Flashcards in Clinical (Week 4) Deck (274):
What is a hamartoma?
A tumour with the correct constituencies of the organ it's from but in wrong distribution
What is the most common renal pelvis tumour?
Transitional cell carcinoma
What is the most common renal parenchymal tumour?
Renal cell carcinoma
What is the most common renal embryonic tumour?
Nephroblastoma (Wilm's Tumour)
What sort of CT is useful in diagnosing a urological malignancy?
Triple phased contrast enhanced
What is the most common benign asymptomatic renal lesion?
Renal cyst (70%)
How do we investigate renal cysts and why can we use this modality?
USS (it is fluid-filled)
When would we biopsy an angiolypoma?
- Risk of bled
What feature of vessels in an angiolypoma make it prone to bleeds?
They are fragile
How can we measure lesion density on a CT of angiolypomas?
What is Wunderlich's Syndrome?
Collapse due to retroperitoneal bleed in an angiolypoma
How does an oncocytoma appear on CT?
- Stellate due to central necrosis
-> No angiogenesis therefore benign
What is the only way to definitively diagnose an oncocytoma and why is a biopsy not totally useful?
Biopsy has a high false negative rate
What is the classic triad of symptoms in a renal cell carcinoma?
Loin pain (40%)
Renal masses (25%)
Frank haematuria (60%)
Which of the following is not a paraneoplastic effect of renal cell carcinoma:
- Weight loss
- Hypercalcaemia (As it produces parathyroid-like hormone)
What is the M:F ratio for the incidence of a renal cell carcinoma?
What is the peak incidence age for renal cell carcinoma?
What type of cancer of a renal cell carcinoma and where is it found?
How do renal cell cancers appear histologically?
If there are bilateral or multifocal renal cell carcinomas, what condition should you suspect and what implications does this have?
- Implications for surgery
What is the first line investigation for renal cell carcinoma, and what is the best investigation?
1st line - USS
- Triple phase contrast CT
What is the downside to using biopsy in the diagnosis of renal cell carcinomas?
High false negative rate
What staging system is used for renal cell carcinomas?
True or false; Direct perinephric fat invasion is rare in renal cell carcinomas?
How do renal cell carcinomas tend to spread?
Where do renal cell carcinomas commonly spread?
Lungs ('Cannon ball' metastases)
What is the standard treatment for a renal cell carcinoma? What does the treatment involve?
Radical nephrectomy (preferably laparoscopically):
- Whole kidney within Gerota's fascia
- Perinephric fat removed
When is the standard treatment for a renal cell carcinoma most often carried out?
Within a month of diagnosis
When would the adrenal gland be removed in the treatment of renal cell carcinoma and why is it not routinely removed?
If it is involved
Reduces the risk of adrenal insufficiency (Addison's syndrome)
How is a partial nephrectomy carried out? What implications does this have on the operation?
Under cold ischaemic:
- Must be done in 20-30 minutes
What is the benefit to a partial nephrectomy?
It is nephron sparing:
- Maintains renal function
- Increases QoL and life expectancy
What surgical approaches can be taken in a partial nephrectomy?
What is the main risk of a partial nephrectomy?
Pseudoaneurysm due to healing vessels
Apart from nephrectomies, what two other treatment options are available for renal cell carcinoma?
How do we measure the performance status in metastatic renal cell carcinoma?
What type of drug is Sunitinib? How does it work?
Tyrosine Kinase inhibitor:
- VEG-F and PDG-F inhibition
- Reduces neovascularisation
What benefit does using Sunitinib in the treatment of renal cell carcinoma have?
26 vs 20 month progression-free survival
What are the five year survival rates of Stage 1-4 renal cell carcinomas?
Stage 1 -> 75%
Stage 2 -> 50%
Stage 3 -> 35%
Stage 4 -> 5%
What are Balanitis Xerotica Obliterans and Leukoplakia?
Pre-malignant cutaneous penile cancers
What is Balanitis Xerotica Obliterans a form of?
Lichen sclerosus et atrophicus (Lichen sclerosus)
How does Balanitis Xerotica Obliterans present?
