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Haroon Phase 2A > GU > Flashcards

GU Flashcards

1
Q

What is the function of the proximal convoluted tubule?

A

Reabsorption of: - some water and Na+ - some other ions - all glucose and amino acids

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2
Q

What is the function of the distal convoluted tubule?

A

Regulating acid-base balance - By secreting H+ and absorbing HCO3- - Also regulates Na+ level

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3
Q

What is the structure of the collecting duct in the kidney?

A

Principal cells: - Regulate Na+ reabsorption and K+ excretion - Respond to aldosterone and ADH Intercalated cells: - Exchange H+ for HCO3-

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4
Q

What is the structure of urothelium?

A
  • Complex stratified epithelium - Can stretch in 3 dimensions - Layer of umbrella cells - make it urine proof
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5
Q

What is the innervation of bladder contraction?

A

Autonomic parasympathetic (cholinergic) - S3-S5 nuclei - Drive detrusor contraction

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6
Q

What is the innervation of bladder relaxation?

A

Autonomic sympathetic (noradrenergic) - T10-L2 nuclei - Urethral contraction (smooth muscle component but remember the main part of the sphincter is skeletal muscle) - Inhibits detrusor contraction

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7
Q

What is the innervation of A-δ fibres (bladder stretch) and C fibres (bladder pain)?

A

Sensory Autonomic - S2-S4 nuclei

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8
Q

Treatment for pyelonephritis

A

Analgesia: Paracetamol - Antibiotics: Ciprofloxacin or co-amoxiclav (if pregnant, give cefalexin) - Refer to hospital if there are signs of sepsis

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9
Q

Treatment for chlamydia

A

First line: doxycycline - if CI or not tolerated: azithromycin - if CI: erythromycin…or ofloxacin but this is CI in pregnancy - Sexual intercourse should be avoided until treatment is complete - Partner must Also be treated

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10
Q

Treatment for gonnorrhoea

A
  • IM ceftriaxone 1g - Refer to GUM clinic
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11
Q

Treatment for early syphilis

A
  • Single deep intramuscular dose of benzathine benzylpenicillin - Refer to GUM clinic - Notify all partners in the last 3 months
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12
Q

What are kidney stones made from?

A

Calcium - Calcium oxalase (80%) - Calcium phosphate (20%) Other types: - Struvite (RF = UTI) (1-5%) - Uric acid (10-20%) - Cystine (1%) - Drug induced (1%)

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13
Q

Aetiology of calcium oxalate stones

A

Low urine volume - Hypercalciuria - Hyperuricosuria - Hyperoxaluria - Hypocitraturia

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14
Q

Aetiology of calcium phosphate stones

A

Low urine volume - Hyperclciuria - Hypocitraturia - High urine pH - Hyperparathyroidism - Renal tubular acidosis

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15
Q

Aetiology of cystine stones

A

Cystinuria, a genetic disorder that causes cystine to leak through the kidneys into the urine

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16
Q

Drugs that impair urine composition

A

Acetazolamide - Allopurinol - Aluminium magnesium hydroxide - Ascorbic acid - Calcium - Furosemide - Laxatives - Vit D - Topiramate

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17
Q

Drugs that crystallise in urine

A

Allopurinol/oxypurinol - Amoxicillin/ampicillin - ceftriaxone - Ephedrine - Indinavir - magnesium trisilicate - Quinolones - Sulphonamides - Triamterene - Zonisamine

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18
Q

Epidemiology of kidney stones

A
  • M:F about 2:1 - Uncommon in children - Age 30-50 but decreasing
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19
Q

Pathophysiology of kidney stones

A
  • Excess solute in collecting duct - Supersaturated urine, favours crystallisation - Stones cause regular outflow obstruction - Hydronephrosis -> dilation + obstruction of renal pelvis
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20
Q

Presentation of kidney stones

A
  • Unilateral loin to groin pain that is colicky (fluctuating) - Patient can’t lie still (DDx = peritonitis) - Haematuria and dysuria - UTI symptoms/recurrent UTIs
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21
Q

Three common obstruction sites for kidney stones

A

Pelvoureteric junction - Pelvic brim (where ureter crosses over iliac vessels) - Vesicoureteral junction

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22
Q

Diagnosis of kidney stones

A

First line: KUBXr - 80% specific for renal stones, cheap + easy Gold standard: Non-contrast CT KUB - 99% specific for stones Bloods: FBC (raised Calcium and Phosphate) U+E (haematuria) Ultrasound if pregnant

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23
Q

Treatment for kidney stones

A
  • Symptomatic -> hydrate, non-opiate analgesia or NSAIDs - Antibiotics if UTI present - Alpha blocker to help stones pass (up to 10mm) - Surgical elective treatment if stones are too big to pass (5mm<)
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24
Q

Methods of surgery for kidney stones

A
  • Extracorporeal shock wave lithotripsy (ESWL) - non-invasive, smaller stones - Percutaneous nephrolithotomy (PCNL) - larger stones, 20mm+ - Uteroscopy (URS) - energy sources including lasers break up stones - Open surgery (last resort when all else fails)
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25
Q

What is acute kidney injury?

