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Year 2 - Renal (DP) > Clinical (Week 4) > Flashcards

Clinical (Week 4) Flashcards

1
Q

What is a hamartoma?

A

A tumour with the correct constituencies of the organ it’s from but in wrong distribution

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2
Q

What is the most common renal pelvis tumour?

A

Transitional cell carcinoma

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3
Q

What is the most common renal parenchymal tumour?

A

Renal cell carcinoma

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4
Q

What is the most common renal embryonic tumour?

A

Nephroblastoma (Wilm’s Tumour)

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5
Q

What sort of CT is useful in diagnosing a urological malignancy?

A

Triple phased contrast enhanced

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6
Q

What is the most common benign asymptomatic renal lesion?

A

Renal cyst (70%)

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7
Q

How do we investigate renal cysts and why can we use this modality?

A

USS (it is fluid-filled)

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8
Q

When would we biopsy an angiolypoma?

A

If fat-sparse:

- Risk of bled

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9
Q

What feature of vessels in an angiolypoma make it prone to bleeds?

A

They are fragile

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10
Q

How can we measure lesion density on a CT of angiolypomas?

A

Hounsfield

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11
Q

What is Wunderlich’s Syndrome?

A

Collapse due to retroperitoneal bleed in an angiolypoma

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12
Q

How does an oncocytoma appear on CT?

A

Central scar:

 - Stellate due to central necrosis
           - > No angiogenesis therefore benign
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13
Q

What is the only way to definitively diagnose an oncocytoma and why is a biopsy not totally useful?

A

Nephrectomy

Biopsy has a high false negative rate

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14
Q

What is the classic triad of symptoms in a renal cell carcinoma?

A 
Loin pain (40%)
Renal masses (25%)
Frank haematuria (60%)
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15
Q

Which of the following is not a paraneoplastic effect of renal cell carcinoma:

  • Weight loss
  • Hyperthyroidism
  • Anaemia
  • Hypertension
  • Hypercalcaemia (As it produces parathyroid-like hormone)
A

Hyperthyroidism

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16
Q

What is the M:F ratio for the incidence of a renal cell carcinoma?

A

2:1

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17
Q

What is the peak incidence age for renal cell carcinoma?

A

65-75 years

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18
Q

What type of cancer of a renal cell carcinoma and where is it found?

A

Adenocarcinoma

The PCT

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19
Q

How do renal cell cancers appear histologically?

A

Clear cells

Papillary subtypes

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20
Q

If there are bilateral or multifocal renal cell carcinomas, what condition should you suspect and what implications does this have?

A

Von Hippel-Lindau:

- Implications for surgery

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21
Q

What is the first line investigation for renal cell carcinoma, and what is the best investigation?

A

1st line - USS
Gold standard:
- Triple phase contrast CT

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22
Q

What is the downside to using biopsy in the diagnosis of renal cell carcinomas?

A

High false negative rate

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23
Q

What staging system is used for renal cell carcinomas?

A

Robson

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24
Q

True or false; Direct perinephric fat invasion is rare in renal cell carcinomas?

A

True

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25
Q

How do renal cell carcinomas tend to spread?

A

Lymphatics

Via IVC

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26
Q

Where do renal cell carcinomas commonly spread?

A

Lungs (‘Cannon ball’ metastases)
Liver
Bone
Brain

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27
Q

What is the standard treatment for a renal cell carcinoma? What does the treatment involve?

A

Radical nephrectomy (preferably laparoscopically):

 - Whole kidney within Gerota's fascia
 - Perinephric fat removed
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28
Q

When is the standard treatment for a renal cell carcinoma most often carried out?

A

Within a month of diagnosis

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29
Q

When would the adrenal gland be removed in the treatment of renal cell carcinoma and why is it not routinely removed?

A

If it is involved

Reduces the risk of adrenal insufficiency (Addison’s syndrome)

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30
Q

How is a partial nephrectomy carried out? What implications does this have on the operation?

A

Under cold ischaemic:

- Must be done in 20-30 minutes

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31
Q

What is the benefit to a partial nephrectomy?

A

It is nephron sparing:

 - Maintains renal function
 - Increases QoL and life expectancy
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32
Q

What surgical approaches can be taken in a partial nephrectomy?

A

Open

Robotic laparoscopy

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33
Q

What is the main risk of a partial nephrectomy?

A

Pseudoaneurysm due to healing vessels

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34
Q

Apart from nephrectomies, what two other treatment options are available for renal cell carcinoma?

A

Radiofrequency ablation

Cryoablation

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35
Q

How do we measure the performance status in metastatic renal cell carcinoma?

A

ECOG

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36
Q

What type of drug is Sunitinib? How does it work?

A

Tyrosine Kinase inhibitor:

 - VEG-F and PDG-F inhibition
 - Reduces neovascularisation
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37
Q

What benefit does using Sunitinib in the treatment of renal cell carcinoma have?

A

26 vs 20 month progression-free survival

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38
Q

What are the five year survival rates of Stage 1-4 renal cell carcinomas?

A

Stage 1 -> 75%
Stage 2 -> 50%
Stage 3 -> 35%
Stage 4 -> 5%

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39
Q

What are Balanitis Xerotica Obliterans and Leukoplakia?

A

Pre-malignant cutaneous penile cancers

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40
Q

What is Balanitis Xerotica Obliterans a form of?

A

Lichen sclerosus et atrophicus (Lichen sclerosus)

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41
Q

How does Balanitis Xerotica Obliterans present?

A

White patches
Fissuring -> Pain
Bleeding
Scarring

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42
Q

Where does Balanitis Xerotica Obliterans occur?

A

Prepuce
Glans
Urethral extension

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43
Q

What is the potential for malignant transformation in Balanitis Xerotica Obliterans?

A

Low

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44
Q

What can predispose to Balanitis Xerotica Obliterans?

A

Poor hygiene

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45
Q

What is Erythroplasia of Queryat?

A

Squamous cell carcinoma in situ on the:

 - Glans
 - Prepuce
 - Shaft
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46
Q

How does Erythroplasia of Queryat appear?

A

Red, velvety patches

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47
Q

What is the name of a squamous cell carcinoma in situ on the rest of the genitalia (ie not Glans, Prepuce or shaft)?

A

Bowen’s Disease

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48
Q

What is it important to differentiate a Squamous cell carcinoma in situ from?

A

Zoon’s Balanitis

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49
Q

When would we circumcise a Squamous cell carcinoma in situ?

A

If present on the prepuce alone

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50
Q

How else can we treat a Squamous cell carcinoma in situ?

A

Topical 5-fluorouracil

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51
Q

Red, raised area on the penis with a foul smelling, fungating mass and phimosis is the typical presentation in what?

A

Penile carcinoma

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52
Q

How do we diagnose a penile carcinoma?

A 
USS
Biopsy (if invasive)
CT -> For distal LNs
MRI
Bone scam
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53
Q

What is the incidence rate and peak age for penile carcinoma?

A

1.5 per 100,000 men

80 years old

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54
Q

What infection is penile carcinoma linked to?

A

HPV 16

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55
Q

What type of cancer is a penile carcinoma?

A

Squamous cell carcinoma

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56
Q

If there is inguinal node invasion of a penile carcinoma, how do we approach the treatment?

A
  1. Assess prognosis
  2. Radionucleotide Sentinel Node Biopsy
  3. Inguinal lymphadenectomy
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57
Q

What chemotherapy agents are used in the treatment of penile cancer?

A

5-Fluorouracil

Cis-platin

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58
Q

What is the most common germ cell testicular tumour?

A

Seminoma

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59
Q

What are some examples of non-seminomatous germ cell tumours?

A

Teratoma
Embryonal
Yolk sac
Choriocarcinoma

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60
Q

What does ITGCN stand for in terms of germ cell testicular tumours?

A

Intra-tubular germ cell neoplasia

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61
Q

How does a testicular tumour typically present?

A

Painless, insensitive testicular swelling

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62
Q

How many testicular tumours are due to metastases and where do they usually come from? How do they present?

A

10%:

 - Neck LNs
 - Dyspnoea
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63
Q

What is the best investigation for testicular tumours?

A

USS (95% sensitivity and specificity)

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64
Q

When would CXR and CT be used in investigation testicular tumours?

A

Staging

Abdominal and thorax metastases

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65
Q

In what germ cell testicular cancer is α-feto protein never raised?

A

Pure seminoma

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66
Q

In what germ cell testicular cancers is hCG raised?

A

5-10% of pure seminomas

60% of teratomas

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67
Q

What can LDH be used to indicate in germ cell testicular cancers?

A

Tumour burden

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68
Q

What are testicular tumour markers usually used to gauge?

A

Effectiveness of therapy

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69
Q

What approach is taken in orchidectomies? Why is this approach taken?

A

Inguinal:

 - Prevents damage to surrounding layers
 - Reduces local recurrance
           - > Due to clamping of cessels
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70
Q

What is the incidence of testicular tumours and what age is the peak incidence?

A

5 per 100,000 men

20-35 years

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71
Q

What is the increase in incidence of testicular tumours if there are undescended testes?

A

30 times risk

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72
Q

What are the three types of teratomas?

A

Differentiated
Intermediate
Undifferentiated

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73
Q

In trophoblastic teratomas, what percentage have a raised hCG?

A

100%

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74
Q

What fraction of residual masses have the following characteristics:

  • Only fibrous tissue
  • Mature (benign) teratoma
  • Residual tumour
A

Only fibrous tissue - A third
Mature (benign) teratoma - A third
Residual tumour - A third

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75
Q

Which of the following does not result from uraemia:

  • Pericarditis
  • Encephalopathy
  • Bronchitis
  • Neuropathy
  • Asterixis
  • Gastritis
A

Bronchitis

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76
Q

What effect does kidney disease have on Vitamin D? What does this result in?

A

Cannot be converted into the active form (Calcitriol)
Results in:
- Bone disease
- Vascular calcification

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77
Q

What effect will kidney failure have on phosphate levels?

A

Phosphate will not be filtered into the filtrate as well so hyperphosphataemia will result

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78
Q

Why does renal failure result in anaemia?

A

Reduced production of erythropoietin

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79
Q

Why can dyspepsia happen in renal failure?

A

Increased risk of peptic ulcers

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80
Q

In renal failure there are a number of urinary tract features, what are they?

A

Frequency

Urgency Polyuria

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81
Q

How do NSAIDs affect the kidneys?

A

Reduced eGFR

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82
Q

What antibiotics can affect the kidneys?

A

Gentamicin -> Toxic
Trimethoprim -> Fluid retention
Penicillins

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83
Q

What happens to JVP in renal failure?

A

It is increased

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84
Q

What is accelerated hypertension classed as?

A

Diastolic BP >120mmHg

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85
Q

What is leukonychia a sign of?

A

Hypoalbuminaemia

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86
Q

Gouty tophi are seen in what kind of kidney disease?

A

CKD

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87
Q

Vasculitis skin rash and systemic vasculitis are signs of what renal disease?

A

Acute glomerulonephritis

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88
Q

What type of vasculitis is HSP?

A

IgA

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89
Q

What is the usual specific gravity of urine and what does this indicate?

A

1.01-1.02

[Urine]

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90
Q

What can cause urine to appear red?

A

Haemoglobin
RBC
Free Hb
Myoglobin

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91
Q

Alkaline urine is seen in what?

A

UTI

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92
Q

If RBCs appear isomorphic in urine microscopy, what does this indicate?

A

It is a lower urinary tract cause

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93
Q

If RBCs appear dysmorphic in urine microscopy, what does this indicate?

A

They are from the glomerulus (been forced out so become misshapen)

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94
Q

What is a normal result of a 24hr urine collection for protein?

A
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95
Q

What is a normal protein:creatinine ratio?

A
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96
Q

What is classed as asymptomatic low grade proteinuria?

A

A protein:creatinine ratio of 0.5-1g/day (100mg/mmol)

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97
Q

What is classed as heavy proteinuria?

A

A protein:creatinine ratio of 1-3g/day (~300mg/mmol)

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98
Q

How is nephrotic syndrome classed in terms of protein:creatinine ratio?

A

> 3g/day

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99
Q

Increased urine protein can indicate what?

A

Increased risk of dialysis need in the future

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100
Q

What causes urinary casts to form? Where is this secreted from?

A

Precipitation of Tamm-Horsfall mucoprotein:

- Renal tubule cells

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101
Q

What causes pronounced formation of urinary casts? What precipitates this?

A

Protein denaturation:

 - Reduced urine flow
 - Low pH
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102
Q

Hyaline casts in the urinary are usually benign; true or false?

A

True

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103
Q

What do RBC urinary casts indicate?

A

Nephritic syndrome

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104
Q

What do leukocyte urinary casts indicate?

A

Infection

Inflammation

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105
Q

What do granular urinary casts indicate?

A

CKD

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106
Q

What chemicals can show up as crystals on urine microscopy? Which is the most common?

