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PHYL2067 > Module 3: Wound Healing, Burns, Pain and Inflammation > Flashcards

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
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2
Q

Layers of Skin

A
  • Epidermis
  • Dermis
  • Papillary layer
  • Reticular layer
  • Hypodermis (superficial fascia)
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3
Q

Epidermis

A
  • Multi layered epithelium consisting primarily of keratinocytes
  • Classified as a stratified squamous epithelium: provides a protective barrier
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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
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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
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6
Q

Layers of Dermis

A
  • Connective tissue beneath the epidermis
  • Papillary dermis
  • Reticular dermis
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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
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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)
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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
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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)
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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)
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12
Q

Four Phases of Wound Healing

A
  1. Inflammatory Phase: Immediate (4-6 days)
  2. Proliferative Phase: (1-14 days)
  3. Proliferative Phase: (4-14 days)
  4. Maturation Phase: (8 days - 1 years)
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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
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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
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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
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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
  1. Heat
  2. Redness
  3. Swelling
  4. Pain
  5. 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:

  1. Damaged cell membranes release phospholipase A2
  2. This forms arachidonic acid which is normal acid in the cell membrane
  3. Arachidonic acid is then released
  4. COX then breaks down arachidonic acid into prostaglandins
  5. 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

PHYL2067 (5 decks)

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