Genitourinary Flashcards
(246 cards)
1
Q
Define nephrolithiasis
A
Renal stones/renal calculi. Stones form in the renal pelvis of the kidney and can travel down the ureters. Majority (80-90%) are calcium oxalate stones (radio-opaque). Other types: calcium phosphate, uric acid (radio-lucent: not seen on x-ray), struvite (produced by bacteria), cystine.
2
Q
Describe the epidemiology of nephrolithiasis
A
Very common. More in men (testosterone > increased oxalate)
3
Q
Describe the aetiology of nephrolithiasis
A
Chronic dehydration, obesity, high protein/salt diet, recurrent UTIs, low urine output, hyperparathyroidism/hypercalcaemia
4
Q
Describe the pathophysiology of nephrolithiasis
A
Excess solute in chronic dehydration causes supersaturated urine which favours crystallisation. Stones cause regular outflow obstruction (hydronephrosis). This leads to dilation and obstruction of renal pelvis. Stones commonly get stuck at pelvo-ureteric junction, vesico-ureteric junction and pelvic brim.
5
Q
What are the key presentations for nephrolithiasis
A
Renal colic = severe colicky unilateral pain originating in loin and radiating to groin. Patient can’t lie still. Haematuria, nausea and vomiting, reduced urine output
6
Q
What is the gold standard investigation for nephrolithiasis
A
Non-contrast CT KUB (kidney, ureter, bladder) – presence of stones. Can only see radio-opaque stones in USS
7
Q
Describe the first line investigations for nephrolithiasis
A
Urine dipstick: haematuria, leukocytes, nitrates. FBC, CRP (infection), U&Es (hypercalcaemia). Abdominal x-ray (will show calcium stones but not uric acid stones as they are radiolucent)
8
Q
Describe the differential diagnosis for nephrolithiasis
A
Peritonitis, appendicitis, UTI
9
Q
Describe the management for nephrolithiasis
A
Symptomatic relief – hydration, NSAIDs (diclofenac). Antiemetics, antibiotics. Watchful waiting – stones under 5mm should pass spontaneously without infection
Elective treatment if too big – Extracorporeal Shock Wave Lithotripsy ESWL (break stone into smaller fragments using shockwaves), ureteroscopy and laser lithotripsy, PCNL (percutaneous nephrolithotomy, use nephoscope to remove stone)
Lifestyle: decrease sodium and protein intake, increase citrus fruit, adequate fluid intake
10
Q
Describe the complications for nephrolithiasis
A
Obstruction (leading to AKI), infection (leading to pyelonephritis)
11
Q
Define acute kidney injury
A
Sudden decline in kidney function determined by increased serum creatinine and decreased urine output. NICE criteria for AKI (KDIGO classification):
Rise in creatinine of >26 micromol/L in 48 hours
Rise in creatinine of >50% from baseline in 7 days
Urine output of <0.5ml/kg/hr for >6 hours
12
Q
Describe the aetiology of acute kidney injury
A
Pre-renal: inadequate blood supply to kidneys – dehydration, hypotension (shock), heart failure
Intra-renal: intrinsic disease in kidney leads to reduced filtration – glomerulonephritis, interstitial nephritis, acute tubular necrosis
Post-renal: obstruction to outflow of urine in kidney causing back pressure and reduced function – obstructive uropathy: kidney stones, cancerous masses, ureter/urethra strictures, enlarged prostate or prostate cancer
13
Q
What are the risk factors for AKI
A
Hypotension, volume depletion, CKD, heart failure, diabetes, cirrhosis, nephrotoxic meds (NSAIDs, ACEi), cancer, trauma
14
Q
Describe the pathophysiology of AKI
A
Pre-renal: low blood volume > decreased perfusion > decreased GFR and creatinine clearance
Intra-renal: kidney damage > decreased oncotic and hydrostatic pressure > decreased GFR
Post-renal: obstruction > back pressure into kidney > decreased hydrostatic pressure > decreased GFR
Decreased GFR leads to build up of normally excreted substances: creatinine, K+ (arrhythmias), urea (confusion, uraemia), fluid (oedema), H+ (acidosis)
15
Q
Describe the key presentations for AKI
A
Reduced urine output, high creatinine, hyperkalaemia (arrhythmias, muscle weakness), uraemia (pericarditis, N+V, encephalopathy), fluid overload (pulmonary and peripheral oedema, hypovolemic shock, orthopnoea), hypotension, sepsis/acute illness
16
Q
Describe the clinical manifestations for AKI
A
Signs: Pre-renal: hypotension, syncope, D+V
Intra-renal: infection, signs of underlying disease
Post-renal: lower urinary tract symptoms (LUTS) – low urine output
Symptoms: Vomiting, nausea, fever, dizziness, altered mental status
17
Q
What is the gold standard investigation for AKI
A
Metabolic profile: U&E (GFR) and creatinine – raised serum creatinine, reduced urine output
18
Q
Describe the first line investigations for AKI
A
NICE criteria for AKI (KDIGO classification):
Rise in creatinine of >26 micromol/L in 48 hours
Rise in creatinine of >50% from baseline in 7 days
Urine output of <0.5ml/kg/hr for >6 hours
Determine cause: urea:creatinine ratio – pre-renal (>100:1), intrarenal (<40:1), post-renal (40-100:1)
Metabolic panel and urine output monitoring: raised serum creatinine, low urine output, raised potassium, metabolic acidosis (raised H+)
Urinalysis: leucocytes and nitrates (infection), proteinuria and haematuria (acute nephritis)
Other: FBC, CRP, renal ultrasound, ECG (hyperkalaemia)
19
Q
Describe the differential diagnosis for AKI
A
Chronic kidney disease, renal stones, tubular necrosis
20
Q
Describe the management for AKI
A
1st line - Treat underlying cause (hypotension, stones, infection). Stop nephrotoxic drugs (NSAIDs, ACEi). Treat complications (electrolyte imbalances).
