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Essentials of Acute Care > test 4 > Flashcards

test 4 Flashcards

1
Q

kidney function is indicated by the

A

GFR (glomerular filtration rate)

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2
Q

The kidneys of children reach adult GFR at approximately

A

1 year of age, but measured GFR vary by age book says 2 years

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3
Q

GFR can be estimated (eGFR) with what equation

A

schwartz equation

eGFR mL/minute/1.73m2 = (k) (height)/serum creatinine

k = constant of 0.413 for all ages/genders

height is measured in cm
serum creatinine is measured in mg/dL

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4
Q

renal blood flow is dependent on

A

intravascular volume and adequate cardiac output with oxygenated blood

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5
Q

equation used to determine whether kidney dysfunction is only a result of hypoperfusion to kidney

A

fractional excretion of sodium

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6
Q

normal BUN-to-creatinine ratio

A

10:1 to 20:1

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7
Q

Elevated BUN-to-creatinine ratios are associated with

A

shock or dehydration with acute kidney failure

can also be from nephrolithiasis or gastrointestinal or pulmonary hemorrhage

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8
Q

Low BUN-to-creatinine ratios are associated with

A

rhabdomyolysis, syndrome of inappropriate antidiuretic hormone secretion, lung disease, malignancy, low dietary protein intake or certain medications

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9
Q

an abrupt cessation or significant decline in the kidneys ability to eliminate waste products, regulate acid-base balance and regulate electrolyte balance

A

Acute renal failure

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10
Q

resorption of electrolytes occurs predominantly where

A

the proximal convoluted tubule

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11
Q

renal wasting of sodium can be due to

A

pseudohypoaldosteronism following a chronic tubular injury (bilat hydronephrosis), true hypoaldosteronism (congenital adrenal hyperplasia) or excessive diuretic use.

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12
Q

acidosis increases serum

A

potassium as hydrogen ion displaces potassium from the intracellular compartment and alkalosis is associated with decreases in serum potassium with reversed cation movement

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13
Q

under hyperkalemic conditions, _____ is secreted and ____ is eliminated by the kidney

A

aldosterone is secreted

potassium is eliminated

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14
Q

tubular reuptake of potassium occurs in the

A

proximal tubule and the thick ascending loop of henle

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15
Q

medications associated with magnesium wasting are associated with

A

natriuresis and/or general tubular epithelial cell damage:

loop and thiazide diuretics, calcineurin inhibitors, cisplatin, ifosfamide, amphotericin B and aminoglycosides

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16
Q

transient wasting of _____ can occur following recover from AKI

A

magnesium

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17
Q

_____ has been associated with hypokalemia due to kaliuresis

A

hypomagnesemia

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18
Q

Development of nephrogenic structures begins

A

3rd-5th week of gestation

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19
Q

Development of nephrogenic structures requires angiotensin II. What maternal medication can cause harm to this process

A

Ace inhibitors can result in fatal renal dysplasia

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20
Q

Fetal kidneys require only ____ of cardiac output

A

10%

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21
Q

At birth, cardiac output _____ and renal vascular resistance ______

A

increases
decreases

increase in GFR and renal blood flow

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22
Q

Renal blood flow is dependent on

A

intravascular volume and sufficient cardiac output

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23
Q

collection of epithelial cells within the distal convoluted tubule that (in conjunction with arterioles) senses the Na levels

A

Juxtaglomerular apparatus (JGA)

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24
Q

renal response to Decreased renal blood flow

A

renin secretion which increases reabsorb of NA which increases intravascular volume

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25
Q

renal response of Sympathetic pathways activated

A

vasoconstriction of renal arterioles → increased GFR/intraglomerular pressure

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26
Q

what are some medications mentioned that affects renal blood flow d/t inhibition of afferent arterioles dilation

A

Prostaglandin inhibitor therapy to promote PDA closure can cause AKI

IV acetaminophen (also used to promote PDA closure) has some transient oliguria noted

ACEs/ARbs can affect intraglomerular pressure by decreasing the efferent arteriolar tone. Using prior to delivery or during neonatal period has been associated with acute kidney failure

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27
Q

eGFR is influenced by the

A

serum creatinine

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28
Q

useful for populations in which creatinine cannot be used (hepatic failure, spina bifida, malnutrition) to detect kidney injury

A

Cystatin C serum concentration

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29
Q

what is testicular torsion

A

twisting of the spermatic cord causing compromised blood flow to the testicle

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30
Q

2 types of testicular torsion

A

intravaginal

extravaginal

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31
Q

spermatic cord twists around the tunica vaginalis

A

intravaginal testicular torsion

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32
Q

spermatic cord twists proximal to the tunica vaginalis (entire scrotal contents)

A

extravaginal testicular torsion

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33
Q

which type of testicular torsion is more commonly seen

A

intravaginal (accounts for 90% of testicular torsion cases)

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34
Q

what happens that allows for a intravaginal testicular torsion to occur

A

it is a congenital malformation resulting in abnormal fixation allowing the epididymis, spermatic cord and testicle to hang freely in the scrotal sac. This allows the structures to twist within the tunica vaginalis

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35
Q

what is the deformity called seen in intravaginal testicular torsion

A

usually a bilateral deformity referred to as “Bell Clapper” deformity

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36
Q

which testicular torsion occurs perinatally during the descent of the testes and may even be present at birth

A

Extravaginal testicular torsion

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37
Q

what are the predisposing factors in testicular torsion

A

trauma

testicular tumor

testicles lying in horizontal plane

history of cryptorchidism and increasing testicular volume

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38
Q

what ages does testicular torsion most commonly present?

A

children < 3 years old

after puberty

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39
Q

clinical presentation of testicular torsion

A

sudden onset of pain in the testis, usually unrelenting

testis is enlarged and tender

absence of cremasteric reflex

affected testicle higher in scrotum

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40
Q

what is gold standard for diagnosis of testicular torsion

A

ultrasound

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41
Q

what ultrasound finding is diagnostic for testicular torsion

A

absence of blood flow to the involved testis; twisting of spermatic cord

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42
Q

treatment for testicular torsion

A

emergent surgical exploration

manual detorsion of testis

affix testis to scrotal wall to prevent recurrence (Orchiopexy)

in most cases, contralateral testis will also be explored and fixed with nonabsorbable sutures to prevent future torsion

if the testicle cannot be salvaged, it is removed. (orchiectomy)

IV fluids, NPO, analgesia when prepping for OR

If loss of testis, support from child life, social/spiritual support may be beneficial

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43
Q

what window do you have before there is irreversible testicular injury in a testicular torsion

A

4-8 hours generally speaking

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44
Q

if the testicle cannot be salvaged, it is removed.

A

orchiectomy

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45
Q

affix testis to scrotal wall to prevent recurrence

A

Orchiopexy

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46
Q

ovarian torsion

A

twisting of adnexal structures compromising blood flow to the ovary

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47
Q

ovarian torsion is usually associated with a

A

cyst or mass

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48
Q

the occurrence of ovarian torsion peaks in

A

adolescence

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49
Q

clinical presentation of ovarian torsion

A

acute onset of abd pain caused by ischemia (more common on R side)

nausea and vomiting

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50
Q

in ovarian torsion the abd pain is more common on what side

A

R

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51
Q

what diagnostic is the definitive study for ovarian torsion

A

Doppler US

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52
Q

what is seen on Doppler US to diagnose ovarian torsion

A

assess for absence of blood flow in the involved ovary or associated ovarian cyst or mass

false negative results are possible depending on severity of torsion

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53
Q

what additional imaging is reserved for patients with nondefinitive findings on US and intermittent symptoms of ovarian torsion

A

Abd CT or MRI

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54
Q

Other than imaging what else will you order when you suspect ovarian torsion and why

A

CBC - evaluate for anemia

Urinalysis to evaluate for UTI

B-hCG to evaluate for pregnancy

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55
Q

Treatment of ovarian torsion

A

medical emergency

Emergent surgical exploration

Detorsion of involved ovary

cystectomy if indicated

rarely is oophorectomy indicated; ovary can often be salvaged for up to 24 hours after the onset of abd pain

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56
Q

an ovary can often be salvaged in ovarian torsion for up to ___ hours after the onset of abd pain

A

24

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57
Q

Hemolytic Uremic Syndrome (HUS) is a disease of the

A

microcirculation

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58
Q

HUS is characterized by

A

hemolytic anemia, thrombocytopenia, and acute renal failure (ARF).

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59
Q

HUS is most frequently seen in

A

children < 4 years of age

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60
Q

HUS is the most common cause of

A

Acute renal failure (ARF)

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61
Q

etiology of HUS

A

contamination of water, meat, fruits and vegetables with infectious bacteria; peak incidence during summer.

E. coli 0157:H7 is the most common etiology of post-diarrheal (D+) HUS

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62
Q

what season is peak occurrence of HUS

A

Summer

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63
Q

what pathogen is the most common etiology of post-diarrheal (D+) HUS

A

E. Coli 0157:H7

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64
Q

what are the 2 types of HUS

A

D+ HUS and

D- HUS

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65
Q

which type of HUS is Postdiarrheal or typical HUS

A

D+

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66
Q

which type of HUS is atypical or sporadic HUS

A

D-

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67
Q

which HUS is more severe

A

D-

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68
Q

which HUS occurs in previously healthy children

what illness did they have recently?

A

D+

gastroenteritis

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69
Q

what pathogen and toxins are associated with D+ HUS

A

Bacterial verotoxins are absorbed through intestinal mucosa (produced by E.coli 0157:H7 infection) - Shiga toxin is the most common cause.

shigella dysenteriae
Citrobacter freundii
other subtypes of E.coli

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70
Q

what toxin is the most common cause of D+ HUS

A

shiga toxin

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71
Q

which type of HUS carries a higher mortality rate

A

D- (50%)

as opposed to D+ (3-5%)

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72
Q

which type of HUS is associated with ESRD

A

D- in 50% of cases

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73
Q

D - is more common in _____ but may also begin in the _____ period

A

adulthood

neonatal period

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74
Q

which type of HUS may have a familial link

A

D-

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75
Q

D- HUS occurs primarily in what season and is associated with what prodrome?

A

Year round

not associated with GI prodrome like D+

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76
Q

causative factors of D- HUS

A

inherited factor H deficiency
(inhibits complement activation, membrane cofactor protein mutations

streptococcus pneumoniae infection

medications including cyclosporine and Tacrolimus

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77
Q

what pathogen is associated with D- HUS

A

streptococcus pneumoniae

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78
Q

what medications are associated with D- HUS

A

Cyclosporine

Tacrolimus

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79
Q

D+HUS occurs as a result of _______, esp ___ ____, absorbed by the intestinal mucosa, which damage _____ cells and ______, producing a prodrome of _____ ________.

A 
verotoxins
Shiga toxin
endothelial cells
erythrocytes
Hemorrhagic enterocolitis
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80
Q

endothelial swelling of the glomerular arterioles in the kidneys secondary to HUS results in a decrease in ________, _________, and __________

A

GFR
Proteinuria
hematuria

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81
Q

In HUS, this characteristic _______ precipitates the release of ____ ____, ___ ___, and ____ ___ in the small vessels of the kidney, gut and CNS, resulting in ___ ____; shearing of RBCs as they pass through narrowed vessels, ______ ______ and ____ and ______.

A 
microangiopathy
clotting factors
platelet aggregation
fibrin deposition 
hemolytic anemia
renal cortical injury
ARF
thrombocytopenia

triad is
thrombocytopenia
ARF
microangiopathic hemolytic anemia

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82
Q

incubation period of D+ HUS in a healthy child with exposure to contaminated source

A

3-5 days

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83
Q

symptoms of D+ HUS

A 
abd pain
watery, nonbloody diarrhea
fever
weakness
lethargy
irritability
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84
Q

In D+ HUS progression to hemorrhagic colitis occurs how long after onset of diarrhea

A

5-7 days

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85
Q

findings in D+HUS

A

pallor
petechiae
ecchymoses
hematuria
oliguria (abnormally small amount of urine)
azotemia (elevated levels of urea and other nitrogen compounds in blood)
HTN

progresses to 
anuria
hepatomegaly
splenomegaly
hematemesis
edema

tremors and seizures (20% of cases)

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86
Q

diagnostic for HUS

A

patient history

presence of microangiopathic hemolytic anemia

ARF

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87
Q

abnormal findings for HUS

A

reticulocytosis

abnormal RBC morphology

schistocytes, burr and helmet cells on smear

fragmented erythrocytes

anemia - decreased plasma haptoglobin

thrombocytopenia

leukocytosis is common

coagulation profile is often normal

stool cultures often positive for E.coli 0157:H7 or other toxin producing bacteria (not always detected)

elevated BUN, serum creatinine, bilirubin, potassium

Coombs negative

microscopic hematuria, proteinuria and casts on urinalysis

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88
Q

what testing should be done at diagnosis of D+ HUS and repeated 2 weeks later and why?

A

Serum ELISA testing to determine the presence of antibodies to Shiga toxin E.coli serotypes

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89
Q

Typical D+ HUS supportive therapy

A

no abx (can stimulate the bacteria to release more toxins that can damage platelets, blood vessels and kidneys)

Dialysis (about 50% of patients)

Correct electrolyte imbalances, azotemia

manage fluid overload

maintain adequate nutrition and caloric intake while observing renal protective diet

correct anemia (75% of patients require PRBC transfusion)

control HTN

Oral Calcium channel blocker (ie) nifedipine

IV calcium channel blocker (ie nicardipine) or nitroprusside

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90
Q

what is the prognosis for D+ HUS

A

90% of pt survive the acute phase

more than 50% recover full renal function

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91
Q

long term follow up for D+ HUS

A

monitor BP and urinalysis

complications are uncommon, however, proteinuria
decreased GFR
HTN
may recur up to 1 year later

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92
Q

D- HUS treatment

A

plasmapheresis - consider for pts with factor H deficiency to limit renal involvement temporarily but does not prevent progression to ESRD and has not been shown to prevent recurrence of D-HUS

Kidney transplant (8-30% if recurrence persists)

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93
Q

Long term care for D-HUS

A

monitoring of BP and urinalysis

Proteinuria, decreased GFR and HTN may recur up to 1 year later

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94
Q

Platelets and HUS

A

Platelet count is low
elevate the bleeding time

bc it only effects primary hemostasis and not secondary, PT/PTT is normal

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95
Q

thrombocytopenia should have platelet counts less than

A

150,000

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96
Q

what do you see clinically when the primary hemostasis is effected in HUS

A

you can be asymptomatic or

mucocutaneous (superficial) bleeding which includes skin bleeding and mucosal bleeding

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97
Q

what type of bleeding occurs when the primary hemostasis is effected in HUS

A

mucocutaneous (superficial) bleeding

no deep or anatomical bleeding - this occurs when secondary hemostasis is effected (hemarthroses, deep muscle bleeding, cranial bleeding)

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98
Q

skin bleeding includes

A

petechiae (1-2 mm)
purpura (0.3-1cm)
ecchymoses (>1cm)

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99
Q

mucosal bleeding includes

A

epistaxis (most common)

bleeding from superficial scratch

easy bruising

gingival bleeding

menorrhagia

GI bleeding

hemoptysis

hematuria

intracranial hemorrhage (severe)

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100
Q

what kind of anemia happens in HUS

A

normocytic

maybe later if sooooo severe it can become microcytic

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101
Q

In HUS is the normocytic anemia

hemolytic or non-hemolytic

A

hemolytic

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102
Q

In HUS is the normocytic anemia

intravascular or extravascular

A

intravascular hemolysis

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103
Q

In HUS is the normocytic anemia

intrinsic or extrinsic (extra-corpuscular)

A

extrinsic (extra-corpuscular)

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104
Q

In HUS is the normocytic anemia

immune or non-immune

A

non-immune

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105
Q

coombs test in HUS will be

A

negative

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106
Q

what is the problem in microangiopathic hemolytic anemia (MAHA) seen in HUS

A

platelets clump together, causing shearing of RBCs (schistocytes) causes destruction of the RBCs (hemolysis) of the hemoglobin forming heme and globin. Heme has iron and protoporphyrin. the protoporphyrin will become unconjugated bilirubin -> liver to become conjugated bilirubin and there is elevated bili levels sometimes.

LDH will rise when there is hemolysis

also there is hemoglobin floating freely in the blood stream that will end up in the kidney tubule leading to hemoglobinuria and the iron can also end up in the kidney tubule causing hemosiderinuria

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107
Q

triad for HUS

A

microangiopathic hemolytic anemia (MAHA)

thrombocytopenia

acute renal failure

and dont forget the bloody diarrhea

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108
Q

anemia - what all is low on blood counts

A

RBC
Hgb
HCT

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109
Q

MCV will be normal, low or high in HUS

A

normal

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110
Q

LDH will be normal, low or high in HUS

A

high

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111
Q

Haptoglobin will be normal, low or high in HUS

A

low

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112
Q

BUN will be normal low or high in HUS

A

high

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113
Q

Creatinine will be normal low or high in HUS

A

high

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114
Q

what should not be transfused in HUS

A

Platelets, will worsen the clotting at the epithelial injury

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115
Q

what common virus can lead to HUS

A

influenzae

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116
Q

bacterial infection of the Upper urinary tract caused by an ascending infection originated in the lower urinary tract

A

pyelonephritis

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117
Q

most common pathogens for pyelonephritis

A

gram positive bacteria: Enterococcus spp. and Staph aureus

Gram negative bacteria: E.coli, Klebsiella spp., Proteus spp. , P. aeruginosa, Serratia spp. and Enterobacter aerogenes

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118
Q

___ to ____% of children with febrile UTI also have ____ _____

A

60-65%

acute pyelonephritis

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119
Q

patho of pyelonephritis

A

bacterial invasion into the upper urinary tract with patchy interstitial inflammation and collections of neutrophils, leading ot tubular necrosis

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120
Q

clinical presentation of pyelonephritis

A 
fever
lethargy
tachycardia
tachypnea
dehydration
pain (abd, suprapubic, flank, and/or costovertebral)
odorous urine
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121
Q

diagnostic eval of pyelonephritis

what tests will you order and what will they show

A

urinalysis - leukocyte esterase and nitrates

Urine culture - critical for determining organism and appropriate abx

BMP - to check kidney function

CBC with diff - evaluation of WBC count and diff

Blood culture - check for bacteremia

CRP - elevated -> indicates inflammatory process

Erythrocyte sedimentation rate (ESR) - elevated indicates an inflammatory process

Renal ultrasound for children 2-24 months

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122
Q

management of pylenonephritis

A

IV abx

Hydration

renal ultrasound

voiding cystourethrography (VCUG) in some cases - for children with recurrent febrile UTI who have evidence of abnormalities on ultrasound

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123
Q

inflammation within the kidney

A

nephritis

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124
Q

types of nephritis

A

primary
secondary
hereditary

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125
Q

which type of nephritis is the most common form and what infection is it most commonly seen with

A

primary

acute poststreptococcal GN

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126
Q

Pathophysiology for _______

deposits of immunoglobulines, complement and cell-mediated immune reactions lead to inflammation and injury

A

nephritis

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127
Q

clinical presentation of nephritis

A

history of recent throat infection

decreased urine output

dark urine

fatigue

headaches

rash on buttocks and posterior legs (specific to secondary gn)

arthralgia (specific to secondary gn)

weight loss (specific to secondary gn)

elevated BP

edema

other signs of fluid overload/CHF

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128
Q

diagnostic evaluation for nephritis

what should you order

A 
electrolyte panel
creatinine
BUN
CBC with diff
Urinalysis 
Urine culture
Throat culture

if acute postreptococcal GN is suspected, a serum antistreptolysin-O (ASO) titer should be checked

To assess for systemic disease, autoimmune panels such as serum complement levels (C3, C4), lupus serologies, anti-DNase B, perinuclear antineutrophil antibody (P-ANCA), cellular antineutrophil cytoplasmic antibody (C-ANCA) and IgA are useful.

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129
Q

low serum C3 levels with respect to nephritis would be indicative of

A

secondary GN

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130
Q

treatment of nephritis

A

ABX - first line is PCN

Treat HTN or acute renal insufficiency

  • judicious fluid mgmt
  • sodium restricted diet
  • diuretics
  • calcium channel antagonists, vasodilators or ACE inhibitors
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131
Q

treatment for secondary forms of glomerulonephritis (GN)

A

corticosteroids
cyclophosphamide

both to counteract the inflammatory process

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132
Q

most common glomerular cause of hematuria

A

Acute poststreptococcal glomerulonephritis

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133
Q

Acute poststreptococcal glomerulonephritis is caused by a prior infection with

A

specific nephritogenic strains of a beta-hemolytic streptococcus of the throat or skin

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134
Q

Acute poststreptococcal glomerulonephritis commonly follows what infection during the cold weather months

A

Group A streptococcal pharyngitis

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135
Q

Acute poststreptococcal glomerulonephritis commonly follows what infection during the warm weather months

A

streptococcal skin infections or pyoderma

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136
Q

clinical presentation of

Acute poststreptococcal glomerulonephritis

A

gross hematuria
edema
HTN
renal insufficiency

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137
Q

diagnostics for Acute poststreptococcal glomerulonephritis

A

urinalysis - RBCs - RBC casts, proteinuria and polymorphonuclear leukocytes

Elevated ASO titer

complement level - C3 initially decreased then returns to normal 6-8 weeks after presentation (sometimes sooner)

Throat culture positive for group A streptococcus can confirm diagnosis

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138
Q

Management for Acute poststreptococcal glomerulonephritis

A

PCN - 10 day course

if allergic to PCN - cephalosporins or macrolides

Acute renal insufficiency - furosemide

HTN - antihypertensives and sodium restriction

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139
Q

group A B-hemolytic streptococci produces what enzyme that does what to RBCs

A

streptolysin that lyses (destroys) RBCs

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140
Q

Group A B-hemolytic streptococci produces what type of reaction

A

Type III hypersensitivity
immune complexes
antibodies (IgG and IgM)
get clogged in the glomerular basement membrane (GBM) (subepithelial) antibodies bind to antigens in the GBM

initiates a inflammatory reaction in the glomerulus - involves C3 complement, cytokines, oxidants and proteases that damages the podocytes (epithelial cells in the glomerular basement membrane)

that damage allows larger molecules to filter through - like RBCs and proteins - causes hematuria and proteinuria. The urine is cola colored. Also oliguria (low urine production)

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141
Q

Acute poststreptococcal glomerulonephritis is a nephrotic syndrome or a nephritic syndrome

A

nephritic syndrome

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142
Q

in Acute poststreptococcal glomerulonephritis you have oliguria…..so this means you have less fluid excreted from the body so you have

A

more fluid retained
peripheral edema
periorbital edema

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143
Q

Acute poststreptococcal glomerulonephritis usually affects what age group?

____ weeks after skin infection such as impetigo and

___ weeks after a throat infection such as pharyngitis

A

children

6 weeks

1-2 weeks after

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144
Q

in Acute poststreptococcal glomerulonephritis

under light microscopy the glomerulus looks

under electron microscopy….

under immunofluorescence …

A

enlarged and hypercellular

subepithelial deposits referred to as “humps”

“starry sky” with a granular appearance

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145
Q

IgA nephropathy usually accompanies what kind of infection

A

Resp or GI infections

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146
Q

kidney filtration disorder in which too much protein is filtered out of the blood, leaking into the urine which results in what?

