Clinical Lab - Exam 1

Front 1

Sodium (Na+)

Back 1

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

Front 2

Presentation of Hypovolemic

Back 2

>2kg in <1 week

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

Dry mouth, dry skin, Skin turgor (↓’ed)
BUN/SCr > 20

Front 3

Presentation of Hypervolemic

Back 3

Acute weight gain

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

BUN/SCr < 20

Front 4

Hypotonic

Back 4

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

Front 5

Hypertonic

Back 5

Na+ > 145 mEq/L

Loss of water and sodium
Na loss >> H2O loss

Front 6

Hypovolemic Hypernatremia

Back 6

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

Front 7

Hypervolemic HYPERnatremia

Back 7

Pathology - Administration of excessive hypertonic fluids

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

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

EC Sodium Gain >> EC Water Gain

Front 8

Euvolemic Hypernatremia

Back 8

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)

Front 9

Presentation of Acute Hypernatremia

Back 9

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

Front 10

Hypovolemic Hyponatremia

Back 10

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)

Front 11

Hypervolemic Hyponatremia

Back 11

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):

Cirrhosis
CHF
Nephrotic syndrome

↑↑EC Water >> ↑↑ EC Sodium (due to impaired Na+2/ H20 excretion)

Front 12

Euvolemic Hyponatremia

Back 12

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

Front 13

Presentation of Acute HYPONATREMIA

Back 13

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

Front 14

Potassium (K+)

Back 14

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+)

Front 15

Magnesium (Mg++)

Back 15

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

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

Renal:
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

Front 16

HYPERkalemia & HYPERmagnesemia

Back 16

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

Cardiovascular
Hypotension
Bradycardia
Cardiac Arrest (asystole)

Neuromuscular
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

Front 17

HYPOkalemia & HYPOmagnesemia

Back 17

Renal Causes:

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

Non-renal Causes:

Metabolic alkalosis (↓ [K+] only)
GI sources (both)
Diarrhea
Vomiting
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)


Cardiovascular:
Hypotension
↑Risk of Digoxin toxicity

Neuromuscular:
Cramps, Weakness

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

Neuromuscular:
Tremors, tetany
Weakness
↑Deep tendon reflexes

CNS:
Irritability, combativeness
Psychosis
Convulsions, coma
*If the patient is having a seizure then Mg levels must be checked and possible given

Front 18

Calcium (Ca+2)

Back 18

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

Front 19

Phosphate (PO4)

Back 19

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

Front 20

HYPOcalcemia & HYPERphosphatemia

Back 20

Renal Causes:

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

Non-renal Causes:

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

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

Neuromuscular:
Tetany, Seizures
↑Deep tendon reflexes
Paresthesias

CNS:
Confusion, hallucinations
Mental instability

Cardiovascular:
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)

Front 21

HYPERcalcemia & HYPOphosphatemia

Back 21

Hypercalcemia (Serum Ca+ > 10.8 mg/L):

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

Calcium < 13 mg/dL:
Asymptomatic

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
Hyperparathyroidism

Neuromuscular:
Weakness, parathesias
Rhabdomyolysis
Cardiac/ Respiratory failure

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

Hematologic:
Hemolysis
WBC & Platelet dysfunction

*Without phosphates, there is little ATP