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1 - MSRA > Nephrology > Flashcards

Nephrology Flashcards

1
Q

Drugs causing acute interstitial nephritis

A

Penicillin
Rifampicin
NSAIDs
Allopurinol
Furosemide

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2
Q

Systemic disease causing acute interstitial nephritis

A

SLE
Sarcoidosis
Sjorgen’s syndrome

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3
Q

Infections causing acute interstitial nephritis

A

Hanta virus
Staphylococci

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4
Q

Features acute interstitial nephritis

A

Fever
Rash
Arthralgia
Hypertension

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5
Q

Blood tests acute interstitial nephritis

A

Eosinophilia
Mild renal impairmentU

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6
Q

Urine acute interstitial nephritis

A

Sterile pyuria
White cell casts

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7
Q

Demographic tubulointerstitial nephritis with uveitis

A

Young females

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8
Q

Symptoms tubulointerstitial nephritis with uveitis

A

Fever
Weight loss
Painful, red eyes

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9
Q

Urinalysis tubulointerstital nephritis with uveitis

A

Positive with leukocytes and protein

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10
Q

Best way to differentiate AKI and CKD

A

Ultrasound - CKD have bilaterally small kidneys

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11
Q

Causes of CKD without bilaterally small kidneys

A
  • Autosomal dominant polycytic kidney disease
  • Diabetic nephropathy
  • Amyloidosis
  • HIV assocaited nephropathy
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12
Q

Blood tests suggesting CKD rather than AKI

A

Hypocalcaemia

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13
Q

AKI criteria

A

Rise in serum creatinine of 26 micromol/L or greater in 48 hours
50% or greater rise in creatinine known or presumed to have happened within past 7 days
Fall in urine output to less than 0.5ml/kg/hour for more than 6 hours

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14
Q

Investigation AKI

A

If no cause or risk of urinary tract obstruction, renal ultrasound within 24 hours of assessment

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15
Q

Drugs that should be stopped in AKI as may worsen renal function

A

NSAIDs
Aminoglycosides
ACE inhibitors
ARBs
Diuretics

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16
Q

Drugs that should be stopped in AKI due to toxicity

A

Metformin
Lithium
Digoxin

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17
Q

Indications for RRT in AKI

A
  • Not responding to medical treatment
  • Complications
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18
Q

Complications of AKI

A

Hyperkalaemia
Pulmonary oedema
Acidosis
Uraemia (pericarditis, encephalitis)

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19
Q

How to differentiate between pre-renal uraemia and acute tubular necrosis?

A
  • In pre-renal uraemia, urine sodium <20mmol/L and urine osmolality >500. In ATN, urine sodium >40 and urine osmolality <350
  • In pre-renal uraemia, good response to fluid challenge. In ATN, poor response
  • In pre-renal uraemia, serum urea:creatinine ratio raised. In ATN, normalN
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20
Q

Stage 1 AKI

A

Increase in creatinine 1.5-1.9x baseline, or
Increase in creatinine ≥26.5, or
Reduction in urine output to <0.5ml/kg/hour for ≥6 hours

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21
Q

Stage 2 AKI

A

Increase in creatinine to 2.0 - 2.9x baseline, or
Reduction in urine output <0.5ml/kg/hour for ≥12 hours

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22
Q

Stage 3 AKI

A

Increase in creatinine ≥3.0 times baseline, or
Increase in creatinine to ≥353.6, or
Reduction in UO to <0.3ml/kg/hour for ≥24 hours. or
Initiation of RRT, or
In patients <18, decrease in eGFR to <35

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23
Q

Criteria for referral to nephrologist AKI

A

Renal transplant
ITU patient with unknown cause of AKI
Vasculitis, glomerulonephritis, tubulointerstitial nephritis, myeloma
AKI with no known cause
Inadequate response to treatment
Complications of AKI
Stage 3 AKI
CKD stage 4 or 5
Qualify for RRT

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24
Q

ADPKD type 1 vs 2

A

ADPKD 1 more common, presents with renal failure earlier

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25
Q

Screening modality ADPKD

A

Ultrasound

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26
Q

Ultrasound diagnostic criteria ADPKD

A
  • 2 cysts, unilateral or bilateral if aged <30
  • 2 cysts in both kidneys if aged 30-59
  • 4 cysts in both kidneys if >60
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27
Q

Management ADPKD

A

Tolvaptan (in select patients)

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28
Q

Purpose of tolvaptan in ADPKD

A

Slow progression of cyst development and renal insufficiency

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29
Q

Criteria for tolvaptan use ADPKD

A

CKD stage 2 or 3
Evidence of rapidly progressive disease
Company provides it with discount agreed in patient access scheme

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30
Q

Features ADPKD

A

Hypertension
Recurrent UTIs
Flank pain
Haematuria
Palpable kidneys
Renal impairment
Renal stones

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31
Q

Extra-renal manifestations ADPKD

A

Liver cysts
Berry aneurysms
Cardiovascular system
Cysts in other organs

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32
Q

ADPKD cardiovascular system

A

Mitral valve prolapse
Mitral/tricuspid incompetence
Aortic root dilatation
Aortic dissection

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33
Q

What other organs get cysts in ADPKD

A

Liver (70%)
Pancreas
Spleen

Rarely:
Thyroid
Oesophagus
Ovary

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34
Q

Inheritance pattern Alport syndrome

A

X-linked dominant

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35
Q

When does Alports syndrome present

A

Childhood

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36
Q

Features Alports syndrome

A

Microscopic haematuria
Progressive renal failure
Bilateral sensorineural deafness
Lenticonus
Retinitis pigmentosa

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37
Q

What is lenticonus

A

Protrusion of the lens surface into the anterior chamber

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38
Q

Investigations Alport syndrome

A

Molecular genetic testing
Renal biopsy

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39
Q

Renal biopsy findings Alport syndrome

A

Longitudinal splitting of lamina densa of GBM, resulting in basket weave appearance

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40
Q

Boys vs girls Alport syndrome

A

Disease more severe in males, females rarely develop renal failure

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41
Q

Cause of failing renal transplant in Alport’s syndrome

A

Presence of anti-GBM antibodies, leading to Goodpastures syndrome like picture

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42
Q

How to calculate anion gap

A

(Sodium + potassium) - (bicarb + chloride)

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43
Q

Normal anion gap

A

8-14

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44
Q

Causes of normal anion gap or hyperchloraemic metabolic acidosis

A

GI bicarb loss - diarrhoea, uterosigmoidostomy, fistula
Renal tubular acidosis
Drugs, e.g. acetazolamide
Ammonium chloride injection
Addison’s disease

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45
Q

Causes of raised anion gap metabolic acidosis

A

Lactate - shock, hypoxia
Ketones - diabetic ketoacidosis, alcohol
Urate - renal failure
Acid poisoning - salicylates, methanol
5-oxoprolone - chronic paracetamol use

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46
Q

Causes of anaemia in renal failure

A
  • Reduced erythropoietin levels
  • Reduced absorption of iron
  • Reduced erythropoiesis due to toxic effects of uraemia on bone marrow
  • Anorexia/nausea due to uraemia
  • Reduced red cell survival
  • Blood loss due to capillary fragility and poor platelet function
  • Stress ulceration leading to chronic blood loss
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47
Q

Targe haemoglobin in CKD

A

10-12

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48
Q

Treatment anaemia in CKD

A

Iron administration (prior to starting…)
Erythropoiesis-stimulating agents

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49
Q

Route of administration of iron

A

Iron if not on ESAs or dialysis. If target Hb not reached in 3 months, switch to IV
If on ESAs or dialysis, IV iron

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50
Q

Examples erythropoiesis stimulating agents

A

Erythropoietin
Darbepoetin

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51
Q

GFR anaemia is seen at in CKD

A

Usually <35 (consider alternative diagnosis if >60

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52
Q

Type of anaemia seen in CKD

A

Normochromic normocytic

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53
Q

Complication anaemia in CKD

A

Left ventricular hypertrophy

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54
Q

Common causes CKD

A

Diabetic nephropathy
Chronic glomerulonephritis
Chronic pyelonephritis
Hypertension
Adult PKD

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55
Q

CKD dietary advice

A

Low protein
Low phosphate
Low sodium
Low potassium

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56
Q

What factors make up GFR

A

Serum creatinine
Age
Gender
Ethnicity

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57
Q

Factors that might affect GFR result

A

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

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58
Q

Stage 1 CKD GFR

A

Greater than 90, with some signs of kidney damage on other testS

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59
Q

Stage 2 CKD

A

60-90, with some sign of kidney damage

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60
Q

Stage 3a CKD

A

45-59

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61
Q

Stage 3b CKD

A

30-44

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62
Q

Stage 4 CKD

A

15-29

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63
Q

Stage 5 CKD

A

Less than 15

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64
Q

First line anti-hypertensive CKD

A

ACE inhibitors

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65
Q

What level of derangement in U&E is acceptable when starting ACEi in CKD

A

Decrease in GFR 25%
Rise in creatinine up to 30%

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66
Q

What to consider if greater derangement in U&E after starting ACEi in CKD

A

Renovascular disease

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67
Q

Role of furosemide CKD

A

Useful as anti-hypertensive, particularly when GFR below 45
Added benefit of lowering potassium

