Renal & Urology Flashcards

Question 1

Q

Define bladder cancer.

Answer

A

Cancer that forms in tissues of the bladder.

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

Question 2

Q

Explain the aetiology / risk factors of bladder cancer.

Answer

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

Question 3

Q

Summarise the epidemiology of bladder cancer.

Answer

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.

Question 4

Q

Recognise the presenting symptoms of bladder cancer.

Answer

A

Presence of risk factors
Haematuria - gross or microscopic
Dysuria
Urinary frequency

Question 5

Q

Recognise the signs of bladder cancer on physical examination.

Answer

A

Presence of risk factors
Haematuria - gross or microscopic
Dysuria
Urinary frequency

Question 6

Q

Identify appropriate investigations for bladder cancer and interpret the results.

Answer

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

Question 7

Q

Define prostate cancer.

Answer

A

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

Question 8

Q

Explain the aetiology / risk factors of prostate cancer.

Answer

A

Risk factors:

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

Question 9

Q

Summarise the epidemiology of prostate cancer.

Answer

A

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

Uncommon in men aged under 50 years.

Question 10

Q

Recognise the presenting symptoms of prostate cancer.

Answer

A

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

Question 11

Q

Recognise the signs of prostate cancer on physical examination.

Answer

A

Elevated PSA
Abnormal digital rectal exam
Palpable lymph nodes
Haematuria

Question 12

Q

Identify appropriate investigations for prostate cancer and interpret the results.

Answer

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

Question 13

Q

Define renal cell carcinoma.

Answer

A

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

Question 14

Q

Explain the aetiology / risk factors of renal cell carcinoma.

Answer

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

Question 15

Q

Summarise the epidemiology of renal cell carcinoma.

Answer

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).

Question 16

Q

Recognise the presenting symptoms of renal cell carcinoma.

Answer

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

Question 17

Q

Recognise the signs of renal cell carcinoma on physical examination.

Answer

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

Question 18

Q

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

Answer

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)

Question 19

Q

Define testicular cancer.

Answer

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.

Question 20

Q

Explain the aetiology / risk factors of testicular cancer.

Answer

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

Question 21

Q

Summarise the epidemiology of testicular cancer.

Answer

A

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

Question 22

Q

Recognise the presenting symptoms of testicular cancer.

Answer

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

Question 23

Q

Recognise the signs of testicular cancer on physical examination.

Answer

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

Question 24

Q

Identify appropriate investigations for testicular cancer and interpret the results.

Answer

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

Question 25

Q

Define testicular torsion.

Answer

A

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.

Question 26

Q

Explain the aetiology / risk factors of testicular torsion.

Answer

A

Risk Factors:

Age under 25 years
Neonate
Bell clapper deformity
Trauma / exercise
Intermittent testicular pain
Undescended testicle
Cold weather

Question 27

Q

Summarise the epidemiology of testicular torsion.

Answer

A

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.

Question 28

Q

Recognise the presenting symptoms of testicular torsion.

Answer

A

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

Question 29

Q

Recognise the signs of testicular torsion on physical examination.

Answer

A

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.

Question 30

Q

Identify appropriate investigations for testicular torsion and interpret the results.

Answer

A

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

Question 31

Q

Generate a management plan for testicular torsion.

Answer

A

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

Question 32

Q

Identify the possible complications of testicular torsion and its management.

Answer

A

Infection
Infertility
Gangrene
Cosmetic deformity
Atrophy
Testicular death

Question 33

Q

Summarise the prognosis for patients with testicular torsions.

Answer

A

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

Question 34

Q

Define AKI.

Answer

A

An acute decline in kidney function, leading to a rise in serum creatinine and/or a fall in urine output.

Spectrum - mild to severe

Question 35

Q

Explain the aetiology / risk factors of AKI.

Answer

A

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)

Question 36

Q

Summarise the epidemiology of AKI.

Answer

A

10,400 per million
Seen in 10-20% of people admitted to hospital as emergencies
Inpatient mortality >20%
ICU incidence - 20-50%, mortality >50%

Question 37

Q

Recognise the presenting symptoms of AKI.

Answer

A

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

Question 38

Q

Recognise the signs of AKI on physical examination.

Answer

A

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

Question 39

Q

Identify appropriate investigations for AKI and interpret the results.

Answer

A

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

Question 40

Q

Generate a management plan for AKI.

