medsurg notes f/e

7/29/2019 medsurg notes F/E

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Topics on blueprint: Ch. 14, 17

Hypovolemiao fluid volume deficit, can occur with abnormal loss of body

fluidso assessment: I/O , monitor pt. for cardiovascular changes,

monitor respiratory status, assessment of neurological

functions includes evaluation of LOC, pupillary response and

voluntary movement of the extremities, degree of muscle

strength and reflexes. Accurate daily weights, inspect for skin

turgor and temperature

o Etiology: inc. insensible water loss or perspiration (high fever,stroke), diabetes insipidus, osmotic diuresis, hemorrhage, GI

losses (diarrhea, vomiting, NG suction, fistula drainage), over

use of diuretics, inadequate fluid intake, and third space fluid

shifts (burns, intestinal obstruction)

o Signs and symptoms: restlessness, drowsiness, lethargy,confusion, thist dry mucous membranes, decr. Skin turgor,

decr. Capillary refill, , postural hypotension, inc. pulse, dec.

CVP, dec. urine output,concentrated urine, inc. respiratory

rate,weakness, dizziness, weightloss, seizures, coma

o Treatments:goal of treatment is to correct the underlyingcause and to replace both water and any needed electrolytes.

Balanced IV solution such as Ringers solution are usually

given. Isotonic (0.9%) sodium chloride is used when rapid

volume replacement is indicated. Blood is administered when

volume loss is due to blood loss.

o Diagnosis deficit fluid volume R/T excessive ECF losses or

decrease fluid intake

decreased cardiac output R/T excessive ECF losses ordecreased fluid intake

risk of deficient fluid volume R/T ECF losses ordecreased fluid intake

potential complications: Hypovolemic shock


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Hypervolemiao Assessment: I/O , monitor pt. for carsiovascular changes,

monitor respiratory status, assessment of neurological

functions includes evaluation of LOC, pupillary response and

voluntary movement of the extremities, degree of musclestrength and reflexes. Accurate daily weights, inspect for skin

turgor and temperature

o Etiology: Fluid volume excess, excessive isotonic or hypotonicIV fluids, Heart failure, renal failure, primary polysipsia,

SIADH, cushings symdrome, longeterm use of corticosteroids.

o Signs and symptoms: headache, confusion, ;ethargy,peripheral edema, jugular venous distention, full and

bounding pulse, inc. BP, inc. CVP, polyuria, dyspnea, crackles,

luminary edema, muscle spasms, weight gain, seizures coma.

o Treatments: goal of treatment is removal of fluids withoutproducing abnormal changes in electrolyte composition or

osmolality of ECF. Diuretics and fluid restriction are the

primary forms of therapy.

o Dietary needs: Restriction of sodium intake may also beindicated

o Diagnosis Excessive fluid volume R/T increased water and/or

sodium retention

Risk for imbalanced fluid volume R/T increased waterand/or sodium retention

Impaired gas exchange R/T water retention leading topulmonary edema

Risk for impaired skin integrity R/T edema Disturbed body image R/T altered body appearance

secondary to edema

Potential complications: pulmonary edema, asciteso Hyponatremia (Na < 135 mEq/L)o Etiology:

Excessive sodium loss: GI losses (diarrhea, vomiting,fistulas, NG suction) Renal losses (diuretics, adrenal


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insufficiency, Na+ wasting renal disease) skin losses

(burns, wound drainage)

Inadequate sodium intake: fasting diets Excessive water gain (dec. sodium concentration):

Excessive hypotonic IV fluids, primary polydipsia Disease states: SIADH, heart failure, primary

hypoaldosteronism.

o Signs and symptoms: Hyponatremia with decreased ECF volume (irritability,

apprehension, confusion, dizziness, personality

changes, tremors , seizures, coma, dry mucous

membranes, postural hypotention, dec. CVP, dec.

jugular venous filing, tachycardia, thread pulse, cold

and clammy skin)

