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Phase 2a > Genitourinary COPY > Flashcards

Genitourinary COPY Flashcards

1
Q

What type of organs are the kidneys? Between which vertebral levels do they lie? What is their blood supply and at which level? What does it contain about a million of?

A
  • Retroperitoneal organs
  • Lie between T11-L3
  • Blood supply from renal artery direct from aorta at L1
  • Contain about a million nephrons
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2
Q

How does urine produced by the kidneys enter the bladder? What type of organ are these?

A
  • Ureters
  • Retroperitoneal organs
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3
Q

What anatomical structures make up the lower urinary tract?

A

Bladder -> bladder neck -> prostate gland -> urethra and urethral sphincter

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4
Q

Give 4 functions of the lower urinary tract.

A
  1. Storage of urine
  2. Converts the continuous process of excretion to an intermittent, controlled and volitional process
  3. Prevents leakage of stored urine
  4. Expulsion of urine
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5
Q

Which muscle is involved in contraction of the bladder during micturition? Describe its actions during storage and voiding.

A
  • Destrusor muscle
  • Storage = relaxed
  • Voiding = contracted
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6
Q

What are the two sphincters in the bladder? How do they differ between male and female? Describe their actions during storage and voiding.

A
  • Internal and external urethral sphincter
  • The EXTERNAL urethral sphincter is the same in both males and females
  • The INTERNAL urethral sphincter differs - MALES (consists of circular smooth rings, thought to prevent seminal regurgitation during ejaculation). FEMALES (thought to be function, i.e. no sphincteric muscle)
  • Storage = urethral sphincters contracted
  • Voiding = urethral sphincters relaxed
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7
Q

What type of epithelium lines the bladder?

A

Urothelium (transitional epithelium)

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8
Q

Describe the nervous control of the bladder and sphincter - which nerves supply the bladder, which vertebral level do they come from, which receptors do they act on and what is their action on the bladder?

A
  • Parasympathetic = make you PEE:
  • Pelvic nerves
  • S2-4
  • Act on M3 receptor
  • Make you PEE, i.e. destrusor muscle contraction
  • Sympathetic = STORAGE:
  • Hypogastric nerves
  • T12-L2
  • Act on B3 receptor
  • STORAGE, i.e. destrusor muscle relaxation
  • Somatic:
  • Pudendal nerve
  • S2-4
  • ACh activates nicotinic receptors
  • Innervates external urethral sphincter
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9
Q

The bladder is in the storage phase 98% of the time. What are the two reflexes that follow from this?

A
  • Appropriate to void = MICTURITION REFLEX
  • Inappropriate to void = GUARDING REFLEX
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10
Q

In the storage phase, why does the pressure remain low as volume increases?

A

RECEPTIVE RELAXATION, i.e. the bladder expands

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11
Q

Describe the micturition phase.

A

Higher volumes = bladder expands = afferent impulses stimulate parasympathetic action of detrusor = contraction. Pudendal nerve is inhibited and the external sphincter relaxes

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12
Q

Describe the guarding relfex.

A
  • Afferent signals from the pelvic nerve are received by the PMC/PAG and transmitted to higher cortical centres
  • If voiding is inappropriate the guarding reflex occurs:
  • Sympathetic (hypogastric) nerve stimulation results in detrusor relaxation
  • Pudendal nerve stimulation results in contraction of the external urethral sphincter
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13
Q

What are lower urinary tract symptoms (LUTS) in men > 50 likely to be due to?

A

Benign prostatic enlargement

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14
Q

What are the lower urinary tract symptoms (LUTS)?

A
  • Storage symptoms:
  • Frequency
  • Nocturia
  • Urgency
  • Urgency incontinence
  • Voiding symptoms:
  • Poor/intermittent stream
  • Post-micturition dribbling
  • Straining
  • Incomplete emptying
  • Hesitancy
  • HAEMATURIA
  • DYSURIA
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15
Q

What might dysuria suggest?

A

Inflammation

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16
Q

What is benign prostatic hyperplasia? How normal is it?

A
  • Benign prostatic hyperplasia = hyperplasia of the inner transitional zone of prostate gland which partially blocks the urethra
  • This is a normal part of ageing for men
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17
Q

What are the complications of benign prostatic hyperplasia?

A
  • Bladder hypertrophy = formation of bladder diverticula
  • Urinary retention = bladder calculi
  • Residual urine can be infection source = recurrent UTIs
  • Hydronephrosis = renal failure
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18
Q

What is the clinical presentation of benign prostatic hyperplasia?

A

LUTS:

  • Storage:
  • Frequency
  • Urgency
  • Nocturia
  • Urgency incontinence
  • Voiding:
  • Poor/intermittent stream
  • Post-micturition dribbling
  • Straining
  • Dysuria
  • Incomplete emptying
  • Hesitancy
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19
Q

What are the investigations for benign prostatic hyperplasia?

A
  • DIGITAL RECTAL EXAM - shows smooth but enlarged prostate
  • PSA - not overly accurate but usually done for completion (remember that you can’t do this at the same time as DRE etc.)
  • Urinalysis
  • Volume charting
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20
Q

Describe the management of benign prostate hyperplasia.

A
  • 1ST LINE = alpha blockers, e.g. tamsulosin - relaxes smooth muscle in bladder neck and prostate
  • 2nd line = 5-alpha reductase inhibitors, e.g. finasteride - blocks conversion of testosterone to dihydrotesterone which decreases prostate size
  • If does not respond to medication consider surgery:
  • TURP (Transurethral resection of prostate) = GOLD STANDARD. Required if there is acute urinary retention, gross haematuria or spreads to kidneys
  • LIFESTYLE - reduce caffeine/alcohol intake, relax when voiding
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21
Q

What is prostate cancer? What is its epidemiology? Which gene mutations is it commonly associated with?

A
  • Prostate cancer = a tumour of glandular origin, situated in the prostate. Most are slow growing but some can be very aggressive and MALIGNANT
  • Most common male malignancy and second most common cause of cancer mortality in men in the U.S.A.
  • Commonly associated with BRCA1/BRCA2 gene mutations
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22
Q

What are the risk factors for prostate cancer?

A
  • Afro-Caribbean
  • Family history/genetics
  • Increasing age
  • Anabolic steroids
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23
Q

Describe the clinical presentation of prostate cancer. Where does it commonly metastasise to?

A
  • LUTS
  • BONE PAIN
  • Weight loss
  • Fatigue
  • Night sweats
  • Commonly metastasises to: bone (SCLEROTIC BONY LESIONS), brain, liver, and lung
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24
Q

Describe the investigations for prostate cancer. What is the grading system?

A
  • DRE (cancerous = hard and craggy) and PSA (this is unreliable, with a high rate of false positives/negatives) are done in community
  • MULTIPARAMETRIC MRI = 1st line
  • TRANSRECTAL USS and BIOPSY = DIAGNOSTIC
  • GLEASON GRADING SYSTEM - the higher the score, the worse the prognosism (8-10 is high)
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25
Q

Describe the management for prostate cancer (local and metastatic). How hormone sensitive is it?

A
  • If local: PROSTATECTOMY (<70), ACTIVE SURVEILLANCE (>70 and low risk), RADIOTHERAPY
  • If metastatic: CHEMOTHERAPY, RADIOTHERAPY, BILATERAL ORCHIECTOMY (gold standard hormonal treatment), Goserelin (suppresses testosterone production as testosterone stimulates growth of prostate cancer), palliative treatments focusing on relieving symptoms, e.g. TURP
  • It is the most hormone sensitive malignancy
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26
Q

What is testicular cancer? Which demographic is it common in? What is the survival rate like? What are the two types of germ cell tumours?

A
  • Testicular cancer arises from the germ cells in the testes. Germ cells are cells that produce gametes (sperm in males). There are other, rare tumours in the testes, e.g. non-germ cell tumours and secondary metastases
  • Most common solid tumour in men aged 20-45
  • Good survival rate (98% 5 year survival)
  • Two types:
  • Seminomas
  • Non-seminomas (most teratomas)
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27
Q

What are the risk factors for testicular cancer?

A
  • Age 20-45
  • Caucasian
  • Cryptorchidism
  • Previous testicular cancer
  • HIV
  • Family history
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28
Q

What is the clinical presentation of testicular cancer?

A
  • PALPABLE LUMP WITHIN THE TESTIS - non-transilluminable (light can’t get through tumour), may be painful/painless
  • Gynaecomastia (especially Leydig cell tumour)
  • Haematospermia
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29
Q

What are the investigations for testicular cancer?

A
  • SCROTAL ULTRASOUND (urgent) is usually the initial investigation
  • CXR if symptomatic for pulmonary metastases
  • Tumour markers (not always raised, not always diagnostic, can be useful to check response before and after surgery) - alpha-fetoprotein, beta-hCG, LDH
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30
Q

Describe the management for testicular cancer.

A

Depending on the staging (Royal Marsden used):

  • URGENT RADICAL INGUINAL ORCHIECTOMY +/- a testicular prosthesis - this is for seminoma
  • CHEMOTHERAPY for non-seminoma (alpha-feto protein)
  • Semen cryopreservation
  • Treatment for metastatic disease - retroperitoneal lymph node dissection if tumour has metastasised to lymph nodes, chemotherapy, radiotherapy
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31
Q

Where does bladder cancer arise from? What is the most common subtype? What are the most common sites of metastasis?

A
  • Bladder cancer = arises from the urothelium
  • Most common subtype is TRANSITIONAL CELL CARCINOMA of the bladder (90%)
  • Most common sites of metastasis = lymph nodes, bones, lung, liver
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32
Q

What are the risk factors for bladder cancer?

A
  • Increasing age
  • Smoking
  • Male
  • Caucasian
  • Exposure to DYES/RUBBER/LEATHER/TEXTILES + PAINT - hairdresser, painter etc. (so question would be painter and painless visible haematuria)
  • Cyclophosphamide (RA/chemotherapy) + previous pelvic radiotherapy
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33
Q

What is the clinical presentation of bladder cancer?

A
  • PAINLESS VISIBLE HAEMATURIA (can be non-visible too, one to remember for exams)
  • Urgency
  • Suprapubic/pelvic mass pain
  • Recurrent UTI
  • Symptoms of systemic spread - bone pain, weight loss etc.
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34
Q

What are the investigations for bladder cancer?

A
  • FLEXIBLE CYSTOSCOPY
  • Bloods
  • Urine sample for microscopy + culture
  • Ultrasound
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35
Q

Describe the management for bladder cancer.

A
  • Psychosocial factors: cancer specialist nurse support, Macmillan support
  • Medical: radiotherapy, chemotherapy (intravesical therapy or systemic) + symptomatic relief
  • Surgical: TRANSURETHRAL RESECTION OF BLADDER TUMOUR (TURBT), radical cystectomy, cystodiathermy
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36
Q

What is the most common type of kidney cancer? How is it usually discovered?

A
  • Most common type is RCC = malignant cancer of proximal convoluted tubule
  • Often asymptomatic and discovered incidentally - 25% have metastasis at presentation
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37
Q

What is the clinical presentation of kidney cancer?

