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FINALS > RENAL AND UROLOGY > Flashcards

RENAL AND UROLOGY Flashcards

1
Q

which drugs are reported to cause acute interstitial nephritis?

A
  • Penicillin.
  • Rifampicin
  • NSAIDs.
  • Diuretics.
  • Allopurinol.
  • Furosemide.
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2
Q

what are the clinical features of acute interstitial nephritis?

A
  • Fever.
  • Macular rash on neck, torso and back.
  • Oedema.
  • Decreased urinary volume.
  • Gross haematuria in 5%
  • Uveitis in TINU syndrome. It occurs in young females.
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3
Q

what is seen on urinalysis in acute interstitial nephritis?

A
  • White cell casts
  • sterile pyuria
  • low grade proteinuria
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4
Q

how is acute interstitial nephritis treated?

A
  • Discontinue triggering medication.
  • Offer a loop diuretic (furosemide) for treatment of fluid retention.
  • Offer a corticosteroid (prednisolone) to improve rate and extent of renal recovery.
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5
Q

What are the causes of pre-renal uraemia?

A
  • Hypovolaemia due to dehydration, haemorrhage, burns or sepsis.
  • Reduced cardiac output due to cardiac failure, liver failure, sepsis, or drugs.
  • Drugs that reduce blood pressure, circulating volume or renal blood flow, such as diuretics, ACE inhibitors and NSAIDs.
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6
Q

what are the causes of intrinsic uraemia?

A
  • Acute tubular necrosis (penicillin, aminoglycosides such as gentamicin).
  • Glomerulonephritis.
  • Acute interstitial nephritis.
  • Vasculitis
  • HUS
  • TTP
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7
Q

what are the causes of post-renal uraemia?

A
  • Urolithiasis.
  • Obstructed urinary catheter.
  • Enlarged prostate.
  • Tumours and other masses.
  • Neurogenic bladder.
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8
Q

what are the complications associated with AKI?

A
  • uraemia
  • hyperkalaemia
  • Other electrolyte abnormalities such as hyponatraemia, hypocalcaemia, hyperphosphataemia, hypermagnesaemia.
  • metabolic acidosis
  • volume overload
  • CKD
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9
Q

what are the risk factors for AKI?

A
  • People aged 65 years or over.
  • History of AKI.
  • Chronic kidney disease.
  • Symptoms or history of urological obstruction.
  • Chronic conditions such as heart failure, liver disease, and diabetes mellitus.
  • Sepsis
  • Hypovolaemia.
  • Nephrotoxic drugs such as diuretics, ACE inhibitors, metformin, NSAIDs (DAMN mnemonic).
  • Cancer and cancer therapy.
  • Immunocompromise (HIV infection).
  • Exposure to iodinated contrast agents within the past week.
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10
Q

what are the clinical features of AKI?

A
  • Often asymptomatic so easily missed.
  • Oliguria.
  • Hypotension.
  • Dizziness and orthostatic symptoms.
  • Nausea and vomiting.
  • Confusion, fatigue, drowsiness.
  • Pericardial rub.
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11
Q

how is pre-renal uraemia managed?

A
  • Start immediate intravenous fluid resuscitation (500 ml intravenous bolus of crystalloid over 15 minutes) with close monitoring to avoid volume overload.
  • Consider vasopressor support (noradrenaline) if patient remains hypotensive despite adequate volume resuscitation.
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12
Q

how is intrinsic renal uraemia managed?

A
  • refer to nephrology
  • Acute interstitial nephritis requires stopping causative drug and managing with a corticosteroid.
  • Acute glomerulonephritis / vasculitis requires management with a cytotoxic or immunomodulating agent.
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13
Q

how is post-renal uraemia managed?

A
  • Insert a catheter if obstruction is suspected and cannot be quickly ruled out by ultrasound.
  • Insert a 3-way urethral catheter for acute clot retention.
  • Refer to urology for nephrostomy or stenting if the patient has pyonephrosis (hydronephrosis, hydroureter) following renal ultrasound.
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14
Q

which patients with AKI should be referred for renal replacement therapy?

A
  • acidosis
  • refractory hyperkalaemia
  • ingestion of toxins
  • fluid overload
  • signs of uraemia (confusion, pericardial rub).
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15
Q

what are the risk factors for the development of acute phosphate nephropathy?

A
  • CKD
  • Dehydration
  • older age
  • hypertension treated with ACE inhibitors and or ARBs and or loop diuretics
  • female gender
  • NSAIDs.
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16
Q

how is acute phosphate nephropathy diagnosed?

A
  • AKI
  • Recent exposure to oral phosphate
  • Renal biopsy findings of acute and chronic tubular injury with abundant calcium phosphate deposits (usually involving more than 40 tubular lumina in a single biopsy),
  • No evidence of hypercalcaemia
  • No other significant pattern of kidney injury on renal biopsy.
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17
Q

what are the risk factors for acute prostatitis?

A
  • Urinary tract infection.
  • Benign prostatic hyperplasia.
  • Urinary tract instrumentation (biopsy, catheterisation, surgical procedures).
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18
Q

what are the clinical features of acute prostatitis?

A
  • Perineal, penile, or rectal pain.
  • Voiding symptoms such as hesitancy, straining, weak stream.
  • Lower back pain, pain on ejaculation.
  • Fever and malaise.
  • Arthralgia and myalgia.
  • Tender prostate on digital rectal examination.
  • Features of a urinary tract infection (dysuria, frequency, urgency).
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19
Q

how is acute prostatitis managed?

A
  • Offer oral ciprofloxacin (500 mg twice daily for 14 days) as first choice oral antibiotic.
  • Recommend an NSAID (ibuprofen) to relive pain and reduce inflammation.
  • Consider catheterisation for patients with voiding symptoms.
  • Refer to hospital for intravenous ciprofloxacin if the patient develops features of a serious illness (sepsis, acute urinary retention, or abscess) or does not improve after 48 hours of starting the antibiotic.
  • Administer intravenous gentamicin if the patient is critically ill.
  • Consider surgical intervention of a prostatic abscess.
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20
Q

what are the clinical features of acute pyelonephritis?

A
  • Fever.
  • Rigors.
  • Loin pain.
  • Nausea and vomiting.
  • Preceding LUTS such as dysuria, frequency and urgency in ascending infection.
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21
Q

how is acute pyelonephritis managed?

A
  • Offer targeted oral antibiotic therapy (cefalexin or cefixime) for mild-to-moderate symptoms with uncomplicated disease.
  • Offer target intravenous antibiotic therapy (cefuroxime or ceftriaxone) for severe symptoms, complicated disease, or pregnant patients.
  • Administer piperacillin/tazobactam or levofloxacin for resistant organisms in complicated disease.
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22
Q

what are the clinical features of pyelonephritis?

A
  • Fever.
  • Rigors.
  • Loin pain.
  • Nausea and vomiting.
  • Preceding LUTS such as dysuria, frequency and urgency in ascending infection.
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23
Q

how is pyelonephritis managed in adults?

A
  • Offer targeted oral antibiotic therapy (cefalexin, or co-amoxiclav, trimethoprim or ciprofloxacin if culture results show susceptibility) for mild-to-moderate symptoms with uncomplicated disease.
  • Offer target intravenous antibiotic therapy (cefuroxime, ceftriaxone, co-amoxiclav, ciprofloxacin and gentamicin) for severe symptoms, complicated disease, or pregnant patients.
  • Administer piperacillin/tazobactam or levofloxacin for resistant organisms in complicated disease.
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24
Q

how is pyelonephritis managed in children?

A
  • In children over 3 months, first choice oral antibiotic is cefalexin or co-amoxiclav
  • First choice IV antibiotics include co-amoxiclav (only if sensitive and in combination), cefuroxime, ceftriaxone and gentamicin
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25
Q

what are the ischaemic causes of acute tubular necrosis?

A
  • Systemic hypoperfusion of the kidneys associated with haemorrhage, burns, and severe dehydration.
  • Pump failure, such as in myocardial infarction and cardiac tamponade.
  • Peripheral vasodilation, such as in sepsis and anaphylaxis
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26
Q

what are the toxic causes of acute tubular necrosis?

A
  • Aminglycosides (gentamicin).
  • NSAIDs
  • Myoglobin secondary to rhabdomyolysis (falls, prolonged seizures, statins).
  • Chemotherapeutic agents.
  • Heavy metals such as lead and mercury.
  • Endogenous filtered portions, such as haemoglobinuria, myoglobinuria, monoclonal light chains (myeloma kidney).
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27
Q

what are the clinical features of acute tubular necrosis?

A
  • Oliguria and anuria.
  • Hypotension.
  • Tachycardia.
  • Anorexia.
  • Malaise.
  • Nausea and vomiting.
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28
Q

how is acute tubular necrosis managed?

A
  • Treat underlying cause of volume contraction or blood loss.
  • Nephrotoxins should be ceased, or if this is not possible, decreased.
  • Administer intravenous volume expansion (sodium chloride) in patients who are haemodynamically unstable.
  • Consider use of vasopressors (noradrenaline) in conjunction with fluids, in patients with vasomotor shock.
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29
Q

what are the clinical features of Alport’s syndrome?

A
  • Gross haematuria.
  • Peripheral oedema.
  • Lenticonus (protrusion of the lens).
  • Sensorineural hearing loss.
  • Fatigue.
  • Malaise.
  • Breathlessness.
  • Hypertension.
  • Foamy urine.
  • Visual disturbances.
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30
Q

how is Alport’s syndrome managed?

A
  • Offer an ACE inhibitor (enalapril) for patients with proteinuria with or without hypertension.
  • Offer dialysis and consider renal transplant for chronic renal failure.
  • Refer to an ophthalmologist and audiologist for visual disturbances and sensorineural hearing loss respectively
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31
Q

what are the clinical features of amyloidosis?

A
  • Lower extremity oedema.
  • Jugular venous distension.
  • Periorbital purpura.
  • Macroglossia.
  • Fatigue.
  • Weight loss.
  • Dyspnoea on exertion.
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32
Q

how is amyloidosis diagnosed?

A

-Perform kidney and heart biopsy to confirm the diagnosis: Positive green birefringence when stained with Congo red.

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33
Q

how is amyloidosis managed?

A
  • Offer myeloblative chemotherapy (melphalan).

- Offer stem cell transplantation for patients who are younger than 70 and have minimal heart failure.

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34
Q

what are the risk factors for the development of balanitis?

A
  • Congenital or acquired dysfunctional foreskin.
  • Uncircumcised state.
  • Poor hygiene
  • Over-washing.
  • HPV infection.
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35
Q

what is balanitis?

A

-inflammation of the glans penis and prepuce

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36
Q

what are the clinical features of balanitis?

A
  • Pruritus.
  • Pain or soreness.
  • Dribbling.
  • Red-scaly patches.
  • Erosions
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37
Q

how is balanitis managed?

A
  • Offer topical hydrocortisone for atopic eczema, contact dermatitis, and psoriasis.
  • Offer topic clobetasol for lichen sclerosis.
  • Offer intramuscular ceftriaxone (or oral cefixime) and oral azithromycin for gonorrhoea.
  • Offer topical ketoconazole for candidiasis.
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38
Q

what are the clinical features of BPH?

A
  • Storage symptoms such as frequency, urgency, nocturia.

- Voiding symptoms such as weak stream, hesitancy, straining, incomplete emptying, terminal dribbling.

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39
Q

what is found on DRE in BPH?

A
  • Asymmetrical enlargement of the lateral lobes
  • Firm rubbery consistency
  • Palpable median groove.
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40
Q

how is BPH managed?

A
  • Offer a behavioural management programme for all patients, which encourages limitation of fluids, bladder training, and treatment of constipation.
  • Manage with ‘watchful waiting’ for mild voiding symptoms
  • Offer an alpha blocker (tamsulosin) as first-line
  • Offer a 5-alpha reductase inhibitor (finasteride) as first line medical treatment in patients with larger prostates
  • Offer combination therapy (tamsulosin + finasteride) for patients who have prostatic enlargement and moderate-to-severe voiding symptoms.
  • Consider adding an antimuscarinic (oxybutynin or tolterodine) for patients who have a mixed picture of both voiding and storage symptoms.
  • Consider urethral catheterisation if medical treatment fails to relieve symptoms.
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41
Q

what are the risk factors for bladder cancer?

A
  • smoking
  • Aromatic amines (anilin dye) used in rubber and dye industries.
  • Polycyclic aromatic hydrocarbons used in aluminium, coal, and roofing industries.
  • Arsenic in drinking water.
  • Pioglitazone.
  • Exposure of the urothelium to carcinogens causes transformation of these cells.
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42
Q

what are the clinical features of bladder cancer?

A
  • Painless haematuria in low-grade tumours.
  • Dysuria (burning) in high-grade tumours.
  • Urinary frequency occurs rarely.
  • Weight loss.
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43
Q

how is bladder cancer diagnosed?

A

-cystoscopy with biopsy

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44
Q

how should non-muscle invasive bladder tumours be treated?

A
  • Perform transurethral resection.

- Administer immediate post-operative intravesical chemotherapy (mitomycin).

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45
Q

how should locally invasive bladder tumours be managed?

A
  • Perform radical cystoprostatectomy in men and radical cystectomy and hysterectomy in women.
  • Offer postoperative chemotherapy (methotrexate, vinblastine, doxorubicin, cisplatin).
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46
Q

what are the causes of CKD?

A
  • diabetes
  • hypertension
  • Cystic disorders of the kidneys such as polycystic kidney disease.
  • Glomerular nephrotic and nephritic syndromes.
  • Nephrotoxic drugs such as aminoglycosides, ACE inhibitors, and bisphosphonates.
  • Multi-system diseases such as SLE, vasculitis, and myeloma.
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47
Q

what complications are associated with CKD?

A
  • anaemia
  • renal osteodystrophy
  • hyperkalaemia
  • secondary or tertiary hyperparathyroidism
  • metabolic acidosis
  • pruritus
  • gout and uraemic pericarditis
  • dialysis dementia
  • malignancy
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48
Q

what are the symptoms of progressive CKD?

A
  • Fatigue.
  • Oedema.
  • Nausea and vomiting.
  • Pruritus.
  • Restless leg syndrome.
  • Anorexia.
  • Arthralgia.
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49
Q

what are the signs of progressive CKD?

A
  • Uraemic odour (ammonia-like smell of breath).
  • Pallor.
  • Cachexia.
  • Cognitive impairment.
  • Dehydration and hypovolaemia.
  • Tachypnoea.
  • Hypertension.
  • Peripheral neuropathy.
  • Frothy urine.
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50
Q

how is stage 1 CKD defined?

A

eGFR >90

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51
Q

how is stage 2 CKD defined?

A

eGFR 60-89

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52
Q

how is stage 3a CKD defined?

A

eGFR 45-59

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53
Q

how is stage 3b CKD defined?

A

eGFR 30-44

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54
Q

how is stage 4 CKD defined?

A

eGFR 15-29

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55
Q

how is stage 5 CKD defined?

A

eGFR <15

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56
Q

what drug management should be implemented in CKD?

A
  • Recommend lifestyle and diet advice such as exercise, achieving a healthy weight and smoking cessation, as well as advice about potassium, calorie and salt intake.
  • Offer an ACE inhibitor (lisinopril) for its renoprotective effects and to keep the blood pressure below 140/90 mmHg in patients with an ACR of less than 70 mg/mmol, and below 130/80 in patients with an ACR of more than 70 mg/mmol.
  • statin therapy
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57
Q

when should an ACE inhibitor be stopped in CKD?

A
  • Serum potassium rises above 6.0 mmol/litre. Reduce the dose if serum potassium rises above 5.0 to 5.9 mmol.litre.
  • eGFR decrease of 25% or more. Do not modify dose if eGFR decreased by less than 25%.
  • Serum creatinine increases more than 30%. Do not modify if serum creatinine increase is less than 30%.
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58
Q

how is anaemia in CKD managed?

A
  • Offer intravenous epoeitin alfa for the treatment of anaemia of erythropoeitin deficiency.
  • Offer intravenous ferrous sulfate for the treatment of iron-deficiency anaemia.
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59
Q

what are the complications associated with haemodialysis?

A
  • Hypotension.
  • Anaphylactic reactions to sterilising agents (ethylene oxide).
  • Air embolus.
  • Dialysis diathesis syndrome due to cerebral oedema.
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60
Q

what are the contraindications to peritoneal dialysis?

A
  • Previous peritonitis causing peritoneal adhesions
  • The presence of a stoma
  • Active intrabdominal sepsis
  • Abdominal hernia
  • Visual impairment
  • Severe arthritis of the hands
  • Crohn’s disease
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61
Q

what are the clinical features of chronic prostatitis?

A
  • Pain or discomfort lasting at least 3 months in the:
  • –Perineum.
  • –Inguinal or suprapubic region.
  • –Scrotum, testis, or penis.
  • –Lower back, abdomen, or rectum.
  • LUTS such as voiding symptoms (straining, hesitancy, weak stream) and storage symptoms (urgency, frequency, nocturia).
  • Sexual dysfunction symptoms such as erectile dysfunction, premature ejaculation, pain during ejaculation, decreased libido.
  • Psychosocial symptoms such as anxiety, stress and depression.
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62
Q

how is chronic pelvic pain in men managed?

A
  • Offer paracetamol or an NSAID for pain relief.

- Offer an alpha blocker (tamsulosin) for 4-6 weeks for significant LUTS.

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63
Q

how is chronic bacterial prostatitis managed?

A
  • Refer to a urologist for specialist assessment.
  • Offer a stool softener (lactulose) if defecation if painful.
  • Offer a single course of antibiotic treatment (trimethoprim or doxocycline) while awaiting referral.
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64
Q

what are the clinical features of chronic pyelonephritis?

A
  • History of vesicoureteral reflux.
  • History of acute pyelonephritis.
  • History of renal obstruction.
  • Nausea.
  • Elevated blood pressure.
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65
Q

how is chronic pyelonephritis managed?

A
  • No specific treatment of pyelonephritis is possible, however treatment of underlying cause (infection or obstruction) is important treated to prevent further damage.
  • Offer percutaneous drainage and intravenous ceftriaxone for emphysematous pyelonephritis.
  • Offer nephrectomy and intravenous ceftriaxone for xanthogranulomatous pyelonephritis.
  • Offer isoniazid with pyridoxine, rifampicin, pyrazinamide and ethambutol for tuberculous pyelonephritis
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66
Q

what are the causes of hypomagnesaemia?

