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Take 2: Electric Boogaloo > Phase 2 - Renal + GU > Flashcards

Phase 2 - Renal + GU Flashcards

1
Q

What is Nephro/Urolithiasis

A

A solid crystellisation of minerals found in the urine - can be:- KIDNEY (from renal pelvis) stones- URETRIC stonesCan get stuck within kidney, ureter, bladder or urethra.10-15% lifetime risk. More common in MALES 30-50 y/o.

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2
Q

Pathophys of Nephrolithiasis + types of stones

A

Solute conc exceed saturation (esp in collecting duct?)-> SUPERSATURATED URINE * FAVOURS CRYSTALISATION (oft triggered by something)Can cause OUTFLOW OBSTRUCTION (within renal parencyma or collecting system -> urinary tract) -> HYDRONEPHROSIS (complication)Formed by deposit of:- CALCIUM OXALATE (radiopaque - 80-90%)- URIC ACID/urate (RADIOLUCENT - much less common - 10%)- CALCIUM PHOSPHATE- STRUVITE (phosphate - 5-10% linked to INFECTIONS esp PROTEUS)- Cystine (derivative of cysteine - uncommon)

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3
Q

What occurs in Hydronephrosis

A

DILATION + OBSTRUCTION of RENAL PELVIS - INCREASED DAMAGE + INFECTION risk(esp as obs causes prostaglandin release which can increase glomerular filtration)

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4
Q

Management of Hydronephrosis

A

Requires SURGICAL DECOMPRESSION ASAP

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5
Q

Where are renal/uretric stones most likely to be found

A
  • Uretropelvic/Pelviuretric junction (RENAL PELVIS MEETS URETER)- PELVIC BRIM- VESICOURETRAL junction (URETER MEETS BLADDER)
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6
Q

Risk factors/causes for renal stones

A
  • ANATOMICAL: - Congenital horseshoe kidney - spina bifida - Obstruction to urinary tract - TRAUMA- CHEMICAL COMPOSITION of urine that favours stone crystalisation - High calcium, urate, oxalate, struvite or cysteine - CHRONIC DEHYDRATION (esp for uric acid stones)- PRIMARY KIDNEY DISEASES (e.g. PKD/renal tubular acidosis)- UTIs (many hydrolyse urea -> ammonium hydroxide) - can form large mixed stones of Magnesium, Ammonium phosphate + Calcium - increased ammonium + alkalinity favour stone formation- DRUGS e.g. diuretics, antacids, acetazolamide, corticosteroids, aspirin, allopurinol, vitamin C/D- Hx/Family Hx of renal stones- Obesity (lowers pH)More specific, focus on above if struggling- Uric acid stone RFx - GOUT (for uric acid stones) or HYPERURICAEMIA - Ileostomy patients -> dehydration + bicarb loss via GI secretion -> acidic urine (uric acid LESS soluble in acid -> stones)- HIGH SALT/OXALATE intake (chocolate, tea, rhubarb) -> HYPEROXALURIA - Low Ca2+ intake can -> decreased binding of oxalate to Ca2+ -> increased oxalate absorption urinary excertion - GI disease e.g. Crohn’s -> increased oxalate GI resorption- HYPERPARATHYROID (hypercalcaemia +/- hypercalciuria)- Cystinuria - autosomal recessive - affects cystein in renal tubule/GI epithelial cells -> excessive urinary excretion/formation of cysteine stonesSlightly more common in MALES; 20-40 y/o (uncommon in children)
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7
Q

Symptoms of renal stones

A

Can be asymp- ACUTE LOIN TO GROIN (/ipsilateral testis/labia) PAIN (Renal colic) - Rapid onset (can be woken from sleep) - COLICKY (in WAVES from ureteric peristalsis) * FLUID/DIURETICS make pain WORSE - CAN’T LIE STILL (diff from peritonitis/biliary) - N + V- Haematuria + dysuria (may get pyuria or other UTI symps)- Recurrent UTIs - esp if voiding impaired- RED FLAG - FEVER (superimposed infection e.g. pyelonephritis)Bowel sounds may be reduced; BP may be low

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8
Q

Diagnosis of renal stones + Diff diagnoses

A

If over 50, assume vascular accident (e.g. AAA) until otherwise proven- PAIN HISTORY- URINALYSIS/dipstick - haematuria, pregnancy (esp ECTOPIC), ovarian cyst (might have torsion) etc. + check for RBCs, protein/glucose - Midstream urine MC+S - for UTI- BLOODS: - FBC - U+E - if DERANGED - suggests HYDRONEPHROSIS - creatinine - Calcium and Uric acid- 1st LINE: Kidney, Ureter, Bladder (KUB) XR - (80% specific, cheap, easy)- GOLD: NON-CONTRAST CT KUB - DIAGNOSTIC - (rapid; no functional info + each scan -> ~18mth background radiation)US rarely used acutely (poor visualisation) - helpful in pregnant/younger RECURRENT patients+ sensitive for hydronephrosisDiff diagnoses:- AAA- Diverticulitis, appendicitis- Ectopic pregnancy (pregnancy test)- Testicular torsion

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9
Q

Complications of stones + Why should you never use contrast for suspected kidney issues

A

Complications:- Pyonephrosis (suppurative (pus producing) upper tract infection), - fistulae, - CKD, - Xanthogranulomatous pyelonephritis (chronic infection of kidneys caused by stones)Contrast needs to be excreted by kidney but is composed of HEAVY metals (large molecules)-> HARMFUL if kidney unable to excrete properly

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10
Q

Treatment of renal stones

A
  • Symptomatic: - IV FLUIDS/HYDRATE - ANALGESIA (NON-OPIATE) * NSAID e.g. IV DICLOFENAC for severe pain - antiemetics if needed - observe for SEPSIS - Nephrostomy if required (tubes inserted in the back and enter kidney pelvis, draining urine) - Ureteric stent – tubes inserted up ureters and bypass stones if necessary- Antibiotics if UTI (e.g. IV CEFUROXIME/GENTAMICIN) - prevent pyonephrotic renal failure/sepsis- If <5mm: - oft pass spontaneously - WATCH + WAITIf too big/causing pain:- Medical expulsive therapy: * ORAL NIFEDIPINE or alpha blocker e.g. ORAL TAMSULOSIN can promote expulsion and reduce analgesia- Surgical elective - EXTRACORPOREAL SHOCK WAVE LITHOTRIPSY (ESWL) * 6-10mm (max 20mm) - URETHROSCOPIC LASER REMOVAL or BASKET EXTRACTION - PERCUTANEOUS NEPHROLITHECTOMY (PCNL) * >20mm/multiple/complex - Consider uretroscopy with YAG laser - NEPHRECTOMY if severe - Laproscopic/open surgery for bladder stones
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11
Q

Why do you not give opiates for kidney problems

A

Opiates renally excreted - if kidney excretion impaired - opiates stay in body -> HARMFUL, can overdose

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12
Q

Where can causes of AKI/CKD originate from AKA classes of AKI/CKD

A
  • Pre-renal- Intrinsic- Post renal
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13
Q

Pre-renal causes of AKI

A

Hypoperfusion- HYPOVOLEMIA/REDUCED Cardia Output - congestive HF - Shock/sepsis - Diarrhoea/vom- RENAL ARTERY STENOSIS- Some DRUGS - REDUCE BP, circ volume or GFR:- Liver failure

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14
Q

Intrinsic/Renal causes of AKI

A
  • Tubular: - ACUTE TUBULAR NECROSIS (ATN) - main (linked iscahemia + some nephrotoxic e.g. Nsaids, contrast, antibiotics) - MYELOMA - RHABDOMYOLYSIS - lymphoma infiltration- Intersitial: - Acute interstitial nephritis (typically presents days-week after drug admin -> oliguria, fever (50%), eosinophilia + sometimes rash) - i.e. allergic reaction - lymphocytic infiltration (hypersensitivity reaction to infection)- VASCULAR - (vasculitis, thrombosis, embolism, dissection)- Glomerular - GLOMERULONEPHRITIS- Toxins + nephrotoxic drugs - NSAIDs - ACE-I (constricts afferent arteriole) - ARBs - loop diuretics - IV contrast- TUMOUR LYSIS syndrome
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15
Q

Post-renal causes of AKI

A

Obstructive- STONES- BENIGN PROSTATIC HYPERPLASIA- External COMPRESSION of URETER (tumours etc)- OCCLUDED indwelling CATHETER- NEUROGENIC BLADDER- Some drugs like anticholinergics + CCBs

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16
Q

Define AKI

A

Abrupt decline in kidney function (hrs - days) - covers a spectrum of injury/causes (it’s a syndrome rather than biochemical diagnosis)- Characterised by: - INCREASED SERUM CREATININE/urea - DECREASED URINE OUTPUT

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17
Q

NICE Diagnostic criteria (KDIGO classification) for AKI

A

Any 1 of below:- INCREASED CREATININE by >= 26 µmol/L in 48 hours- >= 50% INCREASED CREATININE over 7 DAYS- REDUCED URINE OUTPUT: - < 0.5 ml/kg/hour for > 6HR (adults) - < 0.5 ml/kg/hour for > 8HR (kids) - normal = 0.5-1.5 ml/kg/hr

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18
Q

Risk factors for AKI

A
  • CKD- OLDER age (>65)- COMORBIDITIES - DIABETES - LIVER DISEASE - HEART FAILURE- HYPOVOLAEMIA- NEPHROTOXIC DRUGS - NSAIDs + ACE-I - anticholinergics - CCBs - Optiates - CONTRAST- Cognitive impairment
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19
Q

Pathophys of AKI + its complications

A

Decreased filtration/urine output -> ACCUMULATION of usually excreted substances- K+: HYPERKALAEMIA - Arrhythmias- Urea: HYPERURAEMIA - Pruritis from skin deposits + Uremic frost - CONFUSION if severe - (urea -> ammonia -> encephalopathy)- Fluid: OEDEMA- H+: ACIDOSIS

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20
Q

Top 3 causes of AKI

A
  • SEPSIS- CARDIOGENIC SHOCK- MAJOR SURGERY
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21
Q

Signs/symptoms of AKI

A

Remember - all due to SUBSTANCE ACCUMULATION:- ARRHYTHMIAS (K+ accumulation)- METABOLIC ACIDOSIS (H+ retention)- URAEMIA: - ENCEPHALOPTHY - Pericarditis - Skin manifestations (e.g. pruritis)- FLUID OVERLOAD: - or HYPOVOLEMIC SHOCK (pre-renal) - OEDEMA- OLIGURIA (<400 ml/day)/anuria - potentially palpable bladder

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22
Q

Diagnosis of AKI

A
  • 1ST LINE: UREA + ELECTROLYTES - K+, H+, urea - ESTABLISH CAUSE: - UREA:CREATININE (urine dipstick) - >100 = PRE-RENAL - < 40 = RENAL - 40-100 = POST-RENAL- FBC + CRP (infection) - VERY HIGH OR LOW WCC -> SUGGESTS SEPSIS - RENAL BIOPSY (DIAGNOSTIC for INTRARENAL)- USS (DIAGNOSTIC for POST-RENAL)Other tests:- ECG -> HYPERKALAEMIA - Absent P wave, prolonged PR interval, Tall tented T waves, wide QRS complexes- urine dipstick- CXR- ABG
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23
Q

AKI management

A
  • Treat complications: - CALCIUM GLUCONATE - hyperkalaemia - or Insulin with Glucose (milder - insulin shifts potassium into cells but need glucose to stop hypo) - SODIUM BICARB - acidosis - DIURETICS - fluid overload- STOP nephrotoxic DRUGSTreat underlying cause- LAST RESORT - RENA: REPLACEMENT THERAPY - Haemo DIALYSIS - Indicated in: - Acidosis - Fluid overload - Uremia (symptomatic) - K+ >6.5/ ECG change - (think AFUK)
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24
Q

Common Nephrotoxic drugs

A
  • NSAIDS- Aminoglycides- ACE-i- ARB- Loop diuretics- ?Metformin- ?Digoxin- ?Lithium - Any heavy metals can cause damage, esp if kidney is already struggling
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25
Q

Classification of AKI stages

A
  • 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
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26
Q

Define CKD

A

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)

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27
Q

Classification of CKD stages

A

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)

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28
Q

Causes/risk factors of CKD

A

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

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29
Q

Pathophys of CKD

A

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 SCARRINGSymps due to substance accumulation + diabetic nephropathy

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30
Q

Complications of CKD

A
  • ANAEMIA (reduced EPO) -> Pericarditis + effusion if severe- OSTEODYSTROPHY (reduced vit D activation)- NEUROPATHY/ ENCEPHELOPATHY- HTN, ^lipids, vasc calcific -> CVD (highest mortality)
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31
Q

Diagnosis of CKD

A
  • 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
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32
Q

Management of CKD

A

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 - ATORVASTATINIf END-STAGE (stage 5):- RRT (dialysis)- RENAL TRANSPLANT (cure)

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33
Q

Types of RRT

A

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- HaemofiltrationContinuous allows you to add in fluid and better control their fluid volume - needs to be continuously attached to machine

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34
Q

How is RRT typically administered (excluding peritoneal)

A

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)

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35
Q

AKI vs CKD

A
  • 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
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36
Q

Types of incontinence

A
  • 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)
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37
Q

Basic Neuro-urology

A
  • 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
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38
Q

Classification of Lower Urinary Tract Symptoms (LUTS)

A
  • Storage- Voiding- Post-micturitionImportant to learn diff types in each category esp storage + voiding symptoms
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39
Q

Storage related LUTS

A
  • 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
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40
Q

Voiding related LUTS

A
  • SLOW stream/Poor flow- HESITANCY- STRAINING (using abdo muscles)- Intermittency- TERMINAL DRIBBLE(- Splitting/spraying)(- Vesicle tenesmus (incomplete bladder emptying))
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41
Q

Post-micturition related LUTS

A
  • Post-micturition dribble (later than terminal dribble)- Feeling of INCOMPLETE VOIDING (contributes to frequency)
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42
Q

Definition of Over Active Bladder

A

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

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43
Q

How is detrusor overactivity defined

A

A rise in PRESSURE on FILLING on URODYNAMIC TESTING

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44
Q

Briefly, how does urodynamic testing work

A
  • 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 pressureReserved for cases where surgery is considered/bladder safety is potentially compromised
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45
Q

