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My Phase 3a Revision > GU > Flashcards

GU Flashcards

1
Q

Define benign prostatic hyperplasia (BPH)

A

Increase in cell number and size in transitional/peri-urethral prostate area WITHOUT the presence of malignancy

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2
Q

Describe the pathophysiology of Benign prostatic hyperplasia

A

Epithelial and stomal cell increase

Increased A1 adrenoreceptors –> smooth muscle contraction and mass effect of prostate size = obstruction

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3
Q

Give 4 symptoms of BPH

A
  1. Increased frequency of micturition
  2. Nocturia,
  3. Hesitancy
  4. Post-void dribbling
  5. acute urinary retention or retention with overflow incontinence
  6. enlarged smooth prostate
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4
Q

What investigations might you do in someone who you suspect has BPH?

A
  • Digital rectal exam - show smooth but enlarged prostate
  • PSA - not overly accurate but usually done for completion (remember you can’t do this at the same time as DRE)
  • Bladder diaries etc.
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5
Q

What are the aims of the management of BPH?

A

Improve urinary symptoms
Improve QOL
Reduce complications of bladder outflow obstruction

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6
Q

What lifestyle changes can be made to manage symptoms of BPH?

A

Reduce caffeine and alcohol intake
Distraction methods
Bladder training

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7
Q

Describe the treatment for BPH

A

1st line = Alpha-1-antagonists (A-blockers) e.g. tamulosin
- relaxes smooth muscle in bladder neck & prostate

2nd line = 5-alpha-reductase inhibitors e.g. finasteride
- blocks conversion of testosterone to dihydrotestosterone -> decreases prostate size

TURP = gold standard

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8
Q

Give the surgical treatment for BPH

A

Transurethral resection of prostate (TURP)

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9
Q

What are the indications in someone with BPH to do a TURP?

A

RUSHES

  • Retention
  • UTI’s
  • Stones
  • Haematuria
  • Elevated creatinine
  • Symptom deterioration
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10
Q

What is the function of the prostate?

A

Secretes proteolytic enzymes into the semen which breaks down clotting factors in the ejaculate

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11
Q

Define prostate cancer

A

Adenocarcinoma in the peripheral zone of the prostate gland

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12
Q

Where can prostate cancer metastasise to?

A

Lymph nodes and bone

Rarely = brain, liver, lung

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13
Q

By what routes can prostate cancer spread?

A
  1. Lymphatic - to external iliac and internal iliac and presacral node
  2. Haematogenous - to bone, lung. liver, kidneys
  3. Direct - within in the prostate capsule
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14
Q

What can cause prostate cancer?

A
  1. High testosterone levels

2. Family history - 2/3x increased risk if 1st degree relative is affected

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15
Q

what are the symptoms of prostate cancer?

A
  1. LUTS
  2. Bone pain, weight loss, night sweats anaemia = mets
    Most picked up in asymptomatic stage
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16
Q

What investigations might you do in someone who you suspect has prostate cancer?

A

Digital Rectal Exam and PSA are done in community,
Transrectal USS and biopsy = DIAGNOSTIC
Gleason grading system - higher the score the worse the prognosis

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17
Q

What grading system is used in prostate cancer?

A

Gleason grading = higher the score, the more aggressive the cancer

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18
Q

What is the treatment for localised prostate cancer?

A

radical prostatectomy
chemotherapy
radiotherapy

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19
Q

What is the treatment for metastatic prostate cancer?

A
  • prostatectomy
  • chemotherapy
  • radiotherapy
  • zoladex (GnRH agonist)
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20
Q

Give 2 advantages and 1 disadvantage of radical treatment for localised prostate cancer

A

Advantages:

  1. Curative
  2. Reduced patient anxiety

Disadvantages:
1. Can have adverse effects

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21
Q

How do LH antagonists work in treating prostate cancer?

A

First stimulate and then inhibit pituitary gonadotrophin E.g. Leuprolide

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22
Q

Is a raised PSA confirmatory of prostate cancer?

A

NO

Prostate cancer indication

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23
Q

Other than prostate cancer, what can cause an elevated PSA?

A
  1. Benign prostate enlargement
  2. UTI
  3. Prostatitis
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24
Q

Give 2 advantages and 2 disadvantages of screening in prostate cancer

A

Advantages:

  1. Early diagnosis of localised disease (cure)
  2. Early treatment of advanced disease (effective palliation)

Disadvantages:

  1. Over diagnosis of insignificant disease
  2. Harm caused by investigation/treatment
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25
Q

What is PSA?

A

A glycoprotein secreted by the prostate into the blood stream

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26
Q

Name the 2 types of testicular cancers that arise from germ cells

A
  1. Seminoma = most common, slow growing

2. Non-seminoma = yolk sac carcinoma/teratoma, rapid growth

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27
Q

Where does testicular cancer spread?

A

Locally into epididymis, spermatic cord and scortal wall Pelvic and inguinal Metastasises

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28
Q

what are the risk factors for testicular cancer?

A
  1. Cryptorchidism (undescended testes)
  2. Family history
  3. previous testicular cancer
  4. HIV
  5. age 20-45
  6. Caucasian
  7. infant hernia
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29
Q

Give 3 symptoms of testicular cancer

A
  1. Painless testis lump - hard and craggy (non-transilluminable)
  2. Testicular or abdominal pain
  3. haematospermia,
  4. Abdominal mass
  5. Dyspnoea and cough - lung mets
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30
Q

What investigations might you do on someone you suspect to have testicular cancer?

A
  1. Tumour markers = Alpha-fetoprotein (a-FP) and Beta subunit of human chorionic gonadotrophin (B-hCG)
  2. Testicular biopsy
  3. Imaging = US, CT/MRI
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31
Q

How is testicular cancer staged?

A 
1 = no mets 
2 = nodes under diaphragm 
3 = above diaphragm 
4 = lungs
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32
Q

What is the treatment for testicular cancer?

A

Orchidectomy = testis and spermatic cord excised Chemo and radiotherapy

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33
Q

What is epididymitis?

A

Inflammation of the epididymis

Occurs mainly in young males

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34
Q

Give 2 causes of epididymitis

A
  1. E. coli

2. Chlamydia

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35
Q

What is an epididymal cyst?

A

Smooth extra-testicular, spherical cyst in the head of the epididymus

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36
Q

What is hydrocele?

A

Scrotal swelling as a result of excessive fluid in the tunica vaginalis

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37
Q

what is primary hydrocele?

A

In absence of disease in testis
Large and tense testis
Young boys mainly effected
Associated with a patent processus vaginalis, which typically resolves during the 1st year of life

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38
Q

Name 3 causes of secondary hydrocele

A
  1. Testicular tumours
  2. Infection
  3. Testicular torsion
  4. TB
  5. trauma - is rarer and present in older boys and men
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39
Q

What is varicocele?

A

An abnormal enlargement of the pampiniform venous plexus in the scrotum
Caused by venous reflux

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40
Q

Why might renal cell carcinoma cause left sided varicocele?

A

If the renal tumour obstructs where the gonadal vein drains into the renal vein blood can back up and so you may see left sided varicocele

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41
Q

What is testicular torsion?

A

Twisting of the spermatic cord resulting in occlusion of testicular blood vessels
Leads to ischaemia and postnatal loss of testis

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42
Q

Define glomerular disease

A

= Glomerulonephritis

Group of parenchymal kidney diseases that all result in the inflammation of the glomeruli and nephrons

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43
Q

Give 3 consequences of glomerulonephritis

A
  1. Damage to filtration mechanism –> haematuria and proteinuria
  2. Damage to glomerulus restricts blood flow –> hypertension
  3. Loss of usual filtration capacity –> AKI
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44
Q

Briefly describe the pathophysiology of glomerulonephritis

A

Immunologically mediated –> immunoglobulin deposits and inflammatory cells

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45
Q

How can glomerulonephritis present?

A
  1. Nephritic syndrome
  2. Nephrotic syndrome
  3. Asymptomatic haematuria
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46
Q

what are the causes of nephritic syndrome?

A

Renal causes
- IgA nephropathy

Systemic causes

  • SLE
  • Post strep GN
  • Small vessel vasculitis
  • Goodpasture’s/anti-GMB disease
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47
Q

what is the clinical presentation of nephritic syndrome

A

This is a syndrome fitting a clinical picture of inflammation within the kidney.
characterised by:
Haematuria- reflects inflammation of the kidney (red casts on microscopy)
Oliguria- due to reduced GFR
Proteinuria- less than 3g/24 hours
Hypertension –due to fluid overload

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48
Q

What investigations might you do in someone who has nephritic syndrome?

A
  • Urinalysis (dipstick) = haematuria and proteinuria
  • Blood tests = high creatinine and urea
  • Kidney biopsy = diagnostic (crescent shaped glomeruli, Ig depositions, glomerulosclerosis)
  • serology = anti-GBM antibodies, c-ANCA, p-ANCA
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49
Q

How do you manage nephritic syndrome?

A

Treat underlying cause

Blood pressure control- ACE-I/ARB. This reduces proteinuria and preserves renal function

Corticosteroids- this is to reduce the inflammation causing damage to the kidney

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50
Q

Describe the pathophysiology behind nephritic syndrome

A

Kidney inflammation –> large podocytic pores –> RBC, WBC, protein leaks into urine

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51
Q

What are the signs needed in order to make a diagnosis of nephrotic syndrome?

A

proteinuria (>3.5g/day)
hypercholesterolaemia
hypoalbuminemia - results in severe oedema

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52
Q

Describe the pathophysiology of nephrotic syndrome

A
  1. Inflammation – from immune cells (Ab’s, Ig’s - IgG), complement proteins, HTN, atherosclerosis, medications/immunisations, infection
  2. Damage to podocytes – protein leakage (albumin, Ab’s)
  3. Increased liver activity – to increase albumin, - Consequential increase in cholesterol + coagulation factors
  4. Reduced oncotic pressure – oedema - Consequential blood volume decrease, RAAS stimulation, exacerbation
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53
Q

What can nephrotic syndrome be secondary to?

A
  1. DM
  2. SLE
  3. Amyloidosis
  4. Infection
  5. Drugs
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54
Q

what are the primary causes of nephrotic syndrome?

A
  • Minimal change disease
  • Membranous glomerulonephritis
  • focal segmental glomerulosclerosis
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55
Q

What would you see on the needle microscopy taken from someone with minimal change disease?

A

LM - normal
FM - normal
EM - Fused podocyte foot processes

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56
Q

How is minimal change disease treated?

A

High dose corticosteroids = prednisolone

  • Frequent relapse or steroid-dependent disease is treated with CYCLOPHOSPHAMIDE or CICLOSPORIN/TACROLIMUS
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57
Q

What is membranous nephropathy?

A

Thickening of glomerular capillary wall

IgG and C3 complement deposition in sub-epithelial surface –> leaky glomerulus

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58
Q

How would you diagnose membranous nephropathy?

A

Serum anti-PLA2R antibodies

Renal biopsy = thickened glomerular basement membrane (sub epithelial IgG and C3 complement deposits)

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59
Q

What is the management of membranous nephropathy?

A

Managed with ACE-I/ARB in all.

In patients with high risk of progression, prednisolone and cyclopshosphamide.

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60
Q

What are the main symptoms of nephrotic syndrome?

A

Pitting oedema (periorbital, ascites, peripheral)

frothy urine - reflects proteinuria

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61
Q

What investigations might be carried out in someone with nephrotic syndrome?

A

Urinalysis (dipstick) = proteinuria

Blood tests

  • hyperlipidaemia and hypoalbuminaemia
  • protein:creatinine ratio

USS kidney

Needle biopsy and microscopy = GOLD STANDARD

  • light microscopy (LM)
  • fluorescence microscopy (FM)
  • electron microscopy (EM)
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62
Q

Describe the treatment for nephrotic syndrome

A

Fluid and salt restriction

Loop diuretics- to manage oedema

Treat cause

ACE-I/ARB to reduce protein loss

Manage complications

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63
Q

Give 3 complications of nephrotic syndrome

A
  1. Infections (Ig loss, complement activity decrease)
  2. Thromboembolism (more clotting factor) manage with heparin
  3. Hyperlipidaemia - loss of albumin increases cholesterol formation. Manage with statins
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64
Q

What is IgA nephropathy?

A

This is where there is deposition of IgA into the mesangium of the kidney. This results in inflammation and damage

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65
Q

What is the treatment for IgA nephropathy?

A
  • BP control - ACEi / ARB

- steroids if renal function declines

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66
Q

Where can urinary tract stones be found?

A

Upper = renal and ureteric
Lower = bladder, prostatic and urethral
They most commonly are deposited at the pelviureteric junction, pelvic brim and vesicouretertic junction

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67
Q

What are urinary tract stones composed of?

A

80-85% = calcium oxalate (radio-opaque),

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68
Q

Describe the pathophysiology of stone formation in the upper urinary tract?

A

Stones form from crystals in supersaturated urine

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69
Q

Describe the epidemiology of stones in the urinary tract

A 
10-15% lifetime risk 
Males > females (2:1)
Higher prevalence in Middle East due to higher oxalate and lower calcium, containing diet 
Peak prevalence 20-40yrs 
50% risk of recurrence
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70
Q

Give 5 potential causes of urinary tract stones

A
  1. Congenital abnormalities - horseshoe kidney, spina bifida
  2. Hypercalcaemia/high urate/high oxalate
  3. Hyperuricaemia
  4. Infection
  5. Trauma
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71
Q

what is the clinical presentation of urinary tract stones?

A
  • Renal colic = severe unilateral abdominal pain starting in loin + radiating to ipsilateral groin/ testicle/ labia, classically sudden onset early in morning
  • Restlessness,
  • nausea + vomiting,
  • haematuria,
  • dysuria
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72
Q

Give 3 differential diagnosis of urinary tract stones

A
  1. AAA (until proven otherwise)
  2. Diverticulitis
  3. Appendicitis
  4. Ectopic pregnancy
  5. Testicular torsion
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73
Q

What investigations might you do on some who you suspect has a urinary tract stone?

A
  • First line = KUB XR - can see stone in renal tract
  • Gold standard = non-contrast CT KUB, USS KUB in pregnancy (can only see radiopaque stones with USS)
  • Dipstick: haematuria, leucocytes, nitrites
  • Bloods: FBC, CRP, U&Es
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74
Q

Give 5 ways in which urinary tract stones can be prevented

A

thiazide diuretics - reduce Ca levels

  1. Stay well hydrated
  2. Low salt diet
  3. Healthy protein intake
  4. Reduced BMI
  5. Active lifestyle
  6. Urine alkalisation
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75
Q

When are urinary tract stone removed?

A

<5mm = watch and wait

> 5mm:

  • Oral nifedipine (CCB) or alpha blocker (tamsulosin)
  • Extracorporeal shock wave lithotripsy (ESWL) - break stone into smaller fragment using shockwaves
  • Ureteroscopy (laser/basket)
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76
Q

What is renal colic?

A

Pain due to obstruction in the urinary tract

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77
Q

What investigations might you do to find out what is causing someone’s renal colic?

A
  1. Bloods - including calcium, phosphate, urate
  2. Urinalysis
  3. MSU MCS (mid-stream urine microscopy, culture & specificity)
  4. NCCT-KUB (non-contrast CT scan of kidney, ureter and bladder) = gold standard
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78
Q

Describe the treatment for renal colic

A
  1. Analgesia - NSAIDS (diclofenac)
  2. Anti-emetics
  3. Check for sepsis
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79
Q

Give 3 causes of renal colic

A
  1. Urinary tract stones
  2. UTI
  3. Pyelonephritis
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80
Q

Give 3 places where urinary tract stones are likely to get stuck

A
  1. Ureteropelvic junction
  2. Pelvic brim
  3. Vesoureteric junction
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81
Q

Give 5 functions of the kidney

A
  1. Filters and secretes waste/excess substances
  2. Blood volume/fluid management (BP control)
  3. Synthesises Erythropoietin
  4. Acid base regulation (reabsorption go Na, Cl, K, glucose, H2O, AA’s)
  5. Converts 1-hydroxyvitamin D –> 1,25-dihydroxyvitamin D (active)
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82
Q

What is the GFR?

A

Volume of fluid filtered from the glomeruli into Bowman’s space pre unit time

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83
Q

What would you expect a typical GFR to be?

A

120 ml/min

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84
Q

Write an equations for GFR

A

(Um X urine flow rate) / Pm

Um = conc of marker substance in urine
Pm = conc of marker substance in plasma
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85
Q

Give an example of a marker substance for estimating GFR

A

Creatinine

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86
Q

Give 3 essential features of a marker substance for estimating GFR

A
  1. Not metabolised
  2. Freely filtered
  3. Not reabsorbed/secreted
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87
Q

Name a drug that can inhibit creatinine secretion and what is the affect of this on GFR?

A

Trimethoprim (antibiotic to treat UTIs)

Serum creatinine rises and so kidney function (GFR) appears worse

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88
Q

What is the affect on GFR of afferent arteriole vasoconstriction?

A

Decreased GFR

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89
Q

What is the affect on GFR of efferent arteriole vasoconstriction?

A

Increased GFR

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90
Q

What does the eGFR require to be calculated?

A

Steady state

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91
Q

What is the effect of NSAIDs on the afferent arteriole of glomeruli?

A

NSAIDs inhibit prostaglandins and so lead to afferent arteriole vasoconstriction = reduced GFR

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92
Q

What is the effect of AECi on the efferent arteriole of glomeruli?

A

ACEi cause efferent arteriole vasodilation = reduced GFR

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93
Q

Define chronic kidney disease

A

Long standing, usually progressive, impairment in renal function for more than 3 months

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94
Q

How is CKD diagnosed?

A
  • eGFR < 60mL/min/1.73m2,
    or:
  • eGFR < 90mL/min/1.73m2 + signs of renal damage,
    or:
  • Albuminuria > 30mg/24hrs (Albumin:Creatinine > 3mg/mmol)
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95
Q

Briefly describe the pathophysiology causes CKD

A

Hyper-filtration for nephrons that work –> glomerular hypertrophy and reduced arteriolar resistance –> raised intraglomerular capillary pressure and strain –> accelerates remnant nephron failure (progressive)

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96
Q

Name 4 cause of CKD

A
  1. DM - 24% of patients
  2. Hypertension
  3. Glomerulonephritis
  4. Congenital - polycystic kidney disease
  5. Urinary tract obstruction
  6. drugs - NSAIDs, ACEi, antidepressants, many antibiotics
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97
Q

Give 3 signs of CKD

A

Often asymptomatic until very low kidney function

  • Fluid retention
  • oedema and raised JVP
  • Oliguria - 0.5 mL/kg/h or <500mL/day
  • Effects of uraemia
    - pruritus = ureamic frost, yellow/grey complexion, nausea, reduced appetite
  • cardiac arrhythmias - hyperKa
  • Fatigue, pallor - anaemia
  • Bone pain - hyperphosphatemia (CKD-MBD)
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98
Q

What investigations might be done in someone who has CKD?

A

FBC = anaemia
U+Es = raised phosphate, uric acid, urea, creatine and decreased Calcium
Urine dipstick = haematuria and proteinuria
GFR Imaging - USS, CT KUB, ECG, Xrays

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99
Q

Describe the management of CKD

A

Slow progression of disease

  • DM treatment
  • HTN treatment
  • Glumeronephritis treatment

Reduce risk of CVD
- Atorvastatin- 20mg

Manage complications

  • Mineral bone disease- low Vit D
  • HTN
  • Proteinuria
  • Anaemia-> ESA
  • RRT- haemodialysis, peritoneal dialysis, transplant
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100
Q

What is renal replacement therapy?

A

Dialysis or renal transplantation

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101
Q

Name 2 types of dialysis?

A
  1. Haemodialysis

2. Peritoneal dialysis

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102
Q

What is the access point in haemodialysis?

A

AV fistula or tunelled catheter

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103
Q

How does haemodialysis work?

A

Exchange of waste solutes through diffusion into dialysate most common (40%), typically 3x4hrs per week

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104
Q

Give 3 examples of waste products that are removed from the blood in dialysis

A
  1. Urea
  2. Creatinine
  3. Potassium
  4. Phosphate
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105
Q

Give 5 potential complications of haemodialysis

A
  1. Hypotension
  2. Cramps
  3. Nausea
  4. Chest pain
  5. Fever
  6. Blocked or infected dialysis catheter
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106
Q

Give 3 groups of people who haemodialysis is good for?

A
  1. People who live alone/frail/elderly
  2. People who fear operating machines
  3. People who are unsuitable for peritoneal dialysis (abdominal surgery/hernia)
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107
Q

What is the access point for peritoneal dialysis?

A

A peritoneal catheter is placed into the peritoneal cavity through a SC tunnel

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108
Q

what is peritoneal dialysis?

A

peritoneal catheter inserted
Glucose solution pumped in to peritoneum for exchange of solutes across peritoneal membrane
removal of dialysis solution
Continuous or overnight typically

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109
Q

Give 4 potential complications of peritoneal dialysis

A
  1. Infection (peritonitis/catheter exit site infection)
  2. Peri-catheter leak
  3. Abdominal wall herniation
  4. Intestinal perforation
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110
Q

Give 3 groups of people who peritoneal dialysis is good for

A
  1. Young people/those in full time work
  2. People who want control/responsibility of their care
  3. People with severe HF
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111
Q

Where in the abdomen does a transplanted kidney lie?

A

In the iliac fossa

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112
Q

What has to be assessed for a renal transplant to occur?

A

Virology status = CMV, hepatitis, EBV
CVD
TB
ABO and HLA haplotype

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113
Q

What tests can be done to evaluate kidney function in a potential kidney donor?

A
  1. Serum creatinine
  2. Creatinine clearance
  3. Urinalysis
  4. Urine culture
  5. GFR
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114
Q

Give 3 contraindications for renal transplant

A
  1. ABO incompatibility
  2. Active infection
  3. Recent malignancy
  4. Morbid obesity
  5. Age >70
  6. AIDS
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115
Q

What are the 2 main causes of death after a kidney transplant?

A
  1. CV disease

2. Infection

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116
Q

Name 4 potential complications of a kidney transplant

A
  1. Thrombosis
  2. Obstruction
  3. Infections - URTI, chest
  4. Rejection (12% in 1st year)
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117
Q

Why do advanced CKD patients need regular fluid assessment?

A

They may be oliguric or anuric

118
Q

Name a loop diuretic

A

Furosemide - acts on NKCC2 transporter

119
Q

Give 3 potential side effect of furosemide

A
  1. Hypokalaemia
  2. Hypotension
  3. Dehydration
120
Q

What other drug might you prescribe with furosemide in someone with poorly controlled potassium?

A

A potassium sparing diuretic e.g. spironolactone

Work on RAAS not ion channels so help control potassium levels in the blood

121
Q

On which part of the nephron do thiazides act?

A

The distal tubule Act on NCC channels

122
Q

On which part of the nephron do aldosterone antagonists act on?

A

Collecting ducts

123
Q

Define Acute Kidney Injury (AKI)

A

Sudden decline in renal function determined by increased serum creatinine +/- ↓ urine output.
Results in imbalance in electrolytes and azotaemia (↑ creatinine / nitrates)

124
Q

what are the different types of AKI?

A
  1. Pre-renal = decreased blood flow to kidneys –> decreased GFR
  2. Renal = kidney damage
  3. Post-renal = Urinary tract obstruction
125
Q

Give 5 risk factors for AKI

A
  1. Increasing age
  2. CKD
  3. HF
  4. DM
  5. Nephrotoxic drugs - NSAIDs, ACEi
  6. hypertension
126
Q

Give 2 pre-renal causes of AKI

A

low blood volume (bleeding, dehydration, shock, D&V)

low effective circulating volume (cirrhosis, congestive HF)

127
Q

Give 2 renal (intrinsic) causes of AKI

A 
glomerulonephritis
acute tubular necrosis (ATN)
acute interstitial nephritis (AIN), respectively
rhabdomyolysis
tumour lysis syndrome
128
Q

Give 2 post-renal causes of AKI

A
  • kidney stone in ureter or bladder
  • benign prostatic hyperplasia
  • external compression of the ureter
129
Q

How does AKI present?

A
  1. Uraemia (high urea) = fatigue, weakness, vomiting, seizures
  2. Acidosis
  3. Arrhythmias
  4. Oliguria
  5. Oedema
  6. high creatinine
130
Q

What investigations might you do to determine whether someone has AKI?

A
  1. Check potassium
  2. Bloods - Creatinine, U+Es
  3. Urine output and urinalysis
  4. Distinguish whether pre-renal, renal or post renal using imaging (USS, microscopy)
131
Q

What is the affect of AKI on creatinine and urine output?

A

Creatinine = raised

Urine output = reduced

132
Q

What is the diagnostic criteria for AKI?

A

1/3 = diagnostic

  1. Rise in CR >26 mmol/L in 48 hours
  2. Rise in Cr >50% in 48 hours
  3. Urine output fall to < 0.5 ml/kg/h for 6 hours
133
Q

How do you treat AKI?

A

Treat underlying cause – hypotension, infection, stones, obstruction
Stop drugs – NSAIDs, ACEi, ARBs, metformin, lithium, digoxin, loop diuretics
Treat underlying complications – electrolyte imbalances (K+)
Severe = dialysis

134
Q

What is the major complication someone with AKI might develop?

A

Hyperkalaemia

Can lead to arrhythmias ECG = tall tented T waves, increase PR interval and wide QRS complex

135
Q

How can hyperkalaemia be prevented in someone with AKI?

A

Give calcium gluconate to protect myocardium

Give insulin and dextrose (insulins drives K+ into cells and dextrose is to rebalance the blood sugar)

136
Q

Define urinary tract infection

A

Inflammatory response of the urothelium to bacterial invasion, usually associated with bacteriuria and pyuria

137
Q

What determines if a UTI is complicated or uncomplicated?

A

A UTI is deemed complicated if it affects:

  • Someone with an abnormal urinary tract
  • A man
  • Pregnant lady
  • Children
  • Immunocompromised
  • If it is recurrent
138
Q

Describe the pathophysiology of UTI’s

A

Organisms colonise the urethral meatus –> bacterial sent –> bacteriuria

139
Q

Name 3 UTI causative organisms

A

The 5 most common pathogens can remembered with KEEPS:

  • Klebsiella
  • E coli- most common causing >50% of cases
  • Enterococci
  • Proteus
  • Staphylococcus coagulase negative
140
Q

Describe the epidemiology of UTI’s

A

More common in women due to short urethra and its proximity to the anus

141
Q

Give 4 risk factors of UTI’s

A
  1. Catheter
  2. Female
  3. Prostatic hypertrophy (obstructs)
  4. Low urine volume
  5. Urinary tract stones
  6. Pregnancy
142
Q

Give 3 bacterial virulence factors that aid their ability to cause UTI’s

A
  1. Fimbriae/pili that adhere to urothelium
  2. Acid polysaccharide coat resists phagocytes
  3. Toxins (e.g. UPEC releases cytotoxins)
  4. Enzyme production (e.g. urease)
143
Q

What type of pili would you associate with lower UTI?

A

Type 1

Bind to uroplakin

144
Q

What type of pili would you associate with upper UTI?

A

Type P

Bind to glycolipids on urothelium

145
Q

The vagina is heavily colonised with lactobacilli, what is the function of this?

A

Helps maintain a low pH = host defence mechanism

146
Q

Give 2 reasons why a post-menopausal women is more susceptible to a UTI

A
  1. pH rises –> increased colonisation by colonic flora

2. Reduced mucus secretion

147
Q

Give 3 host defence mechanisms against UTIs

A
  1. Antegrade flushing of urine
  2. Tamm-horsfall protein
  3. GAG layer
  4. Low urine pH
  5. Commensal flora
  6. Urinary IgA
148
Q

Define pyuria

A

Presence of pus in urine

149
Q

Name 3 lower urinary tract infections

A
  1. Cystitis
  2. Prostatitis
  3. Urethritis
150
Q

Name a upper urinary tract infection

A

Pyelonephritis

151
Q

what are the classic UTI symptoms

A 
FUNDS: 
frequency, 
urgency, 
nocturia, 
dysuria

Haematuria
Abdominal pain
Malaise
Confusion (old patients)

152
Q

What investigations might you do in someone who you suspect has a UTI?

A
  1. Take a good history
  2. Urinalysis –> haematuria, proteinuria, increased WCC, pH, nitrates, ketones
  3. Microscopy, culture and sensitivity of MSU
  4. In recurrent/complicated UTI = imaging (bladder scan, USS, XR)
153
Q

What is the first line treatment for an uncomplicated UTI?

A

Trimethoprim or nitrofurantoin for 3 days

Increase fluid intake and regular voiding

154
Q

How does trimethoprim work?

A

It affects folic acid metabolism

155
Q

Describe the management for a complicated UTI

A

Culture sample –> Abx for 7 days

156
Q

Define recurrent UTI

A

> 2 episodes in 6 months or >3 in 12 months

157
Q

Describe the management for someone who is having recurrent UTIs

A
  1. Increase fluid intake
  2. Regular voiding
  3. Void pre and post intercourse
  4. Abx prophylaxis
  5. Vaginal oestrogen replacement
158
Q

What is cystitis?

A

Inflammation of the bladder secondary to infection

159
Q

what are the risk factors for cystitis?

A
  1. Urinary obstruction
  2. Previous damage to bladder epithelium
  3. Poor bladder emptying
  4. bladder stones
160
Q

what are the symptoms of cystitis?

A
  1. Dysuria
  2. Frequency and urgency
  3. Suprapubic pain
  4. Offensive smelling/cloudy urine
  5. Haematuria
161
Q

What is the treatment for cystitis?

A

1st line = Trimethoprim or nitrofurantoin (avoid trimethoprim in pregnancy -> teratogenic)

2nd line = ciprofloxacin or Co-amoxiclav

162
Q

what are the causes of prostatitis?

A

acute:

  • streptococcus faecalis
  • e.coli
  • chlamydia

chronic:

  • bacterial (as above)
  • non-bacterial - elevated prostatic pressure, pelvic floor myalgia
163
Q

Give 4 symptoms of acute prostatitis

A
  1. Fever
  2. Rigors
  3. Malaise
  4. Voiding LUTS
  5. Pelvic –> anal pain
  6. pain on ejaculation

very tender prostate

164
Q

Give 3 symptoms of chronic prostatitis

A
  1. Recurrent UTI’s
  2. Pelvic –> anal pain
  3. acute symptoms
    Symptoms for > 3 months
165
Q

What investigations might you do in someone with prostatitis?

A
  1. Urinalysis and MSU = blood, WBC and bacteria
  2. DRE = boggy, tender and hot to touch
  3. STI screen
  4. Microbiology = uropathogens in urine
  5. Imaging - TRUSS +/- CT abdo/pelvis
166
Q

How would you treat prostatitis?

A

Quinolone (ciprofloxacin) or trimethoprim (if unable to take quinolones) for 4-6 weeks
Treat pain = paracetamol/ibuprofen

167
Q

what are the causes of urethritis?

A
  • N. gonorrhoea
  • chlamydia
  • trauma
  • urethral stricture
  • irritation
  • urinary calculi
168
Q

what are the symptoms of urethritis?

A
  • skin lesion
  • dysuria +/- discharge (blood/pus)
  • urethral pain
  • penile discomfort/Pruritis
169
Q

what is the treatment for urethritis?

A

STI treatment = Abx - ceftriaxone and doxycycline

partner notification

170
Q

Define pyelonephritis

A

Infection of the renal pelvis and upper ureter, most commonly acquired by ascending transurethral spread, but can be via blood or lymphatics

171
Q

What can cause pyelonephritis?

A
  • majority caused by UPEC (uropathogenic E.coli)
  • main organisms = KEEPS
    • Klebsiella
    • E.coli - majority
    • Enterococcus
    • Proteus
    • Staphylococcus
172
Q

Give 3 symptoms of pyelonephritis

A

triad of:

  • loin pain (back pain)
  • fever
  • pyuria

may also have:

  • severe headache
  • rigors
  • nausea and vomiting
173
Q

What investigations might you do in someone with pyelonephritis?

A
  1. urine dipstick (1st line)
  2. mid-stream urine MC+S (gold standard)
  3. urgent USS to detect stones, obstruction or incomplete bladder emptying
174
Q

Describe the treatment for pyelonephritis

A

Antibiotics: cefalexin for 7-10 days. Trimethoprim or amoxicillin if sensitive.
Analgesia- paracetamol

175
Q

What can a prolonged pyelonephritis infection cause?

A

Renal abscess

Treatment = drainage

176
Q

what is the management for urinary tract stones?

A
  • Strong analgesia- diclofenac
  • Antibiotics
  • Tamsulosin/nifedipine- relaxes smooth muscle and helps expulsion
  • Percutaneous nephrolithotomy- used to expulse stones over 10mm
177
Q

what are the risk factors for urinary tract stones?

A
  • chronic dehydration
  • obesity
  • high protein/salt diet
  • recurrent UTIs
  • hyperparathyroidism (hypercalcaemia)
  • congenital abnormalities
178
Q

what are the signs for treatment of urinary tract stones?

A
  • intolerable pain/vomiting
  • signs of obstruction/infection
  • AKI (and hyperkalaemia)
179
Q

what is the pathophysiology of pre-renal AKI?

A
  • low blood volume or low effective circulating volume causes decreased perfusion
  • this decreases GFR and creatine clearance which activates RAAS- this increases Na+, urea and BP
180
Q

what is the pathophysiology of post-renal AKI?

A

obstruction

  • stones, prostate enlargement or infection causes back pressure into tubules
  • this decreases hydrostatic pressure which decreases GFR`
181
Q

what is the pathophysiology of intra-renal AKI?

A
  • glomerular - glomerulonephritis
    o this causes barrier damage and protein leakage
    o this decreases oncotic pressure which decreases GFR- tubular
  • necrosis
    o complex blood supply causes cells to infarct, break away and plug tubules
    o this decreases hydrostatic pressure and decreases GFR
  • vascular - vasculitis
    o damaged vasculature decreases O2 which causes necrosis
  • interstitial - acute interstitial nephritis
    o inflammation and immune cells cause damage
182
Q

what are the risk factors for prostate cancer?

A
  • family history
  • increasing age
  • black
  • genetic
  • HOXB13, BRCA2
183
Q

what is the epidemiology of prostate cancer?

A
  • commonest male malignancy
  • 7% of all cancer
  • by age of 80, 80% have malignant prostatic change
  • in most cases malignant foci remain dormant
184
Q

what is the epidemiology of testicular cancer?

A

● Most common cancer in young men
● More than 96% arise from germ cells
● 10% occur in undescended testes
● Main types are seminomas and teratomas

185
Q

what is the epidemiology of benign prostate hyperplasia (BPH)?

A
  • common
  • affects 24% of men 40-60 and 40% of over 60
  • afro-Caribbean men affected more
186
Q

what is the pathophysiology of varicocele?

A

● Abnormal dilation of the testicular veins in the pampiniform venomous plexus caused by venous reflux
● Increased reflux from compression of the renal vein
● Lack of effective valves between testicular and renal veins

187
Q

what is the clinical presentation of varicocele?

A

● Often visible as distended scrotal blood vessels that feel like a bag of worms
● Patient may complain of a dull ache or scrotal heaviness
● Scrotum hangs lower on the side of the varicocele

188
Q

what are the investigations for varicocele?

A

● Venography

● Colour doppler ultrasound to see blood flow

189
Q

what is the management for varicocele?

A

● Surgery if there is pain, infertility or testicular atrophy

190
Q

what is the epidemiology of varicocele?

A

● Left side more commonly affected
● Unusual in boys under 10
● Incidence increases after puberty
● Associated with sub fertility

191
Q

what are the causes of testicular torsion?

A

Underlying congenital malformation
- belt-clapper deformity - where the testis is not fixed to the scrotum completely, allowing for free movement leading to twisting

192
Q

what is the epidemiology of testicular torsion?

A
  • common urological emergency in adolescent boys
  • most common 11-30yrs
  • left side is more commonly affected
193
Q

what is the clinical presentation of testicular torsion?

A
  • sudden onset pain in one testis (walking uncomfortable)
  • pain often starts during sport
  • pain in abdomen
  • nausea and vomiting
  • inflammation of one testis - very tender, hot and swollen
194
Q

what are the investigations for testicular torsion?

A
  • doppler ultrasound - lack of blood flow to testis
  • urinalysis - exclude infection and epididymis
  • prehn’s sign = negative (raising scrotum exacerbates pain)
  • DO NOT DELAY SURGICAL EXPLORATION
195
Q

what is the treatment for testicular torsion?

A
  • surgery
  • expose and untwist testis (6 hour window to save testis)
  • orchidectomy (removal of testis) and bilateral fixation
196
Q

what are the investigations for cystitis?

A
  • dipstick urinalysis = positive leucocytes, blood and nitrites
  • microscopy and sensitivity of mid-stream urine = GOLD STANDARD
197
Q

what are the risk factors for pyelonephritis?

A
  • renal structural abnormalities
  • calculi (stones)
  • catheterisation
  • pregnancy
  • diabetes
  • immunocompromised
198
Q

what is the pathophysiology of pyelonephritis?

A
  • infection mostly due to bacteria from patients bowel flora

- most common via ascending transurethral route but can be blood stream or lymphatics

199
Q

what is the epidemiology of pyelonephritis?

A
  • predominantly females under 35

- unusual in men

200
Q

what is prostatitis?

A

infection and inflammation of the prostate gland

can be acute or chronic

201
Q

what are the risk factors for prostatitis?

A 
STI
UTI
indwelling catheter
post-biopsy
increasing age
202
Q

what is simple hydrocele?

A
  • overproduction of fluid in the tunica vaginalis
203
Q

what is communicating hydrocele?

A

processus vaginalis fails to close, allowing peritoneal fluid to communicate with the scrotal portion

204
Q

what is the clinical presentation of hydrocele?

A
  • non-tender, smooth cystic swelling
  • no pain unless infected
  • transluminates
205
Q

what are the investigations for hydrocele?

A
  • USS

- serum alpha-fetoprotein and hCG to exclude malignant teratomas and germ cell tumours

206
Q

what is the treatment for hydrocele?

A
  • most resolve spontaneously

- therapeutic aspiration or surgical removal

207
Q

what is the epidemiology of epididymal cyst?

A
  • usually develop around 40yrs
  • rare in children
  • not uncommon
208
Q

what is the pathophysiology of epididymal cyst?

A

contain clear and milky fluid - spermatocele

- lie above and behind the testis

209
Q

what is the clinical presentation of epididymal cyst?

A
  • lump
  • may be multiple/bilateral (may be painful)
  • transluminate
  • testis is palpable separately from cyst
210
Q

what are the investigations for epididymal cyst?

211
Q

what is the treatment for epididymal cyst?

A
  • usually not necessary

- if painful/symptomatic then surgical excision

212
Q

what is the pathophysiology of post strep nephritic syndrome?

A
  • most common = strep pyogenes (lancefield group A beta haemolytic)
  • classically occurs 2 weeks after tonsillitis
  • This is nephritic syndrome following an infection, 3-6 weeks prior. This is due to deposition of strep antigens in the glomeruli leading to inflammation and damage.
213
Q

what is the treatment for nephritic syndrome caused by post strep infection?

A

antibiotics - penicillins

supportive therapy

214
Q

what are the clinical features of nephritic syndrome that is specific to SLE?

A
  • rash
  • arthralgia
  • kidney failure
  • neurological symptoms
  • pericarditis
  • pneumonitis
215
Q

what are the investigations for nephritic syndrome that is specific to SLE?

A

ANA positive
DsDNA positive
low complement C3 and C4

216
Q

what is the treatment for nephritic syndrome caused by SLE?

A
  • immunosuppression
  • steroids
  • cyclophosphamide
  • rituximab
217
Q

what is a complicated UTI?

A
  • infection in patients with abnormal urinary tract
  • pregnant women
  • most UTIs in men
  • treatment is more likely to fail and complications are more likely
218
Q

what is an uncomplicated UTI?

A

UTI in a healthy non-pregnant women with normally functioning urinary tract

219
Q

what is urethritis?

A

urethral inflammation due to infectious or non-infectious cause
non-gonococcal > gonococcal

220
Q

what are the investigations for urethritis?

A
  • STI testing
  • microscopy and culture of urethral discharge
  • urine dipstick
  • urethral smear
  • ?flexible cystoscopy
221
Q

what is the clinical presentation of nephrotic syndrome?

A
  • Normal-mild increase in BP
  • Proteinuria > 3.5g/day
  • Normal-mild decrease in GFR
  • Hypoalbuminaemia
  • Pitting oedema of ankles, abdominal wall and sometimes face(periorbital)
  • Frothy urine
222
Q

what are the causes membranous nephropathy?

A
  • idiopathic
  • drugs
  • penicillamine, gold, NSAIDs
  • autoimmune
  • SLE, thyroiditis
  • infection, hep B or C, schistosomiasis
  • cancer
  • lung, colon. stomach, breast
223
Q

what are the causes of focal segmental glomerulosclerosis?

A
  • idiopathic

secondary

  • HIV
  • sickle cell anaemia
  • heroin
  • interferon treatment
224
Q

what are the investigations for focal segmental glomerulosclerosis?

A

needle biopsy = focal sclerosis and GBM thickening

225
Q

what is the pathophysiology of focal segmental glomerulosclerosis?

A
  • Scarring that is focal and only some glomeruli involved and segmental (only part of glomerulus affected)
  • CD80 in podocytes resulting in increased permeability in glomeruli and thus proteinuria and haematuria
  • Secondary hypertension and renal impairment
226
Q

what is the treatment for nephrotic syndrome caused by focal segmental glomerulosclerosis?

A

Give steroids in idiopathic disease

All patients should receive ACE-I/ARB blood pressure control

227
Q

which is the most common cause of nephrotic syndrome in children?

A

minimal change disease

228
Q

what are the risk factors/causes of minimal change disease in nephrotic syndrome?

A
  • can be idiopathic
  • atopy - allergic reaction can trigger
  • drugs - NSAIDs, lithium, antibiotics, bisphosphonates, sulfasalazine
  • hep C, HIV, TB
  • associated with hodgkins lymphoma
229
Q

what is the clinical presentation of minimal change disease?

A
  • Proteinuria
  • Oedema, predominantly around the face
  • Fatigue
  • Frothy urine
230
Q

what is the most common cause of nephrotic syndrome in adults?

A

focal segmental glomerulosclerosis

231
Q

what is the epidemiology of autosomal dominant polycystic kidney disease?

A
  • most common inherited kidney disease
  • autosomal dominant inheritance with high penetrance
  • male > female
232
Q

if 1 parent is affected by autosomal dominant polycystic kidney disease what is the chance of transmission?

A

50% chance

233
Q

if both parents are affects by autosomal dominant polycystic kidney disease, what is the chance of transmission to offspring?

A

50% chance of being affected
25% = normal
25% = homozygous for disease (die in the womb)

234
Q

what are the causes of autosomal dominant polycystic kidney disease?

A
  • mutations in PKD1 gene on chromosome 16 = 85%

- mutations in PKD2 gene on chromosome 4

235
Q

what are the risk factor for autosomal dominant polycystic kidney disease?

A
  • family history of ADPKD- ESRF

- hypertension

236
Q

what is the pathophysiology of autosomal dominant polycystic kidney disease?

A

Cysts develop and grow over time in the tubular portion of the nephron
Compression of renal architecture and vasculature
Progressive impairment - gets bigger and worse with age

237
Q

what is the clinical presentation of autosomal dominant polycystic kidney disease?

A
  • hypertension
  • abdo/flank pain (haemorrhage)
  • LUTS (dysuria, urgency, pain)
  • palpable
238
Q

what are the investigations for autosomal dominant polycystic kidney disease?

A

Renal USS then renal biopsy for genes
<30yrs – at least 2 unilateral or bilateral cysts
30-59yrs – 2 cysts in each kidney
>60yrs – 4 cysts in each kidney

239
Q

what is the treatment for autosomal dominant polycystic kidney disease?

A
  • Treat hypertension – lifestyle, ACEi (ramipril)
  • Infected – Abx or drain
  • Surgical – removal (nephrectomy)
  • Chronic – dialysis or transplant
240
Q

what are the complications of polycystic kidney disease?

A

berry aneurysms
cysts on other organs
50% have ventricular hypertrophy
pre-malignant

241
Q

what is the epidemiology of autosomal recessive polycystic kidney disease?

A
  • rarer than autosomal dominant
  • autosomal recessive inheritance
  • disease of infancy
242
Q

what are the causes of autosomal recessive polycystic kidney disease?

A

PKHD1 mutation on long arm (q) of chromosome 6

243
Q

what is the clinical presentation of autosomal recessive polycystic kidney disease?

A
  • variable
  • many present in infancy with multiple renal cysts and congenital hepatic fibrosis
  • enlarged polycystic kidneys
  • 30% develop kidney failure
244
Q

what are the investigations for autosomal recessive polycystic kidney disease?

A
  • Diagnosed antenatally or neonatally
  • Ultrasound - to see cysts
  • CT & MRI to monitor liver disease
  • Genetic testing
245
Q

what are the treatments for autosomal recessive polycystic kidney disease?

A
  • Currently no treatment available
  • Genetic counselling for family members
  • Laparoscopic removal of cysts to help with pain/nephrectomy (remove entire kidney)
  • Blood pressure control with ACE-inhibitor e.g. RAMIPRIL
  • Treat stones and give analgesia
  • Renal replacement therapy for ESRF
  • Counselling and support
246
Q

what is the specific clinical presentation of pre-renal AKI?

A
  • hypotension (D&V, syncope, pre-syncope)

- signs of liver or heart failure (oedema)

247
Q

what is the specific clinical presentation of intra-renal AKI?

A

infection, signs of underlying disease (vasculitis, glomerulonephritis, DM)

248
Q

what is the specific clinical presentation of post-renal AKI?

A

LUTS (BPH)

249
Q

what are the complications of AKI?

A

end stage renal failure
metabolic acidosis
uraemia
CKD

250
Q

how does diabetes cause CKD?

A

Glycation of glomerular endothelium and efferent arteriole leading to fibrosis (diabetic nephropathy)

251
Q

how does hypertension cause CKD?

A

thickening of afferent arteriole leading to ischaemia. Further fluid overloading due to activation of RAAS

252
Q

what is the treatment for urinary tract stones?

A
  • strong analgesic (IV diclofenac)
  • antibiotics if infection (IV cefuroxime or IV gentomycin)
  • antiemetics
  • stone removal
253
Q

what is stage 1 CKD?

A

eGFR > 90ml/min

254
Q

what is stage 2 CKD?

A

eGFR 60-89ml/min

255
Q

what is stage 3a CKD?

A

eGFR 45-59ml/min

256
Q

what is stage 4 CKD?

A

eGFR 29-15ml/min

257
Q

what is stage 5 CKD?

A

eGFR < 15ml/min

258
Q

which drugs are classed as nephrotoxic?

A
  • NSAIDs
  • aminoglycosides
  • ACEi
  • ARB
  • loop diuretics
  • metformin
  • digoxin
  • lithium
259
Q

what is the clinical presentation of epididymitis?

A

acute pain
unilateral
? previous infection

260
Q

how can you tell the difference between epididymitis and testicular torsion?

A

prehn’s sign - lift scrotum

  • epididymitis = positive (relieves pain)
  • testicular torsion = negative (exacerbates pain)
261
Q

what is the management for epididymitis?

A
  • IM ceftriaxone (if organism is unknown) + doxycycline
262
Q

how does IgA nephropathy present?

A

Presents asymptomatically with microscopic haematuria

263
Q

what are the investigations for IgA nephropathy?

A

diagnosed via biopsy

264
Q

what is the most common cause of nephritic syndrome in high income countries?

A

IgA nephropathy

265
Q

what is goodpastures disease?

A

Caused by autoantibodies to Type IV collagen in glomerular and alveolar membrane

266
Q

what is the clinical presentation of goodpastures disease?

A

Presents with SOB and oliguria due to respiratory and renal damage

267
Q

what are the investigations for goodpasture’s disease?

A

Diagnose with anti-GBM antibodies in bloods and biopsy

268
Q

what is the management for goodpasture’s disease?

A

plasma exchange
steroids
cyclophosphamide (for immune suppression)

269
Q

what is the most common cause of post strep glomerulonephritis?

A
  • most common = strep pyogenes (lancefield group A beta haemolytic)
270
Q

what is the clinical presentation of post strep glomerulonephritis?

A

Presents with haematuria. Can present with acute nephritis

271
Q

what are the investigations for post strep glomerulonephritis?

A

Diagnosed by evidence of strep infection

272
Q

what is the management for post strep glomerulonephritis?

A

Treated with antibiotics to clear the strep, and supportive care.

273
Q

what are the secondary causes of nephrotic syndrome?

A 
DDANI
diabetes
drugs
autoimmune
neoplasia
infection
274
Q

what is the difference between nephritic syndrome vs nephrotic syndrome?

A

NEPHRITIC

  • proteinuria +
  • hypertension
  • haematuria
  • very reduced GFR
  • oedema +

NEPHROTIC

  • proteinuria ++++++
  • hypoalbuminaemia
  • oedema ++++
  • slightly reduced/normal GFR
  • hyperlipidaemia
275
Q

where does bladder cancer spread to?

A

spreads to the iliac and para-aortic nodes, and to the liver and lungs

276
Q

what are the causes/risk factors of bladder cancer?

A
  • Smoking = increases risk 2-4 times, accounts for half of male cases of bladder cancer
  • Age over 55
  • Pelvic radiation
  • Exposure to occupational carcinogens
  • Bladder stone- due to chronic inflammation
277
Q

what is the presentation of bladder cancer?

A
  • Painless haematuria- this is the most common presenting symptom for bladder cancer, assume pt has urothelial tumour till proven otherwise
  • Ask about RF in history
  • UTI symptoms without bacteriuria
278
Q

what are the investigations for bladder cancer?

A

Urinalysis- sterile pyuria
Cystoscopy and biopsy- diagnostic
CTT urogram- allows staging

279
Q

what is the management for bladder cancer?

A

T1: transurethral resection or local diathermy
T2-3: radical cystectomy
T4: palliative chemotherapy and radiotherapy

280
Q

what is the most common bacterial STI?

281
Q

what is the bacteria that causes chlamydia?

A

chlamydia trachomatis

282
Q

what is urolithiasis?

A

presence of stones in urinary tract

283
Q

what is the equation for net filtration pressure for the glomerulus?

A

NFP = GHP - (GCOP + CHP)

NFP = net filtration pressure
GHP = glomerular hydrostatic pressure
GCOP = glomerular colloid oncotic pressure
CHP = capsular hydrostatic pressure
284
Q

what is the gold standard for measuring GFR?

285
Q

which part of the loop of henle is permeable to water?

A

descending limb

286
Q

what is the innervation of the external urinary sphincter?

A

pudendal nerve S2-S4

287
Q

what is the innervation of internal urinary sphincter?

A

pelvic splanchnic nerve S2-S4

288
Q

what is the innervation of the bladder?

A 
sympathetic = sympathetic chain T11-L2
parasympathetic = pelvic splanchnic S2-S4
289
Q

what is the role of intercalated cells of the collecting duct?

A

Intercalated cells are responsible for acid/base balance
Alpha = acid
Beta = basic

290
Q

what cells line the collecting duct?

A

principal cells and intercalated cells

291
Q

what is the physiology of micturation?

A

Pontine micturition centre promotes micturition by activating parasympathetic and deactivating sympathetic and somatic motor activity
Detrusor muscle contracts and sphincters open

292
Q

what is stage 3b CKD?

A

eGFR 30-44ml/min

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