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CP1 > Renal & Urology > Flashcards

Renal & Urology Flashcards

1
Q

Acute pylonephritis presentation

A

Pyrexia
Loin pain + tenderness
Bacteriuria
Rigors, vomiting, oliguria

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2
Q

Cystitis (lower UTI) signs/symptoms

A

Frequency, nocturia, urgency, haematuria, smelly urine, suprapubic pain/tenderness, strangury

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3
Q

Cystitis predisposing factors

A

Female, pregnancy, menopause, urethral obstruction/malformation, catheter, diabetes (glycosuria)

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4
Q

Investigations for UTI

A

MSU dipstick (double +ve nitrites & leucocytes)
Midstream urine MCS
Ask if vaginal discharge (GUM pathology?)
Sepsis 6 if systemically unwell

Further investigations (male, children, treatment-resistant, recurrent, pyelonephritis):
USS - renal scarring/hydronephrosis
CT/IV urography - exclude stones, tumours, diverticula

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5
Q

Causes of sterile pyuria

A

Recently treated UTI, appendicitis, TB, chlamydia, bladder cancer

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6
Q

Common UTI causative organisms

A 
E. Coli - 75%
Proteus
Staphylococcus
Streptococcus
Klebsiella
Pseudomonas
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7
Q

Causes of ureteric obstruction

A

Luminal: calculus, sloughed renal papilla (diabetes/NSAIDs), clot, TCC of renal pelvis/ureter, bladder tumour
Mural: Ureteric stricture (TB, post-calculus, post-surgery), congenital pelviureteric neuromuscular dysfunction, congenital megaureter
Extramural: pelviureteric compression (tumour, diverticulitis, AAA, retroperitoneal fibrosis)

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8
Q

Acute ureteric obstruction signs/symptoms

A

10/10 colicky loin-to-groin pain exacerbated when urine volume increases (alcohol/diuretics)
Anuria if complete bilateral obstruction
Polyuria if hydronephrosis causes post-renal AKI
Palpable hydronephrotic kidney

EXCLUDE: acute scrotum, AAA, pregnancy

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9
Q

Ureteric obstruction investigations

A 
Urine MCS
USS to confirm ureteric dilation
AXR
CT - detailed cause of obstruction
Retrograde pyelogram + cystoscopy
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10
Q

Aetiology of kidney calculi

A

Form in collecting ducts
Classic sites: pelviureteric junction, pelvic brim, vesicoureteric junction
75% calcium oxalate
Magnesium ammonium phosphate (struvite) - Recurrent urease-positive bacteria (eg. proteus mirabilis) infections predispose individuals to struvite renal stones
Urate based
15% lifetime risk, 20-40y, M:F 3:1

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11
Q

Kidney/ureter calculi signs/symptoms

A

Stone in ureter: renal colic, loin-to-groin pain, nausea+vomiting, cannot lie still
Stone in major/minor calyx: dull loin pain
UTI secondary to obstruction

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12
Q

Kidney/ureter calculi risk factors

A

Obesity, dehydration, family/personal history, anatomical abnormalities

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13
Q

Kidney/ureter calculi investigations

A

Bloods (calcium, phosphate, glucose, bicarbonate, urate)
Urine dip (95% +ve for blood), rule out infection
bHCG
Urine MCS
AXR
Non-contrast CT, can exclude abdominal ddx

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14
Q

Bladder calculi presentation

A 
UTI symptoms (frequency, pain, haematuria) at the end of micturition, males at tip of penis
Perineal pain if trigonitis, anuria/bladder distention
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15
Q

Bladder calculi investigations

A

Bloods (calcium, phosphate, glucose, bicarbonate, urate)
Urine dip (95% +ve for blood), rule out infection
bHCG
Urine MCS

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16
Q

Renal cell carcinoma aetiology

A

Vascular tumours arising from the proximal tubular epithelium
90% of renal tumours
Risk factor: prolonged haemodialysis

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17
Q

Renal cell carcinoma presentation

A

50% incidental
10% classic triad - haematuria, loin pain, abdominal mass + B symptoms (pyrexia, night sweats, weight loss)
Invasion of left renal vein = varicocele
Polycythaemia/hypertension if EPO/renin secretion

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18
Q

Renal cell carcinoma investigations

A 
Urine cytology
USS - solid/cystic mass?
CT/MRI
CXR - cannonball mets
Renal angiography if considering nephrectomy
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19
Q

Wilm’s tumour aetiology & presentation

A

20% childhood malignancies
Undifferentiated mesodermal tumour
3.5y, flank pain + abdominal mass
Should not be biopsied

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20
Q

Renal cyst aetiology & presentation

A

50% have a renal cyst by 50y
Causes: polycystic kidney disease, medullary cystic disease (childhood disease leads to ESRF), medullary sponge kidney
Asymptomatic or haematuria/pain

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21
Q

Transitional cell carcinoma aetiology

A

Transitional cell epithelium lines the calyces, renal pelvis, ureter, bladder, urethra
Bladder tumours 50x more common
Risk factors: smoking, aromatic amines, chronic cystitis, pelvic irradiation

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22
Q

Transitional cell carcinoma of the bladder presentation

A

Painless haematuria +/- clots
Reccurrent UTI
Voiding symptoms
Pain from invasion of local structures

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23
Q

Transitional cell carcinoma of the bladder investigations

A

Urine MCS/cytology (sterile pyuria?)
Cystoscopy + biopsy
CT/MRI
Lymphangiography to assess spread

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24
Q

Causes of bladder outlet obstruction

A

Luminal: bladder tumour
Mural: urethral stricture (post-calculus/infection), congenital, neuropathic bladder
Extramural: BPH, prostatic carcinoma, phimosis, paraphimosis

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25
Q

Bladder outlet obstruction signs/symptoms

A

Suprapubic pain, hesitancy/diminished force of stream, terminal dribbling, overflow incontinence, signs of infection due to stasis of urine
Palpable full bladder
Loin tenderness/palpable hydronephrosis
Enlarged prostate on DRE

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26
Q

Bladder outlet obstruction investigations

A

Bloods: FBC (infection, U&Es)
Urine dip and MCS
USS - hydronephrosis?
CT/MRI

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27
Q

Benign prostatic hyperplasia aetiology

A

Benign nodular/diffuse proliferation of glandular layers of the prostate = enlargement of the inner transitional zone
70% of men >70y

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28
Q

Benign prostatic hyperplasia symptoms

A 
Filling symptoms (bladder overactivity): frequency, nocturia, urgency, strangury
Voiding symptoms (bladder outlet obstruction): hesitancy, poor stream, terminal dribble, strangury, retention + overflow incontinence
Symptoms due to complications: haematuria, associated UTI
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29
Q

Benign prostatic hyperplasia investigations

A

DRE
Frequency/volume chart
Bloods: FBC, U&Es, PSA (<4.0ng/mL = normal)
Urinalysis/MCS
Uroflowmetry (requires >150ml. Flow <12ml/2 suggests obstruction or weak detrusor contraction)
Pre/post-void bladder USS
Transrectal USS +/- biopsy to rule out carcinoma

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30
Q

Benign prostatic hyperplasia complications

A

UTI, overflow incontinence, bladder calculi/diverticulae, bilateral hydronephrosis and renal failure

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31
Q

Prostate carcinoma aetiology

A

80% males >80y but only 4% die from it
Most adenocarcinomas arising from peripheral prostate
Peripheral layer enlargement
Spread can be local (seminal vesicles, bladder, rectum), lymphatic, haematogenous - spinal/pelvic mets
Risk factors: family history, raised testosterone

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32
Q

Prostate carcinoma presentation

A

Asymptomatic: DRE/BPH resection histology
Filling, voiding, complication symptoms
Weight loss/bone pain = mets
Hard + craggy prostate

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33
Q

Prostate carcinoma investigations

A

DRE - T stage
PSA - rise >10ng/mL suggestive of tumour (affected by exercise, intercourse, infection, cystoscopy)
Transrectal USS/biopsy - Gleason grading (2 areas of tissue graded/5 to give score/10. Score<6 = low risk. Score>8=high risk.)
D’amico risk stratification: Gleason + stage + PSA
Bone XR/scan + contrast-enhanced MRI for staging

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34
Q

Urethral stricture aetiology

A

Scar of urethral epithelium, commonly extends into underlying corpus spongiosum
Fibroblastic activity leads to shortening of urethral length + narrowing of lumen
Causes: blunt perineal trauma, catheter insertion, gonococcal/non-gonococcal urethritis
Balanitis xerotica obliterans - white atrophic plaques leading to phimosis

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35
Q

Urethral stricture presentation

A

Obstructive voiding symptoms that gradually worsen: dysuria, hesitancy, urinary retention, splayed stream if meatal stricture
OE: firm areas/periurethral scarring
<50y, no prostate abnormalities

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36
Q

Urethral stricture investigation

A

Uroflowmetry
Urethrogram - stricture length, location, calibre, significance
Urethroscopy

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37
Q

Phimosis pathology & presentation

A

Narrowing of the preputial orifice
Causes: idiopathic, congenital, chronic BXO, traumatic forcible retraction of the foreskin
Child presentation: ballooning of foreskin, poor stream
Adult presentation: pain during intercourse, unability to retract the foreskin

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38
Q

Paraphimosis pathology & presentation

A

Pulling a tight foreskin over the glans, obstructing venous return leading to a swollen painful glans
Can occur following erection/catheter insertion

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39
Q

Priapism pathology & presentation

A

Persistant erection of the corpus cavernosa of the penis

Causes: idiopathic, trauma, sickle-cell disease, intracavernosal injections for impotence

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40
Q

Peyronie’s disease pathology & presentation

A

Upward curvature of the penis when erect (1-3% men)

Causes: idiopathic, fibrous scarring following trauma

41
Q

Carcinoma of the penis pathology & presentation

A

Squamous cell carcinomas
Persistent red patch on penis, progressing to infiltrating ulcer. No urethral involvement
Risk factors: 50% cases associated with HPV 16/18, smoking, immunosuppression

42
Q

Varicocele pathology & presentation

A

Varicosities of the pampiniform plexus (commonly left/adolescence), 10% males, increasing with age
Left testicular vein drains horizontally into the left renal vein (c.f. right drains obliquely into IVC)
Valvular incompetency at junction, left renal tumour
Dragging sensation/ache
‘bag of worms’ when palpated standing

43
Q

Hydrocele pathology & presentation

A

Fluctuant fluid that transilluminates - excessive collection of serous fluid in the processus vaginalis
Congenital: associated with hernia sac and patent processus vaginalis - most spontaneously resolve
Primary (idiopathic): ‘vaginal hydrocele’ - seperate from the peritoneal cavity
Secondary: underlying inflammation in the epididymis/testes or underlying cancer

44
Q

Epididymal cyst pathology & presentation

A

Cystic degeneration of epididymal structures
Associated with PKD/CF
Cystic (transilluminates) + seperate from testes (upper pole)
Clear/milky (contains sperm)
Can be painful

45
Q

Pathology and types of testicular tumours

A

Most common solid malignancy in young adults
Risk factors: undescended/ectopic testes (worse if >13y), infertility, hypospadia, family/personal history
Germ cell tumours: seminomas, non-seminomatous germ cell tumours (NSGCTs) (teratomas, yolk sac tumours, choriocarcinomas)
Seminoma - seminiferous tubule cells (30-40y), solid, spermatocyte cells to round cells
Teratoma - totipotent germ cells(20-30y), cystic, variable cell types
Stromal tumours
Lymphoma (older males)
Spread: local - rare. Lymph - para-aortic nodes. Blood - lungs and liver.

46
Q

Testicular tumour presentation

A

Painless lump, hydrocele, haematospermia
Mets symptoms (breathlessness/abdo swelling) - palpable supraclavicular node
Rarely: painful rapidly enlarging; gynaecomastia due to paraneoplastic hormone production

47
Q

Testicular tumour investigations

A

Scrotal USS - reveal mass in presence of hydrocele
Tumour markers: NSGCT (AFP, bHCG), semianomas (never AFP, 10% bHCG)
CT CAP - staging

48
Q

Testicular tortion pathology

A

Usually congenital abnormality (maldescention/bell-clapper testes)
12-18y with history of mild trauma/previous attacks of pain due to partial tortion
Testis twists upon its pedicle obstructing venous return

49
Q

Testicular tortion presentation

A

Sudden onset severe pain in groin/lower abdomen + vomiting
OE: unilateral hot swollen tender testis, sometimes lying high and transverse within the scrotum
Absent cremasteric reflex

50
Q

Testicular tortion investigation

A

Doppler USS - show lack of blood supply to testis

Surgical exploration

51
Q

Testicular appendage tortion pathology + presentation

A

Tortion of embryological remnant
Less painful than testicular tortion
Small blue nodule visible under the scrotum, no elevation of the testis
Classically occurs at start of puberty

52
Q

Epididymo-orchitis pathology

A 
Acute infection (ascending via the vas deferens) followimg gonococcal/non-gonococcal urethritis/E. Coli UTI
Can spread haematogenously (mumps/TB)
53
Q

Epididymo-orchitis presentation

A 
Painful swelling of the epididymis
Secondary hydrocele
History of discharge (STI)/dysuria (UTI)
OE: DRE may reveal co-existent prostatitis
\+ve Phren's sign
54
Q

Epididymo-orchitis investigations

A

First-catch urine MCS and STI screen

USS

55
Q

Acute bacterial prostatitis presentation

A

Pyrexia/rigors, perineal pain, difficulty voiding, UTI symptoms, pain on ejaculation/haematospermia
DRE: prostate exquisitely tender and enlarged
May present alongside epididymo-orchitis (infection passes along vas deferens)

56
Q

What ions do the kidneys decrease the plasma concentration of?

A

creatinine, urea, K+, H+

57
Q

What is the role of the renal corpsucle?

A

Produce glomerular filtrate

58
Q

What is the role of the proximal convoluted tubule?

A

reabsorb water, ions and organic nutrients

59
Q

What is the role of the loop of henle?

A

Descending limb - reabsorption of water

Ascending limb - reabsorption of Na+/Cl-

60
Q

What is the role of the distal convoluted tubule?

A

Secretion of ions, acids, drugs, toxins

Variable reabsorption of water (under control of ADH)

61
Q

What is the role of the collecting duct?

A

Variable reabsorption of water (under control of ADH)

Variable solute reabsorption

62
Q

What are the secondary functions of the kidneys?

A

EPO secretion
Renin secretion
1-alpha-hydroxylation of calcidiol to form calcitriol (vitamin D)

63
Q

What criteria indicate an AKI?

A

Urine output <0.5ml/kg/h for 6 hours
>50% rise in creatinine over 7 days
>26micromol rise in creatinine over 48h

64
Q

Stage 1 AKI criteria

A

Serum creatinine: 150-200% increase or 25micromol/l increase in 48h
Urine output: <0.5ml/kg/h for 6h

65
Q

Stage 2 AKI criteria

A

Serum creatinine: 200-300% increase

Urine output: <0.5ml/kg/h for 12h

66
Q

Stage 3 AKI criteria

A

Serum creatinine: >300% increase or >350micromol/l with acute rise of >45micromol/l in 48h
Urine output: <0.3ml/kg/h for 24h or anuria for 12h

67
Q

AKI aetiology & presentation

A

Risk factors: men, elderly, CKD
Often symptomless with oliguria
Secondary complications: uraemia (vomiting, pruritis, pericarditis, encephalitis), hyperkalaemia (tented T waves), pulmonary oedema (unless pre-renal)

68
Q

Pre-renal AKI aetiology

A

Inadequate renal perfusion (75%)
Shock: hypovolaemic, cardiogenic, distributive
Renovascular obstruction: embolus, aortic dissection, renal artery stenosis (RAS), thrombosis, ACEIs given in bilateral RAS
Prolonged = acute tubular necrosis –> pourous tubular membranes
Initially, urine osmolarity is high (>500mosmol/kg) + low sodium
If ATN occurs, urine is isotonic with plasma + high sodium

69
Q

Post-renal AKI aetiology

A

Urinary tract outflow obstruction –> hydronephrosis
Ureter stones, stricture, clots, malignancy
Bladder outlet obstruction (prostatic enlargement, urethral stricture, phimosis/paraphimosis)

70
Q

Renal AKI - acute tubular necrosis

A

85% of renal AKI
Drugs/toxins damaging tubular cells
Drugs: aminoglycosides (antibiotic ‘-mycin’), cephalosporins (antibiotic ‘cef-‘), radiological contrast mediums, NSAIDs
Toxins: heavy metal poisoning, myoglobinuria, haemolytic uraemic syndrome

71
Q

Renal AKI - interstitial nephritis

A

10% of renal AKI
Drugs bypass basement membrane and cause damage to the interstitium
Causes: antibiotics, diuretics, allopurinol (treats gout), PPIs

72
Q

Myoglobinurea pathology & presentation

A 
Follows rhabdomyolysis (trauma, exercise, medications) releasing myoglobins
Dark urine, precipitates within tubules to cause damage
73
Q

Haemolytic uraemic syndrome pathology & presentation

A

Occurs in children following a diarrhoeal illness caused by verotoxin producing E. Coli O157
In adults following an URTI
Thrombocytopenia (purpura), haemolysis, ATN

74
Q

Nephritic screen components

A

ANCA (ANCA-associated vasculitis) & anti-GBM (Goodpastures) (RPGN)
ANA, dsDNA & complement studies (SLE)
Immunoglobulins, serum electrophoresis (myeloma)
Rheumatoid factor (RA-associated GN)
Hep B/C screen (Mesangiocapillary glomerulonephritis)
ASO (post-strep)
Renal biopsy can be diagnostic if there is uncertainty

75
Q

AKI general first line examinations/investigations

A 
Hypotension/hypertension (CKD)
Palpable bladder?
Bloods: FBC (renal anaemia in CKD), U&amp;Es, bicarbonate, phosphate, CRP, clotting (hepatorenal disease may need invasive procedures), creatine kinase (raised in myoglobinurea)
Nephritic screen if cause unclear
ABG
Urine dip and MCS
ECG (risk of hyperkalaemia)
Renal USS (post-renal causes)
Non-contrast CT (if suspect obstucting calculus)
Echo (if suspect uraemic pericarditis)
76
Q

Common electrolyte abnormalities in AKI

A

Rapidly progressing uraemia (anorexia, vomiting, pruritis, encephalopathy, haemorrhagic episodes)
Hyperkalaemia
Hypernatraemia (unless pre-renal)
Metabolic acidosis
Hypocalcaemia/hypophosphataemia (more in CKD)

77
Q

Hyperkalaemia causes & presentation

A

Pseudohypokalaemia: haemolysis, FBC before U&E, sample taken from drip arm, delay in sample testing
AKI/CKD
Supplements, K sparing diuretics (spironolactone), ACEIs, NSAIDs
Acidosis/DKA
Addison’s (primary adrenal insufficiency), tumour-lysis syndrome, burns
On ECG: tented T waves, widened QRS, flattened P/prolonged PR interval
Untreated: VF + tachycardia

78
Q

How is CKD diagnosed?

A

2 tests (inulin clearance) 3 months apart show reduced eGFR. Staged 1-5

79
Q

CKD stage 1

A

GFR 90+ but other long-term evidence of kidney disease e.g.
proteinurea/haematuria
Genetic diagnosis
Structural abnormality

80
Q

CKD stage 2

A

GFR 60-89 + other long-term evidence of kidney disease e.g.
proteinurea/haematuria
Genetic diagnosis
Structural abnormality

81
Q

CKD stage 3

A

GFR 30-59

82
Q

CKD stage 4

A

GFR 15-29

83
Q

CKD stage 5

A

GFR <15

84
Q

Aetiology of CKD

A 
DM (20-40%)
Hypertension
Chronic glomerulonephritis
Chronic pyelonephritis
Obstructive uropathy
Renovascular disease
Drugs (long-term NSAIDs)
Polycystic kidney disease
85
Q

CKD signs/symptoms

A 
Often asymptomatic until advanced
Vague fatigue and anorexia
Polyuria/nocturia
Restless legs syndrome
Sexual dysfunction
Nausea &amp; pruritis (early uraemia), yellow pigmentation, encephalopathy, pericarditis (severe uraemia)
Pedal oedema/pulmonary oedema (can be cause+symptom)
Pallor (anaemia)
Excoriations (pruritis)
Hypertension/fluid overload signs
Pericardial rub (rare)
86
Q

CKD investigations

A

Bloods: FBC, U&Es, LFTs, calcium, phosphate, PTH levels, glucose
Urinalysis & MCS - quantify proteinurea, exclude infection, look for casts
24h urinary protein/creatinine clearance - assess severity/nephrotic syndrome
CXR if pulmonary oedema suspected
Renal USS is obstructive causes suspected
DTPA scan - investigate vascular supply
Renal biopsy if cause unknown
Bone imaging - renal bone disease

87
Q

Renal anaemia pathology

A

Kidneys normally secrete EPO in response to hypoxia

Kidney partially loses this function in CKD, leading to anaemia

88
Q

Renal bone disease pathology

A

Kidneys produce 1-alpha-hydroxylase: calcidiol from liver –> calcitriol (vit D)
Vit D increases intestinal calcium absorption, increases renal reabsorption of calcium, and bone protective factors
Low vit D –> hypocalcaemia + hyperphosphataemia
Low vit D –> osteomalacia –> 2ndary hyperparathyroidism (raised PTH) –> increased calcium reabsorption from bones and renal tubules
Increased osteoclast activity –> cyst formation and marrow fibrosis: osteitis fibrosis cystica
Long term: tertiary hyperparathyroidism + hypercalcaemia leadimg to osteosclerosis of the spine
End result: osteopenia (detected radiologically)

89
Q

CKD secondary hypertension pathology

A

CKD leads to over-activation of the RAAS leading to hypertension

90
Q

How can diabetes mellitus damage the kidney?

A

Direct glomerular damage: basement membrane thickening, increased permeability of capillary wall + proteinuria, eventual glomerular hyalinisation —> CKD
Ischaemia due to arterial disease: atherosclerosis causes reduced eGFR and glomerular ischaemia
Ascending infection

91
Q

Polycystic kidney disease morphology and pathological consequences

A

AD/AR inheritance. ADPKD 1 in 800 usually bilateral.
Ballottable kidneys, systemic hypertension, CKD, abdominal swelling
Cysts also in liver, lungs, pancreas (asymptomatic)
ARPKD earlier in onset and more malignant course
Liver cysts –> portal hypertension and fibrosis
Associated with berry aneurysms (subarachnoid haemorrhage)

92
Q

Hypertensive renal damage

A

Thickening of renal artery walls –> inelastic rigid afferent arterioles
Chronic ischaemia, progressive loss of glomeruli (replaced by hyaline tissue)
Exacerbated by renal artery stenosis due to atherosclerosis

93
Q

Chronic interstitial nephritis pathology

A

Chronic pyelonephritis, irregular areas of scarring, chronic inflammatory infiltrate
Reflux associated chronic interstitial nephritis: incompetent vesicoureteric valves, predisposing inflammation + scarring. Presents in early adulthood
Obstructive chronic interstitial nephritis: anatomic abnormality leads to recurrent infections (prostate, retroperitoneal fibrosis), stones

94
Q

Glomerulonephritis pathology

A

Common cause of AKI/CKD
Immunological attack by an antibody or T cell attacking an antigen in the glomerulus
Primary (always there) or secondary (acquired/deposited)
Capillary: endothelial cell proliferation (bigger fenestra); capillary wall necrosis; glomerulosclerosis (scarring in the mesangium –> fenestra and capillaries pulled apart)
Basement membrane: thickened (more permeable)
Tubules: deposition of cells in Bowman’s space

95
Q

Secondary factors causing deposition of antigens causing glomerulonephritis

A 
NSAID HSP
Neoplasm
SLE
Amyloid
Infection
Diabetes
Henoch Schonlein Purpura
96
Q

Histological descriptions of glomerular pathology

A

Global: whole glomerulus is diseased
Segmental: small patches of one glomerulus are damaged
Diffuse: >50% glomeruli
Focal: <50% glomeruli

97
Q

Clinical manifestations of glomerulonephritis

A

AKI, CKD, asymptomatic haematuria, nephrotic syndrome, nephritic syndrome, rapidly prgressive glomerulonephritis

98
Q

Nephrotic syndrome pathology

A

TRIAD: proteinurea (3.5g/day), hypoalbuminaemia (<30g/l), oedema (periorbital and peripheral limbs)
Non-proliferative
Renal loss of thromboregulatory proteins (venous thrombosis) and liporegulatory proteins (hyperlipidaemia)
Primary causes: minimal change nephropathy, membranous glomerulonephritis, proliferative glomerulonephitis
Secondary causes: infection, drugs, neoplasm

99
Q

Nephritic syndrome pathology

A

TETRAD: haematuria + red cell casts, oliguria, proteinuria, hypertension
Proliferative (increased cell numbers) + damage to basement membrane –> casts form from blood and protein
Primary causes: IgA nephropathy, Goodpastures
Secondary causes: SLE, HSP

CP1 (12 decks)

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