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MCN SPRINGS2020 > RENAL > Flashcards

RENAL Flashcards

1
Q

renal system

A

kidneys, bladder, ureters, urethra

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2
Q

kidneys

A

mesenchyme; three primitive kidneys:
pronephros (disappears by 4 week GA)
mesonephros (glomeruli, mesonephric tubules and ducts, cloaca, distal portion Wolffian duct)
metanephros (proximal tubule, loop of Henle, distal convoluted tubule, collecting duct

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3
Q

ureters and bladder

A

cloacal division

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4
Q

urine formation and excretion begins when?

A

6-10 weeks GA

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5
Q

when is nephrogenesis complete?

A

full term infant 36GA; FANAROFF: 34GA

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6
Q

GFR

A

Glomerular Filtration Rate: is measured by creatinine clearance, the most consistent marker of GFR in the fetus and neonate
essential for: body fluid homeostasis, electrolyte homeostasis, elimination of drugs;
adult GFR 110-120 reached by 2 years old
postnatal 15-25

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7
Q

renal vasoregulators

A

NO, prostaglandins, ANP, sympathetic nervous system, catecholamines, RAAS

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8
Q

buffer system modulation

A

intracellular: hemoglobin, organic phosphates, bone apatite
extracellular: phosphates, plasma proteins, bicarbonate-carbonic acid system

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9
Q

acid base homeostasis

A

buffer system modulation
respiratory modulation (alveolar ventilation)
renal modulation

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10
Q

functions of the tubular system

A

reabsorption( from the lumen to the blood)
secretion (from the blood to the lumen)
transport (solute through the nephron and into the ureters for excretion as urine)

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11
Q

tubular transport

A

proximal convoluting tubule PCT
loop of Henle LOH
distal tubule DCT
collecting ducts

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12
Q

GENETIC ABNORMALITIES

A

Autosomal Dominant Polycystic Kidney Disease
Autosomal Recessive Polycystic Kidney Disease
Multicystic Dysplastic Kidney Disease
Wilms Tumor
Bartter Syndrome

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13
Q

maternal health influences RENAL

A

prematurity and LBW
GDM, smoking, alcohol, malnutrition: vit A;
drugs: ACE inhibitors and angiotensin, NSAIDs;

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14
Q

Acute Kidney Disease

A

the abrupt deterioration in renal function resulting in the inability to maintain fluid and electrolyte balance
PRERENAL (hemodynamic)
RENAL (intrinsic)
POSTNATAL (obstructive)
S&S: elevated BUN and creatinine, hyperkalemia (peaked T wave); metabolic acidosis

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15
Q

Congenital Hydronephrosis

A

abnormal accumulation of the urine within the collecting system resulting in renal cavity distention

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16
Q

developmental and positional anomalies RENAL

A 
AGENESIS (absence)
DYSPLASIA (errors in renal induction)
HYPOPLASIA (abnormally small)
HORSESHOE KIDNEY (fusion of lower poles)
ureteropelvic junction obstruction
posterior urethral valve disease
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17
Q

ureteral and urachal anomalies

A 
renal duplication (renal duplex)
patent urachus (urine backflow from bladder out to umbilicus)
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18
Q

total body fluids

A

extracellular (interstitial and plasma) and intracellular water.
75% at birth

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19
Q

normal weight loss at birth

A

10% term
15% premie
normal physiological transition process caused by atrial natriuretic peptide

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20
Q

glomerulotubular imbalance

A

physiologic state that is present when the glomerular filtration rate (GFR) exceeds the reabsorptive capacity of the renal tubules

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21
Q

what controls water balance

A

ADH antidiuretic hormone

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22
Q

urinary concentrating ability in preterm infant?

A

diminished preterm and term

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23
Q

urinary diluting ability in preterm infant?

A

diminished in preterm, normal in term

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24
Q

insensible water loss

A

GA, environmental temperature, increase body temperature; skin breakdowns, phototherapy

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25
Q

urine formation depends on what?

A

renal function and the renal solute load

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26
Q

electrolyte requirements

A

sodium and chloride…start after day 1-2

potassium..start after urinary flow is established

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27
Q

third spacing

A

including sepsis, hydrops fetalis, hypoalbuminemia, intra-abdominal infections, and after abdominal or cardiac surgery
infants who accumulate fluid and electrolytes in static body fluid compartments

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28
Q

normal urine specific gravity neonate

A

1.008-1.012

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29
Q

normal urine output

A

1-3 mL/kg

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30
Q

hypo and hyper natremia

A

130-150;

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31
Q

treatment for hyperkalemia

A

potassium above 7
insulin given with glucose; sodium polystyrene sulfonate resin (kayexalate); sodium bicarbonate, if metabolic acidosis is present; and peritoneal dialysis.
if arrhythmeia RX; calcium chloride or calcium gluconate

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32
Q

common diuretics

A

furosemide: loop diuretic, , causes a marked increase in urinary sodium, potassium, and hydrogen ion excretion, leading to hypokalemic metabolic alkalosis.
Chlorothiazide: less potent thiazide diuretic that acts at the distal tubule, also causes a hypokalemic metabolic alkalosis. In contrast to loop diuretics, thiazides decrease urinary calcium excretion.
spironolactone: potassium-sparing aldosterone inhibitor, may be associated with hyperkalemia

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33
Q

nephron

A

functional unit of the kidney: consist:
Renal Corpuscle - a Glomerulus & a Glomerular Capsule (Bowmans Capsule)
Renal Tubule - proximal, loop of Henle, ascending, distal convoluted tubule & collecting duct

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34
Q

maintenance of acid-base balance

A
  1. short: acute compensation, which is accomplished by rapid acid or base buffering by intracellular and extracellular buffers in response to acute decreases or increases in serum pH
  2. long: long-term compensation, which is accomplished by renal excretion of acid or base, including an obligate daily acid load of approximately 1-2 mEq/kg per day
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35
Q

acute compensation

A

intracellular buffers: hemoglobin, organic phosphates, bone hydroxyapatite

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36
Q

kidneys role in acid-base homeostasis

A
  1. Reabsorption of filtered bicarbonate and excretion of excessive bicarbonate in response to metabolic alkalosis
  2. Excretion of the obligate daily acid load and any additional acid load from pathogenic processes, such as lactic acidosis related to sepsis or bicarbonate loss from diarrhea
  3. Compensation for changes in serum pH that result from primary respiratory disorders
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37
Q

acid base maintenance processes in kidneys

A

bicarbonate reabsorption
ammoniagenesis (in liver glutamine converted to ammonium)
production of titratable acids

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38
Q

metabolic acidosis

A

excess acid production or increased loss of base
1. increased anion gap:
-lactic acidosis (hypoxemia, shock, sepsis)
-ketoacidosis
2. normal anion gap
-diarrhea
-renal tubular acidosis
RX: correction of underlying cause: bicarbonate (adverse effects)

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39
Q

metabolic alkalosis

A

loss of acid (hydrochloric) with vomiting, diuretics, chloride deficiency
ingestion of base
contraction of the extracellular volume, with loss fo fluid containing more chloride than bicarbonate
GOES together with: volume depletion: hyperaldosteronism, low potassium, low chloride, respiratory acidosis
RX: dont use ammonium hydrochloride,
ok to use: acetzolamide (CHD), repletion of potassium and chloride

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40
Q

respiratory acidosis and alkalosis

A

respiratory distress syndrome, meconium aspiration syndrome, pulmonary infections, or congenital diaphragmatic hernia
RX with alkali to correct is not appropriate

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41
Q

Renal Tubular Acidosis

A 
disorder characterized by a normal anion gap metabolic acidosis and is the sequela of either impaired reabsorption of bicarbonate or impaired urinary acidification/H+ ion excretion.
TYPES: 
DISTAL
PROXIMAL
HYPERKALEMIC
42
Q

function of prenatal kidneys

A

formation and excretion of urine to maintain an adequate amount of amniotic fluid

43
Q

Urine concentration

A

limited capacity max urinary osmolality 800mOsm/kg

44
Q

urine dilution

A

full ability term: 50mOsm/kg; preterm 70mOsm/kg

45
Q

antenatal drug exposure

A

ACE and ARBs: oligo, renal failure, limb deformities, pulomonary hypoplasia
NSAIDS, epileptic, chemo

46
Q

hypertension caused by ?

A

polycystic kidney disease, acute kidney injury (AKI), renovascular or aortic thrombosis, or obstructive uropathy

47
Q

hypotension caused by ?

A

volume depletion, hemorrhage, sepsis

48
Q

edema caused by ?

A

AKI, hydrops fetalis, congenital nephrotic syndrome

49
Q

ascites caused by ?

A

urinary tract obstruction, congenital nephrotic syndrome, volume overload

50
Q

most common cause of abnormal renal mass?

A

hydronephrosis

51
Q

urinalysis

A

examination of freshly voided urine:
inspection,
urinary dipstick assessment (heme-containing compounds, protein, and glucose)
microscopic analysis (red blood cells, white blood cells, bacteria, casts, or crystals)

52
Q

best way for urine culture?

A

bladder catheterization or suprapubic bladder aspiration

53
Q

when should neonate first void

A

by 48 hours

54
Q

best lab indicator for neonatal kidney function?

