Respiratory Failure:
- Caused by inadequate gas exchange (CO2/O2)
- Known as "hypoxemia" (if there is a drop in blood oxygen)
- Known as "hypercapnia" (if there is a rise in arterial CO2 levels)
- Type I
- Hypoxemia (low blood oxygen)
- High altitude
- Pulmonary embolism
- Alveolar hypoventilation or neuromuscular diseases
- Diffusion difficulty due to disease or infection like pneumonia, ARDS, SARS, etc...
- Shunt (oxygenated blood mixes with unoxygenated blood)
- Type II
- Hypoxemia with hypercapnia (increased blood CO2 levels)
- Decreased pH (respiratory acidosis)
- Caused by inadequate alveolar ventilation
- CO2 builds up in blood and cannot be eliminated
- Increased airway resistance due to COPD, suffocation, asthma, fibrosis, etc...
- Reduced breathing (brainstem injury, lesion, stroke, brain tumor, drugs, extreme obesity, etc...)
- Decreased gas exchange (COPD, emphysema, asthma, chronic bronchitis)
- Neuromuscular problems or diseases
- Deformed chest or chest wall due to scoliosis, kyphosis, injury, flail chest, ankylosing spondylitis, etc...)
- Increased respiratory rate
Some of the causes of respiratory failure include:
- Obstruction to the flow of air in or out of the lungs by a mass or foreign object, drugs, or chest wall changes (trauma, surgery, etc...)
- Thrombus, embolism, right-sided heart failure, myocardial infarction (heart failure/heart attack)
- Lung infections like bronchitis or pneumonia or viruses
- Lung diseases like cancer, interstitial lung disease, COPD, pulmonary edema
Chemistry Tests: CMP, BMP, Lactic Acid (gray-top on ice)
Respiratory Acidosis:
Respiratory acidosis is hypoventilation, or decreased ventilation, which increases the carbon dioxide (CO2) concentration in the blood, thereby decreasing the pH level, resulting in acidosis. Carbon dioxide (CO2) accumulates quickly in the lungs, leading to increased PaCO2, which is also referred to as hypercapnia. Respiratory acidosis is either acute or chronic. Our bodies typically get rid of CO2 through exhalation from the lungs and excretion with the urine, but when these processes are not functioning properly, the following can occur:
Acute Respiratory Acidosis:
Chronic Respiratory Acidosis:
Acute Respiratory Acidosis:
- Rapid onset of ventilation failure
- Central respiratory center depression can cause this
- Stroke
- CVA
- Traumatic brain injury
- Disease like brain abscess, tumor, encephalitis, meningitis, and others
- Neuromuscular diseases such as Guillain-Barre', Muscular Dystrophy, Myasthenia Gravis
- Airway obstruction (choking, drowning, severe asthma, allergic reaction, COPD flare up, suffocation, sudden infant death syndrome)
- Diving
- Asphyxiation
- Blood gas CO2 is >45 mmHg
- Blood pH is <7.35
Chronic Respiratory Acidosis:
- Ongoing conditions
- COPD
- AML
- Interstitial Lung Disease
- Obesity
- Chronic sleep apnea
- Thoracic anomalies
Respiratory Alkalosis:
Respiratory alkalosis is caused by hyperventilation, or exhaling too quickly, resulting in a rapid loss of CO2. Diseases that affect the central nervous system (CNS), such as strokes, brain injuries, or Rett Syndrome, can all cause this condition. The blood pH rises to >7.45 (the normal range is 7.35-7.45). Arterial levels of CO2 decrease. This disrupts the body's acid-base balance. Some causes include the following:
Respiratory alkalosis can be acute or chronic.
- Aspirin (salicylate) toxicity or overdose
- Pulmonary disorders
- An asthma attack
- Drop in blood sugar
- Fever
- A heart disorder
- Liver disease
- Stress
- A panic attack or an anxiety attack
- Burn or chemical injury
- High altitude or altitude sickness
- Exercise intolerance
- Anything that causes shortness of breath
- Obesity
- Improper or lack of mechanical ventilation when needed.
Respiratory alkalosis can be acute or chronic.
Heart Failure:
Heart failure occurs when the heart is unable to pump enough blood to sustain the body's normal functions. This results in ongoing fatigue, dizziness, shortness of breath, fluid build up in the lungs, a cough, swelling in the ankles, legs and abdomen, exercise intolerance, and sometimes chest pain. The most common causes include:
The two types of heart failure include the following:
1) Left Ventricular Dysfunction
2) Normal Ejection Fraction
It can affect the left side, the right side, or be bilateral. There are many different causes. Diagnosis comes about by a physical, chest radiography, echocardiogram, blood tests , and others.
- Coronary Artery Disease (CAD)
- Prior heart attack (Myocardial Infarction)
- Atrial fibrillation
- High blood pressure
- Alcoholism
- A disease that affects the heart valves
- An infection
- Cardiomyopathy
- Lung disorder
- Rheumatory arthritis
The two types of heart failure include the following:
1) Left Ventricular Dysfunction
2) Normal Ejection Fraction
It can affect the left side, the right side, or be bilateral. There are many different causes. Diagnosis comes about by a physical, chest radiography, echocardiogram, blood tests , and others.
- Heart cannot pump enough or with enough force to maintain normal and adequate blood flow in congestive heart failure
- Fatigue, shortness of breath (SOB), weakness, edema, and chest pain are common symptoms
Causes:
- Myocardial infarction
- Coronary artery disease
- Atrial fibrillation
- High blood pressure (chronic/ongoing)
- Alcoholism
- Valvular heart disease
- Heart infections (myocarditis, pericarditis, endocarditis)
- Cardiomyopathy (idiopathic, or unknown cause)
- Trauma
Types:
- Left ventricular dysfunction
- Normal injection fraction
Chemistry Tests:
BNP (will be elevated)
-This test is useful for the detection of congestive heart failure and when the patient has symptoms of angina
Troponin (may be elevated)
-This test is useful for the diagnosis of myocardial infarction (heart attack)
Electrolytes: Potassium (K), Magnesium (Mg), Calcium (Ca), Sodium (Na) (may be decreased)
Kidney function panel (renal panel)
Liver function (liver panel)
Thyroid function tests
C-reactive protein
Vasopressin (elevated)
Glucose, Glucose Metabolism and Diabetes:
Blood glucose levels are one of the most common and frequently performed Chemistry tests in the laboratory. Glucose is a monosaccharide, which is a simple sugar. When our bodies break down the carbohydrates we take in through our diet, monosaccharides are the most simple sugars that exist.
Carbohydrates are absorbed in the small intestine on finger-like projections called microvilli. This is where monosaccharides such as glucose are absorbed. Other monosaccharides, galactose and fructose, are converted by the liver into glucose. Galactose is a sugar found in milk, and fructose is a sugar found in fruit.
Glucose provides the main source of energy for most of our body cells. There are hormones that keep the blood glucose under control, keeping the body in homeostasis, or balance. Insulin is a hormone that is secreted by the pancreas. After we eat, it is secreted, it responds to high glucose levels, and promotes the entry of glucose into cells. There are two types of metabolism that glucose undergoes, depending upon what the needs of the body are. The first type is aerobic respiration, which requires oxygen, and the second is anaerobic respiration, which does not require oxygen. Energy is yielded in the form of ATP (adenosine triphosphate). This process is known as glycolysis.
If glucose is not currently needed, it can be converted into glycogen and stored in the liver until it is needed. This is called glycogenesis. The hormones glucagon, cortisol, and thyroxine work to convert glycogen back into glucose when needed by the body cells. Glucose is also able to be converted into protein and fat as needed and also stored. Glucagon is secreted by the alpha cells of the pancreas, which blocks the action of insulin, and it raises blood glucose levels by causing glycogen stores to break down in the liver.
