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MD2001 > Acute Inflammation > Flashcards

Acute Inflammation Flashcards

1
Q

What are the causes of acute inflammation ?

A
  • Microbial infections
  • Hypersensitivity reactions
  • Physical agents
  • Chemical agents
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2
Q

What are signs/symptoms of acute inflammation?

A
  • Rubor (red) due to dilation of blood vessels (capillaries full and pre-capillary sphincter open)
  • Calor (hot) due to increased blood flow
  • Tumour (swollen) due to oedema
  • Tender (painful) due to stimulation of nerve endings by P and chemical mediators
  • Loss of function
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3
Q

What are the phases of acute inflammation ? Describe eqch

A

1) Vascular phase - dilution and increased permeability

2) Exudative phase - fluids and cells escape from permeable venules

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4
Q

What is the diagnostic feature of acute inflammation ?

A

Neutrophil accumulation in extracellular space

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5
Q

What is the effect of increased vascular permeability compared to when it is normal ?

A

Normally, hydrostatic pressure is high at arterial end, causing fluid to leak out, and low at venous end so fluids leaks back in (but proteins stay in).
With increased permeability, there is a net flow out of both fluid and plasma proteins.

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6
Q

What are the main features of an Exudate ?

A
  • High protein content
  • Proteins include immunoglobins
  • Fibrinogen becomes fibrin (often covers surface of acutely inflamed organs) on extravascular contact
  • High turnover (removed via lympathic. This exudate used in defence)
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7
Q

What are the main differences between exudate and transudate (normal) ?

A
  • Net flow out vs no net flow out
  • Increased vascular permeability vs normal
  • High protein content vs low protein content
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8
Q

How is increased vascular permeability brought about ?

A

Chemical mediators (histamine, bradykinin) stimulate endothelial cell cytoskeleton —-> transient intercellular gaps of 0.1-0.4 microns appear)

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9
Q

Are the endothelial cells damaged in the process of increasing vascular permeability ?

A

NO, the change is transient and reversible, gaps are sealed once the agent is removed and the tight junctions are restored.

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10
Q

Which types of blood cells are “the main site of increased vascular permeability ?”

A

Post-capillary venules

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11
Q

What is the role of the lymphatic system in acute inflammation ?

A
  • Fluid drained from exudate in lymph nodes (hence dilated)
  • Fluid then scrutinized and investigated to see if anythig to make immune response against, (e.g antigens recognised by lymphocytes)
  • Overall, material from site of infection goes through different parts of lymph nodes where different responses made
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12
Q

What is the difference between lymphadenitis and lymphangitis ?

A
  • Lymphadenitis is inflammation of local lymph node

- Lymphangitis is inflammation of walls of lymphatic vessels

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13
Q

What are the functions of neutrophils in inflammation ? How does it do it ?

A
  • Phagocytose organisms/offending agents
  • Kill micro-organisms intracellularly
  • Degrade necrotic tissue with tissue damaging enzymes
  • Produce chemical mediators, toxic oxygen radicals

Does it through chemotaxis (movement), recognition and adhesion to microorganisms, then deals with it

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14
Q

What is margination and what are the steps following it ?

A

1) Margination of neutrophils ( ‘accumulation and adhesion of leukocytes on endothelial cell of blood vessels at site of injury’)
2) Neutrophils in the normal blood flow begin to pavement
3) Pass between endothelial cells to site of inflammation
4) Pass through basal lamina and migrate into adventitia

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15
Q

What are examples of chemotactic compounds ?

A
  • Bacterial products
  • Complement components
  • Product of neutrophil activity
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16
Q

What is chemotaxis ? How does it occur ?

A

Chemotaxis is “ the movement of an organism in response to a chemical stimulus”.

1) Neutrophils within ECM have receptors on surface which may bind on components of infective agent.
2) Components of agent fills receptor on any side of the cell
3) Cell responds by moving toward where receptor occupied = MIGRATION
4) Keeps moving up the gradient (more and more receptors filled) until site of inflammation

17
Q

What are chemical mediators ? What so they cause ?

