Inflammation

Question 1

What is inflammation?

Answer 1

Response of living tissue to injury

Question 2

Acute inflammation features

Answer 2

Immediate
Short
Limits damage
Innate (built in)
Stereotyped - same response each time

Question 3

Phases of inflammation and aims

Answer 3

Vascular phase - changes blood flow, accumulates exudate

Cellular phase - delivers neutrophils

Question 4

How is inflammation controlled

Answer 4

Chemical mediators

Question 5

What’s an cause inflammation

Answer 5

Trauma/foreign body
Microorganisms
Hypersensitivity (allergies)
Other illness (cancer, necrosis)

Question 6

5 clinical signs of inflammation

Answer 6

Rubor (red)
Calor (hot)
Dolor (pain)
Tumor (swelling)
Loss of function

Question 7

Vascular changes in vascular phase and what they achieve

Answer 7

Vasoconstriction (seconds)
Vasodilation (minutes) (redness and heat)
Increased permeability (swelling)

Question 8

Starlings law

Answer 8

Movement of fluid is controlled by:
Hydrostatic pressure and oncotic pressure

(High hydrostatic pressure pushes fluids out, high oncotic pressure pulls fluid in - sponge)

Question 9

What do the vascular changes achieve?

Answer 9

Vasodilation - increased capillary hydrostatic pressure

Increased vessel permeability - plasma proteins move to interstitium (increases interstitial oncotic pressure)

FLUID MOVES OUT OF VESSEL INTO INTERSTITIUM = OEDEMA

Question 10

What happens as a result of fluid moving out of capillaries/vessels?

Answer 10

Increased viscosity of blood

Reduced flow = stasis

Question 11

Exudate (how and what is it)

Answer 11

Caused by increased vascular permeability
Protein rich
Occurs in inflammation

Question 12

Transudate (how and what)

Answer 12

Permeability unchanged
Movement due to - increased capillary hydrostatic pressure/reduced capillary oncotic pressure

Occurs in: heart, hepatic, renal failure

Question 13

How does a vessel wall become permeable? (3 ways)

Answer 13

Retraction of endothelial cells (histamine, nitric oxide, leukotrienes)

Direct injury (burns, toxins, trauma)

Leukocyte dependent injury (enzymes/toxic oxygen species released by active inflammatory cells)

Question 14

Why is the vascular phase effective? (3 ways)

Answer 14

Interstitial fluid increase dilutes toxins

Exudate delivers proteins (fibrin limits spread via mesh prison, immunoglobulins delivered)

Fluid drains to lymph nodes (delivers antigens - stimulate adaptive response)

Question 15

Main cell involved in cellular phase

Answer 15

Neutrophil - trilobed nucleus (appear purple dots on histology)

Question 16

How do neutrophils escape vessels (4 stages)

Answer 16

Margination - move to periphery of vessel

Rolling - via selectins

Adhesion - via integrins

Emigration (diapedesis) - moves to interstitium

Question 17

How do selectins work?

Answer 17

Present on activated endothelial cells
Activated by chemical mediators
Responsible for ROLLING

Question 18

How do integrins work?

Answer 18

Present on neutrophil surface
Change from low affinity to high affinity
Responsible for ADHESION

Question 19

How do neutrophils move through interstitium?

Answer 19

Chemotaxis - Movement along an increasing chemical gradient (low —> high) of chemoattractants

Question 20

Chemoattractants: and what it achieves

Answer 20

Bacterial peptides, inflammatory mediators

Causes rearrangement of neutrophil cytoskeleton to propel itself forward

Question 21

What do neutrophils do?

Answer 21

Phagocytosis
Into vesicle = phagosome
Fuse with lysosomes = phagolysosome
Release lysozymes and digest —> exocytosis

Also release inflators mediators

Question 22

How do neutrophils recognise what to phagocytose?

Answer 22

Opsonins on pathogen - C3b, Fc

Receptors for C3b and Fc are on neutrophil surface

Question 23

Killing mechanisms of neutrophils

Answer 23

Oxygen dependent - ROS ( superoxide, hydroxyl, hydrogen peroxide) or RNS (nitric oxide, nitrogen dioxide)

Oxygen independent - lysozyme, hydrolytic enzymes, defensins

Question 24

Why is the cellular phase effective?

Answer 24

Removes pathogens and necrotic tissue

Releases inflammatory mediators

Question 25

What are inflammatory mediators

Answer 25

Chemical messengers - control and coordinate inflammatory response

Question 26

Where can inflammatory mediators arise from

Answer 26

Activated inflammatory cells Platelets Endothelial cells Toxins (chemoattractants)

Question 27

Inflammatory mediators that cause vasodilation

Answer 27

Histamine Serotonin Prostaglandins Nitric oxide

Question 28

Inflammatory mediators that increase permeability

Answer 28

Histamine Bradykinin Leukotrienes C3a, C5a

Question 29

Mediators that act as chemoattractants

Answer 29

C5a TNF - a IL - 1 Bacterial peptides

Question 30

Inflammatory mediators that cause fever

Answer 30

Prostaglandins IL-1 IL-6 TNF-a

Question 31

Inflammatory mediators that cause pain

Answer 31

Bradykinin Substance P Prostaglandins

Question 32

Complications of inflammation can be:

Answer 32

Local (tissue, organ) or systemic (whole body)

Question 33

Local complications (SELP)

Answer 33

Swelling - compression of tubes (airways, bile duct, intestines) Exudate - compress organs (cardiac tamponade in pericardial sac) Loss of fluid - burns = dehydration Pain - muscle atrophy., psychosocial effects

Question 34

Systemic complications

Answer 34

Fever - pyrogens act on hypothalamus (eg prostaglandins) Leucocytosis - increased white cell production (act on bone marrow IL-6, TNF-a) Acute phase response Septic shock

Question 35

Acute phase response and proteins

Answer 35

Malaise, reduced appetite, altered sleep, tachycardia Induces rest Proteins: C reactive protein (CRP= inflammation severity marker) Fibrinogen A1 antitrypsin

Question 36

Septic shock

Answer 36

``` Huge release of chemical mediators Wide spread VASODILATION Hypotension Tachycardia Multi organ failure FATAL ```

Question 37

After acute inflammation

Answer 37

Resolution Repair with connective tissue Chronic inflammation

Question 38

Complete resolution

Answer 38

Mediators have short half lives Vessel and permeability return to normal Neutrophils = apoptosis and phagocytosed Exudate drains into lymphatics Regeneration of tissue if architecture is preserved

Question 39

Repair with connective tissue

Answer 39

Fibrosis if substantial tissue destruction

Question 40

Chronic inflammation

Answer 40

Prolonged inflammation with repair

Question 41

Itis =

Answer 41

Inflammation

Question 42

appendicitis cause

Answer 42

Blocked lumen from faecolith (solid poo) Accumulation of bacteria and exudate Increased pressure can cause burst appendix

Question 43

Appendicitis symptoms

Answer 43

Vague abdominal pain Sharp tight lower right fossa pain Severe overall pain

Question 44

Cause and symptoms pneumonia

Answer 44

Streptococcus pneumoniae Haemophilus influenzae Shortness of breath Cough Yellow/green sputum Fever

Question 45

Risk factors pneumonia

Answer 45

Smoking | Pre existing lung condition (COPD, asthma, malignancy)

Question 46

Bacteria meningitis causes and symptoms

Answer 46

Cause: Group B streptococcus E.coli Neisseria meningitides ``` Symptoms/signs: Headache Neck stiffness Photophobia (bright lights) Altered mental state ```

Question 47

What happens during meningitis?

Answer 47

Inflammation of meninges (protective layers between skull and brain) DURA, ARACHNOID, PIA (mater) - layers Compression of brain occurs

Question 48

Abscess

Answer 48

Accumulation of dead and dying neutrophils (pus) Liquefactive necrosis Compression of surrounding structures

Question 49

Inflammation of serous cavities

Answer 49

Pleural, peritoneal, pericardium

Question 50

Disorders of acute inflammation

Answer 50

Hereditary angio-oedema Alpha-1 antitrypsin deficiency Chronic granulomatous disease