Fissuring -> Pain
Where does Balanitis Xerotica Obliterans occur?
What is the potential for malignant transformation in Balanitis Xerotica Obliterans?
What can predispose to Balanitis Xerotica Obliterans?
What is Erythroplasia of Queryat?
Squamous cell carcinoma in situ on the:
How does Erythroplasia of Queryat appear?
Red, velvety patches
What is the name of a squamous cell carcinoma in situ on the rest of the genitalia (ie not Glans, Prepuce or shaft)?
What is it important to differentiate a Squamous cell carcinoma in situ from?
When would we circumcise a Squamous cell carcinoma in situ?
If present on the prepuce alone
How else can we treat a Squamous cell carcinoma in situ?
Red, raised area on the penis with a foul smelling, fungating mass and phimosis is the typical presentation in what?
How do we diagnose a penile carcinoma?
Biopsy (if invasive)
CT -> For distal LNs
What is the incidence rate and peak age for penile carcinoma?
1.5 per 100,000 men
80 years old
What infection is penile carcinoma linked to?
What type of cancer is a penile carcinoma?
Squamous cell carcinoma
If there is inguinal node invasion of a penile carcinoma, how do we approach the treatment?
1. Assess prognosis
2. Radionucleotide Sentinel Node Biopsy
3. Inguinal lymphadenectomy
What chemotherapy agents are used in the treatment of penile cancer?
What is the most common germ cell testicular tumour?
What are some examples of non-seminomatous germ cell tumours?
What does ITGCN stand for in terms of germ cell testicular tumours?
Intra-tubular germ cell neoplasia
How does a testicular tumour typically present?
Painless, insensitive testicular swelling
How many testicular tumours are due to metastases and where do they usually come from? How do they present?
- Neck LNs
What is the best investigation for testicular tumours?
USS (95% sensitivity and specificity)
When would CXR and CT be used in investigation testicular tumours?
Abdominal and thorax metastases
In what germ cell testicular cancer is α-feto protein never raised?
In what germ cell testicular cancers is hCG raised?
5-10% of pure seminomas
60% of teratomas
What can LDH be used to indicate in germ cell testicular cancers?
What are testicular tumour markers usually used to gauge?
Effectiveness of therapy
What approach is taken in orchidectomies? Why is this approach taken?
- Prevents damage to surrounding layers
- Reduces local recurrance
-> Due to clamping of cessels
What is the incidence of testicular tumours and what age is the peak incidence?
5 per 100,000 men
What is the increase in incidence of testicular tumours if there are undescended testes?
30 times risk
What are the three types of teratomas?
In trophoblastic teratomas, what percentage have a raised hCG?
What fraction of residual masses have the following characteristics:
- Only fibrous tissue
- Mature (benign) teratoma
- Residual tumour
Only fibrous tissue - A third
Mature (benign) teratoma - A third
Residual tumour - A third
Which of the following does not result from uraemia:
What effect does kidney disease have on Vitamin D? What does this result in?
Cannot be converted into the active form (Calcitriol)
- Bone disease
- Vascular calcification
What effect will kidney failure have on phosphate levels?
Phosphate will not be filtered into the filtrate as well so hyperphosphataemia will result
Why does renal failure result in anaemia?
Reduced production of erythropoietin
Why can dyspepsia happen in renal failure?
Increased risk of peptic ulcers
In renal failure there are a number of urinary tract features, what are they?
How do NSAIDs affect the kidneys?
What antibiotics can affect the kidneys?
Gentamicin -> Toxic
Trimethoprim -> Fluid retention
What happens to JVP in renal failure?
It is increased
What is accelerated hypertension classed as?
Diastolic BP >120mmHg
What is leukonychia a sign of?
Gouty tophi are seen in what kind of kidney disease?
Vasculitis skin rash and systemic vasculitis are signs of what renal disease?
What type of vasculitis is HSP?
What is the usual specific gravity of urine and what does this indicate?
What can cause urine to appear red?
Alkaline urine is seen in what?
