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Year 4 Final > Nephrology > Flashcards

Nephrology Flashcards

1
Q

How much does creatine kinase levels need to be raised to suspect rhabdomylosis?

A

5 times

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2
Q

What does insulin/dextrose infusion do?

A

Shifts potassium from extracellular to intracellular fluid compartments

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3
Q

Bloods in post-streptococcal glomerulonephritis?

A

raised anti-streptolysin O titre are used to confirm the diagnosis of a recent streptococcal infection
low C3

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4
Q

Size of kidneys normally in CKD?

A

Bilaterally small kidneys
Exceptions to this rule include:
autosomal dominant polycystic kidney disease
diabetic nephropathy (early stages)
amyloidosis
HIV-associated nephropathy

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5
Q

Why is increased risk of thromboemobilsm in neprhotic syndrome?

A

Due to loss of antithrombin III and plasminogen in the urine

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6
Q

What is Wilms’ nephroblastoma

A

one of the most common childhood malignancies. It typically presents in children under 5 years of age, with a median age of 3 years old.

Features
abdominal mass (most common presenting feature)
flank pain
painless haematuria
other features: anorexia, fever
unilateral in 95% of cases
metastases are found in 20% of patients (most commonly lung)

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7
Q

Features of acute interstital nephritis?

A

fever, rash, arthralgia
eosinophilia
mild renal impairment
hypertension

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8
Q

What is the treatment of nephrogenic diabetes and why?

A

thiazide diuretic

Why?
In simple terms DI leads to the production of vast amounts of dilute urine which is dehydrating and raises the plasma osmolarity, stimulating thirst. The effect of the thiazide causes more sodium to be released into the urine. This lowers the serum osmolarity which helps to break the polyuria-polydipsia cycle.

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9
Q

What causes haemolytic uraemic syndrome?

A

E coli

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10
Q

Fluid replacement

A

First 10kg 100ml/kg
Second 10kg 50ml/kg
Subsequent kg 20ml/kg

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11
Q

Extra-renal manifestations of Autosomal dominant polycystic kidney disease

A

liver cysts (70% - the commonest extra-renal manifestation): may cause hepatomegaly
berry aneurysms (8%): rupture can cause subarachnoid haemorrhage
cardiovascular system: mitral valve prolapse, mitral/tricuspid incompetence, aortic root dilation, aortic dissection
cysts in other organs: pancreas, spleen; very rarely: thyroid, oesophagus, ovary

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12
Q

Extra-renal manifestations of Autosomal dominant polycystic kidney disease

A

liver cysts (70% - the commonest extra-renal manifestation): may cause hepatomegaly
berry aneurysms (8%): rupture can cause subarachnoid haemorrhage
cardiovascular system: mitral valve prolapse, mitral/tricuspid incompetence, aortic root dilation, aortic dissection
cysts in other organs: pancreas, spleen; very rarely: thyroid, oesophagus, ovary

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13
Q

Normal anion gap metabolic acidosis?

A

gastrointestinal bicarbonate loss: prolonged diarrhoea: may also result in hypokalaemia, ureterosigmoidostomy
fistula, renal tubular acidosis
drugs: e.g. acetazolamide
ammonium chloride injection
Addison’s disease

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14
Q

Management of autosomal dominant polycystic kidney disease?

A

Tolvaptan

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15
Q

Management of minimal change disease?

A

oral corticosteroids: majority of cases (80%) are steroid-responsive
cyclophosphamide is the next step for steroid-resistant cases

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16
Q

Causes of nephrogenic DI

A

genetic:
more common form affects the vasopression (ADH) receptor
less common form results from a mutation in the gene that encodes the aquaporin 2 channel
electrolytes:
hypercalcaemia
hypokalaemia
lithium:
lithium desensitizes the kidney’s ability to respond to ADH in the collecting ducts
demeclocycline
tubulo-interstitial disease: obstruction, sickle-cell, pyelonephritis

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17
Q

Alport memory aid

A

Can’t see- Lenticuonus
Can’t pee- Haematuria/CKD
Can’t hear a high C- Senorineural hearing loss

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18
Q

Most common cause of peritonitis?

