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
Normal urine specific gravity
1.021 to 1.025 in full term infants
26
glycosuria in infants \<34 weeks
common due to decreased tubular reabsorption of glucose
27
Fractional Excretion of Sodium
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
Pre-renal azotemia causes and incidence
85% of AKI (most common) State of hypoperfusion * hypotension * CHF * RDS * Dehydration * Nephrotoxic meds (ACE inhibitors,NSAIDS, COX2 inhibitors, ARBs, aminoglycosides)
29
Intrinsic AKI
* 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
Postrenal AKI
primarily due to obstruction of urine flow * posterior uretheral valves * bilateral ureteropelvic junction obstruction * bilateral ureterovesical junction obstruction * neurogenic bladder * obstructive nephrolithiasis
31
AKI management
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
fluid management for AKI
fluid restriction for low output injury fluid replacement for high-output injury
33
bilateral renal agensis
the failure of renal development or the complete absence of the kidneys associated w/ potter sequence
34
management of bilateral renal agenesis
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
Polycystic Kidney Disease
autosomal recessive cystic kidney disorder; will have a palpable flank mass bilaterally with oliguria or decreased UOP usually occurs bilaterally
36
multicystic dysplastic kidney disease
nongenetic, developmental renal disorder which usually occurs in only one kidney; the cysts are described as “**grape-like” cysts** ## Footnote **usually presents with unilateral abdominal mass** **one of the most common causes of abdominal masses in neonates**
37
Hydronephrosis
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
Ureteropelvic Junction Obstruction
UPJO is one of the most common causes of hydronephrosis; more common in males; obstruction at kidney and ureter junction
39
Posterior urethral valves
most common lower urinary tract obstruction in males; obstruction via membrane blocking the exit from the bladder into the urethra
40
Vesicoureteral Reflux
condition that results in urine backflowing out of the bladder into the ureters
41
Renal Vein Thrombosis
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
Renal Artery Thrombosis
clot in the renal artery, blocks blood flow to the kidney (Frequent w/ UAC) * asymptomatic OR * systemic HTN * hematuria * thrombocytopenia * oliguria or anuria
43
Urinary Tract Infection most common organism
E. Coli (Klebsiella common)
44
UTI Diagnostic
positive urine culture *obtained via sterile bladder tap* or a gram stain with high colony count
45
Prune Belly Syndrome or Eagle-Barrett
a) lack of abdominal wall muscles. b) hydronephrosis with a dilated bladder c) bilateral cryptorchidism
46
Patent urachus
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
chordee
abnormal ventral curvature of the penis
48
Cryptorchidism associated with syndromes
Down, klinefelter, noonan, prader-willi, fetal hydantoin syndrome
49
Renal Tubular Acidosis
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
RTA Types
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
RTA presentation
polyuria, weight loss despite adequate caloric intake; Normal anion gap
52
RTA Treatment
sodium bicarb or bicitra; type 4 may require sodium supplementation and potassium restriction Type 2 - associated with Fanconi anemia - investigate
53
Creatinine levels
\>1.5 indicative of renal impairment, or increase of \>0.3-0.5 rise per day worrisome
54
Fluid challenge
give 10-20ml/kg of NS over 1-2 hours, UOP \<2ml/kg/hr worrisome
55
Hypertension
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
Metabolic acidosis requiring treatment
pH \<7.2 or CO2 \<14, if treating, monitor ionized calcium