Genitourinary Flashcards

1
Q

What is renal colic (nephrolithiasis)?

A

unilateral loin to groin pain that can be excruciating and fluctuates in severity (colicky) as the stone moves and settles - the presenting compliant in symptomatic kidney stones (nephrolithiasis)

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2
Q

What is the epidemiology of renal colic?

A

5-15% of people experience renal colic

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3
Q

What are the risk factors for renal colic/kidney stones?

A

Dehydration
Excess calcium in urine
Diet high in protein, sodium and sugar
Obesity
Certain medications/supplements
GI conditions such as ulcerative colitis or Crohn’s disease
Hyperparathyroidism

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4
Q

What is the most common type of kidney stone?

A

75% calcium oxalate stones (enveloped shaped)

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5
Q

What are the clinical manifestations of renal colic?

A

painful urination
haematuria
cloudy urine
changes in urine (e.g. strong-smelling, increased urgency, reduced/increased frequency)
crystals in urine
fever

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6
Q

What are the investigations for renal colic?

A

computer tomography scan
urine dipstick, kidney USS, abdo XR, renal scan

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7
Q

Where are the most common sites of kidney stones?

A

pelvi-ureteric junction
pelvic brim
vesico-ureteric junction

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8
Q

What is the management for renal colic?

A

Analgesia e.g. paracetamol, NSAIDs
↑ fluid intake
watchful waiting for stones less than 5mm
larger stones (10mm+) require surgical intervention

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9
Q

What are the surgical options for large kidney stones?

A

Extracorporeal shock wave lithotripsy (ESWL) - shock waves break stones into smaller parts so they can be passed

Ureteroscopy and laser lithotripsy - camera inserted via the urethra to identify stone and then targeted lasers used to break it up

Percutaneous nephrolithotomy (PCNL) - nephroscope is inserted via incision through back into kidney to assess ureter - can break up stones

Open surgery - last resort to remove stones

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10
Q

What is acute kidney injury?

A

An acute drop in kidney function characterised by a:
Rise in creatinine of ≥25umol/L in 48hrs
Rise in creatinine of ≥50% in 7 days
Urine output of <0.5ml/kg/hr for >6 hours

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11
Q

What are the pre-renal causes of AKI?

A

[cause inadequate blood supply to kidneys reducing the filtration of blood]
- dehydration
- hypotension
- heart failure

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12
Q

What are the renal causes of AKI?

A

[intrinsic disease in the kidney leading to reduced filtration of blood]
- glomerulonephritis
- interstitial nephritis
- acute tubular necrosis

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13
Q

What are the post-renal causes of AKI?

A

[caused by obstruction to flow of urine out of the kidney]
- kidney stones
- masses such as cancer in the abdomen or pelvis
- ureteral strictures
- enlarged prostate or prostate

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14
Q

What are the risk factors for AKI?

A

Chronic kidney disease
Heart failure
Diabetes
Liver disease
Older age (65+)
Cognitive impairment
Nephrotoxic medications e.g. NSAIDS, ACE-is
use of contrast medium during CT scans

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15
Q

What are the clinical manifestations of AKI?

A

Commonly asymptomatic
Hypotension
Kidney insults
Reduced urine production
Changes in urinary urgency, frequency or hesitancy

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16
Q

What are the investigations for AKI?

A

Urinalysis for protein, blood, (acute nephritis) leukocytes, nitrites (infection) and glucose (diabetes)
USS (look for obstruction)

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17
Q

What is the management for AKI?

A

Stop nephrotoxic medications
Fluid rehydration ( IV fluids in pre-renal AKI)
Relieve obstruction
Severe AKI may require dialysis

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18
Q

What are the potential complications of AKI?

A

hyperkalaemia
fluid overload
heart failure
pulmonary oedema
metabolic acidosis
uraemia (high urea) –> encephalopathy or pericarditis

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19
Q

What is chronic kidney disease?

A

Chronic (>3months) reduction in kidney function with implications for health which tends to be permanent and progressive
Diagnostic characteristics: eGFR <60 or albuminuria

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20
Q

What is the normal urine output?

A

0.5ml/kg/hr

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21
Q

What is the aetiology of CKD?

A

Diabetes
Hypertension
Age-related decline
Glomerulonephritis
Polycystic kidney disease
Medications such as NSAIDS, PPIs + lithium

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22
Q

What are the risk factors for CKD?

A

Older age
Hypertension
Diabetes
Smoking
Use of medications that affect the kidneys

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23
Q

What are the key presentations for CKD?

A

Majority asymptomatic at presentation
Pruritus
Loss of appetite
Nausea
Oedema
Muscle cramps
Peripheral neuropathy
Pallor
Hypertension

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24
Q

What factors affect the progression of CKD?

A

non-modifiable: underlying cause of renal disease, race
modifiable: BP, level of proteinuria, exposure to nephrotoxics, underlying disease activity, further renal insults, dyslipidaemia, ↑phophate, acidosis, anaemia, smoking, glycaemic control if diabetic

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25
What are the investigations for CKD?
Urine ACR (albumin:creatinine ratio) Haematuria Renal ultrasound eGFR (part U&Es) - two tests 3 months <60ml/min apart confirms diagnosis
26
What is the management for CKD?
Treat contributing factors (diabetes, hypertension, glomerulonephritis) Lifestyle changes (exercise, lose weight, stop smoking, diet changes) Depends on severity but usual treatment = ACE-I or Angiotensin-II receptor antagonist Dapagliflozin + statin Dialysis, kidney transplant in severe cases
27
What are the aims of management for CKD?
Slow the progression of disease Reduce risk of cardiovascular disease Reduce risk of complications Treat complications
28
What is the definition of a lower UTI?
bladder infection (cystitis)
29
What is the definition of an upper UTI?
infection of renal pelvis (pyelitis and pyelonephritis)
30
What is the definition of a recurrent UTI?
2+ episodes of UTI in 6 months or 3+ episodes in 1 year
31
What is the definition of an uncomplicated UTI?
infection of the urinary tract by a usual pathogen in a person with a normal urinary tract and with normal kidney function
32
What is the definition of a complicated UTI?
Occurs where anatomical, functional, pharmacological factors predispose the person to persistent infection, recurrent infection or treatment failure
33
What is the epidemiology of UTIs?
1/3 women have UTIs by the age of 24 UTIs are much less common in men
34
What is the aetiology of UTIs?
Majority are caused by E. coli Other causative organisms: Staphylococcus saprophyticus, proteus mirabilis, enterococci Less common causative organisms (more likely in patients with underlying pathology and/or frequent infection): Klebsiella spp. , Proteus vulgaris, Candida albicans, Pseudomonas spp.
35
What are the risk factors for UTIs?
Female Increasing age Recent instrumentation of the renal tract Abnormality of the renal tract Incomplete bladder emptying - particularly by protastic obstruction in men Antibiotic use Use of spermicide Sexual activity Diabetes Presence of catheter Hospitalisation Pregnancy Immunocompromise
36
What are the key presentations of UTIs?
Urinary frequency Pain on urination Dysuria Haematuria Foul-smelling/cloudy urine Urgency Urinary incontinence Suprapubic or loin pain Rigors Pyrexia Nausea + vomiting Acute confused state (elderly patients particularly)
37
What are the investigations for UTIs?
Bladder/kidney exam Urine microscopy Urine culture Urine dipstick (not used when urinary catheter inserted)
38
What are the differential diagnoses for UTIs?
Urethral syndrome or atrophic vaginitis and urethritis in women Other genital tract infections In men, enlarged or inflamed prostate can present similarly
39
What is the general management for UTIs?
Increase fluid intake and personal hygiene behaviours trimethoprim/nitrofurantoin 1 st line antibiotics
40
When can nitrofurantoin not be given for UTI treatment?
pregnancy in third trimester due to risk of neonatal jaundice/haemolysis cant be used in G6PD deficiency
41
What is pyelonephritis?
infection of the renal parenchyma and soft tissues of renal pelvis/upper ureter associated with significant sepsis and systemic upset, rigors predominantly affects women <35
42
What is the classic triad of symptomos seen in pyelonephritis?
loin pain fever pyuria
43
What is nephritic syndrome?
refers to the following symptoms plus inflammation of the kidney without specifying a cause: - haematuria - oliguria (=significantly reduced urine output) - proteinuria <3g.24hrs - fluid retention
44
what are the 3 main signs of nephritic syndrome?
haematuria loss of kidney function signs of fluid overload (oedema)
45
What are 3 three main signs of nephrotic syndrome?
heavy proteinuria >3.5g/24hrs hypoalbuminaemia oedema
46
What is IgA nephropathy?
The presence of dominant or co-dominant mesangial IgA immune deposits which triggers variable degrees of glomerular inflammation and subsequent glomerular and tubulointerstitial scarring.
47
What are the risk factors for IgA nephropathy?
HIV infection FHx of IgAN Asian/white/native american ancestry IgA vasculitis CLD Age 20-30 yrs
48
What are the key presentations of IgA nephropathy?
Visible haematuria 1-2 days after tonsillitis or gastroenteritis viral infection Proteinuria hypertension oedema
49
What is the investigation for IgA nephropathy?
immunofluorescence microscopy shows IgA complex deposition
50
What is the management for IgA nephropathy?
Non-curative, 30% progress to end-stage renal failure BP control (ACE-i)
51
What is post-strep glomerulonephritis?
Acute glomerulonephritis following streptococcal infection is a type III hypersensitivity reaction characterised by the sudden appearance of haematuria, proteinuria, RBC casts in the urine, oedema. and hypertension
52
What are the key presentations of post-strep glomerulonephritis?
visible haematuria 2 weeks after pharyngitis from group A, B haemolytic strep (S. pyogenes) range from asymptomatic urinary to mild "acute nephritis" to a rapidly progressive clinical picture
53
What are the biopsy investigations and results for post-strep glomerulonephritis?
Light microscopy - hypercellular glomeruli e- microscopy - subendothelial immune complex deposition immunofluorescence shows starry sky appearance (IgG, IgM and C3 deposits along glomerular BM and mesangium)
54
What is the management for post-strep glomerulonephritis?
usually self-limiting, sometimes may progress to RGPN (rapidly-progressive glomerulonephritis) Diuretics, salt and water restriction can be given to control fluid overload
55
What is Goodpasture's disease?
a rare autoimmune disorder in which the body makes anti-glomerular basement membrane antibodies which leads to pulmonary-renal syndrome (Goodpasture's syndrome)
56
What are the risk factors for Goodpasture's disease?
FHx Smoking Male 20-30 or 60-70 yrs HLA-DRB or DR4
57
What is the aetiology of goodpasture's disease?
it is caused by an antibody to the alpha-3 chain of type IV collagen which is principally found in the basement membranes of alveoli and glomeruli
58
What are the clinical presentations of Goodpasture's disease?
oliguria haemoptysis oedema crackles on lung examination cough fever nausea
59
What are the investigations for Goodpasture's disease?
Renal function test Renal biopsy (GS) Anti-glomerular basement membrane antibody titre
60
What are the differential diagnoses for Goodpasture's disease?
post-streptococcal glomerulonephritis systemic lupus erythematous microscopic polyangitis
61
What is the management for Goodpasture's disease?
oral corticosteroid, plasmapheresis (remove pathogenic antibody)
62
What is SLE?
Systemic lupus erythematosus is a chronic multisystem autoimmune disorder that most commonly affects women during their reproductive years and is characterised by antinuclear antibodies.
63
What are the clinical presentations of SLE nephropathy?
Haematuria Foamy/cloudy urine (proteinuria) Hypertension Oedema Weight gain (due to excess fluid) High creatinine levels
64
What are the investigations for SLE nephropathy?
Urine sample Blood test for antiphospholipid antibodies and antinuclear antibodies (ANA +ve, anti dsDNA +ve)
65
What is the management for SLE nephropathy
Cyclophosphamide (immunosuppressant) Steroids Hydroxychloroquine (anti-inflammatory)
66
What is nephrotic syndrome?
Kidney disorder which causes the body to pass too much protein in the urine, usually caused by damage to the glomeruli with the following symptoms: Proteinuria (3-15g/day) Hypoalbuminemia Oedema Hyperlipidaemia Weight gain
67
What are the 3 key signs of nephrotic syndrome?
proteinuria oedema hypoalbuminaemia
68
What is the most common cause of nephrotic syndrome in adults?
Focal segmental glomerulosclerosis
69
What is minimal change disease?
Most common form of nephrotic syndrome (a clinical condition characterised by heavy proteinuria, oedema, hypoalbuminemia, hyperlipidaemia) affecting children.
70
What is the aetiology of minimal change disease?
Typically idiopathic but can be secondary to conditions such as Hodgkin’s lymphoma, leukaemia and rarely hep B or C infection.
71
What are the risk factors for minimal change disease?
Viral illness Hx of lymphoma or leukaemia Age 1-8 yrs Hep B or C infection Low birth weight
72
What is the pathophysiology of minimal change disease?
An increase in glomerular permeability to proteins is the main process resulting in proteinuria. Although the pathogenesis of primary nephrotic syndrome is unclear, some evidence suggests that dysregulation of the immune system plays a role in development.
73
What are the key presentations of minimal change disease?
facial /generalised oedema Normal BP Absence of haematuria Proteinuria dyspnoea
74
What are the investigations for minimal change disease?
urinalysis , urine protein/creatinine ratio, serum albumin, lipid profile Renal biopsy + e- microscopy (podocyte effacement + fusion)
75
What are the differential diagnoses for minimal change disease?
Acute glomerulonephritis Focal segmental glomerulosclerosis Congestive heart failure
76
What is the management for minimal change disease?
Corticosteroid therapy Fluid restriction and low salt diet Albumin + furosemide
77
What is focal segmental glomerulosclerosis?
Chronic pathological process caused by injury to podocytes in the renal glomeruli resulting in nephropathy
78
What is the aetiology of focal segmental glomerulosclerosis?
Initiated by injury to podocytes in the renal glomeruli. Primary FSGS: injury produced by unidentified circulating factors which alter the permeability of the glomeruli Secondary FSGS: injury is produced by viruses, toxins, intrarenal haemodynamic changes or a maladaptive response to the loss of functioning nephrons.
79
What are the risk factors for focal segmental glomerulosclerosis?
Male Black race FHx Heroin abuse Causative medications Chronic viral infection e.g. HIV Obesity Solitary or transplanted kidney
80
What is the pathophysiology of focal segmental glomerulosclerosis?
- damage to podocytes triggers apoptosis - podocytes detach from the glomerular basement membrane and are destroyed - the podocyte numbers decline leaving the GBM exposed - maladaptive interactions between the GBM and parietal epithelial cells occurs - the epithelial, endothelial and mesangial cells proliferate - glomerular tuft undergoes sclerosis creating characteristic lesions
81
What are the key presentations of FSGS?
proteinuria oedema hypertension
82
What are the characteristic signs of FSGS?
Muekrcke's lines (white banding on nails due to hypoalbuminaemia) Xanthelasma and xanthomas (skin cholesterol deposits due to hypercholesterolaemia) Lymphadenopathy
83
What are the investigations for FSGS?
urinalysis, serum urea, creatinine, albumin, lipids, GFR light microscopy - segmental sclerosis (NB<50% glomeruli affected)
84
What is the management for FSGS?
treat underlying cuase ACE-i/A-II recetpor antagonist with sodium restriction
85
What is membranous nephropathy?
Chronic immunologically mediated disease of the glomerular basement membrane that may resolve spontaneously, persist with stable renal function or progress to kidney failure Can be either primary (80%) with no identifiable cause or secondary to an underlying cause
86
What is membranous nephropathy?
Chronic immunologically mediated disease of the glomerular basement membrane that may resolve spontaneously, persist with stable renal function or progress to kidney failure Can be either primary (80%) with no identifiable cause or secondary to an underlying cause
87
What are the causes of secondary membranous nephropathy?
Autoimmune: systemic lupus erythematosus, mixed connective tissue disease, rheumatoid arthritis, Sjogren's syndrome Infectious: hepatitis B and C, syphilis Malignancy: solid organ carcinoma (colorectal, lung, etc.), lymphoma, or melanoma Drugs: gold, captopril, lithium, penicillamine, non-steroidal anti-inflammatory drugs (NSAIDs) Other: sarcoidosis, post-renal transplant.
88
What are the risk factors for membranous nephropathy?
Male Age >40 yrs HLA-DR3 Autoimmune disease Hep B or C Syphilis solid organ carcinoma Medications Sarcoidosis Post-renal transplantation
89
What are the clinical presentations of membranous nephropathy?
Oedema Elevated BP Proteinuria or abnormal renal function Xanthelasma Foamy urine Fatigue /malaise Anorexia Muercke’s lines
90
What are the investigations for membranous nephropathy?
urinalysis, serum urea, creatinine, albumin, lipid, urine protein to creatinine ratio light microscopy - thickened GBM e- microscopy - sub-podocyte immune complex depositions, spike + dome appearance
91
What is the management for FSGS?
low salt + protein diet treatment of symptoms/underlying cause
92
What are 2 conditions which can present as both nephrotic and nephritic?
diffuse proliferative glomerulonephritis membrano-proliferative glomerulonephritis
93
What is diffuse proliferative glomerulonephritis?
a histopathologic classification of glomerulonephritis commonly associated with autoimmune diseases, characterised by an increased cellular proliferation affecting >50% of the glomeruli
94
What is the aetiology of diffuse proliferative glomerulonephritis?
Lupus nephritis class IV is the most common cause of DPGN IgA nephropathy Anti-glomerular basement membrane disease Granulomatosis with polyangiitis Microscopic polyangiitis
95
What is the pathophysiology of diffuse proliferative glomerulonephritis?
Immunological attack on the glomerulus —> ↑GBM permeability to protein, RBCs and WBCs Capillary loops become obliterated and sclerosis develops → hypertension and renal failure Fibrinoid necrosis in the glomerular vasculature → vasculitis → ↓renal filtration and function
96
What are the key presentations of DPGN?
Most symptoms result from the decrease in GFR caused by DPGN Nonspecific symptoms: nausea, fatigue, vomiting, oliguria Nephritic symptoms: proteinuria, hypertension, oedema, haematuria
97
What are the investigations for DPGN?
FBC, renal function tests, urinalysis Renal biopsy Renal USS
98
What are the differential diagnoses for DPGN?
Rapidly progressive glomerulonephritis Poststreptococcal glomerulonephritis Membranoproliferative glomerulonephritis
99
What is the management for DPGN?
ACE-i + statin for mild disease Steroids for significant disease IN ESRD - dialysis/kidney transplant
100
What is membranoproliferative glomerulonephritis?
A form of glomerulonephritis caused by an abnormal immune response.
101
What are the characteristic histological features of membranoproliferative glomerulonephritis?
Proliferation of mesangial and endothelial cells and expansion of the mesangial matrix Thickening of the peripheral capillary walls by subendothelial immune deposits and/or intramembranous dense deposits Mesangial interposition into the capillary wall, giving rise to a double-contour or tram-track appearance on light microscopy
102
What is the aetiology of membranoproliferative glomerulonephritis?
May be idiopathic or secondary (more common) in aetiology Autoimmune diseases (systemic lupus erythematosus, scleroderma, Sjogren syndrome) Cancer (leukaemia, lymphoma) Infections (hep b, c, endocarditis, malaria)
103
What are the risk factors for membranoproliferative glomerulonephritis?
Autoimmune disease Hepatitis B or C Cryoglobulinaemia Monoclonal immunoglobulin deposition diseases Subacute bacterial endocarditis Infection of a ventriculoatrial shunt Chronic lymphocytic leukaemia
104
What is the pathophysiology of membranoproliferative glomerulonephritis?
Deposits of antibodies build up in a part of the kidneys called the glomerular basement membrane and cause damage which result in the leakage of blood and protein to leak into the urine.
105
What are the key presentations of membranoproliferative glomerulonephritis
Haematuria Proteinuria Oedema Changes in mental state, decreased alertness Decrease in urine volume Dark urine
106
What are the investigations for membranoproliferative glomerulonephritis?
Urinalysis, Bloods (BUN, creatinine) Kidney biopsy (GS)
107
What is the management for membranoproliferative glomerulonephritis?
Treat underlying condition Steroids (prednisone) for nephrotic-range proteinuria
108
What is benign prostate hyperplasia?
Non-malignant prostate hyperplasia, normal with ageing and usually presents with lower urinary tract symptoms (LUTS).
109
What is the aetiology of benign prostate hyperplasia?
Caused by hyperplasia of the stroma and epithelial cells of the prostate
110
What are the risk factors for benign prostate hyperplasia?
Older age (50+ yrs) Ethnicity FHx Smoking Metabolic syndrome
111
What is the pathophysiology of BPH?
BPH involves hyperplasia of both epithelial and stromal prostatic components which overtime causes bladder outlet obstruction. Obstruction has both a prostatic component due to increased epithelial tissue, particularly in a transition zone and a dynamic component due to increases in stromal smooth muscle tone.
112
What are the key presentations of BPH?
LUTS: Hesitancy, urgency, frequency, intermittency, weak flow Terminal dribbling Incomplete emptying nocturia
113
What are the investigations for BPH?
PSA (unreliable), urine dipstick, urine frequency volume chart DRE (rectal exam) - smooth enlarged prostate (in cancer is hard and irregular) (GS) Abdominal examination
114
What are the differential diagnoses for BPH?
Overactive bladder, prostatitis, prostate cancer, UTI, bladder cancer
115
What is the management for BPH?
Lifestyle changes Decrease caffeine Consider catheter if acute a- blocker (tamsulosin) 5a reductive inhibitors (finasteride) - decreased testosterone production → ↓prostate size Surgery last resort (TURP - transurethral resection of prostate, TUVP/TEVAP - transurethral electrovaporization of the prostate, Holmium laser enucleation of the prostate (HoLEP), open prostatectomy)
116
What is prostate cancer?
Neoplastic , malignant proliferation of the outer zone of the peripheral prostate.
117
What is the epidemiology of prostate cancer?
2nd most common cancer 5th leading cause of cancer mortality in men worldwide
118
What are the risk factors for prostate cancer?
Genetic - BRCA2, HOXB13 ↑age Afrocaribbean ethnicity FHx High dietary fat levels
119
What is the pathophysiology of prostate cancer?
High-grade prostatic intraepithelial neoplasia is considered to be the most likely precursor of invasive prostate cancer. Characterised by cellular proliferation with pre-existing ducts and glands with cytological changes that mimic neoplasm. Prostate cancer tends to spread along the capsular surface of the gland and may invade the seminal vesicles, periprostatic tissue and eventually the bladder neck.
120
What are the key presentations of prostate cancer?
LUTs but with systemic cancer symptoms + bone pain Nocturia, urinary frequency, hesitancy, urgency, dysuria, haematuria Weight loss/anorexia, lethargy, palpable lymphnodes Nodular and asymmetric enlarged prostate on DRE
121
What are the investigations for prostate cancer?
Serum prostate-specific antigen, pre-biopsy multiparametric MRI Prostate biopsy Testosterone, bloods, bone scan, CT/MRI
122
What is the management for prostate cancer?
Local → prostatectomy Metastatic → hormone therapy (↓testosterone = ↓cancer growth/even death) *bilateral orchiectomy (surgical removal of testes) * GNRH receptor agonist e.g. Goserelin radio/chemotherapy
123
What is testicular cancer?
Cancer of the testes which most commonly arises from germ cells (called seminoma) and other types are called non-seminomas. Seminomas make up 90% of cases.
124
what are the risk factors for testicular cancer?
Undescended testes Male infertility Family history Increased height
125
What are the germ and non-germ examples of testicular cancer?
germ = seminoma (90%), teratoma Non-germ = sertoli, leydig, sarcoma
126
What are the key presentations of testicular cancer?
Painless lump on the testicle - non-tender, hard, irregular, non-fluctuant, no transillumination Gynaecomastia May show lung metastasis signs e,g, cough
127
What are the investigations for testicular cancer?
Scrotal USS, tumour markers AFP, BhCG
128
What is the management for testicular cancer?
Urgent radical orchiectomy (+offer sperm storage) always 1st line Adjuvant chemo or radiotherapy
129
What is bladder cancer?
Transitional cell carcinoma (TCC) of bladder 5% are squamous cell carcinoma (higher in areas of schistosomiasis) 2% are adenocarcinoma, sarcoma and SCC
130
What are the risk factors for bladder cancer?
Occupational exposure to dyes/paints/rubber Smoking Chemo + radiotherapy Age male bladder stones (chronic inflammation)
131
What are the key presentations for bladder cancer?
painless haematuria dysuria back pain
132
WHat are the investigations for bladder cancer?
urinalysis flexible cytoscopy + biopsy (GS) CTT urogram (for staging) CT, MRI, bone scan
133
What is the management for bladder cancer
Conservative = support Medical = chemo/radiotherapy Surgery: T1 - transurethral resection (TURBT) or local diathermy T2-3 - radical cystectomy T4 - palliative chemotherapy and radiotherapy
134
What is renal cell carcinoma?
a type of adenocarcinoma arising from the renal tubules
135
What are the subtypes of RCC?
Clear cell (80%) Papillary (15%) Chromophobe (5%)
136
`what are the risk factors for RCC?
Smoking Obesity Hypertension End-stage renal failure Von Hippel-Lindau disease Tuberous sclerosis Hereditary papillary RCC
137
What is the pathophysiology of RCC?
Renal carcinoma tends to spread to the tissues around the kidney, within Gerota’s fascia Often spreads to the renal vein, then to the inferior vena cava “Cannonball metastases” in the lungs are a classic feature of metastatic renal cell carcinoma - they appear as clearly defined circular opacities scattered throughout the lung fields on a chest x-ray
138
What are the key presentations of RCC?
Classic triad of presentation: haematuria, flank pain and palpable mass. (only seen in <10% patients) >50% discovered incidentally on scan Non-specific cancer sx: weight loss, fatigue, anorexia, night sweats Palpable renal mass on examination Paraneoplastic syndromes: polycythaemia, hypercalcaemia, hypertension, Stauffer’s syndrome
139
What are the investigations for RCC?
Bloods, eGFR, urinalysis CT abdo/pelvis (GS) abdo/pelvic USS, MRI abdo/pelvis, CT chest (cannonball mets) biopsy if scan is unclear
140
What is the management for RCC?
4 stages: I: partial or radical nephrectomy II: radical nephrectomy III: radical nephrectomy and adrenalectomy IV: systemic treatment
141
What is transitional cell carcinoma
carcinoma of the upper renal tract presents with haematuria, loin pain, clot colic managed by nephroureterectomy
142
Causes of haematuria
Malignancy (1 in 5) stones infection prostate nephrological cause idiopathic
143
What is polycystic kidney disease?
Genetic condition where the kidneys develop multiple fluid-filled cysts resulting in significant kidney function impairment
144
What is the aetiology of PKD?
Autosomal recessive or dominant (more common) inheritance recessive - disease of infancy or pre-birth with high mortality rate and many congenital abnormalities (Potter's sequence = flattened nose, clubbed feet) dominant - more common in males and presents at 20-30yrs
145
What are the risk factors for PKD?
FHx of mutation FHx of cerebrovascular event
146
What is the pathophysiology of PKD?
PKD1+2 code for polycystin (Ca2+ channel), in cilia of nephron, when filtrate passes through nephron cilia move + polycystin channels on cilia open --> Ca2+ influx which inhibits excessive growth with PKD mutation = Ca2+ influx reduced --> excessive growth of cilia
147
What are the key presentations of PKD?
Renal cysts Hypertension Abdo/flank pain Haematuria Palpable kidneys/abdominal mass Headaches Dysuria Syprapubic pain, fever
148
What are the investigations for PKD?
Urinalysis Bloods (U+E, fasting lipid profile) GS = Renal USS Genetic testing, CT/MRI if USS not confirmatory
149
What are some differentials for PKD?
acquired cystic kidney disease simple cyst tuberous sclerosis complex
150
What is the management for PKD?
Non-curative, manage symptoms (e.g. hypertension, ESRF)
151
What is the cause of chlamydia?
STI caused by the gram-ve bacteria chlamydia trachomatis - intracellular organism which enters and replicates within cells before rupturing the cell and spreading to others.
152
What are the risk factors for chlamydia?
young adults multiple sexual partners sexual activity
153
What are the key presentations of chlamydia in women?
75% are asymptomatic but can present with: Abnormal vaginal discharge Pelvic pain Abnormal vaginal bleeding Painful sex (dyspareunia) Painful urination (dysuria)
154
What are the symptoms of chlamydia in men?
Roughly 50% asymptomatic in men but can present with: Urethral discharge or discomfort Dysuria Epididymo-orchitis (inflammation of epididymis and testicles) Reactive arthritis
155
What are the signs of chlamydia on examination?
Pelvic or abdominal tenderness Cervical motion tenderness Inflamed cervix Purulent discharge
156
What are some differentials for chlamydia?
Bacterial vaginosis, vaginal candidiasis, gonorrhoea
157
What is the management for chlamydia?
Doxycycline 100mg bi-daily for a week Abstain from sex for 7 days Give sexual health advice
158
What are the potential complications of chlamydia?
pelvic inflammatory disease, chronic pelvic pain, infertility, ectopic pregnancy, epididymo-orchitis, conjunctivitis, lymphogranuloma venereum, reactive arthritis
159
What is the aim of the national chlamydia screening programme in england?
To screen every sexually active person under 25yrs for chlamydia annually or when they change their sexual partner
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What is the epidemiology of chlamydia?
chlamydia is the most common STI in the UK
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What is the epidemiology of gonorrhoea?
second most common bacterial STI worldwide
162
What is the aetiology of gonorrhoea?
Caused by neisseria gonorrhoeae, a gram negative diplococcus bacteria which infects mucous membranes with a columnar epithelium such as the endocervix, urethra, rectum, conjunctiva and pharynx. It spreads via contact with mucous secretions from infected areas
163
What are the risk factors for gonorrhoea?
Young adults (20-29yrs) MSM Black ancestry Current or previous Hx of STI Sexually active Multiple sexual partners
164
What are the symptoms of gonorrhoea in women?
50% women are asymptomatic but can present with: Odourless purulent discharge, possibly green or yellow Dysuria Pelvic pain
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What are the symptoms of gonorrhoea in men?
90% men are symptomatic: Odourless purulent discharge, possibly green or yellow Dysuria Testicular pain or swelling (epididymo-orchitis)
166
What are the investigations for gonorrhoea?
Charcoal endocervical swab NAAT (nucleic acid amplification testing) (GS)
167
What are some differentials for gonorrhoea?
Chlamydia, trichomonas, other infectious causes of urethritis, cervicitis, PID, epididymitis, candidal vaginitis or bacterial vaginosis, UTI
168
What is the management for gonorrhoea?
SIngle dose of Intramuscular ceftriaxone 1g (unknown sensitivities) Single oral ciprofloxacin 500mg (for known sensitivities) Sexual health advice
169
What are some potential complications of gonorrhoea?
PID, chronic pelvic pain, infertility, prostatitis, conjunctivitis, urethral strictures, disseminated gonococcal infection, skin lesions
170
What is the cause of syphilis?
Caused by the spirochaetal bacteria Treponema pallidum. Infection is typically acquired through direct person-to-person sexual contact with an individual who has early (primary or secondary) syphilis.
171
How can syphilis be contracted?
It can be contracted through: oral , vaginal or anal sex involving direct contact with infected area Vertical transmission from mother to baby during pregnancy Intravenous drug use Blood transfusions and other transplants (rare)
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What are the risk factors for syphilis?
Sexually active MSM Illicit drug use Commercial sex workers Multiple sexual partners HIV or other STIs
173
What are the different types of syphilis?
Primary Syphilis = painless ulcer (chancre) at original site of infection Secondary= systemic symptoms, particularly of the skin and mucous membranes Latent = occurs after secondary stage where symptoms disappear and the patient becomes asymptomatic despite still being infected (early = within 2 years of infection, late = >2 years following infection) Tertiary = multi-organ symptoms which present many years after initial infection, often includes development of gummas (granulomatous growths which can cause severe tissue damage and deformation) and cardiovascular or neurological symptoms. Neurosyphilis occurs if the infection involves the CNS
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What are the key presentations of primary syphilis?
Painless genital chancre (tends to resolve over 3-8 weeks), local lymphadenopathy
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What are the key symptoms of secondary syphilis?
maculopapular rash, condylomata lata, low-grade fever, lymphadenopathy, alopecia, oral lesions
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What are the key symptoms of tertiary syphilis?
gummatous lesions, aortic aneurysms, neurosyphilis
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What are the symptoms of neurosyphilis?
headache, altered behaviour, dementia, tabes dorsalis, ocular syphilis, paralysis, sensory impairment, argyll-robertson pupil (constricted pupil which doesn’t react to light)
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What are the investigations for syphilis?
Rapid plasma reagin(RPR), venereal disease research lab test (VDRL) Dark-field microscopy swab from lesion (GS)
179
What are some differentials for syphilis?
Genital herpes, chancroid, HIV infection
180
What is the management of syphilis?
Single IM dose of benzathine benzylpenicillin Full screening for other STIs Advice about sexual health Contact tracing
181
What is a hydrocele?
A collection of fluid within the tunica vaginalis (sealed membranous pouch) that surrounds the testes
182
What is the aetiology of hydroceles?
Mostly congenital and resolve within first year of life Most adult hydroceles are acquired
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What are the risk factors for hydrocele?
Premature birth /LBW Male Infants <6 months Late-descending testes Increased intraperitoneal fluid or pressure Inflammation or injury within the scrotum Testicular cancer Connective tissue disorders
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What is the pathophysiology of the 2 types of hydrocele?
Simple hydroceles are common in newborn males - occur where fluid is trapped in the tunica vaginalis, usually resolves itself as fluid is reabsorbed over time Communicating hydrocele - occurs where the tunica vaginalis around the testicle is connected with the peritoneal cavity via a pathway called the processus vaginalis allowing fluid from the peritoneal cavity to enter the hydrocele
185
What are the key presentations of hydroceles?
Soft, smooth, non-tender swelling around teste Swelling is in font and below testicle Simple hydroceles remain one size whereas communicating hydroceles fluctuate in size
186
What are the investigations for hydroceles?
Examination (soft, smooth, non-tender swelling around teste which transilluminates with light) Testicular USS (GS)
187
What are some differentials for hydroceles?
Partially descended testes, inguinal hernia, testicular torsion, haematoma, tumours (rare)
188
What is the management for hydroceles?
Simple hydroceles usually resolve within 2 years without having any lasting negative effects, may require surgery if they are associated with other problems like hernias Communicating hydrocele can be treated with a surgical operation to remove or ligate the connection between the peritoneal cavity and the hydrocele
189
What is a varicocele?
Swelling of the veins of the pampiniform plexus
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What percentage of men are affected by varicocele?
around 15%
191
What are the risk factors for varicocele?
FHx Somatometric parameters (tall/low BMI)
192
What is the pathophysiology of varicocele formation?
Varicoceles are the result of increased resistance in the testicular vein where incompetent valves in the testicular vein allow blood to flow back from the testicular vein into the pampiniform plexus causing swelling of the veins.
193
What are the key presentations of varicocele?
Painless scrotal mass Small testicle Throbbing /dull pain or discomfort, worse on standing Dragging sensation Sub-fertility or infertility
194
What are the investigations for varicocele
Examination (scrotal mass which feels like a bag of worms, more prominent on standing, disappears when lying down, asymmetry in testicular size) Doppler USS (GS) Semen analysis (if fertility concerns), hormonal test (if concerns about function)
195
What is the grading for varicocele?
Subclinical: no clinical abnormality, only detected by Doppler ultrasound Grade I: only clinically palpable with valsalva manoeuvre Grade II: palpable without valsalva manoeuvre Grade III: varicocele is visible through the scrotal skin, easily palpable
196
What is the management for varicocele?
Uncomplicated cases can be managed conservatively (watch and wait) Surgical or endovascular embolisation may be indicted for pain, testicular atrophy or infertility
197
What is an epididymal cyst?
Fluid-filled saac which occurs at the head of the epididymus (above and behind testes) Called a spermatocele if it contains sperm
198
What percentage of men experience epididymal cysts?
30 %
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What are the risk factors for epididymal cysts?
Cystic fibrosis PKD
200
What are the key presentations of epididymal cysts?
mostly asymptomatic soft, round lump at the top of testicle can be painful
201
What are the investigations for epididymal cysts?
Examination : soft round lump at top of testicle associated with the epididymis and transilluminates USS scrotum (GS)
202
What are some differentials for epididymal cysts?
Hydrocele, varicocele, lipoma
203
What is the management for epididymal cysts?
Usually no treatment needed If pain and discomfort surgical removal may be considered Surgical removal if there is torsion of the cyst causing acute pain and swelling
204
What is testicular torsion?
Spermatic cord twists in on itself and occludes the testicular artery causing ischaemia which can lead to gangrene of testis if not dealt with => surgical emergency
205
What are the causes/risk factors for testicular torsion?
Bell-clapper defect (mc) trauma
206
What is the pathophysiology of testicular torsion?
The bell clapper deformity increases the likelihood of torsion because the testicle is freely mobile within the tunica media Intravaginal = testicle rotates within the tunica vaginalis Extravaginal = testicle twists around the spermatic cord as it descends (rare)
207
What are the key presentations of testicular torsion?
Severe unitesticular pain (hurts to walk) Abdominal pain Nausea and vomiting Cremasteric reflex lost (testicle retracts upwards on stroking of inner thig
208
What are the investigations for testicular torsion?
Surgical exploration if there is high risk Doppler USS (check testicular blood flow) = GS
209
What is a major differential for testicular torsion?
Testicular appendix torsion = twisting of a vestigial appendage (seen in 50% males) located along the testicle Also epididymitis or epididymo-orchitis, hydrocele, varicocele, testicular cancer
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What is the management for testicular torsion?
urgent surgery within 6hrs
211
What is the treatment for bell-clapper syndrome?
Bilateral orchiplexy (fixing of testes to scrotal sac to overcome deformity, if testes are non-viable --> orchiectomy
212
What are LUTS?
Lower urinary tract symptoms
213
What are the storage LUTS?
occur when bladder should be storing urine --> urge to urinate - urgency - frequency - incontinence - nocturia
214
What are the voiding LUTS?
occur when bladder outlet is obstructed --> difficulty urinating - poor stream - incomplete emptying - dribbling - hesitancy
215
What are the red flag LUTS?
haemturia dysuria
216
What is incontinence?
Loss of control of urination
217
What are the risk factors for incontinence?
Female Increased age Postmenopausal status Increased BMI Previous pregnancies and vaginal deliveries Pelvic organ prolapse Pelvic floor surgery Neurological conditions (multiple sclerosis) Cognitive impairment and dementia
218
What are the different types of incontinence?
Urge incontinence = overactivity of detrusor muscle → sudden urge to urinate Stress incontinence (sphincter weakness) = leakage of urine due to increased intra-abdominal pressure Mixed incontinence = combination of both Overflow incontinence = overflow of urine when there is chronic urinary retention due to an obstruction to the urine outflow, occurs without the urge to pass urine
219
What are the key presentations of incontinence?
Involuntary urine leakage on effort exertion, sneezing, or coughing Involuntary urine leakage accompanied by or immediately preceded by urgency Frequency of urination Vaginal bulge/pressure Urogenital atrophy
220
What are the investigations for incontinence?
urinalysis, post-void residual measurement, cough stress test Empty supine stress test (valsalva manoeuvre) = GS
221
What is the management for incontinence?
Lifestyle changes - avoid caffeine, diuretics, overfilling of bladder, weight loss (if needed) Pelvic floor exercises Surgery (tension-free vaginal tape (TVT), autologous sling procedures Anticholinergic drugs (oxybutynin, tolterodine, solifenacin)
222
What is urinary retention?
inability to pass urine even when the bladder is full (500+ml)
223
What are the causes of difficulty voiding/urinary retention?
obstruction, stones, BPH, urethral stricture, prolapse, abdominal masses, atonic bladder, neurological flaccid paralysis
224
What is the treatment for urinary retention?
catheterisation
225
What are the investigations for LUTS?
Examination U+Es Urodynamic studies post-void bladder scan bladder diary flowmetry
226
What factors reduce GFR?
renal disease, DM, hypertension (↓ filtration coefficient (Kf)) urinary tract obstruction (kidney stones) (↑serum albumin (↑BCP)) ↓renal blood flow, ↑plasma proteins (↑glomerular osmotic pressure) ↓arterial pressure (small effect) (↓glomerular hydrostatic pressure) ↓angiotensin II (ACEi/ARB) (↓efferent artery resistance) NSAIDS (↑afferent artery resistance)
227
What are the causes of hyperkalaemia?
acute kidney injury drugs: K-sparing diuretics, ACEis, A-II receptor blockers, spironolactone, ciclosporin, heparin metabolic acidosis Addison's disease Rhabdomyolysis Massive blood transfusion
228
What percentage of men with an elevated PSA do not have prostate cancer?
70%
229
What percentage of men with prostate cancer have a normal PSA?
6%
230
What is a potential complication of tamsulosin use?
Postural hypertension and retrograde ejaculation
231
What are some complications of autosomal dominant PCKD?
Polycystic liver disease male infertility subarachnoid haemorrhage
232
What is a wilm's tumour?
rare renal mesenchymal stem cell tumour (nephroblastoma) seen in children under 3 years
233
What are the presentations of Wilm's tumour?
mass in the abdomen abdominal pain haematuria lethargy fever hypertension weight loss
234
What are the diagnostic tests for Wilm's tumours?
USS CT/MRI for staging Biopsy (GS)
235
What is the treatment for Wilm's tumours?
Surgical excision of tumour + nephrectomy of affected kidney Adjuvant chemo and radiotherapy
236
What is epididymo-orchitis?
inflammation of the epididymis, extending to the testes
237
What are the causes of epididymo-orchitis?
E. coli Chlamydia trachomatis Neisseria gonorrhoea Mumps
238
What are the risk factors for epididymo-orchitis?
Multiple sexual partners Unprotected sex History of STI Congenital UT abnormalities Surgery involving the genitals or UT
239
What are the key presentations of epididymo-orchitis?
Gradual onset with unilateral: Testicular pain Dragging or heavy sensation Swelling of testicle and epididymis Tenderness on palpation, particularly over epididymis Urethral discharge Systemic symptoms such as fever and potentially sepsis
240
What signs indicate epididymo-orchitis?
+ve Prem’s sign (pain relieved by elevating testis) Cremaster reflex intact
241
What are the investigations for epididymo-orchitis?
Urine microscopy, culture and sensitivity Chlamydia and gonorrhoea NAAT testing Charcoal swab Saliva swab Serum antibodies USS
242
What is the management for epididymo-orchitis caused by enteric organisms?
ofloxacin for 14 days, levofloxacin for 10 days, co-amoxiclav for 10 days
243
What is the treatment for STI-related epididymo-orchitis?
intramuscular ceftriaxone, doxycycline, ofloxacin
244
What are 2 critical side effects of quinolone antibiotics?
tendon damage and tendon rupture (achilles) lowered seizure threshold
245
What are the potential complications of epididymo-orchitis?
chronic pain, chronic epididymitis, testicular atrophy, sub-fertility or infertility, scrotal abcess
246
What is prostatitis?
Inflammation of the prostate gland Acute bacterial = acute infection in prostate, presenting with a more rapid onset of symptoms Chronic prostatitis = symptoms lasting for longer than 3 months (can be bacterial or not)
247
What is the aetiology of prostatitis?
unclear cause of inflammation of pain may be initially triggered by an infection, with inflammation persisting after the infection has resolved
248
What are the key presentations of chronic prostatitis?
presents with at least 3 months of pelvic pain, LUTS, sexual dysfunction, pain with bowel movements, tender and enlarged prostate
249
What are the key presentations of acute prostatitis?
fever myalgia nausea fatigue sepsis
250
What are the investigations for prostatitis?
urine dipstick urine microscopy, culture and sensitivities chlamydia and gonorrhoea NAAT testing
251
What is the management for acute prostatitis?
Hospital admission for systemically unwell or septic patients - IV antibiotics Oral antibiotics, typically for 2-4 weeks (e.g. ciprofloxacin, ofloxacin or trimethoprim) Analgesia (paracetamol or NSAIDs) Laxatives for pain during bowel movements
252
What are the treatments for chronic prostatitis?
a-blockers (tamsulosin), analgesia, psychological where indicted (CBT, antidepressants), laxatives, antibiotics
253
What are the potential complications for prostatitis?
sepsis, prostate abscess, acute urinary retention, chronic prostatitis
254
What are the GFR categories in CKD staging?
G1: ≥90 (normal + high) G2: 60-89 G3a: 45-59 G3b: 30-44 G4:15-29 G5: <15 (kidney failure)
255
What are the ACR categories in CKD staging?
A1: <3 (normal to mildly increased) A2: 3-30 A3: >30 (severely increased)
256
What is the zone of the prostate affected by BPH?
peripheral zone
257
What is the most common site of metastases for prostate cancer?
bone
258
What is pyuria and what causes it?
Presence of leukocytes in the urine (10 or more WBCs per cubic mm) Associated with infection, pyelonephritis, papillary necrosis, diabetes, renal TB, renal stones, cancer
259
Which bacteria is associated with renal stones and UTIs?
proteus
260
What are casts in the urine? and what do they indicate?
cylindrical protein mouldings formed in the renal tubules cellular and densely granulated casts indicate pyelonephritis or glomerulonephritis RBC casts usually indicate glomerular bleeding epithelial cell and fatty casts accompany tubular necrosis and nephrotic syndrome
261
What are the causes of hyperkalaemia?
Medications (ACE inhibitors, NSAIDs) Acidosis (metabolic + respiratory) Cellular destruction (burns, traumatic injury) Hypoaldosteronism, haemolysis Intake (excessive) Nephrons (renal failure) Excretion (impaired)
262
What are the ECG signs for hyperkalaemia?
Tall tented t waves Wide QRS complex Flattening of P waves Prolonged PR interval
263
What is the gold-standard test for all UTIs?
Midstream microscopy, culture + sensitivity