Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
181 Cards in this Set
- Front
- Back
|
Several functions performed by water in the body and significance (TA 2-1) |
Water in the body functions to maintain body temperature through diaphoresis, remove wastes through urine formation, protect or cushion the brain and fetus, lubricate and cushion joints, transport nutrients and wastes in joints, and maintain pressure in the eye (anterior cavity). - essential to homeostasis and metabolic reactions - movement of body parts |
|
|
Fluid is distributed between the intracellular compartment (ICF - inside the cells) and the extracellular compartment (ECF) |
ECF includes: - Intravascular fluid (IVF) or blood - Interstitial fluid (ISF) or intercellular fluid - Cerebrospinal fluid (CSF) - Transcellular fluids present in various secretions such as those in the pericardial (heart) cavity or the synovial cavities of the joints |
|
|
CSF is formed continuously from the blood and is reabsorbed back into the general circulation |
Which body compartment contains the most water? (TA 2-2) - The Intracellular compartment |
|
|
Suggest why diarrhea may cause a fluid deficit more rapidly than coughing and sneezing with a cold? (TA 2-2) |
A large volume of fluid (review volume of fluid secreted into the gut) is lost with diarrhea, along with electrolytes and proteins, which affects fluid volumes. A very small volume of water and sodium would be lost with a cough or sneeze. |
|
|
Fluid is added to body through - ingestion of solid food and fluids - product of cell metabolism |
Fluid is lost in the - urine and feces - insensible (unapparent) losses through the skin (perspiration) - exhaled air. |
|
|
Control of fluid balance is maintained by |
- thirst mechanism in hypothalamus, osmoreceptor cells: sense the internal environment both fluid volume and concentration and then promote the intake of fluid when needed |
|
|
Control of fluid balance is maintained by |
- the hormone aldosterone: determines the reabsorption of both sodium ions and water from the kidney tubules = these hormones conserve more fluid when there is a fluid deficit in the body. |
|
|
Control of fluid balance is maintained by |
- the hormone, antidiuretic hormone (ADH) which controls the amount of fluid leaving the body in the urine - ADH promotes reabsorption of water into the blood from the kidney tubules |
|
|
Control of fluid balance is maintained by |
- the hormone Atrial Natriuretic Peptide (ANP) which is a hormone synthesized and released by the myocardial cells in the atrium of the heart - ANP reduces workload on heart by regulating fluid, sodium, and potassium levels (homeostasis) - in kidney: ANP increases glomerular filtration rate (GFR) by altering pressure in the glomerular capillaries, - also reduces reabsorption of sodium in the distal convoluted tubules through inhibition of ADH. - renin secretion is reduced and thus renin angiotensin system is inhibited = result is fluid loss from extracellular compartment and lowered blood pressure - also reduces aldosterone secretion leading to retention of potassium |
|
|
Describe how excessive fluid is lost from the body during strenuous exercise on a very hot day. Explain how the body can respond to this fluid loss to maintain homeostasis. What factors may limit such response? (TA 2-3) |
During strenuous exercise on a hot day, the body loses fluid and sodium chloride by diaphoresis or sweating. To maintain homeostasis, the body's hormones, ADH and aldosterone, respond to increase reabsorption of water through the kidneys, and the thirst mechanism is activated. The body must replace Na+ and fluid. Factors limiting these responses include age and body build and the presence of other diseases that impair responses. In addition, the kidneys and hormones may be slow to respond. |
|
|
Fluid circulation throughout the body depends on the |
permeability of the membranes between compartments - filtration or osmosis processes |
|
|
Water moves between the vascular compartment or blood and the interstitial compartment through |
the semipermeable capillary membranes - depending on the relative hydrostatic and osmotic pressures within the compartments *changes in either force will alter movement and volume in compartments |
|
|
Hydrostatic pressure |
pressure exerted by a fluid at equilibrium at a given point within the fluid due to force of gravity = THE "PUSH" FORCE |
|
|
Osmotic pressure |
the minimum pressure which needs to be applied to a solution to prevent the inward flow of water across a semipermeable membrane (tendency of solution to take in water) = THE "PULL" or attraction force in such fluid movements *Proteins and electrolytes contribute to osmotic pressure of a fluid |
|
|
Filtration |
movement of water and solutes from blood (high pressure) to ISF (low pressure) area |
|
|
Diffusion |
Movement of solutes (e.g. Na+, glucose) from high concentration to low concentration |
|
|
Osmosis |
movement of water from low solute concentration (ISF) to high concentration (blood) *difference in electrolyte concentration in interstitial fluid and intracellular fluid change, osmotic pressure change, = osmosis |
|
|
Active Transport |
movement of solute using carrier and energy from low concentration (ISF) to high concentration (cell) |
|
|
At the arteriolar end of capillary - blood hydrostatic pressure (blood pressure) exceeds the opposing interstitial hydrostatic pressure and plasma colloid osmotic pressure of blood = fluid moves OUT from (or pushed out of) the capillary into the interstitial compartment |
At venous end of capillary - hydrostatic pressure is greatly decreased and osmotic pressure higher, = fluid tends to shift (or is pulled) back into the capillary |
|
|
Major factor in the movement of water through cell membranes is |
the difference in osmotic pressure between the cell and the interstitial fluids |
|
|
a) explain how a very high hydrostatic pressure in the venule end of a capillary affects fluid shift (TA 2-4) |
would decrease the amount of fluid returning to the capillary from the interstitial compartment = EDEMA |
|
|
b) Explain how a loss of plasma protein affects fluid shift at the capillaries? (TA 2-4) |
Decreased osmotic pressure of blood promotes movement of fluid out of the capillaries into the areas of higher osmotic pressure and reduces the return of fluid into the capillaries |
|
|
c) Explain how a high concentration of sodium ions in the interstitial fluid affects intracellular fluid levels? |
Fluid could be drawn out of the cells into the ISF by Osmosis |
|
|
Fluid excess occurs in the extracellular comparment and may be referred to as |
Isotonic/iso-osmolar hypotonic/hypo-osmolar hypertonic/hyper-osmolar |
|
|
Edema refers to |
an excessive amount of fluid in the interstitial compartment - cause swelling or enlargement of the tissues - may be localized or generalized - depend on tissue and area: may be highly visible or relatively invisible or not accurately reflect amount of fluid hidden in area |
|
|
Edema is more severe in |
dependent areas of body - force of gravity is greatest - buttocks - ankles - feet (of a person in a wheel chair) |
|
|
First Causes of Edema (1) p 16 |
1. Increased capillary hydrostatic pressure (equivalent to higher blood pressure BP) = prevents return of fluid from interstitial compartment to the venous end of capillary - force excessive amounts of fluid out of capillaries into the tissue. - caused by Pulmonary Edema - hypervolemia = (increased blood volume) associated with kidney failure, pregnancy, congestive heart failure - ascites = fluid in the abdominal cavity |
|
|
Second Cause of Edema (2) p 19 |
2. may be related to loss of plasma proteins (particularly albumin which results in a decrease in plasma osmotic pressure) - plasma proteins usually remain inside capillary and seldom move through semipermeable capillary membrane * the presence of fewer plasma proteins in the capillary allows more fluid to leave the capillary and less fluid to return to the venous end of the capillary. |
|
|
Third Cause of Edema (3) p 19 |
