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AKT > Renal > Flashcards

Renal Flashcards

1
Q

What formula is used to calculate eGFR?

A

Modification of Diet in Renal disease

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2
Q

Which variables are used to calculate eGFR?

A

Serum creatinine
Age
Gender
Ethnicity

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3
Q

Factors that may affect result of eGFR

A

Pregnancy
Muscle mass - amputees, body builders
Eating red meat 12 hours prior to sample being taken

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4
Q

CKD Stage 1 eGFR

A

> 90

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5
Q

CKD Stage 2 eGFR

A

60-90

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6
Q

CKD Stage 3a eGFR

A

45-59

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7
Q

CKD Stage 3b eGFR

A

30-44

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8
Q

CKD Stage 4

A

15-29

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9
Q

CKD Stage 5

A

<15

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10
Q

What increase in creatinine is acceptable following introduction of an ACE inhibitor?

A

30%

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11
Q

What decrease in eGFR is acceptable following introduction of an ACE inhibitor?

A

up to 25%

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12
Q

First line medication for HTN in CKD

A

ACE-I

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13
Q

Collecting an ACR sample

A

First pass morning urine

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14
Q

What qualifies as haematuria in the context of CKD?

A

1+ of blood on 2 out of 3 dipsticks

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15
Q

Causes of transient microscopic haematuria

A

UTI
menstruation
vigorous exercise
sexual intercourse

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16
Q

Causes of persistent microscopic haematuria

A

Cancer - bladder, renal, prostate

Stones

BPH

prostatitis

urethritis

IgA nephropathy

Thin basement membrane disease

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17
Q

Causes of red/orange urine which is not blood

A

Beetroot
Rhubarb
Rifamicin
Doxorubicin

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18
Q

Criteria for urgent referral for haematuria

A

Age ≥45 AND unexplained visible haematuria without UTI or that persists/recurs after treating UTI

Age ≥60 AND unexplained microscopic haemuatira + either dysuria or WCC

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19
Q

Criteria for non-urgent referral for haematuria

A

Age ≥60 with recurrent or persistent unexplained UTI

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20
Q

Features of nephrotic syndrome

A

Proteinuria >3g/day
Hypoalbuminaemia
Oedema

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21
Q

Causes of nephrotic syndrome

A

Primary glomerulonephritis

Diabetes

SLE

Amyloidosis

Gold

Penicillamine

Congenital

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22
Q

Which glomerulonephropathies cause nephrotic syndrome?

A

Minimal change
Membranous
Focal segmental
Membranoproliferative

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23
Q

Features of nephritic syndrome

A

Haematuria and red cell casts

Oedema

Mild hypertension

Oliguria <300ml/day

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24
Q

Causes of nephritic syndrome

A 
Post streptococcal GN
IgA nephropathy
Rapidly progressive GN
Membranoproliferative GN
Henoch-Schonlein purpura
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25
Q

What type of drug is spironolactone?

A

Aldosterone antagonist

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26
Q

Indications for spironolactone

A 
Ascites
Hypertension
Heart failure
Nephrotic syndrome
Conn's syndrome
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27
Q

Side effects of spironolactone

A

Hyperkalaemia

Gynaecomastia

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28
Q

When to refer for suspected renal artery stenosis?

A

Refractory HTN on 3 antihypertensives

Recurrent pulmonary oedema with normal LVSF

Rise of >20% in creat or >15% in eGFR over 12 months, or first 2 months after starting ACEI/ARB

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29
Q

Causes of renal artery stenosis

A

Atherosclerosis

Renal fibromuscular dysplasia

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30
Q

What is Bartter’s syndrome?

A

Inherited cause of severe hypokalaemia

Normotensive

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31
Q

What is Gitelman’s syndrome?

A

Inherited hypokalaemia with hypocalcinuria

Normotensive

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32
Q

What eGFR values should prompt nephrology referral?

A
  • <30
  • Decrease of 25% or more within 12 months
  • Change in eGFR category within 12 months
  • Decrease of 15 within 12 months
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33
Q

What ACR should prompt referral to nephrology?

A

> 70

>30 + persistent haematuria

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34
Q

BP target in patients with CKD and a ACR of >70

A

<130/80

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35
Q

BP targets in patient with CKD and ACR <70

A

<140/90

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36
Q

In CKD what urine ACR is classed as A1?

A

ACR <3

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37
Q

In CKD what urine ACR is classed as A2?

