Breast, Renal & Urology Flashcards

1
Q

Breast cancer

A

most common cancer in women, 2nd most common cause of cancer death in the UK

incidence ↑ with age

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2
Q

Risk factors fro breast cancer

A
↑age
personal history of breast cancer
family history of breast cancer
obesity
nulliparity
1st pregnancy age >30yrs
early menarche / late menopause
COCP
HRT
ionising radiation

Genetics:

  • BRCA 1
  • BRAC2
  • p53 gene mutation
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3
Q

Types of breast cancer

A

Invasive ductal carcinoma

  • most common
  • may be quite aggressive
  • usually unilateral & unifocal

Invasive lobular carcinoma

  • less aggressive
  • often multifocal

Ductal carcinoma in situ (DCIS)

Lobular carcinoma in situ (DCIS)

Medullary breast cancer

  • most common type associated with BRCA1
  • often triple +ve cancer

Mucinous carcinoma

Pagets disease of the nipple
-eczematous changes of the nipple associated with underlying malignancy

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4
Q

Presentation of breast cancer

A

palpable mass
-often non tender, firm

nipple discharge
-bloody discharge is associated strongly with ductal carcinoma

nipple retraction, scaling of the nipple

axillae lymphadenopathy, skin changes e.g. discolouration, dimpling, Peau d’orange, oedema of the arm

NB mastalgia (breast pain) is an uncommon presentation of breast cancer

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5
Q

Screening for breast cancer

A

NHS screening programme for women aged 50-70yrs, who are offered mammography every 3yrs, after age 70 pts are encouraged to make their own mammography appointments

if ↑ breast cancer risk due to FH screening may be offered at younger agre
-e.g. if one 1st degree relative diagnosed at <40y/o or 1st degree male relative diagnosed, or if one 1st degree relative with bilateral cancer at age <50yrs

NB first invitation should be sent to all women before age 53yrs

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6
Q

Investigations for breast cancer

A

mammography

  • bilateral
  • preferred if pt >30y/o

USS of breast + regional lymph nodes

  • often with a biopsy
  • preferred if <30y/o due to denser breast tissue in younger pts

Biopsy

  • fine needle aspration
  • core biopsy (preferred)

Human epithelial growth factor receptor 2 (HER2) status

Hormon receptor testing
-progesterone & oestrogen

genetic testing for BRCA1/BRCA2
-for all women <50y/o with triple -ve breast cancer

NB generally pts will have triple assessment of examination, imaging & biopsy at the breast clinic

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7
Q

Referral for breast cancer pathway

A

age ≥30yrs with unexplained breast lump ± pain
age ≥50yrs with discharge/retraction/other change of one nipple

consider referral if skin changes suggestive of breast cancer or age ≥30yrs with unexplained lump in axilla

NB if <30y/o with unexplained breast lump consider non urgent referral

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8
Q

Management of breast cancer

A

Surgical

  • offered to majority of pts
  • mastectomy ± axillary lymph node clearance
  • if lymph spread suggested = sentinel node biopsy to asses spread during surgery
  • usually also offered breast reconstruction

Radiotherapy
-whole breast radiotherapy is offered to most pts

Hormonal therapy

  • offered as adjuvant therapy if hormone receptor +ve
  • pre-menopause = tamoxifen
  • post-menopause = anastrozole

Biologicals

  • Trastuzumab for HER2 +ve cancer
    • also known as herceptin
    • contraindicated if pt has heart problems

chemotherapy

  • used pre/post op
  • FEC-D is used
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9
Q

Hormonal treatment of breast cancer

A

offered as adjuvant therapy if hormone receptor +ve

pre-menopause = tamoxifen

  • ↑ risk of VTE
  • ↑ risk of endometrial cancer
  • NB also used in males

post-menopausal = aromatase inhibitors e.g. anastrozole

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10
Q

Fibroadenoma

A

a benign breast tumour typically seen in women aged <35 (peak incidence 25-35) accounts for ~10% of all breast masses

presents as highly mobile, firm, smooth & non-tender breast lump (also called a breast mouse)

no ↑ risk of malignancy

generally gets smaller over time, but if >3cm is usually excised

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11
Q

Breast cyst

A

usually seen in women aged 35-50yrs

presents as solitary cyst, usually a discrete small lump that may fluctuate in size

should be referred for imaging at breast clinic

may require aspiration

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12
Q

Fat necrosis

A

usually seen in larger, fatty breasts in overweight women

often after trauma

lump is painless, skin may be red/bruised/dimpled

may require biopsy to confirm diagnosis but then no further management is needed

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13
Q

Ductal papilloma

A

benign warty lesion usually located behind the areola that may cause sticky nipple discharge (discharge is usually from a single duct)

requires triple assessment to rule out cancer

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14
Q

Phyllodes tumour

A

rare tumour that is hard to distinguish from a fibroadenoma but usually occurs in older women

i.e. mobile, small, firm breast lump

treated with wide excision & follow-up

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15
Q

Sclerosis adenosis

A

sclerosis within the lobules causing a lump/pain

can be hard to distinguish from malignancy so biopsy is advised but no ↑ risk of malignancy

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16
Q

Cyclical mastalgia

A

common cause of benign breast pain in young females

breast pain that varies in intensity according to the phases of the menstrual cycle