Severe – renal replacement therapy: haemodialysis (indicated in AFUK: acidosis, fluid overload, uraemia + complications, K+ >6.5)
21
Q
Describe the complications for AKI
A
End-stage renal failure, chronic kidney disease, metabolic acidosis, uraemia > encephalopathy, pericarditis
22
Q
Define bladder cancer
A
Cancer in bladder arising from urothelium. Most common subtype = transitional cell carcinoma. Others = squamous cell carcinoma (schistosomiasis increases likelihood), adenocarcinoma
23
Q
Describe the epidemiology of bladder cancer
A
Old men, people who work in rubber/dye industry
24
Q
Describe the aetiology of bladder cancer
A
Mutation
25
Describe the risk factors for bladder cancer
Exposure to dyes/rubber/leather/textiles/paint (aromatic amines – dye factor worker, hairdresser, painter). Age >65, male, Caucasian, smoking, pelvic radiation
26
What are the key presentations for bladder cancer
Painless haematuria (macro or microscopic), urgency, dysuria, suprapubic/pelvic mass, pelvic pain, recurrent UTI
27
Describe the clinical manifestations for bladder cancer
Signs of metastases: bone pain, weight loss
28
What is the gold standard investigation for bladder cancer
Flexible cystoscopy and biopsy
29
Describe the first line investigations for bladder cancer
urinalysis for microscopy and culture (haematuria), bladder USS
30
Describe the differential diagnosis for bladder cancer
Benign prostatic hyperplasia, UTI, haemorrhagic cystitis
31
Describe the management for bladder cancer
Conservative: cancer support nurse
Medical: chemotherapy, radiotherapy
Surgical: transurethral resection of bladder tumour TURBT, or cystectomy (remove bladder), lymph node dissection if spread
32
Describe the prognosis for bladder cancer
5 year survival rate is 75%
33
Define renal cancer
Renal cell carcinoma is most common type. Adenocarcinoma arising from proximal convoluted tubule
34
Describe the risk factors for renal cancer
Smoking, obesity, hereditary, von Hippel-Lindau
35
What are the key presentations for renal cancer
Triad: Haematuria, flank pain, palpable mass. May have left varicocele
36
Describe the clinical manifestations for renal cancer
Symptoms: Cancer symptoms: weight loss, fatigue, anorexia, night sweats
37
What is the gold standard investigation for renal cancer
CT chest/abdo/pelvis
38
Describe the first line investigations for renal cancer
Abdominal/pelvis ultrasound, bloods: raised RBC, raised calcium, raised LDH
39
Describe the management for renal cancer
1st – nephrectomy/partial nephrectomy
40
Describe the complications for renal cancer
Paraneoplastic changes – polycythaemia, Cushing’s, hypertension, hypercalcaemia
41
Define prostate cancer
Malignant tumour of glandular origin in the prostate. Mostly adenocarcinomas which grow in the peripheral zone of the prostate. Very slow growing.
42
Describe the epidemiology of prostate cancer
Most common cancer in men, most hormone sensitive cancer
43
Describe the aetiology of prostate cancer
Mutation
44
What are the risk factors for prostate cancer
Increasing age, family history, Afro-Caribbean, anabolic steroids
45
Describe the pathophysiology of prostate cancer
Prostate cancer is almost always androgen-dependent, requiring androgen hormones (e.g., testosterone) to grow
46
What are the key presentations for prostate cancer
LUTS – frequency, hesitancy, weak flow, dribbling, nocturia. bone pain, weight loss, fatigue, night sweats
47
Describe the clinical manifestations for prostate cancer
Haematuria, erectile dysfunction, metastases (bone – sclerotic bony lesions, brain, liver, lungs)
48
What is the gold standard investigation for prostate cancer
Transrectal USS and biopsy
49
Describe the first line investigations for prostate cancer
Prostate exam and digital rectal exam (firm, hard, asymmetrical, rough), prostate specific antigen in community (raised), multiparametric MRI
Other: Gleason grading system (based on histology of biopsy. Higher score = worse prognosis)
50
What are the differential diagnosis for prostate cancer
Benign prostatic hyperplasia, chronic prostatitis
51
Describe the management for prostate cancer
Local: prostatectomy (<70), active surveillance (>70 and low risk), external beam radiotherapy, brachytherapy
If metastatic: chemotherapy, radiotherapy, bilateral orchidectomy (gold standard hormonal treatment), androgen deprivation therapy (goserelin – LHRH agonist), palliative treatment to relieve symptoms (e.g., transurethral resection of prostate TURP)
52
Describe the complications for prostate cancer
Metastases (bone, liver, lungs, brain), erectile dysfunction, incontinence
53
Describe the prognosis for prostate cancer
Localised: 100%, metastatic 30%
54
Define testicular cancer
Cancer arising from germ cells in the testes. 90% are germ cell cancers (seminomas, teratomas), rest are non-germ cell cancers (Leydig, Sertoli, lymphoma)
55
Describe the epidemiology of testicular cancer
Young men (15-35)
56
Describe the aetiology of testicular cancer
Mutation
57
What are the risk factors for testicular cancer
Undescended testes (cryptorchidism), male infertility, family history, increased height, HIV
58
What are the key presentations for testicular cancer
Palpable painless lump in testicle which does not transilluminate (light can’t get through)
59
Describe the clinical manifestations for testicular cancer
Haematospermia (blood in semen), gynecomastia
60
What is the gold standard investigation for testicular cancer
Urgent USS (doppler) of testes – testicular mass
61
Describe the first line investigations for testicular cancer
Urgent USS (doppler) of testes, tumour markers (alpha fetoprotein raised in teratomas, beta hCG raised in seminomas and teratomas, lactate dehydrogenase non-specific raised)
Other: Chest x-ray if symptomatic for pulmonary metastases, royal Marsden staging
62
What are the differential diagnosis for testicular cancer
Testicular torsion, epididymo-orchitis, hydrocele
63
Describe the management for testicular cancer
1st line – urgent radical orchidectomy +/- testicular prosthesis
Semen cryopreservation, metastatic – lymph node removal, chemotherapy, radiotherapy
64
What are the complications for testicular cancer
Infertility, hypogonadism, peripheral neuropathy
65
Describe the prognosis for testicular cancer
98% 5 year survival rate
66
Define chronic kidney disease
Chronic reduction in kidney function which is permanent and progressive. >3 months.
Diagnosis: eGFR < 60mL/min/1.73m¬2 or,
eGFR <90mL/min/1.73m2 + signs of renal damage (protein/haematuria, pathology on imaging/biopsy) or,
albuminuria > 30mg/24hrs (albumin:creatinine >3mg/mmol)
67
Describe the aetiology of chronic kidney disease
Diabetes, hypertension, glomerulonephritis, polycystic kidney disease, nephrotoxic drugs (NSAIDs, ACEi), persistent pyelonephritis, obstruction
68
What are the risk factors for chronic kidney disease
Diabetes, hypertension, male, increasing age, smoking
69
Describe the pathophysiology of chronic kidney disease
Many nephrons are damaged causing decreased GFR when increases burden on remaining nephrons. Compensatory RAAS to increase GFR but trans-glomerular pressure is shearing, and a loss of basement membrane permeability causes protein/haematuria.
70
What are the key presentations for chronic kidney disease
Asymptomatic until end-stage (remaining nephrons still work for a while). Symptoms due to substance accumulation: uraemia (pruritis, nausea, uraemic frost, restless legs, encephalopathy, pericarditis), fluid (oedema, raised JVP), potassium (arrhythmias, muscles weakness), oliguria (low urine output), peripheral neuropathy
71
Describe the clinical manifestations for chronic kidney disease
Signs: Haematuria, proteinuria, peripheral neuropathy, hypertension, oedema
Symptoms: Pruritis, loss of appetite, nausea, muscles cramps, pallor, fatigue
72
What is the gold standard investigation for chronic kidney disease
U&E for estimated GFR (eGFR < 60mL/min/1.73m¬2 or, eGFR <90mL/min/1.73m2 + signs of renal damage)
73
Describe the first line investigations for chronic kidney disease
FBC (anaemia of CKD), U&E (raised creatinine, phosphate, potassium. Decreased eGFR), urinalysis (haematuria, proteinuria), raised urine albumin (albumin:creatinine >3mg/mmol), renal USS (bilateral renal atrophy)
Other: GFR function staging. 1: eGFR>90. 2: 60-89, 3a: 45-59, 3b: 30-44, 4: 15-29, 5: <15 (ESRF)
74
What are the differential diagnosis for chronic kidney disease
Diabetic neuropathy, nephrotic syndrome, obstructive uropathy
75
Describe the management for chronic kidney disease
Refer to specialist if eGFR <30, albumin:creatinine ratio >70.
Slow progression and prevent CVD (obesity, hypertension – ACEi, ARB, CCB, diabetes - metformin, diet, statin). Treat complications: anaemia (ferrous sulphate, erythropoietin), oedema (fluid restriction, diuretics), metabolic acidosis (sodium bicarbonate), CKD-mineral bone disease (vitamin D), CVD (statins).
End-stage: renal replacement therapy (eGFR <15) dialysis. Eventually kidney transplant = cure.
76
Describe the complications for chronic kidney disease
Anaemia, CKD-mineral bone disease, neuropathy, encephalopathy, cardiovascular disease
77
Define benign prostatic hyperplasia
Hyperplasia of the stromal and epithelial cells of the prostate causing prostate enlargement which partially blocks the urethra.
78
Describe the aetiology of BPH
Age related hormonal changes
79
What are the risk factors for BPH
Ageing men, smoking, non-Asian race, raised testosterone, family history, castration is protective
80
Describe the pathophysiology of BPH
Inner transitional zone of prostate proliferates and narrows urethra
81
What are the key presentations for BPH
LUTS: Storage - frequency, urgency, incontinence, nocturia. Voiding – dysuria, poor/intermittent stream, dribbling, straining, incomplete emptying, hesitancy
82
What is the gold standard investigation for BPH
Digital rectal exam (smooth, symmetrical but enlarged prostate)
83
Describe the first line investigations for BPH
Digital rectal exam (smooth but enlarged prostate), prostate-specific antigen (raised), urinary frequency volume chart, urine dipstick (rule out infection)
Other: International prostate symptom score
84
What are the differential diagnosis for BPH
Prostate cancer, urinary tract infection, prostatitis
85
Describe the management for BPH
1st line – alpha blockers, e.g., tamsulosin (relaxes smooth muscle in bladder neck and prostate).
2nd line – 5-alpha reductase inhibitors, e.g., finasteride (blocks conversion of testosterone to dihydrotestosterone which decreases prostate size)
Lifestyle – reduce caffeine/alcohol intake
If no response to meds = transurethral resection of prostate (TURP – gold standard)
86
What are the complications for BPH
Postural hypotension (tamsulosin), sexual dysfunction (reduced testosterone from finasteride), retrograde ejaculation from TURP, UTI
87
Describe the epidemiology of pyelonephritis
Females
87
Define pyelonephritis
Upper urinary tract infection. Inflammation of the kidney renal pelvis caused by bacterial infection. Most acquired by ascending transurethral spread. Mostly caused by EPEC – enteropathogenic E. Coli
88
Describe the aetiology of pyelonephritis
KEEPS infection: klebsiella, enterococcus, E. coli (most common), proteus, s. saprophyticus
89
What are the risk factors for pyelonephritis
Female (shorter urethra, urethra near anus), urinary stasis (BPH, stones, cancer), vesicoureteral reflux, instrumentation (catheter)
90
Describe the pathophysiology for pyelonephritis
Pyelonephritis is a complicated UTI as the infection spreads beyond the bladder and urethra to the kidneys and causes damage. Lower UTIs are uncomplicated.
91
What are the key presentations for pyelonephritis
Triad of loin pain, fever and pyuria (urine WBC). Nausea and vomiting. Urgency, frequency, dysuria, suprapubic pain.
92
Describe the clinical manifestations for pyelonephritis
Symptoms: Back pain, headache, nausea and vomiting
93
What is the gold standard investigation for pyelonephritis
Mid-stream urine microscopy and cultures (confirm UTI and identify pathogen)
94
Describe the first line investigations for pyelonephritis
1st line: Urine dipstick (leucocytes, nitrites, maybe haematuria), FBC (raised WCC, CRP)
Other: urgent USS to detect stones, obstruction, incomplete emptying
95
What are the differential diagnosis for pyelonephritis
Lower urinary tract infection, cystitis, prostatitis
96
Describe the management for pyelonephritis
1st line – analgesia, antibiotics (ciprofloxacin, co-amoxiclav)
97
Describe the complications for pyelonephritis
Renal failure, need for catheterisation, renal parenchyma scarring
98
Define cystitis
Lower urinary tract infection causing inflammation of the bladder due to infection, most commonly by enteropathogenic E. coli.
99
Describe the epidemiology of cystitis
Females (shorter urethra, urethra close to bladder).
100
Describe the aetiology of cystitis
KEEPS infection: Klebsiella, enterococci, E. coli, proteus, s. saprophyticus
101
What are the risk factors for cystitis
Female (shorter urethra, urethra near anus), urinary stasis (BPH, stones, cancer), frequent sexual intercourse, instrumentation (catheter), bladder lining damage
102
What are the key presentations for cystitis
Suprapubic pain, dysuria, frequency, urgency, haematuria and polyuria, confusion in elderly
103
What are the gold standard investigations for cystitis
Mid-stream urine microscopy and cultures (confirm UTI and identify pathogen)
104
Describe the first line investigations for cystitis
Urine dipstick (leucocytes, nitrites, blood)
105
What are the differential diagnosis for cystitis
Upper urinary tract infection (pyelonephritis), urethritis, cervicitis
106
Describe the management for cystitis
1st line – trimethoprim/nitrofurantoin (3-day course for women, 7 days for men/women with complications)
In pregnancy, trimethoprim can’t be used in 1st trimester (inhibits folate synthesis), nitrofurantoin can’t be used in 3rd trimester (amoxicillin, cefalexin used instead)
107
Describe the complications for cystitis
Renal infection, sepsis
108
Define prostatitis
Lower urinary tract infection caused by inflammation of the prostate. Usually caused by E. coli
109
Describe the aetiology of prostatitis
KEEPS infection: klebsiella, enterococci, e. coli (mc), proteus, s. saprophyticus
110
What are the risk factors for prostatitis
Benign prostatic enlargement, urinary tract obstruction (stones), catheter, immunosuppression
111
What are the key presentations for prostatitis
LUTS – dysuria, frequency, urgency, diminished stream. Fever, chills, malaise. Pelvic pain (suprapubic, perineum, genitalia). Tender and enlarged prostate
112
Describe the clinical manifestations for prostatitis
Sexual dysfunction, pain with bowel movements
113
What are the gold standard investigations for prostatitis
Mid-stream urine microscopy and cultures (confirm UTI and identify pathogen)
114
Describe the first line investigations for prostatitis
Urine dipstick (leucocytes, nitrites)
115
What are the differential diagnosis for prostatitis
Benign prostatic hyperplasia, prostate cancer, UTI
116
Describe the management for prostatitis
1st line – levofloxacin, ofloxacin or trimethoprim. Also analgesia (NSAIDs)
Signs of sepsis – piperacillin/tazobactam, cephalosporins
117
What are the complications for prostatitis
Sepsis, urinary retention, prostate abscess, chronic prostatitis
118
Define urethritis
Lower urinary tract infection causing inflammation of the urethra. Usually a sexually acquired condition through chlamydia trachomatis (mc) or Neisseria gonorrhoea (lc)
119
Describe the aetiology of urethritis
Non-gonococcal (chlamydia trachomatis) > gonococcal. Also, trauma, urethral stricture, urinary stones.Neisseria gonorrhea
120
What are the risk factors for urethritis
Unprotected sex, MSM, female (shorter urethra, urethra close to anus)
121
What are the key presentations for urethritis
Urethral discharge (blood/pus), dysuria, urethral pain, penile pain/itching
122
What is the gold standard investigation for urethritis
urethral discharge gram stain (raised polymorphonuclear leucocytes confirms urethritis, presence of gram neg cocci = gonorrhoea)
123
Describe the first line investigations for urethritis
1st line urine dipstick (leucocytes), Mid-stream urine microscopy and culture (detect pathogen), Nucleic acid amplification test – detect STI (chlamydia/gonorrhoea)
124
What are the differential diagnosis for urethritis
Urinary tract infection, vaginitis, prostatitis
125
Describe the management for urethritis
Neisseria gonorrhoea = 1g IM ceftriaxone +1g azithromycin
Chlamydia trichomatis = 100mg doxycycline or azithromycin
126
What are the complications for urethritis
Reactive arthritis = triad of conjunctivitis, urethritis, and arthritis (can’t see, can’t pee, can’t climb a tree)
127
Define nephritic syndrome (glumerulonephritis)
A group of glomerulonephritic pathologies that cause inflammation of the kidneys causing both haematuria and proteinuria. increased permeability of glomeruli allows movement of RBCs into filtrate. Key features of nephrotic syndrome: haematuria (5 RBC/uL), proteinuria (1 – 3.5g/day, less than nephrotic syndrome), hypertension
128
Describe the aetiology of nephritic syndrome
IgA nephropathy (Berger’s disease)
Systemic lupus erythematous nephropathy
Post-streptococcal glomerulonephritis
Goodpasture’s syndrome (rapidly progressing glomerulonephritis)
Haemolytic uraemic syndrome
Other: Henoch-Schoenlein purpura, Wegener’s vasculitis, eosinophilic granulomatosis with polyangiitis
129
Describe the pathophysiology of nephritic syndrome
Inflammation > reactive tissue proliferation > break in glomerular basement membrane > crescent formation.
