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Fifth Year Medicine > Renal > Flashcards

Renal Flashcards

1
Q

Stages of CKD?

A 
Stage 1- eGFR >90 if other kidney damage
Stage 2- eGFR 60-89 if other kidney damage
Stage 3- eGFR 30-59
Stage 4- eGFR 15-29
Stage 5- Less than 15, renal failure
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2
Q

Causes of an enlarged kidney

ballotable, moves with respiration

A

Renal carcinoma, nephroblastoma
Hydronephrosis
Pyonephrosis, abscess
Polycystic disease

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3
Q

How does the urea and creatinine ratio in the blood indicate dehydration status?

A

If urea: creatinine is more than 20:1, suggests hypoperfusion or dehydration as urea reabsorption is increased as the urine flows very slowly through the tubules. Creatinine doesn’t get reabsorbed at all so it remains normally excreted at a constant rate.

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4
Q

What does a low urea:creatinine ratio indicate? (

A

Renal damage, as reabsorption of urea is less able to be absorbed

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5
Q

What is the normal albumin creatinine ratio?

A

Men

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6
Q

What causes microalbuminaemia?

A

Diabetes mellitus
Hypertension
Minimal change glomerulonephritis

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7
Q

When would you refer a patient with asymptomatic microscopic haematuria under 40 years?

A

If BP >140/90

EGFR

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8
Q

What will cause a false negative on a urine dip when checking bilirubin?

A

Urine not fresh

Rifampicin (TB)

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9
Q

How may an AKI be diagnosed?

A

Creatinine increase of 26umol/48hours
Creatinine increase 1.5x baseline
Urine output

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10
Q

How is AKI staged with reference to serum creatinine?

A

1- increase of 26umol in 48 hours or 1.5x baseline
2- increase 2-2.9x baseline
3. Increase 3x baseline or >354 umol or on renal replacement therapy

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11
Q

How is AKI staged according to urine output criteria?

A

1-

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12
Q

Risk factors for AKI?

A

Age >75
Urinary symptoms
Poor intake/increased losses
Sepsis

PMH: CKD, liver failure, heart failure
Peripheral vascular disease
Diabetes

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13
Q

Which hypertensive drug is commonly implicated in AKI caused by renal hypoperfusion?

A

ACE-inhibitors

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14
Q

Name three things that may cause acute tubular necrosis leading to an AKI;

A
  1. Aminoglycosides
  2. Contrast
  3. Myoglobunuria (rhadbdomyolysis)
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15
Q

Which things can cause crystal damage to tubules leading to an AKI? Name 4

A

Ethylene glycol poisoning
Uric acid (gout)
Calcium
Myeloma

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16
Q

What size kidney on USS would suggest chronic damage?

A
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17
Q

Indications for renal replacement therapy related to metabolic abnormalities?

A 
Persistent hyperkalaemia (above 7mmol)
Severe metabolic acidosis (pH40mmol) causing pericarditis- pericardial rub or encephalopathy
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18
Q

In likely AKI which drugs should be stopped?

A

NSAIDs
ACE inhibitors
Gentamycin (aminoglycoside)
Amphotericin (antifungal)

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19
Q

When should metformin be stopped in rising creatinine levels?

A

As creatinine goes over 150mmol/L

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20
Q

What volume of fluid do you prescribe for a patient with AKI if it can be determining on an hourly or daily basis?

A

Hourly output + 25mL/h for insensible losses

Daily output + 500mLs for insensible losses

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21
Q

What are the pros and cons of haemodialysis vs haemofiltration?

A

Haemodialysis is faster, but needs patient to be haemodynamically stable

Haemofiltration is less likely to drop BP, as fluid shifts are less significant but is slower so done continuously

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22
Q

Hyperkalaemia ECG changes?

A 
Normally K+ rushes out of cells to repolarise, if outside levels are high the gradient is less steep so movement is slower and HR is slower.
Tall tented T waves
Small absent P wave
Longer PR interval
Widened QRS
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23
Q

Rx of an ECG with tall tented T waves?

A

10mL of 10% calcium gluconate IV via big vein (cardioprotective)
IV insulin + glucose
Salbutamol NEB (but needs high doses, get tachycardic)

Buy time: definitive is correct the cause or dialyse

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24
Q

How long do you need impaired renal function for to classify a CKD?

A

3 months- with abnormal structure or eGF

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25
Q

How low does your eGFR have to be for 3 months for a diagnosis of CKD without structural abnormality?

