Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

MY REVISION - ALL TO DO > TO DO RENAL & GU > Flashcards

TO DO RENAL & GU Flashcards

1
Q

BPH
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

BPH
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

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

A

RUSHES

  • Retention
  • UTI’s
  • Stones (in bladder)
  • Haematuria (refractory to medical therapy)
  • Elevated creatinine
  • Symptom deterioration (despite maximal medical therapy)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

PROSTATE CANCER
What can cause prostate cancer?

A
  1. High testosterone levels
  2. Family history - 2/3x increased risk if 1st degree relative is affected
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

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

A
  • PSA = raised
  • digital rectal exam = asymmetrical, hard, nodular prostate
  • bone profile = hypercalcaemia + raised ALP in metastatic disease
  • liver profile (assess for liver mets)
  • U&Es (assess renal function)
  • multiparametric MRI = first line imaging
  • transrectal ultrasound (TRUS) - guided needle biopsy = gold standard

to consider
- bone scan
- CT abdomen + pelvis/MRI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

PROSTATE CANCER
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

TESTICULAR CANCER
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

TESTICULAR CANCER
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
  8. intersex conditions e.g. kleinfelters syndrome
  9. mumps orchitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

TESTICULAR CANCER
what are the clinical features of testicular cancer?

A

SYMPTOMS
- painless testicular lump
- hyperthyroidism
- gynaecomastia
- bone pain (indicates metastasis)
- breathlessness (indicates lung metastasis)

SIGNS
- firm, non-tender testicular mass (does not transluminate, hydrocele may be present)
- supraclavicular lymphadenopathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

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

A
  • ultrasound testicular doppler = first line
  • tumour markers (beta-HCG, AFP and LDH)

to consider:
- CT chest, abdomen and pelvis (used for staging)

NOTE: fine needle aspiration or needle biopsy must NOT be used due to risk of seeding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

HYDROCELE
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

GLOMERULONEPHRITIS
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

URINARY STONES
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

URINARY STONES
what is the most common type of stone?

A
  1. calcium oxalate
  2. uric acid (radiolucent = not visible on xray)
  3. calcium phosphate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

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

A
  • urinalysis = microscopic haematuria +/- pyuria (culture if septic)
  • CRP = elevated
  • U&Es = raised creatinine
  • bone profile + urate = elevated calcium
  • non-contrast CT KUB = GOLD STANDARD, to be performed within 14hrs

to consider
- 24hr urine monitoring
- renal tract USS
- x-ray KUB
- blood cultures
- coagulation profile

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

URINARY STONES
what is the management for pain?

A

ACUTE
- IV fluids + anti-emetics
- analgesia (NSAID (IM diclofenac), IV paracetamol if NSAID is contraindicated)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

URINARY STONES
what is the management of renal stones?

A
  • < 5mm + asymptomatic = watchful wait
  • 5-10mm = shockwave lithotripsy
  • 10-20mm = shockwave lithotripsy or ureteroscopy
  • > 20mm = percutaneous nephrolithotomy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

URINARY STONES
what is the management of uretic stones?

A
  • <10mm = shockwave lithotripsy (+/- alpha blockers)
  • 10-20mm = ureteroscopy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

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

A
  1. Ureteropelvic junction
  2. Pelvic brim
  3. Vesoureteric junction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

RENAL PHYSIOLOGY
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

RENAL PHYSIOLOGY
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

RENAL PHYSIOLOGY
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

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

A

ACEi cause efferent arteriole vasodilation = reduced GFR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

CKD
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

CKD
Briefly describe the pathophysiology of 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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

DIALYSIS
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

RENAL TRANSPLANT
Give 3 contraindications for renal transplant

A
  1. ABO incompatibility
  2. Active infection
  3. Recent malignancy
  4. Morbid obesity
  5. Age >70
  6. AIDS
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

RENAL TRANSPLANT
Name 4 potential complications of a kidney transplant

A
  1. Thrombosis
  2. Obstruction
  3. Infections - URTI, chest
  4. Rejection (12% in 1st year)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

DIURETICS
On which part of the nephron do thiazides act?