Hyponatremia with normal/ increased ECF volume(headache, apathy, confusion, muscle spasms, seizures,

coma, nausea, vomiting, diarrhea, abdominal cramps,

weight gain, ^ BP ^ CVP)

o Treatments: if caused by water excess all that is needed isfluid restrictions. Drugs that block the activity of ADH

(vasopressin) are used in tx of hyponatremia. Tx of

hyponatremia associated with fluid loss includes fluidreplacement with sodium containing solutions. Conivaptan

(vaprisol) results in ^ urine output w/o loss of electrolytes (it

should not be used in pts. With hypovolemic hyponatremia).

Tolvaptan (Samsca) is used to treat hyponatremia associated

with heart failure, liver cirrhosis, and SIADH.

o Dietary needs: fluid restrictiono Diagnosis

Risk for injusry R/T altered sensorium and decreasedLOC secondary to abnormal CNS function

Risk for electrolyte imbalance R/T excessive loss ofsodium and/ or excessiveintake of water

Potential complication: severe neurologic changes Hypernatremia (Na > 145 mEq/L)


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o Etiology: excessive sodium intake:IV fluids: (hypertonic NaCl,

excessive isotonic NaCl, IV sodium bicarbonate)

hypertonic tube feedings without water supplements,

near-drowning in salt water. Inadequate water intake: unconscious or cognitively

inpaired individuals.

Excessive water loss (^ sodium concentration): ^insensible water loss (high fever, heatstroke, prolonged

hyperventilation), osmotic diuretic therapy, diarrhea

Disease states: diabetes insipidus, primaryhyperaldosteronism, cushings syndrome, uncontrolled

diabetes mellitus.

o Signs and symptoms: Hypernatremia with dec. ECF Volume: restlessness,

agitation, twitching, seizures, coma, intense thirst, dry,

swollen tongue, sticky mucous membranes, postural

hypotention, dec. CVP, weightloss lethargy.

Hypernatremia with normal/ increased ECF Volume:restlessness, agitation, twitching, seizures, coma,

intense thirst, flushed skin, weight gain, peripheral and

pulmonary edema, ^ BP, ^ CVPo Treatments: goal of treatment is to dilute the sodium

concentration with sodium free IV fluids, such as 5% dextrose

in water, and to promote excretion of the excess sodium by

administering diuretics

o Dietary needs: sodium restrictionso Diagnosis:

Risk for injury R/T altered sensorium and seizuressecondary to abnormal CNS function

Risk for electrolyte imbalance R/T intake of sodium and/or loss of water

Potential complication: seizures and coma leading toirreversible brain damage

Hypokalemia (K+


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o Can result from abnormal losses of K from a shift from ECF toICF, or rarely from deficient dietary K intake.

o Most common causes of hypokalemia are abnormal losses, viaeither the kidneys or the GI tract.

o Abnormal losses occur when the patient is diuresing,particularly in a pt. with an elevated aldosterone level.

o Hypokalemia is pften associated with the treatment ofdiabetic ketoacidosis because of a combination of factors,

including an ^ in urinary potassium loss and a shift of

potassium into cells woth the administration of insulin and

correction of metabolic acidosis

o Etiology: Potassium loss: GI losses (diarrhea, vomiting,

fistulas, NG suction) Renal losses (diuretics,

hyperaldosteronism (aldosterone is released when the

circulating blood volume is low; it causes sodium

retention in kidneys, but loss of potassium in the urine),

magnesium depletion(low magnesium stimulates renin

release and subsequently increased aldosterone levels,

which results in k excretion)) skin losses (diaphoresis)

dialysis.

