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14 Cards in this Set
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Edema: an excess of fluid in the interstitial space- may be a manifestation of ECV excess or from other mechanisms.
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Caused by either an increase in the forces that tend to move fluid from capillaries into the interstitial compartment, or
a decrease in forces that tend to move fluid from the interstitial compartment into the capillaries will cause edema Edema may arise from : i.Increased capillary hydrostatic pressure 1.Caused by increased ECV, increased local capillary flow that accompanies inflammation, and by venous congestion ii.Increased interstitial fluid osmotic pressure 1.Occurs when inflammation increases vascular permeability and proteins leak into the interstitial fluid iii.Blockage of lymphatic drainage- 1.Lymphatic vessels usually remove any amount of left over proteins in the interstitial fluid. Blockage of these vessels will cause proteins to accumulate in the interstitial space. 2.Edema resulting from the blockage of lymphatic drainage is usually localized. iv.Decreased capillary osmotic pressure 1.When the plasma proteins are decreased, as in malnutrition or liver disease. |
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Hypocalcemia: if the serum calcium level drops below 4.5 mEq/dl
Calcium is: i. Present in three forms: 1. Bound to plasma proteins (such as albumin) 2. Bound to small organic ions (such as citrate) 3. Or unbound. 4. Only the unbound calcium ions are measured in plasma calcium. The normal range of total plasma calcium in adult is- 4.5-5.5 mEq/dl |
1. Etiology: caused by factors that
a. Decrease calcium intake / absorption i. Diet with insufficient calcium and vitamin D ii. Chronic kidney disease- deficient activated vitamin D iii. Excessive dietary phytates or oxalates iv. Steatorrhea v. Pancreatitis vi. Chronic diarrhea (includes laxative abuse) vii. Malabsorption syndromes b. Decrease physiologic availability of calcium i. Hypoparathyroidism ii. Excessive phosphate intake iii. Tumor lysis syndrome (high phosphate) iv. Hypomagnesmeia v. Alkalosis vi. Large transfusion of citrated blood vii. Rapid infusion of plasma expanders that bind calcium viii. Elevated plasma free fatty acids ix. Chronic kidney disease c. Increase calcium excretion through normal routes i. Steatorrhea ii. pancreatitis 2. Clinical manifestations: Calcium imbalances alter normal neuromuscular excitability. The lower concentration of Ca2+ outside of the cell equalizes the polarity across cell membranes, which is like depolarizing the cell. This makes the action potentials easier to fire. i. Positive Trousseau sign ii. Positive Chvostek sign iii. Paresthesia iv. Muscle twitching and cramping v. Hyperactive reflexes vi. Carpal spasm vii. Pedal spasm viii. Tetany laryngospasm ix. Seizure x. Cardiac dysrhythmias |
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Hypercalcemia: when the serum calcium concentration rises above the upper limit of normal (5.5 mEq/L)
Calcium is: i. Present in three forms: 1. Bound to plasma proteins (such as albumin) 2. Bound to small organic ions (such as citrate) 3. Or unbound. 4. Only the unbound calcium ions are measured in plasma calcium. The normal range of total plasma calcium in adult is- 4.5-5.5 mEq/dl |
1. Etiology: caused by factors that
a. Increase calcium intake or absorption i. Milk-alkali syndrome ii. Vitamin D overdose (includes shark cartilage supplements) b. Cause a shift of calcium from bone to ECF i. Hyperparathyroidism ii. Immobilization iii. Paget disease iv. Bone tumors v. Multiple myeloma vi. Leukemia vii. Nonosseous malignancies that produce bone-reabsorbing factors c. Decreased calcium excretion i. Thiazide diuretics ii. Familial hypocalciuric hypercalcemia 2. Clinical manifestation: causes decreased neuromuscular excitability. It is caused by elevation of the threshold potential of excitable cells (hyperpolarization), making it harder for electrical impulses to send off an action potential a. Anorexia b. Nausea c. Emesis d. Constipation e. Fatigue f. Polyuria g. Muscle weakness h. Diminished reflexes i. Headache j. Confusion k. Lethargy l. Personality change m. Cardiac dysrhythmias |
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Hypomagnesemia: when serum concentration runs below 1.5.
Plasma Magnesium: normal concentration is 1.5- 2.5 mEq/L. magnesium ions are also present in the blood as bound, and unbound ionized forms. |
1. Etiology: caused by
a. Decreased Mg2+ intake i. Chronic alcoholism ii. Malnutrition iii. Prolonged intravenous therapy without magnesium iv. Ileal resection v. Chronic diarrhea (includes laxative abuse) vi. Malabsorption syndromes vii. Steatorrhea viii. pancreatitis b. Decreased physiologic availability of Mg2+ i. Elevated plasma free fatty acid c. Increased Mg2+ excretion i. Renal route 1. Diabetic ketoacidosis 2. Chronic alcoholism 3. Hyperaldosteronism 4. Diuretic therapy ii. Fecal route 1. Steatorrhea 2. Pancreatitis d. And loss of Mg2+ by abnormal route i. Emesis ii. Gastric suction iii. Fistula drainage 2. Clinical manifestation: Mg2+ usually suppresses the release of Ach neurotransmitters and neuromuscular junctions. Too much Mg2+ will cause a lot of Ach to be released, which means the muscles will be stimulated a lot. Signs include: a. Increased neuromuscular excitability b. Insomnia c. Hyperactive reflexes d. Muscle cramps e. Muscle twitching f. Grimacing g. Positive chvostek sign h. Positive Trousseau sign i. Nystagmus j. Dysphagia k. Ataxia l. Tetany m. Seizures 3. It also causes decreased activity of the enzyme that drives the na+/K+ pumps, so intracellular K+ will decrease in myocardium. This will cause a. Spontaneous firing of sinus node b. Shortening of the absolute refractory period |
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Hypermagnesemia: when the serum Mg2+ rises above 2.5
Plasma Magnesium: normal concentration is 1.5- 2.5 mEq/L. magnesium ions are also present in the blood as bound, and unbound ionized forms. |
1. Etiology: major cause is
a. increased mg2+ intake: i. ingestion or aspiration of seawater ii. excessive ingestion of Mg- containing medications iii. excessive intravenous infusion of Mg b. decreased Mg2+ excretion i. Oliguric renal failure ii. adrenal insufficiency 2. Clinical manifestations: since Mg2+ inhibits the release of Ach in neuromuscular junctions, too much Mg2+ inhibits a lot of Ach from coming out. Ach will not be able to act on the muscle, causing: a. Decreased deep tendon reflexes b. Lethargy c. Hypotension d. Flushing e. Diaphoresis f. Drowsiness g. Flaccid paralysis h. Respiratory depression i. Bradycardia j. Cardiac dysrhythmias k. Cardiac arrest |
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Hypophosphatemia: when the plasma phosphate falls below 2.5
Plasma phosphate: the normal range is from 2.5- 4.5 mEq/dl. It is less common than other imbalances |
1. Etiology: caused by
a. Decreased phosphate intake i. Chronic alcoholism ii. Chronic diarrhea iii. Malabsorption syndromes iv. Excessive or long term use of antacids that bind phosphate b. Shift phosphate from extracellular fluid to cells i. Refeeding after starvation (includes anorexia) ii. Total parenteral nutrition iii. Hyperventilation (respiratory alkalosis) iv. Insulin v. Epinephrine vi. Intravenous glucose, fructose, bicarbonate, or lactate c. Increased phosphate excretion i. Alcohol withdrawal ii. Diuretic phase after extensive burns iii. Diabetic ketoacidosis iv. Diuretic therapy d. Loss of phosphate through abnormal routes i. Emesis ii. hemodialysis 2. Clinical manifestations: phosphate is important for the ATP pumps. Signs and symptoms are due to decreased ATP within cells. Or tissues hypoxia caused by decreased 2,3-biphosphoglycerate in RBC a. Anorexia b. Parethesia c. Hemolysis d. Diminished reflexes e. Muscle aches f. Muscle weakness g. Respiratory failure h. Confusion i. Stupor j. Seizures k. Coma l. Impaired cardiac function |
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Hyperphosphatemia: increase of serum phosphate concentration above 4.5
Plasma phosphate: the normal range is from 2.5- 4.5 mEq/dl. It is less common than other imbalances |
1. Etiology: may be caused by
a. Increased phosphate intake i. Overzealous phosphate therapy ii. Excessive use of phosphate-containing enemas or laxatives b. Shift of phosphate from cells or bones to extracellular fluid i. Tumor lysis syndrome ii. Crushing injury iii. rhabdomyolysis c. Decrease phosphate excretion i. Chronic kidney disease ii. Oliguric renal failure iii. Adrenal insufficiency 2. Clinical manifestations: It depends on the effect of the elevated phosphate ions have on calcium ions. b. Typically hyperphosphatemia causes hypocalcaemia c. The signs and symptoms are those of hypocalcaemia Calcium imbalances alter normal neuromuscular excitability. The lower concentration of Ca2+ outside of the cell equalizes the polarity across cell membranes, which is like depolarizing the cell. This makes the action potentials easier to fire. i. Positive Trousseau sign ii. Positive Chvostek sign iii. Paresthesia iv. Muscle twitching and cramping v. Hyperactive reflexes vi. Carpal spasm vii. Pedal spasm viii. Tetany laryngospasm ix. Seizure x. Cardiac dysrhythmias |
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Metabolic acidosis: a condition that tends to cause an increase of metabolic acids
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ETIOLOGY
1. Increase in metabolic acid- it will decrease the normal ratio of bicarbonate to carbonic acid because bicarbonate ions will be used to buffer the additional acids. a. Ex. When caloric intake is insufficient, and the person starts to break down their fats to make ketone. Ketoacids will accumulate in the blood. This also happens with diabetes mellitus, and alcoholism. b. Severe hyperthyroidism c. Severe infection d. Burns e. Circulatory shock f. Tissue hypoxia g. Oliguric renal failure h. Intake of acids or acid precursors (e.g. Methanol, etc). 2. Decrease in base- bicarbs are a type of base. Any condition that causes excessive removal of bicarbonate ions from the body will cause metabolic acidosis. a. Diarrhea b. Gastrointestinal fistula that drains intestinal or pancreatic secretions c. Intestinal decompression d. Renal tubular acidosis 3. Or a combination of increase in metabolic acid and decrease in base 4. Clinical manifestations: a. Headache b. Abdominal pain c. Central nervous system depression – confusion, lethargy, stupor, coma i. This typically occurs in pts with decreased pH of the cerebral spinal fluid of the brain. The enzyme activity will stop, and the proteins will get denatured at such a low pH. 5. Compensatory response: the respiratory compensatory response for metabolic acidosis is hyperventilation. a. The arterial blood gas of a person who has compensated metabolic acidosis show decreased bicarbonate concentration (the primary imbalance) b. the Co2 will decrease (compensation) c. Slightly decreased or even normal pH. |
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Respiratory Acidosis:
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1. Etiology: a condition that tends to cause an excess of carbonic acid. It is caused by factors that
a. Impair the respiratory excretion of carbonic acid i. Impaired gas exchange ii. Inadequate neuromuscular function iii. Impairment of respiratory control in the brainstem b. All these factors decrease the normal 20:1 ration of bicarbonate ion to carbonic acid (which decreases the pH of the blood) 2. Clinical manifestation: a. Headache- occurs because of dilation of blood vessels in the brain, which increases cerebrospinal fluid pressure. b. Tachycardia c. Cardiac dysrhythmias- because of the decreased pH of myocardial cells. d. Neurologic abnormalities such as blurred vision, tremors, vertigo, disorientation, lethargy, or somnolence- this happens because H2Co3 (in the form of Co2 + h2O can cross the blood-brain barrier very easily, decreasing the pH of cerebrospinal fluid. e. Arterial blood gas in patients with respiratory acidosis will show an increased Co2 level (if they’re not compensated) 3. Compensatory response: the renal compensatory response for respiratory acidosis is increased H+ excretion in the urine, which will show as an increased HCo2- level. a. The arterial blood gases of a person who has compensatory respiratory acidosis show increased Pco2 (primary imbalance) b. Increased HCo2- concentration (compensation) c. Slightly decreased or even normal pH. |
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Metabolic alkalosis: a condition that tends to cause a relative deficit of any acid except carbonic acid.
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1. Etiology: it may be caused by
a. An increase in base (bicarbonate ion) i. Increase in ingestion of antacids such as baking soda ii. Massive transfusion with citrated blood iii. Mild or moderate extracellular fluid volume deficit b. Decrease in acid i. Emesis ii. Gastric suction iii. Mild or moderate extracellular fluid volume deficit iv. Hyperaldosteronism v. Hypokelemia – causes metabolic alkalosis by shifting H+ into cells and increasing renal excretion of acid c. Or it may be a combination of both 2. Clinical manifestation: the signs and symptoms of metabolic alkalosis may arise from the extracellular volume deficit: a. Increased neuromuscular excitability b. Fingers and toes may tingle c. Signs of tetany may progress to seizures d. Increased interstitial pH causes increased excitability of nerve cell membrane e. Alkalosis causes more ionized calcium to bind to albumin f. Severe metabolic alkalosis may progress to central nervous system depression- confusion, lethargy, and coma 3. Compensatory response: the compensatory response to metabolic alkalosis is hypoventilation, because there is too little acid, and if you hypoventilate, then you will keep the Co2 in your body, maintaining the pH. a. Respiratory compensation for metabolic alkalosis is usually incomplete. The need for O2 drives ventilation, even though the increased pH tends to repress it. |
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vi. Respiratory Alkalosis:
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1. Etiology: it is a condition that tends to cause a carbonic acid deficit. It is caused by
a. Hyperventilation 2. Clinical manifestation: clinical manifestation of respiratory alkalosis arises from increased neuromuscular excitability. a. Parasthesia: numbness and tingly- around the fingers and mouth b. Carpal and pedal spasms may occur c. Increased extracellular pH has a direct effect of increasing membrane excitability in both central and peripheral neurons d. Alters brain function because of increase e. Cerebral vasoconstriction- reduces blood flow in the brain f. Decreases the availability of ionized calcium g. The CO2 level in people with respiratory alkalosis will be lower than usual. 3. Compensatory Response: the compensatory response to respiratory alkalosis is retaining acid in the urine, which means the bicarbonate level in the blood will be low because of the increase of acid being retained. a. Arterial blood gases of a person who has compensated respiratory alkalosis show decreased PaCo (primary imbalance) b. Decreased bicarbonate concentration (compensation) c. Slightly increased or perhaps normal pH |
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iii. Buffers: chemicals that help control the pH of body fluids. Each buffer system consists of one weak acid, which releases H+ when there is too much base, and a base, that takes up H+ when there’s too much acid.
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There are many buffer systems in the body:
1. Bicarbonate buffers: in the extracellular fluid. This is the most important buffer in our system. a. It works with the base HCO3- (bicarbonate) and H2co3 (carbonic acid) b. HCO3- + H+ ↔ H2CO3 Co2 + H2O c. With the help of carbonic anhydrase, H2co3 turns into CO2 and H2o d. For the pH of the blood to be within normal range, the ratio of bicarbonate ions to carbonic acid MUST BE 20:1 2. Phosphate buffers: in intracellular fluid and urine 3. Hemoglobin buffers: inside RBC 4. Protein buffers: inside cells and blood 5. Buffers are the first line of defense against pH imbalances |
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iv. Respiratory contributions: it is the second defense against acid-base imbalances. Since H2Co3 is able to be turned into CO2 and H2O, the lungs can excrete Co2 and get rid of the acids that way.
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1. The respiratory system adjusts the amount of carbonic acid that remains in the body by altering the rate and depth of respiration
2. The rate and depth of respiration is influenced strongly by chemoreceptors that sense the PaCO2 and the pH of the blood. a. Too much carbonic acid: rate and depth of respiration goes up b. Too little carbonic acid: rate and depth of respiration goes down. c. The body’s correction of a carbonic acid excess or deficit is dependent on normal function of al component of the respiratory system 3. The paCO2 indicates how effectively the respiratory system is excreting carbonic acid (H2CO3) a. If there is too much co2 in the body, then that means there’s too much H2Co3 in the body, which means the rate and depth of the lungs, or there’s some sort of lung disease preventing the person from hyperventilating and getting rid of the excess Co2 b. If there’s too little Co2 in the body, then there’s too little H2co3 in the body. This means some sort of barrier in the lungs is preventing the lungs from retaining Co2 4. The lungs can only excrete Co2 and not any other acids. Carbonic acid (h2co3) is called the volatile gas because it can be excreted as gas. Even though the lungs cannot excrete other acids, they can help balance the pH of the blood by excreting Co2 when the metabolic acids start to accumulate in the body. This is called compensation. a. Compensation does not correct pH disorders, but it does bring the pH back to normal, even though now the other values are abnormal. 5. The compensatory response to any acid other than carbonic acid is hypoventilation. |
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v. Renal contributions: it is the third defense against acid-base disorders at the kidneys. Kidneys can secrete any acid except for carbonic acid. The acids that the kidneys secrete are called metabolic acids.
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1. If metabolic acids accumulate in the blood, then the kidneys will increase their excretion of acids into the urine.
2. The body’s ability to correct an excess or deficit of metabolic acids depends on normal function of the renal system 3. Renal mechanism to accomplish acid secretion: a. In the proximal tubules, renal tubular epithelial cells excrete metabolic acid by secreting H+ ions into the tubule lumen. b. For every H+ that is secreted into the renal tubular fluid (urine), one bicarbonate ion (H2co3) goes back into the interstitial fluid. c. In the tubule fluid, a lot of the H2co3 are reabsorbed during the secretion of acids. d. The kidneys are able to secrete a large amount of metabolic acids, tub it may take a while e. Once the H+ is secreted into the renal tubular fluid, they combine with other chemicals, such as phosphates, bicarbonate ions, and ammonia. This is so that our urine does not get too acidic with the large H+ excretion going on. i. When there is a large secretion of H+, the kidneys will produce more ammonia. 1. Ammonia (NH3) + H+ Ammonium (NH4) 2. NH4 is not lipid soluble, so they can’t go back into the interstitial fluid. This ensures that they stay in the urine. 4. Concentration of HCo3- reflects the effectiveness of renal regulation of metabolic acids. This is because when there is a rise in H+, HCo3- will be there to buffer it and turn it into H2Co3. When there is a lot of H+, then there will be less Hco3-. a. A decreased concentration of HCo3- means that there was a lot of metabolic acids b. An increased concentration of Hco3- means that there were too little metabolic acids (which also means that there’s relatively too little base alkalosis) 5. The compensatory renal response to a high amount of respiratory H+ is to excrete more metabolic H+, which means decreased Hco3- level. This will cause the Hco3- level to be abnormal, but it bring the pH of the overall body back to normal. |
