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ELECTROLYTE IMBALANCES Flashcards

1
Q

What is the normal value of serum potassium

A

3.5mmol/L to 5.0mmol/L

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2
Q

What are the functions of Potassium?

A
  1. Helps with MUSCLE CONTRACTION esp. The heart, Lungs and skeletal muscle
  2. Helps with nerve impulse conduction.

NB : POTASSIUM IS THE MOST ABUNDANT INTRACELLULAR CATION.

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3
Q

What is Hypokalaemia?

A

Hypokalaemia simply means that serum potassium level is below 3.5mmol/L.

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4
Q

What are the drugs that causes Hypolalaemia when its excessively used and how do they do them?

A
  1. DIURETICS- esp the potassium-losing ones. Eg furosimde. It allow the kidney to excrete potassium through urination
  2. CORTICOSTEROIDS - Corticosteroids can cause hypokalaemia by increasing the excretion of potassium in the kidneys. This happens because corticosteroids can enhance the activity of a protein in the kidneys called the renal mineralocorticoid receptor, leading to increased potassium excretion in the urine. This effect can result in lower levels of potassium in the bloodstream, causing hypokalaemia.
  3. Inhaled Albuterol : It stimulates the movement of Potassium from the blood stream to the cells .
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5
Q

What are the conditions (diseases) that can cause hypokalaemia? And how does it happen ?

A
  1. Cushing Syndrome : Cushing syndrome can cause hypokalaemia by increasing the excretion of potassium in the urine. This occurs due to the excess production or administration of glucocorticoids, which are hormones that regulate various processes in the body. In Cushing syndrome, there is an elevated level of cortisol, a type of glucocorticoid, which can lead to increased renal excretion of potassium.

The high levels of cortisol in Cushing syndrome can enhance the activity of the mineralocorticoid receptors in the kidneys, similar to the effect of exogenous corticosteroids. This increased activity of mineralocorticoid receptors promotes potassium excretion in the urine, ultimately resulting in hypokalaemia.

  1. Kidney diseases that affect tubules responsible for reabsorption of potassium : Renal Tubular Acidosis (RTA), Bartter Syndrome and Chronic Kidney Disease (CKD).
  2. Hyperinsulinism : Hyperinsulinism can cause hypokalaemia by promoting the movement of potassium from the bloodstream into the cells. When there is an excess of insulin in the blood, such as in cases of hyperinsulinism, insulin facilitates the uptake of glucose into cells, including muscle cells. This process requires potassium to move alongside glucose into the cells to maintain the proper balance.

As insulin drives glucose and potassium into cells, it can lead to a decrease in the concentration of potassium in the bloodstream, resulting in hypokalaemia. This shift of potassium from the blood into the cells can disrupt the normal potassium levels in the body and lead to associated symptoms and complications of hypokalaemia.

Alkalosis : In alkalosis, the pH of the blood rises, leading to a decrease in hydrogen ions. To compensate for the increased alkalinity, hydrogen ions move from the cells into the bloodstream. In response, potassium ions move from the bloodstream into the cells to maintain electrical neutrality. This movement of potassium into the cells can worsen hypokalaemia, as potassium levels in the blood decrease further.

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6
Q

The other Causes of hypokalaemia that comes from the patient himself.

A
  1. Vomiting, diarrhoea
  2. Excessive diaphoresis.
  3. Fasting
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7
Q

Causes of hypokalemia arising from management of care of the patients.

A
  1. Keeping patients on Nil Per Os.
  2. Prolonged Nasogastric suctioning
  3. Wound drainage .esp gastrointestinal
  4. IV therapy with potassium deficit solutions
  5. Water intoxication.
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8
Q

Assessment findings that indicates Hypokalaemia

A

A. Cardiovascular 🫀: Thready weak irregular pulses, weak peripheral pulses, orthostatic hypotension. Dysrhythmias.

B. Respiratory 🫁 : shallow ineffective respirations that result from profound weakness of the skeletal muscles.

C. Neuromuscular 🧠🦾: Early signs ; Anxeity, Lethargy, confusion, coma
Late signs : Deep Tendon hyporeflexia, loss of tactile discrimination, paraesthesia ( Tingling, pricking, chilling, burning and numbness sensation )

D. Gastrointestinal: decreased motility, hypoactivity and absent bowel sounds, paralytic ileus.
Nausea, vomiting constipation and abdominal distention.

