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Renal > Renal Physiology (main) > Flashcards

Renal Physiology (main) Flashcards

1
Q

What is the main function of the renal tubules?

A

To recover most of the fluid and solutes filtered at the glomerulus

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2
Q

Which cells secrete Tamm-Horsfall glycoprotein?

A

TAL cells

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3
Q

Describe the autonomic innervation of the kidneys

A

The innervation of the kidneys is entirely sympathetic and arises from the celiac plexus. Sympathetic fibers release NE and dopamine into the loose CT near smooth muscle cells of the renal vasculature.

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4
Q

What are the effects of sympathetic stimulation on the kidney?

A
  1. vasoconstriction
  2. enhanced sodium absorption in the proximal tubule
  3. increased renin release (dense accumulation of sympathetic fibers near the granular cells)
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5
Q

Virtual volume of blood plasma (per unit time) needed to supply the amount of solute that appears in the urine

A

Clearance

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6
Q

Clearance formula (mL/min)

A

Cx = (Ux x V)/Px

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7
Q

What approximates RPF?

A

Clearance of PAH

PAH = p-aminohippurate

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8
Q

What approximates GFR?

A

Clearance of Inulin
Inulin is freely filtered, not absorbed or secreted by the renal tubules. Inulin clearance is independent of plasma concentration. Inulin is nontoxic to the kidney.

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9
Q

The volume of fluid filtered into Bowman’s capsule per unit time

A

GFR

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10
Q

Input into Bowman’s space

A

filtered solute load (Fx), expressed in mg/min or mmol/min

Fx = GFR x Px

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11
Q

Reabsorption rate

A

Rx = (GFR x Px) - (Ux x urine flow rate)

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12
Q

Limitations of filtered load calculations

A
  1. If substance has protein binding (Mg, Ca, phosphate, PAH) it is necessary to correct for the nonfilterable fraction of solute
  2. The kidney must not synthesize, degrade or accumulate the solute (ex: ammonium, glutamine & glutamate)
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13
Q

How do NSAIDs induce prerenal disease?

A

Decreased synthesis of prostaglandins which mediate vasodilation, therefore NSAIDs cause vasoconstriction

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14
Q

How do ACE inhibitors cause prerenal disease in bilateral renal artery stenosis?

A

They interfere with the TGF

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15
Q

Normal urine pH

A

5-6.5

In metabolic acidosis, the urine pH should be < 5.3, since excreting acid will normalize the pH of the ECF

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16
Q

Why does urine dipstick underestimate ketone secretion?

A

It only detects 2 of the 3 present (beta-hydroxybutyric acid and acetoacetic acid). It does not detect acetone.

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17
Q

Persistent excretion of 30-300 mg/day of albumin

A

microalbuminuria

Indicates diabetic nephropathy in the patient with diabetes.

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18
Q

the weight of a solution compared to the weight of an equal volume of distilled water

A

specific gravity
It is proportional the the number of solute particles present and their weight.
Note: osmolality only accounts for the number of particles. There may be a disproportionate increase in the SG when larger solutes are present, such as glucose.

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19
Q

Where do urinary casts typically form?

A

The collecting tubules; they are the site at which urine is most concentrated and acidic, both which favor cast formation.

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20
Q

What does fat in the urine indicate?

A

Glomerular disease and nephrotic syndrome. It only occurs when glomerular disease leads to filtration of normally nonfiltered macromolecules.

21
Q

What is the only clinically diagnostic crystal found in urine?

A

hexagonal cystine crystals = cystinuria

22
Q

Fractional excretion of sodium

A

2% means that tubular reabsorption is impaired (ATN). Calculation: (UNa x PCr)/(PNa x UCr)

23
Q

The ratio of the amount of a substance excreted in the urine to the filtered load (another method of determining Fractional Excretion

A

Clearance of substance/GFR

24
Q

What causes concentration of a solute to increase through movement in the tubule?

A

Water reabsorption or solute secretion by the tubule

25
Q

How does a kidney stone cause hydronephrosis?

A

Blockade of ureter outflow causes the ureter to dilate and increases baseline hydrostatic pressure to 70-80 cm H2O over a period of 1-3 hours. This pressure is transmitted retrograde to the nephrons and causes glomerular filtration to halt.

26
Q

How many muscle layers are present in the detrusor muscle?

A

3

27
Q

What makes up the internal sphincter of the bladder?

What nerve innervates it?

A

smooth muscle fibers of the detrusor muscle interspersed with elastic tissue.
Hypogastric

28
Q

What makes up the external sphincter of the bladder?

What nerve innervates it?

A

voluntary, slow-twitch striated muscle fibers.

Pudendal

29
Q

What volume of urine causes urge to void?

A

~ 150 mL causes sensation to void, but >400 mL gives the sensation of fullness

30
Q

When does GFR normalize for body surface area?

A

Around age 2. GFR is low in a newborn due to incomplete development of functioning nephrons.

31
Q

What are the caveats with using creatinine to estimate GFR?

A

It is secreted by the tubules (~20% overestimate) but the methods of detection overestimate plasma creatinine by a similar amount.

32
Q

What is the source of creatinine?

A

normal metabolism of creatine phosphate in muscle. This is why CC is higher in males than females = greater muscle mass.

33
Q

Effects of aging on the bladder

A

Capacity and compliance of bladder decreases with age.
Number of uninhibited contractions increases.
Rate of bladder emptying decreases and residual volume after voiding increases.

34
Q

Two factors that oppose ultrafiltration

A
  1. hydrostatic pressure in Bowman’s space
  2. oncotic pressure in the glomerular capillary
    GFR is the difference between the hydrostatic pressure difference and the oncotic pressure difference.
35
Q

Vasoactive agents produced by mesangial cells

A

prostaglandins & ANG II

36
Q

Volume of filtrate that forms for a given volume of plasma entering the glomeruli

A

Filtration Fraction

FF= GFR/RPF

37
Q

What happens with increased afferent arteriolar resistance?

A

decreased GFR

capillary pressure and RPF both decrease

38
Q

What happens with increased efferent arteriolar resistance?

A

Glomerular capillary pressure increases decreasing RPF. GFR increases. BUT at higher resistances, the GFR falls because the effect of falling RPF dominates.

39
Q

Impermeable to urea

A

TAL, distal tubule, cortical and outer medullary collecting ducts

40
Q

Where is the urea transporter UT1?

A

In the inner medullary collecting ducts. It is activated by ADH and urea is reabsorbed (70%)

41
Q

inherent ability of the afferent arteriole to contract in response to stretch

A

myogenic reflex

42
Q

Why does furosemide make the macula densa “blind?”

A

Furosemide inhibits the Na/K/Cl transporter in the TAL. The macula densa cells also have an apical Na/K/Cl transporter. Since the intracellular concentration of sodium in the macula densa cells determines its response, blocking this cotransmitter makes it unresponsive.

43
Q

What is the overall effect of ANG II?

A

reduce blood flow and GFR

44
Q

Where does AVP cause increased water absorption?

A

principal cells of the collecting tubules and ducts
AVP binds to V2 receptors on the basolateral membrane from ICT to the end of the nephron.
Another action of AVP to increase BP (goal!) vascular smooth muscle contraction, therefore vasoconstriction.

45
Q

What are the effects of ANP?

A
  1. dilates the afferent and efferent arterioles
  2. lowers the sensitivity of the TGF mechanism
    Net effect: increased GFR and RPF. It indirectly decreases release of renin and therefore ANG II. Also, increased blood flow washes out the medullary interstitium and decreases absorption of water and salt.
46
Q

Why does prerenal cause of ARF cause BUN/creatinine > 20:1?

A

Hypoperfusion causes ANG II to be released and a subsequent rise in water reabsorption. Urea follows water so BUN is elevated out of proportion with creatinine.

47
Q

Why does hypercalcemia occur in metabolic acidosis?

A

Calcium binds to albumin and H+ competes for binding sites on albumin

48
Q

Why does PTH promote phosphate excretion in the urine?

A

Calcium and phosphate are at near saturation in the blood. Urinary excretion of phosphate prevents precipitation

Renal (8 decks)

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