Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

FRACP Shuyu > RPA nephrology > Flashcards

RPA nephrology Flashcards

1
Q

Kidney donor risk index; and what is the best predictor of future graft function

A

Donor age - best predictor of future graft function Hypertension Diabetes Last creatinine Cause of death BMI DCD status

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

risk of ESKD in live kidney donor

A

increased risk compared with healthy non donors but still 100 in 100,000 (small absolute risk)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what GN is likely to recur after transplant

A

FSGS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

absolute contraindication to transplant

A

active malignancy

uncontrolled infection (E.g. bronchiectasis)

chronic infections

unacceptable anaesthetic risk

smoking, alcohol, psychological

relative risks: severe sun damage, severe calcular disease, non adherence

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what alleles are assessed in renal transplant

A

A, B, DR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what is the universa plasma donor

A

AB

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what is a more sensitive test than Complement dependent cytotoxicity crossmatch

A

Lminex > Flow cross match > CDC crossmatch

CDC crossmatch only involves adding complement, look for lysis. It is crude and subjective

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

acute cellular kidney rejection histology

A

cellular - tubulitis, intersitital infiltrate

vascular - endothelialitis, glomerulitis, haemorrhage

antibody-mediated - PMNs, C4D+, PTC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

chronic kidney rejection histology

A

glomerulopathy, chronic interstitial inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

type of kidney rejection

A

vascular kidney rejection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

treatment of acute kidney rejection

A
  1. IV methylpred (90% effective)
  2. lymphocyte depleting antibody (ATG)
    1. steroid resistant OR vascular rejection
  3. Adjust immunosuppressants
  4. PLEX, IVIG (for Ab-mediated rejection)
  5. Rescue (high dose tac/myco)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

how does the activated T cell signal for more T cell proliferation (in the context of kidney transplant rejection)

A

release of IL-2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

where does belatacept work

A

fusion protein composed of the Fc fragment of a human IgG1 immunoglobulin linked to the extracellular domain of CTLA-4

blocks the co-stimulation of CD40 to CD40L (between the antigen presenting cell and T cell)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

basiliximab MOA

A

a chimeric (mouse/human) monoclonal antibody which acts as an immunosuppressant by blocking the interleukin-2 receptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what immunosuppresion is better for malignancy or Interstitial fibrosis and tubular atrophy (chronic scarred kidney)

A

mTOR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

main adverse effects of mTOR

A

proteinuria

wound healing problems

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

main adverse effect of mycophenolate

A

bone marrow suppression

GIT symptoms (myfortic may be a slightly better alternative for GI symptoms)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

which transplant immunosuppressant is assoc with a tremor

A

mTOR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

which transplant immunosuppressant is the worst for lipids

A

mTOR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what transplant immuno are ok/not ok for pregnancy

A

pred/tac ok

myco and mTOR contraindicated in pregnancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

primary cells involved in acute kidney rejection

A

CD4T cells - main target of medications as well

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what does glomuerlar scerosis and tubular atrophy suggest

A

dead and chronic changes in glom

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

anatomical abnormality for nephrotic syndrome

A

podocyte

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Nephrotic Ddx

A

minimal change

FSGS

Membranous

Lupus class V

diabetic nephropathy

Amyloid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

causes of nephritic syndrome

A

anca vasculitis

anti GMB

post strep GN

lupus III/IV

TMA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

causes of nephritic/nephrotic overlap

A

IgA

MPGN

Lupus

Myeloma/MGRS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

GN histological classification

A
  1. Glomerular involvement
    1. Diffuse or focal; segmental or generalised
  2. Cell involvement
  3. Changes in non-cellular components of the glomerulus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

GNs that have a mesangial predominance

A

IgA

Mesangioproliferative GN

ImG nephropathy

Clas II lupus nephritis

diabetic nephropathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

is the podocyte on the urine or blood side

A

urine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

what GNs affect the podocytes/epilepthium

A

minimal change

membranous

FSGS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

what GNs affect the endothelial cells

A

these proccesses are usually immune sytem +++

see slides

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

nephrotic ++++ syndrome in young person with acute onset (sometimes with preceeding allergic rhinitis)

A

minimal change disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

minimal change histology

A

light microscopy look normal

EM - flattened podocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

minimal change disease treatment

A

steroid

(second line cyclophosphamide, cyclo/tac, ritux

if not steroid responsive - consider other Ddx ?FSGS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

FSGS histology

A

focal & segmental glomerulosclerosis and hyalinosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

secondary causes of FSGS

A

secondary FSGS (obesity, HTN, previous damage to kidney)

37
Q

FSGS management

A

steroids (less responsive than minimal change)

high dose (60mg) for 6 months

2nd line - cyclophosphamide; cyclo/tac

38
Q

suPAR use

A

to predict FSGS recurrence in transplant

39
Q

most common cause of nephrotic syndrome that’s secondary to a GN

A

primary membranous nephropathy

40
Q

Primary membranous nephropathy histology

A

LM: membranous

IF: granular IgG +/- C3

EM: subepithelial deposits; silver stain has intra-membranous Ig deposits, spikes

41
Q

what are the proteinuria cut offs for risk stratification for membranous GN

A

>8g/day high risk

4.5-8 med risk

42
Q

pathophysiology of primary membranous GN

A

podocyte specific antigen that some people develop an antibody for

causal biomarker is auto Ab to PLA2R. Titre antibody corresponds to the disease activity.

immune deposits on epithelial side

43
Q

anti-PLA2R in GN

A

membranous nephropathy

used for:

diagnosis

risk stratification

differentiating between primary vs secondary

do not need kidney biospy; and only in primary

44
Q

aside from the anti PLA2R, what other antibody is ass with membranous nephropathy

A

TSHD7A Ab (might be assos with malignancies)

45
Q

primary membranous nephropathy treatment

A

cyclophshamide + pred

anticoagulation (warfarin if serum albumin <20mg/day)

HOWEVER, NEJM 2019 compared rituximab with cyclosporine in treatment membraneous nephropathy.

Rituximab was superior (although non inferiority trial). Awaiting PBS

46
Q

secondary membranous GN causes

A

drugs, hepatitis, malignancy

47
Q

most common form of GN worldwide

A

IgA nephropathy

48
Q

pathogenesis of IgA nephropathy

A

O-linked glycans on IgAs are abnormal

the body recognises the abnromality and forms an IgG to this abnormal hinge region.

The immune complex deposits on the mesangium in IgA nephropathy. (it deposits on the endothelium in Henloch Purpura)

Not all people with this O-linked glycans develop IgA

49
Q

treatment of IgA nephropathy

A

ACE-I +/- steroids

50
Q

rapidly progressing glomerunonephriti vs crescentic glomerulonephriti

A

RPGN id the clinical syndrome and crescentic GN is the pathology

51
Q

what is the most common type of RPGN and what age group does that syndrome occur in

A

anca vasculitis

older people 60-70

52
Q

ANCA vs GBM histology

A

LM: - eosinophils + neutrophils

IF: pauciimmune (no immune deposits)

GBM:

IF: linear IgG

53
Q

pathology if the crescents

A

disruption of GBM with proliferation of inflammatory cells and fibrin around the glom and decreases filtering capacity of the glomerulus

54
Q

Treatment of rapidly progressing GN

A

Pred

cyclophosphamide

+/- PLEX (use in pulmonary haemorrhage; anti GBM)

55
Q

ANCA assoc vasculitis

A

small vessel vasculitis, crescentic pauci-immune

56
Q

variants of ANCA vasculitis

A

GPA (Wegner’s) - granulomas - PR3
EGPA (Churg-strauss) - asthma + eosinophilia + granulomas (PR3/MPO)

MPA - no granulomas MPO

PR3 = cANCA (worse prognosis)