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9
Q

Laboratory and investigations that indicate hypokalaemia

A
  1. Serum potassium level : <3.5mmol/L
  2. EKG CHANGES: 1️⃣ ST Depressions
    2️⃣ SHALLOW, FLAT or INVERTED
    T WAVES
    3️⃣ Prominent U waves
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10
Q

What are Precautions and patient teaching when administering Potassium (oral/Iv) ?

A

A. Administer potassium supplements orally.

🔺the oral supplement( tablet/ capsule) may cause nausea and vomiting so encourage the patient to EAT BEFORE taking the medications

🔺DISCONTINUE medication if patient complained of abdominal distention or pain, nausea, vomiting, diarrhoea or abdominal bleeding.

🔺Liquid potassium supplement has UNPLEASANT TASTE. Educate the patient to take it with juice or another liquid.

B. Administer intravenous Potassium.
🔺Assess Renal function before administration of potassium and monitor intake and output during administration

🔺Never give Inj potassium as an IV push (bolus) , intramuscular or subcutaneous route

🔺With already prepared IVF that contains Potassium, rotate and invert the bag before administering and regularly during administration to ensure that potassium is evenly distributed.

🔺 Ensure IV bags containing Potassium are properly labeled

🔺the maximum infusion rate is 5-10mmol/hr. NEVER exceed 20mmol/hr under any circumstance.

🔺Clients should be placed on a cardiac monitor for cardiac changes it receiving more than 10mmol/hr and infusion should be controlled by an infusion device

🔺Potassium infusion causes PHLEBITIS. So access infusion site regularly for signs of phlebitis or infiltration. If it occurs, STOP 🚫 THE Infusion immediately.

🔺K+ replacement is SAFEST infused with a Central line because of increased incidence of IV infiltration

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11
Q

What are the other interventions of Hypokalaemia apart from oral (tablet/Suspension)and iv potassium replacement ?

A

1️⃣monitor electrolytes values
2️⃣Assess renal function before administering and
Monitor intake and output during administration

3️⃣Institute safety measures for patients experiencing muscle weakness

4️⃣if patient is on Potassium-losing diuretic( Furosemide, Torsemide,Bumetamide) , DISCONTINUE and a potassium-sparing diuretic(Spironolactone, Amiloride, Eplerenon, Triamterene) may be prescribed .

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12
Q

Name some foods that contains Potassium

A
  1. All meats
  2. Fish (salmon, cod, sardine, flounder)
  3. Soy products and veggie burgers
  4. Vegetables -winter squash
  5. Fruits -citrus, cantaloupe, Banana 🍌, Kiwi, Prunes, dried Apricot
    5.Milk and Yougurt
    Nuts
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13
Q

Must Know about IV potassium Administration.

A

K+ replacement is safest infused via a central line due to high incidence of infiltration .

NEVER administer K+ by IV push, IM or SC but rather it is always diluted And administered with an IV device .

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14
Q

What is Hyperkalaemia?

A

Serum Potassium level exceeding 5.0mmol/L

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15
Q

What is Hyperkalaemia?

A

Serum Potassium level exceeding 5.0mmol/L

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16
Q

What is Pseudohyperkalaemia?

A

Simply means serum Potassium value exceeds 5.0mmol/L but there are NO CLINICAL SIGNS of hyperkalaemia and this may be due to the wrongful way of redrawing the blood sample or there is cell lysis.
In this case, sample is redrawn and elaluated .

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17
Q

Causes of Hyperkalaemia.?

