notes ch 11 and pp Flashcards
hypotonic over hydration
causes interstitial edema
what creates colloid osmotic pressure in capillaries
albumin
hyperotnic saline does what to water
ICF to ECF into blood stream
rapid resppnse team intervention for hyperkalemia
20 unit insulin in 100 ml 20% dextrose in h2o
high K+ low BS body produces more insuline
low K+ high bs -bodys making less insulin
what would u evaluate that your patient uses if they have high K+( that can lead to high k+)
supplements, diet-, salt substitutes (low sodium high potassium), ACE inhibitors, kidney sparing diuretics, kidney disease
Nursing priority for electrolyte imbalances
–safety– confusion common–
when a patient is taking a K+ sparing diuretic what do they avoid
things that raise K+, ace inhibitors, salt substitutes, high potassium foods and supplements, bananas-
caring for a patient who takes dogoxin and lasix and K+ is 2.5 monitor for what.
lasix spares sodium,
Heart rate
Nurs intervntion for patient with HR failure on loop diuretics (strongest)(lasix)
Excrete sodium and water in loop of henle
daily weight/promote citrus food/monitor serum potassium
ACE inhibitors
used for HTN blocks renin path, which stops excretion of aldosteron which lowers blood volume which lowers BP,
Perfusion risk ..now what
decreases urine output , kidneys release renin- (triggering event-decrease BP reduces perfusion to tissues and organs/reduced blood volume or low oxygen) renin activates angiotensinogen, which is angiotensin I which is activated by angiotensin converting enzyme or ACE to its active form angiotensin II which increases blood pressure and volume(angiotensin II also triggers release of aldosterone.
Insinsible water loss howmuch daily
stool , skin , respirations, sweating, diarrhea, 500-1000ml perday
most important things to monitor during rehydration
HR pusle quality urine output
compare I to O
obligatory urine output
400-600 ml/day
crystalloids
water, minerals and other water soluble ,minerals(electrolytes) with extra stuff like glucose (type of IV fluid) most helpeful for dehydration for ICF and ECF.
Most common type of dehydration
isotonic dehydration-dehydration of ECF ,. ICF is the same
Colloids (IV fludis)
IV fluid with larger non soluble molecules that increase osmotic pressure in plasma volume. maintain plasma volume ECF dehydration.
isotonic IV Fluids
-0.9% saline 5% dextrose in water D5W
5% dextrose in 0.225% saline
ringers lactate
hypotonic IV fluids
-0.45% saline
hypertonic IV fluids
-10% dextrose in water D10W
5%dextrose in 0.9%saline
5% dextrose in 0.45%saline
5%dextrose in ringers lactate
IV therapy in older adults considerations
thinner skin, avoid hands, increased risk for infection, decreased pain perception, avoid multiple sticks, at risk for fluid overload, decreased absorption , kidney heart changes
spironolaCTONE
blocks action of aldosterone. causes excretion of sodium, retention of K+, used for hypertension edema,
adverse effects:
hyperkalemia which can lead to fatal dysrhythmias, not long term -lead to infertility
Thiazide
used for HTN, increases renal excretion of Na K Cl, water, Mg
increases plasma levels of uric acid and glucose less strong than loop diuretics
adverse effects- dehydration, high blood sugar depletion of listed electrolytes
Furosemide(loop diuretic) stongest one
blocks Na and Cl reasorption, by doing this prevents passive reasorption of water, dehydration can occur
use with: pulmonary edema ass with CHF, edema of hepatic cardiac or renal originn that has been unresponsive to less efficacious diuretics,
Side effects: dehydration can promote hypotension, thrombnosis and embolism
(conditions that requre fast water loss) use ful in renal impaired individuals
can promote diuresis unlike thiazide.
Furosemide and electrolytes
promotes excretion of magnesium posing a risk of magnesium deficiency. Symptoms include muscle weakness, tremor, twitching, and dysrhythmias.
increases urinary excretion of calcium. This action has been exploited to treat hypercalcemia.
Furosemide reduces high-density lipoprotein (HDL) cholesterol and raises low-density lipoprotein (LDL) cholesterol and triglycerides.
Sodium
functions-blood pressure/blood volume/ Ph, water balance
muscles, nerves, \
Most abundant cation in EXTRAcellular fluidMaintains osmotic pressure of extracellular fluidRegulates renal retention & excretion of water*Responsible for stimulation of neuromuscular reactions & maintains SBP.
. Vital for muscle and cardiac contraction &nerve impulse transmission.
”. Na levels affects fluid volume/distribution of other electrolytes
Sodium 136-145
Where sodium goes, water follows”
functions-blood pressure/blood volume/ Ph, water balance
muscles, nerves, \
Most abundant cation in EXTRAcellular fluidMaintains osmotic pressure of extracellular fluidRegulates renal retention & excretion of water*Responsible for stimulation of neuromuscular reactions & maintains SBP.
. Vital for muscle and cardiac contraction &nerve impulse transmission.
”. Na levels affects fluid volume/distribution of other electrolytes
Hypernatremia
big bloated
over 145
red/rosy
bid bloated, causes edema, full bounding pulse, flush skin edema, low grade fever, polydypsia(increast thirst),
Late signs_swoolen dry tounge increaser muscle tone, nausea vomiting
Both: restlessness fatigue and GI cramp in both
Hyponatremia below 136
depressed and deflated
depressed and deflated
seizures, coma,
increase HR, weak thready pulse,
resp arrest
Both: restlessness fatigue and GI cramp in both
Both have abdominal cramping
calcium
Normal level: 9.0-10.5 mg/dLAbsorption requires active form of vitamin DStored in bonesParathyroid hormoneThyrocalcitonin
bones,
blood -clotting factors
beats-regulates HR
Hyper calcemia above 10.5
swoolen and slow moans groans stones
Bone pain-leaving bones into blood
Kidney stones, muscle weakness, decreased DTR, constipation
Hypocalcemia below 9
went on vacation
weak bones, risk bleeding, dystrythmias
diarrhea, Trousseaus(BP arm twirk)
Chvosteks(cheek smile when stroke cheek)
circumoral tingling
risk for fractures
risk for bleeding
cardiac dysrythmias-not strong heart beats
Potassium3.5-5
maintain muscle and heart contraction
Some control over intracellular osmolarity and volumeRegulate protein synthesis, glucose use and storage
Hyperkalemia over 5
tight and contracted
heart tight and contracted hypotension and bradycardia, GI tight and contracted: diarrhea hyperactive Bowel tones, Neuromuscular-tight and contracted early-muscles twitch burnoing sensations then numbness hands and feet and around the mouth(paresthesia) Late-muscular paralysis increased DTR profound/severe muscle weakness/heaviness respiratory failure confusion
HYpokalemia below 3.5
low and slow
Heart low and slow-weak pulse, Irregular hr-changes from slow to fast
Dystrythmias
Muscles-weak muscles, muscle cramping, flaccid paralysis
DTR reduced
respiratory failure
confusion-irritability andxiety to altered mental status
GI-low and slow-decreased motility, hypoactive bowel tonesconstipation, abdominalk distension
paralytic ileus-can cause small bowel obsttruction
orthostatic hypotension
Chloride-functions same as sodium- does what sodium does-98-106
Hyper–swoolen dry toungue ,, narusea vomiting, confusion
Hypo-excessive diarrhea, vomiting, sweating
fever-only difference between Cl and Na
Normal level: 98 to 106 mEq/LImbalance occurs as a result of other electrolyte imbalancesTreat underlying electrolyte imbalance or acid-base problem
Magnesium 1.3-2.1
Law and order
calm keep peace
calm keep peace in heart, uterus, DTR
needed for calcium and vit d absorption
best friend calcium
Normal level: 1.3 to 2.1 mg/dLCritical for skeletal muscle contraction, carbohydrate metabolism, ATP formation, vitamin activation, cell growth
hypermagnesiumia
calm and quiet
cardiac-calm and quiet-Heart blocks brady cardia hypoension DTR calm quiet-decreased lungs-depressed shallow respirations GI-calm -hypoactive bowel sounds
Both-neuro confused irritable lungs shallow
hypomagnesiemia
buck wild
cardiac- v-fib-tachycardia- DTR- wild-increased eyes-abnormal eye movement(nystagmus) GI-diarrhea Both-neuro confused irritable lungs shallow
Phosphate/Phosphorus
3-4.5
opposite of calcium
needed for bonew and teeth formation
help regulate calcium
always inverse-if phosphate is high calcium is low
