Renal and urology Flashcards

(165 cards)

1
Q

what are the 3 different types of bladder cancer and which is the most common?

A

transitional cell - most common
SCC
adenocarcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

which regional lymph nodes does bladder cancer extend into?

A

hypogastric
obturator
external iliac
presacral

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what organs does bladder cancer metastasise to?

A

ureter
prostate
bowel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what are the Rf for bladder cancer?

A

Smoking
Analine
Alcohol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

how does bladder cancer present?

A

painless

macroscopic haematuria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

investigations for suspected bladder cancer?

A

cystoscopy + biopsy

CT abdo + pelvis or MRI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

management of bladder cancer?

A

superficial lesions- TURBT

intravesical chemotherapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what are the different anatomical regions of the prostate?

A

central zone - glandular tissue and ejaculatory ducts
peripheral zone
transitional zone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

symptoms of BPH?

A
weak or intermitten urinary flow
straining
hesitancy 
dribbling
incomplete emptying 
urgency 
frequency 
nocturia 
UTI
retention
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what medication is used to treat BPH?

A

alpha-1 antagonist - tamsulosin

5 alpha reductase inhibitors - finasteride

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

MOA of tamsulosin?

A

alpha-1 antagonist - decreases sooth muscle tone (prostate and bladder)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what are some S/E of alpha-1 antagonist?

A

dizziness
postural hypotension
dry mouth
depression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

MOA of finasteride?

A

blocks the conversion of testosterone to dihydrotestosterone which is known to induce BPH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what are some side effects of 5-alpha reductase inhibitors?

A

erectile dysfunction
reduced libido
ejaculation problems
gynaecomastia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

which type of prostate cancer is the most common?

A

adenocarcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

which genetic mutation is most commonly associated with prostate cancer?

A

BRCA 1+2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what are the RF for prostate cancer?

A

obesity
age
FH
high fat and low fibre diet

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what is the most common location for prostate cancer in the prostate?

A

peripheral zone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

how is prostate cancer graded?

What is normal PSA level for each age group?

A

using the gleason grading system where 2 is best prognosis and 10 is the worst prognosis

50-59- <3.0
60-69- <4.0
70+ - <5.0

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

which nodes does prostate cancer spread to?

A

obturator nodes

seminal vesicles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

symptoms of prostate cancer?

A
urgency
frequency 
nocturia 
incomplete emptying 
weak flow
straining 
hesitancy 
pelvic pain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

investigations for prostate cancer?

A

PSA measurement
DRE
trans-rectal USS and biopsy
MRI/CT and bone scan for staging

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what is the criteria for referral for a trans-rectal USS and biopsy?

A

50-69 years
PSA>3
abnormal DRE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

management of prostate cancer?

A

1) watch and wait - elderly, low gleason score
2) radiotherapy (external)
3) radical prostatectomy
4) hormonal therapy
5) active surviellance for low risk males

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
what are the types of hormonal therapy used for prostate cancer?
``` anti-androgens GNRH analogues (goserelin) ```
26
how does hormonal therapy work for prostate cancer?
reduces the amount of testosterone as prostate cancer is believed to be driven by testosterone levels
27
common S/E of radiotherapy for prostate cancer?
erectile dysfunction
28
what is the most common type of testicular cancer?
germ cell cancer
29
what are the two types of germ cell testicular cancer?
seminoma and non-seminoma
30
what is a seminoma?
germ cell tumour of the testicle, that originates from the germinal epithelium of the seminiferous tubules
31
what are non-seminomas?
germ-cell tumour that originate from sex-cord stromal cells
32
what are the 4 types of non-seminoas?
embryonal yolk sac teratoma choriocarcinoma
33
what are the RF for testicular cancer?
``` infertility cryptorchidism FH kleinfelter syndrome mumps orchitis ```
34
what are the presenting features of testicular cancer?
painless lump pain hydrocele gynaecomastia
35
what are the investigations of testicular cancer?
measure AFP, hCG and LDH - raised | testicular USS
36
management of testicular cancer?
chemotherapy radiotherapy orchidectomy retroperitoneal lymph node excision - para-aortic + retroperitoneal lymph nodes
37
where does RCC originate from?
the proximal convoluted tubule
38
what type of histological cancer is RCC?
adenocarcinoma
39
symptoms of RCC?
``` haematuria flank pain abdominal mass pyrexia however may be asymptomatic ```
40
what are the RF for RCC?
smoking obesity hypertension - biggest RF's are these three renal cystic disease that requires dialysis - big risk factor additional: occupational exposure - asbestos genetics - von hippel-lindau syndrome tuberous sclerosis
41
management of RCC?
alpha-interferon and interleukin-2 to reduce the tumour size tyrosine kinase receptor inhibitors (sunitinib) nephrectomy percutaneous ablation active surveillance
42
what is a wilms tumour?
nephroblastoma that usually presents in the first 4 years of life
43
how does wilms tumour present?
mass with haematuria
44
management of wilms tumour?
nephrectomy
45
what is the definition of an AKI?
1) Increase in serum creatinine of 26umol/L or greater within 48 hours 2) Increase in serum creatinine of 50% or greater within the last 7 days 3) A decrease in urine output to less than 0.5ml/kg/hr for more than 6 hours
46
what are the 3 types of causes of AKI?
pre-renal renal post-renal
47
what are some pre-renal causes of AKI?
``` hypovolaemia sepsis CCF RAS cardiogenic shock anaphylaxis (anything that causes ischaemia to the kidneys) ```
48
what are some renal causes of AKI?
inflammation (glomerulonephritis) HUS acute interstitial nephritis - usually due to drugs (NSAIDs) acute tubular necrosis - due to drugs rhabdomyolysis vasculitis drugs (aminoglycosides, heavy-metals, uric acid - cancer tx )
49
what are some post renal causes of AKI?
renal calculi BPH tumour - external compression of the ureter
50
what are the RF for AKI?
CKD Other organ failure e.g. heart failure, liver disease, DM Px AKI use of iodinated contrast agents in last week age > 65 years multiple myeloma
51
what are some investigations of AKI?
``` U+E urinalysis soluble immunology renal biopsy USS ECG- uraemia causes pericarditis ```
52
what are the symptoms and signs of AKI?
reduced urine output pulmonary and peripheral oedema arrhythmias - secondary to potassium and acid-base balance uraemia- fatigue, headache, n+v, lack of appetite etc.
53
management of AKI?
``` ABCDE fluid balance urine output monitoring medication review treat any hyperkalaemia urgently ```
54
name some drugs which should be stopped in AKI as they may worsen the renal function?
``` ACE-I ARB Diuretics NSAIDs Aminoglycosides - gentamycin ```
55
management of hyperkalaemia?
IV calcium gluconate - stabilise the cardiac membrane insulin/dextrose infusion nebulised salbutamol - short term shift in potassium from extracellular to intracellular compartment calcium resonium loop diuretics dialysis - removal of dialysis from body
56
what are the biochemical features of AKI?
uraemia hyponatraemia hyperkalaemia hypocalcaemia -> kidney is unable to produce calcitriol hyperphosphotaemia oedema metabolic acidosis -> H+ ions cannot be excreted
57
what are the stages of CKD?
``` stage I- >90ml/min stage II- 90-60ml/min stage IIIa- 59-45ml/min stage IIIb- 45-30ml/min stage 4- 30-15ml/min stage 5 - <15ml/min - kindey failure ```
58
what components are used to calculate eGFR?
serum creatinine age gender ethnicity
59
what are the causes of CKD?
congenital- PCKD, tuberous sclerosis, alport syndrome pre-existing kidney disease- glomerulonephritis diabetic nephropathy hypertension SLE
