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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

45
Q

Investigation of AKI

A
  • sterile Pyuria
  • white cell casts
46
Q

What is Tublointestital nephritis with uveitis

A
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.

48
Q

Pre-renal causes of AKI

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

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

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

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)

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.

54
Q

Management of AKIs

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

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

57
Q

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

A
  • Metformin
  • Lithium
    -Digoxin

Will not worsen AKI

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

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)
60
Q

• Removal of potassium from the body

A

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

61
Q

• Short-term shift in potassium from extracellular to intra

A

• Combined insulin/dextrose infusion
• Nebulised salbutamol

62
Q

Stabilisation of the cardiac membrane

A

• Intravenous calcium gluconate

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.

64
Q

Germ cell cancer division

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

Non-germ cell tumour

A

Leydig cell tumour
Sarcomas

66
Q

Peak incidence of teratomas

A

25 years

67
Q

Seminomas peak incidence

A

35 years

68
Q

Risk factors for seminomas and teratomas

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

Features of testicular cancer

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

71
Q

Tumour markers in seminomas

A

Chg elevated in 20%

72
Q

Non-tumour cell markers

A

AFP and or beta-hcG in 80-85%

73
Q

Diagnosis of testicular cancer

A

Ultrasound is first line

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

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

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)

77
Q

ADPKD type 1

A

85% of cases
Chromosome 16
Presents with renal failure

78
Q

ADPRK type 2

A

15% of cases
Chromsome 4

79
Q

Investigation for relatives with ADPKD

A

Abdominal ultrasound

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

81
Q

Management of ADPKD

A

Tolaptan (vasopressin receptor 2 agonist)

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.

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)

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
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’

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

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

UKMLA Prep (30 decks)

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