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21 Cards in this Set

  • Front
  • Back
Sodium (Na+)
Normal range: 136-145 mEq/L *or 135*

Most abundant cation in the extracellular fluid

Role in body physiology

Maintains appropriate transmembrane electric potential for neuromuscular function

Major contributor of serum osmolality

Regulates water movement between the extracellular and intracellular compartments
Presentation of Hypovolemic
>2kg in <1 week

Acute weight loss (1 kg = 1 Liter)
Tachycardia, (+) Orthostasis(SBP↓)

Dry mouth, dry skin, Skin turgor (↓’ed)
BUN/SCr > 20
Presentation of Hypervolemic
Acute weight gain

Extremities (all causes)
Pulmonary edema (heart failure)
Ascites (liver failure)
Anasarca (nephrotic syndrome)

BUN/SCr < 20
Na+ < 135 mEq/ L

Loss of water and sodium :
H2O loss >> Na loss

If you loose more water than sodium (sweating, vomiting) hyoptonic fluids, serium sodium will increase leaving you hypovolemic hypernatremia
Na+ > 145 mEq/L

Loss of water and sodium
Na loss >> H2O loss
Hypovolemic Hypernatremia
LOSS of hypotonic fluids AND Patient unable to access Water (Na+ >145)

Presentation of Hypovolemia:
Acute weight loss
Dry mouth, (+) Orthostasis,
BUN:SCr > 20

Common causes:
GI: Vomiting, diarrhea
Skin: ↑ Sweating/ fevers
ALL in patients who cannot access water
Hypervolemic HYPERnatremia
Pathology - Administration of excessive hypertonic fluids

i.e., Hypertonic saline (3% NaCl= 513 mEq of Na+ / Liter) NS is 0.9% and 153 mEq

Excessive hypertonic saline solutions:
i.e.,NaHCO-3 solution
Hypertonic saline enemas

EC Sodium Gain >> EC Water Gain
Euvolemic Hypernatremia
Loss of total body water with minimal loss of total body sodium

NOT enough water loss for dehydration

Seen in conditions promoting Na+-free water loss:

Diabetes insipidus – they cannot retain free water due to the lack of response/production of ADH

Osmotic diuretics

* Loss of Small amount of Water Only (Sodium free water)
Presentation of Acute Hypernatremia
If serum Na+2 < 160 mEq/L
Patient may be asymptomatic

Neuromuscular irritability:

Thirst, Lethargy
Restlessness, hyperreflexia
Irritability, muscle twitching
Seizure, Coma
Due to Cerebral dehydration
Hypovolemic Hyponatremia
Presentation of Hypovolemia:

Acute weight loss
Dry mouth, Orthostasis, BUN:SCr > 20

Common causes:

Overconsumption of hypotonic fluids (i.e., tap water) following severe vomiting, diarrhea, excessive sweating

Overdiuresis (medications)

Commonly Overcorrection of Hypotonic fluid Losses OR
Overdiuresis (Na+ Loss >> Water loss)
Hypervolemic Hyponatremia
Presentation of HYPERvolemia:
Acute weight gain (all causes):

± Ascites (liver failure),
± Pulmonary edema (heart failure)
± Peripheral edema (heart failure)
± Anasarca (nephrotic syndrome)

Common causes (fluid retentive states):

Nephrotic syndrome

↑↑EC Water >> ↑↑ EC Sodium (due to impaired Na+2/ H20 excretion)
Euvolemic Hyponatremia
Slightly increased total body water relative to total body sodium due to impaired secretion

Not enough water retention to cause edema

Impaired excretion due to SIADH:

Syndrome of Inappropriate antidiuretic hormone*
Diseases causes= CNS & pulmonary disease
Drug-induce causes= Chlorpropamide, carbamazepine

*Inappropriate (excessive) ADH (antidiuretic hormone)= aka vasopressin

Slightly ↑ EC Water with normal EC Sodium
NOT enough fluid retention for hypervolemia
Presentation of Acute HYPONATREMIA
125 mEq/L:
nausea, vomiting

*115-120 mEq/L:
headache, tremors
incoordination, lethargy,delirium, obtundation

*110-115 mEq/L:
Seizures, coma

**Symptoms due to Cerebral edema
Potassium (K+)
Normal range 3.5 – 5.0 mEq/L

Primary cation in intracellular space (98%)

Regulates muscle and nerve excitability especially myocardial conduction

Factors effecting regulation:
Renin-angiotensin system (Aldosterone)
Metabolic Acid-Base disorders

Large GI absorption followed by renal filtration
Both with prominent renal reabsorption

Renal (major regulatory system):
Freely filtered, nearly completely reabsorbed
Dependent on aldosterone for regulation

Arterial pH (temporary redistribution):

Metabolic Acidosis (Renal): ↑ Extracellular potassium (< Blood pH = > [H+] = > Serum K+)

Metabolic Alkalosis (GI): ↓ Extracellular potassium (> Blood pH = < [H+] = < Serum K+)
Magnesium (Mg++)
Normal range= 1.5 – 2.2 mEq/L

Bone (50-60%), Intracellular (30-40%)(2nd big)
Extracellular only 1- 2%

Role in neuromuscular and enzymatic function:

Cofactor in ADP to ATP conversion
Helps regulate neuromuscular conduction
Myocardial or skeletal muscle

30% absorption (diet)
60% of elimination (fecal)

Mg+ that is absorbed (30% of intake)
Freely filtered with 97% reabsorption (Loop of Henle)