Shift of Potassium into cell: increased insulin (i.g.,IV dextrose load) , alkalosis (can cause a shift of K into

cells in exchange for hydrogen, thus lowering the K in

the ECF and causing systematic hypokalemia), tissue

repair, ^ epinephrine (e.g. stress)

Lack of Potassium intake: starvation diet low inpotassium, failure to include potassium in parenteral

fluids in NPO.

o Signs and symptoms: Fatigue, muscle weakness, leg cramps, nausea vomiting

paralytic ileus , soft, flabby muscles, parethesias,

decreased reflexes, weak, irregular pulse, polyuria,

hyperglycemia

Electrocardiogram changes: ST segmented depression,flattened T wave, presence of U wave, ventricular


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dysrhythmias (e.g., PVC), bradycardia, enhanced

digitalis effect

Treatments: increasing dietary intake of potassium andpotassium chloride supplements (KCL). KCL can be

given orally or IV. Except in severe deficiencies, KCL isnever given unless there is urine output of at least

0.5mL/ kg of body weight per hour. The preferred

maximum concentration is 40 mEq/L (in severe cases

up to 80 mEq/L). the rate of adm. Should not exceed 10

to 20 mEq per hour and should be administered by

infusion pump to ensure correct administration rate.

(assess iv sites at least hourly for phlebitis and

infiltration) KCL given IV must always be diluted. Never

give in IV push. IV bags must be inverted several times.

Never add a KCL to a hanging IV bag to prevent giving

a bolus dose.

o Dietary needs: potassium rich foodso Diagnosis

Risk for electrolyte imbalance R/T excessive loss ofpotassium

Risk for injury R/T muscle weakness and hyporeflexia Potential complication dysrhythmias

Hyperkalemia (K+ > 5.0 mEq/L)o Most common cause is renal failure.o Potassium sparing drugs and ACE inhibitors are types of drugs

that reduce the kkidneys ability to excrete potassium.

o Must be monitored electrocardiographically to detectdysrhythmias and to monitor the effects of therapy

o Etiology: Excess potassium intake: excessive or rapid

parenteral administration. Potassium-cotaining drugs

(e.g. potassium-penicillin) potassium-containing salt

substitute.


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Shift of potassium out of cells: acidosis, tissuecatabolism (e.g., fever, sepsis, burns) crush injury,

tumor lysis syndrome.

Failure to eliminate potassium: renal disease,potassium-sparing diuretics, adrenal insufficiency, ACEinhibitors.

o Signs and symptoms: Irritability, anxiety, abdominal cramping, diarrhea,

weakness of lower extremeties, paresthesias, irregular

impulse, cardiac arrest if hyperkalemia sudden or

severe.

Electrocardiogram changes: tall, peaked T wave,prolonged PR interval, ST segment depression, loss of P

wave, widening QRS, ventricular fibrillation, ventricular

standstill

o Treatments: administer fluids and possibly diuretics,Kayexalate(administered via the GI tract binds potassium in

exchange for sodium, and the resin is excreted in feces)

o Pts. With moderate hyperkalemia should additionally receiveone of the treatments to force K into cells, usually IV insulin

and glucose.

o The pt. experiencing dangerous cardiac dysrhythmias shouldreceive IV calcium gluconate immediately while the potassium

is being eliminated and forced into cells.

o Hemodialysis is an effective means of removing potassiumfrom the body in the patients with renal failure.

o Dietary needs: withhold potassium from dieto Diagnosis

Risk for electrolyte imbalance R/T excessive retention orcellular release of potassium

Risk for injury R/T lower extremity muscle weaknessand seizures

Potential complication: dysrhythmias Hypocalcemia Ca2+


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o About two thirds of hypercalcemia cases are cause byhyperparathyroidism and one third are caused by malignancy,

especially from breast cancer, lung cancer, and multiple

myeloma.

o Malignancies lead to hypercalcemia trough bone destructionfrom tumor invasion or through tumor secretion of a

parathyroid-related protein, which stimulates calcium release

from bones

o It rarely occurs from increase calcium intake.o Excessive calcium leads to reduced excitability of both

muscles and nerve

o Any pt who has had thyroid or neck surgery must be closelyobserved in the immediate post-op period for manifestations

of hypocalcemia because of the proximity of the surgery to

the parathyroid glands.

