Defence mechanisms of the body Flashcards
What are the 3 lines of defence- skin
Skin (waterproof and impermeable) and mucous membrane- secrete things and trap things to stop pathogens going further
What are the 3 lines of defence- inflammation
non- specific, natural, innate immunity, rapid response
What are the 3 lines of defence- Immunity
specific, acquired immunity, adaptive, slow response
What is inflammation
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.
what are the 5 cardinal signs
redness (rubor), swelling (tumor), warmth (calor), pain (dalor), loss of function (function laesa)
what is the purpose of inflammation
To prevent minor infections becoming overwhelming
to prepare any damaged tissue for repair
Factors that cause inflammation- injury/ trauma
physical/thermal- hot or cold burns/ radiation- flash burns/ electrical trauma/ chemical
Factors that cause inflammation- infection
virus/ bacteria/ rickettsiae- type of organism that is combination of bacteria and virus/ fungi/ protozoa/ worms
Factors that cause inflammation- infraction
lack of oxygen- e.g. myocardial infract which leads to ischaemia
Factors that cause inflammation- immune response
foreign protein hypersensitivity, auto immunity
Factors that cause inflammation- nutrient
nutrient deprivation
Suffix ITIS- Conjunctivitis
infection of eye
Suffix ITIS- tendonitis
inflammation of tendon
Suffix ITIS- osteoarthritis
inflammation of joints
Suffix ITIS- peritonitis
inflammation of abdominal cavity
Suffix ITIS- pericarditis
inflammation of the heart
Suffix ITIS- capsulitis
inflammation of capsule around the joint
What is vascular response
it can be defined as the responsiveness of a blood vessel to a specific stimulus
Vascular response- Transient vasoconstriction- step 1
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
Vascular response- more prolonged vasodilation- step 2
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
Vascular response- increased blood flow and increase in hydrostatic pressure- step 3
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
Vascular response- 4 capillary
opening of capillary beds
Vascular response- bradykinin
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)
Vascular response- plasma-6
leaking of plasma etc.- protein rich exudate
Vascular response- oedema formation-7
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
Vascular response- 8 haemoconcetration
blood flow slows down and almost stops
cellular response- first- neutrophils
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
cellular response- second- WBC squeezing
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
cellular response- third- neutrophil chemotaxis
neutrophils also produce powerful chemotactic chemicals when they die
steps of cellular changes- 1
margination- WBC move to outer part of blood vessel, due to the damaged cells becoming positively charged
steps of cellular changes- 2- rolling
rolling- WBC roll around the edge of the blood vessel
steps of cellular changes- 3
adhesion- WBC become stuck to edge of blood vessel
steps of cellular changes- 4
Pavementation- WBC become flattened on the edge of blood vessel and form a pavement like pattern
steps of cellular changes- 5- chemotaxis
chemotaxis- chemical messages released to draw the required cells to damaged area
steps of cellular changes- 6 psedupod formation
psedupod formation- projection of neutrophils or monocyte will push a little bit through the surface of blood vessel
steps of cellular changes- 7- ameboid action
ameoboid action- WBC wriggle to prevent getting stuck, until it gets to the extracellular fluid
steps of cellular changes- 8- migration
migration- WBC has moved to extracellular fluid (diapedesis- cell walking)- because of vascular changes this can happen
steps of cellular changes- 9- chemotaxis
chemotaxis
What is phagocytosis
the process of ingestion of foreign or particulate matter- done by WBC (macrophage), causes them to die
What is lymphatic drainage
lymphatic system assists in drainage of tissue fluid
How does lymphatic drainage work
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
Cardinal sight- Rubor
Redness- vasodilation; increase blood floe to injured area
Cardinal sight- Calor
Heat- vasodilation; increased blood flow to the injured area
Cardinal sight- dolor
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
Cardinal sight- tumor
oedema, extracellular fluid accumulation often in the tissue as a result of increased permeability
Limitations of blood tests used to detect acute inflammation
They can detect inflammation but not what caused it- used other tests after this
Main blood tests to detect acute inflammation
White blood cell count, erythrocyte sedimentation rate, C- reactive protein (produced by liver)
Blood test used to detect acute inflammation- White blood cell count
reference value- 5000-10,000 /mm3,
changes with inflammation- circulating WBC are increased, often above 10,000 /mm3
Blood test used to detect acute inflammation- white blood cell differential (reference values)
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%
Blood test used to detect acute inflammation- white blood cell differential (changes with inflammation)
measure proportion of each of the 5 types of WBC’s, the proportion of immature neutrophils is increased in comparison to other WWBC types
Blood test used to detect acute inflammation- erythrocyte sedimentation rate (reference value)
0-17 mm/hr for men
1-25 mm/hr for women
44-114 mm/hr in pregnancy
1-13 mm/hr in children
Blood test used to detect acute inflammation- erythrocyte sedimentation rate (changes with inflammation)
Detects RBC clumping or stacking as a result of increased fibrinogen levels; levels increase often above 100mm/hr for those with inflammation
Blood test used to detect acute inflammation- C- reactive protein (produced by liver)- reference value
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
Blood test used to detect acute inflammation- C- reactive protein (produced by liver)- changes with inflammation
> 10mg/L indicates significant inflammatory disease
Blood test used to detect acute inflammation-compliment activity (reference value)
Total compliment 62-145 U/ml
C3 (compromises of 70% of total protein in the compliment system) 80-184 mg/dL
Blood test used to detect acute inflammation-compliment activity changes with inflammation
elevated in inflammation signifying the activation of; compliment over time may decrease, indicating the complement factors are exhausted
Blood test used to detect acute inflammation-prothrombin time (reference value)
measured in time to coagulate approximately 11.2-13.2 seconds
Blood test used to detect acute inflammation- prothrombin time (changes with inflammation)
increased prothrombin result in a reduced time to coagulate
Blood test used to detect acute inflammation- fibrinogen (reference value)
175-400 mg/dL
Blood test used to detect acute inflammation- fibrinogen (changes with inflammation)
elevated during inflammation to promote coagulation
Acute and chronic inflammation- cause
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
Acute and chronic inflammation- onset
Acute- rapid, chronic- slow, insidious
Acute and chronic inflammation- deterioration
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
Acute and chronic inflammation- resolution
acute- full resolution, chronic- fails to resolve
Acute and chronic inflammation- course
acute- follows a definite course, self limiting
chronic- fails to resolve
Acute and chronic inflammation- main cells involved
acute- neutrophils, followed by monocytes- macrophages, chronic- macrophages and fibroblasts
Acute and chronic inflammation- phagocytosis
Acute active phagocytosis, chronic- persistent irritants resistant to phagocytosis, ongoing chemotaxis
Acute and chronic inflammation- outcome
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
Acute and chronic inflammation- examples
acute bronchitis, acute appendicitis, chronic bronchitis, chronic obstructive pulmonary disease
common types of medication for inflammation- aspirin
suppresses inflammatory processes by acting on prostaglandins- lipids produced by damaged tissue
common types of medication for inflammation- NSAIds
non steroid anti- inflammatory drugs (NSAIDs), e.g. ibuprofen, naproxen, diclofenac sodium (voltarol)
common types of medication for inflammation- corticosteroids
this acts by interrupting inflammation process they stop chemical mediator, and suppress phagocytosis, used for chronic inflammation e.g. prednisone
common types of medication for inflammation- immunosuppressants
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
What are the mechanisms of inflammation
vascular response, cellular response, phagocytosis, lymphatic drainage