A
  1. EXCESSIVE POTASSIUM CONTAINING FOOD OR MEDICATIONS
    - potassium chloride or salt
    - Rapid infusion of potassium-containing fluids
  2. DECREASED POTASSIUM EXCRETION
    - Excessive intake of potassium-sparing diuretics
    - Kidney Diseases
    - Adrenal insufficiency: Addisons Disease ; Addison’s disease can lead to hyperkalaemia because it affects the adrenal glands, which are responsible for producing hormones like aldosterone. Aldosterone plays a crucial role in regulating potassium levels in the body. In Addison’s disease, the adrenal glands do not produce enough aldosterone, leading to potassium retention in the body and resulting in high levels of potassium in the blood, known as hyperkalaemia.
  3. MOVEMENT OF POTASSIUM FROM THE INTRACELLULAR FLUID COMPARTMENT TO THE EXTRACELLULAR FLUID
    a. Tissue Damage
    b.Acidosis
    C. Hyperuricemia
    d.hypercatabolism
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18
Q

Classical Assessment Findings of hyperkalaemia

A
  1. Dysrhythmias
  2. Decreased BP
  3. Slow , weak, irregular heartrate
  4. Hyperactive Bowel sounds
  5. Early : Muscle Twitches , cramps , Parasthesias
    late: Profound weakness , ascending flaccid paralysis in the arms and legs
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19
Q

EKG findings of Hyperkalaemia

A

EKG changes - Tall peaked T waves
Flat P waves
Widened QRS complexes
Prolonged PR intervals

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20
Q

What are the Interventions Given to a client with Hyperkalaemia?

A
  1. Monitor serum Potassium level closely in patients who are recieving potassium-sparing diuretics ,potassium oral supplement and IV therapy so that it would be DISCONTINUED when K+ Levels become high.
  2. Educate clients to avoid potassium rich foods and eat potassium restricted foods.
  3. Monitor renal function. If it is good, Prepare to administer potassium losing diuretics.
    When renal function is bad , Prepare to administer SODIUM POLYSTERENE SULPHONATE(oral/rectal) because it is a cation exchange resin that promote GIT sodium absorption and potassium excretion.
    Also, prepare pt for dialysis if potassium level is extremely high.
  4. When there is tall Peaked TWave, administer calcium gluconate slowly to avert myocardial excitability
  5. Prepare to administer hypertonic glucose together with regular/soluble insulin to move excess potassium to cells
  6. If patient is supposed to receive blood products as part of his management but has hyperkalaemia as well, he should recieve fresh blood if possible because older blood products releases potassium which will intend elevate K+ levels .
  7. Instruct client to avoid the use of salt substitutes or other potassium containing substances
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21
Q

What does Sodium do in the body?

A

Sodium is the MOST ABUNDANT extracellular cation which regulates water in the cells of a body .

Wherever sodium goes, water follows so it plays an important role in the BRAIN, NERVES AND MUSCLE CELLS .

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22
Q

Whats HYPONATRAEMIA?

A

Serum potassium level less than 135mmol/L
Sodium imbalances are usually associated with water imbalances .

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23
Q

Causes of hyponatraemia .

A
  1. Increased excretion of sodium. As in a. Excessive diaphoresis
    B. Diuretics
    C. Vomiting and Diarrhea
    D. Wound drainage esp. Gastrointestinal
    E. Kidney diseases
    F. Decreased secretion of aldosterone ( Addisons disease)
  2. Inadequate sodium intake.
    a. Fasting
    b. NPO
    C low salt diet
  3. Dilution of serum sodium .
    a. Excessive ingetion of hypotonic fluids or irrigation with hypotonic fluids.
    b. Kidney diseases
    C. fresh water drowning
    D. Syndrome of Inappropriate Anti-Diuretic Hormone Secretion (SIADHs)
    E. Hyperglycemia
    F. Heart failure
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24
Q

Signs and symptoms of A patient who has hyponatremia?

A

CNS
🔺 SEIZURES
Confusion, Coma, lethargy
Personality changes, Headache

Neuromuscular
- Generalized skeletal muscle weakness that is worse in the extremities.
- Diminished deep tendon reflexes

Integumentary
- DRY MUCUS MEMBRANES

Renal
- Increased urine specific gravity

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25
Q

What do you do if the cause of the patient’s Hyponatraemia is due to fluid volume deficit?

A
  1. IV sodium infusions are prescribed and administered to restore sodium content and fluid volume .
26
Q

What do you do if Patient hyponatremia is due to hypervolaemia

A

Goal : Bring sodium Up, water down.

  1. Administer sodium tabs and high-salt Diet.
  2. Restrict free water and give Osmotic diuretics eg. Mannitol
27
Q

What to do if a patient has severe hyponatremia ?

A
  1. Hospitalization may be required to closely monitor sodium levels while monitoring neurological status closely.
28
Q

What to do if a patient has severe hyponatremia?

A
  1. Hospitalization may be required to closely monitor sodium levels while monitoring neurological status closely.
29
Q

How to monitor neurological status ?

A

Monitoring neurological status involves assessing a person’s brain function to detect changes or abnormalities. Healthcare professionals use a variety of tools and techniques depending on the situation. Here’s an overview of key ways to monitor neurological status:

  • Purpose: Evaluates a person’s level of consciousness based on eye, verbal, and motor responses.
  • Scoring:
    • Eye-opening (1–4)
    • Verbal response (1–5)
    • Motor response (1–6)
  • A total score of 3–15 indicates neurological function, with 15 being fully alert and 3 being deep coma.
  • PERRLA: Pupils should be Perfectly Equal, Round, Reactive to Light, and Accommodating.
  • Observe for abnormal pupil size or reaction to light, which may indicate increased intracranial pressure (ICP) or brain injury.
  • Observation: Is the patient alert, responsive, and oriented to person, place, time, and situation?
  • Changes in LOC can indicate worsening neurological status or conditions like stroke, trauma, or infection.
  • Assess the strength and coordination of muscle movements.
  • Test for symmetry in movements (e.g., hand grasps, leg raises) to detect focal neurological deficits.
  • Testing: Use light touch, pinprick, and temperature tests to assess the patient’s ability to feel sensations.
  • Abnormal findings could indicate nerve or brain damage.
  • Monitor for changes in blood pressure, pulse, and respiratory rate. Abnormal patterns, such as Cushing’s triad (high BP, bradycardia, irregular breathing), may indicate rising intracranial pressure.
  • Assess the 12 cranial nerves responsible for a wide range of functions, including vision, facial movements, and swallowing.
  • Abnormal responses can point to specific areas of brain dysfunction.
  • Test balance and coordination with activities like finger-to-nose or heel-to-shin tests.
  • Monitors brain wave activity, useful for detecting seizures or abnormalities in brain function.
  • Scans provide detailed images of the brain to detect tumors, bleeds, or structural changes.
  • For patients at risk of brain swelling, an ICP monitor can track pressure levels inside the skull.
  • Assess memory, language, problem-solving, and decision-making to evaluate higher brain functions.

Regular monitoring, especially in cases of head injury, stroke, or altered mental status, is critical for detecting early signs of neurological deterioration.

30
Q

You should avoid correcting Hyponatraemia Quickly, why that?

A

Osmotic demyelination syndrome (ODS) is a neurological disorder that results from the rapid correction of severe hyponatremia (low sodium levels in the blood). The disorder affects the myelin sheaths of nerve cells, primarily in the central part of the brain called the pons, although other areas can also be involved.

Key Aspects of Osmotic Demyelination:

1.	Cause:
•	ODS typically occurs when sodium levels are corrected too quickly in patients who have had chronic hyponatremia (a prolonged period of low sodium).
•	The brain adapts to low sodium levels by reducing its osmolality, so when sodium levels are rapidly increased, the brain cannot adjust quickly, leading to dehydration and damage to brain cells and their myelin sheaths.
2.	Myelin Damage:
•	Myelin is the protective covering of nerve fibers (axons), and damage to this sheath can disrupt the transmission of electrical signals in the nervous system.
•	The damage primarily affects the pons (leading to central pontine myelinolysis) but may extend to other areas, resulting in extrapontine myelinolysis.
31
Q

You should avoid correcting Hyponatraemia Quickly, why that?

A

Osmotic demyelination syndrome (ODS) is a neurological disorder that results from the rapid correction of severe hyponatremia (low sodium levels in the blood). The disorder affects the myelin sheaths of nerve cells, primarily in the central part of the brain called the pons, although other areas can also be involved.

Key Aspects of Osmotic Demyelination:

1.	Cause:
•	ODS typically occurs when sodium levels are corrected too quickly in patients who have had chronic hyponatremia (a prolonged period of low sodium).
•	The brain adapts to low sodium levels by reducing its osmolality, so when sodium levels are rapidly increased, the brain cannot adjust quickly, leading to dehydration and damage to brain cells and their myelin sheaths.
2.	Myelin Damage:
•	Myelin is the protective covering of nerve fibers (axons), and damage to this sheath can disrupt the transmission of electrical signals in the nervous system.
•	The damage primarily affects the pons (leading to central pontine myelinolysis) but may extend to other areas, resulting in extrapontine myelinolysis.
32
Q

If Hyponatraemia is caused by SIADH, what do you do ?