A

Endogenous substances released from injured tissue spreading towards uninjured areas.
They cause:
Vasodilation
Emigration of neutrophils into local inflamed tissues where they undergo chemotaxis which is aided by increased vascular permeability
Itching and pain
Oedema and swelling

18
Q

What are plasma factors ?

A

Plasma components that leak out

19
Q

What are the different kinds of enzymatic cascades in plasma factors ?

A

1) Complement systems (triggering/cascade system)
2) Kinins
3) Coagulation factors
4) Fibrinolytic factors

20
Q

What is the main characteristic of neutrophil polymorph ?

A

Lobulated nuclei

21
Q

What helps neutrophils recognise micro-organisms ?

A

Thanks to opsonisation of said organism: Covering them with a substance (opsonins) which binds to major receptors on leukocytes and enhances phagocytosis.

22
Q

Give examples of major opsonis

A

Fc fragment on IgG
C3b (fragment of C3 generated by complement activation)
Collectins- bind to microbial cell walls

23
Q

What are possible types of acute inflammation ?

A

Catarrhal (mucus hypersecretion)
Fibrinous (exudate rich in fibrin)
Hemorrhagic (severe vascular injury)
Membranous (epithelium coated by fibrin)
Pseudomembranous (superficial mucosal slough)
Suppurative (pus)
Serous (protein rich fluid exudate)

24
Q

What is pus made up of ?

A

Neutrophils, bacteria, cellular debris

25
Q

What is an abscess ? What happens when it drains ?

A

Collection of pus surrounded by membrane of sprouting capillaries, neutrophils, and occasional fibroblasts.
Upon draining, it collapses and is obliterated by organisation and fibrosis. If deep seated, might drain along sinus tract or fistula.

26
Q

What are examples of suppurative inflammation ?

A

Empyema of the gallbladder

Certain types of meningitis

27
Q

What is an ulcer ?

A

Excavation of the surface of an organ/tissue due to sloughing off of inflammatory necrotic tissue.

28
Q

What are examples of ulcer ?

A

Inflammatory necrosis of the mucosa

Chronic leg ulcers (in people with circulatory disturbance)

29
Q

What are the pros of acute inflammation ?

A
  • Dilution of toxins allowing them to be carried away by lymphatics
  • Entry of antibodies thanks to increased vascular permeability
  • Fibrin formation impeding movement of microorganisms
  • Transport of drugs thanks to increased vascular permeability
  • Delivery of nutrients and oxygen thanks to fluid flow and increased vascular permeability
  • Stimulation of immune response as fluid exudate containing antigens reaches local lymph nodes (if foreign material, cells migrate from lymph nodes to site of inflammation)
30
Q

What are the cons of acute inflammation ?

A
  • Digestion of normal tissue
  • Swelling (if in airway may hinder breathing)
  • Inappropriate inflammatory response (for instance type 1 hypersensitivity- (IgE recognises pollen as foreign agent and causes degranulation of mast cell, releasing histamine)
31
Q

What are the systemic effects of acute inflammation ?

A
  • Pyrexia (elevation of temperature by few degrees improving the efficiency of leukocyte killing and likely hindering replication of some microorganisms)
  • Constitutional symptoms (malaise, anorexia, nausea)
  • Weight Loss (due to negative Nitrogen balance, especially when extensive chronic inflammation)
  • Reactive hyperplasia (“abnormal increase in volume of a tissue or organ caused by the formation and growth of new normal cell”) of reticuloendothelial system
  • Haematological changes
  • Increased erythrocyte sedimentation rate (become stickier)
  • Anaemia
  • Leukocytosis (increase in WBCs)
32
Q

What are the possible outcomes of Acute Inflammation ?

A 
Resolution
Suppuration (when excessive exudate). After discharge of pus, leads to repair and organisation 
Repair and organisation (when excessive necrosis). Once done, leads to fibrosis.
Chronic inflammation (when persistent causal agent). Once done, leads to fibrosis.

MD2001 (35 decks)

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