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Exam - M - Renal Diseases (Megan) > PassMedicine > Flashcards

PassMedicine Flashcards

1
Q

What is the dose given for maintenance fluids

A

25-30ml/kg/day of water

1mmol/kg/day of potassium and chloride

50-100g/day of glucose

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2
Q

What is the fluid prescribed in a fluid challenge

A

500mls of 0.9% normal saline STAT

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3
Q

What are the paediatric fluid requirements for 24 hours

A

0-10kg = 100ml/kg
11-20kg = 50ml/kg
Anything above = 20ml/kg

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4
Q

What are the features of IgA nephropathy

A
  • 2 days after an infection (URTI)
  • Macroscopic haematuria
  • Caused by mesangial deposition of IgA immune complexes
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5
Q

What are the features of rhabdomyolysis

A

AKI + Disproportionately raised creatinine kinase
CK >5x normal
Tea coloured urine

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6
Q

What are the causes of rhabdomyolysis

A

Statins (especially + clarithromycin)
Seizure
Collapse + Long lie
Crush injury
Ecstasy

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7
Q

What is the management for ADPKD

A

Tolvaptan - To slow down progression to CKD

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8
Q

What is anti-glomerular basement membrane disease

A

AKA Goodpastures syndrome

A rare type of small vessel vasculitis associated with pulmonary haemorrhage and rapidly progressive glomerulonephritis.

Caused by anti GBM antibodies against type IV collagen.

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9
Q

What is the treatment for Anti GBM disease

A

Plasma exchange
Steroids
Cyclophosphamide

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10
Q

What are the signs of good pastures syndrome?

A

Haemoptysis (pulmonary haemorrhage)
Rapidly progressive glomerulonephritis (proteinuria + haematuria + AKI)

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11
Q

How do you calculate the anion gap

A

(Sodium + Potassium) - (Bicarbonate + Chloride)

Normal = 8-14

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12
Q

What are the causes of acidosis with a normal anion gap

A

GI Bicarbonate loss: Diarrhoea, fistula
Renal tubular acidosis
Drugs (acetazolamide)
Ammonium chloride injection
Addisons disease

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13
Q

What are the causes of acidosis with a raised anion gap

A

Lactate (shock, hypoxia)
Ketones (DKA, alcohol)
Urate (renal failure)
Acid poisoning (methanol, salicylates)
Chronic paracetamol use

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14
Q

What causes death in dialysis patients

A

Cardiovascular events (50%)

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15
Q

What are the two main intrinsic causes of AKI

A

Acute interstitial nephritis - inflammatory process (higher white cell count - leukocytes)

Acute tubular necrosis -

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16
Q

What are the features of minimal change disease

A
  • Almost always a nephrotic syndrome
  • 1/3 have only one episode
  • 1/3 have infrequent episodes
  • 1/3 have frequent relapses which stops before adulthood
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17
Q

What is the treatment for minimal change disease

A

Oral corticosteroids - Prednisolone + Urgenzassero outpatient referral to paediatrics

Next line - Cyclophosphamide

Biopsy is only needed if there is no response to treatment

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18
Q

What are the features of post streptococcal glomerulonephritis

A
  • Typically occurs 7-14 days after strep infection
  • Caused by immune complex (IgG, IgM, C3) deposition in the glomeruli
  • Starry sky on immunofluorescence
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19
Q

How is post streptococcal glomerulonephritis

A

Bloods:
- Raised anti-streptolysin O titre
- Low C3

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20
Q

What is the most common presentation of transitional cell carcinoma of the bladder

A

80% present with painless, visible haematuria.

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21
Q

When should someone have an urgent referral for haematuria

A

> 45 years and visible haematuria without UTI
45 and visible haematuria that recurs or persists after treatment for UTI

> 60 years and nonvisible haematuria and either dysuria or raised white cell count on a blood test

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22
Q

When should someone have a non-urgent referral for haematuria

A

> 60 with recurrent or persistent unexplained UTI

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23
Q

What are the symptoms of a Wilms nephroblastoma

A
  • <5 years old
  • Abdominal mass (most common presentation)
  • Flank pain
  • Painless haematuria
  • Anorexia
  • Fever
  • Unilateral 95% of time
  • Metastasis in 20% (most commonly the lungs)
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24
Q

what is CKD stage 1

A

> 90ml + Some sign of kidney damage

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25
Q

what is CKD stage 2

A

60-90ml + Some sign of kidney damage

If kidney tests normal - no CKD (if normal U and E and no proteinuria)

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26
Q

What is CKD stage 3a

A

45-59ml

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27
Q

What is stage 3b CKD

A

30-44ml

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28
Q

What is stage 4 CKD

A

15-29ml

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29
Q

What is stage 5 CKD

A

<15 ml = Established kidney failure.

