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Nursing Science (section 3) > Electrolytes > Flashcards

Electrolytes Flashcards

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1
Q

Hypokalemia ECG changes?

A

“T wave is pushed down”
Inverted T waves
Depressed ST segment
U waves

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2
Q

Potassium deficit caused by?

A

Loop diuretics (furosemide) are potassium wasting

Corticosteroids (retain sodium, therefore waste potassium)

Too much insulin (insulin makes potassium move inside the cell)

Cushing’s ( high cortisol, therefore increases sodium and decreased potassium)

Starvation

Losing through GI suctioning or vomiting

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3
Q

What is Addison’s?

A

Body doesn’t produce enough aldosterone and cortisol, therefore low sodium (and water) and high potassium

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4
Q

What’s in common with AF, junctional rhythms, ventricular rhythms?

A

Absent P waves

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5
Q

What do hypermagnesemia and hyperkalemia do to the QRS?

A

Widen it

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6
Q

Do you bolus K+ IV?

A

Never

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7
Q

Foods high in K+?

A

“POTASSIUM”

Potatoes 🥔 pork 🍖
Oranges 🍊
Tomatoes 🍅
Avocados 🥑
Spinach 🥗
Strawberries 🍓
Fish 🐟
Mushrooms 🍄
Melon (cantaloupe)🍈

And 🥕 , raisins and 🍌

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8
Q

S+S hypercalcemia?

A

“WEAK”

  • weakness of muscles (profound) due to calcium stabilising the sodium channels too well, that there is less depolarisation and excitability.
  • ECG changes (shortened QT interval from decrease in depolarisation potential/more stable membranes and prolonged PR interval)
  • Absent reflexes, absent minded/altered mental status, abdominal distension (constipation, decreased motility)
  • Kidney stone formation
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9
Q

ECG changes of hyperkalemia?

A

“T wave is pulled up”
Flat P waves, prolonged PR intervals, wide QRS and tall, peaked T-waves

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10
Q

Thiazide Diuretics do what to sodium?

A

Cause hyponatremia

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11
Q

What do corticosteroids, cushing’s and hyperaldosteronism have in common?

A

Risk for hypermatremia

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12
Q

Abnormal rhythms from hypokalemia?

A

Low ECF K+ means more Na+, and increased myocardial excitability.
- arrhythmias
- ectopics
- AF, VT, VF, Torsades du Points

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13
Q

Rhythm abnormalities from hyperkalemia?

A

Increased ECF K+ means decreased Na+, there reduced myocardial excitability and depression of pace-making and conduction
- bradycardia
- conduction blocks
- cardiac arrest

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14
Q

Causes of hyperkalemia

A

The body CARED too much about K+

Cellular movement ICF to ECF (burns, tissue damage, rhabdomyolysis: breakdown of muscle with trauma)

Adrenal insufficiency w Addisons (low sodium)

Renal failure (high BUN and creatinine, not excreting, may need dialysis)

Excessive intake

Drugs (K+ sparing diuretics eg spironolactone, ace inhibs, nsaids)

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15
Q

S&S hyperkalemia

A

MURDER

  • Muscle weakness (less Na+ therefore reduced cell excitability/less K+ inside the cell, so reduced excitability)
  • Urine output little or none (renal failure)
  • Respiratory failure (muscle weakness)
  • Decreased cardiac contractility (weak pulse, low heart rate)
  • Early on: muscle twitches/cramps
  • Rhythm changes (pull the “T” waves up: peaked t waves, flat p wave and long pr int and QRS complex) 🤩
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16
Q

Foods Rich in potassium?

A

POTASSIUM

Potatoes, pork
Oranges
Tomatoes
Avocado
Spinach
Strawberries
Fish
Mushrooms
Musk melons - cantaloupe

Plus carrots, raisins, bananas

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17
Q

Nursing interventions for hyperkalemia

A

Monitor cardiac, respiratory, renal and GI status
Stop if potassium and cease supplements
Potassium restricted diet
Prepare patients for dialysis
Kayexalate po or pr, which promotes GI sodium reabsorption and causes potassium excretion
May order k+ wasting drugs like lasix or hydrochlororhiazide.
Administer a hypertonic solution of glucose and regular insulin to pull potassium in to cells

