RENAL AND UROLOGY Flashcards
(287 cards)
1
Q
which drugs are reported to cause acute interstitial nephritis?
A
- Penicillin.
- Rifampicin
- NSAIDs.
- Diuretics.
- Allopurinol.
- Furosemide.
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.
3
Q
what is seen on urinalysis in acute interstitial nephritis?
A
- White cell casts
- sterile pyuria
- low grade proteinuria
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.
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.
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
7
Q
what are the causes of post-renal uraemia?
A
- Urolithiasis.
- Obstructed urinary catheter.
- Enlarged prostate.
- Tumours and other masses.
- Neurogenic bladder.
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
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.
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.
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.
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.
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.
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).
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.
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.
17
Q
what are the risk factors for acute prostatitis?
A
- Urinary tract infection.
- Benign prostatic hyperplasia.
- Urinary tract instrumentation (biopsy, catheterisation, surgical procedures).
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).
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.
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.
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.
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.
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.
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
25
what are the ischaemic causes of acute tubular necrosis?
- 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
26
what are the toxic causes of acute tubular necrosis?
- 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).
27
what are the clinical features of acute tubular necrosis?
- Oliguria and anuria.
- Hypotension.
- Tachycardia.
- Anorexia.
- Malaise.
- Nausea and vomiting.
28
how is acute tubular necrosis managed?
- 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.
29
what are the clinical features of Alport's syndrome?
- Gross haematuria.
- Peripheral oedema.
- Lenticonus (protrusion of the lens).
- Sensorineural hearing loss.
- Fatigue.
- Malaise.
- Breathlessness.
- Hypertension.
- Foamy urine.
- Visual disturbances.
30
how is Alport's syndrome managed?
- 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
31
what are the clinical features of amyloidosis?
- Lower extremity oedema.
- Jugular venous distension.
- Periorbital purpura.
- Macroglossia.
- Fatigue.
- Weight loss.
- Dyspnoea on exertion.
32
how is amyloidosis diagnosed?
-Perform kidney and heart biopsy to confirm the diagnosis: Positive green birefringence when stained with Congo red.
33
how is amyloidosis managed?
- Offer myeloblative chemotherapy (melphalan).
| - Offer stem cell transplantation for patients who are younger than 70 and have minimal heart failure.
34
what are the risk factors for the development of balanitis?
- Congenital or acquired dysfunctional foreskin.
- Uncircumcised state.
- Poor hygiene
- Over-washing.
- HPV infection.
35
what is balanitis?
-inflammation of the glans penis and prepuce
36
what are the clinical features of balanitis?
- Pruritus.
- Pain or soreness.
- Dribbling.
- Red-scaly patches.
- Erosions
37
how is balanitis managed?
- 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.
38
what are the clinical features of BPH?
- Storage symptoms such as frequency, urgency, nocturia.
| - Voiding symptoms such as weak stream, hesitancy, straining, incomplete emptying, terminal dribbling.
39
what is found on DRE in BPH?
- Asymmetrical enlargement of the lateral lobes
- Firm rubbery consistency
- Palpable median groove.
40
how is BPH managed?
- 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.
41
what are the risk factors for bladder cancer?
- 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.
42
what are the clinical features of bladder cancer?
- Painless haematuria in low-grade tumours.
- Dysuria (burning) in high-grade tumours.
- Urinary frequency occurs rarely.
- Weight loss.
43
how is bladder cancer diagnosed?
-cystoscopy with biopsy
44
how should non-muscle invasive bladder tumours be treated?
- Perform transurethral resection.
| - Administer immediate post-operative intravesical chemotherapy (mitomycin).
45
how should locally invasive bladder tumours be managed?
- Perform radical cystoprostatectomy in men and radical cystectomy and hysterectomy in women.
- Offer postoperative chemotherapy (methotrexate, vinblastine, doxorubicin, cisplatin).
46
what are the causes of CKD?
- 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.
47
what complications are associated with CKD?
- anaemia
- renal osteodystrophy
- hyperkalaemia
- secondary or tertiary hyperparathyroidism
- metabolic acidosis
- pruritus
- gout and uraemic pericarditis
- dialysis dementia
- malignancy
48
what are the symptoms of progressive CKD?
- Fatigue.
- Oedema.
- Nausea and vomiting.
- Pruritus.
- Restless leg syndrome.
- Anorexia.
- Arthralgia.
49
what are the signs of progressive CKD?
- Uraemic odour (ammonia-like smell of breath).
- Pallor.
- Cachexia.
- Cognitive impairment.
- Dehydration and hypovolaemia.
- Tachypnoea.
- Hypertension.
- Peripheral neuropathy.
- Frothy urine.
50
how is stage 1 CKD defined?
eGFR >90
51
how is stage 2 CKD defined?
eGFR 60-89
52
how is stage 3a CKD defined?
eGFR 45-59
53
how is stage 3b CKD defined?
eGFR 30-44
54
how is stage 4 CKD defined?
eGFR 15-29
55
how is stage 5 CKD defined?
eGFR <15
56
what drug management should be implemented in CKD?
- 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
57
when should an ACE inhibitor be stopped in CKD?
- 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%.
58
how is anaemia in CKD managed?
- Offer intravenous epoeitin alfa for the treatment of anaemia of erythropoeitin deficiency.
- Offer intravenous ferrous sulfate for the treatment of iron-deficiency anaemia.
59
what are the complications associated with haemodialysis?
- Hypotension.
- Anaphylactic reactions to sterilising agents (ethylene oxide).
- Air embolus.
- Dialysis diathesis syndrome due to cerebral oedema.
60
what are the contraindications to peritoneal dialysis?
- 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
61
what are the clinical features of chronic prostatitis?
- 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.
62
how is chronic pelvic pain in men managed?
- Offer paracetamol or an NSAID for pain relief.
| - Offer an alpha blocker (tamsulosin) for 4-6 weeks for significant LUTS.
63
how is chronic bacterial prostatitis managed?
- 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.
64
what are the clinical features of chronic pyelonephritis?
- History of vesicoureteral reflux.
- History of acute pyelonephritis.
- History of renal obstruction.
- Nausea.
- Elevated blood pressure.
65
how is chronic pyelonephritis managed?
- 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
66
what are the causes of hypomagnesaemia?
- 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.
67
what are the clinical features of hypomagnesaemia?
- Irritability.
- Tremor.
- Carpopedal spasm.
- Hyperreflexia.
- Confusional and hallucinatory states.
- ECG shows prolonged QT interval and broad flattened T waves.
68
how is hypomagnesaemia managed?
- 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.
69
what are the causes of hypermagnesaemia?
- Patients with acute or chronic kidney disease given magnesium-containing laxatives or antacids.
- Magnesium-containing enemas.
- Adrenal insufficiency.
70
what are the clinical features of hypermagnesaemia?
- Weakness.
- Hyporeflexia.
- Narcosis.
- Respiratory paralysis.
- Cardiac conduction defects.
71
how is hypermagnesaemia managed?
- 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.
72
what are the causes of hypophosphataemia?
- Primary hyperparathyroidism.
- Osteomalacia and rickets.
- Vitamin D deficiency.
- Respiratory alkalosis,
- Refeeding syndrome.
- Dent’s disease.
- Diuretics
73
what are the clinical features of hypophosphataemia?
- Diaphragmatic weakness.
- Decreased cardiac contractility.
- Skeletal muscle rhabdomyolysis.
- Left shift in oxyhaemoglobin dissociation curve (reduced 2,3-BPG).
- Haemolysis.
- Confusion.
- Hallucinations.
- Convulsions.
74
how is hypophosphataemia managed?
- Combined therapy with phosphate supplementation and calcitriol administration.
- Administer intravenous phosphate at a maximum rate of 9 mmol every 12 hours.
75
what are the causes of hyperphosphataemia?
- Chronic kidney disease.
- Phosphate-containing enemas.
