Phase 2 - Renal & GU Flashcards

Question

Classification of AKI stages

Answer 1

- 1: - CREATININE 1.5-1.9x Baseline or - Urine REDUCED <0.5 ml/kg/hour for >= 6HR - 2: - CREATININE 2.0-2.9x Baseline or - Urine REDUCED <0.5 ml/kg/hour for >= 12HR - 3: - CREATININE >= 3.0x Baseline or - Urine REDUCED <0.5 ml/kg/hour for >= 24HR

Answer 2

Abnormal kidney structure/function - eGFR <60mL/min/1.73m^2 for >3 MONTHS - OR eGFR <90 ml/min/1.73m2 + signs of renal damage - or Albumin:Creatinine >3mg/mmol (normal = 120)

Answer 3

Based on GFR range: - 1: >90 ml/min (w/ signs of renal damage) - 2: 60-90 ml/min (w/ signs of renal damage) - 3a: 45-59 ml/min - 3b: 30-44 ml/min - 4: 25-29 (severe) - 5: <15 (Kidney FAILURE)

Answer 4

Main: - DIABETES M - HTN Also: - glomerulonephritis - PKD - nephrotoxic drugs (esp NSAIDs)

Answer 5

Many nephrons damaged - REDUCED GFR + INCREASED BURDEN on other nephrons - COMPENSATORY RAAS to RAISE GFR - INCREASED TRANSGLOMERULAR PRESSURE - SHEARING - LOSS OF SELECTIVE PERMEABILITY (protein/haematuria) - ANGIOTENSIN 2 upregulates TGF-beta + Plasminogen activator inhibitor 1 - Causes MESANGIAL SCARRING Symps due to substance accumulation + diabetic nephropathy

Answer 6

- ANAEMIA (reduced EPO) -> Pericarditis + effusion if severe - OSTEODYSTROPHY (reduced vit D activation) - NEUROPATHY/ ENCEPHELOPATHY - HTN, ^lipids, vasc calcific -> CVD (highest mortality)

Answer 7

- FBC (anaemia of chronic disease) - U + E (high urea + creatinine) - raised PTH if stage 3 or more - raised alk phos from bone dystrophy - US (bilateral renal shrinking - can be large if infiltrative e.g. amyloidosis) - GFR FUNCTION STAGING - low eGFR - URINE DIP (PROTEINURIA) - Albumin-Creatinine RATIO >3 = SIG. PROTEINURIA

Answer 8

NO CURE, it's irreversible - treat complications - lifestyle changes - Anaemia: EPO + IRON (give iron first) - Osteodystrophy: Vit D supplements - Oedema: diuretics - CVD: ACE-I + STATINS - ATORVASTATIN If END-STAGE (stage 5): - RRT (dialysis) - RENAL TRANSPLANT (cure)

Answer 9

Non-continuous: - Haemodialysis (short + max solute clearance but haemodynamic instability) - Peritoneal dialysis (slower, less efficient, risk of peritonitis or abdo compartment syndrome but doesn't require vascular access) Continuous - used in ICU: - Haemodiafiltration - Haemofiltration Continuous allows you to add in fluid and better control their fluid volume - needs to be continuously attached to machine

Answer 10

Vascular access - AV Fistula (makes vein larger at connection) - AV Graft (artificial plastic tubing that acts as vein if actual vein too small) - Central venous catheter (temporary plastic tube inserted in large vein, typically in neck but could be in groin - usually only for emergancy haemodialysis)

Answer 11

- Definition: - AKI defined as RAISED SERUM CREATININE + Reduced urine output - CKD = reduced eGFR - Symptom onset: - AKI = shorter onset - CKD = 3+ months - Anaemia: - AKI = NO ANAEMIA - CKD - ANAEMIA OF CHRONIC DISEASE - US: - AKI = NORMAL US - CKD = BILATERAL SMALL ATROPHIED KIDNEYS

Answer 12

- Stress incontinence - related to sphincter weakness - leaks when INTRA-ABDO pressure RISE - (more common in FEMALES) - Urge incontinence - Related to overactive bladder - Mixed - Overflow incontinence (retention -> leaking)

Answer 13

- Cortex - Sensation - Voluntary initiation - **PONTINE MICTURITION CENTRE**/Peri Aquaductal Grey - Co-ordination - Completion of voiding - Spinal Reflexes (S 2-4 - parasymp nerves S3, 4, 5 -> detrusor contraction + sphincter relaxation) - Reflex bladder contraction - Sacral micturition centre - Guarding reflex - Onuf’s nucleus - Receptive relaxation - Sympathetic (T10 - L2) - Inhibits detrusor contraction + smooth muscle sphincter contraction - External urethral sphincter (striated sphincter) - Somatic (skeletal muscle) - overrides autonomic till appropriate to void

Answer 14

- Storage - Voiding - Post-micturition Important to learn diff types in each category esp storage + voiding symptoms

Answer 15

- FREQUENCY - URGENCY (when they need to go, can't hold it long - very desperate) - NOCTURIA - esp in older men (prostate prevents full emptying -> leftover creates need to go at night when everything is relaxed) - INCONTINENCE

Answer 16

- SLOW stream/Poor flow - HESITANCY - STRAINING (using abdo muscles) - Intermittency - TERMINAL DRIBBLE (- Splitting/spraying) (- Vesicle tenesmus (incomplete bladder emptying))

Answer 17

- Post-micturition dribble (later than terminal dribble) - Feeling of INCOMPLETE VOIDING (contributes to frequency)

Answer 18

URGENCY WITH FREQUENCY, with or without nocturia, when appearing in ABSENCE of LOCAL PATHOLOGY Can be wet or dry

Answer 19

A rise in PRESSURE on FILLING on URODYNAMIC TESTING

Answer 20

- Bladder is filled with fluid - Pressure in bladder is measured - Pressure in abdo is also measured (via rectum) - Subtract pressure measured in bladder from intra-abdominal pressure for actual bladder pressure Reserved for cases where surgery is considered/bladder safety is potentially compromised

Answer 21

- NEUROGENIC - Congenital - IATROGENIC (e.g. after prostectomy, leaving catheter in too long) - In FEMALES, oft related to BIRTH TRAUMA: - denervation of pelvic floor/urethral sphincter - weakening of fascial support - oft related to straining e.g. lifting weights

Answer 22

- Men: - ARTIFICIAL SPHINCTER - Women: - Autologous sling - Artificial sphincter CANNOT DO if RISK of UNSAFE bladder (i.e if they have loss of compliance and you add a functional sphincter -> unsafe)

Answer 23

- Behavioural therapy - Bladder diary - reduce caffine/alcohol - ANTI-MUSCARINICS - BLOCK M2/M3 receptors (parasymp) - S/E = dry mouth - B3 AGONIST - MIRABEGRON - increase SYMPATHETIC activity - Botox - muscular PARALYSIS (blocks ACh at neuromuscular junction) - INCOMPLETE BLADDER EMPTHYING -> catheterise 15% - SACRAL NEUROMODULATION (expensive) - neg feedback - shouldn't work in complete spinal injury - Surgery - Augmentation CYSTOPLASTY - may cause retention

Answer 24

- Cut bladder in half (stop contraction) - Put section of bowel in bladder

Answer 25

- Suprapontine (cerebral) - Voiding is CO-ORDINATED but SOCIALLY INAPPROPRIATE - Suprasacral spinal cord conditions (SPASTIC) - upper motor neurone damage - Detrusor-sphincter dyssynergia (loss of co-ord) - Potentially UNSAFE - Sacral spinal cord conditions (FLACCID - conus damaged) - loss of guarding and potentially compliance

Answer 26

Spastic - upper motor neurone lesion - hyper-reflexia - increased tone - No sensation - In bladder - spinal cord telling to squeeze but striated sphincter not relaxed - UNSAFE Flaccid - lower motor neuron lesion - Hyporeflexia - Reduced tone - No sensation - In bladder - no spinal cord control -> fills up, continuous leaking