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18
Q

Causes of hypokalemia

A

body is trying to DITCH potassium

Drugs (loop diuretics - frusemide, laxatives, glucocorticoids, hydrocortisone)

Inadequate intake

Too much water intake

Cushing’s syndrome (causes kidneys to excrete potassium)

Heavy fluid loss (NG suction, vomiting, diarrhoea, wound drainage)

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19
Q

S&S hypokalemia

A

7 L’s (low) slow and low

Lethargy and confusion
Low shallow respirations
Lethal cardiac dysrhythmias (st depression, shallow t wave, projected u wave)
Lots if urine (frequent UO, kidneys are unable to concentrate the urine)
Leg cramps
Limp muscles and decreased deep tendon reflexes
Low blood pressure (severe) and heart rate)

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20
Q

Nursing interventions for hypokalemia

A

Watch cardiac rhythm, RR, neuro, GI, UO, and renal status (BUN and Creatinine)

Watch Mg, who’ll also decrease and hard to get K+ up if Mg low.

Watch gluc, sodium, calcium

Oral K+ supps with food (can cause GI upset) for 2.5 - 3.5

IV for less than 2.5. NEVER via push, IM or SC routes. Give slowly. Monitor ECG. Can cause phlebitis.

Don’t give lasix, thiazides (wastes more potassium)
Don’t give digoxin as can cause toxicity (dig works by ^intracellular sodium to cause ^contractility, and there is already more sodium with hypokalemia).

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21
Q

Causes of hypernatremia?

A

HIGH SALT

Hypercortisolism (Cushings) because cortisol works to maintain BP in times of stress. Plus hyperventilation

Increased intake of salt

GI feeding without adequate water supplements

Hypertonic solutions (and corticosteroids)

Sodium excretion decreased (renal issues)

Aldosterone overproduction (hyperaldosteronism) aka Conn’s. ** opposite of Addison’s

Loss of fluids (dehydration) infection (fever) sweating, diarrhoea, burns, diabetes insipidus **low levels of ADH therefore excessive sodium and urine output.

Thirst impairment

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22
Q

S&S hypernatremia

A

No FRIED foods for you! Too much salt. This is from increased muscle contractions and nerve impulses.

Fatigue
Restless, really agitated (confused, CNS changes)
Increased reflexes (progress to seizures and coma)
Extreme thirst (BIG sign)
Decreased UO, dry mouth/skin.

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23
Q

Nursing interventions for hypernatremia

A

Restrict sodium intake!
Keep pt safe, they will be confused and agitated
Isotonic or hypotonic solutions (0.45%NS) slowly, risk of cerebral edema as fluid shifts back into cells.
Education

24
Q

SIADH what is it?

A

Syndrome of inappropriate (increased) antidiuretic hormone secretion

ADH aka vasopressin retains water in the body as well as causing vasoconstriction. Retaining water dilutes sodium.

25
Q

What’s the Maggie saying to remember common labs?

A

Little Maggie is 1.6-2.6 years old (Mg ++). She ate 3.5-5 bananas (K+) and drank 8.5-10.5 oz of milk (Ca++). Then she took a 135-145 minute nap after swimming in the ocean (Na+)

26
Q

What does sodium regulate?

A

Water in and out of the cell
Muscle contraction
Nerve impulses

27
Q

Vomiting, GI suction (NGT), diarrhoea and sweating cause what?

A

Hyponatremia. There is a lot of sodium in gastric juice (as well as potassium!)

28
Q

What is Addisons?

A
  • Low aldosterone (and cortisol)
  • Normally, aldosterone retains sodium and water to maintain blood volume and pressure
  • low aldosterone means you lose sodium & water but retain potassium
29
Q

What is SIADH? What does it do to sodium?

A

Syndrome of inappropriate (HIGH) anti diuretic hormone.

  • ADH retains sodium and water
  • too much dilutes the blood causing relatively low sodium
30
Q

Causes of sodium dilution?

A

CHF
SIADH
too much hypotonic IVT
renal failure

31
Q

S&S hyponatremia

A

“SALT LOSS”

  • seizures and stupor (decrease in LOC eg confusion, assoc. with slow nerve transmission and swelling of brain cells)
  • abdominal cramping
  • lethargy
  • tendon reflexes diminished
    trouble concentrating
  • loss of urine
    loss of appetite
  • orthostatic hypotension
    overactive bowel sounds
  • shallow respirations (late sign) due to skeletal muscle weakness
  • spasm of muscles
32
Q

What does Cushings do to sodium levels?

