Quarter 2 clinical week 2 reading

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Osmolality

A measure of the total solute concentration per kilogram of solvent

Osmolarity

A measure of the total solute concentration per liter of solution

... must be monitored closely to prevent fluid overload.

Correction of the dehydration with intravenous (IV) fluids ...

The hormones ? and ? are the
major controllers of water/fluid balance.

The hormones ADH and Aldosterone are the
major controllers of water/fluid balance.

Normal water and solute concentrations in body fluids is referred to as an
isotonic/ ? state.

Normal water and solute concentrations in body fluids is referred to as an
isotonic/isosmotic state.

Lost water lowers blood ? and ? to decrease ? output
via low glomerular ? and increased ? activity, both of which act to conserve fluids.

Lost water lowers blood volume and pressure to decrease renal output
via low glomerular filtration and increased ADH activity, both of which act to
conserve fluids.

Hypervolemia simply means too much fluid volume, not always just too much water. If it should occur as a result of too much water, ? mechanisms serve
to correct it. However, if just the volume is expanded and there is no disruption of water concentration, the correction mechanism will differ. Basically, the
expanded volume increases blood pressure and results in increased glomerular filtration in nephrons of the kidney causing increased urine output until the
volume imbalance is corrected.

Hypervolemia simply means too much fluid volume, not always just too much water. If it should occur as a result of too much water, ADH mechanisms serve to correct it. However, if just the volume is expanded and there is no disruption of water concentration, the correction mechanism will differ. Basically, the expanded volume increases blood pressure and results in increased glomerular filtration in nephrons of the kidney causing increased urine output until the volume imbalance is corrected.

? and ? are primarily involved in pH balance

hydrogen and
bicarbonate ions are primarily involved in pH balance

The important role of calcium in this discussion is its control of membrane ?. Being a positive ion, calcium that associates with the plasma membrane and serves to repel other ? ions (like charge repulsions) to help control the membrane's permeability to ? ions.

The important role of calcium in this discussion is its control of membrane permeability. Being a positive ion, calcium that associates with the plasma membrane and serves to repel other positive ions (like charge repulsions) to help control the membrane's permeability to positive ions.

All cells, including excitable cells in the "resting" state (not conducting an action potential), are polarized such that the interior is ? relative to the exterior. This difference in net charge across a cell's membrane is due in part to the ? proteins and ? pH.

All cells, including excitable cells in the "resting" state (not conducting an action potential), are polarized such that the interior is negative relative to the exterior. This difference in net charge across a cell's membrane is due in part to the intracellular proteins and body pH.

Secondary imbalances are usually detected by looking first for ? imbalances. Skin turgor ("tenting" in dehydration and "pitting" in edema) is a good
? balance indicator as are sudden weight changes, blood pressure abnormalities, and peripheral or ? edema.

Secondary imbalances are usually detected by looking first for fluid imbalances. Skin turgor ("tenting" in dehydration and "pitting" in edema) is a good
fluid balance indicator as are sudden weight changes, blood pressure abnormalities, and peripheral or pulmonary edema.

Fluid imbalances often appear on lab reports as changes in ? (percentage of formed elements in blood). A high ? suggests a possible concentration of blood maybe due to dehydration while a low ? can appear with fluid overloads.

Fluid imbalances often appear on lab reports as changes in hematocrit (percentage of formed elements in blood). A high hematocrit suggests a possible concentration of blood maybe due to dehydration while a low hematocrit can appear with fluid overloads.

Hyponatremia - cause:
Decreased intake and ? insufficiency (1 degree ); inappropriate ?; diaphoresis with ? replacement; ? therapy

Hyponatremia - cause:
Decreased intake and adrenal insufficiency (1 degree ); inappropriate ADH; diaphoresis with water replacement; diuretic therapy

Hyponatremia - Clinical manifestation
Cellular swelling with cerebral edema leading to ?, ? and ?; ? weakness; ? thirst; ? if secondary to hypervolemia;

Hyponatremia - Clinical manifestion
Cellular swelling with cerebral edema leading to headache, stupor and coma; muscle weakness; decreased thirst; edema if secondary to hypervolemia;

Hypernatremia - cause
? intake or ? failure (1 degree ); water ?; decreased ?secretion; increased ?; ? failure; ? lesion

Hypernatremia - cause
Increased intake or renal failure (1 degree ); water deprivation; decreased ADH secretion; increased
aldosterone; liver failure; hypothalamic lesion

Hypernatremia - clinical manifestion
Cellular ? with increased CNS irritability; increased thirst; ?tension with ?uria if secondary to hypovolemia

Hypernatremia - clinical manifestion
Cellular shrinking with increased CNS irritability; increased thirst; hypotension with oliguria if secondary to hypovolemia

Hypokalemia - Causes
Decreased intake, adrenal cortex hypo/hyper? function and ? therapy (1 degree ); alkalosis/ acidosis?; vomiting or gastric suction.