Some nephritic syndromes are associated with anti-glomerular basement membrane antibodies which attack the basement membrane (e.g., Goodpasture’s syndrome)
130
What are the key presentations for nephritic syndrome
Visible haematuria, proteinuria, hypertension, oedema (peripheral, pulmonary), oliguria (low urine output), uraemic signs
131
Describe the clinical manifestations for nephritic syndrome
IgA nephropathy: visible haematuria, 1-2 days after viral infection
Post-strep GN: visible haematuria, 2 weeks after strep infection
Rapidly progressing GN (Goodpasture’s, Wegener’s): Fatigue, SOB, cough, haemoptysis, acute kidney failure.
132
What are the first line investigations for nephritic syndrome
1st line: Urinalysis and microscopy (haematuria, proteinuria, dysmorphic RBCs), 24hr urine protein collection, bloods (anaemia, elevated liver enzymes, elevated creatinine)
Serology: anti-GBM (Goodpasture’s), anti-double-stranded DNA (SLE), antinuclear antibody (SLE), ANCA (Wegener’s vasculitis)
IgA: microscopy shows IgA complex deposition
Rapidly progressive GN: microscopy shows crescentic glomerulonephritis
133
What is the gold standard investigation for nephritic syndrome
Renal biopsy (crescent shaped glomeruli, Ig deposits, glomerulosclerosis)
134
Describe the differential diagnosis for nephritic syndrome
Nephrolithiasis, renal cancer, bladder cancer
135
Describe the management for nephritic syndrome
General: hypertension control, proteinuria (ACEi/ARB, loop diuretics, prednisolone), immunosuppression
Specific: Post-streptococcal GN (penicillin), Goodpasture’s (plasmapheresis, corticosteroid immunosuppression), SLE (immunosuppression – rituximab, cyclophosphamide)
136
What are the complications for nephritic syndrome
Acute kidney injury, hypertension, cardiovascular disease, hypercholesterolaemia
137
Define nephrotic syndrome
A group of conditions which cause the glomerular basement membrane to become permeable to protein. It is characterised by: proteinuria, peripheral oedema, hypoalbuminemia, hypercholesteremia.
138
Describe the aetiology of nephrotic syndrome
Primary causes:
* Minimal change disease: KIDS most common. Unclear cause – immune mediated
* Membranous glomerulonephritis: ADULTS. Cause – Abs against SLE, NSAIDs, hepatitis
* Focal segmental glomerulosclerosis: ADULTS most common. Causes – HIV, sickle cell
Secondary causes: diabetic nephropathy
139
Describe the pathophysiology of nephrotic syndrome
Inflammation > damage to podocytes > protein leakage > proteinuria. increased liver activity aiming to increase albumin > consequential increase in cholesterol and clotting factors. Reduced oncotic pressure causes oedema and blood volume loss, which activates the RAAS system.
140
What are the key presentations for nephrotic syndrome
Proteinuria (>3.5g/24hrs): frothy urine, infection. Hypoalbuminemia (<30g/L). Peripheral oedema. Hypercholesterolaemia (xanthelasma – eyes, xanthomata – joints). Haematuria
141
Describe the clinical manifestations for nephrotic syndrome
Signs: Hypercoagulable state, hypogammaglobulinemia, hypertension, thrombosis, hyperlipidaemia
Symptoms: Fatigue, dyspnoea
142
What is the gold standard investigation for nephrotic syndrome
Needle biopsy and microscopy (glomeruli changes – light, fluorescent, electron MS)
Minimal change disease: no change on LM/FM. Podocyte loss (effacement) on EM
Membranous glomerulonephritis: mesangial expansion, capillary wall thickening on LM, IgG and complement 3 deposition spike appearance on FM, GBM thickening on EM
Focal segmental glomerulosclerosis: sclerosis on LM, nothing on FM, GBM thickening on EM
143
Describe the first line investigations for nephrotic syndrome
1st line Bloods: U&E, FBC, CRP, LFT. Mid-stream urinalysis and urine dipstick (proteinuria/haematuria, infection). Kidney USS.