Obstruction of the lymphatic circulation - obstruction usually causes localized edema because excessive fluid and protein are not returned to the general circulation - this develops if a tumor or infection damages lymph node or if lymph nodes are removed |
|
|
Fourth Cause of Edema (4) p 19 |
Increased capillary permeability - usually causes localized edema and may result from an inflammatory response or infection - general increase in capillary permeability can result from some bacterial toxins or large burn wounds, leading to hypovolemia and shock |
|
|
a) in some cases of breast cancer, many of the axillary lymph nodes are removed. Why are injections not usually done on the affected arm? (TA 2-5) |
a) Removal of lymph nodes impairs the flow of lymph and return of excess fluid and protein from the interstitial compartment into the lymphatics No injections are given in the affected arm because edema restricts circulation of blood in the area, and the effectiveness of the injection would be compromised. |
|
|
b) Explain why severe kidney disease may cause generalized edema? (TA 2-5) |
b) Decreased blood flow through a diseased kidney stimulates renin secretion and increased aldosterone levels, resulting in higher sodium and water levels in the ECF (including the ISF) and general vasoconstriction, which increases vascular hydrostatic pressure. Usually plasma proteins are lost in the urine with kidney disease, causing decreased plasma osmotic pressure. If kidney disease causes a significant drop in the GFR, the resultant fluid retention increases blood volume and hydrostatic pressure. |
|
|
c) Explain why the feet may become swollen when one sits for long periods of time, but the swelling decreases when one lies recumbent in bed? (TA 2-5) |
Sitting with the legs dangling causes increased hydrostatic pressure in the leg veins, impairing the return of fluid into the capillaries. When lying down with the legs raised, the force of gravity is reduced, blood flows freely in the veins from the legs, decreasing hydrostatic pressure and promoting fluid return from the tissues. |
|
|
d) Explain how protein-calorie malnutrition results in ascites? |
Reduced plasma proteins result in reduced capillary osmotic pressure, and fluid remains in the ISF. In this case, fluid builds up in the peritoneal cavity, leading to ascites |
|
|
Effects of Edema p 19 |
- local area of swelling may be visible and may be very pale or red in color. - pitting edema: occurs in presence of excess ISF, moves aside when firm pressure is applied by fingers - generalized edema patients significant increase in body weight - indicate a problem before there are other visible signs - functional impairment: restricts movement of joints, interfere with digestion, absorption and function of organs - pain may occur if pressure exerts on nerves locally - sustained edema the arterial circulation may be impaired - difficult to take accurate impressions of dentures - tissue breakdown from pressure, abrasion and external chemicals |
|
|
A) List Three signs of local edema on the knee B) Explain why persistent edema in a leg could cause weakness and skin breakdown (TA 2-6) |
a) swelling or increased size, shiny, taut skin, a feeling of tightness or pressure, and decreased range of movement b) Edema compresses arteries in the area, reducing blood flow, capillary exchange, and supply of nutrients for cell energy, function and reproduction |
|
|
Hypervolemia |
too much fluid in blood |
|
|
Fluid deficit - dehydration p 20 |
insufficient body fluid resulting from inadequate intake or excessive loss of fluids or a combo of the two. - fluid loss measured by change in body weight - loss of electrolytes and sometimes proteins - dehydration |
|
|
Electrolyte losses can influence water balance significantly because |
electrolytes changes lead to osmotic pressure change between compartments - to restore balance, electrolytes and fluid must be replaced |
|
|
Isotonic dehydration |
proportionate loss of fluid and electrolytes |
|
|
Hypotonic dehydration |
loss of more electrolytes than water |
|
|
Hypertonic dehydration |
loss of more fluid than electrolytes |
|
|
Causes of Dehydration |
- vomiting and diarrhea - excessive sweating with loss of sodium and water - diabetic ketoacidosis with loss of fluid, electrolytes, and glucose in urine - insufficient water intake in an elderly or unconscious person - use of a concentrated formula |
|
|
Effects of Dehydration (direct effects) |
- dry mucous membranes in mouth, decreased skin turgor (elasticity) - lower blood pressure, weak pulse, fatigue - increased hematocrit (higher proportion of RBC compared with water in blood) - decreased mental function, confusion, loss of consciousness (brain cell lose water, reduce function) |
|
|
Effects of Dehydration (compensate for fluid loss by) |
-increasing thirst - increasing heart rate - constricting the cutaneous blood vessels, leading to pale and cool skin - producing less urine, concentrating the urine, increasing specific gravity |
|
|
Third-Spacing: fluid deficit and fluid excess p21 |
Third-spacing = fluid shifts out of the blood into a body cavity or tissue where it is no longer available as circulating fluid. Ex: peritonitis, inflammation and infection of peritoneal membranes and burns - lab test: hematocrit and electrolyte concentrations |
|
|
TA 2-8 Describe 3 signs or symptoms of dehydration that are direct effects 3 signs that indicate compensation that is occurring in response to dehydration |
Direct effects are indicated by dry mucous membranes, decreased skin turgor, a weak or thready pulse, and fatigue. Signs of compensation include tachycardia, thirst, oliguria, pallor, and cool skin. |
|
|
TA 2-9 Based on the info given previously on fluid excess and fluid deficit, describe three signs and symptoms of third spacing related to a large burn area |
The fluid deficit in the vascular compartment is indicated by decreased BP, rapid weak pulse, and dizziness whereas the excess ISF (third spacing in this case) would be indicated by edema in the affected area. |
|
|
Electrolyte Sodium Na+ (primary cation in the extracellular fluid) |
Sodium transport across cell membrane controlled by sodium potassium pump or active transport = result in high sodium levels in extracellular fluids and low sodium levels in intracellular (in cell) NA+ = High OUT: low IN |
|
|
Diffusion of sodium occurs |
between the vascular and interstitial fluids - sodium is actively secreted into mucus and other body secretions - exist in body in form of salts: sodium chloride and sodium bicarbonate |
|
|
Sodium levels in body are primarily controlled by |
kidneys through action of aldosterone. |
|
|
Sodium makes up approx 90% of solute in extracellular fluid |
important in maintenance of extracellular volume through its effect on osmotic pressure - essential in conduction of nerve impulses and in muscle contraction |
|
|
Hyponatremia pg 22 |
abnormally low levels of sodium (BELOW 3.8 to 5 mmol per liter or 135 milliequivalent (mEg) per liter |
|
|
Causes of Hyponatremia - sodium deficit result from direct loss of Na+ from body or from an excess of H2O in extracellular compartment = dilution of sodium 1. low sodium in blood 2. low osmotic pressure in extracellular fluid 3. water shifts out of blood 4. more water shifts into cell (from low to high osmotic pressure) 5. cell swells, function decreases and cell ruptures |
Common causes of low serum sodium levels include: - losses from excessive sweating, vomiting and diarrhea - use of certain diuretic drugs combined with low-salt diets - hormonal imbalances such as insufficient aldosterone, adrenal insufficiency and excess ADH secretion - early chronic renal failure - excessive water intake |
|
|
TA (2-10) a high fever is likely to cause deep, rapid respirations, excessive perspiration and higher metabolic rate. How would this affect the fluid and electrolyte balance in the body? |
Fluid loss would occur with hyperventilation and perspiration. Sodium loss in sweat also affects osmotic pressure of the ECF and fluid balance. A higher metabolic rate requires increased turnover of fluid. |