A

Abrupt decline in kidney function (hours-days) characterised by high serum creatinine + urea and low urine output

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26
Q

NICE criteria for acute kidney disease (any one)

A
  • Rise in serum creatinine of > 25μmol/L within 48 hours - 50% or greater rise in serum creatinine over 7 days - A fall in urine output to less than 0.5ml/kg/hour for more than 6 consecutive hours
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27
Q

Risk factors for acute kidney injury

A

65+ - Comorbidities - Cognitive impairment (less water intake) - Hypovolaemia of any cause - Oliguria - Nephrotoxic drug use including contrast agents

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28
Q

Why shouldn’t you use contrast agent when kidney disease is suspected?

A

Contrast would need to be excreted by the kidney

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29
Q

Pathophysiology of acute kidney injury

A

Accumulation of usually excreted substances: - K+ (arrhythmias) - Urea (pruritis + uremic frost, confusion if severe) - Fluid (pul + peripheral oedema) - H+ (acidosis)

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30
Q

Pre-renal AKI

A

Due to hypoperfusion of the kidneys, leading to decreased GFR - Hypovolaemia - Reduced cardiac output (cardiac failure, liver failure, sepsis, drugs) - Drugs that reduce blood pressure (ACE-i, ARBs, NSAIDs, loop diuretics)

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31
Q

Renal AKI

A

A consequence of structural damage to the kidney, eg: tubules, glomeruli, interstitium, bvs. May result from persistent pre-renal and post-renal causes, damaging renal cells - Toxins and drugs (eg: antibiotics, contrast agent, chemo) - Vascular causes (eg: vasculitis, thrombosis, etc) - Glomerular, tubular (MC) or interstitial causes

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32
Q

Post-renal AKI

A

Least common (10%) - due to acute obstruction of the flow of urine -> increased intratubular pressure and decreased GFR - Renal stones - Blocked catheter - Enlarged prostate - GU tract tumours - Neurogenic bladder

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33
Q

Diagnosis of AKI

A
  • Establish cause (pre, intra, post) w KDIGO classification - Check K+, H+, urea, creatining w U+E - FBC + CRP check for infection - Renal biopsy will confirm intrarenal cause, ultrasound for post renal
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34
Q

Best way to establish cause of AKI

A

Urea:Creatinine > 100:1 = Prerenal < 40:1 = Renal 40-100:1 = Postrenal

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35
Q

Treatment for AKI

A

Treat complications - Fluid rehydration with IV fluids for pre-Renal AKI - Stop Nephrotoxic medications - Relieve obstruction in post-Renal AKI - last resort = Renal replacement therapy

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36
Q

When would haemodialysis be given for AKI

A

Acidosis (pH<7.1) Fluid overload (oedema) Uremia K+ >6.5 /ECG change

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37
Q

Normal eGFR

A

120mL/min/1.73m2

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38
Q

When is metformin contraindicated?

A

When eGFR < 30

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39
Q

CKD G scores (eGFR)

A

G1. ≥ 90ml/min/1.73m2 G2. 60-90ml/min/1.73m2 G3a. 45-59ml/min/1.73m2 G3b. 30-44ml/min/1.73m2 G4. 25-29ml/min/1.73m2 G5. <15ml/min/1.73m2

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40
Q

Best clinical readings to quantify CKD

A

eGFR - Albumin:creatinine (more sensitive measurement of proteinurea than PCR)

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41
Q

Aetiology of CKD

A

T2DM - Hypertension - Glomerulonephritis - PKD - Nephrotoxic drugs

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42
Q

Risk factors for CKD (other than diseases)

A

Older Age - Family history - Smoking

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43
Q

Pathophysiology of CKD

A
  • Many nephrons damaged, increased burden on the remaining nephrons - Compensatory RAAS but this increases transglomerular pressure -> shearing and loss of BM selective permeability -> proteinuria/haematuria - Angiotensin 2 upregulates TGF-beta and plasminogen activator-inhibitor-1 -> mesangial scarring
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44
Q

Presentation of CKD

A
  • Asymptomatic early on (lots of nephrons = reserve supply) - Symptoms due to substance accumulation + renal damage (diabetic nephropathy) - Pruritis, loss of appetite, nausea, oedema, muscle cramps, pallor
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45
Q

Complications of CKD

A

Anaemia (Low EPO) - Osteodystrophy (Low Vit D activation) - Neuropathy and encephalopathy - CVD and Hypertension - Haematuria and proteinuria

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46
Q

Diagnosis of CKD

A
  • FBC for anaemia - U+E for eGFR - Early morning urine dipstick for haematuria and albumin:creatinine (>70mg/mmol = significant proteinuria) - Ultrasound shows bilateral renal atrophy
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47
Q

Treatment for CKD

A

No cure so treat complications: - Anaemia: Fe + EPO - Osteodystrophy: Vit D supplements - CVD: ACE-i and statins - Oedema: diuretics - Stop NSAIDs - Stage 5 (end stage renal failure) -> RRT (dialysis) - Ultimately if ESRF, cure is renal transplant

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48
Q

CKD A scores (albumin:creatinine)

A

A1. < 3mg/mmol A2. 3-30mg/mmol A3. >30mg/mmol

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49
Q

A patient has a score of A1 combined with G1 or G2. Can they be diagnosed with CKD?

A

No. They need at least an eGFR of <60 or proteinuria

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50
Q

What is chlamydia caused by?

A

Chlamydia trachomatis, a gram negative intracellular bacillus

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51
Q

Epidemiology and risk factors for chlamydia

A
  • Most common STI in the UK - Under 25 and sexually active - New sexual partner or more than one sexual partner in the last year - Lack of consistent condom use - Unprotected sex
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52
Q

Presentation of chlamydia and gonorrhoea

A

Vaginitis and cervicitis - Proctitis - Epididymo-orchitis - Pelvic inflammatory disease - Pharyngitis - Reactive arthritis

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53
Q

Symptoms of lymphogranuloma venereum (a type of chlamydia)

A

Tenesmus - Anorectal discharge (often bloody) and discomfort - Diarrhoea or altered bowel habits

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54
Q

Diagnosis of chlamydia

A

Nucleic acid amplification testing - Women - vulvovaginal or endocervical swab - Men - first-void urine

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55
Q

What do GUM clinics screen for?

A

Chlamydia - Gonorrhoea - Syphilis (blood test) - HIV (blood test)

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56
Q

What is gonorrhoea caused by?

A

Gram-negative diplococcus Neisseria gonorrhoeae - Spread By penetretive Sexual intercourse Most commonly

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57
Q

Risk factors for gonorrhoea

A

Frequent or unprotected Sexual intercourse - Multiple Sexual partners - MSM - Chlamydial infection

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58
Q

Symptoms in gonorrhoea

A

50% of women and 90% of men are symptomatic

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59
Q

Symptoms of rectal and pharyngeal gonorrhoea infection

A

Rectal infection is usually Asymptomatic but may cause anal discharge and pain or discomfort - Pharyngeal is Asymptomatic in Most cases but is occasionally associated with a sore throat

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60
Q

How do nucleic acid amplification tests work?

A

Check if a gonococcal infection is present or not - By looking at gonococcal RNA or DNA

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61
Q

Diagnosis of gonorrhoea

A

Nucleic acid amplifiction testing - Microscopy shows Gram negative diplococci - Swab infected areas

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62
Q

Pathophysiology of syphilis

A

Spirochete bacteria called Treponema pallidumial - Gets in through skin or mucous membranes, replicates and then disseminates through the body

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63
Q

Risk factors for syphilis

A

MSM - IVDU - Sex workers - Multiple or unprotected Sexual partners

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64
Q

Primary syphilis

A
  • Painless ulcer called a ‘chancre’ at the original site of infection (usually genitals) - Femoral lymphadenopaty - Presents 9-90 days after exposure - Usually resolves spontaneously over 3-10 weeks
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65
Q

Secondary syphilis

A
  • Systemic features, skin lesions, alopecia, mucous patches and early neurosyphilis - Presents 4-12 weeks after initial chancre - Untreated symptoms slowly resolve over 3-12 weeks but may recur
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66
Q

Latent syphilis

A
  • Asymptomatic - Less than 2 years duration from initial infection - Late latent - more than 2 years
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67
Q

Tertiary syphilis

A
  • Gummatous, cardiovascular and neuro syphilis - Presents 15-40 years after initial infection
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68
Q

Diagnosis of syphilis

A

Antibody testing for T.pallidum - Samples from site of infection Can be tested to confirm the presence of T.pallidum with dark field Microscopy and PCR

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69
Q

Five most common UTI pathogens

A

Klebsiella E.coli Enterobacter Proteus S.saphrophyticus MC is uropathogenic e.coli

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70
Q

Why are females more affected by UTIs?

A

Shorter urethra - Closer to anus - Easier for bacteria to colonise

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71
Q

Diagnosis of all types of UTI

A

First line:✨Urine dipstick✨ +ve leukocytes +ve nitrites (bc bacteria break down nitrates into nitrites) +/- haematuria Gold standard: Midstream MC + S - Confirms UTI - Identifies pathogen

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72
Q

What is pyelonephritis?

A

Infection of the renal parenchyma and upper ureter, ascending transurethral spread

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73
Q

Most common causative pathogens of pyelonephritis (most to least common)

A

Uropathogenic E.Coli - Kleblsiella - Proteus - Pseudomonas - Enterobacter

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74
Q

Presentation of pyelonephritis

A

Triad: loin pain, fever, n+v

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75
Q

Patients who have significant symptoms or do not respond to treatment w pyelonephritis

A

Renal abscess - Kidney Stones

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76
Q

What is cystitis?

A

UPEC infection of the bladder - Most common in young sexually active women

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77
Q

Aetiology of cystitis

A

urine stasis - bladder lining damage - Catheters

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78
Q

Presentation of cystitis

A

Suprapubic tenderness and discomfort, worse with a full bladder - High frequency and urgency - Visible Haematuria

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79
Q

Infective vs non-infective urethritis

A

Infective: Gonococcal (LC) and non-gonococcal (MC, chlamydia) Non-infective: Trauma

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80
Q

Risk factors for urethritis

A

MSM and unprotected sex

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81
Q

Presentation of lower urinary tract infections

A
  • Dysuria - Frequency +/- urethral discharge, urethral pain (Urethritis)
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82
Q

Diagnosis of urethritis, epididymo-orchitis and prostatitis

A

Normal diagnosis for UTIs - As well As NAAT (nucleuc acid amplification testing) to detect STI

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83
Q

What is epididymo-orchitis?

A
  • Inflammation of the epididymis, extending to the testes Usually due to: - Urethritis (<35 years) - Cystitis extension (>35 years) - Can also be caused in the elderly from a catheter
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84
Q

Presentation of epididymo-orchitis

A

Unilateral scrotal pain and swelling - Prehn’s sign positive - Cremaster reflex intact - DDx = rule out testicular torsion

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85
Q

Treatment of urethritis and epididymo-orchitis

A

Dependent on cause

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86
Q

Acute vs chronic prostatitis

A
  • Acute bacterial prostatitis - more rapid onset of symptoms - Chronic prostatitis - symptoms lasting for at least 3 months, can be subdivided. Types of chronic prostatitis: - Chronic pelvic pain syndrome - no infection - Chronic bacterial prostatitis - infection
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87
Q

Most common cause of prostatitis

A

E.Coli

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88
Q

Presentation of prostatitis

A

Perineal, penile or Rectal pain - Acute urinary retention, obstructive voiding symptoms - Low back pain, pain on ejaculation - Tender, swollen warm prostate on examination

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89
Q

Functions of the prostate

A
  • Produces testosterone and dihydrotestosterone (5x more potent) - Produces PSA - liquefies semen
90
Q

Risk factors for benign prostatic hyperplasia

A
  • Age (50+) - Men (obviously) - Afrocarribean = high testosterone
91
Q

Pathophysiology of benign prostatic hyperplasia

A

Inner transitional zone of prostate (muscular, gland) proliferates - Causes narrowing of the urethra

92
Q

Presentation of benign prostatic hyperplasia

A

LUTS

93
Q

What happens in benign prostatic hyperplasia if the urethra is totally occluded?

A

Anuria - Retention - Hydronephrosis - UTI - Stones

94
Q

Diagnosis of benign prostatic hyperplasia

A

Digital rectal examination (DRE) - Smooth, enlarged Prostate-specific antigen (PSA) - To rule out prostate cancer (but unreliable as it can be raised in both, but more in cancer)

95
Q

Treatment for benign prostatic hyperplasia

A
  • First line: Alpha blocker (tamsulosin) - Second line: 5 alpha reductase inhibitor (finasteride) - decreases testosterone production and therefore prostate size - Last resort, surgery - TURP - transurethral resection of the prostate (SE = retrograde ejaculation)
96
Q

Risk factors for renal cell carcinoma

A
  • > 40 - Smoking - Obesity - Male - Hypertension - Haemodialysis (15% chance) - Von-Hippel Lindau syndrome (also tuberous sclerosis, Burt Hogge Dube and hereditary papillary RCC)
97
Q

What is Von-Hippel Lindau syndrome?

A
  • Autosomal dominant loss of tumour suppressor gene - ROC (50%) bilaterally - Renal + pancreas cysts - Cerebellum cancers
98
Q

Presentation of renal cell carcinoma

A
  • Often asymptomatic and found incidentally, 25% metastasised cases at presentation - Triad: loin pain, haematuria, abdo mass - May have left sided varicocele - Anaemia (low EPO)
99
Q

Diagnosis of renal cell carcinoma

A

First line: Ultrasound - Gold standard: CT chest/abdo/pelvis

100
Q

Renal cell carcinoma metastases

A
  • Spreads to the tissues around the kidney, within Gerota’s fascia - Often spreads to the renal vein, then IVC - “Cannonball metastases” in the lungs are a classic feature of renal cell carcinoma
101
Q

Staging of renal cell carcinoma

A

img

102
Q

Treatment for renal cell carcinoma

A
  • Sometimes watch and wait - Radiofrequency ablation or cryotherapy (only if tumour is <4cm) - Gold standard: Partial nephrectomy - Radical (full) nephrectomy (most common)
103
Q

What is a Wilms tumour?

A
  • Renal mesenchymal stem cell tumour - Seen in children (<3 years) - Much rarer - Aka: nephroblastoma
104
Q

What type of cancer is renal cell carcinoma?

A

PCR epithelial carcinoma

105
Q

What type of cancer is bladder cancer?

A

transitional cell carcinoma of bladder (mc, and mc subtype is transitional urothelium) - if Patient has schistosomiasis, they are more likely to have squamous cell carcinoma

106
Q

Risk factors for bladder cancer

A
  • Smoking - Age 55+ - Males - Occupational exposure to aromatic amines, eg: painter, hairdresser (dyes), mechanic working with tyres (rubber) - Chemo/radiotherapy (cyclophosphamide)
107
Q

Presentation of bladder cancer

A

Painless Visible Haematuria - LUTS - Recurrent UTIs

108
Q

Diagnosis of bladder cancer

A

Gold standard: flexible cystoscopy + upper tract imaging

109
Q

NICE 2 week wait referral criteria for bladder cancer

A

Age 45 or above with: - Unexplained visible haematuria - or visible haematuria that persists after UTI treatment Age 60 or above with: - Unexplained non-visible haematuria - and either: dysuria or raised white cell count

110
Q

NICE two week wait referral criteria for renal cancer

A

45 or over with: - Unexplained visible haematuria without UTI - or visible haematuria that persists after treated UTI

111
Q

Treatment for bladder cancer

A

T1: Transurethral resection of bladder tumour T2-3: Cystoprostatectomy in men, anterior extentoration in women T4: Palliative or chemo/radiotherapy Intravesical therapy: mitomycin and BCG to reduce recurrence

112
Q

What type of cancer is prostate cancer?

A

Adenocarcinoma of outer peripheral prostate

113
Q

Risk factors for prostate cancer

A

Genetic: BRCA1, BRCA2, HOXB13 - increased Age - Afrocaribbean ethnicity

114
Q

Presentation of prostate cancer

A

LUTS - Systemic cancer symptoms (weight, loss, fatigue, night pain) - Bone pain

115
Q

Prostate cancer metastases

A

Typically to Bone (thick sclerotic lesions) - Typically lumbar back pain - Also liver, lung, brain

116
Q

Diagnosis of prostate cancer

A

DRE + PSA in community - Gold standard: Transrectal Ultrasound - Biopsy gives Gleason score - higher = worse

117
Q

Treatment of metastatic prostate cancer

A

Hormone therapy - Bilateral orchidectomy (best) - GNRH receptor agonist eg: goserelin - Radio/chemo therapy

118
Q

What type of cancer is testicular cancer?

A

Germ cell (90%+) or non germ-cell (<10%) tumour Germ = seminoma (mc) or teratoma Non germ = sertoli, leydig, sarcoma

119
Q

Risk factors for testicular cancer

A
  • Most common cancer in young men 20-45 (more common in caucasians) - Cryptorchidism (undescended testes) - HIV - Previous testicular cancer - Infertility - Family history
120
Q

Presentation of testicular cancer

A
  • Painless, hard, irregular lump in testicle - Does not transilluminate - May show lung metastasis signs, eg: cough -> consider chest x-ray - Gynaecomastia (breast enlargement) if it is a Leydig cell tumour (rare)
121
Q

Diagnosis of testicular cancer

A
  • Examination including lymph nodes, testes and scars from previous orchidopexy- Urgent (Doppler) ultrasound of testes (90% diagnostic) - Bloods for tumour markers - CXR if resp symptoms - Staging: CT chest/abdo/pelvis
122
Q

Tumour markers for testicular cancer

A

beta hCG - raised in seminomas - AFP - raised in teratomas - LDH raised non-specifically

123
Q

Royal Marsden staging system for testicular cancer

A
  1. Isolated to testicle 2. Spread to retroperitoneal lymph nodes 3. Spread to lymph nodes above diaphragm 4. Metastasised to other organs (mc: lymphatics, lungs, liver, brain)
124
Q

Treatment of testicular cancer

A
  • Urgent inguinal orchidectomy (+ offer sperm banking) - Adjuvant chemotherapy Or radiotherapy
125
Q

Most common causes of obstructive uropathy

A

Benign prostatic hyperplasia - Kidney Stones

126
Q

Pathophysiology of obstructive uropathy

A

obstruction - retention and increased Kidney ureter bladder (KUB) pressure - Refluxing/backlogged urine in Renal pelvis - Hydronephrosis - dilated Renal pelvis, more infection prone

127
Q

Treatment of obstructive uropathy

A
  • Relieve kidney pressure -> catheterise urethra, urethral stent - Treat cause/infection
128
Q

Autosomal recessive PKD

A
  • Much less common - Mutated PKHD1 gene on chromosome 6 - Infancy or prebirth - High mortality - Congenital abnormalities - eg: Potter’s sequence: flattened nose + clubbed feet
129
Q

Autosomal dominant PKD

A
  • Most common - Mutated PKD1 (85%) or PKD2 (15%) - More males - Presentation at 20-30 years
130
Q

Pathophysiology of polycystic kidney disease

A

Normally - PKD 1+2 codes for polycystin (Ca2+ channels) - Usually, cilia move and polycystin open - Ca2+ influx inhibits excessive growth PKD - PKD gene mutated - Lack of Ca2+ influx - Excessive growth of cilia - Results in polycysts

131
Q

What is PKD?

A

Cyst formation through Renal parenchyma - Bilateral enlargement and damage

132
Q

Presentation of PKD

A
  • Bilateral flank/back or abdo pain - Hypertension - Haematuria (when cysts rupture), resolves within a few days - Renal stones more common - End stage renal failure at around 50 years
133
Q

Extrarenal cysts

A
  • Particularly in Circle of Willis - Berry aneurysm if rupture -> subarachnoid haemorrhage
134
Q

Diagnosis of PKD

A

Kidney Ultrasound shows enlarged Bilateral kidneys with multple cysts - Also Genetic testing

135
Q

Treatment of PKD

A

non-curative - Manage symptoms

136
Q

Aetiology of nephritic syndrome

A
  • IgA nephropathy/Berger’s disease - mc - Post strep glomerulonephritis - SLE - Goodpasture’s syndrome - Haemolytic uraemic syndrome - All examples of Type 3 hypersensitivity, except for Goodpasture’s which is Type 2
137
Q

Risk factors for IgA nephropathy

A

Asian populations - associated with HIV - Teenagers or young adults

138
Q

Presentation of IgA nephropathy

A
  • Visible haematuria (ribena/coke) - 1-2 days after tonsilitis - Viral infection (or gastroenteritis viral infection)
139
Q

Diagnosis of IgA nephropathy

A

Immunofluorescence Microscopy shows IgA Complex deposition - Biopsy

140
Q

Treatment of IgA nephropathy

A
  • Non-curative - 30% progress to ESRF - First line: BP control (ACE-i)
141
Q

Presentation of post-strep glomerulonephritis

A
  • Visible haematuria - 2 weeks after pharyngitis from Group A, beta-haemolytic strep (S.pyogenes)
142
Q

Diagnosis of post strep glomerulonephritis

A

Light microscope - hypercellular glomeruli - Electron microscope - subendothelial immune Complex deposition - Immunoflorescence - starry sky appearance biopsy???

143
Q

Complications of post strep glomerulonephritis

A

Self limiting usually - Sometimes may progress to rapidly progressing Glomerulonephritis

144
Q

Pathophysiology of SLE nephropathy

A

Lupus nephritis secondary to SLE - ANA deposition in endothelium

145
Q

Diagnosis of SLE nephropathy

A

ANA positive - Anti-ds DNA positive how??? bloods???

146
Q

Treatment of SLE nephropathy

A

Steroids - Hydroxychloroquine - plus immunosuppressants, eg: cyclophosphamide

147
Q

Pathophysiology of Goodpasture’s syndrome

A
  • Presence of autoantibodies (anti-GBM) to alpha-3 chain of Type 4 collagen in glomerular and alveolar membrane - Pulmonary and alveolar haemorrhage, lung fibrosis and glomerulonephritis
148
Q

Treatment for Goodpasture’s syndrome

A
  • Corticosteroids - Plasma exchange (to get rid of anti-GBM antibodies) - Cyclophosphamide (for immune suppression)
149
Q

What is RPGN?

A

Subtype of glomerulonephritis that progresses to ESRF very fast (weeks to months)

150
Q

Diagnosis of RPGN

A

Biopsy shows Inflammatory cresents in Bowman’s space

151
Q

Causes of RPGN

A
  • Wegener’s granulomatosis (c-ANCA +ve) - MPA (pANCA +ve) - Goodpasture’s
152
Q

Aetiology of nephrotic syndrome

A

Primary: - Minimal change disease (mc in children) - Focal segmental glomerulosclerosis (mc in adults) - Membranous nephropathy (caucasian adults) Secondary: - Mc to diabetes

153
Q

Presentation of nephrotic syndrome

A
  • Proteinuria (frothy apple juice🧃) (>3.5g/24hours) - Hypoalbuminaemia (<30g/L) - Oedema (eg: puffy face) - Hyperlipidemia + weight gain
154
Q

Diagnosis of minimal change disease

A

On biopsy: - Light biopsy = no change - Electron biopsy = podocyte effacement + fusion

155
Q

Diagnosis of focal segmental glomerulosclerosis

A

On biopsy: - Light microscopy -> segmental sclerosis - < 50% glomeruli affected

156
Q

Diagnosis of membranous nephropathy

A

On biopsy: - Light microscopy - thickened GBM - Electron microscopy - subpodocyte immune complex deposition, spike + dome appearance

157
Q

Treatment of nephrotic syndrome

A
  • Steroids for 12 weeks with variable response - Minimal change = responds well to them - Focal segmental glomerulosclerosis + membranous nephropathy = less well :(
158
Q

What does a scrotal mass indicate?

A

Cancer until proven otherwise

159
Q

What is an epididymal cyst?

A
  • Extratesticular cyst above and behind testis - Transilluminates - Diagnosed by scrotal ultrasound - Dissolves in 10 days
160
Q

What is hydrocele?

A

Cyst that testicle sits within - Transilluminates - Diagnosed with scrotal Ultrasound

161
Q

Pathophysiology of hydrocele

A

Fluid collection in tunica vaginalis

162
Q

Pathophysiology of varicocele

A

Distended pampiniform plexus - due to increased left Renal vein pressure causing reflux

163
Q

Complication of varicocele

A

Infertility

164
Q

Presentation of varicocele

A

Bag of worms (on left hand side mostly) - Typically Painless, painful when more severe - Diagnosed clinically

165
Q

Pathophysiology of testicular torsion

A

Spermatic cord twists on itself - Occlusion of testicular artery

166
Q

Risk factor for testicular torsion

A

Bell clapper deformity (“horizontal lie” of testes)

167
Q

Presentation of testicular torsion

A
  • Severe unitesticular pain - hurts when walking - Abdo pain - Nausea and vomiting - Cremastering reflex lost - Prehn’s negative
168
Q

Diagnosis of testicular torsion

A

First, surgical exploration - then, Ultrasound to Check testicular blood flow

169
Q

Treatment of testicular torsion

A
  • Urgent surgery within 6 hours (90-100% successful) - All cases require bilateral orchiplexy (fixing of scrotal sac to overcome biclapper deformity) - If testes non-viable = orchidectomy
170
Q

Classification of incontinence

A

Stress incontinence (sphincter weakness) - Urge incontinence (detrusor or bladder overactivity) - Mixed incontinence - Overflow incontinence - Spastic paralysis (neurological UMN lesion)

171
Q

What is retention?

A

Inability to pass urine even when bladder is full (500+mL)

172
Q

Causes of retention

A

obstruction - Stones - BPH - neurological flaccid paralysis (hypotonia of detrusor, As LMN)

173
Q

Treatment of retention

A

Catheterise

174
Q

Storage lower urinary tract symptoms (LUTS)

A

Occur when bladder should be storing urine -> need to pee Frequency Urgency Nocturia Incontinence More common in females

175
Q

Voiding lower urinary tract symptoms (LUTS)

A

Occur when bladder outlets obstructed -> hard to pee Poor Stream Hesitancy Incomplete emptying Dribbling after finishing urination More common in males

176
Q

What diseases can present as both nephrotic and nephritic?

A

Diffuse proliferative Glomerulonephritis - Membranoproliferative Glomerulonephritis

177
Q

General presentation of nephritic syndrome

A
  • Visible/non-visible haematuria (+little proteinuria) - Oliguria (little urine, salt + water retention) - Hypertension - Oedema
178
Q

Difference in pathophysiology of nephrotic vs nephritic syndromee

A

Nephrotic - Podocyte injury - Scarring Nephritic - GBM breaks - Inflammation - Bowman crescents

179
Q

Treatment of post-strep glomerulonephritis

A

Antibiotics to clear the strep - Supportive care

180
Q

Pathophysiology of Henoch Schoenlein purpura

A

Small vessel vasculitis - Affects Kidney and joints due to IgA deposition - IgA nephropathy only in kidneys - HSP everywhere Do Biopsy

181
Q

Presentation of Henoch Schoenlein purpura

A

Purpuric rash on legs - Nephritic symptoms - Joint pain due to IgA deposition

182
Q

Diagnosis of Henoch Schoenlein purpura

A

Diagnosed clinically - Confirmed with Renal Biopsy

183
Q

Treatment of Henoch Schoenlein purpura

A

Corticosteroids - ACE-i/ARB

184
Q

Presentation of Goodpasture’s syndrome

A

Dyspnoea - Coughing problems - Oliguria - Haematuria

185
Q

Diagnosis of Goodpasture’s syndrome

A

lung and Kidney Biopsy - damage and Ig deposition - Serology - Anti-GBM positive

186
Q

What is Prehn’s sign?

A
  • Used to determine the cause of testicular pain - Performed by lifting the scrotum and assessing the consequent changes in pain - Prehn’s sign positive = pain relief upon elevation
187
Q

What is the cremasteric reflex?

A

Stroke inner thigh, ipsilateral testicle should elevate

188
Q

Presentation of epididymitis

A
  • Acute unilateral pain - Sometimes following previous infection - Prehn’s sign positive
189
Q

Treatment of epididymitis

A

Stat IM ceftriaxone (if organism unknown) - plus doxycyline

190
Q

Suprapontine incontinence

A

Mid brain functioning but not controlled By cortex (will present with neuro problems like dementia or cerebral palsy) - reflex bladder and bowel - involuntary urination and defaecation - Coordinated sphincter complete emptying

191
Q

Spastic SCI incontinence

A

Conus functioning but not controlled By brain (sphincter isn’t being told to relax By pons) - reflex bladder and bowel - involuntary urination and defaecation - Dyssynergic sphincter Incomplete emptying

192
Q

Flaccid SCI incontinence

A

Conus destroyed or non-functional - Areflexic bladder and bowel - fill until they Overflow - non-functional sphincter

193
Q

Management of stress incontinence

A

Women:- Pelvic floor re-education/physiotherapy - Duloxetine (caution) - Surgery (last line) Men: - Artifical urinary sphincter

194
Q

Stress incontinence causes

A

Women: - Post-pregnancy trauma Men: - Neurogenic - Iatrogenic (prostatectomy)

195
Q

Management of overactive bladder

A

Behavioural therapy or physiotherapy - Anticholinergic therapy - Mirabegron (B3 agonist) - Botox - Neuromodulation - bladder augmentation

196
Q

Spinal reflexes for bladder

A
  • Reflex bladder contraction - sacral micturition centre - Guarding reflex - onuf’s nucleus (rhabdosphincter - skeletal muscle so somatic) - Receptive relaxation - sympathetic
197
Q

What is an unsafe bladder?

A

One that puts the kidneys at risk - caused by prolonged high pressure

198
Q

Transitional cell carcinoma of the upper tract

A
  • Less common - Same risk factors as bladder cancer - Haematuria, loin pain, “clot colic” - Managed by nephroureterectomy
199
Q

Supportive treatment of nephrotic syndrome

A
  • Control fluids - diuretics, ACE-i/ARB, spironolactone - Statins - Anticoagulation (espesh when albumin <20g/L) - Abx in children
200
Q

What is erectile dysfunction?

A
  • Persistent inability to attain amd maintain an erection sufficient to permit satisfactory sexual performance - Commonly found in men over 40 - Up to 10% of men are affected
201
Q

Pathophysiology of erectile dysfunction

A

Neurogenic - failure to initiate - Arteriogenic - failure to fill (mc) - Venogenic - failure to store

202
Q

Innervation of the penis

A

sympathetic - T11 - L2 - parasympathetic - S2-S4

203
Q

Aetiology of erectile dysfunction

A

Atherosclerosis - Diabetes - Age - Hypogonadism - Trauma to Pelvic plexus - Iatrogenic - surgery that damages Pelvic plexus, drugs - Psychosomatic

204
Q

Treatment of erectile dysfunction

A

Treat underlying cause - Psychosexual counselling if necessary - Intracavernosal injection - Vaccuum assisted device - Implant

205
Q

Treatment of localised prostate cancer

A

Radical prostatectomy - Radiotherapy - external beam, bachytherapy - Watchful waiting

206
Q

What is a consequence of autosomal dominant PCKD?

A

IBS

207
Q

Reactive arthritis (Reiter’s triad)

A
  • Can’t see - conjunctivitis - Can’t pee - urithritis - Can’t climb a tree - arthritis
208
Q

Complications of AKI

A

Hyperkalaemia (Most important) - Rhabdomyolysis

209
Q

Complication of pyelonephritis

A

Hydronephritis from dilated renal pelvis

210
Q

What is pyuria?

A

The presence of leukocytes in the urine

211
Q

Complicated vs uncomplicated UTIs

A

Uncomplicated - non pregnant women Complicated - everyone else

212
Q

Teatment of asymptomatic bacteruria

A

Do not treat if they’re over 65 (???)

213
Q

What to do while waiting UTI test results

A

First line (trimethroprim) if patient is symptomatic

214
Q

Investigations for upper UTI

A

Midstream urine - blood cultures

215
Q

Prevention of uric acid stones

A

Deacidification of urine to pH 7-7-5

216
Q

Prevention of cystine stones

A

Excessive overhydration - urine alkalinisation - Cysteine binders

217
Q

Treatment for cystitis

A
  • Trimethroprim (avoid in pregnancy) or nitrofurantoin (avoid in 3rd trimester) - If pregnant, take amoxicillin instead
218
Q

Treatment for epididymo-orchitis

A

Depends on if it’s caused by an STI (NG/CT) or UTI - treat either appropriately

219
Q

Treatment for urethritis

A

N.Gonorrhoea - IM ceftriaxone or azithromycin - C.Trachomatis - azithromycin (or doxycycline)

220
Q

Symptoms in chlamydia

A

70% of women and 50% of men are asymptomatic

Haroon Phase 2A (14 decks)

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