A

serum creatinine level

term at birth 0/6-1mg/dL then decrease to 0.4

55
Q

radiologic evaluation of kidneys

A

US: anatomy
voiding cystourethrography: use of contrast
tests for vesicoureteral reflux and posterior urethral valves
radioisotopic renal scanning: identified obstruction or scarring
CT: tumor, abscesses

56
Q

Hematuria

A

microscopic

macroscopic

57
Q

Proteinuria

A

urinary dipstick value of at least 1+ (30 mg/dL), with a specific gravity of 1.015 or less, or a urinary dipstick value of at least 2+ (100 mg/ dL), with a specific gravity of more than 1.015

58
Q

persistent heavy proteinuria, edema and hypoalbuminemia, DX?

A

congenital nephrotic syndrome

59
Q

glycosuria

A

presence of glucose on a urinary dipstick

caused by: sepsis or TPN

60
Q

Acute Kidney Injury

A

AKI: sudden decline in kidney function over hours to days, resulting in derangements in fluid, electrolyte, and acid–base balance
3 stages
S&S: oliguria, systemic hypertension, cardiac arrhythmia, evidence of fluid overload or volume depletion, decreased activity, seizure, vomiting, and anorexia.
LABS: elevated serum creatinine and blood urea nitrogen, hyperkalemia, metabolic acidosis, hypocalcemia, hyperphosphatemia, and a prolonged half-life for medications excreted by the kidney

61
Q

causes of AKI

A

prerenal: low volume, hypotension, hemorrhage, sepsis, NEC, CHD, meds
renal: acute tubular necrosis, renal dysplasia
postrenal: obstructive

62
Q

RX for AKI

A

catheter (exclude postrenal obstruction)
fluid challenge: 10-20ml/kg (exclude prerenal
daily weights

63
Q

renal replacement therapy purpose?

A

ultrafiltration (removal of water)

dialysis (removal of solutes)

64
Q

hypertension

A

common in chronic lung disease, renal disease, or a history of umbilical arterial catheterization., coarctation of the Aorta (check BP in 4 extremities), IVH, ECMO, withdrawals
measure BP in the upper arm

BP in 95th% term MAP 72-75

65
Q

nephrocalcinosis SG

A

calcium salt deposition in the renal interstitium

risk factor: hypercalciuria, subcutaneous fat necrosis, hypocitraturia

66
Q

renal vascular thrombosis

A

classic clinical triad: a flank mass, macroscopic hematuria, and thrombocytopenia
LABSL CBC, prothrombin time, activated partial thromboplastin time (aPTT), and fibrinogen concentration

67
Q

renal agenesis

A

the ureteric bud fails to induce proper differentiation of the metanephric blastema,

68
Q

VACTERL

A

vertebral abnormalities, anal atresia, cardiac abnormalities, tracheoesophageal fistula or esophageal atresia, renal agenesis and dysplasia, and limb defects

69
Q

renal dysplasia

A

abnormal renal development in the fetus, leading to replacement of the renal parenchyma by cartilage and disorganized epithelial structures.

70
Q

Multicystic Dysplastic Kidney

A

(MCDK) represents the most severe form of renal dysplasia and is characterized by a nonfunctioning kidney that is devoid of normal renal architecture and composed of multiple large cysts that resemble a cluster of grapes

71
Q

Hydronephrosis SG

A

significant dilation of the upper urinary tract, is one of the most common congenital conditions detected by prenatal ultrasonography

72
Q

hydronephrosis differental DX

A

physiologic hydronephrosis (50%-70% of cases), ureteropelvic junction obstruction (10%-30%), vesicoureteral reflux (10%-40%),
ureterovesical junction obstruction (5%-15%),
multicystic dysplastic kidney (2%-5%),
posterior urethral valves (1%-5%),
ureterocele (1%-3%),
Eagle-Barrett syndrome (<1%)

73
Q

Inherited renal disorders

A

Congenital Nephrotic Syndrome
Polycystic Kidney Disease (enlarged, echogenic kidneys, hypertension)
Neonatal Bartter Syndrome
Renal Tubular Acidosis (defect in reabsorption in bicarb)

74
Q

tumors of the kidneys

A

congenital mesoblastic nephroma, multilocular cystic nephroma, and Wilms tumor (nephroblastoma

75
Q

polycystic kidney disease SG

A

autosomal recassive or dominant; enlarged and echogenic kidneys, oligohydraminios, HPT; hyponatremia

76
Q

exstrophy of the bladder SG

A

mild: epispadias
severe: cloacal exstrophy: omphalocele, bladder exstrophy, imperforated anus, spinal defect

77
Q

potter syndrome SG

A

epicanthal folds, hypertelorism, low-set ears, a crease below lower lip, and a receding chin; oligohydramnios sequence