o Etiology: Decreased total calcium: Chronic kidney disease,

elevated phosphorus, primary hypoparathyroidism, Vit

D deficiency, mag. Deficiency, acute pancreatitis, loop

diuretics (furosemide) chronic alcoholism, diarrhea, dec.

serum albumin (pt is usually asymptomatic due to

normal ionized calcium level) Decreased Ionized Calcium: alkalosis, excess

administration of citrated blood

o Signs and symptoms: Easy fatigability, depression, anxiety, confusion,

numbness and tingling in extremities and region around

mouth, hyperreflexia, muscle cramps, chvosteks sign,

trousseaus sign, laryngeal spasm, tetany, seizures

Electrolycardiogram changes: elongation of STsegment, prolonged QT interval, ventricular tachycardia

o Treatment: oral or IV calcium supplements. (not given IMbecause it can cause severe local reactions like burns,

necrosis, and tissue sloughing) pain and anxiety must be

adequately treated.


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o Diet: a diet in calcium-rich foods is usually ordered alongwith vitamin D supplements

o Diagnosis: risk of electrolyte imbalance related to decreasedproduction of PTH. Risk for injury related to tetany and

seizures potential complications: fracture, respiratory arrest

Hypercalcemia Ca2+ >10.2 mg/dLo Etiology:

Increased total calcium: multiple myeloma,malignancies with bone metastasis, prolonged

immobilization, hyperparathyroidism, Vit D overdose,

thiazide diuretics, Milk-alkali syndrome

Increased ionized calcium: acidosiso Signs and symptoms:

Lethargy, weakness, depressed reflexes, decreasedmemory, confusion, personality changes, psychosis,

anorexia, nausea, vomiting, bone pain, fractures,

polyuria, dehydration, nephrolithiasis, stupor, coma

Electrocardiogram changes: shortened ST segment,shortened QT interval, Ventricular dysrhythmias,

increased digitalis effect.

Treatments: promotion of excretion of calcium in urine byadministration of calcium in urine by administration of a loop

diuretic, and hydration of the patient with isotonic saline infusions.

o The patient must drink 3000 to 4000 mL of fluid daily topromote the renal excretion of calcium and to decrease the

possibility of kidney stone formation.

o Mobilization with weight bearing activity is encouraged toenhance bone mineralization

Nursing diagnosis: risk for electrolyte imbalance r/t excessive bonedestruction.. risk for injury related to neuromuscular and

sensorium changes..potential complications: dysrhythmias

.

Phosphate imbalances

Phosphate is a primary anion in the ICF and is essential to thefunction of muscle, RCBs, and the nervous system. A reciprocal


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relationship exist between phosphorus and calcium in that a high

serum phosphate level tends to cause a low calcium concentration

in the serum.

Hypophosphatemiao Seen in the patient who is malnourished or has

malreabsorption syndrome

o Mild to moderate hypophosphatemia is usually asymptomatic.o Severe hypophosphatemia may be fatal because of

decreased cellular function.

o Etiology: malabsorption syndrome, nutritional recovery syndrome

(reversal or treatment of starvation) glucose

administration, total parenteral nutrition, alcohol

withdrawal, phosphate bounding antiacids, recovery

from diabetic ketoacidosis, respiratory alkalosis

o Signs and symptoms: Central nervous system dysfunction (confusion, coma)

muscle weakness, including respiratory muscle

weakness and difficulty weaning, renal tubular wasting

of magnesium, calcium, HCO3,cardiac problems

(dysrhythmias, dec. stroke volume) osteomalasia,rhabdomyolysis.

o Treatments: management of mild deficiency may involve oralsupplements and ingestion of foods high in phosphorous.