MPO = pANCA

57
Q

ANCA assos vasculitis treatment

A

pred + cyclo or ritux

(ritux can only be given if there’s a contraindication to cyclo or they failed cyclo)

58
Q

ANCA vasculitis maintainence

A

ritux or aza

59
Q

what lupus nephritis to immunosuppress

A

III + IV (diffuse or focal proliferative disease)

Corticosteroids + cyclo/mycophenolate

refractory: steroids + MMF + CNI

60
Q

EM: subepithelial hump diagnosis

A

post-infectious GN

61
Q

membranoproliferative GN histology

A

(same as mesangiocapillary)

describes a histological pattern due to some cause of immune deposition that causes inflammation and the development of a second membrane.

“double coutor” (reduplicaiton of membrane)

cellular proliferation, interstitial damage

if there is positive staining for complement and immunoglobins, look for causes of complexment/immune deposition

62
Q

secondary causes of membranoproliferative GN

A

hep C

SLE

monoclonal gammopathy

63
Q

CLassificaiton of TMA

A

histological diagnosis

classification

primary: hereditary - normally abnormality in complement regulatory genes

Acquired TMA - antibodies to something

64
Q

pregnancy + fragments on blood film

A

HUS

65
Q

diagnosis of atypical HUS

A

observable TMA + end organ damage

ddx TTP

66
Q

eculizumab MOA

A

blocks C5 to stop the conversion to C5b and membrane attack complex

67
Q

kimmelstiel wilson nodules on histology

A

diabetic nephropathy

68
Q

when is eGFR not accurate

A

AKI

Children

extremes of body weight

patients taking extra creatinine/creatining

caution with drug dosing

69
Q

when is the eGFR most useful

A

monitoring in CKD

70
Q

stages of CKD

A
71
Q

what antihypertensives have additional albuminuria reduction properties

A

ACE I/ARB

Non-dihydropyride CCB

Spironolactone

72
Q

daily sodium restriction

A

1500-2000mg/day

73
Q

MOA of thiazides

A

inhibiting reabsorption of sodium (Na+) and chloride (Cl−) ions from the distal convoluted tubules in the kidneys by blocking the thiazide-sensitive Na+-Cl− symporter.

they are vasodilating - but they are more likely to cause diluting hypontraemia

74
Q
A
75
Q

Iron study cut off for iron def in kidney disease

A

TSAT <20%

Ferritin <100

76
Q

most common reason for refractory anaemia to EPO in CKD

A

iron deficiency

(other: chronic inflammation, high PTH, B12/folate, hypothyroid, marrow disorder, malignancy)

77
Q

protein intake recommendations in CKD

A

0.6-0.8g/kg/day

mild reduction in protein is good for kidneys

78
Q

bicarb aim in CKD

A

>21

oral sodibic replacement

79
Q

Ca+, Phos and PTH management in CKD

A

no evidence that any intervention has mortality benefit in RCTs

phosphate binders are only on PBS for dialysis

80
Q
A
81
Q

tolvaptan indications

A

autosomal dominant PCKD

improves eGFR by 1mL/year compared to placebo

PBS for eGFR 30-89

82
Q

resistant hypertension already max dose 3 drugs including diuretic, next step

A

spironolactone

83
Q

which RTA is assos with hyperkalaemia

A

Type 4 RTA

found in hypoaldosteronism which is common in DM

84
Q

Dialysis dysequilibrium syndrome

A

due to the reduction of plasma solute level over a limited time. Plasma becomes hypotonic compared to brain cells and water shifts from the plasma into the brain tissue

85
Q

what drug is assos w SSc renal crisis

A

corticosteroids

86
Q

alport syndrome genetics

A

COL4A5

mostl likely X-linked

87
Q

ATN urinary sodium

A

sodium wasting

(as opposed to hepatorenal - low sodium <10)

88
Q

expect pCO2

A

0.7 [HCO3] + 20 (range: +/- 5)

(or similar to the last 2 digits of the pH)

89
Q
A

FRACP Shuyu (65 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions