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5th Year > Nephrology/Urology > Flashcards

Nephrology/Urology Flashcards

1
Q

What is the triad of symptoms for renal cell carcinoma?

A

Haematuria
Loin pain
Abdominal mass

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2
Q

What are two other symptoms for renal cell carcinoma (not in the triad)?

A

Pyrexia of unknown origin

Left varicocele - due to occlusion of Left testicular vein

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3
Q

What organism causes Haemolytic Uraemic Syndrome?

A

E coli 0157

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4
Q

What is the triad of HUS?

A

AKI
Normocytic haemolytic anaemia
Thrombocytopenia
(all following diarrhoea)

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5
Q

What is the management of HUS?

A

Supportive + fluids

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6
Q

What happens to phosphate in CKD?

A

Increases

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7
Q

How does osteomalacia occur in CKD?

A

Phosphate increases which ‘drags’ calcium into bones

Formation of new, weak bones

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8
Q

What is the management of osteomalacia in CKD?

A

Alendronic acid - decreases bone tunrover

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9
Q

What is indicated by raised phosphate, with low calcium and vitamin D?

A

Secondary Hyperparathyroidism (to CKD)

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10
Q

When should you refer someone with CKD to a nephrologist from GP? (top 4)

A

eGFR <30
eGFR reducing by >5 per year
ACR >70
ACR >30 with haematuria (after UTI excluded)

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11
Q

What cause of CKD will show large/normal size kidney on USS?

A

HIV-associated nephropathy

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12
Q

What is sevelamer?

A

Non-calcium-based phosphate binder

Treats hyperphosphataemia in CKD patients

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13
Q

What is calcium acetate?

A

Calcium-based phosphate binder

Not appropriate is already hypercalcaemic

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14
Q

How is diabetic nephropathy screened?

A

Yearly early morning urine ACR

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15
Q

Why does diabetic nephropathy screening use an early morning sample?

A

To avoid orthostatic proteinuria giving false +ve

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16
Q

What ACR would be classed as microalbuminaemia?

A

ACR >2.5

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17
Q

When should CKD be diagnosed in diabetes?

A

eGFR persistently <60

ACR persistently >3

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18
Q

What are the features of myeloma?

A 
CRAB
Calcium raised
Renal complications
Anaemia
Bone disease
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19
Q

What are the renal features of ADPKD? (5)

A 
HTN
Recurrent UTIs and stones
Abdo pain
Haematuria
CKD
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20
Q

What are the extra-renal features of ADPKD? (4)

A

Liver cysts -> hepatomegaly (70%)
Berry aneurysms -> increased SAH risk (8%)
CVD eg. mitral valve disease, aortic dissection
Cysts elsewhere

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21
Q

What is the triad of nephrotic syndrome?

A

Proteinuria >3g/24hr
Hypoalbuminaemia <30g/L
Oedema

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22
Q

What are the causes of metabolic acidosis with a NORMAL anion gap?

A 
T-DAP
Renal Tubular necrosis
Diarrhoea
Addison's
Pancreatic fistula
\+ Acetazolamide
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23
Q

What might cause metabolic acidosis with a RAISED anion gap?

A

Sepsis
DKA
Salicylate poisoning

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24
Q

How do you distinguish between Acute Tubular Necrosis and pre-renal uraemia?

A

ATN = urinary sodium >40

Pre-renal AKI = urinary sodium <20

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25
How is does the management of ATN and pre-renal AKI differ?
Pre-renal AKIs have good response to fluids, ATN does not
26
What medication can be used to reduce proteinuria?
ACEi | Reduce filter pressure
27
What is an acceptable reduction in kidney function when starting an ACEi?
25% decrease in eGFR | 30% increase in creatinine
28
Nephritic syndrome 1-2 DAYS post URTI?
IgA nephropathy
29
Nephritic syndrome 1-2 WEEKS post URTI?
Post-strep glomerulonephritis
30
What, when found in urine, in pathognomonic for ATN?
Muddy brown casts of epithelial cells
31
Which antibiotic class may cause acute interstitial nephritis?
``` Penicillins Cephalosporins Macrolides Sulfonamides Fluoroquinolones Anti-TB drugs ```
32
What are the symptoms of acute interstitial nephritis?
Back/abdo pain Dysuria Haematuria
33
What is present on urinalysis in acute interstitial nephritis?
``` Eosinophilic casts (sometimes have raised eosinophils on FBC) ```
34
Which renal patients are at risk of squamous cell carcinomas and skin cancers?
Those on long-term immunosuppression suppression eg. transplant patients
35
What could new onset confusion and a pericardial rub indicate in a CKD patient?
Uraemic encephalopathy and pericarditis | These are indications for dialysis
36
What would salicylate poisoning show on an ABG?
Metabolic acidosis with RAISED anion gap
37
What is Goodpasture's syndrome?
Type II Hypersenitivity reaction | Anti-GBM Abs vs Type IV collagen mainly in lungs and kidneys
38
What are the features of Goodpasture's syndrome?
Haemoptysis and haematuria
39
What is the management of hyperkalaemia?
IV calcium glunconate 30mls over 2mins Nebulised salbutamol 5mg B2B 2-4 Actrapid 10 units + 125ml 20% Dextrose infusion
40
How long does an A-V fistula take to start working?
6-8 weeks
41
What are the daily fluid replacement requirements?
Glucose 50-100g/day Water 25-30ml/kg/day Na, K, Cl = 1mmol/kg/day
42
What medication can be used to treat ascites?
Spironalactone
43
When is a micturating cystography used?
If you suspect reflux nephropathy
44
What may be a knock-on effect of renal artery stenosis?
Renal artery stenosis -> increased plasma renin Increased renin -> secondary hyperaldonsteronism Hyperaldosteronism -> Refractory HTN
45
What is eplereone?
Alternative to spironalactone | Used in those who experience gynaecomastia
46
What do the kidneys of someone with diabetic nephropathy appear like on USS?
Bilaterally enlarged
47
What are the criteria for URGENT haematuria urology referrals?
>45yrs with visible haematuria + no UTI | >60yrs with non-visible haematuria + dysuria/rasied WCC
48
What is the criteria for ROUTINE haematuria urology referrals?
>60yrs with recurrent/persistent UTI
49
Where should someone <40yrs with haematuria be referred?
Nephrology (not urology)
50
What are the causes of metabolic acidosis with a RAISED anion gap?
``` LUKA Lactate - shock/hypoxia/sepsis Urate - renal failure Ketones - DKA Acid poisoning - paracetamol/methanol ```
51
What is the prognosis of minimal change disease?
1/3 single episode 1/3 few relapses 1/3 frequent relapses (these stop before adulthood)
52
What is the management of minimal change disease?
Steroids (80% responsive) | Ciclophosphamide = 2nd line
53
What results would indicate diabetes insipidus?
Raised plasma osmolality Reduced urine osmolality Urine osmolality >700 excludes DI
54
How do you differentiate between cranial and nephrogenic diabetes insipidus?
Water deprivation test - cranial DI responds to exogenous vasopressin, nephrogenic does not
55
Which psychiatric medication can result in nephrogenic diabetes insipidus?
Lithium
56
What is an important DDx in an elderly patient who has had a long lie?
Rhabdomyolysis
57
What measures should be taken if someone with CKD requires a contrast-CT?
12hrs IV fluids at 1ml/kg/hr pre- and post-CT | Consider temporary stop of ACEi if eGFR <40
58
Why are those with nephrotic syndrome at increased risk of clotting?
Loss of antithrombin III, protein C and protein S in urine This increases fibrinogen levels which increases clotting risk Require LMWH prophylaxis
59
What is Alport syndrome?
X-linked abnormality in Type IV collagen -> abnormal GBM
60
What are the triad of features of Alport syndrome?
Progressive renal failure Bilateral sensorineural deafness Occular abnormalities
61
What does electron microscopy of the glomerulus show in Alport syndrome?
Basket-weave appearance | Longitudinal splitting of lamina densa of GBM
62
What is the causative organism of peritonitis secondary to peritoneal dialysis?
S. epidermidis
63
What is the management of diabetes insipidus?
Cranial DI = vasopressin | Nephrogenic DI = thiazide diuretic eg. Chlarothiazide
64
What is the most important infection post-organ transplant?
CMV
65
What are the symptoms of post-transplant CMV infection?
Few days unwell + anorexia Hepatitis + jaundice Widespread LNs
66
What is the treatment of post-transplant CMV infection?
Ganciclovir
67
What is alfacalcidol?
Vitamin D analogue | Used in end-stage CKD as does not need kidney reactivation
68
What are the ECG features of hypokalaemia?
Flattened T waves | U waves
69
What is the cut-off for severe hypokalaemia?
<2.5
70
What are the symptoms of hypokalaemia?
Muscle weakness | Palpitations
71
What is the management of hypokalaemia?
Replacement in infusion | Should not exceed 20mmol/hr
72
Which diagnoses are important to consider in someone developing an AKI after starting ACEi?
Young female = fibromuscular dysplasia | Older patients = atherosclerosis
73
What is a hallmark feature of fibromuscular dysplasia?
'String of beads' renal arteries
74
What ABG will Addison's show?
Hyperkalaemic metabolic acidosis | Decreased aldosterone -> increased K retention and increased Na excretion which causes increase H+ retention
75
What should be considered if a patient has persistent sterile pyuria with negative cultures?
Renal TB
76
What may falsely show a decreased eGFR?
Large muscle mass | Due to increased creatinine
77
What do those with nephrotic syndrome require to prevent complications?
LMWH prophylaxis | Low threshold for Abx
78
What are the stages of AKI in terms of urine productions?
Stage 1 = <0.5ml/kg/hr for >6hrs Stage 2 = <0.5ml/kg/hr for >12hrs Stage 3 = <0.3ml/kg/hr for >24hrs OR anuric for >12hrs
79
When does minimal change disease require a biopsy?
When not steroid-responsive Child with nephrotic syndrome only gets biopsy if don't respond to steroids ALL adults get biopsy
80
What is the hallmark feature on biopsy of Rapidly Progressive GN?
Epithelial crescent formation
81
What are 3 causes of RPGN?
Goodpasture's Wegner's SLE
82
What renal(ish) complication might haemochromatosis cause?
Cranial diabete insipidus
83
What are the features of amyloidosis?
50-65yr old Decreased renal function with proteinuria Hepatosplenomegaly COPD
84
How might an amyloidosis patient present?
50-65yrs old with progressive breathlessness and weakness
85
How is amyloidosis diagnosed? (3)
1. Congo red staining = apple green birefringence 2. Serum amyloid precursor (SAP) scan 3. Rectal biopsy
86
What are the features of nephrotic syndrome? (5)
``` Proteinuria >3.5g/day Hypoalbuminaemia Oedema Hyperlipidaemia Lipiduria ```
87
How does SELECTIVE proteinuria develop in minimal change disease?
T-cells release cytokines Podocyte foot effacement Loss of -ve charge barrier CanNOT repel albumin but CAN repel immunoglobulins
88
What type of malignancy is minimal change disease associated with?
Hodgkin's lymphoma
89
What do LM, EM and IF show in minimal change disease?
LM: No change EM: Podocyte effacement IF: -ve
90
What is the management of minimal change disease?
Steroids | Kids respond well, adults also but slower
91
What is Focal Segmental Glomerulosclerosis?
PARTS of SOME glomeruli develop scarring and SCLEROSIS
92
Who is FSGS more common in?
African-americans | Hispanics
93
What are the features of primary (idiopathic) FSGS?
Damaged podocytes become leaky over time Some proteins get trapped in mesangium This causes HYALINOSIS = glassy appearance This turns to SCLEROSIS over time
94
What are the causes of secondary FSGS? (5)
``` Sickle cell disease HIV-associated nephropathy Heroin Kidney hyperperfusion Increased glomerular capillary pressure ```
95
What do LM, EM and IF show in FSGS?
LM: Segmental sclerosis and hyalinosis EM: Foot process effacement IF: Non-specific focal IgM and complement deposits
96
What is the management of FSGS?
Steroids Inconsistent response <10% spontaneously remiss
97
What is membranous GN?
Damage to GBM due to immune complex deposition
98
Who gets membranous GN?
Caucasian adults Generally primary/idiopathic 3rd most common ES-RF cause Lots of causes including SLE
99
What are the two mechanisms of immune complex deposition in membranous GN?
1. AutoAb tageting GBM | 2. Complexes form outside kidneys and carried to GBM
100
What are the two types of AutoAbs targeting the GBM in membranous GN?
M-type phospholipase A2 receptor Neutral endopeptidase Both expresses on podocyte surface
101
What is the main protein involved in immune complex formation outside the kidneys in membranous GN?
Cationic Bovin Serum Albumin | Found in cow's milk and beef protein
102
Where are the immune complex deposits in membranous GN?
Subepithelial
103
How do the immune complex deposits cause kidney damage in membranous GN?
They cause complement activation which forms MACs which damages podocytes and mesangial cells This causes GBM thickening and 'spike and dome' appearance on EM
104
What are the LM, EM and IF features of membranous GN?
LM: GBM thickening EM: Spike and dome appearance IF: Granular complex deposits
105
What is the management of membranous GN?
ACEi Steroids Treat underlying cause
106
What is the prognosis for membranous GN?
1/3 spontaneous remission 1/3 remain proteinuria 1/3 ESRF
107
What is membranoproliferative GN?
Subendothelial immune complex deposition causing inflammation May present as mixed nephrotic/nephritic picture Poor prognosis
108
What are the causes of type 1 membranoproliferative GN?
Cryoglobulinaemia | Chronic Hep C/B
109
What is the pathophysiology of membranoproliferative GN?
SUBENDOTHELIAL deposits by 2 mechanisms: 1. Overactivation of classical complement pathway 2. Inappropriate activation of alternative complement pathway
110
How does over activation of the classical complement pathway cause Type 1 MPGN?
Immune complex formation secondary to chronic infection (eg. HepB/C) deposit in glomerulus This activates the classical complement pathway Results in complex AND complement deposits
111
How does inappropriate activation of the alternative complement pathway occur in Type 1 MPGN?
Nephritis factor (C3NeF) stabilises C3 convertase This causes inappropriate activation Results in complement deposits ONLY
112
What is the difference between the classical and alternative pathway activation causing Type 1 MPGN?
``` Classical = complex AND complement deposits Alternative = complement deposits ONLY ```
113
What is the hallmark feature of MPGN?
Tram-track appearance | Due to splitting of GBM
114
How does GBM occur in MPGN?
Subendothelial deposits cause mesangial proliferation This causes mesangial INTERPOSITION Results in splitting of GBM
115
What do EM and IF of MPGN show?
EM: Tram-track appearance IF: Granular complex deposits
116
What is the hallmark feature of Type 2 MPGN?
'Dense deposits' | Due to complement (NOT complex) deposits
117
What associated features are found in Type 2 MPGN?
Partial lipodystrophy = lose submit tissue from face | Low C3 levels
118
What is the pathophysiology of Type 2 MPGN?
Persistent activation of the ALTERNATIVE complement pathway due to NEPHRITIC FACTOR causes complement deposition and low C3 levels
119
Where are the complement deposits in Type 2 MPGN?
WITHIN the GBM, NOT subendothelial
120
What does EM show in Type 2 MPGN?
INTRAMEMBRANOUS complement deposits = DENSE DEPOSITS
121
What is the hallmark feature of Type 3 MPGN?
Deposits and sub endothelial AND subepithelial
122
What is the management of MPGN?
Steroids = often poor response
123
Why is diabetic nephropathy important?
Leading cause of ESRF in developed world
124
What is the pathophysiology of diabetic nephropathy?
Initial hyperfiltration with increased GFR This causes GBM thickening Results in widened podocyte gaps -> protein can pass Decreases GFR over time
125
Why does initial hyper filtration occur in diabetic nephropathy?
Excess glucose causes glycation of efferent arteriole -> atherosclerosis -> increased glomerular pressure Also afferent arteriole dilates -> increased glomerular pressure Together = hyperfiltration
126
What is the screening for diabetic nephropathy?
Yearly U+E and first-pass ACR
127
When should CKD be diagnosed in diabetic nephropathy?
ACR >3 or eGFR <60 for >3 months
128
What is the management of diabetic nephropathy? (4)
``` Protein restriction Tight glycemic control ACEi - keep BP <130/80 (ARB in Afro-caribbeans) Statin ```
129
What are the features of nephritic syndrome? (6)
``` PHAROH Proteinuria (non-selective) HAEMATURIA Azotemia (increased creatinine and urea) RBC casts in urine OLIGURIA HTN ```
130
What blood tests should be done for someone with nephritic syndrome?
``` Usuals = FBC, U+E, LFT, ESR, CRP Losses = Igs electrophoresis, C3/4 levels Causes = AutoAbs (eg. ANA, ANCA etc), cultures, ASOT, HBsAg, anti-HCV ```
131
What urine tests should be done for someone with nephritic syndrome?
MC&S RBC casts ACR Bence-Jones protein
132
What is ASOT?
Anti-streptolysin O = used for Dx of post-strep GN
133
What is the general management for all nephritic syndromes?
Early nephrology referral Keep BP <130/80 (<125/75 if proteinuria) ACEi
134
What is IgA nephropathy?
Type III hypersensitivity reaction | Mesangial deposits of IgA immune complexes
135
What is another name for IgA nephropathy?
Berger's disease
136
Why is IgA nephropathy important?
Commonest GN worldwide
137
How does IgA nephropathy present?
Macroscopic haematuria in young male 1-2 days following URTI | Nephrotic protein and renal failure are rare
138
What will LM, EM and IF show in IgA nephropathy?
LM: Mesangial proliferation EM: Immune complex deposition IF: IgA and C3 deposits
139
What is the management of IgA nephropathy?
ACEi for HTN control | Steroids are not helpful
140
What is the prognosis for IgA nephropathy?
20% develop ESRF in 20yrs
141
What would suggest a good prognosis in IgA nephropathy?
Frank haematuria
142
What would suggest a worse prognosis in IgA nephropathy? (6)
``` Male Proteinuria HTN Hyperlipidaemia Smokers ACE genotype DD ```
143
How do you differentiate between IgA nephropathy and HSP?
IgA nephropathy = kidneys ONLY | HSP = systemic features
144
What is Post-Strep GN?
Type III Hypersensitivity reaction | Immune complex deposition in glomeruli
145
What makes up the immune complexes deposited in Post-Strep GN?
IgG, IgM and C3
146
How does Post-Strep GN present? (6)
``` Malaise 'Cola-coloured haematuria' Proteinuria Oliguria Peripheral and periorbital oedema 7-14 days post-strep infection ```
147
Who gets Post-Strep GN?
Generally young children
148
Which Strep causes Post-Strep GN?
Strep pyogenes | Group A beta-haemolytic strep
149
What specific bloods with suggest Post-Strep GN?
Low C3 Raised ASO titre Anti-DNAse B +ve
150
Other than strep-throat, what else can post-strep GN present following?
Impetigo - 6 weeks following
151
What is the general prognosis of post-strep GN?
Generally mild - resolves within 1 month
152
What will LM, EM and IF shown post-strep GN?
LM: Enlarges and hypercellular EM: 'Humps' of subendothelial deposits IF: 'Starry sky' granular appearance along GBM
153
What percentage of SLE patients develop kidney disease?
50% | Should be monitored for proteinuria
154
How many WHO classes of SLE-related GN are there?
6
155
Which is the worst WHO class of SLE-related GN?
Class IV = diffuse proliferative GN
156
What specific appearance does Class IV SLE-related GN have on LM?
'Wire-loop' appearance | Due to GBM deposits
157
What type of hypersensitivity reaction is SLE-related GN?
Type III Hypersensitivity | Immune complex deposition, generally subendothelial
158
How does SLE-related GN usual present?
Nephrotic syndrome | But can present as nephritic as well depending on lesion location
159
What is the management of SLE-related GN?
Steroids +/- immunosuppression for Tx of SLE | ACEi for Tx of HTN
160
Why is Rapidly Progressive GN important?
Can cause ESRF over few days
161
What is a specific feature must be present for it to be RPGN?
Glomerular CRESCENTS on LM
162
What causes glomerular crescents in RPGN?
Cell proliferation in Bowman's space
163
What are the 3 types of RPGN?
Type 1 = Anti-GBM disease (3%) Type 2 = Immune complex disease (45%) Type 3 = Pauci-immune disease (50%)
164
What is an example of an Anti-GBM RPGN?
Goodpasture's syndrome
165
What are 3 examples of immune complex RPGN?
SLE-related GN IgA nephropathy HSP
166
What are 2 examples of Pauci-immune RPGN?
``` Granulomatosis with polyangiitis (cANCA +ve) Microscopic polyangiitis (pANCA +ve) ```
167
What does LM show for all RPGN?
Glomerular crescents
168
What does IF show for each type of RPGN?
Type 1 = Linear anti-GBM deposits Type 2 = Granular deposits Type 3 = -ve IF as no deposits
169
What is the general management of all RPGN?
Anticoagulation - prevent fibrin deposits Immunosuppression Plasmaphoresis
170
What is Goodpasture's syndrome?
Type II Hypersensitivity reaction | Anti-GBM Abs vs Type IV collagen
171
What are the features of Goodpasture's syndrome?
Pulmonary haemorrhage then RPGN
172
Who is at increased risk from Goodpasture's syndrome?
Males 20-30yrs and 60-70yrs | Smoking and LRTI increases pulmonary haemorrhage risk
173
Which HLA is Goodpasture's syndrome associated with?
HLA DR2
174
What 2 specific investigations will suggest Goodpasture's syndrome?
Renal biopsy = Linear IgG GBM deposits on IF | Raised transfer factor secondary to pulmonary haemorrhage
175
What is the management of Goodpasture's syndrome?
High-dose IV steroids + cyclophosphamide | Plasma exchange
176
What is the most common type of bladder cancer?
Transitional cell carcinoma (90%) SCC (7%) Adenocarcinoma (2%)
177
What is the most common presentation of bladder cancer?
Painless haematuria
178
Who gets bladder cancer?
50-80yr old males Smokers Aniline dyes
179
What type of bladder tumour is most common?
Papillary (70%) | Mixed/sold growths are more prone to invasion
180
What percentage of females over 50yrs with incidental haematuria, after excluding UTI, will have bladder cancer?
10%
181
How is bladder cancer staged?
Cystoscopy + biopsy Pelvic MRI for local spread CT for mets
182
What is the management of bladder cancer?
Isolated lesion = TURBT High-grade isolated lesion = TURBT + adjuvant BCG PT2+ = radial cystectomy with ill conduit OR radical radiotherapy
183
What is the PT staging system of bladder cancer?
``` PTA = no invasion PT1 = mucosal invasion PT2 = muscle invasion PT3 = serosal invasion PT4 = mets ```
184
What is the 5yr survival of bladder cancer?
``` T1 = 90% T4a = 10-25% N1-2 = 30% ```
185
Where do renal cell cancers arise from?
PCT | Generally upper pole of kidney
186
What is the most common renal cell cancer?
Clear cell tumour (75-85%) | These arise from PCT
187
What type of carcinoma would a renal cell caner arising from the renal pelvis be?
Transitional cell carcinoma
188
Which two syndromes are associated with renal cell cancer?
von Hippel-Lindau | Tuberous sclerosis
189
What is von Hippel-Lindau syndrome?
Dysfunction of VHL gene on Chr3 -> increase IGF-1 | Often get bilateral renal cell cancers
190
What does the increased IGF-1 in vHL syndrome cause?
1. Dysregulated cell growth | 2. Increased VEGF -> angiogenesis
191
What other non-renal cancers is vHL associated with?
Tumours/cysts in eyes and CNS
192
What is the classical triad of renal cell cancer?
Haematuria Loin pain Abdominal mass
193
What 4 endocrine effects are associated with renal cell cancer?
EPO -> polycythaemia PTH -> hypercalcaemia Renin -> HTN ACTH -> Cushing's
194
What non-endocrine paraneoplastic syndrome is associated with renal cell cancer?
Stauffer syndrome | Cholestasis and hepatosplenomegaly secondary to increased IL-6
195
What percentage of patients with renal cell cancer have mets at presentation?
25% | Lungs and bones primarily
196
Why do renal cell cancers met to lungs preferentially?
Grows into renal vein | Lungs are first capillary bed reached
197
How is renal cell cancer staged?
CT chest, abdo and pelvis
198
Would you biopsy a renal cell cancer?
No
199
Why wouldn't you biopsy a renal cell cancer?
High risk of spread and no change to management
200
What is the name of a benign renal tumour with a 'spoke-wheel' pattern on angiography?
Oncocytoma | Preoperative distinction near impossible
201
What is the management of renal cell cancers?
Partial or Total nephrectomy
202
What type of neoadjuvant chemotherapy can be used to shrink a renal cell cancer preoperatively?
Tyrosine kinase inhibitors

5th Year (8 decks)

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