Di Sole 2 Flashcards

1
Q

Kidneys function on conserving water

A
  • the ability of the kidney to form URINE that is MORE CONCentrated than the plasma is essential for survival
  • REQUIRESMENTS for forming conc urin is:
    • HIGH OSMOLARITY of the renal medullary interstitial fluid
    • HIGH level of antidiuretic hormone (ADH) also called vasopressin
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2
Q

Counter multiplier system

A
  • produces a hyperosmotic renal medulla facilitating the concentration of urine
  • vasa recta serve as COUNTER CURRENT EXCHANGERS minimizing washout of solutes from the interstitium
  • U-saped structure of the vessels minimizes loss of solute from the interstitium
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3
Q

ADH hormone

A
  • AN increase in fluid osmolality, plasma sodium conc caused osmoreceptor cells to shink
  • shrinkage of the osmoreceptor cells signals the supraoptic nuclei that release ADH
  • in the kidney, ADH controls the degree of dilution or conc of the urine
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4
Q

ADH feedback mech

A
  • regulation of extracellular fluid osmolarity in response to water defiict
  • Water is conserved in the body, while sodium and other solutes continue to be excreted in the urine
  • Opposite sequence occurs when extracellular fluid become too dilute (hypo-osmotic)
  • with EXCESS OF WATER ingestion and decrease in extracellular osmolarity, less ADH is formed, the renal tubules decrease thier permeability, LESS WATER IS RE-ABSORBED and large volume of urine is formed.
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5
Q

Role of thirst in controlling extracellular fluid Osmolarity

A
  • Fluid intake is regulated by thirst mech
  • the hypothalamus contains THIRST OSMORECEPTORS taht sense ECF osmolarity
  • These cells stimulate other HYPOTHALAMIC NEURONS CAUSING THIRST and INCREASED water intake in response to hyposomolality
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6
Q

stimuli for thirst

A
  • large decrease in circualting blood volume and or blood pressure
  • hemorrhage
  • dryness of the mouth and throat
  • thirst mech and temporarily suppressed after drinking water
    • if insufficient water was drunk the persone become thirsty again until the ECG osmolarity is returned to normal
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7
Q

Renal AUTO-REGULATION

A
  • Kidney regulateds fluid and electrolytes (sodium chloride) homeostasis by MODULATING the RAPPORT BETWEEN GLOMERULI AND TUBULES
    • tubules repsone to glomeruli with Glomerulotubular balance (GTB)
    • Glomeruli response to tubules through the tubuloglomerular feedback (TGF)
  • GTB and TGF are FEEDBACK SYSTEMS TO STABILIZE:
    • single nephrone GFR
    • distal fluid and electrolytes delivery
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8
Q

Glomerulotubular balance function

A
  • GTB enables the function of tubules to COMPENSATE AUTOMATICALLY FOR THE FLUCTUATIONS in FILTRATION RATE in the lomerulus to which it is attached
  • GTB is avheived by tubules via:
    • changes in hydrostatic and colloid osmotic forces
    • luminal factors
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9
Q

Tubularglomerular feedback (TGF) function

A
  • Flucutation in sodium chloride delivery to the distal tubule sensed via the JUXTAGLOMERULAR APPARATUS controls GFR by a feedback mech acting on renal arteriolar resistance
  • justaglomerular complex consists of:
    • macular densa and justaglomerular cells
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10
Q

Angiotensin II

A
  • POWERFUL SODIUM-RETAINING HORMONE
    • increases sodium and water RE-ABSORBITON and helps to return blood pressure and Extracellular fluid volume ot normal by three main effects
      • CONSTRICTS efferent arterioles
      • STIMULATES ALDOSTERONE secretion
      • Stimulates sodium tubular re-absorption
  • REGULATED by chagnes in blood pressure and extracellular fluid volume
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11
Q

Aldosterone

A
  • Secreted by ZONA GLOMERULOSA CELLS of the adrenal cortex
  • Acts on cells of the CORTICAL COLLECTING TUBULE to INCREASE Na+ re-absorption and K+ secretion
    • impaired aldosterone secretion ass with defects in regulation of Na+ and K+ conc
      • adrenal destruction or malfunction (addisons disease); adrenal tumors (conn’s syndrome)
  • Na+ and K+ intake affect the level of aldosterone
    • HIGH Na+ intake DECREASES while HIGH K+ intake INCREASES plasma aldosterone
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12
Q

atrial natriuretic peptide

A
  • atrial natriuretic peptide is secreted by cardiac atria cells in volume expansion conditions
    • increased level of atrial natriuretic peptide INHIBITS RE-ABSORPTION of sodium and water by RENAL TUBULES, especially by the collecting ducts
    • DECREASED SODIUM and water re-Absorption icnreases urinary excretion and helps the blood volume to return to normal
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13
Q

nervous control of kidney

A
  • Increase in activity of renal sympathetic nerves RESULTS in an INCREASE of sodium and water re-absorption due to:
    • reduction in GFR by constriciton of renal arterioles
    • increase in tubular sodium re-absorption
    • increase in renin release and angiotension II formation, which further stimulates tubular sodium re-absorption
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