Renal & Urology Flashcards

(133 cards)

1
Q

Define bladder cancer.

A

Cancer that forms in tissues of the bladder.

Most are transitional cell carcinomas - inner lining of bladder cells.

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2
Q

Explain the aetiology / risk factors of bladder cancer.

A

Risk factors:

  • Tobacco exposure
  • Exposure to chemical carcinogens
  • Age >55 years
  • Pelvic radiation
  • Systemic chemotherapy
  • Schistosoma infection
  • Male sex
  • Chronic bladder inflammation
  • Positive FHx
  • DM Type 2
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3
Q

Summarise the epidemiology of bladder cancer.

A

Ranks ninth in worldwide cancer incidence. Egypt, Western Europe, and North America have the highest incidence rates and Asian countries the lowest rates. More than 90% of new cases occur in people ≥55 years of age.

Over 90% of cancers of the urinary bladder are urothelial carcinoma (previously termed transitional cell carcinoma; UC). Non-muscle-invasive tumours are most common. Low-grade tumours are papillary and generally easy to visualise. High-grade tumours are often flat or in situ, and can be difficult to visualise. If muscle invasion occurs, transurethral resection is insufficient and radical cystoprostatectomy is usually advised.

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4
Q

Recognise the presenting symptoms of bladder cancer.

A
  • Presence of risk factors
  • Haematuria - gross or microscopic
  • Dysuria
  • Urinary frequency
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5
Q

Recognise the signs of bladder cancer on physical examination.

A
  • Presence of risk factors
  • Haematuria - gross or microscopic
  • Dysuria
  • Urinary frequency
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6
Q

Identify appropriate investigations for bladder cancer and interpret the results.

A
  • Urinalysis - red blood cell casts and crenated red cells seen with glomerular bleeding, haematuria, pyuria
  • Urine cytology - +ve in 90% of patients with carcinoma or high-grade tumours, <33% of patients with low-grade transitional cell
  • Renal and bladder ultrasound - bladder tumours/ upper tract obstruction
  • CT urogram - bladder tumours, upper urinary tract tumours, and/or obstruction
  • Cystoscopy
  • IV urogram - filing defects indicative of bladder tumours
  • FBC - normal or mild anaemia
  • Chemistry profile (AlkPhos) - normal or elevated AlkPhos (also give bone scan)
  • CXR
  • CT abdomen and pelvis - rule out stone disease, may reveal primary bladder cancer and/or metastatic disease
  • MRI abdomen and pelvis
  • MR urogram
  • Bone scan - normal or hot spots indicative of bony deposits
  • Urinary markers
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7
Q

Define prostate cancer.

A

A malignant tumour of glandular origin, situated in the prostate.

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8
Q

Explain the aetiology / risk factors of prostate cancer.

A

Risk factors:

  • Age >50 years
  • Black ethnicity
  • North American or Northwest European descent
  • Family history of prostate cancer
  • High levels of dietary fat
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9
Q

Summarise the epidemiology of prostate cancer.

A

Prostate cancer is the second leading cause of cancer mortality in men in the US.

Uncommon in men aged under 50 years.

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10
Q

Recognise the presenting symptoms of prostate cancer.

A
  • Presence of risk factors
  • Nocturia
  • Urinary frequency
  • Urinary hesitancy
  • Dysuria
  • Haematuria
  • Weight loss/anorexia
  • Lethargy
  • Bone pain
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11
Q

Recognise the signs of prostate cancer on physical examination.

A
  • Elevated PSA
  • Abnormal digital rectal exam
  • Palpable lymph nodes
  • Haematuria
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12
Q

Identify appropriate investigations for prostate cancer and interpret the results.

A

1st Line:

  • Serum PSA - >4 micrograms / L
  • Testosterone - baseline test for patients in whom androgen deprivation is considered
  • LFTs - check for risk of hepatitis when giving androgen deprivation
  • FBC - normal except for advanced metastatic disease
  • Renal function - normal except for locally advanced disease causing obstruction
  • Prostate biopsy - malignant cells detected (grade 1-5)

Consider:

  • Bone scan
  • Plain X-rays
  • Pelvic CT scan
  • Pelvic MRI / endorectal MRI
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13
Q

Define renal cell carcinoma.

A

A malignancy arising from renal parenchyma/ cortex, and accounts for about 85% of kidney cancers.

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14
Q

Explain the aetiology / risk factors of renal cell carcinoma.

A

Risk factors:

  • Smoking
  • Male sex
  • Age over 55 years
  • Residence in developed countries
  • Black / American-Indian ethnicity
  • Obesity
  • Hypertension
  • Positive family history of RCC
  • History of hereditary syndrome
  • History of acquired renal cystic disease

Weak risk factors:

  • Asbestos/Cadmium
  • Obstetric history / oestrogen exposure
  • Pelvic radiation
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15
Q

Summarise the epidemiology of renal cell carcinoma.

A

RCC is the seventh most common form of neoplasm in the developed world. The surveillance, epidemiology, and end results (SEER) statistics report that in the US, about 74,000 new cases of kidney cancer were diagnosed in 2019, accounting for 4.2% of all cancer diagnoses (almost double the global average).

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16
Q

Recognise the presenting symptoms of renal cell carcinoma.

A

TRIAD = Flank pain, Haematuria, Palpable Abdominal Mass.

Can be asymptomatic - indicidental finding (>50%)

  • Presence of risk factors
  • Haematuria
  • Flank pain

Non-specific systemic symptoms:

  • Fever
  • Weight loss
  • Sweats
  • Pallor
  • Cachexia
  • Myoneuropathy
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17
Q

Recognise the signs of renal cell carcinoma on physical examination.

A
  • Flank tenderness
  • Palpable abdominal mass
  • Haematuria

Rare:
- Scrotal varicocele

Signs of hepatic dysfunction:

  • Ascites
  • Hepatomegaly
  • Spider angiomata

Signs of IVC involvement:
- Lower limb oedema

Hereditary Syndromes:

  • Dermatological manifestation
  • Birt-Hogg-Dube - papules
  • Hereditary leimyomatous - skin fibromas

Von Hippel Lindau:

  • Vision loss
  • Retinal angiomatosis detected on fundoscopy
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18
Q

Identify appropriate investigations for renal cell carcinoma and interpret the results.

A

BLOODS

  • FBC - paraneoplastic syndrome (reduced Hb or elevated RBC) symptoms such as anaemia of chronic disease, erythrocytosis
  • LDH - >1.5 upper limit
  • Corrected calcium - >2.5mmol/L (>10mg/dL)
  • LFTs - metastatic disease / paraneoplastic syndrome= abnormal

Transaminitis (elevated liver transaminases, aspartate aminotransferase/alanine aminotransferase) and/or poor liver function may be indicative of metastatic lesions.

In the absence of liver metastases, cholestasis (elevated bilirubin, alk phos, gamma-GT), with concomitant elevated prothrombin time, thrombocytosis, and hepatosplenomegaly, is a paraneoplastic presentation of RCC known as Stauffer syndrome.

  • Coagulation - elevated PT in paraneoplastic syndrome

In the absence of liver metastases, cholestasis (elevated bilirubin, alk phos, gamma-GT), with concomitant elevated prothrombin time (PT), thrombocytosis, and hepatosplenomegaly, is a paraneoplastic presentation of RCC known as Stauffer syndrome

  • Creatinine - elevated with reduced creatinine clearance indicating chronic renal insufficiency either preceding or due to RCC (know baseline function)

URINALYSIS

  • Haematuria
  • Proteinuria - seen in CKD and HTN which are risk factors for RCC

IMAGING

  • Abdominal / pelvic US Scan - cyst / mass, lymphadenopathy
  • CT CAP - renal mass, lymphadenopathy, bone or visceral metastases
  • MRI CAP - renal mass, lymphadenopathy, bone or visceral metastases
  • Bone scan - uptake in bone site consistent with metastases (if bone pain or elevated AlkPhos)
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19
Q

Define testicular cancer.

A

Cancer that forms in tissues of one or both testicles. Testicular cancer is most common in young or middle-aged men. Most testicular cancers begin in germ cells (cells that make sperm) and are called testicular germ cell tumors.

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20
Q

Explain the aetiology / risk factors of testicular cancer.