A

Calcium oxalate (most common)
Urate
Phosphate
Cysteine

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107
Q

Hypertension shows ECG changes indicative of what?

A

LVH and strain

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108
Q

What is Stage 1 CKD in terms of description and GFR?

A

Kidney damage with normal or increased GFR

GFR >90

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109
Q

What is Stage 2 CKD in terms of description and GFR?

A

Kidney damage with mildly reduced GFR

GFR 60-89

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110
Q

What is Stage 3 CKD in terms of description and GFR?

A

Moderatley reduced GFR:

- GFR 30-59

111
Q

What is Stage 4 CKD in terms of description and GFR?

A

Severely reduced GFR:

GFR 15-29

112
Q

What is Stage 5 CKD in terms of description and GFR?

A

Kidney failure:

- GFR

113
Q

What is kidney damage in terms of CKD 1 and 2?

A

Evidence of disease:

 - Haematuria
 - Proteinuria
114
Q

What is oliguria classified as?

115
Q

What features need to be present for a patient to have an AKI?

A

Reduction in GFR over hours/days/weeks
+/- Oliguria
With normal/impaired baseline renal function

116
Q

Proteinuria (>3g/day) (mostly albumin), Hypoalbuminaemia, Oedema (limb and periorbital), Hypercholesterolaemia and often normal GFR are signs of what?

A

Nephrotic syndrome

117
Q

AKI, Oliguria, Oedema, Hypertension and Active urinary sediment (RBCs, RBC and granular casts and proteinuria) are signs of what?

A

Nephritic syndrome

118
Q

Can CKD be diagnosed from one eGFR calculation?

119
Q

How is GFR measure directly and why is it not routinely used?

A

Nuclear medicine:

 - Time consuming
 - Expensive
120
Q

How do we usually calculate an eGFR?

A

Creatinine clearance

121
Q

Why does creatinine clearance overestimate GFR?

A

Creatinine is secreted into the tubules

122
Q

What is serum creatinine a product of?

A

Muscle breakdown

123
Q

For white and asian males, what is the calculation for eGFR if creatinine is in mg/dL?

A

186 x Creatinine^-1.154 x Age^-0.203

124
Q

For white and asian males, what is the calculation for eGFR if creatinine is in μmol/L?

A

32788 x Creatinine^-1.154 x Age^-0.203

125
Q

What correction factors are applied to the eGFR calculation for:

  1. Women
  2. Black people
A
  1. Multiply whole equation by 0.742

2. Multiply whole equation by 1.212

126
Q

When is eGFR mostly accurate?

127
Q

If a patient has a low muscle mass, what effect does this have on eGFR?

A

It is overestimated

128
Q

If a patient has a high muscle mass, what effect does this have on eGFR?

A

It is underestimated

129
Q

When is eGFR valid?

A

If [Creatinine]p is stable

130
Q

What percentage of patients are in Stage 1 or 2 CKD?

131
Q

What is Stage 3a of CKD?

A

GFR 45-59ml/min

132
Q

What is Stage 3b of CKD?

A

GFR 30-44ml/min

133
Q

What percentage of patients are in Stage 3 CKD?

134
Q

What percentage of patients are in Stage 4 CKD?

135
Q

What percentage of patients are in Stage 5 CKD?

136
Q

What are some common causes of CKD?

A 
DM
Hypertension
Vascular disease
Chronic glomerulonephritis
Reflux nephropathy
Polycystic kidney disease
137
Q

When do symptoms of CKD tend to appear?

138
Q

Which of the following is not a typical non-specific sign of CKD:

  • Tiredness
  • Poor appetite
  • Itch
  • Weight loss
  • Sleep disturbance
A

Weight loss

139
Q

Impaired urine concentrating in CKD can cause what?

140
Q

What medications can be used to both reduce proteinuria and control BP?

141
Q

What are some cautions when using ACEi/ARB/Spironolactone in CKD?

A

Modest decline in GFR at first

Hyperkalaemia

142
Q

How can CVS risk be reduced in CKD?

A

Control BP and proteinuria
Stop smoking
Statins

143
Q

Apart from erythropoietin, what else should we check as a cause of anaemia in CKD?

A

Vitamin B12

Folate

144
Q

What is the initial treatment for anaemia in CKD?

145
Q

If after the first line treatment for anaemia in CKD the patient is still anaemic, what do we do?

A

Epo. injection (weekly/fortnightly)

146
Q

What is the target Hb in a CKD patient?

A

10.5-12.5g/dL

147
Q

What does CKD initially cause in regards to Vit. D and calcium metabolism?

A

Reduced calcium absorption

Secondary hyperparathyroidism

148
Q

What effect does advanced CKD have on Phosphate and what happens due to this?

A

Increased serum phosphate -> Increased PTH secretion

149
Q

What effect do increased phosphate and calcium have on the cardiovascular system?

A 
Vascular calcification (Become stiff)
(Can also affect heart valves)
150
Q

How can we treat bone disease in CKD?

A

Alfacalcidol (Hydroxylated/Activated Vit D)
Phosphate binders:
- Reduced gut absorption
- eg. Calcium carbonation/acetate + Sevelamer

151
Q

When is dialysis considered?

152
Q

How long does an arteriovenous fistula take to form?

153
Q

How long do you have to wait before the catheter can be used in peritoneal dialysis?

154
Q

How soon can patients be registered for cadaveric kidney transplant?

A

Within 6 months of dialysis beginning

155
Q

What is the definition of AKI?

A

Abrupt (26.4μmol/L

 - OR rise in Cr by 50%
 - OR a decline in urine output
156
Q

What are the 3 criteria that can be used to diagnose Stage 1 AKI (KDIGO staging)?

A 
Serum creatinine criteria:
     - Increase >26μmol/L
     - OR Increase >1.5-1.9 x Reference Cr
Urine output criteria:
     - 6 consecutive hours
157
Q

What are the 2 criteria that can be used to diagnose Stage 2 AKI (KDIGO staging)?

A

Serum creatinine criteria:
- Increase >2-2.9 x Reference Cr
Urine output criteria:
- 12 consecutive hours

158
Q

What are the 5 criteria that can be used to diagnose Stage 3 AKI (KDIGO staging)?

A 
Serum creatinine criteria::
     - Increase >3 x Reference Cr
     - OR Increase to >354μmol/L
     - OR need for renal replacement therapy
Urine output criteria:
     - 24 consecutive hours
     - OR Anuric for 12 hours
159
Q

What can all the pre-renal causes of AKI be classified as?

A

Functional causes

160
Q

The following three conditions all cause pre-renal AKI; how can they come about?

  • Hypovolaemia
  • Hypotension
  • Renal hypoperfusion
A 
Hypovolaemia:
     - Haemorrhage
     - D&V/Burns
Hypotension:
     - Cardiogenic shock
     - Distributive shock (Sepsis/Anaphylaxis)
Renal hypoperfusion:
     - NSAIDs/COX-2
     - ACEi/ARBs
     - Hepatorenal syndrome
161
Q

What is pre-renal AKI essentially?

A

Reversible volume depletion leading to:

 - Oliguria
 - Increased serum creatinine
162
Q

What is oliguria defined as?

163
Q

What effect do ACE inhibitors have on the efferent arterioles and what does this cause? How does renal perfusion affect this?

A

Efferent arteriole vasodilation -> Reduced filtration pressure:

 - If mildly decreased perfusion -> Mildly reduced GFR
 - If hugely decreased perfusion -> Huge GFR drop
164
Q

Put the following steps of the pathophysiology of Pre-renal AKI in order:

  • Reduced effective intravascular volume
  • Sodium and water retention
  • Oliguria
  • Volume depletion/Sepsis
  • Increased levels of ADH and Aldosterone
  • AKI
A
  1. Volume depletion/Sepsis
  2. Reduced effective intravascular volume
  3. Increased levels of ADH and Aldosterone
  4. Sodium and water retention
  5. Oliguria
  6. AKI
165
Q

How much of the cardiac output do the kidneys receive?

166
Q

What is the commonest presentation of AKI and what causes it?

A

Acute Tubular Necrosis

Due to untreated pre-renal AKI

167
Q

What are the common causes of Acute Tubular Necrosis?

A

Sepsis

Severe dehydration

168
Q

What are some less common causes of Acute Tubular Necrosis?

A

Rhabdomyolysis

Drug toxicity

169
Q

What type of AKI is acute tubular necrosis?

170
Q

What feature is pathognomonic of Acute Tubular Necrosis?

A

Muddy brown casts in the urine

171
Q

In acute tubular necrosis, what is the fractional sodium excretion?

A

Above 2-3%

172
Q

In pre-renal AKI, what is the fractional sodium excretion?

173
Q

How can we assess hydration?

A 
BP
HR
Urine output
JVP
Capillary refill
Oedema
174
Q

What solution must we not give as a fluid challenge for hypovolaemia?

A

5% dextrose

175
Q

When should we seek help in treating hypovolaemia?

A

If no change after >1L given

176
Q

What is the underlying pathology behind renal AKI?

A

Inflammation or damage to cells

177
Q

Renal AKI is typically split by the structures affected, what is it divided into?

A

Vascular
Glomerular
Interstitial
Tubular

178
Q

What are vascular causes of renal AKI?

A

Vasculitis

Renovascular disease

179
Q

What are some causes of interstitial nephritis?

A

Drugs
TB
Sarcoidosis

180
Q

What can cause a tubular injury?

A

Ischaemia (Prolonged hypeperfusion [pre-renal AKI])
Gentamicin
Contrast
Rhabdomyolysis

181
Q

Uraemia will have what signs in renal AKI?

A

Itch

Pericarditis

182
Q

What history features may suggest renal disease?

A 
Sore throat
Rash
Joint pains
D&V
Haempotysis
183
Q

What electrolytes on U+Es are markers of renal function?

A

Na+
K+
Urea
Creatinine

184
Q

If, on FBC, there are low platelets, what might be causing the renal AKI?

A

Haemolytic Uraemic Syndrome

Thrombotic Thrombocytopaenic Purpura

185
Q

Abnormal clotting can suggest what in renal disease?

A

Disseminated Intravascular Coagulation

Sepsis

186
Q

When is anaemia seen in renal disease?

A

If CKD

If due to myeloma

187
Q

Haematoproteinuria suggests what?

A

Active glomerulonephritis

188
Q

Anti-GBM antibodies

A

Goodpasture’s

189
Q

How can we test for myeloma and in what age group would we routinely do these investigations?

A

Protein electrophoresis
Bence Jones Protein
In everyone >50 years old

190
Q

What are urgent indications for a renal biopsy?

A

Rapidly progressive glomerulonephritis

Positive immunology and AKI

191
Q

How can we be sure that performing a renal biopsy will be safe?

A

Normal clotting (No Warfarin/Aspirin)
Normotensive
No hydronephrosis

192
Q

If fluid resuscitation doesn’t work in the treatment of AKI, what might we deliver?

A

Inotropes

Vasopressors

193
Q

When is dialysis commenced in AKI?

A 
If anuric and uraemic (>40)
Hyperkalaemia:
     - >7
     - OR >6.5 and unresponsive to therapy
Severe acidosis (pH
194
Q

What is severe acidosis defined as?

195
Q

What is severe uraemia defined as?

A

> 40mmol/L

196
Q

What is the general pathophysiology of post-renal AKI?

A
  1. Urine flow obstruction
  2. Hydropnephrosis
  3. Loss of concentrating ability
197
Q

How is post-renal AKI treated?

A

Catheter
Nephrostomy
Ureteric stenting

198
Q

What is hyperkalaemia defined as?

A

> 5.0mmol/L

199
Q

What is life-threatening hyperkalaemia defined as?

A

> 6.5mmol/L

200
Q

At a serum potassium level of 6-7mmol/L, what ECG changes will be seen?

A

Tented T waves

201
Q

At a serum potassium level of 7-8mmol/L, what ECG changes will be seen?

A

Flattened P waves
Increased PR interval (>0.12-0.20 seconds)
Depressed ST segment
Tented T waves

202
Q

At a serum potassium level of 8-9mmol/L, what ECG changes will be seen?

A 
Atrial standstill (absent P waves)
Prolonged QRS (>0.06-0.10 seconds)
Further tenting of T waves
203
Q

At a serum potassium level of >9mmol/L, what ECG changes will be seen?

A

Sine-wave pattern

204
Q

How do we protect the myocardium in hyperkalaemia?

A

10ml of 10% Calcium Gluconate over 2-3 minutes

OR 5ml 10% Calcium Chloride

205
Q

Can the myocardial protection treatment in hyperkalaemia be repeated?

A

Yes (up to 40ml of calcium gluconate)

206
Q

How long does the protective effect over the myocardium last?

207
Q

How does insulin move K+ back into the cells?

A
  1. Binds to its cellular receptor
  2. Increases Na-K-ATPase activity
  3. K+ taken up into cells
208
Q

How do we administer insulin in hyperkalaemia?

