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Medicine > Renal medicine > Flashcards

Renal medicine Flashcards

1
Q

How is an AKI measured?

A

Using serum creatinine

Rise of >25 micromol/L in 48 hrs

Rise of creatinine >50% in 7 days

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2
Q

How else can a AKI be measured?

A

Urine output <0.5ml/kg/hour for > 6 hours

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3
Q

What are some risk factors for an AKI?

A

CKD

Heart disease

Diabetes

Liver disease

Older age

Nephrotoxic medication e.g. NSAIDs / ACEi

Use of contrast medium e.g. during CTs

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4
Q

What are some causes of pre renal AKI?

A
  • Dehydration
  • Hypotension (shock)
  • HF
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5
Q

What are some renal causes of AKI?

A

- Glomerulonephritis

- Interstitial nephritis

- Acute tubular necrosis

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6
Q

What are some post renal causes of AKI?

A

Kidney stones

Masses e.g. cancer in abdo

Ureter strictures

Enlarged prostate

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7
Q

What are results for UTI dipstick?

A
  • Leucocytes/nitrites suggest infection
  • Protein / blood suggest acute nephritis
  • Glucose suggests diabetes
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8
Q

What can be used to look for obsruction of the urinary tract?

A

Ultrasound

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9
Q

What is the management of AKI?

A

Fluid rehydration with IV fluids in pre-renal

Stop nephrotoxic medications e.g. NSAIDs and ACEi

Relieve obstruction (e.g. insert catheter)

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10
Q

What are some complications from AKI?

A

Hyperkalaemia

Fluid overload

Metabolic acidosis

Uraemia leads to encephalopathy or pericarditis

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11
Q

What are some causes of CKD?

A

Diabetes

Hypertension

Age-related decline

Glomerulonephritis

Polycystic kidney disease

Medications such as NSAIDS, proton pump inhibitors and lithium

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12
Q

What are some risk factors for chronic kidney disease?

A
  • Older age
  • HTN
  • Diabetes
  • Smoking
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13
Q

What are some signs of chronic kidney disease (usually asymptomatic)?

A
  • Pruritis
  • Loss of appetite
  • Nausea
  • Vomiting
  • Oedema
  • Muscle cramps
  • Peripheral neuropathy
  • Pallor
  • HTN
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14
Q

What are some investigations for CKD?

A

eGFR from U&E checked 3 months apart (to confirm diagnosis)

Proteinuria using urine albumin:creatinine ratio (> 3 is significant

Haematuria (dipstick +1 is significant) - prompt investigation for malignancy (e.g. bladder cancer)

Renal ultrasound to investigate patients with accelerated CKD, haematuria, FH of PKD

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15
Q

What eGFR is known as end stage renal failure?

A

<15 (want > 90)

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16
Q

What are some complications of CKD?

A
  • Anaemia
  • Renal bone disease
  • CVD
  • Peripheral neuropathy
  • Dialysis related problems
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17
Q

When would referral to a specialist be considered for CKD?

A

eGFR < 30

ACR > 70 mg/mmol

Uncontrolled hypertensives despite 4 or more anithypertensives

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18
Q

Lifestyle changes to reduce risk of complications from CKD?

A
  • Excercise
  • Maintain healthy weight
  • Stop smoking
  • Offer atorvastatin 20mg for primary prevention of CVD
  • Low phosphate, sodium and potassium diet
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19
Q

How to treat complications in CKD?

A

Oral Sodium bicarbonate to treat metabolic acidosis

Iron and erythropoietin to treat anaemia

Vitamin D to treat bone failure

Dialysis in end stage renal failure

Renal transplant

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20
Q

What is the medication to treat hypertension in CKD patients? What needs to be monitored?

A

ACE inhibitors (aim to keep BP < 140/90)

Serum potassium needs monitoring as CKD and ACEi cause hyperkalaemia

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21
Q

Why does anaemia of chronic disease occur in CKD?

How is it treated?

A

Healthy kidneys produce erythropoietin (stimulates production of RBC)

Exogenous erythropoeitin (blood transfusions should be limites as sensitise immune system “allosensitisation” so transplanted organs more likely to be rejected)

Iron deficiency should be treated before offering erythropoetin

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22
Q

What is:

Osteomalacia

Osteoporosis

Osteosclerosis?

A

Osteomalacia = softening of the bones

Osteoporosis = brittle bones

Osteosclerosis = hardening

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23
Q

What are the x-ray changes in renal bone disease?

A

Spine X-ray = sclerosis of both ends of vertebra (denser white) and osteomalacia in centre of vertebra = classically known as “rugger jersey” spine after stripes found on a rugby shirt

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24
Q

What electrolyte / hormonal abnormalities occur due to CKD?

A

High serum phosphate (low excretion)

Low active vitamin D (kidney metabolises vit D to active form, needed for calcium absorption from intestines / kidneys)

Secondary hyperparathyroidism (due to low calcium) causing increased osteoclast activity

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25
Q

Why does osteomalacia occur in CKD?

A

Increased turnover of bones without adequate calcium supply

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26
Q

Why does osteosclerosis occur in CKD?

Why does osteoporosis occur in CKD?

A

Osteoblasts increase to match osteoclasts by creating new bone but it’s not mineralised due to low calcium level

Osteoporosis = can exist alongside renal bone disease due to other risk factors e.g. age / use of steroids

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27
Q

What is given to patients with CKD?

A

Active vit D (calcitriol)

Low phosphate diet

Bisphosphonates for osteoporosis

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28
Q

What are 2 acute indications for dialysis?

A

AEIOU

Acidosis (not responding to treatment)

Electrolyte abnormalities (hyperkalaemia not responding)

Intoxication (overdose of certain meds)

Oedema (pulmonary)

Uraemia symptoms e.g. seizures

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29
Q

What are the 3 options for dialysis?

A

Continuous ambulatory peritoneal dialysis

Automated peritoneal dialysis

Haemodialysis

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30
Q

What is peritoneal dialysis?

A

Dialysis which uses the peritoneal membrane as the filtration (solution with dextrose added to peritoneal cavity - the solution is then replaced as it filters into cavity)

Continuous = dialysis solution is always in peritoneum (replaced e.g. 2L replaced 4 times a day)

Automated = overnight with a machine replaceing fluid taking 8-10 hours

Involves a Tenckhoff catheter - plastic tube inserted into peritoneal cavity allowing passing of dialysis solution

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31
Q

What are some complications of peritoneal dialysis?

A

Bacterial peritonitis (glucose makes breeding ground)

Peritoneal sclerosis (thickening ans scarring of membrane)

Weight gain due to absorption of carbs in dextrose

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32
Q

How is blood accessed for haemodialysis?

A

AV fistula or tunnelled cuffed catheter

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33
Q

What is a tunnelled cuffed catheter?

A

Tube is inserted into subclavian or jugular vein with tip sitting in SVC or right atrium (two lumens - one for blood entering / leaving)

Ring called “Dacron cuff” surrounding catheter promoting healing and adhesion of tissue to cuff making catheter more permanent

Complications = infection and blood clots

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34
Q

What are the two types of AV fistulas?

A

- Radio-cephalic

- Brachio-cephalic

- Brachio-basilic

Requires 4 week to 4 month maturation

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35
Q

What are some complications of an AV fistula?

A
  • Aneurysm
  • Infection
  • Thrombosis
  • Stenosis
  • STEAL syndrome
  • High output heart failure
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36
Q

What is STEAL syndrome in AV fistula?

A

Ischaemia distal to the AV fistula

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37
Q

What is high output heart failure?

A

Caused by AV fistula increasing pre-load in heart

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38
Q

Can blood be taken from AV fistula?

