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Scarlett's paeds flashcards > Renal > Flashcards

Renal Flashcards

(55 cards)

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1
Q

What is cryptorchidism

A

The absence of one or both testes in the scrotum

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2
Q

What percentage of premature boys have undescended testes

A

22-30%

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3
Q

What is the rate of undescended testes in term infants by 1 years of age

A

1%

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4
Q

What histological changes may be seen in undescended testes after 2 years

A

leydig cell hypoplasia, reduced numbers of germ cells

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5
Q

When is orchidopexy recommended

A

before 2 years of age

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6
Q

What is the most common location for undescended testes to be found in

A

inguinal canal (followed by prescrotal and abdominal)

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7
Q

How is undescended testes investigated

A

Clinical, USS may help if location not determined, bilateral impalpable testes may need BHCG stimulation test or laproscopic exploration

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8
Q

how is cryptorchidism managed

A

PPV ligation at 6m to 1 year

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9
Q

complications of cryptorchidism

A

infertility, malignancy increased risk by 60%

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10
Q

What is encopresis

A

Fecal soiling

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11
Q

What are the 3 types of fecal soiling

A

1) retentive encopresis (due to loss or tolerance of stretch response)
2) non retentive (no constipation)
3) emotional
may be associated with surgical intervention e.g. for hirschsprungs

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12
Q

What may be found on examination in a child with encopresis

A

fecal losing, soft stool in rectum, reduced anal wink and tone, anal sphincter lax due to chronic distension

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13
Q

What investigations for encopresis?

A

anorectal manometry, radionuclear transit scintiography

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14
Q

management for encopresis?

A

constipation management and diet control, laxatives behavioural strategies, biofeedback training,

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15
Q

What are hypospadias

A

abnormal ectopic urethral opening

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16
Q

where on the penis is hypospadias most common

A

distal

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17
Q

what are the causes and genetics of hypospadias

A

environmental and endocrine and genetic. commonly androgen synthesis mutations, higher in IVF babies due to progesterone administration

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18
Q

how is hypospadias investigated

A

RUSS

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19
Q

What is the management for hypospadias

A

DO NOT CIRCUMCISE as foreskin may be used in reconstruction. surgery at 9-12m

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20
Q

What is nePHrOtic syndrome

A

triad of proteinuria, hypoalbuminaemia and oedema

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21
Q

What are the types of primary nephrotic syndrome

A

minimal change disease, focal segmental glomerulosclerosis and membranous nephropathy

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22
Q

what are the types of secondary glomerulonephreitis

A

post infection( malaria, GBS, HepB, VZV, syphillis, HIV, Tb, EBV) , collagen vascular disease, henoch schonlein purpura, congential e.g. alports, sickle cell disease

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23
Q

what is the most common cause of nephrotic syndrome in children

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A

minimal change disease

24
Q

What may you find on examination of someone with nephrotic syndrome

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A

o General: anorexia, oliguria, lethargy, hypertension
o GI: diahrrea, nausea, poor feeding, pain
o Odema: swelling of eyelids, face, ascites, legs and scrotum.
o Complications: infections, renal vein thrombosis, loin pain, haematuria.