Fasting serum plasma glucose level reference ranges are as follows: 70-110 mg/dL. This level naturally increases quickly after a meal rich in carbohydrates. It takes about 1.5-2 hours for it to return back to normal. Hyperglycemia is an increase in blood glucose, common in diabetes. Hypoglycemia is a drop in blood glucose, which falls to <50 mg/dL, which can lead to syncope (fainting) or shock. Too much insulin given to a diabetic patient can result in a rapid drop in blood glucose, leading to hypoglycemia. Insulin lowers the blood sugar.
Carbohydrates are absorbed in the small intestine on finger-like projections called microvilli. This is where monosaccharides such as glucose are absorbed. Other monosaccharides, galactose and fructose, are converted by the liver into glucose. Galactose is a sugar found in milk, and fructose is a sugar found in fruit.
Glucose provides the main source of energy for most of our body cells. There are hormones that keep the blood glucose under control, keeping the body in homeostasis, or balance. Insulin is a hormone that is secreted by the pancreas. After we eat, it is secreted, it responds to high glucose levels, and promotes the entry of glucose into cells. There are two types of metabolism that glucose undergoes, depending upon what the needs of the body are. The first type is aerobic respiration, which requires oxygen, and the second is anaerobic respiration, which does not require oxygen. Energy is yielded in the form of ATP (adenosine triphosphate). This process is known as glycolysis.
If glucose is not currently needed, it can be converted into glycogen and stored in the liver until it is needed. This is called glycogenesis. The hormones glucagon, cortisol, and thyroxine work to convert glycogen back into glucose when needed by the body cells. Glucose is also able to be converted into protein and fat as needed and also stored. Glucagon is secreted by the alpha cells of the pancreas, which blocks the action of insulin, and it raises blood glucose levels by causing glycogen stores to break down in the liver.
Fasting serum plasma glucose level reference ranges are as follows: 70-110 mg/dL. This level naturally increases quickly after a meal rich in carbohydrates. It takes about 1.5-2 hours for it to return back to normal. Hyperglycemia is an increase in blood glucose, common in diabetes. Hypoglycemia is a drop in blood glucose, which falls to <50 mg/dL, which can lead to syncope (fainting) or shock. Too much insulin given to a diabetic patient can result in a rapid drop in blood glucose, leading to hypoglycemia. Insulin lowers the blood sugar.
Diabetes:
Diabetes is an epidemic in our country and cases are on the rise. It poses a problem and challenge in the medical field today. It is currently the 7th leading cause of death in the USA, and it is closely associated with other diseases.
Diabetes Mellitus Type 1:
- B-cell destruction in the pancreas results in total insulin deficiency
- Insulin-dependent (requires regular insulin injections)
- Typically diagnosed during childhood or young adulthood
- Possible genetic link
- Cell-mediated autoimmune destruction of the beta (B) cells in the pancreas
- Increased ketone bodies, which can lead to ketoacidosis, a decrease in blood pH, and/or metabolic acidosis
Diabetes Mellitus Type 2:
- Slow insulin secretory deficiency
- Insulin resistance
- Often controlled first with diet and exercise and close monitoring of blood glucose levels
- Non-insulin-dependent
- Typically diagnosed later in adulthood
- Gradual onset
- Progressive hyperglycemia
- Linked to development of atherosclerosis and an increased risk of coronary artery disease and stroke
Symptoms:
- Polyuria (increased urination)
- Hyperglycemia (increased blood glucose level)
- Glycosuria (urine glucose)-Blood glucose exceeds 160-170 mg/dL, so it spills over into the urine
- Polydipsia (increased thirst)
- Polyphagia (increased hunger)
- Weight loss
- Ketonemia (increased blood ketones)
- Ketonuria (increased urine ketones)
Gestational Diabetes:
- Diagnosed during pregnancy
- Glucose intolerance due to metabolic and hormonal changes during pregnancy
- Can lead to Diabetes Mellitus Type 2 later on
- Can result in birth complications
Diabetes Insipidus:
- This is a type of diabetes that causes a water imbalance in the body
- Characterized by extreme thirst (polydipsia)
- Characterized by a loss of large amounts of diluted urine (polyuria), of up to 15 liters (normally adults excrete about 3 liters of urine per day)
- There is no cure, but it can be managed
- This type of diabetes is completely unrelated to diabetes mellitus
- This type of diabetes is characterized by excessive nocturia (getting up to urinate multiple times at night, or even wetting the bed)
- Damage to or tumors of the pituitary gland or hypothalamus can cause this condition, since it disrupts the normal production, storage and/or excretion of the hormone that controls urine production, ADH
- A defect in the kidney tubules can cause this condition, since they cannot respond normally to the effects of ADH
- There is a rare form of gestational diabetes insipidus caused by an enzyme made by the placenta
- Drinking too much fluid can also cause this condition
- Testing for the body's electrolytes is important in diagnosis and treatment of this type of diabetes
Hyperglycemia and Ketoacidosis:
- Elevated blood glucose levels
- Decreased blood CO2 levels
- Testing for ketones can aid in recognizing this condition, along with other tests such as CO2
- Can be secondary to a traumatic brain injury, disease or illness, liver diseases, overactive adrenal, pituitary or thyroid gland
- Impaired glucose tolerance
- Can be stress-induced
- Common in diabetic patients
Hypoglycemia:
- Decreased blood glucose levels
- Blood glucose level is below the fasting value
- Can be associated with glycogen storage disease (impairment of breakdown of glycogen in the liver)
- Can be associated with islet cell hyperplasia in the pancreas
- Can be associated with insulinoma, resulting in hyperinsulinemia, or increased insulin in the blood
- Can become life-threatening since the brain and cardiac cells depend on glucose for nutrients
- Can lead to nausea, vomiting, weakness, dizziness, shortness of breath, fatigue, muscle spasms, syncope, coma or death
- Premature infants, maternal diabetes, and maternal toxemia can cause this condition in neonates or infants, as can inborn errors of metabolism or ketotic hypoglycemia
Types of Lab Tests for Glucose Levels and Diabetes:
Blood collection for glucose and diabetic testing encompasses capillary whole blood specimens, plasma or serum from a fasting individual. An evacuated gray-top tube containing sodium fluoride is used to collect blood for glucose testing, unless it is a rapid point-of-care test. The sodium fluoride is an additive that blocks glucose metabolism in cells, preserving it for accurate glucose testing. A serum separator tube (SST) or plasma separator tube can be used, but must be processed within 30 minutes of collection.
This test is almost always a fasting test, because glucose increases in the blood after a meal. Blood is drawn 2 hours after a meal if it is not a fasting test. A fasting test means that the individual has not had food or drink for 8-12 hours prior to being drawn. A 4-5 hour oral glucose tolerance test (OGTT) is also a test that can be administered to pregnant women or diabetic individuals or those suspected of being diabetic to check for a pattern of rising serum or plasma glucose.
Glucose can also be tested in body fluids such as CSF and in urine. CSF needs to be tested immediately because should bacteria be present, it will rapidly decrease the levels of glucose. A 24-hour urine collection can be used to test glucose in the urine, because the glucose is preserved by the additive in the 24-hour urine jug. It needs to be stored in the 4-8 degrees refrigerator, because up to 40% of the glucose may be lost in urine that is stored at room temp.
Reference range:
Nonpregnant women: <110 mg/dL fasting or <126 mg/dL 2-hour post-prandial serum or plasma
Point-of-care testing for individuals monitoring their own blood glucose levels at home, as well as monitoring glucose levels in hospitalized patients at the bedside is another form of glucose testing. Capillary blood glucose meters are used for this purpose. This is obtained by finger puncture and involves the use of reagent test strips. Enzymes present on the strip detect glucose levels and cause color changes that can be read by the meter.
Glycosylated hemoglobin testing exists to estimate the longer-term glucose concentration over a period of months. This is called the A1C test or GCHB. Ketone body testing is another test that checks for 3 ketone bodies for acidosis and extremely elevated blood glucose levels or ketoacidosis. Since diabetes can cause renal changes in the kidneys, microalbumin protein testing can be performed to aid in the diagnosis and treatment of diabetic nephropathy.
This test is almost always a fasting test, because glucose increases in the blood after a meal. Blood is drawn 2 hours after a meal if it is not a fasting test. A fasting test means that the individual has not had food or drink for 8-12 hours prior to being drawn. A 4-5 hour oral glucose tolerance test (OGTT) is also a test that can be administered to pregnant women or diabetic individuals or those suspected of being diabetic to check for a pattern of rising serum or plasma glucose.
Glucose can also be tested in body fluids such as CSF and in urine. CSF needs to be tested immediately because should bacteria be present, it will rapidly decrease the levels of glucose. A 24-hour urine collection can be used to test glucose in the urine, because the glucose is preserved by the additive in the 24-hour urine jug. It needs to be stored in the 4-8 degrees refrigerator, because up to 40% of the glucose may be lost in urine that is stored at room temp.
Reference range:
Nonpregnant women: <110 mg/dL fasting or <126 mg/dL 2-hour post-prandial serum or plasma
Point-of-care testing for individuals monitoring their own blood glucose levels at home, as well as monitoring glucose levels in hospitalized patients at the bedside is another form of glucose testing. Capillary blood glucose meters are used for this purpose. This is obtained by finger puncture and involves the use of reagent test strips. Enzymes present on the strip detect glucose levels and cause color changes that can be read by the meter.
Glycosylated hemoglobin testing exists to estimate the longer-term glucose concentration over a period of months. This is called the A1C test or GCHB. Ketone body testing is another test that checks for 3 ketone bodies for acidosis and extremely elevated blood glucose levels or ketoacidosis. Since diabetes can cause renal changes in the kidneys, microalbumin protein testing can be performed to aid in the diagnosis and treatment of diabetic nephropathy.
Electrolyte Imbalances and Pathophysiology:
Our bodies' electrolytes are so important for the normal function of the heart, muscles, and nervous system. Low or high levels can interfere severely with normal function, resulting in rapid or low heartbeat, muscle cramps and pain, and a plethora of other symptoms. Electrolytes are chemical elements that form or exist as ions (charged particles) when dissolved in water. Our bodies are 80% water with dissolved substances. Electrolytes with a positive charge are called cations. Electrolytes with a negative charge are called anions. Cations move toward a cathode, and anions move toward an anode in an electrical field, just like you see with jumper cables and a car battery.
The body strives to keep the electrolytes in balance, which is referred to as homeostasis. It is crucial that the positively charged cations balance/neutralize the negatively charged anions so they cancel each other out. The kidneys and lungs are the major organs that maintain this balance and it is known as the acid-base buffering system. If the body is not able to maintain control over the electrolyte concentration, either through excretion, exhalation or conserving something, then an electrolyte imbalance will happen. This can be harmful and even fatal to the individual since almost all of the body's normal functions depend upon a normal electrolyte balance.
Electrolytes in our bodies include the following:
The body strives to keep the electrolytes in balance, which is referred to as homeostasis. It is crucial that the positively charged cations balance/neutralize the negatively charged anions so they cancel each other out. The kidneys and lungs are the major organs that maintain this balance and it is known as the acid-base buffering system. If the body is not able to maintain control over the electrolyte concentration, either through excretion, exhalation or conserving something, then an electrolyte imbalance will happen. This can be harmful and even fatal to the individual since almost all of the body's normal functions depend upon a normal electrolyte balance.
Electrolytes in our bodies include the following:
- Sodium (Na+)
- The major cation
- Potassium (K+)
- Another major cation
- Calcium (Ca2++)
- Magnesium (Mg2++)
- Chloride (Cl-)
- Major anion
- Bicarbonate (HCO3-)
- Major anion and buffer
- Sulfate (SO-)
- Phosphate (HPO-)
The Cell Membrane, Cells in Solutions, Diffusion, Transport and Osmosis (Electrolyte and Water Balance Occurs, Glucose Transport, Lipoprotein Transport, Etc... Occur Via These Mechanisms):
Passive/Simple Diffusion of Uncharged Particles:
Facilitated Diffusion (Charged Particles and Larger Particles That Need a Little "Help"):
Uniport, Synport, Antiport Transport:
Active Transport:
Osmosis:
Cells in Solutions:
Tonicity and Our Cells:
Tonicity is a measure of the osmotic gradient, or the water potential of two solutions separated by a semipermeable membrane. The cell membrane is a semipermeable membrane, meaning that it only lets certain things in and certain things out as needed. It houses many types of specialized channels and receptors that "recognize" specific molecules and allows them to come in or go out. This keeps the cells, and the body, in homeostasis, or balance. It is when things at the molecular level get out of balance that it causes large scale signs and symptoms and problems in the body that we feel and may or may not recognize.
Molecules are transported across the cell membrane in a variety of different ways, depending upon the size of the molecule and whether or not it has a charge (ion). There are charged particles both inside and outside the cell membrane that play a key role in cardiac function, nerve impulses, and skeletal muscle movement, digestion, and many other functions in the body. Tonicity is the approximate concentration of solutes (particles) dissolved in solvent to create a solution. This determines the extent of transport, which may be passive (simple or facilitated), active (primary or secondary) or via a special "pump". Tonicity only has an effect on solutes that cannot cross the membrane without help of a protein or pump. Solutes that can freely cross the membrane through open channels do not affect tonicity because they always remain equal on both sides of the membrane. When imbalances occur, this results in hypertonic or hypotonic solutions.
Molecules are transported across the cell membrane in a variety of different ways, depending upon the size of the molecule and whether or not it has a charge (ion). There are charged particles both inside and outside the cell membrane that play a key role in cardiac function, nerve impulses, and skeletal muscle movement, digestion, and many other functions in the body. Tonicity is the approximate concentration of solutes (particles) dissolved in solvent to create a solution. This determines the extent of transport, which may be passive (simple or facilitated), active (primary or secondary) or via a special "pump". Tonicity only has an effect on solutes that cannot cross the membrane without help of a protein or pump. Solutes that can freely cross the membrane through open channels do not affect tonicity because they always remain equal on both sides of the membrane. When imbalances occur, this results in hypertonic or hypotonic solutions.
Isotonic Solution:
An isotonic solution is a solution in balance. The solute concentration is the same, or equal, on both sides of the cell membrane. The cell does not swell and it does not shrink. There is no concentration gradient, and cells neither gain nor lose any water. The rate of diffusion of water molecules is the same in both directions. Water molecules can freely cross the membrane through open aquaporins.
Hypotonic Solution:
In a hypotonic solution, the concentration of solutes is lower than in other solutions. The solution outside the cells has a lower concentration of solute molecules than inside the cell, so water rushes into the cell via osmotic pressure to try to balance out of the solute. This causes the cells to swell, and they can lyse/burst. Cells appear bloated due to the turgor pressure of the water pressing against the cell wall. Volume overload, drinking too much water, too much IV saline solution, some types of anemia, and other conditions can cause our red blood cells to swell like this, resulting in poikilocytosis and anisocytosis, or changes in red blood cell size and shape, in which they become larger, swollen, macrocytes. Stomatocytes, ovalocytes, elliptocytes, and target cells are a few examples of this.
Hypertonic Solution:
A hypertonic solution is one in which the concentration of solute is greater outside the cell than inside of it. This means that water rushes out of the cell due to osmotic pressure to try to balance out the concentration on both sides of the cell, so cells shrink or "crenate". A couple of examples of red blood cells that show crenation in the slides shown are echinocytes (Burr cells) and acanthocytes (spur cells).
Sodium (Na+) and Hyponatremia:
Sodium (Na+) is the major cation and positively charged particle in the body. Its highest concentration is in the extracellular fluid. It aids in maintaining healthy osmotic pressure and proper electrolyte balance. Along with chloride (Cl-) and bicarbonate (HCO3-), it aids in maintaining the acid-base balance of the cells of the body.
