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Pathophysiology PH1002 > Defence mechanisms of the body > Flashcards

Defence mechanisms of the body Flashcards

1
Q

What are the 3 lines of defence- skin

A

Skin (waterproof and impermeable) and mucous membrane- secrete things and trap things to stop pathogens going further

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2
Q

What are the 3 lines of defence- inflammation

A

non- specific, natural, innate immunity, rapid response

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3
Q

What are the 3 lines of defence- Immunity

A

specific, acquired immunity, adaptive, slow response

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4
Q

What is inflammation

A

The body’s non- specific protective response to tissue damage, disease or injury in an attempt to destroy, dilute wall off both the injurious agents.

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5
Q

what are the 5 cardinal signs

A

redness (rubor), swelling (tumor), warmth (calor), pain (dalor), loss of function (function laesa)

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6
Q

what is the purpose of inflammation

A

To prevent minor infections becoming overwhelming

to prepare any damaged tissue for repair

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7
Q

Factors that cause inflammation- injury/ trauma

A

physical/thermal- hot or cold burns/ radiation- flash burns/ electrical trauma/ chemical

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8
Q

Factors that cause inflammation- infection

A

virus/ bacteria/ rickettsiae- type of organism that is combination of bacteria and virus/ fungi/ protozoa/ worms

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9
Q

Factors that cause inflammation- infraction

A

lack of oxygen- e.g. myocardial infract which leads to ischaemia

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10
Q

Factors that cause inflammation- immune response

A

foreign protein hypersensitivity, auto immunity

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11
Q

Factors that cause inflammation- nutrient

A

nutrient deprivation

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12
Q

Suffix ITIS- Conjunctivitis

A

infection of eye

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13
Q

Suffix ITIS- tendonitis

A

inflammation of tendon

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14
Q

Suffix ITIS- osteoarthritis

A

inflammation of joints

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15
Q

Suffix ITIS- peritonitis

A

inflammation of abdominal cavity

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16
Q

Suffix ITIS- pericarditis

A

inflammation of the heart

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17
Q

Suffix ITIS- capsulitis

A

inflammation of capsule around the joint

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18
Q

What is vascular response

A

it can be defined as the responsiveness of a blood vessel to a specific stimulus

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19
Q

Vascular response- Transient vasoconstriction- step 1

A

for a small period of time the vessels constrict- muscle tone of arterioles in damaged area to reduce blood flow to reduce the travel of bacteria

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20
Q

Vascular response- more prolonged vasodilation- step 2

A

blood vessels will open back up again- to increase blood flow to allow cells needed to fight infection get to the infection- leads to heat

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21
Q

Vascular response- increased blood flow and increase in hydrostatic pressure- step 3

A

this occurs to dilute down any injurious agent. This puts pressure on cell wall of arteriole- cause things to leak out and leads to swelling

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22
Q

Vascular response- 4 capillary

A

opening of capillary beds

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23
Q

Vascular response- bradykinin

A

gets released as soon as the inflammatory process begins, it is a type of protein/ amino acid and is released as soon as the inflammatory process starts and cause cells within the blood vessel to constrict, this causes capillary endothelium to react (crenelation)

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24
Q

Vascular response- plasma-6

A

leaking of plasma etc.- protein rich exudate

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25
Q

Vascular response- oedema formation-7

A

as oedema gets bigger this means more and more proteins are being let out the cell this leads to the blood being thick and concentrated

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26
Q

Vascular response- 8 haemoconcetration

A

blood flow slows down and almost stops

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27
Q

cellular response- first- neutrophils

A

neutrophils are the first leucocytes (WBC) to emigrate to the site of injury (as they are small and travel fast). They do not last long and often die. They are followed by monocytes which mature into macrophages

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28
Q

cellular response- second- WBC squeezing

A

WBC squeeze through the endothelial gaps by the process of diapedesis (passage of blood cells through the intact walls of the capillary). They are drawn to the site of injury in response to chemical mediators in a process known as chemotaxis

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29
Q

cellular response- third- neutrophil chemotaxis

A

neutrophils also produce powerful chemotactic chemicals when they die

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30
Q

steps of cellular changes- 1

A

margination- WBC move to outer part of blood vessel, due to the damaged cells becoming positively charged

31
Q

steps of cellular changes- 2- rolling

A

rolling- WBC roll around the edge of the blood vessel

32
Q

steps of cellular changes- 3

A

adhesion- WBC become stuck to edge of blood vessel

33
Q

steps of cellular changes- 4

A

Pavementation- WBC become flattened on the edge of blood vessel and form a pavement like pattern

34
Q

steps of cellular changes- 5- chemotaxis

A

chemotaxis- chemical messages released to draw the required cells to damaged area

35
Q

steps of cellular changes- 6 psedupod formation

A

psedupod formation- projection of neutrophils or monocyte will push a little bit through the surface of blood vessel

36
Q

steps of cellular changes- 7- ameboid action

A

ameoboid action- WBC wriggle to prevent getting stuck, until it gets to the extracellular fluid

37
Q

steps of cellular changes- 8- migration

A

migration- WBC has moved to extracellular fluid (diapedesis- cell walking)- because of vascular changes this can happen

38
Q

steps of cellular changes- 9- chemotaxis

A

chemotaxis

39
Q

What is phagocytosis

A

the process of ingestion of foreign or particulate matter- done by WBC (macrophage), causes them to die

40
Q

What is lymphatic drainage

A

lymphatic system assists in drainage of tissue fluid

41
Q

How does lymphatic drainage work

A

during inflammation lymphatic vessels open up assisting drainage of excessive fluid , the products of inflammation and any antigens not dealt with by the inflammatory process. Antigen presenting cells present to immune system, triggering the 3rd line of defence- the specific immune system

42
Q

Cardinal sight- Rubor

A

Redness- vasodilation; increase blood floe to injured area

43
Q

Cardinal sight- Calor

A

Heat- vasodilation; increased blood flow to the injured area

44
Q

Cardinal sight- dolor

A

Pain- increased vascular permeability and accumulation of fluid cases compression in the tissue; chemical mediator can also direct elicit plane response- pain prevent further damage

45
Q

Cardinal sight- tumor

A

oedema, extracellular fluid accumulation often in the tissue as a result of increased permeability

46
Q

Limitations of blood tests used to detect acute inflammation

A

They can detect inflammation but not what caused it- used other tests after this

47
Q

Main blood tests to detect acute inflammation

A

White blood cell count, erythrocyte sedimentation rate, C- reactive protein (produced by liver)

48
Q

Blood test used to detect acute inflammation- White blood cell count

A

reference value- 5000-10,000 /mm3,

changes with inflammation- circulating WBC are increased, often above 10,000 /mm3

49
Q

Blood test used to detect acute inflammation- white blood cell differential (reference values)

A

neutrophils 45-75% bands (immature neutrophils- 0.5%- if high indicates bacterial infection)
Eosinophils- 0-8%
Basophils- 0-3%
Lymphocytes- 16-46%- go up if exposed to virus
monocytes- 4-11%

50
Q

Blood test used to detect acute inflammation- white blood cell differential (changes with inflammation)

A

measure proportion of each of the 5 types of WBC’s, the proportion of immature neutrophils is increased in comparison to other WWBC types

51
Q

Blood test used to detect acute inflammation- erythrocyte sedimentation rate (reference value)

A

0-17 mm/hr for men
1-25 mm/hr for women
44-114 mm/hr in pregnancy
1-13 mm/hr in children

52
Q

Blood test used to detect acute inflammation- erythrocyte sedimentation rate (changes with inflammation)

A

Detects RBC clumping or stacking as a result of increased fibrinogen levels; levels increase often above 100mm/hr for those with inflammation

53
Q

Blood test used to detect acute inflammation- C- reactive protein (produced by liver)- reference value

A

Routine CRP <10MG/L
High sensitivity CRP 0.1-3.8 MG/L
goes up in acute phase of inflammation, can settle back down again and look normal in patients with chronic inflammation

54
Q

Blood test used to detect acute inflammation- C- reactive protein (produced by liver)- changes with inflammation

A

> 10mg/L indicates significant inflammatory disease

55
Q

Blood test used to detect acute inflammation-compliment activity (reference value)

A

Total compliment 62-145 U/ml

C3 (compromises of 70% of total protein in the compliment system) 80-184 mg/dL

56
Q

Blood test used to detect acute inflammation-compliment activity changes with inflammation

A

elevated in inflammation signifying the activation of; compliment over time may decrease, indicating the complement factors are exhausted

57
Q

Blood test used to detect acute inflammation-prothrombin time (reference value)

A

measured in time to coagulate approximately 11.2-13.2 seconds

58
Q

Blood test used to detect acute inflammation- prothrombin time (changes with inflammation)

A

increased prothrombin result in a reduced time to coagulate

59
Q

Blood test used to detect acute inflammation- fibrinogen (reference value)

A

175-400 mg/dL

60
Q

Blood test used to detect acute inflammation- fibrinogen (changes with inflammation)

A

elevated during inflammation to promote coagulation

61
Q

Acute and chronic inflammation- cause

A

Acute- usually known e.g. trauma, surgery, antigen invasion
Chronic- often unknown could be as it has gone on for so long e.g. unresolved acute inflammation, complications of acute inflammation, low grade, persistent irritants

62
Q

Acute and chronic inflammation- onset

A

Acute- rapid, chronic- slow, insidious

63
Q

Acute and chronic inflammation- deterioration

A

Acute- rapid, acute response (vascular changes, oedema and leucocyte infiltration, exudate formation)
Chronic- slower deterioration, lack of an acute responses, irritants unable to penetrate deeply or spread rapidly, proliferation of fibroblasts

64
Q

Acute and chronic inflammation- resolution

A

acute- full resolution, chronic- fails to resolve

65
Q

Acute and chronic inflammation- course

A

acute- follows a definite course, self limiting

chronic- fails to resolve

66
Q

Acute and chronic inflammation- main cells involved

A

acute- neutrophils, followed by monocytes- macrophages, chronic- macrophages and fibroblasts

67
Q

Acute and chronic inflammation- phagocytosis

A

Acute active phagocytosis, chronic- persistent irritants resistant to phagocytosis, ongoing chemotaxis

68
Q

Acute and chronic inflammation- outcome

A

acute- beneficial, prevent invasion, first stage of repair, restoration full function, chronic- destructive scar tissue formation, non- functional- contractures (poor range of movement)- deformities, loss of movement, loss of function

69
Q

Acute and chronic inflammation- examples

A

acute bronchitis, acute appendicitis, chronic bronchitis, chronic obstructive pulmonary disease

70
Q

common types of medication for inflammation- aspirin

A

suppresses inflammatory processes by acting on prostaglandins- lipids produced by damaged tissue

71
Q

common types of medication for inflammation- NSAIds

A

non steroid anti- inflammatory drugs (NSAIDs), e.g. ibuprofen, naproxen, diclofenac sodium (voltarol)

72
Q

common types of medication for inflammation- corticosteroids

A

this acts by interrupting inflammation process they stop chemical mediator, and suppress phagocytosis, used for chronic inflammation e.g. prednisone

73
Q

common types of medication for inflammation- immunosuppressants

A

suppress natural responses- stops WBC from doing what they are supposed to be doing, this is good if they are out of control. however body can be prone to other infections as it is non- specific (global effect) e.g. methotrexate, these also affect RBC

74
Q

What are the mechanisms of inflammation

A

vascular response, cellular response, phagocytosis, lymphatic drainage

Pathophysiology PH1002 (22 decks)

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