A

NO

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39
Q

What are kidney donor matches based off?

A

HLA types (A/B/C) on chromosome 6

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40
Q

In a donated kidney - is the ureter donated also?

A

Yes typically using hockey stick incision

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41
Q

What is the usual lifelong immunosuppression regime for kidney donors?

A

Tacrolimus

Mycophenolate

Prednisolone

(other possibles = cyclosporine, sirolimus, azathioprine)

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42
Q

What are some complications related to a kidney transplant?

A
  • Rejection
  • Failure
  • Electrolyte imbalances
43
Q

What are some complications related to the immunosuppressants used in kidney transplant?

A
  • IHD
  • T2DM (steroids)
  • Infections
  • Non-hodgkin lymphoma
  • Skin cancers particularly squamous cell carcinoma
44
Q

What is nephritis?

A

A general term for inflammation of the kidneys (non-specific term)

45
Q

What is nephritic syndrome?

A

Group of symptoms (not diagnosis):

  • Haematuria
  • Oliguria
  • Proteinuria (moderately raised, less than 3g/24 hrs)
  • Fluid retention
46
Q

What is nephrotic syndrome?

A

- Peripheral oedema

- Proteinuria >3g/24 hours

- Serum albumin less than 25g/L

- Hypercholesterolaemia

47
Q

What is interstitial nephritis?

A

Inflammation in space between cells and tubules (interstitium)

Two types = acute interstitial nephritis and chronic tubulointerstitial nephritis

48
Q

What is glomerulosclerosis?

A

Term to describe scarring of tissue in glomerulus (not a diagnosis)

Causes = any type of glomerulonephritis / obstructive uropathy and by specific disease e.g. FSGS

49
Q

What are some types of glomerulonephritis?

A

Minimal change disease

Focal segmental glomerulosclerosis

Membranous glomerulonephritis

IgA nephropathy (AKA Berger’s disease)

Post streptococcal glomerulonephritis

Rapidly progressive glomerulonephritis

Goodpasture Syndrome

50
Q

How are most types of glomerulonephritis treated?

A

Immunosuppression (e.g. steroids)

Blood pressure control by blocking RAAS (e.g. ACEi or ARBs)

51
Q

What is the most common cause of nephrotic syndrome in children / adults?

A

Children = minimal change disease (usually idiopathic and treated with steroids)

Adults = FSGS

52
Q

What is the most common cause of primary glomerulonephritis?

A

IgA nephropathy (peak in the 20s, histology shoes IgA deposits and glomerular mesangial proliferation)

53
Q

What is the most common type of glomerulonephritis overall?

A

Membranous glomerulonephritis

54
Q

What does membranous glomerulonephritis show on histology? When does it occur?

A

IgG and complement deposits on the basement membrane

Bimodal peak in 20s and 60s (majority idiopathic or can be secondary to malignancy, rheumatoid disorders and drugs e.g. NSAIDs)

55
Q

How does post strep glomerulonephritis present? How does it progress?

A

1-3 weeks after strep infection (tonsillitis / impetigo)

Develop a nephritic syndrome

Usually full recovery

56
Q

What happens in goodpastures syndrome and how does it present?

A

Anti GBM antibodies causing nephritic syndrome and pulmonary haemorrhage (haemoptysis)

57
Q

What can cause AKI and haemoptysis?

A

Goodpasture syndrome (associated with anti-GBM antibodies)

Granulomatosis with polyangiitis (AKA Wegener’s granulomatosis - vasculitis associated with ANCA - also have wheeze, sinusitis and saddle-shaped nose)

58
Q

When does rapidly progressive GN present?

A

Often secondary to goodpastures

Histology shows “cresenteric GN”

Patients are very ill but respond to treatment

59
Q

What is the most common cause of glomerular pathology and what happens?

What is a key feature?