25
How would you investigate nephrotic syndrome
o Bloods: Ues, albumin, FBC, CRPESR high, lipid profile. o Post infectious: ASOT, Thick and thin films, HBV/EBV/HIV serology. o Urine dipstick: high protein, high blood. o MSU: MCS. 24h urine collection for creatinine clearance. o Renal USS and biopsy: other renal disease causing proteinuria (polycyst) biopsy for older children with persistent hematuria. o Doppler USS if renal vein thrombosis suspected.
26
Management of nephrotic syndrome
symptom treatment - low sodium and water diet, monitor BP, U+Es ca, weight, fluid balance, alternating prednisolonen until remission / at least 6 months or cyclophosphamide for steroid resistant patients treat hypertension with ace inhibitors penicillin prophylaxis for peritonitis
27
What are some complications of nephrotic syndrome
renal failure, infection susceptibility, peritonitis, pneumococal sepsis, hypercoaguability leading to renal vein thrombosis and DVTs hyperlipidaemia
28
Why do you get hypercoagulability in nephrotic syndrome
protein loss of antithrombin, proteinc/s
29
what can cause/trigger nephrotic syndrome
URT infection, allergy, insect bite, vaccination, psych stress
30
what is minimal change disease
Minimal change disease accounts for 90% of nephrotic syndrome cases in children <10 years In adults, it may occur without an identified cause (idiopathic), in relation to NSAIDs, or due to Hodgkin's lymphoma. 'Minimal change' refers to light microscopic findings that often reveal normal glomeruli or mild mesangial proliferation. Immunofluorescence typically shows no immune complex deposition.
31
what is focal segmental glomerulosclerosis
FSGS accounts for between 35% and 50% of idiopathic nephrotic syndrome cases in adults Light microscopy shows segmental areas of mesangial collapse and sclerosis affecting some but not all glomeruli (focal disease). FSGS can be either primary (idiopathic) or secondary to HIV, obesity, and reflux nephropathy
32
what is membranous nephropathy
Membranous nephropathy is the most common cause of nephrotic syndrome in adults. Microscopy demonstrates basement membrane thickening without associated cellular proliferation or infiltration. Immunofluorescence reveals diffuse, granular IgG deposition throughout the capillary walls and electron microscopy shows electron dense deposits in the subepithelial space. New basement membrane growth between subepithelial immune deposits leads to the classic 'spike and dome' appearance
33
what are the two types of phimosis
o Physiological phimosis: Foreskin not fully developed at birth, prepitual adhsons cause glans to adhere to foreskin. Rare for neonate foreskin to be retractile fully. Normal until adolescence. o Pathological phimosis: Balantis xerotica obliterans (BXO) unknow aetiology fibrotic disorder.
34
what would you see on examination of phimosis
DO not attempt forceful retraction. Physiological has hx of ballooning and spraying of urine. Distal erythema. Pathological has white fibrotic ring at the distal foreskin. Absence of normal mucosal sprout. Pain and haemorrage. Balantis: often misdiagnosed. True balantis with odema, erythema and generation of purulent material from distal phimotic foreskin.
35
what are the pre renal causes of AKI
* Hypovolaemia (anaphylaxis, haemorrage, GI loss, DKA, burns) * Cardiac failure (coarctaton, HLH, myocarditis) * Hypoxia (pneumonia, RDS)
36
what are the renal causes of AKI
* Acute tubular necrosis ATN due to nephrotoxic drugs or hypoxic injury to tubular cells. * Acute glomerulonephritis (see chapter) * Acute interstitial nephritis (infection, drugs, NSAIDS, frusemide, penicillin) * Small or large vessel obstruction (renal artery stenosis/vein thrombosis, vasculitis, HUS, TTP)
37
What are the post renal causes of AKI
* Neuropathic bladder: transverse myelitis or spinal trauma * Stones: PUJ or ureteral * Urethral prolapse or bladder ureterocele * Iatrogenic: catheter, stent, nephrostomy or surgery.
38
what are the symptoms of aki
Vomiting, nausea, anorexia, oliguria, convulsions, confusion, previous infectious signs PSGN, bloody diahrrea and pallor HUS, ?palpable bladder
39
signs in AKI
1. Skin - livedo reticularis, digital ischemia, butterfly rash, and purpuras to suggest vasculitis. Track marks to suggest endocarditis 2. Eyes and ears - jaundice in liver disease, band keratopathy in multiple myeloma, signs of diabetes mellitus, atheroemboli in retinopathy, and signs of hypertension. Keratitis, iritis, and uveitis in autoimmune vasculitis. Hearing loss in Alport disease. 3. Cardiovascular system - pulse rate, blood pressure, and jugulovenous pulse in establishing volume status. Irregular rhythm may indicate electrolyte imbalance-related arrhythmias. Pericardial friction rub in uremic pericarditis.
40
Investigation aki
