Anti-Diuretic Hormone (ADH) and Fluid Balance: Regulation and Nursing Interventions, Study notes of Anatomy

An in-depth look at the role of Anti-Diuretic Hormone (ADH) in maintaining fluid balance in the body. It covers the functions of ADH, its release mechanisms, and the effects of fluid ingestion and aldosterone on fluid balance. Additionally, it discusses nursing interventions for managing fluid volume deficits and assessing signs and symptoms of electrolyte imbalances.

Typology: Study notes

2019/2020

Uploaded on 10/28/2021

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FLUIDS AND ELECTROLYTES
AMOUNT OF FLUID IN THE BODY:
Fetus 100%
Baby 80-85% (no muscles yet)
Adult 70%
Elderly 50%
> amount of water taken must be equal to the amount of
water lost
WATER INTAKE
Food and drink 2300 mL
Cell Metabolism 200 mL
Total: 2500 mL
OUTPUT
Kidneys 1800 mL
Skin (sweat) 300 mL
Lungs (expiration) 300 mL ( RR, more fluid lost)
GI Tract (feces) 100 mL
TOTAL: 2500 mL
FLUID COMPARTMENT
Intracellular 40% (cytoplasm/protoplasm)
Extracellular 20%
Intravascular 5%
o Plasma (light yellow)
o Cellular components (darkish red)
Interstitial - 15% (third space)
MECHANISMS OF FLUID BALANCE
1. ANTI-DIURETIC HORMONE (ADH)
- Stored in the posterior pituitary gland
- Causes renal tubules to reabsorb water so
that kidneys will not form too much urine
- Released when dehydrated
dehydrated > hypothalamus will feel that
there is in circulating blood volume >
stimulate post. pituitary gland to release
ADH > ADH will have an effect on the renal
tubules to reabsorb water >> urine output
no reabsorption of NA
>> output is less because body is compensating after surgery
2. THIRST MECHANISM
- Compensatory mechanism
perspire > excrete lots of body fluids > thirst
center in the brain (hypothalamus) will be
stimulated > tells us to drink water
blood volume (d/t vomiting, diarrhea, etc)
will cause BP > BP = less blood going to
the kidneys > kidneys will compensate by
releasing renin > RAAS mechanism >
angiotensin 2 > angiotensin 2 stimulates
thirst center
- thirst mechanism MAY NOT work (ex. Patient is
unconscious)
- unconscious patient should receive IV fluids (N/I: do not
slow down)
FLUID INGESTION
Stretch receptors (stomach & intestine) will
send inhibitory signals to the thirst center
Thirst mechanism will stop if stomach and
intestines are stretched (by eating)
3. ALDOSTERONE
- From the adrenal cortex
- Causes reabsorption of NA > water follows
- Hypovolemia > RAAM
hypovolemia (d/t bleeding/vomiting) >
there will be in circulating blood volume =
priority is primary organs = less blood to
secondary organs > kidney will compensate
by releasing renin > renin goes to liver and
converts a precursor protein
(angiotensinogen) to angiotensin 1 (mild
vasoconstrictor) > angiotensin 1 goes to
lungs and converts ACE to angiotensin 2
(potent vasoconstrictor) > angiotensin 2 >
produce aldosterone > reabsorb NA >>
water retention > BP
4. SYMPATHETIC STIMULATION (SNS)
- in blood volume > BP > SNS is stimulated
> trigger adrenal glands > adrenal medulla >
epinephrine and norepinephrine will be
released
Epinephrine causes in cardiac rate > more blood
will be pumped by the heart > more blood will go to
the different organs of the body
Norepinephrine will cause vasoconstriction,
BP more blood will go to the priority organ (brain)
** if less blood is going to the kidneys > less oxygen and
nutrients > less urine
If there is vasoconstriction, assess:
Pale and cold skin because blood is being
directed to the brain
ATRIAL NATRIURETIC PEPTIDE
- cardiac hormone stored in the cells of the atria
- released when atrial pressure is increased
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FLUIDS AND ELECTROLYTES

AMOUNT OF FLUID IN THE BODY:  Fetus – 100%  Baby – 80 - 85% (no muscles yet)  Adult – 70%  Elderly – 50%

amount of water taken must be equal to the amount of water lost WATER INTAKEFood and drink – 2300 mL  Cell Metabolism – 200 mL  Total: 2500 mL OUTPUTKidneys – 1800 mL  Skin (sweat) – 300 mL  Lungs (expiration) – 300 mL (RR, more fluid lost)GI Tract (feces) – 100 mL  TOTAL: 2500 mL FLUID COMPARTMENT Intracellular – 40% (cytoplasm/protoplasm) Extracellular – 20%  Intravascular – 5% o Plasma (light yellow) o Cellular components (darkish red)  Interstitial - 15% (third space)

MECHANISMS OF FLUID BALANCE

  1. ANTI-DIURETIC HORMONE (ADH)
    • Stored in the posterior pituitary gland
    • Causes renal tubules to reabsorb water so that kidneys will not form too much urine
    • Released when dehydrated dehydrated > hypothalamus will feel that there is ᛎ in circulating blood volume > stimulate post. pituitary gland to release ADH > ADH will have an effect on the renal tubules to reabsorb water >> ᛎ urine output no reabsorption of NA

output is less because body is compensating after surgery

  1. THIRST MECHANISM
  • Compensatory mechanism perspire > excrete lots of body fluids > thirst center in the brain (hypothalamus) will be stimulated > tells us to drink water ᛎ blood volume (d/t vomiting, diarrhea, etc) will cause ᛎ BP > ᛎ BP = less blood going to the kidneys > kidneys will compensate by releasing renin > RAAS mechanism > angiotensin 2 > angiotensin 2 stimulates thirst center
  • thirst mechanism MAY NOT work (ex. Patient is unconscious)
  • unconscious patient should receive IV fluids (N/I: do not slow down) FLUID INGESTION  Stretch receptors (stomach & intestine) will send inhibitory signals to the thirst center  Thirst mechanism will stop if stomach and intestines are stretched (by eating)
  1. ALDOSTERONE
  • From the adrenal cortex
  • Causes reabsorption of NA > water follows
  • Hypovolemia > RAAM  hypovolemia (d/t bleeding/vomiting) > there will be ᛎ in circulating blood volume = priority is primary organs = less blood to secondary organs > kidney will compensate by releasing renin > renin goes to liver and converts a precursor protein (angiotensinogen) to angiotensin 1 (mild vasoconstrictor) > angiotensin 1 goes to lungs and converts ACE to angiotensin 2 (potent vasoconstrictor) > angiotensin 2 > produce aldosterone > reabsorb NA >> water retention > ᛏ BP
  1. SYMPATHETIC STIMULATION (SNS)
  • ᛎ in blood volume > ᛎ BP > SNS is stimulated

trigger adrenal glands > adrenal medulla > epinephrine and norepinephrine will be released  Epinephrine – causes ᛏ in cardiac rate > more blood will be pumped by the heart > more blood will go to the different organs of the body  Norepinephrine – will cause vasoconstriction, ∴ ᛏ BP → more blood will go to the priority organ (brain) ** if less blood is going to the kidneys > less oxygen and nutrients > less urine  If there is vasoconstriction, assess:  Pale and cold skin – because blood is being directed to the brain  ATRIAL NATRIURETIC PEPTIDE

  • cardiac hormone stored in the cells of the atria
  • released when atrial pressure is increased
  • opposed the RAAM by ᛎ BP and reducing intravascular blood volume ACTION:
  1. Suppresses serum renin levels
  2. ᛎ aldosterone release from A.G.
  3. ᛏ glomerular filtration w/c ᛏ urine excretion of Na & h2o (when water is reabsorbed, there will be increase pressure in the heart)
  4. ᛎ ADH release from PPG
  5. Reduced vascular resistance by causing vasodilation

released whenever there is ᛏ pressure in the atrium, plenty of blood in the atrium > ANP will oppose RAAM When is atrial pressure increased? > heart failure, COPD

FLUID & ELECTROLYTE IMBALANCES

Extracellular Fluid Volume Deficit

- loss of body fluid from the intravascular and/or interstitial (3rd^ space) compartment > Intravascular – ((bleeding)) > Interstitial – ((diarrhea, vomiting)) ISO-OSMOLAR FLUID VOLUME DEFICIT  When both fluid and Na are lost in equal amounts Example:

  1. Vomiting & diarrhea
  2. GI fistula & GI suctioning
  3. Fever (sweat = ᛏ RR = more fluid loss)
  4. Hemorrhage
  5. Burns
  6. Ascites (fluid accumulation in peritoneal cavity HYPEROSMOLAR FLUID VOLUME DEFICIT  If the amount of water is in excess of the amount of sodium loss, the serum sodium level is increased  Only water is lost Example:
  7. Inadequate fluid intake o Unconscious o Bed Ridden o Giving excess OF
  8. Severe vomiting & diarrhea
  9. Diabetic ketoacidosis o Excess glucose from the blood will go to the kidneys and it will cause osmotic diuresis (glucose that goes to the kidneys attract water to go to the kidneys). And this will cause frequent urination o Complication of Type 1 diabetes
  10. Sweating o More fluid is lost than sodium o ᛏ solute intake (salt & sugar) = attract water  Possible CELLULAR DEHYDRATION - bec. there are plenty of solutes outside, it will attract water from the cells going outside >> will cause shrinkage of cells  Early manifestations of cellular shrinkage: o Restlessness, Apprehension o These neurological manifestations are serious because patient can go into coma and even death ASSESSMENT Signs and symptoms of dehydration  Poor skin turgor  Dry mucous membrane  Slow filling of hand veins  ᛎ urine output o dehydration > hypothalamus will sense it > stimulate PPG to release ADH > ADH prevents kidney from releasing urine by stimulating renal tubules to reabsorb water  Tachycardia - ♡ is compensating to give more blood to the organs of the body NURSING INTERVENTIONS for FLUID VOLUME DEFICIT
  11. Monitor VS every 4 hours. ((If there is volume deficit, BP and CR are decreased))
  12. Promote adequate fluid replacement. ((IV fluids; oral))
  13. Report if urine output is below 250cc/8hrs. ((normal: 30 to 50 cc per hour // 240 to 250 cc per 8 hours))
  14. Monitor lab results such as:  Blood Urea Nitrogen (BUN) - is a parameter that will measure the kidney function (if kidneys are still working) o Urea - waste product of protein metabolism that should be removed by the kidneys o If BUN is high, it means that the kidneys are not working efficiently. (kidneys probably not receiving sufficient amount of blood due to fluid volume deficit to work efficiently)  Hematocrit blood test – determines the percentage of RBCs in the blood o Hematocrit - proportion, by volume, of the blood that consists of red blood cells o Our blood is composed of RBC, WBC, plasma o If there is fluid (plasma) loss, there will be ᛏ hematocrit level
  15. Provide oral hygiene several times per day  Dry mouth causes bad breath (halitosis)  Oral hygiene ᛏ amount of saliva (saliva has plenty of lysosomes w/c can kill bacteria in the mouth)

>> plenty of sodium outside > it will attract water > cells will shrink. To prevent this, the body will compensate. The hypothalamus, where the thirst center is, will be stimulated and you are going to drink a lot of water

  • people who can’t drink voluntarily (unconscious) >> SEVERE HYPERNATREMIA o Infants o Confused elderly people o Unconscious patients  The movement of fluids is from the INTRACELLULAR COMPARTMENT to EXTRACELLULAR COMPARTMENT >> cells will shrink CAUSES OF HYPERNATREMIA:H ypercortisolism (or Cushing’s Syndrome – over cortisol = Hypernatremia, Hyperglycemia, Hypokalemia), Hyperventilation (you lose fluids) ** occurs when the pituitary gland makes too much of the hormone ACTH. ACTH then signals the adrenal glands to produce too much cortisol  I ncreased intake of sodium (Oral / IV)  G I feeding without adequate water supplement  H ypertonic Solution – particles is higher than water ** example: osteorized feeding (TPN) – plenty of salt will attract water  S odium Excretion decreased (you cannot bring out the sodium, ∴ body keeping too much sodium); corticosteroids (when you’re taking steroids, s/e is sodium retention)  A ldosterone Insufficiency (Hyperaldosteronism)  L oss of body fluids (∴ sodium is retained) (dehydrated), infection (Fever), sweating, diarrhea, and diabetes insipidus (deficient; renal tubules will not reabsorb water and this will go to the urine; frequently voiding; Losing plenty of fluids)  T hirst Impairment ASSESSMENT:  GIT → nausea, vomiting, anorexia  Cardiac → ᛏ BP (flow of blood is sluggish, slow perfusion of blood, heart will compensate to give more blood to give to the organs of the body)  CNS → restlessness, agitation, stupor  Neuromuscular → muscular twitching, tremor, hyperreflexion  Skin → dry

SIGNS AND SYMPTOMS

S kin Flushed  A gitation – The water in the cells are being sent out  L ow-Grade Fever  T hirst  Can be as a result of dehydration with no or minimal Na ((accompanied by hemoconcentration in hypernatremia)) Na outside = water will go out = cells will shrink  Moderate to severe hypernatremia can stimulate seizure (WHY? Pulling the water out of the cells in the brain = shrink = seizure)  Correcting hypernatremia too quickly could cause water to shift rapidly into the cells and may cause the brain cells to swell ((treatment = infusion pump)) o Use infusion pump to control delivery of IV to prevent cerebral edema  Correcting water deficit orally should take about 3 days (48-72 hours is safest) o 0.45% NaCl solution allows a more gradual reduction of serum Na, reducing the risk of cerebral edema POTASSIUM (( if many sodium, potassium has to go (hypokalemia) ))

  • promotes transmission and conduction of nerve impulses and the contraction of skeletal, cardiac, and smooth muscles
  • assists in the regulation of intracellular osmolality
  • 98% of body’s K is seen in the intracellular compartment; plenty in the GI tract
  • assists in the maintenance of acid-base balance  Metabolic acidosis – plenty of acid in the body (ex. Having hypovolemic shock (bleeding) > less circulating blood > if there is less circulating blood, plus bleeding, metabolism continues with less o2 > if metabolism goes on with less o2, the body is going to produce lactic acid > anaerobic metabolism  Plenty of hydrogen ions outside so hydrogen ions will go inside the cells > in exchange of the entrance of the hydrogen ions inside the cell, K goes out >> hyperkalemia = cardiac dysrhythmia / cardiac arrest

 K in acid-base balance: K let acid in  Kidneys are damaged that’s why metabolic acidosis > plenty of acid > ᛏ RR > hyperventilate bec. you are removing some of the acid in the form of carbon dioxide  Kidneys also maintain acid-base balance

  • poorly stored in the body; daily intake is important
  • 80%-90% of K is removed by the kidneys; if kidneys are damaged = hyperkalemia
  • 10% is excreted in the feces
  • foods rich in potassium  Cantaloupe  Honeydew  Orange juice  Medium sized potato  Banana  Dried fruits  Raisin  Peaches NORMAL VALUE OF K: 3.5 – 5.3 mEq/L
  • a serum K level less than 2.5 mEq/L or greater than 7. mEq/L can cause cardiac arrest  Nursing intervention: Serum K values need to be closely monitored HYPOKALEMIA
  • plenty of K is excreted CAUSES:  Medications (diuretics - ᛏ urine output)  Dialysis (cleans blood – potassium will be removed in the blood) (protein is also removed)  GI suctioning / Vomiting  NPO / Diarrhea  Cushing’s disease  Hyperventilation  Insulin – bring the glucose with potassium inside the cells, ∴ hypokalemia  Malnutrition  Steroids (cause sodium retention) – Na is retained, K has to go out o “opposing effect” o Stress ᛏ the production of steroids in the body  Cellular damage (surgery, burns) – trauma > bleeding > metabolic acidosis  Laxative abuse (10% of K is excreted through feces)  Ketoacidosis – osmotic diuresis  Trauma – when there is breaking down, K will leave the cells > when tissues are destroyed (trauma), you’re starving it > large quantities of K will leave the cells  “opposing effect ” – when one is retained, the other is excreted HYPOKALEMIA affects cardiac conduction inducing a: o Depressed ST segment o Flat or inverted T waves o Increased U waves P – (ATRIAL DEPOLARIZATION)
  • Impulse is in the atrium (SA node)
  • Atria are contracting (filling the ventricles with blood)
  • Atrioventricular (AV) valves are open
  • Semilunar valves are close (impulse will travel to AV node) PR INTERVAL
  • Impulse is at the AV node
  • Trying to open the atrioventricular valves so more blood can fill the ventricles (impulse will now be received by the Bundle of His and the Purkinje fibers)

