Module 3: Wound Healing, Burns, Pain and Inflammation Flashcards
1
Q
Functions of Skin
A
- Protection: physical, chemical, biological
- Water balance: water resistant barriers; sweating
- Temperature regulation: sweat glands, blood vessels
- Immune function: barrier; Langerhan’s cells
- Sensation: temperature, touch, pain
- Metabolism: vitamin D production
2
Q
Layers of Skin
A
- Epidermis
- Dermis
- Papillary layer
- Reticular layer
- Hypodermis (superficial fascia)
3
Q
Epidermis
A
- Multi layered epithelium consisting primarily of keratinocytes
- Classified as a stratified squamous epithelium: provides a protective barrier
4
Q
Layers of Epidermis
A
Stratum Basale
- Deepest layer
- Single layer of cells
- Contains stem cells for regeneration of the epidermis
Stratum Spinosum
- Prickly layer
- Daughter cells from basale
Stratum Granulosum
- Granular layer
- Contains granules > keratin formation and water resistance
Stratum Lucidum
- Thick skin only
- Clear layer
- Subdivision of the stratum corneum
Stratum Corneum
- Cells lack a nucleus or organelles
- Cell membrane becomes thickened
- Filled with keratin filaments
- Deepest layer coated with lipids to form a water barrier
5
Q
Cell Types of the Epidermis
A
Keratincytes
- Mature over time
- Stem cells divide in stratum basal: daughter cells pushed up (superficially) over time
- Dead, keratinised cells lost from surface
Langerhan’s Cells
- Immune cells
- Initiate an immune response to pathogens and cancer cells
Melanocytes
- Located in the stratum basale
- Produce melanin (pigments)
- Transfer melanin to keratinocytes to protect DNA from UV radiation
Merkel’s Cells
- Located in the stratum basale
- Sensory receptor cells
6
Q
Layers of Dermis
A
- Connective tissue beneath the epidermis
- Papillary dermis
- Reticular dermis
7
Q
Functions of Dermis
A
- Supports the epidermis: blood vessels for nutrient, waste and gas exchange
- Sensory awareness of the environment: tactile, pain and temperature
- Contains hair follicles and glands
8
Q
Hypodermis
A
- Hold integument to underlying tissue and permits movement of skin
- Location of subcutaneous fat
- Protection/padding
- Energy reservoir
- Insulin
- Sensory receptors can be found in the epidermis, dermis and hypodermis
- Sensory receptors detect tactile sensations (e.g. touch, temperature and pain)
9
Q
Location of Hair
A
- Located everywhere except palms, soles, lips and portions of external genitalia
- Nonliving structure produced in hair follicles: surrounded by connective tissue sheath
- Stem cells in the follicle can regenerate the epidermis if required
10
Q
Production of Hair
A
- Hair growth starts at the hair bulb (base of hair follicle)
- Hair papilla is connective tissue containing blood vessels
- Nutrients and chemical signals for epithelial (hair) cell growth
- Epithelial cells divide and push upward; become keratinised (hard and dead)
11
Q
Exocrine Glands of the Skin
A
Sebaceous Glands
- Produce sebum (oily secretion)
- Lubricates hair and skin
Merocrine (Eccrine) Sweat Glands
- Produce sweat (99% water and 1% electrolytes)
- Important for temperature regulation
Apocrine Sweat Glands
- Found in the axilla, nipples, pubic and anal region
- Secretion attracts bacteria (odour)
12
Q
Four Phases of Wound Healing
A
- Inflammatory Phase: Immediate (4-6 days)
- Proliferative Phase: (1-14 days)
- Proliferative Phase: (4-14 days)
- Maturation Phase: (8 days - 1 years)
13
Q
Inflammatory Phase: Immediate (4-6 days)
A
- Formation of blood clot
- Temporary covering
- Protect from pathogens
- Contact with air > scab
- Inflammation
- Increased vascular permeability
- Neutrophils: enzymatic digestion of damaged tissue and bacteria
- Macrophages: phagocytosis of debris and bacteria
14
Q
Proliferative Phase: (1-14 days)
A
- Cell division to replace lost tissue
