NCC content Flashcards

1
Q

non-excretory functions of renal system

A
  • produces renin (regulates blood pressure)
  • produces erythropoietin (initiated by hypoxia, hypovolemia, hypotension)
  • metabolizes vitamin D
  • degrades insulin
  • produces prostaglandins (renal medulla does this)
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2
Q

define nephron

A

functional unit of the kidney

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3
Q

define GFR

A

the rate at which blood flows through capillaries in the nephron
-afferent and efferent arterioles dilate and constrict to control GFR (& BP)

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4
Q

when does nephrogenesis start and finish?

A
  • starts at 7-8 weeks

- completed by 34 weeks

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5
Q

what are the three main functions of the nephron

A
  • filtration
  • reabsorption (occurs through remainder of tubules)
  • secretion (active transport of substances back into the tubules)
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6
Q

what happens in the proximal tubule?

A

major site of reabsorption (Na, H20)

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7
Q

what happens in the descending loop of Henle?

A

reabsorption of H20

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8
Q

what happens in the ascending loop of Henle?

A

reabsorption of Cl, K, Na, Bicarb, Ca

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9
Q

what’s an important characteristic of the ascending loop of Henle?

A

IMPERMEABLE TO H2O

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10
Q

what happens in the distal tubule?

A

reabsorption of H20 & Na

-aldosterone acts on distal tubule to cause it to reabsorb more Na and H20 and to secrete K

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11
Q

what happens in the collecting ducts?

A
  • presence of ADH allows for filtrate within ducts to become more concentrated by making ducts more permeable to H20
  • H20 reabsorbed
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12
Q

How much Na do preterm babies have the ability reabsorb?

A

85-90% vs 95% in term infants

-can’t get rid of excess Na due to decreased GFR

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13
Q

How much of what is filtered by the kidneys (Bowman’s capsule) is reabsorbed by the body?

A

99%

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14
Q

what are the 2 clinical correlates associated with ADH?

A
  • DI

- SIADH

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15
Q

when does GFR reach adult levels (120 ml/min)?

A

around 2 years of age

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16
Q

where is ADH made and stored?

A
  • made in the hypothalamus

- stored in the posterior pituitary

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17
Q

what happens in DI?

A
  • insufficient ADH

- collecting tubules become impermeable to H20 and body can’t reabsorb it

18
Q

what happens in SIADH?

A
  • too much ADH

- collecting tubules are very permeable to H20 so lots of it reabsorbed

19
Q

which babies are prone to SIADH?

A

-CNS abnormality, midline defect, asphyxia, pneumothorax, post-operative babies

20
Q

what does the RAAS system do?

A

regulates the extracellular fluid compartment

  • helps body maintain fluid balance and blood pressure
  • causes systemic vasoconstriction, body hangs on to more Na and H20, increase in intravascular volume
21
Q

how is the RAAS system initiated?

A

release of renin

-produced by the juxtamedullary cells by afferent arterioles

22
Q

How does renin function?

A

after release, it goes systemically to act on angiotensinogen, which is produced by the liver

23
Q

how does angiotensinogen function?

A

it produces angiotensin I

24
Q

how does angiotensin I function?

A

it goes through the pulmonary circulation where angiotensin-converting enzyme (ACE) changes it to angiotensin II

25
Q

how does angiotensin II function?

A

causes vasoconstriction to increase blood pressure and acts on adrenal medulla to release aldosterone

26
Q

how does aldosterone function?

A

causes distal tubule to reabsorb Na and H20

27
Q

normal GFR in a term infant that can maintain homeostasis who isn’t stressed

A

30 ml/min

28
Q

define anuria

A
29
Q

define oliguria

A
30
Q

normal urine output

A

3-5 ml/kg/h

31
Q

define polyuria

A

> 5 ml/kg/h

32
Q

what is acute renal injury/failure?

A
  • loss of water and electrolyte homeostasis

- secondary to abrupt decrease in GFR

33
Q

what causes acute renal injury?

A
  • sepsis
  • perinatal asphyxia
  • hypotension not associated with sepsis
  • just being premature
34
Q

what is most common type of acute renal failure?

A

prerenal (80%)

35
Q

what can happen if prerenal problems aren’t treated appropriately?

A

it can progress to intrinsic ARF

36
Q

in postrenal ARF, where do the obstructions typically take place?

A
  • ureter
  • bladder
  • urethra
37
Q

what is the most common type of intrinsic ARF?

A

acute tubular necrosis

38
Q

what is the most common cause of acute tubular necrosis?

A

untreated prerenal ARF

39
Q

other causes of intrinsic ARF

A
  • infection (fungal balls)
  • aortic/renal artery thrombosis (UAC)
  • renal vein thrombosis (dehydrated babies, babies with perinatal asphyxia, IDM)
  • DIC
  • congenital renal abnormalities
40
Q

what rate of rise is abnormal for creatinine?

A

0.3-0.5 mg/d

41
Q

what does a urinalysis tell you about the tubules?

A

reflects the structure of the tubules/glomerulus

42
Q

what does FeNa tell us?

A

how well the tubules are functioning

  • normally we should have low Na urine levels, so low FeNa levels
  • can be used to differentiate prerenal from intrinsic failure
  • elevated FeNa may indicate intrinsic failure (>2.5%)
  • FeNa