Physio Exam2.txt

  1. neurogenic (central) diabetes insipidus
    • hypothalamic-pituitary (unable to secrete ADH)
    • result of head trauma or intracranial event
  2. nephrogenic diabetes insipidus
    • renal in origin - kidney is unable to respond to ADH
    • defect in V2 receptor or elsewhere
    • plasma ADH high
  3. SIADH
    • syndrome of inappropriate ADH secretion
    • head injury and some lung tumors cause excessive amounts of ADH to be secreted
    • results in: chronic ECF dilution
    • -hyponatremia
    • -expanded ECF volume
    • -excess renal sodium loss (low aldosterone)
    • -dilution and expansion of the ISF
  4. hyponatremia can be caused secondarily by?
    • blood volume depletion
    • excessive free water conservation
    • excessive water intake
  5. causes of hypernatremia
    • loss of water (dehydration, diabetes insipidus)
    • gain of sodium
    • (persistent hypernatremia is rare, excess (Na+) causes hyperosmolarity and thirst, drinking water dilutes back to normal)
  6. micturition: sympathetic fibers
    • relax detrusor muscle (inhibit) during filling
    • contract intrenal sphincter during filling
  7. micturition: PNS
    • PNS is responsible for micturition
    • causes detrusor muscle to contract
    • causes relaxation of internal sphincter
  8. alpha1 receptors
    • receptor for epinephrine
    • cause a shift of K+ out of cells
    • hyperkalemia
  9. beta2 receptors
    • receptor for epinephrine
    • cause a shift of K+ into cells
    • hypokalemia
  10. insulin's effect on K+
    • increases K+ uptake into cells
    • stimulates Na+-K+ ATPase
  11. Aldosterone's effect on K+
    • increases K+ uptake into tubule cells
    • increases K+ excretion
    • stimulates Na+-K+ ATPase
  12. acidosis
    movement of K+ out of cells
  13. alkalosis
    movement of K+ into cells
  14. where does physiological regulation of K+ take place?
    • in the distal tubule and collecting duct
    • (transport in PT and loop of Henle does not change in the face of increased or decreased total body K+)
  15. K+ reabsorption occurs in which cells?
    K+ secretions occurs in which cells?
    • reabsorption: alpha intrecalated cells of distal nephron
    • secretion: principal cells
  16. high K+ diet
    • aldosterone is secreted
    • promotes K+ secretion
    • stimulates Na+-K+ ATPase
    • increases luminal membrane permeability to K+
  17. effects of diuretics
    • increase GFR
    • decrease reabsorption of electrolytes and water by nephron
  18. potentcy of diuretics
    • highest
    • loop diuretics
    • thiazides
    • K+ sparing drugs
    • carbonic anhydrase inhibitors
    • lowest
  19. osmotic diuretics action
    • low MW
    • nonreabsorbable compounds
    • action:
    • retain water in proximal tubule
    • increase Na+ back diffusion
    • increase Na+, water and K+ loss
  20. action of loop diuretics
    • ex. furosemide (Lasix), ethacrynic acid
    • action:
    • inhibits NaCl reabsorption in the thick ascending limb of LOH (blocks Na+,K+,2Cl- cotransporter)
    • also inhibits Ca2+, Mg2+ and water reabsorption
    • increase urine output of electrolytes and water
  21. action of thiazide diuretics
    • ex. chlorothiazide
    • action:
    • inhibits NaCl reabsorption in the early distal tubule
    • increases excretion of Na+, Cl- and K+
    • stimulates Ca2+ reabsorption
  22. action of aldosterone antagonists
    • ex. spironolactone
    • action:
    • competitive inhibition of aldosterone on cortical collecting tubule
    • sodium remains in the tubule and acts as an osmotic diuretic
    • also inhibits K+ secretion
    • used to supplement other diuretics in treatment of edema to prevent K+ wasting
  23. three forms of plasma calcium
    • 50% ionized Ca2+=biologically active
    • 10% complexed to anions (CaPO4)
    • 40% bound to plasma proteins
  24. how much calcium appears in the urine?
    • about 1%
    • reabsorption happens throughout the nephron except the descending limp of the LOH
  25. how is calcium reabsorbed
    • passively with Na+
    • factors that affect Na+ reabsorption also affect Ca+ reabsorption
    • paracellular route
  26. how does calcium cross the apical and basolateral membranes?
    • apical: via Ca2+ channels
    • basolateral: active transport via Ca2+-ATPase or Na+-Ca2+ exchange
    • (PTH stimulates Ca2+ uptake in DT, mediated by cAMP)
  27. Thiazide Diuretics affect on Ca2+ absorption?
    • increase reabsorption of Ca2+
    • inhibits NaCl reabsorption
  28. how is phosphate (PO43-) transported across the luminal membrane and the basolateral membrane?
    • luminal: reabsorption in PT via cotransport with Na+ (2Na+ - 1PO43- symport)
    • basolateral: passive diffusion and PO43- anion antiporter
    • (PTH decreases PO43- reabsorption in proximal tubule and increases PO43- excretion)
  29. what are the normal forms of Mg in the plasma?
    • 20% bound to protein
    • 25% complexed with anions
    • 55% ionized
    • (80% is filterable)
    • (about 1.0mM total in plasma)
  30. how is Mg transported?
    • 30% passively reabsorbed in PT
    • 60% reabsorbed in thick ascending limb
    • 5% of filtered load is excreted
  31. what are the three main homeostatic mechanisms to regulate H+ in the body?
    • buffers: bicarbonate, proteins, phosphates, etc.
    • respiratory compensation: alters CO2 levels
    • renal compensation: alters HCO3- levels
  32. what is normal blood pH?
    • 7.4
    • pH = -log[H+]
  33. what are the sources of H+ in the body?
    • respiratory CO2
    • normal and abnormal processes
    • -degradation of amino acids, exercise, diabetic ketosis, ingestion of acids
    • fixed (non-volatile) acids from:
    • methionine and cysteine catabolism = sulfuric acid
    • phospholipid degradation = phosphoric acid
  34. Bronsted-Lowery definitions of acid/base
    • acid: H+ donor
    • base: H+ acceptor
    • HA = H+ + A-
    • K = [A-][H+]/[A-]
  35. strong acid
    • low affinity for H+
    • H+ dissociate easily
    • lower pK's
  36. weak acid
    • higher affinities for H+
    • do not dissociate as easily
    • higher pK's
  37. buffers
    • first line of defense agains change in pH
    • bicarbonate = most important buffer
    • acid and conjugate base pair: HA/A-
  38. buffers of the blood
    • bicarbonate: pK is low, effective because of its high concentration
    • hemoglobin: imadazole and alpha amino groups are primary buffer sites on proteins
    • proteins: good pK but concentration in blood is low
    • phosphate: unimportant in blood, important in urine
  39. intracellular buffers
    • Primary buffers-
    • proteins: pKs close to 7.4, high [IC]
    • phosphate: same advantages as proteins
    • Secondary buffer-
    • bicarbonate: low concentration
  40. Henderson-Hasselbalck equation
    pH = 6.1 + log([HCO3-]/0.03 x PCO2)
  41. what are metabolic disturbances?
    • changes in [HCO3-]
    • compensated for by kidneys and lungs
    • takes minutes to days
    • lungs=quick, kidney=slow
  42. what are respiratory disturbances?
    • changes in CO2 levels
    • must be compensated for by the kidneys
    • compensation takes days
  43. what happens when plasma HCO3- decreases?
    • respiratory system: increases ventilation to expel CO2
    • kidneys: synthesize new HCO3-
    • (causes: ingestion of acid, formation of metabolic acids like lactic acid)
  44. what happens when plasma HCO3- increases?
    • respiratory system: reduces ventilation to retain CO2
    • kidneys: excrete excess HCO3-
    • (causes: ingestion of excessive antacids, loss of gastric acid from vomiting)
  45. what happens when plasma PCO2 increases?
    • kidneys: synthesize new HCO3- and excrete H+ in urine to raise blood pH
    • (causes: decreased ventilation, drug overdose, airway obstruction)
  46. what happens when plasma PCO2 decreases?
    • kidneys: excrete HCO3- causing urine to become alkaline, blood HCO3- and pH will decrease
    • (causes: hyperventilation, stress, high altitude)
  47. what is respiration regulated by?
    • plasma PCO2
    • elevated PCO2 stimulates respiration
  48. how do the kidneys stabalize HCO3-?
    • 1. complete recovery of filtered bicarbonate when [HCO3-] is less than 26mEq/L
    • 2. synthesis of new HCO3- above and beyond that entering in the glomerular filtrate
    • 3. excretiong of HCO3- when present in excess (greater than 26 mEq/L)
  49. titratable acidity
    • filtered phosphate (excellent for buffering urine)
    • H+ picked up by phosphate allows synthesis of additional HCO3-
  50. Metabolism of glutamine
    • PT cells metabolize glutamine from blood
    • yeilds NH3 and alpha-ketoglutarate
    • NH3 protonated in lument to NH4+
    • alpha-ketoglutarate metabolized to HCO3-
    • yields two HCO3- and two NH4+
    • NH4+ is highly impermeable(lost in urine), HCO3- goes to the blood
    • (acidosis and/or hypokalemia stimulates NH4+ synthesis)
  51. What ratio determines blood pH?
    • [HCO3-]/0.03 x PCO2
    • from Henderson-Hasselbalch equation
    • decreased bicarbonate or increased PCO2 = acidosis
    • increased bicarbonate or decreased PCO2 = alkalosis
  52. mass action rule
    • when PCO2 changes it causes a small change in HCO3- due to mass action
    • CO2 + H2O = H2CO3 = H+ + HCO3-
  53. what is the normal value and range for blood pH?
    • normal value: 7.4
    • normal range: 7.35 - 7.45
    • (outside of normal range = partially compensated, metabolic or respiratory, acidosis or alkalosis)
    • (inside of normal range = completely compensated...)
  54. metabolic alkalosis
    • H+ loss or HCO3- gain
    • causes:
    • ingestion of alkali (ex.antacids)
    • hyperaldosteronism (ex.Conn's syndrome, stimulates H+ loss)
    • ECF volume contraction-vomiting, nasogastric suction, loop or thiazide diuretics
  55. metabolic acidosis
    • gain of H+ or loss of HCO3-
    • causes:
    • ingestion of acids
    • HCO3- lost from the body
    • non-volatile acid accumulation
    • renal HCO3- recovery is reduced
  56. renal tubular acidoses (RTAs)
    • metabolic acidosis from diminished tubular H+ secretion
    • three types:
    • type 1 (distal): ATPase activity is reduced
    • type II (proximal): Na+-H+ antiporter activity is reduced
    • type IV: reduced formation fo NH4+, due to hyperkalemia secondary to aldosterone defeciency, inhibits enzymes that degrade glutamine
  57. anion gap
    • anions shoud = cations
    • AG = [Na+] - [Cl-] - [HCO3-]
    • normal gap = 8-16 mM
  58. causes of anion gap?
    • lactic acidosis: lactic acid
    • ketoacidosis: acetoacetic acid
    • renal failure: accumulation of phosphoric, sulfuric and other non-volatile metabolic acids
    • salicylate poisoning: asprin
    • ethylene glycol poisoning: glycolic and oxalic acids
    • methanol poisoning: formic acid
  59. respiratory alkalosis
    • due to decrease in PaCO2 via increased alveolar ventilation
    • causes:
    • high altitude
    • anxiety
    • hypoxemia
  60. respiratory acidosis
    • due to impaired pulmonary excretion of CO2
    • causes:
    • impairment of central respiratory regulation
    • chest wall dysfunction
    • impaired airway mechanics
    • impaired gas exchange
    • treatment: correct underlying ventilation disorder
  61. hyperaldosteronism (Conn's syndrome)
    • adrenal cortex autonomously secretes too much aldosterone due to tumor
    • when tumor is selectively secreting aldosterone and not all adrenal steriods (Cushing's disease)
    • causes HTN
    • increased Na+ retention
    • increased K+ excretion
    • aldosterone stimulates H+-ATPase in distal tubule
    • partially compensated metabolic alkalosis
  62. diabetic ketoacidosis (DKA)
    • type 1 diabetes, low insulin, formation of ketoacids
    • ketoacids acidify blood, deplete HCO3-
    • increased plasma glucose, increased filtered load, osmotic diuretic, causes volume depletion
    • partially compensated metabolic acidosis
    • excessive anion gap
    • hyperkalemia
  63. contraction alkalosis
    • stomach flu
    • partially compensated metabolic acidosis
    • vomiting causes loss of: fluid(volume), gastric acid(HCl), K+
    • treatment: saline (NaCl or KCl)
  64. MAP=
    MAP=CO x TPR

    CO= HR x SV
  65. defenition of hypertension
    • blood pressure above 140/90
    • primary HTN: variety of unknown factors, no single identifiable cause, multiple defects in BP regulation
    • secondary HTN: caused by secondary well-defined condition, renal, mechanical, or neuroendocrine abnormalities
  66. what hormones does the kidney secrete?
    • renin (granular/juxtaglomerular cells)
    • Erythropoietin (interstitial cells)
    • 1,25 dihydroxycholecalciferol
  67. what two mechanisms regulate RBF and GFR?
    • myogenic mechanism
    • -intrinsic to VSMC contract in response to stretch
    • tubuloglomerular feedback
    • -increase GFR, increase NaCl delivery to LOH, increase resistance in afferent arteriole, decreases RBF and GFR
  68. BUN:Cr ratio
    • should be 10-15
    • high ratio: dehydration, upper GI bleeding, acute obstruction
    • normal ratio: acute tubular necrosis, loss of nephrons
    • low ratio: severe skeletal muscle injury, liver disease, malnutrition
  69. how are organic anions secreted?
    • via tertiary active transport
    • (all organic anions compete for the same transporter)
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Physio Exam2.txt
Physio Exam2