Acute Inflammation Flashcards Preview

ESA2 - Mechanisms Of Disease > Acute Inflammation > Flashcards

Flashcards in Acute Inflammation Deck (58):
1

What is the difference between acute and chronic inflammation?

- ACUTE evolves over hours/days
- CHRONIC evolves over weeks, months and even years

2

What suffix is used to indicate inflammation of an organ/tissue?

-ITIS e.g. inflammation of the appendix would be "appendicitis"

3

Why do chemical mediators (leukocytes, plasma proteins) need to be delivered to a site of injury?

Local defences are not enough to prevent against infection e.g. Epithelia

4

How are leukocytes and fluid signalled to leave the blood cappillary at a site f damage?

- Epithelia release chemical mediators of inflammation (e.g. cytokines, chemokines)
- These signal immune response cells and make the walls of capillaries more permeable so fluid and leukocytes can leak out

5

Name 6 causes of inflammation

- Foreign bodies
- Infections (bacterial, viral etc.)
- Tissue necrosis
- Trauma
- Physical and chemical agents

6

What are the characteristic clinical signs of acute inflammation?

- RUBOR (redness)
- CALOR (heat)
- TUMOUR (swelling)
- DOLOR (pain)
- LOSS OF FUNCTION (promotes rest)

7

What is inflammation?

- Response to injury of a vascularised living tissue
- Delivers defensive materials to a site of injury

8

Describe how an area of inflammation can be come red and hot (RUBOR and CALOR)

- Blood vessels in area of injury dilate
- INCREASED PERFUSION at site of injury to transport chemical mediators and plasma proteins
- Area becomes red from increased blood flow and hot from dilation (more heat loss)

9

What is the role of bradykinins?

- Chemical mediators that stimulate specialised nerve endings at the site of injury causing PAIN
- Increases permeability of vessel walls so exudate leaks out

10

What is the significant of vasodilation of arterioles following inflammation?

- Arterioles dilate and increase perfusion into capillaries so CAPILLARY PRESSURE RISES
- Increased delivery of fluid and plasma proteins to injured tissues

11

Explain how increased leakage of venule walls leads to decrease in perfusion rate upstream

- Plasma proteins escape, leads to increased HAEMATOCRIT of venules and increased RESISTANCE of blood flow
- Increased pressure as outflow is hampered, upstream vessel lumens dilate and blood flow slows
- Increased pressure means greater exudate into tissues so more plasma proteins and fluid delivered

12

What are vasoactive amines? Give 2 examples

- Group of chemical mediators that are the first to appear during inflammation
- Examples are Histamine and Serotonin

13

Where is histamine found?

- Mast cells
- Basophils
- Platelets

14

What can stimulate the release of histamine? (3)

- Physical damage
- Immune/hypersensitivity reactions
- Complement components

15

What is the role of histamine in acute inflammation?

- PAIN, arteriolar dilation and venular leakage
- Causes endothelial cells in capillary walls to CONTRACT and pull apart, forming GAPS which allow plasma proteins and fluid to leak out into tissues (exudate)

16

What is the main difference between the action of histamine and serotonin?

Serotonin can STIMULATE FIBROBLASTS

17

What are prostaglandins and when are they produced?

- Produced during inflammation by cell membrane phospholipids
- Cause VASODILATION, make the skin more sensitive to pain and cause FEVER

18

Describe how NSAIDS such as aspirin work

- Blocks production of prostaglandins from arachnodonic acid by inhibiting cyclo-oxygenase
- This reduces pain and swelling

19

How can the release of histamine be stimulated?

In response to:
- Physical damage
- Immune response/hypersensitivity
- Complement components

20

Explain how vasodilation of arterioles increases the delivery of exudate to an area of injury

- Dilation causes flow to accelerate in capillaries so CAPILLARY PRESSURE RISES
- Capillaries that are normally empty are filled so increases delivery of fluid and leucocytes

21

What is meant by haematocrit?

