Brainscape's Knowledge GenomeTM

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


See full index

Semester 2 Mechanisms Of Disease > W2- Acute Inflammation > Flashcards

W2- Acute Inflammation Flashcards

1
Q

What are the characteristics of acute inflammation? Time etc

A

Innate, immediately, early, stereotyped, short duration (mins-few days)

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

What are the vascualr and cellular reactions of acute inflam?

A

Vascular- accumulate fluid exudate, cellular- invasion of neutrophils

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

What molecules control acute inflam?

A

Chemical mediators from plasma or cells

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

What are the causes of acute inflam?

A

Microbial infections (eg pyogenic- staphylcoccus), acute phase hypersensitivity reactions, physical agents, chemicals, tissue necrosis

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

What are the clinical features of acute inflam?

A

Redness (rubor), swelling (tumour), pain (donor), heat (calor), loss of function- LOCAL CHANGES

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

What 3 changes occur in the tissues during acute inflam?

A

Changes in blood flow, exudation of fluid into tissues, Infiltration of neutrophils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

In the vascular phase of acute inflam, what changes to blood flow occur

A

Transient vasoconstriction of arterioles (few secs), vasodilation of arterioles and then capillaries- increases blood flow (heat and red), increased permeability of blood vessels causes fluid in tissues and swelling, STASIS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What chemicals mediate the immediate early (1/2 hr) vascular response? Where released from? In response to what?

A

HISTAMINE, from MC’s, basophils, platelets, in response to trauma, IR, C3a, C5a, Il-1

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

What effects does histamine have?

A

Vascular dilation, transient increase in vascular permeability, pain

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

Give 2 examples of chemical mediators in the persistent vascular response

A

Leokotrienes, bradykinins

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

What is the purpose of acute inflammation?

A

Response of living tissue to injury to limit damage

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

What is Starling’s Law?

A

Fluid flow across vessel walls is determined by hydrostatic and colloid osmotic pressure comparing plasma and interstitial fluid

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

What does increasing the hydrostatic or oncotic pressure in a vessel do?

A

Increases the fluid flow out of the vessel (protein in interstitium is increased)

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

Why does fluid exudation occur in acute inflam?

A

Arteriolar dilation leads to incrased hydrostatic pressure, increased permeability of vessels leads to proteins in interstitium, net flow of fluid out of vessel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Describe what oedema is and what it is characterised by

A

Excess of fluid in interstitium, transudate or exudate, increased lymphatic drainage.

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

What is Starling’s Law?

A

Fluid flow across vessel walls is determined by hydrostatic and colloid osmotic pressure comparing plasma and interstitial fluid

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

What does increasing the hydrostatic or oncotic pressure in a vessel do?

A

Increases the fluid flow out of the vessel (protein in interstitium is increased)

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

Why does fluid exudation occur in acute inflam?

A

Arteriolar dilation leads to incrased hydrostatic pressure, increased permeability of vessels leads to proteins in interstitium, net flow of fluid out of vessel

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

Describe what oedema is and what it is characterised by

A

Excess of fluid in interstitium, transudate or exudate, increased lymphatic drainage.

20
Q

What is exudate oedema?

A

Fluid loss in inflammation- high protein content in fluid

21
Q

What is transudate oedema? Give an example

A

Fluid loss due to changes in hydrostatic pressure, low protein content of fluid. E.g. Cardiac failure, venous outflow obstruction

22
Q

What 5 mechanisms can cause vascular leakage? (See with slide 17)

A

Endothelial contraction and cytoskeletal reorganisation (gaps), direct injury (burns, chemicals), leukocyte dependent injury, increased transcytosis

23
Q

What is the role of fibrin at a site of injury?

A

Acts as a mesh work to localise inflam mediators and hold proteins at site of injury

24
Q

What is the primary type of WBC involved in inflam?

A

Neutrophil/ polymorph

25
Q

What are the 4 stages of neutrophil infiltration?

A

Margination (line up along blood vessel), rolling (along endothelium), adhesion (to it), emigration (through blood vessel wall-trans endothelial)

26
Q

How do neutrophils escape from vessels?

A

Lreaxation of inter-endothelial cell junctions, digestion of vascular BM, movement

27
Q

Define chemotaxis.

State 3 chemotactants

A

The movement along a c.g of chemoattractants. IE. Neutrophils to site of injury. C5a, LTB4, bacterial peptides

28
Q

What do neutrophils do?

A

Phagocytosis- contact, recognition, internalisation- secondary lysosome. Opsonins (Fc and C3b) facilitate

29
Q

Which free radicals are present in 02 dependent killing mechanism of phagocytosis?

A

Superoxide and hydrogen peroxide

30
Q

What molecules are involved in the 02 independent killing during phagocytosis?

A

Lysozyme, hydrolases, BPI, defending

31
Q

Can neutrophils be harmful to host tissue?

A

Yes- may release toxic metabolites and enzymes

32
Q

What are the main chemical mediators of acute inflam?

A

Histamine, bradykinin, prostaglandins, complement system

33
Q

What chemical mediators increase blood flow?

A

Histamine and prostaglandins

34
Q

What chemical mediators effect vascular permeability?

A

Histamine and leukotrienes

35
Q

Which chemical mediator effects phagocytosis?

A

C3b

36
Q

Which chemical mediators effect neutrophil chemotaxis?

A

C5a, LTB4, bacterial peptides

37
Q

Why is exudation of fluid good?

A

Delivery of nutrients/ plasma proteins/ inflam mediators/ fibrinogen, dilute toxins, incrase lymphatic drainage, deliver antigens to IS and deliver microorganisms to phagocytes

38
Q

Does vasodilation increase temp?

A

Yes

39
Q

Why is pain and loss of function good?

A

Forces rest, reduces chance of further trauma

40
Q

What are the local complications of acute inflam?

A

Swelling (blockage of ducts), compression and serositis from exudate, loss of fluid (burns on skin), pain and loss of function

41
Q

What are the systemic effects of acute inflam?

A

Fever (PG’s, Il-1, TNFalpha), leukocytosis, acute phase response (depresses appetite, increased pulse, sleep disturbances- test CRP), shock (circulatory failure)

42
Q

What are the developmental stages of acute inflam?

A

Complete resolutions, abscess, chronic inflam and fibrous repair, death

43
Q

What happens during resolution after acute inflam?

A

Neutrophils don’t marginate, vascular permeability returns to normal, exudate drains via lymphatic system, fibrin degraded, neutrophils die, damaged tissue may regenerate

44
Q

Give 4 clinical examples of acute inflam (see causative agents from lecture notes and group work)

A

Lobar pneumonia, acute appendicitis, bacterial meningitis, ascending cholangitis and liver abscess

45
Q

Name 3 inherited disorders of acute inflam process

A

RARE: Hereditary angio-oedema, alpha-1 anti trypsin deficiency, chronic granulomatous disease

46
Q

What are the consequences of acute inflam in serous cavities?

A

Exudate pours into pleural/pericardial/peritoneal cavities- respiratory or cardiac impairment, localised fibrin deposition, bread and butter pericarditis

Semester 2 Mechanisms Of Disease (4 decks)

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