Renal Physiology Part 1 Flashcards

1
Q

Distribution of fluids within the body

A
  • ICF: approximately 2/3 of total body water
  • ECF: approximately 1/3 of total body water
  • Interstitial fluid: approximately 3/4 of ECF
  • Plasma Volume: approximately 1/4 of ECF
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2
Q

Extracellular Fluid

A

-plasma and interstitial fluid

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3
Q

Plasma broken down into

A
  • venous compartment

- arterial compartment (effective circulating volume)

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4
Q

Vascular compartment

A

-contains blood volume which is plasma and cellular elements of blood, primarily RBCs

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5
Q

Effective circulating volume (ECV)

A

-the volume of arterial blood effectively perfusing thetissue

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6
Q

Transcellular fluid

A
  • also included in ECF
  • normally contains only a small amount of water such as epithelial secretions, synovial, CSF, etc
  • said to occupy a “third space”
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7
Q

Components of ECF

A

-sodium, chloride, bicarbonate

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8
Q

Components of ICF

A

-potassium, magnesium, phosphate, and organic anions, proteins

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9
Q

Cell membrane between ECF and ICF is

A
  • highly water-permeable
  • not permeable to most electrolytes
  • fluid distribution between 2 compartments is dependent on osmotic effects of Na
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10
Q

Capillary cell membrane

A
  • between ECF compartments is highly permeable to small ions

- fluid distribution is due to balance between capillary hydrostatic pressure and colloid osmotic pressure

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11
Q

Maintenance of body fluid balance is regulated by 2 factors which over NaCl and water balance

A

-ECF volume and ECF osmolarity

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12
Q

Distribution of fluid between ECF and ICF compartments is determined primarily by:

A
  • ion distribution (Na)

- ATPase activity

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13
Q

Distribution of ECF between plasma (vascular space) and interstitial (tissue) compartments is determined by

A
  • balance of hydrostatic vs. oncotic pressures

- intravascular pressure in capillaries vs. plasma protein and solute concentration

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14
Q

Edema

A
  • palpable swelling produced by expansion of interstitial fluid volume caused by:
  • alteration in capillary hemodynamics (altered starling forces with increased net filtration pressure)–fluid moves from vascular space into interstitium due to decreased capillary oncotic pressure
  • renal retention of dietary Na+ and water–expansion of ECF volume
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15
Q

Altered Starling foces role

A
  • edema does not become apparent until interstitial volume is increased by 2.5-3L
  • normal plasma volume is only 3L
  • therefore, edema fluid is not derived from only plsma
  • compensatory renal retention of Na+ and water to maintain plasma volume in response to underling of the vasculature must occur in this situation to cause edema
  • this renal compensation is appropriate to restore tissue perfusion although it exacerbates edema (e.g. congestive heart failure)
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16
Q

Forces for filtration

A

-hydrostatic pressure and oncotic pressure

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17
Q

Hydrostatic pressure (blood pressure) in the capillary (Pc)

A

-directly related to blood flow; venous pressure; blood volume

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18
Q

Oncotic (osmotic) force in the interstitium

A
  • determined by concentration of protein in the interstitial fluid
  • normally the small amount of protein that leaks to the interstitium is minor and is removed by lymphatics
  • thus, under most conditions this is not an important factor influencing the exchange of fluids
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19
Q

Forces for absorption

A

-oncotic pressure of plasma and hydrostatic pressure in interstitium

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20
Q

onctotic (osmotic) pressure of plasma

A
  • the oncotic pressure of plasma solutes that cannot diffuse across the capillary membrane; i.e., the plasma proteins
  • albumin is the most abundant plasma protein and biggest contributor to this force
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21
Q

Hydrostatic pressure in the interstitium

A
  • in most cases close to zero and is not a signficant factor affecting filtration versus reabsorption
  • can become significant if edema is present or it can affect glomerular filtration in the kidney (pressure in Bowman’s space is analogous to interstitial pressure)
22
Q

Renal retention of Na+ and water

A
  • results in overfilling of the vascular tree
  • inappropriate renal fluid retention
  • usually results in elevated blood pressure, expanded plsma and interstitial volumes
  • E.g. primary renal disease (glomerulonephritis, nephrotic syndrome)
23
Q

Non-pitting edema

A

-swollen cells due to increased ICF volume–does NOT respond to diuretics

24
Q

Pitting edema

A
  • increased interstitial fluid volume
  • nephrotic syndrome, CHF, pregnancy, cirrhosis
  • does respond to diuretics
25
Q

