P-T

Question 1

What is Phimosis and foreskin disorders?

Answer 1

Unretractile foreskin due to physiological or pathological problem.

Question 2

What is the aetiology of phimosis and foreskin disorders?

Answer 2

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.

Pathological phimosis: Balantis xerotica obliterans (BXO) unknow aetiology fibrotic disorder.

Question 3

What is the epidemiology of phimosis and foreskin disorders?

Answer 3

Physiological in 50% at 1y, pathological 0.6% at 15y.

Question 4

What History/ Exam/ Investigation findings occur in phimosis and foreskin disorders?

Answer 4

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.

No Ix required

Question 5

What is the pathology of phimosis and foreskin disorders?

Answer 5

BXO: odema and homogenisation of collagen in upper dermis, infiltration of inflammatory cells, atrophy of striatum malphigi and hydropic degeneration of basal cels

HIV: possible protective role of cirumcision in HIV transmission. HIV binds to langerhans cells in surface of foreskin. Lower incidence of cervical carcinoma due to HPV transmission. NO evidence for UTI and penile carcinoma prevention.

Question 6

What is the management of phimosis and foreskin disorders?

Answer 6

Conservatice: no attempts to retract. Variable results fro topical steroids in physiological. Gentle retracton with tissue drying in older boys.

Preputial plasty: small non traumatic dorsal split to widen the meatus

Circumcision: only treatment for BXO. Preformed under GA with sleeve dissection method.

Question 7

What are the complications/ prognosis of phimosis and foreskin disorders?

Answer 7

Pathological: may lead to progressive phimosis and possible urinary retention.

Circumcision: haemorrage, infection, meatal stenosis, glans injury, fistula. Most physiological retract with time, pathological good with surgery.

Question 8

What is acute renal failure?

Answer 8

Significant deterioration in renal functon over hours or days. Increased plasma urea, lower albumin, high phosphate, high creatinine, oliguria. Complete recovery in days to weeks.

Question 9

What are the causes of ARF?

Answer 9

Pre-renal
Renal
Post renal

Question 10

What are the pre-renal causes of ARF?

Answer 10

· Hypovolaemia (anaphylaxis, haemorrage, GI loss, DKA, burns)

· Cardiac failure (coarctaton, HLH, myocarditis)

· Hypoxia (pneumonia, RDS)

Question 11

What are the renal causes of ARF?

Answer 11

· 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)

Question 12

What are the post-renal causes of ARF?

Answer 12

· Neuropathic bladder: transverse myelitis or spinal trauma

· Stones: PUJ or ureteral

· Urethral prolapse or bladder ureterocele

· Iatrogenic: catheter, stent, nephrostomy or surgery.

Question 13

What is the epidemiology of ARF?

Answer 13

1/100k children

Question 14

What is found in the Hx and exam of ARF?

Answer 14

Vomiting, nausea, anorexia, oliguria, convulsions, confusion, previous infectious signs PSGN, bloody diahrrea and pallor HUS, ?palpable bladder.

Assess intravascular volume status, volume depleted, or overloaded. Is patient obstructed? Assess pain and bladder fullness. Ballot kidney.

Question 15

What Ix do you need for ARF?

Answer 15

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.

Blood film: HUS/TTP have RBC fragmentation.

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.

ECG for signs of high K: tented T waves / small absent P waves / PR interval / wide QRS / sine wave pattern / asystole.

Renal USS may detct clot. Biopsy if diagnosis not determined.

Question 16

What is the management of ARF?

Answer 16

Resuscitate ABCDE.

Fluids: allow insensible losses 400ml/m2, replacement of urine output.

Treat cause

Dialysis if

· Severe ECF volume overload, high BP, pulmonary odema or not responding to diuretics.

· Severe high K, uaeamia, metabolic acidosis not controllable with IV NaHCO

· Removal of toxins

Question 17

What are the complications and prognosis of ARF?

Answer 17

Heart failure and pulmonary oedema, GI bleed from plt dysfunction causing gastric ulceration, muscle wasting due to hypercatabolic state, uraemic encephalopathy.

Depends on cause – recovery of renal function following ARF is most likely in pre renal causes, HUS, ATN, AIN or uric acid nephropathy.

Question 18

What is Chronic Renal Failure?

Answer 18

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.

Question 19

What are the stages of CRF?

Answer 19

· 1: GFR 90+

· 2: GFR 60-90

· 3: GFR 30-60

· 4: GFR 15-30

· 5: GFR <15

Question 20

What is the aetiology of CRF in >5y?

Answer 20

> 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.

Question 21

What is the aetiology of CRF in <5y?

Answer 21

<5y: congential abnomalities, hypoplasia, dysplasia, obstruciton, valve malformations.

Question 22

What is the epidemiology of CRF?

Answer 22

Incidence 110/million. High incidence in Asian immingrants into the UK.