Answer 27

Bladder that can cause damage to kidneys via PROLONGED HIGH PRESSURES

Answer 28

Usually in MALES - OBSTRUCTION - stones - BENIGN PROSTATE HYPERPLASIA/enlargement - Abdo masses/prolapse (vaginal/rectal) - Urethral stricture (trauma or infection) - FLACCID PARALYSIS/Atonic bladder - detrusor underactivity

Answer 29

- ALPHA BLOCKERS +/- 5 alpha reductase inhib for BPH - alpha blockers relax muscles around urethra - 5 alpha-reductase inhibitors reduce levels of DiHydroTestosterone (DHT). Prostate shrinks when less DHT present. - Prostatectomy - LONG TERM CATHETERISATION - potentially sacral neuromodulation

Answer 30

Prostate secretes fluid into urethra that nourishes/protects sperm. Normal prostate is around walnut sized, has a midline indent, is symmetrical and the consistancy of the tip of your nose - It produces prostate-specific antigen (PSA) - liqifaction of semen. Raised in serum if cancerous, hyperplastic, inflamed, infected (sexual activity). DHT is the most potent androgen and one that cannot convert to oestrogen. - 5 ALPHA-REDUCTASE converts TESTOSTERONE to DHT in PERIPHERAL TARGET TISSUES (paracrine - only has effect in vincinity of gland secreting it/where it is synthesised). - Mainly in liver - Stimulates sexual differentiation of organs in embryo - Promotes PROSTATE GROWTH, sebaceous gland activity, male pattern baldness and body hair after puberty

Answer 31

Non-malignant prostate hyperplasia (increase in number of epithelial/stromal cells - look up in histology book) - normal w/ aging

Answer 32

- increased AGE - ethnicity (Afro-Caribbean = increased testosterone) CASTRATION is PROTECTIVE

Answer 33

Proliferation of epithelial/stromal cells in INNER TRANSITIONAL ZONE of prostate - causes narrowing of urethra

Answer 34

- LUTS esp VOIDING RELATED - Voiding: - Poor stream; Dribbling - Vesicle tenesmus/incomplete emptying - Straining - Potential dysuria (painful urination) - Storing: - Frequency, urgency, Nocturia (>30%), - Incontinence If totally occluded - may get ANURIA -> RETENTION, HYDRONEPHROSIS, UTI, stones

Answer 35

DRE (digital rectal exam)/PR (per rectal) exam - Prostate feels SMOOTH and ENLARGED, may have very defined or obliterated midline sulcus depending on size (normal prostate is around walnut sized, has a midline sulcus (usually not very defined), is symmetrical and the consistancy of the tip of your nose) PSA to try and rule out cancer (more commonly raised in cancer) but PSA can be raised in both Also exclude things like stones and UTIs

Answer 36

- LIFESTYLE: reduce CAFFINE (it's a diuretic - this is just to reduce urgency/frequency) - May ACUTELY need catheter - Drugs: - 1ST LINE: ALPHA BLOCKER - TAMSULOSIN (relaxes bladder neck) - 2ND LINE: 5 APLHA REDUCATSE INHIB - FINASTERIDE (reduces DHT -> reduces prostate size) - Lowers PSA so may hide cancer + risk of sexual dysfunction - Surgery last resort - TURP - TransUrethral Resection of Prostate - COMPLICATION - retrograde ejaculation

Answer 37

Neoplastic, malignant proliferation of outer PERIPHERAL zone of prostate. Can also affect transitional zone in 20%. (central zone seems pretty resistant to pathologies) - main cause of male malignancy It is usually an ADENOCARCINOMA (glandular epithelium) Spread may be: * Local → Locally advanced: seminal vesicles, bladder and rectum * Via lymph * Haematogenously - bone (sclerotic bony lesions) or less common; brain, liver and lung Androgen receptors on the prostate are responsible for cancerous growth - can get castration-resistant cancer which is still androgen sensitive

Answer 38

- Genetic: mutations in BRCA2, HOXB13 (linked to <55 y/o cancer) - FHx * 3 or more affected relatives or * 2 relatives who have developed early onset - 1 first-degree relative with prostate cancer then 2x risk - Increasing AGE - AFRO-CARIBBEAN ethnicity

Answer 39

- LUTS (same as BPH) - Systemic cancer symptoms - UNEXPLAINED WEIGHT LOSS - Fatigue - NIGHT PAIN - Haematuria - may indicate metastasis - BONE PAIN (indicates METASTASIS) - Typically LUMBAR BACK PAIN

Answer 40

SCLEROTIC LESIONS - thick, looks white on x-rays

Answer 41

- lymph nodes - BONE (particularly sacrum due to interconnected blood flow) - Liver - Lung - Brain

Answer 42

In community: - DRE - can feel HARD, IRREGULAR (nodules) - PSA test (non-specific to cancer + normal levels vary from person to person) - TRANSRECTAL ULTRASOUND w/ BIOPSY (DIAGNOSTIC) - US scan and Biopsy can also be done seperately, Biopsy is the GS

Answer 43

Gleason score - Low = <= 6 - Intermediate = 7 - High/v. high: - Grade group 4 = Gleason score 8 - Grade group 5 = Gleason score 9-10 It is worked out based on histological pattern of cells as they progress from normal to cancerous. Resembles normal = grade 1; So mutated they barely resemble normal = grade 5. - Pathologist identifies the 2 most prominant types of cancer cells in biopsy and adds them together to give overall Gleason score

Answer 44

- If local - PROSTATECTOMY - If metastatic (surgical/medical castration) - HORMONE THERAPY (prostate growth is stimulated by testosterone/DHT so reduced hormones = reduced cancer growth) - GnRH AGONISTS (stops LH/FSH productions by continuously stimulating pituitary -> overcomes pulsatile GnRH release - exogenous suppression of HPG axis) - most common med - GOSERELIN or ZOLADEX (SE - erectile dysfunction, loss of libido etc.) - **Bilateral orchiectomy** (castration - removes testes) - v. effective (remission) - CHEMO/RADIOTHERAPY (typically Radiotherapy) - DOCETAXEL CHEMO (alongside castration if fit enough) - Abiraterone (androgen receptor targeted - alongside castration if not fit enough for chemo) If progresses to castration-resistant disease: - 2nd line androgen receptor targeted hormone therapy: - Abiraterone - Enzalutamide - Further Cytotoxic chemotherapy: **Docetaxel**, Carbazitaxel - Bisphosphonates: Zoledronic Acid - Palliation - castration-resistant = high mortality - need to account for : - pain - spinal cord compression - uretric obstruction - anaemia Cryotherapy is also an option (i would assume for more localised cancer) Often SLOW GROWING so may just do WATCHFUL WAITING (esp if older)

Answer 45

The presence of microorganisms in the urinary tract which produces CLINICAL FEATURES. It can affect the lower tract causing cystitis (bladder), urethritis and prostatitis, and the upper causing pyelonephritis. It can also occur from untreated urolithiasis

Answer 46

Remember with KEEPS: - Klebsiella - E coli- most common causing >50% of cases (UPEC - uropathogenic e coli) - Enterococci - Proteus spp - Staphylococcus coagulase negative (NOT staph aureus) - SAPROPHYTICUS

Answer 47

Remember FUND - Frequency - Urgency - Nocturia - Dysuria

Answer 48

infection and inflammation of the RENAL PARENCHYMA, soft tissues of RENAL PELVIS + UPPER URETER - most often due to ascending UTI from own bowel flora (esp E COLI) - can also infect via blood/lymph - associated with SEPSIS

Answer 49

FEMALE - shorter urethra - closer to anus - easier for bacteria to colonise (+ INFANTS) ELDERLY esp CATHETERISED/INSTITUTIONALISED

Answer 50

- Urine stasis (stones or BPH) - Renal structural abnormalities - Catheters - Diabetes - Pregnancy - Immunocompromised Particularly affects **FEMALES under 35 yrs** Caused by ASCENDING UTI (bacteria move up from urethra); HAEMATOGENOUS spread of pathogens (via blood - esp S. AUREUS, CANDIDA); Lymphatic spread

Answer 51

May be asymp - Classic triad of symptoms: - LOIN PAIN - FEVER (- N+V) - PYURIA (WBC + PUS in urine) on investigation - May get Haematuria - Costovertebral joint/RENAL ANGLE TENDERNESS/pain - Rigors - Significant bacteriuria Oliguria if it causes AKI Septic shock in advanced disease

