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Y4 Medicine > Nephrology > Flashcards

Nephrology Flashcards

1
Q

NICE diagnostic criteria AKI

A
  1. Rise in creatinine >25um/L in 48 hours
  2. Rise in creatinine >50% from baseline in 7 days
  3. Urine output <0.5ml/kg/hr for >6 hours
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2
Q

Nephrotoxic drugs

A

GOD SAD MAN
Gentamicin / Opiates / Diuretics / Sulfonylureas / ACEi & ARBs / DOACs / Metformin / Aldosterone antagonists / NSAIDs

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3
Q

Pre-renal causes of AKI

A

Pre-renal = hypoperfusion
1. True hypoperfusion = GI losses, dehydration, burns, haemorrhage
2. Relative hypoperfusion = NSAIDs + ACEi

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4
Q

Renal causes of AKI

A

Glomerulonephritis
Acute tubular necrosis
Acute interstitial nephritis
Vascular causes e.g HUS or malignant HTN

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5
Q

Post-renal causes of AKI

A

Bilateral pelvic-ureteric obstruction
Bilateral ureteric obstruction
Bladder outflow obstruction
Urethral obstruction

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6
Q

Complications of AKI

A

Hyperkalemia
Hyperphosphatemia
Uremia
Fluid overload
Metabolic acidosis

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7
Q

Classification of CKD

A

Stage 1 = Kidney damage + GFR > 90
Stage 2 = Kidney damage + GFR 60-89
Stage 3 = GFR 45 - 59
Stage 3b = GFR 30 - 44
Stage 4 = GFR 15 - 29
Stage 5 (ESRF) = GFR <15

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8
Q

Which medication can cause rhabdomyolysis

A

Statins

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9
Q

Staging of AKI

A

Stage 1 = Creatinine rise of >26 in 48hours or 1.5-1.99 x increase from baseline in 7 days
Stage 2 = Creatinine rise of 2 - 2.9 x baseline in 7 days
Stage 3 = Creatinine rise 3x of baseline in 7 days or >350 within 48 hours

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10
Q

Indications for dialysis

A

“AEIOU”
Acidosis
Electrolyte derangement resistant to treatment
Intoxication
Pulmonary Oedema
Uremia

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11
Q

What should be prescribed to diabetics with a A:CR of >3

A

ACE inhibitor

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12
Q

Symptoms of uremia

A

Pruritus
Loss of appetite
Metallic taste in mouth
N&V
Neuropathy
Encephalopathy

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13
Q

Management of CKD

A

Optimise risk factors - HTN/diabetes etc
Treat any glomerulonephritis
Reduce CVD risk = Atorvostatin 20mg
Reduce complications risk - Low K+ and phosphate diet, maintain healthy weight, stop smoking etc

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14
Q

Complications of CKD

A

Hypertension
Anemia
Renal bone disease
Hyperkalemia

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15
Q

Management of CKD induced anemia

A

EPO

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16
Q

Side effects of EPO

A

Bone aches
Flu like symptoms
Skin rashes
Hypertension
Iron deficiency anemia

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17
Q

Treatment of renal bone disease

A

Active Vitamin D (calitrol)
Oral calcium supplementation
Bisphosphonates

18
Q

Xray findings in renal bone disease

A

Rugger jersey spine (osteosclerosis at edges of vertebrae with osteomalacia in the center)

19
Q

Management of hyperkalemia

A

IV Insulin + Dextrose infusion
Calcium gluconate - to stabilise cardiac membrane
Nebulised salbutamol
IV fluids
Calcium resonium - removal of K+ from the body

Consider sodium bicarb if acidotic or Dialysis if severe

20
Q

Acute renal transplant failure

A

Presents <6 months after transplant with Proteinuria + Raised leucocytes + Rising creatinine

21
Q

Acute interstitial nephritis

A

Inflammation of the interstitium
Sx = AKI + Hypertension + Hypersensitivity reaction e.g fever, arthralgia, eosinophilia.
Cause = penecillins / NSAIDs usually

Management = Steroids

22
Q

Acute tubular necrosis

A

acute necrosis of the epithlium in the renal tubules leading to an AKI. Classically resulting from ischemia or toxins.

Hypoperfusion causes = shock/sepsis/dehydration/haemorrhage
Toxins = Constrast dye / gentamycin / NSAIDs

Invx = muddy brown casts on urinalysis
Low urine osmolality + high urinary sodium
Fully reversible. Poor response to fluid chalanges

23
Q

Apple-green bifringence on congo red staining

A

Amyloidosis

24
Q

HSP

A

Small vessel vasculitis - has overlap with berger’s disease (IgA nephropathy)

25
Q

Characteristic rash in HSP

A

Palpable purpuric rash over buttocks & extensor surfaces of arms and legs

26
Q

Nephritic syndrome

A

= inflammation of capillary endothelium + GBM
Features:

Proteinuria
Haematuria
Azotemia
Red cell casts
Oliguria
Anti-streptolysin O titre
Hypertension
Sterile pyuria

27
Q

Nephrotic syndrome

A

= Podocyte damage in the GBM

Proteinuria (>3g in 24hours)
Hypoalbuminemia
Oedema

+/- dyslipidemia

28
Q

‘Nephrotic-like’ Glomerulonephritis’

A

Minimal change
Membranous
Focal segmental

29
Q

“Nephritic-like” Glomerulonephritis’

A

Post-streptococcal
Anti-GBM (Goodpastures syndrome)
IgA nephropathy (& HSP)
Rapidly progressive
Small vessel vasculitis (Microscopic polyangitis = pANCA, Granulomatosis with polyangitis = pANCA)

+ Alpert’s syndrome (hearing problems)

30
Q

Mixed nephrotic + nephritic type GN

A

Membranoproliferative
SLE

31
Q

Minimal Change disease

A

Most common cause of nephrotic syndrome in children.

Histology normal
LM normal
EM = fusion of podocyte foot processes

32
Q

Membranous Glomerulonephritis

A

3rd most common cause of ESRF
Caused by immune deposition in GBM causing damage to podocytes.

Invx = Anti-phospholipase A2 antibodies
LM = mesangial expansion
Immunoflourescnce = IgG and C3 deposition
EM = Subepithelial deposits - silver spikes & domes

33
Q

Focal segmental glomerulonephritis

A

Most common cause of nephrotic syndrome in adults. (typically younger adults)
LM = Focal and segmental scarring & hyalinosis
EM = GBM thickening

*ANA levels may be risen if SLE is present (common cause of FSGN)

34
Q

IgA Nephropathy

A

Typified by IgA complexes within the mesangium - type 3 hypersensitivty reactions.

Occurs 1-3 days after a sore throat.
Associated with HSP

Biopsy not needed as clinical diagnosis - but immunoflourescence would should IgA deposition

35
Q

Post-streptococcal GN

A

Occurs 1-3 weeks after a Group A beta-haemolytic streptoccocus infection (usually pyogenes, e.g tonsillitis)

Raised ASO titre
Low C3
Increased anti-DNAaseB

36
Q

Membranoproliferative GN

A

Causes proteinuria +/- Haematuria

T1 = caused by immune complex depositis. EM shows ‘tram-track’ appearance
T2 = C3b nephritic factor

37
Q

Anti-GBM GN (Goodpasture’s syndrome)

A

Typically presents with AKI + Haemoptysis (pulmonary haemorrhage)
Caused by antibodies to T4 Collagen (which is found in glomerular and alveolar basement membranes)

Invx;
- Linear IgG deposition in GBM
- Raised Transfer factor

38
Q

Granulomatosis with Polyangitis (Wegener’s)

A

Features: Sinusitis + Saddle nose deformity + AKI + Haemoptysis + Malaise + Arthralgia

Invx = Raised cANCA
Biopsy = granulomatous inflammation

Management = Steroids + Cyclophosphamide

39
Q

Rapidly progressive GN

A

A term used to describe a rapid decline in renal function + Epithelial crescents in bowmans capsule.

Causes = Goodpastures, Wegeners, Microscopic polyangitis + SLE.

Basically the key finding is Epithelial crescents.

40
Q

Microscopic polyangitis

A

Nephritic GN
No granulomatous inflammation seen
Raised pANCA (target = myeloperoxidase 3)

41
Q

Alport’s syndrome

A

Usually presents in childhood with Microscopic haemturia (nephritic syndrome) + progressive renal failure + bilateral sensorineural hearing loss + lenticonus

Invx = EM shows splitting on lamina densa

Y4 Medicine (22 decks)

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