A

ACR 3-70

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38
Q

In CKD what urine ACR is classed as A3?

A

> 70

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39
Q

Renal cell carcinoma - features

A

Haematuria
Loin pain
Abdominal mass
Left sided varicocele

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40
Q

Renal cell carcinoma - management

A

Partial/total nephrectomy

Alpha interferon and IL2 reduce tumour size

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41
Q

Renal cell carcinoma - associations

A

Middle aged men
Smoking
von Hippel-Lindau syndrome
Tuberous sclerosis

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42
Q

What is granulomatosis with polyangiitis also known as?

A

Wegner’s granulomatosis

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43
Q

What is granulomatosis with polyangiitis?

A

Autoimmune condition

causing necrotising granulomatous vasculitis

affecting upper respiratory tract, lower respiratory tract and kidneys

44
Q

Granulomatosis with polyangiitis - features

A 
Epistaxis
Dyspnoea
Haemoptysis
Rapidly progressive glomerulonephropathy
Saddle shaped nose
Vasculitis
45
Q

What is Henoch-Schonlein Purpura?

A

IgA mediated small vessel vasculitis

46
Q

Who is normally affected by Henoch-Schonlein Purpura?

A

Children after infection

47
Q

Henoch-Schonlein Purpura - features

A

Palpable purpuric rash over buttocks and extensor surfaces of arms and legs

Abdo pain

Polyarthritis

Features of IgA nephropathy = haematuria, renal failure

48
Q

Henoch-Schonlein Purpura - investigations

A

Clinical diagnosis

Raised ESR and raised serum IgA

Check renal function

Urine dipstick for haematuria and proteinuria

Renal biopsy if persistent nephrotic syndrome

49
Q

Henoch-Schonlein Purpura - management

A

Analgesia for arthralgia

Supportive treatment for nephropathy

50
Q

Henoch-Schlonlein Purpura - prognosis

A

Generally excellent

1/3rd will relapse

51
Q

What is Goodpasture’s syndrome?

A

Autoimmune disease caused by anti-glomerular basement membrane antibodies to type IV collagen

52
Q

Goodpasture’s syndrome - features

A

Nephritic syndrome

Pulmonary haemorrhage

Rapidly progressive glomerulonephritis

53
Q

CKD causes

A 
Diabetic nephropathy
Chronic glomerulonephritis
Chronic pyleonephritis
HTN
Adult polycystic kidney disease
54
Q

CKD diagnostic criteria

A

Reduction in renal function to eGFR <60 or proteinuria with ACR >3, for ≥3 months

55
Q

CKD - management of proteinuria

A

ACEI/ARB if ACR>70

56
Q

CKD - which proteinuria should prompt nephrology referal?

A

ACR >70

ACR >30 + haematuria

ACR 3-29 + haematuria + other risk factors

57
Q

CKD - who should get a statin?

A

Everyone with CKD 3, 4 or 5

58
Q

CKD - findings on bone profile

A

Low vit D
Low calcium
High phosphate

59
Q

CKD - protecting against bone mineral disease

A

Non-calcium phosphate binders = sevelamer

60
Q

CKD - first line HTN treatment

A

ACEI

61
Q

CKD - Hb target

A

10-12

62
Q

CKD - main cause of anaemia

A

Reduced epo causing normocytic normochromic anaemia

63
Q

CKD - management

A

Iron replacement

Erythropoiesis stimulating agents = Erythropoeitin, darbepoeitin

64
Q

Causes of cranial diabetes insipidus

A

Idiopathic

Head injury

Pituitary surgery

Craniopharyngiomas

65
Q

Causes of nephrogenic diabetes insipidus

A

Genetic

Hypercalcaemia

Hypokalaemia

Lithium

Demeclocycline

Sickle cell

Pyelonephritis

66
Q

What is cranial diabetes insipidus?

What is nephrogenic diabetes insipidus?

A

Cranial DI = decreased production ADH from pituitary

Nephrogenic DI = insensitivity to ADH

67
Q

Investigations for diabetes insipidius

A

High plasma osmolality
Low urine osmolality
Water deprivation test

68
Q

What urine osmolality excludes diabetes insipidus?

A

> 700

69
Q

Management of cranial diabetes insipidus

A

Desmopressin

70
Q

Management of nephrogenic diabetes insipidus

A

Thiazides

Low salt and low protein diet

71
Q

Features of diabetes insipidus

A

Polyuria

Polydipsia

72
Q

What is Alport’s syndrome?

A

Defect in type IV collagen causing abnormal glomerular basement membrane

73
Q

Alport’s syndrome - inheritance

A

X linked dominant in 85%

74
Q

Alport’s syndrome - features

A

Microscopic haematuria

Progressive renal failure

Bilateral sensorineural deafness

Lenticonus

Retinitis pigmentosa

75
Q

What is lenticonus?

A

Protrusion of lens surface into the anterior chamber

76
Q

Alport’s syndrome - diagnosis

A

Genetic testing

Renal biopsy = splitting of lamina propria causing ‘basket weave’ appearance

77
Q

Alport’s syndrome - management

A

Control HTN
ACE-I
Dialysis
Transplant

78
Q

Why does renal transplant fail in Alport’s syndrome?

A

Anti-GBM antibodies leading to a goodpasture’s syndrome like picture

79
Q

Autosomal dominant polycystic kidney disease - renal features

A

HTN

recurrent UTI

abdo pain

renal stones

haematuria

CKD

80
Q

Autosomal dominant polycystic kidney disease - extra renal manifestations

A 
Liver cysts
Berry aneuryms
MV prolapse
Aortic root dilation, aortic dissection
Cysts in other organs
81
Q

Autosomal dominant polycystic kidney disease - screening test for family members

A

Abdominal ultrasound

82
Q

Autosomal dominant polycystic kidney disease - diagnostic criteria

A

In patients with positive family history:

  • 2 cysts, unilateral or bilateral, if <30y
  • 2 cysts in both kidneys if 30-59y
  • 4 cysts in both kidneys if >60y
83
Q

Autosomal dominant polycystic kidney disease - management

A

Tolvaptan (vasopressin receptor 2 antagonist) IF

  • CKD 2 or 3
  • rapidly progressing disease
  • drug company agree discount cost
84
Q

Renal papillary necrosis - features

A

Visible haematuria

Loin pain

Proteinuria

85
Q

What is Berger’s disease also called?

A

IgA nephropathy

86
Q

What is IgA nephropathy also called?

A

Berger’s disease

87
Q

IgA nephropathy - presentation

A

Young male with recurrent macroscopic haematuria

Recent respiratory tract infection

88
Q

IgA nephropathy - investigations

A

Urine dipstick - protein, blood

Increased plasma IgA

24h urine - proteinuria

Renal biopsy

89
Q

IgA nephropathy - management if isolated haematuria with no/minimal haematuria and normal egfr

A

No treatment

monitor renal function

90
Q

IgA nephropathy - management if persistent proteinuria with normal or slightly reduced egfr

A

ACE-I

91
Q

IgA nephropathy - management if active disease with falling eGFR or not responding to ACE-I

A

Corticosteroids

92
Q

IgA nephropathy - associations

A

Alcoholic cirrhosis

Coeliac disease

Dermatitis herpetiformis

Henoch-Schlonlein purpura

93
Q

IgA nephropathy - prognosis

A

25% develop ESR

94
Q

IgA nephropathy - markers of good prognosis

A

Frank haematuria

95
Q

IgA nephropathy - markers of poor prognosis

A

Male

Proteinuria

HTN

Hyperlipidaemia

AE genotype DD

96
Q

Post-streptococcal glomerulonephritis - when does it occur?

A

In young children

7-14 days after strep infection

97
Q

Post-streptococcal glomerulonephritis - what is the most common cause?

A

strep pyogenes

98
Q

Post-streptococcal glomerulonephritis - features

A

nephritic syndrome

visible haematuria

proteinuria - may cause oedema

oligouria

99
Q

Post-streptococcal glomerulonephritis - investigations

A

low C3

increased ASO titre

Urine red cell casts

Renal biopsy

100
Q

Post-streptococcal glomerulonephritis - management

A

supportive
may need dialysis

95% recover renal function

101
Q

Minimal change disease - features

A

Nephrotic syndrome - oedema

Normotension

102
Q

Minimal change disease - investigations

A

Proteinuria

Renal biopsy - normal on LM, fusion of podocytes on EM

103
Q

Minimal change disease - management

A

80% cases steroid responsive

Cyclophosphamide if not

104
Q

Minimal change disease - causes

A

Idiopathic

NSAIDS

rifampicin

Hodgkin’s lymphoma

Thyoma

Infectious mononucleosis

105
Q

Minimal change disease - prognosis

A

1/3 have one episode
1/3 have infrequent episodes
1/3 have frequent relapses which stop before adulthood

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