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Year 2 - Renal > Week 3 > Flashcards

Week 3 Flashcards

1
Q

What are some of the key features that distinguish glomerulonephritis from pyelonephritis?

A

Glomerulonephritis

  • Non-infective
  • Presents as glomerular tufts with secondary tubulointerstitial changes
  • Usually diffuse, may be focal
  • Immunological mechanisms are often implicated but there doesn’t seem to be any one single cause

Pyelonephritis

  • Bacterial infection of the renal pelvis, calyces, tubules and interstitium. E. coli is the most common causative organism
    • also Pseudomonas and Strep. faecalis
  • Can be acute or chronic
  • Patchy distribution
  • More common in females
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2
Q

Why are females more predisposed to developing UTIs?

A

They have shorter, wider urethras

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3
Q

What are some of the risk factors for developing pyelonephritis?

A

Age and sex

Pregnancy

Urinary tract obstructions e.g. calculi, strictures, neoplasms, congenital abnormalities etc.

Compromised uretero-vesical valves and vescio-ureteric reflux

Diabetes

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4
Q

How might someone with chronic pyelonephritis present?

What would be the appearance on renal imaging?

A

Often no previous history of UTI, and symptoms are vague

Hypertension and/or uraemia

Large volume of dilute urine

On renal imaging, coarse cortical scarring and distortion of the calyces is seen

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5
Q

If a patient presented with vague symptoms such as weight loss, fever, loin pain and dysuria, and on imaging caseating granulomatous inflammation was seen in the kidneys, what might the diagnosis be?

A

Tuberculous Pyelonephritis

Caseous foci are identical to those seen in the lung of tuberculosis patients - slow growth with progressive renal destruction which can spread to ureters, bladder and other viscera

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6
Q

What bacterial species can cause cystitis?

A

E. coli

Klebsiella

Proteus

Psuedomonas

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7
Q

What tropical infection can predispose to numerous urothelial malignancies?

A

Schistosomiasis

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8
Q

Urinary tract obstruction can eventually lead to what in the kidney?

A

Hydronephrosis

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9
Q

Patient presents with haematuria! What questions do you ask them?

A

How long?

Is it painful? (a.k.a. dysuria)

Changes in urinary frequency?

Any symptoms of infection?

Other consitutional symptoms?

Where in the strain of urine? Beginning, end, or throughout?

Does it occur every time you go the bathroom?

What are the clots like? e.g. shape, colour

Lifestyle factors/Occupation - smoking, drinking, exposure to various chemicals e.g. dyes, diesel fumes etc.

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10
Q

What are “storage symptoms” related to? Give some examples of these symptoms

A

Related to bladder function

Frequency of urination

Urgency

Incontinence

Nocturia

Sense of incomplete empyting

Pain with filling of the bladder

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11
Q

What are “voiding symptoms” related to? Give some examples of these symptoms

A

Related to urinary flow e.g. due to obstruction

Hesitancy

Poor flow

Post-urination dribbling

Intermittent stream

Spraying/deviation of stream

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12
Q

Patient presents with a lump in the groin! What questions do you ask?

A

Quick or gradual appearance?

Changing size?

Bilateral?

Painful? Signs of skin change e.g. redness etc.

Recent trauma or infection?

Soft or hard lump - NB: testicular cancer lumps are described as being stone-like

Constitutional symptoms?

STIs? Discharge?

Does it go away at any point e.g. when lying down?

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13
Q

What is the “classic triad” of renal tumours?

Why is it not actually that great diagnostically?

A

Classic triad

  • Pain
  • Lump in loin
  • Frank haematuria

Not great because it’s only seen in ~20% patients with renal tumours - most present asymptomatically

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14
Q

What are the three concepts of dialysis?

What toxins are removed, and what is infused?

A
  1. Diffusion
  2. Convection
  3. Adsorption

Potassium, urea and sodium are all removed, and bicarbonate is infused

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15
Q

Simple cysts in kidneys are very common/very uncommon

Do they usually cause functional disturbance?

A

Simple cysts in kidneys are very common, can be multiple and large and usually cause no functional disturbance

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16
Q

How is infantile polycystic kidney disease inherited?

What gene is involved?

How does it present in the kidneys?

A

Inherited in an autosomal recessive manner (ARPKD)

Mutation is in the PKDH2 gene on chromosome 6

Causes bilateral renal enlargement, elongated cysts and dilatation of the medullary collecting ducts

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17
Q

What other congenital condition is Infantile Polycystic Kidney Disease/ARPKD associated with?

A

Also associated with congenital hepatic fibrosis

The Liver is the most common site for cysts to develop in alongside the kidney

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18
Q

What are the two potential gene defects that can result in development of autosomal dominant polycystic kidney disease (ADPKD)? Which of these defects is more common?

