Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Conditions > Genitourinary > Flashcards

Genitourinary Flashcards

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Describe the epidemiology of nephrolithiasis

A

Very common. More in men (testosterone > increased oxalate)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Describe the aetiology of nephrolithiasis

A

Chronic dehydration, obesity, high protein/salt diet, recurrent UTIs, low urine output, hyperparathyroidism/hypercalcaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Describe the differential diagnosis for nephrolithiasis

A

Peritonitis, appendicitis, UTI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Describe the complications for nephrolithiasis

A

Obstruction (leading to AKI), infection (leading to pyelonephritis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the risk factors for AKI

A

Hypotension, volume depletion, CKD, heart failure, diabetes, cirrhosis, nephrotoxic meds (NSAIDs, ACEi), cancer, trauma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the gold standard investigation for AKI

A

Metabolic profile: U&E (GFR) and creatinine – raised serum creatinine, reduced urine output

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Describe the differential diagnosis for AKI

A

Chronic kidney disease, renal stones, tubular necrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Describe the complications for AKI

A

End-stage renal failure, chronic kidney disease, metabolic acidosis, uraemia > encephalopathy, pericarditis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Describe the epidemiology of bladder cancer

A

Old men, people who work in rubber/dye industry

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Describe the aetiology of bladder cancer

A

Mutation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Describe the risk factors for bladder cancer

A

Exposure to dyes/rubber/leather/textiles/paint (aromatic amines – dye factor worker, hairdresser, painter). Age >65, male, Caucasian, smoking, pelvic radiation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What are the key presentations for bladder cancer

A

Painless haematuria (macro or microscopic), urgency, dysuria, suprapubic/pelvic mass, pelvic pain, recurrent UTI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Describe the clinical manifestations for bladder cancer

A

Signs of metastases: bone pain, weight loss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is the gold standard investigation for bladder cancer

A

Flexible cystoscopy and biopsy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Describe the first line investigations for bladder cancer

A

urinalysis for microscopy and culture (haematuria), bladder USS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Describe the differential diagnosis for bladder cancer

A

Benign prostatic hyperplasia, UTI, haemorrhagic cystitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Describe the management for bladder cancer

A

Conservative: cancer support nurse
Medical: chemotherapy, radiotherapy
Surgical: transurethral resection of bladder tumour TURBT, or cystectomy (remove bladder), lymph node dissection if spread

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Describe the prognosis for bladder cancer

A

5 year survival rate is 75%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Define renal cancer

A

Renal cell carcinoma is most common type. Adenocarcinoma arising from proximal convoluted tubule

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Describe the risk factors for renal cancer

A

Smoking, obesity, hereditary, von Hippel-Lindau

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What are the key presentations for renal cancer

A

Triad: Haematuria, flank pain, palpable mass. May have left varicocele

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Describe the clinical manifestations for renal cancer

A

Symptoms: Cancer symptoms: weight loss, fatigue, anorexia, night sweats

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What is the gold standard investigation for renal cancer

A

CT chest/abdo/pelvis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Describe the first line investigations for renal cancer

A

Abdominal/pelvis ultrasound, bloods: raised RBC, raised calcium, raised LDH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Describe the management for renal cancer

A

1st – nephrectomy/partial nephrectomy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Describe the complications for renal cancer

A

Paraneoplastic changes – polycythaemia, Cushing’s, hypertension, hypercalcaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Define prostate cancer

A

Malignant tumour of glandular origin in the prostate. Mostly adenocarcinomas which grow in the peripheral zone of the prostate. Very slow growing.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Describe the epidemiology of prostate cancer

A

Most common cancer in men, most hormone sensitive cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Describe the aetiology of prostate cancer

A

Mutation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What are the risk factors for prostate cancer

A

Increasing age, family history, Afro-Caribbean, anabolic steroids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Describe the pathophysiology of prostate cancer

A

Prostate cancer is almost always androgen-dependent, requiring androgen hormones (e.g., testosterone) to grow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What are the key presentations for prostate cancer

A

LUTS – frequency, hesitancy, weak flow, dribbling, nocturia. bone pain, weight loss, fatigue, night sweats

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Describe the clinical manifestations for prostate cancer

A

Haematuria, erectile dysfunction, metastases (bone – sclerotic bony lesions, brain, liver, lungs)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What is the gold standard investigation for prostate cancer

A

Transrectal USS and biopsy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Describe the first line investigations for prostate cancer

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What are the differential diagnosis for prostate cancer

A

Benign prostatic hyperplasia, chronic prostatitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Describe the management for prostate cancer

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Describe the complications for prostate cancer

A

Metastases (bone, liver, lungs, brain), erectile dysfunction, incontinence

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Describe the prognosis for prostate cancer

A

Localised: 100%, metastatic 30%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Define testicular cancer

A

Cancer arising from germ cells in the testes. 90% are germ cell cancers (seminomas, teratomas), rest are non-germ cell cancers (Leydig, Sertoli, lymphoma)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Describe the epidemiology of testicular cancer

A

Young men (15-35)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Describe the aetiology of testicular cancer

A

Mutation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What are the risk factors for testicular cancer

A

Undescended testes (cryptorchidism), male infertility, family history, increased height, HIV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

What are the key presentations for testicular cancer

A

Palpable painless lump in testicle which does not transilluminate (light can’t get through)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Describe the clinical manifestations for testicular cancer

A

Haematospermia (blood in semen), gynecomastia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

What is the gold standard investigation for testicular cancer

A

Urgent USS (doppler) of testes – testicular mass

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Describe the first line investigations for testicular cancer

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

What are the differential diagnosis for testicular cancer

A

Testicular torsion, epididymo-orchitis, hydrocele

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Describe the management for testicular cancer

A

1st line – urgent radical orchidectomy +/- testicular prosthesis
Semen cryopreservation, metastatic – lymph node removal, chemotherapy, radiotherapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

What are the complications for testicular cancer

A

Infertility, hypogonadism, peripheral neuropathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Describe the prognosis for testicular cancer

A

98% 5 year survival rate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Define chronic kidney disease

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Describe the aetiology of chronic kidney disease

A

Diabetes, hypertension, glomerulonephritis, polycystic kidney disease, nephrotoxic drugs (NSAIDs, ACEi), persistent pyelonephritis, obstruction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

What are the risk factors for chronic kidney disease

A

Diabetes, hypertension, male, increasing age, smoking

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Describe the pathophysiology of chronic kidney disease

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

What are the key presentations for chronic kidney disease

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Describe the clinical manifestations for chronic kidney disease

A

Signs: Haematuria, proteinuria, peripheral neuropathy, hypertension, oedema
Symptoms: Pruritis, loss of appetite, nausea, muscles cramps, pallor, fatigue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

What is the gold standard investigation for chronic kidney disease

A

U&E for estimated GFR (eGFR < 60mL/min/1.73m¬2 or, eGFR <90mL/min/1.73m2 + signs of renal damage)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Describe the first line investigations for chronic kidney disease

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

What are the differential diagnosis for chronic kidney disease

A

Diabetic neuropathy, nephrotic syndrome, obstructive uropathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Describe the management for chronic kidney disease

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

Describe the complications for chronic kidney disease

A

Anaemia, CKD-mineral bone disease, neuropathy, encephalopathy, cardiovascular disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

Define benign prostatic hyperplasia

A

Hyperplasia of the stromal and epithelial cells of the prostate causing prostate enlargement which partially blocks the urethra.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

Describe the aetiology of BPH

A

Age related hormonal changes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

What are the risk factors for BPH

A

Ageing men, smoking, non-Asian race, raised testosterone, family history, castration is protective

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

Describe the pathophysiology of BPH

A

Inner transitional zone of prostate proliferates and narrows urethra

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

What are the key presentations for BPH

A

LUTS: Storage - frequency, urgency, incontinence, nocturia. Voiding – dysuria, poor/intermittent stream, dribbling, straining, incomplete emptying, hesitancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

What is the gold standard investigation for BPH

A

Digital rectal exam (smooth, symmetrical but enlarged prostate)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

Describe the first line investigations for BPH

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

What are the differential diagnosis for BPH

A

Prostate cancer, urinary tract infection, prostatitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

Describe the management for BPH

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

What are the complications for BPH

A

Postural hypotension (tamsulosin), sexual dysfunction (reduced testosterone from finasteride), retrograde ejaculation from TURP, UTI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

Describe the epidemiology of pyelonephritis

A

Females

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

Define pyelonephritis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

Describe the aetiology of pyelonephritis

A

KEEPS infection: klebsiella, enterococcus, E. coli (most common), proteus, s. saprophyticus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

What are the risk factors for pyelonephritis

A

Female (shorter urethra, urethra near anus), urinary stasis (BPH, stones, cancer), vesicoureteral reflux, instrumentation (catheter)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

Describe the pathophysiology for pyelonephritis

A

Pyelonephritis is a complicated UTI as the infection spreads beyond the bladder and urethra to the kidneys and causes damage. Lower UTIs are uncomplicated.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

What are the key presentations for pyelonephritis

A

Triad of loin pain, fever and pyuria (urine WBC). Nausea and vomiting. Urgency, frequency, dysuria, suprapubic pain.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

Describe the clinical manifestations for pyelonephritis

A

Symptoms: Back pain, headache, nausea and vomiting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

What is the gold standard investigation for pyelonephritis

A

Mid-stream urine microscopy and cultures (confirm UTI and identify pathogen)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

Describe the first line investigations for pyelonephritis

A

1st line: Urine dipstick (leucocytes, nitrites, maybe haematuria), FBC (raised WCC, CRP)

Other: urgent USS to detect stones, obstruction, incomplete emptying

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

What are the differential diagnosis for pyelonephritis

A

Lower urinary tract infection, cystitis, prostatitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

Describe the management for pyelonephritis

A

1st line – analgesia, antibiotics (ciprofloxacin, co-amoxiclav)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

Describe the complications for pyelonephritis

A

Renal failure, need for catheterisation, renal parenchyma scarring

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

Define cystitis

A

Lower urinary tract infection causing inflammation of the bladder due to infection, most commonly by enteropathogenic E. coli.

99
Q

Describe the epidemiology of cystitis

A

Females (shorter urethra, urethra close to bladder).

100
Q

Describe the aetiology of cystitis

A

KEEPS infection: Klebsiella, enterococci, E. coli, proteus, s. saprophyticus

101
Q

What are the risk factors for cystitis

A

Female (shorter urethra, urethra near anus), urinary stasis (BPH, stones, cancer), frequent sexual intercourse, instrumentation (catheter), bladder lining damage

102
Q

What are the key presentations for cystitis

A

Suprapubic pain, dysuria, frequency, urgency, haematuria and polyuria, confusion in elderly

103
Q

What are the gold standard investigations for cystitis

A

Mid-stream urine microscopy and cultures (confirm UTI and identify pathogen)

104
Q

Describe the first line investigations for cystitis

A

Urine dipstick (leucocytes, nitrites, blood)

105
Q

What are the differential diagnosis for cystitis

A

Upper urinary tract infection (pyelonephritis), urethritis, cervicitis

106
Q

Describe the management for cystitis

A

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
Q

Describe the complications for cystitis

A

Renal infection, sepsis

108
Q

Define prostatitis

A

Lower urinary tract infection caused by inflammation of the prostate. Usually caused by E. coli

109
Q

Describe the aetiology of prostatitis

A

KEEPS infection: klebsiella, enterococci, e. coli (mc), proteus, s. saprophyticus

110
Q

What are the risk factors for prostatitis

A

Benign prostatic enlargement, urinary tract obstruction (stones), catheter, immunosuppression

111
Q

What are the key presentations for prostatitis

A

LUTS – dysuria, frequency, urgency, diminished stream. Fever, chills, malaise. Pelvic pain (suprapubic, perineum, genitalia). Tender and enlarged prostate

112
Q

Describe the clinical manifestations for prostatitis

A

Sexual dysfunction, pain with bowel movements

113
Q

What are the gold standard investigations for prostatitis

A

Mid-stream urine microscopy and cultures (confirm UTI and identify pathogen)

114
Q

Describe the first line investigations for prostatitis

A

Urine dipstick (leucocytes, nitrites)

115
Q

What are the differential diagnosis for prostatitis

A

Benign prostatic hyperplasia, prostate cancer, UTI

116
Q

Describe the management for prostatitis

A

1st line – levofloxacin, ofloxacin or trimethoprim. Also analgesia (NSAIDs)
Signs of sepsis – piperacillin/tazobactam, cephalosporins

117
Q

What are the complications for prostatitis

A

Sepsis, urinary retention, prostate abscess, chronic prostatitis

118
Q

Define urethritis

A

Lower urinary tract infection causing inflammation of the urethra. Usually a sexually acquired condition through chlamydia trachomatis (mc) or Neisseria gonorrhoea (lc)

119
Q

Describe the aetiology of urethritis

A

Non-gonococcal (chlamydia trachomatis) > gonococcal. Also, trauma, urethral stricture, urinary stones.Neisseria gonorrhea

120
Q

What are the risk factors for urethritis

A

Unprotected sex, MSM, female (shorter urethra, urethra close to anus)

121
Q

What are the key presentations for urethritis

A

Urethral discharge (blood/pus), dysuria, urethral pain, penile pain/itching

122
Q

What is the gold standard investigation for urethritis

A

urethral discharge gram stain (raised polymorphonuclear leucocytes confirms urethritis, presence of gram neg cocci = gonorrhoea)

123
Q

Describe the first line investigations for urethritis

A

1st line urine dipstick (leucocytes), Mid-stream urine microscopy and culture (detect pathogen), Nucleic acid amplification test – detect STI (chlamydia/gonorrhoea)

124
Q

What are the differential diagnosis for urethritis

A

Urinary tract infection, vaginitis, prostatitis

125
Q

Describe the management for urethritis

A

Neisseria gonorrhoea = 1g IM ceftriaxone +1g azithromycin
Chlamydia trichomatis = 100mg doxycycline or azithromycin

126
Q

What are the complications for urethritis

A

Reactive arthritis = triad of conjunctivitis, urethritis, and arthritis (can’t see, can’t pee, can’t climb a tree)

127
Q

Define nephritic syndrome (glumerulonephritis)

A

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
Q

Describe the aetiology of nephritic syndrome

A

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
Q

Describe the pathophysiology of nephritic syndrome

A

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
Q

What are the key presentations for nephritic syndrome

A

Visible haematuria, proteinuria, hypertension, oedema (peripheral, pulmonary), oliguria (low urine output), uraemic signs

131
Q

Describe the clinical manifestations for nephritic syndrome

A

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
Q

What are the first line investigations for nephritic syndrome

A

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
Q

What is the gold standard investigation for nephritic syndrome

A

Renal biopsy (crescent shaped glomeruli, Ig deposits, glomerulosclerosis)

134
Q

Describe the differential diagnosis for nephritic syndrome

A

Nephrolithiasis, renal cancer, bladder cancer

135
Q

Describe the management for nephritic syndrome

A

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
Q

What are the complications for nephritic syndrome

A

Acute kidney injury, hypertension, cardiovascular disease, hypercholesterolaemia

137
Q

Define nephrotic syndrome

A

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
Q

Describe the aetiology of nephrotic syndrome

A

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
Q

Describe the pathophysiology of nephrotic syndrome

A

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
Q

What are the key presentations for nephrotic syndrome

A

Proteinuria (>3.5g/24hrs): frothy urine, infection. Hypoalbuminemia (<30g/L). Peripheral oedema. Hypercholesterolaemia (xanthelasma – eyes, xanthomata – joints). Haematuria

141
Q

Describe the clinical manifestations for nephrotic syndrome

A

Signs: Hypercoagulable state, hypogammaglobulinemia, hypertension, thrombosis, hyperlipidaemia
Symptoms: Fatigue, dyspnoea

142
Q

What is the gold standard investigation for nephrotic syndrome

A

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
Q

Describe the first line investigations for nephrotic syndrome

A

1st line Bloods: U&E, FBC, CRP, LFT. Mid-stream urinalysis and urine dipstick (proteinuria/haematuria, infection). Kidney USS.

144
Q

What are the differential diagnosis for nephrotic syndrome

A

Minimal change disease, membranous glomerulonephritis, focal segmental glomerulosclerosis, diabetic nephropathy, nephritic syndrome causes

145
Q

Describe the management for nephrotic syndrome

A

Treat underlying cause – 12 weeks corticosteroids (prednisolone)
Treat complications – oedema (low salt and protein intake, diuretics), hyperlipidaemia (statins), hypercoagulable state (anticoagulants), infection (antibiotics)

146
Q

Describe the complications for nephrotic syndrome

A

Chronic kidney disease, end-stage liver failure, hypovolaemia, thrombosis, infection

147
Q

Define polycystic kidney disease

A

Inherited disease where multiple fluid-filled cysts form within the kidneys. Two types – autosomal dominant (mc) and autosomal recessive

148
Q

Describe the aetiology of polycystic kidney disease

A

Autosomal dominant: PKD-1 chromosome 16 (85%). PKD-2 chromosome 4 (15%)
Autosomal recessive: gene on chromosome 6

149
Q

What are the risk factors for polycystic disease

A

Family history of PKD or cerebrovascular events

150
Q

Describe the pathophysiology of polycystic kidney disease

A

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
Q

What are the key presentations for polycystic kidney disease

A

Painless haematuria. Hypertension, bilateral abdominal/flank pain, headaches, LUTS (dysuria, urgency, pain), palpable kidneys

152
Q

Describe the clinical manifestations for polycystic kidney disease

A

Signs: Extra-renal manifestations: cerebral aneurysms (berry), hepatic splenic pancreatic ovarian and prostatic cysts, cardiac murmur, abdominal hernia, hepatomegaly

153
Q

What is the gold standard investigation for polycystic kidney disease

A

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
Q

Describe the further investigations for polycystic kidney disease

A

Genetic testing, urinalysis (albuminuria, haematuria, proteinuria, bacteriuria)

155
Q

What are the differential diagnosis for polycystic kidney disease

A

Acquired renal cystic disease, tuberous sclerosis, von Hippel-Lindau

156
Q

Describe the management for polycystic kidney disease

A

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
Q

Describe the complications for polycystic kidney disease

A

Berry aneurysm rupture > subarachnoid haemorrhage, cysts on other organs, left ventricular hypertrophy, end-stage renal failure, cardiovascular disease

158
Q

Define epididymal cyst

A

Smooth extra testicular cyst at the top of the testicle (epididymis). Contains clear and milky fluid

159
Q

Describe the epidemiology for epididymal cysts

A

Middle-aged men

160
Q

What are the key presentations for epididymal cysts

A

Contains clear and milky fluid, pain, transilluminates (fluid filled), soft round lump at top of testicle, palpated separate to testicle

161
Q

What is the gold standard investigation for epididymal cyst

A

USS scrotum

162
Q

What are the differential diagnosis for epididymal cysts

A

Hydrocele, variocele, testicular cancer

163
Q

Describe the management for epididymal cysts

A

No treatment. Surgical removal if causing pain

164
Q

Define hydrocele

A

Abnormal collection of fluid in the tunica vaginalis which surrounds the testis.

Simple: overproduction of fluid
Communicating: peritoneal fluid and scrotum are connected

165
Q

Describe the aetiology of hydrocele

A

Idiopathic or secondary to: testicular torsion, testicular cancer, epididymo-orchitis, trauma

166
Q

What are the key presentations for hydrocele

A

Non-tender smooth scrotal swelling. Painless unless infected. Transilluminates. No bowel sounds (not a hernia)

167
Q

What is the gold standard investigation for hydrocele

A

Clinical diagnosis, USS scrotum

168
Q

What are the differential diagnosis for hydrocele

A

Testicular cancer, variocele, inguinal hernia

169
Q

Describe the mangement for hydrocele

A

Observation or surgery/aspiration for larger symptomatic hydroceles

170
Q

Define variocele

A

Abnormal dilation of testicular veins in pampiniform venous plexus

171
Q

Describe the aetiology for variocele

A

Increased resistance in testicular vein, incompetent valves in testicular vein causing reflux

172
Q

Describe the pathophysiology for variocele

A

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

173
Q

What are the key presentations for variocele

A

Scrotal mass that feels like a bag of worms, dragging, heaviness of scrotum, throbbing/dull pain, worse on standing

174
Q

Describe the first line investigations for variocele

A

Clinical diagnosis

175
Q

Describe the further investigations for variocele

A

USS with doppler, semen analysis for fertility, hormone tests for testicular function

176
Q

What are the differential diagnosis for variocele

A

Testicular mass, hydrocele, inguinal hernia

177
Q

Describe the management for variocele

A

1st line – observation or surgical repair if there is pain, infertility, or atrophy

178
Q

What are the complications for variocele

A

Infertility, testicular atrophy

179
Q

Define testicular torsion

A

Twisting of the spermatic cord with rotation of the testis. Urological emergency.

180
Q

Describe the epidemiology for testicular torsion

A

Teenage boy

181
Q

What are the risk factors for testicular torsion

A

Bell clapper deformity (horizontal lie of testicles)

182
Q

Describe the pathophysiology for testicular torsion

A

Torsion causes occlusion of testicular artery which leads to ischaemia, necrosis, gangrene

183
Q

What are the key presentations for testicular torsion

A

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

184
Q

Describe the clinical manifestations for testicular torsion

A

Symptoms: Abdominal pain, nausea and vomiting

185
Q

What is the gold standard investigation for testicular torsion

A

Scrotal ultrasound (whirlpool sign – spiral appearance of spermatic cord and blood vessels)

186
Q

What are the differential diagnosis for testicular torsion

A

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

186
Q

Describe the first line investigations for testicular torsion

A

Immediate surgical exploration if there is increased risk

187
Q

Describe the management for testicular torsion

A

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

188
Q

Describe the complications for testicular torsion

A

Ischaemia, necrosis, sub/infertility, loss of testicle

189
Q

Define obstructive uropathy

A

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.

190
Q

Describe the aetiology for obstructive uropathy

A

Renal stones, benign prostatic hypertrophy

191
Q

Describe the pathophysiology for obstructive uropathy

A

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

192
Q

What are the key presentations for obstructive uropathy

A

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.

193
Q

Describe the first line investigations for obstructive uropathy

A

Urinary dipstick, renal USS, urea and creatinine, FBC

194
Q

Describe the management for obstructive uropathy

A

1st line – relieving pressure on kidneys: urethral catheter, ureteric stent, nephrostomy tube.
Treat underling cause: renal stones, benign prostatic hypertrophy. Treat infection

195
Q

Define Von Hippel-Lindau

A

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

196
Q

Describe the clinical manifestations for Von Hippel-Lindau

A

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
197
Q

Describe the management for Von Hippel-Lindau

A

Depends on lesion type

e.g. surgical removal for RCC or laser treatment for haemangioblastomas in the eye

198
Q

Define incontinence

A

Urinary incontinence is a problem where the process of urination, also called micturition, happens involuntarily. There are 2 types of incontinence, urge and stress.

199
Q

Define urge continence

A

Overactive bladder due to uninhibited detrusor muscle

200
Q

Define stress incontinence

A

Urine leaks out due to high abdominal pressure

201
Q

Describe the risk factors for incontinence

A
  • 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
202
Q

Describe the management for incontinence

A

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.

203
Q

Define chlamydia

A

Sexually transmitted infection caused by chlamydia trachomatis - gram negative bacteria. Most common STI in UK

204
Q

Describe the pathophysiology for chlamydia

A

Intracellular organism - enters and replicates in cells before rupturing the cell and spreading to others.

204
Q

Describe the risk factors for chlamydia

A

Young, sexually active, having multiple partners, unprotected sex

204
Q

Describe the aetiology of chlamydia

A

Chlamydia trachomatis

205
Q

What are the key presentations for chlamydia

A

Asymptomatic.
Women: abnormal vaginal discharge (yellow, cloudy), vaginal bleeding, cervical inflammation, painful sex and urination
Men: penis discharge, painful urination

206
Q

What is the gold standard investigation for chlamydia

A

Nucleic acid amplification test (NAAT) – swabs check directly for DNA or RNA of organism (swabs: endocervical, vulvovaginal, first-catch urine sample, urethral in men)

207
Q

Describe the management for chlamydia

A

1st line – doxycycline 100mg twice a day for 7 days. Doxycycline contraindicated in pregnancy and breastfeeding, instead use: clarithromycin, azithromycin, amoxicillin

208
Q

Describe the complications for chlamydia

A

Infertility, pelvic inflammatory disease, ectopic pregnancy

209
Q

Define epididymo-orchitis (UTI)

A

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)

210
Q

Describe the epidemiology of epididymo-orchitis (UTI)

A

STI in < 35, E.coli in>35

211
Q

Describe the aetiology for UTIs

A

E.coli, Neisseria gonorrhoea, chlamydia trachomatis, mumps

212
Q

Describe the risk factors for UTIs

A

Unprotected sex, bladder outflow obstruction (stones, BPH), catheter

213
Q

What are the key presentations for epididymo-orchitis (UTI)

A

Gradual onset unilateral scrotal pain and swelling, pain relieved with elevated testis (Prehn’s sign), dragging heavy sensation

214
Q

Describe the clinical manifestations for UTIs

A

Signs: Cremaster reflex intact, urethral discharge, fever, tenderness
Symptoms: Dysuria, frequency, urgency

215
Q

What is the gold standard investigation for UTIs

A

NAAT testing, urine microscopy and cultures

216
Q

Describe the first line investigations for UTIs

A

1st line: Urine dipstick (leucocytes, nitrites, blood)

Other: USS to rule out testicular torsion

217
Q

What are the differential diagnosis for epididymo-orchitis

A

Testicular torsion, infected hydrocele, testicular tumour

217
Q

Describe the management for epididymo-orchitis

A

Neisseria gonorrhoea = 1g IM ceftriaxone +1g azithromycin
Chlamydia trichomatis = 100mg doxycycline or azithromycin
E. coli = 500mg levofloxacin

218
Q

Describe the complications for epididymo-orchitis

A

Chronic pain, infertility, testicular atrophy

219
Q

Define gonorrhoea

A

Sexually transmitted infection caused by Neisseria gonorrhoea – gram negative diplococcus

220
Q

Describe the aetiology for gonorrhoea

A

Neisseria gonorrhoea

221
Q

Describe the risk factors for gonorrhoea

A

Young, sexually active, having multiple partners, unprotected sex

222
Q

Describe the pathophysiology for gonorrhoea

A

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.

223
Q

What are the key presentations for gonorrhoea

A

Women: odourless purulent discharge (green/yellow), painful urination, pelvic pain
Men: odourless purulent discharge (green/yellow), painful urination, testicular pain or swelling (epididymo-orchitis)

224
Q

What is the gold standard investigation for gonorrhoea

A

Nucleic acid amplification test (NAAT) – checks for RNA or DNA of organism. Swabs: endocervical, vulvovaginal, first-catch urine, urethral (men)

225
Q

Describe the first line investigations for gonorrhoea

A

Charcoal swab for microscopy, culture and antibiotic sensitivities

226
Q

Describe the management for gonorrhoea

A

1st line – IM ceftriaxone (cephalosporin) 1g if sensitivities are not known. Oral ciprofloxacin 500mg if sensitivities are known.

227
Q

Describe the complications for gonorrhoea

A

Pelvic inflammatory disease, infertility, ectopic pregnancy, disseminated gonococcal infection (spread to skin and joints)

228
Q

Define LUTS

A

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

229
Q

Describe the epidemiology of incontinence and retention

A

Incontinence – women. Retention - men

230
Q

Describe the aetiology of incontinence and retention

A

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)

230
Q

What are the key presentations for LUTS

A

Lower urinary tract symptoms:
* Storage: frequency, urgency, nocturia, incontinence
* Voiding: poor stream, hesitancy, incomplete emptying, dribbling

231
Q

What are the red flag LUTS

A

Red flags: dysuria and haematuria

232
Q

Describe the management for LUTS

A

Incontinence: stress – surgery (tension free vaginal tape or urethral bulking injections), urge – anticholinergic medication (oxybutynin, tolterodine, solifenacin)
Retention: catheterisation

232
Q

Define syphilis

A

Sexually transmitted infection caused by Treponema pallidum – spirochaete bacterium which gets through skin and mucous membranes

233
Q

Describe the aetiology of syphilis

A

Treponema pallidum

234
Q

Describe the risk factors for syphilis

A

Young, sexually active, having multiple partners, unprotected sex, IVDU

235
Q

Describe the pathophysiology for syphilis

A

Spirochaete bacteria which gets through skin and mucous membranes, replicates then disseminates throughout the body. Transmission: sex, vertical transmission, IVDU, blood transfusions

236
Q

What are the key presentations for syphilis

A

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

237
Q

What is the gold standard investigation for syphilis

A

Antibody testing for T. pallidum: dark field microscopy, serum treponema assay/agglutination, or PCR

238
Q

Describe the management for syphilis

A

1st line – IM benzathine benzylpenicillin. Penicillin allergy: Ceftriaxone, amoxicillin and doxycycline (contraindicated in pregnancy/breastfeeding)

239
Q

Describe the complications for syphilis

A

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

Conditions (9 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions