Week 2 Flashcards
What is sublethal injury?
Alters function without causing cell destruction. Injury potentially reversible if harmful stimulus is removed.
What is a lethal injury?
Irreversible process that causes cell death.
What is hypertrophy?
An expansion in the size of cells, which results in increased tissue mass without cell division.
What is physical hypertrophy?
Results from increased workload on an organ or tissue that is not caused by disease.
What is hyperplasia?
A multiplication of cells as a result of increased cellular division.
What is atrophy?
A decrease in the size of a tissue or organ as a result of a reduction in the number or size of individual cells.
What is metaplasia?
The transformation of one cell type into another in response to a change in physiological condition or an external irritant.
What is dysplasia?
Abnormal differentiation of dividing cells that results in changes in their size, shape, and appearance.
What is anaplasia?
Cell differentiation to a more immature or embryonic form.
What is apoptosis?
Programmed cell death.
What is necrosis?
Tissue death that results from traumatic injury, infection or exposure.
What is gangrene?
Can result from degenerative changes that occur with certain chronic diseases, such as atherosclerosis or diabetes.
What is wet gangrene?
Occurs as the result of sudden rapid elimination of blood flow, seen in severe burn or traumatic crush injury.
What is the inflammatory response?
A biological response to cell injury caused by pathogens, irritants, chronic health conditions.
What is selectins?
Cell surgace carbohydrate binding proteins that mediate cell adhesion, involved in leukocyte extraversion during the immune response.
What are integrins?
cell receptors that mediate attachment between endothelial cells and surrounding tissues, also involved in leukocyte extraversion during the immune response.
What is regeneration?
The replacement of lost cells and tissues with cells of the same type.
What is repair?
Healing as a result of lost cells being replaced by connective tissue
What are fibroblasts?
Immature connective tissue cells that migrate into the healing site and secrete collagen.
What are adhesions?
Bands of scar tissue that form between or around organs.
What is dishence?
The separation and distribution of previously joined wound edges.
What is evisceration?
occurs when wound edges separate to the extent that intestines protrude through the wound.
What are fistulas?
Abnormal passage that forms between organs or a hollow organ and the skin.
What is a hypertrophic scar?
Inappropriately large, red, raised, and hard scar.
What is a keloid?
a protrusion of scar tissue that extends beyond the wound edges and may form tumour like masses of scar tissue.
What is a pressure sore?
Localized injury to the skin or underlying soft tissue, usually a boney prominence or related medical or other devices as a result of pressure or pressure in combination with shear, friction, or both.
What is shearing force?
Pressure exerted on the skin when it adheres to the bed and the underlying skin layers slide in the direction of body movement, friction and excessive moisture.
What is pathological hypertrophy?
result of disease. Ex. enlargement/ thickening of heart ventricle from chronic hypertension.
What is compensatory hypertrophy?
result from increased workload caused by reduced function. Ie. when a kidney is removed, remaining kidney enlarges due to increased workload.
What is physical hyperplasia?
adaptive response to normal body changes. Ex. cells during pregnancy.
What is pathological hyperplasia?
result of disease. Eg. endometrial hyperplasia caused by excess estrogen.
What is compensatory hyperplasia?
process whereby cells of certain organs regenerate. Ie. the liver.
What is metaplasia?
Transformation of one cell type in the response to a change in physiological conditions.
What are the adaptive processes?
Hypertrophy, hyperplasia, atrophy, metaplasia.
What are maladaptive processes?
Dysplasia, anaplasia.
What are causes of lethal cell injury?
Heat, cold, radiation, electrothermal injury, mechanical trauma, chemical injury, viruses, bacteria, antigen, autoimmune response.
What is the mononuclear phagocyte system?
Monocytes and macrophages, considered fixed or free,. Functions include recognition and phagocytosis of foreign materials, immune response and removal of old damaged cells.
What do the arterioles do in the vascular response to inflammation?
Arterioles undergo transient vasoconstriction, which is stimulated by the SNS.
What does firbin-platelet clot release?
Histamine.
What does the release of histamine cause?
Hyperemia, which results in increased filration pressure, causing endothelial cell retraction, and increases capillary permeability.
When is fibrin formed?
When fibrinogen leaves the blood.
What does fibrin do?
Fibrin strengthens the blood clot formed by platelets.
What does the clot in the healing process do?
Traps bacteria, prevents spread, releases growth factors, begins healing process.
What does nitric oxide do?
Used to inhibit vascular smooth muscle contraction and growth, platelet aggregation and leukocyte adhesion to endothelium. Released by phagocytes.
What do cytokines do?
released by macrophages, cause endothelial cells to express cellular adhesion molecules selectins and integrins.
What do neutrophils do?
first WBCs to arrive at injury site (6-12 hrs after injury). They phagocytize bacteria, foreign material and damaged cells. Dead neutrophils form pus. To keep up, bone marrow produces more neutrophils, thus resulting in an elevated WBC.
What do monocytes do?
arrive to the site 3-7 hrs after injury, transform to macrophages upon entering the cell. Assist phagocytes in clearing debris. Cleans area before healing begins. Can form into giant cell, turning into a granuloma, which can cause chronic inflammation.
What do lymphocytes do?
arrive later at site. Assist with humoral and cell-mediated immunity.
What do eosinophils do?
eosinophils released in large quantities during allergic reaction. Release chemicals to control effects of histamines and serotonin. Also involved in phagocytosis of allergen-antibody complex. Eosinophils contain chemicals that can destroy parasites cell surfaces.
