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147 Cards in this Set
- Front
- Back
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Analyte
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Substance measured by the test
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Biomarker
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Measuring a process
A substance is measured and serves as an indicator of that process. Ex: A1C, CA-125 (cancer marker) |
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Units
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Method of reporting lab results
Traditional: mg/dL, mEq/L International System (SI): mmol/L |
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Specimen
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Sample used for lab analysis
- venous blood, urine, arterial blood, sputum |
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Reference range
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Normal range of a lab value, usually the mean value from a standard population +/- 2 standard deviations.
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Critical value
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Needs to be addressed urgently
Lab result outside of reference range upon which immediate action usually needs to take place. |
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Accuracy of a test
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Test is close to the correct lab value.
A test can be accurate but not precise. |
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Precision
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Relates to being able to duplicate the same results.
A test can be precise but not accurate. |
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Qualitative
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Reports results as either positive or negative - yes or no
Ex: urine pregnancy Hcg test |
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Quantitative
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Results reported as an exact numeric measurement.
Ex: blood pregnancy Hcg test |
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Semi-quantitative
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Results reported as either negative or with varying degrees of positivity.
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Sensitivity
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True positives
TP/(TP+FN) true pos/(true pos + false neg) Ex: If 100 patients known to have a disease were tested, and 43 test positive, then the test has 43% sensitivity. |
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Specificity
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True negatives
TN/(FP+TN) true neg/(false pos + true neg) Ex: If 100 with no disease are tested and 96 return a negative result, then the test has 96% specificity. |
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Screening tests
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Performed on healthy patients.
Do NOT provide a definitive answer or diagnosis. High sensitivity, detects disease at early state. |
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Diagnosis tests
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Performed on at-risk individuals.
Provide a definitive answer or diagnosis. High specificity, can detect disease at late stage. |
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Rationale for ordering tests
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Establishing baseline health
Confirming a suspected diagnosis Differentiating among possible diagnoses --- have a differential in mind Determining the stage, activity or severity of disease Detecting disease recurrence Assessing the effectiveness of therapy Guiding the course of therapy |
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Interpreting lab results
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Baseline studies
Lab value compared to reference range Rate of change of lab value Isolated results versus trends Spurious results |
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Metabolic panel
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Give providers information about the patients: kidney, liver, protein, electrolyte, glucose, and acid/base balance.
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Basic metabolic panel (BMP/Chem 8)
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Na, K, Cl, CO2, BUN, creatinine, glucose, calcium
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Complete metabolic panel (CMP/Chem 14)
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BMP+ liver function tests (LFT)
LFT: AST, ALT, Albumin, total protein, Alkaline phosphatase, bilirubin |
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What does CMP assess?
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glucose, calcium, proteins, electrolytes, kidney function, and liver function
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What electrolytes and renal functions does the CMP assess?
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Sodium
Potassium Chloride Bicarbonate Magnesium Calcium Phosphate BUN Creatinine |
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Normal range for Na
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136-145 mEq/L
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What function does Na have?
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Most abundant cation in extracellular fluid
Major regulating factor for water balance Vital to normal body processes, including nerve and muscle function. Volume status is important! |
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Complications of low Na
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Altered mental status
Seizures |
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What is the importance of volume status?
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CHF
Swollen but dehydrated - ECF overloaded - Intravascular (in the vessel) depleted |
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How can you determine volume status?
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Edema
Turgor Blood pressure Heart rate Mucous membranes Urine color |
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Causes of hypernatremia
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Impaired thirst
Water loss Sodium gain Transcellular water shift (rare) |
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Hypernatremia
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Serum sodium in excess of 145 mmol/liter, and represents a hyperosmolality.
Due to primary sodium gain or water deficit Normal response to hypernatremia - Increased water intake by thirst and excretion of the minimum volume of maximally concentrated urine. - As a result of vasopressin secretion due to osmotic stimulus. |
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How does impaired thirst cause hypernatremia?
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Hyperosmolality typically is mild unless thirst mechanism is abnormal or access to water is limited. Common in the elderly and infants. Primary hypodipsia (rare) a result of damage to the hypothalamic osmoreceptors that control thirst. Due to vascular occlusions, tumors, granulomatous diseases and others.
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How does non-renal water loss cause hypernatremia?
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Nonrenal water loss
Insensible loss (skin, respiratory, or GI tract) Increased with - Fever, exercise, heat exposure, and burns Diarrhea is the most common cause: specifically osmotic diarrhea ( due to lactulose, sorbitol, or malabsorption of carbohydrates) and viral gastroenteritis (resulting in water loss that exceeds loss of NA+ or K+) |
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What is the most common cause of hypernatremia?
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Renal water loss
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How does renal water loss cause hypernatremia?
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Osmotic diuresis
Diabetes insipidus |
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What is the most common cause of non-renal water loss?
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Diarrhea
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Osmotic diuresis
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The most common cause being hyperglycemia and glucosuria in poorly controlled diabetes mellitus.
Must control the fluid first!!! |
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Diabetes insipidus
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Nonosmotic urinary water loss usually due to central diabetes insipidus (CDI) with impaired vasopressin secretion or neprhogenic diabetes insipidus (NDI) from resistance to action of vasopressin (anti-diuretic).
The most common cause of CDI is destruction of the neurohypophysis as a result of trauma, neurosurgery, granulomatous disease, neoplasms, ischemia, or infection. |
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What is vasopression?
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A hormonal anti-diuretic
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How does sodium gain contribute to hypernatremia?
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Infrequent and seen mostly in patients with diabetic ketoacidosis and osmotic diuresis that is treated with normal saline.
Inadvertent hypertonic saline or sodium bicarbonate. Sodium chloride tablets or ingestion of sea water. |
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How does transcellular water shift contribute to hypernatremia?
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Usually due to seizures or rhabdomyolysis.
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Clinical approach to hypernatremia
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Refer to flow chart on slide 16.
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Symptoms of hypernatremia
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Neurologic
- Altered mentation, weakness, neuromuscular irritability, coma, seizures Polyuria and thirst |
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Signs of increased volume status due to hypernatremia
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Edema
Dyspnea Tachypnea Rales JVD |
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Hyponatremia
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Serum sodium in less than 135 mmol/liter in the absence of hyperglycemia. Usually reflects hypo-osmolar state and increased ICF volume
Normal response is excretion of solute free water by reabsorption of NaCl without water in the ascending loop of Henle and maintenance of dilute urine |
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Symptoms of hyponatremia
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Nausea and vomiting, headache, altered mentation, lethargy, fatigue, loss of appetite, restlessness and irritability, muscle weakness, spasms, or cramps, seizures, and decreased consciousness or coma.
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What corrections are needed for hydration calculations?
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Glucose
Lipids Protein contents Could indicate pseudohyponatremia. MedCalc |
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Causes of hyponatremia
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Hypovolemic states
Euvolemic states Hypervolemic states |
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Hypervolemic states (low volume)
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Low plasma osmolality.
Have an effective decreased arterial volume leading to thirst and vasopressin release. CHF, cirrhosis, nephrotic syndrome, renal insufficiency |
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Euvolemic states (normal volume)
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Low plasma osmolality
SIADH, hypothyroidism, adrenal insufficiency, primary polydipsia, reset osmostat, acute hypoxia or hypercapnia, medication Elevated plasma osmolality Hyperglycemia, mannitol (needs correction value) Normal plasma osmolality Hyperproteinnemia, hyperlipidemia (pseudohyponatremia) |
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Hypovolemic states
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Decreased arterial volume stimulates vasopressin release which impairs capacity to excrete a dilute urine (results electrolyte free water reabsorption).
Low plasma osmolality Extrarenal sodium loss- (low urine sodium) - Remote diuretic use, remote vomiting Renal losses (elevated urine sodium) Sodium wasting nephropathy, hypoaldosternoism, diuretic, vomiting. |
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What factors should you consider with hyponatremia?
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1. Volume status
2. Plasma osmolality |
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What factors should you consider with hypernatremia?
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1. Volume status
2. Urine osmolaity |
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Clinical approach to hyponatremia
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Refer to flow chart on slide 18.
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Normal range for K
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3.5-5.0 mEq/L
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What function does K have?
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Primary cation in the intracellular space.
Secretion regulated by aldosterone and hyperkalemia. Major role is regulation of muscle and nerve excitability Vital to cell metabolism and muscle function. |
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What is the most critical complication of a K imbalance?
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Heart conditions/problems
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S/S of hyperkalemia
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Cardiac toxicity
- Arrythmias - Peaked T waves - Prolonged PR or QRS Weakness Paralysis Hypoventilation |
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What is the primary cause of hyperkalemia?
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Decreased renal loss
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How does increased intake cause hyperkalemia?
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Rarely isolated cause
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Pseudohyperkalemia
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Due to K+ movement out of cell with venipuncture
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How does transcellular shift cause hyperkalemia?
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Tumor lysis syndrome and rhabdomyosysis lead to K+ release from cells.
- leads to a destruction of cells Metabolic acidosis associated with hyperkalemia Insulin deficiency Beta antagonist-treat with beta agonist (albuterol) - May contribute to elevation with other primary cause. Medication - succynylcholine (paralytic med) - once drug wears off, it improves |
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How does decreased renal excretion cause hyperkalemia?
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Decreased secretion results from either impaired Na+ reabsorption or increased Cl- reabsorption.
Impaired Na+ reabsorption- decreased aldosterone synthesis (Addison’s), Heparin, K+ sparing diuretics, ACE inhibitors, NSAIDS, other medication Impaired Cl- reabsorption- in renal insufficiency, diabetic nephropathy, or chronic tubulointerstitial disease. |
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Treatment of hyperkalemia
***NOT ON EXAM*** |
Short-term treatment
- Treat with insulin - D-50 (glucose to counteract insulin) - Give Calcium Cl/gluconate Long-term treatment - Kaxoliate - Dialysis |
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Hypokalemia
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Serum potassium <3.5mmol/liter
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S/S of hypokalemia
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Fatigue, myalgia, lower extremity muscular weakness, arrhythmias, rhabdomyolysis.
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Causes of hypokalemia
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Decreased net intake
Shift into cells Increased net loss |
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How does diminished intake cause hypokalemia?
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Seldom occurs as isolated cause
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How does transcellular shift cause hypokalemia?
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Typically a transient intracellular shift without affecting total body content.
Metabolic alkalosis Insulin therapy Beta agonists Stress induced catecholamine release |
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How does non-renal loss cause hypokalemia?
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GI loss as in vomiting or NG suction (loss of gastric contents results in volume depletion and metabolic alkalosis both promote kaliuresis.
Hypovolemia stimulates aldosterone release which increases secretion by cells and kaliuresis). |
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How does renal loss cause hypokalemia?
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Diuretic use
Primary hyperaldosteronism Hyperreninemia Hypomagnesemia Other |
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Normal range for Cl
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96-106 mEq/L
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Functions of Cl
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Most abundant extracellular anion
Role is balancing out positive charges in the extracellular fluid, and by passively following sodium, it helps to maintain extracellular osmolality Helps to regulate the amount of fluid in the body and maintain the acid-base balance. |
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Most important functions of Cl
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Follows Na
Maintains osmolality Maintains acid-base balance |
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Hyperchloridemia
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Serum level >106mmol/liter
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Causes of hyperchoridemia
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Hyperchloremic metabolic acidosis
Respiratory alkalosis Renal disease Severe dehydration Diabetes insipidus IV saline |
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Hypochloridemia
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Serum levels <96 mmol/liter
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Causes of hypochloridemia
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Renal loss- loop diuretics salt wasting nephropathies
GI loss- NG suction, gastric outlet obstruction, congenital chloride losing enteropathy, secretory diarrhea, Zollinger-Ellison, other |
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Normal range of bicarbonate (CO2)
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24-30 mmol/L
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Functions of CO2
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Serum CO2 values approximate the value of bicarbonate in the blood
Helps to maintain the body’s acid-base balance (pH) - Increases pH (alkaline) |
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Metabolic acidosis
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Acidotic patient with low bicarb
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Low bicarbonate
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In metabolic acidosis
Mildly deceased in chronic respiratory alkalosis with compensation |
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High bicarbonate
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In metabolic alkalosis
Mildly increased in chronic respiratory acidosis with compensation. |
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Normal range of magnesium
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1.5-2.2 mEq/L
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Functions of magnesium
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Cation, predominantly intracellular.
More than 50% stored in bone, most of the rest in soft tissues. Role in maintaining neuromuscular functions, enzyme functions, cofactor for ADP→ATP (helps regulate energy). |
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Hypermagnesium
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Serum levels >2.2 mEq/L
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S/S of hypermagnesium
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Weakness, nausea, vomiting, arrhythmias, decreased respirations, decreased DTR’s, brachycardia.
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Causes of hypermagnesium
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Acute or chronic renal failure (most common cause)
Adrenal insufficiency Medications with magnesium salts other |
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Hypomagnesium
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Serum levels <1.5 mEq/liter
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S/S of hypomagnesium
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Weakness, cramps, arrhythmias, tremors, jerking, nystagmus, increased DTR’s, tachycardia, hallucinations, tetany, seizures
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Causes of hypomagnesium
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Excessive urinary losses
Decreased intake Increased intestinal losses Alterations in distribution |
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How does excessive urinary loss cause hypomagnesium?
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Alcoholism
Renal tubular acidosis Interstitial renal diseases Hypercalcemic states Drugs Other |
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How does decreased intake cause hypomagnesium?
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Protein-calorie malnutrition
Starvation Pregnancy |
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How do increased intestinal losses cause hypomagnesium?
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Malabsorption syndromes
Surgical resection of small bowel (short bowel syndrome) NG suctioning (prolonged) Laxatives Diarrhea |
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How do alterations in distribution cause hypomagnesium?
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Sepsis syndrome
Multiple blood transfusions Pancreatitis Thermal injury |
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Major issues associated with magnesium
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Heart
Rate DTR Kidney problems Malnutrition/absorption issues |
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Normal range for Ca
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Normal range 8.5-10.8 mg/dL
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Functions of Ca
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Cation, 99.5% is integrated into bone. Other 0.5% mostly extracellular.
Role in neuromuscular activity, endocrine function, coagulation and bone and tooth metabolism |
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Hypercalcemia
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Typically due to both increased entry of calcium into the ECF and decreased renal clearance.
Serum level >10.8mg/dL |
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Causes of hypercalcemia
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Primary hyperparathyroidism- most common cause in ambulatory medicine
Malignancy- most common cause in hospitalized patients Less common – sarcoidosis, Vitamin D toxicity, lithium, hyperthyroidism, milk-alkali syndrome |
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S/S of hypercalcemia
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Stones (kidney and biliary), bones (pain), abdominal groans (N/V/constipation), thrones (polyuria), and psychiatric tones (depression, AMS, coma, insomnia)
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What is the most common cause of hypercalcemia in hospitalized patients?
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Malignancy due to breakdown of bone
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Hypocalcemia
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Serum level <8.5mg/dL
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S/S of hypocalcemia
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Asymptomatic to tetany, paresthesias, carpopedal spasms.
Trousseaus’ sign Chvostek’s sign |
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Causes of hypocalcemia
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Most commonly hypoalbuniemia
Renal failure, hypoparathyroidism, severe hypomagnesaemia, acute pancreatitis, tumor lysis syndrome, vitamin D deficiency, other. |
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Chvostek’s sign
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Twitching of facial muscles when the facial nerve is tapped anterior to the ear.
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Trousseaus’ sign
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Carpal spasm when a BP cuff is inflated above systolic pressure for 3 minutes.
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Normal range of phosphate
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2.6-4.5 mg/dL
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Functions of phosphate
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Major intracellular anion, 85% of phosphate is contained in bone
Involved in formation of ATP, component of phospholipid membranes, part of 2,3-DPG which regulates release of O2 from hemoglobin, important for cellular metabolism, bone formation |
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Hyperphosphatemia
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Most often due to renal failure, but also occurs in hypoparathyroidism, rhabdomyolysis, tumor lysis syndrome, acidosis, and excess administration
S/S: those attributed to hypocalcemia |
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S/S of hypophosphatemia
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Muscular abnormalities-weakness, rhabdo, respiratory failure, heart failure.
Neurologic- paresthesia, confusion, stupor, seizure, coma, dysarthria |
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Causes of hypophosphatemia
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Impaired intestinal absorption
Increased renal excretion redistribution in to cells (alcohol abuse, respiratory alkalosis, malabsorption, aluminum-containing antacids which bind to phosphate, severe burns) |
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Normal range of BUN
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8-20 mg/dL
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Functions of BUN (blood urea nitrogen)
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Measures kidney function
Produced by liver during breakdown of protein or ammonia Extra nitrogen is expelled from the body through urea (reflects serum nitrogen level) Kidney excretes urea in the urine |
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Low BUN
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SIADH
Liver disease Over hydration Anabolic hormones Malnutrition Pregnancy |
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High BUN
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Renal disease
Prerenal azotemia- GI hemorrhage, Shock, tissue necrosis, 3rd degree burn, dehydration, etc.. Addison’s disease Steroid therapy High protein diet Post-renal (renal vein thrombosis, urinary obstruction Medication (creatinine help differentiate prerenal from renal disease) |
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How do you determine if BUN is elevated?
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Look at creatinine along with it
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Normal range for creatinine
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0.7-1.5 mg/dL
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Functions of creatinine
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Measures kidney function
Non-protein nitrogenous biochemical in the blood Produced in the muscle as a spontaneous decomposition product of creatine and creatine phosphate Liver→creatine→creatine phosphate in muscles→ creatinine Inverse relationship between creatinine and kidney function Level also affected by muscle mass, sex, age, race, drugs, low-protein diets Useful in evaluation of GFR (glomerular filtration rate) |
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Low creatinine
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Small muscle mass
Cachectic patients Amputees Muscle disease |
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High creatinine
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Increased in renal disease, muscle necrosis and hypovolemia.
Renal failure (AKI, CKD, ESRD) Medications falsely elevate (cephalosporins) |
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AKI
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Acute Kidney Injury
(formerly kidney failure) |
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ESRD
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End-stage Renal Disease
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How can you determine location of renal problem?
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Consider BUN/creatinine ratio (see slide 36)
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Liver functions
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Synthesizes amino acids to proteins
Involved in breakdown of excess amino acids (to ammonia and urea) Plays role in carbohydrate metabolism Synthesizes cholesterol Primary location for detoxification and excretion of drugs and toxins |
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Pancreas functions
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Exocrine glands produce enzymes for digestion (e.g., lipase, amylase)
Endocrine glands produce insulin and glucagon |
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LFT for protein synthesis
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Albumin
Prealbumin PT/INR (clotting proteins) - used to measure coumadin therapy |
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LFT for excretion into bile ducts
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Bilirubin
Alkaline phosphatase - elevated in gallbladder disease |
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LFT for hepatocellular injury
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Transaminases
AST (aspartate aminotransferase) ALT (alanine aminotransferase) |
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LFT for detoxification
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Ammonia
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Normal range for albumin
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3.5-5.5 g/dL
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Functions of albumin
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Major plasma protein
Involved in maintaining plasma oncotic pressure and binding/transport of numerous hormones and drugs Long half-life (20 days) Low: causes fluid retention/ascites - treat with albumin for ascites |
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Normal range of prealbumin
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19.5-35.8 mg/dL
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Functions of prealbumin
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Involved in binding/transport of various solutes (thyroxin, retinol)
Used to assess protein calorie nutrition Shorter half-life (2 days) |
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Normal range for prothrombin time/INR
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PT 11.1-13.1 sec
INR 0.1-1.1 |
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Functions of PT/INR
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Measure speed of a set of reactions in the coagulation cascade which require clotting factors and vitamin K
Prolongation reflects clotting abnormalities |
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What lab evaluates synthetic liver function?
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Prothrombin time/INR
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What lab evaluates excretory liver function and cholestasis?
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Alkaline phosphatase
Bilirubin |
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Normal range for alkaline phosphatase
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30-120 IU/L
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Functions of alkaline phosphatase
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Enzyme found in liver, bone, placenta, WBCs, etc
Elevation may be related to: - Cholestasis - Bone growth, fracture, disease - Placental function in pregnancy - Infection |
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Normal range of bilirubin
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total 0.3-1 mg/dL
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Functions of bilirubin
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Breakdown product of heme pigments (e.g., hemoglobin)
Unconjugated (indirect) Normal range 0.2-0.7 mg/dL Insoluble Conjugated (direct) Normal range 0.1-0.3 mg/dL Linked to glucuronic acid by liver Soluble Excreted in stool |
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Gilbert's disease
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Increased indirect bilirubin
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What labs evaluate for hepatocellular injury?
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Aminotransferases (AST, ALT)
AST aspartate aminotransferase ALT alanine aminotransferase |
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What labs evaluate pancreatic inflammation?
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Amylase
Lipase |
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Amylase
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Normal range 60-180 IU/L
Breaks down starch Secreted by pancreas (40%) and salivary glands (60%) |
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Lipase
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Normal range <160 IU/L
Catalyzes hydrolysis of triglycerides to fatty acids and glycerol - more related to pancreas - test this for alcoholic pancreatitis |
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Functions of ALT/AST
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Enzymes in hepatic cells which assist with various metabolic pathways
Released into the serum in greater quantities when there is hepatocyte damage Very sensitive and may be mildly elevated with minimal hepatic damage |
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Normal range for ALT/AST
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<35 IU/L
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