Answer

A

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)

Question 41

Q

Identify the possible complications of AKI and its management.

Answer

A

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

Question 42

Q

Summarise the prognosis for patients with AKI.

Answer

A

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

Question 43

Q

What is Resuscitation, Replacement or Routine Maintenance, when you’re prescribing IV fluid therapy?

Answer

A

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.

Question 44

Q

Define urinary catheterisation.

Answer

A

A flexible tube used to empty the bladder and collect urine in a drainage bag.

Urethral or suprapubic (small opening in tummy).

Question 45

Q

Summarise the indications for urinary catheterisation.

Answer

A

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

Question 46

Q

Identify the possible complications of urinary catheterisation.

Answer

A

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

Question 47

Q

Define amyloidosis.

Answer

A

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

Question 48

Q

Explain the aetiology / risk factors of amyloidosis.

Answer

A

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

Question 49

Q

Summarise the epidemiology of amyloidosis.

Answer

A

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

Question 50

Q

Recognize the presenting symptoms of amyloidosis.

Answer

A

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

Question 51

Q

Recognize the signs of amyloidosis on physical examination.

Answer

A

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

Question 52

Q

Identify appropriate investigations for amyloidosis and interpret the results.

Answer

A

Tissue biopsy - congo red stain, immunohistochemistry (diagnose amyloidosis, identify amyloid fibril protein)
Urine (proteinuria, free immunoglobi light chains in AL)
Blood (CRP, ESR, RF, Ig levels, serum protein electrophoresis, LFTs, U&E, SAA levels)
123I-SAP Scan - radiolabeled SAP localizes to the deposits enabling quantitative imaging of amyloidotic organs throughout the body

Question 53

Q

Define UTI.

Answer

A

Characterised by presence of >100,000 of colony-forming units per milllitre of urine.

May affect bladder (cystitis), kidney (pyelonephritis) or prostate (prostatitis).

Question 54

Q

Explain the aetiology / risk factors of UTI.

Answer

A

Transurethral ascent of normal colonic organisms.

Escherichia coli
Proteus mirabilis
Klebsiella
Enterococci (hospitals)

Question 55

Q

Summarise the epidemiology of UTI.

Answer

A

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).

Question 56

Q

Recognise the presenting symptoms of UTI.

Answer

A

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.

Question 57

Q

Recognise the signs of UTI on physical examination.

Answer

A

May be asymptomatic.

Cystitis:

Fever
Abdominal / suprapubic / loin tenderness
Bladder distension

Pyelonephritis

Fever
Loin / flank tenderness

Prostatitis:

Tender
Swollen prostate

Question 58

Q

Identify appropriate investigations for UTI and interpret the results.

Answer

A

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

Question 59

Q

Generate a management plan for UTI.

Answer

A

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

Question 60

Q

Identify the possible complications or UTI and its management.

Answer

A

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

Question 61

Q

Summarise the prognosis for patients with UTI.

Answer

A

Mostly resolve with treatment. Among pregnant women, 20% develop acute pyelonephritis if not treated, however there is a high relapse rate.

Question 62

Q

Define epididymitis and orchitis.

Answer

A

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.

Question 63

Q

Explain the aetiology / risk factors of epididymitis and orchitis.

Answer

A

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

Question 64

Q

Summarise the epidemiology of epididymitis and orchitis.

Answer

A

Usually unilateral.

Answer 65

A

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

Answer 66

A

Common

Unilateral scrotal pain
Tenderness
Hot
Erythematous
Swollen hemiscrotum

Uncommon

Pyrexia
Fluctuant swelling or induration of scrotal tissue
Enlarged or tender prostate

Answer 67

A

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

Answer 68

A

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

Answer 69

A

Scrotal abscess and pyocele
Testicular infarction
Fertility problems
Testicular atrophy
Cutaneous fistulization from rupture of abscess through tunica vaginalis
Recurrence, chronic epididymitis and orchialgia

Answer 70

A

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.

Answer 71

A

The abnormal dilation of the internal speratic veins and pampiniform plexus that drain blood from the testis.

Answer 72

A

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

Answer 73

A

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.

Answer 74

A

Painless scrotal mass
Left-sided signs / symptoms
Small testicle
Infertility
Age > 12 years
Scrotal or groin pain

Answer 75

A

Painless scrotal mass
Left-sided signs / symptoms
Small testicle
Infertility
Age > 12 years
Scrotal or groin pain (uncommon)

Answer 76

A

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

Answer 77

A

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.

