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Phase 2a > Renal + urogenital > Flashcards

Renal + urogenital Flashcards

1
Q

Explain what tubuloglomerular feedback is

A

Macula densa cells of DCT lie between afferent/efferent arterioles + detect NaCl using it as indicator of GFR.

  • NaCl raised = afferent arteriole constriction.
  • NaCl reduced, renin secretion from juxtaglomerular cells.
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2
Q 
URINARY INCONTINENCE
What is...
i) Urgency incontinence?
ii) Stress incontinence?
iii) Overflow incontinence?
A

i) Strong desire to void (F>M).
ii) Increased abdominal pressure stimulates need to urinate (F»M).
iii) Leaking small amounts of urine + so outflow obstruction (M>F).

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3
Q

URINARY INCONTINENCE

What could the aetiology of these urinary incontinences be?

A 
Urgency = over active bladder from detrusor overactivity (urgency + frequency ± nocturia wen appearing in absence of pathology).
Stress = laughing, coughing, sneezing, lifting (increasing abdominal pressure).
Overflow = benign prostatic hyperplasia, tumour.
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4
Q

URINARY INCONTINENCE

What investigations and treatments would you do for these urinary incontinences?

A
  • Over active bladder = bladder retraining, diary + exercises, cut out caffeine/alcohol, bladder diary urodynamics.
  • Stress = pelvic floor strengthening.
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5
Q

URINARY TRACT STONE

What is the pathophysiology of renal stones?

A
  • Formed when urine extremely saturated with salt + minerals like calcium oxalate.
  • Calcium oxalate precipitates from in the basement membrane of loops of Henle > Randall’s plaque in renal papillae > develop into stone.
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6
Q

URINARY TRACT STONE

What is the pathophysiology of bladder stones?

A
  • Most commonly, urinary stasis due to failure of optimal emptying leading to precipitation, consider in women with UTI.
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7
Q

URINARY TRACT STONE

What are the classic places where calculi are likely to get stuck?

A
  • Ureteropelvic junction (junction between pelvis + top of ureter).
  • Pelvic brim (where ureter passes over iliac vessels).
  • Vesoureteric junction (ureter passes into bladder).
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8
Q

URINARY TRACT STONE

What is the aetiology or renal calculi?

A

Hypercalciuria…
- Hypercalcaemia (primary hyperparathyroidism).
- Excessive dietary calcium.
- Excessive bone resorption (long-term immobilisation).
Uric acid by hyperuricaemia.
Cystine stones by cystinuria (AR).

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9
Q

URINARY TRACT STONE

What is the aetiology of bladder calculi?

A
  • Usually due to foreign bodies, obstruction or infection.
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10
Q

URINARY TRACT STONE

What is the clinical presentation or urinary tract stones?

A
  • Renal colic = sudden, severe pain “from loin to groin” due to stones causing dilatation, stretching + spasm of ureter.
  • UTI symptoms (dysuria, urgency, frequency).
  • Haematuria, proteinuria.
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11
Q

URINARY TRACT STONE

What is the prevention of urinary tract stones?

A
  • Stay well hydrated.
  • Low salt diet.
  • Healthy protein intake.
  • Reduce BMI + active lifestyle.
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12
Q

URINARY TRACT STONE

What are the investigations of urinary tract stones?

A

Bloods…

  • U+E >calcium, phosphate, urate.
  • Urine dipstick = haematuria.
  • Mid-stream sample of urine with microscopy + culture.
  • Non-contrast CT abdomen/KUB = gold standard.
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13
Q

URINARY TRACT STONE

What is the treatment for urinary tract stones?

A
  • Analgesic like diclofenac, fluids.
  • Extracorporeal shock wave lithotripsy (ESWL) to fragment stones.
  • Percutaneous nephrolithotomy (PCNL) if large.
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14
Q

ACUTE KIDNEY INJURY

What is the AKI?

A
  • Abrupt deterioration in renal function, usually over hours/days, which is reversible but may cause sudden, life-threatening biochemical disturbances.
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15
Q 
ACUTE KIDNEY INJURY
What is the pathophysiology of...
i) pre-renal
ii) renal
iii) post-renal

AKI?

A

i) Impaired perfusion to kidneys causing reduced GFR. Occurs due to decreased vascular volume/CO, systemic vasodilation or renal vasoconstriction.
ii) Damage to kidney apparatus which impairs ability function.
iii) Urinary outflow obstructed either intrinsically or extrinsically (compression).