Answer 52

- ABDO EXAM - Tender loins + renal angle tenderness (+ rule out outher abdo pathology) - BLOODS - elevated inflam markers - URINALYSIS/URINE DIPSTICK - white cells; Nitrites (bacteria break down nitrates -> nitrites); microscopic haematuria (protein) - leucocyte elastase - foul smelling - MID STREAM URINE SAMPLE, CULTURE + MICROSCOPY (gold - diagnostic) RENAL/UPPER TRACT USS - to rule out urinary tract obstruction or stones, abnormal anatomy, incomplete bladder emptying

Answer 53

Rest FLUID REPLACEMENT (Cranberry juice?, lots of water) ANALGESIA (paracetamol NOT opiods) Antibiotics (BROAD SPECTRUM): - CIPROFLOXACIN or **CO-AMOXICLAV** (both ORAL) - IV **GENTAMICIN** or CO-AMOXICLAV if SEVERE - CEFALEXIN for 7-10 days if PREG - Trimethoprim or amoxicillin if sensitive. Surgery to drain abscesses/remove calculi if required - May need catheter If CHRONIC -> NEPHRECTOMY Complications: - Renal abscess - Emphysematous pyelonephritis (Gas accumulation in renal parenchyma, collecting system or perinephritic tissue due to necrotizing infection of renal parenchyma) - Kidney fibrosis - Sepsis

Answer 54

Infection of the urinary bladder - it is most common in young sexually active women Oft a UPEC (uropathogenic e coli) infection

Answer 55

- Urine stasis (from obstruction)/poor emptying - Catheters - Bladder epithelium damage History of UTI Diabetes Frequent sexual intercourse? Pregnancy

Answer 56

- Dysuria- discomfort, pain, burning on urination - Frequency - Urgency - Cloudy smelly urine - Haematuria - **Suprapubic tenderness/discomfort** - abdo/loin as well potentially

Answer 57

Urine dipstick- if positive for nitrites or WBCs and RBCs then UTI likely - unreliable in women over 65 so don’t bother MID STREAM Urine Microscopy, culture and sensitivity (gold)

Answer 58

Antibiotics: - 3 days of TRIMETHOPRIM, or NITROFURANTOIN or CEFALEXIN. - avoid nitrofurantoin at TERM in pregnancy. - TRIMETHOPRIM CONTRAINDICATED in pregnancy - 2nd LINE = CIPROFLOXACIN or Co-AMOXICLAV - amoxicilin if pregnant

Answer 59

Usually a SEXUALLY ACQUIRED INFECTION - Non-gonococcal: - CHLAMYDIA TRACHOMATIS (main - esp 15-24 y/o) - Mycoplasma genitalium - Ureaplasma urealyticum - Trichomonas vaginalis - Gonococcal: NESSERIA GONORRHOEA (less common) Non-infective cause = Trauma, stricture, irritation, stones

Answer 60

UNPROTECTED SEX - MSM esp male

Answer 61

- DYSURIA +/- URETHRAL DISCHARGE (blood/pus) - Urethral pain - penile discomfort - potential skin lesions - may get systemic symptoms Chlamydia: - Men = TESTICULAR pain - Voiding symptoms, dysuria - 50% asymp - Women = VAGINAL discharge and dysuria - white, yellow or green discharge - 70% are asymp Gonorrhoea: - more LIKELY to be ASYMP (90-95%) - Men = dysuria, frequency, discharge - Women = VAGINAL discharge, dysuria, PELVIC pain

Answer 62

- NAAT (nucleic acid amplification test) - GOLD - Detects STI if present - Female - SELF COLLECTED VAGINAL SWAB (best), endocervical swab, first void urine - Male - FIRST VOID URINE - URINALYSIS/DIP STICK (to exclude UTI) - Blood cultures (??- MID STREAM CULTURE + SENSITIVITY) For Gonorrhoea - need to SWAB infected areas and CULTURE/MICROSCOPY - urethral smear

Answer 63

- N. Gonorrhoea: - single IM CEFTRIAXONE dose + ORAL AZITHROMYCIN - partner notification, patient education + contact tracing - C. Trachomatis: - Single dose of 1g AZITHROMYCIN - 7 days of DOXYCYCLIN (bi-daily) - test for other STIs - avoid sex till finished + contact tracing - If PREGNANT: - ORAL ERYTHROMYCIN 14 days - or ORAL AZITHROMYCIN STAT

Answer 64

REACTIVE ARTHRITIS - Can't see, can't pee, can't climb a tree - conjunctivitis, urethritis, arthritis

Answer 65

Inflammation of epididymus extending to testes - Usually due to urethritis (STI) or MAINLY Extension of Cystitis (KEEPS) Most common in MALE 15-30 yrs (STIs) and OVER 60s (KEEPS - UTIs) Also: MUMPS, TRAUMA, CATHETER in ELDERLY RFx: - Previous infection - Indwelling catheter - Structural/functional abnormality of urinary tract - Anal intercourse (MSM esp)

Answer 66

- Unilateral scrotal PAIN + PALPABLE SWELLING (subacute) - Pain RELIEVED upon ELEVATING SCROTUM (+ve Prehn's sign) - tender on examination - Cremaster reflex intact - May get sweats/fever If STI - may have urethritis/urethral discharge If MUMPS: - HEADACHES, FEVER - UNI/BI-LATERAL PAROTID SWELLING

Answer 67

- NAAT - Intracellular G -VE DIPLOCOCCI = GONORRHOEA - Urine dip - MC + S (mid stream sample) - for UTI symps - US to rule out abscess - Urethral smear/swab RULE OUT TESTICULAR TORSION: - typically teste torsion has -ve Prehn's sign - If any doubt -> Surgical Scrotal Exploration

Answer 68

Antibiotics depending on which STI/UTI is affecting - Analgesia - NSAIDs - Scrotal support (supportive underwear) - Abstain from sexual intercourse - Partner notification/testing

Answer 69

Inflammation and swelling of the prostate gland, most commonly caused by **E coli** - can be acute or chronic

Answer 70

- Very tender prostate: on DRE **intensely tender prostate gland**, may feel hot. May be boggy/nodular in places. - SYSTEMIC Sx: fever, rigors, malaise - significant VOIDING Sx (poor intermittent stream, hesitancy, straining, dribbling, incomplete emptying, dysuria etc.) - PAIN on EJACULATION - PELVIC pain In CHRONIC: - Symps for >3 months - Recurrent UTIs

Answer 71

- DRE: - Prostate is **tender** or hot to tough - Hard from calcification (in chronic?) - Urinalysis and MID STREAM culture - shows blood, WBCs, and bacteria - Blood cultures- in patients who are febrile - NAAT - esp for chlamydia - Trans-urethral US scan (TrUSS)

Answer 72

Acute: - IV GENTAMICIN + IV CO-AMOXICLAV or IV TAZOCIN or IV CARBAPENEM (depending on severity/resistence) - CIPROFLOXACIN or levofloxacin for 2-4 weeks afterwards - 2ND LINE = TRIMETHOPRIM - TRUSS guided abscess drainage if necessary Chronic: - 4-6 week course of quinolone e.g. CIPROFLOXACIN (antibiotic) - BUT they don’t tend to respond as well to antibiotics - +/- Alpha-blocker e.g. TAMSULOSIN - NSAIDs e.g. IBUPROFEN

Answer 73

Urinary retention

Answer 74

Uncomplicated: - UTI in healthy non-pregnant woman with normally functioning urinary tract Complicated UTI: - Infection in patients with ABNORMAL urinary TRACT e.g. stones, obstruction or SYSTEMIC DISEASE involving the KIDNEY e.g. diabetes mellitus, sickle-cell, or VIRULENT organism e.g. Staphylococcus Aureus - TREATMENT FAILURE is more likely - COMPLICATIONS are more likely e.g. renal papillary necrosis and renal abscess - Majority of UTI’s in MEN are considered complicated - associated with urological abnormalities such as bladder outlet obstruction

Answer 75

- Surface attachment molecules: - Fimbriae/P PILLI to allow ureteral ascent - Afimbrial attachments e.g. glycocalix - Avoidance of host defences: - Acid polysaccharide coat (CAPSULE) that resists phagocytosis - TOXINS - release cytotoxins - directly toxic - Aerobactin - for Fe acquisition - Haemolysin- for pore formation

Answer 76

* Urothelium * Vaginal epithelium * Vaginal mucus

Answer 77

* Oestrogen depletion due to the loss of lactobacilli and pH change: - Seen post-menopause where the pH rises and there is increased colonisation by colonic flora and a reduction in vaginal mucus secretion - Results in increased susceptibly to UTI * Those with HLA-A3 blood group antigen - tend to have recurrent UTIs

Answer 78

- Gram-negative: Proteus, Klebsiella & Pseudomonas - Gram-positive: Staphylococci & Mycoplasma Increases risk of stone formation

Answer 79

- **Antegrade flushing of urine** - forward flow of urine - Tamm-Horsfall protein - has antimicrobial properties - Low urine pH and high osmolarity - Urinary IgA

Answer 80

A syndrome fitting a clinical picture of **inflammation within the kidney** - typically in subendothelial space. Involves AKI, active dipstick results, hypertension/fluid overload or oliguria. Defined by presence of: - Haematuria- reflects inflammation of the kidney - even if non-visible red cell casts seen on microscopy - Proteinuria- less than 3g/24 hours (>3.5g/24hr = nephrotic range) - RBC casts can be seen on urine microscopy (glomerular bleeding) - Hypertension –due to Fluid overload (from suppression of RAAS -> sodium retention) - can have vision changes/heart issues - Oliguria- due to reduced GFR (not necessarily all at same time)

Answer 81

Can have systemic or renal causes - COMMONEST PRIMARY CAUSE is (Cresentic) IgA nephropathy/Henoch Schonlein purpura (RENAL) - in developed/high income countries Systemic causes: - Infective: - Post strep glomerulonephritis (typically PYOGENES/GROUP A STREP) - Other bacteria e.g. MRSA, typhoid, secondary syphilis - HEP B/C - Schistosomiasis - Malaria - Infective endocarditis - SLE - Systemic SCLEROSIS - Small vessel vasculitis (ANCA associated vasculitis) - Goodpasture's/anti-GBM disease

Answer 82

* Typical case of post-streptococcal glomerulonephritis occurs in a child 1-3 weeks after streptococcal infection (pharyngitis or cellulitis) with a Lancefield group A beta-haemolytic streptococcus e.g. streptococcus pyogenes * Occurs classically **2 weeks after tonsillitis** * Bacterial **antigen deposited** in **glomerulus** leading to **diffuse proliferative glomerulonephritis (inflammation/damage)** -> HAEMATURIA + potential acute nephritis DIAGNOSE via evidence of STREP INFECTION Treat with ANTIBIOTICS + SUPPORTIVE

Answer 83

Presentation (systemic inflammation): - Rash, - arthralgia, - kidney failure, (30-50% have renal disease at presentation) - neurological symptoms, - pericarditis and pneumonitis Most common in AFRICAN, HISPANIC, ASIAN descent - 15-45 Y/O FEMALES (10:1 ratio against males) Serology: * Anti-nuclear antibody (ANA) positive and Double stranded DNA positive * Low complement C3 & C4 Classification: - Class 1: Normal on LM, mesangial immune deposits on IF - Class 2: Mesangial Hypercellularity + immune deposits - Class 3: Focal segmental proliferative lupus nephritis - 4: Diffuse proliferative lupus nephritis - 5: Membranous lupus - 6: Advance sclerosing lupus nephritis Treatment (no specific): - **Immunosuppression; steroids**, cyclophosphamide, rituximab, (mycophenolate)

Answer 84

* ANA positive, Anti-Scl 70 positive * **Severe hypertension** - may lead to strictures * **‘Onion skin’ changes on renal biopsy**, raynauds phenomenon, fibrotic skin, oesophageal dysmotility

Answer 85

ANCA ASSOCIATED VASCULITIS (**Anti-Neutrophil Cytoplasmic Antibodies**). Also associated with PR3/MPO. Attacks small vessels in the kidney and eye (and systemically). May be granulomatous. Oft affects caucasians >50 y/o. Presents with systemic inflam +/- features of other organ system involvement. Complications = haemorrhaging under nails, lungs etc. Diagnosis: - serum ANCA (changes in titre correlate with disease activity) - Biopsy: segmental glomerular necrosis - cresent formation. Degree of active lesions, fibrosis + tubular atrophy - prognostic markers Treatment: - **Immunosuppression**, steroids, cyclophosphamide, rituximab, (give for 2-3 years then remove - immune function may come back after 2-15 years or other, v variable) plasma exchange (to remove antibodies) - Not v useful if already very fibrosed - treatment works best if current high immune activity

Answer 86

- caused by autoantibodies directed against Type IV COLLAGEN (intrinsic to basement membrane of both kidney and lung) -> Rapidly progressive kidney failure (days/weeks) - presents with SOB + OLIGURIA - active dipstick - Haemoptysis * Co-existence of **acute glomerulonephritis** and **pulmonary alveolar haemorrhage** DIAGNOSE: - anti-GBM (glomerular basement membrane) ANTIBODIES (bloods/biopsy) - BIOPSY - IgG staining - immunoflurescence

Answer 87

- Remove antibody via plasma exchange - Immunosuppression - Steroids/cyclophosphamide (give sperm presarvation before giving cytotoxic meds)

Answer 88

- IgA glycosylation abnormality - Kidney attacked by IgA DEPOSITION in MESANGIUM (bit that provides structural support to glomerulus) -> HAEMATURIA Can be nephritic, nephrotic (5%), asymptomatic (60-80% benign) or a progressive chronic kidney disease (20-30%) - commonest cause of glomerulonephritis worldwide - associated with TONSILITIS (synpharingitic haematuria) Diagnose with BIOPSY (may be unecessary if haematuria present - could only be IgA or thin membrane disease) - Diffuse mesangial IgA deposits, subendothelial and sub epithelial deposits on EM is not uncommon - also do kidney US + urine dipstick to check

Answer 89

- BP control - ACE inhibitors/angiotensin receptor blockers e.g. RAMIPRIL/CADESARTAN - SGLT2 inhibs can also help - Steroids/fish oil if persistent after 3-6 months - Immunosuppression if aggressive e.g. CYCLOPHOSPHAMIDE (no specific treatment)

Answer 90

- Haematuria (mild macrocytic) - Proteinuria - usually less than 2g in 24 hours - Hypertension (moderate-severe increase) and Oedema (periorbital, leg or sacral) caused by salt and water retention - Increased JVP + may have crepitations in lungs from pulmonary oedema - Bleeding into lungs/joints can also present as nose bleeds, coughing, painful joints etc. - Oliguria (little urine) - Uraemia and symptoms of it: * Anorexia * Pruritus * Lethargy and nausea Deteriorating kidney function - Moderate-severe decrease in GFR

Answer 91

- Take history to determine cause - Measure **eGFR, proteinuria, serum urea & electrolytes and albumin** - to determine current status and monitor progress - **Culture** - swab from throat or infected skin - **Urine dipstick** to detect proteinuria and haematuria - Renal biopsy if necessary

Answer 92

Depends on the cause - outlined previously - Autoimmune causes treated with immunosuppression or plasma exchange - Infective causes treated with Antibiotics or antivirals **Blood pressure control** to reduce proteinuria and preserve renal function (and reduce fluid retention) - ACE-I/ARB - SALT RESTRICTION - LOOP DIURETICS (e.g. ORAL FUROSEMIDE) - CCB e.g. AMLODIPINE **Corticosteroids**- this is to reduce the inflammation causing damage to the kidney

Answer 93

It's a broad term that refers to a group of parenchymal kidney diseases that all result in the inflammation of the glomeruli and nephrons - common cause of end stage renal failure (ESRF) - 25%

