Renal Tract Conditions Flashcards

1
Q

What is a urinary tract infection

A

Infection of the urinary tract system (bladder, urethra, kidneys), generally caused by bacteria (especially E. coli)

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2
Q

How common are UTIs

A

Lifetime incidence of UTIs in adult women is 50% to 60%

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3
Q

Who are affected by UTIs

A

Women are at high risk due to a shorter urethra and the proximity of the anal and genital regions

Prevalence increases with age with women over 65 x2 as likely as rest of female population

Children with chronic constipation

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4
Q

What causes UTIs

A

Bacteria:
Infection ascends from the urethra to the bladder and can ascend further to the ureters and the renal pelvises (pyelonephritis)
E. coli is usually the causative organism
Staph Saprophyticus is 2nd

Viral:
Immunocompromised ptx and children most susceptible
Adenovirus, cytomegalovirus and BK virus are commonly involved in haemorrhagic cystitis

Yeast:
Rare (usually Candida species)

Abacterial:
Intersitial cystitis

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5
Q

What are the risk factors for UTIs

A
Sexual intercourse
Indwelling urinary catheres
Pregnancy
Abnormalities of the urinary tract
- prevent bladder emptying 
- resulting in urinary stasis
- EG Urinary bladder diverticulum, Benign prostatic hyperplasia, congenital malformations causeing vesicoureteral reflux
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6
Q

How do UTIs present

A

Clinical findings depend on which part of the tract is affected and who is presenting

Lower:

  • Dysuria
  • Haematutia
  • Suprapubic pain
  • Urinary urgency
  • Increased urinary frequency

Upper:

  • Same symptoms as above plus the following
  • Fever
  • Flank pain
  • Fatigue/malaise
  • Nausea and vomiting

In males they may have prostatic/perineal area pain

In children:

  • Urinary incontinence
  • Malodorous urine
  • Irritability
  • Poor feeding
  • Failure to thrive

In elderly:
- Delirium/ acute confusion

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7
Q

What are potential signs on examination of those with suspected UTI

A

Pyuria (white blood cells can cause cloudiness)
Bacteriuria
Positive leukocyte esterase and nitrites on urinalysis

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8
Q

What are the differentials of UTi

A

If experiencing the fever and flank pain then take this as a sign of more serious infection eg pyelonephritis

Interstitial cystitis (painful bladder syndrome)

Asymptomatic bacteriuria

Vaginitis

Pelvic inflammatory disease

Prostatitis

Trauma

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9
Q

How would a patient with suspected UTI be investigated

A
Urinalysis
Urine culture
Imaging:
- CT without contrast
- Ultrasound
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10
Q

How would UTI be explained to the patient and what would be discussed

A

Infection of the urinary tract system (bladder, urethra, kidneys), generally caused by bacteria (especially E. coli)

Easily treatable

Pregnant women need immediate antibiotics no matter severity of symptoms

Non-pregnant women can be given antibiotics if sever symptoms or a back up prescription to take if symptoms do not start to improve within 48 hours or if they worsen

Self-care:

  • Drink enough fluids to not feel thirsty
  • Take paracetamol or ibuprofen for pain relief

Safety net:

  • Call healthcare services if
    • Shivering, chills muscle pain
    • Confusion, or drowsiness
    • No urine passed in 24hrs
    • Vomitting
    • Blood in urine
    • Temp high (>38) or low (<36)
    • Kidney pain in back or under ribs
    • Worsening UTI symptoms
    • No improvement after 48hours of antibiotics
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11
Q

What is the treatment for a UTI

A

First-line empiric antibiotic therapy for uncomplicated UTIs includes outpatient therapy with oral trimethoprim-sulfamethoxazole, nitrofurantoin or fosfomycin for up to 7 days

For complicated UTIs antibiotic therapy should be extended for 7-14 days

Pregnant women with cystitis should be screened and treated if positive for asymptomatic bacteriuria

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12
Q

What is pyelonephritis

A

A severe infectious inflammatory disease of the renal parenchyma, calcices and pelvis that can be acute, recurrent or chronic.

Refers specificaly to infections in the kidney

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13
Q

Who is affected by pyelonephritis

A

Hospitalisation as a result of acute is 5x more common in women than men however women show a much lower mortality rate.

Complicated acute pyelonephritis tends to occur in med, older people, pregnant women and those with underlying anatomical or physiological abnormalities, immunosuppression, obstruction, catheteriation, incorrect abx selection and usage and resistant organisms

Slightly more than 20% of renal transplant patients suffer from acute pyelonephritis within 2 months of surgery.

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14
Q

What causes pyelonephritis

A

Acute:
- Enteric bacteria (eg E coli) that ascend from the lower urinary tract or that spread haematogenously to the kidney

Complicated infections can result from:

  • Underlying medical problems (eg diabetes, HIV)
  • Genitourinary anatomical abnormalities
  • Obstruction (eg benign prostatic hypertrophy, calculi)
  • Multi-drug-resistant pathogens
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15
Q

What are the risk factors for pyelonephritis

A

Strong:

  • UTI
  • Diabetes
  • Stress incontinence
  • Foreign body in urinary tract (eg calculus, catheter)
  • Anatomical/ functional urinary abnormality
  • Immunosuppressive state
  • Pregnancy
  • Frequent sexual intercourse

Weak:

  • Maternal family history of UTI
  • New sex partner
  • Spermicide use
  • Age between 18 and 50 years
  • Age >60years
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16
Q

How does pyelonephritis present

A
Fever
Presence of risk factors 
Nausea and vomiting
Dysuria, frequency, or urgency
Flank pain or costovertebral angle tenderness
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17
Q

Which other conditions present similarly to pyelonephritis

A

Chronic vs acute pyelonphritis

Pelvic inflammatory disease

Pelvic pain syndrome

Cystitis

Acute prostatitis

Lower lobe pneumonia

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18
Q

How is suspected pyelonephritis investigated

A

1st line investigations:

  • urinalysis
  • gram stain
  • urine culture
  • full blood count
  • erythrocyte sedimentation rate
  • CRP
  • procalcitonin
  • blood culture

Investigations to consider:

  • renal ultrasound
  • contrast enhanced spiral computed tomography
  • magnetic resonance imaging

Emerrging tests:

  • interleukin
  • copeptin
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19
Q

How would pyelonephritis be discussed with patient

A

If taken abx then follow and complete regimen so recurrent infection is prevented

Should be aware and alert their doctor of concerning symproms such as fever or flank pain

If pregnant, UTI may ascend to the kidney and may be sever so important to seek routine antenatal testing and treatment in such situations

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20
Q

How is pyelonephritis treated

A

Goals of treatment are infection control and symptom reduction

Indications for hospitalisation:

  • Inability to maintain oral hydration or adherence to meds regimen
  • Hypotension
  • Vomiting
  • Dehydration
  • Sepsis
  • High WBC count
  • Temp >39
  • Severly ill with multiple comorbidities
  • Pregnancy
  • Uncertain about diagnosis
  • Older and/or immunocompromised

Start abx before results of blood or urine cultures are returned in order to prevent ptx deterioration

Mild to moderate and uncomplicated pyelonephritis:

  • Oral antibiotics:
    • Fluoroquinolones
    • Cephalosporins
    • Sulphonamides

Severe and complicated pyelonephritis and pregnant ptx:

  • hospitalisation and treatment with IV agents
  • Choice of abx regimen based on blood/urine cultures and localised resistence patterns
  • Possible regimens:
    • Fluoroquinolones
    • Extended spectrum cephalosporins
    • Aminoglycosides with or without ampicillin
    • Aminopenicillins
    • Antipseudomonal penicillins
    • Carbapenems
  • Two week course of IV abx often sufficient
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21
Q

What is the prognosis of pyelonephritis

A

Complications:

  • obstruction requiring catheterisation
  • spesis
  • renal failure
  • abscess formation
  • antibiotic failure

Recurrence:

  • Usually occurs within 1-2 weeks
  • Most likely cause is insufficient duration of initial treatment
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22
Q

What is hydronephrosis

A

Swelling of a kidney due to a build up of urine. It happens when urine cannot drain out from the kidney to the bladder froma blockage or obstruction. Can occur in one or both kidneys

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23
Q

How common is hydronephrosis

A

Prevalence in general population is 0.15% to 0.67%

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24
Q

What causes hydronephrosis

A

Usually caused by another underlying illness or risk factor:

  • Kidney stone
  • Congenital blockage
  • Blood clot
  • Scarring of tissue due to injury or previous surgery
  • Tumor or cancer (bladder, cervical, colon, or prostate)
  • BPH
  • Pregnancy
  • UTI
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25
Q

What are the risk factors for hydronephrosis

A

Renal calculi
External compression from abdominal and pelvic masses and tumors
Diabetes
Neurogenic bladder
Congenital anomalies of kidneys and urinary tract

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26
Q

How does hydronephrosis present

A

Pain in back or side (may be sudden and sever or may be a dull ache that comes and goes over time) (may get worse after drinking lots of fluid)

UTI symptoms

Haematuria

Decrease in urinary frequency or with a weaker stream

Does not tend to cause symptoms in babies

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27
Q

What are the differential diagnoses for hydronephrosis

A

Renal sinus cysts
Extrarenal pelvis
Pseudohydronephrosis

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28
Q

How is suspected hydronephrosis investigated

A
Ultrasound usualling confirms diagnosis
Can also use Xray, CT or MRI
Cystoscopy
FBC
U and E
CRP
LFT
Urinalysis
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29
Q

How is hydronephrosis treated

A

Address underlying cause

Abx for any infection cause

May require surgery to remove any kidney stones

Catheterisation in cases of sever blockage or nephrostomy bag to drain urine directly from kidney

Key to treatment is address issue asap to avoid any permanent damage to kidneys

Can lead to kidney failure in severe cases in which case will need dialysis or kidney transplant, however most people recover from hydronephrosis if treated promptly.

30
Q

What is acute kidney injury

A

An acute decline in kideny function, leading to a rise in serum creatinine and/or a fall in urine output

It is a specturm from milf kidney injury to severe kidney failure

31
Q

How common is acute kidney injury

A

Estimated to be 10400 per million population in UK

Seen in 10-20% people admitted to hospital as emergencies with an inpatient mortality of >20%

32
Q

What are the causes of AKI for each type

A

Prerenal:
Any condition leading to decreased renal perfusion
- Hypovolaemia
- Hypotension
- Renal artery stenosis
- Drugs affecting glomerular perfusion (NSAIDs, ACE inhibitors, cyclosporin)

Intrinsic:
Any disease that leads to sever direct kidney damage
- Acute tubular necrosis (most comonly caused by sepsis, infection, ischemia or nephrotoxins)
- Glomerulonephritis
- Vascular (haemolytic uremic syndrome, vasculitis, malignant hypertension, thrombotic thrombocytopenic purpura)
- Acute tubulointerstitial nephritis (drug-induced, infectious, immunologica)

Postrenal:
Any condition that results in bilateral obstruction of urinary flow from the renal pelvis to the urethra
-Congenital malformations
-Acquired obstructions (benign prostatic hyperplasia, Tumors, stones, catheter associated injuries)
-Neurogenic bladder

33
Q

What are the risk factors for AKI

A
Strong:
Advanced age
Underlying kidney disease
Diabetes mellitus
Sepsis
Iodinated contrast
Exposure to nephrotoxins
Excessive fluid loss
Surgery
Haemorrhage
Recent vascular intervention
Cardiac arrest
Pancreatitis
Trauma
Malignant hypertension
Myeloproliferative disorders (eg multiple myeloma)
Connective tissue disease
Sodium-retaining states (eg congestive heart failure, cirrhosis, nephrotic syndrome)
Drug overdose
Nephrolithiasis
Weak:
Drug abuse
Alcohol abuse
Excessive exercise
Recent blood transfusion
Malignancy
Genetic susceptibility
Use of renin-angiotensin system inhibitors
Proton pump inhibitors
Herbal therapy
34
Q

How does AKI present

A

Usually occurs in patients with intercurrent illness, without symptoms or signs specific to the kidneys and is only diagnosed when kidney function tests are performed

May present in many different ways:

  • sepsis
  • hypotension
  • decreased urine output
  • lower UTI symptoms
  • oedema
35
Q

What are the differentials in suspected AKI

A

Chronic kidney disease
Increase muscle mass
Drug side effect

36
Q

How is suspected AKI investigated

A

1st investigation:

  • basic metabolic profile (U and E, LFT)
  • serum potassium
  • FBC
  • Bicrabonate
  • CRP
  • Blood culture
  • Urinalysis
  • Urine culture
  • Urine output monitoring
  • Fluid challenge (good response supports diagnosis of pre-renal AKI)
  • Venous blood gas
  • Chest X ray
  • ECG
37
Q

What should be discussed with AKI patients

A

Inform patient of episode of AKI, giving cause and prevention measures needed to avoid further episode

Discuss immediate treatment options, monitoring and prognosis; and long term treatment options, monitoring, self-management and support in collaboration with MDT

Info to those needing renal replacement therapy after discharge (fistula, peritoneal catheter, frequency and length of dialysis)

Discuss risk of future AKI

38
Q

How is AKI treated

A

STOP AKI anogram:

Sepsis:
- Perform urgent screening and implement local guidelines within 1 hour of suspected sepsis

Toxins:
- identify and stop any nephrotoxic drugs and nephrotoxins

Optimise volume status and blood pressure:

  • if hypovolaemic give immediate IV bolus of crystalloid
  • Withhold drugs that may exacerbate AKI (ACE inhibitors or angiotensin-II receptor antagonists
  • Consider withholding diuretics and other antihypertensive medications
  • Escalate to critical care for consideration of vasopressors if pt remains severly hypotensive

Prevent harm:

  • Identify and treat reversible causes (eg UTI)
  • Treat life threatening compliactions (hyperkalaemia and acidosis)
  • Review and modify doses of all meds in line with degree of kidney injury
39
Q

What is chronic renal failure

A

Abnormality in kidney function or structure for at least three months

40
Q

How common is chronic renal failure

A

9-13% of adults worldwide

41
Q

Who is most affected by chronic renal failure

A

Black people, Hispanic people and FH of kidney disease have higher prevalence.
Those with an episode of AKI are most likely to be at risk of CKD and end-stage kidney disease in the future.

42
Q

What causes CKD

A

Diabetic nephropathy: most common, cause accounts for 44% of cases

Hypertensive nephropathy: 28%

Glomerulonephritis: 8%

Polycystic kidney disease/ hereditary: 2%

Urological disease: 0.5%

Other causes:
Amyloidosis
Toxins
Chronic inflammation

43
Q

What are the risk factors for CKD

A

Strong:

  • Diabetes
  • Hypertension
  • Age > 50yo
  • Childhood kidney disease

Weak:

  • Smoking
  • Obesity
  • Black or Hispanic ethnicity
  • Family history of CKD
  • Autoimmune disorders
  • Male
  • Long term use of NSAIDs
  • High uric acid levels
44
Q

How does CKD present

A
Often asymptomatic until later stages
Common:
Fatigue
Oedema
Nausea w/ or without vomiting
Pruritus
Restless legs
Anorexia
Uncommon:
Foamy-appearing urine
Cola coloured urine
Rashes
Dyspnoea
Orthopnoea
Seizures
Retinopathy
45
Q

What signs may be a CKD patient have no examination

A
Hypertension
Peripheral oedema
Pulmonary oedema
Clinical features of uremia
Pigmented spots
Pruritus
Anemia
Uremic pericarditis
Pleuritis
Asterixis
Encephalopathy 
Peripheral neuropathy
GI symptoms (nausea, vomiting)
46
Q

What other conditions present similarly to CKD

A
Diabetic kidney disease
Hypertensive nephrosclerosis
Ischemic nephropathy
Obstructive uropathy
Nephrotic syndrome
Glomerulonephritis
47
Q

How is suspected CKD investigated

A

Blood tests:

  • FBC
  • U and E (compare trend of eGFR and creatinine)
  • CRP
  • Bicarbonate
  • Urine tests (dipstick, urinalysis - Protein creatinine ratio and albumin creatinine ratio to accurately measure levels of protein leakage from kidneys)

Ultrasound (size- shrunken in chronic presentation)

ECG (electrocardiogram)

Echocardiogram

Vit D is activated by kidneys and this is needed for calcium absorption so if kidneys aren’t functioning then there will be low calcium levels and therefore high parathyroid hormone

Renal biopsy to determine underlying cause

Classification based on glomerular filtration rate
Stage GFR) (mL/min/1.73 m2) Description
1 > 90 Normal or high
2 60 to 89 Mildly decreased
3 30 to 59 Moderately decreased
4 15 to 29 Severely decreased
5 < 15 Kidney failure

Classification based on albuminuria
Stage Urinary albumin excretion (mg/day) Description
A1 < 30 Normal
A2 30 to 300 Mildly increased (microalbuminuria)
A3 > 300 Severely increased (macroalbuminuria)

48
Q

What should be discussed with CKD patients

A

Patients must be proactive in the management of their disease and monitor their progression. Dietary therapy is indicated from stage 3 onwards. Lifestyle changes are the leading factors in delaying progression of CKD. From stage 4, they will be trained in types of dialysis and may be evaluated for transplant and the referral made for this.
It is a chronic lifelong condition which they will suffer with long term.
When they go on to dialysis, this can be incredibly limiting for the patient and their quality of life due to either regular hospital attendance (haemodialysis) or regular dialysis 3-4 times a day (CAPD) or overnight (APD)

49
Q

What are the consequences of CKD

A

MAD HUNGER

  • Metabolic Acidosis
  • Dyslipidaemia
  • High potassium
  • Uraemia
  • Na+/H2O retention
  • Growth retardation
  • Erythropoietin failure (anaemia)
  • Renal osteodystrophy
50
Q

How is CKD managed

A

Conservative:
- Diet: salt restriction, potassium restriction, fluid restriction

Medical:

  • Nephrotoxic substance avoidance: NSAIDs, Nicotine, Sulfonamide antibiotics, aminoglycosides, vancomycin, acyclovir, cisplatin
  • Blood pressyre control
  • Vaccinations: Pneumococcal every 5 years, Flu jab, hep B

If eGFR of 17 then start education on dialysis and transplant
Starting dialysis is a decision based on how the patient feels not purely on numbers from tests

51
Q

What is benign prostatic hyperplasia

A

Lower urinary tract symptoms caused by bladder outlet obstruction due to benign prostatic hyperplasia, also known as benign due to benign prostatic enlargement, are due to two components:

  • a static component related to increase in beign prostatic tissue narrowing the urethral lumen
  • a dynamic component related to an increase in prostatic smooth muscle tone mediated by alpha-adrenergic receptors

Symtoms related to bladder outlet obstruction may also be contributed to by bladder over-activity

52
Q

How common is benign prostatic hyperplasia

A

Approx 42% men aged 51-60 years
82% men aged 71-80 years
Global lifetime prevalence is around 25%

53
Q

Who is affected by BPH

A

Usually seen in older men

54
Q

What causes BPH

A

Hyperplasia of the epithelial and stromal compartments, particularly in the transitional zone, may be attributed to various factors including shifts in age related hormal changes creating androgen/oestrogen imbalances.

Changes in prostatic stromal-epithelial interactions that occur with ageing and increases in prostatic stem cell numbers are also potential causes.

Progression from pathological BPH to clinical BPH (ie symptomatic) may require additional factors such as prostatitis, vascular effects and changes in the glandular capsule

55
Q

What are the risk factors for BPH

A

Strong:
Age >50 years

Weak:
Family history
Non-asian race
Smoking
Male pattern baldness
Metabolic syndrome
56
Q

How does BPH present

A
Frequency
Urgency
Nocturia
Weak stream
Hesitency
Intermittency
Straining
Incomplete emptying
Post void dribbling
57
Q

What are the differentials in suspected BPH

A
Overactive bladder
Prostatitis
Prostate cancer
UTI
Bladder cancer
Neurogenic bladder
Urethral stricture
58
Q

How is suspected BPH investigated

A

1st investigations:

  • Urinalysis
  • Prostate specific antigen
  • International prostate symptom score (pt questionaire)
  • Global bother score (pt questionaire)
  • Volume charting

Investigations to consider:

  • Ultrasound
  • CT abdomen/pelvis
  • Cytoscopy
  • Uroflowmetry
  • Urodynamic study
59
Q

What should be discussed with BPH patients

A

Openly discuss bother and treatment effects during regular follow-ups

Caution pt on side effects of medications (dizziness, impotence)

Acute progression of symptoms should alert patient to impending urinary retention for ehich catheterisation may be required

Pt symptoms are key indicator for therapy need and should keep diary of voiding wherever possible

60
Q

How is BPH managed

A

Goal is to improve LUTS, both voiding and storage issues, in order to improve QOL of pt

Fluid limitations

Watchful waiting

Alpha-blockers

5-alpha-reductase inhibitors for those with prostate >30grams to reduce prostate size

Anticholinergic therapy may benefit men with LUTS that are primarily irritative (frequency and urgency) without elevation to post-void residual volume.

Drug therapy and response should be reassessed every 6 to 12 months

Refer to urologist for therapeutic invasive therapy if:

  • chosen surgery as primary treatment
  • refactory response to medication or unwilling to use it
  • complications attributed to BPH
61
Q

What is prostate carcinoma

A

A malignant tumour of glandular origin, situated in the prostate

62
Q

How common is prostate carcinoma

A

6th leading cause of cancer mortality in US and second leading cause among men in US

Lifetime risk of developing prostate cancer in the US is approximately 12%

63
Q

Who is affected by prostate carcinoma

A

Most commonly seen in older men with median age at diagnosis being 66 years old

Highest incidence seen among black men.

64
Q

What causes prostate carcinoma

A

Exact cause is unknown

Suggested factors:

  • High fat diet
  • Genetic factors
65
Q

What are the risk factors of prostate carcinoma

A
Age >50 yo
Black ethnicity
North American or Northwest European descent
Family History of prostate cancer 
High levels dietary fat
66
Q

How does prostate carcinoma present

A

Common:

  • Nocturia
  • Urinary frequency
  • Urinary hesitancy
  • Dysuria

Uncommon:

  • Haematuria
  • Weight loss
  • Lethargy
  • Bone pain
67
Q

What signs will be on examination of prostate carcinoma

A

Common:

  • Abnormal digital rectal examination (asymmetrical, nodular prostate)
  • Elevated prostate specific sntigen (PSA)

Uncommon:
-Palpable lymph nodes

68
Q

What are the differentials in suspected prostate carcinoma

A

Benign prostatic hyperplasia

Chronic prostatitis

69
Q

How is suspected prostate carcinoma investigated

A

1st investigations:

  • Serum prostate specific antigen (PSA)
  • Testosterone
  • LFTs
  • FBC
  • Renal function
  • Prostate biopsy

Investigations to consider:

  • Bone scan
  • Plain x-rays
  • Pelvic CT scan
  • Pelvic MRI/endorectal MRI

Emerging tests:

  • Urinary biomarkers
  • Serum biomarkers
  • 18F-sodium fluoride PET/CT and 11C-choline PET/CT
  • Prostate cancer antigen 3 (PCA3) assay
  • TMPRSS2-ERG gene fusions
  • Prostate health index (PHI)
  • 4Kscore test
70
Q

How is prostate carcinoma discussed with patient

A

It is a curable cancer
Survival depend on initial stage of disease at the time of diagnosis
Overall 5 year survival rate is around 100% for local and regional stage prostate cancer and around 30% for distant stage prostate cancer

71
Q

How is prostate carcinoma treated

A

Treatment may consist of:

  • observation
  • active surveillance
  • androgen deprivation therapy
  • external beam radiotherapy
  • brachytherapy
  • radical prostatectomy
  • or a combination of 2 or more of these modalities