Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

ESA2 Emily > MOD Week 2 acute inflammation > Flashcards

MOD Week 2 acute inflammation Flashcards

1
Q

Define acute inflammation

A

Response of a living tissue to injury which is initiated to limit tissue damage.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the characteristics of acute inflammation?

A

innate
immediate and early
stereotyped
short duration

Often activated in response to vascular and cellular reactions; controlled by chemical mediators (derived from plasma cells) and is protective but can lead to local complications and systemic effects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the purpose of acute inflammation

A

deliver defensive mechanisms to a site of injury to protect the body from infection (particularly bacterial) and aid in tissue repair.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Why is there initially swelling with acute inflammation?

A

Initially fluid pours out of the blood vessels and then leukocytes follow within a few minutes through pores to aid in reducing inflammation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Name the causes of acute inflammation.

Hint: My happy plant can talk

A

Microbial infections e.g. pyogenic organisms
Hypersensitivity reactions (inniate the acute inflammatory response)
Physical agents
Chemicals and drugs e.g. drinking bleach
Tissue necrosis (ALWAYS results in acute inflammation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the clinical signs of acute inflammation?

A 
Rubour= redness
Tumour= swelling
Color= heat
Dolor= pain
LOSS OF FUNCTION (as a result of  the above)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What tissue changes occur as a result of acute inflammation? Describe them all thoroughly.

A
  1. Changes in blood flow:
    - Initial vasoconstriction (seconds)
    - Vasodilation of arterioles and capillaries meaning blood vessels become dilated and increase perfusion. This causes rubor and color.
    - Increased permeability of blood vessels allowing exudation of protein-rich fluid into tissues e.g. leucocytes and slowing of circulation due to swelling.
    - Increased concentration of RBC in small vessels and increased viscosity of blood results in STASIS.
  2. Formation of fluid exudate, from Starling’s Law:
    - Fluid flow across vessel walls determined by balance of hydrostatic and colloid osmotic pressure.
    - Both are increased.
    - Vasodilation of arterioles by vasoactive mediators such as histamine
    - Arteriole flow increases, meaning capillary pressure rises and so more fluid and leukocytes are delivered to place of injury.
    - After vasodilation, arterioles become leaky and plasma can escape through endothelial gaps
    - increased haemocrit in venules.
    - Increased resistance to blood flow in venules
    - Upstream blood pressure rises
    - Increased pressure in vessels means there is greater exudation of fluid into spaces, which allows more delivery of plasma proteins to an injury site.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What chemical mediators are released into blood stream immediately?

A

Within 30 mins…
HISTAMINE is released from mast cells, basophils and platelets. This may be in response to physical damage, immunological reactions, C3a, C5a, IL-1 and factors from neutrophils and platelets.

It causes vascular dilations and transient increase in vascular permeability as well as PAIN.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What causes increased hydrostatic pressure in acute inflammation?

A

Arteriolar dilatation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What leads to loss of protein into the interstitium in acute inflammation?

A

increased permeability of vessel walls

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the main consequence of vascular leakage?

A

Oedema= excess of fluid in interstitium
can be transudate (such as in heart failure) or exudate (such as in acute inflammation, resulting in a protein rich fluid).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the result of oedema on lymphatic system?

A

Increased lymphatic drainage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Compare exudate and transudate oedema

A

Exudate is fluid loss due to inflammation (or cancer) with a high protein content.
Transudate is fluid loss due to hydrostatic imbalance with a low protein content. For example, in cardiac failure or venous outflow obstruction. Lack of pores in capillaries prevent plasma proteins being filtered out.

An exudate oedema is more dangerous than transudate.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the mechanisms of vascular leakage?

A 
Endothelial contraction (histamine)
Cytoskeletal reorganisation (cytokines IL-1 and TNF)
Direct injury (toxic burns, chemicals)
Leukocyte dependent injury (Toxic oxygen species and leucocyte enzymes)
Increased transcytosis (formation of channels across endothelial cytoplasm allowing macromolecules to move). e.g. VEGF
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What proteins are commonly found in exudate?

A

Opsonins (which coat foreign materials to make phagocytosis easier)
Complement (which produce a bacteria-perforating structure)
Antibodies (which bind to surface of micro-organisms to act as opsonins).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the primary type of white blood cell, involved in inflammation?

A

Neutrophil leucocyte

A type of granulocyte also known as polymorphonuclear leucocyte

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is another name for a neutrophil?

A

Polymorph

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is margination of neutrophils and what causes it?

A

Neutrophils lining up onlong the edge of blood vessels, along the ENDOTHELIUM. Caused by stasis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Describe the steps following infiltration of neutrophils

A
  1. Stasis of blood causing neutrophil margination
  2. Neutrophils role along endothelium to stick to it intermittently= ROLLING.
  3. Adhesion of neutrophils (sticking more avidly)
  4. Emigration of neutrophils through the vessel wall
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

How do neutrophils escape from vessels?

A

Relaxation of inter-endothelial cell junctions
Digestion of vascular basement membrane
Movement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Define chemotaxis

A

Movement along a concentration gradient of chemoattractants to the source of inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What form of exudate may form as a post-operative complication?

A

Seroma, a tissue space filled with a clear fluid of serous exudate.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is starlings law?

A

Describes the forces involved in equilibrium of fluid exchange in microcirculation. Acute inflammation disrupts this.

24
Q

How do neutrophils phagocytose?

A
  1. contact
  2. recognition
  3. internalisation

Facilitated by opsonins Fc and C3b and cytoskeletal changes.

25
Q

What are secondary lysosomes?

A

Phagosomes fuse with lysosomes to produce secondary lysosomes.

26
Q

What are the killing mechanisms involved in acute inflammation?

A

oxygen dependent:

  • superoxide and hydrogen peroxide produced
  • H2O2-Myeloperoxidase-Halide system which produces HOCl (free radical)

Oxygen independent:

  • lysozyme and hydrolases
  • bacterial permeability increasing protein (BPI)
  • Cationic proteins (defensins)
27
Q

What is starlings law dependent on?

A

capillary pressure
interstitial free fluid pressure
plasma colloid osmotic pressure
interstitial fluid colloid osmotic pressure `

28
Q

What is inflammation of the lymph nodes called and when does this occur?

A

Lymphadenitis

occurs when inflammation containing exudate drains into the lymph nodes.

29
Q

What is the life span of a neutrophil?

A

12-20 hours

30
Q

How many granules of bacterial substances are contained in each neutrophil?

A

2000

31
Q

What chemical mediators of acute inflammation are produced in the liver and are regarded as plasma proteins?

A

Proteases such as kinins, complement system proteins and coagulation/fibronolytic system proteins

32
Q

Give an example of a prostroglandin as a chemical mediator

A

Metabolites of arachiodonic acid

33
Q

What chemical mediator is produced by white blood cells?

A

Cytokines and chemokines such as interleukins, TNF-a

34
Q

What chemical mediators increase blood flow?

A

Hint: The word help can only see first and last letters because blood is flowing so fast!!

histamine
prostaglandins

35
Q

What chemical mediators increase vascular permeability?

A

Hint: The word help can only see 1st and 3rd letter because there is holes in the word in correspondence with vascular permeability

Histamine
Leukotrienes

36
Q

What chemical mediators increase neutrophil chemotaxis?

A

Hint: Class 5a read Lustigens Taschenbuch 4. This week it was about bacterial peptides! :O

C5a, LTB4, bacterial peptides

37
Q

What chemical mediators increase phagocytosis?

A

Hint: Chloe 3 bellies

C3b

38
Q

How can you tell is an infection is bacterial or viral?

A

Do a blood test for what kind of leukocyte is most prominent:

Many polymorphs/neutrophils- BACTERIAL
Many lymphocytes- VIRAL

39
Q

What chemical mediators increase release of leukocytes from bone marrow?

A

IL-1 and TNF-a

40
Q

What are the systemic effects of acute inflammation?

A

Decreased appetite
Raised pulse rate
Altered sleep pattern
Changes in plasma concentrations of acute phase proteins.

41
Q

What is aranchonic acid?

A

Fatty acid found in cell membranes released from cell membranes during normal metabolic processes, cell death or injury.

42
Q

What are eicosanoids? What are their types?

A

Derivatives of aranchonic acid which are critical in modulating inflammation

Leukotrinens and protaglandins

43
Q

What can happen following acute inflammation?

A
  1. complete resolution
  2. continued acute inflammation with chronic inflammation
  3. chronic inflammation and fibrous repair and possibly tissue regeneration
  4. death
44
Q

When is complete resolution, following acute inflammation not possible?

A

If tissue architecture has been destroyed

45
Q

Discuss the full role of neutrophils in inflammation

A
  1. Chemotaxis (directional movement towards a chemotaxin) e.g. endotoxin, clotted blood, complement fragments and leukotriene B4
  2. Activation- rush of calcium and sodium into a cell following chemotaxin binding to make it swell and reorganise the cytoskeleton by sending out pseudopodia and making activated cells stickier than normal.
  3. Margination, rolling and adhesion
  4. Diapedesis- leukocytes leaving venules by digging themselves out by producing collagenase to digest basement membrane. The leukocytes pull themselves along collagen fibres of other tissue structures.
  5. Recognition and attachment, using oponins which make targets more easily recognisable by phagocytes.
  6. Phagocytosis
  7. Killing with or without oxygen
46
Q

Describe the action of bradykinin

A

A vasoactive peptide which causes pain by stimulating specialised nerve endings and increasing vascular permeability.

47
Q

What is prostoglanin blocked by to reduce pain and swelling?

A

NSAIDs, e.g. aspirin

48
Q

What mechanism of action does NSAIDs utilise?

A

Inhibit cyclo-oxygenase (an enzyme which produces prostaglandins from arachadonic acid)

49
Q

How does the complement system cause bacteria to die?

A

Uses chemicals which punch holes in their cell membranes

50
Q

Describe lobar pneumonia

A

Causative organism: Streptococcus pneumonia
Presents with worsening fever, prostration (extreme weakness), hypoxaemia over a few days, dry cough and breathlessness.

If treated, the condition can resolve completely.

Down a microscope, excudate will be visable in the alveoli instead of a clear slided, showing air present.

51
Q

Define ascites

A

Accumulation of fluid in peritoneal cavity, causing abdominal swelling

52
Q

Acute inflammation in serous cavities is characterised by what?

A

Respiratory or cardiac impairment

Localised fibrin deposition

53
Q

How is fever different from hyperthermia?

A

Fever is controlled by the body as an internal mechanism

Hyperthermia is not controlled and you cannot decrease your temperature

54
Q

What does pyrogenic mean?

A

Inducing fever

55
Q

State some pyrogenic cytokines

A

TNF
Interleukin 1

Produced by macrophages

56
Q

What happens when inflammatory mediators spread throughout the whole body?

A

SHOCK
Dramatic drop in blood pressure, widespread vasodilation and increased vascular permeability.
OFTEN FATAL.

57
Q

Following acute inflammation, if parenchymal cells are damaged beyond repair, what will form in their place?

A

Scar

ESA2 Emily (8 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions