tissue reponse to injury Flashcards
signs of inflammation
redness swelling tenderness increase temperature loss of function
chemical mediators
histamine, leukotrienes and cytokines
inflammation response phases
inflammation: day 1-4
fibroblastic repair phase: day 4 to week 6
maturation-remodling phase: 4 weeks to 3 years
histamine
released from the injured mast cells, causes vasodilation and increased cell permeability, owing to a swelling to endothelial cells and then separation between the cells
margination
leukotrienes and prostaglandins are responsible for margination: leukocytes (neutrophils and macrophages) adhere along the cell walls this will increase cell permeability affecting the passage of fluid, proteins and neutrophils though cell walls
diapedisis
movement of white blood cells OUT of small arterial vessels
exudate
accumulation of fluid that penetrates through vessel walls into joining extravascular space
neutrophils
a type of white blood cell that engulf invading microbes and contributes to the nonspecific defences of the body against disease
phagocytes
a type of white blood cell that ingests invading microbes
vasoconstriction
narrowing of blood vessels
inflammation response sequence
- injury to cell
- chemical mediators liberated (histamine, leukotrienes and cytokines)
- vascular reaction (vasoconstriction, vasodilation and exudate creates stasis)
- plateelts and leukocytes adhere to vascular wall
5 phagocytosis - clot formation
blood clot coagulation
thromboplastin prothrombin thrombin fibrinogen insoluble fibrin clot
collagen
structural protein found in the skin and connective tissue
type 1: found in skin, fascia, tendon, bone, ligaments, cartilage, and interstitial tissues (*found most in fibroblastic repair phase)
type 2: found in hyaline cartilage and vertebral disks
type 3: found in skin, smooth muscle, nerves and blood vessels (less tensile strength)
granulation tissue
fibroblasts, collagen and capillaries
extracellular matrix
collagen, elastic, ground substance, proteoglycans, glycosaminoglycans
maturation - remodling phases
a realignment or remodeling of the collagen fibers that make up scar tissue according to the tensile forces to which that scar is subjected
fibroblastic repair phase
along with increased oxygen delivery comes an increase in blood flow, which delivers nutrients essential for tissue regeneration in the area. The formation of a delicate connective tissue called granulation tissue occurs with the breakdown of the fibrin clot. granulation consists of fibroblasts, collagen and capillaries.
factors that impede healing
extent of injury (micro/macro tears) edema hemorrhage poor vascular supply separation of tissue muscle spasm atrophy corticosteriods kelod/hypertrophic scars infection humidity/climate/oxygen tension health/age/nutrition
ligament healing
- immediately after injury, ~72 hrs thee is a loss of blood from damaged vessels and attraction of inflammatory cells
- next 6 weeks, vascular proliferation w/ new capillary growth begins to occur along with fibroblastic activity, forming a fibrin clot
- gradually there is a decrease in fibroblastic activity, decrease in vascularity, and max increas in collagen density of a scar
- maturation of a scar may require at least 12 mos
myelinated axon
transmission of action potential travels- acts as a catalyst to make these signals travel quicker
schwann cell
supporting cells of the peripheral nervous system responsible for the formation of myelin
NSAIDS
nonsteroidal antiinflammatory drugs
therapeutic modalities
machines, devices, or substances that are used to enhance recovery from an injury
*heat facilitates an acute inflammatory response and cold slows down the inflammatory response
bone healing
- blood vessels are broken at the fracture line, the blood clots and forms hematoma
- blood vessels grow into the fracture and fibrocartilage soft callus forms
- fibrocartilage becomes ossified and forms a bony callus made up of spongy bone
- osteoclasts remove excess tissue from the bony callus and the bon eventually resembles its original appearance
acute pain
episode of pain that lasts from seconds to less than 6 months
chronic pain
episode of pain that lasts for 6 months or longer
may be intermittent or continuous
myofascial pain
small hyper-irritable areas within a muscle in which nerve impulse bombard the central nervous system and are expressed as a referral pain
gate control theory
sensory information coming FROM cutaneous receptors in the skin enteres the ascending AB afferents and is carried to the substantia gelatinosa in the dorsal horn of the spinal cord.
likewise pain messages from the nociceptors are carried along the Ad and C afferent fibers and enter the dorsal horn.
sensory information coming from AB fibers overrids or inhibits the “pain information” carried along Ad/C fibers thus inhibiting or effectively “closing the gate” to, the transmission of pain information to second order neurons.
Pain information is not transmitted and never reaches sensory centers in the brain
this theory occurs at the spinal cord level
neurotransmitters
serotonin, norepinephrine, substance P, enkephalins, beta-endorphins
first order neurons
first-order or primary afferents tranmist impulses from a nociceptor to the dorsal horn of the spinal cord.
4 types:
- Aalpha * LARGE DIAMETER
- Abeta *LARGE DIAMETER
- Adelta *small
- C *smal
efferent nerve fibers
nerve fiber, such as motor neurons, transmits impulses FROM the spinal cord TOWARDS the periphery
afferent nerve fibers
nerve fibers transmit impulses FROM the nociceptors TOWARD the spinal cord
A-Delta fibers
transmit sensation of pain and temperature
small
originate from nociceptors located in skin and transmit fast pain
C-fibers
small
pain and temperature
orginate from both superficial tissure (skin) and deeper tissue (ligaments and muscles) and transmit slow pain
neural transmission
first order (nociceptors to dorsal horn of spinal cord second order (afferent carries sensory message from dorsal horn to brain and are then categorized as nociceptor specific neuron synapse with third order which carry information via ascending spinal tracts to various brain centers, where the input is integrated, interpreted and acted upon
descending pathway pain control
previous experiences, emotional influences, sensory perception, and other factors could influence the transmission of pain messages and thus the perception of pain
the information coming from higher centers in the brain along efferent descending pathways in the spinal cord causes a release of two neurotransmitter like substances, enkephalin and norepinephrine, into the dorsal horn, which together block or inhibit the synaptic transmission of impulses from the Adelta and C afferent to second-order afferent neurons
beta endorphin
pain (noxious) stimulation of nociceptors resultant in the transmission of the pain information along adelta and C afferents can stimulate the release of an opiate like chemical called beta endorphin from the hypothalamus and anterior pituitary. Beta-endorphin is endogenous to the central nervous system and is konwn to have strong analgesic effects. The exact mechanism by which beta-endorphin produces these potent analgesic effect are unclear. Acupuncture, acupressure, point stim using electrical currents are all techniques that may stimulate the release of beta endorphin.
