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Pocket MSRA - Book 1 > Nephrology > Flashcards

Nephrology Flashcards

1
Q

What is an AKI?

A

Potentially reversible acute decline in kidney function, measured by creatinine and urine output

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2
Q

What are the KDIGO criteria for stage 1 AKI?

A

Cr increase >26 w/i 48hrs OR Cr increase >1.5-2x baseline
Urine output <0.5ml/kg/hr for 6 consecutive hours

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3
Q

What are the KDIGO criteria for stage 2 AKI?

A

Cr increase >2-3x baseline
Urine output <0.5ml/kg/hr for 12 consecutive hours

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4
Q

What are the KDIGO criteria for stage 3 AKI?

A

Cr increase >3x baseline OR Cr increase >354 OR requiring RTT
Urine output <0.3ml/kg/hr for 24hrs OR anuric >12hrs

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5
Q

How does AKI present?

A

Uraemia
Acidosis
Hyperkalaemia
Fluid overload
Anuric

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6
Q

What risk factors are there for AKI?

A

Old patients
Volume depletion
Cardiac failure
Nephrotoxic medications
Iodine contrast
Systemic illness

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7
Q

What are the three types of AKI?

A

Pre-renal (66%)
Renal (20%)
Post-renal

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8
Q

How can the causes of a pre-renal AKI be classified?

A

Volume depletion
Systemic vasodilation
Intrarenal vasoconstriction
Fluid redistribution

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9
Q

What is the main sequelae of un-treated pre-renal AKI?

A

Acute tubular necrosis

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10
Q

How can the causes of a renal AKI be classified?

A

Glomerular
Interstitial disease
Tubular disease
Vascular disease

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11
Q

What are the glomerular causes of a renal AKI?

A

GPA/SLE
Anti-GBM
Post-strep

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12
Q

What are the tubular causes of a renal AKI?

A

Nephrotoxics - NSAIDs, PPIs, cephalosporins, penicillins
EBV/CMV/HIV
Sarcoid
Allergic

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13
Q

What are the vascular causes of a renal AKI?

A

RV thrombosis
Scleroderma
Atheroembolic disease
Shock
HUS
TTP
Vasculitis

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14
Q

How can the causes of a post-renal AKI be classified?

A

Intrarenal
Bilateral tract
Urethral obstruction
Others - TB, post-op, neuropathy

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15
Q

What are the intrarenal causes of a post-renal AKI?

A

Light chain precipitation
Urate sludge
Tumour lysis

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16
Q

What are the bilateral tract causes of a post-renal AKI?

A

Stones
Retroperitoneal fibrosis
Papillary necrosis

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17
Q

What are the urethral obstruction causes of a post-renal AKI?

A

Post valve
Retroperitoneal fibrosis
BPH
Prostate ca
Urethral strictures

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18
Q

How should AKI be investigated?

A

Pre-renal - BP, volume status
Renal - urine dip
Post-renal - USS + bladder scan

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19
Q

What are the options for imaging the kidneys?

A

USS - 1st choice
CTKUB - no contrast, pick up stones
CTU - contrast, not-effective if eGFR low

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20
Q

How can a pre-renal AKI be distinguished from ATN?

A

Pre-renal - lower urinary Na and Urea, higher urine osmolality
ATN - higher urinary Na, urinary/plasma osmolality equal, urinary casts

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21
Q

How should an AKI be managed?

A

A-E
Stop DAMN (diuretics, ACEi/ARB, metformin, NSAIDs)
Treat reversible cause
Monitor UO (catheter)
Dialysis

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22
Q

When should dialysis be considered in AKI?

A

AEIOU
Acidosis (pH <7.2)
Electrolytes (refractory K+ >6.5)
Intoxication (poisoning e.g. Aspirin)
Oedema (pulmonary)
Uraemia (encephalopathy, pericarditis)

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23
Q

What is nephrotic syndrome?

A

Heavy proteinuria causing hypoalbuminaemia and oedema

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24
Q

How does nephrotic syndrome present?

A

Polyuria
Polydipsia
Frothy urine
Oliguria/anuria
SOB/fatigue (pulmonary oedema)

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25
Q

What are the potential complications of nephrotic syndrome?

A

Infection
Hypercoagulability (VTE)
Hypocalcaemia

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26
Q

What is the management of nephrotic syndrome?

A

Na/fluid restrict
Diuretics
LMWH
Trial steroids - if no response –> biopsy

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27
Q

What are the histopathological classifications of 1o nephrotic syndrome?

A

Minimal change
Membranous nephropathy
Focal segmental glomerulosclerosis (FSGS)

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28
Q

What are the risk factors for minimal change nephrotic syndrome?

A

Hodgkin’s lymphoma
NSAIDs
Common in children
Prev. episodes (2/3 recur)

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29
Q

What is the treatment for minimal change nephrotic syndrome?

A

Steroids (80% respond) –> cyclophosphamide if resistant

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30
Q

What is the outcome for minimal change nephrotic syndrome?

A

1/3 1x episode
1/3 infrequent recurrence
1/3 frequent recurrence

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31
Q

What is the treatment for membranous nephrotic syndrome?

A

Combination steroid + cyclophosphamide

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32
Q

What are the 2o causes of nephrotic syndrome?

A

Infection (bacterial, parasitic)
Immune/inflammatory (SLE, RA)
Metabolic (DM)
Malignant
Drugs (NSAIDs, penicillamine, heroin etc.)
Toxins
Pregnany
Transplant rejection

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33
Q

What is the treatment for FSGS?

A

Combination steroid + cyclophosphamide
Often causes ESRF

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34
Q

What are the 5 stages of diabetic nephropathy?

A

1 - Hyperfiltration (increase eGFR)
2 - Silent stage (early histological change)
3 - Incipient nephropathy/microalbuminuria (30-300mg/24hr)
4 - Overt nephropathy/persistent proteinuria. eGFR decline/HTN
5 - ESRF

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35
Q

What are the presenting features of nephritic syndrome?

A

Haematuria
Reduced eGFR
Oliguria
Uraeia
Fluid retention
HTN –> headache, LVH

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36
Q

What are the causes of nephritic syndrome?

A

Post infection w/ Group A Strep (proliferative)
Infections (bacterial, viral, parasitic)
Immune/inflammatory (RA, SLE)

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37
Q

What is IgA Nephropathy?

A

Most common form of idiopathic glomerulonephritis leading to CKD

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38
Q

What are the risk factors for IgA Nephropahty?

A

Commonly occurs post URTI
Coeliac disease
Young patients
Male

39
Q

What is Haemolytic Uraemic Syndrome?

A

Most common cause of AKI in paeds
Triad of
-thrombocytopenia
-AKI
-microangiopathic haemolytic anaemia (Coomb’s negative)

40
Q

What are the risk factors for HUS?

A

Post e.coli infection (0157:H7)
Tumours
Pregnancy
Ciclosporin
SLE
HIB

41
Q

How should HUS be managed?

A

Supportive therapy only
No need for a/b

42
Q

What is tubulointerstitial nephritis?

A

Inflammation of renal interstitium

43
Q

What are the causes of tubulointerstitial nephritis?

A

Drugs (nephrotoxics, abx - Pen, Rifampicin)
Infections (staph, strep, CMV/EBV)
Immune
Chronic TIN fibrosis 2o reflux/DM

44
Q

How does tubulointerstitial nephritis present?

A

Polyuria
Nocturia
Polydipsia
Glycosuria
Urticaria
Fever
Arthralgia

45
Q

How is tubulointerstitial nephritis treated?

A

Stop offending drugs
Fluids
Prednisolone

46
Q

What is renal tubular acidosis?

A

Acidaemia 2o failure of kidneys to form acidic urine

47
Q

What are the two types of renal tubular acidosis?

A

Distal
-most common
-unable to excrete H+
Proximal
-unable to resorb HCO3-

48
Q

What are the risk factors for distal RTA?

A

1o
Marfan’s
SLE
Sjogren’s

49
Q

What are the risk factors for proximal RTA?

A

Sjogren’s
Myeloma
Nephrotic syndrome
Wilson’s disease

50
Q

How does RTA present?

A

Polyuria
Acidotic
Arrhythmias (K+)
Renal calculi
Muscle weakness

51
Q

What is polycystic kidney disease?

A

Most common inherited cause of renal disease

52
Q

What is the inheritance pattern of PKD?

A

Autosomal dominant
High/complete penetrance

53
Q

What are the two types of PKD?

A

Type 1 - Chromosome 16 (80%)
Type 2 - Chromosome 4

54
Q

How dose PKD present?

A

Typically w/ complications
Loin pain
Palpable kidneys
Gross haematuria (following trauma)
UTI
Stones
ESRF - 70% by 70y/o

55
Q

What are the extrarenal manifestations of PKD?

A

HTN
Infertility
Liver cysts
Mitral valve prolapse/aortic root dilation –> aortic dissection
Berry aneurysm –> SAH

56
Q

How is PKD diagnosed?

A

Imaging - USS/CT
If <30 - FHx +ve and 2 cysts
If 30-59 - 2 cysts both kidneys
If >60 - 4 cysts both kidneys

57
Q

What is the management of PKD?

A

Counselling/risk factor modification
MRA screen for berry aneurysm
STatin/Aspirin
Laparoscopic cyst removal
ESRF (50%)

58
Q

What is CKD?

A

Abnormal kidney function/structure
Diagnosis based on reduced function/evidence kidney damage

59
Q

What are the stages of CKD?

A

1 - eGFR >90 (but proteinuria)
2 - eGFR 60-90 (but proteinuria)
3 - eGFR 30-59
4 - eGFR 15-29
5 - eGFR <15

60
Q

How is CKD diagnosed?

A

eGFR measurements + proteinuria
2 values at 3/12

61
Q

How is CKD managed?

A

Slow progression (BUPA)
-blood pressure control
-underlying illness control
-protein intake
-avoid obstruction/dehydration/infection/nephrotoxics

62
Q

What is the first line drug for BP control in CKD?

A

ACE inhibitors

63
Q

What are the contraindications for ACEi in CKD?

A

Fixed renal aa stenosis
Pregnancy
Oligohydramnios
Prev. hypersensitvity/angioedema

64
Q

What are the complications of CKD?

A

Anaemia
Bones - fractures, deformity, 2o hyperparathyroidism
CVD
Drug-related side effects (reduced excretion)
Emotional dysregulation (sexual dysfunction)
Fluids (Pulmonary oedema –> IV Furosemide)
Growth restriction
HTN
Immunosuppression
Joint problems
Killed by kidneys (death)
Legs restless (Clonazepam)

65
Q

What are the options for RRT?

A

Haemodialysis
Peritoneal dialysis
Renal transplant

66
Q

Describe the structure of haemodialysis

A

3 treatments/week
3-5hrs/treatment
Done at hospital/satellite site
Requires AVF

67
Q

Describe the structure of peritoneal dialysis

A

Ambulatory exchange/exchange episodes t/o day
8hr exchange o/n (8-20L)
Requires peritoneal catheter insertion

68
Q

When is peritoneal dialysis considered preferable?

A

1st 2 years of dialysis (preserves renal function)
Haemodynamic instability
Poor veins

69
Q

What are the advantages of peritoneal dialysis?

A

Flexibility
No diet restriction/needles

70
Q

What are the negative aspects of haemodialysis?

A

Fixed schedule
Travel to hospitals
Permanent access/recurrent needle sticks
Diet/fluid restriction
Haemodynamic instability
AVF creation

71
Q

What are the common problems w/ arterio-venous fistulas?