A

Nephrotic syndrome

proteinuria
edema
hyperlipidemia

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147
Q

etiologies of nephrotic syndrome

A

idiopathic (90%)

believed to have immunopathogenesis

genetic disorders

secondary causes include infection, drugs, immunologic/allergic disorders, associated with malignant disease, glomerular filtration

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148
Q

idiopathic causes of childhood nephrotic sydnrome

A 
IgA nephropathy
minimal change disease
focal segmental glomerulosclerosis
membranoproliferative GN (MPGN)
mesangial proliferative
membranous nephropathy
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149
Q

secondary causes of childhood nephrotic syndrome

A 
diabetes
Henoch-schonlein purpura
hepatitis B or C
SLE - systemic lupus erythematosus (lupus)
malignancy
vasculitis
streptococcal infection
Human immunodeficiency syndrome
congenital syphilis, toxoplasmosis, cytomegalovirus, rubella
malaria
certain meds
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150
Q

what medications can be secondary causes of nephrotic syndrome

A 
penicillamine
gold
nonsteroidal anti inflammatory medications
interferon
mercury
pamidronate
lithium
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151
Q

what are some genetic causes for childhood nephrotic syndrome

A

Nail-patella syndrome

Pierson syndrome

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152
Q

patho of nephrotic syndrome

A

injury to podocytes which cause collapse of the podocyte structure -> spacing and fracture of protein barrier -> allows neg charged proteins to move free across the disrupted filtration membrane -> proteinuria, edema, decreased circulating albumin -> increased interstitial edema -> increased synthesis of lipoproteins and decreased lipid catabolism -> hyperlipidemia

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153
Q

clinical presentation of nephrotic syndrome

A

edema - most notably periorbital edema

frothy or foamy urine

sudden increase in weight with edema

HTN

Hypoalbuminemia

Hyperlipidemia (LDL and triglycerides)

(can also have ascites and pleural effusions)

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154
Q

nephrotic syndrome diagnostics

A

Urine dipstick to look for proteinuria

24 hour urine collection (ideal) - >3.5g/day (book says > 4g/day for older children and adults and 40mg/m2/hr or 50mg/kg/day in young children)

CBC with diff

complete metabolic panel with serum albumin

Serum C3/C4 complement

antinuclear antibody

hepatitis B and C

HIV testing

Immunologic studies (IgG, IgM, IgE)

kidney biopsy

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155
Q

management of nephrotic syndrome

A

high dose steroids (prednisone 2mg/kg/day for 6 weeks divided into 3 doses) (book says divided into 2 doses)

treatment is continued until pt is in remission (3 days with zero trace protein via urine dipstick)

once proteinuria is resolved -> maintenance dose of steroids - 2mg/kg every other morning, then tapered off over 6 weeks

if no remission after initial treatment or have frequent relapses -> pt is considered steroid resistant -> begin cytotoxic medications such as cyclosporine A (relapse is high when this med is discontinued), cyclophosphamide or chlorambucil. Other options are levamisole (however not common due to risk of drug induced vasculitis), mycophenolate mofetil, sirolimus, tacrolimus and are usually given with high-dose methylprednisolone to induce remission.

supportive therapy includes ACE inhibitors/ARBS, statins, diuretics and restricting dietary sodium to 1500 to 2,000 mg/day

severe edema can require treatment with 25% albumin and diuretics - monitor for HTN, pulmonary edema and CHF

Furosemide and other diuretics can cause electrolyte imbalances (hypokalemia, hyponatremia, deplete intravascular volume -> puts pt at higher risk for kidney failure)

OTC antacids or H2 blockers to protect gastric mucosa from prolonged steroid use

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156
Q

hallmark of nephrotic syndrome is (labs)

A

massive proteinuria and decreased circulating albumin levels

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157
Q

nephritis that includes systemic vasculitis of the small vessels

A

Henoch-Schonlein Purpura nephritis

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158
Q

Henoch-Schonlein Purpura nephritis is seen in what age group

A

any age from infancy to adulthood but overwhelmingly a childhood disease

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159
Q

Henoch-Schonlein Purpura nephritis is mediated by the formation of what

A

immune complexes containing IgA within the skin, intestines and glomeruli

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160
Q

Henoch-Schonlein Purpura nephritis symptoms usually present _ to __ weeks after what 2 infections with what pathogens

A

1-3
URI
Gastrointestinal infection such as
(Epstein-Barr virus, Parvovirus B19, Helicobacter pylori infection, Yersinia infection, Shigella infection, Salmonella infection) or environmental allergen exposure (medications, foods, insect bites)

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161
Q

what kind of rash is associated with Henoch-Schonlein Purpura nephritis

A

raised, non-blanching, purpuric rash most prominent on buttocks and lower legs

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162
Q

what other symptoms are associated with Henoch-Schonlein Purpura nephritis other than rash

A

abd pain
arthralgias
glomerulonephritis

(may be acute or insidious)

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163
Q

diagnostics of Henoch-Schonlein Purpura nephritis

A

clinical presentation

gross hematuria

urinalysis: microscopic or gross hematuria and proteinuria

CBC: Leukocytosis with eosinophilia, thrombocytosis

D-dimer - increased

PT and PTT - decreased

IgA levels -may be increased

stool guaiac - occult blood

kidney biopsy findings are indistinguishable from IgA nephropathy

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164
Q

Henoch-Schonlein Purpura nephritis management

A

resolves spontaneously in >90% patients

symptomatic management of systemic complications is treatment of choice

prednisone 1-2mg/kg/day for 14 days in some cases (more severe)

Plasmapheresis, high dose IVIG and immunosuppressant therapy may be needed for refractory cases

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165
Q

Recurrence of symptoms in Henoch-Schonlein Purpura nephritis

A

as many as 1/3 of patients may have recurrence of symptoms

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166
Q

what can cause isolated hematuria

A

IgA nephropathy (or it can cause nephritic syndrome)

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167
Q

why is 24 hr urine collection optimal

A

a dipstick can tell you that their is protein in the urine, a 24 hour urine collection can quantify it

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168
Q

what range of proteinuria is associated with nephrotic syndrome

A

severe proteinuria
>3.5g/day

(book says > 4g/day for older children and adults and 40mg/m2/hr or 50mg/kg/day in young children)

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169
Q

what range of proteinuria is associated with nephritic syndrome or isolated proteinurea

A

Moderate proteinuria

1-3.5g/day

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170
Q

what is an alternative to 24 hour protein collection (in young children the first urine of the day is often used)

A

Urine protein/urine creatinine ratio using spot urine samples

normal levels - 0.2mg protein/mg creatinine in children older than 2

less than 0.5 mg protein/mg creatinine in children age 6 months to 2 years

any abnormal numbers needs further eval

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171
Q

macroscopic vs microscopic hematuria

A

macroscopic can be seen by the eye

microscopic can be seen in dipstick testing or microscopy.

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172
Q

if the blood is coming from the Glomeruli, the RBCs are usually

A

dysmorphic or RBCs casts

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173
Q

If the hematuria are due to kidney stones the RBCs are

A

not dysmorphic and there are no RBC casts

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174
Q

isolated hematuria f/u

A

it can persist so urinalysis is repeated in 1-4 weeks

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175
Q

when is transient isolated hematuria seen

A

excessive exercise

abdominal trauma

cancer (higher risk if older than 50)

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176
Q

transient isolated proteinuria is _- _ g of protein lost per day

A

1-2

repeat in a few days

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177
Q

orthostatic proteinuria is seen in

A

individual below age 30 when pt is in an upright position - most common cause is orthostatic proteinuria and does not require medical attention

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178
Q

clinical signs of nephritic syndrome

A

peripheral edema

periorbital edema

HTN

Oliguria (80-400mL/day)

Urinalysis shows glomerular hematuria and proteinuria

24 hour protein test shows 1-3g/day

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179
Q

Rapidly progressive glomerulonephritis falls under what category

A

nephritic syndrome

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180
Q

clinical signs in rapidly progressive glomerulonephritis

A

rapidly decrease in eGFR over a few days to 3 months

fatigue

peripheral edema

gross hematuria

HTN

decreased urine output

urinalysis - glomerular hematuria

24 hour protein collection shows 1-2g/day

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181
Q

what streptozyme tests are elevated in throat infections (looking at poststreptococcal glomerulonephritis)

which 2 out of those are for the skin

A

Antistreptolysin-O

Anti-Hyaluronidase (for both)

Anti-nicotinamide adenine dinucleotidase (ANTI-NAD)

Anti-DNAse B Antibodies (for both)

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182
Q

serum C3 and C4 can be high or low in nephritic syndromes

A

low

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183
Q

symptoms of IgA nephropathy

A

gross hematuria
flank pain
in someone who has a URI

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184
Q

Henoch-Schonlein Purpura nephritis is AKA

A

IgA vasculitis

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185
Q

in IgA vasculitis what does the CBC , PT, PTT look like

A

normal - rules out thrombocytopenia and coagulopathies

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186
Q

isolated hematuria
nephritic syndrome
plus systemic symptoms like symmetrical rashes, palpable purpura, migratory arthritis, GI symptoms (n/v/abd pain)

think

A

IgA vasculitis (Henoch-schonlein purpura nephritis)

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187
Q

what is diagnostic for IgA vasculitis

A

skin biopsy showing leukocytoclastic vasculitis and IgA deposition

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188
Q

what is alport sydnrome

A

isolated persistent hematuria

genetic condition seen in children that can lead to renal failure and hearing loss

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189
Q

eye exam finding seen in alport syndrome

A

anterior lenticonus

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190
Q

you suspect alport syndrome

C3 and C4 levels are low

ANA antibodies are seen or not seen

what is done to confirm the diagnosis

A

kidney biopsy

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191
Q

you suspect alport syndrome

C3 and C4 levels are normal

ANA antibodies are negative

what is done to confirm the diagnosis

A

genetic testing

a kidney biopsy can also be done

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192
Q

symptoms of SLE (lupus)

A 
migratory polyarticular arthritis
arthralgias
butterfly rash
delirium 
psychosis
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193
Q

edema occurs when the plasma oncotic pressure _____ due to ______________, causing ___________ which ______

A

drops due to the loss of circulating albumin, causing fluid to shift into the interstitial space

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194
Q

edema occurs when the plasma oncotic pressure _____ due to ______________, causing ___________ which ______

(nephrotic syndrome)

A

drops due to the loss of circulating albumin, causing fluid to shift into the interstitial space which further depletes the intravascular volume leading to renal hypoperfusion and stimulates the Renin-angiotensin-aldosterone cycle to retain more sodium and thus more water

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195
Q

In nephrotic syndrome, in addition to abnormal water excretion, there is an increased level of _____ that also contributes to water retention

A

vasopressin

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196
Q

what causes hyperlipidemia in nephrotic syndrome

A

increased synthesis of lipoproteins in the liver in response to intravascular protein loss

and

decreased lipid catabolism in response to a loss of lipoprotein lipase (enzyme necessary for lipid breakdown)

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197
Q

if nephrotic syndrome presents within the first 3 months of life, it is caused by _________, and requires ______

A

specific genetic defects

kidney transplantation

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198
Q

nephrotic syndrome that presents within months 4-12 of life is considered

A

infantile nephrotic syndrome

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199
Q

Nephrotic syndrome that presents after 1 year is considered

A

childhood nephrotic syndrome

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200
Q

childhood nephrotic syndrome most common between _ and _ years

A

2-8

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201
Q

what special populations/gender/age are most likely to get nephrotic syndrome

A

children

males

Asian, arabian, indian and african american have a higher incidence of idiopathic NS than children of european descent

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202
Q

what races have a higher risk of steroid resistant Nephrotic syndrome and FSGS

A

African American

Hispanic

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203
Q

due to low serum albumin, ascites, impaired immune system, patients with nephrotic syndrome are at higher risk of

what are the symptoms

associated pathogens

A

spontaneous bacterial peritonitis

fever
severe abd pain
peritoneal signs
possible sepsis

streptococcus pneumoniae

gram negative organisms

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204
Q

in nephrotic syndrome a renal biopsy is recommended for children ages ____ and older because ____

A

12 and older
they are more likely to have a diagnosis of FSGS rather than MCNS which puts them at higher risk for progressive kidney failure

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205
Q

nephrotic syndrome relapse is defined as

A

a recurrence of urine Pr/Cr ratio >= 2 or urine protein >= 2 for 3-5 consecutive days after initial remission

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206
Q

frequently relapsing nephrotic syndrome is defined as

A

2 or more relapses within the first 6 months of initial treatment or 4 or more relapses in a 12 month period.

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207
Q

teaching that goes with nephrotic syndrome

A

monitoring proteinuria at home with urine dipsticks

common childhood illnesses and infections can trigger a relapse such as otitis media and sinusitis

immunizations esp yearly flu and pneumococcal vaccines are very important to prevent bacterial peritonitis

No live viral vaccines while on steroid therapy

side effects of long term steroid use - appetite stimulation, bone demineralization, cushingoid appearance, mood changes, decreased immune function, growth retardation, night sweats, HTN, cataracts
rare side effects - pseudotumor cerebri, depression, steroid psychosis, steroid-induced diabetes

importance of tapering steroid use after extended therapy

maintain physical activity and avoid bed rest to prevent blood clot formation (risk of DVT, renal vein thrombosis, pulmonary embolism)

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208
Q

risks associated with nephrotic syndrome (complications)

A

obesity

delayed bone growth

dyslipidemia ->increased risk of cardiovascular disease

higher risk of infections

thromboembolism ( loss of antithrombin III factor in the urine, increased fibrinogen, platelet hyperaggregability from volume depletion)

osteoporosis

HTN

decreased visual acuity from cataracts and myopia

males treated with immunosuppressive therapy are at risk for decreased sperm count and motility

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209
Q

what forms of nephrotic syndrome are the most severe

A

SRNS (steroid resistant nephrotic syndrome)

FSGS (focal segmental glomerulosclerosis)

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210
Q

children with biopsy proven ___ nephrotic syndrome have a 25% chance of relapse after puberty

A

MCNS (minimal change nephrotic syndrome)

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211
Q

what is the most common form of acute glomerulonephritis (GN)

A

poststreptococcal glomerulonephritis (PSGN)

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212
Q

what is the most common form of chronic glomerulonephritis (GN)

A

immunoglobulin (Ig)A nephropathy

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213
Q

most common identifiable lower urinary tract causes of hematuria include

A

UTI
kidney stones
hypercalciuria

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214
Q

which type of GN occurs most frequently in children 2-12 years of age and is more common in boys. manifestations are typical of acute GN and develop 5-21 days (average 10 days) after ______ infection or 4-6 weeks after _____

A

poststreptococcal glomerulonephritis (PSGN)

streptococcal pharyngitis (GAS)

impetigo

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215
Q

In PSGN, pay close attention to ______ because it can become severe enough to cause _____ ____, ____

A

blood pressure

heart failure

seizures

encephalopathy

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216
Q

asymptomatic microscopic hematuria or recurrent gross hematuria

concurrent with a URI

A

IgA nephropathy

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217
Q

typical features of acute GN where renal insufficiency progresses more quickly and severely.

renal biopsy shows glomerular epithelial cell proliferation with crescents

A

rapidly progressive glomerulonephritis (RPGN)

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218
Q

early recognition of RPGN is crucial to prevent

A

progression to ESRD that occurs without prompt treatment

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219
Q

typically caused by x linked chromosome mutations but also has been associated with mutations of genes for type IV collagen, both leading to abnormal glomerular basement membrane (GBM).

may present with microscopic or gross hematuria

males typically develop progressive renal failure and sensorineural hearing loss during adolescence and young adulthood

females typically have a more benign course but usually have at least microscopic hematuria

A

alport syndrome

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220
Q

caused by mutations leading to isolated glomerular basement membrane thinning

these mutations are often autosomal dominant with hematuria frequently noted in first degree relatives

typically not progressive and usually has an excellent prognosis

A

thin basement membrane disease

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221
Q

painless gross hematuria may be seen in

A

strenuous exercise

sickle cell trait/disease

Wilms tumor

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222
Q

hematuria may be associated with pain when due to bleeding from ____ or ____

A

renal cysts

nutcracker syndrome (renal vein compression)

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223
Q

Gross hematuria following trauma may signify more

A

severe renal or lower urinary tract injury

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224
Q

associated with dysuria and urinary frequency

A

UTI

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225
Q

may be associated with asymptomatic hematuria or with flank or abd pain

A

urolithiasis

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226
Q

can cause both gross and microscopic hematuria and may be associated with urinary tract symptoms such as dysuria and urinary frequency or may be asymptomatic

A

Hyperalciuria

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227
Q

all patients with hematuria should have

A

careful history

physical including BP

urinalysis including microscopic evaluation to identify RBCs

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228
Q

glomerular hematuria is suggested by

A

brownish (tea or cola colored) urine and presence of RBC casts and/or dysmorphic RBCs on urine microsopy

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229
Q

a urine color that is more bright red without RBC casts or dysmorphic RBCs is more suggestive of

A

lower urinary tract source

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230
Q

presence of low C3 complement narrows the differential diagnosis to

A

PSGN

membranoproliferative GN

lupus nephritis

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231
Q

children with isolated, asymptomatic microscopic hematuria may be observed with

A

repeat urinalyses - if persistent, additional evaluation may be appropriate

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232
Q

microscopic hematuria may persist for ____ after resolution of PSGN

A

for months or even years

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233
Q

children with IgA nephropathy and other forms of chronic Gn have greater risk of progression to

A

ESRD

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234
Q

the presence of persistent, heavy proteinuria, HTN, decreased kidney function and severe glomerular lesions on biopsy is associated with

A

poor outcomes

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235
Q

long term follow up for idiopathic isolated asymptomatic microscopic hematuria or suspected thin basement membrane disease

A

yearly urinalysis to r/o proteinuria and blood measurement to exclude progressive forms of renal disease

excellent prognosis

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236
Q

Lupus Nephritis has ___ stages determined by a _____

A

6

kidney biopsy

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237
Q

if pt presents with red urine/hematuria

cause not apparent on H&P

urinalysis negative for blood

A

urate crystals in infants

from medications, foods, dyes

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238
Q

if pt presents with red urine/hematuria

cause not apparent on H&P

urinalysis positive for blood

what should be ordered next

A

order urine microscopy

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239
Q

if pt presents with red urine/hematuria

cause not apparent on H&P

urinalysis positive for blood

urine microscopy

RBCs confirmed

they are asymptomatic

what is it?

what is the follow up?

what should be done if hematuria persists

A

isolated microscopic hematuria

repeat urinalysis x 2 at least one week apart

if symptoms persist…consider

urine calcium to creatinine ratios

test first degree relatives for hematuria

Hgb electrophoresis to r/o sickle cell

serum chemistries

renal us

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240
Q

if pt presents with red urine/hematuria

cause not apparent on H&P

urinalysis positive for blood

urine microscopy

RBCs confirmed

they are symptomatic (symptomatic microscopic hematuria or gross hematuria)

what orders should come next?

A

urine culture

urine calcium to creatinine ratio

urine protein to creatinine ratio

serum chemistries

serum albumin

C3 and C4 complement

CBC

renal US

Renal biopsy in selected cases

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241
Q

HTN is a red flag in the presence of hematuria that the etiology might be ____ in origin

A

renal

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242
Q

Growth retardation or recent rapid weight gain in the presence of hematuria can be signs of

A

kidney disease

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243
Q

If urine is positive for RBCs , RBC casts and proteinuria and there is a history of edema and hypertension, then what labs would you order to further evaluate kidney function

A 
electrolytes
bicarbonate
BUN
Creatinine
glucose
total and ionized calcium
albumin
phosphorous
eGFR
CBC and diff
protein-creatinine ratio
complement C3 &C4
Antistreptolysin O titer
244
Q

hypocalcemia is usually r/t ________ and amenable with _____ and ______

A

hyperphosphatemia

Vit D

phosphate binders

245
Q

an abrupt cessation or significant decline in the kidney’s ability to eliminate waste products, regulate acid - base balance, and regulate electrolyte balance

A

acute renal failure

246
Q

sudden sustained decrease in the GFR occuring over a period of hours to days

A

AKI

247
Q

acute renal failure and AKI

A

term used changed from acute renal failure to AKI

248
Q

what criterion was the first step towards defining AKI

A

Rifle Criteria

249
Q

KDIGO AKI defininition

A

increase in SCr by >0.3 mg/dl within 48 hours
or
increase in SCr to x 1.5 times baseline within the prior 7 days
or
urine volume <0.5ml/kg/h for 6 hours

250
Q

Evaluation of AKI

A

medication history looking for nephrotoxic agents

vital signs

Fluid balance - urine output

serum electrolytes and CBC

consider hepatic panel if concern for hepatorenal syndrome

chest x ray if resp symptoms

251
Q

KDIGO-AKI staging

Stage 1

A

Serum creatinine
1.5-1.9 times baseline
>0.3 mg/dl (>26.5mmol/l) increase

and/or

urine output
<0.5ml/hg/h for 6-12 hours

252
Q

KDIGO - AKI staging

stage 2

A

Serum creatinine 2.0-2.9 times baseline

and/or

urine output <0.5ml/kg/h for 12 hours

253
Q

KDIGO AKI staging

stage 3

A

SCr 3 times baseline

increase in Serum creatinine to >4.0mg/dl

initiation of renal replacement therapy

<18 yrs - decrease in eGFR to <35ml/min per 1.73m2

and/or

urine output
<0.3ml/kg/h x 24 hours
anuria for x 12 hours

254
Q

management of AKI

A

judicious fluid mgmt to restore intravascular volume or diuresis depending on clinical status (urine output replacement and calculated insensible losses may be warranted)

treat electrolyte imbalances

treat HTN

renal support if indicated

adjust meds that are excreted renally

255
Q

what calculation can you use to guide fluid management

A

calculation of fractional excretion of sodium

256
Q

prerenal kidney disease causes of acute renal failure in children

A

dehydration/depleted intravascular volume

distributive volume issues/decreased effective intravascular volume

257
Q

intrinsic kidney disease causes of acute renal failure in children

A

acute tubular necrosis

ischemia/hypoxia in kidneys

medication/drug-induced

infection (HUS, PSGN)

INterstitial nephritis

GN

renal artery or venous thrombosis

endogenous toxins (myoglobin)

exogenous toxins (methanol, ethylene glycol)

idiopathic

258
Q

obstructive uropathy causes of acute renal failure in children

A

bilat ureteral obstruction

kidney obstruction

259
Q

specific genetic conditions associated with acute renal failure

A

polycystic kidney disease

alport syndrome

nephrotic syndrome (focal segmental glomerulosclerosis, membranoproliferative GN)

SLE

Diabetes

260
Q

presenting symptoms of acute renal failure

A

oliguria/anuria

edema

electrolyte abnormalities

decreased appetite

nausea

fatigue

SOB

HTN

confusion

261
Q

Hyponatremia is common in acute renal failure, what are you at risk for at what level

how do you treat?

A

risk for seizure activity if serum sodium is <125mEq/L. Treat with hypertonic saline (ie) 3% saline)

262
Q

Hyperkalemia EKG findings

A

peaked T waves

prolongation of PR interval

widening of QRS complex

flattening of P waves

263
Q

what can be used to shift potassium into cells to avoid ventricular tachycardia/fibrillation

A

glucose

sodium bicarbonate

insulin

albuterol

264
Q

what med can stabilize the cardiac cell membrane in the presence of hyperkalemia setting of acute renal failure

A

calcium chloride

265
Q

what med can exchange potassium and sodium in the colon in the presence of hyperkalemia setting of acute renal failure

A

sodium polystyrene

266
Q

emergent dialysis is often indicated for serum potassium levels

A

> 7mEq/L

267
Q

HTN therapy in acute renal failure

A

avoid ACE inhibitors. Goal is normal blood pressure for gender and height

268
Q

name some nephrotoxic medications

A 
aminoglycosides
Vancomycin
Bactrim
Zosyn
anticholinergics
amphotericin
immunosuppressive agents
chemo
NSAIDS
RAAS blockers (ACE ARB)
IV contrast
Diuretics
269
Q

PMH r/t AKI focusted history

A 
Heart disease
liver disease
oncologic disease
BMT
spinal cord injury
recent surgery
CKD
Previous AKI episodes 
Previous kidney stones
270
Q

HPI specific to kidney

A

change in urination pattern-frequency

urgency

stream

drippling

feeling incomplete emptying

dysuria

flank pain

271
Q

HPI specific to AKI

A 
recent illnesses 
n/v/d
oral intake
fever
UOP
rashes
hemodynamic changes
weight gain
edema
272
Q

AKI workup (from lecture)

A

urinalysis

urine protein/creatinine ratio

urine myoglobin/hemoglobin

Fe (fractional excretion) of Na, FeUrea (Diuretic)

CPK, uric acid, free hemoglobin

Urine microscopy: muddy brown casts in ATN, RBC casts in AGN

Renal US

Bladder Catheterization

Bladder pressure

273
Q

completely filtered at the glomerulus, taken up and metabolized by proximal convoluted tubule

filtration marker

no affected by muscle mass, age or hydration status

used in critically ill patients to predict AKI development

used for CF patients to predict aminoglycoside associated nephrotoxic AKI

A

Cystatin C

274
Q

used for CF patients to predict aminoglycoside associated nephrotoxic AKI

A

Cystatin C

275
Q

Peritoneal dialysis uses ______ ____ solution to infuse into the peritoneal cavity to facilitate the removal of _____, _____ and ________.

A

hyperosmolar dialysate solution

electrolytes
toxins
free water

276
Q

Peritoneal dialysis uses the peritoneal space as the

A

semipermeable membrane filter

277
Q

solutes move from the intravascular space into the peritoneal space over a prescribed period of time referred to as the _____ ______ and then are passibley drained into an external drainage collection system

A

dwell time

278
Q

percutaneous or surgically inserted flexible single-lumen catheter allows for peritoneal dialysis fluid into the peritoneal space, dwells for a prescribed period of time and then drains into an external collection bag

A

Tenckhoff catheter

279
Q

for the Tenckhoff catheter healing takes approximately

A

2 weeks

280
Q

Typical volumes for a Tenckhoff catheter of __________may be used immediately after insertion; after peritoneal lining is healed, _________ may be used

A

10mL/kg/cycle

20-40 mL/kg/cycle

281
Q

2 settings on the cycler machines for peritoneal dialysis

A

CCPD - continuous cycling peritoneal dialysis via machine

CAPD - continuous ambulatory peritoneal dialysis

282
Q

which setting for cycler machine used in peritoneal dialysis is used to maximize fluid and toxin removal

A

CAPD - continuous ambulatory peritoneal dialysis

283
Q

which setting for cycler machine used in peritoneal dialysis is used in either Nighttime-only therapy or nighttime and periodic day treatment

A

CCPD - continuous cycling peritoneal dialysis via machine

284
Q

how many cycles with what dwell time for CCPD

A

8-10 cycles with dwell times of 30 - 45 minutes

285
Q

what are the types of peritoneal dialysis fluid

A

1.5%
2.5%
4.25%
glucose solutions

286
Q

dialysis fluid is _______ to serum and contains a high concentration of ______

A

hyperosmolar

carbohydrates

287
Q

peritoneal dialysis promotes _______

A

ultrafiltration

288
Q

higher the percentage of carbohydrate solution, greater the volume of

A

fluid removed

289
Q

benefits of peritoneal dialysis

A

fluid removal
urea, creatinine and potassium clearance

clearance of toxins

treatment may be provided at home, outpatient or inpatient

may be used in neonates and infants

290
Q

complications of peritoneal dialysis

A

abd discomfort

peritonitis

electrolyte imbalance, hyperglycemia, protein loss

inguinal/abd hernia

resp compromise

long term peritoneal fibrotic tissue may limit functional dialysis

Peritoneum may lose its selectivity over time (decreased clearance, increased proteinemia)

contraindicated in patients with significant abd pathology

291
Q

in peritoneal dialysis when should the pt be weighed

A

prior to and immediately after therapy

292
Q

Peritoneal dialysis must end with _____ cycle

A

drain cycle

293
Q

For a pt who is on peritoneal dialysis, what should you monitor

A

fluid
electrolytes
hemodynamic status

294
Q

for peritoneal dialysis access the peritoneal catheter using ____ or ___ technique

A

aseptic

sterile

295
Q

for peritoneal dialysis monitor for _____

A

sepsis

296
Q

may treat peritonitis for someone who receives peritoneal dialysis

A

by adding abx to dialysis fluid

297
Q

kidney biopsy is most commonly performed _______; needle inserted through ____, through _____ and into _____

A

percutaneously
skin
tissue
kidney

298
Q

kidney biopsy may be performed ____ using_____ or with the assistance of

A

blindly
landmarks
imaging guidance using ultrasound, CT or fluoroscopy

occasionally through an open procedure

299
Q

contraindications to a kidney biopsy

A

coagulation disorders with increased risk of procedural bleeding

operative kidney tumors (could spread the malignant cells)

hydronephrosis - risk of perforating large renal pelvis r/i urine leak requiring surgical repair

UTI: risk of spreading infection

300
Q

Potential complications of kidney biopsy

A

hemorrhage - kidney is highly vascular

unintended puncture of surrounding organ (liver, lung, bowel, inferior vena cava)

301
Q

Preop for kidney biopsy

A 
NPO
coag studies
CBC
type and cross/type and screen
Sedation may not be required in older cooperative children
302
Q

postop kidney biopsy

A

pressure over puncture site for 20 min followed by a pressure dressing

limited movement/activity for 24 hours after procedure

monitor for signs of hemorrhage

evaluate abd for signs of hemorrhage or bowel perforation

303
Q

indications for kidney transplant

A

irreversible kidney failure

most common etiologies are congenital, urologic and inherited disorders

304
Q

evaluation for kidney transplant begin when the estimated creatinine clearance is

A

<60 mL/min/1.73m2

305
Q

if circumstances allow ________ prior to dialysis requirement is ideal to avoid associated morbidities

A

transplantation

306
Q

contraindications to kidney transplant

A

malignancy

chronic illness with shortened life expectancy

severe brain damage

inability to improve quality of life

307
Q

evaluation of someone looking at kidney transplant

A

diagnosis of kidney failure or ESRD and eval for multisystem involvement

  • Lab sampling
  • Anti-human leukocyte antigen antibodies and panel-reactive antibodies: evaluated for sensitization to determine which donor antigens should be avoided to prevent rejection
  • Radiologic eval
  • US - look for urinary tract abnormalities
  • Echocardiogram
  • electrocardiogram

invasive studies

  • cardiac cath in select patients
  • angiogram in select patients

discussion of prognosis and appropriateness of transplantation

Psychosocial eval - ability to adhere to posttransplant therapies and f/u appts, readiness, religious or cultural beliefs that may impact transplant, resources, barriers

308
Q

what lab is used to evaluated for sensitization to determine which donor antigens should be avoided to prevent rejection

A

Anti-human leukocyte antigen antibodies and panel-reactive antibodies

309
Q

what type of donors are preferred in kidney transplant and why

A

live - improved graft survival unless high suspicion of recurrent disease

310
Q

when a live donor is used for kidney transplant focus on

A

overall donor health
must be>=18 years of age unless an identical twin
may be exceptions with the evaluation by an ethics team

311
Q

Preparing for tranplantation

A

achieve optimal physical and mental health state prior to transplant with financial planning

312
Q

living donor eval

A

preliminary labs for
blood type
human leukocyte antigen typing, crossmatch

referral to unbiased physician

313
Q

Posttranplant care

A

maintenance immunosuppression

calcineurin inhibitor, usually in conjunction with a second agent such as an antiproliferative agent (mycophenolate mofetil) or mTOR inhibitor (rapamune)

314
Q

Calcineurin inhibitors (mycophenolate mofetil) are

A

nephrotoxic

levels require monitoring

315
Q

Cadaveric kidney differences

A

graft function - poor initial graft function is more common - can indicate acute tubular necrosis

dialysis may be required in the first few weeks after transplant; typically only temp

starting of immunosuppression often differs between living and cadaveric donors

316
Q

common kidney rejection signs and symptoms

A 
HTN
fever
proteinuria
oliguria
graft nonfunction

must always be on your differential list of transplant patients

317
Q

definitive diagnosis of kidney rejection is

A

biopsy

318
Q

type of rejection that occurs minutes to hours after transplant

A

hyperacute

319
Q

type of rejection that occurs 3-90 days post tranplant

A

acute

320
Q

type of rejection that occurs >60 post tranplant

A

chronic

321
Q

Posttranplant infection

fever days after transplant think

A

atelectasis

322
Q

posttransplant infection

fever
weeks after transplant think

A

foreign objects

323
Q

posttransplant infection

fever
2-6 weeks post transplant think

A

fungal

324
Q

posttransplant infection

fever
6-8 weeks post transplant think

A

viral

325
Q

signs and symptoms of post-transplant infection these 2 staples then varies

A

fever

elevated WBC

326
Q

when you think post-transplant infection

think ____ vs ____ vs _____

A

primary
reactivation
reinfection

327
Q

result of an inherited or acquired defect that affects the kidneys ability to filter bicarbonate or excrete ammonia

A

renal tubular acidosis

328
Q

can be a genetic cause of renal tubular acidosis

A

Sickle cell anemia

329
Q

Acquired cases of renal tubular acidosis

A

certain medications
obstructive uropathy
autoimmune diseases

330
Q

often associated with presence of UTI

A

renal tubular acidosis

331
Q

relatively uncommon clinical syndrome characterized by defects in the renal tubules as a result of failure to maintain a normal serum bicarbonate level despite the consumption of a regular diet and normal metabolism and acid production

A

renal tubular acidosis

332
Q

in renal tubular acidosis the defects in renal tubules lead to a ______ __________ __________ with a normal to moderately decreased GFR and normal anion gap

A

hyperchloremic metabolic acidosis

333
Q

decrease in acid excretion

A

Type I RTA (distal)

334
Q

failure of bicarbonate reabsorption with decreased ammonium absorption

A

Type II RTA (proximal)

335
Q

Aldosterone deficiency or impairment of its effects, resulting in reduced potassium excretion, hyperkalemia and acidosis

A

Type IV RTA

336
Q

what types of renal tubular acidosis are most common in children

A

types I and II

337
Q

clinical presentation of renal tubular acidosis

A

Polyuria

polydipsia

preference of savory foods

hypokalemia

refractory rickets

metabolic acidosis

338
Q

RTA that is linked to multiple genetic disorders (sensorineural hearing loss and nephrocalcinosis); FTT or short stature, anorexia, vomiting, dehydration

A

type I RTA

339
Q

RTA with FTT, hyperchloremic acidosis with hypokalemia
rarely nephrocalcinosis
rickets or osteomalacia may indicate _____ _______

A

Type II RTA

Fanconi Syndrome

340
Q

RTA - HTN common if child has underlying _____ syndrome, renal parenchymal disease or mineralocorticoid dysfunction

A

Type IV RTA

Gordon syndrome

341
Q

RTA type linked to multiple genetic disorders

A

Type I RTA

342
Q

diagnostic evaluation of renal tubular acidosis

A

serum and urine electrolytes

fractional excretion of bicarbonate and urine pH

Urine glucose and protein, calcium-to-creatinine ratio.

