PAIN, INFLAMMATION, AND TISSUE HEALING Flashcards
PHASES OF TISSUE HEALING
Inflammation Phase (1 - 6th day)
Proliferation Phase (3rd to 20th day)
Maturation Phase (9th day onwards)
What are the goals of Infllamation phase?
Restore function in 3 ways
(1) eliminate the pathological insult
(2) replacing damaged tissue
(3) restore function to promote regeneration of normal tissue structure
Phase ion tissue healing wherei it prepares the wound injured tissue for healing
Inflammation Phase (1 - 6th day)
T or F
Calor (Heat, it increases the metabolic rate),
Rubor (Redness,),
TRUE
Cardinal signs of Inflammation
Calor
Rubor
Tumor
Dolor
Functio Laesa
T or F
Tumor (loss of function, pain and swelling impedes the ROM)
Dolor (Pain, pain receptors are stimulated by chemical and mechanical stimuli),
Functio Laesa (Swelling, vasodilation and and increase capillary permeability)),
FALSE
Tumor (Swelling, vasodilation and and increase capillary permeability)),
Dolor (Pain, pain receptors are stimulated by chemical and mechanical stimuli),
Functio Laesa (loss of function, pain and swelling impedes the ROM)
Inflammation Phase (1 - 6th day)
: it prepares the wound injured tissue for healing
initiates the healing process also called __or inflam___mo (to set alight or set on fire)
called Inflammer or inflammo (to set alight or set on fire)
What occurs during the Inflammatory phase?
Vasoconstriction of injured BV
Vasodilation of adjacent uninjured BV
Clot formation
Phagocytosis by WBCs
Alteration in the anatomy and function of the microvascular system
Goal; INCREASE THE MOVEMENT OF PLASMA PROTEINS AND FLUID OUT OF THE VASCULAR SPACE INTO THE SITE OF INJURY
Vascular Response
Psychological response: Hemostatic Response to ruptured/injured skin
controls blood loss when vessels are injured
clot information
Fibrin + Fibronectin + Collagen will form?
Fibrin Lattice Formation
4 mechanisms that cause increased permeability
endothelial cell contraction
result of direct endothelial injury
leukocyte-dependent endothelial injury
Leakage by regenerating capillaries that lack differentiated endothelium
Which is correct?
Neutrophils - 3rd line of defense
Basophils - release antigen I
Monocyte - premature (inactive) macrophages
All are correct
All are wrong
Neutrophils - 1st line of defense
Basophils - release histamine
Monocyte - premature (inactive) macrophages
T of F
Monocytes - promote phagocytosis
FALSE
Macrophages - promote phagocytosis
LEUKOCYTIC EVENTS DURING INFLAMMATION (4)
Pavementing
Margination
Diapedesis
Chemotaxis
3 MAJOR CONSEQUENCES OF INFLAMMATION
->Fibrin, Fibronectin, and collagen crosslink to form a Fibrin Lattice that limits blood abd provides the wound with initial strength
-> Neutrophils followed by macrophages begin to remove damaged tissue
-> Endothelial cells and fibroblasts are recruited and are stimulated to divide
T or F
Fibroblast - produces collagen
TRUE
Goal of the Proliferation Phase
Achieve coalescence and closure of injured area
Involves epithelial cells and connective tissue
The wound is covered, and the injury site starts to regain some of some of its initial strength
Rebuilds damaged structures and strengthen the wound
Proliferation Phase
Burn patients will likely die from?
Dehydration
Reestablishment of epidermis
Create new epithelial cells.
these are under Proliferation phase of healing in what event?
Epithelialization
During Epithelialization will all types of wound under go this at the same phase?