78
Q

Posterior Urethral Valves SG

A

the most common cause of lower urinary tract obstruction

postnatal RX: securing adequate drainage of the urinary tract

79
Q

Eagle-Barrett Syndrome SG

A

triad of genitourinary abnormalities (markedly enlarged bladder with poor contractility without urethral obstruction, megaureters, and renal dysplasia), deficiency of abdominal wall musculature, and cryptorchidism

80
Q

Bartter Syndrome SG

A

autosomal recessive; hypokalemic tubulopathy; s&s: salt wasting, polyuria, hypokalemia, hypercalciuria

81
Q

patent urachus SG

A

opening between the bladder and the belly button (navel); the urachus is a tube between bladder and belly button present before birth

82
Q

patent urachus SG

A

opening between the bladder and the belly button (navel); the urachus is a tube between bladder and belly button present before birth

83
Q

Fanconi Syndrome SG

A

Renal Tubular Acidosis, Type II/Proximal

84
Q

renal failure lab values SG

A

infant under 120 days of age as an increase in serum Cr more or equal to 0.3mg/dL or 50% or more from the previous lowest value and/or urine output less than 0.5ml/kg/hr

85
Q

kidneys US SG

A

when? abnormal antenatal; abdominal mass, AKI, HPT, hematuria, congenital and UT anatomy
DX: hydronephrosis, cystic kidney disease, size an positon, nephrocalcinosis

86
Q

kidneys VCOG SG

A

voiding cystourethtography
why? evaluate urethea and bladder for vesicoureteral reflux and posterior urethral valves
significant hydronephrosis, hydroureter, documanted UTI
how? contrast via urinary cath;

87
Q

HYPOnatremia SG

A

etiology: decreased GFR caused by AKI
increased proximal tubular fluid and Na re-absorption associated with volume depletion
RX: Na+ volume depletion= increase fluide
Na+oliguria= fluid restriction

Bartter syndrome, Congenital Adrenal Hyperplasia, Pseudohyopaldesteronism (ALDOSTERONE)

88
Q

ALDOSTERONE

A

promotes hydrogen secretion

resposnible for Na and K homeostasis

89
Q

Fractional Excretion of Na

A

FE Na normal less than 1%; renal sodium loss is proportional to GA; younger the age more negative sodium balance and decreased Na

90
Q

ADH

A

Antidiuretic Hormone:
controls water balance
controls water absorption in the collecting duct
where? hypothalmus, baroreceptors of carotic sinus and Left Artium
increased osmolarity= increased ADH

91
Q

Non-excretory kidney

functions

A 
Produces Renin
Produces erythropoietin
Metabolizes vitamin D
Degrades insulin
Produces prostaglandins
92
Q

Excretory functions kidneys

A

maintain plasma osmolarity
Maintain electrolyte balance
Maintain water balance
Excretes nitrogenous end products

93
Q

Renin Angiotensin Aldosterone

System (RAAS)

A 
Stimulation leads to:
– Systemic vasoconstriction
– Sodium retention
– Expansion of ECF
Renin
– Juxtaglomerular cells
– Walls of afferent arteriole
94
Q

LASIX

A 
Loop diuretic
– Blocks reabsorption of Cl-
– Increases RBF
– Impairs Ca++ &amp; Mg++ reabsorption
– Onset of action &amp; duration differs in neonates
95
Q

Thiazides

A

Acts on distal tubule
Augment K+ wasting
Stimulate Ca++ resorption

96
Q

K+ sparing

A

competitive inhibition of aldosterone

Potassium retained

97
Q

Theophylline

A

Mild diuretic effect

Inhibits Na+ reabsorption

98
Q

Dopamine

A

Dilation of renal arteries
Inhibits Angiotension II
Inhibits ADH release

99
Q

Indocin

A 
Inhibits cyclooxygenase pathway
Decreases GFR
Increases ADH secretion
 SIADH
 reabsorption of H20 &amp; decreased UOP
100
Q

Creatinine

A

Best clinical measure of GFR
– Five days to reflect neonatal values
– Levels above 130 mmol/l (1.5mg/dl) considered
indicative of renal impairment in the newborn
 Levels influenced by gestation and postnatal age
 Gestation –and-age based reference charts should be
used in interpretation of creatinine values in the VLBW
  0.3-0.5 mg/day abnormal

101
Q

Urinalysis

A 
reflects structure of tubules
– Protein
– Blood
– Pyuria
– Microscopic exam
 Epithelial cells
 Casts
102
Q

fluid challenge

A

 10 ml to 20 ml/kg NS IV over 1-2 hours
 Lasix 1 Lasix 1-2 mg/kg should oliguria persist 2 mg/kg should oliguria persist
 Response is defined as UOP > 2 ml/kg/hr

MCN SPRINGS2020 (1 decks)

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