Patho unit 2

  1. 2/3 of the body's water is composed of what?
    Intracellular fluid (ICF)
  2. 1/3 of the body's water is composed of what?
    Extracellular fluid (ECF)
  3. 2 main ECF compartments are what?
    • interstitial fluid compartment
    • intravascular fluid compartment
  4. Define the Total Body Water (TBW)
    Sum of fluids within all compartments
  5. What makes infants more susceptible to dehydration?
    • 1) high metabolic rate,
    • 2) accelerated turnover of body fluids from greater body surface area in proportion to body size,
    • 3) renal mechanisms that regulate fluid and electrolyte conservation may not be mature enough to counter fluid losses.
  6. What makes older adults more prone to dehydration?
    • 1) increased amount of body fat
    • 2) decreased muscle mass
    • 3) decreased ability to regulate sodium and water balances
    • 4) kidneys are less efficient in producing concentrated urine and responses for conserving sodium become sluggish.
  7. The movement of water between ICF and ECF is primarily a function of what?
    Osmotic forces
  8. Define aquaporins
    water channel proteins that provide permeability to water allowing for osmosis
  9. Sodium is the most abundant ion in which compartment?
    ECF and is responsible for osmotic balance of the ECF
  10. Potassium maintains osmotic balance of what compartment?
  11. Osmotic forces within the capillary are balanced by what?
    Hydrostatic pressure produced by cardiac contraction
  12. What is responsible for plasma effective osmolality and why?
    Plasma proteins (albumin) generate plasma oncotic pressure because water, sodium and glucose readily move across the capillary membrane
  13. What are the forces favoring filtration (movement of water out of the capillary and into the interstitial space)?
    Capillary hydrostatic pressure and interstitial oncotic pressure
  14. What are the forces opposing filtration?
    plasma oncotic pressure (pressure of plasma proteins) and the interstitial hydrostatic pressure
  15. Describe Starling hypothesis
    • Net filtration = forces favoring filtration - forces opposing filtration
    • It is the movement of fluid back and forth across the capillary membrane wall to maintain equilibrium between spaces. There is arterial filtration and venous reabsorption, therefore, the arterial end of the capillary has a greater hydrostatic pressure than cappillary oncotic pressure causing water to filter into the interstitial space. Likewise, at the venous end of the capillary, oncotic pressure exceeds hydrostatic pressure causing water to filter back into the circulation leading to equilibrium between the spaces.
  16. Describe the 4 causes of interstitial edema.
    • It is a problem of fluid distribution rather than fluid excess.
    • 1) increased capillary hydrostatic pressure (fluid moves out of the capillary into the interstitial space)
    • 2) decreased plasma oncotic pressure (decreased amount of fluid moving back into capillary)
    • 3) increased capillary membrane permeability (permits the escape of plasma proteins into the interstititial space)
    • 4) lymphatic obstruction (decreases amount of plasma proteins able to move into the lymphatics and return to the circulation - accumulates in the interstitial space)
  17. What effect does venous obstruction have on hydrostatic pressures? Explain
    It increases hydrostatic pressure of fluid within the capillaries and causes fluid to escape into the interstitial space
  18. What effect does salt and water retention have on the hydrostatic pressure?
    Increases hydrostatic pressure causing fluid to escape into the interstitium causing edema.
  19. What are some causes of decreased plasma oncotic pressure?
    loss (nephrotic syndrome, hemorrhage, burns) or decreased production of plasma albumin (liver disease or protein malnutrition) causing decreased oncotic attraction of fluid within the capillary, thus fluid moves into the interstitial space.
  20. A patient has suffered a severe burn. Why is he experiencing extreme edema as well as hypotension?
    Burns cause increase in capillary permeability due to the inflammatory immune response. This causes proteins to escape from the plasma and produce edema through the loss of oncotic pressure and a gain in interstitial fluid proteins. This makes it appear that the he is in a state of dehydration because the fluid is in the interstitial spaces and unavailable for metabolic processes or perfusion causing hypotension.
  21. What is responsible for the regulation of sodium balance?
    The renal effects of aldosterone from the adrenal cortex and natriuretic peptides.
  22. What regulates water balance?
    antidiuretic hormone (ADH) fromthe posterior pituitary
  23. What is the most abundant ECF cation?
  24. What are some important functions of sodium?
    • 1) regulates osmolality (interstitial and intravascular fluid vol)
    • 2) maintains neuromscular irritibility for conduction of nerve impulses along with K+ and Ca+.
    • 3) regulates acid-base balance (NaHCO3 and NaPO4)
    • 4) participates in cellular chemical reactions and membrane transport
    • 5) indirectly regulates water balance thru regulation of extracellular osmotic forces with Cl- and bicarb.
  25. What influences aldosterone secretion and what are its actions?
    • It is secreted when sodium levels are low, potassium levels are high, or renal perfussion is decreased.
    • It is released form the adrenal cortex and increases the reabsorption of sodium and secretion of potassium by the distal tubules. This makes sodium concentration in ECF enhanced and potassium is excreted in the urine.
  26. Describe the renin-angiotensin-aldossterone system.
    When circulating blood volume or BP decreases, renin is secreted by the kidney. Renin stimulates the release of Angiotensin 1 which is then converted to Angiotensin II. Angiotensin II then stimulates the secretion of aldosterone and causes vasoconstriction. Aldosterone promotes sodium and water reabsorption, conserving blood volume. The vasoconstriction increases BP and restores renal perfusion. This inhibits further release of renin.
  27. What are natriuretic peptides?
    hormones (ANP) produced by the myocardial atria, (BNP) produced by the myocardial ventricles, and urodilatin within the kidney.

    They decrease blood pressure and increase sodium and water excretion. Therefore, they are natural antagonists to the renin-angiotensin system.
  28. What are the three factors in sodium regulation?
    Increased glomerular filtration, aldosterone, and natriuretic peptides.
  29. What is the major anion in the ECF?
    Chloride - it follows the active transport of sodium so that its changes are proportional to that of sodium.
  30. What are the primary factors in regulation of water balance?
    Secretion of ADH and perception of thirst.
  31. What are the actions of osmoreceptors?
    neurons located in the hypothalamus that are stimulated by increased osmolality. When released, they cause thirst which leads to drinking water to restore plasma volume and dilutes the ECF osmolality. Addionally, they cause release of ADH which then increases permeability of renal tubular cells to water and sodium. Water is then reabsorbed into the plasma causing increased urine concentration and decreased plasma osmolality.
  32. What are the actions of baroreceptors?
    They are stretch receptors located in the aorta, pulmonary arteries, and carotid sinus. When there is decreased atrial or aortic pressure, it stimulates release of ADH which inturn leads to reabsorption of water and promotes restoration of plasma volume.
  33. What happens when isotonic alerations occur?
    Changes in TBW are accompanied by proportional changes in electrolytes and water. For example, if a person loses pure plasma (hemorrhage) or ECF (sweating), fluid volume is depleted, but the number and type of electrolytes (sodium) and osmolality remains within normal range.
  34. What happens with hypertonic fluid alterations?
    the osmolality of the ECF is elevated causing water to move from intracellular space to extracellular space. This causes ICF dehydration/ECF overload leading to symptoms of hypervolemia.

    Causes: 1) hypernatremia (from hypertonic IVF, hyperaldosteronism, cushing syndrome) which leads to osmotic attraction of water and symptoms of hypervolemia, 2) ECF free water deficit (from DI, hyperventilation) which leads to hypovolemia.
  35. What are some common causes of hypernatremia?
    • 1) inadequate free water intake (causes ICF and ECF dehydration)
    • 2) excessive administration of hypertonic saline solution (sodium bicarb)
    • 3) hyperaldosteronism (causes conservation of sodium and reabsorption of water in the renal tubules)
    • 4) cushing syndrome (caused by excess secretion of ACTH which also causes increase secretion of aldosterone)
  36. Describe clinical manifestations and symptoms of hypernatremia?
    • Serum sodium > 147 mEq/L
    • Seizures, coma, pulmonary edema from primary hypernatremia
    • Thirst, fever, dry mucous membranes, hypotension, tachycardia from hypernatremia secondary to water loss.
  37. How would you treat a patient who is hypotensive, tachycardic, serum sodium is 152, serum Cl- is 112, low urine output with specific gravity of 1.035, Hct is elevated?
    This is a hypernatremic state with dehydration possibly from water loss. It is treated with isotonic salt-free fluid (D5W) until the serum sodium level returns to normal. Additionally, attempt to stop the source of the water loss. Must be treated slowly to prevent rapid movement of fluid into brain cells causing cerebral edema, seizures and brain death.
  38. What causes hypotonic alterations?
    When the osmolality of the ECF is less than normal causing fluid to shift from the ECF to the ICF (where osmotic pressure is greater) leading to cellular swelling.

    Causes: 1) hyponatremia which causes osmotic pressure of the ECF to decrease and water moves into the cell. Plasma volume then decreases, leading to symptoms of hypovolemia. 2) Free water excess which causes both the ICF and ECF volume increase leading to symptoms of hypervolemia and water intoxication with cerebral and pulmonary edema.
  39. What are some causes of hyponatremia?
    • 1) pure sodium deficit: diuretics and extrarenal losses such as vomitting, diarrhea, GI suctioning, burns.
    • 2) Inadequate intake of dietary sodium (rare)
    • 3) Dilutional hyponatremias: with excess of TBW compared with total body sodium or a shift of water from the ICF to ECF (mannitol), excessive replacement with D5W, excessive use of hypotonic solutions like 0.45 NS, excessive sweating may stim thirst and lead to intake of large amounts of water.
    • 4) Hypotonic hyponatremia: when TBW exceeds the increase in sodium as in renal failure
    • 5) Hypertonic hyponatremia: when the shift of water from the ICF to ECF occurs with hyperglycemia, hyperlipidemia, and hyperproteinemia. Water is attracted to the ECF from the ICF compartment causing dilutional hyponatremia and other electrolytes.
  40. Your patient is admitted with 3 day h/o vomitting and diarrhea. She is hypovolemic, hypotensive, tachycardic, and has decreased UOP. Her labs show an elevated HCT, sodium of 130, Cl- level of 90 (nl is 97-105), she has a bicarb of 17, pH of 7.32, CO2 33, and urine spec gravity is < 1.010. What is her diagnosis and how would you treat it?
    She is in an isotonic hypovolemic state with hyponatremia, hypochloremia, metabolic alkalosis. She needs IVF replacement with hypertonic 0.9 NS until her sodium returns to normal, NPO, possibly give her bicarb suppliment. All this while taking care not to increase her sodium level too quickly.
  41. Describe SIADH.
    • Conditions such as fear, pain, acute infection, brain trauma, surgery, drugs, ADH secreting tumor cells in the lung, pancreas, or other tissues cause increased ADH secretion which leads to increased renal reabsorption of water.
    • Amount of ADH is inappropriate in relation to serum sodium levels. Serum sodium levels and osmolality are reduced from dilution. The kidneys continue to secrete sodium making urine sodium and osmolality elevated. Body fluid volume is increased because of reabsorption of water and urine volume is decreased.
  42. What are the clinical manifestations and treatments for hyponatremia from water excess?
    serum and urine sodium will be decreased. Serum and urine osmolality are decreased because water is in excess of sodium therefore diluting the sodium. Hct will be reduced as well. Treatment would be to withhold water for 24 hours. For more severe forms showing CNS effects, hypertonic saline (3%) can be used. Arginine vasopressin receptor antagonist can be used for SIADH.
  43. What are 4 major roles of potassium?
    • 1) regulation of ICF osmolality
    • 2) provides balance for intracellular electrical neutrality in relation to hydrogen and Na+
    • 3) required for glycogen deposition in the liver and skeletal muscle cells
    • 4) maintains resting membrane potential
  44. What 3 things effect regulation of potassium balance?
    • 1) the kidney
    • 2) aldosterone levels
    • 3) changes in pH and thus hydrogen ion concentration
  45. How do changes in pH effect serum potassium levels?
    • During acidosis: hydrogen is moving into the cell, therefore K+ moves out of the cell into the ECF. Decreased ICF K+ results in decreased K+ secretion by the kidneys leading to hyperkalemia.
    • During alkalosis: hydrogen moves out of the cell causing K+ to move into the cell. Distal tubular cells increase their secretion of K+ into the urine leading to hypokalemia.
  46. How does aldosterone help with potassium regulation?
    When potassium levels are increased , aldosterone is released stimulating secretion of potassium into the urine by the distal tubules of the kidney. Additionally, it increases the secretion of K+ from sweat glands.
  47. What 3 hormones promote movement of potassium movement from ECF to ICF?
    aldosterone, insulin, epinephrine
  48. What effect does insulin have on potassium movement?
    it stimulates the Na+/K+ ATPase pump, thereby promoting the movement of potassium into the liver and muscle cells simultaneously with glucose transport after eating.
  49. What effects do catecholamines have on potassium balance?
    • Beta 1 adrenergics (epinepherine) stimulate movement of K+ into cells
    • Alpha adrenergics shift K+ out of cells.
  50. What happens to potassium levels during DKA?
    Since it is a state of acidosis, H+ moves into the cell in exchange for K+ moving out of the cell in attempt to accomodate the acidotic state. Normal level of potassium is maintained in the plasma, but continues to be lost in the urine causing a deficit in total body K+. If insulin is given for treatment of DKA, the insulin will drive the potassium into the cells and causing severe hypokalemia. K+ replacements must be given as well.
  51. What are 5 causes of hypokalemia?
    • 1) decreased po intake
    • 2) increased movement of K+ into cells from ECF (as with alkalosis).
    • 3) loss of total body K+ stores (as with GI and renal disorders)
    • 4) increased aldosterone secretion (as with stress, dehydration and hyponatremia, etc)
    • 5) increased renal K+ excretion (diuretics or low Mag)
  52. What are some symptoms of kypokalemia?
    • decreased hepatic and skeletal muscle glycogen synthesis,
    • impaired renal function
    • polyuria (increased urine with low spec grav)
    • polydipsia (increased thirst with dehydration)
    • neuromuscular excitability
    • skeletal muscle weakness,
    • cardic dysrhythmias
  53. What are the cardiac changes exhibited with hypokalemia?
    SB, AV block, PAT, depressed T-wave, U-wave increases, ST depression, peaked P-wave, prolonged QRS

    * slows the Na/K pump
  54. How is hypokalemia treated?
    correction of acid-base balance is first and foremost
  55. What are some causes of hyperkalemia?
    • 1) increased intake
    • 2) shift of K+ from ICF to ECF
    • 3) decreased renal excretion of K+
  56. What are some causes of hyperkalemia from movement from ICF to ECF?
    cell trauma or change in cell membrane permeability, acidosis, insulin deficiency, cell hypoxia, burns, crush injuries
  57. What will Addison's disease do to K+ concentrations in the body?
    Since Addison's results in decreased production and secretion of aldosterone, there will be a tendency toward hyperkalemia. Aldosterone promotes the movement of K+ from the ECF to ICF with hyperkalemia so that the plasma K+ can then be filtered out by the kidneys and K+ can be secreted in the urine.
  58. What are some symptoms of hyperkalemia?
    Muscle weakness, restlessness, diarrhea, muscle paralysis, cardiac arrythmias: narrow and peaked T-waves, shortened QT interval, depressed ST segment, prolonged PR interval, widened QRS, VF, cardiac arrest. it also causes hypopolarized cell (increased excitability).
  59. What effects does Calcium have on the cell and K+ in the cell?
    • It influences the threshold potential by augmenting or overriding the effects of hyperkalemia. for example, hypocalcemia makes the threshold potential more negative thereby enhancing the neuromuscular effects of hyperkalemia (more muscle weakness). Hypercalcemia makes the threshold potential less negative, thereby counteracting the effects of hyperkalemia on resting membrane potential.
    • K+ effects resting membrane potential versus Ca+ effects threshold potential.
  60. What are some treatments for hyperkalemia?
    • 1) Calcium gluconate: retores normal neuromuscular irritibility.
    • 2) glucose: stimulates insulin secretion
    • 3) glucose and insulin: facilitates cellular entry of potassium
    • 4) Sodium bicarb: corrects metabolic acidosis and lowers serum potassium
  61. Where is intracellular calcium located and what are its functions?
    • Located primarily in the mitochondria.
