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MSRA revision > Renal/urology > Flashcards

Renal/urology Flashcards

1
Q

What is sterile pyuria?

A

A urine dip positive for leucocytes, or leucocytes seen on microscopy - but no bacteria grown on culture.

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2
Q

What are the features of epididymal cyst?

A
  • palpated separately to the testes
  • transilluminates
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3
Q

What is a spermatocele?

A
  • fluid, filled cyst
    like an epididymal cyst, it is palpated separately to the testes
  • fluctuant, cystic
  • usually asymptomatic
  • milky fluid on aspiration
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4
Q

What is a positive Prehn’s sign?

A
  • helps you to identify cause of testicular pain
  • Lifting up the scrotum relieves the pain
  • Positive - associated with epididymitis
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5
Q

What is the cremasteric reflex?

A

Stroke the inner medial thigh below the scrotum causes the ipsilateral testicle (same side) to retract/pull up
- ABSENT in testicular torsion

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6
Q

Key features of Epididymitis?

A
  • unilateral painful, swollen testicle
  • fever
  • dysuria
  • urinary frequency
  • urethral discharge
  • US shows increased blood flow
  • PREHN’S SIGN POSITIVE
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7
Q

What are the key features of testicular torsion

A
  • SUDDEN ONSET, painful, unilateral testicle
  • nausea and vomiting
  • abdominal pain
  • testicle may appear in horizontal position or high riding
  • Prehn’s sign is negative
  • cremasteric reflex ABSENT
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8
Q

how do you diagnose testicular torsion?

A

Ultrasound however not to delay if high clinical suspicion- urgent surgical scrotal exploration

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9
Q

What is appendix testes and appendix epididymis?

A

The appendix testis is a small appendage of that is usually located on the upper pole between the testis and epididymis

The appendix epididymis is a small appendage on the top of the epididymis

They are embryological remnants and don’t serve any function, like the appendix.

They can both develop torsion, but appendix testis is more likely to.

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10
Q

What are the main features of appendix testis torsion?

A
  • symptoms are similar to testicular torsion but onset may be more gradual
  • pain and tenderness is often localized to the upper pole of the testis or epididymis.
  • however for torsions of either appendages, the presentation is usually in pre-pubertal boys (whereas testicular torsion more commonly occurs in adolescent boys)
  • blue dot sign
  • cremasteric reflex usually intact
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11
Q

What is the management of torsion of the tetsicular appendages?

A

conservative management
The testicular appendage tends to calcify and degenerate over two weeks

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12
Q

What are the main causes of acute scrotal pain to know?

A
  • epididymitis
  • testicular torsion
  • appendix testis torsion
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13
Q

What is the blue dot sign?

A
  • can be seen in testicular appendix torsion
  • Torsion –> ischaemia of the appendage –> appears as a blue dot underneath the skin
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14
Q

What is the most common cause of epididymitis?

A
  • Most common cause overall: E.coli
  • Young, sexually active - chlamydia/gonorrheoa
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15
Q

What is a hydrocele?

A
  • fluid accumulates between the visceral and parietal layers of the tunica vaginalis
  • this is caused by incomplete closure of the processus vaginalis
  • can be classified into communicating and non-communicating
  • communicating with the peritoneal cavity or does not communicate with the peritoneal cavity
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16
Q

What are the key features of hydrocele?

A
  • usually asymptomatic
  • can be unilateral or bilateral
  • painless, swelling of scrotum
  • feels like a water balloon
  • TRANSILLUMINATES
  • most commonly presents in infants (congenital)
  • in adults it is usually idiopathic
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17
Q

What is a varicocele?

A

dilatation of the pampiniform venous plexus

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18
Q

What are the key symptoms of varicocele?

A
  • Usually on the left side
  • feels like a bag of worms
  • dragging sensation
  • disappears on lying down (drains)
  • DOES NOT TRANSILLUMINATE
  • can lead to infertility due to increasing scrotal temperature
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19
Q

What is the difference between the drainage of the left and right testicles?

A

right testicular veins drain directly into the IVC
Left testicular veins drain into the left renal vein which then drains into the IVC

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20
Q

What is the cause of Varicocele?

A
  1. primary - idiopathic
  2. obstruction of the renal veins due to renal tumour or thrombosis
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21
Q

What are the clinical findings of a testicular tumour

A
  • painless swelling
  • does NOT transilluminate as it is solid
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22
Q

What is cryptorchidism

A
  • Undescended testes
  • Three percent of males will be born with an undescended testicle. Most of these will descend within the first months of life, and no treatment is indicated.
  • Rarely, physiologic descent does not occur, and surgery is indicated to prevent complications such as reduced fertility or testicular cancer.
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23
Q

Cryptorchidism increases the risk of what?

A

increased risk of
- Testicular cancer
- infertility
- torsion

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24
Q

what is a penile fracture?

A

Traumatic rupture of corpus cavernosum - urological emergency

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25
Q

what are the symptoms of a penile fracture?

A
  • snapping sound followed by swelling and bruising of the penis
  • eggplant appearance - due to swelling and discolouration
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26
Q

what is the cause of mechanism of contrast induced nephropathy?

A

acute tubular necrosis

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27
Q

On what chromosome is the mutation involved in PCKD?

A

PKD1 on chromosome 16 (85%
PKD 2 on chromosome 4 (15%)

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28
Q

What is the inheritance of PCKD?

A

Autosomal dominant

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29
Q

What are the key features of PCKD?

A
  • cysts on the kidneys bilaterally - palpable masses in the flanks
  • haematuria (due to cyst rupture)
  • Intracranial berry aneurysms - can lead to SAH
  • increased risk of colonic diverticula
  • increased risk of renal cell carcinoma
  • mitral valve prolpase
  • hypetension
  • progressive kidney failure
  • benign hepatic cysts
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30
Q

what are some causes of a raised PSA?

A
  • old age
  • acute urinary retention
  • catheterisation
  • BPH
  • prostatitis
  • prostate cancer
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31
Q

What are the causes of urethral injuries?

A

Can be classified into
- posterior urethral injury - affecting the prostatic and membranous portion of the urethra - typically due to RTA causing pelvic fractures
- anterior - affecting the urethra distal to the membranous region - typically due to straddle injuries or direct blunt trauma

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32
Q

What are the symptoms of urethral injury?

A
  1. blood at the urethral meatus
  2. acute urinary retention
  3. palpable bladder
  4. Scrotal or perineal haematoma/bruising
  5. high riding prostate on DRE
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33
Q

What is the most common cause of bladder rupture?

A

Usually due to blunt trauma (such as RTA) + are associated with pelvic fracture in most cases.

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34
Q

What are the two types of bladder rupture?

A

extraperitoneal - more common (80%)
- associated with pelvis fracture
- typically occurs at base of bladder
- Mx: short term Foley catheter to allow bladder to heal

Intraperitoneal bladder rupute
- Less common -20%
- Associated with direct blow onto distended bladder
- typically occurs at bladder dome
- can lead to peritonitis
- Mx: surgical as will typically not heal with just a catheter

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35
Q

What investigation do you do if you suspect bladder rupture?

A

CT cystogram

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36
Q

What are the symptoms of bladder rupture?

A
  • usually History of blunt force trauma
  • haematuria
  • difficulty voiding
  • suprapubic pain
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37
Q

What is Wilm’s tumour?

A
  • malignancy that occurs in childhood - nephroblastoma
  • malignant proliferation of metanephric blastema cells (primitive embryologic cells in the kidney)
  • rare, but the most common primary renal tumour in children
  • typical onset age 2-4 years old
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38
Q

How does Wilm’s tumour present

A
  • palpable abdominal mass
  • hypertension (cells may secret renin)
  • fever due to tumour necrosis
  • haematuria
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39
Q

What is the most common type of renal cancer?

A

Renal cell carcinoma (80%)
Of the 3 subtypes, clear cell is the most common

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40
Q

What is the other less common types of renal cancer?

A

Transitional cell carcinoma (occurs in the renal pelvis), Wilm’s tumour, sarcoma or benign tumours

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41
Q

What is the most common risk factor for renal cell carcinoma?

A

smoking

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42
Q

What paraneoplastic syndrome is associated with RCC?

A

Cells secrete EPO which can lead to secondary polycythemia (high RBCs)
Can also get hypercalaemia

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43
Q

Unlike most other cancers, how does RCC spread?

