1) Definition of hypokalemia
Potassium is the major intracellular cation. Hypokalemia means that the amount of potassium in the blood is less than normal.
Normal potassium levels are 3.5 to 5.5 meq/liter.
About 98% of the body’s potassium is located inside the cell.
During the formation of nerve tissue and converting glucose to glycogen, potassium enters the cell.
As tissue breaks down, potassium is released from the cell. This mainly includes any trauma, dehydration.
Definition of hyperkalemia
Hyperkalemia is a condition in which the potassium level of the body or blood exceeds the normal potassium levels.
Normal potassium levels are 3.5 to 5.5 meq/liter.
In hyperkalemia potassium levels are greater than 5.5 meq/liter.
causes/Etiology
Due to excessive consumption of salt containing potassium.
The intake of potassium in the body is high and if the kidney cannot excrete that much potassium from the body.
Due to excessive use of oral or intravenous potassium supplementation.
Acute renal failure.
chronic renal failure.
Adrenal gland insufficiency.
Glomerulonephritis (Glomerulonephritis := Infection and inflammation of glomerulus, the filtering part of the kidney is called glomerulonephritis).
metabolic acidosis.
rejection of kidney transplant.
Lack of aldosterone.
additions disease.
type 1 diabetes burns.
hemolytic conditions.
rhabdomyolysis
(Breakdown of muscle tissues) from drugs, alcoholism, coma, or certain infection.
Certain types of medication such as:
ACE inhibitors,
Potassium chloride,
Heparin,
captopril,
NSAIDs,
Use of potassium sparing diuretic (ex:= spironolactone).
clinical manifestation/ sign and symptoms
Irregular heartbeat,
A slow heart rate,
low blood pressure,
nausea,
vomiting,
palpitations,
Muscle twitches and cramps.
Diarrhea.
Cardiac arrhythmia.
Ecg changes.
Muscular weakness and paralysis occur.
Confusion and coma.
Ventricular dish arrhythmias and cardiac arrest.
respiratory failure.
tingling and numbness sensation.
fluid paralysis.
cardiac arrest.
Anemia.
Diagnostic evaluation
history taking and physical examination.
Serum potassium levels are (greater than) > 5.5 meq.
Metabolic acidosis-serum pH falls below 7.35.
ecg changes:=
Elevated T waves,
Widened qrs complx,
Prolong pR interval,
Flattened or absent p waves,
Depressed St segment.
medical management
Treatment of hyperkalemia depends on its cause, the severity of the hyperkalemia, its symptoms, and the patient’s overall health.
The patient should have a low potassium intake in the diet.
Continuous cardiac monitoring of the patient should be done.
The patient should be adequately fluidized intravenously.
Continuous ECG monitoring of the patient should be done.
Medicines that reduce the amount of potassium in the body should be provided to the patient.
If the patient has severe hyperkalemia, dialysis is also required.
Intravenous calcium gluconate should be administered to people if the amount of potassium is not reduced by medication.
The patient should also be provided with sodium bicarbonate to allow potassium to temporarily shift into the cell.
The patient’s serum potassium level should be checked continuously.
Medications that increase potassium levels in the body should be discontinued.
The patient should be administered 25% or 50% glucose and insulin intravenously to allow potassium to re-enter the cell from the extracellular space.
Intravenous calcium should be provided for a short period of time to reduce the effects of hyperkalemia to protect the heart and muscles.
Providing diuretic medicine to the patient.
nursing care for hyperkalemia
Assess the patient’s intake output chart.
Avoiding potassium by the patient’s oral or parenteral route.
Avoid taking the patient’s potassium rich food eg fruit juice.
Assess the patient’s pain level and provide comfort measures.
To assess the patient’s vital signs.
Monitor for fluid excess if patient is taking sodium bicarbonate.
To check the patient’s heart rhythm.
calcium imbalance
Calcium is the most abundant mineral in the human body.
This is good for critical and health.
IN Body normal calcium level is 9 to 11mg/dl or 4.5 to 5.5 meq/liter.
Calcium is a mineral that is mainly found in bones and teeth.
More than 99% of calcium is in bones (skeleton system).
Calcium is an important component of bones and teeth.
Calcium plays an important role in nerve impulses and contraction and relaxation of muscles and is also involved in cardiac muscles.
Calcium plays an important role in blood clotting, muscle and nerve function.
1) Define hypocalcemia. (Define hypocalcemia.)
2) Explain the causes/Etiology, Clinical manifestation, And diagnostic evaluation of hypocalcemia.
3) Explain the management of hypocalcemia. (Write management of hypocalcemia.)
1) Define hypocalcemia.
definition:=
When the amount of calcium in the body and blood is low, it is called hypocalcemia.
Hypokalemia is a condition in which the level of calcium in the body is less than the normal level, it is called hypo calcium.
Normal calcium level 4.5 to 5.5 meq/liter, or 9 to 11mg/dl.
(In hypocalcemia the level of calcium in blood is less than 9mg/dl or 4.5 meq/liter.)
Etiology/cause
Thyroid gland is underactive due to damage due to any disease or surgery.
Due to excessive binding of calcium to iron.
large amount of citrate blood.
hypoalbuminemia (decrease in albumin level).
alkalosis (alkalosis).
Hyperphosphatemia (the amount of Phosphate is more).
