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Yr3 - General Medicine > Renal > Flashcards

Renal Flashcards

1
Q

AAV

A

ANCA Associated Vasculitis

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2
Q

ACR

A

Albumin:Creatinine Ratio

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3
Q

ADPKD

A

Autosomal Dominant Polycystic Kidney Injury

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4
Q

APD

A

Automated Peritoneal Dialysis

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5
Q

ANA

A

Anti-Nucleic Antibody

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6
Q

ANCA

A

Anti-Neutrophilic Cytoplasm Antibody

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7
Q

ATN

A

Acute Tubular Necrosis

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8
Q

AVF

A

AterioVenous Fistula

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9
Q

CAPD

A

Continuous Ambulatory Peritoneal Dialysis

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10
Q

CKD

A

Chronic Kidney Disease

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11
Q

CMV

A

Cytomegalovirus

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12
Q

CNI

A

Calcineurin Inhibitors

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13
Q

CHr

A

Hypochormnic Red Cells

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14
Q

eGFR

A

Estimated Globerular Filtration Rate

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15
Q

ESA

A

Erythropoeitin Stimulating Agent

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16
Q

ESRF

A

End Stage Renal Failure

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17
Q

GN

A

GlomeruloNephritis

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18
Q

GPA

A

Glomerulomatous PolyAngitis

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19
Q

HUS

A

Haemolytic Uraemic Syndrome

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20
Q

MMF

A

Mycophenolate Mofetil

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21
Q

MPA

A

Microscopic PolyAngitis

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22
Q

NODAT

A

New-Onset Diabetes After Transplantation

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23
Q

PCR

A

Protein: Creatinine Ratio

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24
Q

PD

A

Peritoneal Dialysis

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25
Q

PND

A

Paroxysmal Nocturnal Dyspnoea

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26
Q

RRT

A

Renal Replacement Therapy

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27
Q

RPGN

A

Rapidly Progressive GlomeruloNephritis

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28
Q

RTA

A

Renal Tubular Acidosis

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29
Q

SIADH

A

Syndrome of Inappropriate Anti-Diuretic Hormone

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30
Q

SLE

A

Systemic Lupus Erythematosus

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31
Q

SVCO

A

Superior Vena Cava Obstruction

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32
Q

TIN

A

TubuloInterstital Nephritis

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33
Q

TTP

A

Thrombotic Thrombocytopenic Purpura

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34
Q

Features to ask out dyspnoea

A 
Exercise tolerance
Triggers
Relieving factors
Diurnal variation
Orthopnoea
PND
Associated symptoms
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35
Q

Features to ask about leg swelling

A

Site
Severity
Time of onset
Amount of fluid intake

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36
Q

Features to ask about N+V

A 
Triggers
Relieving factors
Able to keep down food
Frequency
Associated symptoms
Bowel frequency
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37
Q

Features to ask about ENT symptoms

A 
Nasal secretions
Sinusitis
Epistaxis
Haemoptysis
Sore throat
Visual disturbances
Hearing loss
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38
Q

Features to ask about constitutional symptoms

A 
Fever
Joint pains
Muscle aches
Weight changes
Lethargy
Night sweats
Pruritus
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39
Q

Features to ask about lower urinary tract symptoms

A 
Dysuria
Frequency
Quantity of urine
Colour of urine
Frothiness
Haematuria
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40
Q

Features to ask about flank pain

A 
Duration
Radiation
Associated symptoms
Intensity
Aggravating/relieving factors
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41
Q

Presenting complaints of renal history

A 
Dyspnoea
Leg swelling
N+V
Upper airway symptoms
Constitutional symptoms
Lower urinary tract symptoms
Flank pain
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42
Q

Features of PMH of renal histroy

A 
Previous AKI - hospitalisation, requiring dialysis
CKD stage
Cause of CKD/ESRD
CVS risk factors - DM, HTN, Hypercholesterolaemia
Recurrent UTIs
Childhood infections
Surgery 
Cancer
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43
Q

Types of haemodialysis lines

A 
Perm-cath
- tunelled under skin
- long term
Vas-cath
- non-tunelled
- short term
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44
Q

Signs of advanced renal disease

A

Brown nails
Discolouration of skin from uraemia
Under-nutrition leading to muscle wasting
Uraemic frost - urea from sweat crystallises on the skin
Hyper-reflexia, pericardial rub, GI ulceration and bleedin

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45
Q

How to calculate anion gap

A

[Na+] - ([Cl-] + [HCO3])

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46
Q

Normal anion gap

A

8-12

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47
Q

What does high anion gap mean

A

Acidosis caused by increased acid

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48
Q

Causes of high anion gap

A 
Lactic acidosis
- anaerobic exercise
- sepsis
- organ ischaemia
Ketoacidosis
- diabetic
- alcohol abuse
- starvation
Toxins
- ethylene glycol
- methanol
- isoniazid
- aspirin
- salicylate
Renal failure
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49
Q

What causes a normal anion gap in acidosis

A

Reduced alkali

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50
Q

Causes of normal anion gap in acidosis

A 
GI losses of HCO3
- vomiting
- diarrhoea
Renal losses of HCO3
- renal tubular acidosis
- mineralocorticoid deficiency (Addison's)
Toxins
- ammonium chloride
- acetazolamide
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51
Q

Causes of hypernatraemia

A

Usually water deficit

  • cellular dehydration - osmotic drag
  • vascular shear stress - bleeding and thrombosis
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52
Q

Symptoms of hypernatraemia

A 
Thirst
Apathy
Irritability
Weakness
Confusion
Reduced consciousness
Seizures
Hyperfreflexia
Spasticity
Coma
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53
Q

Causes of hypovolaemic high Na+

A 
Renal free water losses
- osmotic diuresis (NG feed)
- loop diuretics
- intrinsic renal disease
Non-renal free water losses
- excess sweating
- burns
- diarrhoea
- fistulas
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54
Q

Causes of euvolaemic high Na+

A 
Renal losses
- diabetes insipidus
- hypodipsia
Extra-renal losses
- insensible
- respiratory losses
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55
Q

Causes of hypervolaemic high Na+

A 
Primary hyperaldosteronism
Cushing's syndrome
Hypertonic dialysis
Hypertonic sodium bicarbonate
Sodium chloride tablets
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56
Q

Features of diabetes insipidus

A

Dilute urine - urine osmolatlity < 300
Polydipsia
Polyuria - not always hypernatraemic

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57
Q

Causes of cranial DI

A

Impaired release of ADH

  • trauma/post op
  • tumours
  • cerebral sacroid/TB
  • infections - meningitis/encephalitis
  • cerebral vasculitis - SLE/Wegener’s
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58
Q

Causes of nephrogenic DI

A

Resistance to ADH

  • congenital
  • drugs - lithium, amphoterecin, demeclocycline
  • hypokalaemia
  • hypercalcaemia
  • tubulointestinal disease
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59
Q

Treatment of hypernatraemia

A

Free water

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60
Q

Symptoms of hyponatraemia

A 
Decreased perception and gait disturbance
Yawning
Nausea
Reversible ataxia
Headache
Apathy
Confusion
Seizures
Coma
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61
Q

Features of pseudohyponatraemia

A

Low plasma sodium (<135 mmol/L) due to increased plasma lipid and/or plasma protein concentration

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62
Q

Causes of hypovolaemic hyponatraemia

A

Renal loss - [Urine Na+ > 20 mmol/L]
- diuretics - thiazides
- osmotic diuresis - gluocse, urea in recovering ATN
- Addison’s disease - mineralocorticoid deficiency
Non-renal loss - [Urine Na+ < 20 mmol/L]
- diarrhoea
- vomiting
- sweating
- third space losses - burns, bowel obstruction, pancreatitis

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63
Q

Treatment of hypovolaemic hyponatraemia

A

IV fluids - 0.9% NaCl at 1-3 nl/kg/hour

Give K+ if necessary

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64
Q

Causes of euvolaemic hyponatraemia

A

Hypothyroidism
Primary polydipsia - urine osmolality < 100
Glucocorticoid deficiency - adrenal insufficiency, SIADH

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65
Q

Features of SIADH

A

Low serum osmolality
Inappropriately concentrated urine - urine osmolality > 100
Urine Na+ > 20
Clinical euvolaemia
Not on diuretics
Diagnosis of elimination - normal renal, thyroid and adrenal function

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66
Q

Management of SIADH

A

Fluid restrict < 800 ml/day
PO sodium chloride
May give furosemide
Demeclocycline induces DI - reversing ADH effect

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67
Q

Causes of hypervolaemic hyponatraemia

A

CCF
Nephrotic syndrome
Liver cirrhosis

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68
Q

Treatment of hypervolaemic hyponatraemia

A

Fluid restrict

Consider furosemide

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69
Q

Rate of correcting hyponatraemia

A

<12 mmol/L/day

- too rapid correction leads to central pontine/osmotic myelinosis

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70
Q

Treatment of hyponatraemia

A

Acute
- 3% hypertonic salive IV bolus +/- furosemide
Chronic
- hypertonic saline bolus if having seizures
- isotonic saline and furosemide
Asymptomatic
- water restriction
- stop offending drug
- restore volume if dehydrated
- Na+, water restriction and diuretics if overloaded

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71
Q

Causes of hyperkalaemia

A 
CKD
- rich diet with CKD - dried fruit, potatoes, oranges, tomatoes, avocados, nuts
Drugs
- ACEi
- ARBs
- Spironolactone
- Amiloride
- NSAIDs
- Heparin
- B-blockers
Hypoaldosteronism
Addison's disease
Acidosis
DKA
Massive haemolysis
Rhabdomyolysis
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72
Q

Features of hyporeninaemic hypoaldosteronism

A

Decreased angiotensin 2 production as well as intra-adrenal dysfunction
Hypertensive with increased extra-cellular fluid volume
- renin down-regulated by fluid overload

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73
Q

Causes of hyporeninaemic hypoaldosteronism

A 
Diabetic nephropathy
NSAIDs
Ciclosporin
Sickle cell
Lupus nephritis
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74
Q

Treatment of hyporeninaemic hypoaldosteronism

A

Low K+ diet

Loop diuretic if overloaded

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75
Q

ECG changes of hyperkalaemia

A 
Tented T waves
Prolonged QRS 
Slurring of ST segment
Loss of P waves
Asystole
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76
Q

Treatment of hyperkalaemia

A

Stabilising myocardium - prevent arrhythmias
- 10mls of 10% calcium gluconate over 5-10 mins
Shifting K+ back to intracellular space
- 10 units fast acting insulin IV (actrapid) and IV glucose/dextrose 50% 50mls
- 500mls 1.4% sodium bicarbonate - if acidotic
- 5-10mg salbutamol via nebuliser
Eliminating K+ from body
- 15-45g oral or rectal Calcium Resonium - mixed with sorbitol or laculose
- 20-80mg Furosemide - depending on hydration status
- dialysis if resistant to medical treatment

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77
Q

Symptoms of hypokalaemia

A 
Fatigue
Constipation
Proximal muscle weakness
Paralysis
Cardiac arrhythmias
Worsened glucose control in diabetics
Hypertension
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78
Q

Causes of hypokalaemia

A 
Pseudohyokalaemia
- acute leukaemia
Extra-renal losses
- inadequate PO intake
- gut losses 
Redistribution
- delirium tremens
- beta agonists
- insulin
- caffeine
- doxazosin
Refeeding syndrome
Primary hyperaldosteronism
Cushing's syndrome
Renal losses
- diuretics
- RTA
- glucocorticoids
- hypomagnesaemia
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79
Q

ECG changes in hypokalaemia

A

Small T waves
U wave
Increased PR interval

80
Q

Treatment of hypokalaemia

A

Replace magnesium
Oral K replacement
IV K replacement - 0.9% NaCl

81
Q

Risk factors for AKI

A 
Diabetes
CKD
IHD / CCF
Elderly > 75
Sepsis
Medications
- ACEi
- ARBs
- NSAIDs
- Antibiotics
82
Q

Stages of AKI

A 
Stage 1
- 1.5-1.9 x baseline serum creatinine
- or 26.5 μmol/L increase
- urine output < 0.5ml/kg/hr for 6-12 hours
Stage 2
- 2.0-2.9 x baseline serum creatinine
- urine output < 0.5ml/kg/hr 12 hours
Stage 3
- 3 x baseline serum creatinine
- or 353.6 μmol/L increase
- or initiation of renal replacement therapy
- urine output < 0.3ml/kg/hr for > 24 hours 
- or anuria for > 12 hours
83
Q

Prerenal causes of AKI

A 
Hypovolaemia
Decreased CO
Decreased effective circulating volume
- CCF
- liver failure
Impaired renal autoregulation
- NSAIDs
- ACEi/ARBs
- Cycloporine
84
Q

Postrenal causes of AKI

A

Bladder outlet obstruction

Bilateral pelvoureteral obstruction - unilateral obstruction of solitary functioning kidney

85
Q

Intrinsic causes of AKI

A 
Glomerular
- acute glomerulonephritis
Tubules and interstitium
- ischaemia
- sepsis
- nephrotoxins
Vascular
- vasculitis
- malignant hypertension
- TTP-HUS
86
Q

Nephrotoxins that can cause AKI

A 
Exogenous
- iodinated contrast
- aminoglycosides
- cisplatin
- amphotericin B
Endogenous
- haemolysis
- rhabdomyolysis
- myeloma
- intratubular crystals
87
Q

Investigations in AKI

A

Urine dip - abnormal protein and blood
Daily bloods - FBC, U&Es, LFTs, bone profile, CRP
Urine - PCR, MC+S, USS KUB

88
Q

Management of AKI

A

Discontinue nephrotoxic agents if possible
Ensure volume status and perfusion pressure
- if dehydrated give IV fluids
- if overloaded give diuretics
Be aware of 3rd space losses
- patient may look overloaded but JVP and BP low
Monitor urine output
Avoid hyperglycaemia
Treat underlying cause

89
Q

Indications for renal replacement therapy in AKI

A 
Resitant to medical therapy
- hyperkalaemia
- metabolic acidosis
- fluid overload
Uraemic pericarditis
Uraemic encephalopahty
Intoxications
90
Q

Symptoms of uraemic encephalopathy

A

Vomiting
Confusion
Drowsiness
Reduced consciousness

91
Q

Features of nephrotic syndrome

A

Oedema
Albumin < 30
Urine PCR > 350
Hypercholesteraemia

92
Q

Complications of nephrotic syndrome

A 
Higher risk of infection
Venous thromboembolism
Progression of CKD
Hypertension
Hyperlipidaemia
93
Q

Causes of nephrotic syndrome

A

Minimal change disease - commonest form in children
Focal segmental glomerulosclerosis
Membranous nephropathy
Membranoproliferative glomerulonephritis - commonly presents as nephritic syndrome
Lupus nephritis

94
Q

Presentation of nephritic syndrome

A 
AKI
Mild to moderate oedema
Proteinuria < 3.5g/24hrs
Hypertension
Sometimes visible haematuria
95
Q

Causes of nephritic syndrome

A 
Post-infectious GN
IgA nephropathy
Small vessel vasculitis
Anti-GBM disease
Thin basement membrane disease
Alport syndrome
Lupus nephritis
Membranoproliferative glomerulonephritis
96
Q

Associations of post-infectious GN

A 
Weeks after group A, B-haemolytic streptococci infections
- 1-2 weeks post tonillitis/pharyngitis
- 3-4 weeks post impetigo/cellulits
Usually children 3-12 yrs
Can lead to PRGN in some cases
97
Q

Investigation findings of post-infectious GN

A

Postive anti-streptococcal antibodies
Low serum C3
Biopsy - immune complex deposition
- IgG, IgA, C3

98
Q

Treatment for post-infectious GN

A

Usually self limiting
Supportive therapy
- ACEi/ARB for proteinuria and hypertension
- low sodium diet

99
Q

Associations for IgA nephropathy

A

Episodic gross haematuria during or directly after URT and GI infections or strenuous exercise
Male > Female
2nd-3rd decade of life

100
Q

Investigation findings for IgA nephropathy

A

Asymptomatic michrochaematuria with intermittent visible haematuria
Increase serum IgA
Normal C3 and C4
Biopsy
- mesangial immune complex depositis in glomeruli

101
Q

Treatment for IgA nephropathy

A

Supportive therapy

- ACEi/ARB for proteinuria and hypertension

102
Q

Types of small vessel vasculitis (ANCA associated)

A

Granulomatosis with polyangitis (GPA)
Microscopic polyangitis (MPA)
Eosinophilic granulmatosis with polyangitis (Churg-Stauss syndrome)

103
Q

Associations with GPA

A

Pulmonary and nasopharyngeal involvement

  • haemoptysis
  • nasal ulcers / polyps
104
Q

Investigation findings for GPA

A

c-ANCA (PR3)
Biopsy
- segmental necrotising GN

105
Q

Associations for MPA

A

Usually only mild respiratory symptoms

106
Q

Investigation findings for MPA

A

p-ANCA (MPO)
Biopsy
- segmental necrotising GN

107
Q

Associations for eosinophilic granulomatosis with polyangitis

A

Patients have

  • asthma
  • allergic rhinitis
  • purpura
  • peripheral neuropathy
108
Q

Investigation findings for eosinophilic granulomatosis with polyangitis

A 
p-ANCA
Bloods
- eosinophilia
Biopsy
- segmental necrotising GN
109
Q

Treatment for ANCA associated vasculitis

A

Immunosuppression

110
Q

Associations for anti-GBM disease (Goodpasture syndrome)

A

Two peaks - 3rd and 7th decade
Antibodies against type IV collagen
- react with pulmonary basement membrane causing pulmonay haemorrhage
Can lead to PRGN

111
Q

Investigation findings for anti-GBM disease

A

Anti-GBM antibodies
Pulmonary infiltrates on CXR
Biopsy
- linear deposition of IgG along basement membrane

112
Q

Treatment for anti-GBM disease

A

Plasma exchange

Immunosuppression

113
Q

Associations for thin basement membrane disease

A

Heriditary
Abnormalities of type IV collagen
Good prognosis

114
Q

Investigations for thin basement membrane disease

A

Persistent microscopic haematuria
- possible intermittent visible haematuria
Biopsy
- diffuse thining of GBM

115
Q

Treatment for thin basement membrane disease

A

Monitor renal function

Supportive treatment

116
Q

Associations for Alport syndrome

A

X-linked - usually affects males
Mutation in gene coding for type V collagen
Associated with hearing loss and abnormalities of the eyes
Often leads to ESRF

117
Q

Investigation findings for alport syndrome

A

Persistent microscopic haematuria with intermittent visible haematuria
Sensorineural hearing loss
Biospy
- splitting of GBM
- alternating thickening and thinning of GBM
Genetic studies - family history

118
Q

Treatment for alport syndrome

A

Supportive treatment
Renal replacement therapy
Renal transplant
- can lead to development of anti-GBM sdisease

119
Q

Associations for lupus nephritis

A

Complication of SLE

Can be nephrotic or nephritic

120
Q

Investigation findings for lupus nephritis

A

ANA and anti-dsDNA postitive
Biopsy
- 6 different classes have different presentation

121
Q

Treatment for lupus nephritis

A

Supportive therapy

Immunosuppressive therapy based on classification/presentation

122
Q

Management of glomerulonephritis

A 
Supportive
- ACEi/ARB for proteinuria
- control BP
- salt and water restriction if fluid overloaded
- diuretics for fluid overload
- statins for hypercholesterolaemia
Immunosuppressive
- specific to cause
- oral corticosteriods, IV pulsed methylprednisolone, tacrolimus, ciclosporin, reiuximab, MMF, azathioprine
Invasive
- RRT / haemodialysis - severe AKI or ESRF
- plasma exchange for AAV and anti-GBM
123
Q

Definition of CKD

A

Presence of kidney damage

  • manifested by abnormal albumin excretion or decreased kidney function
  • quantified by eGFR
  • persists for more than 3 months
124
Q

CKD classification

A 
ACR categories
- A1 = < 3
- A2 = 3-30 
- A3 = > 30 
GFR categories
G1 = > 90
G2 = 60-89 
G3a = 45-59
G3b = 30-44
G4 = 15-29
G5 = < 15 (kidney failure)
125
Q

Causes of CKD

A 
Diabetes 
Hypertension
Glomerulonephritis
Renovascular disease
Polycystic kidney disease
Obstructive nephropathy - urological problems
Chronic/recurrent pyelonephritis
126
Q

Complications of CKD

A

Anaemia of chronic kidney disease
Chronic kidney disease - mineral and bone disease
Secondary and tertiary hyperparathyroidism
Hypertension
CVS disease
Malnutrition/sarcopenia
Dyslipidaemia

127
Q

Complications of advanced CKD

A 
Electrolyte disturbances
Fluid overload
Metabolic acidosis
Uraemic pericarditis
Uraemic encephalopathy
128
Q

Management of CKD

A 
Treat underlying disease
Reduced CVS risk
- statin, control BP and diabetes, weight loss and exercise, stop smoking
Reduce progression of CKD
- reduce proteinuria - ACEi/ARB
- monitor blood and BP
Prevent complications
- low phosphate/potassium diet
- phosphate binders
- IV iron/folate/vit B12
- EPO
129
Q

Features of diabetic nephropathy

A

Type 1 or long duration type 2
Associated with other diabetic microvascular complications
- retinopathy
- peripheral neuropathy

130
Q

Diagnosis of diabetic nephropathy

A

Most diabetic patients will undergo screening for diabetic nephropathy

  • raised urine albumin:creatinine ratio
  • evidence of long standing/poorly controlled DM
  • evidence of other microvascular disease
131
Q

Treatment of diabetic nephropathy

A

ACEi/ARB - reduce proteinuria
Anti-hypertensives - BP control
CVS risk modification
Screen for other microvascular complications

132
Q

Features of hypertensive nephropathy

A

Chronic raised BP causing nephrosclerosis

- hard to tell if HTN caused renal impairment or renal impairment caused HTN

133
Q

Investigations for hypertensive nephroapthy

A

24 hour urinary metanephrines - phaeochromocytoma
Aldosterone:renin ratio - primary aldosteronism
Cortisol and dexamethasone suppression test - Cushing’s syndrome
TSH - hyperthyroidism
MRA - renal artery stenosis

134
Q

Features of polycystic kidney disease

A

2 types - autosomal dominant
- type 1 - PKD1 mutation on chromosone 16
- type 2 - PKD2 mutation on chromosone 4
Symptoms related to
- size of kidney
- infection of cysts - flank pain, haematuria, fever
- asymptomatic

135
Q

Diagnosis of polycystic kidney disease

A

Family history

USS

136
Q

Treatment of polycystic kidney disease

A

Control BP
Tolvaptan - vasopression recptor-2 antagonist
Genetic counselling and testing

137
Q

Features contributing to anaemia of chronic kidney disease

A

Decreased production of erythropoietin from the kidney
Absolute iron deficiency - poor absorption and malnutrition
Functional iron deficiency - inflammation, infection
Blood loss
Shortened red blood cell survival
Bone marrow suppression from uraemia
Medication induced
Deficiency of vit B12 and folate

138
Q

Management of anaemia of CKD

A

Measure haematinics - vitamin B12, folate, ferritin, iron, transferrin saturation, CHr
Replacement of any deficiencies
Aim for Hb 100-120

139
Q

Diagnosis of CKD mineral bone disease

A

Abnormalities of calcium, phosphate, alkaline phosphatase, PTH or vitamin D metabolism
Vascular and/or soft tissue calcification
Abnormalities in bone turnover, metabolism, volume, linear growth or strength
- low turnover states
- adynamic bone disease
- osteomalacia
- high turnover states
- osteitis fibrosa

140
Q

Featues of CKD MBD

A 
Increased fibroblast growth factor 23
Increased alkaline phosphatase and PTH
Increased phosphate
Decreased serum calcium
Decreased 1,25-vitamin D
141
Q

Causes of tertiary hyperparathyriodism

A

PTH release continues despite raised serum calcium levels

  • parathyroid gland nodular hyperplasia
  • advanced CKD
142
Q

Management of CKD MBD

A

Reduce occurrence/severity of renal bone disease

CVS morbidity and mortality caused by elevated serum levels of PTH and high phosphate levels and calcium overload

143
Q

Features of peritoneal dialysis

A

Reliant on patients own peritoneal membrane
Solutes move from patients blood across peritoneal membrane, down concentration gradient
Osmotic gradient created by high concentration of glucose in dialysate fluid - removes water from patient

144
Q

Advantages of peritoneal dialysis

A

Quality of life
Good when patients have some residual native renal function
Regimes designed on a more individual basis

145
Q

Disadvantages of peritoneal dialysis

A

Patients need to be able to manage technical aspects of dialysis
Unsuitable in patients with stoma/previous surgery
Risk of infection

146
Q

Complications of peritoneal dialysis

A 
Drianage problems
Malposition
Leaks
Herniae
Hydrothorax
Long term use -> encapsulating peritoneal sclerosis
147
Q

Features of automated PD

A

Automated cycler machine performed at night

- 10-12L exchanged over 8-10 hours

148
Q

Features of continuous ambulatory PD

A

4-5 dialysis exchanges per day - 2L each

Regular intervals throughout day with long overnight dwell

149
Q

Advantages of haemodialysis

A

Efficient

Unit-based - plenty of support from staff

150
Q

Disadvantages of haemodialysis

A

Less freedom - fixed days at haemodialysis unit
Food and fluid restrictions
Use of needles

151
Q

Complications of haemodialysis

A 
Infection/bacteraemia
Haemodynamic instability
Reaction to dialysers
Haematomas
Risk of bleeding
Muscle cramps
Anaemia - clotted lines
AVF steal syndrome
SCVO - central lines
152
Q

Advantages of renal transplantation

A

Near normal lifestyle

Better mortality/morbidity

153
Q

Disadvantages of renal transplantation

A 
Criteria to meet suitability to safely undergo operatio
Compliance with lifelong medication
Risk of rejection
Risk of malignancies over time
Risk of infection - immunosuppression
Long waiting times for cadaveric organ
154
Q

Active conservative management

A

When RRT offers no survival benefit

- insuitable for or choose not to have invasive therapy

155
Q

Considerations for active conservative management

A

Age > 08

WHO performance score of 3 or more

156
Q

Features of active conservative management

A 
Symptom control to enhance quality of life
Respect patients preferred place of care
Advanced care plan
MDT approach
Support for patient and family
157
Q

Contraindications for kidney transplanation

A

Active infection or malignancy
Severe heart disease - not suitable for correction
Severe lung disease
Reversible renal disease
Uncontrolled substance abuse, psychiatric illness
On-going treatment non-adherence
Short life expectancy

158
Q

Types of kidney transplant

A

Living related donor
Living unrelated donor
Cadaveric donor

159
Q

Features of living related donor transplant

A

Best possible option
- elective procedure
- may have good compatibility
Time to transplantation - months

160
Q

Features of living unrelated donor transplant

A

Comparable outcomes to live-related donors

Time to transplantation - months

161
Q

Types of living unrelated donor transplant

A

Live-donor paired exchange
Live-donor/deceased-donor exchange
Live-donor change
Altruistic donation

162
Q

Features of deceased donor transplant

A

60%
Little time for preparation
Time to transplantation - years
Survival of kidney allograft and patients are significantly low compared to live donor transplantation

163
Q

Induction treatment for renal transplant

A

At the moment of transplantation - potent immunosuppression to create tolerance of the graft

  • methylprenisolone
  • basiliximab
  • thymoglobulin
  • alentuzumab
  • rituximab
164
Q

Maintenance treatment for renal transplant

A 
Steroids
- prednisolone
Calcineurin inhibitors
- tacrolimus
- cyclosporine
- voclosporin
Antimetabolite medications
- mycophenolate
- azathioprine
Rapamycin inhibitors
- sirolimus
- everolimus
T-cell regulation
- belatacept 
- belimumab
165
Q

Long term care for renal transplant patient

A

Monitor GFR, CNI levels, proteinuria, Ca, phosphate, PTH, lipids and glucose
Screen for infections
Vaccination - except live or live attenuated viral vaccines
Monitor CVS disease, bone and mineral metabolism disease
Screen for malignancies
- 3x more likley to have cancer
- anunual skin checks
Contraception obligatory in 1st year
- counsel about pregnancy after

166
Q

Causes of mortality for transplant patient

A

CVS disease
Infections
Malignancy

167
Q

Acute complications of transplant

A

Surgical complications
Infection
- < 4 weeks - nosocomial infections or related to donor
- 1-12 months - activation of latent infections, relapsed, residual or opportunistic infections
- > 12 months - community aquired

168
Q

Common pathogens in post transplant infection

A 
CMV
Hepatitis B
HSV
Varicella zoster
EBV
BK
Aspergillus
Listeria
TB
169
Q

Chronic complications post renal transplantation

A

New-Onset Diabetes After Transplant (NODAT)

Malignancy

170
Q

Simultaneous kidney transplantation options

A 
Liver-kidney
- liver failure or cirrhosis and ESFR
Pancreas-kidney
- selected patients with type 1 DM
- simultaneous or sequential
Re-transplant
- transplant patients who progress into ESRF
171
Q

Examples of loop diuretics

A

Furosemide
Bumetanide
Torsemide

172
Q

Main indications of loop diuretics

A

Fluid overload

173
Q

Action of loop diuretics

A

Inhibits Na+K+Cl- transporter in Loop of Henle

174
Q

Pharmacokinetics of loop diuretics

A

Metabolised - kidney and liver

Excreted - urine

175
Q

Common side effects of loop diuretics

A 
Hyponatraemia
Hypokalaemia
Diuresis
Dehydration
Alkalosis
176
Q

Features of loop diuretics

A

Furosemide 40mg = Bumetanide 1mg
IV better absorbed if gut oedema present
Protein-bound = low volume of distribution

177
Q

Examples of thiazide and thiazide-like diuretics

A

Bendroflumethiazide

Indapamide

178
Q

Main indications of thiazide and thiazide-like diuretics

A

Hypertension

Fluid overload

179
Q

Method of action of thiazide and thiazide-like diuretics

A

Inhibits NaCl channel in distal convoluted tubule

180
Q

Pharmacokinetics of thiazide and thiazide-like diuretics

A

Metabolised - kidney

Excreted - urine

181
Q

Common side effects of thiazide and thiazide-like diuretics

A 
Hyponatraemia
Hypokalaemia
Dehydration
Hypercalcaemia
Hyperuricaemia
Hypomagnesaemia
Alkalosis
182
Q

Examples of K-sparing diuretics

A

Aldosterone antagnosists
- spironolactone
Epithelial Na channel blockers
- amiloride

183
Q

Main indications of K-sparing diuretics

A

K-losing tubulopathies
Hypertension
Heart failure

184
Q

Method of action of K-sparing diuretics

A

Block epithelial Na channel

Antagonises the action of aldosterone at mineralocorticoid recptors

185
Q

Common side effects of K-sparing diuretics

A

Hyperkalaemia
- caution when combined with ACEi/ARBs
Gynaecomastia

186
Q

Examples of carbonic anhydrase inhibitors

A

Acetazolamide

Brinzolamide

187
Q

Main indications of carbonic anhydrase inhibitors

A

Glaucoma

Benign intracranial hypertension

188
Q

Method of action of carbonic anhydrase inhibitors

A

Inhibits carbonic anhydrase
- causes increased renal excretion of Na, K, HCO3 and H2O
Decreases production of aqueous humour

189
Q

Common side effects of carbonic anhydrase inhibitors

A

Flushing
Metabolic acidosis
Agranulocytosis
Liver failure

190
Q

Examples of corticosteriods

A

Prednisolone - PO
Hydrocortisone - IV, IM
Dexamethasone - PO, IV
Triamcinolone - IM

191
Q

Main indications of corticosteriods

A

Supress inflammation, allergy and immune responses

192
Q

Method of action of corticosteriods

A

Alters gene transcription

  • anti-inflammatory
  • immunosuppressive
  • increased gluconeogenesis
  • decreased glucose utilisation
  • increased liver protein catabolism
193
Q

Pharmacokinetics of corticosteriods

A

Metabolised - liver

Excreted - urine

194
Q

Common side effects of corticosteriods

A 
Adrenal suppression - courses > 3 weeks
Hyperglycaemia
Psychosis
Insomnia
Indigestion
Mood swings
195
Q

Long term side effects of corticosteriods

A 
Diabetes
Cataracts
Glaucoma
Peptic ulceration
Susceptibility to infections
Osteoporosis
Muscle wasting
Skin thinning
Cushingoid appearance
196
Q

Cautions of long term corticosteriods

A

Long-term course should not be withdrawn abruptly
Additional medication
- PPI - GORD
- Bisphosphonates - bone protection

Yr3 - General Medicine (9 decks)

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