60
symptoms of CKD?
``` anaemia bruising nausea + vomiting pruritis parasthesia haemorrhage ```
61
what are some biochemical abnormalities seen in CKD?
``` hyponatraemia hyperkalaemia hypocalcaemia hyperphosphataemia metabolic acidosis normocytic normochromic anaemia high creatinine uraemia ```
62
how does CKD affect the bones?
reduced vit D hydroxylation in kidneys due to disease + low calcium due to lack of vitamin D leads to secondary hyperparathyroidism which results in osteomalacia and osteoporosis - can lead to a brown tumour (bony lesion)
63
how does CKD cause anaemia?
reduced EPO levels (EPO stimulates stem cells to mature into RBC) reduced absorption of iron
64
what is the target haemoglobin in renal failure?
10-12 g/dl
65
what is the management of CKD?
``` lifestyle- reduce salt intake, increase exercise and diet vit D supplementation ACE-I (BP control) reduce CVS risk- statin and aspirin if severe- renal replacement therapy ```
66
what are some drugs that need to be avoided in CKD?
metformin tetracylcines (doxycycline)/nitrofurantoin lithium NSAIDs
67
how is CKD diagnosed?
eGFR<60 on 2 seperate occasions, 2 weeks apart, within 3 months
68
what are the different types of renal stones?
``` calcium oxalate cystine uric acid calcium phosphate struvite ```
69
which is the most common type of renal stone?
calcium oxalate
70
what are the RF for renal calculi?
``` anatomical anomalies - horseshoe kidney or ureteral stricture FHx of renal stones HTN gout - uric acid stones (high purine) hyperparathyroidism (hypercalciuriea) dehydration immobilisation ```
71
symptoms of renal stones?
``` Renal colic- severe pain in loin at costovertebral angle and moves towards the groin Haematuria Tenderness of lion or renal angle Dysuria Rigors + fever N+V ```
72
Investigations of renal stones?
urine dip test - haematuria (red cell casts) MSSU - for sensitivity and cultures Non-enhanced CT-KUB within 14 hours of admission
73
management of renal stones?
NSAID's- first line relief (diclofenac and ibuprofen) Anti-emetics if needed Stones < 5mm will usually pass spontaneously Stones > 5 mm - shockwave lithotripsy, uretoscopy, percutaneous nephrolithotomy
74
how do struvite stones form?
infection stones that form when proteus bacteria use urease to break down urea. This causes the urine to be more acidic and so predisposes to stone formation.
75
what is the appearance of struvite stones?
stag-horn shape extending across the calculi dirty-white radio-opaque
76
what colour are calcium oxalate stones and what is their appearance on x-ray?
black/brown colour | radio-opaque on x-ray
77
what colour are uric acid stones and was is their appearance on x-ray?
red-brown colour | radio-luscent on x-ray
78
which 3 areas of the renal system are likely to become obstructed by renal stones?
1) uretopelvic junction 2) junction where the ureters cross the iliac vessels 3) uretovesical junction
79
what is nephrotic syndrome characterised by?
proteinuria oedema hypoalbuminaemia - triad additional features: hyperlipidaemia + hypercoaguable state
80
what are some examples of kidney disease within nephrotic syndrome?
``` Minimal change disease Membranous GN Focal segmental glomerulosclerosis Amyloidosis Diabetic nephropathy ```
81
what is the most common cause of nephrotic syndrome in children?
Minimal change glomerulonephritis
82
what is the pathophysiology of minimal change disease?
T-cell and cytokine mediated damage to the glomerular basement membrane leads to increased glomerular permeability to serum albumin
83
Presentation of minimal change disease?
``` nephrotic syndrome: proteinuria, oedema (peri-orbital and scrotal) vomiting pale skin hyperlipidaemia ```
84
investigations for nephrotic syndrome?
urine dip | renal biopsy- light and electron microscopy
85
what are the findings on light and electron microscopy of minimal change disease?
normal - light microscopy | fusion of podocytes and effacement of foot processes- electron microscopy
86
management of nephrotic syndrome/minimal change disease?
high dose prednisolone 6-14 weeks | cyclophosphamide if non-responsive to steroids
87
what is membranous nephropathy?
Presence of subepithelial immunoglobulin-containing deposits along the GBM.
88
what can b seen on renal biopsy of membranous nephropathy/glomerulonephritis?
thickened GBM due to sub-epithelial deposits - causing a spike and dome appearance
89
causes of membranous nephropathy/glomerulonephritis?
``` idiopathic infections- hep B, malaria, syphilis malignancy- lung cance, lymphoma, leukaemia drugs- gold, penicillamine, NSAID's autoimmune diseases ```
90
management of membranous glomerulonephritis?
ACE-I or ARB | Corticosteroids + cyclophosphamide
91
what are the causes of focal segmental glomerulosclerosis?