Due to not getting enough calcium in the diet.
Due to insufficient intake of vitamin D in the diet.
Due to chronic renal failure.
Due to non absorption of proper amount of calcium in gastero intestinal track.
Intestinal fistula. (Fistula means abnormal connection of two organs).
crohn’s disease, chronic inflammatory bowel disease.
Due to deficiency of parathyroid hormone and vitamin D.
severe burns or infection.
Osteoporosis (this is a bone condition in which bones are weak and fragile that break down easily).
Due to infection of pancreas
Kidney failure.
Due to low level of magnesium in the blood.
Certain medications such as diuretics, estrogen replacement therapy, glucose, calcium channel blockers, insulin, and magnesium are responsible for conditioning hypo calcium.
Due to drinking too much alcohol, nutrition cannot be taken in adequate amount.
Biphosphate therapy.
Certain types of leukemia (blood cancer) and blood disorders.
Toxic shock syndrome.
clinical manifestation/ sign and symptoms
osteoporosis (bones become weak and fragile that break down easily due to calcium deficiency).
Anxiety and irritability.
Pathogenic fracture (any kind of disease that weakens the bone and can break down easily).
Tetany (tetany: spasm in muscles due to calcium deficiency and underactive parathyroid gland).
Tingling sensation occurs around the nose and on the tip of the finger.
Tingling and numbness sensation also occurs in hands, feet.
Muscle spasm.
Heart rate is irregular and increases.
Nausea, vomiting.
Increase in blood pressure.
Changes in mental status.
Deep tendon reflexes become hyperactive.
The size of the gasterointestinal track increases.
G.I. Diarrhea and abdominal cramps occur due to increased motility of the G.i. track.
Cardiac arrhythmias.
Laryngospasm (difficulty in speech due to spasm in the vocal cord).
Hypotension.
Dry skin.
Dermatitis (inflammation of the skin).
skin hyperpigmentation.
Chvostek sign ( Chvostek sign :=
This sign is seen when the amount of calcium in the body is in a low amount (hypocalcemia), facial muscles twitch when a person is tapped on the cheek and in front of the ear.
trousseau’s sign
This symptom is seen when there is a condition of hypo calcium in the body.
(Carpopedal spasm is a severe spasm in the hand muscles.)
Neurological symptoms like depression, personality change, seizures, loss of movement control.
Spasm in body muscles.
Diagnostic evaluation
history taking and physical examination.
Serum sodium level is less than <8.5 mg/dl.
low platelet count.
increase parathyroid hormone level.
Ecg shows lengthened Qt interval, Prolong St segment, arrhythmias.
There are also changes in serum protein levels as serum calcium is slightly bound to albumin.
medical management
A person who is deficient in calcium should take calcium supplementation.
Taking vitamin D in proper amount.
Provide intravenous calcium gluconate or calcium chloride to a person with acute or severe hypocalcemia.
Calcium supplements should be provided one to two hours after a meal to increase intestinal absorption.
If the patient has severe hypocalcemia with cardiac arrhythmias and tetany, the patient should be given calcium salts immediately.
Provide calcium carbonate in the initial stage of hypocalcemia.
Calcium carbonate at 250 or 500 mg/tablet.
Provide calcium gluconate and calcium chloride to the patient.
If there is a serious condition, provide calcium chloride to the patient.
Provide calcium carbonate in the initial stage of hypocalcemia.
Vitamin D therapy should be taken in proper amount.
Consuming foods rich in vitamin D, such as milk or dairy products, will allow calcium to be absorbed properly.
nursing management
To check patient’s vital sign and blood pressure.
Administer calcium to the patient intravenously.
Monitor the patient’s airway and respiratory status.
Provide education about sources of calcium to the patient and his family members.
If the patient has undergone thyroid or neck surgery, monitor the patient for signs and symptoms of hypocalcemia or not.
Ask the patient to do proper exercises.
Providing work and quiet environment to Nishant.
Keeping the patient’s bed at a low level and providing a side rail.
Ask the patient to avoid alcohol.
Ask the patient to avoid caffeine intake.
Smoking reduces the amount of calcium in the body so ask the patient to avoid smoking.
Ask the patient to take a proper calcium rich diet.
1) define hypercalcemia
2) Explain the etiology, sign and symptoms, and diagnostic evaluation of hypercalcemia. (Write the causes of hypercalcemia, its signs and symptoms and diagnostic evolution.)
3) Explain the management of hypercalcemia. (Write management of hypercalcemia.)
Definition of hypercalcemia.
Hypercalcemia is a condition in which the level of calcium in the blood and body is
If it is more than 11 mg/deciliter (11mg/dl) or 5.5 equivalent per liter (5.5 meq/liter), it is called hypercalcium.
In normal level serum calcium level is (9 to 11 mg/dl or 4.5 to 5.5meq/liter).
(in hypercalcemia the level of calcium is greater than > 11mg/dl or 5.5 meq/liter)
Etiology/cause
Over active parathyroid gland.
Bone cancer causes excessive release of calcium from the bone.
Dehydration, loss of water from the body.
Multiple myeloma,
multiple fractures,
immobilization,
Intake more calcium in the diet.
Prolong bed rest.
Excessive absorption of calcium due to high amounts of vitamin D.
tumor that destroy bone.
Excessive calcium and vitamin D intake.
repeated transmission with citrated blood.
Excessive consumption of milk products.
chronic kidney failure.
alkalosis.
Dietary excessive intake of calcium
Vitamin D increases the amount of calcium absorbed.
chronic kidney disease.
use of certain medication such as thiazide diuretic.
inherited kidney or metabolic condition.
clinical manifestation/sign and symptoms.
Heart rate increases.
Blood pressure increases.
Muscle weakness.
Loss of appetite.
bone pain and pathological fracture.
Constipation (constipation).
Vomiting.
Abdominal pain.
body ache.
Decreased ability of blood to clot.
Nausea and vomiting.
Body ache.
Passing too much urine (polyuria) and feeling very thirsty (polydypsia).
Lethargy.
Stones are formed in the kidney and the waste product builds up in the body itself.
Confusion.
Heart block.
Difficulty speaking.
Very sleepy.
headache.
irritability.
Depression.
Memory is impaired.
Mood swings.
Confusion.
psychosis.
renal stones.
decrease deep tendon reflexes.
coma.
Diagnostic evaluation
history taking and physical examination.
Serum calcium level is greater than 10.5 mg/dl.
ECG shows signs of heart block. Shortened QT interval and ST segment.
X-ray may reveal the presence of osteoporosis, bone cavitation or urinary calculi.
urinalysis.
Decreased parathyroid hormone.
Sulkowitch urine test shows increased calcium precipitation.
Medical management
If the patient has a severe hypercalcic condition, he needs immediate hospitalization.
Maintain hydration status of patients with severe or acute hypercalcemia by providing normal saline.
If the patient has nausea, vomiting, polyuria, provide normal saline.
Individuals who are taking diuretic medicine or Lasix (frusemide) should be provided so that the amount of calcium is excreted from the body.
Using drugs that bind calcium and release it from the body.
Ask the patient to ambulate.
Ask the patient to provide plenty of fluids.
Providing reinsurance to the client and his family members.
Calcitonin helps lower serum sodium levels.
Biphosphate helps to increase the amount of calcium absorbed in the bone.
administer glucocorticoids.
dialysis.
Nursing management
Maintaining intake output chart of patient.
Ask the patient to increase fluid intake.
Tell the patient to take a low calcium diet.
Reassurance to client and family members of the patient.
Ask the patient to increase fluid intake.
If the patient’s serum calcium level rises above 5.5 meq/liter, check the patient for cardiac arrhythmias.
If the patient is using a diuretic or normal saline, check the patient for signs and symptoms of heart failure.
If the patient is receiving a glycoside, observe for toxicity such as loss of appetite, nosia, vomiting, bradycardia, etc.
If the patient’s bones are weak, change the patient’s position carefully.
If the patient is bedridden, change the patient’s position frequently and ask the patient to do range of motion exercises.
To check patient’s vital sign.
Assess the patient’s respiratory status.
To check the patient’s heart sound.
Ask the patient to do physical activity to maintain weight.
Ask the patient to take enough fiber rich food to relieve constipation.
Ask the patient to take a low calcium diet and fluid intake.
Asking the patient to be active so that calcium can be reduced from the body.
1) Define hypomagnesemia.
2) Explain Etiology, Clinical manifestation, and diagnostic evaluation of hypomagnesemia. (Write the causes of hypomagnesia, its signs and symptoms, and diagnostic evaluation.)
3) Explain the management of hypomagnesemia. (Write management of hypomagnesaemia.)
Introduction of Magnesium
Magnesium is an essential component that regulates over 300 enzymes that are responsible for many body functions.
Magnesium works as a cofactor for many body enzymes.
Magnesium plays an important role in the metabolic activity of the body.
Magnesium is important for the relaxation of smooth muscles such as those surrounding the bronchial tubes.
And skeletal muscle contraction and neurons that are located in the brain.
Magnesium converts what is in the body into energy and helps build up in protein and maintains the level of calcium in the blood.
Magnesium prevents cardio vascular disease and prevents irregular heart beat.
Magnesium helps prevent heart attacks.
Magnesium prevents the condition of stroke.
(the normal value for serum magnesium is 1.5 to 2.5 meq/liter) or (1.8-3.0mg/dl) if magnesium
If there is an imbalance, it is called hypomagnesemia.
Or called hypermagnesemia (hypermagnesemia).
Hypomagnasemia is an electronic disturbance.
Those who have abnormally low levels of magnesium have less than normal magnesium levels in the blood.
(The normal adult values for Magnesium is 1.5-2.5meq/liter.)
(In hypomagnasemia level of Magnesium is (less than) <1.5 meq/liter.)
Etiology/cause
Due to excessive loss of magnesium from the body.
Due to low intake of magnesium.
Due to protein calorie mal nutrition.
Due to lack of proper absorption in intestine.
Due to my nutrition or starvation.
Due to excessive fluid loss from the body.
Due to excessive excretion of urine from the body.
Severe diarrhea.
Crohn’s disease.
Due to giving too much diuretic.
use of certain medication including amphotericin,
Cisplatin, Aminoglycoside.
Gastrointestinal fistula.
Renal damage.
ostomies.
Total parenteral nutrition.
Excessive urination (polyuria).
Alcoholism.
Malabsorption.
Due to high blood calcium level in the body.
hyperaldosteronism.
Clinical manifestation/sign and symptoms
positive trousseau’s and chovostek signs.
Loss of appetite.
Nausea.
Vomiting.
weakness.
apathy.
Muscle weakness.
paresthesia (tingling or numbness sensation).
The moment is slow and involuntary.
hyperirritability,
tetany,
leg and foot cramps.
to be startled
Trams,
Ataxia: Absence of normal coordination.
carpopedal spasm.
Depression.
Irritability.
Psychotic behavior.
to be startled
vertical nystagmus (vertical nystagmus := involuntary movement of eye ball.
Cardiac dysrhythmias.
Extreme agitation.
Insomnia
delirium.
Auditory and visual hallucinations.
diagnostic evaluation
history taking and physical examination.
serum magnesium lower than 1.5 meq/liter (hypomagnesemia),
hypocalcemia,
hypokalemia,
low urine Magnesium and calcium.
low magnesium in cerebrospinal fluid and muscles.
Decrease serum albumin level.
nuclear magnesium resonance spectroscopy.
Electrocardiogram may show:=
A.) Prolong PR and QT interval,
B) widening QRS,
c) ST segment depression.
D) Flattened T waves.
E) prominent U wave.
Medical management
Treatment of hypo magnesium is provided based on its deficiency and clinical effect.
The goal of treatment is to identify and eliminate the cause of hypomagnesemia and replace the amount of magnesium in the body.
Provide oral magnesium replacement to patients with mild symptoms.
Replacement of intravenous magnesium in patients with very senior signs and symptoms.
And asking a person with a condition of mild hypomagnesia to take a diet rich in magnesium.
Like := green leafy vegetable 🥗,
Nuts,
Legumes 🫛 (legumes),
Whole grain
Sea food (🍢),
Ask to take magnesium rich diet like etc.
Magnesium preparations such as magnesium oxide should be taken as they contain higher amounts of magnesium.
Provide magnesium sulfate intravenously (10 to 40 meq/liter) to patients who have severe hypo magnesium conditions.
If the patient has Cardiac arrhythmia Obstetrics problem Electrolyte disturbance, Asthma.
If there is a condition like etc. then provide magnesium sulphate intravenously.
Nursing management
Ask the patient to take magnesium rich food.
Monitor the patient’s level of consciousness.
Monitoring the patient’s breathing pattern.
ASSESS ECG CHANGES OF THE PATIENT To assess Ecg changes in a person taking digitalis group of medicines.
Refrain from taking excessive diuretic and laxative.
Monitor the patient’s bowel sound and abdominal distension.
Check the patient’s reflexes before infusing magnesium.
Provide patient work, quiet and dark room.
Provide a low bed of the patient and keep his side wells high to prevent the patient from falling down if he faints.
1) define hypermagnesemia. (Define and hypermagnesemia).
2) Explain etiology, clinical manifestation, and diagnostic evaluation of hypermagnesemia. (Write down the causes of hypermagnesium, its signs and symptoms, and diagnostic evaluation.)
3) Explain the management of hypermagnesemia. (Write management of hypermagnesemia.)
Define hypermagnesemia: (Define hypermagnesemia).
Hypermagnesia is an electronic imbalance in which magnesium levels in the body exceed 2.5 meq/liter.
A normal level of magnesium in the body is important for the function of the heart and nervous system.
(in hypermagnesemia the level of magnesium is greater than > 2.5 meq/liter).
Etiology/cause
hemolysis,
renal insufficiency,
More Magnesium Vada due to overuse of antacids and laxatives.
Hypothyroidism.
lithium therapy.
diabetic ketoacidosis.
adrenal insufficiency.
overdose with magnesium salts.
severe dehydration.
chronic renal insufficiency.
clinical manifestation / sign and symptoms
nausea and vomiting,
weakness,
difficulty breathing,
Low blood pressure (hypotension),
bradypnea,
feel tired,
falling asleep,
skeletal muscle weakness,
diminished reflexes,
facial paresthesias,
flaccid muscle paralysis,
hypercalcemia,
arrhythmia,
Decreased deep tendon reflexes.
Bradycardia.
Bridging is a cell.
bradycardia.
cardiac failure.
diagnostic evaluation
history taking and physical examination.
Serum magnesium level is greater than 2.5 meq/liter.
coexisting Elevated potassium and calcium levels.
ECG changes:= prolonged PR interval ,Tall t waves, Prolonged QT interval and Widened QRS.
medical management
Ask the patient to increase fluid intake.
Provide diuretic medicine to the patient.
Infuse calcium gluconate to prevent magnesium toxicity.
A person who cannot pass magnesium through urine, i.e. if his kidney function is impaired, then diet should be provided to him.
Nursing management
Monitoring the patient’s care fully.
To maintain an intake output chart of Tisant.
Tell the patient not to take magnesium rich food.
To assess the patient’s reflexes.
Monitor the patient for lethargy or drowsiness.
Avoid over-the-counter drugs that contain magnesium.
To check patient’s vital sign.
To assess the patient’s respiratory function.
monitor Ecg changes like:=( prolonged PR, Prolonged QRS, and prolonged QT.)
Ask the patient to take a low-magnesium diet.
Explain phosphorus
Phosphorus is an intracellular anion.
Phosphorus is required for the normal functioning of the cell.
Phosphorus is mainly in combination with calcium which is mainly found in teeth and bones.
Phosphorus is the primary anion of the intracellular fluid.
About 85% of phosphorus is in bones and teeth.
About 14% is in the soft tissues and less than 1% is in the extracellular fluid (ECF).
Phosphorus is responsible for a very important function.
Phospharus also supports the formation of ATP (ATP := adenosine triphosphate) and bones and teeth.
Phosphorus plays an important role in the utilization of vitamin D, in acid-base homeostasis, nerve, and muscle activity, and in the metabolism of carbohydrate, protein, and fat.
Normal serum phospharus level 2.5 to 4.5 mg/dl (0.8-1.5 mol./liter), due to Phospharus imbalance.
Hypophosphatemia (lower than normal amount of phosphorus).
A condition like hyperphosphatemia (as in phospharus) may arise.
1) Define phospharus deficit (hypophosphatemia). Define hypophosphatemia.
2) Explain Etiology, Clinical manifestation, Diagnostic evaluation of hypophosphatemia. (List the causes of hypophosphatemia, its signs and symptoms, and* its diagnostic evaluation.)
3) Explain the management of hypophosphatemia. (Write Hypo Phosphatemia Management)
Definition of hypophosphatemia Define hypophosphatemia.
Hypo phosphataemia is a condition in which the level of phosphorus in the body is less than the normal level.
Hypo phosphate is mainly caused by starvation and alcoholism.
(Normal Phosphate level is 2.5 to 4.5 mg/dl (0.8-1.5 mmol/liter))
In mild hypophosphatemia (2-2.5mg/dl or 0.65-0.81 mmol/liter),
In moderate Hypophosphatemia (1-2mg/dl or 0.32-0.65 mmol/liter),
In severe hypophosphatemia (<1mg/dl or 0.32 mmol/liter).
Etiology/ cause
Administer intravenous fluid without phosphorus.
hyperparathyroidism: This is a condition in which the parathyroid gland secretes too much parathyroid hormone.
respiratory alkalosis..
Due to poor kidney function
A condition of hypophosphatemia may occur due to which the renal tubule cannot reabsorb phosphorus in an adequate amount.
Recovery from certain types of disease such as diabetes ketoacidosis or severe burns can condition hypophosphatemia.
Due to overuse of diuretic medicine.
Due to lack of intake of adequate amount of phosphorus due to long-term alcoholism and poor nutrition.
Any intestinal abnormality in which the intestine cannot absorb adequate amounts of phosphorus. Ex:=chronic diarrhoea.
clinical manifestation/(sign and symptoms)
hunger,
Weakness in skeleton and smooth muscles.
tingling sensation.
numbness.
paresthesia (feeling of tingling and numbness sensation).
tremors.
bone pain.
Weakness.
respiratory insufficiency.
Impair neurologic function.
Confusion.
Memory loss.
to be startled
Coma.
peripheral neuropathy and paralysis.
Hemolytic anemia.
Impaired leukocytes and platelet count.
Diagnostic evaluation
history taking and physical examination.
Serum Phosphate level is less than 2.5 mg/dl.
Urin Phosphate level grayer than 1.3 g/24 hours.
medical management
Ask the patient to take phosphate in his diet.
Provide patient with medication supplementation if phosphate replacement is not achieved through diet.
If not cured by meditation, provide phosphate to the patient intravenously.
Tell the patient to take nephosphare rich.
Ex:= green leafy vegetable 🥦,
peas
beans(🫘),
nuts,
chocolate,
beef liver,
Ask to take phosphate rich food etc.
in case of severe hypophosphatemia so administer Phosphate intravenously.
the dose of kpo4 2.5 mg/dl every 6 hourly.
If the patient has hyperparathyroidism, surgical removal of the parathyroid gland.
nursing management
Checking the patient’s serum electrolyte level.
Ask the patient to take Phosphate rich food in the diet.
To check whether the patient has muscle weakness or not.
Checking the mental status of the patient.
To check patient’s vital signs.
Maintain patient’s intake output chart.
1) Define hyper phosphatemia (phosphorus excess). Define hyperphosphatemia.
2) Explain Etiology, Clinical manifestation, And sign and symptoms of hyperphosphatemia. (Write the causes of hyperphosphatemia, its signs and symptoms and diagnostic evaluation.)
3) Explain the management of hyperphosphatemia.
Definition of hyperphosphatemia. (Define hyperphosphatenia.
Hyperphosphatemia is a condition in which the level of phosphorus in the body and blood increases beyond the normal level.
Hyperphosphatemia occurs due to excessive absorption of phosphorus, low loss from the body, and excessive production.
A major cause of hyperphosphatemia is renal failure.
Etiology/cause
renal failure,
chemotherapy,
hypothyroidism (due to low thyroid level),
respiratory acidosis,
Diabetic ketoacidosis,
Due to excessive intake of phosphate.
Profound muscle necrosis.
Hypophosphatemia is a condition caused by overuse of laxatives and enemas that contain phosphate.
Phosphorus is not excreted from the body due to kidney failure and due to magnesium deficiency.
Hypoparathyroidism is a condition in which the parathyroid gland does not produce adequate amounts of parathyroid hormone.