24 hour urine sample

radiographies of long bone or wrists for eval of rickets

abd us (kidneys)

genetic or chromosomal eval

343
Q

mgmt of RTA

A

emergent or inpatient mgmt for children with hyperchloremic, non-anion gap acidosis requiring bicarbonate replacement IV

slow rehydration and electrolyte replacement, sodium bicarbonate or citrate, diuretic, phosphate replacement in children with rickets

344
Q

without proper therapy, chronic acidity in the blood results in

A

growth retardation

nephrolithiasis

bone disease

chronic renal failure

345
Q

which type of RTA - a lot of bicarbonate lost through the urinary tract

A

Type II Renal tubular acidosis

346
Q

which type of RTA are too many hydrogen ions retained

A

Type I and IV renal tubular acidosis

347
Q

In Type I RTA, there is a build up of ___ ions in the blood leading to _____ which causes _____ _____. There is an increase of _____ excretion

A

H+
Acidemia
Metabolic acidosis
potassium

348
Q

metabolic acidosis will increase ____ excretion w/o increasing calcium ____

A

urine calcium excretion

calcium absorption

349
Q

which RTA involves osmotic diuresis -> mild hypovolemia -> activates RAAS -> sodium reabsorption and K excretion -> hypokalemia

A

Type II RTA

350
Q

which RTA is r/t a aldosterone deficiency or resistance in the collecting ducts

A

Type IV

351
Q

what is the most common cause of GN in older children and adults

A

Membranoproliferative glomerular nephritis (MPGN)

352
Q

this form of nephritis results in ongoing glomerular injury that leads to glomerular destruction and ESRD

A

Membranoproliferative glomerular nephritis (MPGN)

353
Q

Etiology of Membranoproliferative glomerular nephritis (MPGN)

A

Autoimmune disease (SLE, scleroderma, Sjogren syndrome, sarcoidosis)

malignancy (leukemia, lymphoma)

infectious (hepatitis B, C, endocarditis, malaria)

354
Q

clinical presentation of Membranoproliferative glomerular nephritis (MPGN)

A

nephrotic syndrome

gross hematuria or asymptomatic microscopic hematuria

Proteinuria

Renal function may be normal or decreased

HTN is common

Serum C3 may be low

355
Q

diagnostic eval for Membranoproliferative glomerular nephritis (MPGN)

A

kidney biopsy is gold standard for diagnosis

356
Q

mgmt Membranoproliferative glomerular nephritis (MPGN)

A

systemic steroids for children and antiplatelets for adults

additional therapies include plasmapheresis and plasma infusion

357
Q

an extracorporeal blood purification therapy intended to substitute for impaired renal function over an extended period of time.

A

continuous renal replacement therapy

358
Q

Continuous renal replacement therapy is used to treat

A 
fluid overload
acute renal failure
chronic renal failure
life threatening electrolyte imbalances
intoxications (molecule size dependent)
concomitant sepsis
multiorgan failure
359
Q

continuous renal replacement therapy is used only in what setting?

administered for _____ hours

can be given for how much time?

A

only in critical care setting

administered continuously, 24 hours a day

administered for days or weeks but not a long term therapy

360
Q

what criteria for AKI is used for necessitating use of continuous renal replacement therapy

A

RIFLE

estimated creatinine clearance decreased by 50% urine output <0.5mL/kg/hour x 16 hours

361
Q

In sepsis with hemodynamic instability what is continuous renal replacement therapy used for

A 
cytokine removal
reduces hemodynamic instability
allows precise volume control
toxin removal
effective control of uremia, hypophosphatemia, hyperkalemia
362
Q

in uremia with encephalopathy, how does continuous renal replacement therapy help

A

removal of urea and toxins

363
Q

what criteria for Acute renal failure is used for necessitating the use of continuous renal replacement therapy

A

RIFLE

estimated creatinine clearance by 75% or urine output <0.3ml/kg/hour for 24 hours or anuric for 12 hours

364
Q

for continuous renal replacement therapy to be effective in the case of intoxication, the molecular size must be able to

A

be cleared by filter for effective treatment

365
Q

complications of continuous renal replacement therapy

A

hypotension
hypothermia
bleeding
electrolyte imbalance
central line infection (hemodialysis catheter)
venus thrombus
-consider PRBCs transfusion prior to start of continuous renal replacement therapy (CRRT) - esp if <=10kg

Hyperthermia unit may be added to CRRT machine to warm the blood being returned to the pt

366
Q

what placement of the hemodialysis catheter can be temp or permanent?

A

internal jugular

367
Q

what placement of the hemodialysis catheter is temp access only

A

femoral vein

368
Q

during CRRT maintenance of anticoagulation

A

sodium citrate

369
Q

how does sodium citrate work in anticoagulation for CRRT

A

it combines with calcium ion to render clotting factors inactive within the filter

370
Q

how is citrate processed

A

through the liver

371
Q

when using sodium citrate for anticoagulation during CRRT, what must you have continually infusing and why

A

calcium outside of the circuit to maintain normal calcium levels

372
Q

Prior to initiating sodium citrate in the CRRT circuit, the patients ionized calcium should be

A

> =1.1 mmol/L

373
Q

benefits of using sodium citrate

A

minimal bleeding risks

extended filter life

374
Q

risk of using sodium citrate for anticoagulation during CRRT

A

metabolic alkalosis
-citrate is buffered into bicarbonate

citrate lock

  • rising total calcium with dropping ionized calcium
  • delivery of citrate exceeds hepatic metabolism and CRRT clearance

hypocalcemia
hypernatremia
hyperglycemia
-monitor CRRT ionized calcium levels, serum ionized and total calcium, sodium and glucose levels

375
Q

treatment for metabolic alkalosis for someone on CRRT (risk when using sodium citrate for anticoagulation)

A

eliminate acetate and bicarbonate sources

376
Q

treatment for citrate lock during CRRT

A

increase dialysis by 20-30%

decrease or stop citrate for 3-4 hours and restart at 70% of prior rate

377
Q

what levels must be monitored closely during CRRT

A

CRRT ionized calcium levels

serum ionized calcium

serum total calcium

sodium

glucose

378
Q

how does heparin work in anticoagulation for CRRT

A

acts indirectly at multiple sites in both intrinsic and extrinsic coagulation pathways to prolong coagulation

379
Q

goal for heparin in CRRT

A

achieve activated clot time (ACT) 180-220 milliseconds (commonly used to maintain the circuit)

380
Q

benefits for using heparin in CRRT

A

may be used in liver failure

381
Q

risks for using heparin in CRRT

A

bleeding

382
Q

monitoring heparin in CRRT

A

anticoagulation (ACT, protime, prothrombin time)

383
Q

kidney dysfunction results in

A

electrolyte imbalance

anasarca

accumulation of uremic toxins

384
Q

blood and dialysis fluid enter hemodialysis filter in a _____ approach which does what??

A

countercurrent

maximizes the concentration gradient between the blood and dialysis fluid

385
Q

typically hemodialysis will run for __- __ hours each session

A

3-4

386
Q

indications for hemodialysis

A

hypervolemia: resp compromise, heart failure, HTN, hyponatremia and/or anasarca

electrolyte abnormalities: Hyperkalemia, hyperphosphatemia, hypocalcemia
and/or acidosis

symptomatic azotemia or uremia: confusion, bradycardia, platelet dysfunction, pericardial effusion

asymptomatic azotemia or uremia (ie-acute or chronic renal failure)

toxicity of non-protein bound medications, poisons or ammonia

malnutrition: decreased intake due to volume restriction, increased metabolic demands, catabolic metabolism or malabsorption

387
Q

placement options for hemodialysis catheter

A

short term

tunneled (internal jugular or superior vena cava)

arteriovenous fistula or graft - internal vascular access surgical connection joining an artery and a vein for hemodialysis use

388
Q

Blood flow rate and dialysis rate for hemodialysis treatment

A

150-350mL/min

500mL/hour

389
Q

Hemodialysis treatment requires at least a __Fr catheter to allow appropriate flood flow rate

A

7

390
Q

ideally a pt receiving hemodialysis weighs more than

A

10kg

391
Q

hemodynamic stability is optional or required prior to initiation of hemodialysis treatment

A

required

392
Q

Hemodialysis can be done where and by who

A

inpatient (acute or critical care) or outpatient facility by a hemodialysis technician

393
Q

benefits of hemodialysis

A 
fluid removal
urea
creatinine
potassium
toxin clearance
394
Q

complications of hemodialysis

A

disequilibrium syndrome

hypotension

bleeding

electrolyte imbalance

catheter infection

vessel thrombosis

baroreceptor dysfunction

395
Q

what is disequilibrium syndrome

A

dialysis induced cerebral edema

396
Q

symptoms of disequilibrium syndrome

A

nausea
headache
confusion
seizures

in someone who is receiving dialysis

397
Q

treatment for disequilibrium syndrome

A

mannitol infusion (poorly cleared by dialysis) and short session with low blood flow rate without ultrafiltration

398
Q

why is hypotension a potential complication of hemodialysis

A

caused by rapid removal of fluid from intravascular space

399
Q

symptoms of hypotension listed for hemodialysis prior to the hypotension

A

tachycardia

nausea

crampy abd pain

emesis

400
Q

treatment for hypotension with hemodialysis

A

small fluid boluses

decrease in ultrafiltration

if shock occurs, treat with fluid and discontinue dialysis

401
Q

how do you monitor for electrolyte imbalances for hemodialysis

A

pre- and post dialysis weights

fluid, electrolyte and hemodynamic monitoring

402
Q

how do you prevent vessel thrombosis for hemodialysis pt

A

heparinize catheter after use

403
Q

symptoms of baroreceptor dysfunction

A

this may happen with chronic renal failure

bradycardia

404
Q

treatment for baroreceptor dysfunction in hemodialysis pt

A

atropine
or

epinephrine

to restore perfusion

405
Q

when kidneys have sustained damage in structure or function for over 3 months, this is referred to as

A

chronic kidney disease

406
Q

causes of CKD are divided into 3 categories

A

Prerenal

intrarenal

postrenal

407
Q

prerenal cause of CKD is due to?

what are 2 examples

A

decrease in renal perfusion

heart failure
cirrhosis

408
Q

Intrarenal cause of CKD

A

renal vascular disease

  • HTN
  • Renal artery stenosis

Glomerular disease

  • Nephritic disease
  • nephrotic disease

Tubulointerstitial disease
-polycystic kidney disease

nephrotoxic substances

409
Q

Postrenal cause of CKD

A

prostatic disease

repeated episodes of pyelonephritis

410
Q

stages of CKD based on GFR

A 
Stage 1 (G1) - >=90 mL/min/1.73m2 
(underlying kidney disease)
Stage 2 (G2) - 60-89 mL/min/1.73m2 
(mildly decreased)

Stage 3a(G3a) - 45-59
mL/min/1.73m2
(mild-moderately decreased)

Stage 3b (G3b) - 30-44
mL/min/1.73m2
(moderately-severely decreased)

Stage 4(G4) - 15-29
mL/min/1.73m2
(severely decreased)

Stage 5 (G5) - <15
mL/min/1.73m2
ESRD

if on dialysis its staged as G5D

411
Q

what is referred to as G stages

A

eGFR for staging of chronic kidney disease

412
Q

CKD can cause anemia, why

A

kidney not making enough erythropoietin

hemodialysis - regular blood loss

prone to iron deficiency anemia

  • diet low in iron
  • blood loss
  • impaired absorption of iron
413
Q

CKD can cause mineral and bone disorder (CKD-MBD)

tell me about it

A

hyperphosphatemia

hypocalcemia

skeletal abnormalities

extra -skeletal calcifications such as coronary artery calcifications

kidneys cannot excrete the phosphate so this leads to hyperphosphatemia and improper conversion of 25-hydroxyvitamin D to activate calcitriol (active version of vit D) -> leads to hypocalcemia ->

hyperphosphatemia + hypocalcemia = increased levels of parathyroid hormone (leads to secondary - as these increase more (hypertrophied parathyroid) this can lead to hypercalcemia