Hyponatremia is a low sodium level, detected in the blood and/or urine. Blood levels fall to <135 mmol/L. It is severe if it drops to <120 mmol/L. Kidney disease, liver disease, heart failure, ADH insufficiency, adrenal diseases or dysfunctions, hypothyroidism, volume depletion can all cause this condition, and many symptoms may accompany it. Some common conditions that cause it include:
Hyponatremia is a low sodium level, detected in the blood and/or urine. Blood levels fall to <135 mmol/L. It is severe if it drops to <120 mmol/L. Kidney disease, liver disease, heart failure, ADH insufficiency, adrenal diseases or dysfunctions, hypothyroidism, volume depletion can all cause this condition, and many symptoms may accompany it. Some common conditions that cause it include:
- Severe polyuria
- Metabolic acidosis
- Addison's disease
- Diarrhea
- Renal tubular disorders
- Diuretics
- Caffeine excess
Hypernatremia:
Hypernatremia is a high sodium level, detected in the blood and/or urine. Blood levels rise to >145 mmol/L as detected by the chemistry BMP. Severe symptoms occur if it rises to >160 mmol/L. There are many causes and many symptoms. Some of the most common causes include:
- Cardiac failure
- Congestive heart failure
- Liver disease with ascites fluid
- Renal disease
- Nephritic syndrome
- Cushing's syndrome
- Severe dehydration
- Brain injury
- Diabetic coma after insulin therapy
- Excess treatment with sodium salts
Blood chemistry and urine chemistry tests, including osmolality tests, aid in the diagnosis of hyponatremia and hypernatremia. Na+ is the major cation and it is found in the highest concentration in extracellular fluid between cells. Water retention results in sodium retention, conversely water loss results in sodium loss. Fluid buildup is known as edema.
The kidneys basically have the ability to either excrete or conserve large amounts of sodium, depending on the concentration of Na+ in the extracellular fluids and the needs of the body. Atop each kidney sits a triangular-shaped gland known as the adrenal cortex. Along with the pituitary and hypothalamus glands in the brain, the adrenal cortex glands secrete or store hormones that aid in the conservation or excretion of sodium and water. Diseases, disorders involving these glands and others, or injury can affect the acid-base balance of the body.
Osmolality is the physical property of a solution dependent upon the concentration of solutes (materials dissolved in a liquid) per kilogram of solvent (the dissolver/liquid). This is the condition upon which the hypothalamus in the brain responds, and it is the body's thermostat. Regulation of osmolality affects the Na+ concentration in the plasma. This regulates important mechanisms in the body, including:
The kidneys basically have the ability to either excrete or conserve large amounts of sodium, depending on the concentration of Na+ in the extracellular fluids and the needs of the body. Atop each kidney sits a triangular-shaped gland known as the adrenal cortex. Along with the pituitary and hypothalamus glands in the brain, the adrenal cortex glands secrete or store hormones that aid in the conservation or excretion of sodium and water. Diseases, disorders involving these glands and others, or injury can affect the acid-base balance of the body.
Osmolality is the physical property of a solution dependent upon the concentration of solutes (materials dissolved in a liquid) per kilogram of solvent (the dissolver/liquid). This is the condition upon which the hypothalamus in the brain responds, and it is the body's thermostat. Regulation of osmolality affects the Na+ concentration in the plasma. This regulates important mechanisms in the body, including:
- Thirst mechanism and intake of water in response
- Excretion of water in the form of urine, which is mainly influenced by the hormone antidiuretic hormone
- Regulation of blood volume, which occurs via a number of hormone, including aldosterone, angiotensin II, and atrial natriuretic peptide
Edema (Swelling):
Isotonic Saline Solution: 0.9% NaCl
Potassium (K+) and Hypokalemia:
Potassium (K+) is the body's major intracellular cation. Some is also found in the extracellular fluid. Along with sodium (Na+), the two cations form a sodium-potassium pump which plays a key role in the muscle activity of the heart and movement of the skeletal muscles.
Hypokalemia is abnormally low levels of potassium (K+) in the blood. This can result from prolonged vomiting and/or diarrhea or from potassium deficiency. Also, use of diuretics can result in excess potassium loss from the body. The kidneys already naturally excrete potassium from the body, even if the body is deficient. The body is unable to protect itself. We must get a regular intake of potassium in the diet.
Seen in the following conditions:
Hypokalemia is abnormally low levels of potassium (K+) in the blood. This can result from prolonged vomiting and/or diarrhea or from potassium deficiency. Also, use of diuretics can result in excess potassium loss from the body. The kidneys already naturally excrete potassium from the body, even if the body is deficient. The body is unable to protect itself. We must get a regular intake of potassium in the diet.
Seen in the following conditions:
- Aldosteronism
- Diarrhea
- Vomiting
- Cushing's Syndrome
- Diuretic therapy (long-term)
- Too much ingestion of licorice (black licorice)
- Heart arrhythmia
Hyperkalemia:
Hyperkalemia is elevated levels of potassium (K+) in the blood. Conditions that cause potassium levels to become elevated include kidney dysfunction or urinary obstruction. Renal dialysis removes excesses from the blood plasma.
Potassium levels are important because they play a role in heart, muscle and nerve function.
Conditions seen in:
Conditions seen in:
- Burn injuries
- Crush injuries
- Diabetic ketoacidosis
- Myocardial infarction
- Renal failure
- Addison's Disease
- Blood transfusions involving large amounts of blood (massive transfusion)
Hypomagnesemia:
Hypomagnesemia is lower levels of magnesium in the blood.
- Often seen in hospitalized ICU patients receiving diuretics or on digitalis therapy
- Rare in non-hospitalized patients
- Serum levels fall below 0.5 mmol/L
- Affects the cardiovascular system
- Affects the neuromuscular system
- Can result in secondary metabolic conditions, including depression, agitation, psychosis, neurosis, hyponatremia, hypokalemia, hypocalcemia)
Hypermagnesemia:
Hypermagnesemia is higher levels of magnesium in the blood.
- Rare and not seen as often as hypomagnesemia
- Usually results from decreased renal function
- May result from excessive intake of dietary Mg supplements or antacids such as TUMS or Rolaids
- AVOID HEMOLYSIS because the concentration of Mg is TEN TIMES HIGHER inside the cell than outside of it
- Collect blood for testing in light green lithium heparin or dark green sodium heparin evacuated tube
Chloride (Cl-):
Chloride is found in the serum, plasma, CSF, urine, and tissues of the body. Its concentration in the extracellular fluid is important since it aids in maintaining the acid-base balance of the body. If there is a decrease in CO2, there will be an increase in bicarbonate (HCO3-), and vice versa. This major anion counterbalances the positive sodium cation. Chloride aids in maintaining osmotic pressure and distribution of water inside and outside the cells, and it maintains electrical neutrality of the body. It aids in buffering when CO2 exchange occurs in the red blood cells.
Acid-Base Balances and Chloride Shift:
The normal hydrogen ion concentration (H+) in the blood and extracellular body fluids ranges from 7.35 to 7.45 on the pH scale. Anything less than that results in acidosis. Anything greater than that results in alkalosis. The lungs and kidneys control and excrete H+ to maintain pH homeostasis. The body has a buffer system as a first line of defense to provide against extreme changes in H+ ions. Buffers consist of a weak acid, such as carbonic acid, and a base or salt, such as bicarbonate. Another buffer is the phosphate buffer system.
When CO2 exchange occurs in the red blood cells, chloride aids in buffering and this is referred to as the chloride shift. Bicarbonate leaves the plasma and enters RBCs at the same time that blood receives oxygen and chloride moves from the RBCs to the plasma. If this did not occur, cells would lyse (burst/explode) or crenate (shrink and dry up). This aids in keeping red blood cells in an isotonic solution.
Imbalances in chloride levels are seen in the following conditions:
When CO2 exchange occurs in the red blood cells, chloride aids in buffering and this is referred to as the chloride shift. Bicarbonate leaves the plasma and enters RBCs at the same time that blood receives oxygen and chloride moves from the RBCs to the plasma. If this did not occur, cells would lyse (burst/explode) or crenate (shrink and dry up). This aids in keeping red blood cells in an isotonic solution.
Imbalances in chloride levels are seen in the following conditions:
- Dehydration
- Decreased renal blood flow
- Congestive heart failure
- Too much dietary supplementation with Cl-
- Chronic pyelonephritis
- An inborn metabolic acidotic condition
- Diabetic acidosis
- Renal failure
- Prolonged vomiting
Bicarbonate (HCO3-):
Bicarbonate is the other major extracellular anion that maintains the body's acid-base buffering system. This is filtered by the kidneys and most of it is reabsorbed.
Anion Gap:
The anion gap is a mathematical calculation and difference between the anions Cl- and HCO3- and the cations Na+ and K+. Cl- and HCO3- are summed up and subtracted from the sum of Na+ and K+. The difference should be <16 mmol/L. The normal anion gap should range between 10-20 mmol/L.
Increased in:
Decreased in:
The anion gap can be used for quality control (QC) for the electrolytes.
Increased in:
- Ketoacidosis
- Lactic acidosis
- Salicylate (aspirin) intoxication
- Methanol ingestion
- Uremia
- Increased plasma proteins
Decreased in:
- Increase in Mg+ or Ca+
- Decrease in the unmeasured anions
The anion gap can be used for quality control (QC) for the electrolytes.
Metabolic Acidosis:
Metabolic acidosis is a condition that results from the body's buildup of acids or the kidney is not removing enough of them. It can lead to the more severe condition of acidemia. Blood pH falls to <7.35. There are many things that can cause it, but it can result in coma and death if it goes unchecked. There is an increase in the anion gap. Several types of metabolic acidosis include:
- lactic acidosis
- ketoacidosis
- rhabdomyolysis
- kidney failure resulting in uremia
- drug OD, particularly of aspirin/acetaminophen
- alcoholism
- ingestion of antifreeze
Metabolic Alkalosis:
Metabolic alkalosis is a condition in which the blood pH rises to >7.45. Many conditions can cause it, including:
- Vomiting
- Diarrhea
- Cystic Fibrosis
- Excess alkaloids, such as TUMS
See the other tab on clinical chemistry tests to see which color evacuated tube blood should be collected in for the tests on electrolytes. Green-top lithium heparinized plasma is the most common.
Electrolyte Profile:
- Sodium
- Stable in serum for 1 week (room temp/fridge) or 1 year (frozen)
- Light green lithium heparin evacuated tube for plasma
- Serum
- Urine (24-hour)
- CSF
- Other body fluids
- Don't use sodium heparin evacuated tube (dark green) since it will interfere with the test
- Stable in serum for 1 week (room temp/fridge) or 1 year (frozen)
- Potassium
- Light green lithium heparin or dark green sodium heparin tube
- Serum can be used
- Stable for 1 week at room temp. or in fridge or frozen for up to 1 year
- 24-hour urine can be tested
- Avoid hemolysis BECAUSE the concentration of potassium in the RBC's is about 20x that in serum or plasma!!!!!!!!!!!!!!!!!!!! It can interfere with the test
- Separate the cells from the plasma or serum within THREE HOURS of collection to avoid the shift of potassium from the RBC's into the serum or plasma
- DO NOT have the patient open and close the fist when collecting blood for potassium levels, since the muscular pumping action can increase the plasma potassium level by 10-20%
- Light green lithium heparin or dark green sodium heparin tube
- Chloride
- Can use lithium or sodium heparin
- Can use an SST tube
- Serum, plasma, urine, sweat or other body fluids can be tested
- Hemolysis does not really affect it
- Can use lithium or sodium heparin
- Bicarbonate
- Can use lithium or sodium heparin
- Can use serum
- Test IMMEDIATELY upon opening the tube to minimize losses of CO2 and HCO3-
- Can use lithium or sodium heparin
The Other Electrolytes:
- Calcium (Ca+) (free calcium ions)
- Needed for proper cardiac function
- Regulated by three hormones:
- parathyroid hormone (PTH)
- vitamin D
- calcitonin
- Test serum
- Ionized Calcium (ICA)
- Decreased level impairs cardiac function
- Decreased level causes tetany (muscle spasms)
- Test whole blood (calcium exists as ionized calcium; 45%)
- Magnesium (Mg+)
- This is the 4th most common cation in the body
- Intracellular ion
- Found in bone and muscle
- Cofactor of >300 enzymes
- Essential for proper cardiovascular and neuromuscular function
- This is the 4th most common cation in the body
Hypocalcemia:
- Low serum or blood levels of calcium
- Results in neuromuscular irritability
- Cardiac irregularities
Hypercalcemia:
- High serum or blood levels of calcium
- Results from primary hyperparathyroidism
- Results from several types of malignancies
Reference Ranges:
Check with your particular lab for reference ranges, which is based on specific instruments and specimen types.
Multi-Organ Failure:
This is the failure of two or more organs, and there are four clinical stages. Septic shock, sepsis, renal failure, liver failure, lactic acidosis, respiratory and metabolic acidosis or alkalosis, all play a key role in multi-organ failure.
Stages:
Mortality: 30-100%
Stages:
- Respiratory alkalosis, oliguria (absence of urine), hyperglycemia
- Tachycardia (rapid heart beat), Hypoxemia (lack of oxygen to tissues), hypocapnia (low CO2), liver dysfunction, hematology (blood) changes in CBC w/diff
- Shock, azotemia, acid-base balance is off, coagulation abnormalities
- Oliguria, needs vasopressin, lactic acidosis, ischemic colitis due to lack of motion of the smooth muscles found in the intestines
Mortality: 30-100%
Kidney (Renal) Function and Kidney Failure:
Many people in the USA are affected by renal (kidney) diseases and dysfunctions. It affects >8 million people. Kidney failure causes mortality in more people than many cancers. Chronic kidney disease and renal failure increase an individual's risk of cardiovascular disease as well, since toxins build up in the blood. Renal function is measured by the BUN (blood urea nitrogen) chemistry test, serum creatinine and creatinine clearance, the glomerular filtration rate and cystatin C.
Urea is a major waste product of metabolism, and is normally excreted with the urine. Because urea is a waste product and a toxin, its buildup in the bloodstream can have negative consequences on a patient's health. It is the major constituent of a group of metabolic waste products along with nitrogen, amino acids, uric acid, creatinine, creatine, and ammonia. Most of the urea is excreted through the kidneys (a tiny amount is excreted in sweat and some through the lungs).
The liver makes urea and the liver is our major detoxification organ. Once protein breaks down into its simpler form of amino acids, ammonia is formed. Ammonia is toxic to the body so it is removed in the liver or combined with amino acids then converted to urea. The liver contains enzymes that act upon these larger metabolites to break them down into simpler ones. The kidneys then remove them. If there is a buildup of these toxins in the blood, it indicates that the kidneys are not functioning properly. It also means that the filtering system of the kidneys may be compromised. If the glomerular filtration rate drops to at least 50%, at that point urea will show up as a significant increase in concentration. Diet, hydration, and protein metabolism also affect this.
High nitrogen levels in the blood result in a condition called uremia. Significant plasma increases in urea and creatinine is called azotemia and indicates kidney insufficiency. Decreased levels are seen in liver damage or pregnancy. It can also occur from prerenal, renal or postrenal causes.
Prerenal Azotemia:
- Poor perfusion of the kidneys
- Decreased GFR (glomerular filtration rate)
- Dehydration
- Shock
- Congestive heart failure
- Fever
- Stress
- Severe burn
- Trauma or traumatic injury
- Blood volume loss
Renal Azotemia:
- Decreased GFR
- Acute renal disease
- Chronic renal disease
- Acute glomerulonephritis
- Chronic glomerulonephritis
- Polycystic kidney disease
- Nephrosclerosis
Postrenal Azotemia:
- Any obstruction, such as a kidney stone, a tumor, a stricture, or an enlarged prostate gland
- Urea is reabsorbed and goes back into the bloodstream
BUN:
- Test directly from serum lithium heparin, sodium heparin, plasma, or urine
- Don't use a gray top, since sodium fluoride will interfere with the urease reaction
Creatinine:
- Serum, heparinized plasma, or dilute urine can be used to test for
- Results from formation from creatine and creatine phosphate
- Its clearance from the plasma is an indicator of the glomerular filtration rate (GFR)
- Hemolysis can interfere and cause results to be falsely increased
- Originates in the muscles of the body and filtered through the kidneys
- Excretion is impaired with renal disease, so its concentration will be increased in the blood
- Creatinine clearance is an index that relates creatinine excretion to muscle mass
- Tested in 24-hour urine collection preserved by refrigeration
- Also measured in the blood about 12 hours into urine collection
- Calculated
GFR:
- Estimated by substances in the plasma and urine and calculated
Creatine:
- Made mostly by the liver
- Taken to other tissues of the body
- Drives metabolic reactions
- Increased levels found in muscle diseases or injury
Uric Acid:
- Pruine nucleoside metabolism waste product
- Elevated in:
- Gout
- Renal disease
- Increased catabolism of nucleic acids
Ammonia:
- Waste product from the breakdown of amino acids
- Toxic to the neurological system
- Indicates hepatic (liver) failure (most common cause of ammonia buildup in the blood)
- Indicator of Reye's syndrome
- Indicator of inherited deficiencies of urea cycle enzymes (hyperammonemia)
Diseases and Disorders of the Adrenal Glands (Sit Atop the Kidneys):
Aldosteronism:
Aldosteronism is a disorder which may be primary or secondary, involve hyperplasia of the adrenal glands, be hypoaldosteronism or salt-losing syndrome. The adrenal glands are triangular-shaped glands that sit atop the kidneys and secrete hormones that aid in the conservation and/or excretion of salt and water.
The adrenal glands are endocrine glands and part of the endocrine system. They secrete adrenaline (the "fight or flight" hormone) and the steroids aldosterone and cortisol. They secrete mineralocorticoids, glucocorticoids, and androgens. The mineralocorticoid aldosterone aids in maintaining blood pressure/blood volume and electrolyte balance/salt balance. Angiotensin II and extracellular potassium actually regulate aldosterone. The regulating system is known as the renin-angiotensin-aldosterone system. The hypothalamus and pituitary glands, along with the adrenal glands, play this role in the body.
The glucocorticoids cortisol and corticosterone aid in regulating metabolism and suppressing the immune system. They also play a role in regulating blood sugar levels along with the hormones secreted by the pancreas. They are anti-inflammatory and conserve calcium. Cortisol levels are also regulated somewhat by the hormone ACTH produced by the pituitary gland, because bursts of the hormone can be secreted and released in response to it. Its secretion is affected by Circadian rhythm, and its levels are naturally highest in the morning. The corticosteroids all share cholesterol (a sterol) as a starting precursor. The androgens are the male and female sex hormones that are secreted by the adrenal glands, then converted to their respective male or female hormones (testosterone or estrogen) in the gonads (testes in men and ovaries in women). Adrenaline and noradrenaline produced by the adrenal glands are catecholamines that aid the body in responding quickly to stress.
The adrenal glands are endocrine glands and part of the endocrine system. They secrete adrenaline (the "fight or flight" hormone) and the steroids aldosterone and cortisol. They secrete mineralocorticoids, glucocorticoids, and androgens. The mineralocorticoid aldosterone aids in maintaining blood pressure/blood volume and electrolyte balance/salt balance. Angiotensin II and extracellular potassium actually regulate aldosterone. The regulating system is known as the renin-angiotensin-aldosterone system. The hypothalamus and pituitary glands, along with the adrenal glands, play this role in the body.
The glucocorticoids cortisol and corticosterone aid in regulating metabolism and suppressing the immune system. They also play a role in regulating blood sugar levels along with the hormones secreted by the pancreas. They are anti-inflammatory and conserve calcium. Cortisol levels are also regulated somewhat by the hormone ACTH produced by the pituitary gland, because bursts of the hormone can be secreted and released in response to it. Its secretion is affected by Circadian rhythm, and its levels are naturally highest in the morning. The corticosteroids all share cholesterol (a sterol) as a starting precursor. The androgens are the male and female sex hormones that are secreted by the adrenal glands, then converted to their respective male or female hormones (testosterone or estrogen) in the gonads (testes in men and ovaries in women). Adrenaline and noradrenaline produced by the adrenal glands are catecholamines that aid the body in responding quickly to stress.
Addison's Disease:
Addison's Disease in underproduction of cortisol. It is also called primary adrenal insufficiency. It can be secondary if it involves the angiotensin-renin-aldosterone system and other glands. This is usually an autoimmune condition in which the body's own immune system attacks the tissues of the glands. It can also be caused by tuberculosis. Signs and symptoms include:
- Hyperpigmentation of the skin
- Fatigue
- Adrenal crisis with hypovolemic shock ( a medical emergency)
- Untreated, this can lead to a coma or even death
- Managed with injections of hydrocortisone
Cushing's Syndrome:
Cushing's Syndrome is overproduction of cortisol. It can be caused by certain medications, but the most common cause is a pituitary tumor called an adenoma, which is often benign. This causes excessive production of ACTH, which in turn causes too much cortisol to be released. Signs and symptoms include:
- Puffiness
- Obesity
- Increased blood pressure
- Diabetes
- Excessive body hair
- Osteoporosis
- Depression
- Stretch marks
- Thinning of the skin
Conn's Syndrome:
Conn's Syndrome is another term for primary aldosteronism. Excessive growth of the tissue of both adrenal glands is the cause, or aldosterone-producing tumors called adenomas, which may be benign. High blood pressure, electrolyte imbalance, sodium retention (hypernatremia), and potassium deficiency (hypokalemia) are the symptoms.
Uric Acid and Gout:
Uric acid buildup in the blood and uric acid crystals seen in body fluids are linked to gout.
Liver Function, Bilirubin Metabolism, and Jaundice:
One of the most frequent chemistry lab tests used in the assessment of liver function is bilirubin (direct and total). This is tested on the serum. Bilirubin comes from the heme (iron-containing) portion of hemoglobin carried by red blood cells. Heme is released when red blood cells are broken down. Bilirubin complexes with the protein albumin, forming unconjugated bilirubin, where it is taken to the liver and processed into conjugated bilirubin by the cells of the liver. It then enters bile fluid to be taken to the small intestines, where most of it is converted to urobilinogen.
Icterus, or jaundice, is a yellowish discoloration of the skin, mucous membranes, whites of the eyes, and plasma. Buildup, retention of bilirubin, or abnormal metabolism of bilirubin result in this condition. Jaundice can be:
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Liver Enzymes:
There are tests for a variety of liver enzymes that aid in the diagnosis of liver disease. They include the following:
- Alkaline phosphatase
- Increased in cholestasis
- Increased in bone degeneration
- Lactate dehydrogenase
- Aspartate Aminotransferase (AST)
- Kick off the conversion of aspartate to oxaloacetate
- Found in the liver, heart, kidneys and muscles
- Increased in viral jaundice and chronic active hepatitis
- Alanine Aminotransferase (ALT)
- Kick of the conversation of alanine to pyruvate
- Found primarily in the liver
- Increased in viral jaundice and chronic active hepatitis
- Gamma-glutamyltransferase
- Increased in blockages of bile flow, cholestasis, or chronic alcoholism
- Bile acids
- Triglycerides
- Cholesterol
- Serum proteins
- Urea
- Ammonia
- Coagulation proteins
- Hepatitis Acute Panel (Tests for Hep A, B and C)
Hypoproteinemia:
- Decreased protein levels in the blood
- May indicate renal disease, inflammation, loss of blood or a severe burn
- Dietary deficiency can cause or malnutrition
- Intestinal malabsorption can cause
- Liver disease can cause
Hyperproteinemia:
- Increased protein levels in the blood
- Most common cause is dehydration
Pancreatic Function and Pancreatic Diseases:
- Pancreatitis
- Amylase
- Lipase
- Amylase
- Cystic Fibrosis
- Sweat chloride
- Sweat chloride
- Pancreatic carcinoma
- Amylase
- Lipase
- Amylase
The Thyroid and Thyroid Hormones:
The thyroid is a butterfly-shaped endocrine gland found in the neck just below the Adam's Apple. It secretes thyroid hormones, which regulate metabolism and protein synthesis. The thyroid hormones are T3 (triiodothyronine) and T4 (thyroxine). Iodine and tyrosine (an amino acid) are precursors of these hormones. We obtain iodine from the diet, mostly from iodized salt. It is also naturally found in seafood and in kelp. The thyroid produces the hormone calcitonin as well, which regulates calcium levels in the body. The thyroid itself is regulated by the pituitary gland and its hormonal secretions, mainly thyroid stimulating hormone (TSH), secreted by the anterior (front portion) of the pituitary gland, which itself is regulated by the thyrotropin-releasing hormone (THR) released by the hypothalamus, the body's master gland.
The thyroid is protected by flexible cartilage, the hyoid bone (only non-connected, free-floating bone in the body), supported by muscles and ligaments that enable it to move up and down when you breathe and swallow. Thyroid cartilage sits just above it and cricoid cartilage below it, as well as the trachea. The cricoid cartilage is a complete ring of cartilage around the trachea. A thin, fibrous capsule surrounds and protects the bilobed thyroid gland as well. Four parathyroid glands, two on each side, sit atop the thyroid gland. It is rich in blood supply from the thyroid and common carotid arteries. The thyroid consists of three types of cells: follicular, parafollicular and follicles. Follicles secrete thyroglobulin (precursor of the thyroid hormones T3 and T4) and iodinated glycoprotein. Follicular cells secrete T3 and T4 hormones under the influence of thyroid stimulating hormone (TSH) released by the pituitary gland. Parafollicular cells secrete calcitonin. Thyroid function tests are panels of tests designed to measure levels of T3, T4 and TSH in the blood. High T3 and T4 levels may indicate hyperthyroidism. Low T3 and T4 levels may indicate hypothyroidism. Normal T3 and T4 with low TSH may indicate subclinical hyperthyroidism. TSH is the most sensitive indicator of thyroid dysfunction, however. CT scans with guided biopsies are often the choice to rule out thyroid cancer or goiter. The Free T4 chemistry lab test is designed to detect thyroxine (T4) circulation in the blood as a mixture of free and serum protein bound to hormone. Free T4 is absorbed by target cells it acts upon, and the body maintains homeostasis by recirculating free T4. Free T4 values aid in the indication of thyroid dysfunction. T4 is less sensitive to changes in the serum binding proteins than T3. Calcitonin assays are useful in aiding in the diagnosis of thyroid nodular diseases, including goiter and medullary carcinoma of the thyroid. Triiodothyronine (T3):
Thyroxine (T4):
Calcitonin:
The body cannot function without these hormones, so diseases that affect the hormone can have numerous signs and symptoms and individuals who suffer from thyroid diseases must have synthetic hormones as treatment when necessary. |
Hypothyroidism:
In hypothyroidism, the thyroid gland is not producing enough thyroid hormone. It is a disorder of the endocrine system. There may be a nodule or nodules on the thyroid gland called a goiter. A goiter puts an individual at higher risk of developing thyroid cancer later on so it is closely monitored. Thyroid-stimulating hormone (TSH) and thyroxine levels are closely monitored by chemistry lab tests. Iodized salt is a good way to provide iodine needed to stimulate production of these hormones. Too little iodine intake in the diet is the most common cause. Oftentimes, sea salt does not contain iodine. Other causes include:
Hypothyroidism related to iodine deficiency is one of the main underlying causes of a dietary deficiency-related intellectual disability, which is easily preventable and treatable.
- Autoimmune Hashimoto's Thyroiditis (the second most common cause)
- Prior treatment with radioactive iodine
- Unprotected neck exposure to radiation during X-rays
- Injury to the hypothalamus
- Injury to the pituitary gland
- A birth defect
- Certain medications
- Prior thyroid surgery
- Nodules
- Cancer
Hypothyroidism related to iodine deficiency is one of the main underlying causes of a dietary deficiency-related intellectual disability, which is easily preventable and treatable.
Hyperthyroidism:
Hyperthyroidism is the excess production of thyroid hormone by the thyroid gland.
Causes and conditions seen in include the following:
Checked in the chemistry lab by TSH levels, T3 and T4. The TSH is often low, and the T3 and T4 are often raised.
Causes and conditions seen in include the following:
- Grave's Disease (40-80% of the time)-autoimmune
- Multi-nodular goiter
- Inflammation of the thyroid (thyroiditis)
- Pregnancy or post-pregnancy (temporary)
- Toxic adenoma
- Excess iodine in the diet (kelp)
- Too much synthetic thyroid hormone (given to those with hypothyroidism, but levels are monitored throughout the lifetime in case it goes to the other extreme of hyperthyroidism and levels are frequently adjusted)
- Certain drugs
- Cancer
Checked in the chemistry lab by TSH levels, T3 and T4. The TSH is often low, and the T3 and T4 are often raised.
Medullary Carcinoma:
Parathyroid Glands:
For the parathyroid diseases, PTH levels, calcium levels, and serum albumin levels are tested in the blood.
Hypoparathyroidism:
Hypoparathyroidism is underproduction of parathyroid hormone (PTH). This may lead to a drop in the calcium level in the blood, resulting in muscle cramps. Calcium is then leached from the bones, which can cause the bones to thin and weaken and ache. Muscles may spasm painfully or go into tetany. Causes may include:
- Autoimmune attack
- Prior thyroid surgery
- It can be a genetic condition (inherited)
Hyperparathyroidism:
Hyperparathyroidism is increased parathyroid hormone (PTH) in the blood. There are 4 parathyroid hormones that lie on top of the back of the thyroid glands. Either the parathyroid glands are making too much PTH, or it can be secondary due to other causes. Symptoms may include kidney stones, weak bones, increased urination, weakness, depression, bone pain, nausea, vomiting, fatigue, muscle soreness, loss of appetite and confusion may occur. Primary causes include:
- A benign tumor called an adenoma, as seen in the image below
- Cancer
- Vitamin D deficiency
- Chronic kidney disease
- Low blood calcium
- Can cause calcification in the brain, as seen in the scan below
Drug and Alcohol Assays:
Drug assays and troughs are performed on serum, plasma or urine to test for recreational or street drug use or overdose, and are also used to monitor levels in patients who are on prescription medications to adjust levels if needed, and to monitor whether someone is developing an addiction or overuse of a drug. Alcohol (ETOH) assays are used to monitor blood alcohol levels and can aid in the diagnosis of alcoholism. These tests may involve chain of custody paperwork, and legal documentation.
Tumor Markers:
- Lactate dehydrogenase (elevated)
- Neuron-specific enolase
- Alkaline phosphatase
- ACTH
- AFP
- B-hcG
- CA 15-3
- CA 27.29
- CA 19-9
- CA 125
- PSA
- CEA
- Many others
Lipids, Cholesterol, Triglycerides, Lipoproteins and Their Clinical Significance:
Cardiac Disease and Cardiac Markers:
When an individual experiences chest pain or other symptoms of a myocardial infarction (MI), or heart attack, there is a short window of time in which the cardiac markers released from the myocardial tissue are elevated at their highest and can aid in the diagnosis of the MI. The images below show the areas in which the patient may complain of pain or numbness or heaviness, and show the damage caused by a myocardial infarction, or heart attack, which is irreversible damage.
