enzymes and o2 radicals
28
Q

What are Neutrophil Extracellular Traps (NETs)?

A

neutrophil release nuclear material (lose their nuclei), forming extracellular traps for bacteria.

29
Q

What is the role of lymphatics?
How does is stay open?
What is a disadvantage?
What is bacteraemia?
When does sepsis occur?

A
  • fluid, plasma, debris, leucocyte and bacteria move to lymph nodes
  • exudation in inflamed tissues is paralleled by increased drainage, limiting swelling
  • fibrils tether lymph vessels to surrounding tissue, maintaining patency
  • bacteria may also spread through lymphs, could cause inflammation of lymph vessels and nodes. could invade blood stream and bacteremia.
  • sepsis occurs if there’s the continuous entry of bacteria into circulation
30
Q

What is lymphangitis?

A

the infection spread through lymph vessels

31
Q

What are the major cellular sources of chemical medicators?

A
  • neutrophils
  • monocytes/ macrophages
  • mast cells
  • platelets
  • most epithelial cells can also be activated to produce mediators
32
Q

Where for mediators originate?

A

plasma or cells

33
Q

provide examples of preformed and newly synthesised mediators

A

preformed in intracellular granules that must be secreted (histamine)

new synthesised in response to an inflammatory stimulus (prostaglandins, leukotrienes, cytokines, o2 radicals)

34
Q

Where do mediators bind to? What are 2 exceptions?

A

specific receptors on target cells.
except lysosomal enzymes and reactive o2 species

35
Q

What can mediators stimulate the release of?

A

secondary mediators. leading to amp or inhib of response

36
Q

What is the life-span of most mediators? How do they die, provide examples.

A

short-lived, die by decay, enzymatic inactivation, scavenging or inhibition

37
Q

What are 2 important plasma-derived mediator pathways?

A

Factor XII and Complement pathway

38
Q

What does activation of coagulation factor xii-activated pathway give rise to?

A

Kinins and Fibrinopeptites

39
Q

How is the complement system activated?

A
  • classically - antigen/ antibody
  • alternative - microbial surfaces, lysosomal proteases, aggregates immunoglobins, plasmin)
  • lectin pathway
40
Q

What happens when the complement system is activated?

A

cascade of enzymes (C1-C9) form membrane attack complex -> lyse microbes -> anaphylatoxins (C3a and C5a) release histamine from mast cells -> cause vasodilation and increase permeability

41
Q

What are 6 important cell-derived mediators?

A
  • histamine
  • Pgs
  • Leukotrienes
  • NO
  • Cytokines
42
Q

Histamine;

  • Source
  • Stimuli
  • Action
A
  • mast cells
  • trauma, cold, heat, allergic reaction, inflammatory mediators
  • vasodilation, increased vascular permeability, endothelial activation
43
Q

Prostaglandins and leukotrienes;

  • Source
  • Action
A
  • arachnoid acid, membrane phospholipids
  • Pgs: vasodilation, pain
  • Ls: increase vascular permeability, smooth muscle contraction
44
Q

Interleukin-1 and Tumour necrosis factor-alpha;

  • Source
  • respond to
  • local effects
  • systemic effects
  • septic shock role
A
  • activate macrophages
  • endotoxins, antigen-antibody complex, microbial toxins, trauma
  • adhesion, chemokines, pgs, no, leucocytes
  • fever, anorexia, neutrophilia, hepatic protein synthesis, septic shock
  • hypotension, reduced tissue perfection, multiple organ dysfunction, thrombosis
45
Q

Platelet-activating factor;

  • Source (3)
  • Action (3)
  • Human impact
A
  • membrane phospholipids in activated leucocytes, endothelial cells, platelets
  • increase vascular permeability
  • leucocyte adhesion-> chemotaxis -> activation
  • boost Pgs and Ls production
  • these findings are only based on animal studies
46
Q

NO;

  • Source
  • pro-inflam
  • anti-inflam
A
  • endothelial, neurons
  • microbicidal, tissue damage, septic shock
  • inhibit leucocyte recruitment
47
Q

What are the systemic effects of acute inflammation (3)?

A
  • fever
  • hepatic protein synthesis
  • leucocytosis
48
Q

What causes fever?

A

IL-1 and TNF-a reach hypothalamus -> produces PGE@ -> resets hypothalamic thermostat -> increased sympathetic outflow -> vasoconstriction and shivering

49
Q

What causes hepatic protein synthesis?

A

IL-1, IL-6, TNF-a -> synthesis fibrinogen and CRP (increases 100-fold)

50
Q

What causes neutrophilia?

A

IL-1, TNF-a accelerate neutrophil reserve pool from bone marrow -> also induces granulocyte colony stimulating factor

51
Q

What are acute complications of tissue damage in acute inflammation (2)? Give disease examples of these.

A
  • tissue damage, gangerous appendicitis
  • abscess, brain absess
52
Q

What is an abscess? Causes? Complications?

A
  • localised collection of pus
  • pyogenic bacterial infection, obstructed drainage
  • sinus/ fistula, pyaemia, sepsis
53
Q

What is an empyema thoracis?

A

an infection of the pleural space that is most commonly a complication of pneumonia (parapneumonic)

54
Q

When does onset of recovery occur?

A
  • dilution/neutralisation of pathogen by exudate
  • phagocytosis/destruction by leucocytes
  • drainage via lymphatics
  • medical treatment
55
Q

When will resolution occur?

A
  • tissue architecture intact
  • exudate effectively removed
  • organ has the capacity to regenerate
56
Q

If a tissue cant recover, how does it repair?

A
  • repair by granulation
57
Q

What does granulation tissue consist of?

A
  1. new-thin walled blood vessels
  2. fibroblasts producing collagen
  3. macrophages and other mononuclear inflammatory cells
58
Q

When does inflammation progress to chronicity?

A

when irritants can’t be removed

Path2201 (6 decks)

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