    • 1) major cation for the structure and function of bones and teeth
    • 2) enzymatic cofactor for blood clotting
    • 3) hormone secretion and function of cell receptors
    • 4) membrane stability and permeability
  62. What is normal serum phosphate level?
    2.5 - 4.5 mg/dl
  63. What are the functions of phosphate?
    acts as an intracellular and extracellular anion buffer in the regulation of acid-base balance, provides energy for muscle contraction in the form of ATP
  64. What 3 hormones regulate Calcium and phosphate concentrations?
    • 1) PTH (secreted in response to low calcium - causes reabsorption of calcium and inhibition of phosphate reabsorption leading to increase in serum calcium and urinary excretion of phosphate.)
    • 2) Vitamin D (secreted in response to low phosphate levels, low calcium, and PTH secretion to further enhance absorption of calcium in the small intestine, bone, and renal tubules of the kidney)
    • 3) calcitonin (decreases calcium levels by inhibiting osteoclasitic activity in bone)
  65. What is the normal serum calcium level?
    8.5 - 12mg/dl
  66. Calcium deficits are related to what?
    • 1) inadequate intestinal absorption
    • 2) deposition of ionized calcium into bone or soft tissue
    • 3) blood administration
    • 4) decreases in PTH and vit. D.
  67. What happens to Calcium levels with excessive amounts of phosphorus intake?
    Calcium binds with it making absorption of calcium and phos by the body impossible or difficult.
  68. How do blood transfusions cause hypocalcemia?
    the citrate in the blood products binds to the calcium so it is unavailable for absorption
  69. How do pancreatitis and bone metastases cause hypocalcemia?
    Pancreatitis leads to the release of lipases into soft tissue spaces and free fatty acids are formed which bind the calcium.

    Bone mets inhibit bone resorption and increase calcium deposits into bone, thereby decreasing serum calcium levels.
  70. Your patient has a vitamin D deficiency and has had a parathyroidectomy. What lab value would you expect to be low?
    Calcium would be low due to decreased intestinal absorption of calcium (vit D) and the loss of PTH.
  71. Your patient is septic, in a metabolic alkalosis, and has peripheral edema with hypoalbuminemia. Would you expect hyper or hypocalcemia? Why?
    • Hypocalcemia because the increase in pH enhances protein binding of iCa.
    • Low protein levels decrease the amount of bound calcium in the plasma.
  72. Would you expect hyperreflexia or hyporeflexia with hypocalcemia and why?
    Hyperreflexia due to increased neuromuscular excitability from a lower threshold potential approaching resting membrane potential.
  73. Chvostek sign and Trousseau sign is an indication of what?

    • Positive Chvostek: tapping on facial nerve just below the temple to elicit twitch of the nose or lip
    • Positive Trousseau: contraction of the hand and fingers when the arterial blood flow in the arm is occluded for 5 minutes.
  74. Do the following diseases cause hyper or hypocalcemia? (Hyperparathyroidism, bone mets from breast, prostate, cervical, or hematological cancers, sarcoidosis, excess vitiamin D.)
  75. What does acidosis do to calcium?
    Decreases serum binding of calcium to albumin which increases ionized calcium thus causing hypercalcemia.
  76. What are the most common causes of hyperphosphatemia?
    • intestinal malabsorption
    • increased renal excretion of phosphate
  77. What symptoms are exhibited with hypophosphatemia?
    hypoxia, bradycardia, heart arrhythmias (especially heart block) due to decreased ATP levels which diminish release of oxygen to the tissues. May also show muscle weakness, respiratory failure, irritibility, confusion, coma, convulsions.
  78. Normal phosphate levels are what?
    2 - 4.5 mg/dl
  79. What organ(s) are responsible for regulating magnesium levels?
    small intestine and kidney
  80. What is normal Magnesium level?
    1.8 - 2.4
  81. What is the relationship between Mg and K?
    Mg inhibits potassium channels, therefore, hypomagnesemia causes movement of K out of the cell. The kidneys then excrete the potassium and it results in hypokalemia.
Card Set
Patho unit 2
alterations in fluids/electrolytes/acid/base balance