Renal Flashcards

(174 cards)

1
Q

AKI

A

defined as an acute drop in kidney function (under 48 hours). It is diagnosed by measuring the serum creatinine.

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2
Q

AKI criteria

A
  1. Rise in creatinine of ≥ 26.4 micromol/L in 48 hours (>1.5-1.9 x reference) or <0.5ml/kg/hr for >6 hours
  2. Rise in creatinine of ≥ 50% (>2-2.9 x reference) in 7 days or Urine output of < 0.5ml/kg/hour for > 12 hours
  3. Increase >3 x reference SCr or increase to >354 and <0.3ml/Kg/hr for >24 hours
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3
Q

risk factors for AKI

A
  1. CKD
  2. Heart failure
  3. Diabetes
  4. Liver disease
  5. Previous AKI
  6. Peripheral vascular disease
  7. Older age (above 65 years)
  8. Cognitive impairment
  9. Nephrotoxic medications such as NSAIDS and ACE inhibitors
  10. Use of a contrast medium such as during CT scans
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4
Q

Pre-renal (inadequate supply of blood to kidneys reducing filtration of blood)

A
  1. Hypovolaemia: Haemorrhage, volume depletion (e.g. D&V, burns and dehydration)
  2. Hypotension: cardiogenic shock and distributive shock (sepsis or anaphylaxis)
  3. Renal Hypoperfusion: Heart failure, NSAIDs/ACEi/ARBs/hepatorenal syndrome
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5
Q

Renal causes of AKI

A
  1. Glomerulonephritis
  2. Interstitial nephritis: Drugs (NSAIDs, antibiotics, PPI), Infection (TB) and systemic (sarcoidosis)
  3. Tubular injury: Ischaemia, drugs (gentamicin), contrast and rhabdomyolysis
  4. Acute tubular necrosis
  5. Vasculitis/renovascular
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6
Q

Post renal causes (obstruction to outflow of urine from the kidney, causing back-pressure into the kidney and reduced kidney function)

A
  1. Kidney stones
  2. Ureter or urethral strictures
  3. Enlarged prostate or prostate cancer
  4. Masses such as cancer in the abdomen or pelvis
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7
Q

sign/symptoms of AKI

A
  1. Constitutional symptoms e.g. Anorexia, weight loss, fatigue, lethargy
  2. Nausea & Vomiting
  3. Itch
  4. Fluid overload: Oedema, SOB

Signs

  1. Fluid overload incl hypertension, Oedema, Pul oedema, effusions (pleural & pulmonary)
  2. Uraemia incl itch, pericarditis
  3. Oliguria
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8
Q

AKI Iv

A

Urinalysis: protein, blood, nitrites, glucose, WCC

U&E

FBC and coagulation screen

immunology: ANA, ANCA, GBM

protein electrophoresis and BJP

USS

biopsy

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9
Q

Management of AKI

A
  1. assess for hydration: BP, HR, UO, JVP, CRT, Oedema
  2. IV Fluid hydration (fluid challenge for hypovolaemia) - crystalloid (0.9% NaCl) or colloid: not 5% dextrose
    - bolus of fluid, if >1000mls and no improvement, seek help
    - heart failure: fluid overload be careful
  3. Stop nephrotoxic medications e.g. NSAIDS and ACEi
  4. Relive obstruction in post renal AKI
  5. Dialysis: anuria or uraemia
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10
Q

AKI complications

A

Hyperkalaemia
fluid overload, heart failure and pulmonary oedema
metabolic acidosis, uraemia (encephalopathy or pericarditis)

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11
Q

CKD

A

abnormal kidney function and/or structure

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12
Q

CKD risk factor

A
AKI
CVD disease
diabetes 
hypertension
Glomerulonephritis
Polycystic kidney disease 
age related decline
Medication: NSAIDs, ACEi/ARBs and lithium 
Smoking 
Untreated urinary outflow tract obstruction 
proteinuria
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13
Q

CKD Iv

A

U&Es and eGFR (2 tests + 3 months apart)

Proteinuria (ACR) and Haematuria (dipstick)

renal USS

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14
Q

ACR stages

A

A1: <3
A2: 3-30
A3: >30

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15
Q

CKD stages

A
G1: >90
G2: 60-89
G3a: 45-59
G3b: 30-44
G4: 15-29
G5: <15`
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16
Q

Accelerated CKD

A

sustained decrease in GFR of 25% or more and a change in GFR category within 12 months

Or

a sustained decrease in GFR of 15 ml/min/1.73m2 per year

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17
Q

Renal consequences of CKD

A
  • Local – pain/ haemorrhage/ infection
  • Urinary – haematuria/ proteinuria
  • Impaired salt and water handling
  • Hypertension
  • Electrolyte abnormalities
  • Acid-base disturbance → ESRD (End stage renal disease)
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18
Q

slowing CKD management

A
  1. ACEi - Reduce proteinuria
  2. Treat glomerulonephritis
  3. Exercise, maintain a healthy weight and stop smoking
  4. Special dietary advice about phosphate, sodium, potassium and water intake
  5. Offer atorvastatin 20mg
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19
Q

Anaemia of CKD

A

Target 100-120Hb, exclude B12 and folate, check ferritin (>100) and TSats > 20%

  1. Oral iron - IV iron - EPO
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20
Q

Bone disease of CKD

A
  1. Osteomalacia occurs due to increased turnover of bones without adequate calcium supply.
    Osteosclerosis occurs when the osteoblasts respond by increasing their activity to match the osteoclasts by creating new tissue in the bone, however due to the low calcium level this new tissue is not properly mineralised.
  2. Osteoporosis can exist alongside the renal bone disease due to other risk factors such as age and use of steroids.
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21
Q

CKD: Bone disease management

A
  1. Active forms of vitamin D (alfacalcidol and calcitriol) – don’t need activation by kidneys
  2. Phosphate binders
  3. Salt reduction, K+ and fluid restriction
  4. Bisphosphonates
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22
Q

Dialysis 3 main purposes

A

excess fluid, solutes and waste products.

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23
Q

Dialysis based on

A
  1. Diffusion e.g. urea, K+, Na+ and infusion of HCO3-
  2. Convection: water across semipermeable membrane
  3. Adsorption: atoms, ions or molecules from a substance
    adhere to a surface of the adsorbent
    e.g. plasma proteins
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24
Q

Dialysis indications

A

A – Acidosis (severe and not responding to treatment)

E – Electrolyte abnormalities (severe and unresponsive hyperkalaemia)

I – Intoxication (overdose of certain medications)

O – Oedema (severe and unresponsive pulmonary oedema)