A

coagulase-negative staphylococci such as Staphylococcus epidermidis is the most common cause. Staphylococcus aureus is another common cause

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19
Q

Anion gap?

A

(Na+ + K+) - (Cl- + HCO-3)

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20
Q

What are eosinophilic casts a qsign of?

A

Tubulointerstitial nephritis

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21
Q

How does acute tubular necrosis respond to fluid challenge?

A

Poorly

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22
Q

HyperK >6.5? Remember CAN

A
  1. Calcium gluconate 10% 10ml by slow IV titrated to ECG response
  2. Actrapid 10U in 50ml 50% glucose in 15minutes
  3. Neb Salbutamol
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23
Q

Next step if blood sample 6.4

A

Perform an ECG

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24
Q

Causes of focal segmental glomerulosclerosis?

A

idiopathic
secondary to other renal pathology e.g. IgA nephropathy, reflux nephropathy
HIV
heroin
Alport’s syndrome
sickle-cell

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25
Q

Management of proteinuria in CKD?

A

Ace inhibitors

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26
Q

Ratio used when identifying patients with proteinuria?

A

Albumin:creatinine ratio

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27
Q

Drug that stabilises cardiac membrane?

A

IV calcium gluconate

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28
Q

Risk if 0.9% saline is used?

A

if large volumes are used there is an increased risk of hyperchloraemic metabolic acidosis

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29
Q

Post-streptococcal glomerulonephritis cause?

A

immune complex (IgG, IgM and C3) deposition in the glomeruli

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30
Q

Features of post strep glomeulonephritis?

A

general
headache
malaise
visible haematuria
proteinuria
this may result in oedema
hypertension
oliguria

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31
Q

What is Dialysis disequilibrium syndrome

A

rare complication and usually affects those who have recently started renal replacement therapy. It is caused by cerebral oedema, but the exact mechanism is unclear. Therefore this is a diagnosis of exclusion.

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32
Q

Causes of renal artery stenosis in an old guy?

A

Atherosclerosis

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33
Q

What does kidney sense in renal artery stenosis?

A

Hypotension
Therefore RAAS system activated
Then leads to hypertension

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34
Q

Causes of secondary hyperparathyroidism?

A

Higher blood phosphorus levels
The kidneys cannot make active vitamin D (needed to absorb calcium)
Lower blood calcium levels

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35
Q

Recommended fluid challenge for patients with no clincial signs or documentation of HF?

A

500 ml of normal saline stat

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36
Q

Causes of intrinsic AKI?

A

glomerulonephritis
acute tubular necrosis (ATN)
acute interstitial nephritis (AIN), respectively
rhabdomyolysis
tumour lysis syndrome

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37
Q

What rate shoild maintaince fluids be prescribed?

A

30 ml/kg/24hr.

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38
Q

Screening for diabetic nephropathy?

A

all patients should be screened annually using urinary albumin:creatinine ratio (ACR)
should be an early morning specimen
ACR > 2.5 = microalbuminuria

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39
Q

Treatment of clot retention?

A

Continueous bladder irrigation

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40
Q

What is hyperacute rejection?

A

occurs minutes to hours after re-vascularisation of the transplanted kidney. It is due to pre-existing antibodies in the recipient’s blood, such as ABO antibodies. This type of rejection is very rare now due to the sensitivity of cross-matching but risk factors include:
Previous blood transfusions
Previous transplants
Multiple pregnancies

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41
Q

Pre renal uraemia urine osmolarity

A

More than 500mOsm/kg

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42
Q

Urine sodium in pre-renal uraemia?

A

Urine sodium less than 20

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43
Q

Symptoms of a negative fluid balance?

A

Hypotension
Oliguria
Sunken eyes and reduced skin turgor
Tachycardia

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44
Q

What does calcium resonium do?

A

removal of potassium from the body, rather than shifting potassium between fluid compartments in the short-term

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45
Q

IV fluid resusistation how long give inital bolus

A

Over less than 15 minutes

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46
Q

Does hypocalcemia suggest CKD and AKI?

A

CKD

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47
Q

A helpful mnemonic to remember the drugs to stop in AKI is DAMN AKI:

A

Diuretics
Aminoglycosides and ACE inhibitors
Metformin
NSAIDs.

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48
Q

Why is tea coloured urine present in rhabdomylosis?

A

Due to the presence of myoglobin in the urine

49
Q

Henoch schonlein purpura presents with what?

A

abdominal pain, arthritis, haematuria and a purpuric rash over the buttocks and extensor surfaces of arms and legs

50
Q

Stage 1 AKI?

A

Increase in creatinine to 1.5-1.9 times baseline, or
Increase in creatinine by ≥26.5 µmol/L, or
Reduction in urine output to <0.5 mL/kg/hour for ≥ 6 hours

51
Q

When prescribing fluids the potassium requirement per day is what?

A

1 mmol/kg/day

52
Q

Causes of cranial DI?

A

idiopathic
post head injury
pituitary surgery
craniopharyngiomas
infiltrative
histiocytosis X
sarcoidosis
DIDMOAD is the association of cranial Diabetes Insipidus, Diabetes Mellitus, Optic Atrophy and Deafness (also known as Wolfram’s syndrome)
haemochromatosis

53
Q

Drugs that remove potassium from the body?

A

calcium resonium (orally or enema)
enemas are more effective than oral as potassium is secreted by the rectum
loop diuretics
dialysis
haemofiltration/haemodialysis should be considered for patients with AKI with persistent hyperkalaemia

54
Q

What may slow progression of ADPKD in some patients

A

Tolvaptan

55
Q

Features of acute interstital neprhitis?

A

fever, rash, arthralgia
eosinophilia
mild renal impairment
hypertension

56
Q

Investigation findings ijn acute interstital nephritis?

A

sterile pyuria
white cell casts

57
Q

Pathophysiology of Alport’s?

A

due to a defect in the gene which codes for type IV collagen resulting in an abnormal glomerular-basement membrane

58
Q

Why does lithium cause DI?

A

lithium desensitizes the kidney’s ability to respond to ADH in the collecting ducts

59
Q

What changes IN nephrotic syndrome predispose patients to VTE?

A

Loss of antithrombin-III, proteins C and S and an associated rise in fibrinogen levels

60
Q

Indications for spironlactone?

A
  • ascites: patients with cirrhosis develop a secondary hyperaldosteronism. Relatively large doses such as 100 or 200mg are often used
  • hypertension: used in some patients as a NICE ‘step 4’ treatment
  • heart failure (see RALES study below)
  • nephrotic syndrome
  • Conn’s syndrome
61
Q

What Stabilisation of the cardiac membrane?

A

IV calcium gluconate

62
Q

Short-term shift in potassium from extracellular (ECF) to intracellular fluid (ICF)
compartment

A

combined insulin/dextrose infusion
nebulised salbutamol

63
Q

Removal of potassium from the body

A

calcium resonium (orally or enema)
enemas are more effective than oral as potassium is secreted by the rectum
loop diuretics
dialysis
haemofiltration/haemodialysis should be considered for patients with AKI with persistent hyperkalaemia

64
Q

Most common cause of glomeruloneprhtisi?

A

IgA nephropathy

65
Q

How does IgA nephropathy present?

A

macroscopic haematuria in young people following an upper respiratory tract infection.

66
Q

How many days presentation of IgA nephropathy vs post strep glomeruloneprhitis?

A

IgA is 1-2 days
Post strep glomeruloneprhtisi is 1-2 weeks

67
Q

Features of henoch schonlein purpura?

A

palpable purpuric rash (with localized oedema) over buttocks and extensor surfaces of arms and legs
abdominal pain
polyarthritis
features of IgA nephropathy may occur e.g. haematuria, renal failure

68
Q

Factors which may affect the result of an eGFR

A

pregnancy
muscle mass (e.g. amputees, body-builders)
eating red meat 12 hours prior to the sample being taken

69
Q

Causes of a normal anion gap or hyperchloraemic metabolic acidosis

A

gastrointestinal bicarbonate loss: diarrhoea, ureterosigmoidostomy, fistula
renal tubular acidosis
drugs: e.g. acetazolamide
ammonium chloride injection
Addison’s disease

70
Q

Causes of a raised anion gap metabolic acidosis

A

lactate: shock, hypoxia
ketones: diabetic ketoacidosis, alcohol
urate: renal failure
acid poisoning: salicylates, methanol
5-oxoproline: chronic paracetamol use

71
Q

If a patient has a urine output of < 0.5ml/kg/hr postoperatively the first step is

A

to consider a fluid challenge, if there are no contraindications or signs of haemorrhage etc

72
Q

Refer to a nephrologist if any of the following apply:

A

Renal tranplant
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 (see guideline for details)
CKD stage 4 or 5
Qualify for renal replacement hyperkalaemia / metabolic acidosis/ complications of uraemia/ fluid overload (pulmonary oedema)

73
Q

Detection of AKI

A

U and Es
Urinalysis
Imaging: Renal US

74
Q

Haemolytic uraemic syndrome triad?

A

acute kidney injury
microangiopathic haemolytic anaemia
thrombocytopenia

75
Q

Signs of rejection within the immediate (24-48h) post-transplant period should always raise suspicions of what?

A

hyperacute rejection, the rapidity of which is caused by pre-existing of antibodies against a donor’s ABO/HLA antigens.

76
Q

Management of salicylate posioning?

A

IV sodium bicarbonate

77
Q

Mechanism of action to ifferentate bwtween ITP, TTP and HSP?

A

ITP and TTP have petichae and purpura caused by thrombocytopenia.
However, with HSP, it is a small vessel vasculitis which occurs in children and often precedes a URTI (group A strep). As it is inflammatory, you get a reactive rise in the platelets. The petichae and purpura are not caused by haemostasis imbalance as such but inflammation of the small blood vessels. This is also why that in ITP the petichae and purpura is flat against the skin and in HSP it is PALPABLE.
Other differentiating symptoms include: HSP has a classical distribution over the buttocks and lower extremities, is associated with arthritis/arthralgia, colicky abdominal pain, and IgA nephropathy i.e. blood in urine!

78
Q

Salicylate poisoning (ASPIRIN) does what to anion gap?

A

raised anion gap metabolic acidosis

79
Q

Where does spirnolactone act?

A

aldosterone antagonist which acts in the cortical collecting duct.

80
Q

Indications for spirnolactone?

A

ascites: patients with cirrhosis develop a secondary hyperaldosteronism. Relatively large doses such as 100 or 200mg are often used
hypertension: used in some patients as a NICE ‘step 4’ treatment
heart failure (see RALES study below)
nephrotic syndrome
Conn’s syndrome

81
Q

Side-effects of erythropoietin

A

accelerated hypertension potentially leading to encephalopathy and seizures (blood pressure increases in 25% of patients)
bone aches
flu-like symptoms
skin rashes, urticaria
pure red cell aplasia* (due to antibodies against erythropoietin)
raised PCV increases risk of thrombosis (e.g. Fistula)
iron deficiency 2nd to increased erythropoiesis

82
Q

Features of acute interstitial neprhitis?

A

fever, rash, arthralgia
eosinophilia
mild renal impairment
hypertension

83
Q

Managing proteinuria in CKD?

A

ACE inhibitors (or angiotensin II receptor blockers) are key in the management of proteinuria
they should be used first-line in patients with coexistent hypertension and CKD, if the ACR is > 30 mg/mmol
if the ACR > 70 mg/mmol they are indicated regardless of the patient’s blood pressure

84
Q

What agent is used to prevent nephrotoxicity due to cotnrast media?

A

intravenous 0.9% sodium chloride at a rate of 1 mL/kg/hour for 12 hours pre- and post- procedure. There is also evidence to support the use of isotonic sodium bicarbonate

85
Q

Membranous nephropathy is caused by what?

A

the thickening of a part of the glomerular basement membrane

86
Q

Management of minimal change disease?

A

oral corticosteroids: majority of cases (80%) are steroid-responsive
cyclophosphamide is the next step for steroid-resistant cases

87
Q

pathophysiology of minimal change disease

A

T-cell and cytokine-mediated damage to the glomerular basement membrane → polyanion loss
the resultant reduction of electrostatic charge → increased glomerular permeability to serum albumin

88
Q

Causes of nephrogenic DI

A

genetic:
more common form affects the vasopression (ADH) receptor
less common form results from a mutation in the gene that encodes the aquaporin 2 channel
electrolytes
hypercalcaemia
hypokalaemia
lithium
lithium desensitizes the kidney’s ability to respond to ADH in the collecting ducts
demeclocycline
tubulo-interstitial disease: obstruction, sickle-cell, pyelonephritis

89
Q

When prescribing fluids, the glucose requirement is what

A

50-100 g/day

90
Q

In the 2013 guidelines NICE recommend the following requirements for maintenance fluids:

A

25-30 ml/kg/day of water and
approximately 1 mmol/kg/day of potassium, sodium and chloride and
approximately 50-100 g/day of glucose to limit starvation ketosis

91
Q

May have to be stopped in AKI as increased risk of toxicity (but doesn’t usually worsen AKI itself)

A
  • Metformin
  • Lithium
  • Digoxin
92
Q

All patients with chronic kidney disease should be started on what

A

statin

93
Q

Nephrotic syndrome is associated with a hypercoagulable state due to what

A

loss of antithrombin III via the kidneys

94
Q

Differentiating between ATN and acute intersittial neprhitis?

A

Acute interstitial nephritis is an inflammatory process so there is a higher white cell content in the urine, while acute tubular necrosis is not so the urine has no cellular component. A glomerulonephritis would induce a nephritic syndrome with blood present in the urine.

95
Q

presence of protein effectively rules out what in a urine dip

A

pre-renal or post-renal cause

96
Q

What is alport’s syndrome?

A

defect in the gene which codes for type IV collagen resulting in an abnormal glomerular-basement membrane (GBM). The disease is more severe in males with females rarely developing renal failure.

97
Q

Alport’s syndrome usually presents in childhood. The following features may be seen

A

microscopic haematuria
progressive renal failure
bilateral sensorineural deafness
lenticonus: protrusion of the lens surface into the anterior chamber
retinitis pigmentosa
renal biopsy: splitting of lamina densa seen on electron microscopy

Can’t see : lenticonus
Can’t pee: progressive renal failure, microscopic haematuria
Can’t hear a bee: sensorineural hearing loss

98
Q

What are hyaline casts seen in?

A

consist of Tamm-Horsfall protein (secreted by distal convoluted tubule)
seen in normal urine, after exercise, during fever or with loop diuretics

99
Q

When prescribing fluids, the potassium requirement per day is

A

1 mmol/kg/day

100
Q

Basic problems in chronic kidney disease (CKD):

A

1-alpha hydroxylation normally occurs in the kidneys → CKD leads to low vitamin D
the kidneys normally excrete phosphate → CKD leads to high phosphate

This, in turn, causes other problems:
the high phosphate level ‘drags’ calcium from the bones, resulting in osteomalacia
low calcium: due to lack of vitamin D, high phosphate
secondary hyperparathyroidism: due to low calcium, high phosphate and low vitamin D

101
Q

What is the most likely outcome following the diagnosis of minimal change nephropathy in a 10-year-old male?

A

Full recovery but latent recurrent episodes

102
Q

The maximum recommended rate of potassium infusion via a peripheral line is

A

10 mmol/hour, whereas rates above 20 mmol/hour require cardiac monitoring

103
Q

Treatment for hyperacute rejection?

A

no treatment is possible and the graft must be removed

104
Q

Treatment for acute graft failure?

A

may be reversible with steroids and immunosuppressants

105
Q

Management of anaemia in CKD?

A

the 2011 NICE guidelines suggest a target haemoglobin of 10 - 12 g/dl
determination and optimisation of iron status should be carried out prior to the administration of erythropoiesis-stimulating agents (ESA).
oral iron should be offered for patients who are not on ESAs or haemodialysis. If target Hb levels are not reached within 3 months then patients should be switched to IV iron
patients on ESAs or haemodialysis generally require IV iron
ESAs such as erythropoietin and darbepoetin should be used in those ‘who are likely to benefit in terms of quality of life and physical function’

106
Q

Screening for diabetic nephropathy?

A

all patients should be screened annually using urinary albumin:creatinine ratio (ACR)
should be an early morning specimen
ACR > 2.5 = microalbuminuria

107
Q

Why can membranous glomeruloneprhtitis cause derrnaged TFTs

A

due to urinary loss of thyroid-binding globulins, leading to a low total T4 level.

108
Q

Detect acute kidney injury, in line with the (p)RIFLE, AKIN or KDIGO definitions, by using any of the following criteria:§§

A

a rise in serum creatinine of 26 micromol/litre or greater within 48 hours
a 50% or greater rise in serum creatinine known or presumed to have occurred within the past 7 days
a fall in urine output to less than 0.5 ml/kg/hour for more than 6 hours in adults and more than

109
Q

Collecting an ACR sample for CKD

A

by collecting a ‘spot’ sample it avoids the need to collect urine over a 24 hour period in order to detect or quantify proteinuria
should be a first-pass morning urine specimen
if the initial ACR is between 3 mg/mmol and 70 mg/mmol, this should be confirmed by a subsequent early morning sample. If the initial ACR is 70 mg/mmol or more, a repeat sample need not be tested.

110
Q

wHAT SHOULD be monitord in HSP?

A

blood pressure and urinanalysis should be monitored to detect progressive renal involvement

111
Q

When prescribing maintenance fluids, HOW much water is typically required

A

25-30 ml/kg/day

112
Q

What is amyloidosis?

A

term which describes the extracellular deposition of an insoluble fibrillar protein termed amyloid
amyloid is derived from many different precursor proteins
in addition to the fibrillar component, amyloid also contains a non-fibrillary protein called amyloid-P component, derived from the acute phase protein serum amyloid P
other non-fibrillary components include apolipoprotein E and heparan sulphate proteoglycans
the accumulation of amyloid fibrils leads to tissue/organ dysfunction

113
Q

PRE RENAL uraemia vs ATN features

A
114
Q

Urea to creatinine ratio above what is important ?

A

100 Increases ratio indicates a pre renal cause

115
Q

What is ATN?

A

most common cause of acute kidney injury. It is caused by the necrosis of tubular cells due to ischaemia or nephrotoxins. Hence, the tubule would not be capable of reabsorbing urea. On blood tests, you would expect to see normal serum urea : creatinine ratio.

116
Q

Level for severe hyperkalaemia?

A

More than 6.5 mmol/L

117
Q

All patients with severe hyperkalaemia (≥ 6.5 mmol/L) or with ECG changes should have emergency treatment with what?

A
  • IV calcium gluconate: to stabilise the myocardium
  • insulin/dextrose infusion: short-term shift in potassium from ECF to ICF
  • other treatments such as nebulised salbutamol may be given to temporarily lower the serum potassium
118
Q

Features of acute interstitial nephritis?

A
  • fever, rash, arthralgia
  • eosinophilia
  • mild renal impairment
  • hypertension
119
Q

Systemic lupus erythematosus with proteinuria on urinalysis - consider what?

A

Lupus nephritis

Year 4 Final (39 decks)

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