Applied Bioscience 263 # 2

Front 1

Describe the vascular changes in an acute inflammatory response.

Back 1

Vasodilation
increased blood supply
elimination of pathogens
redness & heat

Front 2

List four types of inflammatory mediators and state their function.

Back 2

Histamine: increases vascular permeability, smooth muscle constriction
Chemotacic factors: attract inflammatory cells to the site
Leukotrines: same as histamine
Nitric oxide: vasodilation, suppresses release of inflammatory molecules from mast cells

Front 3

Describe healing by primary and secondary intention.

Back 3

P: restoration of original tissue and function
S: heal by the process of repair, scar formation

Front 4

Explain the effects of soluble mediators and the extracellular matrix on tissue repair and wound healing

Back 4

SM =
Opsonins: bind and tag microorgranisms for efficent phagocyte recognition
Inflammatory cytokines: short half life ensures that excessive immune responses and systemic activation don't occur
Acute-phase proteins: increase in number and immaturity of circulating neutrophils

Front 5

Trace the wound-healing process through the inflammatory, proliferative, and remodelling phases.

Back 5

I: platelet aggression & activation, leukocyte migration, phagocytosis, mediator release, venule dilation, exudative, lymphatic blockade, primary retention lasts 4 days, secondary retention continues until epithelisation is complete
P: fibroblast proliferation stimulated by macrophage which releases growth factors, increased collagen synthesis, granulation tissue & neuvascularisation
R: intermolecular cross-linking of collagen via vitamin C deep hydroxylation, increase in tensile strength, tertiary collagen replaced with primary, scar flattens

Front 6

Explain the effects of malnutrition; ischemia and oxygen deprivation; impaired immune and inflammatory responses and infection, wound separation and foreign bodies on wound healing/pressure ulcers

Back 6

insufficent repair, excessive repair or function
related to predisposing or acquired condition or numerous drugs and nutrients

repair delays healing by reactivating inflammatory processes

Front 7

Identify factors that may delay or improve wound healing across the lifespan.

Back 7

Neonates: depressed inflammatory response, neutrophil chemotaxis & alternative complement pathway activity
Infants: greater body surface/mass and decreased subcutaneous fat results inability to conserve heat
Elderly: chronic illnesses cause risk to impaired wound healing, poor responses to environmental extremes

Front 8

State the clinical manifestations of wound healing and the pathophysiology associated with the different stages

Back 8

acute inflammation: localised vasodilation, increased vascular permeability & diapedesis

reconstructing phase: wound begins to heal

maturation phase: wound is remodelled

Front 9

Outline wound classification

Back 9

Accurate wound length, width and depth measurements, tunneling of the complement, underlying cause of the wound, surface, exudate, description,

Front 10

Explain pharmacological and non-pharmacological treatment to promote wound healing.

Back 10

non: education, pain assessment, lowered stress, drainage & debriding regularly, reassess meds, vistors, distractions
pharma: antibiotic ointments/tablets to fight infection, iodine and silver to promote healing

Front 11

Explain the impact of impaired mobility and how it effects wound healing

Back 11

Immobility complications: Lungs inspiratory muscles working in different plane - additional stress abdominal contents
push against diaphragm - shallower breathing collapse of alveoli (atelectasis) poor coughing predisposition to
infection.

Front 12

Describe nursing interventions and rationale to promote wound healing and or mobility

Back 12

Management: Assessment - Sequential Repositioning. Pressure relieving devices –foam, air mattress, sheepskin, and gel pad, hygiene and increase movement

Front 13

What is kelois?

Back 13

elevated, rounded, and firm with irregular claw like margins that extend beyond original site of injury

Front 14

Discuss the functional fluid compartments of the body

Back 14

Total body water is made up of intracellular and extracellular. Extracellular encompasses interstitial and intravascular fluid and fluids from major organs and tracts.

Front 15

Discuss the regulatory processes for sodium and water balance in the body, including the
role of antidiuretic hormone.

Back 15

i. Regulated by the secretion of ADH (antidiuretic hormone).
ii. Osmoreceptors stimulate thirst and release of ADH from pituitary gland
iii. ADH secreted when plasma osmolality increases or circulating blood volume decreases and BP drops.

Front 16

Define hypotonic, isotonic and hypertonic alterations in water balance and give an example of each.

Back 16

Occurs when the osmolality of the extra cellular fluid (ECF) is less than normal (280 mOsm).
ii. Hypotonic IV fluids have a lower osmolality than plasma
iii. Water is pulled out of vessels into cells
iv. Decrease vascular volume, increase fluid in cell

Front 17

Identify the basic causes and clinical manifestations of hypernatraemia and hyponatremia.

Back 17

Hypo: thirst, fever, dry mucous membranes, restlessness
Caused by sodium loss, inadequate sodium intake, or dilution of sodium level by water excess (dilutional hyponatremia)

Hyper: caused more by inappropriate administration of hypertonic saline solution or over secretion of aldosterone

Front 18

Discuss the clinical manifestations of hyperkalaemia and hypokalaemia.

Back 18

Hyper: muscle weakness, loss of muscle tone, paralysis, decreased cardiac conductions (arrythmias), restlessness, intestinal cramping, diarrhea (mild loss)

Hypo: neuromuscular or cardiac effects, skeletal muscle weakness, smooth muscle atony, and cardiac dysrhythmias (or arrythmias), respiratory arrest, metabolic dysfunctions, carbohydrate metabolism is affected

Front 19

Describe how fluid balance differentiates in the infant and the ageing individual.

Back 19

Infant: Immature kidneys and high body surface area contribute to fluid losses. Dehydration is serious

Ageing: Limited fluid intake, kidneys less able to reabsorb water

Front 20

Identify common clinical manifestations of fluid and electrolyte imbalance and the
underlying pathophysiology in children.

Back 20

Dehydration: thirst, decreased urine output, decreased body weight, decreased skin elasticity.
Renal mechanisms not mature enough to deal with abnormal losses.
High metabolic rate and higher body surface area leads to greater fluid intake and output compared to their size

Front 21

Discuss the therapeutics, including nursing interventions, which are used in the management
of fluid and electrolyte dysfunction.

Back 21

IV fluids, patients drinking water, sports drinks,

Front 22

Briefly discuss complications of fluid and electrolyte disturbance.

Back 22

UTI'S: retrograde movement of bacteria into bladder and urethra.
UTO'S: Obstruction anywhere in the urinary tract
Glomerular disorders: Diseases related to the glomerulus
Chronic kidney disease: Progressive loss of renal function
Acute kidney injury: Range of changes ass w/rapid decline in renal function
Structural abnormalities:
Tumors:

Front 23

Site Cannon's 4 features of homeostasis

Back 23

Constancy in an open system, such as our bodies represent, requires mechanisms that act to maintain this constancy. Cannon based this proposition on insights into the ways by which steady states such as glucose concentrations, body temperature and acid-base balance were regulated.
Steady-state conditions require that any tendency toward change automatically meets with factors that resist change. An increase in blood sugar results in thirst as the body attempts to dilute the concentration of sugar in the extracellular fluid.
The regulating system that determines the homeostatic state consists of a number of cooperating mechanisms acting simultaneously or successively. Blood sugar is regulated by insulin, glucagons, and other hormones that control its release from the liver or its uptake by the tissues.
Homeostasis does not occur by chance, but is the result of organized self-government.

Front 24

Describe the components of a control system, including the function of a negative feedback system.

Back 24

Sensor - a neuron that detects the variable
Control centre - in the CNS, matches info from sensor with normal range to see if needs to be changed
Effector - CNS sends signals to regions of body to make response

Front 25

State Selye’s definition of stress

Back 25

Alarm: flight or fight response, SNS activated, cortisol and aldosterone released to meet threat
Resistance: PNS returns functions to normal, BGL's remain high, cortisol and aldosterone continue at levels, increased HR, BP and resps
Exhaustion: body cannot keep up stress for too long

Front 26

Outline the physiological complications of prolonged stress, depression and anxiety for those experiencing illness and or disease.

Back 26

Increased HR and widespread vasodilation: increases venous return, BP and cardiac output
Increased BR: bronchodilation to maximise airway
Renin activation: increased reabsorption of Na and H2O, blood volume
Hormones cause BSL's and lipid levels to rise
Stress = immunosuppressant
Increased cortisol = increases allergic responses and inflammation

Front 27

Cite two factors that influence the nature of the stress response.

Back 27

Sympathetic = physical changes
Hypothalamic-pituitary-adrenal axis = psychological

Front 28

Explain the interactions among components of the nervous system in mediating the stress response.

Back 28

SNS = altered levels in the body
Hypothalamic-pituitary-adrenal axis = hormone changes

Front 29

Describe the stress responses (clinical manifestations) of the autonomic nervous system, the endocrine system, the immune system, and the musculoskeletal system.

Back 29

autonomic nervous system: involuntary vital functions (SNS and PNS)
endocrine system: glucose, insulin and BGL's
immune system: infections due to cortisol
musculoskeletal system: vasodilation and glucose

Front 30

Explain the purpose of adaptation.

Back 30

Allow us to get used to scenarios without constantly having elevated stress levels

Front 31

Identify the difference between anxiety, depression and stress.

Back 31

Anxiety: multi-system response to a percieved threat, reflects combination of biochemical changes in the body, patient's personal history, memory and social situation
Depression: low mood and eversion to activity that affects a person's thoughts, feelings, actions and wellbeing
Stress: state of affairs that arise when a person relates to situations in a certain way. How the individual appraises and reacts to situations.

Front 32

Describe the physiologic and psychological effects of a chronic stress response.

Back 32

Cortisol elevation: affects mood, behaviour; changes in cognition, appetite, sleep, insomnia, hyperinsomnia, sensory perception alterations, impair memory processes

Front 33

List five non pharmacologic methods of treating stress.

Back 33

communication, psychological support, organisation, relaxing time, socialising.

Front 34

• State the main pharmacological treatments available in Australia to treat depression, anxiety and stress.

Back 34

Depression: Diazepam, interacts with most other drugs. 1 - 10mg up to 3 times daily.
Stress: Zoloft (sertaline), 50mg once daily.

Front 35

Describe the nursing implication caring for those experiencing stress, depression and or anxiety.

Back 35

Be patient, no extra pressure, caring, supportive, listen, clear explaination, relaxation techniques, correct medication