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Phase 2a > Renal + urogenital > Flashcards

Renal + urogenital Flashcards

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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
CHRONIC KIDNEY DISEASE | What is the clinical presentation of CKD?
- Anaemia (pallor, lethargy). - Amenorrhoea/erectile dysfunction. - HTN. - Nocturia, polyuria, oedema.
26
CHRONIC KIDNEY DISEASE | What are the investigations for CKD?
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.
27
CHRONIC KIDNEY DISEASE | What is the treatment for CKD stages 1–4?
- Maintain BP targeting RAAS. - Control blood sugar if DM. - Smoking cessation. - Eat healthy, exercise. - Stop nephrotoxic drugs. - Antiplatelets/coagulants, statins, vitamin D.
28
CHRONIC KIDNEY DISEASE | What is the treatment for end-stage renal failure?
- Dialysis. | - Transplant.
29
CHRONIC KIDNEY DISEASE | What are the two types of dialysis?
- Haemodialysis, AV fistula, 3x/week | - Peritoneal dialysis, peritoneal catheter, daily (as one long exchange or shorter ones).
30
CHRONIC KIDNEY DISEASE | What are the complications with the 2 types of dialysis?
- Haemo = hypotension, nausea, fever, impact on daily life (frequent dialysis). - Peritoneal = peri-catheter leak, abdominal wall herniation, intestinal perforation.
31
CHRONIC KIDNEY DISEASE | What are the benefits with the 2 types of dialysis.
- 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.
32
CHRONIC KIDNEY DISEASE | What are the 2 types of kidney transplants?
- 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.
33
CHRONIC KIDNEY DISEASE | What treatment do you need to go on post-kidney transplantation and what is the effect of this?
Chronic immunosuppression. - Malignancy. - Infection. - Side effects of other drugs.
34
RENAL CELL CARCINOMA | What is the pathophysiology of RCC?
- 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.
35
RENAL CELL CARCINOMA | What is the epidemiology + risk factors for RCC?
- 90% renal cancers, 55y/o M:F = 2:1. - Smoking. - Obesity. - HTN.
36
RENAL CELL CARCINOMA | What genetic condition is linked to RCC?
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.
37
RENAL CELL CARCINOMA | What is the clinical presentation of RCC?
- Haematuria. - Abdominal mass. - Loin pain. - Cancer (weight loss, malaise).
38
RENAL CELL CARCINOMA | What are the investigations for RCC?
- BP from increased renin. - Abdominal/pelvis USS. - Urinalysis. - Flexible cystoscopy + biopsy.
39
RENAL CELL CARCINOMA | What is the treatment for RCC?
- Radical nephrectomy. | - Cryotherapy + radiofrequency ablation for unfit/unwilling patients.
40
TRANSITIONAL CELL CARCINOMA | What is the pathophysiology of TCC?
- Arises from bladder (50%), ureter + renal pelvis. | - Common metastases = lymph nodes, lung, breast, skin.
41
TRANSITIONAL CELL CARCINOMA | What is the epidemiology + risk factors for TCC?
- M:F = 4:1, >40y/o. - Smoking. - Occupational exposure (rubber factories due to aromatic amines). - Male. - Family Hx.
42
TRANSITIONAL CELL CARCINOMA | What is the clinical presentation of TCC?
- PAINLESS haematuria. - Frequency/urgency/dysuria. - Urinary tract obstruction.
43
TRANSITIONAL CELL CARCINOMA | What are the investigations for TCC?
- Cystoscopy + biopsy = diagnostic. - Urine cytology. - CT urogram.
44
TRANSITIONAL CELL CARCINOMA | What is the treatment for TCC?
- Trans-urethral resection of bladder tumour (TURBT) with chemotherapy. - Radical cystectomy (radiotherapy if unfit/unwilling) if muscle invasive. - Palliative if invasion beyond bladder.
45
TESTICULAR CARCINOMA | What is the pathophysiology of testicular carcinoma?
- 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.
46
TESTICULAR CARCINOMA | What are the risk factors for testicular carcinoma?
- Undescended testes. | - Family Hx.
47
TESTICULAR CARCINOMA | What is the clinical presentation of testicular carcinoma?
- Painless lump in testicle (CANCER TILL PROVEN OTHERWISE). | - Can present with metastases in lungs = cough, dyspnoea, para-aortic lymph nodes causing back pain.
48
TESTICULAR CARCINOMA | What are the investigations of testicular carcinoma?
- Ultrasound scrotum - Serum concentrations of tumour markers alpha-fetoprotein (seminomas only) + beta-human chorionic gonadotrophin elevated. - CXR/CT chest, abdomen + pelvis for staging.
49
TESTICULAR CARCINOMA | What is the treatment for testicular carcinoma?
- Orchidectomy, offer sperm banking. - Seminoma radiotherapy if spread below diaphragm, chemotherapy if above. - Teratoma = chemotherapy if metastases.
50
PROSTATIC CARCINOMA | What is the pathophysiology of prostatic carcinoma?
- Most are adenocarcinomas typically affecting peripheral zone of prostate. - Commonly metastasise to lymph nodes + bone (can spread locally bladder, rectum).
51
PROSTATIC CARCINOMA | What is the aetiology of prostatic carcinoma?
- Genetic, family history. | - Can develop from benign prostatic hypertrophy.
52
PROSTATIC CARCINOMA | What is the screening for prostate carcinoma?
- 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.
53
PROSTATIC CARCINOMA | What PSA levels are normal/abnormal?
PSA > 4.0ng/mL = abnormal, >10ng/mL = 50% men have prostate cancer.
54
PROSTATIC CARCINOMA | What are the advantages + disadvantages of screening in prostate carcinoma?
- Can lead to early diagnosis, treatment + so cure. | - Uncertain natural history, screening leads to over diagnosis + treatment.
55
PROSTATIC CARCINOMA | What is the clinical presentation of prostate carcinoma?
- Nocturia, hesitancy, poor stream, terminal dribbling, obstruction. - Weight loss ± bone pain suggest metastases.
56
PROSTATIC CARCINOMA | What are the investigations for prostate carcinoma?
- Serum PSA elevated. - Digital rectal examination = hard, irregular, craggy prostate. - Transrectal ultrasound + biopsy. - Gleason grading, higher score = more aggressive.
57
PROSTATIC CARCINOMA | What is the treatment for prostate carcinoma?
If localised, watchful waiting or radical prostatectomy or radiotherapy. - Metastatic = palliative treatment like hormone therapy.
58
BPH | What is the pathophysiology of benign prostatic hyperplasia (BPH)?
- Benign nodular or diffuse proliferation of musculofibrous + glandular layers of the prostate, it's the inner (transitional) zone which enlarges, median lobe.
59
BPH | What is the clinical presentation of BPH?
LUTS... - Nocturia, frequency, urgency, post-micturition dribbling, poor stream/flow, hesitancy, overflow incontinence, haematuria. - Bladder stones, UTI.
60
BPH | What are the investigations for BPH?
- 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
BPH | What is the generic treatment for BPH?
- 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
BPH | What is the medical therapy for BPH?
- Alpha-blockers like doxazosin + tamsulosin to those with severe voiding problems (first line). - 5-alpha reductase inhibitor like finasteride.
63
BPH | What is the surgical treatment for BPH?
- Transurethral resection of prostate (TURB). - Transurethral incision of prostate (TUIP). - Transurethral laser-induce prostatectomy (TULIP). - Retropubic prostatectomy (open surgery) if v large.
64
URINARY TRACT INFECTIONS | What is the pathophysiology of UTI?
- Inflammatory response of urothelium to bacterial invasion, usually associated with bacteriuria + pyuria. - Organisms colonise the urethral meatus + ascend via transurethral route.
65
URINARY TRACT INFECTIONS | What are bacterial virulent factors in UTI?
- Fimbriae/pilli that adhere to urothelium. - Acid polysaccharide coat which resists phagocytosis. - Toxins. - Enzyme production (urease).
66
URINARY TRACT INFECTIONS | What is the aetiology of UTI? Why is it more common in women?
- Strains of uropathogenic E. coli, can be proteus or klebsiella. - Shorter urethra + proximity to anus.
67
``` URINARY TRACT INFECTIONS What is the aetiology of... i) pyelonephritis? ii) Cystitis? iii) Prostatitis? iv) Urethritis? ```
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
URINARY TRACT INFECTIONS | What classifies a UTI as being recurrent or complicated?
- 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
URINARY TRACT INFECTIONS | What are the risk factors for UTIs?
- Female. - Sexual activity. - Catheter. - Stones. - Immunosuppression.
70
URINARY TRACT INFECTIONS | What is the clinical presentation of pyelonephritis?
- Loin pain/tenderness. - Fever/nausea. - Pyuria.
71
URINARY TRACT INFECTIONS | What is the clinical presentation of cystitis?
- Dysuria, frequency + urgency. - Suprapubic pain. - Haematuria.
72
URINARY TRACT INFECTIONS | What is the clinical presentation of prostatitis?
- Pelvic/penile/rectal pain. - Dysuria. - Systemically unwell (fever, nausea, malaise).
73
URINARY TRACT INFECTIONS | What is the clinical presentation of urethritis?
- Urethral discharge (if gonoccoal). - Urethral pain. - Dysuria w/ smell
74
URINARY TRACT INFECTIONS | What are the investigations for UTI?
- Urine dipstick, cloudy, offensive smell, fresh sample not catheter. - Midstream specimen of urine culture + sensitivity sample. - Bloods (CRP raised), urine dipstick.
75
URINARY TRACT INFECTIONS What are the investigations for... i) prostatitis? ii) recurrent/complicated UTI?
i) Semen cultures ± STI screen, digital rectal exam. | ii) Post-void bladder scan, USS renal tract/pelvis, flexible cystoscopy.
76
URINARY TRACT INFECTIONS | What is the treatment for UTI?
``` Uncomplicated... - Trimethoprim/nitrofurantoin. - If fails, Abx sensitive to culture. Pyelonephritis... - Co-amoxiclav, drain obstructed kidney. Prostatitis... - Ciprofloxacin as can penetrate prostatic fluid. ```
77
URINARY TRACT INFECTIONS | What are the cautions of trimethoprim + nitrofurantoin in pregnancy?
- Avoid trimethoprim 1st trimester. | - Avoid nitrofurantoin 3rd trimester.
78
URINARY TRACT INFECTIONS | What is the treatment for recurrent UTIs?
- Increase fluid intake + regular voiding. - Void pre + post intercourse. - Abx prophylaxis.
79
EPIDIDYMO-ORCHITIS | What is the pathophysiology of epididymo-orchitis?
- Inflammation of epididymis + testicle, most common route of infection is spreading from urethra, second is from bladder.
80
EPIDIDYMO-ORCHITIS | What is the aetiology of epididymo-orchitis?
- Most commonly STI in men <35y/o. | - >35y/o then gram -ve enteric organisms (UTI), viral.
81
EPIDIDYMO-ORCHITIS | What is the clinical presentation of epididymo-orchitis?
- Unilateral scrotal pain + swelling. - Sweats/fever. - Dysuria. (If STI urethral discharge).
82
EPIDIDYMO-ORCHITIS | What are the investigations for epididymo-orchitis?
RULE OUT TORSION. - First-void urine, uretrhal swba, MSU. Treatment = STI advice, if UTI = ciprofloxacin.
83
NEPHRITIC SYNDROME | What is the pathophysiology of nephritic syndrome?
- 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
NEPHRITIC SYNDROME | What is the aetiology of nephritis syndrome?
- IgA nephropathy. - Goodpasture's syndrome (anti-glomerular basement membrane disease). - Post-strep infection. - SLE. - Anti-neutrophil cytoplasmic antibody (ANCA).
85
NEPHRITIC SYNDROME | What is Goodpasture's syndrome
- Autoantibodies to type IV collagen which is present in glomerular + alveolar basement membranes are produced causing damage.
86
NEPHRITIC SYNDROME | What is the clinical presentation of nephritis syndrome?
- Haematuria. - Proteinuria. - HTN (compensatory as glomerulus damage restricts blood flow). - Oedema.
87
NEPHRITIC SYNDROME | What are the investigations for nephritis syndrome?
- Urine dipstick (protein + blood). - Urine MC&S, RBC cast, Bence Jones protein. - Serum autoantibodies. - Renal biopsy = diagnostic.
88
NEPHRITIC SYNDROME | What is the treatment for nephritic syndrome?
- Treat underlying. - Treat HTN with salt restriction, loop diuretics + ACEi/ARB. - Corticosteroids.
89
NEPHROTIC SYNDROME | What is the pathophysiology of nephrotic syndrome?
- Massively increased filtration of macromolecules across the glomerular capillary wall due to structural + functional abnormalities of the glomerular podocytes.
90
NEPHROTIC SYNDROME | What can nephrotic syndrome be primary to?
- Minimal change disease. - Membranous nephropathy. - Focal segmental glomerulosclerosis (FSGS). - Membranoproliferative glomerulonephritis.
91
NEPHROTIC SYNDROME | What is minimal change disease?
- Abnormal function of the podocytes (diffuse loss of podocyte foot processes, vacuolation + appearance of microvilli).
92
``` NEPHROTIC SYNDROME What is... i) membranous nephropathy? ii) FSGS? iii) membranoproliferative glomerulonephritis? ```
i) Immune-mediated damage. ii) Podocyte injury/death. iii) Pathology in the glomerular basement membrane/endothelial cells.
93
NEPHROTIC SYNDROME | What are secondary causes of nephrotic syndrome?
- DM. - Drugs like NSAIDs. - Autoimmune like SLE.
94
NEPHROTIC SYNDROME | What is the clinical presentation of nephrotic syndrome?
Triad of... - Heavy proteinuria >3g/24h. - Hypoalbuminaemia. - Oedema (ankles/face/abdomen).
95
NEPHROTIC SYNDROME | What are the potential complications of nephrotic syndrome?
- Thromboembolism. - Infection. - Hyperlipidaemia.
96
NEPHROTIC SYNDROME | What are the investigations for nephrotic syndrome?
- Serum albumin, U+Es, eGFR. - Urine dipstick. - Serum autoantibodies. - Renal biopsy.
97
NEPHROTIC SYNDROME | What is the unique feature seen in minimal change disease?
- Light microscopy shows no change. | - Electron microscopy shows fused podocytes.
98
NEPHROTIC SYNDROME | What is the treatment for nephrotic syndrome?
Reduce oedema... - Fluid + salt restriction, loop diuretic. Treat underlying cause... - Corticosteroids in minimal change disease. Reduce proteinuria... - ACEi/ARBs.
99
NEPHROTIC SYNDROME | How do you prevent complications in nephrotic syndrome?
- Thromboembolism with anti-coagulation (LMWH, warfarin). - Infection with vaccinations. - Hyperlipidaemia with statins.
100
POLYCYSTIC KIDNEY DISEASE | What is the pathophysiology of ADPKD?
- 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
POLYCYSTIC KIDNEY DISEASE | What is the pathophysiology of ARPKD?
- 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
POLYCYSTIC KIDNEY DISEASE | What is the pathophysiology of acquired PKD?
- Renal injury/ischaemia leads to abnormal cell proliferation where cysts develop over time.
103
POLYCYSTIC KIDNEY DISEASE | What is the aetiology of PKD?
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
POLYCYSTIC KIDNEY DISEASE | What is the renal clinical presentation of ADPKD?
- Loin pain (cyst haemorrhagE). - Haematuria (visible). - HTN. - Renal calculi. - Palpable costovertebral masses.
105
POLYCYSTIC KIDNEY DISEASE | What is the extra-renal clinical presentation of ADPKD?
- Liver cysts. | - Intracranial aneurysms like subarachnoid haemorrhage as polycystin involved in production of berry aneurysms.
106
POLYCYSTIC KIDNEY DISEASE | What is the clinical presentation of ARPKD?
Presents ante/perinatally... - Renal cysts + enlargement. - Hepatic fibrosis > portal HTN. - Poor prognosis.
107
POLYCYSTIC KIDNEY DISEASE | What is the clinical presentation for acquired polycystic kidney disease?
- No genetic mutation, family history. - Normal kidney size. - Risk factor for RCC.
108
POLYCYSTIC KIDNEY DISEASE | What are the investigations for PKD?
- Family Hx, HTN. - Urinalysis. - USS kidney preferred. - Total kidney volume = prognostic.
109
POLYCYSTIC KIDNEY DISEASE | What is the treatment for ADPKD?
- Treat BP NOT CCB. - Antibiotics if infection. - Water intake 3–4L/day may suppress cyst growth. - Tolvaptan to help slow kidney function decline.
110
TESTICULAR TORSION | What is the pathophysiology + aetiology of testicular torsion?
- 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
TESTICULAR TORSION | What is the clinical presentation of testicular torsion?
- Sudden, severe pain in one testis. - Acute swelling of scrotum. - Vomiting.
112
TESTICULAR TORSION | What is the major complication of testicular torsion?
- If left untreated >6h testicular atrophy can result meaning testicle may not be viable requiring semi-urgent orchidectomy.
113
TESTICULAR TORSION | What are the investigations and treatment for testicular torsion?
- Examination sufficient > surgical exploration + manually reduced, verify by scrotal doppler USS.
114
EPIDIDYMAL CYST | What is the pathophysiology + aetiology of epididymal cyst?
- 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
EPIDIDYMAL CYST | What is the clinical presentation + investigations of epididymal cyst?
- Lump, often multiple + bilateral, usually asymptomatic. | - Scrotal USS, transilluminate scrotum.
116
HYDROCELE | What is the pathophysiology of hydrocele? What is the difference between primary/secondary?
- 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
HYDROCELE | What is the clinical presentation of hydrocele?
- Scrotal enlargement with a non-tender, smooth cystic swelling. - Anterior to + below the testis transilluminate.
118
HYDROCELE | What are the investigations + treatment of hydrocele?
- Scrotal USS, transilluminate. | - Spontaneously or aspiration.
119
VARICOCELE | What is the pathophysiology of varicocele?
- 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
VARICOCELE | What is the aetiology of varicocele?
- Venous reflux. - More common on left due to angle of left testicular vein entering left renal vein, if obstructed (RCC) can cause backflow.
121
VARICOCELE | What is the clinical presentation of varicocele?
- Visible distended scortal blood vessels. - Scrotum feels like 'a bag of worms'. - Affected side hangs lower.
122
VARICOCELE | What are the investigations + treatment of varicocele?
- Observation, scrotal USS. | - Repair via surgery or embolisation.
123
ALPHA-1 BLOCKERS | What is the mechanism? Give an example. What are the side effects?
- Cause vasodilation + reduce smooth muscle tone in prostate + bladder so there's reduced resistance to bladder outflow. - Doxazosin, tamsulosin. - Hypotension, depression, retrograde ejaculation.
124
5-ALPHA-REDUCTASE INHIBITOR | What is the mechanism. Give an example. What are side effects and caution?
- Decreased conversion of testosterone to the more potent androgen dihydrotestosterone, reduces prostate size. - Finasteride. - Decreased libido, impotency, excreted in semen so use condoms.
125
ERECTILE DYSFUNCTION | What are the causes of erectile dysfunction? What are the risk factors?
- Organic (vasculogenic, neurogenic, hormonal, anatomical). - Psychogenic. - Obesity, lack of exercise, smoking, DM
126
ERECTILE DYSFUNCTION | What are the characteristics of psychogenic erectile dysfunction?
- Sudden. - Situational. - Younger males.
127
ERECTILE DYSFUNCTION | What is the non-pharmacological treatment for erectile dysfunction?
- Lose weight. - Stop smoking. - Education + counselling of pt and partner.
128
ERECTILE DYSFUNCTION What is the... i) first line ii) second line iii) third line pharmacological treatment for erectile dysfunction?
i) Phosphodiesterase inhibitor (sildenafil, viagra), vasodilation and so increased arterial blood flow to penis. ii) Intracavernous injections, vacuum device. iii) Penile prosthesis implantation.
129
STIs | What is the generic rule of thumb for STIs? What are the risk factors?
- Discharge = chlamydia/gonorrhoea. - Ulcers = syphilis/herpes. - <25y/o, MSM.
130
STIs | What are the investigations for STIs?
- Female = vaginal swab. - Male = first-void urine. - Nucleic acid amplification test (NAAT). - Other relevant swabs.
131
STIs What is the treatment for... i) Chlamydia? ii) Gonorrhoea? iii) Syphilis?
i) Doxycycline. ii) IM ceftriaxone, PO azithromycin. iii) IM penicillin.

Phase 2a (12 decks)

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