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MRCOG - Part 2 > AKI and NSAIDs > Flashcards

AKI and NSAIDs Flashcards

1
Q

the causes of AKI in pregnancy

A
  • Preeclampsia
  • HELLP syndrome
  • acute retention
  • placental abruption
  • acute fatty live in Pg
  • thrombotic microangiopathy (HUS,TTP)
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2
Q

Methods of gestational assessment of renal function

A

The use of estimated glomerular filtration rate is also not valid in pregnancy, and serum creatinine and change in creatinine are the only parameters that can be used for gestational assessment of renal function.

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3
Q

Serum creatinine in pregnancy

A

Serum creatinine falls by 35 micromol/l in pregnancy
leading to an average creatinine in pregnancy of 53 micromol/l.

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4
Q

Most common cause of AKI in pregnancy??

A

PE 1.4%

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5
Q

creatinine value diagnostic for AKI in pregnancy

A

90 micromol/l

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6
Q

The clinical approach to a pregnant woman with AKI involves:

A
  1. fluid status assessment
  2. medication review
  3. consideration of fluid replacement
  4. appropriate diagnostic work-up
  5. early involvement of a nephrologist for patients who do
    not respond to initial management.
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7
Q

Drugs doses reduction in case of AKI

A

Drug doses may need to be adjusted for a decrease in glomerular filtration rate below 30 ml/minute including antibiotics, anticoagulants, insulin and opiates. The use of NSAIDs, which often form part of a standard postpartum analgesic protocol, is contraindicated in AKI

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8
Q

Which NSAID has best safety profile

A

Ibuprofen

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9
Q

What is the average creatinine in pregnancy

A

53 micromol/L

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10
Q

when does NASIDs is contraindicated

A
  • AKI
  • 3rd trimester
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11
Q

What is the commenest glomerular disease world wide?

A

PE

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11
Q

What is the prevalence of pre eclampsia due to AKI

A

1.5-2%

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11
Q

What findings you will get on renal biopsy in case of pre eclampsia AKI

A

Renal biopsy reveals endothelial cell swelling, termed glomerular endotheliosis

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12
Q

How we manage the dose of MgSO4 based on creatinine levels

A

MgSO4 is renally excreted.
if the urine output falls to below 20 ml/hour
or if the creatinine is higher than 90 micromol/l

a 50% dose reduction in magnesium sulphate infusion should be considered from 1 g/hour to 0.5 g/hour.

in severe PE or eclampsia, the usual loading bolus dose of 4 g is given.

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13
Q

in severe PE or eclampsia, the usual loading bolus dose given is

A

4 g

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14
Q

in severe PE or eclampsia, the usual loading bolus dose given is

A

4 g

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15
Q

In the context of AKI, how often is the monitoring of the serum magnesium level should be undertaken

A

every 4 to 6 hours, or whenever there is clinical concern regarding toxicity.

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16
Q

Serum magnesium concentrations advised in AKI

A

Serum magnesium concentrations may not correlate with toxicity but a level of **2–3.5 mmol/l **is advised.

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17
Q

Women with pre eclampsia should be “kept dry” means

A

IV hydration:
* isn’t benificial in case of PE w/ oliguria
* in women with PE is associated with pulmonary oedema and increased maternal mortality.

fluid restriction of 80 ml/hour is recommended peripartum.

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18
Q

When the natural diuresis occur in postpartum period

A

36–48 hours postpartum

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19
Q

Immediate postpartum period what level of urinary output we consider normal .

A

a urine output >40 ml in 4 hours is sufficient in the immediate postpartum period.

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20
Q

Define HELLP syndrome

A

a constellation of haemolysis, elevated liver enzymes and low platelets, and is a variant of severe pre- eclampsia.

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21
Q

The incidence of renal impairment in HELLP

A

3-15%

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22
Q

risk factors of AKI in HELLP

A

abruption, disseminated intravascular coagulation, sepsis, haemorrhage or intrauterine death

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23
Q

What will be the findings on renal biopsy in cases of HELLP

A

glomerular endotheliosis of pre-eclampsia with additional thrombotic microangiopathy.

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24
Q

If HELLP is the diagnosis then when its symptoms start to detriorate postpartum

A

48 hours postpartum

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25
Q

If the symptoms doesn’t recover after 48 hours postpartum what do we consider

A

Consider TTP/HUS

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26
Q

Pregnancy-associated thrombotic microangiopathy

A

1 in 25K

27
Q

In which conditions do we encounter thrombotic microangiopathy

A

HUS/TTP

28
Q

In TTP and HUS, what complications does it cause

A
28
Q

In TTP and HUS, what complications does it cause

A
29
Q

What is the abnormality in TTP

A

In TTP there is abnormality in ADAMTS13/(a disintegrim and metalloproteinase with thrmbospondin type 1 motif member 13)

30
Q

What is abnormality in HUS

A

Complement pathway overactivation that causes endothelial injury and damage

31
Q

What is the mechanism in which ADAMTS13 is required ..how its abnormality lead to AKI

A

**VwB is hemostatic protein that induce the formation of platelet plug **
Usually it undergoes rapid breakdown by ADAMST13 protein
Where the ADAMST13 protein is deficient deposition of platelet rich thrombinoccur in the microcirculation leading to TTP
LEvels of ADAMST13 decrease in normal pregnancy during the 2nd and 3rd trimester and pregnancy associated TTP manifests during these trimester or in the postpartum period
AKI develop in 30 to.80% of cases of pregnancy associated TTP.

32
Q

Levels of ADAMTS13 in normal pregnancy

A

Levels of ADAMTS13 decrease in normal pregnancy during the second and third trimester, and pregnancy-associated TTP manifests during these trimesters or in the postpartum period.

33
Q

Incidence of AKI to happen in prenant woman with TTP

A

30-80% (which is higher than TTP without pregancy)

34
Q

percentage of women with pregnancy-associated HUS have a detectable complement gene mutation

A

86%

35
Q

Percentage of patients with microangiopathy and complement abnormalities progress to end-stage renal failure.

A

76%

36
Q

How are TTP and HUSa managed

A

with fresh frozen plasma infusion and/or plasma exchange.
Also, eculizumab is licensed for the treatment of atypical HUS.

37
Q

Which drug is licensed for the treatment of atypical HUS

A

Eculizumab

38
Q

Which drug is licensed for the treatment of atypical HUS

A

Eculizumab

39
Q

Action of Eculizumab in treating atypical HUS

A

inhibits activation of the complement pathway via an antiC5 blocking antibody.

40
Q

What is Acute fatty liver of pregnancy

A

disorder linked to fetal homozygosity for disorders of beta-fatty acid oxidation leading to an excessive fatty acid load in the mother

41
Q

Incidence of AFLOP

A

is a rare obstetric emergency with 5 per 100000 maternities in the UK.

42
Q

What Histological examination of the kidney in acute fatty liver of pregnancy reveals

A

Tubular free fatty acid deposition, which links with the pathogenesis in the liver.

43
Q

The main differential diagnosis of acute fatty liver of pregnancy is

A

HELLP (because of low platelets and deranged liver function)

44
Q

C/P that is suggestive of AFLP more than HELLP

A
  • low serum glucose,
  • raised serum ammonia
  • prodromal vomiting
45
Q

Management of AFLP

A

early diagnosis, supportive care and prompt delivery.
In most women there is recovery of liver function and resolution of AKI after delivery

46
Q

Define SLE

A

Idiopathic autoimmune condition with multi organ involvement

47
Q

What % of cases of SLE have renal involvement?

A

20-49%

48
Q

If lupus nephritis present first time during pregnancy what are its symptoms

A

AKI, proteinuria and hypertension

49
Q

What drugs we use to treat lupus nephritis?

A
  • # 1st Predinsolone
  • hydroxychloroquine
  • tacrolimus
50
Q

Is Mycophenolate mofetil safe in pregnancy

A

NO, it’s teratogenic
should be substituted with azathioprine prepregnancy.

51
Q

Define Obstructive nephropathy

A

Renal dysfunction from urinary tract obstruction

52
Q

What are Obstructive nephropathy complications

A
  • AKI
  • urosepsis as a result of abscess formation
  • pyonephrosis
53
Q

Which position of uterus causes acute urinary retention in first trimester??

A

Retroflexion

54
Q

Which position of uterus causes acute urinary retention in first trimester??

A

Retroflexion

55
Q

What is the first diagnostic step of AKI In catheterized women

A

excluding a blockage of the catheter

56
Q

What are the features of pathological obstruction

A

renal colic or infective symptoms

57
Q

Pathological obstruction is suggested on ultrasound if?

A
  • if ureter is dilated distal to brim
  • If the obstruction doesn’t decompress by positioning the women on all fours
  • if urteric jets are absent even in the contralateral position
58
Q

What are the indications for intervention in pregnancy

A
  • AKI
  • Infection
59
Q

What are the interventions we can do to obstructive nephropathy during pregnancy

A

percutaneous nephrostomy or delivery if near term

60
Q

most common cause of acute interstitial nephritis and kidney injury.

A

Drugs

61
Q

Which drugs are responsible for AKI during pregnancy and postpartum

A

penicillins, cephalosporins, proton-pump inhibitors and H2 receptor antagonists.

62
Q

Till what gestation we can prescribe NSAID and in what type of cases

A

Before 30 weeks
pleuritic pain, fibroid degeneration or musculoskeletal pain.

63
Q

Which NSAID has highest risk of nephrotoxicity??

A

Naproxen

64
Q

What are the side effects of indomethacin and fenoprofen?

A
  • Indomethacin causes nephritis and hyperkalemia
  • Fenoprofen causes nephrosis
65
Q

The mechanism of action of NSAIDs

A

inhibition of prostaglandin biosynthesis. This is mediated by preventing the prostaglandin precursor arachidonic acid from binding to the cyclooxygenase (COX) enzyme.

66
Q

Which iv analgesic is preffered in AKI

A

Fentanyl

MRCOG - Part 2 (45 decks)

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