If RBCs appear isomorphic in urine microscopy, what does this indicate?
It is a lower urinary tract cause
If RBCs appear dysmorphic in urine microscopy, what does this indicate?
They are from the glomerulus (been forced out so become misshapen)
What is a normal result of a 24hr urine collection for protein?
What is a normal protein:creatinine ratio?
What is classed as asymptomatic low grade proteinuria?
A protein:creatinine ratio of 0.5-1g/day (100mg/mmol)
What is classed as heavy proteinuria?
A protein:creatinine ratio of 1-3g/day (~300mg/mmol)
How is nephrotic syndrome classed in terms of protein:creatinine ratio?
Increased urine protein can indicate what?
Increased risk of dialysis need in the future
What causes urinary casts to form? Where is this secreted from?
Precipitation of Tamm-Horsfall mucoprotein:
- Renal tubule cells
What causes pronounced formation of urinary casts? What precipitates this?
- Reduced urine flow
- Low pH
Hyaline casts in the urinary are usually benign; true or false?
What do RBC urinary casts indicate?
What do leukocyte urinary casts indicate?
What do granular urinary casts indicate?
What chemicals can show up as crystals on urine microscopy? Which is the most common?
Calcium oxalate (most common)
Hypertension shows ECG changes indicative of what?
LVH and strain
What is Stage 1 CKD in terms of description and GFR?
Kidney damage with normal or increased GFR
What is Stage 2 CKD in terms of description and GFR?
Kidney damage with mildly reduced GFR
What is Stage 3 CKD in terms of description and GFR?
Moderatley reduced GFR:
- GFR 30-59
What is Stage 4 CKD in terms of description and GFR?
Severely reduced GFR:
What is Stage 5 CKD in terms of description and GFR?
What is kidney damage in terms of CKD 1 and 2?
Evidence of disease:
What is oliguria classified as?
What features need to be present for a patient to have an AKI?
Reduction in GFR over hours/days/weeks
With normal/impaired baseline renal function
Proteinuria (>3g/day) (mostly albumin), Hypoalbuminaemia, Oedema (limb and periorbital), Hypercholesterolaemia and often normal GFR are signs of what?
AKI, Oliguria, Oedema, Hypertension and Active urinary sediment (RBCs, RBC and granular casts and proteinuria) are signs of what?
Can CKD be diagnosed from one eGFR calculation?
How is GFR measure directly and why is it not routinely used?
- Time consuming
How do we usually calculate an eGFR?
Why does creatinine clearance overestimate GFR?
Creatinine is secreted into the tubules
What is serum creatinine a product of?
For white and asian males, what is the calculation for eGFR if creatinine is in mg/dL?
186 x Creatinine^-1.154 x Age^-0.203
For white and asian males, what is the calculation for eGFR if creatinine is in μmol/L?
32788 x Creatinine^-1.154 x Age^-0.203
What correction factors are applied to the eGFR calculation for:
2. Black people
1. Multiply whole equation by 0.742
2. Multiply whole equation by 1.212
When is eGFR mostly accurate?
If a patient has a low muscle mass, what effect does this have on eGFR?
It is overestimated
If a patient has a high muscle mass, what effect does this have on eGFR?
It is underestimated
When is eGFR valid?
If [Creatinine]p is stable
What percentage of patients are in Stage 1 or 2 CKD?
What is Stage 3a of CKD?
What is Stage 3b of CKD?
What percentage of patients are in Stage 3 CKD?
What percentage of patients are in Stage 4 CKD?
What percentage of patients are in Stage 5 CKD?
What are some common causes of CKD?
Polycystic kidney disease
When do symptoms of CKD tend to appear?
Which of the following is not a typical non-specific sign of CKD:
- Poor appetite
- Weight loss
- Sleep disturbance
Impaired urine concentrating in CKD can cause what?
What medications can be used to both reduce proteinuria and control BP?
What are some cautions when using ACEi/ARB/Spironolactone in CKD?
Modest decline in GFR at first
How can CVS risk be reduced in CKD?
Control BP and proteinuria
Apart from erythropoietin, what else should we check as a cause of anaemia in CKD?
What is the initial treatment for anaemia in CKD?
If after the first line treatment for anaemia in CKD the patient is still anaemic, what do we do?
Epo. injection (weekly/fortnightly)
What is the target Hb in a CKD patient?
What does CKD initially cause in regards to Vit. D and calcium metabolism?
Reduced calcium absorption
What effect does advanced CKD have on Phosphate and what happens due to this?
Increased serum phosphate -> Increased PTH secretion
What effect do increased phosphate and calcium have on the cardiovascular system?
Vascular calcification (Become stiff)
(Can also affect heart valves)
How can we treat bone disease in CKD?
Alfacalcidol (Hydroxylated/Activated Vit D)
- Reduced gut absorption
- eg. Calcium carbonation/acetate + Sevelamer
When is dialysis considered?
How long does an arteriovenous fistula take to form?
How long do you have to wait before the catheter can be used in peritoneal dialysis?
How soon can patients be registered for cadaveric kidney transplant?
Within 6 months of dialysis beginning
What is the definition of AKI?
- OR rise in Cr by 50%
- OR a decline in urine output
What are the 3 criteria that can be used to diagnose Stage 1 AKI (KDIGO staging)?
Serum creatinine criteria:
- Increase >26μmol/L
- OR Increase >1.5-1.9 x Reference Cr
Urine output criteria:
- 6 consecutive hours
What are the 2 criteria that can be used to diagnose Stage 2 AKI (KDIGO staging)?
Serum creatinine criteria:
- Increase >2-2.9 x Reference Cr
Urine output criteria:
- 12 consecutive hours
What are the 5 criteria that can be used to diagnose Stage 3 AKI (KDIGO staging)?
Serum creatinine criteria::
- Increase >3 x Reference Cr
- OR Increase to >354μmol/L
- OR need for renal replacement therapy
Urine output criteria:
- 24 consecutive hours
- OR Anuric for 12 hours
What can all the pre-renal causes of AKI be classified as?
The following three conditions all cause pre-renal AKI; how can they come about?
- Renal hypoperfusion
- Cardiogenic shock
- Distributive shock (Sepsis/Anaphylaxis)
- Hepatorenal syndrome
What is pre-renal AKI essentially?
Reversible volume depletion leading to:
- Increased serum creatinine
What is oliguria defined as?
What effect do ACE inhibitors have on the efferent arterioles and what does this cause? How does renal perfusion affect this?
Efferent arteriole vasodilation -> Reduced filtration pressure:
- If mildly decreased perfusion -> Mildly reduced GFR
- If hugely decreased perfusion -> Huge GFR drop
Put the following steps of the pathophysiology of Pre-renal AKI in order:
- Reduced effective intravascular volume
- Sodium and water retention
- Volume depletion/Sepsis
- Increased levels of ADH and Aldosterone
1. Volume depletion/Sepsis
2. Reduced effective intravascular volume
3. Increased levels of ADH and Aldosterone
4. Sodium and water retention
How much of the cardiac output do the kidneys receive?
What is the commonest presentation of AKI and what causes it?
Acute Tubular Necrosis
Due to untreated pre-renal AKI
What are the common causes of Acute Tubular Necrosis?
What are some less common causes of Acute Tubular Necrosis?
What type of AKI is acute tubular necrosis?
What feature is pathognomonic of Acute Tubular Necrosis?
Muddy brown casts in the urine
In acute tubular necrosis, what is the fractional sodium excretion?
In pre-renal AKI, what is the fractional sodium excretion?
How can we assess hydration?
What solution must we not give as a fluid challenge for hypovolaemia?
When should we seek help in treating hypovolaemia?
If no change after >1L given
What is the underlying pathology behind renal AKI?
Inflammation or damage to cells
Renal AKI is typically split by the structures affected, what is it divided into?
What are vascular causes of renal AKI?
What are some causes of interstitial nephritis?
What can cause a tubular injury?
Ischaemia (Prolonged hypeperfusion [pre-renal AKI])
Uraemia will have what signs in renal AKI?
What history features may suggest renal disease?
What electrolytes on U+Es are markers of renal function?
If, on FBC, there are low platelets, what might be causing the renal AKI?
Haemolytic Uraemic Syndrome
Thrombotic Thrombocytopaenic Purpura
Abnormal clotting can suggest what in renal disease?
Disseminated Intravascular Coagulation
When is anaemia seen in renal disease?
If due to myeloma
Haematoproteinuria suggests what?
How can we test for myeloma and in what age group would we routinely do these investigations?
Bence Jones Protein
In everyone >50 years old
What are urgent indications for a renal biopsy?
Rapidly progressive glomerulonephritis
Positive immunology and AKI
How can we be sure that performing a renal biopsy will be safe?
Normal clotting (No Warfarin/Aspirin)
If fluid resuscitation doesn't work in the treatment of AKI, what might we deliver?
When is dialysis commenced in AKI?
If anuric and uraemic (>40)
- OR >6.5 and unresponsive to therapy
Severe acidosis (pH
What is severe acidosis defined as?
What is severe uraemia defined as?
What is the general pathophysiology of post-renal AKI?
1. Urine flow obstruction
3. Loss of concentrating ability
How is post-renal AKI treated?
What is hyperkalaemia defined as?
What is life-threatening hyperkalaemia defined as?
At a serum potassium level of 6-7mmol/L, what ECG changes will be seen?
Tented T waves
At a serum potassium level of 7-8mmol/L, what ECG changes will be seen?
Flattened P waves
Increased PR interval (>0.12-0.20 seconds)
Depressed ST segment
Tented T waves
At a serum potassium level of 8-9mmol/L, what ECG changes will be seen?
Atrial standstill (absent P waves)
Prolonged QRS (>0.06-0.10 seconds)
Further tenting of T waves
At a serum potassium level of >9mmol/L, what ECG changes will be seen?
How do we protect the myocardium in hyperkalaemia?
10ml of 10% Calcium Gluconate over 2-3 minutes
(OR 5ml 10% Calcium Chloride)
Can the myocardial protection treatment in hyperkalaemia be repeated?
Yes (up to 40ml of calcium gluconate)
How long does the protective effect over the myocardium last?
How does insulin move K+ back into the cells?
1. Binds to its cellular receptor
2. Increases Na-K-ATPase activity
3. K+ taken up into cells
How do we administer insulin in hyperkalaemia?
- 10-15IU in 50ml of 50% Dextrose over 30mins
How long does insulins affect last for in the treatment of hyperkalaemia?
How regularly can insulin therapy be used in hyperkalaemia?
Every 4 hours
How regularly must we check blood glucose after insulin therapy (for hyperkalaemia) and what do we do in it drops?
Every 6 hours
Infuse 10% glucose if glucose drops
How else can we move K+ back into cells?
Nebulised salbutamol for 90 minutes
What does calcium resonium do?
Reduces gut absorption of K+
If a 25 year old IVDU is found collapsed at home and his renal function has deteriorated, what is the most likely cause?
Which of the following does not cause hyperkalaemia:
What is the second most common cause of Stag 5 CKD (after DM)?
What is glomerulonephritis?
Immune mediated disease affecting the glomeruli with secondary tubulointerstitial damage
How does humoral glomerulonephritis arise?
Intrinsic or Planted Ag results in the deposition of circulating immune complexes
What causes a proliferative glomerulonephritis and what is the main presenting feature?
Damage to endothelial/mesangial cells
Haematuria (+/- proteinuria)
What causes a non-proliferative glomerulonephritis and what is the main presenting feature?
Damage to podocytes
Proteinuria (NO haematuria)
What would you expect to see on urine microscopy of a patient with glomerulonephritis?
RBC + granular casts
What is microalbuminaemia defined as?
What kind of glomerulonephritis can present as an AKI?
Rapidly Progressive Glomerulonephritis (RPGN)
Nephritic syndrome is indicative of what kind of process; proliferative or non-proliferative?
Nephrotic syndrome is indicative of what kind of process; proliferative or non-proliferative?
How can nephrotic syndrome result in more infections?
Loss of opsonising antibodies
Which of the following is not a complication of nephrotic syndrome:
- Renal vein thrombosis
- Pulmonary embolism
- Volume depletion
- Vitamin D deficiency
Hyperthyrodisim (actually causes subclinical hypothyroidism
What are the majority of cases of GN?
What is secondary GN associated with?
- ANCa associated vasculitis
What type of ANCA is PR3 and what is it seen in (mainly)?
What type of ANCA is MPO and what is it seen in (mainly)?
Microscopic polyangiitis and EGPA
What do proliferative and non-proliferative GN refer to?
Absence or presence of mesangial cell proliferation
What is cresenteric GN?
Presence of crescents:
- Epithelial cell extracapillary proliferation
eg. RPGN in vasculitis
What are the target BPs in GN?
What sort of supplements might have a benefit in GN?
Omega-3 fatty acids
What corticosteroids are used in GN?
What alkylating agents are used in GN?
What calcineurin inhibitors are used in GN?
Cyclosporin A (CSA)
What two other drugs are used in GN (ie. Not steroids/alkylating agents/calcineurin inhibitors)?
Mycophenalate Mofetil (MMF)
What other non-drug immunosuppression can be used in the treatment of GN?
- IV Ig
- Monoclonal T or B cell antibodies
Which of the following is not used in the general treatment of nephrotic syndrome:
- Fluid and salt restriction
- IV albumin
Statins (though anticoagulation use is questionable)
What is complete remission of nephrotic syndrome?
What is partial remission of nephrotic syndrome?
Who is minimal change nephropathy most common in?
Children (77% of cases)
On renal biopsy, how does minimal change nephropathy appear?
- Light microscopy
Foot process fusion (podocyte) on electron microscopy
What drug treatment will induce remission in 94% of patients with minimal change nephropathy?
What are the second line drugs for minimal change nephropathy if the first line doesn't work?
Cyclosporin A (CSA)
True or false; minimal change nephropathy will not cause progressive renal failure?
What is the possible cause of minimal change nephropathy?
Who is focal segmental glomerulosclerosis most common in?
Adults (35% of cases)
What can causes secondary focal segmental glomerulosclerosis?
What does focal segmental glomerulosclerosis appear like on renal biopsy?
- Minimal Ig deposition
- Minimal complement deposition
How many cases of focal segmental glomerulosclerosis will be induced into remission by oral steroids?
How many cases of focal segmental glomerulosclerosis progress to ESRD and how long does this take?
50% in 10 years
What is the aetiology of focal segmental glomerulosclerosis?
Soluble urokinae plasminogen activator receptor (suPAR) in 67%
Who is membranous nephropathy most common in?
- 2nd commonest cause of nephrotic syndrome
What infections are secondary causes of V?
What connective tissue disease is linked to membranous nephropathy?
What malignancies are associated with membranous nephropathy?
What drugs are associated with membranous nephropathy?
How does membranous nephropathy appear on renal biopsy?
Subepithelial immune complex deposition in BM (making it appear thicker)
How is membranous nephropathy treated?
B-cell monoclonal antibodies
How many cases of membranous nephropathy progress to ESRD and how long does this take?
30% in 10 years
What can precipitate microscopic haematuria in IgA nephropathy?
Where is IgA nephropathy most common?
Worldwide (most common cause of GN worldwide)
What is IgA nephropathy associated with and how would it present?
How does IgA nephropathy appear on renal biopsy?
- Mesangial cell proliferation and expansion
- IgA deposits in mesangium
How many cases of IgA nephropathy progress to ESRD and how long does this take?
25% in 10 years
How is IgA nephropathy treated?
What is present in the urine of Rapidly Progressive Glomerulonephritis patients?
- RBC + granular casts
How does Rapidly Progressive Glomerulonephritis appear on renal biopsy?
What are some ANCA-positive causes of Rapidly Progressive Glomerulonephritis?
What are some ANCA-negative causes of Rapidly Progressive Glomerulonephritis?