  • pain rapidly resolves with the start of menstruation
  • pain generally diffuse & bilateral

management includes supportive bras, topical/oral analgesia (NSAIDs/paracetamol)

consider referral if no improvement after 3 months, specialists may consider danazol or bromocriptine

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17
Q

Puerperal mastitis

A

inflammation of the breast, often secondary to nipple fissures, affecting ~10% of breast feeding mothers

presents with ≥1 week postpartum in one breast with painful/tender, red, hot breast with pain during breastfeeding, fever and malaise

women should be encouraged to continue breast feeding

give Abx (flucloxacillin, 10-14days) if systemically unwell / nipple fissure / symptoms not improving 12-24h post effective milk removal

NB if untreated may cause breast abscess

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18
Q

Breast abscess

A

may be a consequence of untreated Puerperal mastitis or mammary duct ectasia

presents with purulent nipple discharge, a fluctuating mass, pain and fever

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19
Q

Non lactational mastitis

A

usually seen in smokers or those with nipple rings usually are of reproductive age

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20
Q

mammary duct ectasia

A

due to dilation of breast ducts, usually seen in perimenopausal women (age 40-50yrs)

presents as tender lump around areola with green nipple discharge ± blood

usually no treatment needed unless recurrent/persistent then may need surgical excision

may progress to breast abscess

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21
Q

Testicular cancer

A

most common malignancy in men aged 20-30yrs

95% are germ cell tumours e.g. seminomas or non seminomas (e.g. embryonal, teratoma)

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22
Q

Risk factors for testicular cancer

A
infertility
cryptorchidism
Fh of testicular cancer 
mumps orchitis 
Klinefelters syndrome
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23
Q

Presentation, investigations & management of testicular cancer

A

Presentation:

  • painless testicular lump
  • hydrocele
  • gynaecomastia
  • NB pain is a rare symptom

Investigations:

  • testicular USS (1st line)
  • Tumour markers
    - Seminomas = ↑hCG
    - non-seminomas = ↑AFP / beta-hCG
    - germ cell tumours = ↑LDH

Management:
-orchidectomy ± chemo/radiotherapy

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24
Q

Hydrocele

A

presents as a fluctuating, painless transilluminating mass, usually possible to get above the mass on examination

investigated with USS in younger men to exclude cancer

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25
Q

Varicocele

A

abnormal enlargement of pampiniform plexus, most common cause of scrotal enlargement

generally presents as painless enlargement or with dull aching pain of hemiscortum
-most commonly left sided

feels like bag of worms on palpation, with negative transillumination

diagnosed with USS

management is generally conservative but surgery may be required if painful

NB there is an increased risk of subfertility/infertility

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26
Q

Bening prostatic hyperplasia (BPH)

A

a non-neoplastic glandular & stromal hyperplasia of the transition zone to the prostate

common enough to be considered normal with increasing age
~50% of 50y/o mean have evidence of BPH, but unusual before age 45

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27
Q

Presentation of Bening prostatic hyperplasia (BPH)

A

lower urinary tract symptoms (LUTS)

  • urinary frequency
  • urinary urgency
  • hesitancy
  • incomplete emptying
  • weak/intermittent stream
  • straining
  • terminal dribble
  • nocturia

PR examination
-symmetrically enlarged, smooth, firm, non tender prostate

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28
Q

Assessment of Bening prostatic hyperplasia (BPH)

A

International prostate symptom score (IPSS)

  • used to assess the severity of LUTS
  • assess impact on QoL
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29
Q

Investigations for Bening prostatic hyperplasia (BPH)

A

Prostate specific antigen (PSA)

  • indicated if pt is worried about prostate cancer
  • usually ↑

Prostate USS
-done pre surgery

Urinalysis (normal usually)
post-void residual bladder scan
urinary frequency - volume chart
uroflowmetry
U&Es, FBC, LFTs
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30
Q

Management of Bening prostatic hyperplasia (BPH)

A

Minimal symptoms
-watchful waiting

Pharmacological (trialed before surgery)

  • Alpha-1 antagonist (1st line)
    • e.g. Tamsulosin or alfuzosin
    • improve symptoms in ~70% of men
    • ↓ muscle tone of prostate & bladder
    • side effects: dizziness, hypotension, dry mouth
  • 5-alpha reductase inhibitors (2nd line)
    • e.g. finasteride
    • block conversion of testosterone→dihydrotestosterone
    • ↓ prostate volume
    • side effects: erectile/ejaculation dysfunction, ↓ libido
    • can be combine with Alpha-1 antagonist if severe BPH

Surgery (2nd line)

  • generally only after failed medical treatment
  • transurethral resection of prostate (TURP) = procedure of choice
  • may consider UroLift system
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31
Q

Prostatitis

A

an inflammation of the prostate gland that may be of infectious or non infectious

infectious causes are commonly due to E.coli (may also be STI causes e.g. Chlamydia/Gonorrhoea especially in <35y/o men, while non infectious may be inflammatory response post UTI

presents generally with fever, malaise, dysuria / frequency / urgency (due to bladder irritation, with pain radiating to lower back, perineum, rectum or penis

DRE may reveal a tender, boggy prostate gland

treatment includes STI screening and a 14day course of quinones if bacterial, and NSAIDs

