Overview of Urinary System (B2: W4) Flashcards

1
Q

What percentage of nephrons are cortical versus juxtamedullary?

A
  • 85% of nephrons are cortical
  • 15% are juxtamedullary
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2
Q

What is responsible for generating the interstitial osmotic gradient in the kidney?

A

Juxtamedullary nephrons

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3
Q

What determines the relative ability of water and particles to move via a paracellular route in the neprhons?

A

The expression patter of tight junction proteins along the nephron

The permeability of tight junctions between epithelial cells differs throughout the nephron

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4
Q

What is the relationship of resistance to water flow through the nephron and the segment of the nephron?

A

Resistance to flow increases as you move through the nephron

  • 0 resistance in glomerulus
  • 1000x more resitant in the collecting duct
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5
Q

What is osmotic permeability in the nephron?

A

The ability of water to move through the nephron

Moves from proximal tubule to the collecting duct

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6
Q

What is the osmotic permeability of the neprhon starting from the proximal tubule to the collecting duct?

A

Proximal tubule - high osmotic permeability, low resistance to flow

As you move down the neprhon - low permeability, high resistance

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7
Q

What element increases water permeability in the collecting duct?

A

Antidiruetic hormone (ADH) aka arginine vasopressin (AVP)

Forms aquaporins that allow water to go through the cells

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8
Q

Where is aquaporin AQP2 located, and how is it modulated?

A

It is located on the luminal, apical surface of the collecting duct cells

Regulated by ADH

Three are several different AQPs present in the proximal tubule and collecting duct, but only AQP2 is modulated by ADH/AVP

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9
Q

Describe the blood flow from the renal artery and out the renal vein

A
  • Blood travels in through renal artery
  • Afferent arterioles split off, creating resistance
  • Travels through the glomerulus
  • Out the efferent arteriole, which creates more resistance
  • Travels through the peritubular capillaries
  • Exits via renal vein

In a juxtamedullary nephron, there is also the vasa recta for blood to travel through before returning to the vein

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10
Q

What is the function of the macula densa cells?

A

These are specialized cells tha sense flow in the distabl tubule

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11
Q

Which cells secrete renin?

A

Juxtaglomerular cells

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12
Q

What other types of cells surround the arterioles?

A

Mesangial cells

Granular cells

Smooth muscle cells

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13
Q

What is tubuloglomerular feedback (TGF)?

A

A mechanism that serves to maintain a relatively constant GFR by sensing NaCl levels in the distal nephron and releasing substances that feed back on to the glomerulus to modify arteriolar resistance

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14
Q

What are the downstream effects of a decrease in arterial pressure, and what does TGF do to correct them?

A

Downstream decrease in glomerular hydrostatic pressure

  • Less filtrate goes in nephron
  • GFR goes down
  • NaCl delivery is decreased (at macula densa cells)
    • Decrease in afferent arteriolar resistance
    • Increase in efferent arteriolar resistance
      • Renin secretion increased
      • Angiotensin II increased
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15
Q

What is the effect of angiotensin II on vascular smooth muscle?

A

Causes vasoconstriction

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16
Q

What happens when tubular flow increases, and how does TGF correct for it?

A
  • Flow is faster, so there is less time for NaCl reabsorption
    • More NaCl is delivered
  • Transporters move salt into macula densa cells
    • More Na/K ATPase activity
  • Adenosine binds to receptor on mesangial cells
  • Ca increases - afferent arteriole contracts
  • Less flow, and renin secretion goes down
17
Q

How does the configuration of arterioles and capillareis affect vascular pressure gradients within the kidney?

A
  • The glomerulus is a high pressure capillary
    • Filtration occurs
  • Peritubular capillaries are low pressure
    • Reabsorption occurs

These resistances are in series

Net flow affected by Starling forces

18
Q

What is the pressure profile in the renal circulation as compared to other vascular beds?

A

Sharp decreases in pressure at glomerular capillaries and peritubular capillaries

19
Q

How is blood flow within the kidneys calculated?

A

Change in pressure divided by the sum of the resistance of the afferent and efferent arterioles

Resistance of either arteriole will affect renal blood flow

20
Q

What are the effects of raising the afferent arteriolar resistance?

A

When afferent arteriole dilates

  • Renal blood flow increases
  • Glomerular pressure increases
  • GFR increases

The opposite occurs when the afferent arteriole constricts

21
Q

What are the effects of a decrease in efferent arteriolar resistance?

A

Efferent arteriole dilates

  • Renal blood flow increases
  • Glomerular pressure decreases
  • Small decrease in GFR

The opposite occurs upon constriction of the efferent arteriole

22
Q

What is filtration fraction, and how is it calculated?

A

The percentage of renal plasma flow that enters the tubule

Filtration Fraction = GFR/Renal Plasma Flow

Usually about 20% of plasma gets filtered into glomerulus, the rest goes through

23
Q

What happens to the filtration fraction if the efferent arteriole contracts? If it dilates?

A
  • Increase in Re (constriction): increase in GFR, decrease in renal plasma flow
    • Filtration fraction increases
  • Decrease in Re (dilation): decrease in GFR, increase in renal plasma flow
    • Filtration fraction decreases
24
Q

Which blood vessel is crucial for autoregulation of blood flow?

A

Afferent arteriole - increases resistance as renal artery pressure goes up

There are a range of perfusion pressure over which renal blood flow remains relatively constant, as does GFR

25
Q

What are the primary mechanisms underlying autregulation of RBF?

A
  1. Myogenic response
    1. Gets stretched, then contracts
    2. Keeps pressure in glomerulus constant
  2. TGF
    1. Regulates afferent areteriolar resistance
26
Q

Can nerves affec renal blood flow?

A

Yes

Normally, we don’t have a lot of sympathetic control of flow in the kidneys

  • Sympathetic activation is not an everyday occurence - can happen with hemorrhage
27
Q

What afactors regulate renin release?

A
  1. Decreased stretch in afferent arteriole
  2. Decreased NaCl delivery –> TGF
  3. Increased sympathetic nerve activity

All of this goes back to a decrease in volume or pressure

28
Q

What effects does angiotensin II have in increasing the blood pressure?

A
  • Causes vasoconstriction
  • Enhances thirst and ADH release (increase in water retention)
  • Stimulates adrenal gland to release adlosterone (sodium retention), NE, and Epi
  • Stimulates sympathetic nerves to release NE
29
Q

What is acute renal failure?

A

Abrupt loss of kidney function that results in the retention of urea and other nitrogenous waste products and in the dysregulation of extracellular volume and electrolytes

30
Q

What is the role of prostaglandins in kidneys?

A

Dilation

  • When there is a decrease in extracellular fluid volume, renin increases angiotensin II and baroreceptors stimulate sympathetic activity
  • There is a balance between relaxation and contraction of arterioles
    • Ang II primarily contracts efferent arteriole
    • PGs dilate afferent arteriole
  • Renal blood flow is maintained
31
Q

What happens to patients with a decreased extracellular fluid volume take NSAIDS?

A
  • Prostaglandins cause headache, so patient takes NSAIDS for pain
  • These block prostaglandins - constriction
  • Renal blood flow goes down
  • Leads to acute renal failure
  • Solution: stop taking ibuprofen
32
Q

What is secondary hyper aldosteronism?

A
  • Renal artery stenosis causes pressure in the afferent arteriole to go down
  • Less stretch –> release of renin –> Ang II –> Aldosterone
    • This feedback cause high aldosterone
    • Hypertension is a consequence
33
Q

What happens to patients who have renal artery stenosis and are treated with ACE inhibitors?

A
  • ACE inhibitor given for hypertension
  • Stops the formation of Ang II and aldosterone
  • Efferent arteriole does not contract, low GFR
  • GFR can be reduced enough to cause acute renal failure
34
Q

What is the relationship between oxygen consumption and sodium reabsorption?

A
  • As renal blood flow increases, oxygen consumption increases
    • Greater GFR
  • The reabsorption of sodium is getting the most oxygen
    • Energy needed to fuel Na/K ATPase