Causes of Stress incontinence

A
  • 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
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46
Q

Treatment of Stress incontinence (+ main contraindication)

A
  • Men: - ARTIFICIAL SPHINCTER- Women: - Autologous sling - Artificial sphincterCANNOT DO if RISK of UNSAFE bladder (i.e if they have loss of compliance and you add a functional sphincter -> unsafe)
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47
Q

Management of urge incontinence

A
  • 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
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48
Q

Briefly, what happens in a cystoplasty

A
  • Cut bladder in half (stop contraction)- Put section of bowel in bladder
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49
Q

3 categories of neurogenic bladder conditions

A
  • 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
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50
Q

Spastic vs Flaccid

A

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

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51
Q

What is an unsafe bladder

A

Bladder that can cause damage to kidneys via PROLONGED HIGH PRESSURES

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52
Q

What causes voiding problems

A

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

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53
Q

Treatment of voiding LUTS

A
  • 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
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54
Q

Normal role/anatomy prostate and the role of DHT

A

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

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55
Q

Define benign prostatic hyperplasia

A

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

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56
Q

Risk factors for BPH

A
  • increased AGE- ethnicity (Afro-Caribbean = increased testosterone)CASTRATION is PROTECTIVE
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57
Q

Pathophys of BPH

A

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

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58
Q

Presentation of BPH

A
  • LUTS esp VOIDING RELATED - Voiding: - Poor stream; Dribbling - Vesicle tenesmus/incomplete emptying - Straining - Potential dysuria (painful urination) - Storing: - Frequency, urgency, Nocturia (>30%), - IncontinenceIf totally occluded - may get ANURIA -> RETENTION, HYDRONEPHROSIS, UTI, stones
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59
Q

Investigation of BPH

A

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 bothAlso exclude things like stones and UTIs

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60
Q

Treatment for BPH

A
  • 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
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61
Q

Define/pathophys of prostate cancer

A

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 malignancyIt 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 lungAndrogen receptors on the prostate are responsible for cancerous growth- can get castration-resistant cancer which is still androgen sensitive

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62
Q

Risk factors for prostatic cancer

A
  • 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
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63
Q

Presentation of Prostate cancer

A
  • 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
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64
Q

What kind of bone lesions does prostate cancer cause

A

SCLEROTIC LESIONS- thick, looks white on x-rays

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65
Q

Which areas does prostate cancer typically metastesise to

A
  • lymph nodes- BONE (particularly sacrum due to interconnected blood flow)- Liver- Lung- Brain
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66
Q

Diagnosis of prostate cancer

A

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

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67
Q

What grading system is used for prostate cancer

A

Gleason score- Low = <= 6- Intermediate = 7- High/v. high: - Grade group 4 = Gleason score 8 - Grade group 5 = Gleason score 9-10It 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

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68
Q

Treatment of prostate cancer

A
  • 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 - anaemiaCryotherapy is also an option (i would assume for more localised cancer)Often SLOW GROWING so may just do WATCHFUL WAITING (esp if older)
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69
Q

Define what a UTI is

A

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

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70
Q

What are the 5 most common pathogens that cause UTIs

A

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

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71
Q

What are the storing LUTS commonly seen in UTIs

A

Remember FUND- Frequency- Urgency- Nocturia- Dysuria

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72
Q

Define Pyelonephritis

A

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

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73
Q

Risk factor for UTIs in general

A

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

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74
Q

Risk factors/causes for Pyelonephritis

A
  • Urine stasis (stones or BPH)- Renal structural abnormalities- Catheters- Diabetes- Pregnancy- ImmunocompromisedParticularly affects FEMALES under 35 yrsCaused by ASCENDING UTI (bacteria move up from urethra); HAEMATOGENOUS spread of pathogens (via blood - esp S. AUREUS, CANDIDA); Lymphatic spread
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75
Q

Presentation of Pyelonephritis

A

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 bacteriuriaOliguria if it causes AKISeptic shock in advanced disease

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76
Q

Investigations for Pyelonephritis

A
  • 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
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77
Q

Treatment for pyelonephritis + Complications

A

RestFLUID 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 catheterIf CHRONIC -> NEPHRECTOMYComplications:- Renal abscess- Emphysematous pyelonephritis (Gas accumulation in renal parenchyma, collecting system or perinephritic tissue due to necrotizing infection of renal parenchyma)- Kidney fibrosis- Sepsis

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78
Q

Define Cystitis

A

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

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79
Q

Risk factors for Cystitis

A
  • Urine stasis (from obstruction)/poor emptying- Catheters - Bladder epithelium damageHistory of UTIDiabetesFrequent sexual intercourse?Pregnancy
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80
Q

Presentation of Cystitis

A
  • Dysuria- discomfort, pain, burning on urination- Frequency- Urgency- Cloudy smelly urine - Haematuria- Suprapubic tenderness/discomfort - abdo/loin as well potentially
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81
Q

Diagnosis of Cystitis

A

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

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82
Q

Management of Cystitis

A

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

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83
Q

Causes of Urethritis

A

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

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84
Q

Risk factors for Urethritis

A

UNPROTECTED SEX- MSM espmale

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85
Q

Presentation of Urethritis/common STIs

A
  • DYSURIA +/- URETHRAL DISCHARGE (blood/pus)- Urethral pain- penile discomfort- potential skin lesions- may get systemic symptomsChlamydia:- Men = TESTICULAR pain - Voiding symptoms, dysuria - 50% asymp- Women = VAGINAL discharge and dysuria - white, yellow or green discharge - 70% are asympGonorrhoea:- more LIKELY to be ASYMP (90-95%)- Men = dysuria, frequency, discharge- Women = VAGINAL discharge, dysuria, PELVIC pain
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86
Q

Diagnosis of Urethritis

A
  • 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
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87
Q

Treatment of Urethritis

A
  • 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
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88
Q

What condition is urethritis often linked to

A

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

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89
Q

Define Epididymo-Orchitis + it’s aetiology + risk factors

A

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 ELDERLYRFx:- Previous infection- Indwelling catheter- Structural/functional abnormality of urinary tract- Anal intercourse (MSM esp)

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90
Q

Presentation of Epididymo-Orchitis

A
  • Unilateral scrotal PAIN + PALPABLE SWELLING (subacute) - Pain RELIEVED upon ELEVATING SCROTUM (+ve Prehn’s sign) - tender on examination- Cremaster reflex intact- May get sweats/feverIf STI - may have urethritis/urethral dischargeIf MUMPS: - HEADACHES, FEVER - UNI/BI-LATERAL PAROTID SWELLING
91
Q

Diagnosis of Epididymo-Orchitis

A
  • NAAT - Intracellular G -VE DIPLOCOCCI = GONORRHOEA- Urine dip- MC + S (mid stream sample) - for UTI symps- US to rule out abscess- Urethral smear/swabRULE OUT TESTICULAR TORSION:- typically teste torsion has -ve Prehn’s sign- If any doubt -> Surgical Scrotal Exploration
92
Q

Treatment of epididymo-orchitis

A

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

93
Q

Prostatitis

A

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

94
Q

Presentation of prostatitis

A
  • 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 painIn CHRONIC:- Symps for >3 months- Recurrent UTIs
95
Q

Investigations of Prostatitis

A
  • 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)
96
Q

Management of Prostatitis

A

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 necessaryChronic:- 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

97
Q

Complications of Prostatitis

A

Urinary retention

98
Q

Complicated vs Uncomplicated UTI

A

Uncomplicated:- UTI in healthy non-pregnant woman with normally functioning urinary tractComplicated 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

99
Q

What special factors do UPEC have

A
  • 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
100
Q

Where do bacteria typically adhere to in GU tract

A
  • Urothelium* Vaginal epithelium* Vaginal mucus
101
Q

Higher rates of bacterial adhesion in GU tract occurs in what states

A
  • 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
102
Q

Which UTI causing pathogens secrete urease and what does it do

A
  • Gram-negative: Proteus, Klebsiella & Pseudomonas- Gram-positive: Staphylococci & MycoplasmaIncreases risk of stone formation
103
Q

Host defense mechanisms against UTIs

A
  • Antegrade flushing of urine - forward flow of urine- Tamm-Horsfall protein - has antimicrobial properties- Low urine pH and high osmolarity- Urinary IgA
104
Q

Define Acute NehphrItic syndrome

A

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)

105
Q

Aetiology of Nephritic syndrome

A

Can have systemic or renal causes- COMMONEST PRIMARY CAUSE is (Cresentic) IgA nephropathy/Henoch Schonlein purpura (RENAL) - in developed/high income countriesSystemic 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

106
Q

Post-strep glomerulonephritis pathophys + management

A
  • Typical case of post-streptococcal glomerulonephritis occurs in a child1-3 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 nephritisDIAGNOSE via evidence of STREP INFECTIONTreat with ANTIBIOTICS + SUPPORTIVE
107
Q

SLE

A

Presentation (systemic inflammation):- Rash, - arthralgia, - kidney failure, (30-50% have renal disease at presentation)- neurological symptoms, - pericarditis and pneumonitisMost 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 & C4Classification:- 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 nephritisTreatment (no specific):- Immunosuppression; steroids, cyclophosphamide, rituximab, (mycophenolate)

108
Q

Systemic sclerosis

A
  • ANA positive, Anti-Scl 70 positive* Severe hypertension - may lead to strictures* ‘Onion skin’ changes on renal biopsy, raynauds phenomenon, fibrotic skin, oesophageal dysmotility
109
Q

Multisystem small vessel vasculitis

A

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 markersTreatment:- 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

110
Q

What is Goodpastures disease

A
  • 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 haemorrhageDIAGNOSE:- anti-GBM (glomerular basement membrane) ANTIBODIES (bloods/biopsy)- BIOPSY - IgG staining - immunoflurescence
111
Q

Treatment of Goodpastures

A
  • Remove antibody via plasma exchange- Immunosuppression - Steroids/cyclophosphamide (give sperm presarvation before giving cytotoxic meds)
112
Q

What is IgA nephropathy

A
  • IgA glycosylation abnormality- Kidney attacked by IgA DEPOSITION in MESANGIUM (bit that provides structural support to glomerulus) -> HAEMATURIACan 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
113
Q

Treatment for IgA nephropathy

A
  • 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)
114
Q

Presentation of Nephritic syndrome

A
  • 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 nauseaDeteriorating kidney function- Moderate-severe decrease in GFR
115
Q

DIagnosis of Nephritic syndrome

A
  • Take history to determine cause- Measure eGFR, proteinuria, serum urea & electrolytes and albumin - todetermine current status and monitor progress- Culture - swab from throat or infected skin- Urine dipstick to detect proteinuria and haematuria- Renal biopsy if necessary
116
Q

Treatment of Nephritic syndrome

A

Depends on the cause - outlined previously- Autoimmune causes treated with immunosuppression or plasma exchange- Infective causes treated with Antibiotics or antiviralsBlood 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. AMLODIPINECorticosteroids- this is to reduce the inflammation causing damage to the kidney

117
Q

Define glomerulonephritis

A

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%

118
Q

What outcomes can glomerulonephritis cause

A
  • 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
119
Q

How can glomerulonephritis present

A
  • Acute Nephritic Syndrome (Acute glomerulonephritis)- Nephrotic syndrome- Asymptomatic urinary abnormalities - haematuria, proteinuria or both- Chronic kidney disease (CKD) - can present as stage 3/4
120
Q

Causes of glomerulonephritis

A
  • IgA nephropathy- Goodpasture’s disease- Post-streptococcal glomerulonephritis- Henoch Schoenlein purpura (small vessel vasculitis)
121
Q

What is Henoch Schoenlein purpura

A
  • 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
122
Q

How is Henoch Schoenlein purpura diagnosed

A

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

123
Q

How is Henoch Schoenlein purpura treated

A

CORTICOSTEROIDS and ACE-I/ARBs

124
Q

Define Nephrotic syndrome

A

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 severeALL 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 cholesterolLeaking huge amount of protein but kidney function remains same so no kidney failure- 25% have NO VISIBLE CHANGES on BIOPSYPretty rare

125
Q

Risk factors for Nephrotic syndrome

A

DIABETES MELLITUS (most common 2ndry cause)

126
Q

Aetiology of Nephrotic syndrome

A

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

127
Q

Pathophys of Nephrotic syndrome

A
  • 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
128
Q

Presentation of Nephrotic syndrome

A
  • 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
129
Q

Diagnosis of nephrotic syndrome

A
  • 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 guidedBP normal/slightly raisedCXR or ultrasound for pleural effusion or ascitesSerum + urine electrophoresis - amyloid, myelomaANA, double-stranded DNA antibody, complement C3 and C4 indicates SLEAntiphospholipase A2 receptor antibody indicates membranous nephropathyHepB surface antigen, HepC antibody or HIV (can cause cryoglobinaemia - proetins clump at low temps)
130
Q

Management of Nephrotic syndrome

A

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

131
Q

Complications of nephrotic syndrome

A
  • 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.
132
Q

What is membranous nephropathy

A
  • Presents with asymptomatic proteinuria/nephrotic syndrome +/- microscopic haematuria, hypertension and renal impairmentDeposition 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
133
Q

Diagnosis of membranous nephropathy

A

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

134
Q

Management of Membranous nephropathy

A

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

135
Q

What is Focal segmental glomerulosclerosis

A

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

136
Q

Diagnosis of Focal segmental glomerulosclerosis

A

RENAL BIOPSY - scarring of glomerui (FOCAL SCLEROSIS)

137
Q

Treatment of Focal segmental glomerulosclerosis

A
  • ACE-I/ARB - for BP control- CORTICOSTROIDS esp if idiopathic - potentially other immunosuppression e.g. cyclophosphamide or ciclosporin
138
Q

What is Minimal change disease

A
  • A primary cause of nephrotic syndrome (commonest cause in children) - esp in BOYS OVER 5 y/o- 20% of nephrotic syndrome in adults
139
Q

Risk factors/causes of Minimal change disease

A
  • 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
140
Q

Pathophys of Minimal change disease

A
  • Disrupted podocyte ACTIN CYTOSKELETON -> FUSION of FOOT PROCESSES- seen only on electron microscopyAppear to be caused by IMMATURE DIFFERENTIATING CD35 STEM CELLS
141
Q

Presentation of Minimal change disease

A
  • Proteinuria- Oedema, predominantly around the face- Fatigue- Frothy urinei.e. same as Nephrotic syndrome as minimal change disease causes nephrotic syndrome
142
Q

Diagnosis of minimal change disease

A

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

143
Q

Treatment of minimal change disease

A
  • High dose corticosteroids e.g. PREDNISOLONE - can reverse proteinuria in 95% - majority relapse- Frequent relapse/steroid-dependent disease treated with: CYCLOPHOSPHAMIDE or CICLOSPORIN/TACROLIMUS
144
Q

What are asymp urinary abnormalities

A
  • 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
145
Q

Causes of asymp urinary abnormalities

A
  • IgA nephropathy- Thin membrane disease (membrane thin - more likely to leak into urine)
146
Q

What tissue does renal cell carcinoma oft originate from

A

Also known as Hypernephroma and Grawitz tumour90% arise from PROXIMAL CONVOLUTED TUBULAR EPITHELIUM

147
Q

Epidemiology of renal cancer

A
  • 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
148
Q

Risk factors/causes of renal cancer

A
  • Smoking- Obesity- Hypertension- Renal failure & haemodialysis (15% develop RCC)- Polycystic kidneys- Genetic: - Von Hippel Lindau (VHL) syndrome - Tuberous sclerosis - Hereditary Papillary RCC
149
Q

What is Von Hippel Lindau syndrome

A
  • 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
150
Q

Pathophys of Renal cancer

A
  • 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
151
Q

Presentation of RCC

A

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

152
Q

Diff diagnosis of RCC

A
  • Transitional cell carcinoma, - Wilms’ tumour (young kids - to do with embryogenesis leftovers), - renal oncocytoma (benign), - leiomyosarcoma (smooth muscles)
153
Q

Diagnosis of RCC

A
  • 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
154
Q

Treatment of RCC

A
  • 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
155
Q

What is the Mayo prognostic risk score for RCC

A

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

156
Q

What is Wilms’ tumour

A
  • 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
157
Q

What is bladder cancer

A
  • 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 TCCCan also get squamous cell carcinoma from Schistosomiasis
158
Q

Risk factors for TCC

A
  • 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
159
Q

Pathophys of bladder cancer (spread)

A
  • Tumour spread: * Local → to pelvic structures * Lymphatic → to iliac and para-aortic nodes * Haematogenous → to liver and lungs
160
Q

Presentation of bladder cancer

A
  • 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
161
Q

Diagnosis of Bladder cancer

A
  • 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
162
Q

Diff diagnosis of bladder cancer

A
  • Haemorrhagic cystitis, - renal cancer, - UTI, - urethral trauma(cause main symp is haematuria)
163
Q

Treatment of TCC/bladder cancer

A

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

164
Q

Testicular tumours/cancer - epidemiology

A
  • 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
165
Q

Risk factors for testicular cancer

A
  • 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
166
Q

Presentation of testicular cancer

A
  • 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
167
Q

Diff diagnosis of testicular cancer

A
  • Testicular torsion, (presents with ACUTE PAIN)- lymphoma, - hydrocele, (can be non-cacner related - oft reactive to infection/tumour)- Varicocele- epididymal cyst- Trauma
168
Q

Diagnosis of testicular cancer

A
  • 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
169
Q

Treatment of testicular cancer

A
  • 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
170
Q

What is non-malignant scrotal disease

A

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

171
Q

How to initially differentiate between testicular masses on examination

A

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

172
Q

What is an epididymal cyst

A

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

173
Q

Epidemiology of epididymal cyst

A
  • Usually develop around the age of 40- Not uncommon- Rare in children
174
Q

Pathophys of epididymal cyst

A
  • Contain clear fluid (if milky = spermatocele)- Lie above and behind the testis
175
Q

Presentation of epidiymal cysts

A
  • 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)
176
Q

Diff diagnosis of epididymal cyst

A
  • 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
177
Q

Diagnosis of epididymal cyst

A
  • transillumination to eliminate hydrocele- scrotal US
178
Q

Treatment of epididymal cyst

A
  • Usually not necessary- If painful and symptomatic then surgical excision
179
Q

Define hydrocele

A

Abnormal collection of fluid within the TUNICA VAGINALIS

180
Q

Epidemiology of hydroceles

A
  • Clinically apparent scrotal hydroceles are evident in 6% of term males beyond the newborn period- Most paediatric hydroceles are congenital
181
Q

Causes of hydroceles

A
  • 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
182
Q

Pathophys of hydrocele

A
  • Overproduction of fluid in tunica vaginalis (simple hydrocele)- Processus vaginalis fails to close -> peritoneal fluid communicates freely with the scrotal portion (communicating hydrocele)
183
Q

Presentation of hydrocele

A
  • 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
184
Q

Diff diagnosis of hydrocele

A

Main - TESTICULAR TORSION + strangulated hernia

185
Q

Diagnosis of hydrocele

A
  • Ultrasound- Serum alpha-fetoprotein and human chorionic gonadotrophin to help exclude malignancy
186
Q

Treatment of hydrocele

A
  • Oft resolve spontaneously - congenital oft by 2 y/o- Therapeutic aspiration or surgical removal
187
Q

Define varicocele

A

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

188
Q

Epidemiology of varicocele

A
  • 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
189
Q

Causes of varicocele

A
  • 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 veinsOft related to renal cancers, stones etc.
190
Q

Presentation of varicocele

A
  • 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
191
Q

Diff diagnosis of varicocele

A

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

192
Q

Diagnosis of varicocele

A
  • Venography- Colour doppler ultrasound (see blood flow)
193
Q

Treatment of varicocele

A

Surgery IF there is PAIN, INFERTILITY or TESTICULAR ATROPHY

194
Q

Define testicular torsion

A

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

195
Q

What times should testicular torsion surgery be performed within to optimise salvagability

A

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

196
Q

Epidemiology of Testicular torsion

A
  • 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
197
Q

Causes of testicular torsion

A

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

198
Q

Presentation of testicular torsion

A

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 retractedWith 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

199
Q

Differential diagnosis of testicular torsion

A
  • 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
200
Q

Diagnosis of testicular torsion

A
  • Doppler ultrasound may demonstrate lack of blood flow to testis- Urinalysis to exclude infection and epididymis- DO NOT DELAY SURGICAL EXPLORATION
201
Q

Treatment of testicular torsion

A
  • SURGERY - expose + untwist (6HR WINDOW)- Orchidectomy (removal) if needs be- Bilateral fixation
202
Q

Define erectile dysfunction

A

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

203
Q

Epidemiology of erectile dysfunction

A

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

204
Q

Categories of ED

A

Neurogenic - failure to initiateArteriogenic - failure to fillVenogenic - failure to store(oft multifactorial)

205
Q

Aetiology of Erectile dysfunction

A

AgeDIabetesHypertensionHyperlipidaemiaHypogonadism (endocrine)Trauma (including iatrogenic)Drugs (anti-androgenic: finasteride, b-blockers, anti-depressants, statins etc.)PsychosomaticNeurological (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.

206
Q

Diagnosis/assessment of ED

A

Patient centred approach: Identify undelying modifiable co-morbiditiesHistory (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.)

207
Q

Treatment of ED

A

Underlying cause - Psychosexual counselling (if needed)Viagra (1st line) - PDE-5 inhib (improves SM relaxation) - CONTRAINDICATED if recent MI/stroke - take only 30min before intercourseHypogonadism - 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

208
Q

What organisms are commonly associated with UTIs

A

50% E coliRemember KEEPSKlebsiellaE coliEnterococciProteusStaph SaprophyticusStaph aureus and Pseudomonas Aeruginosa can also cause UTIs but rarer

209
Q

Risk factors for UTIs

A
  • Pregnancy- Sex- Catheterisation (Catheters can induce biofilm formations)- Structural abnormalities of urinary tracts- Previous UTI- Stones (can become site of infection)Associated with Diabetes
210
Q

Investigations to be done for UTIs in general

A
  • 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
211
Q

Treatment for UTIs in general/overview

A

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

212
Q

What is the target 24hr urine output for a 70kg adult patient

A

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

213
Q

NSAIDs are most likely to cause which type of renal injury

A

INTERSTITIALNSAIDs cause a decrease in prostaglandins, which results in unopposed constriction of theafferent arterioles

214
Q

Define Polycystic kidney disease

A

Cyst formation throught renal parenchyma-> bilateral enlargement + swelling

215
Q

Aetiology + RFx of PKD

A

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)

216
Q

Pathophys of ADPKD

A

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 ciliaPKD mutation impairs polycystin function -> reduced Ca2+ influx -> disorientated cell division/EXCESSIVE CILIA GROWTH -> loss of planar polarity -> cyst initiation -> fluid secreted by epithelial cells -> cystMechanical compression + apoptosis of healthy tissie + reactive fibrosis -> progressive loss of renal function (so rapidly growing cysts = faster renal function decline)

217
Q

PKD1 vs PKD2

A

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

218
Q

Brief explanation of ARPKD + Potter’s sequence

A

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

219
Q

Presentation of ADPKD

A

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 failureComplications: - 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

220
Q

Diagnosis of PKD (same for both)

A
  • 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
221
Q

Treatment of PKD (same for both)

A

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

222
Q

Diff diagnosis of ADPKD

A
  • Acquired and simple cysts of the kidneys- Autosomal recessive PKD- Medullary sponge kidney- Tuberous sclerosis
223
Q

What is fanconi syndrome

A

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)

224
Q

What is fanconi syndrome

A

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)

Take 2: Electric Boogaloo (20 decks)

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