BMD 420 Module 2 (Chapter 2) Flashcards

Fluid inside cells

Fluid outside cells including intravascular and interstitial fluid

Force that pushes fluid out of capillaries into tissues

Force that pulls water toward higher solute concentration

Excess fluid accumulation in interstitial tissue causing swelling

Increased hydrostatic pressure; decreased plasma proteins; lymphatic obstruction; increased capillary permeability

Indentation remains after pressing swollen tissue

Insufficient body fluid due to low intake or excessive loss

Equal loss of water and electrolytes

Greater electrolyte loss than water causing diluted plasma

Greater water loss than electrolytes causing concentrated plasma

Vomiting, diarrhea, sweating, diabetic ketoacidosis, inadequate H2O intake

Dry mucous membranes, decreased skin turgor, fatigue, low BP, increased hematocrit

Increased thirst, increased heart rate, vasoconstriction, concentrated urine

Fluid shift from bloodstream into tissues or cavities where it cannot be used for circulation

Hypovolemia despite fluid present in body

Burns peritonitis severe inflammation

Primary extracellular cation controlling fluid balance and nerve conduction

Low serum sodium levels below 135 mEq/L which causes fluid to shift into the cells.

Excessive sweating, diarrhea, and vomiting. Low Na+ Diet. Diuretic drugs. Low aldosterone (Not reabsorbing Na+), excess ADH (Increases the amount of H2O retained and not excreted), and adrenal insufficiency (responsible for producing aldosterone). Renal failure and drinking too much H2O.

Fatigue, cramps, impaired nerve conduction, fluid imbalances, low blood volume since the fluid shifted into the cells like brain cells.

1. Low Na+ in blood (Less pull of H2O from the vasculature). 2. Low osmotic pressure (pull) in the ECF. 3. H2O shifts out of the blood. 4. Cells in the ECF have a higher osmotic pressure (pull) due to the K+ inside which pulls H2O inside the cell. 5. Cell swells and ruptures

High serum sodium levels above 145 mEq/L which causes fluid to shift out of cells causing dehydration of tissues

Ingesting too much Na+. High H2O loss. Low ADH (Excreting a lot of fluid and leaving high levels of Na+ behind). Loss of thirst mechanism (Not drinking enough water). Diarrhea.

Weakness, agitation, Firm tissue, increased thirst with dry mucous membranes, and decreased urine output due to normal ADH secretion.

Primary intracellular cation critical for cardiac and muscle function

1. High H+ [ ] in blood. 2. H+ shifts out of the capillary and into the ECF. 3. In a cell in the ECF, the H+ will enter and displace the K+ that was already in there. 4. K+ is now in the ECF after being kicked out and will travel into the blood. 5. High K+ [ ] in the blood

Low serum potassium levels below 3.5 mEq/L

Diuretics, diarrhea, low intake of K+, excessive aldosterone (Promotes Na+ retention and K+ loss), insulin therapy (causes cells to uptake more K+=less K+ in the blood)

Cardiac dysrhythmias, fatigue, muscle weakness, Paresthesia (abnormal touch sensations, feeling of "pins and needles", decreased GI motility, Impaired renal functions (Can't concentrate urine or increased urine output), and respiratory weakness

Prolonged PR interval, ST depression, shallow T wave, prominent U wave

High serum potassium levels above 5 mEq/L

Renal failure (Not releasing enough K+=increased K+ amount in blood), tissue damage (leakage of intracellular K+ into ECF), acidosis (Displacement of K+ cells), potassium sparing diuretic drugs (Everything but K+ is getting excreted), Aldosterone deficit (body id not releasing enough K+)

Cardiac dysrhythmias, fatigue, muscle weakness, paresthesia, nausea

Wide P wave, prolonged PR interval, decreased R wave height, widened QRS, Depressed ST segment, and tall peaked T wave

Bone strength nerve stability muscle contraction clotting enzyme function. Balance maintained by: Parathyroid hormone (PTH) which increases Ca2+ absorption, and Calcitonin which lowers Ca2+.

