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Year 3 Medicine > Renal > Flashcards

Renal Flashcards

1
Q

What systems in particular should be reviewed in renal patients?

A

GI: bowels, appetite, weight loss
MSK: joint pains, rashes (purpuric/urticarial/malar rash)

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2
Q

What hand signs may be present in renal patients?

A

Clubbing
Peripheral cyanosis
Uraemic flap
Cogwheel rigiditiy

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3
Q

When examining an arteriovenous fistula, what should you be checking?

A 
Size
Colour
Thrill
Evidence of recent use
Working or failed
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4
Q

What type of HD access in renal patients is tunneled under the skin?

A

Perm-cath

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5
Q

What type of haemodyalysis acsess in renal patients is non-tunneled?

A

Vas-cath

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6
Q

What should be included when fluid assessing a renal patient?

A

Vitals: BP, pules (character and rate), RR, UO, lying and standing BP
JVP assessment
Heart sounds (murmurs, gallop, added sounds)
Chest ascultation (pulmonary odema: fine crackles, pleural effusion: decreased air entry, dull percussion, increased vocal ressonance)
Oedema (peripheral/sacral/scortal)
Evidence of ascites

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7
Q

On in abdominal exmaination, what may be remarkable in renal patients?

A 
PD tube
Palpable polycystic kidney
ENlarged, cystic lvier
Scars from surgery (nephrecotomy, transplant, previous PD tube insertions)
Palpable transplanted kidney
INdwelling catheter
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8
Q

What are some (rare) signs of advanced renal disease on examination?

A

Brown nails
Uraemic discolouration of the skin (yellow-brown)
Muscle wasting secondary to under nutrition
Uraemic frost (urea from sweat crystalises on skin)
Hyper-reflexia
Pericardial rub
GI uleceration and bleeding

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9
Q

What might an US-KUB show us?

A

Peri-nephritic collections
Kidney size
Corticomedullary differentiation
Hydronephrosis

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10
Q

How might we investigate a renal patients urine?

A

Dipstick - Infection (nitrites, leukocytes), glomerular pathology (blood, protein)
Protien:Creatinine - quantifies the amount of all protein in the urine
Albumin:Creatinine - quantifies just albumin, useful for diagnosing and monitoring diabetic nephropathy
Urine microscopy, culture and sensitivity

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11
Q

What bloods should be done in renal patients?

A

FBC - anaemia (CKD), infection, allergic reactions
Haematinics - folate/iron/B12 def.
U&Es - Potassium, urea, creatinine, bicarbonate
Bone profile: Calcium, phosphate, PTH, alkaline phosphate
CRP - infection/inflammation
HbA1c - diabetic control

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12
Q

Renal loss causes of metabolic alkalosis?

A

Primary hyperaldosteronism
Tubular transporter defects
Diuretics

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13
Q

How does IgA neuropathy usually present?

A

Nephritic syndrome
Recurrent gross of microscopic haematuria (12-72hours) following an URTI
+/- haematuria

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14
Q

What is found on renal biopsy of a patient with IgA nephropathy?

A

IgA and C3 deposits in the sub-endothelium of the glomerulus

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15
Q

How do IgA nephropathy and PSGN present differently in terms of timeline relative to URTI?

A

IgA nephropathy occurs 1-2 days post infection

PSGN occurs 1-3 weeks post-infection

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16
Q

How do IgA nephropathy and PSGN present differently in terms of renal biopsy?

A

IgA nephropathy shows IgA immune deposits

PSGN shows IgG immune deposits

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17
Q

What conditions can cause a nephritic picture?

Hint: SHARP AIM

A 
SLE
Henoch-Schonlein purpura
Anti glomerular basement membrane disease (Good pastures)
Rapidly progressive GN
PSGN
Alport's syndrome
IgA nephropathy (AKA Berger's disease)
Membranoproliferative GN
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18
Q

How are nephrotic syndromes characterised?

A

Proteinuria (>3g/d),
Hypoalbuminaemia sufficient to cause:
1. Odema
2. Hyperlipidemia

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19
Q

How are nephrotic syndromes managed?

A 
BP control
Reduction in proteinuria using ACEi
COntrol of hyperlipidemia 
Anticoagulation if hypercoagulable 
Treatment of underlying cause
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20
Q

Why is the risk of thrombosis increased in patients with nephrotic syndromes?

A

Hypoalbuminaemia - risk of thrombosis increases as albumin decreases

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21
Q

Why do patients with nephrotic syndromes have hyperlipidemia?

A

Increased hepatic lipoprotien synthesis secondary to protein losses

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22
Q

How are nephritic syndromes characterised?

A

Oliguria/anuria
Hypertension
Heamaturia (microscopic or macroscopic)
(+ fluid retention, seen as facial odema, uraemia, (proteinuria))
Patients may also complain of loin pain, headaches and general malise

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23
Q

Mainstay treatment of nephritic syndromes?

A

Steroids

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24
Q

What is the most common cause of GN?

A

IgA Nephropathy

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25
Q

Pathophysiology of Berger’s disease?

A

Raised IgA synthesis secondary to infection
Form immune complexes, more easily lodges in the mesangium of the glomerulous, causing proliferation
This combined with the activation of the alternative compliment pathway causes glomerular injury

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26
Q

How can IgA nephropathy be diagnosed histalogically?

A

Immunoflorecence shows IgA depositied in a granular pattern in the mesangium

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27
Q

What will be seen in the urine of patients with Berger’s disease?