Severe deficiency can be serious and may require IV

administration of sodium phosphate or potassium phosphate.

Frequent monitoring levels is necessary to guide IV therapy.

o Dietary needs: Hyperphosphatemia

o Major condition that can lead to Hyperphosphatemiao Is acute or chronic renal failure that results in an altered

ability of the kidney to excrete phosphate.

o Etiology: Renal failure, chemotherapeutic agents, enemas

containing phosphorus (e.g., fleet enema) excessive


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ingestion (e.g., milk, phosphate containing laxatives)

large Vit D intake, hypoparathyroidism

o Signs and symptoms: Hypocalcemia, muscle problems; tetany, deposition of

calcium-phosphate precipitates in skin, soft tissue,cornea, vicera, blood vessels.

o Treatments: aimed at identifying and treating the underlyingcause. Adequate hydration and correction of hypo calcemic

conditions can enhace the renal excretion of phosphate

through the action of PTH

o Dietary needs: restriction of foods and fluids high inphosphorus

Osmolality: measures the osmotic force of solute per unit ofweight of solute. Used to describe fluids inside the body.

o Assessment: normal plasma osmolality is between 275 and295 mOsm/kg a value greater than 295 indicates that the

concentrationof particle is too great or the water content is

too little (water deficit). A value less than 275 indicates too

little solute for the amount of water or too much water for the

amount of solute (water excess). Because the major

determinants of the plasma osmolality are sodium andglucose, one can calculate the effective plasma osmolality

based on the concentration of those substances.

o Isotonic: fluids with the same osmolality as the cell interioro Hypotonic: solutes are less concentrated than the cells.o Hypertonic: solutes more concentrated than cell.

Spacing a term used to describe the disruption of body water.o First spacing describes the normal distribution of fluid in the

ICF and ECF

o Second spacing refers to an abnormal accumulation ofinterstitial fluid (edema)

o Third spacingoccurs when fluid accumulates in a portion ofthe body from which it is not easily exchanged with the rest

of the ECF. It is trapped and unavailable for functional use


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(ascites, sequestration of fluid in the abdominal cavity with

peritonitis, and edema associated with burns, traumas, or

sepsis)

Arterial blood gases and interpretationo pH: 7.35- 7.45o PaCO2: 35- 45 mm Hgo Bicarbonate: 22-26 mEq/Lo Pao2: 80-100 mm Hgo SaO2: >95%

Antidiuretic hormone (actions/effects)o Water balance is maintained via the finely tuned balance of

water intake and excretion. A body fluid deficit or increase in

plasma osmolality is sensed by the osmoreceptors in the

hypothalamus, which in turn stimulate thirst and antidiuretic

hormone release (ADH). Thirst causes the patient to drink

water. ADH ,which is synthesized in the hypothalamus and

stored in the posterior pituitary, acts in the renal distal and

collecting tubules causing water reabsorption. Together these

factors result in increased free water in the body and

decreased plasma osmolality. If the plasma osmolalitydecreased or there is water excess, secretion of ADH is

suppressed , resulting in urinary excretion of water

o Under the hypothalamic control, the posterior pituitaryreleases ADH, which regulates water retention by the kidneys.

The distal tubules and collecting ducts in the kidney respond

to ADH by becoming more permeable to water so that water

is reabsorbed from the tubular filtrate into the blood and not

excreted in urine. Other factors that stimulate ADH release

include stress, nausea, nicotine, and morphine. These factors

usually result in shifts of osmolality within the range of

normal values. It is common for the postoperative patient to

have low serum osmolality after surgery, possibly because of

the stress and opioid analgesia.

SIADH:


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o Etiology: a pathologic condition Syndrome of inappropriateantidiuretic hormone secretion are cause by abnormal ADH

production in CNS disorders (brain tumors, brain injury) and

certain malignancies (small cell lung cancer)

o The inappropriate ADH causes water retention, whichproduces a decrease in plasma osmolality below the normal

value and a relative increase in urine osmolality with a

decrease in urine volume .

o Signs and symptoms:o Treatments

RAAS and its relationship of potassium/ sodiumo Aldosterone is a mineralocorticoid with potent sodium

retaining and potassium excreting capabilities. Secretions of

aldosterone may be simulated by the decreased renal

perfusion or decreased sodium delivery to the distal portion of

the renal tubule. The kidneys respond by secreting renin into

the plasma. Angiotensinogen, produced in the liver and

normally found in the blood is acted on by the renin to form

angiotensin I which is converted to angiotensin II. It then

stimulates the adrenal cortex to secrete aldosterone.

Acid-Base Balanceo Metabolic acidosiso Occurs when an acid other than carbonic acid accumulates in

the body or when bicarbonate is lost from body fluids, In bith

cases a bicarbonate deficit results. Ketoacid accumulate in

diabetic ketoacidosis and lactic acid accumulation with shock

are examples of accumulation of acids. Severe diarrhea

results in loss of bicarbonate and secrete hydrogen ions.

o Gain of fixed acid, inability to excrete acid or loss of base. S/S: neurologic (drowsiness, confusion, headache,

coma), Cardiovascular (dec. bp, dysrhythmias[re;ated

to hyperkalemia from compensation], warm flush skin

[r/t peripheral vasodilation] ) GI (nausea, vomiting,


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diarrhea, abdominal pain) Respiratory (deep, rapid

respirations [compensatory action by the lungs])

Etiology: diabetic ketoacidosis, lactic acidosis,starvation, severe diarrhea, renal tubular acidosis, renal

failure, GI fistulas, shock Blood gas interpretations: plasma pH: dec., PaCO2

normal, HCO3 dec.

o Metabolic alkalosiso Occurs when a loss of acid or a gain in bicarbonate occurs.o Loss of strong acid or gain of base

S/S: neurologic ( dizziness, irritability, nervousness,confusion) cardiovascular (tachycardia, dysrhythmias

r/t hypokalemia from compensation) GI (nausea,

vomiting, anorexia) neuromuscular (tetany, tremors,

tingling of fingers and toes, muscle cramps, hypertonic

muscles and seizures)

Etiology: severe vomiting, excessive gastric suctioning,diuretic therapy, potassium deficit, excessive NaHCO3

intake, excessive mineralo-corticoids

Blood gas interpretations: plasma pH: ^, PaCO2normal, HCO3: ^

o Respiratory acidosiso Occurs when there is hypoventilation. Hypoventilation results

in a buildup of carbon dioxide; subsequently, carbon acid

accumulates in the blood. Carbonic acid dissociates, liberating

hydrogen ios, and there is a decrease in pH. If carbon dioxide

is not eliminated from the blood, acidosis results from

accumulation of carbonic acid.

o Patho: CO2 retention from hypoventilation S/S: neuro (drowsiness, disorientation, dizziness,

headache, coma) Cardiovascular ( dec. bp, ventricular

fibrillation [related to hyperkalemia from compensation]

warm flush skin r/e peripheral vasodilation)

neuromuscular (seizures) Repiratory (hypoventilation


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with hypoxia (lungs are unable to compensate when

there is a resp. problem))

Etiology:causes: chronic obstructive pulmonary disease,barbiturate or sedative overdose, chest wall abnormality

(obesity), severe pneumonia, atelectasis, respiratorymuscle weakness, mechanical hypoventilation

Blood gas interpretations: plasma pH dec., PaCO 2 ^,HCO3 normal (uncompensated)

o Respiratory alkalosiso Occurs with hyperventilation. The primary cause of

respiratory alkalosis is hypoxemia from acute pulmonary

disorders. Anxiety, CNS disorders, and the mechanical

overventilation also increase the ventilation rate and decrease

the partial pressure of arterial carbonic acid and alkalosis.

o Increased CO2 excretion from hyperventilationo Patho: increased CO2 excretion from hyperventilation

S/S: neurologic (lethargy, light-headedness, confusion )cardiovascular (tachycardia, dysrhythmias r/t

hypokalemia from compensation) GI (Nausea, vomiting,

epigastric pain) Neuromuscular (tetany, numbness,

tingling of extremities, hyperreflexia, seizures)respiratory (hyperventilation [lungs are unable to

compensate when there is a respiratory problem])

Etiology: causes: hyperventilation (caused by hypoxiapulmonary emboli, anxiety, fear, pain, exercise, fever)

stimulated respiratory caused by septicemia,

encephalitis, brain injury, salicylate poisoning,

mechanical hyperventilation

Blood gas interpretations:plasma pH ^, PaCO2 dec,HCO3 normal (uncompensated)

Fluid volume status??? (I dont know what she I s looking for in thisI cant find anything in the nook that says this specifically. If you

guys can find it let me know )

o Components


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o Indicatorso Monitoring

Geneticso Study of inheritance; study of geneso Autosomal recessive: are caused by mutations of two gene

pairs on a chromosome. A person who inherits one copy of

the recessive allele does not develop the disease because the

normal allele predominates however this person is a carrier.

Males and females are affected equally heterozygotes are

carriers and usually asymptomatic. Affected individuals will

have unaffected parents. 25% chance offspring of 2

heterozygous parents will be affected. 50% they will be

carriers. Frequently there is a negative family history for

disease.

Examples: cystic fibrosis, tay-sachs disease, sickle celldisease.

o Autosomal dominant: are caused by a mutation of a singlegene pair on a chromosome. Males and females are equally

affected. More common than recessive disorders and usually

less severe. Affected individuals show variable expression.

Incomplete penetrance in some conditions affected individualsmay have an affected parent. Children of a heterozygous

(affected parent) will have a 50% chance of being affected.

Examples: Huntingtons disease, Breast and ovariancancer related to BRCA genes

o X-linked recessive: are caused by a mutation on the xchromosome. Usually only males are effected by this disorder

because women who carry the mutated gene on one x

chromosome have another x chromosome to compensate for

the mutation. Women who carry the gene can transmit the

mutation to their offspring

Examples: Hemophilia, wiskott-aldrich syndromeo X-linked dominant: are very rare. (nothing in book or

slides)


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o Stem cells: cells in the body that have that ability to divideand remain a stem cell or differentiate into specialized cells

such as brain cell o muscle cell. Perhaps the most important

potential application of human stem cells is the generation of

tissues that could be used for cell-based therapies. Embryonic stem cells have the ability to become any

one of the hundreds of types of cells in the human

body. They are derived from human embryo cells that

are 4-5 days old. They are pluripotent and can

differentiate into any cell type that they are stimulated

to become

Adult stem cells are undifferentiated cells that are foundin small numbers in many adult organs and tissues

including the brain, bone marrow, peripheral blood,

blood vessels, skeletal muscles, skin, teeth, heart, gut,

liver, ovarian epithelium, and testis. Their primary role

is to maintain and repair tissue in which they are found.

They are usually thought of as multipotent cells, giving

rise to a closely related family of cells within the tissue.

o GINA The genetic information nondiscrimination act prohibitsdiscrimination in health care coverage and employment based

on genetic information. It prevents health insurers fromdenying coverage, adjusting premiums , and discriminating

against a person solely based on his or her genetic or family

history information. Prevents insurers from requesting that a

person have a genetic test. Prohibits employers from using

genetic information for hiring, firing, or promoting decisions

regarding terms of employment. GINAs health coverage

nondiscriminatory protection does not extend to life

insurance, disability insurance, and long-term care insurance.


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2/3/2013 9:32:00 AM

Med-surg study guide

Chapter 14, 17


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2/3/2013 9:32:00 AM

medsurg notes f/e

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