Session 2 - Acute Inflammation

Question 1

What are 6 causes of acute inflammation?

Answer 1

Foreign bodies 
Immune reactions 
Infections
Tissue necrosis
Trauma
Physical and chemical agents

Question 2

What are the 5 signs of acute inflammation?

Answer 2

Redness 
Heat
Swelling
Pain
Loss of function

Question 3

What is rubor?

Answer 3

Redness

Question 4

What is calor?

Answer 4

Heat

Question 5

What is tumor?

Answer 5

Swelling

Question 6

What is dolor?

Answer 6

Pain

Question 7

What is inflammation?

Answer 7

Response of living tissue to injury

Question 8

What are 2 phases of inflammation?

Answer 8

Vascular

Cellular

Question 9

What happens during vascular phase with regard to blood flow?

Answer 9

Brief vasoconstriction for seconds
Longer lasting vasodilation, causing heat and redness
Increased permeability so fluid and cells can escape

Question 10

What is Starling’s Law?

Answer 10

Movement of fluid is controlled by the balance of hydrostatic pressure and oncotic pressure

Question 11

What is hydrostatic pressure?

Answer 11

Pressure exerted on a vessel wall by a fluid, pushing fluid away from blood vessels

Question 12

What is oncotic pressure?

Answer 12

Pressure exerted by proteins, drawing fluid towards blood vessels

Question 13

Why does heat and redness present during acute inflammation?

Answer 13

Vasodilation

Question 14

Why does oedema present during acute inflammation?

Answer 14

Vasodilation increases capillary hydrostatic pressure, increased vessel permeability allows plasma proteins to move into interstitial, causing increased interstitial oncotic pressure, hence fluid moves out of vessel into interstitial fluid

Question 15

What is stasis?

Answer 15

Reduced flow through vessel

Question 16

Why does acute inflammation cause stasis?

Answer 16

Fluid moves out of vessel, increasing viscosity of blood

Question 17

What is exudate?

Answer 17

Protein rich fluid occurring in inflammation when vascular permeability increases

Question 18

What is transudate?

Answer 18

Ultrafiltrate of plasma occurring during organ failure as fluid moves due to increased capillary hydrostatic pressure and decreased capillary oncotic pressure, and vascular permeability is unchanged

Question 19

What are 3 ways of increasing permeability of vessel walls?

Answer 19

Retraction of endothelial cells
Direct injury
Leukocyte dependent injury

Question 20

What are 3 main components that makes vascular phase effective?

Answer 20

Interstitial fluid
Exudate
Lymph nodes

Question 21

What is the role of interstitial fluid during acute inflammation?

Answer 21

Dilutes toxins

Question 22

What are the 2 roles of exudate in acute inflammation?

Answer 22

Delivers proteins

• fibrin to limit spread of toxin
• immunoglobulins from adaptive immune response

Question 23

What is the role of lymph nodes in acute inflammation?

Answer 23

Fluid drains to lymph nodes, stimulating adaptive immune response

Question 24

What is the primary white blood cell involved in cellular phase of acute inflammation?

Answer 24

Neutrophils

Question 25

What are the 4 steps of neutrophils escaping vessels?

Answer 25

1. Margination 2. Rolling 3. Adhesion 4. Emigration / diapedesis

Question 26

What are the 2 main adhesion molecules used by neutrophils to escape from vessels?

Answer 26

Selections Integrins

Question 27

What do selectins do?

Answer 27

Responsible for rolling, expressed on activated endothelial cells and are activated by chemical mediators

Question 28

What do integrins do?

Answer 28

Found on neutrophil surface, changes from low affinity to high affinity, responsible for adhesion

Question 29

How do neutrophils move through the interstitium?

Answer 29

Chemotaxis, along an increasing chemical gradient of chemoattractants

Question 30

How do neutrophils recognize what to phagocytose?

Answer 30

Opsonisation - toxin covered in C3b and Fc and neutrophils have the respective receptors on its surface

Question 31

What are the 2 types of opsonins?

Answer 31

C3b and Fc

Question 32

What are 2 ways neutrophils destroy pathogens?

Answer 32

Oxygen dependent Oxygen independent

Question 33

What are the 2 molecules that oxygen dependent killing mechanisms use?

Answer 33

Reactive oxygen intermediates and nitrogen intermediates

Question 34

What are the 3 types of molecules used in oxygen independent killing mechanisms?

Answer 34

Lysosome Hydrolytic enzymes Defensins

Question 35

What are 2 ways that cellular phase is effective in acute inflammation?

Answer 35

Removal of pathogens and necrotic tissue Release of inflammatory mediators

Question 36

What are inflammatory mediators?

Answer 36

Chemical messengers that control and coordinate inflammatory response

Question 37

What are 3 examples of mediators that controls vasodilation?

Answer 37

Histamine Serotonin Prostaglandins

Question 38

What are 3 mediators that increases vascular permeability?

Answer 38

Histamine Bradykinin Leukotrienes

Question 39

What are 3 mediators that controls chemotaxis?

Answer 39

C5a TNF-a IL-1

Question 40

What are 3 mediators that causes systemic responses?

Answer 40

Prostaglandins IL-6 IL-1

Question 41

What are 3 mediators that control pain?

Answer 41

Bradykinin Substance P Prostaglandin

Question 42

What are 4 types of local complications of acute inflammation?

Answer 42

Swelling can cause compression of tubes, exudate compresses organs, loss of fluid, pain can lead to psychosocial consequences

Question 43

What are 4 forms of systemic effects of acute inflammation?

Answer 43

Fever - pyrogens act on hypothalamus to increase temperature Leucocytosis - mediators act on bone marrow to increased production of white cells Acute phase response - reduced appetite, altered sleep to induce rest Septic shock - dramatic drop in BP due to widespread vasodilation

Question 44

What are 3 possible outcomes after acute inflammation?

Answer 44

1. Complete resolution 2. Repair with connective tissue (fibrosis) 3. Progression to chronic inflammation (prolonged inflammation with repair)

Question 45

What is hereditary angio-oedema?

Answer 45

Inherited deficiency of C1-esterase inhibitor

Question 46

What is alpha-1 antitrypsin deficiency?

Answer 46

Low levels of alpha-1 antitrypsin, a protease inhibitor which deactivates enzymes released from neutrophils at the site of inflammation, so proteases act unchecked and destroy normal parenchyma tissue

Question 47

What are the symptoms of alpha-1 antitrypsin deficiency?

Answer 47

Emphysema

Question 48

What is chronic granulomatous disease?

Answer 48

Phagocytes cannot generate free radical superoxide, bacteria phagocytosed but phagocytes cannot kill them as they cannot do oxygen burst, results in many chronic infections

Question 49

How does appendicitis occur?

Answer 49

Lumen is blocked by faecolith, accumulation of bacteria and exudate leads to increased pressure and eventually perforation

Question 50

What are 2 organisms that cause pneumonia?

Answer 50

Streptococcus Pneumoniae | Haemophilus influenzae

Question 51

What are 4 symptoms of pneumonia?

Answer 51

Shortness of breath Cough Sputum Fever

Question 52

What are 2 risk factors of pneumonia?

Answer 52

Smoking | Pre existing lung infection

Question 53

What is bacterial meningitis?

Answer 53

Inflammation of meningitis

Question 54

What are 3 causative organisms of bacterial meningitis?

Answer 54

Group B streptococcus E. Coli Neisseria meningitides

Question 55

What are 4 symptoms of bacterial meningitis?

Answer 55

Headache Neck stiffness Photophobia Altered mental state

Question 56

What are abscesses?

Answer 56

Accumulation of dead and dying neutrophils with associated liquefaction necrosis