68
Q

Causes of cranial DI

A

Idiopathic
Post head injury
Pituitary surgery
Craniopharyngiomas
Infiltrate - histiocytosis X, sarcoidosis
Wolframs syndrome
Haemochromatosis

69
Q

What is Wolframs syndrome

A

Association of;
- Cranial DI
- Diabetes mellitus
- Optic atrophy
- Deafness

70
Q

Causes nephrogenic DI

A

Genetic
Hypercalcaemia
Hypokalaemia
Lithium
Demeclocycline
Tubulo-interstitial disease - obstruction, sickle cell, pyelonephritis

71
Q

Investigation DI

A

High plasma osmolality, low urine osmolality
Water deprivation test

72
Q

What urine osmo excludes diabetes insipidus

A

> 700

73
Q

Management nephrogenic diabetes insipidus

A

Thiazides
Low salt/protein diet

74
Q

Management central diabetes insipidus

A

Desmopressin

75
Q

Maintenance fluid requirements

A

25-30ml/kg/day water
1mmol/kg/day potassium, sodium, chloride
50-100g/day glucose

76
Q

Risk of large volumes of 0.9% saline

A

Hyperchloraemic metabolic acidosis

77
Q

Causes of transient or spurious non-visible haematuria

A

UTI
Mensturation
Vigorous exercise
Sexual intercourseC

78
Q

Causes of persistent non-visible haematuria

A

Cancer (bladder, renal, prostate)
Stones
Benign prostatic hyperplasia
Prostatitis
Urethritis, e.g. Chlamydia
Renal causes - IgA nephropathy, thin basement membrane disease

79
Q

Causes of red/orange urine with neg blood dipstick

A

Foods - beetroot, rhubarb
Drugs - rifampicin, doxorubicin

80
Q

What is defined as persistent non-visible haematuria

A

Blood being present in 2 out of 3 samples tested 2-3 weeks apart

81
Q

Further investigations haematuria

A

Bloods - renal function, albumin:creatinine ratio or protein:creatinine ratio, BP

82
Q

Limitation urine microscopy in haematuria

A

Time to analysis significantly affects number of RBC detectedU

83
Q

Criteria 2WW with haematuria

A

Age ≥45 with:
- Unexplained visible haematuria without UTI
- Visible haematuria that persists or recurs after successful treatment of UTI

Age ≥60 and unexplained non-visible haematuria and either dysuria or raised WCC on bloods

84
Q

Criteria non-urgent referral for haematuria

A

Age ≥60 with recurrent or persistent unexplained urinary tract infection

85
Q

Triad seen in HUS

A

AKI
Microangiopathic haemolytic anaemia
Thrombocytopenia

86
Q

Causes HUS

A

Most cases secondary:
Shiga toxin-producing E coli 0157:H7 (90% of cases in children)
Pneumococcal infection
HIV
SLE
Drugs
Cancer

Primary HUS due to complement dysregulation

87
Q

Investigation in HUS

A

Blood film (most useful test)
U&E
Stool culture

88
Q

Blood film finding in HUS

A

Intravascular red blood cell fragmentation → formation of schistocytes
Hb <80
Thrombocytopenia

89
Q

U&E in HUS

A

AKI

90
Q

Stool culture in HUS

A

May show evidence of STEC infection

91
Q

Management HUS

A

Supportive treatment - fluids, blood transfusion, dialysis

92
Q

Indications for plasma exchange in HUS

A

Complicated - in general, reserved for severe cases of HUS not associated with diarrhoea

93
Q

Medicine used in treatment of HUS

A

Eculizumab - greater efficacy than plasma exchange alone in treatment of adult atypical HUS

94
Q

What is HSP

A

IgA mediated small vessel vasculitis

95
Q

Features HUS

A

Palpable purpuric rash with localised oedema over buttocks and extensor surfaces of arms and legs
Abdominal pain
Polyarthritis
Features of IgA nephropathy may occur - haematuria, renal failure

96
Q

Treatment HUS

A

Supportive

97
Q

Prognosis HUS

A

Usually excellent - self-limiting condition, esp in children without renal involvement