- Tumour lysis and rhabdomyolysis
76
how is hyperphosphataemia managed?
-Gut phosphate binder for chronic hyperphosphataemia.
77
what are the risk factors for epididymitis?
- Unprotected sexual intercourse.
- Benign prostatic hyperplasia.
- Catheterisation and cystoscopic procedures.
78
what are the clinical features of epididymitis?
- Unilateral scrotal pain and swelling that develops over a few days.
- Pain is relieved through scrotal elevation.
- Tenderness.
- Hot, erythematous, swollen, hemiscrotum.
79
how is epididymitis managed?
- 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).
80
is focal segmental glomerulosclerosis nephrotic or nephritic?
-Nephrotic
81
what are the clinical features focal segmental glomerulosclerosis?
- 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.
82
how is focal segmental glomerulosclerosis managed?
- 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.
83
what is haemolytic uraemic syndrome?
a triad of acute renal failure, microangiopathic haemolytic anaemia and thrombocytopenia.
84
what are the clinical features of HUS?
- Bloody diarrhoea.
- Abdominal pain.
- Nausea.
- Vomiting.
85
what is seen on FBC and blood film in HUS?
- anaemia
- thrombocytopenia
- Schistocytes
86
how is HUS managed?
- 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.
87
what are the clinical features of a hydrocele?
- 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.
88
how is a hydrocele managed in children under 2?
-Observation is appropriate as most resolve spontaneously
89
how is a hydrocele managed in children between 2 and 11?
-Perform elective surgical repair for persistence of a hydrocele beyond 2 years of age to avoid complications.
90
how is a hydrocele managed in an adolescent?
- Observation is appropriate.
- Perform elective surgical repair only if the hydrocele is very large and uncomfortable.
- Perform aspiration for post-varicocelectomy.
91
how is a hydrocele managed in adults?
- Observation is appropriate.
| - Perform elective surgical repair only if the hydrocele is very large and uncomfortable.
92
what are the causes of decreased renal excretion of potassium?
- 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.
93
what are the causes of decreased cellular entry of potassium?
- Metabolic acidosis in exchange for hydrogen ions.
- Hyperglycaemia due to hyperosmolarity.
- Digoxin overdose which inhibits Na+-K+-ATPase.
94
what are the clinical features of hyperkalaemia?
- Muscle weakness.
- Kussmaul respiration when associated with metabolic acidosis.
- Hypotension.
- Bradycardia.
- Sudden death from systolic cardiac arrest.
95
what is seen on ECG in hyperkalaemia?
- Peaked T waves
- Wide QRS complex
- Sine wave appearance which indicates pre-arrest
- Prolonged PR interval
- Reduced P waves
- Ventricular fibrillation
- Asystole.
96
what is the management of hyperkalaemia?
- 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.
97
what are the causes of hypernatraemia?
- free water loss (diabetes insidious, diarrhoea, peritoneal dialysis)
- inadequate free water intake
- sodium overload
98
what are the clinical features of hypernatraemia?
- Nausea and vomiting.
- Confusion.
- Fever.
99
how can urine osmolality aid the diagnosis of hypernatraemia?
- 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.
100
how is hypernatraemia managed?
- 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.
101
what are the causes of increased potassium excretion?
- 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.
102
what are the causes of increased potassium entry into cells?
- metabolic or respiratory alkalosis
- Beta-adrenergic activity
- insulin
- anabolic states
- hypothermia
103
what are the clinical features of hypokalaemia?
- Usually asymptomatic.
- Muscle weakness in severe hypokalaemia.
- Atrial and ventricular ectopic beats.
- Increased risk of digoxin toxicity.
- Rhabdomyolysis.
- Interstitial renal disease.
104
what are the ECG features of hypokalaemia?
- 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.
105
what are the causes of hyponatraemia with hypovolaemia?
- 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.
106
what are the causes of hyponatraemia with euvolaemia?
- 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.
107
what are the causes of hyponatraemia with hypervolaemia?
- Acute kidney injury and chronic kidney disease.
- Congestive heart failure.
- Cirrhosis.
- Nephrotic syndrome.
108
what is the cause of pseudohyponatraemia?
- high serum or lipid levels
| - hyperosmolarity due to severe hyperglycaemia.
109
what are the clinical features of acute hyponatraemia?
- Nausea and vomiting.
- Seizures.
- Coma.
- Confusion.
- Headache.
110
what are the clinical features of chronic hyponatraemia?
- Gait instability.
- Falls.
- Concentration and cognitive deficits.
111
how can the different types of hyponatraemia be distinguished using serum osmolality?
- Less than 275 mmol/kg indicates hypotonic hypernatraemia
- More than 295 indicates hypertonic hypernatraemia
- Normal serum osmolality suggests pseudohyponatraemia.
112
how can urine sodium concentration distinguish the cause of hypovolaemic hyponatraemia?
- 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).
113
how can urine sodium concentration distinguish the cause of hypervolaemic hyponatraemia?
- More than 20 mmol/L indicates AKI or CKD
| - Less than 20 mmol/L indicates heart failure, liver failure, or nephrotic syndrome.
114
how is hypernatraemia managed?
- 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.
115
what are the clinical features of HSP?
- 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
how is HSP managed?
- Offer prednisolone for severe oedema or abdominal pain
| - Offer methylprednisolone sodium succinate and cyclophosphamide for rapidly progressive nephritis
117
what are the clinical features of HSP?
- 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
how is IgA nephropathy managed?
- 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
what are the clinical features of lupus nephritis?
- Oedema.
- hypertension
- features of SLE
120
is lupus nephritis a nephritic or nephrotic syndrome?
nephritic
121
how is lupus nephritis managed?
- Offer cyclophosphamide, prednisolone and hydroxychloroquine to induce remission.
- Offer mycophenolate motefil and prednisolone as a maintenance regimen.
122
what are the clinical features of membranous nephropathy?
- Oedema of the lower extremities and peri-orbital regions.
- Xanthelasma.
- Foamy urine.
- Hypertension.
123
what is seen on silver staining in membranous nephropathy?
-Black spikes
124
how is membranous nephropathy managed?
- 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
Define metabolic acidosis
- 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
what are the causes of a metabolic acidosis with a normal anion gap?
- Diarrhoea due to increased GI bicarbonate loss).
- Renal tubular acidosis.
- Addison’s disease.
127
how is plasma anion gap calculated?
{[Na+] + [K+]} - {[HCO3-] + [Cl-]}
128
how can the causes of a metabolic acidosis with a normal anion gap be distinguished from each other?
- Diarrhoea causes a decreased urinary anion gap
| - Renal tubular acidosis causes an increased urinary anion gap
129
how is urinary anion gap calculated?
{Urinary [Na+] + Urinary [K+] - Urinary [Cl-]}
130
what are the causes of a metabolic acidosis with a high anion gap?
- 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
how is metabolic acidosis managed?
- 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
what is a metabolic alkalosis?
- an arterial pH of more than 7.45
| - increase in plasma bicarbonate level.
133
what are the causes of a chloride responsive metabolic alkalosis?
- Vomiting.
- Gastric drainage.
- Villous adenoma of the colon.
- Cystic fibrosis.
- Post-diuretic therapy.
- Post-hypercapnia.
134
what are the causes of a chloride resistant metabolic alkalosis?
- 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
how is chloride responsive metabolic alkalosis treated?
- Administer isotonic saline therapy if there is extracellular depletion.
- Administer hydrochloride acid or ammonium chloride if there is fluid overload.
136
how is chloride resistant metabolic alkalosis treated?
- 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
what are the complications associated with minimal change disease?
- 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
what are the clinical features of minimal change disease?
- Facial oedema (puffy eyes in the morning)
- Scrotal, vulval, leg and ankle oedema
- Anasarca (oedema involving the entire body).
- Ascites
- Breatlessness
- Xanthelasmata.
139
how is minimal change disease managed?
- 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
when should steroid sparing agents be given and give examples of these drugs
- With frequent relapse.
- Who are unresponsive to steroids.
- Who have severe steroid side effects.
e. g. cyclophosphamide, levamisole, tacrolimus, ciclosporin, mycophenolate mofetil
141
what is phimosis?
the prepuce cannot be retracted over the glans penis
142
what is paraphimosis?
- when a tight prepuce is retracted behind the glans
| - leading to obstruction of the venous return from the glans and the prepuce.
143
what are the risk factors for development of a phimosis or paraphimosis?
- Lack of circumcision.
- Urinary catheterisation.
- Phimosis .
- Poor hygiene.
- Bacterial or parasitic infection.
- Diabetes.
- Haemangiomas.
144
what are the clinical features of phimosis/paraphimosis?
- Penile pain.
- Band of retracted foreskin tissue beneath the glans.
- Swollen glans penis.
- Indwelling catheter.
- Erythema.
- Voiding symptoms e.g. ballooning on micturition
145
how is phimosis/paraphimosis managed?
- 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
what are the medical indications for circumcision?
- recurrent balanoposthitis
- recurrent UTI
- phimosis
147
what are the complications associated with ADPKD?
- 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
what are the clinical features of ADPKD?
- 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
what are the diagnostic criteria on USS on ADPKD?
- 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
How is ADPKD screened for in asymptomatic people with positive family history?
-ultrasound kidney
151
how is ADPKD managed?
- 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
how long after an streptococcal throat infection does post-streptococcal glomerulonephritis occur?
-2 weeks
153
what are the clinical features of post-streptococcal glomerulonephritis?
- 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
how is post-streptococcal glomerulonephritis diagnosed?
- low c3 on measuring complement levels
- elevated antistreptolysin O antibody
- sub-epithelial humps on renal biopsy
155
how is post-streptococcal glomerulonephritis managed?
- 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
define priapism
- prolonged and persistent penile erection
- lasting more than 4 hours
- unassociated with sexual interest or situation.
157
what are the risk factors for priapism?
- 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
what are the clinical features of priapism?
- 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
how does corpus cavernous blood analysis appear in ischaemic priapism?
- Decreased oxygen
- increased carbon dioxide
- acidosis
160
how is priapism managed?
- 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
what are the risk factors associated with prostate cancer?
- High fat diet.
- Obesity.
- Family history of prostate cancer (BRCA2 mutation).
162
what are the clinical features of prostate cancer?
- 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
when should PSA not be measured?
- active UTI
- prostate biopsy in the last 6 weeks
- exercised vigorously within the past 48 hours
- ejaculated within the past 48 hours
164
how is low-intermediate risk prostate cancer managed?
- watchful waiting
- active surveillance
- radical prostatectomy
- external beam radiotherapy
- brachytherapy
165
how is high risk prostate cancer managed?
- Offer radical prostatectomy
- radiotherapy with 6 months of androgen deprivation therapy including a GnRH agonist (goserelin) and androgen receptor blockers (flutamide)
166
what are the risk factors for the development of renal artery stenosis?
- Smoking.
- Dyslipidaemia.
- Hypertension.
- Male gender.
- Increasing age (greater than 55 years).
- History of malignant hypertension.
167
what are the clinical features of renal artery stenosis?
- Flash pulmonary oedema.
| - Progressively difficult-to-control hypertension
168
how is renal artery stenosis diagnosed?
- 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
how is renal artery stenosis managed with atherosclerotic disease?
- 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
how is renal artery stenosis managed with fibromuscular dysplasia?
- 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
what is the classic triad of symptoms associated with renal cell carcinoma?
- Flank pain
- Haematuria.
- Palpable abdominal mass.
172
what are the clinical features, other than the classic triad, of renal cell carcinoma?
- 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
how is renal cell carcinoma diagnosed?
CT abdomen and pelvis
174
how is renal cell carcinoma managed?
- 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
what are the clinical features of Wilms' tumour?
- 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
how is Wilms' tumour managed?
- initial chemotherapy
| - followed by delayed nephrectomy
177
what are the causes of type 1 renal tubular acidosis?
- rheumatoid arthritis
- systemic lupus erythematosus
- Sjogren’s syndrome.
178
what are the causes of type 2 renal tubular acidosis?
- Fanconi’s syndrome
| - Wilson’s disease
179
what are the causes of type 3 renal tubular acidosis?
-hereditary carbonic anhydrase II deficiency
180
what are the causes of type 4 renal tubular acidosis?
-aldosterone deficiency
181
what are the risk factors for the development of renal tubular acidosis?
- Childhood.
- Urinary tract obstruction.
- Diabetes mellitus.
- Primary biliary cholangitis.
- Amphotericin-B therapy.
- Toxic exposure to heavy metals.
- Untreated adrenal insufficiency.
182
what are the clinical features of renal tubular acidosis?
- Growth retardation.
- Failure to thrive.
- Sensorineural hearing loss.
- Muscle weakness (due to hyperkalaemia in type 4 renal tubular acidosis).
- Kussmaul respiration.
183
what is seen on blood gas in renal tubular acidosis?
- serum bicarbonate: Less than 21 mmol/L.
- arterial blood pH: Less than 7.35
- normal anion gap
184
how is type 4 renal tubular acidosis managed?
- 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
how is type 1 and 2 renal tubular acidosis managed?
-Offer sodium bicarbonate and citric acid (Shohl’s solution)
186
what is stage 1 testicular cancer?
-tumour confined to testis
187
what is stage 2 testicular cancer?
-Involvement of testis and para-aortic lymph nodes
188
what is stage 3 testicular cancer?
-Involvement of mediastinal and or supraclavicular nodes
189
what is stage 4 testicular cancer?
-Pulmonary or other visceral metastasis.
190
what are the risk factors for developing testicular cancer?
- Crypto-orchidism (failure of testis to descend from abdomen into scrotum)
- Family history.
- Infertility.
- Testicular atrophy.
- HIV infection.
191
what are the clinical features of testicular cancer?
- 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
which testicular tumours secrete beta-hCG?
- seminoma
| - choriocarcinoma
193
which testicular tumours secrete AFP?
- embryonal and yolk sac tumours
| - teratoma
194
how is testicular cancer managed?
- 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
what are the clinical features of testicular torsion?
- 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
how is testicular torsion managed?
- 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
what are the risk factors for UTI in young/pre-menopausal women?
- Sexual intercourse.
- UTI in childhood.
- Mother with a history of UTI
198
what are the risk factors for UTI in elderly/post-menopausal women?
- UTI before menopause.
- Urinary incontinence.
- Atrophic vaginitis.
- Cystocele.
- Increased post-void urine volume.
- Urine catheterisation.
199
what are the key clinical features of a UTI in women under 65?
- Dysuria.
- New nocturia.
- Cloudy-looking urine.
200
what are the key clinical features of a UTI in women over 65?
- Dysuria.
- New frequency or urgency.
- New incontinence.
- New or worsening delirium.
- New suprapubic pain.
- New haematuria.
201
how is UTI managed in women?
- 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
how is UTI managed in pregnancy?
- 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
how should symptomatic catheter associated UTIs be treated?
- 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
how should catheter associated UTIs with upper UTI symptoms be treated?
- 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
what are the risk factors for UTI in men?
- 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
how is UTI managed in men?
- 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
what are the risk factors for UTI in children?
- Voiding dysfunction (neurogenic bladder, voluntary withholding of urine, chronic constipation, indwelling foreign bodies).
- Vesicoureteral reflux.
- Sexual activity.
- Immunosuppression.
208
what are the clinical features of UTI in infants?
- Fever
- Vomiting
- Lethargy or irritability
- Poor feeding
- Jaundice
- Septicaemia
- Offensive urine
- Febrile convulsion (>6 months)
209
what are the clinical features of UTI in children?
- 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
what investigations should be performed in children with suspected UTI?
- urine dipstick
- MSC
- ultrasound if atypical UTI
- If abnormal ultrasound, function scans such as MCUG and DMSA after 4-6 months
211
how is UTI managed in children under 3 months?
-Immediate hospital admission for intravenous antibiotics (ampicillin and gentamicin).
212
how is lower UTI managed in children over 3 months?
- 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
how is upper UTI managed in children over 3 months?
- 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
which drugs promote calcium oxalate stone formation?
- loop diuretics
- antacids
- glucocorticoids
- theophylline
- acetazolamide
215
which drugs promote rate stone formation?
- Thiazide diuretics
| - salicylates
216
what are the risk factors for developing kidney stones?
- 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
what are the clinical features of kidney stones?
- 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
how are kidney stones diagnosed?
- CT KUB
| - USS first line in pregnancy and children
219
how is pain managed in kidney stones?
- 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
how should kidney stones less than 5mm be managed?
-watchful waiting
221
how should kidney stones less than 10mm be managed?
- medical expulsion therapy with an alpha blocker (tamsulosin)
- shock wave lithotripsy
- ureteroscopy in pregnancy only
222
how should kidney stones more than 10mm be managed?
-ureteroscopy
223
how should kidney stones more than 20mm be managed?
-percutaneous nephrolithotomy
224
what is a varicocele?
an abnormal dilation of the internal spermatic veins and pampiniform plexus of veins around the spermatic cord.
225
what are the clinical features of a varicocele?
- Painless scrotal mass, typically on the left side.
- Palpation above the testicle reveals a ‘bag of worms’ appearance.
- Small testicle.
- Reduced fertility.
226
what is a grade 1 varicocele?
only palpable with Valsalva manoeuvre
227
what is a grade 2 varicocele?
palpable without Valsalva manoeuvre.
228
what is a grade 3 varicocele?
visible through the scrotal skin.
229
what is a subclinical varicocele?
only detected by Doppler ultrasound.
230
how is a varicocele managed?
- 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
what is acute urinary retention?
a medical emergency characterised by the abrupt development of the inability to pass urine (over a period of hours).
232
what are the risk factors for developing acute urinary retention?
- 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
what are the clinical features of acute retention?
- 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
how is acute urinary retention managed?
- 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
how is chronic urinary retention managed?
- intermittent catheterisation
- indwelling catheter
- alpha adrenoreceptor blockers
- urostomy
236
what is enuresis?
- 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
what are the causes of enuresis?
- Lack of attention to bladder sensation
- detrusor instability
- bladder neck weakness
- neuropathic bladder
- UTI
- constipation
- ectopic ureter
238
how is enuresis managed?
- 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
what are the causes of secondary enuresis?
- 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
what is overflow incontinence?
-leakage of urine from a full distended bladder
241
what is functional incontinence?
passage of urine occurs owing to inability to get to a toilet because of disability, unavailability of facilities or dementia
242
what is stress incontinence?
involuntary leakage of urine on effort or exertion, or on sneezing or coughing.
243
what are the clinical features of stress incontinence?
- 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
how is stress incontinence managed?
- weight loss
- treat cause of chronic cough
- Pelvic floor muscle training
- duloxetine
- surgery
245
what is an overactive bladder?
urgency, with or without urge incontinence, usually with frequency or nocturia, in the absence of proven infection.
246
what are the clinical features of overactive bladder?
- 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
how is overactive bladder managed?
- reduce fluid intake
- void to a timetable
- anticholinergics or beta-3-adrenergic receptor agonist
- botox
248
how should bilateral undescended testes at birth be managed?
-urgent referral to a paediatrician within 24 hours
249
how should bilateral undescended testes at 6-8 weeks of age be managed?
-Arrange urgent referral to a paediatrician to be seen within 2 weeks.
250
how should a unilateral undescended testis be managed:
a) at birth
b) at 6-8 weeks
c) at 4-5months
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
define paediatric hypertension
blood pressure above 95th percentile for height, age and sex.
252
what are the symptoms of hypertension in children?
- vomiting
- headaches
- facial palsy
- hypertensive retinopathy
- convulsions or proteinuria
- failure to thrive.
- cardiac failure
- palpitations and sweating in pheochromocytoma
253
what are the renal causes of hypertension in children?
- Renal parenchymal disease
- Renovascular disease
- PKD
- nephritic syndrome
254
what are the cardiac causes of hypertension in children?
-Coarctation of the aorta
255
what are the malignant causes of hypertension in children?
- Phaemochromocytoma
| - Neuroblastoma
256
what are the endocrine causes of hypertension in children?
- CAH
- Cushing’s syndrome/Steroid therapy
- Hyperthyroidism
257
how is hypertension in children managed?
- correct underlying cause
| - ACE inhibitors
258
what are the clinical features of fanconi syndrome?
- Polydipsia and polyuria
- Salt depletion and dehydration
- Hyperchloraemic metabolic acidosis
- Rickets
- Failure to thrive/poor growth.
259
what is seen on blood gas in fanconi syndrome?
- Hyperchloraemic metabolic acidosis
- normal serum anion gap
- hypophosphataemia
- hypokalaemia.
260
how is fanconi syndrome managed?
- 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
what are the causes of rhabdomyolysis?
- 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
what are the clinical features of rhabdomyolysis?
-Often of the cause, with muscle pain, swelling, tenderness, and red- brown urine.
263
how is rhabdomyolysis managed?
-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
what are the adverse effects of loop diuretics?
- 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
in which patients should loop diuretics be used cautiously?
- 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
with which other drugs do loop diuretics interact with?
- 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
what are the adverse effects of thiazide like diuretics?
- Hyponatraemia
- Hypokalaemia
- Erectile dysfunction
- Rarely agranulocytosis
- Rarely pancreatitis.
268
in which patients should thiazide diuretics be used cautiously?
- 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
what are the adverse effects of potassium sparing diuretics?
- GI upset
- Hypotension
- Urinary symptoms
- Electrolyte disturbances.
270
in which patients should potassium sparing diuretics be used cautiously?
- Avoid in severe renal impairment
- Avoid in hyperkalaemia
- Avoid in hypovolaemia.
271
with which drugs do potassium sparing diuretics interact?
- Potassium supplements
- Aldosterone antagonists
- Altered renal clearance of digoxin and lithium.
272
what are the adverse effects of oral potassium?
- GI disturbance
- Gi obstruction
- GI ulceration and bleeding
- Over-treatment can cause hyperkalaemia and risk of arrhythmias.
273
with which drugs do oral potassium supplements interact with?
- Potassium elevating drugs including IV NaCl
- aldosterone antagonists
- potassium-sparing diuretics
- ACE inhibitors and ARAs.
274
what are the adverse effects of anti-muscarinics?
- Dry mouth
- Tachycardia
- Constipation
- Blurred vision
- Urinary retention.
275
in which patients should anti-muscarincs be used cautiously?
- 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
what are the adverse effects of alpha-blockers?
- Postural hypotension
- Dizziness
- Syncope.
277
what are the adverse effects of 5 alpha reductase inhibitors?
- Impotence
- Reduced libido
- Gynaecomastia
- Hair growth
- Breast cancer.
278
what are the adverse effects of phosphodiesterase type 5 inhibitors?
- 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
in which patients should phosphodiesterase type 5 inhibitors be used cautiously?
- 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
with which drugs do phosphodiesterase type 5 inhibitors interact?
- 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
what are the normal daily fluid requirements?
- 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
what is a stage 1 AKI?
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
what is a stage 2 AKI?
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
what is a stage 3 AKI?
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
how is a diagnosis of AKI confirmed?
- 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
what are the risk factors for erectile dysfunction?
- 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
how is erectile dysfunction managed?
- modify risk factors
- psychosexual therapy
- lifestyle advice
- PDE5i
- vacuum erection device
- alprostadil
- penile prosthesis
