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Finals > Renal > Flashcards

Renal Flashcards

1
Q

What are the causes of CKD?

A 
Diabetes 
HTN
renal artery stenosis
SLE
glomerular diseases 
PCKD
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2
Q

How do the kidneys appear in CKD? When is that not the case?

A

bilaterally small

This is not the case in diabetics

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3
Q

What are the signs and symptoms of CKD?

A

polyuria (eventually progress to oliguria)
ankle oedema
itching
insomnia

anaemia: fatigue, SOB
bone disease: bone pain, fragility fractures
neuro: seizures
uraemia: N&V, cramps, anorexia

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4
Q

What are the stages of CKD?

A

1: >90 + need proteinuria or symptoms
2: 60-90 + need proteinuria or symptoms
3: 30-60
4: 15-30
5: <15 +will have uraemic symptoms

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5
Q

What blood results would you expect to see in CKD?

A 
normocytic normochromic anaemia
raised creatinine and urea
raised potassium
low eGFR
low calcium, high phosphate, high PTH
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6
Q

What is the management of CKD?

A

control risk factors i.e. good diabetes and HTN control
avoid nephrotoxic drugs
loop diuretics for oedema
eventually renal replacement therapy

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7
Q

How would you identify CKD patients with proteinuria?

A

albumin-creatinine ratio

This is a first pass morning urine sample

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8
Q

How is proteinuria in CKD managed? At what point for varying groups of CKD patients would you initiate this treatment?

A

ACE-I
if diabetic then ACR >3
if HTN then ACR >30
if no comorbidities then ACR >70

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9
Q

What can give a false +ve albumin-creatinine ratio?

A

UTI

recent exercise

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10
Q

Anaemia in CKD is what type of anaemia? At what eGFR would you expect the patient to start becoming anaemic?

A

normocytic normochromic

eGFR <35

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11
Q

Why does anaemia occur in CKD?

A
  • reduced EPO production
  • poor iron absorption
  • reduced intake due to anorexia seen with uraemia
  • reduced erythropoiesis as uraemia is toxic to marrow
  • increased RBC destruction due to HD
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12
Q

How is anaemia in CKD managed?

A

first optimise iron with IV iron infusion
then give EPO

(EPO will be useless if low iron)

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13
Q

How is HTN in CKD managed?

A

ACE-I (reduce filtration pressure so reduce workload)

furosemide to balance the potassium

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14
Q

What is the pathophysiology of CKD bone disease?

A
  1. reduced vit D (kidney unable to hydroxylate) and increased phosphate (kidney unable to actively excrete)
  2. reduced Ca
  3. raised PTH and osteomalacia
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15
Q

How is CKD related bone disease managed?

A

bisphosphonates if osteomalacia
Vitamin D
phosphate binders (Sevelamer is a non-calcium containing one that is used to stop calcium associated vessel calcification)

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16
Q

What are the hallmarks of an AKI?

A

uraemia - enough to cause symptoms

oliguria - <0.5ml/kg/hr

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17
Q

What are the causes of AKI?

A

PRE-RENAL:
hypovolaemia/shock
renal artery stenosis

RENAL:
nephrotoxic drugs
IV contrast
rhabdomyolysis
tumour lysis syndrome
vasculitis 
glomerulonephritis
POST-RENAL:
Stones 
BPH
strictures
tumours
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18
Q

Why is creatinine not a good marker for AKI in elderly?

A

they have a low muscle mass and so a low creatinine doesn’t necessarily mean their kidneys are not struggling

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19
Q

What blood results would you expect in AKI?

A

raised creatinine and urea

raised K

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20
Q

How (on bloods) do you differentiate between an acute and a chronic drop in kidney function?

A

the calcium

it only goes low in chronic disease

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21
Q

Compare the urea and creatinine in an AKI vs dehydration

A

AKI: +++creatinine
dehydration: +++urea

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22
Q

What would urine microscopy show in AKI?

A

pre-renal: hyaline casts
renal: muddy brown casts
post renal: red cell casts

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23
Q

Compare the urine sodium levels in pre-renal vs renal AKI. Why does this happen?

A

in pre-renal your kidney holds on to sodium in an attempt to increase intravascular volume therefore urine sodium is low

in renal the urine sodium is high

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24
Q

Compare the urine osmolality in pre-renal vs renal AKI

A

pre-renal: concentrated (trying to hold on to water)

renal: dilute

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25
Q

Compare the serum urea:creatinine ratio in pre-renal vs renal AKI

A

pre-renal: raised i.e. proportionally serum urea is high

renal: normal

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26
Q

What is the appearance of the urine in pre-renal vs renal AKI?

A

pre-renal: normal

renal: brown granular casts

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27
Q

When would someone be considered for renal replacement therapy?

A

Raised urea + symptoms or uraemia
Raised potassium
Metabolic acidosis
Pulmonary oedema

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28
Q

What are the complications of AKI?

A

Pulmonary oedema
Metabolic acidosis
Arrhythmias resulting from hyperkalaemia
uraemic symptoms e.g. seizures

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29
Q

What else could cause a raised urea?

A

GI bleed
high protein diet
increased protein catabolism i.e. fever, stress, steroids

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30
Q

What is fibromuscular dysplasia?

A

Stenosis and aneurysm of medium sized arteries

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31
Q

How would fibromuscular dysplasia present?

A

Young females
Slow onset CKD or HTN or they may present acutely following ACE-I initiation
Flash pulmonary oedema

32
Q

What would an MR angiogram of fibromuscular dysplasia show?

A

String on beads i.e. they artery is stenosed but with aneurysms

33
Q

Compare the presentation and urine dip results of HSP, IgA nephropathy and post-strep glomerulonephritis

A

HSP: young males with haematuria + purpuric rash over buttocks and extensors + joint pain

IgA nephropathy: young males, 1/2 days post strep infection with visible haematuria

post-strep: 1-2 weeks post strep infection, malaise, proteinuria (oedema) and visible haematuria, HTN

34
Q

What is Alport syndrome? How does it present on biopsy?

A

x-linked collagen defect leading to an abnormal glomerular basement membrane
There is splitting of the lamina densa of the GBM

35
Q

What are the signs and symptoms of alport syndrome?

A

renal failure
microscopic haematuria
bilateral sensorineural deafness
retinitis pigmentosa

36
Q

What is Goodpastures?

A

vasculitis

There are anti-glomerular basement membrane antibodies

37
Q

How does Goodpastures present?

A

glomerulonephritis (rapid onset AKI, proteinuria and haematuria)
pulmonary haemorrhage

38
Q

What is the management of Goodpastures?

A

steroids and plasma exchange

39
Q

What are the hallmark features of nephrotic syndromes?

A

proteinuria
hypoalbuminaemia
oedema
frothy urea

40
Q

How does the oedema in nephrotic syndrome compare to HF?

A

it is worse in the morning in nephrotic syndrome

41
Q

What are the causes of minimal change glomerulonephritis?

A

Hodgkins
Infectious mononucleosis
NSAIDs

42
Q

How is minimal change glomerulonephritis managed?

A
  1. steroids

2. cyclophosphamide

43
Q

What is an ADR of cyclophosphamide?

A

haemorrhagic cystitis

44
Q

What are some risk factors/associations with focal segmental glomerulonephritis?

A

Obesity
HIV
Heroin

45
Q

What are the causes of membranous glomerulonephritis?

A

Malignancy (prostate, lung, haematological)
Hepatitis, malaria, syphilis
SLE
Penicillamine given in Wilson’s disease

46
Q

Compare the pathophysiology (briefly) of the 3 types of nephrotic syndrome

A

minimal change: podocyte damage

focal segmental: fibrosis or glomerular tufts

membranous: thickened BM and sub epithelial deposits giving “spike and dome appearance”

47
Q

What are some complications of nephrotic syndrome?

A

Infections: lost immunoglobulins in urine
Thrombosis: lost protein C and S and antithrombin in urine
Anaemia
Hypocalcaemia
Reduced total T4

48
Q

How is nephrotic syndrome managed (aside from steroids/immunosuppression)

A

Heparin (due to being pro-thrombotic)
ACE-i
Fluid and salt control

49
Q

How is membranous glomerulonephritis managed?

A

ACE-I to reduce proteinuria

Steroids or cyclophosphamide

50
Q

What are the hallmark features of nephritic syndrome?

A

Haematuria and mild proteinuria
Hypertension
Raised creatinine

51
Q

What would make a UTI “complicated”

A 
Male
Catheter associated 
Renal pathology
Immunosuppressed
Abnormal organism
52
Q

How are UTI’s managed?

A

Uncomplicated: 3 days trimethoprim or nitrofurantoin
Lower complicated: 7 days of trimethoprim or nitrofurantoin
Upper complicated: 14 days ciprofloxacin

53
Q

How are UTI’s managed in pregnancy?

A

Nitrofurantoin until the third trimester

Cefalexin near term

54
Q

What channels and where in the kidney do the various diuretics work on?

A

Loop: NKCC2 in the loop of henle
Thiazide: sodium-chloride cotransporter in early DCT
Aldosterone antagonists: eNaC in late DCT and CD

55
Q

What are the side effects of loop diuretics?

A 
(hypotension, AKI)
Hypokalaemia 
Hypocalcaemia 
Gout
Ototoxic
Glucose intolerance
56
Q

What are the side effects of thiazide diuretics?

A 
(hypotension, AKI)
Hypokalaemia
Hypercalcaemia
Gout
Glucose intolerance 
pancreatitis 
thrombocytopenia
57
Q

What are the side effects of aldosterone antagonists?

A

(hypotension, AKI)
Hyperkalaemia
Gynecomastia

58
Q

How does ADPKD present?

A

Haematuria
Flank pain
Recurrent UTI
HTN

NOT ANAEMIA (EPO production preserved)

59
Q

What are the extra-renal complications of ADPKD?

A 
berry aneurysms
Liver cysts
mitral regurg/prolapse 
aortic root dilation and dissection 
Abdominal wall hernias
60
Q

What should you consider in persistent sterile pyuria with persistent negative urine cultures?

A

Renal TB

61
Q

How long does an AV fistula take to mature?

A

4-8 weeks

62
Q

What are the pros and cons of HD?

A

+ Not responsible
+ Get days off
+ Can be done in emergency through CVC

  • unsightly fistula
  • risk of haemorrhage
  • risk of thrombosis
  • multiple days in hosptial/week
  • air embolus
  • anaphylactoid reaction to dialysis fluid
  • steal syndrome (cold, crampy extremities)
63
Q

What are the pros and cons of PD?

A

+ Can do it at home
+ No needles
+ Less long term CVS risk as constantly dialysed

  • risk of peritonitis
  • obesity (due to ++glucose in dialysis fluid)
  • pleural effusion
  • hernias
  • you’re responsible
  • peritoneal membrane eventually fails
64
Q

What would indicate someone was underdialysed?

A

insomnia
itching
fatigue
sensory neuropathy and restless legs

65
Q

What are some complications of a renal transplant?

A 
Thrombosis 
Urine leakage 
UTIs
ATN of the graft
Side effects of the anti-rejection medications
66
Q

Describe a hyperacute renal transplant rejection (timing, reason, management)

A

Within minutes to hours
Due to ABO or HLA incompatibility which causes thrombosis of the graft vessels
Need to remove the graft

67
Q

Describe an acute renal transplant rejection (timing, reason, presentation, management)

A

<6 months
HLA mismatch or CMV infection
Rise in creatinine, fevers, graft pain
High dose methylprednisolone

68
Q

Describe a chronic renal transplant rejection (timing, reason, presentation)

A

> 6 months
Recurrence of the underlying pathology or fibrosis
Gradual rise in creatinine and protein

69
Q

What are the causes of rhabdomyolysis?

A 
Long lie
Crush injury
Seizure
Ecstasy 
Statins when given with clarithromycin
70
Q

How does rhabdomyolysis present? (in terms of blood results and blood gas)

A

AKI with +++ creatinine
Raised K, phosphate
Low calcium

Metabolic acidosis

71
Q

How is rhabdomyolysis managed?

A

Fluids

urinary alkalanisation

72
Q

What is acute interstitial nephritis?

A

A cause of AKI where there is interstitial oedema and infiltrate

73
Q

How does acute interstitial nephritis present?

A

Fever, malaise and arthralgia
rash
mild renal impairment
eosinophilia

74
Q

What are the causes of acute interstitial nephritis?

A

Drugs:

  • penicillin
  • NSAIDS
  • allopurinol
  • furosemide

SLE and sarcoid

75
Q

What characteristic urine and blood results are seen in acute interstitial nephritis?

A

Sterile pyuria
White cell casts
Eosinophilia

Finals (16 decks)

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