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KSAP July 2020 > Questions > Flashcards

Questions Flashcards

1
Q

How is flow fraction calculated? In what dialysis modality is it most useful?

A

Qd/Qb. A low flow fraction ratio is deemed useful in low dialysate volume therapies such as home HD.

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2
Q

How is filtration fraction calculated where UF is significant?

A

(Qd + UF)/Qb; remembering that where UF is significant, clearance occurs with it.

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3
Q

What is the problem with linkage analysis for PKD genetics in the case of potential living donation? What is a better option?

A

It requires three affected family members across two generations. Direct mutation analysis is preferred.

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4
Q

What is the sensitivity of US without cysts under the age of 30 in ADPKD due to (1) PKD1, and (2)PKD2?

A

The sensitivity of an ultrasound without cysts under the age of 30 is 94% in PKD1 and 70% in PKD2

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5
Q

What are the main causes of pseudohyponatraemia?

A
  • Hyperglycaemia,
  • hyperproteinaemia (as is found in MM),
  • hypertriglyceridaemia,
  • elevated lipoprotein X (as in obstructive jaundice)
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6
Q

How might you improve the efficacy of piperacillin-tazobactam in a patient on CRRT?

A

By administering piperacillin-tazobactam as a prolonged infusion (over 3hours). Beta lactam antibiotics demonstrate time dependent bacterial killing. You should aim to exceed the minimal inhibitory concentration (MIC) for at least 50% of the dosing interval.

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7
Q

How do you calculate clearance of a drug by CVVH?

A

C = effluent rate x sieving coefficient

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8
Q

How is the equation for drug clearance on CVVH modified for pre-filter fluid replacement?

A

C = effluent rate x sieving coefficient x Qb/(Qb + prefilter replacement)

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9
Q

Can you name a class of antibiotic that would be better delivered by bolus on CVVH?

A

Aminoglycosides- you are looking to achieve a higher peak concentration as these drugs demonstrate concentration dependent rather than time dependent killing.

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10
Q

What are the indications for dialysis in Li toxicity?

A
  • Level ≥ 4 +
  • AKI +/or
  • altered mentation +/or seizure +/or
  • dysarhytmias (regardless of level)
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11
Q

What is the volume of distribution of Li?

A

0.5L/kg (therefore, quite high), not protein bound.

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12
Q

How would you dialyse a person with Li toxicity?

A

Qb 350ml/min, 6 hour treatment (if levels not readily available), if levels are, continue until measured Li level is <1.

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13
Q

How would you sub-classify the causes of MPGN based on immunoglobulin and complement deposition?

A
  1. Ig and Complement deposition: LN (polyclonal), PCD (monoclonal), Hep C MPGN (polyclonal)
  2. Ig negative, complement positive: C3G
  3. Ig and C negative: TMA
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14
Q

What is Liddle syndrome?

A

Rare autosomal dominant cause of hypertension. Phenotype caused by an activating mutation in the ENaC of the distal nephron. Typified by hyporeninaemic, hypoaldosteronism. The treatment is with ENaC blockade (not MRA).

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15
Q

Why are MRAs ineffective in Liddle syndrome?

A

The resultant volume expansion in Liddle syndrome leads to hypoaldosteronism.

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16
Q

How do you calculate the urinary anion gap? What is its significance?

A

([Na+] + [K+]) - [Cl-]. The UAG, if negative in states of metabolic acidosis, normally means that the cause for NAGMA is non-renal. The gap is thought to be representative of renal ammonia secretion, but may be superseded by direct ammonia measurements.

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17
Q

What is the phenotype of T1 DRTA?

A
  • NAGMA with high UAG

- urine pH >5.5 because of inability to excrete acid load.

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18
Q

What is the normal osmolal gap?

A

<10

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19
Q

How do you calculate osmolal gap?

A

OG = 2x[Na+] + Glucose (mg/dl)/18 + BUN (mg/dl) / 2.8 + Ethanol (mg/dl) / 4.6

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20
Q

What are the toxic metabolites of ethylene glycol?

A

Glycolic acid and oxalic acid

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21
Q

What role do pyridoxine and thiamine play in EG toxicity?

A

Promote the conversion of glycolic acid to less toxic metabolites

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22
Q

In what time frame should you aim to discontinue steroids in AAV?

A

Within 6 months. Study of 150 patients showed no impact on time to relapse, relapse, ESKD, or death if continued beyond that timeframe.

23
Q

Amyloidosis is associated with increased bleeding risk in kidney biopsy. True/False

A

False. A large retrospective analysis found that this observation was likely due to a reporting bias.

24
Q

PEXIVAS showed a benefit for TPE in AAV. True/False

A

False.

25
Q

How does heparin and LMWH lead to hyperkalaemia?

A

Direct toxicity to the ZG cells of the adrenal gland.

26
Q

What other therapies, apart from steroids, can be used to reduce the conversion of 25-OH vitamin D to 1,25-OH vitamin D?

A

Ketoconazole and hydroxychloroquine

27
Q

What other therapies can be used in the treatment of sarcoidosis in the patient intolerant of steroids?

A

Azathioprine, infliximab, and MMF

28
Q

What metabolic abnormality is associated with Sjogren syndrome?

A

Type 1 Distal RTA

29
Q

What is the principle difference between anti-GBM disease occurring in native kidneys and that which occurs in a patient with Alport syndrome?

A

Native disease Ab are against a3 chain of T4 collagen; transplant Alport’s Abs are against the a5 chain.

30
Q

What is the risk of ESKD in the female X-linked carrier of Alport’s?

A

30% at 60 yrs, 40% at 80yrs; therefore, donation is discouraged in females under the age of 40 who are heterozygous carriers of the disease.

31
Q

What is patiromer?

A

It is a potassium binding polymer that uses calcium sorbitol as an exchange resin; it generally lowers the serum K by 0.5-1 over a 3day to two week period.

32
Q

What is the prevalence of ICA among patients with ADPKD vs the general population?

A

Prevalence of 9-12% versus 2-3% of the gen pop.

33
Q

What are the KDIGO guidelines for screening for ICA in ADPKD?

A

Family history of ICA/SAH
Patients who wish to be screened
High risk occupation

34
Q

What are the intervals for screening for ICA in ADPKD?

A

Family history, no aneurysm: 5-10 years
Aneurysm <7mm, high risk occupation, planning conception or transplant: 5 years
>10 mm aneurysm: urgent NS referral for coiling, high risk of rupture.

35
Q

How do you calculate FWD in hypernatraemia?

A

FWD = 0.6(weight)([serumNa/140] - 1)

36
Q

How does Li cause hypercalcaemia?

A

Binds and inhibits the CaSR in the Parathyroid gland; enhanced release of PTH and consequent hypercalcaemia. (may cause or aggravate PHPTH). Also inhibits the CaSR in the loop of Henle, which leads to reduced paracellular absorption of Ca2+.

37
Q

What is the normal effect of hypercalcaemia on the CaSR in the loH?

A

inhibitor of the ROMK; reduced K+ for the Na/K/Cl co-transporter in the luminal membrane; decrease in paracellular Ca2+.

38
Q

What is the metabolic abnormality in salicyclate toxicity?

A

Metabolic acidosis and respiratory alkalosis

39
Q

Positive staining for C4d in the peritubular capillaries indicates ABMR. True/False

A

True

40
Q

The measurement of RNA polymerase III is useful in the diagnosis of which connective tissue disease?

A

Scleroderma; it is also predictive of development of SRC and worsening, progressive cutaneous disease

41
Q

What percentage of patients with scleroderma develop scleroderma renal crisis?

A

10%

42
Q

What is the more sensitive test for diffuse SS: Topoisomerase (Scl-70) Ab or anti-centromere Ab?

A

Scl-70; anti centromere is positive in 50% of cases of limited SS.

43
Q

What condition is required for the formation of struvite stones?

A

These stones can only form in the presence of urease-producing bacteria such as Proteus, Corynebacterium, Haemophilus, and others (but never Escherichia coli).

44
Q

What is the appearance of struvite crystals on urine microscopy?

A

Coffin lid appearance.

45
Q

When might you consider chemolysis with hemacidrin in struvite stone disease?

A

If small fragments remain that cannot be surgically removed, chemolysis with hemacidrin, an acid substance used to dissolve calculi, can be infused via a nephrostomy tube or a catheter in the ureter. Chemolysis is not without side effects and is only considered after significant surgical debulking of the stone has been performed and if the patient is medically stable.

46
Q

What can be given to limit cysteinuria in patients with cysteine stones?

A

Tiopronin

47
Q

What side effects are associated with sirolimus?

A

Proteinuria, edema, and pneumonitis

48
Q

What is the infectious disease society of America’s definition of a CAUTI?

A

A catheter-associated urinary tract infection (CAUTI) is defined by the presence of ≥103 CFU/mL of pathogenic bacteria and symptoms that are compatible with a UTI

49
Q

What urine chemistries are useful in the diagnosis of proximal tubulopathy?

A 
FE Uric Acid (<10% suggests normal tubular function)
FE Phosphate (<5% suggests normal tubular function)
50
Q

What is the effect of switching a CNI to a mTORi on eGFR and graft survival?

A
  • A systematic review of 29 studies found that patients who were converted from a CNI to an to a mammalian target of rapamycin inhibitor within 1 year after transplant had a higher GFR at 1 year compared with those who continued taking a CNI. However, there was no difference in graft survival, an observation also made in the CONVERT trial.
51
Q

What medications are associated with CUA?

A
  • corticosteroids,
  • warfarin,
  • calcitriol,
  • calcium-containing supplements and phosphate binders, and
  • IV iron
52
Q

What is the evidence for IV bicarbonate in AKI?

A

Correction of severe acidosis (<7.2) in a subgroup of patients with moderate or severe AKI was found to be beneficial in the BICAR-ICU trial.

53
Q

What are the suggestive features of BKVAN?

A
  • The combination of BK viremia of >10,000 copies/mL and allograft dysfunction (3-6months) is highly suspicious for this diagnosis.
54
Q

What staining is used to help diagnose BKVAN on kidney biopsy?

A
  • Anti SV40

KSAP July 2020 (1 decks)

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