A

Diabetes - chronically high glucose passing through causing scarring (glomerulosclerosis)

Proteinuria

60
Q

What is the treatment of choice for diabetics with poor blood pressure?

A

ACEi (should be started in diabetics even if BP normal)

61
Q

What is interstitial nephritis?

What are the two types?

A

Inflammation of the space between cells and tubules

Acute interstitial nephritis and chronic tubulointerstitial nephritis

62
Q

How does acute interstitial nephritis present?

What is it usually caused by?

What is the management?

A

Presents = AKI, hypertension (other features of hypersentitivity = rash, fever, eosinophilia)

Hypersensitivity reation to drugs (NSAIDs or abx) or an infection

Management = steroids

63
Q

What is acute tubular necrosis?

A

Necrosis of the epithelial cells of the renal tubules

64
Q

What are some causes of ATN?

A
  • Shock
  • Sepsis
  • Dehydration
65
Q

Which toxins can cause ATN?

A

Gentamicin

NSAIDs

Radiology contrast dye

66
Q

What is found on urinalysis for ATN?

A

Muddy brown casts (pathognomonic)

67
Q

What is the management for ATN?

A
  • IV fluids
  • Stop nephrotoxic medication
  • Treat complications
68
Q

What is renal tubular acidosis?

A

Metabolic acidosis due to pathology in the tubules of the kidneys (tubules responsible for balancing hydrogen and bicarbonate ions between blood and urine)

69
Q

What is type 1 renal tubular acidosis?

A

Distal tubule is unable to excrete hydrogen ions

70
Q

What are the causes of renal tubular acidosis?

A
  • Genetic
  • SLE
  • Sjogren’s
  • Primary biliary cirrhosis
  • Hyperthyroidism
  • Sickle cell anaemia
  • Marfan’s syndrome
71
Q

How does type 1 renal tubular acidosis present?

A
  • Failure to thrive in children
  • Hyperventilation to compensate for metabolic acidosis
  • CKD
  • Bone disease (osteomalacia)
72
Q

What are the lab results for type 1 renal tubular acidosis?

A
  • Hypokalaemia
  • Metabolic acidosis
  • High urinary pH (above 6)
73
Q

What is the treament of type 1 renal tubular acidosis?

A

Oral bicarbonate

74
Q

What is the problem in type 2 renal tubular acidosis?

What is the main cause?

What are the lab results?

What is the treatment

A

Proximal tubule is unable to reabsorb bicarbonate from urine into blood

Faconi’s syndrome is main cause

Results = hypokalaemia, metabolic acidosis, high urinary pH > 6

Treat with oral bicarbonate

75
Q

What is type 2 renal tubular acidosis?

A

Combination of type 1 and type 2 (rare)

76
Q

What is type 4 renal tubular acidosis?

A

Reduced aldosterone

77
Q

What can cause type 4 renal tubular acidosis?

A

Adrenal insufficiency

ACEi

Spironolactone

SLE

Diabetes

HIV

78
Q

What are the results in type 4 renal tubular acidosis?

A

Hyperkalaemia

High Chloride

Metabolic acidosis

Low urinary pH

79
Q

What is the treatment for type 4 renal tubular acidosis?

A

Fludrocortisone

Sodium bicarbonate and treatment of the hyperkalaemia

80
Q

What is haemolytic uraemic syndrome?

A

When there is thrombosis in small blood vessels throughout the body

81
Q

What is haemolytic uraemic syndrome usually caused by?

A

Shiga toxin

82
Q

What is the classic triad seen in haemolytic urarmic syndrome?

A

Haemolytic anaemia

Acute kidney injury

Thrombocytopenia (low platelets)

83
Q

Where does the shiga toxin come from?

A

E.Coli 0157 (and shigella)

84
Q

How does haemolytic uraemic syndrome present?

