renal and urology Flashcards

1
Q

stage 5 ckd

A

0-15 eGFR

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2
Q

stage 4 ckd

A

15-30 eGFR

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3
Q

stage 3 ckd

A

3a = 45-60 eGFR
3b = 30-45 eGFR

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4
Q

causes of CKD

A

diabetic nephropathy
chronic glomerulonephritis
chronic pyelonephritis
hypertension
adult polycystic kidney disease

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5
Q

features of renal bone disease

A

osteomalacia
osteoporosis
osteosclerosis

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6
Q

spine x-ray in renal bone disease

A

“rugger jersey” spine
sclerosis of both ends of the vertebra (denser white) and osteomalacia in the centre of the vertebra (less white)

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7
Q

metabolic probs in ckd

A

low VD
high phosphate
LOW calcium
secondary hyperparathyroidism

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8
Q

ckd bone disease tx

A

reduce dietary phosphate
phosphate binders (sevelamer)
give VD (eg alfacalcidol, calcitriol)
bisphosphonates (alendronic acid)

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9
Q

hypercalcaemia tx

A

Fluids

Calcitonin (reduces serum calcium levels by inhibiting osteoclast activity)

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10
Q

nice criteria for AKI

A

Rise in creatinine of ≥ 25 micromol/L in 48 hours
Rise in creatinine of ≥ 50% in 7 days
Urine output of < 0.5ml/kg/hour for > 6 hours

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11
Q

RFs AKI

A

Chronic kidney disease
Heart failure
Diabetes
Liver disease
Older age (above 65 years)
Cognitive impairment
Nephrotoxic medications such as NSAIDS and ACE inhibitors
Use of a contrast medium such as during CT scans

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12
Q

pre renal causes AKI

A

inadequate BS:
Dehydration
Hypotension (shock)
Hypovolaemia - D+V
Heart failure
Renal artery stenosis

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13
Q

renal causes AKI

A

Glomerulonephritis
Interstitial nephritis
Acute tubular necrosis (most common)
Rhabdomyolysis
tumour lysis syndrome

drugs - ACEi, NSAIDs, nephrotoxic abx (gentamicin, vancomycin, tetracyclines)

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14
Q

post renal causes AKI

A

obstruction to outflow:
Kidney stones
Masses such as cancer in the abdomen or pelvis
Ureter or uretral strictures
Enlarged prostate or prostate cancer

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15
Q

what drugs to stop in AKI

A

NSAIDs (except if aspirin at cardiac dose e.g. 75mg od)
* Aminoglycosides
* ACE inhibitors
* Angiotensin II receptor antagonists
* Diuretics

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16
Q

eGFR variables

A

CAGE - Creatinine, Age, Gender, Ethnicity

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17
Q

inheritance pattern of PKD

A

autosomal dominant
- more common
- assoc w cerebral haemorrhage

autosomal recessive
- more severe, usually presents antenatally or at birth
- less likely to have FHX

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18
Q

when is contrast CI

A

renal impairment

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19
Q

most signif cause of anaemia in CKD

A

reduced erythropoietin

(carry out iron studies b4 giving EPO)

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20
Q

stages to classify AKI

A

Stage 1 - 1.5-1.9x baseline creatinine - All in the 1’s

Stage 2 - 2-2.9x baseline creatinine - All in the 2’s

Stage 3 - 3x baseline creatinine - All in the 3’s

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21
Q

when to send a urine culture in UTI

A

if pregnant
visible or non-visible haematuria
> 65 yrs
if male

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22
Q

UTI tx non-pregnant women

A

trimethoprim or nitrofurantoin for 3 days

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23
Q

how long to give UTI abx if catheterised

A

7 days

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24
Q

UTI tx males

A

trimethoprim or nitrofurantoin 7 days

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25
Differentiating between IgA nephropathy and post-streptococcal glomerulonephritis
post-streptococcal glomerulonephritis presents after 1-2 WEEKS, IgA nephropathy after 1-2 DAYS (post RTI) post-strep has low complement post- strep has more proteinuria
26
prostatitis presentation+ what is a common cause
chronic if > 3mths Prostatitis: perineal or prostatic pain Lower urinary tract symptoms: dysuria, frequency, urgency Symptoms of systemic upset: fever, myalgia E. coli is common cause
27
prostatitis ix
Focussed history Digital rectal examination: tender, warm, swollen prostate Midstream sample of urine Screening for sexually transmitted infections (gonorrhoea can cause prostatitis)
28
acute prostatitis mx
Hospital admission for systemically unwell or septic patients (for bloods, blood cultures and IV antibiotics) Oral abx 14 days (quinolone) = ciprofloxacin 1st line (ofloxacin or trimethoprim)
29
chronic prostatitis mx
Alpha-blockers (e.g., tamsulosin) Analgesia Psychological treatment Antibiotics if less than 6 months of symptoms or a history of infection (e.g., trimethoprim or doxycycline for 4-6 weeks) Laxatives
30
how to measure proteinuria in CKD
albumin:creatinine ratio (ACR)
31
when to prescribe ACEi in CKD
if they have an albumin:creatinine ratio (ACR) > 30 mg/mmol + existing HTN ACR > 70 regardless
32
valvular abnormality w PKD
Mitral valve prolapse mitral regurgitation
33
AKI mx
stop nephrotoxic drugs careful fluid balance fluid resus espesh if pre-renal cause tx hyperkalaemia specialist if cause is not known or is severe haemodialysis when not responding to med tx of comps if fluid overload consider - loop diuretics e.g. furosemide - adrenaline - inotrope like dobutamine to increase BP
34
AKI ix
U&Es - sodium - potassium - urea - creatinine - for dx urine output urinalysis - blood + protein (nephritic syndrome?) no identifiable cause for the deterioration or are at risk of urinary tract obstruction they should have a renal ultrasound
35
when to refer AKI to nephrologist
Renal tranplant ITU patient with unknown cause of AKI Vasculitis/ glomerulonephritis/ tubulointerstitial nephritis/ myeloma AKI with no known cause Inadequate response to treatment Complications of AKI Stage 3 AKI (see guideline for details) CKD stage 4 or 5 Qualify for renal replacement hyperkalaemia / metabolic acidosis/ complications of uraemia/ fluid overload (pulmonary oedema)
36
features to differentiate AKI from CKD
renal ultrasound in CKD will have bilateral small kidneys apart from: AD PKD diabetic nephropathy (early stages) amyloidosis HIV-associated nephropathy CKD will have hypocalcaemia due to lack of VD
37
what can cause hyperkalaemia
AKI CKD (stage 4 or 5) Rhabdomyolysis Adrenal insufficiency - addisons Tumour lysis syndrome metabolic acidosis disease massive blood transfusion drugs*: , ACEis, ARBs, spironolactone (K+ sparing), ciclosporin, heparin *BBs interfere with K+ transport into cells + can potentially cause hyperkalaemia in renal failure patients - remember beta-agonists, e.g. Salbutamol, are sometimes used as emergency treatment
38
what foods are high in K+
salt substitutes (i.e. Contain potassium rather than sodium) bananas, oranges, kiwi fruit, avocado, spinach, tomatoes
39
ECG hyperkalaemia
Peaked or 'tall-tented' T waves (occurs first) Loss of P waves Broad QRS complexes Prolonged PR interval Sinusoidal wave pattern (v severe) Ventricular fibrillation
40
mx hyperkalaemia below 6.5mmol/L + no ECG changes
tx underlying cause for example, treating acute kidney injury and stopping medications (e.g., spironolactone or ACE inhibitors)
41
mx hyperkalaemia above 6.5 or w ECG changes
IV CALCIUM GLUCONATE + INSULIN WITH DEXTROSE INFUSION INSULIN drives potassium from the extracellular space to the intracellular space DEXTROSE is required to prevent hypoglycaemia while on insulin CALCIUM GLUCONATE stabilises the cardiac muscle cells and reduces the risk of arrhythmias other options: Nebulised salbutamol temporarily drives potassium into cells Oral calcium resonium reduces potassium absorption in the GI tract (this is slow and causes constipation) Sodium bicarbonate (in acidotic patients on renal advice) drives potassium into cells as it corrects the acidosis Haemodialysis may be required in severe or persistent cases
42
what albumin:creatinine ratio means
proteinuria >3 mg/mmol
43
what albumin:creatinine ratios to refer to a nephrologist
>70 mg/mmol - unless known to be caused by diabetes + already approp tx >30 mg/mmol w persistent haematuria 3-29 mg/mmol w persistent haematuria + other RFs e.g. declining eGFR/CVD
44
what is rhabdomyolysis
skeletal muscle breaking down + releasing various chemicals into the blood. Muscle cells (myocytes) undergo cell death (apoptosis), releasing: Myoglobin Potassium Phosphate Creatine kinase
45
complications of rhabdomyolysis
hyperkalaemia - arrythmias + arrest AKI - myoglobin is toxic in high concs DIC compartment syndrome
46
causes of rhabdomyolysis
Anything that causes significant damage to muscle cells: Prolonged immobility, particularly frail patients who fall + spend time on the floor before being found Extremely rigorous exercise beyond the person’s fitness level (e.g., endurance events or CrossFit) Crush injuries Seizures Statins
47
features of rhabdomyolysis
Muscle pain Muscle weakness Muscle swelling Reduced urine output (oliguria) Red-brown urine (myoglobinuria) Fatigue Nausea and vomiting Confusion (particularly in frail patients)
48
ix rhabdomyolysis
Creatine kinase (CK) blood test for dx - normally <150 U/L. In rhabdomyolysis, it can be 1,000-100,000 U/L - typically rises in the first 12 hours, then remains elevated for 1-3 days, then gradually falls - higher the CK, the greater the risk of kidney injury Myoglobinuria - urine dipstick will test +ve for blood U&Es for AKI + hyperkalaemia ECGs- hyperkalaemia
49
tx rhabdomyolysis
IV fluids hyperkalaemia tx
50
what is haemolytic uraemic syndrome (HUS)
thrombosis in small BVs throughout the body, usually triggered by Shiga toxins from either E. coli O157 or Shigella Most often affects children following an episode of gastroenteritis. Abx and anti-motility medication (e.g., loperamide) used to treat gastroenteritis caused by E. coli O157 or Shigella increase the risk of HUS.
51
triad in HUS
Microangiopathic haemolytic anaemia (thrombi causes RBCs to ruptures as they pass through small BVs) AKI Thrombocytopenia (low platelets) (as they are used to form the thrombus)
52
HUS presentation
E. coli O157 + Shigella cause gastroenteritis. Diarrhoea is the first symptom, which turns bloody within 3 days. Around a week after the onset of diarrhoea, the features of HUS develop: Fever Abdominal pain Lethargy Pallor Reduced UO Haematuria Hypertension Bruising Jaundice (due to haemolysis) Confusion
53
mx HUS
Medical emergency + requires hospital admission + supportive management: Hypovolaemia (e.g., IV fluids) Hypertension Severe anaemia (e.g., blood transfusions) Severe renal failure (e.g., haemodialysis) It is self-limiting, and most patients fully recover with good supportive care.
54
ix HUS
stool culture to establish causative organism FBC = anaemia - haemoglobin level less than 8 g/dL with a negative Coomb's test, thrombocytopenia Fragmented blood film = schistocytes and helmet cells U&Es = AKI
55
features of nephritic syndrome
Haematuria - microscopic or macroscopic Oliguria Proteinuria, <3g per 24 hours (higher protein suggests nephrotic syndrome) Fluid retention
56
what is nephritic syndrome
a group of features that occurs w nephritis (inflammation of the kidneys)
57
what is nephrotic syndrome
occurs when the basement membrane in the glomerulus becomes highly permeable, resulting in significant proteinuria. It refers to a group of features without specifying the underlying cause
58
features of nephrotic syndrome
NO blood Proteinuria (>3kg in 24hr) = FROTHY urine Low serum albumin (<25g per litre) Peripheral oedema Hypercholesterolaemia
59
what does nephrotic syndrome predispose px to
thrombosis - loss of antithrombin III (a protein that will be lost in urine) - it inhibits coagulation by inhibiting the enzymatic activity of thrombin hypertension hyperlipidaemia - due to overproduction in the liver infection risk - due to urinary immunoglobulin loss
60
most common cause of nephrotic syndrome
minimal change disease
61
top causes of nephrotic syndrome in adults + other causes
Membranous nephropathy Focal segmental glomerulosclerosis Membranoproliferative glomerulonephritis Henoch-Schönlein purpura (HSP) Diabetes Infection (e.g., HIV)
62
what is IgA nephropathy (Berger’s disease)
commonest cause of primary glomerulonephritis worldwide (nephritic syndrome)
63
IgA nephropathy presentation
young male, recurrent episodes of macroscopic haematuria typically associated with a recent/current RTI nephrotic range proteinuria is rare renal failure is unusual and seen in a minority of patients
64
histology in IgA nephropathy
IgA deposits and glomerular mesangial proliferation
65
what is membranous nephropathy
deposits of immune complexes (IgG + complement) in the glomerular basement membrane -> thickening + malfunctioning of the membrane, proteinuria usually idiopathic
66
histology in membranous nephropathy
IgG and complement deposits on the basement membrane
67
histology in Rapidly progressive glomerulonephritis
glomerular crescents
68
what is goodpasture syndrome
also known as anti-glomerular basement membrane (anti-GBM) disease Anti-GBM antibodies attack the glomerulus + pulmonary basement membranes. It causes glomerulonephritis and pulmonary haemorrhage
69
goodpastures syndrome histology
renal biopsy: linear IgG deposits along the basement membrane
70
goodpastures syndrome presentation
patient in their 20s or 60s with acute kidney failure and haemoptysis (coughing up blood) can be exacerbated by a RTI
71
systemic diseases that can cause glomerulonephritis