- Keratinocytes in stratum basale migrate and proliferate along wound edge
- Proliferate under scab to form an intact layer
- Proliferation in the dermis
- Angiogenesis (sprouting of new blood vessels from existing ones)
- Migration and proliferation of fibroblasts to the wound site
- Deposition of new collagen by fibroblasts
15
Q
Proliferative Phase: (4-14 days)
A
- Granulation tissue in the dermis is characteristic of the proliferative phase
- Extensive capillary bed
- High proportion of fibroblasts to make new connective tissue
- Oedematous
16
Q
Maturation Phase: (8 days - 1 year)
A
- Granulation tissue replaced by scar tissue
- Capillaries recede > white appearance
- Connective tissue is remodelled
- Stronger collagen fibres
- More organised
- Increased tensile strength
17
Q
Types of Burns
A
- Thermal
- Chemical
- Electrical
18
Q
Types of Burns Based on Depth
A
1st Degree: Superficial
- Tissue depth = epidermis
- Skin function = intact
- Tactile and pain receptors = intact
- Healing time = 3-5 days
- Scar potential = none
2nd Degree: Superficial Partial Thickness
- Tissue depth = epidermis and upper dermis
- Skin function = absent
- Tactile and pain receptors = intact
- Healing time = 21-28 days
- Scar potential = minimal
2nd Degree: Deep Partial Thickness
- Tissue depth = epidermis and most dermis
- Skin function = absent
- Tactile and pain receptors = intact but diminished pain receptors
- Healing time = months
- Scar potential = high due to slow healing
3rd Degree: Full Thickness
- Tissue depth = epidermis, dermis and hypodermis
- Skin function = absent
- Tactile and pain receptor = absent
- Healing time = most will not heal without surgical intervention
- Scar potential = variable
19
Q
Responses to Burns
A
Zone of Coagulation
- Irreversible tissue damage
- Coagulative necrosis
Zone of Stasis
- Tissue is compromised and ischaemic (decreased blood flow)
- Outcome is variable: can worsen
Zone of Hyperaemia
- Dilated blood vessels but no structural change in tissue
- Will heal
20
Q
Burn Shock
A
- Severe burns can cause burn shock which can result in death without treatment
- Systemic response
- Fluid shift
- Decreased cardiac output
21
Q
Detecting Pain
A
Sensory information is detected by receptors
- Convert environmental stimuli into electrical stimuli
- Pain receptors are called nociceptors
- Nociceptors can respond to three classes of stimuli:
1. Mechanical
2. Thermal
3. Chemical
22
Q
Fast Pain
A
- Sharp, prickling pain
- Initiated by mechanical or thermal stimuli
- Easily localised
- Occurs first
- Carried by A-delta fibres (small diameter and myelinated axons)
23
Q
Slow Pain
A
- Dull, aching, burning pain
- Initiated by mechanical, thermal or chemical stimuli
- Poorly localised
- Occurs second and persists for longer
- Carried by C-fibres (small diameter and unmyelinated axons)
24
Q
Lateral Sensory Discriminative Pathway
A
- Painful stimuli activate neurons that ultimately synapse at the somatosensory cortex
- Perception (awareness) of pain
- Localisation of pain
- Intensity of pain
- This pathway is primarily initiated by A-delta fibres
*1st Order Neuron (nociceptor) Peripheral tissue > spinal cord *2nd Order Neuron Spinal cord > thalamus *3rd Order Neuron Thalamus > somatosensory cortex
25
Q
Medial Affective Motivational Pathway
A
- The affective motivational aspect of pain requires the stimulation of additional brain structures
- Hypothalamus (autonomic and behavioural response to pain)
- Limbic system (emotional response to pain)
- Reticular formation (heightened alertness)
- This pathway is primarily initiated by C-fibres and is poorly localised
26
Q
Five Main Features of Inflammation
A
- Heat
- Redness
- Swelling
- Pain
- Loss of function
27
Q
Inflammatory Response
A
Vasodilation
- Local blood vessels dilate
- Increases supply of inflammatory cells and chemicals to site of injury
Increased Vascular Permeability
