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Year 2 MBChB > Renal > Flashcards

Renal Flashcards

1
Q

What antibodies are present in Good-pastures?

A

Anti-glomerular basement membrane

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2
Q

What is the presentation of Good-pastures?

A

Haemoptysis, nephritic syndrome

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3
Q

What investigations are done in Good-pastures?

A

Anti-GBM,

IgG along the basement membrane

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4
Q

What is the investigation of choice in a suspected glomerulonephritis?

A

Renal biopsy

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5
Q

What investigations are done in microscopic polyangitis?

A

p-ANCA

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6
Q

What is the presentation of nephrotic syndrome?

A

POO (proteinuria, oedema, nephrOtic)

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7
Q

What are the causes of minimal change disease?

A

Hodgkin’s, NSAIDS, assoc with atopy

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8
Q

What investigation is done in minimal change disease?

A

Electron microscopy: fused podocytes

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9
Q

Which GN is assoc with FSGS?

A

HIV

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10
Q

What is the presentation of FSGS?

A

Nephrotic syndrome - may be associated with haematuria, hypertension, poor renal function

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11
Q

How is FSGS investigated?

A

Specific segments of certain glomeruli develop sclerosed lesions

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12
Q

What is membranous GN caused by?

A

Immune complex deposition –> complement activation against glomerular basement membrane proteins

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13
Q

What can membranous GN be secondary to?

A

SLE, Hep B, penicillin amine, gold & malignancy

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14
Q

How is membranous GN investigated?

A

Thickened glomerular basement membrane, immunofluorescence: increased IgG uptake

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15
Q

What is the most common GN in adults?

A

IgA nephropathy

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16
Q

When does IgA nephropathy often appear?

A

1-2 days after URTI

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17
Q

What is the presentation of IgA nephropathy?

A

Nephritic syndrome: macroscopic haematuria, hypertension

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18
Q

What investigations are done in IgA nephropathy?

A

Microscopy: increased mesangial cells and matrix, IgA deposits in matrix

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19
Q

What is the presentation of post-strep GN?

A

Nephritic syndrome, AKI

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20
Q

When does post-strep Gn occur?

A

1-2 weeks after URTI (commonly strep pyogenes)

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21
Q

What is membranoproliferative GN caused by?

A

Subendothelial deposition of immune complexes

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22
Q

What is membranoproliferative GN associated with?

A

Decreased C3 levels

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23
Q

How is membranoproliferative GN investigated?

A

Thickened BM and mesangium, IgG deposition

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24
Q

How can the causes of AKI be split up?

A

Prerenal, intrinsic, postrenal

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25
Q

What are some pre renal causes of AKI?

A

Hypovolaemia, renal artery stenosis

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26
Q

What are some intrinsic renal causes of AKI?

A

GN, Acute tubular necrosis, acute interstitial nephritis, rhabdomyolysis, tumour lysis syndrome

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27
Q

What are some post renal causes of AKI?

A

stones, BPH, external compression of ureter (tumour)

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28
Q

Define oliguria

A

Urine output < 0.5ml/kg/hour

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29
Q

What are the signs and symptoms of AKI?

A

Reduced urine output, oedema, arrhythmias (secondary to electrolyte abnormalities), features of uraemia

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30
Q

Which drugs should be stoped in AKI?

A

NSAIDs, ACEIs, diuretics, aminoglycosides, angiotensin II receptor antagonists

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31
Q

Which drugs may have to be stopped in AKI due to increased risk of toxicity?

A

Metformin, lithium, digoxin

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32
Q

When should haemodialysis be considered in AKI?

A

Hyperkalaemia, acidosis, uraemia

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33
Q

How is AKI managed?

A

Careful fluid balance, stopping drugs, finding cause (urinalysis, U&Es, renal USS), management of hyperkalaemia

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34
Q

What is the buzzword for acute tubular necrosis?

A

Brown granular casts

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35
Q

What is the criteria for diagnosing AKI in adults?

A

Rise in creatinine of 26 or more in 48 hours OR at least 50% rise in creatinine over 7 days OR oliguria for more than 6 hours

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36
Q

What is the final pathway in AKI?

A

Tubular cell death

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37
Q

What is the best way to differentiate between acute and chronic renal failure?

A

Renal ultrasound - chronic have bilateral small kidneys usually

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38
Q

Which chromosome is affected in ADPKD type 1?

A

Chromosome 16

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39
Q

What are the features of ADPKD?

A

Hypertension, recurrent UTIs, abdo pain, renal stones, haematuria, CKD

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40
Q

How is Alport’s syndrome inherited?

A

X-linked dominant

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41
Q

What is Alport’s syndrome due to?

A

Defect in the gene which codes for type IV collagen –> abnormal GBM

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42
Q

What are the features for Alport’s?

A

Microscopic haematuria, progressive renal failure, bilateral SN deafness, lenticonus

43
Q

What is amyloidosis?

A

Extraceullular deposition of an insoluble fibrillar protein (amyloid)

44
Q

How is amyloidosis diagnosed?

A

Congo-red staining - apple green birefringence, SAP scan

45
Q

What are common causes of CKD?

A

Diabetic nephropathy, chronic GN, chronic pyelonephritis, hypertension, PCKD

46
Q

Define stage 1 CKD

A

eGFR > 90 with some sign of kidney damage on other tests

47
Q

Define stage 2 CKD

A

eGFR 60-90 with some sign of kidney damage on other tests

48
Q

Define stage 3a CKD

A

eGFR 45 - 59

49
Q

Define stage 3b CKD

A

eGFR 30-44

50
Q

Define stage 4 CKD

A

eGFR 15-29

51
Q

Define stage 5 CKD

A

eGFR < 15

52
Q

What factors may affect the eGFR result?

A

Pregnancy, muscle mass, eating red meat 12 hours prior to sample

53
Q

Which drugs are first line in hypertension with CKD?

A

ACEIs

54
Q

What eGFR change is OK with ACEIs in CKD?

A

eGFR decrease of up to 25%

55
Q

What investigations are done in diabetes insipidus?

A

High plasma osmolality, low urine osmolality, water deprivation test

56
Q

What is diabetes insipidus caused by?

A

Deficiency of ADH (cranial), or insensitivity to ADH (nephrogenic)

57
Q

How are diabetics screened for diabetic nephropathy?

A

Albumin:creatinine ration in early morning specimen

58
Q

What is used to treat anaemia associated with CKD?

A

EPO

59
Q

Which renal problem is HSP associated with?

A

IgA nephropathy

60
Q

What are the features of HSP?

A

purpuric rash peripherally, abdominal pain, polyarthritis, IgA nephropathy

61
Q

What are the ECG changes of hypokalaemia?

A

U waves, small T waves, prolonged PR, ST depression

62
Q

What does hypokalaemia predispose patients to?

A

Digoxin toxicity

63
Q

When does hyper acute acute graft rejection occur?

A

minutes to hours

64
Q

What is hyper acute ate graft rejection due to?

A

Pre-existent antibodies against donor HLA Type 1 antigens (type II hypersensitivity)

65
Q

What is acute graft failure due to?

A

Usually mismatched HLA (cell-mediated), can be CMV

66
Q

When does acute graft failure occur?

A

Within 6 months

67
Q

What is chronic graft failure due to?

A

Both antibody and cell mediated mechanisms cause fibrosis to the transplanted kidney

68
Q

When does chronic graft failure occur?

A

> 6 months

69
Q

What is the management of rhabomyolsis?

A

IV fluids, sometimes urinary alkalinization

70
Q

Where does spironolactone act?

A

Cortical collecting duct

71
Q

Where do loop diuretics act?

A

Ascending loop of Henle

72
Q

Where is glucose reabsorbed?

A

Proximal convoluted tubule

73
Q

Where is most water reabsorbed?

A

proximal convoluted tubule

74
Q

What is the management of UTI in non-pregnant women?

A

Trimethoprim/nitrofurantoin for three days

75
Q

How is pyelonephritis managed?

A

IV amor + gent, step down to PO co-trimoxazole

76
Q

What is the make up of the majority of renal stones?

A

Calcium oxalate

77
Q

What is the first line management of renal stones?

A

USS

78
Q

What is the investigation of choice in renal stones to confirm diagnosis?

A

Non contrast CT

79
Q

What drugs should be given for renal colic?

A

Diclofenac

80
Q

How are stones managed (< 5mm)?

A

Usually will pass within 4 weeks

81
Q

How are stones managed ( >5mm)?

A

Lithotripsy (less than 2cm), ureteroscopy (less than 2cm pregnancy), percutaneous nephrolithotomy (complex stones + staghorn)

82
Q

What is the most common renal malignancy?

A

Renal cell carcinoma

83
Q

How are renal cancers investigated?

A

CT chest, abdo, pelvis

84
Q

What decade of life do renal cancers most commonly affect?

A

60s

85
Q

What are causes of bilateral hydropnephrosis?

A

SUPER: stenosis of urethra, urethral valve, prostate, extensive bladder tumour, retroperitoneal fibrosis

86
Q

What are causes of unilateral hydronephrosis?

A

PACT: pelvic-ureteric obstruction, aberrant renal vessels, calculi, tumours of renal vessels

87
Q

What are the investigations done in hydronephrosis?

A

USS, IVU

88
Q

What does nephrotic syndrome occur due to?

A

Protein loss through abnormally permeable capillary basement membranes

89
Q

What is the most common renal cell carcinoma?

A

Clear cell

90
Q

What is a sarcomatous renal cancer?

A

Renal cell cancer that contains muscles, nerves, fat, blood vessels

91
Q

What are the features of a WIlms’ tumour?

A

Abdo mass, painless haematuria, flank pain

92
Q

When does Wilms’ tumour occur?

A

Typically under 5 years of age

93
Q

How are Wilms’ tumours treated?

A

Nephrectomy

94
Q

Do Wilms’ tumours metastasise?

A

yes - early, usually to lung

95
Q

What are paraneoplastic features of renal cell carcinoma?

A

Hypertension and polycythaemia

96
Q

What is an angiomyolipoma?

A

Tumour composed of blood vessels, smooth muscle, and fat

97
Q

What are the different parts of the urethra (proximal)?

A

Prostatic –> membranous –> bulbous –> penile

98
Q

What is the descending loop of henley responsible for?

A

Highly permeable to water, impermeable to NaCl

99
Q

Where do thiazide diuretics act?

A

Distal tubule

100
Q

Where do potassium sparing diuretics act?

A

Collecting tubule

101
Q

Where do loop diuretics act?

A

Thick ascending loop of Henley

102
Q

What does beading of the renal artery indicate?

A

Fibromuscular dysplasia

103
Q

What does apple green birefringence on congo red stain indicate?

A

Amyloidosis

Year 2 MBChB (8 decks)

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