98
Q

Monitoring HUS

A

BP and urinalysis to detect renal involvement

99
Q

ECG changes hyperkalaemia

A

Tall tented T waves
Loss of P waves
Broad QRS
Sinusoidal wave pattern

100
Q

Treatment to stabilise myocardium in hyperkalaemia

A

IV calcium gluconate

101
Q

Treatment to short-term shift potassium ECF → ICF in hyperkalaemia

A

Insulin/dex
Salbutamol nebs

102
Q

Treatment to remove potassium from body

A

Calcium resonium (orally or enema)
Loop diuretics
Dialysis

103
Q

Features hypokalaemia

A

Muscle weakness
Hypotonia

104
Q

ECG hypokalaemia

A

U waves
Small or absent T waves
Prolonged PR interval
ST depression

105
Q

Conditions associated with IgA nephropathy

A

Alcoholic cirrhosis
Coeliac disease/dermatitis herpetiformis
HSP

106
Q

IgA nephropathy also known as

A

Berger’s disease

107
Q

Classic presentation IgA nephropathy

A

Macroscopic haematuria in young people following URTI

108
Q

Histology IgA nephropathy

A

Mesangial hypercellularity, positive immunoflourescence for IgA and C3

109
Q

IgA nephropathy vs post-streptococcal glomerulonephritis

A

Post streptococcal glomerulonephritis associated with low complement levels
Main symptom in post-streptococcal glomerulonephritis is proteinuria
Typically interval between URTI and onset of renal problems in post-streptococcal glomerulonephritis

110
Q

When is no treatment needed IgA nephropathy

A

Isolated haematuria, no or minimal haematuria (less than 1000mg/day), and normal GFR

Just f/u to check renal function

111
Q

Treatment IgA nephropathy when persistent proteinuria but normal/slightly reduced GFR

A

ACE inhibitors

112
Q

Treatment IgA nephropathy if active disease (falling GFR) or failure to respond to ACEi

A

Immunosuppression with corticosteroids

113
Q

Prognosis IgA nephropathy

A

25% develop ESRF

114
Q

Markers of good prognosis IgA nephropathy

A

Frank haematuria

115
Q

Markers of poor prognosis IgA nephropathy

A

Male gender
Proteinuria, esp >2g/day
Smoking
Hypertension
Hyperlipidaemia
ACE genotype DD

116
Q

Cause normal anion gap metabolic acidosis

A
  • GI bicarb loss (diarrhoea, ureterosigmoidoscopy, fistula)
  • Renal tubular acidosis
  • Drugs, e.g. acetazolamide
  • Ammonium chloride injection
  • Addison’s disease
117
Q

Causes raised anion gap metabolic acidosis

A
  • Lactate - shock, sepsis, hypoxia
  • Ketones - diabetic ketoacidosis
  • Urate - renal failure
  • Acid poisioning - salicylates, methanol
118
Q

Division of metabolic acidosis secondary to high lactate

A

Type A - sepsis, shock, hypoxia, burns
Type B - metformin

119
Q

Causes minimal change disease

A

Majority of cases idiopathic

In 10-20% cases, cause found:
- Drugs
- Hodgkin’s lymphoma
- Thymoma
- Infectious mononucleosis

120
Q

Drugs causing minimal change disease

A

NSAIDs
Rifampicin

121
Q

Features minimal change disease

A

Nephrotic syndrome
Normotension
Highly selective proteinuria

122
Q

Features of proteinuria in minimal change disease

A

Only intermediate sized proteins such as albumin and transferrin leak through the glomerulus

123
Q

Renal biopsy in minimal change disease

A

Normal glomeruli on light microscopy
Electron microscopy shows fusion of podocytes and effacement of foot processes

124
Q

First line treatment minimal change disease

A

Oral corticosteroids

80% steroid responsive

125
Q

Second line treatment minimal change disease

A

Cyclophosphamide

126
Q

Definition contrast media nephrotoxicity

A

25% increase in creatinine occurring within 3 days of intravascular administration of contrast media

127
Q

Management of metformin around contrast procedures

A

Hold 48 hours before and until renal function normal - reduce risk of lactic acidosis

128
Q

Complications peritoneal dialysis

A

Peritonitis
Sclerosing peritonitis

129
Q

Most common cause of peritonitis in peritoneal dialysis

A

Coagulase neg staph e.g. Staphylococcis epidermidis

130
Q

Antibiotics peritonitis caused by peritoneal dialysis

A

Vanc (or teic) + ceftazidime added to dialysis fluid

or

Vancomycin added to dialysis fluid and ciprofloxacin by mouth

131
Q

Bacteria causing post-streptococcal glomerulonephritis

A

Group A beta haemolytic streptococcus, usually streptococcus pyogenes

132
Q

Timeline post-streptococcal glomerulonephritis

A

Typically 7-14 days after infection

133
Q

Pathophysiology post-streptococcal glomerulonephritis

A

Immune complex (IgG, IgM, C3) deposition in glomeruli

134
Q

Features post-streptococcal glomerulonephritis

A
  • Headache
  • Malaise
  • Proteinuria, may result in oedema
  • Hypertension
  • Oliguria
135
Q

Bloods post-streptococcal glomerulonephritis

A

Raised anti-streptolysin O titre (confirm recent streptococcal infection)
Low C3

136
Q

Renal biopsy in post-streptococcal glomerulonephritis

A

Acute, diffuse proliferative glomerulonephritis
Endothelial proliferation with neutrophils
Subepithelial humps caused by lumpy immune deposits on electron microscopy
Granular or starry sky appearance on immunoflourescence

137
Q

Post-op renal transplant problems

A

ATN graft
Vascular thrombosis
Urine leakage
UTI

138
Q

When does hyperacute rejection of renal transplant occur

A

Minutes to hours

139
Q

Cause hyperacute rejection renal transplant

A

Pre-existing antibodies against ABO or HLA antigens

140
Q

What kind of hypersensitivity reaction hyperacute rejection renal transplant

A

Type II hypersensitivity reaction

141
Q

Pathophysiology hyperacute rejection renal transplant

A

Widespread thrombosis of graft vessels → ischaemia and necrosis of transplanted organ

142
Q

Management hyperacute rejection renal transplant

A

No treatment possible, graft must be removed

143
Q

Timeline acute graft failure renal transplant

A

<6 months

144
Q

Cause acute graft failure renal transplant

A

Usually mismatched HLA causing cell-mediated (cytotoxic T cells) reaction
Other causes include CMV infection

145
Q

Presentation acute graft failure renal transplant

A

Usually asymptomatic, picked up with rising creatinine, pyuria, proteinuria

146
Q

Treatment acute graft failure renal transplant

A

May be reversible with steroids and immunosuppressants

147
Q

Timeline chronic graft failure

A

> 6 months

148
Q

Causes chronic graft failure

A
  • Chronic allograft nephropathy
  • Recurrence of original renal disease
149
Q

What happens in chronic graft nephropathy

A

Both antibody and cell-mediated mechanisms cause fibrosis to the transplanted kidney

150
Q

Initial immunosuppression renal transplant

A

Ciclosporin/tacrolimus with monoclonal antibody

151
Q

Maintenance immunosuppression renal transplant

A

Ciclosporin/tacrolimus with mycophenolate mofetil or sirolimus

152
Q

When should steroids be added renal transplant immunosuppression

A

If more than one steroid responsive acute rejection episdoe

153
Q

Advantages tacrolimus over ciclosporin

A

Lower incidence of acute rejection
Less hypertension and hyperlipidaemiai

154
Q

Disadvantages tacrolimus over ciclosporin

A

High incidence of impaired glucose tolerance and diabetes

155
Q

SEs mycophenolate mofetil

A

GI and marrow suppression

156
Q

SEs sirolimus

A

Hyperlipidaemia

157
Q

Complications long term immunosuppression

A

Cardiovascular disease
Renal failure
Malignancy

158
Q

Malignancy advice for patients on immunosuppressants after renal transplant

A

Education about minimising sun exposure to reduce risk of squamous cell carcinoma and basal cell carcinoma

159
Q

Causes rhabdomyolysis

A

Seizure
Collapse/coma
Ecstasy
Crush injury
McArdle’s syndrome
Drugs

160
Q

Drugs causing rhabdo

A

Statin, esp if co-prescribed with clarithromycin

161
Q

Features rhabdomyolysis

A

AKI with disproportionately raised creatinine
Elevated CK (at least 5x upper limit of normal)
Myogloburia
Hypocalcaemia
Elevated phosphate
Hyperkalaemia
Metabolic acidosis

162
Q

Management rhabdomyolysis

A

IV fluids to maintain good urine output
Urinary alkalinisation sometimes used

163
Q

Indications spironolactone

A

Ascites
Hypertension
Heart failure
Nephrotic syndrome
Conn’s syndrome

164
Q

Adverse effects spironolactone

A

Hyperkalaemia
Gynaecomastia

165
Q
A

1 - MSRA (23 decks)

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