A

Formation (takes 6-8/52 to mature)
Infection
Thrombosis
Stenosis
Steal syndrome

72
Q

What is steal syndrome?

A

Distal ischaemia 2o insertion of AVF
-blood preferentially flows through AVF

73
Q

What are the potential complications of haemodialysis?

A

Sepsis
Blood loss
Infective endocarditis
Disequilibration syndrome
Bioincompatability (interaction b/w machines and blood)

74
Q

What is Disequilibration syndrome?

A

Neurological sx post dialysis
-confusion
-headache
-dizziness
-coma
-convulsions

75
Q

What are the contraindications to peritoneal dialysis?

A

Major intrabdominal problems (e.g. adhesions)
Poor motivation/hygiene
Emactiona
COPD
Stoma in-situ

76
Q

What are the potential complications of peritoneal dialysis?

A

Hernia
Encapsulating peritoneal sclerosis
Infection/blockage
PD peritonitis

77
Q

What virology needs checking prior to renal transplant?

A

CMV
HCV
HBV
HIV
VZV
EBV

78
Q

What is the prognosis post renal transplant?

A

Best prognosis of RRT
95% survival 1yr, 90% graft survival
15yr graft srvival

79
Q

What are the potential complications of renal transplant?

A

Bleeding
Graft thrombosis
Infection
Leaks
Rejection

80
Q

Describe hyperacute transplant rejection

A

Minutes-hrs
Type II HR (IgG)
Causes vessel thrombosis

81
Q

Describe acute transplant rejection

A

<6/12
Type IV HR (T-cell)
Treated w/ steroids/immunosuppression

82
Q

Describe chronic transplant rejection

A

> 6/12
Antibody/cell fibrosis to kidney (chronic allograft nephropathy
Recurrence of CKD

83
Q

How should prescribing in CKD change?

A

Consider reducing maintenance dose (reduced metabolism/excretion)
Increase doses of diuretics/renally acting drugs
Reduce doses of nephrotoxics

84
Q

What are the causes of Hypokalaemia?

A

Reduced intake
Excessive losses (sweating, GI, endocrine, renal)
Transcellular shifts

85
Q

How does Hypokalaemia present?

A

Cramps
Tetany
Weakness
Palpitations (arrhythmias)
Nephrogenic Diabetes insipidus

86
Q

How should Hypokalaemia be managed?

A

Mild - Sando K+, K+ sparing diuretics
Severe - IV K+
Magnesium

87
Q

What are the causes of Hyperkalaemia?

A

Excess intake (TPN, a/b, idiopathic, blood transfusion)
Reduced losses (addisons, ACE-i, spironolactone, AKI)
Transcellular shift (acidosis, haemolysos, rhabdomyolsis)

88
Q

How does Hyperkalaemia present?

A

Palpitations/arrhythmias
Cardiac arrest

89
Q

How shoulder Hyperkalaemia be managed?

A

Stop nephrotoxics
Calcium gluconate (10ml 10% IV)
Salbutamol nebs
50ml 50% IV Dextrose
Actrapid 10 units
Calcium resonium - non-invasive, takes days
Haemodialysis

90
Q

When should haemodialysis be considered for Hyperkalaemia?

A

If K+ >7 (esp. if ECG changes) OR refractory

91
Q

How is anion gap calculated?

A

(Na + K) - (Cl + HCO3)

92
Q

What are the causes of a non-anion gap metabolic acidosis?

A

GI loss of HCO3- (diarrhoea)
Saline infusion (hyperchloraemic metabolic acidosis)
Chronic pancreatitis
Renal tubular acidosis

93
Q

What are the causes of a high anion-gap metabolic acidosis?

A

Lactic acidosis
Ketoacidosis e.g. DKA
Alcohol (methanol toxicity, ketoacidosis)
Iron toxicity/Isoniazid
Salicylate toxicity
Ethanol/ethylene toxicity
Renal causes

Pocket MSRA - Book 1 (7 decks)

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