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Urology > Renal > Flashcards

Renal Flashcards

1
Q

What is glomerulonephritis?

A

This is inflammation of the glomerulus

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2
Q

What is the difference between primary and secondary glomerulonephritis?

A

It may be secondary or primary. Primary is where the cause is unknown and secondary is when there is another disease in the body.

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3
Q

What are the kidney cells most likely to be damaged in glomerulophritis?

A

If podocytes are damaged, there can be a lot of protein in the urine.

If parietal cells are dameged, there will be a crescent shape.

Endothelial cells are usually damaged in systemic disease.

Mesangial cells.

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4
Q

What are some investigations for glomerulonephritis?

A

A full medical and drug (including recreational) history.

Basics – UEs, dip urine for blood, quantify proteinuria, check albumin, check USS

Glomerulonephritis screen:
o	ANCA
o	Anti-GBM 
o	ANA / dsDNA
o	Complement
o	Anti-PLA2R
o	Immunoglobulins
o	Rheumatoid factor
o	Virology – hep B, C, HIV

Others: Myeloma screen, HbA1c.

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5
Q

Describe a kidney biopsy is carried out

A

This is done as a day case. The patient will lie on their tummy and it is ultrasound guided. It is done under local anaesthetic. The patient takes a breath in as the kidneys move when you breath.

It doesn’t matter which kidney is biopsied as both kidney will be affected. However, the left kidney is easier to reach.

The main risk is bleeding as the kidney is a very vascular organ. There is around a 1% chance of a significant bleed.

This is required for clinical diagnosis of glomerulonephritis.

Biopsy of kidney cortex examined under
• Light microscopy (glomerular and tubular structure)
• Immunofluorescence (looking for Ig and complement)
• Electron microscopy (glomerular basement membrane and deposits)

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6
Q

What is the main risk of a kidney biopsy?

A

The main risk is bleeding as the kidney is a very vascular organ. There is around a 1% chance of a significant bleed.

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7
Q

What does light microscopy look at in the kidney?

A

Glomerulus and tubular structure

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8
Q

What does immunoflorescene look at in the kidney?

A

Looking for IgG and complement

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9
Q

What does electron microscopy look at in the kidney?

A

Glomerulus BM and deposits.

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10
Q

What is synpharyngitic?

A

Sore throat and Coca Cola urine

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11
Q

How is nephrotic syndrome classified?

A

This is classified as:

  1. 3.5g proteinuria per 24h (urine PCR >300)
  2. Serum albumin <30
  3. Oedema
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12
Q

Why is there oedema in nephrotic syndrome?

A

Urinary loss of albumin results in a decrease in oncotic pressure. This results in peripheral oedema.

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13
Q

What is nephritic syndrome?

A
  • Hypertension
  • Blood and protein in urine
  • Declining kidney function
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14
Q

What cells are damaged in nephrotic syndrome?

A

Podocytes

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15
Q

Is IgA nephropathy nephrotic or nephritic?

A

Nephritis.

This is the most common primary glomerular disease.

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16
Q

What is deposited in the mesangium in IgA nephropathy?

A

IgA (abnormal production)

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17
Q

About cases of IgA nephropathy will progress to ESFR?

A

One third

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18
Q

What is the BP aim for IgA nephorapthy?

A

The most important control is tight BP control. The aim is 125/75. ACEi is the top choice.

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19
Q

Is membranous GN nephritic or nephrotic?

A

Nephrotic

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20
Q

What antibody is present in membranous GN?

A

Anti-Phospholipase A2 receptor antibody

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21
Q

What are the possible outcomes of membranous GN?

A

Variable natural history.
• A third spontaneously remit.
• A third progress to ESRF over 1-2 years.
• A third persistent proteinuria maintain GFR.

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22
Q

What are the treatment options for membranous GN?

A
  1. Treat underlying disease if secondary
  2. Supportive non-immunological – ACEi, statin, diuretics, salt restriction
3.	Specific immunotherapy (6 months)
•	Steroids
•	Alkylating agents (cyclophosphamide)
•	Alternative agents – rituximab, anti-CD20 MAb
•	Cyclosporin

Outcomes – Complete remission, partial remission, ESRD, relapse, death.

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23
Q

What are some examples of conditions that can lead to membranous GN?

A

10% occur due to secondary to malignancy, CTD and drugs.

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24
Q

What is the commonest GN in children?

A

Minimal change disease

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25
Q

What type of syndrome does minimal change disease cause?

A

Nephrotic

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26
Q

What does Minimal change disease show on light microscopy?

A

Light microscopy is normal whereas electron microscopy shows effacement of podocyte foot processes.

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27
Q

Can Minimal change disease follow an URTI?

A

Yes

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28
Q

What percentage of people with Minimal change disease will relapse?

A

50%

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29
Q

What is the treatment of Minimal change disease ?

A

The treatment is high dose steroids. Prednisolone 1mg/kg for up to 8 weeks.

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30
Q

What type of syndrome does Rapidly progressive GN cause?

A

Nephritic

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31
Q

What does Rapidly progressive GN show on biopsy?

A

Crescent shape

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32
Q

What are some causes of Rapidly progressive GN?

A 
Common causes: 
•	ANCA vasculitis (MPO / PR3)
•	Goodpasture’s syndrome (anti-GBM)
•	Lupus nephritis
•	Infection associated: steph and staph
•	HSP nephritis: IgA nephroapthy
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33
Q

What are the antibodies made in Antineutrophil cytoplasmic antibodies (ANCA)?

A

Antineutrophil cytoplasmic antibodies (ANCA) are a group of autoantibodies produced when a person’s immune system mistakenly targets and attacks its own neutrophil proteins. Two of the most commonly targeted proteins are myeloperoxidase (MPO) and proteinase 3 (PR3). This results in the production of antibodies to MPO (microscopic polyangiitis) and/or PR3 (GPA)

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34
Q

What is the difference between MPO and PR3?

A

This results in the production of antibodies to MPO (microscopic polyangiitis) and/or PR3 (GPA)

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35
Q

What is Goodpastures’ syndrome?

A

Goodpasture’s syndrome is very rare. This is where auto-antibodies target type IV collagen in the glomerular and alveolar basement membrane. There can commonly be lung diease too.

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36
Q

What do antibodies target in Goodpasture’s syndrome?

A

Type IV collagen.

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37
Q

What are the three embryological structures of kidney development?

A
  • Pronephros
  • Mesonephros
  • Metanephros
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38
Q

When does urine production occur?

A

10 weeks

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39
Q

What does nephrogenesis commence?

A

Week 10

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40
Q

Are there new nephrons at week 36?

A

No

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41
Q

When does a child achieve an adult GFR?

A

2 years

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42
Q

What is renal agenesis?

A

This is congenital absence of renal parenchymal tissue. It occurs at the metanephric stage.

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43
Q

What is renal hypoplasia?

A

This is the reduction in the number of nephrons. There will be a normal architecture.

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44
Q

What is renal dysplasia?

A

This is malformed renal tissue

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45
Q

What is hypodysplasia?

A

Renal Hypodysplasia is congenitally small kidneys with dysplastic features.

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46
Q

What is the inhertitance of ARPKD?

A

Autosomal recessive

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47
Q

What is oligohydraminois?

A

Low lowels of amniotic fluid

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48
Q

What are some features of ARPKD?

A 
Clinical presentation:
–	Antenatal:
•	Antenatal US
•	Oligohydramnios: low levels of amniotic fluid 
–	Infancy:
•	Large palpable renal mass
•	Respiratory distress
•	Renal failure:
•	HT
•	Hyponatremia: urinary concentrating defect
–	Childhood:
•	Renal failure
•	HT
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49
Q

Is congenital hepatic fibrosis associated with ARPKD?

A

Yes

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50
Q

What is the rate of progresion to ESRF from ARPKD?

A

50%

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51
Q

What is the genetic associated with ADPKD?

A

– PKD1 mutation – cc 16: 85% ; polycystin 1

– PKD2 mutation – cc 4: 10-15%; polycystin 2

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52
Q

What is the most common mutation in ADPKD?

A

PDK1

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53
Q

What is seen on ultrasound with ADPKD?

A

Large echogenic kidneys and microcytes

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54
Q

Where do cysts form from in ADPKS?

A

Tubules

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55
Q

What are some associated anomalies with ADPKS?

A 
Assoc. Anomalies:
–	Mitral valve prolapse
–	Cerebral Aneurysm
–	AV malformation
–	Hepatic/pancreatic cysts
–	Colonic diverticula/hernia
–	Management
–	Supportive
–	Directed : Tolvaptan
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56
Q

What is hydronephrosis?

A

Swelling of the kidney due to a build of fluid

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57
Q

What sex is more affected with hydronephrosis?

A

Males

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58
Q

What is PUJ obstruction?

A

This occurs in 1 in 500 births. There is partial/total blockage of urine at ureter junction with kidney.

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59
Q

What sex is more affected by PUJ obstruction?

A

Males

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60
Q

How much is the uterer dilated in VUJ obstruction?

A

> 7mm

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61
Q

What are some symptoms of posterior urethral valves?

A 
Some symptoms include:
•	an enlarged bladder, so that it can be felt through the abdomen as a lump
•	urinary tract infections (UTIs)
•	difficulty urinating
•	a weak stream of urine
•	unusually frequent urination
•	bed wetting after toilet training has been successful
•	poor weight gain
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62
Q

What is Vesico-ureteric Reflux?

A

This is retrograde passage of urine from bladder into upper urinary tract.

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63
Q

How many grades are in Vesico-ureteric Reflux?

A

5

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64
Q

What sex is more affected by UTIs under 3 months?

A

Boys

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65
Q

What sex is more affected by UTIs over 3 months?

A

Girls

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66
Q

Does circumcision increase or decrease the risk of getting a UTI?

A

Decrease

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67
Q

What are some symptoms of an upper tract UTI?

A 
•	Upper Tract
–	Pyrexia (Rigors)
–	Vomiting
–	Systemic upset
–	Abdo pain
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68
Q

What are some symptoms of an lower tract UTI?

A 
•	Lower Tract
–	Dysuria
–	Frequency
–	Haematuria
–	Wetting
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69
Q

What is Von Hippel Lindau?

A

Von Hippel Lindau: rare, AD.
Multisystem – kidneys, pancreas and genital tract.
Multiple cysts – benign with potential for malignant transformation (clear cell carcinoma). Tumours tend to appear in early adulthood.

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70
Q

What tumour is at increased risk in Von Hippel Lindau?

A

Clear cell carcinoma

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71
Q

What is the hesitance of Von Hippel Lindau??

A

AD

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72
Q

What is the inheritance of Tuberous Sclerosis?

A

AD

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73
Q

What is Tuberous Sclerosis?

A

Tuberous Sclerosis: AD and is multisystem.
Benign tumours – brain, kidneys, heart, eyes, skin.
Seizures, developmental delay, Kidneys – tumours called angiomyolipomas. Risk of haemorrhage.
Rarely to progress to ESRD.

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74
Q

What type of tumours are at increased risk in Tuberous Sclerosis?

A

Angiomyolipomas

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75
Q

What chromosome is PDK one on?

A

16

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76
Q

What chromosome is PDK two on?

A

4

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77
Q

What do the gene PKD code for?

A

Polycystin

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78
Q

What are some extra-renal manifestations of APKD?

A
  • intracranial aneurysms
  • HTN
  • valvular abnormalities
  • hepatic cysts and pancreatic cysts
  • bronchioctasis
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79
Q

What is Tolvaptan?

A

This is a vasopressin V2 receptor antagonist.
the side effects are hepatotoxicity and hypernatremia.
People will have to drink 6-8 litres a day.

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80
Q

What is the inheritance of Alport’s syndrome?

A

X-linked

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81
Q

What is mutated in Alport’s syndrome?

A

COL3A5 which codes for collagen four

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82
Q

Can there be deafness in Alport’s syndrome?

A

Yes: sensorineural

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83
Q

What is the inheritance of Fabrys?

A

X-linked

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84
Q

What is deficient in Fabry’s disease?

A

Alpha galactosidase A deficiency causing accumulation of Gb3

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85
Q

What are some functions of the kidney?

A
  • metabolic waste excretion
  • endocrine functions
  • drug metabolism/excretion
  • BP control
  • acid/base
  • control of solutes and fluid status
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86
Q

Describe the Glomerular filtration barrier

A

The renal corpuscle contains the glomerulus and Bowman’s capsule.

The glomerulus is supplied by the afferent artery. the capillaries are fenestrated. This means that red and white blood cells are unbale to pass through.

The basement membrane, which is under the endothelium, is negatively charged. This means that plasma proteins are unable to pass through.

Bowman’s capsule is made up of a visceral and parietal layer. The visceral layer is made of podocytes. In-between are nephrin proteins.
The podocytes have long process and pedicles which wrap around the capillaries and leave filtration slits.

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87
Q

What protein does urine dip sick detect?

A

albumin

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88
Q

Is creatinine affected by diet?

A

Slightly

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89
Q

What is creatinine a breakdown product of?

A

Muscle

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90
Q

What is the MDRD4 formula based on?

A

Plasma creatine concentration, age, gender and race

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91
Q

How is MDRD4 formula expressed?

A

It is given as ml/min per 1/73m2 body surface area.

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92
Q

Is GRF exponential with creatinine?

A

Yes

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93
Q

Is eGFR accurate when it is <60ml?

A

No

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94
Q

Is eGFR accurate when under 18 years?

A

No

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95
Q

What is the normal GFR?

A

100ml

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96
Q

What is CKD 1?

A

> 90

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97
Q

What is CKD 2?

A

60-89

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98
Q

What is CKD 3?

A

30-59

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99
Q

What is CKD 4?

A

15-29

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100
Q

What is CKD 5?

A

<15

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101
Q

What percentage of diabetes are diagnosed with kidney problems?

A

30-40%

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102
Q

What is the first sign of diabetes nephroapthy?

A

Microalbunuria (not detected by a stranded dip stick)

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103
Q

What is the pathogenesis of diabetic nephropathy?

A

Hyperglycaemia leads to increased growth factors, RAAS activation, production of advanced glycosylation end-products and oxidative stress.
This causes increase glomerular capillary pressure, podocyte damage and endothelial dysfunction.
Albuminuria is the first sign. There will then be nodule formation and fibrosis.

The process is:
	Hyperglycaemia
	Volume expansion
	Intraglomerular hypertension
	Hyperinfiltration
	Proteinuria
	Hypertension and renal failure
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104
Q

Will an ACEi deterioration renla artery stenosis?

A

Yes

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105
Q

is RAAS unregulated in renal artery stenos?

A

Yes

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106
Q

What is the effect on renal size in renal artery stenosis?

A

> 1.5cm

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107
Q

What is the treatment of renal artery stenos?

A

Management:

Medical:
• BP control (not ACEi/ARB)
• statin
• if diabetic, good glycaemic control

Lifestyle
• smoking cessation
• exercise
• (low sodium diet)

Angioplasty
• rapidly deteriorating renal failure
• uncontrolled ↑BP on multiple agents
• flash pulmonary oedema

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108
Q

How long are amyloid fibrils?

A

8-10nm

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109
Q

How is amyloid stained?

A

congo red

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110
Q

What are the two types of amyloidosis?

A

There are two types:

  • AL: light chain see nin Myeloma
  • AA: too much serum amyloid associated protein that is seen in inflammatory diseases for example TB, RA and IBD
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111
Q

What are some examples of antibodies present in systemic lupus?

A

There is the presence of many antibodies for example direct against double stranded DNA (dsDNA).

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112
Q

What sex is more affected by systemic lupus arythmatosus?

A

Females

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113
Q

Why is there a low count of C4 in SLE?

A

There are immune complexes that accumulate and activate complement. This results in low C4 and renal damage.

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114
Q

What is a common presentation of SLE?

A

Presentation:

  • Rash
  • Photosensitivity
  • Ulcers
  • Arthritis
  • Serositis
  • CNS effects
  • Cytopenia’s
  • Renal disease
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115
Q

What is acute kidney injury?

A

Acute kidney injury is a syndrome of decreased renal function, measured by serum creatinine or urine output, occurring over hours-days.

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116
Q

What are the three features of AKI?

A

AKI:

  • Rise in creatinine >26umol/L within 48 hours
  • Rise in creatinine >1.5 x baseline within 7 days
  • Urine output <0.5mL/kg/hour for 6 consecutive hours
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117
Q

What are some causes of AKI?

A
  • sepsis
  • major surgery
  • cariogenic shock
  • drugs
  • hepatorenal syndrome
  • obstruction
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118
Q

What is oliguria defined as?

A

Oliguria is urine output that is less than 1 mL/kg/h in infants, less than 0.5 mL/kg/h in children, and less than 400 mL or 500 mL per 24h in adults.

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119
Q

Out of oliguric and non-oliguric, which is easier to mange?

A

Non-oliguric

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120
Q

What are e-Alerts?

A

Electronic alerts (e-alerts) for AKI have been introduced in the UK in order to facilitate earlier detection and improve management.

This is calculated:

  • Serum creatinine ≥1.5 times higher than the median of all creatinine values 8–365 days ago
  • Serum creatinine ≥1.5 times higher than the lowest creatinine within 7 days
  • Serum creatinine >26 µmol/L higher than the lowest creatinine within 48 h
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121
Q

Give some examples of pre-renal causes of AKI?

A
  • haemorrhage
  • D and V
  • burns
  • cariogenic shock
  • sepsis
  • drugs and toxins
  • hypotension
  • hypoxia
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122
Q

What is the pathology of pre-real causes of AKI?

A

There is decreased vascular volume and cardiac output. There will be systemic vasodilation and renal vasoconstriction

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123
Q

What is the pathology of renal causes of AKI?

A

There is damage to the kidney cells

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124
Q

What are some causes of renal AKI?

A
  • GM
  • ATN
  • Drugs
  • Vasculitis
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125
Q

What is the pathology of post-renal causes of AKI?

A

There is obstruction.

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126
Q

What is the causes of post-renal causes of AKI?

A
  • stones
  • malignancy
  • clot
  • lymph nodes
  • prostate
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127
Q

What is the most common cause of post-renal AKI in males?

A

Prostate

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128
Q

What is the most common causes of intrinsic AKI?

A

Acute tubular necrosis accounts for 80%

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129
Q

Can gentamicin cause AKI?

A

Yes

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130
Q

What is rhabdomyolysis?

A

Skeletal muscle is broken down very quickly. There is then the release of the contents into the extracellular space. An increase in cytokine ad decrease in NO cause renal vasoconstriction. Myoglobin will be filtered by the glomeruli causing obstruction and inflammation.

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131
Q

What is acute tubular necrosis?

A

There is prolonged renal hypo-perfusion causing intrinsic renal damage.

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132
Q

What are some causes of ATN?

A
  • Hypotension
  • Sepsis
  • Toxins
  • Or often, all three
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133
Q

What are some examples of exogenous toxins that can cause AKI?

A
  • Drugs (eg, NSAID’s gentamicin, ACEinh)
  • Contrast
  • Poisons (eg, metals, antifreeze)
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134
Q

What are some examples of endogenous toxins that can cause AKI?

A 
Endogenous
•	Myoglobin
•	Hemoglobin
•	Immunoglobins
•	Calcium
•	Urate
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135
Q

Why can’t NSAIDs be used in AKI?

A

When pressure falls, prostaglandins dilate the afferent arteriole to increase flow.

NSAIDs reversibly inhibit the production of renal prostaglandins via their inhibition of COX-1 and COX-2. Renal prostaglandins cause dilatation of the renal afferent arteriole. This mechanism is important for maintaining GFR when renal blood flow is reduced.

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136
Q

Why can’t ACE inhibitors be used in AKI?

A

Angiotensin II constricts the efferent to allow the kidney to deal with hypoperfusion. Therefore, ACEi are contraindicated.

137
Q

What are some investigations for AKI?

A 
Investigations:
•	Acute or chronic?
•	Bloods – both urea and creatinine ↑
•	Potassium
•	Urine output (usually <400ml/day)
•	Clinical assessment of fluid status
	(BP, JVP, oedema, heart sounds)
•	Underlying diagnosis (history, exam, meds)
•	GN screen
•	Renal ultrasound
138
Q

What is the treatment of AKI?

A

Immediate treatment:
• Airway and Breathing
• Circulation – shock - restore renal perfusion
• hyperkalemia
• pulmonary oedema
• Remove causes
• drugs
• sepsis
• Exclude obstruction & consider ‘renal’ causes
• are the pre-renal causes sufficient to account for AKI?
• Ask for help: ICU or renal unit

139
Q

What is the significant of potassium and AKI?

A

Decreased GFR will result in potassium retention. There will be tall tented T waves.
If the potassium is <6, it does show abnormality but there is no immediate concern. It the potassium is 6-6.4, there is a risk of arrhythmia and there is needs to be immediate treatment (especially if there are ECG changes).
It the potassium is >6.5 this is a medical emergency.

140
Q

What is the treatment of hyperkalaemia in AKI?

A

Treatment:

  • Reduce absorption from gut – Calcium Resonium 15g 4x day orally (or enema), new drugs coming
  • Insulin 10-15units actrapid+ 50ml 50% dextrose moves potassium into cells (watch BM)
  • Calcium gluconate 10ml 10% as cardiac membrane stabiliser
141
Q

Why is there oedema in AKI?

A

There is retention of sodium and water

142
Q

What is the treatment of metabolic acidosis in AKI?

A

There is a risk of metabolic acidosis as there is reduced capacity to secrete hydrogen ions and generate bicarbonate.

There should be bicarbonate supplementation:
- Iv NaBicarb 1.26% iv

143
Q

What concentration of potassium means that there has to be dialysis?

A

> 6,5

144
Q

What percentage of AKI returns to baseline kidney function?

A

85%

145
Q

Describe the polyuric stage of AKI?

A

Recovery:
• Often a polyuric phase for 48-72hr: increased urine production
• May be up to 6l urine/day
• Often subsequent low K, Ca, Mg as ‘low quality urine
• Tubules fail to concentrate urine

146
Q

What staging is used for AKI?

A

KDIGO

147
Q

What level of potassium is a medical emergency?

A

> 6.5

148
Q

Why should a renal ultrasound be carried out in AKI?

A

Renal ultrasound:

This should be done to exclude obstruction. This also gives indication on the size of the kidney.
Loss of cortico-medullar differentiation suggests CKD.

149
Q

Should kidney dialysis e given in AKI if there is refractory pulmonary oedema?

A

Yes

150
Q

What defines CKD?

A

CKD = kidney damage or GFR<60ml/min per 1.73m2 for 3 months or more.

151
Q

What GFR defines CKD?

A

<60

152
Q

What is serum creatine a product of?

A

Muscle metabolism

153
Q

What are some problems of serum creatine for determining GFR?

A

Exponential relationship leads to:

  1. Slow recognition of loss of the first 70% of renal function ie LAG TIME
  2. Surprise at the sudden rise in creatinine with late renal referral

Effect of muscle mass leads to:

  1. Overestimation of function in women
  2. Overestimation of function in the elderly
  3. Overestimation in other low muscle mass groups e.g. amputees, para/quadriplegics, rheumatoid arthritis
154
Q

Is there over or under estimation of the GFR in low muscle group people?

A

Over estimation

- this is because the creatinie is inversely proportional to GFR

155
Q

What four factors make the MDRD-4 formula?

A

serum creatine, are, sex, race

156
Q

What are some problems with eGFR (MDRD)?

A

Problems with eGFR:
• Only validated in whites and African Americans
• Mean age 50 ie not validated in elderly
• Values above 60ml/min not distinguishable so reported as eGFR >59ml/min
• Drug dosing – doesn’t take weight into account
• AKI – not valid
• Pregnancy

157
Q

What is stage one CKD?

A

> 90

158
Q

What is stage two CKD?

A

60-89

159
Q

What is stage three CKD?

A

30-59

160
Q

What is stage four CKD?

A

15-29

161
Q

What is stage five CKD?

A

<15

162
Q

What eGFR means there is established renal failure?

A

<15

163
Q

How much protein in the urine is normal?

A

<150mg/day

- about 2/3 is albumin

164
Q

Does proteinuria need to be quantified?

A

Yes

165
Q

What is the normal ACR?

A

<2.5

166
Q

What is the normal PCR?

A

<20

167
Q

What ACR shows albuminuria?

A

> 30

168
Q

What are some causes of CKD?

A
  • diabetic nephropathy
  • renovascular disease
  • chronic GM
  • reflux
  • ADPKD
  • obstructive
169
Q

What are some symptoms of advanced CKD?

A

Symptoms of advanced CKD

  • Pruritus
  • Nausea, anorexia, weight loss
  • Fatigue
  • Leg swelling
  • Breathlessness: Kussmauls due to metabolic acidosis
  • Nocturia
  • Joint/bone pain: less calcitriol produced
  • Confusion
170
Q

Why is there bone pain in advanced CKD?

A

Less calcitriol produced

171
Q

What are some signs of advanced CKD?

A
  • Peripheral and pulmonary oedema
  • Pericardial rub
  • Rash/excoriation
  • Hypertension: increased water and sodium retention
  • Tachypnoea
  • Cachexia
  • Pallor &/or lemon-yellow tinge
172
Q

Why is there hypertension in advanced CKD?

A

There is sodium and water retention

173
Q

What drug can be used in CKD for hypertension?

A

ACE inhibitors

174
Q

What is the treatment of anaemia in chronic renal disease?

A

This is common, particularly when eGFR <30.

Iron absorption & utilisation suboptimal

Replace iron, B12, folate first if low

ESA eg Darbepoietin alfa (EPOD) 30microg every 2 weeks. The trigger is usually Hb <100g/l and the target Hb 100-120g/l.

175
Q

What are some examples of phosphate binders for CKD?

A

• Phosphate binders: target phosphate 0.9-1.5 mmol/l and inhibit absorption
Calcium based : calcium carbonate/acetate
Non-calcium : sevelamer, lanthanum, aluminium

176
Q

Why may parathyroid surgery be carried out in CK?

A

• Parathyroidectomy: Parathyroid surgery in patients with end-stage kidney disease (ESKD) is an effective therapy for normalization or stabilization of calcium and parathyroid hormone (PTH) metabolism, and for improving renal osteodystrophy

177
Q

What is the most common mutation in ADPKD?

A

PKD1

178
Q

What should the diet of someone on dialysis have?

A

Should be low in potassium, sodium and phosphate

179
Q

What are some mediccal conditions that means kidney transplant is contraindicated?

A 
Medical contraindications:
•	Hyertension
•	Hypotension
•	Disease that will recur in the transplant 
•	Cancer
180
Q

What are some temporal conditions that means kidney transplant is contraindicated?

A

Temporary:

  • Active infection
  • HIV with viral replication
  • Unstable CVD
181
Q

What is the difference in management of type one and two diabetic kidney disease?

A

One: transplanted clinic
Two: dialysis

182
Q

What are some conditions for a kidney transplant from a deceased donor?

A

Decreased doners:

  • Brain stem death – heart beating/non-heart beating
  • No malignancy or unidentified/untreated infections
  • Good kidney function – you only get one kidney
183
Q

What is the average waiting time for a kidney transplant?

A

2-3 years

184
Q

What type of donor can type A blood get?

A

A and O

185
Q

What type of donor can type B blood get?

A

B and O

186
Q

What type of donor can type AB blood get?

A

O, A, B and AB

187
Q

What type of donor can type O blood get?

A

O

188
Q

What HLA are aimed to be matched for kidney transplant?

A

HLA-A, B and DR

189
Q

What is the mechanism of action of basiliximab?

A

This is a monoclonal antibody abasing IL-2

190
Q

What is the mechanism of action of tacrolimus?

A

Tacrolimus – calcineurin inhibitor

191
Q

What is the mechanism of action of Mycophenolate?

A

inhibitor of inosine-5’-monophosphate dehydrogenase - depletes guanosine nucleotides in T and B lymphocytes and inhibits proliferation

192
Q

When there is rejection in kidney transplant, what is the treatment?

A

Increase immunosuppression

193
Q

When there is infection in kidney transplant, what is the treatment?

A

The treatment is to reduce immunosuppresion and treat with antibiotic/anti-viral

194
Q

When there is malignancy in kidney transplant, what is the treatment?

A

The treatment is to reduce immunosuppression with +/- rituximab or chemotherapy.

195
Q

What is uraemia?

A

Uraemia is a clinical syndrome marked by elevated concentrations of urea in the blood and associated with fluid, electrolyte, and hormone imbalances and metabolic abnormalities, which develop in parallel with deterioration of renal function.

196
Q

What GFR is dialysis usually started on?

A

5-10

197
Q

can uraemia cause a metallictaste?

A

Yes

198
Q

What is haemodiaylsis?

A

Blood is passed over a semi-permeable membrane against dialysis fluid in the opposite direction.
Diffusion of solutes occurs down the concentration gradient. A hydrostatic gradient is used to clear excess fluid as required.

199
Q

Where is access achieved for haemodiaylsis?

A

Access is achieved via an arteriovenous fistula (artery and vein connection),

This should be created before the need for dialysis to avoid infection risk associated with central venous dialysis.

200
Q

How often is haemodiaylsis? required?

A

HD is required three times a week for 4 hours.

Multiple other options – mainly home based:
• 6h 3 times a week
• Short daily dialysis
• Daily overnight

201
Q

What are the aims of harm-dialysis?

A

The aims:
• Removal of solutes – e.g. potassium, urea: DIFFUSION
• Removal of fluid ‘ultrafiltration’ - pressure: HYDROSTATIC FILTRATION

202
Q

How are solutes removed during haemodialysis?

A

Diffusion

203
Q

What are some complications of haemodialysis?

A 
Complications:
•	‘Crash’  (acute hypotension)
•	Access problems
•	Cramps
•	Fatigue
•	Hypokalemia
•	Blood loss
•	Dialysis disequilibrium
•	Air embolism
204
Q

Describe peritoneal dialysis?

A

This uses the peritoneum as a semi-permeable membrane. A Cather is inserted into the peritoneal cavity and fluid infused.

Solutes diffuse slowly across.

Ultrafiltration is achieved by adding osmotic agents to the fluid.

It is a continuous process with intermittent drainage and refilling of the peritoneal cavity, performed at home

205
Q

How is ultrafiltration achieved in peritoneal dialysis?

A

Adding osmotic agents

206
Q

What is the difference between APD and CAPD (peritoneal dialysis)?

A

APD, Automated Peritoneal Dialysis is a type of Peritoneal dialysis. You exchange fluid during the night.
CAPD, Continuous Ambulatory Peritoneal Dialysis is a type of Peritoneal dialysis where you exchange fluid four times a day.

207
Q

What are some complications of peritoneal dialysis?

A

Complications:

  • Infection - peritonitis
  • Glucose load – development or worsening control of diabetes
  • Mechanical – hernia, diaphragmatic leak, dislodged catheter
  • Peritoneal membrane failure
  • Hypoalbuminaemia
  • Encapsulating peritoneal sclerosis
208
Q

Is glucose overload a complication of peritoneal dialysis?

A

Yes

209
Q

What are some examples of patients that are not suitable for peritoneal dialysis?

A 
Some patients not suitable:
•	Grossly obese
•	Intra-abdominal adhesions
•	Frail
•	Home not suitable
210
Q

Is anaemia supplemented by dialysis?

A

• Anaemia: Need erythropoiesis supplementing agents and iron

211
Q

Is renal bone disease supplemented by dialysis?

A

• Renal bone disease: Need phosphate binders and vitamin D

212
Q

Is neuropathy supplemented by dialysis?

A

N

213
Q

Is endocrine disturbance supplemented by dialysis?

A

No

214
Q

What are some pros and cons of kidney dialysis?

A 
Pros:
•	No dialysis
•	Better level of renal function
•	Can live much more independently
•	Better life expectancy
•	Fertility better
Cons:
•	Immunosuppressive medication for duration of transplant
•	Increased cardiovascular risk
•	Increased infection
•	Post transplant diabetes
•	Skin malignancies and others
215
Q

What is the commonest male malignancy?

A

Prostate cancer

216
Q

What is the ten year survival of prostate cancer?

A

84%

217
Q

What is the incidence of prostate cancer?

A

1 in 6 men

218
Q

What are some risk factor for prostate cancer?

A
  • increasing age (uncommon less than 50)
  • family history
  • BRCA, PTEN and TP53
  • african american men
  • industria chemicals for example cadmium and UV
  • hormonal
  • men who become sexually active at a younger age
  • high fat diet
  • elevated 5-reductase levels
219
Q

Why are most men asymptomatic with prostate cancer?

A

This is because there s early screening with PSA

220
Q

What are some local suymptoms of prostate cancer?

A

Local (66%) and locally advanced (27%) : OFTEN ASYMPTOMATIC
• Painful or slow micturition, Urinary retention (may cause anuria, uraemia), Urinary tract infection
• Haematuria

221
Q

What is the most common symptom of metastatic prostate cancer?

A

Bone pain

222
Q

What are some investigations for prostate cancer?

A

Diagnosis and Screening:

  • DRE - digital rectal examination
  • PSA - prostate-specific antigen
  • PIRADS - Prostate MRI
  • TRUS - guided needle biopsy
223
Q

What is the most common type of cancer is the prostate?

A

Adenocarcinoma

224
Q

Where is the most common location of prostate cancer?

A

Peripheral zone

225
Q

Describe the Gleason grading system

A

The Gleason score is the sum of the two most prominent Gleason grades seen histologically in a sample. Gleason scores provide useful prognostic information.

Gleason score = the most common grade + the highest other grade in the samples
For example, if the biopsy samples show that:
• most of the cancer seen is grade 3, and
• the highest grade of any other cancer seen is grade 4, then
• the Gleason score will be 7 (3+4).

226
Q

What does a gleason stage of <4 show?

A

Well differentiated

227
Q

What does a gleason stage of 5-7 show?

A

Moderalty differentiated

228
Q

What does a gleason stage of >7 show?

A

Poorly differentiated

229
Q

What is PSA?

A

This is a Serine protease (33kD) secreted into seminal fluid. It is responsible for liquefaction of seminal coagulation.
Small proportion leaks into circulation

230
Q

What is the link of PSA and age?

A

It will tend to rise with age.

231
Q

What is the advantage of PSA screening?

A

PSA measurements can provide information about prostate cancer from the initial screening and early detection through to the staging of the disease. It can also be used to monitor the progression.

232
Q

What is localised prostate cancer?

A

Localised prostate cancer is cancer that’s inside the prostate and hasn’t spread to other parts of the body.

233
Q

What are the treatment options for localised prostate cancer?

A 
•	Watchful waiting
•	Active Surveillance
•	Radiotherapy (with or without LHRH analogue)
o	external beam
o	brachytherapy
•	Radical prostatectomy 
•	Cryotherapy/HIFU
•	TURP if symptomatic
234
Q

What are some metastatic complications of prostate cancer?

A 
Spinal cord compression:
o	Urological emergency
o	Severe pain
o	Off legs
o	Retention
o	Constipation
o	Urgent MRI
o	Radiotherapy vs spinal decompression surgery

Ureteric obstruction
• Anorexia, weight loss, raised creatinine
• To nephrostomize or not and then to stent or not
• Temporary measure will not improve cancer progression

235
Q

What is Orchidectomy ?

A

The removal of the testes

236
Q

What are some treatment options of advanced prostate cancer?

A

Advanced prostate cancer:

Orchidectomy and LHRH analogue treatment produce good responses in 70-80% patients, but long-term outcome is less favourable as remission is not usually maintained.

  • Androgen ablation therapy - medical castration (LHRH analogue) or surgical castration (orchidectomy)
  • Chemotherapy
  • TURP for relief of symptoms
  • Radiotherapy
237
Q

Describe the Hypothalamic pituitary testicular axis

A

Luteinising hormone-releasing hormone (LHRH) is secreted from the hypothalamus. LHRH then stimulates the pituitary gland to produce luteinising hormone (LH) and follicle-stimulating hormone (FSH). In turn, LH and FSH stimulate the testes to secrete testosterone.

Adrenocorticotrophic hormone (ACTH) is released from the pituitary gland after stimulation by corticotrophin-releasing hormone (CRH) which is secreted from the hypothalamus.1

ACTH regulates secretion of adrenal androgens, some of which are converted to testosterone.

238
Q

What are some risk factors for bladder cancer?

A

Risk factors:

  • Age – rare <50yrs, most common 80th decade
  • Male > Female
  • Race- more common in Caucasians
  • Chronic inflammation- stones, infection (schistosomiasis), long term catheters
  • Drugs-cyclophosphamide, pioglitzone
  • Pelvic radiotherapy
  • Occupation
239
Q

What occupation can give an increased risk of bladder cancer?

A

Occupational exposures to polycyclic aromatic hydrocarbons (PAH) increased the risk of bladder cancer. There is a 25-45 year latency.

240
Q

What are some drugs that can increase the risk of bladder cancer?

A

Pioglitazone and cyclophosphamide

241
Q

What are some features of bladder cancer?

A
  • Classically painless frank haematuria

* Some present with microscopic haematuria (5% serious causes)

242
Q

What is the most common cancer of the bladder?

A

Transitional cell carcinoma: 75% superficial and 25% invasive

243
Q

What is the staging of bladder cancer?

A

NMIBC:
Non-muscle invasive Bladder Cancer
MIBC:
Muscle Invasive Bladder Cancer

244
Q

What is TURBT?

A

A trans urethral resection of bladder tumour (TURBT) is usually the first treatment you have for early bladder cancer. Your surgeon removes the tumour in your bladder through the urethra. The urethra is the tube that carries urine from the bladder to the outside of your body.

245
Q

What is mitomycin C?

A

Mitomycin C:

This is a type of chemotherapy drug. It inhibits DNA synthesis. It is given once off or as a 6-week course.

246
Q

What is BCG therapy?

A

BCG therapy:

This is a type of immunotherapy. This causes a cell mediated immune response. There is induction and maintenance.

247
Q

What is radical cystectomy?

A

Radical cystectomy:

This is where the bladder and prostate/uterus removed. The urine is diverted.

The mortality 2%.

Sometimes required after radiotherapy failure “salvage cystectomy”.

248
Q

What are some risk factors for renal cancer?

A

Risk factors:

  • Smoking (RR 1.4-3.0): this causes choric hypoxia and DNA damage
  • Obesity (RR 1.5-3.0)
  • Hypertension
  • Acquired renal cystic disease (RR 4)
  • Haemodialysis
249
Q

What are some features of bladder cancer

A

Presentation:

80% incidental
<25% systemic symptoms-
• Night sweats, Fever, Fatigue,Weight loss
• 10% classic triad- mass, pain, haematuria
• Varicocele
• Lower limb oedema

• Paraneoplastic syndrome

250
Q

What is paraneoplastic syndromes in bladder canceR?

A

Paraneoplastic syndromes: this occurs when the tumour releases a hormone

• Polycythaemia:(3-10%)
• Hypercalcaemia:(3-13%) either from a PTH-like substance, or from osteolytic hypercalcaemia
• Hypertension:(Up to 40%) renin secretion
• Deranged LFT’s: Stauffer’s syndrome, from hepatotoxic tumour products
• Rare:
o ACTH (Cushing’s syndrome)
o enteroglucagon (protein enteropathy)
o prolactin (galactorrhoea)
o insulin (hypoglycaemia)

251
Q

What are some investigation for Renal cancer?

A

Diagnosis and Investigation:

•	Initial diagnosis:
o	Usually on USS
•	CT kidneys +/- MRI RV
•	Renal Biopsy
•	CT Chest
252
Q

What is the most common cancer of kidneys?

A

Clear cell

253
Q

What stage is renal cancer gone into the renal vein?

A

Stage three

  • b is below the diaphargm
  • c is above the diaphragm
254
Q

What is Nephron sparing surgery?

A

Nephron sparing surgery (NSS), also known as partial nephrectomy, is kidney surgery where only part of the kidney is removed. It is most often performed as a first step in the treatment certain types of kidney cancer.

255
Q

Can tyrosine kinase inhibitor be used in metastatic kidney disease?

A

Tyrosine kinase inhibitors can be used in metastatic kidney disease.

256
Q

What are some risk factors for testicular cancer?

A 
Risk factors:
•	Age 20-45yo
•	Cryptorchidism
•	HIV
•	Caucasian population
257
Q

What are some tumour markers of testicular cancer?

A

Tumour markers:
 Alpha-fetoprotein (50-70% Teratoms and Yolk Sac Tumours)
 Beta hCG (40% Teratoma, 15% Seminoma)
 LDH (10-20% Seminoma)

258
Q

Is alpha-fetoprotein a tumour marker of testicular cancer?

A

Yes

259
Q

Is beta hCG a tumour marker of testicular cancer?

A

Yes

260
Q

What is the most common testicular cancer?

A

Germ cell: seminoma and teratoma

261
Q

What type of tumours can be in testes?

A
  • germ cell: seminma, teratoma
  • stroma: leydig, sortoli
  • lymphoma
262
Q

What is the treatment of testicular caner?

A

Treatment:

  • Radical Orchidectomy
  • Chemotherapy
  • Para-aortic nodal radiotherapy
  • Retroperitoneal Lymph Node Dissection
263
Q

What is the treatment of penile cancer?

A

Treatment:

  • Circumcision
  • Topical treatment CO2/5FU
  • Penectomy +/- reconstruction
  • Lymphadenectomy
  • Chemo-radiotherapy
264
Q

What is Penile cancer associated with?

A

This is rare (0.2% male cancers in the west).

It is associated with HPV infection (16,18,21) and smoking.

265
Q

Is penile cancer rare in circuited males?

A

Yes

266
Q

What is bacteriuria?

A

Bacteria in the urine

267
Q

What is the difference between uncomplicated and complicated UTI?

A

Uncomplicated UTI
⬜ Lower UTI, normal structure & neurology

Complicated UTI: there will be a structural/functional abnormality
⬜ UUTI +/- systemic signs and symptoms
⬜ CAUTI: catheter associated UTI

268
Q

When is bacteriuria common?

A

This is common in preschool age, girls being affected more than boys.
Adults:
- Non pregnant females (1.3%)
- Males (0.1%)

Other risk groups:
	Hospitalized
	Catheterized 
	Diabetics
	Anatomical abnormalities
	Pregnant patients
269
Q

When should asymptotic bacteriuria be treated?

A

Management:

Treat asymptomatic bacteriuria only in 
•	Preschool children
•	Pregnancy
•	(Renal transplant)
•	(Immunocompromised)
270
Q

Is ascending or descending UTIs more common?

A

UTIs develop by either ascending or descending bacterial invasion into the urinary tract. The more common mode of infection is the ascending pathway, where faecal flora gain access to the urinary tract via colonization of the urethra. Rarely, a UTI occurs by way of the descending pathway.

271
Q

Describe ascending UTI?

A 
Ascending
•	Urethral colonization 
•	female>male
•	Multiplication in bladder
•	Ureteric involvement
272
Q

Describe descending UTI?

A

Descending/hematogenous:

  • Blood-born infections
  • Involvement of renal parenchyma
273
Q

95% if UTIs are caused by a single organism. What are some causes of multiple organisms?

A

Multiple organisms in
o Long term catheters
o Recurrent infection
o Structural/ neurological abnormalities

274
Q

What are some features of a UTI?

A 
Features:
o	Suprapubic discomfort
o	Dysuria
o	Urgency
o	Frequency
o	Cloudy, blood stained, smelly urine
o	Low-grade fever
o	Sepsis

Failure to thrive, jaundice; in
neonates.
Abdominal pain and vomiting in children.

Nocturia, incontinence, confusion in the elderly

275
Q

What is the most common cause of UTI?

A
  • E coli

This is a gram negative bacilli.

276
Q

What are some investigations for an uncomplicated UTI for non-pregnant women?

A

Non-pregnant women

1st presentation, culture not mandatory
 Dipstick, high false positive rate
 Check previous culture results
 Antibiotic 3-7/7

No response to treatment
• Urine culture
• Change antibiotic

277
Q

What are some investigations for an uncomplicated UTI for children and men?

A

Children and men
Send urine for each and every presentation
■ Treat appropriately

278
Q

What are some investigations for an uncomplicated UTI for pregnant women?

A

Pregnant women:

This is common and send urine sample with each presentation.

Treat for 7-10 days
• Amoxicillin and cefalexin relatively safe
• Avoid Trimethoprim in 1st trimester
• Avoid Nitrofurantoin near term

May need hospital admission for IVs if severe.

Can develop into pyelonephritis (~30%).

279
Q

How is a recurrent UTI defined as?

A

• ≥2 episodes in six months
• ≥3 episodes/year
This mostly affects women.

280
Q

What is the management of recurrent UTI?

A 
Management:
•	Send sample with each episode
•	Encourage hydration
•	Encourage urge initiated and post coital voiding
•	Intravaginal/oral oestrogen
•	Urology investigation

Self-administered single dose/short course therapy. Single dose post coital abx.

Prophylactic antibiotics If simple measures fail. Ideally six months
■ Trimethoprim
■ Nitrofurantoin: Associated risk with long term use

There is a risk of development of antimicrobial resistance.

281
Q

Describe a catcher associated UTI

A

Catheter associated UTI:

Millions of catheter insertions/year.

Colonization common and treatment not required.

Infection (HAI, 35%)
• Disturbance of the flushing system
• Colonization of the urinary catheter
• Biofilm production by bacteria

Likely organisms
• Patient’s flora
• Healthcare environment

282
Q

What are some complication of catheters?

A
  • CAUTI
  • Obstruction-hydronephrosis
  • Chronic renal inflammation
  • Urinary tract stones
  • Long term risk of bladder cancer
283
Q

What are some preventative measures of catheter infections?

A

Prevention of catheter infections:

o	Catheterize only if necessary
o	Remove when no longer needed “Forgotten catheter”
o	Remove/replace if causing infection
o	Catheter care (bundles)
o	Hand hygiene
284
Q

What is the treatment of catheter infections?

A

Treatment of catheter related UTI:

  • Check recent /previous microbiology
  • Start empirical antibiotics
  • Remove catheter if not needed
  • Replace catheter under antibiotic cover

Will need antibiotics.

285
Q

What is acute pyelonephritis?

A

This is an upper urinary tract infection and it is moderate to severe.

This is an ascending infection involving the pelvis of the kidney. There is an enlarged kidney and abscesses on the surface.

286
Q

What is the management of acute pyelonephritis?

A

Management:

  • Check previous/recent microbiology results
  • Send urine +/- blood culture+/- imaging
  • Community: Co-amoxiclav/ Ciprofloxacin/ /Trimethoprim
287
Q

What is the difference in treatment for uncomplicated and completed pyelonephritis?

A

Uncomplicated pyelonephritis, 7-14/7 antibiotic

Complicated pyelonephritis, ≥ 14/7 therapy +/- radiological/surgical intervention

288
Q

Is renal access a complication of pyelonephritis?

A

Yes

289
Q

What are some risk factors for

Perinephric abscess?

A 
Risk factors
•	Untreated LUTI,
•	anatomical abnormalities
•	Renal calculi
•	Bacteraemia, haematogenous spread
290
Q

What are some invesitgatins for a complicated UTI?

A

All patients
• FBC, U+Es, CRP
• Urine sample
o Urethral, CSU, Suprapubic, Nephrostomy
• Blood culture if pyrexia or hypothermic
• Renal ultrasound
• CT KUB: CT of kidneys, ureters and bladder
• Antibiotic therapy 14/7 or more

291
Q

What is Pyuria?

A

Pus in the urine

292
Q

What is the difference in route of administration of antibiotic for uncomplicated and complicated UTI?

A

Uncomplicated is Oral and complicated is IV

293
Q

What is prostatitis?

A

Inflammation of the prostate gland

294
Q

Describe Acute bacterial prostatitis?

A

This is a localised infection and it is usually spontaneous. It is most llkey caused by E coli.

295
Q

What are some investigations of Acute bacterial prostatitis??

A 
Investigations 
•	Urine culture, usually positive
•	Blood culture
•	Trans-rectal U/S
•	CT/ MRI
•	Obtaining prostatic secretions NOT advisable
296
Q

What are some complications of Acute bacterial prostatitis??

A 
Complications:
•	Prostatic abscess
•	Spontaneous rupture: Urethra, rectum
•	Epididymitis
•	Pyelonephritis 
•	Systemic sepsis
297
Q

What is the most common treatment for acute bacterial prostatitis?

A

• Ciprofloxacin/ Ofloxacin (no streptococcus cover)

298
Q

What does chronic prostatitis usually follow?

A

• Ciprofloxacin/ Ofloxacin (no streptococcus cover)

299
Q

What is epididymis?

A

This is inflammation of the epididymis

300
Q

What are some causes of epididymis?

A

Aetiology
• Ascending infection from urethra
• Urethral instrumentation

301
Q

What are some symtpoms of epididymis?

A

Symptoms
• Pain, fever, swelling, penile discharge
• Symptoms of UTI/ urethritis

302
Q

What are some common organisms of epididymis?

A

Common organisms:
• GNB, enterococci, staphylococci
• TB in high risk areas and individuals
• In sexually active men: Rule out Chlamydia and N.gonorrhoea (urethritis)

303
Q

What is orchitis?

A

Inflammation of the testes

304
Q

What are some symptoms of orchitis?

A 
Symptoms include:
•	Testicular pain and swelling
•	Dysuria 
•	Fever
•	Penile discharge
305
Q

What is the most common viral cause of orchitis?

A

Mumps

306
Q

Describe bacterial orchitis

A 
Pyogenic (pus)
•	Complication of epididymitis 
•	Acutely unwell
•	Rule out sexually transmitted bacteria
•	Intravenous antibiotics
o	As per complicated UTI
•	Urgent urological review

Complications
• Testicular infarction
• Abscess formation

307
Q

What is Fournier’s gangrene?

A

This is a form necrotising fasciitis and it is usually >50 years.
There is a rapid onset and spreading of infection.

308
Q

What are some risk factors for Fournier’s gangrene?

A 
Risk factors:
•	UTI
•	Complications of IBD
•	Trauma
•	Recent Surgery
309
Q

What is the fist line management for Fournier’s gangrene?

A

Surgical debridement

310
Q

Describe the anatomy of the kidneys

A

The kidneys are paired retroperitoneal organs located between T12-L3.

The right lies lower than the left.

They are normally 10-12cm length, 5-7cm wide and 3cm thick

Gerota’s Fascia covers the kidneys and adrenal glands. This is deficient inferiorly.

The upper pole of the kidney is more posterior and medial. Medal surface is more anterior.

311
Q

What are the three parts of the ureters?

A

proximal, mid and distal

312
Q

What are the four layers f he ureters?

A 
4 layers – vary depending on site
•	Urothelial mucosa
•	Lamina propria 
•	Muscular layer
•	Adventitial layer
313
Q

What are the three most common places of ureteric stones?

A
  • pelvis
  • crossing of iliac artery
  • uretero-vescilar junction
314
Q

What are some intrinsic risk factor for kidney stones?

A 
Intrinsic factors:
•	Sex (males affected twice as much)
•	Age: peak is 20-50
•	family history : 25%
•	Comorbid conditions
315
Q

What are some extrinsic isk factor for kidney stones?

A 
Extrinsic factors
o	Fluid intake
o	Diet: high animal protein (high oxalate, low pH, low citrate), high salt and low calcium diets
o	Lifestyle: sedentary
o	Climate: higher in hot climates 
o	Country of residence (USA highest)
316
Q

Do males have a higher oxalate production?

A

Yes

317
Q

What is the rate of recurrence of a kidney stone?

A

The prevalence is increasing. Once a stone has formed, 50% will form another 10 years.

318
Q

Why is there a higher rate of kidney stones in summer?

A

In summer, there is higher urinary concentration and a lower pH. The water intake will also be lower.

319
Q

What are some symptoms of renal stones?

A

Symptoms

  • Persistent ache in lower back
  • Renal colic
  • Restlessness
  • Nausea
  • More frequent urination
  • Dysuria
  • Haematuria
320
Q

What is the most common type of renal stones?

A

Calcium oxalate stones

321
Q

Can uric acid stones be seen on x-ray?

A

NO

322
Q

Describe calcium renal stones

A

This is caused by too much calcium in the urine and this can be due to hypercalciuria, overactive parathyroid gland, kidney disease, sarcoidosis and cancer.

Calcium will usually bind to negative oxalate ion. This forms a black/brown stone which is radio opaque. These are more likely to be found in acidic urine.
Oxalate is found in some fruit, vegetables, nuts and chocolate.

Calcium can also bind to phosphate. These are dirty white, radiopaque and more likely to form in alkali urine.

323
Q

What foods can oxalate be found in?

A

Fruit, veg, nuts and chocolate

324
Q

Describe uric acid stones

A

These are red/brown and radiolucent.

Uric acid can lose a hydrogen ion and become a urea ion which binds to sodium, forming monosodium urate which crystallises.

Uric acid is a breakdown product of purines and hence eating high urine foods (shellfish, anchovies, red meant, organs) can increase the risk.

Gout is associated with uric acid stones.

325
Q

Describe struvite stones

A

These are a mix of magnesium, ammonium and phosphate (all three are known as struvite). This is caused by a variety of bacteria which use urease to break urea into carbon dioxide and ammonia.
The ammonia makes the urine more alkali and favours precipitation of magnesium, ammonium and phosphate.
These are known as staghorns. The staghorn means that the stones are branched that fill all or part of the renal pelvis and branch into several or all of the calyces. They are most often composed of struvite.

326
Q

What three compounds are in struvite stones?

A

Magnesium, ammonium and phosphate

327
Q

Can Struvite stones be seen on x-ray?

A

No

328
Q

When are Struvite stones common?

A

After a UTI

329
Q

Describe cystine stones

A

They can be seen on x-ray and These are caused by inherited cystinuria.

330
Q

Describe Xanthine stones

A

These are caused by enzyme deficiency that causes the build-up of xanthine deposits.

331
Q

Describe silica stones

A

These are rare and caused by certain medications of herbal supplements.

332
Q

What are some investigations for renal stones?

A

Investigations

  • History and examination
  • Bloods:U&E, CRP, FBC
  • Urine: Non visible haematuria= 85%
  • Imaging: Gold standard = CT KUB (non contrast)
First stone:
•	U&amp;E
•	Calcium
•	Urate
•	Urine dip
•	MSSU
•	(Sodium nitroprusside – Cystine)
•	Stone analysis
Recurrent:
•	U&amp;E
•	Calcium
•	Urate
•	venous bicarbonate
•	24 hour urine analysis
333
Q

What is the main imaging for renal stones?

A

Imaging:

CT KUB
• 94-100% sensitivity
• 92-100% specificity

Other benefits
•	Stone diameter
•	Skin to stone distance
•	Hounsefield units
•	No contrast
•	Lower radiation dose

Ultrasound:
• 45% - Sensitivity
• 88-94% specificity

X-ray KUB
o 44-77% sensitivity
o 80-87% specificity
o Better for follow up of known stone

334
Q

Does a CT KUB have a lower radiation dose than CT?

A

Yes

335
Q

Can analgesia be given for renal stones?

A

Yes

336
Q

What are some surgical management for renal stones?

A

Surgical: there are various options depending on location and size
• Ureteroscopy and basket: scope inserted into bladder and collect the stone
• Ureteroscopy and fragmentation
• FURS – flexible ureteroscopy
• ESWL – extracorporeal shockwave lithotripsy
• PCNL – percutaneous nephrolithotomy: scope used
• Emergency stent or nephrostomy

337
Q

What is a nephrostomy?

A

A nephrostomy is an artificial opening created between the kidney and the skin which allows for the urinary diversion directly from the upper part of the urinary system (renal pelvis).

Ureteric stents, also known as double J stents or retrograde ureteric stents, is a urological catheter that has two “J-shaped” (curled) ends, where one is anchored in the renal pelvis and the other inside the bladder.

338
Q

Describe ESWL

A

This produces a shockwave: Electrohydraulic, Electromagnetic and Piezoelectric

They have a direct effect: Shearing and Spalling/

Cavitation effect:
o Shockwave in fluid causes a microbubble
o Dissolved gas in fluid around bubble expands into bubble
o Bubble collapses
o Microjets
o Pit stone surface

339
Q

When would admission be required for kidney stones?

A

When admission is required?

o	Uncontrollable pain
o	Fever or signs of sepsis
o	Solitary kidney with a ureteric stone 
o	Bilateral ureteric stones
o	Renal failure caused by an obstructing stone

If discharging a patient be sure to give them clear worsening advice and when to come back to hospital

Urology (1 decks)

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