The ideal markers for diagnosis of an acute myocardial infarction (MI), or heart attack, include:
OTHER CARDIAC MARKERS:
The ideal markers for diagnosis of an acute myocardial infarction (MI), or heart attack, include:
- Myoglobin
- Indicator of muscle damage
- Found in skeletal and cardiac muscles
- Early marker of injury
- Rises 1-3 hours after the event
- Not cardiac-specific
- Increased levels found in trauma, renal failure, any type of muscle damage
- Troponins
- Complex of three proteins
- TnT
- TnI
- Largest portion of troponin released into blood circulation after damage to myocardial tissue
- Complexes with cTnC
- Stay elevated in the blood for 4-10 days post-MI
- TnC
- Bind to the thin filaments of striated cardiac or skeletal muscle
- Regulate muscle contraction
- Complex of three proteins
- CK isoenzyme (CKMB)
- Increases after tissue injury
- Aids in early diagnosis of myocardial cell death
- Cardiac-specific
- Sensitive 4-6 hours after onset of symptoms of MI
OTHER CARDIAC MARKERS:
- Homocysteine
- Also an aid in diagnosis of MI
- Amino acid in the blood
- Increased in folate, vitamin B deficiencies, and linked to higher risk of stroke, heart attack, and peripheral vascular disease
- Damages inner lining of arteries
- Promotes blood clots and atherosclerosis
- C-Reactive Protein
- Inflammation
- Risk for cardiovascular disease
- Brain Natriuretic Peptides (BNP)
- Heart failure
- Fibrinogen
- Inflammation
- D-Dimer
- Blood clot and thrombus formation
- Microalbumin
- Independent risk factor in patients with diabetes and hypertension
Congestive (Right-Sided) Heart Failure Affects the Pulmonary System (Lungs):
Acute Pancreatitis:
Acute pancreatitis is a rapid onset of inflammation of the pancreas. Gallstones blocking the common bile duct are the primary cause of acute pancreatitis. Other causes include alcoholism, disease, cancer/tumors or trauma. It may occur just once, occur again, or become chronic.
As long as the acute pancreatitis is mild, hospitalization, pain medication, and IV fluids tend to be successful treatment for the condition. Severe pancreatitis often results in a stay in the ICU, where the disease progress and treatment can be closely monitored, especially if there are secondary complications due to the nature of the disease. Severe pancreatitis is linked to a high mortality rate, even with proper treatment.
Signs and symptoms may include the following:
As long as the acute pancreatitis is mild, hospitalization, pain medication, and IV fluids tend to be successful treatment for the condition. Severe pancreatitis often results in a stay in the ICU, where the disease progress and treatment can be closely monitored, especially if there are secondary complications due to the nature of the disease. Severe pancreatitis is linked to a high mortality rate, even with proper treatment.
Signs and symptoms may include the following:
- Severe epigastric pain, often radiating to the back or shoulder (may present with symptoms similar to a heart attack)
- Nausea and vomiting
- Loss of appetite
- Fever
- Chills
- Shock
- Rapid heart beat
- Hiccups
- Peritonitis
- Respiratory distress syndrome
Hepatitis:
The Hepatitis Virus strains are infections of the liver. Some result in acute infections, some in chronic, and some in carrier states. Hepatitis C and B are linked to liver cancer. There are vaccinations available against Hepatitis B.
Hepatitis A has the ability to remain infectious outside the host for months. It is spread via the fecal-oral route. Hepatitis B has the ability to remain infectious outside the host for 7 days. Hepatitis C has the ability to remain infectious outside the host for 21 days.
Hepatitis A has the ability to remain infectious outside the host for months. It is spread via the fecal-oral route. Hepatitis B has the ability to remain infectious outside the host for 7 days. Hepatitis C has the ability to remain infectious outside the host for 21 days.
Hepatitis A:
Hepatitis A is spread via the fecal-oral route. In addition to reactive Hepatitis A, the patient's liver enzymes AST and ALT will also be elevated. Anti-HAV total measures both the IgG and IgM. Anti-HAV (IgM) measures just the IgM and is an infection marker that indicates acute infection if positive. If negative, it means the patient has immunity to Hepatitis A from vaccination or a previous infection.
If the HBsAG is negative, the Anti-Hbs is positive, the Anti-HAV IgM is positive, and the Anti-HAV IgG is negative, this means the patient has acute Heptitis A.
If the HBsAG is negative, the Anti-Hbs is positive, the Anti-HAV IgM is positive, and the Anti-HAV IgG is negative, this means the patient has acute Heptitis A.
Hepatitis B:
The Hepatitis B surface antibody quantifies the detection of antibodies to the Hepatitis B surface antigen in serum and plasma. It is used to determine whether or not an immunization or series of Hep. B vaccinations was successful, providing immunity, or to detect recent illness or recovery from Hepatitis B infection. Values of <10.0 mlu/mL are non-reactive, whereas values of >10.0 mLU/mL are reactive.
The Hepatitis B surface antigen qualifies detection of antigen on the surface of Hepatitis B virus particles in serum and plasma. This is the first serological marker for post-infection with Hepatitis B Virus. This appears 1-10 weeks post-exposure at levels strong enough to be detected in serum or plasma. Detection can occur 2-8 weeks before a patient experiences any symptoms. It can also detect a chronic carrier state of >6 months. Anti-HBe, if positive, means that the patient is in the recovery phase of Hepatitis B infection.
A Hepatitis B surface antigen confirmatory test is a specialty antibody-neutralization test used to confirm the presence of Hepatitis B surface antigen in the blood. Molecular Biology DNA tests by PCR can determine the viral load.
The Hepatitis B vaccination with successful immunity will result in a reactive Anti-Hbs and a nonreactive Anti-HBc. The vaccine contains Hepatitis B surface antigen (Ag) protein so it is the only antibody produced. It takes about 6-7 weeks for the serum to fully seroconvert post-vaccination.
Chronic state will result in a reactive Anti-HBc (IgM) and a reactive HBsAG. Approximately 7 months later, other reactive tests include Anti-HBs, Anti-HBe, and Anti-HBC (total). Antibodies in the serum are present against surface antigen present on the virus particle. e-Antigen is ONLY present during the ACUTE phase. The acute phase lasts <6 months.
Following an exposure or post-needlestick, both the phlebotomist and the patient should be tested for Hepatitis. If the patient is reactive for Hep. B, the person who was stuck should be monitored for several weeks for HBsAG, because it takes a few weeks for seroconversion to occur, and HBsAG is the earliest marker to become reactive in infection. The patient tested is the SOURCE.
The Hepatitis B surface antigen qualifies detection of antigen on the surface of Hepatitis B virus particles in serum and plasma. This is the first serological marker for post-infection with Hepatitis B Virus. This appears 1-10 weeks post-exposure at levels strong enough to be detected in serum or plasma. Detection can occur 2-8 weeks before a patient experiences any symptoms. It can also detect a chronic carrier state of >6 months. Anti-HBe, if positive, means that the patient is in the recovery phase of Hepatitis B infection.
A Hepatitis B surface antigen confirmatory test is a specialty antibody-neutralization test used to confirm the presence of Hepatitis B surface antigen in the blood. Molecular Biology DNA tests by PCR can determine the viral load.
The Hepatitis B vaccination with successful immunity will result in a reactive Anti-Hbs and a nonreactive Anti-HBc. The vaccine contains Hepatitis B surface antigen (Ag) protein so it is the only antibody produced. It takes about 6-7 weeks for the serum to fully seroconvert post-vaccination.
Chronic state will result in a reactive Anti-HBc (IgM) and a reactive HBsAG. Approximately 7 months later, other reactive tests include Anti-HBs, Anti-HBe, and Anti-HBC (total). Antibodies in the serum are present against surface antigen present on the virus particle. e-Antigen is ONLY present during the ACUTE phase. The acute phase lasts <6 months.
Following an exposure or post-needlestick, both the phlebotomist and the patient should be tested for Hepatitis. If the patient is reactive for Hep. B, the person who was stuck should be monitored for several weeks for HBsAG, because it takes a few weeks for seroconversion to occur, and HBsAG is the earliest marker to become reactive in infection. The patient tested is the SOURCE.
Hepatitis C:
Anti-HCV, if reactive, and if Hepatitis C RNA is nonreactive, or <15 IU/L, this indicates a past infection with Hepatitis C. The body has cleared the virus, the patient is currently aviremic, however, they will be positive (or a carrier) of the virus for life.
Hepatitis D:
Fulminant Hepatitis:
Fulminant Hepatitis is caused by infection of the liver with the hepatitis virus, exposure to toxins, including fungal mycotoxins, or drug-induced injury. It causes massive necrosis of the liver cells, resulting in a decrease in the size of the liver, an acute atrophy, and rapid liver failure, which occurs within days or weeks, which can be life-threatening.