A

Initial gastroenteritis with bloody diarrhoea

then:

  • Reduced urine output
  • Haematuria
  • Abdo pain
  • Lethargy
  • Confusion
  • Hypertension
  • Bruising
85
Q

What is the treatment of haemolytic uraemic syndrome?

A
  • Antihypertensives
  • Blood transfusions
  • Dialysis
86
Q

In rhabdomyolysis what do the cells release?

A
  • Myoglobin
  • Potassium
  • Phosphate
  • Creatine Kinase
87
Q

What is the most immediately dangerous breakdown product?

A

Potassium - arrhythmias

88
Q

What is released in rhabdomyolysis which is toxic to the kidneys?

A

Myoglobin

89
Q

What can cause rhabdomyolysis?

A
  • Prolonged immobility
  • Rigorous exercise

- Crush injury

- Seizures

90
Q

What are some signs of rhabdomyolysis?

A
  • Muscle aches and pains
  • Oedema
  • Fatigue
  • Confusion
  • Red/brown urine
91
Q

What are the investigations for rhabdomyolysis?

A

CK blood test

Myoglobin on dipstick (myoglobinurea)

U&Es for hyperkalaemia and AKI

ECG

92
Q

What is the treatment for rhabdomyolysis?

A

IV fluids (to encourage filtration of breakdown products)

Treat hyperkalaemia (can cause VF)

Consider IV sodium bicarbonate (makes urine more alkaline reducing toxicity of myoglobin on kidneys)

Consider IV mannitol (increases GFR to help flush breakdown products and reduces oedema)

Treat complications

93
Q

What are some causes of hyperkalaemia?

A

AKI

CKD

Rhabdomyolysis

Adrenal insufficiency

Tumour lysis syndrome

94
Q

What medications can cause hyperkalaemia?

A

Aldosterone antagonists

ACE inhibitors

Angiotensin II receptor blockers

NSAIDs

95
Q

What are the ECG changes (required if potassium > 6) in hyperkalaemia?

A
  • Tall T waves
  • Flattened P waves
  • Broad QRS complexes
96
Q

What are the main treatment options for lowering potassium?

A

Insulin and dextrose

IV calcium gluconate stabalises the heart

97
Q

What are some other options for lowering serum potassium?

A

Nebulised salbutamol (drives potassium into cells)

IV fluids (increases urine output thus loss from kidneys)

Oral calcium resonium draws potassium out of gut into stools (suitable for milder cases of hyperkalaemia)

Sodium bicarbonate (IV / oral) to drive potassium into cells as acidosis is corrected

Dialysis if severe / persistent case associated with renal failure

98
Q

What is associated with PKD?

A

Hepatic cysts

Cerebral aneurysms

99
Q

How is PKD diagnosed? What is the mode of inheritance?

A

Ultrasound / genetic testing

Dominant (more common) or recessive

100
Q

What are some complications of PKD?

A
  • Chronic loin pain
  • HTN
  • CVD
  • Gross haematuria (cyst rupture)
  • Renal stones
  • End stage renal failure
101
Q

When does autosomal recessive PKD present?

What does it result in?

A

Preganancy with oligohydraminos

Underdevelopment of lungs causing respiratory failure

Causes end stage renal failure before reaching adulthood

102
Q

What is the main treatment for PKD?

A

Tolvaptan (vasopressin receptor antagonist) slows development of cysts and progression of renal failure

103
Q

How are the complications of PKD managed?

A
  • Antihypertensives for HTN
  • Analgesia for renal colic
  • Abx for infection
  • Dialysis for end stage renal failure
  • Renal transplant
104
Q

What are some other management steps for PKD?

A

Genetic counselling

Avoid contact sports due to the risk of cyst rupture

Avoid anti-inflammatory medications and anticoagulants

Regular ultrasound to monitor

Regular bloods to monitor function

Regular blood pressure to monitor for hypertension

MR angiogram can be used to diagnose intracranial aneurysms in symptomatic patients or those with a family history

Medicine (12 decks)

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