Answer 94

- Damage to the filtration mechanism resulting in HAEMATURIA and PROTEINURIA - RBC CASTS on URINE MICROSCOPY = characteristic - Damage to the glomerulus restricts blood flow -> compensatory HYPERTENSION - Loss of the usual filtration capacity -> ACUTE KIDNEY INJURY

Answer 95

- Acute Nephritic Syndrome (Acute glomerulonephritis) - Nephrotic syndrome - Asymptomatic urinary abnormalities - haematuria, proteinuria or both - Chronic kidney disease (CKD) - can present as stage 3/4

Answer 96

- IgA nephropathy - Goodpasture's disease - Post-streptococcal glomerulonephritis - Henoch Schoenlein purpura (small vessel vasculitis)

Answer 97

- A **small vessel vasculitis** that affects the kidney and joints due to **IgA deposition** - Presents with a purpuric rash on legs, nephritic symptoms, and joint pain due to IgA deposition

Answer 98

Via presence of clinical signs (rash, nephritic symptoms, joint pain) Confirmed with RENAL BIOPSY (IgA deposition)

Answer 99

CORTICOSTEROIDS and ACE-I/ARBs

Answer 100

A syndrome where there is a **structural/functional issue with the filtration barrier**, esp the **podocytes**, which results in **leaking of protein** into the urine. This results in the triad characterising nephrotic syndrome: - **Proteinuria >3g/24 hours** - **Hypoalbuminaemia (<25g/L)** - due to loss of albumin in urine - **Oedema** - loss of oncotic pressure. This can be rapid and severe ALL THREE NEED TO BE PRESENT to be defined as Nephrotic syndrome/ Severe **hyperlipidaemia/hypercholesterolaemia** often present: - Liver goes into overdrive due to albumin loss and other protein loss which increases risk of blood clots and produces raised cholesterol Leaking huge amount of protein but kidney function remains same so no kidney failure - 25% have NO VISIBLE CHANGES on BIOPSY Pretty rare

Answer 101

DIABETES MELLITUS (most common 2ndry cause)

Answer 102

Primary causes (due to primary renal disease - affects podocytes): - MINIMAL CHANGE DISEASE - commonest cause in children (but also seen in adults) - MEMBRANOUS NEPHROPATHY (adults) - FOCAL SEGMENTAL GLOMERULOSCLEROSIS (esp black adults) Secondary causes (anything systemic that causes kidney damage/post-glomerular scarring): * Diabetes mellitus (MOST COMMON SECONDARY CAUSE) * Amyloidosis * Infections e.g. Hep B or C and HIV * SLE, Rheumatoid Arthritis (autoimmune) * Drugs e.g. gold, penicillamine, NSAIDs and ACE-inhibitors * Malignancy

Answer 103

- PODOCYTE INJURY -> probs main cause of proteinuria - Podocytes wrap around the glomerular capillaries and maintain the filtration barrier - preventing large molecular weight proteins from entering the urine - Damage to podocyte foot processes or loss of podocytes can cause heavy protein loss

Answer 104

- Pitting oedema of ankles, genital, abdominal wall and sometimes face (periorbital) - can get pulm odeoma - Frothy urine (proteinuria) On investigation: - Normal-mild increase in BP - Proteinuria > 3.5g/day - Normal-mild decrease in GFR - Hypoalbuniaemia

Answer 105

- Urinalysis/dip stick - Urine Protein: creatinine ratio- to quantify the degree of proteinuria (high) - Blood tests - renal function (normal/mildly impaired), - SERUM ALBUMIN = LOW - serum creatinine - eGFR (normal/slightly low) - Glucose levels - elevated lipids - **Renal biopsy**- gives cause - typically lower lobe, 3 samples, imaging guided BP normal/slightly raised CXR or ultrasound for pleural effusion or ascites Serum + urine electrophoresis - amyloid, myeloma ANA, double-stranded DNA antibody, complement C3 and C4 indicates SLE Antiphospholipase A2 receptor antibody indicates membranous nephropathy HepB surface antigen, HepC antibody or HIV (can cause cryoglobinaemia - proetins clump at low temps)

Answer 106

Supportive then specific - Reduce oedema: * Fluid and salt restriction while giving diuretics * Loop diuretics e.g. IV FUROSEMIDE - IV - gut oedema may prevent oral absorption (* Thiazide diuretics e.g. IV BENDROFLUMETHIAZIDE) - Reduce proteinuria: * ACE inhibitor e.g. RAMIPRIL * or Angiotensin receptor blocker e.g. CANDESARTAN (* Normal NOT high protein diet) - Reduce risk of complications: * Prophylactic anticoagulation with WARFARIN, especially when albumin is low (<20g/l) e.g. membranous, amyloid * Reduce cholesterol with statins e.g. SIMVASTATIN * Treat infections promptly + vaccinate where necessary - prophylactic antibiotics in children - Treat underlying cause

Answer 107

- HYPERLIPIDAEMIA - Low albumin = Low oncotic pressure -> HEPATIC LIPOPROTEIN SYNTHESIS = INCREASED COLESTEROL + TRIGLYCERIDES - give STATINS - THROMBOEMBOLISM - Loss of albumin puts liver into overdrive -> INCREASED CLOTTING FACTORS -> HYPERCOAGUABLE STATE - E.g. DVT, PE, renal vein thrombosis - HEPARIN PROPHYLAXIS - RISK OF INFFECTION - Loss of Ig in urine + immunosuppressive treatment -> low serum IgG, decreased complement activity + reduced T cell function - e.g. Cellulitis, Strep, Spontaneous bacterial peritonitis etc.

Answer 108

- Presents with asymptomatic proteinuria/**nephrotic syndrome** +/- microscopic haematuria, hypertension and renal impairment Deposition of IgG and C3 along outer aspect of glomerular basement membrane (subepithelial) -> Thickening of glomerular capillary wall -> LEAKY GLOMERULUS (IMMUNE MEDIATED) Can be: - Idiopathic: PLA2R antigen (in podocyte membrane) attacked - anti-PLA2R antibody - Secondary * Drugs e.g. penicillamine, gold or NSAIDs * Autoimmune - SLE, thyroiditis * Infection e.g. hepatitis B or C, schistomiasis * Neoplasia e.g. lung, colon, stomach and breast

Answer 109

RENAL BIOPSY - thickened basement membrane SERUM **Anti phospholipase A2 receptor antibody (Anti-PLA2R Ab)** (70-80%) Both are diagnostic

Answer 110

30% spontaneous remission - ACE-I/ARB - If high risk of progression, give additional immunosuppression - PREDNISOLONE + CYCLOPHOSPHAMIDE

Answer 111

Commonest primary cause of nephrotic syndrome found on biopsy: - Oft IDIOPATHIC - Secondary to: HIV, Lithium, Heroin - Causes scarring that is focal + only some glomeruli involved - segmental (only part of glomerulus affected) - CD80 molecules in podocytes -> INCREASED PERMEABILITY in glomeruli -> PROTEIN/HAEMATURIA -> SECONDARY HTN + RENAL IMPAIRMENT

Answer 112

RENAL BIOPSY - scarring of glomerui (FOCAL SCLEROSIS)

Answer 113

- ACE-I/ARB - for BP control - CORTICOSTROIDS esp if idiopathic - potentially other immunosuppression e.g. cyclophosphamide or ciclosporin

Answer 114

- A primary cause of nephrotic syndrome (commonest cause in children) - esp in BOYS OVER 5 y/o - 20% of nephrotic syndrome in adults

Answer 115

- Idiopathic - Atopy (predisposition to immune response) present in 30% of cases -> allergic reactions can trigger nephrotic syndrome - Drugs: * NSAIDs * Lithium * Antibiotics e.g. cephalosporins, rifampicin and ampicillin * Bisphosphonates * Sulfasalazine - Hep C, HIV and TB are rare causes - associated with Hodgkin's lymphoma

Answer 116

- Disrupted podocyte ACTIN CYTOSKELETON -> FUSION of FOOT PROCESSES - seen only on electron microscopy Appear to be caused by IMMATURE DIFFERENTIATING CD35 STEM CELLS

Answer 117

- Proteinuria - Oedema, predominantly around the face - Fatigue - Frothy urine i.e. same as Nephrotic syndrome as minimal change disease causes nephrotic syndrome

