Basic Chemistry Flashcards

(51 cards)

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

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
Clinical manifestations of Hyper-K
irritability, N/V/D, intestinal colic & rarely flaccid paralysis
26
Hyper- K EKG manifestations
peaked T waves, widened or biphasic waves of the QRS complex
27
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+
28
Hyper- K Treatment planning
depends on (1) degree of hyperkalemia (2) degree of cardiac & neuromuscluar involvement (3) duration of the hyperkalemia
29
Mild Hyper-K Tx
if K+ is < 6.5 mEq/L & no ECG changes, usually safe to try correcting underlying cause & restrict K+ intake
30
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
31
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+
32
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
33
Clinical manifestations of Hypochloremia and Tx
seldom a primary problem therefore the sgs/sxs will depend Tx – treat the underlying cause, IV fluids
34
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
35
Clinical manifestations of Hyperchloremia and Tx
Clinical manifestations - acid-base alterations Tx – treat the underlying cause
36
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-
37
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)
38
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)
39
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
40
Calculation of serum osmolality
2 (Na+) + Glucose/18 + BUN/2.8 Serum osmolality ↑ with dehydration & ↓ with overhydration
41
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)
42
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
43
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
44
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
45
Dcreased BUN levels implications
Liver failure Acromegaly Malnutrition Impaired GI absorption Overhydration Interfering factors – Diets, ↓ in children & women, pregnancy, aggressive IVF, many drugs
46
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
47
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
48
Increased Creatinine levels implications
Impaired renal function Urinary tract obstruction Muscle disease, rhabdomyolysis CHF, shock, dehydration
49
Decreased Creatinine levels implications
Small stature Decreased muscle mass Inadequate dietary protein Pregnancy
50
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
51
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