Renal & Genitourinary ( 10% ) Flashcards

1
Q
  1. Membranous glomerulonephritis
  • a. Is always due to an underlying renal condition.
  • b. Is idiopathic in 10% of cases.
  • c. Leads to chronic renal failure in 60% of patients.
  • d. Has a typically aggressive disease progression
  • e. Is the most common cause of nephrotic syndrome in adults.
A

e. Is the most common cause of nephrotic syndrome in adults.

Other answers seem wrong, as per R&C FSCS is most common (35%), MG second (30%), ‘other’ third (17%)

  • a. Is sometimes due to an underlying renal condition, but can be a systemic condition - 75% idiopathic, remainder is SLE or drugs
  • b. Is idiopathic in 75% of cases.
  • c. Leads to chronic renal failure in 40% of patients; takes decades
  • d. Has a typically slow disease progression - decades to develop renal failure
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2
Q
  1. Acute nephritic syndrome has all of the following features EXCEPT:
  • a. Proteinuria
  • b. Haematuria
  • c. Hypertension
  • d. Hyaline casts
  • e. Oliguria
A

d. Hyaline casts

  • These are clear and are formed in low-flow urine, concentrated urine, or an acidic environment, eg dehydration or after exercise, and may be seen in normal people.*
  • Nephritic may have RBC cases, WBC casts, or epithelial (tubular) casts*
  • Also have haematuria and proteinuria.*
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3
Q
  1. Regarding nephrotic syndrome, which of the following is TRUE?
  • a. Albumin is lost and other globulins unaffected
  • b. Hypertension
  • c. Alteration in serum lipid levels
  • d. Sodium and water excretion
  • e. Haematuria
A

c. Alteration in serum lipid levels

Hyperlipidaemia and lipiduria seen in nephrotic syndome, secondary to protein loss and generalised oedema

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4
Q
  1. Regarding acute glomerulonephritis
  • a. White blood cells dominate the urinary sediment.
  • b. Post streptococcal GN usually appears 6-8 weeks after a strep infection.
  • c. Patients have a normal or low BP.
  • d. Henoch Schonlein Purpura is most frequent in children and young adults
  • e. Acute GN is not associated with systemic lupus erythematosus.
A

d. Henoch Schonlein Purpura is most frequent in children and young adults

  • a. Red blood cells dominate the urinary sediment, though WBC can also be present
  • b. Post streptococcal GN usually appears 1-4 weeks after a strep infection
  • c. Patients have an elevated BP
  • e. Acute GN can be associated with systemic lupus erythematosus.
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5
Q
  1. With respect to streptococcal infection
    * a. May result in glomerulonephritis 3 weeks post infection
A

a. May result in glomerulonephritis 3 weeks post infection

(Group A beta haemolytic strep)

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6
Q
  1. Acute glomerulonephritis
  • a. Occurs 1-4 weeks after impetigo
  • b. Due to toxic effects of streptolysin on basement membrane
  • c. Due to group B alpha haemolytic strep
  • d. Leads to renal failure usually
A

a. Occurs 1-4 weeks after impetigo

(Gp A Strep)

  • b. Due to toxic effects of exotoxin B in glomerulus, causing an immune-reaction (type II HSR)
  • c. Due to group A beta haemolytic strep
  • d. Leads to renal failure in 5% of children and 40% of adults
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7
Q

The following are features of the nephrotic syndrome EXCEPT

  • Hypoalbuminaemia
  • Hypolipidaemia
  • Hypernatraemia
  • Thrombotic complications
A

Hypolipidaemia

  • Get hyperlipidaemia and lipiduria in nephrotic syndrome*
  • Thrombotic complications are idiopathic and thought to be multifactorial*
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8
Q

The most like cause of the nephrotic syndrome is

  • Focal segmental glomerulosclerosis in children. Adults
  • Systemic disease in adults
  • Primary disease in children
  • Minimal change disease in adults
A

Primary disease in children

95% of nephrotic syndrome (5% due to systemic disease)

  • Focal segmental glomerulosclerosis in Adults (most common, 35%)
  • Systemic disease in adults - 40% of cases (60% primary)
  • Minimal change disease in children (most common - 75%)
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9
Q

Alport syndrome is associated with all EXCEPT

  • A conductive hearing loss.
  • Blindness due to opacification in the eyes
  • Haematuria
  • Renal failure
A

A conductive hearing loss.

Sensorineural

‘Alport syndrome is a genetic disorder affecting around 1 in 5,000-10,000 children, characterized by glomerulonephritis, end-stage kidney disease, and hearing loss. Alport syndrome can also affect the eyes, though the changes do not usually affect sight, except when changes to the lens occur in later life. Blood in urine is universal. Proteinuria is a feature as kidney disease progresses.’

Due to inherited defect in type IV collagen

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10
Q

Post streptococcal glomerulonephritis

  • Is initially caused by an infection with group B α-haemolytic streptococci.
  • An example of a type II hypersensitivity reaction.
  • Will cause rapidly progressing disease in 10%
  • Occurs 1-4 weeks after the initial infection
A

Occurs 1-4 weeks after the initial infection

  • Is initially caused by an infection with Beta haemolytic group A streptococci.
  • An example of a type III hypersensitivity reaction (immune-complex deposition)
  • Will cause rapidly progressing disease in 5% of children and 40% of adults (these numbers are for progression to CKD, unsure about RPD)
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11
Q
  1. Concerning acute tubular necrosis.
  • a. Cephalosporins are not a causative agent
  • b. Nephrotoxic causes are associated with a poor prognosis.
  • c. Casts are found in the loop of Henle.
  • d. Rhabdomyolysis is not a cause
  • e. Ischaemic tubular necrosis is uncommon after haemorrhagic shock
A

C or E listed as answer, both seem wrong

?a) - R&C lists only gentamicin, radiocontrst, heavy metals, poisons as drug causes (no definitive list of medications)

  • a. Cephalosporins ?can be a causative agent
    • Drugs: sulphonamides, NSAID, synthetic penicillins, diuretics
  • b. Nephrotoxic causes are associated with a relatively good prognosis - 95% survival (cf 50% as part of MODS)
  • c. Casts are found in the DCT and CD
  • d. Rhabdomyolysis is a cause (myoglobin causes ATN)
  • e. Ischaemic tubular necrosis is common after haemorrhagic shock
    • Hypovolemic shock listed as a cause of ATN in R&C
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12
Q
  1. Regarding acute tubular necrosis
  • a. It is associated with hyperkalaemia not hypokalaemia in recovery.
  • b. Non-oliguric has a better recovery
  • c. It is associated with ischaemic cortical cells
  • d. 80% are associated with anuria
A

b. Non-oliguric has a better recovery

  • a. It is associated with hypokalaemia in recovery due to return of GFR but an inability of the tubules to reabsorb -> loss of Na, K, and polyuria
  • c. It is associated with ischaemic cortical cells
    • Depends on type (nephrotoxic vs ischaemic) but generally PCT and LoH
  • d. 80% are associated with anuria
    • Dont know exact number but anecdotally speaking, much less.
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13
Q
  1. Ischaemic tubular necrosis is associated with
  • a. Maintenance stage with polyuria.
  • b. Predominantly proximal necrosis.
  • c. Intact basement membranes
  • d. Tubular cast obstruction
  • e. Distal necrosis only.
A

d. Tubular cast obstruction

I think both types are

  • a. Maintenance stage with Oliguria
  • b. Predominantly desc and thick asc limb necrosis.
    • Toxic type causes proximal ischaemia
  • c. Rupture of basement membranes.
  • e. LoH necrosis (see answer to B)
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14
Q
  1. Regarding the hepatorenal syndrome
  • a. It is irreversible
  • b. One loses the ability to concentrate urine
  • c. Urine has a high sodium concentration
  • d. The urine is hyperosmolar
  • e. The favoured theory of its generation involves increased renal blood flow
A

d. The urine is hyperosmolar

  • Hepatorenal syndrome (HRS) is a type of progressive kidney failure seen in people with severe liver damage, most often caused by cirrhosis. As the kidneys stop functioning, toxins begin to build up in the body. Eventually, this leads to liver failure.*
  • Low urine volume (<500ml/day)*
  • Low urinary sodium concentration + plasma sodium <130*
  • Urine osmolarity > plasmam*
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15
Q
  1. Acute loss of 30% of renal capacity in a young person
  • a. Worsens with ACE inhibitors.
  • b. Can still produce a normal urine output and maintain normal electrolytes
A

b. Can still produce a normal urine output and maintain normal electrolytes

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16
Q
  1. In chronic renal failure, morphology includes:
  • a. Glomerular hyperplasia with dilation of tubules
  • b. Slowing of filtrate through loop of Henle
  • c. Decreased pressure in glomerulus
  • d. Hyaline connective tissue changes in glomeruli, tubular atrophy
A

d. Hyaline connective tissue changes in glomeruli, tubular atrophy

This is what is found in nephrosclerosis

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17
Q
  1. Renal failure morphology:
    * a. Nephron dilation and hypertrophy
A

a. Nephron dilation and hypertrophy

Apparently

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18
Q
  1. ischaemic acute renal tubular necrosis is characterized by
  • a. occlusion of tubular lumens by casts
  • b. acute tubular injury is most obvious in the proximal convoluted tubule.
  • c. absence of eosinophilic hyaline casts.
  • d. large continuous areas of epithelial necrosis.
  • e. sparing of the parts of the tubule in the renal medulla.
A

a. occlusion of tubular lumens by casts

  • b. In Toxic ATI acute tubular injury is most obvious in the proximal convoluted tubule (ischaemic LoH)
  • c. Presence of eosinophilic hyaline casts
  • d. Discontinuous (skip lesion) areas of epithelial necrosis
  • e. Involvement of outer proximal medulla
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19
Q
  1. Nephrotoxic ATN is caused by all EXCEPT:
  • a. Erythromycin
  • b. Contrast
  • c. Carbon tetrachloride
  • d. Gentamicin
  • e. Lead
A

a. Erythromycin

Penicillins can though

20
Q

Acute tubular necrosis

  • Is more benign if associated with polyuria
  • Initially has elevated urine output with reduced urea.
  • Leads to renal failure in 95% of cases caused by a nephrotoxic agent.
  • Accounts for 25% of cases of acute renal failure in hospital. 50%
A

Is more benign if associated with polyuria

  • Initially has Oliguria, followed by polyuria
  • Leads to renal failure in 5% of cases caused by a nephrotoxic agent.
  • Accounts for 50% of cases of acute renal failure in hospital.
21
Q

Acute tubular necrosis

  • Has a mortality rate of 20% with associated multiorgan failure due to shock.
  • Critical events are tubular injury and ischaemia regardless of the underlying cause
  • Red cell casts are usually found in the renal glomerulus.
  • Accounts for 80% of cases of acute renal failure in hospital.
A

Critical events are tubular injury and ischaemia regardless of the underlying cause

  • Has a mortality rate of 50% with associated multiorgan failure due to shock.
  • Red cell casts are not found in the renal glomerulus - it is a tubular pathology
  • Accounts for 50% of cases of acute renal failure in hospital.
22
Q
  1. Regarding pyelonephritis
  • a. Uncontrolled hypertension is a major predisposing factor
  • b. The microscopic changes in chronic pyelonephritis are pathognomonic
  • c. Staphylococci and streptococcus faecalis are common pathogens.
  • d. In the first year of life, it is more common in females
  • e. It is generally a benign and self limited condition
A

e. It is generally a benign and self limited condition

As per R&C, generally benign if appropriate abx given

All other options seem wrong - staph and strep are rare causes

23
Q
  1. In pyelonephritis
  • a. 85% of infections are caused by Gram negative bacteria
  • b. ureteral obstruction makes haematogenous infection less likely.
  • c. ureteral obstruction allows bacteria to ascend the ureter into the pelvis
  • d. infection is less likely during pregnancy
  • e. papillary necrosis and perinephric abscess are common sequelae.
A

a. 85% of infections are caused by Gram negative bacteria

  • b. ureteral obstruction makes haematogenous infection more likely.
    • Haematogenous spread more likely to occur in sepsis, endocarditis, ureteral obstruction, immunosuppressed and non-enteric organisms
  • c. ureteral obstruction allows bacteria to ascend the ureter into the kidney, out of the pelvis
  • d. infection is more likely during pregnancy
  • e. papillary necrosis and perinephric abscess are uncommon but possible sequelae
24
Q