- Blood vessels become “leaky”
- Causes swelling (oedema)
Migration of Inflammatory Cells (Diapedesis)
- Through leaky capillaries to site of injury
- Phagocytosis of infection agents
28
Q
Inflammatory Chemicals and Pain
A
- Stimulate nociceptors and cause pain
- Sensitise the nociceptors by lowering the threshold for action potential generation
- Sensitisation results in:
- Hyperalgesia = heightened pain from a painful stimulus
- Allodynia = pain from a non-painful stimulus
29
Q
Inflammatory Mediators that cause Pain
A
- Histamine: increase blood flow; increase vascular permeability
- Prostaglandis: increase vascular permeability; attracts neutrophils
- Bradykinin: increase vascular permeability; dilates blood vessels
30
Q
Non-Steroid Anti Inflammatory Drugs (NSAIDS)
A
- e.g. aspirin, ibuprofen
- Inhibits cycle-oxygenase (COX) enzymes
- Blocks the production of prostaglandins
- Reduces sensitisation of nociceptors
- NSAIDS work by blocking the action of COX enzymes, thus reducing the production of prostaglandins
Process:
- Damaged cell membranes release phospholipase A2
- This forms arachidonic acid which is normal acid in the cell membrane
- Arachidonic acid is then released
- COX then breaks down arachidonic acid into prostaglandins
- This then causes pain and inflammation
31
Q
Pharmaceutical Opioids
A
- Opioid drugs bind to opioid receptors in the spinal cord and brain to decrease pain perception and alter the emotional response to pain
- e.g. morphine, codeine
32
Q
Visceral Pain
A
- Localised damage (e.g. surgical incision) rarely causes severe pain
- Diffuse activation of pain nerve endings causes extreme pain
- Causes of visceral pain:
- Ischemia (chemical stimuli > lactic acid and chemicals from tissue damage)
- Muscle spasm (produced cramping pain)
- Over distention
- Visceral pain is transmitted through C-fibres and is therefore dull, aching pain
- Visceral pain is often referred to the body surface
33
Q
Referred Pain
A
- When a person feels pain in an area that is remote to the site of tissue damage
- Why is visceral pain referred?
- 2nd order neuron in the spinal cord receive pain signals from both visceral nociceptors and cutaneous nociceptors
- Pain from the viscera is perceived to originate from the corresponding cutaneous nociceptors
34
Q
Acute Pain
A
- Onset = usually sudden
- Characteristics = generally sharp, localised, may radiate
- Physiological response = raised blood pressure, raised respiratory and heart rate, sweating, pallor, dilated pupils, increased muscle tension
- Emotional/Behavioural Response = anxiety and restlessness, focus on pain, cries, grimaces, moans
- Therapeutic goals = relief of pain, prevent transition to chronic pain, sedation often desirable
35
Q
Chronic Pain
A
- Onset = longer duration
- Characteristics = dull, aching, persistent, diffuse
- Physiological response = often absent: normal blood pressure, normal respiratory and heart rate; normal pupils, dry skin
- Emotional/ Behavioural Response = can be depressed, withdrawn, expressionless and exhausted, no report of pain unless questioned
- Therapeutic goals = prevention of pain; improve quality of life, sedation not usually wanted
36
Q
Chronic Nociceptive Pain
A
- Nociceptors are chronically activated
- Pain has a peripheral cause (e.g. chronic inflammation)
- e.g. osteoarthritis, cancer
37
Q
Chronic Neuropathic Pain
A
- Pain arising from damage to the nervous system, which persists after the injury has healed
- Can result in spontaneous pain (no stimulus), hyperalgesia and allodynia
- Can result in changes to the pain pathway:
- Changes in ion channel expression (e.g. increase sodium channels in nociceptor nerve endings) and neurotransmitter receptor expression (increase glutamate receptors in 2nd order neurons)
- e.g. Diabetes, AIDS, MS, traumatic injury, shingles
