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Y1S1 > Acute Inflammation > Flashcards

Acute Inflammation Flashcards

1
Q

Name the four causes of acute inflammation

A

Microbial Infections
Hypersensitivity reactions
physical agents
chemical agents

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2
Q

What are the 5 main things to look for in regards to acute inflammation

A
  • Red - dilation of the blood vessels
  • Hot - peripheral increase in temperature due to increased blood flow (hyperaemia)
  • Swollen - due to oedema and contribution from inflammatory cells
  • Painful - Stimulation of nerve endings by pressure and chemical mediators
  • Loss of function
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3
Q

What are the two phases of acute inflammation

A

Vascular phase = dilation and increased permeability

Exudative phase = fluid and cells escape from permeable venules

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4
Q

What cell type is characteristic of acute inflammation

A

neutrophil Polymorph, in the extracellular space

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5
Q

What is capillaries import to note

A

They are not always open, during acute inflammation the precapillary spinchter is OPEN meaning most capillaries are full. During a normal homeostasis these remain closed.

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6
Q

What happens to plasma proteins during acute inflammation

A

There is a NET flow out of the capillary as the plasma proteins move out due to increased permeability of capillaries

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7
Q

What is the Exudate composed of? (the thing that leaves the capillary due to increased permeability

A

High protein content (including immunoglobulins = for the destruction of invading bodies)
Fibrinogen > Fibrin (this occurs on extravascular contact - inflamed organ surfaces are commonly covered in fibrin)
High turn over as this is continuously removed by the lymphatic system

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8
Q

Give me some features of exudate

A

– Net flow out
– Increased vascular permeability
– High protein content

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9
Q

Give me some features of transudate

A

– Net flow out
– Normal vascular permeability
– Low protein content

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10
Q

What does an increased vascular permeability mean?

A
  • due to chemical mediators like histamine and bradykinin
  • stimulation of endothelial cell cytoskeleton by said mediators
  • confined to post capillary venules
  • Transient, intracellular gaps (approx 0.1 - 0.4 microns)
    Endothelial cells are NOT DAMAGED in the process
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11
Q

What happens in the lymphatic system during inflammation

A
  • Becomes dilated
  • Drain fluid from exudate
  • Antigens carried to lymph nodes
  • Recognised by lymphocytes
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12
Q

Lymphangitis

A

infection of the lymphatic channel

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13
Q

lymphadenitis

A

Inflammation of a lymphatic gland

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14
Q

What do chemotactic compounds include

A
  • Bacterial products
  • Some complement components
  • Products of neutrophil activity
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15
Q

How do neutrophils move

A

along a concentration gradient

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16
Q

What does the spread of acute inflammation suggest following injury?

A

chemical substances released from the injured tissues spread outwards into uninjured areas

17
Q

What do these endogenous chemical mediators cause?

A 
Vasodilation
Emigration of neutrophils 
Chemotaxis
Increased vascular permeability 
Itching and pain
18
Q

What are the four enzymatic cascade systems that plasma contains

A
  1. The complement system
  2. the kinins
  3. the coagulation factors
  4. The fibrinolytic system
19
Q

What do neutrophils do?

A
  • Kill organisms
  • degrade nectrotic tissue
  • ingest offending agents
  • produce chemical mediators, toxic oxygen radicals and enzymes
20
Q

How do neutrophils achieve this?

A

Movement (chemotaxis
recognition pf and adhesion to micro-organisms
phagocytosis
intracellular killing micro-organisms

21
Q

What causes microorganisms to be recognised

A

not recognised until being coated in opsonins

22
Q

What are opsonins

A

these bind to specific receptors on leucocytes and greatly enhance phagocytosis

23
Q

Name some major opsonins

A

Fc Fragment of IgE

Collectins - plasma proteins that bind to cell walls

24
Q

Define phagocytosis

A

The process whereby cells such as neutrophils and macrophages ingest solid particles

25
Q

Name me the symptoms of inflammation

A 
serous = proteins rich exudate
catarrhal = mucus hyper secretion
fibrinous = exudate contains lots of fibrin
haemorrhagic = severe vascular injury 
suppurative = production of pus 
membranous = epithelium is coated by fibrin
pseudomembranous = superficial mucosal slough
26
Q

What is caused by a fibrous clot

A

Herpes ulceration

27
Q

Tell me more about suppuration

A

Causative stimulus virtually always infective agent
A collection of pus surrounded by a membrane of sprouting capillaries , neutrophils and occasional fibroblasts is called an abscess

28
Q

What happens when a suppuration is drained

A

the abcess cavity collapses and is obliterated by organisation and fibroisis
Deep seated abscesses may drain along side a sinus tract or fistula

29
Q

Whats ulceration caused by

A

Sloughing of inflammatory necrotic tissue

30
Q

What are the most common types of ulceration

A

the mucosa - mouth, stomach, intestine

Chronic leg ulcers in those with circulatory disturbance

31
Q

What are the benefits of Acute inflammation

A
  • dilution of toxins as carried away by lymphatics
  • entry of antibodies - due to increased vascular permeability
  • fibrin formation - impedes movement of microorganisms
  • transport of drugs- e.g. antibiotics
  • delivery of nutrients and o2 - aided by increased fluid flow
  • stimulation of the immune system as fluid exudate contains antigens which reach local lymph nodes
32
Q

Disadvantages of acute inflammation

A

Digestion of normal tissues
Swelling - laryngeal oedema, Brian swelling
Inappropriate hypersensitive inflammatory response

33
Q

What is pyrexia

A

A fever
Elevation in temperature of even a few degrees may improve the efficiency of leukocyte killing and probably impairs the replication of many offending microorganisms

34
Q

What are the systematic effects of acute inflammation

A

Constitutional symptoms include:
- malaise (feeling of discomfort)
- anorexia
- nausea
weight loss due to negative nitrogen balance
reactive hyperplasia (increase in size of an organ) of the reticuloendothelial system (immune cell system)
Haemotological changes
Increased erythrocyte sedimentation rate Anaemia
Leukocytosis

Y1S1 (71 decks)

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