Hypoparathyroidism (underproduction of PTH which increases Ca2+ absorption), Malabsorption syndrome, Deficit serum albumin (Ca2+ often bound to these proteins), Increased pH (alkalosis), and renal failure (increased phosphate retention and loss of Ca2+)

Muscle twitching, hyperactive reflexes, Chvostek sign (Spasm of the lip or face), Trousseau sign (carpopedal spasm when BP cuff blocks circulation to the hand), laryngospasm, arrhythmias (weak heart contractions)

Neoplasms (malignant bone tumors due to uncontrolled Ca2+ release), Hyperparathyroidism (overproduction of PTH which increases Ca2+ absorption), decreased stress to bone, increased Ca2+ intake, Milk-alkali syndrome (High milk and antacid intake)

Muscle weakness, lethargy, personality changes, kidney stones, dysrhythmias (increased strength of cardiac contractions), polyuria (high Ca2+ interferes with ADH),

Intracellular cation affecting neuromuscular function and linked to calcium and potassium

Due to malabsorption or malnutrition. Diuretics, diabetic ketoacidosis, hyperparathyroidism, and hyperaldosteronism

Neuromuscular irritability, tremors, insomnia, personality changes, arrhythmias (Increased heart rate)

Renal failure

Depressed neuromuscular function, decreased reflexes, lethargy, cardiac arrhythmias

Located in bone but circulates in ICF and ECF. Functions: Bone mineralization, ATP metabolism, buffer system, cell membranes

Malabsorption, diarrhea, too many antacids, alkalosis, hyperthyroidism

Tremors, weak reflexes, paresthesia, confusion, poor blood cell function, anorexia

Renal failure or tissue destruction releasing intracellular phosphate

Neuromuscular irritability, tremors, insomnia, personality changes, arrhythmias (Increased heart rate)

Major extracellular anion important for acid-base balance and follows sodium

Early stages vomiting, alkalosis, excessive sweating

Nausea, vomiting, diarrhea, muscle twitching, confusion, sleepiness

Excess sodium chloride intake or dehydration

Edema and weight gain

1. Vomiting (loses HCl). 2. Stomach has low HCl levels. 3. Cl- moves from ECF to gastric secretions (stomach). 4. Cl- shifts from plasma to ECF. 5. Bicarbonate ions (HCO3-) moves out of RBC to replace the lost Cl-. 5. Increased HCO3- in blood leads to alkalosis

7.35 to 7.45

Blood pH below normal range

Blood pH above normal range

Sodium Bicarbonate carbonic acid buffer system

20 to 1

Chemoreceptors (Peripheral/Carotid bodies and Central/Medulla oblongata) detect an increase in CO2 (decrease in pH) which stimulates increased respiration rate to drive off more CO2=raises pH

Respiratory rate reduced and more CO2 retained=lowering blood pH

Increased CO2 retention from pneumonia, airway obstruction, opiates, chronic obstructive pulmonary disease

Decreased availability of bicarbonate ions. Diarrhea, renal failure, lactic acid ketoacidosis, bicarbonate loss

Hyperventilation caused by anxiety, fever, aspirin overdose

Vomiting, hypokalemia, excessive antacid intake

Deep rapid breathing to remove CO2

Arterial blood gas analysis

Respiratory cause= change in CO2 levels. Metabolic cause= change in bicarbonate levels

Failure of lungs and kidneys to restore pH leading to life threatening imbalance

This mechanism responds to osmoreceptors that detect changes in blood plasma osmolality. As the high plasma osmolality increases that triggers the thirst mechanism which results in low available H2O meaning we need to increase the amount of H2O intake.

This hormone is produced by the hypothalamus and released from the posterior pituitary gland in response to high plasma osmolality. It increases water reabsorption which reduces urine production.

It is a hormone released by the adrenal cortex and increases Na+ and H2O reabsorption in the kidneys.

It is a hormone released by cardiac muscle fibers in the atria when it senses pressure/stretch in the chamber and in response to high blood volume/pressure by the kidneys increasing renal sodium excretion which brings blood volume and BP down.