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Year 2 - Renal (DP) > Clinical (Week 5) > Flashcards

Clinical (Week 5) Flashcards

1
Q

How quickly does blood flow through the dialysis machine?

A

300ml/min

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2
Q

The following ions are in the dialysate, but are they in higher or lower concentrations than the patients blood:

  • Na+
  • Bicarbonate
  • K+
  • Glucose
A

Na+ is lower
Bicarbonate is higher
K+ is lower
Glucose is about equal (if not slightly higher)

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3
Q

How is water removed from the patient?

A

Dialysate hydrostatic pressure

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4
Q

Why is pure water used for the dialysate?

A

No cytokines, bacteria or toxins present that may damage the patients

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5
Q

How efficient is dialysis?

A

Not very:

- 10-12ml/min/1.73m^2

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6
Q

If a patient was on dialysis 3hrs/3times/week, what would their absolute death risk increase be?

A

6% (1% for each half hour and they would be 3 hours down)

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7
Q

If a patient on dialysis is anuric, what must their fluid intake be restricted to?

A

1L per day

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8
Q

What foods contain high levels of K+ so should be avoided when a patient is on dialysis?

A

Bananas
Chocolate
Potatoes
Avacado

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9
Q

Why should a low phosphate diet be observed when on dialysis?

A

It isn’t dialysed well

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10
Q

What should be avoided as they are high in phosphate?

A

Ready meals

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11
Q

When are phosphate binders taken and what do they do?

A 
With meals (6-12 per day):
     - Prevent GI phosphate absorption
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12
Q

What is the main con of using a Scribner shunt for dialysis?

A

Eventually clogs

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13
Q

When is a Scribner shunt still used?

A

For dialysis in AKI or ESRD

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14
Q

What veins can a tunnelled venous catheter be inserted into and which is preferred?

A

Jugular (preferred)
Subclavian
Femoral

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15
Q

Which of the following can be used in dialysing and AKI patient:

  • Scribner shunt
  • Fistula
  • Tunnelled venous catheter
A

Scribner shunt

Tunnelled venous catheter

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16
Q

In which of the following is infection most likely and with what organism:

  • Scribner shunt
  • Fistula
  • Tunnelled venous catheter
A

Tunnelled venous catheter

Staph. aureus

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17
Q

If a dialysis site gets infected, what can result?

A

Endocarditis

Discitis

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18
Q

How is an infected dialysis line treated?

A

Vancomycin

Line removal

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19
Q

How does intradialytic hypotension arise?

A

ICF -> ECF -> Intravascular -> Hypotension

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20
Q

If a patient becomes fluid overloaded on dialysis, what can result?

A

Pulmonary oedema
Hypertension
Appearance of LVF

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21
Q

What drug should not be given if a patient on dialysis becomes fluid overloaded?

A

Furosemide

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22
Q

What are some other complications of dialysis?

A

Blood leaks -> Exsanguination?
Loss of vascular access
Hypokalaemia -> Cardiac arrest

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23
Q

What drives water removal across the peritoneal membrane in peritoneal dialysis?

A

High [Glucose] in the dialysate fluid

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24
Q

How is continuous peritoneal dialysis carried out?

A

4 bag exchanges per day
Fluid drained then replaced
30 minutes per exchange

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25
Q

How is automated peritoneal dialysis carried out?

A

1 bag left in all day

Overnight machine drains it in and out (over 9hrs)

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26
Q

What are the benefits of continuous peritoneal dialysis?

A

Simpler
Lower-tech
Cheaper

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27
Q

Where can infection arise in peritoneal dialysis?

A

Peritonitis

Exit site

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28
Q

What are typical contaminants that cause infection in peritoneal dialysis patients?

A

Staph
Strep
Diphtheroids

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29
Q

What gut bacteria can cause infection in peritoneal dialysis patients?

A

E. coil

Klebsiella

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30
Q

What must we do before treating infection in peritoneal dialysis?

A

Culture PD fluid

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31
Q

What is the treatment for peritoneal dialysis infections?

A

Intraperitoneal antibiotics:

- Vancomycin + Gentamicin

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32
Q

In what peritoneal dialysis infections must the catheter be removed?

A

Staph

Pseudomonas

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33
Q

Why can peritoneal dialysis only last so long?

A

Peritoneal membrane thickens -> Inability to remove enough fluid

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34
Q

What can an increased intra-abdominal pressure on standing cause in peritoneal dialysis?

A

Hernia

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35
Q

What symptoms may indicate the need for dialysis?

A 
Fatigue
Fluid overload
Vomiting
Itch
Nausea
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36
Q

How long does the 1st session of haemodialysis usually last?

A

2 hours

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37
Q

Why is the 1st session of haemodialysis shorter?

A

Prevent disequilibrium syndrome:

 - Cerebral oedema
 - Seizures
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38
Q

Which of the following might indicate the need for withdrawal from dialysis:

  • PVD
  • Cerebrovascular disease
  • CVD
  • Cancer
  • Liver failure
  • Increased patient fragility
  • Palliative care
A

Liver failure

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39
Q

How is overt diabetic nephropathy defined?

A

Persistent albuminaemia:

 - 300mg/24hr
           - > On >2 occasions
                      - > 3-6 months apart
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40
Q

How does autonomic neuropathy present in diabetes?

A

Gastroparesis
Silent MI
Urogenital abnormalities

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41
Q

What haemodynamic changes are involved in diabetic nephropathy?

A
  1. Afferent arteriolar vasodilation:
    • Mediated by vasoactive chemicals (IGF-1)
  2. Hyperflitration
  3. Increased GFR
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42
Q

What causes renal hypertrophy in diabetic nephropathy?

A

Increased plasma glucose -> Renal growth factors

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43
Q

What is a Kimmelstiel-Wilson Lesion?

A

Nodular diabetic glomerulosclerosis

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44
Q

What does proteinuria indicate in diabetic nephropathy?

A

GBM thickening

Podocyte dysfunction

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45
Q

How can we try and prevent diabetic nephropathy?

A

Glycaemic control:

- HbA1c

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46
Q

What is the most common causes of renovascular hypertension?

A

Renal artery stenosis

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47
Q

What causes ischaemic nephropathy?

A

Reduced GFR associated with renal hypoperfusion beyond level of autoregulatory compensation

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48
Q

What can ischaemic nephropathy result in?

A

Renal atrophy

Progressive CKD

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49
Q

What is the prevalence of fibromuscular dysplasia?

A

4:1000

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50
Q

What people are most commonly affected by fibromuscular dysplasia?

A

Females aged 15-50yrs

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51
Q

What percentage of fibromuscular dysplasia cases are familial and how do they tend to present?

A

10%

Involving both renal arteries

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52
Q

What is fibromuscular dysplasia associated with?

A

Ehlers-Danlos

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53
Q

If fibromuscular dysplasia involves the cerebral arteries, what can happen?

A

Carotid artery dissection

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54
Q

What patients does atherosclerotic renovascular disease tend to affect?

A

Caucasian males aged >50yrs

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55
Q

With what do patients with renovascular disease tend to present?

A

AKI after ACEi treatment

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56
Q

How can patients with atherosclerotic renovascular disease present?

A

Renovascular hypertension
Flash pulmonary oedema
Microscopic haematuria
Renal bruit

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57
Q

Which of the following is not useful in screening for ischaemic renal disease?

  • Renal USS
  • Renal artery duplex studies
  • Urine microscopy
  • CT/MRI angiography
  • Angiography
A

Urine microscopy

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58
Q

How are the majority of ischaemic renal disease patients treated?

A

Medical therapy

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59
Q

What surgical options are useful in treating ischaemic renal disease?

A

Angioplasty (+/- stenting)

Stenting alone

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60
Q

When are ACEi inhibtiors contra-indicated in renovascular disease?

A

Bilateral renal artery stenosis

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61
Q

What is myeloma?

A

Cancer of plasma cells

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62
Q

How does myeloma cause disease?

A

Abnormal plasma cells accumulate in bone marrow:

- Interfere with normal RBC production

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63
Q

What antibody can also be produced by myelomas?

A

Paraprotein

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64
Q

Which of the following is not a sign of myeloma:

  • Anaemia
  • Recurrent infections
  • Haematuria
  • Renal failure
  • Amyloidosis
  • Hypercalcaemia
A

Haematuria

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65
Q

Which of the following is not a symptom of myeloma:

  • Bone pain
  • Weakness
  • Fatigue
  • Nausea
  • Weight loss
A

Nausea

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66
Q

On blood tests, what are the signs of myeloma?

A 
Normocytic anaemia (in 75%)
Rouleaux formation (chains of RBCs) (in 50%)
Increased CRP/PV (in 30%)
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67
Q

Apart from blood testing, what other investigations can be carried out for myeloma?

A

Protein electrophoresis
BJP in urine
Lytic lesions on skeletal survey

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68
Q

What are the peak ages of myeloma incidence in males and females?

A

Males - 80 years

Females - 70 years

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69
Q

In what populations is the risk of myeloma doubled?

A

Blacks

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70
Q

What percentage of myeloma patients have renal impairment at presentation?

A

50%

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71
Q

What percentage of myeloma patients need dialysis at presentation?

A

10%

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72
Q

Which of the following is not a renal manifestation of myeloma:

  • AKI (secondary to hypercalcaemia)
  • Monoclonal Ig Deposition disease
  • Glomerulonephritis
  • Cast nephropathy
  • Amyloidosis
A

GN

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73
Q

What is the pathology of amyloidosis?

A

Deposition of proteinaceous material in extracellular spaces

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74
Q

How is amyloidosis classified?

A

By type of precursor protein that makes up the main component of the fibrils

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75
Q

What are the two classes of renal amyloidoses?

A 
Primary amyloid (Amyloid Light-chain [AL])
Secondary amyloid (Serum Amyloid A [AA])
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76
Q

What is the classical histological appearance of amyloidosis?

A

Positive Congo-Red staining:

 - Showing apple-green birefringence
           - > Under polarised light
77
Q

What nephrotoxins need stopped in myeloma with acute renal failure?

A

NSAIDs

Diuretics (increase risk of cast formation)

78
Q

How do we treat hypercalcaemic in myeloma?

A

IV saline for volume resuscitation

IV pamidronate

79
Q

What can reduce the tumour load in myeloma?

A

Chemotherapy

High dose dexamethasone

80
Q

What can plasma exchange do in the treatment of myeloma?

A

Removes amyloid light chains

81
Q

What is GPA?

A

Necrotising granulomatosis inflammation

82
Q

Where does GPA most commonly affect?

A

Respiratory tract

83
Q

How does EGPA usually present?

A

Asthma (>95%) and eosinophilia

84
Q

What percentage of EGPA patients have skin involvement and what skin features would be present?

A

66%
Palpable purpura
S/C nodules

85
Q

Is microscopic polyangiitis necrotising?

A

No

86
Q

Why can microscopic polyangiitis result in pulmonary haemorrhage?

A

Alveolar capillary involvement

87
Q

In what two small vessel vasculitides is renal involvement more common?

A

GPA

MPA

88
Q

How does small vessel vasculitis-related renal disease present?

A

Haematuria
Proteinuria
AKI

89
Q

How do small vessel vasculitides appear on renal biopsy?

A

Segmental necrotising GN (crescent)

90
Q

What percentage of SLE patients have renal involvement at presentation?

A

50%

91
Q

What percentage of SLE patients will have some renal involvement during the course of their disease?

A

60%

92
Q

What is the most common presentation of lupus nephritis?

A

Proteinuria

93
Q

In the ISN classification of lupus nephritis, what do each of the Classes I-VI mean?

A 
Class I -> Minimal mesangial
Class II -> Mesangial proliferative
Class III -> Focal proliferative
Class IV -> Diffuse proliferative
Class V -> Membranous
Class VI -> Advanced sclerosing
94
Q

What antihypertensive treatment is used in lupus nephritis and what is the target BP?

A

ACEi/ARBs

130/80

95
Q

How do we induce immunosuppression in lupus nephritis?

A

High dose steroids
Cyclophosphamide/MMF
Azathioprine, Rituximab + Tacrolimus

96
Q

How do we maintain immunosuppression in lupus nephritis?

A

Steroids

MMF/Azathioprine

97
Q

Which of the following is not a poor prognostic factor in systemic disease:

  • Renal disease
  • Female
  • Young/Old
  • Poor socio-economic status
  • Antiphospholipid syndrome
  • High disease activity
A

Female (Being male is a poor prognostic factor)

98
Q

What drugs can cause intrarenal failure?

A

Gentamicin
Sulphonamides
Aspirin

99
Q

What drugs can cause post-renal failure?

A

Methysergide

Chemotherapy

100
Q

Which type of adverse drug reaction has a high mortality?

A

Type B (Bizarre reactions)

101
Q

What are some examples of Type B adverse drug reactions?

A

Rashes
Bone marrow aplasia due to Chloramphenicol
Hepatic necrosis due to Halothane

102
Q

Give examples of Type C adverse drug reactions (chronic)?

A

Steroids -> Cushing’s
β-Blockers -> Diabetes
NSAIDs -> Hypertension

103
Q

What types of affects are usually seen in Type D adverse drug reactions?

A

Teratogenic

Carcinogenic

104
Q

What are some examples of Type D adverse drug reactions?

A

Secondary malignancies post-chemotherapy

Craniofacial abnormalities in kids of women taken isotretinoin

105
Q

What can β-blocker therapy withdrawal result in?

A

Angina

106
Q

What can steroid therapy withdrawal result in?

A

Addisonian crisis

107
Q

What drugs does theophylline commonly interact with?

A

Macrolide antibiotics (Clarithromicin, Eryhtromicin)

108
Q

What drugs do statins commonly interact with?

A

Macrolides and Fibrates

109
Q

What drugs do ACEi commonly interact with?

A

Sulphonylureas

110
Q

What drugs does clopidogrel commonly interact with?

A

PPIs

111
Q

What drugs can exacerbate CHF?

A

NSAIDs
COX-2
TZDs

112
Q

What drugs can cause urinary retention in BPH?

A

Decongestants

Anticholinergics

113
Q

What drugs can worsen constipation?

A

Calcium channel blockers

Anticholinergics

114
Q

Potassium rich foods (bananas, oranges and green leafy vegetables) interact with what drugs?

A

ACEi/ARBs

K+ sparing diuretics

115
Q

Vitamine E and K rich foods (apples, chickpeas, spinach, nuts, kiwi and broccoli) interact with what drug?

A

Warfarin

116
Q

Foods that alter pH (chicken, turkey, milk, soy, cheese, yoghurt) interact with what drugs?

A

Antibiotics
Thyroid medications
Digoxin
Diuretics

117
Q

Which foods interact with cytochome P450 and what drugs can this affect?

A

Grapefruit, apple, orange and cranberry:

 - Statins
 - Antihistamines
118
Q

What is the first stage of drug development and what are features of this stage?

A

Pre-clinical:

 - Most efficient
 - Least attrition (Financial cost, morbidity/mortality)
119
Q

What phases of drug development are clinical tries and what are some features of these stages?

A 
Phases 1-3
Limited sample size:
     - Low frequency adverse drug reactions
     - Time lag ADR
Exclusion of frail patients
120
Q

What are some features of post-marketing surveillance?

A

Less efficient
High attrition:
- Financial cost, morbidity/mortality
Most data available

121
Q

What is LD50?

A

The amount of ingested substance/drug that kills 50% of a test sample

122
Q

What is ED50?

A

The effective dose for 50% of people receiving the drug

123
Q

How is the therapeutic index calculated?

A

LD50/ED50

124
Q

What is Phase 1 of drug metabolism?

A

Usually through cytochrome P450:

- Oxidation, Reduction and Hydrolysis

125
Q

What is Phase 2 of drug metabolism? What does it allow?

A

Conjugation -> Water soluble

Enables excretion in urine or bile

126
Q

During what phase of drug metabolism do most adverse drug reaction occur?

A

Phase 1

127
Q

What two mutations can result in ADPKD and what chromosomes do they appear on?

A

PKD1 gene mutations (85% of cases):
- Chromosome 16
PKD2 gene mutations:
- Chromosome 4

128
Q

Which mutation causing ADPKD results in earlier ESKD?

A

PKD1 gene mutations

129
Q

What is the pathology of ADPKD?

A

Large kidneys
Epithelial-lined cysts arise from a small number of tubules
Benign adenomas (25% of kidneys)

130
Q

What is the mean age for hypertension in ADPKD?

A

31

131
Q

What can cause haematuria in ADPKD?

A

Cyst rupture
Cystitis
Stones

132
Q

Is ADPKD painful?

A

Yes it can be

133
Q

What is the most common extra-renal manifestation of ADPKD and when do they appear?

A

Hepatic cysts ten years after renal cysts

134
Q

What can hepatic cysts in ADPKD cause?

A

SoB
Pain
Ankle swelling

135
Q

True or false; Hepatic cysts in ADPKD often allow the liver to continue function?

A

True

136
Q

What percentage of ADPKD patients can suffer from intracranial aneurysms?

A

4-8%

137
Q

Where do ADPKD-related intracranial aneurysms tend to arise?

A

Anterior circulation territory

138
Q

When would you screen for ADPKD-related intracranial aneurysms?

A

If FHx

139
Q

What cardiac disease can result due to ADPKD?

A

Mitral/Aortic valve prolapse
Valvular disease:
- Collagenous/Myxomatous degeneration

140
Q

What can profoundly increase the risk of diverticular disease in ADPKD?

A

If they are on dialysis

141
Q

By what percentage is the incidence of abdominal and inguinal hernias increased in ADPKD?

A

45%

142
Q

What renal changes can be seen on USS of ADPKD?

A

Multiple, bilateral cysts

Renal enlargement

143
Q

What genetic investigations can be done into ADPKD?

A

Linkage analysis

Mutation analysis

144
Q

Early onset ADPKD presents in what patients?

A

In utero

Kids in their 1st year of life

145
Q

How can early onset ADPDK be distinguished from ARPKD?

A

USS:

- ARPKD shows congenital hepatic fibrosis

146
Q

How is ADPKD diagnosed in children?

A

One cysts on USS in a high risk patient

147
Q

How common are cerebral aneurysms in early onset ADPDK?

A

Rare

148
Q

What is the main treatment for ADPKD?

A

Rigorous hypertension control

149
Q

What does Tolvaptan do?

A

Reduces cyst volume and progression

150
Q

If a patient with ADPKD is in renal failure, what treatments can be offered?

A

Dialysis
Transplant
Cardiovascular and Cerebrovascular disease prevention

151
Q

Who does ARPKD present in?

A

Young children

152
Q

How common are hepatic lesions in ARPKD?

A

Very!

153
Q

What is the incidence of ARPKD?

A

1:20,000

154
Q

What is the genetic linkage in ARPKD?

A

PKDH1 (On chromosome 6)

155
Q

Where do the cysts arise from in ARPKD?

A

Collecting ducts

156
Q

Which of the following is not a common presenting sign in ARPKD:

  • Kidneys always palpable
  • Hypertension
  • Recurrent UTI
  • Chronic pain
  • Slow decline in GFR
A

Chronic pain

157
Q

What percentage of ARPKD patients die in the 1st year of life?

A

9-24%

158
Q

If a patient with ARPKD survives the 1st year of life, what is the chance the patient will survive >15 years?

A

80%

159
Q

What is Alport’s syndrome?

A

Hereditary nephritis due to a disorder of Type IV collagen matrix

160
Q

What percentage of patients with ESKD have Alport’s syndrome?

A

1-2%

161
Q

What is the most common inheritance of Alport’s syndrome?

A

X-linked (85%)

162
Q

What is the common gene mutation in Alport’s syndrome and what does it cause?

A

COL4A5:

- Deficient collagenous matrix

163
Q

What is the characteristic feature of Alport’s syndrome?

A

Haematuria

164
Q

When does proteinuria occur in Alport’s syndrome and what is it a sign of?

A

Later

Bad prognostic indicator

165
Q

What are some extra-renal manifestations of Alport’s syndrome?

A

Sensorineural deafness
Ocular defects:
- Anterior lenticonus -> Conical protrusion of lens
- Keratoconus -> Conical corneal protrusion
Leiomyomatosis of oesophagus/genitals (rare)

166
Q

When should Alport’s syndrome be suspected?

A

Haematuria +/- Hearing loss

167
Q

How does Alport’s syndrome appear on renal biopsy?

A

Variable thickness GBM (characteristic)

Lamina densa splitting

168
Q

How is Alport’s syndrome treated?

A 
Aggressive treatment of:
     - BP
     - Proteinuria
Dialysis
Transplant
169
Q

What is Anderson Fabrys Disease?

A

Inborn error of glycosphingolipid metabolism:

 - α-galactosidase A deficiency
 - Lysosomal storage disease
170
Q

What type of inheritance is Anderson Fabrys Disease?

A

X-linked

171
Q

Which of the following does Anderson Fabrys Disease not affect:

  • Kidneys
  • Heart
  • Liver
  • Lungs
  • Eryhtrocytes
A

Heart

172
Q

How will a renal biopsy appear in Anderson Fabrys Disease?

A

Concentric lamellar inclusions within lysosomes

173
Q

What is the main cutaneous feature of Anderson Fabrys Disease?

A

Angiokeratomas

174
Q

What are some cardiovascular features of Anderson Fabrys Disease?

A

Cardiomyopathy

Valvular disease

175
Q

What are some neurological features of Anderson Fabrys Disease?

A

CVA

Acroparaesthesia

176
Q

How can Anderson Fabrys Disease be diagnosed?

A

Plasma leukocyte α-GAL activity
Biopsy:
- Renal
- Skin

177
Q

What is an angiokeratoma?

A

A benign cutaneous lesion of capillaries, resulting in small marks of red to blue color; characterized by hyperkeratosis

178
Q

How is Anderson Fabrys Disease treated?

A

Fabryzyme

Complication management

179
Q

What pattern of inheritance does Medullary Cystic Kidney show?

A

Autosomal dominant

180
Q

What is the pathology behind Medullary Cystic Kidney?

A

Abnormal renal tubules -> Fibrosis

Cysts in the corticomedullary junction and medulla

181
Q

What size are kidneys in Medullary Cystic Kidney?

A

Normal/Small

182
Q

How is Medullary Cystic Kidney diagnosed?

A

FHx

CT

183
Q

When does Medullary Cystic Kidney present?

A

~28 yers of age

184
Q

What is the best treatment for Medullary Cystic Kidney?

A

Transplant

185
Q

What sort of inheritance does medullary sponge kidney show?

A

Sporadic

186
Q

What is the pathology behind medullary sponge kidney?

A

Dilatation of collecting ducts

187
Q

What do the cysts have in medullary sponge kidney?

A

Calculi

188
Q

How is medullary sponge kidney diagnosed?

A

IV urography
OR
Contrast-enhanced CT

Year 2 - Renal (DP) (15 decks)

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