Answer 78

A

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

Answer 79

A

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

Answer 80

A

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

Answer 81

A

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

Answer 82

A

1st line:
- Clinical diagnosis - features of hydrocele

Consider:
- Ultrasound - confirm prescence via scrotal or inguinal ultrasound

Answer 83

A

Lower urinary tract symptoms (LUTS) caused by bladder outlet obstruction (BOO) due to benign prostatic hyperplasia (also known as BPE).

Answer 84

A

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

Answer 85

A

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.

Answer 86

A

LUTS

STORAGE SYMPTOMS

Frequency
Urgency
Nocturia
Incontinence

VOIDING SYMPTOMS

Weak stream
Dribbling
Dysuria
Straining

Uncommon:

Fever with dysuria
Urinary retention

Answer 87

A

Prostate volume > 30g
Nodules or tenderness suspicious of prostate cancer or prostatitis
Abdominal examination for palpable bladder
DRE
Neurological assessment

Answer 88

A

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

Answer 89

A

Acute urinary retention
Long-term chronic urinary retention
UTI
Renal damage
Renal stones

Answer 90

A

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.

Answer 91

A

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)

Answer 92

A

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

Answer 93

A

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

Answer 94

A

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.

Answer 95

A

Fatigue
N&V
Pruritus
Restless legs
Anorexia
Infection-related glomerular disease
Oedema
Arthralgia
Enlarged prostate gland
Foamy-appearing urine
Coca-coloured urine

Answer 96

A

Fatigue
N&V
Pruritus
Restless legs
Anorexia
Infection-related glomerular disease
Oedema
Arthralgia
Enlarged prostate gland
Foamy-appearing urine
Coca-coloured urine

Answer 97

A

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

Answer 98

A

Glomerular injury.

Characterised by inflammatory changes in glomerular capillaries and glomerular basement membrane.

Answer 99

A

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

Answer 100

A

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.

Answer 101

A

Presence of risk factors
Haematuria
Oedema
Hypertension
Oliguria
Anorexia
Nausea
Malaise
Weight loss
Fever
Skin rash
Arthralgia
Haemoptysis
Abdominal pain
Sore throat
Hypervolaemia

Answer 102

A

Presence of risk factors
Haematuria
Oedema
Hypertension
Oliguria
Anorexia
Nausea
Malaise
Weight loss
Fever
Skin rash
Arthralgia
Haemoptysis
Abdominal pain
Sore throat
Hypervolaemia

Answer 103

A

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)

Answer 104

A

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.

Answer 105

A

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.

Answer 106

A

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.

Answer 107

A

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

Answer 108

A

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

Answer 109

A

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

Answer 110

A

Part of a heterogeneous group of disorders characterised by:

RENAL CYSTS
SYSTEMIC AND EXTRARENAL MANIFESTATIONS

Answer 111

A

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

Answer 112

A

More common = autosomal dominant PKD

Answer 113

A

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

Answer 114

A

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

Answer 115

A

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

Answer 116

A

Resection from within the prostatic urethra.

May be achieved using a variety of methods - e.g. electrocautery, laser.

Answer 117

A

Acute urinary retention
Failed voiding trials
Recurrent gross haematuria
Urinary tract infection
Renal insufficiency secondary to obstruction

Answer 118

A

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

Answer 119

A

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.

Answer 120

A

Due to atherosclerotic disease or fibromuscular dysplasia.

Often presents with accelerated or difficult-to-control hypertension.

Risk factors:

Dyslipidaemia
Smoking
Diabetes
Female sex

Answer 121

A

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).

Answer 122

A

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

Answer 123

A

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

Answer 124

A

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

Answer 125

A

Aka. Nephrolithiasis or urolithiasis.

The presence of crystalline stones (calculi) within the urinary system (kidneys and ureter).

Answer 126

A

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

Answer 127

A

Adult men more commonly than adult women.

Common.

Answer 128

A

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!

Answer 129

A

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!

Answer 130

A

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

Answer 131

A

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)

Answer 132

A

Abcess formation
Pyelonephritis
Urinary fistula formation
ureteral scarring
Ureteral stenosis
Ureteral perforation
Extravasation
Urosepsis
Obstruction

Answer 133

A

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.

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Renal & Urology Flashcards

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