Urinary tract infection

  • Is never caused by gram positive bacteria.
  • Is usually caused by Enterobacter.
  • Is caused by normal intestinal bacterial in 60%.
  • Can be caused by fungal and viral infections
A

Can be caused by fungal and viral infections

  • Is rarely caused by gram positive bacteria like Staph saprophyticus and strep
  • Is usually caused by E coli
  • Is caused by normal intestinal bacterial in 85%
25
Q

Urinary tract infection

  • Is usually from haematogenous spread.
  • Is not associated with catherization
  • Will be pyelonephritis if there is tubular necrosis
  • Has a rate of 20-40% in pregnancy
A

Will be pyelonephritis if there is tubular necrosis

  • Is uncommonly from haematogenous spread.
  • Is associated with catherization
  • ??Has a rate of 20-40% in pregnancy
26
Q
  1. Hypertensive renal disease
  • a. 15% is secondary to renal artery stenosis.
  • b. 60% of renovascular hypertension is due to fibromuscular hyperplasia.
  • c. malignant hypertension only arises if previous hypertension.
  • d. onion skinning correlates with degree of renal failure
  • e. glomerulonephritis occurs 1-3 weeks post group B strep infection
A

d. onion skinning correlates with degree of renal failure.

Onion-skinning = fibro-elastic hyperplastic arteriosclerosis

  • a. 5% is secondary to renal artery stenosis.
  • b. 30% of renovascular hypertension is due to fibromuscular hyperplasia, 70% due to atherosclerosis
    • c. malignant hypertension does not require previous hypertension. Hypertensive emergency doesn’t have to occur in pre-existing hypertension – different pathologies
  • e. glomerulonephritis occurs 1-3 weeks post group A strep infection.
27
Q
  1. Urolithiasis
  • a. Presence of hypercalcaemia implies renal insufficiency.
  • b. A patient with leukaemia is likely to make cystine calculi.
  • c. Calcium is the major component of 35% of calculi
  • d. Struvite stones are made up of magnesium-ammonium-phosphate
  • e. Hypercalcaemia is found in most patients who make renal calculi.
A

d. Struvite stones are made up of magnesium-ammonium-phosphate

  • a. Presence of hypercalcaemia does not implies renal insufficiency
  • b. A patient with leukaemia is likely to make uric acid calculi, due to high rate of nucleic acid turnover
  • c. Calcium is the major component of 70% of calculi
  • e. Hypercalcaemia is found in a minority of patients who make renal calculi - 55% have hypercalcuria without hypercalcaemia (calcium stones)
28
Q
  1. Alkaline urine causes precipitation of
  • a. Magnesium-ammonium-phosphate stones
  • b. calcium stones
  • c, urate stones
  • d. rolling stones
  • e. cystine stones
A

a. Magnesium-ammonium-phosphate stones

aka struvite

UTI (proteus, Klebs) → alkaline urine -> precipitates magnesium-ammonium-phosphate, can lead to staghorn calculi

29
Q
  1. Renal calculi occur in the presence of
  • a. An alkaline pH of urine.
  • b. Large residual volume of urine
  • c. Urinary obstruction
  • d. Usual concentrations of urinary constituents
  • e. Deficiency of inhibitors of crystal formation in urine
A

e. Deficiency of inhibitors of crystal formation in urine

  • a. An alkaline pH of urine.
    • Can be but also in acidic, so therefore not a general rule
    • Alkaline urine -> struvite, acidic urine -> uric acid
  • b. Large residual volume of urine
  • c. Urinary obstruction
  • d. Increased concentrations of urinary constituents
30
Q
  1. renal calculi
  • a. 50% with high calcium get calcium oxalate stones
  • b. they are bilateral in 80%.
  • c. 30% have protease splitting bacteria.
A

Nick lists a) as correct, however it seems that 5% of people with hypercalcaemia and hypercalcuria get calcium stones, 55% with hypercalciuria alone do, and that 50% of calcium stones are associated with idiopathic calciuria (question is unclear where the high calcium is)

  • a. 50% with high calcium get calcium oxalate stones
  • b. they are bilateral in 20%
  • c. 10% have protease splitting bacteria (this is what causes struvite stones, which make 10% of all total stones)
31
Q
  1. Renal stones
  • a. Are unilateral in 60% of patients.
  • b. Formation is enhanced by a deficiency of inhibitors of crystal formation in urine
  • c. Are least commonly composed of magnesium ammonium phosphate.
  • d. Can be formed by urea splitting organisms such as Proteus and Klebsiella
  • e. Formed of calcium are radiolucent.
A

d. Can be formed by urea splitting organisms such as Proteus and Klebsiella

This causes struvite stones

  • a. Are unilateral in 80% of patients.
  • b. Formation is enhanced by a deficiency of inhibitors of crystal formation in urine
  • c. Are least commonly composed of cystine (1%), then magnesium ammonium phosphate (10%), uric acid (10%), calcium (70%)
  • e. Formed of calcium are Radio-opaque
32
Q

Regarding renal calculi

  • Most stones will contain magnesium ammonium and phosphate
  • All stones contain an organic component
  • Formation is not hereditary.
  • Uric acid stones form in alkaline urine.
A

All stones contain an organic component

Organic mucoprotein making up 5-10% of stone by weight is present in all stones

  • 10% of stones will contain magnesium ammonium and phosphate.
  • Formation has a Genetic component
  • Uric acid stones form in acidic urine, struvite stones in an alkaline one (due to urea splitting bacteria)
33
Q

Regarding renal calculi

  • Calcium oxalate stones are commonly associated with hypercalciuria
  • Triple stones form in the acid urine produced by the action of bacteria.
  • Most patients with uric acid stones will have hyperuricaemia.
  • Uric acid stones are usually radiopaque.
A

Calcium oxalate stones are commonly associated with hypercalciuria

(50% of calcium stones; 10% in hypercalciuira + hypercalcaemia)

  • Triple stones (aka struvite) form in the alkaline urine produced by the action of bacteria
  • A minority of patients with uric acid stones will have hyperuricaemia.
  • Uric acid stones are usually radioLucent
34
Q
  1. Which of the following is seen in Nephrotic syndrome (2000, 2004)
  • (a) Albumin is lost in the urine, while other globulins are unaffected
  • (b) Early hypertension
  • (c) A reduction in serum lipid levels
  • (d) Sodium and water retention
  • (e) gross haematuria
A

(d) Sodium and water retention, which exacerbates the oedema

Several mechanisms, such as increased aldosterone secretion

  • (a) Albumin is lost in the urine, but other globulins are also lost
  • (b) Early hypertension - marker of disease
  • (c) A rise in serum lipid levels
  • (e) gross haematuria - this is seen in cystitis or nephritis syndome.
35
Q
  1. In the diagnosis of renal hypertension (x2)
  • (a) acute glomerulonephritis whilst causing nephrotic syndrome, does not generally cause hypertension
  • (b) 60% of cases of renovascular hypertension are due to fibromuscular dysplasia
  • (c) Malignant hypertension only occurs in patients with previous hypertension
  • (d) Onion skinning is proportional to the degree of renal failure
  • (e) none of the above is true
A

(d) Onion skinning (also known as hyperplastic arteriolitis) is proportional to the degree of renal failure

  • (a) acute glomerulonephritis, renal artery stenosis, vasculitis and renin producing tumours are all a cause of renal hypertension
  • (b) renovascular hypertension is due to aortic insufficiency, polyarteritis nodosa, or coarctation of the aorta. Hyperplastic arteriosclerosis is due to actions of PDGF, and other mitogenic factors which cause hyperplasia of smooth muscle cells.
  • (c) Malignant hypertension generally occurs in patients with previous hypertension, but may occasionally develop in previously normotensive individuals.
36
Q
  1. Malignant hypertension
  • (a) 75% recover with no loss of renal function
  • (b) is associated with abnormal renin levels
  • (c) is always seen in those patients with pre-existing hypertension (d) is not associated with morbidity
  • (e) affects 1-5% of patients with hypertension
A

(b) is associated with markedly elevated plasma renin levels

(e) affects 1-5% of all patients with elevated blood pressure

  • (a) 50% recover with pre-crisis renal function
  • (c) is is occasionally seen in previously healthy individuals but is mostly seen in those patients with pre-existing hypertension
  • (d) is associated with morbidity, and previously had a very high mortality rate
37
Q
  1. In chronic renal failure the morphology includes
  • (a) hyperplasia of nephrons
  • (b) hypertrophy of nephrons
  • (c) reduction in the connective tissue surrounding arterioles
  • (d) metaplasia within nephrons
  • (e) none of the above
A

(b) hypertrophy of remaining nephrons

  • (a) hyperplasia of nephrons does not occur (hypertrophy does)
  • (c) increase in the connective tissue surrounding arterioles (arteriosclerosis)
  • (d) metaplasia within nephrons (wrong - hypertrophy)
38
Q
  1. Acute tubular necrosis is not caused by
  • (a) erythromycin
  • (b) lead
  • (c) carbon tetrachloride
  • (d) IV contrast
  • (e) gentamycin
A

(a) erythromycin

Heavy metals, organic solvents, IV contract, aminoglycosides do cause it.

39
Q
  1. Concerning acute tubular necrosis
  • (a) cephalosporins are not a causative agent
  • (b) nephrotoxic causes are associated with poor outcomes
  • (c) casts are found in the loop of Henle
  • (d) rhabdomyolysis is not a cause
  • (e) ischaemic tubular necrosis is uncommon after haemorrhagic shock
A

(a) cephalosporins are not a causative agent

  • (b) nephrotoxic causes are associated with better outcomes than ischaemic (95% receovery if no other organs involved)
  • (c) casts are found in the DCT
  • (d) rhabdomyolysis is a cause
  • (e) ischaemic tubular necrosis is common after haemorrhagic shock
40
Q
  1. Regarding acute tubular necrosis
  • (a) it is associated with hyperkalaemia in recovery
  • (b) non-oliguric type has a better recovery
  • (c) it is associated with ischaemic cortical cells
  • (d) 80% of cases are associated with anuria
  • (e) intrarenal vasodilation is a major cause of ATN
A

(b) non-oliguric type has a better recovery

  • (a) it is associated with hyperkalaemia in maintenence, and hypokalaemia in recovery, due to an inability to concentrate urine leading to polyuria
  • (c) it is associated with ischaemic thick limb of the medullary cells
  • (d) ?? of cases are associated with initial oliguria then polyuria.
    • ​<80% have anuria, probably much less.
  • (e) intrarenal vasoconstriction is a major cause of ATN
41
Q
  1. Ischaemic tubular necrosis is characterised by which feature
  • (a) tubular cast obstruction
  • (b) distal necrosis only
  • (c) an intact basement membrane
  • (d) predominantly proximal necrosis
  • (e) a maintenance stage consisting of polyuria
A

(a) tubular cast obstruction

Have reworded the question as ‘which feature’, from ‘all of the following except’ as only a) seemed to be correct.

ITN is associated with:

  • (a) tubular cast occlusion
  • (b) mostly proximal tubule and thick ascending medulla necrosis
  • (c) an intact basement membrane in parts, but patchy rupture is also seen
  • (d) toxic shows predominantly proximal necrosis, whereas ischaemic is some PT and ALoH
  • (e) an
    • initial phase with increased BUN and decreased urine,
    • a maintenance phase, with a reduction in urine out put to as little as 40mL/day, then
    • a recovery stage consisting of polyuria, up to 3L/day. Recovery is possible due to the maintenance of most of the basement membrane.
42
Q
  1. In pyelonephritis
  • (a) 85% of infections are caused by gram-negative bacteria
  • (b) ureteric obstruction makes haematogenous infection less likely
  • (c) ureteric obstruction allows bacteria to ascend the ureter into the renal pelvis
  • (d) infection is less likely during pregnancy
  • (e) papillary necrosis and perinephric abscesses are common sequelae
A

(a) 85% of infections are caused by gram-negative bacteria

  • (b) ureteric obstruction makes haematogenous infection more likely
  • (c) ureteric obstruction is a predisposing risk factor, but as for inducing stasis and therefore infection, it is not stated
  • (d) infection is more likely during pregnancy
  • (e) papillary necrosis and perinephric abscesses are possible but uncommon sequelae
43
Q
  1. Urolithiasis
  • (a) and the presence of hypercalcaemia implies renal insufficiency
  • (b) in a patient with leukaemia is likely to be made up of cystine
  • (c) is calcium based in 35% of calculi
  • (d) made up of magnesium ammonium phosphate are struvite stones,
  • (e) by calcium oxalate stones is primarily due to hypercalciuria
A

(d) made up of magnesium ammonium phosphate are struvite stones

(e) by calcium oxalate stones is primarily due to hypercalciuria

  • (55% of calcium stones have idiopathic hypercalciuria, 10% have both hypercalcaemia and hypercalciuria)*
  • They dont acknowledge e) as being right but it would appear so*
  • ??(a) and the presence of hypercalcaemia implies renal insufficiency
  • (b) in a patient with leukaemia is likely to be made up of urate
    • ​cystine usually due to genetic defects
  • (c) is calcium based in 70% of calculi
44
Q
  1. Regarding renal stones
  • (a) most calcium stones form in patients with hypercalcaemia
  • (b) urate stones form in the plasma from uric acid crystals
  • (c) 80% are unilateral
  • (d) struvite stones are generally small and pass easily
  • (e) most staghorn calculi form idiopathically
A

(c) 80% are unilateral

  • (a) only 10% of calcium stones form in patients with hypercalcaemia
  • (b) urate stones form in the urine from uric acid crystals
  • (d) struvite stones are generally large and may develop into staghorn calculi
  • (e) most staghorn calculi form secondary to infections with urea-splitting bacteria
45
Q
  1. Which stones form preferentially at a high pH
  • (a) cysteine
  • (b) urea
  • (c) calcium oxalate
  • (d) calcium phosphate
  • (e) magnesium ammonium phosphate
A

(e) magnesium ammonium phosphate, as the urea-splitting bacteria (proteus and some staphylococci) convert urea to ammonia.

  • (a) cysteine stones form at a low pH, and are due to genetic defects in amino acid resorption
  • (b) urate (predisposing factors: high cell turnover, gout)
  • (c) calcium oxalate and phosphate (predisposing factors: ​hypercalciuria and hypercalcaemia)
46
Q
  1. In hepatorenal syndrome
  • (a) it is irreversible
  • (b) one loses the ability to concentrate urine
  • (c) urine has a high sodium concentration
  • (d) the urine is hyperosmolar
  • (e) the favoured theory for the pathogenesis is increased renal blood flow
A

(d) the urine is hyperosmolar, devoid of proteins and sediment and low in sodium

  • (a) It is reversible, but the outlook is poor (not specifically mentioned in text)
  • (b) the ability to concentrate urine is retained
  • (c) the urine is surprisingly low in sodium
  • (e) the favoured theory is the decrease in renal blood flow, secondary to systemic vasodilation
47
Q
  1. Regarding acute renal failure
  • (a) glomerulonephritis is usually immune mediated
  • (b) glomerular filtration rate is usually 20-50% of normal
  • (c) it is often irreversible
  • (d) caused by acute tubular necrosis is irreversible
  • (e) none of the above is true
A

(a) glomerulonephritis is usually immune mediated

  • (b) glomerular filtration rate is usually 20-25% of normal
  • (c) it is frequently reversible
  • (d) caused by acute tubular necrosis is reversible, as the basement membrane is usually intact