Henoch-Schönlein purpura (HSP) Vasculitis (e.g., microscopic polyangiitis or granulomatosis with polyangiitis) Lupus nephritis (associated with systemic lupus erythematosus)
72
what is post-streptococcal glomerulonephritis
Occurs 7-14 days following a group A beta-haemolytic Streptococcus infection (Strep pyogenes) Caused by immune complex (IgG, IgM and C3) deposition in the glomeruli Usually young children
73
Membranoproliferative glomerulonephritis
It involves immune complex deposits and mesangial proliferation.
74
post-streptococcal glomerulonephritis sx
headache malaise visible haematuria proteinuria (less commonly signif) this may result in oedema hypertension oliguria
75
ix in post-strep glomerulonephritis
bloods - raised anti-streptolysin O titre are used to confirm the diagnosis of a recent streptococcal infection - low C3 renal biopsy - electron microscopy: subepithelial 'humps' caused by lumpy immune complex deposits - immunofluorescence: 'starry sky' appearance
76
significant AKI, haemoptysis + p-ANCA antibodies
microscopic polyangiitis (diff from egwp which is also p-ANCA, similar sx to gwp which is c-ANCA)
77
significant AKI, haemoptysis + c-ANCA antibodies
granulomatosis with polyangiitis
78
what is tumour lysis syndrome
usually triggered by intro of combo chemo - occurs from the breakdown of tumour cells -> release of chemicals from the cell -> high potassium and high phosphate level in the presence of a low calcium. Suspect in any patient presenting with an AKI in the presence of a high phosphate and high uric acid level.
79
what is serum urea-creatinine ratio used for
urea and creatinine both freely filtered at the glomerulus creatinine is not reabsorbed (it is removed from body entirely by the kidneys therefore v high if kidneys are not working) urea reabsorbed by tubules (urea absorption increased compared to creatinine in pre-renal) can be used as an indicator of the likely cause of renal failure
80
high urea-creatinine ratio
PRE- RENAL FAILURE - dehydration corticosteroids GI haemorrhage protein-rich diet severe catabolic state
81
low urea-creatinine ratio
intrinsic renal damage severe liver dysfunction malnutrition pregnancy low protein diet SIADH rhabdomyolysis
82
spironolactone mechanism of action
aldosterone antagonist
83
what does renal artery stenosis cause
secondary hyperaldosteronism due to disproportionately low BP in the kidneys -> HTN as excessive renin is released
84
what is renal artery stenosis
narrowing of the artery supplying the kidney, usually due to atherosclerosis
85
where do renal stones most commonly get stuck
vesico-ureteric junction
86
most common type of kidney stone
calcium based - Calcium oxalate (more common) - Calcium phosphate Opaque on XR (can be seen)
87
other types of kidney stone (apart from calcium)
Uric acid – these are not visible on x-ray Struvite – produced by bacteria, therefore, associated with infection (stag horn shape) Cystine – associated with cystinuria, an autosomal recessive disease (semi-opaque ground glass on XR)
88
what is a staghorn calculus + what is it made from
where a renal stone forms in the shape of the renal pelvis - body sits in the renal pelvis with horns extending into the renal calyces occurs with stones made of struvite In recurrent URTIs, the bacteria can hydrolyse the urea in urine to ammonia, creating the solid struvite
89
renal stones presentation
may be asx Renal colic is the usual complaint: - Unilateral loin to groin pain that can be excruciating - Colicky (fluctuating in severity) as the stone moves and settles May also be: - haematuria - N&V - reduced urine output - sx of sepsis if infection present
90
renal stones ix
Non-contrast computer tomography (CT) of the kidneys, ureters and bladder (CT KUB) = INITIAL IX OF CHOICE FOR DX, do within 24 hrs pres US KUB (preg women or children) urine dipstick = haematuria (but normal does not exclude) bloods - infection + U&Es, Ca (hypercalcaemia is a cause) Abdo XR (wld not show uric acid stones, + may not show small stones) Analyse stone
91
mx renal stones
NSAIDs best analgesia = IM diclofenac Antiemetics = metoclopramide, prochlorperazine or cyclizine Abx if infection Watch + wait if < 5mm + uncomplicated Consider tamsulosin (alpha blocker) to aid spontan passage (only if <10mm) 5-10mm shockwave lithotripsy Surgical (e.g. ureteroscopy, Percutaneous nephrolithotomy) if >10mm, do not pass spontan or complete obstruction (hydronephrosis shown by dilation of renal pelvis) / infection
92
advice to px who get recurrent renal stones
Increase oral fluid intake (2.5 – 3 litres per day) Add fresh lemon juice to water (citric acid binds to urinary calcium reducing the formation of stones) Avoid carbonated drinks (cola drinks contain phosphoric acid, which promotes calcium oxalate formation) Reduce dietary salt intake (less than 6g per day) Maintain a normal calcium intake (low dietary calcium might increase the risk of kidney stones) For calcium stones – reduce the intake of oxalate-rich foods (e.g., spinach, beetroot, nuts, rhubarb and black tea) For uric acid stones – reduce the intake of purine-rich foods (e.g., kidney, liver, anchovies, sardines and spinach) Limit dietary protein
93
medications for recurrent renal stones
POTASSIUM CITRATE in patients with calcium oxalate stones and raised urinary calcium Thiazide diuretics (e.g., indapamide) in patients with calcium oxalate stones and raised urinary calcium (can increase distal tubular calcium resorption)
