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YR6 Rotations > Renal > Flashcards

Renal Flashcards

1
Q

What are the 2 main types of dialysis?

A

Haemodialysis
Peritoneal dialysis

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2
Q

What is required for haemodialysis?

A

Dialysis machine (patient’s blood is pumped OUTSIDE body through this machine)

Vascular access is required via an AV fistula (longterm), or a temporary CVC

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3
Q

What happens inside a haemodialysis machine (broadly)?

A

Blood flows through tiny semi-permeable tubes surrounded by a dialysis solution (dialysate)
Filtration occurs via osmosis + diffusion- dialysis fluid contains solutes at a similar level to the level they would be in a healthy patient’s blood
Can add bicarbonate (to combat acidosis), EPO + drugs if needed
Heparin always added

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4
Q

How often should haemodialysis be performed?

A

4h treatment 3x per week

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5
Q

How many weeks does an AV fistula take to mature?

A

6-8w

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6
Q

How does peritoneal dialysis work?

A

Dialysis solution injected into abdo cavity through a permanent catheter.

High dextrose conc. of the solution draws waste products from blood into abdo cavity across the peritoneum.

After several hours of dwell time, the solution is drained, removing waste products from body, + exchanged for new dialysis solution.

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7
Q

What is continuous ambulatory peritoneal dialysis (CAPD)?

A

Patient operated- each exchange 30-40 mins + each dwell time 4-8h.
Patient can do normal activities with dialysis solution inside their abdomen

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8
Q

What is automated peritoneal dialysis (APD)?

A

dialysis machine fills + drains the abdomen while patient is sleeping, performing 3-5 exchanges over 8-10h each night

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9
Q

Give 5 complications of haemodialysis

A

Site infection
Stenosis at site
Bleeding
AV access steal syndrome
Dialysis disequilibrium syndrome

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10
Q

What is Steal syndrome?

A

painful ischemia of the hand secondary to AV fistula or graft shunting blood away from the distal limb

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11
Q

What is Dialysis disequilibrium syndrome?

A

acute cerebral oedema secondary to rapid extraction of osmotically active substances (e.g., urea, NaCl) from the blood

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12
Q

Give 3 advantages of PD

A

Offers more flexibility (can be done overnight
Is better tolerated by patients
Less expensive

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13
Q

What is a Tesio line?

A

Tunneled dual lumen central line
Used as a ‘bridge’ before an AV fistula can be put in
1 lumen enters the right atrium, the other sits outside the RA in the vena cava
Both lumens exit the body

(with a central line, only 1 lumen enters the skin)

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14
Q

Why is a normal vein unsuitable for haemodialysis, and why is an AV fistula used?

A

Normal vein would easily collapse/ thrombose with recurrent venepuncture
Vein in an AV fistula hypertrophies in response to turbulent flow of blood from artery + so can withstand repeated venepuncture

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15
Q

What are the most common causes of AKI?

A

STOP

Sepsis/ dehydration

Toxins (NSAIDs, Nephrotoxic drugs)

Obstruction in the urinary tract

Parenchymal kidney disease

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16
Q

What are the most common causes of CKD?

A

Diabetic nephropathy

HTN

(PKD)

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17
Q

What are the primary functions of the kidney?

A

Salt + water balance

Acid base homeostasis

Endocrine function: vitamin D, EPO, renin-angiotensin system

Excrete waste

Electrolyte homeostasis

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18
Q

What symptoms might you expect from someone in CKD? (7)

A

Anaemia: SOB, fatigue, LoC, headache

Uraemia: encephalopathy, N+V, confusion, pruritis, pericarditis

Fluid overload: pedal oedema, pleural effusion, ascites, tiredness

Hyperkalaemia: palpitations, cardiac arrest, asymptomatic

Acidosis: N+V, tiredness

Increased drug action: opioid side effects

Reduced urine output

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19
Q

List 5 indications for emergency dialysis

A

A – Acidosis

E – Electrolyte imbalance (K+ >6.5, refractory to medical Mx)

I – Intoxication (certain drugs require dialysis to clear the blood)

O – Overload of fluid (refractory to diuretic Tx)

U – Uraemic encephalopathy + pericarditis

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20
Q

What mnemonic can be used for drugs that can be dialysed out?

A

BLAST
Barbiturates
Lithium
Alcohol
Salicylates
Theophylline

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21
Q

What diet should be followed in patients with very low creatinine clearance?

A

Low phosphate
(eg. avoid chocolate, shellfish, nuts)

Low K+ (avoid chocolate, bananas etc)

Fluid restricted (avoid alcohol + too much tea/ coffee)

Low salt (avoid processed foods)

Can take phosphate binders if diet restriction alone doesn’t succeed

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22
Q

Name 1 phosphate binder

A

Sevelamer

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23
Q

How does CKD affect phosphate and vitamin D?

A

1-alpha hydroxylation normally occurs in kidneys → leads to LOW vitamin D

kidneys normally excrete phosphate → leads to HIGH phosphate

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24
Q

What problems arise from high phosphate and low vitamin D in CKD?

A

High phosphate level ‘drags’ calcium from bones→ osteomalacia

Low calcium: due to lack of vitamin D + high phosphate

Secondary hyperparathyroidism: due to low calcium, high phosphate + low vitamin D

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25
Q

Define acute kidney injury

A

Sudden decrease in GFR manifested by an increase in serum creatinine or oliguria over a period of hours/ weeks

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26
Q

What causes should be excluded first in AKI? Why?

A

Pre renal (hypovolaemia, sepsis) + post renal (stones, cancer)
Renal causes require a biopsy

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27
Q

How can AKI secondary to blood loss be differentiated into pre-renal and renal cause?

A

Pre: LOW urinary Na+ (hypovolaemia: kidneys hold on)

Renal: HIGH urinary Na+ (ischaemia of tubules: loss)

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28
Q

How are intrinsic renal causes of AKI classified?

A

Glomerulonephritis: MCD, Membranous GN

ATN: affects tubules

AIN: affects surrounding tissue

Vascular: small (microangiopathic- HUS, TTP) or large (obstructive- thrombosis/ emboli)

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29
Q

What is nephritic syndrome?

A

Subtype of intrinsic AKI with BLOOD + PROTEIN in urine indicative of glomerular disease

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30
Q

What is nephrotic syndrome?

A

Proteinuria (>3.5g/ 1.73m^2 body surface area/ 24h)
Hypoalbuminaemia (<30g/L)
Oedema
(+ Hyperlipidaemia)

31
Q

What causes the high level of proteinuria in nephrotic syndrome?

A

Injury of the podocyte
(provides most of the protein filter barrier of the glomerulus)

32
Q

Give 3 primary renal diseases presenting with nephrotic syndrome

A

Minimal change disease
Membranous glomerulonephritis
Focal Segmental Glomerular Sclerosis

33
Q

Give 2 systemic causes presenting with nephrotic syndrome

A

Diabetes
Amyloidosis

34
Q

What is chronic kidney disease?

A

Decrease in GFR present >3 months

35
Q

Which 4 variables are used in the modification of diet in renal disease (MDRD) formula for eGFR?

A

Creatinine (serum)
Age
Gender
Ethnicity

36
Q

List 3 factors that will affect the MDRD estimation of GFR

A

Pregnancy
Muscle mass (e.g. amputees (lower Cr), body-builders (higher Cr))
Eating red meat 12h prior to the sample being taken

37
Q

What is Proliferative glomerulonephritis characterised by?

A

Increased no. cells in glomerulus
Presents with NEPHRITIC syndrome

38
Q

What is Non-proliferative glomerulonephritis characterised by?

A

Lack of glomerular cell proliferation
Presents with NEPHROTIC syndrome

39
Q

Give 6 causes of proliferative glomerulonephritis

A

IgA nephropathy

Post-infectious glomerulonephritis

Membranoproliferative glomerulonephritis

Rapidly progressive glomerulonephritis (RPGN)

Anti-GBM disease

Vasculitic disorders (GPA + microscopic polyangitis)

40
Q

What is IgA nephropathy aka? In which patient group is it usually seen?

A

Bergers disease
Most common form of glomerulonephritis in adults
Often young adults

41
Q

How does IgA nephropathy usually present?

A

Haematuria
24-48h after URTI

42
Q

Mx of IgA nephropathy with isolated hematuria, no/ min. proteinuria (<500-1000 mg/day) and normal GFR

A

No Tx needed
F/U to check renal function

43
Q

Mx of IgA nephropathy with persistent proteinuria (>500-1000 mg/day), and normal/ slightly reduced GFR

A

ACE inhibitors

44
Q

Mx of IgA nephropathy with active disease (falling GFR) or failure to respond to ACEi

A

High dose Prednisolone

45
Q

What is the prognosis in IgA nephropathy?

A

25% develop ESRF within 20-25y

46
Q

What investigations are required for IgA nephropathy?

A

Renal biopsy (definitive): increased no. mesangial cells

Urinalysis: haematuria

47
Q

What is Post-infectious glomerulonephritis most commonly associated with?

A

Group A beta-haemolytic Streptococcus infection (usually Strep. pyogenes)

48
Q

How does Post-infectious glomerulonephritis usually present?

A

Gross haematuria
Proteinuria + Oedema
Oliguria
Headache + malaise
1-2w after strep infection

49
Q

What is the pathophysiology of Post-streptococcal glomerulonephritis?

A

immune complex (IgG, IgM + C3) deposition in the glomeruli.

50
Q

What investigations can be used for Post-streptococcal glomerulonephritis?

A

anti-streptolysin titre (ASOT).
low C3

Biopsy
Diffuse proliferative + exudative glomeronephritis
EM: subepithelial humps- lumpy complex deposition

51
Q

Mx and prognosis in post-streptococcal glomerulonephritis

A

Self limiting

Good prognosis

52
Q

What is Membranoproliferative glomerulonephritis?

A

group of immune-mediated disorders characterised by GBM thickening + proliferative changes on light microscopy.

53
Q

Membranoproliferative glomerulonephritis is associated with which 2 diseases

A

Hepatitis C

SLE

54
Q

How can membranoproliferative glomerulonephritis present?

A

Nephrotic syndrome
Haematuria
Proteinuria

55
Q

Give 3 typical findings on renal biopsy in membranoproliferative glomerulonephritis

A

Thickened basement membrane
Thickened mesangium
“Tram tracking” appearance: electron dense material deposition

56
Q

Mx for membranoproliferative glomerulonephritis

A

Children (with nephrotic-range proteinuria): corticosteroids

Adults: dipyridamole + aspirin

Kidney transplantation for patients with ESRF

57
Q

What is Rapidly progressive glomerulonephritis (RPGN) aka?

A

Crescentic glomerulonephritis

58
Q

What is RPGN?

A

rapid loss of renal function a/w formation of epithelial crescents in the majority of glomeruli within weeks-months

59
Q

List 4 causes of RPGN

A

Goodpasture’s syndrome
Wegener’s granulomatosis
SLE
Microscopic polyarteritis

60
Q

How does RPGN present?

A

Nephritic syndrome: haematuria with red cell casts, proteinuria, HTN, oliguria

Features specific to underlying cause (e.g. haemoptysis with Goodpasture’s, vasculitic rash or sinusitis with Wegener’s)

61
Q

What is Anti-GBM antibody disease aka?

A

Goodpasture’s syndrome if lungs + kidneys involved

62
Q

What is Goodpasture’s syndrome?

A

small-vessel vasculitis a/w pulmonary haemorrhage + rapidly progressive glomerulonephritis.

Caused by anti-GBM antibodies against type IV collagen.

63
Q

Describe epidemiology of Goodpasture’s syndrome

A

M > F 2:1
Bimodal 20-30 + 60-70
HLA DR2 association

64
Q

How does Goodpasture’s syndrome usually present?

A

Pulmonary haemorrhage: Haemoptysis

RPGN: rapid onset AKI=
nephritis → proteinuria + haematuria

65
Q

What investigations can be used for Goodpasture’s syndrome?

A

Immunohistochemistry: Linear IgG deposits along basement membrane

Antibodies: anti-GBM antibodies

66
Q

Mx for Goodpasture’s syndrome

A

Prednisolone
Plasmapheresis
Cyclophosphamide

67
Q

Give 5 risk factors for pulmonary haemorrhage in Goodpasture’s syndrome

A

Smoking
LRTI
Pulmonary oedema
Inhalation of hydrocarbons
Young males

68
Q

What are the small vessel ANCA-associated vasculitides?

A

Microscopic polyangiitis (MPA)

Granulomatosis with polyangiitis (GPA-Wegener’s granulomatosis)

Eosinophilic granulomatosis with polyangiitis (EGPA- Churg-Strauss syndrome)

69
Q

What is the pathophysiology of the ANCA associated vasculitides?

A

Anti-neutrophil cytoplasmic antibodies target myeloperoxidase + proteinase 3

70
Q

What is GPA characterised by?

A

necrotising vasculitis with granulomas
Affects ENT, lungs, kidneys, skin, eyes, nervous system

71
Q

How does GPA present?

A

FLAW

ENT: nasal crusting + discharge, otitis media, sensorineural deafness

Pulmonary: cough, dyspnoea, haemoptysis

Renal: haematuria, proteinuria, nephritic syndrome

72
Q

Ix for GPA

A

Biopsy: leukocytoclastic vasculitis with necrotic changes + granulomatous inflammation

ANCA serology

73
Q

Mx for GPA

A

Induction: Methylprednisolone, Prednisolone + Rituximab/ Cyclophosphamide

Maintenance: Prednisolone + Rituximab/ Methotrexate

YR6 Rotations (1 decks)

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