Pathophysiology Flashcards
Layers
- Epidermis - 4-5 layers- stratified squamous epithelium
- stratum germinativum- deepest layer=melanocytes (protect from UV), keratinocytes (water repellent and toughness)
- stratum spinosum- polygonal cells attached by desmoses
- stratum granulosum- glycolipids (slow water loss)
- stratum Lucidum - transparent layer with no nuclei, only present in thick skin (hands, soles feet)
- stratum corneum- outermost layer (thickest and filled with dead keratin fragments
- function- protect, prevent water loss, skin colour, converts cholesterol to Vit D, phagocytes to destroy bacteria
*basement membrane - adherent and mechanical support layer, plays role in regulating transfer of proteins, oxygen and nutrients
- dermis- connective tissue- blood cells, nerve fibres, lymphatic vessels, sweat glands, hair follicles, sebaceous glands
- papillary layer- receptors for pain and touch
- reticular layer- blood vessels, sweat and sebaceous glands, deep pressure receptors
- function- regulate body temp, transmit signals to CNS
- hypodermis-subcutaneous layer-large blood vessels, storage of fat deposits
- function- protective layer for underlying organs, insulate, regulate temp
- sebaceous glands- found with hair follicles, secrete sebum
- sweat glands- eccrine (numerous on forehead, palms and soles, secretes water, antibodies, sodium, metabolic waste, Vit C) and apocrine (axillary, Anal, genital area. Secrete same as eccrine but with proteins and fatty acids)
- ceruminous- ear wax
Wound healing
1- inflammation- platelets that contact damage tissue aggregate, fibrin deposits and forms thrombus, inhibits bleeding. Local vasodilation and vessel permeability, neutrophils and macrophages infiltrate and remove dead cells and secrete growth factor that stimulates proliferation of fibroblasts
2- reconstruction- 2-3days - granulation tissue begins to form with complete re-epithelialisation in this stage. Epithelial cells cover wound and join to other epithelial cells to reach other side of wound
3- remodelling or maturation- years- collagen fibres laid down in proliferation stage are reorganised to improve tensile strength of wound. Scar contracts and fades in colour. Excessive scars can form- hypertrophic or keloid
4- post burn itch- mediators are released when keratinocytes are damaged (histamine, interleukins, protease activated receptors and nerve growth factors
Major burns
Extensive loss of skin=infections, hypothermia, fluid and electrolyte loss. Cytokines release into systemic system creating systemic effects such as cardiac arrhythmia, circulatory failure, hyper metabolic state- nutritional deficit,
GI- paralytic ileus or hyperacidity leading to ulcers, translocation of gut bacteria due to increased cell permeability can lead to infection, dehydration leads to decreased glomeruli filtration rate and reduced toxic waste removal
Systemic response to major burns
Skin- if microcirculation intact then cools skin once heat source removed, if microcirculation lost then deep burns continue even after heat source removed
Hypovolaemia- fluid shift from vascular and intracellular to interstitial, reduced perfusion and oxygenation of tissues, leads to multi organ failure if not treated. Potassium, sodium, and albumin leak into interstitial space. Haemolysed RBC release potassium into extracellular spaces. If fluid replacement is adequate cell membranes become selectively permeable again and stop leakage. Fluid is reabsorbed (24hrs post)- diuresis stage, potassium is slow to return to normal and hypokalaemia can occur, sodium also lost in urine at this stage
Cardiovascular- hyper metabolic state with increase O2 consumption, increased blood viscosity and impairment of microcirculation, rhythm alterations due to release of mediators, hormones and O2 free radicals. Electric burns alter rhythm due to heat damage and interference with electrical activity, compartment syndrome due to arterial compression resulting in decreased blood to area.
Respiratory- cells damaged, cilia inactivated, congestion/infection develops. Pulmonary oedema develops secondary, surfactant inactivated and atelectasis and alveolar collapse.
GI- gut bacteria relocation=sepsis, malnutrition, hyper metabolism- leads to catabolic state and decreased wound healing, splanchnic hypoperfusion as a result of intravascular, paralytic ileus (early enteral feeding can reduce this), curlings ulcers
Renal- GFR reduced, urine output decreased, serum creatinine blood urea nitrogen increase, myoglobinuria/haemoglobinuria-pigments can occlude renal tubules leading to renal failure
Immune system- circulating immunoglobulin is decreased and WBC function impaired
Metabolism- high energy expenditure through increased production of catecholamines, glucocorticoids and glucagon, hyperglycaemia. Two phases- ebb phase- decrease O2 consumption, fluid imbalance, shock and inadequate circulating volume, gut function slows. Flow phase- adequate resuscitation occurs and increased cellular activity and protein catabolism, lipolysis, and gluconeogenesis
Wound assessment
Type- surgical, venous ulcer, pressure
Location-
Appearance/size/depth
Exudate- serous (serum from cells damaged and releasing), haemoserous (damaged small capillaries in dermis), sanguineous (damage of blood vessel)
Delayed healing- infection, blood supply, nutrition/vitamin deficiency, tissue hypoxia, inflammatory and immune response, co-mornidities (diabetes, cardiac)
Wound heat
Vasodilator, increased capillary permeability, increases cellular metabolism, increase inflammation, sedative effect, <20mins
Wound cold
Vasoconstriction, decreases capillary permeability, decreases cellular metabolism, slows bacteria growth and decrease inflammation, local anaesthetic effect. 15 degrees
