Volume regulation.txt

  1. Purpose of CVMP activation of the sympathetic drive
    • Transfer volume to central circulation
    • Cardiac inotropy, chronotropy
  2. Purpose of CVMP activation of sympathetic and endocrine outflow to the kidney
    • Preserve GFR
    • Produce concentrated, Na+-free urine
  3. Pathway by which sympathetic outflow to kidney causes increased GFR
    Sympathetic stimulation of JGA → renin secretion → AI → AII → constriction of afferent/efferent arterioles → secretion of PGI → dilation of afferent arteriole → increase GFR
  4. Effect of antiotensin II on the PCT
    Stimulate Na/H counter-transporter → increase Na+ reabsorption
  5. Aldosterone causes increased Na+ reabsorption in these nephron segments
    Medullary and cortical collecting ducts
  6. In times of dehydration, the kidney can preserve up to [%] of the filtrate
  7. What brainstem region might be involved in the salt appetite that accompanies thirst?
    Nucleus of the solitary tract
  8. Increased extracellular fluid volume (ECFV) leads to inactivation of [?] and increased secretion of [?]
  9. Atrial natriuretic peptide (ANP):
    Stimulation for secretion
    Effect on CCD and MCD
    Relationship to ADH
    Effect on afferent arteriole
    • Atrial stretch
    • Antagonize aldosterone
    • Antagonize ADH → decreased water reabsorption
    • Decrease resistance → increased GFR
  10. What effect does increased renal blood flow have on the medullary osmotic gradient?
    Washes it out → decreased water reabsorption
  11. Severe intravascular volume depletion - Effects on:
    Supine BP
    Inferior vena cava filling
    Pulmonary capillary wedge pressure (PCWP)
    • Reduced (systolic < 80 mm Hg)
    • Underfilling
    • Reduced
  12. Sign of decreased systemic interstitial volume
    Decreased skin turgor
  13. Signs of decreased transcellular volume
    • Dry mouth, mucous membranes
    • Diminished intraocular pressure
    • Absent axillary sweat
  14. Intravascular volume overload – Effects on:
    Heart sounds
    Jugular venous pressure
    Hepatojugular reflux
    • Hypertension
    • S3 gallop (due to ventricular distension)
    • Increased
    • Present
  15. What is hepatojugular reflux?
    Press on the liver → jugular veins distend
  16. Signs of increased systemic interstitial volume
    • Dependent pitting edema
    • Hepatic congestion
  17. Signs of increased pulmonary interstitial volume
    • Rales
    • Wheezing
  18. Define ascites
    Fluid accumulation in the peritoneal cavity (e.g., secondary to increased extracellular fluid volume)
  19. Generalized, pitting edema:
    Represents ECF overload of at least [#] L
    Symmetric or asymmetric?
    Noticeable or not?
    • 3 L
    • Symmetric
    • Depends on the size of the person
  20. 3 contributing factors to generalized, pitting edema
    • Altered Starling balance
    • Continued intake of salt and water
    • Renal retention of salt and water
  21. Equation for Starling’s law of transcapillary volume flux (net flux, JV)
    JV = σ Kf (ΔP – Δπ)

    • σ = solute reflection coefficient
    • Kf = capillary permeability
    • ΔP = hydrostatic pressure gradient
    • Δπ = oncotic pressure gradient
  22. T/F: Renal retention of salt and water can be triggered either during intravascular volume depletion or during intravascular volume overload
  23. Why is generalized, pitting edema termed “dependent”?
    It shifts around, based on your body position
  24. Generalized, pitting edema can accumulate in which spaces?
    Peritoneal (ascites) or pleural (pleural effusion)
  25. Causes of localized, pitting edema
    • Damage to a capillary bed
    • Local obstruction of lymphatic or venous drainage
  26. Non-pitting swelling reflects increased [ICF or ECF]
  27. In non-pitting swelling, there is [more or less] excess water than excess salt
  28. How can hypothyroidism cause non-pitting swelling (myxedema)?
    Interstitial mucopolysaccharides accumulate → trap water, albumin
  29. What disease process is associated with severe peri-orbital edema?
    Nephrotic syndrome (you’re losing albumin through the nephron)
  30. 3 disease processes that result in massive edema
    • Congestive heart failure
    • Nephrotic syndrome
    • Cirrhosis
  31. What happens to the ECFV in a normal patient on a high-Na+ diet or mineralcorticoid (over several days)? Why?
    • ECFV increases by a maximum of 2.5 L, then it remains stable
    • Inactivate CVMP, increase ANP
  32. T/F: You can have increased salt intake without experiencing increased thirst
  33. What happens to the ECFV in a patient with CHF, nephrotic syndrome, or cirrhosis, on a high-Na+ diet or mineralcorticoid (over several days)? Why?
    • Generalized edema
    • Failure to inactivate CVMP and/or failure to respond to ANP
  34. Mechanisms of ineffective intravascular volume
    • Baroreceptor malfunction
    • Volume shunted into circulation without baroreceptors
    • CVMP/kidney receives an overriding stimulus
    • Kidney misinterprets signals
  35. Baroreceptor stimulation → [activation or inhibition] of CVMP
  36. Mechanism by which the baroreceptor can misinterpret a pressure waveform
    • CHF → desynchronized cardiac contraction → abnormal waveform
    • Densensitivity of the baroreceptor to increased pressure, over time
  37. 2 places volume can be shunted, where it is undetectable by baroreceptors
    • Splanchnic vessels
    • Arterial-venous fistulae
  38. 2 circumstances in which splanchnic shunting could occur
    • Cirrhosis
    • Sepsis
  39. Effective perfusion = [?] x [?]
    (cardiac output) x (systemic vascular resistance)
  40. In cirrhosis, hepatic venous outflow obstruction + A-V fistulae → activation of the [?] reflex for salt retention
  41. Increased portal venous pressure (in cirrhosis) causes [?]-[?] venous shunting, resulting in [signs]
    porto-systemic; hemorrhoids, varices
  42. In cirrhosis, what pathologic liver changes cause increased portal pressure?
    • Distortion/fibrosis of the sinusoids
    • Decreased clearance of vasoconstrictors/dilators
  43. T/F: Ascites is a sign of cirrhosis
  44. The cirrhotic liver is [underperfused or overperfused]
  45. How does an underperfused, cirrhotic liver ultimately result in increased Na/water retention?
    • Distressed liver sends signal to kidney → kidney retains salt and water (hepato-renal reflex)
    • Example of an “overriding” stimulus leading to failure to inactivate CVMP
  46. T/F: Arterial-venous fistulae form in cirrhosis
  47. Describe the normal pathogenesis of nephrotic syndrome, leading to edema
    Loss of albumin → fluid seeps out of capillaries → decreased IVF → CVMP activation → Na/water retention
  48. How can nephrotic syndrome result in edema when albumin is not very low?
    IVF overfill → secretion of ANP; but patients have acquired ANP resistance and the kidneys cannot respond to ANP
  49. In patients with acquired ANP resistance + nephrotic syndrome, the edema subsides [before or after] the proteinuria, if the patient regains ANP sensitivity
  50. Define pre-renal azotemia
    Rise in BUN despite good renal function
  51. BUN:
    Stands for…
    Is an indication of…
    • Blood urea nitrogen
    • Ability to clear nitrogenous waste
  52. T/F: An increase in BUN always correlates with decreased glomerular filtration
    False – GFR can be normal; the nephron is simply reabsorbing more urea into the bloodstream
  53. What hormone controls urea reabsorption in the nephon?
  54. Effect of increased BUN on:
    Urine volume
    Urine Na+ content
    Urine osmolarity
    Acid/base balance
    Urine K+ content
    • Decreased
    • Decreased
    • Increased
    • Metabolic alkalosis
    • Decreased
  55. You should look for the symptoms of pre-renal azotemia in patients with…
    Severe heart failure
  56. What hormones cause hypokalemia and metabolic alkalosis in pre-renal azotemia?
    Aldosterone, AII
  57. What hormone causes hyponatremia and azotemia in pre-renal azotemia?
  58. CVMP activation results in the release of…
    Aldosterone and catecholamines
  59. How does aldosterone induce metabolic alkalosis?
    Increases ammoniagenesis (increase in H+ secretion and HCO3­- production)
  60. How do aldosterone and ADH cause an increase in the medullary osmotic gradient?
    • Aldosterone → increased Na+ reabsorption into interstitium
    • ADH → increased urea reabsorption into interstitium
  61. What transporters are upregulated by aldosterone in the cortical collecting duct?
    Apical ENaC and ROMK1, basolateral Na/K ATPase
  62. In the collecting duct, why does an increase in Na+ reabsorption contribute to hypokalemia and alkalosis?
    Increases the transcellular electrical gradient favoring K+ and H+ secretion into the tubule lumen
  63. Cardio-renal syndrome results from acutely worsening [?]
Card Set
Volume regulation.txt
Volume regulation