A

The distal tubule Act on NCC channels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

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

A

Collecting ducts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

AKI
what are the pre-renal causes of AKI?

A
  • hypovolaemia (reduced oral intake, haemorrhage, GI loss, renal loss, burns)
  • reduced cardiac output (heart failure, liver failure, sepsis, drugs)
  • drugs that reduce BP, circulating volume or renal blood flow (ACEi, ARBs, loop diuretics, aldosterone antagonists)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

AKI
What are the renal (intrinsic) causes of AKI?

A
  • toxins + drugs (antibiotics, contrast, chemotherapy)
  • vascular (vasculitis, theromboembolism)
  • tubular (acute tubular necrosis, rhabdomyolysis, myeloma)
  • interstitial causes (interstitial nephritis, lymphoma infiltration)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

AKI
what are the post-renal causes of AKI?

A

OBSTRUCTION
- renal stones
- blocked urinary catheter
- enlarged prostate
- GU tract tumours
- retroperitoneal fibrosis
- neurogenic bladder

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

AKI
What is the diagnostic criteria for AKI?

A

1/3 = diagnostic

  1. Rise in creatinine >26 mmol/L in 48 hours
  2. Rise in creatinine >1.5 x in last 7 days
  3. Urine output fall to < 0.5 ml/kg/h for more than 6 hours
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

AKI
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

AKI
what are the indications for renal replacement therapy?

A

AEIOU
- acidosis (refractory)
- electrolyte imbalance (refractory)
- ingestion of toxins
- oedema/overload
- uraemia (refractory)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

UTI
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

UTI
What is the first line treatment for an uncomplicated UTI?

A

NON-PREGNANT FEMALE
- 1st line = NITROFURANTOIN (if eGFR>45) or TRIMETHOPRIM for 3 days
- 2nd line = NITROFURANTOIN (if not used 1st line + eGFR>45) or PIVIMECILLINAM or FOSFOMYCIN for 3 days

PREGNANT FEMALE
- 1st line = NITROFURANTOIN (if eGFR>45 + avoid near term) for 7 days
- 2nd line = AMOXICILLIN (only if culture-sensitive) or CEFALEXIN for 7 days

CATHETERISED FEMALE
- 1st line = NITROFURANTOIN or TRIMETHOPRIM for 7 days

MALE
- 1st line = TRIMETHOPRIM or NITROFURANTOIN for 7 days
- 2nd line = AMOXICILLIN (only if culture sensitive) or CEFALEXIN for 7 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

CYSTITIS
what are the risk factors for cystitis?

A
  1. Urinary obstruction
  2. Previous damage to bladder epithelium
  3. Poor bladder emptying
  4. bladder stones
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

CYSTITIS
What is the treatment for cystitis?

A

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

2nd line = ciprofloxacin or Co-amoxiclav

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

PROSTATITIS
what are the causes of prostatitis?

A

acute:

  • streptococcus faecalis
  • e.coli (most common)
  • chlamydia

chronic:

  • bacterial (as above)
  • non-bacterial - elevated prostatic pressure, pelvic floor myalgia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

PROSTATITIS
How would you treat prostatitis?

A

1st line
- fluoroquinolone antibiotic (CIPROFLOXACIN), alternatives are trimethoprim + ofloxacin
- acute = 2-4 weeks
- chronic = 12 weeks

other treatment
- alpha blockers (TAMSULOSIN)
- NSAIDs
- stool softeners

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

URETHRITIS
URETHRITIS
what are the causes of urethritis?

A
  • N. gonorrhoea
  • chlamydia
  • trauma
  • urethral stricture
  • irritation
  • urinary calculi
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

URETHRITIS
what is the treatment for urethritis?

