Inflammation Flashcards

1
Q

3 lines of defence

A

1- skin and mucous membranes
Skin is physical barrier and waterproof
Mucous membranes secrete things and trap viruses and bacteria
Eg, tears wash away particles, eyelashes trap particles, blink reflex, enzymes neutralise harmful substances and skin stops entry of pathogens
2- inflammation
Non-specific, natural, innate immunity and rapid response

3- immunity
Specific, acquired immunity, adaptive and slow response

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2
Q

Define inflammation

A

Body’s non specific protective response to tissue damage, disease or injury in attempt to destroy, dilute or wall off injurious agent and injured tissue

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3
Q

5 cardinal signs of inflammation

A

Acronym: We See Really Painful Legs

Warmth / calor - increased blood flow, either specific or whole body (Pyrexia)
Swelling/ tumor- oedema, leaky fluid
Redness/ rubor- increased blood flow
Pain/ dolor - locally by compression of nerve endings + chemical release
Loss of function / function leasa

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4
Q

Why do we have inflammation?

A

Prevents minor infections from becoming unmanageable

Prepares damaged tissue for repair

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5
Q

5 factors that cause inflammation

A

Injury / trauma- physical (sports), thermal (ice burns), radiation (flash burns), electrical and chemical

Infection- virus, bacterium, rickettsiae, fungi, Protozoa or worms

Infarction- lack of oxygen to damaged tissue eg, MI leads to ischaemia

Immune reactions- foreign protein hypersensitivity like allergies and auto immune conditions like RA or ankylosing spondylitis or chrons disease

Nutrient deprivation

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6
Q

ITIS

A

Means inflammation

Eg
Conjunctivitis - eye inflammation 
Arthritis- inflammation in joints 
Tendinitis- inflamed tendons
Appendicitis - inflamed appendix 
Peritonitis - inflamed abdominal cavity 
Pericarditis- inflamed heart 
Capsulitis - inflamed capsules of joints
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7
Q

Mechanism of inflammation

A

Vicky Can’t Pick Lemons

Vascular response- changes in blood flow and protein rich exudation
Cellular response - leucocyte emigration
Phagocytosis - starts clear up process of causative agent
Lymphatic drainage - rid of excess fluid and gives protection

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8
Q

Steps in vascular response

A

TRANSIENT VASOCONSTRICTION- few seconds
MORE PROLONGED VASODILATION
INCREASE BLOOD FLOW AND HYDROSTATIC PRESSURE
OPENING OF CAPILLARY BEDS
INCREASED VASCULAR PERMEABILITY
BRADYKININ- amino acid so Capillary endothelium retracts (crenallation). Causes muscles in blood vessel walls to constrict so gaps are larger in vessels.
Leaking plasma- protein rich exudate
Oedema formation - fluid retention at injury site
Haemoconcentration - more proteins lost from blood , blood gets thicker and more concentrated
Stasis - blood flow slows and then stops

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9
Q

Cellular response

A

Basically, neutrophils get to site first, they are small and travel quickly in blood. Drawn by chemotaxis. Neutrophils also produce chemotactic chemicals.
then monocytes, which last longer but take longer to arrive as larger
Turns into macrophages

WBC travel on inside normally
Chemotaxis - WBCs to rim of vessel in MARGINATION
Endothelial cells positive charge and WBC negative
ROLL of WBCs as cant move smoothly
ADHESION- WBCs stick to vessel walls
PAVEMENTING- Flattens WBCs at walls
All due to chemotaxis
WBCs struggle to get through gaps in blood vessels and form projections called pseudopods
WBCs wriggle in amoeboid actions
WBCs pass through gaps by emigration and diapedesis cell walking (from blood vessel into extracellular fluid to site of injury)
Chemotaxis encourages more WBCs to area to destroy damaged cells or pathogen

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10
Q

Phagocytosis

A

Neutrophils and monocytes become macrophages at injury site

Macrophage ingests + destroys antigen, remove damaged tissue etc.

Macrophages die in process

This is non specific

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11
Q

Lymphatic drainage

A

Lymph system beside vascular, runs through lymph nodes like femoral triangle, popliteal fossa, cubital fossa etc.

Lymphatic system drains tissue fluid, products of inflammation and antigens not dealt with

Antigen presenting cells present to immunity - 3rd line of defence

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12
Q

WHY RUBOR?

A

Increased blood flow to area via vasodilation

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13
Q

Why calor?

A

More blood flow to area via vasodilation. It can be local or pyrexia (whole body increases in temperature)

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14
Q

Function leasa

A

Because of tissue damage, swelling and pain

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15
Q

Dolor

A

More vascular permeability and fluid = compressed tissue and compresses nerves. Chemical mediators elicit pain on nerve endings

Pain prevents more inflammation

Diabetics have reduced pain

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16
Q

Tumor

A

Increased vascular permeability of vessels

Extra cellular fluid accumulates in tissues to form an oedema

17
Q

Blood tests that detect inflammation

A

HIGH WHITE BLOOD CELL COUNT (leucocytosis) above 10,000 mm2

WHITE BLOOD CELL DIFFERENTIAL- proportions of different WBCs . In inflammation proportion of immature neutrophils increases more than others,

ERYTHROCYTES SEDIMENTATION- red blood cells sediment. With inflammation, more fibrinogen causes clumping of RBCs. So RBCs sediment at faster rate. Above 100mmhr

C REACTIVE PROTEIN- protein produced by liver in acute inflammation more than 10mg/L

COMPLIMENT ACTIVITY- activation of compliment in inflammation. Over time this may decrease as compliment factors exhausted.

PROTHROMBIN TIME- increased prothrombin means reduced time to coagulate

FIBRINOGEN- elevated during inflammation to promote coagulation

18
Q

CAUSE OF ACUTE INFLAMMATION

A

Often known like trauma, surgery or antigen invasion

19
Q

CAUSES OF CHRONIC INFLAMMATION

A

Often unknown, like unresolved acute or persistent irritants

20
Q

Onset of acute

A

Rapid onset

21
Q

Onset of chronic

A

Slow

22
Q

Deterioration of acute inflammation

A

Rapid acute response (VCPL)

Exudate formation

23
Q

Deterioration of chronic

A

Slow and lack of acute response

Proliferation of fibroblasts

24
Q

Resolution of acute

A

Fully resolved

25
Q

Resolution of chronic

A

Fails to resolve

26
Q

Course of acute

A

Definite course

27
Q

Course of chronic

A

Slow unremitting

28
Q

Main cells in acute

A

Neutrophils, monocytes and macrophages

29
Q

Main cells I chronic

A

Macrophages and fibroblasts

30
Q

Acute phagocytosis

A

Active phagocytosis

31
Q

Phagocytosis of chronic

A

Irritant resistant to phagocytosis

Ongoing chemotaxis

32
Q

Outcome of acute

A

Beneficial
Prevent invasion
1st stage of tissue repair

33
Q

Outcome of chronic

A

Destructive scar tissue

Loss of movement

34
Q

Examples of acute

A

Acute tonsillitis
Acute appendicitis
Acute sprain

35
Q

Examples of chronic

A

Chronic bronchitis
RA
COPD
Ankylosing spondylitis

36
Q

Medication for inflammation

A

Aspirin- suppresses inflammatory response. Prostaglandins

NSAIDS
Ibuprofen
Diclofenac sodium
Naproxen

Corticosteroids
Prednisolone- interrupts inflammation chronic. Stops chemical mediators
Suppresses phagocytosis

Immunosuppressants- methotrexate
Suppresses natural response but can make prone to other infections, non specific