A

Actrapid:

- 10-15IU in 50ml of 50% Dextrose over 30mins

209
Q

How long does insulins affect last for in the treatment of hyperkalaemia?

210
Q

How regularly can insulin therapy be used in hyperkalaemia?

A

Every 4 hours

211
Q

How regularly must we check blood glucose after insulin therapy (for hyperkalaemia) and what do we do in it drops?

A

Every 6 hours

Infuse 10% glucose if glucose drops

212
Q

How else can we move K+ back into cells?

A

Nebulised salbutamol for 90 minutes

213
Q

What does calcium resonium do?

A

Reduces gut absorption of K+

214
Q

If a 25 year old IVDU is found collapsed at home and his renal function has deteriorated, what is the most likely cause?

A

Rhabdomyolysis

215
Q

Which of the following does not cause hyperkalaemia:

  • Spironolactone
  • Ramipril
  • Amiloride
  • Furosemide
  • Atenolol
A

Furosemide

216
Q

What is the second most common cause of Stag 5 CKD (after DM)?

A

Chronic glomerulonephritis

217
Q

What is glomerulonephritis?

A

Immune mediated disease affecting the glomeruli with secondary tubulointerstitial damage

218
Q

How does humoral glomerulonephritis arise?

A

Intrinsic or Planted Ag results in the deposition of circulating immune complexes

219
Q

What causes a proliferative glomerulonephritis and what is the main presenting feature?

A

Damage to endothelial/mesangial cells

Haematuria (+/- proteinuria)

220
Q

What causes a non-proliferative glomerulonephritis and what is the main presenting feature?

A

Damage to podocytes

Proteinuria (NO haematuria)

221
Q

What would you expect to see on urine microscopy of a patient with glomerulonephritis?

A

Dysmorphic RBCs
RBC + granular casts
Lipiduria

222
Q

What is microalbuminaemia defined as?

A

30-300mg Albumin/day

223
Q

What kind of glomerulonephritis can present as an AKI?

A

Rapidly Progressive Glomerulonephritis (RPGN)

224
Q

Nephritic syndrome is indicative of what kind of process; proliferative or non-proliferative?

A

Proliferative

225
Q

Nephrotic syndrome is indicative of what kind of process; proliferative or non-proliferative?

A

Non-proliferative

226
Q

How can nephrotic syndrome result in more infections?

A

Loss of opsonising antibodies

227
Q

Which of the following is not a complication of nephrotic syndrome:

  • Renal vein thrombosis
  • Pulmonary embolism
  • Volume depletion
  • Vitamin D deficiency
  • Hyperthyroidism
A

Hyperthyrodisim (actually causes subclinical hypothyroidism

228
Q

What are the majority of cases of GN?

A

Idiopathic/Primary

229
Q

What is secondary GN associated with?

A 
Infections/Drugs
Malignancy
Systemic disease:
     - ANCa associated vasculitis
     - SLE
     - Goodpasture's
     - HSP
230
Q

What type of ANCA is PR3 and what is it seen in (mainly)?

A

c-ANCA

GPA

231
Q

What type of ANCA is MPO and what is it seen in (mainly)?

A

p-ANCA

Microscopic polyangiitis and EGPA

232
Q

What do proliferative and non-proliferative GN refer to?

A

Absence or presence of mesangial cell proliferation

233
Q

What is cresenteric GN?

A

Presence of crescents:

 - Epithelial cell extracapillary proliferation eg. RPGN in vasculitis
234
Q

What are the target BPs in GN?

235
Q

What sort of supplements might have a benefit in GN?

A

Omega-3 fatty acids

Fish oil

236
Q

What corticosteroids are used in GN?

A

PO prednisolone

IV methylprednisolone

237
Q

What alkylating agents are used in GN?

A

Cyclophosphamide

Chlorambucil

238
Q

What calcineurin inhibitors are used in GN?

A 
Cyclosporin A (CSA)
Tacrolimus
239
Q

What two other drugs are used in GN (ie. Not steroids/alkylating agents/calcineurin inhibitors)?

A 
Azathioprine
Mycophenalate Mofetil (MMF)
240
Q

What other non-drug immunosuppression can be used in the treatment of GN?

A

Plasmapharesis
Antibodies:
- IV Ig
- Monoclonal T or B cell antibodies

241
Q

Which of the following is not used in the general treatment of nephrotic syndrome:

  • Fluid and salt restriction
  • Statins
  • Diuretics
  • ACEi/ARBs
  • Anticoagulation
  • IV albumin
A

Statins (though anticoagulation use is questionable)

242
Q

What is complete remission of nephrotic syndrome?

243
Q

What is partial remission of nephrotic syndrome?

244
Q

Who is minimal change nephropathy most common in?

A

Children (77% of cases)

245
Q

On renal biopsy, how does minimal change nephropathy appear?

A

Normal on:
- Light microscopy
- Immunofluorescence
Foot process fusion (podocyte) on electron microscopy

246
Q

What drug treatment will induce remission in 94% of patients with minimal change nephropathy?

A

Oral steroids

247
Q

What are the second line drugs for minimal change nephropathy if the first line doesn’t work?

A 
Cyclophosphamide
Cyclosporin A (CSA)
248
Q

True or false; minimal change nephropathy will not cause progressive renal failure?

249
Q

What is the possible cause of minimal change nephropathy?

250
Q

Who is focal segmental glomerulosclerosis most common in?

A

Adults (35% of cases)

251
Q

What can causes secondary focal segmental glomerulosclerosis?

A

HIV
Heroin
Obesity
Reflux nephropathy

252
Q

What does focal segmental glomerulosclerosis appear like on renal biopsy?

A

Light microscopy:
- Minimal Ig deposition
Immunofluorescence:
- Minimal complement deposition

253
Q

How many cases of focal segmental glomerulosclerosis will be induced into remission by oral steroids?

254
Q

How many cases of focal segmental glomerulosclerosis progress to ESRD and how long does this take?

A

50% in 10 years

255
Q

What is the aetiology of focal segmental glomerulosclerosis?

A

Soluble urokinae plasminogen activator receptor (suPAR) in 67%
Increased integrins
Podocytes effacement

256
Q

Who is membranous nephropathy most common in?

A

Adults:

 - 2nd commonest cause of nephrotic syndrome
 - 15-30%
257
Q

What infections are secondary causes of V?

A

Hepatitis

Prasites

258
Q

What connective tissue disease is linked to membranous nephropathy?

259
Q

What malignancies are associated with membranous nephropathy?

A

Carcinomas

Lymphoma

260
Q

What drugs are associated with membranous nephropathy?

A

Gold

Penicillamine

261
Q

How does membranous nephropathy appear on renal biopsy?

A

Subepithelial immune complex deposition in BM (making it appear thicker)

262
Q

How is membranous nephropathy treated?

A

Steroids
Alkylating agents
B-cell monoclonal antibodies

263
Q

How many cases of membranous nephropathy progress to ESRD and how long does this take?

A

30% in 10 years

264
Q

What can precipitate microscopic haematuria in IgA nephropathy?

A

Respiratory/GI infection

265
Q

Where is IgA nephropathy most common?

A

Worldwide (most common cause of GN worldwide)

266
Q

What is IgA nephropathy associated with and how would it present?

A

HSP:

 - Arthritis
 - Colitis
 - Purpura
267
Q

How does IgA nephropathy appear on renal biopsy?

A

Light microscopy:
- Mesangial cell proliferation and expansion
Immunofluorescence:
- IgA deposits in mesangium

268
Q

How many cases of IgA nephropathy progress to ESRD and how long does this take?

A

25% in 10 years

269
Q

How is IgA nephropathy treated?

A

BP control
ACEi/ARB
Fish oil

270
Q

What is present in the urine of Rapidly Progressive Glomerulonephritis patients?

A

Active sediment:

 - RBCs
 - RBC + granular casts
271
Q

How does Rapidly Progressive Glomerulonephritis appear on renal biopsy?

A

Glomerular crescents

272
Q

What are some ANCA-positive causes of Rapidly Progressive Glomerulonephritis?

A

GPA

Microscopic polyangiitis

273
Q

What are some ANCA-negative causes of Rapidly Progressive Glomerulonephritis?

A

Goodpasture’s
HSP/IgA
SLE

274
Q

How is Rapidly Progressive Glomerulonephritis treated?

A

Steroids:
- IV Methylprednisolone/PO Prednisolone
Cytotoxics:
- Cyclophsphamide/MMF/Azathioprine
Rituximab (B-cell CD20 receptor monoclonal antibodies)
Plasmapharesis

Year 2 - Renal (DP) (15 decks)

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