Breast, Renal & Urology Flashcards

(129 cards)

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
Varicocele
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
26
Bening prostatic hyperplasia (BPH)
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
27
Presentation of Bening prostatic hyperplasia (BPH)
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
28
Assessment of Bening prostatic hyperplasia (BPH)
International prostate symptom score (IPSS) - used to assess the severity of LUTS - assess impact on QoL
29
Investigations for Bening prostatic hyperplasia (BPH)
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 ```
30
Management of Bening prostatic hyperplasia (BPH)
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
31
Prostatitis
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
32
Pharmacological treatment of Benign prostatic hyperplasia (BPH)
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
33
Prostate cancer
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
34
Location of prostate lesions
Prostate cancer: -peripheral zone BPH -transitional zone
35
Epidemiology & Risk factors for Prostate cancer
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
36
Presentation of prostate cancer
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
37
DRE examination findings for prostate pathology
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
38
Investigations for prostate cancer
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
39
Management of prostate cancer
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
40
Bladder cancer
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
41
Risk factors for bladder cancer
smoking exposure to aniline dyes e.g. 2-naphthylamine rubber manufacturing cyclophosphamide
42
Risk factor for squamous cell bladder cancer
Indwelling catheters | schistosomiasis**
43
Presentation of bladder cancer
painless macroscopic haematuria dysuria urinary frequency other voiding symptoms NB painless haematuria is cancer until proven otherwise
44
Investigations for bladder cancer
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
45
Management of bladder cancer
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
46
Renal cell carcinoma (RCC) also known as hypernephroma
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
47
Risk factors for Renal cell carcinoma (RCC)
smoking obesity HTN also associated with von Hippel-Lindau syndrome & tuberous sclerosis
48
Presentation of Renal cell carcinoma (RCC)
``` 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
49
Investigations for Renal cell carcinoma (RCC)
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 ```
50
Management of Renal cell carcinoma (RCC)
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
51
Nephrolithiasis (renal stones)
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
52
Epidemiology of Nephrolithiasis (renal stones)
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
Risk factors for Nephrolithiasis (renal stones)
``` 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
Presentation of Nephrolithiasis (renal stones)
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
Investigations for Nephrolithiasis (renal stones)
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
Management of Nephrolithiasis (renal stones)
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
Urinary tract infection (UTI)
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
Aetiology of Urinary tract infection (UTI)
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
Risk factors of Urinary tract infection (UTI)
``` ↑ age recent instrumentation of the renal tract renal tract abnormalities sexual activity diabetes institutionisation catheterisation pregnancy immune suppression ```
60
Presentation of Urinary tract infection (UTI)
``` 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
Investigations for Urinary tract infection (UTI)
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
Management of Urinary tract infection (UTI)
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
Management of Urinary tract infection (UTI) in non pregnant women
3 days pf trimethoprim / nitrofurantoin NB send cultures if age >65yrs or macro.microscopic haematuria
64
Management of Urinary tract infection (UTI) in pregnant women
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
Management of Urinary tract infection (UTI) in men
offer 7 days of trimethoprim or nitrofurantoin
66
Management of Urinary tract infection (UTI) in catheterised pts
DO NOT treat asymptomatic bactiuria if symptomatic = 7 days of Abx
67
Acute kidney injury (AKI)
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
Pre-renal causes of Acute kidney injury (AKI)
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
Intrinsic renal causes of Acute kidney injury (AKI)
2nd most common glomerulonephritis, HUS, acute tubular necrosis following prolonged ischaemia, nephrotoxins (e.g. NSAIDs, infection), vasculitis, malignant hypertension, polyarteritis nodosa, eclampsia
70
Post-renal causes of Acute kidney injury (AKI)
Least common causes ``` calculi papillary necrosis urethral stricture BPH/Prostate cancer bladder tumour radiation fibrosis ```
71
Risk factors for Acute kidney injury (AKI)
``` ↑ 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
Presentation of Acute kidney injury (AKI)
Often asymptomatic ``` ↓ urine output pulmonary & peripheral oedema oliguria/anuria dyspnoea uraemia (anorexia, nausea, encephalopathy, asterix, pericarditis) fatigue confusion lethargy ```
73
Investigations for Acute kidney injury (AKI)
U&Es - ↑ creatinine - ↑ urea - ↑ K+ ``` FBC, CRP, Coagulation urinalysis urine output measurement urine MC&S ABG/VBG CXR ECG ```
74
Staging of Acute kidney injury (AKI)
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
Management of Acute kidney injury (AKI)
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
Chronic kidney disease (CKD)
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
Staging of Chronic kidney disease (CKD)
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
Staging of Chronic kidney disease (CKD)
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
Presentation of Chronic kidney disease (CKD)
often asymptomatic ``` oedema polyuria lethargy pruritis anorexia insomnia hypertension sexual dysfunction ```
80
Investigations for Chronic kidney disease (CKD)
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
Management of Chronic kidney disease (CKD)
``` 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
Monitoring of Chronic kidney disease (CKD)
monitored with eGFR & creatinine as well as ACR frequency determined by severity of CKD
83
Complications of Chronic kidney disease (CKD)
``` anaemia (↓EPO) hypetension secondary hyperparathyroidism coagulopathy fluid overload ```
84
Renal replacement therapy (RRT)
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
Haemodialysis
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
Peritoneal dialysis (PD)
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
Renal transplant
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
Indications for acute dialysis
``` Hyperkalaemia pulmonary oedema pericarditis symptomatic uraemia severe acidosis ``` (obviously pt also has to be in renal failure)
89
Nephrotic syndrome
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
Key features of nephrotic syndrome
Proteinuria >3.5g/24h Hypoalbuminaemia ≤30g/L (≤3g/dL) Oedema
91
Aetiology of Nephrotic syndrome
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
Presentation of Nephrotic syndrome
Peripheral oedema -in children often starts with periorbital oedema frothy urine leukonychia SOB dyspnoea hypercoaguability -e.g. DVT, PE
93
Investigations for Nephrotic syndrome
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
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Management of Nephrotic syndrome
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
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Nephritic syndrome
characterised by glomerular capillary damage leading to - haematuria* - pyuria - water retention - hypertension* - oedema
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Aetiology of Nephritic syndrome
``` 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)
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Presentation of Nephritic syndrome
intermittent gross haematuria -cola-coloured urine hypertension pitting oedema oliguria
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Investigations for Nephritic syndrome
Urinalysis - blood ++ - protein <3.5g/24h urinary sediment - red cell casts - sterile pyuria U&Es - ↓eGFR - ↑ creatinine Renal biopsy
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Management of Nephritic syndrome
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
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Glomerulonephritis
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
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IgA nephropathy (Bergers disease)
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
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Post-streptococcal glomerulonephritis
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
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Anti-glomerular basement membrane disease (Goodpastures disease)
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
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Focal segmental glomerulosclerosis (FSGS)
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)
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Membranous glomerulonephritis
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
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Minimal change disease
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
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Membranoproliferazive glomerulonephritis (mesangiocapillary glomerulonephritis)
uncommmon associated with ↓C3 levels generally treated with ACE-Is/ARBs
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Rapidly progressive gvomerulonpoehritis
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
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Alport Syndrome
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
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Diuretics
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
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Carbonic anhydrase inhibitors
Examples: -acetazolamide MOA: -inhibits carbonic anhydrase in kidney, eyes and brain Indications: - acute glaucoma - altitude sickness - Idiopathic intracranial hypertension (IIH)
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Osmotic diuretics
Examples: -mannitol, urea MOA: -↑osmolality of tubular fluid = ↑ urine production Indications: - ↑ICP e.g. in cerebral oedma - acute glaucoma NB can lead to dehydration
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Loop diuretics
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
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Thiazide diuretics
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
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Potassium sparing diuretics
2 subtypes - Aldosterone antagonist e.g. spironolcatone/epleronone - epithelial Na+ channel blockers e.g. amiloride Side effects: -↑K+
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Aldosterone antagonist (a type of Potassium sparing diuretic)
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
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Epithelial Na+ channel blockers (a type of Potassium sparing diuretic)
Examples: -amiloride Indications: -used with other diuretics as alternative to K+ supplements Side effects: -↑K+
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Polycystic kidney disease (PKD)
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
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Types of Polycystic kidney disease (PKD)
Autosomal dominant PKD (ADPKD) - most common form - onset usually age >30yrs Autosomal recessive PKD (ARPKD) -more likely to present in childhood
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Presentation of Polycystic kidney disease (PKD)
``` 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
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Screening for Polycystic kidney disease (PKD)
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
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Investigations for Polycystic kidney disease (PKD)
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 ```
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Management of Polycystic kidney disease (PKD)
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
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Pyelonephritis
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
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Risk factors for Pyelonephritis
structural renal abnormalities -e.g. vesicoureteric reflux (VUR ``` calculi urinary catheterisation stents pregnancy diabetes ```
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Presentation of Pyelonephritis
``` Fever, chills, rigors flank pain / loin pain dysuria, weakness costovertebral angle tenderness suprapubic tenderness nausea & vomiting tachycardia, hypotension ```
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Investigations for Pyelonephritis
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
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Management of Pyelonephritis
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
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Prophylaxis for Pyelonephritis
usually in women with ≥3 episodes in a year | usually with trimethoprim