Ratio of volume of erythrocytes to total volume of blood within the vessel

22

Explain how leaky venules can lead to an increase in resistance of blood flow within them

- Plasma can escape through tiny gaps between endothelial cells
- INCREASED HAEMATOCRIT within venules to blood is more viscous, leading to resistive flow

23

Explain the vascular changes that occur in acute inflammation

- Vasodilation of arterioles to increase blood flow to site of injury
- Increased permeability of venules leads to increased loss of exudate from vessel; blood is more viscous and flow slows at site of injury - STASIS
- Reduced rate of outflow so exudate can be delivered

24

What 4 forces are involved in Starling's Law?

- Capillary pressure
- Interstitial free fluid pressure
- Plasma colloid osmotic pressure
- Interstitial fluid colloid osmotic pressure

25

What are the main forces involved in driving fluid IN and OUT of the capillary?

- IN - Plasma colloid osmotic pressure of plasma proteins (e.g. increased plasma proteins inside capillary)
- OUT - hydrostatic pressure of the blood (capillary pressure e.g. increased pressure of fluid)

26

Describe the lymphatic role of the tissue fluid in acute inflammation

- Exudate contains microorganisms and antigens, which are drained into the lymphatics
- Foreign antigens are presented to the immune system within the lymph nodes which aids the immune response

27

What do you call inflammation of the lymph nodes?

Lymphadenitis

28

Name 3 plasma proteins present in the exudate

- Opsonins
- Complement
- Antibodies

29

What is the name given to tissue fluid that contains no plasma proteins? Where might this be seen?

- TRANSUDATE (ultrafiltration of plasma that occurs in normal tissue)
- Seen in HEART FAILURE due to increased hydrostatic pressure of capillaries

30

Name 4 chemical mediators that induce vascular leakage

- Histamine
- Bradykinin
- Serotonin
- Complement C3a, C4a, C5a

31

What is the primary type of leucocyte involved in acute inflammation?

NEUTROPHIL

32

What does the presence of neutrophils in tissue suggest?

- Normally ONLY found in the blood and bone marrow
- Indicates INVASION BY BACTERIA/PARASITE and/or TISSUE INJURY

33

What is chemotaxis?

- Directional movement towards a chemical attractant (chemotaxins) at the site of injury
- These include bacterial products (e.g. ENDOTOXIN), injured tissues and substances released from leucocytes (CYTOKINES)

34

What is the role of chemotaxins? Give 4 examples

- Released by cells or bacteria to attract and recruit inflammatory cells at the site of injury
- Complement C3a, C5a; Endotoxin; Thrombin and FDPs, Leukotriene B4

35

What powerful chemotaxin is produced by leucocytes?

Leukotriene B4

36

What is Endotoxin?

Lipopolysaccharide CHEMOTAXIN released from outer membrane of Gram Negative bacteria

37

How do chemotaxins work to direct neutrophils to the site of injury?

- Chemotaxin binds to receptors on neutrophils and stimulates influx of Na+ and Ca2+
- Cell swells and cytoskeleton is reorganised into a triangular shape pointing in the direction of the chemotacic stimuli

38

Briefly describe margination, rolling and adhesion of neutrophils

- Endothelial wall is coated in adhesion molecules such as SELECTIN and INTEGRIN
- Neutrophils marginate at periphery of vessel and stick to the wall, binding to integrins and roll along wall binding to selectins until they become trapped

39

Describe the process of diapedesis

- Leucocytes DIG their way out of venules as they cannot escape through the gaps which exudate flows (too big)
- Produce COLLAGENASE which digests the basement membrane
- Pull themselves along collagen fibres of other tissues to reach site of injury

40

What is the role of opsonins? Give 2 examples

- Substances which bind to foreign bodies and allow them to be recognised by phagocytes and phagocytosed
- e.g. IgG antibody, complement C3b
- When not present, phagocyte recognises surface antigens

41

What is degranulation?

Digestion of a foreign body by granules of phagosomes - inject bactericidal substances into particle and destroys them

42

Describe 2 ways (one O2 dependant, one O2 independent) by which phagocytes can kill phagocytosed organisms

- OXYGEN DEPENDANT - production of ROS such as superoxide, H2O2 and OH- and release into phagosome
- OXYGEN INDEPENDENT - use of ENZYMES such as proteases and lysozyme

43

What is meant by an inflammatory mediator?

Any molecule produced during inflammation that modulates an inflammatory response

44

Name 3 common responses of cells to chemical inflammatory mediators

- Chemotaxis
- Phagocytosis
- Contraction/Relaxation (e.g. smooth muscle cells, venous endothelial cells)

45

Give 5 examples of groups of endogenous mediators of inflammation

- Vasoactive amines (histamine)
- Vasoactive peptides (bradykinin)
- Complement (C3a, C3b, C5a)
- Clotting factors and fibrinolytic cascades
- Cytokines and chemokines

46

What are the main sources and roles of inflammatory mediators?

- Vasodilation of arterioles
- Increased vascular permeability
- Chemotaxis
- Phagocytosis
- Pain

47

List 4 local complications of acute inflammation

- DAMAGE TO NORMAL TISSUE due to substances released by neutrophils
- OBSTRUCTION OF TUBES AND COMPRESSION caused by swelling and fluid accumulation
- LOSS OF FLUID due to increased tissue pressure so fluid leaks from surface wound
- PAIN/LOSS OF FUNCTION to enforce rest

48

Explain how a fever occurs in acute inflammation

- Macrophages stimulated by exogenous pyrogens and produce PYROGENIC CYTOKINES
- Stimulates production of PROSTAGLANDIN E2 from anterior hypothalamus which causes fever, pain and increased vascular permeability

49

What systemic effects can arise from acute inflammation? (4)

- Fever
- Leucocytosis
- Change in level of plasma proteins (acute phase response)
- Shock

50

Describe how neutrophilia can lead to leucocytosis

- Occurs during bacterial infection
- Colony stimulating factors produced by macrophages and endothelial cells stimulate bone marrow to produce more neutrophils
- Number of circulating leucocytes increases, causing leucocytosis

51

What is the acute phase response and what are the resulting symptoms?

- Change in level of plasma proteins produced by the LIVER within hours of injury
- Produced by CYTOKINES released during inflammation and cause tiredness and lack of appetite

52

Give examples of proteins which have an altered synthesis during the acute phase response

- DECREASED PRODUCTION - Albumin
- INCREASED PRODUCTION - fibrinogen, complement C3, ceruloplasmin, α-1 antitrypsin, C-reactive protein (CRP)

53

Explain how shock can occur in acute inflammation

- Spread of bacteria products and mediators around systemic circulation
- Leads to inflammation throughout body
- DRAMATIC DROP IN BLOOD PRESSURE due to widespread vasodilation and increased vascular permeability with resultant fluid exudate
- Often FATAL

54

Describe how acute inflammation is resolved

- Mediators and neutrophils have SHORT LIFESPAN so do not persist
- Once removed, vascular permeability returns to normal and exudate is reabsorbed or drained into lymphatics
- Neutrophils undergo apoptosis and are phagocytosed (along with necrotic debris) by macrophages

55

Name the 4 types of exudate and explain their appearance

- PUS/ABSCESS - creamy/white (rich in neutrophils)
- HAEMORRHAGIC - red (where vascular damage has occurred)
- SEROUS - clear (contains plasma proteins but no leucocytes)
- FIBRINOUS - friction between serosal surfaces (due to deposition of fibrin) e.g. bread and butter pericarditis

56

What is hereditary angio-oedema and what are the symptoms?

- Rare autosomal dominant deficiency of C1-ESTERASE INHIBITOR (complement protein)
- Attacks of non-itchy cutaneous angio-oedema and recurrent abdo pain (intestinal oedema)

57

Explain the consequences of α-1 antitrypsin disorder

- Deficiency in protease so enzymes released from neutrophils cannot be broken down
- Neutrophil enzymes can damage parenchymal tissue causing emphysema, liver disease or cirrhosis

58

Explain the pathophysiology of chronic granulomatous disease

- Genetic condition where phagocytes are unable to produce ROS superoxide so CANNOT GENERATE A RESPIRATORY BURST
- Chronic infections (as bacteria cannot be destroyed) and numerous granulomas formed