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32
Q

Pharmacological treatment of Benign prostatic hyperplasia (BPH)

A

1st line = Alpha-1 antagonist

  • e.g. Tamsulosin or alfuzosin
  • improve symptoms in ~70% of men
  • ↓ muscle tone of prostate & bladder
  • side effects: dizziness, hypotension, dry mouth

2nd line = 5-alpha reductase inhibitors

  • e.g. finasteride
  • block conversion of testosterone→dihydrotestosterone
  • ↓ prostate volume
  • side effects: erectile/ejaculation dysfunction, ↓ libido

If severe symptoms then both drug types can be combined

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33
Q

Prostate cancer

A

a malignant tumour of glandular origin situated in the prostate, most commonly adenocarcinomas arising in the peripheral zone of the prostate

most common site of metastasis = bones & lymph nodes

most common cancer in men (~27% of all male cancer)
especially common in black males
usually seen at age >50yrs

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34
Q

Location of prostate lesions

A

Prostate cancer:
-peripheral zone

BPH
-transitional zone

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35
Q

Epidemiology & Risk factors for Prostate cancer

A

most common cancer in men (~27% of all male cancer)
especially common in black males
least common in asian men
usually seen at age >50yrs

2nd most common cause of cancer death in males

Risk factors:

  • ↑ age
  • afro-carribbean origin
  • afro-american origin
  • Family history
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36
Q

Presentation of prostate cancer

A

typically asymptomatic

LUTS (hesitancy, weak stream, incomplete emptying, frequency)
haematuria
flank pain
weight loss
↓ appetite
Bone pain (if metastasis)

PR examination

  • may remain normal even in advanced disease
  • hard irregular prostate with lobar asymmetry
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37
Q

DRE examination findings for prostate pathology

A

Prostate cancer

  • may remain normal even in advanced disease
  • hard irregular prostate with lobar asymmetry

BPH
-symmetrically enlarged, smooth, firm, non tender prostate

Prostatitis
-tender, boggy prostate gland

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38
Q

Investigations for prostate cancer

A

Prostate specific antigen (PSA) ↑

multi parametric MRI*
-1st line imagine now

transurethral ultrasound guided biopsy

  • biopsy is grade with Gleason scale
  • Gleason scale goes from 1-10
  • used as prognostic indicator
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39
Q

Management of prostate cancer

A

Localised prostate cancer

  • active monitoring
  • watchful waiting

Locally advanced cancer

  • radical prostatectomy
    • commonly causes erectile dysfunction
  • radiotherapy
    • external beam & brachytherapy

Metastatic prostate cancer

  • hormonal therapy with anti androgen therapy
    • GnRH agonist e.g. goserelin*
    • bicalutamide (non steroidal anti androgen)
    • cryptoterone acetate, abiraterone
    • enzalutamide (NICE recommended)
  • bilateral orchidectomy
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40
Q

Bladder cancer

A

most common malignancy of the urinary tract

Types:

  • transitional cell (urothelial) carcinoma (~90% of cases)
  • squamous cell carcinoma (~8% of cases)
  • adenocarcinoma (~2% of cases)

NB these can occur anywhere in the urinary tract but bladder is most common place

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41
Q

Risk factors for bladder cancer

A

smoking
exposure to aniline dyes e.g. 2-naphthylamine
rubber manufacturing
cyclophosphamide

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42
Q

Risk factor for squamous cell bladder cancer

A

Indwelling catheters

schistosomiasis**

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43
Q

Presentation of bladder cancer

A

painless macroscopic haematuria
dysuria
urinary frequency
other voiding symptoms

NB painless haematuria is cancer until proven otherwise

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44
Q

Investigations for bladder cancer

A

Urinalysis

  • haematuria
  • may show pyuria

cystoscopy ± biopsy
urine cytology
CT/MRI chest/abdo/pelvis
U&Es, FBC

NB incidental microscopic haematuria is still associated with bladder cancer and should be treated as such especially in those aged >60

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45
Q

Management of bladder cancer

A

Non-invasive
-transurethral resection of bladder tumour (TURBT)

Invasive cancer

  • neo-adjuvant chemotherapy
  • radical cystectomy

Metastatic disease
-treated with cisplatin based chemo

NB pts should be followed up post TURBT with cystoscopy every 3 months as superficial transitional cell carcinoma may recur in ~80% of pts

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46
Q

Renal cell carcinoma (RCC)

also known as hypernephroma

A

a renal malignancy arising from the renal parenchyma/cortex (usually proximal tubular epithelium) accounting for ~90% of renal cancers

Most common kidney cancer in adults (NB in children Wilm’s tumour is most common)

~85% are clear cell carcinomas

usually seen in males, aged 60-70yrs

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47
Q

Risk factors for Renal cell carcinoma (RCC)

A

smoking
obesity
HTN

also associated with von Hippel-Lindau syndrome & tuberous sclerosis

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48
Q

Presentation of Renal cell carcinoma (RCC)

A
Triad of
-haematuria
-loin pain
-loin/abdo mass
        plus
fatigue, weight loss, varicocele (L sided usually), pyrexia of unknown origin, oedema 

~25% of pts have metastatic disease

  • haemoptysis
  • bone pain
  • pathological fractures

NB paraneoplastic features e.g. hepatic dysfunction or polycythaemia (↑EPO production) may be present

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49
Q

Investigations for Renal cell carcinoma (RCC)

A

FBC
-Hb ↓

urinalysis
-haematuria ± proteinuria

CT kidney with contrast 
MRI/USS kidney
U&Es (usually normal)
LFTs (may be abnormal)
Urine MC&S
CT/MRI chest/abdo/pelvis
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50
Q

Management of Renal cell carcinoma (RCC)

A

confined disease
-partial/total nephrectomy depending on tumour size
if <7cm = partial

advanced/metastatic disease

  • receptor kinase inhibitors (1st line)
    - e.g. surafenib / sutinib
  • alpha-interferon & interleukin 2
    - help ↓ tumour size
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51
Q

Nephrolithiasis (renal stones)

A

encompasses te formation of all types of urinary calculi in the kidney / urinary system

 - ~80% of stones are calcium containing 
 - calcium oxalate stones are most common type

very common condition, usually age 40-60yrs
more common in men (3:1 male:female ratio)
most common in white people

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52
Q

Epidemiology of Nephrolithiasis (renal stones)

A

very common condition
more common in men (3:1 male:female ratio)
most common in white people
peak age 40-60yrs
calcium oxalate are the most common stones

53
Q

Risk factors for Nephrolithiasis (renal stones)

A
dehydration
↑ Ca2+
hyperparathyrodisim
renal tubular acidosis 
FH of urinary tract stones
cystinuria
diet high in urate/calcium/sodium/animal protein
gout (RF for urate stones)
Drugs (generally ↑ Ca2+ excretion) 
-loop diuretics, steroids, acetazolamide, theophylline
54
Q

Presentation of Nephrolithiasis (renal stones)

A

Renal colic

  • sudden severe flank pain radiating to ipsilateral groin
  • often intermittent
  • pain recedes to dull ache in between attacks

rigours, fever
dysuria, haematuria, urinary retention
nausea & vomiting

NB pt generally unable to lie/sit still and frequently moves i.e. writhing in pain

55
Q

Investigations for Nephrolithiasis (renal stones)

A

Urinalysis

  • haematuria
  • leukocytosis
  • nitrates
  • pH <5 suggestive of uric acid stones

non enchanted CT

  • imaging of choice
  • non contrast CT KUB should be done within 14h of admission

USS
-imaging of choice in children/young adults/pregnant women

FBC, U&Es Ca2+
CRP, coagulation

56
Q

Management of Nephrolithiasis (renal stones)

A

Pain relief
-NSAIDs e.g. diclofenac = 1st line

-Stones <5mm generally pass spontaneously

  • ureteric obstruction + infection = requires urgent surgical decompression
    • nephrostomy tubes or ureteric stent

Non emergency management:

  • shock wave lithotripsy, ureteroscopy, percutaneous nephrolithotomy
  • stone <2cm = lithotripsy
  • stone <2cm & pregnant = ureteroscopy
  • complex stone/staghorn calculi = percutaneous nephrolithotomy

Prevention
-if ↑Ca2+ thiazide diuretics & good fluid intake can reduce reoccurrence

57
Q

Urinary tract infection (UTI)

A

an inflammatory reaction of the urinary tract epithelium in response to infection

very common especially in women
men are much less likely to get UTIs but if they do its more serious

58
Q

Aetiology of Urinary tract infection (UTI)

A

E. Coli (most common)

staph saprophyticus, proteus mirabilis, klebsiella

NB non E.coli infection more often seen in pts with underlying pathologies, immunosuppression or those who are catheterised

59
Q

Risk factors of Urinary tract infection (UTI)

A
↑ age
recent instrumentation of the renal tract
renal tract abnormalities 
sexual activity 
diabetes
institutionisation 
catheterisation 
pregnancy 
immune suppression
60
Q

Presentation of Urinary tract infection (UTI)

A
dysuria (burning/stinging on urination)
urinary frequency 
urinary urgency
cloudy/offensive smelling urine
fever (often low grade)
malaise
suprapubic / loin pain
rigors

in elderly pts UTIs may present as an acute confusional state / delirium

61
Q

Investigations for Urinary tract infection (UTI)

A

Urinalysis

  • nitrates +
  • leukocytes +
  • sufficient to diagnose UTI in healthy women
  • NB this is not used to diagnose UTI in catheterised pts

urine MC&S

  • shows organism + sensitivity
  • should be done for all men, pregnant pts, immunosuppressed pts, or if empirical treatment fails
62
Q

Management of Urinary tract infection (UTI)

A

Non pregnant women
-3 days of trimethoprim / nitrofurantoin

Pregnant women

  • Symptomatic:
    • 1st line = nitrofurantoin
    • 2nd line = amoxicillin / cefalexin
  • Asymptomatic bacteriuria
    • 7 days of nitrofurantoin + follow up culture as evidence of cure

Men
-offer 7 days of trimethoprim or nitrofurantoin

catheterised pts

  • DO NOT treat asymptomatic bactiuria
  • if symptomatic = 7 days of Abx
63
Q

Management of Urinary tract infection (UTI) in non pregnant women

A

3 days pf trimethoprim / nitrofurantoin

NB send cultures if age >65yrs or macro.microscopic haematuria

64
Q

Management of Urinary tract infection (UTI) in pregnant women

A

Symptomatic:

  • 1st line = nitrofurantoin
  • 2nd line = amoxicillin / cefalexin

Asymptomatic bacteriuria
-7 days of nitrofurantoin + follow up culture as evidence of cure

NB trimethoprim is contraindicated in pregnancy but used instead of nitrofurantoin in breastfeeding women

65
Q

Management of Urinary tract infection (UTI) in men

A

offer 7 days of trimethoprim or nitrofurantoin

66
Q

Management of Urinary tract infection (UTI) in catheterised pts

A

DO NOT treat asymptomatic bactiuria

if symptomatic = 7 days of Abx

67
Q

Acute kidney injury (AKI)

A

an acute deterioration in kidney function leading to ↑ serum creatinine, and/or ↓ urine output

causes may be pre-renal (most common), intrinsic renal or post-renal

68
Q

Pre-renal causes of Acute kidney injury (AKI)

A

Most common, account for ~90% of cases)

Volume depletion
-haemorrhage, burns, D&V, dehydration

Hypotension
-sepsis, cardiogenic shock

oedematous state
-HF, cirrhosis, nephrotic syndrome

renal hypoperfusion
-Renal artery stenosis, NSAIDs, ACE-I/ARBs

69
Q

Intrinsic renal causes of Acute kidney injury (AKI)

A

2nd most common

glomerulonephritis, HUS, acute tubular necrosis following prolonged ischaemia, nephrotoxins (e.g. NSAIDs, infection), vasculitis, malignant hypertension, polyarteritis nodosa, eclampsia

70
Q

Post-renal causes of Acute kidney injury (AKI)

A

Least common causes

calculi
papillary necrosis
urethral stricture
BPH/Prostate cancer
bladder tumour
radiation fibrosis
71
Q

Risk factors for Acute kidney injury (AKI)

A
↑ age (especially >65yrs)
CKD (especially eGFR <40)
history of AKI
co-existing illness e.g. HF, liver disease, diabetes 
neurological impairment 
reliance on carers
use of NSAIDs
use of ACE-Is/ARBs
use of diuretics
72
Q

Presentation of Acute kidney injury (AKI)

A

Often asymptomatic

↓ urine output 
pulmonary & peripheral oedema
oliguria/anuria 
dyspnoea
uraemia (anorexia, nausea, encephalopathy, asterix, pericarditis)
fatigue
confusion 
lethargy
73
Q

Investigations for Acute kidney injury (AKI)

A

U&Es

  • ↑ creatinine
  • ↑ urea
  • ↑ K+
FBC, CRP, Coagulation
urinalysis 
urine output measurement
urine MC&S
ABG/VBG
CXR
ECG
74
Q

Staging of Acute kidney injury (AKI)

A

Staged via KDIGO criteria

Stage I

  • ↑ creatinine to 1.5-1.9x baseline or
  • ↑ creatinine by ≥26.5 µmol/L, or
  • ↓ urine output to <0.5 mL/kg/hour for ≥ 6 hours

Stage II

  • ↑ creatinine to 2.0 to 2.9 times baseline, or
  • ↓ urine output to <0.5 mL/kg/hour for ≥12 hours

Stage III

  • ↑ creatinine to ≥ 3.0 times baseline, or
  • ↑ creatinine to ≥353.6 µmol/L or
  • ↓ urine output to <0.3 mL/kg/hour for ≥24 hours or
  • initiation of kidney replacement therapy or,
  • patients <18 years, ↓ eGFR to <35 mL/min/1.73 m2
75
Q

Management of Acute kidney injury (AKI)

A

management is largely supportive

Stop medications

  • NSAIDs, ahminoglycosides, ACE-Is/ARBs, diuretics
  • Also stop lithium, metformin, digoxin due to ↑ risk of toxicity

monitor K+, Na+, Ca2+, glucose

optimise fluid balance
-e.g. with IV fluids

nephrology referral to treat underlying cause or if considering renal replacement therapy

76
Q

Chronic kidney disease (CKD)

A

an abnormality in kidney structure or function persisting >3 months

accelerated progression of CKD = sustained ↓ in GFR ≥25% or ↓ in GFR of >15 per year

common causes include diabetic nephropathy, hypertension, chronic glomerulonephritis/pyelonephritis and adult PKD

77
Q

Staging of Chronic kidney disease (CKD)

A

Stage I
-GFR >90ml/min with some signs of kidney damage on other tests

Stage II
-GFR 60-90ml/min with some signs of kidney damage

Stage III

  • a = GFR 45-59ml/min
  • b = GFR 30-44ml/min

Stage IV
-GFR 15-29ml/min

Stage V
-GFR <15ml/min

NB if all kidney tests are normal there is no CKD

78
Q

Staging of Chronic kidney disease (CKD)

A

Stage I
-GFR >90ml/min with some signs of kidney damage on other tests

Stage II
-GFR 60-90ml/min with some signs of kidney damage

Stage III

  • a = GFR 45-59ml/min
  • b = GFR 30-44ml/min

Stage IV
-GFR 15-29ml/min

Stage V
-GFR <15ml/min

NB if all kidney tests are normal there is no CKD

79
Q

Presentation of Chronic kidney disease (CKD)

A

often asymptomatic

oedema
polyuria
lethargy
pruritis
anorexia
insomnia
hypertension 
sexual dysfunction
80
Q