414
Q

hyperkalemia symptoms

A

palpitations
paresthesias
muscle weakness

415
Q

medications listed in book to cause AKI

A

prostaglandin synthetase inhibitors (naproxen, ibuprofen, mefenamic acid, indomethacin)

ACE inhibitors (-pril)

Cyclosporin A (immunosuppressive drug)

Diuretics

another found in video
aminoglycosides (-mycin)

416
Q

leading causes of anemia in CKD

A

iron deficiency

Erythropoietin (EPO) defieciencies

417
Q

what type of failure is most common cause of AKI

A

prerenal failure

(book lists the following as prerenal causes of AKI)
gastroenteritis
gastrointestinal damage
DKA
hypoproteinemia
hemorrhage
third space losses

peripheral vasodilation
impaired cardiac output
bilat renal vessel occlusion

418
Q

medications that can be used to reduce serum potassium level or stabilize the cardiac membrane

A

sodium bicarb

albuterol

glucose

insulin

all of the above work by shifting potassium into cell

sodium polystyrene exchanges sodium for potassium in the colonic mucosa

419
Q

emergency dialysis is needed if serum potassium level is above ____ with ____

A

6-7 mEq/L with tall peaked T waves, prolongation of PR interval, flattening of P waves or widening of the QRS complex on ECG

420
Q

continued hyperkalemia will result in

A

ventricular tachycardia

ventricular fibrillation

421
Q

chronic metabolic acidosis which is a bicarb level of

A

22
bicarbonate
acids

422
Q

In CKD, metabolic acidosis contributes to bone disease by

acidosis also causes a resistance to ____ hormone and _____ factors

A

releasing calcium in an attempt to buffer the acidosis

growth
insulin - like growth

423
Q

____ and _____ intake should be limited in kidney insufficiency. Special formulas with low _____ and ____ can help with nutrition mgmt in infants.

A

potassium
phosphorous

potassium
phosphorous

424
Q

what factors affect growth in children with CKD

A

malnutrition

persistent metabolic acidosis

end organ growth hormone resistance

renal bone disease

even with correction of malnutrition and acidosis children with CKD grow poorly

425
Q

optimizing ____ and managing ____ abnormalities in early childhood allows for the greatest linear growth when supplementing with recombinant growth hormone.

A

nutrition

metabolic

426
Q

pediatric patients with CKD and HTN have greater variation in _______ and decreased variation in_______.

A

blood pressure

heart rate

427
Q

recommended cardiovascular management in CKD includes

A

24 hour ambulatory BP measurements

dyslipidemia screening as a part of their cardiovascular risk assessment

RAAS inhibitors for HTN mgmnt

428
Q

In G3 CBC is checked to look for

A

normocytic anemia

normochromic anemia

429
Q

the lack of EPO is a reflection of

A

dysfunctional kidney and poor GFR

430
Q

what is a good indicator of iron stores

A

calculating the serum transferrin saturation

divide serum iron by total iron binding capacity and multiply by 100

431
Q

labs for iron deficiency

A

serum iron (low)
TIBC (high)
ferritin (low)

432
Q

to evaluate CKD-MBD what levels are checked

A

phosphate
calcium
PTH
vit D

433
Q

At stage 3 what do the following levels look like

A

Phosphate and calcium remain normal

high PTH
low vit D

434
Q

at what G level do you start to see hyperphosphatemia and hypocalcemia

A

G4

435
Q

US used in CKD - what do they US and what are they looking for

A

abd US to check size of kidneys and look for signs of hydronephrosis

Parathyroid US to look for large parathyroid

436
Q

anemia for CKD

elemental iron replacement should be delivered

A

2-3mg/kg (up to 6mg/kg) with the ferritin level at least 100ng/mL and a transferrin saturation of 20%

437
Q

dont give iron with _____ due to decreases gi aborption

A

calcium binders

438
Q

Recombinant EPO should be started at -___-____ units/kg weekly by subcutaneous or IV injection adjusted to reach a desired hgb level of 11-12 gm/dL

A

80-120

439
Q

The correction of anemia has been associated with

A

better exercise tolerance

physical performance

school attendance

improved quality of life

440
Q

caloric intake to slow progression of renal disease

A

30-35kCal/kg/day

this is to help manage body weight

441
Q

protein restriction for an CKD pt who is not on dialysis

A

0.8g/kg/day

442
Q

CKD with HTN/volume overload

sodium restriction

A

2g/day (roughly 1/3 of a tablespoon of salt daily)

443
Q

calcium intake to prevent tissue deposition should be

A

<1g/day

444
Q

if the eGFR < 30mL/min/1.732 then the max potassium intake is

A

4g/day

445
Q

at what G stage should the pt be on a statin

A

G3

446
Q

pediatric hypertension is defined as

A

systolic or diastolic BP measurement exceeding the 95% percentile for gender age and height on 3 occasions

447
Q

book for children 1-12

normal BP

A

<90th percentile

448
Q

book for children 1-12

elevated BP

A

BP>=90th percentile to <95th percentile or 120/80 to <95th (whichever is lower)

449
Q

book for children 1-12

stage 1 HTN

A

> = 95th percentile to <95th percentile +12mmHg, or 130/80-139/89 (whichever is lower)

450
Q

book for children 1-12

stage 2 HTN

A

> =95th percentile + 12mmHg, or >140/90 (whichever is lower)

451
Q

book for children >= 13

normal BP

A

<120/<80

452
Q

book for children >= 13

elevated BP

A

120/<80 - 129/<80

453
Q

book for children >= 13

Stage 1 HTN

A

130/80 - 139/89

454
Q

book for children >= 13

Stage 2 HTN

A

> = 140/90

455
Q

if the initial bp measurement is >=90% what should you do?

A

auscultatory bp should be measured 2 additional times at the same visit and the average of the 2 readings should be used to categorize the BP

456
Q

Patients with elevated BP should have theri BP rechecked by auscultation every ___ months for ___ yr(s)

A

6 months

1 year

457
Q

Stage 1 HTN is re-evaluated on repeated visits on ??? to confirm

A

1-2 weeks after initial check and then again 3 months later to confirm

if elevated still -> further eval and/or referral to specialist is warranted

458
Q

Stage 2 HTN should have a repeat bp measurement within _____ and be referred for further eval if their bp remains within stage 2 criteria

A

1 week

459
Q

determinants of BP

A

cardiac output

peripheral vascular resistance

460
Q

the most common type of HTN in children and adolescents in the US

A

primary HTN

461
Q

what can you take iron supplements with in improve absorption

A

orange juice

462
Q

secondary HTN is most commonly seen with

A

kidney disease

463
Q

most common cardiac cause of HTN

A

coarctation of aorta

464
Q

most common endocrine cause of HTN

A

hyperthyroidism

465
Q

genetic disorders associated with HTN

A

Liddle syndrome

Gordon syndrome

466
Q

neoplasms associated with HTN

A

Wilms tumor

pheochromocytoma

467
Q

neonatal HTN can be due to factors such as

A

umbilical catheter-associated thromboembolism

congenital lesions of the renal vasculature or parenchyma

bronchopulmonary dysplasia

exposure to medications

maternal drug use

468
Q

education for fistula arm

A

should not use for Blood draw

Should not use for BP checks

should not sleep on that arm

should not carry anything >5lbs

469
Q

when should a healthy child over the age of 3 have their bp checked

A

annually

pretty much everyone else is at every visit

470
Q

comorbidities associated with HTN

A

obesity
kidney disease
diabetes
aortic coarctation

471
Q

History that predisposes to HTN

A

prematurity

congenital heart disease

kidney disease

transplant

malignancy

evidence of Intracranial pressure

recurrent UTIs

medications with HTN side effects

472
Q

BP should be measured with an appropriately sized cuff, after ___ min of rest in what position

A

5
seated position with feet resting on the floor and with the R arm supported at the level of the heart and uncovered above the BP cuff

473
Q

what is the preferred device/method for BP measurement

A

auscultation because oscillometric devices use proprietary algorithms to calculate BP from measured MAP and can vary in accuracy

474
Q

Patient history on an H&P for HTN should include

A

gestational age

birth weight

complications for preg, delivery

nutritional

physical activity

psychosocial factors such as anxiety and situational stressors

familial history

475
Q

HTN can be secondary to medications such as

A

steroids

decongestants

oral contraceptives

chronic NSAID use

drug use

caffeine

stimulants

476
Q

what labs should be ordered for all patients with confirmed HTN

A

UA and chemistry panel

477
Q

those less than 6 years old with HTN or have abnormal UA or kidney function should also have a

A

renal US

478
Q

an ____ should be obtained at the time of consideration of pharmacologic therapy for HTN

A

echocardiogram

479
Q

HTN….in addition to the evaluation for underlying causes and end organ damage, evaluation for comorbidities such as _____ and ______ should be considered

A

dyslipidemia

obstructive sleep apnea (OSA) - associated with HTN independent of obesity status

480
Q

other symptoms of Obstructive sleep apnea

A

HTN
snoring
daytime tiredness in older children
hyperactivity in younger children

481
Q

lifestyle changes for HTN

A

weight reduction
regular physical activity
diet modification

482
Q

pharm treatment for HTN is indicated in children with

A

symptomatic HTN

stage 2 HTN without an identified modifiable factor

comorbidities such as DM or CKD

or who remain Hypertensive after a trial of lifestyle modifications

483
Q

Treatment for HTN should be initiated with a ___ at a ___ dose with dose adjustments every __-___ weeks

A

single
low
2-4

484
Q

pharm classes for treating pediatric HTN

A

ACE inhibitor
ARB
Long acting CCB
or Thiazide diuretic

485
Q

what antihypertensives are not recommended as initial treatment in children

A

B blockers

486
Q

____ and _____ are renoprotective and are preferred in pt with HTN and CKD, proteinuria or diabetes unless there is a contraindication (what are those)

(Book)

A

ACE and ARBs

use with caution in children with volume depletion, bilat renal artery stenosis or hyperkalemia

contraindicated in pregnancy and angioedema

487
Q

what race may need a higher dose of ACE due to possible decreased response

A

African American children

488
Q

elfin faces think

when eval for HTN

A

Williams syndrome

489
Q

moon face think

when eval for HTN

A

cushing syndrome

490
Q

thyroid enlargement think

when eval for HTN

A

hyperthyroidism

491
Q

webbed neck think

when eval for HTN

A

Turner syndrome

492
Q

tonsillar hypertrophy think

when eval for HTN

A

OSA,

493
Q

retinal changes think

when eval for HTN

A

severe HTN and secondary etiology

494
Q

papilledema think

when eval for HTN

A

intracranial HTN

495
Q

Acne, hirsutism, striae think

when eval for HTN

A

cushing syndrome

steroid use

496
Q

cafe -au-lait spots and/or neurofibromas

when eval for HTN

A

neurofibromatosis

497
Q

ash leaf spots and/or adenoma sebaceum

when eval for HTN

A

tuberous sclerosis

498
Q

rash think

when eval for HTN

A

secondary kidney disease
Lupus erythematosus
henoch-schonlein purpura

499
Q

acanthosis nigricans think

when eval for HTN

A

Type 2 DM

500
Q

murmur think

when eval for HTN

A

coarctation of aorta

501
Q

apical heave think

when eval for HTN

A

L ventricular hypertrophy

502
Q

abdominal bruit think

when eval for HTN

A

renovascular disease

503
Q

abd mass think

when eval for HTN

A

hydronephrosis
polycystic kidney disease
kidney tumors
neuroblastoma

504
Q

Pulse in lower extrem

A

coarctation of aorta

505
Q

asymmetry of limbs think

when eval for HTN

A

Beckwith-Weideman syndrome

506
Q

Arthritis think

when eval for HTN

A

henoch-schonlein purpura
collagen vascular disease
lupus erythematosus

507
Q

muscle weakness think

when eval for HTN

A

Liddle syndrome

Hyperaldosteronism

508
Q

Ascending paralysis

when eval for HTN

A

guillain - barre syndrome

509
Q

diminished pain response

when eval for HTN

A

familial dysautonomia

510
Q

Pt should be seen every __-_ weeks while titrating medications and every ___ -___ months thereafter if on medications for HTN

A

4-6 weeks

3-4 months

511
Q

Pt attempting lifestyle mods for HTN should be seen every _-__

A

3-6 months

512
Q

The AHA recommends restricting competitive sports participation in athletes with

A

LVH beyond what is seen with typical athletic Heart until BP is controlled and restriction those with stage 2 HTN even without LVH from participating in high static sports (weight lifting, boxing, wrestling) until BP is controlled.

513
Q

when can children and adolescents with HTN participate in sports

A

once target organ damage and risks have been assessed

514
Q

bacterial or fungal infection in any part of the urinary tract (urethra, ureters, bladder, kidney)

A

UTI

515
Q

a UTI that migrates to the kidney results in ______ which is what type of UTI

A

pyelonephritis

upper urinary tract infection

516
Q

uncircumcised males have the highest incidence in the first 3 months of life

A

UTI

517
Q

what is associated with higher incidence of UTI

A

genetic predisposition

history of dysfunctional voiding or elimination

518
Q

in otherwise healthy children, UTI may indicate an underlying abnormality in the urinary tract such as

A

vesicoureteral reflux (VUR) disease

519
Q

most common etiology of UTI

A

colonic organisms

520
Q

pathogens commonly cause UTI

A

gram neg bacteria

E.Coli
Klebsiella species
Pseudomonas aeruginosa

gram positive bacteria
enterococcus
Staph aureus
group B streptococcus

Candida
adenovirus
herpes simplex

521
Q

in a UTI pathogens infiltrate the _____ of the ____, resulting in an _____ response

A

mucosa
bladder
inflammatory

522
Q

clinical presentation of UTI in infants/young children

A 
fever
irritability
fussiness
decreased appetite
lethargy
changes in activity level
jaundice
weight loss
523
Q

clinical presentations of UTI in preschool/young school age

A

abd pain
n/v
urinary frequency

524
Q

clinical presentations of UTI in older children

A 
urinary frequency
dysuria
urgency
suprapubic pain
n/v
525
Q

evaluate history for UTI

A

structural abnormalities of UT

baths

voiding/elimination dysfunction

sexual activity

maltreatment risk

526
Q

physical exam evaluation for UTI

A

evaluate for sacral dimple

costovertebral angle tenderness

suprapubic tenderness

527
Q

Urinalysis evaluation for UTI

A

presence of leukocyte esterase

nitrites

> 5 WBCs

bacteria/hpf

528
Q

Urine culture for UTI

A

identifies pathogen and evaluates abx sensitivity/resistance

529
Q

what tests are recommended to determine presence of a UTI

A

UA and UC

530
Q

when is a renal US indicated in a UTI

A

children 2 mos - 2yrs

531
Q

US evaluates what in UTI

A

anatomy

kidney size/shape

evidence of hydronephrosis

areas of inflammation and signs of pylelonephritis

532
Q

when would you order a voiding cystourethrography

A

if renal and bladder US show hydronephrosis, scarring or evidence of high grade VUR or obstructive uropathy

all infants 2 months to 2 yrs with recurrence of febrile UTI

533
Q

what is a dimercaptosuccinic acid (DMSA) scintigraphy

A

nuclear medicine scan used to evaluate for renal scarring

534
Q

mgmt for UTI- duration is determined by

A

determined by pt age, severity of illness, local resistance patterns, associated underlying disorders

535
Q

Uncomplicated UTI duration of therapy is

A

7-10 days

2-4 days according to some studies

536
Q

complicated UTI duration of therapy

A

14 days

537
Q

initial oral therapy abx selection for UTI

A

Bactrim
Augmentin
Cefixime

538
Q

initial parenteral therapy for UTI treatment

A

ceftriaxone
cefotaxime
gentamicin

539
Q

in general, oral abx are just as effective or less effective than pareneral

A

equally

540
Q

recommended medication for discomfort or fever in UTI

A

acetaminophen

541
Q

when is hospitalization recommended for UTI

A

when unable to tolerate oral meds
or maintain adequate hydration

fail to improve outpatient
evidence of sepsis

underlying medical that may complicate management

542
Q

Pt family education for UTI

A

signs of UTI

hygiene

limiting bubble baths

constipation prevention

urination after intercourse if sexually active

close clinical f/u after 7-10 days of abx to evaluate for recurrent UTI

543
Q

why are underlying urinary tract abnormalities important to recognize early

A

so they do not lead to renal scarring

544
Q

prophylactic abx do/do not reduce risk of recurrent UTI,. How about in cases of mild to moderate VUR

A

do not

even in cases of mild to moderate VUR

545
Q

1 in = ___ cm

A

2.54cm

546
Q

proximal tubule job

A

water and electrolyte reabsorption

547
Q

the job of the distal convoluted

A

primary site of vasopressin response so urine concentration

548
Q

Sodium Polystyrene aka

A

kayexalate

549
Q

eCCl decrease by 25% or decrease in urine output <0.5ml/kg/h for 8 hours

A

pRIFLE risk

550
Q

eCCl decrease by 50% or decrease in urine output <0.5ml/kg/h for 16 hours

A

pRIFLE injury

551
Q

eCCl decrease by 75% or eCCl <35 ml/min/1.73m2 or decrease in urine output <0.3ml/kg/h for 24 hours or anuric for 12 hours

A

pRIFLE failure

552
Q

persistent failure > 4 weeks

A

pRIFLE loss

553
Q

persistent failure >3months

A

pRIFLE End stage renal disease

554
Q

retrograde flow of urine from the bladder up the ureter, sometimes into the kidney – usually results from congenital incompetence of the ureterovesical junction (matures in early childhood), renal dysplasia, or neurogenic bladder

A

Vesicoureteral reflux:

555
Q

Vesicoureteral reflux causes

A

renal scarring even with one UTI

556
Q

Vesicoureteral reflux exposes the kidney to increased

A

hydrodynamic pressure during voiding and increases likelihood of infection d/t incomplete emptying of ureter and bladder

557
Q

diagnosis Vesicoureteral reflux diagnosis

A

renal ultrasound (best method) → VCUG (direct measurement of VUR)

us - if there is reflux
VCUG - how severe it is

558
Q

Treatment Vesicoureteral reflux

A

+/- prophylactic antibiotic therapy (bactrim) for mild to moderate VUR, monitor for complications (HTN, CKD)

559
Q

what is the significance of evaluating for the sacral dimple on physical exam in UTI

A

spina bifida is at increased risk for UTI secondary to neurogenic bladder

560
Q

more than 50, 000 colony-forming units/mL of a single organism and pyuria

A

Positive urine culture for a UTI

561
Q

organism mentioned in UTI but not in pyelonephritis

A

Group B streptococcus

562
Q

organisms mentioned in pyelonephritis not mentioned for UTI

A

Proteus spp.

Serratia spp.

563
Q

lab to evaluate kidney function

A

BMP

564
Q

most severe type of UTI

why?

A

Pyelonephritis

d/t irreversible renal damage that can occur

565
Q

Pyelonephritis can lead to

A

tubulointerstitial nephritis (TIN) which can lead to ESRD

566
Q

inflammation affecting the interstitium and renal tubules of the kidney – leads to inability to concentrate urine, salt wasting, and metabolic acidosis

A

tubulointerstitial nephritis (TIN)

567
Q

symptoms of tubulointerstitial nephritis (TIN)

A

maculopapular rash, joint pain with flexion or extension, uveitis (eye inflammation)

568
Q

if they have a UTI and fever what MUST be r/o

A

pyelonephritis

569
Q

treatment for nephritis if allergic to pcn

A

macrolides

cephalosporins

570
Q

clot formation as a result of endothelial cell injury or hypercoagulable/sludging state where the thrombus forms in the intrarenal circulation and can extend to inferior vena cava or main renal vein

A

renal artery/vein thrombosis

571
Q

acute occlusion of the renal artery d/t thrombus formation leading to renal infarction and irreversible loss of renal function

A

renal artery thrombus

572
Q

clinical presentation of renal artery/vein thrombosis

A 
abrupt onset hematuria
flank mass, unilat or bilat
flank pain
oliguria
HTN
573
Q

diagnostic of renal artery/vein throbosis

A

doppler US of kidneys

574
Q

what is associated with renal artery/vein thrombosis

A 
history of 
asphyxia
sepsis
shock
dehydration
hypercoagulable state
indwelling umbilical catheters
maternal diabetes in newborns/infant
nephrotic syndrome
congenital heart
Factor V Leiden deficiency
exposure to contrast
after kidney transplants
575
Q

management of renal artery/vein thrombosis

A

monitor and maintain fluid and electrolytes

BP monitoring

treat with anticoagulants (heparin) or thrombolytics

inferior vena cava thrombus may require thrombectomy

treat underlying

576
Q

complication of renal artery/vein thrombosis

A 
PE
renal atrophy (affected side)
577
Q

what do you treat type II RTA

A

HCTZ

578
Q

Type III RTA treat with

A

thiazide diuretics

579
Q

Type I RTA treat with

A

bicarb

580
Q

priapism is common with what disease

A

sickle cell

581
Q

management of priapism

A

warm sitz baths
analgesics
aggressive hydration

582
Q

when do you consult urology in priapism

A

erection lasting 4 hours

583
Q

how does urology fix priapism

A

aspirate blood from corpora and irrigate with saline or dilute adrenergic solution

shunt placement may be considered in refractory cases

584
Q

priapism with sickle cell who else do you consult

A

hematology

may use a simple or exchange transfusion

585
Q

ical pt in CRRT should be around

A

1.2

586
Q

ical of circuit in CRRT should be around

A

.4

587
Q

ionized calcium and total calcium

A

ionized calcium is what the body can use

citrate binds the calcium so the body cant use this. A healthy liver clears the citrate

total calcium includes what is bound to citrate

so a high total calcium with dropping ionized calcium -> citrate lock

588
Q

CRRT

removal of free water from blood

A

slow continuous ultrafiltration

589
Q

CRRT

plasma and metabolites are removed from blood via ultrafiltration

A

continuous venovenous hemofiltration

590
Q

CCRT
plasma and metabolites are removed from blood via dialysis

effective small molecule clearance

A

continuous venovenous dialysis

591
Q

CRRT
plasma and metabolites are removed from blood via filtration and dialysis

uses replacement fluid to limit the increased blood viscosity within the hemodialysis filter

Blood volume reconstituted by IV fluid as replacement fluid with desired electrolytes

replacement fluid is not returned to the pt

most efficient solute clearance

A

Continuous venovenous hemodiafiltration (CVVHDF)

592
Q

how do you evaluate for rejection after kidney transplant

A

kidney biopsy

593
Q

normal pH urine

A

4.6-8

594
Q

normal protein urine

A

0-8mg/dL

595
Q

normal protein in urine 24 hour at rest

A

50-80mg/24 hr

596
Q

normal protein in urine 24 hour during exercise

A

<250mg / 24 hr

597
Q

normal wbc urine

A

0-4 per low power field

598
Q

RBC normal urine

A

<2

599
Q

RBC normal casts urine

A

none

600
Q

WBC casts urine normal

A

none

601
Q

low c3 is seen in

A

acute post streptococcal GN
post infectious GN
MPGN
lupus nephritis

602
Q

normal bicarb (Hco3)

A

22-26

603
Q

pH normal serum

A

7.35-3.45

604
Q

PaO2 serum

A

75-100

605
Q

PaCO2

A

35-45

606
Q

normal albumin

A

3.5-5

607
Q

serum K

A

3.6-5.2

Essentials of Acute Care (9 decks)

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