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(SG) condensed phase 2a > Genitourinary > Flashcards

Genitourinary Flashcards

1
Q

Define urinary tract stones

A

Calculi form that cause symptoms by blocking and abrasing structures.

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2
Q

Types of urinary tract stones

A

Renal.

Bladder.

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3
Q

How do urinary tract stones clinically present?

A

Many asymptomatic.

Haematuria possible.

Renal colic: Sudden, severe pain in the loin -> groin.

More painful if the stone is moving. They tend to writhe around in agony rather than lie still.

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4
Q

Urinary tract stones - bladder - note

A

5% of UT stones.

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5
Q

Pathophysiology of urinary tract stones - renal

A

Formed when the urine is super saturated with salt and minerals (calcium oxalate, calcium phosphate, magnesium ammonium phosphate (struvite), uric acid and cystine).

Additionally, calcium oxalate precipitates form in the basement membrane of loops of henle -> (Randall’s plaque) in the renal papillae -> Develops into a stone.

Renal colic: Caused by the stones in the kidney, renal pelvis or ureter causing dilatation, stretching and spasm of the ureter.

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6
Q

Pathophysiology of urinary tract stones - bladder

A

Most commonly, urinary stasis due to failure of optimal emptying -> Precipitation.

Consider in women with UTI.

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7
Q

Cause of urinary tract stones - renal

A

Calcium: Hypercalcaemia. Excessive dietary calcium.

Excessive bone resorption (long term immobilisation).

Uric acid: Hyperuricaemia (possibly with gout)

Cystine stones: Cystinuria (autosomal recessive)

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8
Q

Cause of urinary tract stones - bladder

A

Usually occur because of foreign bodies, obstruction or infection.

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9
Q

Epidemiology of urinary tract stones - renal

A

Common.

10% lifetime incidence.

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10
Q

Diagnostic test for urinary tract stones

A

Midstream urine culture.

CT is gold standard.

Chemical analysis of passed stones to determine composition.

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11
Q

Treatment of urinary tract stones

A

NSAIDs (diclofenac) for pain.

Allow stones to pass spontaneously.

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12
Q

Complications of urinary tract stones

A

Irreversible renal damage.

Long term blockage -> Sepsis.

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13
Q

Sequelae of urinary tract stones

A

Recurrence.

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14
Q

Define acute kidney injury

A

Rapid deterioration of renal function.

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15
Q

Define chronic kidney disease

A

Longterm,

usually progressive impairment of kidney function (>3 months of evidence of kidney damage).

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16
Q

How does acute kidney injury clinically present?

A

Oliguria common.

Anuria possible.

Nausea, vomiting.

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17
Q

How does chronic kidney disease clinically present?

A

Anaemia: Pallor, lethargy.

CNS: Confusion, coma (severe)

CVS: Hypertension

Renal: Nocturia, polyuria, haematuria(?)

Renal osteodystrophy: Osteomalacia, bone pain, hyperparathyroidism

Skin: Pruritus

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18
Q

Pathophysiology of acute kidney injury

A

Prerenal: Impaired perfusion of the kidneys.

Kidneys require adequate perfusion to maintain glomerular filtration

Renal: Damage to kidney apparatus impairs ability to function

Postrenal: Urinary outflow obstructed

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19
Q

Pathophysiology of chronic kidney disease

A

Anaemia: Reduced erythropoietin production and increased blood loss.

Bone disease: Renal phosphate retention and impaired production of 1,25 - dihydroxyvitamin D -> Fall in serum calcium concentration -> Compensatory release of PTH -> Sustained skeletal decalcification.

Neuro: Peripheral paraesthesiae and weakness.

Advanced uraemia -> depressed cerebral function, myotonic twitching and fits.

Median nerve compression caused by amyloidosis.

CVS: Increased frequency of hypertension, dyslipidaemia and vascular calcification

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20
Q

Cause of acute kidney injury

A

Prerenal: Volume depletion (vomiting/diarrhoea), hypotension, cardiac failure

Renal: Glomerular disease, tubular injury, nephritis (NSAIDs), vascular disease

Postrenal: Calculus, urethral stricture

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21
Q

Cause of chronic kidney disease

A

Various.

Congenital: Polycystic kidney disease, tuberous sclerosis

Renal: Glomerular disease, urinary tract obstruction

CVS: Hypertension, arteriopathic renal disease

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22
Q

Epidemiology of acute kidney injury

A

15% of adults admitted to hospital develop AKI.

More common in elderly.

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23
Q

Epidemiology of chronic kidney disease

A

Common (varying severity).

Increases with age.

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24
Q

Diagnostic test for acute kidney injury

A

Serial serum creatinine readings: Acute rise.

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25
Q

Diagnostic test for chronic kidney disease

A

Bloods: Normochromic, normocytic anaemia. Serum calcium, phosphate and uric acid.

GFR: Assess renal function

Renal ultrasound: Check for damage.

Dipstick: Haematuria, proteinuria

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26
Q

Treatment of acute kidney injury

A

Conservative.

Treat underlying cause.

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27
Q

Treatment of chronic kidney disease

A

Renoprotection: Maintain blood pressure at less than 120/80 mmHg (antihypertensive)

Bone: Vitamin D supplements, bisphosphonates

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28
Q

Complications of acute kidney injury

A

Volume overload.

Metabolic acidosis.

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29
Q

Complications of chronic kidney disease

A

Hypertension,

renal osteodystrophy,

uraemic encephalopathy,

dialysis amyloid deposition.

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30
Q

Define nephritic syndrome

A

Inflammation of the kidney.

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31
Q

Define nephrotic syndrome

A

Oedema and loss of protein due to increased glomerular permeability.

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32
Q

Define minimal change disease

A

Loss of podocyte foot processes,

vacuolation

and appearance of microvilli in the glomerulus.

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33
Q

How does nephritic syndrome clinically present?

A

Haematuria,

proteinuria (slight),

hypertension,

low urine volume,

uraemia,

can occur 1-3 weeks after strep infection

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34
Q

How does nephrotic syndrome clinically present?

A

Proteinurea,

hypoalbuminaemia,

oedema,

hyperlipidemia.

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35
Q

How does minimal change disease clinically present?

A

Presents as nephrotic syndrome.

Proteinurea,

hypoalbuminaemia,

oedema,

hyperlipidemia.

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36
Q

Nephritic syndrome - note

A

Loss of a lot of blood

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37
Q

Nephrotic syndrome - note

A

Loss of a lot of protein

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38
Q

Minimal change disease - note

A

Named since minimal change can be seen under a light microscope.

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39
Q

Pathophysiology of nephritic syndrome

A

Inflammation

-> Podocytes develop large pores,

which allows blood to flow into the urine.

Red cell casts; characteristic.

Low renal function -> Low urine volume

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40
Q

Pathophysiology of nephrotic syndrome

A

Gaps in podocytes allow proteins to leak into urine.

Albumin lost

  • > hypoalbuminemia
  • > decreased intravascular oncotic pressure
  • > fluid moves into surrounding tissue causing oedema.

Additionally, hypoalbuminema

  • > liver compensation
  • > (s/e) increased lipid production
  • > hyperlipidemia.
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41
Q

Pathophysiology of minimal change disease

A

Three hallmarks:

Diffuse loss of podocyte foot processes,

Vacuolation

and Appearance of microvilli.

Podocyte losses may account for proteinuria.

Considered idiopathic.

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42
Q

Causes of nephritic syndrome

A

Inflammation of the glomerulus.

Streptococcus, viral infection, parasitic infection ->

antigen becomes trapped in the glomerulus.

Any of above.

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43
Q

Causes of nephrotic syndrome

A

Primary renal disease: Minimal change disease

Secondary: Diabetes, toxins, SLE.

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44
Q

Cause of minimal change disease

A

Unknown

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45
Q

Epidemiology of nephrotic syndrome

A

Mainly adults.

Twice as common in men.

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46
Q

Epidemiology of minimal change disease

A

Accounts for 80% of all nephrotic syndrome in children, and 20% in adults.

Peak incidence 2-3 years.

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47
Q

Diagnostic test for nephritic syndrome

A

Urine dipstick

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48
Q

Diagnostic test for nephrotic syndrome

A

Urine dipstick

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49
Q

Diagnostic test for minimal change disease

A

Light microscope - no change

Electron microscope of biopsy - abnormal podocytes.

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50
Q

Treatment of nephritic syndrome

A

Treat underlying disease.

Allow spontaneous recovery.

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51
Q

Treatment of nephrotic syndrome

A

Treat underlying disease.

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52
Q

Treatment of minimal change disease

A

Supportive care (reduce oedema).

Prednisolone (can halt process).

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53
Q

Complications of nephritic syndrome

A

Depends on underlying disease.

Generally; AKI,

decreased resistance to infection.

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54
Q

Complications of nephrotic syndrome

A

Depends on underlying disease

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55
Q

Complications of minimal change disease

A

Nephrotic syndrome.

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56
Q

Define polycystic kidney disease

A

Multiple renal cysts

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57
Q

Define epididymal cyst

A

Extratesticular, spherical cysts in the head of the epididymis.

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58
Q

Types of polycystic kidney disease

A

Autosomal Dominant

Autosomal Recessive

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59
Q

How does autosomal dominant polycystic kidney disease clinically present?

A

Presents at any age after 20s.

Acute loin pain (cyst haemorrhage),

abdominal discomfort,

hypertension.

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60
Q

How does autosomal recessive polycystic kidney disease clinically present?

A

Highly variable.

Presents at any age.

Consistently; renal enlargement.

Less commonly; liver disease.

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61
Q

How does an epididymal cyst clinically present?

A

Lump.

Often multiple and bilateral.

Often asymptomatic.

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62
Q

Pathophysiology of autosomal dominant polycystic kidney disease

A

PKD1 codes polycystin, an integral membrane protein which regulates tubular and vascular development in kidneys and other organs.

Cysts develop throughout both kidneys

  • > Increase in size with age
  • > Renal enlargement
  • > progressive destruction of renal tissue.
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63
Q

Pathophysiology of autosomal recessive polycystic kidney disease

A

Dilatation and elongation of renal collecting ducts

-> bilaterally enlarged and cystic kidneys.

At birth, the interstitium and the rest of the tubules are normal,

but can later develop interstitial fibrosis and tubular atropy ->

End stage kidney disease.

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64
Q

Cause of autosomal dominant polycystic kidney disease

A

Autosomal dominant.

PKD1 gene most common.

Possibly PKD2.

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65
Q

Cause of autosomal recessive polycystic kidney disease

A

Autosomal recessive.

Fibrocystin gene, responsible for tubulogenesis.

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66
Q

Cause of an epididymal cyst

A

Possibly obstruction of the epididymis.

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67
Q

Epidemiology of autosomal dominant polycystic kidney disease

A

Most common cause of inherited serious renal disease.

1/1000 individuals.

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68
Q

Epidemiology of autosomal recessive polycystic kidney disease

A

10/100,000 births.

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69
Q

Epidemiology of epididymal cyst

A

Onset at age 40.

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70
Q

Diagnostic test for autosomal dominant polycystic kidney disease

A

Examination.

Ultrasound.

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71
Q

Diagnostic test for autosomal recessive polycystic kidney disease

A

Ultrasound.

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72
Q

Diagnostic test for epididymal cyst

A

Ultrasound.

Transilluminate.

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73
Q

Treatment of autosomal dominant polycystic kidney disease

A

Control blood pressure.

Many eventually require renal replacement.

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74
Q

Treatment of autosomal recessive polycystic kidney disease

A

Nephrectomy may be necessary.

Fluid overload can be managed with diuretics and continuous renal replacement therapy.

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75
Q

Treatment of an epididymal cyst

A

Not usually necessary.

Surgical excision.

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76
Q

Complications of autosomal dominant polycystic kidney disease

A

Subarachnoid haemorrhage:

polycystin involved in the production of berry aneurysms.

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77
Q

Complications of autosomal recessive polycystic kidney disease

A

Infant death if congenital.