94
what is a hydrocele
collection of fluid within the tunica vaginalis that surrounds the testes usually painless and present with a soft scrotal swelling communicating + non-communicating
95
hydrocele examination
The testicle is palpable within the hydrocele Soft, fluctuant, may be large Irreducible + has no bowel sounds (distinguishing it from a hernia) Transilluminated by shining torch through the skin, into the fluid (the testicle floats within the fluid)
96
mx hydrocele
exclude serious causes (cancer) If idiopathic - conservative mx only if uncertainty/hard to palpate - do an USS
97
what type of hydrocele may you get in newborn males
communicating - caused by patency of the processus vaginalis allowing peritoneal fluid to drain down into the scrotum usually resolve in 1st few mths so reassure (think about surgical repair if not resolved in 1-2 yrs)
98
what is a varicocele
occurs where the veins in the pampiniform plexus become swollen as a result of increased resistance in the testicular vein (incompetent valves / obstruction by tumour?)
99
comps in varicocele
can cause impaired fertility - due to disrupting the temperature in the affected testicle may result in testicular atrophy, reducing the size and function of the testicle
100
what is the pampiniform plexus
a venous plexus found in the spermatic cord and drains the testes (drains into the testicular vein) plays a role in regulating the temperature of blood entering the testes by absorbing heat from the nearby testicular artery
101
which side do most varicoceles occur on
LEFT due to increased resistance in L testicular vein (R drains into IVC, L drains into L renal vein)
102
varicocele presentation
Throbbing/dull pain or discomfort, worse on standing A dragging sensation Sub-fertility or infertility
103
varicocele examination
A scrotal mass that feels like a “bag of worms” More prominent on standing Disappears when lying down Asymmetry in testicular size if the varicocele has affected the growth of the testicle
104
when to refer varicocele urgently to urology
Varicoceles that do not disappear when lying down - as they raise concerns about retroperitoneal tumours obstructing the drainage of the renal vein
105
varicocele ix
Ultrasound with Doppler imaging can be used to confirm the diagnosis Semen analysis if there are concerns about fertility Hormonal tests (e.g., FSH and testosterone) if there are concerns about function
106
varicocele tx
Uncomplicated cases can be managed conservatively. Surgery or endovascular embolisation may be indicated for pain, testicular atrophy or infertility.
107
what is an epididymal cyst
fluid filled sac that occurs at the head of the epididymis if it contains sperm it is called a spermatocele
108
epididymal cyst presentation
mostly asx may present having felt a lump, or they may be found incidentally on ultrasound for another indication.
109
epididymal cyst examination
Soft, round lump Typically at the top of the testicle Associated with the epididymis Separate from the testicle May be able to transilluminate large cysts (appearing separate from the testicle)
110
epididymal cyst tx
Usually harmless and are not associated with infertility or cancer. They may cause pain or discomfort where removal wld be considered.
111
indications for short-term dialysis
A – Acidosis (severe and not responding to treatment) E – Electrolyte abnormalities (particularly treatment-resistant hyperkalaemia) I – Intoxication (overdose of certain medications) O – Oedema (severe and unresponsive pulmonary oedema) U – Uraemia leading to pericarditis or encephalitis - sx such as seizures or reduced consciousness
112
options for long term dialysis
Haemodialysis for long term access use: - Tunnelled cuffed catheter - Arteriovenous fistula Peritoneal dialysis
113
AV fistula features to examine in OSCE
Skin integrity Aneurysms Palpable thrill (a fine vibration felt over the anastomosis) A “machinery murmur” on auscultation over the fistula
114
comps of AV fistula
Aneurysm Infection Thrombosis Stenosis STEAL syndrome High-output heart failure
115
what is STEAL syndrome
occurs when there is inadequate blood flow to the limb distal to the fistula. The AV fistula “steals” blood from the rest of the limb. Blood is diverted away from the part of the limb it was supposed to supply -> ischaemia. Instead, it flows through the fistula and into the venous system.
116
what is high-output heart failure
caused by blood flowing quickly from the arterial to the venous system through an A-V fistula. There is a rapid return of blood to the heart, increasing the pre-load -> hypertrophy of the heart muscle and heart failure.
117
comps of peritoneal dialysis
Bacterial peritonitis (infections in the high-sugar environment are common and serious) Peritoneal sclerosis (thickening and scarring of the peritoneal membrane) Ultrafiltration failure (the dextrose is absorbed, reducing the filtration gradient, making ultrafiltration less effective) Weight gain (due to absorption of the dextrose) Psychosocial implications
118
what does the dialysis solution that goes into peritoneal cavity contain
dextrose
119
most common cause of peritonitis secondary to peritoneal dialysis
Staphylococcus epidermidis
120
LUTS
occur w prostate pathology Hesitancy – difficult starting and maintaining the flow of urine Weak flow Urgency – a sudden pressing urge to pass urine Frequency – needing to pass urine often, usually with small amounts Intermittency – flow that starts, stops and varies in rate Straining to pass urine Terminal dribbling – dribbling after finishing urination Incomplete emptying – not being able to fully empty the bladder, with chronic retention Nocturia – having to wake to pass urine multiple times at night
121
initial assessment of man presenting w LUTS
Digital rectal examination (prostate exam) to assess the size, shape and characteristics of the prostate Abdominal examination to assess for a palpable bladder and other abnormalities Urinary frequency volume chart, recording 3 days of fluid intake and output Urine dipstick to assess for infection, haematuria (e.g., due to bladder cancer) and other pathology Prostate-specific antigen (PSA) for prostate cancer, depending on the patient preference
122
common causes of raised PSA
Prostate cancer Benign prostatic hyperplasia Prostatitis Urinary tract infections Vigorous exercise (notably cycling) Recent ejaculation or prostate stimulation
123
difference between exam in benign + cancerous prostate
A benign prostate feels smooth, symmetrical and slightly soft, with a maintained central sulcus A cancerous prostate may feel firm/hard, asymmetrical, craggy or irregular, with loss of the central sulcus
124
medical mx of BPH
Alpha-blockers (e.g., tamsulosin) relax smooth muscle, with rapid improvement in symptoms (tx of immediate sx) 5-alpha reductase inhibitors (e.g., finasteride) gradually reduce the size of the prostate (tx of the enlargement, takes 6 mths)
125
how long does finasteride take to improve sx in BPH
6 mths
126
SE tamsulosin
postural hypotension as alpha blocker
127
SE finasteride
sexual dysfunction (due to reduced testosterone). as a 5-alpha reductase inhibitor it stops the conversion testosterone to dihydrotestosterone (DHT) (more potent version)
128
what to monitor in HSP
blood pressure and urinanalysis
129
HIV-associated nephropathy (HIVAN) features
massive proteinuria resulting in nephrotic syndrome normal or large kidneys focal segmental glomerulosclerosis with focal or global capillary collapse on renal biopsy elevated urea and creatinine normotension
130
which form of renal impairment is most commonly assoc w hep C
Membranoproliferative glomerulonephritis
131
which form of renal impairment is most commonly assoc w HIV
focal segmental glomerulosclerosis
132
what can invalidate eGFR
Eating red meat the evening before a blood test
133
Rfs for prostate cancer
Increasing age Family history Black African or Caribbean origin Tall stature Anabolic steroids
134
prostate cancer presentation
asx LUTS Haematuria Erectile dysfunction Symptoms of advanced disease or metastasis (e.g., weight loss, bone pain or cauda equina syndrome)
135
first line ix for suspected prostate cancer
Multiparametric MRI of prostate results reported on a Likert scale 1 – very low suspicion 2 – low suspicion 3 – equivocal 4 – probable cancer 5 – definite cancer
136
when to perform a prostate biopsy
MRI findings (e.g., Likert 3 or above) and the clinical suspicion (i.e. examination and PSA level)
137
what to do if suspicion of cancer on DRE
Refer for 2-week wait appointment and advise urgent multiparametric MRI
138
gleason grading system
prostate cancer grading system based on histology from biopsies The greater the Gleason score, the more poorly differentiated the tumour is + the worse the prognosis - 1 (closest to normal) to 5 (most abnormal) made up of 2 nos from different samples 6 is considered low risk 7 is intermediate risk (3 + 4 is lower risk than 4 + 3) 8 or above is deemed to be high risk
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RFs bladder cancer
increased age smoking aromatic amines - dye + rubber - transitional cell carcinoma Schistosomiasis causes squamous cell carcinoma
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types of bladder cancer
Transitional cell carcinoma (90%) Squamous cell carcinoma (5% – higher in areas of schistosomiasis)
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bladder cancer key presentation
Painless haematuria
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when to do a 2 week wait referral for bladder cancer
>45 with unexplained visible haematuria, either without a UTI or persisting after treatment for a UTI >60 with microscopic haematuria PLUS: - Dysuria or; - Raised white blood cells on a full blood count consider a non-urgent referral in >60 with recurrent unexplained UTIs
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bladder cancer dx
Cystoscopy
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tx of non-muscle invasive bladder cancer
Transurethral resection of bladder tumour (TURBT) Intravesical chemotherapy is often used after a TURBT procedure to reduce the risk of recurrence.
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tx for invasive bladder cancer
radical cystectomy
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immunotherapy in bladder cancer
Intravesical BCG Giving the BCG vaccine (the same one as for tuberculosis) into the bladder is thought to stimulate the immune system, which in turn attacks the bladder tumours.
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most common renal tumour
Renal adenocarcinoma
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Renal Cell Carcinoma presentation
haematuria, flank pain and a palpable mass
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RFs Renal Cell Carcinoma
Smoking Obesity Hypertension End-stage renal failure Von Hippel-Lindau Disease Tuberous sclerosis
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when to do 2 week wait for renal cell carcinoma
>45 with unexplained visible haematuria, either without a UTI or persisting after treatment for a UTI
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classic feature of metastatic renal cell carcinoma
“Cannonball metastases” in the lungs - appear as clearly-defined circular opacities scattered throughout the lung fields on a chest x-ray.
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paraneoplastic features of renal cell carcinoma
Polycythaemia – due to secretion of unregulated erythropoietin Hypercalcaemia – due to secretion of a hormone that mimics the action of parathyroid hormone Hypertension – due to various factors, including increased renin secretion, polycythaemia and physical compression Stauffer’s syndrome – abnormal liver function tests (raised ALT, AST, ALP and bilirubin) without liver metastasis
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types of renal cell adenocarcinoma
Clear cell (around 80%) Papillary (around 15%) Chromophobe (around 5%)
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how to calc urea:creatinine ratio
plasma urea (mmol/L) / (plasma creatinine (μmol/L) divided by 1000)
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mx for confined renal cancer
a partial or total nephrectomy depending on the tumour size - patients with a T1 tumour (i.e. < 7cm in size + confined to kidney) are typically offered a partial nephrectomy
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Alport's syndrome presentation
microscopic haematuria, bilateral sensorineural deafness, and lenticonus
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drug causes of acute interstitial nephritis
PENICILLIN rifampicin NSAIDs allopurinol furosemide
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acute interstitial nephritis presentation
allergic picture may have just had penicillin abx fever, rash, arthralgia EOSINOPHILIA mild renal impairment hypertension
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ix results in acute interstitial nephritis
sterile pyuria white cell casts in urine
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what to use in px who have troubling gynaecomastia on spironolactone
Eplerenone
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what cells does testicular cancer usually come from
germ cells in the testes
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2 types of testicular cancer
Seminomas Non-seminomas (mostly teratomas)
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RFs testicular cancer
Undescended testes Male infertility Family history Increased height
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presentation testicular cancer
lump on testicle - non-tender - arising from testicle - hard - irregular - non-fluctuant - no transillumination rarely can get gynaecomastia - espesh in Leydig cell tumours
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ix testicular cancer
SCROTAL USS initial ix staging CT scan
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tumour markers for testicular cancer
Alpha-fetoprotein – may be raised in teratomas (not in pure seminomas) Beta-hCG – may be raised in both teratomas and seminomas Lactate dehydrogenase (LDH) is a very non-specific tumour marker
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Royal Marsden Staging System testicular cancer
Stage 1 – isolated to the testicle Stage 2 – spread to the retroperitoneal lymph nodes Stage 3 – spread to the lymph nodes above the diaphragm Stage 4 – metastasised to other organs
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Extra-renal manifestations of PKD
berry aneurysms Hepatic, splenic, pancreatic, ovarian and prostatic cysts (LIVER CYSTS ARE THE MOST COMMON EXTRA THING) Mitral regurgitation Colonic diverticula
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comps of PKD
Chronic loin/flank pain Hypertension Gross haematuria can occur with cyst rupture (usually resolves within a few days) Recurrent urinary tract infections Renal stones End-stage renal failure occurs at a mean age of 50 years
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ix PKD
Ultrasound and genetic testing are used for diagnosis.
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mx ADPKD
tolvaptan - vasopressin receptor antagonist - can slow progression of cysts + progression of renal failure tx HTN analgesia abx if infections drainage if sx dialysis renal transplant
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conservative mx PKD
Genetic counselling Avoiding contact sports due to the risk of cyst rupture Avoiding NSAIDs and anticoagulants MR angiography (MRA) can be used to screen for cerebral aneurysms
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what is pyelonephritis
inflammation of the kidney resulting from bacterial infection - affects the renal pelvis (join between kidney and ureter) and parenchyma (tissue)
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RFs pyelonephritis
Female sex Structural urological abnormalities Vesico-ureteric reflux (urine refluxing from the bladder to the ureters – usually in children) Diabetes
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most common cause pyelonephritis
E. coli - gram-negative, anaerobic, rod-shaped bacteria that are part of the normal lower intestinal microbiome (found in the faeces + can easily spread to bladder)
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presentation pyelonephritis
Lower UTI sx - dysuria, suprapubic discomfort and increased frequency + Fever Loin or back pain (bilateral or unilateral) Nausea / vomiting Patients may also have: Systemic illness Loss of appetite Haematuria Renal angle tenderness on examination
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ix pyelonephritis
Urine dipstick = nitrites, leukocytes, blood. Midstream urine (MSU) for microscopy, culture and sensitivity testing to establish the causative organism Raised white blood cells and raised inflammatory markers ultrasound or CT scan to exclude other things
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1st line for mx pyelonephritis in community
cefalexin for 7-10 days co-amoxiclav if culture results trimethoprim if culture results ciprofloxacin (keep tendon damage and lower seizure threshold in mind) hx if thinking sepsis!
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what to use to assess for renal damage in recurrent pyelonephritis
Dimercaptosuccinic acid (DMSA) scans
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what is orchitis
inflammation of the testicle
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what does the epididymis do
Sperm mature and are stored in the epididymis (released from testicle into its head). The epididymis drains into the vas deferen
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causes of epididymo-orchitis
Escherichia coli (E. coli) Chlamydia trachomatis Neisseria gonorrhoea Mumps - usually just testicle
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presentation epididymo-orchitis
gradual onset, over minutes to hours, with unilateral: Testicular pain Dragging or heavy sensation Swelling of testicle and epididymis Tenderness on palpation, particularly over epididymis - positive Prehn's sign (relief of pain upon lifting the scrotum) Presence of the cremasteric reflex (stroking the inner thigh, testicle moves upwards) - both differentiate from torsion Urethral discharge (should make you think of chlamydia or gonorrhoea) Systemic symptoms such as fever and potentially sepsis
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tx for epididymo-orchitis when it is most likely caused by an enteric organism (e.g., E. coli)
Ofloxacin for 14 days Levofloxacin for 10 days Co-amoxiclav for 10 days (where quinolones are contraindicated)
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causes of non-gonococcal urethritis (NGU)
Chlamydia trachomatis Ureaplasma urealyticum Mycoplasma genitalium
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tx urethritis
either oral doxycycline for 7 days or single dose of oral azithromycin
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exceptions to the rule that most patients with CKD have bilateral small kidney
autosomal dominant polycystic kidney disease diabetic nephropathy (early stages) amyloidosis HIV-associated nephropathy
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features that suggest CKD rather than AKI
bilateral small kidneys (apart from exceptions) hypocalcaemia (due to lack of vitamin D)
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what is acute tubular necrosis
most common renal cause of an AKI damage to the tubular cells from prolonged ischaemia/presence of toxins. The kidneys are no longer able to concentrate urine or retain sodium leading to high urinary sodium and low urine osmolality (more dilute).
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what happens if you correct chronic hypernatraemia too fast
cerebral oedema
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plasma sodium in dehydration
high (however not if there is salt loss eg D+V)
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acute tubular necrosis presentation
AKI with the presence of muddy brown casts in the urine.
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what can cause acute tubular necrosis
Ischaemia due to hypoperfusion (e.g., dehydration, shock or heart failure) Nephrotoxins (e.g., gentamicin, radiocontrast agents or cisplatin)
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surgical mx renal stones
Treatment Stone <5mm = expectant treatment Stone <2cm = lithotripsy (wave to break stone) Stone <2cm + pregnant = ureteroscopy (camera passed through urethra) Stone complex = percutaneous nephrolithotomy (invasive, camera passed though kidney from back) hydronephrosis/infection = nephrostomy (drainage of urine from kidney) as needs urgent decompression
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pain reliever in renal stones
IM Diclofenac
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comp of radiotherapy of the prostate + how does that comp present
proctitis (inflammation in the rectum) pain, altered bowel habit, rectal bleeding and discharge (Prednisolone suppositories can help reduce inflammation)
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tx testicular torsion
Emergency bilateral orchidopexy - surgical fixation of both testes to the posterior wall (need both done to prevent further risk)