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Week 3_Peds Nephro

Terms in this set (42)

What is enuresis and how does it compare to urinary incontinence?
Involuntary loss of large amounts of urine
Urinary incontinence is involuntary loss of small amount of urine.
What is primary vs secondary enuresis?
Primary = in children never toilet-trained before
Secondary = in children who have been continent for >6 months
7 year old boy wets bed every night. Has no UTIs. Pees large amounts. Has never been dry at night before. Has no day-time accidents. His Father was a primary wetting until 11 years. Kid is a Deep sleeper. What is the diagnosis?
Primary Nocturnal enuresis.
Delay in achievement of nocturnal continence
8 year old girl. Wet bed every night. No UTIs.
Was dry day & night at 3 years old now wet several times a day - small amounts. Runs to bathroom "squats". What is the diagnosis?
2ndary noturnal and diurnal incontinence
If the renal ultrasound indicated structural abnormalities such as: upper tract dilatation,
thickened bladder wall and residual volume, what would be the diagnosis?
Bladder dysfunction.
If there is a History of
- no intermittent flow
- incontinence associated with holding maneuver and the Ultrasound indicated no residual volume, what would be the diagnosis?
Uninhibited detrusor contractions
How can primary nocturnal enuresis be managed?
explain
nocturnal enuresis alarm
DDAVP
Minimise punishment
How can uninhibited contractions be managed?
Timed voiding
Oxybutinin
Prophylactic antibiotics if UTIs
How are UTIs and bladder dysfunction connected?
UTIs -> Acute dysfunction (Dysuria, Frequency, Urge, Incontinence) -> Chronic dysfunction
-> Reflux -> UTIs
9 year old girl Wets bed every night. Asymptomatic UTIs. Dry day & night at 3 years old. Wet several times a day. infrequent voids
prolonged, interrupted void significant residual volume.
Bloodwork: Elevated creatinine
VCUG: Bilateral vesicoureteric reflux
Ultrasound: Reflux nephropathy
Urodynamics: detrusor sphincter dyssynergy
large capacity bladder, huge residual volume
Secondary diurnal and nocturnal bladder dysfunction
Detrusor-sphincter dyssynergy
Detrusor failure or "lazy bladder"
How can diurnal and nocturnal bladder dysfunction secondary to detrusor-sphincter dyssynergy be managed?
Prophylactic antibiotics
Clean intermittent catherizations
trial of prazosin
How can sphincter incontinence be managed?
Ephedrine
Define Hematuria
>/ 5RBCs/hpf, in three consecutive centrifuged urine samples
What is the Ddx for hematuria?
What are the 3 layers of filteration in the glomerulus?
Endothelium
Basement membranes
Podocytes
Define proteinuria.
qualitative: 1+ in dilute, 2+ in concentrated urine (specific gravity> 1.015)
quantitative: >4 mg/m2/h on timed urine (>40 mg/m2/his nephrotic range)
______ assesses risk of progressive glomerulonephropathy in diabetes.
Microalbuminuria
True or false. Progressive proteinuris is indicative of renal disease.
True
What are the potential causes of transient proteinuria?
due to fever (>38.3°C/101 °F),
dehydration,
exercise,
seizures,
stress
What are the potential causes of persistent proteinuria?
Orthostatic
(more common in adolescents - usually benign):
- elevated protein excretion when
- upright and normal when recumbent;
Glomerular
- nephrotic syndrome,
- glomerulonephritis
Tubulointerstitial
- Fanconi syndrome,
- ATN
Structural abnormalities of urinary tract
Hydronephrosis
What is the most common cause of acute renal failure in children?
Hemolytic uremic syndrome
What is the clinical presentation of hemolytic uremic syndrome?
triad: acute renal failure, thrombocytopenia, MAHA

- abdominal pain, diarrhea, followed by bloody diarrhea
Hx: weakness, lethargy, oliguria
PE: pallor, jaundice (hemolysis), edema, petechiae, hypertension
What is the most likely cause of HUS?
E.coli O157, or shiga toxin
What is the treatment options for HUS?
• supportive treatment; nutritional support; monitor electrolytes; dialysis if electrolyte abnormality cannot be corrected, fluid overload, or BUN> 100 mg/dL; PRBC for symptomatic anemia
• steroids not helpful; antibiotics not indicated
What are the presentation of nephritic syndrome?
PHAROH
Proteinuria
Hematuria
Azotemia
RBC casts
Oliguria
Hypertension
What are the risk factors and pathophysiology of post-strep glomerulonephritis?
Risk factors
most common in children
Occurs 1-3 weeks following group A beta-hemolytic streptococcal infection of skin or throat
Pahthophysiology
Antigen-antibody mediated complement activation
Diffuse, proliferative glomerulonephritis
How is post-strep glomerulonephritis diagnosed?
Elevated serum levels of antibody titres of strep antigens.
How is nephritic syndrome managed?
• symptomatic treatment: fluid restriction, antihypertensives, diuretics
• in severe cases: hemodialysis or peritoneal dialysis may be necessary
• eradication of infection (penicillin or erythromycin)
What are the major causes of acute glomerulonephritis?
What is the clinical presentation of nephritic syndrome?
PALE
Proteinurira
Hypoalbuminemia
Dyslipidemia
Edema (initially face swelling = periorbital and pretrial edema)
What are the several etiologies of primary nephrotic syndrome?
Minimal change disease
Membranous glomerulonephritis
Focal segmental glomerular sclerosis (FSGS)
Membranoproliferative glomerulonephritis
What etiologies are responsible for secondary nephrotic syndrome?
Vasculitis
Infections (e.g. hepatitis Band C, syphilis, HIV)
Medications (e.g. captopril, penicillamine, NSAIDs, anticonvulsants)
Malignancy
Hereditary (e.g. sickle cell disease, Alpert syndrome)
Metabolic, inflammatory (e.g. lupus nephropathy; rheumatoid arthritis)
What are the complications of nephrotic syndrome?
Hypercoagulable state (low volume + Antithrombin III depletion)
Hypotension, shock, renal failure
Side effects of drugs (Diuretics, Steroids, Immunsuppresants)
Risk of Infections
When should kidney biopsies be considered?
• HTN (higher risk ofFSGS), steroid resistant, frequent relapses (>2 relapses in 6 month period), low serum complement, severely decreased renal function
• presentation before first year of life (high likelihood of congenital nephrotic syndrome)
• presentation after 10 years of age to rule out more serious renal pathology than MCD
How can minimal change disease be managed?
Oral prednisone
A negative tuberculin skin test should be performed before starting steroid medications
A measurable decrease in protein excretion may take at least 7 to 10 days following initiation of treatment, and proteinuria clears by third week of oral prednisone
What are the long term adverse effects of Minimal change disease?
Up to 2/3 of patients experience relapses
Hence long term steroids can lead to cushing's syndrome.
How does MCD progress to FSGS?
Where is the site of injury if hematuria is present in:
Terminal part of the stream
Initial part of the stream
Bright red clots
Tea or Cola coloured clots
Initial part = Uretheral origin
Terminal part = bladder
Bright red clots = Lower urinary tract in origin
Tea or cola coloured = Renal parenchymal origin
What are the etiologies of persistent microscopic hematuria?
Benign familial hematuria
Alport's disease
What is the presentation of Alport's disease?
Present with hematuria (exercise)
Sensorineural hearing loss
ESRD in males by the 4th decade
What are the different kinds of gross hematurias?
with pharyngitis = PSGN
With diarrhea = HUS
With URTI = IgA nephropathy
What are the different kinds of antibody-mediated glomerular diseases?
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