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78
Q

Define Hydrocele

A

Abnormal collection of fluid within the remnants of the processus vaginalis.

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79
Q

Define Varicocele

A

Abnormal dilatation of the testicular veins in the pampiniform plexus.

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80
Q

Types of Hydrocele

A

Simple

Communicating

Non-communicating

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81
Q

How does simple hydrocele clinically present?

A

Scrotal enlargement with a non-tender, smooth cystic swelling.

Anterior to and below the testis transilluminate.

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82
Q

How does communicating hydrocele clinically present?

A

As simple hydrocele.

Vacillates in size and is usually related to ambulation.

83
Q

How does varicocele clinically present?

A

Usually asymptomatic.

Scrotum feels like ‘a bag of worms’.

Side affected hangs lower.

84
Q

Pathophysiology of simple hydrocele

A

Accumulation of fluid within tunica vaginalis.

Usually disappears in the first 2 years of life.

85
Q

Pathophysiology of communicating hydrocele

A

Persistence of the processus vaginalis allows peritoneal fluid to communicate freely with the scrotal portion of the processus.

86
Q

Pathophysiology of varicocele

A

Heat generated by varicocele affects sperm quality.

Proteins required for healthy sperm are reduced.

87
Q

Causes of simple hydrocele

A

Congenital.

Trauma, testicular torsion.

Also possibly due to generalised oedema from other cause.

88
Q

Cause of communicating hydrocele

A

Congenital.

Can present in older males as a result of intra-abdominal pressure or fluid overload.

89
Q

Cause of non-communicating hydrocele

A

Imbalance between secretion and reabsorption of fluid.

Also secondary to trauma, torsion.

90
Q

Cause of varicocele

A

Venous reflux.

More common on the left, due to the angle of the left testicular vein entering the left renal vein.

Can be due to problems with the valves causing backflow of blood.

This causes swelling due to excessive pressure.

91
Q

Epidemiology of hydrocele

A

1-2% of male neonates.

92
Q

Epidemiology of varicocele

A

Incidence increases after puberty.

93
Q

Diagnostic test for hydrocele

A

Ultrasound.

Transilluminate.

94
Q

Diagnostic test for varicocele

A

Observation.

More accurate: Ultrasound.

95
Q

Treatment of hydrocele

A

Observation for first 2 years.

Surgical removal.

96
Q

Treatment of varicocele

A

If symptomatic: Surgery.

Avoid if possible; surgery can cause testicular damage.

97
Q

Complications of hydrocele

A

Infection.

Depending on underlying pathology; infertility or testicular atrophy due to trauma.

98
Q

Complications of varicocele

A

Left untreated - can cause infertility.

99
Q

Define testicular torsion

A

Torsion of the spermatic cord.

100
Q

Define benign prostatic hyperplasia

A

Increase in the size of the prostate gland without malignancy.

101
Q

How does testicular torsion clinically present?

A

Acute swelling of the scrotum.

Sudden severe pain in one testis.

Often follows sport or physical activity.

102
Q

How does benign prostatic hyperplasia clinically present?

A

Frequent urination,

incomplete emptying,

intermittent stream,

weak stream,

urgency,

nocturia

and straining (I-PSS grading).

103
Q

Pathophysiology of testicular torsion

A

Occlusion of the testicular blood vessels.

104
Q

Pathophysiology of benign prostatic hyperplasia

A

Glandular epithelial cells and stromal cells undergo hyperplasia.

Usually the median lobe is affected.

105
Q

Cause of testicular torsion

A

Trauma.

RF: High insertion of the tunica vaginalis.

106
Q

Cause of benign prostatic hyperplasia

A

Not fully known.

Assumed relationship to androgens, possibly promoting cell proliferation in the prostate.

107
Q

Epidemiology of testicular torsion

A

1/4000 males under 25.

108
Q

Epidemiology of benign prostatic hyperplasia

A

Affects QOL of 40% of men in 50s,

and 90% of men in 90s.

109
Q

Diagnostic test for testicular torsion

A

Examination is often sufficient.

110
Q

Diagnostic test for benign prostatic hyperplasia

A

History.