Normal level: 3.0-4.5 mg/dLFound in bonesActivates vitamins and enzymes; assists in cell growth and metabolismPlasma levels of calcium and phosphorus exist in a balanced reciprocal relationship
Hyperphosphatemia(low calcium too)
Trousseaus sign
Chvosteks sign
diarrhea
Weak bones risk for fractures
Weak blood decreased clotting-risk for bleeding
Heart beats weak dysrhythmias
Hypophosphatemia(high calcium)
swoolen slow- COnstipatioon decreased dtr muscle weakness decreased heart rate and respiratory rate Increased BP kidney stones from renal calculi
Filtration
Movement of fluid through cell or blood vessel membrane because of differences in water pressure (hydrostatic pressure) This is related to water volume pressing against confining walls
Hydrostatic pressure
Water-pushing pressure”Force that pushes water outward from a confined space through a membraneAmount of water in any body fluid space determines pressureExample: Blood pressureMoving whole blood from the heart to capillaries where filtration occurs to exchange water, nutrients, and waste products between the blood and tissues
Edema
Develops with changes in normal hydrostatic pressure differences
Diffusion
Free movement of particles (solute) across permeable membrane from area of higher to lower concentrationImportant in transport of most electrolytes; other particles diffuse through cell membranesSodium pumpsGlucose cannot enter most cell membranes without help of insulin
Osmosis & Filtration
Act together at capillary membrane to maintain normal ECF and ICF volumesThirst mechanism is example of how osmosis helps maintain homeostasisFeeling of thirst caused by activation of brain cells responding to changes in ECG osmolarity
Insensible water loss
nsensible water loss – Through skin, lungs, stool
Fluid loss
Minimum?
Minimum urine amount needed to excrete toxic waste products = 400 to 600 mL/day
Fluid balance
Closely linked to/affected by electrolyte concentrationsFluid intakeFluid loss
Aldosterone
Aldosterone is secreted by the adrenal cortex whenever sodium levels in the extracellular fluid (ECF) are low. Aldosterone prevents both water and sodium loss. When aldosterone is secreted, it acts on the kidney nephrons, triggering them to reabsorb sodium and water from the urine back into the blood. This action increases blood osmolarity and blood volume. Aldosterone also promotes kidney potassium excretion.
ADH
Antidiuretic hormone (ADH), or vasopressin, is released from the posterior pituitary gland in response to changes in blood osmolarity. The hypothalamus contains the osmoreceptors that are sensitive to changes in blood osmolarity. Increased blood osmolarity, especially an increase in the level of plasma sodium, results in a slight shrinkage of these cells and triggers ADH release from the posterior pituitary gland. Because the action of ADH retains just water, it only indirectly regulates electrolyte retention or excretion.
ADH acts on kidney nephrons, making them more permeable to water. As a result, more water is reabsorbed by these tubules and returned to the blood, decreasing blood osmolarity by making it more dilute.
osmolarity decreases with low plasma sodium levels, the osmoreceptors swell slightly and inhibit ADH release. Less water is then reabsorbed, and more is excreted in the urine, bringing extracellular fluid (ECF) osmolarity up to normal.
NPH
Natriuretic peptides (NPs) are hormones secreted by special cells that line the atria of the heart (atrial natriuretic peptide [ANP]) and the ventricles of the heart. (The peptide secreted by the heart ventricular cells is known as brain natriuretic peptide [BNP].) These peptides are secreted in response to increased blood volume and blood pressure, which stretch the heart tissue. NP binds to receptors in the nephrons, creating effects that are opposite of aldosterone. Kidney reabsorption of sodium is inhibited at the same time that urine output is increased. The outcome is decreased circulating blood volume and decreased blood osmolarity.
A major regulator of fluid balance, also known as the renin-angiotensin system (RAS).
most important body fluids to keep in balance for optimal function are the blood volume (plasma volume) and the fluid inside the cells (intracellular fluid).
Maintaining blood volume at a sufficient level for blood pressure to remain high enough to ensure adequate PERFUSION is critical for life.
the kidney is a major regulator of water and sodium balance to maintain blood pressure and perfusion to all tissues and organs, the kidneys monitor blood pressure, blood volume, blood oxygen levels, and blood osmolarity (related to sodium concentration).
When kidneys sense that any one of these parameters is getting low, they secrete a substance called renin that sets into motion a group of hormonal and blood vessel responses to ensure that blood pressure is raised back up to normal.
triggering event for renin sectrion
any change in the blood indicating that PERFUSION is at risk. Low blood pressure is a triggering event- it reduces perfusion to tissues and organs.
Anything that reduces blood volume (e.g., dehydration, hemorrhage) below a critical level always lowers blood pressure.
Low blood oxygen levels also are triggering events because with too little oxygen in the blood it cannot supply the needed oxygen and the tissues and organs could die.
A low blood sodium level also is a triggering event because sodium and water are closely linked. Where sodium goes, water follows.
So anything that causes the blood to have too little sodium prevents water from staying in the blood. The result is low blood volume with low blood pressure and poor tissue perfusion.
kidneys sense that PERFUSION is at risk, cells in the kidney tubule secrete renin into the blood.
Renin then activates angiotensinogen.
Activated angiotensinogen is angiotensin I, which is activated by the enzyme angiotensin-converting enzyme or ACE to its most active form, angiotensin II
Angiotensin II starts several actions to increase blood volume and blood pressure.
First it constricts arteries and veins throughout the body which increases peripheral resistance and reduces the size of the vascular bed, which raises blood pressure as a compensatory mechanism without adding more blood volume.
Angiotensin II constricts the size of the arterioles that feed the kidney nephrons which results in a lower glomerular filtration rate and a huge reduction of urine output. Decreasing urine output prevents further water loss so more is retained in the blood to help raise blood pressure.
Angiotensin II also causes the adrenal glands to secrete the hormone aldosterone.
Aldosterone is nicknamed the “water-and-sodium-saving hormone” because it causes the kidneys to reabsorb water and sodium, preventing them from being excreted into the urine.
This response allows more water and sodium to be returned to the blood, increasing blood pressure, blood volume, and PERFUSION.
triggering event for renin sectrion
any change in the blood indicating that PERFUSION is at risk. Low blood pressure is a triggering event- it reduces perfusion to tissues and organs.
Anything that reduces blood volume (e.g., dehydration, hemorrhage) below a critical level always lowers blood pressure.
Low blood oxygen levels also are triggering events because with too little oxygen in the blood it cannot supply the needed oxygen and the tissues and organs could die.
A low blood sodium level also is a triggering event because sodium and water are closely linked. Where sodium goes, water follows.
So anything that causes the blood to have too little sodium prevents water from staying in the blood. The result is low blood volume with low blood pressure and poor tissue perfusion.
kidneys sense that PERFUSION is at risk, cells in the kidney tubule secrete renin into the blood.
Renin then activates angiotensinogen.
Activated angiotensinogen is angiotensin I, which is activated by the enzyme angiotensin-converting enzyme or ACE to its most active form, angiotensin II
Angiotensin II starts several actions to increase blood volume and blood pressure.
First it constricts arteries and veins throughout the body which increases peripheral resistance and reduces the size of the vascular bed, which raises blood pressure as a compensatory mechanism without adding more blood volume.
Angiotensin II constricts the size of the arterioles that feed the kidney nephrons which results in a lower glomerular filtration rate and a huge reduction of urine output. Decreasing urine output prevents further water loss so more is retained in the blood to help raise blood pressure.
Angiotensin II also causes the adrenal glands to secrete the hormone aldosterone.
Aldosterone is nicknamed the “water-and-sodium-saving hormone” because it causes the kidneys to reabsorb water and sodium, preventing them from being excreted into the urine.
This response allows more water and sodium to be returned to the blood, increasing blood pressure, blood volume, and PERFUSION.
Renin-angiotensin II pathway is greatly stimulated with shock, or when stress response is stimulated
ACE inhibitors
Disrupt renin-angiotensin II pathway by reducing amount of ACE produced
With less angiotensin II, less vasoconstriction and reduced peripheral resistance
Greater excretion of water and sodium in urine
By locking angiotensin II receptors, blood pressure lowersPatients with hypertension often take ACE-inhibitor medications
dehydration: Collaborative Care
Fluid intake/retention does not meet body’s fluid needs; results in fluid volume deficit Assessment History Physical assessment/clinical manifestations: Cardiovascular Respiratory Skin Neurologic Renal
Diuretics on koidneys
Mannitol-proximal convoluted tubule Na Cl out 65%
Furosemide
thick segment ascending limb of henlies loop Na Cl out20%
Thiazides
early distyal convvoluted tubule-Na Cl out 10 %
Spironolactone Triamterene
late distal convoluted tubule and collecting duct (distal nephron) 1-5%
water to pound weight
1 L of water weighs 2.2 lb, equal to 1 kgWeight change of 1 lb = fluid volume change of about 500 mL
Fluid overload
AssessmentPatient safetyPulmonary edemaDrug therapyNutrition therapyMonitoring of intake and output (I&O)
PLasma volume
3.5-5.5L osmolarity-270-310 NA-135-145 K 3.5-5 Cl-96-109 Ca-8.5-10 Mg-1.6 protein-7-8
Interstitial fluid
volume 10L Osmolarity-270-310 Na-135-145 K-3.5-5 Cl-118 Ca-7-9 Mg-1.3 Prpotein-2
Intracellular fluid
volume-30 L osmo-270-310 Na-14 K-140 Cl-4-6 Ca-1-8 Mg-6-30 Protein-16
considerations for older adults
At risk for most electrolyte imbalances from age-related organ changes Have less total body water than younger adults; more at risk for fluid imbalances; more likely to be taking drugs affecting fluid or electrolyte balance
While monitoring a patient who has fluid overload, the nurse would be most concerned about which assessment finding?
While monitoring a patient who has fluid overload, the nurse would be most concerned about which assessment finding?A.Bounding pulse B.Neck vein distentionC.Pitting edema in the feet
D.Presence of crackles in the lungs
A patient has been having frequent liquid diarrhea for the last 24 hours. A stool sample was sent to the laboratory to confirm possible Clostridium difficile infection. The nurse should monitor the patient for which electrolyte imbalance?
A.Dehydration
B.Hypokalemia
*C.Hyponatremia
D.Hypocalcemia
A 25-year-old student has been taken to an urgent care clinic because of dehydration. She says she has had “the flu,” with vomiting and diarrhea “all night” and has had very little to eat or drink. She says the GI symptoms have subsided, but she feels weak. The nurse expects which type of rehydration to occur?
A.IV fluid replacement
B.Oral rehydration therapy with tea
C.Oral rehydration therapy with water
*D.Oral rehydration therapy with a solution containing glucose and electrolytes
How diuretics work:
Most diuretics share the same basic mechanism of action: blockade of sodium and chloride reabsorption. By blocking the reabsorption of these prominent solutes, diuretics create osmotic pressure within the nephron that prevents the passive reabsorption of water. Hence, diuretics cause water and solutes to be retained within the nephron and thereby promote the excretion of both
Diuretics make you pee!!
The increase in urine flow that a diuretic produces is directly related to the amount of sodium and chloride reabsorption that it blocks.
drugs that act early in the nephron have the opportunity to block the greatest amount of solute reabsorption. As a result, these agents produce the greatest diuresis.
Adverse effects:
can cause hypovolemia (from excessive fluid loss), acid-base imbalance, and altered electrolyte levels.
***These adverse effects can be minimized by using short-acting diuretics and by timing drug administration such that the kidney is allowed to operate in a drug-free manner between periods of diuresis. Both measures will give the kidney periodic opportunities to readjust the ECF so as to compensate for any undesired alterations produced under the influence of diuretics.
Loop Diuretics:
These drugs produce more loss of fluid and electrolytes than any other diuretics. They are known as loop diuretics because their site of action is in the loop of Henle.
Furosemide:
: Furosemide acts in the thick segment of the ascending limb of Henle’s loop to block reabsorption of sodium and chloride. By blocking solute reabsorption, furosemide prevents passive reabsorption of water.
Use of furosemide can produce excessive loss of sodium, chloride, and water. Severe dehydration can result. Dehydration can promote hypotension, thrombosis, and embolism.
Furosemide is a powerful drug that is generally reserved for situations that require rapid or massive mobilization of fluid.
Conditions that justify use of furosemide include
(1) pulmonary edema associated with congestive heart failure (CHF); (2) edema of hepatic, cardiac, or renal origin that has been unresponsive to less efficacious diuretics; and (3) hypertension that cannot be controlled with other diuretics.
especially useful in patients with severe renal impairment, since, unlike the thiazides (see later in the chapter), the drug can promote diuresis even when renal blood flow and glomerular filtration rate (GFR) are low
Use of furosemide can produce excessive loss of sodium, chloride, and water. Severe dehydration can result. Dehydration can promote hypotension, thrombosis, and embolism.
Electrolytes
and furosemide
Furosemide increases urinary excretion of magnesium, posing a risk of magnesium deficiency. Symptoms include muscle weakness, tremor, twitching, and dysrhythmias.
Furosemide increases urinary excretion of calcium. This action has been exploited to treat hypercalcemia.
Furosemide reduces high-density lipoprotein (HDL) cholesterol and raises low-density lipoprotein (LDL) cholesterol and triglycerides.
Nurse monitors/does:
Monitor for signs of dehydration- Signs of evolving dehydration include dry mouth, unusual thirst, and oliguria (scanty urine output). Impending dehydration can also be anticipated from excessive loss of weight.
Signs of hypotension include dizziness, light-headedness, and fainting. If blood pressure falls precipitously, furosemide should be discontinued
Hypokalemia can be minimized by consuming potassium-rich foods (e.g., dried fruits, nuts, spinach, potatoes, bananas), taking potassium supplements, or using a potassium-sparing diuretic.
Because of the risk of hearing loss, caution is needed when loop diuretics are used in combination with other ototoxic drugs
When furosemide is taken by a diabetic patient, he or she should be especially diligent about monitoring blood glucose content.
Older adults
Diuretics are the most common cause of adverse medication reactions and interactions in older adults. Monitor closely for dehydration and cardiac dysrhythmias.
Children/adolescents
Diuretics can be used safely in children, just in smaller doses. Side effect profiles are similar to those for adults.
Pregnant women
Animal studies revealed that furosemide can cause maternal death, abortion, and fetal resorption. Risks and benefits must be considered for administration during pregnancy.
Breast-feeding womenBreast-feeding women
Furosemide may decrease breast milk production through excessive diuresis. Data are lacking regarding transmission of drug from mother to infant via breast milk.
Adverse effects:
Furosemide can produce excessive loss of sodium, chloride, and water. Severe dehydration can result.
Dehydration can promote thrombosis and embolism.
If dehydration occurs, furosemide should be withheld.
The risk of dehydration and its sequelae can be minimized by initiating therapy with low doses, adjusting the dosage carefully, monitoring weight loss every day, and administering furosemide on an intermittent schedule.
Furosemide can cause a substantial drop in blood pressure. At least two mechanisms are involved: (1) loss of volume and (2) relaxation of venous smooth muscle, which reduces venous return to the heart.
Hypokalemia.Potassium is lost through increased secretion in the distal nephron. If serum potassium falls below 3.5 mEq/L, fatal dysrhythmias may result.
Ototoxicity.- Rarely, loop diuretics cause hearing impairment.
Hyperglycemia- Elevation of plasma glucose is a potential, albeit uncommon, complication of furosemide therapy.
Hyperuricemia- Elevation of plasma uric acid is a frequent side effect of treatment. patients predisposed to gout, elevation of uric acid may precipitate a gouty attack
Pregnancy- In animals loop diuretics have caused maternal death, abortion, fetal resorption, and other adverse effects- only use if you have to.
thiazide diuretics (also known as benzothiadiazides
have effects similar to those of the loop diuretics. Like the loop diuretics, thiazides increase renal excretion of sodium, chloride, potassium, and water. In addition, thiazides elevate plasma levels of uric acid and glucose. The principal difference between the thiazides and loop diuretics is that the maximum diuresis produced by the thiazides is considerably lower than the maximum diuresis produced by the loop diuretics. In addition, whereas loop diuretics can be effective even when urine flow is decreased, thiazides cannot.
Uses:
Hydrochlorothiazide promotes urine production by blocking the reabsorption of sodium and chloride in the early segment of the distal convoluted tubule
The primary indication for hydrochlorothiazide is hypertension
Thiazides are preferred drugs for mobilizing edema associated with mild to moderate heart failure.
Diabetes insipidus is a rare condition characterized by excessive production of urine. In patients with this disorder, thiazides reduce urine production by 30% to 50%.
Thiazides promote tubular reabsorption of calcium and may thereby decrease the risk of osteoporosis in postmenopausal women. thiazides promote renal calcium retention, they may counteract the calcium loss associated with menopause and may thereby help preserve bone integrity.
Adverse effects
Thiazides increase excretion of magnesium, sometimes causing magnesium deficiency. Symptoms include muscle weakness, tremor, twitching, and dysrhythmias.
Loss of sodium, chloride, and water can lead to hyponatremia, hypochloremia, and dehydration.
Hypokalemia- thiazides can cause hypokalemia from excessive potassium excretion.
Hyperglycemia-thiazides can elevate plasma levels of glucose. Significant hyperglycemia develops only in diabetic patients, who should be especially diligent about monitoring blood glucose.
Hyperuricemia-The thiazides, like the loop diuretics, can cause retention of uric acid, thereby elevating plasma uric acid.
Thiazides can increase levels of LDL cholesterol, total cholesterol, and triglycerides.
Spironolactone [Aldactone] -Potassium-Sparing Diuretics
blocks the actions of aldosterone in the distal nephron. Since aldosterone acts to promote sodium uptake in exchange for potassium secretion, inhibition of aldosterone has the opposite effect: retention of potassium and increased excretion of sodium
Therapeutic Uses
Hypertension and edema- used most commonly in combination with a thiazide or loop diuretic.
In patients with severe heart failure, spironolactone reduces mortality and hospital admissions.
spironolactone can be used for primary hyperaldosteronism, premenstrual syndrome , polycystic ovary syndrome, and acne in young women.
Adverse Effects
can cause a variety of endocrine effects, including gynecomastia, menstrual irregularities, impotence, hirsutism, and deepening of the voice.
The potassium-sparing effects of spironolactone can result in hyperkalemia, a condition that can produce fatal dysrhythmias- monitor heart.
If serum potassium rises above 5 mEq/L or if signs of hyperkalemia develop (e.g., abnormal heart rhythm), spironolactone should be discontinued and potassium intake restricted. Injection of insulin can help lower potassium levels by promoting potassium uptake into cells.
When given long term to rats in doses 25 to 250 times those used in humans, spironolactone has caused benign adenomas of the thyroid and testes, malignant mammary tumors, and proliferative changes in the liver.
To promote safe administration, NIOSH suggests donning a protective gown and two sets of gloves when cutting or crushing tablets.
Colloids
are IV fluids that contain larger non–water-soluble molecules that increase the osmotic pressure in the plasma volume. These fluids are most useful in helping to maintain plasma volume with a lower infused volume.
crystalloids
Crystalloids are IV fluids that contain water, minerals (electrolytes), and sometimes other water-soluble substances such as glucose. These fluids rapidly disperse to all body fluid compartments and are most useful when dehydration includes both the intracellular and extracellular compartments.
The two most important areas to monitor during rehydration are pulse rate and quality and urine output.
normal serum osmolarity for adults is between 270 and 300 mOsm/L. Parenteral solutions within that normal range are isotonic
fluids greater than 300 mOsm/L are hypertonic
fluids less than 270 mOsm/L are hypotonic.
Hypertonic solutions are used to correct altered FLUID AND ELECTROLYTE BALANCE and acid-base imbalances by moving water out of the body’s cells and into the bloodstream. Parenteral nutrition solutions are hypertonic.
hypotonic infusates move water into cells to expand them.
Patients receiving either hypertonic or hypotonic fluids are at risk for phlebitis and infiltration.
