Tissue injury and wound healing Flashcards
Adaptive growth patterns
- Hypertrophy - increases cell and tissue size
- Hyperplasia - increase cell number (cell division)
- Atrophy - decrease in cell size, numbers (death)
- Metaplasia - change in cell differentiation, better equipped for environmental stress
- Dysplasia - distorted growth pattern, increased mitoses (abnormal hyperplasia)
Hypertrophy and metaplasia are adaptive and therefore reversible
Cell types/populations
- Labile - Continuous cell proliferation (skin, gut, respiratory tract, bone), always proliferating so can regenerate if damaged. At risk in chemo treatment for cancer (targets regen).
- Stable - Do not normally proliferate (adult) but are able to undergo cell proliferation (liver, kidney, smooth muscle). Grow to a point then stay there. Slow cell turnover but can mostly proliferate and replace what’s lost
- Permanent - No (or little) capacity to divide in adult tissue (neurons, cardiac muscles). Don’t repair and therefore have to rebuild.
Cell death
- Apoptosis - Active process (cell suicide), pump water out, membrane bound body fragments for use in other cells
- Necrosis, cells swell to cause membrane rupture. Often results in inflammation
Injury vs death
Both injury and cell death have similar causes. The duration, severity and the cell type will determine the outcome.
- Lack of oxygen and ischemia
- Toxicity of chemicals and drugs
- Mitochondrial damage, depletion of energy (ATP)
Injury can be reversible or nonreversible (cell death)
Gouty arthritis
Gouty arthritis - metabolic products like urate crystal form in the joint. Pain and loss of function
Body’s response to cell and tissue death
want to repair the injury meaning regenerating the tissue if possible (cant with permeant cells). Or can rebuild with fibre (fibrosis) when regeneration isn’t possible.
Local signs of inflammation
- Redness
- Swelling
- Heat
- Loss of function and pain
Systemic signs of inflammation
- Fever
- Leukocytosis
- Acute phase proteins
- Sleepiness and hypotension
Mechanism of inflammation
- Changes in blood vessel
- Increased fluid from vessels
- Increase leucocytes (neutrophils, lymphocytes) in inflamed area
Chemotaxis
Chemotaxis allows inflammatory cells (responsible for initiating vessel and cellular changes) to move to site of injury. Movement via a chemical gradient, the concentration of this gradient is highest near site of injury .
Meningitis
Infection in meninges, inflammatory response, oedema. Oedema causes increased pressure (headaches). Haemorrhaging in brain.
Laryngitis
Infection in larynx. Inflammatory response resulting in airway obstruction
Granulation tissue
New connective tissue and new blood vessels that form during wound healing. Granulation tissue is able to fill wounds of almost any size (extensive scarring). It consists of new vessels and chronic inflammatory cells such as new and active macrophages and fibroblasts.
Healing by first and second intention
Mostly related to the scarring. Healing by second has extensive scarring caused by excess fibrosis (needing to rebuild a lot of tissue)
Fibrosis
Development of fibrous connective tissue as a reparative response to injury or damage. This results from chronic inflammation (needs chronic inflammatory cells). Fibrosis in would healing with granulation tissue. Not the same as scar tissue.
End stage disease
Healing pushed past its limit and patient needs a transplant. Chronic inflammatory cell population persist. Function tissue replaced by fibrous scar tissue.
Restrictive pulmonary disease
Pneumoconiosis (black lung disease). High concentration of coal particles causes chronic inflammation (macrophages) leading to fibrosis.
Bone remodelling
Continuous process throughout life. Osteogenic cells in periosteum of the bone response to trauma or stress to the bone. With stress osteogenic cells secret more osteoid to form new bone tissue. At the same time osteoclasts in the endosteum breakdown bone tissue to maintain the thickness of the bone and to make to make the medullary cavity large enough.
Osteomalacia/Rickets
Softening of bone from a deficiency in vitamin D which can cause failure to replace the turnover of calcium and phosphorus in the organic matrix of bone.
Factors that influence healing
- Nutrition, age, blood supply. disease (diabetes, cancer), hormones
- Infection, mechanical factors (movement around wounds), foreign bodies, size and location
Peripheral neuropathy
- Damage to peripheral nervous system
- Causes include certain medication (cancer meds), diabetes, infection, auto immune disease that lead to nerve damage (lupus and rheumatoid arthritis)
- Symptoms, numbness, tingle, sensitivity to touch, burning pain (night), muscle atrophy, exhaustion
segmental demyelination
Schwann cell injury results in segmental demyelination
Wallerian degeneration
Damage to axons, failure of nerve impulse transmission, traumatic disruption (cut). When cut distal axon breaks down and this is termed Wallerian degeneration.
Can axons regenerate
In PNS, axon function may be restored but function not likely restored in the CNS.
Gillian Barre Syndrome (GBS)
Inflammatory cell infiltrates in the peripheral nerve, roots, sensory and autonomic ganglia. Life threatening, follows viral illness. Autoimmune infection affecting nerve roots, myelin degeneration. Begins in distal limbs with ascending paralysis which can involved respiratory muscles.
Causes (60-70%) from influenza like virus.
Symptoms include tingling or prickly sensation in fingers and toes, muscle weakness in legs that travels to upper body and gets worse over time.
Infection polyneuropathies:
- Poliomyelitis - highly infection, can cause paralysis in hours. Enters in mouth and multiples in intestines. Targets and destroys lower motor neurones, nerve dysfunction, wasting of muscle.
- Leprosy - chronic inflammation swelling, destruction of nerve, loss of sensation, occasional sever injury to peripheries, treat with steroids if found early
- Chickenpox - can remain in nerve cells as latent infection, causes sever vesicular rash
Muscle pathologies
- Denervation atrophy - atrophy of muscle units, muscle fibres remain viable. If never disfunction returns myocytes can return to normal (disuse atrophy)
- Myopathy - Direct injury of muscle fibres is termed myopathy. Examples are inflammatory, autoimmune, drugs and ethanol
- Hypertrophy - overuse of muscle building causes cells to hypertrophy beyond their capacity (limits oxygen transmission)
Muscular dystrophies
Duchenne and Becker are X linked. Boys develop weakness by age 5, progressive inability to walk and death in early 20s. Duchenne is a full loss of dystrophin gene and has muscle fibre necrosis and regeneration. Becker is much milder.
Myotonic dystrophy
Myotonic dystrophy - Most common form of muscular dystrophy and begins in adulthood (20-30). Progressive muscle weakness or loss (droopy face and man breasts in men)
Type 1 - involvement in legs, hands, neck and face
Type 2 - involvement in neck, shoulders, elbows and hips (milder than type 1)
Myasthenia gravis (MG)
Myasthenia gravis (MG) - disease of neuromuscular junction, grave muscle weakness that increases during period of activity and improves with rest. It is an auto immune disease which antibodies develop to the acetlycholine receptor f the NMJ
Ocular myasthenia gravis (OMG)
Ocular myasthenia gravis (OMG) - Contained to eye muscles (one or both)
