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Nephrology & Urology > Nephrology > Flashcards

Nephrology Flashcards

1
Q

What is counted in eGFR?

A

Age
Gender
Ethinicity
Cr clearance

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2
Q

What are 2 measures of kidney function/

A 
Creatine clearance (eGFR)
ALb:Cr ration
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3
Q

What are 5 functions of kidney?

A 
Blood volume control
Toxin excretion
RBC production
Vit D metabolism
Acid base regulation
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4
Q

What BP is aimed for in diabetics?

A

140/90

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5
Q

How is BP managed in diabetic nephropathy?

A

ACEi or ARB or CCB then A&C then A & C & D

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6
Q

Why does CKD cause anaemia?

A

CKD caused by increaed liver toxins reducing bowel absorbtion and caused by decreaed erythropoetin

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7
Q

WHat stage CKD to refer to nephrology?

A 
4
Or
Renal artery stenosis
HTN on 4 agents
A:Cr ratio >70
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8
Q

What are contraindications to kidney transplant?

A

CJD
Blood cancer
Other cancers if active or recent

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9
Q

What is main point of renal diet?

A

Low postassium

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10
Q

How is pain releif given in AKI?

A

Fentanyl

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11
Q

How does myeloma cause an AKI?

A

Cast nephropathy

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12
Q

What is eGFR of each stage or KD?

5-3a

A 
5--- <15
4---15-40
3b--- 30-45
3a--- 45-60- 
ALL Stages of Kidney failure must have some sign of renal damage too (1 and 2) or reduction in function (3-5)
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13
Q

What is normal urine output?

A

0.5ml/kg/hour

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14
Q

How do you define an AKI?

A

Serum Cr >26,4 above baseline

Creatinine increase of over 50% or oligouria

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15
Q

What are the 3 subdivisions of AKI and give examples of each

A

Pre renal- under perfusion- CCF, D&V, hypovolaemia, se[sis, bleeding)

Renal- Glomerular disease, Drugs

Post Renal- Calculi, Tumours, BPH, urinary retention

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16
Q

What is most common cause of nephropathy in adults?

A

IgA (post UTI)

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17
Q

Which nephropathy has IgG deposits?

A

Membranous Glomerulonephropathy
complement activated against GBM
Thickened GBM on microscopic analysis

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18
Q

What are vasculitis causes of nephropathy and what are autoabs??

A

Wegeners- cANCA

Microscopic Polyangitis - pANCA

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19
Q

How are vasculitic and Goodpasture’s managed?

A

Steroids

Cyclophosphamide

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20
Q

What autoab is seen in goodpastures?

A

antiGBM

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21
Q

What is the difference between IgA nephropathy and post infectious?

A

IgA is after GI infection

Post Infection is after strep pyogenes (URTI)

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22
Q

How is post infectious nephropathy managed?

A

conservatively, resolves after 2-3 weeks

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23
Q

What is the umbrella term for the effects of SLE, Hepatitis etc on the kidney that results in end stage failure?

A

Membranoproliferative Glomerularnephritis.

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24
Q

What is the definition of a proliferative glomerularnephritis?

A

Increased number of cells in glomerulus= presents with nephritis

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25
Q

Name 6 causes of nephritis (proliferative glomerularnephropathy)

A 
IgA
Wegeners
Microscopic Polyangitis
Goodpastures
Post Infectious
Membranoproliferative Glomerularnephritis
26
Q

What is the definition of non proliferative glomerular nephropathy?

A

Lack of proliferative cells at glomerulus

Nephotic syndromes

27
Q

Name 3 causes of nephrotic syndrome

A

Minimal change disease
Focal Segmental Glomerular Schlerosis (FSGS)
Membranous Glomerular Nephritis (MGN)

28
Q

What is histology of minimal change disease?

A

Fused podocytes on electron microscopy

29
Q

How is minimal change disease managed?

A

Prednisolone

30
Q

What is the main cause of steroid resistant nephotic syndrome?

A

FSGS

31
Q

What is the cause of FSGS?

A

Genetics

32
Q

What is management of FSGS?

A

Diuretics for oedema
Antihypertensives
Statins
No steroids work, but some cytotoxics

33
Q

How is FSGS ultimately managed?

A

Transplant

34
Q

What are the causes of membranous glomerularnephritis?

A 
Hep B
SLE
Malaria
Penecillamine
Idiopathic
35
Q

What is pathophysiology of MGN?

A

Immune complex (IgG) deposition thickening basement membrane. Immunofluorescence demonstrates this

36
Q

What is management of MGN?

A

Steroids slow disease process

37
Q

What is prognosis of MGN?

A

1/3 progress
1/3 chronic
1/3 remission

38
Q

Which 3 diseases can quickly progress to end stage crescenteric glomerularnepritis?

A

Wegeners
Goodpastures
Microscopic Polyangitis

39
Q

How long after URTI infection does IgA nephropathy occur and how long does it last?

A

24-48 hours

several months recurrent

40
Q

How is IgA nephropathy confirmed?

A

IgA deposits on membrane in biospy

41
Q

How long does it take for post infectious glomerular nephritis to present?

A

2 weeks

42
Q

How is diagnosis of post infectious made?

A

Proliferation of mesangial cellsm neutrophils and monocytes and bowmans space impaired on light microscopy- classic crescenteric glomerularnephritis

43
Q

Why is there hyperlipidaemia in nephrotic syndrome?

A

Hypoalb causes liver to increase alb production, and there fore also increasing lipid production causing hyperlipidaemia

44
Q

What is a key sign of nephritic syndrome?

A

RBC casts in urine indicating glomerular damage

Low urine output

45
Q

What is seen in Alport’s Syndrome?

A

Abnormal collagen metabolism leading to abnormal GBM (basketweave)
More common in men
Presents in childhood with
- 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

46
Q

How is Alport’s inherited?

A

X linked Dom

47
Q

What prophylaxis is needed in nephrotic syndrome?

A

LMWH against VTE

48
Q

How is Autosomal Dominamant PCKD screened for

A

USS

49
Q

How is PCKD managed in adults?

A

For select patients, tolvaptan (vasopressin receptor 2 antagonist) may be an option. NICE recommended it as an option for treating ADPKD in adults to slow the progression of cyst development and renal insufficiency only if:
they have chronic kidney disease stage 2 or 3 at the start of treatment
there is evidence of rapidly progressing disease

50
Q

What is Recessive PCKD?

A

Causes end stage renal failure in childhood, detected in prenatal USS or born and present with Potter’s Syndrome

51
Q

What rate should maintenance fluids be given ar?

A

30 ml/kg for a 24 hours period

52
Q

What are causes of acute tubular necrosis?

A

Ischaemia
Sepsis
Nephrotoxins- rhabdomyolitis, aminoglycosides, lead, contrasts

53
Q

What are signs of ATN?

A

Brown casts in urine

Raised urea, creatinine and potassium (=SIGNS OF AKI)

54
Q

What are the phases of ATN?

A

oliguric phase
polyuric phase
recovery phase

55
Q

How do you distingiush between pre renal AKI and ATN?

A 
PRE RENAL:
Low urine sodium(<20)
Good response to fluid challenge
High urine osmolality
Raised urea:cr ratio in blood
56
Q

What is acute interstitial nephritis?

A

Large cause of AKI

Interstitial oedema and inflitrate

57
Q

What causes acute interstitial nephritis (AIN)?

A

Most commonly drugs: penicillin, rifampicin, NSAIDs, allopurinol, furosemide
Systemic disease: SLE, sarcoidosis, and Sjögren’s
infection: Hanta virus , staphylococci

58
Q

How does AIN present?

A 
fever, rash (diffuse maculopapular), arthralgia
eosinophilia
mild renal impairment
hypertension
sterile pyuria
white cell casts
59
Q

What are Renal atherothrombus signs?

A

Livedo reticularis

White cell casts in urine

60
Q

What are addiotional features seen in PCKD?

A 
Hepatomegaly due to cysts
Large kidneys causing large volume occupied and therefore early satiety
Divertoculosis
Ovarian cysts
Intercranial aneurysms
61
Q

What does nephrotic syndrome increase the risk of generally and specific to kidneys?

A

Hypercoagulable state

Therefore renal vein thrombosis

62
Q

WHat constitutes hyperkalaemia?

A

> 6.5

If lower than this just do an ECG to assess

Nephrology & Urology (3 decks)

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