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16
Q 
ACUTE KIDNEY INJURY
What is the aetiology of
i) pre-renal
ii) renal
iii) post-renal

AKI?

A

i) Hypotension, heart failure, atherosclerosis, sepsis.
ii) Glomerular disease (glomerulonephritis), interstitial (nephrotoxic drugs ACEi, NSAIDs, infection), vessels (vasculitis).
iii) Stone, renal tract malignancy, prostatic hypertrophy.

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17
Q

ACUTE KIDNEY INJURY

What are the risk factors for AKI?

A
  • Increasing age.
  • CKD.
  • Heart failure.
  • DM.
  • Nephrotoxic drugs.
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18
Q

ACUTE KIDNEY INJURY

What is the clinical presentation of AKI?

A
  • Oliguria.
  • Increased JVP, oedema.
  • Systemic (nausea, vomiting).
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19
Q

ACUTE KIDNEY INJURY

What are the serious complications with AKI?

A

Hyperkalaemia which can lead to arrhythmias + cardiac arrest.
- Give calcium gluconate to protect myocardium + insulin + dextrose.
Volume overload + metabolic acidosis.

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20
Q

ACUTE KIDNEY INJURY

What are the investigations for AKI?

A

Bloods…

  • U+E = rise in creatinine (acutely/gradually), hyperkalaemia.
  • Reduced urine output >6h consecutively.
  • Urinalysis ?infection.
  • ?USS renal
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21
Q

ACUTE KIDNEY INJURY

What is the treatment for AKI?

A
  • Best management = prevention, optimise fluid balance.
  • Treat symptoms (IV fluids, diuretics).
  • Stop nephrotoxic medication.
  • Dialysis if all else fails.
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22
Q

CHRONIC KIDNEY DISEASE

What is the pathophysiology of CKD?

A
  • Abnormal kidney structure/function present for >3 months with implications for health.
  • Irreversible loss of nephron/function - glomerulosclerosis.
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23
Q

CHRONIC KIDNEY DISEASE

What is the aetiology of CKD?

A
  • DM.
  • HTN.
  • Congenital like polycystic kidney disease.
  • Long term NSAID use.
  • Kidney diseases (chronic pyelonephritis).
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24
Q

CHRONIC KIDNEY DISEASE

What are the classifications of CKD?

A

Stage 1+2 = only CKD if signs of kidney damage.

  • Stage 1, GFR>90, asymptomatic.
  • Stage 2, 60≤GFR<90, asymptomatic.
  • Stage 3a 45≤GFR<60, some symptoms mild-moderate damage.
  • Stage 3b 30≤GFR<45, some symptoms moderate-severe damage
  • Stage 4 15≤GFR<30, symptoms, severe damage.
  • Stage 5 GFR<15, kidney failure.
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25
Q

CHRONIC KIDNEY DISEASE

What is the clinical presentation of CKD?

A
  • Anaemia (pallor, lethargy).
  • Amenorrhoea/erectile dysfunction.
  • HTN.
  • Nocturia, polyuria, oedema.
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26
Q

CHRONIC KIDNEY DISEASE

What are the investigations for CKD?

A

Bloods…
- Normochromic/cytic anaemia.
- U+E with urea + creatinine high, low calc, high pTH.
Urine dipstick (haematuria, proteinuria = infection).
GFR to assess function.
Renal USS, biopsy for damage.

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27
Q

CHRONIC KIDNEY DISEASE

What is the treatment for CKD stages 1–4?

A
  • Maintain BP targeting RAAS.
  • Control blood sugar if DM.
  • Smoking cessation.
  • Eat healthy, exercise.
  • Stop nephrotoxic drugs.
  • Antiplatelets/coagulants, statins, vitamin D.
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28
Q

CHRONIC KIDNEY DISEASE

What is the treatment for end-stage renal failure?

A
  • Dialysis.

- Transplant.

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29
Q

CHRONIC KIDNEY DISEASE

What are the two types of dialysis?

A
  • Haemodialysis, AV fistula, 3x/week

- Peritoneal dialysis, peritoneal catheter, daily (as one long exchange or shorter ones).

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30
Q

CHRONIC KIDNEY DISEASE

What are the complications with the 2 types of dialysis?

A
  • Haemo = hypotension, nausea, fever, impact on daily life (frequent dialysis).
  • Peritoneal = peri-catheter leak, abdominal wall herniation, intestinal perforation.
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31
Q

CHRONIC KIDNEY DISEASE

What are the benefits with the 2 types of dialysis.

A
  • Haemo = people who live alone/frail/elderly, unsuitable for peritoneal (previous surgery).
  • Peritoneal = good for young people/full time workers who want control of care.
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32
Q

CHRONIC KIDNEY DISEASE

What are the 2 types of kidney transplants?

A
  • Living donor = blood relative, ABO compatible, HLA identical + excellent medical condition
  • Cadaveric donor = irreversible brain damage, normal renal function, ABO compatible, best possible HLA match.
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33
Q

CHRONIC KIDNEY DISEASE

What treatment do you need to go on post-kidney transplantation and what is the effect of this?

A

Chronic immunosuppression.

  • Malignancy.
  • Infection.
  • Side effects of other drugs.
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34
Q

RENAL CELL CARCINOMA

What is the pathophysiology of RCC?

A
  • Arises from the proimal renal tubular epithelium.
  • Can secrete PTH (hypercalcaemia), ACTH (Cushing’s-like syndrome), EPO (polycythaemia), renin (HTN).
  • Common metastases = lymph nodes, lung, breast, bone.
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35
Q

RENAL CELL CARCINOMA

What is the epidemiology + risk factors for RCC?

A
  • 90% renal cancers, 55y/o M:F = 2:1.
  • Smoking.
  • Obesity.
  • HTN.
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36
Q

RENAL CELL CARCINOMA

What genetic condition is linked to RCC?

A

Von Hippel Lindau disease.
- AD condition can cause RCC as loss of tumour suppressor gene VHL allowing lots of benign cysts to grow, may develop into cancer.

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37
Q

RENAL CELL CARCINOMA

What is the clinical presentation of RCC?

A
  • Haematuria.
  • Abdominal mass.
  • Loin pain.
  • Cancer (weight loss, malaise).
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38
Q

RENAL CELL CARCINOMA

What are the investigations for RCC?

A
  • BP from increased renin.
  • Abdominal/pelvis USS.
  • Urinalysis.
  • Flexible cystoscopy + biopsy.
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39
Q

RENAL CELL CARCINOMA

What is the treatment for RCC?

A
  • Radical nephrectomy.

- Cryotherapy + radiofrequency ablation for unfit/unwilling patients.

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40
Q

TRANSITIONAL CELL CARCINOMA

What is the pathophysiology of TCC?

A
  • Arises from bladder (50%), ureter + renal pelvis.

- Common metastases = lymph nodes, lung, breast, skin.

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41
Q

TRANSITIONAL CELL CARCINOMA

What is the epidemiology + risk factors for TCC?

A
  • M:F = 4:1, >40y/o.
  • Smoking.
  • Occupational exposure (rubber factories due to aromatic amines).
  • Male.
  • Family Hx.
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42
Q

TRANSITIONAL CELL CARCINOMA

What is the clinical presentation of TCC?

A
  • PAINLESS haematuria.
  • Frequency/urgency/dysuria.
  • Urinary tract obstruction.
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43
Q

TRANSITIONAL CELL CARCINOMA

What are the investigations for TCC?

A
  • Cystoscopy + biopsy = diagnostic.
  • Urine cytology.
  • CT urogram.
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44
Q

TRANSITIONAL CELL CARCINOMA

What is the treatment for TCC?

A
  • Trans-urethral resection of bladder tumour (TURBT) with chemotherapy.
  • Radical cystectomy (radiotherapy if unfit/unwilling) if muscle invasive.
  • Palliative if invasion beyond bladder.
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45
Q

TESTICULAR CARCINOMA

What is the pathophysiology of testicular carcinoma?

A
  • 96% seminomas which arise from germ cells, remainder are teratomas composed of tissue not normally present at that site (teeth, hair).
  • Most common cancer in young men.
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46
Q

TESTICULAR CARCINOMA

What are the risk factors for testicular carcinoma?

A
  • Undescended testes.

- Family Hx.

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47
Q

TESTICULAR CARCINOMA

What is the clinical presentation of testicular carcinoma?

A
  • Painless lump in testicle (CANCER TILL PROVEN OTHERWISE).

- Can present with metastases in lungs = cough, dyspnoea, para-aortic lymph nodes causing back pain.

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48
Q

TESTICULAR CARCINOMA

What are the investigations of testicular carcinoma?

A
  • Ultrasound scrotum
  • Serum concentrations of tumour markers alpha-fetoprotein (seminomas only) + beta-human chorionic gonadotrophin elevated.
  • CXR/CT chest, abdomen + pelvis for staging.
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49
Q

TESTICULAR CARCINOMA

What is the treatment for testicular carcinoma?

A
  • Orchidectomy, offer sperm banking.
  • Seminoma radiotherapy if spread below diaphragm, chemotherapy if above.
  • Teratoma = chemotherapy if metastases.
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50
Q

PROSTATIC CARCINOMA

What is the pathophysiology of prostatic carcinoma?

A
  • Most are adenocarcinomas typically affecting peripheral zone of prostate.
  • Commonly metastasise to lymph nodes + bone (can spread locally bladder, rectum).
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51
Q

PROSTATIC CARCINOMA

What is the aetiology of prostatic carcinoma?

A
  • Genetic, family history.

- Can develop from benign prostatic hypertrophy.

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52
Q

PROSTATIC CARCINOMA

What is the screening for prostate carcinoma?

A
  • Done by annual measurement of serum prostate-specific antigen (PSA) which is glycoprotein expressed by normal + neoplastic prostate tissue secreted into blood stream.
  • Digital rectal examination.
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53
Q

PROSTATIC CARCINOMA

What PSA levels are normal/abnormal?

A

PSA > 4.0ng/mL = abnormal, >10ng/mL = 50% men have prostate cancer.

54
Q

PROSTATIC CARCINOMA

What are the advantages + disadvantages of screening in prostate carcinoma?

A
  • Can lead to early diagnosis, treatment + so cure.

- Uncertain natural history, screening leads to over diagnosis + treatment.

55
Q

PROSTATIC CARCINOMA

What is the clinical presentation of prostate carcinoma?

A
  • Nocturia, hesitancy, poor stream, terminal dribbling, obstruction.
  • Weight loss ± bone pain suggest metastases.
56
Q

PROSTATIC CARCINOMA

What are the investigations for prostate carcinoma?

A
  • Serum PSA elevated.
  • Digital rectal examination = hard, irregular, craggy prostate.
  • Transrectal ultrasound + biopsy.
  • Gleason grading, higher score = more aggressive.
57
Q

PROSTATIC CARCINOMA

What is the treatment for prostate carcinoma?

A

If localised, watchful waiting or radical prostatectomy or radiotherapy.
- Metastatic = palliative treatment like hormone therapy.

58
Q

BPH

What is the pathophysiology of benign prostatic hyperplasia (BPH)?

A
  • Benign nodular or diffuse proliferation of musculofibrous + glandular layers of the prostate, it’s the inner (transitional) zone which enlarges, median lobe.
59
Q

BPH

What is the clinical presentation of BPH?

A

LUTS…

  • Nocturia, frequency, urgency, post-micturition dribbling, poor stream/flow, hesitancy, overflow incontinence, haematuria.
  • Bladder stones, UTI.
60
Q

BPH

What are the investigations for BPH?

A
  • Bloods like FBC, U+E, serum PSA elevated.
  • Digital rectal examination.
  • International Prostate Symptom Score (I-PSS) looks at LUTS + how they affect daily life.
  • Transrectal USS ± biopsy.
61
Q

BPH

What is the generic treatment for BPH?

A
  • Watchful waiting.
  • Avoid caffine, alcohol (reduce urgency/nocturia).
  • Relax when voiding + void twice in row to aid emptying.
  • Control urgency by practicing distraction methods.
62
Q

BPH

What is the medical therapy for BPH?

A
  • Alpha-blockers like doxazosin + tamsulosin to those with severe voiding problems (first line).
  • 5-alpha reductase inhibitor like finasteride.
63
Q

BPH

What is the surgical treatment for BPH?

A
  • Transurethral resection of prostate (TURB).
  • Transurethral incision of prostate (TUIP).
  • Transurethral laser-induce prostatectomy (TULIP).
  • Retropubic prostatectomy (open surgery) if v large.
64
Q

URINARY TRACT INFECTIONS

What is the pathophysiology of UTI?