A
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26
Q

What symptoms occur with rising urea levels?

A

Vomiting, anorexia
Restless legs
Fatigue, weakness
Pruritis, bone pain

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27
Q

What can cause a chronically damaged kidney to look large rather than small and fibrosed on ultrasound?

A

Infiltration: amyloid, myeloma
Adult polycystic kidney disease
Diabetes mellitus

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28
Q

When would you think about biopsying a kidney in impaired function?

A

If rapidly progressive disease

Unclear cause + normal sized kidneys

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29
Q

What are the stages of CKD?

A 
GFR values
1. >90 with evidence of other renal damage
2. 60-89
3a. 45-59
3b. 30-44
2. 15-29
1.
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30
Q

In stage 1 kidney disease, GFR may be >90 with evidence of kidney damage, what might that evidence be?

A

Proteinuria, haematuria

Abnormal anatomy

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31
Q

Target BP if
A. Having CKD
B. Has CKD + diabetoc
C. Has CKD + proteinuria (ACR>70)

A

A.

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32
Q

Rx for renal bone disease?

A

Calcichew = binder to reduce gut absorption of PO4-
Vit D analogues
Ca2+ supplements = reduce high PTH and bone disease

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33
Q

For those with CKD what can you give to reduce progression in patients with
A. Diabetes
B. Cardiovascular disease (IHD)

A

A. ACEi or ARB even if BP is normal

B. If lipids are raised, statin

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34
Q

CI to kidney biopsy

A

Abnormal clotting, current neoplasms
BP> 160/>90
CKD with kidneys

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35
Q

Name some drugs that are renally excreted and may accumulate in renal failure?

A 
Aminoglycosides (gentamycin) + cephalosporin
Heparin
Lithium
Opiates
Digoxin
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36
Q

What substance accumulating in dialysis can lead to carpal tunnel syndrome, arthralgia and fractures?

A

Amyloid

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37
Q

What is the difference in presentation of IgA nephropathy Vs post-strep glomerulonephritis?

A

IgA tends to be young man, haematuria whilst having a sore throat
Post-strep tends to be 1 month after a sore throat or skin infection

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38
Q

Difference between IgA nephropathy and post-strep glomerulonephritis on histology?

A

IgA nephropathy- mesangial proliferation (+ IgA deposition)

Post-strep- mesangial + endothelial proliferation (IgG deposits)

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39
Q

Name the nephritic syndromes:

A

A Hen SLEeps in the Pastures after the MeAn cock is aggressive

IgA nephropathy (sore throat)
Henoch Schonlein (purpuric rash)
SLE (anti- smith, anti dsDNA)
Goodpastures (anti GBM)
Post strep (1 month after skin/throat infection)
Mesangiocapillary (tramlines, via complement of immune complex)
Rapidly progressive (crescents)

40
Q

In Goodpasture’s disease, what type of collagen is the antibody against?

A

Type IV in basement membranes of lungs and kidney

41
Q

Which diseases are associated with immune complex deposition leading to mesangiocapillary glomerulonephritis?

A

Hepatitis C
SLE
Gammopathies (including myeloma)

42
Q

What retinal changes may be observed in someone with mesangiocapillary glomerulonephritis?

A

Drusen (yellow white spots)

In complement mediated Mesangiocapillary glomerulonephritis

43
Q

On a renal biopsy what causes tram-lining of the glomerulus? (A clear circumferential gap around the outside

A

Mesangiocapillary glomerulonephritis

44
Q

Which glomerulonephritidies would you consider giving IV cyclophosphamide as Rx for?

A

SLE (with high dose prednisolone)
Mesangiocapillary (if rapidly reducing eGFR)
Rapidly progressive GN

45
Q

Which glomerulonephritidies would you give ACEi in?

A

Henoch-Schonlein Purpura (IgA- small vessel vasculitis)
IgA nephropathy
Mesangiocapillary GN

46
Q

Which glomerulonephritidies would you consider plasma exchange for?

A

Goodpasture’s (get rid of the anti-GBM)

Rapidly progessive GN (crescents on biopsy)

47
Q

Causes of nephrotic syndrome

A

It’s not gunan taken, a minimal change, to remember + get it all in my BRANE, exams so MeAN, I gotta FOCUS, after all this, gunna have SCLEROSIS (be scarred), or diabetes, since I have no SLEep, Amyloid any HElP?

Primary: Minimal change, membranous nephropathy, mesangiocapillary GN, focal segmental glomerulosclerosis

Secondary: diabetes, SLE, amyloid, Hep B/C, drugs

48
Q

Which drugs may cause nephrotic syndrome?

A

NSAIDs
Anti-TNF (rheumatoid, IBD, ank spond, psoriasis)
Gold (rheumatoid)
Penicillamine (rheumatoid, Wilsons)

49
Q

Causes of rapidly progressive glomerulonephritis?

A
  1. Immune complex: post-infectious, SLE, IgA, Henoch
  2. Pauci-immune: Wegener’s (c-ANCA, saddle shaped nose)
    Microscopic polyangiitis (p-ANCA)
    Churg-strauss (rhinitis/asthma, p-ANCA)
  3. Goodpastures (anti-GBM)
50
Q

How is suspected Henoch-Schonlein glomerulonephritis confirmed?

A

Immunofluorescence of skin or renal biopsy shows C3 and IgA

Same as IgA nephropathy

51
Q

What proportio of those with IgA nephropathy develop end stage renal failure in their life?

A

20%

52
Q

What serology findings might occur in post-strep glomerulonephritis?

A

Anti-streptolysin O

Also C3 may be raised

53
Q

Differential of nephrotic syndrome?

A

Congestive cardiac failure- raised JVP, pulmonary oedema, mild proteinuria

Liver failure- low albumin

54
Q

What clinical features suggest a child with seeming nephrotic syndrome does not have minimal change?

A

PC:

55
Q

What are the difficulties of renal biopsy in an adult with nephrotic syndrome?

A 
Grossly oedematous (no albumin)
Hypercoagulable (increased clotting factors, liver response to low oncotic pressure)
56
Q

What happens to cholesterol levels in nephrotic syndrome?

A

Cholesterol increases, may be >10mmol/L

Due to liver response to low oncotic pressure trying to compensate

57
Q

Rx for frequently-relapsing or steroid-dependent disease in nephrotic syndrome?

A 
Cyclophosphamide
Or Ciclosporin (gum hypertrophy)/ tacrolimus
58
Q

What type of nephrotic syndrome do patient with renal transplant get?

A

Focal segmental glomerulosclerosis

59
Q

Site of action of loop diuretics?

A

Block Na+/K+/2Cl- cotransporter in thick ascending limb

60
Q

What ABG picture does loop diuretics give?

A

Hypokalaemic metabolic alkalosis (less ion uptake, includes H+ and K+)

61
Q

Where do thiazide diuretics act?

A

Na+/Cl- transporter in the distal convoluted tubule

62
Q

Which type of diuretic (loop or thiazide) increases urine calcium excretion?

A

Loop- can be used in severe hypercalcaemia

Thiazide increases Ca uptake, so in patient’s with hypercalcaemia, it reduces stone formation

63
Q

Why do thiazide diuretics increase likelihood of gout?

A

They reduce uric acid excretion (more reabsorbed)

64
Q

Old man has muscle ache after falling and being on the floor for some hours, plasma CK comes back >1000. What needs to be excluded?

A

Myocardial infarction (via troponin)

65
Q

What combination of dipstick and microscopy findings suggest cola-coloured urine is due to rhabdomyolysis?

A

Dipstick +ve blood

Microscopy no RBCs (all been turned into myoglobin)

66
Q

Complications of rhabdomyolysis?

A

Hyperkalaemia
AKI- from myoglobin (may use IV NaCO3 to alkinize urine and prevent the toxic form of myoglobin forming)
DIC
Compartment syndrome from muscle injury

67
Q

What Rx can be given in rhabdomyolysis to reduce myoglobin toxicity damaging the kidney and causing an AKI?

A

IV sodium bicarbonate to alkalinize urine to pH >6.5 which stabilised the less toxic form
Maintain urine output at 300mL/hr

68
Q

Patient is recently started on antibiotics, they are noted to have a rising GFR, fever and rash. Renal biopsy shows inflammatory infiltrate in the interstitium. Diagnosis?

A

Acute interstitial nephritis- eosinophilic inflammation of tissue between the tubules in response a new drug starting

69
Q

Commonest cause of haemolytic uraemic syndrome?

A

E Coli 0157 (often after undercooked meat)

PC: abdo pain, bloody diarrhoea, AKI
Low Hb, low platelets, blood/protein on dip

70
Q

Cause of thrombotic thrombocytopenic purpura?

A

Deficiency in ADAM13 protease needed to cleave von Willebrand factor = vWF multimers, platelet aggregation and fibrin deposition

71
Q

Rx of thrombotic thrombocytopenic purpura?

A

Plasma exchange
Steroids
? Ecluzumab (targets C5 pathway)

72
Q

How often should you check diabetics for microalbuminaemia?

A

Yearly- sign of CKD

73
Q

Volume of albumin excreted in 24 hours in a diagnosis of microalbuminaemia?

A

30-300mg

74
Q

What are the USS criteria for diagnosing autosomal dominant polycystic kidney disease by age?

A

18-39 years = >3 cysts in total across both kidneys
40-59 years = >2 cysts in each kidney
>60 years = >4 cysts in each kidney

75
Q

What extrarenal structural abnormalities are associated with polycystic kidney disease?

A

Intra-cranial aneurysm (risk of sub-arachnoid haemorrhage)
Liver + ovarian cysts
Mitral valve prolapse

76
Q

Which type of polycystic kidney disease more typically presents in infancy?
What is ti associated with?

A

Autosomal recessive PCK

Associated with congenital hepatic fibrosis

77
Q

Which neuroectodermal syndromes are associated with renal cysts?

A 
Tuberous sclerosis (angiofiroma, epilepsy, periungual fibroma)
Von hippel-lindau (phaeochromocytoma, cranioangiomas, renal + pancreatic cysts, RCC)
78
Q

Deaf child has been getting haematuria, what rare syndrome could it be?

A

Alport’s: leads to focal segmental glomerulosclerosis

May also get ocular defects- bulging lens capsule on slit lamp

79
Q

Inheritance and cause of Alport’s syndrome?

A

X-linked mutation in the a5 chain of type IV collagen

Associated with sensorineural deafness, ocular defects and kidney disease

80
Q

What complication are children with alport’s syndrome at risk of after a kidney transplant?

A

Goodpasture’s disease (anti-GBM) as Alport’s is due to a mutation in type IV collagen, so may form anti-GBM antibodies

81
Q

In diabetics, what in source of the damage to the kidneys in pathological terms?

A

Glycosylation of proteins from high glucose levels that is not mediated by enzymes triggers an inflammatory response and deposition of collagen.

82
Q

What kind of kidneys can you only ever feel?

A

Polycystic kidneys that are HUGE or if they’ve had a transplants

(Ballot through abdomen palpation)

83
Q

Which nerve roots carry kidney pain from the capsule or parenchyma?

A

T10-L1 nerve roots

84
Q

How big is a kidney typically on ultrasound?

A

10-12cm

85
Q

First imaging modality if kidney damage is suspected?

A

Ultrasound to determine whether’s it’s an acute or chronic condition (will be shrunken with fibrosis)

86
Q

MRI is good for looking at what component of the kidney?

A

The vasculature, ie renal artery stenosis

Kidney will look smaller if artery is stenosed

87
Q

What kind of hormones do the kidneys break down?

A

Insulin and parathyroid hormone

88
Q

What kind of pH abnormalities does kidney failure cause?

A

Metabolic acidosis- as no longer excreting hydrogen ions

Will breath fast to compensate

89
Q

What tests indicate nephrotic syndrome?

A

HOP
Serum albumin (low)
Oedema (examination)
Proteinuria (urine dipstick/ ACR)

90
Q

What immunoglobulin gets deposited on the membrane in membranous glomerulopathy?

A

IgG

91
Q

What is the pathology of tubular necrosis?

A

When the epithelial cells lining the tubules slough off

Causes an AKI

92
Q

What is the difference between a high creatinine and a high creatinine kinase?

A

Creatinine indicates kidney injury

Creatinine kinase is an enzyme released from muscle damage ie in rhabdomyosis

93
Q

What part of the metabolism of vitamin D does the kidney do?

A

It hydroxlates the 1st carbon on 1,25 dihydroxy vitamin D3

94
Q

How does tertiary hyperparathyroidism occur in CKD and how is it treated?

A

Secondary hyper-PTH leads to autonomous production by the PTH gland
Driving it is raised phosphate (not excreted), low vit D3 and low Ca2+ (from no VitD)

95
Q

Standard medical treatment for CKD?

A 
Sodium bicarbonate- metabolic acidosis (from failure to excrete H+)
Antihypertensives
Diuretics (fluid retension)
Phosphate binders (reduce high PTH)
VitD3 analogs
Erythropoetin

Fifth Year Medicine (32 decks)

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