Electrolytes Flashcards

1
Q

Potassium

general

A

In kidneys, the majority of filtered K+ is resorbed in the proximal tubular system

Selective secretion or absorption in the distal tubule determines net K+
Limit of renal K+ excretion 10 mEq/ L
Excretion affected by circulating Aldosterone, cellular and extracellular K+, tubular urine flow rates, & acid-base disturbances

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2
Q

potassium

normal range

A

3.5-5.0 mEq/L

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3
Q

Potassium

Function

A

NA+/K+-ATPase
Nerve transmission
Skeletal muscle contraction
Cardiac muscle function
Renal and fluid ion balance
Potassium channels
Nerve action potentials

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4
Q

Hypokalemia

causes

A

K level < 3.5 mEq/L

Hypokalemia occurs from one of 3 pathologic mechanisms:
Deficient intake
Anorexia, alcohol use disorder

Increase excretion
Diuretics, Hyperglycemia, 1° or 2° Aldosteronism, Elevated ACTH, Corticosteroid excess

GI loss
Colon, rectum- high K content
Gastric- hypokalemic hypochloremic met. Alkalosis

Other: Licorice, Acute Leukemia, Iatrogenic

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5
Q

Hypokalemia

Clinical Symptoms

A

Skeletal muscle weakness/malaise
Fatigue
Weakness/cramps
Paresthesias
Paralysis (flaccid paralysis if severe)
N/V/C – paralytic ileus
Polydipsia
Polyuria/Nocturia

Usually asymptomatic until < 3.0 mEq/L

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6
Q

Hypokalemia

Clinical Signs

A

hypotension
Diminished/ absent DTRs

Cardiac abnormalities-EKG changes
Ventricular arrhythmias, flatten T waves, U waves, depressed ST segments, and ventricular ectopy, cardiac arrest

May be acidotic

Usually asymptomatic until < 3.0 mEq/L

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7
Q

hypokalemia

ECG changes

A

Although the ECG is a fairly good indicator of hyperkalemia, it is not reliable for detecting hypokalemia. However, when ECG changes are seen they tend to be those that are shown in this figure.

A : normal
B : shows flattening of the T wave, which is the earliest change
C and D :A “U wave” then develops, associated with ST-T wave flattening and sometimes slight ST depression. A “pseudo P-pulmonale” pattern may be seen.
E and F : ST depression is more noticeable and the U wave increases in amplitude until ultimately the U wave overtakes the T wave. At this point distinguishing between the T wave and U wave may be almost impossible (“Q-U” prolongation).

Note - The ECG changes of hypomagnesemia are identical to those of hypokalemia.

with K think t wave

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8
Q

Hypokalemia

Treatment

A

Replace potassium (10 mEq of KCl will increase serum K approximately 0.1 mEq/L)

Orally (preferred)
Normal renal fxn
Do not exceed 40 mEq/h

IV (if emergent)
Do not exceed 10 mEq/h
Repeat as often as necessary
ECG monitor, mandatory if rate > 10 mEq/h
Avoid dextrose solutions-will drop K level

Rapid correction
Hyperkalemia
Arrhythmias

Make sure Mg is normal. If not, correct hypomagnesemia (K+ will normalize)

Correct hypocalcemia and hypokalemia together

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9
Q

hypokalemia

A

if oral - should take 4 hours for K/ 24 hours for Mg
if IV - should take 1 hour for K/

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10
Q

Hyperkalemia

general and causes

A

K level > 5.2 mEq/L

Physiologic Response
Rapid urinary excretion

Etiology
Impaired renal potassium excretion
Hypoaldosteronism
Shift from inside cells to extracellular fluid
Medications : ACE/ARB/Spironolactone

Laboratory error:
Hemolysis
Patients with hyperkalemia and no kidney injury/disease who are not taking medications that cause hyperkalemia should have repeat blood draw to rule out spurious hyperkalemia

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11
Q
A
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12
Q

Hyperkalemia

Clinical Manifestations

A

Peripheral muscle weakness and fatigue
SOB/Respiratory paralysis

CARDIAC abnormalities
EKG with peaked T waves at K of 6.0-7.0
flat p wave
increased PR interval
decreased QT interval
wide QRS
depressed ST segment
K of 8.0 or higher the QRS merge with T , V-fib, cardiac arrest

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13
Q

hyperkalemia

A

A: normalB: shows peaking of the T wave, which is the earliest change (K+ about 6-7 mEq/L)

C: The T wave becomes taller and more peaked (K+ about 7-8 mEq/L); it almost looks like the Empire State building (tall, peaked, with a narrow base). Contrast with the T wave that is sometimes seen in healthy individuals as a normal variant (shaded box) in which the T wave is rounded, its sides are not symmetric, and it has a broad base.