A
  • Inflammatory response of urothelium to bacterial invasion, usually associated with bacteriuria + pyuria.
  • Organisms colonise the urethral meatus + ascend via transurethral route.
65
Q

URINARY TRACT INFECTIONS

What are bacterial virulent factors in UTI?

A
  • Fimbriae/pilli that adhere to urothelium.
  • Acid polysaccharide coat which resists phagocytosis.
  • Toxins.
  • Enzyme production (urease).
66
Q

URINARY TRACT INFECTIONS

What is the aetiology of UTI? Why is it more common in women?

A
  • Strains of uropathogenic E. coli, can be proteus or klebsiella.
  • Shorter urethra + proximity to anus.
67
Q 
URINARY TRACT INFECTIONS
What is the aetiology of...
i) pyelonephritis?
ii) Cystitis?
iii) Prostatitis?
iv) Urethritis?
A

i) Infection usually from bladder, in children most likely reflux or structural/functional abnormalities.
ii) Can be caused from incomplete bladder emptying.
iii) Usually gram -ve like E.coli, enterobacter, sometimes STI like Neisseria gonorrhoea, chlamydia trachomatis.
iv) Gonococcal = neisseria gonorrhoeae, non-gonococcal = chlamydia trachomatis.

68
Q

URINARY TRACT INFECTIONS

What classifies a UTI as being recurrent or complicated?

A
  • Recurrent UTI = (>2 episodes in 6m, >3 in 12m) caused by re-infection, bacterial persistence or unresolved infection.
  • Complicated UTI = affects someone with an abnormal urinary tract, man, pregnant lady, child, immunocompromised.
69
Q

URINARY TRACT INFECTIONS

What are the risk factors for UTIs?

A
  • Female.
  • Sexual activity.
  • Catheter.
  • Stones.
  • Immunosuppression.
70
Q

URINARY TRACT INFECTIONS

What is the clinical presentation of pyelonephritis?

A
  • Loin pain/tenderness.
  • Fever/nausea.
  • Pyuria.
71
Q

URINARY TRACT INFECTIONS

What is the clinical presentation of cystitis?

A
  • Dysuria, frequency + urgency.
  • Suprapubic pain.
  • Haematuria.
72
Q

URINARY TRACT INFECTIONS

What is the clinical presentation of prostatitis?

A
  • Pelvic/penile/rectal pain.
  • Dysuria.
  • Systemically unwell (fever, nausea, malaise).
73
Q

URINARY TRACT INFECTIONS

What is the clinical presentation of urethritis?

A
  • Urethral discharge (if gonoccoal).
  • Urethral pain.
  • Dysuria w/ smell
74
Q

URINARY TRACT INFECTIONS

What are the investigations for UTI?

A
  • Urine dipstick, cloudy, offensive smell, fresh sample not catheter.
  • Midstream specimen of urine culture + sensitivity sample.
  • Bloods (CRP raised), urine dipstick.
75
Q

URINARY TRACT INFECTIONS
What are the investigations for…
i) prostatitis?
ii) recurrent/complicated UTI?

A

i) Semen cultures ± STI screen, digital rectal exam.

ii) Post-void bladder scan, USS renal tract/pelvis, flexible cystoscopy.

76
Q

URINARY TRACT INFECTIONS

What is the treatment for UTI?

A 
Uncomplicated...
- Trimethoprim/nitrofurantoin.
- If fails, Abx sensitive to culture.
Pyelonephritis...
- Co-amoxiclav, drain obstructed kidney.
Prostatitis...
- Ciprofloxacin as can penetrate prostatic fluid.
77
Q

URINARY TRACT INFECTIONS

What are the cautions of trimethoprim + nitrofurantoin in pregnancy?

A
  • Avoid trimethoprim 1st trimester.

- Avoid nitrofurantoin 3rd trimester.

78
Q

URINARY TRACT INFECTIONS

What is the treatment for recurrent UTIs?

A
  • Increase fluid intake + regular voiding.
  • Void pre + post intercourse.
  • Abx prophylaxis.
79
Q

EPIDIDYMO-ORCHITIS

What is the pathophysiology of epididymo-orchitis?

A
  • Inflammation of epididymis + testicle, most common route of infection is spreading from urethra, second is from bladder.
80
Q

EPIDIDYMO-ORCHITIS

What is the aetiology of epididymo-orchitis?

A
  • Most commonly STI in men <35y/o.

- >35y/o then gram -ve enteric organisms (UTI), viral.

81
Q

EPIDIDYMO-ORCHITIS

What is the clinical presentation of epididymo-orchitis?

A
  • Unilateral scrotal pain + swelling.
  • Sweats/fever.
  • Dysuria.
    (If STI urethral discharge).
82
Q

EPIDIDYMO-ORCHITIS

What are the investigations for epididymo-orchitis?

A

RULE OUT TORSION.
- First-void urine, uretrhal swba, MSU.
Treatment = STI advice, if UTI = ciprofloxacin.

83
Q

NEPHRITIC SYNDROME

What is the pathophysiology of nephritic syndrome?

A
  • There is immune complex deposition in glomerular capillary leading to neutrophil recruitment + inflammation causing damage to the glomerular capillary memrabne – podocytes develop large pores.
  • This allows blood with RBCs, WBCs, protein etc. to leak into Bowman’s capsule + excreted into urine.
84
Q

NEPHRITIC SYNDROME

What is the aetiology of nephritis syndrome?

A
  • IgA nephropathy.
  • Goodpasture’s syndrome (anti-glomerular basement membrane disease).
  • Post-strep infection.
  • SLE.
  • Anti-neutrophil cytoplasmic antibody (ANCA).
85
Q

NEPHRITIC SYNDROME

What is Goodpasture’s syndrome

A
  • Autoantibodies to type IV collagen which is present in glomerular + alveolar basement membranes are produced causing damage.
86
Q

NEPHRITIC SYNDROME

What is the clinical presentation of nephritis syndrome?

A
  • Haematuria.
  • Proteinuria.
  • HTN (compensatory as glomerulus damage restricts blood flow).
  • Oedema.
87
Q

NEPHRITIC SYNDROME

What are the investigations for nephritis syndrome?

A
  • Urine dipstick (protein + blood).
  • Urine MC&S, RBC cast, Bence Jones protein.
  • Serum autoantibodies.
  • Renal biopsy = diagnostic.
88
Q

NEPHRITIC SYNDROME

What is the treatment for nephritic syndrome?

A
  • Treat underlying.
  • Treat HTN with salt restriction, loop diuretics + ACEi/ARB.
  • Corticosteroids.
89
Q

NEPHROTIC SYNDROME

What is the pathophysiology of nephrotic syndrome?

A
  • Massively increased filtration of macromolecules across the glomerular capillary wall due to structural + functional abnormalities of the glomerular podocytes.
90
Q

NEPHROTIC SYNDROME

What can nephrotic syndrome be primary to?

A
  • Minimal change disease.
  • Membranous nephropathy.
  • Focal segmental glomerulosclerosis (FSGS).
  • Membranoproliferative glomerulonephritis.
91
Q

NEPHROTIC SYNDROME

What is minimal change disease?

A
  • Abnormal function of the podocytes (diffuse loss of podocyte foot processes, vacuolation + appearance of microvilli).
92
Q 
NEPHROTIC SYNDROME
What is...
i) membranous nephropathy?
ii) FSGS?
iii) membranoproliferative glomerulonephritis?
A

i) Immune-mediated damage.
ii) Podocyte injury/death.
iii) Pathology in the glomerular basement membrane/endothelial cells.

93
Q

NEPHROTIC SYNDROME

What are secondary causes of nephrotic syndrome?

A
  • DM.
  • Drugs like NSAIDs.
  • Autoimmune like SLE.
94
Q

NEPHROTIC SYNDROME

What is the clinical presentation of nephrotic syndrome?

A

Triad of…

  • Heavy proteinuria >3g/24h.
  • Hypoalbuminaemia.
  • Oedema (ankles/face/abdomen).
95
Q

NEPHROTIC SYNDROME

What are the potential complications of nephrotic syndrome?

A
  • Thromboembolism.
  • Infection.
  • Hyperlipidaemia.
96
Q

NEPHROTIC SYNDROME

What are the investigations for nephrotic syndrome?

A
  • Serum albumin, U+Es, eGFR.
  • Urine dipstick.
  • Serum autoantibodies.
  • Renal biopsy.
97
Q

NEPHROTIC SYNDROME

What is the unique feature seen in minimal change disease?

A
  • Light microscopy shows no change.

- Electron microscopy shows fused podocytes.

98
Q

NEPHROTIC SYNDROME

What is the treatment for nephrotic syndrome?

A

Reduce oedema…
- Fluid + salt restriction, loop diuretic.
Treat underlying cause…
- Corticosteroids in minimal change disease.
Reduce proteinuria…
- ACEi/ARBs.

99
Q

NEPHROTIC SYNDROME

How do you prevent complications in nephrotic syndrome?

A
  • Thromboembolism with anti-coagulation (LMWH, warfarin).
  • Infection with vaccinations.
  • Hyperlipidaemia with statins.
100
Q

POLYCYSTIC KIDNEY DISEASE

What is the pathophysiology of ADPKD?

A
  • Mutation in PKD1 which codes polycystin, an integral membrane protein which regulates tubular + vascular development in kidneys + other organs.
  • Cysts develop throughout both kidneys + increase in size with age causing renal enlargement + progressive destruction of renal tissue.
101
Q

POLYCYSTIC KIDNEY DISEASE

What is the pathophysiology of ARPKD?

A
  • Dilation + elongation of renal collecting ducts leads to bilaterally enlarged + cystic kidneys.
  • Normal at birth, can later develop interstitial fibrosis + tubular atrophy > end-stage renal failure.
102
Q

POLYCYSTIC KIDNEY DISEASE

What is the pathophysiology of acquired PKD?

A
  • Renal injury/ischaemia leads to abnormal cell proliferation where cysts develop over time.
103
Q

POLYCYSTIC KIDNEY DISEASE

What is the aetiology of PKD?

A

ADPKD…
- PKD1 (chromosome 16) in 85%, more severe ESRF by 50s.
- PKD2 (chromosome 4), slower course, ESRF by 70s.
ARPKD…
- Fibrocystin gene (PKHD1, responsible for tubulogenesis).

104
Q

POLYCYSTIC KIDNEY DISEASE

What is the renal clinical presentation of ADPKD?

A
  • Loin pain (cyst haemorrhagE).
  • Haematuria (visible).
  • HTN.
  • Renal calculi.
  • Palpable costovertebral masses.
105
Q

POLYCYSTIC KIDNEY DISEASE

What is the extra-renal clinical presentation of ADPKD?

A
  • Liver cysts.

- Intracranial aneurysms like subarachnoid haemorrhage as polycystin involved in production of berry aneurysms.

106
Q

POLYCYSTIC KIDNEY DISEASE

What is the clinical presentation of ARPKD?

A

Presents ante/perinatally…

  • Renal cysts + enlargement.
  • Hepatic fibrosis > portal HTN.
  • Poor prognosis.
107
Q

POLYCYSTIC KIDNEY DISEASE

What is the clinical presentation for acquired polycystic kidney disease?

A
  • No genetic mutation, family history.
  • Normal kidney size.
  • Risk factor for RCC.
108
Q

POLYCYSTIC KIDNEY DISEASE

What are the investigations for PKD?

A
  • Family Hx, HTN.
  • Urinalysis.
  • USS kidney preferred.
  • Total kidney volume = prognostic.
109
Q

POLYCYSTIC KIDNEY DISEASE

What is the treatment for ADPKD?

A
  • Treat BP NOT CCB.
  • Antibiotics if infection.
  • Water intake 3–4L/day may suppress cyst growth.
  • Tolvaptan to help slow kidney function decline.
110
Q

TESTICULAR TORSION

What is the pathophysiology + aetiology of testicular torsion?

A
  • Occlusion of testicular blood vessels from torsion of spermatic cord, can lead to ischaemia.
  • Trauma, often follows sport or physical activity.
  • RF = high insertion of tunica vaginalis.
111
Q

TESTICULAR TORSION

What is the clinical presentation of testicular torsion?

A
  • Sudden, severe pain in one testis.
  • Acute swelling of scrotum.
  • Vomiting.
112
Q

TESTICULAR TORSION

What is the major complication of testicular torsion?

A
  • If left untreated >6h testicular atrophy can result meaning testicle may not be viable requiring semi-urgent orchidectomy.
113
Q

TESTICULAR TORSION

What are the investigations and treatment for testicular torsion?

A
  • Examination sufficient > surgical exploration + manually reduced, verify by scrotal doppler USS.
114
Q

EPIDIDYMAL CYST

What is the pathophysiology + aetiology of epididymal cyst?

A
  • Extra-testicular, spherical cyst in the head of the epididymis.
  • May contain clear or milky (spermatocele) fluid, they lie above + behind testis.
  • Possibly obstruction of epididymis.
115
Q

EPIDIDYMAL CYST

What is the clinical presentation + investigations of epididymal cyst?

A
  • Lump, often multiple + bilateral, usually asymptomatic.

- Scrotal USS, transilluminate scrotum.

116
Q

HYDROCELE

What is the pathophysiology of hydrocele? What is the difference between primary/secondary?

A
  • Abnormal collection of fluid within the tunica vaginalis.
    Primary (congenital)…
  • Associated with a patent processus vaginalis, typically resolves in first year of life.
    Secondary…
  • Testis tumour/trauma/infection.
117
Q

HYDROCELE

What is the clinical presentation of hydrocele?

A
  • Scrotal enlargement with a non-tender, smooth cystic swelling.
  • Anterior to + below the testis transilluminate.
118
Q

HYDROCELE

What are the investigations + treatment of hydrocele?

A
  • Scrotal USS, transilluminate.

- Spontaneously or aspiration.

119
Q

VARICOCELE

What is the pathophysiology of varicocele?

A
  • An abnormal dilatation of the testicular veins in the pampiniform plexus in the scrotum.
  • Heat generated by varicocele affects sperm quality + proteins required for healthy sperm are reduced.
120
Q

VARICOCELE

What is the aetiology of varicocele?

A
  • Venous reflux.
  • More common on left due to angle of left testicular vein entering left renal vein, if obstructed (RCC) can cause backflow.
121
Q

VARICOCELE

What is the clinical presentation of varicocele?

A
  • Visible distended scortal blood vessels.
  • Scrotum feels like ‘a bag of worms’.
  • Affected side hangs lower.
122
Q

VARICOCELE

What are the investigations + treatment of varicocele?

A
  • Observation, scrotal USS.

- Repair via surgery or embolisation.

123
Q

ALPHA-1 BLOCKERS

What is the mechanism? Give an example. What are the side effects?

A
  • Cause vasodilation + reduce smooth muscle tone in prostate + bladder so there’s reduced resistance to bladder outflow.
  • Doxazosin, tamsulosin.
  • Hypotension, depression, retrograde ejaculation.
124
Q

5-ALPHA-REDUCTASE INHIBITOR

What is the mechanism. Give an example. What are side effects and caution?

A
  • Decreased conversion of testosterone to the more potent androgen dihydrotestosterone, reduces prostate size.
  • Finasteride.
  • Decreased libido, impotency, excreted in semen so use condoms.
125
Q

ERECTILE DYSFUNCTION

What are the causes of erectile dysfunction? What are the risk factors?

A
  • Organic (vasculogenic, neurogenic, hormonal, anatomical).
  • Psychogenic.
  • Obesity, lack of exercise, smoking, DM
126
Q

ERECTILE DYSFUNCTION

What are the characteristics of psychogenic erectile dysfunction?

A
  • Sudden.
  • Situational.
  • Younger males.
127
Q

ERECTILE DYSFUNCTION

What is the non-pharmacological treatment for erectile dysfunction?

A
  • Lose weight.
  • Stop smoking.
  • Education + counselling of pt and partner.
128
Q

ERECTILE DYSFUNCTION
What is the…

i) first line
ii) second line
iii) third line

pharmacological treatment for erectile dysfunction?

A

i) Phosphodiesterase inhibitor (sildenafil, viagra), vasodilation and so increased arterial blood flow to penis.
ii) Intracavernous injections, vacuum device.
iii) Penile prosthesis implantation.

129
Q

STIs

What is the generic rule of thumb for STIs? What are the risk factors?

A
  • Discharge = chlamydia/gonorrhoea.
  • Ulcers = syphilis/herpes.
  • <25y/o, MSM.
130
Q

STIs

What are the investigations for STIs?

A
  • Female = vaginal swab.
  • Male = first-void urine.
  • Nucleic acid amplification test (NAAT).
  • Other relevant swabs.
131
Q

STIs
What is the treatment for…

i) Chlamydia?
ii) Gonorrhoea?
iii) Syphilis?

A

i) Doxycycline.
ii) IM ceftriaxone, PO azithromycin.
iii) IM penicillin.

Phase 2a (12 decks)

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