o Bloods: low Hb, low albumin, high creatinine, high urine, high WCC and CRP, blood cultures for sepsis, high P, high K, low Mg, blood gas for acidosis, clotting studies, ASOT. o Blood film: HUS/TTP have RBC fragmentation. o Urinalysis (blood and protein) glucose if interstitial nephritis, microscopy for casts in GN, urine Na,creat,and urea to distinguish between pre renal and renal. o ECG for signs of high K: tented T waves / small absent P waves / PR interval / wide QRS / sine wave pattern / asystole. o Renal USS may detct clot. Biopsy if diagnosis not determined.
41
How is CKD defined
Chronic renal failure is described as either GFR<60ml/min/1.73m2 for >3 months or as kidney damage. Kidney damage is seen using damage markers in urine and blood tests
42
What are the 5 stages of GFR
* 1: GFR 90+ * 2: GFR 60-90 * 3: GFR 30-60 * 4: GFR 15-30 * 5: GFR <15
43
aetiology of CKD
<5y: congential abnomalities, hypoplasia, dysplasia, obstruction, valve malformations. >5y: • Vascular: vasculitis, renal artery stenosis • Glomerular: glomerulonephritis, amyloid, SLE, diabetes • Tubulointerstitial disease: pyelonephritis, TB, nephrocalcinosis • Obstruction: myeloma, HIV nephropathy, gout, scleroderma, renal tumor • Vesciculoureteral reflux. • Hereditary: Aloprt’s and PCKD.
44
examination CKD
Systemic: Kussmaul’s breathing (acidosis) signs of anaemia, odema, screatch marks, pigmentation Hands: Leukonykia and brown lines distally Palpable kidneys, pallor, odema, pigmentaton, scratch marks, growth retardation
45
Investigations and CKD
FBC: Iron deficiency anaemia, high creatinine, low albumin. UE (low urea/creaitnine) eGFR (using MDRD calculator), low Ca, high Phos, ALP and PTH. Aetiology: immunological studies (ANA/ANCA) and blood glucose 24h urine: creatinine clearance (for GFR) and protein Imaging: uraemic pericardial effusion and pulmonary odema. Bone scan for sings of hyperparathyroidism or osteomalacia. Renal USSL size and obstruction Renal biopsy: for disease specific pathology
46
treatment CKD
Treat underlying cause (ie. Control diabetes and hypertension) ABCDDE • Anaemia: EPO injections • BP: ACEi and AT2 blockers (CAREFUL with RAStenosis) • Calcium: Hypocalcaemia: replace calcitriol to normalize Ca and PTH. • Diet: high energy intake. Low protein. Low K (may need NaHCO3) low Phosphate (use binders ie. CaHCO3 or ALOH) • Drugs: avoid nephrotoxic drugs (ie. NSAIDS) and adjust dosage for other kidney excreted drugs • Edema: diuretics ie. Frusemide, metolazone Renal replacement therapy: peritoneal dialysis, haemodialysis, renal transplantation
47
renal causes of urinary tract abnormalities
* Multicystic dysplastic kidneys: MCDK, renal medullary and hepatic cysts. Early ureteric obstruction. * Medullary sponge kidney: cystic dilation of the collecting ducts, multiple calculi * Nephronophitosis: multiple cyst formation at corticomedullary junction with progressive glomerular sclerosis. * Unilateral renal agenesus: absence of a kidney * Ectopic or horseshoe kidney: Fusion of lower poles leading to symmetrical or asymmetrical horseshoe.
48
Non renal causes of urinary tract abnormalities
* PUJ obstruction: stenosis or stresia of proximal ureter. * Veso-ureteric reflux: with associated hydronephrosis, graded 1-4. * Non obstructed non refluxin primary megaureter: aperistaltic megaureter * Bladder outlet obstruction: posterior urethral vale malformation, congenital lesion with variable obstruction. * Uterterocele: Intrabladder hernia ot cystic ballooning at the lower end of ureter. * Hypospadias or epispadias: abnormal ectopic urethral opening. Ventral is hypo, dorsal is epispadias.
49
signs/symptoms of urinary tract abnormalities
Antenatal: common oligohydramnios, decreased fetal urine output. Pulmonary hypoplasia in severe cases. Antenatal diagnosis of hydronephrosis. Postnatal: intra abdominal masses, UTI, pain, hematuria, calculi, renal failure, HTN, hepatosplenomegaly, liver fibrosis, voiding dysfunction,
50
investigations for urinary tract abnormalities
o USS: non invasive, visualize kidney. o IVUG: Visualise majority of anomalis including VUN/PUV that are not seen in USS. Nuclear imaging: DMSA Tc-99m DMSA (2,3 dimercaptosuccinic acid) is a technetium radiopharmaceutical used in renal imaging to evaluate renal structure and morphology, o and MAG3 for assessment of kidney function and perfusion. Overestimate function in obstructed system.
51
Most common organisms in UTI
Usually transurethral ascent of colonic organisms. Most common are E.coli, then Proteus mirabilis, Klebsiella and Enterococci.
52
symptoms of UTI
``` o Cystitis: frequency, urgency, dysuria, haematuria, suprapubic pain, smelly urine o Pyelonephritis (acute): fever, loin pain o Prostatitis: fever, lower back pain, irritative (urgency, frequency) and obstructive (hesitancy, dribbling, poor flow) LUTS. ```
53
Examination UTI
o May be asymptomatic. o Cystitis: fever, suprapubic or loin tenderness, bladder distension o Pyelonephritis: fever, loin tenderness o Prostatitis: fever, tender painful prostate.
54
Cystitis management
o Cystitis: if symptomatic, consider microbiological policies (cotrimetazole, trimetopham, amoxicillin win women)
55
pyelonephritis management
o Pyelonepritis: IV gentamicin, cefuroxime or ciproflaxin

Scarlett's paeds flashcards (5 decks)

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