If yes, What will decide which will under go first?
initiation depends on the depth of wound
if the wound is superficial, epithelialization occurs immediately, if deep, it occurs later
Process of Epithelialization
Basal cells attach themselves on basal membrane
Holds the parent cells and pulls to the center to close the wound
Contact inhibition - cells will stop moving after contact
Basal cells will differentiate and proliferate
Walang
Strongest type of Collagen
Type 1 collagen
*also most abundant
TImeline of increase in tissue tensile strength,
increase in amount of collagen -> increase tensile strength
7th Day
TImeline of increase in tissue tensile strength
Type III collagen is replaced by type I collagen
12th Day
TImeline of increase in tissue tensile strength,Maximal Production of collagen but strength is 20%
21st Day
What will happen to the tissue tensile strength in the injkured area after 8 weeks
strength is at 80%
no longer gain 100% strength, pero sa fx keribellz except
what theory is this,
cells that margin/around ng wound, they will tend to move inward
Picture Frame Theory
3 types of Healing
Healing by Primary intention
healing by secondary intention
tertiary or delayed healing intention
Type of healing where:
combination of primary and tertiary intention
allowing sutures to stay open a few days
tertiary or delayed healing intention
Type of healing:
sugat may infection
wound must undergo wound contraction
*normal MOI
healing by secondary intention
What type of healing is this,
minimal tissue loss
Minimal wound contaction
surgical
Healing by Primary intention
neovascularization occurs in 1 of 3 mechanism, What are these mechanism?
Generation of new vascular network
anastomosis to pre-existing vessels
Coupling of vessels in the injured area
The process of Formation of new BVs
Occurs in 1 of 3 mechanisms
neovascularization
What causes the sensation of itch in wound healing? and why?
Contraction of the wounds, cause the pain receptors to be stimulated because itch has the same pathway with pain
Phase where the modification of scar tissue into its mature form. To restore the prior function of the tissue.
Maturation Phase
COLLAGEN SYNTHESIS IS ___ DEPENDENT⭐️⭐️⭐️
COLLAGEN LYSISIS IS NOT ___ DEPENDENT
COLLAGEN SYNTHESIS IS O2 DEPENDENT⭐️⭐️⭐️
COLLAGEN LYSISIS IS NOT O2 DEPENDENT
T or F
Partner always si collagen (tensile strength) and elastin (for elasticity) . Pag too much collagen results in a decrease in ROM.
TRUE
Theory where:
scar attempts to mimic the characteristics of the tissue it is healing
Induction theory
Theory where:
internal and external stresses placed on the injured area during the maturation phase determine the final tissue structure
Tension theory
ATTRIBUTES TO BE CONSIDERED IN THE SELECTION OF PHYSICAL AGENTS
Goals and effects of treatment
↓
Contraindications and precautions
↓
Evidence for physical agent use
↓
Cost, convenience and availability
Types of pain
Acute pain
Chronic Pain
PRIMARY CHRONIC NINCEPT
PERIPHERAL NEUROPATHIC:
peripheral sensitization
central sensitization
Psychosocial pain
Triggered by cognition, emotion, context, and environment
psychosocial factors may have some influence but doesn’t predominate
Psychosocial pain
Type of pain:
pain that often has no clear anatomical
can be worsened by cold, can spread or worsen without identifiable cause
central sensitization
Type of pain:
pain arising from peripheral nerves conduct nociceptive impulses to the CNS
injured tissues release chemicals that stimulate nociceptors
peripheral sensitization
Type of pain:
arises as a direct consequence of a lesion or disease affecting the peripheral nerve
Two types:
PERIPHERAL NEUROPATHIC:
type of pain that is;
Direct result from actual or potential injury and/or disease
May last less than 12 weeks
Well located and defined*
ACute
Type of pain:
Persistent or recurring pain existing 3 to 6 months; persists beyond the normal time expected for healing injured tissue
Associated with structural and functional changes of CNS
Chronic
pain that occurs at a site remote from the source of the disease or injury
convergence of nerves and nerve roots
Referred Pain
pain that often has no clear anatomical
can be worsened by cold, can spread or worsen without identifiable cause
central sensitization
Type of pain
Triggered by cognition, emotion, context, and environment
psychosocial factors may have some influence but doesn’t predominate
some features are similar to central sensitization
Psychosocial pain
Fast pain vs slow pain
Fast Pain - Application of pain
Slow pain - lingering pain
PROCESS OF NOCICEPTION
Transduction
Transmission
Perception
Modulation