Investigations for Chronic kidney disease (CKD)

A

renal ultrasound
-small kidneys on USS are indicative of CKD

U&Es

  • often severely deranged
  • pts often tolerate this due to chronicity

FBC

  • anaemia usually
  • if not anaemic points more to AKI
eGFR ↓
Ca2+ (usually ↓)
urinalysis 
urine albumin
glucose
81
Q

Management of Chronic kidney disease (CKD)

A
annual CVD assessment 
nutrition & exercise adjustment 
Vit D & Calcium supplements 
20mg statin 
consider oral anticoagulant 

control BP

  • target 130/80, requires ≥2 meds mostly
  • use ACE-Is
  • if eGFR <45 consider furosemide

If severe = renal replacement therapy (RRT)

82
Q

Monitoring of Chronic kidney disease (CKD)

A

monitored with eGFR & creatinine as well as ACR

frequency determined by severity of CKD

83
Q

Complications of Chronic kidney disease (CKD)

A
anaemia (↓EPO)
hypetension
secondary hyperparathyroidism 
coagulopathy
fluid overload
84
Q

Renal replacement therapy (RRT)

A

RRT is indicated when kidneys transiently or persistently lose function to remove toxins, metabolites and water from the body

~10% of CKD pts develop renal failure (GFR <15ml/min)

Types:

  • haemodialysis
  • peritoneal dialysis
  • renal transplant
85
Q

Haemodialysis

A

most common form of RRT

involves haemofiltration at hospital ~3x per week for 3-5h

requires formation of arteriovenous fistula at least 8 weeks before

86
Q

Peritoneal dialysis (PD)

A

filtration occurs in via pts peritoneum with dialysis solution injected into abdominal cavity via a permanent catheter

can be continuous PD (CAPD) where fluid is exchanged every 48h
OR
automated PD (APD) where dialysis machine performs 3-5 exchanges as pt sleeps
87
Q

Renal transplant

A

kidney can be from live or deceased donor, average wait list is ~3years

donated kidney usually transplanted into the groin & the vessel connected to external iliac arteries with the failing kidneys left in place

lifespan of donated kidney is 10-12yrs from deceased donor & 12-15yrs from live donor

pt on lifelong immunosuppression e.g. Tacrolimus, Cyclosporine, Mycophenolate

88
Q

Indications for acute dialysis

A
Hyperkalaemia 
pulmonary oedema
pericarditis 
symptomatic uraemia
severe acidosis 

(obviously pt also has to be in renal failure)

89
Q

Nephrotic syndrome

A

A collection of signs & symptoms indicating damage to the glomerular filtration barrier

characterised by:

  • Proteinuria >3.5g/24h
  • Hypoalbuminaemia ≤30g/L (≤3g/dL)
  • Oedema
90
Q

Key features of nephrotic syndrome

A

Proteinuria >3.5g/24h
Hypoalbuminaemia ≤30g/L (≤3g/dL)
Oedema

91
Q

Aetiology of Nephrotic syndrome

A

Focal segmental glomerulosclerosis = most common cause in adults

Minimal change disease = most common cause in children

Other causes
-membranoproliferative glomerulonephritis, membranous nephropathy

Secondary causes
-diabetic nephropathy, lupus nephritis, amyloid nephropathy

92
Q

Presentation of Nephrotic syndrome

A

Peripheral oedema
-in children often starts with periorbital oedema

frothy urine
leukonychia
SOB
dyspnoea

hypercoaguability
-e.g. DVT, PE

93
Q

Investigations for Nephrotic syndrome

A

Urinalysis

  • proteinuria +++
  • haematuria may be +

serum albumin
- ≤30g/L

24h urine protein
->3.5g

lipid profile
-commonly shows hyperlipidaemia

renal biopsy
-shows definitive cause often

FBC, U&Es, LFts, glucose, CRO
urine MC&S

94
Q

Management of Nephrotic syndrome

A

Dietary sodium restriction
fluid restriction

high dose diuretics

  • 1st line furosemide ± spironolactone
  • can also consider other loop diuretics e.g. bumetanide

In children:

  • corticosteroids
  • ~80% of children have relapses so consider cyclophosphamide when relapsing
  • most are initially steroid sensitive

consider ACE-Is in adults

95
Q

Nephritic syndrome

A

characterised by glomerular capillary damage leading to

  • haematuria*
  • pyuria
  • water retention
  • hypertension*
  • oedema
96
Q

Aetiology of Nephritic syndrome

A
IgA nephropathy (burgers disease)
-most common cause

post-streptococcal glomerulonephritis
-usually seen in children ~1-2 weeks post strep throat/skin infections

small vessel vasculitis e.g. WEgners / Churg strauss
Goodpastures disease (anti-GBM antibodies)
Alport syndrome
rapidly progressing glomerulonephritis (RPGN)

97
Q

Presentation of Nephritic syndrome

A

intermittent gross haematuria
-cola-coloured urine

hypertension
pitting oedema
oliguria

98
Q

Investigations for Nephritic syndrome

A

Urinalysis

  • blood ++
  • protein <3.5g/24h

urinary sediment

  • red cell casts
  • sterile pyuria

U&Es

  • ↓eGFR
  • ↑ creatinine

Renal biopsy

99
Q

Management of Nephritic syndrome

A

low sodium diet
water restriction

ACE-Is/ARBs
-for HTN & proteinuria

Plasmapheresis
-for anti-GBM & RPGN

acute streptococcal glomerulonephritis in children is usually self limiting and doesn’t require treatment

100
Q

Glomerulonephritis

A

denotes glomerular injury and applies to a group of diseases that are generally charcterised by inflammatory changes in the glomerular capillaries & glomerular basement membrane

can cause both nephrotic or nephritic syndromes

101
Q

IgA nephropathy (Bergers disease)

A

Most common cause of glomerulonephritis world wide

classically presents 1-2 days post URTI/GI infection in young people (especially men) with recurring episodes of macroscopic haematuria + flank pain ± nephritic syndrome

diagnostic include ↑IgA levels, normal C3/C4 complement levels & renal biopsy (showing mesangial IgA deposition)

management includes ARBs/ACE-Is for BP control and steroids

102
Q

Post-streptococcal glomerulonephritis

A

typically occurs 1-2 weeks post group A strep infection (strep progenes), especially in young children

due to immune complex (IgG, IgM, C3 complement) deposition in the glomeruli

presents with proteinuria, haematuria, HTN and oedema

Investigations include ↓C3/C4 complement levels, ↑ASO titre & biopsy (often not required but shows starry-sky appearance)

usually self limiting with good prognosis

103
Q

Anti-glomerular basement membrane disease (Goodpastures disease)

A

a type of small vessel vasculitis associated with pulmonary haemorrhage & rapidly progressing glomerulonephritis caused by anti-GBM antibodies

presents with pulmonary haemorrhage & nephritic syndrome

diagnostics include normal ESR (normally ↑ in vasculitis), +ve anti-GBM antibodies, CXR, renal biopsy (showing linear IgG deposits along basement membrane)

managed with plasma exchange, steroids and cyclophosphamide

104
Q

Focal segmental glomerulosclerosis (FSGS)

A

most common cause of nephrotic syndrome in adults, due to injury of podocytes

often idiopathic but may be due to HIV, heroin use or sickle cell

presents wit nephrotic syndrome (proteinuria, oedema)

diagnostics include renal biopsy showing focal & segmental sclerosis with podocyte effacement

managed with steroids ± immunosuppressants

NB noted to have high reoccurrence rate in renal transplants)

105
Q

Membranous glomerulonephritis

A

most common cause of nephrotic syndrome in european & middle easter ppl

usually presents with nephrotic syndrome

diagnostics include renal biopsy, showing thickened basement membrane (spike & dome appearance), and if idiopathic may have +ve anti-phospholipase A2 antibodies

managed with ACE-Is/ARBs, immunosuppression (steroids + cyclophosphamide)

poor prognosis with 1/3 pts progressing to end stage renal failure

106
Q

Minimal change disease

A

most common cause of nephrotic syndrome in children
generally idiopathic

presents with nephrotic syndrome (proteinuria, hypoalbuminaemia, oedema)

diagnosis include renal biopsy (normal appearance on light microscopy with podocyte fusion & effacement on electron microscopy)

managed with steroids (~80% of cases are steroid sensitive) or cyclophosphamide if steroid resistant

107
Q

Membranoproliferazive glomerulonephritis (mesangiocapillary glomerulonephritis)

A

uncommmon

associated with ↓C3 levels

generally treated with ACE-Is/ARBs

108
Q

Rapidly progressive gvomerulonpoehritis

A

rapid ↓ renal function associated with formation of epithelia crescents

causes include good pastures, Wegners, SLE

presents with nephritic syndrome (HTN, haematuria)
& features of underlying cause

generally treated with steroids & cyclophosphamide

109
Q

Alport Syndrome

A

most common inherited nephritis
X-linked recessive condition usually presenting in childhood

presents with progressive renal failure & bilateral sensorineural hearing loss/deafness

no definitive treatment available

110
Q

Diuretics

A

a group of drugs that ↑ urine production, they are generally categorised by what renal structures they affect

Types:

  • Loop diuretics e.g. furosemide/bumetanide
  • Thiazide diuretics e.g. bendroflumathiazide
  • Thiazide-like diuretics e.g. indapamide/chlortalidone
  • Aldosterone antagonist e.g. spironolcatone/epleronone
  • epithelial Na+ channel blockers e.g. amiloride
  • Osmotic diuretics e.g. mannitol
  • Carbonic anhydrase inhibitors e.g. acetazolamide
111
Q

Carbonic anhydrase inhibitors

A

Examples:
-acetazolamide

MOA:
-inhibits carbonic anhydrase in kidney, eyes and brain

Indications:

  • acute glaucoma
  • altitude sickness
  • Idiopathic intracranial hypertension (IIH)
112
Q

Osmotic diuretics

A

Examples:
-mannitol, urea

MOA:
-↑osmolality of tubular fluid = ↑ urine production

Indications:

  • ↑ICP e.g. in cerebral oedma
  • acute glaucoma

NB can lead to dehydration

113
Q

Loop diuretics

A

Examples:
-Furosemide, Bumetanide

MOA:
-inhibit Na-K-Cl cotransporter in the thick ascending loop of Henle

Indications:

  • HF
  • resistant hypertension (especially in pts with renal impairment)
  • fluid retention in CKD
  • Oedema

Side effects:

  • ↓ Na+
  • ↓ K+
  • ↓ Ca2+
  • hypochloraemic alkalosis
  • gout
114
Q

Thiazide diuretics

A

Examples:

  • bendroflumathiazide
  • Thiazide like diuretics e.g. Indapamide / Chlortalidone are now preferred

MOA:
-inhibit thiazide sensitive Na+-Cl- symporters in distal convoluted tubules

Indications:

  • hypertension
  • severe HF in combination with loop diuretics

Side effects:

  • ↓ Na+
  • ↓ K+
  • ↓ Ca2+
  • postural hypotension
  • impotence
  • impaired glucose tolerance
115
Q

Potassium sparing diuretics

A

2 subtypes

  • Aldosterone antagonist e.g. spironolcatone/epleronone
  • epithelial Na+ channel blockers e.g. amiloride

Side effects:
-↑K+

116
Q

Aldosterone antagonist (a type of Potassium sparing diuretic)

A

Examples:
-spironolcatone, epleronone

Indications:

  • ascites (large doses of 100-200mg)
  • HF (if ↓K+)
  • Hypertension (if ↓K+)
  • nephrotic syndrome
  • conns syndrome

Side effects:

  • ↑K+
  • spironolactone can cause endocrine disturbances e.g. gynaecomastia, amenorrhoea, erectile dysfunction

NB epleronone does not cause frequently cause endocrine disturbances so can be used instead of spironolactone

117
Q

Epithelial Na+ channel blockers (a type of Potassium sparing diuretic)

A

Examples:
-amiloride

Indications:
-used with other diuretics as alternative to K+ supplements

Side effects:
-↑K+

118
Q

Polycystic kidney disease (PKD)

A

a heterogenous group of disorders characterised by renal cysts and numerous system & extra renal manifestation

Types:

  • Autosomal dominant PKD (ADPKD)
    • most common form
    • onset usually age >30yrs
  • Autosomal recessive PKD (ARPKD)
    • more likely to present in childhood

NB ADPKD is the most common inherited serious renal disease, and is responsible for ~10% of end stage renal failure

119
Q

Types of Polycystic kidney disease (PKD)

A

Autosomal dominant PKD (ADPKD)

  • most common form
  • onset usually age >30yrs

Autosomal recessive PKD (ARPKD)
-more likely to present in childhood

120
Q

Presentation of Polycystic kidney disease (PKD)

A
hypertension
recurrent UTIs
abdo pain
renal stones
haematuria
CKD
flank pain / loin pain
palpable enlarged kidneys

hepatomegaly
-due to bening liver cysts

cerebral berry aneurysms
-can cause SAH

121
Q

Screening for Polycystic kidney disease (PKD)

A

In relatives of pts with PKD using renal USS

Diagnostic criteria in pt with +ve family history

  • 2 cysts, unilateral/bilateral if age <30yrs
  • 2 cysts in both kidneys if age 30-59yrs
  • 4 cysts in both kidneys if age >60yrs
122
Q

Investigations for Polycystic kidney disease (PKD)

A

FBC
-may be ↑Hb due to ↑ EPO secretion

Renal USS

  • diagnostic method of choice
  • shows renal cysts
Urinalysis 
Urine MC&S
U&Es
Bone profile
genetic testing
123
Q

Management of Polycystic kidney disease (PKD)

A

screening family members
pt & relative education

Tolvaptan

  • used in selected pts
  • usually CKD stage 1-3 with rapid progression

ACE-Is/ARBs

  • for HTN
  • target BP 130/80
124
Q

Pyelonephritis

A

an infection of the renal pelvis & parenchyma that is usually associated with an ascending UTI, generally more common in women (in neonates more common in boys)

Causes usually same as UTIs
-E.coli*, Klebsiella, proteus, enterococcus

NB repeated episodes of acute pyelonephritis can lead to chronic pyelonephritis which involves destruction & scarring of renal tissue due to repeated inflammation and can lead to CKD

125
Q

Risk factors for Pyelonephritis

A

structural renal abnormalities
-e.g. vesicoureteric reflux (VUR

calculi 
urinary catheterisation 
stents
pregnancy
diabetes
126
Q

Presentation of Pyelonephritis

A
Fever, chills, rigors 
flank pain / loin pain
dysuria, weakness
costovertebral angle tenderness
suprapubic tenderness 
nausea & vomiting
tachycardia, hypotension
127
Q

Investigations for Pyelonephritis

A

Urinalysis

  • leukocytes +
  • nitrites +
  • WCC casts
  • haematuria

FBC

  • WCC ↑
  • neutrophilia

Renal USS
-if blood in urine or urine unclear

CRP/ESR (↑)
Contrast enhanced CT
Urine MC&S
Blood cultures

128
Q

Management of Pyelonephritis

A

Supportive

  • IV fluids
  • Analgesia

Empirical Abx
-1st line = co-amoxiclav or ciprofloxacin for 7days

Surgery
-may be needed to drain renal abscesses or perinephric abscesses

NB in children 1st line = co-amoxiclav and 2nd line is cefixime

129
Q

Prophylaxis for Pyelonephritis

A

usually in women with ≥3 episodes in a year

usually with trimethoprim