A

RBC (dysmorphic, suggestive of bleeding in the glomerulous)
WBC
Associated casts

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28
Q

Gold standard to diagnose Berger’s disease?

A

Renal biopsy

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29
Q

Management of Berger’s disease?

A

Monitoring and optimising fluid balance
Optimise BP
ACEi/ARB to reduce proteinuria and protect renal function
Corticosteroids can also help decrease proteinuria

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30
Q

How can CKD be differentiated from AKI using renal ultrasound?

A

ESRD shows bilateral shrunken kidneys on USS

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31
Q

Up to which stage of CKD do patients tend to remain asymptomatic?

A

4 or 5

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32
Q

What is the eGFR in Stage 1 of CKD?

A

> 90ml/min/1.73m2

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33
Q

What is the eGFR in Stage 2 of CKD?

A

60-89ml/min/1.73m2

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34
Q

What is the eGFR in Stage 3a of CKD?

A

45-59ml/min/1.73m2

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35
Q

What is the eGFR in Stage 3b of CKD?

A

30-44ml.min/1.73m2

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36
Q

What is the eGFR in Stage 4 of CKD?

A

15-30ml/min/1.73m2

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37
Q

What is the eGFR in Stage 5 of CKD?

A

<15ml/min/1.73m2

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38
Q

How can the causes of CKD be classified?

A

Glomerular - primary (Berger’s disease), secondary (SLE)
Vascular - vasculitis, renal artery stenosis
Tubulointestinal - amyloidosis and myeloma
Congenital - polycystic kidney disease
Systemics - DM, HTN
Developmental - vesico-urteric reflux causing chronic pyelonephritis

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39
Q

What are the four most common causes of CKD?

A

DM
HTN
Chronic GN
Polycystic kindey disease

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40
Q

What are the complications of CKD, in relation to the kidney’s function?

A

Waste and excretion - uraemia, hyperphosphataemia
Regulation of fluid balance - HTN, peripheral/pulmonary oedema
Acid-base balance - metabolic acidosis
EPO production - anaemia
Activation of vitamin D - hypocalcemia

ALSO: CVD, renal osteodystrophy, electrolyte disturbance (acidosis, hyperkalemia), leg restlessness, sensory neuropathy

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41
Q

Features of renal osteodystrophy?

A

Reduced bone density - osteoperosis
Reduced bone mineralisation - osteomalcia
Secondary/tertiary hyperparathyroidism
May get spinal osteosclerosis: Ruffer Jersey spine

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42
Q

Management of oedema?

A

Fluid restriction
Salt restriction
Diuretics e.g. furosemide

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43
Q

Management of anaemia in CKD?

A

Monthly sub-cut EPO

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44
Q

How are hypocalcaemia and hyperphosphatemia managed in CKD?

A

Dietary potassium restriction (dairy products, eggs)
Sevelamer (phosphate binder)
Alfacalcidol (a 1- hydroxylated vitamin D analogue)
Parathyroidectomy (tertiary hyperparathyroidsim, PTH>28 mmol/L)

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45
Q

What is the first line treatment for BPH?

A

Alpha-blocker (e.g. Tamsulosin) or an 5-alpha reductase inhibitor

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46
Q

General causes of urinary retention?

A 
Neurological
Obstructive 
Infectious
Drugs
Post-op
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47
Q

What class of medication typically causes acute urinary retention and why?

A

Anticholinergic medications

Block parasympathetic activity on the detrusor muscle and their inhibitory effects on the bladder sphincters

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48
Q

Drugs with what properties can cause acute urinary retention?

A

Alpha agonist properties

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49
Q

How should acute urinary retention be investigated?

A 
Bladder scan
DRE
Urinalysis
Post void residual 
Specific investigations will depend on the accompying symptoms
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50
Q

What should be considered in patients with signs of fluid overload and AKI?

A

Haemofiltration

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51
Q

What level of creatinine rise from baseline is indicative of AKI Stage 1?

A

x1.5

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52
Q

What level of creatinine rise from baseline is indicative of AKI Stage 2?

A

x2

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53
Q

What level of creatinine rise from baseline is indicative of AKI Stage 3?

A

x3

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54
Q

What urine output is indicative of AKI stage 1?

A

<0.5ml/kg/hour for 6 hours

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55
Q

What urine output is indicative of AKI stage 2?

A

<0.5ml/kg/hour for 12 hours

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56
Q

What urine output is indicative of AKI stage 3?

A

<0.3ml/kg.hour for 24 hours

Or anuria for 12 hours

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57
Q

What serum creatinine is indicative of AKI stage 3, regardless of baseline?

A

> 354umol/dl

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58
Q

Risk factors for AKI?

A 
CKD
DM with CKD
HF
Renal transplant 
Over 75
Hypovolemia
Contrast administration
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59
Q

Pre-renal causes of AKI? (55% of cases)

A

SHock (hypovolemic, cardiogenic, distributive)

Renovascular disease

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60
Q

Renal causes of AKI (35%)?

A 
Dysfunction of the glomeruli, such as in acute GN
Tubules (acute tubular necrosis)
Interstitial (such as acute interstitial nephritis)
Renal vessels (such as in haemolytic uraemia syndrome of vasculitides)
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61
Q

What are the post renal causes of AKI (20% of cases)

A

Caused by an obstruction to urinary flow (stricture, bladder stones)
Luminal (kidney stone)
Mural (tumour of urinary tract)
External compression (BPH)

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62
Q

What investigations should be done in a pt with an AKI?

A

Bloods: FBC, U&E, LFT, glucose, clotting, calcium, ESR
ABG: hypoxia, acidosis, potassium
Urine: dip, MCS, chemistry (U&E, CRP, osmolality, BJP)
ECG - hyperkalemia
CXR: Pulmonary odema
Renal USS: renal size, hyronephrosis
Glomerularnephritis screen if cause unclear

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63
Q

Why can kidney pathology cause hypoxia?

A

Pulmonary odema

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64
Q

Examples of common renally excerted drugs?

A

Lithium, metformin, digoxin

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65
Q

Examples of common nephrotoxic drugs (should be suspended in AKI)?

A

NSAIDs
Aminoglycosides (gentamicin)
ACEi/ARB
Diuretics

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66
Q

What are the indications for dialysis in AKI?

Hint: AEIOU

A

Acidosis (severe metabolic acidosis with pH of less than 7.20)
Electrolyte imbalance (persisten hyperkalemia, 7mM+)
Odema (refractory pulmonary odema)
Uraemia (encepalopathy or pericarditis)

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67
Q

Clincal features of cystitis?

A 
Urinary frequency
Dysuria 
Foul smelling urine 
Suprapubic pain
Suprapubic tenderness
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68
Q

Clinical features of pyelonephritis?

A 
Fever/rigors
Malaise
Lin/flank pain
Vommiting 
Loin/flank tenderness
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69
Q

What causes pyelonephritis?

A

Trans-urethral ascent of colonic commensals, most commonly E-coli

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70
Q

How to differentiate pyelonephritis from cystitits?

A

In cystitis pt is unlikely to be pyrexial or have flank/loin tenderness, or abnormal vital signs

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71
Q

How to investigate pyelonephritis?

A 
Urine dipstick (+leukocytes, +nitrites)
FBC (raised WCC, U&Es, blood cultures)
A renal USS can be performed to look for hydronephrosis if severe infection occurs with AKI
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72
Q

How is pyelonephritis managed?

A

IVABx

Broad spectrum cephalosporin/a quinolone/gentamicin

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73
Q

What is painless intermittent haematuria in a male smoker suggestive of? How should this be investigated?

A

Transitional cell carcinoma of the bladder

Cytoscopy

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74
Q

How can TCC of the bladder cause urinary retention?

A

Clot retention
Tumour growth
Tumour prolapse

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75
Q

Modifiable risk factors for UTI?

A

Contraceptive diaphragm
Recurrent sexual intercourse
Urethral instrumentation/catheterisation

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76
Q

What typically causes acute tubular necrosis?

A

Nephrotoxic drugs

Ischemia

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77
Q

How does ATN present?

A

Hypotension, unresponsive to fluid challange
Oliguria, uraemia, electolyte imblanace - AKI
Raised urea and creatinine with maintained urea:creatinine rato
Raised eosionophils
Low urine sodium (inadequete reabsorption)

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78
Q

How is ATN treated?

A

Fluid support
Cessation of nephrotoxic agent
RRT

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79
Q

Ischemic causes of ATN?

A

Hypotension
Shock - haemorrhagic, cardiogenic, sepetic
Direct vascular injury - surgery trauma

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80
Q

Nephrotoxic drugs?

A 
Aminoglycocide antibiotics e.g. gentamicin
Chemotherapy agents - e.g. cisplatin
NSAIDs
ACEi e.g. ramipril
ARB e.g. cabdesartan
Statins
Contrast
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81
Q

How does rhabdomyolysis cause AKI?

A

Myoglobin is nephrotoxic and can also precipitate in the glomerulus causing renal obstruction

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82
Q

Why will urine dips be false positive for blood in rhabdomyolysis?

A

Myoglobinuria

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83
Q

What is the most common cause of hypernatremia?

A

Water deficit

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84
Q

Indications for RRT in AKI?

A

Hyperkalemia refractory to medical therapy
Metabolic acidosis refractory to medical therapy
Fluid overload refractory to diuretics (anuric pts)
Uraemic encephalopathy - vommiting, confusion, drowisness, reduced conciousness
Intoxications - ethylene glycol, methanol, salicylates, lithium

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85
Q

Indications for RRT in AKI?

A

Hyperkalemia refractory to medical therapy
Metabolic acidosis refractory to medical therapy
Fluid overload refractory to diuretics (anuric pts)
Uraemic encephalopathy - vommiting, confusion, drowisness, reduced conciousness
Intoxications - ethylene glycol, methanol, salicylates, lithium

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86
Q

Potential complications of nephrotic syndromes?

A 
Higher risk of infection
Venous thromboembolism 
Progression of CKD
HTN
Hyperlipidemia
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87
Q

Causes of nephrotic syndrome?

A

Minimal change disease
Focal segmental glomerular nephritis
Membranous Nephropathy
Amylodosis/myeloma/diabetes (may have nephrotic range proteinuria but not necessarily other nephrotic features?

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88
Q

What can cause nephritic syndromes?

A 
Post-infectious glomrerularnephritis 
IgA Nephropathy 
Small vessel vasculitis(ANCA associated)
Anti-GBM disease (goodpastures syndrome)
Thin basement membrane disease
Alport syndrome
Lupus nephritis
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89
Q

Investigation findings in post-infectious GN

A

Positive anti-streptococcal antibodies (ASO titre)
Low serum C3
Biopsy: immune complex deposition: IgG IgM C3

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90
Q

Complication of PSGN?

A

RPGN

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91
Q

Complication of PSGN?

A

RPGN

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92
Q

Complication of PSGN?

A

RPGN

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93
Q

Investigation findings in IgA nephropathy

A 
Asymptomatic microhaematuria
Intermittent visable haematuria
Increase serum IgA
Normal C3, C4
Mesangial immune complex deposits in glomeruli
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94
Q

In what types of nephritic syndromes would you find c-ANCA and segmental necrotizing GN?

A 
Granulomatosis with polyangitis (GPA)
Microscopic polyangitis (MPA)
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95
Q

In what types of nephritic syndromes would you find c-ANCA and segmental necrotizing GN?

A 
Granulomatosis with polyangitis (GPA)
Microscopic polyangitis (MPA)
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95
Q

In what types of nephritic syndromes secondary to small vessel vasculitis would you find c-ANCA and segmental necrotizing GN?

A

Granulomatosis with polyangitis (GPA)
Microscopic polyangitis (MPA)
Eosinophillic granulomatosis with polyangitis (Chur-Strauss syndrome) (focal)

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96
Q

How to treat small vessel vasculitis?

A

Immunosupression

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97
Q

How to treat Goodpasture Syndrome?

A

Plasma exchange

Immunosupression

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98
Q

Thin basement membrane disease causes what to be abnormal?

A

Type IV collagen

Heriditary

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99
Q

What is the inheritance pattern of Alports syndrome?

100
Q

What type of collagen is abnormal in Alport syndrome?

101
Q

What is associated with Alport syndrome?

A

ESRF
Hearing loss - sensioneural
Eye abnormality

102
Q

What is found on biopsy of a kidney in a patient with Alport syndrome?

A

Splitting of GBM

Alternate thickening and thinning of the GBM

103
Q

What is found on biopsy of a kidney in a patient with Alport syndrome?

A

Splitting of GBM

Alternate thickening and thinning of the GBM

104
Q

What is found on biopsy of a kidney in a patient with Alport syndrome?

A

Splitting of GBM

Alternate thickening and thinning of the GBM

105
Q

How is Alport syndrom managed?

A

RRT
Transplant
Supportive treatment

106
Q

When should patinets with GN be considered for LMWH therapy?

A

<20g/dl hypoalbuminaemia

Higher risk for VTE

107
Q

What is CKD?

A

Chronic kidney disease, is defined as the presence of kidney damage, manifested by abnormal albumin excretion or decreased kidney function, quantified by measured or estimated GFR that persists for more than three months.

108
Q

Causes of CKD?

A 
Diabetes 
HTN
GN
Renovascular disease
Obstructive nephropathy -urological problems
CHronic/recurrenty pyelonephrtis 
Others
109
Q

Complications of CKD

A
  • Anaemia of Chronic Kidney Disease
  • Chronic Kidney Disease – Mineral & Bone Disease
  • Secondary & Tertiary Hyperparathyroidism
  • Hypertension
  • Cardiovascular Disease – No 1 cause of Mortality
  • Malnutrition/sarcopenia
  • Dyslipidaemia
  • As CKD progresses
  • Electrolyte disturbances
  • Fluid overload
  • Metabolic acidosis
  • Uraemic pericarditis
  • Uraemic encephalopathy
110
Q

What can be used to treat/prevent the complications of CKD?

A

Dietary advice regadring low phosphate/low potassium diet
Phosphate binders
IV Iron/FOlate/Vit B12 replacement
EPO
Replace Vitamin D deficiency
Consider calcimimetics for tertiary hyperparathyroidism
Dietician input

111
Q

How is acute interstitial nephritis typically caused?

A

Antibiotic use

112
Q

How is polycystic kidney disease inherited?

A

Polycystic kidney disease is inherited in an autosomal dominant pattern

113
Q

What is the diagnostic criteria for AKI in adults?

A

↑ creatinine > 26µmol/L in 48 hours
↑ creatinine > 50% in 7 days
↓ urine output < 0.5ml/kg/hr for more than 6 hours

114
Q

Features of Henoch-Scholein purpara?

A

palpable purpuric rash (with localized oedema) over buttocks and extensor surfaces of arms and legs
abdominal pain
polyarthritis
features of IgA nephropathy may occur e.g. haematuria, renal failure

115
Q

What should you suspect when a patient presents with normocytic anaemia, thrombocytopaenia and AKI following diarrhoeal illness

A

Haemolytic uraemic syndrome

Specifically microangipathic haemolytic anaemia

116
Q

Causes of HUS

A

Primary (uncommon) complement dysregulation

Secondary - Ecoli (STEC) (90%), HIV, pneumococcal infection, cancer, drugs

117
Q

How will the kidneys of patients with diabetic nephropathy appear on USS?

A

Bilaterally enlarged or normal sized (unlike most patients with CKD who will have shrunken kidneys)

118
Q

How will the kidneys of patients with diabetic nephropathy appear on USS?

A

Bilaterally enlarged or normal sized (unlike most patients with CKD who will have shrunken kidneys)

119
Q

What causes minimal change disease?

A

idiopathic
drugs: NSAIDs, rifampicin
Hodgkin’s lymphoma, thymoma
infectious mononucleosis

120
Q

What is seen in biopsy in a patient with minimal change disease?

A

Podocyte fusion and effacement of foot processes on electron microscopy

121
Q

How does Goodpastures syndrome typically present?

A

Anti-GBM disease typically presents with haemoptysis + AKI/proteinuria/haematuria

122
Q

How much maintained fluid should be prescribed to a NBM peadiatric pt

A

100ml/kg for the first 10kg, 50ml/kg for the next 10kg and 20ml/kg for every subsequent kg

123
Q

How much fluid should a adult have per day for maintence?

A

25-30ml/kg/day

124
Q

What should be assessed in a patient with bilateral urinary obstruction?

A

Renal function must be assessed in a patient with potential bilateral urinary tract obstruction

124
Q

What should be assessed in a patient with bilateral urinary obstruction?

A

Renal function must be assessed in a patient with potential bilateral urinary tract obstruction

125
Q

Over what time period does acute graft failure occur and how does it present?

A

Acute graft failure happens within months, is usually asymptomatic and is picked up by a rising creatinine, pyuria and proteinuria

126
Q

Over what time period does acute graft failure occur and how does it present?

A

Acute graft failure happens within months, is usually asymptomatic and is picked up by a rising creatinine, pyuria and proteinuria

127
Q

How is CKD managed in terms of treating underlying disease?

A 
Treat and monitor diabetic control
Treat HTN
Treat infections promptly
Tolvaptan if meets criteria for ADPKD
Immunosupression for GN if appropriate
128
Q

How is cardiovascular risk reduced in CKD?

A 
Statin
Control HTN
Improve diabetic control
Advise weight loss
Advise exercise
Smoking cessation
129
Q

How can the progression of CKD be managed?

A

Reduce proteinuria - ARB/ACEi
Monitor blood tests
Control BP

130
Q

How can the progression of CKD be managed?

A

Reduce proteinuria - ARB/ACEi
Monitor blood tests
Control BP

131
Q

How might CKD patients plan for the future?

A

Start discussions of what options they have if they reach ESR|F
Home care team input
Discuss advantages and disadvantages of RRT
Referal for fistula
Refer for PD tube insertion
Work up for transplant

132
Q

What would alert you to possible diabetic nephropathy?

A

Raised urine albumin:creatinine ratio / PCR
Evidence of long-standing/poorly controlled DM
Evidence of other microvascular diease (Retinopathy, peripheral neuropathy)

133
Q

What is hypertensive nephropathy?

A

Chronic raised BP causing nephroscleorisis

134
Q

How would you investigate HTN nephropathy to decide if the HTN caused the nephropathy or if the nephropathy has caused the HTN?

A

24 hour urinary metanephrines (phaeochromocytoma)
Aldosterone: renin ratio (primary aldosteronisms)
Cortisol & dexamethasone supression test (CUshins syndrome)
TSH (hyperthyroidism)
MRA (renal artery stenosis)

135
Q

What is tolvaptan and how is it used in CKD?

A

Vasopressin receptor-2 antagonist, slows progression of CKD

136
Q

What factors contribute to anaemia of Chronic Kidney disease?

A 
Decreased production of erythropoietin from the kidney
Absolute iron deficiency 
Functional iron deficiency
Blood loss
Shortened red blood cell survival
Bone marrow supression from uraemia 
Medication induced
Deficiency of Vit B12 and folate
137
Q

Management of anaemia of CKD?

A

Measure haematinics - Vitamin B12, folate, ferritin, iron, transferrin saturation, CHr
If deficient in any of the above - replace this first (IV iron may be tolerated better than PO)
Discuss with renal team regarding starting ESA
Aim HB 100-120

138
Q

What is the diagnostic criteria for CKD Mineral bone disease:

A

Evidence of one or more:
- 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 strench
Low turnover states: Adynamic bone disease, osteomalacia
High turnover states: osteitis fibrosa

139
Q

Why does CKD sometimes lead to CKD-MBD?

A 
CKD leads to:
Increased fibroblast growth factor-23
Increased alkaline phosphatase and PTH
Increases phosphate
Decreased serum calcium
Decreased 1,25 - Vitamin D

As CKD develops, disturbances in the homeostatic pathways lead to hypocalcemia, hyperphosphataemia, Vitamin D deficiency and the development of secondary hyperparathyroidism

140
Q

When does tertiary hyperparathyroidism occur in renal patients?

A

Advanced CKD:
Parathyroid gland nodular hyperplasia leading to
PTH release continues despite raised serum calcium levels (independelty)

141
Q

What is the focus of management of CKD-MBD?

A

Focus is to reduce
The occurence and/or severity of renal bone disease
CVD morbiditity and mortality caused by elevated serum levels of PTH and high phosphate levels and calcium overload

142
Q

What is peritoneal dialysis?

A

A home based therapy
Reliant on the patient’s own peritoneal membrane acting as the dialysis membrane
Solutes (electrolytes, urea, creatinine) move from the patient’s own blood, across the peritoneal membrane, down the concentration gradient into the dialysate fluid
Osmotic gradient is created by high concentration of glucose in diaiysate fluid, which removes water from the patient

143
Q

What are the advantages of PD?

A

Quality of life
Good first choice for patients with some residual native renal function
Regimes are designed on a much more individualised basis than patients on HD?

144
Q

Disadvantages of PD?

A

Patients need to be able to manage the technical aspects of dialysis
Unsuitable for patients with stoma/previous surgery
Risk of infection (PD peritonitis)
Complications - drainage problems, malposition, leak, hearnia, hyrothorax, long term use associated with encapsulating preitoneal sclerosis

145
Q

Types of PD?

A

Automated PD
- Carried out with an automated cycler machine performed at night
- 10-12L eachanged over 8-10 hours
- Lifestyle advantages - leaves daytime free
Continous ambulatory PD
- usually consiting of 4-5 dialysis exchanges per day (aprox 2L each)
- Exchanges are performed at regular intervals throughout a day, with a long overnight dwell
Assisted automated PD
- Trained HCAs visit a patient’s home to help with setting up APD

146
Q

How does HD work?

A

Dialysis machine pumps blood from the patient
Through disposable tubing
Through a dialyser or artifical kidney
Back into the patient
Waste solute, salt and excess fluid is removed from the blood as it passes through the dialyser

147
Q

Advantages for HD?

A

Efficient

Unit bases - support from staff

148
Q

Disadvantages of HD?

A 
Dialysis access needs to be secured 
Infection/bactereamia
Haemodynamis instability 
Reactions to dialysers
Haematomas/risk of bleeding
Muscle cramps
Anaemia due to clotted lines/haemolysis
AVF steal syndrome
SVCO from central lines
149
Q

Advantages of renal transplant?

A

Near normal lifestyle

Better mortality/morbidity

150
Q

Disadvantages of renal transplant?

A 
Criteria to meet suitability to safely undergo operation
Complience with lifelong medication
Risk of rejection
Risk of malignancies over time 
Risk of infection (on immunosupression)
Long waiting times of cadaveric organ
151
Q

When does RRT offer no survival benefit?

A

Age>80

WHO performance score of 3 or more

152
Q

Why is it important to document immunisation episodes (blood transfusion, pregnancies, prior transplant)

A

Immunised patients are more difficult to cross-match

153
Q

Contraindications for kidney transplant?

A

Active infection or malignancy
Severe heart disease no suitable for correction
Severe lung disease
Reversible renal disease
Uncontrolled substance abuse, psychiatric illness
On-going treatment non-adherence
Short life expectancy

154
Q

Living related donor transplantation time?

155
Q

What are the four forms of living unrelated donor transplantation?

A

a) live-donor paired exchange
b) live-donor/deceased donor exchange
c) live-donor chain
d) alturistic donation

156
Q

Disadvantage of deceased donor transplantation?

A

Survival of kidney allograft and patients are significantly low compared to live donor transplantation
Time to transplantation happens in years
Transplant protocol are important to keep updated regulary

157
Q

Why is hyperacute kidney transplant rejection rarely seen?

A

At the moment of transplantation, potent immunosupression drugs are used to create tolerance to the graft
Methyprednisolone in combination with one of:
basiliximab and thymoglobulin
alentuzumab and rituximab

158
Q

What maintenance treatment is used after transplantation to long term to prevent acute or chronic rejection?

A

Steroids: prednisolone or prednisone
Calcineurin inhibitors (CNI): tracolimus, cyclosporine, voclosporin
Antimetabolite medications: mycophenolate, azathiprine
Rapamycin inhibitors: sirolimus and everolimus
T-cell regulation: belatacept and belimumab

159
Q

How often should renal transplant patients be followed up?

A

Follow up happens several times a month for the first 6 months
Less often after this

160
Q

What should be monitored in renal transplant patients?

A 
GFR
CNI levels
Proteinuria
Ca
Phosphate and PTH
Lipids and glucose
Screen for infections
CVD, bone mineral metabolism disease
Screen for malignancies (pts three times more likely to have any cancer)
Annual skin check for skin cancers
161
Q

Renal transplant patients should be up to date with vaccinations, with the exception of what?

A

Live or live attenuated viral vaccines

162
Q

What is mortality related to in renal transplant patients?

A

CVD
Infection
Mallignancies

163
Q

For how long ins contraception compulsory following a kidney transplant?

A

One year

Pregnancy counselling after this

164
Q

What are the possible compliactions of renal transplant?

A

Within one month: surgery or infection related
Within one year: new onset diabetes after transplant
Mallignancy )skin, cervix, breast, prostate, renal and urothelial, liver, colorectal, lymphoproliferative diease (strong association with EBV))

165
Q

What are the potential sources of infection in a kidney transplantation, in relation to the time of transplant?

A

<4 weeks: nosocominal infections or relation to donor
1 to 12 months: activation of latent infections, relapsed, residual or opportunistic infections, community
>12 months: community aquired

166
Q

Important germs to consider in kidney transplantation?

A 
CMV
Hep B
HSV
VZ
EBV
BK
Aspergillus
Pneumocystis jirovecii
Listeria
Mycobacterium tuberculosis
Toxoplasma gondii
167
Q

Examples of loop diuretics?

A

Furosemide
Bumetanide
Toresmide

168
Q

Main indications for loop diuretucs?

A

Fluid overload

169
Q

How are loop diuretics metabolised?

A

Liver and kidney

170
Q

How do loop diuretics work?

A

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

171
Q

Common side effects of loop diuretics?

A

Hyponatraemia, hypokalaemia, diuresis, dehyrdation, alkalosis

172
Q

Which is more potent, furosemide or bumetanide?

A

Bumetanide (x40)

173
Q

When in particular is IV loop diuretic indicated?

A

When gut odema is present

174
Q

Why do loop diuretics have a low volume of distribution?

A

Protein-bound

175
Q

Examples of thizide/thiazide like diuretics?

A

Bendroflumethiazide, Indapamide

176
Q

Main indications for thiazide/thiazide like diuretics?

A

HTN

Fluid overload

177
Q

How are thiazide-like/thiazide diuretics metabolised?

178
Q

Common side effects of thiazide/thiazide like diuretics?

A 
Hyponataemia
Hypokalemia 
Dehydration
Hypercalcemia
Hyperuricaemia
Hypomagnesaemia
Use with caution alongside loop diuretics
179
Q

Examples of K-sparing diuretics

A

Aldosterone antagonists - Spironolactone

Epethilial Na channel blockes - Amiloride

180
Q

Main indications for K+ sparing diuretics?

A

K+-losing tubulopathies
Hypertension
HF

181
Q

Common side effects of K+ sparing diuretics?

A

Hyperkalemia

Gynaecomastia

182
Q

Why should K+ sparing diuretics be used with caution alongside ACEi/ARB

A

Increased risk of hyperkalaemia

183
Q

Examples of carbonic anhydrase inhibitors?

A

Acetazolamide

Brinzolamide

184
Q

Main indications for use of carbonic anhydrase inhibitors?

A

Galucoma

Benign intracranial hypertension

185
Q

How do thizaide diuretics work?

A

Inhibit NaCl channel in distal convuluted tubule

186
Q

How does sprinolactone act?

A

Anatagonises the action of aldosterone at mineralcortocoid receptors

187
Q

How does Amiloride act?

A

Blocks epithelial Na Channel

188
Q

How do carbonic anhydrase inhibitors work/

A

Inhibits carbonic anhydrase

Also decrease production of aqueous humour

189
Q

Common side effects of CAi?

A

Flushing
Metabolic acidosis
Agranulocytosis
Liver failure

190
Q

What do CAi increase the renal excretion of?

A

Na
K
HCO3
H20

191
Q

Examples of corticosteroids?

A

Prednisolone (PO)
Hydrocortisone (IV/IM)
Dexamethasone (PO/IV)
Triamciolone (IM)

192
Q

Main indications of corticosteroids?

A

Supress inflammation

Allergy and immune respones

193
Q

How do corticosteroids act?

A

Alters gene transcription

194
Q

Effects of corticosteroids?

A 
Anti-inflammatory 
Immunsupressive
Increase gluconeogenesis
Decreased glucose utilisation
Increased protein catabolism
195
Q

How are corticosteroids metabolised?

196
Q

Side effects of corticosteroids?

A 
Adrenal supression
Hyperglycemia
Spychosis
Insomnia
Indegestion
Mood swings 
Diabetes
Cataracts
Gaucoma
Peptic ulceration
Osteoperosis
Susceptibility to infections
Muscle wasting
Skinn thinning
Cushingoid appearance
197
Q

What may need to be perscribed alongside corticosteorids?

A

May need PPI to reduce GORD

BIphosphonates for bone protection

198
Q

What is the most effective analgesia in renal colic/urinary calculi?

A

NSAIDs- IM diclofenac

199
Q

Glomerulonephritis features

A

Haematuria
Oedema
HTN
Oliguria

200
Q

How can PSGN be investigated?

A

Anti streptolysin titre (ASOT)

201
Q

What antibiotic causes a creatinine rise but not a change in eGFR?

A

Trimethoprim

202
Q

Morphine is contraindicated in patients with moderate to severe renal failure, as its active metabolites accumulate in renal failure, what can be used instead?

A

Tramadol as this is metabolised by the liver

203
Q

Which anti-hypertensive agent is most likely to cause dehydration and intravascular depletion?

A

Loop diuretic - Furosemide

204
Q

What is the most common cause of kidney cancer?

A

Renal cell carcinoma 80-85%

205
Q

How does rhabdomyolysis cause AKI?

A

Muscle damage produced myoglobin
Filters through the kidneys
It is nephtoxic
Worsened by associated hypovolaemia due to inadeuqete fluid replacement can also worsen the AKI

206
Q

Long term side effect of calcineurin inhbiitors?

A

Direct nephrotoxicity, resulting in tubular atrophy and fibrosis
Symptoms of uraemia

Gum hypertrophy, HTN, atheroslecorsis

Ciclosporin is given to inhibit T lymphocyte proliferation to prevent transplant rejection

207
Q

When does tertiary hyperparathyroidsim occur?

A

Longstanding seconday hyperparathyroidism and renal disease

208
Q

How can cystic fibrosis be diagnosed?

A

Sweat test - positive if abnormally high sodium

209
Q

Signs/features of cystic fibrosis?

A

Recurrent chest infections since birth
Signs of chronic hypoxia (e.g.) clubbing
recurring chest infections.
wheezing, coughing, shortness of breath and damage to the airways (bronchiectasis)
difficulty putting on weight and growing.
yellowing of the skin and the whites of the eyes (jaundice)
diarrhoea, constipation, or large, smelly poo.

210
Q

How does osmotic diuresis occur?

A

Certain substances such as glucose, maninitol are found in high concentration in the renal tubules, preventing water from being reabsorbed. This results in hypovolemic hypernatremia and can be secondary to pathological states such as HHS and DKA.

211
Q

What is the only cause of metabolic acidosis that has a RAISED anion gap?

A

TCA overdose (exogenous acid ingested, increase in anions not involved in the anion gap calculation

212
Q

What is renal artery stenosis? Which patients is it found in and why? How can diagnosis be confirmed?

A

Renal artery stenosis is a narrowing of the artery supplying the kidney. This is usually found in patients with atherosclerosis, as an atherosclerotic plaque causes narrowing of this vessel similar to the narrowing of the coronary arteries found in angina. This can be confirmed with a doppler ultrasound, CT angiogram or magnetic resonance angiography (MRA).

213
Q

What can be used in peritoneal dialysis as the dialysate fluid?

A

Osmotic agent such as 1/5% glucose solution

Helps to draw water across partially permeable membrane (peritoneal membrane), avoiding fluid overload

214
Q

What is the most common complication of haemodyalysis?

A

Dialysis induced hypotension

215
Q

Why does dialysis induced hypotension occur?

A

Rapid reduction of blood volume during ultrafiltiration

and the decrease in extracellular osmolality during dialysis.

216
Q

What common drugs may cause hyperkalemia?

A

ACEi
Beta blockers
Sprinolactone

217
Q

Acute vs chronic graft vs host disease timing

A

acute within 100 days

218
Q

Classical presentation of acute graft vs host disease?

A

Fever
D and V
Maculopapular rash on palm and soles
Jaundice

219
Q

What is the mechanism of action of ondansetron?

A

Serotonin antagonist

220
Q

Causes of HUS?

A

MOst common E-coli 0157 (shigea toxin)

Shigella

221
Q

Variables included in Modification of Diet in Renal Disease (MDRD) equation?

A

eGFR variables - CAGE - Creatinine, Age, Gender, Ethnicity

222
Q

What cancer can cause cannonball mets?

A

Renal cell carcinoma can metastasise to the lungs, causing ‘cannonball metastases’

223
Q

A potassium above 6mmol/L should prompt what in a patient with CKD?

A

cessation of ACE inhibitors

224
Q

Management of hyperkalemia?

A

HyperK >6.5? Remember CAN

  1. Calcium gluconate 10% 10ml by slow IV titrated ti ECG response
  2. Actrapid 10U in 50ml 50% glucose in 15minutes
  3. Neb Salbutamol

HyperK <6.5 -> do ECG first

225
Q

How might ramipril disturb serum potassium?

A

Hyperkalemia

226
Q

Treatment of nephrogenic DI?

A

thiazides are used to treat nephrogenic DI

desmopressin cranial

227
Q

Screening for adult polycystic kidney disease?

A

Ultrasound is the screening test for adult polycystic kidney disease

228
Q

What is an acceptable change in renal function after starting and ACEi?

A

NICE suggest that a decrease in eGFR of up to 25% or a rise in creatinine of up to 30% is acceptable, although any rise should prompt careful monitoring and exclusion of other causes (e.g. NSAIDs).

229
Q

ATN response to fluid challenge?

230
Q

Treating rhabdomyalysis?

A

The mainstay of rhabdomyolysis treatment is rapid IV fluid rehydration - normal saline pref

231
Q

What albumin:creatine ratio shows hyperalbuminuria

A

> 2.5 mg/mmol in men, >3.5 mg/mmol in women

232
Q

Stages of diabetic nephropaphy?

A
  1. Hyperfiltration (increase in eGFR)
  2. Latent phase
  3. Microalbuminuria (ACR 30-300 urine dip negative)
  4. Proteinuria (ACR>300mg/day)
  5. Progression to ESRF
233
Q

Mechanism of anaemia in CKD?

A 
Reduced EPO - most significant - normocytic 
Reduce erythropoesis
B12 def
Iron def
Red cell lifespan
234
Q

Urinary hyaline casts are usually an innocuous finding on urine microscopy, especially in conjunction with a negative urine dipstick, and may be caused by what?

A

Loop diuretics such furosemide.
May also be seen after exercise
IN a fever

NOT TO BE CONFUSED WITH BROWN GRANULAR CASTS - ATN

235
Q

Treatment of diabetic nephropathy?

A

Lifestyle changes
Control diabetes
Control CVS risk factors
ACEi to treat microalbuminaemia

236
Q

How are ACEi useful in diabetic nephropathy?

A

As proteinuria increases, renal function deteriorates
Mechanism is via dilating the efferent arterioles and the reducing the glomerular capilary filtration pressure
This reduces the GFR and and reduced the long term risk of glomerulosclerosis and further deterioration in kidney function

237
Q

Membranous glomerularopathy is seen in which pts?

A

Older age groups

238
Q

What happens in minimal change disease

A

Increased fenstrations
Podocyte effacement
Proteins can get through glomerular basement mebrane

239
Q

What might be seen on CT in pyelonephritis

A

Gas in renal parenchymea

240
Q

Most common organisms in pyelonephritis

A

Ecoli
Klebsiella
Proteus
Enterobacter

241
Q

How might ATN present?

A 
Occurs in days 
Oliguria
HTN
Fluid retention
Haematyrua
Proteinuria
242
Q

Acid base distrubances in aspirin overdose

A

Initialy respiratory alkalosis due to central respiratory centre stimulation
In later stages metabolic acidosis develops as a result of direct effect of the metabolite salicylic acid and more complex disruption of normal cellular metabolism

243
Q

Causes of atrophic kidney

A 
Long term scarring
Generally occurs over years
Renal artery stenosis
Recurrent pyelonephritis
(Congenital)
244
Q

USS KUB indications?

A

Pyelonephritis
Nephrotic syndrome to assess kidney size prior to renal biopsy
?Hydronephrosis
Renal tumours

245
Q

What hpens in PSGN

A

Group A haemolytic strep antibodies against this bind to glomerular basement membrane

246
Q

Peritonitis secondary to PD causative organisms?

A

Coagulase-negative Staphylococcus is the most common cause of peritonitis secondary to peritoneal dialysis

Year 3 Medicine (8 decks)

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