How do patients with ADPKD present?

A

PKD gene 1 present on Chromosome 16 (accounts for 90% of ADPKD)

PKD gene 2 present on Chromosome 4 (accounts for the remaining 10%)

Patients present usually in middle adult life with abdominal mass, haematuria, hypertension and chronic renal failure

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19
Q

Where else might cysts present in a patient with ADPKD? What pathologies may develop?

A

Cysts can develop in the liver, pancreas and lung, usually with no functional effect

Cysts can also develop in the brain, known as Berry aneurysms of the Circle of Willis, and this can result in the development of subarachnoid haemorrhages

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20
Q

Name some types of benign renal tumour

A

Fibroma - common, medullary origin, seen as white nodules

Adenoma - seen as yellowish nodules and more cortical

Angiomyolipoma - mix of fat, muscle and blood vessels.

Juxtaglomerular cell tumour (JGCT)

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21
Q

If you suspected a patient had a benign renal tumour and were trying to differentiate between a fibroma and an adenoma, how would you tell these two apart?

A

Fibroma - white nodules and medullary origin

Adenoma - yellowish nodules and cortical origin

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22
Q

What other disease are angiomyolipomas associated with?

A

Tubular sclerosis

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23
Q

JGCTs produce what?

How does this present clinically?

A

JGCTs produce renin

This results in the development of secondary hypertension

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24
Q

What are the 3 mechanisms by which renin is released?

A
  1. Baroreceptor mechanism - decreased pressure in the afferent arteriole in the kidneys prompts renin release
  2. Sympathetic nerve mechanism - beta1-adrenergic nerves stimulate renin release (think fight or flight and increased blood pressure etc.)
  3. Macula densa mechanism - sense drops in NaCl in distal convoluted tubule and promote renin release
25
Q

Very generally, describe the Renin-Angiotensin-Aldosterone System

A

Renin produced by juxtaglomerular cells in kidney

Angiotensinogen produced by liver, converted to angiotensin I by renin.

Angiotensin I is converted to Angiotensin II by Angiotensin Converting Enzyme produced by the lungs

Angiotensin II acts on the adrenal glands to cause the release of Aldosterone, which promotes the retention of Na+ and thus increases blood pressure

26
Q

What vertebral level are the kidneys?

A

Right kidney - T12-L2

Left kidney - T11-L1

27
Q

Name some types of malignant renal tumour

A

Nephroblastoma (Wilm’s Tumour)

Urothelial carcinomas - present in the renal pelvis and calyces

Renal cell carcinoma - a.k.a. clear cell ca, hypernephroma, Grawitz tumour. Arises from renal tubular epithelium

28
Q

What malignant renal tumour is the most common intra-abdominal tumour in children?

A

Nephroblastoma (Wilm’s Tumour)

29
Q

What is the most common primary renal tumour in adults?

Who gets it?

How does it present?

A

Renal Cell Carcinoma a.k.a. Grawitz tumour, Clear Cell ca. etc.

Most common in people age 55-60. M:F 2:1

Presents with abdominal pain, haematuria, flank pain, general features of malignant disease

30
Q

What are some paraneoplastic features of renal cell carcinoma?

A

Polycythaemia (increased number of RBCs in the blood due to erythropoetic stimulating substance)

Hypercalcaemia

31
Q

Where might a renal cell tumour extend to?

A

Extension via the renal vein into the IVC and eventually end up in right atrium - confers a worse prognosis

32
Q

What is the most common form of bladder cancer? What is its most common presenting feature?

What are some of the risk factors?

A

Most common form of bladder cancer is Transitional Cell Carcinoma (TCC) - 90% of bladder cancers.

Most common presenting symptom is haematuria

Risk factors

  • Aniline dyes
  • Working in the rubber industry
  • Benzidine
  • Cyclophosphamide
  • Schistosomiasis
  • Smoking
33
Q

Where do most TCCs occur?

How does this present?

A

75% of TCCs occur in the trigone

This can cause ureteric obstruction

34
Q

What is the most common malignant bladder cancer in children?

A

Embryonal Rhabdomyosarcoma

35
Q

What is more likely to present with haematuria - prostate cancer or benign prostate hyperplasia?

A

BPH more commonly presents with haematuria (20%), while prostate cancer is less common (0.7%)

36
Q

Can sport cause haematuria?

A

Yes! Both contact and non-contact sports can cause haematuria

Non-contact a.k.a. Jogger’s haematuria

Disappears on its own after 7-10 days

37
Q

Where is the likely source of the bleed if a patient presents with haematuria…

  • at initial urination
  • at terminal urination
A

Initial - bladder

Terminal - prostate

38
Q

Development of what type of cancer is associated with schistosomiasis and Aristolochia (a plant)?

A

TCC

39
Q

What is the “Israel Triad” of symptoms associated with renal cancer?

A

Pain

Haematuria

Renal mass (lump in loin)

40
Q

Working interiorly to exteriorly, what are the 3 layers of fibres in the detrusor muscle?

A

Inner longitudinal muscle fibres

Circular muscle fibres

Outer longitudinal muscle fibres

41
Q

What are ‘phimosis’ and ‘paraphymosis’?

A

Phymosis - inability to retract the foreskin back past the glans of the penis

Paraphymosis - inability to return the foreskin back after having retracted it over the glans of the penis

42
Q

What are voiding symptoms related to? Are they more common in males or females?

Give some examples

A

Related to flow and stem from a blockage. Obstruction is more common in males

  • Poor flow
  • Intermittent stream
  • Spraying/deviation of stream
  • Hesitancy
  • Post-micturation dribbling
43
Q

What are storage symptoms related to? Are they more common in males or females?

Give some examples

A

Storage symptoms are related to the bladder (e.g. overactivity) and are more common in females

  • Frequency
  • Urgency
  • Nocturia
  • Urge incontinence
  • Sense of incomplete emptying
  • Pain with filling of the bladder
44
Q

What are the two types of haematuria?

A

Microscopic (non-visible)

Macroscopic/Visible (gross/frank etc.)

45
Q

What questions do you need to ask specifically about the bleeding in a patient presenting with frank haematuria?

A

Presence of clots?

Mild, moderate or severe?

Shape of clots?

Is it painful or painless?

At what point in the stream does the blood appear? (nb - terminal bleeding is specific to prostate)

46
Q

How is microscopic haematuria diagnosed?

A

Dipstick shows 3-5 RBCs per HPF (high-power field)

47
Q

How can benign prostatic hyperplasia be treated?

A

Alpha blockers (relax the muscles of the prostate and bladder neck)

Finasteride (blocks the conversion of testosterone to dihydrotestosterone and reduces prostate size)

TURP (transurethral resection of the prostate)

48
Q

What are the various zones of the prostate?

A

Transitional Zone - gives rise to BPH, and only ~20% of prostate cancers arise from here

Central Zone - only 1-5% of prostate cancers arise from here

Peripheral Zone - makes up the majority of prostatic glandular tissue and is the origin for up to 70% of prostatic cancers

49
Q

In general, benign changes in the prostate occur in the ____ zone and malignant changes occur in the ____ zone

A

Bengin - central/transitional zone

Malignant - peripheral zone

50
Q

What age group is prostatic cancer most commonly seen in?

A

Peak is 70-74, with 85% of cases occuring in patients over 65

Rare in under 50s

51
Q

How are the majority of prostate cancers picked up clinically?

How might prostate cancer present clinically?

A

Most are asymptomatic and found by PSA tests and abnormal DRE findings

May present with lower urinary tract symptoms, haematuria/haematospermia, bone pain, anorexia/weight loss etc.

52
Q

Where is PSA produced and what is its function?

How to serum levels of PSA change in prostate cancer?

Is PSA a good marker for prostate cancer?

A

Produced by secretory epithelial cells in the prostate gland and functions to liquefy sperm

In a healthy individual, PSA levels will be high in semen and low in the blood, however PSA in the blood will increase with prostate cancer

PSA isn’t great for diagnosing prostate cancer - it has good sensitivity (90%) but isn’t very specific (40%)

53
Q

In what other conditions might a raised serum PSA be seen in?

What is required when considering PSA measurement in an asymptomatic individual

A

BPH

Prostatitis/UTIs

Urinary retention

Catheterisation

In an asymptomatic individual, PSA counselling is essential due to the low specificity of the test

54
Q

How is diagnosis of prostate cancer confirmed in a patient with raised PSA and abnormal findings on DRE?

A

With a TRUS (Trans-rectal ultrasound-guided) biopsy

10 biopsies are taken, 5 from each lobe of the prostate

55
Q

What type of cancer are the majority of prostate cancers?

A

Multifocal adenocarcinomas (>95%)

56
Q

How are prostate cancers graded?

A

Using Gleason’s Scoring (1-5)

Two most abundant cell types are added together to give a score between 2 and 10

Very good predictor of prognosis

57
Q

What benign renal pathology can be identified by the appearance of a central scar on CT

A

Oncocytoma

58
Q

If a young patient presented with multiple bilateral renal cell carcinomas or other renal cancers e.g. phaeochromocytoma, what autosomal dominant condition might you suspect?

What genetic defect would be seen in this condition?

A

You might suspect Vonn Hippel Lindau

This is caused by a defect in the VHL gene due to a deletion in 3p25

VHL is a tumour suppressor gene, and this defect results in VEGF, PDGF and angiogenesis

59
Q
A

Year 2 - Renal (6 decks)

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