A

Classical triad:

  • HAEMATURIA
  • Vague LOIN PAIN
  • PALPABLE mass in abdomen/lower back
  • May present with VARICOCELE - invasion of left renal vein leads to compression of left testicular vein
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38
Q

What are the investigations for kidney cancer?

A
  • USS (1st line)
  • CT chest/abdomen/pelvis (more sensitive than USS)
  • RENAL BIOPSY = diagnostic
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39
Q

Describe the management for kidney cancer.

A

Surgery to remove the tumour is first line:

  • PARTIAL NEPHRECTOMY = part of the kidney removed
  • RADICAL NEPHRECTOMY = entire kidney removed plus surrounding tissue
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40
Q

What are the complications of kidney cancer?

A

PARANEOPLASTIC CHANGES - polycythaemia, HTN, hypercalcaemia, Cushing’s

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41
Q

What are the 7 functions of the kidney? What is the acronym for this?

A
  • AWETBED:
  • Acid-base balance
  • Water removal
  • EPO
  • Toxins
  • BP - produces renin
  • Electrolyte balance, e.g. sodium, potassium
  • Vitamin D activation

(Urea excretion as well)

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42
Q

What is the basic unit of the kidney? In which parts of the kidney are these found?

A
  • Nephron = basic unit of the kidney
  • Millions of nephrons in the cortex + medulla:
  • Renal corpuscle (glomerulus within Bowman’s capsule) = filter
  • Proximal convoluted tubule = for reabsorbing solutes
  • Loop of Henle = for concentrating urine
  • Distal convoluted tubule = for reabsorbing more water and solutes
  • Collecting duct = for reabsorbing water + controlling acid-base + ion balance
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43
Q

What is the cardiac output in L/min? What is the renal blood flow? How about urine flow?

A
  • Cardiac output = 5L/min
  • Renal blood flow = 1L/min
  • Urine flow = 1ml/min
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44
Q

What is the pathway of the renal artery to the glomerular and peritubular artery?

A

Renal artery –> interlobar artery –> arcuate artery –> interlobular artery –> afferent arteriole –> (nephron) glomerular capillary and peritubular capillary

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45
Q

What is glomerular filtration?

A

Passage of fluid from the blood into Bowman’s space to form the filtrate

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46
Q

What does the filtration barrier of the glomerulus consist of?

A
  • Endothelium - fenestrated
  • Glomerular basement membrane - T4 collagen, -ve charge
  • Epithelium - podocytes with foot processes
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47
Q

What can and can’t pass through the filtration barrier?

A
  • Small molecules + ions up to 10kDa can pass freely, e.g. glucose, uric acid, potassium, creatinine
  • Larger molecules increasingly restricted
  • Fixed negative charge in glomerular basement membrane repels negatively charged anions
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48
Q

What is the glomerular filtration rate (GFR)? How is it calculated? What is the average GFR in a 70kg person?

A
  • The volume of fluid filtered from the glomerulus to the Bowman’s Space per unit time
  • GFR = Kf (Pgc - Pbs - Pi gc) - P is hydrostatic pressure, Pi is oncotic pressure
  • In a 70kg person the average GFR = 125ml/min
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49
Q

What are the factors affecting GFR?

A
  • Blood pressure = increase in BP –> increased hydrostatic pressure –> increase in GFR
  • Size of substance = albumin + all that is attached (lipophilic molecules) to it is unable to cross
  • Charge of substance = BM is negatively charged, repels other -vely charged substances, e.g. albumin
  • Attachment to protein = albumin
  • Capillary permeability
  • Surface area
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50
Q

What do we use to measure GFR and why? Which substance do we use clinically? What is the gold standard for measuring inulin?

A
  • Use of a marker substance: free filtered (not attached to large proteins), not metabolised + not secreted/reabsorbed
  • Amount excreted per minute = amount filtered per minute
  • GFR = Um (concentration of marker substance in urine) x urine flow rate / Pm (concentration of marker substance in plasma)
  • Clinically: CREATININE (muscle metabolite)
  • GOLD STANDARD = INULIN
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51
Q

Give an example of a marker substance used for estimating GFR.

A

Creatinine

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52
Q

Estimating GFR: Give 3 essential features of a marker substance.

A
  1. Not metabolised
  2. Freely filtered
  3. Not reabsorbed/secreted
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53
Q

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

A

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

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54
Q

What is the effect on GFR of afferent arteriole vasoconstriction?

A

Decreased GFR

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55
Q

What is the effect on GFR of efferent arteriole vasoconstriction?

A

Increased GFR

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56
Q

What is renal clearance? How is this calculated?

A
  • Volume of plasma from which a substance is completely removed by the kidney per unit time
  • Marker substance is freely filtered at the glomerulus + is neither reabsorbed nor secreted in the tubule, so all the marker substance that is filtered will end up in the urine, no more (as it is not secreted) and no less (as it is not reabsorbed)
  • Clearance = urine concentration x urine volume / plasma concentration
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57
Q

Where in the nephron does the bulk of reabsorption occur?

A

PCT

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58
Q

What 7 things are reabsorbed at the PCT?

A
  1. Sodium
  2. Chlorine
  3. Potassium
  4. Glucose
  5. Water
  6. Amino acids
  7. Bicarbonate
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59
Q

What happens in the loop of Henle? In which nephrons are these found? What are the two cell types lined by?

A
  • 2 parts: descending and ascending
  • Descending: H2O reabsorption (impermeable to ions)
  • Ascending: Na+, K+ and Cl- reabsorption, has thin (simple squamous epithelium) + thick (low cuboidal) part
  • Found only on juxtamedullary (15%) nephrons, cortical (85%) nephrons do not extend into medulla
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60
Q

What happens in the distal convoluted tubule? What is the macula densa?

A
  • Fine tuning, absorption of solutes - beginning to concentrate the urine. Acidified the urine by secreting H+ ions into it
  • Exchanges urinary Na+ for body K+, this effect is mediated by aldosterone
  • Macula densa = detects Na+ concentration. If low (indicator of low GFR) –> sends signals to release renin –> RAAS –> increase in BP –> increase GFR
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61
Q

What happens in the collecting duct? What are the two cell types and what do they do? What are the cells lined by?

A
  • Acid secretion and concentration of urine, hormones such as aldosterone and ADH act here
  • 2 cells:
  • Principal cells (respond to aldosterone = exchanging Na+ for K+ and ADH = increasing water reabsorption)
  • Intercalated cells (responsible for exchanging acid for base). Alpha intercalated cells secrete acid, beta intercalated cells secrete bicarbonate
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62
Q

What is nephrolithiasis? Who are they more common in? How do they come about?

A
  • Nephrolithiasis = kidney stones. They are hard stones that form in the renal pelvis, where the urine collects before travelling down the ureters
  • Slightly more common in men (testosterone -> increased oxolate)
  • Stones form when solutes precipitate out as crystals in urine
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63
Q

What are the different types of nephrolithiasis?

A
  • Calcium stones:
  • CALCIUM OXOLATE (more common) (80%)
  • Calcium phosphate
  • Other types of kidney stones include:
  • Uric acid – these are not visible on x-ray
  • Struvite – produced by bacteria, so associated with infection
  • Cystine – associated with cystinuria, an autosomal recessive disease
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64
Q

What are the risk factors for nephrolithiasis?

A
  • Raised serum calcium (hypercalcaemia, hyperparathyroidism)
  • Reduced urine output (chronic dehydration, high protein/salt diet)
  • Recurrent UTIs
  • Congenital abnormalities
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65
Q

What are the two key complications of nephrolithiasis?

A
  • OBSTRUCTION leading to acute kidney injury
  • INFECTION with obstructive pyelonephritis
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66
Q

What is the clinical presentation of nephrolithiasis?

A
  • RENAL COLIC. This UNILATERAL LOIN TO GROIN PAIN that can be excruciating (“worse than childbirth”) and COLICKY (fluctuating in severity) as the stone moves and settles
  • Restlessness
  • N+V
  • Haematuria
  • Dysuria
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67
Q

What are the investigations for nephrolithiasis? What would these show?

A
  • Urine dipstick usually shows HAEMATURIA
  • Bloods: FBC, CRP, U+Es - check for hypercalcaemia and infection
  • GOLD STANDARD = NON-CONTRAST CT of the kidneys, ureters and bladder (KUB)
  • Abdominal X-ray will show calcium stones but not uric acid stones (radiolucent)
  • Ultrasound KUB is less preferred
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68
Q

Describe the management for nephrolithiasis.

A
  • NSAIDs = most effective analgesia, e.g. IM diclofenac
  • Antiemetics for N+V, antibiotics if infection
  • Watchful waiting for stones <5mm as they usually pass - tamsulosin (alpha-blocker) can help with this
  • If do not pass, >10mm, or complete obstruction or infection = SURGERY:
  • ESWL (Extracorporeal shock wave lithotripsy) = break stone into smaller fragments using shockwaves
  • Uteroscopy
  • PCNL (percutaneous nephrolithotomy) = nephroscope inserted to remove stone
  • Lifestyle: decrease sodium and protein intake, increased citrus fruit, adequate fluid intake
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69
Q

What is chronic kidney disease? What is the aetiology?

A
  • Abnormal kidney function present for >3 MONTHS
  • Aetiology:
  • Diabetes
  • Hypertension
  • Age-related decline
  • Glomerulonephritis
  • Polycystic kidney disease
  • Medications such as NSAIDS, proton pump inhibitors and lithium
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70
Q

What are the risk factors for chronic kidney disease?

A
  • Older age
  • Hypertension
  • Diabetes
  • Smoking
  • Use of medications that affect the kidneys, e.g. NSAIDS
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71
Q

Describe the presentation of chronic kidney disease.

A
  • Usually CKD is ASYMPTOMATIC and diagnosed upon testing. Signs and symptoms usually due to uraemia:
  • Pruritus
  • Nausea
  • Reduced appetite
  • Oedema
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72
Q

What are the investigations for CKD?

A
  • Bloods: U+E to check the ESTIMATED GLOMERULAR FILTRATION RATE (eGFR):
  • G1 = >90 mL/min/1.73m^2
  • G2 = 60-89 mL/min/1.73m^2 (<60 = CKD)
  • G3a = 45-59 mL/min/1.73m^2
  • G3b = 30-44 mL/min/1.73m^2
  • G4 = 15-29 mL/min/1.73m^2
  • G5 = <15 mL/min/1.73m^2 = end-stage renal failure
  • Urinalysis:
  • Proteinuria can be checked using urine albumin:creatinine ratio
  • Haematuria can be checked using a urine dipstick
  • Renal ultrasound
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73
Q

What are the complications of CKD?

A
  • Anaemia
  • Renal bone disease
  • Cardiovascular disease
  • Peripheral neuropathy
  • Dialysis related problems
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74
Q

Describe the management for CKD.

A
  • ACE inhibitors are FIRST LINE
  • CKD is irreversible in many:
  • Slowing the progression of the disease: optimise diabetic control, optimise hypertensive control, treat glomerulonephritis
  • Reducing the risk of complications: exercise, maintain a healthy weight and stop smoking, special dietary advice about phosphate, sodium, potassium and water intake, offer atorvastatin 20mg for primary prevention of cardiovascular disease
  • Treating complications: ORAL SODIUM BICARBONATE to treat metabolic acidosis, IRON supplementation and EPO to treat anaemia, vitamin D to treat renal bone disease, dialysis in end stage renal failure, renal transplant in end stage renal failure
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75
Q

Who is renal replacement therapy considered for? What are the different types?

A
  • Considered for patients with: END STAGE RENAL FAILURE (eGFR< 15 = stage 5), acidosis not responsive to bicarb, persistent electrolyte disturbances, persistent oedema, severe symptoms of uraemia (seizures, LOC)
  • RRT = therapy that replaces the normal blood-filtering function of the kidney:
  • Haemodialysis - most common
  • Peritoneal dialysis
  • Renal transplant
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76
Q

What unit is used to express eGFR?

a) mL/sec/1.73m2
b) mL/min/1.73m2
c) m2/min
d) mL/min

A

B) mL/min/1.73m^2

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77
Q

What is the most common cause of CKD?

A

Diabetes

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78
Q

What is acute kidney injury?

A

Acute kidney injury (AKI) is defined as an acute drop in kidney function. It is diagnosed by measuring the serum CREATININE +/- decreased urine output. Results in IMBALANCE IN ELECTROLYTES and azotaemia (increased creatinine/nitrates) = BAD

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79
Q

What is creatinine?

A

Creatinine is a waste product made by your muscles as part of everyday activity. Normally, your kidneys filter creatinine from your blood and send it out of the body in your urine. If there is a problem with your kidneys, creatinine can build up in the blood

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80
Q

What are the risk factors for AKI?

A
  • CKD
  • Diabetes
  • Hypertension
  • Older age (> 65 years)
  • Nephrotoxic medications, e.g. NSAIDs, ACEi
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81
Q

What are the three types of causes of AKI?

A
  • Pre-renal
  • Intra-renal
  • Post-renal
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82
Q

Describe the pre-renal causes of AKI.

A

Pre-renal pathology is the MOST COMMON cause of acute kidney injury. It is due to inadequate blood supply to kidneys reducing the filtration of blood. Inadequate blood supply may be due to:

  • Dehydration
  • Hypotension (shock)
  • Heart failure

(decreased volume = decreased perfusion = decreased GFR and decreased creatinine clearance = RAAS activation = increased Na+, urea + BP)

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83
Q

Describe the intra-renal causes of AKI.

A

This is where INTRINSIC DISEASE in the kidney is leading to reduced filtration of blood. It may be due to:

  • Glomerulonephritis - barrier damage + protein leakage = decreased oncotic pressure = decreased GFR
  • Interstitial nephritis = inflammation and immune cells =
  • Acute tubular necrosis
  • Vasculitis
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84
Q

Describe the post-renal causes of AKI.

A

Post renal acute kidney injury is caused by OBSTRUCTION TO THE OUTFLOW of urine from the kidney, causing back-pressure into the kidney and reduced kidney function. This is called an OBSTRUCTIVE UROPATHY. Obstruction may be caused by:

  • Kidney stones
  • Masses such as cancer in the abdomen or pelvis
  • Ureter or urethral strictures
  • Enlarged prostate or prostate cancer
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85
Q

What is the clincal presentation of AKI?

A
  • Universal: OLIGURIA (<0.5 mL/kg/hr >6hrs), HIGH CREATININE, hyperkalaemia, uraemia
  • Pre-renal: hypotension, signs of liver or heart failure (oedema)
  • Intra-renal: infection, signs of underlying disease
  • Post-renal: LUTS (BPH)
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86
Q

What are the investigations for AKI?

A
  • URINALYSIS for protein, blood, leucocytes, nitrites and glucose:
  • Leucocytes and nitrites suggest infection
  • Protein and blood suggest acute nephritis (but can be positive in infection)
  • Glucose suggests diabetes
  • U+E - eGFR
  • CREATININE levels - a rise in serum creatinine of 26 micromol/L or greater within 48 hours
  • Ultrasound of the urinary tract is used to look for obstruction
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87
Q

What is the NICE criteria for AKI?

A
  • Rise in creatinine of ≥ 25 micromol/L in 48 hours
  • Rise in creatinine of ≥ 50% in 7 days
  • Urine output of < 0.5ml/kg/hour for > 6 hours
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88
Q

Describe the management for AKI.

A
  • First step = identify and treat underlying cause:

  • FLUID REHYDRATION with IV fluids in pre-renal AKI
  • STOP NEPHROTOXIC MEDICATIONS such as NSAIDS and antihypertensives that reduce the filtration pressure (i.e. ACE inhibitors)
  • RELIEVE OBSTRUCTION in a post-renal AKI, e.g. insert a catheter for a patient in retention from an enlarged prostate
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89
Q

Describe the complications of AKI.

A
  • Hyperkalaemia
  • Fluid overload, heart failure and pulmonary oedema
  • Metabolic acidosis
  • Uraemia (high urea) can lead to ENCEPHALOPATHY or PERICARDITIS
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90
Q

Describe 1 pre-renal cause, 1 renal, 1 post-renal cause of AKI.

A
  • Pre-renal: hypotension
  • Intra-renal: glomerulonephritis
  • Post-renal: kidney stones
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91
Q

List 3 risk factors for AKI.

A
  • CKD
  • Hypertension
  • Diabetes
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92
Q

Which 2 factors are important for the diagnosis of AKI?

a. Polyuria, serum creatinine
b. Serum creatinine, oliguria
c. Polyuria, eGFR
d. Oliguria, urine creatinine
e. eGFR, serum creatinine

A

E

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93
Q

What are the different types of urinary tract infections?

A
  • Pyelonephritis - infection of the kidneys
  • Urethritis – infection of the urethra
  • Cystitis – infection of the bladder
  • Prostatitis - infection of the prostate
  • Vaginitis – infection of the vagina
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94
Q

What is pyelonephritis? What does it affect? How is it most commonly acquired?

A
  • Pyelonephritis refers to inflammation of the kidney resulting from bacterial infection. The inflammation affects the renal pelvis (join between kidney and ureter) and parenchyma (tissue)
  • Most commonly acquired via ASCENDING TRANSURETHRAL SPREAD but can be via blood or lymphatics
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95
Q

What are the common causes of pyelonephritis?

A
  • Majority are caused by UPEC (gram negative, anaerobic, rod-shaped bacteria)
  • Other causes:
  • Klebsiella pneumoniae (gram-negative anaerobic rod)
  • Enterococcus
  • Pseudomonas aeruginosa
  • Staphylococcus saprophyticus
  • Candida albicans (fungal)
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96
Q

Describe the presentation of pyelonephritis.

A
  • Similar presentation to lower UTIs (i.e. dysuria, suprapubic discomfort and increased frequency) plus the ADDITIONAL TRIAD OF SYMPTOMS:
  • Fever, loin pain, N+V
  • Patients may also have: systemic illness, loss of appetite, haematuria, renal angle tenderness on examination
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97
Q

Describe the investigations for pyelonephritis.

A
  • 1st line = urine dipstick (will show signs of infection)
  • GOLD STANDARD - mid-stream urine for MC+S (microscopy, culture and sensitivity)
  • Blood tests will show raised WBCs + raised inflammatory markers, e.g CRP
  • Urgent USS to detect stones, obstruction or incomplete bladder emptying
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98
Q

Describe the management for pyelonephritis.

A

Referall to hospital if there are features of sepsis (SEPSIS SIX (3 tests, 3 treatments):

  • Three tests: blood lactate level, blood culture, urine output
  • Three treatments: oxygen to maintain oxygen saturations of 94-98% (or 88-92% in COPD), empirical broad-spectrum IV antibiotics (according to local guidelines), IV fluids
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99
Q

What is urethritis? What are the causes?

A
  • Urethral inflammation due to infectious or non-infectious cause
  • Infectious: gonococcal (NEISSERIA GONORRHOEA) or non-gonococcal (CHLAMYDIA TRACHOMATIS)
  • Non-infectious: trauma, chemical irritation
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100
Q

What are the risk factors for urethritis?

A
  • Biologically male, young
  • Multiple sexual partners
  • Partner with a sexually transmitted disease (STD)
  • Unprotected sexual intercourse
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101
Q

Describe the clinical presentation of urethritis.

A
  • Skin lesion
  • Dysuria +/- discharge (blood/ pus)
  • Urethral pain
  • Penile discomfort/pruritus
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102
Q

What are the investigations for urethritis?

A
  • Nucleic acid amplification tests (NAAT)
  • Microscopy and culture of urethral discharge
  • Urine dipstick to exclude UTI
  • STI testing
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103
Q

Describe the management for urethritis.

A

Management of underlying cause - antibiotics, e.g. azithromycin and partner notification

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104
Q

What is the major complication of urethritis?

A

Reactive arthritis - triad of conjuctivitis, urethritis and arthritis - ‘can’t see, can’t pee, can’t climb a tree’

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105
Q

What is cystitis? Who are more susceptible? What are the causes?

A
  • Cystitis is a chronic condition causing inflammation in the bladder
  • Women are more susceptible due to SHORTER URETHRA and SHORT PROXIMITY to anus which allows bacteria transfer
  • Causes: KEEPS: Klebsiella, E.coli (most common), Enterococci, Proteus species, Staph aureus/saprophyticus
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106
Q

Describe the clinical presentation of cystitis.

A
  • SUPRAPUBIC PAIN, worse with a full bladder and often relieved by emptying the bladder
  • FREQUENCY of urination
  • URGENCY of urination
  • Confusion (in elderly)
  • Dysuria
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107
Q

Describe the investigations for cystitis.

A
  • 1st line = urine dipstick = increased leukocytes/blood/nitrates
  • Gold standard = MID-STREAM MC+S
  • Cystoscopy - for bladder cancer
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108
Q

Describe the management for cystitis.

A
  • Antibiotics: TRIMETHOPRIM/NITROFURANTOIN (3 day course for women, 7 day for men/complicated women). In pregnancy = trimethoprim cannot be used in 1st trimester (inhibits folate synthesis), nitrofurantoin cannot be used in 3rd trimester - amoxicillin, cefalexin can both be used
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109
Q

What is prostatitis? What are the two types?

A
  • Prostatitis refers to inflammation of the prostate. It can be classed as:
  • Acute bacterial prostatitis – acute infection in the prostate, presenting with a more rapid onset of symptoms
  • Chronic prostatitis – symptoms lasting for at least 3 months
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110
Q

Describe the clinical presentation of acute and chronic prostatitis.

A
  • Chronic prostatitis presents with at least 3 months of: pelvic pain, LUTS, sexual dysfunction, pain with bowel movements + tender and enlarged prostate
  • Acute prostatitis = more acute presentation of similar symptoms and systemic symptoms of infection, e.g. fever, myalgia
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111
Q

What are the investigations for prostatitis?

A
  • Urine dipstick testing can confirm evidence of infection
  • Urine MC&S can identify the causative organism and the antibiotic sensitivities
  • Chlamydia and gonorrhoea NAAT testing on a first pass urine, if sexually transmitted infection is considered
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112
Q

Describe the management of acute and chronic prostatitis.

A
  • Acute:
  • Hospital admission for systemically unwell or septic patients
  • Oral antibiotics, typically for 2-4 weeks (e.g., ciprofloxacin, ofloxacin or trimethoprim)
  • Analgesia (paracetamol or NSAIDs)
  • Laxatives for pain during bowel movements
  • Chronic:
  • Alpha-blockers (e.g., tamsulosin) relax smooth muscle, with rapid improvement in symptoms
  • Analgesia (paracetamol or NSAIDs)
  • Psychological treatment, where indicated (e.g., cognitive behavioural therapy and / or antidepressants)
  • Antibiotics if less than 6 months of symptoms or a history of infection (e.g., trimethoprim or doxycycline for 4-6 weeks)
  • Laxatives for pain during bowel movements
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113
Q

What is the difference between complicated and uncomplicated UTI?

A
  • Uncomplicated UTI — UTI caused by typical pathogens in people with a normal urinary tract and kidney function, and no predisposing co-morbidities
  • Complicated UTI — UTI with an increased likelihood of complications such as persistent infection, treatment failure and recurrent infection
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114
Q

What are the scrotal diseases to study?

A
  • Varicocele
  • Testicular torsion
  • Epididymal cyst
  • Epididymitis
  • Hydrocele
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115
Q

What is a varicocele? Which side is more affected and why?

A
  • A varicocele is the abnormal dilation of the internal spermatic veins and pampiniform plexus that drain blood from the testis
  • Left side more commonly affected (angle that left testicular vein enters the left renal vein = increased flow resistance)
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116
Q

What is varicocele the most common cause of in young adults?

A

Scrotal enlargement

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117
Q

What are the complications of varicocele?

A

Testicular damage = atrophy = poor sperm production + quality = infertility

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118
Q

What is the clinical presentation of varicocele?

A
  • Feels like a BAG OF WORMS
  • Dragging/soreness/heaviness of the scrotum
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119
Q

What are the investigations for a varicocele?

A
  • Clinical diagnosis
  • Doppler ultrasound
  • Semen analysis
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120
Q

Describe the treatment for varicocele.

A

Surgical repair if there is pain, infertility, or testicular atrophy

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121
Q

What is testicular torsion? What does a delay in treatment cause?

A
  • Testicular torsion refers to twisting of the spermatic cord with rotation of the testicle
  • It is a urological emergency - delay in treatment increases the risk of ischaemia and necrosis of the testicle, leading to sub-fertility or infertility
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122
Q

Describe a cause of testicular torsion.

A
  • A BELL-CLAPPER DEFORMITY is one of the causes of testicular torsion

Normally, the testicle is fixed posteriorly to the tunica vaginalis. A bell-clapper deformity is where the fixation between the testicle and the tunica vaginalis is absent. The testicle hangs in a horizontal position (like a bell-clapper) instead of the typical more vertical position. It is also able to rotate within the tunica vaginalis, twisting at the spermatic cord. As it rotates, it twists the vessels and cuts off the blood supply

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123
Q

What is the clinical presentation of testicular torsion?

A
  • Sudden onset of acute, severe pain
  • Firm swollen testicle (on examination)
  • Elevated (retracted) testicle (on examination)
  • Absent cremasteric reflex (on examination)
  • Abnormal testicular lie - often horizontal (on examination)
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124
Q

What are the investigations for testicular torsion?

A

UNNECESSARY IF CLINICAL FINDINGS ARE STRONGLY SUGGESTIVE:

  • Colour Doppler ultrasound - absent of decreased blood flow in affected testicle. Can show a whirlpool sign (spiral appearance to spermatic cord and blood vessels)
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125
Q

Describe the treatment for testicular torsion.

A
  • SURGICAL DETORSION within 6 hours
  • Orchiopexy (correcting the position of the testicles and fixing them in place)
  • Orchidectomy (removing the testicle) if the surgery is delayed or there is necrosis
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126
Q

What is an epididymal cyst? What does it contain? Are they confined to one testis? What is the treatment?

A
  • Smooth extra testicular spherical cyst at the epididymis (top of the testicle)
  • Contains clear and milky fluid - TRANSLUMINATES (fluid-filled)
  • May be multiple and bilateral. When they get large can be painful. Can palpate the cyst and testis separately
  • No treatment is usually necessary
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127
Q

What is epididymitis? What are the causes?

A
  • Inflammation of the epididymis
  • Causes:
  • Infectious, e.g. E.coli, Chlamydia trachomatis
  • Non-infectious, e.g. trauma, autoimmune disease
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128
Q

What is the clinical presentation of epididymitis?

A
  • Usually unilateral scrotal pain, sometimes radiates to abdomen with/without swelling
  • Fever, chills
  • LUTS
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129
Q

Describe the investigations for epididymitis.

A
  • Gram stain of urethral secretions
  • Urine dipstick test, microscopy, and culture
  • Colour Doppler ultrasound - enlarged, thickened epididymis with increased blood flow = excludes testicular torsion
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130
Q

Describe the treatment for epididymitis.

A
  • Infectious epididymitis: ceftriaxone, doxycycline
  • Non-infectious: treat underlying cause
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131
Q

What is a hydrocele? What are the two types?

A
  • A hydrocele is a collection of fluid within the tunica vaginalis that surrounds the testes:
  • Simple hydrocele: processus vaginalis is closed and more fluid is being produced by the tunica vaginalis (fluid trapped in the tunica vaginalis) than is being absorbed
  • Communicating hydrocele: the tunica vaginalis is connected with the peritoneal cavity via the processus vaginalis. This allows fluid to travel from the peritoneal cavity into the hydrocele, allowing the hydrocele to fluctuate in size
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132
Q

In hydrocele, what is found upon examination of the testes?

A
  • Non-tender smooth cystic swelling
  • Painless unless infected
  • TRANSILLUMINATES with light
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133
Q

What are the key differential diagnoses of a scrotal or inguinal swelling in a neonate?

A
  • Hydrocele
  • Partially descended testes
  • Inguinal hernia
  • Testicular torsion
  • Haematoma
  • Tumours (rare)
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134
Q

What is a useful investigation for hydrocele?

A

After clinical diagnosis, ULTRASOUND is useful for confirmation of diagnosis and excluding other causes

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135
Q

Describe the management for simple and communicating hydrocele.

A
  • Simple hydroceles = usually resolve within 2 years without having any lasting negative effects. They may require surgery if they are associated with other problems, such as a hernia
  • Communicating hydroceles = can be treated with a surgical operation to remove or ligate the connection between the peritoneal cavity and the hydrocele (the processus vaginalis)
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136
Q

What is the difference between a complicated and non-complicated UTI?

A
  • Uncomplicated UTI — UTI caused by typical pathogens in people with a normal urinary tract and kidney function, and no predisposing co-morbidities
  • Complicated UTI — UTI with an increased likelihood of complications such as persistent infection, treatment failure and recurrent infection
137
Q

In complicated and uncomplicated UTIs, do we need to send samples for culture?

A
  • Complicated = always send sample for culture
  • Uncomplicated = not necessary to send for culture, can treat empirically
138
Q

What is glomerulonephritis?

A

Glomerulonephritis is an umbrella term applied to conditions that cause inflammation of or around the glomerulus and nephron. There are many conditions that can be described as glomerulonephritis, e.g. IgA nephropathy, minimal change disease, Goodpasture’s syndrome

139
Q

What is the difference between nephritic and nephrotic syndrome?

A
  • The glomerulonephritides (glomerulonephritis) classically present on a spectrum ranging from nephrosis to nephritis
  • Nephritic syndrome refers to a group of symptoms, not a diagnosis. It simply means the patient does not fit a clinical picture of having inflammation of their kidney and it does not represent a specific diagnosis or give the underlying cause. Unlike nephrotic syndrome, there are no set criteria
  • Nephrotic syndrome refers to a group of symptoms without specifying the underlying cause. Therefore, nephrotic syndrome is not a disease, but is a way of saying “the patient has these symptoms”, which indicates there is an underlying disease present but doesn’t specify the disease.
140
Q

What are the systemic and renal causes of nephritic syndrome?

A
  • Renal: IgA nephropathy (Berger’s disease)
  • Systemic
  • Post-streptococcal glomerulonephritis
  • Goodpasture’s syndrome
  • SLE nephropathy
  • Small vessel vasculitis
141
Q

What are the key features in nephritic syndrome?

A
  • HAEMATURIA means blood in the urine. This can be microscopic (not visible) or macroscopic (visible)
  • OLIGURIA
  • PROTEINURIA. In nephritic syndrome, there is less than 3g / 24 hours. Any more and it starts being classified as nephrotic syndrome
  • FLUID RETENTION
142
Q

What is IgA nephropathy (nephritic syndrome)? How common is it?

A
  • IgA nephropathy (Berger’s disease) is where abnormal IgA forms -> deposits in kidneys -> kidney damage
  • COMMONEST cause of PRIMARY glomerulonephritis (not caused by another disease) worldwide
143
Q

What is the clinical presentation of IgA nephropathy?

A
  • Haematuria
  • Proteinuria usually <1g
144
Q

What are the investigations for IgA nephropathy? What would the histology show?

A

Renal biopsy (diagnostic) - histology shows ‘IgA deposits and glomerular MESANGIAL proliferation’

145
Q

Describe the treatment for IgA nephropathy.

A
  • ACEi/ARB to reduce proteinuria
  • Corticosteroids if persistent proteinuria
146
Q

What is Henoch-Schonlein purpura? What is its presentation? How about its investigations and management?

A
  • Systemic variant of IgA nephropathy with IgA deposition in the skin/joints/gut in addition to the kidney
  • Presentation = purpuric rash (typically on the legs)
  • Investigations and management are the same as IgA nephropathy
147
Q

What is post-streptococcal glomerulonephritis (a.k.a. diffuse proliferative glomerulonephritis)? What is its presentation?

A
  • Occurs 3-6 weeks after a streptococcal infection. Streptococcal antigen deposits in the glomerulus leading to immune complex formation and inflammation
  • Presentation: varies from HAEMATURIA to acute nephritis (haematuria, oedema, oliguria)
148
Q

What are the investigations for post-streptococcal glomerulonephritis? Describe the treatment for post-streptococcal glomerulonephritis.

A
  • Investigations: urinalysis - qualitative haematuria, proteinuria and evidence of STREP infection
  • Treatment: ACEi/ARB to reduce proteinuria, penicillins
149
Q

What is Goodpasture’s syndrome? What is the clinical presentation?

A
  • Anti-GBM (glomerular basement membrane) antibodies attack glomerulus and pulmonary basement membranes. This causes glomerulonephritis and pulmonary haemorrhage
  • In exam, there may be a patient that presents with acute kidney failure and haemoptysis (coughing up blood)
  • Presentation: SOB and OLIGURIA
150
Q

What are the investigations for Goodpasture’s syndrome? Describe the treatment for Goodpasture’s syndrome.

A
  • Investigations: renal biopsy and anti-GBM antibodies
  • Treatment: plasma exchange, corticosteroids and cyclophosphamide
151
Q

What is SLE nephropathy (lupus nephritis)? What can it progress to?

A
  • SLE nephropathy is inflammation of the kidneys caused by SLE
  • It can progress to end-stage renal failure
152
Q

What are the investigations for SLE nephropathy?

A
  • Urine protein:creatinine ratio
  • Renal biopsy
  • Urinalysis = nephritic picture
153
Q

Describe the treatment for SLE nephropathy.

A
  • Prednisolone to reduce proteinuria
  • Monoclonal antibodies
154
Q

What is diffuse proliferative glomerulonephritis? What are its causes? What are its investigations and what do they show? Describe its treatment.

A
  • Diffuse proliferative glomerulonephritis, a histopathologic classification of glomerulonephritis commonly associated with autoimmune diseases, is characterized by an increased cellular proliferation affecting > 50% of the glomeruli
  • Caused by IgA nephropathy, Henoch-Schonlein purpura, lupus nephritis etc.
  • Renal biopsy: LM = hypercellularity of endothelial and mesangial cells, IM = granular deposition of Ig, complement, and fibrin along the GBM, EM = electron-dense deposits
  • Treat underlying disease
155
Q

To have a nephrotic syndrome, what criteria must the patient have?

A
  • PERIPHERAL OEDEMA from hypoalbuminaemia
  • PROTEINURIA more than 3g/24 hours
  • HYPOALBUMINAEMIA - SERUM ALBUMIN less than 25g/L
  • HYPERCHOLESTERAEMIA
156
Q

How does nephrotic syndrome occur? What is the pathophysiology of nephrotic syndrome?

A
  • Nephrotic syndrome occurs when the basement membrane in the glomerulus has podocyte damage, making it highly permeable to proteins:
  • Inflammation - from immune cells, HTN etc.
  • This causes DAMAGE to PODOCYTES = protein leakage (albumin)
  • Increased liver activity to increase albumin. Consequential increase in cholesterol + coagulation factors
  • Reduced oncotic pressure - oedema. Consequential blood volume decreases, RAAS stimulation, exacerbation
157
Q

What are the primary causes of nephrotic syndrome to study?

A
  • Minimal change disease
  • Focal segmental glomerulosclerosis
  • Membranous nephropathy
  • Membranoproliferative glomerulonephritis
158
Q

What are the secondary causes of nephrotic syndrome?

A
  • DDANI:
  • Diabetic nephropathy
  • Drugs
  • Autoimmune
  • Neoplasia
  • Infection
159
Q

What does nephrotic syndrome generally present as?

A
  • FROTHY URINE (from proteinuria)
  • OEDEMA (from hypoalbuminaemia)
  • Pallor
160
Q

What are the general investigations for nephrotic syndrome?

A
  • GOLD STANDARD = needle biopsy and microscopy - light microscopy (LM), fluorescence microscopy (FM) and electron microscopy (EM)
  • General:
  • Bloods: U+E, FBC, LFT, CRP, Ca2+, glucose
  • MSU
  • Dipstick
  • USS kidney
161
Q

Describe the general management for nephrotic syndrome.

A
  • Treatment of underlying cause - 12 WEEKS CORTICOSTEROIDS - PREDNISOLONE
  • Treatment of complications:
  • Oedema (LOW SALT INTAKE/LOW PROTEIN DIET)
  • Hyperlipidaemia (STATINS if prolonged)
  • Hypercoagulable state (PROPHYLACTIC ANTICOAGULANTS - apixaban, LMWH (immediate effect), warfarin (delayed effect)
  • Infection (ABx)
162
Q

What are the general complications of nephrotic syndrome?

A
  • HYPERLIPIDAEMIA - loss of albumin increases cholesterol formation. Manage with statins
  • VTE - due to increased clotted factors. Give heparin
163
Q

What is minimal change disease? What are its causes? What are its investigations and what do they show? Describe its management.

A
  • Most common cause of nephrotic syndrome in CHILDREN
  • Mainly idiopathic
  • Needle biopsy = NO CHANGE on LM/FM. EM = loss of podocytes (effacement)
  • PREDNISOLONE
164
Q

What is focal segmental glomerulosclerosis? Is it found more in adults or children? What are its causes? What are its investigations and what will they show? Describe its treatment.

A
  • COMMONEST glomerunephritis seen on renal biopsy. Adults
  • Causes = idiopathic or HIV, heroin, lithium, lymphoma
  • Needle biopsy: LM = SCLEROSIS (plaques), FM = nothing, EM = GBM thickening
  • ACEi/ARBs, corticosteroids only in idiopathic disease
165
Q

What is membranous nephropathy? What are its causes? What are its investigations and what do they show? Describe its treatment.

A
  • 25% of adult nephrotic syndrome
  • Primary (idiopathic) or secondary to malignancy, infection (e.g. hepatitis), immunological disease (SLE, RA), drugs
  • ANTI-PHOSPHOLIPASE A2 RECEPTOR in 70-80% of idiopathic disease. Diffusely thickened GBM due to subendothelial deposits. ‘Spikes’ on silver stain
  • ACEi/ARBs in all. Immunosuppression (corticosteroids + cyclophosphamide) only in those at high risk of progression
166
Q

What is membranoproliferative glomerulonephritis? What is it divided into? What are its investigations? Describe its treatment.

A
  • 10% of adult nephrotic syndrome
  • Divided into immune-complex associated (e.g. infection) and C3 glomerulonephropathy
  • Needle biopsy: LM = mesangial expansion, capillary wall thickening, FM = IgG and COMPLEMENT 3 (C3) staining (granular appearance), EM = GBM thickening
  • ACEi/ARBs in all, underlying cause in immune-complex disease
167
Q

Which are the key clinical signs of nephritic syndrome?

a. Haematuria, recurrent UTIs, dysuria
b. Microalbuminaemia, proteinuria, oedema
c. Proteinuria, haematuria, hypertension
d. Polydipsia, polyuria, dehydration

A

C

168
Q

Which is not a cause of nephritic syndrome?

a. Membranous glomerulonephritis
b. Eosinophilic granulomatosis with polyangiitis
c. Post-streptococcal glomerulonephritis
d. System lupus erythematosus

A

A

169
Q

What is the most common primary cause of nephrotic syndrome in adults?

a. Minimal change disease
b. Amyloidosis
c. Membranous glomerulonephritis
d. Focal segmental glomerulosclerosis
e. Diabetes mellitus

A

D

170
Q

Which of these triads makes up nephrotic syndrome?

a. Hypoalbuminuria, hypercholesterolaemia, proteinuria
b. Hyperproteinaemia, hypercholesterolaemia, hypoalbminuria
c. Hypocholesterolaemia, hypoalbuminaemia, proteinuria
d. Hypercholesterolaemia, hyperalbuminaemia, proteinuria
e. Proteinuria, hypoalbuminaemia, hypercholesterolaemia

A

E

171
Q

Which of these is not a treatment for nephrotic syndrome?

a. Prednisolone
b. Low salt diet
c. High protein diet
d. Atorvastatin
e. Prophylactic anticoagulants

A

C

172
Q

What is the gold standard investigation for nephrotic syndrome?

A

Needle biopsy and microscopy

173
Q

Compare nephrotic and nephritic syndrome.

A
  • Nephritic = proteinuria <3g/24hrs, haematuria, hypertension, oliguria
  • Nephrotic = proteinuria >3g/24hrs, hypoalabuminaemia, oedema, hypercholesteraemia
174
Q

What is polycystic kidney disease? What are the two types and what are their causes?

A
  • Polycystic kidney disease is a genetic condition where the kidneys develop clusters of fluid-filled cysts
  • AUTOSOMAL DOMINANT: PKD1 (85%) and PKD2 (polycystin) genes - chromosome 16
  • AUTOSOMAL RECESSIVE: caused by mutation on PKHD1 gene on chromosome 6 that codes for fibrocystin. Younger patients - usually found on antenatal screening
175
Q

What is the pathophysiology of 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
176
Q

What is the presentation of both autosomal recessive and dominant polycystic kidney disease?

A
  • Autosomal recessive: OLIGOHYDRAMNIOS (lack of amniotic fluid) and polycystic kidneys on antenatal scans. Lack of amniotic fluid leads to POTTER’S SYNDROME
  • Autosomal dominant: HYPERTENSION, abdo/flank pain (haemmorrhage), headaches, LUTS
177
Q

What are the investigations for polycystic kidney disease?

A

Renal USS and 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
178
Q

Describe the management for polycystic kidney disease.

A
  • TOLVAPTAN can slow the development of cysts and the progression of renal failure in autosomal dominant polycystic kidney disease. Recommended in certain situations
  • Antihypertensives for hypertension
  • Infected - Abx or drain
  • Surgical removal - nephrectomy
  • Chronic - dialysis (first-line renal replacement therapy) or transplant
179
Q

What are the complications of polycystic kidney disease?

A
  • Associated with BERRY ANEURYSMS - rupture causing a SUB-ARACHNOID HAEMORRHAGE
  • Cysts on other organs, e.g. ovaries
  • 50% have ventricular hypertrophy
  • Pre-malignant
180
Q

What is Von Hippel-Lindau disease? What is its aetiology?

A
  • Genetic disorder - mutation of tumour suppressor gene VHL (chr 3). Benign tumours and cysts in many organs, as well as malignant tumours in certain locations
  • Autosomal dominant, 20% de novo mutation
181
Q

What is the pathophysiology of Von Hippel-Lindau disease?

A

VHL normally regulates hypoxia inducible factor (HIF). HIF promotes transcription of PDGF and VEGF

182
Q

Where are the tumour locations in Von Hippel-Lindau syndrome?

A

Tumour locations:

  • CNS (haemangioblastoma)
  • Liver
  • Lungs
  • Pancreas (malignant neuroendocrine)
  • Adrenals (phaeochromocytoma)
  • Clear renal cell carcinoma (malignant) in 70% of people with VHL mutation - bilateral, multifocal tumours
183
Q

What is the presentation of Von Hippel-Lindau syndrome?

A
  • Renal cell carcinoma - haematuria, flank pain, abdominal mass (advanced stage typically)
  • B SYMPTOMS - weight loss, fever, fatigue, night sweats & disturbed sleep
  • CNS - ataxia, headaches, nausea & vomiting
  • Phaeochromo. - headaches, sweating, palpitations, HTN
184
Q

What are the investigations for Von Hippel-Lindau syndrome (for renal cell carcinoma)?

A
  • Screening - annual BP and abdominal USS (1st line)
  • CT head, chest and abdo
  • MRI – baseline scan; tumour staging
  • Bloods – FBC, U&Es, LFTs
  • Renal biopsy – histology of tumour (diagnostic)
185
Q

Describe the management of Von Hippel-Lindau disease (renal cell carcinoma).

A

Surgical excision once renal cell carcinoma > 3cm. Usually asymptomatic prior to this and numerous small tumours and cysts may be present. Partial/radical nephrectomy (1st line)

186
Q

What is chlamydia? How many cases are asymptomatic?

A
  • Chlamydia trachomatis is a gram-negative bacteria. Chlamydia is the most common sexually transmitted infection in the UK and a significant cause of infertility
  • Being young, sexually active and having multiple partners increase the risk of catching the infection. 50% of men and 75% of woman are aysmptomatic, though they can still pass the infection on
187
Q

What is the clinical presentation of chlamydia in men and women?

A
  • Women: abnormal vaginal discharge, pelvic pain, abnormal vaginal bleeding (intermenstrual or postcoital), painful sex (dyspareunia), painful urination (dysuria)
  • Men: urethral discharge or discomfort, painful urination (dysuria), epididymo-orchitis, reactive arthritis
188
Q

What are the investigations for chlamydia?

A

NUCLEIC ACID AMPLIFICATION TESTS (NAAT). This can involve a vulvovaginal swab, endocervical swab, first-catch urine sample (in women or men), urethral swab in men etc.

189
Q

Describe the management for chlamydia.

A

1st line for uncomplicated chlamydia is DOXYCYCLINE 100MG TWICE A DAY FOR 7 DAYS

190
Q

Name some complications of chlamydia.

A
  • Pelvic inflammatory disease
  • Chronic pelvic pain
  • Infertility
  • Ectopic pregnancy
  • Epididymo-orchitis
  • Conjunctivitis
191
Q

What is gonorrhoea? How does it spread?

A

Neisseria gonorrhoeae is a Gram-negative diplococcus bacteria. It infects mucous membranes with a columnar epithelium, such as the endocervix in women, urethra, rectum, conjunctiva and pharynx. It spreads via contact with mucous secretions from infected areas

192
Q

What is the clinical presentation of gonorrhoea in men and women?

A
  • Women (50% are symptomatic):
  • Odourless purulent discharge, possibly green or yellow
  • Dysuria
  • Pelvic pain
  • Men (90% are symptomatic):
  • Odourless purulent discharge, possibly green or yellow
  • Dysuria
  • Epididymo-orchitis
193
Q

What are the investigations for gonorrhoea?

A
  • NATT is used to detect the RNA or DNA of gonorrhoea, but no specific information - endocervical, vulvovaginal or urethral swabs, or in a first-catch urine sample
  • A standard charcoal endocervical swab should be taken for microscopy, culture and antibiotic sensitivities before initiating antibiotics - important due to high rates of antibiotic resistance and to idenitfy the specific bacteria
194
Q

Describe the management of gonorrhoea.

A
  • A single dose of INTRAMUSCULAR CEFTRIAXONE 1g if the sensitivities are NOT known
  • A single dose of ORAL CIPROFLOXACIN 500mg if the sensitivities ARE known
195
Q

Name some complications of gonorrhoea.

A
  • Pelvic inflammatory disease
  • Chronic pelvic pain
  • Infertility
  • Epididymo-orchitis (men)
  • Prostatitis (men)
  • GONOCOCCAL CONJUNCTIVITIS in neonates - medical emergency associated with sepsis, perforation of the eye and blindness
196
Q

What is syphilis? What are the different stages?

A
  • Syphilis is caused by bacteria called Treponema pallidum
  • Stages:
  • Primary syphilis = PAINLESS ULCER at site of infection
  • Secondary syphilis = systemic symptoms
  • Latent syphilis = symptoms disappear
  • Tertiary syphilis = many years after initial infection
  • Neurosyphilis = occurs if the infection involves the central nervous system, presenting with neurological symptoms
197
Q

Describe the clinical presentations of the different stages of syphilis.

A
  • Primary syphilis = painless genital ulcer (chancre)
  • Secondary syphilis typically starts after the chancre has healed, with symptoms of: maculopapular rash, CONDYLOMATA LATA (grey wart-like lesions around the genitals and anus), low-grade fever
  • Tertiary syphilis can present with several symptoms depending on the affected organs: GUMMATOUS LESIONS (GUMMAS are granulomatous lesions that can affect the skin, organs and bones), aortic aneurysms, neurosyphilis
  • Neurosyphilis can occur at any stage if the infection reaches the CNS and present with symptoms of: headache, altered behaviour, dementia, TABES DORSALIS (demyelination affecting the spinal cord posterior columns), OCULAR SYPHILIS, ARGYLL-ROBERTSON PUPIL
198
Q

What are the investigations for syphilis?

A

ANTIBODY TESTING for antibodies to T.pallidum - DARK FIELD MICROSCOPY and POLYMERASE CHAIN REACTION (PCR)

199
Q

Describe the management for syphilis.

A
  • A single DEEP INTRAMUSCULAR dose of BENZATHINE BENZYLPENICILLIN. Alternative regimes and types of penicillin are used in different scenarios
  • All patients should be managed and followed up by specialist service, such as GUM. As with all other STIs, patients need: full screening for STIs, advice about avoiding sexual activity until treated, contact tracing, prevention of future infections
200
Q

What is pelvic inflammatory disease? What are its causes and risk factors?

A
  • Pelvic inflammatory disease is inflammation and infection of the organs of the pelvis, caused by infection spreading up through the cervix
  • Causes: STIs, e.g. neisseria gonorrhoeae, chlamydia trachomatis. Non-STIs, e.g. haemophilus influenza, e.coli
  • Risk factors = same for STIs, e.g. not using barrier contraception, multiple sexual partners, younger age, previous STIs
201
Q

Describe the clinical presentation of pelvic inflammatory disease.

A
  • Women may present with symptoms of:
  • Pelvic or lower abdominal pain
  • Abnormal vaginal discharge
  • Abnormal bleeding (intermenstrual or postcoital)
  • Pain during sex (dyspareunia)
  • Fever
  • Dysuria
202
Q

What are the investigations for pelvic inflammatory disease?

A
  • Patients with pelvic inflammatory disease should have testing for causative organisms and other sexually transmitted infections:
  • NAAT swabs for gonorrhoea and chlamydia (and Mycoplasma genitalium if available)
  • HIV test
  • Syphilis test
203
Q

Describe the management for pelvic inflammatory disease.

A
  • Where appropriate patients should be referred to a genitourinary medicine (GUM) specialist service for management and contact tracing. Antibiotics are started empirically, before swab results are obtained, to avoid a delay and complications:
  • A single dose of intramuscular ceftriaxone 1g (to cover gonorrhoea)
  • Doxycycline 100mg twice daily for 14 days (to cover chlamydia and Mycoplasma genitalium)
  • Metronidazole 400mg twice daily for 14 days (to cover anaerobes such as Gardnerella vaginalis)
  • Ceftriaxone and doxycycline will cover many other bacteria, including H. influenzae and E. coli
204
Q

What are the complications of pelvic inflammatory disease?

A
  • Sepsis
  • Abscess
  • Infertility
  • Chronic pelvic pain
  • Ectopic pregnancy
  • Fitz-Hugh-Curtis syndrome
205
Q

Mrs A Vrige (23 years old) has been complaining of dysuria, urgency and frequency passing urine. Similar urinary symptoms over the last few months were treated with 3 days of Cephalexin by another GP. She is in a stable relationship with her husband and takes the oral contraceptive pill.

Which antibiotic do you use while awaiting results?

A. Ciprofloxacin

B. Trimethoprim

C. Nitrofurantoin

D. Tazocin

E. No antibiotic needed

A

C

206
Q

After 24 hours, yellow colonies are growing on the agar plate. A Gram film is made. What do you see?

A. Gram negative bacilli

B. Gram negative cocci

C. Gram positive bacilli

D. Gram positive cocci

E. No organisms seen

A

D

207
Q

Which organism from the list is/are most likely in view of the plate and the Gram stain appearance?

A. E.coli

B. Pseudomonas aeruginosa

C. Proteus mirabilis

D. Staphylococcus saprophyticus

E. Klebsiella pneumoniae

A

D

208
Q

Mr C Docalot is a 65 year old man with benign prostatic hyperplasia for which he has been prescribed tamsulosin for several years. He presents with 3 days of increased urinary frequency and lower back pain. On examination he is unwell and agitated: T 390C and BP 90/50 and there is right renal angle tenderness.

What key samples should be taken?

A. MSU and blood culture

B. Sputum and MSU

C. CSU

D. Blood culture

E. All of the above

A

A

209
Q

Describe what is seen on the gram film.

A. Gram negative cocci

B. Gram negative bacilli

C. Gram positive cocci

D. Gram positive bacilli

E. All of the above

A

B

210
Q

What culture medium have these bacteria been grown on and what does the culture show?

A. Blood agar and Pink lactose fermenting colonies

B. Blood agar and non lactose fermenting colonies

C. CLED and lactose fermenting colonies

D. MacConkey and pink lactose fermenting colonies

E. None of the above

A

D

211
Q

Put the clinical presentation, blood culture and urine results together to form a diagnosis.

A. Proteus UTI

B. Proteus pyelonephritis

C. E.coli UTI

D. E.coli urosepsis

E. E.coli Pyelonephritis

A

E

212
Q

What would you treat with first line and for how long?

A. Trimetoprim 7 days

B. Nitrofurantoin 14 days

C. Co-amoxiclav 14 days

D. Co-amoxiclav 7 days

E. Ciprofloxacin 7 days

A

C

213
Q

Mr E.Home is an 84 year-old man who has become confused and agitated. He has been sent to the frailty unit and you assess him. Other than the confusion, the only significant finding from history and examination is that he has a long-term urinary catheter.

The nurse uses a dipstick to assess the urine. This will give her an indication if an infection is present or not:

A. True

B. False

A

False

214
Q

The nurse completes the form and sends the urine sample to the Microbiology lab who inoculate some culture plates and dispose of the sample. Should Microscopy be performed on the sample?

A. Yes

B. No

A

B. No

215
Q

Look at the CLED plate below. Is there pure growth on the plate?

A. Yes

B. No

A

B. No

216
Q

What is growing on the blood agar below?

A. Proteus

B. E.coli

C. Staphylococcus saprophyticus

D. Enterococcus

E. Klebsiella

A

A

217
Q

Is the specimen diagnostic?

A. Yes

B. No

A

B. No

218
Q

Mrs B.gravid is a 37 year old, 28 weeks pregnant women in the antenatal clinic who has brought a urine sample with her. She is otherwise well.

Urinalysis shows leukocytes and protein. This indicates:

A. Nothing - this is expected in pregnancy

B. Pre-eclampsia

C. UTI

D. Possibility of pre-eclampsia and UTI

E. Obstetric cholestasis

A

D

219
Q

The microscopy shows epithelial cells but no pus cells, this suggests:

A. Definite infection

B. Pyelonephritis

C. Pre-eclampsia

D. Sample contamination

E. None of the above

A

D

220
Q

Based on this sample, the patient should be treated as a UTI.

A. True

B. False

A

B. False

221
Q

The risk of pyelonephritis in untreated asymptomatic bacteriuria in pregnancy is:

A. 5-10%

B. 20-40%

C. 50-60%

D. 60%

E. 70-75%

A

B. 20-40%

222
Q

Who needs urgent treatment?

A. Paul, 66M, imaging showed 3mm stone, complaining of severe discomfort and can’t sit still

B. Jane, 54F, imaging showed a unilateral 15mm stone, describes the pain as worse than childbirth, afebrile

C. Mike, 36M, imaging showed a 8mm stone, bloods show high WCC, elevated creatinine, urea and potassium

A

C.

A should be small enough to pass spontaneously, B is likely too big to pass spontaneously but not urgent - elective, but C has signs of infection + AKI

223
Q

Martin is a 76 year old retired painter who pays a visit to the haematuria outpatient clinic with suspected bladder cancer. Which of these is not a routine investigation within this clinic?

A. CT urogram

B. Flexible cystoscopy

C. Ultrasound

D. Urine microscopy + culture

A

A. CT urogram

224
Q

Amy, 26F. On dipstick you find she is positive for leukocytes and nitrites, with a slight trace of blood. She complains of dysuria and is slightly febrile. First line drug? What about if she was 6 weeks pregnant?

A
  • Trimethoprim
  • Cefalexin
225
Q

What is the mechanism of action of Tamsulosin?

A. Blocks conversion of testosterone to dihydrotestosterone decreasing size

B. Selective inhibitor of PDE5

C. Relaxes the smooth muscle in the bladder neck and prostate

D. Blocks calcium from entering the cells of the bladder neck and prostate

A

C. Relaxes the smooth muscle in the bladder neck and prostate

226
Q

81M complaining of lower back pain, strains when he goes to the toilet which is more often than usual. What is the gold standard investigation?

A. PSA

B. Transrectal USS and biopsy

C. Digital rectal examination

D. MRI spine

A

B. Transrectal USS and biopsy

227
Q

Which of these is not a cause of raised PSA?

A. BPH

B. DRE

C. Drinking alcohol

D. Ejaculation

A

C

228
Q

71M undergone cystoprostatectomy for bladder cancer. Which of these is not a sign of sepsis as a post-operative complication?

A. New confusion

B. Fever

C. Tachycardia

D. Low RR

A

D

229
Q

39F, BMI 50 with a past medical history of hyperparathyroidism and autoimmune hepatitis. What is the most likely type of kidney stone?

A. Calcium oxolate

B. Struvite

C. Uric acid

D. Cholesterol

A

A. Calcium oxolate

230
Q

Which is the most common way for pyelonephritis to be acquired?

A. Ascending transurethral

B. Lymphatics

C. Blood

A

A. Ascending transurethral

231
Q

A 45-year-old man presents to his A&E with swelling around his eyes and ankles. He has previous travel to South East Asia. He admits to vomiting and diarrhoea (which is clay coloured) and pain in his RUQ. Blood and urine tests were run and a kidney needle biopsy was performed. Fluorescence microscopy showed IgG and C3 deposits in the glomerulus. What is the most likely diagnosis?

A. Minimal change disease

B. Membranous glomerulonephritis

C. AKI

D. Diabetes nephropathy

E. Gallstones

A

B. Membranous glomerulonephritis

232
Q

Which of the following is an intra-renal cause of AKI?

A. Streptococcal tonsillitis

B. Massive haemorrhage

C. Liver failure

D. Diarrhoea and vomiting

E. Benign prostate hyperplasia

A

A. Streptococcal tonsillitis

233
Q

Histology of a renal biopsy shows depositions of IgA complexes and mesangial proliferation. Which features of the patient’s history are most likely?

A. Dizziness when standing and palpitations

B. Frothy urine, long term IV drug use

C. Bloody urine preceded by tonsillitis

D. Flank pain and increased urgency to urinate

A

C. Bloody urine preceded by tonsillitis

234
Q

A patient attends the renal clinic having been diagnosed with chronic kidney disease stage 4, secondary to long-standing hypertension and diabetes. She asks about the diet she should be keeping to. What is the most appropriate piece of advice about her diet she should be given?

A. Low potassium, high sodium

B. High protein, low sodium, high potassium

C. High phosphate, low potassium

D. Low protein, low potassium, low phosphate

A

D. Low protein, low potassium, low phosphate

235
Q

Describe hyperkalaemia on an ECG.

A

Med school love this

  • Tall ‘tented’ T waves
  • P wave flattening
  • PR elongation
  • Wide QRS complex
236
Q

Explain the mechanism by which Insulin corrects the raised electrolyte level and why Dextrose is always given at the same time.

A

Med school love this.

Insulin shifts potassium into cells by stimulating the activity of Na+-H+ antiporter on cell membrane, promoting the entry of sodium into cells, which leads to activation of the Na+-K+ ATPase, causing an electrogenic influx of potassium. IV insulin leads to a dose-dependent decline in serum potassium levels.

Dextrose is given to prevent hypoglycaemia.

237
Q

What is breast cancer? What are its risk factors?

A
  • Breast cancer is the most common form of cancer in the UK. It mostly affects women and is rare in men (about 1% of UK cases). Around 1 in 8 women will develop breast cancer in their lifetime.
  • Risk factors:
  • Female (99% of breast cancers)
  • Increased oestrogen exposure (earlier onset of periods and later menopause)
  • More dense breast tissue (more glandular tissue)
  • Obesity
  • Smoking
  • Family history (first-degree relatives)
  • Oral contraceptive pill (but risk returns to normal after 10 years)
  • Combined HRT
238
Q

Mutations in which genes are associated with breast cancer?

A
  • BRCA refers to the BReast CAncer gene. The BRCA genes are tumour suppressor genes. Mutations in these genes lead to an increased risk of breast cancer (as well as ovarian and other cancers):
  • BRCA1 gene is on chromosome 17
  • BRCA2 gene is on chromosome 13
  • There are other rarer genetic abnormalities associated with breast cancer (e.g., TP53 and PTEN genes).
239
Q

What are the different types of breast cancer?

A
  • Ductal carcinoma in situ
  • Lobular carcinoma in situ
  • Invasive ductal carcinoma
  • Invasive lobular carcinoma (NST - no specific type)
  • Inflammatory breast cancer
  • Paget’s disease of the nipple
240
Q

What is the clinical presentation of breast cancer?

A
  • Lumps that are hard, irregular, painless or fixed in place
  • Lumps may be tethered to the skin or the chest wall
  • Nipple retraction
  • Skin dimpling or oedema (peau d’orange)
  • Lymphadenopathy, particularly in the axilla
241
Q

Who is breast cancer screening offered to? What does it involve?

A
  • The NHS breast cancer screening program offers a MAMMOGRAM every 3 years to women aged 50 – 70 years
  • There are different recommendations for screening patients with a higher risk, i.e. those with first-degree relatives
242
Q

What are the criteria for a two week wait referral for breast cancer? What happens once the patient has been referred?

A
  • The NICE guidelines (updated January 2021) recommend a two week wait referral for suspected breast cancer for:
  • An unexplained breast lump in patients aged 30 or above
  • Unilateral nipple changes in patients aged 50 or above (discharge, retraction or other changes)
  • An unexplained lump in the axilla in patients aged 30 or above
  • Skin changes suggestive of breast cancer
  • Once a patient has been referred for specialist services under a two week wait referral for suspected cancer, they should initially receive a triple diagnostic assessment comprising of:
  • CLINICAL ASSESSMENT (history and examination)
  • IMAGING (ultrasound or mammography) - US better in younger women, mammogram better in older women
  • BIOPSY (fine needle aspiration or core biopsy)
243
Q

What are the common sites of metastases for breast cancer?

A
  • You can remember the notable locations that breast cancer metastasis occur using 2 Ls and 2 Bs:
  • L - Lungs
  • L - Liver
  • B - Bones
  • B - Brain
244
Q

Describe the treatment for breast cancer.

A
  • Surgery:
  • BREAST-CONSERVING SURGERY (e.g., wide local excision), usually coupled with radiotherapy. Can be offered reconstruction
  • MASECTOMY (removal of the whole breast), potentially with immediate or delayed breast reconstruction - breast implants or flap reconstruction
  • Axillary clearance if cancer cells found in the nodes
  • Radiotherapy
  • Chemotherapy
  • Hormone treatment - for patients with OESTROGEN-RECEPTOR POSITIVE breast cancer:
  • TAMOXIFEN for PREMENOPAUSAL WOMEN
  • AROMATASE INHIBITORS for POSTMENOPAUSAL WOMEN
245
Q
A

B

246
Q
A

A. Renal papilla, minor calyx, major calyx, renal pelvis, ureter, bladder, urethra

247
Q
A

B. 10mmHg

248
Q
A

D. Inulin

249
Q
A

C. Thick ascending loop of Henle

250
Q
A

D. Amino acids are reabsorbed with a K+ co-transporter

251
Q
A

E. Somatic pudendal nerve (S2-S4)

252
Q
A

D. Aldosterone causes decreased reabsorption of Na+

253
Q
A

D. The medulla has two centres involved in the control of micturition; the storage and micturition centre

254
Q
A

B. ADH promotes the release of aquaporins to decrease water retention

255
Q
A

B. Hypovolaemia

256
Q
A

B. Increased resorption of K+

257
Q
A

D. Proximal part of the distal convoluted tubule

258
Q
A

C. Bed rest

259
Q
A

D. Urolithiasis

260
Q
A

C. Ampulla

261
Q
A

D. Suspensory ligament

262
Q
A

B

263
Q
A

E. Seminiferous tubules, rete testis, epididymis, vas deferens, urethra

264
Q
A

D. Thickens cervical mucus

265
Q
A

C. Tunica albuginea

266
Q
A

E. Lutenizing hormone (LH)

267
Q
A

B. Prolactin is normally inhibited by GABA

268
Q
A

D. Menstrual, proliferative and secretory

269
Q
A

C. Human chorionic gonadotrophin (hCG)

270
Q
A

B. Vaginal candidiasis

271
Q
A

E. Primordial germ cells

272
Q
A

B. Varicocele

273
Q
A

C. 10cm

274
Q
A

D. Phosphodiesterase type 5 (PDE-5) inhibitor

275
Q
A

D. Increased FSH:LH ratio

276
Q
A

A. Suspensory ligaments

277
Q
A

B. Laparoscopy

278
Q
A

A. Cortical reaction

279
Q

When starting patients on an alpha blocker (e.g. doxazosin) for benign prostatic hyperplasia, what side-effect should you warn the patient about?

a) Bradycardia
b) Hypertension
c) Hypotension
d) Tachycardia

A

C) Hypotension. (Postural) hypotension – SEs include (postural hypotension), dizziness, dry mouth

280
Q
A

A. Chronic kidney disease

281
Q
A

A. A hard and irregular mass

282
Q
A

C. Refer to urology for surgery immediately

283
Q
A

C. Cephalexin

284
Q
A

A. Chemotherapy

285
Q
A

A. Phosphodisesterase inhibitor (sildenafil)

286
Q
A

A. 50%

287
Q
A

C. IgA nephropathy

288
Q
A

A. Prostatitis and Escherichia coli

289
Q
A

A. Varicocele

290
Q
A

A. Renal colic

291
Q
A

A. CT KUB

292
Q
A

A. Pyelonephritis

293
Q
A

A. Intra renal acute kidney injury

294
Q
A

B. Renal cell carcinoma

295
Q
A

A. Transitional cell carcinoma

296
Q
A

A. DRE

297
Q
A

C. Ceftriaxone 500mg IMI with Azithromycin 1 gram orally STAT

298
Q
A

A. Prednisolone

299
Q
A

B. Prophylactic antibiotics for Pneumocystic pneumonia

300
Q

Pre-renal, intrinsic, or post-renal?