U – Uraemia symptoms such as seizures or reduced consciousness

eGFR < 7ml/min

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25
Haemodiafiltration (HDF)
haemodialysis is primarily diffusive, haemodiafiltration is increasingly convective, in nature. greater the convective force, the greater will be the generated volume of the pressure-driven ‘ultrafiltrate’. • Large volumes of ultrafiltrate add enormously to solute drag - especially for the larger “middle molecule” solute classes
26
different types of PD
continuous (2L x 4times per day) vs automated (overnight)
27
types of renal transplant
Deceased Heart Beating Donors (Brain stem death (DBD)) Non-Heart Beating Donors (DCD) Live Donation (altruistic)
28
Lifelong immunosuppression for kidney transplant
Induction Consolidation Maintenance
29
Transplant rejection types
1. Hyperacute - preformed antibodies 2. Acute rejection: cellular or antibody mediated, treated with immunosuppression 3. Chronic rejection: antibody mediated slowly progressive decline in renal function.
30
CMV infection - transplant
1st 3 months - Prophylactic PO valganciclovir in higher risk patients - IV ganciclovir if evidence of infection
31
Nephritic syndrome
``` Haematuria oliguria Proteinuria (<3g) Oedema Hypertension affect endothelial cells (proliferative process) ```
32
Nephrotic syndrome
``` Peripheral oedema Proteinuria >3g Hypoalbuminemia (<25g/L) Hypercholesterolaemia affects podocytes (non-proliferative process) ```
33
Minimal change disease
usually idiopathic, most common nephrotic syndrome in children, secondary to hodgkins lymphoma, leukaemia and a virus EM: foot fusion 1st line: steroids 2nd line: cyclophosphamide
34
Focal segmental glomerulosclerosis
small sections of each glomerulus (filter), and only a limited number of glomeruli are damaged at first. Commonest cause of nephrotic syndrome in adults (35%) primary (more common) or secondary (HIV/Heroin use/Obesity/ Reflux nephropathy)
35
Focal segmental glomerulosclerosis diagnosis and management
Small areas of mesangial collapse and sclerosis steroids
36
Membranous glomerulonephritis
2nd commonest cause of nephrotic syndrome in adults (15-30%) 1. idiopathic (majority) 2. Infections (Hep B), malignancies, Connective tissue diseases and drugs (gold/penicillamine)
37
Membranous glomerulonephritis diagnosis
Renal biopsy: subepithelial immune complex deposition in the basement membrane Anti PLA2r antibody: forms immune complex stuck between podocytes and basement membrane (blood) LM: Diffuse thickening of GBM. “spikes” with special silver stains IF: “IgG and complement (C3) deposits on the basement membrane” EM: Electron dense sub-epithelial deposits
38
Membranous glomerulonephritis Mx
immunosuppression e.g. Steroids/Alkylating agents/B cell monoclonal Ab (rituximab: stop antibody production and therefore damage) • 30% progress to end stage renal failure in 10 years
39
IgA nephropathy
Commonest GN in the world (Nephritis)
40
IgA nephropathy signs/symptoms
Asymptomatic microhaematuria  non-nephrotic range proteinuria Macroscopic haematuria after resp/GI infection Young adult and tonsillitis AKI (red cells clogging tubes up)/CKD Associated with Henoch-Schonlein Purpura (HSP) (arthritis/colitis/ purpuric skin rash)
41
IgA nephropathy Ix and management
LM: Diffuse mesangial IgA deposition IF: IgA and C3 deposition EM: Electron dense deposits in mesangium - BP control/ ACE inhibitors & ARBs/ Fish oil - Corticosteroids if persistent proteinuria >1g 3-6 months of ACE-i/ARB and GFR>50
42
Post streptococcal glomerulonephritis (AKA diffuse proliferative glomerulonephritis)
Skin or throat infection: 1-3 weeks after a streptococcal infection (e.g. tonsillitis or impetigo) Strep endocarditis: immune complex (bacterial antigen and antibody) – circulates and lodges into the kidney They develop a nephritic syndrome Can cause rapid decline unlike IgA Complement levels are lower in this but normal in IgA nephropathy
43
Post streptococcal glomerulonephritis Ix
Evidence of strep infection: increase ASOT, anti-DNAse B or decrease C3 CRP (less in IgA) and more in raise in this Fever, AKI, CRP, low complement Echo: for endocarditis
44
Mesangiocapillary glomerulonephritis
Idiopathic Secondary to Autoimmune e.g. SLE, RA, Cancer Mixed nephrotic/ nephritic syndrome
45
Mesangiocapillary glomerulonephritis diagnosis
LM: Mesangial proliferation, neutrophils and monocytes, thickened capillary walls. “tram track” GBM IF: Granular deposits of C3 EM: Electron dense sub-endothelial deposits +/- sub-epithelial +/- mesangial
46
Mesangiocapillary glomerulonephritis management
ACE-i/ARB and BP control Treat underlying cause Trial of immunosuppression if no underlying cause is found and progressive decline in function
47
Rapidly progressive glomerulonephritis
ANCA-Positive: Systemic Vasculitis, Wegener’s granulomatosis (Granulomatosis with polyangiitis) and Microscopic polyangiitis ANCA-Negative: Goodpasture’s disease-Anti-GBM, Henoch Scholein Purpura HSP/IgA, IgA & membranous (transforms into this) and Systemic Lupus Erythematosus SLE crescentic glomerulonephritis
48
Rapidly progressive glomerulonephritis signs/symptoms
Rapid deterioration in renal function over days/weeks Active urinary sediment (RBC’s, RBC & Granular Casts) It presents with a very acute illness with sick patients but it responds well to treatment
49
Rapidly progressive glomerulonephritis management
• Immunosuppression - Steroids (IV Methylprednisolone / Oral Prednisolone) - Cytotoxic (Cyclophosphamide/ Mycophenolate/ Azathioprine - dialysis
50
Goodpasture Syndrome
Anti-GBM (glomerular basement membrane) antibodies attack glomerulus and pulmonary basement membranes due to type IV collagen
51
Goodpasture Syndrome Mx
Imunosuppression - Steroids (IV Methylprednisolone / Oral Prednisolone) - Cytotoxic (Cyclophosphamide/ Mycophenolate/ Azathioprine - dialysis
52
Diabetic nephropathy
chronic high level of glucose passing through the glomerulus causes scarring. This is called glomerulosclerosis. Haemodynamic changes – increased GFR and initial decrease in creatinine – afferent arteriolar vasodilation mediated by range of vasoactive mediators. Renal hypertrophy due to raised plasma glucose which stimulates growth factors, renin-angiotensin aldosterone activation, production of advanced glycation products and oxidative stress
53
Diabetic nephropathy screening
albumin: creatinine ratio and U&Es. Overt diabetic nephropathy is characterised by persistent albuminuria (300mg/24 hours on at least 2 occasions separated by 3-6 months)
54
Diabetic nephropathy management
optimising blood sugar levels (Hb1Ac below 53 mmol to reduce microvascular complications) and blood pressure (ACE inhibitors) Lipid control: statins
55
Myeloma
Cancer of plasma cells: a type of WBC normally responsible for producing antibodies Excess production of immunoglobins (proteins) Collections of abnormal plasma cells accumulate in the bone marrow
56
Myeloma diagnosis
FBC, U&Es, LFTS Bloods: Serum Protein Electrophoresis and Serum Free light chains Urine: Bence Jones Protein Bone Marrow Biopsy
57
Myeloma management
Stop nephrotoxic medication e.g. NSAIDs – don’t give for the back pain Diuretics in view of risk increasing cast formation – flush calcium out as well Manage hypercalcaemia (saline +/- bisphosphonates [inhibit osteoclasts] ) - Chemotherapy to reduce tumour load - High dose dexamethasone may help reduce tumour load - Thalidomide/bortezomib: monoclonal antibodies - Stem cell transplant
58
Amyloidosis
extracellular amyloid (insoluble protein fibrils) in tissues or organs Occurs due to abnormal folding of proteins which aggregate and become insoluble
59
Amyloidosis types
1. Primary / Light chain (AL) 2. Secondary / Systemic / Inflammatory (AA) 3. Dialysis (Aβ2M) 4. Hereditary and old age (ATTR)
60
Amyloidosis complications
Renal – (nephrotic range) proteinuria +/- impaired renal function Cardiac – Restrictive Cardiomyopathy Nerves – peripheral or autonomic neuropathy Hepatomegaly / Splenomegaly GI – malabsorption
61
Amyloidosis Iv
Urinalysis + uPCR (urine protein creatinine ratio) Blood tests – renal function, markers of inflammation, protein electrophoresis, SFLC (Serum free light-chain measurement) Renal Biopsy: Congo red staining (apple green under polarised light) [Other biopsy - abdominal fat pad or rectal biopsy] SAP scan – Scintigraphy with radiolabelled serum amyloid – shows extent of disease
62
Vasculitis Mx
Corticosteroids Cyclophosphamide/Rituximab Azathioprine/Methotrexate used for maintenance Plasma Exchange – dialysis machine
63
SLE diagnosis
High index of suspicion: young lady with non-specific symptoms Blood: Raised inflammatory markers, Immunology – ANA +ve, anti-dsDNA ab (~70%) and Complement – low levels Urinalysis: protein: ACR >30 and PCR>50 Renal biopsy:
64
Interstitial nephritis
inflammation of the space between cells and tubules (the interstitium) within the kidney.
65
Acute interstitial nephritis
presents with AKI and hypertension acute inflammation of tubules and interstitium hypersensitivity reaction to: - drugs (NSAIDs or antibiotics) - Infection e.g. strep - autoimmune
66
Acute interstitial nephritis other signs/symptoms
``` o Rash o Fever o Eosinophilia on blood test o Arthralgia AKI + hypertension ```
67
Acute interstitial nephritis management
treat underlying cause | steroids
68
Chronic Tubulointerstitial Nephritis
chronic inflammation of the tubules and interstitium. Presents as CKD. Autoimmune, infectious, iatrogenic and granulomatous disease causes
69
Chronic Tubulointerstitial Nephritis management
ACEi/ARB (BP control), glucose control and lipids (statins) | steroids
70
Acute tubular necrosis
damage and death (necrosis) of the epithelial cells of the renal tubules. Most common cause of AKI Cause: ischaemia or toxins reversible: regenerates after 7-21 days
71
Acute tubular necrosis Iv
- Urinalysis: “Muddy brown casts” | - renal tubular epithelial cells in urine
72
Acute tubular necrosis management
``` Same as AKI supportive IV fluids stop nephrotoxins treat complications ```
73
Renal tubular acidosis
metabolic acidosis due to pathology in the tubules of the kidney.
74
Type 1 renal tubular acidosis
pathology in the distal tubule. The distal tubule is unable to excrete hydrogen ions that cause acidosis - hyperventilate to compensate for metabolic acidosis (blow CO2)
75
Type 1 renal tubular acidosis Ix + Mx
Hypokalaemia, metabolic acidosis and high urinary pH Mx: Oral bicarbonate
76
Type 2 renal tubular acidosis
The proximal tubule is unable to reabsorb bicarbonate from the urine into the blood. Excessive bicarbonate is excreted in the urine leads to acidosis in the blood due bicarbonate normally lowers pH Fanconi’s syndrome is the main cause
77
Type 2 renal tubular acidosis Ix + Mx
Hypokalaemia Metabolic acidosis High urinary pH Mx: oral bicarbonate and K+ replacement
78
Type 3 RTA
Type 3 renal tubular acidosis is a combination of type 1 and type 2 with pathology in the proximal and distal tubule.
79
Type 4 Renal Tubular Acidosis
Reduced aldosterone (stimulates sodium absorption and excretion of K+ and H+) and affects the distal tubule. Lower levels of K+ and H+ becomes excreted in the urine from the blood leading to hyperkalaemic renal tubule acidosis Causes: adrenal insufficiency, ACEi, spironolactone, SLE, diabetes or HIV
80
Type 4 Renal Tubular Acidosis Ix and Mx
- Hyperkalaemia – how to distinguish between type 1 and 4 - High chloride - Metabolic acidosis - Low urinary pH – reduced ammonia (suppressed by K+ -normally counter balances H+ acidity) production and less in urine Mx: - Fludrocortisone – synthetic corticosteroid medication that works similar to aldosterone - Sodium bicarbonate - Treatment of the hyperkalaemia may also be required
81
Haemolytic Uraemic Syndrome
thrombosis (blood clots) in small blood vessels throughout the body (especially glomerulus capillaries). 1. Haemolytic anaemia 2. AKI (haematuria and proteinuria) 3. Low platelet count
82
HUS signs/symptoms
``` Reduced urine output – due to AKI Haematuria or dark brown urine Abdominal pain Lethargy & irritability Confusion Hypertension Bruising ```
83
HUS management
anti-hypertensives blood transfusions dialysis
84
Rhabdomyolysis
skeletal muscle tissue breaks down and releases breakdown products into the blood. Myocytes undergo apoptosis - myoglobin, K+, P+, CK
85
Causes of Rhabdomyolysis
Prolonged immobility Extremely rigorous exercise Crush injuries Seizures
86
signs/symptoms of Rhabdomyolysis
``` Muscle aches & pain Oedema Fatigue Confusion Red-brown urine ```
87
Rhabdomyolysis Ix and Mx
CK blood test Myoglobinuria U&Es ECG Mx IV fluids: rehydrate and encourage filtration IV NaCl (reduce myoglobin toxicity) IV mannitol
88
Causes of hyperkalaemia
``` Acute kidney injury Chronic kidney disease Rhabdomyolysis Adrenal insufficiency Tumour lysis syndrome Medications a lot ```
89
hyperkalaemia ECG results
Tall peaked T waves Flattening or absence of P waves Broad QRS complexes
90
Hyperkalaemia management
calcium gluconate 10mls 10% - stabilise myocardium Insulin (actrapid) and dextrose (50mls of 50%) ``` Nebulised salbutamol IV fluids Oral calcium resonium Sodium bicarbonate Dialysis ```
91
Polycystic Kidney Disease chromosomes
PKD-1: chromosome 16 | PKD-2: chromosome 4
92
Polycystic Kidney Disease extra renal manifestations
Cerebral aneurysms Hepatic cysts: SOB, ankle swelling and pain Cardiac valve disease (aortic/mitral regurgitation/Aortic root dilatation) Colonic diverticula and colonic perforation- Abdominal and inguinal hernias
93
Polycystic Kidney Disease management
``` Tolvaptan: slow the development of cysts and renal failure Antihypertensives Hydration Analgesia Antibiotics Dialysis Renal transplant ```
94
Autosomal recessive polycystic kidney disease (ARPKD) chromosome
6 Young children and constantly associated with hepatic lesions renal: bilateral and symmetrical small cysts appearing from collecting duct system
95
Autosomal recessive polycystic kidney disease (ARPKD) signs/symptoms
Kidneys always palpable Hypertension Recurrent Urinary Tract Infections Slow Decline in GFR -less than 1/3 reach dialysis It often presents in pregnancy with oligohydramnios as the fetus does not produce enough urine. They can have dysmorphic features such as underdeveloped ear cartilage, low set ears and a flat nasal bridge.
96
Autosomal recessive polycystic kidney disease (ARPKD) management
dialysis in the first few days | tolvaptan
97
ALPORTS SYNDROME (HEREDITARY NEPHRITIS)
genetically heterogeneous disorder characterized by nephritic syndrome X linked inheritance (85%) Disorder of Type IV collagen matrix Mutation (COL4A5 gene) leads to deficient collagenous matrix
98
ALPORTS SYNDROME signs/symptoms
Haematuria - characteristic feature. Proteinuria seen later but confers bad prognosis Sensorineural deafness Ocular defects Leiomyomatosis of oesophagus/genitalia-rare Suspect in haematuria and hearing loss
99
ANDERSON FABRYS DISEASE
Uncommon Inborn error of Glycosphingolipid metabolism (deficiency of a-galactosidase A) X linked disease lysosomal storage disease Look for angiokeratomas
100
ANDERSON FABRYS diagnosis and Mx
Plasma /Leukocyte: a-GAL activity in blood Enzyme replacement - Fabryzyme
101
MEDULLARY CYSTIC KIDNEY
Autosomal Dominant inheritance Morphologically abnormal renal tubules leading to fibrosis Cysts are in the corticomedullary junction/medulla - not essential for diagnosis
102
Oncocytoma: benign tumour
Spherical, capsulated, brown/tan colored CT scan: Spoke wheel pattern (Has got central scar (stellate): strands come out from the center. Necrosis in the middle – can’t revascularize)
103
Angiomyolipoma (AML)
Blood vessels, muscle and fats: typical hamartoma associated with TS
104
Angiomyolipoma (AML) Mx
4 cm is considered cut off: rough guide Elective: Embolization/Partial nephrectomy Emergency: Embolization / emergency nephrectomy: usually the whole
105
Renal cell carcinoma
adenocarcinoma of renal cortex (arise from proximal convoluted tube)
106
Types of RCC
``` Clear cell: loss of VHL Papillary Chromophobe Collecting duct Medullary cell ```
107
RCC signs/symptoms
Haematuria, vague loin pain and mass (3 together: less than 10% in cases) Non-specific symptoms of cancer (e.g. weight loss, fatigue, anorexia, night sweats) Pyrexia of unknown origin (8-9 %) Varicocoele: causing pressure on left gonadal vein. Left gonadal vein drains in left renal vein. Left sided renal tumours can cause these Paraneoplastic syndrome (30%): weight loss, anaemia, HT and hypercalcemia
108
RCC Ix
USS CT: Chest, abdo and pelvis FBC: Hb
109
RCC Mx
small tumours 3-4cm: - surveillance (elderly) - ablation - partial nephrectomy >3-4cm - surveillance (elderly) - ablation - partial nephrectomy - Radical Nephrectomy >7cm - radical nephrectomy
110
RCC adjuvant therapy
TKI (Tyrosine kinase inhibitors) e.g. Sunitinib | - Reduces neovascularisation
111
RCC paraneoplastic syndromes
Polycythaemia (RCC secretes unregulated erythropoietin) Hypercalcaemia (RCC secretes a hormone that mimics the action of PTH)
112
Wilms tumour
* Under 5 * Mass in the abdomen (parents noticed or presenting with signs/symptoms) * Abdominal pain * Haematuria * Lethargy * Fever * Hypertension * Weight loss
113
Prostate cancer pathology
adenocarcinomas originating in peripheral zone local extension through the prostatic capsule, to the urethra, bladder base and seminal vesicles and with perineural invasion along autonomic nerves. pelvic lymph nodes
114
Prostate cancer sign/symptoms
Majority asymptomatic Lower urinary tract symptoms: bladder outflow obstruction: hesitancy, poor stream, terminal dribbling, frequency, nocturia, urinary retention or obstruction Hematuria/Haematospermia Bone pain, Anorexia, Weight loss and fatigue ED
115
Prostate cancer diagnosis
``` PSA PR exam Prostate biopsy TMN: T1-4 - Gleason grading system (1-5) ```
116
Prostate cancer management
Organ confined - watchful waiting - active surveillance - Radical prostatectomy - Radical radiotherapy Locally advanced - radiotherapy - watchful waiting - hormonal therapy Metastatic disease - GNRH analogues e.g. Goserelin - Anti-androgens - Steroidal: cyproterone acetate - Non-steroidal: nilutamide and bicalutamide - bilateral subcapsular orchidectomy - maximal androgen blockade Cytotoxic chemotherapy with docetaxel Abiraterone (androgen synthesis inhibitor)
117
Bladder cancer
arise from the endothelial lining (urothelium) - transitional cell carcinoma (papillary 80% and non papillary 20%) - squamous cell carcinomas Urachal
118
Bladder cancer risk factors
- smoking - hair dyes - schistosomiasis -
119
Bladder cancer signs/symptoms
painless haematuria | bladder mass and palpable kidney
120
bladder cancer diagnosis
Cystoscopy and biopsy (transurethral resection of bladder tumour) Urine cytology During a CT urogram Retrograde pyelogram
121
Bladder cancer Mx
Not invading the muscle - Superficial bladder – resected endoscopically with repeated cystoscopic surveillance to detect surveillance to detect recurrence - Transurethral Resection of a Bladder Tumour (TURBT) - Chemo into bladder after surgery (use barrier contraception afterwards) - Weekly treatments for 6 weeks with BCG vaccine squirted into the bladder via catheter, then every six months for 3 years. Muscle-invasive bladder cancer - Radical cystectomy with ileal conduit+/- removal of other pelvic contents - Radiotherapy (as neoadjuvant, primary treatment or palliative) - IV chemotherapy as neoadjuvant or palliative
122
Testicular cancer risk factors
previous TC Cryptorchidism HIV FH
123
Types of TC
``` Seminoma Non-seminomatous - Teratoma - Yolk sac - Choriocarcinoma ```
124
Testicular Cancer signs/symptoms
Asymmetry or slight scrotal discoloration o Hard without flatulence or transillumination, non-tender, irregular mass mostly intratesticular o Assess involvement of epididymis, spermatic cord and scrotal skin. o Secondary hydrocoele o Abdominal mass – advanced disease
125
TC bloods
Alpha-fetoprotein: teratomas and yolk sac Beta-hCG - choriocarcinoma
126
TC mx
Orchidectomy - radicular inguinal orchidectomy - chemo/radio
127
Penile cancer
Squamous cell carcinoma Kaposi sarcoma BCC
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Penile cancer risk factors
``` Age: 5-6 th decade Pre-malignant conditions in 40% cases Phimosis (unable to retract foreskin): Chronic inflammation Geography: Asia, Africa, South America Human Papilloma virus: Types 16 and 18 Smoking Immunocompromised patients ```
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Squamous carcinoma in situ Mx
Circumcision: if prepuce alone (foreskin) Topical 5 fluorouracil
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Invasive Squamous carcinoma Mx
Prepucial lesions: Circumcision Glans lesions - Superficial: Glans resurfacing - Deep: Glansectomy More advanced disease: - Total penile amputation with formation of perineal urethrostomy - Inguinal lymphadenectomy - If involved lymph nodes. Also in high risk penile cancer cases even when not involved.
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Upper Urinary Obstructive Uropathy
Loin to groin/flank pain on affected side (stretching/irritation of ureter and kidney) pain on affected side (stretching/irritation of ureter and kidney) Reduced / no urine output Non-specific symptoms (e.g. vomiting) Reduced renal function on bloods
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Lower Urinary Tract Obstruction (i.e. bladder / urethra)
Acute urinary retention (unable to pass urine and increasingly full bladder) Lower urinary tract symptoms (e.g. poor flow, difficulty initiating urination, terminal dribbling) Reduced renal function on bloods
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Benign Prostatic Hyperplasia
hyperplasia of the stromal and epithelial cells of the prostate
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BPH key questions
Storage - Urgency: If you are watching your favourite TV Programme, and get the feeling of wanting to pass urine, can you delay until the programme is finished? - Frequency: How often do you pass urine from the time you wake up in the morning until the time you go to sleep at night? - Nocturia: How many times, on average are you woken from sleep because you need to pass urine? Voiding - Hesitancy - Poor flow - Intermittency - Straining to void - Terminal dribbling - Incomplete emptying
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Red flags in urinary tract obstruction
- haematuria - bedwetting (high pressure chronic retention) - suprapubic pain - recurrent urinary tract infections - back pain and neurological symptoms
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BPH Ix
``` Urine dipstick PSA Rectal exam IPSSS Serum creatinine Frequency - volume chart USS Cystoscopy ```
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BPH Mx
- Alpha blockers (relax smooth muscle; e.g. tamsulosin 400 mcg once daily) - 5-alpha reductase inhibitors (block testosterone and reduce the size of the prostate; e.g. finasteride) - Anticholinergic (Inhibits bladder smooth muscle contraction) - Beta agonist (Inhibits bladder smooth muscle contraction) Surgery - Transurethral resection of the prostate (TURP)
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Acute Urinary Retention
complication of BPH, prostate cancer and urethral stricture (women: pelvic prolapse, mass or post surgery for stress incontinence) - spontaneous vs precipitated - painful (acute) vs painless (chronic)
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Acute Urinary Retention Ix
FBC, renal functions (usually normal in acute urinary retention) urine dipstick DRE: Prostate and pelvic mass: anal tone & perianal sensation (S2-3): Cauda equina
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Acute Urinary Retention Mx
catheter and record residual volume | treat cause
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Chronic retention signs/symptoms
Painless and may not feel any difficulty: renal impairment in high pressure chronic retention Nocturnal enuresis Sometimes smell slightly like urine due to leakage Tense, palpable bladder, hypertension, and progressive renal impairment associated with bilateral hydronephrosis and hydroureter commonly leading to uraemia and death
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Chronic retention Mx
Admit cathertise , monitor post obstruction diuresis (>200ml/hr for 2 consecutive hours or >3L/24h) Definitive: LTC/ISC/Surgery (after at least 6 weeks)
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Renal stones signs/symptoms
asymptomatic and never cause an issue Renal colic Excruciating loin to groin pain Colicky (fluctuating in severity) as the stone moves and settles May have haematuria, nausea, vomiting and oliguria May have symptoms of sepsis if infection present (i.e. fever)
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Renal stones diagnosis
Urine dipstick: haematuria and infection Bloods: FBC, U&Es, CRP, urate and calcium CT KUB
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Renal stones Mx
``` NSAIDs e.g. PR diclofenac+/- anti-opiate Antiemetic Fluids Antibiotics if infection ``` - No pain, no sepsis or AKI = manage conservatively (watchful waiting and Tamsulosin to aid passage) - Surgical Interventions if stone has not passed in one month and AKI/sepsis/refractory pain: aim to decompress kidney in immediate management Indications to treat urgently: Pain unrelieved, Pyrexia, Persistent nausea/vomiting and High-grade obstruction - Extracorporeal Shock Wave Lithotripsy - Ureteroscopy and Laser Lithotripsy - Percutaneous Nephrolithotomy (under GA in theatre) - Open Surgery
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Testicular torsion signs/symptoms
Acute/sudden onset of unilateral testicular pain - nausea/vomiting - May be referral of pain to lower abdomen - Acutely tender testicle (often difficult to examine due to extent of tenderness) - Firm testicle - Absent cremasteric reflex - Abnormal lie and Horizontal lie - Rotated so that epididymis is not in normal posterior position - Elevated (retracted) testicle - Acute hydrocoele + oedema may obliterate landmarks
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Testicular torsion Mx
Immediate surgical scrotal exploration | - orchiplexy and possible orchiectomy if delayed surgery
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Torsion of appendage
twisting of a vestigial appendage that is located along the testicle. This appendage has no function, yet more than half of all boys are born with one
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Torsion of appendage
very similar to torsion seen early, may have localised tenderness at superior pole and “blue dot” sign Testis should be mobile and cremasteric reflex present
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Paraphimosis
Painful swelling of the foreskin distal to a phimotic ring
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Paraphimosis Mx
Iced glove, granulated sugar for 1-2hrs (facilitates manual reduction – osmotic gradient), multiple punctures in oedematous skin Manual compression of glans with distal traction on oedematous foreskin Dorsal slit (relieve strangulation of the glans)
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Priapism
• Prolonged erection (> 4hrs), often painful and not associated with sexual arousal
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Priapism classification
Ischaemic (Vascular stasis in penis and decreased venous outflow) Non-ischaemic (arterial or high-flow)
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Priapism Mx
Ischaemic - Aspiration +/- irrigation with saline - Injection of alpha-agonist, e.g. phenylephrine 100-200ug every 5-10 mins up to max 1000ug after aspiration: reduce blood flow to penis - Surgical shunt Non-ischaemic - Observe, may resolve spontaneously - Selective arterial embolization with non-permanent materials
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Fournier’s gangrene
necrotizing fasciitis occurring about the male genitalia
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Emphysematous pyelonephritis
acute necrotizing parenchymal and perirenal infection caused by gas-forming uropathogens, usually E coli
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Bladder injury
Commonly associated with pelvic fracture - Suprapubic/abdominal pain + inability to void - Suprapubic tenderness, lower abdominal bruising, guarding/rigidity, diminished bowel sounds
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Bladder injury Mx
Large-bore catheter | Antibiotics
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Urethral injury
Posterior urethral injury often associated with fracture of pubic rami Post. urethra fixed at urogenital diaphragm and puboprostatic ligaments, so bulbomembranous junction most vulnerable
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Penile fracture
Typically happens during intercourse – buckling injury when penis slips out of vagina and strikes pubis
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Complicated UTI
- systemic symptoms (infection goes into the bloodstream) or | - urinary structural abnormality /stones
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Common organisms of UTI
Escherichia coli is the most common cause Klebsiella Proteus: struvite stones – calculi: Produces urease which breaks down urea to form ammonia, which increases urinary pH - precipitation of salts (swarming cultures) Enterococcus: hospital acquired infections Pseudomonas: associated with catheters and instrumentation – needs ciprofloxacin
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UTI diagnosis
>105 - probale UTI <103 - not significant UTI 104 - contamianed? infection? repeat?
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Empirical antibiotic treatment for UTI Female
Nitrofurantoin or trimethoprim orally (3 days)
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Empirical antibiotic treatment for UTI Uncatheterised male UTI
nitrofurantoin or trimethoprim orally (7 days)
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Complicated UTI or pyelonephritis (GP) Mx
com-amox or co-trimoxazole (14 days)
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Complicated UTI or pyelonephritis (Hospital)
Amoxicillin (enterococci) and gentamicin (coliforms) IV for 3 days - (co-trimoxazole and gentamicin if penicillin allergy), stepdown as guided by antibiotic sensitivities
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Abacterial cystitis/Urethral syndrome + Mx
• Pus cells present in urine, but no significant growth on culture - alkalinising urine and stop the thing causing it
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Asymptomatic bacteriuria
Patient is asymptomatic, therefore condition is detected incidentally ``` Significant bacteriuria (>105 orgs/mL) No pus cells in urine ```
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Asymptomatic bacteriuria Mx
treat in pregnancy
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UTI in catheterised patients
Catheterised patients with >105 orgs/mL should ONLY be given antibiotics if there is supporting evidence of UTI (fever, symptoms etc.) Unnecessary antibiotics result in the catheter becoming colonised with increasingly resistant organisms
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Pyelonephritis
Infection in the renal pelvis (join between kidney and ureter) and parenchyma (tissue)
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Pyelonephritis Ix
- Specimen collection – mid stream as first stream most likely to be contaminated - Blood cultures - Urine dipstick - CT scan - USS - DMSA scans
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Pyelonephritis Mx
Broad spectrum: IV amoxicillin + Gentamicin (IV Co-trimoxazole + Gentamicin) adimt, iV fluids, analgesia and antipyretics