|
|
TA (2-10) List several reasons why drinking a fluid containing water, glucose and electrolytes would be better than drinking tap water after vomiting? |
Electrolytes could replace lost sodium, restoring better balance in the body. Water alone would dilute electrolytes in the ECF, decreasing osmotic pressure and leading to further fluid shifts in the body. Glucose provides nutrients for the cells with a higher metabolic rate, thus reducing the risk of acidosis. (acidosis = increased acidity in blood and tissue) |
|
|
Effects of Hyponatremia |
- low sodium levels impair nerve function and result in fluid imbalances (manifestations include fatigue, muscle cramps, abdominal discomfort or cramps with nausea and vomiting) - decreased osmotic pressure in the extracellular compartment may cause a fluid shift into cells = hypovolemia and decreased blood pressure - brain cells may swell, causing confusion, headache, weakness or seizures |
|
|
Hypernatremia |
excess sodium level in the blood and extracellular fluids (more than 145 mEq per liter |
|
|
Causes of Hypernatremia |
- excess sodium results from ingestion of large amounts of sodium without proportionate water intake or a loss of water from the body that is faster than the loss of sodium - insufficient ADH = large volume of dilute urine (diabetes insipidus) - loss of thirst mechanism - watery diarrhea - prolonged periods of rapid respiration |
|
|
TA 2-11 Hypernatremia accompanied by an elevated hematocrit value indicates what fact about body fluids? |
Excessive loss of water from the vascular compartment has resulted in a relatively higher proportion of sodium and RBCs in the blood. |
|
|
Signs of Hyponatremia - anorexia, nausea, cramps - fatigue, lethargy, muscle weakness - headache, confusion, seizures - decreased blood pressure |
Signs of Hypernatremia - thirst; tongue and mucosa are dry and sticky - weakness, lethargy, agitation - edema - elevated blood pressure |
|
|
TA 2-12 Compare the effects of aldosterone with those of ADH on serum sodium levels |
Aldosterone would likely increase serum sodium levels or maintain a normal value if an equivalent amount of water is added. (The total amount of sodium in the body would increase.) ADH would decrease serum sodium levels because increased water reabsorption reduces the concentration of sodium. |
|
|
TA 2-12 List the signs and symptoms common to both hyponatremia and hypernatremia and also any signs that differentiate the two states |
Signs that occur in both include restlessness, weakness, confusion, and convulsions. Hyponatremia, caused by loss of sodium, leads to hypovolemia. Note that the signs depend on the cause and relative change in water balance. Hyponatremia is indicated by abdominal cramps, nausea, and diarrhea. Hypernatremia causes thirst and dry mucosa, oliguria, and increased body temperature. Hypernatremia, resulting from increased sodium in the body, leads to edema, weight gain, and increased blood pressure. |
|
|
Potassium (K+) is a major intracellular cation serum levels are very low (3.5 to 5 mEq per liter or 3.5 to 5 mmol per liter) - potassium levels influenced by acid-base balance in body |
Potassium is ingested in foods and excreted primarily in the urine under influence of Aldosterone hormone - Insulin promotes movement of K+ into cells = insulin reduces serum Potassium Levels |
|
|
Acidosis (more H+ in blood) |
- shift potassium ions K+out of the cell into the extracellular fluids - many hydrogen ions diffuse form blood into ISF because of high hydrogen ion concentration in the blood = when H+ move into the cell, displace K+ out of the cell to maintain electrochemical neutrality. - promotes hydrogen ion excretion by the kidneys and retention of potassium in the body |
|
|
Alkalosis (less H+ in blood) |
- shifts more potassium into the cell |
|
|
Hyperkalemia |
excess potassium ions in the ISF diffuse into the blood |
|
|
Potassium |
- assists in the regulation of intracellular fluid volume, metabolic processes in the cell - important in nerve conduction and contraction of all muscle types - determine membrane potential - abnormal potassium levels have serious effect on contractions of cardiac muscle causes changes in the electrocardiogram (ECG) and cardiac arrest or standstill |
|
|
Hypokalemia |
serum level of potassium is less than 2 mmol per liter or 3.5 mEq per liter |
|
|
Causes of Hypokalemia |
- diarrhea - diuresis associated with certain diuretic drugs - presence of excessive aldosterone or glucocorticoids in the body (in Cushing's syndrome) - decreased dietary intake (alcoholism, eating disorder, starvation) - treatment of diabetic ketoacidosis with insulin |
|
|
Effects of Hypokalemia p24 |
- cardiac dysrhythmias are serious typical ECG pattern: prolonged repolarization and may lead to cardiac arrest. - hypokalemia interferes with neuromuscular function, muscle become less responsive to stimuli (fatigue and muscle weakness) - Paresthesias "pins and needles" abnormal sensation develop - decreased digestive tract motility causes decreased appetite (anorexia) and nausea - respiratory muscle becomes weak, leading to shallow respirations (in people with severe K+ deficits) - renal function is impaired, lead to failure to concentrate the urine, and increased urine output (polyuria) (severe cases) |
|
|
Hyperkalemia |
serum level of potassium is greater than 2.6 mmol per liter or 5 mEq per liter |
|
|
Causes of Hyperkalemia p25f |
- renal failure - deficit of aldosterone - use of "potassium-sparing" diuretic drugs - prevent potassium from being excreted in adequate amounts - leakage of Intracellular K+ into Extracellular fluids in patients with extensive tissue damage such as traumatic crush injuries or burns - displacement of K+ from cells by prolonged or severe acidosis |
|
|
Effects of Hyperkalemia |
- ECG show typical cardiac dysrhythmias which may lead to cardiac arrest - muscle weakness common, progressing to paralysis as hyperkalemia advances and impairs neuromuscular activity - fatigue, nausea, and paresthesias common |
|
|
TA 2-13 a) Compare the manifestations of hyponatremia and hypokalemia. |
Hyponatremia causes a movement shift of water into cells, resulting in muscle cramps, weakness and fatigue, abdominal cramps, and nausea. Increased intracellular fluid in the nervous system causes lethargy, confusion, and headache. Hypokalemia causes muscle weakness and paresthesias, nausea, abdominal distention, and decreased bowel sounds. Hypokalemia causes serious cardiac arrhythmias, polyuria, and metabolic alkalosis. |
|
|
b) Why is any small change in potassium level considered a serious problem? TA 2-13 |
Potassium is primarily an intracellular ion, and the normal range for potassium is very low (see Ready References). Any change in the content has a significant effect. Both hyperkalemia and hypokalemia cause cardiac dysrhythmias and possible cardiac arrest. |
|
|
Calcium Ca2+ very important extracellular cation - ingested in food, esp in milk products, stored in bones and excreted in the body in the urine and feces. |
Calcium balance is controlled by - parathyroid hormone (PTH) - calcitonin - influenced by vitamin D and phosphate ion levels |
|
|
Function of PTH |
if blood calcium levels are low, stimulate the secretion of PTH = increases calcium absorption from digestive tract and kidneys and promote reabsorption from bone |
|
|
Vitamin D |
may be ingested or synthesized in the skin in presence of UV but must be activated in the kidneys - promotes calcium movement from bone and intestines into blood |
|
|
Calcium and phosphate ions in the extracellular fluid have a reciprocal relationship |
If calcium levels are high, phosphates are low - if calcium and phosphate levels increase, crystals of calcium phosphate precipitate in soft tissues |
|
|
Important functions of Calcium |
- provides structural strength essential for bones and teeth - maintain stability of nerve membranes, controlling permeability and excitability needed for nerve conduction - required for muscle contractions - necessary for many metabolic processes and enzyme reactions such as blood clots |
|
|
TA 2-14 When nerve membranes become more permeable, is the nerve more or less easily stimulated? |
The nerve is more easily stimulated because ions move more freely across the membrane. |
|
|
Hypocalcemia |
Serum calcium level is less than 2.2 mmol er liter or below 4 mEq per liter - decrease in number of free Ca2+ ions |
|
|
Causes of Hypocalcemia |
- Hypoparathyroidism - decreased PTH results in decreased intestinal calcium absorption - Malabsorption syndrome - result in decrease intestinal absorption of Vitamin D or Calcium - Deficient serum albumin - Increased serum pH = Alkalosis *occurs in renal failure: retention of phosphate ion, loss of Ca2+ and Vitamin D not activated = decrease intestinal absorption of calcium |
|
|
Effects of Hypocalcemia |
- low serum calcium levels increase the permeability and excitability of nerve membranes = spontaneous stimulation of skeletal muscle - leads to muscle twitching, carpopedal spasm (atypical contraction of fingers) and hyperactive reflexes. - Chvostek's sign spasm of the lip or face when the face is tapped in front of the ear - Trouseau's sign, carpopedal spasm when a blood pressure cuff blocks circulation to hand - tetany (skeletal muscle spasm) - severe calcium deficits may cause laryngospasm - obstruct the airway - Paresthesias and abdominal cramps are common - heart contraction become weak owing to insufficient calcium for muscle action, conduction is delayed, arrhythmias develop and blood pressure drops |
|
|
Skeletal muscle spasms result from the increased irritability of the nerves associated with the muscle fibers, whereas the weaker contraction of cardiac muscle (lack nerves) is directly related to the calcium deficit |
Adequate calcium is stored in the skeletal muscle cells to provide for contractions, whereas contraction of cardiac muscle relies on available extracellular calcium ions passing through the calcium channels |
|
|
Explain the different effects of low serum calcium on skeletal muscle and cardiac muscle (TA 2-15) |
- Hypocalcemia increases neural excitability, causing skeletal muscle spasms. Calcium is stored in skeletal muscle; therefore, it is readily available for muscle contraction. - Contraction of cardiac muscle depends on the movement of calcium from the blood into muscle fibers; therefore, hypocalcemia results in a weak cardiac contraction and arrhythmias. *Nerves are not involved in cardiac contraction. |
|
|
Hypercalcemia |
serum calcium is greater than 5 mEq per liter or greater than 2.5 mmol per liter |
|
|
causes of hypercalcemia |
- uncontrolled release of calcium ions from the bones due to neoplasms - hyperparathryoidism - immobility, may decrease stress on the bone, leading to demineralization. -increased intake of calcium due to excessive Vitamin D or to excess dietary calcium |
|
|
Effects of Hypercalcemia |
- depress nueromuscular activity, leading to muscle weakness, loss of muscle tone, lethargy, stupor, often personality changes, anorexia and nausea - interfere with function of ADH in kidneys = less absorption of water an din polyuria - cardiac contractions increase in strength and dysrhythmias may develop. - effects on bone vary: if excess PTH is the cause, bone density will be decreased, spontaneous fractures may occur (in weight bearing areas) causing bone pain. if intake of Ca2+ is high, PTH levels will be low, and more calcium will be stored in bone, maintaining bone strength. |
|
|
Signs of Calcium Imbalance Hypocalcemia - Tetany: involuntary skeletal muscle spasm, Carpopedal spasm, Laryngospasm -Tingling fingers - Mental confusion, irritability - Arrhythmias, weak heart contractions |
Signs of Calcium Imbalance Hypercalcemia - Apathy (lack of interest), lethargy - Anorexia, nausea, constipation - Polyuria, thirst - Kidney stones - Arrhythmias, prolonged strong cardiac contractions, increased blood pressures |
|
|
Think About 2-16 Describe the effect of each of the following conditions on serum calcium levels and on bone density 1. hyperparthyroidism 2. renal failure 3. very large intake of vitamin D |
1. Hyperparathyroidism draws calcium from bone stores, increasing serum calcium levels and reducing bone density. 2. Renal failure results in decreased active vitamin D; therefore, there is less absorption of calcium from the intestines and renal tubules, leading to low serum calcium levels. Also, serum phosphate is retained, increasing serum phosphate levels and resulting in low serum calcium levels. Hypocalcemia stimulates increased secretion of parathyroid hormone, leading to decreased bone density. 3. Excessive intake of vitamin D causes hypercalcemia and increased bone density. |
|
|
Other Electrolytes: Magnesium |
an intracellular ion that has normals serum level of 0.7 to 1.1 mmol per liter - about 50% of Mg2+ is stored in the bone - serum levels linked to both potassium and calcium levels - found in green vegetables and important in many enzyme reactions and protein and DNA synthesis |
|
|
Hypomagnesemia (low Mg2+ levels) |
results form malabsorption or malnutrition, - often associated with chronic alcoholism - use of diuretics, diabetic ketoacidosis, hyperparathyroidsm and hyperaldosteronism - neuromuscular hyperirritability with tremors or chorea (involuntary repetitive movements), insomnia, personality changes and increased heart rate with arrhythmias |
|
|
Hypermagnesemia (high Mg2+ levels) |
- occurs with renal failure - depress neuromuscular function - lead to decreased reflexes, lethargy and cardiac arrthymias |
|
|
Phosphate ions HPO4- and H2PO4- - located primarily in bone but circulate in both intracellular and extracellular fluids |
serum level normally 0.85 to 1.45 mmol per liter |
|
|
phosphate is important in |
- bone and tooth mineralization - many metabolic processes, particularly those involving cellular energy source, ATP - phosphate buffer system for acid-base balance, has a role in removal of hydrogen ions from body through kidneys - integral part of the cell membrane - in its reciprocal relationship with serum calcium |
|
|
Hypophosphatemia |
low serum phosphate levels may result from malabsorption syndromes, diarrhea, or excessive use of antacids - alkaloses ad hyperparathyroidsm are other causes - neurological function is impaired, causing tremors, weak reflexes (hyporefelxia), paresthesias (abnormal sensation), confusion and stupor (unconsciousness), anorexia and difficulty swallowing (dysphagia) - blood cells function less effectively - oxygen transport decreases and clotting and phagocytosis decrease |
|
|
TA 2-17 Explain how serum calcium levels are affected by low phosphate levels? |
Low serum phosphate levels cause increased serum calcium levels because of the reciprocal relationship of their concentrations. The product of their content is always a constant. If the levels of both ions increase, they deposit as a salt in the soft tissues. Similarly, high phosphate causes low calcium in the blood. |
|
|
Hyperphosphatemia |
high serum phosphate often results from renal failure - tissue damage or cancer chemotherapy may cause release of intracellular phosphate - manifestations of hyperphosphatemia are the same as those of hypocalcemia |
|
|
Chloride ion (Cl-) |
major extracellular anion with normal serum level of 98 to 106 mmol per liter - chloride ions tend to follow sodium because the attraction between electrical charge on the ions = high sodium levels usually lead to high chloride levels |
|
|
Chloride and bicarbonate ions are both negatively charged, can exchange places as blood circulates through the body to assist in maintaining acid-base balance |
as bicarbonate ions are used up in binding with metabolic acids, chloride ions diffuse out of the red blood cells in the serum to maintain the same number of negative ions in the blood |
|
|
Reverse: serum chloride levels decrease and bicarbonate ions leave erythrocytes to maintain electrical neutrality |
thus low serum chloride leads to high serum bicarbonate or alkalosis = Chloride Shift |
|
|
Hypochloremia |
low serum chloride is usually associated with alkalosis in the early stages of vomiting when hydrochloric acid is lost form the stomach - excessive perspiration associated with fever or strenuous labor on a hot day can lead to loss of sodium chloride = Hypernatremia and hypochloremia, = dehydration |
|
|
TA 2-18 a) state one cause of hypomagnesemia b) state one cause of hyperphosphatemia c) list and describe two signs of hypophosphatemia |
a) Hypomagnesemia can be caused by malabsorption syndrome or malnutrition. b) Hyperphosphatemia is caused by cell destruction associated with tumors, increased intake, or renal failure, high intake. c) Signs of hypophosphatemia include paresthesia (abnormal sensations such as tingling), hyporeflexia (weak responses of skeletal muscles), intention tremors (involuntary shakiness when making a voluntary movement), and confusion (decreased neurologic function). |
|
|
Acid-base is essential to homeostasis because cell enzymes can function only within a very narrow pH range |
Normal serum pH is 7.35 to 7.45 |
|
|
Death usually results if serum pH is below 6.8 or above 7.8. |
pH of less than 7.35 depresses central nervous system function and decreases all cell enzyme activity |
|
|
Acidosis = serum pH is less than 7.4 more hydrogen ions H+ present *body normally has tendency towards acidosis/lower pH because cell metabolism is constantly producing CO2 and H2CO3 carbonic acid and nonvolatile metabolic acids (lactic acid, ketoacids, sulfates or phosphate) |
Alkalosis = serum pH greater than 7.4 is more basic fewer hydrogen ions H+ present Alkalosis=increase serum pH but decrease H+ |
|
|
Lactic Acid results from the anaerobic metabolism (without oxygen) of glucose, ketoacids results from incomplete oxidation of fatty acids and proteins metabolism may produce sulfates or phosphates from Acidosis |
TA 2-19 a) When Hydrogen ions are decreased, is the pH higher or lower? = Higher (less H+ = basic = alkalosis) b) State the optimal range of serum pH and effects on normal cell function if serum pH is not in the optimal range = 7.35 to 7.45 when level serum pH is out of levels normal range, cell enzymes cannot function for normal metabolism |
|
|
Three mechanisms control or compensate for pH |
1. The buffer pairs circulating in the blood respond to pH changes immediately 2. The respiratory system can alter carbon dioxide levels (carbonic acid) in the body by changing the respiratory rate (lungs) 3. The kidneys can modify the excretion rate of acids and the production and absorption of bicarbonate ion. (kidney slow but most effective because hey can excrete all types of acids) and can adjust serum bicarbonate levels |
|
|
TA 2-20 How does the respiratory rate change when more hydrogen ions enter the blood and how does this change affect acid levels in the body? |
An increased respiratory rate blows off CO2, thereby decreasing carbonic acid levels and the total number of free hydrogen ions in the blood. |
|
|
Buffer Systems |
to control serum pH in blood = is a combination of a weak acid and its alkaline salt - reacts with any acids or alkali added to blood, neutralizing them and maintaining relative constant pH |
|
|
The body has 4 major buffer pairs 1. Sodium bicarbonate-carbonic acid system 2. Phosphate system 3. Hemoglobin system 4. Protein system |
Bicarbonate system (carbonic acid + bicarbonate ion) - major extracellular fluid buffer - used clinically to assess client's acid-base status - composed of carbonic acid (from combination of carbon dioxide and water) and bicarbonate ion (present as sodium bicarbonate) |
|
|
Bicarbonate system bicarbonate ion (HCO3-) = base and carbonic acid (H2CO3) = acid = controlled by respiratory system and the kidneys |
Cell metabolism produces CO2 which diffuses into the ISF and blood where it reacts with H2O to form H2CO3 carbonic acid. - then dissociates immediately under influences of the enzyme carbonic anhydrase to form 3 H+ and 2 bicarbonate ion (per molecule of carbonic acid) |
|
|
In the Lungs, - this reaction can be reversed to form CO2, which is expired along with water, reducing the total amount of carbonic acid or acid in the body. |
In the Kidneys, - reaction need to form more hydrogen ions promoted by enzymes = resultant H+ are excreted in the urine and bicarbonate ions are return to blood to restore buffer levels (neutralize) |
|
|
Ratio of biocarbonate ion to carbonic acid (carbon dioxide) need to be ratio of 20:1 bicarbonate:carbonic acid H+ = 1 Bicarbonate = 20 |
If respiration is impaired. cause increase in CO2 in blood - kidney must increase serum bicarbonate levels to compensate for the change |
|
|
TA 2-21 If bicarbonate ion is lost from the body, how will carbonic acid levels change? = Carbonic acid levels decrease in compensation for the bicarbonate loss. |
Respiratory System - when CO2 or H+ levels increase, chemoreceptors stimulate the respiratory control center to increase the respiratory rate = removing more carbon dioxide or acid from the body |
|
|
When Alkalosis develops (decreased H+) - respiratory rate decreases, retaining more CO2 and increasing acid in the body. Alkalosis=increase serum pH but decrease H+ Major Causes of |
Renal System Kidneys can reduce the acid content of body, by exchanging H+ for Na+ under influence of aldosterone and can remove H+ by combining them with ammonia and other chemicals - kidney provide bicarbonate ion for buffer pair needed |
|
|
Urine pH may range from 4.8 to 8.0 - kidney compensate for metabolic conditions and dietary intake. |
Lungs: carbon dioxide + water <-> carbonic acid <-> hydrogen ions + bicarbonate ions: kidneys |
|
|
TA 2-22 1) reduced blood flow through the kidneys for a long time will have what effect on serum pH why? - The serum pH decreases because the kidney cannot excrete as much acid or produce as much base bicarbonate ion for buffering. |
TA 2-22 2) How would the lungs and kidneys respond to the ingestion of large quantities of antacid? - A large amount of antacid (base) increases the serum pH; therefore, the respiratory rate slows, and the kidneys excrete fewer acids (remember, acids are constantly produced during cell metabolism). |
|
|
Respiratory rate decreases when increase in serum pH (decrease H+ = more basic- Alkalosis) |
Respiratory rate (CO2 Levels) increases when decrease in serum pH (increase H+ = more acidic - Acidosis) due to Respiratory Problems - bad metabolic or renal problems Metabolic Acidosis Major Causes: Diabetic ketoacidosis, lactic acidosis, loss of base (bicarbonate), renal tubular acidosis, poisons (ethylene glycol and methanol) |
|
|
TA 2-22 3. How is the kidney more effective in maintaining serum pH than the lungs? = Kidneys can excrete all types of acids and provide bicarbonate ions for buffer. = Lungs can only excrete carbonic acid in the form of carbon dioxide and water. |
Acid Base Imbalance (4 types) - Compensation - Decompensation - Acidosis - Alkalosis |
|
|
Acidosis - increase in H+ or decrease in serum pH - can result either from an increase in CO2 levels (more acidic) due to respiratory problems or from decrease in bicarbonate ions (base) because of metabolic or renal problems Respiratory Acidosis caused by: Lung disorders, (COPD, severe asthma, pneumonia or pulmonary edema), sleep disordered breathing - apnea, Guillain-Barre syndrome or amyotrophic lateral sclerosis, overdose of drugs (alcohol, opioids and strong sedatives) |
Alkalosis - decrease in H+ or increase serum pH - if serum bicarbonate increases = metabolic alkalosis - if increased respirations, cause a decrease in carbon dioxide (less acidic) |
|
|
TA 2-23 Name or state the category of the imbalance resulting from each of the following 1) increased respiratory rate = cause respiratory alkalosis; CO2 reduced (0.5) 2) renal failure = cause metabolic acidosis; bicarbonate ion reduced (10) 3) excessive intake of bicarbonate and state resulting change in the 20:1 ratio = excessive intake of antacid causes metabolic alkalosis; bicarbonate ion is increased (25) |
Compensation - assessed by the subsequent change in the second part of the ratio and requires function of body systems not involved in the cause |
|
|
For ex: if patient has respiratory disorder causing acidosis, lungs cannot compensate effectively, but kidneys can (20:1 ratio maintained and serum pH is normal) - compensation is limited and patient must be monitored carefully if ongoing threat to homeostasis |
Decompensation - imbalance: if kidneys and lungs cannot compensate adequately, ratio changes, serum pH moves out of the normal range = affecting cell metabolism and function - intervention is essential if homeostasis is to be regained. |
|
|
TA 2-24 a) if an individual with very low blood pressure or circulatory shock, blood flow to cells is very poor, resulting in increased lactic acid. Briefly describe the compensations that will take place = Increased lactic acid levels cause deep rapid respirations to remove some acid (carbonic) and the kidneys to excrete more acids (nonvolatile; e.g., lactic and carbonic acids) from the urine and to increase production and absorption of bicarbonate ion to buffer the acids. |
TA 2-24 b) What changes in the bicarbonate ratio and serum pH indicate that decompensation has occurred? - The ratio is no longer 20:1, and serum pH is outside the normal range (in this case below 7.35 |
|
|
Respiratory Causes of Acidosis - slow shallow respirations (eg drugs) - respiratory congestion - pneumonia, COPD (emphysema) |
Respiratory Effect of Acidosis = increased PCO2 |
|
|
Respiratory Compensation of Acidosis = kidneys excrete more H+ and reabsorb more bicarbonate |
Respiratory Laboratory of Acidosis = Elevated PCO3 - Elevated serum bicarbonate - compensated serum pH = 7.35 to 7.4 - decompensated serum pH less than 7.35 |
|
|
Metabolic Causes of Acidosis - shock - diabetic ketoacidosis - renal failure - diarrhea |
Metabolic Effects of Acidosis - decreased serum bicarbonate ion |
|
|
Metabolic compensation of Acidosis - rapid, deep respirations - kidneys excrete more acid and increase bicarbonate absorption |
Metabolic Laboratory Acidosis - low serum bicarbonate - low PCO2 - Compensated serum pH = 7.35 to 7.4 - Decompensated serum pH less than 7.35 |
|
|
Respiratory Causes of Alkalosis - hyperventilation (anxiety, aspirin overdose) |
Respiratory effect of Alkalosis - decreased PCO2 |
|
|
Respiratory Compensation of Alkalosis - kidneys excrete less H+ and reabsorb less bicarbonate |
Respiratory Laboratory of Alkalosis - Low PCO2 - Low serum bicarbonate - Compensated serum pH = 7.4 to 7.45 - Decompensated serum pH greater than 7.45 |
|
|
Metabolic Causes of Alkalosis - vomiting (early stage) - excessive antacid intake |
Metabolic Effect of Alkalosis - increased serum bicarbonate ion |
|
|
Metabolic Compensation of Alkalosis - slow, shallow respirations - kidneys excrete less acid and decrease bicarbonate absorption |
Metabolic Laboratory of Alkalosis - elevated PCO2 - elevated serum bicarbonate - compensated serum pH = 7.4 to 7.45 - decompensated serum pH greater than 7.45 |
|
|
Chapter 4 |
Pain - serves as one of body's defense mechanisms = result from stimulation of nociceptors by ischemia, chemical mediators, or distention of tissue (enlarged/swollen) |
|
|
Pain may be felt - inflammation - infection - ischemia (inadequate blood supply to organ) - tissue necrosis - stretching of tissue - chemicals - burns |
In skeletal muscle, pain may result from - ischemia or hemorrhage In organs: liver, kidney, or brain pain receptors in covering capsule, felt when capsule is stretched by inflammation In stomach and intestines: pain result from inflammation of the mucosa, ischemia, distention or muscle spasm |
|
|
Somatic pain may arise from - skin (cutaneous) or - deeper structures (bone or muscle) to be conducted by sensory nerves |
Visceral Pain originates from the organs that travels by sympathetic fibers |
|
|
Nociceptors = pain receptors - free sensory nerve endings that are present in most tissues of body - may stimulated by thermal, chemical or physical means |
Thermal means; extreme temperatures Mechanical means: pressure Chemical sources: acids or compounds produced in body (bradykinin, histamine, or prostaglandin) |
|
|
Pain threshold: = level of stimulation required to activate the nerve ending sufficiently for the individual to perceive pain - nerve fibers sends signals to spinal cord and brain Pain perception (and response) : subjective but can compared from day-to-day in same person (depend on conditioning of individual) |
Pain Tolerance: = ability to withstand pain or the perception of its intensity or duration - may be increased by endorphin release - may be reduced because of fatigue or stress - varies considerably with past pain experience and overall state of health (varies among people and different situations) |
|
|
Afferent Fibers: (2 types) = conduct pain impulses toward the center (CNS) 1. Myelinated A delta fibers - transmit impulses rapidly 2. Unmyelinated C fibers - transmit impulses slowly. |
A delta fibers: Acute pain - sudden, sharp, localized pain related to thermal and physical stimuli primarily from skin and mucous membranes |
|
|
C fibers: = chronic pain - often experienced as diffuse, dull, burning or aching sensation - receive thermal, physical and chemical stimuli from muscle, tendons, the myocardium and digestive tract and skin |
Peripheral nerves transmit - afferent pain impulse to dorsal root ganglia and into spinal cord through dorsal horn (substantia gelatinosa) |
|
|
Dermatone = each spinal nerve conducts impulses from a specific area of the skin - area of skin innervated by each spinal nerve - somatosensory cortex is "mapped" to correspond to areas of body so that source can be interpreted in the brain - dermatone used to test area of sensory loss or pain sensation = determine site of damage after spinal cord injuries |
Efferent Fibers: - moving away from the center: efferent nerve fibers carry motor impulses back to muscles - at spinal cord synapse, a reflex response to sudden pain results in a motor efferent impulse back to muscle that initiates an involuntary muscle contraction to move the body away from the source of pain |
|
|
Reflex response - Involuntary muscle contraction away from pain source - Involuntary muscle contraction to guard against movement |
After sensory impulse reaches synapse - connecting neurons transmit across spinal cord to ascending tracts to the brain 2 types of tracts in the spinothalamic bundle |
|
|
2 types of Tracts in Spinothalamic Bundle 1. Paleospinothalamic Tract - slower impulses for chronic or dull pain 2. Neospinothalamic Tract - fast impulses for acute sharp pain Double pathway experiences with an injury to skin, initial sharp severe pain, followed by a duller but persistent throbbing or aching pain. |
Reticular formation - the two spinothalamic bundle tracts connect with brain stem, hypothalamus, thalamus and other structures as they ASCEND to the somatic sensory area in cerebral cortex of PARIETAL LOBE of brain. = location and characteristics of pain are perceived. |
|
|
Acute Pain - Usually sudden and severe, short term - Indicates tissue damage - May be localized or generalized - Initiates physiologic stress response ↑ Blood pressure and heart rate; cool, pale, moist skin; ↑ respiratory rate; ↑ skeletal muscle tension - Vomiting may occur. - Strong emotional response may occur. |
Chronic Pain - Occurs over extended time; may be recurrent - Usually more difficult to treat than acute pain - Often perceived to be generalized - Individual may be fatigued, irritable, depressed - Sleep disturbances common - Specific cause may be less apparent. - Appetite may be affected. - Can lead to weight gain or loss - Frequently affects daily activities - Accommodation and pacing of activities may be required. - Periods of acute pain may accompany chronic pain conditions. - Usually reduces tolerance to additional pain |
|
|
|
|
|
Phantom Pain - Usually in adults - More common if chronic pain has occurred - Can follow an amputation - Pain, itching, tingling - Usually does not respond to common pain therapies - May resolve within weeks to months - Phenomenon not fully understood |
RAS: Reticular Activating System - arousal state - in reticular formation in the pons and medulla influences the brain's awareness of incoming pain stimuli - many drugs depress RAS, decreasing the pain experienced |
|
|
Hypothalamus - role in response to pain through its connections with the pituitary gland and sympathetic nervous system - response to pain involves a stress response and emotional response (crying, moaning, anger) |
Thalamus - processes many types of sensory stimuli as they enter brain - important in emotional response to pain thru limbic system |
|
|
Describe your response to sudden severe pain in own experience (injury) Describe your physical response and emotional reactions - Example responses are faint and dizzy, rapid heart rate and breathing, nauseous, pale and diaphoretic, and anxious. |
Using knowledge of normal physiology, list effects of increased sympathetic nervous system = Effects include increased heart rate and contractility, increased BP, cutaneous and visceral vasoconstriction, bronchodilation, pupil dilation, increased BMR, and increased blood glucose level.c. Monitoring the sympathetic re |
|
|
Suggest how monitoring for sympathetic nervous system changes assist you in evaluating a person's level of pain = Monitoring the sympathetic response gives a more accurate indication of the level of pain because it is less subjective and not modified as much by the individual’s tolerance and conditioning factors. |
Gate-Control Theory = Control systems, “gates” built into normal pain pathways - Can modify pain stimuli conduction and transmission in the spinal cord and brain - Gates open = Pain impulses transmitted from periphery, then spinothalamic tract then ascend to brain - Gates closed = Reduces or modifies the passage of pain impulses: or stimulus blocked (response to other sensory stimuli along competing nerve pathways may diminish pain sensations or by modulating or inhibiting impulses |
|
|
Referred Pain - Source may be difficult to determine. - Pain may be perceived at site distant from source - Characteristic of visceral damage in the abdominal organs - Heart attack or ischemia in the heart |
TENS: Transcutaneous Electrical Nerve Stimulation = therapeutic intervention that increases sensory stimulation at a site, thus blocking pain transmission - brain can inhibit or modify incoming pain stimuli by producing efferent or outgoing transmissions through reticular formation |
|
|
Key to Analgesia System (blocking of pain impulses to brain) - release of a number of opiate-like chemicals (OPIODS) secreted by interneurons within the central nervous system = block conduction of pain impulses into CNS - resemble drug Morphine (derived from opium used as analgesic) |
Endogenous or endorphins = originating from body = morphine like substances produced in body that block pain stimuli at sites in the brain and spinal cord - include Enkephalins, dynorphins, and beta-lipotropins |
|
|
Enkephalins - released in spinal cord and is attached to opiate receptors on afferent neuron thus blocking release of the Neurotransmitter Substance P at synapse = prevents transmission of pain stimulus into spinal cord |
Serotonin - another chemical released in the spinal cord that acts on other neurons in spinal cord to increase the release of enkephalins. |
|
|
Clinical Depression - chronic pain due to reduction in serotonin levels in brain = natural opiate receptors found in many areas of brain, as are secretions of endorphins (can block pain impulses at that level) |
3 Methods of "closing the gate" and reducing pain = presence of other sensory stimuli (e.g., pressure or cold), particularly from the same body region, inhibitory impulses from the brain, distraction by other activities, and drugs. |
|
|
Signs and Symptoms and Diagnosis of Pain - Nausea and vomiting - May occur with acute pain - Fainting and dizziness - May occur with acute painAnxiety and fear - Frequently evident in people with chest pain or trauma - Location of pain - Descriptive terms: Aching, burning, sharp, throbbing, widespread, cramping, constant, periodic, unbearable, moderate - Timing of pain - Association with an activity - Physical evidence of pain - Pallor and sweating, High blood pressure, tachycardia (excessive rapid heartbeat) - Clenched fists or rigid faces - Restlessness or constant motion - Guarding area to prevent stimulation of receptors |
Young Children and Pain (pg 57) - Infants respond physiologically - Examples: tachycardia, increased blood pressure, facial expressions - Great variations in different developmental stages: - Different coping mechanisms - Range of behavior - Often have difficulty describing the pain - Withdrawal and lack of communication in older children |
|
|
Referred Pain (pg 57) - Source may be difficult to determine or can be localized to specific area = Pain may be perceived at site distant from source - Characteristic of visceral damage in the abdominal organs - Heart attack or ischemia in the heart - usually pain originates in a deep organ/muscle and perceived on surface of body in a different area |
TA 4-4 a) from your ow experience describe sharp pain, an aching pain and cramping pain = Sharp pain may be described as severe and stabbing, aching pain is dull and constant, and cramping pain is characterized by intermittent waves of pain that increase and decrease. |
|
|
TA 4-4 b) list factors that often make pain seem more severe = Fatigue, hunger, fear, and multiple problems or stressors may make pain more severe. |
TA 4-4 c) differentiate pain threshold from pain tolerance = Pain threshold is the level of stimulation of a pain receptor required before pain is perceived. Pain tolerance refers to the level of pain that precipitates action by the individual. |
|
|
TA 4-5 Compare the characteristics of acute and chronic pain = Acute pain is sudden and severe but usually temporary, and it activates the stress response. = Chronic pain is persistent and may not be as localized or as severe. It often is associated with depression and irritability. Tolerance is reduced by chronic pain, making coping often more difficult. |
Headache (pg 60) = common type of pain - Congested sinuses, nasal congestion, eye strain - Muscle spasm and tension - From emotional stress - In temporal area - Temporomandibular joint syndrome (TMI) - Migraine - Abnormal cerebral blood flow and metabolism in the brain (increased neural activity) - Intracranial headaches - Increased pressure inside the skull - many precipitating factors: atmospheric changes, stress, menstruation, dietary choices and hunger |
|
|
Methods of Managing Pain (pg 61) - Remove cause of pain as soon as possible - Use of analgesic medications (most common) - Orally, Parenterally (injection), Transdermal patch - Analgesic Classified by ability to relieve = Mild pain, Moderate pain, Severe pain |
Methods for Managing Pain Continued (pg 61) -Sedatives and antianxiety drugs - Adjuncts to analgesic therapy - Promote rest and relaxation - May reduce dosage requirements for analgesic - Chronic and increasing pain - May occur in cancer - Stepwise fashion to reduce pain - Tolerance to narcotics develops over time - Increase dose requirements - New drug may be required |
|
|
Moderate Pain is managed - codeine commonly used either alone or combo with acetaminophen or aspirin - codeine: a narcotic, a morphine derivative, acting at the opiate receptors in CNS - Adverse effects: cause nausea, constipation, high doses: respiratory depression - taking with food/milk reduce gastric irritation - Oxycodone (syntehtic narcotic combined with acetaminophen or aspirin) = drug affects perception of pain and emotional response = relaxation, sense of well-being, dependency. *significant problem |
Mild pain is usually managed with - acetaminophen (Tylenol) or acetylsalicylic acid (ASA, aspirin) - act primarily at the peripheral site - useful when inflammation is present - fewer side effects *Even in high doses, not effective for severe pain |
|
|
Severe Pain Managing - morphine, hydromorphine or other narcotics favored - drugs block pain pathways in spinal cord and brain, alter perception of pain in positive manner - tolerance develops with long-term use (require higher doses) - addiction - Meperidine helpful for short-term pain - lead to buildup of toxic metabolite |
NSAIDS (Naproxen, ibuprofen) - widely used to treat both acute and chronic pain - particularly when inflammation is present (lower body temp - fever = antipyretic action) *Even in high doses, not effective for severe pain ASA Aspirin (aceytlsalicylic acid) - acts as a platelet inhibitor reducing blood clotting (lower body temp - fever = antipyretic action) *Even in high doses, not effective for severe pain |
|
|
Treatment of Migraine Pain - mild migraine treat with NSAIDS (Ibuprofen- advil, motrin,) Acetaminophen (Tylenol) - moderate pain: combo of Acetaminophen, codeine, and caffeine or Acetaminophen, aspirin and caffeine |
Treatment of Severe Migraine Pain - difficult - ergotamine can be effective if it is administered immediately after onset of headache - drug of choice: triptans that act on some 5-HT (5-hydroxytriptamine) receptors to block the vasodilation and release of vasoactive peptides in the brain = these drugs relieve nausea and light sensitivity as well as pain and nausea Ex: almotriptan (Axert), rizatriptan (Maxalt), sumatriptan (Imitrex), naratriptan (Amerge), zolmitriptan (Zomig), frovatriptan (Frova) and eletriptan (Relpax) |
|
|
Preventative medication for Migraines (on daily basis or just before) - several cardiovascular drug groups usually used for hypertension, the beta-blockers, and calcium channel blockers |
Intracranial headaches (pg 60) result from - increased pressure inside skull - any space-occupying mass stretches cerebral vascular walls or meninges covering brain - causes: trauma with edema or hemorrhage, tumors, infections (meningitis) or inflammation resulting form toxins such as alcohol. - Headaches may be occipital or frontal |
|
|
Central Pain - pain that is caused by dysfunction or damage to brain or spinal cord - lesion: abscess, infarction, hemorrhage, tumor or damage resulting from direct injury - persistent, irritating - can be very localized or involve large area of body |
Neuropathic Pain (pg 61) - caused by trauma or disease involving peripheral nerves - tingling, burning, severe shooting pain (varies) - stimulated by movement or injured nerves - Neuralgias: extreme painful conditions result of damage to peripheral nerves caused by infection/disease - Causalgia: type of neuralgia involves severe burning pain triggered by normally "nontraumatic" stimuli |
|
|
Ischemic Pain - from profound, sudden loss of blood flow to an organ or tissues in specific area of body - results in hypoxia (tissue damage and release of inflammatory and pain-producing substances) - aching, burning, prickling to strong shooting pain - Atherosclerotic disorders can cause ischemic pain = improve blood flow and prevent / reduce tissue hypoxia to manage pain |
Cancer-Related Pain pg 61 - usually chronic - pain caused by advance of disease and resultant damage to body (most common) - pain associated with treatment of disease - pain that is the result of a coexisting disease unrelated to the cancer |
|
|
PCA - Patient -controlled analgesia for SEVERE PAIN - many patients with severe pain administer their own medications as needed - small pumps attached to vascular access sites *lessen overal consumption of narcotics |
Intractable pain: cannot be controlled with medications = surgical intervention procedures: rhizotomy or cordotomy to sever sensory nerve pathway in spinal nerve/cord |
|
|
Anesthesia pg 62 Local anesthesia - Injected or applied topically to skin or mucous membranes Spinal or regional anesthesia - Blocks pain from legs or abdomen General anesthesia - Causes loss of consciousness (gas or injection) Neuroleptanesthesia - Patient can respond to commands. - Relatively unaware of procedure, no discomfort |
General Anesthesia (pg 63) - administering a gas to be inhaled (Nitrous Oxide or injecting a barbiturate such as sodium pentothal intravenously) - loss of consciousness Type: Neuroleptanesthesia (patient can respond to commands but is relatively unaware of procedure or of any discomfort) |
|
|
Alkalosis: - excessive blood alkalinity caused by overabundance of bicarbonate in blood - or loss of acid from blood (metabolic alkalosis) - or by low level of CO2 in blood = rapid or deep breathing (respiratory alkalosis) |
Major Causes Of Metabolic Alkalosis - loss of acid due to vomiting, or drainage of stomach - overreactive adrenal gland (due to Cushing syndrome and some adrenal tumors) - use of diuretics (ex: thiazides, furosemide, ethacrynic acid) *develops when body loses too much acids or gains too much base |
|
|
Major Causes of Respiratory Alkalosis - hyperventilation (rapid deep breathing) causes too much CO2 to be expelled - anxiety or panic attacks - aspirin overdose (early stages) - fever or infection - low O2 levels in blood - pain |
Aspirin Overdose can cause BOTH Respiratory Alkalosis and Metabolic Acidosis |
|
|
Symptoms of Alkalosis - irritability - muscle twitching and cramps - tingling in fingers, toes and round lips (Paresthesia) - severe alkalosis: painful muscle spasm (tetany) |
The control of fluid balance is maintained by - the thirst mechanism in hypothalamus - ADH hormone - ANP hormone - Aldosterone hormone |
|
|
Renal failure is a common cause of = hyperkalemia |
Three types of Anesthesia include - local - spinal/regional - general |
|
|
Local Anesthetic - Ex: Lidocaine; injected/topical; may add epinephrine - Effects: block nerve conduction (sensory) in a peripheral nerve - Purpose: removal of a skin lesion; tooth extraction |
General Anesthetic - Ex: Intravenous- thiopental sodium inhalation (gas) nitrous oxide - Effects: affects brain- partial or total loss of consciousness - Purpose: general surgery, no pain/awareness when combined with analgesic |
|
|
Relative or Neurolept-anesthesia - Ex: Diazepam or droperidol - effects: can respond |
Spinal Anesthesia - Ex: local anesthetic injected into subarachnoid or epidural space around lower spinal cord - Effects: blocks nerve conduction (sensation) at and below level of injection - purpose: surgery on lower part of body: labor and delivery |
|
|
Spinothalamic Tract - bundle of sensory nerve fibers conducting afferent pain impulses up the spinal cord to the brain. |
Parietal lobe - is the somatosensory area of the brain where pain characteristics and location are identified. |
|
|
Endorphins and Enkephalins - opioids or morphine-like substances produced in the CNS that can block the pain pathway naturally |
Define and give an example of Referred Pain Referred pain is perceived in an area some distance away from its origin; for example, cardiac pain is perceived in the left arm and shoulder. |
|
|
Differentiate characteristics of acute and intractable pain
Acute: sudden and severe, often temporary, and usually arises from a specific cause and responds to appropriate treatments. Intractable: may have an unknown cause and does not respond to the usual methods of treatment. It is chronic and may be disabling. |
List several factors that can alter the perception of pain and response to pain - prior experience with pain, - age, - physiological status, - the cause of pain, anxiety or fear - conditioning. |
|
|
Briefly describe six possible methods of pain control |
- analgesics, anti-inflammatory drugs, anesthetics, application of heat or cold, massage, surgery, acupuncture, relaxation techniques, hypnosis, and distracting activities. |
|
|
Proportion of Blood (to body weight) in an adult male? = 4% plasma |
Serum Potassium Levels are affected by - aldosterone - serum H+ level - insulin levels |
|
|
Insensible fluid loss refers to water loss through = perspiration and expiration |
One of the factors involved in the increased need for water in infants is = higher metabolic rate |
|
|
Pain tolerance = degree of pain that is endured before an individual takes action |
One cause of Edema = increased capillary permeability |
|
|
Young infants typically respond to pain with tachycardia and increased blood pressure. |
a headache that is related to changes in cerebral blood flow is classified as a ________ headache - migraine |