A

Suggest medications that antagonise ADH.
They are VAPTANS

Eg. Tolvaptan, conivaptan, Lexivaptan, Mozivaptan .

33
Q

What is the Key information to know about Lithium and hyponatremia

A

Monitoring lithium levels in a patient with hyponatremia is crucial because sodium and lithium are closely related in how they are handled by the kidneys. Any change in sodium levels can significantly affect lithium pharmacokinetics and increase the risk of lithium toxicity.

For a patient who is already on lithium but has hyponatremia, it is important to monitor Lithium toxicity because the kidney tries to reabsorb sodium during hyponatremia which would intend reabsorb lithium as well.

The normal lithium level is 0.6 to 1.2 mmol/L

34
Q

What is Hypernatraemia

A

Hypernatraemia simply means serum sodium level exceeds 145mmol/L

35
Q

What are the causes of hypernatraemia?

A
  1. Decreased sodium excretion. As in;
    a. Excessive intake of corticosteroids
    b. Cushing syndrome
    c. Hyperaldosteronism
    d. Kidney disease.
  2. Increased sodium intake
    a. Excessive oral sodium ingestion
    b. Excessive administration of Sodium containing IV fluids
  3. Decreased water intake
    a. NPO
    b Fasting
  4. Increased water loss
    a. Increased rate of metabolism
    b. Hyperventilation
    c. Infection
    d. Excessive Diaphoresis
    e. Diabetes Insipidus
    F. Watery diarrhoea
36
Q

Name the must know assessment findings noted on a patient with hypernatraemia.

A

CNS: 🔺Altered cerebral function
Integumentary:🔺Dry and sticky tongue & mucus membrane. 2. Dry and flushed skin.

37
Q

Name some interventions given to a patient with hypernatraemia.

A

Goal: Find the cause of >Na+ and treat accordingly.

  1. Fluid loss? , Give IV infusions eg D5W. But monitor sugars in a patient with DM .
  2. Inadequate renal excretion? Diuretics: Thiazide diuretics, loop diuretics.
  3. Too much sodium intake? Restrict them
38
Q

What are some facts about calcium??

A

🔺 Calcium is Absorbed in the GIT, stored in the bones and finally, its excreted by the kidneys.

🔺Calcium is controlled by the parathyroid hormone and Cholecalciferol( Vitamin D)

🔺 Calcium and phosphate has inverse relationship with each other

🔺 Magnesium and calcium are like best fiends in terms of the hormones that release them, storage and absorption BUT calcium is found outside cells and magnesium is in the cells.

39
Q

What are some facts about calcium??

A

🔺 Calcium is Absorbed in the GIT, stored in the bones and finally, its excreted by the kidneys.

🔺Calcium is controlled by the parathyroid hormone and Cholecalciferol( Vitamin D)

🔺 Calcium and phosphate has inverse relationship with each other

🔺 Magnesium and calcium are like best fiends in terms of the hormones that release them, storage and absorption BUT calcium is found outside cells and magnesium is in the cells.

40
Q

What is the normal level of calcium in the blood?

A

9-10.5mg/dl( 2.25 to 2.75mmol/L

41
Q

What is the normal level of calcium in the blood?

A

9-10.5mg/dl( 2.25 to 2.75mmol/L

42
Q

What are the causes of Hypocalcemia?

A
  1. Inhibition of calcium from absorbing in the GIT
    a. Malabsorption syndrome : Cohrons disease, Celiac Spuree
    b. Inadequate calcium intake
    c. Lactose intolerance.
    d inadequate vitamin D intake
    e. End-stage Kidney disease
    f. Alcoholism
    g anorexia and bulimia nervousa
  2. Increased calcium excretion
    a kidney disease, polyuric phase
    b. Diarrhoea
    c. Stearrhoea
    d. Gastrointestinal wound drainage
  3. Conditions that decrease the ionized fraction of calcium.
    a Hyperproteinemia/ Hyperalbumimaemia
    b. Alkalosis
    c Medications. Such as calcium chelators/Binders
    d. Acute pancreatitis
    e. Hyperhosphataemia
    f removal or destruction of the parathyroid gland
43
Q

Common signs and symptoms of Hypocalcemia

A

🔺Patient is irritable

Seizure, weak bones, positive trousseau’s and Chvostek’s signs

EKG changes: Prolonged ST and QT intervals

44
Q

How does high albumin levels affect calcium levels in the blood?