D: P wave amplitude decreases, the PR interval lengthens, and the QRS widens (K+ >8 mEq/L).

E: P waves disappear (sino- ventricular rhythm) and the QRS becomes sinusoid (K+ >10 mEq/L).V Fib usually follows.

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14
Q

Hyperkalemia-

work up
Labs – to determine cause

A

To determine potential cause (Electrolytes and EKG done)

Renal function assessment for renal failure

Urine K, Na, and osmolality

CBC (low Hg, Hct, or abnormal red cell suggests hemolysis/severe leukocytosis or a questions if it is pseudo-hyperkalemia

Metabolic panel – low bicarb (metabolic acidosis), hyperglycemia, elevated LDH, uric acid, phosphate, ALT, CK (rhabdomyolysis)

Serum cortisol, renin, aldosterone (adrenal insuff.)

check Mg as well

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15
Q

Hyperkalemia

Treatment
mild/moderate vs severe

calcium gluconate** will correct hyper K in 5 minutes. likely to see on PANCE
A

Mild to Moderate (no cardiac abnormalities)
Restrict K+ intake, stop K+ sparing diuretics, address volume or acid-base disorders
Give K+ wasting diuretics

Severe or if cardiac abnormalities present
10% calcium gluconate IV over 5 min to reduce muscle excitability
Use 10 to 30 mL, action is quick (1-2 min)
Redistribute potassium from extracellular space to intracellular space
Using rapid-acting insulin (5 to 10 U) drives K+ into the cells
Given with 25 g glucose 50% IV over 5 min
Sodium bicarb IV (helpful if acidotic)
β₂-adrenergic agonist (Albuterol) 0.5% 20 mg in 4mL normal saline by nebulizer (onset is 15-30 min)

Dialysis (Decrease total body potassium level)
Identify and treat correctable causes

Kayexalate by mouth or enema binds and removes K- gives diarrhea

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16
Q

Hypochloremia

General and Causes

A

Normal serum chloride 98-110 mEq/L
Hypochloremia < 98 mEq/L

Due to
Loss of gastric contents (N/V, NGT)
Excess extracellular water (hypotonic fluid admin., SIADH)
Renal losses caused by diuretics
Renal failure
During respiratory acidosis (kidneys resorb bicarb, Cl- excreted)

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17
Q

Hypochloremia

Clinical Sx and Tx

A

No specific S/S
(typically co-exist with Na def – Na and Cl stick together)

TX: NaCl or KCl (if K def too)

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18
Q

Hyperchloremia

general and causes

Sx / Tx

A

Serum Cl- >110 mEq/L
Uncommon in the surgical pt
Most commonly caused by administration of chloride rich IV fluids (0.9% NaCl)
In association with hyperchloremic metabolic acidosis, RTA, hypernatremia, iatrogenic,

No specific s/s

Treat underlying disorder. Used balanced solutions.

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19
Q

Calcium

general

A

Normal serum calcium 8.5-10.5 mEq/L (ionized 4.75-5.30mg/dL)
Hypocalcemia < 8.5 mEq/L (corrected for albumin)
Hypercalcemia >11 mEq/L
Most found in hydroxyapatite crystals in bone

40% bound to plasma protein (albumin)
Correct serum Ca++ in hypoalbuminemic pts
Corrected serum Ca++ = measure Ca++ + (0.8 X [4-measured albumin in g/dL])

50% ionized and physiologically active

Resorption Increased by
PTH or metabolic alkalosis

Half of serum calcium is free while the other half is bound to albumin

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20
Q

calcium

function

A

Neural signaling
Bone mineralization
Cardiac function
Skeletal muscle contraction
Digestive system function

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21
Q

Physiology of Calcium

A

Stimulates osteoclasts to break down bone – releasing calcium and phosphorus

Increases reabsorption of calcium by kidneys

Blocks reabsorption of phosphate by kidneys, leading to urinary phosphate loss.