Question 23

What would you find on Hx and Exam in CRF?

Answer 23

Clinical presentaiton: antenata diagnosis, fail to thrive, delayed puberty, malaise, anorexia, incidental dx on blood test or urinalysis.

Systemic: Kussmal’s breathing (acidosis) signs of anaemia, odema, screatch marks, pigmentation

Hands: Leukonykia and brown lines distally

Palpable kidneys, pallor, odema, pigmentaton, scratch marks, hrowth retardation

Question 24

What Ix for CRF?

Answer 24

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

Question 25

What is the management of CRF?

Answer 25

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

Question 26

What are the complications of CRF?

Answer 26

Haematological: Anaemia (low EPO, low marrow activity, platelet malfunction)

CVS: accelerated atherosclerosis, high BP, pericarditis

Neuromuscular: neuropathy, myopathy

Renal osteodystrophy: low 1a hydroxylase activity, therefore low calcitriol. Secondary hyperparathyroidism. Hypocalcaemia and hyperphosphataemia. Leads to decreased bone depositition with formation of areas of sclerosis.

Endocrine: amenhorrea

Peritoneal dialysis: protein loss, peritornitis

Haemodialysis:

· acute: hypotension,

· chronic: atherosclerosis, sepsis, amyloidosis (due to low removal of B2 microblogulin) and aluminium toxicity form dialysate and potassium binders.

Transplantation and immunosuppression: high BP, opportunistic infections, side effcts of individual drugs (ie, steroids causing CUshings) recurrence of renal disease (eg. Goodpastures)

Question 27

What is the prognosis of CRF?

Answer 27

Depends on complications. Early treatment improves prognosis.

Question 28

What is testicular torsion?

Answer 28

Rotation of testicle aorund vascular pedicle causing strangulation.

Question 29

What is the aetiology of torsion?

Answer 29

Usually this is a torsion of the spermatic cord in a congenitally abnormal testis, often maldescended or hanging like a bell clapper within a completely investing tunica vaginalis.

· Occasionally, true torsion of the testis occurs without involving the cord, when there is an extensive mesorchium between the testis and epididymis.

Torsion is more common in undescended and ectopic testes. It is probably impossible for torsion to occur in an anatomically completely normal testis.

Question 30

What would you find in the history and exam of torsion?

Answer 30

Torsion of the testis is a surgical emergency, which usually occurs in children or adolescents.

· There may be a history of mild trauma to the testis or of previous attacks of pain in the testis due to partial torsion and spontaneous untwisting.

· Cycling, straining, lifting and coitus are typical precipitants.

· Hx: sudden pain in the groin and lower abdomen ,often accompanied by vomiting.

· The abdominal pain occurs because the nerve supply of the testis is mainly from the T10 sympathetic pathway. Rarely, the pain is limited to the abdomen.

· Torsion of right testis can be commonly mistaken for appendicitis, because the testis has not been examined with care, or more often not at all. 


· Examination of the scrotum reveals a swollen testis, painful to touch and lying high in the scrotum.

Question 31

What are the Ddx of torsion?

Answer 31

Epididymitis (acute)
Torsion of testicular appendage
Strangulated inguinal hernia

Question 32

What is acute epididymitis?

Answer 32

o The testis does not lie so high in the scrotum, there is a systemic reaction with pyrexia and leucocytosis and there is usually a history of urinary infection with pus cells and organisms in the urine.

o A useful factor in differential diagnosis is the age of the patient, as torsion of the testis is unusual after the age of 20 years, whereas epididymitis is rare before that age.

Question 33

What is torsion of testicular appendage?

Answer 33

o Two embryological remnants exist around the testis, the appendix testis and the appendix epididymis, which may themselves twist.

o They present in a similar fashion to testicular torsion, but on examination the testis does not lie high in the scrotum, and a dark blue pealike swelling may be visible through the scrotal skin.

Question 34

What is a strangulated inguinal hernia?

Answer 34

o Torsion may also mimic a strangulated inguinal hernia.

o Colour Doppler ultrasound of the testis may be helpful in diagnosis, provided it can be carried out rapidly by an experienced operator, and without delaying surgical exploration.

Question 35

What is the treatment of torsion?

Answer 35

If there is any doubt as to the diagnosis, it is best to explore the testis as soon after admission as possible, because every hour increases the likelihood of irreversible damage to the testis.
If still viable, the testis is untwisted and sutured to the tunica vaginalis. If infarcted, it is removed. In every case, fixation of the other testis should be performed at the same time, since any congenital anomaly is likely to be bilateral and torsion of the opposite testis may therefore occur.

Question 36

What are the complications/ prognosis of torsion?

Answer 36

Untreated, the testis undergoes irreversible infarction within a few hours and there is a typical transudation of blood‐stained fluid into the tunica vaginalis.