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1
Q

BPH
Describe the pathophysiology of Benign prostatic hyperplasia

A

Epithelial and stomal cell increase
Increased A1 adrenoreceptors –> smooth muscle contraction and mass effect of prostate size = obstruction

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2
Q

BPH
Describe the treatment for BPH

A

1st line = Alpha-1-antagonists (A-blockers) e.g. tamulosin
- relaxes smooth muscle in bladder neck & prostate

2nd line = 5-alpha-reductase inhibitors e.g. finasteride
- blocks conversion of testosterone to dihydrotestosterone -> decreases prostate size

TURP = gold standard

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3
Q

BPH
What are the indications in someone with BPH to do a TURP?

A

RUSHES

  • Retention
  • UTI’s
  • Stones (in bladder)
  • Haematuria (refractory to medical therapy)
  • Elevated creatinine
  • Symptom deterioration (despite maximal medical therapy)
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4
Q

PROSTATE CANCER
What can cause prostate cancer?

A
  1. High testosterone levels
  2. Family history - 2/3x increased risk if 1st degree relative is affected
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5
Q

PROSTATE CANCER
What investigations might you do in someone who you suspect has prostate cancer?

A
  • PSA = raised
  • digital rectal exam = asymmetrical, hard, nodular prostate
  • bone profile = hypercalcaemia + raised ALP in metastatic disease
  • liver profile (assess for liver mets)
  • U&Es (assess renal function)
  • multiparametric MRI = first line imaging
  • transrectal ultrasound (TRUS) - guided needle biopsy = gold standard

to consider
- bone scan
- CT abdomen + pelvis/MRI

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6
Q

PROSTATE CANCER
Give 2 advantages and 2 disadvantages of screening in prostate cancer

A

Advantages:

  1. Early diagnosis of localised disease (cure)
  2. Early treatment of advanced disease (effective palliation)

Disadvantages:

  1. Over diagnosis of insignificant disease
  2. Harm caused by investigation/treatment
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7
Q

TESTICULAR CANCER
Name the 2 types of testicular cancers that arise from germ cells

A
  1. Seminoma = most common, slow growing

2. Non-seminoma = yolk sac carcinoma/teratoma, rapid growth

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8
Q

TESTICULAR CANCER
what are the risk factors for testicular cancer?

A
  1. Cryptorchidism (undescended testes)
  2. Family history
  3. previous testicular cancer
  4. HIV
  5. age 20-45
  6. Caucasian
  7. infant hernia
  8. intersex conditions e.g. kleinfelters syndrome
  9. mumps orchitis
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9
Q

TESTICULAR CANCER
what are the clinical features of testicular cancer?

A

SYMPTOMS
- painless testicular lump
- hyperthyroidism
- gynaecomastia
- bone pain (indicates metastasis)
- breathlessness (indicates lung metastasis)

SIGNS
- firm, non-tender testicular mass (does not transluminate, hydrocele may be present)
- supraclavicular lymphadenopathy

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10
Q

TESTICULAR CANCER
What investigations might you do on someone you suspect to have testicular cancer?

A
  • ultrasound testicular doppler = first line
  • tumour markers (beta-HCG, AFP and LDH)

to consider:
- CT chest, abdomen and pelvis (used for staging)

NOTE: fine needle aspiration or needle biopsy must NOT be used due to risk of seeding

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11
Q

HYDROCELE
Name 3 causes of secondary hydrocele

A
  1. Testicular tumours
  2. Infection
  3. Testicular torsion
  4. TB
  5. trauma - is rarer and present in older boys and men
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12
Q

GLOMERULONEPHRITIS
Give 3 consequences of glomerulonephritis

A
  1. Damage to filtration mechanism –> haematuria and proteinuria
  2. Damage to glomerulus restricts blood flow –> hypertension
  3. Loss of usual filtration capacity –> AKI
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13
Q

URINARY STONES
Give 5 potential causes of urinary tract stones

A
  1. Congenital abnormalities - horseshoe kidney, spina bifida
  2. Hypercalcaemia/high urate/high oxalate
  3. Hyperuricaemia
  4. Infection
  5. Trauma
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14
Q

URINARY STONES
what is the most common type of stone?

A
  1. calcium oxalate
  2. uric acid (radiolucent = not visible on xray)
  3. calcium phosphate
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15
Q

URINARY STONES
What investigations might you do on some who you suspect has a urinary tract stone?

A
  • urinalysis = microscopic haematuria +/- pyuria (culture if septic)
  • CRP = elevated
  • U&Es = raised creatinine
  • bone profile + urate = elevated calcium
  • non-contrast CT KUB = GOLD STANDARD, to be performed within 14hrs

to consider
- 24hr urine monitoring
- renal tract USS
- x-ray KUB
- blood cultures
- coagulation profile

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16
Q

URINARY STONES
what is the management for pain?

A

ACUTE
- IV fluids + anti-emetics
- analgesia (NSAID (IM diclofenac), IV paracetamol if NSAID is contraindicated)

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17
Q

URINARY STONES
what is the management of renal stones?

A
  • < 5mm + asymptomatic = watchful wait
  • 5-10mm = shockwave lithotripsy
  • 10-20mm = shockwave lithotripsy or ureteroscopy
  • > 20mm = percutaneous nephrolithotomy
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18
Q

URINARY STONES
what is the management of uretic stones?

A
  • <10mm = shockwave lithotripsy (+/- alpha blockers)
  • 10-20mm = ureteroscopy
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19
Q

URINARY STONES
Give 3 places where urinary tract stones are likely to get stuck

A
  1. Ureteropelvic junction
  2. Pelvic brim
  3. Vesoureteric junction
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20
Q

RENAL PHYSIOLOGY
Give 5 functions of the kidney

A
  1. Filters and secretes waste/excess substances
  2. Blood volume/fluid management (BP control)
  3. Synthesises Erythropoietin
  4. Acid base regulation (reabsorption go Na, Cl, K, glucose, H2O, AA’s)
  5. Converts 1-hydroxyvitamin D –> 1,25-dihydroxyvitamin D (active)
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21
Q

RENAL PHYSIOLOGY
Write an equations for GFR

A

(Um X urine flow rate) / Pm

Um = conc of marker substance in urine
Pm = conc of marker substance in plasma
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22
Q

RENAL PHYSIOLOGY
What is the effect of NSAIDs on the afferent arteriole of glomeruli?

A

NSAIDs inhibit prostaglandins and so lead to afferent arteriole vasoconstriction = reduced GFR

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23
Q

RENAL PHYSIOLOGY
What is the effect of AECi on the efferent arteriole of glomeruli?

A

ACEi cause efferent arteriole vasodilation = reduced GFR

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24
Q

CKD
How is CKD diagnosed?

A
  • eGFR < 60mL/min/1.73m2,
    or:
  • eGFR < 90mL/min/1.73m2 + signs of renal damage,
    or:
  • Albuminuria > 30mg/24hrs (Albumin:Creatinine > 3mg/mmol)
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25
CKD Briefly describe the pathophysiology of CKD
Hyper-filtration for nephrons that work --> glomerular hypertrophy and reduced arteriolar resistance --> raised intraglomerular capillary pressure and strain --> accelerates remnant nephron failure (progressive)
26
DIALYSIS Give 4 potential complications of peritoneal dialysis
1. Infection (peritonitis/catheter exit site infection) 2. Peri-catheter leak 3. Abdominal wall herniation 4. Intestinal perforation
27
RENAL TRANSPLANT Give 3 contraindications for renal transplant
1. ABO incompatibility 2. Active infection 3. Recent malignancy 4. Morbid obesity 5. Age >70 6. AIDS
28
RENAL TRANSPLANT Name 4 potential complications of a kidney transplant
1. Thrombosis 2. Obstruction 3. Infections - URTI, chest 4. Rejection (12% in 1st year)
29
DIURETICS On which part of the nephron do thiazides act?
The distal tubule Act on NCC channels
30
DIURETICS On which part of the nephron do aldosterone antagonists act on?
Collecting ducts
31
AKI what are the pre-renal causes of AKI?
- hypovolaemia (reduced oral intake, haemorrhage, GI loss, renal loss, burns) - reduced cardiac output (heart failure, liver failure, sepsis, drugs) - drugs that reduce BP, circulating volume or renal blood flow (ACEi, ARBs, loop diuretics, aldosterone antagonists)
32
AKI What are the renal (intrinsic) causes of AKI?
- toxins + drugs (antibiotics, contrast, chemotherapy) - vascular (vasculitis, theromboembolism) - tubular (acute tubular necrosis, rhabdomyolysis, myeloma) - interstitial causes (interstitial nephritis, lymphoma infiltration)
33
AKI what are the post-renal causes of AKI?
OBSTRUCTION - renal stones - blocked urinary catheter - enlarged prostate - GU tract tumours - retroperitoneal fibrosis - neurogenic bladder
34
AKI What is the diagnostic criteria for AKI?
1/3 = diagnostic 1. Rise in creatinine >26 mmol/L in 48 hours 2. Rise in creatinine >1.5 x in last 7 days 3. Urine output fall to < 0.5 ml/kg/h for more than 6 hours
35
AKI How can hyperkalaemia be prevented in someone with AKI?
Give calcium gluconate to protect myocardium | Give insulin and dextrose (insulins drives K+ into cells and dextrose is to rebalance the blood sugar)
36
AKI what are the indications for renal replacement therapy?
AEIOU - acidosis (refractory) - electrolyte imbalance (refractory) - ingestion of toxins - oedema/overload - uraemia (refractory)
37
UTI Give 2 reasons why a post-menopausal women is more susceptible to a UTI
1. pH rises --> increased colonisation by colonic flora | 2. Reduced mucus secretion
38
UTI What is the first line treatment for an uncomplicated UTI?
NON-PREGNANT FEMALE - 1st line = NITROFURANTOIN (if eGFR>45) or TRIMETHOPRIM for 3 days - 2nd line = NITROFURANTOIN (if not used 1st line + eGFR>45) or PIVIMECILLINAM or FOSFOMYCIN for 3 days PREGNANT FEMALE - 1st line = NITROFURANTOIN (if eGFR>45 + avoid near term) for 7 days - 2nd line = AMOXICILLIN (only if culture-sensitive) or CEFALEXIN for 7 days CATHETERISED FEMALE - 1st line = NITROFURANTOIN or TRIMETHOPRIM for 7 days MALE - 1st line = TRIMETHOPRIM or NITROFURANTOIN for 7 days - 2nd line = AMOXICILLIN (only if culture sensitive) or CEFALEXIN for 7 days
39
CYSTITIS what are the risk factors for cystitis?
1. Urinary obstruction 2. Previous damage to bladder epithelium 3. Poor bladder emptying 4. bladder stones
40
CYSTITIS What is the treatment for cystitis?
1st line = Trimethoprim or nitrofurantoin (avoid trimethoprim in pregnancy -> teratogenic) 2nd line = ciprofloxacin or Co-amoxiclav
41
PROSTATITIS what are the causes of prostatitis?
acute: - streptococcus faecalis - e.coli (most common) - chlamydia chronic: - bacterial (as above) - non-bacterial - elevated prostatic pressure, pelvic floor myalgia
42
PROSTATITIS How would you treat prostatitis?
1st line - fluoroquinolone antibiotic (CIPROFLOXACIN), alternatives are trimethoprim + ofloxacin - acute = 2-4 weeks - chronic = 12 weeks other treatment - alpha blockers (TAMSULOSIN) - NSAIDs - stool softeners
43
URETHRITIS URETHRITIS what are the causes of urethritis?
- N. gonorrhoea - chlamydia - trauma - urethral stricture - irritation - urinary calculi
44
URETHRITIS what is the treatment for urethritis?
oral doxycycline for 7 days of single dose of azithromycin
45
PYELONEPHRITIS Describe the treatment for pyelonephritis
MILD DISEASE - ORAL ANTIBIOTICS - oral cefalexin - 500mg BD or TDS for 7-10 days - oral ciprofloxacin - 500mg BD for 7 days SEVERE DISEASE - IV ANTIBIOTICS - IV gentamicin (dosage based of body weight + renal function) - IV ciprofloxacin 400mg TDS ADJUNCT THERAPY - hydration = oral or IV - analgesia = PR DICLOFENAC
46
AKI what is the pathophysiology of pre-renal AKI?
- low blood volume or low effective circulating volume causes decreased perfusion - this decreases GFR and creatine clearance which activates RAAS- this increases Na+, urea and BP
47
PROSTATE CANCER what are the risk factors for prostate cancer?
- family history - increasing age - black - genetic - HOXB13, BRCA2
48
TESTICUAR TORSION what are the causes of testicular torsion?
Underlying congenital malformation - belt-clapper deformity - where the testis is not fixed to the scrotum completely, allowing for free movement leading to twisting
49
TESTICULAR TORSION what is the clinical presentation of testicular torsion?
SYMPTOMS - testicular (usually unilateral, sudden onset, excruciating, can be intermittent) - Nausea + vomiting - lower abdominal pain (referred) SIGNS - swollen, high-riding and tender testicle - skin may be erythematous - prehn's negative (pain NOT relieved on lifting ipsilateral testicle) - absent cremasteric reflex
50
HYDROCELE what is communicating hydrocele?
processus vaginalis fails to close, allowing peritoneal fluid to communicate with the scrotal portion
51
EPIDIDYMAL CYST what is the clinical presentation of epididymal cyst?
- soft, round lump - typically at the top of the testicle, posteriorly - may be multiple/bilateral (may be painful) - transluminate (for large cysts, appearing separate from the testicle) - testis is palpable separately from cyst
52
POLYCYSTIC KIDNEY what are the causes of autosomal dominant polycystic kidney disease?
- mutations in PKD1 gene on chromosome 16 = 85% | - mutations in PKD2 gene on chromosome 4
53
POLYCYSTIC KIDNEY what is the treatment for autosomal dominant polycystic kidney disease?
- Treat hypertension – lifestyle, ACEi (ramipril) - Infected – Abx or drain - Surgical – removal (nephrectomy) - Chronic – dialysis or transplant
54
POLYCYSTIC KIDNEY what are the causes of autosomal recessive polycystic kidney disease?
PKHD1 mutation on long arm (q) of chromosome 6
55
CKD how does diabetes cause CKD?
Glycation of glomerular endothelium and efferent arteriole leading to fibrosis (diabetic nephropathy)
56
CKD how does hypertension cause CKD?
thickening of afferent arteriole leading to ischaemia. Further fluid overloading due to activation of RAAS
57
CKD what is stage 1 CKD?
eGFR > 90ml/min
58
CKD what is stage 2 CKD?
eGFR 60-89ml/min
59
CKD what is stage 3a CKD?
eGFR 45-59ml/min
60
CKD what is stage 4 CKD?
eGFR 29-15ml/min
61
CKD what is stage 5 CKD?
eGFR < 15ml/min
62
GOODPASTURES what is goodpastures disease?
Caused by autoantibodies (anti-GBM) to Type 4 collagen in glomerular and alveolar membrane
63
GOODPASTURES what is the clinical presentation of goodpastures disease?
Presents with SOB and oliguria due to respiratory and renal damage
64
GOODPASTURES what are the investigations for goodpasture's disease?
bloods = anti-GBM antibodies biopsy = linear deposits of antibodies along GBM
65
GOODPASTURES what is the management for goodpasture's disease?
plasma exchange steroids cyclophosphamide (for immune suppression)
66
POST STREP GLOMERULONEPHRITIS what are the findings?
Bloods = anti-streptolysin O titres, low complement Biopsy = granular subepithelial immune complex deposits (lumpy bumpy)
67
POST STREP GLOMERULONEPHRITIS what is the management for post strep glomerulonephritis?
Treated with antibiotics to clear the strep, and supportive care.
68
NEPHRITIC VS NEPHROTIC what is the difference between nephritic syndrome vs nephrotic syndrome?
NEPHRITIC - proteinuria + - hypertension - haematuria - very reduced GFR - oedema + NEPHROTIC - proteinuria ++++++ - hypoalbuminaemia - oedema ++++ - slightly reduced/normal GFR - hyperlipidaemia
69
BLADDER CANCER where does bladder cancer spread to?
spreads to the iliac and para-aortic nodes, and to the liver and lungs
70
BLADDER CANCER what are the investigations for bladder cancer?
- urinalysis = haematuria - urinary cytology = cancer cells - FBC = anaemia (in chronic bleeding) - U&Es (assess renal failure) - bone profile = hypercalcaemia + raised ALP with bone mets - LFTs + coagulation screen = deranged in liver mets - flexible cystoscopy = to confirm tumour further staging - CT abdomen + pelvis - CT urogram - Pelvic MRI - PET scan - bone scan
71
BLADDER CANCER what is the management for bladder cancer?
SUPERFICIAL/NON-MUSCLE INVASIVE - trans-urethral resection of bladder tumour with post-op dose of intravesical mitomycin C - low risk = no further treatment - intermediate risk = 6 doses intravesical mitomycin C - high risk = intravesical BCG or radical cystectomy MUSCLE-INVASIVE - radical cystectomy (with neoadjuvant chemo) - will require urostomy - radical radiotherapy (with neoadjuvant chemo) LOCALLY ADVANCED OR METASTATIC - chemotherapy (cis-platin based) - palliative treatment (radiotherapy for symptom control)
72
RENAL PHYSIOLOGY what is the equation for net filtration pressure for the glomerulus?
NFP = GHP - (GCOP + CHP) ``` NFP = net filtration pressure GHP = glomerular hydrostatic pressure GCOP = glomerular colloid oncotic pressure CHP = capsular hydrostatic pressure ```
73
RENAL PHYSIOLOGY which part of the loop of henle is permeable to water?
descending limb
74
RENAL PHYSIOLOGY what is the innervation of the external urinary sphincter?
pudendal nerve S2-S4
75
RENAL PHYSIOLOGY what is the innervation of internal urinary sphincter?
pelvic splanchnic nerve S2-S4
76
RENAL PHYSIOLOGY what is the innervation of the bladder?
``` sympathetic = sympathetic chain T11-L2 parasympathetic = pelvic splanchnic S2-S4 ```
77
RENAL PHYSIOLOGY what is the role of intercalated cells of the collecting duct?
Intercalated cells are responsible for acid/base balance Alpha = acid Beta = basic
78
RENAL PHYSIOLOGY what is the physiology of micturation?
Pontine micturition centre promotes micturition by activating parasympathetic and deactivating sympathetic and somatic motor activity Detrusor muscle contracts and sphincters open
79
CKD what is stage 3b CKD?
eGFR 30-44ml/min
80
DIALYSIS what is the most common causative organism of peritonitis secondary to peritoneal dialysis?
staphylococcus epidermidis s.aureus is another common cause
81
DIALYSIS what is the management of peritonitis secondary to peritoneal dialysis?
vancomycin + ceftazidime added to dialysis fluid OR vancomycin added to dialysis fluid + oral ciprofloxacin
82
EPIDIDYMO-ORCHITIS what is the management?
ANTIBIOTICS - STI related = ceftriaxone 500mg-1g IM single dose + doxycycine 100mg BD for 10-14 days - UTI related = oflaxacin 200mg BD for 14 days or levofoxacin 500mg OD for 10 days SUPPORTIVE CARE - analgesia (paracetamol + NSAIDS) - safety net - referral
83
BLADDER CANCER what are the 2WW referral criteria?
>45 + unexplained visible haematuria without UTI >45 + visible haematuria that persists/recurs after successful treatment of UTI >60 + unexplained microscopic haematuria + dysuria or raised WCC
84
EPIDIDYMAL CYST what conditions are associated with epididymal cysts?
- polycystic kidney disease - cystic fibrosis - von Hippel-Lindau syndrome
85
AKI what are the different stages of AKI?
STAGE 1 - Cr rise to 1.5-1.9 x baseline - Cr rise by 26umol/L - fall in urine to <0.5ml/kg/hr for >6hrs STAGE 2 - Cr rise to 2.0-2.9 x baseline - fall in urine output to 0.5ml/kg/hr for >12 hrs STAGE 3 - Cr rise to >3.0 x baseline - Cr rise to >353.6umol/L - fall in urine to <0.3ml/kg/hr for >24hrs - in patients <18yr, fall in eGFR to <35ml/min/1.73m2
86
RENAL CELL CARCINOMA what are the risk factors?
- increasing age - male - black ethnicity - smoking - obesity - hypertension - end-stage renal failure - Von Hippel-Lindau disease - Tuberous sclerosis
87
RENAL CELL CARCINOMA what is the management?
LOCALISED DISEASE - partial nephrectomy (standard for T1 tumours) - radical nephrectomy (standard for T2-4) +/- lymph node dissection + adenalectomy if involved - minimally invasive procedures (radiofrequency ablation or embolisation) if unfit for surgery METASTATIC DISEASE - molecular therapy (sunitinib or pazopanib) - radiotherapy - cytoreductive surgery
88
RENAL CELL CARCINOMA what are the endocrine associations?
EPO = polycythaemia PTH hormone-related peptide (PTHrP) = hypercalcaemia ACTH = cushings syndrome renin
89
URINARY STONES what are the risk factors?
- dehydration - previous kidney stones - stone-forming foods (chocolate, rhubarb, spinach, tea, most nuts) - genetic - crohns disease - hypercalcaemia - hyperparathyroidism - kidney related disease (polycystic kidney) - drugs (loop diuretics, acetazolamide, protease inhibitors) - gout
90
NEPHRITIC SYNDROME what is the predominant symptom in nephritic syndrome?
haematuria
91
NEPHRITIC SYNDROME what are the causes?
- IgA nephropathy - post-streptococcal GN - anti-GBM antibody disease (goodpastures syndrome) - alport's syndrome - lupus nephritis - granulomatosis with polyangiitis (GPA) - microscopic polyangiitis (MPA) - eosinophilic granulomatosis with polyangiitis (eGPA) - MPGN
92
NEPHRITIC SYNDROME what are the features of IgA nephropathy?
- IgA levels rise secondary to recent (in last 7 days) GI/resp infection - associated with coeliac disease - most common glomerulonephritis worldwide
93
NEPHRITIC SYNDROME what are the findings for IgA nephropathy?
Blood = high IgA titres, normal complement Biopsy = mesangial deposits of IgA complexes
94
NEPHRITIC SYNDROME what is the management of IgA nephropathy?
no proteinuria = no treatment required proteinuria 0.5-1g/day = ACEi failure to respond to treatment = corticosteroids
95
NEPHRITIC SYNDROME what are the features of alport's syndrome?
comprises of triad of ophthalmological issues, auditory issues and nephritic syndrome x-linked dominant inheritance
96
NEPHRITIC SYNDROME what are the findings for Alport's syndrome?
- renal biopsy = gold standard (basket-weave appearance under electron microscope) - genetic testing = mutation in alpha chain of type IV collagen
97
NEPHRITIC SYNDROME what are the findings for lupus nephritis?
- loop wire appearance
98
NEPHRITIC SYNDROME what are the features of granulomatosis with polyangiitis (Wegener's granulomatosis)?
- small vessel vasculitis - affects lungs, nasopharynx and kidneys - saddle nose deformity
99
NEPHRITIC SYNDROME what are the findings for granulomatosis with polyangiitis?
c-ANCA positive renal biopsy = segmental necrotising glomerulonephritis
100
NEPHRITIC SYNDROME what are the features of microscopic polyangiitis?
small vessel vasculitis affects lungs and kidneys
101
NEPHRITIC SYNDROME what are the findings for microscopic polyangiitis?
p-ANCA positive
102
NEPHRITIC SYNDROME what are the features of eosinophilic granulomatosis with polyangiitis (Churg-Strauss syndrome)?
characterised by: - asthma - allergic rhinitis - nasal polyps - eosinophilia - small vessel vasculitis
103
NEPHRITIC SYNDROME what are the findings for eosinophilic granulomatosis with polyangiitis (Churg-Strauss syndrome)?
- p-ANCA positive - eosinophilia
104
NEPHRITIC SYNDROME what are the general clinical features?
SYMPTOMS - pink, red or 'coke' tinged urine (haematuria) - foamy urine (proteinuria) SIGNS - oliguria (urine output <0.5ml/kg/hr) - hypertension - haematuria
105
NEPHROTIC SYNDROME what is the classic triad for nephrotic syndrome?
- proteinuria (>3.5g/day) - hypoalbuminaemia (<30g/L) - leads to severe oedema - hyperlipidaemia
106
NEPHROTIC SYNDROME what is the predominant feature for nephrotic syndrome?
proteinuria
107
NEPHROTIC SYNDROME what are the causes?
- minimal change disease (most common in children) - focal segmental glomerulosclerosis - membranous nephropathy - membranoproliferative GN - diabetes - amyloidosis
108
NEPHROTIC SYNDROME what are the general clinical features?
SYMPTOMS - frothy urine - facial and peripheral oedema - recurrent infections (due to hypogammaglobinaemia) - predisposition to VTE SIGNS - HTN (more common in nephritic) - proteinuria - limited/absent haematuria -
109
NEPHROTIC SYNDROME what are the investigations?
- urinalysis = proteinuria - 24hr urine protein collection = >3.5g protein - urine albumin-creatinine ratio (ACR) = raised - U&Es (to monitor eGFR) - LFTs = hypoalbuminaemia <25m/L - lipid profile = hypercholesterolaemia - renal USS to consider - renal biopsy (light + electron microscopy) - assess for underlying cause
110
NEPHROTIC SYNDROME what is the most common cause in children?
minimal change disease
111
NEPHROTIC SYNDROME what is the most common cause in adults?
focal segmental glomerulosclerosis
112
NEPHROTIC SYNDROME what are the features of minimal change disease?
- most common cause in children - responds excellent to steroids - may be preceded by URTI - associated with hodgkins lymphoma
113
NEPHROTIC SYNDROME what are the findings for minimal change disease?
- light microscopy = normal glomeruli - electron microscopy = effacement of foot processes
114
NEPHROTIC SYNDROME what are the findings for focal segmental glomerulonephritis?
- light microscopy = focal + segmental glomerular sclerosis - electron microscopy = effacement of foot processes
115
NEPHROTIC SYNDROME what are the findings in membranous nephropathy?
- light microsopy = thick glomerular basement membrane - electron microscopy = subepithelial immune complex deposition (spike + dome pattern)
116
NEPHROTIC SYNDROME what are the findings for amyloidosis?
- apple-green birefringence under polarise microscopy with congo red stain
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NEPHROTIC SYNDROME what is the management?
LIFESTYLE - low salt, protein and fat diet - improve CVD risk factors ADJUNCTIVE THERAPIES - diuretics (relief of fluid overload) - ACEi (reduce proteinuria) MINIMAL CHANGE DISEASE - corticosteroids FOCAL SEGMENTAL GLOMERULONEPHRITIS - corticosteroids - ciclosporin if not responsive to steroids MEMBRANOUS NEPHROPATHY - corticosteroids + cyclophosphamide
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RENAL TRANSPLANT FAILURE what is the management of acute graft failure?
may be reversible with steroids and immunosuppressants
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RENAL TUBULAR ACIDOSIS what is it?
a group of conditions that all result in a hyperchloraemic metabolic acidosis with a normal anion gap
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RENAL TUBULAR ACIDOSIS what is the blood results for renal tubular acidosis?
hyperchloraemic metabolic acidosis with normal anion gap
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RENAL TUBULAR ACIDOSIS what are the different types?
- type I (distal) - type II (proximal) - type III (mixed) - type IV (hyperkalaemic)
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RENAL TUBULAR ACIDOSIS what is type I RTA?
- defective H+ secretion in distal tubule - causes hypokalaemia
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RENAL TUBULAR ACIDOSIS what are the causes of type I RTA?
- idiopathic - RA - SLE - Sjogren's - amphotericin B toxicity - analgesic nephropathy
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RENAL TUBULAR ACIDOSIS what are the complications of type I RTA?
nephrocalcinosis renal stones
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RENAL TUBULAR ACIDOSIS what is type II RTA?
- decreased HCO3- reabsorption in proximal tubule - causes hypokalaemia
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RENAL TUBULAR ACIDOSIS what are the causes of type II RTA?
- idiopathic - fanconi syndrome - wilson's disease - cystinosis - outdated tetracyclines - carbonic anhydrase inhibitors (acetazolamide, topiramate)
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RENAL TUBULAR ACIDOSIS what are the complications of type II RTA?
- osteomalacia
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RENAL TUBULAR ACIDOSIS what is type 3 RTA?
- extremely rare - caused by carbonic anhydrase II deficiency - results in hypokalaemia
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RENAL TUBULAR ACIDOSIS what is type IV RTA?
- reduction in aldosterone leads in turn to reduction in proximal tubular ammonium excretion
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RENAL TUBULAR ACIDOSIS what are the causes of type IV RTA?
- hyperaldosteronism - diabetes
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RENAL TUBULAR ACIDOSIS does it cause hypo or hyperkalaemia?
Type 1 = hypokalaemia Type 2 = hypokalaemia Type 3 = hypokalaemia Type 4 = hyperkalaemia
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RENAL TUBULAR ACIDOSIS what is the clinical presentation?
- often asymptomatic - children may present with poor growth or rickets - alkaline urine = recurrent UTIs - osteomalacia (bone pain, # risk + weakness)
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RENAL TUBULAR ACIDOSIS what are the investigations?
- blood gas - urinary pH + electrolytes - ECG - U&Es - bone profile - magnesium - aldosterone + renin - USS KUB
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RENAL TUBULAR ACIDOSIS what is the management?
- stop causative medications - treat electrolyte imbalance - Type 1 + 2 = bicarbonate (or potassium citrate) - type 4 = lifelong mineralocorticoid + glucocorticoid replacement
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ACUTE INTERSTITIAL NEPHRITIS what is it?
A cause of intrinsic AKI where there is acute tubulo-interstitial inflammation It most commonly occurs due to a hypersensitivity reaction to certain medications
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ACUTE INTERSTITIAL NEPHRITIS what are the causes?
MEDICIATIONS - antibiotics (beta-lactams, cephalosporins, fluoroquinolones) - NSAIDs - diuretics - rifampicin - allopurinol - PPIs - ranitidine - warfarin - phenytoin AUTOIMMUNE - Sjogren - SLE - sarcoidosis INFECTIONS
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ACUTE INTERSTITIAL NEPHRITIS what are the clinical features?
- rash (macular or maculopapular + fleeting) - fevers (low grade) - oliguria - flank pain or sensation of fullness - arthralgia - peripheral oedema (esp in NSAIDs) - hypertension - eosinophilia
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ACUTE INTERSTITIAL NEPHRITIS what are the investigations?
URINE - microscopy = pyuria + white cell casts - culture = negative (sterile pyuria) BLOODS - FBC = eosinophilia - U&Es - autoimmune screen IMAGING - renal USS
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ACUTE INTERSTITIAL NEPHRITIS what is the management?
CONSERVATIVE - stop any causative medications - supportive fluid management - refer to specialist renal services MEDICAL - if autoimmune = steroids - fluid overload = furosemide
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ACUTE TUBULAR NECROSIS/INJURY what is it?
the most common cause of intrinsic AKI renal tubular epithelial cells are damaged either due to nephrotoxic agent or ischaemic insult
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ACUTE TUBULAR NECROSIS/INJURY what are the risk factors?
- hypovolaemia - older age - CKD - recent use of nephrotoxic drugs
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ACUTE TUBULAR NECROSIS/INJURY what are the causes?
ISCHAEMIC - hypovolaemia - diarrhoea/vomiting - haemorrhage - dehydration - burns - anaphylaxis - sepsis - surgery NEPHROTOXIC CAUSES - aminoglycosides (e.g. gentamicin) - antifungals (e.g. amphotericin) - chemotherapy - antivirals - NSAIDs - contrast agents - myoglobin - haemoglobin
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ACUTE TUBULAR NECROSIS/INJURY what are the clinical features?
Lethargy and malaise Nausea and vomiting Oliguria or anuria (polyuria may be seen in the recovery phase) Confusion Drowsiness Peripheral oedema
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ACUTE TUBULAR NECROSIS/INJURY what are the investigations?
URINE - dipstick = may be false positive for blood - microscopy = muddy brown granular casts and renal tubular epithelial cells - osmolality = low - urinary sodium = high BLOODs - blood gas - U&Es - urea:creatinine ratio - FBC IMAGING - ECG - USS KUB
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ACUTE TUBULAR NECROSIS/INJURY what is the management?
CONSERVATIVE - identify + treat cause - avoid nephrotoxic meds - fluid balance monitoring MEDICAL - IV fluids - blood if haemorrhage
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CKD how would you manage HTN complication from CKD?
1. ACEi 2. furosemide
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CKD what change in eGFR and creatinine is acceptable when starting ACEi?
- decrease in eGFR up to 25% - rise in creatinine up to 30%
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CKD how would you manage proteinuria in CKD?
1. ACEi 2. SGLT-2
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CKD what level of albumin-creatinine ratio (ACR) would you begin treatment for proteinuria?
if ACR > 30mg/mol + HTN if ACR>70mg/mol even without HTN
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CKD how would you manage CVD in CKD?
statin (+ aspirin)
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CKD what is the management of bones in CKD?
reduce dietary phosphate intake vitamin D can use phosphate binders
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DIFFUSE PROLIFERATIVE GLOMERULONEPHRITIS what is it?
can be nephritic or nephrotic syndrome it is the most common manifestation of lupus nephritis
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DIFFUSE PROLIFERATIVE GLOMERULONEPHRITIS what are the findings?
bloods = anti-dsDNA, ANA biopsy = wire loop capillaries

MY REVISION - ALL TO DO (21 decks)

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