144
What are the differential diagnosis for nephrotic syndrome
Minimal change disease, membranous glomerulonephritis, focal segmental glomerulosclerosis, diabetic nephropathy, nephritic syndrome causes
145
Describe the management for nephrotic syndrome
Treat underlying cause – 12 weeks corticosteroids (prednisolone)
Treat complications – oedema (low salt and protein intake, diuretics), hyperlipidaemia (statins), hypercoagulable state (anticoagulants), infection (antibiotics)
146
Describe the complications for nephrotic syndrome
Chronic kidney disease, end-stage liver failure, hypovolaemia, thrombosis, infection
147
Define polycystic kidney disease
Inherited disease where multiple fluid-filled cysts form within the kidneys. Two types – autosomal dominant (mc) and autosomal recessive
148
Describe the aetiology of polycystic kidney disease
Autosomal dominant: PKD-1 chromosome 16 (85%). PKD-2 chromosome 4 (15%)
Autosomal recessive: gene on chromosome 6
149
What are the risk factors for polycystic disease
Family history of PKD or cerebrovascular events
150
Describe the pathophysiology of polycystic kidney disease
Cysts develop and grow over time into the tubular portion of the nephron. Compression of renal architecture and vasculature. Progressive impairment – gets bigger and worse with age
151
What are the key presentations for polycystic kidney disease
Painless haematuria. Hypertension, bilateral abdominal/flank pain, headaches, LUTS (dysuria, urgency, pain), palpable kidneys
152
Describe the clinical manifestations for polycystic kidney disease
Signs: Extra-renal manifestations: cerebral aneurysms (berry), hepatic splenic pancreatic ovarian and prostatic cysts, cardiac murmur, abdominal hernia, hepatomegaly
153
What is the gold standard investigation for polycystic kidney disease
Kidney ultrasound (enlarged bilateral kidneys with multiple cysts). Age 15-39 (at least 3 cysts unilateral or bilateral), 40-59 (at least 2 in each kidney), 60+ (at least 4 in each kidney)
154
Describe the further investigations for polycystic kidney disease
Genetic testing, urinalysis (albuminuria, haematuria, proteinuria, bacteriuria)
155
What are the differential diagnosis for polycystic kidney disease
Acquired renal cystic disease, tuberous sclerosis, von Hippel-Lindau
156
Describe the management for polycystic kidney disease
Tolvaptan (ADH receptor antagonist) to slow development of cysts and progression of renal failure.
Supportive: antihypertensives, antibiotics if infected, drainage of cysts, analgesic for renal colic, surgical removal of cysts, dialysis or transplant for ESRF
157
Describe the complications for polycystic kidney disease
Berry aneurysm rupture > subarachnoid haemorrhage, cysts on other organs, left ventricular hypertrophy, end-stage renal failure, cardiovascular disease
158
Define epididymal cyst
Smooth extra testicular cyst at the top of the testicle (epididymis). Contains clear and milky fluid
159
Describe the epidemiology for epididymal cysts
Middle-aged men
160
What are the key presentations for epididymal cysts
Contains clear and milky fluid, pain, transilluminates (fluid filled), soft round lump at top of testicle, palpated separate to testicle
161
What is the gold standard investigation for epididymal cyst
USS scrotum
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What are the differential diagnosis for epididymal cysts
Hydrocele, variocele, testicular cancer
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Describe the management for epididymal cysts
No treatment. Surgical removal if causing pain
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Define hydrocele
Abnormal collection of fluid in the tunica vaginalis which surrounds the testis.
Simple: overproduction of fluid
Communicating: peritoneal fluid and scrotum are connected
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Describe the aetiology of hydrocele
Idiopathic or secondary to: testicular torsion, testicular cancer, epididymo-orchitis, trauma
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What are the key presentations for hydrocele
Non-tender smooth scrotal swelling. Painless unless infected. Transilluminates. No bowel sounds (not a hernia)
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What is the gold standard investigation for hydrocele
Clinical diagnosis, USS scrotum
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What are the differential diagnosis for hydrocele
Testicular cancer, variocele, inguinal hernia
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Describe the mangement for hydrocele
Observation or surgery/aspiration for larger symptomatic hydroceles
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Define variocele
Abnormal dilation of testicular veins in pampiniform venous plexus
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Describe the aetiology for variocele
Increased resistance in testicular vein, incompetent valves in testicular vein causing reflux
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Describe the pathophysiology for variocele
Left side more commonly affected due to the angle that the left testicular vein enters the left renal vein. Varicocele can cause infertility because it disrupts the temperature in the testicles for producing sperm. Pampiniform plexus regulates temperature of blood entering testes by absorbing heat from testicular artery
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What are the key presentations for variocele
Scrotal mass that feels like a bag of worms, dragging, heaviness of scrotum, throbbing/dull pain, worse on standing
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Describe the first line investigations for variocele
Clinical diagnosis
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Describe the further investigations for variocele
USS with doppler, semen analysis for fertility, hormone tests for testicular function
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What are the differential diagnosis for variocele
Testicular mass, hydrocele, inguinal hernia
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Describe the management for variocele
1st line – observation or surgical repair if there is pain, infertility, or atrophy
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What are the complications for variocele
Infertility, testicular atrophy
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Define testicular torsion
Twisting of the spermatic cord with rotation of the testis. Urological emergency.