  1. T2DM and HTN, low urine osmolality, high urine Na+, high blood K+
  2. Normal Na+, raised urea and creatine. Responds well to fluid therapy
  3. Loin -> groin acute colicky pain, microscopic haematuria
A
  1. Intrinsic
  2. Pre-renal
  3. Post-renal
301
Q

a) Nephritic syndrome is characterised by _______ of the kidney and is diagnosed by _____ _______
b) A child presenting with haematuria 4 weeks after a skin infection has ____ __________ ________
c) ___ ________ is the most common cause of nephritic syndrome in the UK

A

a) Nephritic syndrome is characterised by inflammation of the kidney and is diagnosed by renal biopsy
b) A child presenting with haematuria 4 weeks after a skin infection has post streptococcal nephritis
c) IgA nephritis is the most common cause of nephritic syndrome in the UK

302
Q

a) A patient with nephrotic syndrome presents with _____ and ______ ______
b) ____/_____ are used to reduce protein loss and slow progression of renal disease
c) 25% of cases of nephrotic syndrome have __ ______ _______ __ _____

A

a) A patient with nephrotic syndrome presents with oedema and frothy urine
b) ACE-I/ARB are used to reduce protein loss and slow progression of renal disease
c) 25% of cases of nephrotic syndrome have no visible changes on biopsy

303
Q

a) Bladder cancer classically presents with ______ __________
b) Kidney cancer presents with a triad of ________, ______ ____ and ______
c) FUNDS stands for ________, ______, _____, and ______
d) Cystitis should be treated with _______ and _______

A

a) Bladder cancer classically presents with painless haematuria
b) Kidney cancer presents with a triad of haematuria, flank pain, palpable abdominal mass
c) FUNDS stands for frequency, urgency, nocturia, and discharge
d) Cystitis should be treated with cefalexin and analgesia

304
Q

a) Kidney stones are commonly found at the _____ ______ ________, the _____ ______, and the vesicoureteral junction
b) The diagnostic test for STI’s is _______ ____ _________ ________
c) 85% of patients with kidney stones present with ________

A

a) Kidney stones are commonly found at the pelvic ureteric junction, the pelvic brim, and the vesicoureteral junction
b) The diagnostic test for STI’s is Nucleic acid amplification testing
c) 85% of patients with kidney stones present with haematuria

305
Q
A

D. Ultrasound KUB

306
Q
A

A. Tamsulosin

307
Q
A

B. 5 alpha reductase inhibitor

308
Q
A
309
Q
A

E. Hydrocele

310
Q
A

C. Prostatitis

311
Q
A

A. Infertility

312
Q
A

D. Cytoscopy with biopsy

313
Q
A

B. Non-contrast helical CT scan

314
Q
A

A. Rhabdomyolysis

315
Q
A

a) Calcium gluconate

316
Q
A

a. IgA nephropathy

317
Q
A

A. Acute interstitial nephritis

318
Q
A

A. Renal biopsy

319
Q
A
  1. Calcium, phosphate, alkaline phosphatase, PTH
320
Q
A

A. Normal renal function

321
Q
A

C. Oral iron replacement

322
Q
A

C. Secondary hyperparathyroidism

323
Q
A

D. Surgical removal

324
Q
A

B. Chlamydia trachomatis

325
Q
A

E. Pyelonephritis

326
Q

You are a junior doctor in general practice. A 70-year-old man presents to you, complaining of having to go to the toilet several times during the night. He states that when he goes to the toilet, it takes time for the stream to start and when it does start, it isn’t as strong as it used to be. He denies any other symptoms. Which of the following would be the first treatment?

A. Sildenafil

B. Tamsulosin

C. Oxybutynin

D. Ibuprofen

E. Alprostadil

A

B. Tamsulosin

327
Q

A 16-year-old boy presents to A&E with severe pain in his left groin area that started when he was playing football with his friends. On examination, the left side of his scrotum is red and swollen and his cremasteric reflex was absent on the left. What is the diagnosis?

A. Hydrocele

B. Varicocele

C. Epididymitis

D. Testicular torsion

E. Epididymal cyst

A

D. Testicular torsion

328
Q

A 52-year-old man presents after having another episode of severe pain down the left side of his abdomen. He previously had an episode a few days ago. He says the episodes don’t last very long but when they happen, he can’t get comfortable and describes the pain as the worst pain he has ever felt in his life. He says he sometimes feels sick when the pain happens. What would be the best investigation to perform?

A. Non-contrast CT of the kidneys, ureter, and bladder

B. Ultrasound

C. Contrast CT of the kidneys, ureter, and bladder

D. MRI

E. Urine dip

A

A. Non-contrast CT of the kidneys, ureter, and bladder. This presentation is consistent with kidney stones. NCCT-KUB is the gold standard investigation for kidney stones. An ultrasound would be done instead of a CT if the patient was a pregnant person

329
Q

A 72-year-old man has recently been diagnosed with chronic kidney disease (CKD). Some blood tests have been done which show his glomerular filtration rate (GFR) is 48ml/min/1.73m2. Which stage of CKD is this?

A. 1

B. 2

C. 3a

D. 3b

E. 4

A

C. 3a

330
Q

Joe (35M) presents to A&E after he noticed blood in his urine. He denies pain or fever associated with the bleed, but has had a sore throat for the past 3 days. He has not had a similar episode previously.

Blood pressure is 158/101mmHg, and urinalysis with microscopy finds mild proteinuria with red cell casts present.

Which of the following can also cause the clinical syndrome Joe has?

A. Diabetic nephropathy

B. Post-streptococcal glomerulonephritis

C. Minimal change disease

D. Membranous nephropathy

E. Focal segmental glomerulosclerosis

A

B. Post-streptococcal glomerulonephritis

331
Q

A 34-year-old woman who is otherwise healthy has had a fever, nausea, and right-sided back pain for 2 days. The physical examination shows a temperature of 39.0ºC, blood pressure of 120/60 mm Hg, pulse of 110 and respiratory rate of 18. Dipstick urinalysis is positive for leukocytes, nitrites, and blood.

Which of the following is most appropriate empirical antibiotic therapy in this patient?

A. Trimethoprim

B. Ciprofloxacin

C. Flucloxacillin

D. Doxycycline

E. Nitrofurantoin

A

B. Ciprofloxacin

332
Q

John, (65M) is admitted to hospital for an elective knee replacement. He has a past medical history of:

MI 2 years ago, on aspirin.

Chronically elevated BP of 180/109mmHg, never been managed.

3 days after the operation, John becomes very unwell. His temperature has spiked, he appears dehydrated and has developed an elevated serum creatinine, oliguria and hyperkalaemia.

It is believed that John is suffering acute kidney injury secondary to sepsis. Which of the following are you least likely to offer John?

A. Insulin + dextrose

B. Given fluids

C. Stop aspirin

D. Start ACEi for high blood pressure

E. Give sodium citrate for acidosis

A

D. Start ACEi for high blood pressure

333
Q

A 25-year-old man presents after experiencing a burning sensation when he urinates and noticing an odd discharge from his urethra for the past few days. Upon questioning, he mentions he has multiple sexual partners. You send off samples for testing which confirm a diagnosis of gonorrhoea.

A. What is the name of the organism that causes gonorrhoea? (1 mark)

B. What would the gram stain appearance of this organism be? (2 marks)

C. What antibiotic would you prescribe for this man and how would it be administered? (2 marks)

D. What other advice would you give to this man? (3 marks)

A

A. Neisseria gonorrhoea

B. Gram-negative diplococci

C. Ceftriaxone as an intramuscular injection

D. Advise him to attend a genitourinary clinic or specialist sexual health service, use condoms whenever he has sex, get regular STI testing whilst sexually active, abstain from sex until treatment has been completed

334
Q

The causes of acute kidney injury (AKI) can be split into several different categories.

A. What are these categories? (3 marks)

B. Name 5 causes of acute kidney injury? (5 marks)

A

A. Pre-renal, intra-renal, post-renal

B. Pre-renal -> hypotension (sepsis, etc), hypovolaemia (dehydration, acute blood loss, etc), low cardiac output (heart failure), low renal perfusion (NSAIDs, ACEIs)

Renal -> glomerulonephritis, vasculitis, acute tubular necrosis (can be ischaemic or nephrotoxic [gentamicin, radiocontrast media, cisplatin, etc])

Post-renal -> stones (renal or bladder), BPH, prostate cancer, bladder cancer, blood clots, urethral stricture

335
Q

A 67-year-old man presents to you in general practice after a one-month history of noticing blood in his urine. He has also been going to the toilet more frequently. His wife states that she thinks he has lost some weight as his clothes are a bit looser now. He denies any pain.

A. What would be the most likely diagnosis? (1 mark)

B. What is the best investigation to confirm this diagnosis? (1 mark)

C. What options for management of this condition are there

i. Surgically? (2 marks)
ii. Medically? (4 marks)

A

A. Bladder cancer

B. Flexible cytoscopy

C. i) Transurethral resection of the bladder tumour (TURBT) is the surgical option for non-muscle invasive cancer. Radical cystectomy can be done in higher risk cancer and muscle-invasive cancers

ii) For non-muscle invasive cancers, mitomycin C can be given around the time of TURBT. For higher risk, non-muscle invasive cancers, BCG can be given. For muscle-invasive cancers, MVAC (methotrexate, vinblastine, doxorubicin, cisplatin) chemotherapy can be given

336
Q

A. What is the most common cause of glomerulonephritis worldwide? (1mark)

B. What are the four main components of nephrotic syndrome? (4 marks)

A

A. IgA nephropathy (Berger’s disease)

B. 1. Heavy proteinuria (>3.5g/24hrs) – shown on dipstick as ACR.

  1. Hypoalbuminaemia (<30g/L) – lost in urine.
  2. Oedema – reduced oncotic pressure due to low albumin.
  3. Hypercholesterolaemia – cholesterol is bound to albumin and synthesis goes wrong.

Also, haematuria is usually mild or absent.

337
Q

A 66yr old female presents with urinary urgency and frequency. She needs to urinate up to 12 times per day and 2-3 times at night. Recently the urgency comes on so suddenly and strongly she cannot make it to the toilet and leaks urine.

A. Describe how oxybutynin works in treating urge incontinence? (2marks)

B. Give two side-effects of this type of drug? (2marks)

A

A. It is an anticholinergic drug. By inhibiting parasympathetic nervous system, it decreases detrusor excitability, preventing symptoms of urgency.

B. Dry eyes and tachycardia. Others = dry mouth, dilated pupils/blurred vision, constipation, dizziness (postural hypotension), confusion

338
Q

Simon is a 78yr old male. He presents to GP complaining of worsening urgency and nocturia. This has been going on for the last 5 years but he has noticed a sudden decline in symptoms over the last 3 weeks. He also thinks he has lost some weight and has noticed some new pain in the centre of his lower back.

A. Describe some of the positives and negatives of PSA screening. (4 marks)

B. What is the gold standard method for diagnosing prostate cancer and which grading system is used to assess prostate cancer? (2 marks)

A

A. Positives: early detection of prostate ca, leads to better outcomes, simple, widely available blood test, cheap. Negatives: high rate of false positives, can cause anxiety, prostate ca often slow growing and never spread beyond the prostate, not requiring treatment

B. Transrectal US guided prostate biopsy - Gleason grading

Phase 2a (25 decks)

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