A

oral doxycycline for 7 days of single dose of azithromycin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

PYELONEPHRITIS
Describe the treatment for pyelonephritis

A

MILD DISEASE - ORAL ANTIBIOTICS
- oral cefalexin - 500mg BD or TDS for 7-10 days
- oral ciprofloxacin - 500mg BD for 7 days

SEVERE DISEASE - IV ANTIBIOTICS
- IV gentamicin (dosage based of body weight + renal function)
- IV ciprofloxacin 400mg TDS

ADJUNCT THERAPY
- hydration = oral or IV
- analgesia = PR DICLOFENAC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

AKI
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

PROSTATE CANCER
what are the risk factors for prostate cancer?

A
  • family history
  • increasing age
  • black
  • genetic
  • HOXB13, BRCA2
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

TESTICUAR TORSION
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

TESTICULAR TORSION
what is the clinical presentation of testicular torsion?

A

SYMPTOMS
- testicular (usually unilateral, sudden onset, excruciating, can be intermittent)
- Nausea + vomiting
- lower abdominal pain (referred)

SIGNS
- swollen, high-riding and tender testicle
- skin may be erythematous
- prehn’s negative (pain NOT relieved on lifting ipsilateral testicle)
- absent cremasteric reflex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

HYDROCELE
what is communicating hydrocele?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

EPIDIDYMAL CYST
what is the clinical presentation of epididymal cyst?

A
  • soft, round lump
  • typically at the top of the testicle, posteriorly
  • may be multiple/bilateral (may be painful)
  • transluminate (for large cysts, appearing separate from the testicle)
  • testis is palpable separately from cyst
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

POLYCYSTIC KIDNEY
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

POLYCYSTIC KIDNEY
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

POLYCYSTIC KIDNEY
what are the causes of autosomal recessive polycystic kidney disease?

A

PKHD1 mutation on long arm (q) of chromosome 6

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

CKD
how does diabetes cause CKD?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

CKD
how does hypertension cause CKD?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

CKD
what is stage 1 CKD?

A

eGFR > 90ml/min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

CKD
what is stage 2 CKD?

A

eGFR 60-89ml/min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

CKD
what is stage 3a CKD?

A

eGFR 45-59ml/min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

CKD
what is stage 4 CKD?

A

eGFR 29-15ml/min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

CKD
what is stage 5 CKD?

A

eGFR < 15ml/min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

GOODPASTURES
what is goodpastures disease?

A

Caused by autoantibodies (anti-GBM) to Type 4 collagen in glomerular and alveolar membrane

63
Q

GOODPASTURES
what is the clinical presentation of goodpastures disease?

A

Presents with SOB and oliguria due to respiratory and renal damage

64
Q

GOODPASTURES
what are the investigations for goodpasture’s disease?

A

bloods = anti-GBM antibodies
biopsy = linear deposits of antibodies along GBM

65
Q

GOODPASTURES
what is the management for goodpasture’s disease?

A

plasma exchange
steroids
cyclophosphamide (for immune suppression)

66
Q

POST STREP GLOMERULONEPHRITIS
what are the findings?

A

Bloods = anti-streptolysin O titres, low complement

Biopsy = granular subepithelial immune complex deposits (lumpy bumpy)

67
Q

POST STREP GLOMERULONEPHRITIS
what is the management for post strep glomerulonephritis?

A

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

68
Q

NEPHRITIC VS NEPHROTIC
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
69
Q

BLADDER CANCER
where does bladder cancer spread to?

A

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

70
Q

BLADDER CANCER
what are the investigations for bladder cancer?

A
  • urinalysis = haematuria
  • urinary cytology = cancer cells
  • FBC = anaemia (in chronic bleeding)
  • U&Es (assess renal failure)
  • bone profile = hypercalcaemia + raised ALP with bone mets
  • LFTs + coagulation screen = deranged in liver mets
  • flexible cystoscopy = to confirm tumour

further staging
- CT abdomen + pelvis
- CT urogram
- Pelvic MRI
- PET scan
- bone scan

71
Q

BLADDER CANCER
what is the management for bladder cancer?

A

SUPERFICIAL/NON-MUSCLE INVASIVE
- trans-urethral resection of bladder tumour with post-op dose of intravesical mitomycin C
- low risk = no further treatment
- intermediate risk = 6 doses intravesical mitomycin C
- high risk = intravesical BCG or radical cystectomy

MUSCLE-INVASIVE
- radical cystectomy (with neoadjuvant chemo) - will require urostomy
- radical radiotherapy (with neoadjuvant chemo)

LOCALLY ADVANCED OR METASTATIC
- chemotherapy (cis-platin based)
- palliative treatment (radiotherapy for symptom control)

72
Q

RENAL PHYSIOLOGY
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
73
Q

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

A

descending limb

74
Q

RENAL PHYSIOLOGY
what is the innervation of the external urinary sphincter?

A

pudendal nerve S2-S4

75
Q

RENAL PHYSIOLOGY
what is the innervation of internal urinary sphincter?

A

pelvic splanchnic nerve S2-S4

76
Q

RENAL PHYSIOLOGY
what is the innervation of the bladder?

A 
sympathetic = sympathetic chain T11-L2
parasympathetic = pelvic splanchnic S2-S4
77
Q

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

A

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

78
Q

RENAL PHYSIOLOGY
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

79
Q

CKD
what is stage 3b CKD?

A

eGFR 30-44ml/min

80
Q

DIALYSIS
what is the most common causative organism of peritonitis secondary to peritoneal dialysis?

A

staphylococcus epidermidis

s.aureus is another common cause

81
Q

DIALYSIS
what is the management of peritonitis secondary to peritoneal dialysis?

A

vancomycin + ceftazidime added to dialysis fluid

OR

vancomycin added to dialysis fluid + oral ciprofloxacin

82
Q

EPIDIDYMO-ORCHITIS
what is the management?

A

ANTIBIOTICS
- STI related = ceftriaxone 500mg-1g IM single dose + doxycycine 100mg BD for 10-14 days

  • UTI related = oflaxacin 200mg BD for 14 days or levofoxacin 500mg OD for 10 days

SUPPORTIVE CARE
- analgesia (paracetamol + NSAIDS)
- safety net
- referral

83
Q

BLADDER CANCER
what are the 2WW referral criteria?

A

> 45 + unexplained visible haematuria without UTI
45 + visible haematuria that persists/recurs after successful treatment of UTI
60 + unexplained microscopic haematuria + dysuria or raised WCC

84
Q

EPIDIDYMAL CYST
what conditions are associated with epididymal cysts?

A
  • polycystic kidney disease
  • cystic fibrosis
  • von Hippel-Lindau syndrome
85
Q

AKI
what are the different stages of AKI?

A

STAGE 1
- Cr rise to 1.5-1.9 x baseline
- Cr rise by 26umol/L
- fall in urine to <0.5ml/kg/hr for >6hrs

STAGE 2
- Cr rise to 2.0-2.9 x baseline
- fall in urine output to 0.5ml/kg/hr for >12 hrs

STAGE 3
- Cr rise to >3.0 x baseline
- Cr rise to >353.6umol/L
- fall in urine to <0.3ml/kg/hr for >24hrs
- in patients <18yr, fall in eGFR to <35ml/min/1.73m2

86
Q

RENAL CELL CARCINOMA
what are the risk factors?

A
  • increasing age
  • male
  • black ethnicity
  • smoking
  • obesity
  • hypertension
  • end-stage renal failure
  • Von Hippel-Lindau disease
  • Tuberous sclerosis
87
Q

RENAL CELL CARCINOMA
what is the management?