``` idiopathic secondary to renal pathology - IgA nephropathy, reflux nephropathy HIV Heroin Alport syndrome Sickle cell ```
92
what is focal segmental glomerulosclerosis?
scarring of the renal glomeruli, that occurs in small stages are first
93
what can be seen on renal biopsy in focal segmental glomerulosclerosis?
light microscopy- focal and segmental scleorsis | electron microscopy- effacement of podocytes
94
management of focal segmental glomerulosclerosis?
``` high dose steroids BP control (ACE-I/ARB) immunosuppression if severe ```
95
what is renal amyloidosis?
deposition of amyloid protein in the kidney due to disordered protein folding- can be systemic or local (to an organ such as the kidney)
96
what is seen on biopsy in amyloidosis?
light microsopy- eosinophil deposits in mesangium | electron microscopy- amyloid deposits
97
management of amyloidosis?
BP control and stem cell transplant | If not for stem cell transplant, then chemotherapy and steroids
98
what is diabetic nephropathy and what are some of the physiological changes of the glomerulus?
Poorly controlled blood glucose levels causes constriction of the efferent arteriole and dilation of the afferent arteriole which leads to glomerular hypertension. This causes thickening of the basement membrane of the glomerulus, widening of the slit membranes of the podocytes and an increase in the mesangial cells.
99
signs and symptoms of diabetic nephropathy?
``` nocturia - usually first symptom fatigue headaches n+v pruritis peripheral oedema ```
100
what are the RF of diabetic nephropathy?
``` poorly controlled diabetes uncontrolled high BP T1D onset before 20 smoking FHx ```
101
Investigations of diabetic nephropathy?
urinary albumin: creatinine ratio - abnormal levels of urinary albumin in diabetic indicates diabetic neprhopathy eGFR
102
management of diabetic nephropathy?
ACE-I and ARB - to reduce glomerular hypertension BP control (aim for <130/80mmHg) Control dyslipidaemia e.g. statins Reduce dietary intake of salt
103
Features of nephritic syndrome?
haematuria + red cell clasts oliguria HTN
104
what are some examples of nephritic syndrome?
rapidly progressive glomerulonephritis IgA nephropathy Alport Syndrome
105
Pathophysiology of rapidly progressive glomerulonephritis?
term used to describe a rapid loss of renal function associated with the formation of epithelial crescents in the majority of the glomeruli
106
what are the causes of rapidly progressive glomerulonephritis?
good pastures syndrome Wegeners granulomatosis SLE
107
what is seen on biopsy in rapidly progressive glomerulonephritis?
epithelial crescents in the glomerulus
108
Management of progressive glomerulonephritis?
corticosteroids + cylophosphamide
109
what is the most common cause of glomerulonephritis worldwide?
IgA nephropathy
110
what is the pathophysiology of IgA nephropathy?
mesangial deposition of IgA immune complexes
111
typical presentation of IgA nephropathy?
young male with recurrent episodes of macroscopic haematuria 1-2 days following a URTI
112
what is alport syndrome?
genetic condition leading to abnormal production of type IV collagen, which results in an abnormal basement membrane production in the ears, kidneys, and eyes
113
what is the inheritance pattern of alport's syndrome?
X-linked dominant
114
presentation of alport's syndrome?
haematuria renal failure bilateral sensorineural deafness retinitis pigmentosa/catarracts
115
what is seen on renal biopsy in alport's syndrome?
electron microscopy- splitting of the lamina densa of the glomerular basement membrane resulting in "basket weave appearance"
116
management of alport's syndrome?
ACE-ARB dialysis renal transplant
117
what is post-strep glomerulonephritis?
excessive immune complex deposition in the glomerulus following a group A beta-haemolytic strep throat infection
118
when does post-strep glomerulonephritis present?
7-14 days after and group A beta-haemolytic streptococcus infection (usually strep pyogenes)
119
what are the features of post-strep glomerulonephritis?
``` haemturia proteinuria low complement levels (C3) headache malaiase HTN ```
120
what investigations are conducted for post-strep glomerulonephritis?
electron microscopy - immune complex deposits immunoflouresence - starry sky appearance urine dip
121
what is good pastures disease?
production of anti-GBM antibodies against type IV collagen found in the alveolar and renal basement membranes
122
presentation of good pastures disease?
pulmonary haemorrhage - haemoptysis, SOB | renal disease- haematuria
123
investigations for good pastures disease?
anti-GBM antibodies (serum) | biopsy- crescents
124
management of good pastures disease?
plasma exchange corticosteroids cyclophosphamide
125
what genetic loci have been identified in ADPKD?
PKD1 and PKD2
126
presentation of ADPKD?
``` HTN recurrent UTI stones liver cysts berry aneurysms CVS- mitral valve collapse or incompetence ```
127
investigations for ADPKD?
USS - visualise cysts | genetic testing
128
management of ADPKD?
tolvaptan (vasopressin receptor antagonist) - thought to inhibit a molecule involved in the enlargement of the cysts (not widely used) control BP dialysis kidney transplant
129
pathophysiology of renal tubular acidosis?
defects in the tubular transport of HCO3- and or H+
130
which types or renal tubular acidosis is the most common?
Type 4 RTA
131
what is deficient in Type 4 RTA?
aldosterone deficiency and/or resistance
132
what is the potassium abnormality in type 4 renal tubular acidosis?
hyperkalaemia
133
management of type 4 renal tubular acidosis?
furosemide mineralcorticoid replacement- fludrocortisone low potassium diet
134
presentation of pyelonephritis?
fever rigors loin pain vomiting
135
what is found in the urine in pyelonephritis?
white cell casts
136
investigations of acute pyelonephritis?
urinalysis - cloudy offensive urine FBC- ESR/CRP Blood cultures USS KUB
137
which organisms usually cause acute pyelonephritis?
E.coli Klebsiella Proteus Enterococcus
138
RF for acute pyelonephritis?
``` pregnancy calculi catherterization diabetes prostate enlargement structural abnormalities vesicoureteric reflux ```
139
management of acute pyelonephritis?
ciprofloxacin or co-amoxiclav for 7 days | trimethoprin may be used if sensitive
140
what is acute tubular necrosis?
necrosis of tubular epithelial cells due to ischaemia
141
what is pathognomonic for ATN?
muddy brown casts in the urine !!!!!!!
142
what are the causes of ATN?
toxic- nephrotoxic drugs (aminoglycoside, rhabdomyolysis, radiocontrast agents, lead) ischaemia- sepsis, shock
143
what are the histopathological features of ATN?
tubular epithelium necrosis - loss of nuclei and detachment of the tubular cells from the basement membrane
144
management of ATN?
correct underlying abnormality supportive care renal-replacement therapy if needed
145
investigations of ATN?
``` metabolic profile urine creatinine: albumin ration urine sodium conc- high urine osmolality - decreased FBC ```
146
what is HSP?
systemic deposition of IgA and small cell vasculitis
147
symptoms of HSP?
abdominal pain D+V purpura rash on back of leg and buttocks haematuria
148
management of HSP?
supportive analgesia corticosteroids
149
signs of ckd on examination?
``` excoriations (pruritis) pallor uraemic inge peripheral oedema bruising ```
150
describe the process of dialysis?
blood and dialysis fluid flow either side of a semi-permeable membrane, molecules diffuse down their conc gradient causing the plasma biochemistry to change to become more like the dialysis fluid
151
complications of peritoneal dialysis?
``` bacterial peritonitis local infection at catheter site constipation failure sclerosing peritonitis ```
152
what does life long immunosuppression increase the risk of?
SCC
153
what are the 3 main actions of PTH?
increase osteoclast activity increases ca and phosph reabsorption via kidney increased hydroxylation of vit D
154
what is renal osteodystrophy?
damage to bone in patients with CKD
155
management of renal dystrophy?
restrict dietary phosp phosphate binders vit D analogues calcium supplements
156
what is tertiary parathyroidism?
prolonged secondary hyperparathyroidism causes the glands to undergo adenomatous or hyperplastic change, causing high levels of PTH to be released even in the presence of normal or high calcium
157
what are the life threatening complications of AKI?
hyperkalaemia | pulmonary oedema
158
what are the indications for dialysis in AKI?
``` pulmonary oedema hyperkalaemia severe metabolic acidosis uraemic encephalopathy uraemic pericarditis ```
159
how does rhabdomyolysis cause AKI?
skeletal muscle breakdown results in creatinine kinase myoglobin and other components to be released in the bloodstream. The myoglobin is filtered through the glomerulus obstructing the tubules causing acute tubular necrosis
160
Ix for rhabdomyolysis?
urinary myoglobin
161
causes of rhabdomyloysis?
``` exercises crush injury long lie burns seizures neuroleptic malignant syndrome ```
162
what is the management of rhabdoymyolysis?
IV fluids
163
what are the ECG changes in hyperkalaemia?
tall tented t waves flattened p waves wide QRS prolonged PR interval
164
what are some complications of nephrotic syndrome?
hyperlipidaemia - give statin | thrombo-embolic event (due to increased fibrinogen)- consider anticoagulation
165
how to assess fluid status?
urine output input chart look for: dehydration signs, peripheral oedema, JVP, pulmonary oedema U+E- osmolality etc.