A

In hypoalbuminaemia/hyperproteinaemia, there is too much albumin the blood which calcium binds to, making the active ones (calcium ) in the blood become few which leads to hypocalcemia .

45
Q

What are the interventions given to a patient with hypocalcemia

A

1 Check albumin levels in the blood and when it is low, calcium levels should be corrected by administration of oral calcium supplement or IV.
When administering the IV, warm the infusion to body Temperature and administer SLOWLY while the Patient has been placed on an EKG monitor to monitor for signs of hypercalcemia.
Also, check the infusion site for infiltration .

  1. Administer drugs that increases calcium absorption.
    a. Aluminium hydroxide
    b. Vitamin D
  2. 🔺initiate seizure precautions and provide a very quiet environment to reduce environmental stimuli

🔺 Because of weakness in the bones, move patient slowly and carefully while observing them for signs for a pathological fracture

  1. Keep 10% calcium gluconate available for treatment of acute calcium deficit
  2. Instruct them to eat food high in Calcium eg Tofu, diary products etc
46
Q

What is Hypercalcemia?

A

Serum calcium level greater than 2.75mmol/L(10.5mg/dl)

47
Q

What are the causes of hypercalcemia?

A
  1. Increased Intake of Calcium and vitamin D
  2. Kidney disease that causes retention of calcium
  3. THIAZIDE DIURETICS🔺
  4. hyperparathyroidism
  5. Hyperthyroidism
  6. Malignancy
  7. Immobility: weak bones, increased release of calcium
  8. Addison disease
  9. Dehydration
  10. LITHIUM INTAKE 🔺
48
Q

Assessment Findings in Hypercalcaemia? 🐢

A

🔑 EVERYTHING IN THE BODY SYSTEMS SLOWS DOWN.

Neuro- lethargy, Coma, Disorientation, profound muscle weakness, Diminished or absent deep tendon reflexes.

GIT: Decreased motility and hypoactive bowel sounds, Anorexia, Nausea abd distension, Constipation.

Resp: Ineffective respiratory movement

Cardio: bradycardia, DVT, Cyanosis

Urinary: Renal Calculi

49
Q

Interventions given to Clients with Hypercalacemia

A

Look for cause and deal with it!!!

Dehydration? Give isotonic fluids as prescribed

Too much calcium food, IVs and Oral? Discontinue them.

They have the potential to get PATHOLOGICAL FRACTURE, keep them safe.

They have the potential to get KIDNEY STONES, monitor for signs like flank or abdominal pain, and strain urine to check for stones.

On drugs like Thiazide diuretics? Anticipate for a change to loop diuretics.

Lithium? Adjust dosage.

DRUGS GIVEN TO COUNTERACT THE ALREADY EXISTING HYPERCALCAEMIA ARE ; 🔺Phosporus
🔺Calcitonin, 🔺Biphosphanate.

Severe and all interventions aint giving fruitful results? Recommend Dialysis

50
Q

Must know about CALCIUM IMBALANCES?

A

Clients are at risk of pathological fracture so handle them with care ‼️

51
Q

Quick Facts About Magmesium in relation to calcium

A

Magnesium and calcium are closely related when it comes to how they are absorbed, magnesium is required for the release of parathyroid hormone

BUT Calcium is required for muscle contraction and Magnesium is required for muscle relaxation that is why CALCIUM GLUCONATE IS THE ANTIDOTE FOR HYPERMAGNESEMIA ‼️

Magnesium is found in the intracellular fluid compartment whilst calcium is in the extracellular compartment

52
Q

The normal Magnesium level is

A

1.8 to 2.6mEq/dl (0.74 to 1.07mmol/l

53
Q

Causes of Hypomagnesemia

A

Issues related to its absorption:
Malnutrition, starvation, vomiting, diarrhoea, Crohn’s disease, celiac disease, malabsorption syndrome

Issues related to too much excretion:
alcoholism, diuretics

Issues related to movement from the serum to cells:
HyperInsulinism / insulin administration
Hyperglycemia
Sepsis

54
Q

Assessment findings of Hypomagnesemia ?

A

🔺 REMEBER THAT MG IS NEEDED IN MUSCLE RELAXATION, hence if its low, means muscles can’t relax but will be Agitated

Neuro: Hyperreflexia, Twitches, paresthesias, POSITIVE TROUSSEAUS &CHOVSTECKS SIGNS, Tetany, seizures.

CNS: irritability, confusion

Cardio; Tachycardia, TORSADE DE POINTS. HPT

RESP: shallow resps

ECG changes : TORSADE DE POINT, tall Twaves, depressed ST segments

55
Q

Interventions given to clients with Hypomagnesemia .

A

🔺 ALWAYS REMEMBER THAT HYPOCALCEMIA ACCOMPANIES HYPOMAGNNESEMIA SO INTERVENTIONS SHOULD AIM AT RESTORING CALCIUM LEVELS.

At risk of seizure 🔺, initiate seizure precautions.

magnesium sulphate is prescribed and give it slowly via IV route. IM route causes pain&tissue damage and monitor for signs of Hypermagnesemia which is DIMINISHED DEEP TENDON REFLEXES during administration of the drug.

Oral magnesium supplements: causes diarrhoea, hold when severe diarrhoea occurs

Increase foods high in mg : dark green leafy vegetables, milk, whole grains

🔑 when TORSADE THE POINTE IS SEEN ON THE MONITOR, Give mgsO4 faster else cardiac status will be lost.

56
Q

What is Hypermagnesemia

A

Too much magnesium in the blood. Mg level exceeding 1.07mmol/L

57
Q

Causes of Hypermagnesemia?

A

Caused by either a problem with its excretion or too much intake of it.

  1. Excessive intake of mg containing foods, drugs or IV administration
  2. Kidney is compromised and cannot excrete magnesium hence retaining them.
58
Q

Assessment findings of Hypermagnesemia ?

A

🔺Remember that magnesium is responsible for muscle relaxation so in Hypermagnesemia, the muscles become Too RELAXED.

Classical signs is DIMINISHED DEEP TENDON REFLEXES.

CNS: drowsiness, lethargy that progresses to coma.

Cardio: Bradycardia, dysrhythmia, cardiac arrest, hypotension.

Resp: respiratory insufficiency, when the skeletal muscle of respiration is involved.

EKG changes : prolonged PR interval, widened QRS complexes

59
Q

Interventions given to pts with Hypermagnesemia.

A

Stop foods, and drugs that are rich is magnesium

Diuretics to increase magnesium excretion

🔺CALCIUM GLUCONATE TO COUNTERACT THE EFFECT OF TOO MUCH MAGNESIUM IN THE BLOOD.

60
Q

Facts about Phosphorus

A

It is the major cellular metabolism and energy producer (Adenosine triphosphate. ATP) and makes up the cell membrane phospholipid bilayer.

It has an Inverse relationship with Calcium.

Normal serum phosphorus level is 3.0 to 4.5mg/dl

61
Q

Causes of hypophosphataemia?

A

Inadequate phosphorus intake: starvation, Malnutrition.

Increased phosphorus excretion:
1. hyperparathyroidism ,

  1. malignancy ( the release of Fibroblast Growth Factor 23 impairs phosphate re absorption in the kidneys, leading to phospaturia )
  2. Use of magnesium / aluminium Hydroxide based antacid .

Intracellular fluid shift.: hyperglycaemia ( insulin administration)

Respiratory Alkalosis

62
Q

Intervention of hyperphospataemia

A

Intervention entails the management of hypocalcemia.

Administer phosphate binding medications that increase fecal excretion of phosphorus by binding them from foods in the GIT.
🔺Sevelamer Carbonate ( Renvela) & Sevelamer hydroxide (Renagel) but give them stool softeners & laxatives as Sevelamer causes constipation.

Instruct the client to avoid phosphate containing food and medications ( laxatives and enemas )

Instruct client to take phosphate binders with food of immediately after food.

FLUID AND ELECTROLYTES (4 decks)

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