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NNP Board Exam Review > Renal > Flashcards

Renal Flashcards

1
Q

Kidney begins functioning at …

A

9-10 weeks of gestation

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2
Q

nephrogenesis, the process of ___________, is complete by about ______ weeks GA

A

process of nephron formation, completed by 34-36 weeks

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3
Q

Bladder formation begins at ______ weeks gestation

A

4-6 weeks

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4
Q

uretheral development is complete by _____ weeks

A

12-13 weeks

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5
Q

the major determinate of GFR

A

blood pressure in the peritubular capillary system

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6
Q

Tubular function: proximal tubules

A

are generally re-absorptive and absorb water, sodium, potassium glucose, amino acids, bicarb, phosphorous, magnesium, chloride, and calcium

secreted: organic acids, hydrogen ions

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7
Q

distal tubular function

A

secrete potassium and hydrogen ions
reabsorb: water in the presence of arganine vasopressin, variable sodium reabsorption (dependent on presence of aldosterone)

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8
Q

ADH system

A

regulates renal blood flow through the renin-angiotensis-aldosterone-AHD system

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9
Q

ADH system: in the ascending loop of henle, a drop in sodium chloride will cause a ______ of the afferent arteriole, allowing for _______ blood flow

A

relaxation —–increased

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10
Q

ADH system: the macula dense cells will stimulate the juxtaglomerular cells to release _______ activating the ADH system.

A

renin

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11
Q

The goal of the ADH system is to maintain adequate renal perfusion by _______ sodium chloride and water _______ by the peritubular capillaries to increase intravascular volume, increasing cardiac output and blood pressure.

A

increasing sodium chloride and increasing water reabsorption

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12
Q

Renin

A

released in response to decreased renal blood flow; converts angiotensinogen from the liver to angiotensin I

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13
Q

angiotensin I

A

undergoes further conversion to angiotensin II in the lungs and renal endothelium by enzyme angiotensin-converting-enzyme (ACE)

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14
Q

Angiotensin II

A

a potent vasoconstrictor of peripheral blood vessels and the efferent arteriole that increases tubular sodium, chloride, and water reabsorption

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15
Q

Aldosterone

A

a mineral corticoid hormone released by the adrenal cortex in response to angiotensin II, adrenocorticotropic hormone, or hyperkalemia.

aldosterone increases intravascular volume through sodium, chloride, and water reabsorption and excretion of potassium and hydrogen ions

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16
Q

Arginine Vasopressin

A

increases the permeability of the collecting ducts to water, and allows for water reabsorption into the peritubular capillaries, increasing intravascular volume

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17
Q

Atrial natriuretic Protein and B natriuretic protein

A

reverse the action of the ADH system

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18
Q

Elevated maternal serum or amniotic alpha-fetoprotein levels indicate (renal)

A

obstructive uropathy, renal agenesis, or congenital nephrotic sydrome

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19
Q

oligohydramnios associated with

A

renal agenesis, dysplasia, polycystic kidney disease or urinary tract obstruction

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20
Q

polyhydramnios may be associated with (renal)

A

due to renal tubular dysfunction and decreased ability to concentrate urine

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21
Q

Elevated BUN

A

may be seen in AKI or hypercatabolic states or with increased protein intake

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22
Q

An increase in serum creatinine

A

increase >0.2mg/dL per day or creatinine >1.5 indicate renal dysfunction

creatinine at birth reflective of mother but should either remain the same or decrease after that (depending on GA)

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23
Q

BUN / Creatinine ratio

A

disproportionate rise - prerenal azotemia

proportionate rise - intrinsic AKI

24
Q

Potassium in AKI

A

often elevated in AKI due to impaired excretion

25
Q

Normal urine specific gravity

A

1.021 to 1.025 in full term infants

26
Q

glycosuria in infants <34 weeks

A

common due to decreased tubular reabsorption of glucose

27
Q

Fractional Excretion of Sodium

A

amount of urinary sodium excretion is a percentage of the filtered sodium, reflecting the balance between glomerular filtration and tubular reabsorption of sodium

(urine sodium x plasma creatinine) / plasma Na x urine creatinine x 100%

FENa >3% indicative of intrinsic renal injury

FENa <2.5% indicative of pre-renal injury

28
Q

Pre-renal azotemia causes and incidence

A

85% of AKI (most common)

State of hypoperfusion

  • hypotension
  • CHF
  • RDS
  • Dehydration
  • Nephrotoxic meds (ACE inhibitors,NSAIDS, COX2 inhibitors, ARBs, aminoglycosides)
29
Q

Intrinsic AKI

A
  • renal dysfunction due to direct structural damage
  • may result from prolongation of prerenal causes of renal injury,
  • congenital defects,
  • inflammation / infection due to viral or yeast infections
  • vascular ischemia/hypoperfusion such as aortic or artery thrombosis
  • nephrotoxic administration of meds in utero or postnatal
  • ATN may be due to perinatal asphyxia
30
Q

Postrenal AKI

A

primarily due to obstruction of urine flow

  • posterior uretheral valves
  • bilateral ureteropelvic junction obstruction
  • bilateral ureterovesical junction obstruction
  • neurogenic bladder
  • obstructive nephrolithiasis
31
Q

AKI management

A

fluid challenge for prerenal AKI

renal ultrasound to assess for presence of urine in bladder

low of low-dose dopamine may be used to increase renal blood flow

treat underlying condition

lasix for fluid overload

32
Q

fluid management for AKI

A

fluid restriction for low output injury

fluid replacement for high-output injury

33
Q

bilateral renal agensis

A

the failure of renal development or the complete absence of the kidneys

associated w/ potter sequence

34
Q

management of bilateral renal agenesis

A

oligohydramnios leads to compression of the fetus leading to pulmonary hypoplasia

comfort measures, dialysis if pulmonary hypoplasia is not severe

almost always 100% mortality

35
Q

Polycystic Kidney Disease

A

autosomal recessive cystic kidney disorder; will have a palpable flank mass bilaterally with oliguria or decreased UOP

usually occurs bilaterally

36
Q

multicystic dysplastic kidney disease

A

nongenetic, developmental renal disorder which usually occurs in only one kidney; the cysts are described as “grape-like” cysts

usually presents with unilateral abdominal mass

one of the most common causes of abdominal masses in neonates

37
Q

Hydronephrosis

A

damage to the kidney from a congenital obstruction of the flow of urine which causes urine to backup into the kidneys which dilates the renal pelvis and calyces

38
Q

Ureteropelvic Junction Obstruction

A

UPJO is one of the most common causes of hydronephrosis; more common in males; obstruction at kidney and ureter junction

39
Q

Posterior urethral valves

A

most common lower urinary tract obstruction in males;

obstruction via membrane blocking the exit from the bladder into the urethra

40
Q

Vesicoureteral Reflux

A

condition that results in urine backflowing out of the bladder into the ureters

41
Q

Renal Vein Thrombosis

A

usually unilateral thrombosis, usually on left side;

  • abdominal flank mass
  • possible abdominal distention
  • significant hematuria
  • thrombocytopenia

high HCT at birth may contribute

If clots occur with UVCs, often occur in the IVC

42
Q

Renal Artery Thrombosis

A

clot in the renal artery, blocks blood flow to the kidney (Frequent w/ UAC)

  • asymptomatic OR
  • systemic HTN
  • hematuria
  • thrombocytopenia
    • oliguria or anuria
43
Q

Urinary Tract Infection most common organism

A

E. Coli (Klebsiella common)

44
Q

UTI Diagnostic

A

positive urine culture obtained via sterile bladder tap or a gram stain with high colony count

45
Q

Prune Belly Syndrome or Eagle-Barrett

A

a) lack of abdominal wall muscles. b) hydronephrosis with a dilated bladder c) bilateral cryptorchidism

46
Q

Patent urachus

A

appearance of clear fluid / urine from the umbilicus at birth; at risk of developing UTI or excoriation of skin; supportive care and surgical closure after 1 year of age

47
Q

chordee

A

abnormal ventral curvature of the penis

48
Q

Cryptorchidism associated with syndromes

A

Down, klinefelter, noonan, prader-willi, fetal hydantoin syndrome

49
Q

Renal Tubular Acidosis

A

Normal kidneys excrete hydrogen ions and reabsorb bicarb to compensate for acidosis. RTA is a failure to to respond or attempt to compensate for acidosis

50
Q

RTA Types

A

Type 1 - distal RTA - inability to secrete hydrogen

type 2 - proximal RTA - defect in the ability to reabsorb bicarb

Type 3 - a combination of types 1 and 2

type 4 - hyperkalemic tubular type is due to a problem with aldosterone (deficiency or resistence) that results in high levels of potassium

51
Q

RTA presentation

A

polyuria, weight loss despite adequate caloric intake; Normal anion gap

52
Q

RTA Treatment

A

sodium bicarb or bicitra; type 4 may require sodium supplementation and potassium restriction

Type 2 - associated with Fanconi anemia - investigate

53
Q

Creatinine levels

A

>1.5 indicative of renal impairment, or increase of >0.3-0.5 rise per day worrisome

54
Q

Fluid challenge

A

give 10-20ml/kg of NS over 1-2 hours, UOP <2ml/kg/hr worrisome

55
Q

Hypertension

A

Term: 100/70 Preterm: 90/60 ; most common cause is acute renal damage, or fluid overload; ARF is most common cause, tx w/ Hydralazine

56
Q

Metabolic acidosis requiring treatment

A

pH <7.2 or CO2 <14, if treating, monitor ionized calcium

NNP Board Exam Review (19 decks)

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