Increases conversion of inactive to active 1,25 vitamin D (which then increases calcium absorption from gut)

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22
Q

Hypocalcemia

general and causes

A

Serum calcium < 8.5 mg/dL

Normal physiologic Response

Etiology
Malabsorption
Decreased intake
Vitamin D deficiency
Bowel surgery
Hypoparathyroidism
Decreased serum albumin
Chronic kidney disease
Decreased calcitriol
Hyperphosphatemia

Often seen in surgical patient/hospitalized patients
May be acute or chronic

Acute pancreatitis
Hypoparathyroidism
Severe soft tissue infections (necrotizing fasciitis)
Renal Insufficiency
Malabsorption syndromes
Chronic Diarrhea
Vitamin D def.
Hypomagnesemia
Hyperphosphatemia
Blood transfusion
Adverse effects of drugs
rhabdomyolysis
Tumor lysis syndrome
rickets
Genetic disorders
Chronic Diarrhea
Osteoblastic metastases
Prostate and breast cancer
DiGeorge syndrome
IBD
Fluid loss from pancreatic/ intestinal fistulas

23
Q

Hypocalcemia

Classifications of mild vs severe

A

Mild
Calcium level of 8.5-8.0
asymptomatic

Severe
Calcium level below 7.6
Symptomatic at any level below normal

24
Q

hypocalcemia

Clinical Manifestations

A

Circumoral tingling
Numbness/ tingling of fingertips
Muscle cramps
Wheezing/Dyspnea
Seizures
Palpitations/Chest pain
Confusion
Depression
Trousseau’s Sign :Carpal spasm elicited by inflation of BP cuff to 20 mmHg above systolic pressure for 3 min

Chvostek Sign :Twitching of circumoral muscles in response to tapping facial nerve anterior to ear

Wheezing
Irregular heart rhythm
Hyperactive DTRs
Tetany
Prolonged QT on EKG

25
# Hypocalcemia Diagnostic evaluation
Serum Calcium or ionized Calcium Identify cause: Serum albumin, K, Mg, Phos, Alk, Vit D, PTH, Cr, CK Urinary calcium
26
#Hypocalcemia Tx
Treatment depends on severity, how acutely it developed, and the degree of neuromuscular irritability. Treatment given to: **Asymptomatic patients with calcium < 7.6 mg/dL** Symptomatic pts **Preferred tx: Calcium gluconate 10 mL 10% (slow injection over 5 min)** Calcium gluconate diluted in 50 mL of 5% dextrose or 0.9% NaCl Monitor calcium levels. If persistent, may give calcium gluconate infusion 1.2 to 1.6 mg/kg of elemental Ca infused over 4 to 6 hrs increases serum Ca by 2 to 3 mg/dL If Ca persists (or likely to), give oral Vitamin D supplementation. If pt is also hypomagnesemic, must correct Mg first. If Chronic, give supplemental Ca with Vit D.
27
# Hypercalcemia general and causes
Serum Ca > 10.5 mEq/L No formal classification, but may be described as mild, moderate, or severe Mild < 12 Moderate 12-14 Severe > 14 Occurs from one of three mechanisms: 1) increased bone resorption (example, lytic bone lesions) 2) Increased GI absorption of Ca (excessive PTH effects on 1,25 (OH)2D 3) Decreased renal Ca excretion (thiazide diuretics) May be classified if PTH are elevated or reduced PTH elevated: primary or tertiary hyperparathyroidism PTH reduced: malignancy, excess Vit. D, Drugs (thiazides. Lithium, estrogens/testosterone, milk-alkali syndrome, thyrotoxicosis, pheochromocytoma, acute adrenal insuf. Most common causes are primary hyperparathyroidism and malignancy.
28
# Hypercalcemia clinical manifestations
Asymptomatic Symptomatic: Gastrointestinal Constipation Anorexia Renal Nephrolithiasis Neurologic Anxiety, lethargy Cardiac Arrhythmia – Short QT interval “moans, groans, pains, and stones”
29
# Calcium
30
# Hypercalcemia treatment
Restrict Ca++ Hydrate- IV ½ NS or NS Enhances urinary calcium excretion Saline diuresis lead to hypokalemia, hypomagnesemia, or other electrolyte imbalance Avoid fluid overload If severe, use bisphosphonates. (not used if hyperparathyroid) Drugs of choice are pamidronate and zoledronic acid. Corticosteroid-used long term to suppress calcium release from bone but take 1-2 weeks to show results Treat underlying cause
31
# Magnesium general and function
2nd most abundant cation of the intracellular fluid Mg++ is tightly regulated by the gut, kidney, and bone. Function Activates enzymes ATP function in combination with phosphate Signal transduction pathways Nerve transmission
32
# Hypomagnesemia general and cause | mild/mod/severe
Normal 1.8-2.1 mg/dL Mild 1.5-1.8 mg/dL Moderate 1-1.4 mg/dL Severe < 1mg/dL Common in critically ill pts Etiology Diminished absorption or intake Increased renal loss
33
# Hypomagnesemia Clinical Manifestations
Most frequently, asymptomatic Clinical manifestations appear with more severe symptoms: N/V Anorexia Weakness Lethargy Cramps Fasciculations, tetany Carpopedal spasm Paresthesias Irritability, inattention Confusion
34
# hypomagnesemia Cardiac Arrhythmias
(variety of atrial and ventricular arrhythmias – flattened T waves, prolonged QT interval, ST depression, and widened QRS complexes)
35
# Hypomagnesemia Treatment
TX: oral, IV magnesium sulfate, hydration-watch in renal failure Management Chronic, asymptomatic PO Magnesium oxide Symptomatic IV Magnesium sulfate in 5% dextrose or normal saline Calcium and potassium replacement may be required, but patients with hypokalemia and hypocalcemia do not recover without magnesium supplementation Dose adjustments for patients with advanced chronic kidney disease
36
# Hypermagnesemia general and causes
Serum magnesium > 2.2 mg/dL Rare However, magnesium toxicity is potentially fatal. Persistent hypermagnesemia most often seen in chronic renal insufficiency. These patients are taking large amounts of magnesium. May occur in patients given large doses of IV magnesium (ie, preeclampsia) May be seen in oral supplementation; however, the kidney is typically able to excrete excess magnesium. May be caused by: Eclampsia treatment Renal failure Rhabdomyolysis Dehydration Severe metabolic acidosis Adrenal Insufficiency Antacids
37
# Hypermagnesemia Clinical Findings
Impaired neurologic function Muscle weakness Decreased deep tendon reflexes Obtundation, confusion Flaccid paralysis Impaired gastrointestinal function Ileus Cardiac abnormalities Prolonged QT interval Severe Respiratory paralysis Hypotension, cardiac arrest
38
# Hypermagnesemia Tx
Discontinue exogenous sources Antacids, laxatives IV **Calcium chloride** Antagonizes magnesium Avoid use of magnesium in advanced chronic kidney disease Hemodialysis
39
# Phosphorus general and function
Normal 3 to 4.5 mg/dL Total body content: 85% in bone, 14% intracellular, and 1% extracellular Daily intake is 800 to 1500 mg Present in many foods: dairy products, meats, grains Kidney secretes phosphorus Most filtered at the glomerulus **PTH increases renal phosphate excretion Vitamin D enhances intestinal phosphate absorption**
40
# Hypophosphatemia etiology
Caused by : Decreased intake Impaired intestinal absorption Antacid use, TPN, Vit D. def Redistribution into cells or bone Hyperparathryoidism, cancer, steroids Renal losses Diuretics, hyperaldosteronism, burns, renal transplant, resp. alkalosis, SIADH, steroids Frequently depleted in alcoholism poor diet and renal loss Common in surgical pt Associated with Potassium and Magnesium losses
41
# Hypophosphatemia clin man
Clinical Manifestations: Only observed if severe (< 1 mg/dL) Encephalopathy, dilated cardiomyopathy, generalized muscle weakness, rhabdomyolysis, and hemolysis.
42
# hypophospatemia Dx
often done with history and physical exam Can measure 24 hr urine or fractional excretion in spot urine for phosphate normal response is for kidneys to reduce phosphate excretion to less than 100 mg/day
43
# hypophosphatemia Tx
Treatment: If mild, no treatment – decrease intake. If symptomatic or having ongoing loss, Oral repletion: Na or KPO4 salts or skimmed milk IV phosphorus If on dialysis, use phosphate-containing dialysate
44
# Hyperphosphatemia general and causes
Common Caused by: Excessive phosphate intake Increased intestinal absorption Laxatives and enemas, intoxication with Vit. D Redistribution from intracellular stores Massive cell lysis (rhabdomyolysis, tumor lysis syndrome), DKA Impaired renal excretion Acute or chronic renal failure, primary hypoparathyroidism Pseudohyperphosphatemia may occur in hemolytic specimens or hyperglobulinemic states (ie, multiple myeloma)
45
# Hyperphosphatemia clin man
May cause Acute Renal Failure. Can cause hypocalcemia – tetany, hypotension, seizures, & cardiac arrhythmias
46
# hyperphosphatemia Treatment
If acute, asymptomatic, and normal renal function, hyperphosphatemia will most likely resolve spontaneously. If symptomatic and impaired renal function, extracorporeal therapy to remove excess phosphate. Chronic Minimize dietary phosphorus intake Phosphate binders (calcium salts, lanthanum carbonate, or sevelamer) Aluminum hydroxide effective phosphate binder, but prolonged use leads to aluminum accumulation. (may cause encephalopathy and osteomalacia) hemodialysis
47
1. Which of the following electrolyte abnormalities is commonly associated with hypomagnesemia? a. Hypercalcemia b. Hypernatremia c. Hypochloremia d. Hypokalemia
d. Hypokalemia
48
1. Which of the following electrocardiogram findings is most associated with hypercalcemia? a. Elevated ST segment b. Increased QRS voltage c. Lengthened PR interval d. Short QT interval e. Widened T-waves
d. Short QT interval
49
1. Which of the following is the most appropriate initial treatment of cardiac arrhythmia in a patient with hyperkalemia? a. Calcium gluconate b. Furosemide (Lasix) c. Insulin with glucose d. Sodium polystyrene (Kayexalate) e. Triamterene (Dyrenium)
a. Calcium gluconate
50
Which of the following mediations is most likely to cause hyperkalemia? a. Acetazolamide (Diamox) b. Eplerenone (Inspra) c. Furosemide (Lasix) d. Hydrochlorothiazide (Microzide)
b. Eplerenone (Inspra)
51
A 72-year old man is hospitalized for severe malnutrition. The patient is started on **total parenteral nutrition**. Which of the following electrolyte abnormalities should you be monitoring vigilantly? a.-hyperkalemia b. Hypermagnesemia c. Hypocalcemia d. hypophosphatemia
all of them
52
Which of the following electrolyte abnormalities is associated with diuretic therapy ? a. Hyperkalemia b. Hypermagnesemia c. Hypomagnesemia d. hyperchloremia
c. Hypomagnesemia
53
A 75-year-old man is admitted with congestive heart failure. His home medications include furosemide 80 mg daily and digoxin 0.125 mg daily. His admitting ECG reveals **flattened T waves and the prescence of U wave**. Which of the following serum electrolyte abnormalities is most likely for this patient? a. K 2.4 mEq/L b. K 5.7 mEq/L c. Calcium 12mg/dL d. Magnesium 1.2
a. K 2.4 mEq/L
54
A 57-year-old woman presents to clinic with weight loss, fatigue, and recurrent nephrolithiasis. Her physical exam is unremarkable. Her laboratory evaluations reveals normal renal and hepatic function, ESR of 52 mm/h, TSH of 2.0, and a serum calcium of 17mg/dL. Which of the following is the most likely cause of the patient’s hypercalcemia? a. Thyrotoxicosis b. Hyperparathyroidism c. Excessive calcium supplements d. malignancy
d. malignancy | stones, bones, abdominal moans