Ultrasound.

DRE.

111
Q

Treatment of testicular torsion

A

Reduce manually (twist).

Verify by doppler ultrasound.

112
Q

Treatment of benign prostatic hyperplasia

A

Watchful waiting.

Alpha blockers (doxazosin) to those with severe voiding problems.

5-alpha reductase inhibitor (finasteride)

Surgery: Large prostate/failure to respond.

Transurethral resection of the prostate.

113
Q

Complications of testicular torsion

A

Infarction of the affected testicle followed by atrophy

114
Q

Complications of benign prostatic hyperplasia

A

Recurrent UTI.

Bladder calculi.

115
Q

Define bladder carcinoma

A

Cancer of the bladder.

116
Q

Define renal carcinoma

A

Cancer of the kidney.

117
Q

Types of renal carcinoma

A

Renal cell carcinoma

Transitional cell carcinoma

118
Q

How does bladder carcinoma clinically present?

A

Painless haematuria.

Advanced disease may have voiding symptoms.

Classic cancer symptoms.

119
Q

How does renal carcinoma clinically present?

A

Haematuria,

abdominal mass,

lethargy,

anorexia,

weight loss,

abdo pain.

120
Q

Renal cell carcinoma - note

A

Arises from the renal tubule

121
Q

Transitional cell carcinoma - note

A

Arises from the renal pelvis

122
Q

Pathophysiology of bladder cancer

A

Arises from the transitional cells of the mucosal urothelium.

Can invade the muscle to cause voiding symptoms. Has a high propensity for metastasis.

123
Q

Pathophysiology of renal cell carcinoma

A

Can secrete PTH (hypercalcaemia),

ACTH (Cushings like syndome),

EPO (polycythaemia),

renin (HTN).

Common metastases:

Lymphoma, lung, breast, skin

124
Q

Pathophysiology of transitional cell carcinoma

A

Common metastases:

Lymphoma, lung, breast, skin.

125
Q

Cause of bladder carcinoma

A

Genetic (no specific gene).

Strong link with smoking.

Aromatic amines and polycyclic aromatic hydrocarbons (working in a dye factory) are renally excreted.

Also associated with increasing age.

126
Q

Cause of renal carcinoma

A

RF: Regular NSAID use,

obesity,

FH

127
Q

Epidemiology of bladder carcinoma

A

Smokers and dye factory workers.

128
Q

Diagnostic tests for bladder carcinoma

A

Cystoscopy: Examine for signs of tumour

Biopsy: Determine cell type, confirm diagnosis

Urine cytology: Rule out infection

129
Q

Diagnostic tests for renal carcinoma

A

IVU: Dye stains kidney -> passes into ureters.

Blurs the outline.

Ultrasonography: Solid or cystic

CT: Preoperative staging

130
Q

Treatment of bladder carcinoma

A

Non-invasive: Transurethral resection

Invasive: Cystectomy (with orthotopic bladder substitute).

Chemotherapy (cisplatin).

131
Q

Treatment of renal carcinoma

A

Surgical.

Radio/Chemo.

132
Q

Complications of bladder carcinoma

A

Urinary retention.

UTI.

Recurrence.

Metastasis.

133
Q

Define prostatic carcinoma

A

Cancer of the prostate

134
Q

Define testicular carcinoma

A

Cancer of the testicle

135
Q

Types of testicular carcinoma

A

Seminoma

Teratomas

136
Q

How does prostatic carcinoma clinically present?

A

Serum PSA elevated.

Bladder outflow obstruction (I-PSS grading).

Occasionally; presents with metastases (usually to bone).

137
Q

How does testicular carcinoma clinically present?

A

Classic cancer symptoms.

Painless lump in the testicle.

Possible mestastasis to the lung.

138
Q

Pathophysiology of prostatic carcinoma

A

Adenocarcinoma.

Androgen driven.

Mostly affects the lateral lobes (in constrast to BPH).

Can spread through lymphatics, haematogenously, local invasion.

139
Q

Pathophysiology of seminoma - type of testicular carcinoma

A

96% arise from germ cells.

140
Q

Pathophysiology of teratomas - type of testicular carcinoma

A

Composed of tissue not normally present at the site (teeth and stuff).

141
Q

Cause of prostatic carcinoma

A

Genetic (no specific gene).

Can develop from benign prostatic hyperplasia.

142
Q

Cause of testicular carcinoma

A

Unknown.

RF: Undescended testes, FH.

143
Q

Epidemiology of prostatic carcinoma

A

Most common cancer in men.

144
Q

Epidemiology of testicular carcinoma

A

Most common cancer in young men.

145
Q

Diagnostic tests for prostatic carcinoma

A

DRE: hard irregular gland.

Ultrasound.

Serum PSA: raised (markedly if metastasis).

146
Q

Diagnostic test for seminoma - type of testicular carcinoma

A

Ultrasound.

CXR/CT: Tumour staging; check metastases.

Serum conc. Of beta-hCG: Raised.

147
Q

Diagnostic test for teratomas - type of testicular carcinoma

A

No markers.

CXR/CT: Tumour staging; check metastases.

148
Q

Treatment of prostatic carcinoma

A

Microscopic: Watchful waiting

Confined to gland: Prostatectomy or radiotherapy

Metastatic: Androgen suppression (surgical/chemical castration).

149
Q

Treatment of seminoma - type of testicular carcinoma

A

Surgery: Orchidectomy (offer sperm banking).

Metastasis: Radiotherapy (Chemo if advanced).

150
Q

Treatment of teratomas - type of testicular carcinoma

A

Surgery: Orchidectomy (offer sperm banking)

Metastasis: Chemotherapy.

151
Q

Complications of prostatic carcinoma

A

Metastasis and death.

152
Q

Complications of testicular carcinoma

A

Metastasis and death.

153
Q

Define Pyelonephritis

A

Infection within the renal pelvis.

154
Q

Define Cystitis

A

Infection causing inflammation of the bladder.

155
Q

Define Prostatitis

A

Bacterial infection of the prostate gland.

156
Q

Types of Pyelonephritis

A

Acute.

Chronic.

157
Q

How does acute pyelonephritis clinically present?

A

Rapid, loin, suprapubic or back pain.

Fever, malaise, nausea, anorexia.

Possibly lower UTI, with frequent dysuria, haematuria or hesitancy.

158
Q

How does chronic pyelonephritis clinically present?

A

As acute pyelonephritis.

Failure to thrive.

Possibly hypertension.

159
Q

How does cystitis clinically present?

A

Frequent urination, urgency, dysuria.

Abdominal tenderness, swollen bladder, confusion (elderly).

160
Q

How does prostatitis clinically present?

A

Macroscopic haematuria, fever, dysuria, pyrexia.

Sharp pelvic/penile/anal pain.

161
Q

Pathophysiology of acute pyelonephritis

A

Often, infection will rise from the bladder to the renal pelvis.

Haematogenous spread also possible.

Local infection will cause inflammation and damage.

162
Q

Pathophysiology of chronic pyelonephritis

A

Chronic infection can cause characteristic scarring of the kidney.

163
Q

Pathophysiology of cystitis

A

Infection of urine stored in the bladder.

Can be ‘washed out’ with frequent fluids.

164
Q

Cause of acute pyelonephritis

A

Infection by UTI organisms (Escherischia coli, Klebsiella, Proteus, Enterococcus).

RF: Calculi, catheterisation, pregnancy, diabetes

165
Q

Cause of chronic pyelonephritis

A

As acute pyelonephritis.

Infection by UTI organisms (Escherischia coli, Klebsiella, Proteus, Enterococcus).

RF: Calculi, catheterisation, pregnancy, diabetes

166
Q

Cause of cystitis

A

Can be caused from incomplete emptying.

167
Q

Cause of prostatitis

A

Usually gram negative organisms; Escherichia coli, Enterobacter, Serratia.

Sometimes STI: Neisseria gonorrhoeaeand

Chlamydia trachomatis.

168
Q

Epidemiology of acute pyelonephritis

A

Can occur at any age.

Generally more frequent in females, except in neonates.

169
Q

Epidemiology of chronic pyelonephritis

A

4/100,000 asymptomatic adults.

170
Q

Epidemiology of cystitis

A

Very common.

171
Q

Epidemiology of prostatitis

A

15% of men experience symptoms at some point in life.

172
Q

Diagnostic test for acute pyelonephritis

A

Urine dipstick.

Urine is cloudy with an offensive smell.

Midstream culture.

173
Q

Diagnostic test for chronic pyelonephritis

A

Urine dipstick.

Midstream culture.

174
Q

Diagnostic test for cystitis

A

History.

Midstream culture.

175
Q

Diagnostic test for prostatitis

A

DRE: Gland can feel nodular, ‘boggy’, tender and hot.

176
Q

Treatment of acute pyelonephritis

A

Support.

Antibiotics, empirically.

Ciprofloxacin / co-amoxiclav first line.

177
Q

Treatment of chronic pyelonephritis

A

Blood pressure control to slow progression of renal failure.

Antibiotics, empirically.

178
Q

Treatment of cystitis

A

Often resolves without treatment.

Fluids and possibly antibiotics.

179
Q

Treatment of prostatitis

A

Antibiotics, empirically.

Quinolones, first line.

180
Q

Complications of acute pyelonephritis

A

Septicaemia,

renal abscess.

181
Q

Complications of chronic pyelonephritis

A

Septicaemia,

progressive renal scarring,

secondary hypertension.

182
Q

Complications of prostatitis

A

Chronic infection.

183
Q

Define Urethritis

A

Urethral inflammation.

184
Q

Define Epididymo-orchitis

A

Pain,

swelling

and inflammation of the epididymis.

185
Q

Types of urethritis

A

Gonococcal.

Non-gonococcal.

186
Q

How does gonococcal urethritis clinically present?

A

May be asymptomatic.

Usually is asymptomatic in women.

Urethral discharge, more noticeable after holding urine overnight.

Dysuria.

187
Q

How does non-gonococcal urethritis clinically present?

A

As gonococcal urethritis, no discharge.

188
Q

How does epididymo-orchitis clinically present?

A

Unilateral scrotal pain and swelling.

In STI: urethral discharge also.

Tenderness to palpation on affected side.

Palpable swelling.

189
Q

Pathophysiology of epididymo-orchitis

A

Most common route of infection is infection spreading from the urethra.

Second is from the bladder.

190
Q

Cause of gonococcal urethritis

A

Neisseria gonorrhoeae.

As a result of STI.

191
Q

Cause of non-gonococcal urethritis

A

Number of organisms.

Chlamydia trachomatis,

Mycoplasma genitalium most commonly.

192
Q

Cause of epididymo-orchitis

A

In men under 35, most commonly STI.

Over 35, gram negative enteric organisms.

Can also be viral.

193
Q

Epidemiology of non-gonococcal urethritis

A

Most common condition diagnosed and treated in men in genitourinary.

194
Q

Epidemiology of epididymo-orchitis

A

25/10,000 (likely dropped now).

195
Q

Diagnostic test for urethritis

A

Urethral smear.

Screen for STIs.

196
Q

Diagnostic test for epididymo-orchitis

A

Culture urethral smear.

197
Q

Treatment of gonococcal urethritis

A

Antibiotics, empirically.

Quinolones, first line.

198
Q

Treatment of non-gonococcal urethritis

A

Antibiotics.

Specifically ceftriaxone.

199
Q

Treatment of epididymo-orchitis

A

Check for torsion.

STI advice.

Empirical antibiotics if appropriate.

200
Q

Complications of gonococcal urethritis

A

Epididymitis,

prostatitis,

gonococcal arthritis.

201
Q

Complications of non-gonococcal urethritis

A

Epididymitis,

prostatitis.

202
Q

Complications of epididymo-orchitis

A

Reactive hydrocele,

abscess formation.

203
Q

Sequelae of gonococcal urethritis

A

If untreated, can remit spontaneously.

204
Q

Sequelae of non-gonococcal urethritis

A

10-20% become recurrent.

(SG) condensed phase 2a (9 decks)

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