What do basophils do?
carry histamine and heparin in granules, which are released during inflammation.
What is histamine?
stored in granules of basophils, mast cells, platelets. Causes vasodilation and increased vascular permeability by stimulating contraction of endothelial cells and creating widened gaps between cells.
what does serotonin do?
stored in granules of basophils, mast cells, platelets. Causes vasodilation and increased vascular permeability by stimulating contraction of endothelial cells and creating widened gaps between cells.
What does kinins do?
produced from precursor factor kininogen as a result of activation of Hageman factor of clotting system. Causes smooth muscle contratction and dialation, stimulates pain.
What do complement components do?
Anaphylatoxic agents generated from complement pathway activation. Stimulate histamine release, stimulate chemotaxis.
What do fibropeptides do?
produced from activation of the clotting system. Increase vascular permeability; stimulate chemotaxis for neutrophils and monocytes.
What do prostaglandins and leukotrines do?
produced from arachidonic acid. Prostaglandins E1 and E2 cause vasodilation; leukotriene B4 stimulates chemotaxis.
What do cytokines do?
secreted by WBCs and other cells. Act as messengers between cell types, instruct cells to alter their proliferation differentiation, secretion or activity.
What is the complement system?
an enzymatic cascade consisting of pathways to mediate inflammation and destroy invading pathogens. Major functions include advanced phagocytosis, chemotaxis, cellular lysis.
What are anaphylotoxins in the complement system?
C3a, C4a and C5a, bind to receptors on mast cells and basophils, triggering histamine release.
What are the clinical manifestatons of inflammation?
redness, swelling, heat and pain. Systematic manifestations include leukocytosis w/ shift to left, malaise, nausea, fever, high pulse and rr.
What causes general symptoms of malaise?
Interleukin-1, interleukin-6 and tumour necrosis factor.
What are the benefits of fever?
killing microorganisms, increased phagocytosis via neutrophils, increased proliferation of T cells, and enhances interferon
Explain the process of fever.
Fever-release of cytokines initiates metabolic changes in temp-regulating center of hypothalamus. PGE2 has direct effect on fever. Hypothalamus activates ANS to stimulate shivers, and decrease sweating. Adrenaline released to increase metabolic rate. Body basically picks a new temperature to regulate to, hence why someone can feel cold, but is burning hot. Cytokines and fever trigger bodies defence mechanisms.
What is acute inflammation?
healing occurs in 2-3 weeks, no residual damage. Neutrophils dominant.
What is subacute inflammation?
same as acute, but lasts longer.
What is chronic inflammation?
Weeks to years. Persistant injury to tissue. Lymphocytes and macrophages predominant. Ie, RA, TB. May alter immune response.
What are the phases of primary intention?
inflammatory, granulation, maturation phase and scar contraction.
What is the inflammation phase?
3-5 days. Incision is aligned and sutured.
What is the granulation phase?
5 days to 3 weeks. Includes proliferating fibroblasts, proliferating capillary sprouts, various types of WBCs. Wound is pink and vascular.
What is maturation and scar contraction?
Overlaps with granulation phase. 7 days post injury. The scaring process.
What is secondary intention?
Wounds that are not well approximated. Ie. Chronic wounds. Debriding may need to take place. Essentially the same as primary intention. Healing takes place outside in, bottom up.
What is teritary intention?
delayed primary intention. Occurs when wound is intentionally left open (ie. animal bite). Results in larger scar.
What are complications of wound healing?
- Adhesions
- Contractures
- Dehiscence - 3 potential causes, infection, granulation tissue, obseity.
- Excess granulation
- Fistula formation
- Infection
- Hemorrhage
- Formation of hypertrophic scars and keloids.
What are some factors that delay healing?
- Vit C deficiency- delays formation of collagen fibres and capillary development.
- Protein deficiency- decreases supply of amino acids for tissue repair.
- Zinc deficiency- impairs epithelization.
- Inadequate blood supply- decreases supply of nutrients to injured area, removal of debris, inhibits inflammatory response.
- Smoking- nicotine is vasoconstrictor and stops blood flow in areas.
- Corticosteroid drugs- impair phagocytosis by WBCs, inhibit fibroblast proliferation and function, depress formation of granulation tissue, inhibit wound contraction.
- Infection- increase inflammatory response and tissue destruction
- Anemia- reduces supply of oxygen
- Age- slows collagen, synthesis of fibroblasts, impairs circulation, alters phagocytosis and immune response.
- Obesity- decreases supply in fatty tissues.
- Diabetes- decreases collagen synthesis, impairs phagocytosis due to hyperglycemia.
- Poor general health
- Mechanical friction on wound
- Cold Temperature
- Excessive moisture
What are the stages of fever?
- Prodrome: non-specific complaints, headache, fatigue, malaise.
- Chill: cutaneous vasoconstriction, pale skin, feeling chilled, generalized shivering,
- Flushing: overall warming, flushing of the skin, person feels warm
- Defervescence: sweating, causes body temp to lower.
What is a tool you can use to assess wounds?
Measure height, width, depth
Exudate
Appearance of wound bed (red, yellow, black, mixed)
Suffering, pain, quality and intensity
Undermining
Reevaluate
Edge
What are factors that enhance wound healing?
- Good diet, low fat, high fluid intake
- Add carbs, vit A and C, Zinc, watch for vit B deficiency
- Clean wound
- No friction
- Good moisture
- Regular blood glucose