A

High cortisol, stress hormone (maintains BP in inflammatory process for eg)
- too much causes sodium retention and inversely potassium wasting

33
Q

What is Conn’s syndrome?

A

Aka primary aldosteronism and opposite of Addisons.

  • high aldosterone means sodium & water retention and potassium excretion
34
Q

What role does Chloride play in the body?
What’s it’s relationship with sodium?

A

Sticks with Sodium! ** NaCl**
If there’s a loss of sodium there’s generally a loss of chloride, with a lot of overlapping causes, and S&S.

  • acid base balance (relationship with bicarb)
  • digestion (need it to make hydrochloric acid)
  • fluid balance (with the help of sodium)
35
Q

What controls chloride levels?

A

Kidneys, sweat and GI juices

36
Q

Hypochloremia caused by

A

GI related vomiting, loss of gastric juice (suctioning) and ileostomy (bowel effluent rich in NaCl)

Diuretics “thiazides” same as hyponatremia

Burns

Cystic fibrosis (lose a lot of chloride through sweat)

Fluid volume overload dilutes the chloride (heart failure, SIADH - retaining water)

Metabolic alkalosis (high bicarbonate, therefore low chloride as they have opposite relationships)

37
Q

How do chloride and bicarbonate react?

A

They shift into and out of red blood cells to influence gas exchange

38
Q

S&S hypochloremia

A

Same as hyponatremia!

Eg Dehydration S&S (^heart rate, decreased blood pressure, fever, vomit, diarrhoea, lethargy)

39
Q

Causes of hyperchloremia

A

Increased sodium intake (hypertonic fluids)

No water intake or losing too much (causes dehydration and highly concentrated sodium and chloride in the blood)

Decreased bicarbonate (^chloride) eg diarrhea

Conn’s syndrome (^aldosterone) therefore retaining sodium therefore chloride (and excreting potassium)

Corticosteroids (retaining sodium to keep BP up)

Metabolic acidosis due to low bicarbonate therefore high chloride

Renal issues

40
Q

S&S hyperchloremia

A

Similar to hypernatremia and acidosis

41
Q

Function of calcium, & normal level?

A

Health of bones and teeth
Muscle and nerve conduction
Clotting

8.5-10.5mg/dL

42
Q

Where is calcium absorbed and stored? What are the essentials needed to absorb calcium?

A

In the gut, and then stored in the bones.

Vitamin D to absorb calcium.
Calcitonin produced by the thyroid gland, parathyroid hormone (PTH) produced by the parathyroid glands.

If these glands are harmed by trauma or surgery there can be issues with the calcium levels

43
Q

Causes of hypocalcemia?

A
  • decreased PTH (thyroidectomy)
  • decreased intake (lactose intolerance)
  • low vitamin D
  • CKD (wasting too much calcium)
  • Bisphosphonates (meds used to treat osteoporosis by slowing down the bones release of calcium into the bloodstream)
  • Aminoglycosides (antibiotics that end in “mycin”, cause Ca++ wasting via kidneys)
  • Anticonvulsants (phenobarbital, phenytoin: affect vitamin D levels)
44
Q

S&S hypocalcemia?

A

“CRAMPS” as muscles and nerves are affected

  • convulsions (low calcium in the extracellular space causes increased excitability, resulting from more unstable sodium channels therefore easier depolarisation)
  • reflexes hyperactive
  • arrhythmias (prolonged QT interval from calcium channels staying open for longer)
  • muscle spasms in calves/feet (tetany)
  • positive signs (chvostek’s: facial twitch when tapping cranial nerve 7 & trousseau’s: inflate BP cuff to >SBP for 3 min, wrist and hand will flex but not fingers)
  • sensation of tingling/numbness in fingers and toes (parasthesia)
45
Q

Causes of hypercalcemia?

A
  • Hyperactive PTH releases too much calcium into the blood from bones
  • Excess Vitamin D, supplements
  • Bone cancer
  • Thiazide diuretics promote calcium reabsorption
  • Lithium (increases PTH secretion)
46
Q

What does magnesium do in the body and it’s normal range?

A

1.5-2.5 mg/dL

Resides mainly IN the cell (with potassium) and is used to activate ATP for the sodium potassium pump (bringing 3 sodium into the cell and sending 2 potassium out during depolarisation).

Plays a role in muscular contraction (maintaining blood pressure in the vessels and at the neuromuscular junction)

Normally, there are calcium channels on the neuron, that are held stable by magnesium (binding to the site and not letting too much calcium into the neuron to fire neurotransmitter to cause the muscle to fire)

47
Q

Causes of hypomagnesemia?

A

Not consuming enough Mg++
Other electrolyte imbalances (calcium or potassium tend to throw magnesium off too)
Malabsorption in small intestine
PPI (proton pump inhibitor: prevent magnesium reabsorption as a side effect of inhibiting the H+/K+ ATPase proton pump)
Alcoholism (reduces reabsorption of magnesium)

48
Q

S&S hypomagnesemia?

A

“TWITCH” as everything will be hyperactive/excited

  • Trousseau’s and Chvosteks sign (also related to hypocalcemia)
  • weakness
  • increased deep tendon reflexes
  • torsades de pointes (alcoholism) / tetany / seizures / EKG changes related to low Ca++ and K+
  • calcium and potassium levels low
  • hypertension (magnesium helps keep BP normal and having low Mg++ can cause increased vessel contraction)
49
Q

What is Torsades de Pointes?

A

A polymorphic ventricular tachycardia that can terminate spontaneously or degenerate into VF, caused by excess of positive ions inside the cell = prolonged repolarisation phase PLUS an ectopic in this repol phase. Different to VF as it can spontaneously resolve.

50
Q

Causes of Hypermagnesemia?

A

Rare condition:
Trying to correct magnesium deficiency or OB patient with pre-eclampsia who’s receiving magnesium sulfate (monitor levels and check DTR’s to ensure they aren’t absent)

Renal function can cause magnesium build up in the blood.

51
Q

S&S hypermagnesemia?

A

“LETHARGY” symptoms only present in severe cases

  • lethargic (profound)
  • ECG changes (prolonged PR/QT intervals and wide QRS: slow conduction)
  • tendon reflexes absent/grossly diminished
  • hypotension
  • arrhythmias (bradycardia/heart blocks)
  • red and hot face (flushing)
  • GI issues (nausea and vomiting)
  • impaired breathing (skeletal muscle weakness)
  • confusion (neurological impairment)
52
Q

Function of phosphate, where is it stored, and normal range?

A

Teeth and bone building, as well as a component of DNA, RNA and ATP.
Stored in bones
2.5-4.5 mg/dL

53
Q

Causes of hypophosphatemia?

A
  • Aluminium antacids (neutralises excess gastric acid) can block absorption of phosphate from food
  • Starvation/refeeding syndrome (which happens after starvation, refeeding can increase glucs. Insulin uses phosphate to change glucose into energy, therefore this syndrome can cause low phosphate stores)
  • Overactive parathyroid: too much inhibition on kidneys reabsorbing phosphate, wasting too much phosphate in urine.
  • Low vitamin D, as vit D helps absorb phosphate.
54
Q

S&S hypophosphatemia?

A

“BONE”

  • bone pain and fractures
  • osteomalacia (bone softening/leg bowing “rickets” in children affecting growth
  • neuro status changes (irritability, confusion, seizures, related to ATP depletion)
  • erythrocyte destruction aka haemolytic anemia
55
Q

Causes of hyperphosphatemia?

A
  • overuse of phosphate containing laxatives (fleet enema) therefore watch in patients with renal failure
  • excess Vitamin D
  • rhabdomyolysis (muscles become damaged from trauma (eg) and break down, the contents of the muscle go to the kidneys, and damage kidneys)
  • hypoparathyroidism (instead of normally being able to inhibit phosphate reabsorption via the kidneys, body will retain phosphate)
56
Q

S&S hyperphosphatemia?

A

Similar to HYPOcalcemia

  • convulsions
  • hyperactive reflexes
  • arrhythmias
  • muscle spasms (calves/feet, tetany, seizures
  • pruritus (itching, renal failure)
  • trousseau’s and Chovstek’s

Nursing Science (section 3) (5 decks)

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