A
  • Bartter’s syndrome.
  • Familial hypomagnesaemia, hypercalciuria and nephrocalcinosis (FHHNC).
  • Malabsorption.
  • Malnutrition.
  • Drugs such as diuretics, digoxin, and proton pump inhibitors.
  • Diabetic ketoacidosis.
  • Hyperaldosteronism.
  • Syndrome of inappropriate ADH secretion.
  • Severe diarrhoea.
  • Acute pancreatitis.
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67
Q

what are the clinical features of hypomagnesaemia?

A
  • Irritability.
  • Tremor.
  • Carpopedal spasm.
  • Hyperreflexia.
  • Confusional and hallucinatory states.
  • ECG shows prolonged QT interval and broad flattened T waves.
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68
Q

how is hypomagnesaemia managed?

A
  • Withdrawal of precipitating agents such as diuretics.
  • If symptomatic give a parenteral infusion of 50 mmol of magnesium chloride in 1 L of 5% glucose or other isotonic fluid over 12-24 hours.
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69
Q

what are the causes of hypermagnesaemia?

A
  • Patients with acute or chronic kidney disease given magnesium-containing laxatives or antacids.
  • Magnesium-containing enemas.
  • Adrenal insufficiency.
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70
Q

what are the clinical features of hypermagnesaemia?

A
  • Weakness.
  • Hyporeflexia.
  • Narcosis.
  • Respiratory paralysis.
  • Cardiac conduction defects.
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71
Q

how is hypermagnesaemia managed?

A
  • Withdrawal of magnesium therapy.
  • An intravenous injection of 10ml of calcium gluconate 10%.
  • Glucose and insulin (as for hyperkalaemia).
  • Dialysis in patients with severe kidney disease.
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72
Q

what are the causes of hypophosphataemia?

A
  • Primary hyperparathyroidism.
  • Osteomalacia and rickets.
  • Vitamin D deficiency.
  • Respiratory alkalosis,
  • Refeeding syndrome.
  • Dent’s disease.
  • Diuretics
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73
Q

what are the clinical features of hypophosphataemia?

A
  • Diaphragmatic weakness.
  • Decreased cardiac contractility.
  • Skeletal muscle rhabdomyolysis.
  • Left shift in oxyhaemoglobin dissociation curve (reduced 2,3-BPG).
  • Haemolysis.
  • Confusion.
  • Hallucinations.
  • Convulsions.
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74
Q

how is hypophosphataemia managed?

A
  • Combined therapy with phosphate supplementation and calcitriol administration.
  • Administer intravenous phosphate at a maximum rate of 9 mmol every 12 hours.
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75
Q

what are the causes of hyperphosphataemia?

A
  • Chronic kidney disease.
  • Phosphate-containing enemas.
  • Tumour lysis and rhabdomyolysis
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76
Q

how is hyperphosphataemia managed?

A

-Gut phosphate binder for chronic hyperphosphataemia.

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77
Q

what are the risk factors for epididymitis?

A
  • Unprotected sexual intercourse.
  • Benign prostatic hyperplasia.
  • Catheterisation and cystoscopic procedures.
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78
Q

what are the clinical features of epididymitis?

A
  • Unilateral scrotal pain and swelling that develops over a few days.
  • Pain is relieved through scrotal elevation.
  • Tenderness.
  • Hot, erythematous, swollen, hemiscrotum.
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79
Q

how is epididymitis managed?

A
  • Offer intramuscular ceftriaxone and oral azithromycin for suspected gonorrhoea.
  • Offer oral doxycycline for suspected chlamydia.
  • Offer ofloxacin for suspected enteric organisms.
  • Supportive measures include:
  • –Paracetamol.
  • –Bed rest.
  • –Scrotal elevation (supportive underwear).
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80
Q

is focal segmental glomerulosclerosis nephrotic or nephritic?

A

-Nephrotic

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81
Q

what are the clinical features focal segmental glomerulosclerosis?

A
  • Perform urinalysis: Proteinuria.
  • Measure urine protein/creatinine ratio: More than 2.
  • Perform 24-hour urinary protein: More than 3g per 24 hours inn symptomatic patients.
  • Measure serum albumin: Low.
  • Perform a serum lipid profile: Elevated triglyceride and cholesterol.
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82
Q

how is focal segmental glomerulosclerosis managed?

A
  • Offer an ACE inhibitor (enalapril) for asymptomatic patients with proteinuria < 3g/24 hours.
  • Offer a corticosteroid (prednisolone 1 mg/kg orally once daily) for symptomatic patients or proteinuria > 3g/24 hours. Offer an adjunct ACE inhibitor.
  • Give adjunct furosemide and a statin.
  • Offer cyclosporin as a second line management in symptomatic patients who do not achieve remission after 4 months of steroid treatment. These patients should be treated for 4 to 6 months.
  • Consider mycophenolate in patients with steroid resistant disease, who cannot tolerate cyclosporin.
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83
Q

what is haemolytic uraemic syndrome?

A

a triad of acute renal failure, microangiopathic haemolytic anaemia and thrombocytopenia.

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84
Q

what are the clinical features of HUS?

A
  • Bloody diarrhoea.
  • Abdominal pain.
  • Nausea.
  • Vomiting.
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85
Q

what is seen on FBC and blood film in HUS?

A
  • anaemia
  • thrombocytopenia
  • Schistocytes
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86
Q

how is HUS managed?

A
  • Administer an intravenous crystalloid (sodium chloride).
  • Perform a red cell transfusion for anaemia.
  • Perform plasmapheresis or plasma infusion for acute kidney injury.
  • Consider renal transplantation for irreversible acute kidney injury.
  • Offer eculizumab for patients with atypical HUS.
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87
Q

what are the clinical features of a hydrocele?

A
  • Scrotal swelling that is soft and non-tender.
  • Transillumination.
  • Swelling enlarges throughout day and with increased intra-abdominal pressure (coughing, straining, crying).
  • Testes may not be palpable.
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88
Q

how is a hydrocele managed in children under 2?

A

-Observation is appropriate as most resolve spontaneously

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89
Q

how is a hydrocele managed in children between 2 and 11?

A

-Perform elective surgical repair for persistence of a hydrocele beyond 2 years of age to avoid complications.

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90
Q

how is a hydrocele managed in an adolescent?

A
  • Observation is appropriate.
  • Perform elective surgical repair only if the hydrocele is very large and uncomfortable.
  • Perform aspiration for post-varicocelectomy.
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91
Q

how is a hydrocele managed in adults?

A
  • Observation is appropriate.

- Perform elective surgical repair only if the hydrocele is very large and uncomfortable.

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92
Q

what are the causes of decreased renal excretion of potassium?

A
  • Acute kidney injury or chronic kidney disease as the GFR begins to decline below 60 ml/ minute.
  • Reduction in plasma aldosteronism, such as Addison’s disease.
  • Pseudohypoaldosteronism, such as Gordon’s syndrome, which is a mirror image of Gitelman’s syndrome.
  • Drugs such as potassium sparing diuretics, NSAIDs, ACE inhibitors, heparin and trimethoprim.
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93
Q

what are the causes of decreased cellular entry of potassium?

A
  • Metabolic acidosis in exchange for hydrogen ions.
  • Hyperglycaemia due to hyperosmolarity.
  • Digoxin overdose which inhibits Na+-K+-ATPase.
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94
Q

what are the clinical features of hyperkalaemia?

A
  • Muscle weakness.
  • Kussmaul respiration when associated with metabolic acidosis.
  • Hypotension.
  • Bradycardia.
  • Sudden death from systolic cardiac arrest.
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95
Q

what is seen on ECG in hyperkalaemia?

A
  • Peaked T waves
  • Wide QRS complex
  • Sine wave appearance which indicates pre-arrest
  • Prolonged PR interval
  • Reduced P waves
  • Ventricular fibrillation
  • Asystole.
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96
Q

what is the management of hyperkalaemia?

A
  • Eliminate the source of hyperkalaemia.
  • Administer 10% calcium chloride or gluconate to block the membrane effects of hyperkalaemia.
  • Administer nebulised salbutamol or intravenous insulin/glucose to lower the serum potassium value.
  • –This should be done urgently if potassium is greater than 6.5mmol/l or in the presence of ECG changes

-Offer a potassium exchange resin (sodium zirconium cyclosilicate) as maintenance therapy to keep potassium down after emergency treatment.

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97
Q

what are the causes of hypernatraemia?

A
  • free water loss (diabetes insidious, diarrhoea, peritoneal dialysis)
  • inadequate free water intake
  • sodium overload
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98
Q

what are the clinical features of hypernatraemia?

A
  • Nausea and vomiting.
  • Confusion.
  • Fever.
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99
Q

how can urine osmolality aid the diagnosis of hypernatraemia?

A
  • Less than 150 mmol/kg indicates diabetes insipidus.
  • 200 - 500 mmol/kg indicates renal concentrating defect.
  • More than 500 mmol/kg indicates pure volume depletion.
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100
Q

how is hypernatraemia managed?

A
  • Administer desmopressin in ADH deficiency.
  • Give slow infusion of 0.9% saline in severe hypernatraemia typically caused by severe volume depletion.
  • Administer dextrose 5% for most patients who do not have severe or symptomatic hypernatraemia.
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101
Q

what are the causes of increased potassium excretion?

A
  • Loss of potassium from the GI tract including vomiting, villous adenoma or a vasoactive intestinal peptide secreting tumour.
  • Renal loss of potassium include loop and thiazide diuretic therapy, primary hyperaldosteronism, salt-wasting nephropathies, and metabolic acidosis.
  • Skin loss due to sweating, cystic fibrosis, burns, eczema or psoriasis.
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102
Q

what are the causes of increased potassium entry into cells?

A
  • metabolic or respiratory alkalosis
  • Beta-adrenergic activity
  • insulin
  • anabolic states
  • hypothermia
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103
Q

what are the clinical features of hypokalaemia?

A
  • Usually asymptomatic.
  • Muscle weakness in severe hypokalaemia.
  • Atrial and ventricular ectopic beats.
  • Increased risk of digoxin toxicity.
  • Rhabdomyolysis.
  • Interstitial renal disease.
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104
Q

what are the ECG features of hypokalaemia?

A
  • Treat the underlying cause.
  • Offer slow release oral potassium replacement for severe hypokalaemia.
  • For severe hypokalaemia where there is arrhythmia, muscle weakness, or severe DKA:
  • –Give 40 mmol intravenous potassium chloride over 4 hours (a rate that does not exceed 10 mmol/hour).
  • –Give 3 bags of 0.9% saline.
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105
Q

what are the causes of hyponatraemia with hypovolaemia?

A
  • Gastrointestinal fluid loss such as severe diarrhoea (Legionnaire’s disease) or vomiting.
  • Third spacing of fluids, such as in pancreatitis.
  • Addison’s disease.
  • Salt-wasting nephropathy.
  • Cerebral salt wasting syndrome.
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106
Q

what are the causes of hyponatraemia with euvolaemia?

A
  • Medications such as thiazide diuretics, vasopressin, and antidepressants.
  • Hypothyroidism.
  • Syndromes of inappropriate ADH secretion, resulting from malignancy, CNS disorders, pulmonary disease.
  • High fluid intake due to prolonged physical activity, surgery, or primary polydipsia, or beer potomonia.
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107
Q

what are the causes of hyponatraemia with hypervolaemia?

A
  • Acute kidney injury and chronic kidney disease.
  • Congestive heart failure.
  • Cirrhosis.
  • Nephrotic syndrome.
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108
Q

what is the cause of pseudohyponatraemia?

A
  • high serum or lipid levels

- hyperosmolarity due to severe hyperglycaemia.

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109
Q

what are the clinical features of acute hyponatraemia?

A
  • Nausea and vomiting.
  • Seizures.
  • Coma.
  • Confusion.
  • Headache.
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110
Q

what are the clinical features of chronic hyponatraemia?

A
  • Gait instability.
  • Falls.
  • Concentration and cognitive deficits.
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111
Q

how can the different types of hyponatraemia be distinguished using serum osmolality?

A
  • Less than 275 mmol/kg indicates hypotonic hypernatraemia
  • More than 295 indicates hypertonic hypernatraemia
  • Normal serum osmolality suggests pseudohyponatraemia.
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112
Q

how can urine sodium concentration distinguish the cause of hypovolaemic hyponatraemia?

A
  • More than 20 mmol/L indicates renal sodium loss (e.g. diuretics)
  • Less than 20 mmol/L indicates extrarenal sodium loss (e.g. GI loss).
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113
Q

how can urine sodium concentration distinguish the cause of hypervolaemic hyponatraemia?

A
  • More than 20 mmol/L indicates AKI or CKD

- Less than 20 mmol/L indicates heart failure, liver failure, or nephrotic syndrome.

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114
Q

how is hypernatraemia managed?

A
  • Administer hypertonic (3%) saline infusion for acute or symptomatic hyponatraemia over 10 minutes.
  • Administer isotonic (0.9%) saline infusion for hypovolaemic hyponatraemia at a rate of 3-6 mmol/L/day.
  • Ensure fluid restriction for hypervolaemic or euvolaemic hyponatraemia. Consider a vasopressin receptor antagonist (tolvaptan) if fluid restriction fails.
  • Stop treatment and administer desmopressin if there is an overcorrection serum sodium concentration of more than 8 - 12 mmol/L/day.
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115
Q

what are the clinical features of HSP?

A
  • fever
  • rash, characteristically palpable and symmetrically distributed over the buttocks, arms, legs and ankles.
  • joint pain
  • periarticular oedema
  • colicky abdominal pain
  • haematemesis and melaena
  • intussusception
  • IgA nephropathy
116
Q

how is HSP managed?

A
  • Offer prednisolone for severe oedema or abdominal pain

- Offer methylprednisolone sodium succinate and cyclophosphamide for rapidly progressive nephritis

117
Q

what are the clinical features of HSP?

A
  • Microscopic and sometimes macroscopic haematuria following an upper respiratory tract infection.
  • Proteinuria, which is rarely nephrotic, and rarely causes oedema.
  • Hypertension in chronic kidney disease.
  • Haematuria.
118
Q

how is IgA nephropathy managed?

A
  • Observe patients with low risk of progression (proteinuria less than 0.5 grams per day).
  • Offer ACE inhibitors (captopril) for patients with medium risk of progression (proteinuria less than 1 gram per day).
  • Offer prednisolone to patients with high risk of progression, who have proteinuria greater than 1 gram per day following ACE inhibitor therapy.
  • Offer combined immunosuppressive therapy (prednisolone, cyclophosphamide and azathioprine for patients presenting with acute kidney injury with crescentic IgA nephropathy.
119
Q

what are the clinical features of lupus nephritis?

A
  • Oedema.
  • hypertension
  • features of SLE
120
Q

is lupus nephritis a nephritic or nephrotic syndrome?

A

nephritic

121
Q

how is lupus nephritis managed?

A
  • Offer cyclophosphamide, prednisolone and hydroxychloroquine to induce remission.
  • Offer mycophenolate motefil and prednisolone as a maintenance regimen.
122
Q

what are the clinical features of membranous nephropathy?

A
  • Oedema of the lower extremities and peri-orbital regions.
  • Xanthelasma.
  • Foamy urine.
  • Hypertension.
123
Q

what is seen on silver staining in membranous nephropathy?

A

-Black spikes

124
Q

how is membranous nephropathy managed?

A
  • Offer an ACE inhibitor (enalapril) and recommend a low-salt diet for hypertension.
  • Offer a statin (simvastatin) for hyperlipidaemia.
  • Offer a loop diuretic (furosemide) for oedema.
  • Consider prednisolone and cyclophosphamide only where there is declining renal function.
125
Q

Define metabolic acidosis

A
  • a pH of less than 7.35
  • a decrease in plasma bicarbonate and or a marked increase in the serum anion gap.
  • It occurs due to the accumulation of an acid other than carbonic acid.
126
Q

what are the causes of a metabolic acidosis with a normal anion gap?

A
  • Diarrhoea due to increased GI bicarbonate loss).
  • Renal tubular acidosis.
  • Addison’s disease.
127
Q

how is plasma anion gap calculated?

A

{[Na+] + [K+]} - {[HCO3-] + [Cl-]}

128
Q

how can the causes of a metabolic acidosis with a normal anion gap be distinguished from each other?

A
  • Diarrhoea causes a decreased urinary anion gap

- Renal tubular acidosis causes an increased urinary anion gap

129
Q

how is urinary anion gap calculated?

A

{Urinary [Na+] + Urinary [K+] - Urinary [Cl-]}

130
Q

what are the causes of a metabolic acidosis with a high anion gap?

A
  • Uraemic acidosis (sulfate and phosphate) due to kidney failure.
  • Lactic acidosis (lactate) due to sepsis following tissue hypoxia or metformin accumulation.
  • Ketoacidosis (acetoacetic acid) due to insulin deficiency, alcohol excess, and starvation.
  • Salicylate (aspirin) and alcohol toxicity.
  • A mixed picture is seen in cholera, where gastrointestinal loss of bicarbonate causes a normal anion gap acidosis, but the anion gap is often increased owing to renal failure and lactic acidosis as a result of hypovolaemia.
131
Q

how is metabolic acidosis managed?

A
  • Offer oxygen therapy in lactic acidosis due to poor tissue perfusion.
  • Offer insulin in diabetic ketoacidosis.
  • Offer ethanol in methanol and ethylene glycol poisoning.
  • Offer dialysis for removal of salicylates.
  • Consider administration of intravenous sodium bicarbonate when H+ is above 126 nmol/L (pH < 6.9).
132
Q

what is a metabolic alkalosis?

A
  • an arterial pH of more than 7.45

- increase in plasma bicarbonate level.

133
Q

what are the causes of a chloride responsive metabolic alkalosis?

A
  • Vomiting.
  • Gastric drainage.
  • Villous adenoma of the colon.
  • Cystic fibrosis.
  • Post-diuretic therapy.
  • Post-hypercapnia.
134
Q

what are the causes of a chloride resistant metabolic alkalosis?

A
  • potassium depletion
  • Primary hyperaldosteronism.
  • Secondary hyperaldosteronism.
  • Renal artery stenosis.
  • Cushing’s syndrome.
  • Liddle’s syndrome.
  • Bartter’s syndrome.
  • Gitelman’s syndrome.
  • Current loop or thiazide diuretic therapy.
  • Post starvation refeeding syndrome.
135
Q

how is chloride responsive metabolic alkalosis treated?

A
  • Administer isotonic saline therapy if there is extracellular depletion.
  • Administer hydrochloride acid or ammonium chloride if there is fluid overload.
136
Q

how is chloride resistant metabolic alkalosis treated?

A
  • Offer oral potassium chloride for mild to moderate hypokalaemia.
  • Offer intravenous potassium chloride for severe hypokalaemia, with the presence of cardiac arrhythmia or generalised weakness.
137
Q

what are the complications associated with minimal change disease?

A
  • Bacterial infections such as Pneumococcus pneumonia, due to loss of immunoglobulin in the urine.
  • Renal vein thrombosis due to hyper-coagulability of the blood
  • Hypertension.
138
Q

what are the clinical features of minimal change disease?

A
  • Facial oedema (puffy eyes in the morning)
  • Scrotal, vulval, leg and ankle oedema
  • Anasarca (oedema involving the entire body).
  • Ascites
  • Breatlessness
  • Xanthelasmata.
139
Q

how is minimal change disease managed?

A
  • Offer prednisolone 60 mg per square metre of body surface area daily for either 6 weeks or until urine is protein-free for 3 days, followed by 40 mg per square metre of body surface area for 4 weeks on alternate days as the first line treatment.
  • Recommend a low salt diet and fluid restriction.
140
Q

when should steroid sparing agents be given and give examples of these drugs

A
  • With frequent relapse.
  • Who are unresponsive to steroids.
  • Who have severe steroid side effects.
    e. g. cyclophosphamide, levamisole, tacrolimus, ciclosporin, mycophenolate mofetil
141
Q

what is phimosis?

A

the prepuce cannot be retracted over the glans penis

142
Q

what is paraphimosis?

A
  • when a tight prepuce is retracted behind the glans

- leading to obstruction of the venous return from the glans and the prepuce.

143
Q

what are the risk factors for development of a phimosis or paraphimosis?

A
  • Lack of circumcision.
  • Urinary catheterisation.
  • Phimosis .
  • Poor hygiene.
  • Bacterial or parasitic infection.
  • Diabetes.
  • Haemangiomas.
144
Q

what are the clinical features of phimosis/paraphimosis?

A
  • Penile pain.
  • Band of retracted foreskin tissue beneath the glans.
  • Swollen glans penis.
  • Indwelling catheter.
  • Erythema.
  • Voiding symptoms e.g. ballooning on micturition
145
Q

how is phimosis/paraphimosis managed?

A
  • Perform emergency surgery if there is ischaemia and necrosis.
  • If there is not ischaemia or necrosis:
  • Perform manual manipulation to reduce swelling and to replace foreskin over the glans penis as first line management.
  • Perform the puncture technique as second line management.
  • Perform surgical reduction and circumcision (or preputioplasty in older boys who are able to regular retract their own forskin) as third line management.
146
Q

what are the medical indications for circumcision?

A
  • recurrent balanoposthitis
  • recurrent UTI
  • phimosis
147
Q

what are the complications associated with ADPKD?

A
  • Pain
  • Cyst infection.
  • Renal calculi.
  • Hypertension.
  • Progressive chronic kidney disease.
  • Polycystic liver disease (most common)
  • Berry aneurysms development and rupture leading to subarachnoid haemorrhage.
  • Mitral valve regurgitation.
148
Q

what are the clinical features of ADPKD?

A
  • Family history of ADPKD.
  • Family history of subarachnoid haemorrhage.
  • Acute loin pain or haematuria owing to haemorrhage into a cyst, cyst infection or stone formation.
  • Loin discomfort owing to increase size of the kidneys.
  • Dysuria, suprapubic pain, fever owing to UTI.
  • Hypertension
  • hepatomegaly
  • cardiac murmur
149
Q

what are the diagnostic criteria on USS on ADPKD?

A
  • Younger than 30: 3 or more unilateral or bilateral cysts.
  • Between 30 and 59 years of age: At least 2 cysts in each kidney.
  • Over 60: At least 4 cysts in each kidney.
150
Q

How is ADPKD screened for in asymptomatic people with positive family history?

A

-ultrasound kidney

151
Q

how is ADPKD managed?

A
  • Tolvaptan is recommended as an option for slowing the progression of cyst development and renal insufficiency in the presence of stage 2 or 3 CKD or rapidly progressing disease.
  • For hypertension: ACE inhibitor (captopril) or ARB (losartan).
  • For UTI: Antibiotic therapy (nitrofurantoin or trimethoprim).
  • For infected renal or hepatic cysts: Antibiotic therapy (ciprofloxacin).
  • For end-stage rental disease: Renal transplant
152
Q

how long after an streptococcal throat infection does post-streptococcal glomerulonephritis occur?

A

-2 weeks

153
Q

what are the clinical features of post-streptococcal glomerulonephritis?

A
  • Macroscopic haematuria 2 weeks following a streptococcal throat infection (nephritic syndrome).
  • Proteinuria that may be severe enough to produce nephrotic syndrome.
  • Oliguria.
  • Oedema.
  • Hypertension.
  • Headache and malaise.
154
Q

how is post-streptococcal glomerulonephritis diagnosed?

A
  • low c3 on measuring complement levels
  • elevated antistreptolysin O antibody
  • sub-epithelial humps on renal biopsy
155
Q

how is post-streptococcal glomerulonephritis managed?

A
  • offer an ACE inhibitor (enalapril) as a first-line treatment to treat hypertension.
  • Offer a loop diuretic (furosemide) and encourage a low-salt diet for oedema.
  • Consider a corticosteroid (prednisolone) if recovery is slow.
156
Q

define priapism

A
  • prolonged and persistent penile erection
  • lasting more than 4 hours
  • unassociated with sexual interest or situation.
157
Q

what are the risk factors for priapism?

A
  • Haemoglobinopathies including sickle cell disease and thalassaemia.
  • Vasoactive drugs including sildenafil, hydralazine, antidepressants and antipsychotic, alcohol, cocaine.
  • Perineal or penile trauma.
  • Malignancies including prostatic adenocarcinoma, urothelial carcinoma.
  • Local infection.
  • Spinal cord disease such as cauda equina syndrome.
158
Q

what are the clinical features of priapism?

A
  • Prolonged erection greater than 4 hours.
  • Rigid and tender penis in ischaemic priapism.
  • Penis is usually neither painful nor tender is non-ischaemic priapism
  • History of risk factors.
159
Q

how does corpus cavernous blood analysis appear in ischaemic priapism?

A
  • Decreased oxygen
  • increased carbon dioxide
  • acidosis
160
Q

how is priapism managed?

A
  • Perform aspiration and administer intracavernosal phenylephrine every 3-5 minutes for ischaemic or stuttering priapism.
  • Perform a surgical penile shunt (Winter shunt) if intracavernosal injection of a sympathomimetic has failed.
  • Perform cavernosal artery embolisation for non-ischaemic priapism.
  • Administer a GnRH agonist (leuprorelin) for recurrent stuttering priapism in adults.
161
Q

what are the risk factors associated with prostate cancer?

A
  • High fat diet.
  • Obesity.
  • Family history of prostate cancer (BRCA2 mutation).
162
Q

what are the clinical features of prostate cancer?

A
  • Lower urinary tract symptoms such as frequency, urgency, hesitancy, terminal dribbling, and or overactive bladder.
  • Lower back pain.
  • Anorexia and weight loss.
  • Haematuria.
  • Lethargy.
  • Erectile dysfunction.
163
Q

when should PSA not be measured?

A
  • active UTI
  • prostate biopsy in the last 6 weeks
  • exercised vigorously within the past 48 hours
  • ejaculated within the past 48 hours
164
Q

how is low-intermediate risk prostate cancer managed?

A
  • watchful waiting
  • active surveillance
  • radical prostatectomy
  • external beam radiotherapy
  • brachytherapy
165
Q

how is high risk prostate cancer managed?

A
  • Offer radical prostatectomy
  • radiotherapy with 6 months of androgen deprivation therapy including a GnRH agonist (goserelin) and androgen receptor blockers (flutamide)
166
Q

what are the risk factors for the development of renal artery stenosis?

A
  • Smoking.
  • Dyslipidaemia.
  • Hypertension.
  • Male gender.
  • Increasing age (greater than 55 years).
  • History of malignant hypertension.
167
Q

what are the clinical features of renal artery stenosis?

A
  • Flash pulmonary oedema.

- Progressively difficult-to-control hypertension

168
Q

how is renal artery stenosis diagnosed?

A
  • abdominal examination: Abdominal bruit lateral to the midline above the umbilicus.
  • Perform duplex ultrasound: Greater than a 50% reduction in vessel diameter.
  • Perform conventional CT or MR angiography: Greater than a 50% reduction in vessel diameter.
169
Q

how is renal artery stenosis managed with atherosclerotic disease?

A
  • Offer an ACE inhibitor (captopril) plus lifestyle modification.
  • Offer a statin (atorvastatin).
  • Offer an anti-platelet agent (aspirin).
  • Consider renal artery stenting if there is refractory hypertension on a multi drug regimen, or progressive chronic kidney disease, or acute kidney injury.
170
Q

how is renal artery stenosis managed with fibromuscular dysplasia?

A
  • Offer an ACE inhibitor (captopril) and percutaneous renal artery balloon angioplasty as the first-line therapy.
  • Offer surgical reconstruction of the renal arteries in complex disease that extends into the segmental arteries.
171
Q

what is the classic triad of symptoms associated with renal cell carcinoma?

A
  • Flank pain
  • Haematuria.
  • Palpable abdominal mass.
172
Q

what are the clinical features, other than the classic triad, of renal cell carcinoma?

A
  • Left sided painless scrotal mass with ‘bag of worms’ appearance
  • Polycythaemia.
  • Vision loss due to von Hippel Lindau disease.
  • Malaise.
  • Anorexia and weight loss.
  • Hypertension due to renin secretion
  • Pyrexia.
173
Q

how is renal cell carcinoma diagnosed?

A

CT abdomen and pelvis

174
Q

how is renal cell carcinoma managed?

A
  • Perform radical nephrectomy, unless there are bilateral tumours or the contralateral kidney functions poorly, in which case conservative surgery such as a partial nephrectomy may be indicated
  • Offer targeted therapy (avelumab with axitininib) for patients with stage 4 metastatic disease.
  • Offer a bisphosphonate (zoledronic acid) for patients with bone metastases.
175
Q

what are the clinical features of Wilms’ tumour?

A
  • Unilateral upper abdominal or flank mass that is painless and non-tender
  • Abdominal distension.
  • Anorexia
  • Abdominal pain
  • Anaemia due to haemorrhage into mass
  • Haematuria
  • Hypertension
176
Q

how is Wilms’ tumour managed?

A
  • initial chemotherapy

- followed by delayed nephrectomy

177
Q

what are the causes of type 1 renal tubular acidosis?

A
  • rheumatoid arthritis
  • systemic lupus erythematosus
  • Sjogren’s syndrome.
178
Q

what are the causes of type 2 renal tubular acidosis?

A
  • Fanconi’s syndrome

- Wilson’s disease

179
Q

what are the causes of type 3 renal tubular acidosis?

A

-hereditary carbonic anhydrase II deficiency

180
Q

what are the causes of type 4 renal tubular acidosis?

A

-aldosterone deficiency

181
Q

what are the risk factors for the development of renal tubular acidosis?

A
  • Childhood.
  • Urinary tract obstruction.
  • Diabetes mellitus.
  • Primary biliary cholangitis.
  • Amphotericin-B therapy.
  • Toxic exposure to heavy metals.
  • Untreated adrenal insufficiency.
182
Q

what are the clinical features of renal tubular acidosis?

A
  • Growth retardation.
  • Failure to thrive.
  • Sensorineural hearing loss.
  • Muscle weakness (due to hyperkalaemia in type 4 renal tubular acidosis).
  • Kussmaul respiration.
183
Q

what is seen on blood gas in renal tubular acidosis?

A
  • serum bicarbonate: Less than 21 mmol/L.
  • arterial blood pH: Less than 7.35
  • normal anion gap
184
Q

how is type 4 renal tubular acidosis managed?

A
  • Offer fludrocortisone as aldosterone replacement.
  • Offer a loop diuretic (furosemide) for patients with mineralocorticoid resistance.
  • Recommend a low potassium diet and the avoidance of salt substitutes.
185
Q

how is type 1 and 2 renal tubular acidosis managed?

A

-Offer sodium bicarbonate and citric acid (Shohl’s solution)

186
Q

what is stage 1 testicular cancer?

A

-tumour confined to testis

187
Q

what is stage 2 testicular cancer?

A

-Involvement of testis and para-aortic lymph nodes

188
Q

what is stage 3 testicular cancer?

A

-Involvement of mediastinal and or supraclavicular nodes

189
Q

what is stage 4 testicular cancer?

A

-Pulmonary or other visceral metastasis.

190
Q

what are the risk factors for developing testicular cancer?

A
  • Crypto-orchidism (failure of testis to descend from abdomen into scrotum)
  • Family history.
  • Infertility.
  • Testicular atrophy.
  • HIV infection.
191
Q

what are the clinical features of testicular cancer?

A
  • Non-specific testicular discomfort.
  • Painless testicular mass that is smooth and firm that does not transilluminate.
  • Bone pain with skeletal metastasis.
  • Low extremity swelling in venous occlusion
  • Supraclavicular lymph node enlargement.
  • Gynaecomastia.
  • Sudden onset painful swelling if there is associated haemorrhage or infection.
192
Q

which testicular tumours secrete beta-hCG?

A
  • seminoma

- choriocarcinoma

193
Q

which testicular tumours secrete AFP?

A
  • embryonal and yolk sac tumours

- teratoma

194
Q

how is testicular cancer managed?

A
  • radical inguinal orchidectomy in patients with a testicular lesion suspicious for malignant neoplasm and a normal contralateral testis.
  • adjuvant carboplatin chemotherapy post orchidectomy for early stage seminoma.
  • retroperitoneal lymph node dissection post-orchidectomy for early stage non- seminoma.
  • post-orchidectomy combination chemotherapy (bleomycin, etoposide and cisplatin) for advanced or metastatic cancer.
  • salvage chemotherapy (vinblastine, ifosfamide, mesna, cisplatin for relapsing disease.
195
Q

what are the clinical features of testicular torsion?

A
  • Severe scrotal pain that is sudden onset, unilateral and not relieved by elevation (absent Prehn sign).
  • Testis may have a transverse lie and may be higher riding than unaffected testis
  • Nausea and vomiting.
  • Absent cremasteric reflex.
  • Scrotal oedema and erythema.
  • Abdominal pain.
196
Q

how is testicular torsion managed?

A
  • Perform surgical exploration and fixation of both testis to optimise testicular salvageability.
  • The contralateral testis is fixed to the posterior wall to prevent bilateral testicular torsion, a bell-clapper deformity is often bilateral
  • Consider manual de-torsion were surgery is not available within 6 hours
  • Consider orchidectomy if there is extensive testicular damage.
197
Q

what are the risk factors for UTI in young/pre-menopausal women?

A
  • Sexual intercourse.
  • UTI in childhood.
  • Mother with a history of UTI
198
Q

what are the risk factors for UTI in elderly/post-menopausal women?

A
  • UTI before menopause.
  • Urinary incontinence.
  • Atrophic vaginitis.
  • Cystocele.
  • Increased post-void urine volume.
  • Urine catheterisation.
199
Q

what are the key clinical features of a UTI in women under 65?

A
  • Dysuria.
  • New nocturia.
  • Cloudy-looking urine.
200
Q

what are the key clinical features of a UTI in women over 65?

A
  • Dysuria.
  • New frequency or urgency.
  • New incontinence.
  • New or worsening delirium.
  • New suprapubic pain.
  • New haematuria.
201
Q

how is UTI managed in women?

A
  • Offer nitrofurantoin 100 mg twice daily for 3 days if eGFR is greater than 45/ml/minute or more.
  • Offer trimethoprim 200 mg twice daily for 3 days if there is a low risk of resistance.
  • Consider pivmecillinam or fosfomycin if there is no improvement in lower UTI symptoms on first choice taken for at least 48 hours, or when first choice is unsuitable.
202
Q

how is UTI managed in pregnancy?

A
  • Offer nitrofurantoin 100 mg twice daily for 7 days in the first and second trimester of pregnancy, as it can cause haemolytic anaemia in the third trimester.
  • Offer amoxicillin (only if cultures show sensitivity) or cefalexin 500 mg twice daily for 7 days if there is no improvement in lower UTI symptoms on first choice taken for at least 48 hours, or when first choice is unsuitable.
  • Offer trimethoprim 200 mg twice daily for 7 days in the second and third trimester of pregnancy, as it can be teratogenic in the first trimester.
203
Q

how should symptomatic catheter associated UTIs be treated?

A
  • consider removing or changing catheter.
  • Offer nitrofurantoin or trimethoprim for 7 days.
  • Consider pivmecillinam if there is no improvement in lower UTI symptoms on first choice taken for at least 48 hours, or when first choice is unsuitable.
204
Q

how should catheter associated UTIs with upper UTI symptoms be treated?

A
  • Offer cefalexin for 7 days.
  • Consider IV cefuroxime if there is no improvement in symptoms on first choice taken for at least 48 hours, or when first choice is unsuitable.
205
Q

what are the risk factors for UTI in men?

A
  • Age over 50 years.
  • Benign prostatic hyperplasia and other causes of urine outflow obstruction (calculi, stricture).
  • Catheterisation.
  • Previous urinary tract surgery.
  • Previous UTI.
  • Anal sex.
  • Diabetes mellitus.
  • Immunosuppression.
  • Recent hospitalisation.
  • Uncircumcised men.
  • Vaginal sex.
206
Q

how is UTI managed in men?

A
  • Prescribe nitrofurantoin 100 mg twice daily for 7 days if eGFR is greater than 45/ml/minute or more.
  • Prescribe trimethoprim 200 mg twice daily for 7 days if there is a low risk of resistance.
207
Q

what are the risk factors for UTI in children?

A
  • Voiding dysfunction (neurogenic bladder, voluntary withholding of urine, chronic constipation, indwelling foreign bodies).
  • Vesicoureteral reflux.
  • Sexual activity.
  • Immunosuppression.
208
Q

what are the clinical features of UTI in infants?

A
  • Fever
  • Vomiting
  • Lethargy or irritability
  • Poor feeding
  • Jaundice
  • Septicaemia
  • Offensive urine
  • Febrile convulsion (>6 months)
209
Q

what are the clinical features of UTI in children?

A
  • Dysuria and frequency
  • Abdominal pain or loin tenderness
  • Fever with or without rigors
  • Lethargy and anorexia
  • Vomiting and diarrhoea
  • Haematuria
  • Offensive or cloudy urine
  • Febrile convulsion
  • Recurrence of enuresis
210
Q

what investigations should be performed in children with suspected UTI?

A
  • urine dipstick
  • MSC
  • ultrasound if atypical UTI
  • If abnormal ultrasound, function scans such as MCUG and DMSA after 4-6 months
211
Q

how is UTI managed in children under 3 months?

A

-Immediate hospital admission for intravenous antibiotics (ampicillin and gentamicin).

212
Q

how is lower UTI managed in children over 3 months?

A
  • Offer trimethoprim if there is low risk of resistance for 3 days.
  • Offer nitrofurantoin if eGFR is greater than 45ml/minute for 3 days.
  • Offer cefalexin for 3 days as a second line option.
213
Q

how is upper UTI managed in children over 3 months?

A
  • Offer cefalexin for 7-10 days.
  • Offer co-amoxiclav for 7-10 days if results are available and susceptible.
  • Offer cefuroxime 7-10 days as a second line option.
214
Q

which drugs promote calcium oxalate stone formation?

A
  • loop diuretics
  • antacids
  • glucocorticoids
  • theophylline
  • acetazolamide
215
Q

which drugs promote rate stone formation?

A
  • Thiazide diuretics

- salicylates

216
Q

what are the risk factors for developing kidney stones?

A
  • Male gender (3:1).
  • White ethnicity.
  • Increasing age, with peak onset between 40 and 60 years.
  • Diet, with excessive intake of oxalate (rhubarb and spinach), urate (alcohol, seafood, meat), sodium (associated with high urinary sodium and calcium levels, and low citrate).
  • Chronic dehydration, fluid intake is inversely proportional to the risk of stone formation.

Obesity.

-Family history.

217
Q

what are the clinical features of kidney stones?

A
  • Abrupt onset of severe unilateral abdominal pain originating in the loin or flank and radiating to the labia in women and to the groin or testicle in men.
  • Painful episode lasts minute to hours and occurs in spasms with intervals of no pain or dull ache.
  • Nausea and vomiting.
  • Haematuria.
  • Recurrent urinary tract infections.
218
Q

how are kidney stones diagnosed?

A
  • CT KUB

- USS first line in pregnancy and children

219
Q

how is pain managed in kidney stones?

A
  • Offer NSAIDs by any route as first line (rectal diclofenac is gold standard)
  • If NSAIDs contraindicated or ineffective, give IV paracetamol
  • If IV paracetamol and NSAIDs contraindicated or ineffective, give opioids
220
Q

how should kidney stones less than 5mm be managed?

A

-watchful waiting

221
Q

how should kidney stones less than 10mm be managed?

A
  • medical expulsion therapy with an alpha blocker (tamsulosin)
  • shock wave lithotripsy
  • ureteroscopy in pregnancy only
222
Q

how should kidney stones more than 10mm be managed?

A

-ureteroscopy

223
Q

how should kidney stones more than 20mm be managed?

A

-percutaneous nephrolithotomy

224
Q

what is a varicocele?

A

an abnormal dilation of the internal spermatic veins and pampiniform plexus of veins around the spermatic cord.

225
Q

what are the clinical features of a varicocele?

A
  • Painless scrotal mass, typically on the left side.
  • Palpation above the testicle reveals a ‘bag of worms’ appearance.
  • Small testicle.
  • Reduced fertility.
226
Q

what is a grade 1 varicocele?

A

only palpable with Valsalva manoeuvre

227
Q

what is a grade 2 varicocele?

A

palpable without Valsalva manoeuvre.

228
Q

what is a grade 3 varicocele?

A

visible through the scrotal skin.

229
Q

what is a subclinical varicocele?

A

only detected by Doppler ultrasound.

230
Q

how is a varicocele managed?

A
  • Offer reassurance for a subclinical or grade 1 varicocele.
  • Observation is appropriate for a group 2 or 3 varicocele with symmetrical testicles.
  • Perform open surgical repair for a group 2 or 3 varicocele with asymmetrical testicles.
231
Q

what is acute urinary retention?

A

a medical emergency characterised by the abrupt development of the inability to pass urine (over a period of hours).

232
Q

what are the risk factors for developing acute urinary retention?

A
  • BPH
  • Constipation
  • Medication such as anticholinergic agents, narcotic analgesia and alpha receptor antagonists
  • Ureteric calculi
  • Neurological disease
  • Malignancy
  • Posterior urethral valves
  • Meatal stenosis
  • Pregnancy
  • Haematuria and clot retention
  • Bladder hernia
  • Cystocele
  • Iatrogenic injury
  • Urethral instrumentation
  • Retroperitoneal fibrosis
233
Q

what are the clinical features of acute retention?

A
  • Pain
  • Tense and distended lower abdomen
  • Inability to pass urine for many hours
  • If due to BPH or urethral stricture there will be recent worsening of LUTS
  • Costovertebral angle tenderness
  • Overflow incontinence
234
Q

how is acute urinary retention managed?

A
  • Urinary catheterisation to empty the bladder
  • Alpha blockers (such as tamsulosin) should be started in men over 65 at least 24 hours before attempting to remove the catheter
  • Treat the underlying cause of retention
  • Use a 3-way catheter to relieve clot retention
  • Patients with obstruction and sepsis require antibiotic treatment
235
Q

how is chronic urinary retention managed?

A
  • intermittent catheterisation
  • indwelling catheter
  • alpha adrenoreceptor blockers
  • urostomy
236
Q

what is enuresis?

A
  • lack of bladder control during the day in a child old enough to be continent (over the age of 3–5 years).
  • Nocturnal enuresis is also usually present.
237
Q

what are the causes of enuresis?

A
  • Lack of attention to bladder sensation
  • detrusor instability
  • bladder neck weakness
  • neuropathic bladder
  • UTI
  • constipation
  • ectopic ureter
238
Q

how is enuresis managed?

A
  • If rapid or short term control is required, offer desmopressin to be taken at bedtime
  • A small portable alarm with a pad in the pants, which is activated by urine, can be used when there is lack of attention to bladder sensation for long term treatment
  • Anticholinergic drugs, such as oxybutynin, or imipramine (TCA) can be used to damp down bladder contractions, may be helpful if other measures fail.
239
Q

what are the causes of secondary enuresis?

A
  • Emotional upset, the commonest cause
  • UTI
  • Polyuria from an osmotic diuresis in diabetes mellitus or a renal concentrating disorder, e.g. sickle cell disease or chronic renal failure.
240
Q

what is overflow incontinence?

A

-leakage of urine from a full distended bladder

241
Q

what is functional incontinence?

A

passage of urine occurs owing to inability to get to a toilet because of disability, unavailability of facilities or dementia

242
Q

what is stress incontinence?

A

involuntary leakage of urine on effort or exertion, or on sneezing or coughing.

243
Q

what are the clinical features of stress incontinence?

A
  • Incontinence associated with coughing, sneezing, laughing and exercise
  • There may also be frequency, urgency or urge incontinence. It
  • Examination with a Sims’ speculum:
  • –cystocoele or urethrocoele.
  • –Leakage of urine with coughing may be seen.
  • –The abdomen is palpated to exclude a distended bladder.
244
Q

how is stress incontinence managed?

A
  • weight loss
  • treat cause of chronic cough
  • Pelvic floor muscle training
  • duloxetine
  • surgery
245
Q

what is an overactive bladder?

A

urgency, with or without urge incontinence, usually with frequency or nocturia, in the absence of proven infection.

246
Q

what are the clinical features of overactive bladder?

A
  • Urgency and urge incontinence, frequency and nocturia
  • Some patients leak at night or at orgasm.
  • A history of childhood enuresis is common, as is faecal urgency.
  • Examination: is often normal, but an incidental cystocoele may be present.
247
Q

how is overactive bladder managed?

A
  • reduce fluid intake
  • void to a timetable
  • anticholinergics or beta-3-adrenergic receptor agonist
  • botox
248
Q

how should bilateral undescended testes at birth be managed?

A

-urgent referral to a paediatrician within 24 hours

249
Q

how should bilateral undescended testes at 6-8 weeks of age be managed?

A

-Arrange urgent referral to a paediatrician to be seen within 2 weeks.

250
Q

how should a unilateral undescended testis be managed:

a) at birth
b) at 6-8 weeks
c) at 4-5months

A

a) re-examine at 6-8 weeks
b) re-examine at 4-5 months
c) arrange referral to paediatric surgery or urology to be seen by 6 months

251
Q

define paediatric hypertension

A

blood pressure above 95th percentile for height, age and sex.

252
Q

what are the symptoms of hypertension in children?

A
  • vomiting
  • headaches
  • facial palsy
  • hypertensive retinopathy
  • convulsions or proteinuria
  • failure to thrive.
  • cardiac failure
  • palpitations and sweating in pheochromocytoma
253
Q

what are the renal causes of hypertension in children?

A
  • Renal parenchymal disease
  • Renovascular disease
  • PKD
  • nephritic syndrome
254
Q

what are the cardiac causes of hypertension in children?

A

-Coarctation of the aorta

255
Q

what are the malignant causes of hypertension in children?

A
  • Phaemochromocytoma

- Neuroblastoma

256
Q

what are the endocrine causes of hypertension in children?

A
  • CAH
  • Cushing’s syndrome/Steroid therapy
  • Hyperthyroidism
257
Q

how is hypertension in children managed?

A
  • correct underlying cause

- ACE inhibitors

258
Q

what are the clinical features of fanconi syndrome?

A
  • Polydipsia and polyuria
  • Salt depletion and dehydration
  • Hyperchloraemic metabolic acidosis
  • Rickets
  • Failure to thrive/poor growth.
259
Q

what is seen on blood gas in fanconi syndrome?

A
  • Hyperchloraemic metabolic acidosis
  • normal serum anion gap
  • hypophosphataemia
  • hypokalaemia.
260
Q

how is fanconi syndrome managed?

A
  • Offer sodium bicarbonate to correct acidosis
  • Offer potassium and phosphate supplementation for hypokalaemia and hypophosphataemia
  • Allow free access to water to prevent dehydration
  • Hydrochlorothiazide to prevent volume expansion, but can increase potassium loss
  • Vitamin D replacement
261
Q

what are the causes of rhabdomyolysis?

A
  • Embolism
  • Clamp on artery during surgery
  • Trauma
  • Prolonged immobilization (eg after falling)
  • Burns
  • Crush injury
  • Excessive exercise
  • Uncontrolled seizures
  • Drugs and toxins: statins, alcohol, ecstasy, heroin, snake bite, carbon monoxide
  • Neuroleptic malignant syndrome
  • infections: Coxsackie, EBV, influenza
  • Myositis
  • Malignant hyperpyrexia
  • Inherited muscle disorders: McArdle’s disease, Duchenne’s muscular dystrophy.
262
Q

what are the clinical features of rhabdomyolysis?

A

-Often of the cause, with muscle pain, swelling, tenderness, and red- brown urine.

263
Q

how is rhabdomyolysis managed?

A

-Urgent treatment for hyperkalaemia.

  • IV fluid rehydration is a priority to prevent AKI:
  • –maintain urine output at 300mL/h until myoglobinuria has ceased
  • If oliguric, CVP monitoring is useful to prevent fluid overload.
  • IV sodium bicarbonate is used to alkalinize urine to pH >6.5, to stabilize a less toxic form of myoglobin.
  • Dialysis may be needed.
264
Q

what are the adverse effects of loop diuretics?

A
  • Dehydration
  • Hypotension
  • Low electrolyte state
  • Hearing loss and tinnitus as it blocks a Na+K+2Cl- transporter that regulates endolymph composition in the inner ear.
265
Q

in which patients should loop diuretics be used cautiously?

A
  • Avoid in patients with severe hypovolaemia or dehydration
  • Caution in patients with hepatic encephalopathy where hypokalaemia can worsen coma
  • Caution in patients with hypokalaemia and/or hyponatraemia
  • Caution in patients with gout as they inhibit uric acid excretion.
266
Q

with which other drugs do loop diuretics interact with?

A
  • Reduced urinary excretion of lithium
  • Reduce urinary excretion of digoxin with increased risk of digoxin toxicity
  • Reduce urinary excretion of aminoglycosides with increased risk of ototoxicity or nephrotoxicity of aminoglycosides.
267
Q

what are the adverse effects of thiazide like diuretics?

A
  • Hyponatraemia
  • Hypokalaemia
  • Erectile dysfunction
  • Rarely agranulocytosis
  • Rarely pancreatitis.
268
Q

in which patients should thiazide diuretics be used cautiously?

A
  • Avoid in patient with hypokalaemia and hyponatraemia
  • Avoid in patients with hypercalcaemia
  • Avoid in patients with Addison’s disease
  • Caution in patients with gout due to reduced uric acid excretion.
269
Q

what are the adverse effects of potassium sparing diuretics?

A
  • GI upset
  • Hypotension
  • Urinary symptoms
  • Electrolyte disturbances.
270
Q

in which patients should potassium sparing diuretics be used cautiously?

A
  • Avoid in severe renal impairment
  • Avoid in hyperkalaemia
  • Avoid in hypovolaemia.
271
Q

with which drugs do potassium sparing diuretics interact?

A
  • Potassium supplements
  • Aldosterone antagonists
  • Altered renal clearance of digoxin and lithium.
272
Q

what are the adverse effects of oral potassium?

A
  • GI disturbance
  • Gi obstruction
  • GI ulceration and bleeding
  • Over-treatment can cause hyperkalaemia and risk of arrhythmias.
273
Q

with which drugs do oral potassium supplements interact with?

A
  • Potassium elevating drugs including IV NaCl
  • aldosterone antagonists
  • potassium-sparing diuretics
  • ACE inhibitors and ARAs.
274
Q

what are the adverse effects of anti-muscarinics?

A
  • Dry mouth
  • Tachycardia
  • Constipation
  • Blurred vision
  • Urinary retention.
275
Q

in which patients should anti-muscarincs be used cautiously?

A
  • Avoid in urinary tract infection
  • Caution in dementia as CNS side effects such as drowsiness and confusion can be problematic
  • Caution in angle-closure glaucoma due to dangerous rise in intraocular pressure
  • Caution with arrhythmias.
276
Q

what are the adverse effects of alpha-blockers?

A
  • Postural hypotension
  • Dizziness
  • Syncope.
277
Q

what are the adverse effects of 5 alpha reductase inhibitors?

A
  • Impotence
  • Reduced libido
  • Gynaecomastia
  • Hair growth
  • Breast cancer.
278
Q

what are the adverse effects of phosphodiesterase type 5 inhibitors?

A
  • Flushing
  • Headache
  • Dizziness
  • Nasal congestion
  • Hypotension
  • Tachycardia
  • Palpitations
  • Risk of cardiovascular and cerebrovascular event
  • Priapism requiring urgent medical assistance
  • Visual disorders including colour distortion due to inhibition of PDE6 in the retina.
279
Q

in which patients should phosphodiesterase type 5 inhibitors be used cautiously?

A
  • Avoid with recent stroke
  • Avoid with recent acute coronary syndrome
  • Avoid with history of cardiovascular disease
  • Caution in people with hepatic or renal impairment in whom sildenafil metabolism and excretion is reduced.
280
Q

with which drugs do phosphodiesterase type 5 inhibitors interact?

A
  • Marked arterial vasodilation with other drugs that increase nitric oxide such as nitrates or nicorandil
  • Increased risk of hypotension with other vasodilators such as alpha blockers and calcium channels blockers

Increased plasma concentrations with CP450 inhibitors such as amiodarone, diltiazem and fluconazole.

281
Q

what are the normal daily fluid requirements?

A
  • 25 - 30 ml/kg/day of water.
  • 1 mmol/kg/day of sodium, potassium, and chloride.
  • 50 - 100 g/day glucose (e.g. glucose 5% contains 5 g/100ml)
282
Q

what is a stage 1 AKI?

A

Creatinine rise of 1.5 - 2.0 times the baseline within 7 days or a urine output of less than 0.5 ml/kg/hour for more than 6 hours.

283
Q

what is a stage 2 AKI?

A

Creatinine rise of 2.0 - 2.99 times within 7 days or a urine output of less than 0.5 ml/ kg/hour for more than 12 hours.

284
Q

what is a stage 3 AKI?

A

Creatinine rise of 3 times the baseline or more within 7 days or a urine output of less than 0.3 ml/kg/hour for more than 12 hours.

285
Q

how is a diagnosis of AKI confirmed?

A
  • A rise in serum creatinine greater than 26 micromol/l within 48 hours.
  • A rise in serum creatinine greater than 1.5 times the baseline within 7 days.
  • A fall in urine output to less than 0.5 ml/kg/hour for more than 6 hours.
  • A 25% of greater fall in eGFR in children and young children within past 7 days.
286
Q

what are the risk factors for erectile dysfunction?

A
  • Coronary artery disease
  • Peripheral arterial disease
  • Psychosexual problems
  • Excess alcohol
  • Hypertension
  • Hyperlipidaemia
  • Diabetes
  • Smoking
  • Metabolic syndrome
  • Neurological disease
  • Pelvic surgery
  • Spinal cord injury
  • Peyronie’s disease – causes penile deformity
  • Depression
  • Hypogonadism
  • Antihypertensive use
  • Antidepressant use
  • Anti-androgenic use
  • BPH
287
Q

how is erectile dysfunction managed?

A
  • modify risk factors
  • psychosexual therapy
  • lifestyle advice
  • PDE5i
  • vacuum erection device
  • alprostadil
  • penile prosthesis

FINALS (18 decks)

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