Answer 118

RENAL BIOPSY: * Normal under light microscopy * Electron microscopy shows FUSED PODOCYTE FOOT PROCESSES

Answer 119

- High dose corticosteroids e.g. PREDNISOLONE - can reverse proteinuria in 95% - majority relapse - Frequent relapse/steroid-dependent disease treated with: CYCLOPHOSPHAMIDE or CICLOSPORIN/TACROLIMUS

Answer 120

* Incidental finding of dipstick haematuria +/- proteinuria * Kidney function and blood pressure are NORMAL * Diagnosis is usually clinical, don’t biopsy unless kidney function abnormal or significant proteinuria

Answer 121

- IgA nephropathy - Thin membrane disease (membrane thin - more likely to leak into urine)

Answer 122

Also known as Hypernephroma and Grawitz tumour 90% arise from PROXIMAL CONVOLUTED TUBULAR EPITHELIUM

Answer 123

- MOST COMMON renal tumour = PROXIMAL CONVOLUTED TUBULE - Accounts for 2-3% of all malignancies - 7th most common in uk - 34% preventable - More common in **MALES** than females - Usually present **after 50 y/o** - Rare before 40 yrs - Average age at presentation is **55 yrs** (- Highest incidence is in the **Czech republic**) - Rates increasing

Answer 124

- **Smoking** - Obesity - **Hypertension** - Renal failure & **haemodialysis** (15% develop RCC) - Polycystic kidneys - Genetic: - Von Hippel Lindau (VHL) syndrome - Tuberous sclerosis - Hereditary Papillary RCC

Answer 125

- AUTOSOMAL DOMINANT mutation of chromosome 3 on short arm * **Loss of both copies of tumour suppressor gene** * 50% develop RCC (renal cell cancer) that is often bilateral and multifocal * Renal and pancreatic cysts as well as cerebellar malignancy also arise

Answer 126

- Malignant cancer of the proximal convoluted tubular epithelium (usually) - Spread may be direct (renal vein), via lymph or haematogenous (bone, liver, lung) - **25% have metastases at presentation**

Answer 127

Oft asymp - discovered incidentally on scan (>50%) Characteristic triad (<10%): - HAEMATURIA, FLANK/LOIN PAIN, PALPABLE ABDO MASS Systemic: - Anorexia, malaise, unexplained weight loss RARE: - invasion of LEFT RENAL VEIN -> compression of LEFT Testicular vein -> VARIOCELE Paraneoplastic syndrome: - Polycythaemia in 5% - Hypertension in 30% - due to renin secretion by tumour - Anaemia due to depression of erythropoietin

Answer 128

- **Transitional cell carcinoma**, - Wilms’ tumour (young kids - to do with embryogenesis leftovers), - renal oncocytoma (benign), - leiomyosarcoma (smooth muscles)

Answer 129

- Bloods: * FBC - possible polycythaemia and anaemia due to EPO increase/decrease (* ESR may be raised) (* Liver biochemistry may be abnormal) - BP may be high from increased renin - Ultrasound: * To distinguish simple cyst from complex cyst or tumour - **CT chest and abdomen with contrast**: * More sensitive than ultrasound in detecting renal mass + will show involvement of renal vein or inferior vena cava, if present * contrast shows kidney function since in normal kidney should see it being taken up and excreted well * Tumour staging (can stage with CT chest. abdo, pelvis etc) - MRI if extending into vein - can also see mets in brain/bone - CXR shows Cannonball mets in lungs if present - renal biopsy - if unsure on scan or prior to ABLATION/SYSTEMIC therapy - NOT if it is a cystic mass - risk of seeding - IF signs of bone issue OR hypercalcaemia -> Bone scan

Answer 130

- Survaillance - slow growing, esp in older - Localised = SURGERY * Radical Nephrectomy (open, laproscopic, robotic) unless tumours bilateral * If bilateral involvement then _partial_ nephrectomy - If patients can't tolerate surgery = ABLATIVE TECHNIQUES - only works if <4cm or to stop bleeding in palliative - e.g. CRYOABLATION or RADIO THERAPY - can harm kidney function - Metastatic/locally advanced: * **Interleukin-2 + Interferon alpha** - produce remission in 20% * Biological angio-genesis targeted therapy: - SUNITINIB, BEVACIZUMAB and SORAFENIB * TEMSIROLIMUS (mTOR inhibitor) - found to improve survival more than interferon * Last 2 options given if patients do not respond to 1st - Palliative - embolisation esp if bleeding

Answer 131

Predicts survival + determines treatment option - Stage I: partial or radical nephrectomy - Stage II: radical nephrectomy - Stage III: radical nephrectomy and adrenalectomy - Stage IV: systemic treatment

Answer 132

* Childhood tumour of the primitive renal tubules and mesenchymal cells * Seen within the first 3 years of life - main abdo malignancy in children * Presents as an abdominal mass and less commonly with haematuria * Diagnosis established by ultrasound, CT and MRI * Treated with a combination of nephrectomy, radiotherapy and chemotherapy

Answer 133

* 90% are urothelial/transitional cell carcinoma (TCC) - responsible for 3% of deaths from malignancy * The calyces, renal pelvis, ureter, bladder and urethra are ALL lined by transitional epithelium and are all susceptible to transitional cell carcinoma - BLADDER tumour most COMMON TCC Can also get squamous cell carcinoma from Schistosomiasis

Answer 134

- **Smoking (2-4x)** - Occupational exposure to carcinogens: * Beta-napthylamine, benzidine, azo dyes, aromatic hydrocarbons * Workers in petroleum, chemical, cable and rubber industries are particularly at risk (including hairdressers) - Exposure to drugs e.g. phenacetin and **cyclophosphamide** - Pelvic radiation - Chronic inflammation of urinary tract e.g. schistomiasis (usually associated with squamous carcinoma), indwelling catheter or stone - > 55 yrs (peaks in 80s) - 49% preventable - Male - Family history

Answer 135

- Tumour spread: * Local → to pelvic structures * Lymphatic → to iliac and para-aortic nodes * Haematogenous → to liver and lungs

Answer 136

- Painless visible haematuria - MOST COMMON SYMPTOM, however, pain may result due to clot retention - Any patient over 40 presenting with haematuria - assume urothelial tumour until proven otherwise! - Recurrent UTI’s (esp post-menopausal women, esp >60 y/o) - Voiding irritabiliity/UTI symptoms without bacteriuria - LUTS

Answer 137

- Urinalysis- sterile pyuria - CYSTOSCOPY + BIOPSY - diagnostic - CT urogram (contrast) - allows staging + can be diagnostic - urinary tumour markers (e.g. bladder tumour antigen -> detects complement factor H-related protein - elevated) - MRI/lymphangiography (may show pelvic node involvement) - CT/MRI of pelvis if pelvic metastasis suspected

Answer 138

- Haemorrhagic cystitis, - renal cancer, - UTI, - urethral trauma (cause main symp is haematuria)

Answer 139

Depends on staging - Non-muscle invasive bladder cancer (T1) - less dangerous: * Surgical resection (transurethral - or local diathermy) - also diagnostic * +/- Chemotherapy: - **MITOMYCIN** (cytotoxic antibiotic - reduces recurrance), DOXORUBICIN and CISPLATIN to reduce recurrence - Localised muscle invasive disease (T2-3): * Radical cystectomy (oft cystoprostectomy in males, anterior extenoration in females) - GOLD STANDARD - high morbidity, need stoma afterwards (ileal conduit diversion for urostomy or orthotopic neobladder - also from bowel): - Post-op chemotherapy = M-VAC: - METHOTREXATE, VINBLASTINE, ADRIAMYCIN and CISPLATIN * Radical radiotherapy - if not fit for surgery * Chemotherapy = CMV: - CISPLATIN, METHOTREXATE, VINBLASTINE - Metastatic bladder cancer (T4): * Palliative chemotherapy and radiotherapy

Answer 140

- Most common cancer in males aged 15-44 yrs - 10% occur in undescended testes - More than 96% arise from **germ cells**: * Seminomas - 25-40 yrs and 60 yrs * Teratomas - infancy - 4% arise from non-germ cells: * Leydig cell tumours * Sertoli cell tumours * Sarcomas

Answer 141

- Undescended testis - cryptorchidism (undescended because it is abnormal) - Infant hernia - Infertility - Family history - HIV - 12x risk if already have cancer in one testicle - Caucasian males

Answer 142

- PAINLESS LUMP (common) - Testicular pain and/or abdominal pain - Hydrocele - Cough and dyspnoea - indicative of **lung metastases** - Back pain - indicative of **para-aortic lymph node metastasis** - Abdominal mass

Answer 143

- Testicular torsion, (presents with ACUTE PAIN) - lymphoma, - hydrocele, (can be non-cacner related - oft reactive to infection/tumour) - Varicocele - epididymal cyst - Trauma

Answer 144

- Examination: - Lymphnodes - supraclavicular + groin - scars from previous orchidopexy (bringing down undescended testes) - chast/abdo examination (checking metastasis) + examine testes - **Ultrasound** (urgent, oft same day): * differentiate between masses body of testes and other intrascrotal swellings - Biopsy and histology - risk of seeding - Serum tumour markers: * Alpha-fetoprotein (AFP) and/or Beta subunit of human chorionic gonadotrophin (B-hCG): - Raised AFP & B-hCG in teratomas - B-hCG in minority of those with seminomas - AFP is not elevated in those with pure seminomas - LDH may be high - CXR - resp symptoms - CT - staging

Answer 145

- RADICAL ORCHIDECTOMY via inguinal approach - (risk of seeding tumour if done via scrotum) - Oft do chemo/radio (esp in peritoneal lymph node mets) therapy as neoadjuvant therapy - chemosensitive patients - **Seminomas with metastases below diaphragm** - *only treated with radiotherapy* - More widespread tumours treated with chemo - Also do radical orchidectomy to control metastatic disease - Teratomas treated with chemo - Sperm storage offered

Answer 146

Any scrotal lumps that are not cancer - A testicular lump is CANCER until proven otherwise

Answer 147

Can you get above it? Is it separate from the testis? Cystic or solid? * Cannot get above - Inguinoscrotal hernia or proximally extending hydrocele * Separate & cystic - Epididymal cyst * Separate & solid - Epididymitis or Varicocele * Testicular and cystic - Hydrocele * Testicular & solid - **Tumour**, haematocele

Answer 148

Smooth, extratesticular, spherical cyst in the head of the epididymis

Answer 149

- Usually develop around the age of 40 - Not uncommon - Rare in children

Answer 150

- Contain clear fluid (if milky = spermatocele) - Lie above and behind the testis

Answer 151

- Normally present having noticed a lump - Often are multiple, may be bilateral - Small cysts may remain undetected and asymptomatic - Once large, may be painful - Well defined and will transluminate since fluid-filled - Testis is palpable separately from cyst (unlike hydrocele where testis is palpable within fluid filled swelling)

Answer 152

- Spermatocele: * Fluid and sperm filled cyst in the epididymis * No way clinically to differentiate between epididymal cyst vs spermatocele * Can be differentiated as sperm are present in the milky fluid aspirate of a spermatocele - Hydrocele - collections of fluid surrounding entire testicle - Varicocele - dilated veins that increase with increases in abdominal pressure

Answer 153

- transillumination to eliminate hydrocele - scrotal US

Answer 154

- Usually not necessary - If painful and symptomatic then surgical excision

Answer 155

Abnormal collection of fluid within the TUNICA VAGINALIS

Answer 156

- Clinically apparent scrotal hydroceles are evident in 6% of term males beyond the newborn period - Most paediatric hydroceles are congenital

Answer 157

- Primary hydrocele: * More common and larger * Usually in younger men * Associated with a patent processus vaginalis - typically resolves during 1st year of life - Secondary hydrocele: * Rarer and present in older boys and men * Secondary to: - Testis tumour - Trauma - Infection - TB - Testicular torsion - Generalised oedema

Answer 158

- Overproduction of fluid in tunica vaginalis (simple hydrocele) - Processus vaginalis fails to close -> peritoneal fluid communicates freely with the scrotal portion (communicating hydrocele)

Answer 159

- SCROTAL ENLARGEMENT: NON-TENDER, SMOOTH, CYSTIC - pain only present if INFECTED - Testis are usually palpable but may be difficult to palpate in large hydrocele - Lies anterior to + below testis + will TRANSLUMINATE

Answer 160

Main - TESTICULAR TORSION + strangulated hernia

Answer 161

- Ultrasound - Serum alpha-fetoprotein and human chorionic gonadotrophin to help exclude malignancy

Answer 162

- Oft resolve spontaneously - congenital oft by 2 y/o - Therapeutic aspiration or surgical removal

Answer 163

Abnormal dilation of the testicular veins in the pampiniform venomous plexus, caused by venous reflux

Answer 164

- Left side MORE COMMONLY AFFECTED (due to connection with renal vein being more prone to blockage/reflux) - Unusual in boys under 10 yrs - Incidence increases after puberty - Associated with sub fertility

Answer 165

- More common on the left - Angle at which the left testicular vein enters the left renal vein - Increased reflux from compression of renal vein - Lack of effective valves between the testicular and renal veins Oft related to renal cancers, stones etc.

Answer 166

- Often visible as distended scrotoal blood vessels that feel like ‘a bag of worms’ (hold scrotum steady with other hand to palpate properly) - Patient may complain of a dull ache or scrotal heaviness - Scrotum hangs lower on the side of the varicocele

Answer 167

Secondary to other pathological processes blocking the testicular vein e.g. kidney tumours and other retroperitoneal tumours

Answer 168

- Venography - Colour doppler ultrasound (see blood flow)

Answer 169

Surgery IF there is PAIN, INFERTILITY or TESTICULAR ATROPHY

Answer 170

Twisting of spermatic cord resulting in OCCLUSION of testicular blood vessels -> can rapidly lead to ISCHAEMIA/INFARCT + loss of testes (germ cells most susceptible cell line to ischaemia) need to try to recognise before cardinal symptoms fully manifest - prompt surgery saves testes

Answer 171

**<6HRS** - salvage rate 90-100% if >24hrs salvage 0-10%

Answer 172

- Common UROLOGICAL EMERGENCY among adolescent boys and young men - Typically in neonates or post-pubertal boys but can occur in all ages - **most common at 11-30yrs** - LEFT SIDE more commonly affected

Answer 173

BELL CLAPPER DEFORMITY (congenital) - testes not fixed completely to scrotum -> free movement + twisting A genetic risk factor

Answer 174

Any boy presenting with abdo pain - testes should be checked - SUDDEN onset of ACUTE, SEVERE PAIN in ONE testis (unilateral) - makes walking uncomfortable - Prehn's sign negative (not releived by lifting testis) - Pain often comes on during sport or physical activity - Pain in abdomen, nausea and vomiting are common - Inflammation of one testis - it is **very tender, hot and swollen** - Testis may lie **high and transversely**(more horizontal)/slightly retracted With intermittent torsion the pain may have passed on presentation - but if it was severe and the lie is horizontal then prophylactic fixing may be wise

Answer 175

- EPIDIDYMO-ORCHITIS (main) - usually in older patients + may have UTI symps + more gradual onset of pain - Tumour, trauma or acute hydrocele - Torsion of testicular/epididymal appendage (remnant of Mullerian duct): * Usually in boys 7-12yrs - less painful * Small blue nodule under scrotum * Caused by surge in gonadotrophins that signal the onset of puberty - Idiopathic scrotal oedema (usually 2-10 y/o) - benign - differentiate by ABSENCE of pain + tenderness

Answer 176

- Doppler ultrasound may demonstrate lack of blood flow to testis - Urinalysis to exclude infection and epididymis - DO NOT DELAY SURGICAL EXPLORATION

Answer 177

- SURGERY - expose + untwist (6HR WINDOW) - Orchidectomy (removal) if needs be - Bilateral fixation

Answer 178

The persistent inability to attain and maintain an erection sufficient to permit satisfactory sexual performance (goes on a while)

Answer 179

10% men 40-70 y/o - increasing prevelance with age

Answer 180

Neurogenic - failure to initiate Arteriogenic - failure to fill Venogenic - failure to store (oft multifactorial)

Answer 181

Age DIabetes Hypertension Hyperlipidaemia Hypogonadism (endocrine) Trauma (including iatrogenic) Drugs (anti-androgenic: finasteride, b-blockers, anti-depressants, statins etc.) Psychosomatic Neurological (MS, corda equina, parkinson's etc) Inflammation (prostatitis) Mechanical: Peyronie's disease (painful scarring around tunica albigenae) RFx: Smoking, Alcohol + illicit drugs, obesity, depression, CVD etc.

Answer 182

Patient centred approach: Identify undelying modifiable co-morbidities History (time/duration of onset, medication, stress, age, situational, trigering events, RFx) - do they have early morning erections - if yes means all physiology is working - a psychological issue - may be situational e.g. performance anxiety with new partner - check effect on mental health - check nature of dysfunction (aforementioned categories) Examination: - Height, weight, BMI - Thyroid, Pulmon, Cardiac - Abdo exam (hepatosplenomegaly) - Peno-scrotal exam (peyronie's, hypogonadism) - Rectal exam (tumour could press on pelvic plexus) Tests: - International index of ED - Urinalysis - Fasting glucose (diabetes) - Lipid profile - Morning testosterone (if low then prolactin, FSH, LH as well) Suspect arterial cause - Doppler ultrasonography (check if penile artery stenoised) Rigiscan - measures frequency, ridgidity + dureation of erections (at home, at night etc.)

Answer 183

Underlying cause - Psychosexual counselling (if needed) Viagra (1st line) - PDE-5 inhib (improves SM relaxation) - CONTRAINDICATED if recent MI/stroke - take only 30min before intercourse Hypogonadism - testosterone replacement (edno referral) If nowt works: - Intraurethral suppository (localised, improves vasc flow - ALprostadil) - Intracavernosal injection - Vaccuum assisted device (increases flow, prevents outflow - bruising, may only work short time) - Last line: Implant into corpus cavernosus (can fill with water - infection, eroding out through skin) - oft used for spinal injuries

Answer 184

50% E coli Remember KEEPS Klebsiella E coli Enterococci Proteus Staph Saprophyticus Staph aureus and Pseudomonas Aeruginosa can also cause UTIs but rarer

Answer 185

- Pregnancy - Sex - Catheterisation (Catheters can induce biofilm formations) - Structural abnormalities of urinary tracts - Previous UTI - Stones (can become site of infection) Associated with Diabetes

Answer 186

- Urine dipstick – leukocytes/ nitrates present, blood - Microscopy o Leukocytes (>10^4 wbc/ml) o RBC o Casts (indicates Upper tract infection) o Bacteria o Epithelial cells – if present indicate contamination - Urine culture - Antibiotic sensitivity test

Answer 187

Asymptomatic Bacteriuria: - Do Not Treat in >65s Uncomplicated Infection: - 3 days antibiotics: nitrofurantoin (first line in sheffield due to increased resistance to trimethoprim), trimethoprim - Alter if antibiotic resistance is identified Complicated infection: - 7 day antibiotics course: nitrofurantoin, trimethoprim - Alter if antibiotic resistance is identified UTIs in pregnancy - Asymptomatic bacteriuria Is treated - Avoid Nitrofurantoin - poor renal function (Creatinine clearance: <45ml/min)

Answer 188

840 - 2520ml (normal 24hr urine volume range is 800-2000 mL - with normal fluid intake of ~2L) - Target urine output for adult is 0.5-1.5 mL/kg/hour

Answer 189

INTERSTITIAL NSAIDs cause a decrease in prostaglandins, which results in unopposed constriction of the afferent arterioles

Answer 190

Cyst formation throught renal parenchyma -> bilateral enlargement + swelling

Answer 191

Familial inherited PKD mutation - Autosomal dominant (main) - PKD 1 (85%) - PKD 2 (15%) - more MALES - typically presents 20-30 Y/O - Autosomal recessive (less common) - infancy/pre-birth - High mortality - many congenital abnormalities (e.g Potter's sequence - flattened nose + clubbed feet)

Answer 192

PKD 1 + 2 code for polycystin 1 (regulates tubuler/vasc development) + 2 respectively (Ca2+ CHANNELS) In the nephron there are cilia present with polycystin channels on them. When filtrate passes, the cilia move and the polycystin channels OPEN. This causes a Ca2+ INFLUX into the cilia which allows signelling + INHIBITS EXCESSIVE GROWTH of cilia PKD mutation impairs polycystin function -> reduced Ca2+ influx -> disorientated cell division/EXCESSIVE CILIA GROWTH -> loss of planar polarity -> cyst initiation -> fluid secreted by epithelial cells -> cyst Mechanical compression + apoptosis of healthy tissie + reactive fibrosis -> progressive loss of renal function (so rapidly growing cysts = faster renal function decline)

Answer 193

PKD 2 typically has milder symptoms but the symptoms also have more delayed onset than in PKD 1 -> delayed diagnosis PKD 1 - larger kidneys

Answer 194

PKHD1 mutation (long arm - chromosome 6) Fetus/infant has fluid filled kidney cysts (+/- congenital hepatic fibrosis) -> kidneys too enlarged -> poor/failing kidney function (but variable Px) - with this presentation should also consider Multicystic dysplasia, Hydronephrosis and renal vein thrombosis (things thant cause fluid collection) Potter's sequence is to do with lack of amniotic fluid linked to poor kidney function (kidneys circulate amniotic fluid) -> compression of baby -> deformities

Answer 195

Asymp for many years - oft present >= 20 Y/O - BILATERAL FLANK/BACK or ABDO PAIN (as kidneys enlarge) - +/- HTN and HAEMATURIA (from haemorrhage into cyst, infection or stone) -> renal colic from clots - Excessive water/salt loss -> dehydration hence increased risk of renal stones esp URIC ACID stones -> progressive renal failure Complications: - May get EXTRARENAL CYSTS - esp in CIRCLE OF WILLIS (berry aneurysm - rupture -> SUB ARACHNOID HAEMORRHAGE) - 70% -> polycystic liver disease - Ovarian cysts - Pancreatitis; Diverticular disease - Mitral valve prolapse (and LVH) - possibly from HTN

Answer 196

- History - FHx of ADPKD, ESRF, HTN - genetic testing (but big gene + many mutations) - may have HTN - Kidney US - bilateral enlarged w/ multiple cysts - DIAGNOSTIC for at risk ppl if: - 15-39yrs ≥ 3 cysts (uni/bilateral) - 40-59yrs ≥ 2 cysts (each kidney) - > 60yrs ≥ 4 cysts (each kidney) - EXCLUDE ADPKD if: ≥ 40yrs < 2 cysts - CANNOT EXCLUDE via US if <30 YRS - ARPKD - ante/neonatal US - CT/MRI for liver disease

Answer 197

Non-curative Manage Sx: - ACE-I for HTN - Analgesia for stones - Laproscopic cyst removal/nephrectomy (to reduce pain) - RRT or transplant for endstage renal failure Children and siblings of patients with the disease should be offered screening by renal ultrasound in their 20s + counselling/support for affected

Answer 198

- Acquired and simple cysts of the kidneys - Autosomal recessive PKD - Medullary sponge kidney - Tuberous sclerosis

Answer 199

Dysfunction of the renal proximal tubule resulting in urinary loss of substances normally reabsorbed by the kidney e.g.. bicarb, glucose, amino acids, phosphate, small proteins, uric acid. This often results in salt wasting, potassium wasting and VOLUME DEPLETION (secondary effects)

Answer 200

Dysfunction of the renal proximal tubule resulting in urinary loss of substances normally reabsorbed by the kidney e.g.. bicarb, glucose, amino acids, phosphate, small proteins, uric acid. This often results in salt wasting, potassium wasting and VOLUME DEPLETION (secondary effects)

Brainscape's Knowledge GenomeTM

Phase 2 - Renal & GU Flashcards

Brainscape's Knowledge Genome^TM