A

Haematogenously - via the renal vein which drains into the IVC
Most cancers spread via the lymphatic system

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44
Q

What are the symptoms of RCC?

A
  • palpable mass
  • flank pain
  • haematuria
  • can present as varicocele if left sided
45
Q

What are the most common sites of RCC metastases?

A

Lung (classically you see cannon ball mets) and bone

46
Q

What hereditary syndromes are associated with RCC?

A

Von Hippel Lindau syndrome - they can get bilateral RCC
Tuberous sclerosis

47
Q

What is angiomyolipoma?

A

Benign tumour of the kidney - made up of blood vessels, smooth muscle and adipose tissue
80% occur sporadically
20% are associated with hereditary conditions such as tuberous sclerosis

48
Q

What is tuberous sclerosis?

A

Autosomal dominant genetic disorder - mutation of hamartin and tuberin which are tumour suppressor genes - this results in multiple benign tumours around the body

49
Q

What are the key features of tuberous sclerosis?

A
  • benign tumours - symptoms caused by compressive effect
  • Cutaneous manifestations
  • Seizures due to cortical hamartomas
  • renal angiomyolipomas
  • lung
  • liver
  • heart (rhabdomyomas)
  • developmental delay
50
Q

What are Ash leaf spots?

A
  • occur in tuberous sclerosis
  • white, flat skin lesions - hypo pigmented macular lesions
  • earliest cutaneous sign
51
Q

What is a Shahgreen patch?

A
  • raised, leathery, skin coloured skin lesion
  • Found in tuberous sclerosis
52
Q

What is the most common type of bladder cancer?

A
  • Transitional cell carcinoma - 90%
    Transitional cell carcinoma can also occur in the renal pelvis and ureter where these cells are found
53
Q

What are some risk factors for transitional cell carcinoma?

A
  • smoking (just like RCC)
  • aniline dyes used in the manufac- ture of some plastics
  • medications such as cyclophosphamide (a chemotherapeutic agent and immunosuppressant).
54
Q

How do you classify testicular cancer?

A

classified into germ call 95%
and non-germcell

Germ cell is sub classified into:
- seminoma - 55%
- non-seminoma

Non-seminoma
- teratoma (post pubertal type)
- embryonal carcinoma
- choriocarcinoma
- yolk sac tumours (post pubertal type)

55
Q

What tumour marker do you use in monitoring testicular teratoma?

A

AFP

(not found in seminomas)

56
Q

What tumour marker do you use to monitor testicular seminoma?

A

HCG

57
Q

What are the key features of testicular seminoma

A
  • Most common germ cell tumour
  • malignant
  • typically occurs in men aged 30-50
  • Beta HCG is elevated
  • painless, unilateral enlarged testicle
  • friend egg appearance on histology
58
Q

What are the key features of testicular teratoma

A
  • a type of germ cell tumour
  • derived from one or more germinal layers (endoderm, mesoderm, and ectoderm).
  • they are MALIGNANT in adult MEN
  • Benign in women and children
59
Q

What is Alport syndrome?

A
  • most commonly X-linked inherited disorder
  • Mutation in gene responsive for type IV collage
  • This results in an abnormal glomerular basement membrane - irregular thinning and splitting
60
Q

What are the key features of Alport syndrome?

A
  • anterior lenticonus (abnormal lens in the eye)
  • sensorineural hearing loss (deaf)
  • Glomerulonephritis and renal failure
  • Microscopy: GBM has a “basket-weave” appearance

“can’t see, can’t pee, can’t hear a bee”

61
Q

What is granulomatosis with polyangiitis (GPA?)

A
  • Aka Wegener’s granulomatosis
  • Affects children and adolescents
  • affects lungs AND Kidneys (not just upper airways)
  • medium vessel vasculitis
  • different from polyarteritis nodosa because the lung (both upper airway and lung parenchyma) is affected in GPA.
  • chronic sinusitis with nasal septal perforation (saddle-nose deformity)
  • recurrent epistaxis
  • hemoptysis from lung involvement (alveolar hemorrhage)
  • hematuria from renal involvement c-ANCA is a marker of disease.
  • Treat with cyclophosphamide and steroids.
  • Remember the Cs of gPA: c-ANCA, corticosteroids, cyclophosphamide.
62
Q

What is Churg Strauss syndrome and what are main clinical features ?

A

Churg Straus syndrome - aka eosinophilic granulomatosis with polyangiitis (EGPA)
- small vessel vasculitis
- adult onset asthma - precedes onset of vasculitis by 3-9 years
- allergic rhinitis
- sinusitis
- nasal polyps
- can get peripheral neuropathy
-oesinophilia
- Raised IgE
- p-ANCA positive

(kidneys not commonly affected, lung parenchyma less commonly affected)

63
Q

What is Henoch schonlein purpura? (HSP)

A
  • small vessel vasculitis caused by IgA immune complex deposition in capillaries leading to inflammation
  • most common vasculitis in children
  • typically occurs in children <10 years old
  • classically occurs following a viral URTI (rapid onset - whereas PSGN occurs 1-2 weeks later)

Management: conservative

64
Q

What are the main symptoms of henoch schonlein purpura (HSP?)

A

Tetrad:
1. palpable purpura on the legs and buttocks from inflamed hemorrhagic vessels (100%) - non-blanching
2. arthritis from inflammation of vessels leading to joints (75%)
3. abdominal pain +/- bloody stool from affected gut vessels (50%)
4. renal disease from renal vessel involvement (50%)

The inflamed intestines can also lead to intussusception because the swelling can act as a lead point to drag itself into the adjacent loop of bowel.

65
Q

What is polyarteritis nodosa?

A
  • necrotising vasculitis affecting medium sized vessels
  • associated with hepatitis B infection in 5-10% of cases
  • More common in men
  • affects multiple organs (hence POLY) but does NOT affect pulmonary vessels
66
Q

What are some of the main clinical features of polyarteritis nodosa?

A
  • system symptoms such as fever, weight loss
  • Diffuse myalgia
  • Most commonly affects renal arteries –> renal failure
  • Skin: livedo reticularis (web/lace like skin discolouration)
  • neuropathy - can be mono or poly
  • testicular pain or tenderness
  • hepatitis B positive
  • diastolic Bp >90mmHg
  • MI if cardiac arteries affected
  • Treatment: steroids, cyclophosphamide, anti-virals for Hep B infection
67
Q

What is Kawasaki disease?

A
  • small to medium vessel vasculitis that typically occurs in children
  • More common children of asian descent
  • can get coronary artery involvement - which can lead to aneurysms and MI
68
Q

What are the clinical features of Kawasaki disease?

A

Acute phase (1-2 weeks)
“CRASH and burn (fever)”
- High fever of 39 or higher for at least 5 days
- Conjunctivitis (bilateral, non exudative)
- Rash - polymorphous, widespread rash
- Adenopathy (cervical
- Hand and feet swelling
- mucosal involvement - strawberry tongue and fissured lips

Subacute phase (2-4) weeks
- fever, rash and lymphadenopathy settle
- desquamation of the rash
- cardiac abnormalites can present at this stage MI, sudden cardiac death

69
Q

What is the treatment for Kawasaki disease?

A
  • IV immunoglobulins
  • aspirin
70
Q

What is the cause of post-streptococcal glomerulonephritis?

A

An immune reaction that occurs 1-2 weeks after infection with group A beta haemolytic streptococcus (strep progenies)

Type III hypersensitivity reaction

  • Antibody–antigen complexes deposit in the glomerular basement membrane.
  • Edema and hematuria are the main features.
  • Cannot be prevented with antibiotics.
71
Q

What are the symptoms/signs of PSGN?

A
  • most commonly in children
  • sore throat
  • fever
  • Coca Cola urine
  • oedema - usually peri-orbital but can be peripheral as well
  • hypertension
  • resolves spontaneously.
72
Q

What are the clinical findings in PSGN?

A
  • AKI
  • high titers of antistreptolysin O (ASO) antibodies
  • Low complement
  • RBC casts in urine
73
Q

What is goodpasture’s syndrome

A
  • Type II hypersensitivity reaction - autoimmune disorder
  • Anti-glomerular basement membrane antibodies (anti-GBM)
74
Q

What are the main clinical features of good pasture’s syndrome?

A

Triad
1. rapidly deteriorating renal function
2. lung haemorrhage - haemoptysis
3. Anti-GBM antibodies

75
Q

What is the treatment for good pasture’s syndrome?

A

immunosuppressive agents + plasma exchange to remove the anti-GBM autoantibodies

76
Q

What is IgA nephropathy?

A

Most common glomerulonephritis.

Can occur or recur after viral upper respiratory infection or gastroenteritis (usually within 1 wk).

IgA immune-complex deposition in glomerular mesangial cells that results in its proliferation

Results in a nephritic syndrome

77
Q

How to tell apart nephritic vs nephrotic syndrome?

A

nephritic - glomerulonephritis - acute inflammation of kidney
LOSING BLOOD IN URINE
lose a bit of protein and have a bit of oedema
also HTN is a major feature

nephrotic - proteinuria - OEDEMA
LOSING A LOT OF PROTEIN IN URINE

78
Q

What are the features of nephritic syndrome?

A
  1. RBC casts in urine
  2. Mild proteinuria
  3. Mild oedema
  4. HTN
  5. Raised JVP
  6. Oliguria
  7. Raised urea + creatinine
79
Q

What are the features of nephrotic syndrome?

A
  1. massive proteinuria
    - low albumin
    - frothy urine
  2. significant oedema
  3. high cholesterol and triglycerides
  4. hypercoagulability
  5. increased risk of infection (loss of IgG antibodies in urine)

Causes by:
Loss of negative charge of the basement membrane

80
Q

Causes of nephrotic syndrome

A
  1. Minimal change disease
  2. focal segmental glomerulosclerosis
  3. Membranous nephropathy
  4. diabetes mellitus
  5. amyloidosis
81
Q

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

A

Minimal change disease

Responds well the steroids.

82
Q

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

A

Focal segmental glomerulosclerosis

83
Q

What is the mechanism of action of tamsulosin?

A

Alpha receptor anagonist

Causes smooth muscle relaxation in the prostate

84
Q

What is the mechanism of action of Finasteride?

A

5 alpha reductase inhibitor
5 alpha reductase converts testosterone to DHT which stimulates prostatic growth
helps reduce size of the prostate gland

85
Q

What is Peyronie disease?

A
  • fibrous tissue develops in the penis
  • causes the penis to curve when erect
  • painful erections
86
Q

On which part of the nephron does aldosterone act?

A

The principle cells of the collecting duct s- Na+ is reabsorbed (into blood stream) and K+ is excreted into urine

Aldosterone upregulates this in an effort to increase intravascular volume by reabsorbing more sodium, but in the process it causes K+ secretion
Aldosterone also stimulates H+ secretion in the α-intercalated cells

Thus in hyperaldosteronism (e.g. Conn’s syndrome) you can get hypernatraemia, hypokalaemia and metabolic alkalosis

87
Q

On which part of the nephron does ADH act?

A

The collecting duct
Increases water reabsorption

88
Q

What is the function of angiotensin II

A
  • causes system vasoconstriction
  • preferentially causes vasoconstriction of efferent arteriole to increase glomerular filtration pressure
  • stimulates aldosterone release from the adrenal gland
  • also directly acts on the kidney in the proximal tubule to increase sodium and water reabsorptipn
  • stimulates thirst

(With high levels of AT II (e.g., in severe hypotension), the afferent arteriole will constrict as well, which lowers the GFR because the blood is needed elsewhere (e.g., the brain).)

(Some stimuli can directly stimulate aldosterone secretion. For example, an increased plasma ion concentration of K+ and a reduced plasma concentration of Na+ directly stimulate aldo- sterone secretion from the adrenal cortex)

89
Q

What is the pathophysiology of renal artery stenosis

A

renal artery stenosis –> renal hypo perfusion - JG cells around the afferent arteriole detect less stretch –> they increase renin secretion –> renin converts angiotensin I to angiotensin II via ACE (enzyme) –> Angiotensin 2 causes preferential constriction of efferent arteriole, system vasoconstriction, acts directly on kidneys and stimulates aldosterone release from adrenal gland which increases sodium reabsorption in the kidney –> the total effect is increasing intravascular volume and BP - in RAA this can result I’m hypertension that is refractory to treatment

90
Q

What is the most common cause of renal artery stenosis?