Due to this, there is an inability of the kidneys which cannot respond to the parathyroid hormone due to which there is no excretion of phosphorus from the body.
And the amount of phosphorus in the body increases.
The amount of phosphate in the body also increases due to the condition of hypocalcemia.
clinical manifestation/sign and symptoms
tetany,
Tingling sensation in finger tips.
Loss of appetite.
Nausea.
vomiting,
Muscle weakness.
hyperreflexia.
Tachycardia.
Decreased urine output.
Difficulty seeing.
Palpitation.
Depression.
Memory loss.
Convergence to come.
Calcification of soft tissue.
Arteriosclerosis.
Arteriosclerosis can cause heart attacks and strokes.
Severe itching.
diagnostic evaluation
history taking and physical examination.
Serum Phosphate level is greater than 4.5 mg/dl.
Serum calcium level is less than 9mg/dl.
X Ray,
decrease parathyroid hormone,
Check blood urea nitrogen level (BUN) and creatinine level.
medical management
Provide vitamin D preparation to the patient to reduce phosphate levels.
Use an oral phosphate binder that can absorb phosphorus from the GI tract.
Lanthanum carbonate provides to the dialysis patients.
Using calcium salts such as (calcium carbonate, gluconate, and chloride) that bind phosphate from the blood stream and lower blood phosphorus levels.
Use albumin salts like albumin hydroxide which can bind phosphorus.
Observe the patient for severe hyperphosphatemia and provide calcium gluconate intravenously to the patient.
Dialysis is an important treatment to remove excess phosphate from the blood.
Foods that are phosphate rich including dairy products, meat, nuts and other high protein foods should be avoided.
nursing management
Assess the patient’s serum phosphorus level.
Checking the patient for signs and symptoms of hypocalcemia.
Properly monitor patients who are at high risk for hyperphosphatemia.
Ask the patient to take a low phosphorus diet.
Phosphorous fridge food like 🧀 cheese,
cream,
nuts,
whole grain,
cereals,
dried fruits,
vegetables,
sweetbreads,
Ask not to take phosphorus rich food like milk food.
When the phosphorus level of the patient is normal, instruct the patient to avoid laxatives and enemas that are high in phosphate.
Instruct the patient to check whether there are any signs and symptoms of hypo calcium and assess whether there are any changes in the patient’s urine output.
Ask the patient to take low phosphorus food.
Chloride imbalance
Chloride is the major extracellular fluid anion.
And this mainly from blood. It is present in large amount in intestine and lymph fluid.
Chloride A mainly
Gastricr, pancreatic
It is present in juice and sweat.
Sodium and chloride are present in water as ECF and contribute to osmotic pressure.
The amount of chloride causes dilution of extra cellular fluid and changes in its concentration.
Due to this, sodium content also changes.
Due to the secretion of aldosterone, the reabsorption of sodium occurs, due to which the reabsorption of chloride also goes away.
The choroid plexus (the chloride plexus) is formed.
It depends on the concentration of sodium and chloride.
Because sodium and chloride increase its water absorption.
Due to this, cerebrospinal fluid is formed.
Bicarbonate has an inverse relationship with chloride.
Chloride moves from the plasma into the red blood cells, while bicarbonate moves back into the plasma.
Then the formation of hydrogen ions occurs which helps in the release of oxygen from the hemoglobin.
Now when one of these three electrolytes (sodium, bicarbonate, or chloride) is disturbed, the other two electrolytes are also affected.
1) Define chloride deficit (hypochloremia). (Define hypochloremia.
2) Explain Etiology, Clinical manifestation, Diagnostic evaluation of hypochloremia. Write the causes of hypochloremia, its signs and symptoms, and diagnostic evaluation.
3) Explain the management of hypochloremia.
Define chloride deficit (hypochloremia). (Define hypochloremia.
The concentration of chloride depends on its intake.
Excretion of fluoride and its reabsorption takes place in the kidneys.
Chloride is produced in the stomach as hydrochloric acid and a small amount of chloride is lost in the feces.
Hypochloride is an electrolyte imbalance.
In which the chloride in the body and blood is at a low level, more than the normal level is seen.
(Normal chloride level in adult is 97-107meq/liter. )
(In hypochloremia the level of chloride is less than 97 meq/liter.)
Hypochloremia If the chloride level is less than 97 meq/liter, it is called hypochloremia.
cause/Etiology
Due to low intake of chloride.
Due to the low absorption of chloride.
Due to low sodium intake.
Due to low potassium intake.
Due to prolonged use of diuretic medicine.
Metabolic alcoholosis.
Due to release of excess chloride from the body due to diarrhoea.
vomiting,
Gastric absorption.
Gastric surgery.
sign and symptoms/ clinical manifestation
confusion,
apathy (loss of interest),
Disc Orientation.
Oversleeping.
to be startled
To sit in one’s place.
Muscle wasting.
atrophy (decrease in size of muscles and tissue).
Hypotonia.
Tetanus.
Dependent reflexes are hyperactive.
Weakness.
twitching.
Muscle Crèmes.
Cell bridging.
Hyponatremia.
Hypokalemia.
Mussels Crèmes.
cardiac dysrhythmias.
Caesar (siezer).
diagnostic evaluation
History taking and physical examination.
