Basic Chemistry Flashcards
Chem 7 - how it’s collected
panel test of serum level of 7 substances.
6-10ccs of venous blood in red speckled or gold top tube. (after clots - spun in centrifuge and serun tested)
*fluid balance, renal function, and acid-base status
Chem 7 substances
- soduim,
- potassium
3.chloride
4.CO2 - BUN
- creatinine
- glucose
Sodium
reference values and general functions
Reference Range: 136 – 145 mEq/L
Critical Values: <120 or >160 mEq/L
Na+ is the major extracellular cation - responsible for fluid movement between the ICF and ECF
Main function - controls the maintenance of osmotic P°, acid-base balance and the initiation of action potentials
Hyponatremia -
symptoms and clinical manifestations
↓ in Na+ levels <135 mEq/L
Sxs usually develop once the Na+ level drops below 125 mEq/L
Clinical manifestations - include weakness, confusion, muscle cramps, HA, personality changes, apprehension, depression and lethargy which can progress to coma
Hyponatremia association with hypertonicity, normotonicity & hypotonicity
Hypertonic – Results from an osmotic shift of water from ICF to ECF (high blood glucose)
Normotonic (Isotonic) – Usually due to ↑ lipids or proteins present in the blood sample which causes an artificial dilution in the sodium levels
Hypotonic – most common form of hyponatremia; it is caused by water retention & characterized by a ↓ in serum osmolarity
Hypertonic causes
Hyperglycemia
Mannitol
Sorbitol
Glycerol
Maltose
Radiocontrast agents
Isotonic causes
Hyperproteinemia
Hyperlipidemia
Hypotonic causes
Dehydration
diarrhea
vomiting
diuretics
ACEi
Aldosterone decrease
SIADH
Hypothyroid
CHF
Liver Disease
Nephrotic Syndrome
Advanced Renal Failure
Symptomatic Hyponatremia Tx
increase serum Na no more than 1-2mEq/L per hour and no more than 25-30mEq/L in the 1st 2 days
Hypertonic saline + furosemide
Asymptomatic Hyponatremia Tx
Restrict water intake to 0.5 – 1 L/d;
Normal (0.9%) saline with furosemide may be used in asymptomatic pts with serum Na+ <120 mEq/L
Hypernatremia
↑ in Na+ level >145 mEq/L
Characterized by hypertonicity of ECF & almost always causes cellular dehydration
3 main mechanisms of hypernatremia
Excessive water losses
Decreased water intake
Excessive Na+ intake
Clinical manifestations –hypernatremia
Dry mucous membranes, thirst, agitation, restlessness, convulsions, oliguria or anuria, tachycardia, weak & thready pulses, ↓BP, HA, hyporeflexia, coma
Sxs of dehydration are most common
Hypernatremia Tx
0.9% saline; if cause is ↑ Na+ intake then limit intake & can use free water or Dextrose5 Water
Potassium
reference values and general functions
Reference Range: 3.5 – 5.0 mEq/L
Panic Values: < 2.5 or > 6.5 mEq/L
K+ is principle intracellular cation & the primary buffer within the cell
Small amts are found in serum and bone
Due to small extracellular content, small minor ↑ or ↓ can have significant consequences
Other important potassium roles
K+ - important role in nerve conduction, muscle function, protein synthesis, osmotic pressure and acid/base balance
Along with Ca²+ and Na+, K+ controls the rate & force of cardiac contractions
85% of cellular K+ excreted in urine via the glomeruli, remainder is excreted in the stool & sweat
Reabsorption takes place in the proximal tubule and in the thick ascending limb of Henle
Potassium level components
K+ concentration depends on aldosterone, Na+ reabsorption, acid/base balance
When performing venipuncture educate pt not to open & close hand AFTER the tourniquet is applied
Hemolysis of blood during venipuncture or lab processing will falsely ↑ K+ levels
Hypo-K
↓ in K+ < 3.5 mEq/L or a falling trend of 0.1 – 0.2 mEq/L/d
Most frequent cause of deficiency is GI loss
Most frequent cause of depletion is IVF administration without K+ supplementation
Clinical manifestations of Hypo - K
muscle weakness & cramps, fatigue, constipation, ileus, flaccid paralysis, hyporeflexia, hypercapnia,
Hypo K manifestations on EKG
broadened T waves, U waves, PVCs & depressed ST segments
Hypo K causes
Vomiting, diarrhea, laxative abuse
Increased postprandial or self-administration of insulin
Alkalosis
Trauma (via beta-adrenergic stimulation)
Increased aldosterone (mineralcorticoid) effects
Primary hyper-aldosteronism
Secondary aldosteronism (dehydration, heart failure)
Renovasucular & malignant hypertension
Ectopic ACTH-producing tumor (Cushing’s Syndrome)
Renin-producing tumor
Diuretucs
Hypomagnesemia
Renal Tubular Acidosis
Hypo-K Tx
mild-mod deficiency treat with oral K+ which is very easily absorbed;
severe hypokalemia - IV K+ replacement
(also when PO supplementation cannot be taken)
Check Mg²+ levels first!!!!
Any patient receiving IV K+ should have continuous ECG monitoring
Check serum K+ Q3-6°
Hyper-K
↑ K+ > 5.0 mEq/L
Most frequently due to renal failure or cell damage
Commonly associated with acidosis
Clinical manifestations of Hyper-K
irritability, N/V/D, intestinal colic & rarely flaccid paralysis
Hyper- K EKG manifestations
peaked T waves, widened or biphasic waves of the QRS complex
Hyper-K Causes
Hemolysis
Repeated fist clenching during phlebotomy
Specimen drawn above IV line containing K+ infusion
Renal failure (acute & chronic)
Hypoaldosteronism (primary or secondary)
Heparin
Drugs that inhibit K+ excretion (spirinolactone, triamterene, ACE-I
ARBs, NSAIDs, and trimethoprim)
Rhabdomyolysis
Severe infection
Vigorous exercise
Metabolic acidosis
Insulin deficiency
Excessive intake of K+
Hyper- K Treatment planning
depends on (1) degree of hyperkalemia (2) degree of cardiac & neuromuscluar involvement (3) duration of the hyperkalemia
Mild Hyper-K Tx
if K+ is < 6.5 mEq/L & no ECG changes, usually safe to try correcting underlying cause & restrict K+ intake
Severve Hyper-K Tx
when K+ is > 6.5 mEq/L with EKG changes or > 7.0 mEq/L without EKG changes.
Monitor the EKG continuously
Ca+ (CaCl- or Ca²+ gluconate 5-30 mL IV)
Sodium Bicarbonate (NaHCO3)
Regular insulin (5-10 units IV) + glucose 50% (D5W, D5 1/2NS, or D5NS)
Can also administer albuterol
Promote K+ elimination with Na+ polystyrene
(Kayexalate) or dialysis in patients with coexistent renal failure
Chloride reference values and general functions
Reference Range: 96 – 106 mEq/L
Panic Values: < 70 or > 120 mEq/L
Major extracellular anion; important in cellular hyperpolarization (especially neurons)
Moves in & out of cells; forms NaCl-, hydrochloric acid, KCl- & CaCl-
Important in CSF formation & in GI secretions
Changes in Na+ commonly affect Cl- levels b/c it is commonly attached to the + charge of Na+
Hypochloremia
↓ Cl- levels < 96 mEq/L
Always associated with a metabolic alkalosis & oftens results in a paradoxic aciduria
Cl- is measured to calculate the anion gap
Causes - vomiting, gastric suction, burns, CHF, water intoxication
Clinical manifestations of Hypochloremia and Tx
seldom a primary problem therefore the sgs/sxs will depend
Tx – treat the underlying cause, IV fluids
Hyperchloremia
↑ Cl- levels > 106 mEq/L
Usually associated with a tendency towards acidosis (HCO3 loss)
Causes – dehydration, Cushing’s syndrome, hyperventilation, diarrhea, diabetes insipidus, hyperparathyroidism, & salicylate intoxication
Clinical manifestations of Hyperchloremia and Tx
Clinical manifestations - acid-base alterations
Tx – treat the underlying cause
CO2 and HCO3 - Ref. values and behavior
Serum Reference Range: 22 – 29 mEq/L
CO2 is transported in 3 forms (1) attached to Hgb (2) dissolved CO2 in plasma (3) and as HCO3- in the plasma
Dissolved CO2 & HCO3- make up about 77% of the CO2 that is transported in the extracellular fluid
90% of CO2 in blood is in the form of HCO3-
Increased and Decreased levels of CO2 and HCO3
Increased levels – metabolic alkalosis, respiratory acidosis (hypoventilation states), severe vomiting or gastric drainage
Decreased levels – metabolic acidosis, respiratory alkalosis (disorders causing hyperventilation)
Anion Gap
Anion Gap = Sodium – (Chloride + CO2)
Normal Anion Gap is between 8 – 14 mEq/L
Difference between cations & anions reflects concentrations of other anions that are present in ECF but are not routinely measured, but may become ↑ in the acidotic state
Helps distinguish type of metabolic acidosis (wide anion gap vs. normal anion gap)
Serum Osmolality
Reference Range: 275 – 295 mOsmol/kg
Measured osmolality is the measure of the number of dissolved solute particles in solution
Predominant osmotically active particles in the ECF are Na+ & its attendant anions (Cl- & HCO3-), BUN, & glucose
Calculation of serum osmolality
2 (Na+) + Glucose/18 + BUN/2.8
Serum osmolality ↑ with dehydration & ↓ with overhydration
Osmolar gap
Difference between measured & calculated serum osmolality is called the osmolar gap (usually < 10 mOsm)
Presence of gap > 10 mOsm suggests the presence of an unmeasured osmotically active substance (ETOH, acetone, mannitol)
Renal Function Tests
BUN interpreted in conjunction with creatinine
BUN – creatinine ratio provides useful diagnostic info
BUN is less accurate & specific for renal fx compared with creatinine
Less interfering factors that can alter creatinine levels
BUN Ref Values + notes
Blood Urea Nitrogen (BUN)
Reference Range: 6 – 20 mg/dl
Panic Values: > 100 mg/dl
Synthesized in liver & along with CO2, constitutes final product of protein metabolism
Proteins→ amino acids→ free ammonia→ urea → deposited in blood & renal excretion
The amount of excreted urea varies directly with protein intake
Increased BUN levels implications
Impaired renal function
Chronic renal disease
Urinary tract obstruction
Hemorrhage into GI tract
Diabetes mellitus with ketoacidosis
⇑ protein intake or catabolism
Anabolic steroids
Dehydration
Dcreased BUN levels implications
Liver failure
Acromegaly
Malnutrition
Impaired GI absorption
Overhydration
Interfering factors – Diets, ↓ in children & women, pregnancy, aggressive IVF, many drugs
Creatinine Ref. Values + notes
Reference Range: 0.5 – 1.2 mg/dl
Critical Values: > 4 mg/dl
Catabolic product of creatine phosphate used in skeletal muscle contraction
Creatinine is removed from plasma entirely by the kidneys & excreted in urine without reabsorption by the tubules
Creatinine behavior
Does not ⇑ until renal function is impaired
Unlike BUN the creatinine level is minimally affected by hepatic function
If the value doubles, the renal function has fallen to one-half of its normal state
Aminoglycosides, cephalosporins, & nephrotoxic drugs can increase levels
Increased Creatinine levels implications
Impaired renal function
Urinary tract obstruction
Muscle disease, rhabdomyolysis
CHF, shock, dehydration
Decreased Creatinine levels implications
Small stature
Decreased muscle mass
Inadequate dietary protein
Pregnancy
BUN:Creatinine Ratio
Normal 10:1
Ratios > than 15:1 represent prerenal conditions
Ratios < 10:1 occur in persons with liver disease,
pregnancy, SIADH & those who receive a low-protein diet or chronic dialysis
Azotemia
Accumulation or elevation of nitrogenous wastes in the blood
Pre-renal: elevation of wastes due to pathologic conditions BEFORE it gets to kidney
Intrarenal (intrinsic): primary renal disease
Post-renal: elevation of wastes due to pathologic conditions of the urinary tract distal to kidneys