A

LOCALISED DISEASE
- partial nephrectomy (standard for T1 tumours)
- radical nephrectomy (standard for T2-4) +/- lymph node dissection + adenalectomy if involved
- minimally invasive procedures (radiofrequency ablation or embolisation) if unfit for surgery

METASTATIC DISEASE
- molecular therapy (sunitinib or pazopanib)
- radiotherapy
- cytoreductive surgery

88
Q

RENAL CELL CARCINOMA
what are the endocrine associations?

A

EPO = polycythaemia
PTH hormone-related peptide (PTHrP) = hypercalcaemia
ACTH = cushings syndrome
renin

89
Q

URINARY STONES
what are the risk factors?

A
  • dehydration
  • previous kidney stones
  • stone-forming foods (chocolate, rhubarb, spinach, tea, most nuts)
  • genetic
  • crohns disease
  • hypercalcaemia
  • hyperparathyroidism
  • kidney related disease (polycystic kidney)
  • drugs (loop diuretics, acetazolamide, protease inhibitors)
  • gout
90
Q

NEPHRITIC SYNDROME
what is the predominant symptom in nephritic syndrome?

A

haematuria

91
Q

NEPHRITIC SYNDROME
what are the causes?

A
  • IgA nephropathy
  • post-streptococcal GN
  • anti-GBM antibody disease (goodpastures syndrome)
  • alport’s syndrome
  • lupus nephritis
  • granulomatosis with polyangiitis (GPA)
  • microscopic polyangiitis (MPA)
  • eosinophilic granulomatosis with polyangiitis (eGPA)
  • MPGN
92
Q

NEPHRITIC SYNDROME
what are the features of IgA nephropathy?

A
  • IgA levels rise secondary to recent (in last 7 days) GI/resp infection
  • associated with coeliac disease
  • most common glomerulonephritis worldwide
93
Q

NEPHRITIC SYNDROME
what are the findings for IgA nephropathy?

A

Blood = high IgA titres, normal complement
Biopsy = mesangial deposits of IgA complexes

94
Q

NEPHRITIC SYNDROME
what is the management of IgA nephropathy?

A

no proteinuria = no treatment required

proteinuria 0.5-1g/day = ACEi
failure to respond to treatment = corticosteroids

95
Q

NEPHRITIC SYNDROME
what are the features of alport’s syndrome?

A

comprises of triad of ophthalmological issues, auditory issues and nephritic syndrome

x-linked dominant inheritance

96
Q

NEPHRITIC SYNDROME
what are the findings for Alport’s syndrome?

A
  • renal biopsy = gold standard (basket-weave appearance under electron microscope)
  • genetic testing = mutation in alpha chain of type IV collagen
97
Q

NEPHRITIC SYNDROME
what are the findings for lupus nephritis?

A
  • loop wire appearance
98
Q

NEPHRITIC SYNDROME
what are the features of granulomatosis with polyangiitis (Wegener’s granulomatosis)?

A
  • small vessel vasculitis
  • affects lungs, nasopharynx and kidneys
  • saddle nose deformity
99
Q

NEPHRITIC SYNDROME
what are the findings for granulomatosis with polyangiitis?

A

c-ANCA positive
renal biopsy = segmental necrotising glomerulonephritis

100
Q

NEPHRITIC SYNDROME
what are the features of microscopic polyangiitis?

A

small vessel vasculitis
affects lungs and kidneys

101
Q

NEPHRITIC SYNDROME
what are the findings for microscopic polyangiitis?

A

p-ANCA positive

102
Q

NEPHRITIC SYNDROME
what are the features of eosinophilic granulomatosis with polyangiitis (Churg-Strauss syndrome)?

A

characterised by:
- asthma
- allergic rhinitis
- nasal polyps
- eosinophilia
- small vessel vasculitis

103
Q

NEPHRITIC SYNDROME
what are the findings for eosinophilic granulomatosis with polyangiitis (Churg-Strauss syndrome)?

A
  • p-ANCA positive
  • eosinophilia
104
Q

NEPHRITIC SYNDROME
what are the general clinical features?

A

SYMPTOMS
- pink, red or ‘coke’ tinged urine (haematuria)
- foamy urine (proteinuria)

SIGNS
- oliguria (urine output <0.5ml/kg/hr)
- hypertension
- haematuria

105
Q

NEPHROTIC SYNDROME
what is the classic triad for nephrotic syndrome?

A
  • proteinuria (>3.5g/day)
  • hypoalbuminaemia (<30g/L) - leads to severe oedema
  • hyperlipidaemia
106
Q

NEPHROTIC SYNDROME
what is the predominant feature for nephrotic syndrome?

A

proteinuria

107
Q

NEPHROTIC SYNDROME
what are the causes?

A
  • minimal change disease (most common in children)
  • focal segmental glomerulosclerosis
  • membranous nephropathy
  • membranoproliferative GN
  • diabetes
  • amyloidosis
108
Q

NEPHROTIC SYNDROME
what are the general clinical features?

A

SYMPTOMS
- frothy urine
- facial and peripheral oedema
- recurrent infections (due to hypogammaglobinaemia)
- predisposition to VTE

SIGNS
- HTN (more common in nephritic)
- proteinuria
- limited/absent haematuria
-

109
Q

NEPHROTIC SYNDROME
what are the investigations?

A
  • urinalysis = proteinuria
  • 24hr urine protein collection = >3.5g protein
  • urine albumin-creatinine ratio (ACR) = raised
  • U&Es (to monitor eGFR)
  • LFTs = hypoalbuminaemia <25m/L
  • lipid profile = hypercholesterolaemia
  • renal USS

to consider
- renal biopsy (light + electron microscopy)
- assess for underlying cause

110
Q

NEPHROTIC SYNDROME
what is the most common cause in children?

A

minimal change disease

111
Q

NEPHROTIC SYNDROME
what is the most common cause in adults?

A

focal segmental glomerulosclerosis

112
Q

NEPHROTIC SYNDROME
what are the features of minimal change disease?

A
  • most common cause in children
  • responds excellent to steroids
  • may be preceded by URTI
  • associated with hodgkins lymphoma
113
Q

NEPHROTIC SYNDROME
what are the findings for minimal change disease?

A
  • light microscopy = normal glomeruli
  • electron microscopy = effacement of foot processes
114
Q

NEPHROTIC SYNDROME
what are the findings for focal segmental glomerulonephritis?

A
  • light microscopy = focal + segmental glomerular sclerosis
  • electron microscopy = effacement of foot processes
115
Q

NEPHROTIC SYNDROME
what are the findings in membranous nephropathy?

A
  • light microsopy = thick glomerular basement membrane
  • electron microscopy = subepithelial immune complex deposition (spike + dome pattern)
116
Q

NEPHROTIC SYNDROME
what are the findings for amyloidosis?

A
  • apple-green birefringence under polarise microscopy with congo red stain
117
Q

NEPHROTIC SYNDROME
what is the management?

A

LIFESTYLE
- low salt, protein and fat diet
- improve CVD risk factors

ADJUNCTIVE THERAPIES
- diuretics (relief of fluid overload)
- ACEi (reduce proteinuria)

MINIMAL CHANGE DISEASE
- corticosteroids

FOCAL SEGMENTAL GLOMERULONEPHRITIS
- corticosteroids
- ciclosporin if not responsive to steroids

MEMBRANOUS NEPHROPATHY
- corticosteroids + cyclophosphamide

118
Q

RENAL TRANSPLANT FAILURE
what is the management of acute graft failure?

A

may be reversible with steroids and immunosuppressants

119
Q

RENAL TUBULAR ACIDOSIS
what is it?

A

a group of conditions that all result in a hyperchloraemic metabolic acidosis with a normal anion gap

120
Q

RENAL TUBULAR ACIDOSIS
what is the blood results for renal tubular acidosis?

A

hyperchloraemic metabolic acidosis with normal anion gap

121
Q

RENAL TUBULAR ACIDOSIS
what are the different types?

A
  • type I (distal)
  • type II (proximal)
  • type III (mixed)
  • type IV (hyperkalaemic)
122
Q

RENAL TUBULAR ACIDOSIS
what is type I RTA?

A
  • defective H+ secretion in distal tubule
  • causes hypokalaemia
123
Q

RENAL TUBULAR ACIDOSIS
what are the causes of type I RTA?

A
  • idiopathic
  • RA
  • SLE
  • Sjogren’s
  • amphotericin B toxicity
  • analgesic nephropathy
124
Q

RENAL TUBULAR ACIDOSIS
what are the complications of type I RTA?

A

nephrocalcinosis
renal stones

125
Q

RENAL TUBULAR ACIDOSIS
what is type II RTA?

A
  • decreased HCO3- reabsorption in proximal tubule
  • causes hypokalaemia
126
Q

RENAL TUBULAR ACIDOSIS
what are the causes of type II RTA?

A
  • idiopathic
  • fanconi syndrome
  • wilson’s disease
  • cystinosis
  • outdated tetracyclines
  • carbonic anhydrase inhibitors (acetazolamide, topiramate)
127
Q

RENAL TUBULAR ACIDOSIS
what are the complications of type II RTA?

A
  • osteomalacia
128
Q

RENAL TUBULAR ACIDOSIS
what is type 3 RTA?

A
  • extremely rare
  • caused by carbonic anhydrase II deficiency
  • results in hypokalaemia
129
Q

RENAL TUBULAR ACIDOSIS
what is type IV RTA?

A
  • reduction in aldosterone leads in turn to reduction in proximal tubular ammonium excretion
130
Q

RENAL TUBULAR ACIDOSIS
what are the causes of type IV RTA?

A
  • hyperaldosteronism
  • diabetes
131
Q

RENAL TUBULAR ACIDOSIS
does it cause hypo or hyperkalaemia?

A

Type 1 = hypokalaemia
Type 2 = hypokalaemia
Type 3 = hypokalaemia
Type 4 = hyperkalaemia

132
Q

RENAL TUBULAR ACIDOSIS
what is the clinical presentation?

A
  • often asymptomatic
  • children may present with poor growth or rickets
  • alkaline urine = recurrent UTIs
  • osteomalacia (bone pain, # risk + weakness)
133
Q

RENAL TUBULAR ACIDOSIS
what are the investigations?

A
  • blood gas
  • urinary pH + electrolytes
  • ECG
  • U&Es
  • bone profile
  • magnesium
  • aldosterone + renin
  • USS KUB
134
Q

RENAL TUBULAR ACIDOSIS
what is the management?

A
  • stop causative medications
  • treat electrolyte imbalance
  • Type 1 + 2 = bicarbonate (or potassium citrate)
  • type 4 = lifelong mineralocorticoid + glucocorticoid replacement
135
Q

ACUTE INTERSTITIAL NEPHRITIS
what is it?

A

A cause of intrinsic AKI where there is acute tubulo-interstitial inflammation
It most commonly occurs due to a hypersensitivity reaction to certain medications

136
Q

ACUTE INTERSTITIAL NEPHRITIS
what are the causes?

A

MEDICIATIONS
- antibiotics (beta-lactams, cephalosporins, fluoroquinolones)
- NSAIDs
- diuretics
- rifampicin
- allopurinol
- PPIs
- ranitidine
- warfarin
- phenytoin

AUTOIMMUNE
- Sjogren
- SLE
- sarcoidosis

INFECTIONS

137
Q

ACUTE INTERSTITIAL NEPHRITIS
what are the clinical features?

A
  • rash (macular or maculopapular + fleeting)
  • fevers (low grade)
  • oliguria
  • flank pain or sensation of fullness
  • arthralgia
  • peripheral oedema (esp in NSAIDs)
  • hypertension
  • eosinophilia
138
Q

ACUTE INTERSTITIAL NEPHRITIS
what are the investigations?

A

URINE
- microscopy = pyuria + white cell casts
- culture = negative (sterile pyuria)

BLOODS
- FBC = eosinophilia
- U&Es
- autoimmune screen

IMAGING
- renal USS

139
Q

ACUTE INTERSTITIAL NEPHRITIS
what is the management?

A

CONSERVATIVE
- stop any causative medications
- supportive fluid management
- refer to specialist renal services

MEDICAL
- if autoimmune = steroids
- fluid overload = furosemide

140
Q

ACUTE TUBULAR NECROSIS/INJURY
what is it?

A

the most common cause of intrinsic AKI

renal tubular epithelial cells are damaged either due to nephrotoxic agent or ischaemic insult

141
Q

ACUTE TUBULAR NECROSIS/INJURY
what are the risk factors?

A
  • hypovolaemia
  • older age
  • CKD
  • recent use of nephrotoxic drugs
142
Q

ACUTE TUBULAR NECROSIS/INJURY
what are the causes?

A

ISCHAEMIC
- hypovolaemia
- diarrhoea/vomiting
- haemorrhage
- dehydration
- burns
- anaphylaxis
- sepsis
- surgery

NEPHROTOXIC CAUSES
- aminoglycosides (e.g. gentamicin)
- antifungals (e.g. amphotericin)
- chemotherapy
- antivirals
- NSAIDs
- contrast agents
- myoglobin
- haemoglobin

143
Q

ACUTE TUBULAR NECROSIS/INJURY
what are the clinical features?

A

Lethargy and malaise
Nausea and vomiting
Oliguria or anuria (polyuria may be seen in the recovery phase)
Confusion
Drowsiness
Peripheral oedema

144
Q

ACUTE TUBULAR NECROSIS/INJURY
what are the investigations?

A

URINE
- dipstick = may be false positive for blood
- microscopy = muddy brown granular casts and renal tubular epithelial cells
- osmolality = low
- urinary sodium = high

BLOODs
- blood gas
- U&Es
- urea:creatinine ratio
- FBC

IMAGING
- ECG
- USS KUB

145
Q

ACUTE TUBULAR NECROSIS/INJURY
what is the management?

A

CONSERVATIVE
- identify + treat cause
- avoid nephrotoxic meds
- fluid balance monitoring

MEDICAL
- IV fluids
- blood if haemorrhage

146
Q

CKD
how would you manage HTN complication from CKD?

A
  1. ACEi
  2. furosemide
147
Q

CKD
what change in eGFR and creatinine is acceptable when starting ACEi?

A
  • decrease in eGFR up to 25%
  • rise in creatinine up to 30%
148
Q

CKD
how would you manage proteinuria in CKD?

A
  1. ACEi
  2. SGLT-2
149
Q

CKD
what level of albumin-creatinine ratio (ACR) would you begin treatment for proteinuria?

A

if ACR > 30mg/mol + HTN
if ACR>70mg/mol even without HTN

150
Q

CKD
how would you manage CVD in CKD?

A

statin (+ aspirin)

151
Q

CKD
what is the management of bones in CKD?

A

reduce dietary phosphate intake
vitamin D

can use phosphate binders

152
Q

DIFFUSE PROLIFERATIVE GLOMERULONEPHRITIS
what is it?

A

can be nephritic or nephrotic syndrome

it is the most common manifestation of lupus nephritis

153
Q

DIFFUSE PROLIFERATIVE GLOMERULONEPHRITIS
what are the findings?

A

bloods = anti-dsDNA, ANA

biopsy = wire loop capillaries

MY REVISION - ALL TO DO (21 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions