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Kidneys Flashcards

1
Q

List six functions of the kidneys.

A 
metabolic waste excretion
endocrine functions
drug metabolism/excretion
control of solutes and fluid status
blood pressure control
acid/base balance
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2
Q

What is the normal amount of protein excreted from the kidneys over 24 hours?

A

150mg

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3
Q

Name the three ways that urinary protein excretion is measured.

A
  • 24hr urine collection (g/24h)
  • protein:creatinine ratio on morning spot sample
  • albumin:creatinine ratio
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4
Q

Differentiate between non-visible haematuria and visible haematuria.

A
  • non: can be blood detectable on dipstick only

- visible: can come from anywhere in the urinary tract

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5
Q

List causes of visible haematuria.

A

kidney stones, infection, malignancy, cysts, inflammation

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6
Q

Define renal clearance (GFR) and how it is calculated.

A

= volume of plasma which would be cleared of the substance per unit of time

(urine conc of substance x urine volume) / plasma conc of substance

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7
Q

The MDRD*4 formula for estimation of GFR from plasma creatinine concentration is based on which 4 factors?

A

plasma creatinine conc.
age
gender
race

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8
Q

Describe the staging of chronic kidney disease using eGFR.

A

1: eGFR > 90 ml/min normal
2. 60-89 normal unless evidence of kidney disease
3. 30-59 moderate impairment
4. 15-29 severe impairment
5. < 15 advanced renal failure

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9
Q

List some of the secondary causes of GN.

A
  • diabetes
  • haem: myeloma, CLL, PRV
  • bacterial endocarditis
  • resp: bronchiectasis, lung cancer, TB
  • gastro: ALD, IBD, coeliac
  • drugs: NSAIDs, bisphosphonates, heroin
  • rhemu: RA, lupus, amyloid
  • ID: hepatitis, HIV, antibiotics, malaria
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10
Q

Following presentation and history, what is required to make a diagnosis of GN?

A

kidney biopsy

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11
Q

What are the three ways in which the kidney cortex biopsy is examined?

A
  • light microscopy (glomerular and tubular structure)
  • immunofluorescence (looking for Ig and complement)
  • electron microscopy (BM and deposits)
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12
Q

Describe how different types of GN present including RPGN, nephritic and nephrotic.

A
  • RPGN: rapid rise in serum creatinine, crescentic damage, vasculitis, lupus, IgA
  • nephritic: blood and protein in urine, high BP, rising sCr, proliferative/acute inflammation, IgA, lupus, post-infectious
  • nephrotic: >3,5mg proteinuria, low sAlb, oedema, non-proliferative, podocyte damage, minimal change/FSGS/membranous
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13
Q

List the four criteria used to define nephrotic syndrome.

A
  1. 3.5g proteinuria per 24hr
  2. Serum albumin <30
  3. Oedema
  4. Hyperlipidaemia
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14
Q

What are the two main risks associated with nephrotic syndrome?

A

risk of venous thromboembolism

increased risk of infection

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15
Q

What are the possible therapeutic strategies of GN in relation to the stage:

  • insult precipitant e.g. infection, antibody
  • injury
  • response to injury
  • outcome
A
  • control infection
  • remove AB/IC
  • steroids, cytotoxics, anti-hypertensives
  • dialysis, transplantation, slow progression, resolution
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16
Q

Describe the four stage spectrum of IgA nephropathy.

A

1 minor urinary abnormalities
2 hypertension
3 renal impairment and heavy proteinuria
4 rapidly progressive GN

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17
Q

What is the most common primary glomerular disease?

A

IgA nephropathy causing mesangial disease

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18
Q

What causes IgA nephropathy?

A

precipitated by infection - Occurring intercurrently with an episode of pharyngitis (synpharyngitic)
secondary = HSP, cirrhosis, coeliac

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19
Q

Describe the brief pathophysiology of IgA nephropathy and how it presents.

A

abnormal/over-production of IgA1 leading to mesangial deposition and subsequent proliferation

haematuria, hypertension, proteinuria

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20
Q

What treatment is available for IgA nephropathy?

A

no specific therapy

antihypertensive Rx - ACEi

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21
Q

How does membranous GN present?

A

nephrotic syndrome

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22
Q

Which antibody is seen in 70% of cases of membranous GN?

A

anti-phospholipase A2 receptor antibody

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23
Q

Which type of GN is secondarily caused by malignancy, connective tissue diseases and drugs?

A

membranous

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24
Q

In membranous GN, where are immune complexes located?

A

in basement membrane and sub-epithelial space

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25
Q

Describe the variable natural history of membrane GN.

A 
1/3 = spontaneously remit
1/3 = progress to ESRF over 1-2 years
1/3 = persistent proteinuria, maintain GFR
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26
Q

What are the three stages in treating membranous GN?

A

1 underlying cause if secondary
2 supportive non-immunological e.g. ACEi, statins, diuretics, salt restriction
3 immunotherapy e.g. steroids, alkylating agents, cyclosporin, rituximab (anti-CD20 MAB)

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27
Q

What is the commonest form of GN in children?

A

minimal change

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28
Q

What are the main pathological features seen in minimal change GN?

A

podocyte foot process fusion
T cell cytokine mediated - target glom. epithelial cell
causes nephrotic syndrome

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29
Q

How might minimal change GN present?

A

acute - may follow URTI

GFR normal or reduced due to intravascular depletion

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30
Q

Describe the treatment for minimal change GN.

A

high dose steroids - prednisolone 1mg/kg for up to 8 weeks

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31
Q

List the five commonest causes of crescentic/rapidly progressive GN.

A 
ANCA vasculitis
Goodpasture's syndrome (anti-GBM disease)
Lupus nephritis
infection associated
HSP nephritis
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32
Q

What is RPGN?

A

group of conditions which demonstrate glomerular crescents on kidney biopsy

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33
Q

Discuss the approach to the patient in suspected glomerulonephritis.

A
  • full medical and drug history
  • basics: UEs, dip urine for blood, quantify proteinuria, check albumin, check USS
  • glomerulonephritis screen
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34
Q

In a glomerulonephritis screen, many diseases may be detected. What are these and what substance are they associated with?

A
  • diabetic nephropathy: HbA1c
  • ANCA/anti-GBM: vasculitis
  • ANA/PLA2R/virology: membranous
  • complement/ANA/dsDNA: lupus
  • complement/virology(hep B, C, HIV)/Igs/RF: MPGN, FSGS
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35
Q

Discuss the different types of glomerulonephritis including proliferative and non-proliferative.

A 
proliferative = nephritic syndrome e.g. IgA nephropathy, post-infectious, RPGN
non-proliferative = nephrotic syndrome e.g. minimal change disease, focal segmental GN, membranous GN
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36
Q

What is the triad of nephritic syndrome?

A

1 haematuria
2 decreased urine production
3 hypertension
leading to end-stage kidney failure

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37
Q

List four of the main systemic diseases associated with renal dysfunction.

A

diabetes mellitus
atheromatous vascular disease
amyloidosis
SLE

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38
Q

Briefly describe how diabetes leads to renal failure.

A

hyperglycaemia, volume expansion, intra-glomerular hypertension, hyperfiltration, proteinuria, hypertension and renal failure

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39
Q

Describe the structural changes seen in diabetic kidney disease.

A

thickening of glomerular BM
fusion of foot processes
loss of podocytes with denuding of the glomerular BM
mesangial matrix expansion

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40
Q

How might the risk of diabetic nephropathy be reduced?

A

tight glycaemic control
good BP control
SGLT2 inhibitors e.g. empagliflozin

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41
Q

Describe how SGLT2 inhibition leads to cardiac and renal protection.

A
  • glycosuria and natriuresis

- weight loss, lower HbA1c, lower BP, decreased intraglomerular hypertension, decreased atherosclerosis

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42
Q

List three causes of non-proteinuric AKI.

A
  • obstruction
  • renovascular disease - renal artery stenosis
  • interstitial nephritis
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43
Q

Discuss the pathogenesis of renovascular disease.

A

1 progressive narrowing of renal arteries with atheroma
2 perfusion falls, GFR falls but tissue oxygenation of cortex and medulla maintained
3 RA stenosis 70%, cortical hypoxia causes microvascular damage and activation of inflammatory pathways
4 parenchymal inflammation and fibrosis irreversible

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44
Q

Describe the 3 point management of renal artery stenosis.

A
  1. Medical - BP control (not ACEi/ARB), statin
  2. Lifestyle - smoking cessation, exercise
  3. Angioplasty - in rapidly deteriorating renal failure, uncontrolled hypertension, flash pulmonary oedema
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45
Q

What is amyloidosis and what organs does it affect?

A

deposition of highly stable insoluble proteineous material in extracellular space
kidney, heart, liver, gut

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46
Q

Describe the specific ultrastructural features of amyloid.

A

8nm linear aggregated fibrils of variable length forming a felt-like structure made of beta-pleated sheets

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47
Q

What type of amyloid is seen from previous TB and familial Mediterranean fever?

A

AA amyloid

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48
Q

How is amyloidosis detected using microscopy?

A

light microscopy: congo red stain = apple green birefringence
electron microscopy: amyloid fibrils 8nm cause mesangial expansion

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49
Q

Differentiate between the two classes of amyloidosis, AA and AL and how they are treated.

A 
AA = systemic amyloidosis (inflammation/infection). Treat underlying infection source.
AL = Ig fragments from haematological conditions e.g. myeloma. Treat underlying haematological condition.
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50
Q

What is systemic lupus erythematosis?

A

auto-immune disease, immune complex mediated glomerular disease

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51
Q

What are the autoantibodies present in SLE directed against?

A

DNA, histones, snRNPs, transcription/translation factors

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52
Q

Describe the pathophysiology of lupus nephritis.

A
  • autoantibodies produced against dsDNA or nucleosomes (anti-dsDNA, anti-histone)
  • form intravascular immune complexes or attach to GBM
  • activate complement
  • renal damage
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53
Q

How is SLE treated?

A

immunosuppression - steroids, MMF, cyclophosphamide, rituximab

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54
Q

Describe the presenting features of urinary tract infections to include both cystitis and pyelonephritis.

A
  • cystitis: dysuria, frequency, urgency, suprapubic pain, haematuria
  • pyelonephritis: the above PLUS fever, chills/rigors, flank pain, costo-vertebral angle tenderness, N+V
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55
Q

What are the risk factors to developing a UTI?

A
  • infancy
  • abnormal urinary tract
  • female
  • bladder dysfunction
  • ‘foreign’ body e.g. catheter
  • diabetes mellitus
  • renal transplant
  • immunosuppression
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56
Q

How is the diagnosis of UTI made?

A
  • multistix: leucocytes + nitrites
  • microscopy/flow cytometry: pus cells + bacteria
  • urine culture - in all children <3 years if clinical suspicion
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57
Q

Which organism is the most likely cause of UTI?

A

E. coli

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58
Q

What criteria must be reached from the urine culture to define UTI?

A

single organism > 10^5 CFU/ml

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59
Q

Discuss the antibiotic treatment for UTI.

A

oral unless vomiting, severely unwell, infant <3 months = trimethoprim, co-amoxiclav, nitrofurantoin, cephalosporin

IV = 3rd gen cephalosporin e.g. ceftriaxone, gentamicin

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60
Q

What is the importance of investigation and management of UTI in childhood?

A
  • imaging: US, micturating cystourethrogram (gold standard for VUR and PUV), nuclear medicine imaging e.g. DMSA (scarring)
  • antibiotic prophylaxis: not in simple UTI, consider for CAKUT, trimethoprim, nitrofurantoin
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61
Q

What is vesico-ureteric reflux?

A

a condition in which urine flows retrograde, or backward, from the bladder into the ureters/kidneys

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62
Q

Give examples of two congenital abnormalities of kidney and urinary tract.

A
  • vesico-ureteric reflux

- obstruction of urinary drainage tracts

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63
Q

What is oligohydramnios and what does it suggest?

A

deficiency of amniotic fluid

significant renal impairment

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64
Q

Describe the medical and surgical management of VUR and UTI.

A
  • medical: antibiotic prophylaxis for high grade VUR until toilet trained
  • surgical: if recurrent, proven febrile UTI and/or new scarring on meds, ‘STING’ procedure - narrows ureteric orifice
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65
Q

List common causes of bladder outlet obstruction.

A
  • prostatic hypertrophy
  • functional obstruction: neurogenic bladder (spina bifida, trauma etc), prune belly syndrome
  • posterior urethral valve
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66
Q

What is Prune Belly Syndrome?

A

triad of:

  1. Megacystis/megaureters
  2. Absent abdominal wall muscles
  3. Bilateral cryptochidism
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67
Q

How does a posterior urethral valve present?

A

antenatal hydronephrosis
urinary tract infection
poor urinary stream
renal dysfunction

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68
Q

How is a posterior urethral valve managed?

A

valve resection
antibiotic prophylaxis
CKD care

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69
Q

What is the commonest cause of hydronephrosis in children?

A

pelvi-ureteric junction obstruction

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70
Q

What are the complications associated with PUJO?

A

abdominal mass, pain, haematuria, UTI

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71
Q

What does VUJO stand for?

A

vesico-ureteric junction obstruction

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72
Q

Describe the management of ureteric obstruction.

A
  1. PUJO
    - observant: USS, DMSA, MAG3 diuresis renogram
    - surgical: pyeloplasty
  2. VUJO
    - observant: most resolve, USS, DMSA, MAG3 diuresis renogram
    - surgical: for symptoms or increasing dilatation, stent insertion, resection or re-implantation
73
Q

What is a kidney cyst and what problems can they cause?

A
  • sac-like structure containing fluid arising from the tubules
  • compressing other structures, replacing useful tissues, becoming infected, bleeding, pain
74
Q

Is adult polycystic kidney disease AD or AR?

A

autosomal dominant

75
Q

What gene mutations are associated with APKD and what do they code for?

A
  • PKD1 on c16 - polycystin 1
  • PKD2 on c4 - polycystin 2
  • 25% no FHx
76
Q

How do the PKD gene mutations lead to APKD?

A
  • polycystins are located in renal tubular epithelium
  • overexpressed in cyst cells
  • membrane proteins involved in intracellular calcium regulation
77
Q

How is APKD diagnosed?

A

US: If FHx US at age 21:
- age 15-30: 2 unilateral or bilateral cysts
- age 30-59: 2 cysts in each kidney
- over age 60: 4 cysts in each kidney
No FHx: 10 or more cysts in both kidneys, renal enlargement, liver cysts

78
Q

What are the clinical consequences of APKD?

A
  • renal complications - ESRD
  • hypertension
  • intracranial aneurysms
  • mitral valve prolapse
  • aortic incompetence
  • diverticular disease
  • liver/pancreas cysts
79
Q

Discuss the management of APKD.

A
  • supportive management
  • early detection and BP management
  • treat complications
  • renal replacement therapy
  • ?tolvaptan - vasopressin V2 receptor antagonist
80
Q

What are the potential implications of using tolvaptan as a drug therapy for APKD?

A
  • delay onset of RRT by around 4-5 years
  • heavy monitoring
  • SE: hepatotoxicity, hypernatraemia
  • very expensive
81
Q

List four other rare kidney cystic diseases.

A

Von Hippel Lindau
tuberous sclerosis
AR PKD
medullary cystic disease

82
Q

What is Von Hippel Lindau disease?

A

visceral cysts and benign tumours with potential for subsequent malignant transformation
AD

83
Q

What is tuberous sclerosis?

A

multiple benign tumours - brain, eyes, heart, kidney, skin
epilepsy and LD
AD

84
Q

What is AR PKD?

A

rare inherited childhood condition, where the development of the kidneys and liver is abnormal - hepatic fibrosis

85
Q

What is medullary cystic disease?

A

AD
cysts in medulla not cortex
small to normal sized kidney
gout

86
Q

What gene mutations are associated with Alport’s syndrome?

A 
usually X-linked
collagen 4 abnormalities
- alpha 3
- alpha 4 (COL3A4)
- alpha 5 (COL3A5)
87
Q

What are the clinical consequences of Alport’s syndrome?

A

deafness (sensorineural hearing loss)
renal failure (microscopic haematuria and proteinuria)
50% on dialysis by 25y

88
Q

Describe the changes seen in the basement membrane in Alport’s.

A

defect in collagen 4 = abnormally split and laminated GBM

89
Q

What is Fabry’s disease?

A

X-linked storage disorder

alpha-galactosidase A deficiency resulting in accumulation of globotriaosylceramide (Gb3)

90
Q

How does Fabry’s disease lead to renal failure?

A

Gb3 accumulated in glomeruli, particularly podocytes causing proteinuria and ESRF

91
Q

What extra-renal features are associated with Fabry’s syndrome?

A

neuropathy
cardiac
skin - angiokeratoma

92
Q

How is Fabry’s disease diagnosed and managed?

A

diagnosis:

  • measure alpha-Gal A activity in leucocytes
  • renal biopsy - inclusion bodies of Gb3

management: enzyme replacement therapy

93
Q

Define AKI according to UKRA guidelines.

A

decline of renal excretory function over hours or days.. recognised by the rise in serum urea and creatinine

94
Q

What are the three stages of AKI severity according the KDIGO?

A
  1. Serum creatinine 1.5-2x AKI baseline
  2. 2-3x AKI baseline
  3. > 3x AKI baseline
95
Q

Can you give examples of causes of:

  1. pre-renal AKI
  2. intrinsic AKI
  3. post-renal AKI?
A
  1. hypovolaemia + hypotension, reduced circulatory volume, drugs, renal artery stenosis
  2. glomerulonephritis, tubular dysfunction, myeloma, sarcoid, acute tubular necrosis
  3. renal papillary necrosis, kidney stones, cervix carcinoma, prostatic hypertrophy, urethral strictures
96
Q

ATN is always due to under perfusion of the tubules and/or direct toxicity. What are the three main causes of this?

A

hypotension, sepsis, toxins

97
Q

What happens to glomerular filtration as pressure falls?

A

prostaglandins dilate afferent arteriole to increase flow as MAP falls towards 80mmHg

98
Q

Describe the effects of NSAIDs and ACEis on the glomerulus.

A
  • NSAIDs: block dilatation of afferent arterioles

- ACEi: block constriction of efferent arterioles

99
Q

Describe the treatment of AKI.

A
  • restore renal perfusion (hyperkalaemia and pulmonary oedema)
  • remove causes (drugs and sepsis)
  • exclude obstruction and consider ‘renal’ causes
100
Q

Discuss the diagnostic process of AKI.

A
  • need for urgent action may take precedence over making final diagnosis
  • history and exam
  • drugs
  • urinalysis
  • renal US
  • ‘GN’ screen
101
Q

What features of a clinical exam would make you suspect AKI?

A

sepsis, rashes, haemoptysis, rhabomyolysis

102
Q

What level of serum potassium is classified as a medical emergency?

103
Q

How would you treat hyperkalaemia?

A
  • reduce absorption from gut - calcium resonium
  • insulin - moves K+ into cells
  • calcium gluconate - cardiac membrane stabiliser
104
Q

Raised potassium levels can lead to acidosis. How is this treated?

A

IV NaBicarc 1.26%

105
Q

What is the definition of CKD?

A

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

106
Q

What is the criteria for albuminuria?

107
Q

List some causes of CKD.

A
  • diabetic nephropathy
  • renovascular disease/ischaemic nephropathy
  • chronic glomerulonephritis
  • chronic pyelonephritis
  • ADPKD
  • obstructive uropathy
108
Q

What are the symptoms of advanced CKD?

A

pruritus, nausea, anorexia, weight loss, fatigue, leg swelling, breathlessness, nocturia, joint/bone pain, confusion

109
Q

What are the signs of advanced CKD?

A

peripheral and pulmonary oedema, pericardial rub, rash/excoriation, hypertension, tachypnoea, cachexia, pallor and/or lemon yellow tinge

110
Q

What methods of management are available to slow down progression of CKD?

A
  • BP control: ACEi/ARB
  • diabetic control
  • diet
  • smoking cessation
  • lowering cholesterol
  • treat acidosis
111
Q

Anaemia is common in CKD, especially as eGFR falls below 30. Describe its management.

A
  • replace iron, B12, folate

- darbopoietin

112
Q

CKD leads to increased levels of PTH leading to secondary hyperparathyroidism and metabolic bone disease. How can this be treated?

A
  • vit D supplements
  • Mg supplements
  • phosphate binders
  • calcimimetic
  • parathyroidectomy
113
Q

What are the indications for starting renal replacement therapy?

A
  1. medically resistant hyperkalaemia
  2. medically resistant pulmonary oedema
  3. medically resistant acidosis
  4. uraemic pericarditis
  5. uraemic encephalopathy
  6. GFR between 5-10 ml/min/1.73m2
114
Q

Name the main RRT modalities.

A
  • haemodialysis
  • peritoneal dialysis
  • renal transplant
115
Q

What are the two main points of access for haemodialysis?

A
  • TCVC Tunneled Central Venous Catheter

- AVF arteriovenous fistula

116
Q

What is the standard amount of times that a patient requires HD a week?

A

4 hours 3 times a week

117
Q

What are some of the complications associated with haemodialysis?

A
  • ‘crash’ - acute hypotension
  • access problems
  • cramps, fatigue
  • hypokalaemia
  • blood loss
  • dialysis disequilibrium
  • air embolism
118
Q

List the complications associated with PD.

A
  • peritonitis
  • glucose load: development or worsening control of diabetes
  • mechanical: hernia, diaphragmatic leak, dislodged catheter
  • peritoneal membrane failure
  • hypoalbuminaemia
119
Q

What patients are not suitable for peritoneal dialysis?

A
  • grossly obese
  • intra-abdominal adhesions
  • frail
  • home not suitable
120
Q

What issues associated with kidney disease are not helped by dialysis?

A
  • anaemia
  • renal bone disease
  • neuropathy
  • endocrine disturbances
121
Q

Discuss the pros and cons of renal transplantation.

A
  • pros: no dialysis, better level of renal function, independence, better life expectancy
  • cons: immunosuppression, increased CV and infection risk, skin malignancies
122
Q

Name three immunosuppressive medications typically used in renal transplantation.

A

cyclosporin
tacrolimus
MPA

123
Q

What is the most effective form of RRT?

A

transplant

124
Q

What is urosepsis?

A

complicated UTI

  • temp > 38
  • HR > 90
  • RR > 20
  • WBC > 12 or < 4
125
Q

What are the common organisms that cause UTI?

A
  1. Gram -ve bacilli e.g. E. coli, Klebsiella sp, Proteus sp., Pseudomonas sp.
  2. Gram +ve e.g. staph, strep
  3. Anaerobes
  4. Candida sp.
126
Q

UTI during pregnancy is common and is usually treated with amoxicillin or cephalexin. Which antibiotics should be avoided?

A

trimethoprim in 1st trimester

nitrofurantoin near term

127
Q

What is the definition of recurrent UTI?

A

> 2 episodes in 6 months

128
Q

What advice should be given to women who suffer from recurrent UTI?

A

hydration, urge-initiated and post-coital voiding, intravaginal/oral oestrogen

129
Q

What antibiotic therapy is available from recurrent UTI?

A
  • self-administered single dose/short course therapy
  • single dose post coital abx
  • prophylactic antibiotics
130
Q

What are some of the complications associated with catheters?

A
  • CAUTI
  • obstruction-hydronephrosis
  • chronic renal inflammation
  • urinary tract stones
  • long term risk of bladder cancer
131
Q

What measures can be taken to prevent catheter infections?

A
  • only if necessary
  • remove when no longer needed
  • remove/replace if causing infection
  • hand hygiene
132
Q

How would you treat catheter related UTI?

A
  • check recent/previous microbiology
  • start empirical antibiotics
  • remove catheter if not needed
  • antibiotics: broad spectrum, historically gent/cipro
133
Q

What is the standard treatment for community acute pyelonephritis?

A

co-amoxiclav/ciprofloxacin/trimethoprim

134
Q

What are the complications associated with pyelonephritis?

A

renal and perinephric abscess

135
Q

What are the risk factors for developing a perinephric abscess?

A
  • untreated LUTI, anatomical abnormalities
  • renal calculi
  • bacteraemia, haematogenous spread
136
Q

How is a perinephric abscess treated?

A

treat empirically as complicated UTI - poor response -> surgical management

137
Q

Which antibiotics are effective against uncomplicated UTI?

A

PO amoxicillin, trimethoprim, nitrofurantoin

138
Q

What antibiotics should be used in complicated UTI?

A

IV

  • amoxicillin/vancomycin
  • gentamicin/aztreonam/temocillin
139
Q

What are the signs of acute bacterial prostatitis?

A

fever, perineal/back pain, UTI, urinary retention, diffuse oedema

140
Q

What are the likely organisms to have caused acute bacterial prostatitis?

A
  • gram -ve bacilli
  • S. aureus
  • N. gonorrhoea
141
Q

List the complications associated with acute bacterial prostatitis.

A
  • prostatic abscess
  • spontaneous rupture
  • epididymitis
  • pyelonephritis
  • systemic sepsis
142
Q

Describe the antibiotic management of acute bacterial prostatitis.

A

ciprofloxacin - no strep cover

143
Q

Chlamydia urethritis is associated with which chronic condition?

A

chronic prostatitis

144
Q

What is epididymitis and describe its aetiology?

A
  • inflammatory reaction of the epididymis
  • ascending infection from urethra
  • urethral instrumentation
145
Q

Describe the symptoms associated with epididymitis.

A

pain, fever, swelling, penile discharge - symptoms of UTI/urethritis

146
Q

What are the organisms commonly associated with epididymitis?

A
  • GNB, enterococci, staphylococci
  • TB in high risk areas
  • chlamydia, gonorrhoea
147
Q

Orchitis is inflammation of one or both testicles. What would the symptoms of this be?

A

testicular pain and swelling, dysuria, fever, penile discharge

148
Q

What are the complications of bacterial orchitis?

A

testicular infarction and abscess formation

149
Q

What is Fournier’s gangrene?

A

a type of necrotizing fasciitis or gangrene affecting the external genitalia and/or perineum

150
Q

What are the risk factors to developing Fournier’s gangrene?

A
  • > 50
  • UTI
  • complications of IBD
  • trauma
  • recent surgery
151
Q

Describe the management of Fourier’s gangrene.

A
  • blood cultures, urine, tissue/pus
  • surgical debridement
  • broad spectrum Abx initially
152
Q

Describe the range of drugs which must be avoided or dose reduced in renal disease.

A
  • avoid: metformin, NSAIDs

- reduce dose: antibiotics, LMWH, digoxin, phenytoin

153
Q

What changes should be made to dose and dosage interval in:

  1. Renal disease
  2. Hepatic disease
A
  1. Dose = none. Dosage interval = increase

2. Dose = decrease. Dosage interval = increase

154
Q

Why do kidney stones form?

A

abnormal urine, urinary obstruction, urinary infection

155
Q

Describe the composition of urine that leads to stone formation.

A
  • low volume, low pH, low citrate, low Mg

- high uric acid, high calcium, high oxalate

156
Q

What are the congenital and acquired urinary obstructions that lead to stone formation?

A

congenital: medullary sponge kidney, PUJO, mega-ureter, ureterocele
acquired: ureteric stricture, anastamotic stricture

157
Q

Which organisms can increase the possibility of kidney stone formation?

A
  • urease producing organisms

- proteus mirablis: splits urea to form ammonia, raises urine pH, struvite

158
Q

List the different types of kidney stones.

A
  • calcium: calcium oxalate monohydrate or dihydrate, calcium phosphate
  • infection stones: struvite
  • uric acid stone - metabolic syndromes
  • cystine - genetic
159
Q

Describe the presentation of a patient with kidney stones.

A
  • pain: colic, radiates from loin to groin, cannot settle, unable to stay still
  • haematuria
  • UTI or sepsis
  • often incidental
160
Q

How are kidney stones managed non-surgically?

A
  • small/asymptomatic = observation
  • medical = dissolution therapy (urate)
  • pain: analgesia, NSAIDs
161
Q

What are the surgical treatments available for kidney stones?

A
  • extracorporeal shockwave lithotripsy
  • ureteroscopy
  • percutaneous nephrolithotomy
  • emergency stent and nephrostomy
162
Q

What are the risk factors for development of prostate cancer?

A
  • elderly men
  • genetics: HPC1, BRCA2, PTEN, TP53?
  • westernised nations
163
Q

What are the symptoms of prostate cancer?

A
  • often asymptomatic
  • painful or slow micturition
  • UTI
  • haematuria
  • urinary retention
  • lympdoedema
  • metastatic: bone pain, renal failure
164
Q

Name three processes of diagnosing and screening for prostate cancer.

A
  • digital rectal exam
  • prostate-specific antigen
  • TRUS guided needle biopsy
165
Q

Describe the pathology of prostatic cancer.

A
  • primary adenocarcinoma

- usually arises in peripheral zone of prostate

166
Q

What are the treatment options available for prostate cancer?

A
  • active surveillance
  • RTx
  • radical prostatectomy
  • cryotherapy
  • TURP if symptomatic
  • androgen ablation therapy in advanced
167
Q

What are the metastatic complications of prostatic cancer?

A
  • spinal cord compression: urological emergency, severe pain, retention, constipation, urgent MRI
  • ureteric obstruction: anorexia, weight loss, raised creatinine
168
Q

Name 3 risk factors for the development of bladder cancer.

A

smoking, old age, caucasian, environmental carcinogens, stones, long term catheters, drugs e.g. cyclophosphamide, pelvis RTx

169
Q

Describe the presentation of bladder cancer and subsequent investigation.

A
  • classically painless frank haematuria

- cystoscopy and renal USS

170
Q

Describe the pathology of bladder cancers.

A
  • 90% transitional cell carcinoma
  • 5% squamous carcinoma
  • 2% adenocarcinoma
171
Q

How are bladder cancers treated?

A
  • urgent TURBT

- intravesical mitomycin reduces risk of recurrence

172
Q

What are the risk factors to developing renal cancer?

A

smoking, obesity, hypertension, acquired renal cystic disease, haemodialysis, genetics (VHL)

173
Q

How does renal cancer present?

A
  • 80% incidental
  • <25% systemic = night sweats, fever, fatigue, weight loss, haemoptysis
  • 10% triad of mass, pain, haematuria
  • varicocele
  • lower limb oedema
174
Q

What are the paraneoplastic syndromes associated with kidney cancer?

A

polycythaemia, hypercalcaemua, hypertension, deranged LFTs, Cushing’s

175
Q

What are the risk factors to developing testicular cancer?

A
  • men 20-45 y/o
  • cryptorchidism
  • HIV
  • caucasian
176
Q

What is the main clinical presentation of testicular cancer and how it this investigated?

A
  • painless lump

- investigations: scrotal US, tumour markers = AFP, beta-hCG, LDH

177
Q

Describe the treatment available for testicular cancer.

A
  • radical orchidectomy
  • chemotherapy
  • para-aortic nodal RTx
  • retroperitoneal lymph node dissection
178
Q

What infection is associated with penile cancer?

A

HPV 16 + 18

179
Q

What is the treatment available for penile cancer?

A

circumcision, topical treatment, penectomy +/- reconstruction

Phase 3 (10 decks)

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