Primary causes of peripheral edema

A
  • increased capillary hydrostatic pressure
  • increased interstitial oncotic pressure
  • decreased vasscular oncotic pressure
  • increased capillary permeability (k)
  • lymphatic obstruction/removal (lymphedema)
26
Q

Increased capillary hydrostatic pressure (Pc)

A
  • marked increase in blood flow, e.g., vasodilation in a given vascular bed
  • increased venous pressure, e.g., venous obstruction or heart failure
  • elevated blood volume (typically the result of Na+ retention), e.g., heart failure
27
Q

Increased interstitial oncotic pressure

A

primary cause is thyroid dysfunction (elevated mucopolysaccharides in interstitium)

  • act as osmotic agents resulting in fluid accumulation and a non-pitting edema
  • lymphedema can also increase this
28
Q

Decreased vascular oncotic pressure

A
  • liver failure

- nephrotic syndrome

29
Q

Increased capillary permeability

A

-circulating agents, e.g., tumor necrosis factor alpha, bradykinin, histamine, cytokines related to burn trauma, etc., increase fluid filtration resulting in edema

30
Q

Lymphatic obstruction/removal (lymphedema)

A
  • filarial
  • bacterial lymphangitis
  • trauma
  • surgery
  • tumor
31
Q

When there is a net gain of fluid by the body

A
  • ECF volume always enlarges

- a net loss of body fluid decreases ECF volume

32
Q

Intracellular volume is only altered if

A

extracellular osmolality changes

33
Q

If ECF osmolality increases

A

cells lose water and shrink

34
Q

If ECF osmolality decreases

A

cells gain water and swell

35
Q

Renal microcirculation

A
  • 2 sets of arterioles, 2 sets of capillaries in series
  • first capillary network (glomerular capillaries)
  • second capillary network (peritubular capillaries)
36
Q

Glomerular capillaries

A

-high hydrostatic pressure; large fluid volume filtered into Bowman’s capsule

37
Q

Peritubular capillaries

A

-low hydrostatic presuure; large amounts of water and solute are reabsorbed

38
Q

Renal sympathetic innervation

A

-sympathetic neurons synapse on smooth muscle (causing arteriolar constriction) and granular cells (causing renin secretion) in afferent arterioles

39
Q

Sensory fibers from bladder wall and posterior urethra are activated by

A

stretch

40
Q

Parasympathetic fibers from sacral micturition center

A
  • S2-S4 (pelvic nerve)

- stimulate detrusor muscle, inhibits contraction of internal urethral sphincter

41
Q

Sympathetic fibers

A
  • hypogastric nerve

- inhibits detrusor constriction; constricts INTERNAL urethral sphincter

42
Q

Somatic motor neurons

A
  • voluntary; pudendal nerve

- constrict external urethral sphincter

43
Q

Glomerular membrane

A
  • free passage of water, small solutes (glucose, amino acids, electrolytes): concentration are the same on both sides of membrane
  • passage of large molecules (proteins) are formed elements is impeded
  • normally, only very small amounts of protein are filtered into Bowman’s capsule
44
Q

Structure of glomerular membrane

A
  • 3 distinct layers
  • fenestrated capillary endothelium: highly permeable to water, dissolved solutes
  • glomerular basement membrane: collagen, proteoglycans contain anionic negative charges
  • podocyte epithelium: slit pores between podocytes restrict large molecules
45
Q

Physical forces affecting glomerular filtration

A
  • GFR is remarkably high
  • GFR is product of 3 physical factors
    1. hydraulic conductivity (Lp) of glomerular membrane
    2. surface area for filtration (product of 1 and 2 is ultrafiltration coefficient Kf)
    3. capillary ultrafiltration pressure (Puf)
  • GFR=Kf x Puf
46
Q

A primary glomerular disease may

A

-lower GFR by decreasing the surface area available for filtration due to damage to glomerular membrane

47
Q

Ultrafiltration pressure (Puf)

A
  • driving force for glomerular filtration
  • determined by hydrostatic and colloid osmotic pressures in glomerular capillaries, Bowman’s capsule
  • Puf=Pgc-(Pbc + oncotic pressure in glomerular capillaries)
  • the difference of 3 pressures–>net filtration pressure
48
Q

Net filtration pressure

A

glomerular hydrostatic pressure- (bowman’s capsule pressure- glomerular oncotic pressure)

49
Q

Mechanisms for altering GFR

A
  • altered Kf: mesangial cell contraction–shortens capillary loops, lowers Kf and thus lowers GFR
  • altered Puf changes in Pgc
50
Q

Pgc determined by 3 factors

A

renal arterial blood pressure
afferent arteriolar resistance
efferent arteriolar resistance