A
  1. atherosclerosis - especially in older people and/or smokers
  2. Fibromuscylar dysplasia - in young, middle aged women
91
Q

What is the typical presentation of RAA?

A
  • can present as sudden/recurrent pulmonary oedema
  • resistant HTN + acute worsening of renal function after starting an ACE inhibitor
92
Q

Why does an ACEi worsen renal function in RAA?

A

RAA results in reduced renal perfusion and subsequent activation of the RAA pathway - angiotensin II Is causing constriction of the efferent arteriole to try to maintain GFP
ACE inhibitor - inhibits ACE and reduced Angiotensin II production
Thus you get relative dilatation of the efferent arteriole + also system vasodilatation - further reducing renal perfusion - resulting in a decrease in kidney function

93
Q

What are some contraindications to ACEinhibitors?

A
  • pregnancy (risk of fatal renal agencies)
  • bilateral renal artery stenosis
94
Q

On which part of the nephron do loop diuretics act on?

A
  • Acts on the thick ascending loop of henle
  • Inhibits the Na+/K+/2Cl- cotransporter (which normally pumps these ions into the lumen)
  • Thus inhibiting Na+ reabsorption and therefore water
95
Q

On which part if the nephron do thiazide diuretics act on?

A

Thiazide diuretics inhibit the Na+/Cl- co-transporter in the distal convoluted tubule
This prevents Na+ reabsorption and its osmotically related water

96
Q

What markers do you use to grade chronic kidney disease?

A

eGFR and albumin/creatinine ratio.

97
Q

What is acute interstitial nephritis?

A

immune mediated renal inflammation - type IV hypersensitivity reaction- leading to AKI - most commonly drug induced e.g NSAIDs, penicillin

98
Q

What are the clinical features of acute interstitial nephritis?

A
  • Presents 1-2 weeks after starting the drug
    FARE
  • Fever
  • Arthralgia
  • Rash
  • Eosinophilia
  • Tx: stop the drug +/- steroids
99
Q

What is fanconi syndrome?

A

Proximal tubule of the nephron is impaired
Can be inherited or acquired
In children - typically inherited/genetic defect - commonly due to cystinosis
In adults - typically acquired (e.g. due to medications)

Proximal tubule is unable to re-absrob HCO3- - bicarb wasting in urine

100
Q

What are the clinical features of Fanconi syndrome

A
  • Rickets in children (Vitamin D which is produced in the proximal tubule and urinary excretion of calcium + phosphate)
  • Osteomalacia in adults
  • Low Phosphate
  • Type 2 renal tubular acidosis - bicarb wasting in urine
  • hypokalaemia
101
Q

What is Congo red staining used to test for?

A

Used to detect amyloid in tissues such as muscles/brain

102
Q

Renal biopsy shows apple green birefringence under polarised light after Congo red stain. What is this indicative of?

A

Renal amyloidosis.

103
Q

What is meant by functional incontinence?

A

Physical or mental barriers to getting to the toilet in time
- impaired mobility
- difficulty removing clothes before urinating
- dementia or mental illness resulting in loss of awareness of needing the toilet.

104
Q

What are the features of normal pressure hydrocephalus?

A

WET WACKY WOBBLY

  1. urinary incontinence
  2. dementia
  3. wide based shuffling abnormal gait
105
Q

What vaccine is used in the treatment of bladder cancer?

A

BCG vaccine (Bacillus Calmette-Guérin) which is also used to prevent TB
Used to treat non muscle invasive bladder ca

Given directly into the bladder via a catheter

106
Q

What are the electrolyte findings in chronic kidney diseas?

A
  • hyperkalaemia (impaired excretion)
  • hyperphosphataemia (impaired excretion + secondary hyperparathyroidism)
  • Low HCO3 levels
  • Uraemia
  • Metabolic acidosis (low HCO3-)
  • ## Hypocalcaemia (impaired Vit D activation - reduced ca2+ absorption from gut)
107
Q

What enzyme activates vitamin D in the kidneys?

A

1-α-hydroxylase

108
Q

What is the first line investigation if you suspect renal stone?

A

CT KUB without contrast

109
Q

How do you definitively diagnose the cause of nephrotic syndrome?

A

Renal biopsy

MSRA revision (25 decks)

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