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Describe the epidemiology for testicular torsion
Teenage boy
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What are the risk factors for testicular torsion
Bell clapper deformity (horizontal lie of testicles)
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Describe the pathophysiology for testicular torsion
Torsion causes occlusion of testicular artery which leads to ischaemia, necrosis, gangrene
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What are the key presentations for testicular torsion
Severe unilateral testicular pain, hurts to walk, cremasteric reflex lost – stroke inner thigh, ipsilateral testicle should retract upwards. No pain relief with elevating testis (-ve prehn sign). Firm, swollen testicle
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Describe the clinical manifestations for testicular torsion
Symptoms: Abdominal pain, nausea and vomiting
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What is the gold standard investigation for testicular torsion
Scrotal ultrasound (whirlpool sign – spiral appearance of spermatic cord and blood vessels)
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What are the differential diagnosis for testicular torsion
Testicular appendage torsion (twisting of testicular appendage – small tissue above testicle. Pain superior on testicle. No N+V. blue dot sign). Varicocele, hydrocele, testicular cancer
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Describe the first line investigations for testicular torsion
Immediate surgical exploration if there is increased risk
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Describe the management for testicular torsion
1st line – urgent surgery: surgical exploration of scrotum, orchiopexy (correcting the position of testicles), orchidectomy (removing the testicle) if surgery is delayed or if there is necrosis
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Describe the complications for testicular torsion
Ischaemia, necrosis, sub/infertility, loss of testicle
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Define obstructive uropathy
Blockage of urinary flow. Can affect one or both kidneys depending on level of obstruction. If only one kidney is blocked, urine output may remain normal with normal serum creatinine. When kidney function is affected, this is obstructive uropathy.
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Describe the aetiology for obstructive uropathy
Renal stones, benign prostatic hypertrophy
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Describe the pathophysiology for obstructive uropathy
Obstruction leads to urinary retention which increases kidney, ureter, or bladder pressure. Refluxing of urine into the renal pelvis causes hydronephrosis – dilation or renal pelvis, which is more infection prone
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What are the key presentations for obstructive uropathy
Obstruction! Flank pain, fever, lower urinary tract symptoms (LUTS) – slowed/intermittent stream, straining to pee, frequency, bladder never feels empty. May be asymptomatic if only one kidney affected.
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Describe the first line investigations for obstructive uropathy
Urinary dipstick, renal USS, urea and creatinine, FBC
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Describe the management for obstructive uropathy
1st line – relieving pressure on kidneys: urethral catheter, ureteric stent, nephrostomy tube.
Treat underling cause: renal stones, benign prostatic hypertrophy. Treat infection
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Define Von Hippel-Lindau
Von Hippel Lindau disease is a rare autosomal dominant disorder characterised by a mutation in a tumour suppressor gene which leads to the formation of cysts and benign tumours in various parts of the body like the eye, CNS, kidneys, adrenal glands and pancreas
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Describe the clinical manifestations for Von Hippel-Lindau
Depends on lesion:
- Refer to RCC for RCC symptoms
- Sympathetic symptoms e.g. headaches, sweating, palpitations, hypertension if paragangliomas present
- Deafness if cystadenomas in ear
- Blindness with haemangioblastomas affecting the eye
- Ataxia (loss of balance) if haemangioblastoma is in cerebellum
- Headaches, nausea and vomiting if haemangioblastoma blocks flow of CSF
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Describe the management for Von Hippel-Lindau
Depends on lesion type
e.g. surgical removal for RCC or laser treatment for haemangioblastomas in the eye
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Define incontinence
Urinary incontinence is a problem where the process of urination, also called micturition, happens involuntarily. There are 2 types of incontinence, urge and stress.
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Define urge continence
Overactive bladder due to uninhibited detrusor muscle
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Define stress incontinence
Urine leaks out due to high abdominal pressure
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Describe the risk factors for incontinence
- **Increased age**
- **Postmenopausal status**
- **Obesity**
- **Pregnancy**
- **Vaginal delivery**
- **Prostate surgery**
- **Pelvic floor surgery**
- **Pelvic organ prolapse**
- **Neurological conditions, such as multiple sclerosis**
- **Cognitive impairment and dementia**
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Describe the management for incontinence
Lifestyle changes such as losing weight and cutting down on caffeine and alcohol. Pelvic floor exercises, where you strengthen your pelvic floor muscles by squeezing them. Bladder training, where you learn ways to wait longer between needing to urinate and passing urine.
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Define chlamydia
Sexually transmitted infection caused by chlamydia trachomatis - gram negative bacteria. Most common STI in UK
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Describe the pathophysiology for chlamydia
Intracellular organism - enters and replicates in cells before rupturing the cell and spreading to others.
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Describe the risk factors for chlamydia
Young, sexually active, having multiple partners, unprotected sex
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Describe the aetiology of chlamydia
Chlamydia trachomatis
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What are the key presentations for chlamydia
Asymptomatic.
Women: abnormal vaginal discharge (yellow, cloudy), vaginal bleeding, cervical inflammation, painful sex and urination
Men: penis discharge, painful urination
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What is the gold standard investigation for chlamydia
Nucleic acid amplification test (NAAT) – swabs check directly for DNA or RNA of organism (swabs: endocervical, vulvovaginal, first-catch urine sample, urethral in men)
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Describe the management for chlamydia
1st line – doxycycline 100mg twice a day for 7 days. Doxycycline contraindicated in pregnancy and breastfeeding, instead use: clarithromycin, azithromycin, amoxicillin
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Describe the complications for chlamydia
Infertility, pelvic inflammatory disease, ectopic pregnancy
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Define epididymo-orchitis (UTI)
Lower urinary tract infection caused by inflammation of the epididymis and testicles. Usually caused by sexually transmitted organisms (gonorrhoea, chlamydia) or by enteric pathogens (E. coli)
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Describe the epidemiology of epididymo-orchitis (UTI)
STI in < 35, E.coli in>35
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Describe the aetiology for UTIs
E.coli, Neisseria gonorrhoea, chlamydia trachomatis, mumps
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Describe the risk factors for UTIs
Unprotected sex, bladder outflow obstruction (stones, BPH), catheter
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What are the key presentations for epididymo-orchitis (UTI)
Gradual onset unilateral scrotal pain and swelling, pain relieved with elevated testis (Prehn’s sign), dragging heavy sensation
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Describe the clinical manifestations for UTIs
Signs: Cremaster reflex intact, urethral discharge, fever, tenderness
Symptoms: Dysuria, frequency, urgency
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What is the gold standard investigation for UTIs
NAAT testing, urine microscopy and cultures
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Describe the first line investigations for UTIs
1st line: Urine dipstick (leucocytes, nitrites, blood)
Other: USS to rule out testicular torsion
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What are the differential diagnosis for epididymo-orchitis
Testicular torsion, infected hydrocele, testicular tumour
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Describe the management for epididymo-orchitis
Neisseria gonorrhoea = 1g IM ceftriaxone +1g azithromycin
Chlamydia trichomatis = 100mg doxycycline or azithromycin
E. coli = 500mg levofloxacin
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Describe the complications for epididymo-orchitis
Chronic pain, infertility, testicular atrophy
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Define gonorrhoea
Sexually transmitted infection caused by Neisseria gonorrhoea – gram negative diplococcus
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Describe the aetiology for gonorrhoea
Neisseria gonorrhoea
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Describe the risk factors for gonorrhoea
Young, sexually active, having multiple partners, unprotected sex
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Describe the pathophysiology for gonorrhoea
Gram negative diplococcus which infects mucous membranes with a columnar epithelium, e.g., endocervix, urethra, rectum, conjunctiva and pharynx. Spreads via contact with mucous secretions from infected areas.
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What are the key presentations for gonorrhoea
Women: odourless purulent discharge (green/yellow), painful urination, pelvic pain
Men: odourless purulent discharge (green/yellow), painful urination, testicular pain or swelling (epididymo-orchitis)
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What is the gold standard investigation for gonorrhoea
Nucleic acid amplification test (NAAT) – checks for RNA or DNA of organism. Swabs: endocervical, vulvovaginal, first-catch urine, urethral (men)
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Describe the first line investigations for gonorrhoea
Charcoal swab for microscopy, culture and antibiotic sensitivities
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Describe the management for gonorrhoea
1st line – IM ceftriaxone (cephalosporin) 1g if sensitivities are not known. Oral ciprofloxacin 500mg if sensitivities are known.
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Describe the complications for gonorrhoea
Pelvic inflammatory disease, infertility, ectopic pregnancy, disseminated gonococcal infection (spread to skin and joints)
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Define LUTS
LUTS: array of symptoms found in conditions affecting the quality and control of micturition.
Incontinence: loss of control of urination. Stress incontinence – weakness of pelvic floor and sphincter muscles allowing urine to leak when increased pressure on the bladder, e.g., cough, laugh. Urge incontinence – overactivity of detrusor muscle, feeling constant urge to pee.
Retention: inability to pass urine even with a full bladder, due to obstruction of outflow. Chronic urinary retention leads to overflow of urine and incontinence occurs without the urge to pass urinate. Also known as overflow incontinence
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Describe the epidemiology of incontinence and retention
Incontinence – women. Retention - men
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Describe the aetiology of incontinence and retention
Incontinence: previous pregnancy and vaginal delivery, pelvic organ prolapse, pelvic floor surgery, neurological conditions (multiple sclerosis), cognitive impairment/dementia, increasing age, BMI
Retention: obstruction – kidney stones, benign prostatic hyperplasia, neurological conditions (MS, diabetic neuropathy, spinal cord injury)
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What are the key presentations for LUTS
Lower urinary tract symptoms:
* Storage: frequency, urgency, nocturia, incontinence
* Voiding: poor stream, hesitancy, incomplete emptying, dribbling
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What are the red flag LUTS
Red flags: dysuria and haematuria
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Describe the management for LUTS
Incontinence: stress – surgery (tension free vaginal tape or urethral bulking injections), urge – anticholinergic medication (oxybutynin, tolterodine, solifenacin)
Retention: catheterisation
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Define syphilis
Sexually transmitted infection caused by Treponema pallidum – spirochaete bacterium which gets through skin and mucous membranes
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Describe the aetiology of syphilis
Treponema pallidum
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Describe the risk factors for syphilis
Young, sexually active, having multiple partners, unprotected sex, IVDU
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Describe the pathophysiology for syphilis
Spirochaete bacteria which gets through skin and mucous membranes, replicates then disseminates throughout the body. Transmission: sex, vertical transmission, IVDU, blood transfusions
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What are the key presentations for syphilis
Primary syphilis: painless genital ulcer (chancre), lymphadenopathy
Secondary: maculopapular rash, condylomata lata (grey wart-like lesions around genitals), fever, lymphadenopathy
Tertiary: gummatous lesions (granulomatous lesions on skin, organs, bones), abdominal aortic aneurysm
Neurosyphilis: headache, altered behaviour, dementia, tremor, paralysis
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What is the gold standard investigation for syphilis
Antibody testing for T. pallidum: dark field microscopy, serum treponema assay/agglutination, or PCR
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Describe the management for syphilis
1st line – IM benzathine benzylpenicillin. Penicillin allergy: Ceftriaxone, amoxicillin and doxycycline (contraindicated in pregnancy/breastfeeding)
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Describe the complications for syphilis
Jarisch Herxheimer reaction. The Jarisch–Herxheimer reaction is the abrupt onset of fever, chills, myalgia, headache, tachycardia, hyperventilation, flushing, and mild hypotension 1–2 hours after treatment of a spirochetal infection with penicillin or other antimicrobial agents
