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Osha 2a > Renal + Urogenital > Flashcards

Renal + Urogenital Flashcards

1
Q

What is the function of the urinary tract?

A
  • to collect continuously produced urine
  • to store it under safe conditions
  • to expel urine when socially acceptable
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2
Q

What are the key features in the filling of a normally functioning bladder?

A
  • continence
  • sensation of bladder volume
  • receptive relaxation: relaxes to allow larger volume without increased pressure
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3
Q

What are the key features in the voiding of a normally functioning bladder?

A
  • voluntary initiation
  • complete emptying
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4
Q

What incontinence problems can occur in neuropathic bladder management?

A
  • incontinence: neurogenic detrusor overactivity ( sphincter contracts by itself
  • stress incontinence: when pressure inc in abdomen e.g. coughing, urine leaks out - normally prevented by guarding reflex
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5
Q

What upper tract injury problems can occur in neuropathic bladder management?

A
  • infection
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6
Q

What are the 5 main functions of the kidney?

A
  • fluid balance and BP control
  • waste, toxin and drug removal
  • red cell production (generates erythropoietin)
  • vit D metabolism
  • acid-base regulation
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7
Q

Why are most people with advanced CKD anaemic?

A
  • not enough EPO to stimulate bone marrow to produce RBC
  • leads to normocytic anaemia
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8
Q

What is acute kidney injury?

A
  • acute drop in kidney function over hours or days
  • diagnosed by measuring serum creatinine
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9
Q

What are the NICE criteria for AKI?

A
  • rise in creatinine of ≥25µmol/L in 48h
  • rise in creatinine of ≥50% in 7 days
  • urine output of < 0.5ml/kg/hr for > 6hrs
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10
Q

What are risk factors for AKI?

A
  • CKD
  • heart failure
  • diabetes
  • liver disease
  • older age
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11
Q

What are pre-renal causes of renal failure?

A
  • due to inadequate blood supply to the kidneys, reducing filtration of blood
  • hypovolaemia
  • reduced CO
  • drugs that reduce BP
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12
Q

What are causes of renal failure?

A
  • intrinsic disease leads to reduced filtration of blood
  • Glomerulonephritis
  • Interstitial nephritis
  • Acute tubular necrosis
  • rhabdomyolysis: CK in skeletal muscle is nephrotoxic
  • nephrotoxic drugs and antibiotics
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13
Q

What are post-renal causes of AKI?

A
  • caused by obstruction to the outflow of urine causing back pressure and reduced kidney function
  • renal stones
  • cancer
  • enlarged prostate
  • blocked catheter
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14
Q

What are symptoms of AKI?

A
  • nausea
  • dehydration and less urination
  • diarrhoea
  • confusion and drowsiness
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15
Q

How is AKI investigated?

A
  • urinalysis
  • leucocytes and nitrites: infection
  • protein and blood: acute nephritis
  • glucose: diabetes
  • ultrasound for obstruction
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16
Q

How is AKI managed?

A
  • fluid rehydration if pre-renal
  • stop nephrotoxic medication
  • relieve obstruction if post renal
  • dialysis if serious
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17
Q

How is CKD investigated?

A
  • eGFR calculated using U&E
  • proteinuria using albumin:creatinine ratio (≥3mg/mmol)
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18
Q

Which LUTS fall into storage?

A
  • frequency
  • urgency
  • nocturia
  • incontinence
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19
Q

Which LUTS fall into voiding?

A
  • poor flow
  • intermittency
  • straining
  • terminal dribbling
  • hesitancy
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20
Q

Which LUTS fall into post micturition?

A
  • sensation of incomplete voiding
  • post-micturition dribbling
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21
Q

What can cause difficulty voiding?

A
  • benign prostatic hyperplasia
  • urethral stricture
  • masses
  • prolapse
  • non-obstructive: atonic bladder: insufficient detrusor contraction
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22
Q

What is stress incontinence?

A
  • weakness of the pelvic floor and sphincter muscles
  • leads to urine leakage when there is inc pressure on the bladder
  • occurs when laughing, coughing, sneezing
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23
Q

What is urge incontinence?

A
  • overactivity of detrusor leads to sudden urge to pass urine
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24
Q

What is overflow incontinence?

A
  • occurs in chronic urinary retention
  • due to obstruction of outflow of urine
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25
Q

What are the risk factors for renal cell carcinoma?

A
  • smoking
  • obesity
  • genetic
  • more common in males
  • hypertension
  • dialysis
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26
Q

How does renal cell carcinoma present?

A
  • triad: haematuria, loin pain, palpable mass
  • mostly found incidentally on scan
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27
Q

How is renal cancer staged?

A
  • Stage 1: tumour diameter < 7cm
  • Stage 2: diameter > 7cm
  • Stage 3: local size, spread to nearby tissues and veins
  • Stage 4: metastasis occurred
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28
Q

How is renal cancer investigated?

A
  • CT TAP used for staging
  • MRI if needed
  • biopsy
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29
Q

How is renal cancer managed?

A
  • active surveillance if slow growing and treatment would be detrimental
  • radiofrequency ablation, cryotherapy, arterial embolisation
  • partial or radical nephrectomy
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30
Q

What are the types of renal cell carcinoma?

A
  • clear cell carcinoma
  • papillary carcinoma
  • chromophobe
  • collecting duct
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31
Q

What paraneoplastic features are associated with renal cell carcinoma?

A
  • polycythaemia: unregulated EPO
  • hypercalcaemia: PTH mimic
  • hypertension: inc renin secretion and physical compression
  • Staffer’s syndrome: abnormal LFTs without liver metastasis
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32
Q

What are common complications of renal cell carcinoma?

A
  • spread to renal vein, IVC
  • cannonball metastases appear as defined circular opacities scattered through lung fields on CXR
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33
Q

What are the risk factors for bladder cancer?

A
  • smoking
  • exposure to aromatic hydrocarbons, dyes, rubber,
  • industrial exposures: hairdressers, leather and chemical workers
  • drugs e.g. cyclophosphamide
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34
Q

How does bladder cancer present?

A
  • painless, visible haematuria
  • LUTS without cause
  • recurrent UTIs
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35
Q

Where does bladder cancer occur and what are the types?

A
  • transitional cell carcinoma = 90%: affects urothelium
  • squamous cell carcinoma: dysplasia from irritation e.g. stones, schistosomiasis
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36
Q

How is bladder cancer investigated?

A
  • flexible cystoscopy: direct visualisation which is very quick
  • ultrasound
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37
Q

What are the surgical management options for bladder cancer?

A
  • transurethral resection (TURBT) is used for non muscle invasive bladder cancer
  • tumour removal during cystoscopy
  • radical cystectomy: removal of entire bladder
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38
Q

How is bladder cancer staged?

A
  • non-muscle invasive bladder cancer vs muscle invasive bladder cancer
  • T1: sub epithelial only: low risk
  • T2: muscle invasive
  • T3a/b through the muscle / invading perivesical fat
  • T4a/b invading prostate / pelvic side wall
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39
Q

What are the non surgical management options for bladder cancer?

A
  • intravesical chemotherapy: given through catheter to reduce recurrence risk
  • intravesical BCG: BCG vaccine used as immunotherapy
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40
Q

What is the most common way to divert urine following cystectomy?

A
  • draining urine from the kidney, bypassing the ureters, bladder and urethra
  • creating ileal conduit
  • urine drains from kidneys > ureters > separated ileum > urostomy bag
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41
Q

What are the types of testicular cancer?

A
  • germ cell: seminoma or non seminoma
  • Non seminoma: teratoma, yolk sac tumour, choriocarcinoma
  • Leydig, and Sertoli cell are rare
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42
Q

How does testicular cancer present?

A
  • painless testicular lump: non-tender, hard, irregular
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43
Q

What are risk factors for testicular cancer?

A
  • cryptorchidism
  • family history
  • HIV
  • previous testicular cancer
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44
Q

How is testicular cancer investigated?

A
  • scrotal ultrasound
  • tumour markers: α fetoprotein, β hCG, LDH
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45
Q

What is the epidemiology of testicular cancer?

A
  • caucasian males
  • aged 15-35
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46
Q

How is testicular cancer staged?

A
  • X-ray
  • 1: isolated to testicle
  • 2: spread to retroperitoneal lymph nodes
  • 3: spread to lymph nodes above diaphragm
  • 4: metastasised to other organs
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47
Q

How is testicular cancer managed?

A
  • radical inguinal orchidectomy
  • platinum based chemotherapy
  • sperm banking due to possible infertility
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48
Q

What are key risk factors for prostate cancer?

A
  • increasing age
  • family history
  • Black African/Caribbean origin
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49
Q

How does prostate cancer present?

A
  • LUTS (similar to benign prostatic hyperplasia)
  • haematuria
  • erectile dysfunction
  • symptoms of metastasis
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50
Q

How is prostate cancer diagnosed?

A
  • PSA
  • DRE
  • MRI
  • transrectal ultrasound guided prostate biopsy
  • histopathology: Gleason grading
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51
Q

What type of cancer is prostate typically?

A
  • adenocarcinoma
  • typically occurs in peripheral zone of prostate
  • multifocal, occurs with a dominant nodule
  • metastasises to lymph nodes, bone, brain, lungs
  • firm, hard, irregular and loss of central sulcus in DRE
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52
Q

What is the Gleason scoring system?

A
  • tissue grading for prostate cancer
  • looks to see how close the tissue is to normality
  • grade: how the cancer is likely to behave
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53
Q

What is the staging for prostate cancer?

A
  • T1: no palpable tumour on DRE, present on biopsy
  • T2: visible nodule, palpable on DRE but confined to prostate
  • T3: palpable tumour extending beyond capsule
  • T4: invading local structures: sphincter, rectum
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54
Q

How is prostate cancer managed?

A
  • surveillance: if early
  • external beam radiotherapy: can lead to proctitis
  • brachytherapy or hormone therapy
  • radical prostatectomy
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55
Q

What is glomerulonephritis?

A
  • broad term referring to a group of conditions concerning inflammation and damage to the glomeruli and nephrons
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56
Q

What is IgA nephropathy?

A
  • most common cause of primary glomerulonephritis
  • abnormality in IgA glycosylation leads to deposition in the mesangium
  • leads to haematuria and proteinuria
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57
Q

How does IgA nephropathy present and how is it diagnosed?

A
  • episodic macroscopic haematuria
  • stimulated by illness e.g. sore throat
  • nephrotic syndrome rare
  • biopsy
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58
Q

How is IgA nephropathy treated?

A
  • controlling BP: ACE-i, ARBs
  • steroids and immunosuppression
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59
Q

What are the types of erectile dysfunction?

A
  • neurogenic: failure to initiate
  • arteriogenic (most common): failure to fill
  • venogenic: failure to store
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60
Q

What is the epidemiology of erectile dysfunction?

A
  • affects 10% of men aged 40-70
  • increasing prevalence with age
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61
Q

What is a UTI?

A
  • combination of clinical features and the presence of bacteria in the urine
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62
Q

How can UTIs be classified?

A
  • asymptomatic bacteriuria
  • uncomplicated
  • complicated
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63
Q

What is pyuria?

A
  • presence of leucocytes in the urine
  • associated with infection
  • can have sterile pyuria: finding white cells but not detecting any bacteria e.g. if non-infective cause
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64
Q

What are some examples of complicated UTIs?

A
  • pregnant women
  • men and children
  • catheterised
  • immunocompromised or persistent infection
65
Q

Which bacteria commonly cause UTIs?

A
  • E. coli >50%
  • Proteus (if repeated suggests renal stones)
  • Klebsiella (tend to be catheter associated)
  • Enterococci
  • Staph. saprophytic (young women)
  • S. aureus
  • Pseudomonas aeruginosa
66
Q

What is the capacity of the bladder?

A
  • 500ml in women
  • 700ml in men
67
Q

What is the aetiology of UTIs?

A
  • catheterisation: cystitis > UTI
  • short female urethra
  • stones reduce flow and capacity
68
Q

Why does reduced flow cause UTI and what are some causes?

A
  • reduced flow and capacity leads to inflammation and inc frequency
  • means bacteria isn’t washed away
  • renal, ureteric and bladder stones
  • obstruction from prostatic hypertrophy
  • low urine vol
69
Q

What are symptoms of lower UTIs?

A
  • painful urination (dysuria: stinging, burning)
  • haematuria
  • cloudy/foul smelling urine
  • frequency + urgency
  • more localised
70
Q

What are symptoms of upper UTIs?

A
  • haematuria
  • fever
  • more systemically unwell
71
Q

How are UTIs diagnosed?

A
  • urine sample > dipstick
  • microscopy > cultures
  • sensitivities to find treatment
72
Q

What factors are considered in urinalysis?

A
  • bloods
  • protein
  • pH
  • glucose and ketones
  • leucocytes and nitrates
73
Q

What are the types of urine sampling?

A
  • MSU: midstream urine
  • CSU: catheter stream
  • clean catch/bag: children
  • SPA aspirate: suprapubic
74
Q

What is early morning urine used for?

A
  • looks for TB
  • 3x samples
  • large volume of urine due to no urination overnight
  • higher no. of bacilli on first void of day
75
Q

How are uncomplicated UTIs treated?

A
  • most can be treated empirically with 1st line antibiotics > 3 day course
  • inc fluid intake > inc frequency
  • voiding pre and post intercourse
  • keeping good hygiene
76
Q

What antibiotics are used to treat UTIs?

A
  • avoid broad spectrum
  • nitrofurantoin (contraindicated in 3rd trimester pregnancy & low creatinine clearance)/trimethoprim
  • 3 days if uncomplicated, 7 if male, pregnant, catheter
77
Q

What is pyelonephritis?

A
  • bacterial infection causing inflammation of kidney
  • affects renal parenchyma and soft tissues of renal pelvis + upper ureter
78
Q

What are the causes/risk factors for pyelonephritis?

A
  • young women who are fluid depleted
  • structural urological abnormalities
  • vesico-ureteric reflux
  • diabetes
79
Q

What are the classic triad of symptoms of pyelonephritis?

A
  • loin pain
  • fever
  • nausea/vomiting
80
Q

What are other signs of pyelonephritis?

A
  • upper UTIs present with systemic illness
  • loss of appetite
  • haematuria
81
Q

What are the possible causes of pyelonephritis?

A
  • ascending: urethra colonised with bacteria
  • haematogenous: S. aureus or Candida
  • lymphatic spread is rare
82
Q

How is pyelonephritis investigated?

A
  • abdo exam: loin and renal angle tenderness
  • bloods inc cultures
  • Ultrasound
  • Mid stream urine
  • urine dipstick: nitrites, leukocytes, blood
83
Q

How is pyelonephritis treated?

A
  • fluid replacement
  • IV antibiotics: broad spectrum e.g. co-amoxiclav ± Gentamicin: 1-2 weeks
  • drain the obstructed kidney
  • catheter and analgesia
84
Q

Where do stones occur in the urinary tract?

A
  • anywhere from collecting duct to external urethral meatus
  • renal and ureteric stones in upper urinary tract
  • bladder, prostatic and urethral stones in lower
85
Q

What are the causes of urinary tract stones?

A
  • congenital: due to stasis of urine
  • acquired: obstruction, trauma and reflux
  • urinary: calcium, oxalate, urate, cystine
  • dehydration
  • infection
86
Q

What are urinary tract stones made of?

A
  • crystals of normal urinary constituents
  • Most are calcium based with oxalate and phosphate
  • some from uric acid
87
Q

How can stones be prevented?

A
  • over hydration (based on urine output)
  • low salt diet
  • healthy protein and normal dairy intake
  • reduce BMI and keep an active lifestyle
88
Q

What are the symptoms of urinary tract stones?

A
  • loin pain (radiating to groin)/flank pain
  • reduced urine output
  • renal colic
  • UTI symptoms: dysuria, urgency, frequency
  • recurrent UTIs
  • haematuria
89
Q

What is testicular torsion?

A
  • twisting of the spermatic cord and rotation of the testicle which cuts off the blood supply
  • can lead to ischaemia, necrosis and infertility
90
Q

What is the epidemiology and aetiology of testicular torsion?

A
  • typically occurs in teenage boys
  • triggered by activity e.g. sport
  • Bell-clapper deformity: absence of fixation between testicle and tunica vaginalis
91
Q

What is the presentation of testicular torsion?

A
  • acute, rapid onset of unilateral testicular pain
  • abdo pain and vomiting
  • firm, swollen testicle
  • testicle lying high and horizontal
  • absent cremasteric reflex
92
Q

How is testicular torsion investigated?

A
  • doppler ultrasound to rule out epididymitis (but can delay surgery)
  • absent cremasteric reflex
  • surgical exploration mandatory as urological emergency
93
Q

How is testicular torsion managed?

A
  • surgery
  • surgical exploration of scrotum
  • orchiopexy (correction of position)
  • orchidectomy (removal) if necrosis
94
Q

What is benign prostatic hyperplasia?

A
  • hyperplasia of the stromal and epithelial cells of the prostate
95
Q

How is BPH investigated?

A
  • international prostate symptom score (IPSS)
  • DRE
  • PSA
  • urine dipstick and bladder diary
96
Q

What can cause a raised PSA?

A
  • prostate cancer
  • BPH
  • prostatitis
  • UTI
  • vigorous exercise
  • recent ejaculation or prostate stimulation
97
Q

How is BPH treated?

A
  • α blockers e.g. tamsulosin relaxes smooth muscle
  • 5-α reductase inhibitors reduce size of prostate: convert testosterone to DHT e.g. finasteride
98
Q

What is felt in a prostate exam that differentiates BPH and cancer?

A
  • BPH: smooth, symmetrical, slightly soft with central sulcus
  • cancer: hard, asymmetrical, irregular, loss of central sulcus
99
Q

What is an epididymal cyst?

A
  • occur at head of epididymis (top of testicle)
  • fluid filled sac
  • soft, round lump - separate from testicle
  • harmless
100
Q

What is a hydrocele?

A
  • collection of fluid in tunica vaginalis
  • can be idiopathic
  • cause: cancer, torsion, epididymo-orchitis, trauma
101
Q

How does a hydrocele present?

A
  • testicle palpable within hydrocele
  • painless and soft scrotal swelling
  • irreducible and no bowel sounds
  • transilluminated by torch
102
Q

What is a varicocele?

A
  • veins in pampiniform plexus become swollen
  • veins drain into testicular vein and regulate temp in testes
  • caused by inc resistance in testicular vein/incompetent valves
  • 90% occur in LHS
103
Q

How does a varicocele present?

A
  • throbbing pain, dragging sensation
  • more prominent on standing and disappears when lying down
  • scrotal mass that feels like bag of worms
104
Q

How are varicoceles investigated?

A
  • US with doppler imaging
  • semen analysis
  • hormonal tests
105
Q

What complications can arise from varicoceles?

A
  • testicular atrophy
  • reduction in size and function of testicle
  • infertility/impaired fertility due to temperature disruption
106
Q

What diseases are included in an STI screen?

A
  • chlamydia
  • gonorrhoea
  • syphilis
  • HIV
107
Q

What is the national chlamydia screening programme?

A
  • screens every sexually active person under 25 for chlamydia annually or when they change sexual partner
  • positive cases retested after 3 months
108
Q

What is the public health response to gonorrhoea?

A
  • referral to GUM clinic for testing, treatment and contact tracing
  • treatment with ciprofloxacin
  • NAAT testing to check if cured due to antibiotic resistance
109
Q

How is syphilis managed?

A
  • full STI screen
  • advice and contact tracing
  • deep IM dose of benzathine benzylpenacillin
110
Q

How is syphilis tested for?

A
  • antibody testing for Abs to T. palladium
  • dark field microscopy and PCR
111
Q

How is syphilis transmitted?

A
  • Oral, vaginal or anal sex
  • Vertical transmission
  • IV drug use
  • Blood transfusions (rare)
112
Q

What is nephritic syndrome?

A
  • a group of symptoms
  • haematuria (smoky coloured urine)
  • oliguria
  • proteinuria
  • fluid retention
113
Q

What is Goodpasture’s syndrome?

A
  • rare, genetic, autoimmune condition
  • glomerulonephritis and alveolar haemorrhage with circulating anti-GBM antibodies
114
Q

What is post streptococcal glomerulonephritis?

A
  • patients under 30 y/o
  • occurs 1-3 weeks after streptococcal (S. pyogenes) infection
  • patients develop a nephritic syndrome and usually have a full recovery
115
Q

What are the types of prostatitis?

A
  • acute bacterial: rapid onset
  • chronic: symptoms last > 3 months
  • chronic bacterial
116
Q

How does chronic prostatitis present?

A
  • pelvic pain
  • LUTS
  • sexual dysfunction
  • pain with bowel movements
  • tender and enlarged prostate
117
Q

How is chronic prostatitis managed?

A
  • α blockers (tamsulosin)
  • analgesia
  • antibiotics
  • laxatives for pain during bowel movement
118
Q

How is prostatitis investigated?

A
  • urine dipstick testing
  • urine microscopy, cultures and sensitivities
  • chlamydia and gonorrhoea NAAT testing
119
Q

What is epididymo-orchitis and what are the causes?

A
  • inflammation of the epididymis and testicle on one side
  • E. coli, chlamydia trachomatis, neisseria gonorrhoea, mumps
120
Q

What is the aetiology of nephrotic syndrome?

A
  • minimal change disease
  • focal segmental glomerulosclerosis
  • membranous nephropathy
121
Q

What is the triad of nephrotic syndrome symptoms?

A
  • proteinuria >3g/24hr
  • hypoalbuminaemia <30g/L
  • oedema
122
Q

What is the management of nephrotic syndrome?

A
  • high dose steroids
  • low salt diet
  • diuretics
  • albumin infusions
  • ACE-i
123
Q

What are the genetics and epidemiology behind autosomal dominant polycystic kidney disease?

A
  • mutation in PKD1/2 gene on chromosome 16
  • more common in males, presents age 20-30
124
Q

What is the presentation of ADPKD?

A
  • cystic enlargement of collecting ducts
  • liver cysts
  • intracranial aneurysms: subarachnoid haemorrhage
  • abdo pain ± haematuria
  • bilateral flank pain
125
Q

What is the pathophysiology behind the presentation of ADPKD?

A
  • PKD 1 + 2 code for polycystin (Ca channel)
  • when filtrate passes, channels open and calcium influx inhibits excessive growth
  • PKD mutation: Ca reduced so excess cilia growth > cysts
126
Q

How is ADPKD diagnosed and treated?

A
  • kidney USS
  • treat hypertension (ACE-i)
  • treat end stage renal failure (transplant)
  • laparoscopic cyst removal
127
Q

What are the genetics behind ARPKD?

A
  • mutation of PKDH1 on chromosome 6
  • codes for proteins creating tubules and healthy epithelial tissue
128
Q

What is the pathophysiology behind ARPKD?

A
  • oligohydraminos is lack of amniotic fluid
  • leads to Potter syndrome
  • leads to underdeveloped lungs and resp failure
129
Q

What are the symptoms of ARPKD?

A
  • cystic enlargement of collecting ducts
  • oligohydraminos
  • pulmonary hyperplasia
  • congenital liver fibrosis
  • Potter syndrome
130
Q

What is Potter syndrome?

A
  • dysmorphic features
  • underdeveloped ear cartilage and low set ears
  • flat nasal bridge
  • skeletal abnormalities
131
Q

What is the extrarenal presentation of ARPKD?

A
  • liver failure
  • portal hypertension
  • progressive renal failure
  • hypertension
  • chronic lung disease
132
Q

What is chronic kidney failure?

A

a permanent and progressive reduction in kidney function

133
Q

What are aetiologies of chronic kidney failure?

A
  • diabetes
  • hypertension
  • age
  • glomerulonephritis
  • PKD
  • meds: NSAIDs, PPIs, lithium
134
Q

What are risk factors for chronic kidney failure?

A
  • older age
  • diabetes
  • hypertension
  • smoking
  • nephrotoxic medication
135
Q

What is the pathophysiology behind chronic kidney disease?

A
  • damaged nephrons > reduced GFR
  • inc burden on remaining nephrons
  • compensatory RAAS to inc GFR causes inc transglomerular pressure and damages basement membrane selectiveness
  • leads to proteinuria and haematuria
  • mesangial scarring
136
Q

What is the presentation of chronic kidney disease?

A
  • pruritus
  • loss of appetite
  • nausea
  • oedema
  • muscle cramps
  • hypertension
  • pallor
137
Q

What investigations are done in chronic kidney disease?

A
  • eGFR with U&E: 2 tests 3 months apart
  • urine dipstick: haematuria
  • albumin:creatinine >3mg/mmol
  • renal USS
138
Q

What is the criteria for chronic kidney disease?

A

eGFR <60mL/min/1.73m^2

139
Q

What is the management of chronic kidney disease?

A
  • treat diabetes, htn, oedema and glomerulonephritis
  • exercise and dietary advice
  • atorvastatin for prevention of CVD
140
Q

How is anaemia of chronic disease treated?

A
  • IV/oral iron and erythropoietin
141
Q

What are the 5 stages of chronic renal disease?

A
  • G1 = >90
  • G2 = 60-89
  • G3a = 45-59
  • G3b = 30-44
  • G4 = 15-29
  • G5 = <15 (end-stage renal failure)
142
Q

What is the pathophysiology behind renal bone disease?

A
  • high serum phosphate due to reduced excretion and low vit D > less calcium absorbed
  • 2º hyperparathyroidism > inc osteoclast activity
143
Q

What are the features of renal bone disease?

A
  • osteomalacia
  • osteoporosis
  • osteosclerosis
144
Q

Where do renal stones most commonly get stuck?

A
  • vesico-ureteric junction
145
Q

What are the common complications of renal stones?

A
  • obstruction > AKI
  • infection > obstructive pyelonephritis
146
Q

What is the cause of renal stones?

A
  • hypercalcaemia is a common cause esp when paired with low urine output
147
Q

What types of kidney stones most commonly occur?

A
  • calcium oxalate (80%)
  • calcium phosphate
  • uric acid, struvite, cystine
148
Q

How do renal stones present?

A
  • unilateral loin to groin pain
  • colicky pain
  • haematuria
  • nausea, vomiting
  • reduced urine output
  • patient can’t lie still
149
Q

What investigations are done for renal stones?

A
  • urine dipstick: haematuria
  • bloods: FBC, U&Es
  • KUB CT
150
Q

What is the management of renal stones?

A
  • NSAIDs
  • extracorporeal shock wave lithotripsy
  • percutaneous nephrolithiotomy
  • tamsulosin can be used to help passage
151
Q

What are the NICE guidelines for the prevention of renal stones?

A
  • inc oral fluid intake (2-3L/day)
  • normal calcium intake (low intake inc risk)
  • lower oxalate intake (spinach, beetroot, nuts)
152
Q

Which medications can be used to prevent renal stones?

A
  • potassium citrate
  • thiazide diuretics
153
Q

What is membranous glomerulonephritis?

A
  • bimodal peak age 20 and 60
  • IgG and complement deposits on basement membrane
  • usually idiopathic
154
Q

How is glomerulonephritis/nephritic/nephrotic syndrome treated?

A
  • immunosuppression
  • blood pressure control (ACE-i or ARBs)
  • furosemide if oedema
155
Q

How is glomerulonephritis/nephritic/nephrotic syndrome investigated?

A
  • renal biopsy
  • to check for minimal change disease
156
Q

What is the pathophysiology behind nephrotic syndrome?

A
  • basement membrane in glomerulus becomes highly permeable to protein
  • proteins leak from blood > urine
  • leads to frothy urine
157
Q

What is focal segmental glomerulosclerosis?

A
  • tissue scarring in glomerulus
  • light microscope shows segmental sclerosis
  • treated by corticosteroids
158
Q

What are the investigations done in nephrotic syndrome?

A
  • light microscopy
  • electron microscopy
159
Q

What is seen on electron microscopy in minimal change disease and membranous nephropathy?

A
  • MCD: podocyte effacement + fusion
  • MN: subpodocyte immune complex deposition

Osha 2a (15 decks)

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