Hypokalemia - Causes
Decreased intake, adrenal cortex hyperfunction and diuretic therapy (1 degree ); alkalosis; vomiting/gastric suction

Hypokalemia - Clinical manifestation
Cardiac ? (lower T and appearance of U wave due to slow repolarization) and ? weakness;

Hypokalemia - Clinical manifestation
Cardiac arhythmia (lower T and appearance of U wave due to slow repolarization) and muscle weakness;

Hyperkalemia - Causes
Increased intake or ? failure and hyper/ hypoaldosteronism ? (1 0 ); alkalo/ acidosis ?; RBC ?;

Hyperkalemia - Causes
Increased intake or renal failure and hypoaldosteronism (1 0 ); acidosis; RBC hemolysis;

Hyperkalimia - Clinical manifestation
Cardiac ? (shallow, wide QRS with elevated T due to exaggerated repolarization); ? and/or ?

Hyperkalimia - Clinical manifestation
Cardiac depression (shallow, wide QRS with elevated T due to exaggerated repolarization); paresthesia (a sensation of tingling, tickling, prickling, pricking, or burning of a person's skin with no apparent long-term physical effect) and/or paralysis

buffers become the body's ? line of defense against pH changes and are considered responsible for pH "regulation." By controlling levels of acidic ? and alkaline ? ion, the ? and ? systems also contribute to pH regulation. However, these two organ systems are also of major importance in pH "?" when normal regulatory buffer mechanisms are overwhelmed.

buffers become the body's first line of defense against pH changes and are considered responsible for pH "regulation." By controlling levels of acidic carbon dioxide and alkaline bicarbonate ion, the respiratory and renal systems also contribute to pH regulation. However, these two organ systems are also of major importance in pH "compensation" when normal regulatory buffer mechanisms are overwhelmed.

In normal individuals, pH is controlled by two major and related processes; pH ? and pH ?.

In normal individuals, pH is controlled by two major and related processes; pH regulation and pH compensation.

Given that normal body pH is slightly ? and that normal metabolism produces? waste products such as carbonic acid (carbon dioxide reacted with water) and ? acid, body pH is constantly threatened with shifts toward ?.

Given that normal body pH is slightly alkaline and that normal metabolism produces acidic waste products such as carbonic acid (carbon dioxide reacted with water) and lactic acid, body pH is constantly threatened with shifts toward acidity.

Carbonic acid is described as a ? acid since it has a vapor phase. The vapor phase exists because it can be converted into carbon dioxide and ? vapor, both of which are volatile (gaseous) and can be removed across the lungs.

Carbonic acid is described as a volatile acid since it has a vapor phase. The vapor phase exists because it can be converted into carbon dioxide and water vapor, both of which are volatile (gaseous) and can be removed across the lungs.

The ? participate in normal pH regulation by the
secretion of ? ions into the urine as blood is processed by ?.

CO 2 + H 2 O <=> H 2 CO 3 <=> H + + HCO 3-

CO2 = Volatile
H2CO3 = carbonic acid
H+ & HCO3- = ?

The kidneys participate in normal pH regulation by the
secretion of hydrogen ions into the urine as blood is processed by nephrons.

CO 2 + H 2 O <=> H 2 CO 3 <=> H + + HCO 3-

CO2 = Volatile
H2CO3 = carbonic acid
H+ & HCO3- nonvolatile Intermediate

Bicarbonate ion is also ?, and must be eliminated or retained by the ? as pH changes dictate. When a bicarbonate ion is formed in blood or body fluid from carbonic acid, a free hydrogen ion is generated which must be taken up by ? to
prevent pH shifts toward the acid side of the scale (review the hemoglobin/oxyhemoglobin buffer).

Bicarbonate ion is also nonvolatile, and must be eliminated or retained by the kidneys as pH changes dictate. When a bicarbonate ion is formed in blood or body fluid from carbonic acid, a free hydrogen ion is generated which must be taken up by hemoglobin to prevent pH shifts toward the acid side of the scale (review the hemoglobin/oxyhemoglobin buffer).

Hypocalcemia - Causes
Decreased intake (1o ), vit. ?
deficiency, hypo/hyper ? parathyroid; hypo/hyper ? albuminemia; ? abuse or ? failure

Hypocalcemia - Causes
Decreased intake (1o), vit. D
deficiency, hypoparathyroid; hypoalbuminemia; alcohol abuse or liver failure

Hypocalcemia - Clinical manifestation
Increased neuromuscular activity (possible convulsions); skeletal muscle tetany;

Hypocalcemia - Clinical manifestation
Increased neuromuscular activity (possible convulsions); skeletal muscle tetany;

Hypercalcemia - Causes
Increased intake (1o ); immobility; hypo/ hyper ?parathyroidism; ? malignancies; ? failure

Hypercalcemia - Causes
Increased intake (1o ); immobility; hyperparathyroidism; bone malignancies; renal failure

Hypercalcemia - Clinical manifestation
Decreased ? activity (stupor to coma); ?; increased ? risk

Hypercalcemia - Clinical manifestation
Decreased neuromuscular activity (stupor to coma); renal calculi; increased fracture risk

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