Dialysis or transplant most likely needed

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30
Q

When is haemodialysis indicated

A

Stage 5 CKD

AEIOU
Acidosis
Electrolyte imbalance (hyperkalaemia >6.5)
Intoxication
Overload (of fluid - can be pulmonary)
Uraemia (pericarditis or encephalopathy)

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31
Q

What is used to treat hyperphosphataemia in CKD

A

Sevelamer

Phosphate is really excreted so will build up if there is impaired renal function. This drags the calcium out of the bone and causes osteomalacia.

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32
Q

What is used in CKD to supplement a lack of vitamin D

A

Alfacalcidol

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33
Q

What are the mineral bone diseases that occur with CKD

A

Low vitamin D - Causes low calcium
High Phosphate

Secondary Hyperparathyroidism: Due to low calcium, high phosphate, high vitamin D

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34
Q

how is ADPKD diagnosed

A

Ultrasound

diagnostic criteria (in patients with positive family history):

  • two cysts, unilateral or bilateral, if aged < 30 years
  • two cysts in both kidneys if aged 30-59 years
  • four cysts in both kidneys if aged > 60 years
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35
Q

what investigation should be done for patients with AKI of unknown origin

A

ultrasound

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36
Q

What is the criteria for a stage 1 AKI

A

Increase in creatinine 1.5-1.9x baseline

Increase in creatinine by >26umol/L

Reduction in urine output to <0.5ml/kg/hour for > 6 hours

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37
Q

What is the criteria for stage 2 AKI

A

Increase in creatinine to 2-2.9x baseline

Reduction in urine output to <0.5ml/kg for > 12 hours

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38
Q

What is the criteria for stage 3 AKI

A

Increase in creatinine >3x baseline

Increase in creatinine to >353.6umol/l

Reduction in urine output to <0.3ml/kg/hour for > 24 hours

Initiation of kidney replacement therapy

eGFR <35ml in patients < 18 years

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39
Q

what are the causes of peritonitis in peritoneal dialysis

A

Staphylococcus epidermidis - most common cause

Staphylococcus aureus

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40
Q

what is the pH of prolonged diarrhoea

A

Metabolic acidosis with hypokalaemia

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41
Q

What is diabetes insipidus

A

A condition where either:
- Theres a decreased secretion of ADH from the pituitary gland

OR

  • Theres an insensitivity to ADH from the kidney
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42
Q

What are the pre-renal causes of an AKI

A

Ischaemia:
- Hypovolaemia secondary to diarrhoea or vomiting
- Renal artery stenosis
- DEHYDRATION

NORMAL URINE OSMOLARITY
URINE SODIUM <20

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43
Q

What are the intrinsic causes of an Aki

A
  • Glomerulonephritis
  • Acute tubular necrosis
  • Acute interstitial nephritis
  • Rhabdomyolysis
  • Tumour lysis syndrome
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44
Q

What are the post renal causes of an AKI

A
  • Kidney stone in the ureter or bladder
  • BPH
  • External compression of the ureter
45
Q

Which drugs have a nephrotoxic potential

A

NSAIDs
Aminoglycosides
ACE inhibitors
ARBs
Diuretics

46
Q

When should Hartmanns solution not be used

A

In patients with hyperkalaemia (Contains potassium)

47
Q

What are the features of an acute Graft failure

A
  • < 6 months
  • Usually due to mismatched HLA
  • Asymptomatic + picked up by rising creatinine, pyuria and proteinuria
  • may be reversible with steroids and immunosuppressants
48
Q

What are the features of chronic graft failure

A
  • > 6 months
49
Q

What is dialysis

A

A method for performing the filtration of the blood artificially in patients with renal failure

It removes excess fluid, solutes and waste products

50
Q

What is peritoneal dialysis

A

A dialysis solution (containing dextrose) is added into the peritoneal cavity.

Ultrafiltration occurs across the peritoneal membrane into the dialysis solution.

The solution is then replaced and the waste products are taken away.

51
Q

How is peritoneal dialysis done

A

Via a tenckhoff catheter.

  1. Continuous ambulatory peritoneal dialysis - Where dialysis solution is in the peritoneum at ALL TIMES. The fluid is then changed at regular intervals.
  2. Automated dialysis - Occurs overnight. A machine continuously replaces fluid to optimise filtration. This takes 8-10 hours.
52
Q

What are the complications of peritoneal dialysis

A

Bacterial Peritonitis
Peritoneal sclerosis
Ultrafiltration failure - If the patient absorbs the dextrose in the solution, this reduces the filtration gradient
Weight gain
Psychosocial effects

53
Q

What is haemodialysis

A

When the blood is filtered using a machine.

This requires good access to an abundant blood supply.

54
Q

What are the main access points for haemodialysis

A

Tunnelled cuffed catheter:
- Tube inserted into the subclavian or jugular vein with a tip that sits in the SVC or right atrium.
- Two lumens - one where blood exits (red) and one where blood enters (blue).

Can cause infection and blood clots.

A-V Fistula

55
Q

What are the features of an A-V Fistula

A
  • Connection between artery and vein
  • Bypasses the capillary system - allows blood to flow under higher pressure
  • Requires surgery
  • 4 -1 week maturation period without use
  • Radiocephalic
  • Brachio-cephalic
  • Brachio-basilic
56
Q

What should be done when examining an AV fistula

A
  • Skin integrity
  • Aneurysm
  • Palpable thrill (fine vibration)
  • Machinery murmur on auscultation
  • Pin prick marks - to suggest active use
  • Blood supply to distal limb

Murmur and thrill will be absent if the fistula is thromboses or has been surgically ligated like after a renal transplant

57
Q

What are the complications of A-V fistulas

A
  • Aneurysm
  • Infection
  • Thrombosis
  • Stenosis
  • STEAL syndrome - Inadequate blood flow to the limb distal to the AV fistula
  • High-output cardiac failure - increased preload and hypertrophy of the heart muscle
58
Q

Which organism most commonly causes bacterial peritonitis

A

Staphylococcus epidermidis

59
Q

What are the physiological functions of the kidney

A
  1. Remove waste products/medications - urea
  2. Reabsorbs vital nutrients - Sodium, Potassium, water
  3. Hormone secretion - Erythropoietin, Renin, Calcitriol
60
Q

What is acute interstitial nephritis

A

An acute inflammation of the tubules and interstitium

Usually a hypersensitivity reaction

61
Q

What are the signs of acute interstitial nephritis

A
  • Urticarial-like rashes
  • Fever
  • Arthralgia
  • Elevated white cell count in urine
  • Eosinophils
  • IgE elevated
  • Hypertension
  • Sterile pyuria
  • White cell casts (eosinophilic casts)
62
Q

What are the causes of acute interstitial nephritis

A

Drugs - Especially antibiotics
Penicillin
Rifampicin
NSAIDs
Allopurinol
Furosemide

63
Q

What is the main cause of anaemia in CKD

A

Due to reduced erythropoietin levels

Normochromic, normocytic anaemia.

Occurs when the eGFR is <35ml/min.

Predisposes the patient to left ventricular hypertrophy

64
Q

What is the management of anaemia in CKD

A

Optimising iron status first

Erythropoietin

65
Q

What is Henoch-Schonlein Purpura

A

An IgA mediated small vessel vascilutus.

Causes a purpuric rash in the buttocks and lower limbs.

Often triggered by URTI or a gastroenteritis.

IgA deposits in blood vessels causing inflammation:
- Skin
- Kidneys
- GI Tract

66
Q

What are the features of Henoch-Schonlein Purpura

A
  • Usually seen in children after infection
  • Palpable purpuric rash over buttocks and extensor surfaces of arms and legs
  • Abdominal pain
  • Poly arthritis
  • Some features of IgA nephropathy (haematuria, renal failure)
  1. Purpura (100%)
  2. Joint pain (75%)
  3. Abdominal pain (50%)
  4. Kidney involvement (50%) - IgA nephritis (microscopic or macroscopic haematuria, and proteinuria)
67
Q

What is the treatment for henoch-Schonlein Purpura

A

Analgesia
Supportive

Blood pressure and urinalysis should be monitored to detect progressive renal involvement.

68
Q

What are the differentials for a nonblancing rash

A

Meningococcal septicaemia
Henoch-schonlein purpura
idiopathic thrombocytopenia purpura
leukaemia
Haemolytic uraemia syndrome

69
Q

How is the diagnosis of henoch-schnlein purpura made

A

Rule out other more serious causes of a non blanching rash:
- FBC
- Blood film
- Albumin
- CRP
- Blood cultures
- Urine dipstick
- Blood pressure
- Urine protein : creatinine ratio

70
Q

What is the criteria for henoch-schonlein purpura

A

Palpable purpura

+ 1 other from:
- Diffuse abdominal pain
- arthritis or arthralgia
- IgA deposit on histology
- Proteinuria/Haematuria

71
Q

What are the complications of hence-schonlein purpura

A
  • 1/3rd have a reoccurrence within 6 months
  • a small minority of patients develop end stage renal failure
  • most get better within 4-6 weeks
72
Q

What is haemolytic uraemia syndrome

A

Occurs when there is thrombosis within small blood vessels throughout the body. Usually trigger by the shiga toxin (E. coli 0157).

Increased risk if used antibiotic or loperamide to treat gastroenteritis.

Triad:
- Haemolytic anaemia (caused by the breakdown of RBCs)
- Acute kidney injury
- Thrombocytopenia

73
Q

What is the presentation of HUS?

A

E. coli 0157 - presents as a bloody diarrhoea (gastroenteritis)

Haemolytic uraemia syndrome usually develops 5 days later:
- Reduced urine output
- Haematuria
- Abdominal pain
- Lethargy
- Hypertension
- Confusion
- Bruising

74
Q

What is the treatment

A

Medical emergency - mortality 10%

Supportive:
- Haemodialysis if AKI
- Blood transfusion if severe anaemia
- Antihypertensive medication

70-80% make a complete recovery

75
Q

What are signs of dehydration in a blood test

A

The increase in urea is proportionately higher than the rise in creatinine

(dehydration causes a release in ADH which also increases urea absorption at the collecting ducts)

76
Q

What are some of the main features between AKI and CKD

A

Ultrasound:
- Most patients with CKD will have bilateral small kidneys
- Exceptions to this are - ADPKD, early stages of diabetic nephropathy, amyloidosis, HIV associated nephropathy

Calcium will be LOW in CKD (due to lack of vitamin D) but normal in AKI

77
Q

What are signs of ADPKD

A

Hypertension
Recurrent UTIs
Flank pain
Haematuria
Palpable kidneys
Renal impairment
Renal stones

Extra renal manifestations:
Liver cysts (most common extra Rena manifestation)
Berry aneurysm (can cause SAH)
Mitral valve prolapse
Aortic dissection
Aortic root dilatation
Mitral-tricuspid incompetence

Cysts: Pancreas, spleen, thyroid, oesophagus, ovary

78
Q

What is idiopathic thrombocytopenia purpura

A

It is a spontaneous low platelet count which causes a purpuric (non-blanching) rash.

It is a type II hypersensitivity reaction. Caused by antibodies that destroy platelets.

Can be spontaneously or triggered by a viral infection.

79
Q

What is the presentation of idiopathic thrombocytopenia purpura

A
  • Usually presents in <10 years old
  • Often a history of recent viral infection
  • Onset over 24-48 hours:
    Bleeding (gums, epistaxis, menorrhagia), bruising, petichael or purpuric rash.
80
Q

What is the difference between petichae, purpirae and ecchymoses

A

ALL are non-blanching lesions

Petechiae - pin prick (1mm)

Purpura - larger (3-10mm)

Eccymoses - Large (>10mm)

81
Q

What does diarrhoea cause

A

Metabolic acidosis with hypokalaemia

82
Q

What is the prognosis of minimal change disease

A

1/3rd - have only one episode
1/3rd - have frequent relapses that stop before adulthood
1/3rd - have infrequent replaces

83
Q

Which medications are usually safe to continue in an AKI

A

Paracetamol
Aspirin
Warfarin
Statin
Aspirin (at cardio protective dose 75mg)
Clopidogrel
beta blockers

84
Q

Which drugs may have to be stopped in AKI for risk of toxicity (rather than kidney injury)

A

Metformin
Lithium
Digoxin

85
Q

Which drugs should be stopped in an AKI because they worsen renal function

A

NSAIDs (except aspirin at 75mg)
Aminoglycosides
ACE inhibitors
Angiotensin II receptor antagonists
Diuretics

86
Q

What is aport syndrome

A

An X-linked disease caused by a defect in type IV collagen

This causes an abnormal glomerular basement membrane

87
Q

What are the features of aport syndrome

A
  • Microscopic haematuria
  • Progressive renal failure
  • Bilateral sensorineural deafness
  • protrusion of the lens surface into the anterior chamber
88
Q

What is one of the common ways to tell the difference between acute tubular necrosis (renal cause) and a pre-renal cause

A

Pre- renal: A fluid challenge would cause an increase in urine

Renal: There is a poor response to fluid challenge

89
Q

What is the management of IgA nephropathy

A

Isolated haematuria, no proteinuria:
- No treatment needed
- Follow up to check renal function

Persistent proteinuria, normal or slightly reduced eGFR:
- Treatment with ACE inhibitors

Active disease (falling eGFR) or failure to respond to ACE inhibitors:
- Immunosuppression with corticosteroids

90
Q

What is the prognosis of IgA nephropathy

A

25% develop end stage renal failure

91
Q

How is proteinuria tested for in CKD

A

Urinary albumin:Creatinine ratio testing.

Positive if ACR is >3mg/mmol.

92
Q

What is an autologous transplant

A

From one donor to themselves

93
Q

What is an allogenic transplant

A

From one donor to another recipient

94
Q

What is an isograft transplantation

A

From one donor to their genetically identical recipient

95
Q

What is a xenotransplantation

A

From a donor to another species

96
Q

What are the signs of acute graft failre

A

Asymptomatic:
Picked up by a rising creatinine
Pyuria
Rising urea

97
Q

What is acute tubular necrosis

A

the most common cause of acute kidney injury.

caused by the necrosis of tubular cells due to ischaemia or nephrotoxins.

On blood tests, normal serum urea:creatinine ratio would be expected. On urine tests, sodium levels higher than 40 mmol/, low osmolality, and muddy brown casts would be expected.

98
Q

what can be used to determine whether a kidney injury is acute or chronic

A

Calcium will be LOW in chronic kidney disease

99
Q

What measures should be taken for patients at. risk of contrast induced nephrotoxicity

A
  • 0.9% sodium chloride at 1ml/kg/hr for 12 hours pre and post procedure
  • Withhold metformin for a minimum of 48 hours and until renal function has been checked (due to lactic acidosis)
100
Q

Who is at risk of contrast induced nephrotoxicity

A

known renal impairment (especially diabetic nephropathy)
age > 70 years
dehydration
cardiac failure
the use of nephrotoxic drugs such as NSAIDs

101
Q

what is the most common cause of death in patients receiving haemodialysis

A

Ischaemic hear disease

102
Q

How is cranial diabetes insipidus treated

A

Desmopressin

103
Q

How is nephrogenic diabetes insipidus treated

A

Thiazides (chlorothiazide)

104
Q

why are patients with nephrotic syndrome at an increased risk of thromboembolism

A

Loss of antithrombin III

105
Q

What bone mineral problems are seen in CKD

A

Low vitamin D (Kidney usually converts vitamin D)

High phosphate (kidney usually excretes phosphate)

106
Q

What steps should be taken in CKD to increase vitamin D

A

Increase dietary consumption

Supplements:
- Alfacalcidol
- Calcitriol

107
Q

What steps should be taken in CKD to reduce phosphate

A

First line - recommend a low phosphate diet

Supplementation:
- phosphate binders - sevelamir is now used

Severe cases - parathyroidectomy

108
Q

what medication should be given if someone has nephrotic syndrome

A

prophylactic low molecular weight heparin

Puts you at an increased VTE - due to a decrease in antithrombin III

109
Q

what is one of the signs of acute tubular necrosis

A

A poor response to fluid challenge

Exam - M - Renal Diseases (Megan) (16 decks)

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