Serum Mg and K = highly dependent on normal oral intake and renal elimination for maintenance of normal serum concentrations
ONLY Serum K+ significantly affected by metabolic acid-base disorders
HYPERkalemia & HYPERmagnesemia
Renal Causes:

Renal failure
↑ [K+] and ↑[Mg+]
Acute & Chronic failure
ESRD – End Stage Renal Disease

Non-renal Causes:

Metabolic acidosis (↑ [K+] only)
Medications (↑ [K+] only )
ACE inhibitors/ ARBs
Excessive Intake
Excess K+ or Mg+ suppliments

Hyperkalemia Presentation (Serum K+> 5.0 mEq/L):

EKG Abnormalities
Widened QRS complex
ST Segment depression
Peaked T waves

Cardiac Arrest (asystole)

Cramps, Weakness

*Peaked T waves – represents the cardiac cells continually repolarizing due to high K levels.
NaCO2 can be given to promote alkylosis and drive K intracellular

Hypermagnesemia Presentation(serum Mg+2 >2.2 mEq/L):

Magnesium < 5.0 mEq/L:
Rarely symptomatic

Magnesium = 6- 10 mEq/L:
Drowsiness, ↓DTR, Bradycardia

Magnesium = 10 - 15 mEq/L:
PR & QRS Prolongation, Paralysis

Magnesium > 15 mEq/L:
Respiratory arrest, Asystole
HYPOkalemia & HYPOmagnesemia
Renal Causes:

Drug- induced (Drug-induced acute tubular necrosis or overdiuresis)
Diuretics (ALL)

Non-renal Causes:

Metabolic alkalosis (↓ [K+] only)
GI sources (both)
Decrease Intake (Both)
Anorexia, Alcoholism

Hypokalemia Presentation (Serum K+ < 3.5 mEq/L):

EKG Abnormalities:
PR Prolongation
ST segment depression
Flattened T –waves
Prominent U-waves (U wave is another attempt to repolarize the cell)

↑Risk of Digoxin toxicity

Cramps, Weakness

Hypomagnesemia Presentation (Serum Mg+2 < 1.5 mEq/L):

Tremors, tetany
↑Deep tendon reflexes

Irritability, combativeness
Convulsions, coma
*If the patient is having a seizure then Mg levels must be checked and possible given
Calcium (Ca+2)
Normal range 8.5 – 10.8 mg/dL

99.5% of body calcium is integrated within bones (0.5% extracellular)

Major physiologic roles:
Neuromuscular/ Myocardial functions
Blood coagulation
Bone Metabolism

Extracellular Ca+2 is 40% protein bound (54% unbound)
Unbound “ionized” fraction is physiologically active

Unbound fraction is affected by available serum albumin
Must correct total calcium level when albumin levels are low:

Corrected Ca = [(4-albumin) x 0.8] + CaMeasured

Vitamin D3 & PTH = ↑Calcium resorption (bone), absorption (GI), & reabsorption (renal)

*Chronic renal failure = ↓’ed Vitamin D3 activation and ↓’ed response to PTH
Phosphate (PO4)
Normal range 2.6 – 4.5 mg/dL

85% of body’s phosphate is integrated within bones with 15% found intracellular

Major physiologic roles:
Forms high energy bonds for ATP
Essential component of nucleic acids
HYPOcalcemia & HYPERphosphatemia
Renal Causes:

Chronic renal failure
Kidneys are responsible for eliminating phosphate’s ESRD

Non-renal Causes:

↓’ed Intake (Vit D & Ca+)
Excess Intake (PO4 supplimt)

Hypocalcemia Presentation:(serum Ca+2 < 8.5 mg/dL)

Tetany, Seizures
↑Deep tendon reflexes

Confusion, hallucinations
Mental instability

Hypotension, Bradycardia
Cardiac arrhythmias
Heart failure (depressive)

*These symptoms are similar to hypomagnesium

Hyperphosphatemia Presentation: (serum PO4 > 4.5 mg/dL)

Mostly asymptomatic (symptoms of concurrent hypocalcemia)

Extracellular PO4 complexes with extracellular Ca+2 to form a crystal IF their product (Ca x PO) > 55

i.e. Phosphate = 8 mg/dL & Calcium = 9 mg/dL (Product= 72)

Ca+2-PO4 crystals deposit:
Bone (arthritis-like)
Skin (Rash, ischemic ulcers)
Eyes (“Redeye”/ conjunctivitis)
Vascular (may lead to cardiac arrhythmias)
HYPERcalcemia & HYPOphosphatemia
Hypercalcemia (Serum Ca+ > 10.8 mg/L):

Malignancy (i.e, bone)
Highly symptomatic for cancer

Calcium < 13 mg/dL:

Calcium 13- 15 mg/dL:
Renal effects=
Polyuria, nocturia, polydipsia
GI complaints
Nausea, vomiting, constipation

Calcium > 15 mg/dL:
Lethargy, obtundation
Acute renal failure
Coma, death

Hypophosphatemia (Serum PO4 < 2.6 mg/L):

Phosphate binders – antacids (Mg)
Refeeding syndrome – patient has not eaten in weeks and then suddenly eats lowers phosphates

Weakness, parathesias
Cardiac/ Respiratory failure

Confusion, hallucinations
Delirium, Seizures (often masked by hyper-Ca+)

WBC & Platelet dysfunction

*Without phosphates, there is little ATP