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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
Ix CKD?
ACR >3mg/mmol + diabetes >30mg/mmol + HTN >70mg/mmol
26
Consequences of CKD?
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
27
Screening for PCKD?
ABDOMINAL USS >=2 cysts age <30 >= 2 cysts in both kidneys age 30-59 >=4 cysts in both kidneys >60
28
Features of PCKD?
liver cysts berry aneurysms mitral valve prolapse renal failure signs
29
Mx PCKD?
tolvaptan (slows progresion)
30
what are the features of ADPKD1?
85% CASES Chr16 (PKD1 gene) presents earlier with renal failure
31
what are the features of ADPKD2?
15% cases | Chr4 (PKD2 GENE)
32
What is the most common glomerulonephritis?
IgA nephropathy | IgA and IgG complex and deposit in organs
33
S/S IgA Nephropathy?
purpuric rash - urticarial, maculopapular, spares trunk arthralgia- large joints abdominal pain - colicky, melena, intussusception glomerulonephritis - micro/macroscopic haematuria
34
Ix IgA nephropathy?
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
Mx IgA nephropathy?
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
When are hyaline casts seen in urine?
``` tamm-horsfall protein (secreted by DCT) NORMAL urine after exercise during fever with loop diuretics ```
37
When are brown granular casts seen in urine?
ATN
38
when are red cell casts seen in urine?
nephritic syndrome
39
What is the most common renal tumour?
RCC (85% of all renal malignancies) | clear cell carcinoma
40
S/S renal carcinoma?
``` loin pain frank haematuria abdominal mass may see haemoptysis if cannonball mets VHL ```
41
associated features RCC?
``` LEFT varicocele (obstruction of testicular vein), PUO, metastasis paraneoplastic: EPO, PTHrp, renin, ACTH ```
42
Management of bladder Ca?
in situ - trans-urethral resection | ex situ - radical cystectomy
43
Ix bladder cancer
CT IVU
44
Bladder Ca associations?
dyes rubber chemical smoking schistosomiasis (SCC bladder)
45
Who is nephroblastoma common in?
80% of GU malignancies <15y
46
S/S npehroblastoma ?
``` flank mass (90%) HTN (50%) ```
47
Ix nephroblastoma?
USS | CT
48
Mx nephroblastoma?
resection + chemotherapy
49
Where does neuroblastoma arise from?
adrenal gland
50
Ix neuroblastoma?
MIBG | CT (calcified)
51
Mx neuroblastoma?
resection chemotherapy radiotherapy
52
Staging of Renal cell carcinoma?
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
Complications of haemodialysis?
``` site infection endocarditis stenosis at site hypotension arrhythmia air embolus anaphylactic reaction disequilibration syndrome ```
54
Complications of peritoneal dialysis?
``` peritonitis sclerosing peritonitis catheter infection catheter blockage constipation fluid retention hyperglycaemia hernia back pain malnutrition ```
55
What is contrast media nephrotoxicity?
Contrast media nephrotoxicity may be defined as a 25% increase in creatinine occurring within 3 days of the intravascular administration of contrast media.
56
RF contrast media nephrotoxicity?
known renal impairment (especially diabetic nephropathy) age > 70 years dehydration cardiac failure the use of nephrotoxic drugs such as NSAIDs
57
which procedures may cause may cause contrast-induced nephropathy?
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
prevention of contrast media nephrotoxicity?
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
what does minimal change disease present as?
a nephrotic syndrome | 75% of cases in children and 25% in adults
60
what causes minimal change disease?
Majority idiopathic drugs: NSAIDs, rifampicin Hodgkin's lymphoma, thymoma infectious mononucleosis
61
Features of minimal change?
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
Management of minimal change?
majority of cases (80%) are steroid-responsive | cyclophosphamide is the next step for steroid-resistant cases
63
Prognosis of minimal change?
1/3 have just one episode 1/3 have infrequent relapses 1/3 have frequent relapses which stop before adulthood
64
Types of peritoneal dialysis?
APD (automated peritoneal dialysis) | CAPD (continuous ambulatory peritoneal dialysis)
65
Complications of peritoneal dialysis?
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
Management of nephrogenic diabetes insipidus?
nephrogenic diabetes insipidus: thiazides (chlorothiazide), low salt/protein diet - central diabetes insipidus can be treated with desmopressin
67
Causes of nephrogenic diabetes inspidus?
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
What is the screening for diabetic retinopathy?
all patients should be screened annually using urinary albumin:creatinine ratio (ACR) should be an early morning specimen ACR > 2.5 = microalbuminuria
69
what is the management of diabetic retinopathy?
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
what are some causes of hyperkalaemia?
``` 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
What changes in patients with nephrotic syndrome predispose to the development of venous thromboembolism?
Loss of antithrombin-III, proteins C and S and an associated rise in fibrinogen levels predispose to thrombosis
72
what is the difference between AKI and CKD on ultrasound?
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
what are the causes of acute interstitial nephritis?
``` 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
What are the features of acute interstitial nephritis?
fever, rash, arthralgia eosinophilia mild renal impairment hypertension
75
what are the investigations for acute interstitial nephritis?
sterile pyuria | white cell casts
76
What is Tubulointerstitial nephritis with uveitis?
occurs in young females. Symptoms include fever, weight loss and painful, red eyes. Urinalysis is positive for leukocytes and protein.
77
Side effects of EPO?
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
Why might EPO therapy be ineffective?
``` iron deficiency inadequate dose concurrent infection/inflammation hyperparathyroid bone disease aluminium toxicity ```

Year 6 Medicine (18 decks)

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