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
Management of proteinuria in CKD?
Ace inhibitors
26
Ratio used when identifying patients with proteinuria?
Albumin:creatinine ratio
27
Drug that stabilises cardiac membrane?
IV calcium gluconate
28
Risk if 0.9% saline is used?
if large volumes are used there is an increased risk of hyperchloraemic metabolic acidosis
29
Post-streptococcal glomerulonephritis cause?
immune complex (IgG, IgM and C3) deposition in the glomeruli
30
Features of post strep glomeulonephritis?
general headache malaise visible haematuria proteinuria this may result in oedema hypertension oliguria
31
What is Dialysis disequilibrium syndrome
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.
32
Causes of renal artery stenosis in an old guy?
Atherosclerosis
33
What does kidney sense in renal artery stenosis?
Hypotension Therefore RAAS system activated Then leads to hypertension
34
Causes of secondary hyperparathyroidism?
Higher blood phosphorus levels The kidneys cannot make active vitamin D (needed to absorb calcium) Lower blood calcium levels
35
Recommended fluid challenge for patients with no clincial signs or documentation of HF?
500 ml of normal saline stat
36
Causes of intrinsic AKI?
glomerulonephritis acute tubular necrosis (ATN) acute interstitial nephritis (AIN), respectively rhabdomyolysis tumour lysis syndrome
37
What rate shoild maintaince fluids be prescribed?
30 ml/kg/24hr.
38
Screening for diabetic nephropathy?
all patients should be screened annually using urinary albumin:creatinine ratio (ACR) should be an early morning specimen ACR > 2.5 = microalbuminuria
39
Treatment of clot retention?
Continueous bladder irrigation
40
What is hyperacute rejection?
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
41
Pre renal uraemia urine osmolarity
More than 500mOsm/kg
42
Urine sodium in pre-renal uraemia?
Urine sodium less than 20
43
Symptoms of a negative fluid balance?
Hypotension Oliguria Sunken eyes and reduced skin turgor Tachycardia
44
What does calcium resonium do?
removal of potassium from the body, rather than shifting potassium between fluid compartments in the short-term
45
IV fluid resusistation how long give inital bolus
Over less than 15 minutes
46
Does hypocalcemia suggest CKD and AKI?
CKD
47
A helpful mnemonic to remember the drugs to stop in AKI is DAMN AKI:
Diuretics Aminoglycosides and ACE inhibitors Metformin NSAIDs.
48
Why is tea coloured urine present in rhabdomylosis?
Due to the presence of myoglobin in the urine
49
Henoch schonlein purpura presents with what?
abdominal pain, arthritis, haematuria and a purpuric rash over the buttocks and extensor surfaces of arms and legs
50
Stage 1 AKI?
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
When prescribing fluids the potassium requirement per day is what?
1 mmol/kg/day
52
Causes of cranial DI?
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
Drugs that remove potassium from the body?
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
What may slow progression of ADPKD in some patients
Tolvaptan
55
Features of acute interstital neprhitis?
fever, rash, arthralgia eosinophilia mild renal impairment hypertension
56
Investigation findings ijn acute interstital nephritis?
sterile pyuria white cell casts
57
Pathophysiology of Alport's?
due to a defect in the gene which codes for type IV collagen resulting in an abnormal glomerular-basement membrane
58
Why does lithium cause DI?
lithium desensitizes the kidney's ability to respond to ADH in the collecting ducts
59
What changes IN nephrotic syndrome predispose patients to VTE?
Loss of antithrombin-III, proteins C and S and an associated rise in fibrinogen levels
60
Indications for spironlactone?
* 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
What Stabilisation of the cardiac membrane?
IV calcium gluconate
62
Short-term shift in potassium from extracellular (ECF) to intracellular fluid (ICF) compartment
combined insulin/dextrose infusion nebulised salbutamol
63
Removal of potassium from the body
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
Most common cause of glomeruloneprhtisi?
IgA nephropathy
65
How does IgA nephropathy present?
macroscopic haematuria in young people following an upper respiratory tract infection.
66
How many days presentation of IgA nephropathy vs post strep glomeruloneprhitis?
IgA is 1-2 days Post strep glomeruloneprhtisi is 1-2 weeks
67
Features of henoch schonlein purpura?
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
Factors which may affect the result of an eGFR
pregnancy muscle mass (e.g. amputees, body-builders) eating red meat 12 hours prior to the sample being taken
69
Causes of a normal anion gap or hyperchloraemic metabolic acidosis
gastrointestinal bicarbonate loss: diarrhoea, ureterosigmoidostomy, fistula renal tubular acidosis drugs: e.g. acetazolamide ammonium chloride injection Addison's disease
70
Causes of a raised anion gap metabolic acidosis
lactate: shock, hypoxia ketones: diabetic ketoacidosis, alcohol urate: renal failure acid poisoning: salicylates, methanol 5-oxoproline: chronic paracetamol use
71
If a patient has a urine output of < 0.5ml/kg/hr postoperatively the first step is
to consider a fluid challenge, if there are no contraindications or signs of haemorrhage etc
72
Refer to a nephrologist if any of the following apply:
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
Detection of AKI
U and Es Urinalysis Imaging: Renal US
74
Haemolytic uraemic syndrome triad?
acute kidney injury microangiopathic haemolytic anaemia thrombocytopenia
75
Signs of rejection within the immediate (24-48h) post-transplant period should always raise suspicions of what?
hyperacute rejection, the rapidity of which is caused by pre-existing of antibodies against a donor's ABO/HLA antigens.
76
Management of salicylate posioning?
IV sodium bicarbonate
77
Mechanism of action to ifferentate bwtween ITP, TTP and HSP?
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
Salicylate poisoning (ASPIRIN) does what to anion gap?
raised anion gap metabolic acidosis
79
Where does spirnolactone act?
aldosterone antagonist which acts in the cortical collecting duct.
80
Indications for spirnolactone?
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
Side-effects of erythropoietin
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
Features of acute interstitial neprhitis?
fever, rash, arthralgia eosinophilia mild renal impairment hypertension
83
Managing proteinuria in CKD?
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
What agent is used to prevent nephrotoxicity due to cotnrast media?
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
Membranous nephropathy is caused by what?
the thickening of a part of the glomerular basement membrane
86
Management of minimal change disease?
oral corticosteroids: majority of cases (80%) are steroid-responsive cyclophosphamide is the next step for steroid-resistant cases
87
pathophysiology of minimal change disease
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
Causes of nephrogenic DI
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
When prescribing fluids, the glucose requirement is what
50-100 g/day
90
In the 2013 guidelines NICE recommend the following requirements for maintenance fluids:
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
May have to be stopped in AKI as increased risk of toxicity (but doesn't usually worsen AKI itself)
* Metformin * Lithium * Digoxin
92
All patients with chronic kidney disease should be started on what
statin
93
Nephrotic syndrome is associated with a hypercoagulable state due to what
loss of antithrombin III via the kidneys
94
Differentiating between ATN and acute intersittial neprhitis?
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
presence of protein effectively rules out what in a urine dip
pre-renal or post-renal cause
96
What is alport's syndrome?
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
Alport's syndrome usually presents in childhood. The following features may be seen
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 ## Footnote Can't see : lenticonus Can't pee: progressive renal failure, microscopic haematuria Can't hear a bee: sensorineural hearing loss
98
What are hyaline casts seen in?
consist of Tamm-Horsfall protein (secreted by distal convoluted tubule) seen in normal urine, after exercise, during fever or with loop diuretics
99
When prescribing fluids, the potassium requirement per day is
1 mmol/kg/day
100
Basic problems in chronic kidney disease (CKD):
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
What is the most likely outcome following the diagnosis of minimal change nephropathy in a 10-year-old male?
Full recovery but latent recurrent episodes
102
The maximum recommended rate of potassium infusion via a peripheral line is
10 mmol/hour, whereas rates above 20 mmol/hour require cardiac monitoring
103
Treatment for hyperacute rejection?
no treatment is possible and the graft must be removed
104
Treatment for acute graft failure?
may be reversible with steroids and immunosuppressants
105
Management of anaemia in CKD?
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
Screening for diabetic nephropathy?
all patients should be screened annually using urinary albumin:creatinine ratio (ACR) should be an early morning specimen ACR > 2.5 = microalbuminuria
107
Why can membranous glomeruloneprhtitis cause derrnaged TFTs
due to urinary loss of thyroid-binding globulins, leading to a low total T4 level.
108
Detect acute kidney injury, in line with the (p)RIFLE, AKIN or KDIGO definitions, by using any of the following criteria:§§
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
Collecting an ACR sample for CKD
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
wHAT SHOULD be monitord in HSP?
blood pressure and urinanalysis should be monitored to detect progressive renal involvement
111
When prescribing maintenance fluids, HOW much water is typically required
25-30 ml/kg/day
112
What is amyloidosis?
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
PRE RENAL uraemia vs ATN features
114
Urea to creatinine ratio above what is important ?
100 Increases ratio indicates a pre renal cause
115
What is ATN?
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
Level for severe hyperkalaemia?
More than 6.5 mmol/L
117
All patients with severe hyperkalaemia (≥ 6.5 mmol/L) or with ECG changes should have emergency treatment with what?
* 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
Features of acute interstitial nephritis?
* fever, rash, arthralgia * eosinophilia * mild renal impairment * hypertension
119
Systemic lupus erythematosus with proteinuria on urinalysis - consider what?
Lupus nephritis