A

Risk factors:

  • Cryptorchidism
  • Gonadal dysgenesis
  • Family history of testicular cancer
  • Personal history of testicular cancer
  • Testicular atrophy
  • White ethnicity
  • HIV infection
  • Chemical carcinogens and low sperm count
  • Rural residence
  • Higher socioeconomic status
  • Inguinal hernia
  • Genetic abnormality
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21
Q

Summarise the epidemiology of testicular cancer.

A

The most common malignancy in young adult men (20 to 34 years of age), and highly curable when diagnosed early.

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22
Q

Recognise the presenting symptoms of testicular cancer.

A
  • Presence of risk factors
  • Age 20-34 years
  • Testicular mass - 55% on right side, 2% bilateral, 85% painless, 10% acute pain
  • Extratesticular manifestation - e.g. bone pain, extremity swelling (venous occlusion), supraclavicular lymph nodes, hyperthyroidism, gynaecomastia
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23
Q

Recognise the signs of testicular cancer on physical examination.

A
  • Presence of risk factors
  • Age 20-34 years
  • Testicular mass - 55% on right side, 2% bilateral, 85% painless, 10% acute pain
  • Extratesticular manifestation - e.g. bone pain, extremity swelling (venous occlusion), supraclavicular lymph nodes, hyperthyroidism, gynaecomastia
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24
Q

Identify appropriate investigations for testicular cancer and interpret the results.

A
  • Ultrasound with colour Doppler of testis - testicular mass
  • CXR - mediastinal and lung mass suggestive of metastasis
  • CT Scan (AP) - enlarged retroperitoneal lymph nodes
  • Serum beta-hCG - >0.7 IU/L - elevated in all choriocarcinomas, 5-10% of seminomas
  • Serum AFP - >25microgram / L - elevated by embryonal carcinoma, yolk sac tumours, combined tumours but NOT choriocarcinomas and seminomas
  • Serum LDH - only elevated marker in 10% of non-seminomas, elevated in 50% of all cases
  • Histological examination of testicular mass post-rochiectomy
  • Serum placenta AlkPhos - elevated in 40% patients with advanced disease
  • Serum gamma-GT - >85 U/L in 1/3 cases of seminoma
  • MRI AP - staging tool
  • CT Chest - show metastatic lesions
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25
Define testicular torsion.
A urological emergency caused by the twisting of the testicle on the spermatic cord leading to constriction of the vascular supply and time-sensitive ischaemia and/or necrosis of testicular tissue.
26
Explain the aetiology / risk factors of testicular torsion.
Risk Factors: - Age under 25 years - Neonate - Bell clapper deformity - Trauma / exercise - Intermittent testicular pain - Undescended testicle - Cold weather
27
Summarise the epidemiology of testicular torsion.
Testicular torsion is a well known emergency in urology and can occur at any age. Our study shows that the incidence was 2.9 cases per 100,000 person years of males <25 yr of age and 1.1 cases per 100,000 person years at all ages. Most common at ages 11-30 years.
28
Recognise the presenting symptoms of testicular torsion.
- Sudden onset of pain in one testis - Intermittent or acute on-and-off pain - No pain relief upon elevation of scrotum - Walking uncomfortable - Abdominal pain - Nausea - Vomiting - Fever - Increased urinary frequency
29
Recognise the signs of testicular torsion on physical examination.
- Scrotal swelling or oedema - Inflammation of one testis - very tender, hot and swollen - Testis may lie high and tranversely NB: With intermittent torsion, the pain may have passed on presentation, but if it was severe, and the lie is horizontal, prophylactic fixing may be wise.
30
Identify appropriate investigations for testicular torsion and interpret the results.
- Doppler US - may demonstrate lack of blood flow to the testis - Only perform US if diagnosis equivocal - do not delay surgical exploration - Urinalysis, FBC, CRP - check for infection
31
Generate a management plan for testicular torsion.
- Ask consent for possible orchidectomy + bilateral fixation (orchidopexy) - At surgery exposure and untwist the testis - If colour looks good, return the testis to the scrotum and fix both testes to the scrotum
32
Identify the possible complications of testicular torsion and its management.
- Infection - Infertility - Gangrene - Cosmetic deformity - Atrophy - Testicular death
33
Summarise the prognosis for patients with testicular torsions.
If testicular torsion is treated right away—at best within six hours—the testicle may be saved. But if blood flow is cut off for more than six hours, the testicle may lose its ability to function
34
Define AKI.
An acute decline in kidney function, leading to a rise in serum creatinine and/or a fall in urine output. Spectrum - mild to severe
35
Explain the aetiology / risk factors of AKI.
Impaired clearance and regulation of metabolic homeostasis, altered acid / base and electrolyte regulation and impaired volume regulation. Caused by: - Impaired kidney perfusion - Exposure to nephrotoxins - e.g. aminoglycosides, vancomycin + piperacilliin-tazobactam, cancer therapies, NSAIDs, ACE inhibitors - Outflow obstruction - Intrinsic kidney disease Risk Factors: - Advanced age - Underlying kidney disease - DM - Sepsis - Iodinated contrast - Exposure to nephrotoxins - Excessive fluid loss - Sugrery - Haemorrhage - Recent vascular intervention - Cardiac arrest - Pancreatitis - Trauma - Malignant hypertension - Myeloproliferative disorders - e.g. multiple myeloma - Connective tissue disease - Sodium-retaining states - e.g. congestive heart failure, cirrhosis, nephrotic syndrome - Drug overdose - Nephrolithiasis Staging on the basis of Creatinine: Stage 1 - rise of>26micromol/L within 48 hours or 1.5-1.9x baseline Stage 2 - rise to 2-2.9x baseline Stage 3 - rise to >3x baseline or >354 micromol/L or initiated on RRT (irrespective of staging)
36
Summarise the epidemiology of AKI.
10,400 per million Seen in 10-20% of people admitted to hospital as emergencies Inpatient mortality >20% ICU incidence - 20-50%, mortality >50%
37
Recognise the presenting symptoms of AKI.
- Hypotension - Risk factors - Kidney insults - Reduced urine production - Lower urinary tract symptoms - e.g. urgency, frequency, hesitancy - Symptoms of volume overload or pulmonary oedema - e.g. orthopnoea, swollen ankles, crackles on auscultation of lungs, tachypnoea - N&V - Fever - Rash - Arthralgia - Haematuria - visible or non-visible - Palpable bladder and/or enlarged prostate and/or abdominal distension
38
Recognise the signs of AKI on physical examination.
- Hypotension - Risk factors - Kidney insults - Reduced urine production - Lower urinary tract symptoms - e.g. urgency, frequency, hesitancy - Symptoms of volume overload or pulmonary oedema - e.g. orthopnoea, swollen ankles, crackles on auscultation of lungs, tachypnoea - N&V - Fever - Rash - Arthralgia - Haematuria - visible or non-visible - Palpable bladder and/or enlarged prostate and/or abdominal distension
39
Identify appropriate investigations for AKI and interpret the results.
- Basic metabolic profile - includes urea, creatinine (HIGH), LFTs (hepatorenal syndrome) - K+ serum - HIGH - >6mmol/L or ECG changes = urgent treatment - FBC - leukocytosis (sepsis), low platelets (haemolytic uraemic syndrome, thrombotic thrombocytopenic purpura, cryoglobulinaemia), anaemia (haemolytic uraemic syndrome, myeloma, vasculitis) - Bicarbonate - LOW = acidosis - CRP - HIGH (sepsis, infection, vasculitis) - Blood culture - bacterial pathogen causing sepsis - Urinalysis - RBCs, WBCs, celllular casts, proteinuria, positive nitrile, leukocyte esterase - Urine culture - bacterial growth with antibiotic sensitivity - Urine output monitoring - hourly if catheterised, 4-hourly if not - <0.5ml/kg/hour for 6 hours at least - Fluid challenge - kidney function improves rapidly - Venous blood gases (metabolic acidosis) - anion gap acidosis - CXR - infection, pulmonary oedema, haemorrhage, cardiomegaly - ECG - peaked T waves, increased PR interval, widened QRS, atrial arrest, deterioration to a sine wave pattern = hyperkalaemia Measure serum creatinine to check for AKI if - compare to baseline over 3 months (if none, repeat within 12 hours): - >65 years - History - CKD, heart failure, liver disease, diabetes, dementia - Previous AKI - Exposure to iodinated contrast agent, nephrotoxins, RAS modifying agent, diuretic - History of urological obstruction - Sepsis - Hypovolaemia (with/without hypotension) - Hypotenison (SBP <90mmHg or a fall of >40mmHg from baseline BP) - Oliguria - urine output <0.5ml/kg/hour - Acute rise in NEWS >5 CKD Features (doesn't exclude): - Rise in serum creatinine over a long period of time - Hypocalcaemia - Hyperphosphataemia - Anaemia - Small kidneys on ultrasound, sometimes scarred NB: CKD is a risk factor for AKI. Check for: - Recent use of trimethoprim - false positive rise - Creatinine falls during pregnancy, so a rise in creatinine after recent delivery - false positive rise Serum K+ 5.5 to 5.9 mmol/L indicates mild hyperkalaemia 6.0 to 6.4 mmol/L indicates moderate hyperkalaemia ≥6.5 mmol/L indicates severe hyperkalaemia To catheterise or not to catheterise? - Benefits - sustained fall in urine output suggests AKI, difficult to measure without, diagnostic and therapeutic for bladder neck obstruction, assessment of response to treatment, urinalysis performed on samples - Risks - infection, trauma, falls risk
40
Generate a management plan for AKI.
Treat sepsis, optimization of volume status, correction of acidaemia or electrolyte complications, avoidance of nephrotoxins and relief of any obstruction. STOP AKI S = Sepsis - implement Sepsis Six within 1 hour, source and treat infection T = Toxins - stop nephrotoxins O = Optimise volume status /BP - assess and give IV fluids, hold antihypertensives and diuretics, consider vasopressors if not responding P = Prevent harm - treat complications and cause If HYPOVOLAEMIC - e.g. sepsis, fluid loss, reduced fluid intake(pre-kidney): - Mild hyperkalaemia (5.5-5.9) - fluid resus (500mL bolus over 15mins, wide bore cannula, crystalloid, reassess) , review meds, stop nephrotoxins (e.g. aminoglycoside antibiotics, NSAIDs, iodinated contrast agents, ACEi, ARB, diuretics), treat cause, vasoactive drug (e.g. noradrenaline, vasopressin, dobutamine), blood transfusion, specialist referral, cation-exchange resin (e.g. calcium polystyrene sulfonate to remove K+ from body) - Moderate hyperkalaemia (6.0-6.4) and no ECG changes - fluid resus, review meds, stop nephrotoxins, identify and treat cause, vasoactive drug, blood transfusion, specialist referral, insulin / glucose (to push potassium intracellularly, give over 15 mins, acts within 10-20 mins, lasts 4-6 hours) , salbutamol (to push potassium intracellularly) - Moderate (6.0-6.4) or Severe hyperkalaemia (>6.5) and associated ECG changes - fluid resus, review meds, stop nephrotoxins, identify and treat cause, vasoactive drug, blood transfusion, specialist referral, calcium chloride or gluconate (IV over 5-10 mins for cardiac protection vs arrhythmias), insulin/glucose, salbutamol - Metabolic acidosis - fluid resus, review medications, stop nephrotoxins, identify and treat cause, vasoactive drug, blood transfusion, specialist referral, sodium bicarbonate (if pH <7.2, refer to ICU possibly?, venous bicarb <16mmol/L with no volume overload) - Uraemia, refractory severe hyperkalaemia etc - fluid resus, review meds, stop nephrotoxins, identify and treat cause, vasoactive drug, blood transfusion, specialist referral, renal replacement therapy (if end-organ complications of uraemia, severe hyperkalaemia, refractory acidosis that is not responding - give intermittent haemodialysis [4hrs, fast removal of toxins] or continuous RRT [24-72hours, slower blood flow] or peritoneal dialysis) If HYPERVOLAEMIC - e.g. obstruction to urinary flow (post-renal): - Pulmoary oedema - loop diuretic (furosemide), sodium restriction, treat cause, renal replacement therapy (on basis of condition, not urea or creatinine value - intermittent haemodialysis, CRRT, peritoneal dialysis), upright positioning, high-flow oxygen (15L/min via resevoir mask, CPAP), glyceryl trinitrate IV (aim for SBP >95mmHg) - Mild hyperkalaemia (5.5-5.9) - loop diuretic (furosemide), sodium restriction, treat cause (review meds, restrict dietary intake, monitor K+ and glucose), renal replacement, cation-exchange resin (calcium polystyrene sulfonate - remove K+ from the body) - Moderate hyperkalaemia (6.0-6.4) and no ECG changes - loop diuretic (furosemide), sodium restriction, RRT, treat cause, insulin & glucose (push potassium intracellularly, give over 15 mins, acts within 10-20 mins, lasts 4-6 hours) , salbutamol (drive potassium intracellularly) - Severe hyperkalaemia (>6.5) or moderate hyperkalaemia (6.0-6.4) and associated ECG changes - loop diuretic (furosemide), sodium restriction, RRT, treat cause, calcium (for cardiac protection vs arrhythmias- can be calcium chloride or calcium gluconate), insulin & glucose, salbutamol - Metabolic acidosis - loop diuretic, sodium restriction, treat cause, RRT, specialist advice (once obstruction relieved, diuresis progressing, renal team decides whether to use sodium bicarbonate)
41
Identify the possible complications of AKI and its management.
- Renal replacement therapy if do not respond to medical management - Hyperkalaemia - Acidaemia - Uraemic encephalopathy - Pericarditis - Pulmonary oedema - Volume overload - Electrolyte and acid-base disturbances - Hyponatraemia - Metabolic acidosis - Nutritional and gastrointestinal disturbances - Anaemia - Bleeding diathesis - Infection - Sepsis - Death - Multi-organ failure - Arrythmias - Muscle weakness
42
Summarise the prognosis for patients with AKI.
Prompt recognition and treatment is important. AKI occurs in 10% to 20% of emergency admissions and has an inpatient mortality >20%. Important to monitor: - Review haemodynamic status, including postural BP - Weight monitroing - Fluid input / out put chart - Urea and electrolytes - ECG changes - Dietary intake - avoid K+ rich foods
43
What is Resuscitation, Replacement or Routine Maintenance, when you're prescribing IV fluid therapy?
Resuscitation fluid therapy is aimed at re-establishing haemodynamic stability by restoring intravascular volume. Replacement fluid therapy provides daily maintenance water and electrolyte requirements and replaces any ongoing abnormal fluid losses. Maintenance fluid therapy must provide daily ongoing water and electrolyte requirements (i.e., sodium 1 mmol/kg, potassium 1 mmol/kg, and water 25-35 mL/kg) Never give maintenance fluids at a rate of >100 mL/hour.
44
Define urinary catheterisation.
A flexible tube used to empty the bladder and collect urine in a drainage bag. Urethral or suprapubic (small opening in tummy).
45
Summarise the indications for urinary catheterisation.
- Acute urinary retention - e.g. BPH, blood clots - Chronic obstruction that causes hydronephrosis - Initiation of continuous bladder irrigation - Intermittent decompression for neurogenic bladder - Hygienic care of bedridden patients
46
Identify the possible complications of urinary catheterisation.
- Allergy or sensitivity to latex - Bladder stones - Blood infections (septicaemia) - Blood in urine (haematuria) - Kidney damage (long-term) - Urethral injury - Urinary tract or kidney infections
47
Define amyloidosis.
Heterogenous group of diseases characterized by extracellular deposition of amyloid fibrils. Can be systemic or localised - e.g. pancreatic islets of Langerhans, cerebral cortex, cerebral blood vessels, bones and joints Pancreatic Islets of Langerhans - T2DM Cerebral Cortex - Alzheimer's Cerebral Blood Vessels - amyloid angiopathy Bones & Joints - long-term dialysis caused by B2 microglobulin
48
Explain the aetiology / risk factors of amyloidosis.
Amyloid fibrils are polymers comprising low-molecular-weight subunit proteins. Amyloid fibril subunits are derived from proteins that undergo conformational changes to adopt anti-parallel B-pleated sheet configuration. Amyloid fibril subunits associated with GAGs and serum amyloid P-component (SAP), and their sdeposition progressively disrupts the structure and function of nromal tissue. Classification: - AA - serum amyloid A protein - e.g. Chronic inflammatory (RA, seronegative arthritides, Crohn's, familial Mediterranean fever), chronic infections (TB, bronchiectasis, osteomyelitis), malignancy (Hodgkin's disease, renal cancer) - AL - monoclonal immunoglobulin light chains fibril protein - e.g. subtle monoclonal plasma cell dyscrasias, multiple myeloma, Waldenstrom's macroglobulinaemia, B-cell lymphoma - ATTR (familiar amyloid polyneuropath) - genetic-variant transthyretin - autosomal dominantly transmitted muttaions in the gene for transthyretin (TTR), variable penetrance Risk factors: - Monoclonal gammopathy of undetermined significance (MGUS) - Inflammatory polyarthropathy - Chronic infections - IBD
49
Summarise the epidemiology of amyloidosis.
AA = 1-5% incidence among patients with chronic inflammatory disease AL = estimated annual incidence of about 3,000 cases in US, 300-600 cases in UK Hereditary - 5% of patients with systemic amyloidosis
50
Recognize the presenting symptoms of amyloidosis.
Renal - Proteinuria - Nephrotic syndrome - Renal failure Cardiac - Restrictive cardiomyopathy - Heart failure - Arrythmia - Angina - due to accumulation of amyloid in coronary arteries GI - Macroglossia - characteristic of AL - Hepatomegaly - Splenomegaly - Gut dysmotility - Malabsorption - Bleeding Neurological - Sensory and motor neuropathy - Autonomic neuropathy - symptoms of bowel or bladder dysfunction, postural hypotension - Carpal tunnel syndrome Skin - Waxy skin - Easy brusing - Purpura around the eyes - characteristic of AL - Plaques - Nodules Joints - Painful asymmetrical large joint - Shoulder pad sign - enlargement of the anterior shoulder Haematological - Bleeding diathesis - factor X deficiency due to binding on amyloid fibrils primarily in the liver and spleen and reduce synthesis of coagulation factors in patients with advanced liver disease
51
Recognize the signs of amyloidosis on physical examination.
Renal - Proteinuria - Nephrotic syndrome - Renal failure Cardiac - Restrictive cardiomyopathy - Heart failure - Arrythmia - Angina - due to accumulation of amyloid in coronary arteries GI - Macroglossia - characteristic of AL - Hepatomegaly - Splenomegaly - Gut dysmotility - Malabsorption - Bleeding Neurological - Sensory and motor neuropathy - Autonomic neuropathy - symptoms of bowel or bladder dysfunction, postural hypotension - Carpal tunnel syndrome Skin - Waxy skin - Easy brusing - Purpura around the eyes - characteristic of AL - Plaques - Nodules Joints - Painful asymmetrical large joint - Shoulder pad sign - enlargement of the anterior shoulder Haematological - Bleeding diathesis - factor X deficiency due to binding on amyloid fibrils primarily in the liver and spleen and reduce synthesis of coagulation factors in patients with advanced liver disease
52
Identify appropriate investigations for amyloidosis and interpret the results.
1. Tissue biopsy - congo red stain, immunohistochemistry (diagnose amyloidosis, identify amyloid fibril protein) 2. Urine (proteinuria, free immunoglobi light chains in AL) 3. Blood (CRP, ESR, RF, Ig levels, serum protein electrophoresis, LFTs, U&E, SAA levels) 4. 123I-SAP Scan - radiolabeled SAP localizes to the deposits enabling quantitative imaging of amyloidotic organs throughout the body
53
Define UTI.
Characterised by presence of >100,000 of colony-forming units per milllitre of urine. May affect bladder (cystitis), kidney (pyelonephritis) or prostate (prostatitis).
54
Explain the aetiology / risk factors of UTI.
Transurethral ascent of normal colonic organisms. Escherichia coli Proteus mirabilis Klebsiella Enterococci (hospitals)
55
Summarise the epidemiology of UTI.
30% of women experience UTI at some point in their lives. 5% of pregnant women, 2% of non-pregnant women, 20% elderly living at home, 50% institutionalized elderly. Rare in children and young men (if present, suspect an underlying cause).
56
