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Year 6 Medicine > Nephrology > Flashcards

Nephrology Flashcards

1
Q

What are the prerenal causes of AKI?

A

dehydration
shock - sepsis, blood loss
renal artery stenosis - often triggered by ACEi/NSAIDS

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2
Q

What are the intrinsic renal causes of AKI?

A 
INTRINSIC
Ischaemia
Nephrotoxic Abx
Tablets ( NSAIDS, ACEi)
Radiological contrast
Injury (rhabdomyolysis)
Negatively birefringent crystals
Syndromes (glomerulonephritis)
Inflammation (vasculitis)
Cholesterol emboli
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3
Q

What are some postrenal causes of AKI?

A

Lumen: sloughed papilla or stone
In wall: tumour (renal cell, transitional cell), fibrosis
External pressure: BPH, prostate ca, aneurysm, lymphadenopathy

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4
Q

Indications for dialysis?

A 
MUH FC
metabolic acidosis [pH<7.1]
uraemic symptoms [encephalopathy, nausea, pruritic, malaise, pericarditis]
hyperkalaemia
fluid overload
CKD stage 5 [GFR <15]
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5
Q

what are the types of peritoneal dialysis?

A

CAPD - continuous ambulatory peritoneal dialysis

APD - automated peritoneal dialysis

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6
Q

what sort of catheter is used for peritoneal dialysis

A

Tenckhoff catheter

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7
Q

what are the complications of an AV fistula?

A

thrombosis, stenosis, infection, bleeding, aneurysm, steal syndrome

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8
Q

what are the complications of a tesio line?

A

sepsis, peritonitis, DIC, fluid overload, DDS

Dialysis disequilibrium syndrome = cerebral oedema

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9
Q

what is a tesio line?

A

central line to internal jugular and right atrium, tunnelled under skin with two lumens entering skin

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10
Q

what is a swan gantz line and where is the entry point?

A

3 lumen line into subclavian vein

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11
Q

what technique is used to insert lines?

A

seldinger
LA + US guidance
CXR

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12
Q

which drugs can be used for immunosuppression in transplant?

A

calcineurin inhibitors
anti-proliferative (MMF, azathioprine)
steroids

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13
Q

Which HLAs are most important to match before transplant?

A

DR>B>A

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14
Q

Complications of transplant?

A

surgical
anaesthetic
transplant (failure or rejection)
immunosuppression (GvHD, SCC)

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15
Q

What are the types of rejection?

A

Hyper acute (<24h)
Acute (<6m)
Chronic (>6m)

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16
Q

RFs for hyper acute rejection?

A

previous blood transfusion, previous transplant, multiple pregnancies

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17
Q

Mx acute rejection?

A 
antibody mediated:
IVIG
plasmapheresis
anti-CD20
anti-c5

T cell mediated: (more common)
steroids
OKT3
ATG

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18
Q

Intrinsic causes of ARF?

A

vasculitis: small vessel - HUS, TTP, DIC, GPA, eGPA/ large vessel - renal artery/vein thrombosis
glomerulonephritis: minimal change (children), membranous
ATN
AIN/interstitial nephritis: drugs (75%)/ rash, fever, eosinophilia, sterile pyuria, nephrotic syndrome

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19
Q

how to differentiate between pre-renal and intrinsic renal AKI?

A

URINARY SODIUM
pre-renal:<20 (low as kidneys hold on to sodium)
intrisinc [ATN]: >40 (ischaemia of tubules means loss of sodium)

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20
Q

Which drugs may precipitate AKI?

A 
DAMN
Diurtics
ACEi/ARB
Metformin
NSAIDs
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21
Q

what are the CKD stages?

A 
eGFR
stage 1: >90 + other signs damage
stage 2: 60-90 + other signs damange
stage 3a: 45-60
stage 3b: 30-45
stage 4: 15-30
stage 5: <15
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22
Q

In CKD when should routine referral to nephrology be made?

A

eGFR <30mL/min/1.73m^2

eGFR decrease >25% or >15ml/min in 12m

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23
Q

Management of CKD?

A

Diet: reduce phosphate, Na, K, fluid restrict. AvoidETOH, tea, coffee, chocolate and banana
PO binders- sevelamar (binds and prevents absorption)
Vit D
Parathyroidectomy (rarely)

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24
Q

Mx CKD

A

ACEi

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25
Q

Ix CKD?

A

ACR
>3mg/mmol + diabetes
>30mg/mmol + HTN
>70mg/mmol

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26
Q

Consequences of CKD?

A
  1. failure of homeostatic function: acidosis, hyperkalaemia
  2. failure of hormonal function: anaemia, renal bone disease
  3. cardiovascular disease: vascular calcification, renal osteodystrophy
  4. uraemic cardiomyopathy
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27
Q

Screening for PCKD?

A

ABDOMINAL USS
>=2 cysts age <30
>= 2 cysts in both kidneys age 30-59
>=4 cysts in both kidneys >60

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28
Q

Features of PCKD?

A

liver cysts
berry aneurysms
mitral valve prolapse
renal failure signs

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29
Q

Mx PCKD?

A

tolvaptan (slows progresion)

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30
Q

what are the features of ADPKD1?

A

85% CASES
Chr16 (PKD1 gene)
presents earlier with renal failure

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31
Q

what are the features of ADPKD2?

A

15% cases

Chr4 (PKD2 GENE)

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32
Q

What is the most common glomerulonephritis?

A

IgA nephropathy

IgA and IgG complex and deposit in organs

33
Q

S/S IgA Nephropathy?

A

purpuric rash - urticarial, maculopapular, spares trunk
arthralgia- large joints
abdominal pain - colicky, melena, intussusception
glomerulonephritis - micro/macroscopic haematuria

34
Q

Ix IgA nephropathy?

A

Urinalysis: RBCs, proteinuria, casts, urea, Cr, 24h protein (rule out meningococcal)
1st: FBC, clotting screen, urine dip, U&E
Increase IgA, normal coag

follow up: weekly for 1m, 2weekly for 2m, 3m, 6m, 12m with bP and urine measurements

35
Q

Mx IgA nephropathy?

A

resolve spontaneously within 4w (most)
joint pain - NSAIDs
scrotal involvement/oedema/abdo pain - oral prednisolone
renal involvement - IV corticosteroids (nephrotic proteinuria or declining renal Fx)

36
Q

When are hyaline casts seen in urine?

A 
tamm-horsfall protein (secreted by DCT)
NORMAL urine
after exercise
during fever
with loop diuretics
37
Q

When are brown granular casts seen in urine?

38
Q

when are red cell casts seen in urine?

A

nephritic syndrome

39
Q

What is the most common renal tumour?

A

RCC (85% of all renal malignancies)

clear cell carcinoma

40
Q

S/S renal carcinoma?

A 
loin pain
frank haematuria
abdominal mass 
may see haemoptysis if cannonball mets
VHL
41
Q

associated features RCC?

A 
LEFT varicocele (obstruction of testicular vein), PUO, metastasis
paraneoplastic: EPO, PTHrp, renin, ACTH
42
Q

Management of bladder Ca?

A

in situ - trans-urethral resection

ex situ - radical cystectomy

43
Q

Ix bladder cancer

44
Q

Bladder Ca associations?

A

dyes
rubber chemical
smoking
schistosomiasis (SCC bladder)

45
Q

Who is nephroblastoma common in?

A

80% of GU malignancies <15y

46
Q

S/S npehroblastoma ?

A 
flank mass (90%)
HTN (50%)
47
Q

Ix nephroblastoma?

48
Q

Mx nephroblastoma?

A

resection + chemotherapy

49
Q

Where does neuroblastoma arise from?

A

adrenal gland

50
Q

Ix neuroblastoma?

A

MIBG

CT (calcified)

51
Q

Mx neuroblastoma?

A

resection
chemotherapy
radiotherapy

52
Q

Staging of Renal cell carcinoma?

A

T1: tumour <=7cm and confined to kidney
T2: tumour >7cm AND CONFINED TO kidney
T3: tumour extends to major veins but not into adrenal or beyond gerota’s fascia
T4: tumour invades beyond gerota’s fascia

53
Q

Complications of haemodialysis?

A 
site infection
endocarditis
stenosis at site
hypotension
arrhythmia
air embolus
anaphylactic reaction
disequilibration syndrome
54
Q

Complications of peritoneal dialysis?

A 
peritonitis
sclerosing peritonitis
catheter infection
catheter blockage
constipation
fluid retention
hyperglycaemia
hernia
back pain 
malnutrition
55
Q

What is contrast media nephrotoxicity?

A

Contrast media nephrotoxicity may be defined as a 25% increase in creatinine occurring within 3 days of the intravascular administration of contrast media.

56
Q

RF contrast media nephrotoxicity?

A

known renal impairment (especially diabetic nephropathy)
age > 70 years
dehydration
cardiac failure
the use of nephrotoxic drugs such as NSAIDs

57
Q

which procedures may cause may cause contrast-induced nephropathy?

A

CT with contrast
coronary angiography/percutaneous coronary intervention (PCI)
around 5% of patients who’ve undergone PCI develop a transient rise in the plasma creatinine concentration of more than 88 µmol/L

58
Q

prevention of contrast media nephrotoxicity?

A

intravenous 0.9% sodium chloride at a rate of 1 mL/kg/hour for 12 hours pre- and post- procedure.
isotonic sodium bicarbonate
hold metformin for 48 h after until renal function normal

59
Q

what does minimal change disease present as?

A

a nephrotic syndrome

75% of cases in children and 25% in adults

60
Q

what causes minimal change disease?

A

Majority idiopathic
drugs: NSAIDs, rifampicin
Hodgkin’s lymphoma, thymoma
infectious mononucleosis

61
Q

Features of minimal change?

A

nephrotic syndrome
normotension - hypertension is rare
highly selective proteinuria
only intermediate-sized proteins such as albumin and transferrin leak through the glomerulus
renal biopsy
normal glomeruli on light microscopy
electron microscopy shows fusion of podocytes and effacement of foot processes

62
Q

Management of minimal change?

A

majority of cases (80%) are steroid-responsive

cyclophosphamide is the next step for steroid-resistant cases

63
Q

Prognosis of minimal change?

A

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

64
Q

Types of peritoneal dialysis?

A

APD (automated peritoneal dialysis)

CAPD (continuous ambulatory peritoneal dialysis)

65
Q

Complications of peritoneal dialysis?

A

peritonitis (s.epidermidis > S.aureus > gram -ve)

the BNF recommends vancomycin (or teicoplanin) + ceftazidime added to dialysis fluid OR vancomycin added to dialysis fluid + ciprofloxacin by mouth

66
Q

Management of nephrogenic diabetes insipidus?

A

nephrogenic diabetes insipidus: thiazides (chlorothiazide), low salt/protein diet
- central diabetes insipidus can be treated with desmopressin

67
Q

Causes of nephrogenic diabetes inspidus?

A

genetic: the more common form affects the vasopression (ADH) receptor, the 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

68
Q

What is the screening for diabetic retinopathy?

A

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

69
Q

what is the management of diabetic retinopathy?

A

dietary protein restriction
tight glycaemic control
BP control: aim for < 130/80 mmHg
ACE inhibitor or angiotensin-II receptor antagonist
should be start if urinary ACR of 3 mg/mmol or more
dual therapy with ACE inhibitors and angiotensin-II receptor antagonist should not be started
control dyslipidaemia e.g. Statins

70
Q

what are some causes of hyperkalaemia?

A 
acute kidney injury
drugs*: potassium sparing diuretics, ACE inhibitors, angiotensin 2 receptor blockers, spironolactone, ciclosporin, heparin**
metabolic acidosis
Addison's disease
rhabdomyolysis
massive blood transfusion
71
Q

What changes in patients with nephrotic syndrome predispose to the development of venous thromboembolism?

A

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

72
Q

what is the difference between AKI and CKD on ultrasound?

A

Most patients with CKD have bilateral small kidneys. Exceptions to this rule include:
autosomal dominant polycystic kidney disease
diabetic nephropathy (early stages)
amyloidosis
HIV-associated nephropathy

Other features suggesting CKD rather than AKI
hypocalcaemia (due to lack of vitamin D)

73
Q

what are the causes of acute interstitial nephritis?

A 
drugs: the most common cause, particularly antibiotics
penicillin
rifampicin
NSAIDs
allopurinol
furosemide
systemic disease: SLE, sarcoidosis, and Sjögren's syndrome
infection: Hanta virus , staphylococci
74
Q

What are the features of acute interstitial nephritis?

A

fever, rash, arthralgia
eosinophilia
mild renal impairment
hypertension

75
Q

what are the investigations for acute interstitial nephritis?

A

sterile pyuria

white cell casts

76
Q

What is Tubulointerstitial nephritis with uveitis?

A

occurs in young females. Symptoms include fever, weight loss and painful, red eyes. Urinalysis is positive for leukocytes and protein.

77
Q

Side effects of EPO?

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

78
Q

Why might EPO therapy be ineffective?

A 
iron deficiency
inadequate dose
concurrent infection/inflammation
hyperparathyroid bone disease
aluminium toxicity

Year 6 Medicine (18 decks)

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