 Cardiac monitor must be used to ensure safety For severe K deficit:  10 - 20 mEq of KCl can be given every hour  Dilute in IV fluids NURSING INTERVENTIONS:  K products should be mixed well to prevent unintended bolus administration  IV K should be diluted with N.S.  Site should be changed every 72 hours or sooner if tenderness occurs  Potassium-rich foods:

  • Cantaloupe - Fish
  • Avocado - Spinach
  • Beans - Banana
  • Orange Juice
  • Med. sized potato Hypokalemia/Hyperkalemia  CARDIAC DYSRHYTHMIA – irregular heartbeat o Causes ᛎ in cardiac output If cardiac dysrhythmia isn’t corrected immediately, it can cause cardiac arrest  Cardiac arrest - when the heart suddenly stops pumping blood round the body, commonly because of a problem with electrical signals in the heart  When the heart stops pumping blood, the brain is starved of oxygen. This causes unconsciousness and to stop breathing Heart attack - happens when blood supplying the heart muscle is cut off due to a clot in one of the coronary arteries INSERT CARDIAC CYLE HYPERKALEMIA
  • causes ᛏ cardiac rate  Respiratory/Metabolic Acidosis o hyperkalemia > cardiac dysrhythmia > ᛏ cardiac rate > ᛎ cardiac output > less oxygen & nutrients going to the body > hypoxemia > px will become weak because there is less oxygen > anaerobic metabolism > lactic acid is produced > metabolic acidosis o Anaerobic metabolism - creation of energy through the combustion of carbohydrates in the absence of oxygen

lactic acid is produced  patient will be given o  HOW METABOLIC ACIDOSIS LEADS TO HYPERKALEMIA?

  • Anaerobic metabolism > lactic acid is produced > metabolic acidosis > plenty of H+^ ions (acid) > plenty H+^ ions will be filling the blood > H+^ will go into the cells > entrance of H+^ will push K outside > hyperkalemia  Medication (to correct acidosis)
  • Na HCO 3 (ᛏ base)
  • since the acid-base balance is corrected, the K that went out goes back in  CAUSES OF METABOLIC ACIDOSIS o If kidneys are damaged. 1)^ kidneys function in maintaining acid-base balance by excreting waste products like uric acid & urea (these are going to flood blood) || 2)^ Kidneys produce bicarbonates (base) o Lungs. Lungs control acid in the form of CO 2. o Bleeding o Diarrhea (removes bicarbonates) CAUSES OF HYPERKALEMIA:  IV K infusion  ᛎ renal function

 Metabolic acidosis  Severe traumatic injury (bleeding) o Ex. Burns – cells are destroyed > K goes out > hyperkalemia o Bleeding - (less blood circulating > anaerobic metabolism > lactic acid <metabolic acidosis)  Blood for transfusion that is 1-3 weeks old o Old RBC > K goes out of blood cells ASSESSMENT FINDINGS:GIT – ab cramps, chronic diarrhea (lose HCO 3 ), nausea  Cardiac – tachycardia later bradycardia (heart weakens = ᛎ BP) & finally cardiac arrest o Medications: ( beta-blockers – olol)  (-) inotropic: ᛎ contractility of heart  (-) chronotropic: ᛎ CR  Renal – oliguria (ᛎ urine output *600cc and below in 24hrs); anuria (absence of urine *50cc in 24hrs) o There’s oliguria because of the tachycardia effect of hyperkalemia. Increase cardiac rate closes the AV valves immediately so less blood is filling the ventricles from the atrium > less blood output > less blood going to the kidney (secondary organ) > kidney will not function well  Neuromuscular – weakness, numbness, muscle cramps ECG manifestations:

5.5 – 6.0 mEq/L

o Tall, peaked T waves

6.0 – 7.0 mEq/L

o Prolonged PR interval

o Widened QRS interval

ᛏ 8.0 mEq/L

o Complete heart block & cardiac arrest

MANAGEMENT:

(MILD) 5.5 – 6.5 mEq/L

  • Restrict K intake

(MOD) 6.5 – 7.5 mEq/L

  • Give Kayexalate or Kalimate (1 sachet in

100cc of water)

o Kayexalate lowers the K in the body

by binding K in the intestine

o Kalimate

  • Give diuretics: furosemide
  • Give beta-2 agonist (salbutamol, albuterol)

through nebulization

o Causes K to move from ECF to ICF

(SEVERE) ᛏ 7.5 mEq/L

  • Calcium gluconate (10mL/ampule in 10%

solution)

o Given because effect of

hyperkalemia is cardiac dysrrythmia;

o Slow IV push

 Rapid administration may

cause hypotension

o ᛎ the antagonistic effect of K excess

on the myocardium when the

cardiac disturbance is due to ᛏK

o Ca ᛎ the irritability of the

myocardium resulting from ᛏK

o Not promote K loss

  • Glucose insulin (50mL)

o Insulin is given as a treatment for

the hyperkalemia

o Insulin will carry the K to enter the

cell (one way of decreasing the K in

the blood)

o Since insulin is also a carrier of

glucose, the glucose in the blood is

  • calcitonin inhibits the reabsorption of Ca from bones and decrease serum Ca level > Ca will go to kidneys, therefore prone to develop renal calculi PTH:
  • ᛏ calcium absorption from the GIT
  • ᛏ calcium reabsorption from the renal tubules
  • releases calcium from the bone  NORMAL CALCIUM LEVEL: 8.5 to 10.5 mg/dL low Ca – parathyroid is stimulated > bone resorption high Ca – thyroid is stimulated > secrete calcitonin  Calcium and phosphates have an opposing effect o Phosphates are being removed by the kidneys o Foods rich in protein = rich in phosphates o If kidneys are damaged, phosphates level will be high > calcium will become low o Kidneys damaged > for calcium to be absorbed, doctors will give an active vitamin D (calcitriol) and they will remove phosphates (calcium carbonate) and this will lower the phosphates > once phosphates are lowered, calcium will be absorbed

HYPOCALCEMIA

CAUSES:

 Chronic diarrhea  Hypoalbuminemia (main prob: edema)  Renal failure (kidneys are resp. for activation of vitamin D w/c is needed for Ca reabsorption)  Citrated blood transfusion

  • Citrate is added to stored blood to prevent clotting, binds with Ca and renders it unavailable for use
  • Combine with ionized calcium and temporarily remove it from circulation
  • 1 or 2 bags of blood transfusion in a day won’t have an effect in decreasing the serum Ca level
  • 3 or more bags in one day > citrate is increased in level > possible hypocalcemia (because there’s so much citrate and this will bind with the calcium)
  1. Alkalosis
  2. Hypoparathyroidism  Patient receiving massive blood trnsfusion are at risk for hypocalcemia  Calcium gluconate (med given) o Additional calcium given bec of the binding factor of the citrate to Ca may cause hypocalcemia MANIFESTATIONS of hypocalcemia: LATE SIGNS  Chvostek’s sign o Tap the px  Trosseau’s sign o Apply BP cuff > increase systolic pressure 20mmHg to normal > leave for 3 - 5 minutes > indicate there is TETANY ASSESSMENT FINDINGS:  Anxiety, irritability  Tetany (EARLY SIGNS) o twitching around the mouth o tingling & numbness of fingers  Laryngeal spasm (brief spasm in the vocal chords (larynx/voice box) – there will be DOF, px can die), spasmodic contraction  Abdominal cramps  Muscle cramps

ECG READING

HYPOCALCEMIA

o < 8.5 mg/dL

  • lengthening ST
  • lengthening QT HYPERCALCEMIA o > 10.5 mg/dL
  • shortened ST
  • shortened QT HYPOCALCEMIA TREATMENT o CHRONIC TREATMENT  Ca carbonate – given because there’s low Ca; Calci-Aid & Calsan (antacid)  Active vitamin D3 – Calcitriol

o I.V. Ca Chloride  Given very slowly because it may cause extravasation  In general, Ca gluconate is preferred then Ca chloride because it is less likely to cause tissue necrosis

MANAGEMENT

I.V. CALCIUM SUPPLEMENT

 Ca solution are highly irritating to vein. Administer the solution SLOWLY.  Frequently assess IV site.  Close monitor the patient because too rapid infusion can cause cardiac arrest  Ca SHOULD NOT BE GIVEN with saline solution because S.S. increase Ca loss  Ca SHOULD BE GIVEN in big vein. (phlebitis)

ORAL CALCIUM SUPPLEMENT

 Administer at least 30 minutes prior to a meal to enhance intestinal absorption  Teach patient to eat foods rich in Ca, vit. D and protein  Check for prolonged bleeding or reduced clot formation. (Ca can cause clotting of the blood) CALCIUM-RICH FOODS

  • Okra
  • Broccoli
  • Cabbage
  • Coconut meat
  • Almonds
  • Pumpkin seeds
  • Avocado
  • Celery
  • Onions
  • Spinach NURSING INTERVENTION  Limit alcohol and caffeine intake. (Limit calcium absorption)  Limit cigarette smoking w/c increases urinary excretion of Ca  Avoid laxatives and antacids that contain phosphorus because they decrease Ca absorption. o Antacids – should never be given with other drugs because antacids decreases the absorption of other drugs  Give 1 hour before or 2 hours after all drugs  Handle the patient gently. (severe bone calcium loss makes the bone soft and brittle)  Use bed sheet to lift patient.

HYPERCALCEMIA

CAUSES:

 Excess use of Ca supplement  Use of thiazide (mild diuretic used for HTN patient to remove excess fluids) – decreases the excretion of Ca  Prolonged immobilization – lose calcium in the bone because bone is not being used, Ca goes out)  Hyperparathyroidism - increasing the workload of parathyroid > always giving out parathormone > parathormone will remove Ca from the bone > Ca will be in the blood  Steroid therapy – mobilize Ca absorption from the bone o Taking steroids for more than 3 months will cause osteoporosis ASSESSMENT FINDINGS  Abdominal cramps and constipation. (Hypercalcemia can decrease the peristalsis)  Anorexia, nausea & vomiting  Confusion, lethargy  Bone pain (bec the bone loses Ca)  Extreme thirst  Muscle weakness (because muscles are connected to the bones through ligaments and tendons)  Increase BP – Ca is + inotropic DANGER SIGNS  Arrythmia – bradycardia  Cardiac arrest  Coma  Paralytic ileus MANAGEMENT0.9 NaCl solution o 200 – 300 cc/hr o Na in the solution inhibits the renal tubular reabsorption of Ca o To achieve urine output of 200 cc/hr o To dilute the serum Ca concentration (Ca may crystallize)  Furosemide o 20 – 40 mg, 8-16hrs after volume re

o Diarrhea o Fistula  Fluid from the lower GI tract has a higher concentration of Mg (10-14 mEq/L) than the upper tract, so loss from diarrhea and intestinal fistulas are likely to induce ᛎ Mg

  1. Disruption in small bowel function  Major site of Mg absorption – distal small bowel o Intestinal resection o Inflammatory bowel disease
  2. Withdrawal from alcohol  chronic alcohol abuse – major cause of symptomatic ᛎ Mg o N/I: serum Mg level should be measured at least every 2 or 3 hours (may be normal on admission but may ᛎ as a result of metabolic changes, such as the intracellular shift of Mg associated with IV glucose administration)
  3. Nutritional replacement  The major cellular electrolytes move from the serum to newly synthesized cells o Administration of tube feedings or parenteral nutrition ( o TPN o Prolonged IV fluid therapy
  4. DM (d/t osmotic diuresis) o Increase urination > Mg is lost in urine 40% > Decrease Na+, K+, Mg+ = electrolyte imbalance
  5. Inadequate intake of Mg MAGNESIUM-RICH FOODS
  • Almonds
  • Spinach
  • Soybeans
  • Cashews
  • Avocados
  • Potatoes
  • Brown rice ASSESSMENT FINDINGS  3T’s and hyperactive DTR’s o Tremors o Twitching o Tetany o Hyperactive deep tendon reflexes Tonicity refers to what the cell does in a certain environment. If the environment is hypertonic, the cell will shrink due to water leaving the cell. Hypotonic means water enters the cell and caused it to expand and possibly explode. Osmolarity refers to the relative concentration of two solutions. If the outer environment is hyperosmotic, the concentration of solutes outside the cell is greater than the concentration inside the cell. Tonicity and osmolarity generally will have the same prefix. However, there are some solutes that will act oddly and can create a situation where the system is hypertonic and isoosmotic. Just look at what the cell does and relative concentration of each solution, and you can figure it out.