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Lab Medicine > Basic Chemistry > Flashcards

Basic Chemistry Flashcards

1
Q

Chem 7 - how it’s collected

A

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

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2
Q

Chem 7 substances

A
  1. soduim,
  2. potassium
    3.chloride
    4.CO2
  3. BUN
  4. creatinine
  5. glucose
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3
Q

Sodium
reference values and general functions

A

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

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4
Q

Hyponatremia -
symptoms and clinical manifestations

A

↓ 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

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5
Q

Hyponatremia association with hypertonicity, normotonicity & hypotonicity

A

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

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6
Q

Hypertonic causes

A

Hyperglycemia
Mannitol
Sorbitol

Glycerol
Maltose
Radiocontrast agents

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7
Q

Isotonic causes

A

Hyperproteinemia
Hyperlipidemia

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8
Q

Hypotonic causes

A

Dehydration
diarrhea
vomiting

diuretics
ACEi
Aldosterone decrease

SIADH
Hypothyroid
CHF

Liver Disease
Nephrotic Syndrome
Advanced Renal Failure

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9
Q

Symptomatic Hyponatremia Tx

A

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

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10
Q

Asymptomatic Hyponatremia Tx

A

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

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11
Q

Hypernatremia

A

↑ in Na+ level >145 mEq/L
Characterized by hypertonicity of ECF & almost always causes cellular dehydration

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12
Q

3 main mechanisms of hypernatremia

A

Excessive water losses
Decreased water intake
Excessive Na+ intake

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13
Q

Clinical manifestations –hypernatremia

A

Dry mucous membranes, thirst, agitation, restlessness, convulsions, oliguria or anuria, tachycardia, weak & thready pulses, ↓BP, HA, hyporeflexia, coma

Sxs of dehydration are most common

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14
Q

Hypernatremia Tx

A

0.9% saline; if cause is ↑ Na+ intake then limit intake & can use free water or Dextrose5 Water

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15
Q

Potassium
reference values and general functions

A

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

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16
Q

Other important potassium roles

A

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

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17
Q

Potassium level components

A

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

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18
Q

Hypo-K

A

↓ 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

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19
Q

Clinical manifestations of Hypo - K

A

muscle weakness & cramps, fatigue, constipation, ileus, flaccid paralysis, hyporeflexia, hypercapnia,

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20
Q

Hypo K manifestations on EKG

A

broadened T waves, U waves, PVCs & depressed ST segments

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21
Q

Hypo K causes

A

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

22
Q
A
23
Q

Hypo-K Tx

A

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°

24
Q

Hyper-K

A

↑ K+ > 5.0 mEq/L

Most frequently due to renal failure or cell damage

Commonly associated with acidosis

25
Q

Clinical manifestations of Hyper-K

A

irritability, N/V/D, intestinal colic & rarely flaccid paralysis

26
Q

Hyper- K EKG manifestations

A

peaked T waves, widened or biphasic waves of the QRS complex

27
Q

Hyper-K Causes

A

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+

28
Q

Hyper- K Treatment planning

A

depends on (1) degree of hyperkalemia (2) degree of cardiac & neuromuscluar involvement (3) duration of the hyperkalemia

29
Q

Mild Hyper-K Tx

A

if K+ is < 6.5 mEq/L & no ECG changes, usually safe to try correcting underlying cause & restrict K+ intake

30
Q

Severve Hyper-K Tx

A

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

31
Q

Chloride reference values and general functions

A

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+

32
Q

Hypochloremia

A

↓ 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

33
Q

Clinical manifestations of Hypochloremia and Tx

A

seldom a primary problem therefore the sgs/sxs will depend

Tx – treat the underlying cause, IV fluids

34
Q

Hyperchloremia

A

↑ 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

35
Q

Clinical manifestations of Hyperchloremia and Tx

A

Clinical manifestations - acid-base alterations

Tx – treat the underlying cause

36
Q

CO2 and HCO3 - Ref. values and behavior

A

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-

37
Q

Increased and Decreased levels of CO2 and HCO3

A

Increased levels – metabolic alkalosis, respiratory acidosis (hypoventilation states), severe vomiting or gastric drainage

Decreased levels – metabolic acidosis, respiratory alkalosis (disorders causing hyperventilation)

38
Q

Anion Gap

A

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)

39
Q

Serum Osmolality

A

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

40
Q

Calculation of serum osmolality

A

2 (Na+) + Glucose/18 + BUN/2.8

Serum osmolality ↑ with dehydration & ↓ with overhydration

41
Q

Osmolar gap

A

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)

42
Q

Renal Function Tests

A

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

43
Q

BUN Ref Values + notes

A

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

44
Q

Increased BUN levels implications

A

Impaired renal function
Chronic renal disease
Urinary tract obstruction
Hemorrhage into GI tract

Diabetes mellitus with ketoacidosis
⇑ protein intake or catabolism
Anabolic steroids
Dehydration

45
Q

Dcreased BUN levels implications

A

Liver failure
Acromegaly
Malnutrition
Impaired GI absorption

Overhydration
Interfering factors – Diets, ↓ in children & women, pregnancy, aggressive IVF, many drugs

46
Q

Creatinine Ref. Values + notes

A

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

47
Q

Creatinine behavior

A

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

48
Q

Increased Creatinine levels implications

A

Impaired renal function
Urinary tract obstruction
Muscle disease, rhabdomyolysis
CHF, shock, dehydration

49
Q

Decreased Creatinine levels implications

A

Small stature
Decreased muscle mass
Inadequate dietary protein
Pregnancy

50
Q

BUN:Creatinine Ratio

A

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

51
Q

Azotemia

A

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

Lab Medicine (6 decks)

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