Serum chloride level is less than 97 meq/liter.
serum ph is greater than 7.45.
serum co2 level is greater than 32 meq/liter.
Serum Bicarbonate.
serum electrolytes.
urine electrolyte.
urine osmolarity.
medical management
Ask the patient to take salty food orally.
Administer 0.9% sodium chloride intravenously to the patient.
Administer ammonium chloride to the patient.
Administer potassium chloride to the patient.
Administer potassium chloride orally or intravenously to the patient.
Administer 10- 40 meq/liter potassium chloride.
If potassium chloride is to be administered intravenously, it should not exceed 20 meq/liter.
Uretic drugs that excrete chloride from the body should be avoided.
Food which contains high amount of chloride should be given to the patient like:
Tomato juice (🍅),
salty broth,
canned vegetables,
processed meat,
Provide food like fruits, etc.
Bottled water excretes more chloride from the body, so such water should be avoided.
Ammonium chloride an acidifying agent may be used for metabolic alkalosis.
The patient’s excessive chloride diet should be intake.
nursing management
Maintaining intake output chart of patient.
Assess the patient’s arterial blood gas value.
Checking the patient’s serum electrolyte level.
Checking the patient’s level of consciousness.
Checking the patient’s muscle strength and moment.
If any changes are observed, report to the physician immediately.
To monitor patient’s vital signs properly.
Provide patient education or intake of high chloride diet.
1) Define hyperchloremia. (Define hyperchloremia.)
2) Explain Etiology, Clinical manifestation, Sign and symptoms of hyperchloremia. Write the causes, signs and symptoms and diagnostic evaluation of hyperchloremia.
3) Explain the management of hyperchloremia.
Define hyperchloremia. Define hyperchloremia.
Hyperkaloremia is an electrolyte imbalance in which the level of chloride in the blood and body exceeds the normal value.
(Normal chlorine level is 97-107 meq/liter).
(In hyperchloremia the value of chlorides greater than 108 meq/liter)
Loss of bicarbonate from the body along with hypernatremia and metabolic acidosis increase chloride levels.
Etiology/cause
due to excessive chloride intake.
Because too much chloride is absorbed into the body.
Hyperingestion of ammonium chloride.
ureterointestinal anastomosis.
Ingesting large amounts of chloride through any route of the body like intravenously.
Orally,
Nasophastric tube,
Enema etc.
Due to taking certain types of medicine such as cadiuretic.
due to dehydration.
vomiting,
diarrhea,
sweating,
high fever,
metabolic acidosis,
brain stem injury causes hyperventilation and hyperparathyroidism,
clinical manifestation/ sign and symptoms
Tachypnea (increase respiratory rate),
weakness,
feel tired,
deep and rapid respiratory rate.
Diminished thinking power.
Hyper tension.
Hypervolemia.
hypernatremia,
hyperchloremia,
Decreased cardiac output.
dysrrhythemias.
Coma.
Fluid retention.
diagnostic evaluation
history taking and physical examination.
serum chloride level greater than 108 meq/liter.
Serum level is less than 7.35.
Serum carbon dioxide level is less than 22 meq/liter.
Serum sodium level is greater than 145 meq/liter.
serum Bicarbonate level is less than 22 meq/liter.
increase urine chloride excretion.
medical management
If there is severe hyperchloremic acidosis, its treatment involves sodium bicarbonate intravenously to increase the level of bicarbonate due to chloride ion excretion through the kidneys.
If there is mild amount of hyperchloremia then administration of ringer lactate solutions which enter the carbonate in the liver and due to this the condition of acidosis is treated.
Administer a diuretic to eliminate chloride.
Take or restrict sodium, fluid and chloride in small amounts.
It is necessary to correct the cause of hyperchlorination and maintain electrolyte and acid-base balance.
nursing management
To monitor patient’s vital signs.
Checking the patient’s arterial blood gas value.
To assess the patient’s intake output.
Assess the patient’s respiratory, neurologic and cardiac systems. And if there are any changes in it, to report it to the physician immediately.
Educating the patient on diet.
Explain acid base balance
Acids and bases are formed as part of normal metabolic processes in the body.
Acids are formed as end products of glucose, fat and protein.
And these are called fixed acids because they do not undergo any changes once they are formed.
Weak acid, carbonic acid. Carbon dioxide of cellular metabolism is formed by combining with water.
These acids are not fixed because they change back to bicarbonate and hydrogen.
Explain Acid-base Imbalance. (Describe acid base imbalance)
Acids and bases are formed in the body as part of a normal metabolic process.
Kidneys secrete hydrogen ions (acid) to maintain acid and base balance. Sodium reabsorbs iron and bicarbonate ion (base). Phosphate acidifies the salt and produces ammonium ions.
due to these the normal blood pH is between 7.35 to 7.45 maintain in body.
Respiratory imbalance occurs when there is a problem in the oxygenation of the blood. Ex:= hyperventilation,
Stagnation of blood flow, etc.
Metabolic imbalance occurs when kidney function breaks down.
Imbalance occurs in the injection (ingestion) and loss (loss) of fluid.
And due to other problems in body organs.
A patient’s acid-base status can be obtained by taking the following sample from arterial blood.
1) ph ( normal 7.35 to 7.45 ):= measure hydrogen ion concentration.
2)PCO2 (normal 40 mmhg):= partial pressure of carbon dioxide.
3) Bicarbonate (normal 27meq/liter)
1) Explain the respiratory acidosis. Describe respiratory acidosis.
2) Explain Etiology, Clinical manifestation, Diagnostic evaluation of respiratory acidosis. (Describe the causes of respiratory acidosis, its signs and symptoms and diagnostic evaluation.
3) Explain the management of respiratory acidosis. (Write management of respiratory acidosis.
Describe respiratory acidosis.
Respiratory acidosis is a condition that occurs when the lungs cannot remove all the carbon dioxide produced in the body from the body.
Respiratory acidosis is a medical condition.
In which the ventilation of the body is reduced (hypoventilation).
And the amount of carbon dioxide in the blood increases and due to this the blood ph decreases. This condition is called acidosis.
Alveolar ventilation is reduced.
In respiratory acidosis the blood pH falls below 7.35.
Pco2 is greater than 42 mmhg.
This causes acid-base imbalance.
And because of that body fluid
And specially blood is acidic.
Carbon dioxide is produced as the body’s cells repair, and carbon dioxide accumulates if there is not enough carbon dioxide.
Alveolar ventilation cannot expel the drug from the body.
So alveolar hypoventilation occurs.
Due to this, the amount of PACO2 (paco2) in the body increases (hypercapnea).
type of respiratory acidosis
1) Acute respiratory acidosis
2) chronic respiratory acidosis. (Chronic Respiratory Acidosis)
1) Acute respiratory acidosis:=
Acute respiratory acidosis occurs when ventilation suddenly fails.
In acute respiratory acidosis paco2 is elevated above the upper limit of reference range (over 47 mmhg) (ph <7.35).
Acute respiratory acidosis is caused by hypo ventilation.
And it is mainly due to the disease of the central secretory center which is located in the cerebral cavity.
or due to any drugs,
May be due to myasthenia gravis, Gulin bar syndrome etc. or Airway obstruction due to
Copd (cronic obstruction pulmonary disease) can also be due.
2) cronic respiratory acidosis (chronic respiratory acidosis)
Chronic secretory acidosis can be due to pulmonary disease or any chronic disease or secondary to any other disease.
In chronic respiratory acidosis the pco2 exceeds the normal range.
Normal blood pH (7.35 to 7.45). Elevated serum Bicarbonate (hco3->30mm hg).
Chronic respiratory acidosis is caused by all disorders including COPD (cronic obstruction pulmonary disease).
Chronic restorative acidosis is also seen due to secondary obesity, hypoventilation syndrome, neuromuscular disorder, ventilatory defects and intestinal fibrosis, and thoracic deformity.
And it is also seen due to lung disease.
cause/ Etiology
drugs := narcotics,
Anesthetic,
Hypnotics,
Sedative etc.
Central nervous system trauma such as medullary injury that impairs ventilatory drive.
Airway obstruction.
parenchymal lung disease.
A chest wall disorder.
Severe kyphoscoliosis status post thoracoplasty.
Flail Chest.
alkalosis spondylitis.
Chronicmetabolic alkalosis which reduces alveolar ventilation.
Neuromuscular diseases like Gulin Barr syndrome, Poliomyelitis,
In this disease, the respiratory muscles cannot contract properly, causing hypo ventilation.
chronic obstructive pulmonary disease (copd),
Asthma, adult respiratory distress syndrome.
Chronic bronchitis.
large pneumothorax.
extensive pneumonia.
Pulmonary Edema.
clinical manifestation/ sign and symptoms
difficulty breathing,
shortness of breath,
feel very tired,
chronic cough,
wheezing,
confusion,
irritability,
lethargy,
Increase in pulse rate,
Respiratory rate increase,
increase blood pressure,
mental confusion,
felling of fullness in head,
anxiety,
delirium,
confusion,
papilloedema,
Superficial blood vessels should be dilated.
Diagnostic evaluation
history taking and physical examination
Arterial blood gas analysis.
pco2 greater than 45 mmhg.
ph is below the normal limit 7.35 to 7.45.
complete blood count tests.
monitoring of serum electrolyte level.
chest X Ray,
Pulmonary function test,
ct scanning,
mri of brain,
fluoroscopy,
Ecg identify any cardiac involvement.
medical management
The goal of treatment is to correct the source of alveolar hypoventilation.
Correct any dis order if any.
provide ebronchodilatore medicine to patient.
provide antibiotics medicine.
administration supplementary oxygen therapy.
Ask to avoid smoking.
Ask to lose weight.
provide non-invasive positive pressure ventilation.
Dialysis to eliminate toxic drugs.
provide endotracheal intubation.
tracheostomy.
mechanical ventilation.
provide antibiotic 💊 medicine.
Administer chest tube to administer pneumothorax.
PEEP := to prevent alveolar collapse.
for pulmonary emboli thrombolytics or anticoagulant therapy.
Bronchoscopy to remove excessive secretion.
provide bronchodilator medicine.
administration B agonist like ipratropium, bromide, methylxanthines.
Provide oxygen therapy and corticosteroids to the patient.
nursing management
Monitoring the patient’s arterial blood gas analysis.
Assess the patient’s respiratory status.
Provide semifolder position of the patient.
Provide oxygen therapy to the patient properly.
To auscultate the breathing sound of the patient.