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UKMLA Prep > Renal and urology > Flashcards

Renal and urology Flashcards

Conditions and Presentations

1
Q

Haematuria

A

-Microscopic or dipstick positive haematuria is increasingly termed non-visible haematuria

  • macroscopic haematuria is termed visible haematuria
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2
Q

Causes of transient or spurious non-visible haematuria

A

urinary tract infection
menstruation
vigorous exercise (this normally settles after around 3 days)
sexual intercourse

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3
Q

Causes of persistent non-visible haematuria

A
  • Cancer (bladder, renal, prostate)
  • stones
  • benign prostatic hyperplasia
  • prostatitis
  • urethritis e.g. Chlamydia
  • renal causes: IgA nephropathy, thin basement membrane disease
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4
Q

Spurious causes - red/orange urine, where blood is not present on dipstick

A

foods: beetroot, rhubarb
drugs: rifampicin, doxorubicin

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5
Q

Testing of haematuria

A

urine dipstick is the test of choice for detecting haematuria
persistent non-visible haematuria is often defined as blood being present in 2 out of 3 samples tested 2-3 weeks apart
renal function, albumin:creatinine (ACR) or protein:creatinine ratio (PCR) and blood pressure should also be checked
urine microscopy may be used but time to analysis significantly affects the number of red blood cells detected

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6
Q

Urgent referral within 2 weeks haematauria

A
  • Ages >= 45 years and

unexplained visible haematuria without urinary tract infection, or
visible haematuria that persists or recurs after successful treatment of urinary tract infection

Aged >= 60 years AND have unexplained nonvisible haematuria and either dysuria or a raised white cell count on a blood test

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7
Q

Non- urgent referral when haematauria is observed

A

Aged 60 >= 60 years with recurrent or persistent unexplained urinary tract infection

Since the investigation (or not) of non-visible haematuria is such as a common dilemma a number of guidelines have been published. They generally agree with NICE guidance, of note:
patients under the age of 40 years with normal renal function, no proteinuria and who are normotensive do not need to be referred and may be managed in primary care

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8
Q

Nephrotic syndrome

A
  1. Proteinuria (> 3g/24hr) causing
  2. Hypoalbuminaemia (< 30g/L) and
  3. Oedema
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9
Q

Primary causes of nephrotic syndrome

A

inimal change disease, focal segmental glomerulosclerosis (FSGS), membranous nephropathy.

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10
Q

Secondary causes of nephrotic syndrome

A

Diabetes mellitus, systemic lupus erythematosus (SLE), amyloidosis, infections (HIV, hepatitis B and C), drugs (NSAIDs, gold therapy).

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11
Q

Pathophysiology of nephrotic synrome

A

he underlying mechanism involves damage to the glomerular basement membrane and podocytes, leading to increased permeability to proteins.
This proteinuria, in turn, results in hypoalbuminaemia and subsequent oedema due to reduced plasma oncotic pressure.
Loss of antithrombin-III, proteins C and S and an associated rise in fibrinogen levels predispose to thrombosis
Loss of thyroxine-binding globulin lowers the total, but not free, thyroxine levels

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12
Q

What are the initial investigations for nephrotic syndrome

A

Urine dipstick: proteinuria and check for microscopic haematuria
MSU to exclude urinary tract infection.
Quantify proteinuria using an early morning urinary protein:creatinine ratio or albumin:creatinine ratio.
FBC and coagulation screen
Urea and electrolytes

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13
Q

Calcium oxalate renal stones

A

Opaque on radiograph
Frequency of 40%

Urine dipstick: proteinuria and check for microscopic haematuria
MSU to exclude urinary tract infection.
Quantify proteinuria using an early morning urinary protein:creatinine ratio or albumin:creatinine ratio.
FBC and coagulation screen
Urea and electrolytes

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14
Q

Cystine renal stones

A

Inherited recessive disorder of transmembrane cystine transport leading to decreased absorption of cystine from intestine and renal tubule
Multiple stones may form
Relatively radiodense because they contain sulphur

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15
Q

Uric acid renal stones

A

Uric acid is a product of purine metabolism
May precipitate when urinary pH low
May be caused by diseases with extensive tissue breakdown e.g. malignancy
More common in children with inborn errors of metabolism
Radiolucent

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16
Q

Calcium phosphate renal stones

A

May occur in renal tubular acidosis, high urinary pH increases supersaturation of urine with calcium and phosphate
Renal tubular acidosis types 1 and 3 increase risk of stone formation (types 2 and 4 do not)
Radio-opaque stones (composition similar to bone)

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17
Q

Struvite renal stones

A

Stones formed from magnesium, ammonium and phosphate
Occur as a result of urease producing bacteria (and are thus associated with chronic infections)
Under the alkaline conditions produced, the crystals can precipitate
Slightly radio-opaque

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18
Q

Effects of urinary pH on stone formation

A
  • urine pH typical varies from 5-7

Calcium phosphate Normal- alkaline >5.5
Calcium oxalate Variable 6
Uric acid Acid 5.5
Struvate Alkaline >7.2
Cystine Normal 6.5

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19
Q

Management of renal stones - pain management

A

BAUS and NICE recommend an NSAID as the analgesia of choice for renal colic

NSAIDs can increase the risk of cardiovascular events and should be considered before prescribing

NSAIDs are contraindicated or not giving sufficient pain relief NICE recommend IV paracetamol

Intramuscular diclofenac

Alpha blockers (promotes smooth muscle relaxation and dilation of the ureter) use when distal uterine stones are less than 10mm in size

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20
Q

Investigation of renal stones

A

serum creatinine and electrolytes: check renal function
FBC / CRP: look for associated infection
calcium/urate: look for underlying causes
stone analysis should be considered once the stone has passed
also: clotting if percutaneous intervention planned and blood cultures if pyrexial or other signs of sepsis

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21
Q

Imaging of renal stones

A
  • non contrast KUB (within 24 hours of admission)
  • immediate KUB if solitary kidney or fever
  • ultrasound for children or pregnant women
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22
Q

Management (breakdown) of renal stones

A

Renal stones
watchful waiting if < 5mm and asymptomatic
5-10mm shockwave lithotripsy
10-20 mm shockwave lithotripsy OR ureteroscopy
> 20 mm percutaneous nephrolithotomy

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23
Q

Management (breakdown) of uteric stones

A

shockwave lithotripsy +/- alpha blockers>< 10mm shockwave lithotripsy +/- alpha blockers
10-20 mm ureteroscopy

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24
Q

Will renal stones pass spontaneously?

A

Stones < 5 mm will usually pass spontaneously.

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25
Q

Shockable lithotripsy

A

A shock wave is generated external to the patient, internally cavitation bubbles and mechanical stress lead to stone fragmentation
The passage of shock waves can result in the development of solid organ injury
Fragmentation of larger stones may result in the development of ureteric obstruction
The procedure is uncomfortable for patients and analgesia is required during the procedure and afterwards.

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26
Q

Ureteroscopy

A

A ureteroscope is passed retrograde through the ureter and into the renal pelvis
It is indicated in individuals (e.g. pregnant females) where lithotripsy is contraindicated and in complex stone disease
In most cases a stent is left in situ for 4 weeks after the procedure.

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27
Q

Percutaneous nephrolithotomy

A

In this procedure, access is gained to the renal collecting system
Once access is achieved, intra corporeal lithotripsy or stone fragmentation is performed and stone fragments removed.

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28
Q

Prevention of calcium stones

A

high fluid intake
add lemon juice to drinking water
avoid carbonated drinks
limit salt intake
potassium citrate may be beneficial NICE
thiazides diuretics (increase distal tubular calcium resorption)

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29
Q

Prevention of oxalate stones

A

cholestyramine reduces urinary oxalate secretion
pyridoxine reduces urinary oxalate secretion

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30
Q

Uric acid stones prevention

A

allopurinol
urinary alkalinization e.g. oral bicarbonate

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31
Q

Risk factors for renal stones in general

A

dehydration
hypercalciuria, hyperparathyroidism, hypercalcaemia
cystinuria
high dietary oxalate
renal tubular acidosis
medullary sponge kidney, polycystic kidney disease
beryllium or cadmium exposure

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32
Q

Risk factors of urate stones

A

gout
ileostomy: loss of bicarbonate and fluid results in acidic urine, causing the precipitation of uric acid

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33
Q

Drugs causes of renal stones

A

drugs that promote calcium stones: loop diuretics, steroids, acetazolamide, theophylline
thiazides can prevent calcium stones (increase distal tubular calcium resorption)

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34
Q

What are the features of lower UTI in adults?

A

urinary frequency
urinary urgency
cloudy/offensive smelling urine
lower abdominal pain
fever: typically low-grade in lower UTI
malaise
in elderly patients, acute confusion is a common feature

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35
Q

Urine dipstick (what do nitrites, leukocytes and blood mean)

A

positive for nitrite or leukocyte and red blood cells → UTI likely
negative for nitrite and positive for leukocyte → UTI is equally likely to other diagnoses
negative for all nitrite, leukocyte and red blood cells → UTI is less likely

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36
Q

Who can have a urine dipstick

A

Women < 65 years of age, who do not have risk factors for complicated UTI

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37
Q

When not to use urine dipsticks

A

Diagnosis of UTI in women > 65 years, men and catheterised patients

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38
Q

When should a urine culture be taken?

A

women aged > 65 years
recurrent UTI (2 episodes in 6 months or 3 in 12 months)
pregnant women
men
visible or non-visible haematuria

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39
Q

Management of UTI

A
  • women 3 days of nitrofuratonin
  • Men 7 days of nitrofuroatonin
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40
Q

AKI

A

Reduction in renal function following an insult to the kidneys

Causes are pre renal, intrinsic and post renal causes

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41
Q

What drugs cause UTIs

A

the most common cause, particularly antibiotics
penicillin
rifampicin
NSAIDs
allopurinol
furosemide

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42
Q

Other causes of AKIs

A

SLE, sarcoidosis, and Sjögren’s syndrome
infection: Hanta virus , staphylococci

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43
Q

Pathophysiology of AKI

A

histology: marked interstitial oedema and interstitial infiltrate in the connective tissue between renal tubules

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44
Q

Features of AKI

A

fever, rash, arthralgia
eosinophilia
mild renal impairment
hypertension

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45
Q

Investigation of AKI

A
  • sterile Pyuria
  • white cell casts
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46
Q

What is Tublointestital nephritis with uveitis

A
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47
Q

Presentation of Tubulointerstitial nephritis with uveitis

A

Tubulointerstitial nephritis with uveitis (TINU) usually occurs in young females.
Symptoms include
-fever
- weight loss
-painful, red eyes.

Urinalysis is positive for leukocytes and protein.

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48
Q

Pre-renal causes of AKI

A
  • ischaemia
  • any cause of reduced blood flow
    -renal artery stenosis
  • hypovolaemia secondary to diarrhoea and vomiting
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49
Q

Intrinsic causes of AKI

A

Damage within the kidney itself

glomerulonephritis
acute tubular necrosis (ATN)
acute interstitial nephritis (AIN), respectively
rhabdomyolysis
tumour lysis syndrome

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50
Q

Postrenal causes of AKI

A

Obstruction of the urine coming from the kidney

kidney stone in ureter or bladder
benign prostatic hyperplasia
external compression of the ureter

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51
Q

Who is at increased risk for AKIs?

A

chronic kidney disease
other organ failure/chronic disease e.g. heart failure, liver disease, diabetes mellitus
history of acute kidney injury
use of drugs with nephrotoxic potential (e.g. NSAIDs, aminoglycosides, ACE inhibitors, angiotensin II receptor antagonists [ARBs] and diuretics) within the past week
use of iodinated contrast agents within the past week
age 65 years or over

oliguria (urine output less than 0.5 ml/kg/hour)
neurological or cognitive impairment or disability, which may mean limited access to fluids because of reliance on a carer

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52
Q

Signs and symptoms of AKI

A

reduced urine output
pulmonary and peripheral oedema
arrhythmias (secondary to changes in potassium and acid-base balance)
features of uraemia (for example, pericarditis or encephalopathy)

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53
Q

Detection of AKIs

A

sodium
potassium
urea
creatinine

all patients with suspected AKI should have urinalysis

if patients have no identifiable cause for the deterioration or are at risk of urinary tract obstruction they should have a renal ultrasound within 24 hours of assessment.

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54
Q

Management of AKIs

A
  • largely supportive
  • fluid balance to ensure kidneys work properly
  • stop appropriate drugs
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55
Q

What drugs are usually safe to continue in AKI

A

Paracetamol
• Warfarin
• Statins
• Aspirin (at a cardioprotective dose of 75mg od)
• Clopidogrel
• Beta-blockers

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56
Q

What drugs should be stopped as they may worsen AKIs?

A

NSAIDs (except if aspirin at cardiac dose e.g. 75mg od)
• Aminoglycosides
• ACE inhibitors
• Angiotensin II receptor antagonists
• Diuretics

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57
Q

What drugs may have to be stopped in AKI due to toxicity?

A
  • Metformin
  • Lithium
    -Digoxin

Will not worsen AKI

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58
Q

NOT RECOMMENDED treatment for AKIs

A

Loop diuretics (to artificially boost urine output) and low-dose dopamine (in an attempt to increase renal perfusion).

Note that Loop diuretics can be used in patients with significant fluid overload

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59
Q

When is renal replacement therapy (haemodialysis) needs to be used

A
  • patient is not responding to treatment:
  • hyperkalaemia
  • pulmonary oedema
  • acidosis or uraemia (e.g pericarditis and encephalopathy)
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60
Q

• Removal of potassium from the body

A

Calcium resonium (orally or enema)
• Loop diuretics
• Dialysis

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61
Q

• Short-term shift in potassium from extracellular to intra

A

• Combined insulin/dextrose infusion
• Nebulised salbutamol

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62
Q

Stabilisation of the cardiac membrane

A

• Intravenous calcium gluconate

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63
Q

Testicular cancer

A

most common malignancy in men aged 20-30 years. Around 95% of cases of testicular cancer are germ-cell tumours.

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64
Q

Germ cell cancer division

A
  • seminomas
  • non- seminomas- including embryonic, yolk sac, teratomas and chorizo carcinoma
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65
Q

Non-germ cell tumour

A

Leydig cell tumour
Sarcomas

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66
Q

Peak incidence of teratomas

A

25 years

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67
Q

Seminomas peak incidence

A

35 years

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68
Q

Risk factors for seminomas and teratomas

A
  • infertility
  • cryptorchidism
  • family history
  • Klinefelter’s syndrome
  • mumps orchitis
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69
Q

Features of testicular cancer

A
  • painless lump
  • hydrocele
  • pain in minority of men
  • gynaecomastia (increased oestrogen: androgen ratio)
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70
Q

Pathophysiology of gynaecomastia of testicular cancer

A

this occurs due to an increased oestrogen:androgen ratio
germ-cell tumours → hCG → Leydig cell dysfunction → increases in both oestradiol and testosterone production, but rise in oestradiol is relatively greater than testosterone
leydig cell tumours → directly secrete more oestradiol and convert additional androgen precursors to oestrogens

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71
Q

Tumour markers in seminomas

A

Chg elevated in 20%

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72
Q

Non-tumour cell markers

A

AFP and or beta-hcG in 80-85%

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73
Q

Diagnosis of testicular cancer

A

Ultrasound is first line

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74
Q

Management of testicular cancer

A

treatment depends on whether the tumour is a seminoma or a non-seminoma
orchidectomy
chemotherapy and radiotherapy may be given depending on staging and tumour type

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75
Q

Prognosis of testicular cancer

A

5 year survival for seminomas is around 95% if Stage I
5 year survival for teratomas is around 85% if Stage I

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76
Q

Autosomal dominant polycystic kidney cancer (ADPKD)

A

Most common inherited cause of kidney disease, affecting 1 in 1,000 Caucasians

Two main diseases affected PKD1 and PDK2 (code for polycystin-1 and polycystin-2 respectively)

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77
Q

ADPKD type 1

A

85% of cases
Chromosome 16
Presents with renal failure

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78
Q

ADPRK type 2

A

15% of cases
Chromsome 4

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79
Q

Investigation for relatives with ADPKD

A

Abdominal ultrasound

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80
Q

Ultrasound diagnostic criteria

A

two cysts, unilateral or bilateral, if aged < 30 years
two cysts in both kidneys if aged 30-59 years
four cysts in both kidneys if aged > 60 years

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81
Q

Management of ADPKD

A

Tolaptan (vasopressin receptor 2 agonist)

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82
Q

NICE guidelines around tx in ADPKD

A

-they have chronic kidney disease stage 2 or 3 at the start of treatment

-there is evidence of rapidly progressing disease

-the company provides it with the discount agreed in the patient access scheme.

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83
Q

CKD anaemia

A
  • reduced erythropoietin levels
  • normochromic anaemia
  • GFR less than 35ml/min (other causes of anaemia should be considered if the GFR is > 60 ml/min)

CKD can also predispose of left ventricular hypertrophy- (increase in three fold increase in mortality)

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84
Q

Causes of anaemia in renal failure

A
  • reduced erythropoietin
  • reduced absorption of iron
    -reduced erythropoiesis due to toxic effects of uraemia on bone marrow
  • anorexia/ nausea due to uraemia
  • reduced red cell survival (especially in haemodialysis)
  • blood loss due to capillary fragility and poor platelet function)
  • stress ulceration leading to chronic blood loss
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85
Q

Management of CKD anaemia

A
  • target haemoglobin (10-12g/dl)
  • determination and optimisation of iron status should be carried out prior to the administration of erythropoiesis-stimulating agents (ESA).

oral iron should be offered for patients who are not on ESAs or haemodialysis. If target Hb levels are not reached within 3 months then patients should be switched to IV iron
patients on ESAs or haemodialysis generally require IV iron
ESAs such as erythropoietin and darbepoetin should be used in those ‘who are likely to benefit in terms of quality of life and physical function’

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86
Q

CKD bone disease

A

-low vitamin D (1-alpha hydroxylation normally occurs in the kidneys)
-high phosphate
-low calcium: due to lack of vitamin D, high phosphate
-secondary hyperparathyroidism: due to low calcium, high phosphate and low vitamin D

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87
Q

Ostetits fibrosa cystica (CKD)

A

hyperparathyroid bone disease

88
Q

A dynamo CKD

A

reduction in cellular activity (both osteoblasts and osteoclasts) in bone
may be due to over treatment with vitamin D

89
Q

Osteomalacia

A

Low vitamin d

90
Q

Common causes of CKD

A

-diabetic nephropathy
-chronic glomerulonephritis
-chronic pyelonephritis
-hypertension
-adult polycystic kidney disease

91
Q

EGFR and classification

A
  • serum creatine may not be able to provide an accurate estimation of renal function due to difference in muscle mass
92
Q

Modification of Diet in Renal Disease (MDRD)

A

-serum creatinine
-age
-gender
-ethnicity

Equation which takes the following into account to get a better understanding of eGFR

93
Q

Factors which can affect MORD result

A
  • pregnancy
  • muscle mass (amputees and body builders
  • eating red meat 12 hours before sample is taken
94
Q

CKD stage 1

A

Greater than 90 ml/min, with some sign of kidney damage on other tests (if all the kidney tests* are normal, there is no CKD)

95
Q

What is normal eGFR value

A

120ml/min

96
Q

Stage 2 CKD

A

60-90 ml/min with some sign of kidney damage (if kidney tests* are normal, there is no CKD)

97
Q

Stage 3a CKD

A

45-59 ml/min, a moderate reduction in kidney function

98
Q

Stage 3b CKD

A

30-44 ml/min, a moderate reduction in kidney function

99
Q

Stage 4 CKD

A

15-29 ml/min, a severe reduction in kidney function

100
Q

Stage 5 CKD

A

Less than 15 ml/min, established kidney failure - dialysis or a kidney transplant may be needed

101
Q

Features of CKD

A
  • typically asymptomatic (usually diagnosed by abnormal urea and electrolyte result)
  • late stage make be symptomatic

Possible features include

oedema: e.g. ankle swelling, weight gain
polyuria
lethargy
pruritus (secondary to uraemia)
anorexia, which may result in weight loss
insomnia
nausea and vomiting
hypertension

102
Q

Management of mineral bone disease management in CKD

A

Aim is to reduce phosphate and parathyroid hormone levels

reduced dietary intake of phosphate is the first-line management
phosphate binders
vitamin D: alfacalcidol, calcitriol
parathyroidectomy may be needed in some cases

103
Q

Phosphate binders

A

aluminium-based binders are less commonly used now
calcium-based binders
problems include hypercalcemia and vascular calcification

104
Q

Sevelamer

A

a non-calcium based binder that is now increasingly used
binds to dietary phosphate and prevents its absorption
also appears to have other beneficial effects including reducing uric acid levels and improving the lipid profiles of patients with chronic kidney disease

105
Q

Management of proteinuria in CKD

A
  • ACE inhibitors (angiotensin II receptor blockers)
  • SGLT-2 inhibitors
106
Q

ACE inhibitors in CKD

A

should be used first-line in patients with coexistent hypertension and CKD, if the ACR is > 30 mg/mmol
if the ACR > 70 mg/mmol they are indicated regardless of the patient’s blood pressure

107
Q

SGLT-2 inhibitors in CKD

A

patients who have proteinuric CKD (with or without diabetes) may benefit from treatment with SGLT2 inhibitors
they primarily act by blocking reabsorption of glucose in the proximal tubule → lowers the renal glucose threshold → glycosuria
by blocking the cotransporter, they also reduce sodium reabsorption → natriuresis reduces intravascular volume and blood pressure, but it also increases the delivery of sodium to the macula densa → normalizes tubuloglomerular feedback and thereby reduces intraglomerular pressure

108
Q

Proteinuria; when to refer to nephrologist

A

a urinary albumin:creatinine ratio (ACR) of 70 mg/mmol or more, unless known to be caused by diabetes and already appropriately treated
a urinary ACR of 30 mg/mmol or more, together with persistent haematuria (two out of three dipstick tests show 1+ or more of blood) after exclusion of a urinary tract infection
consider referral to a nephrologist for people with an ACR between 3-29 mg/mmol who have persistent haematuria and other risk factors such as a declining eGFR, or cardiovascular disease

109
Q
A
110
Q

Acute urinary retention

A

medical emergency typified by a sudden inability to pass urine, frequently observed in older males who have undergone recent surgery

111
Q

Causes of urinary retention

A

Luminal causes (stone, blood clot, tumour, UTI)
Mural causes (stricture, neuromuscular dysfunction)
Extra-mural (abdominal/pelvic mass/tumours, retroperitoneal fibrosis)
Neurological pathologies (cauda equina, MS)
Obstructive pathologies
Infectious diseases including UTIs
Medications

112
Q

Drugs which cause urinary retention

A
  • anti cholingeric medications
  • morphine
  • alpha agonists
  • alcohol
113
Q

Signs and symptoms of urinary retention

A

Inability to pass urine
Lower abdominal discomfort
Pain or distress
Suprapubic tenderness
Suprapubic mass (due to an enlarged bladder)
Delirium (hypoactive or hyperactive)

114
Q

Urinary retension investigation

A

Bladder scan/USS renal tract
Digital Rectal Exam
Urinalysis and urine MCS
Evaluation of post-void residual
Bloods tests: FBC, renal profile (renal function is often preserved due to the acuity, unlike in chronic urinary retention), CRP
Consider non-contrast CT KUB if stones suspected

115
Q

Management of acute urinary retention

A
  • underlying cause correction
  • catheter
  • obstruction: medical management with alpha-blockers
    *TURP if this fails
  • Neurogenic- surgery
116
Q

Balanoposthitis

A

inflammation of the glans penis and the prepuce.

117
Q

Balanoposthitits infective causes

A

Bacterial infections (e.g., Streptococcus, Staphylococcus)
Fungal infections, predominantly Candida species
Viral infections, such as human papillomavirus (HPV) or herpes simplex virus (HSV)

118
Q

Non infective causes of balanoposthitis

A

Dermatological conditions such as psoriasis, lichen planus, or lichen sclerosus
Chemical irritants
Poor hygiene
Phimosis (tight foreskin)

119
Q

balanoposthitis features

A

Redness and swelling of the glans penis and prepuce
Pain or discomfort
Itching
Presence of a foul-smelling discharge
Difficulty retracting the foreskin (phimosis)

120
Q

Investigation balanoposthitis

A

Swab for culture
Antibiotics

121
Q

Management of balanoposthitis

A
  • hygiene
  • avoid irritants
  • skin biopsy may be necessitated for a comprehensive diagnosis
122
Q

BPH

A

non-cancerous enlargement of the prostate gland, particularly the transition zone, leading to the compression of the urethra and subsequent lower urinary tract symptoms (LUTS).

123
Q
A

Increase in incidence after age 40

124
Q

Aetiology of BPH

A

Age

dihydrotestosterone

125
Q

Features of BPH

A

Hesitancy
Weak stream
Frequency
Urgency
Nocturia
Sensation of incomplete emptying

126
Q

IPPS

A

International Prostate Symptom Score (IPSS):
Assessing the severity of LUTS.
Score 20–35: severely symptomatic.
Score 8–19: moderately symptomatic.
Score 0–7: mildly symptomatic.

127
Q

Investigators of BPH

A
  • DRE
  • ipps
    *PSA
    *2WW
128
Q

Management of BPH

A
  • Alpha-blockers (tamsulosin)
  • 5-alpha reductase inhibitor for enlarged prostate
  • TURP) or laser prostatectomy for moderate to severe symptoms.
129
Q

Bladder cancer

A

Malignant growth
Most common is transitional cell carcinoma

130
Q

Risk factors bladder cancer (transitional cell)

A

Smoking
Exposure to aromatic amines (employed in rubber, dyes, and chemical industry)
Use of Cyclophosphamide

131
Q

Risk factors for SCC bladder e

A

Schistosomiasis infection
Long-term catheterisation (10+ years)

132
Q

Bladder cancer adenocarcinoma risk

A

Presence of other types of bladder cancer
Local bowel cancer

133
Q

Risk factors for Small Cell Bladder Cancer

A

Association with other types of bladder cancer

134
Q

signs and symptoms of bladder cancer

A

Painless haematuria
Recurrent UTIs
Hydronephrosis
Unintended weight loss
Night sweats

135
Q

Investigations of bladder cancer

A
  • CT urogram
  • flexible cystoscopy
136
Q

Bladder cancer 2ww criteria

A

45 years and over and have:
Unexplained visible haematuria without urinary tract infection, or
Visible haematuria that persists or recurs after successful treatment of urinary tract infection.

60 years and over and have unexplained non-visible haematuria and either dysuria or a raised white cell count on a blood test.
Consider non-urgent referral for bladder cancer in people aged 60 years and over with recurrent or persistent unexplained urinary tract infection.

137
Q

Bladder cancer classification

A

Non-muscle invasive: Tis (non-invasive, in situ), Ta – non-invasive, T1 – tumour invades inner lining and connective tissues.
Muscle invasive: T2 (tumour invades muscle), T3 (invades perivesical fat and LN), T4 (metastatic spread).

138
Q

CIS, Ta, and T1 and is managed

A

Surgery: Transurethral resection of the bladder tumour (TURBT) is the gold standard.
Chemotherapy: The bladder can be instilled with chemotherapeutic agents such as Mitomycin C (single dose if low risk, 6 week course if intermediate risk).
Immunotherapy: BCG immunotherapy can be instilled into the bladders of patients with high-risk non-muscle invasive cancers or carcinoma in situ (CIS).
If there is high-risk muscle non-muscle invasive cancer/CIS a radical cystectomy may still be considered.

139
Q

Muscle invasive bladder cancer

A

gold standard treatment is a radical cystectomy with urinary diversion,

140
Q

How much drug to give when pt has hyperkalaemia

A

Calcium gluconate
30mg of 10%

141
Q

AEIOU dialysis reasons

A
  • Acid base disturbance
  • Electorlyye
  • Intoxication
  • Overload of volume
  • Uraemia (pericarditis, encephalopathy )
142
Q

What eGFR needed for transplant

A

Less than 25 eGFR

143
Q

What is a fistula

A

Abnormal structure to allow connection between two epithelial surfaces

144
Q

Steal syndrome

A

Blood from the body goes to the fistula instead which causes the most intense pain.

145
Q

Three concerns with peritoneal dialysis

A

Abdominal pain
Fever
Cloudy periotenium space

146
Q

how long can someone be on peritoneal dialysis for?

A

3-4 years

147
Q

how long can someone be on peritoneal dialysis for?

A

3-4 years

148
Q

Polycystic kidney disease

A
  • genetic condition
  • healthy kidney tissue is replaced with many fluid-filled cysts.
  • palpable kidneys
149
Q

Absolute contradictions for kidney transplant

A

Untreated malignancy
Active infection

Untreated HIV infection or AIDS

Any condition with a life expectancy <2 years

Malignant melanoma within the previous 5 years

150
Q

Relative contradictions for kidney transplant

A
  • Co-morbidities, e.g. diabetes mellitus
    Age >65 years

Obesity

HBV or HCV infection

Previous malignancy (depending on type)

151
Q

Delayed graft function

A
  • need for dialysis in the first week after transplantation
152
Q

survival of donation after brain stem death

A

DBD transplant recipients is around 97% and for living donor transplant recipients is around 99%

153
Q

Autosomal dominant kidney disease

A

PKD1 gene on chromosome 16 (85% of cases)
PKD2 gene on chromosome 4 (15% of cases)

154
Q

Autosomal recessive kidney disease

A

polycystic kidney and hepatic disease 1 (PKHD1) gene on chromosome 6.

155
Q

Oligohydramnios

A
  • reduced amniotic fluid volume due to reduced urine output
  • dysmorphic features, such as underdeveloped ear cartilage, low-set ears and a flat nasal bridge.
  • End-stage renal failure usually occurs before reaching adulthood.
156
Q

Global management of PKD

A

Genetic counselling
Avoiding contact sports due to the risk of cyst rupture
Avoiding NSAIDs and anticoagulants
MR angiography (MRA) can be used to screen for cerebral aneurysms

157
Q

Acute management of PKD

A

Antihypertensives for hypertension (e.g., ACE inhibitors)
Analgesia for acute pain
Antibiotics for infections (e.g., UTIs or cyst infections)
Drainage of symptomatic can be performed by aspiration or surgery
Dialysis for end-stage renal failure
Renal transplant for end-stage renal failure

158
Q

Slow progression of renal failure in autosomal dominant PKD

A

Tolvaptan

159
Q

Extra-renal manifestations PKD

A

Cerebral aneurysms
Hepatic, splenic, pancreatic, ovarian and prostatic cysts
Mitral regurgitation
Colonic diverticula

160
Q

Conditions Cause hyperkalemia

A

Acute kidney injury
Chronic kidney disease (stage 4 or 5)
Rhabdomyolysis
Adrenal insufficiency
Tumour lysis syndrome

161
Q

Medications cause hyperkalemia

A

Aldosterone antagonists (e.g., spironolactone and eplerenone)
ACE inhibitors (e.g., ramipril)
Angiotensin II receptor blockers (e.g., candesartan)
NSAIDs (e.g., naproxen)

162
Q

ECG changes hyperkalemia

A

Tall peaked T-waves
Flattening or absence of P waves
Prolonged PR interval
Broad QRS complexes

163
Q
A

A- flattened p waves
B- tall peaked T waves
C- broad QRS complex

164
Q

When do patients need urgent treatment for hyperkalaemia

A

ECG changes
Serum potassium above 6.5 mmol/L

165
Q

Urgent Management of hyperkalemia

A
  • insulin and dextrose infusion
  • IV calcium gluconate:
166
Q

“ relaxed management “ of hyperkalemia

A

Nebulised salbutamol temporarily drives potassium into cells
Oral calcium resonium reduces potassium absorption in the GI tract (this is slow and causes constipation)
Sodium bicarbonate (in acidotic patients on renal advice) drives potassium into cells as it corrects the acidosis
Haemodialysis may be required in severe or persistent cases

167
Q

Rhabdomyolysis

A

skeletal muscle breaking down and releasing various chemicals into the blood. Myocytes undergo cell apoptosis

168
Q

what is released during rhabdomylosis?

A

Myoglobin
Potassium
Phosphate
Creatine kinase

169
Q

What is benign prostatic hyperplasia (BPH)?

A

A common condition seen in older men.

170
Q

What are the risk factors for BPH?

A
  • Age
  • Ethnicity: black > white > Asian
171
Q

What percentage of 50-year-old men have evidence of BPH?

A

Around 50%

172
Q

What symptoms are categorized as voiding symptoms in BPH?

A
  • Weak or intermittent urinary flow
  • Straining
  • Hesitancy
  • Terminal dribbling
  • Incomplete emptying
173
Q

What are the storage symptoms associated with BPH?

A
  • Urgency
  • Frequency
  • Urgency incontinence
  • Nocturia
  • Post-micturition dribbling
174
Q

What complications can arise from BPH?

A
  • Urinary tract infection
  • Retention
  • Obstructive uropathy
175
Q

What assessments are commonly used for BPH?

A
  • Dipstick urine
  • U&Es
  • PSA
  • Urinary frequency-volume chart
  • International Prostate Symptom Score (IPSS)
176
Q

What does an IPSS score of 20-35 indicate?

A

Severely symptomatic

177
Q

What are the management options for BPH?

A
  • Watchful waiting
  • Alpha-1 antagonists (e.g., tamsulosin)
  • 5 alpha-reductase inhibitors (e.g., finasteride)
  • Combination therapy
  • Antimuscarinic drugs
  • Surgery (e.g., TURP)
178
Q

What is TURP syndrome?

A

A rare and life-threatening complication of transurethral resection of the prostate surgery.

179
Q

What are the risk factors for developing TURP syndrome?

A
  • Surgical time > 1 hr
  • Height of bag > 70cm
  • Resected > 60g
  • Large blood loss
  • Perforation
  • Large amount of fluid used
  • Poorly controlled CHF
180
Q

What is the most common urological cancer?

A

Bladder cancer

181
Q

What age group is most affected by bladder cancer?

A

Males aged between 50 and 80 years

182
Q

What is the most important risk factor for urothelial carcinoma of the bladder?

A

Smoking

183
Q

Which type of carcinoma accounts for over 90% of bladder cancers?

A

Urothelial (transitional cell) carcinoma

184
Q

What is the TNM stage T3 in bladder cancer?

A

Tumour extends to perivesical fat

185
Q

What are common presentations of bladder cancer?

A

Painless, macroscopic haematuria

186
Q

What is the prognosis for T2 bladder cancer?

A

60%

187
Q

What are the major criteria for diagnosing multiple myeloma?

A
  • Plasmacytoma
  • 30% plasma cells in a bone marrow sample
  • Elevated levels of M protein
188
Q

What does the mnemonic CRABBI stand for in multiple myeloma?

A
  • Calcium
  • Renal
  • Anaemia
  • Bleeding
  • Bones
  • Infection
189
Q

What initial investigations are done for nephrotic syndrome?

A
  • Urine dipstick
  • MSU
  • Quantify proteinuria
  • FBC and coagulation screen
  • Urea and electrolytes
190
Q

What is the triad of nephrotic syndrome?

A
  • Proteinuria (> 3g/24hr)
  • Hypoalbuminaemia (< 30g/L)
  • Oedema
191
Q

What is the primary treatment for multiple myeloma?

A
  • Induction therapy
  • Targeted drugs
  • Chemotherapy
  • Steroids
192
Q

What is the typical age at presentation for multiple myeloma?

A

70 years old

193
Q

What is the most common cause of renal impairment in myeloma?

A

Monoclonal production of immunoglobulins leading to light chain deposition

194
Q

What are common complications of nephrotic syndrome?

A
  • Increased risk of thromboembolism
  • Hyperlipidaemia
  • Chronic kidney disease
  • Increased risk of infection
195
Q

What is the normal upper limit for PSA?

A

4ng/ml

196
Q

What is the annual diagnosis rate of prostate cancer in men in the UK?

A

Approximately 50,000 men are diagnosed with the condition each year

Up to 9,000 will die in the UK from the condition per year.

197
Q

What are common symptoms of metastatic prostate cancer?

A

Bone pain

Metastatic disease may present as bone pain.

198
Q

What diagnostic tools are used for prostate cancer?

A
  • Prostate specific antigen measurement
  • Digital rectal examination
  • Trans rectal ultrasound (+/- biopsy)
  • MRI/CT and bone scan for staging
199
Q

What is the normal upper limit for PSA?

A

4 ng/ml

This value may include patients with benign disease and localized prostate cancer.

200
Q

What percentage of free to total PSA is suggestive of cancer?

A

< 20%

Values of <20% are suggestive of cancer, and biopsy is advised.

201
Q

What is the most common type of prostate cancer?

A

Adenocarcinoma (95% of cases)

In situ malignancy may be found in areas adjacent to cancer.

202
Q

What grading system is used for prostate cancer pathology?

A

Gleason grading system

Two grades are awarded: 1 for the most dominant grade and 2 for the second most dominant grade.

203
Q

What are the treatment options for low-risk prostate cancer?

A
  • Watch and wait
  • Radiotherapy
  • Surgery
  • Hormonal therapy
204
Q

What is the standard treatment for localized prostate cancer?

A

Radical prostatectomy

Surgical removal of the prostate is the standard treatment.

205
Q

What is the preferred option for low-risk men according to NICE?

A

Active surveillance

Particularly suitable for men with clinical stage T1c, Gleason score 3+3, and PSA density < 0.15 ng/ml/ml.

206
Q

What are common risk factors for prostate cancer?

A
  • Increasing age
  • Obesity
  • Afro-Caribbean ethnicity
  • Family history (5-10% of cases)
207
Q

What symptoms may indicate localized prostate cancer?

A
  • Bladder outlet obstruction
  • Haematuria
  • Pain in back, perineal, or testicular regions
208
Q

What is the traditional investigation method for suspected prostate cancer?

A

Transrectal ultrasound-guided biopsy (TRUS)

Recent guidelines now advocate for the use of multiparametric MRI.

209
Q

What are potential complications of TRUS biopsy?

A
  • Sepsis (1% of cases)
  • Pain lasting >= 2 weeks (15% of cases)
  • Fever (5%)
  • Haematuria and rectal bleeding
210
Q

What is the recommended first-line investigation for clinically localized prostate cancer?

A

Multiparametric MRI

211
Q

What are the treatment options for localized advanced prostate cancer (T3/T4)?

A
  • Hormonal therapy
  • Radical prostatectomy
  • Radiotherapy (external beam and brachytherapy)
212
Q

What is one key aim of treating advanced prostate cancer?

A

Reducing androgen levels

213
Q

What are examples of anti-androgen therapies?

A
  • Goserelin (GnRH agonist)
  • Bicalutamide (non-steroidal anti-androgen)
  • Cyproterone acetate (steroidal anti-androgen)
  • Abiraterone (androgen synthesis inhibitor)
214
Q

What is the PSA testing recommendation for men older than 50?

A

PSA testing should be offered to men older than 50 years of age who request a PSA test

215
Q

What are age-specific PSA thresholds for men with possible symptoms of prostate cancer?

A
  • < 40: Use clinical judgement
  • 40–49: > 2.5 ng/ml
  • 50–59: > 3.5 ng/ml
  • 60–69: > 4.5 ng/ml
  • 70–79: > 6.5 ng/ml
  • > 79: Use clinical judgement
216
Q

True or False: Around 15% of men with prostate cancer have a normal PSA level.

A

True

217
Q

What factors can raise PSA levels?

A
  • Benign prostatic hyperplasia (BPH)
  • Prostatitis
  • Ejaculation
  • Vigorous exercise
  • Urinary retention
  • Instrumentation of the urinary tract

UKMLA Prep (39 decks)

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