Recognise the presenting symptoms of UTI.
- Silent - asymptomatic bacteruria Cystitis: - Frequency - Urgency - Dysuria - pain on micturition - Haematuria - Suprapubic pain - Smelly urine Pyelonephritis (acute): - Feber - Malaise - Rigors - Loin / flank pain Prostatitis: - Fever - Low back / perineal pain - Irritative and obstructive symptoms - e.g. hesitancy, urgency, intermittency, poor stream, dribbling Elderly: - Malaise - Nocturia - Incontinence - Confusion Up to 30% of women with UTI symptoms may not have bacteruria.
57
Recognise the signs of UTI on physical examination.
May be asymptomatic. Cystitis: - Fever - Abdominal / suprapubic / loin tenderness - Bladder distension Pyelonephritis - Fever - Loin / flank tenderness Prostatitis: - Tender - Swollen prostate
58
Identify appropriate investigations for UTI and interpret the results.
MSU - Dipstick test - blood, protein, leucocytes, nitrites - Microscopy, culture and sensitivity - >10^5 colonies/mL indicates significant bacteriuria, but with UTI symptoms threshold becomes lower = women (>10^2/mL), men (>10^5/mL) - If there is sterile pyuria (pus cells with no organisms), consider if this may be partially treated UTI, tuberculosis stones, tumour, interstitial nephritis, renal papillary necrosis Imaging - Renal USS or IV urogram if women with frequent UTI and children/men
59
Generate a management plan for UTI.
Cystitis: - Local microbiological polices - Commonly used: oral co-trimoxazole, trimethoprim, nitrofurantoin, amoxicilliin, ciprofloxacin (males) Pyelonephritis: - IV gentamicin, cefuroxime, ciprofloxacin Catheterized patients: - Obtain culture - Change catheter - Do not treat unless patient is symptomatic Prophylaxis: - High fluid intake - Regular micturation to keep bladder empty - Cranberry-based products reduced frequency of recurrence - Low-dose long-term (6-12 months) antibiotics if frequently having UTIs Surgical: - Rarely necessary - May be necessary for relief of any obstruction and removal of any renal calculi
60
Identify the possible complications or UTI and its management.
- Renal papillary necrosis - in those with underlying renal disease - e.g. DM, stones - Renal / perinephric abscess - seen on renal USS - Pyonephritis - pus in palvicalyceal system - Gram-negative septicaemia
61
Summarise the prognosis for patients with UTI.
Mostly resolve with treatment. Among pregnant women, 20% develop acute pyelonephritis if not treated, however there is a high relapse rate.
62
Define epididymitis and orchitis.
Epididymitis - inflammation of the epididymis Orchitis - inflammation of one or both testicles Acute epididymitis - inflammation of the epididymis characterized by scrotal pain and swelling of less than 6 weeks' duration. Acute Epididymo-orchitis - if concurrent inflammation of the testis is present.
63
Explain the aetiology / risk factors of epididymitis and orchitis.
Sexually active men - most commonly caused by: - Chlamydia trachomatis - Neisseria gonorrhoea - Mycoplasma genitalium Older men - most commonly caused by enteric pathogens: - Bladder outlet obstruction - Recent instrumentation of the urinary tract - Systemic illness RISK FACTORS: - Unprotected sexual intercourse - Bladder outflow obstruction - Instrumentation of urinary tract - Immunosuppression - Vasculitis - Amiodarone - Mumps - Exposure to TB
64
Summarise the epidemiology of epididymitis and orchitis.
Usually unilateral.
65
Recognise the presenting symptoms of epididymitis and orchitis.
- Irritative lower urinary tract symptoms - Urethral discharge (purulent) - Fever Common - Presence of risk factors - Age >19 years - Gradual onset - Symptoms <6 weeks' duration - Frequent and painful micturition
66
Recognise the signs of epididymitis and orchitis on physical examination.
Common - Unilateral scrotal pain - Tenderness - Hot - Erythematous - Swollen hemiscrotum Uncommon - Pyrexia - Fluctuant swelling or induration of scrotal tissue - Enlarged or tender prostate
67
Identify appropriate investigations for epididymitis and orchitis and interpret the results.
1st line: - Gram stain of urethral secretions - >5 WBC per oil immersion field, intracellular gram-negative diplococci - Urine dipstick test - positive leukocyte esterase tests shown as colour change on the reagent strip - Urine microscopy - >10 WBC per high-power field - Urine culture - Isolate of causative organism - NAAT (nucleic acid amplification test) of urethral secretions or first-void urine - Chalmydia trachomatis, Neisseria gonorrhoea, Mycoplasma genitalium DNA / RNA detected - Culture of urethral secretions - positive culture for N.gonorrhoea Consider: - Colour duplex US - epididymis is enlarged, hyperaemic, low-resistance monophasic arterial waveform pattern, good for localising areas of inflammation - Surgical exploration - oedematous epididymis with vascular congestion and evidence of surrounding inflammatory reaction, with no evidence of testicular torsion - 3 early morning urine samples for acid-fast bacilli staining, culture and NAAT - may be positive - HIV test - may be positive - Syphilis test - may be positive
68
Generate a management plan for epididymitis and orchitis.
BACTERIAL INFECTION - Abx - Supportive measures - paracetamol or naproxen or ibuprofen NB: Abx Gonorrhoea / Chlamydia suspected - ceftriaxone and doxycycline Gonorrhoea / Chlamydia suspected, Gonorrhoea likely - ceftriaxone, doxycycline and azithromycin Gonorrhoea / Chlamydia / Enteric organisms suspected - ceftriaxone, ofloxacin / levofloxacin Enteric organisms suspected - ofloxacin or levofloxacin M Genitalium suspected - moxifloxacin AMIODARONE-INDUCED - Discontinuation or dose reduction - Supportive measures - paracetamol or naproxen or ibuprofen UNDERLYING VASCULITIS - Specialist referral to rheumatologist - can be due to Behcet's Syndrome or Henoch-Schonlein purpura - Supportive measures - paracetamol or naproxen or ibuprofen IDIOPATHIC OR VIRAL - Supportive measures - paracetamol or naproxen or ibuprofen TB - Anti-TB antibiotics - guidelines! - Specialist referral - Supportive measures - paracetamol or naproxen or ibuprofen
69
Identify the possible complications of epididymitis and orchitis and its management.
- Scrotal abscess and pyocele - Testicular infarction - Fertility problems - Testicular atrophy - Cutaneous fistulization from rupture of abscess through tunica vaginalis - Recurrence, chronic epididymitis and orchialgia
70
Summarise the prognosis for patients with epididymitis and orchitis.
Most epididymitis cases clear up within 3 months. However, more invasive treatment may be needed in some cases. If an abscess has formed on the testicles, your doctor can drain the pus using a needle or with surgery. Surgery is another option if no other treatments have been successful.
71
Define varicocoele.
The abnormal dilation of the internal speratic veins and pampiniform plexus that drain blood from the testis.
72
Explain the aetiology / risk factors of varicocoele.
Caused by defective valves in the veins within the scrotum, just above the testicles. May impede adolescent testicular growth and affect adult sperm parameters and testosterone production. Risk factors: - Somatometric parameters - e.g. tall, low BMI - Family history of varicocele
73
Summarise the epidemiology of varicocoele.
15% of adolescent boys and adult men. 90% cases left side. 10% bilateral. 40% of men being evaluated in a male fertility clinic will have a varicocele.
74
Recognise the presenting symptoms of varicocoele.
- Painless scrotal mass - Left-sided signs / symptoms - Small testicle - Infertility - Age > 12 years - Scrotal or groin pain
75
Recognise the signs of varicocele on physical examination.
- Painless scrotal mass - Left-sided signs / symptoms - Small testicle - Infertility - Age > 12 years - Scrotal or groin pain (uncommon)
76
Identify appropriate investigations for varicocoele and interpret the results.
1st line: - Clinical diagnosis - inspection of spermatic cord above the testicle may reveal "bag of worms appearance", Valsalva manoeuvre to elicit small ones Consider: - Scrotal ultrasound with colour flow Doppler imaging - identification of sub-clinical varicocele - Semen analysis - reduced sperm count, impaired sperm motility - Serum FSH and GnRH stimulation - high (suggesting testicular dysfunction) - Serum testosterone - may be low - DNA fragmentation index (DFI) - high - CT abdomen / pelvis - exclude abdominal, pelvic or retroperitoneal mass - MRI abdomen / pelvis - exclude abdominal, pelvic or retroperitoneal mass - Retroperitoneal USS - exclude retroperitoneal mass
77
Define hydrocoele.
A collection of serous fluid between the layers of the membrane (tunica vaginalis) that surrounds the testis or along the spermatic cord. Similar collection in females along the canal of Nuck.
78
Explain the aetiology / risk factors of hydrocoele.
x2 Types: COMMUNICATING - Patent processus vaginalis connects peritoneum with tunica vaginalis - Allows peritoneal fluid to flow freely between both structures - Abdominal contents may enter the groin = inguinal hernia (direct or indirect) - Direct - hernial sac medial to inferior epigastric artery and deep inguinal ring - Indirect - hernial sac lateral to inferior epigastric artery NON-COMMUNICATING - Clossed processus vaginalis - More fluid is being produced by tunica vaginalis than is being absorbed Risk factors: - Male sex - Prematurity and low birth weight - Infants < 6 months of age - Infants whose testes descend relatively late - Increased intraperitoneal fluid or pressure - Inflammation or injury within the scrotum - Testicular cancer - Connective tissue disorders - Varicocelectomy - Failariasis - Maternal exposure to polybrominated biphenyl
79
Summarise the epidemiology of hydrocoele.
Common in male infants and the newborn. Most are congenital and resolve within the first year of life. May occur in adult men where they are found secondary to: - Minor trauma - Infection - Testicular torsion - Epididymitis - Varicocele operation - Testicular tumour
80
Recognise the presenting symptoms of hydrocoele.
- Painless - Swollen scrotum - On one or both sides - Feels like a water-filled balloon - Transillumination - Enlargement of scrotal mass following activity - Variation in scrotal mass during the day
81
Recognise the signs of hydrocoele on physical examination.
- Painless - Swollen scrotum - On one or both sides - Feels like a water-filled balloon - Transillumination - Enlargement of scrotal mass following activity - Variation in scrotal mass during the day
82
Identify appropriate investigations for hydrocoele and interpret the results.
1st line: - Clinical diagnosis - features of hydrocele Consider: - Ultrasound - confirm prescence via scrotal or inguinal ultrasound
83
Define benign prostatic hyperplasia.
Lower urinary tract symptoms (LUTS) caused by bladder outlet obstruction (BOO) due to benign prostatic hyperplasia (also known as BPE).
84
Explain the aetiology / risk factors of BPH.
- Smooth muscle hyperplasia - Prostatic enlargement - Bladder dysfunction - Input from CNS 2 COMPONENTS: - Static component - increase in benign prostatic tissue narrowing urethral lumen - Dynamic component - increase in prostatic smooth muscle tone mediated by alpha-adrenergic receptors May also be due to bladder overactivity. Risk factors: - >50 years - Family history - Non-Asian race - Cigarette smoking - Male pattern baldness - Metabolic syndrome
85
Summarise the epidemiology of BPH.
Clinical benign prostatic hyperplasia (BPH) is one of the most common diseases in ageing men and the most common cause of lower urinary tract symptoms (LUTS). The prevalence of BPH increases after the age of 40 years, with a prevalence of 8%–60% at age 90 years.
86
Recognise the presenting symptoms of BPH.
LUTS STORAGE SYMPTOMS - Frequency - Urgency - Nocturia - Incontinence VOIDING SYMPTOMS - Weak stream - Dribbling - Dysuria - Straining Uncommon: - Fever with dysuria - Urinary retention
87
Recognise the signs of BPH on physical examination.
- Prostate volume > 30g - Nodules or tenderness suspicious of prostate cancer or prostatitis - Abdominal examination for palpable bladder - DRE - Neurological assessment
88
Identify appropriate investigations for BPH and interpret the results.
1st line: - Urinalysis - normal in BPH, haematuria in cancer, pyuria in UTI - PSA - elevation greater than age guideline - International Prostate Symptom Score - defines severity of symptoms - Global bother score - defines degree of bother to patient - Volume charting - diary of frequency and volume of voiding Consider: - USS - hydronephrosis, mass, urolithiasis, post-void residual - CT AP - mass, hydronephrosis, urolithiasis - Cystoscopy - mass, stone, stricture - Uroflowmetry - < 15ml/second - Urodynamic study - abnormal bladder pressure, abnormal bladder voiding
89
Identify the possible complications of BPH and its management.
- Acute urinary retention - Long-term chronic urinary retention - UTI - Renal damage - Renal stones
90
Summarise the prognosis for patients with BPH.
The outlook for benign prostatic hyperplasia is good; although it can cause significant discomfort, the condition is benign. As the prostate gland grows in size, symptoms may become worse, warranting medication or surgery.
91
Generate a management plan for patients with BPH.
NON-BOTHERSOME - Watchful waiting - yearly follow up - Behavioural management programme - limit fluids, bladder training, treatment of constipation BOTHERSOME + NO SURGERY - Alpha blocker - terazosin, doxazosin, alfuzosin, tamsulosin, silodosin - Behavioural management programme - 5-alpha-reductase inhibitor - finesteride, dutasteride - Phosphodiesterase-5 (PDE-5) inhibitor - sildenafil, tadalafil, vardenafil - Anti-cholinergic agent - tolterodine, fesoterodine, oxybutynin, solifenacin - Combination! BOTHERSOME + SURGERY + PROSTATE VOLUME < 30g - Minimally invasive therapy: TUIP BOTHERSOME + SURGERY + PROSTATE VOLUME 30-80g - Minimally invasive therapy: PVP, PUL, TUMT, water vapour thermal therapy - Moderately invasive therapy: TURP, TUVP, laser vaporisation (HoLEP, ThuLEP, PVP) BOTHERSOME + SURGERY + PROSTATE VOLUME > 80g - Open prostatectomy or laser enucleation (HoLEP or ThuLEP)
92
Define CKD.
Abnormalities of kidney structure of function, present for >3 months, with implications for health. Glomerular filtration rate < 60ml/min/1.73m^2. Presence of one or more of the markers of kidney damage: - Albuminuria - Proteinuria - Urine sediment abnormalities - e.g. haematuria - Electrolyte abnormalities due to tubular disorders - Abnormalities detected by histology - Structural abnormalities detected by imaging - History of kidney transplantation
93
Explain the aetiology / risk factors of CKD.
Common causes: - DM - Hypertension - Glomerulonephritis - Chronic pyelonephritis - Medullary cystic kidney disease - Obstructive nephropathy - Obesity-related nephropathy - Ischaemic nephropathy - Acute uric acid nephropathy Risk factors: - DM - Hypertension - Age > 50 years - Childhood kidney disease - Smoking - Obesity - Black or Hispanic ethnicity - Family history of CKD - Autoimmune disorders - Male sex - Long-term use of NSAIDs - High uric acid levels
94
Summarise the epidemiology of CKD.
CKD is more common in people aged 65 years or older (38%) than in people aged 45–64 years (13%) or 18–44 years (7%). CKD is more common in women (15%) than men (12%). CKD is more common in non-Hispanic blacks (16%) than in non-Hispanic whites (13%) or non-Hispanic Asians (12%). About 14% of Hispanics have CKD.
95
Recognise the presenting symptoms of CKD.
- Fatigue - N&V - Pruritus - Restless legs - Anorexia - Infection-related glomerular disease - Oedema - Arthralgia - Enlarged prostate gland - Foamy-appearing urine - Coca-coloured urine
96
Recognise the signs of CKD on physical examination.
- Fatigue - N&V - Pruritus - Restless legs - Anorexia - Infection-related glomerular disease - Oedema - Arthralgia - Enlarged prostate gland - Foamy-appearing urine - Coca-coloured urine
97
Identify appropriate investigations for CKD and interpret the results.
1st line: - Renal chemistry - high renal creatinine, electrolyte abnormalities (metabolic acidosis develops) - Estimation of GFR- < 60ml?min/1.73m^2 - Serum cystatin C and cystatin C-based estimation of GFR - reduced muscle mass (overestimation), increased muscle mass (underestimation) - Urinalysis - haematuria, proteinuria - Urinary albumin - moderately increased [AER 30-300 mg/day; ACR 30-300 mg/g] - Renal ultrasound - small kidney size, presence of obstruction/hydronephrosis, kidney stones Consider: - Kidney biopsy - variable depending on aetiology - Plain Abdo XR - calcium-containing kidney stones - Abdo CT - reveal kidney stones, renal masses, cysts - Abdo MRI - mass lesions in kidney
98
Define glomerulonephritis.
Glomerular injury. Characterised by inflammatory changes in glomerular capillaries and glomerular basement membrane.
99
Explain the aetiology / risk factors of glomerulonephritis.
Can involve part or all of the glomeruli or the glomerular tuft. Inflammatory changes mostly immune mediated. Group of diseases: - Membranous GN - Minimal change disease - Focal and segmental glomerulosclerosis - Immunoglobulin A nephropathy - Rapidly progressive GN - vasculitis and anti-GBM disease - Lupus nephritis Risk factors: - Group A beta-haemolytic Streptococus - Respiratory infections - GI infections - HBV - HCV - Infective endocarditis - HIV - SLE - Systemic vasculitis - Hodgkin's lymphoma - Lung cancer - Colorectal cancer - Non-Hodgkin's lymphoma - Leukaemia - Thymoma - Haemolytic uraemic syndrome - Drugs - penicillamine, gold sodium thiomalate, NSAIDs, captopril, mitomycin C, cocaine, anabolic steroids
100
Summarise the epidemiology of glomerulonephritis.
The mean age of prevalent and incident patients with GN from a systemic immunologic disease was 55.2 and 58.0 years, respectively. For primary GN, 41.7% of prevalent and 40.4% of incident patients were female; for GN from a systemic immunologic disease, 69.0% of prevalent and 58.0% of incident patients were female.
101
Recognise the presenting symptoms of glomeruloneprhitis.
- Presence of risk factors - Haematuria - Oedema - Hypertension - Oliguria - Anorexia - Nausea - Malaise - Weight loss - Fever - Skin rash - Arthralgia - Haemoptysis - Abdominal pain - Sore throat - Hypervolaemia
102
Recognise the signs of glomerulonephritis on physical examination.
- Presence of risk factors - Haematuria - Oedema - Hypertension - Oliguria - Anorexia - Nausea - Malaise - Weight loss - Fever - Skin rash - Arthralgia - Haemoptysis - Abdominal pain - Sore throat - Hypervolaemia
103
Identify appropriate investigations for glomerulonephritis and interpret the results.
- Urinalysis and urine microscopy - haematuria, proteinuria, dysmorphic RBCs, leukocytes, RBC casts - Comprehensive metabolic profile - normal or renal failure, elevated liver enzymes, hypoalbuminaemia - GFR - normal or reduced - FBC - normocytic normochromic anaemia - Lipid profile - hyperlipidaemia or normal - Spot urine albumin:creatinine ratio (ACR) - normal or high (>220mg/mmol) - Ultrasound of kidneys - small kidneys or normal Consider: - ESR/CRP - elevated or normal - Complement levels - low or normal C3 in immune complex diseases - Rheumatoid factor - positive or normal (rheumatoid arthritis or cryoglobulinaemia) - Anti-neutrophil cytoplasmic antibody - positive or normal (pacui-immune or anti-GBM disease) - Anti-glomerular basement membrane (GBM) antibody - positive or normal ( anti-GBM, Goodpasture's) - Anti-streptolysin O antibody - high or rising titres indicate post-strep GN - Anti-hyaluronidase - high or rising titres indicate post-strep GN - Anti-DNAse - positive indicate post-strep GN - Anti-double-stranded DNA - positive (SLE) or normal - Anti-nuclear antibody - high titres = SLE - Cryoglobins - positive or normal (cryoglobulinaemia) - HCV and HBV serology - positive or normal - HIV serology - antibody to HIV or normal - Electrophoresis - monoclonal or polyclonal gammopathy or normal - Drug screen - positive or normal (if suspected drug or medication toxicity) - Renal biopsy - characteristic findings - Anti-phoshplipase A2 receptor antibodies - positive or nomral (idiopathic membranous GN) - CT Chest Abdo - normal or positive for malignancy (exclude in normal patients)
104
Define nephrotic syndrome.
The presence of proteinuria (>3.5g / 24 hours), hypoalbuminaemia (<30g/L) and peripheral oedema. PROTEINURIA HYPOALBUMINAEMIA PERIPHERAL OEDEMA NB: Contrast to nephritic syndrome (AKI + hypertension + active urinary sediment of red cells/casts) = NEPHROTIC SYNDROME HAS NO CELLS OR CASTS IN URINE.
105
Explain the aetiology / risk factors of nephrotic syndrome.
Causes: - Minimal change disease - Focal segmental glomerulosclerosis - Membranous nephropathy (most common cause in adults) - Diabetic nephropathy (both 1 and 2) - Amyloidosis PATHOPHYSIOLOGY There are 3 categories of proteinuria: glomerular, tubular, and overflow. Glomerular proteinuria develops when the components of the filtration barrier are disrupted by disease. The primary insult leading to the development of nephrotic syndrome is the development of high-grade glomerular proteinuria, and the heavier the protein loss the more likely the development of the full-blown syndrome and worsening of renal function. Patients become hypoalbuminaemic due to the urinary loss of albumin. The liver tries to compensate for this protein loss by increasing the synthesis of albumin, as well as other molecules including LDL and VLDL and lipoprotein(a), contributing to the development of lipid abnormalities including hypercholesterolaemia and hypertriglyceridaemia. Lipiduria occurs in the form of: lipid sediment, fatty casts, oval fat bodies, or free fat droplets in the urine (which appear as Maltese crosses under polarised light). Hypercoagulability results from the loss of inhibitors of coagulation in the urine and increased synthesis of procoagulatory factors by the liver. The oedema is due to a combination of a decrease in oncotic pressure from the hypoalbuminaemia, as well as a primary renal sodium retention in the collecting tubules. Patients with nephrotic syndrome are also at increased risk of infection due to loss of immunoglobulins and complement and other compounds being lost in the urine.
106
Summarise the epidemiology of nephrotic syndrome.
The most common cause in children is minimal change disease.[1] In adults, primary glomerular diseases are more frequent in males (55%), whereas secondary glomerular disease is more frequent in females (72%). The most common cause in younger adults is FSGS, followed by minimal change nephropathy. Membranous nephropathy is the most common cause in older people,[2][3] and diabetic nephropathy in adults with a history of long-standing diabetes.
107
Recognise the presenting symptoms of nephrotic syndrome.
- History of long-standing diabetes, end-organ damage, renal disease, malignancy, SLE, HIV infection, multiple myeloma, connective tissue diseases, amyloidosis - Medications - pamidronate, lithium, gold, penicillamine, NSAIDs, interferon alfa, heroin, mercury, formaldehyde - Oedema - Foamy urine - Symptoms suggestive of occult malignancy - cough, weight loss, night weats, tarry stools - Symptoms suggestive of SLE - rash, photosensitivity, arthralgias - Symptoms suggestive of Fabry's disease - painful neuropathy - Family history of Fabry's disease, amyloidosis, renal disease
108
Recognize the signs of nephrotic syndrome on physical examination.
- Mild oedema or severe oedema (anasara) - peri-orbital oedema - White banding of the nails from hypoalbuminaemia - Muehrcke's lines - Xanthelasmata - severe HCL - Weight gain due to simultaneous oedema with protein malnutrition lean body mass loss - Rash (SLE) - Easy bruising (amyloidosis) - Neuropathy (amyloidosis) - Haem-positive stool (GI malignancy) - Fundoscopic examination shows diabetic retinopathy
109
Identify appropriate investigations for nephrotic syndrome and interpret the results.
To establish a diagnosis of nephrotic syndrome, initial evaluation includes: - Careful history and physical examination - Quantification of proteinuria by either a 24-hour urine collection (normal <150 mg/day, nephrotic range >3.5 g/day) or alternatively a spot urine protein-to-creatinine ratio on a random urine specimen (this closely correlates with a 24-hour urine protein). - Urinalysis (fresh urine) with microscopy to check for the presence of cellular casts. - Urine should also be sent for urine protein electrophoresis ``` - Serological studies, including: auto-immune screen (ANA, complement screen, cryoglobulins) serum free light chains syphilis serology hepatitis B and C serology. ``` - Renal biopsy to determine the type of nephrotic syndrome
110
Define polycystic kidney disease.
Part of a heterogeneous group of disorders characterised by: - RENAL CYSTS - SYSTEMIC AND EXTRARENAL MANIFESTATIONS
111
Explain the aetiology / risk factors of polycystic kidney disease.
x2 TYPES: - Autosomal-dominant PKD - Autosomal recessive PKD RESULTS IN: - RENAL CYSTS - EXTRARENAL CYSTS - INTRACRANIAL ANEURYSMS - DOLICHOECTASIAS - elongated and distended arteries - AORTIC ROOT DILATION - ANEURYSMS - MITRAL VALVE PROLAPSE - ABDOMINAL WALL HERNIAS Risk Factors: - Family history of autosomal-dominant PKD - Family history of cerebrovascular event
112
Summarise the epidemiology of polycystic kidney disease.
More common = autosomal dominant PKD
113
Recognise the presenting symptoms of polycystic kidney disease.
- FHx of autosomal-dominant PKD or end-stage renal disease - FHx of cerebrovascular event - Renal cysts - Hypertension - Abdominal / flank pain - Haematuria - Palpable kidneys / abdominal mass - Headaches - Dysuria, urgency, suprapubic pain, fever - Cardiac murmur - Abdominal hernia or rectus abdominis diastasis - Hepatomegaly - Chest pain
114
Recognise the signs of polycystic kidney disease on physical examination.
- FHx of autosomal-dominant PKD or end-stage renal disease - FHx of cerebrovascular event - Renal cysts - Hypertension - Abdominal / flank pain - Haematuria - Palpable kidneys / abdominal mass - Headaches - Dysuria, urgency, suprapubic pain, fever - Cardiac murmur - Abdominal hernia or rectus abdominis diastasis - Hepatomegaly - Chest pain
115
Identify appropriate investigations for polycystic kidney disease and interpret the results.
1st line: - Renal ultrasound - <30 years = at least 2 uni/bilateral cysts, 30-59 yrs = 2 cysts in each kidney, >60 years = 4 cysts in each kidney - CT scan of abdomen / pelvis - absence of FHx: >10 cysts in each kidney; presence of FHx: <30 years of age - at least 2 unilateral or bilateral cysts; 30 to 59 years of age: 2 cysts in each kidney; >60 years of age: 4 cysts in each kidney - MRI of abdomen / pelvis - >10 cysts in each kidney - Urinalysis / Gram stain and urine culture - bacteriuria if UTI, microscopic haematuria, proteinuria, increased urinary albumin excretion - Serum electrolytes, urea, creatinine - normal or elevated - Fasting lipid profile - normal or elevated (prognostic marker) - ECG - LVH changes in setting of CV complications - CT scan of brain - positive for intracranial bleed in setting of ruptured intracranial aneurysm Consider: - Genetic testing - PKD1 or PKD2 mutation - Echocardiogram - mitral valve prolapse, aortic root dilation, diastolic dysfunction, LVH - 24 hour urine collection - low citrate, high uric acid, oxalate in setting of stones, proteinuria - KUB XR and tomogram - radiopaque stones on KUB, radiolucent identified on tomogram - Dual-energy CT - differences in attenuation values differentiate between stones if present - LP and cerebrospinal fluid analysis - elevated cerebrospinal fluid pressure or xanthochromia in setting of ruptured intracranial aneurysm - MR angiogram of brain - bleeding vessel or intracranial aneurysm identified - CRP - >5 mg/dL suggests infection - PET scan - increased uptake suggests infection
116
Define transurethral resection of the prostate (TURP).
Resection from within the prostatic urethra. May be achieved using a variety of methods - e.g. electrocautery, laser.
117
Summarise the indications for transurethral resection of the prostate (TURP).
- Acute urinary retention - Failed voiding trials - Recurrent gross haematuria - Urinary tract infection - Renal insufficiency secondary to obstruction
118
Identify the possible complications of transurethral resection of the prostate (TURP).
- Bladder injury - Hemorrhage - primary, reactionary or secondary - Haematuria - Electrolyte abnormalities - Infection - Loss of erections (ED) - Painful or difficult urination - Retrograde ejaculation - goes into the bladder and not out the penis - Clot retention - Incontinence - TUR syndrome - seizures or cardiovascular collapse caused by hypervolaemia and hyponatremia due to absorption of glycine irrigation fluid - Urethral stricture
119
Define renal artery stenosis.
A narrowing of the renal artery lumen. Significant if >50% reduction in vessel diameter present. Ischaemic nephropathy - chronic reduction in glomerular filtration rate that occurs from a narrowing in the renal artery. Renovascular hypertension is hypertension mediated by high levels of renin and Angiotensin II, produced by an underperfused kidney supplied by a stenosed renal artery.
120
Explain the aetiology / risk factors of renal artery stenosis.
Due to atherosclerotic disease or fibromuscular dysplasia. Often presents with accelerated or difficult-to-control hypertension. Risk factors: - Dyslipidaemia - Smoking - Diabetes - Female sex
121
Summarise the epidemiology of renal artery stenosis.
Image result for epidemiology of renal artery stenosis The prevalence of renal artery stenosis ranges from 14% to 42% in studies performed on patients with aortic (abdominal) or peripheral vascular disease (10–16). It is somewhat less (11% to 23%) in patients with documented coronary artery disease (17–19).
122
Recognise the presenting symptoms of renal artery stenosis.
- Onset of hypertension age >55 years - History of accelerated, malignant or resistant hypertension - History of unexplained kidney dysfunction - History of unexplained kidney dysfunction - History of multi-vessel coronary artery disease - History of another peripheral vascular disease - Abdominal bruit - Sudden or unexplained recurrent pulmonary oedema - Onset of hypertension age < 30 years - Absence of family history of hypertension - History of AKI after ACE or ARB - History of unexplained congestive heart failure - Refractory angina - History of hypokalaemia
123
Recognise the signs of renal artery stenosis on physical examination.
- Onset of hypertension age >55 years - History of accelerated, malignant or resistant hypertension - History of unexplained kidney dysfunction - History of unexplained kidney dysfunction - History of multi-vessel coronary artery disease - History of another peripheral vascular disease - Abdominal bruit - Sudden or unexplained recurrent pulmonary oedema - Onset of hypertension age < 30 years - Absence of family history of hypertension - History of AKI after ACE or ARB - History of unexplained congestive heart failure - Refractory angina - History of hypokalaemia
124
Identify appropriate investigations for renal artery stenosis and interpret the results.
1st Line: - Serum creatinine - normal or elevated - Serum potassium - low or normal (hypokalaemia may suggest due to activation of RAAS) - Urinalysis and sediment evaluation - normal in absence of diabetic nephropathy or hypertensive glomerulosclerosis - Aldosterone-to-renin ratio - <20 (excludes primary aldosteronism as cause of hypertension and hypokalaemia) Investigations to consider: - Duplex ultrasound - >50% reduction in vessel diameter - Gadolinium-enhanced MRA - >50% reduction in vessel diameter - CT angiography - >50% reduction in vessel diameter - Conventional angiography - >50% reduction in vessel diameter - CO2 angiography - >50% reduction in vessel diameter - Non-contrast magnetic resonance angiography - >50% reduction in vessel diameter - Captopril radionuclide renal scan - delayed time to max radiotracer activity, asymmetry of peak activity of each kidney, marked cortical retention, marked reduction in cGFR
125
Define urinary tract calculi.
Aka. Nephrolithiasis or urolithiasis. The presence of crystalline stones (calculi) within the urinary system (kidneys and ureter).
126
Explain the aetiology / risk factors of urinary tract calculi.
Composed of varying amounts of crystalloid and organic matrix. Originate in kidney and pass down into the ureter. Risk factors: - Chronic dehydration - Diet - high salt intake - Obesity - Positive family history - Specific medicines - antacids, carbonic anhydrase inhibitors, sodium and calcium containing medications, vitamins C and D, protease inhibitors - Metabolic abnormalities - Male - Crystalluria - White ancestry - Warm climate
127
Summarise the epidemiology of urinary tract calculi.
Adult men more commonly than adult women. | Common.
128
Recognise the presenting symptoms of urinary tract calculi.
- Acute, severe flank pain - Previous episodes - N&V - Urinary frequency / urgency - Haematuria - Testicular pain - Obesity - Family history of nephrolithiasis - Precipitation medications - antacids, carbonic anhydrase inhibitors, sodium and calcium containing medications, vitamins C and D, protease inhibitors - Groin pain - Fever - Tachycardia - Hypotension - Costovertebral angle and ipsilateral flank tenderness - loin to groin!
129
Recognise the signs of urinary tract calculi on physical examination.
- Acute, severe flank pain - Previous episodes - N&V - Urinary frequency / urgency - Haematuria - Testicular pain - Obesity - Family history of nephrolithiasis - Precipitation medications - antacids, carbonic anhydrase inhibitors, sodium and calcium containing medications, vitamins C and D, protease inhibitors - Groin pain - Fever - Tachycardia - Hypotension - Costovertebral angle and ipsilateral flank tenderness - loin to groin!
130
Identify appropriate investigations for urinary tract calculi and interpret the results.
1st line: - Non-contrast helical CT scan (non-pregnant) - calcification seen in renal collecting system or ureter, hydronephrosis, perinephric stranding (indicative of inflammation or infection) - Renal ultrasound (pregnant or child) - calcification within the urinary tract, along with dilation - Urinalysis - leukocytes, nitrates, blood (majority), microscopic WBC/FBC or bacteria - FBC with differential - high WCC suggests pyelonephritis or urinary tract infection - Serum electorlytes, urea and creatinine - hypercalcaemia (hyperPTH), hyperuricaemia (gout) - Urine pregnancy test - negative Consider: - Stone analysis - stone composition - Plain abdominal radiograph (KUB) - calcification seen within the urinary tract - MRI - filling defect seen in the collecting system - Spot urine for cystine - cystinuria
131
Generate a management plan for urinary tract calculi.
INITIAL - acute renal colic, nonpregnant - Hydration - Analgesia - NSAIDs (ibuprofen, diclofenac), IV paracetamol, Morphine ACUTE 1) Confirmed renal or ureteric stone, with evidence of obstruction, non-pregnant WITH INFECTION - Urgent decompression via stent or percutaneous nephrostomy tube - Urgent antibiotic therapy - empirical broad-spectrum pending sensitivity results WITHOUT INFECTION - Urgent decompression 2) Confirmed renal stone, no evidence of obstruction, non-pregnant - Hydration - Analgesia - NSAIDs (ibuprofen, diclofenac), IV paracetamol, Morphine - Antibiotic therapy - depends on infection, patient factors, local resistance patterns - Watchful waiting if asymptomatic <5mm or 5-10mm and patient consent - Surgical intervention - shock wave lithotripsy, ureteroscopy, percutaneous nephrolithotomy 3) Confirmed ureteric stone, no evidence of obstruction, non-pregnant - Hydration - Analgesia - NSAIDs (ibuprofen, diclofenac), IV paracetamol, Morphine - Antibiotic therapy - depends on infection, patient factors, local resistance patterns - Medical expulsive therapy - alpha-blocker (tamsulosin or alfuzosin) for distal ureteric stones <10mm - Surgical intervention - shock wave lithotripsy, ureteroscopy, percutaneous nephrolithotomy 4) Pregnant - Specialist referral - ureteric strent or percutaneous nephrolithotomy tube if not controlled with oral analgesia or obstructing stone or infection - 48-80% of stones pass spontaneously during pregnancy ONGOING - following an acute episode, non-pregnant - Hydration - add lemon juice - Dietary modification - avoid high protein, lots of fruit & veg, - Alkalinisation - potassium citrate, sodium bicarbonate (dissolves uric acid stones) - Preventative medical therapy - potassium citrate, sodium bicarbonate, thiazide diuretics (>50% calcium oxalate, hypercalciuria), oxalate chelator (hyperoxaluria), cystinuria (thiol binding agent and potassium citrate)
132
Identify the possible complications of urinary tract calculi and its management.
- Abcess formation - Pyelonephritis - Urinary fistula formation - ureteral scarring - Ureteral stenosis - Ureteral perforation - Extravasation - Urosepsis - Obstruction
133
Summarise the prognosis for patients with urinary tract calculi.
The usually quoted recurrence rate for urinary calculi is 50% within 5 years and 70% or higher within 10 years, although a large, prospective study published in 1999 suggested that the recurrence rate may be somewhat lower at 25-30% over a 7.5-year period.